2
Dear Readers,
You now hold the result of the dedicated work of numerous physicians from a wide range of
medical, not only surgical, departments. Each author is deeply committed to facilitating your
orientation within surgical topics and fostering a comprehensive understanding to guide you
effectively toward accurate surgical reasoning and action.
The aim of this work extends beyond merely reflecting the dynamic evolution of the field of
surgery. Above all, it seeks to impart key insights rooted in the rich surgical tradition of Brno – to
authentically highlight the historical significance of what we consider the "crown jewel" of surgery
at the Faculty of Medicine, Masaryk University.
These materials are by no means a substitute for the mandatory and recommended literature;
rather, they serve as an overview and supplement, designed primarily as a guide to assist you in
preparing for questions on the state examinations in surgery (the number of the official state exam
question can be found in brackets after the chapter title).
Finally, we kindly request your feedback – an evaluation of each chapter in terms of both
scope and content. Your input is invaluable and will greatly contribute to the improvement of this
resource. We welcome any suggestions for revisions, proposals for additions or improvements,
whether by condensing or expanding particular sections. Beyond constructive criticism, we are, of
course, equally appreciative of any questions or positive feedback.
Your feedback will be invaluable in guiding this text's further development and refinement.
Please send your thoughts to our email address: chirmuni@group.muni.cz, and we will respond to
each message.
We wish you joy in achieving grown understanding and the creative inspiration it brings as
you use this resource to enhance your surgical knowledge and skills.
The Editors,
Tomáš Ledvina, Jan Ledvina, Petr Krsička, Petra Kurečková and Teodor Horváth
VERSION UPDATED TO 7.1.2025
3
RECOMMENDED LITERATURE:
PAFKO, Pavel. Základy speciální chirurgie. 1. vyd. Praha: Galén, 2008, 385 s.
ISBN 9788072624027.
ŠNAJDAUF, Jiří a Richard ŠKÁBA. Dětská chirurgie. 1. vyd. Praha: Galén, 2005, 395 s.
ISBN 807262329X.
HOCH, Jiří a Jan LEFFLER. Speciální chirurgie: učebnice pro lékařské fakulty. 2. vyd. Praha:
Maxdorf, 2003, 224 s. ISBN 8085912066.
MARKO, Ľubomír a Peter KOTHAJ. Atlas miniinvazívnej chirurgie a chirurgickej endoskopie. 1.
vyd. Banská Bystrica: Marko, 1998, 156 s. ISBN 8096807609.
KABELKA, Miroslav. Dětská chirurgie: učebnice pro lékařské fakulty. 1. vyd. Praha: Karolinum,
1992, 320 s. ISBN 8070665610.
4
TEAM OF AUTHORS
University Hospital Brno - Bohunice:
• Surgical Clinic: MUDr. Cabanová Lucia; MUDr. Csölle Jakub; MUDr. Farkašová Martina;
MUDr. Gregora Jakub; MUDr. Grolich Tomáš, Ph.D.; MUDr. Hlavsa Jan, Ph.D.; doc.
MUDr. Horváth Teodor, CSc.; MUDr. Ivanecká Dominika; MUDr. Jaborník Martin; MUDr.
Konečná Drahomíra; MUDr. Kurečková Petra; MUDr. Mgr. Kysela Petr, Ph.D.; MUDr.
Linhartová Marcela, Ph.D.; MUDr. Marek David; MUDr. Marek Filip, Ph.D.; MUDr. Mitáš
Ladislav, Ph.D.; MUDr. Moravčík Petr; MUDr. Petríková Laura; MUDr. Poláchová
Veronika; MUDr. Pospíšil Jan; MUDr. PharmDr. Potrusil Martin; doc. MUDr. Procházka
Vladimír, Ph.D.; MUDr. Svatoň Roman; MUDr. Svoboda Martin; MUDr. Španková
Markéta; MUDr. Štefela Horváthová Erika; MUDr. Trenz Aleš; MUDr. Vaverka Vítězslav;
MUDr. Vysloužil Pavel; MUDr. Vytešníková Martina; MUDr. Zatloukal Martin
• Clinic of Radiology and Nuclear Medicine: MUDr. Andrašina Tomáš, Ph.D.; MUDr. Bárta
Radek; MUDr. Hanžlová Barbora; MUDr. Matkulčík Peter; MUDr. Rohan Tomáš
• Deparment of Gastroenterology and Internal Medicine: doc. MUDr. Dastych Milan,
CSc., MBA; doc. MUDr. Kroupa Radek, Ph.D.; MUDr. Skutil Tomáš
• Urology Clinic: doc. MUDr. Fedorko Michal, Ph.D., FEBU; MUDr. Kašík Marek; MUDr.
Moravčíková Mária; MUDr. Trinh Tuan; MUDr. Varga Gabriel, Ph.D., FEBU; MUDr.
Wasserbauer Roman
• Clinic of accident surgery: MUDr. Dobiášek Miroslav; doc. MUDr. Krtička Milan, Ph.D.;
MUDr. Rak Václav, Ph.D.; MUDr. Staňa Martin; MUDr. Študent Petr; MUDr. Tručka
Robert Clinic of burns and reconstructive surgery: MUDr. Dubovská Nikola; MUDr.
Ferkodičová Iveta; MUDr. Hokynková Alica, Ph.D.; MUDr. Holoubek Jakub; MUDr. Mager
Radomír, Ph.D.; MUDr. Matysková Dominika; doc. MUDr. Streit Libor Ph.D.; doc. MUDr.
Šín Petr, Ph.D., MBA; MUDr. Topolčaniová Lenka; MUDr. Váňa Vladimír
• Clinic of Neurosurgery: doc. MUDr. Fadrus Pavel, Ph.D.; prof. MUDr. Smrčka Martin,
Ph.D., MBA
• Orthopedic clinic: doc. MUDr. Chaloupka Richard, CSc.; MUDr. Parížek Dominik; MUDr.
Ryba Luděk, Ph.D.
• Institute of Laboratory Medicine - Bacteriology Section: MUDr. Horváthová Beáta
• Hospital Pharmacy - Clinical Pharmacy Section: PharmDr. Musilová Karolína
5
University Hospital Brno - Children's Hospital:
• Clinic of paediatric surgery, orthopedics and traumatology: MUDr. Bibrová Štěpánka,
Ph.D.; MUDr. Doušek Robert; MUDr. Husár Matej; MUDr. Ledvina Jan; MUDr. Mareček
Lukáš; MUDr. Marek Ondřej, Ph.D.; prof. MUDr. Plánka Ladislav, Ph.D.; MUDr. Starý
David, Ph.D., MUDr. Tůma Jiří, CSc.; MUDr. Turek Jakub, Ph.D.; MUDr. Urbášek Karel,
Ph.D.; MUDr. Václav Ondrej
• Clinic of paediatric anesthesiology and resuscitation: MUDr. Klabusayová Eva, DESAIC;
MUDr. Kořínková Bianka; MUDr. Šoltysová Jana; prof. MUDr. Štourač Petr, Ph.D., MBA,
FESAIC
St. Anne’s University Hospital Brno:
• 1st Dept. of Surgery: MUDr. Berková Alena, Ph.D.; MUDr. Glombová Katarína; MUDr.
Hasara Roman; MUDr. Hemmelová Beáta, Ph.D.; MUDr. Chovanec Zdeněk, Ph.D.; MUDr.
Kašpar Michal; MUDr. Konečný Jan, Ph.D.; MUDr. Křenek Adam; MUDr. Musil Tomáš;
doc. MUDr. Penka Igor, CSc.; MUDr. Peštál Adam, Ph.D.; MUDr. Prudius Vadim, Ph.D.,
MUDr. Reška Michal, Ph.D.; MUDr. Urbánek Libor; doc. MUDr. Veverková Lenka, Ph.D.;
MUDr. Vlček Petr, Ph.D.; MUDr. Vojtaník Pavol; MUDr. Vystrčilová Tamara; MUDr. Žák
Jan, Ph.D.
• 2nd Dept. of Surgery: MUDr. Novotný Tomáš, Ph.D.
• Dept. of Neurosurgery: MUDr. Barák Martin; prof. MUDr. Brichtová Eva, Ph.D.
• 1st Dept. of Orthopedic: MUDr. Jindra Jakub; MUDr. Kubíček Marian; MUDr. Liskay
Jakub; MUDr. Mahdal Michal, Ph.D.; MUDr. Martinek Lukáš; MUDr. Nachtnebl Luboš,
Ph.D.; MUDr. Pazourek Lukáš, Ph.D.; doc. MUDr. Tomáš Tomáš, Ph.D.
• Dept. of Plastic and Aesthetic Surgery: MUDr. Bayezid Can Kadir; MUDr. Berkeš Andrej;
doc. MUDr. Dvořák Zdeněk, Ph.D.; MUDr. Janeček Pavel; MUDr. Klabusay Filip, Kubát
Martin; MUDr. Menoušek Jan; MUDr. Streit Libor, Ph.D.
Center for Cardiovascular and Transplant Surgery: MUDr. Fila Petr, Ph.D.; doc. MUDr. Němec
Petr, CSc., MBA
Masaryk Memorial Cancer Institute:
• Department of Surgical Oncology: doc. MUDr. Coufal Oldřich, Ph.D.; doc. MUDr. Fait
Vuk, CSc; MUDr. Gabrielová Lucie; MUDr. Hrabec Roman, FEBU; MUDr. Krésová
Pavlína, Ph.D.; MUDr. Krsička Petr; MUDr. Rothová Veronika; doc. MUDr. Staník Michal,
Ph.D.; MUDr. Šimůnek Radim; MUDr. Zapletal Ondřej; prof. MUDr. Žaloudík Jan, CSc
6
Trauma Hospital in Brno:
• Dept. of Traumatology: MUDr. Kelbl Martin, Ph.D.; MUDr. Pavlacký Tomáš; prof. MUDr.
Veselý Radek, Ph.D.; prof. MUDr. Wendsche Peter, CSc.; MUDr. Zukal Radek
Ivančice Hospital:
• Dept. of Surgery: MUDr. Koloděj Daniel; MUDr. Ledvina Tomáš; MUDr. Majerčák Lukáš;
MUDr. Musilová Zuzana, Ph.D.
University Hospital Ostrava:
• Dept. of Imaging Methods: MUDr. Zavadil Jan
Tábor Hospital, Inc.:
• Dept. of Surgery: MUDr. Laššáková Zuzana
Academican Ladislav Dérer Hospital:
• Surgical Clinic of SZU and UNB: MUDr. Kučera Adam
External Contributors: MUDr. Melichar Jindřich, CSc.
7
SPECIAL SURGERY......................................................................................................................................................... 9
NEUROSURGERY ............................................................................................................................................................ 10
Neural tube defects (10)............................................................................................................................................ 11
Brain vascular malformation (13) ............................................................................................................................. 14
Brain ischemia (14).................................................................................................................................................... 16
Intracrania hypertension, brain edema (9) ............................................................................................................... 20
Hydrocephalus – pathophysiology, clinical signs, treatment modalities (11) ........................................................... 24
Scull fractures (15)..................................................................................................................................................... 27
Concussion, contusion and diffuse axonal injury (16) ............................................................................................... 29
Intracranial bleeding (17).......................................................................................................................................... 32
Brain abscess, subdural empyema (18)..................................................................................................................... 35
Central nervous system tumours (12) ....................................................................................................................... 38
Lumbar disc herniation, complications, failed back surgery syndrome (19) ............................................................. 42
Pepipheral nerve injury (20) ...................................................................................................................................... 46
CARDIOTHORACIC SURGERY AND TRANSPLANTATION.................................................................................................. 50
Congenital anomalies of the heart and great vessels (21) ........................................................................................ 51
Surgical treatment of heart valve diseases (22)........................................................................................................ 56
Surgical treatment for coronary artery disease (23) ................................................................................................. 61
Surgical treatment of aortic disease (24) .................................................................................................................. 65
Cardiopulmonary bypass, mechanical cardiac support (28) ..................................................................................... 70
Cardiac and great vessel injuries (25)........................................................................................................................ 74
Transplantation of heart, lung and liver (26) ............................................................................................................ 77
Organ donors, surgical technique of organ procurement (27).................................................................................. 82
UROLOGY ....................................................................................................................................................................... 86
Congenital defects of the urogenital tract (29) ......................................................................................................... 87
Male infertility and sexual dysfunction (32).............................................................................................................. 89
Vesicoureteral reflux, hydronephrosis (34)................................................................................................................ 94
Urolithiasis, renal colic (33)....................................................................................................................................... 98
Hydrocele, epididymitis, orchitis, testicular torsion (35) .........................................................................................102
Benign prostatic hyperplasia (30)............................................................................................................................105
Urogenital tumors (31)............................................................................................................................................109
Urological trauma (36)............................................................................................................................................114
ORTHOPAEDICS............................................................................................................................................................118
Congenital deformities of musculoskeletal system (2)............................................................................................119
Scoliosis and other spine deformities (3).................................................................................................................123
Orthopaedic treatment of degenerative and rheumatic diseases (8) .....................................................................125
Neuro-orthopaedic surgery (7)................................................................................................................................129
8
Aseptic bone necrosis, enthesopathy and tendinitis (5) ..........................................................................................133
Paediatric orthopaedic conditions of hip joint (6) ...................................................................................................137
Bone tumours – types, diagnostic, treatment modalities (1) ..................................................................................141
Back pain – differential diagnosis (4) ......................................................................................................................145
TRAUMATOLOGY .........................................................................................................................................................147
Neck injuries (54).....................................................................................................................................................148
Spinal cord and spine injuries, including vertebral fractures (55) ...........................................................................151
Chest injuries (52)....................................................................................................................................................155
Abdominal injuries (51) ...........................................................................................................................................158
Gastrointestinal tract injuries (53) ..........................................................................................................................164
Tendon injuries, Dupuytren's contracture (56)........................................................................................................168
Clavicle, scapula, and shoulder injuries (57)............................................................................................................172
Humerus and elbow injuries (58).............................................................................................................................176
Forearm and hand injuries (59)...............................................................................................................................180
Pelvic and hip injuries (60).......................................................................................................................................186
Femur, thigh, and knee injuries (61)........................................................................................................................190
Tibia, ankle, and foot injuries (62)...........................................................................................................................195
Non-specific bone inflammation, specific inflammations of bones and joints (63).................................................199
PLASTIC SURGERY.........................................................................................................................................................204
Congenital nevus, malignant melanoma, skin tumours (47)...................................................................................205
Skin grafts and local skin flaps (46).........................................................................................................................211
Nerve repair, grafting and transfers (50) ................................................................................................................215
Hand and finger injuries and amputations (48) ......................................................................................................220
Replantation surgery (including transport of the patient and amputated body parts) (49) ...................................223
PEDIATRIC SURGERY.....................................................................................................................................................227
Congenital diaphragmatic hernia, abdominal wall defects in children (42) ...........................................................228
Gastrointestinal congenital defects (41) .................................................................................................................231
Hirschsprung's disease (44).....................................................................................................................................236
Pyloric stenosis, intussusception (43)......................................................................................................................239
Necrotizing enterokolitis in children (40) ................................................................................................................242
Undescended testicles, phimosis, paraphimosis (38) ..............................................................................................246
Pediatric urology (45)..............................................................................................................................................250
Pediatric tumors (39)...............................................................................................................................................252
Pediatric fractures (37)............................................................................................................................................256
9
10
11
NEURAL TUBE DEFECTS (10)
Barák Martin, Brichtová Eva
Congenital nervous system defects can involve various abnormalities in the brain, spinal cord, spine,
or skull. These defects often occur in combination or may be part of complex genetic syndromes.
Their development is associated with various stages of embryonic development and can be
influenced by external and internal factors, with some having a hereditary basis. The most severe
brain development disorders often result in miscarriage or death of the child shortly after birth. Some
of these defects can be diagnosed prenatally, allowing the mother to make informed decisions
regarding the continuation of the pregnancy.
The most common congenital nervous system defects requiring neurosurgical intervention include:
- Spinal dysraphism
- Craniosynostosis
Spinal dysraphisms encompass a wide spectrum of congenital disorders characterised by
incomplete neural tube closure, from which the spinal cord later develops. They most commonly
manifest as an absence of the vertebral arch or other tissues surrounding the spinal cord. These
defects are called “spina bifida” and can lead to partial or complete neurological impairments below
the lesion level. They most frequently occur in the lumbosacral region and develop between the 14th
and 40th day of gestation. The causes of these defects are not fully understood, but risk factors
include folic acid deficiency, exposure to teratogens during pregnancy (e.g., antiepileptic drugs),
substance abuse, obesity, and maternal diabetes.
Classification of spinal dysraphism
Open Spina Bifida (Spina Bifida Aperta, Cystica): Defects in which the skin covering is very thin
or absent, allowing direct contact of the spinal cord with the external environment. This category
includes:
- Myelomeningocele: A defect of the vertebral arch with herniation of the spinal cord
and nerve roots. Neurological impairment is common, often associated with hydrocephalus
and Chiari II malformation—high risk of infection and cerebrospinal fluid hypotension.
- Meningocele: A defect of the vertebral arch with protrusion of the meninges without
neural structures. Neurological impairment is milder with a better prognosis.
Hidden Spina Bifida (Spina Bifida Occulta): Defects of the vertebral arch where the skin covering
is intact, but cutaneous stigmata are often present at the lesion site. These defects are often diagnosed
later in life. This category includes:
- Dermal Sinus (skin dimpling with communication to nervous tissue)
12
- Tethered Cord Syndrome
- Diastematomyelia (spinal cord duplication)
- Lipomyelomeningocele
Prenatal diagnostic techniques include amniocentesis, serum alpha-fetoprotein level measurement,
ultrasound examination, and prenatal MRI (contraindicated in the first trimester). Postnatal
diagnostics involve clinical examination, ultrasound through the fontanelle (to rule out associated
hydrocephalus), spinal MRI, and electrophysiological testing.
Treatment:
- Open Spina Bifida (Spina Bifida Aperta): Treatment is primarily surgical, aiming to
close the defect by reconstructing the spinal meninges and skin. In cases of extensive defects,
collaboration with a plastic surgeon is required. Surgery should be performed within 24 hours
after birth.
- Hidden Spina Bifida (Spina Bifida Occulta): Surgical intervention is indicated in
clinical symptoms or as a preventive measure. The type of surgery depends on the specific
defect, and intraoperative monitoring of spinal cord and nerve root function using
electrophysiological methods is necessary.
Craniosynostosis
The cranial vault consists of flat bones joined by cranial sutures, which prevent premature skull
fusion. These sutures usually fuse in adulthood, except for the metopic suture, which ossifies around
18 months. Craniosynostosis arises from the premature fusion of one or more cranial sutures, leading
to abnormal head shape and potential impact on brain development.
Classification according to the affected cranial suture:
- Sagittal suture – scaphocephaly, dolichocephaly (the most common type)
- Coronal suture – brachycephaly, anterior plagiocephaly
- Metopic suture – trigonocephaly
- Lambdoid suture – posterior plagiocephaly (rare)
- Multiple craniosynostosis – oxycephaly
- Syndromic craniosynostosis – associated with other congenital anomalies (e.g.,
syndactyly, polydactyly), such as Apert syndrome or Crouzon syndrome
The diagnosis is based on clinical examination (typical shape deformity, palpable bony ridge along
the course of the ossified suture, and possibly facial deformities such as hypertelorism or maxillary
hypoplasia). The anthropometric examination is primarily used to compare preoperative and
13
postoperative conditions. It is performed either with a craniometer or an optical 3D scanner.
Prematurely fused sutures are well visualised by X-ray and CT scans, which, however, expose the
patient to radiation; therefore, the necessity of such imaging must be carefully considered.
Surgical treatment focuses on correcting the skull shape and preventing any secondary damage to
brain development. The optimal timing for surgery is at 6 months of age for simple craniosynostosis,
whereas syndromic forms require later and often repeated interventions. Currently, two surgical
techniques are used: calvarial remodelling (a comprehensive procedure involving resection of the
affected part of the skull, reshaping it, and fixing it with absorbable plates) or endoscopic surgery
(endoscopically assisted resection of the affected suture) followed by treatment with a remodelling
head orthosis. The greatest risk of surgery is blood loss, which necessitates preoperative
haematological preparation, meticulous anaesthetic management, and subsequent intensive care.
14
BRAIN VASCULAR MALFORMATION (13)
Fadrus Pavel, Smrčka Martin
Cerebral vascular malformations include:
1/ Arteriovenous malformations (AVM)
2/ Cavernous haemangiomas (cavernomas)
3/ Telangiectasias and venous anomalies.
However, only the first two diagnoses are of clinical significance.
Arteriovenous Malformations (AVM)
Pathophysiology: AVMs arise due to disordered embryonic development of the brain's vascular
network. A pathological communication forms between the arterial and venous systems without
a normal capillary bed, allowing arterial blood to flow rapidly through a pathological tangle of thinwalled
vessels (referred to as the nidus of the malformation) directly into the veins. Due to the high
flow, the feeding arteries and draining veins are usually markedly dilated and tortuous, and
arterialised bright red blood is often seen in the veins. In some patients, AVMs have been shown to
develop later in life.
Clinical symptoms: AVMs typically present with haemorrhage (in 70% of cases), usually
originating from the nidus or the venous component of the malformation, causing spontaneous
intracerebral haemorrhage, less commonly subarachnoid haemorrhage (SAH). The cumulative risk
of AVM bleeding is 2-3% per year. Spontaneous intracerebral haemorrhage from an AVM, unlike
hypertensive haemorrhage, typically occurs in the brain's lobes and affects younger individuals with
normal blood pressure. Other possible presentations include hemiparesis, aphasia, or epilepsy, more
commonly seen in larger malformations due to the so-called "steal phenomenon." As most of the
blood flows through the malformation, the surrounding brain tissue is poorly perfused, leading to
cellular dysfunction at the ion channel level, manifesting as deficit-related (hemiparesis) or irritative
(epilepsy) symptoms.
Diagnosis: Diagnosis is established via CT, MRI, and mainly with cerebral panangiography. A
pathognomonic feature is a visualisation of the draining veins during the arterial phase on
angiography alongside the nidus of the malformation. Based on angiographic and MRI findings, the
Spetzler-Martin grading system (Grades I-V) assesses AVM size, venous drainage, and eloquence
of the nidus's location.
Treatment: The Spetzler-Martin grading influences treatment choice. It is essential to weigh the
risks of the natural disease course against those of the selected therapeutic approach. AVM grades I
15
and II are suitable for surgical resection. Surgery involves interrupting the feeding arteries near the
nidus and excising it. This procedure is often complex, with difficulty increasing with higher AVM
grades. For grades III-V, a combination of surgery and endovascular methods is preferable.
Endovascular therapy involves selectively catheterising feeding arteries close to the nidus and
performing embolisation, usually with glue. While eliminating an AVM solely via embolisation is
challenging, this method can significantly reduce blood flow through the malformation, facilitating
subsequent surgery. Small (up to 3 cm), deep, and eloquently located AVMs with high surgical risk
may be better treated with gamma knife radiosurgery. Obliteration of the malformation occurs after
irradiation through endothelial proliferation and thrombosis. However, in cases where the AVM has
caused significant bleeding, time is of the essence, as complete obliteration following gamma knife
therapy takes approximately two years, during which the patient remains at risk of further bleeding.
Cavernous Haemangioma (Cavernoma)
Pathophysiology: A cavernoma is a well-demarcated vascular lesion composed of thin-walled
caverns through which blood flows very slowly. The lesion is supplied by small arterioles and
drained by small venules. Due to the very slow blood flow through the cavernoma, this malformation
is not visible on cerebral angiography. Cavernomas are typically located deep within the brain
parenchyma, often near the ventricles, with a predilection for the brainstem. Cavernomas may
enlarge over time and can be multiple. Multiple cavernomas may have a genetic basis and can be
hereditary.
Clinical symptoms: Cavernomas typically present with recurrent small bleeding, which irritates the
surrounding brain tissue and leads to epileptic episodes. In some cases, cavernomas may manifest as
worsening focal neurological signs (hemiparesis, aphasia) or with bulbar symptoms and cranial nerve
involvement (when located in the brainstem).
Diagnosis: Diagnosis is primarily via MRI, where the lesion is particularly well visualised on T2weighted
images. On CT, cavernomas can often be missed.
Treatment: Options include observation, particularly if the cavernoma is located in a highly
eloquent area with high surgical risk, or if it is an incidental finding. Surgery is required for
symptomatic cavernomas. In the brainstem or other eloquent locations, surgery is warranted after
repeated haemorrhagic episodes with progressive clinical deterioration. Cavernoma excision is
relatively straightforward. The surrounding brain tissue is typically stained rust-coloured by
haemosiderin from previous haemorrhages. Stereotactic navigation is often beneficial for better
surgical orientation. Gamma knife irradiation of cavernomas is considered ineffective.
16
BRAIN ISCHEMIA (14)
Fadrus Pavel, Smrčka Martin
Ischaemic stroke is a considerable health problem, being the third most common cause of death in
developed countries and the main cause of disability. The primary risk factor for ischaemic stroke is
hypertension, followed by coronary artery disease, atrial fibrillation, diabetes mellitus,
hyperlipidaemia, obesity, and smoking.
Pathophysiology: Cerebral ischaemia occurs when cerebral blood flow (CBF) is reduced to a level
that cannot maintain adequate oxygen delivery for cellular functions. The physiological value of
CBF is 50 ml/100 g/min. When it drops to 30 ml/100 g/min, somnolence occurs. The ischaemic
threshold is crossed below 20 ml/100 g/min, leading to the "penumbra" stage, where electrical
activity in the neuron’s ceases; however, their anatomical integrity remains intact. This stage is
reversible. Acute therapeutic intervention focuses on the brain tissue within the penumbra. Necrotic
cells are irreversibly lost. CBF below 10 ml/100 g/min results in irreversible brain damage.
• Ischaemic stroke: A permanent neurological deficit resulting from inadequate perfusion in
the corresponding brain region.
• Reversible ischaemic neurological deficit (RIND): Lasts more than 24 hours but less than
one week.
• Transient ischaemic attack (TIA): A transient focal neurological deficit lasting less than 24
hours, typically a few minutes.
The most common cause of ischaemic stroke is atherosclerosis, though a cardiogenic origin is also
significant. Arteritis or fibromuscular dysplasia are rare. The causes of ischaemia include:
• Embolism: The source is often an unstable substance from a stenotic internal carotid plaque
or thrombi forming in the heart in atrial fibrillation and bacterial endocarditis.
• Thrombosis: Occurs in hypertensive patients at sites of tight stenosis in large intracranial
arteries.
• Lacunar infarcts affect small penetrating arteries in the basal ganglia.
• Haemodynamic infarcts: Result from a drop in mean arterial pressure exceeding the limits
of autoregulation. These occur with extracranial internal carotid artery occlusion and an
insufficient Circle of Willis. Global ischaemia, known as "brain hypoxia", due to prolonged
hypotension, also falls into this category.
17
Diagnosis: 1/ Imaging the extent of infarction:
• CT: The basic method for determining the extent and location of the infarct. Its advantages
include availability, the ability to differentiate haemorrhage, and speed. However, it is less
sensitive than MRI. In the acute phase, within a few hours of the event, CT changes may be
minimal or subtle, such as a loss of grey-white matter differentiation, disappearance of gyri,
and mild expansion. CT perfusion improves sensitivity in early infarct detection and can
distinguish between penumbra and necrosis. The brain tissue in the penumbra is the target of
acute therapeutic intervention. CT angiography can identify the location of major arterial
occlusions.
• MRI: Diffusion – and perfusion-weighted MRI can detect ischaemia in the acute phase. It is
more precise than CT in identifying the penumbra. Additionally, MRI can detect smallvolume
lesions, such as lacunar infarcts, which are not seen on CT. FLAIR MRI visualises
subacute and chronic ischaemic lesions.
2/ Imaging vascular pathology:
• Carotid ultrasound: The basic screening test for extracranial vessels. In the hands of an
experienced sonographer, it has high sensitivity and specificity, and it is minimally invasive.
• Angiography (DSA): Provides detailed and reproducible imaging of vascular pathology.
Unlike ultrasound, it also visualises intracranial vessels and provides the surgeon with an
excellent anatomical overview. Its disadvantages include invasiveness and associated risks,
such as stroke and inguinal haematoma.
• CT or MR angiography: CT angiography has largely replaced DSA in determining the
degree of carotid stenosis. In cases where CT angiography is contraindicated (e.g., contrast
allergy), MR angiography can be used.
• Transcranial Doppler (TCD): Visualises intracranial vessels and measures blood flow
speed and direction.
3/ Functional diagnostics:
• Perfusion CT under stress, SPECT, or TCD under stress: These tests identify patients at
risk of haemodynamic stroke. In response to reduced cerebral perfusion pressure (CPP),
patients compensate by dilating cerebral arterioles to maintain adequate cerebral blood flow
(CBF). This is the basis of CBF autoregulation.
Therapy: 1/ Surgical treatment of cerebral ischaemia Most strokes are treated conservatively.
Surgical treatment can be divided into elective and acute procedures.
a/ Elective procedures: After the resolution of stroke, transient attack, or ocular symptoms, surgery
aims to prevent the recurrence of clinical symptoms.
18
• Stenosis of the internal carotid artery
• Carotid endarterectomy: Patients who have experienced a cerebral TIA (transient
hemiparesis contralateral to the carotid lesion) or ocular TIA, known as amaurosis fugax,
where there is transient blindness in the ipsilateral eye due to embolism in the central retinal
artery, undergo evaluation of the carotid arteries. Confirmation of more than 50% stenosis of
the internal carotid artery is an indication for surgery. The procedure should be performed
within 14 days of the event to prevent the recurrence of the stroke. Asymptomatic carotid
stenosis (incidental findings on ultrasound) is rarely the cause of stroke over time with
modern medical treatment (antiplatelet therapy, statins). Therefore, the decision for surgery is
strictly individualised. Patients with stenosis over 60% are indicated for surgery if other risk
factors for stroke are present (e.g., unstable carotid plaque, atypical Circle of Willis, male
gender, etc.). Carotid surgery is preventive, aimed at preventing a threatened stroke. Patients
who are non-ambulatory with severe residual neurological deficits are unlikely to benefit
from surgery.
• 2/ Carotid artery stenting: The method involves disrupting the plaque by dilating the
stenosis with an angioplasty balloon and implanting a stent into the vessel wall. Indications
include restenosis after previous carotid surgery (a difficult and risky procedure for both the
surgeon and patient), a high bifurcation of the carotid artery that is surgically difficult to
access, and polymorbid patients for whom open surgery would pose a greater risk.
• 3/ Kinking (bending) of the carotid artery: If it causes ischaemic symptoms, it requires
resection of the redundant vessel wall and reimplantation into the common carotid artery. The
cause of kinking, like stenosis, is atherosclerosis.
• 4/ Coiling of the carotid artery: This is usually not the cause of stroke and, therefore, does
not typically require surgical intervention. Resection of the coil is justified if recurrent strokes
occur despite maximum medical therapy (dual antiplatelet therapy).
• 5/ Extra-intracranial bypass: This is indicated in patients with chronic occlusion of the
carotid artery and recurrent minor strokes or TIAs despite maximal medical therapy. The
indication for surgery is the depletion of cerebrovascular reserve capacity. In this procedure,
one of the branches of the superficial temporal artery is dissected and anastomosed end-toside
to a recipient branch of the middle cerebral artery (MCA).
b/ Acute procedures:
• Acute carotid thrombendarterectomy: This is performed relatively rarely and is most often
done in already hospitalised patients with minor stroke or TIA who experience a sudden
deterioration in clinical status due to occlusion of a previously stenotic internal carotid artery.
19
• Intravenous thrombolysis: Intravenous administration of recombinant tissue plasminogen
activator (rtPA) is recognised as the treatment of choice for severe strokes, based on positive
results from European and American studies, provided there is no haemorrhage on CT and
the time interval between stroke onset and treatment is no more than 4.5 hours. This method
is highly effective.
• Mechanical thrombectomy: In cases where stroke is caused by occlusion of a large arterial
trunk (e.g., internal carotid artery, MCA), intravenous thrombolysis may not be successful. In
such cases, prompt intervention with mechanical thrombectomy is performed. The method
involves introducing a stent retriever through the arterial system beyond the occlusion site.
The stent dilates, allowing the embolus or thrombus to be captured and then removed
retrogradely from the circulation via the femoral artery. The time window for this procedure
is up to 6 hours from stroke onset, but there is no strict time limitation in the case of basilar
artery occlusion. Stroke care and comprehensive cerebrovascular centres are concentrated in
stroke centres, where intravenous thrombolysis can also be administered. Efficient logistics
and cooperation are crucial, following the principle that "time is brain." Stroke care in the
Czech Republic is currently well organised.
• Decompressive craniectomy for expansively behaving ischaemia: This is performed when
the ischaemic volume involves the entire MCA territory and behaves expansively,
compressing the brainstem. Clinical deterioration typically occurs 48–72 hours after the
stroke, primarily due to the development of oedema. The patient becomes somnolent and
eventually falls into a coma, with signs of temporal herniation. Removing the bone flap and
dura mater reconstruction at this stage is life-saving. Decompressive craniectomy reduces
intracranial pressure and ensures adequate cerebral perfusion. The residual neurological
deficit is usually significant.
20
INTRACRANIA HYPERTENSION, BRAIN EDEMA (9)
Fadrus Pavel, Smrčka Martin
Intracranial and perfusion pressure
An adult lying down has normal intracranial pressure (ICP) values between 7-15 mmHg. In the
upright position, ICP may drop below atmospheric pressure values. In children, normal ICP is 3-7
mmHg. During sneezing, coughing or other types of Valsalva manoeuvre, ICP rises physiologically
up to values of around 60 mmHg. ICP values higher than 20 mmHg are generally accepted as
pathological (intracranial hypertension).
In 1783, Monro was the first to describe the relationship between volume and pressure inside the
cranial cavity. Later, this theory was supplemented by Kellie (1823) and Burrows (1848) and the
Monro-Kellie hypothesis was created. According to this theory, the cranial cavity is a rigid box of
fixed volume containing three incompressible compartments: brain tissue, blood, and cerebrospinal
fluid. If the volume of one of these compartments increases, another must decrease if the pressure
inside the skull is to remain stationary. This ability is used under physiological circumstances during
cardiac activity. With each heartbeat, about 15 ml of new blood flows into the brain, the increase in
volume being quickly compensated by the movement of cerebrospinal fluid and venous blood out of
the cranial cavity. The most common cause of increased intracranial pressure is an intracranial
expansion lesion (tumour, hematoma, cyst, abscess), cerebral oedema or cerebrospinal fluid passage
disorder (hydrocephalus).
The effect of volume changes inside the cranial cavity on intracranial pressure is dependent on the
state of compensatory mechanisms. It depends on how much cerebrospinal fluid can still be moved
from the cranial cavity to the spinal canal, how much the cerebral blood volume (CBV) can be
reduced in the cerebral vessels (especially the venous system) and what is the state of elasticity of the
brain tissue. After compensatory mechanisms have been exhausted, the rapidly increasing
intracranial pressure can cause displacement of the brain mass and the formation of brain
herniation. If the expansive lesion acts unilaterally, there is a midline shift of the brain mass. A
subfalcine (cingulate) herniation can occur when the brain tissue of the frontal or parietal lobe is
hidden under the free edge of the falx, referred to as the signum falcis.
This may result in ischemia in the basin of pericallosal arteries (aa. pericallosae). Herniation of the
temporal lobe into the tentorial notch (tentorial herniation, conus temporalis) is common. It was
first described by Meyer in 1920. In its frequent form, the medial part of the temporal lobe is pushed
into the tentorial notch. At the same time, the brainstem and the oculomotor nerve on the ipsilateral
side are compressed. The posterior cerebral artery is often closed by direct pressure against the edge
21
of the tentorium, and an ipsilateral infarction occurs in its basin. Clinically, the temporal cone
syndrome is manifested by severe impairment of consciousness (usually GCS 3–5), ipsilateral
mydriasis, contralateral hemiparesis and often also disorders of vital functions. In the
pathophysiological mechanism, however, the pressure of the opposite edge of the tentorium on the
brainstem and the contralateral oculomotor nerve can also be applied. This syndrome must be
understood as an expression of decompensated intracranial hypertension. A tonsillar herniation
(occipital cone) may occur during expansions in the posterior cranial fossa or as a continuation of
mass transfer from the supratentorial compartment. The cerebellar tonsils reach below the level of
the foramen magnum, obliteration of the large cistern occurs, and mainly direct pressure on the
elongated spinal cord. This mechanism can very quickly manifest as sudden respiratory arrest and
death. Tonsillar herniation can be provoked if we perform a lumbar puncture in a patient with
intracranial hypertension. For this reason, lumbar puncture is contraindicated in these patients.
In addition to intracranial pressure, Cerebral Perfusion Pressure (CPP) is also important in the
pathophysiology of neurosurgical diseases. CPP is calculated as the difference between arterial
pressure and venous pressure. In practice, it is difficult to determine the venous pressure in the
cortical veins, but it is only slightly higher than the intracranial pressure value. CPP is therefore
defined as MABP - ICP (MABP, Mean Arterial Blood Pressure). In all patients, we try to keep
CPP above 60 mmHg (if we monitor ICP and MABP). CPP is important because it relates to cerebral
blood flow (CBF). The relationship between CBF and CPP is reflected in the autoregulation curve,
when between about CPP 40-160 mmHg CBF remains unchanged, below 40 mmHg CBF decreases
dramatically.
The quantity that mediates the relationship between CBF and CPP is cerebrovascular resistance.
According to Poiseuille's law, it is inversely proportional to the fourth power of the diameter of the
vessel. Changes in cerebrovascular resistance are the essence of autoregulation of cerebral blood
flow. In practice, this means that as CPP is reduced, vasodilation occurs gradually to maintain CBF.
Vasodilatation is maximal at the lower end of the plateau phase of the autoregulation curve, when the
compensatory capacity of the vascular wall is exhausted. In many cerebral disorders (injuries,
cerebral ischemia), the autoregulatory ability of the cerebral vessels is impaired.
Clinically, intracranial hypertension may not show any symptoms at first. In the later stages,
headaches, nausea or vomiting appear, and gradually there is a disturbance of consciousness. One of
the late symptoms of intracranial hypertension is the Cushing's reflex - hypertension and
bradycardia. This is a reflex effort of the organism to maintain sufficient CPP. During an
ophthalmological examination, after a certain duration of intracranial hypertension (usually at least
22
two days), we find the prominence of the papilla of the optic nerve (congestion on the fundus), which
is indicated in diopters.
Cerebral oedema
The most important types of cerebral oedema are vasogenic and cytotoxic oedema (Klatzo, 1967).
Cerebral oedema contributes to increased intracranial pressure by increasing the volume of the brain
mass and reducing the viscoelastic properties of the parenchyma (compliance).
Vasogenic oedema appears primarily in the white matter of the brain. It is common, for example,
after an injury, but it is typical for tumours and infections. Mechanical trauma to the brain tissue,
tumour growth or infectious influences will disrupt the integrity of the blood-brain barrier. This
results in extravasation of fluid and plasma proteins into the extracellular space. These proteins
further exacerbate oedema based on an altered oncotic gradient. The cause of the disruption of the
blood-brain barrier is not only mechanical, but substances released from damaged brain tissue such
as bradykinin, arachidonic acid, histamine and free radicals are also involved in the increase in
vascular permeability. Type IV collagenase is also apparently involved in this type of oedema by
dissolving the basal lamina of the capillary bed. On CT, it appears as a hypodense area in the brain's
white matter. Corticoids are effective for this type of oedema, especially in tumours or abscesses.
Post-traumatic oedema, on the other hand, does not respond to corticoids, apparently because it is a
combination of vasogenic and cytotoxic oedema.
Cytotoxic oedema is most pronounced in the grey matter of the brain. It is sometimes called
ischemic because a disorder of cerebral blood flow causes it. This leads to deterioration of cellular
metabolism and malfunction of membrane ion channels. Together with sodium, water enters the
intracellular space, and oedema occurs. Another possibility is that cytotoxic oedema occurs
secondary to vasogenic oedema, which causes microcirculation to collapse. We demonstrate
cytotoxic oedema on CT as hypodensity in the grey and white matter of the brain.
Cerebral hyperemia (swelling) can be another cause of brain swelling. It is more common in
children but can also occur in adult patients. Pathophysiologically, it is a different entity from brain
oedema. There is an idea that the cause is direct damage to the hypothalamus and brainstem with
vasoregulatory centres. This will result in vasoparalysis with a subsequent increase in cerebral blood
flow and cerebral blood volume, to the extent that it manifests as an increase in intracranial pressure
and obstruction of venous outflow. Eventually, decompensation, a decrease in cerebral perfusion
pressure, and cerebral ischemia occur. On CT, the hyperemic brain appears as a homogeneous
isodense or hyperdense mass with lost gyrification and obliterated basal cisterns.
23
Intracranial pressure monitoring
The only way to determine intracranial pressure values is by directly measuring it using a sensor
inserted into the intracranium. Previously used epidural sensors are not very accurate; subdural
sensors have slightly better results. We record the most accurate ICP measurements using fibre-optic
intraparenchymal or intraventricular sensors. In the case of intraventricular administration, derivation
of cerebrospinal fluid is also possible. If possible, both intraparenchymal and intraventricular leads
are inserted from the Kocher point, usually in the non-dominant hemisphere. This point is located
about 3 cm lateral to the midline and 2 cm ventral to the coronary suture. This is the site that is
commonly used for ventricular puncture or ventriculostomy (Fig):
Current monitors used in the ICU for invasive monitoring already continuously record the ICP curve
in mmHg without difficulty. If the patient also has invasive BP monitoring installed (e.g. in the radial
artery), the monitor continuously calculates the mean arterial blood pressure and relates it to the ICP.
This also gives us a continuous CPP curve. Based on the knowledge of the current values of ICP and
CPP, we can carry out treatment measures.
24
HYDROCEPHALUS – PATHOPHYSIOLOGY, CLINICAL SIGNS, TREATMENT MODALITIES (11)
Barák Martin, Brichtová Eva
The term "hydrocephalus" originates from the Greek words "hydro" meaning water, and "kephale"
meaning head. It refers to an abnormal accumulation of cerebrospinal fluid (CSF) within the cranial
cavity, either in the brain's ventricles or in the external CSF spaces.
Cerebrospinal fluid is primarily produced in the lateral ventricles by the choroid plexus. It then flows
from the lateral ventricles through the foramen of Monro (intraventricular foramen) into the third
ventricle, continues via the aqueduct of Sylvius (cerebral aqueduct) to the fourth ventricle, and
passes through the foramina of Luschka (laterally) and foramen of Magendie (medially) into the
subarachnoid spaces (cerebral cisterns). From there, it is absorbed predominantly into the venous
system through the arachnoid granulations (Pacchionian granulations) into the cerebral venous
sinuses. The total amount of CSF in the ventricles and subarachnoid spaces of an adult is
approximately 150 mL and it is renewed three times a day.
Types and basic classification of hydrocephalus:
By etiology - Congenital
- Acquired
By pathogenesis
- Obstructive hydrocephalus (non-communicating) – a blockage within
the ventricular system leading to the obliteration of the normal flow of
cerebrospinal fluid (causes include congenital malformations, tumors,
hemorrhage with clot formation).
- Communicating hydrocephalus – further divided into two subtypes:
o Hyporesorptive – impaired absorption of CSF due to fibrotic
changes in the subarachnoid spaces (following subarachnoid
hemorrhage and/or inflammation, such as meningitis and
meningoencephalitis).
o Hypersecretory – increased production of CSF (e.g., tumors of the
choroid plexus).
o A specific type is termed normal pressure hydrocephalus (NPH).
The clinical manifestation of hydrocephalus is associated with symptoms of intracranial
hypertension (depends on the patient's age and the progression of hydrocephalus). Symptoms include
headache, vomiting, visual disturbances, behavioral changes, cognitive decline, psychiatric
25
symptoms, and, in severe cases, loss of consciousness. In neonates and infants with an open anterior
fontanelle, there could be head enlargement (macrocephaly), a bulging and tense fontanelle, and
prominent scalp veins. Infants can be irritable or lethargic, sleepy, and exhibit delayed psychomotor
development. Decompensated hydrocephalus may present with the “setting sun” sign (eyes deviated
downward with the lower part of the iris covered by the lower eyelid) and Parinaud's syndrome
(impaired upward gaze).
Diagnosis is based on clinical examination and imaging methods: MRI of the brain (to identify
obstruction, especially at the aqueduct of Sylvius, and dynamic sequences for CSF flow), CT of the
brain (quick and accessible but with radiation exposure), and cranial ultrasound through the anterior
fontanelle in children (non-invasive and allows repeated assessments to monitor hydrocephalus
dynamics). Fundoscopic examination to assess for papilledema is often performed.
Therapeutic management - symptomatic (active) hydrocephalus requires neurosurgical intervention
for CSF drainage. This can be either temporary (external ventricular drainage, external lumbar
drainage) or permanent (internal drainage - shunt, where the CSF is diverted to another body cavity,
most commonly the peritoneal cavity or the circulatory system).
A permanent internal drainage system (shunt) consists of three parts: a proximal catheter (inserted
into the brain ventricle, cyst, external CSF spaces, or dural sac in the lumbar region – known as a
lumboperitoneal shunt), a one-way valve (fixed or programmable), and a distal catheter (leading to
the peritoneal cavity – VP shunt or to the right atrium – ventriculoatrial (VA) shunt). Complications
of internal shunt systems are mechanical (catheter or valve obstruction due to scarring or blood clots,
or disruption of shunt continuity) or infectious (dehiscence with shunt exposure, ventriculitis, sepsis).
Endoscopic surgery, aimed at creating a new drainage pathway for CSF, is an alternative treatment
for obstructive hydrocephalus. The most common procedure is endoscopic third ventriculostomy
(ETV), which involves perforation of the floor of the third ventricle to drain into the prepontine
cistern. If a tumor obstructs CSF flow, the treatment involves surgical excision of the tumor.
A specific subtype of hydrocephalus is normal pressure hydrocephalus (NPH), a form of
communicating hydrocephalus characterized by ventricular enlargement with abnormal CSF
dynamics (intracranial pressure is normal or only episodically elevated), accompanied by a
characteristic triad of clinical symptoms. It primarily occurs in older patients (over 60 years) and its
exact pathogenesis is unknown (a risk factor includes a history of elevated intracranial pressure due
to trauma, inflammation, or hemorrhage).
26
Clinical symptoms of NPH: Hakim's triad – dementia (memory impairment and cognitive decline),
gait disturbances (short steps, wide base, instability), and urinary incontinence.
Diagnosis: based on clinical symptomatology, imaging studies (brain MRI, CT), and functional CSF
assessment:
- CSF resistance tests (LIT – increased resistance is typical for NPH).
- Lumbar puncture (normal initial pressure) and the so-called TAP test (symptomatic
improvement after the removal of 30-50 mL of CSF during lumbar puncture; an
alternative is a multi-day lumbar drainage).
A typical clinical presentation and positive functional CSF tests are indications for VP shunt
implantation.
27
SCULL FRACTURES (15)
Fadrus Pavel, Smrčka Martin
A plain skull X-ray, typically performed in two projections, can establish the diagnosis. However,
this is now rarely used in practice. The most reliable imaging for craniofacial skeletal and
intracranial structure injuries is a CT scan.
Skull fractures are divided into linear (fissures) and depressed fractures. Depressed fractures are
often comminuted (fragmented).
1/ Linear fractures do not require surgery and will heal spontaneously. However, they require
monitoring as they can lead to an epidural haematoma. This may arise from injury to the meningeal
artery by the bone edge or, more slowly, due to bleeding from the diploe.
2/ Some depressed fractures are also treated conservatively. This is usually the case when the bone
fragment depression is less than the thickness of the bone or when the depression occurs at the site of
venous sinuses, where elevation of the fragments could result in difficult-to-control bleeding.
Surgical treatment is necessary if the depression is greater than the thickness of the skull if it causes
focal neurological symptoms or epilepsy, or if it presents a cosmetically unfavourable appearance.
Surgery is also recommended for a growing fracture, which occurs in young children. In this
condition, the dura mater becomes entrapped at the fracture site, and due to the pulsation of
intracranial contents, the defect enlarges as the bone edges progressively separate — a "ping-pong
ball" fracture that normally heals spontaneously. A craniotomy is typically performed around the
depressed bone plate. The bone is then fixed with bone stitches or mini-plates. In significant,
comminuted, or infected fractures, bone fragments are removed. Large bone defects are typically
reconstructed using custom-made 3D implants fabricated from various materials, such as titanium,
Medpor, or PEEK.
Basilar Skull Fractures
Clinically, basilar skull fractures may present with raccoon eyes (periorbital haematoma),
retroauricular haematoma (Battle's sign), haemotympanum, or cerebrospinal fluid (CSF) leakage
(nasal or otorrhoea). Fractures involving a tear in the dura mater and CSF leakage carry a high risk of
meningitis and brain abscess. CT is the most reliable diagnostic tool. The presence of
pneumocephalus suggests a breach in the paranasal sinus walls and typically indicates a tear in the
dura mater.
Conservative management is appropriate for basilar skull fractures without CSF leakage or with
resolving leakage. Conservative therapy for CSF leakage includes fluid restriction, bed rest with
head elevation, avoiding activities that increase abdominal pressure, administration of Diluran (to
28
reduce CSF production), and Framycetin nasal drops to prevent infection. Healing can be supported
by inserting a spinal drain to divert a certain amount of CSF daily (typically around 100–200 ml over
24 hours).
Fractures with persistent CSF leakage require surgery. Surgery is also recommended for patients
with a history of head trauma who develop recurrent meningitis, even if the injury occurred years
ago and there is no evidence of CSF leakage. Other indications include pneumocephalus (which may
also be valvular), orbital roof fractures associated with impaired ocular movement, enophthalmos, or
exophthalmos.
The procedure involves the reconstruction of the anterior cranial fossa. A bifrontal craniotomy is
performed, with the scalp reflected from the hairline to the supraorbital margins. Only loose bone
fragments are removed from the base of the skull. If a dural tear is identified, it is sutured with nonabsorbable
material. Complications of basilar skull fractures can be severe and include recurrent CSF
leakage, meningoencephalitis, and epilepsy. Transverse fractures of the petrous bone can cause
injury to cranial nerves V, VI, VII, and VIII, while longitudinal fractures can result in conductive
hearing loss. Injuries to cranial nerves I and II can occur with fractures of the anterior cranial fossa,
and injuries to cranial nerves IX-XII can occur with condylar fractures. Less common vascular
complications include traumatic carotid-cavernous fistula, false aneurysm of the petrous or
cavernous segment of the carotid artery, and carotid artery occlusion.
29
CONCUSSION, CONTUSION AND DIFFUSE AXONAL INJURY (16)
Barák Martin, Brichtová Eva
Craniocerebral injuries (or TBI – traumatic brain injury) occur due to the impact of blunt force
or as a result of penetrating head injuries, leading to structural damage to the CNS or CNS
dysfunction. TBIs are often associated with injuries to the soft tissues of the head or skull, and
cervical spine injuries are also frequently concurrent. These injuries are of significant
epidemiological concern—TBI is the leading cause of death among children and young adults in all
types of trauma (10% of TBIs are fatal; 50% of patients are initially unconscious), and survivors
often suffer lifelong consequences.
Classification of TBIs:
By severity (most commonly assessed using neurological status/Glasgow Coma Scale GCS –
not a linear scale):
- Mild (GCS 14-15; loss of consciousness/amnesia)
- Moderate (GCS 9-13; or focal neurological deficit)
- Severe (GCS 3-8; coma)
By pathophysiology:
- Primary injury – brain injury occurring at the time of trauma; the primary cause cannot
be influenced.
- Secondary injury – indirect brain injury resulting from pathophysiological changes
caused by the acute CNS insult; clinical management aims to minimize the development
of secondary injury (e.g., brain edema, hypoxia of brain tissue)
By extent of brain damage:
- Focal injuries – brain contusion, intracranial hemorrhage (intracerebral hematoma,
traumatic subarachnoid hemorrhage, subdural hemorrhage, epidural hemorrhage)
- Diffuse injuries – concussion, diffuse axonal injury (DAI)
Typical causes of TBI include falls (including those during intoxication), car accidents, and acts of
violence. The specific injuries depend on the force exerted and the mechanism of trauma. Risk
factors include older age, use of anticoagulant/antiplatelet medications, internal comorbidities, and
intoxication.
Clinical presentation depends on the type and severity of the TBI. Classic symptoms may include
headaches, nausea and vomiting, focal neurological symptoms (e.g., limb paresis, speech
disturbances), seizures (with the risk of developing late epilepsy), and, in the most severe cases,
impaired consciousness.
30
Common complications include bleeding, which typically manifests within 24 hours of the initial
injury, and the risk of developing brain oedema with subsequent intracranial hypertension syndrome,
epilepsy, hydrocephalus, and infectious complications.
Diagnosis relies heavily on a history of the injury and includes a neurological examination to stratify
the severity of the condition and topically localize the injury. Imaging techniques—particularly CT
(trauma protocol)—play a crucial role. CT is the method of choice in acute conditions and can
clearly identify the most common types of brain injuries that require urgent neurosurgical
intervention. In cases of TBI, CT of the cervical spine is always necessary (5% of head traumas are
associated with severe cervical spine injuries); otherwise, the patient must be managed as if they
have a cervical spine injury (semi-rigid cervical collar).
Brain concussion (commotio cerebri) represents a reversible functional disorder characterized by a
brief loss of consciousness without evident traumatic anatomical changes (negative CT findings).
Loss of consciousness may last only a few seconds and rarely exceeds 30 minutes. Clinical signs
include headaches and memory impairment (typically retrograde amnesia—patients do not remember
the injury), as well as nausea/vomiting. Some patients exhibit late sequelae of concussion (so-called
post-concussion syndrome), with headaches, concentration difficulties, and sleep disturbances
persisting for several months post-trauma. Diagnosis is based on injury history and normal
neurological findings, with the need to exclude other traumas on brain CT that would require
neurosurgical intervention. Treatment is fully conservative; patients are usually hospitalized for 24
hours for observation and analgesic therapy.
Brain contusion due to bruising of the brain tissue, ranging from minor lesions to extensive,
multiple contusions. It typically occurs on the convexity of the brain, most commonly in the
temporal and frontal lobes (coup—where the brain impacts the hard skull during sudden movement),
and contusions may also develop on the opposite side of the impact site (contre-coup). Less
commonly, contusions result from depressed skull fractures. Clinical symptoms depend on injury
severity—minor contusions may be entirely asymptomatic. Typical manifestations include focal
neurological symptoms, such as motor and speech disorders (depending on the affected eloquent
area), headaches, behavioral disturbances, and impaired consciousness. Structural damage to the
cerebral cortex is also a risk factor for seizure development. Larger contusions can lead to brain
edema and subsequent intracranial hypertension. Diagnosis is based on CT findings—typically
showing signs of bleeding within brain tissue on the convexity (hyperdensity on brain CT); however,
contusion lesions may not be visible on initial examination and can develop over several hours,
warranting additional CT scan within 24 hours. Anamnesis of the injury and neurological symptoms
corresponding to the affected brain region are also crucial. Treatment is predominantly conservative,
31
requiring clinical monitoring and prevention of secondary damage (especially blood pressure
correction; in the case of anticoagulant or antiplatelet medication use, reversing their effects).
Surgical intervention is indicated in specific cases of developing intracranial hypertension from
expansively behaving contusions —decompressive craniectomy is indicated in severe TBIs
(supratentorial) with signs of intracranial hypertension unresponsive to antiedema therapy. In cases
of expansive contusion in the posterior cranial fossa (risk of brainstem compression), decompression
of the posterior cranial fossa with surgical treatment of the hemorrhage/contusion is required.
Diffuse Axonal Injury (DAI) is characterized by multiple axonal damages resulting from trauma.
DAI typically follows high-energy trauma, involving shear forces and mechanical damage to brain
pathways. The clinical picture is marked by post-traumatic unconsciousness, which may persist for
months, depending on the injury's severity. Neurological findings also depend on specific neural
pathway damage (focal lesions, decortication or decerebration symptoms, and brainstem
involvement). Consciousness impairment (vegetative coma) or severe neurological deficits can
persist long-term, representing a highly unfavorable prognosis. DAI diagnosis is based on trauma
history and clinical status (persistent unconsciousness after TBI with exclusion of other causes). DAI
patients may present minimal or negative findings on initial brain CT (necessary to exclude other
urgent conditions requiring surgical intervention, such as SDH/EDH), which do not explain the
neurological deficit. Specific DAI changes can be observed only on brain MRI (typically in the
corpus callosum and basal ganglia). The initial therapeutic goal is to ensure vital function stability
(mechanical ventilation and circulatory support) and overall clinical stabilization. Due to the risk of
developing intracranial hypertension, intracranial pressure monitoring and appropriate treatment of
intracranial hypertension are recommended. Patients often require subsequent intensive care with an
uncertain neurological outcome.
32
INTRACRANIAL BLEEDING (17)
Barák Martin, Brichtová Eva
Intracranial hemorrhage can be classified by etiology into traumatic and non-traumatic
(spontaneous). Based on location, intracranial hemorrhage is divided into extracerebral (EDH,
SDH, SAH) and intracerebral (ICH, IVH). The most common cause of extracerebral hemorrhage is
trauma.
Epidural Hematoma (EDH) – An epidural hematoma occurs due to bleeding into the space
between the dura mater and the skull. Under normal conditions, this space does not exist because the
dura mater firmly adheres to the skull. Epidural hematomas occur in approximately 1–6% of all head
injuries and are most commonly caused by bleeding from the meningeal artery, which is damaged by
a skull fracture. EDH can also result from bleeding from a damaged skull or an injury to a venous
sinus. The most typical localization is the temporal region, where the source of bleeding is usually
the middle meningeal artery, or its branches damaged by a fracture. However, a skull fracture is not a
necessary condition for the development of EDH (up to 40% of cases have no fracture). The clinical
presentation may resemble that of acute subdural hematoma (aSDH), but EDH often includes a socalled
lucid interval (seen in 10–27% of patients). This interval is characterized by a brief loss of
consciousness immediately following the injury, followed by a period of full consciousness, and then
a subsequent loss of consciousness due to EDH. In the temporal region, EDH is most dangerous
because even minor pressure on the temporal lobe can lead to its displacement and compression of
the brainstem, resulting in severe neurological symptoms. If symptomatic EDH is not promptly and
adequately treated, it usually results in death. Treatment involves evacuation of the hematoma via
craniotomy, cessation of bleeding, and suturing the dura to the bone edges to prevent recurrence.
