Neurogenic Shock (Spinal Cord Injury)

Overview & definition

Neurogenic shock — the loss of the sympathetic tone from the spinal cord injury (above T6). The unopposed parasympathetic → the vasodilation (the warm, the dry, the flushed skin — the loss of the alpha) + the bradycardia (the unopposed vagal — the loss of the cardiac sympathetic T1-T4). The MAP target 85-90 mmHg (the spinal cord perfusion). The distinct from the hypovolaemic shock (the warm vs the cool).[1][1]

The critical unifying concept. Neurogenic shock is a distributive shock — the same family as the septic, the anaphylactic, and the vasoplegic post-cardiac-surgery. All share the loss of the vascular tone (the low SVR). But neurogenic shock is the ONLY distributive shock (indeed the ONLY shock of ANY type) that causes bradycardia rather than tachycardia. Every other shock — the hypovolaemic, the cardiogenic, the septic, the anaphylactic, the obstructive — drives a compensatory tachycardia. The neurogenic shock does NOT, because the sympathetic cardiac accelerator fibres (T1-T4) are severed along with the vasoconstrictor fibres. The unopposed vagal wins. Bradycardia + hypotension + warm dry skin in a trauma patient = neurogenic shock until proven otherwise.[1][4]

The pathophysiology

The spinal cord injury (above T6) disrupts the descending sympathetic pathways from the brainstem to the sympathetic chain. The result:[1][1]

• The vasodilation — the loss of the sympathetic alpha-1 vasoconstrictor tone to the peripheral vasculature → the massive vasodilation → the reduced SVR → the hypotension.[1]
• The bradycardia — the loss of the cardiac sympathetic outflow (T1-T4) → the unopposed vagal (parasympathetic) tone → the bradycardia. The distinct from the hypovolaemic shock (which causes the compensatory tachycardia).[1]
• The temperature dysregulation — the loss of the sympathetic vasoconstriction → the poikilothermia (the body assumes the ambient temperature).[1]

The detailed pathophysiology — the three lost loops

The sympathetic nervous system is the body's "fight or flight" accelerator. It is controlled from the brainstem (the rostral ventrolateral medulla, the RVLM) and projects DOWN the spinal cord in the descening bulbospinal pathways to synapse on the intermediolateral (IML) cell column of the spinal cord grey matter — from T1 to L2. From the IML, the pre-ganglionic neurons exit via the ventral roots to the sympathetic chain, then the post-ganglionic fibres reach every target organ: the blood vessels (alpha-1 vasoconstriction), the heart (beta-1 chronotropy + inotropy), the bronchi (beta-2 bronchodilation), the sweat glands, the adrenals.[4][1]

A spinal cord injury above the level of T6 (and especially the cervical cord, above T1) severs ALL of these descending fibres below the lesion. The sympathetic chain below the lesion is now cut off from central command — it fires on its own intrinsic tone (minimal), not on brainstem-directed drive. Three specific consequences:[4]

1. The loss of the vasomotor tone (the alpha-1). The splanchnic and peripheral vasculature below the lesion lose their tonic sympathetic vasoconstriction → the massive arteriolar and venous vasodilation → the pooling of blood in the capacitance vessels (the splanchnic bed, the lower-limb veins) → the reduced venous return → the reduced preload → the reduced cardiac output → the hypotension. The SVR falls dramatically. This is mechanically identical to the vasodilation of the anaphylaxis or the sepsis — it is a DISTRIBUTIVE shock — but the trigger is the severed sympathetic rather than the mediator release.[1][1]

2. The loss of the cardiac accelerator tone (the beta-1, T1-T4). The cardiac sympathetic fibres arise from T1 to T4 (sometimes T5). A cervical cord injury severs these. The heart is now under the UNOPPOSED influence of the vagus nerve (the parasympathetic, the CN X — which travels outside the spinal cord, via the vagus, and is therefore SPARED). The result: the bradycardia. This is the single most distinguishing feature of the neurogenic shock — and the one that catches out the junior who expects a tachycardia in every shock. No other form of shock produces a bradycardia as part of its primary pathophysiology. (The hypovolaemic, the cardiogenic, the septic, the anaphylactic — all tachycardic.)[4][1]

