Even when the mechanism is highly suggestive for significant spinal injury, the shocked major trauma patient is haemorrhaging until proven otherwise; cue blood products and damage control resuscitation.
When there is no evidence of external haemorrhage in the primary survey, the EFAST is negative, and the trauma series CT shows no evidence of bleeding, a diagnosis of neurogenic shock can be considered, particularly if there is obvious focal neurological deficit.
It should always be a diagnosis of exclusion due to it’s rarity; mislabelling a hypovolaemic trauma patient with neurogenic shock will result in a bad outcome very rapidly. Having said that, the nuances of managing neurogenic shock run against the grain when compared to other major trauma principles. Thus, a sound understanding of the underlying pathophysiology is crucial if one fancies him/herself a half-decent traumatologist.
What is neurogenic shock?
Neurogenic shock is distributive in nature, much like septic or anaphylactic shock. It occurs exclusively in patients with spinal cord injuries, and results from loss of sympathetic tone to the heart and vasculature. The unopposed vagal innervation results in a deadly triad of hypotension, bradycardia and peripheral vasodilation.
Sympathetic outflow originates from the lateral horn of spinal cord segments T1 to L2 – the ‘sympathetic cord’. As sympathetic innervation of the heart arises from T1-T5 it is theorised that neurogenic shock can only occur when the spinal cord injury is at T5 or above.
In the haemorrhagic, hypovolaemic major trauma patient, a restrictive fluid regimen is employed as per principles of permissive hypotension; and the fluid of choice should always be a blood product. In contrast, managing the neurogenic shock patient is pretty similar to managing septic shock, minus the antibiotics.
The goals of therapy are to restore and maintain tissue perfusion, and in doing so, prevent secondary cord injury. Unlike other types of distributive shock where the vasculature is ‘leaky’, neurogenic shock is purely vasoplegic with no hypovolaemic component. Therefore, the mainstay of therapy is judicious crystalloid with early vasopressors. Overzealous fluid administration can result in iatrogenic pulmonary oedema.
In real life, these patients are rarely ‘either or’. The multiply injured will usually be juggling haemorrhage, pain and anxiety, which wreak havoc on the vital signs, obscuring the characteristic bradycardia/hypotension combination one would expect to see in neurogenic shock.
It is complex, life threatening, and notoriously difficult to identify.
Recent EMJ paper – Taylor et al, October 2016
An interesting recent EMJ publication tackles this issue by exploring the nature of neurogenic shock presentations in a UK-based major trauma centre over a 3-year period. Appropriate patients were selected from the hospital’s TARN database, and their clinical notes were subsequently interrogated.
Out of 33 patients identified as sustaining a spinal cord injury, only 15 experienced neurogenic shock. This was despite a pretty wide net being cast in terms of criteria; an episode was defined as: systolic blood pressure <100mmHg and heart rate of <80bpm recorded concurrently.
Naturally, this tiny study group prevents any concrete conclusions being drawn from the data, but it’s reflective of the remarkably rare nature of neurogenic shock – which in itself is an important point to appreciate.
Vital signs were looked at from the prehospital and ED environments, which is unique to this study – previous similar publications have only investigated patients in spinal injury units. As such, they found that time of presentation was highly variable in these patients. The earliest appearance of neurogenic shock was 13 minutes post-injury, and the latest appearance was 263 minutes post-injury. In many of the patients that presented later, they had normal vital signs prior to going into neurogenic shock.
Four patients had anatomic lesions below T5 (1 at T9, 3 at L1), which contradicts the theory that neurogenic shock can only occur from spinal cord injuries at T5 and above. The authors suggest that this is explained by the fact that the whole length of the sympathetic cord supplies innervation to the vasculature, and interruption at any level has the capacity to induce shock, independent of heart involvement (i.e. entirely vasoplegic). Two-thirds of patients had cervical cord injuries.
Perhaps predictably, patients with complete spinal cord injuries were significantly more likely to experience neurogenic shock when compared to those with incomplete injuries. However, the authors were unable to identify any clues that predicted severity of neurogenic shock (judged by presence of marked/persistent bradycardia or hypotension); this included type of injury (i.e. complete or incomplete) and vitals when neurogenic shock first presented. However, it’s worth remembering how small the studied cohort was.
Neurogenic shock is an elusive diagnosis to confidently make, particularly when there is a cloudy ‘mixed-shock’ picture. We must remember to consider it in patients with a suggestive mechanism of injury, and appropriately tailor management when it’s likely to be in play.
It’s unpredictable, variable in onset and should be considered in shocked patients with any type of spinal injury, regardless of anatomical level. Awareness of these nuances will improve outcomes.