Management of Acute Severe Traumatic Brain Injury

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Management of acute severe traumatic brain injury

Author: Venkatakrishna Rajajee, MBBS
Section Editors: Michael J Aminoff, MD, DSc, Maria E Moreira, MD, Alejandro A Rabinstein, MD
Deputy Editor: Janet L Wilterdink, MD
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Aug 2019. | This topic last updated: Jun 13, 2019.
INTRODUCTION AND DEFINITION
Traumatic brain injury (TBI) is a leading cause of death and disability. In 2013, there were approximately 2.5 million emergency
department (ED) visits, 282,000 hospitalizations, and 56,000 deaths related to TBI in the United States [1]. Many survivors live with
significant disabilities, resulting in major socioeconomic burden as well. In 2010, the economic impact of TBI in the United States was
estimated to be $76.5 billion in direct and indirect costs [2,3]. More severe TBI carries a disproportionately greater economic toll.
The severity of TBI is most commonly graded using the Glasgow Coma Scale (GCS), assessed following the initial resuscitation and
within 48 hours of injury (table 1) [4]. Severe TBI is typically defined by a GCS score <9 [5], while a GCS score of 9 through 12
represents moderate injury and a GCS score of 13 through 15 mild injury [6].
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 [7-10]. The Brain Trauma Foundation (BTF) updated its
guidelines for the management of severe TBI in 2016 [11]. The intent of these guidelines has been to use existing evidence to provide
recommendations for management 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
several treatment concepts is relatively weak. Despite this, there is evidence that treatment in centers with neurosurgical support,
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especially in neurointensive care units that operate based on guideline-driven protocols, is associated with better patient outcomes [12-
19].
Patients with severe head injury may frequently have other traumatic injuries to internal organs, lungs, limbs, or the spinal cord. These
are discussed in separate topic reviews. (See "Initial management of trauma in adults" and "Initial management of moderate to severe
hemorrhage in the adult trauma patient" and "Overview of inpatient management of the adult trauma patient".)
This topic discusses the management of acute severe TBI. The epidemiology and pathophysiology of TBI, the management of mild TBI,
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 "Acute mild traumatic brain injury (concussion) in adults" and "Acute traumatic
spinal cord injury" and "Skull fractures in adults".)
INITIAL EVALUATION AND TREATMENT
Prehospital — The primary goal of prehospital management for severe TBI is the prevention and treatment of hypotension and
hypoxia, two systemic insults known to be major causes of secondary injury after TBI [20-25]. The injured brain is especially vulnerable
to secondary insults in the first 24 hours. In a meta-analysis of clinical trials and population-based studies, hypoxia (PaO2 <60 mmHg)
and hypotension (systolic blood pressure [BP] <90 mmHg) were present in 50 and 30 percent of patients, respectively, and were each
associated with a higher likelihood of a poor outcome: hypoxia (odds ratio [OR] 2.14); hypotension (OR 2.67) [21]. Even low-normal BP
may be associated with poor outcomes. An analysis of 5057 patients with TBI entered into a European trauma registry revealed that the
odds of death tripled with an admission systolic BP <90 mmHg, doubled with a systolic BP <100 mmHg, and were 1.5 times greater
with an admission systolic BP <120 mmHg, after controlling for potential confounders [26].
Changes in prehospital management that aim to normalize oxygenation and BP may be associated with improved outcomes [27-31]:
● Prehospital airway management – Prehospital endotracheal intubation is recommended in patients with TBI and a Glasgow
Coma Scale (GCS) score <9, an inability to protect their airway, or an SpO2 <90 percent despite the administration of supplemental
oxygen [32]. Patients who are not intubated should receive supplemental oxygen as necessary to maintain an SpO2 >90 to 93
percent.

When intubation is indicated but adequate expertise is unavailable, or an attempt at intubation is unsuccessful, bag-mask
ventilation should be performed in conjunction with basic airway-opening maneuvers or airway adjuncts.
The benefit of prehospital intubation is uncertain, with studies finding conflicting results [33]. Large observational studies have not
found a benefit [34] and in some cases found harm to be associated with prehospital intubation [35]. One analysis suggested that
prehospital intubation performed by aeromedical crews (often more experienced in the management of critically ill patients than
ground crews) was associated with better outcomes [36]. In a randomized trial of 312 patients with severe TBI transported by
ground in Australia, prehospital rapid-sequence intubation by paramedics was associated with better functional outcome at six
months compared with intubation in hospital (51 versus 39 percent of patients with favorable outcome on the extended Glasgow
Outcome Scale [E-GOS]) [37].
Thus, the following factors should be considered by emergency medical service (EMS) systems when developing protocols that
address the use of prehospital intubation in patients with severe TBI [34]:
• Appropriate hands-on training of prehospital providers in rapid-sequence intubation, along with ongoing maintenance of skills,
is essential.
• Both hypoventilation and hyperventilation should be avoided following intubation. Quantitative capnography may be useful in
this situation.
• Hemodynamic instability may occur following rapid-sequence intubation, and immediate measures should be taken to correct
hypotension prior to emergency department (ED) arrival.
• While patients with more severe injury and a lower GCS score are more likely to require intubation, the GCS should not be the
sole factor in making decisions on prehospital intubation. Patients with a poor initial neurologic exam will often improve prior to
ED arrival.
Factors that may influence the decision to intubate by a trained provider include:
- Low GCS

- Poor chest rise despite the use of airway repositioning and basic adjuncts (oropharyngeal airway device, nasopharyngeal
airway device, suctioning)
- SpO2 <90 to 93 percent despite the use of supplemental oxygen
- Clinical signs of cerebral herniation (see 'Impending cerebral herniation' below)
- Evidence of aspiration
- Long transport time
• The use of a supraglottic airway device may be lifesaving when intubation is indicated but cannot be performed. (See
"Extraglottic devices for emergency airway management in adults", section on 'Supraglottic airways'.)
Other aspects of prehospital intubation in adult trauma patients are discussed separately. (See "Prehospital care of the adult
trauma patient", section on 'Airway support'.)
● Blood pressure management – Prevention of hypotension in the prehospital setting is best accomplished by adequate fluid
resuscitation using isotonic crystalloids. While hypertonic saline has theoretical benefits, including the need for a lower volume to
achieve intravascular filling in patients with ongoing blood loss, randomized controlled trials in the prehospital setting have not
suggested benefit [38,39].
● Neurologic assessment – 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 GCS can be helpful for early triage decisions (table 1).
Other aspects of the prehospital management of the trauma patient are discussed in detail separately. (See "Prehospital care of the
adult trauma patient".)
Emergency department — In the early hospital admission phase of patients with severe head injury, treatment and diagnostic
assessment are performed according to the Advanced Trauma Life Support (ATLS) protocol. Important considerations specific to TBI
include:

● Endotracheal intubation should be performed at this time for all patients with a GCS score <9, inability to protect the airway,
inability to maintain SpO2 >90 percent despite the use of supplemental oxygen, or clinical signs of cerebral herniation. Adequate
oxygenation (PaO2 >60 mmHg) continues to be a priority. Specific aspects of this procedure in this setting are described
separately. (See "Emergency airway management in the patient with elevated ICP".)
● Vital signs including heart rate, BP, respiratory status (pulse oximetry, capnography), and temperature require ongoing monitoring.
Hypoxia, hypoventilation, hyperventilation, and hypotension are scrupulously avoided [20].
● The patient should be assessed for other systemic trauma, per the ATLS algorithm. (See "Initial management of trauma in adults".)
● A neurologic examination should be completed as soon as possible to determine the clinical severity of the TBI. The GCS is
commonly used to assess and communicate neurologic status in this setting (table 1). The pupillary examination is crucial in the
patient with TBI.
The Full Outline of UnResponsiveness (FOUR) score is an alternative scale for the assessment of patients with severe TBI (table
2) [40]. Potential advantages over the GCS include the ability to grade injury in intubated patients and to assess brainstem
function. Prospective comparisons with the GCS in TBI have suggested an equivalent ability to predict long-term outcomes [41,42].
Neurologic status should be frequently assessed. Deterioration is common in the initial hours after the injury. Interruption of
sedative infusions may be required to obtain an examination that best reflects the actual neurologic status of the patient.
● Evaluation and management of increased intracranial pressure (ICP) should begin in the ED. Immediate lifesaving measures must
be instituted in patients demonstrating clinical signs of impending or ongoing cerebral herniation [43]. These signs include
significant pupillary asymmetry, unilateral or bilateral fixed and dilated pupils, decorticate or decerebrate posturing, respiratory
depression, and the "Cushing triad" of hypertension, bradycardia, and irregular respiration. Patients who fulfill criteria may undergo
placement of an ICP monitor in the ED. (See 'Initial treatment' below and 'Impending cerebral herniation' below and 'ICP and CPP
monitoring' below.)
● A complete blood count, electrolytes, glucose, coagulation parameters, blood alcohol level, and urine toxicology should be
checked. Efforts to reverse a coagulopathy should begin immediately. (See 'Management of coagulopathy' below.)
Patients with TBI should be transferred to a hospital with neurosurgical services as soon as they are hemodynamically stable [12-16].
Neuroimaging — Computed tomography (CT) is the preferred imaging modality in the acute phase of head trauma and should be
performed as quickly as possible, as certain lesions will indicate potentially lifesaving neurosurgical interventions. (See 'Surgical
treatment' below.)
A noncontrast CT scan will detect skull fractures, intracranial hematomas, and cerebral edema (image 1A-D). Current guidelines
recommend head CT in all TBI patients with a GCS score 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 [44-48]. While there is no clear indication for routine follow-up CT
scans in the absence of clinical change or changes in physiologic parameters such as ICP, practice varies considerably in this regard
[49,50]. In the absence of clinical deterioration, repeat imaging in six hours is reasonable in patients with a hematoma present on the
initial scan, particularly in patients with a GCS <9 [51]. Although contrast is not typically used, parenchymal contrast extravasation, as
with spontaneous intracerebral hemorrhage (ICH), may predict a higher risk of hemorrhage progression [52]. (See "Spontaneous
intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis", section on 'Hemorrhage enlargement'.)
Screening for blunt cerebrovascular injury — Injury to the carotid and vertebral arteries most commonly occurs as a result of skull
base or vertebral fractures that involve vulnerable segments of these vessels. While blunt cerebrovascular injury (BCVI) may result in
stroke at the time of injury, a latency of several hours to several days between the trauma and cerebrovascular event is common.
Because antithrombotic therapy during this latent period may prevent subsequent ischemic strokes, BCVI is important to identify.
We use the expanded Denver criteria to identify patients at high risk for BCVI, and perform multislice CT angiography of the head and
neck to screen for such injury (algorithm 1). In patients with severe TBI who have BCVI, we typically initiate aspirin 81 mg daily when
such injury is discovered and if no contraindications exist; anticoagulation with heparin is typically contraindicated in the setting of acute
severe TBI. Other aspects of treatment and monitoring of carotid or vertebral artery injury with or without ischemic stroke are discussed
separately. (See "Blunt cerebrovascular injury: Mechanisms, screening, and diagnostic evaluation" and "Blunt cerebrovascular injury:
Treatment and outcomes".)
SURGICAL TREATMENT

Indications 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 computed tomography (CT) criteria such as large hematoma volume or thickness and
evidence of mass effect including midline shift (image 1A):
● Epidural hematoma – Surgical guidelines recommend evacuation of an epidural hematoma (EDH) (image 1D) larger than 30 mL
in volume regardless of a patient's GCS score; emergency surgical evacuation is recommended for patients with acute EDH and
coma (GCS score ≤8) who have pupillary abnormalities (anisocoria) [53]. (See "Intracranial epidural hematoma in adults", section
on 'Management'.)
● Subdural hematoma – Acute subdural hematomas (SDHs) >10 mm in thickness or associated with midline shift >5 mm on CT
should be surgically evacuated, regardless of the patient's GCS score (image 1A) [54]. 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 if the patient
presents with asymmetric or fixed and dilated pupils, or intracranial pressure (ICP) measurements are consistently >20 mmHg.
(See "Subdural hematoma in adults: Prognosis and management", section on 'Acute SDH'.)
● Intracerebral hemorrhage – Surgical evacuation of a traumatic intracerebral hemorrhage (ICH) in the posterior fossa is
recommended when there is evidence of significant mass effect (brainstem compression, obliteration of the fourth ventricle,
effacement of the basal cisterns, or obstructive hydrocephalus) [55].
For traumatic ICH involving the cerebral hemispheres (image 1C), surgical indications are not as clearly defined. Consensus
surgical guidelines recommend craniotomy with evacuation if the hemorrhage exceeds 50 cm3 in volume, or if the GCS score is 6
to 8 in a patient with a frontal or temporal hemorrhage greater than 20 cm3 with midline shift of at least 5 mm and/or cisternal
compression on CT scan [56].
● Penetrating injury – Superficial debridement and dural closure to prevent cerebrospinal fluid (CSF) leak is generally
recommended [57]. 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 is routine in this setting and is believed to have contributed to the reduced incidence of
infection [58]. (See "Skull fractures in adults", section on 'Penetrating injuries'.)

