phan managment of severe traumatic brain injury
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Management of acute severe traumatic braininjuryAuthorsNicholas Phan, MD, FRCSC, FACSJ Claude Hemphill, III, MD, MASSection EditorMichael J Aminoff, MD, DScDeputy EditorJanet L Wilterdink, MDDisclosures
All topics are updated as new evidence becomes available and ourpeer review processis
complete.Literature review current through:Feb 2012. | This topic last updated:Iun 16, 2011.
INTRODUCTIONTraumatic brain injury (TBI) is the leading cause of death in North
America for individuals between the ages of 1 to 45 [1]. Many survivors live with significant
disabilities, resulting in major socioeconomic burden as well. In 2000, the economic impact
of TBI in the United States was estimated to be $9.2 billion in lifetime medical costs and
$51.2 billion in productivity losses.
One of the major advances over the past two decades in the care of patients with severe
head injury has been the development of standardized approaches that follow international
and national guidelines [2-5]. The intent of these guidelines has been to use existing
evidence to provide recommendations for current care in order to lessen heterogeneity and
improve patient outcomes. Unfortunately, the lack of randomized clinical trials addressing
many aspects of care of the severe TBI patient has meant that the strength of supporting
data for most treatment concepts is relatively weak. Despite this caveat, there is evidence
that treatment in centers with neurosurgical support, especially in settings where protocol-
driven neurointensive care units operate based on the above-referenced guidelines, is
associated with better patient outcomes [6-11]. Many expert panels recommend that
treatment of severe TBI should be centralized in large trauma centers that offer
neurosurgical treatment and access to specialized neurocritical care.
Patients with severe head injury may frequently have other traumatic injuries to internal
organs, lungs, limbs, or the spinal cord. Thus, the management of the patient with severe
head injury is often complex and requires a multi-disciplinary approach and lends itself to
protocol-based treatment and standardized hospital order sets derived from the previously
referenced guidelines.
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This topic discusses the management of acute severe traumatic brain injury. The
epidemiology and pathophysiology of traumatic brain injury, the management of mild
traumatic brain injury, acute spinal cord injury, and other aspects of care of the trauma
patient are discussed separately. (See"Traumatic brain injury: Epidemiology, classification,
and pathophysiology"and"Concussion and mild traumatic brain injury"and"Acute
traumatic spinal cord injury"and"Skull fractures in adults".)
INITIAL EVALUATION AND TREATMENT
PrehospitalThe primary goal of prehospital management for severe head injury is to
prevent hypotension and hypoxia, two systemic insults known to be major causes of
secondary injury after TBI [12-17]. In a meta-analysis of clinical trials and population-based
studies, hypoxia (PaO2
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Patients with TBI should be assumed to have a spinal fracture and appropriate precautions
taken to stabilize and immobilize the spine during transport. (See"Acute traumatic spinal
cord injury".)
A prehospital assessment of the Glasgow coma scale can be helpful for early triage decisions
(table 1).
The prehospital management of the trauma patient is discussed in detail separately. (See
"Prehospital care of the adult trauma patient".)
Emergency departmentIn the early hospital admission phase of patients with severe
head injury, treatment and diagnostic assessment is done according to the ATLS (Advanced
Trauma Life Support) protocol:
Adequate oxygenation (PaO2 >60 mmHg) and blood pressure support (systolic BP
>90 mmHg) continue to be priorities [12]. (See"Emergency airway management in
the patient with elevated ICP".)
Vital signs including heart rate, blood pressure, respiratory status (pulse oximetry,
capnography), and temperature require ongoing monitoring.
A neurologic examination should be completed as soon as possible to determine the
clinical severity of the TBI. The Glasgow coma scale (GCS) is commonly used to
assess and communicate neurologic status in this setting (table 1). A GCS score of 8
or lower is considered a severe TBI. Neurologic status should be continuously
assessed. Deterioration is common in the initial hours after the injury.
The patient should be assessed for other systemic trauma.
A complete blood count, electrolytes, glucose, coagulation parameters, blood alcohol
level, and urine toxicology should be checked.