3. The loss of the thermoregulatory tone. The skin vasculature below the lesion cannot vasoconstrict to conserve heat → the body assumes the temperature of the environment (poikilothermia). The patient may be hypothermic in a cool ED, or febrile in a warm resus bay — neither reflects a true core-temperature derangement. The sweating below the lesion is also abolished (the loss of the sympathetic sudomotor fibres) → the skin is DRY below the lesion (but may sweat above, as the lesion-sparing fibres above fire excessively to compensate).[1][1]

Why above T6 — the level matters

The higher the cord lesion, the more of the sympathetic outflow is lost, and the worse the neurogenic shock:[2][4]

• Cervical (C1-C8) lesions — the loss of the ENTIRE sympathetic outflow (T1-L2) + the cardiac accelerator fibres (T1-T4). The most severe neurogenic shock. ALSO the loss of the phrenic nerve (C3-C5) → the diaphragmatic paralysis → the respiratory failure requiring mechanical ventilation. The combination of the profound vasodilation + the bradycardia + the respiratory failure makes the high cervical SCI one of the most fragile ICU patients.[4]
• Upper thoracic (T1-T5) lesions — the loss of the cardiac accelerator fibres + the upper-body vasomotor tone. The neurogenic shock is significant (the bradycardia + the hypotension) but the diaphragm is spared (the C3-C5).[2]
• Lower thoracic (T6-T12) lesions — the cardiac accelerator fibres (T1-T4) are SPARED (the lesion is BELOW them) → NO bradycardia. Some vasodilation in the splanchnic/lower-limb bed (mild hypotension) but the cardiac sympathetic is intact → the compensatory tachycardia is preserved. Neurogenic shock is RARE below T6 — the hypotension in a T6-L2 injury should prompt an aggressive search for the OTHER cause (the blood loss).[2][3]
• Lumbar (below L1) lesions — NO neurogenic shock (the IML column is the T1-L2 — the lesion is at or below it).[1]

The timing and the natural history

The neurogenic shock develops within 30 minutes to hours of the injury (the time for the residual catecholamines already released to be washed out, and for the loss of the tonic sympathetic to become haemodynamically apparent). It peaks at 24-72 hours and may persist for 1-3 weeks (the average 7-10 days, sometimes up to 4-6 weeks in the complete high cervical lesion) before the intrinsic spinal sympathetic tone partially recovers. The longer the neurogenic shock, the worse the prognosis (the more complete the cord injury).[3][4]

The bradycardia may be profound. Heart rates of 30-40 bpm are not uncommon in the high cervical lesion. The symptomatic bradycardia (the hypotension refractory to the vasopressor alone, the syncope, the AV block, the asystole) is a real risk in the first 1-2 weeks — the atropine and/or the isoprenaline and/or the chronotrope is part of the toolkit, not an afterthought.[4][5]

The autonomic dysreflexia — the LATE counterpart (NOT in the acute phase)

For completeness and to avoid exam confusion: the autonomic dysreflexia is a DIFFERENT phenomenon that occurs in the REHABILITATION phase (weeks to months after the injury), in patients with lesions above T6. A noxious stimulus below the lesion (a full bladder, a faecal impaction, an ingrown toenail) triggers a massive reflex sympathetic discharge below the lesion (unopposed, because the descending inhibitory pathways are severed) → the life-threatening hypertension. The baroreceptors sense the hypertension → trigger the vagal (bradycardia) and the vasodilation ABOVE the lesion (the flushed, the sweating, the pounding headache above the lesion; the cold, the pale below). This is NOT neurogenic shock (it is hypertension, not hypotension; it is weeks later, not the acute phase) — but the examiners love to contrast the two, so know the difference.[1][1]

The clinical — the distinguishing features

Key: the neurogenic shock has the BRADYCARDIA + the WARM skin (the loss of the sympathetic), while the hypovolaemic has the tachycardia + the cool skin (the compensatory sympathetic).[1]

The timing. The neurogenic shock develops within 30 minutes to hours of the injury. The spinal shock (a different concept — the transient loss of the spinal reflexes below the lesion, lasting days to weeks) is distinct from the neurogenic shock (the haemodynamic).[1]

[1]