Acute Subdural Hemorrhage (aSDH) – This type of hemorrhage occurs between the dura mater
and arachnoid. It is usually caused by bleeding from a bridging vein or from a cerebral contusion. On
CT imaging, it appears as a hyperdense crescent of blood that follows the brain surface. Smaller
aSDH may be asymptomatic, while larger ones typically lead to impaired consciousness,
contralateral hemiparesis, and ipsilateral pupillary dilation (mydriasis). The development of
ipsilateral mydriasis is a poor prognostic sign, indicating brain shift and compression of the third
cranial nerve (oculomotor nerve). Brain compression caused by aSDH can also trigger epileptic
seizures. Symptomatic hematomas must be surgically removed via craniotomy and the source of
bleeding surgically managed, sometimes requiring decompressive craniectomy. Smaller aSDH may
resolve spontaneously or gradually evolve into chronic subdural hematomas.
33
Chronic Subdural Hematoma (chSDH) – A chronic subdural hematoma is defined as a hematoma
persisting for more than three weeks after injury. In some cases, trauma may not be evident in the
patient's history. This type of hematoma is relatively common in neurosurgical settings and
frequently occurs in patients with brain atrophy, where even minor head trauma can cause bleeding,
usually from a bridging vein. This condition mainly affects elderly individuals, alcoholics, and
patients with coagulopathies. Chronic coughing, such as in asthmatics, can also contribute to the
development of chSDH. These hematomas do not undergo spontaneous resorption; instead, they
gradually become encapsulated, with the capsule being richly vascularized due to neovascularization.
This process can lead to gradual hematoma enlargement due to recurrent minor bleeding and osmotic
activity drawing fluid from the surroundings. Clinical symptoms can be subtle for a long time and
are often mistaken for dementia, presenting typically as progressive headaches, psychological
changes, gait disturbances, and falls, leading to decompensation of chSDH and ultimately
neurological deficits that prompt diagnosis. On CT, chSDH appears as an iso- or hypodense crescentshaped
collection around the hemisphere, often with components of various ages and signs of recent
bleeding. Membranes and septations within the hematoma, visible on CT, may complicate treatment.
Despite subtle clinical signs, chSDH is a severe condition that, without treatment, can be fatal.
Decompensation, such as further bleeding into the hematoma, can quickly worsen the clinical
picture. Treatment involves evacuating the hematoma through burr holes, washing the subdural
space, and inserting drainage, which remains in the subdural space for 24–72 hours. In cases of
septated hematomas, repeat surgery or more radical craniotomy may be required.
Traumatic Subarachnoid Hemorrhage (traumSAH) – Trauma can also lead to traumatic
subarachnoid hemorrhage, involving bleeding between the pia mater and arachnoid. It is crucial to
exclude other causes of subarachnoid hemorrhage, such as ruptured cerebral aneurysms, especially
when trauma history is unclear or when SAH is located in the cisterns or Sylvian fissure, as purely
traumatic SAH is usually found on the convexity. It should be recognized that falls or trauma might
occur as a result of aneurysm rupture or other causes. Traumatic SAH is treated conservatively.
Intraventricular Hemorrhage (IVH) – Intraventricular hemorrhage involves bleeding into the
cerebral ventricles. It can be caused by head trauma or, in the case of spontaneous IVH, by rupture of
an intracerebral hemorrhage into the ventricles. Massive hemorrhage may lead to obstructive
hydrocephalus, necessitating the insertion of a temporary external ventricular drain to divert
cerebrospinal fluid.
Intracerebral Hemorrhage (ICH) – Intracerebral hemorrhage accounts for 15-30% of all
cerebrovascular accidents (the remainder are ischemic). ICH refers to bleeding directly into brain
34
parenchyma and has significantly higher mortality than ischemic strokes. ICH can be classified
etiologically into: a) primary (predominantly due to uncontrolled arterial hypertension) and b)
secondary (due to vascular malformations – aneurysms, arteriovenous malformations, CNS tumors,
coagulopathies including iatrogenic from anticoagulants, or complications of neurosurgical
procedures). Primary (spontaneous) ICH typically occurs in the basal ganglia, thalamus, or brainstem
and is associated with significant neurological deficits, including impaired consciousness. Clinically,
hemorrhagic stroke is challenging to distinguish from ischemic stroke, though ICH usually shows
clinical progression over minutes to hours, with headache and altered consciousness (in contrast to
ischemic stroke, which typically has sudden onset with maximum initial deficit). Diagnosis relies on
non-contrast CT of the brain showing hyperdensity in the parenchyma; CT angiography may be
required if a vascular cause is suspected, particularly in younger patients without hypertension
history. Primary ICH is usually managed conservatively, with ICU admission, stabilization of vital
functions, prevention of secondary brain injury, and control of hypertension. Anticoagulant reversal
is necessary if applicable. Surgical intervention is indicated for cerebellar hemorrhages with
brainstem compression or atypical superficial hematomas to relieve pressure on surrounding brain
tissue.
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BRAIN ABSCESS, SUBDURAL EMPYEMA (18)
Barák Martin, Brichtová Eva
Inflammatory diseases of the brain and spine constitute a group of severe infectious conditions that
require prompt diagnosis and treatment due to their potentially fatal course. The most common
inflammatory diseases of the brain include meningitis, brain abscess, cranial osteomyelitis, and
subdural empyema.
Central nervous system (CNS) infections can be categorized based on their cause. In neurosurgery,
the most frequently encountered infections are a) Spontaneous infections (typically brain abscess),
b) Postoperative complications (commonly meningitis), c) Post-traumatic complications
(typically meningitis). These mechanisms are associated with different infection sources: a)
Continuous spread of infection (ENT area - otogenic origin such as otitis media, paranasal sinuses,
or dental complications), b) Infections caused by direct trauma (presence of cerebrospinal fluid
leak or open injuries), and c) Hematogenous infections (chronic inflammation such as urinary tract
infection or endocarditis).
Clinical manifestations of CNS infections include general symptoms of infectious disease (fever,
malaise and fatigue). Depending on the infection site, focal neurological symptoms may develop,
such as hemiparesis, speech disturbances, epileptic seizures, or meningeal signs (positive upper and
lower meningeal signs, such as neck stiffness, Lasegue's, Kernig's, and Brudzinski's signs).
Progressive disease can lead to consciousness impairment, signs of intracranial hypertension,
cerebral edema, and death. The proximity of anatomical structures increases the risk of irreversible
neurological deficits, intracranial vessel thrombosis, and systemic infectious complications, such as
sepsis.
Diagnosis is based on a combination of clinical, paraclinical, and imaging methods. A
comprehensive neurological examination is essential, with imaging techniques such as CT and MRI
(including contrast enhancement) playing a central role in the initial localization of lesions and their
monitoring over time. Laboratory findings typically include elevated inflammatory markers
(leukocytosis, C-reactive protein) and an inflammatory profile in lumbar puncture (presence of
polymorphonuclear cells, elevated lactate, decreased glucose levels). In many cases, biopsy sampling
for microbiological examination is necessary to confirm the diagnosis, allowing targeted antibiotic
therapy.
36
Treatment strategies differ among the specific nosological units and usually involve a combination
of neurosurgical intervention (drainage of the abscess via craniotomy or stereotactic puncture;
drainage of subdural empyema from craniotomy; surgical revision in postoperative inflammatory
complications; extraction of osteomyelitic bone plates; duraplasty in traumatic cerebrospinal fluid
leaks) followed by antibiotic therapy (empirically using Ceftriaxone + Metronidazole, with potential
adjustments based on microbiological results). Epilepsy prophylaxis with antiepileptic drugs (e.g.,
Levetiracetam) is also recommended.
Brain Abscess represents a purulent focal inflammation of brain tissue with direct tissue destruction.
The clinical picture depends on the anatomical location and size of the abscess. A distinguishing
feature of brain abscesses is the absence of meningeal signs, such as meningeal irritation. Treatment
consists of surgical drainage of the abscess (stereotactic puncture, evacuation, and drainage)
followed by antibiotic therapy. There is a significant risk of irreversible neurological deficits and
septic complications.
Subdural Empyema is a rare infection characterized by the accumulation of pus in the subdural
space. Due to the absence of anatomical barriers in the subdural space, there is a high risk of rapid
progression. The clinical presentation reflects this risk, often progressing quickly to septic shock.
The primary goal of treatment is emergent surgical evacuation and drainage of the subdural space,
followed by antibiotic therapy.
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38
CENTRAL NERVOUS SYSTEM TUMOURS (12)
Barák Martin, Brichtová Eva
Central nervous system (CNS) tumours include those arising from brain tissue (intra-axial tumours)
and those outside the brain parenchyma (extra-axial tumours, e.g., meningeal tumours). These
tumours are classified based on their origin into a) primary CNS tumours and b) secondary CNS
tumours (metastases) and by their biological behaviour into a) benign tumours and b) malignant
tumours. A unique aspect of neuro-oncology is that even biologically benign tumours can clinically
present similarly to malignant tumours, exhibiting significant clinical symptoms and progressive
clinical deterioration over time (limited intracranial space).
CNS tumours constitute approximately 3% of all adult tumours. In adults, secondary tumours are
more common, with CNS metastases observed in 15-30% of patients in the late stages of other
systemic cancers. In the pediatric population, CNS tumours are the most common solid
malignancy (20% of all tumours) and the second most common cancer after hematologic
malignancies. Unlike adults, CNS tumours in children are typically infratentorial (in the posterior
fossa below the tentorium cerebelli), compared to the predominantly supratentorial location seen in
adults.
The clinical presentation of CNS tumours is influenced by the pathophysiological principles of an
expanding process within the intracranial space. Due to the constraints of the skull, the tumour's
growth leads to increased intracranial pressure, resulting in symptoms of intracranial hypertension
such as headache, nausea and vomiting, and altered consciousness. Local destruction or compression
of surrounding brain tissue by the tumour or infiltration results in specific focal neurological
symptoms corresponding to the location of eloquent brain areas.
MRI with contrast is the gold standard for diagnosis, while CT with contrast may be useful in acute
situations. Histological examination, incorporating both histopathological and molecular-genetic
analyses, is crucial for diagnosis and therapeutic planning, as it allows for tumour classification into
specific groups and subtypes.
Treatment decisions are based on imaging findings, tumor location (resectable vs. non-resectable
due to anatomical constraints), patient history (e.g., prior oncological disease suggesting metastasis),
and overall patient status. Surgical resection is generally the cornerstone of treatment for most
tumours, aiming for disease remission. In specific cases, an initial diagnostic biopsy may be
performed to determine the tumour’s nature. Comprehensive oncological care, including CHT and
RT, is provided in the Czech Republic in specialized comprehensive cancer centres.
39
Pediatric CNS Tumors
Pilocytic Astrocytoma – This is the most common benign CNS tumour in children. It typically
grows slowly and is commonly located in the cerebellum. Clinical symptoms arise from its
anatomical location, including cerebellar symptoms, hydrocephalus, signs of intracranial
hypertension, behavioural disturbances, and failure to thrive in children. The primary goal is radical
surgical resection, usually without the need for subsequent oncological treatment. The prognosis for
patients is generally favourable.
Pediatric Diffuse Gliomas – This heterogeneous group of tumours varies in biological behaviour.
The more aggressive subtypes are often unfavourably located in the brainstem, making them largely
unresectable from a surgical perspective. Despite CHRT, the prognosis remains extremely poor.
Ependymal tumours (Ependymomas) are typically benign and occur in the region of the fourth
ventricle. Symptoms arise from this typical location, including obstructive hydrocephalus, signs of
intracranial hypertension, and cerebellar symptoms. The goal is maximal radical surgical resection,
with subsequent oncological therapy considered based on histological findings.
Embryonal tumours include the most common malignant tumour in children - medulloblastoma.
Medulloblastoma is found in the vermis on the roof of the fourth ventricle. It is an aggressive tumour
with often poor prognosis, especially in cases of large tumours, late diagnosis, and in younger
patients. There is also a risk of secondary metastasis spreading along the entire craniospinal axis (socalled
drop metastases). The clinical course is determined by its anatomical location, manifesting as
obstructive hydrocephalus, intracranial hypertension, cerebellar symptoms (ataxia), and in younger
children, behavioural changes, irritability, lethargy, and macrocephaly. In the case of metastatic
spinal involvement, paraparesis or paraplegia may develop (requires MRI of the entire craniospinal
axis). The therapeutic aim is maximal radical resection; however, resection must be limited in cases
of brainstem invasion to prevent neurological damage. Treatment also includes comprehensive
oncological management, including CHRT, and targeted therapy depending on specific molecular
subtypes.
Benign CNS Tumors in adults
Meningiomas are the most common benign brain tumours in adults. These are slow-growing, wellcircumscribed
tumours that can occur anywhere along the meninges (originating from arachnoid
cells). Their incidence increases with age and is more common in women; they are also more
frequently seen in patients with a history of head and neck radiotherapy. Clinically, they are usually
asymptomatic (an incidental finding on MRI), but further progression may lead to headaches, focal
neurological symptoms (depending on the tumour's location), and epileptic seizures. Diagnosis is
based on brain MRI, where a direct connection of the tumour to the dura mater is observed.
40
Symptomatic meningiomas often require surgical resection aimed at tumour removal, including
treatment of the adjacent dura mater with the tumour origin.
Vestibular schwannoma is a benign tumour originating from Schwann cells of the
vestibulocochlear nerve located in the cerebellopontine angle. Its incidence increases with age. It
may occur sporadically, while bilateral vestibular schwannomas are associated with genetic
syndromes (neurofibromatosis). Clinical symptoms result from damage to anatomical structures in
the cerebellopontine angle—primarily gradually progressive hearing loss and vertigo (both related to
the CN VIII), CN VII palsy, and, less frequently, CN V impairment. Large tumours can compress the
brainstem, cerebellum, or cerebrospinal fluid pathways, posing a risk of hydrocephalus development.
Diagnosis is based on MRI, and audiometry is necessary to assess hearing impairment objectively.
The primary treatment for larger tumours is surgical resection, with intraoperative monitoring of
cranial nerve VII and VIII functions to prevent neurological damage. Stereotactic radiosurgery is an
alternative for smaller tumours.
A pituitary adenoma is a benign tumour located in the sella turcica. These tumours are classified as
microadenomas (less than 1 cm) or macroadenomas (greater than 1 cm) and are further categorized
based on hormonal activity (most commonly prolactin, ACTH, GH) or inactivity. Clinical symptoms
arise from local effects—compression of the optic chiasm (visual disturbances), damage to cranial
nerves, headaches, and hormonal manifestations (hyperprolactinemia, acromegaly,
panhypopituitarism). Diagnostic evaluation includes imaging studies, endocrine assessment, and
visual field testing. Therapeutic management is multimodal, combining pharmacological (dopamine
agonists for prolactinomas) and neurosurgical approaches. Progressive or symptomatic tumours are
indicated for neurosurgical intervention, which can be approached either classically via craniotomy
or via endoscopic transsphenoidal access. Patients require endocrinological follow-up with potential
initiation of hormone replacement therapy as needed.
Malignant tumours in adults and secondary tumours
Adult Gliomas (glioblastoma, astrocytoma, oligodendroglioma) comprise a heterogeneous group of
the most common primary CNS tumours in adults. They are generally characterized by diffusely
infiltrating growth into the surrounding brain tissue.
Glioblastoma is the most common malignant primary CNS tumour, accounting for 50% of
malignant primary tumours in adults. Its incidence increases with age. Glioblastoma is known for its
rapid progression and extensive infiltration of surrounding brain tissue. Clinically, it presents with
headaches, focal neurological deficits, signs of intracranial hypertension, epilepsy, behavioural
changes, and impaired consciousness. Diagnosis is based on MRI with contrast. The goal is maximal
radical surgical resection followed by CHRT. The extent of resection may be limited by the
41
proximity to critical anatomical structures and the risk of neurological deficits. If the tumour is
inoperable, a diagnostic biopsy is performed. The prognosis remains extremely poor despite
comprehensive treatment.
Astrocytomas include subtypes with varying biological behaviour. Unlike glioblastomas,
astrocytomas tend to occur in younger patients, typically under the age of 40, and can gradually
progress to more aggressive variants. Clinical presentation, diagnosis and treatment are like those for
glioblastoma. The prognosis is more favourable compared to glioblastoma.
Oligodendroglioma is a specific subtype arising from oligodendrocytes. It is a slowly growing
tumour with a risk of progression to more aggressive forms. Typical clinical manifestations include
epilepsy and focal neurological symptoms. The aim of surgical therapy is maximal radical resection
followed by oncological treatment.
CNS Lymphomas are a group of haematological malignancies occurring within CNS tissue. Clinical
symptoms depend on the tumour's location, often presenting with seizures. The goal of surgical
intervention is biopsy confirmation, followed by comprehensive oncological treatment, including
CHRT.
Metastases (secondary CNS tumours) are the most common type of brain tumours, accounting for
approximately 50% of all brain tumours. There are often multiple cases at the time of diagnosis.
Incidence increases with age and with improved diagnostics (MRI) and oncological care. Metastatic
spread typically occurs haematogenously to the brain parenchyma or meninges, less frequently via
local extension or cerebrospinal fluid pathways. Lung carcinoma is the most common primary site,
followed by breast and prostate cancer, melanoma, renal cell carcinoma, and colorectal cancer.
Clinical symptoms progress gradually, including headaches, focal neurological deficits, and signs of
intracranial hypertension. MRI is crucial in the diagnostic process, as CT lacks sufficient resolution
to assess metastatic involvement. The therapeutic management depends on the patient’s overall
condition, primary cancer type, and the extent of metastatic spread. Surgical intervention is limited to
solitary metastases accessible through a single craniotomy or in cases of multiple metastases where
one lesion significantly impacts patient survival (e.g., brainstem compression). In the absence of a
known primary malignancy, solitary lesions may be biopsied to establish the primary cancer
diagnosis.
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LUMBAR DISC HERNIATION, COMPLICATIONS, FAILED BACK SURGERY SYNDROME (19)
Fadrus Pavel, Smrčka Martin
Pathophysiology: From the second decade of life, the vascular supply to the intervertebral disc
becomes impaired, first affecting the nucleus pulposus and later the annulus fibrosus. Gradually,
degeneration of the annulus fibrosus occurs to the point where a portion of the disc may herniate into
the spinal canal. If herniation does not occur, the height of the disc continues to decrease. Eventually,
osteochondrosis, uncovertebral neoarthrosis, osteophyte formation, and spondyloarthrosis develop.
These processes ultimately lead to the compression of neural structures within the spinal canal. The
neurosurgeon's role in treating these patients is primarily to relieve the compression of the neural
structures (decompression).
A/ Degenerative Disease of the Cervical Spine
Disc herniations in the cervical spine most commonly occur at the C5/6 and C6/7 levels. Once the
neural structures in the cervical spine are compressed, a radicular (nerve root) syndrome or
myelopathy develops. These syndromes may occur either in isolation or concurrently.
Radicular syndrome is characterised by irritation—pain radiating into a specific dermatome of the
upper limb (cervicobrachial syndrome). It may also present with motor and sensory deficits
(weakness, atrophy, reduced reflexes in certain muscles, sensory disturbances). Radicular syndrome
develops particularly when the compression is located laterally within the spinal canal.
Myelopathy arises from medial spinal cord compression. The greatest pressure is exerted on the
pyramidal tracts, leading to spasticity and pyramidal irritative signs. In advanced myelopathy, there
is progressive gait disturbance.
Diagnosis: Plain X-rays may reveal osteophytes on the vertebral bodies and, in some cases,
narrowing of the intervertebral foramina. CT scans are even more sensitive to these changes and can
demonstrate the relationship between osteoproductive degenerative changes in the cervical spine and
the contents of the spinal canal. MRI is essential for diagnosing degenerative disease of the cervical
spine. It can reveal disc herniations, the degree of spinal canal stenosis, and changes within the spinal
cord (e.g., hyperintense areas on T2-weighted images), indicative of advanced myelopathy. If there is
any doubt, electrophysiological testing (e.g., electromyography, evoked potentials) is recommended.
Treatment: Surgery is usually performed through an anterior approach. This allows for
decompression of both the dural sac and exiting nerve roots. A cage made of polymer or metal filled
with osteoconductive material is inserted into the space of the removed disc, and the segment can be
stabilised with a metal plate. The goal of the surgery is to fuse two adjacent vertebrae. Some centres
43
insert mobile artificial disc replacements. With appropriate indications, surgery is successful in 90%
of patients.
In certain cases, surgery is indicated through a posterior approach, especially for lateral disc
herniations causing monoradicular involvement of a specific nerve root.
B/ Degenerative Disease of the Lumbosacral Spine
The disease typically begins with pain in the lower lumbar spine, commonly called lumbago. When
the integrity of the annulus fibrosus is disrupted, part of the disc herniates into the spinal canal. The
disc herniation may remain beneath the intact posterior longitudinal ligament (subligamentous
herniation), or a disc fragment may migrate into the spinal canal (epidural sequestration). Disc
herniations most commonly occur at the L5/S1 (50%) and L4/5 (45%) levels, with a smaller
percentage at L3/4 and even fewer at L2/3.
Clinically, the lumboischiadic syndrome (LIS) is characterised by pain radiating into the
corresponding dermatome (irritative symptoms), sensory disturbances in that dermatome, reduced or
absent reflexes, and paresis (loss of function symptoms).
Failed Back Surgery Syndrome (FBSS) refers to persistent back or leg pain in patients who have
undergone surgery for degenerative spinal disease. One serious complication is cauda equina
syndrome, which presents with perianogenital hypoaesthesia or anaesthesia and sphincter
disturbances, manifesting acutely as urinary retention. This syndrome requires immediate surgery.
Diagnosis of disc herniation is primarily based on MRI, which provides a detailed view of the entire
lumbosacral spine. MRI reveals not only disc herniations but also lumbar stenosis or various
instabilities of the lumbosacral spine. It is particularly useful in recurrent disc herniations, as it can
distinguish scar tissue from a true recurrent herniation (especially after contrast administration).
Treatment of lumboischiadic syndrome is initially conservative, which is effective in up to 70% of
patients.
If there is no significant improvement after several weeks of conservative treatment, surgery is
indicated. Most disc herniations are operated on through a transligamentous approach (through the
yellow ligament). Surgery usually involves a single level, as a herniation of a single disc causes 95%
of symptoms. In recent years, endoscopic techniques have been increasingly used, whereby an
endoscope is introduced transcutaneously to the herniated disc and the herniated portion is removed
through the working channel of the endoscope. This avoids the need for extensive dissection of
paravertebral muscles and the removal of larger portions of the lamina and yellow ligament. Two
main approaches are used—transforaminal and translaminar, which mirror the traditional
microdiscectomy approach.
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In strictly indicated cases, minimally invasive, often CT-guided, percutaneous methods may be used
to treat lumboischiadic syndrome. These methods are reserved for patients with disc protrusion,
causing leg pain primarily in the seated position when disc pressure is highest. The condition
requires an intact, non-fragmented disc and no annulus fibrosus rupture. This is confirmed by
discography (injecting contrast directly into the disc under CT guidance), where no contrast should
escape outside the disc. These methods involve the percutaneous introduction of a needle or
electrode into the disc (under CT guidance) and removing the nucleus pulposus through electrical
thermocoagulation, laser vaporisation, or chemonucleolysis (chymopapain).
80-90% of patients experience significant relief from lumboischiadic syndrome following disc
herniation surgery due to decompression of the nerve root. However, back pain (lumbago) may
persist, as surgery does not address the underlying cause of this pain.
In a small number of patients (less than 1%), postoperative discitis (infection of the operated
intervertebral space) may occur. Symptoms typically develop 5-7 days postoperatively and include
severe lumbar pain without radiation to the legs, low-grade fever, and significantly elevated ESR.
MRI confirms the diagnosis. Treatment involves extended bed rest (several weeks) and prolonged
administration of anti-staphylococcal antibiotics. The prognosis is usually good.
Lumbar stenosis is a more serious degenerative condition of the lumbosacral spine than simple disc
herniation. It primarily affects older patients over 60 years old. Stenosis in these patients develops
from long-term degeneration across multiple lumbar segments. Osteoproductive changes
(spondylosis, spondyloarthrosis) and often multilevel disc protrusions narrow the canal to just a few
millimetres.
Clinically, the condition may present as back pain and radicular involvement of certain nerve roots,
but the most common symptom is neurogenic claudication. Patients can only walk short distances
before stopping and usually find relief in a flexed position. Diagnosis relies on MRI, which shows
the degree of canal stenosis (in millimetres) and its extent (number of segments involved). Like
lumbar stenosis, treatment is initially conservative. If symptoms worsen, surgery is indicated,
focusing on decompression of the neural structures. Surgery is performed with the patient prone
under general anaesthesia and involves complete dorsal exposure of the dural sac and exiting nerve
roots—laminectomy (removal of vertebral arches and spinous processes). In cases of severe stenosis
or laminectomy spanning more than two segments, lumbar stabilisation with transpedicular screw
instrumentation and intervertebral disc replacement is often considered. Most of these procedures are
performed through a posterior approach, using techniques such as PLIF (posterior lumbar interbody
fusion), TLIF (transforaminal lumbar interbody fusion), and XLIF (extreme lateral interbody fusion).
45
An alternative is the anterior retroperitoneal approach, ALIF (anterior lumbar interbody fusion).
These operations typically result in significant pain relief and improved walking ability.
Some patients with degenerative lumbosacral spine disease develop significant spondyloarthritis with
pronounced instability between the vertebrae of the lower lumbar spine—spondylolisthesis. These
patients primarily experience back pain, which is often worse when walking. Typical radicular
symptoms may also be present. Diagnosis involves functional X-rays, CT, and MRI. If conservative
treatment and rehabilitation fail, surgery is indicated. This involves decompression of the dural sac,
disc replacement with a cage, reduction of vertebral slippage, and transpedicular fixation of the
adjacent vertebrae in the affected spine segment.
46
PEPIPHERAL NERVE INJURY (20)
Fadrus Pavel, Smrčka Martin
Anatomical Notes: A peripheral nerve's basic morphological and functional unit is the neuron. It
consists of the nerve cell body, peripheral nerve fibre (axon), and terminal branching, which ends at
an effector (in the case of motor fibres) or begins at a receptor (in the case of sensory fibres). The
bodies of the neurons forming peripheral nerves are located either in the spinal cord or in the spinal
ganglia. The axons form the basic functional unit of the peripheral nerve. Axons are covered by a
myelin sheath, which is produced by Schwann cells in the peripheral nervous system. The
interruptions in the myelin sheath are called Nodes of Ranvier. Individual nerve fibres are covered by
a layer of reticular and collagen fibres called the endoneurium. Multiple nerve fibres form bundles
called fascicles, which are covered by the perineurium. Several fascicles combine to form the
peripheral nerve, and its outer covering is called the epineurium.
Pathophysiology of Nerve Injuries: The neuron in the anterior horn of the spinal cord or in the
spinal ganglia, together with its peripheral fibres and the motor end plate or receptor, forms a
functional unit. After the axon is severed, distal to the site of injury, it undergoes degradation known
as Wallerian degeneration.
Proximally to the site of axonal transection (the so-called central or proximal stump), Wallerian
degeneration begins. From the end of the Node of Ranvier, fibrils grow from the axon and are
directed into the Büngner bands. Suppose the nerve ends do not reconnect; an amputation neuroma
forms at the proximal stump. This occurs through the proliferation of connective tissue from the
epineurium, into which the proximal axons grow, eventually encased by fibrous tissue. Axons
regenerate at a rate of 1 mm per day, with a delay of 4-6 weeks at the suture site.
Classification of Nerve Injuries
The simplest classification is the Seddon classification, which categorises injuries from least to most
severe:
1. Neurapraxia: A reversible injury where the axons are not severed. The impairment is
functional, comparable to a concussion in the central nervous system. Recovery typically
occurs within six weeks, resulting in full restoration of nerve function.
2. Axonotmesis: An injury where the axons are severed, but the endoneurial tubes remain
intact. Wallerian degeneration occurs distally, but the macroscopic structure of the nerve is
preserved. Regeneration occurs spontaneously within six months.
3. Neurotmesis: A complete anatomical severing of the nerve. Wallerian degeneration ensues,
and spontaneous regeneration is not possible without surgical intervention.
47
Diagnosis: Diagnosing a peripheral nerve injury involves taking a thorough history (mechanism of
injury) and performing a detailed clinical examination. Electrophysiological testing is not indicated
in the acute phase and is essential in delayed surgeries. Electromyography (EMG) helps monitor the
progress of regeneration. Evidence of distal nerve conduction supports a conservative approach (e.g.,
external neurolysis, the release of scar tissue around the nerve). At the same time, the absence of
potentials necessitates aggressive resection of the neuroma with defect repair using grafts.
Surgical Technique: Successful surgery requires microsurgical techniques. Fine, atraumatic sutures
such as Ethilon 8-10/0 are used, and tension-free suturing is crucial. If a nerve defect is present, it is
bridged using autografts, typically the sensory sural nerve. The graft acts as a conduit for neurofibril
growth during Wallerian degeneration.
Brachial Plexus Injury (C5-Th1)
Brachial plexus injuries are among the most severe peripheral nerve injuries. They are classified as
supraclavicular and infraclavicular injuries.
EMG, nerve action potentials (NAP), CT myelography, and MRI are useful in diagnosing brachial
plexus injuries.
Conservative management is indicated if clinical and laboratory evidence (EMG) shows
improvement. Surgery is indicated for open injuries and closed injuries where there is no
improvement. Infraclavicular injuries have a better prognosis than supraclavicular ones.
Radial Nerve Injury (C5-8)
This is the largest nerve in the upper limb, responsible for motor control of the elbow, wrist, finger
extension, thumb extension, and abduction.
Surgery: In relatively rare open injuries, acute revision is clearly indicated. Indications are more
challenging in radial nerve palsy associated with humeral fractures. It is often difficult to determine
whether paralysis occurred immediately after the injury (due to traction and nerve contusion) or as a
result of iatrogenic injury during surgery. The first scenario typically resolves spontaneously
(axonotmesis), whereas the second requires revision. Delayed surgery should be supported by
intraoperative electrophysiological testing.
Ulnar Nerve Injury (C8-Th1)
The ulnar nerve is a mixed nerve, essential for fine finger movements.
Treatment: Open injuries require urgent revision. Injuries to the nerve at the wrist are often
associated with ulnar artery transection, and it is advisable to treat the nerve while performing an
arterial anastomosis. Ligating the artery can impair the regeneration of the ulnar nerve due to
ischemia.
48
Median Nerve Injury (C5-Th1)
The median nerve is a mixed nerve that branches in the forearm. Median nerve injuries are typically
lacerations at the wrist or forearm. Motor impairment includes difficulty with volar abduction of the
thumb, and a positive "grinding test" may occur when the thumb cannot rotate around the other
fingers. Patients often experience sensory disturbances, causalgia, and trophic changes in the skin,
which become cyanotic and atrophic. Neuroma pain is intense, and patients tend to avoid using the
affected hand.
Treatment: In open injuries (typically at the wrist), surgical treatment is required. In closed injuries,
treatment is individualised.
Compression Syndromes
These syndromes occur when there is a mismatch between the volume of the peripheral nerve and
the anatomical space it occupies. Many compression syndromes are described, but only the most
clinically significant are mentioned here due to their high prevalence.
Carpal Tunnel Syndrome (CTS)
The carpal tunnel is bordered on the volar site (vertically) by the transverse carpal ligament and
dorsolaterally by the carpal bones.
Treatment: For mild symptoms, conservative treatment may be attempted. This involves addressing
the underlying condition, reducing stress on the limb, immobilisation (night splints), physiotherapy
(mobilisation of carpal bones), and anti-inflammatory medication, either orally or through local
injections.
Surgical treatment involves dividing the transverse carpal ligament under direct vision or
endoscopically. This procedure is usually performed on an outpatient basis under local anaesthesia.
Nerve decompression is achieved by dissecting the entire length of the transverse carpal ligament.
The most common postoperative complication is insufficient symptom relief, usually due to
incomplete division of the ligament, which results in residual syndrome rather than a recurrence.
Occasionally, injury to the palmar cutaneous branch occurs, causing pain in the base of the thenar
area. Anomalous courses of the recurrent branch of the median nerve must be considered. Direct
injury to the median nerve is rare.
A rare but serious postoperative complication is complex regional pain syndrome (CRPS),
characterised by motor, sensory, and autonomic disturbances that can lead to severely impaired
mobility and necrosis of the skin in the affected area, accompanied by intense pain.
49
Cubital Tunnel Syndrome
The ulnar nerve is compressed at the elbow as it passes behind the medial epicondyle, where it lies
superficially and is vulnerable to trauma. The condition initially presents with paraesthesias in the
fourth and fifth fingers, which worsen with elbow flexion.
Treatment: Conservative management involves immobilisation in a splint and limiting activity.
Surgical options include simple nerve decompression (sometimes with resection of part of the medial
epicondyle of the humerus) or transposition of the ulnar nerve (less commonly). For post-traumatic
deformities, medial epicondylectomy may be added. Long-term studies have not shown a significant
benefit of transposition over simple decompression. Intramuscular transposition is indicated in cases
of reoperation for progressive neurological symptoms.
Overall, surgical outcomes for cubital tunnel syndrome are somewhat less favourable than for carpal
tunnel syndrome.
Compression of the Ulnar Nerve in Guyon's Canal
Guyon's canal is bordered volarly by the aponeurosis and dorsolaterally by the pisiform and hamate
bones. The ulnar nerve divides here into motor and sensory branches. Differentiation from more
proximal compression is confirmed by the preserved function of the flexor digitorum profundus and
normal sensation on the dorsal ulnar side of the hand. The site of compression is confirmed by
electrophysiological testing (EMG).
Treatment: After conservative options are exhausted, surgical decompression involves dissecting
the aponeurosis.
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51
CONGENITAL ANOMALIES OF THE HEART AND GREAT VESSELS (21)
Fila Petr, Němec Petr
Congenital heart disease (CHD) affects approximately 0.6-0.8% of newborns.
Basic classification (only the most common defects are listed)
1. defects without shunt (congenital aortic valve stenosis, coarctation of the aorta), defects with left to
right shunt (patent ductus arteriosus, ventricular septal defect, atrial septal defect) and defects with
right to left shunt (tetralogy of Fallot, transposition of the great arteries).
2. Cyanotic and non-cyanotic defects
3. Critical and other defects
Defects without shunt
Congenital stenosis of the aortic valve:
Depending on the location, this may be subvalvular, valvar (most commonly bicuspid) or supravalvar
aortic stenosis (AS). The narrowing causes pressure overload in the left ventricle.
The defect may be clinically silent for a long time, but may later present with dyspnoea on exertion or
arrhythmias. Less commonly, it may be a critical stenosis requiring urgent treatment.
Treatment: Critical stenosis requires urgent treatment (balloon dilatation), where a balloon is inserted
through the inside of the artery into the narrowed valve and inflated to dilate the valve. The planned
surgical solution consists of incision of the fused valve cusps, reconstruction of the valve (valvular
AS), resection of the connective membrane or muscular part of the septum (subvalvular AS), or
dilatation of the ascending aorta with a patch (supravalvular AS). Definitive treatment of aortic stenosis
can be achieved by replacing the aortic valve with an artificial valve.
Coarctation of the aorta
Coarctation of the aorta is the presence of a significant narrowing at the end of the arch, most
commonly behind the left subclavian artery. It may be found in isolation or in combination with various
CHD´s.
A small coarctation may not be clinically manifest and is sometimes an incidental finding in adulthood.
In front of the narrowing there is high blood pressure in the aorta (increased blood pressure in the
vessels leading to the head increases the risk of haemorrhagic stroke, epistaxis is typical). In contrast,
the pressure behind the stenosis is low. There is a weak to non-palpable pulse in the lower extremities.
52
An echocardiogram of the heart may show congestion of the left half of the heart, enlargement of the
heart, and sometimes the narrowing of the aorta itself. CT angiography or MRI angiography of the
aorta is useful for confirmation.
Treatment is predominantly surgical (resection of the affected segment via a left-sided thoracotomy
and end-to-end suture (Fig. 1). In neonates or older patients, catheter-based treatment is also possible
- balloon angioplasty or stent or stent graft implantation.
Left-to-right shunt diseases
Patent ductus arteriosus (PDA)
During fetal development, this connection between the aorta and the pulmonary artery allows blood to
bypass the lungs. In healthy newborns, it closes spontaneously during the first 24 to 96 hours of life.
However, in some children, especially those born prematurely, it remains open and causes failure to
thrive in a milder form and signs of heart failure in a more severe form. Treatment is mainly
conservative (indomethacin, ibuprofen). However, if this is not successful, the PDA must be closed
surgically, either by ligation or resection.
Atrial septal defect (ASD)
In ASD, the septum that separates the atria is not fully formed. This causes shunting from left to right
and can lead to congestion of the right side of the heart.
Increased blood flow through the pulmonary circulation can result in increased pulmonary artery
pressure and even the development of pulmonary fibrosis. In the terminal phase, Eisenmenger's
syndrome may occur when the peripheral resistance of the pulmonary circulation is already so high
that the pressures in both atria equalise and the shunt changes to left-to-right. In such patients, repair
of the atrial septal defect is no longer contraindicated because of the risk of right ventricular failure.
Depending on the localisation of the defect, there are two basic types:
1. Ostium primum defect - localised above the atrioventricular valve and often associated with a
mitral valve defect.
2. Ostium secundum defect - is more common and can be located anywhere at the level of the
atrial septum.
Small openings in the atrial septum may be asymptomatic (detected by auscultation due to the presence
of a murmur) and manifest with increased dyspnoea or arrhythmias in adolescence or adulthood.
The first manifestation may also be what is known as paradoxical embolism. This occurs when a
thrombus from the deep venous system of the lower limbs passes through the orifice into the left atrium
53
and from there into the left ventricle and the systemic circulation as a result of increased pressure in
the right-sided compartments (Valsalva manoeuvre).
Treatment of the defect consists of closing the defect with a suture (in the case of a small defect) or
with a patch of autologous or bovine pericardium. Recently, if the localisation is favourable, the defect
can be closed by catheter with an occluder (Fig. 2).
The atrial septal defect of the primum type is divided into incomplete and complete, with several
intermediate stages in between. In a complete defect, the adjacent part of the ventricular septum is
missing and the mitral or even the tricuspid valve is developmentally damaged. This type of defect is
diagnosed in infancy and treatment is surgical and consists of complex reconstruction - closure of the
defect between the atria and ventricles and reconstruction of the damaged mitral and tricuspid valves.
Ventricular septal defect (VSD)
VSD is the most common congenital heart disease in which there is a defect in the septum that separates
the chambers of the heart, causing a shunt from left-to-right. It can be an isolated or a part of a complex
heart malformation. It can be located in the area between the membranous and muscular parts of the
septum (perimembranous defect) or in the muscular part of the septum (muscular defect).
VSD may be asymptomatic and is diagnosed by a systolic murmur on auscultation, or it may cause
decreased exercise capacity or dyspnoea on exertion. The diagnosis is confirmed by echocardiography.
Treatment: for very small defects without significant clinical signs, the child can be followed regularly
as the defect may close spontaneously, especially in the muscular region. Larger defects that cause
clinical symptoms need to be closed surgically, usually with a pericardial or dacron patch. As the edge
of the defect is crossed by the conduction system, there is a risk of grade III a-v block. Exceptionally,
the defect can be closed by catheterisation with an occluder.
Right-to-left shunt diseases
Tetralogy of Fallot (F4)
F4 is an example of a complex cyanotic heart defect involving a VSD, aortic seeding over the defect
and stenosis of the pulmonary artery causing right ventricular hypertrophy.
Symptoms: The presence of a high proportion of deoxygenated blood in the systemic circulation causes
cyanosis, particularly of the face, lips, mucous membranes and fingers (club fingers). There may also
be fatigue and mild dyspnoea, and sudden attacks of shortness of breath with pallor and loss of
consciousness.
This needs to be treated by surgery. In the past, a shunt was created between the pulmonary and
systemic circulations to increase the flow through the lungs in the critical state, thereby increasing the
54
amount of oxygenated blood. The current approach is to perform what is called a radical correction,
i.e. a procedure that leads to normalisation of the anatomical and functional conditions in the heart.
The VSD is closed and the stenosis of the pulmonary artery is removed either by a direct procedure on
the pulmonary artery or by a patch on the outflow tract of the right ventricle. This significantly
improves the prognosis. However, patients need to be followed up by a cardiologist after surgery, as
about 25% of patients need reoperation in adulthood. The most common reason is pulmonary
insufficiency, in which case the pulmonary valve must be a biological prosthesis or homograft. In
appropriate morphological conditions, transcatheter valve implantation is also possible.
Transposition of great arteries - uncorrected:
Transposition of the great arteries is another serious cyanotic congenital heart defect where the
branches of the great arteries from the ventricles are switched. The aorta is transposed from the right
ventricle and the pulmonary artery is transposed from the left ventricle. In this defect, blood collects
from the body into the superior and inferior vena cava, goes through the right atrium into the right
ventricle, into the aorta and throughout the body. From the lungs, blood flows through the pulmonary
veins into the left atrium, through the mitral valve into the left ventricle, into the pulmonary artery,
and again into the lungs. This creates two independent circuits. This would not be a condition
compatible with life, but usually other shunt defects are present that allow at least partial mixing of the
blood (ASD, VSD or PDA). If none of these defects are present, the shunt must be artificially created
immediately (a catheter is used to create a defect at the level of the atria).
Surgical treatment previously consisted of correction at the atrial level, i.e. the right ventricle became
a systemic ventricle. However, this caused problems in the long term, so now the correction is
performed at the level of the great arteries, i.e. the aorta (including the coronary arteries) is repositioned
over the left ventricle and the pulmonary artery over the right. This creates a physiological circulation.
Transposition of the great arteries - corrected:
This type of defect is relatively rare and both the great arteries and the ventricles are transposed. Blood
from the left atrium flows into the right ventricle and aorta, and blood from the right atrium flows into
the left ventricle and pulmonary artery. In this case, we are not talking about the right and left
ventricles, but the systemic and pulmonary ventricles. The right ventricle does not have an evolved
wall to cope with the work of the systemic ventricle in the long term, so dilatation, atrioventricular
valve insufficiency and heart failure gradually develop. Surgical treatment consists of replacement of
the insufficient valve or, in later stages, heart transplantation.
55
Treatment: transposition of the great arteries is corrected as early as possible in the neonatal period by
complex cardiac surgery aimed at normalising the anatomical conditions.
Fig. 1 Coarctation of the aorta and end-to-end anastomosis after correction
Fig. 2 Closing of the ASD by catheter with an occluder
56
SURGICAL TREATMENT OF HEART VALVE DISEASES (22)
Fila Petr, Němec Petr
Heart valves play a key role in maintaining unidirectional blood flow during the cardiac cycle. Their
dysfunction leads to impaired haemodynamics, which can result in heart failure (HF), atrial
fibrillation, pulmonary hypertension and other complications.
The valve is not only made up of leaflets from a functional point of view. In the aortic valve, the
functional parts are the cusps, the anulus, the aortic root and the sinotubular junction (where the
aortic root joins the tubular part of the ascending aorta). In the mitral valve, the cusps attach to the
anulus, and the cusps are connected by chordae tendinae that branch from the papillary muscles,
which attach to the wall of the left ventricle (LV). Pathology in any of the functional parts of the
valve can cause valvular regurgitation, and an understanding of the functional parts is also important
for the correct surgical management of valvular regurgitation, especially when the goal is to repair
the valve.
The prevalence of valvular heart disease is estimated at 2-3% of the population and increases with
age.
Pathophysiology of valvular disease
Valvular disease can be divided into two main categories: stenosis and insufficiency.
• stenosis is characterised by a narrowing of the valve orifice, resulting in an increased pressure
gradient and restricted blood flow.
• insufficiency is a condition in which the valve does not close sufficiently, causing blood to
flow backwards. In the atrioventricular valves (mitral and tricuspid), a distinction is made
between primary insufficiency (involvement of the tips, tendons, papillary muscles) and
secondary insufficiency (dilatation of the anulus and left or right ventricle).
Often, however, these defects are combined (stenoinsufficiency) with a possible predominance of
one or the other component.
Heart valve replacement
The primary goal of surgical treatment is to repair the valve. If reconstruction (valve repair) is not
possible, the solution is valve replacement. There are two basic types of valve replacement:
• mechanical prosthesis - require lifelong anticoagulation, have unlimited durability but higher
rates of thromboembolic and haemorrhagic complications, more suitable for younger patients
• biological prosthesis - do not require lifelong anticoagulation, have limited durability,
preferable for older patients
Aortic valve stenosis
57
The narrowing of the opening of the aortic valve restricts blood flow from the LV to the aorta and
then to the systemic circulation, increasing the workload on the LV, which must exert more pressure
to overcome the resistance of the valve. This can lead to LV hypertrophy and eventually LV
dysfunction. It affects 3-5% of people over the age of 65. The incidence increases with age, with
degenerative calcification of the aortic valve being the dominant cause. Severe stenosis is defined by
an orifice area of less than 1.0 cm² and a maximum gradient above 40 mmHg.
Etiology
• degenerative calcification - in older patients, calcium deposits accumulate on the valve,
reducing its mobility and functionality.
• congenital - bicuspid or unicuspid aortic valve (presence of two/one cusps instead of three)
leads to early development of stenosis.
• postrheumatic fever - streptococcal infection that damages the valves and causes thickening
and adhesions of the valve cusps, rare due to availability of ATB treatment.
Symptoms: shortness of breath, angina, syncope
Diagnosis: auscultatory systolic murmur over the aorta, ECG with signs of LV hypertrophy,
echocardiography, catheterisation to evaluate the gradient between the LV and the aorta.
Treatment
Surgical valve replacement: standard for symptomatic patients or patients with severe stenosis,
mechanical or biological valve. Selected patients may be offered the Ross procedure, in which the
patient's pulmonary valve is used to replace the aortic valve. The pulmonary valve is then replaced
with an allograft from a tissue bank (Fig 1). This procedure is mainly indicated in young patients
with aortic valve dysfunction, where the long-term durability of the valve and the absence of the
need for anticoagulation are an advantage.
Transcatheter aortic valve replacement (TAVI): catheter-based valve implantation (on beating heart,
without extracorporeal circulation) for patients over 75 years of age or for polymorbid patients at
high surgical risk.
Aortic valve insufficiency
Aortic insufficiency (AI), or aortic regurgitation, blood volume flows backwards into the LV leads to
increased LV volume and congestion. Over time, dilation and hypertrophy of the LV may occur,
initially maintaining cardiac output but later leading to decompensation and HF.
Etiology: congenital bicuspid/unicuspid valves, degenerative changes of the leaflets, dilatation of the
annulus, root or sinotubular junction, infective endocarditis or, rarely post-rheumatic involvement.
58
Symptoms: in the early stages the patient may be asymptomatic. Gradually patients may experience
shortness of breath on exertion, fatigue, palpitations and signs of HF. Sometimes acute AI can occur,
often associated with severe dyspnoea, hypotension and signs of cardiogenic shock. Acute AI often
follows aortic dissection or endocarditis and requires urgent surgical intervention.
Diagnosis: auscultation of the heart may reveal a diastolic murmur in the third or fourth intercostal
space to the left of the sternum. Echocardiography is the basic diagnostic method. Magnetic
resonance imaging may be used to assess regurgitant volumes.
Surgical treatment: in severe symptomatic regurgitation or in patients with left ventricular
dilatation, surgical reconstruction (aortic valve repair) of the aortic valve is method of choice. In the
case of dilatation of the cusp, root or ascending aorta, aortic valve replacement surgery is performed,
including the David and Yacoub operations (aortic valve-sparing operations). Surgical replacement is
the solution if the valve cannot be preserved (repaired).
Mitral stenosis
is mainly a consequence of rheumatic fever, when the mitral orifice is narrowed by calcification and
fibrosis. The non-rheumatic cause of mitral stenosis is degenerative calcification of the valve.
Clinically severe mitral stenosis has a valve area of less than 1.5 cm², with symptoms such as
dyspnoea on exertion, pulmonary hypertension and HF occurring at values below 1.0 cm². Mitral
stenosis increases left atrial pressure, leading to subsequent atrial fibrillation and thromboembolic
complications.
The most common surgical treatment for mitral stenosis is replacement with a mechanical or
biological valve.
Mitral insufficiency
also known as mitral regurgitation (MR), resulting in a backward flow of blood from the LV to the
left atrium during systole. This backward blood flow causes congestion in the left atrium and LV,
which can lead to the development of HF, pulmonary hypertension and other complications.
Etiology: prolapse of the mitral valve cusp (degenerative changes), chordal rupture, post-infarction
papillary muscle rupture, infective endocarditis, post-rheumatic involvement - primary. LV dilatation
with anulus dilatation or even a change in LV geometry (dilatation) and subsequent traction on the
papillary muscles leads to MR - secondary.
Correct determination of the cause of MR in relation to the functional parts of the valve is a
prerequisite for correct treatment (repair) of the valve.
Symptoms: shortness of breath, fatigue, palpitations or progressive signs of HF. In acute MR cardiogenic
shock, pulmonary oedema
59
Diagnosis: Auscultation of a holosystolic murmur over the apex, echocardiography (to assess the
severity and cause of regurgitation, and to assess the size and function of the left atrium and LV).
Treatment: the principle of surgical treatment is primarily reconstruction (repair) of the valve. The
prolapsed part of the tip can be resected, the ruptured/elongated chord can be replaced with a
neochord. An annuloplasty with implantation of a mitral ring is almost always performed. A mitral
valve that cannot be repaired is replaced with a mechanical or biological valve.
For patients at high surgical risk, less invasive mitral valve procedures (transapical implantation of
the valve in the mitral position, on a beating heart) or the more common catheter-based implantation
of a clip that anchors the anterior and posterior cusps (i.e. MitraClip), creating a double orifice mitral
valve, have recently emerged.
Tricuspid stenosis
This is a rare disease of the tricuspid valve. It is caused by post-rheumatic disease, endocarditis,
tumours or carcinoid syndrome. The solution is usually replacement with a bioprosthesis.
Tricuspid insufficiency
Primary tricuspid regurgitation (TR) results from involvement of the cusps, chords or papillary
muscles. Secondary TR is more common with dilatation of the tricuspid annulus. Clinically
significant TR leads to the development of right-sided HF, oedema and ascites. Surgical treatment
consists of implantation of an annuloplasty tricuspid ring to correct the dilatation of the annulus.
Pulmonary valve defects are rare. They are mostly associated with congenital heart disease.
60
Fig. 1 Ross procedure - diseased aortic valve is replaced with the patient's own pulmonary valve.
This is followed by the replacement of the pulmonary valve with a pulmonary allograft from tissue
bank.
Fig. 2 Transcatheter aortic valve replacement (TAVI) – transfemoral or transapical access
61
SURGICAL TREATMENT FOR CORONARY ARTERY DISEASE (23)
Fila Petr, Němec Petr
Introduction
Ischaemic heart disease (IHD) is a disorder in which there is an imbalance between the demand for
oxygen and the supply to the myocardium. The most common cause of IHD is atherosclerosis. Acute
and chronic forms of IHD are distinguished.
Besides preventing IHD in patients, we use conservative medical treatment, percutaneous coronary
intervention (PCI) and surgery.
One or more coronary artery bypass graft (CABG) are used in the surgical treatment of IHD. The
principle of coronary artery bypass grafting is to bridge the affected coronary artery using an arterial
or venous graft. The peripheral anastomosis of the bypass graft is placed on the coronary artery distal
to the affected coronary artery (stenosis, occlusion). For venous graft, the central anastomosis is
placed on the ascending aorta. In arterial bypasses, the central end is left in situ or anastomosed to
the ascending aorta or connected to another bypass.
Indication for CABG
Patients with severe coronary artery disease are referred for surgical revascularization. Most
commonly:
- left main disease
- two-vessel disease with stenosis or occlusion of the proximal segment of the left anterior
descending artery (LAD)
- three-vessel disease (i.e. involvement of the LAD, circumflex artery and right coronary artery)
In patients with acute coronary syndrome, surgical revascularisation is preffered when percutaneous
coronary intervention (PCI) was not technically feasible or in the presence of mechanical
complications of myocardial infarction. In addition to coronary involvement, the general condition of
the patient (age, comorbidities) must be taken under consideration in the decision-making process.
Grafts (conduits) for revascularisation
Arterial grafts: internal thoracic artery (ITA), radial artery (RA), gastroepiploic artery, inferior
epigastric artery.
Venous grafts: great saphenous vein (GSV), small saphenous vein.
Arterial conduits have better long-term patency due to their wall structure (more than 90% of
bypasses remain patent after 10 years). In venous conduits, neointimal hyperplasia develops after a
62
few years and can lead to stenosis or occlusion of the bypass (about 50% of bypasses remain patent
after 10 years).
Harvesting conduits for revascularisation
Arterial conduits are harvested either as free grafts (e.g. right-sided ITA, RA) or left in-situ. The
most commonly used left in-situ arterial graft is the left-sided ITA. Centrally, its origin from the
subclavian artery is preserved, while the peripheral end of the artery is cut at the lower edge of the
sternum and sutured to the coronary artery, usually the LAD.
The radial artery is harvested as a free graft, usually from the non-dominant limb. Prior to harvesting
the RA, a thorough assessment of the arteries of the forearm (Allen's test, ultrasound examination)
should be performed to ensure a good arterial supply to the hand via ulnar artery.
The right gastroepiploic and inferior epigastric arteries are rarely used as grafts.
Lower extremity vein grafts can be harvested openly from one or more skin incisions or
endoscopically. Endoscopic harvesting of GSVs is the minimally invasive technique, which has the
advantage of less postoperative pain, faster recovery and better cosmetic effect. Patients with obesity,
diabetes or chronic lower limb ischaemia may benefit from this technique.
Types of procedures in the surgical revascularisation of the heart
CABG using extracorporeal circulation (ECC): during surgery, the patient is connected to an ECC
and cardioplegic cardiac arrest is induced. Distal vascular graft anastomoses are constructed on the
arrested heart and central anastomoses are sutured to the ascending aorta once the aortic cross-clamp
is released and hearts starts to beat. After weaning from the ECC, the cannulas through which the
ECC was connected are removed. The advantage of this technique is a stable and bloodless surgical
field. The disadvantages are an increased risk of embolism due to manipulation of the aorta and a
higher inflammatory response of the body to blood contact with the artificial surfaces of the ECC.
CABG without the use of ECC (off-pump CABG) is performed on a beating heart. During suturing
of distal anastomoses, this area of the heart must be partially stabilised with various devices. Once
the artery is opened, an intracoronary shunt is placed in the lumen to control bleeding while
maintaining peripheral blood supply to the myocardial tissue. This type of operation is particularly
important in high-risk patients after a stroke or in patients with renal failure. The disadvantage is that
it is more technically challenging.
Minimally invasive CABG: This is a gentle surgical approach that is used to reduce the stress of the
surgery and allow a faster recovery. This includes a procedure known as MIDCAB (Minimally
Invasive Direct Coronary Artery Bypass Grafting) - a procedure in which the anterior wall of the
63
heart (usually the LAD or diagonal artery) is revascularised using a left-sided ITA. The surgical
approach is an anterior left-sided thoracotomy in the 4th intercostal space. ITA is harvested
thoracoscopically or directly through the thoracotomy. The anastomosis is performed on the beating
heart as described above. In some units, the same type of operation is being done using a robotic
system.
Complications of acute myocardial infarction:
1/ Acute mechanical complications of acute myocardial infarction are rare but very serious
complications with a high mortality rate.
• left ventricular free wall rupture - a large rupture results in death due to massive cardiac
tamponade. Pericardiocentesis is indicated for small tears with gradual leakage of blood into
the pericardial cavity. The definitive surgical solution is to close the left ventricle with
pledgeted sutures or to close the defect with a patch. If the tear in the left ventricular wall
(and blood leakage) occurs gradually over several days or in case of pericardial adhesions,
encapsulation of the site may occur with subsequent development of a false aneurysm
(pseudoaneurysm).
• post-infarction ventricular septal defect - occurs as a complication of a large myocardial
infarction in the territory of the LAD or the right coronary artery. A left-to-right shunt occurs
at the site of the defect, resulting in volume overload of the right ventricle and low cardiac
output of the left ventricle. Patients in cardiogenic shock require immediate surgical
intervention to close the defect with a patch. Currently, the most common alternative to this
procedure is to connect the patient to mechanical heart support (extracorporeal membrane
oxygenation - ECMO) and postpone surgery. This has the advantage of allowing some
healing and strengthening of the defect area, which makes the surgery safer for defect
closure. In patients with a small septal defect in whom surgery can be delayed, we administer
inotropic support or introduce an intra-aortic balloon counter-pulsation device.
• acute mitral valve regurgitation - occurs as a complication of post-infarction rupture of the
papillary muscle. Acute mitral regurgitation leads to postcapillary pulmonary hypertension
and pulmonary oedema with dyspnoea and hypoxia. As blood returns to the left atrium in
systole, forward cardiac output decreases and organ hypoperfusion occurs. Emergent surgical
management is indicated, consisting of mitral valve replacement with potential myocardial
revascularisation.
2/ Left ventricular aneurysm is a late complication of transmural myocardial infarction. It is caused
by the remodelling of the heart muscle into scar tissue. This leads to thinning of the left ventricular
64
wall and paradoxical bulging during systole. The main clinical symptoms are low cardiac output
(some blood remains in the aneurysm and is not ejected during systole), systemic embolism from
mural thrombosis in the aneurysm and ventricular arrhythmias. Symptomatic left ventricular
aneurysm is referred for surgery - resection of the aneurysm with or without patch closure of the
defect.
