US Neurology - Volume 5 Issue 2

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Brain Trauma
right frontal white matter if there are no focal lesions, or in an area close BP increase (as occurs when pressure autoregulation is impaired), a
to a lesion or contusion if there is focal pathology. The PbtO
2
readings are decision is made balancing the risks of higher ICP and low PbtO
2
based
allowed to settle for one hour before any intervention is planned. FiO
2
is on the absolute values of each. If hemoglobin is less than 10g/dl, we
increased to test the monitor for an appropriate response to PaO
2
. A head transfuse the patient to examine the effect of higher hemoglobin on
CT scan is performed when the patient is stable to confirm the location of PbtO
2
. If ICP is controlled, we allow the PaCO
2
to be maintained at a
the catheter tip. higher level in the hope that this will promote cerebral vasodilation. If the
above methods are not effective, or as a temporary intervention while
Treatment of Low Brain Tissue Oxygen other therapies are prepared, we increase the FiO
2
to increase the partial
Our approach to low PbtO
2
emphasizes individualization of patient care. pressure of oxygen in the tissues.
The type of injury, profiles of ICP and BP, status of pressure auto-
regulation, metabolic dysregulation, and systemic injury/disease are but Interpretation of Other Variables
some of the issues that influence decisions in the individual patient. In In addition to the treatment of low PbtO
2
, we have found the response of
general terms, we begin with a search for a possible reversible cause for PbtO
2
helpful to interpret other monitored variables or interventions. For
low PbtO
2
, such as high or borderline ICP, low CPP, low hemoglobin, low example, high ICP may be due to several factors. If PbtO
2
is also high
PaO
2
, low PaCO
2
, subclinical seizures, or cerebral vasospasm. If there is (especially if transcranial Doppler flow velocities are elevated), this
an apparent cause for low PbtO
2
that can be identified, we address this suggests the high ICP may be due to hyperemia. In this case, lowering
first. In the absence of these, we elevate the CPP by 5–10mmHg and PaCO
2
may be a useful strategy, and monitoring PbtO
2
may add a degree
observe its effect on PbtO
2
and ICP. If PbtO
2
improves and ICP is either of safety while doing this. When transcranial Doppler velocities are
unchanged or marginally increased, we continue at the higher CPP. If elevated, PbtO
2
may help distinguish between hyperemia and vasospasm.
PbtO
2
does not improve, artificial elevation of CPP may not be beneficial Low PbtO
2
in the face of high ICP may be due to the rise in ICP, or both
and only the adverse effects remain. If ICP increases in tandem with the may be caused by a third factor, such as subclinical seizures. n
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