Topic Progress:

Pathophysiology

 

Traumatic Brain Injury (TBI) occurs when a traumatic insult causes the brain to move rapidly inside the skull, causing damage.  Brain function may either be immediately impaired by direct  brain parenchyma damage (primary  injury) or by further cellular damage (secondary injury) which may occur shortly thereafter from the cascade of intracranial events triggered by the initial insult (eg. oedema), or as a result of hypoxia and hypotension. 

TBI can cause traumatic intracranial haemorrhages (extra dural, subdural or subarachnoid) and cerebral oedema which increases the intracranial pressure (ICP).  The Monro-Kellie doctrine (below) is an important principle to understand.

The cranial vault is fixed in size (constrained by the skull) and encases non-compressible CSF and minimally compressible brain tissue.  Any swelling from oedema or an intracranial lesion has nowhere to expand and thus increases the ICP and compromises the cerebral perfusion pressure (CPP).   

 

Cerebral perfusion is highly regulated across a wide range of mean arterial blood pressure, typically between 50 and 150 mmHg by neurohormonal changes in cerebral vascular resistance.  In traumatic brain injury, this autoregulation is grossly disturbed and the relationship between cerebral blood flow and blood pressure becomes more linear.  To prevent secondary injury, we target a CPP.  

CPP = MAP – ICP.

In TBI, the ICP is often higher than the central venous pressure (CVP) which establishes a new gradient of pressure that determines CBF across the vasculature.  This is a pathological state that can remain for many weeks; we assume that by targeting the CPP within the normal range we achieve a satisfactory state of tissue blood flow.  It is important to realise that this is not always guaranteed, and higher CPPs may be necessary in those who have untreated hypertension, where the autoregulatory curve may have moved to the right

 

The graph below demonstrates the relationship between cerebral blood flow and cerebral perfusion pressure.

 

With this basic physiology in mind and thinking about your patient Jake,   what blood pressure would you be aiming for during intubation?  If Jake wasn’t just an isolated head injury (ie. he was a multitrauma with chest and abdominal injuries)  would your blood pressure target be different?

[az_accordion_section] [accordion title=”Answer” id=”acc-1″]You presume that Jake’s intracranial pressure is elevated based on his presentation and posturing. If you estimate that his ICP is around 20 mmHg, to ensure adequate cerebral perfusion (CPP> 60 mmHg), he will need a mean arterial pressure of approximately 80 mmHg. You may not have invasive blood pressure monitoring at the time of intubation, but if not, a systolic blood pressure of approximately 110-120mmHg should ensure an adequate CPP, assuming an elevated ICP. If there is concomitant chest, abdominal or pelvic trauma with haemorrhage, it is a matter of juggling haemorrhage control and circulation with adequate cerebral perfusion pressure. As such, blood pressure parameters are often lower with a systolic blood pressure of 90-100 mmHg an acceptable compromise. [/accordion] [/az_accordion_section]

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