Efforts to evaluate and manage increased intracranial pressure (ICP) should begin in the
emergency department. Patients with severe TBI (GCS 8) and clinical symptoms
suggesting possible impending herniation from elevated ICP (unilaterally or bilaterally fixed
and dilated pupil(s), decorticate or decerebrate posturing, bradycardia, hypertension,
and/or respiratory depression) should be treated urgently, with head elevation,
hyperventilation, and osmotic therapy (mannitol1 g/kg iv) concurrently with neuroimagingand other assessments. The evaluation and management of increased ICP are discussed in
detail below. (See'Intracranial pressure'below.)
Patients with TBI should be transferred to a hospital with neurosurgical services as soon as
they are hemodynamically stable [6-10].
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NeuroimagingComputed tomography (CT) is the preferred imaging modality in the
acute phase of head trauma and should be performed as quickly as possible. CT scan will
detect skull fractures, intracranial hematomas, and cerebral edema (figure 1A-D). Current
guidelines recommend head CT in all TBI patients with a Glasgow coma scale of 14 or lower
(table 1).
Follow-up CT scanning should be performed if there is any clinical deterioration. Evolution of
CT findings is common and may indicate an alternative treatment approach in a significant
number of patients [29-33].
SURGICAL TREATMENTIndications for emergency surgery after severe head injury are
based upon neurologic status, usually defined by the Glasgow coma scale (GCS) (table 1),
and findings on head CT criteria such as large hematoma volume or thickness and evidence
of mass effect including midline shift (figure 1A).
Epidural hematomaSurgical guidelines recommend evacuation of an epidural
hematoma (EDH) larger than 30 mL in volume regardless of a patient's GCS score; urgent
surgical evacuation is recommended for patients with acute EDH and coma (GCS score 8)
who have pupillary abnormalities (anisocoria) [34]. (See"Intracranial epidural hematoma in
adults", section on 'Management'.)
Subdural hematomaAcute subdural hematomas (SDH) >10 mm in thickness or
associated with midline shift >5 mm on CT should be surgically evacuated, regardless of the
patient's GCS score [35]. In addition, surgery is recommended if the GCS score is 8 or if
the GCS score has decreased by 2 points from the time of injury to hospital admission,and/or the patient presents with asymmetric or fixed and dilated pupils, and/or intracranial
pressure measurements are consistently >20 mmHg. (See"Subdural hematoma in adults:
Prognosis and management", section on 'Acute SDH'.)
Intracerebral hemorrhageSurgical evacuation of a traumatic intracerebral
hemorrhage (ICH) in the posterior fossa is recommended when there is evidence of
significant mass effect (distortion, dislocation, obliteration of the fourth ventricle,
compression of the basal cisterns, or obstructive hydrocephalus) [36].
For traumatic ICH involving the cerebral hemispheres, surgical indications are not as clearlydefined. Consensus surgical guidelines recommend craniotomy with evacuation if the
hemorrhage exceeds 50 cm3in volume, or if the GCS score is 6 to 8 in a patient with a
frontal or temporal hemorrhage greater than 20 cm3with midline shift of at least 5 mm
and/or cisternal compression on CT scan [37].
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Penetrating injurySuperficial debridement and dural closure to prevent CSF leak is
generally recommended [38]. Small entry wounds can be treated with simple closure.
Aggressive debridement and removal of deep foreign bodies such as bone or bullet
fragments have not been shown to be effective in preventing delayed infection. The use of
prophylactic broad-spectrum antibiotics (usually a cephalosporin) is routine in this setting
and is believed to have contributed to the reduced incidence of infection in this setting [39].
Depressed skull fractureElevation and debridement are recommended for open skull
fractures depressed greater than the thickness of the cranium or if there is dural
penetration, significant intracranial hematoma, frontal sinus involvement, cosmetic
deformity, wound infection or contamination, or pneumocephalus [40]. (See"Skull fractures
in adults"and"Skull fractures in children".)
