Page 1610 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

CHAPTER 118: Head Injury 1129

in the incidence of late PTS, despite therapeutic phenytoin levels in most of there are no clear data to support the use of a particular parameter,
these patients. The adverse drug effects during the first 2 weeks of treat- intervention or device. 5,84-87 As such, the choice of monitor(s) depends
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ment were not significantly different for placebo versus treated patients. on the technology available, the preferences and expertise of the staff,
The overall mortality rates were also not significantly different. Another and individual patient considerations. The integration of information
smaller study also found no significant reduction in late PTS using phe- from multiple monitors in real-time using bioinformatics techniques to
nytoin or phenobarbital prophylaxis. The majority of information is on analyze data has been proposed ; however, improvements in the indi-
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clinically evident PTS. There is a paucity of data concerning nonconvulsive vidual monitoring technologies will also be needed to improve clinical
seizures after TBI 67,68 and studies of the role of continuous electroencepha- care. A brief description of the major bedside neuromonitoring modali-
lography monitoring post TBI and antiseizure therapy are needed. 69,70 ties organized by parameter is provided below.
Currently, antiseizure prophylaxis with phenytoin is recommended
for the prevention of early PTS, that is, within 7 days of the TBI. Routine
prophylaxis later than 1 week following TBI is not recommended. INTRACRANIAL PRESSURE MONITORING
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Levetiracetam is a newer antiepileptic agent that has been evaluated Intracranial pressure (ICP) monitoring remains a cornerstone in neuro-
for prophylaxis in TBI and appears to be effective. 71,72 However, further monitoring after severe TBI. The normal ICP in a supine adult ranges
studies are needed to establish the efficacy of levetiracetam as monother- from 7 to 15 mm Hg. Elevated ICP or intracranial hypertension (IH)
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apy. Phenytoin appears to be more cost-effective than levetiracetam. (ie, ICP >20-25 mm Hg) causes brain injury by ischemic mechanisms
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Levetiracetam may be reserved for patients with adverse reactions to either by reducing cerebral perfusion or causing herniation of brain
phenytoin. tissue, compressing the brain stem and leading to cardiopulmonary
If late PTS occur, they should be managed with the standard approach arrest. IH after TBI indicates severe brain injury and is a major predic-
used for new onset seizures. tor of mortality and neurological morbidity. 90-93 IH occurs in 40% of
■ GLUCOCORTICOIDS patients after severe TBI. After TBI, comatose patients (GCS ≤8) with
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TBI, as with other tissue injuries, is associated with complex inflam- an abnormal CT scan have the highest risk for IH (53%-63%). Patients
with a normal CT scan on admission have a lower incidence of IH
matory pathways involving pro- and anti-inflammatory cytokines, (13%). After TBI, when increases in the mean ICP in 5 mm Hg incre-
5
free radical formation, complement factors, adhesion molecules, and ments were compared against outcome using stepwise ordinal logistic
other pathways. Glucocorticoids have anti-inflammatory properties, regression, a 20-mm Hg cutoff was found to optimally predict poor
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can reduce free radical production, and have been shown to reduce outcome (GOS) in the largest prospectively collected, observational
ICP by reducing vasogenic edema associated with brain tumors ; study to date. Smaller, noncontrolled reports also suggest a range of
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however, there is no evidence that glucocorticoids reduce the cytotoxic 15 to 25 mm Hg. 86,96,97
edema associated with TBI or improve the clinical outcome. 77,78 Trials After TBI, persistent ICP >20 is associated with poor outcome and
using high-dose methylprednisolone, high-dose dexamethasone, there are limited data—class II and III level evidence—that patients
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the synthetic glucocorticoid triamcinolone, and the 21-aminosteroid responding to ICP lowering treatments have a lower mortality and better
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tirilazad have not demonstrated an overall beneficial effect of steroids outcome. 5,97-100 Level II evidence supports ICP monitoring in salvage-