Fig. 1: Basic principles of surgical myocardial revascularisation: 1 - left ITA to the LAD, 2 - right
ITA as Y-graft to the circumflex artery, 3-vein graft (or radial artery) from ascending aorta to the
right coronary artery (ITA-internal thoracic artery, LAD-left anterior descending artery)
65
SURGICAL TREATMENT OF AORTIC DISEASE (24)
Fila Petr, Němec Petr
The most common types of acquired aortic disease encountered by cardiac surgeons are aortic
aneurysm and aortic dissection. These diseases have different etiologies, clinical manifestations, and,
most importantly, prognosis.
1. Aortic aneurysm
Aortic aneurysm is a localized enlargement of the aorta. Most aneurysms of the thoracic aorta are
true, meaning they involve all aortic wall layers. The etiology is usually idiopathic (degenerative).
Genetic predisposition (Marfan syndrome, Loeys-Dietz syndrome, bicuspid aortopathy…) is
associated with aneurysms, especially in younger people. Inflammatory causes of aneurysm
(infectious or non-infectious) are rare.
Thoracic aneurysms are usually asymptomatic and are diagnosed during routine physical
examinations for other reasons. It is less common for them to be manifested by pain or signs of
compression of the surrounding structures. The aneurysm may be filled with thrombi that can
embolize.
The aneurysm puts the patient at risk of rupture, with the development of massive bleeding,
dissection due to weakening of the aortic wall, embolization of mural thrombi, and, in the region of
the aortic bulb, development of aortic valve regurgitation. Diagnosis is usually based on
echocardiography, CT, or MRI.
The risk of aneurysm rupture increases with the size of the aorta. The indication for surgery is mainly
determined by the diameter of the aneurysm - over 50 mm in the thoracic aorta and 40 mm in the
abdominal aorta.
Resection of the aneurysmal aorta and its replacement with a prosthesis is the main principle of
surgical treatment of aortic aneurysms. This principle is common to all surgical procedures.
However, due to the specific nature of the individual parts, we divide the aorta into three parts: - the
aortic root with ascending aorta, the aortic arch, and the descending aorta (thoracic and abdominal).
In clinical practice, it is widespread for the aneurysm to affect more than one of these sections and
the procedure performed will be a combination of the procedures described below.
1.1 Aortic root and ascending aorta
The most common procedure in this area involves replacing the aortic valve and ascending aorta and
reimplantation of the coronary arteries into a prosthesis (Bentall operation).
66
This procedure uses a composite graft consisting of a mechanical or biological valve and an attached
vascular prosthesis. After aortic valve excision, this graft is implanted like a simple aortic valve
replacement. The coronary arteries are then reimplanted into the prosthesis. Patients with normal
aortic valves can undergo a valve-sparing operation in which the aortic valve is preserved, and only
the aortic wall is replaced.
These operations are more beneficial for the patient in the long term but are technically more
challenging.
In the region of the ascending aorta, there are no branches from the sinotubular junction to the
brachiocephalic trunk. The primary surgical procedure is to resection the aneurysm and replace it
with a graft with end-to-end anastomosis at both ends.
PEARS (personalized external aortic root support) is the modern method for preventing further aortic
dilatation. This custom-made mesh (based on the patient's aortic CT scan) is implanted externally to
the aorta to cover the root and ascending aorta. This method is suitable if the aorta is not too dilated
and the aortic valve is without haemodynamic pathology.
1.2. Aortic arch
The principle of surgical treatment of aortic arch aneurysms is resection of the aorta and its
replacement with a vascular prosthesis, with reimplantation of the branch arteries.
These surgical procedures are complex because arteries supplying the brain branch off from this
region of the aorta. This requires adequate protection of the brain during surgery. There are basic
ways to protect the brain during aortic arch surgery: deep hypothermia (18°C) with circulatory arrest
and orthograde cerebral perfusion. Currently, the most commonly used method is orthograde cerebral
perfusion, in which the brain is perfused with oxygenated blood from the extracorporeal circulation
(ECC) through cannulae inserted into the supra-aortic branches (brachiocephalic trunk, left common
carotid artery and eventually the left subclavian artery) during circulatory arrest. This ensures
adequate oxygenation of the brain. We combine orthograde cerebral perfusion with varying degrees
of hypothermia. This has a protective effect on the lower half of the body, which is not perfused
during circulatory arrest, and creates space for a brief interruption of orthograde cerebral perfusion,
for example, during cannula insertion or suture finishing. Hypothermia in the range of 26 to 28°C is
most used.
1.2 Descending aorta
The principle of surgical treatment of descending aortic aneurysms is still the resection of the dilated
part and its replacement with a prosthesis. These procedures are performed through a left
67
thoracotomy, with or without the use of ECC. A specific feature of operations on the descending
thoracic aorta is the presence of the arteries supplying the spinal cord and the associated risk of
spinal ischaemia with the subsequent development of paraplegia. If a larger part of the thoracic aorta
is replaced, the branches supplying the spinal cord must be reimplanted into the prosthesis. The risk
of paraplegia can also be reduced by drainage of the cerebrospinal fluid. For descending aortic
aneurysms, endovascular treatment is strongly advocated, in which a stent graft (coated stent) is
introduced into the descending aorta by way of the femoral artery, deployed there, and anchored at
both ends in the non-expanded part of the aorta, thereby excluding the aneurysm from the flow and
preventing its rupture.
In the case of aneurysms (thoracoabdominal), we must also reimplant the visceral arteries (celiac
trunk, superior mesenteric artery, renal arteries) and ensure adequate perfusion of these outlying
branches during surgery. Thoracoabdominal aortic replacement is a technically demanding procedure
that also requires a sizeable surgical approach (thoraco-freno-laparotomy). Therefore, interventional
endovascular treatment with stent grafts or the so-called hybrid treatment (combination of open
surgical and endovascular treatment) is beginning to be promoted in the abdominal aorta.
2. Aortic dissection
Acute aortic dissection is a life-threatening disorder in which a tear in the intima ('entry') and the
blood flow causes a longitudinal 'split' of the layers of the vessel wall in the tunica media. The tunica
adventitia remains intact. This creates a 'true' and a 'false' aortic lumen, which rapidly fills with blood
and the pressure of which pushes the layers of the thoracic aortic wall apart, causing the dissection to
spread proximally and distally. Proximally, the dissection may extend to the aortic valve annulus and
distally to the femoral bifurcation. Distally, another intimal tear (re-entry) usually connects the true
and false lumens. The true lumen is often significantly compressed by the false lumen.
Risk factors for dissection include inadequately treated hypertension, aortopathy causing aortic
dilatation, and atherosclerosis. The disease usually begins with a sharp pain behind the sternum or in
the back between the shoulder blades, often associated with physical exertion or a rise in blood
pressure.
The patient's life is threatened by the rupture of the thin tunica adventitia and subsequent bleeding
into the surrounding areas (pericardial cavity, pleural cavity, retroperitoneal space). Ischaemic
involvement of organs whose supplying artery branches off the dissected aortic segment and is
obliterated by a false lumen may also occur (Fig 1). The dissection thus manifests as ischaemia from
the basin of these arteries, i.e. myocardial infarction, neurological symptoms (stroke, lower limb
paraplegia), signs of splanchnic ischaemia, anuria or lower limb ischaemia. If the dissection extends
68
proximally to the aortic bulb, it may cause a commissural tear of the aortic valve, resulting in acute
aortic regurgitation. Dissection is diagnosed by CT and echocardiography.
According to the location of the intimal tear, the Standford classification (Fig. 2) divides dissections
into type A, when the ascending aorta is involved in the dissection, and type B, when the ascending
aorta is not involved in the dissection. This classification is crucial for treatment. Patients with type
A dissection are indicated for emergent surgery, as 50% of patients die in the first 48 hours without
surgery.
The principle of surgical treatment is resection and replacement with a vascular graft of the part of
the thoracic aorta where the primary intimal tear (entry) is located. If the tear is in the ascending
aorta, we replace the ascending aorta during. The aortic arch is replaced if the tear is in the intimal
region of the arch. The dissected distal part of the aorta (descending), which we do not replace, can
be left to thrombotomise the false lumen. In patients with an intimal tear in the aortic arch and a
dissection extending into the descending aorta, we can use the "frozen elephant trunk" method. In
this technique, we place a composite stent graft into the descending aorta during circulatory arrest
after the aortic arch is excised and position it so that the stent-reinforced portion is dissected into the
descending aorta, and then use the other portion with the prosthesis to perform the aortic arch
replacement. This method has the advantage of being more radical, with a greater likelihood of
thrombosis of the false sac and healing of the descending aorta.
In patients with type B dissection, conservative treatment or stent graft implantation is preferred.
Only rupture or organ or limb ischaemia is an indication for surgical treatment.
The operative mortality of acute thoracic aortic dissection is high, at 10-20%. Post-operative
morbidity is also relatively high, mainly because we are leaving the dissected aorta in the descending
part, the wall of which has already been damaged by the dissection.
69
Fig. 1. Aortic disection with entry (1), reentry (2), true (3) and false (4) lumen impairing blood flow
to the branches
Fig. 3. Aortic dissection classification
70
CARDIOPULMONARY BYPASS, MECHANICAL CARDIAC SUPPORT (28)
Fila Petr, Němec Petr
1. Cardiopulmonary bypass (CPB)
CPB is a complex method that temporarily replaces the function of the heart and lungs by directly
connecting the patient's circulatory system to an external device. The principle of CPB during
cardiac surgery is to divert blood outside the patient's heart (body), oxygenate it, remove carbon
dioxide, and return it to the systemic circulation. The heat exchanger, a part of the CPB, allows
regulation of the patient’s body temperature.
Components of CPB (Fig. 1):
Venous (drainage) cannula/cannulae – inserted into the venous system (right atrial appendage,
superior and inferior vena cava, or femoral vein).
Venous line – tubing set connecting the venous cannula to the venous reservoir.
Reservoir – acts as a blood reservoir for the CPB system.
Pumps – CPB usually consists of one main pump and several auxiliary pumps. The main pump
provides the flow of blood from the venous reservoir through the oxygenator and heat exchanger into
the patient’s arterial system. Auxiliary pumps are used for suction blood from the surgical field.
Oxygenator and heat exchanger
Arterial line – tubing set connecting the oxygenator to the arterial cannula.
Arterial cannula – inserted into the ascending aorta or femoral artery.
Additional devices – include filters, hemoconcentrators, blood cardioplegia system
Anticoagulation.
The activation of the coagulation cascade upon contact with CPB components usually leads to blood
clotting and system thrombosis. Therefore, heparin is administered to the patient at the start of
surgery at a dose of 3-4 mg/kg.
2. Myocardial protection during cardiac surgery
Under normal circumstances, the heart is supplied with blood through the coronary arteries that arise
from the aortic root. To stop the heart, it is necessary to halt blood flow into the coronary arteries,
which is achieved by placing a cross-clamp on the ascending aorta. From this moment, when the
coronary arteries are not perfused with warm oxygenated blood, cardioprotective measures must be
taken to prevent irreversible myocardial damage.
Myocardial protection is mainly ensured by administering cardioplegic solutions.
71
The basic principles of myocardial protection are:
- Electromechanical arrest.
- Prevention of cellular oedema and stabilization of cell membranes.
- Adequate cooling of the myocardium (thus slowing metabolism) or ensuring sufficient energy
supply while maintaining normothermia.
Cardioplegic solutions can be categorized based on:
Composition:
Intracellular: Low sodium concentration and absence of calcium reduce action potential conduction
and contractile force.
Extracellular: Higher potassium concentration (up to 40mmol/L) leads to depolarization of the cell
membrane.
Solutions are mildly alkalic to compensate the acidosis, which occurs due to lactate accumulation in
muscle during anaerobic metabolism. Cellular oedema results from ischemia, so these solutions must
be slightly hyperosmolar to ensure fluid transport out of the cell, with glucose or mannitol added for
this purpose. Procaine may be added to stabilize cell membranes.
Blood-based: A blood-based cardioplegic solution is created by mixing the patient’s blood with a
crystalloid solution high in potassium in a predetermined ratio (commonly 1:4). This combination
reduces hemodilution, provides better buffering capacity, protects against oxygen radicals through
endogenous antioxidants, and maintains physiological pH.
In most cardioplegic solutions, local hypothermia is used in addition to their composition.
Administration methods:
-Antegrade: Cardioplegic solution is delivered through a specialized cannula into the ascending aorta
(between the aortic root and the clamp) or, after opening the aorta, directly into the coronary ostia.
Retrograde: A cannula is inserted into the coronary sinus, and cardioplegia is administered
retrogradely through the heart’s venous system, with pressure not exceeding 50mmHg.
Combined: A combination of antegrade and retrograde administration ensures the best distribution of
the cardioplegic solution in the myocardium.
The effect of cardioplegic solution is time-limited, so its administration must be repeated based on
the duration of the surgery.
3. Mechanical circulatory supports (MCS)
MCS encompasses a range of devices used when the heart cannot provide sufficient perfusion to the
body's organs and tissues. The general indication is medically unmanageable heart failure, often
resulting from myocardial damage.
72
Indications for MCS use:
1. Cardiogenic shock after heart surgery or cardiogenic shock of another origin (e.g., postmyocardial
infarction, unsuccessful PCI, myocarditis).
2. Hemodynamic deterioration in patients on the heart transplant waiting list or those selected for
destination therapy.
3. Acute rejection or heart failure immediately after transplantation.
MCS Classification (Table 1):
- Based on duration of the use, they are divided into short-term supports (for acute heart failure,
where heart function is expected to recover) and long-term supports (for patients awaiting
transplantation for months/years). Permanent devices are for patients contraindicated for
transplantation.MCS can support the function of the left ventricle (left-side MCS), the right ventricle
(right-side MCS), or both (biventricular support).
A specific type of MCS is the total artificial heart, where both ventricles and valves are removed and
replaced by the device.
Purpose-based MCS classification:
1. Bridge to Decision (BTD) – for patients with acute heart failure pending evaluation of further
therapeutic options, neurological status, and organ functions.
2. Bridge to Recovery (BTR) – for acute but reversible heart failure cases. Recovery of heart
function leads to MCS removal.
3. Bridge to Transplantation (BTT) – to support patients on the waiting list for heart transplantation
until a suitable donor heart is available.
4. Destination Therapy (DT) – permanent MCS use for patients in the terminal phase of heart failure
who are not candidates for transplantation.
Most commonly used MCS:
-Short-term: Intra-aortic balloon pump (IABP), extracorporeal membrane oxygenation (ECMO), leftside
MCS with a centrifugal pump.
Long-term: Left-side MCS with an intracorporal centrifugal pump (LVAD), where the patient is
connected to an external power supply by a cable.
Future of MHS: This field is rapidly evolving due to the growing number of patients with heart
failure who could benefit from this treatment. If the problem of transcutaneous energy transfer can be
solved, long-term MHS may become an alternative
73
Fig. 1 Schema of Extracorporeal Circulation Systém
1 – arterial cannula, 2 – venous cannula, 3 – reservoir, 4 – pump, 5 -oxygenator and heat exchanger
Duration Support Localisation Character of the
flow
Short-term
- Reversible failure
- Possibility of recovery
Long-term
- Bridge to transplant
Destination
- Not suitable for heart
transplant
Left-side
Right-side
Biventricular
Paracorporal
Implantable
Pulse flow
Continuous flow
Table 1 Mechanical circulatory support classification
74
CARDIAC AND GREAT VESSEL INJURIES (25)
Fila Petr, Němec Petr
Heart injuries can be divided into penetrating and blunt injuries according to the mechanism of
injury. The consequences of these injuries can range from clinically silent arrhythmias to immediate
death at the site of injury.
Penetrating injuries
These are caused directly (stabbing, gunshot) or indirectly (by sharp fragments of ribs or sternum in
chest trauma). Due to anatomical relationships, the right ventricle is most commonly injured. The left
ventricle, atria and great vessels may also be affected. Of the coronary arteries, the left anterior
descending artery is most commonly injured. The patient is at risk of haemorrhagic shock or cardiac
tamponade. Possible sequelae of penetrating cardiac injury include haemothorax/pneumothorax,
myocardial infarction, arrhythmias, valvular injury or projectile embolism from a gunshot. Diagnosis
is based on clinical examination, noting the open chest wall and epigastric wound, signs of severe
skeletal chest injury, attenuation of cardiac echoes, jugular venous filling, respiratory impairment
and absence of peripheral pulsations. Tachycardia and hypotension are present. Of the imaging
modalities, transthoracic echocardiography (TTE) is of great diagnostic importance. The detection of
pericardial effusion may be an indicator of cardiac injury. CT angiography is part of the protocol for
the investigation of severe chest trauma and reliably detects associated injuries. An ECG helps to
detect arrhythmias.
In patients with proven tamponade, pericardiocentesis can be performed under TTE control. As a last
resort, emergent left-sided thoracotomy is performed to allow evacuation of the tamponade,
temporary hemostasis (digital compression, clamp loading, Foley catheter), clamp loading of the
descending aorta to centralise circulation and direct cardiac massage. The definitive treatment is
surgical from a mid-longitudinal sternotomy, which allows access to all cardiac compartments and
possible connection to the extracorporeal circulation. Cardiac injury is treated with polypropylene
mattress sutures over pericardial or Teflon felts (Fig 1). Coronary artery injuries require ligation of
the arteries and bypass grafting. The affected valve may be repaired or replaced. Any foreign bodies
in the chambers of the heart will need to be removed.
Blunt injuries
The mechanism of occurrence includes direct impact on the precordium, deceleration, compression
of the heart between the sternum and the spine, and rapid filling of the heart with venous blood as the
lower half of the body is compressed. They occur as a result of chest trauma.
75
They are particularly likely to occur in cases of sternal fracture or avulsion of the anterior segment of
the ribs with the sternum.
Myocardial coma is manifested by malignant ventricular arrhythmias with no morphological basis,
followed by sudden death. Myocardial contusion is the most common form of blunt cardiac injury.
Diagnosis is based on the description of the mechanism of injury, abnormal ECG findings (nonspecific
ST segment changes, negative T wave, supraventricular or ventricular extrasystoles, newonset
block, ischaemic changes) and/or elevation of cardiac-specific enzymes (troponin). The patient
is at risk of developing malignant arrhythmias or heart failure with more extensive bruising;
therefore, continuous monitoring of vital signs and ECG is necessary.
Therapy should focus on treating arrhythmias (pharmacological or electrical cardioversion, pacing
for high-grade block) and haemodynamic stabilisation. In severe myocardial contusion, blunt injury
to the coronary artery with its thrombosis may occur, leading to myocardial infarction with all its
consequences and possible complications. Treatment depends on the coronary findings. Other blunt
trauma modalities are rare.
Traumatic rupture of the ventricular wall is often lethal; survivors present with cardiac tamponade
and require urgent surgical management.
Traumatic septal defects often present with a time latency and treatment is then deferred (depending
on the size of the defect and the significance of the left-to-right shunt) - conservative, transcatheter
occlusion or surgical closure.
Rupture of the pericardium can lead to herniation of the heart into the pleural or abdominal cavity
and torsion of the great vessels. Clinical manifestations include haemodynamic instability and
cardiac arrest. Treatment involves repositioning of the heart and suturing of the defect.
Blunt valve injuries most commonly affect the aortic and mitral valves with the development of
acute regurgitation, which in severe cases can lead to left heart failure, cardiogenic shock and
pulmonary oedema. Depending on the perioperative findings, treatment is either surgical
(reconstruction) or prosthetic (replacement).
Large vessel injury
The major intrathoracic vessels include the aorta and the branches of the aortic arch, the superior
vena cava and its tributaries, the inferior vena cava, the pulmonary artery and its branches, and the
pulmonary veins.
Penetrating injuries may be direct or indirect, as in the heart. They often result in exsanguination at
the site of injury. Surviving patients in haemorrhagic shock or after successful initial resuscitation
are transferred directly to the operating theatre. Only haemodynamically stable patients with large
76
vessel injuries are referred to the operating theatre for a chest CT with CT angiography as part of the
trauma protocol. The principle of treatment is direct suturing of the injured vessel, interposition of a
vascular prosthesis, reconstruction of the vessel with a patch or bypass surgery. In patients with a
prolonged course, endovascular therapy - stentgraft implantation - may be considered.
Blunt aortic injury (car accidents, fall-related injuries) is caused by shearing forces at the junction of
the mobile aortic arch and the fixed descending aorta - behind the left subclavian artery. Complete
transection is a life-threatening injury with massive haemorrhage ending in exsanguination. In
incomplete subadventitial transection, therapy consists of controlled hypotension with systolic blood
pressure levels below 100 mmHg and sten graft placement to bridge the defect in the aortic wall.
Cardiac surgery is required for arch injury at the site of the great vessel outflow.
Fig. 1. Ventricle suture using U-stitches using of teflon felt supporting the suture
77
TRANSPLANTATION OF HEART, LUNG AND LIVER (26)
Fila Petr, Němec Petr
Currently heart, liver, lung, kidney and pancreas transplants are routinely performed. It is also
possible to transplant the uterus or intestine. In case of multiple organ failure so-called multi-organ
transplant can be performed most commonly kidney + pancreas or liver + kidney combination. In
certain specific situations a multivisceral transplant may be carried out which involves the transplant
of the liver, stomach, small intestine and pancreas.
Patients in the terminal stage of a disease which cannot be treated otherwise and who have no
contraindications are indicated for organ transplantation.
General contraindications for transplantation:
Malignant disease
Chronic infection
Active infection or sepsis
Poor patient compliance
Patient’s age
Nowadays most contraindications are considered relative with the overall biological condition of the
patient being crucial. The patient must undergo comprehensive examination be assessed by a
multidisciplinary committee and if no contraindications are found they are placed on the waiting list.
Heart Transplant (HT)
The first successful orthotopic heart transplant (HT) was performed in 1967 by Ch. Barnard in South
Africa. The results of early transplants were poor due to the lack of adequate immunosuppressive
therapy. Since the 1980s, with the introduction of new immunosuppressants, heart transplantation
has gradually become an established treatment method for patients in the terminal stage of heart
failure (classified as NYHA III or IV) refractory to medical treatment and where no other surgical
options exist.
Indications for heart transplantation:
Patients most commonly indicated for transplantation have:
Ischemic heart disease with surgically untreatable coronary artery damage and low ejection fraction
(usually below 20%)
Dilated cardiomyopathy with a low ejection fraction
Less common indications include other types of cardiomyopathy, surgically untreatable valvular or
congenital heart defects and patients with malignant arrhythmias.
78
Specific contraindications for heart transplantation:
Increased pulmonary vascular resistance
Severe extracardiac disease (CNS, liver, lungs etc.)
HT procedure:
Heart transplantation is performed using cardiopulmonary bypass and cannulation of ascending aorta
and both vena cava. After clamping the ascending aorta and stopping the blood flow to the coronary
arteries the diseased heart is excised leaving long stumps of the aorta, pulmonary artery and both
vena cava. The posterior part of the left atrium is also preserved (Fig 1). The new graft is then
transplanted with sutures done in the following order: left atrium, inferior and superior vena cava,
pulmonary artery and aorta. This so-called bicaval technique replaced the original method where the
entire atria were preserved, which led to frequent arrhythmias.
Surgical outcomes are excellent given the patients' condition with early mortality under 10%. Oneyear
survival is between 80-90% and about 70% of recipients survive five years. After a successful
transplant patients experience dramatic improvements in health and mostly are able to fully return to
social and work life.
Liver Transplant (LT)
The first liver transplant was performed in 1967 in Denver, and the first LT in the Czech Republic
was carried out in 1982 at the 2nd Surgical Clinic at university hospital St. Anna in Brno.
Indications for liver transplantation:
Patients with terminal liver failure, most commonly caused by:
Liver cirrhosis due to cholestatic diseases, viral hepatitis, excessive alcohol consumption, etc.
Metabolic diseases (e.g., Wilson's disease, hemochromatosis)
Polycystic liver disease, Budd-Chiari syndrome, or liver failure of unknown etiology
Other indications include liver tumours (unresectable primary hepatocellular carcinoma or carcinoma
in cirrhosis).
LT procedure:
Access to the abdominal cavity is carried out via a subcostal incision extending across the midline.
The structures in the hepatoduodenal ligament (hepatic artery, portal vein and bile duct) are isolated
and cut. The liver is then detached from the inferior vena cava (IVC), which is left in situ. A new
liver is implanted by suturing the anastomoses in the following order: IVC of the graft end-to-side to
the IVC of recipient, portal vein, hepatic artery, and finally a bile duct end-to-end anastomosis is
created. Most patients with liver cirrhosis have coagulation disorders, requiring precise surgical
technique and careful control of bleeding.
79
Surgical outcomes are excellent with early mortality ranging from 5-10%. Five-year survival rates
are 80% and approximately 60% of patients survive ten years. Most patients experience a significant
improvement in quality of life and return to normal daily activities.
Lung Transplant (LuT)
The first successful lung transplant was performed in 1983 in Toronto.
Indications for lung transplantation:
Restrictive lung disease (e.g., cystic fibrosis)
Obstructive lung disease (primary or secondary pulmonary emphysema)
Pulmonary vascular disease (e.g., primary pulmonary hypertension)
Specific contraindications include smoking, extreme cachexia, or obesity.
LuT procedure:
A transplant can involve one or both lungs (bilateral transplant is now preferred). Lung
transplantation is performed via thoracotomy (bilateral thoracotomy for both lungs). After dissection
of pulmonary hilum the pulmonary artery, pulmonary veins, and main bronchus are cut, and the lung
is removed. End-to-end anastomoses of the pulmonary artery, pulmonary veins (directly to the left
atrium), and bronchus are created. For bilateral lung transplants, extracorporeal membrane
oxygenation (ECMO) is used to ensure stable circulation and oxygenation of the patient.
The results of lung transplants are also very good, with one-year survival rates between 70-80% and
five-year survival rates around 50%.
Kidney Transplant (KT)
Kidney transplantation is not a life-saving procedure because patients with terminal kidney failure
can be treated with regular dialysis.
Indications for kidney transplantation: Chronic kidney failure of various aetiologies. Patients can be
transplanted after being included in a dialysis program or even before (preemptive transplantation).
KT procedure:
A single kidney is transplanted which is functionally sufficient. The transplant is performed
heterotopically (in a different location than the original kidneys which are usually left in place). After
incision above inquinale ligament the external iliac artery and vein are isolated. The kidney is placed
in the pelvic region and an anastomosis is created to connect the graft's vessels end-to-side with the
recipient's pelvic vessels. The ureter is implanted directly into the urine bladder.
80
Early results of kidney transplants are excellent and it is proven that successful kidney transplants
significantly improve quality of life long-term survival and reduce healthcare costs compared to
dialysis treatment.
Long-term Post-Transplant Care
After all organ transplants patients must take lifelong immunosuppressive therapy to prevent graft
rejection. However, this therapy carries certain complications such as hypertension, diabetes,
impaired kidney function, obesity and hypercholesterolemia. Therefore, it is essential to regularly
monitor the levels of immunosuppressive drugs and combine different medications to minimize their
side effects.
For early diagnosis of rejection biopsies are necessary (tacking of several small pieces of the tissue).
In the long-term follow-up the patients are in risks of infection, chronic rejection (manifesting
differently in each organ) a higher incidence of tumours and the side effects of chronic
immunosuppressive therapy.
Specific postoperative monitoring:
For heart transplants, regular endomyocardial biopsies are performed, taking samples from the right
ventricle. Coronary angiography is done annually.
For lung transplants, regular transbronchial biopsies are performed.
For liver transplants, biopsies are only done if acute rejection is suspected. The most common
postoperative complications involve bile ducts, including anastomotic leaks and strictures.
For kidney transplants, biopsies are also only done when rejection is suspected. The most common
complication is an anastomotic leak between the ureter and the urine bladder.
81
Fig. 1 After excision of the heart with preservation of long stumps of the aorta, pulmonary artery and
both vena cava. The posterior part of the left atrium is also preserved. The new heart after the bicaval
technique of transplantation
82
ORGAN DONORS, SURGICAL TECHNIQUE OF ORGAN PROCUREMENT (27)
Fila Petr, Němec Petr
The issue of organ donation in the Czech Republic is governed by Act No. 285/2022 Sb. According
to this law, every person can be considered an organ donor unless they have expressed objection to
organ donation during their lifetime (presumed consent principle). Objection can be made by for
example registering in the National Registry of Persons Objecting to Postmortem Tissue and Organ
Donation.
The number of donors in all countries worldwide is lower than the number of transplants needed
which is why there is an effort to maximize the use of all patients with a hopeless prognosis who
meet the criteria for donation. The process of donation and transplantation is concentrated in
transplantation centres. There are seven in the Czech Republic. Each centre has its designated region
where it conducts these activities.
Organ donors can be divided into two groups:
Living Donors
From a living donor, either a paired organ (kidney) or part of another organ with regenerative ability
(liver segments or lobe) can be taken. The donor must undergo a thorough examination to ensure that
their health will not be harmed. The donor must give a consent to the procedure.
The main advantages of transplantation from a living donor include that both the procurement and
transplant can be planned as elective procedure, with both the donor and recipient in optimal
condition and minimal cold ischemia. This results in better long-term transplant outcomes.
Deceased Donors
Organs can be procured from a deceased donor if their death has been confirmed. Death is
determined by two independent physicians based on the irreversible cessation of circulation or the
irreversible cessation of brain function, including the brainstem.
Donors after Circulatory Death (DCD)
Donation follows cardiopulmonary failure under defined conditions. Patients with a hopeless
prognosis receive palliative care. If cardiac arrest occurs (two of the three criteria must be met:
asystole on ECG, flat arterial curve or a stopped heart on echocardiographic examination) a fiveminute
no-touch interval follows. Afterward the time of death is recorded and organ procurement can
begin.
Donors after Brain Death (DBD)
83
A donor is a patient who has suffered irreversible brain injury, resulting in coma and loss of
brainstem reflexes.
Before inclusion in the donor program, potentially reversible causes (intoxication, drug effects, and
metabolic imbalances) must be ruled out.
This irreversible loss of consciousness is considered as brain death which is regarded as the
biological death of the person.
Brain death must be confirmed through:
Clinical examination – Neurological examination of central nerves (demonstrating areflexia above
C1), apnoea test
One of imaging methods – Cerebral angiography, perfusion scintigraphy, evoked potentials, or
transcranial Doppler ultrasound.
Once all these conditions are met, the patient can be considered brain-dead and included in the donor
program. Brain death presents challenges such as hemodynamic instability, thermoregulatory issues,
metabolic and endocrine changes, which need to be managed during intensive care.
Transplant Coordination Centre (KST)
KST is an independent body responsible for coordinating donation and transplantation, maintaining
legally mandated registries, identifying the most suitable recipients for procured organs, and ensuring
international cooperation and coordination.
Contraindications for Donation
Medical: Sepsis, HIV-positive, systemic viral infection, most cancers
Non-medical: Patient objection, family objection (even though this type of objection is not legally
recognized, it is generally respected)
Types of Donors:
Ideal Donor: Under 60 years of age, with no organ diseases.
Marginal Donor: Over 60 years old and/or with mild clinical or laboratory abnormalities. This type
of donor has become more common due to the general population's health status. The risks and
benefits of transplantation from such donors must be carefully weighed.
Organ Procurement
84
Due to the larger number of patients on waiting lists than available donors there is a push to always
perform multi-organ procurement where all viable organs from the donor are collected.
Multi-organ procurement is logistically complex procedure as it involves several surgical teams from
different hospitals. Close cooperation with the anaesthesiologist is essential to ensure optimal organ
quality.
Surgical Technique:
In multi-organ procurement, an incision is made from the jugular to the symphysis. The abdominal
and thoracic cavities are assessed macroscopically to exclude any unexpected pathological findings
(e.g., tumour). All the organs being removed are partially isolated and their macroscopic appearance
is assessed. After administering heparin, large vessels (abdominal aorta for abdominal organs,
ascending aorta for the heart, pulmonary artery for the lungs) are cannulated. Clamps are applied to
these vessels to stop blood flow to the organs which are then flushed with cold preservation solution
and externally cooled with ice slush. Once adequately flushed the organs are sequentially explanted
in this order: heart, lungs, liver, pancreas and kidneys.
Between Procurement and Transplantation, Organs Are Stored:
- In a cold solution
- Connected to a perfusion device (hypothermic or normothermic perfusion). The advantage of
this method is better organ quality, though it is logistically and economically demanding.
Time Intervals:
For successful transplantation, it is crucial to minimize the time between organ procurement and
transplantation. Two key intervals are monitored:
Cold Ischemic time: The time from the start of organ perfusion with preservation solution to the
restoration of blood flow in the organ (maximum tolerated time varies by organ—shortest for the
heart at 2-4 hours, longest for the kidney at 18-24 hours).
Warm Ischemic time: The time from cessation of blood flow in the organ to the start of perfusion
with preservation solution. Ideally, this is zero; in living donor procedures and DCD, it is acceptable
up to 30-60 minutes.
Waiting List
Each patient waiting for a transplant must be placed on a waiting list in one of two categories:
Elective: A patient in a stable condition waiting at home
Urgent: A patient in critical condition requiring hospitalization. Criteria for urgent status vary by
organ. For example, a patient waiting for a heart transplant must be on intravenous therapy
(inotropes, diuretics) or have mechanical heart support.
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Organ Allocation (Matching Donor and Recipient)
Organ allocation is a process that considers many factors and must be entirely transparent, based
solely on medical criteria. Allocation criteria differ for each organ.
Factors considered include blood type (identical or at least compatible), body weight (for example,
donor and recipient should be of similar build for heart or lung transplants), recipient’s clinical
condition (urgent or elective status; urgent status always takes precedence), and waiting time on the
list. For kidneys, HLA matching is also considered.
Once an organ is allocated to a specific patient, the transplantation procedure begins. According to
law, transplantation centres must respect the anonymity between the donor and recipient.
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87
CONGENITAL DEFECTS OF THE UROGENITAL TRACT (29)
Husár Matej
Congenital defects of the genitourinary system are most often the result of a defect in the interaction
between the developing ureteric bud and the metanephrogenic blastema or a defective ascent of the
kidneys. A distinction is made between upper and lower urinary tract anomalies.
Upper urinary tract anomalies
- Numerical abnormalities: supernumerary kidney, unilateral renal agenesis, bilateral renal agenesis
(incompatible with life)
- Disorders of kidney migration: ectopic kidney (pelvic/lumbar dystopia), crossed ectopia
- Fusion anomalies of the kidney: most commonly horseshoe kidney (ren arcuatus)
- Rotational renal anomalies (malrotation)
Many upper urinary tract anomalies are asymptomatic and their detection is incidental. In
symptomatic defects, the defect can results is obstructive or reflux uropathy. The severity of renal
involvement depends on the function, obstruction of urinary outflow, risk of infection, vesicoureteral
reflux and formation of stones. Ultrasonography is used in the diagnosis, which can detect some
congenital renal defects prenatally. Ultrasonography is used not only for diagnosis but also for
monitoring the dynamics the obstruction. In case of diagnostic discrepancy, MRI or CT can be used.
Dynamic scintigraphy is used to determine renal functions in obstructive uropathies and static
scintigraphy in reflux uropathies.
The most common obstructive uropathy in childhood is hydronephrosis that is an obstruction in the
pyeloureteral junction. If the obstruction is urodynamically significant, pyeloplasty is performed resection
of the pyeloureteral junction and anastomosis of the ureter to the renal pelvis.
Hydronephrosis may manifest clinically in children as pyelonephritis, usually detected prenatally on
ultrasonography. If hydronephrosis arises suddenly, it manifests as renal colic, which is most
commonly seen in nephrolithiasis.
The second common nephropathic defect is vesicoureteral reflux, It is the return of urine from the
bladder to the ureters and the hollow system of the kidneys. We distinguish between primary and
secondary reflux. Primary reflux occurs on the basis of short course of the ureter through the bladder
wall and ectopic location of the ureteral orifice, which is usually gaping. Secondary reflux is caused
by bladder dysfunction or subvesical obstruction (posterior urethral valve, urethral stricture...). In
children, the reflux is most often detected after the first pyelonephritis or as an incidental finding on
ultrasound as dilatation of the ureters and the hollow renal system. Currently, the only reliable
method to confirm vesicoureteral reflux is micturition cystourethrography. Treatment is initiated
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with antibiotic prophylaxis medication. Another option is minimally invasive endoscopic antireflux
injection. In limited indications, ureteral reimplantation is performed, where the ureters are
submucosally reimplanted to ensure antireflux positioning of the ureters in the bladder wall. The
indication for each therapy depends on several factors, namely the function of the kidney, the degree
of reflux, the effect of antibiotic prophylaxis and the cooperation of the family in the treatment of the
child.
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MALE INFERTILITY AND SEXUAL DYSFUNCTION (32)
Kašík Marek
Infertility
Infertility is defined by the inability of a sexually active, non-contraceptive couple to achieve
spontaneous pregnancy within twelve months. It affects 12-15% of couples worldwide, the male
factor is responsible in half of the cases either alone, or associated with infertility issues of woman as
well. In majority of the cases it is connected to pathologic semen analysis. Physiologic parameters
are shown in table 1. Asthenozoospermia refers to low sperm motility or an insufficient amount of
sperm with overall progressive movement. Teratozoospermia is defined as less than 4% of sperm
with normal morphology. Oligospermia refers to low sperm count and cryptozoospermia is a
condition where spermatozoa are detected only after centrifugation of semen. Azoospermia is
defined as the absence of sperm in ejaculate. These pathological conditions are sometimes occurring
at the same time and termed OAT syndrome (oligoasthenoteratozoospermia). Etiology can be
congenital, acquired or idiopathic. The last one constitutes around 30-40% of cases. Hypogonadism
refers to a condition that is characterized by the diminished levels of testosterone and is one of the
causes of infertility. Hypogonadism can be divided into primary, in which testicles are affected, and
secondary, which is caused by a disorder of the hypothalamus or pituitary gland. Causes of primary
and secondary hypogonadism are summarized in tables 1 and 2, respectively.
Varicocele
Varicocele refers to dilation of veins of the pampiniform venous plexus accompanied by some
degree of reflux of blood in the scrotum. It is not an uncommon finding, as much as 20% of men are
affected. Varicocele occurs typically on the left side, less commonly on the both sides. Isolated
right-sided varicocele is rare – the incidence is around 2%. This condition is caused by venous
insufficiency and so called nutcracker phenomenon. Secondary varicocele forms as a result of
compression of veins that are responsible for venous drainage from the scrotum or vein blockage
due to thrombus associated with kidney tumour. This type of varicocele occurs on the both side with
the same incidence rate. Diagnostic work-up includes physical examination, the patient must be
examined in the standing position. We can differentiate 3 grades of varicocele. Varicocele is usually
asymptomatic, although it may cause discomfort and pain in the scrotum propagating to lower
abdomen. Scrotal ultrasound examines size of the testes, dilated veins and presence of reflux during
Valsalva maneuver. Furthermore, semen analysis is done, as varicocele can be associated with
infertility.
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Cryptorchidism
Cryptorchidism is the most common congenital anomaly of male genitalia; the incidence is
around 1% at the age of 1. Approximately 50% of patients with bilateral cryptorchidism are
infertile.
Azoospermia
Azoospermia, defined as the absence of sperm in ejaculate. It is be divided into obstructive and nonobstructive.
Obstructive azoospermia is less common (15-20% of cases), laboratory results show
normal levels of FSH, LH and testosterone. Testes are a normal size and the epididymis is usually
enlarged. The site of obstruction is within the testes or epididymis, ductus deferens can also be
obstructed (post-vasectomy, cystic fibrosis or iatrogenic injury during surgery of inguinal hernia) as
well as ejaculatory ducts. Non-obstructive azoospermia is a complex pathological condition with
multifactorial etiology involving genetic disorders, hormonal imbalances or scrotal injury.
Diagnostics and therapy
Examination includes inspection of the patient’s body (absence of body hair, gynecomastia etc.) and
external genitalia. We evaluate the size of the testes and epididymis and assess any pathological
conditions by palpation (varicocele, absence of ductus deferens). Doppler ultrasonography is used to
examine the scrotum, additionally, we perform a transrectal ultrasonography of the prostate and the
seminal vesicles. Laboratory examination includes hormone tests and a semen culture test.
Antibiotic therapy is warranted in case of proven infection. In selected cases hormonal therapy is
indicated. In patients with hypergonadotropic hypogonadism we use human chorionic gonadotropin
usually in combination with recombinant FSH. Surgical therapy includes reconstructive surgery and
sperm retrieval procedures. MESA (microsurgical epididymal sperm aspiration) is indicated in case
of obstruction of ductus deferens or epididymis, TESE (testicular sperm extraction) is performed in
case of intratesticular obstruction. Acquired sperm is subsequently used for techniques of
assisted reproduction. Reconstructive procedures include vasovasostomy, vasoepididymostomy and
transurethral resection of ejaculatory ducts (TURED). Varicocele is usually managed
conservatively. Surgery is recommended only in selected cases - clear indications for
varicocelectomy are infertility, testicular hypotrophy or symptomatic varicocele. Dilated veins of
the pampiniform plexus or the internal spermatic vein are ligated during the surgery. Inguinal or
subinguinal microsurgical lymphatic and artery sparing varicocelectomy is considered ‘gold
standard’ treatment. Suprainguinal open or laparoscopic surgery is also feasible. Sparing the
lymphatic vessels lowers the risk of postoperative
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hydrocele. Other treatment option is sclero-embolisation of the internal spermatic vein performed by
an interventional radiologist.
Sexual dysfunction
Erectile dysfunction
Erectile dysfunction (ED) is defined as an inability to attain or sustain an erection long enough for
satisfactory sexual intercourse. It occurs in as much as 50% of men above 50 years old, although it
can affect younger men as well. Erectile dysfunction can develop gradually or all of a sudden.
Recognized risk factors are stress, depression, obesity, lack of physical activity, smoking, drug
abuse, atherosclerosis, diabetes, liver disease and pelvic surgery (radical prostatectomy).
Oftentimes, ED can be an adverse effect of certain medications. Loss of erectile function can be a
symptom of other illnesses, particularly cardiovascular diseases.
Diagnostic work-up relies on the patient´s history, inquiring about nighttime and morning erections,
rigidity and duration of erections, issues with ejaculation or orgasm. Furthermore, it is necessary to
assess signs of hypotestosteronism and the mental health of a patient. The presence of morning
erections and normal rigidity during masturbation may help to distinguish organic from psychogenic
etiology. We examine external genitalia – testes size, presence of pubic hair, pathological conditions
such as Peyronie´s disease etc. A crucial laboratory examination is testing the testosterone level,
lipid panel and fasting glycaemia. Moreover, the standardized IIEF questionnaire is used
(international index of erectile function).
The first stage of treating erectile dysfunction should involve having a healthy active lifestyle and
a healthy diet. Testosterone replacement therapy is indicated if hypogonadism is detected.
Untreated prostate cancer is a contraindication to testosterone supplementation. Patients with
mental health issues can be referred to a psychologist or sex therapist. Inhibitors of
phosphodiesterase 5 (PDE5-I) are used as first line treatment of erectile dysfunction. They induce
relaxation of smooth muscle in the corpora cavernosa, resulting in increased penile arterial blood
flow. Different PDE5-I agents, namely sildenafil (first one discovered), tadalafil, vardenafil and
avanafil, differ in onset and duration of action. They are taken on-demand, before planned sexual
intercourse. Alternatively, tadalafil can be taken daily in lower dose. Common side effects include
headaches, flushing and nasal congestion. Vacuum erector device is another treatment option for
men with erectile dysfunction. After using the device, constriction ring can be used to maintain the
erection. The ring should not be placed for longer than 30 minutes. Intracavernosal alprostadil
injection is a second-line treatment
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after failure of PDE5-I. Erection occurs 5-15 minutes after administration and duration depends on
the dose. Complications include pain, hematoma, fibrosis of corpora cavernosa, prolonged erection
and even priapism. Penile implants represent last-line treatment of ED, they can be classified into
semi-rigid and inflatable prosthesis.
Peyronie´s disease
Peyronie´s disease, also called induratio penis plastica, is a disorder that may cause difficult or
impossible sexual intercourse. It is characterized by occurrence of fibrous calcified plaques in the
tunica albuginea, leading to curvature, shortening of the penis and erectile dysfunction. Precise
underlying cause in unknown. Repeated microtrauma of tunica albuginea is thought to play role in
the pathogenesis. There is an association with other fibromatous disorder such as Dupuytren’s
contracture. Peak incidence is around 55-60 years of age. Disease is divided into two stages – acute
and chronic. . The first is the active (acute) stage characterized by painful erections and changing of
the deformity. The second stage is the stable (chronic) phase, in which the deformity is stabilized
and pain during erection disappears. Diagnosis is determined by patient’s history (onset of
symptoms, painful erection, bending or shortening of the penis) and physical examination. Penile
examination is done to evaluate the presence of palpable nodule or plaque. An objective assessment
of penile curvature during erection is necessary, this is obtained by a home (self) photography in two
planes. Doppler ultrasonography is used to assess localization, size and number of plaques.
Conservative management is feasible in patients who are able to have sexual intercourse. Use of oral
treatment (vitamin E, colchicine, potassium para-aminobenzoate) is controversial as there is no
convincing evidence about the efficacy. Intralesional treatment allows a localised delivery of a
particular agent directly into the plaque and leads to improvement of the curvature. Steroids, calcium
channel antagonists, clostridium collagenase and interferon α-2b are used. Surgical treatment is
considered if conservative treatment fails.
There are two types of surgical repair: penile shortening and penile lengthening procedures. Penile
shortening procedures include the resection or plication techniques performed on the convex side of
the penis. Penile lengthening procedures are performed on the concave side of the penis using a
graft. Patients with a complex deformity are offered implantation of penile prosthesis. Shock wave
treatment is a novel therapeutic modality for Peyronie´s disease.
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VESICOURETERAL REFLUX, HYDRONEPHROSIS (34)
Kašik Marek, Fedorko Michal
Vesicoureteral reflux
We define vesicoureteral reflux (VUR) as the backflow of urine from the bladder into the ureter, or
up to the collecting system of the kidney. Prevalence of VUR in a healthy pediatric population is not
known, estimates range from 0.4% to 1.8%. In children with a proven urinary tract infection (UTI),
VUR occurs quite often, especially in children with acute pyelonephritis, where it is present in 29-
50% of those affected and its occurrence is inversely proportional to the age of the child. Reflux is
more often diagnosed in girls, on the contrary, prenatal diagnosis of VUR is more common in
newborn boys. In the pathogenesis of VUR, genetic predisposition plays a role, its familial
occurrence is proven in many children, however the mechanism of transmission is not known.
VUR does not show specific symptoms, it is characterized by recurrent UTIs, through reflux of
infected urine, bacteria reach the kidney. Increased backpressure during VUR leads to intrarenal
reflux (IRR), which is the propulsion of urine from the apex of the renal papilla in the pelvis towards
the collecting ducts and kidney parenchyma.
The presence of triads – VUR, IRR and UTI is a high risk for early onset parenchymatous scars in
the kidney and the development of so-called reflux nephropathy. The result of the harmful effect of
reflux on the kidney is the slowing down of its growth with the formation of a "small shrivelled
kidney", in then bilateral impairment with the possibility of developing chronic renal insufficiency.
VUR without UTI usually does not lead to scarring. The first symptom of kidney damage from
reflux can also be hypertension, which is suffered by up to 15% of children with VUR. One of the
dominant signs in infants may be failure to thrive. A rare symptom of reflux can also be bedwetting.
According to the pathophysiology, we distinguish between primary VUR (it arises in case of
congenital insufficiency of the ureterovesical connection) and secondary (occurs during other
pathological changes of the urinary tract, e.g. with subvesical obstruction, UTI, neurogenic
micturition disorders, after trauma or iatrogenic damage, etc.).
The diagnostic method for detecting VUR is classic X-ray voiding cystourethrography
(VCUG), which alone can determine the degree of VUR and should help in differentiation of
primary VUR from secondary. According to the international classification, we recognize 5 grades:
VUR (Fig. 1):
1. Reflux into the lower part of the undilated ureter
2. Reflux into the renal pelvis, which is not dilated.
3. Reflux with mild dilation of ureter and pelvis, the contour of the calyces is preserved
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4. Reflux with significant dilatation of the ureter and pelvis, blunting of the calyces, but they
are still concave
5. Reflux with massive dilatation of the collecting system of the kidney, the calyces are convex
Reflux can be passive, when retrograde urine flow to the kidney occurs when filling the bladder with
contrast material, or active, when VUR appears only during micturition.
Other investigative methods include urethrocystoscopy in boys when subvesical obstruction is
suspected or to evaluate the shape of the ureteral orifices. Urodynamic evaluation is performed in
case of suspicion of more serious dysfunction of the lower urinary tract.
The goal of VUR treatment is to prevent morphological and functional kidney damage, to secure
their normal development and growth, adjust the function of the ureterovesical junction and
eliminate infection.
Today, conservative therapy is mostly recommended - long-term application of prophylactic dosage
of antibacterial drugs. After eradication of the infection, low doses of furantoin or co-trimoxazole are
most often administered prophylactically. This approach is based on the theory of maturation of the
intravesical ureter, which anticipates that maturation of antireflux mechanisms make take up to 12
years. Therefore, in cases of VUR grades I – III spontaneous resolution can be expected, but higher
grades of VUR require surgical treatment. Surgery includes transurethral operations (submucosal
injections, Fig. 2), open operations (antireflux reconstructions) and laparoscopic operations.
Hydronephrosis
Hydronephrosis means dilatation of the excretory system of the kidney, i.e. calyces and pelvis, due to
urinary retention. The extent of dilatation of the pelvicalyceal system (PCS) does not always
correspond to the severity of the obstruction in the upper urinary tract. The etiology may be primary
(congenital) or secondary. Individual causes are listed in Table 1.
Most cases of primary hydronephrosis are asymptomatic and diagnosed during prenatal or postnatal
newborn screening. Less often, the first symptom is acute pyelonephritis, abdominal pain, palpable
resistance in the abdomen or failure to thrive.
The symptomatology of secondary hydronephrosis depends on the cause. As a rule, these symptoms
are nephralgia, hematuria, renal colic, acute pyelonephritis. Recurrent urinary tract infections with
fever, abdominal pain, hematuria and pyuria may also occur. In the case of a solitary kidney, the
symptom may be oliguria or anuria if the obstruction is absolute, as well as in bilateral
hydronephrosis.
Ultrasonography (USG) is the most widely used for diagnosis of hydronephrosis, both prenatal and
postnatal. According to the ultrasound findings, we distinguish 4 grades of hydronephrosis from a
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slightly enlarged pelvis up to significant dilatation of the collecting system with reduction of renal
parenchyma.
Newborns are recommended to be examined at the earliest after 48 hours of life, preferably on the
3rd or 4th day, due to lower hydration and physiological oliguria in the first days of life.
Another examination method is dynamic scintigraphy of the kidneys - mutual comparison of the
functional capacity of the kidneys. It shows the kinetics of an intravenously administered
radiopharmaceutical (MAG3) and its transport through the urinary tract. In case of unclear findings,
obstruction can be confirmed or ruled out by administration of a diuretic (furosemide). Excretory
urography is currently rarely used.
Most primary hydronephrosis tend to resolve spontaneously. Patients undergo repeated USG and
isotope examinations. Surgical treatment is indicated in cases with low relative function (< 35%) of
affected kidneys detected at the first isotope examination, kidneys with extreme dilatation of the PCS
(≥ 50 mm in the anteroposterior dimension) or if during the follow-up the dilatation progresses or the
relative function of the kidney decreases. Furthermore, patients with symptomatic congenital
hydronephrosis (pain, recurrent pyelonephritis, etc.) are also indicated for surgery. The most
common the procedure is pyeloplasty due to obstruction of the ureteropelvic junction. Part of the
renal pelvis, ureteropelvic junction and part of the proximal ureter are removed. The ureter is then
pulled upwards, spatulated and sutured to the remaining part of the renal pelvis. In adulthood, the
method of choice is a laparoscopic or robotic approach. Endoscopic treatment consists of incising the
stenosis with a knife or laser either by antegrade or retrograde approach. The aperistaltic section of
the ureter is managed with reconstructive surgery in childhood. In secondary hydronephrosis, the
management involves eliminating the cause. Acute drainage of the upper urinary tract due to
hydronephrosis can be achieved by introducing a JJ stent or nephrostomy.
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Figure 1 Stages of VUR, source: Kočvara R., Drlík M.: Pediatric urology. Maxdorf. 2023
Primary
hydronephrosis
Obstruction of the ureteropelvic junction
• Stenosis
• compression by an aberrant vessel supplying the lower pole of the
kidney
• high insertion of ureter into renal pelvis
• persistent and fixed fetal folds of the ureter
Vesicoureteral junction obstruction
• aperistaltic juxtavesical section of the ureter
• ureterocele
Vesicoureteral reflux
Secundary
hydronephrosis
Ureterolithiasis
Ureteral stricture and stenosis
Extramural compression of the ureter, e.g. by a tumour
Subvesical obstruction
Table 1
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UROLITHIASIS, RENAL COLIC (33)
Trinh Tuah, Fedorko Michal
1. Epidemiology and risk factors
The lifetime prevalence of urolithiasis ranges from 1% to 15%, varying by age, race, sex and
geographical location (prevalence in the Czech Republic is about 5%). The causes of the formation
and growth of urinary stones are multifactorial and can be divided into internal and external factors.
Internal factors include age, sex, the presence of obesity and genetic influences. Urinary calculi
occur most commonly in male patients of working age however, the occurrence of urolithiasis in
childhood or old age is not rare. External factors may include local climate, season (high prevalence
in summer), low fluid intake, dietary habits and also the work environment (typically in workers in
hot environments).
2. Pathophysiology of stone formation and composition
2.1 Pathophysiology of stone formation
The basic prerequisite for the formation of stones is hypersaturation of urine with lithogenic
substances. Free stone-forming crystals can be detected in most urine samples, and yet the majority
individuals do not form stones. In patients with urolithiasis, there are more crystals of lithogenic
substances in their urine and they have a higher risk of aggregation. The crystal theory of the
formation of urolithiasis has several stages.
- supersaturation is a state where a substance is present in a solution several times more than its
own solubility
- crystal nucleation from supersaturated urine (crystallization)
- crystal growth - increase in volume
- crystal aggregation
Urinary stones consist of a crystalline and a non-crystalline component (the so-called matrix). The
Matrix is composed of organic matter - a combination of mucoproteins, proteins, carbohydrates and
urine inhibitors.
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Citrate inhibits the formation of calcium oxalate and calcium
phosphate stones, especially by forming complexes
with calcium, thereby reducing its availability
Phosphate, pyrophosphate, magnesium bind to oxalates, reducing aggregation and crystal
growth
Nephrocalcin and Tamm-Horsfall
glycoprotein, osteopontin (uropontin)
inhibit the aggregation of calcium oxalate crystals
Tab. 1: examples of crystallization inhibitors
2.2 Composition of urolithiasis
Analysis of the composition of urinary stones is important for further diagnosis and treatment. It is
performed in specialized laboratories, mainly infrared microscopy and polarization spectroscopy are
used. The stones are often of a mixed nature. The most common component of urinary of stones is
calcium. The most common compositions of urinary stones include:
• calcium oxalate – approx. 80%
• calcium phosphate – approx. 22%
• urate – 15-20%
• struvite – 7-10%
2.3 Metabolic disorders related to stone formation
2.3.1 Calcium oxalate and calcium phosphate stones
Hypercalciuria – the most common disorder, we distinguish 3 types
• absorptive (excessive absorption from the intestines)
• renal (excessive losses of calcium through the kidneys)
• resorptive (excessive mobilization of calcium from bones)
• examples of diseases: primary hyperparathyroidism, immobilization, sarcoidosis, hypervitaminosis
D, Cushing's syndrome, treatment with corticoids, hyperthyroidism, multiple myeloma,
malignancies
Hyperoxaluria - causes an increase in urine saturation with calcium oxalate
• primary hyperoxaluria – AR hereditary disease
• enteric hyperoxaluria - e.g. Crohn's disease, chronic pancreatitis, ileal resection
• dietary hyperoxaluria - increased absorption from food rich in oxalates (nuts, chocolate, spinach,
rhubarb)
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Hypocitraturia - citrates reduce the amount of ionized calcium in the urine, thus preventing the
formation of calcium-oxalate complex, occurs in 15-63% of patients with nephrolithiasis
• disease example: distal renal tubular acidosis
Renal tubular acidosis – a disorder of urine acidification, a higher pH causes urine hypersaturation
calcium and phosphate
2.3.2 Urate stones
Hyperuricemia, hyperuricosuria – excess uric acid, low urine pH (5.5 ± 0.4) and low diuresis
increases the formation of urolithiasis
• example of a disease: gout (50% of patients with urate stones have gout), myeloproliferative
disease
2.3.3 Rare types of urolithiasis
• xanthine - the cause is a xanthine oxidase defect, AR hereditary disorder
• cystine - AR hereditary disorder, hypercystinuria
• infectious – magnesium ammonium phosphate (struvite) stones, formed by the action of urease
produced by bacteria, e.g. Proteus mirabilis strain, etc.
3. Renal colic
3.1 Symptoms
Small kidney stones usually asymptomatic, larger stones can cause indeterminate symptoms dull
pain (nephralgia). A renal colic occurs when kidney stones are released into the pelvis and travel to
the ureter. Renal parenchyma do not have pain receptors, kidney pain originates from of the fibrous
capsule of the kidney, which responds to distension and local irritation. The pain is localized to the
area of the ipsilateral costovertebral angle below the 12th rib near the spine. Renal colic is
characterized by sudden, sharp, spasmodic pain in the lumbar region of fluctuating intensity,
pulsating in nature and shooting into the surroundings, with propagation up to the labia or testicles.
Accompanying symptoms may be hematuria (microscopic or macroscopic), dysuria or GIT problems
(nausea, vomiting). Infectious stone occurs in severe complications such as pyonephrosis, septicemia
or perinephritic abscess.