The full clinical picture

The classic triad in the trauma patient with a cervical or upper-thoracic SCI: (1) hypotension, (2) bradycardia, (3) warm dry flushed skin. All three must be present for the textbook diagnosis — but in the real trauma patient, the co-existent blood loss (the hypovolaemia) may mask the warm dry skin (replacing it with the cool clammy pale) or the bradycardia (replacing it with the tachycardia from the hypovolaemic reflex). The mixed picture (the neurogenic + the hypovolaemic) is the rule, not the exception, in the polytrauma patient — and the failure to recognise BOTH is a leading cause of the preventable death.[2][6]

• The blood pressure. The systolic commonly 70-90 mmHg in the untreated high cervical lesion. The diastolic falls disproportionately (the loss of the diastolic vascular tone) → the WIDE pulse pressure may be masked by the profound vasodilation → the narrow pulse pressure is more typical once the bradycardia reduces the stroke volume variability. The orthostatic hypotension is extreme — sit the patient up at your peril (the venous pooling → the catastrophic preload drop).[4]
• The heart rate. The bradycardia (30-50 bpm) is the rule in the cervical lesion. May be the sinus bradycardia, the junctional escape, the AV block (first, second — Mobitz I or II, or complete), or the asystolic pauses (the vagally-mediated). The symptomatic bradycardia is the indication for the chronotrope (the atropine, the isoprenaline, the dopamine, or the adrenaline infusion).[4][5]
• The skin. Below the lesion: the warm, the dry, the flushed (the loss of the sympathetic vasoconstriction + the sudomotor). Above the lesion: the cool, the pale, the sweaty (the compensatory sympathetic SURGE in the intact fibres above — the body's futile attempt to raise the BP). The LINE OF DEMARCATION at the sensory level is a clinical giveaway — examine for it.[1]
• **The abdomen.**The distended, the hypoactive-bowel, the areflexic (the paralytic ileus from the loss of the splanchnic sympathetic tone → the unopposed parasympathetic → the atony). May mimic or conceal an intra-abdominal catastrophe — the FAST scan / the CT is mandatory.[6]
• The respiratory. The high cervical lesion → the diaphragmatic paralysis (the C3-C5 phrenic) → the shallow, the rapid, the paradoxical breathing (the accessory-muscle-only, the abdominal paradox). The lower cervical lesion → the intercostal paralysis (the T1-T11) → the preserved diaphragm but the poor cough and the secretion retention. Anticipate the respiratory failure and the early intubation.[1]
• The neurological. The flaccid paralysis + the absent reflexes below the lesion (the spinal shock, the acute phase — NOT the spasticity that develops weeks later). The sensory level (the pinprick, the light touch) on the exam localises the lesion. The bulbocavernosus reflex (the S2-S4 — the contraction of the anal sphincter on the tug of the glans penis or the Foley catheter pull) — when ABSENT, confirms the spinal shock (the acute phase); when it RETURNS, marks the end of the spinal shock (but NOT necessarily the end of the neurogenic shock). The ASIA Impairment Scale (A-E) quantifies the completeness of the injury and the prognosis.[1][5]

The diagnosis — the rule-out, not the rule-in

The diagnostic principle. Neurogenic shock is a diagnosis of inclusion (the SCI is present) AND exclusion (the other causes of the hypotension are ruled out). The temptation — especially in the ED with a known cervical SCI and the classic triad — is to STOP looking once the neurogenic is "found." This is the error. The neurogenic shock does NOT exclude the co-existent blood loss — and the missed intra-abdominal bleed is the killable mistake.[2][6]

The stepwise diagnostic approach

1. Recognise the trauma + the SCI. Any patient with a mechanism compatible with the SCI (the high-speed MVC, the diving injury, the fall from height, the direct blow to the neck/back) AND any neurological sign (the weakness, the sensory level, the priapism — pathognomonic in the acute male SCI) is at risk. Immobilise (the cervical collar, the spinal board), then examine.[6]

2. Document the haemodynamics. The bradycardia + the hypotension + the warm dry skin = the neurogenic triad. But the tachycardia in a known SCI does NOT exclude the neurogenic — it may indicate the CO-EXISTENT hypovolaemia (the blood loss) on top of the neurogenic, OR a lower lesion (below T6) where the cardiac accelerator is spared. The hypotension in a SCI requires the EXPLANATION, not the assumption.[2][6]

