Spinal Cord Injury Daniel Ira Department of Trauma Surgery University Hospital Brno logo Incidence n10 - 15 per million n 18 - 35 years n Male - 3:1 n RTA 51% - cars n Domestic 16% n Industrial 11% nSports 16% - diving incidents nSelf harm 5% n Types nCervical 40% nThoracic 10% nLumbar 3% nDorso lumbar 35% nAny 14% nInjury – osseus/ligamentousus nSCIWORA Syndrome n (Spinal Cord Injury w/o Radiologic Abnormality) n Anatomy nSpinal cord ends below lower border of L1 nCauda equina is below L1 n n nMechanical injury - early ischaemia, cord edema - cord necrosis C:\Users\Katka\Pictures\spinal-cord2.gif C:\Users\Katka\Pictures\spinal-cord3.gif C:\Users\Katka\Pictures\spinal-cord5.jpg Spinal Cord Injury pathophysiology nPrimary injury nInitial insult to cord n nLocal deformation n nEnergy transformation PSWebImageBitMap0001 Spinal Cord Injury pathophysiology nSecondary injury n nBiochemical cascade n nCellular processes Theories for secondary injuries nLipid Peroxidation and Free Radicals nAbnormal Electrolyte Fluxes and Excitotoxicity nAbnormal Vascular Perfusion nAbnormal Intracellular Sodium Concentration nAssociated Inflammatory and Immune Response Level of Spinal injury nNeurological level is at the most lowest segment with normal motor & sensory function n nDifficult to determine : n - as most muscle efferents receive fibres from more than one level n - Closed cord lesions may extend over several cms. n - Dermatomes have imprecise boundaries. Cord level n C2 – C7 = add +1 for cord level n n T1 – T6 = add +2 n T7 – T9 = add +3 n nT10 = L1, L2 level nT11 = L3, L4 level n nL1 = sacro coccygeal segments n C:\Users\Katka\Pictures\spinal-cord.gif C:\Users\Katka\Pictures\dermatome(2).jpg C:\Users\Katka\Pictures\dermatomes.jpg C:\Users\Katka\Pictures\spaceball.gif site of compression. http://www.ebmedicine.net/spaw/uploads/aboutUs/Cervical%20And%20Lumbosacral%20Dermatomes%20And%20My otomes%20Emergency%20Medicine%20Practice_1.JPG ASIA Score nBased on key muscle strength & key sensory points nUseful for following improvement or deterioration asia motor asia sensory Degrees of injury n Complete - flaccid paralysis + total loss of sensory & motor functions n nIncomplete - mixed loss n - Anterior sc syndrome n - Posterior sc syndrome n - Central cord syndrome n - Brown sequard’s syndrome n - Cauda equina syndrome Anterior spinal cord syndrome nFlexion rotational force to spine n nDue to compression fracture of vertebral body or anterior dislocation n nAnterior spinal artery compression n nLoss of power, reduced pain and temperature below the lesion. posterior cord Posterior cord syndrome nHyperextension injuries n nPosterior vertebral body fracture n nLoss of proprioception and vibration sense n nSevere ataxia anterior cord syndrome Central cord syndrome nOlder age with cervical spondylosis n nHyperextension with minor trauma n nCord is compressed by osteophytes from vertebral body against thick ligamentum flavum. n nDamages the central cervical tract n central cord Brown sequards syndrome nHemisection of the cord n nStab injury and lateral mass fractures n nUninjured side has good power but absent pinprick and temperature n nIpsilateral weakness and position sense loss nContralateral pain and temperature loss n brown sequard Neurogenic shock nLesions above Th6 nMinutes – hours (fall of catecholamines may take 24 hrs) nDisruption of sympathetic outflow from Th1 - L2 nUnapposed vagal tone nPeripheral vasodilatation nHypotension, Bradycardia & Hypothermia n nBUT consider haemmorhagic shock if – injury below Th6, other major injuries, hypotension with spinal fracture alone without neurological injury. Spinal shock nTransient physiological reflex depression of cord function – ‘concussion of spinal cord’ n nLoss anal tone, reflexes, autonomic control within 24-72hr n nFlaccid paralysis bladder & bowel and sustained priapism n nLasts even days till reflex