● Depressed skull fracture – Elevation 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 [59]. (See "Skull fractures in adults", section on 'Depressed
fractures' and "Skull fractures in children: Clinical manifestations, diagnosis, and management".)
● Refractory intracranial hypertension – Decompressive craniectomy may be lifesaving in patients with refractory elevations of
ICP. (See 'Decompressive craniectomy' below.)
INTENSIVE CARE MANAGEMENT
A principal focus of critical care management for severe TBI is to limit secondary brain injury. In general, treatment efforts are aimed at
intracranial pressure (ICP) management and maintenance of cerebral perfusion, as well as optimizing oxygenation and blood pressure
(BP) and managing temperature, glucose, seizures, and other potential secondary brain insults.
Other aspects of the general medical care of the trauma patient are discussed in detail separately. (See "Overview of inpatient
management of the adult trauma patient".)
Other extracranial traumatic injuries are managed simultaneously. (See appropriate topic reviews.)
Hemodynamic management
● Fluids – Isotonic fluids (normal saline) should be used to maintain euvolemia. Saline may be preferable to albumin; the latter was
associated with increased mortality (42 versus 22 percent, p <0.001) in a post hoc analysis of patients with TBI enrolled in the
SAFE clinical trial, which compared saline with albumin for fluid resuscitation in the intensive care unit (ICU) [60].
While balanced crystalloid solutions (eg, lactated Ringer's and plasmalyte) are used to decrease the risk of acute kidney injury in
other critically ill patients, normal saline is preferred in TBI, since balanced solutions are relatively hypotonic and may worsen
cerebral edema. In the SMART ICU trial comparing saline with balanced solutions in the critically ill, exclusion of patients with TBI
was permitted [61]. Among the TBI patients enrolled in SMART ICU, no benefit was seen with the use of balanced fluids.
Electrolyte imbalances are common in patients with TBI and should be regularly assessed along with other laboratory parameters.

● Blood pressure – The avoidance of hypotension remains a priority in the ICU. Guidelines recommend maintaining the systolic BP
≥100 mmHg for patients 50 to 69 years old and ≥110 mmHg for patients 15 to 49 or >70 years old [11].
● Cerebral perfusion pressure – Through autoregulation, the normal cerebral vasculature maintains an adequate cerebral blood
flow (CBF) across a wide range (50 to 150 mmHg) of mean arterial pressure (MAP). Cerebral autoregulation is disrupted in
approximately one-third of patients with severe TBI [62-64]. In these patients, a rise in MAP can lead to elevated ICP due 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 MAP and the ICP (CPP = MAP – ICP), is a useful surrogate. Episodes of hypotension
(low MAP), raised ICP, and/or low CPP are associated with secondary brain injury and worse clinical outcomes [27,28,65].
A goal CPP of 60 to 70 mmHg is recommended to improve survival and favorable outcomes [11]. Targeting a goal CPP >70 mmHg
appeared to reduce mortality and morbidity in some earlier studies [66,67]. However, subsequent studies have suggested that
routine use of this strategy does not improve outcomes and may increase the risk of acute hypoxic respiratory failure [67-69].
Efforts to optimize CPP should first focus on treatment of ICP elevation [70]. Patients with more severely impaired autoregulation
and suboptimal CPP are best managed with efforts to lower ICP, rather than by elevating MAP with vasopressors; hypertension is
more likely to worsen cerebral edema when protective autoregulation is impaired [68]. (See 'Intracranial pressure management'
below.)
Continuous monitoring of cerebral oximetry or the pressure reactivity index (PRx) may help determine the adequacy of
autoregulation and identify the optimal CPP in individual patients. (See 'Advanced neuromonitoring' below.)
Ventilation — Most patients with severe TBI are sedated and artificially ventilated during the first several days [71]. Since acute
hypercarbia may result in elevations in ICP, and hypocarbia may precipitate cerebral ischemia, the use of end-tidal carbon dioxide
(ETCO2) monitoring should be considered for all ventilated TBI patients. Hypoxia should also be avoided, and the PaO2 maintained >60
mmHg [20].

