CTB in OOHCA and rhabdo management

1. What are the indications for a head CT (or other imaging) and an EEG in our patients who have had an OOHCA of a suspected cardiac cause?

2. In patients undergoing treatment for rhabdomyolysis is there a role for alkalinisation of the urine and/or mannitol?


I’ll attempt question 2, based on a recent case summary I wrote. This is my own intepretation of the literature, but I’d be very interested to hear the opinions of others more experienced than me.

The evidence base for any therapy to prevent renal injury in rhabdomyolysis is severely limited by the lack of standard definition of both rhabdomyolysis and acute renal failure. As an example, there is an up to twenty-fold difference in the CK cut-off used to define rhabdomyolysis – >500 U/L vs > 10000 U/L, resulting in very different patient populations.

The main justification for using sodium bicarbonate stems from animal studies dating back to the 1940s and 50s showing that myoglobin precipitates in acidic urine, and that rabbits fed on a diet which produced an acidic urine (and which also caused a reduced baseline urine output) were susceptible to fatal renal failure following IV myoglobin infusion, whereas control animals were not. Subsequent animal studies have variably supported and conflicted with these findings.

No appropriately-designed prospective or retrospective studies in human subjects have shown benefit of sodium bicarbonate administration over aggressive early fluid resuscitation alone, and a few have shown an absence of benefit. There are quite a few papers out there purporting to demonstrate that sodium bicarbonate works, but these are all case series with no control groups and so can’t answer the question being asked. The only three prospective controlled studies, none of which showed benefit, used a combination of sodium bicarbonate and mannitol for the treatment arms.

The pathogenesis of acute kidney injury in rhabdomyolysis is still a matter of some debate, and it’s far from clear that tubular myoglobin precipitation is anything more than an epiphenomenon. It’s possible that urinary alkalinisation might address some of the other hypothesised mechanisms, but again, this hasn’t been demonstrated in practice. It also isn’t at all clear that sodium bicarbonate is terribly effective at alkalinising your urine, depending of course on how much you give and on patient factors. Some retrospective studies have shown no difference in urinary pH between patients receiving and not receiving sodium bicarbonate.

There might, of course, be plenty of other good reasons to give a rhabdo patient sodium bicarbonate – to treat hyperkalaemia, or as a temporising measure for metabolic acidosis. But I don’t think there is any compelling reason to use it, or mannitol, specifically to prevent progression to renal failure.

Best reviews on the subject:

Holt S, Moore K. Pathogenesis of renal failure in rhabdomyolysis: the role of myoglobin. Nephron Experimental Nephrology. 2000;8(2):72-6.

Scharman EJ, Troutman WG. Prevention of kidney injury following rhabdomyolysis: a systematic review. Annals of Pharmacotherapy. 2013 Jan;47(1):90-105.


I think the question of CT and EEG in OOHCA is a complicated and thorny issue, with a lot of personal perspective and opinion overlaying it. However, I will try and summarise my views.
I think there are some not very contentious points:
1. CT is indicated within the first 48 hours for diagnostic (rather than prognostic) reasons. For example, if the arrest was unwitnessed, the presentation was atypical or an alternative/additional pathology is possible. We have had massive PE’s and SAH’s present as OOHCA. Additionally, we have had one OOHCA who managed to fracture their C-spine on the way down.
2. There is no single investigation or examination finding that is definitive. Obviously there are exceptions to this for example a CT that showed tonsillar herniation or massive intra cerebral bleed. However these are not technically OOHCA and don’t occur that commonly. Therefore a multimodal approach is far more robust and fits with current ILCOR recommendations.
3. Clinical examination is the cornerstone of prognostication. Consistently abnormal neurology is far more indicative of eventual poor outcome that early CT or EEG. Absence of neurology (i.e. GCS 3 not doing anything at all) is not the same as presence of abnormal neurology (myoclonic jerking, extensor posturing etc). Giving more time often yields better impressions.

There are some other somewhat more contentious points:
1. EEG can demonstrate “malignant” rhythms- status epilepticus, burst suppression, Generalised supression and alpha coma. 88% of non-survivors will have a malignant EEG
2. Lack of reactivity also adds weight to a dodgy EEG
3. CT done too early may be falsely reassuring, or demonstrate “early hypoxic change” that is not prognostic. However, the later the CT is done and the more severe the changes, the more helpful it becomes. Severe loss of grey-white matter differentiation at 72 hours is a poor feature.
4. There are a number of clinical features that demonstrate poor outcome but they are so devastating that I do not think they add much. For example, loss of pupillary reflex or corneal reflex consistently at 72 hours have a false positive rate approaching 0%. However, this happens very infrequently and is as obvious as saying a patient whose head has come off has a survival rate approaching 0%.
5. Status myoclonus refractory to treatment also has a poor outcome but there is no definition of what status myoclonus is, and what refractory to treatment consists of- I haven’t encountered many myoclonic situations that do not resolve with increasing doses of Keppra.

With these in mind I take the following approach-
a. CT prior to ICU admission only if alternative diagnosis is possible.
b. At least 24 hours of sedation and temperature management post-arrest.
c. Stop sedation and assess neurology first- those that appear to be emerging don’t get any further investigations.
d. Patients who show no neurology get an EEG and CT at the 48-72 hour mark
e. Patients who show abnormal neurology still get an EEG and CT with me, though I am aware that this is not the case with all of my colleagues.
f. The information gained from these three aspects (neurology, CT, EEG) are used in concert with family discussion and previous wishes to determine next steps.
g. MRI is only requested if situation is equivocal or family are unaccepting.


Thanks B, great summary of a sensible treatment pathway.

Just wondered where evoked somatosensory potentials fit into this pathway…….my understanding was that they were a better test than EEG. Are you using them routinely in Leeds?

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