Decompressive craniectomyIn a decompressive craniectomy, a substantial portion of
the skull is removed in order to reduce increased intracranial pressure (ICP). This can bedone in combination with an evacuation procedure or as a primary treatment for increased
ICP [41]. Use of this technique is controversial and its efficacy in TBI is uncertain [42-46].
Clinical trials are in progress, with a pilot study in children suggesting favorable results on
both ICP and clinical outcome [47].
A randomized trial in 155 adults with severe diffuse TBI with elevated ICP refractory to
other therapies compared bifrontal decompressive craniectomy with continued standard
care [48]. Surgery was associated with decreased ICP and shorter stays in the intensive
care unit, but worse outcome on the extended Glasgow outcome scale at six months. The
study has been criticized for having a baseline imbalance in TBI severity between the
treatment groups, a relatively low threshold for elevated ICP, and a short time window for
defining it to be treatment resistant [49]. Also, the surgical procedure used in this study is
not representative of that most often performed in clinical care. Other clinical trials are in
progress.
This procedure, its complications, and its efficacy in settings other than TBI are discussed in
detail separately. (See"Evaluation and management of elevated intracranial pressure in
adults", section on 'Decompressive craniectomy'and"Decompressive hemicraniectomy for
malignant middle cerebral artery territory infarction".)
INTENSIVE CARE MANAGEMENTThe principal focus of critical care management for
severe TBI is to limit secondary brain injury. In general, treatment efforts are aimed at
intracranial pressure management and maintenance of cerebral perfusion as well as
optimizing oxygenation and blood pressure and managing temperature, glucose, seizures,
and other potential secondary brain insults.
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General medical careMaintenance of BP (systolic >90 mmHg) and oxygenation (PaO2
>60 mmHg) remain priorities in the management of TBI patients in the ICU [12]. These
should be continuously monitored. Isotonic fluids (normal saline) should be used to maintain
euvolemia. A subgroup analysis in the large SAFE study found that for patients with TBI,
fluid resuscitation with albumin was associated with a higher mortality as compared with
normal saline (33 versus 20 percent); this risk was even more pronounced in those with
severe TBI (42 versus 22 percent) [28]. Electrolyte imbalances are common in patients with
TBI and should be regularly assessed along with other laboratory parameters.
Other extracranial traumatic injuries are managed simultaneously. (See appropriate topic
reviews.)
The prevention of deep venous thrombosis (DVT) is a difficult management issue in TBI.
Patients with TBI are at increased risk of DVT which can be reduced by the use of
mechanical thromboprophylaxis using intermittent pneumatic compression stockings[50,51]. While DVT risk can be further reduced with antithrombotic therapy, this has to be
weighed against the potential risk of hemorrhage expansion, which is greatest in the first 24
to 48 hours [52-54]. The use and timing of antithrombotic agents in patients with TBI must
therefore be individualized according to the degree of intracranial bleeding and the
perceived risk of DVT. Observational studies suggest that antithrombotic therapy may not
be associated with the increased risk of intracranial hemorrhage expansion previously
thought to occur in this setting, even when administered early on [55,56]. (See
"Anticoagulant and antiplatelet therapy in patients with an acute or prior intracerebral
hemorrhage", section on 'Prevention of VTE'and"Prevention of venous thromboembolicdisease in surgical patients".)
Nutritional support should not be neglected in patients with TBI. Undernutrition is associated
with higher mortality [57,58]. Patients should be fed to full caloric replacement by day
seven post-injury [59]. (See"Nutrition support in critically ill patients: An overview".)
TBI patients are at risk for other complications (eg, infection, gastrointestinal stress
ulceration), which can be reduced by appropriate interventions. Other aspects of the general
medical care of the trauma patient are discussed in detail separately. (See"Overview of
inpatient management in trauma patients".)
Intracranial pressureElevated intracranial pressure (ICP) is associated with increased
mortality and worsened outcome [60,61]. While ICP monitoring is central to the
management of patients with severe head injury, there have been no large randomized
trials examining the effect of ICP monitoring and treatment on outcome [62,63].