While hyperventilation can be used to reduce ICP, guidelines recommend avoiding hyperventilation because of safety concerns,
especially in the acute phase (the first 24 to 48 hours) following TBI. Mild to moderate hyperventilation can be considered at later
stages, but PaCO2 of less than 30 mmHg should be avoided, except as a temporary intervention to help resolve ICP crises [72]. (See
'Impending cerebral herniation' below.)
With hyperventilation, PaCO2 decreases, leading to cerebral vasoconstriction, which then results in decreased cerebral blood volume
and ICP. However, hyperventilation-induced vasoconstriction may also cause secondary ischemia and may thereby worsen outcomes
[73-75]. Hyperventilation can also increase extracellular lactate and glutamate levels that may contribute to secondary brain injury [76].
In one randomized study, patients hyperventilated to a PaCO2 of 25 mmHg for five days had a worse clinical outcome than
nonhyperventilated controls [77]. The use of multimodality monitoring of cerebral oxygenation and metabolism should also be
considered when using therapeutic hyperventilation, to monitor its effects and prevent ischemic episodes [74,75,78]. (See 'Advanced
neuromonitoring' below.)
While patients with TBI frequently suffer acute hypoxic respiratory failure and require higher levels of positive end-expiratory pressure
(PEEP), a theoretical concern has been that elevated intrathoracic pressures will hamper venous return from the brain and worsen ICP.
Studies of applied PEEP up to 15 to 20 cm H2O [79-81], as well as ventilator modes such as airway pressure release ventilation
(APRV) [82], have not revealed a consistent effect on ICP, although patients with severe lung injury did demonstrate a small but
statistically significant positive relationship between PEEP and ICP (0.31 mmHg rise in ICP for every 1 cm H2O rise in PEEP) in one
retrospective study [79]. The use of PEEP in TBI patients with acute respiratory distress syndrome (ARDS) does, however, seem to
significantly improve brain tissue oxygenation [81]. Our practice, therefore, is to use PEEP up to 15 to 20 cm H2O, as well as APRV
when clinically appropriate, for the management of ARDS in patients with TBI in conjunction with monitoring of ICP.
Antiseizure drugs and electroencephalography monitoring — Antiseizure drugs are generally recommended to prevent and treat
post-traumatic seizures in the setting of severe TBI. We typically use levetiracetam [83]. Patients with TBI who develop any seizures will
require ongoing antiseizure therapy. The duration of antiseizure drug therapy in severe TBI patients who do suffer seizures is not well
established; this is discussed separately. (See "Post-traumatic seizures and epilepsy", section on 'Management'.)
The incidence of early post-traumatic seizures (within the first week or two) may be as high as 30 percent in patients with severe TBI
[84-86]. In addition, case series suggest that approximately 15 to 25 percent of patients with coma and severe head injury will have
nonconvulsive seizures identified on continuous monitoring with electroencephalography (EEG) [86-88]. While the clinical significance
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of clinically silent electrographic seizures is unclear, we monitor patients with EEG if there is persistent impaired consciousness that is
disproportionate to the extent of injury visible on imaging. We generally continue antiseizure drugs if there are electrographic seizures.
The assessment and treatment of nonconvulsive status epilepticus is discussed separately. (See "Nonconvulsive status epilepticus",
section on 'Treatment'.)
The use of antiseizure drugs 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 [89,90]. 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 [86]. In addition, recurrent seizures may
increase CBF 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.
While certain guidelines recommend phenytoin to prevent early post-traumatic seizures for the first seven days following injury [11], we
prefer levetiracetam in this setting. Studies of phenytoin use in other conditions such as subarachnoid hemorrhage have revealed an
adverse association between higher cumulative dosing of phenytoin and worse long-term functional and cognitive outcomes [91]. A
randomized clinical trial that compared levetiracetam with phenytoin for seizure prophylaxis in neurosurgical ICU patients (89 percent
with TBI) revealed equivalent efficacy for seizure prevention but improved six-month functional outcomes with levetiracetam [83]. A
subsequent single-center randomized clinical trial did not demonstrate a reduction in inpatient adverse events with levetiracetam
compared with phenytoin, but did not assess long-term functional outcomes [92]. A subsequent meta-analysis that included
observational studies revealed fewer adverse drug events with levetiracetam [93].
Post-traumatic seizures and epilepsy are discussed in detail separately. (See "Post-traumatic seizures and epilepsy".)
Venous thromboembolism prophylaxis — Patients with TBI are at increased risk of venous thromboembolism (VTE). We initiate
mechanical prophylaxis with intermittent pneumatic compression on admission for all patients with TBI, and chemoprophylaxis with
either unfractionated heparin 5000 units three times daily or with enoxaparin 40 mg daily 24 hours following admission in most TBI
patients with stability confirmed on repeat imaging.
The efficacy and safety of mechanical thromboprophylaxis using intermittent pneumatic compression is discussed separately [94,95].
(See "Prevention of venous thromboembolic disease in adult nonorthopedic surgical patients".)

While VTE 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 [96-98]. Data examining this trade-off in patients with severe TBI are limited.
While some observational studies suggest that antithrombotic therapy may not be associated with increased risk of intracranial
hemorrhage expansion [99-101], others have found a higher rate of hemorrhage progression with the use of low molecular weight
heparin [102]. One pilot study randomly assigned 62 patients with low-risk TBI to enoxaparin or placebo [103]. Subclinical, radiographic
progression of intracranial hemorrhage was nonsignificantly more common in the treated patient group; no patient suffered a clinical
progression; one patient in the placebo group developed deep vein thrombosis (DVT). A more recent meta-analysis of clinical trials and
observational studies concluded that the use of pharmacologic VTE prophylaxis was safe when initiated within 24 to 48 hours of injury
in TBI patients with stability demonstrated on repeat imaging [104]. (See "Prevention of venous thromboembolic disease in adult
nonorthopedic surgical patients".)
Management of coagulopathy — Coagulation parameters should be measured in the emergency department (ED) in all patients with
severe TBI, and efforts to correct any identified coagulopathy should begin immediately.
Approximately one-third of patients with severe TBI demonstrate a coagulopathy, which is associated with an increased risk of
hemorrhage enlargement, poor neurologic outcomes, and death [105-110]. The coagulopathy may result from existing patient
medications such as warfarin or antiplatelet agents. Acute TBI is also thought to produce a more subtle coagulopathy through the
systemic release of tissue factor and brain phospholipids into the circulation leading to inappropriate intravascular coagulation and a
consumptive coagulopathy [110-112].
● Patients taking warfarin may be managed with prothrombin complex concentrate (PCC) and vitamin K as recommended for
patients with warfarin-associated intracerebral hemorrhage (ICH). (See "Reversal of anticoagulation in intracranial hemorrhage".)
Reversal of direct oral anticoagulants is discussed separately. (See "Management of bleeding in patients receiving direct oral
anticoagulants", section on 'Major bleeding'.)
● In patients with thrombocytopenia, some centers choose to maintain a platelet count >75,000/microL with platelet transfusions if
necessary. In one cohort analysis, a platelet count of <135,000/microL was associated with a 12.4 times higher risk of hemorrhage
expansion, while a platelet count of <95,000/microL identified patients who were 31.5 times more likely to require neurosurgical
intervention [113]. There is insufficient evidence at this time to support the routine use of a specific goal platelet count.

The utility of platelet transfusions in TBI patients who arrive on antiplatelet medications is not known, although the incidence of
neurologic worsening is greater in such patients [113,114]. (See "Use of blood products in the critically ill", section on 'Platelets'.)
Recommendations for coagulation reversal in other categories of patients with severe TBI are limited by lack of evidence [115]. When a
coagulopathy is identified, it is reasonable to use fresh frozen plasma (FFP), PCC, and/or vitamin K as for warfarin reversal. A
reasonable, if somewhat arbitrary, target is an international normalized ratio (INR) <1.4. A phase II dose-escalation clinical trial of
recombinant factor VIIa in TBI patients demonstrated a nonsignificant trend towards limiting hematoma expansion but no mortality
benefit, although this was not directed exclusively at patients with TBI-related INR elevation [116].
Hemostatic therapy in noncoagulopathic patients with severe TBI is discussed separately. (See 'Hemostatic treatments' below.)
Glucose management — Avoidance of both hypo- and hyperglycemia is appropriate in patients with severe TBI, 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, we target a range of 140 to 180 mg/dL. (See "Glycemic control and intensive insulin therapy in critical illness".)
Both hyper- and hypoglycemia are associated with worsened outcome in a variety of neurologic conditions including severe TBI [117-
119]. 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 barrier
permeability.
We do not use intensive insulin therapy to target a glucose level between 80 to 110 mg/dL. 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 [120]. Moreover, this approach is associated with a greater risk of
hypoglycemia and worse outcomes in other critically ill patients. (See "Glycemic control and intensive insulin therapy in critical illness".)
Temperature management — Fever should be avoided. Fever is associated with worse outcome after stroke and probably severe
head injury, presumably by aggravating secondary brain injury [27]. Fever also worsens ICP control through an increase in metabolic
demand, blood flow, and blood volume.
Maintenance of normothermia should be attempted with the use of antipyretic medications, surface-cooling devices, or endovascular
temperature management catheters. While induced normothermia using endovascular cooling and a continuous feedback-loop system

