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

1. Rutland-Brown W, Langlois JA, Thomas KE, Xi YL. Incidence of traumatic brain injury in theUnited States, 2003. J Head Trauma Rehabil 2006; 21:544.

2. Brain Trauma Foundation, American Association of Neurological Surgeons, Congress ofNeurological Surgeons, et al. Guidelines for the management of severe traumatic braininjury. Introduction. J Neurotrauma 2007; 24 Suppl 1:S1.

3. Maas AI, Dearden M, Teasdale GM, et al. EBIC-guidelines for management of severe headinjury in adults. European Brain Injury Consortium. Acta Neurochir (Wien) 1997; 139:286.

4. Newcombe R, Merry G. The management of acute neurotrauma in rural and remotelocations: A set of guidelines for the care of head and spinal injuries. J Clin Neurosci 1999;6:85.

5. Adelson PD, Bratton SL, Carney NA, et al. Guidelines for the acute medical management ofsevere traumatic brain injury in infants, children, and adolescents. Chapter 1: Introduction.Pediatr Crit Care Med 2003; 4:S2.

6. Patel HC, Bouamra O, Woodford M, et al. Trends in head injury outcome from 1989 to 2003and the effect of neurosurgical care: an observational study. Lancet 2005; 366:1538.

7. Suarez JI, Zaidat OO, Suri MF, et al. Length of stay and mortality in neurocritically illpatients: impact of a specialized neurocritical care team. Crit Care Med 2004; 32:2311.

8. Thillai M. Neurosurgical units working beyond safe capacity. BMJ 2000; 320:399.9. Varelas PN, Conti MM, Spanaki MV, et al. The impact of a neurointensivist-led team on a

semiclosed neurosciences intensive care unit. Crit Care Med 2004; 32:2191.
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