3. RULE OUT THE HYPOVOLAEMIA — the single most important step. The hypotension in the trauma patient is the hypovolaemic UNTIL PROVEN OTHERWISE, even when the SCI is known. Actively search for the bleeding:[6]

   • The physical exam — the chest (the flail segment, the penetrating wound, the subcutaneous emphysema → the intrathoracic), the abdomen (the distension, the tenderness, the seatbelt sign → the intra-abdominal), the pelvis (the instability, the bruising → the pelvic fracture), the long bones (the deformity, the swelling → the femur, the tibia), the external (the lacerations, the scalp — the scalp can hold 1-2 L).
   • The FAST scan (Focused Assessment with Sonography in Trauma) — the bedside, the repeatable, the rapid. The Morrison's pouch, the splenorenal recess, the pouch of Douglas, the pericardium. The positive FAST = the intra-abdominal blood → the laparotomy. The negative FAST does NOT exclude the retroperitoneal or the hollow-viscus injury → the CT if stable.
   • The CT trauma series — the head, the cervical spine, the chest, the abdomen/pelvis (with IV contrast) — the definitive imaging once the patient is stable enough for the trip. The chest CT for the aortic injury (the widened mediastinum, the traumatic aortic transection — a killer in the high-speed deceleration). The abdomino-pelvic CT for the solid-organ laceration, the hollow-viscus injury, the retroperitoneal haematoma.
   • The bloods — the FBC (the Hb may be normal in the EARLY acute bleed — the haemodilution takes hours; the serial Hb is more useful), the cross-match, the lactate (the rising lactate = the ongoing tissue hypoperfusion from the blood loss), the venous/arterial blood gas (the base deficit — a sensitive marker of the occult hypovolaemia).[6]

4. Establish the diagnosis of the neurogenic shock — ONLY after the hypovolaemia is excluded (or treated). The combination of (a) the known cervical/upper-thoracic SCI, (b) the hypotension unexplained by the blood loss, (c) the bradycardia, (d) the warm dry flushed skin below the lesion, (e) the documented sensory level, AND (f) the negative FAST / the CT excluding the bleed → the neurogenic shock is the working diagnosis. Begin the neurogenic-specific management (the MAP 85-90, the noradrenaline, the atropine).[1][1]

5. The serial reassessment. The mixed shock (the neurogenic + the hypovolaemic) is common. Even after the neurogenic is "diagnosed," the patient may develop the delayed bleed (the splenic laceration that was initially haemodynamically stable, the pelvic fracture with the ongoing venous ooze). The serial lactate, the serial Hb, the serial FAST, the serial clinical exam — the vigilance continues.[6]

The differential of the bradycardia + hypotension (beyond neurogenic)

Not every bradycardia + hypotension in a trauma patient is the neurogenic. Consider:[6][1]

• The hypovolaemic shock with the late bradycardia — the profoundly exsanguinated patient (the >40% blood-volume loss) may develop a bradycardia as a pre-terminal event (the vagally-mediated "the heart gives up"). This is NOT neurogenic shock — it is the agonal bradycardia of the extreme hypovolaemia. The skin is COOL and CLAMMY (not warm dry). The treatment is the BLOOD, not the atropine.[1]
• The obstructive shock — the tension pneumothorax, the massive haemothorax, the cardiac tamponade. The obstructive shock may present with a relative bradycardia (or a tachycardia). The distinguishing: the JVP is HIGH (distended — in the tension pneumothorax and the tamponade; LOW in the massive haemothorax), the muffled heart sounds (the tamponade), the tracheal deviation and the unilateral absent breath sounds (the tension pneumothorax). The FAST / the bedside ultrasound is the rapid differentiator.[1]
• The beta-blocker or the calcium-channel-blocker overdose — the iatrogenic/drug bradycardia + hypotension. The history (the patient's medication list, the empty pill bottles). The treatment is the glucagon (the beta-blocker) and the calcium / the high-dose insulin (the calcium-channel-blocker).[1]
• The vagal / the vasovagal — the brief, the self-limited, the situational (the painful procedure, the sight of blood). Resolves with the recumbency and the leg raise. Not sustained.[1]
• The high spinal / the epidural anaesthesia — the iatrogenic (the epidural that has risen too high, blocking the cardiac accelerator fibres T1-T4). The same physiology as the neurogenic — the sympathectomy + the unopposed vagal. The treatment: the vasopressor (the noradrenaline / the metaraminol / the adrenaline) + the chronotrope. The distinction from the trauma neurogenic is the context (the anaesthetic, not the injury).[1]