3.2 Diagnosis
Taking a patient history, physical and laboratory examination (urine, blood serum) is crucial. Upon
first contact with the patient, we perform an ultrasound of the kidneys and bladder (or the entire
abdomen). Obstruction of the excretory urinary tract manifests itself as dilatation of the calico-pelvic
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system (hydronephrosis). A non-contrast CT scan of the abdomen and pelvis is the gold standard
for confirming or ruling out urolithiasis. In case of suspected infectious complications associated
with obstruction of the urinary system, abdominal CT with contrast material is indicated.
3.3 Therapy of renal colic and urolithiasis
The basis is the administration of spasmo-analgesics, which relieves the patient of pain. First-line
analgesic agents are non-steroidal anti-inflammatory drugs: metamizole, diclofenac, indomethacin or
ibuprofen. Second-line analgesic agents: opiates (hydromorphine, pentazocine, tramadol).
Conservative (expulsive) treatment can be chosen for small ureterolithiasis (usually up to 5 mm), the
treatment aims to expel the stone by administering alpha-blockers (e.g. tamsulosin) and antiedematous
drugs, it is important to increase fluid intake and exercise. In case of refractory pain, signs
of incipient sepsis, renal failure, obstruction of a solitary kidney or general alteration of the patient's
condition it is necessary to relief the obstruction (introduction of a nephrostomy or double J stent).
Active stone removal means performing an endoscopic procedure, or extracorporeal shock wave
lithotripsy (ESWL). Commonly performed endoscopic procedures are ureteroscopy (flexible or
semi-rigid) and percutaneous nephrolithotripsy. Laparoscopic and open surgery for urolithiasis are
currently rarely performed.
3.4 Prevention of urolithiasis
Primary prevention (prophylaxis) consists in sufficient fluid intake (around 2.5 litres daily),
movement, adherence to the principles of healthy nutrition and lifestyle with an emphasis on limiting
intake of simple sugars, animal proteins and saturated fats. Adequate consumption of dairy products
and foods containing calcium are beneficial (restricted calcium intake leads to an increase in
available intestinal oxalate and subsequent increase in oxalate absorption). Specific pharmacological
prevention (metaphylaxis) is based on the knowledge of the stone composition and the detected
metabolic disorder after assessment. The goal is to prevent recurrence of stones. It is necessary to
monitor metabolic parameters in urine and blood.
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HYDROCELE, EPIDIDYMITIS, ORCHITIS, TESTICULAR TORSION (35)
Morančíková Mária, Fedorko Michal
Hydrocele – fluid collection between parietal and visceral layer of tunica vaginalis.
The typical signs are the enlargement of the scrotum and a feeling of weight or pressure. The
enlargment is gradual and there is no palpable change of the testicle. Hydrocele can be congenital,
caused by patent processus vaginalis leading to a communication between the scrotal and peritoneal
cavity. It usually spontaneously resolves itself within 18 months after birth. Primary hydrocele is
idiopathic and secondary type is associated with other pathological conditions such as epididymitis
or testicular tumour. Hydrocele can be diagnosed by palpation and ultrasonography, it is important to
rule out the presence of a testicular tumor or intestines, therefore ruling out indirect scrotal hernia.
Surgery is a mainstay of therapy. Hydrocelectomy is done under general or spinal anesthesia through
a scrotal incision. The sac is opened, drained, and partially excised and the edges of are sewn
together behind the spermatic cord so that the hydrocele does not reoccur.
Epididymitis – inflammation of epididymis
Clinical hallmarks of epididymitis are pain, swelling, and higher temperature of the epididymis, but
the condition can spread to the testicle and affect the whole hemiscrotum. It is usually not possible to
differentiate the testis and epididymis during palpation if the whole hemiscrotum is inflamed.
Laboratory results show CRP and white blood cell count elevation, there may be a finding of
leukocytes in urinary sediment and positive urine culture. The route of infection is the ascent of
pathogens from the lower urinary tract. The most common pathogens are Chlamydia trachomatis
(accounts for sexual transmission in younger men) and E. coli (in older men related to incomplete
voiding due to prostate enlargement and the spread of infection from the urinary bladder). Excluding
testicular torsion or tumor is of utmost importance. The use of Doppler ultrasonography is essential.
The patient has to be inquired about risky sexual encounters. This condition can be preceded by
urethritis, which manifests as dysuria, a burning sensation in the urethra (even between voidings),
and urethral discharge. The main focus in elderly men is on voiding symptoms, which usually
uncovers some lower urinary tract symptoms or dysuria before the epididymitis. Antimicrobial
therapy should be chosen according to the most anticipated pathogen. If there is suspicion of Ch.
trachomatis or Mycoplasma genitalium infection, doxycycline is the antibiotic of the first choice. In
the case of gonorrhea, parenteral application of third-generation cephalosporine is an effective
treatment. If inpatient treatment is necessary, parenteral administration of aminopenicillin with
aminoglycoside is the most appropriate therapy. Treatment includes placement of a suprapubic
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catheter if high post-void residual urine is detected. Sexual abstinence is necessary until the
completion of treatment.
Orchitis – inflammation of the testicle
Isolated orchitis is relatively rare. In most cases, it is accompanied by a concurrent infection of the
epididymis. This condition is referred to as orchiepidymitis. It is typically bacterial in origin, and its
signs, symptoms, and management are the same as epididymitis. Isolated infection of the testicles is
a complication of a viral mumps infection and it affects 20-30% of men with mumps after puberty.
In this case, the inflammation is usually bilateral, associated with malaise, fever, preauricular
tenderness, and palpable swelling of the scrotum. Ultrasonography of the scrotum is necessary in all
cases to rule out a testicular tumor or torsion. Orchitis is managed conservatively, treatment is
symptomatic and includes bed rest, local cooling, and scrotal support.
Testicular torsion
Testicular torsion along the axis of a spermatic cord leads to venous and arterial occlusion, with
subsequent ischemia and infarction. It occurs mainly in the neonatal period and during puberty. It is
caused by the contraction of the cremasteric muscle, which is bound to the spermatic cord. Its spasm
can occur during sports, other physical activity, even getting up from a bed, or during sleep. The
affected testis is usually twisted medially. Predisposing conditions are cryptorchidism, proximal
attachment of tunica vaginalis on a spermatic cord, long mesorchium, or insufficient gubernacular
fixation of testis in a scrotum. It is crucial to take action within 6 hours of the onset of symptoms.
Irreversible changes in the testicle start to develop after 6 hours, which strongly reduces the
probability of saving the affected testicle. The sudden onset of strong testicular pain and swelling are
typical symptoms. Pain can propagate to the groin or lower abdomen, and is usually accompanied by
nausea and vomiting. It is therefore necessary to examine the genitals in male patients with lower
abdominal pain. There is no dysuria or fever. Upon physical inspection, there is visible asymmetric
swelling of the scrotum, with or without skin erythema. Palpation of the affected testicle is
extremely painful and the testicle itself lays higher in the scrotum (Brunzel sign). Depending on the
degree of torsion, the testicle can change its original vertical axis to horizontal. The cremasteric
reflex is almost always absent. Elevation of the testis does not relieve the pain as in the case of
epididymitis (Prehn sign). Laboratory findings in urine sediment are normal. The absence of blood
perfusion of the affected testicle on the scrotal Doppler ultrasonography test is the most important
finding in diagnostic work-up. It is useful to compare perfusion on both sides. Besides this, an
ultrasound scan can detect other pathology, e.g. hydrocele, scrotal hernia, tumor, or torsion of the
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appendix testis. Immediate scrotal explorative surgery is required to untwist the testicle and assess
its vitality. Before surgery, manual detorsion may be attempted (with mediolateral rotation) and, if
successful, it leads to immediate pain relief. However, even in this case surgery is mandatory. The
highest chance for testicle salvage is when the surgery is performed within 6 hours after onset of the
symptoms. During surgery, we evaluate the perfusion and vitality of the testicle, in case of torsion it
is of livid or even black color. After making sure the perfusion is normal again (it appears as a colour
change), we perform orchidopexy, which fixates the testicle to the inner scrotal layer to prevent a
recurrence. The contralateral testicle is fixated as well in the same time or as a secondary surgery
later. In a case of necrosis, the colour of a testicle after detorsion remains black, orchiectomy is
performed as well as orchidopexy of a contralateral testicle.
Torsion of an appendix testis
Testicular and epididymal appendices are small rudimental residues of a Müllerian duct. They
usually measure just a few millimeters, but in the case of longer peduncles, there is a possibility of
their torsion as well. Clinically there is not much difference from testicular torsion, as there is also
acute onset of pain. The swollen appendix is usually palpable by the upper pole of a testicle and its
ischemia can be visible through the skin as a „blue-dot sign“. This condition, although it does not
pose a risk for testicular vitality, is often hard to differentiate from a testicular torsion. Doppler
ultrasonography shows normal testicular perfusion with hypervascularization of an appendix, which
is usually clearly visible due to edema. Ischemia of appendix leads to atrophy over time. Because of
frequent uncertainty about torsion of the testicle, exploration surgery is often inevitable. The necrotic
appendix is then excised. If the diagnosis is clear and the pain is moderate, management can be
conservative with scrotal cooling and pain relief with NSAID administration.
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BENIGN PROSTATIC HYPERPLASIA (30)
Wasserbauer Roman, Fedorko, Michal
Benign prostatic hyperplasia (BPH) is the most common benign condition that affects men as they
age. Hyperplasia of predominantly stromal cells of the prostate leads to the diverse set of symptoms
called LUTS (lower urinary tract symptoms). These symptoms are associated with a worsened
quality of life. The incidence is increasing with age. At the age of 65, about 30% of men have a
worse quality of life and this amount doubles every decade. This progressive disease is characterized
by decreased flow of urine, increased post-void residual urine, enlarged prostate and LUTS.
Terminology:
- benign prostatic enlargement (BPE) – increased size of the prostate due to
BPH
- bladder outlet obstruction (BOO) – decreased flow of urine without specific reason
- benign prostatic obstruction (BPO) – obstruction caused by BPH
Etiology:
Increasing age and the presence of androgens (testosterone) definitely plays a role, but etiology
seems to be multifactorial. Other presumed causes include an increased amount of prostatic stem
cells, clonal expansion of proliferating cells, growth reactivation trough embryonic induction and the
effect of growth factors.
Pathophysiology:
BPH is a histologic diagnosis defined as an increase in the total number of stromal and glandular
epithelial cells within the transition zone of the prostate gland. Hyperplasia is induced by the
presence of androgens during puberty and then later in life. Men with defective androgen production
or boys castrated before puberty never develop BPH. Growth occurs in the periurethral transition
zone of the prostate and leads to compression of the adjacent zone towards the capsule. Prostatic
hyperplasia leads not only to BPE, BOO and LUTS, but also to the development of bladder
dysfunction and urinary retention (acute or chronic). The mechanism of subvesical obstruction due to
BPH involves two different components: mechanic (compression of the urethra by enlarged prostate)
and dynamic (increased smooth muscle tone). There are secondary changes of detrusor muscle due to
subvesical obstruction and this, alongside with age and altered nervous system function, leads to
worse LUTS and complications associated with BPH.
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Diagnostics:
Symptomatology - there are various lower urinary track symptoms (LUTS):
- obstructive symptoms – weak stream, straining, hesitancy, intermittent stream, terminal
dribbling, incomplete voiding, urinary retention, overflow incontinence
- irritative symptoms - urgency, frequency, nocturia, urge incontinence
Urinalysis
IPSS (international prostate symptom score): questionnaire consisting of 7 questions evaluating
how bothersome are urinary symptoms, 8th
question enquires about quality of life
DRV (digital rectal examination): assessment of size, shape, symmetry, tenderness, consistency,
palpable nodules and possibly extracapsular extension
PSA: diagnostics and follow-up of patients with prostate cancer
Post-void residual urine (PVR): the amount of urine retained in the bladder after voiding, measured
by catheterization or ultrasonography
Uroflowmetry (UFM): measurement of urine flow during urination ,evaluating maximum flow rate
and other parameters, voided volume of at least 150ml is required for valid results
Pressure-flow studies: urodynamic invasive examination allowing more detailed assessment of
bladder function and evaluating bladder outlet obstruction
Transabdominal ultrasound: measurement of prostate size, configuration, post-void residual urine,
examination of upper urinary tract. Transrectal ultrasound: more accurate measurement of prostate
size. It may reveal suspicious prostatic lesions.
Endoscopy: diagnostics of other causes of subvesical obstruction or hematuria (possibility of a
bladder tumor)
Therapy:
Watchful waiting (WW): it can be offered to men with mild or moderate LUTS, that are minimally
troubled by their symptoms. In 85% of cases, men are clinically stable for one year, however,
progression occurs in 65% of cases over a period of five years. WW includes education, calming
down the patient, follow-up and drinking enough fluids.
Pharmacotherapy:
- alpha-1 blockers: by antagonizing the effect of endogenous catecholamine on smooth
muscle of the prostate and bladder neck they induce relaxation of prostatic muscle tone and therefore
effect dynamic component of subvesical obstruction. They are offered to men with moderate to
severe symptoms. These medications may cause retrograde ejaculation as an adverse effect.
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- 5-alfa reductase inhibitors: inhibition of testosterone to dihydrotestosterone leads to
apoptosis and results in reduction of prostate size as well as lowered PSA levels.
They are suitable for men with moderate to severe symptoms and prostate size at least 40ml. Full
effect can be observed after 6 months from the onset of treatment. Low libido and erectile
dysfunction are the most notable adverse effects.
- antimuscarinic drugs: block the effect of acetylcholine on the muscarinic receptors, thereby
reducing detrusor hyperactivity
- combination therapy: used for patients who complain of persisting LUTS despite
monotherapy, overall effect of pharmacotherapy is increased in combination therapy
- phytotherapy: use of herbal extracts, that have anti-inflammatory, anti-androgenic or
estrogenic effect, effectivity was not usually proven in vivo and mechanism of action is unclear,
nevertheless, some patients benefit from this therapy
Surgical therapy: indications are LUTS refractory to pharmacotherapy, urinary retention, recurrent
urinary tract infections, increased post-void urinary volume, recurrent hematuria, bladder stones,
renal insufficiency caused by BPH
- TURP (transurethral prostate resection): first described in 1932, using monopolar or
bipolar resectoscope prostatic tissue of transitional zone is resected. Long-term efficacy and safety of
this surgery is evidence-based and it is considered ‘gold standard’ surgical treatment of BHP in
patients with prostate up to 70g. Possible complications include bleeding, TUR syndrome (caused by
absorption of irrigation fluid through blood vessels, does not occur when bipolar resectoscope is
used), urinary retention or urinary tract infection.
- TUIP (transurethral prostate incision ): this procedure is used in patients with prostate size
smaller than 30g, bladder neck is incised using incision knife, removing obstruction at bladder outlet
obstruction is removed. Figure 1
- Open prostatectomy: the oldest surgical method for treatment of BPH, ideal for patients
with prostate larger than 80g. It starts with suprapubic midline incision, after dissection, the bladder
wall is revealed and incised, subsequently using index finger prostatic adenomas are separated from
the capsule and removed. This method is proven to have long term effectiveness. Figure 2
- HoLEP: transurethral procedure that uses holmium laser fiber (wavelength 2140nm),
enabling precise incision, dissection and resection. Adenomas are removed as a whole, then moved
to bladder cavity and evacuated using morcellator. It is an alternative to open prostatectomy. Other
type of laser, such as a thulium laser, can be used.
- Mini-invasive methods: procedures done in local anesthesia indicated in patients with
smaller prostate size, high-risk patients or young patients who wish to avoid possible complications
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such as erectile dysfunction or incontinence. Another currently used technique is called Rezum, it
works by inserting water vapor into the prostate and causing coagulation necrosis with subsequent
absorption of adenomatous tissue. Furthermore, a method called Urolift (prostatic urethral lift) uses
an implant that is permanently inserted in prostatic urethra and pushes the prostate lobes towards
capsule. HIFU (high-intensity focused ultrasound), TUMT (transurethral microwave thermotherapy),
or aquablation are other surgical treatment options worth mentioning.
Figure 1: transurethral incision of the prostate (source: Fedorko, 2020)
Figure 2: Open prostatectomy (source: Fedorko, 2020)
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UROGENITAL TUMORS (31)
Staník Michal
I. PROSTATE CANCER
Prostate cancer (PCa) is the most common solid tumour in men and the second leading cause of
cancer-related death, following lung cancer. Risk factors include the presence of male sex hormones
and a family history of PCa. The incidence of PCa increases with age, being relatively rare in men
under 50.
Pathology
The most common malignant tumour of the prostate is adenocarcinoma (90%). Less common
tumours include neuroendocrine carcinoma, which has a significantly worse prognosis and is often
resistant to hormone therapy. Unlike other solid tumours where tumour grading is used, PCa is
assessed based on the architectural disruption of the prostate glands, using a 1-5 scale known as the
Gleason grade. The two most prevalent Gleason grades observed in a tumour are combined to create
a Gleason score ranging from 6 to 10, which reflects the tumour's aggressiveness (see Table 1). For
simplification, the Gleason score is expressed as the ISUP (International Society of Urological
Pathology) grade, which ranges from 1 to 5. ISUP grade 1 indicates an indolent, slow-growing
tumour, while ISUP grades 4-5 represent the most aggressive forms of the disease.
Gleason score ISUP grade Risk groups
2-6 1 Low-risk
7 (3+4) 2 Intermediate-risk
7 (4+3) 3
8 4 High-risk
9-10 5
Table 1 Comparison of Gleason score classification, ISUP grading, and risk group classification for
prostate cancer
Clinical manifestation
Early stages of PCa are most often asymptomatic. Urinary symptoms such as dysuria, urgency, and
obstructive voiding are nonspecific and can be mistaken for benign prostatic hyperplasia. In locally
advanced stages, symptoms may arise from tumour infiltration into surrounding tissues, causing
lower urinary tract symptoms, pelvic pain, or hematuria. In metastatic disease, bone pain and
pathological fractures are common due to bone metastases. Spinal cord compression can lead to
neurological symptoms that require urgent intervention. Other nonspecific signs include weight loss
and cachexia.
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Diagnosis
The main diagnostic tools include digital rectal examination (DRE), prostate-specific antigen (PSA),
prostate MRI, and subsequent prostate biopsy. DRE is performed on every patient, although it only
detects around 20% of PCa cases. With a threshold of 3 ng/mL, PSA testing has a high sensitivity for
identifying men at risk for PCa. In men with elevated PSA, pre-biopsy MRI reduces unnecessary
biopsies and enhances the detection of high-grade tumours while minimising the identification of
indolent cancer. Prostate biopsy remains necessary for histological confirmation of PCa. Biopsy
methods include transrectal or transperineal ultrasound-guided biopsies and MRI-targeted biopsies,
with the latter improving accuracy by focusing on MRI-detected lesions. A CT scan of the abdomen
and pelvis and bone scintigraphy are performed to assess for metastatic spread (the lymph nodes and
bones).
Early detection and screening
PCa screening based on PSA testing can reduce mortality by identifying cancer at an early stage
when treatment is more effective. However, it also poses risks of overdiagnosis, detecting cancers
that may not cause harm (indolent cancer), and overtreatment.
Treatment
For localised prostate cancer, treatment options include:
1. Active surveillance - recommended for men with low-risk, indolent tumours. It involves regular
monitoring with PSA, DRE, and repeat MRI and biopsies.
2. Radical prostatectomy – most often performed robotically, involving complete removal of the
prostate gland and seminal vesicles (in men with intermediate- to high-risk PCa).
3. Radiation therapy - external beam radiation or brachytherapy (implanting radioactive seeds). It
can be used alone or in combination with hormone therapy for higher-risk cases.
Metastatic PCa often initially responds to hormone deprivation therapies that lower androgen levels.
However, over time, the disease can progress from a hormone-sensitive state to castrationresistant
prostate cancer (CRPC), marked by continued cancer progression despite low levels of
circulating androgens. The treatment approaches include:
1. Androgen Deprivation Therapy (ADT): It can be achieved through surgical castration
(orchiectomy) or medical options, including luteinising hormone-releasing hormone (LHRH)
agonists/antagonists and anti-androgens.
2. Chemotherapy: Chemotherapy such as docetaxel or cabazitaxel may be used for aggressive
disease.
3. Next-Generation Hormonal Therapies: Drugs like enzalutamide and abiraterone are used
to further suppress androgen signalling in combination with ADT.
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II. KIDNEY CANCER
Kidney cancer accounts for about 2-3% of adult cancers worldwide. It is more common in men than
women, typically diagnosed between ages 50-70. Risk factors include smoking, obesity,
hypertension, and family history.
Pathology
The most frequent benign renal tumours are papillary adenomas, renal oncocytomas and
angiomyolipomas. Renal cell carcinoma (RCC) is the most common malignant tumour, comprising
subtypes such as clear cell (70%), papillary (15%), and chromophobe (5%).
Clinical manifestation
In the early stages, RCC is often asymptomatic and discovered incidentally during imaging for other
conditions. The classic triad in advanced cases includes hematuria, flank pain, and a palpable
abdominal mass. Other symptoms can include unexplained weight loss, fever, and fatigue.
Paraneoplastic syndromes include hypercalcemia or anaemia.
Diagnosis
Suspicion for RCC usually arises from an ultrasound examination. To confirm the diagnosis, the
standard imaging tests are a CT scan of the abdomen or an MRI. A biopsy is rarely done, typically
only if thermal ablation is considered or in metastatic settings before systemic treatment.
Additionally, a CT scan of the thorax is used to rule out pulmonary metastases.
Treatment
In localised renal cancer, the primary treatment is the surgical removal of the tumour. This can
involve a partial nephrectomy, where only the tumour is removed, or radical nephrectomy. In some
cases, thermal ablation (radiofrequency or cryoablation) or active surveillance may be used for
smaller tumours or patients who are not surgical candidates. In metastatic renal cancer, treatment
typically involves targeted therapies (tyrosine kinase inhibitors) or immunotherapy (immune
checkpoint inhibitors). Cytoreductive nephrectomy may be considered in select cases, followed by
systemic treatment to manage distant metastases and prolong survival.
III. BLADDER CANCER
Bladder cancer (BC) is the 10th most common cancer worldwide, with a higher incidence in men
than women. It is most prevalent in older adults after age 65. Smoking and occupational exposure to
chemicals like aromatic amines are the leading risk factors.
Pathology
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Benign bladder tumours include urothelial papillomas and leiomyomas. The most frequent types of
BC are urothelial carcinoma (90%), squamous cell carcinoma (5%), and adenocarcinoma (2%). BC
is classified into three stages: non-muscle invasive (NMIBC), muscle-invasive (MIBC), and
metastatic disease. NMIBC remains confined to the bladder's mucosa and submucosa, while MIBC
invades deeper into the muscle layer.
Clinical manifestation
Painless gross hematuria is the most common symptom, which always warrants thorough
examination to rule out cancer. Other symptoms may include frequent urination, urgency, dysuria,
and pelvic pain. Signs like lower back pain (due to ureteral obstruction), weight loss, and fatigue
may develop in advanced stages.
Diagnosis
Cystoscopy is the primary test, allowing direct visualisation and biopsy of bladder lesions. Urinalysis
and cytology help detect blood or cancer cells. Imaging tests like CT urography or MRI evaluate the
tumour's extent and assess the upper urinary tract. CT scans of the abdomen and thorax are
performed to rule out metastases (the lymph nodes and lungs).
Treatment
Generally, the first step involves transurethral resection of the bladder tumour (TURBT) to obtain
histology. In NMIBC, this is followed by intravesical therapy with chemotherapy to prevent
recurrence in selected patients. MIBC is usually treated by radical cystectomy combined with
cisplatin-based neoadjuvant chemotherapy. A bladder-sparing approach with chemoradiation is an
option. After cystectomy, urinary diversion options include an ileal conduit (ureteroileostomy) or an
ileal neobladder, which allows normal urination through the urethra. Metastatic BC treatment
includes cisplatin-based chemotherapy and immune checkpoint inhibitors.
IV. TESTICULAR CANCER
Testicular cancer (TC) is a rare malignancy, constituting about 1% of all male cancers. It primarily
affects younger men, typically between 15 and 35 years old. Risk factors include family history and
finding of undescended testis.
Pathology
Testicular cancer is primarily classified into germ-cell tumours and non-germ-cell tumours. Germ
cell tumours are further divided into seminomas, which are the most frequent type of TC, and nonseminomas,
which include embryonal carcinoma, yolk sac tumour, choriocarcinoma, and teratoma.
Non-germ cell tumours, like Leydig and Sertoli cell tumours, are rare.
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Clinical manifestation
Testicular cancer often presents as a painless lump or swelling in one testicle, which may be
accompanied by discomfort or a feeling of heaviness. Advanced cases might present with back pain,
cough, gynecomastia or other systemic symptoms due to metastasis.
Diagnosis
The diagnosis of TC is based on a physical examination, scrotal ultrasound, and serum tumour
markers [e.g., alpha-fetoprotein (AFP), human chorionic gonadotropin (hCG), and lactate
dehydrogenase (LDH)]. If TC is suspected, a radical orchiectomy via an inguinal approach is
performed. CT of the thorax and abdomen is used to assess for metastasis, with the most frequent
sites being lymph nodes, pulmonary, and hepatic metastases. Stage I is confined to the testicle, Stage
II involves regional lymph nodes, and Stage III indicates distant metastases.
Treatment
Treatment for Stage I involves a radical orchiectomy. Afterward, patients may undergo active
surveillance or chemotherapy to prevent recurrence. In metastatic testicular cancer (Stage II and III),
treatment involves a radical orchiectomy followed by chemotherapy. In non-seminoma cases,
residual disease in the retroperitoneum is often surgically removed through retroperitoneal
lymphadenectomy.
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UROLOGICAL TRAUMA (36)
Varga Gabriel, Fedorko Michal
Kidney trauma
Etiology: Renal trauma presents around 1-5% of all trauma cases. It results most commonly from
road traffic accidents, falls, sporting injuries. Motor vehicle accidents can lead to deceleration
injuries causing contusion, laceration of renal parenchyma or renal pedicle injury. Stabbing or
gunshot trauma is the most common cause of penetrating injury. Iatrogenic trauma most frequently
results from percutaneous nephrostomy, renal biopsy, percutaneous stone extraction,
endopyelotomy and endovascular interventions (vascular injury)
Diagnostics: Medical history (flank pain, mechanism of injury, presence of hematuria), physical
examination can show abrasions, penetrating gunshot wounds, stabbing or blunt force trauma of
the upper abdomen or flank area, injured thorax or broken ribs. Vital signs monitoring is essential.
(possible hemodynamic instability)
Laboratory examination: Urinalysis, complete blood count (hematocrit), creatinine (kidney
function before the injury)
Imaging tests: abdominal ultrasound (subcapsular hematoma, perirenal hematoma,
hemoperitoneum), CT urography (grading of renal trauma, evaluating extravasation of contract dye
as an evidence of active bleeding, assessing function of contralateral kidney), single shot
intraoperative excretory urography in unstable patients. MRI is as effective in diagnostics of renal
trauma as CT, however, it is not routinely used in diagnostic algorithm. The severity of renal injury
is classified into 5 grades depending on presence of different characteristics such as perirenal
hematoma, laceration of parenchyma, collecting system rupture, injury of the main vessels or
shattered kidney.
Conservative management: Blunt renal trauma
Hemodynamic stability is crucial criterion for the management of all renal injuries. Non-operative
management has become the treatment of choice for most cases (Grade I-IV). In stable patients, this
means a period of bed rest, observation and close monitoring in the ICU unit. Renal injuries grade
IV-V in polytrauma patients usually require exploration surgery and nephrectomy. Conservative
approach is recommended in case of traumatic unilateralcomplete renal artery thrombosis.
Angiography with selective embolization is a minimally invasive treatment used especially in
iatrogenic injuries.
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Surgical management: Penetrating injuries
Penetrating wounds have traditionally been managed surgically. The goals of exploration following
renal trauma are vascular control and renal salvage. Feasibility of renal reconstruction should be
judged during the operation. Repair should be attempted in patients with a solitary kidney or
bilateral injuries, even in grade V vascular injuries. A nephrectomy is performed if reconstructive
procedure is not possible.
Ureteral trauma
Etiology: Trauma to the ureters is relatively rare. Iatrogenic injury during open, laparoscopic and
endoscopic surgery is responsible for the majority of cases. The injury is often missed intra-operatively.
Penetrating external ureteral trauma is predominantly caused by gunshot wounds. About one-third of
cases of external trauma to the ureters are caused by blunt trauma, mostly road traffic accidents. Common
mechanisms of iatrogenic ureteral trauma include ligation with a suture, crushing by instruments, partial
or complete transection, thermal injury, or ischemia due to devascularization. Gynecological operations
are the most common cause of significant iatrogenic ureteral injury. Risk factors for iatrogenic trauma
include malignancy, prior surgery or irradiation, diverticulitis, endometriosis, anatomical abnormalities,
and hemorrhage.
Clinical picture and diagnostics: In penetrating injuries, the diagnosis is made intra-operatively,
while it is often delayed in blunt and iatrogenic cases. The patient may present with flank pain,
vaginal or drain urinary leakage, hematuria, fever and uremia. Extravasation of contrast dye on CT
scan is the hallmark sign of ureteral trauma. Furthermore, urinoma, hydronephrosis or ascites may be
present. In unclear cases, a retrograde or antegrade ureterography can confirm the injury.
Therapy: Immediate intraoperative diagnosis can be managed by a repair and stent placement. A
partial transection is repaired by suture and insertion of a JJ stent. Stenting decreases the risk of
stricture. Injuries that are diagnosed late are treated first with a nephrostomy tube and
reconstruction is performed in 6-12 weeks. The type of reconstructive surgery depends on the
extent and localization of the injury.
Bladder trauma
Etiology: Majority of cases (around 75%) are blunt trauma occurring when the bladder is full.
Motor vehicle accidents are the commonest cause of blunt bladder injury, followed by falls,
industrial pelvic crush injuries and blows to the lower abdomen. 60-90% of patients have
associated pelvic fractures. Children are particularly at risk of bladder trauma due to higher
position of bladder (above pubic symphysis).
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Classification: According to the location, bladder injuries are classified into two distinct types.
Intraperitoneal injury usually occurs at the apex of the bladder and leads to leak of urine into the
peritoneal cavity. Extraperitoneal injury is almost always associated with pelvic fractures and
usually caused by distortion of the pelvic ring or direct rupture due to bone fragments. Iatrogenic
injury results from urologic (TUR - transurethral resection) or gynecologic (cesarean section,
sling surgery) procedures.
Clinical picture and diagnostics: Gross hematuria is present in 80-95% of cases. Other clinical
signs include suprapubic pain, inability to void, edema or hematoma of perineum, scrotum or thighs.
Iatrogenic injury is recognized as low return of irrigation fluid during TUR and abdominal
distention. During a laparoscopy, bladder injuries may be identified as filling of a urine drainage bag
with gas. The key examination in the diagnostic algorithm (following taking medical history and
physical examination) is retrograde cystography. CT scan is used as well because of the common
association with pelvic fractures, and in fact, CT imaging is routinely used in polytrauma cases. In
intraperitoneal injuries, free contrast medium is visible in the abdomen, outlining bowel loops and
abdominal viscera.
Therapy: Extraperitoneal injuries are managed conservatively with continuous bladder drainage (7-
14 days) using a transurethral or suprapubic catheter and antibiotic prophylaxis. In case of an
extraperitoneal injury with pelvic fractures treated by internal fixation, repair of the bladder is
recommended. Intraperitoneal ruptures and penetrating bladder injuries are always managed by
surgical repair as well. Iatrogenic injuries recognized intra-operatively are immediately repaired.
Urethral trauma
Etiology: Anterior urethral injuries in males are caused by blunt trauma (fall or kick to the
perineum). Penetrating injuries are rare (gunshot trauma). Trauma by inserting foreign bodies or
penile fractures are also uncommon. Furthermore, transurethral catheterization or endoscopic
surgery can lead to iatrogenic urethral injury. Posterior urethral injury in males is associated with
pelvis fracture. Urethral injuries in females are extremely rare and the main cause is pelvis fracture.
Classification: Urethral trauma can be divided into injury of anterior urethra (penile and
bulbar) and posterior urethra (membranous and prostatic). From a surgical aspect, there can be
a complete or partial rupture. In case of complete urethral rupture there is a gap between the
ends of the urethra. Partial rupture is associated with urethral elongation, mucosal injury and
partial tear in urethral wall.
Complications: Late complications include stricture, incontinence and erectile dysfunction.
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Diagnostics: Major symptoms are blood at the meatus, inability to pass urine, palpable overfilled
bladder, hematuria, painful urination, ecchymosis, potentially edema in scrotal and perineal region,
or difficult catheterization. Upon digital rectal examination there may be finding of so-called high
riding prostate. Retrograde urethrography is a standard diagnostic examination to evaluate urethral
injury. It can assess extent and localization of injury. Flexible cysto-urethroscopy may evaluate
urethral injury as well and additionally, it enables placement of urethral catheter if necessary.
Management of anterior urethral injuries: Suprapubic urinary diversion or early endoscopic realignment
with transurethral catheter placement are treatment options in case of anterior urethral
trauma. Partial or complete ruptures require urinary diversion for at least 2-3 weeks. Penetrating
injuries are managed with immediate repair. Small lacerations and stabbing injuries can be repaired
by simple closure. Short defects of bulbar (<2-3cm) and penile (<1,5cm) urethra can be managed
with spatulation and primary anastomotic repair. In the case of longer defects or apparent infection,
a deferred repair is needed.
Management of posterior urethral injuries: It can be divided into immediate repair (< 48 hours
after injury), delayed surgery (2 day to 2 weeks after injury) and deferred treatment (>3 months
after injury). Immediate management is carried out by ultrasound-guided suprapubic cystostomy.
Partial ruptures of posterior urethra can be managed with insertion of suprapubic or transurethral
catheter. Retrograde uretrography is used after 2 weeks, until injury is not healed up. Residual or
consequent stricture is managed either with direct vision internal uretrotomy or anastomotic
urethroplasty, depending on the length of the stricture. Complete rupture of posterior urethra is
treated with early endoscopic realignment (approximation of urethral ends over catheter) or early
urethroplasty (suturing ends of the urethra). Early urethroplasty is difficult because of poor
visualization and the inability to accurately assess the degree of urethral disruption, due to
extensive swelling. Standard treatment is deferred one-stage urethroplasty (at least 3 month after
injury) - perineal anastomotic repair represents the surgical technique of choice.
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CONGENITAL DEFORMITIES OF MUSCULOSKELETAL SYSTEM (2)
Urbášek Karel
Congenital malformations of the musculoskeletal system refer to a diverse range of conditions
characterized by abnormal development of the bones, muscles, joints, and connective tissues present
at birth. These malformations can affect various parts of the body, including the limbs, spine, skull,
and pelvis. The severity and specific manifestations of these malformations can vary widely, ranging
from minor single limb abnormalities to more complex systemic and debilitating conditions. The
causes of congenital musculoskeletal malformations are multifactorial and can involve a combination
of genetic, environmental, and developmental factors. Here we present examples of the most
common pathologies.
Pes Equinovarus Congenitus (Clubfoot)
Is most common musculoskeletal birth defect. Overall incidence is 1:1.000 with male:female ratio
approximately 2:1. Half of the cases are bilateral. In 80%, clubfoot is an isolated deformity.
Genetic component is strongly suggested, unaffected parents with affected child have 2.5% - 6.5%
chance of having another child with a clubfoot. In 20% is associated with conditions such as
arthrogryposis, diastrophic dysplasia, myelodysplasia, tibial hemimelia, amniotic band syndrome
(Streeter dysplasia) etc. And it is called syndromic clubfoot.
Diagnosis is made clinically. It is a complex deformity consisting of Cavus (tight intrinsics, FHL,
FDL), Adductus of forefoot (tight tibialis posterior), Varus (tight tendoachilles, tibialis posterior,
tibialis anterior) and Equinus (tight tendoachilles). The gold standard treatment is Ponseti method
casting (casts changing at weekly intervals with gradual correction of deformity) followed by
achillotomy to correct residual equinus. Subsequently, it is necessary to use a special brace until the
age of 5 years to maintain the correction. Supplemental surgical procedures such tibialis anterior
tendon transfer may be required during treatment to correct residual deformity. The overall success
rate of the Ponseti method is over 90%.
Congenital Femoral Deficiency (CFD)
Congenital femoral deficiency (CFD) is a rare birth longitudinal postaxial defect that is characterized
by a short femur, associated with hip and knee deformity, deficiency, or instability. Leg length
difference can reach 40-50 cm. The more severe types were previously known as proximal femoral
focal deficiency (PFFD). The incidence is 1:40.000. The cause of an isolated single-limb abnormality
is generally unknown and is usually not associated with a genetic abnormality. CFD is often
associated with Fibular Hemimelia. The treatment strategies for CFD depend on the severity. In all
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but the most extreme cases, deformity correction surgery and limb lengthening are the preferred
treatment method. The use of orthotics is also an option.
Fibular Hemimelia (FH)
Fibular hemimelia is a longitudinal postaxial defect where part or all of the fibula is missing. The
Incidence is 1:40.000. Bilateral fibular hemimelia is even rarer. It is assumed that genes guiding the
formation of the limb are activated in an abnormal order. FH is not heritable.
Major problems associated with FH are foot and ankle deformities, limb length discrepancy and knee
deformities. The treatment strategies FH depend on the severity. Deformity correction surgery
(reorientation of ankle joint, talo-calcaneal osteotomy, knee stabilization) and limb lengthening are
the preferred treatment method. The use of orthotics is also an option.
Tibial Hemimelia (TH).
Is the least common longitudinal bone defect. The incidence is1:250.000-1.000.000. Almost all TH
will need surgery to help children stand and walk. The type of surgery needed depends mainly on
how much of the tibia is present and the condition of the knee and ankle joints.
Congenital Pseudarthrosis of the Tibia (CPT)
Pseudarthrosis usually develops prenatally or within the first two years of life. The incidence of CPT
is 1:250.000 births. The cause of CPT is currently unknown; however, there is a strong association
with neurofibromatosis in 50% of cases and an association with fibrous dysplasia in 10% of cases.
The difficulty of treatment lies in the weak healing power at the fracture site, a tendency to refracture
after treatment, and the difficulty of stabilizing small osteoporotic bone fragments in small children.
The most promising treatment is the "Cross-union" method which combines surgical and
pharmacological approaches. With the aim of fusing the tibia and fibula with a bone graft from the
iliac crest and fixing the tibia with a telescopic nail and plate.
Radial Club Hand (RCH)
Is a longitudinal deficiency of the radius. It includes a spectrum of deficiencies involving the radius,
the radial side of the carpus, and the thumb. The incidence is 1:30.000–100.000. Fifty percent are
bilateral and are usually associated with other upper extremity deformities and deficiencies,
including absent or hypoplastic thumb, TAR syndrome, Fancomi’s anemia etc. RCH is an
aesthetically unappealing deformity that also results in significant functional impairment (due to
absent or hypoplastic thumb) and instability and restricted motion in the elbow, wrist, and finger
joints. The aim of the surgery is to correct the position of the hand and stabilize it and reconstruct the
gripping ability of the thumb.
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Achondroplasia
Accounts for about 75% of all dwarfisms, affecting 1 out of 10.000–50.0000 live births. It is caused
by a mutation in the fibroblast growth factor receptor 3 (FGFR3) gene that results in impaired
endochondral bone growth. Most cases (80%) are spontaneous mutations.
The average adult height for men is 131 cm and for women is 125 cm. Limb deformities, frontal
bossing, midface hypoplasia, hyper-lordosis, spinal stenosis, and normal intellect are typical.
For diagnosis physical exam. and X-rays are sufficient, genetic testing confirms the diagnosis.
Treatment: new drug is available, applied daily subcutaneously, it antagonizes downstream FGFR3
signaling and thus alleviates the symptoms of achondroplasia.
Traditionally treatment focuses on any problems or complications and includes guided growth,
osteotomy, limb lengthening, spinal cord decompression, etc.
Osteogenesis Imperfecta (OI)
Is an inherited (genetic) bone disorder that is present at birth. It is also known as Brittle bone disease.
The incidence is 1:10.000-20.000. Mutations in the COL1A1 and COL1A2 genes cause
approximately 90% of all cases. These genetic changes reduce the amount of type I collagen.
Patients have soft bones that are not formed normally and fracture easily, and other problems. Signs
and symptoms may range from mild to progressively deforming to perinatally lethal. The spine is
commonly affected.
The main goal of treatment is to prevent deformities and fractures. Bisphosphonates are used in the
symptomatic treatment of OI to reduce the number of fractures. Of the surgical interventions, the
most common are deformity corrections secured by pediatric telescopic intra-medullary nails.
Arthrogryposis Multiplex Congenita (AMC)
AMC is a descriptive term for the development of nonprogressive contractures affecting two or more
different areas of the body. The incidence is approximately 1:3000. A contracture completely or
partially restricts the movement of the affected joint. Specific symptoms and physical findings can
differ greatly in range and severity. The legs are affected more often than the arms and the jaws and
back may also be affected. Variants in over 400 genes have been identified as responsible for
different types of arthrogryposis. One-third of individuals with AMC may have structural or
functional abnormalities of the central nervous system.
Treatment: A multidisciplinary approach is best. Standard physical therapy, removable splints and
serial casting to mobilize stiff joints is helpful. In some patients, surgery may be necessary to
improve joint motion and avoid muscle atrophy.
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Congenital Scoliosis (CS)
It occurs in 1 in 10.000 newborns and is much less common than juvenile idiopathic scoliosis.
There are 2 main causes of CS: Incomplete Formation of Vertebrae: part of one vertebra (or more)
may not form completely and hemivertebra developed. More than one hemivertebra can sometimes
balance each other out and make the spine more stable.
Failure of Separation of Vertebrae: the spine forms first as a single column of tissue that later
separates into segments. If this separation is not complete, the result may be a partial fusion (boney
bar) joining two or more vertebrae together, preventing spine from growing on one side.
Combination of Bars and Hemivertebrae: causes the most severe growth problem. These cases can
require surgery at an early age to stop the increased deformity.
In rare cases there may be a problem with the spinal cord or nerves that produces weakness,
numbness, or a loss of coordination. CT scans and MRI are mandatory in treatment planning.
Nonsurgical Treatment: Braces are not effective in treating the curvature caused by the congenitally
abnormal vertebrae, but they are sometimes used to control compensatory curves.
Surgical Treatment: The important goal of surgery is to allow the spine and chest to grow as much as
possible. Surgical options include hemivertebra removal and spinal fusion etc.
Myelomeningocele (MMC)
Is the most common central nervous system congenital condition. It is a type of spina bifida. The
incidence is 1:1.500. The cause of MMC is still unknown, but it’s a complex combination of genetic,
nutritional and environmental factors that are being considered. MMC most commonly occurs in
lumbar and sacral areas. Hydrocephalus is also a problem.
Treatment involves surgery to repair the opening in spine. (fetal or postnatal surgery). MMC causes
moderate to severe disabilities, such as muscle weakness, loss of bladder or bowel control,
and/or paralysis. Most common orthopedic complications are hip dislocation, contractures and spine
deformities. Most patients are wheelchair-bound, but there are some who are able to walk
independently.
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SCOLIOSIS AND OTHER SPINE DEFORMITIES (3)
Chaloupka Richard, Ryba Luděk, Parížek Dominik
Scoliosis is a three-dimensional spinal deformity (in frontal, sagittal and transverse planes).
Curvature in the frontal plane is called scoliosis, in the sagittal plane lordosis and kyphosis and in the
transverse plane it´s rotation of vertebrae. In the forward bend – flexion test, scoliosis is manifested
by a prominence (hump), so-called gibbus. It occurs in the population with a frequency of about 3%.
The most commonly used classification of scoliosis is based on etiopathogenesis: 1/ Idiopathic (the
most common) 2/ Congenital 3/ Neuromuscular (CP - cerebral palsy, muscular dystrophies,
myopathies).
Diagnosis is based on anamnesis, clinical examination and imaging. When taking a medical history,
we focus on the family anamnesis, in the personal history we focus on the patient's period of
psychomotor development. We ask about the patient's current difficulties (pain, respiratory
insufficiency, fatigue), previous kinds of treatment and date of the first occurrence of a problem.
During the clinical examination we focus mainly on the limbs and spine. We perform a forward
bending test (Adams test) and side bends. During the examination we focus mainly on symmetry (Is
the spine misaligned? Are the shoulder blades/glutes/shoulders at the same height? Is there a
difference in limb length? Is the pelvis oblique?), the condition of the musculature, not forgetting the
orientation neurological examination. If a prominence is present, measure it in cm. From the imaging
methods we choose X-ray examination, using long formats capturing the whole spine, images are
taken standing in anteroposterior and lateral projection, the size of the deformity is determined by the
Cobb angle measurement (see figure).
Treatment is either 1/ conservative or 2/ surgical.
Conservative treatment is chosen for less severe deformities. It mainly includes physiotherapy,
continuous daily exercise, change of habits and posture, sparing of the spine, alternating regime. We
use bracing during the growth period at curve values of 20-40°, the minimum duration of brace use is
16 hours per day, physiotherapy and daily exercises are necessary. We choose surgical treatment for
severe deformities, it serves as a prevention of oppression of internal organs (abdominal, lungs restriction
of breathing functions), prevention of development of spine degenerative changes. The
operation is indicated in growing children with a curve above 40°. In children under 10-12 years of
age we use GGS (Guided Growth Systems, instrumentation without vertebral fusion – transpedicular
screws and rods in majority of cases). For patients over 10-12 years of age, we perform definitive
treatment from a posterior approach with transpedicular fixation and vertebral fusion. For idiopathic
and congenital scoliosis we make sure to keep instrumentation and fusion as short as possible.
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For neuromuscular scoliosis, we choose long construct/intrumentation with the possibility of fixation
also to the sacrum and iliac bone (in case of an oblique pelvis or instability of the sitting position,
pelvic fixation improves the stability of the sitting position).
Wrong posture is a common cause of spinal deformity. It manifests itself as a flexible deformity
with muscular imbalance. The deformity disappears when lying down and when muscles are
activated (correction occurs). Treatment consists of rehabilitation, stretching of shortened muscles
(especially pectoral and knee flexors), strengthening of abdominal and back muscles. It is important
to pay attention to correct posture, continuous daily exercises, correct movement regime, regular
changing of activities and positions.
Morbus Scheuermann (kyphosis dorsalis juvenilis) is genetically determined enlargement of the
thoracic kyphosis due to incorrect ossification. X-ray imaging plays a key role in the diagnosis; we
use long formats in two standing projections. On the X-ray we can observe wedge-shaped vertebrae,
disc reduction, and irregularity of the end plates of vertebrae.
For flexible kyphosis (we perform lateral X-ray in lying position with reclination with the wedge at
the apex of the kyphosis) in range of 50-70 degrees is the method of choice bracing and
physiotherapy during the growth period of the patient. Surgical treatment is chosen when the
kyphosis is above 70 degrees.
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ORTHOPAEDIC TREATMENT OF DEGENERATIVE AND RHEUMATIC DISEASES (8)
Liskay Jakub, Tomáš Tomáš
Degenerative joint disease (osteoarthritis) is a non-inflammatory degenerative joint disease
characterized by degradation of articular cartilage, subchondral sclerosis, osteophyte formation and
soft tissue changes involving the synovial membrane, joint capsule, joint ligaments and muscles. It is
a very common disease that increases with age, affecting more women with characteristic changes in
the small joints of the hands, weight-bearing joints and spine. Risk factors include age, gender,
genetic predisposition, biomechanical disorders, trauma, obesity, as well as ethnic and geographical
influences. The disease is uncommon in those under 40 years of age but is the most common chronic
disease in older patients. More than 80% of people over 75 years of age are affected.
Osteoarthritis is divided into primary (cause unknown - affects the small proximal and distal
interphalangeal joints of the hands, 1. Carpometacarpal joint of the thumb, cervical C5-6 and lumbar
L5-S1 spine, hip and knee joints) and secondary ( cause is known - metabolic diseases (gout,
hemochromatosis), hormonal conditions (acromegaly, diabetes) , recurrent bleeding in the joint,
inflammatory process, mechanical factors (intra-articular fractures, coxa vara congenita, conditions
after developmental dislocation of the hips, conditions after aseptic necrosis of the femoral head,
overweight, after total menisectomy)
Clinical manifestations - at the beginning there is a slight pain in the joint, which increases with
exertion and weather changes, morning stiffness, with progression the pain is higher, limping, the
patient cannot stand, the muscles react with a protective spasm, the joint stiffens, joint contractures
are formed, the joint swells and during movement there are audible jerks.
Diagnosis - the basic imaging method is X-ray, it divides osteoarthritis into I- IV grades according to
Kellgren- Lawrence classification, MRI examination.
Treatment - conservative therapy is usually the method of first choice of treatment of osteoarthritis.
Conservative treatment is divided into non-pharmacological and pharmacological treatment. Nonpharmacological
treatment is based on the modification of the life and work regime, reduction of the
vertical load on the weight-bearing joints (weight reduction, canes, crutches), regular exercise,
prevention of contractures, appropriate sports (cycling, swimming, pool exercises), physical
treatment (magnetotherapy, radiation). Pharmacological treatment has an anti-inflammatory and
analgesic effect (Paracetamol, Metamizol). To suppress the inflammatory component, the application
of non-steroidal anti-inflammatory drugs (NSAIDs) is appropriate. NSAIDs are divided according to
their mechanism of action into cyclooxygenase 1 inhibitors - ibuprofen, indomethacin, diclofenac,
and cyclooxygenase 2 inhibitors (preferential - meloxicam, nimesulid, selective - celecoxib).
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The use of opioid analgesics (Tramadol, DHC, Durogesis) is possible. Opioid analgesics (Tramadol,
DHC, Durogesis) may be used in high grades of osteoarthritis. Pharmacological therapy must be
used with caution in view of side effects, drug interactions and associated diseases. Another group of
drugs are SYSADOA (symptomatic slow acting drugs in osteoarthritis). These include glucosamine,
chondroitin sulphate and diacerein. Corticosteroids have a strong anti-inflammatory effect. Intraarticular
administration of depot corticosteroids (e.g. methylprednisone) may provide temporary pain
relief. The strong anti-inflammatory effect of corticosteroids is useful in acute synovialitis.
Hyaluronic acid provides lubrication of the joint, shock absorption and is an important component of
the extracellular matrix of cartilage. Hyaluronic acid derivatives are injected into the joint and are
obtained from various sources (cock's comb, bacterial fermentation, etc.).
Surgical treatment - indicated in case of failure of conservative treatment, divided into primary
preventive procedures, secondary preventive procedures, palliative procedures and definitive surgical
solution.
Preventive primary procedures are procedures to prevent the development of arthrosis. They include
the correct treatment of intra-articular fractures, the correct treatment of ligament ruptures and
luxations, ligament stabilisation and resurfacing for joint instability, treatment of meniscal ruptures,
treatment of chondromalacia deposits, removal of loose bodies, early procedures for congenital and
developmental defects ensuring an anatomically and functionally normal joint (especially early
surgical treatment of developmental dysplasia of the hip - VDKK , Morbus Perthes, coxa vara
adolescentium)
Preventive secondary surgery is surgery in the field of arthritic changes or changes that will clearly
lead to arthrosis, with the aim of slowing or stopping the progression of these changes. These include
surgical correction of the axis (valgus osteotomy of the proximal tibia at the genu varum, varus
osteotomy of the distal femur at the genu valgus, osteotomy of the proximal femur, pelvis.), late
procedures in the context of congenital and developmental defects providing correction in order to
delay the onset of secondary degenerative changes (e.g. Chiari osteotomy or tectum repairs in
developmental hip dysplasia), synovectomy in rheumatoid arthritis.
Palliative surgeries are procedures for advanced arthritic changes that are symptomatic, do not affect
the progression of the disease, but delay the need for definitive resolution. These procedures include
arthroscopic debridement of articular cartilage and menisci, synovectomy for osteoarthritis,
styloidectomy and denervation of the carpus or e.g. Man surgery for hallux rigidus.
The definitive treatment of osteoarthritis is resection arthroplasty (e.g. Keller's operation for arthrosis
of the metatarsophalangeal joint of the thumb, Girdlestone operation), arthrodesis, partial joint
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replacement (hemiarthroplasty) and total joint replacement, which has the best clinical results
especially in the hip and knee joints.
Arthrodesis is the artificial induction of joint ossification between two bones by surgery. The
surgical principle is the removal of cartilage debris, the modification of articular surfaces with the
revival of bone surfaces, the possible use of bone grafts, the correct axial and rotational positioning
with respect to limb function and the provision of resting to solid bone healing by means of stable
osteosynthesis (LCP, compression plates, compression screws, staples, possibly biological autograft
using a fibula in ankle arthrodesis). Arthrodesis is the method of choice as a definitive solution in the
wrist (arthrosis of the RC joint and carpus), the tibiofemoral joint, the subtalar joint as a triple
arthrodesis and the metatarsophalangeal joint of the big toe. Arthrodesis is also used as final surgery
especially in joint infections in resistant cases.
Rheumatic diseases
Rheumatoid arthritis is an inflammatory disease of the joints of the extremities in which the
infectious agents causing the disease have not been identified or cultured. For the actual diagnosis,
the following criteria must be fulfilled: morning stiffness for at least 1 hour for at least 6 weeks,
swelling of at least three joints for at least 6 weeks, symmetrical swelling for at least 6 weeks,
rheumatic nodules, evidence of rheumatic factors, radiographic changes in the hands.
Clinical manifestations - joints have all the signs of inflammation except redness in the acute phase.
Subsequently, swelling, subluxation, deformity and ankylosis occur. Some deformities are typical,
e.g. "swan neck" in the fingers, ulnar deviation in the metacarpophalangeal joints, palmar flexion in
the wrist, flexion contractures in the IP and dorsal in the MTP joints of the foot, semiflexion
contractures in the knees and elbows or flexion/adduction in the hips. Life-threatening is instability
of the atlantoaxial joint.
Therapy - NSAIDs are the first-choice drugs, DMARDs (disease-modifying antirheumatic drugs) patients
with active synovialitis (Methotrexate, Sulfasalazine, glucocorticoids) are designated for
therapy with so-called basal drugs. Surgical therapy - synovectomy is the extirpation of the
hypertrophic inflammatory lining of the affected joint( carpometacarpal joints, knee joint) in order to
reduce the volume of inflammatory tissue as much as possible and prevent joint destruction ,
reconstruction of the forefoot and hindfoot (e.g. procedures to correct hallux valgus - arthrodesis of
the metatarsophalangeal joint, resection of the metatarsal heads at the flatfoot, arthrodesis of the
subtalar joint and ankle), implantation of total replacement of large joints and small joints of the
hand (silicone implants), osteotomy, tenotomy.
Ankylosing spondylitis (Bechterew’s disease) is an autoimmune disease with the production of
antibodies against its own tissue, where the target tissues are the ligament attachments of the spine
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and the sacroiliac joints (SI joints). The result is ankylosis of the spine. Males are predominantly
affected, and the disease begins in the 2nd to 3rd decade of life. The SI joints and spine are the main
structures affected, but extraskeletal manifestations such as uveitis are also part of the disease;
pulmonary restriction is a secondary affliction of reduced thoracic capacity. The underlying process
is inflammatory involvement of the intervertebral joints and progressive calcification of the spinal
ligaments with the development of spondylophytes. Gradually, with bridging of the intervertebral
spaces, calcification of the anulus fibrosus of the intervertebral disc occurs, the final picture of which
may be ankylosis of the spine (“bamboo stick" ). The disease progresses most commonly in a
caudocranial direction.
Therapy - Surgical therapy of spinal deformities in ankylosing spondylarthritis is very challenging.
It consists of osteotomy (OT) of the spine with eventual deliberation and is burdened with a high
incidence of neurological complications.
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NEURO-ORTHOPAEDIC SURGERY (7)
Chaloupka Richard, Ryba Luděk, Parížek Dominik
Neuro-orthopedics is a field that merges neurology and orthopedics, focusing on conditions that
involve both the nervous system and the musculoskeletal system. Disorders in this area often require
multidisciplinary care to improve motor function, alleviate pain, and enhance overall quality of life.
Among the most significant conditions in this area are cerebral palsy, entrapment syndromes, and
birth-related brachial plexus injuries like Erb's palsy and Klumpke's palsy.
1. Cerebral Palsy
Overview:
Cerebral palsy (CP) is one of the most common neuro-orthopedic conditions. It refers to a group of
permanent movement disorders that appear in early childhood, primarily affecting motor function
due to brain injury or malformation during, or shortly after birth. The injury typically occurs either
before, during, or shortly after birth. The condition is non-progressive, but its effects can lead to
progressive musculoskeletal deformities.
Diagnosis:
The diagnosis of cerebral palsy is often made based on clinical observation of motor development
and neurological functions. Symptoms include poor coordination, stiff or weak muscles, and
exaggerated reflexes. MRI and CT scans are often used to detect brain abnormalities. Diagnosis
usually occurs in early childhood when motor delays become evident. Additional diagnostic tests,
such as EEG, may be used to rule out other related conditions.
Treatment:
Cerebral palsy cannot be cured, but treatment focuses on improving the quality of life and mobility
of the affected individual. A combination of physical therapy, which is essential and must be longterm
(such as the Vojta method), occupational therapy, speech therapy, and medical interventions are
used to improve motor function and coordination. Orthopedic surgeries, such as tendon lengthening
or correction of bone deformities, may be necessary to manage spasticity and improve mobility.
Injections of botulinum toxin (Botox) and intrathecal baclofen therapy are often used to relax spastic
muscles. In severe cases, selective dorsal rhizotomy (SDR) surgery, which involves cutting the nerve
fibers causing spasticity, may be performed.
Orthopedic Care:
Children with cerebral palsy often suffer from musculoskeletal problems such as scoliosis, hip
dislocations, or foot deformities. Regular monitoring by orthopedic specialists is essential for
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preventing or correcting deformities, with orthopedic interventions, such as braces or surgeries, used
to maintain mobility and function. For lower limb contractures, surgeries such as adductor tenotomy,
hamstring lengthening, and Achilles tendon lengthening are indicated by the age of 6, followed by 3-
6 weeks of plaster immobilization and subsequent rehabilitation to enable walking.
