Clinical Case 055: Tolchock to the gulliver

The title for this post comes from Anthony Burgess’ classic dystopian novel A Clockwork Orange.  In the lingo of the novel’s antihero a “tolchock to the gulliver” is a blow to the head – it is a violent, fascinating book, with a great moral.  Check it out if you have not already.  Anyway onto the case…

42 yo. man presents to the ED after a domestic argument resulting in a bit of a brawl.  He was wrestling with his brother-in-law when a ‘bysander’ struck him with a cricket bat to the head.  Being a little bit drunk, and dazed he then layed on the ground fro 5 minutes before getting up to rejoin the party.  Having lost the battle he then drank another 6 cans before vomiting and having a syncopal collapse.

On arrival by ambulance he is very drunk, slurring his words and uncoordinated. An initial GCS is calculated at 13 (E4, V4, M5).  He is a bit combative and not keen to be examined.  He has a small laceration to his right temple with underlying haematoma.  As you try and get some IV access he pulls the blanket over his head and grumbles about the bloke with the cricket bat.

On closer examination – his pupils are symmetrical and reactive.  He has no palpable skull fracture, but a growing haematoma above his ear. No haemotympanum, no Battle’s sign etc.  You leave him in peace for a few minutes to see a sick-looking baby in the next bay.

When you return to the bedside he is drowsy he is now GCS 8 (E1, V3, M4) and maybe his right pupil is a little bigger than the left.  A bedside US of his ONSD shows 7.5mm on the right and 6 on the left (average 6.75mm)… see UltraSound for ICP post

Not good – we need to do something pronto. Broome has a CT machine, but the closest neurosurgeon is ~2000 km away.

Intubation seems like a good idea – he is dropping his GCS and might have an intracranial bleed – he needs either a CT or transfer soon, but both of these need a secure airway.

So here is the first clinical question from this case – what is the evidence for achieving an intubated airway in this scenario?  Which drugs? Strategies for maintaining cerebral perfusion?  Ventilation options?

The concept of pretreatment for intubation of raised ICP / head-injured patient is an old one. The drugs that usually get used are lignocaine or the shorter opiates – fentanyl / remifentanil.  The literature on this is not great – lot of it is looking at ICU-measured ICP in patients during suctioning, or patients with ICP due to  head tumours – not trauma RSI.  The summary of the evidence is that there are not many directly applicable studies out there. Summary: no enough evidence to support routine use lignocaine.

I think most of us are already using an opiate such as fentanyl pre-induction for other reasons.  Evidence for using it in TBI? – once again – no direct evidence.  If you are trying to block the catecholamine surge – then you need big doses – 3mcg/kg.  But beware of the potential for hypotension

If you want detail – check out Brain Lin’s lecture on Neuroprotective RSI via Free Emergency Talks (here).

Most of us are still using some type of paralytic for RSI in trauma / head injury. In the past sux has been used but there has always been the nagging question about tis potential to cause a rise in ICP (hence drop CPP). There was a trend to “pretreating” with a small dose of non-depolarising agent – but this was never really validated in humans. Here is a paper from 2001 that reviewed this question Emerg Med Journ.  Once again – no clear positive evidence, it remains unproven and not recommended.

Now with the trend towards using rocuronium as 1st line in RSI – is this debate obsolete?  Can we just use roc and not worry about the sux issues?

The selection of an appropriate dose is probably the most important factor – you do not want to drop the BP at all, the brain’s perfusion relies on maintaining a decent BP.  The literature on what constitutes a ‘decent BP’ varies but 90 – 100 mmHg are widely used minimum systolic BP you should allow.  [Important note: head-injury means you have to run with a higher MAP than we teach for other trauma ie. 65 mmHg]

Traditionally agents such as thiopentone and propofol have been used in Australia – we do not have etomidate. Ketamine has been widely not used due to the theory that it increases ICP. But what does the evidence show? Flianovsky et al did a nice lit review on the topic in CJEM in 2010 – they concluded it did no harm and had ideal haemodynamic profile to maintain CPP – so no positive evidence, but sounds like a good agent. 

Keep patient head up 20 – 30 degrees

Avoid any constrictive ties / dressings around the neck that can impede venous drainage of the skull

Preferably no CVC in the jugulars

Monitor – BP (MAP), RR, heart rate closely – an arterial line will assist with accurate BP assessment and gas monitoring

Monitor ECG for arrhythmias

OK. That is enough for one post.  Case 055 is to be continued…. oodles of evidence in the next part.  Sorry there is not much in the literature for the stuff above.

Love to hear your comments on the management thus far.

There is a great twitter debate going on if you are keen to follow – @broomedocs  6/6/12





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