Welcome back to the tasty morsels of critical care podcast. This is number 50, so for all 7 of you out there, well done for making it this far especially when you can’t even get CPD points for it.

Today we’ll look at Oh’s Manual Chapter 80 written by the one and only Oli Flower of SMACC and CODA fame.

Like TBI we can split up spinal cord injury into primary and secondary injury. Primary injuries include direct mechanical injury like compression, haematoma, laceration, traction or even complete transection which is thankfully rare.

Secondary injuries include local ischaemia that begins at site but extends progressively in both directions (ie the cord level of injury can get worse). There is loss of autoregulation of blood supply and lots of inflammatory stuff. In addition there is often bleeding into the cord with oedema.

The assessment of SCI is driven by the ASIA score which is a systematic severity assessment tool that includes pictures and tells you what all the dermatomes and myotomes are so you don’t need to actually carry them all in your brain. It is a useful and at this stage well validated tool for motor prognosis that forms the cornerstone of assessing SCI. It spits out a grade A to E which is unhelpfully the opposite of what you want in your A Levels as a grade A is a complete injury with very low chance of recovery. B is described as sensory incomplete, which again is confusingly named as it suggests that there is an incomplete sensory injury but in reality it means a severe motor injury with preservation of sensory function below the level of injury. C and D are varying degrees of motor preservation below the injury and grade E is normal

A further key point to help us speak the language of the spinal surgeons is that of neurological level of injury. The Neurological level of injury = most caudal segment with normal sensory and antigravity (ie 3+ ) motor function. Remember that the neurological level does not usually equal the radiological level as the spinal cord is much shorter than the spinal column.

There are a variety of cord syndromes described that are certainly exam worthy and worth knowing about. The central cord syndrome consists of

weakness and sensory loss in the arms>legs,
the useful mnemonic is MUD (motor, upper, distal)
think hyperextension in a grotty neck with pre existing arthritis
the pathophys here is central ischaemia/haematoma

The anterior cord syndrome looks like

loss of motor, pain, temp below injury.
can also seen in aortic pathology

The brown-seqard syndrome is more notable for teaching anatomy than it is for clinical practice but for completeness look for

ipsilateral loss of motor, proprioception and find touch
contralateral pain and temperature loss

Diagnosis and imaging these days is all about CT and MRI. There is still a robust literature in well done plain films for exclusion of c-spine injury in the lower risk patients, but by now I think everyone has just moved to CT. The controversy in ICU at this stage is whether a CT is sufficient. Oh cites a 4% miss rate for CT, ie injuries not seen on CT that will show up on MRI but more importantly only 0.3% actually need an intervention. CT remains better for bones but MRI is brilliant for cord and ligaments.

In general, from what I have seen, if the patient has a neck but is unconscious, then they end up getting an MRI, generally several days after the original injury and normal CT c spine. This leads to a prolonged and somewhat hard to quantify decrement in the patient’s care as maintaining spinal precautions is challenging in the ICU patient. The EAST group makes a conditional recommendation for clearance of the C-spine following a normal CT c-spine but this doesn’t seem to have made it across the Atlantic to our orthopaedic teams even if it seems our local neurosurgeons have embraced the idea. Bottom line is that this remains a topic of controversy where there is a very small (but not zero) risk of removing the collar without the MRI.

One thing to remember when ordering imaging is vertebral artery injury. While not routine you should have a low threshold for adding an angio when there is a fracture of the transverse foramen, base of skull, facet joint, or preexisiting spinal disease. It is not good form to wake them up two days later to find they’ve stroked from a dissection.

Moving onto management. An incomplete injury with compression on imaging needs urgent decompression. The term “urgent” is somewhat ill defined in this statement but it doesn’t seem to be a 3am urgent in my experience.

Managing an SCI patient in the ICU is best broken up by systems. At least it is for exam purposes.

From a respiratory point of view if it is a high c spine injury, then expect loss of the diaphragm and apnoea, If the diaphragm is preserved then there will still be loss of cough. Somewhat paradoxically, they generally breath better flat rather than upright. When supine the abdominal contents push the diaphragm up giving it mechanical advantage for respiration. Expect to see reduced vital capacity and FRC with atelectasis, reduced chest wall compliance with spasticity of chest wall muscles. There is often wheeze due to sympathetic loss (ie the beta outflow) and 75% of cervical injuries will need intubation. Ventilation is often done with higher Vt (eg 10/kg) to prevent atelectasis and allow lower PEEP (again, giving the diaphragm the advantage). If they are extubatable then extubation to NIV is reasonable. If you have a complete injury above C5 almost all need trache so perhaps best to crack on and do it early. Expect a prolonged wean.

When it comes to haemodynamics, the loss of sympathetic outflow can cause profound vasoplegia, hypotension and bradycardia. Asystole is common with simple suction in first week and then resolves with time rather than a pacemaker typically. Keeping the MAP>85 might help and has some low level data in support and has a guideline recommendation for 7 days post injury. This can often lead to a request for a critical care bed for an otherwise well patient who needs some noradrenaline and an art line to meet the MAP targets. Neurogenic shock is of course a real thing in the immediate post injury phase but as always in the immediate post injury phase you should be thinking bleeding first second and third before considering that as a diagnosis.

Autonomic dysreflexia describes hypertension due to symapthetic stimulation in pts with injuries above T6. It only occurs after the initial period has settled. There is sympathetic vasoconstriction below level of the lesion, and parasympathetic reaction above the lesion (brady, sweating and vasodilation). Bladder and bowel stimuli are the main culprits but remember ureteric stones can also do it. Treatment involves sitting them up and using agents like GTN and captopril. IV SNP andGTN can be used if unresponsive.

Finally, as I’ve gone on too long already, a note on outcomes. Hospital survival is 90%. The clinical exam (ie the ASIA score, even on day 1) rather than things like MRI, remains the best predictor of outcome. There is a 7% conversion from ASIA A (complete) to B (some sensation) at one year with none progressing to C (ie an ASIA A will not get motor recovery). That is indeed a bit miserable but on the brighter side 50% of ASIA B convert to C or D within a year. Even improving a level of injury (ie from a C8 to a C7) will lead to a significant improvement in hand function and ultimately quality of life.

Reading

Oh’s Manual Chapter 80

Anatomy for emergency medicine series on the spinal cord

Eastern Association for Surgery for Trauma 2015 systematic review

THE FORGING TABLE | Romans 3:1-8 (Ep. 855)

Undaunted.Life: A Man's Podcast by Kyle Thompson

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