Dr Eanna Mac Suibhne

Peer review and editor: Dr Luke Phillips

Welcome to Fast Fridays – a case-based, rapid review of a topic. The cases have been adapted from real patients but have been changed for anonymity and to emphasise key learning points. 

The Case

A 30 year old  bricklayer has fallen 3m off scaffolding onto the hard ground below and has been unable to mobilise since the incident. The patient presents complaining of back pain with associated altered motor function and sensation to his lower limbs.  

He is GCS 15 and his vital signs read a BP 80/40 mmHg, Heart Rate 47bpm, Oxygen Saturations of 100% on room air and his temperature is 37 degrees Celsius. He has warm hands and feet. 

On examination you notice that power of his lower limbs is 0/5 in all myotomes and he cannot appreciate sensation below the dermatome level of T4.  

What is the likely source of this patient’s shock?

You saw spinal trauma in the blog title and went straight for neurogenic shock, and you are right…however, following a mechanism such as this, it is important to rule out other sources of shock in trauma. Common things being common, ongoing bleeding and the resultant haemorrhagic shock will most often be the culprit. Things that may go against this are the patient’s heart rate and their warm peripheries. 

It follows that resuscitation management priorities should continue along these lines until occult haemorrhage has been definitively ruled out. Falling into the tunnel vision trap in a scenario such as this can easily happen. So, following a rehearsed approach to trauma care is pivotal to ensuring a comprehensive assessment of the patient’s injuries. 

Spinal vs Neurogenic shock: same thing, right?
These terms are often, incorrectly, used interchangeably.  

Neurogenic shock is a form of distributive shock and results from the spinal cord injury disrupting autonomic pathways. This results in a decrease in vascular tone and unopposed parasympathetic stimulation. The outcome of this is hypotension, bradycardia and poikilothermia. The level of injury required for neurogenic shock to occur is usually above T6.  

Spinal shock, which is akin to a concussive injury of the spinal cord is a mimicker of a complete spinal cord injury and produces complete neurological dysfunction distal to the site of injury. The neuropraxia can often last hours- weeks.  

Figure 1 – Neurogenic shock is the result, in most cases, of the high spinal cord injury (above T6) that presents with medullary shock (plegia or paresis), hyperextensibility and hypo or deep osteotendinous and superficial cutaneous injury below the lesion. There are also reports of trauma to the lumbar spinal cord.


The patient is still hypotensive, what are the management priorities?

Before considering circulation, ensure that there is a plan in place from an airway viewpoint. If a patient has sustained a SCI above C5, close monitoring of respiratory efficacy is needed and a definitive airway is likely to be required as diaphragmatic function will be compromised. 

Options for hypotension with neurogenic shock involve fluid boluses as first line with escalation to vasopressor and inotropic support as second line. Fluid administration compensates for the vasogenic dilation that occurs. When considering second line options, no single agent is recommended. Noradrenaline, is an agent which boasts both alpha and beta (weak) action and treats both hypotension and bradycardia. A popular choice. Adrenaline could be considered if the patient is profoundly bradycardic.  

Recommendations vary, but, keeping the mean arterial pressure (MAP) at 85 to 90 mmHg for the first 7 days is optimal to enhance spinal cord perfusion and prevent secondary injury(1). Other targets to keep in mind are those of maintaining organ perfusion (normal mentation, warm peripheries, urine output >0.5 mL/kg/h)(2). Boluses of atropine 0.6mg can also be your friend here in the short-term.  

How do I describe a Spinal Cord Injury?

We classify spinal cord injuries as primary vs secondary and complete vs incomplete 

A primary injury arises from the immediate effect of the trauma. This occurs through compression, contusion, transection or shearing of the spinal cord. 

Secondary injuries arise following the initial injury and can occur within minutes to hours. This results from spinal cord ischaemia, hypoxia, inflammation, and oedema. Our management priorities are aimed at reducing the evolution of these secondary injuries. 

The examination findings of a complete SCI would involve complete loss of motor and sensory function below the level of the lesion, however bearing in mind that motor and sensory changes can a appear at separate dermatomal and myotomal levels depending on the size and distribution of the associated haematoma. In describing and documenting your findings, you should refer to the standardised assessment tool developed by the American Spinal Injury Association (ASIA). This is a universal classification tool for spinal cord injuries based on a standardized sensory and motor assessment. A copy of the tool can be found here.

Incomplete spinal cord lesions can often be classified into one of three clinical syndromes which are outlined in the table below(2):



A CT has been performed:

Case courtesy of RMH Core Conditions, Radiopaedia.org. From the case rID: 30238

What are the key findings on this image?
Comminuted burst fracture T6. Anterior 1/3 of body is severely displaced anteroinferiorly and to the right, lying anterior and to the right of the upper body of T7.

Moderately large posterior mediastinal/paravertebral haematoma. 

Posterior body is retropulsed with narrowing of spinal canal by approximately 30%. No obvious intracanal haemorrhage. 

The Outcome

Once alternative potential causes for shock were out ruled and our patient was deemed to have neurogenic shock arising from a primary SCI at the level of T6, the neurosurgery team were contacted for input and consideration for urgent decompression. Recent studies reveal a significant greater recovery in patients who had early decompression (<24 h after spinal injury) compared with those who had late surgery (≥24 h after spinal injury), in terms of both motor and sensory function

References and Further Reading:

  1. Andrew,I R Maas et al, Surgical decompression in acute spinal cord injury: earlier is better, The Lancet Nuerology; Volume 20, Issue 2, P84-886, Feb 01, 2021
  2. Agarwal, Y et al, Radiologic Imaging in Spinal Trauma in ISCoS Textbook of Comprehensive Management of Spinal Cord Injuries, Publisher: Wolters Kluwer, May 2015, 
  3. Nickson, Chris.  “Traumatic Spinal Injury Overview, Initial Assessment and Management.” LifeInTheFastLane, March 21, 2012.
  4. Yue JK, Tsolinas RE, Burke JF, Deng H, Upadhyayula PS, Robinson CK, Lee YM, Chan AK, Winkler EA, Dhall SS. Vasopressor support in managing acute spinal cord injury: current knowledge. J Neurosurg Sci. 2019 Jun;63(3):308-317
Eanna Mac Suibhne

Eanna Mac Suibhne

Eanna is an Irish-trained Emergency physician whose interests broadly include trauma, toxicology and sports injury management. The search of experiencing working in an MTC has resulted in sticks being upped and his recent move to Melbourne. The freely available great coffee was a happy coincidence.