neural arcs below the level recovers. Assessment & Managemnt nFailure to suspect leads to failure to detect injuries nABCDE – Logroll and remove the spinal board nLook for markers of spinal injury nSecondary survey nAdequate Xray’s nEmergency treatment nSurgery nDefinitive care & rehab. Clinical features nPain in the neck or back radiating due to nerve root irritation n nSensory disturbance distal to neurological level n nWeakness or flaccid paralysis below the level Signs in an Unconcious patients nDiaphragmatic breathing nNeurological shock (Low BP & HR) nSpinal shock - Flaccid areflexia nFlexed upper limbs (loss of extensor innervation below C5) nResponds to pain above the clavicle only nPriapism n Signs of spinal injury nForehead wounds – think of hyperextension injury n nLocalized bruise n nDeformities of spine - Gibbus, feel a step & Priapism n n n Emergeny Care nCareful manual handling especially if unconcious nJaw thrust is safer nCorrect gross spinal deformities nCall the anaesthetist if diaphragmatic paralysis or RR>35 nUse flexible fibreoptic scopes in unstable fractures nRyles tube if abdominal distension causes respiratory probl nCathetrize to avoid overstretching of detrusor nIV fluids – paralytic ileus in first 48hrs. nPassive movements to rule out fractures nSmall iv doses of opiates Assessment nDocument the level of injury n nRule out other injuries – CT/FAST in abdominal injuries as there is paralytic ileus and absent peritioneal irritation. n nAssociated injuries in dorsal spine fracture are : n - Renal injuries n - Chest and Sternal injuries n - Wide Mediatinum due to fracture haematoma. n - Retroperitoneal injuries Therapy nPharmacologic Interventions nDecompression nProspects of Spinal Cord Regeneration Emergency treatment nABCDE nKeep warm nTreat if BP<80mmHg & HR <50bpm nH2 Antagonists & Heparin n n The National Acute Spinal Cord Injury Study (NASCIS) nMethylprednisolone 30mg/kg iv bolus over 15min immediately n45minutes after the bolus a 5.4mg/kg/h infusion over 23 hrs in first 3 hours after the injury. n5.4mg/kg/hr for 47hrs if 4 - 8hrs following the injury. n n nSteroids nSteroids mainly act by prevention of lipid peroxidation by free radicals and membrane stabilisation. They may help prevent apoptosis by checking calcium fluxes, improving vascular perfusion, and are thought to help reduce white matter oedema, and enhance Na/KATPase activity n n nNaloxone nNaloxone is an opiate receptor that was included in one treatment arm of the NASCIS studies nFound to be effective in the subgroup of patients with incomplete spinal cord injuries n nGangliosides nThese are glycosphingolipids at the outer cellular membranes of the central nervous system nThere is some evidence that gangliosides may have neuroprotective action, with more speedy recovery of motor and sensory function in partial cord injuries nCalcium Channel Blockers nThought to work by improvement in blood flow via vessel dilatation n nAntagonists of Glutamate Receptors nWorks by prevention of excitotoxicity as a result of glutamate accumulation – helps to prevent abnormal sodium and calcium fluxes, which may prove lethal to cells n nOthers nInhibition of cyclo-oxygenase nMinocycline nSodium channel blockers nErythropoietin nCyclosporin Augmentation of Regenerative Ability of CNS Neurons Neurotrophic Factors nEpidermal growth factor n nFibroblast growth factor 2 n nBDGF: brain derived growth factor n nCyclic AMP Kojima, J Neurotrauma, 2002 Whiplash injury nSudden hyperextension and flexion nIncreasing neck pain for the first 24hours nAssociated headache, pain radiating to both shoulders and paraesthesia in hands nReduced lateral flexion nAnterior longitudinal ligaments are torn causes dysphagia nForward flexion against resistance is painful n90% are asymptomatic after 2years n10% still have pain nSome still claim money hence the need for proper documentations.