Shock,MOF,SIRS,sepsis, compartment syndrome Klinika úrazové chirurgie FN Brno-Bohunice Shock nMajor cause of death of critically ill patients nCondition in which the cardiovascular system fails to perfuse tissues adequately nLife threatening decrease of blood perfusion in internal organs, systemic state of hypoperfusion nImbalance between demand and supply of oxygen for organ tissues nCentralisation of volume circulation - brain, heart, lungs n Shock pathofysiology ncellular hypoxemia – energy deficit, > aerobic metabolism switch to anaerobic, > lactic acid accumulation – metabolic acidosis > cellular function failure, Na/K pump impaired > mitochondria damage, cell death n n n n n n n Compensatopry mechanisms nBaroreceptors , volumoreceptors i aorta – afferental signaling to CNS – sympathetic stimulation, Adrenaline – vasoconstriction / defensive responce/ n n n n Sympathetic stimulation Classification of shock nBased on initiating mechanism nHypovolemic nCardiogenic nObstrctive nDistributive n Septic n Anaphylaxis n Neurogenic n nHypovolemic shock nreduced circulating volume ( Empty tank ) due to haemorrhagic/ non haemorrhagic causes (dehydration) --1. blood loss – trauma -- 2. fluid loss – diarrhea, nausea and vomiting n n n n Severity estimation nAllgower shock index ( PR/SBP ) n60/120 – 0,5 normal condition n100/100 – 1 – impending – loss of 30% of volime n120/80 – 1,5 – moderate/severe shock – life threatening n nEstimation of blood loss nhumerus 200-1000 ml forearm 400 ml shin 500-1000 ml n pelvis 2000-3000 ml / more femur 1500-2000 ml n I II III IV Blood loss ml <750 750-1000 1500-2000 >2000 Blood loss % <15 15-30 30-40 >40 HR <100 >100 >120 >140 BP normal orthostatic hypotension Severe hypotension Mental status normal anxious confused coma Urine output normal normal reduced anuric Lactic acidosis + ++ ++ +++ nObstructive shock - mechanical obstruction nPE nTension PNO nCardiac tamponade n Tension pneumothorax noccurs when air enters the pleural space from a lung injury or through the chest wall without a means of exit nresults in death if it is not immediately recognized and treated nwhen air is allowed to leak into the pleural space during inspiration and becomes trapped during exhalation, an increase in the pleural pressure results n Tension pneumothorax nincreased pleural pressure produces mediastinal shift nmediastinal shift results in: n - compression of the uninjured lung n - kinking of the superior and inferior vena n cava, decreasing venous return to the n heart nprogression of simple or open pneumothorax n pneumothorax Tension pneumothorax download n Tension pneumothorax nmanagement nemergency care is directed at reducing the pressure in the pleural space n nocclude open wound nneedle thoracostomy ntube thoracostomy – in-hospital management n4nd intercostal space in mid-axillary line nTOP OF RIB n n Pulmonary embolism pulmonary_embolism Pulmonary embolism ØECG ØX-ray Ø D-Dimery Ø CT pulmonary angiogram (CTPA) Ø ECHO n n Pericardial tamponade n nrestriction to cardiac filling caused by blood or other fluid within the pericardium noccurs in <2% of all serious chest trauma nhowever, very high mortality nresults from tear in the coronary artery or penetration of myocardium nblood seeps into pericardium and is unable to escape n200-300 ml of blood can restrict effectiveness of cardiac contractions n n n n n n Pericardial tamponade nsigns and symptoms n - tachycardia n - respiratory distress n - Becks triad - narrowing pulse pressure n - neck vein distention n - muffled heart sounds n - ECG changes n n n n n Pericardial tamponade nmanagement nhigh flow O2 nIV therapy npericardiocentesis – needle insertion through the skin incision directed toward the left shoulder at a 45 degree angle to the abdominal wall. n n n n n n n Cardiogenic shock n n primary failure of heart pump ,( IM, valvular disease, malignant arrhytmia ) Distributive shock Distributive shock n n nBlood vessel problem - hypoperfusion due to periferal vasodilation with hypotension nCardiac pump and blood volume are normal but blood is not