2. Entrapment Syndromes
Overview:
Entrapment neuropathies are conditions where nerve becomes compressed or restricted, leading to
pain, numbness, or muscle weakness. These syndromes can occur in various parts of the body and
affect both children and adults. Examples include carpal tunnel syndrome, cubital tunnel syndrome,
and tarsal tunnel syndrome. While these conditions are more commonly associated with adults, they
can also occur in children, often due to trauma or congenital deformities.
Diagnosis:
The diagnosis of entrapment syndromes is based on a combination of physical examination, medical
history, and nerve conduction studies. Electromyography (EMG) and nerve conduction velocity
(NCV) tests are often used to determine the extent of nerve damage. Imaging studies, such as
ultrasound or MRI, can help identify the precise location of nerve compression.
Treatment:
The treatment of entrapment syndromes varies depending on the severity and location of the nerve
compression. Non-surgical options include physical therapy, splinting, anti-inflammatory
medications, and corticosteroid injections. In more severe cases, surgery may be necessary to relieve
the compressed nerve and alleviate symptoms. Common surgical procedures include carpal tunnel
release and cubital tunnel release.
3. Brachial Plexus Injuries
Erb's Palsy
Overview:
Erb's palsy is a type of brachial plexus injury that affects the upper arm and shoulder. It is usually a
result of birth trauma, occurring when the baby's neck is stretched to one side during a difficult
delivery. This injury primarily affects the upper part of the brachial plexus (nerve roots C5-C6),
which control the movement and sensation of the arm and shoulder.
Diagnosis:
Diagnosis is usually made at birth based on the infant's inability to move the affected arm. EMG and
nerve conduction studies may be performed to determine the extent of nerve damage.
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Treatment:
Treatment for Erb's palsy begins with physical therapy to encourage movement and prevent muscle
atrophy. If there is no significant improvement within the first few months, surgical options such as
nerve grafts or nerve transfers may be considered to restore function. Many children with Erb's palsy
regain partial or complete function with early rehabilitation.
Klumpke's Palsy
Overview:
Klumpke's palsy is a rarer form of brachial plexus injury that affects the lower nerves (C8-T1). It
results in weakness or paralysis of the forearm and hand muscles. Like Erb's palsy, Klumpke's palsy
is often associated with birth trauma but can also occur in older children due to trauma or stretching
of the lower brachial plexus.
Diagnosis:
The clinical presentation includes a "claw hand" deformity, where the forearm and hand muscles are
weak or paralyzed. Diagnostic tests are the same as for Erb's palsy.
Treatment:
Physical therapy is the mainstay of treatment to maintain joint mobility and muscle strength. In cases
where function does not improve within the first year, surgical intervention may be necessary, such
as nerve or tendon transfers to improve hand function.
4. Other Neuro-Orthopedic Conditions
Spina Bifida and Myelomeningocele:
Spina bifida is a congenital condition where the vertebral arch fails to close. Mild forms do not
require treatment. If the defect is larger, leading to a herniation of the dural sac and spinal cord,
surgical intervention after birth is required. Children with myelomeningocele may suffer from leg
paralysis or weakness, bladder and bowel dysfunction, and orthopedic deformities such as congenital
clubfoot (pes equinovarus) or scoliosis. Early diagnosis through prenatal screening or at birth allows
for early treatment, often involving a combination of surgery, physical therapy, and orthopedic
procedures to manage musculoskeletal deformities.
Duchenne Muscular Dystrophy:
Duchenne muscular dystrophy (DMD) is a genetic disorder characterized by progressive muscle
degeneration and weakness, primarily affecting boys. DMD requires a multidisciplinary approach
that includes physical therapy, corticosteroids to slow muscle loss, and orthopedic surgery to correct
contractures or scoliosis.
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Spinal Muscular Atrophy (SMA):
Spinal muscular atrophy (SMA) is a genetic disorder affecting motor neurons, leading to progressive
muscle atrophy. Orthopedic complications, such as scoliosis and joint contractures, often arise as
muscles weaken. Recent advances in gene therapy, such as Spinraza and Zolgensma, have
significantly improved the prognosis for children with SMA, but orthopedic care remains crucial to
ensure mobility and prevent deformities.
Conclusion
Neuro-orthopedics plays a vital role in treating a wide range of conditions that affect both the
nervous system and the musculoskeletal system. Disorders such as cerebral palsy, Duchenne
muscular dystrophy, and spinal muscular atrophy require a multidisciplinary approach that involves
neurologists, orthopedic surgeons, and rehabilitation specialists. Early diagnosis and intervention are
key to optimizing outcomes and improving the quality of life for affected individuals. Effective
treatment often involves a combination of physical therapy and surgical procedures tailored to the
specific needs of the patient.
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ASEPTIC BONE NECROSIS, ENTHESOPATHY AND TENDINITIS (5)
Lukáš Martinek, Luboš Nachtnebl
Aseptic bone necrosis
Aseptic bone necrosis (osteonecrosis) is a degenerative bone disease characterized by the death of
cellular components of bone due to interruption of the subchondral blood supply. Synonyms are
avascular necrosis or ischemic bone necrosis. It affects predilectively the epiphysis of the long bones
of the weight-bearing joints. In the most severe cases, bone destruction or collapse of the entire joint
occurs. The most common sites for avascular bone necrosis are the femoral head, the knee joint
(femoral condyles), the talus, the wrist region and the humeral head.
Risk factors includes: chemo-, radiotherapy, smoking, intraarticular fractures, arterial and venous
abnormalities, intraarticular bleeding, use of high doses of corticosteroids, metabolic diseases
(Gaucher disease), dyslipidemia, bleeding disorders, sickle cell anemia, autoimmune conditions,
repetitive microtrauma during overuse activities, etc. In a small percentage of cases, mutations in the
COL2A1 gene, which affects the production of type 2 collagen, have been shown to have autosomal
dominant inheritance. However, in a large percentage of cases the cause is not clear.
Pathophysiologically, a decrease of subchondral blood circulation causes a state of hypoxia in the
bone, leading to loss of cell membrane integrity, cell necrosis and an increase in neutrophiles and
macrophages. Macroscopically, subchondral bone collapse occurs with subsequent degenerative joint
involvement. Macroscopic changes visible on X-ray and CT imaging usually detect more advanced
stage of the disease. On MRI, signal changes due to edema and ischemia of fat cells in the bone
marrow detect disease earlier.
The clinical state is dominated by pain in the affected area of subjectively varying intensity and often
difficult localisation. The early stages of the disease are usually difficult to diagnose by clinical
examination, that‘s why there is often a delay in establishing the correct diagnosis. For this reason, it
is extremely important to take a correct history of the patient, focusing on the occurrence of the
above-mentioned diseases in the past or present and to identify previous traumatic conditions or
sports and work stress on the musculoskeletal system.
The most common aseptic bone necrosis:
Aseptic necrosis of the femoral head - often asymptomatic in the early stages. In case of atraumatic
etiology, up to 70% of cases are bilateral. Pain localized to the hip and groin already indicates a
progressive stage of the disease. Irradiation of pain to the thighs, buttocks and rest pain, signs of
stiffness and changes in gait stereotype are often present.
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Aseptic necrosis of the knee (condyles of the femur) - characterized by pain in the knee under load
and at rest at night. On examination, the pain in the vast majority of cases is localized in the area of
the medial femoral condyle (morbus Ahlbäck), imitating meniscal rupture with possible palpation of
the painful area during knee flexion with movement deficit. The most common types are
spontaneous and post-traumatic. Iatrogenic after an arthoscopic meniscectomy is relatively rare.
Treatment depends on the affected area. In general, the strategy for conservative treatment or salvage
procedures is to try to revascularise the affected site. However, these procedures have numerous
limitations depending on the losalisation.
• For the hip joint, lightweighting and limitation of motion are indicated as part of
conservative treatment. Treatment with a combination of bisphosphonates remains
controversial, although some papers have shown benefit. Among surgical treatments in the
early stages, when the affected area is small, revascularization procedures with
decompression of the affected head or in combination with autologous or allogeneic grafts or
biologic agents may be used. For larger lesions, if diversion of the supporting surface is
possible, rotational osteotomies in the intertrochanteric area can be used. In irreversible
conditions with head collapse or failure of previous methods, total joint replacement is the
only solution.
• For the knee joint (medial femoral condyle) in case of spontaneous necrosis, some cases are
treated with lightening and physiotherapy with a focus on quadriceps strengthening. In the
case of elderly patients in whom spontaneous necrosis is more frequent, unicompartmental
joint replacement provides good results. For larger lesions with more degenerative
destruction of the entire joint, total arthroplasty is the solution. In younger ones at the
precollapse stage, arthroscopy and decompression using an osteochondral autograft may be
helpfull. When the mechanical axis is impaired, the procedure often needs to be
supplemented with a high tibial osteotomy.
Enthesopathy and tendon inflammations
Tendons and tendon attachments are anatomical structures of the human body providing leveraged
transmission of muscle force to the skeleton, thus enabling locomotion. Another function is to absorb
shock and limit muscle damage by overloading.
Etiologically, one of the most important factors in the development of the disease is age-related
degeneration and frequent excessive mechanical stress. Most often, the development of these
diseases occurs with a change in the style or intensity of physical activity.
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Pathological-anatomical changes include microcracks, dystrophic changes, mechanical damage of
Sharpey fibers, periostitis, ossifications, and metaplastic changes.
Diagnosis consists in taking a proper history of the patient. We are interested in trauma, cyclic
mechanical overload with regard to jobs, sports activities. With age-related degeneration, patients
may not experience any changes in movement habits or activities. On clinical examination, we can
see palpatory tenderness, swelling, crepitus, and positivity of tension and resistance tests.
On imaging, we are interested in changes in the skeleton, ossification or calcification in the tendon or
tendon attachment, or changes in the tendon-to-bone transition and the formation of traction spurs. In
the ultrasound image, inflammatory changes are visible by hypoechogenicity of the image, we can
observe thinning, echogenicity changes in degenerative diseases, hyperechogenic calcifications, fluid
rim in tenosynovialitis, or neovascularization in the ultrasound image. MRI examination has
significantly improved the diagnosis of tendon pathologies. It allows to differentiate tendinosis,
peritendinitis or partial tendon rupture.
Treatment options depend on the affected area and the patient should always be warned of the very
likely possibility of a long healing process. When treatment is initiated, it is ideal to eliminate
processes causing the difficulty. Calmness and elimination of congestion relieves symptoms and
starts the reparative processes. Modification of workload, training activities, sports equipment or
exercise regimen at work is necessary. Long-term fixation is inappropriate due to the possibility of
atrophy. Targeted rehabilitation is aimed at increasing tensile strength and developing adaptation to
the activity performed. Stretching, eccentric exercise with mechanical cooling after the performed
exercise is important. Exercising in cycles of increasing load will gradually eliminate symptoms as
the patient is exposed to the load. Among physical methods, therapeutic ultrasound, electrotherapy,
magnetotherapy, cryotherapy in the initial stages and thermotherapy in the later stages of the disease
are used as an adjunct. Non-steroidal antiinflammatory drugs are generally recommended in the
initial stages of the disease. Local application of corticosteroids may be used if initial treatment fails.
Application should be limited to 2 to 3 doses to an identical area with a minimum interval of 6
weeks. After their application, intense exertion should be avoided for some time. Some areas Achilles
tendon, ligamentum patellae are contraindicated for corticosteroid application due to the
possibility of tendon rupture. If conservative therapy is ineffective and symptoms persist beyond 6-
12 months, surgical treatment is indicated.
The most common enthesopathies and tendonitis and their treatment:
Radial and ulnar epicondylitis of the humerus (tennis or golfers elbow) - in addition to racket
sports players, it affects also patients performing repetitive unilateral movements in the workplace
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(assemblers, plumbers, etc.). The pathological process mainly affects m. carpi radialis brevis in the
case of tennis elbow, m. pronator teres and m. flexor carpi radialis in the case of golfers elbow. It is
characterised by collagen fibre disruption, neovascularisation and mucoid degeneration. It affects the
outer respectively inner side of the elbow with the possibility of irradiation proximally and distally.
Typical is pain of the epicondyle and positivity of resistance tests - chair test, painful extension or
flexion of the wrist against resistance. Therapy consists in the acute phase in pain relief - NSAIDs,
icing, resting the limb, short-term use of a brace is usually appropriate. If the pain persists, local
application of corticosteroids is indicated. After relief of acute manifestations, the rehabilitation
process is followed by physical therapy (ultrasound, electro-magnetic therapy). If conservative
treatment fails, surgical treatment may be indicated, consisting in the shift of the origo with
débridement and distalization of the tendon, usually accompanied by resection of part of the
ligamentum anulare in the case of tennis elbow.
Peritendinitis of the Achilles tendon - the maximum painfulness is localized 3-5 cm above the
tendon, the tendon on the calcaneus is also painful. A single overload leads to the development of
acute peritendinitis, diffuse seepage and swelling. The tendon is painful to pressure, crepitations may
be palpable. In chronic state, the pain is less intense, swelling may be absent, spindle-shaped
swelling may be present. Therapy consists in interruption of activity, general or local using of
NSAIDs. Local application of corticosteroids is contraindicated. Treatment of the chronic form is
more difficult, sometimes rigid fixation is necessary. Physical therapy is also helpfull. When
conservative treatment fails, peritenonectomy is indicated. However, the results of surgical treatment
are far from 100%.
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PAEDIATRIC ORTHOPAEDIC CONDITIONS OF HIP JOINT (6)
Václav Ondrej, Urbášek Karel
A limping child is one of the most common reasons for visiting a pediatric orthopedist. In addition to
the injury, we always think about hip disease. The trouble may be caused by benign transient
synovitis, or it may be a serious problem like SCFE that can affect future quality of life, all the way
up to life-threatening septic coxitis.
Dysplasia of the Hip (DDH)
DDH is a disorder of hip joint development occurring both prenatally and postnatally, with an annual
incidence of 10-20 per 1000 newborns. It represents a group of various forms – may manifest as
acetabular dysplasia (disorder of the acetabular development where the "steep" bony roof does not
properly cover the femoral head) which can be associated with a certain degree of hip joint
decentration – subluxation (partial dislocation) or luxation (complete dislocation) of the femoral
head, with the need to further differentiate between reducible dislocations (so-called unstable hip)
and irreducible dislocations.
The disease typically exhibits a dynamic evolution, sometimes pathology identified at birth
spontaneously corrects, while at other times, the decentration may worsen.
The etiopathogenesis of DDH remains unclear, favoring multifactorial theories involving genetic,
mechanical, hormonal, and constitutional factors.
In Czech Republic, the diagnostic process is part of the mandatory newborn screening. Early
detection shortens the treatment duration and reduces the need for surgical intervention, thereby
decreasing the risk of early degenerative changes in the hip joint (pre-arthrosis) in the future. The
process involves clinical and sonographic examination, known as the triple stage examination. The
initial examination takes place at birth, the second at 6-8 weeks of age, and the third at 3-4 months.
In medical history, we explore the occurrence of disease in the family and the course of pregnancy.
During the clinical examination, we observed the positioning and movement of the lower limbs and
muscle tone, an indirect sign may be asymmetry of skin folds. The fundamental diagnostic maneuver
is the Barlow sign – during flexion of the hip and knee joints, the knee on the dislocated side is
lower; the Barlow test (dislocate) – applying pressure along the longitudinal axis of the thigh and
adducting the hip leads to the femoral head slipping out of the acetabulum; and the Ortolani test
(reduce) – moving the hip from adduction to abduction leads to reduction of the femoral head into
the acetabulum with an accompanying palpable phenomenon in the case of a reducible dislocation.
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The goal of ultrasonographic examination is to elucidate morphological changes in the hip joint, with
findings categorized according to Graf’s classification, from Type I (physiological) to Type IV
(dislocation).
After introduction of national screening program, the radiographic examination is indicated only in
cases of diagnostic uncertainty or for treatment monitoring, due to radiation exposure and the
predominance of the non-ossified skeleton.
The aim of therapy is to achieve a stable and properly centered femoral head in the acetabulum.
Conservative treatment should be initiated as soon as possible after birth, utilizing so-called
abduction devices, keeping femur correctly centered in the socket until proper development is
completed. In early stages (from birth to 3 months of age), the Frejka pillow is used, and in later
stages (3 months to 1 year of age), Pavlik harness is used. In cases of irreducible dislocation or
persistent hip joint instability, vertical (overhead) traction is indicated, which involves continuous
pulling of the lower limb using weighted loads to release juxtaarticular contractures, followed by
repositioning of the femoral head into the acetabulum. The traction regime is conducted during
hospitalization and followed by arthrography (contrast X-ray examination of the hip joint) under
general anesthesia, to reveal non-ossified articular structures. If successful repositioning is achieved,
the limb is fixed with a plaster cast for approximately 6 weeks.
Surgical therapy, an open hip reduction, is reserved for cases where reduction cannot be achieved
or maintained conservatively. It involves joint revision, removal of reduction obstacles, and
reduction of the femoral head, with possible additional procedures such as osteotomy of the proximal
femur and/or pelvis.
Complications of DDH depend on the extent of joint damage. Generally, DDH is considered a prearthritic
condition with the risk of early degenerative changes in the hip joint and development of
coxarthrosis. A feared complication of DDH therapy is avascular necrosis of the femoral head.
Legg-Calvé-Perthes Disease (LCPD)
This is an idiopathic aseptic (avascular) necrosis of the femoral head, with an annual incidence of 1-
25/100 000. It affects children aged 4 to 12, with the peak occurrence between the ages of 5 and 8.
Boys are more commonly affected, and approximately 10% of cases are bilateral.
The etiopathogenesis remains unknown, hypothesis involves the role of coagulation factors.
The first subjective symptom is usually load-related joint pain, often initially referred to more distal
areas (thigh, knee). Clinically we can explore restriction in the range of motion of the hip joint and a
characteristic "Perthes limp," which involves limping on the affected limb due to a combination of
antalgic and Trendelenburg gait caused by hip abductor muscles insufficiency.
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Paraclinical examination is based on X-ray imaging in 2 projections – anteroposterior and the socalled
Lauenstein or "frog-leg" view. In the early stages of the disease, skeletal changes may not be
visible on standard X-rays. MRI or bone scintigraphy, which allow for early diagnosis and prompt
treatment, have higher sensitivity. Ultrasound examination often reveals synovitis with intra-articular
effusion.
The course of the disease is individual, typically lasting several months and progressing through four
stages - the stage of necrosis and fragmentation, during which the femoral head becomes
mechanically vulnerable and may deform or collapse, followed by the stages of re-ossification and
remodeling, during which the bone structure is reconstituted.
In the differential diagnosis, transient synovitis, SCFE, infectious conditions such as septic arthritis
and osteomyelitis of the proximal femur, and rare forms of skeletal dysplasia (e.g.,
spondyloepiphyseal dysplasia) must be ruled out.
Treatment is based on the "containment" principle, which involves maintaining full coverage of the
femoral head by the acetabulum to prevent deformity and its associated consequences. This can be
achieved either conservatively or surgically, with the treatment method chosen based on the severity
of the disease and the patient's age.
Generally, for children under 6 years of age, conservative treatment predominates. This includes
relieving weight from the affected limb using crutches, physical rehabilitation, and possibly orthotic
devices (e.g., the Atlanta brace). For children over 6 years old and/or with significant involvement of
the femoral head, surgical treatment may be necessary. This typically involves relatively complex redirectional
osteotomy of the proximal femur and/or pelvis.
Complications and consequences of the disease include femoroacetabular impingement due to joint
surface incongruence from bone deformity, and the early development of secondary coxarthrosis.
Slipped Capital Femoral Epiphysis (SCFE, Coxa Vara Adolescentium, CVA)
SCFE is an acquired hip joint condition characterized by idiopathic non-traumatic slip of the femoral
head (epiphysis). It typically occurs in obese individuals (more frequently in boys) during the period
of growth acceleration (ages 13-15 for boys and 11-13 for girls) with an incidence of 1-10 per 100
000 children. Approximately 30% of cases are bilateral. The etiology is unknown, but hormonal
influences are evident. SCFE is more frequently observed in individuals with adiposogenital
dysmorphia. The pathogenesis involves transient subcapital growth plate weakening, resulting in
slippage of the femoral head into retroversion and varus (backward, downward and medial) during
period of rapid growth, often associated with significant overweight (high BMI).
Typically, the condition is categorized as:
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Chronic: symptoms develop over weeks to months (groin pain, often referred to the thigh and knee,
restricted hip joint movement), a hallmark is so-called Drehman sign (flexion of the hip joint is only
possible with external rotation)
Acute: prodromal symptoms develop for 2-3 weeks, often followed by sudden deterioration
accompanied by severe pain like that of a fracture (fracture-like pain)
Acute on a chronic basis: long-term issues with sudden worsening, with radiographic evidence of
remodeling changes in the growth cartilage
Diagnosis involves clinical examination and radiographic imaging of both hips (to compare sides
and assess the risk of bilateral occurrence) in two basic projections – anteroposterior and axial
(abduction). From both projections, the Southwick angle (HSA, head-shaft angle, between the axis of
the femoral diaphysis and epiphysis) can be calculated. The degree of slippage determines the
severity of the condition, classified as Grade I (mild, 0-30°), Grade II (moderate, 30-60°) and Grade
III (severe, >60°). The term "pre-slip" is used to describe changes in the growth cartilage without
measurable slip.
Differential diagnosis includes physeal trauma (epiphyseolysis), as well as Legg-Calvé-Perthes
disease or infectious hip joint conditions such as osteomyelitis or septic arthritis. A thorough medical
history is essential, considering any potential trauma and the patient’s age.
The principle of therapy is to restore the position of the femoral head and stabilize the growth plate.
For stable Grade I slippage, fixation with Kirschner wires or screws ("pinning in situ") is used. For
more severe slips, corrective osteotomy of the proximal femur is necessary. Only in unstable (acute)
slips can a closed reduction and pinning with Kirschner wires be performer.
Complications include chondrolysis – necrosis of the articular cartilage, which is often
spontaneously reversible, and the feared avascular necrosis of the femoral head due to damage to
the retinacular vessels supplying the epiphysis. This can lead to secondary deformity resulting in
femoroacetabular impingement and the development of early degenerative changes in the articular
cartilage (pre-arthrosis).
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BONE TUMOURS – TYPES, DIAGNOSTIC, TREATMENT MODALITIES (1)
Marian Kubíček, Lukáš Pazourek
According to the WHO classification of 2020, primary bone tumours are divided into 9 groups
according to the type of cell population that the tumour generates and more than 20 subtypes are
described.
Detailed knowledge of the WHO classification is beyond the scope of this paper.
Basic subdivision of bone tumours including an overview of the most common types:
A. BENIGN
• chondroma (osteochondroma/enchondroma), osteoma, osteoid osteoma, …
• SEMIMALIGNANT (locally aggressive) - benign histological picture of the tumour,
aggressive growth, high tendency to local recurrence when intralesional resection is
performed, rarely can form pulmonary metastases - giant cell tumour of bone,
chondroblastoma, osteoblastoma, ...
B. MALIGNANT
PRIMARY
• osteosarcoma (OSA) - the most common bone sarcoma in children and adolescents (usually
2nd decade), typically affects the metaphyses of the long bones in the knee (distal femur,
proximal tibia)
chondrosarcoma (CHoSA) - the most common sarcoma in adults, affecting mostly the flat
bones and proximal parts of the limb skeleton (typically pelvis, scapula, femur and proximal
humerus)
Ewing's sarcoma (ES) - the most common primary malignant bone tumour under 10 years of
age (usually 5-25 years), typically affecting flat bones (pelvis, scapula) and the
metadiaphyses of long bones
• haematological malignancies - they fall within the competence of haematooncology, the basis
of their therapy is systemic treatment, in some cases radiotherapy is also used, the surgeon is
mainly involved in the management of pathological or impending pathological fractures multiple
myeloma (the most common primary malignant bone tumour representing up to 1%
of all malignancies), primary bone lymphoma, ...
• - other very rare ones - chordoma, adamantinoma, angiosarcoma, ...
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SECONDARY (metastatic bone disease)
• typically breast cancer (osteolytic/mixed lesions), prostate cancer (osteoplastic
lesions - low risk of pathological fracture), lung cancer (osteolytic/mixed lesions), kidney
and thyroid cancer (osteolytic lesions, high vascularity)
Bone tumours can be lined up according to their incidence as follows: benign > secondary malignant
> primary haematological malignancies > primary sarcomas (rare, representing only 0.2-0.3 % of all
malignant tumours, up to 100 cases diagnosed annually in the Czech Republic)
The basis of diagnosis is a well taken medical history, clinical and paraclinical examination. Pain is
one of the most common symptoms, in malignant tumours it is often nocturnal, intermittent,
localized in depth and gradually worsening. Later, swelling, redness, palpable pain resistance or
impaired limb function may occur. Malignant tumours are usually accompanied by general nonspecific
symptoms (fever, loss of appetite, weight loss, leukocytosis, increased sedimentation,
elevation of CRP, ...). Bone tumours may be clinically silent for a long time and the first
manifestation may be a pathological fracture or, in the case of malignant forms, distant metastases.
Especially in benign and slow-growing lesions, they are also rarely captured as incidental findings on
imaging modality. The basis of non-invasive paraclinical examinations is X-ray or supplemented by
MRI/CT examination. Malignant tumours are characterized by an aggressive growth, periosteal
reaction, erosion of cortex and endosteal irregularities (scalloping). As part of staging, lung Xray/CT,
skeletal scintigraphy, and abdominal ultrasonography are supplemented. The collection of
material for histological examination can be performed by needle biopsy or excisional biopsy. Bone
tumours are a rare and often neglected diagnosis. It is necessary to think of this disease in differential
diagnosis - i.e. to have an oncological reflex. In particular, it is important to avoid prolonged
ineffective conservative therapy without having an X-ray or other imaging modality done.
Treatment should take place in specialized centers under the direction of an experienced
multidisciplinary team. The treatment strategy is chosen individually for each patient, often based on
the decision of a multidisciplinary tumour board.
Local treatment options include mainly surgery, radiotherapy and methods such as embolization or
radiofrequency ablation. According to the oncological radicality, surgical resection can be radical,
wide, marginal or intralesional and according to the degree of mutilation we distinguish:
A, ablative procedures (amputation, exarticulation)
B, limb-preserving procedures (curettage with cemento- or spongioplasty, resection without
replacement or with replacement using bone graft or endoprosthesis).
In systemic therapy, chemotherapy, hormone therapy, bisphosphonates and biological therapy are
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mainly used. In general, the principles of therapy vary according to the biological nature and type of
tumour.
OSA is a radioresistant tumour. The method of choice for low malignant OSA is radical surgery.
Treatment of highly malignant OSA is multimodal in the sequence: neoadjuvant chemotherapy surgery
(wide resection) - adjuvant chemotherapy.
CHoSA is a chemo-/radioresistant tumour. The method of choice is radical surgery.
ES is characterized by high chemo/radiosensitivity. After combined neoadjuvant chemotherapy,
local treatment takes place. Surgery is preferred over radiotherapy. Consolidation treatment is
followed by adjuvant chemotherapy/radiotherapy.
Bone metastases - indication for surgical treatment is most often pathological or impending
pathological fracture, less often resection of solitary or oligometastatic lesions in some types of
tumours. Bone metastases are surgically treated according to the extent of the disease and the
prognosis of the patient. In the case of bone solitary metastases and good prognosis of the underlying
disease, care is taken to ensure radicality of surgical therapy. Patients with multiple metastases and a
less favorable prognosis undergo the simplest possible procedure with early mobilization. The basis
of treatment is of course systemic oncological treatment of the underlying disease. Radiotherapy is
also often used.
Benign affections can be treated by intralesional procedures, most often by curettage of the lesion.
To reduce the number of local recurrences, it is advisable to combine curettage with the use of local
adjuvants (cryosurgery, application of phenol, bone cement, argon beam, ...).
A large proportion of benign tumours do not need surgical treatment or histological verification and
are often only observed.
In the case of localized forms of highly malignant OSA and ES, approximately 70-75% of patients
survive 5 years. If metastases are already present, approximately 30% of patients survive 3 years.
The prognosis for low malignant CHoSA is favorable if wide resection is possible. 90% of patients
survive 10 years. In highly malignant forms with a higher risk of dissemination and no possibility of
systemic treatment, the prognosis is significantly worse. Survival time in secondary bone tumours
depends on the extent of the underlying disease and the treatment options. With advances in systemic
cancer treatment, survival of patients with disseminated oncological disease is generally prolonged.
The goal of the orthopaedic surgeon is to ensure the quality of life of these patients.
Bone tumours in the spine form a separate chapter. The spine is a typical site of bone metastases and
multiple myeloma, on the other hand, the occurrence of primary bone sarcomas is very rare. The
main difference from other sites is mainly in the principles of surgical therapy.
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Patients without nerve findings undergo a multidisciplinary tumour board meeting where further
management is recommended. If a progressive, severe nerve finding is present, surgery is
performed within 24 hours of the onset of plegia or severe paresis. Surgery is performed by an
anterior approach (resection of the body, adjacent discs, replacement with special cages), posterior
(Th and L spine, transpedicular fixation) or combined approaches. Of course, systemic oncological
treatment and radiotherapy are also an integral part of the care and are indicated based on
histological examination and extent of the disease.
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BACK PAIN – DIFFERENTIAL DIAGNOSIS (4)
Chaloupka Richard, Ryba Luděk, Parížek Dominik
The basic step in the differential diagnosis of back pain is a thorough examination. It includes
medical history, physical examination, imaging methods and laboratory tests.
Medical history: Was there an injury? Is the pain at rest, at night (tumors, inflammations)? Assess
pain intensity (e.g.: VAS - visual analogue scale 0-10) and character of pain.
Physical examination: we evaluate the shape of the spine and its deformities (scoliosis?), the
condition of the muscles (symmetry, amount of muscle mass, spasm), mobility of the spine, limbs
(difference in length?), orientation neurological examination (is it a root irritation? is the sensitivity
(a)symmetrical? weakening of the limbs?)
Imaging methods: X-ray examination in standing position in 2 projections (anteroposterior and
lateral), especially for the lumbar spine. In trauma cases we need X-ray and CT examination, in some
cases MRI. For nerve involvement, inflammation, tumors we indicate MRI scanning. Bone
densitometry is useful for the diagnosis of osteoporosis.
Laboratory tests: used mainly to exclude inflammatory etiology, i.e. KO and CRP - blood count and
C reactive protein. In osteology, these are bone remodeling markers (BTM - Bone Turnover
Markers).
Pain is divided according to its duration into acute (up to 3 months duration) and chronic (over 3
months).
According to the etiology, we divide pain into nociceptive, neuropathic and mixed. Nociceptive pain
is caused by irritation of pain receptors by trauma, inflammation or tumor. Neuropathic pain is
caused directly by nervous system involvement (damaged nerve). Back pain may be isolated, without
irradiation (cervicalgia, thoracalgia, lumbalgia), or may radiate to varying degrees to the extremities
(pseudoradicular, radicular pain). Pseudoradicular pains do not follow a root distribution, they are
only in the proximal parts of the limbs. Radicular irritation has a typical localization (according to
the dermatome), in the same place it can be accompanied by tingling, burning. With severe nerve
oppression, there may neurological deficiency as hypesthesia or paresis.
The impairment may be functional, structural or combined. In functional impairment, we assess
mobility, range of motion and muscle status (symmetry, muscle strength). Structural impairment is
mainly revealed by imaging (X-ray, CT, MRI, densitometry).
Causes of back pain according to the affected tissue: vertebrogenic, discogenic (disc prolapse),
myogenic (most common, muscle imbalance), neurogenic, vascular, pain transmitted from internal
organs (e.g.: renal colic), psychosomatic, psychogenic (rare).
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Causes of back pain according to the pathological-anatomical division: congenital defects (e.g.:
scoliosis), degenerative disorders, tumors (most commonly metastases), injuries, metabolic diseases,
inflammatory diseases. Inflammatory diseases are divided into rheumatic inflammation (rheumatoid
arthritis, m. Bechterew's), non-specific inflammation (caused most often by staphylococci) and
specific inflammation (most often TB - tuberculosis).
We always treat back pain according to the etiology. In the differential diagnosis of back pain, we
must first exclude severe causes - trauma, inflammation, tumor or pathological fractures in
osteoporosis and tumors. The basis of treatment is rehabilitation, paying attention to correct posture,
regular stretching and strengthening of the abdominal and back muscles. It is important to exercise
daily. Rest only for the necessary time (few days), then active rehabilitation and return to normal
activities as soon as possible. Regimen measures such as sparing of the spine and changing positions
are important. Medication and braces are used only temporarily.
We indicate surgery when there is a clear cause of pain - injuries, inflammation, tumors, deformities,
spinal instability, worsening of neurological findings. In the cervical spine, treatment from the
anterior approach with vertebral fusion predominates. In the thoracic and lumbar spine, the posterior
approach with transpedicular fixation and vertebral fusion predominates.
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148
NECK INJURIES (54)
Urbanek Libor
In patients with a neck injury, only soft tissues or also deeper structures can be affected - vascular
injuries and injuries to the proximal GIT and airway may be life-threatening
The main causes of neck injuries include:
• Traffic accidents
• Professional injuries
• Sports and leisure activities
• Hobbies
• Crimes
• Suicides
We divide neck injuries into 2 main groups:
• Blunt trauma – skin surface without discontinuity
• Sharp trauma – characterized by open wounds affecting the skin and underlying tissues in
various depth
Blunt neck injury
• No open wounds
• Soft tissues are damaged by external pressure against underlying bony or cartilaginous
structures of the larynx and spine
• Simple contusions are very common
• Small or weak external signs may not correlate with the severity of the injury (minimal skin
changes, no visible hematomas, swelling, etc.)
• We must rule out lesions of deep neck structures (main vessels, larynx, trachea, spine,
proximal GIT) always in patients with a history of blunt neck trauma or the possibility of it
• Acute suffocation can occur as a result of edema, hematoma, or traumatic structural changes
Injuries to the larynx
These injuries can be both closed and open. A frequent etiology is suicide or as a result of
interpersonal conflicts. The thyroid cartilage is most often damaged. Damage to the larynx can result
in severe breathing problems, up to apnea, and even death. Blunt trauma to the larynx may be
followed by reflex cardiac arrest. Trauma can also cause edema or hematoma, which will lead to
narrowing of the airway. In severe neck injuries, destruction of the larynx structure, mucosal
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disruption associated with severe trauma and bleeding to the airways, and cartilage fractures may
occur.
Sharp neck injury
Sharp trauma causes open wounds. These can be of variable depth and direction and can therefore
affect different structures and organs of the neck. Heavy bleeding can occur especially when large
vessels are involved (opening of the ACC leads to death within 30 seconds without emergency first
aid). Various types of wounds such as vulnus lacerum, scissum, sectum, contusolacerum, etc. may
occur according to the traumatic mechanism.
Neck injury management
As part of the treatment, it is primarily necessary to control bleeding, which can be life-threatening.
Furthermore, possible suffocation must be urgently managed. It is mostly difficult to secure the
airways in the case of primary or secondary obstruction (edema, hetatoma, lacerations, injury and
deformation of the larynx cartilages). Orotracheal intubation is often impossible, coniotomy and/or
emergent tracheostomy must be performed. After basic stabilization (respiratory tract, bleeding,
blood pressure), it is necessary to rule out further injuries and treat open wounds. Revision to exclude
deeper and structural injury, removal of tissue debris and damaged tissue, lavage to clean the wound
and suturing. Heavily contaminated with severe tissue destruction should not be closed immediately.
Antitetanus prophylaxis should be a matter of course.
As part of the long-term consequences, post-traumatic stenosis of the larynx and trachea may
develope, and permanent tracheostomy can be long-term consequence
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CT scan -laryngeal trauma-fracture of the thyroid cartillage, destruction of arytenoids, laryngeal
obstruction due to oedema and haematoma, emphysema in soft tissues
3D reconstruction - oblique fracture of the thyroid cartillage
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SPINAL CORD AND SPINE INJURIES, INCLUDING VERTEBRAL FRACTURES (55)
Veselý Radek, Kelbl Martin, Wendsche Peter
Spine and spinal cord injuries
Spine injuries are serious disabilities that can lead to permanent consequences such as chronic pain,
deformities, motor and sensory impairments of varying degrees. Epidemiologically, there are 85
cases of spinal fractures per 100,000 inhabitants per year, 2/3 of the injured are men. The thoracic
and lumbar spine is injured in 75 % of cases, of which 50 % are Th11-L2 fractures.
1. Mechanisms of injury
• Compression: forces applied in the craniocaudal axis of the spine - typical mechanisms
include falling on the buttocks or extended lower limbs
• Hyperflexion and hyperextension: extreme anteroposterior or lateral bending of the spine
can lead to ligament injuries, more complex vertebral fractures or spinal cord compression. A
typical mechanism is a fall from a height onto the back
• Rotation: violent rotation of the spine can cause vertebral dislocation or fracture. Most
commonly high-energy injuries e.g. in road traffic accidents.
• Penetrating trauma: gunshot or stab wounds with direct damage to the spinal cord and
vertebrae
2. Classification of spinal fractures
The AO classification is the most used.
Due to the complex and unique anatomical conditions, upper cervical spine injuries are separately
classified (C0-C2). An example of an injury is the fracture of a dens axis in low-energy head injuries
in the elderly population.
The lower cervical (C3-7), thoracic and lumbar spine have a classification divided into 3 types:
• Type A - Compression fractures: these fractures primarily affect the anterior portion of the
vertebral body, leaving the posterior elements (vertebral arches and spinal processes) intact.
• A0: Isolated vertebral process fractures
• A1: Fractures of one end plate without injury to the posterior wall of the vertebra
• A2: Pincer fractures of the vertebral body
• A3: Fractures of a single end plate with posterior wall involvement (incomplete burst)
• A4: Cominuted fractures involving both end plates and posterior wall (complete
burst)
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• Type B - Distraction Injuries: These include damage to the spine resulting from excessive
stretching (extension) or bending (flexion) of the spine. These fractures can damage both the
anterior and posterior structures of the spine, and often result in a disruption of the stabilizing
ligaments.
• B1: Purely bony injury to one vertebra (Chance fracture)
• B2: Bone and/or ligamentous injury to posterior structures
• B3: Extension injuries (typical of m. Bechterev)
• Type C - Dislocated injuries with translation or rotation: these are the most severe
injuries that are caused by high-energy violence with a combination of rotational forces and
other mechanisms (compression, distraction). These fractures are accompanied by
neurological deficits in up to 90%.
3. Stability of the injury
An unstable injury is a case where the physiological range of motion results in abnormal mobility of
the injured segment and a threat to the spinal cord or other neural structures. Unstable injuries are
usually indicated for surgical treatment.
4. Clinical manifestations
Clinical manifestations depend on the site and severity of the injury. The main manifestations
include:
Soreness at the site of injury, deformity (gibus), local haematoma, palpable defect in the area of the
posterior structures of the spine. The most serious are neurological symptoms:
• Paraplegia: transverse spinal cord lesions below the C8 level, complete sensory and motor
deficits below the injured segment of the thoracic or lumbar spine.
• Tetraplegia: transversal spinal cord lesions above Th1 level, complete sensory and motor
deficits of trunk and lower limbs, varying severity of upper limb involvement depending on
the level of injury
• Paraparesis and tetraparesis: incomplete spinal cord lesions (some function preserved)
• Root syndromes: irritation or paresis of the injured nerve root according to the level of
injury (pain in the relevant dermatoma, loss of sensation or motor function of the relevant
root).
• Caudae equinae syndrome: multiple nerve roots below the L2 level are affected,
characterized by impaired sensation, motor skills, impaired urinary and anal sphincters.
5. Diagnostics
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• Clinical examination: based on the history and mechanism of injury, the physician assesses
local findings, pain, motor and sensory functions, autonomic functions and general
neurological status
• Radiological examination:
• X-ray in two projections - basic overview of fractures and dislocations
• CT including 2D and 3D reconstructions to show bone injuries in more detail, show
sites difficult to access on X-ray (e.g. C-Th level).
• Until a fracture is clearly ruled out, treat the patient after major mechanisms of
trauma as if they have a spinal injury (immobilization, hard collar)
• MRI provides the best view of soft tissues such as the spinal cord, intervertebral discs
and ligamentous structures. In severe acute conditions, the usefulness is limited due to
lower availability and the length of the examination
• Other examination - neurological, EMG, motor and sensory evoked potentials (MEP, SEP)
6. Treatment
• Conservative management - wherever stability is not significantly compromised, no risk of
deformity, no neurological symptoms, contraindications to surgery (internal, age, non-
cooperation).
• Hard cervical collar (Philadelphia) - stable C spine injury
• Halo-apparatus - more stable fixation of the C spine - 4 screws fixing the halo ring to the
skull and then connected to the halo-vest on the trunk
• SOMI - sternal-occipital-mandibular-immobilization - a brace consisting of a cervical
collar and thoracic stabilizer, used to immobilize the upper thoracic spine (above Th6)
• Jewett brace - orthosis for fixation of Th and L spine fractures
• Surgical stabilization
• Isolated anterior approach - the gold standard for cervical spine injuries and some types
of Th/L spine injuries. It consists of repositioning, removal of the vertebral body or
intervertebral disc, replacement with a bone graft or other implant and stabilization with a
bridging plate. The aim is to create a fusion of the damaged segment of the spine.
• Isolated posterior approach - a typical procedure in thoracic and lumbar spine injuries,
consists of inserting screws into the pedicles above and below the injured segment,
repositioning the axis and height of the vertebral body and connecting the screws with
rods.
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• Combined approach - in severe injuries with significant comminution, a posterior
approach is followed by the addition of an anterior approach.
• Rehabilitation: an important part of the treatment is physiotherapy and rehabilitation aimed at
restoring function, preventing muscle atrophy and improving the patient's quality of life.
Obr.: AO Spine Thoracolumbar Injury Classification System
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CHEST INJURIES (52)
Peštál Adam
Nosology a
Concept - A chest injury is a trauma affecting the thorax or intrathoracic organs.
Etiology - Mechanical impairment of the chest is caused by contusion, compression or deceleration.
Pathogenesis - chest trauma may result in severe conditions associated with impaired ventilation and
circulation. Causes of ventilation impairment include airway injury, lung compression, lung
contusion, and inadequate breathing mechanics. Circulatory failure is caused by hypovolemia in
hemorrhage or cardiac injury, cardiac tamponade. Subsequent complications of injury can result in
very serious conditions such as ARDS, SIRS, MOF.
Severe chest injuries are divided into critical: massive intrathoracic haemorrhage, tension
pneumothorax, airway obstruction, cardiac tamponade, chest wall instability. And potentially lifethreatening
conditions: aortic injury, diaphragmatic rupture with herniation of abdominal organs,
tracheobronchial injury, oesophageal injury.
Nosology b
Clinic - the clinical manifestations of the injury are very varied, but conditions associated with
impaired ventilation or circulation are in the foreground. Manifestations are dyspnoea,
hyposaturation, hypercapnia, hypoxaemia, chest or tachycardia, hypotension. On examination, we
monitor respiratory excursions, jugular venous filling, assess chest stability, crepitations,
subcutaneous emphysema by palpation, and investigate auscultatory findings. The mechanism of
chest injury should always be considered. Great caution is needed in the initial diagnosis of
penetrating chest injury in the area medial to the medioclavicular line. The injury is often associated
with cardiac or large vessel involvement. In fractures of the caudal ribs, injury to intra-abdominal
organs - liver or spleen - should be thought of.
Laboratory examination - standard basic laboratory examination is extended by Astrup blood test
and determination of cardioenzymes.
Imaging methods - in the care of patients with chest trauma requiring admission to the high
threshold UP, FAST or direct CT is the method of choice - the so-called trauma protocol, e.g.
triphasic hybrid protocol. In other cases, chest X-ray and chest ultrasound are used. Chest X-ray is
also performed in lateral projection, to exclude fracture of sternum, thoracic vertebrae.
Treatment - in the case of a mild injury, treatment is conservative, i.e. physical examination, relief
in a semi-sitting position, sufficient analgesic therapy (pleural pain is very intense due to the
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sensitive innervation of the pleura), conservative treatment is also possible in the case of serial rib
fractures and so-called door fractures (double serial fractures). In the situation of an unstable chest
with significant impairment of respiratory mechanics with hypoventilation or extensive reduction of
pleural volume, surgical stabilization of the ribs with osteosynthetic splints is indicated. In case of
minor PNO or haemothorax, conservative therapy is possible provided very careful observation of
the patient. As a rule, however, these findings require thoracic drainage, ideally modo Elander, even
in the case of PNO! Drainage in the V intercostal space in the anterior or middle axillary line. Before
drainage, the position of the diaphragm should be known (to exclude diaphragmatic rupture or the
presence of diaphragmatic hernia). It is necessary to master the correct technique of chest drain
insertion. In PNO, one should always think of a form of so-called pressure overload PNO with
mediastinal compression, this situation can also occur gradually over time! It is necessary to monitor
the patency of the drain, the nature of the secretion, its quantity and the general condition of the
patient - shock curve, anaemia, ventilation parameters. In case of continued bleeding, it is necessary
to search for the cause of bleeding we perform control angio CT to identify active bleeding from the
injured intercostal artery, lung... Often a surgical revision is necessary. Surgical revision is always
indicated for penetrating chest trauma. In the case of a stable patient, revision is also possible by
VATS. Treatment of tracheal and main bronchial injuries is conservative (observation, lesion gluing,
stenting) or operative. It depends on the extent of the injury and symptomatology. If surgical
treatment is necessary, right-sided thoracotomy is the most common approach. Urgent thoracotomy
is indicated in case of suspected cardiac tamponade (clinical picture - Beck's triad, ultrasound
examination). The approach is complete longitudinal sternotomy or anterolateral thoracotomy in the
Vth intercostal space. Separate chapters of the scripts are devoted to the treatment of oesophageal
and spinal injuries. Patients with severe chest trauma are often treated in the ICU or the ARC
according to their respiratory status. Targeted ATB therapy, respiratory care, adequate nutrition and
rehabilitation are an integral part of treatment.
Nosology c)
Complications - a potentially very diverse spectrum resulting from the nature of individual injuries,
generally the risk of rebleeding, the development of infectious complications in the sense of
pneumonia, pleural empyema, infections in the wound.
Prognosis - some types of chest injuries are fatal, especially avulsion injuries of the aorta or VCS
with deceleration mechanism. Cardiac injury is often fatal. In the case of combined trauma or
polytrauma, chest injury significantly increases both morbidity and mortality. In view of the
advances in medical care, especially in the field of ARO (ECMO, UPV, elimination methods...) and
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in the field of microbiology, the prognosis of patients with severe chest trauma is incomparably more
favourable than in earlier times. Active surgical treatment also contributes to the success of
successful cure of patients.
Prevention - specific prevention consists in the use of available protective equipment both at work
and in sport. In traffic, the use of seat belts. When working at heights, correctly stabilized so-called
approach aids (ladder, scaffolding...) or the use of "climbing" belay.
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ABDOMINAL INJURIES (51)
Konečná Drahomíra, Mihalčin Matúš, Horváth Teodor
Abdominal trauma includes penetrating and blunt injuries of the abdominal wall, injuries to
the parenchymatous abdominal organs, gastrointestinal (GI) tract and its vascular supply, starting
with the cardia and ending with the rectum and anus.
A subgroup of abdominal trauma is retroperitoneal (RP) organ injuries, with the magistral vessels
running in the RP and pelvic organs. The hemoperitoneum is a life-threatening internal bleeding with
an accumulation of blood in the abdominal cavity. It arises from traumas of the spleen, liver or the
vessels of the GI tract. The clinical signs of massive bleeding are abdominal pain, pale-coloured skin,
tachycardia, and arterial hypotension, with physical findings corresponding to the mechanism of
injury. The laboratory methods and imaging confirm this diagnosis.
The multidetector computed tomography (MDCT) is employed in modern diagnostics,
especially in polytrauma patients. The extent of the injury is shown, and its classification is enabled –
creating basic conditions for the exact decision-making process of appropriate treatment options
1/conservative, i.e. nonoperative 2/ damage control surgery (DCS) 3/surgical anatomical reparation.
Careful follow-up is included in the choice of conservative treatment.
Damage control surgery (DCS) is represented by the life-saving arrangement of actions in
patients with critical polytrauma. It aims to restore the physiological functions before anatomical
restoration in the following order:
Hemostasis, contamination control by lavage and drainage, prevention of hypothermia, renewal of
homeostasis, including coagulation, preventing abdominal compartment syndrome in the case of the
need for a temporary closure of the abdominal wall. An integral part of the treatment is the
prevention of Deep Vein Thrombosis (DVT).
LIVER
Conservative treatment can be undertaken in hemodynamically stable patients with blunt
liver injury of Grade I and II (see Fig Fix1) with small hemoperitoneum (no circulatory response).
Follow-up is required.
For patients with continuing bleeding, surgical intervention is indicated with surgical revision
of all particular anatomical structures. Performed through the upper midline or transversal incision,
the surgery starts with hemostasis by manually compressing the liver against the posterior abdominal
wall. The operating surgeon then searches for other injuries and sources of the bleeding.
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If, in liver wounds, there is extensive bleeding or the source of the bleeding cannot be found,
the Pringle manoeuvre is a solution. This is the insertion of a vascular clamp across the porta
hepatis en bloc, followed by management of the vascular structures and the branches of the bile duct.
Small vessels can be cauterised or ligated. Managing greater liver veins requires a vascular suture on
the vascular clamp. Then, an anatomical reconstruction of the parenchyma is performed using
absorbable adaptation mattress sutures. If the Pringle manoeuvre does
not stop the bleeding but only reduces it, this indicates retrohepatic venous trauma.
In the case of greater liver resection, there is a need to avoid 1/ the interlobar plane being endangered
by injury of the middle hepatic vein and 2/ the plane of the falciform ligament where there is a
danger of damage to the portal vein.
The liver packing using gause pacs or abdominal towels is indicated in the circumstances of
1/diffuse nonsurgical oozing, 2/developed coagulopathy, 3/if a less experienced surgeon needs to
stabilise the patient who is waiting for a specialist or before the transfer to a more specialised
hospital, e.g. university hospital.
The omentoplasty: After significant bleeding has been controlled, oozing can be stopped
with the omentum used
as a living pack and obliteration of dead space (bolster sutures).
Debridement: Small fragments of necrotic tissue should be removed from the wound.
Nonsurgical hemostasis can utilise (porcine) gelatine foam, oxidised cellulose, microfibrillar
collagen, human thrombin, fibrin glue, and autologous concentrated fibrin platelet enriched fibrin
sealants and medical technologies such as monopolar or bipolar electrocautery using high-frequency
electric current or Argon beam generator - the procedure destroying tissue with high-frequency
electric current passed through a stream of argon gas to the tissue.
Liver drainage: Every Grade III or greater liver laceration should be put in the drain to
monitor postoperative bleeding (PB) and biliary secretion. Early PB usually comes from an
undiscovered injury of the hepatic artery. Late PB can be a consequence of arterial pseudoaneurysm
manifested by hemobilia. In such cases, invasive radiology with catheter
embolisation of the right or left hepatic artery branches is considered.
SPLEEN
Conservative treatment is indicated in hemodynamic stable patients after blunt abdominal
trauma with no or minimal bleeding into the peritoneal cavity without continuation (Fig 2, Grade I).
Surgical treatment: The access to the spleen is enabled by upper midline or left subcostal
incision.
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Except the hilar branching of the splenic artery is not constant, keep surgeon in mind the vessels of
gastrosplenic, splenocolic, phrenicosplenic, and splenorenal ligaments and the presence of pancreatic
tail near the hilus of the spleen. For the assessment of the splenic injury, mobilisation is needed by
cutting all upper mentioned ligaments, removing the clots from injured areas, and ligating injured
vessels.
According to features of the injury (Fig 2, Grade II, III, IV), the following treatments options may be
used:
A. Splenic salvage
Splenorrhaphy by individual mattress sutures with viable omental plug and Teflon pledges.
Its success is limited by the fragility of splenic parenchyma.
Splenic capping with absorbable polyglycolic acid mesh or nonabsorbable teflon wrapped
around the spleen to tamponade the injury. Drainage is needed after splenic salvage operations.
To stop the nonsurgical bleeding, the same pharmaceutical products and technologies are
mentioned under the subsection liver.
Partial or Hemisplenectomy using an ultrasonic surgical aspirator or laser is represented by
segmental vessel ligation, resection, and mattress sutures. The omentum, splenic capping and
wrapping can be utilised.
B. Splenectomy
The splenectomy is clearly indicated in the case of a completely shattered or avulsed spleen
or hilar laceration (Fig 2, Grade V). This procedure is performed as one fastest, especially in higher
grade spleen injury in patients with current serious trauma of the neurocranium, thorax, and pelvis,
and in patients with coagulopathy.
The risk of Overwhelming PostSplenectomy Infection (OPSI) is lifelong. Immediate
postoperative prevention is represented by wide spectrum antibiotics (ATB); prospective protection
means routine vaccination against Streptococcus pneumoniae, Haemophilus influenzae, and
Neisseria meningitidis and annually against influenza and COVID-19, both with a predisposition to
bacterial superinfections. Before the discharge, the patient should 1/ get notified of the necessity of
seeking medical attention at the elevation of body temperature to 38°C (100°F) and to be equipped
with the prescription of emergency reserve of ATB; these will be used no later than 2 hours after the
onset of the fever.
As emergency antibiotics (ABx) are chosen, amoxicillin/clavulanate 1 gram tablet to be taken every
6-8 hours or cefuroxime/axetil 500mg tablet to be taken every 6-8 hours Whereas, in patients with
penicillin allergy, moxifloxacin 400mg tablet per day.
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VESSELS
The vascular trauma is manifested by hematoma or intraabdominal bleeding with obvious
signs of acutely damaged abdomen and hypovolemia. It is not usually isolated. Midline (central)
supramesocolic hematomas, including haemorrhage into the lesser sac and inframesocolic
hematomas, should be opened and explored by midline incision from the xiphoid process to
symphysis.
Periduodenal, periportal, and right-sided pericolic hematomas are clarified by Kocher
manoeuvre – i.e. the releasing and medial rotation of the duodenum and the head of the pancreas.
Cutting of parietal peritoneum from hepatic flexure laterally longitudinally alongside right colon
down to caecum uncovers inferior vena cava. The operation continues with tamponade, followed by
revision. A vascular suture or venous patch treats the solitary lesion. In a dramatically hemodynamic
unstable patient with more injuries of the inferior vena cava, there is no other way except its ligation.
Collateral vessels will develop.
The source of the hematoma or haemorrhage in the region of the right upper abdominal
quadrant is the superior mesenteric artery or vein. For the overview, digital compression is needed
between the index and middle finger placed into foramen Winslow behind the head of the pancreas
and thumb on its anterior surface. Discovered injury can be tamponaded with a finger or controlled
with a Satinsky clamp and sutured.
The simple suture of the vein (venorrhaphy) or venous patch is indicated in a circulatory
stable patient. The ligature of the portal vein is possible in the circulatory unstable patient.
Central inframesocolic hematomas are accessible after retracting the transversal colon
cephalad and small bowel to the right. They may be caused by injury of visceral vessels or the aorta.
If the vitality of the bowel is damaged, resection is needed.
The assessment of bowel vitality is facilitated by the fluorescence of the indocyanine green
(ICG) dye administered into the circulation through the peripheral vein. The fluorescence is
generated by irradiating the operating field with near-infrared electromagnetic waves (806 nm). ICG
absorbs the waves, and its energy is emitted in the visible part of the light spectrum. The intense
green colour of the bowel confirms physiological blood perfusion.
COMMENTS AND CONTROVERSIES
There are different classifications of liver and spleen injury. The illustrative examples of their
complexity were chosen here.
Quite small subcapsular hematoma of the spleen or liver can break too in a time period of
some hours to some weeks, giving rise to bleeding or even two-stroke rupture.
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Figure 1: Liver Injury Scale by Arthur J. Donovan
GRADE
I Hematoma Subcapsular, nonexpanding, <10% surface area (SA)
Laceration Capsular tear, nonbleeding, <1 cm parenchymal depth
II Hematoma Subcapsular, nonexpanding, 10% to 50% SA
Laceration Capsular tear, active bleeding
1 to 3 cm parenchymal depth, < 10 cm in length
III Hematoma Subcapsular, >50% surface area or expanding
Ruptured subcapsular hematoma with active bleeding
Intraparenchymal hematoma >2cm or expanding
Laceration >3 cm parenchymal depth
IV Hematoma Ruptured intraparenchymal hematoma with active bleeding
Laceration Parenchymal disruption involving 25% to 50% of hepatic lobe
V Laceration Parenchymal disruption involving > 50% of hepatic lobe
Vascular Juxtahepatic venous injuries (i.e. retrohepatic vena cava, major hepatic veins)
VI Vascular Hepatic avulsion
Figure 2: Splenic Organ Injury Scale by American Association for the Surgery of Trauma
GRADE
I Nonexpanding subcapsular hematoma involving <10% of surface area (SA)
Nonbleeding capsular laceration with <1 cm deep parenchymal involvement
II Nonexpanding subcapsular hematoma involving 10% to 50% of SA
Nonexpanding intraparenchymal hematoma <2 cm in diameter
Bleeding capsular tear or parenchymal laceration 1 to 3cm deep without of
trabecular vessel involvement
III Expanding subcapsular (subcaps.) or intraparenchymal hematoma
Bleeding subcaps. hematoma or subcaps. hematoma involving > 50% of SA
Intraparenchymal hematoma > 2 cm in diameter
Parenchymal laceration >3 cm deep or involving trabecular vessels
IV Ruptured intraparenchymal hematoma with active bleeding
Laceration involving segmental or hilar vessels producing major
devasculari sation (> 25% splenic volume)
V Completely shattered or avulsed spleen
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Hilar laceration that devascularizes entire spleen
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GASTROINTESTINAL TRACT INJURIES (53)
Penka Igor
Injury to the gastrointestinal tract can affect any part of the digestive apparatus, whether it is the
parenchymatous organs (liver, spleen, pancreas) or the intestinal tract at any level. It can be open –
penetrating injuries from stabbing, cutting, cutting or gunshot wounds, but also blunt injuries from
contusions of the abdominal wall, where the intensity of the injury mechanism plays a crucial role.