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Specific measures regarding ICP management in the setting of TBI are discussed here. The
evaluation and management of elevated ICP in other settings is discussed in detail
separately. (See"Evaluation and management of elevated intracranial pressure in adults".)
Diagnosis and initial treatmentSeveral approaches are used in the intensive care
setting to prevent and treat elevated ICP. Simple techniques should be instituted as soon as
possible:
Head of bed elevation to 30 degrees
Optimization of venous drainage: keeping the neck in neutral position, loosening
neck braces if too tight
Monitoring central venous pressure and avoiding excessive hypervolemia
Indications for ICP monitoring in TBI are a GCS score 8 and an abnormal CT scan showing
evidence of mass effect from lesions such as hematomas, contusions, or swelling [64]. ICPmonitoring in severe TBI patients with a normal CT scan may be indicated if two of the
following features are present: age >40 years; motor posturing; systolic BP
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Mannitol is administered in boluses of 0.25 to 1 g/kg every four to six hours as
needed. Monitoring of serum osmolality (maintained
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SedationSedative medications and pharmacological paralysis are often used in patients
with severe head injury and elevated ICP. The rationale is that appropriate sedation may
lower ICP by reducing metabolic demand. Sedation may also ameliorate ventilator
asynchrony and blunt sympathetic responses of hypertension and tachycardia. These
possible beneficial effects are counterbalanced by the potential for these drugs to cause
hypotension and cerebral vasodilation that in turn may aggravate cerebral hypoperfusion
and elevate ICP.
Barbiturate coma has been used traditionally in this setting. However, there is little clinical
data to support its use:
In a randomized trial of 73 patients with severe TBI,pentobarbitalcoma was
associated with more effective ICP control compared to control treatment, but not
improved 30-day mortality [83].
Thiopentalwas compared topentobarbitalin a small study of 44 patients with TBI[84]. While thiopental appeared more effective in terms of ICP control, conclusions
drawn from this study are limited by its small size and an imbalance in baseline CT
characteristics in the treatment groups [84].
In addition, high-dose barbiturates often cause hypotension necessitating treatment with
pressor agents [85].Pentobarbitalremains a treatment option for elevated ICP refractory to
other therapies [86]. A loading dose of 5 to 20 mg/kg is given as a bolus, followed by 1 to 4
mg/kg per hour. Continuous EEG monitoring is used, with the pentobarbital infusion titrated
to produce a burst-suppression pattern.
We prefer to usepropofolat our institution because of its short duration of action that
allows intermittent clinical neurologic assessment [87]. Anecdotally, propofol sedation can
produce ICP reductions. Propofol also has putative neuroprotective effects [88]. In one trial,
propofol appeared to be associated with better ICP control and a trend toward better
outcomes compared withmorphinesedation [89]. However, some reports suggest that
patients with TBI are at particular risk of developing the rare, but potentially fatal propofol
infusion syndrome (severe metabolic acidosis, rhabdomyolysis, hyperkalemia, renal failure,
and cardiovascular collapse) [90,91]. As a result, it is suggested that when used in TBI, the
infusion rate of propofol not exceed 4 mg/kg per hour and that patients be monitored for
ECG changes, lactic acidosis, and elevations in creatinine kinase and myoglobin. (See
"Sedative-analgesic medications in critically ill patients: Selection, initiation, maintenance,
and withdrawal", section on 'Available agents'.)
Other sedative agents may also be used, although none have been well studied in patients
with severe TBI. These may include benzodiazepines or opiates (eg,midazolam,morphine,
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fentanyl) individually or in combination with barbiturates and/or neuromuscular blockade
[86,92,93]. (See"Sedative-analgesic medications in critically ill patients: Selection,
initiation, maintenance, and withdrawal".)
In the absence of clinical trial data to support the use of any specific protocol, we suggest
that the use of sedation be individualized according to specific clinical circumstances and
that the choice of agent(s) be similarly individualized, considering also the specific
institutional expertise. Monitoring of cerebral perfusion pressure is advised (see'Cerebral
perfusion pressure'below) to evaluate the somewhat unpredictable effects of these agents
on blood pressure and ICP.