reaching the tissues n n Distributive shock nSeptic shock – infectious agent (endotoxines, SIRS) provoked periferal vasodilation, sepsis + acute circulatory failure with hypotension n Anaphylactic shock – a type of shock that results from widespread systemic allergic reaction to an antigen n Neurogenic shock - a type of shock that results from the loss or suppression of sympathetic tone Septic shock – risk factors nAge nMalnutrition nUse of invasive catheters nTraumatic wounds nDrug therapy Septic shock – risk factors nInitiated by G neg. or G posit. Bacteria, fungi or viruses nCell walls of organism contain endotoxins – endotoxins release inflammatory mediators – vasodilatation and increase capillary permeability leads to shoc due to alteration in peripherial circulation and massive dilation nInflammation – complex defensive reactio of n vascularized tissue to harm nInfection – inflammation with identified microorganism in host tissue nBacteremia – presence of bacterias in bloodtream nSIRS – systematic inflammatory responce syndrom nSepsis Inflammation n- Rapid, complex biological response of body tissue to harmful stimulus - n- elimination of harm causes, clear out damaged tissues and cells, prepare site for reparation of tissue defects, n n- innate defensive responce and reparative process, complex of immune cells and blood vessels and molecular mediators n Inflammatory reaction nInjured tissue cells release chemokines, histamin, etc., n nVascular phase – activation of endothelial cells – adjacent capillaries dilate, increase blood flow, endothelial cells contract, increase intercellular gaps, increase permeability, exudation of fluids, solubile proteins to soft tidssue n - activation of endothelial surface n SIRS (Systemic Inflammatory Response Syndrome) n n Massive tissue inflammation, long lasting – overproduction of proinflammatory cytokines – all tissues affected. SIRS nSIRS to infection manifested by two or more of following - nBT > 38 / < 36 dg. nHR > 90/min nTachypnea > 20/min nLeukocytosis > 12 0000 or leukopenia < 4 000 n-------------------------------------------------------------- n n n n Sepsis nLife threatening clinical syndrome nSpecific type of SIRS condition + confirmed infection n nClinical signs nLab / CRP, Procalcitonin / n Imaginig / X-rax, CT scan / n prove of infection nSepsis n nSevere sepsis – sepsis + new-onset organ dysfunction n nSeptic shock – severe sepsis + acute circulatory failure with hypotension n nMODS n C:\Users\Martin\Desktop\obr. orthobull\sirs-mods-sepsis-27-638.jpg C:\Users\Martin\Desktop\obr. orthobull\sirs-mods-sepsis-28-638.jpg Clinical signs nTachycardia – BP >100/min nHypotension – SBP < 90 torr nAltered mental status nPallor, cold sweat, capillary refill nTachypnea, hyperventilation > 20/min nOliguria(<500ml/d or 30ml/h) nAnuria (<100ml/d or 0,5ml/h/kg) nDecrease CVP <2cm H2O, /5-7/ nLactate > 2mmol/l hypoxia, > 4 mmol/l n n n n nMonitoring n- ECG, n- cont. saturation, n- hourly urine output n n nInvasive monitoring n- CVP n- invasive arterial BP n- Cardiac output n- Lactate, Base deficit, n therapy nSigns of shock - begin therapeutic management + complete dif. dg. of shock cause n nFluid resuscitation - refill volume nDynamic fluid responce – 500ml /20min, maesure response nAdequate oxygenation nSurgical management nPharmacological therapy – inadequate effect of volume refill n vascular resistance – Noradrenaline / Norepinephrine n sepsis first choise nInotropic suppurt – low CO - Dobutamine Septic shock management nSigns of shock n vital signs + lactate level nMicrobiological exam samples nEmpiric ATB nFluid resuscitation 20ml/kg nCVP 8-10 n MODS (Multipl Organ Dysfunction Syndrome)/ MOF (multiple organ failure) n most severe condition , high mortality rate > 60% n n 2 or more organ systems dysfunction in acutely ill patients such that homeostasis cannot be maintained without intervention n nComplication of prolonged shock n n MODS (Multipl Organ Dysfunction Syndrome) nPrimary MODS – direct insult/ injury to organ causing failure of function / aspiration…/ n nSecondary