The most serious are high-energy injuries from traffic accidents and falls from heights, which is a
very important anamnestic data in itself. In these cases, gastrointestinal tract (GIT) injury is usually
part of a serious associated injury or part of polytrauma. Iatrogenic injuries during instrumental
diagnosis and therapy (endoscopic and radiointerventional procedures and invasive procedures in
any field) also form a significant group. Of the GIT injuries, the most serious are those that lead to
leakage of the contents of the gastrointestinal tract into the environment – mediastinum, free
abdominal cavity, retroperitoneum. All of these conditions are extremely serious and are
immediately life-threatening. Symptomatology and diagnosis. The difficult fact is that the
symptomatology of these events can be relatively poor at the beginning and the only data on which
the surgeon can rely is the anamnestic data of the insult and almost always pain of varying intensity
in the immediate period after the injury. A slightly later symptom is usually fever, sometimes
associated with shivering. Also, during clinical examination, the picture is initially poor and nonspecific.
Peritoneal symptoms also appear with a certain delay. In laboratory examination, an
increase in inflammatory indicators – CRP and leu – is characteristic. However, the greatest support
for diagnosis can be found in imaging methods – especially in contrast CT scans. Of the native X-ray
methods, X-ray of the lungs with pathognomonic enlargement of the mediastinum in mediastinitis
will help. In perforation of the GIT, native X-ray subphrenis in a standing position, which
demonstrates a more massive pneumoperitoneum. In cases where we suspect a possible injury of the
gastrointestinal tract supported by clear apathic data even with poor symptomatology and almost
negative clinical examination, we do not hesitate to request a contrast CT scan on the suspicious area
(chest, abdomen, retroperitoneum). If the patient is circulatory stable and there is no danger of delay,
there may be room for diagnostic laparoscopy (thoracoscopy), which also carries significant
therapeutic potential in the form of laparoscopic treatment. In the case of severe concomitant injuries
or polytraumas, often associated with circulatory instability or unconsciousness, the requirement for
contrast whole-body CT examination is usually implemented in emergency departments with
concomitant circulatory restitution of the patient.
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Surgical treatment. It has already been said that GIT perforation events are among the most serious
conditions in surgery and are indicated for urgent surgical treatment.
The extent of perforation is absolutely essential – from small perforations in the range of a few mm
to extensive devastation of long sections of the GIT with destruction, bruising and devitalization of
the wall of the GIT organ in the immediate vicinity of the perforation hole. A timely surgical revision
allows suture to be performed – with a single or continuing suture, or with the stapler technique. The
later the surgical revision is performed, the more extensive changes in the vitality of the perforation
area can be expected, in addition to the progressive development of infection in the immediate
vicinity of the defect. After 24 hours, the hope of the suture being successful is small and later it is
not even advisable to attempt suture. In cases of a time delay, there are only the options of surgical
drainage as a definitive treatment, or, on the contrary, complex extensive resection procedures,
usually with the establishment of a derivation of the more oral sections of the GIT - a stoma with the
prospect of temporariness, which is in many cases relative. It is always necessary to keep in mind the
invaluable assistance of interventional radiology and endoscopy with the therapeutic potential of
stent insertion (mainly in cases of esophageal injury). In cases of severe concomitant injuries and
polytraumas, perforation injuries of the gastrointestinal tract are evaluated as rather secondary
concomitant injuries, which must be treated surgically during urgent surgical revisions – of course,
according to the principles of Damage Control Surgery. This represents the fastest possible closure
of the GIT perforation (stapler resection of the intestine), without any reconstruction, which is
performed in the second period after stabilization of the patient. Oesophageal injury: not a common
injury, but not an isolated one. Examples are burns of the esophagus by acid or lye or swallowing of
foreign bodies. Both either by mistake or as part of self-harm. Serious perforation injuries occur most
often during endoscopic procedures. From the perforations of the esophagus, it is necessary to
mention the not quite exceptionally occurring so-called Oesophagus perforation. Boerhaave
syndrome – spontaneous rupture of the distal esophagus due to excessive vomiting, mostly
postprandial in allocoholics. Chemical burns – acid causing coagulation necrosis, alkalis causing
colic necrosis. The mucous membrane of the esophagus is affected first, but if a larger amount is
used and prolonged exposure to noxa, necrosis of the entire esophageal wall can occur. It is always
necessary to rule out perforation of the esophagus – p.o. contrast CT scan or X-ray contrast
examination with aqueous solution, careful gastrofibroscopic examination to assess the extent of
oesophageal involvement, including the stomach. In non-perforating cases, it is possible to proceed
conservatively and carefully monitor whether perforation develops. Therapy consists of
administering analgesics, treatment of the shock state. Immediately after the burn, chemical
neutralization can be attempted. For acids, it is best to use water or soda (sodium bicarbonate), for
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alkalis, significantly diluted with vinegar water. It is necessary to ensure nutrition - in mild cases it is
possible to take fluids after the disease, in more severe cases it is necessary to provide enteral
nutrition by nasojejunal tube.
In case of suspicion of perforation, it is necessary to administer antibiotics and surgical solution,
which is very difficult in the most severe cases with extirpation of the esophagus and establishment
of a derivative cervical esophagostomy and a nourishing gastrostomy (jejunostomy) with the
prospect of reconstructive surgery in the second period. Injury to the duodenum. It is similar to
oesophageal injury in incidence, diagnostic and therapeutic severity, including high mortality. It can
occur with blunt and penetrating abdominal trauma and can be associated with injury to surrounding
organs, including major vessels. It also occurs following instrumental endoscopic procedures of the
duodenum, biliary tract and pancreas (ERCP and papillotomy, extraction of choledocholithiasis and
placement of stents in the biliary and pancreatic ducts). The most serious are, of course, perforating
injuries of the duodenum with extraluminal leakage of duodenal contents - with development of
peritonitis in the case of leakage into the free abdominal cavity, or - development of retroperitoneal
phlegmon in the case of leakage of duodenal contents into the retroperitoneum. Surgical treatment, as
with oesophageal treatment, depends on the extent and location of the perforation and the vitality of
the duodenal wall around the perforation. Suturing of the duodenal wall can be performed in the
mildest cases, while more extensive, devastating injuries may require complex resection and
reconstruction procedures (anastomosis with the small bowel). Gastric injuries are considered for
penetrating injuries and blunt abdominal injuries – blows to the front abdominal wall, injuries caused
by car belts in traffic accidents. The most serious are certainly perforations with leakage of gastric
contents and the development of acute peritonitis. All of the above applies to the diagnosis and is
rather based on the detection of pneumoperitoneum, which is in itself an indication for urgent
surgery. The stomach is usually easily accessible and suture of even larger defects is usually well
done. In more severe cases, it is necessary to perform a resection with a connection of the stomach
with a thin loop. The issue of thin loop injuries is practically identical. However, in the case of colon
injuries, in the case of more extensive perforations, often with nine-fold perforation and insufficient
vitality of the intestinal wall around the perforation, we cannot avoid a resection procedure and,
above all, the need for a colostomy. Anorectal injury is relatively rare. It most often comes as a
foreign body injury and as an iatrogenic injury during diagnostic-therapeutic colonoscopy.
Perforation injury of the intraperitoneal part of the rectum leads to the development of stercoral
peritonitis. Injury to the extraperitoneal part of the rectum leads to infection in the area of the small
pelvis with the formation of pararectal, periproctal abscesses. In the diagnosis, anamnesis and
clinical examination play a crucial role, with an emphasis on per rectum examination, which often
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shows a palpable rectal defect. It is beneficial to perform ano-rectoscopy as soon as possible.
Contrast CT imaging is also a standard diagnostic method – in case of uncertainty, magnetic
resonance imaging (MRI) may be important. The aim of surgical treatment is to treat the rectal
defect, prevent infection, maintain continence and evacuation function of the rectum.
A crucial role, as in the case of the oesophagus and duodenum, is played by the extent and location
of the affliction. Minor perforations of the intraperitoneal rectum can be treated by simple surgical
suture, extensive devastation by difficult resection procedures, in the vast majority of cases with
simultaneous establishment of a derivation stoma. Extraperitoneal rectal injury with the development
of abscesses is treated by drainage (CT-guided or transanal), in more extensive injuries it is
necessary to establish a derivation stoma. Very serious injuries with relatively high morbidity include
almost exclusively iatrogenic injuries of the biliary tract – most often in laparoscopic
cholecystectomy. Quite exceptionally, hepatocholedochus injury also occurs during biliary tract
instrumentation during ERCP or difficult extractions of bulky choledocholithiasis. Now in the era of
laparoscopic cholecystectomy, the frequency of biliary tract injuries has practically increased – 0.7%
of LSK cholecystectomy. Diagnosis is based on the postoperative course - abnormal abdominal drain
waste, increase in obstructive liver enzymes, elevation of serum bilirubin values. An acute ERCP
examination and contrast CT examination with an assessment of arterial supply to the liver play a
crucial role in the diagnosis. If it is a bile duct injury with preserved continuity, then the method of
treatment is endoscopic treatment or interventional radiology options (ERCP, stent insertion or PTD
drainage under CT navigation). In the case of complete rupture of the bile duct or even loss injury,
the method of choice is a surgical solution with anastomosis of the severed ends of the bile duct end
to end on a T drain, or the establishment of a biliodigestive shunt. Injury to the omentum and
suspension apparatus of the intestine. It occurs in penetrating and blunt rather high-energy injuries.
In most cases, it is associated with injury to surrounding organs. It is manifested by bleeding from
injured blood vessels – hemoperitoneal syndrome. In cases of mesentery and mesocolon injuries, the
main vessels may be affected, resulting in necrosis of the intestinal wall with perforation and leakage
of GIT contents into the abdominal cavity – perforation peritonitis syndrome. Diagnosis and
treatment are governed by the principles of the affected organ – see above.
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TENDON INJURIES, DUPUYTREN'S CONTRACTURE (56)
Menoušek Jan, Kubát Martin
Dupuytren's contracture is a benign, slowly progressive fibroproliferative disease of the palmar
aponeurosis, event. other localities (plantar aponeurosis – Lederhose’s disease, penis - Peyron's
disease). It is characterized by the formation of retracted skin in the palm, as well as the formation of
nodules and bands in the palmar and digital fascia, which shorten and lead to finger contracture and
thus limitation of hand function. The flexor tendons are not involved in the contracture and are intact.
The disease is named after the French surgeon Guillaume Dupuytren.
Dupuytren's contracture is an autosomal dominant disease with variable penetrance. Negative
influences promoting the onset of the disease are heavy manual labor, smoking, diabetes, epilepsy,
and repetitive trauma to the hand. Rheumatoid arthritis is considered to be a protective influence.
The disease is referred to as Viking disease and the highest prevalence is in Scandinavia and
Western Europe. The disease has a median age of onset of 50 years, with the incidence of the
disease increasing with advancing age. The earlier the disease manifests, the more aggressive the
disease behaves and the risk of recurrence increases. The incidence in males is 10-15 times higher
than in females and the white race has the highest incidence, unlike other races where the
incidence is more sporadic. The disease progresses in three stages. Proliferative - fibroblastic
proliferation and nodule formation. Involutional - fibroblasts are not regulated and transform into
myofibroblasts. Residual stage - type III collagen begins to be deposited and this connective tissue
begins to organize into bands that the fingers of the hand subsequently contract.
Classification of Dupuytren's contracture according Karfík (it is not very accurate and does not
allow to evaluate the postoperative outcome): This classification consists of three types of hand
involvement: palmar, simple and complex. The Tubiana complex classification seems to be the most
appropriate.
Indications for surgery: a) a positive "table top test" (the patient does not touch the table with the
entire palm surface when placing the hand on the table), b) painful nodules in the palm - painful
gripping when the neurovascular bundle is compressed, c) 30st flexion contracture in the MP, or
any other contracture in the PIP, d) as soon as the patient starts to be bothered by the disease.
Treatment of the disease can be conservative, minimally invasive, surgical and enzymatic
(collagenase application). Follow-up rehabilitation is an integral part of the treatment.
Fasciectomy (on the finger) and aponeurectomy (in the palm of the hand) are the most commonly
used invasive surgical procedures in which surgical removal of the pathological contractile band
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from the finger ray is performed. According to the extent, they are divided into limited, regional
(usually ulnar half of the palm) or total.
The disadvantage of this method is a long convalescence, the advantage is the immediate and longterm
effect of the operation. Dermofasciectomy is a surgical solution in which the contracting bands
and nodes are removed with the skin and the defect is covered with a skin graft. Percutaneous
aponeurotomy is a minivascular method in which the pathological contracting bands are cut through
and released from the skin by means of a needle through tiny punctures in the skin. The advantage of
the method is a very short recovery time and a limited amount of scarring. The disadvantage is early
recurrence. It can be complemented by lipografting, in which a small amount of fat is additionally
removed from the abdomen or buttocks using the lipoaspiration technique, the fat is centrifuged or
sedimented and then infiltrated into the operated area using a special application cannula.
Rehabilitation: varies from one surgical procedure to another and according to the surgeon's habits.
After fasciectomy/aponeurectomy, a splint is applied immediately after surgery volarly with
compression, where the fingers are flexed as if holding a ball in the hand. Flexion and compression is
important because of the attachment of the skin flaps to the underlying skin and because of the lack
of skin cover (in extension, it would be necessary to cover the volar defects with a skin graft). After
all sutures are removed (3 weeks after surgery), we begin full finger rehabilitation with intermittent
splinting. Patients actively warm up the fingers during the day and leave the hand in an extension
splint overnight.
Recurrence: postoperative recurrence rates have been reported to range from 10 to 77%, with no
uniform criteria for recurrence. Some authors consider recurrence to be secondary to a flexion
contracture or knot, but this does not affect the functionality of the hand. Furthermore, the recurrence
rate varies from year to year after surgery
Tendon injuries
Flexors
The flexors are divided into extrinsic and intrinsic muscles, depending on the location of the origin.
Extrinsic muscles originates on the humerus, radius, ulna, and interosseous membrane and are
responsible for the overall flexion of the fingers, especially at the IP joints. Intrinsic muscles have
orrigin and attachment to the hand. We divide them into lumbrical and interosseous muscles, which
both help flexion in the MP joints and extension in the IP joints. An important part of the flexor
apparatus are pulleys (annular and crossed), which serve to keep the tendon close to the bone and
thus prevent the formation of a "bowstring". ¨
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Flexor tendon injuries by location. Three phalangeal fingers: zone 1 – distal to the PIP (contains
only the FDP), zone 2 – from the PIP joint to the distal palmar groove, the so-called "no man's land",
zone 3 – between the distal palmar groove of the palm and the distal edge of the carpal tunnel., zone
4 – area carpal tunnel. Injury in this area usually also includes injury to the median nerve, zone 5 –
forearm proximal to the carpal tunnel.
Thumb: zone T1 - distal to the IP joint, zone T2 - area above the proximal phalanx from the A1 loop
to the IP joint, zone T3 - thenar groove - distal edge of the carpal tunnel, zone T4 and T5 are the
same as the finger zones.
Diagnosis and surgical treatment of flexor injuries. In an FDP injury, there is a failure of flexion
of the distal joint in the DIP. When the FDS is injured, there is a loss of flexion in PIP. In the case of
a combined injury, there is a loss of flexion in the DIP and in the PIP while flexion in the MP is
preserved (flexion using intrinsic muscles). We always treat flexor injuries with a 4strand suture,
which we divide into primary (within 24 hours), delayed primary (1st to 14th day) and secondary,
which requires tendon replacement using a tendon transplant.
Extensors. The muscles originates at the humerus, radius, ulna and interosseous membrane and pass
through the dorsum of the hand to the fingers. The thumb has 3 extensors attach at different levels.
The abductor attaches at the base of the 1st metacarpal, the EPB at the base of the basal joint and the
EPL at the base of the distal joint. The index and little fingers have 2 extensors. II. -V. extensors
have junctions between them on the back of the hand and therefore there may not be a complete loss
of extension upon interruption. Extensors II.-V. of the finger form distally from the MP joints
together with the attachments of the intrinsic muscles, the so-called dorsal aponeurosis.
Extensor tendon injuries by location – 8 zones of injury. Three-jointed fingers. zone 1 - DIP,
zone 2 - middle joint, zone 3 - PIP, zone 4 - base joint, zone 5 - MCP, zone 6 - metacarpals, zone 7 retinaculum,
zone 8 - distal forearm. Inch. zone T 1 - IP joint, zone T 2 - base joint, zone T 3 - MCP
joint, zone T 4 - metacarpal area, zone T 5 - CMC (carpo-metacarpal joint), zones 6 to 8 are identical
to the zones of three-jointed fingers
Treatment of extensor injuries can be treated closed (splitting, Kirschner wires). Avulsion extensor
injury of the distal joint in zone I is called mallet finger. Most often, it is a closed injury, tearing of
the dorsal aponeurosis with semiflexion in the DIP. Treatment consists of immobilizing the middle
and distal joint in DIP hyperextension for 6 - 8 weeks, followed by night splinting for 4 weeks. An
open injury in zone II of the middle strip of the dorsal aponeurosis, when the lateral strips remain in
continuity, which slide palmarly on the sides of the PIP joint, causing its flexion and hyperextension
in the DIP, the so-called buttonhole (boutonnière). Swan neck deformity is characterized by PIP
hyperextension with DIP semiflexion. It arises on FDS imbalance, dorsal aponeurosis and
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lengthening of the PIP volar plate, when the shortened deep flexor pulls the distal joint. The therapy
is conservative(splinting) and surgical.
Rehabilitation of the hand is an integral part of the treatment of tendon injuries. We distinguish
between early (within 5 days from the suture) and delayed (after 3 weeks). Further to active and
passive, when the tendons slide in the channels on the base of the extension. In early rehabilitation,
one must think about the strength of the tendon suture, which is least strong between the 9th and 15th
POD.
Rehabilitation after flexor suture: 1. strict 4-week immobilization (after replantation, in children
under 10 years, patient noncompliance 2. passive mobilization according to Duran-Hauser 3. passive
mobilization according to Kleinert 4. active mobilization according to Strickland, "place and hold"
technique.
Rehabilitation of extensors: 6 weeks of hyperextension immobilization followed by very gentle
active flexion for zone I. In zone III. active DIP flexion at zero PIP extension with a static splint by
week 6. Followed by active exercises of the DIP and MP joints with active extension in the PIP joint
with continued splinting of the PIP joint until the end of the 12th week. In zone V., VI., and VII.
volar extension plate. From the 4th week, dynamic splint, static at night. From the 6th to the 12th
week, active exercise of the MP joints with active flexion and passive extension is performed.
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CLAVICLE, SCAPULA, AND SHOULDER INJURIES (57)
Dobiášek Miroslav
Injuries to the clavicle, scapula and shoulder can be collectively referred to as shouder girdle injuries.
The latter is formed by the junction of these 3 parts and the adjacent chest wall. Injuries range can by
from contusions and soft tissue injuries, to fractures (closed, open), luxation fractures and traumatic
amputations.
Clavicular injuries
Anatomy: The clavicle connects the brachial girdle to the trunk. It provides abduction of the arm,
mobility of the limb, stability of the shoulder and protects the neurovascular structures.
Epidemiology and aetiology: Fractures are common, accounting 5% of all fractures. Injuries are
most often caused by direct violence or by a figurative fall on an outstretched limb.
Clinical picture and diagnosis: Clavicle contusion is manifested by swelling, pain, haematoma and
more or less restriction of movement. In fractures, there is also defiguration, crepitations and
pathological movement in the clavicle area. They may be associated with a breach of the skin
covering, intrathoracic injury or injury to the subclavian vessels or brachial plexus. They are divided
into 3 types. The most common type I is injury of the middle part (diaphysis). Type II is injury of the
lateral part and the least common medial type III. Examination of the periphery is an integral part.
The imaging modality of choice is radiography in two projections.
Therapy and complications: Treatment of the contusion consists of temporary wearing sling until
the pain subsides and local physical therapy. In the past, fracture therapy has been only conservative.
Today, it has a place in non-dislocated or minimally dislocated and stable fractures. It consists in
fixation of the limb with an anti-rotation sling, Gilchrist or Delbet rings fixation, depending on the
localization of the fracture. The immobilization period is 3-4 weeks with subsequent rehabilitation.
In children, fixation for 2-3 weeks is sufficient. Open fractures, fractures with threatening injury to
the skin cover, injuries to the neurovascular bundle and dislocated fractures (shortening of more than
2 cm and dislocation ad latus by the width of the bone) are indicated for surgical treatment.
Osteosynthesis is performed either by intramedullary or splint osteosynthesis. Complications may
include skin cover injury, neurovascular injury, infection, pseudoartrosis and osteosynthesis failure.
AC joint injuries
Anatomy: The acromioclavicular joint is secured by the acromioclavicular (AC) and
coracoclavicular (CC) ligaments.
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Epidemiology and aetiology: The injury is most often caused by a fall on the shoulder or on an
outstretched limb. These are common sports injuries. We use the Tossy or Rockwood classification.
Tossy's type I: distortion-injury of the joint capsule of the AC joint, AC and CC ligament intact, type
II: subluxation-tearing of the joint capsule and AC ligament, CC ligament intact, type III: luxationtearing
of all 3 structures including the CC ligament.
Clinical picture and diagnosis: Swelling, pain, prominence of the lateral clavicle and piano key
symptom. X-rays are performed, possibly with stress images or comparison with the healthy limb.
MRI may also be added.
Therapy and complications: Fix in a sling or shoulder brace for 3 weeks with subsequent
rehabilitation. Surgical treatment is reserved for type III. We stabilize the AC joint using tension
cerclage, "hook" splint or minimally invasive anchors.
A rare injury in the clavicular region is luxation in the sternoclavicular joint. It is caused either by
direct force on the clavicle or by a fall on the shoulder. Anterior (presternal) and posterior
(retrosternal) types are distinguished. The anterior type can be closed repaired, the posterior type is
treated by open repositioning and at the same time stabilization with a splint.
Scapula injury
Anatomy: The scapula connects the chest to the upper limb and is essential for free movement at the
shoulder joint. It is protected by a large number of muscles.
Epidemiology and aetiology: Fractures are rare and are caused by a direct impact on the scapula
from behind or by a fall on the shoulder. Often associated with intrathoracic injury.
Clinical picture and diagnosis. Imaging methods include X-ray and more detailed CT scanning.
Fractures of the scapula are divided into 5 groups: fractures of the process, body, neck, glenoid and
combined fractures. An interesting type of injury is the "floating shoulder" when the bony and
ligamentous apparatus of the upper limb is separated from the axial skeleton (in double injury of the
upper suspensory apparatus or simultaneous fracture of the clavicle and glenoid).
Therapy and complications. We indicate for surgery dislocated glenoid fractures with deficit on the
articular surface of more than 2 mm and double injury of the superior suspensory complex. We use
splints and tension screws using 3D printing to treat scaphoid fractures. Postoperative fixation tends
to be for 3-4 weeks with subsequent rehabilitation. Complications can include pseudoartrosis,
implant failure, infections or post-traumatic arthrosis.
Shoulder injury
Due to the complexity of the area and the variability of injuries, we will select the 4 most common
ones:
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1. Rotator cuff injury:
Anatomy: The rotator cuff is composed of the muscles m. subscapularis, m. supraspinatus, m.
infraspinatus and teres minor, which provide rotational movements and elevation of the limb.
Epidemiology and aetiology: Acute traumatic rupture with high load during limb elevation is rare.
Chronic irritation of the subacromial bursa and progressive fibrotization with impaired rotator cuff
function is more common.
Clinical picture and diagnosis: Long-term shoulder pain with progressive deterioration of function
is typical. We investigate with resistance tests, drop test, Cyriax pain arc helps to differentiate. X-ray,
ultrasound and MRI are performed.
Therapy and complications: On the basis of the examination, we decide between conservative
treatment, which is suitable only for partial ruptures, and surgical treatment, which is arthroscopic
suture.
2. Injury to the m. biceps brachii
We divide it into injuries in the proximal part, the muscular middle part and the distal part.
Proximally, the long head of the biceps brachii is injured, which is manifested by a typical "bump"
deformity in the medial part of the arm. Therapy is predominantly conservative with short-term
immobilization of the limb. Surgical treatment is possible by refixation. Injury to the medial part of
the muscle is most often caused by a direct mechanism. Swelling and haematoma may be present.
Therapy is conservative. Injury to the distal biceps tendon most often occurs when lifting heavy
loads. Clinically, there is a significant limitation of muscle strength, hematoma in the distal part of
the arm and an impalpable tendon. Therapy is surgical with refixation of the tendon to the tuberositas
radii. In addition to the typical clinical picture, ultrasound examination is used in the diagnosis.
3. Luxation of the shoulder joint:
Anatomy. Static (joint capsule, labrum, ligaments) and dynamic stabilisers (muscles) ensure the
stability of the joint.
Epidemiology and aetiology: Etiologically, the most common is a fall on an outstretched limb, but
luxation can occur without an injury mechanism (habitual luxations).
Clinical picture and diagnosis: Pain, shoulder defiguration and palpable empty joint socket are
present. There are 4 types of luxations (anterior, posterior, superior and inferior). Anterior luxation is
the most common. It is diagnosed by X-ray.
Therapy and complications. Surgical treatment is necessary for irreversible luxations and for
concomitant vascular injury. Injury to the brachial complex or vascular injury may be the most
common complication. Recurrent luxations are also not rare.
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4. Fractures of the proximal humerus
Epidemiology and aetiology. They represent a relatively large number of fractures (5-6%). The
cause is most often a trivial fall on the shoulder, predominantly in elderly patients.
Clinical picture and diagnosis: They present with pain, limitation of mobility, haematoma, and in
luxation fractures an empty joint socket can be palpated. It is important to examine the periphery to
exclude nerve or vascular lesions. The basic imaging modalities are X-ray and CT to verify and plan
the management of the fracture. The classifications used are AO and more commonly Neer's (types
I-VI). They use the division of the proximal humerus into head, diaphysis, greater and lesser
tuberosity.
Therapy and Complications: Evaluation and treatment must be approached on a strictly individual
basis. Conservative treatment is the appropriate treatment for up to 75% of fractures. It is indicated
for all non-dislocated fractures, dislocated fractures in elderly patients with lower expectations of a
good functional outcome and polymorbid patients. Surgical treatment is most commonly performed
from a deltoideopectoral approach. The choice is between splint osteosynthesis, which is suitable for
all types of dislocated fractures in younger patients (up to 65-75 years). Hemiarthroplasty, which
provides good pain relief, but the functional outcome is limited - suitable for patients with
multifractured fractures without the possibility of osteosynthesis. The last option is reverse total
endoprosthesis, which has a better functional outcome. They are indicated in elderly patients (65-75
years) with the requirement for the best possible functional outcome, in failed osteosyntheses and in
luxating four fragments fractures. The recommended immobilization with a sling or shoulder brace
for conservative therapy is for 2-4 weeks, with passive exercise initiated after 1-2 weeks, followed
by active rehabilitation. For postoperative conditions, fixation and rehabilitation are individually
selected. Early complications include vascular and nerve injuries. Late ones include the development
of avascular necrosis, healing in malposition, pseudoartrosis or failure of osteosynthesis.
Comments and controversy: When treating injuries, it is important to make an individual
assessment and weigh the benefits and risks to the patient of the proposed therapy (especially
surgery). We should ascertain the patient's expectations for the future and respect the patient's
wishes.
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HUMERUS AND ELBOW INJURIES (58)
Reška Michal
Humerus injury
1. Fractures of the proximal humerus
Diagnostics:
- Clinically, pain localized to the shoulder or proximal part of the arm with limitation of range
of motion. Swelling may be present, and the hematoma usually resolves after a few days. It is
always important to examine the neurocirculation of the limb up to the periphery.
- X-ray: the minimum is two projections perpendicular to each other - anteroposterior +
transthoracic , but three perpendicular images are recommended - anteroposterior, lateral
transscapular and axial.
- CT with 3D reconstruction will clarify the findings, help the therapist. Balance sheet
- USG functional to examine the rotator cuff
- MR before reconstructive procedures, assessment of rota. cuffs and head vitality.
- epi- or electrocution patients
Classification: AO classification: 11 A, B, C see. www.aosurgery.org, Neer classification: Neer I-VI
Therapy: The aim is to restore the function of the shoulder joint as best as possible.
- Functionally conservative treatment
Immobilization with a Desault bandage event. three-point shoulder brace ( Gilchrist ) usually for 3
weeks. Abduction splint. Hanging plaster ( hanging cast ) especially in neck fractures with
shortening - it has no significance in lying patients.
- Operative treatment
The basic principle of surgical treatment is the reposition of fragments, including bumps with muscle
attachments, and their adequate fixation. Choice of commonly known implants – K. wires, screws,
plates incl. angularly stable, special intramedullary nails. In case of non-reconstructable fractures,
especially of the head, replacement of the head or frame is necessary . joint.
Rehabilitation:
After conservative therapy, we start passive rehabilitation first, gradually depending on the condition
and X-ray checks with the addition of a muscle component. After surgical treatment, it is necessary
to approach individually and take into account the procedure performed - for example, with adaptive
osteosynthesis, you must first start with passive rehabilitation, on the contrary, with stable
osteosynthesis, you can rehabilitate early and actively.
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Complication:
Early: - vascular injury, nerve injury
Late: - avascular necrosis of the head, healing in dislocation, impingement you are subacromial
space, hip joint, failure of osteosynthesis, adhesive capsulitis
2. Fractures of the diaphysis of the humerus
Diagnostics:
Clinically, crepitation, pain, deformity, pathol . momentum, X-ray in two projections. Examination
of the neurocirculation of the limb periphery!
Classification: AO: 12- A, B, C - see. www.aosurgery.org.
Therapy:
Conservative therapy requires patient cooperation and more frequent X-ray checks due to the
possibility of redislocation.
- high plaster fixation with epaulet over the shoulder, functional treatment according to
Sarmiento - orthosis ( Brace )
Operative treatment - technique : Open reposition with radial nerve revision and plate
osteosynthesis, intramedullary anterograde or retrograde nailing , external fixator mostly single-plane
, possibility of extension to the forearm in case of combined injury with the elbow joint.
Complication:
radial nerve paresis , complications during implant insertion
Rehabilitation:
Early after surgery – after the surgery has healed. wounds pac. passively rehabilitates the shoulder
and elbow joint. After splinting, full weight bearing until the fracture heals. After nailing, you can
exercise actively right away, only the rotation of the arm is limited until the bone heals.
3. Distal humerus injury
Diagnostics:
- Injury history
- Swelling, hematoma, deformation, dysfunction
- X-ray image in two projections for basic orientation
- CT examination for closer verification of intra-articular involvement
Classification: AO classification 13- A, B, C - see. www.aosurgery.org
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Therapy:
Conservative therapy is rarely possible for non-dislocated extra-articular fractures. But the vast
majority of these fractures require surgical treatment.
Note: treatment of type C fractures in the area of dist . humerus and elbow is a problem of special
traumatology.
4. Proximal forearm injury
Radial head injury
Diagnostics:
- Clinically, pain, limitation of function, typical pain targeted above the head of the radius and
in rotation
- X-ray in two projections, it is advisable to perform an X-ray of the elbow and forearm watch
out for the Essex- Lopresti fracture (fracture of the head of the radius with rupture of
the interosseous membrane, typ. widening of the radio -ulnar distance on the X-ray)
Classification: according to AO.
Therapy:
- Conservative therapy: for non-dislocated fractures without instability, short-term
immobilization for 14 days with early rehabilitation, initially excluding rotational movements
of the forearm.
- Operative treatment for comminuted or significantly displaced fractures:
Pronatio dolorosa
Typical for children, popping out of the head of the radius from the ligamentum annulare , especially
during traction and rotation behind the extentoxed forearm. Clinically, pain is manifested by rotation
of the forearm and pain above the head. The therapy is head repositioning and short-term
immobilization for 7-14 days.
Fractures of the proximal ulna
Process fractures coronoid
Diagnostics: X-ray, CT
Therapy: reposition and osteosynthesis, most often with a tension screw, in the case of a more
massive fragment, a splint synthesis can also be chosen
Olecranon fractures ulnae
Most often, they enter by falling directly on the elbow. Dislocation by traction of the triceps muscle
proximally is typical .
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Diagnostics:
- Clinical swelling, hematoma, palp . defect, crepitation
- X-ray in two projections
Therapy:
Conservative therapy with plaster fixation exceptionally, in the vast majority of cases of surgery.
Dislocation of the elbow joint
Diagnostics:
- Typical clinical picture with deformity corresponding to anterior or posterior dislocation
- X-ray elbow and dist . humerus in two projections
- Considering the possibility of injury to the median nerve and ulnaris nerve , it is always
necessary to examine the periphery of the limb as well
- In old patients, the combination with a fracture of the dist . humerus
Therapy: Urgent reduction under general anesthesia
Complications: Vascular injury (necessary angiographic examination), paresis of the ulnar nerve ,
compartment syndrome on the forearm especially after prolonged dislocation, paraarticular
ossification and stiffness of the elbow joint
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FOREARM AND HAND INJURIES (59)
Pavlacký Tomáš, Zukal Radek, Veselý Radek
PROXIMAL FOREARM INJURY
Fractures of the proximal radius
The radius head is an important stabilizer of the elbow and forearm. These fractures are caused by
the application of force either directly to the elbow or more commonly indirectly through the
forearm. Therefore, they are often associated with other injuries of upper limb.
Diagnostics: Clinical examination with pressure on the radial head during forearm rotations. X-ray
of the elbow, forearm and wrist simultaneously with respect to associated injuries.
Therapy: A) Conservative - for non-displaced fractures with joint incongruence up to 2 mm,
without ligamentous instability of the elbow. Immobilization for 7-10 days and early functional
treatment otherwise stiffness occurs. Relieving aspiration remains controversial.
B) Surgical - for dislocated or comminuted fractures. Isolated screws and LCP plates
(2.7 mm or 2.0 mm). In severe comminution extirpation and replacement of the head.
Cave: 1) Essex-Lopresti – complex injury of the radial head, interosseous membrane and radioulnar
junction, which always requires surgical treatment. 2) After resection of the head, proximalization of
radius, valgus deformity and limitation of forearm function occur.
Fractures of the proximal ulna
Coronoid fractures
They are most often part of a luxating elbow injury. Their therapy depends on the extent and
localization of the fractured fragment and the degree of dislocation.
Diagnostics: Clinical examination, including instability. In case of therapeutic uncertainty, it is
advisable to supplement the X-ray with CT reconstruction.
Therapy: A) Conservative - non-dislocated, up to 5mm. POP for 2 weeks
B) Surgical – plate fixation, isolated screws or anchor.
Olecranon fractures
Almost always intra-articular fractures, that arise from a direct impact on the elbow.
Diagnostics: Clinical findings are significant: swelling, hematoma, sometimes palpable defect and
disturbance of extension. X-ray in precise projections is sufficient for isolated injuries.
Therapy: A) Conservative - very limited, only for non-displaced fractures or patients with
contraindications to surgery. Plaster fixation in semiflexion for 3 weeks and subsequent functional
treatment. Healing is often associated with pseudoarthrosis and associated limitation of movement,
but it is surprisingly well tolerated by elderly patients.
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B) Surgical – preferred approach. The aim is to restore the joint congruence. For
simple fractures, the so-called tension band wire (Fig.1) is used. It consists of two parallel K-wires
and a cerclage wire. In this way, the distraction on the outer cortices is converted to compression on
the inner cortices during flexion, thus exploiting the principle of absolute stability on the articular
surface. For comminuted fractures, angle-stable splints, alternatively, a nail fusion, isolated screws or
an external fixator are used.
Elbow dislocations
It is the third most common dislocation after shoulder and finger dislocation. It usually occurs in
younger patients because the distal humerus rather fractures than dislocates in the older age group
with the same mechanism of injury. The most common mechanism is a fall on the extended forearm,
when the anterior joint capsule loosens and the olecranon, which is encased in the olecranon fossa,
travels dorsally. Less commonly, a fall on the olecranon with the elbow joint flexed results in
anterior luxation. Isolated luxation is rather rare, more often there are associated fractures of the
proximal forearm.
Diagnostics: Clinical examination reveals obvious deformity and limitation of movement. Stability,
neurovascular state and X-ray examinations need to be repeated after the reposition.
Therapy: A) Conservative - in patients without residual instability, rigid fixation for 10-14 days,
then brace with limited range of motion
B) Surgical – suture or reinsertion of the collateral ligaments in acute elbow
instability, using an anchor. Anatomical reconstruction of associated fractures is important. Chronic
instability is resolved by the substitution of associated ligament with a graft or tape.
Cave: Associated median and ulnar nerve injuries, possible compartment syndrome.
FOREARM INJURIES
The forearm is a complex unit consisting not only of the forearm bones, but also their proximal and
distal articulation and the interosseous membrane. Therefore, its injuries should be perceived as
similarly complex. Thus, an indirect mechanism, although less common, may result in a complex
osteoligamentous injury in several stages. (Fig.2) In contrast, fractures resulting from the more
common direct violence to the forearm, usually cause isolated fractures of the diaphysis of the radius
and ulna.
Diagnostics: On clinical examination, marked defiguration, swelling and crepitations are often
present. Radiographs in two perpendicular projections with a consistent view of the elbow, forearm
and wrist are necessary.
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Therapy: A) Conservative - only for non-dislocated fractures, plaster fixation in neutral position
from the metacarpophalangeal joints to above the elbow to prevent rotation for 4-6 weeks with early
realignment and release of the elbow in the vertical axis.
B) Surgical - the aim is to restore axis, length and rotation. Plate osteosynthesis is used
to achieve absolute or relative stability depending on the nature of the fracture.
Cave: 1) Forearm fractures have the highest incidence of open injuries in the upper limb
2) Galeazzi's fracture - fracture of the diaphysis of the radius with simultaneous luxation of the ulna
head, solved exclusively by surgical osteosynthesis of the radius and transfixation of the distal
radioulnar joint in the correct position. 3) Monteggio fracture - fracture of the proximal ulna with
simultaneous luxation of the radial head. We also first perform a stable osteosynthesis of the ulna. It
is subsequently supplemented by revision and possible suture of the ligamentum anulare in case of
persistent luxation of the radial head.
FRACTURES OF THE DISTAL RADIUS
Distal radial fracture is the most common skeletal injury of the upper limb with a bimodal
distribution. It occurs less frequently in younger patients as part of a high-energy injury. More often
it is a classic osteoporotic fracture, typical of older patients with a female predominance.
Diagnostics: Clinical examination, X-ray in two perpendicular projections clearly defines the
stability criteria and possible indications for surgery. CT scan in intra-articular fractures.
Therapy: Before the final decision, the fracture is reduced in LA with 1% Mesocaine injected into
the hematoma. Subsequently, traction and counter traction are used to reposition the fracture using
the ligamentotaxis. Finaly, repositioning is completed by direct manipulation.
A) Conservative - for minimally dislocated, stable fractures. The limb is fixed for 4-6 weeks
in plaster fixation extending from the distal palmar crease below the elbow. Initially it is cut because
of the swelling onset.
B) Surgical - for dislocated, unstable fractures. Most often by volar approach using a preshaped,
LCP plate. For open and grossly comminuted fractures, treatment with an external fixator
inserted into the diaphysis of the radius and second metacarpal bone is possible.
Cave: Fractures in this location are often characterized by eponyms. (Fig.3) 1) Colles’ fracture–
extraarticular fracture with bayonet-like deformity and dislocation of the periphery dorsally and
radially. 2) Smith's fracture– inverse to Colles’ fracture - it is an extraarticular fracture with volar
dislocation. It is more often unstable.
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HAND INJURY
Scaphoid fractures
The scaphoid is the most injured bone of the carpus. Majority of the fractures pass through the
middle third and are caused by a fall on the wrist in extension. The clinical presentation is associated
with tenderness over the fossa la tabatière and may be relatively subtle in the early stages. The
standard of care for imaging is radiographs in 3 projections supplemented by CT scanning whenthe
fracture is suspected and to facilitate classification. Conservative treatment is reserved for nondisplaced
fractures. Cast fixation immobilizes the thumb and elbow joints in addition to the wrist and
is usually left in place for 6 weeks. Surgical treatment belongs to all the remaining categories, with
the so-called Herbert screw used for fixation, allowing compression of the fracture due to two
threads with unequal lengths and steepness (Fig.4).
Luxation of the wrist
These are severe and complex osteoligamentous injuries. They are divided into perilunate luxations
in which the lunate remains in contact with the radius and the rest of the carpus is dislocated
dorsally, and lunate luxations in which the lunate is dislocated ventrally, and the rest of the carpus
remains in place. The cornerstone of therapy is early diagnosis, which from plain radiographs can be
relatively difficult especially in the AP plane. This is followed by acute closed reposition and then
early operative revision of the injured ligaments.
Metacarpal fractures
It is one of the most common hand injuries with typical dislocation. The eponyms describe the most
frequent units such as Boxer's fracture in the region of the fifth metacarpal and Bennett's or Roland's
fractures in the region of the base of the first metacarpal. Therapy is frequently conservative with
plaster fixation in "safe position" (Fig.5) for 4-5 weeks. For dislocated fractures, we use a
combination of K-wires, small screws or plates for osteosynthesis.
Fractures and dislocations of phalanges
They are similar in character to metacarpal fractures. The more common conservative therapy is
fixation for 3 weeks with an aluminium splint at the level of interphalangeal joints. In the aMCP joint
a plaster fixation in "safe position" is mechanically preferable. Given the minimal soft tissue cover
and the high risk of adhesions, the surgical treatment is done using K-wires or small screws. It is
most often indicated for rotational deviation or significant intra-articular inequality. In this location,
there is a low correlation between clinical and radiographic signs of healing. Luxation of
interphalangeal joint is one of the most common injuries. Reposition is usually easily accomplished
with traction and counter traction followed by fixation for 3 weeks with an aluminium splint or
brace.
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Fig. 1 Scheme of tension band wire, screw and plate fixation in olecranon fracture.
Fig. 2 Types of forearm fractures
Fig. 4 Herbert screw used in scaphoid fracture
Fig. 5 Safe position for fixation of hand injuriesFig. 3 Types of distal radial fractures
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PELVIC AND HIP INJURIES (60)
Rak Václav
Fractures of the pelvis
Anatomy
The pelvis is made up of two pelvic bones (os ilium, os ischii and os pubis) and the sacrum (os
sacrum), forming a confined space containing some abdominal organs.
Epidemiology and etiology
Pelvic fractures account for about 2% of all fractures, but occur in 20% of polytrauma cases. They
are most commonly caused by road traffic accidents or falls from height, where high energy trauma
is the cause.
Classification
According to the stability of the fracture, there are three categories - stable A, whereby individual
bones are injured, - partially stable B (this includes open book fractures), - unstable C, which have a
mortality rate of over 25%.
Clinical picture and diagnosis
In stable fractures, pelvic injury is manifested by pain and haematoma, and the patient usually cannot
walk due to pain. The diagnosis is confirmed by X-ray (anteroposterior, inlet and outlet projections)
and possibly by a refining CT scan. In types B and C, the patient is often in a state of shock from
massive haemorrhage, with pain in the sacral region or in the symphysis and lower abdomen if
conscious. Pelvic instability is determined by clinical examination, evident by pressure on the iliac
crests or symphyseal defect, which is confirmed by radiological methods.
Therapy and complications
Conservative treatment with bed rest is chosen for type A fractures. Displaced fractures can be
treated with repositioning and osteosynthesis. Type B and C already require anti-shock treatment,
stopping bleeding (angioembolization or extraperitoneal tamponade) and stabilization of the pelvic
ring with an external fixator. With a delay after stabilization of the condition, splint osteosynthesis
follows, where type C is solved by stabilizing the anterior segment with a splint, the posterior
segment with screws, splint or screws. The diagnostic and therapeutic procedure is illustrated in the
diagram below. In pelvic surgery, we choose, for example, from an anterior or posterior approach.
Due to the proximity of organs of the urogenital and gastrointestinal systems, blood vessels and
nerves, pelvic injuries are often accompanied by damage to these structures, which can lead to
serious complications, most commonly e.g. injury to the urinary bladder, rectum, blood vessels
threatening acute bleeding, thrombosis or embolization.
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Fractures of the acetabulum
Epidemiology and etiology
As intra-articular fractures, acetabular fractures usually occur by an indirect mechanism when the
femoral head strikes the acetabular socket (typically in car accidents). It accompanies hip luxation in
50%. When the femoral head breaks through the acetabulum, we speak of the so-called central
luxation.
Classification
According to clinical anatomy, we distinguish between the anterior and posterior pillar of the
acetabulum, which is also used in the classification. There are 3 categories - partial intra-articular
fractures affecting one pillar, - transverse fractures passing through both pillars, - intra-articular
fractures of both pillars (so-called floating acetabulum).
Clinical picture and diagnosis
The patient suffers from sharp pain in the hip and cannot step on the foot. The limb is in a position of
relief (abduction, external rotation). When the acetabulum breaks through, a shortening of the limb is
seen. X-ray focus on the anterior (oblique iliac) or posterior (oblique obturator) edge of the
acetabulum. CT and 3D reconstruction are used for better clarity.
Therapy and complications
Non-displaced fractures can be treated conservatively - bed rest and rehabilitation. Dislocated
fractures are indicated for surgery, when we choose osteosynthetic splints or screws. Because of the
localization, post-traumatic arthrosis often occurs, often resolved by total endoprosthesis.
Hip injury
The hip joint (articulatio coxae) is a spherical synovial joint connecting the lower limb and pelvis. It
allows movement and provides stability to the body. It consists of the head of the femur (caput
femoris) and the socket (acetabulum).
Anatomy of the proximal femur
The proximal femur consists of the femoral head, neck and body. The head forms the articular
surface on which the socket for the ligamentum capitis femoris is located. The vascular supply comes
from the arteria femoralis through the arteria circumflexa femoris medialis and lateralis. Their
preservation during injury plays a role in the viability of the femoral head and the potential risk of
avascular necrosis. The neck makes an angle of 125-135° with the body of the femur (the
collodiaphyseal angle). An important structure is the Adams' arch, the strongest trabecular part of the
bone on the medial side, which plays a role in stabilizing osteosynthesis. On the body of the bone,
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we distinguish the trochanter major and trochanter minor humps, which are important for fracture
classification and influence fracture stability.
Epidemiology and etiology
Fractures of the proximal femur are common, especially in older women (7th-8th decade). In
younger patients, they are the result of high-energy injuries (car accidents, falls). In older people, on
the other hand, they often occur in less severe falls, usually as a result of osteoporosis. Head fractures
are the rarest. Trochanteric fractures account for over half of proximal femur fractures and heal very
well.
Classification
According to Pipkin, head fractures are categorized into four types. According to Pauwels and
Garden, we classify cervical fractures, and we further divide them into intra- and extracapsular.
According to the course of fracture through the trochanteric mass we divide trochanteric fractures.
For a more detailed classification with therapeutic management see the diagram below.
Clinical picture and diagnosis
Typical symptoms are limb shortening, external rotation and semiflexion. The patient cannot step on
the limb. Diagnosis includes X-ray (AP and axial projection) including the other side for comparison
and possibly CT scan for more accurate determination.
Therapy and complications
Conservative treatment is chosen for stable wedged fractures, but it is associated with a high risk of
complications and is nowadays chosen only minimally. Surgical treatment is indicated for all
dislocated fractures and includes osteosynthese or alloplasty. Osteosynthese is performed with
dynamic hip screws (DHS) or intramedullary femoral nails (IMFN). Alloplasty (CCP - cervicocapital
prosthesis, TEP - total endoprosthesis) is the method of choice for dislocated intracapsular neck
fractures, for proximal femur fractures with the presence of more advanced arthrosis and for some
pathological fractures. Complications also include the development of avascular necrosis of the head
in case of injury to the vascular supply, but here it is more rare. Head fractures are often associated
with hip luxation or acetabular injury. The healing of fractures may be complicated by the formation
of a pseudoarthrosis, or the fracture may heal in a varus position and cause long-term complications
even after healing, e.g. a shortened limb.
Hip luxation is a separate chapter. It is a rare injury. It occurs in younger patients in high-energy
trauma. It is divided into simple or complex occurring with fractures of the acetabulum or proximal
femur. We further divide it into posterior and anterior luxation, with the posterior occurring much
more frequently. It is manifested by severe and sudden pain, the patient is unable to walk, the limb is
shortened and in pathological rotation. For diagnosis we use X-ray or CT scan for clarification. For
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Femoral neck
fractures
Extracapsular
(basicervical)
surgery - DHS
Intracapsular
(subcapital,
mesocervical)
Conservative
therapy
Surgery
Osteosynthese
(screws, DHS)
Alloplasty (CCP,
TEP)
Head fractures
Conservative therapy
(Nondisplaced fractures)
Surgery
Screws, or possibly
together with
acetabular
osteosynthese
Alloplasty (CCP, TEP)
Per-/Intertrochanteric
fractures
Subtrochanteric
fractures
Osteosynthese
(IMFN, DHS)
Pelvic injury
•Polytrauma
•Unstable patient
Emergency
department
Primary survey
•A - Airways
•B - Breathing
•C - Circulation
•D - Disability
•E - Exposure
Emergency
department
Secondary survey
•Physical examination
•Pelvic belt loading
•Imaging (X-ray, CT
scan)
Operating theatre
Acute treatment
•Bleeding stopping,
angioembolisation,
extraperitoneal
tamponade
•Stabilisation, external
fixator, clamp
Operating theatre
Definitive treatment
•Osteosynthese:
Splint, screws,
possibly combination
with external fixator
therapy we choose emergent repositioning under general anaesthesia, failing which we choose open
repositioning followed by stabilisation.
Fracture of the proximal femur – classification and therapy
Management of a patient with pelvis injury
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FEMUR, THIGH, AND KNEE INJURIES (61)
Konečný Jan
I. Femur injuries
a) Proximal femur
1. Head fractures - rare, usually with hip luxation. Mechanism - most commonly axial violence in
high-energy trauma, 95% of patients have other injuries requiring hospitalization. DG - x-ray - only a
rough guide, CT scan is required. Treatment - according to fragment size, fragment location,
breakage site, age and general condition. Repositioning of the luxated hip is necessary, the sides of
the fracture can be treated conservatively and surgically. Complications - osteonecrosis of the
fragment or head, development of arthrosis
2. Femoral neck fractures - common in the elderly, average age between 70 and 80 years, more
common in women. Mechanism - low-energy trauma in the elderly, high-energy trauma in the
younger. Investigation - history - may not indicate major fall, sometimes associated with impaired
consciousness, chest pain etc. Ascertain patient's pre-injury condition and mobility. Clinically typical
position of the injured limb - external rotation, anteflexion at the hip and shortening of the
limb, reported pain from hip to knee, worsening on movement. Always examine pelvic stability,
blood supply and innervation of both hips. DG - X-ray - injured hip, clear image of the whole pelvis
(exclusion of pelvic fracture and assessment of arthrosis of the secondary hip), according to the clinic
X-ray of the whole femur and knee. CT scan - only when unclear. Classification - basic division according
to the fracture site in relation to the joint capsule - a/intracapsular - subcapital or
mediocervical - risk of head necrosis, b/extracapsular - basicervical or laterocervical - no risk of head
necrosis. Further classification - according to the direction of fracture and stability of the fracture according
to Pauwels - I.st. - the fracture has an angle with the horizontal up to 30°, II.st. 30-70°,
III.st. more than 70°. According to dislocation - according to Gardena - risk of compromising the
vitality of the head. Garden I - incomplete fracture - medial cortical fracture, valgus angulation laterally
the neck is impaction into the head, Garden II - complete fracture without dislocation.
Garden III - fracture with dislocation - the neck remains in contact with the head, Garden IV dislocated
fracture - the neck loses contact with the head. Treatment -intracapsular fractures - risk of
subsequent necrosis of the head with dislocation, treatment according to the Garden classification. G
I - conservative treatment (in case of secondary dislocation implantation of TEP or CKP), G II osteosynthesis.
G III and IV - risk of subsequent necrosis of the head - procedure according to the
age, general condition of the patient, time since the injury and arthrosis - osteosynthesis,
implantation of TEP - total hip replacement, implantation of CKP - replacement of the head and neck
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(lifetime of the implant about 5 years). Extracapsular fractures - without a greater risk of disruption
of the nutrition of the head - osteosynthesis, as pertrochanteric fractures.
3. Pertrochanteric fractures - fractures of the area between the trochanters. About 50% of prox. femur
fractures - like neck fractures, average age slightly lower - around 70 years. Mechanism predominantly
fall from standing to the ground with direct impact on the region of the greater
trochanter in the elderly, in young high-energy. Examination and X-ray diagnosis as for cervical
fractures. Treatment- surgical - osteosynthesis with the use of special implants - most often PFN
(Proximal Femoral Nail), less often DHS (Dynamic Hip Screw) splints.
Without osteosynthesis, the elderly, often polymorbid patient is immobile for a long time - high risk
of complications with a relatively high mortality rate (bronchopneumonia, TEN, decubitus,
uroinfections, etc.). Surgery for "vital indication" in the broader sense. Temporal aspect - the least
complications are in surgery within 3 days of injury. Do not postpone surgery unless follow-up and
preparation of the patient will clearly reduce the risks of surgery and postoperative course. This
applies to all fractures of the neck and trochanteric region of the femur.
4.Isolated trochanteric fractures - rare - breakage of the greater trochanter by direct impact - femur
stability not compromised, isolated fracture of the lesser trochanter - avulsion - muscle pull.
Conservative procedure.
5. Subtrochanteric fractures - up to 5cm distal to the lesser trochanter - cortical bone with little blood
supply is highly stressed by a combination of compression and tensile forces, usually dislocated by
strong muscle pull. Mechanism - older patients - low energy - "minimal" falls, young - high energy
injuries, pathological fractures - more common than elsewhere. Examination - often significant
deformity, possibly significant blood loss - hypovolemic shock. X-ray of pelvis, hip and femur
including knee. Treatment - under first aid and point C in ABCDE procedure - acute, temporary
stabilisation of limb in traction. Non-operative - skeletal traction - in adults rarely. Operative - in
adults mostly - intra-articular ridging - aim for closed repositioning. Early surgery reduces blood
loss. Complications - relatively common - failure to heal/healing with deformity - high demands on
stability of osteosynthesis.
(b) Femoral diaphysis
Fractures - most commonly high energy trauma, less commonly pathological fractures - especially in
the elderly after 'small falls', usually dislocated and unstable. Examination - due to the mechanism of
careful overall - frequent simultaneous injury to multiple organ systems, There is considerable blood
loss even in closed fractures - 1000-2000ml - average 1200ml. Often the same knee is also injured.
DG - X-ray - whole femur with both joints in 2 projections. Treatment - first aid - repositioning and
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stabilising the fracture with traction - significantly reduces blood loss (point C from ABC algorithm),
risk of secondary soft tissue injuries, pain etc.. Definitive treatment - operative - most commonly
intramedullary nailing.
c) Distal femur
Fractures - extraarticular - supracondylar , intraarticular . Large muscle forces - typical dislocation of
fragments by traction - m.gastrocnemius - dorsal displacement and angulation, m.quadriceps femoris
and hamstrings - traction proximally - shortening. Examination - possibility of vascular injury in
typical dislocation of dist. fragment. DG - X-ray - baseline, CT - relationship to articular surface.
When vascular injury is suspected angiography. MRI only subsequently - diagnosis of soft knee
injury. Treatment - conservative - incomplete or undislocated stable fractures - immobilization, for
dislocated fractures - skeletal traction for 6-12 weeks - high risk of local and overall complications therefore
rare in adults. Surgical - mostly, type of osteosynthesis - special implants - splints (LCP),
spikes, for smaller fragments screws, or a combination of methods. External fixator - in vascular
reconstructions and in polytrauma or open fractures - usually temporary, after stabilisation
conversion to internal osteosynthesis.
II. Thigh injuries
Muscle injuries - mostly incomplete muscle ruptures, direct mechanism - impact, or indirect excessive
muscle contraction. Treatment mostly conservative - icing, immobilization, gradual
mobilization. Quadriceps tendon rupture - most common in over 40 years of age, 2cm proximal to
the patella. Examination - palpable defect, complete rupture - loss of active extension in the knee. Xray
- to rule out fractures, ultrasound (MRI) may help, but clinical examination is most important.
Treatment - complete rupture - surgical - suture or reinsertion, incomplete rupture - conservative immobilization
of the knee with a brace and gradual mobilization (about 6 weeks). Ligamentum
Patellae - much less common, approach similar.
III. Knee injuries
Fractures of the patella - indirect mechanism - muscle traction - most common - dislocation, direct
mechanism - impact, often incomplete fractures, combined mechanism. Examination - extensor
apparatus - managing active extension in the knee, possibility of injury to the same hip, tibia, leg in
high energy injuries. DG - X-ray - 2 projections. Treatment - conservative - non-displaced fractures
without violation of extensor apparatus - fixation - brace for 6 weeks with gradual mobilization.
Operative - dislocated fractures with violated extensor apparatus - open repositioning and
osteosynthesis - tension cerclage, screws.
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Soft knee injuries
Luxation of the knee - not common but threatens the limb - close to blood vessels and nerves, often
spontaneous repositioning. Often with fractures of prox. tibia and fibula. Mechanism - high-energy
injuries, or sports. Examination - reposition as soon as possible, examination of blood supply to limb
- in 20-60% of a.popliteal injuries - reconstruction required within 8h, only then examination of
ligamentous apparatus, examination of innervation - n.peroneus - not rushed - most often
neurapraxia, complete lesions rare - usually cons. procedure. DG - X-ray - 2 projections, when
fracture sides are unclear CT, when vascular lesion is suspected angiography, MRI diagnosis of
ligamentous injury only at second time. Treatment - urgent closed repositioning - during
investigation, fixation with brace, in case of instability external fixator, vascular reconstruction as
needed, open repositioning - if not possible closed - exceptionally. Treatment of ligamentous injury
only afterwards.
Patella luxation - more common in women - hypermobility, anatomical predisposition, muscle pull lateral,
medial by direct force, risk of osteochondral fractures of the patella or femur, often
spontaneous reposition. Examination - clinic, X-ray. Treatment - repositioning in knee extension,
fixation with brace. In recurrent - surgical solution - arthroscopy, correction of patello-femoral
instability.