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on outcome. There is level I evidence that high-dose methylpred- able patients after severe TBI that have a GCS ≤8 after resuscitation
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nisolone increases mortality after moderate to severe TBI, although the and have CT evidence of edema, herniation, contusions, hematomas,
cause was not apparent. 78,79 The negative results of corticosteroid trials or compressed basal cisterns or that have a normal CT scan, but are
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may be related to their side effects and trials of more targeted anti- at high risk of developing intracranial hypertension—that is, have two
inflammatory agents are needed. 75 or more of the following on admission: age >40, unilateral or bilateral
■ NEUROMONITORING ISSUES motor posturing, or hypotension (SBP <90 mm Hg). In patients with
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traumatic subarachnoid hemorrhage (SAH), ICP monitoring was the
Severe TBI sets into motion a cascade of injurious events including first indicator of evolving lesions in 20% of the severe TBI group, with
inflammatory, excitotoxic, edema forming and apoptotic processes that 80% of these having operative intervention. Patients presenting with
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result in an imbalance between cerebral oxygen and nutrient supply diffuse axonal injury after TBI, without associated mass lesions, are less
and brain tissue metabolic demand. Intracranial hemodynamics is also likely to develop ICP elevation and may not need ICP monitoring. 102
dependent on alterations in systemic hemodynamics resulting in a very There is no level I evidence, that is, randomized prospective con-
complex milieu. trolled clinical trial, that treatment based on ICP monitoring improves
Prevention of secondary injury via the early detection, treatment, and outcome after TBI. The results of a recently published Washington
5
possible prevention of adverse intracranial pathophysiological events are University-sponsored multicenter, controlled trial of patients aged ≥13
the goals of bedside neuromonitoring. The brain, however, is a very deli- with severe TBI randomized to treatment based upon direct intraparen-
cate structure surrounded by blood vessels and encased within a bony chymal ICP monitoring (target ICP ≤20 mm Hg) versus protocolized
vault and remains very difficult to safely and accurately interrogate at the care based on imaging and clinical examination demonstrated no
bedside. Multimodality neuromonitoring aims to improve the reliability significant between-group difference in survival, impaired conscious-
of information by simultaneously using two or more techniques to assess ness, functional exam at 3 and 6 months post-TBI, or ICU length of stay.
the state of the intracranial environment, the brain, and the response to The use of hyperosmolar agents and hyperventilation was significantly
therapeutic measures or changes in systemic hemodynamics. higher in the imaging and clinical examination group. Thus, for patients
Typical neuromonitors include measurement of ICP—the most com- with severe TBI, it appears that pressure-targeted ICP monitoring is not
monly used neuromonitor in TBI, quantitative or qualitative CBF, jugu- superior to care based on neurological exam and serial CT imaging. 103
). ICP cannot be reliably predicted by physical exam or CT scan alone.
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lar venous bulb oximetry (Sj O 2 ), and brain tissue oxygenation (Pbt O 2
Continuous EEG monitoring can be used in the detection and treat- Treating for presumed intracranial hypertension without actual monitoring
ment of nonconvulsive seizures and status epilepticus. Other potential of ICP may lead to the inappropriate application of hyperventilation,
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monitoring techniques have significant technical limitations (eg, cere- hyperosmolar therapy, or sedation (barbiturates) leading to delete-
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bral oximetry via near infrared spectroscopy [NIRS]) or are primarily rious effects on cerebral blood flow or unnecessary paralytics that may
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research tools (eg, cerebral microdialysis). increase ICU stay. ICP monitoring permits the following of changes
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The parameters to measure, the devices proposed to monitor them, in the intracranial vault in patients who are comatose or sedated and
the integration of this data, and its application to bedside management paralyzed. Monitoring ICP may help detect worsening brain edema and
remain the subject of much clinical and laboratory research. Currently the development of surgical mass lesions and allow for calculation of
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