Head injury

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One way to conceptualise this:
After head injury most patients have a oligaemic cerebral circulation 
due to vasospasm or raised pressure, however some patients have 
cerebral hyperaemia due to loss of local vascular reflexes. To add to the 
confusion patients may move between these states, and different parts 
of the same brain may be in different states.

Dropping CO2 by hyperventilation to cause further cerebral 
vasoconstriction seems like a bad idea if the cerebral circulation is 
already oligaemic. However, in hyperaemia hyperventilation, creating 
some vasoconstriction, may be just the ticket.

Our problem is that we have no easy way of determining the state of 
the cerebral circulation so treatment has to be pretty 'blind'. Trans-
cranial doppler, trans-cranial oximetry and jugular bulb oxygen 
saturations give some idea of the state of the cerebral circulation and 
the effect of treatment - but none are easy or very satisfactory 
(especially acutely).

A high CO2 is probably bad for both groups of patients, so keeping the 
CO2 at the bottom of the normal range is being used as a compromise. 
For an individual patient it may or may not be the optimum level. Until 
we have better neuro-monitoring we will not be able to individualise 
acute treatment.

Tim.
> 
>   Clive,
> 
>   Hyperventilation decreases intracranial volume (and thus, to some
>   degree, pressure) by decreasing cerebral blood flow.  As one might
>   expect, it's not typically a fair trade.
> 
>   Hyperventilation should only be used to achieve eucapnea (PaCO2
>   35-45).  As such, it should only be undertaken in settings where it
>   can be controlled and monitored.
> 
>   Who's still telling you to do it, and under what circumstances?
> 
>   Pret Bjorn
>   Trauma Coordinator
>   EMMC Trauma Program
>   489 State Street
>   Bangor, ME 04401
> 


Timothy J Coats MD FRCS FFAEM
Senior Lecturer in Accident and Emergency / Pre-Hospital Care
Royal London Hospital, UK.

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