Injuries - of the menisci, ligaments and cartilage of the knee joint
Mechanism - from high-energy - luxation, to sports injuries - ligament and meniscus injuries, to
minimal trauma - meniscus injuries. Sports injuries - about 70%. Most often indirect mechanism.
Injuries according to the direction and magnitude of the force applied and the position of the knee
joint. Examination - history - description of the injury event, difficulties - pain during a certain
movement, swelling after loading, etc. Objective - Special manoeuvres on the menisci (if 2
manoeuvres are positive, the probability of injury is over 90%). Imaging - X-ray - skeletal trauma
and bone position, MRI - shows ligaments, cartilage and menisci - over 90% yield. Ultrasound - not
beneficial. Arthroscopy - the pinnacle of diagnosis and resolution at the same time. Treatment of
meniscal injuries - operative - arthroscopy - procedure according to type of rupture, age and
comorbidities - attempt salvage surgery (sutures), resection procedures - removal of loose part of
meniscus. Treatment of ligament injuries: lateral ligaments - LCM and LCL - mostly conservatively
- immobilization with a brace with gradual mobilization - 6 weeks in total, surgically rarely. Crossed
ligaments LCA and LCP - acute, mostly conservative procedure, followed by ligament replacement
with an interval of several months - most often with the use of tendons m.semitendinosus,
m.quadriceps femoris, or lig. patellae - indication according to age, comorbidities and degree of
instability.
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TIBIA, ANKLE, AND FOOT INJURIES (62)
Zukal Radek, Pavlacký Tomáš, Veselý Radek
Fractures of the proximal tibia are most often caused by falls and side impacts on the knee joint,
and there is often a rotational force present. Skeletal injuries are often accompanied by ligament and
meniscal injuries. A distinction is made between extra-articular and partially or completely intraarticular
fractures. A significant proportion of fractures are comminuted fractures.
Diagnosis is based on clinical examination, when we find an altered contour of the knee joint, limited
movement, impossibility of weight-bearing, pain and swelling, or hemarthrosis. The state of
innervation and vascular supply at the periphery of the limb should always be carefully examined.
The standard radiological examination includes X-ray in two projections, followed by CT scanning
when intra-articular fracture is confirmed.
The main aim of therapy is to restore the smooth articular surface, physiological axis and stability of
the knee joint, which leads to the preservation of the best possible knee function and allows early
rehabilitation. The conservative approach is chosen only when surgery is contraindicated, e.g. due to
severe comorbidities of the patient or in case of a non-displaced fracture (infraction). The preferred
solution is surgical treatment with osteosynthesis with condylar buttress plates, separate screws or
their combination and treatment of the soft knee with special suture material. Preferably, the surgery
is arthroscopically assisted. In the case of extensive soft tissue injury or open fractures, a two-stage
approach is necessary, whereby a thorough debridement is performed in the first stage and the knee
is fixed with a bridging external fixator. Complications include paresis of the n. fibularis, injury to
the popliteal vessels (especially in luxation fractures) and compartment syndrome.
Fractures of the diaphyseal part of the tibia are among the most common diaphyseal fractures in
general. Due to the poor soft tissue cover in the ventromedial part of the shank, they are largely open
fractures. Usually both bones are fractured simultaneously; isolated injury to one bone occurs mainly
due to direct violence. The tibia is the predominant injury; the diaphyseal part of the fibula is of little
clinical significance as it is not a weight-bearing bone.
Clinical diagnosis is usually not difficult; pain, crepitations, contour changes and pathological
movement are present. X-rays are useful to evaluate the type of fracture and to choose the
therapeutic approach, and it is advisable to capture the entire fibula. We choose surgical treatment
for almost all tibial fractures, because only this way we avoid complications from long-term
immobilization and it allows early mobilization of adjacent joints. Temporary cast fixation must be
applied over the knee and the ankle with thorough padding at the malleoli, heel and fibula head. For
osteosynthesis, closed reduction and the use of an intra-medullar secured nail is the most common
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method of choice; open reduction and plate osteosynthesis are also possible in some cases. In the
case of open fractures or closed fractures with a greater degree of soft tissue contusion, usage of an
external fixator is indicated.
Increased attention in tibial injuries should be paid to the so-called compartment syndrome, where,
as a result of soft tissue swelling in closed osteofascial spaces, muscle ischemia and oppression of
vascular and nerve structures occur. Late or insufficiently radical intervention may result in
permanent functional damage to the limb, in extreme cases even amputation. Diagnosis is mainly
clinical, with symptoms dominated by swelling and severe pain unresponsive to analgesic therapy.
Sensory and motor disturbances are present only at an advanced stage of this condition when there is
already developed mostly unrepairable damage to nerve structures. Beware, pulsations in the
periphery may be preserved. Treatment is surgical, consisting of dermofasciotomy and pressure relief
in all four compartments of the shank.
Fractures of the distal tibia (pilon) are often caused by a high-energy mechanism of injury with
soft tissue damage and the presence of comminuted zones and articular surface defects; in most
cases, a fibula fracture is also present.
Similarly to the previous types, we find the presence of clear deformity and crepitations; we perform
X-ray imaging, and in case of more complex multifragmentary or intra-articular fractures, we also
perform CT scanning. Often, swelling and damage to the skin cover is caused directly by the
mechanism of injury or secondarily by the pressure of dislocated fragments; early reduction and
fixation can prevent skin bullae or necrosis of entire skin regions.
Conservative therapy in plaster cast fixation is acceptable only in non-dislocated extraarticular
fractures; its disadvantage is the long period of immobilization of the ankle with subsequent difficult
rehabilitation. The surgical solution most often consists of open reduction and stabilization with
screws and various types of plate. Initial usage of an external fixator is indicated in similar situations
as for other parts of the shank.
Injury to the ankle is one of the most common injuries to the lower limb. Usually, it is caused by
distortion mechanism during a misstep or fall even from a small height. Depending on the
mechanism of injury, distension or partial rupture of the ligamentous structures of the ankle occurs,
most often the anterior fibulotalar ligament in supination injuries and the superficial portion of the
deltoid ligament in pronation injuries. Distension of the ligament from a partial rupture can be
distinguished clinically by the degree of swelling and the local presence of a haematoma in partial
rupture, whereas ankle instability may be present in complete rupture. To determine the severity of
ligamentous injury, sonography and MRI are useful imaging modalities. In ankle injuries, we should
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always perform an X-ray to rule out possible skeletal injury. In the case of soft tissue injury, we most
often indicate fixation in a brace with crutches for two to three weeks.
Fractures in the upper ankle joint have similar mechanisms of formation as the above-mentioned
soft tissue injuries, often they are luxation open fractures, which is due to the thin skin cover in this
area. In closed fractures, the vitality of the skin is compromised by the pressure of the dislocated
fragments; therefore, early, at least approximate, reduction is indicated.
The classification of fractures is based on the Danis-Weber categorization according to the type of
distal fibula fracture: below the tibiofibular syndesmosis (type A), at the height of the syndesmosis
(B), above the syndesmosis (C).
In bimalleolar fractures, in addition to the fibula fracture, there is also a fracture of the medial
malleolus (or rupture of the deltoid ligament) present, in trimalleolar fractures, a fracture of the
dorsal edge of the articular surface of the distal tibia is also present. These fractures are considered
intra-articular fractures and CT scanning is often necessary to determine the extent of damage.
Conservative treatment in cast fixation is indicated only for isolated type A fractures or for
nondisplaced type B fractures without medial side injury and without asymmetry of the ankle
mortise. Surgical management consists of open reduction and stabilization with plates, separate
screws and Kirschner wires.
A special type of fracture of the ankle is the Maissonneuve fracture, i.e. a high type C fracture.
Clinically, we find pain in the medial ankle area, on the X-ray we find a fracture of the medial ankle
with asymmetry of the ankle mortise, or the X-ray is without evidence of a fracture (only a rupture of
the deltoid ligament is present on the medial side). In this fracture, the interosseous membrane
between the tibia and fibula is torn and the fibula is fractured in its proximal third. Therefore, during
the ankle examination, we do not forget to investigate any pain in the area of the proximal fibula, and
in case of an isolated medial ankle injury, we carry out X-ray of the entire shank. A Maissonneuve
fracture requires operative treatment, otherwise it results in ankle instability.
In most cases, Achilles tendon injuries occur when there are degenerative changes to the tendon
present (e.g. local or systemic corticosteroid therapy); open injuries are also possible.
The diagnosis is based on the anamnestic data of the circumstances of the injury, clinically we find
palpation pain and a palpable defect, Thompson's test is positive (there is no passive plantar flexion
when the calf is compressed). Active plantar flexion is usually preserved to a limited extent by
m.plantaris activity. If in doubt, we perform sonography.
The scope of therapy ranges from conservative treatment in plaster or special vacuum fixation (with
gradual conversion from full plantar flexion to full ankle movement) to surgical solution with open
suture or minimally invasive solution from mini-incision or percutaneous suture.
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Talus fractures are usually the result of high-energy trauma, typically a fall from a height or in a car
accident. Most common talus fractures occur in the cervical region. For an accurate diagnosis, a CT
scan is necessary, treatment consists of osteosynthesis with individual screws.
Fractures of the calcaneus also occur most often as a result of car accidents or falls from heights.
Clinically, we find swelling and pain in the heel area, on the lateral X-ray we usually find a
straightening of Böhler's angle, for a precise diagnosis a CT scan is necessary. Conservative therapy
is reserved for minimally dislocated fractures and, conversely, highly comminuted fractures where
operative treatment does not usually lead to better functional results. Other types of fractures are
indications for surgical treatment, which is usually complex and involves a range of osteosynthetic
material and is associated with the risk of problematic wound healing due to inferior vascular supply
to the skin in this area. Fractures of the calcaneus, despite all efforts and care, are not infrequently
burdened with permanent consequences.
Luxations in the tarsal area (talus luxation, Chopart joint luxation) and luxations and fractures in
the Lisfranc joint area are usually the result of low-energy (sports injuries) or high-energy trauma,
depending on the severity of the injury. X-ray and CT scan will provide a diagnosis after a thorough
clinical examination. Conservative treatment is chosen only for stable and non-displaced injuries,
otherwise surgical transfixation with Kirschner wires or screws is indicated.
Fractures of the metatarsal bones are most often caused by direct force, dropping of heavy objects
on the foot and in this area we also encounter so-called stress fractures resulting from long-term
fatigue. Diagnostics is provided by X-rays, conservative treatment with plaster cast fixation or
special walking braces is reserved only for fractures without major dislocation, otherwise surgical
stabilization is recommended.
Toe fractures or luxations are caused by direct force, often by tripping during sporting activity. For
the proper function of the foot, the big toe is the most important, therefore we pay the most attention
to its injuries; in some more serious injuries, surgical treatment is indicated for the big toe, while for
most injuries and for other toes we are satisfied with conservative treatment. Instead of fixation with
a plaster cast, we prefer adhesive bandage fixation, where the adjacent healthy toe serves as a support
for the injured toe. Keep in mind that toe luxations should be reduced as soon as possible (by pulling
in the physiological axis of the toe) because of the risk of ischemic damage.
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NON-SPECIFIC BONE INFLAMMATION, SPECIFIC INFLAMMATIONS OF BONES AND JOINTS (63)
Jindra Jakub, Mahdal Michal
Osteomyelitis is an inflammatory disease of the bone; if the inflammation penetrates into the relevant
joint, it causes its inflammation - arthritis. Inflammation of the spine with involvement of the
intervertebral disc is called spondylodiscitis.
Depending on the mechanism of origin, osteomyelitis is divided into haematogenous and exogenous
(occurring after trauma to the skeleton - e.g. open fractures).
The course of osteomyelitis can be divided into:
1. acute - the patient's symptoms manifest in the first 14 days to 12 weeks of the disease
2. chronic - often an extension of the acute phase, become chronic (lasting more than 6 months)
3. sub-acute - the time of manifestation is given as 12 weeks from the onset of the disease.
The causative agent of non-specific diseases is most often a bacterium (Staphylococcus aureus,
Staphylococcus epidermidis, Streptococcus pyogenes), the causative agent of a less common group
of specific inflammations is e.g. Mycobacterium tuberculosis.
The mechanism of infection is the colonisation of bone tissue by pathogenic organisms. Leukocytes
are attracted to the bone and enzymes are produced at the site to destroy the bacteria. There are
produced cytokines. As a result, blood flow to the areas is reduced and devitalised necrotic bone
forms, known as sequestra (infected necrotic bone). Antibiotics have little penetration into the
avascular bone and their effect is limited (hence the surgical approach to treatment). The body's
defence against infection is to seal the infection by forming new bone around the sequestrum. This
new bone is called the involucral bone. If the sequestrum drains through the sinus to the surface, a
fistula is formed.
Symptoms of OM
General febrillia, inappetence, general alteration of the organism, weight loss in
chronic patients, night sweats, hepatorenal insufficiency, MODS
Local pain, redness, oedema, fluctuating resistance with abscess formation,
synovialitis and joint filling with restriction of movement, possibly with
contracture formation
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The treatment of osteomyelitis is based on combination of antibiotic therapy and surgical
intervention. In addition to antibiotic treatment, surgical intervention may be necessary to address
the necrotic masses (debridement) and introduce a lavage (a supply and drainage drain into the cavity
or joint space, followed by lavage with a dilute disinfectant solution to eliminate the bacterial load).
In case a bone defect is present, it can be filled (bone grafts or a bioscaffold). Antibiotics are only
effective until a pus-filled deposit is formed; they do not penetrate avascular tissue. Such deposits
require surgical removal.
Antibiotics can be applied locally in carriers to the site of infection during surgery. It is
recommended that antibiotic administration be continued after surgery.
Acute haematogenous osteomyelitis
Acute haematogenous osteomyelitis occurs mainly in paediatric patients. The course of acute
haematogenous OM varies with age due to the different blood supply to the bones (neonates,
children, adults):
In neonates, the purulent process penetrates the cortical bone intracapsularly or along the periphery
of the epiphysis into the epiphysis and perforates the joint (pyarthrosis). The joint is severely affected
by the infection and, despite appropriate treatment, the prognosis is usually poor. Joint deformities
and limb length discrepancy occur during growth.
Prematurity is a risk factor for the development of the disease. Prenatal, perinatal and postnatal
infections (most commonly umbilical sepsis, purulent skin disease, enterocolitis or pneumonia) can
often be identified in the medical history. Treatment consists of immobilisation of the limb and
administration of ATB. If pyarthrosis is suspected, an acute puncture of the joint is performed and if
pus is aspirated, an acute revision of the joint with lavage and introduction of lavage is indicated.
Early surgical intervention minimises joint damage.
Osteomyelitis in childhood predominantly affects the metaphysis. The growth plate presents an
insurmountable barrier to the advancing infection, which enters the joint only where the joint capsule
Diagnosis of OM
Laboratory detect and monitor the overall inflammatory activity of the organism (e.g.:
CRP, leukocytosis, procalcitonin, erythrocyte sedimentation rate)
Imaging X-ray, CT, MRI, scintigraphic imaging
Microbiological
examination
culture, PCR
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reaches the metaphysis. The focus of infection may be a skin, ENT or genitourinary infection. Chills,
high fever, redness and inflammatory oedema over the affected area are present. The site is palpable
and painful. Haemoculture is positive in about 50% of cases. If acute haematogenous OM is
suspected, puncture of the lesion - subperiosteal abscess or bone marrow - is indicated. Surgical
treatment (debridement, lavage) is necessary in sequestration.
The clinical presentation and radiological findings may appear identical to those of Ewing's
sarcoma, and only a biopsy and histological examination can provide definitive differentiation.
Acute haematogenous OM is a rare occurrence in adults. The infectious focus may be located in the
ENT region, the genitourinary tract, the dental area, or in a cutaneous inflammatory condition. The
condition predominantly affects the bones of the appendicular skeleton, with the vertebrae being the
most commonly affected bones. Infection of long bones is an uncommon occurrence. Those at
increased risk of developing this condition include patients with diabetes mellitus, lower limb
ischaemic disease, liver disease, immunosuppression or HIV infection. The process initiates at the
peridiskal portion of the vertebra, where blood flow is reduced in the broad venous plexuses. The
process then progresses to the penetration of the vertebral body, resulting in the destruction of the
disc. It may subsequently extend along the disc periphery to the adjacent vertebral body. The process
is frequently referred to as spondylodiscitis, given that there is always concomitant involvement of
the disc and the adjacent vertebral body. Localised abscesses may arise in the pre-vertebral or
epidural region, which may result in neurological symptoms. Magnetic resonance imaging (MRI) is
the most effective method for diagnosis. The standard treatment is conservative, comprising corset
application (Jewett corset, TLS brace) and long-term (3-6 months) administration of antibiotics
(ATB). Surgical revision is indicated when conservative treatment has failed, signs of dural sac
compression are present, or when kyphotic progression is evident.
Acute exogenous osteomyelitis is a disease that occurs following soft tissue injuries, open fractures
and surgical procedures on bones. It is caused by direct contamination of the affected area with
bacteria or their penetration from a nearby site. The most common causative agents are
Staphylococcus aureus and S. epidermidis, although there is also a significant proportion of
nosocomial infections with resistance, including enterococci, E. coli, Acinetobacter, Pseudomonas,
and Klebsiella. In open fractures, infectious complications occur in up to 30% of cases, with a
particularly high incidence observed in open fractures of grades II and III according to Tscherne's
classification. Infections manifest between three and 14 days following surgical or traumatic
procedures. The patient reports a sensation of heat, burning, and twitching in the wound,
accompanied by a feeling of tension. Clinically, the presence of swelling, redness, fluctuation and
possibly secretion from the wound can be observed. Concurrently, the presence of febrile symptoms,
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elevation of laboratory inflammatory parameters and alteration of general condition can be
documented. In order to facilitate optimal therapeutic outcomes, the following measures should be
undertaken: the release of sutures, performance of an incision, evacuation of the hematoma or pus,
debridement and flushing of the wound with a disinfectant solution. The administration of antibiotic
therapy represents an essential component of the therapeutic approach.
Secondary chronic osteomyelitis arises from the transition from acute haematogenous or, more
commonly, exogenous osteomyelitis (OM) after open fractures or infected osteosyntheses. The
underlying cause is the delayed recognition or inadequate treatment of acute osteomyelitis (OM) or
the inappropriate management of open fractures and infected osteosyntheses. It occurs in three
distinct forms:
1) The inflammatory process subsides, but recurs with an interval of months to years, and the fistula
either does not develop or appears intermittently.
2. The inflammation is at an inactive state, yet persistent in its formation of fistulae.
3) The fistula persists, and recurrent exacerbations occur. The disease is long-lasting, frequently
lasting a lifetime, and often resulting in the loss of a limb. We are not talking about the cure of
chronic OM, but about its transformation into a resting stage. Surgical intervention is indicated when
the outcome of conservative treatment is inadequate, when there is pus retention, when exacerbations
are more frequent and prolonged, or when sequestrum is clearly evident.
Specific inflammations of bones and joints
The main agent of specific inflammation is Mycobacterium tuberculosis, another agent is Treponema
pallidum. Tuberculous inflammation most frequently manifests as spinal disease (spondylitis anterior
profunda) when the primary focus is situated in the peridiskal region of the vertebral body. However,
in its early stages, the inflammatory process perforates the annulus fibrosus and spreads to the disc,
resulting in TBC spondylodiscitis. The infection subsequently spreads to other vertebral bodies. The
infected vertebrae are filled with necrotic material and undergo gradual collapse, predominantly in
the ventral region. Cold abscesses are formed, which spread prevertebrally and paravertebrally. Due
to the action of gravity, these abscesses converge from the cervical spine to the retropharyngeal
space, from the thoracic spine to the mediastinum, and through the diaphragm to the
retroperitoneum. The infection may also spread from the lumbar spine along the m. psoas through
the trigonum femorale to the thigh, or it may perforate the lig. longitudinale posterior and pass into
the spinal canal, where it causes dural sac oppression with neurological symptoms. The classic
course of this affliction may result in the so-called Pott triad, which comprises an abscess, kyphosis,
and paraplegia. The second most common site for tuberculosis of the bone is the knee joint. The
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process is initiated by primary involvement of the synovial membrane and develops into exudative
synovialitis with hydrops.
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CONGENITAL NEVUS, MALIGNANT MELANOMA, SKIN TUMOURS (47)
Rothová Veronika, Fait Vuk, Zapletal Ondřej, Krsička Petr
MALIGNANT MELANOMA
Malignant melanoma (MM) is one of the most malignant tumours. It mainly affects the skin, but it
can also affect the eye, ear, leptomeninges, gastrointestinal tract and mucous membrane of the mouth
or genitals. Malignant melanoma develops through (by) the proliferation of melanocytes. It can be
malignisation of an already present melanocytic nevus or, more often, de novo in more than 70% of
cases. Melanoma cells most often spread through the lymphatic vessels from the primary tumour.
Initially, it is creating regional nodal metastases. Later, it also spreads through the bloodstream and
forms (creates) distant metastases in other organs (lungs, liver, brain).
Development and spread of cancer: Genetic factors and environmental factors contribute to its
development. Genetic factors include a family history of malignant melanoma (FAM syndrome –
familial MM syndrome), a proven mutation in the CDKN2A gene, and a BRCA 2 mutation. The
most significant external factor is exposure to sunlight (UVA and UVB). This is further related to the
increased sensitivity of the skin to sunlight (skin phototype I and II), increased exposure to sunlight
during childhood, skin burns, increased number of dysplastic nevi or large congenital nevus,
immunosuppression, phototherapy (treatment of psoriasis PUVA - psoralens + UVA radiation),
overusing a solarium.
Epidemiology: The incidence of MM is increasing dramatically and mainly affects the Caucasian
population. In 2021, the incidence was about 24 cases/100,000 inhabitants in the Czech Republic.
Mortality was 4 cases/100,000 inhabitants. However, the highest incidence of MM is in Australia
and New Zealand. In patients of African, African American and Asian descent, melanoma is mostly
found on the soles of the feet, palms and under the nail plates (Acral lentiginous type), which is, in
contrast, rare in the Caucasian population.
The most common clinical variants of melanoma:
● Superficial spreading melanoma (SSM) – is the most common and accounts for about 70% of
all melanomas. It has the classic ABCDE warning signs (see below).
● Nodular melanoma (NMM) – is the second most common variant of melanoma, accounting for
about 15-30%. It is characterized by rapid vertical growth and the formation of nodules that
enlarge rapidly.
● Lentigo malignant melanoma (LMM) mainly affects older individuals over 65 years of age. It
appears mainly in the head and neck, rarely on the backs of the hands and feet. It arises from
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lentigo maligna, which is carcinoma in situ; the transition to invasion takes (in) an average of 10-
15 years.
● Acral lentiginous melanoma (ALM) is a melanoma that mainly affects the soles, palms, and
subungual areas. Diagnosis is often challenging and delayed, as ALM is frequently misdiagnosed
as subungual haematoma, bloody verruca, or clavus. Subungual melanoma is manifested by a
diffuse change of colour under the nail plate. The spread of pigment to the proximal or lateral
nail plate is referred to as Hutchinson's sign. It is very important to distinguish subungual
melanoma from subungual hematoma. The basic difference is that the subungual hematoma
deposit gradually grows, shrinks and disappears, whereas subungual melanoma does not.
Differential diagnosis: Melanoma needs to be distinguished from pigmented basocellular
carcinoma, spinocellular carcinoma, seborrheic keratosis, dysplastic nevus, hemangioma, and
subungual hematoma.
Diagnosis: This includes clinical and dermatoscopic examination using a dermatoscope, which
focuses on examining the skin of the entire body, including the palms, soles (feet), and scalp.
An ABCDE rule was created that evaluates the warning signs of melanoma:
● A - Asymmetry
● B - Border (edges) - irregular edges,
● C - Colour - spotted colouring,
● D - Diameter - diameter greater than 6 mm,
● E – Evolution (development) – permanent increase in time.
If 3-4 of the above parameters are met, the suspicion of melanoma is high.
Excisional biopsy and histological examination are necessary in case of unclear clinical findings. It
is performed by complete excision of a suspicious skin lesion with a margin of 1-3 mm under local
anaesthesia and closure of the defect with a linear suture. When this is not possible due to the size or
unfavourable location of the skin lesion, an excisional biopsy - a smaller biopsy from the most
suspicious part of the lesion - is recommended. If subungual acral lentiginous melanoma is
suspected, a biopsy is taken after fenestration of the nail.
Histopathological examination must include one of the most important prognostic factors, which is:
● The thickness of the tumour in millimetres according to the Breslow thickness.
● The histological subtype of the tumour.
● The presence of ulceration on the tumour surface.
● The depth of invasion according to the Clark scale.
● The mitotic index (the number of mitoses per 1 mm2).
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● The presence of microscopic satellites.
● The presence of regression.
Imaging methods for staging to diagnose distant metastases are X-ray, ultrasound, CT, PET/CT, and
MR; however, in advanced disease, PET/CT is most appropriate. The indication is considered
individually.
Melanoma stages: The international TNM classification for melanoma is determined as follows: T
(tumour) is determined by the tumour's thickness (Breslow thickness), N is the status of the draining
lymph nodes, and M describes whether the cancer cells have spread and made as distant metastases.
After completing the TNM classification, patients are, based on the findings, divided into Stages 1-4.
The stage provides information on how big the tumour is and how far it has spread. Treatment
management is then determined based on the stage and clinical condition of the patient.
Treatment: The basis is surgical treatment:
a) Surgery to remove primary tumour - wide local excisions / re-excision of margins. This
procedure aims for the complete removal of the tumour with a sufficient margin of healthy tissue or
re-excision of the scar at the site of the primary melanoma and subsequent closure of the skin defect.
The ideal option is a primary linear suture; in case of larger defects, plastic surgery methods, such as
skin graft or flap reconstruction, must be used. The recommended clinical margin is between 1-2cm,
determined by the thickness of the melanoma, and can be modified considering anatomical site and
functional needs. According to many statistics, a larger hem is not of fundamental importance for the
occurrence of further recurrences and the prognosis of the disease. A specific situation is subungual
acral lentiginous melanoma when exarticulation of the distal limb of the finger is recommended.
b) Surgery to remove lymph nodes:
– Sentinel Lymph Node Biopsy (SLNB) - is primarily a diagnostic method. The goal is to identify or
rule out metastatic involvement in the regional lymphatic basin. Sentinel lymph node biopsy (SLNB)
is recommended for melanomas with nodularity, ulceration or regression and in the case of
histologically verified melanomas with a thickness (Breslow) of more than 0.8 mm. Several methods
can be used to identify the sentinel lymph node (SLN). In the 1990s, Morton et al. developed the first
method for identifying SLB, which was based on using lymphatic mapping with dye (patent blue or
methylene blue). Subsequently, another option, using a radio-colloid labelled with the isotope
technetium (Tc-99), was developed. For the most accurate identification of SLNB, numerous
specialists use a combination of both methods. Other techniques, such as the ICG fluorescence or
Semtimag technique, are not commonly used in routine practice. The localization substance
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infiltrates the vicinity of the tumour/scar, from where it reaches the first lymph node via the
lymphatic channels. Subsequently, SN is detected and extirpated using a radiocolloid using a gamma
probe.
Among the most common locations are the axilla, groin, head and neck area, the iliac area, or, less
commonly, the popliteal area. If metastasis in SN has not been confirmed, there is a high probability
that other lymph nodes are not affected. Initially, SN involvement used to be an indication for
complete lymphadenectomy. However, nowadays, those patients more frequently receive adjuvant
systemic therapy - immunotherapy rather than for further radical surgery.
– regional dissection (lymphadenectomy) - therapeutic performance is indicated in case of evidence
of recurrence metastases in the regional lymphatic region. Evidence of metastases can be clinical or
sonographic with biopsy verification. According to the location, the following are most often
performed: Axillary Lymph Node Dissection (ALND), ilio-inguinal dissection (ILD) and cervical
dissection, rarely popliteal dissection. Undesirable consequences include limb lymphedema,
neuropathy, and limitations in movement.
c) Managing locoregional relapses - Melanomas tend to relapse often, even after several years.
Patients might develop local recurrences, regional nodal relapses, in-transit metastases, multiple limb
relapses, and distant metastases that can occur anywhere (predilection lungs, liver, brain). Primarily,
the solution is always surgical. If surgical resection is no longer possible, local radiotherapy is
recommended. In exceptional cases, the hyperthermic isolated perfusion method can be used for limb
relapses. In the case of solitary metachronous distant metastases, the finding can be solved by
resection procedures.
Systemic oncological treatment: In recent years, targeted treatment and modern immunotherapy
have been used for advanced disease (stage III and IV). The indication for targeted treatment is
linked to the presence of a BRAF oncogene mutation (positivity is present in about 40% of patients).
In the case of immunotherapy, these are monoclonal antibodies. If these treatment options cannot be
indicated, palliative chemotherapy and the use of cytostatics can still be offered. Irradiation of, for
example, brain metastases, skin, bone or nodal metastases can also be indicated as a palliative
treatment.
Prognosis: The prognosis corresponds to the clinical stage, or melanoma thickness - for a tumour
with a thickness < 1 mm, the probability of 10-year survival is 92%. On the contrary, for a melanoma
> 4 mm, it is approx. 50%. Patients with affected lymph nodes have a worse prognosis. The
prognosis with disseminated melanoma is very poor, and approximately 10% of patients survive 5
years. Recently, with the advent of modern oncological treatment, survival has improved
significantly.
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NON-MELANOMA SKIN TUMOURS
Among the most common are basocellular carcinoma (basaliomas) and squamous cell carcinomas
(spinalioma). The main risk factor is UV radiation, which mostly affects elderly patients. Basaliomas
grow slowly (within years) - locally invasive and destructive growth is rare, and they do not produce
distant metastases. Spinal tumours can grow exophytically and have a greater disposition to
metastasize. The basis of diagnosis is clinical and histological examination. In advanced spinal
tumours, an ultrasound examination of the lymph nodes is performed for the risk of lymphogenic
dissemination. The basic treatment is surgical removal of the skin tumour with a border to healthy
tissue. If surgical treatment is not possible, cryotherapy or curative radiotherapy can be used.
Systemic targeted treatment can be used for locally advanced and metastatic basal cell carcinomas.
In the case of a disseminated spinal tumour, palliative systemic chemotherapy is recommended. The
prognosis for both skin tumours is excellent. 90-95% of patients are cured by radical excision
without affecting the nodes.
CONGENITAL NEVI
These are benign melanocytic skin tumours. If they do not change or enlarge, it is not necessary to
remove them. However, their excision is usually performed for cosmetic reasons. In excision, a
minimal margin into healthy tissue is sufficient. Dysplastic nevi (DN) is a separate group - a clinical
unit between melanocytic nevus and melanoma. Their clinical appearance resembles melanoma in
situ. DN carriers have a higher risk of developing melanoma than the general population. Excision is
indicated in case of clinical and dermatoscopic uncertainty. Correct histological evaluation by an
experienced pathologist is important.
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SKIN GRAFTS AND LOCAL SKIN FLAPS (46)
Hokynková Alica, Streit Libor, Šín Petr, Matysková Dominika
Skin grafting and flap plasty are used in the reconstruction of skin and soft tissue defects of various
origins, extents, and locations with the aim of restoring the damaged skin coverage. In reconstructive
surgery, there are a number of reconstructive techniques, and their selection is guided by the
reconstruction ladder, meaning from the simplest technique to the most complex (Fig. 1). Defects of
limited extent can be closed with direct suturing. Larger defects can be reconstructed by
autotransplantation of a skin graft without a vascular supply, or by a skin flap, which has a vascular
supply, and due to the included subcutaneus tissue the reconstruction is more complex than in the
case of a skin graft (Fig. 2).
Skin Grafting
Skin grafting is a surgical procedure aimed at restoring the integrity of the skin by transferring it
from a healthy area to a damaged area. A skin graft always consists of a full layer of the epidermis
and varying layers of the dermis. The transfer of skin graft is facilitated by the fact that skin without
subcutaneous tissue remains temporarily viable until capillaries grow into the graft from the base of
the wound, ensuring its nourishment. Unlike flap plasty, skin grafts do not have their own blood
supply. Skin grafting is indicated for reconstructing skin defects of various etiologies, such as burn
injuries, traumatic defects, infectious complications, venous ulcers, etc. It is not applied to defects
exposing deeper structures, such as tendons, nerves, blood vessels, and bones. Harvesting is
performed using an air- or electro-dermatome, Watanabe knife, or Humby knife, or scalpel for
smaller defects. Skin grafts are fixed itno the wound with stitches or metal clips and are slightly
compressed against the base of the defect. Uncomplicated healing typically takes about 7–10 days.
Skin grafts are classified according to the type of donor into: 1. Autotransplantation (autograft):
This is the most commonly used type of transplantation, where skin is taken from one part of the
patient's body and transferred to the skin defect, making the skin donor also the recipient; 2.
Allotransplantation (allograft): In this type of transplantation, skin graft is taken from the body of
another person; in the case of identical twins, the graft is referred to as an isograft. Allografts are
applied only temporarily (until autotransplantation can be performed) to prevent rejection; 3.
Xenotransplantation (xenograft): This type of transplantation uses skin from another species, most
frequently from pigs, and is applied only temporarily.
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Types of Autografts by Thickness and Contained Tissue:
Dermoepidermal Skin Graft (Split-thickness skin graft - STSG): This type includes only the
epidermis and part of the dermis (thin 0.15–0.3 mm, moderately thick 0.23–0.45 mm, thick 0.45–0.6
mm). For extensive defects, the harvested graft is expanded using meshing with a mesh dermatome,
allowing for the graft to spread over a larger area through multiple small incisions (mesh), that
enable fluid drainage and quicker adherence of the graft to the base. These grafts heal faster but are
less mechanically durable than full-thickness grafts. They are suitable for covering large surface
defects. The donor area (usually the ventral side of the thighs) is typically healed by
reepithelialization in about 14 days.
Full-thickness Skin Graft (Full-thickness graft - FTSG): The full-thickness skin graft includes the
entire epidermis and dermis (0.6 mm and more). The graft is only perforated with the point of a
scalpel to allow fluid drainage from the base of the defect. These skin grafts are primarily used in the
reconstruction of defects in the head area, showing better aesthetic results and greater durability.
They are suitable for covering smaller defects. The donor area (retroauricular, supraclavicular area,
groin, etc.) is sutured.
Flap plasty
Flap plasty utilize the transfer of tissue (skin and subcutaneous fat, sometimes also fascia, muscle,
etc.) from a donor site to the defect. A flap always has its own blood supply (fasciocutaneous,
myocutaneous, direct cutaneous), which is crucial during its planning and preparation. Flaps are
categorized according to various criteria, including distance (local, distant), tissue content (skin,
fasciocutaneous, myocutaneous, osteomusculocutaneous-composite, visceral, etc.), blood supply
(random, axial, myocutaneous, fasciocutaneous), method of transfer (rotational, transpositional, free,
etc.), function (sensory, innervated muscle, transfer of a toe from the foot to the hand, etc.), and the
time interval from the injury, etc. Local flaps utilize surrounding tissue for reconstructing defects.
They can have various shapes and methods of transfer, such as island (unidirectional or
bidirectional), rotational, transpositional, sliding, and island "keystone flaps," etc. Local flaps can
also be combined with one another to close defects. Local flaps are very frequently used to
reconstruct defects after skin cancer removal, typically in facial area, but it can iclude larger volumes
of transferred tissue, such as the rotational fasciocutaneous gluteal flap in the reconstruction of sacral
pressure ulcers. An example of the use of a double transpositional flap is Z-plasty, which is used to
address the distribution and elongation of contracted scars (Fig. 3b). Distant flaps are characterized
by the use of tissue that is located away from the defect site. They are utilized in cases where local
flaps cannot be used. Distant flaps can be direct, where the flap is directly connected to the defect
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and a temporary pedicle remains preserved between the defect and the donor site, allowing for the
growth of neocapillaries between the defect and the flap. Subsequently, after 3-5 weeks, the pedicle
of the flap is severed. An example is the inguinal flap used for reconstructing defects on the hand. In
this specific case, the flap is sewn onto the defect on the hand (Fig. 4).The most technically
demanding are free flaps, where the composite tissue is dissected on a specific nutrient pedicle,
transferred to the defect site, where it is connected to recipient vessels using an operating
microscope. These operations are discussed in the chapter "Microsurgical Reconstruction: Free Flaps
and Allogenic Transplantation", which is part of the Addendum to this book.
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Fig. 1: Reconstructive ladder Fig. 2: Blood supply of a flap
Fig. 3: Local flaps: a) Reconstruction of the nasal defect with double transpositional „bilobed“ flap b) Z-plasty
Fig.4: Distant flaps
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NERVE REPAIR, GRAFTING AND TRANSFERS (50)
Janeček Pavel, Klabusay Filip, Dvořák Zdeněk, Streit Libor, Bayezid Can Kadir
The principle of repairing a damaged nerve
The basic prerequisite for successful peripheral nerve repair is the restoration of nerve continuity in
case of nerve severance. The rule of thumb is the use of microsurgical technique with adequate
magnification, the use of microinstrumentation and suture material of 8/0 - 10/0 thickness (0.2 mm
thread thickness). A tension-free suture is essential for a successful suture of the nerve, and partial
mobilization of the nerve can be performed to facilitate suturing. In the event that the loss of injury is
so great that tension-free suture of the nerve cannot be achieved, it is preferable to proceed with the
use of a nerve graft. Depending on the size of the nerve, we choose 2 types of suture. For smaller
nerves where motor and sensory fascicles cannot be identified, we choose the epineural type of
suture, in which we adapt the nerve ends to each other behind the epineurium with several (usually
four) single sutures. For larger nerves, an interfascicular suture can be used, in which we suture the
individual fascicles together.
epineural type interfascicular type
Timing of nerve reconstruction
The best therapeutic results are achieved with immediate nerve reconstruction. The actual shape and
position of the fascicles and the vascular network on the nerve surface allow proper coaptation of the
nerve stumps.
With early reparation, retraction of the nerve stumps and the formation of a neuroma does not occur.
In addition, motor fascicles can be differentiated by stimulation within 72 hours after injury.
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In situations where adequate primary treatment is not possible, nerve stumps should be approximated
to prevent retraction and subsequent reparation delayed until the general condition of the patient or
wound allows, preferably within 3 weeks of injury. On subsequent revision, the resulting neuroma
must be resected down to healthy tissue. The mechanism of peripheral nerve injury also has a
significant effect on the final outcome, with the best results being those in which there is a sharp
break in the nerve and the worst results in crush or avulsion type injuries.
Nerve grafts
If the nerve stumps are too far apart and a tension-free suture cannot be achieved, nerve grafts should
be used to reconstruct the nerve. The grafts are placed in the defect according to the position of the
fascicles. To avoid loss of part of the axons before distal anastomosis by branching, it is advisable to
rotate the inserted nerve graft 180°. Nerve grafts are divided into autografts, allografts and conduits.
Autographs
Nerve grafts taken from another part of the patient's body. For the purpose of a nerve graft, we
usually use nerve-sensitive nerves, mainly because of the morbidity of the donor site (the loss of
surface sensation is less severe for the patient than the loss of motor function of a particular muscle).
The most commonly used donor nerve is the sural nerve, from which a graft 30-40 cm long can be
obtained in an adult and can be removed by a special forceps from small incisions. After its removal,
there is a sensory loss on the lateral ankle and lateral
heel side, the extent of which diminishes with time. For
smaller nerve defects, the lateral cutaneous
antebrachial nerve from the forearm can be used. The
usual length of the graft obtained is approximately 8
cm. Another variant is medial cutaneous antebrachial
nerve (in the groove between triceps muscle and biceps
muscle), in this way a graft of up to 20 cm length can
be obtained. Of the motor nerves, the distal part of the
interosseous antebrachial anterior nerve or intercostal
nerve can be used for graft harvesting.
Allographs
Nerve grafts from cadaveric donors. Sterilized and decellularized, they essentially serve as a matrix
into which the axons of the proximal end of the injured nerve grow. Due to the decellularization
method, there is no need to worry about graft rejection or other immunogenic reaction. The use of
allografts has similar results to autografts.
sural nerve
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Conduits
Nerve graft made of artificial material (most often collagen). Not immunogenic, it can be purchased
in multiple diameters and lengths. Compared to autografts and allografts, they have poorer
regenerative results according to available studies, and their other disadvantage is their high cost.
Nerve transfers
Nerve transfers (neurotization)
are most often indicated for very
proximal peripheral nerve injury
or for avulsion of nerve roots
from the spinal cord. In these
cases, a nerve transfer will
facilitate better reinnervation of
the effector organ (muscle) than
would be achieved with the use
of a nerve graft.
In motor nerve transfer, donor
nerves are used, i.e., nerves that
are detached from the functional
muscle that is dispensable and, when connected to the distal stump of the injured nerve, will
innervate the desired muscle unit. Because of the speed of regeneration, we try to perform the nerve
coaptation as close as possible to the motor discs of the reinnervated muscle, and the use of a motor
nerve of a synergistic muscle is also an advantage. One example is the Oberlin tranfer for elbow
flexion recovery, which is used in brachial plexus injuries when the n. ulnaris is preserved. Thus, part
of the motor fibers of the n. ulnaris are reconnected to the biceps muscle branch of the n.
musculocutaneus.
conduit
Oberlin transfer
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Failure of peripheral nerve reconstruction
For motor nerves, it should be remembered that the lifetime of neuromuscular discs in skeletal
muscle without innervation is a maximum of 2 years, and it also depends on the age of the patient.
The earlier the reconstruction is performed, the better the chance of success. The electrostimulation
of the affected muscle is indispensable and should be carried out until its full reinnervation. The time
aspect must be taken into account, where we can approximate a nerve regeneration rate of 1mm/s
and a delay in the anastomosis of approximately one month. If successful reinnervation of the muscle
does not take place, it is effectively lost forever as a motor unit for the organism. In this case,
reconstruction of the lost function can be accomplished by free microvascular transfer of the motor
unit, i.e., the functional muscle, which can be sacrificed (e.g., m. gracilis) or the muscle function is
replaced by tendon transfers. Their principle is to reconnect the tendon apparatus of the less
important functional muscle to the tendon apparatus of the non-functional key muscle. In the case of
sensory nerves, reconstruction can be performed at any time during life, and there are known cases of
tissue regaining sensitivity even after 40 years. All these techniques belong to the field of highly
specialized reconstructive surgery.
Facial Paralysis
The resting position and movement of a healthy face are determined by the actions of the muscles of
facial expression, which are innervated by the facial nerve. A lesion of the facial nerve hampers the
ability to generate facial expressions. Facial palsy is a distressing condition that causes both
functional and aesthetic issues, posing significant challenges to the patient’s quality of life. Facial
palsy can be subclassified as central or peripheral, depending on the location of the lesion. Central
paresis results from damage to the brain center or fibers above the nerve nucleus (lesion of the upper
motor neurons). In the case of peripheral palsy, the facial nerve is damaged at the level of the lower
motor neurons during its course after arising from the pons. Peripheral palsies are more common and
manifest on the affected side. In complete peripheral palsy, we observe drooping of the eyebrow and
modiolus, an effaced nasolabial fold and absent function of the orbicularis oculi. The eyelids do not
close, blinking disappears, and the protective functions of the eyelids are impaired. The prognosis of
paralysis can range from persistent complete (flaccid) paralysis to the full return of normal facial
function. However, there is a wide range of clinical presentations, from hypoactivity to hyperactivity,
between these two extremes in spastic facial palsy.
The aim of complex surgical treatment for flaccid facial palsy is to restore the resting position and
symmetry of the face, recover the protective functions of the eyelids, and, ideally, also restore facial
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movement and the ability to smile. To correct incomplete closure of the eyelids (lagophthalmos),
oculoplastic operations are performed, most often using lateral tarsorrhaphy, passive suspension of
the lower eyelid, and/or implantation of a platinum weight in the upper eyelid. To restore movement,
facial reanimation surgery is performed within 2 years of the onset of paralysis, most commonly in
the form of neurotization procedures. These procedures aim for tensionless nerve coaptation of the
interrupted or missing section of the facial nerve, either through end-to-end anastomosis or other
anastomotic approaches involving nerve grafts, enabling the connection of the distal end of the nerve
stump to the healthy contralateral facial nerve. A different approach involves connecting the
peripheral branches of the facial nerve to other cranial nerves on the ipsilateral side (e.g., the
masseteric nerve). After 2 years from the onset of paralysis, irreversible changes occur in the motor
end plates of the facial muscles, leading to permanent atrophy and fibrosis. A reconstructive
procedure to replace the mimetic muscles is required. An example of such an operation is
reanimation by so-called lenghtening temporalis myoplasty or a free muscle transfer (most often the
gracilis muscle). The spastic type of facial nerve palsy, characterized by synkinesis, arises as a
result of aberrant nerve regeneration, which most often occurs after viral palsy or Bell's palsy. The
treatment of this type of paresis typically consists of neuromuscular training, the application of
botulinum toxin, and, in resistant cases, selective neurectomy of the distal branches of the facial
nerve.
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HAND AND FINGER INJURIES AND AMPUTATIONS (48)
Hokynková Alica, Šín Petr, Matysková Dominika
Injuries of the hand may involve defects in the skin, connective tissues, tendons, intrinsic hand
muscles, blood vessels, nerves, or the skeletal system. These injuries are typically caused by trauma,
often resulting from occupational accidents, and can range from minor superficial wounds to severe,
devastating injuries, including amputations (for more detailed information, refer to the chapter on
Replantation). The cornerstone of preoperative evaluation is a thorough clinical examination of the
injured hand. This assessment includes evaluating the size, depth, and location of the defect, as well
as the functional status of key structures—such as mobility (e.g., flexion, extension, abduction,
adduction, radial and ulnar deviation), blood circulation (assessed by skin color, temperature, and
capillary refill), and sensory function (evaluating the distribution areas of the median, radial, and
ulnar nerves). Scars from previous injuries or surgeries should also be carefully documented. For
severe injuries in the hand area, it is necessary to think about the risk of compartment syndrome. In
the indicated cases of severe hand injury, it is necessary to perform releasing fasciotomies of
individual compartments in the forearm and hand area. The aim is to relieve the pressure in the
fascial loci due to increasing swelling of the muscle groups, ev. also to release the carpal tunnel by
dissection of the carpal ligament to prevent median nerve retraction.Additionally, a detailed history
of the trauma is essential, including the mechanism of injury (e.g., avulsion, laceration by sharp or
blunt objects, animal bites, or complex trauma involving mechanical, pressure, or thermal
components such as burns from hot rollers), as well as the time of injury and, if relevant, the duration
of tourniquet application in cases of severe hemorrhage. The dominant hand should be identified, and
a complete personal history, including age, comorbidities, smoking habits, occupation, hobbies, and
tetanus vaccination status, should be obtained. In cases where skeletal involvement is suspected,
radiographic imaging in both anteroposterior and lateral views is performed, with additional
projections or imaging modalities considered if indicated. The management of hand injuries is
performed in an operating room, under antibiotic prophylaxis, in sterile conditions, and using
appropriate anesthesia—whether local, regional (e.g., digital block, wrist block, axillary block), or
general—depending on the extent of the injury and the planned reconstructive procedure. As a
general principle, surgery is carried out under bloodless conditions, achieved using a tourniquet, and
magnification (such as magnifying loupes) is often utilized. The surgical exploration involves
extending the wound proximally and distally to properly visualize the extent of the injury and assess
the nature and amount of tissue loss. This evaluation guides the choice of the reconstructive method,
which may range from simple direct suturing to more complex procedures such as free flap
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reconstruction. Whenever possible, the reconstructive procedure is performed immediately, provided
the condition of the wound permits. However, in cases involving severe contamination, infection, or
anticipated necrosis of the surrounding tissue, temporary wound management techniques are applied.
These may include the use of synthetic wound coverings, moist wound healing methods, or negative
pressure wound therapy (vacuum-assisted closure). Definitive reconstructive surgery is then delayed
until a later stage, when the wound is more suitable for intervention.
Superficial Skin defects
Superficial skin defects of the hand refer to injuries where the skin layers (epidermis, dermis, or
subcutaneous tissue) are absent, but crucial underlying structures—such as tendons, ligaments, joint
capsules, blood vessels, nerves, and bone—remain intact. These injuries commonly result from sharp
instruments such as glass, knives, or woodworking tools like planers. In cases of minor injuries,
direct suturing of the defect may be feasible after mobilization of the surrounding tissue, although
this is often limited in the palmar region. Small, superficial wounds—such as those on the
fingertip—can be allowed to heal by secondary intention, typically managed with antiseptic
ointments. For excoriation injuries limited to the epidermis, a conservative approach is preferred.For
larger superficial defects that are not infected, skin grafting may be indicated. Either full-thickness or
split-thickness skin grafts are applied and secured to the wound bed using metal clips or sutures,
along with gauze compression. Skin grafts generally take 7 to 10 days to heal, with full-thickness
grafts requiring more time. The final outcome typically results in a flat scar with some degree of
contraction, which tends to be more pronounced with thinner grafts. Comprehensive scar
management, including the use of silicone gels, compression sleeves, pressure massage, and even
laser therapy, may be required. Rehabilitation plays a critical role in preventing contractures, which
could otherwise limit the range of motion, particularly in the hand and fingers.
Deep Skin Defects
Deep skin defects are characterized by the absence of skin coverage, with exposed or damaged
deeper structures. These injuries require reconstruction using flap techniques, transferring wellvascularized
tissue to the site of the defect. Depending on the nature and extent of the injury, local,
distant, or free flaps may be employed (see chapter on Skin Flaps and Transplantation).
Local Flaps
Local flaps utilize tissue from the surrounding area of the defect. Examples include the V-Y
advancement flap (for fingertip reconstruction, either unilaterally or bilaterally), the Moberg flap
(used to move volar thumb skin to cover a thumb tip defect), rotation flaps, Limberg flaps,
transposition flaps, and reverse forearm flaps (based on radial, ulnar, or posterior interosseous
arteries). Additional examples are the Kite flap, based on the second dorsal metacarpal artery, and
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others.
Distant Flaps
Distant flaps involve tissue from more remote areas of the body that remain connected to both the
donor and defect sites for a period, typically around three weeks, after which surgical detachment is
performed. Examples include cross-finger flaps, tarsal flaps, and inguinal flaps, among others.
Free Flaps
Free flaps are often employed in the reconstruction of severe or complex hand injuries, especially in
cases of large or combined defects. These flaps not only restore skin coverage but can also help
reconstruct functional units, such as through free transfer of a toe to the hand. These procedures are
among the most intricate reconstructive techniques, often requiring several hours. The vascular
pedicle of the flap is meticulously connected to recipient vessels near the defect through
microsurgical techniques. Examples include the SCIP (superficial circumflex iliac perforator) flap
from the groin area, the ALT (anterolateral thigh) flap nourished by perforators from the descending
branch of the lateral circumflex femoral artery, and the fascia of the serratus anterior or temporalis
muscle.
Loss of Functional Structures
Hand injuries may involve the loss of functional structures, such as bone, tendons, or nerves. When
bone is lost, bone grafting or shortening may be performed. In cases of tendon loss, tendon
transposition surgeries can replace the missing tendon with another, such as using the extensor
indicis or extensor digiti minimi, or with a tendon graft, such as the palmaris longus or plantaris
tendon. This may be done either at the time of injury or as a staged procedure following the insertion
of a temporary silicone replacement. Similarly, missing blood vessels may be replaced by a venous
graft from the nearby area or from the lower limb. If part of a nerve is lost, a nerve graft, often
harvested from the sural nerve, may be used.
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REPLANTATION SURGERY (INCLUDING TRANSPORT OF THE PATIENT AND AMPUTATED BODY PARTS)
(49)
Dvořák Zdeněk, Berkeš Andrej
Introduction and definition of terms
Replantation and revascularization of amputated limbs is a standard procedure for restoring hand
grip. These procedures are performed in specialised replantation centres and the following terms
need to be defined for communication with them:
Amputee - separated acral part of a limb (separated fingers, palm, whole hand, forearm…)
Total amputation - the amputate and stump are completely separated and not connected by any
tissue. The procedure to restore the integrity of the body is called replantation.
Subtotal amputation - the amputate and stump are conected by tissue without sufficient nutrition
(bone, tendon, nerve, skin bridge up to 1/ circumference of the finger) and blood vessels are
interrupted. The amputate is not perfused, replantation is needed to restore integrity.
Severe combined injuries with interruption of blood vessels - severe injuries of the limb with
disruption of functional anatomical structures and interruption of major blood vessels, but with blood
supply to the semi-amputated part of the limb by way of collaterals. The procedure to restore blood
supply is called revascularisation.
Replantation - includes all procedures to restore the continuity, function and nutrition of the
replanted part, i.e. osteosynthesis of bone, suturing of tendons or muscles, anastomosis of blood
vessels, microsuturing of nerves and reconstruction of the skin covering.
Revascularisation - a procedure to improve blood supply to the periphery in injuries where vascular
supply is significantly restricted but other functionally important structures are fully or largely
preserved.
Warm ischaemia - is a condition in which the amputee is uncooled, left at body temperature. The
duration of warm ischaemia (during which the amputate can still be replanted) is approximately 10
hours for fingers and 6 hours for amputates containing muscle tissue.
Cold ischaemia is a condition in which the amputee is separated from the body and cooled to 4°C.
The duration of cold ischaemia should be less than 24 hours for fingers and 10 hours for an amputee
containing muscle tissue.
Replantation surgery, indications and contraindications for surgery
The good status of the structures of the amputated tissue is important for the success of replantation.
Another factor is the maintenance of a period of warm or cold ischemia of the amputate. The general
condition of the patient is also important (extent of injury, other injuries, associated diseases -
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atherosclerosis, diabetes mellitus, hypertension, vascular disease, etc.). It is necessary to take into
account the age of the patient, his ability to undergo the procedure. Replantation of a single finger
takes approximately 2 - 4 hours, replantation of the hand in the palm of the hand 6 - 10 hours, higher
amputation 6 - 8 hours, with thrombosed anastomoses the procedure is prolonged and there is a
higher risk of subsequent revisions.
The suitability of replantation is related to the mechanism of injury, as there are variations in the
success rate of the procedure ranging from smooth cut, sawing off, circular sawing to crushing
injuries. The highest percentage of replant failures occurs with the avulsion injury mechanism.
The indications for replantation are categorized into absolute and relative. Absolute indications for
replantation include thumb amputation, multi-finger amputation, palmar amputation, wrist
amputation, distal forearm amputation, and all amputations in children. Relative indications for
replantation are high amputations, amputation of one finger or part of it, and isolated amputation of
the index finger across the PIP joint. Contraindications to replantation are psychiatric disease,
advanced age, heavy smoking, severe stage diabetes, or severe polytrauma.
Management of the treatment
Most of the injured are primarily treated by an ambulance with a doctor. After administering of first
aid, the patient is transferred to the nearest surgical outpatient clinic, where the surgeon assesses the
severity of the injury, the condition of the amputated parts and contacts the replantation centre. He or
she then communicates the following facts to the replantation centre by telephone. Nowadays, it is
also possible to send electronically photodocumentation of the case. After considering all the
circumstances, the surgeon of the replantation centre will decide whether to transfer the patient for
replantation. Replantation centers with 24/7 service are:
q Department of Plastic and Aesthetic Surgery, St. Anne's Hospital, Brno
q Department of Plastic Surgery, FN Královské Vinohrady, Prague
The Department of Plastic Surgery of the Ostrava University Hospital and the Traumatology
Department of the České Budějovice Hospital offer replantation on a regular basis. Due to the small
size of the Czech Republic, transport by ambulance is suitable both for surgical treatment and
subsequently transfer to the nearest replantation centre. Air transport of the patient is indicated only
if the patient is in severe state or if the nearest replantation centre is busy treating another patient and
transport by ambulance would be too long.
Principles of amputation and stump treatment
A completely amputated parts should be treated by wrapping it in sterile gauze moistened with
saline, then it should be placed in a bag, which is placed in a second bag with water and ice. The
ratio of water to ice should be approximately 2:1, aiming for a cooling temperature of 4°C. The
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stump of the limb should be treated with a sterile gauze cover and compression bandage (see Fig. 1).
When treating the stump, do not interrupt any skin or tissue that maintain continuity in subtotal
amputation, do not apply disinfectant to the wound area, ensure good haemostasis (compression
dressing), avoid the use of a tourniquet if possible (time of application should be indicated if used).
The tourniquet is used only in high amputations with continued arterial bleeding and the risk of
hypovolemic shock. Also, immobilization of the injured part is performed and elevation of the limb
during transport is ensured.
Fig. 1 - Correct treatment of amputees. The amputee is placed in gauze moistened with saline and
then placed in a plastic bag. The bag containing the finger amputates is then placed in another bag
with a 2:1 solution of water and ice.
Principles of replantation and specifics of amputation injuries
Most replantation procedures are performed under general anaesthesia; exceptionally, local or
regional anaesthesia (axillary block) may be used. During replantation, the skeleton is first shortened
and then osteosynthesized, most often using K-wires for fingers. Skeletal shortening is always
necessary because of deficit of the soft tissue. A minimum 4-strand flexor tendon suture is
performed to allow early rehabilitation. The volar neurovascular bundles are identified and a
microsuture of usually one dominant (thicker) digital artery is performed. If the vessel is destroyed in
a longer distance, then the damaged part of artery is replaced with a vein graft. The surgery continues
with microsuturing of both digital nerves and suturing of the dorsal aponeurosis of the finger. To
provide venous drainage, microsuturing of the veins on the dorsum of the finger is performed, most
commonly at a ratio of 2 veins per supply artery. At the end of the operation, an skin cover suture is
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performed and the blood supply to the replanted tissue is monitored. If the amputated part is
containing muscle tissue, the time of ischemia must be respected. Rapid osteosynthesis of the
skeleton is performed, then the procedure continues with reconstruction of the artery and suturing of
the thick vein. This is followed by reconstruction of tendons, nerves and the remaining stuctures.
Replantation procedure can be performed for all acral losses on the human body. Replantation of the
lower limb, scalp, auricle, nose or even the penis could be performed.