has been shown to lower the fever burden and improve ICP control following TBI [121], this approach has not been systematically
tested with regard to clinical outcome. Our preference is to use surface cooling with adhesive pads and continuous feedback-loop
regulation to maintain normothermia in patients with severe TBI and elevated ICP.
Shivering may complicate these treatments and can increase metabolic demand and worsen brain tissue oxygenation [122]. The
management of shivering is discussed separately. (See "Post-cardiac arrest management in adults", section on 'Sedation and
suppression of shivering'.)
Noninduced hypothermia has been associated with an increase in mortality after TBI [123], but the efficacy of efforts to avoid this
complication has not been evaluated.
The role of therapeutic induced hypothermia is discussed separately. (See 'Hypothermia' below.)
Paroxysmal sympathetic hyperactivity — Previously referred to as "sympathetic storms," paroxysmal sympathetic hyperactivity
(PSH) is characterized by episodes of hypertension, tachycardia, tachypnea, hyperthermia, diaphoresis, increased tone, and posturing,
of varying severity [124]. This phenomenon, which is thought to be a result of disinhibition and sympathetic release, occurs in
approximately 10 percent of patients with TBI [125-127]. The occurrence of PSH correlates with severity of injury and predicts
increased length of stay and worse outcomes [125,128].
Our preference is to use intermittent doses of midazolam and fentanyl to abort severe PSH episodes that last longer than a few
minutes. In patients with recurrent episodes, we typically initiate therapy with a nonselective beta blocker that crosses the blood-brain
barrier, such as propranolol, at a starting dose of 10 mg thrice daily, in conjunction with an alpha-2 receptor agonist such as clonidine,
at a starting dose of 0.1 mg twice daily [129]. The use of these agents is frequently limited by hypotension. We use a combination of
gabapentin (starting dose 100 to 300 mg thrice daily) and bromocriptine (starting dose 1.25 to 2.5 mg twice daily) in patients who do not
tolerate propranolol and clonidine. Others have also reported success in using these agents in individual patients [124-128].
Nutritional support — Guidelines recommend that basic nutritional goals be attained no later than five to seven days from injury, and
that transpyloric enteral nutrition be considered to decrease the rate of ventilator-associated pneumonia [11,130]. There is some
evidence that early enteral nutrition may decrease rates of pneumonia [131] as well as mortality [132] following TBI, although a
randomized controlled trial did not demonstrate a reduction in complications [133]. (See "Nutrition support in critically ill patients: An
overview".)
INTRACRANIAL PRESSURE MANAGEMENT
Elevated intracranial pressure (ICP) is associated with increased mortality and worse outcome [134-136].
Specific measures regarding ICP management in the setting of TBI are discussed here. The evaluation and management of elevated
ICP in other settings are discussed in detail separately. (See "Evaluation and management of elevated intracranial pressure in adults".)
A tiered approach to management of elevated ICP in severe TBI is shown in the algorithm (algorithm 2).
Initial treatment — Simple techniques should be instituted as soon as possible:
● Head of bed (HOB) elevation to 30° to permit adequate venous drainage from the brain while not compromising cerebral perfusion
● Optimization of venous drainage: keeping the neck in neutral position, loosening neck braces if too tight
Impending cerebral herniation — All patients should be quickly assessed for impending cerebral herniation; such assessments
should be performed every one to two hours in the first days after severe TBI. Clinical signs of impending herniation include significant
pupillary asymmetry, unilateral or bilateral fixed and dilated pupils, decorticate or decerebrate posturing, respiratory depression, and the
"Cushing triad" of hypertension, bradycardia, and irregular respiration. In such patients, the following measures must be taken
immediately:
● Endotracheal intubation, if not already performed, keeping in mind the specific considerations outlined above. (See 'Emergency
department' above.)
● Elevation of the HOB to 30 to 45°, with the head maintained in the neutral position, to permit adequate venous drainage from the
brain while not compromising cerebral perfusion.
● Brief hyperventilation to a pCO2 of approximately 30 mmHg (end-tidal carbon dioxide [ETCO2] 25 to 30 mmHg), as a lifesaving
measure. Hyperventilation will rapidly and reliably lower the ICP in the setting of cerebral herniation [43]. However, prolonged use
is potentially harmful and is not recommended. (See 'Ventilation' above.)

● Use of a bolus dose of an osmotic agent capable of transiently reversing cerebral herniation. The two agents that have
demonstrated efficacy in published studies to acutely reverse herniation are:
• Mannitol: 1 to 1.5 g/kg [137]
• 23.4 percent sodium chloride (NaCl): 30 to 60 mL administered over 10 minutes [138]
Since mannitol may result in volume depletion, we prefer 23.4 percent NaCl, particularly in trauma patients with ongoing blood loss,
hemodynamic instability, or renal failure. Excessively rapid administration of 23.4 percent NaCl can, however, provoke transient but
profound hypotension [138]. Guidelines recommend that mannitol use prior to the initiation of ICP monitoring be restricted to the
management of cerebral herniation or acute neurologic deterioration that is not attributable to extracranial causes [11].
● Maintenance of a higher mean arterial pressure (MAP), to approximately 80 to 100 mmHg, to maintain an adequate cerebral
perfusion pressure (CPP), since the ICP may be extremely high in the setting of cerebral herniation. Both fluid resuscitation and
vasopressor use are frequently necessary in this setting.
Such interventions are a temporizing measure pending more definitive interventions, including neurosurgical treatment.
ICP and CPP monitoring — Indications for ICP monitoring in TBI are a Glasgow Coma Scale (GCS) score ≤8 and an abnormal
computed tomography (CT) scan showing evidence of mass effect from lesions such as hematomas, contusions, or swelling. ICP
monitoring 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 blood pressure (BP) <90 mmHg [7]. These indications, endorsed by prior guidelines, were derived from older
studies that identified independent predictors of intracranial hypertension [139]. While current Brain Trauma Foundation (BTF)
guidelines recommend that information from ICP monitoring be used to guide the management of patients with severe TBI, in order to
reduce in-hospital and two-week postinjury mortality [11], they did not re-endorse these specific indications for the use of ICP
monitoring.
A ventricular catheter, also known as an external ventricular drain (EVD), connected to a strain gauge transducer is the most accurate
and cost-effective method of ICP monitoring and has the therapeutic advantage of allowing for cerebrospinal fluid (CSF) drainage to
treat rises in ICP (figure 1) [140]. Intraparenchymal ICP monitors are technically easier to place and are associated with a lower risk of
hemorrhage and infection than EVDs. An intraparenchymal catheter may be an acceptable alternative when the risk of bleeding or