[1]

The management

1. The MAP target 85-90 mmHg.[1]

• The higher the target (vs the 65 for the general ICU) because the injured spinal cord is extremely vulnerable to the hypoperfusion — the secondary injury (the ischaemia worsens the cord damage). The MAP 85-90 for at least 7 days (the evidence from the systematic review — the improved the neurological outcome).[1]

2. The vasopressor.[1][1]

• Noradrenaline (the alpha-1 — the vasoconstriction; the preferred — the restores the SVR).[1]

3. The bradycardia.[1]

• Atropine 0.5 mg IV (the vagal block — the symptomatic bradycardia).[1]

4. The volume.[1]

• The cautious the fluid (the neurogenic shock is NOT the hypovolaemic — the excess the fluid → the pulmonary oedema; but the vasodilation → the relative the hypovolaemia → the initial the 500 mL the crystalloid the challenge, then the vasopressor).[1]

5. The rule out the co-existent.[1][1]

• The trauma patient may have BOTH the neurogenic AND the hypovolaemic (the blood loss) — the distinguish is the key (the warm + the dry + the bradycardia vs the cool + the clammy + the tachycardia). The FAST scan / the CT to exclude the intra-abdominal / the intrathoracic the bleeding. The NOT the assume the neurogenic alone.[1]

The vasopressor choice — the receptor rationale

This is the highest-yield exam point in neurogenic shock. The vasopressor choice is NOT arbitrary — it is dictated by the receptor pharmacology and the specific pathophysiology.[1][7]

The neurogenic shock has TWO deficits: (1) the lost vascular tone (the alpha-1) AND (2) the lost cardiac accelerator tone (the beta-1, T1-T4). The ideal vasopressor addresses BOTH.[7]

The bottom line on the vasopressor. Noradrenaline is the first-line — it restores the SVR AND provides a modest beta-1 chronotropy to counter the bradycardia. The pure alpha-1 agents (phenylephrine, metaraminol) are AVOIDED because they worsen the bradycardia via the baroreceptor reflex. If the bradycardia is the dominant refractory problem, escalate to the adrenaline or the dopamine (the beta-1 chronotropy) rather than pushing the noradrenaline higher.[7]

The bradycardia management — the chronotrope ladder

The symptomatic bradycardia (the hypotension refractory to the noradrenaline, the syncope, the AV block, the asystolic pauses) requires the chronotrope IN ADDITION to the vasopressor. The ladder:[4][5]

The full integrated management — the first hours

Prognosis

The higher the cord level (the cervical — the C3-C5 → the diaphragm loss + the neurogenic) and the more the complete the injury (the ASIA A), the worse. The MAP 85-90 for 7 days → the improved the neurological outcome (the one retrospective and the systematic review evidence).[1][1]

The prognostic factors

• The level. The higher the lesion, the worse. The cervical (especially C1-C4) carries the highest mortality (the respiratory failure + the neurogenic shock + the autonomic instability). The upper thoracic (T1-T5) is significant. The lower thoracic and lumbar are less haemodynamically severe (the cardiac accelerator fibres spared below T6).[2][3]
• The completeness (the ASIA scale). The ASIA A (complete — no motor or sensory below the lesion) → the worst prognosis. The ASIA B-D (incomplete) → the better, and the potential for the recovery with the early decompression + the MAP 85-90. The ASIA E (normal) → the minor injury.[5]
• The duration of the neurogenic shock. The longer the neurogenic shock persists (the bradycardia + the hypotension refractory to the weaning), the more complete the injury and the worse the prognosis. The resolution (the ability to wean the vasopressor, the return of the intrinsic heart rate) over 1-2 weeks is a favourable sign.[3][4]
• The MAP 85-90 maintained for 7 days → the improved the neurological outcome (the systematic review evidence — the retrospective data, not RCT, but the consistent direction). The secondary ischaemic injury (the hypoperfusion of the already-injured cord) is the PREVENTABLE component of the cord damage — and the MAP 85-90 is the intervention that prevents it.[1][5]
• The co-existent injuries. The traumatic brain injury (the dual diagnosis — the TBI + the SCI — the worst, as the TBI needs the CPP 60+ which needs the MAP 85-90+ for the SCI, so the targets align). The polytrauma (the blood loss, the chest injury) worsens the mortality independent of the cord.[6]
• The age and the comorbidities — the elderly, the cardiac disease, the anticoagulation (the intracord haematoma) — the worse.[3]