Postoperative care and complications
Postoperative care after replantation is performed in specialized ICU, where, the blood supply to the
replanted part is intensively monitored. The patient is heparinized and is using Acetylsalic acid 100
mg p.o. in one daily dose from the third postoperative day for 3 weeks after surgery. The blood
supply to the replant is assessed by capillary reflow, color, temperature and skin turgor. The principle
of assessing capillary reflow is to experss the blood from the capillaries by pressure and to monitor
its re-entry, which is possible when the blood perfusion in the capillaries is sufficient. Its normal time
is about 1 second. The prolongation of capillary reflow is observed in ischemia, while its shortening
is observed in venostasis. Complications of replantation could be venous and arterial thrombosis,
vasospasm, infection, bleeding or failure of replantation. Most of these states require urgent surgical
revision.
The importance of replantations
Replantation is a standard reconstructive procedure for upper limb injuries. It contributes to the
restoration of upper limb function by improving the gripping ability of the injured hand. These
factors, together with a favourable appearance, contribute significantly to the psychological
stabilisation of the patient and enable him to return to work.
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CONGENITAL DIAPHRAGMATIC HERNIA, ABDOMINAL WALL DEFECTS IN CHILDREN (42)
Turek Jakub, Plánka Ladislav
Definition
A congenital diaphragmatic hernia (CDH) is a malformation in which the abdominal content herniates
into the thoracic cavity due to incomplete development of the foetal diaphragm, leading to pulmonary
hypoplasia with alteration of the development of pulmonary vascular structures. Bohdalek's hernia
(about 70%) represents a herniation in the posterolateral part of the diaphragm (preferably on the left
side), Morgagni's hernia arises based on a defect in the anteromedial part of the diaphragm.
Aetiology
The aetiology of the occurrence is probably multifactorial. It may occur as an isolated malformation
or as part of chromosomal abnormalities (Turner syndrome, trisomy 13. and 18.), chromosomal
aberrations (e.g. Fryns or Cornelia de Lange syndromes). Exposure to teratogens (lithium, allopurinol)
during pregnancy may be associated with the development of this malformation.
Pathogenesis
The diaphragmatic hernia is caused by a defect in the continuity of the pleuroperitoneal membrane,
which results in herniation of the abdominal contents into the thoracic cavity, compromising the
normal development of the lung tissue and the pulmonary vessels, leading to thickening of vessel wall
and resulting in persistent pulmonary hypertension.
Clinical manifestation
More than 50% of CDH is diagnosed during the prenatal screening between 18 and 24 weeks of
gestation by ultrasound, which may be supplemented by foetal MRI if in doubt. Mothers may also
present with low α-fetoprotein levels at 18th gestation or polyhydramnios.
Postnatally, CDH manifests as worsening respiratory insufficiency, cyanosis, disappearance of the
auscultatory finding on the lungs on the affected side and dislocation of the cardiac echoes.
CDH is confirmed on a native chest X-ray, which shows intestinal villi in the thoracic cavity and
mediastinal shift. In case of diagnostic confusion, CT or MRI may be added.
Course
Management depends on prenatal recognition of the malformation. If the diagnosis of CDH is
confirmed at the screening examination, the option is to transfer the child to children surgery centres
for foetal surgery - tracheal occlusion. After birth, the clinical manifestation is significant and as soon
as the patient is stabilized, surgical management is considered. Patients are primarily transferred to
centres where neonatal ECMO is available for postoperative care.
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Complications
Long-term complications in patients include chronic lung disease, aspiration pneumonia, pulmonary
hypertension, and obstructive lung disease. Gastrointestinal complications can include GERD or
growth disturbances. Recurrence is another risk that can occur in months to years after surgery. Later,
the orthopaedic problems such as chest deformities or scoliosis may occur after CDH repair.
Prognosis
Prognosis depends on many factors. Negative prognostic features include a low Apgar score, the
presence of severe pulmonary hypertension, shock, and the need for ECMO.
Differential diagnosis
The differential diagnosis may include congenital cystic adenomatoid malformation,
bronchopulmonary sequestration, bronchogenic cyst, bronchial atresia or teratomas.
Treatment
Surgical treatment is the only alternative for patients with CDH. Surgery is performed after control of
pulmonary hypertension. The defect is approached from a subcostal incision, but recently minimally
invasive - thoracoscopic approaches have come to the fore. For smaller defects, marginal suture is
performed, while for larger defects, a patch must be implanted, both from artificial materials (Goretex)
and biological materials.
Prevention
The only possible prevention is to avoid carcinogens in pregnancy and to undergo prenatal screening,
which can detect most cases of CDH and thus time the delivery in perinatal centres.
Gastroschisis
Definition
This is a paraumbilical defect in the entire thickness of the abdominal wall with protrusion of the
intestines, which are not covered by any membrane.
Aetiology
The exact aetiology is unknown. Gastroschisis is caused by a malformation of the ventral part of the
abdominal wall. Risk factors for this diagnosis include smoking, environmental influences (exposure
to certain substances such as nitrosamines), or the use of certain medications during pregnancy
(aspirin, ibuprofen, decongestants).
Clinical manifestations
The clinical picture is typical - after delivery, a defect is observed in the abdominal wall area, usually
paraumbilical to the right, the intestines are herniated extracorporeally, macerated and oozing, not
covered by a membrane. In addition to the intestines, other organs of the abdominal cavity may be
herniated. The picture of herniation is evident in prenatal screening.
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Progress
After the diagnosis is made, the pregnant woman is monitored at the perinatology centre, delivery is
planned based on the baby's condition, often the delivery is induced. Based on the study, with a
standard course of pregnancy, there is no contraindication to vaginal delivery.
Prognosis
Compared to other abdominal wall defects, patients with gastroschisis have the best prognosis and
more than 95% of patients survive.
Differential diagnosis
Gastroschisis must be differentiated from omphalocele. In the differential diagnosis, we must also
think of umbilical hernia, bladder exstrophy or cloacal exstrophy.
Treatment
The therapy is the closure of the defect primarily or by means of a temporary cover - a silo, which
gradually closes with the expansion of the volume of the abdominal cavity and the repositioning of the
contents into the abdominal cavity.
Omphalocele
Definition
This is a defect of the abdominal wall in which prothorax of the intestinal villi from the base of the
umbilical stump occurs and the herniated contents are covered by the amniotic membrane.
Aetiology
Unlike gastroschisis, omphalocele is associated with some genetic syndromes such as BeckwidtWiedemann
or trisomy 13., 18. and 21. chromosomes. Omphalocele occurs when there is no rotation
and repositioning of the physiologically herniated intestines after the 12th
week of gestation.
Clinical manifestation
It is the herniation of intestines (rarely by other organs of the abdominal cavity) through the umbilical
stump, which are covered by the amniotic sac. This condition is recognizable in prenatal screening.
Prognosis
Depends on the size of the defect and the associated conditions within the syndromes.
Differential diagnosis
It is most important to differentiate omphalocele from gastroschisis. We must also think of other
diagnoses such as umbilical hernias or umbilical cord anomalies.
Treatment
The therapy is similar to that of gastroschisis, i.e. closure of the defect primarily or in several steps
with the help of a so-called silo.
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GASTROINTESTINAL CONGENITAL DEFECTS (41)
Marek Ondřej, Plánka Ladislav
Definition of the term
Congenital malformations of the digestive tract include many separate diseases. Atresia and
stenosis of the different parts of the GIT are most commonly encountered. These include atresia of the
esophagus, duodenum and other parts of the small intestine. Another separate unit is anorectal
malformations. Other congenital anomalies of the digestive tract include pylorostenosis, duplications
of individual parts of the GIT. Malrotations - a failure of the physiological rotation of the small and
large intestine, which includes nonrotation, compression of the duodenum, congenital volvulus of the
small intestine, Ladd's syndrome and internal hernias are also included in this group. The last important
congenital anomaly of the digestive tract is intestinal aganglionosis - Hirschsprung's disease.
Atresia of the oesophagus
Definition of the term
It is the most common congenital malformation of the esophagus. It is a failure of a
differentiation during embryonic development. It occurs in approximately 1:5000 live births. We most
commonly use the Vogt or Gross classification to classify this disease. We encounter 85% of
esophageal atresia with lower tracheoesophageal fistula (Vogt IIIb). The second most common in
about 10% is isolated esophageal atresia without fistula (Vogt II). Recently, prenatal diagnosis has
advanced and most esophageal atresia is detected during prenatal ultrasound screening.
Associated congenital anomalies, including congenital heart defects, urogenital, skeletal and
other gastrointestinal defects, may also be seen. When multiple anomalies occur together, we refer to
VATER or VACTERL syndrome.
Clinical manifestation
Newborn infants do not tolerate the first dose of milk. Patients have increased salivation,
coughing, tachypnea and desaturation can be observed. There is a risk of developing aspiration
pneumonia in case of fistulas.
Prenatal screening reveals most esophageal atresia. After birth, the nasogastric probe
encounters resistance or rolls back. In the most common atresia with lower tracheoesophageal fistula,
a coiled probe in the oral esophageal stump and gas in the aboral parts of the GIT can be seen on plain
chest and abdominal X-ray. In atresia without fistula, no gas is seen in other parts of the GIT. Only in
case of diagnostic doubt, it is possible to use 0.5 ml of aqueous contrast fluid injected into the
nasogastric probe and the X-ray reveals the diagnosis definitively.
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Complications
The most common surgical complications include stricture at the anastomosis. And repeated
endoscopic dilatations are necessary. We can also observe dehiscence of the anastomosis or recurrent
tracheoesophageal fistula.
Prognosis
If it is an isolated anomaly, the prognosis depends on the type of atresia, the birth weight of the
child and the distance between the esophageal stumps. With low birth weight and greater distance
between stumps, the risk of anastomotic stricture and recurrent dilatation is greater. Patients are also
more likely to experience dyskinetic movements of the esophagus and more likely to suffer from
respiratory tract infections.
Differential diagnosis
Esophageal stenosis, esophageal diverticulum, esophageal duplication,
laryngotracheoesophageal cleft.
Treatment
Treatment is exclusively surgical. In the most common type of atresia with lower
tracheoesophageal fistula, an end-to-end anastomosis from the right-sided posterolateral thoracotomy
or thoracoscopic approach is usually performed within 24-48 hours after birth. In long-distance atresia
or without fistula, ligation of the tracheoesophageal fistula and creation of a nutritive gastrostomy is
appropriate, and esophageal continuity is restored postponed. Most often, this involves replacement of
the esophagus with the stomach. Increasingly, especially in long-gap or atresia without fistula, a
thoracoscopic approach and gradual closure of both esophageal stumps using sliding knots is being
used.
Atresia and stenosis of the duodenum
Definition of the term
A congenital disorder of patency in the duodenum that manifests early after birth as a sudden
obstruction of the digestive tract. It is probably on the basis of incorrect vacuolization and
recanalization of the GIT during embryonic development. Three types of duodenal atresia are
encountered. Intraluminal mucosal membrane, two blind ends of the duodenum connected by a
ligamentous strand or two blind ends of the duodenum that are not connected and there is a "V" shaped
defect in the mesentery. Stenosis of the duodenum is most often caused by external compression.
Clinical manifestation
Vomiting in the first few hours after birth, most often with admixture of gall, because the
obstruction is more often placed infrapapillary.
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In later diagnosis and repeated vomiting, are observed signs of dehydration and hypochloremic
alkalosis. The diagnosis begins by plain abdominal X-ray or laterogram. Two bubbles (double bubbles)
are typical. Possible stenosis is differentiated by administration of a contrast fluid.
Complications
They occur in the form of dehiscence of the anastomosis or injury to the papilla.
Duodenogastric reflux and other complications may manifest themselves later. Other complications
may be associated with associated anomalies.
Differential diagnosis
Other types of atresia or stenosis in the GIT area, malrotation.
Treatment
Insertion of nasogastric probe and adjustment of the internal environment. Subsequently,
reconstruction of GIT continuity, most commonly duodenoduodenal anastomosis from a transverse
laparotomy in the right epigastrium. The membrane can be excised from the duodenotomy, but only if
it is possible to locate the Vater's papilla quite safely.
Small intestine atresia
Definition of the term
Atresia of the small intestine occurs in 1:5000 newborns. Most often they result from
intrauterine ischemia or after trauma (twisting, torsion...) and it is classified according to Grosfeld into
types 1-4, see. Fig. 1.
Clinical manifestation
After birth, occurs persistent vomiting with a gall admixture and abdominal distention. In
developed vomiting, signs of dehydration and hypochloremic alkalosis appear. A plain abdominal
photograph shows widely dilated levels of small intestines.
Complications
Postoperative ileus, stricture or dehiscence of the anastomosis.
Prognosis
Generally good for isolated defects, for complex defects it depends on the most severe defect.
Differential diagnosis
Ladd's syndrome, Hirschsprung's disease, congenital volvulus of the small intestine, meconium
ileus.
Treatment
Insertion of nasogastric probe, adjustment of internal environment. Reconstruction of
continuity by intestinal anastomosis, usually with the necessity of modelling (tapering) of the oral and
aboral part of the intestine.
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Anorectal malformations
Definition of the term
It is a congenital disease of the rectum and anus resulting in the absence of an external anal
opening and anomalous placement of the anorectum on the perineum or into the lower urinary or
genital tract. The incidence is 1:5000 live births. Several classifications are encountered.
Malformations can be divided into low, medium and high, according to the location of the atretic
stump. In boys, perineal, rectourethral, rectoprostatic and rectovesical fistulae are distinguished; in
girls, perineal, vestibular or vaginal fistulae.
Clinical manifestation
Depending on the type of malformation, stool may not pass after birth. A detailed clinical
examination of the external genital area and perineum is necessary. In atresia where stool cannot be
derived, we will add an X-ray and ultrasound examination to reveal the type of malformation. We can
use MRI to assess the pelvic conditions.
Complications
Various types of incontinence, obstipation, wound dehiscence and ileus may occur with
colostomy.
Prognosis
The incontinence depends on the type of anorectal malformation and associated defects.
Treatment
In atresia without the possibility of stool derivation, sigmoidostomy is necessary. Subsequently,
around six months of age, the patient undergoes laparoscopically assisted or conventional
posterosagittal anorectoplasty. Subsequently, a colostomy is closed after approximately 2 months. In
patients with a fistula where stool derivation is possible, we can perform the reconstructive surgery
directly, without a temporary colostomy, usually around three months of age.
Malrotation
A congenital abnormality of the physiological rotation of the small and large intestine, which
may manifest as a sudden abdominal accident or ileus.
Nonrotation is the arrest of physiological rotation after the first phase. The entire small intestine
is located in the right half of the abdominal cavity and the large intestine in the left half. This defect
may not manifest clinically and may be an incidental finding during abdominal surgery.
Ladd's syndrome is a combination of congenital volvulus with compression of the duodenum
by an underrotated cecum. It manifests clinically as an ileus. Treatment is surgical and often urgent
because of possible ischemia of the small intestinal in the case of volvulus. Derotation of the bowel
and dissection of the peritoneal strips leading from the cecum to the posterior abdominal wall in the
235
region of the liver and gallbladder are performed, and duodenal release is also performed. The
duodenum is placed vertically, to the right of the spine, and the bowel are placed in a nonrotational
position. The small intestine in the right half of the abdominal cavity and the large intestine on the left.
Fig. 1: Classification of small intestine atresia according to Grosfeld
ŠNAJDAUF, Jiří a ŠKÁBA, Richard. Dětská chirurgie. Praha: Galén, c2005. ISBN 80-7262-329-x.
236
HIRSCHSPRUNG'S DISEASE (44)
Turek Jakub, Tůma Jiří
Definition
Hirschsprung disease (HD) is a congenital intestinal aganglionosis in which ganglion cells of the
myenteric Auerbach's and submucosal Meissner's plexus are absent. It always affects terminal rectum,
i.e. from the linea dentata of the anal canal and extends proximally. The incidence of the disease is
1:5000 - 10,000 live births. Depending on the length of the affected segment of the intestine, several
forms are distinguished: the ultra-short form (1-3 cm long aganglionic segment), the classical rectosigmoideal
form (rectum and distal part of the colon sigmoideum), the long form (up tp ½ colon
transversum), aganglionosis of the whole colon or even the extensive aganglionosis of the NTBA type
(nearly total bowel aganglionosis).
Aetiology
The aetiology is not fully understood. 70% of the disease occurs as an isolated disorder without any
associated syndromes. Familial occurrence is 8-20% and in approximately 12% the disease is
associated with chromosomal abnormalities, mainly trisomy of 21. chromosome. To date, several
genes regulating neural tube and nerve cell development have been discovered, the most important of
which is the RET proto-oncogene.
Pathogenesis
In HD, there is the failure of migration of neuroblasts from the neural crest or in the mis-differentiation
of neuroblasts into ganglion cells leading to their accelerated apoptosis. The migration of neuroblasts
occurs in a craniocaudal direction, which explains the different types of disease according to the length
of the affected segment. The earlier the failure of migration occurs, the longer the segment of the
intestine remains without intervention.
Clinical manifestation
The clinical picture is based on the nature of the disease, where the affected segment is permanently
spastic, impossible to relax and pass stool. It acts as a functional barrier that can only be overcome by
increased effort of the oral segment of the bowel, which gradually hypertrophies, and a megacolon can
develop. The clinical picture depends on the age of the child and the length of the affected section. In
the most common, the rectosigmoid form, the symptoms occur early after birth – late passage of
meconium or the meconium does not leave in proper portions, the child is nauseous or vomits, the
abdomen is markedly distended, and there are extensive peristaltic movement of bowel. Massive
amounts of stool and gas are passed after insertion of a rectal tube or rectal thermometer. Eating
disorders, chronic anaemia or intermittent vomiting are typical for older children.
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Paraclinical findings
- Imaging methods
The primary imaging modality is a contrast study - irrigographic examination. The image of the classic
form is typically a narrowed rectum funnelling into a dilated colon sigmoideum.
- Histological diagnosis
Biopsy may be performed as a full-thickness biopsy of the rectal wall, or biopsy of mucosa and
submucosa as part of a colonoscopy examination, or by the method of suction biopsy. In the latter 2
cases, immunohistochemistry for AChE reaction (elevated levels in the absence of positive findings)
or detection of calretinin (negative findings in the absence of an aganglionic segment) is used.
- Rectal manometry
This examination monitors the rectosphincteric inhibitory reflex, the presence of which rules out
Hirschsprung's disease, whereas its absence does not confirm the diagnosis.
Course
In patients with suspected Hirschsprung's disease, surgical resection of the affected segment of bowel
is the definitive method of treatment. On per rectum examination, gentle sphincter divulgence can
temporarily improve symptoms but does not eliminate them. When patients are decompensated, they
may even develop an ileus.
Complications
Complications are mainly related to enormous dilatation of the intestines, which can lead to ileus or
HAEC (Hirschsprung's associated enterocolitis) with subsequent sepsis and shock. Other
complications related to the surgical procedure include rectal stricture, dehiscence of the anastomosis,
chronic constipation or, conversely, faecal incontinence in the long term follow up.
Prognosis
It is mainly determined by the length of the affected segment and the correct performance of the
surgery. However, the long-term functional results are favourable and more than 50% of patients are
completely free of difficulties.
Differential diagnosis
In the differential diagnosis, we must exclude other forms of neonatal intestinal obstruction, namely
Ladd bands, meconium ileus, meconium plug syndrome, congenital intestinal hypoganglionosis and
isolated intestinal neuronal dysplasia type B.
Therapy
Definitive therapy is surgery to remove the affected segment into the healthy tissue, remove the
sphincteroachlasia of the internal sphincter by partial resection and suture the colon anastomosis. The
most common techniques used are the techniques according to Swenson, Duhamel or Soave. The
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surgery can be performed transrectally in certain circumstances, but often the bowel needs to be
released in the abdominal cavity by laparotomy or laparoscopic approach.
Prevention
As this is a congenital disease, prevention of the disease is difficult to achieve.
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PYLORIC STENOSIS, INTUSSUSCEPTION (43)
Marek Ondřej, Plánka Ladislav
Pylorostenosis
Definition of the term
Hypetrophy of the pyloric channel usually in newborns and infants most commonly between
4 and 6 weeks of age. It is the most common cause of vomiting in neonatal and early infancy.
Etiology and pathogenesis
The exact etiology is not yet clarified. One theory postulates that increased acidity of gastric
juices leads to muscle spasm and thus muscle hypertrophy. A protective effect of breast milk is
assumed. Pylorostenosis may be congenital or acquired. It occurs in about 1:5000 births and affects
boys about four times more often. The muscle of the pylorus is thickened, edematous - the muscle
fibers are hypertrophied.
Clinical manifestation
Milder vomiting may occur as early as around the 2nd week of life, but characteristic is bow
vomiting of engorged milk without gall admixture between the 4th and 6th week of life. Vomiting
occurs shortly after eating. Patients stop gaining weight and may show signs of dehydration.
Sometimes a "pyloric tumor" can be palpated right below the rib arch.
In laboratory tests, hypochloremic alkalosis and hypokalemia are typical.
Of the imaging modalities, the first priority is the abdominal ultrasound, where the radiologist
assesses the width and length of the muscle of the pyloric channel. We speak of mature
pylorostenosis when the length of the pyloric canal muscle exceeds 17 mm and the width exceeds 4
mm. Another option is examination with a contrast fluid under X-rays.
Course
The patient typically develops recurrent bow vomiting between 4 and 6 weeks of life and
stops gaining weight. On ultrasound examination, pylorostenosis is confirmed. The patient is
admitted to the intensive care unit, the internal environment is modified with infusion therapy before
surgery, and a nasogastric probe is inserted for recurrent vomiting. Surgical treatment is followed by
laparotomy or laparoscopic pyloromyotomy. In 12 hours after surgery, if uncomplicated, gradual oral
intake is started.
Complications
The most common complication of surgical treatment is injury to the pyloric mucosa, which
is treated with a suture and pyloromyotomy at another location in the pylorus. Another complication
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is inadequate pyloromyotomy, which manifests as continued vomiting with another surgery and a
new pyloromyotomy out of the original scar.
Prognosis
The prognosis is good; recurrence or complications are rare.
Differential diagnosis
Overfeeding of the child, gastroesophageal reflux, or other obstructions in the aboral parts of
the gastrointestinal tract.
Treatment
Definitive treatment is surgical. Before the procedure, it is necessary to stabilize the patient,
infusion therapy, adjustment of the internal environment and, in case of repeated vomiting, insertion
of a nasogastric probe. Surgical treatment is longitudinal pyloromyotomy of the pyloric hypertrophic
muscle. The procedure can be performed by laparotomy or laparoscopically. With sufficient
pyloromyotomy, the gastric mucosa is interposed between the muscle fibers along the entire length
of the pylorus.
Prevention
Prevention of this disease is not yet known. A protective effect of breast milk is assumed.
Intussusception (Invagination)
Definition of the term
Intussusception is the telescopic insertion of the oral part of the intestine into the aboral part
following the direction of peristalsis. It is a combination of mechanical ileus by invagination with
strangulation of the vessels of the retracted mesentery. Most commonly encountered is ileocolic
intussusception, less frequently with small or large bowel (ileoileal or colocolic) intussusception.
Etiology
Intussusception is typical in children under three years of age. The exact etiology is often
unknown, so we speak of idiopathic intussusception. Among the causes of Intussusception we can
include the intensification of peristalsis or the multiplication of mesenteric lymph nodes. In older
children, the cause is the leading point - Meckel's diverticulum, polyp and others.
Pathogenesis
Retracted bowel - invaginate causes obstruction and retracted mesentery causes impaired
blood outflow, venostasis and subsequent swelling of the bowel. In case of late diagnosis, ischemia
and necrosis of the bowel may occur due to hypoperfusion.
Clinical manifestation
241
Intussusception is characterised by severe colicky pain at intervals. In between the pains,
children are usually free of difficulties. With prolonged duration, vomiting also occurs, initially
reflex, then more from a developed ileus. Another sign is "raspberry jelly" - hemorrhagic mucus with
venostatic edema of the intestinal wall, which we detect on per rectum examination.
Laboratory tests may be unremarkable. When vomiting develops, hypochloremic alkalosis
and hypokalemia are encountered. Of the imaging tests, the method of choice is abdominal
ultrasound with a target image. On X-ray, we observe an ileus. Another option is irrigography, which
is also a conservative treatment.
Course
Typically, the patient is between the sixth week to the second year of age with a picture of
severe colicky pain. Ultrasound examination reveals ileocolic invagination. The patient undergoes
hydrostatic desinvagination under general anaesthesia under ultrasound control. If it fails or if there
are repeated episodes of recurrence, treatment is surgical.
Complications
With late diagnosis, ischemia and necrosis of the intestinal wall may occur. Invaginations
may recur during a single hospitalization or with intervals.
Prognosis
The prognosis for idiopathic and early diagnosed invaginations is good, they may only recur
usually within 10%. For invaginations with a leading point, the prognosis depends on the point itself.
In late-diagnosed invaginations, ischemia and perforation of the intestine with all its consequences
may occur.
Differential diagnosis
Enterocolitis.
Treatment
In stable children, hydrostatic desinvagination under general anesthesia and under ultrasound
control is the treatment of choice. In children with a developed ileus, stabilization, insertion of a
nasogastric probe, adjustment of the internal environment and infusion therapy are in place first.
Hydrostatic desinvagination is retrograde filling of the colon with a contrast fluid up to 100 cm of
water column. In addition to ultrasound, skiagraphy can be used for control. If hydrostatic
desinvagination fails, surgery is indicated.
Prevention
There is no prevention in this disease.
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NECROTIZING ENTEROKOLITIS IN CHILDREN (40)
Bibrová Štěpánka, Starý David
Definition: Necrotizing enterocolitis is one of the most common and serious abdominal episodes in
children of neonatal age. It is a life-threatening disease, affecting 5-12% of preterm newborns with
very low birth weight (below 1,500 g). It usually manifests in the 2nd -3rd week of life, worldwide it
occurs in 0.3-2.4/1,000 live births, 70% of witch are babies born before 36 week gestation.
Aetiology: It is an inflammatory disease and at the same time an ischemic disability or necrosis of
the intestinal wall cells which are caused by the penetration of bacteria into the wall of the affected
part of the digestive tract. In the most severe cases even perforation of the intestinal wall, leakage of
intestinal contents into the abdominal cavity and secondary peritonitis may occur. Especially in
premature babies, immaturity of the digestive tract wall, including the immune system, plays a role.
In term infants, it often occurs in the first days of life and a history of hypoxic episode is often given.
The most commonly affected compartment is the terminal ileum and caecum but NEC can arise in
any part of the gastrointestinal tract.
Pathogenesis: NEC arises on a multifactorial basis, when various noxes affected the immature
gastrointestinal tract. Inadequate production of gastric acid and digestive enzymes prevents
elimination of ingested pathogens and antigens, insufficient mucus production may lead to increased
microbial adherence, and slower peristalsis makes it easier for bacteria to penetrate the intestinal
wall.
The primary risks are low birth weight, low gestational age, artificial pulmonary ventilation and
artificial nutrition (especially with high osmolality), chorioamnionitis. Other risk factors include
intestinal immaturity, genetic predisposition, abnormal and delayed microbial colonization (e.g. after
administration of broad-spectrum antibiotics, delayed enteral and artificial nutrition), abnormal
changes in microvascularization during the transition to ex utero life (e.g. Perinatal asphyxia in nonprogressive
or premature labour). Maternal prenatal and perinatal risks include pre-eclampsia,
premature amniotic fluid outflow, placental abruption, drug exposure (e.g. Indomethacin,
corticosteroids), abuse (e.g. cocaine). Other risk factors include congenital and acquired
abnormalities of the cardiopulmonary system (e.g. RDS, shock, hypotension, congenital hear disease,
patent dictus arteriosus).
Clinical manifestation: Signs and symptoms of NEC are often nonspecific, variable and
inconspicuous. Gastrointestinal symptoms include pain, abdominal distension, inappetence, transient
food intolerance, delayed gastric emptying, nausea and vomiting, occult or even major bleeding in
stools, change in stool pattern, diarrhoea. With the development of the disease, there is also a general
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reaction of the organism, the development of sepsis and shock. Systemic symptoms include lethargy,
respiratory failure, thermal instability, circulatory failure, cyanosis, unconsciousness and ultimately
multiorgan failure.
Based on the clinical findings and imaging results, there are 3 grades of NEC (Bell´s criteria
modified by Kliemann) – see the table below.
Physical examination of the abdomen shows abdominal distention, intestinal villi are visible through
the skin, sometimes the abdominal wall is red coloured. Abdomen is painful on palpation, there may
be palpable resistance. Bowel sounds may be weakened.
Laboratory tests tend to diagnose acidosis (metabolic or respiratory), hyperglycaemia, neutropenia,
thrombocytopenia, also DIC or positive haemoculture may be detected.
Among imagine methods, X-ray and ultrasound examinations are used to diagnose NEC. The
specific symptom on a plain abdominal radiograph is the finding of pneumatosis intestini (gas seen
in the intestinal wall), a subileous or ileous state. Also a specific, adverse sign is the appearance of
gas in the portal tract. Pneumoperitoneum is indicative of intestinal perforation. Gas in the portal
tract can also be diagnosed by ultrasound examination.
Course: The course may be mild to peracute.
Therapy: Primary care is to ensure patient´s vital function, provide venous access, resuscitation
therapy if necessary, fluid resuscitation in hypotension, endotracheal intubation and mechanical
ventilation in respiratory failure.
When NEC is suspected and in mild forms, conservative therapy is indicated. In the first place,
enteral nutrition must be discontinued, nasogastric tube should be inserted (to decompress the dilated
bowel), broad-spectrum antibiotics are administered intravenously, usually in two or three
combinations according to the patient´s general condition. Adequate paternal nutrition is essential. If
conservative therapy is successful, enteral nutrition can be continued after resolution of infectious
symptoms. In case of failure conservative therapy, deterioration of the intestine, surgical therapy is
indicated. The aim of laparotomy is revision of the abdominal cavity, resection of the perforated or
clearly necrotic part of the affected bowel and stitching of the stoma. Primary anastomosis is not
recommended because of the high risks of ischemia at the anastomosis site and subsequent
complications. When resecting the bowel, we try to take the gentlest approach and preserve as much
of the bowel as possible.
In critically ill, unstable patients with pancolitis, laparotomy may be contraindicated. In these
patients with proven bowel perforation or pneumoperitoneum, only peritoneal drainage is
recommended, followed by laparotomy after stabilization of the condition.
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Complications: Surgical therapy and the need to remove large parts of the affected bowel can lead to
short bowel syndrome. Resections can lead to gastrointestinal dysmotility, bacterial overgrowth,
digestive enzyme deficiency, gastric acid hypersecretion, overgrowth of intestinal bacteria and their
translocation into the bloodstream, which can cause sepsis. Patients with NEC are at high risk of
failure to thrive, fistulas, strictures and adhesions. In addition to gastrointestinal difficulties, there is a
risk of delayed psychomotor development and cognitive changes are observed.
Differential diagnosis: If the differential diagnosis i tis necessary to exclude other congenital
developmental defects of the digestive tract (e.g. malrotation, intestinal volvulus, atresia). In
raticular, gastroenteritis, meningitis, urinary tract infection or sepsis of other aetiology should be
excluded from infectious causes.
Prognosis: A 10-50% mortality rate is generally reported, which depends on the timeliness of
diagnosis and therapy of NEC. In fulminant course the prognosis is very negative.
Prevention: Multidisciplinary collaboration is important for early diagnosis and treatment of NEC to
minimalize complications. Early administration of colostrum and natura breast milk, which contain
high levels of immune mediators that contribute to bacterial and anti-inflammatory protection of the
gut wall, is a preventive factor for NEC. The growth factors contained in colostrum stimulate the
development of the digestive tract. The administration of probiotics also helps to regulate the
pro.inflammatory response.
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Classification of NEC (Bell´s criteria modif. Kliemann)
Grade General signs Abdominal signs X-ray signs
I. grade –
Suspicious
NEC
A
temperature instability,
lethargy, bradycardia,
apnoe
gastric residue, vomiting,
abdominal distension,
occulte bleeding
normal findings or
mild dilatation of
intestinal villi, ileus
B as IA
IA + macroscopic bleeding
in stool
as IA
II. grade -
Cinfirmed
NEC
A as IA
inaudible intestinal
peristalsis ± palpation
sensitivity
as IA
B
as IIA +
trombocythopenia and
mild metabolic acidosis
clear palpatory sensitivity
± redness, abdominal skin
phlegmona ± palpable
resistence in the right lower
quadrant
gas in v. portae ±
ascites
III. grade -
Developed
NEC
A
respiratory failure,
hypotension,
bradycardia,
combinated respratory
and metabolic acidosis,
DIC, neutropenia
diffuse peritonitis,
abdominal distension,
marked panifulness
clear ascites
B as IIIA as IIIA pneumopertoneum
Table 1 – Clasiffication of NEC
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UNDESCENDED TESTICLES, PHIMOSIS, PARAPHIMOSIS (38)
Bibrová Štěpánka
Undescended testicle
Definition: Undescended, retined testicle is one of the most common congenital defects of the male
external genitalia and crytorchism. I tis divided into abdominal and inquinal retention according to
the level of fit, and may occur unilaterally or bilaterally. I tis more often diagnosed in premature
infrants or is part of another disability (e.g. Klinefelter´s syndome).
Etiology and pathogenesis: Embryonic gonadal development begins with the indiferent stage,
followed by the stage of differentiation of the base into the testis or ovary. The initially high-based
gonád descends into the genital mounds. At the beginning of the 4th intrauterine month, i tis located
at the entrance to the canalis inquinalis, where it remains until the 7th month and i tis usually
abbreviated at the end of the 8th to 9th month of intrauterine development. Mechanical influences,
hormonal action of androgens anf progressive histological changes in the testis gubernaculum are
involved in the descent of the testis. Due to a transient increase in hormonal levels after birth (usually
by the 3rd month), testicular descent may continue after birth.
Clinical manifestation and course: Diagnosis is based on anamnestic data and careful physical
examination by palpation. The patient is examined supine and in the Turkish sitting position (a
decrease in the cremaster reflex can distinguish a retractile testis from a non-descended testis).
Sometimes other sings of insufficient masculanisation may by present (e.g. hypospadias,
micropenis). Among paraclinical methods, ultrasound examination can sometimes help in diagnosis.
In the case of abdominal retention, laparoskopy is also used for dagnosis. The presence of functional
Leydig cells can be demonstrated by the hCG stimulation test in the presence og bilateral
nonpalpable testis.
Therapy: Treatment is mainly surgical – orchidopexy, fixation of the testicle in the scrotum. The goal
is to correctly position the testicle in the scrotum until the child is 1-1,5 years old. The inquinal
appoach is used for the palpable testicle during the inquinal canal, for the nonpalpable testicle a
diagnostic laparoskopy is performed. Abdominal retention is usually treated with a two-stage
operation. In the first time, the internal testicular vessels are interrupted laparoscopically, the testi sis
inserted into the internal anulum of the inquinal canal and in the second time (usually after about 2
months) an orchidopexy is performed. In case of finding of hypotrophic or atrophied testis,
orchiectomy is indicated. Hormone therapy, fromerly widely used, is nowadays hardly used
anymore, but may have a positive effect on future fertility.
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Complications: After surgical therapy, testicular atrophy, torsion of the spermatic funikulus (e.g.
scarring, insufficient relaxation) may occur, and fertility may be impaired if the fallopian tube is
injuried. In the case of untreated crytorchidism, there is an incerased risk of developing a mailgnant
testucular tumor, a seminoma (especially after puberty).
Prognosis: In case of orchidopexy, the risk of malignancy of testicular tissue is reduced. In case of
orchiectomies, testicular protheses can be implanted into the scrotum after puberty.
Differential diagnosis: Differentiation from other causes of cryptorchidism – ectopic testis, anorchia
(testicular atrophy or agenesis), acquired cryptorchidism after inquinal surgery (e.g. hernioplasty,
hydrocele surgery). Furthermore, i tis necessary to distinguish a retractable (bouncing) testis (by the
action of increased cremaster reflex, a transient withdrawal of the testis into the inquinal canal).
Bilateral retention may be part of a metabolic disease (e.g. congenital hypopituirtarism, CAH).
Prevention: Early detection and therapy by careful clinical examination of newborns and infants as
part of preventive pediatric checkups.
Phimosis
Definition: Inability to pull the foreskin of the penis over the glans penis. It is a disproportion
between the circumference of the foreskin of the penis and the glans.
Etiology: 2 form occur – primary, naurally in most newborn boys, and secondary due to scar tissue
formation (e.g. in systemic disease, postinflammatory, forced pulling).
Pathogenesis: At birth, the foreskin is assiciated with the glans penis, encircling it. By multifactorial
action (gradual detachment of the epithelial layers of the inner leaf and glans, formation of the
smegma, nocturnal erection), the adhesions gradually relax spontaneously and the circumference of
the foreskin expands. Secondary phimosis is induced by the pathological action of inflammatory
processes, microtrauma and trauma to the fereskin and external genitalia.
Clinical manifestation: A careful, gentle physical examination of the patient is important. We detect
the presence of coglutination, between the inner leaf of the feroeskin and the glans penis, elasticity of
the foreskin orifice and formation of ragades. Durin urination, transient expansion of the foreskin sac
may occur. In secondary phimosis, we observe rigid collagenous ligaments that prevent overstreting
of the foreskin. A history of recurrent balanoposthitis may be found.
Therapy: In asymptomatic cases, observation only and natural development in monitored. In
symptomatic patients (e.g. pain, recurrent balanoposthitis), treatment – conservative or surgical – is
necessary. The aim of the conservative pharmacological therapy is to achieve relaxation of the
constricted part of the foreskin, corticosteroids are applied locally for 6-8 weeks. Conglutination of
the foreskin is mechanically released on an outpatient department, under local anaesthesia.
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Surgery is performed by partial resection of the foreskin (removal of only the stenotic part of the
foreskin and its plastics) or complete circumscission. Cpmplete circumscission is contraindicated in
conditions where the foreskin can be used for reconstructive procedures (e.g. disorders of sex
development, hypospadias, epispadias, recessed penis).
Complications: The most common complcation of phimosis is recurrent balanitis, difficulty
urinating. Infectious complcations may occur after cirrcumcision, scarring with poor cosmetic
outcome, skin bridges, urethral stenosis. More serious postoperative complications include
hemorrhage, injury to the glans, necrosis of the penis, and formation of ureterocutaneous fistulas.
Prognosis: Depends on the duration, development of ischemic changes. In most cases, i tis good. In
caase of repeated failure of conservative therapy or rcurence of phimosis within 2-6 months after its
completion, surgicle treatment is the method of choice. Complete circumcision is necessary in
balanitis xerotica obliterans.
Differential diagnosis: We must distinguish paraphimosis, hypospadias, epispadias, balanitis from
phimosis.
Prevention: Observance of meticulous hygiene, non-voilent retraction, early detection and therapy of
balanitis.
Paraphimosis
Definition: This is an acute affection of the penis, the foreskin is overstretched beyond the edge of
the glans penis and cannot be repaired back.
Etiology: Paraphimosis can occur after prolonged overstretching of the foreskin (especially at the
tighter orifices), when irritation of the foreskin (e.g. inflammation, intercourse, allergic reaction)
causes swlling and repositioning cannot be performed.
Pathogenesis: The overstretched outh of the foreskin behind the edge of the glans acts as a
stragulating ring, restricting lymphatic and venous drainage from the foreskin and glans penis. The
condition may progress to massive swelling, ischemia of the affected tissues (including the gland and
glandular urethra) and development of necrosis of the foreskin and penile skin.
Clinical manifestation and course: Massive, circular swelling of the foreskin, in stages, venostasis,
discoloration of the penile foreskin and gland and superficial skin defects may occur.
Therapy: In paraphimosis, manual compression of the foreskin and glans penis and repositioning of
the foreskin back as early as possible is neccessary. In case of impossibility of manual reposition,
early surgical therapy is performed – dorsal dissection of the strangilating ring of the foreskin
followed by complete circumscission at a second time.
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Complications: postischemic changes of the glans penis with the appearance of deformities, necrosis
of the penile skin, urethral stricrures.
Prognosis: Mostly good.
Differential diagnosis: It is necessary to distinguish balanitis, phimosis in particular.
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PEDIATRIC UROLOGY (45)
Husár Matej
Almost 30% of all birth defects in boys are urological diagnoses. Some diseases can be detected
prenatally by ultrasound, such as the more severe obstructive and reflux nephropathies, megavesica
and bladder exstrophy. Postnatally, external genital examination is performed as a part of neonatal
screening to detect congenital adrenal hyperplasia (CAH) in children, and testicular descensus in
boys and exclusion of hypospadias. If CAH is found, or bilateral non-palpable testes with
hypospadias, endocrinological and genetic testing should be added. Endocrinological examination in
boys is best to be performed during the minipuberty period (around the 2nd-3rd month after birth)
due to activation of the hypothalamic-pituitary-gonadal pathways. For more details on congenital
defects in terms of obstructive uropathy and cryptorchidism, see the next questions.
Infancy and toddlerhood
In this age, febrile urinary tract inflammations of the character of pyelonephritis are quite common.
According to the guidelines, it is currently recommended to perform micturating cystourethrography
to diagnose vesicoureteral reflux (VUR) after the first attack. A child with VUR should be provided
with a prophylactic dose of ATB to prevent another attack of pyelonephritis. Surgical management
of VUR is performed at an older age, taking into account the degree of VUR, recurrence of
inflammation and the clinical condition of the child. It is possible to perform minimally invasive
submucosal antireflux injection into the ureteral orifice or to perform ureteral reimplantation. Severe
obstructive uropathy resulting in hydronephrosis or megaureters is solved by acute urinary diversion
- puncture nephrostomy or puncture epicystostomy, and the actual surgical solution is indicated after
stabilization of the patient and according to the evolution of the severity of the obstruction.
In infancy and toddlerhood, correction of cleft defects of the external genitalia is performed, and at
the end of the first year of life, cryptorchidism begins to be solved.
At this age, we must think about metabolic defects that can result in the formation of urolithiasis.
The most common metabolic defect with concrement formation is cystinuria.
Preschool and school age
The most critical period for the development of Wilms tumour (nephroblastoma of the kidney) is the
4th-10th year of life. Most often a palpable bulky mass extruding into the abdominal wall is found.
Current oncologic treatment protocol is: neoadjuvant chemotherapy, nephrectomy, followed by
chemotherapy/radiotherapy. In addition to renal tumours, testicular and paratesticular tumours
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(sarcomas) and bladder tumours are also found. For testicular and paratesticular tumors, a safe high
orchiectomy from the inguinal approach is performed. For bladder tumours, a biopsy is performed
first to typify the tumour and then surgical intervention.
Urinary tract infections in pre-school and school age are mainly suffered by girls, they are often
associated with inadequate or improper hygiene, lower urinary tract dysfunction (most often
overactive bladder) and also due to urethral stenosis or persistent synechiae of labia minora. Also,
one already needs to think about sexually transmitted infections.
In boys, phimosis, whether physiological or due to inflammation of the foreskin or due to lichen
planus (balanitis xerotica obliterans), is often addressed.
After the 5th year of life, bedwetting begins to be addressed in children. Clean bedwetting, without
daytime micturition problems, can be significantly improved by regimen measures - no drinking in
the evening, proper urination, or waking up at night and urinating. If there is no effect, it can be
helped by putting on an adiuretine hormone.
At the age when children are already beginning to develop sports activities, trauma occurs. The most
common are blunt impacts to the lumbar region with injury to the kidneys, or injuries to the external
genital area associated with urethral injury. Most renal trauma is treated conservatively (strict bed
rest, haemodynamic therapy, antibiotics), only when urinary extravasation and haemodynamically
unstable bleeding could require surgical intervention. Urethral injuries are also treated
conservatively, only in case of complete urethral rupture urethroplasty is needed or late
complications in terms of post-traumatic ruptures need to be solved.
A final note for this age is urolithiasis, which is most often associated with low diuresis on the basis
of low fluid intake (oxalate stones). Exceptionally, there is a metabolic basis for lithiasis or the
formation of stones due to repeated infections (struvite stones).
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PEDIATRIC TUMORS (39)
Doušek Robert, Tůma Jiří
Childhood tumours are a very heterogeneous group of diseases. Children with cancer show
significant differences from adult patients - they have different tumour types with different biological
behaviour, they are treated differently, they respond differently to treatment, they process
experiences differently psychologically. The most common childhood tumours are of haematogenous
origin, followed by tumours of central nervous origin, neuroblastoma, sarcomas, nephroblastoma and
germ cell tumours.
The general paediatric surgeon treats paediatric patients mainly with tumours of the thoracic and
abdominal cavities and some limb tumours. Patients with tumours in other locations are operated on
by a neurosurgeon, orthopaedic surgeon, otorhinolaryngologist, urologist, gynaecologist and others.
Approximately one hundred years ago, surgery was the only treatment option for pediatric tumors;
today, surgery is part of multimodal cancer therapy. This text deals mainly with the surgical aspects
of the care of pediatric cancer patients.
The surgeon (as well as the physician of other specialties) can play an important role in the early
detection of childhood cancer. The tumor typically manifests nonspecifically, either by a solitary
symptom or a combination of symptoms. The most common symptoms include tactile resistance,
pain, stagnation or weight loss, behavioural changes, fatigue, dry cough, changes in movement
patterns, vomiting, and defecation disorders.
The clue to suspecting a correct diagnosis should be a correct reflection of the observation that
symptoms attributed to a more trivial disease do not disappear after the usual period of treatment or
recur.
Various imaging and laboratory tests are used in the diagnostic process. Key investigations
(histology, molecular biology) leading to an accurate diagnosis usually require a sample of tumour
tissue. Properly performed biopsy has its own rules - selection of the collection site with the least
traumatization of the patient, sufficient sample size - typically 1 cm3
, collection of vital tumor tissue
instead of necrosis, gentle handling of the sample to prevent its destruction, prevention of
contamination of surrounding tissues, careful hemostasis and suture, delivery of the sample without
fixation, correct labeling and, if necessary, orientation of the sample. In some situations, it may be
appropriate to request a frozen section biopsy.
At important junctions in the cancer patient's journey, a panel of experts from different specialties
(the oncology committee) meets, evaluates what has been learned so far and proposes a course of
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action. The surgeon has the opportunity to request further necessary examinations, specify the risk
level of the considered surgical solution, etc.
The main benefit of the oncology committee (MDT) for the paediatric patient is the multidisciplinary
discussion with the search for consensus on the most appropriate treatment approach.
A common difficult decision for cancer patients is whether it is better to perform a biopsy or a
definitive resection procedure. Generally, in smaller tumours, definitive resection is the first choice,
whereas in advanced disease, non-surgical oncological treatment follows biopsy, and definitive
surgical treatment is usually followed by oncological therapy once the tumour has reduced in size.
The actual surgical procedure with therapeutic intent has common general patterns, but in some
aspects the principles differ significantly depending on the type of tumour. The general principles
include the choice of the optimal surgical approach, early ligation of supply and drainage vessels,
sufficient radicality with the least invasiveness, prevention of injury and contamination of
surrounding organs, careful haemostasis, and correct transfer of the tumour for further examination.
The differences according to the type of tumour can be illustrated by the example of soft tissue
sarcomas and neuroblastoma (the basic explanation for the different surgical approaches is the
different sensitivity of tumours to non-surgical treatment).
For patients with sarcoma, a sufficiently radical removal of the pathological lesion en bloc with a rim
of healthy tissue (R0 resection) is a vital principle. If part of the tumor tissue remains in the patient's
body (microscopic (R1) or macroscopic (R2) residue), the risk of difficult-to-treat local recurrence
increases substantially. After insufficiently radical surgery, we consider so-called primary radical
reexcision. Furthermore, due to the biological nature of sarcomas, we are actively looking for
lymphatic metastases.
On the other hand, in neuroblastoma we do not necessarily need to achieve maximum radicality;
95% resection is a frequent goal, with deliberate retention of small remnants of tumor tissue on vital
structures. The emphasis is on preserving the integrity and function of the surrounding organs. It is
not necessary to remove the tumour en bloc; resection is facilitated by the piecemeal technique,
whereby removal of several accessible portions of the tumour allows the originally inaccessible part
of the lesion to be safely resected. The main pitfall of neuroblastoma tends to be its intimate
relationship to major blood vessels (aorta and inferior vena cava and their branches).
A special subchapter is represented by young patients who are born with the tumour. The treatment
of these patients combines the principles of oncological and neonatal surgery (extremely gentle
tissue manipulation, emphasis on minimal blood loss, special instruments, optimal timing of
surgery). The most common neonatal tumour is sacrococcygeal teratoma.
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The general hierarchy of surgical treatment goals (saving life takes precedence over saving health,
and health takes precedence over cosmetic outcome) is also valid for paediatric cancer patients, yet
only rarely are mutilation operations indicated (resulting in ablation or loss of function of an
important organ), as a similar therapeutic effect can usually be achieved by a combination of less
invasive surgery and non-surgical treatment.
In the 1990s, the indications of the newly developed minimally invasive surgery (e.g. thoracoscopy,
laparoscopy) gradually expanded. Initially, the presence of malignant disease was taken as a
contraindication to the minimally invasive approach; nowadays, minimally invasive surgery has a
firm place in the treatment of paediatric patients with cancer.
Surgical intervention is necessary to ensure quality vascular access for the administration of cancer
therapy. Most commonly, this involves the insertion of a central venous catheter, a tunneled central
catheter or a venous port.
The surgeon also encounters pediatric patients treated in palliative care. Typical procedures include
drainage of thoracic effusion or ascites, bypass surgery, construction of an ostomy for nutrition or,
conversely, for derivation of intestinal contents, and arrest of bleeding.
Pediatric tumors carry the risk of many complications and acute conditions. We mention some
requiring surgical intervention. The tumor may make itself known by rupture, violent hemorrhage,
ileus, urinary retention, suppurative inflammation, torsion of an important organ, compression of the
spinal cord. Serious complications may arise from the resection surgery itself. Complications of
chemotherapy include, among others, hemorrhagic cystitis, acute pancreatitis, neutropenic colitis
with the necessity of resection of the necrotic section of the intestine, invasive aspergillosis requiring
radical surgical removal of all foci persisting after antifungal therapy.
The overall survival prognosis is highly variable, generally more favourable in a paediatric cancer
patient than in an adult cancer patient. The variability in prognosis is illustrated by neuroblastoma
tumors with two extremes: patients with an unfavorable biological profile of small localized
neuroblastoma may have a poor prognosis, whereas other patients with neuroblastoma will be cured
spontaneously without any therapeutic intervention. Along with efforts to further reduce mortality,
there has been a recent emphasis on substantially reducing treatment morbidity, as surviving
pediatric patients carry more long-term sequelae into their lives than their adult counterparts.
In the future, pediatric oncologic surgery can be expected to intensify its efforts to provide
maximally effective surgical treatment with the least invasiveness and least morbidity. This goal
could be achieved, for example, by refinement of navigation techniques including 3D imaging,
further development of minimally invasive and robotic surgery, prophylaxis of later fertility
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disorders and the use of precision medicine (based on molecular-biological specification of the
disease) in direct combination with surgery.
Despite all the technical advances, the therapeutic relationship is based on fundamental medical
principles, treating a unique human being at a fragile age.
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PEDIATRIC FRACTURES (37)
Mareček Lukáš, Plánka Ladislav
Definition and introduction
The composition of a pediatric skeleton varies from an adult skeleton especially by a large content of
cartilaginous tissue and the presence of growth cartilages, which ensure the bone growth. Bones are
also more elastic in childhood. For these reasons, different types of fractures occur in childhood and
require a specific therapeutic approach.
Specific types of child age fractures:
a) Subperiosteal fractures (Torus/Buckle fracture) - an incomplete fracture with cortical injury on
one side of the bone,
b) Bowing fractures - no obvious fracture line, the angulation of a bone is greater than
physiologically,
c) Greenstick fractures - one side of the cortical bone is broken, the other side is only angulated,
d) Epiphyseal separation and fractures - injuries in the region of the growth cartilage, according
to Salter and Harris they are classified into five types,
e) Avulsion fractures - when a muscle or ligament is overpulled, a bone fragment is displaced
instead of soft tissue being injured.
Fractures typically occur in children when they fall or by an object impaction, or during pathological
movement, similarly to adult patients. Pathological fractures (e.g. in the field of a bone cyst) or stress
fractures (from overload) are exceptions. Atypical fractures result from an intentional violence.
Diagnostics
Diagnosing fractures in children is similar to adult patients. However, we emphasize on physical
examination and low radiation dose in imaging methods.
Medical history - we ask about the problem’s development, it’s circumstances and changes over the
time.
Physical examination - we look for certain signs (obvious bone fragment, pathological mobility,
change in shape) or uncertain signs of fracture (swelling, hematoma, palpation or tenderness).
X-ray examination - basic imaging examination method. The great advantage is a low dose of ionizing
radiation, however obtaining only 2D images of bones and the absence of cartilaginous tissue imaging
is the disadvantage.
Ultrasound examination – frequently it is the first diagnostic method in epiphyseal region imaging in
a case of growing skeleton.
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Other imaging methods - in case of complicated fractures, uncertain X-ray findings or in case of
polytrauma, CT scan is the method of choice. MRI has its place in investigating pathologies and
complications of pediatric fractures, such as bone bridge formation or fractures of the neonatal
skeleton.
Pediatric fractures therapy
In the treatment of pediatric fractures, it is necessary to take an advantage of the propitious healing
potential and remodelling abilities of the pediatric skeleton. Most of the fractures in the child age is
treated conservatively. If surgery is necessary, it must be performed in a such way to minimize injury
in the area of the active growth plate by the osteosynthetic material.
Conservative approach
The fixation time for healing pediatric fractures depends on the patient’s age and the localization of
the injury. The healing rate and required fixation time increases with age, with the distance of the
fracture site from the growth cartilage and with a reduced vascular supply to the injured area.
Location Standard fixation time
Metaphysis / Epiphysis 2,5–4 weeks
Diaphysis 5–7 weeks
Scaphoid bone / Talus 6–9 weeks
The fixation can be made of different materials. However, at the beginning of the treatment, a noncircular,
ideally plaster splint is required because of the swelling and the risk of compartment syndrome
development. Once the swelling has subsided, fixation with lighter materials can be used for fractures
without risk of dislocation. A preformed splint can be used for uncomplicated finger injuries. Some
traction techniques may be applied in the treatment of diaphyseal fractures of long bones in small
patients (up to 15 kg).
Surgical approach
Unstable and potentially unstable fractures need to be fixed with osteosynthetic materials. If possible,
the operation is perfomed from a small skin incision or percutaneously. A drilling thin Kirschner wire
is the most frequently used material in the treatment of epiphyseal fractures. The ESIN method is used
in the treatment of diaphyseal fractures in long bones (usually a Prévot nail is implanted into the
intramedullary cavity of long bones). Another possible methods include cancellous, usually cannulated
screws, or rigid intramedullary nails (if the growth plate is closed), and rarely applied are plating
systems or external fixators.
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Typical fractures of children age:
Birth injuries - during difficult fetus delivery, a fracture of the clavicle or the humerus diaphysis may
occur. These fractures are treated by fixing the limb to the body for 2-3 weeks. Supracondylar
fracture of the humerus - the most common fracture in the elbow region in children. A displaced
fracture requires precise repositioning and osteosynthesis under general anaesthesia. This type of
fracture is dangerous by a neurovascular injury and a risk of healing in residual dislocation (especially
rotational), which may lead to permanent consequences (limitation of full mobility in the elbow joint).
Monteggia lesion - fracture of the ulnar bone with injury to the humeroradial joint. Usually, a fracture
of the ulnar bone is associated with luxation or subluxation of the radial head. Avulsion fracture of
SIAS/SIAI - fracture typical for adolescent patients. Hypercontraction of the m. quadriceps femoris
occurs during rapid acceleration or braking and its onset tears a bone fragment from the hip bone.
Impressive skull fracture (ping-pong fracture) - a fracture of the neurocranium typically occurs
when an infant or toddler falls from a greater height on an obstacle by the top of the head. It requires
a head CT scan to rule out other intracranial injuries. Depending on the degree of impingement,
operative therapy is indicated.
Complications of pediatric fractures
Acute complications include injury to blood vessels, nerves and soft tissues (partial or complete
laceration by the mechanism of injury, injury caused by bone fragments or osteosynthetic material).
Late complications include bone bridge, which occurs when the injured part of the growth plate
undergoes necrosis. During healing, a conjunction of the epiphysis and metaphysis occurs and the
growth stops in the injured region. Depending on its location, the bone bridge then causes impaired
bone growth in length, angulation, or a combination of both, and thus shortening or curvature of one
of the limbs. A non-union is the name given to a fracture that does not heal in six months or more and
requires surgical treatment. Axial deformity, or malunion, is the result of a fracture healing in an
inconvenient position in which the skeletal remodelling capabilities are insufficient. Bone synostosis
is caused by transverse ossification of the long bones of the forearm or lower leg and it is caused by
hematoma ossification connecting the bones with an injured periosteum.
Generally it can be said it is more difficult to diagnose and classify the children fractures than to operate
them. The major mastery consists in the art of conservative treatment methods usage and especially
some specific types of fractures should be treated in the pediatric skeletal traumatology centers.
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Image references:
(Figures no. 1 – 4) - Archive of Department of Radiology and Nuclear Medicine, The University Hospital Brno
(Figure no. 5) - AO Surgery Reference website
(https://media.aofoundation.org/-/jssmedia/surgery/p13/p13_p010_i1200.png?w=400)
(Figure no. 6) - Little JT, Klionsky NB, Chaturvedi A, Soral A, Chaturvedi A. Pediatric distal forearm and wrist injury:
an imaging review. Radiographics. 2014 Mar-Apr;34(2):472-90. doi: 10.1148/rg.342135073. PMID: 24617692.
Distal humerus
supracondylar fracture
Distal forearm
subperiostal fracture
Distal ulnar greenstick
fracture with complete
metaphyseal distal
radius fracture
Supracondylar facture
fixation with Kirschner
wires
Epiphyseal separation
of distal radius SH II
Fig. 1 Fig. 2 Fig. 3
Fig. 4 Fig. 5
Fig. 6