infection is thought to be higher than usual, or when EVD placement is unsuccessful because of technical difficulty. Significant midline
shift and ventricular collapse ("slit ventricles") will increase the technical difficulty of EVD placement. Intraparenchymal catheters have
been preferentially used for ICP monitoring of severe TBI patients in some resource-limited settings because of the perceived high
baseline risk of infection [141,142]. However, low-cost techniques of external ventricular drainage for ICP monitoring are also
recommended in these settings [143]. Other monitor types are discussed separately. (See "Evaluation and management of elevated
intracranial pressure in adults", section on 'Types of monitors'.)
An ICP goal ≤22 mmHg is recommended as the threshold that predicts survival and favorable outcome following TBI [11,144].
Therapeutic measures are initiated in a stepwise manner to attain this goal, starting with CSF drainage, sedation, and analgesia as
described in sections below.
ICP monitoring allows ongoing assessment of CPP, itself an approximation of the more clinically relevant cerebral blood flow (CBF).
Targeting a goal CPP of 60 to 70 mmHg appears to reduce mortality and morbidity [11,66,67]. Efforts to optimize CPP should first focus
on treatment of ICP elevations [70]. Patients with more severely impaired autoregulation and suboptimal CPP are best managed with
efforts to lower ICP, rather than by elevating MAP with vasopressors; hypertension is more likely to worsen cerebral edema when
protective autoregulation is impaired [68].
While ICP monitoring has long been central to the management of patients with severe head injury, the strength of this recommendation
has been limited by the lack of large randomized trials examining the effect of ICP monitoring and treatment on outcome [145-147]. One
randomized study of 324 patients older than 12 years with severe TBI hospitalized in Bolivia or Ecuador (BEST TRIP) found no
differences in outcomes among those patients assigned to management guided by invasive ICP monitoring consistent with guidelines
versus patients assigned to a treatment protocol based on high-intensity clinical and imaging evaluation [141]. While this trial
demonstrated the feasibility of managing patients in low-resource environments using frequent clinical and imaging evaluations, as an
alternative to invasive ICP monitoring, its findings are not considered to be generalizable to the management of severe TBI in other
settings. Other important limitations of the trial include limited use of CSF drainage, multiple statistically significant differences in
therapeutic measures between treatment arms that may have impacted outcomes, and limitations in the availability of rehabilitative
services following discharge. By contrast, registry-based studies from New York and India [142,148] have demonstrated decreased in-
hospital mortality with the use of invasive ICP monitoring to guide therapy, even after controlling for potential confounders.

Several noninvasive techniques of ICP monitoring have been evaluated [149]. Sonographic measurement of the optic nerve sheath
diameter (ONSD) has shown promise in some studies; however, wide variability in diagnostic thresholds limit its clinical applicability
[150-152]. Transcranial Doppler has also been evaluated for noninvasive ICP assessment, with variable results [153-155]. All of these
techniques are currently considered investigational and should not be used to direct clinical management.
Cerebrospinal fluid drainage — In patients with a ventricular catheter, drainage of CSF is generally the first intervention for lowering
ICP. Drainage may be continuous or intermittent, with a limited volume of CSF drained in response to elevations in ICP above goal.
Based on observational data, guidelines recommend continuous CSF drainage for better control of ICP compared with intermittent
drainage [11,156]. Continuous drainage is particularly recommended in patients with a GCS score <6 in the first 12 hours [11]. Caution
must be utilized with continuous drainage, however, since excessive drainage can lead to ventricular collapse and malfunctioning or
occlusion of the catheter in the setting of cerebral edema and small ventricles.
Sedation and analgesia — Protocol-based analgosedation is recommended by 2018 guidelines from the Society of Critical Care
Medicine to decrease duration of mechanical ventilation and intensive care unit (ICU) length of stay [157]. Analgosedation may consist
of either analgesia-first sedation or analgesia-based sedation. With analgesia-first sedation, an opioid such as fentanyl is used before,
then often in conjunction with, a sedative infusion to achieve sedation goals. Analgesia-based sedation consists of the use of an opioid
infusion alone, titrated to high enough doses to achieve a sedation goal without a concomitant sedative infusion. While either approach
is a reasonable first step in the management of the intubated patient with severe TBI, patients with significant ICP elevation should be
managed with an effective sedative agent in conjunction with the opioid infusion. Appropriate analgesia and sedation may lower ICP by
reducing cerebral metabolic demand, and thereby CBF and cerebral blood volume [158]. Sedation may also ameliorate ventilator
asynchrony and blunt sympathetic responses of hypertension and tachycardia.
Effective analgesia is a critical first step, since patients with TBI often have pain that goes unrecognized. Fentanyl infusions are
commonly used in this setting for greater efficacy compared with morphine, and to minimize hemodynamic instability. (See "Pain control
in the critically ill adult patient".)
Propofol may be the preferred sedating agent in this setting because of its efficacy in decreasing cerebral metabolic demand and ICP,
as well as its short duration of action that allows intermittent clinical neurologic assessment [159]. In one trial, propofol appeared to be
associated with better ICP control and a trend toward better outcomes compared with morphine alone [160]. Propofol also has putative