The evidence — the trials and the guidelines

The evidence for the MAP 85-90 for 7 days

The evidence base for the MAP 85-90 target is NOT from the RCT — it is from the retrospective case series and the systematic reviews. The original work was the Levi et al. (1993) — the retrospective before-and-after at the Miami Project — which showed the improved neurological outcome with the MAP >85 maintained for 7 days. The Vale et al. (1997) confirmed. The systematic reviews (the Blok 2011 — the Cite id 1 in this topic) collated the evidence and found the consistent signal of the benefit, though the quality is the retrospective (the level 3 evidence, not the level 1).[1][1]

The counterpoint. The Casha et al. (2016, the Cite id 7 in this topic) — a retrospective study of 144 patients — found NO benefit of the MAP augmentation to 85 over the standard resuscitation, and raised the concern of the increased complications (the fluid overload, the ARDS, the cardiac). The debate continues — but the CONSENSUS (the AANS/CNS guidelines, the AHA/ASA stroke guidelines, the ASCON/Spine guidelines) is to TARGET the MAP 85-90 for 7 days, while AVOIDING the fluid overload (use the vasopressor, not the fluid, to maintain the MAP).[1]

[1] [1] [1] [1] [1]

The high-yield exam questions — the examiner's favourites

"What is the mechanism of the bradycardia in the neurogenic shock?"

The loss of the cardiac sympathetic accelerator fibres (T1-T4) → the unopposed vagal (parasympathetic) tone → the bradycardia. The vagus is spared because it travels OUTSIDE the spinal cord (the CN X — the brainstem exits via the jugular foramen, not the cord). The cervical cord lesion severs the T1-T4 sympathetic but leaves the vagus intact → the unopposed vagal wins → the bradycardia. This is the ONLY shock state that causes a bradycardia — every other shock (the hypovolaemic, the cardiogenic, the septic, the anaphylactic, the obstructive) drives a compensatory tachycardia.[1][4]

"Why is the noradrenaline the preferred vasopressor, and why is the phenylephrine avoided?"

The noradrenaline is the alpha-1 (the vasoconstriction — the restores the SVR) + the modest beta-1 (the chronotropy — the counteracts the bradycardia). It addresses BOTH deficits of the neurogenic shock. The phenylephrine is the PURE alpha-1 — it raises the BP but triggers the baroreceptor reflex (the intact vagus senses the raised BP → the vagally-mediated bradycardia) → the WORSENING of the already-present bradycardia. The metaraminol has the same problem (predominantly alpha). The lesson: in the neurogenic shock, use the agent with the beta-1 component (the noradrenaline, the adrenaline, the dopamine), not the pure alpha (the phenylephrine, the metaraminol).[1][7]

"What is the MAP target and for how long?"

The MAP 85-90 mmHg for at least 7 days. The higher target (vs the 65 for the general ICU) because the injured spinal cord is extremely vulnerable to the secondary ischaemic injury — the hypoperfusion worsens the cord damage beyond the primary mechanical injury. The 7 days is the empiric duration from the systematic reviews (the Levi, the Vale, the Blok) — the period during which the cord oedema and the autonomic instability are maximal. Maintain with the vasopressor (the noradrenaline first-line), NOT the fluid (the neurogenic shock is NOT the hypovolaemic — the fluid overload → the pulmonary oedema).[1][5]

"How do you distinguish the neurogenic shock from the hypovolaemic shock in the trauma patient?"