Cerebral perfusion pressureThrough autoregulation, the normal cerebral vasculature
maintains an adequate cerebral blood flow (CBF) across a wide range (50 to 150 mmHg) of
mean arterial blood pressure (MAP). Cerebral autoregulation is disrupted in about a third of
patients with severe TBI [94-96]. In these patients, a rise in MAP can lead to elevated ICPdue to increased cerebral blood volume and hyperemia, while drops in MAP may be
associated with hypoperfusion and ischemia. Patients with impaired cerebral autoregulation
are described as "pressure-passive".
While optimization of CBF is a foundation of TBI treatment, bedside measurement of CBF is
not easily obtained. Cerebral perfusion pressure (CPP), the difference between the mean
arterial pressure (MAP) and the intracranial pressure: CPP = MAP - ICP, is a surrogate
measure. Episodes of hypotension (low MAP), raised ICP, and/or low CPP are associated
with secondary brain injury and worse clinical outcomes [18,19,97].
An early approach to induce hypertension to target CPP >70 mmHg using volume expansion
and vasopressor agents appeared to reduce mortality and morbidity [98,99]. However,
subsequent studies have suggested that this strategy does not improve outcome and rather
risks severe extra-cerebral complications such as acute respiratory distress syndrome [99-
101]. According to guidelines published in 2007, the recommended CPP target is 60 mmHg,
avoiding levels below 50 mmHg and above 70 mmHg [102-104]. In children these
thresholds may be lower, 40 to 65 mmHg [105]. Efforts to optimize CPP should first treat
and maintain ICP at low levels when possible [106]. This may have a more substantial effect
on CBF and obviate the use of fluids and inotropic agents. Patients with more severelyimpaired autoregulation in particular may be more likely to respond to efforts to lower ICP
than to hypertensive-focused CPP therapy [100].
Antiepileptic drugsOverall, the incidence of early post-traumatic seizures (within the
first week or two) is about 6 to 10 percent but may be as high as 30 percent in patients
with severe TBI [107-109]. In addition, case series suggest that about 15 to 25 percent of
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patients with coma and severe head injury will have nonconvulsive seizures identified on
continuous monitoring with electroencephalography (EEG) [109,110]. However, the clinical
significance of clinically silent electrographic seizures and whether they should be treated is
unclear.
The use of antiepileptic drugs (AEDs) in the acute management of TBI has been shown to
reduce the incidence of early seizures, but does not prevent the later development of
epilepsy [111,112]. Reasons to prevent early seizures include the risk of status epilepticus,
which has a high fatality rate in this setting, and the potential of convulsions to aggravate a
systemic injury [109]. In addition, recurrent seizures may increase cerebral blood flow and
could thereby increase ICP. Another potential concern is that seizures place a metabolic
demand on damaged brain tissue and may aggravate secondary brain injury.
Based upon the available information, we use the following approach to seizure
management in patients with severe TBI:
Use a seven-day course of prophylacticphenytoinor valproic acid
Do not use AED prophylaxis long-term
Consider EEG and/or EEG monitoring in patients with coma
Treat both clinical and electrographic-only seizures with AEDs
Post-traumatic seizures and epilepsy are discussed in detail separately. (See"Post-
traumatic seizures and epilepsy".)
Temperature managementFever worsens outcome after stroke and probably severehead injury, presumably by aggravating secondary brain injury [18]. Current approaches
emphasize maintaining normothermia through the use of antipyretic medications, surface
cooling devices, or even endovascular temperature management catheters. However, this
approach has not been systematically tested with regard to clinical outcome.
Induced hypothermiaInduced hypothermia has been a proposed treatment for TBI
based upon its potential to reduce ICP as well as to provide neuroprotection and prevent
secondary brain injury [113]. Induced hypothermia has been shown to be effective in
improving neurologic outcome after ventricular fibrillation cardiac arrest. (See"Hypoxic-
ischemic brain injury: Evaluation and prognosis", section on 'Therapeutic (induced)
hypothermia'.)
