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1132 PART 10: The Surgical Patient

microelectrode within a semipermeable membrane at the bedside via the oxygen treatment group. Cerebral microdialysis studies also sug-
140
a cranial bolt or in the operating room, into the brain surface usually gest that after severe TBI, the brain may show signs of ischemia if the
in an area expected to be the most prone to ischemia (Fig. 118-15). CPP trends below 50 mm Hg; however, no significant benefits are appar-
is an alternative way to monitor the effects of ICP on brain tissue ent from elevating the CPP above this threshold. 85,141
Pbt O 2
oxygenation.
monitoring is that a very small
An important limitation of Pbt O 2 TREATMENT OF INTRACRANIAL HYPERTENSION
volume of tissue surrounding the probe, about 1 mm , is sampled.
3
Changes that affect a clinically insignificant (ie, small) area at the elec- Treatment of elevated ICP should take into account the risks of hernia-
trode site can lead to over interpretation of results and clinically signifi- tion, which are determined by the location, asymmetry, and size of the
cant changes that are distant to the small sample area will be undetected. mass lesion as well as the absolute ICP. Herniation can occur at ICP
values (eg, <10-15 mm Hg) 134,135 <20 to 25 mm Hg and pupillary abnormalities have been reported with
In terms of outcome after TBI, low Pbt O 2
142
of longer duration (eg, >30 minutes) are associated with higher mor- ICP values as low as 18 mm Hg. An individualized approach taking
135
tality rates (56% vs 9%) and less favorable neurological outcomes (GOS into account ICP in the context of the clinical exam and CT imaging
84 levels <15 mm Hg lasting ≥4 hours may over time is necessary; however, current Brain Trauma Foundation
4-5). TBI patients with Pbt O 2
136 have also (BTF) guidelines recommend treatment of IH after TBI at an upper
have a 50% mortality. Greater than 5% reductions in Pbt O 2
86
been reported after TBI during patient transport between ICU and the ICP threshold of 20 to 25 mm Hg and maintaining ICP <20 mm Hg.
radiology suite, and the effect appears to be associated with preexisting A recent meta-analysis of trials and case series reported after 1970, in
and reduced lung function. 137 which patients were treated for severe closed TBI, found a consistent
low Pbt O 2
may include high concentrations 12% lower mortality and 6% higher favorable outcomes among the
Treatment aimed at improving Pbt O 2
143
of inspired oxygen, ventilator manipulation, sedation, CPP augmenta- aggressive ICP monitored and treated patients. However, a recently
tion, or ICP reduction. 84,138 Although maintaining Pbt O 2 >25 mm Hg has published multicenter, randomized controlled trial of ICP-directed
been reported to significantly decrease mortality (44% vs 25%) in TBI monitoring in patients with severe TBI did not demonstrate any signifi-
patients treated with a high oxygen concentration protocol, outcome cant difference in outcome versus treatment based on serial neurological
139
103
-directed treatment are inconclusive due to nonrandom- exam and CT imaging. The role of ICP monitoring after severe TBI
studies on Pbt O 2
ized controlled design and lack of medium or longer-term outcome needs reassessment and further study. 103
84 , the goal is to maintain In addition to general measures including head in midline posi-
measures. However, when monitoring Pbt O 2
levels ≥15 mm Hg. 84 tion and elevated to 30° to avoid compromising venous drainage, ICP
Pbt O 2 lowering treatments include sedation, muscle relaxants, CSF drainage,
■ CEREBRAL MICRODIALYSIS hyperventilation, hyperosmolar therapy, neurosurgical decompression,
Cerebral microdialysis is primarily a research technique performed by barbiturate coma, and hypo- or normothermia.
ing room or via burr hole near damaged or “at risk” cerebral cortex to ■ SEDATION, ANALGESIA, AND PARALYTICS
inserting a tiny semipermeable intracranial catheter(s) in the operat-
extract and measure brain metabolites (via dialysis). One study in TBI Although sedatives and sedating analgesics may be avoided in more
patients demonstrated that 100% inspired oxygen within 6 hours of stable patients to allow close monitoring of the neurological examina-
admission was associated with an improvement in metabolic parameters tion, critically ill patients with severe TBI will require sedation to control
including increased brain glucose and decreased glutamate, lactate, and agitation (encephalopathy), reduce pain, improve oxygenation and ven-
lactate/pyruvate ratio but a nonsignificant improvement in outcome in tilation via ventilator synchrony, reduce oxygen consumption, allow for
procedures and imaging, and minimize ICP via sedative and analgesic
effects, decreased cerebral metabolic rate, and decreased CBF. In cases of
refractory intracranial hypertension, high-dose barbiturates (see below)
may be used to reduce ICP by deep suppression of CMR. The effects of
sedatives on blood pressure may be beneficial in controlling systemic
hypertension or deleterious if they result in systemic hypotension with
reduced CPP. After TBI the interrelationships between ICP, hetero-
geneous distribution of autoregulation dysfunction, CBF, and CMR
make the prediction of the effect of decreased CPP difficult. The ability
to regionally monitor cerebral metabolism at the bedside is needed to
assess what are likely individual responses to TBI. In the meantime,
conservative control of parameters and maintenance of homeostasis
are recommended. Critically ill patients, particularly those with SIRS or
sepsis, have a tendency to become hypotensive with sedation and will
need vasopressors along with sedation to maintain the desired MAP/
CPP. Vasopressors should be prepared and ready to infuse just before
sedation in patients with low normal BP or frank hypotension. Bolus
doses of sedative analgesics should be avoided in patients with critical
reductions in intracranial compliance since they have a greater tendency
to decrease MAP and increase ICP. 144,145
The commonly used sedatives are short-acting benzodiazepines such as
) monitor inserted via a bolt into the midazolam and lorazepam. They are used to control agitation and improve
FIGURE 118-15. A. Brain tissue oxygen (Pbt O 2
of 15.3 mm Hg after insertion. Brain tissue oxygen ventilator synchrony. Midazolam is preferred for continuous intravenous
frontal region. B. Monitor showing a Pbt O 2
readings (top number) require an approximately four-hour period after insertion to equilibrate dosing because the stabilizing agent in lorazepam, propylene glycol, may
due to the clearance of microtrauma around the catheter tip. Readings should not be heeded lead to metabolic acidosis when infused for prolonged periods.
prior to this time period. If there is concern about whether the brain tissue oxygen probe is The most widely used narcotic in the acute setting has been mor-
challenge can be performed. With a functioning probe, this phine sulfate and limited studies suggest a high level of analgesic
functioning, a 2-minute 100% Fi O 2
. Brain temperature (bottom number) is efficacy and safety in this setting; however, rebound increase in
challenge will show an appropriate rise in the Pbt O 2
accurate immediately after insertion. CBF and ICP may occur with withdrawal of morphine. Fentanyl
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