neuroprotective effects [161]. Hypotension is common with propofol, and fluids and vasopressors should be used as appropriate to
maintain CPP goals. The propofol infusion syndrome (severe metabolic acidosis, rhabdomyolysis, hyperkalemia, renal failure, and
cardiovascular collapse) is a rare complication that is more likely to occur with the use of high rates of infusion over extended periods of
time [162]. Other considerations in the selection of sedative agents in the critical care setting are discussed separately. (See "Sedative-
analgesic medications in critically ill adults: Selection, initiation, maintenance, and withdrawal".)
In general, light sedation, to a goal Richmond Agitation-Sedation Scale (RASS) (table 3) of 0 to -2, is recommended when the ICP is
adequately controlled [158]. Deeper levels of sedation, to a RASS of -4 to -5, are often necessary when ICP elevation is refractory to
light sedation.
Dosing and administration of sedative and analgesic agents in the critical care setting is described in detail separately (table 4). (See
"Sedative-analgesic medications in critically ill adults: Properties, dosage regimens, and adverse effects".)
Neuromuscular blockade may decrease ICP elevations associated with ventilator dyssynchrony and coughing. However, the routine
use of paralytic medications is discouraged, since these agents may result in prolonged neuromuscular weakness and delay weaning
from mechanical ventilation. (See "Neuromuscular weakness related to critical illness".)
Osmotic therapy — Osmotic therapy (mannitol or hypertonic saline) is generally utilized in TBI patients who are clinically symptomatic
from cerebral edema or have documented ICP elevation that does not respond to initial measures such as CSF drainage, analgesia,
and sedation.
Intravascular injection of hyperosmolar agents (hypertonic saline, mannitol) creates an osmolar gradient, drawing water across the
blood-brain barrier [163]. This leads to a decrease in brain volume and a decrease in ICP.
Protocols — We use an infusion of 3 percent NaCl to achieve a sodium goal of 145 to 155 mEq/L in patients with elevated ICP. In
addition, we use supplemental 30 mL bolus doses of 23.4 percent NaCl, administered over 10 minutes, to treat acute ICP elevations.
Mannitol is an acceptable alternative. No specific hyperosmolar treatment protocol has been shown to improve function outcome or
mortality in clinical trials.
The effect of hyperosmolar therapy diminishes with time, as a compensatory increase in brain osmoles occurs within 24 hours
[164,165]. Thus, hyperosmolar agents should be weaned slowly after prolonged use to prevent a reversal in the osmotic gradient and

consequent rebound cerebral edema.
● Hypertonic saline is an effective hyperosmolar agent for the control of elevated ICP [82,142,164,166-175]. This agent has been
used in a wide range of concentrations, from 3 percent, most commonly used as a continuous infusion, to 23.4 percent, which is
typically used in intermittent boluses [176,177]. When used as a continuous infusion, 3 percent NaCl may be titrated to an initial
sodium goal of approximately 145 to 155 mEq/L. Hypertonic saline should be administered via a central venous catheter because
of the risk of extravasation injury when used with peripheral intravenous (IV) access. Short-term use via peripheral IV access is
permissible in the setting of acute ICP elevation, however, while central access is obtained.
Hypertonic saline has several theoretical advantages over mannitol [164]. In particular, volume depletion and hypovolemia do not
occur, which makes this agent safer in the trauma patient with ongoing blood loss, hypovolemia, or hypotension. Hypertonic saline
has a reflection coefficient of 1.0 (compared with 0.9 for mannitol), and is therefore less likely to leak into brain tissue. Potential
adverse effects include circulatory overload and pulmonary edema, and an increased chloride burden, which may result in a non-
anion gap metabolic acidosis [178]. (See 'Monitoring and complications' below.)
● Mannitol has also been shown to reduce ICP and improve CBF [146,179-183]. Mannitol is administered in boluses of 0.25 to 1 g/kg
every four to six hours as needed.
A serious albeit theoretical concern with mannitol use is leakage into brain tissue in patients with disruption of the blood-brain
barrier, with consequent reversal of the osmolar gradient and rebound cerebral edema [184,185]. Judicious administration of
mannitol, on an as-needed basis for elevations in ICP, is advisable to minimize this potential risk. (See "Evaluation and
management of elevated intracranial pressure in adults", section on 'Mannitol'.)
In the aggregate, multiple observational studies [171,174], small randomized clinical trials [166,167,172,175], meta-analyses [169,173],
and systematic reviews [170] have not found compelling evidence to suggest superiority of either agent to improve outcomes such as
mortality or functional recovery. The majority of studies do suggest improved ICP control with hypertonic saline [166,167,170-174],
along with possible improvements in cerebral perfusion [172,174] and brain tissue oxygenation [174].
Monitoring and complications — Serial measurement of electrolytes, often at four- to six-hour intervals, is primarily performed for
safety, to prevent excessive elevation of sodium and chloride levels, and to detect and correct other derangements such as
hypokalemia. Ongoing fluid balance should also be closely monitored. Hypernatremia is associated with increased mortality in severe
TBI [186]. This association may reflect an effect of diabetes insipidus (DI) [186], often a marker of more extensive brain injury that
includes the hypothalamic-pituitary axis.
In addition, for patients receiving mannitol, serum osmolality should be monitored and maintained <320 mmol/L to minimize
complications. Renal function tests are checked daily. As an osmotic diuretic, mannitol may cause dehydration and acute kidney injury.
(See "Complications of mannitol therapy".)
Hypernatremia should be corrected gradually, if at all. Severe rebound cerebral edema may occur when the sodium level, and therefore
serum osmolality, is lowered too quickly. There is no high-quality evidence for a specific upper limit of sodium that necessitates
correction in this setting, and management should be individualized. Patients with renal failure may be at higher risk for complications
from hyperchloremia [61]. Patients with DI should also be managed more aggressively, primarily to treat hypovolemia and the free
water deficit. (See "Treatment of central diabetes insipidus".)
In the absence of these conditions and in the setting of elevated ICP or severe cerebral edema, we rarely correct a sodium level under
160 to 165 mEq/L. When the sodium level is lowered, we avoid correction by more than 5 mEq/L in a 24-hour period, and we closely
monitor the patient's neurologic status and ICP. (See "Treatment of hypernatremia in adults".)
Refractory ICP elevation — Patients with elevated ICP that is refractory to the measures described above may be managed with
decompressive craniectomy, barbiturate coma, or hypothermia.
Decompressive craniectomy — Decompressive craniectomy is effective in controlling ICP and is potentially lifesaving in patients
who have failed medical therapy. While many patients who require decompressive craniectomy as a lifesaving procedure will suffer
severe disability, some survivors will attain a functional outcome of independence within the home or better. Decompressive
craniectomy should be considered in TBI patients with ICP elevation refractory to medical therapy, after appropriate counseling of
patient surrogates and a discussion of the entire range of possible long-term outcomes that includes survival with severe disability and
minimally conscious or vegetative states.
In a decompressive craniectomy, a substantial portion of the skull is removed to allow brain tissue to swell beyond the confines of the
cranial vault, which otherwise restricts the total volume contained within (the Monro-Kellie doctrine). A craniectomy of sufficient size can
rapidly relieve intracranial hypertension. A "primary" or prophylactic craniectomy is performed in anticipation of elevated ICP, most often
at the time of hematoma evacuation, or on the basis of clinical or imaging findings on presentation that suggest the presence of life-
threatening intracranial hypertension [187,188]. A "secondary" or therapeutic decompressive craniectomy is performed to control
proven ICP elevation (measured using invasive monitoring) that is refractory to medical therapy.
Attention to specific technical considerations is particularly important [187,188], since an ineffective decompression will expose the
patient to the risks of the procedure without the anticipated benefit:
● The site and extent of bone removal should be tailored to the predominant location of injury and edema. A hemicraniectomy
(removal of one side of the skull) is performed for predominantly unilateral injury, while a large bifrontal craniectomy, with variable
extension into the temporal and parietal bones, is necessary for bifrontal or diffuse injury.
● The craniectomy must be of sufficient size. An insufficient skull defect may be ineffective in resolving intracranial hypertension,
while causing additional injury when cortical veins are compressed against the edge of the skull defect, leading to venous
infarction. A defect of at least 11 to 12 cm diameter is recommended when performing a hemicraniectomy.
● The middle cranial fossa should be adequately decompressed to minimize the risk of uncal herniation, which may occur despite
normal ICP.
● A generous durotomy must be performed, since most of the reduction in ICP is achieved by opening the dura. The dural defect is
then covered using loosely applied hemostatic material or a duraplasty.
Clinical trials of decompressive craniectomy in TBI suggest that the procedure is effective in controlling ICP and is lifesaving in patients
who have failed medical therapy. However, patients who require decompressive craniectomy for the management of intracranial
hypertension following TBI have suffered particularly severe brain injury and may be left in a state of severe disability or worse.
Conclusions from clinical trials are somewhat limited because of short follow-up time; functional recovery following severe TBI may be
delayed beyond one year of follow-up. (See 'Outcomes' below.)
● A randomized trial (DECRA) in 155 adults with severe diffuse TBI and ICP >20 mmHg for 15 minutes within a one-hour period
despite first-tier therapies compared bifrontal craniectomy with continued medical care [189]. Surgery was associated with a
decreased burden of intracranial hypertension and shorter stays in the ICU, but worse outcome on the extended Glasgow Outcome
Scale (E-GOS) at six months. Patients judged to require surgical evacuation of an intracranial hematoma were excluded, limiting
the applicability of these findings. Other limitations of this trial included a low ICP threshold for eligibility, use of a very extensive