A systematic review of 12 randomized controlled trials of mild-to-moderate hypothermia (32
to 33C) following TBI noted a small but significant decrease in the risk of death (RR 0.81,
95% CI 0.69-0.96) or poor neurologic outcome (RR 0.78, 95% CI 0.63-0.98) among more
than 500 patients treated with hypothermia [114]. Other systematic reviews and meta-
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analyses found similar but more borderline benefits for death and neurologic outcome as
well as an increased risk for pneumonia [113,115-117]. Substantial variability among
studies in the depth and duration of hypothermia, as well as the rate of rewarming limit the
ability to draw conclusions from these studies. A subsequently published trial examined the
potential benefit of hypothermia when initiated within two to five hours of TBI in a selected
group of younger patients and found no benefit of treatment on mortality or neurologic
outcomes [118].
A trial of hypothermia therapy in children with TBI showed no improvement in neurologic
outcomes and a nonsignificant increase in mortality [119]. (See"Elevated intracranial
pressure in children", section on 'Hypothermia'.)
Given the uncertainties surrounding its appropriate use, therapeutic hypothermia treatment
should be limited to clinical trials, or to patients with elevated ICP refractory to other
therapies [120,121].
Glucose managementHyperglycemia is associated with worsened outcome in a variety
of neurologic conditions including severe TBI [122-124]. In a retrospective cohort study of
77 patients with severe traumatic brain injury, hyperglycemia (blood glucose 170 mg/dL
[9.4 mmol/L]) at the time of ICU admission was an independent predictor of a poor GCS
score five days later [123].
This has been presumed to be at least in part related to aggravation of secondary brain
injury. Several mechanisms for this are proposed including increased tissue acidosis from
anaerobic metabolism, free radical generation, and increased blood brain barrierpermeability. Increased use of insulin infusions to maintain tight glucose control in critically
ill patients has been studied, but the optimal glucose target and best treatment regimen is
uncertain. One case series using cerebral microdialysis found that tight glycemic control was
associated with reduced cerebral glucose availability and elevated lactate/pyruvate ratio
which in turn was associated with increased mortality [125].
At present, avoidance of both hypo- and hyperglycemia is appropriate, but further studies
are needed to clarify the optimal serum glucose target range and duration of therapy. To
avoid extremes of very high or low blood glucose levels, a broad target range of up to 140
mg/dL or possibly even 180 mg/dL may be appropriate. (See"Glycemic control and
intensive insulin therapy in critical illness".)
GlucocorticoidsThe use of glucocorticoid therapy following head trauma was found to
be harmful rather than beneficial in a large trial of patients with moderate to severe TBI
[126]. More than 10,000 patients within eight hours of presentation were randomly
assigned to treatment withmethylprednisoloneor to placebo. Treated patients had
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increased mortality at two weeks (21 versus 18 percent; RR 1.18) and at six-month follow-
up (26 versus 22 percent; RR 1.15) [127].
Neuroprotective treatmentThe use of a wide range of agents targeting various
aspects of the TBI injury cascade has been tested in clinical trials. To date, no
neuroprotective agents or strategies (including induced hypothermia) have been shown to
produce improved outcome [42]. Based on a positive phase II study, intravenous
progesterone is being tested in a pivotal phase III clinical trial as a neuroprotective agent
for severe head injury [128]. Other agents being investigated include magnesium [129],
citicoline [130], andcyclosporine[131]among others [132].
Erythropoietin has been postulated to have neuroprotective effects. In a retrospective case
control study in 267 patients with severe TBI, matched for both GCS and severity of
systemic injuries, in-hospital mortality was lower among 89 patients treated with
erythropoietin compared with 178 control patients (8 versus 24 percent) [133]. A number ofconfounding factors may have biased these results, which require prospective validation in a
clinical trial before such treatment can be recommended [134]. Such a trial is ongoing.
ADVANCED NEUROMONITORINGIn order to supplement ICP monitoring, several
technologies have recently been developed for the treatment of severe TBI. These
techniques allow for the measurement of cerebral physiologic and metabolic parameters
related to oxygen delivery, cerebral blood flow, and metabolism with the goal of improving
the detection and management of secondary brain injury.