MODS – complication, distant organ affected due to profound SIRS/sepsis C:\Users\Martin\Desktop\obr. orthobull\sirs-mods-sepsis-48-638.jpg Organ dysfunction nLungs – ARDS nKidneys – AKI – acute tubular necrosis nCvS – shock nCNS – metabolic encephalopathy nCoagulation – DIC nEndocrine – adrenal insufficiency nLiver - cholestasis nSkeletal muscle – rhabdomyolysis nGIT – gastroparesis, ileus, ulcer ARDS/ ALI (Adult Respiratory Distress Syndrom/ Acute lung injury) nChest trauma, aspiration, sepsis n Pulmonary endothelial cell reactio to inflammatory mediators, hypoxia, acidosis nMost common, lung first filter n n nDynamic acute formation in 12-48 h. nX-ray/ CT – bilateral flaky/patchy n infiltrates n n n n n n n n C:\Users\Martin\Desktop\obr. orthobull\5e7cfb6d90bbcf70e73493819e691a_thumb.jpg nCreate higher permeability of pulmonary vessels – exudate, progresion of gas exchange imparement, interstitial pulmonary oedema, loss of pneumocytes > lack of suffactant > alveolar pulmonary oedema, n or athelectasis n n C:\Users\Martin\Desktop\obr. orthobull\ards_clinical_pathology1318419263671.jpg nStage I - latent – dyspnoe, mild hypoxemia, hyperventilation, X-ray – flaky opacities aroun hilus nStage II – ortopnoe, moderate hypoxemia, cyanosys, tachacardia, tachypnoe, X-ray – pulmonary oedema nStage III – terminal – sebere hypoxia, shock, AV , X-ray diffuse infiltrates n nEnd-stage – global respiratory insufficiency – reductio of alveolar surface, fibrosis n n nTh -Oxygen support -artefitial lung ventilation+ PEEP -Glucocorticoids - prone position n - n DIC (Disseminated Intravascular Coagulation) nAcquired coagulopathy – multiple systemic formation of blood clots – trombus- in microvascular circulation – consumption of coagulation factors – diffuse tissue/parenchamal bleeding n periferal tissue ischemia nHematologic examination (fibrinogen, DD, FDP, aPTT, INR, AT) InR >1,5, aPTT > 60sec, PLT < 80 000 nLMWH nSupplementation of AT III, FFP, EBR, fibrinogen, platelets nTherapy of primar cause DIC C:\Users\Martin\Desktop\obr. orthobull\images.jpg C:\Users\Martin\Desktop\obr. orthobull\images 2.jpg AKI / Acute kodnes injury nKidney vessels – autoregulation - perfusion maintain in BP 50-180mmHg n nPrerenal failure - low volume nIntrincis cause – acute tubular necrosis – ischemic/ toxic – muddy brown cast during urinanalysis n nOligoanuria, /<500/50ml/, fluid balance, uremia, creatinin > 177 n nRRT - iRRT/ CVVH Liver failure nDue to hepatocyte necrosis – impairement of excretion function – icterus due to hyperbilirubinemia, n bilirubin > 35mmol/l n nImparement of synthetic and metabolic function n - hypoceagulation, haemorrhage, hypoglycemia n nLiver ecephalopaty - due to hyperamonemia n nSymptomatic therapy, supplemtally therapy n Metabolic complications nHyperglycemia nInsulinoresistence nCatabolic reactions - rhabdomyolysis GiT nStress gastric ulcer – upper GiT haemorrhage n nGut ischemis - loss of barrier finction against intestinal bacterias and toxins > translocation, inflmmatory response, souce of bacteremia and sepsis of critically ill patients n n PPI n early enteral nutrition / glutamin/ n Local/ infectious complication nI.v. ATB therapy , high dose, sensitivity n nSurgical debridement of necrotic tissue/ drainage of abscess n nSurgical management of initial harmful insult n / surgical bleeding, PNO, pleural effusion / n Compartment syndrome nA condition in which increased compartment pressure within a confined space, compromises the circulation and viability of the tissues within that space Compartment syndrome nIncrease in volume of contents n and/or nReduction in size of compartment n ↓ nincreased pressure within the compartment n ↓ ncompression of muscles, nerves & vessels n ↓ nimpaired blood flow n ↓ nischemia & necrosis Compartment syndrome Symptoms nPain nParaesthesia nParesis nPulses present nFunctional failure Compartment syndrome-pressure monitoring Compartment syndrome- Therapy n nSurgical decompression with a fasciotomy is the definitive treatment n Compartment syndrome- Therapy Compartment syndrome- abdominal