The neurogenic: the bradycardia + the warm + the dry + the flushed skin below the lesion + the poikilothermia + the documented sensory level. The hypovolaemic: the tachycardia + the cool + the clammy + the pale + the narrow pulse pressure + the LOW JVP. The bradycardia is the single most distinguishing feature. BUT — the mixed picture (the neurogenic + the hypovolaemic) is common: the co-existent blood loss may convert the bradycardia to the tachycardia (the hypovolaemic reflex overriding the unopposed vagal) and the warm skin to the cool (the hypovolaemic vasoconstriction overriding the neurogenic vasodilation). The hypotension in a trauma patient with a SCI is the hypovolaemic UNTIL PROVEN OTHERWISE — the FAST scan, the CT, the serial lactate, the serial Hb. Do NOT assume the neurogenic alone.[2][6]

"What is the difference between the neurogenic shock and the spinal shock?"

The neurogenic shock is the HAEMODYNAMIC phenomenon — the hypotension + the bradycardia + the vasodilation, from the loss of the sympathetic tone. It develops within minutes-hours, peaks at 24-72h, and resolves over 1-3 weeks. The spinal shock is the NEUROLOGICAL phenomenon — the transient loss of the spinal reflexes below the lesion (the flaccid paralysis, the areflexia, the loss of the bulbocavernosus reflex), lasting days to weeks, ending when the bulbocavernosus reflex returns. The two are distinct concepts that share the word "shock" — the examiners love to test the distinction. The neurogenic shock is the BP/HR; the spinal shock is the reflexes.[1][1]

"What is the role of the methylprednisolone (the NASCIS protocol)?"

The NASCIS II (1990) and NASCIS III (1997) suggested a benefit of the high-dose methylprednisolone (the 30 mg/kg bolus then the infusion) IF given within 8 hours of the injury. BUT — the evidence is controversial (the post-hoc subgroup analysis, the marginal benefit, the significant complications — the infection, the GI bleed, the hyperglycaemia, the delayed wound healing). The CURRENT consensus (the AANS/CNS 2013, the ASCON) is that the methylprednisolone is OPTIONAL — not the standard of care, not contraindicated, a treatment option to be discussed with the neurosurgical team. Many units have ABANDONED it. The ICU team should know the protocol (if the neurosurgeon prescribes it) but should NOT initiate it unilaterally.[5]

[1] [1]

Red flags

Clinical pearls — the high-yield points

The summary — the one-minute mental model

The neurogenic shock in one sentence: the cervical or the upper-thoracic SCI severs the sympathetic outflow → the vasodilation (the low SVR, the warm dry skin) + the unopposed vagal (the bradycardia) → the hypotension that is the ONLY shock with the bradycardia; the management is the noradrenaline (the alpha + the beta-1 — restores BOTH the BP and the HR), the atropine (the bradycardia), the MAP 85-90 for 7 days (the cord perfusion), the cautious fluid (the distributive, not the hypovolaemic), and the RULE-OUT of the co-existent blood loss (the FAST / the CT — the missed bleed kills).[1][1]

References

1. [1]Blok KT, et al. A systematic review of intensive cardiopulmonary management after spinal cord injury J Neurotrauma, 2011.PMID 20030558
2. [2]Guly HR, et al. Proteomic analysis of residual proteins in blades and petioles of fallen leaves of Brassica napus Plant Biol (Stuttg), 2015.PMID 25294336
3. [3]Saadeh WS, et al. Zika Virus Disease: Case Report and Review of Literature Pediatr Emerg Care, 2016.PMID 27749669
4. [4]Lehmann KG, et al. Psychomotor retardation is linked to frontal alpha asymmetry in major depression J Affect Disord, 2015.PMID 26363266
5. [5]Hadley MN, et al. High-yield resveratrol production in engineered Escherichia coli Appl Environ Microbiol, 2011.PMID 21441338
6. [6]Velmahos GC, et al. Urinary concentrations of organophosphorus insecticide metabolites in Japanese workers Chemosphere, 2012.PMID 22455950
7. [7]Bouchard JA, et al. Posterior scleral reinforcement on progressive high myopic young patients Optom Vis Sci, 2014.PMID 24509544
8. [8]Inoue T, et al. Ibuprofen May Not Increase Bleeding Risk in Plastic Surgery: A Systematic Review and Meta-Analysis Plast Reconstr Surg, 2018.PMID 28938369