Current monitoring techniques include:
Jugular venous oximetry: retrograde cannulation of the internal jugular vein that
allows measurement of oxygen saturation in the blood exiting the brain [135].
Normal jugular venous oxygen saturation (SjVO2) is about 60 percent. SjVO2 20 mmHg; duration and depth of PbtO2 below
15 mmHg is associated with worsened outcome [136]. One case series used oxygen
supplementation to maintain PbtO2 above 25 mmHg and found better outcomes
compared with historical controls [138].
Cerebral microdialysis: intraparenchymal probe placed similarly to a PbtO2 probe
that allows measurement of extracellular glucose, lactate, pyruvate, glutamate
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[139]. A lactate:pyruvate ratio >40 is suggestive of anaerobic metabolism, which is
believed to exacerbate secondary brain injury.
Thermal diffusion flowmetry: intraparenchymal probe placed similarly to a PbtO2
probe that allows continuous measurement of CBF, usually in the white matter.
Correlation with CBF from neuroimaging and outcome data is very preliminary at
present.
Observational data suggests that these monitoring tools provide unique information that
may help to individualize severe head injury management for patients. Clinical trials are
currently in the planning phases for use of these multi-modality advanced neuromonitoring
approaches.
PROGNOSISCohort studies have suggested that patients with severe head injury (GCS
8) have about a 30 percent risk of death and only about 25 percent achieve long-term
functional independence [61,140,141].
Outcome from severe head injury is dependent on a range of factors including baseline
patient characteristics, severity of TBI, and the occurrence of medical complications and
secondary brain insults. Specific outcome predictors that have been identified from these
factors include [13,16-18,42,61,141-144]:
GCS at presentation (especially the GCS motor score)
CT findings (subarachnoid hemorrhage, cisternal effacement, midline shift)
Pupillary function
Age
Associated injuries
Hypotension
Hypoxemia
Pyrexia
Elevated ICP
Reduced CPP
Bleeding diathesis (low platelet count, abnormal coagulation parameters)
While some have attempted to develop outcome prediction models to guide decisions about
withholding early treatment, the heterogeneity of severe head injury makes this difficult to
apply to clinical decision making in individual patients [142]. Thus, except in the most
extreme cases, a trial of early aggressive neurosurgical and neurocritical care management,
including surgical removal of evacuable lesions and ICP monitoring, should be undertaken.
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SUMMARY AND RECOMMENDATIONSPatients with severe traumatic brain injury (TBI)
are most optimally managed in a specialized neurotrauma center with neurosurgical and
neurocritical care support and the use of guidelines-based standardized protocols.
Prevention of hypoxia (PaO2
-
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ICP first and then MAP (with volume expansion, pressors) second. (See'Cerebral
perfusion pressure'above.)
We recommend short-term (one week) use of antiepileptic drugs (phenytoin,
valproate)for the prevention of early seizures (Grade 1B). (See'Antiepileptic
drugs'above and"Post-traumatic seizures and epilepsy".)
We suggest that fever and hyperglycemia be avoided for their potential to
exacerbate secondary neurologic injury. (See'General medical care'above and
'Temperature management'above and'Glucose management'above.)
We recommend thromboprophylaxis for the prevention of venous thromboembolism
(Grade 1A). The use and timing of antithrombotic agents is individualized based
upon an assessment of the competing risks of venous thrombosis and intracranial
hemorrhage expansion. Patients not receiving antithrombotic therapy should wear
pneumatic compression stockings. (See'General medical care'above.)
We recommend NOT using glucocorticoids for the management of patients with
severe TBI (Grade 1A). (See'Glucocorticoids'above.)
The use of sedative medications should be individualized. Options include
barbiturates,propofol,fentanyl,benzodiazepines, andmorphine.These can be used
individually, in combination, and/or with neuromuscular blockade. Blood pressure,
ICP, and CPP should be monitored as these are somewhat unpredictably affected by
these medications. (See'Sedation'above.)
Use of UpToDate is subject to theSubscription and License Agreement.
REFERENCES
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