Acute Spinal Cord Injury and Neurogenic Shock — Comprehensive ICU Management

Also known as Spinal cord injury · SCI · Neurogenic shock · ASIA impairment scale · Autonomic dysreflexia · Cervical spine injury · Spinal cord perfusion pressure · STASCIS

Acute spinal cord injury (SCI) — traumatic damage to the spinal cord causing motor/sensory deficit below the injury level ± autonomic dysfunction. Neurogenic shock: loss of sympathetic tone below the lesion (cervical or upper thoracic SCI) → VASODILATION (hypotension) + BRADYCARDIA (unopposed parasympathetic/vagal tone) — DISTRIBUTES differently from other shock types (warm, dry skin + bradycardia vs cold/clammy/tachycardic of hypovolaemic shock). ASIA Impairment Scale (A=complete, B=sensory incomplete, C=motor incomplete non-functional, D=motor incomplete functional, E=normal). Management: (1) ATLS primary survey + spinal precautions (cervical collar + logroll + spinal board), (2) NEUROGENIC SHOCK: noradrenaline (alpha + beta — restores BP AND HR) + atropine (for symptomatic bradycardia) + target MAP 85-90 mmHg for 7 days (maintain spinal cord perfusion — controversial but widely practiced), (3) EARLY SURGICAL DECOMPRESSION (STASCIS trial — within 24h improves neurological outcomes), (4) METHYLPREDNISOLONE (controversial — NASCIS II/III — high-dose within 8h may improve outcomes but increases infection risk — many centres have abandoned routine use), (5) VTE prophylaxis (high risk — LMWH is the first-choice anticoagulant), (6) prevent secondary injury (avoid hypotension/hypoxia/hyperthermia). Autonomic dysreflexia (T6 or above): noxious stimulus below lesion → massive sympathetic discharge → hypertensive crisis → intracranial haemorrhage/stroke. Management: sit upright + identify/remove trigger + rapid-acting antihypertensives (nitroglycerin ointment, nifedipine).

high29 referencesUpdated 19 Aug 202635 min readVerification in progress

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8 MCQs

The one-paragraph exam answer

Acute spinal cord injury (SCI) is traumatic cord damage causing motor and sensory loss below the lesion, and the exam-defining complication is neurogenic shock: loss of sympathetic tone below a cervical or upper-thoracic lesion produces the triad hypotension plus bradycardia plus warm dry skin — the only shock state that bradys, and distinct from the cold, clammy, tachycardic hypovolaemic shock you must exclude in every trauma patient. Resuscitate with ATLS plus spinal precautions, treat neurogenic shock with noradrenaline (alpha plus beta) and atropine for symptomatic bradycardia — never pure alpha-agonists, and never fluid boluses — and hold the mean arterial pressure at 85 to 90 mmHg for 7 days to keep the pressure-passive injured cord perfused. Early surgical decompression within 24 hours (STASCIS) is the one intervention that changes neurological outcome; high-dose methylprednisolone is controversial, with practice varying widely between centres and countries. These patients carry a very high venous thromboembolism risk and must never receive succinylcholine after 24 hours.^[1]^[5]^[15]^[13]

Meet the patient

A 28-year-old man dives into a shallow lake and does not surface. Friends pull him out awake but unable to move his arms or legs. In resus he is tetraplegic at C5 (ASIA A), blood pressure 78/42, heart rate 46, and his skin is warm and dry to the fingertips. The CT shows a C5 burst fracture with cord compression.^[1]

The single question that decides his first hour is the one every fellowship stem turns on: is this neurogenic shock or hypovolaemic shock? The bradycardia plus the warm dry skin answers it — and the answer chooses your drug. Hold that one question and the whole topic slots into place.^[1]

References29Show

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