Page 1616 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

CHAPTER 118: Head Injury 1135

lateralization, something not studied in the DECRA trial. Bifrontal a strong correlation of duration and degree of hyperthermia with poor
craniectomies may be best reserved for patients with severe edema and outcome. After TBI, brain temperature can be elevated as much as 0.5
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mass effect related to bifrontal contusions. A second randomized, con- to 2°C above core body temperature and can potentiate ischemic neuronal
trolled study, RESCUEicp, is still enrolling patients. This trial involves damage. “Induced normothermia” has been suggested to maintain body
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performing DC after maximal medical management has failed, using a or brain temperatures within normal range (36-37.5°C) during the early
25-mm Hg ICP threshold for treatment. postinjury period. Such cooling has also been effective in reducing ICP
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Despite the paucity of level 1 or 2 evidence, DC is a viable alternative and the differential between brain and body temperature. 194
treatment for IH in select patients with refractory ICP. DC can be used The potential benefits of hypothermia need to be tempered by the
as part of the initial surgery for hematoma evacuation, especially in potential complications and evidence of clinical benefit. The potential
patients who have evidence of severe global brain swelling as evidenced risks of hypothermia include increased susceptibility to cardiac arrhyth-
by effaced or compressed basilar cisterns on computed tomography or mias, infection, and hemodynamic instability. 195-197 There are significant
shift that is disproportionate to the size of the space-occupying mass differences between studies in cooling methods, temperature targets,
lesion. Delayed hemicraniectomy, or secondary hemicraniectomy, can and cooling duration. The major limitations include poorly described
be used in patients who exhibit intractable ICP with maximal medi- randomization, inadequate descriptions of the differences in baseline
cal therapy. Since some third-tier approaches, such as high-dose bar- prognostic factors between groups including baseline temperature and
biturates and moderate hypothermia, require significant monitoring no blinding of outcome assessors. A pseudo-lowering of the admission
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and hemodynamic support, DC can be considered prior to initiating GCS in patients who are baseline hypothermic may lead to misclassifi-
these methods to reduce the therapeutic intensity imposed by medical cation of the severity of TBI and the reported improvements in GOS
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management. attributed to induced hypothermia may not be valid. Prophylactic hypo-
■ BARBITURATES thermia after TBI is not significantly associated with decreased mortal-
ity when compared to normothermic controls. Further clinical trials
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Barbiturates can lower the ICP when surgical and other medical of improved design are underway to determine the potential benefits of
therapies have failed and have been in use for over 75 years. The therapeutic hypothermia in TBI. 199
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main mechanism is by reducing the cerebral metabolic rate leading Currently, we routinely maintain normal body and brain temperatures
to reduced CBF, decreased cerebral blood volume, and hence reduced (as measured by a brain tissue oxygen monitor, Fig. 118-15) in severe
ICP. Barbiturates may also have additional cerebroprotective effects TBI patients for up to a week after injury by placing a surface cool-
including inhibition of free radical-mediated lipid peroxidation and ing device when temperatures are noted to rise. Intravascular cooling
excitotoxicity. However, there are no randomized prospective trials catheters have also been used with good effect. 193,194 Hypothermia and
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that indicate, beyond the known reductions in ICP, an improvement in induced normothermia can mask infection, and cultures are drawn
neurological outcome. 105,146 when the cooling device temperature is disproportionately low, indicat-
After TBI, high-dose barbiturate administration is recommended to ing a greater effort by the device to cool the patient. As an advantage
control IH refractory to maximum standard medical and surgical treat- over moderate hypothermia, induced normothermia does not require a
ment but not as prophylaxis to prevent elevated ICP. This is based slow rewarming phase and can be discontinued after much of the threat
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on two randomized control trials of early, prophylactic administration of intracranial hypertension has passed.
of pentobarbital after TBI that reported no significant improvement in
outcome, but a much higher incidence of hypotension or increased
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mortality with diffuse injury in the pentobarbital treated group. VENOUS THROMBOEMBOLISM PROPHYLAXIS
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Patients with refractory IH post severe TBI (GCS of 4-8) given high-
dose barbiturates were twice as likely to achieve ICP control and those TBI is the second highest risk factor for the development of venous
achieving ICP control had lower mortality. 98 thromboembolism (VTE), second only to acute spinal cord injury. The
The most common barbiturate used is pentobarbital. The load- risk of developing VTE after TBI is estimated to be about 3% to 5% in
ing dose for refractory IH is pentobarbital 10 mg/kg over 30 minutes patients that receive pharmacologic prophylaxis within the first 2 days
followed by a maintenance dose of 1 mg/kg per hour with further titra- after TBI and up to 15% when initiation of pharmacologic prophylaxis
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tion to achieve burst suppression on EEG, an indicator of near-maximal is delayed beyond 48 hours. In a recent study of 939 patients post-
reduction in cerebral metabolism and hence CBF. Hemodynamic TBI treated with mechanical prophylaxis and 677 followed with weekly
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monitoring with maintenance of adequate BP is required before and duplex ultrasound scans commencing 7 to 10 days after admission, deep
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during barbiturate therapy. Cardiac output measurements at repeated venous thrombosis (DVT) was present in 31.6%. Patients with head
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intervals are advised due to the cardiac depressant effects of barbiturates and extracranial injuries had a higher incidence of DVT (34.3%) than
and this may be an indication to place a pulmonary artery catheter or those with isolated head injuries (25.8%). Older age, males, higher injury
a transpulmonary (thermodilution or lithium dilution) device. In addi- severity scores, subarachnoid hemorrhage, and lower-extremity injury
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tion, such patients can also experience intestinal paresis necessitating were risk factors associated with developing DVT. The incidence of
total parenteral instead of enteral nutrition. pulmonary embolism during the acute hospitalization period after TBI
Sedatives such as propofol can be used to control of ICP but as for has been reported to be 0.38%. 202
any agent it is important to monitor the effect on ICP and CPP—since Despite these VTE risks, TBI patients are at high risk of intracranial
all sedatives can lower BP but also decrease CMR, it is not clear, without bleeding or expansion of posttraumatic intracranial hematomas that
better means to monitor ischemia, that they are of benefit or harm. may require neurosurgical intervention or result in death. Mechanical
prophylaxis with elastic stockings (ES) or intermittent pneumatic com-
pression devices (IPC) prevents sizable numbers of nonfatal VTE events,
PROPHYLACTIC HYPOTHERMIA at the expense of skin complications, but without increasing bleeding
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AND INDUCED NORMOTHERMIA risks and is recommended for all patients with severe TBI. The
current recommendations for VTE prophylaxis post-TBI are mechanical
The rationale for hypothermia after TBI includes lowering of ICP and prophylaxis, preferably with IPC, over no prophylaxis when not contra-
neuroprotection. Preventing pyrexia, or systemic hyperthermia, within indicated by lower-extremity injury. Mechanical prophylaxis via IPC
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the first few days to 1 week after TBI is an important consideration in criti- is safe and does not appear to increase ICP. Mechanical prophylaxis is
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cal care management. Studies have shown that hyperthermia can nega- effective at reducing the incidence of DVT after TBI. 203,205
tively affect outcome in patients with stroke and TBI. 190-192 A retrospective However, VTE prophylaxis with pharmacological agents is more
analysis of 1626 patients in the Chinese Head Trauma Data Bank showed effective than mechanical measures alone. Pharmacologic prophylaxis

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