bilateral craniectomy not reflective of typical clinical practice, and a baseline imbalance in patients admitted with bilateral fixed
pupils suggestive of devastating injury [190].
● The RESCUEicp trial used more broadly applicable eligibility criteria; 408 patients 10 to 65 years old with refractory ICP >25 mmHg
for 1 to 12 hours despite medical therapy were randomized to continued medical therapy or craniectomy appropriate to the type of
injury [191]. Patients requiring hematoma evacuation were included. Control of ICP was improved in the surgical arm. At six
months, patients in the surgical group had lower mortality (27 versus 49 percent) but higher rates of vegetative state (8.5 versus
2.1 percent), lower severe disability (dependent on others for care in the home; 22 versus 14 percent), and upper severe disability
(independent within but not outside of the home; 15 versus 8 percent), these outcomes likely reflecting those of patients who would
have not otherwise survived. Rates of moderate disability and good recovery were similar between the two groups (23 versus 20
percent and 4 versus 7 percent, respectively). The intention-to-treat analysis with 37 percent crossover from medical to surgical
treatment likely diluted the apparent treatment effect. A prespecified analysis of outcomes at one year revealed that the surgical
group had a higher rate of favorable outcomes (defined as better than lower severe disability or, ie, functionally independent within
the home or better) of 45 versus 32 percent.
Barbiturate coma — Pentobarbital and thiopental infusions may be used to manage elevated ICP refractory to other therapies.
While effective for the control of ICP, the use of barbiturate coma has not been shown to improve outcomes following TBI [192]. Our
practice is to consider barbiturate coma for ICP control only when first-line measures, including hyperosmolar therapy as well as a
propofol infusion titrated to deep sedation (RASS score of -5), have been ineffective and surgical decompression is not feasible.
These agents profoundly decrease cerebral metabolic demand, CBF, and cerebral blood volume [193]. A loading dose of 5 to 20 mg/kg
of pentobarbital is typically administered, followed by 1 to 4 mg/kg per hour. Continuous electroencephalography (EEG) monitoring is
used, with the pentobarbital infusion titrated to produce a burst-suppression pattern. While effective for the control of ICP, pentobarbital
infusions are associated with morbidity. The neurologic examination is precluded for an extended period of time because of the long
half-life of this drug. This may also result in delays in the determination of brain death. Other common side effects include hypotension
requiring vasopressor support, adynamic ileus, and poor pulmonary mucus clearance, with the consequent risk of ventilator-associated
pneumonia [194]. Severe metabolic acidosis from propylene-glycol toxicity has been reported with the use of pentobarbital infusions
[195,196].

Hypothermia — Induced or therapeutic hypothermia has been proposed as a treatment for TBI based upon its potential to reduce
ICP as well as to provide neuroprotection and prevent secondary brain injury [197]. Therapeutic hypothermia does appear effective for
the control of ICP [198] but has not been convincingly shown to improve outcomes. Therapeutic hypothermia treatment should,
therefore, be limited to clinical trials, or to patients with elevated ICP refractory to other therapies, after discussion with family and other
patient surrogates [199-201].
A systematic review of 37 randomized controlled trials, including 3110 subjects, of mild to moderate hypothermia (32 to 35°C) following
TBI concluded that there was no high-quality evidence that hypothermia is beneficial following TBI for the goal of improving meaningful
long-term outcomes [202]. Other systematic reviews and meta-analyses found borderline benefits for death and neurologic outcome,
but also an increased risk for pneumonia [197,203-206]. Substantial variability among studies in the depth and duration of hypothermia,
as well as the rate of rewarming, limits the ability to draw conclusions from these studies. Two subsequently published trials found no
benefit of induced hypothermia in specific subgroups of patients with TBI; in one, hypothermia was not beneficial when initiated within
two to five hours of TBI in a selected group of younger patients (age 16 to 45 years) [207]. In another trial, there was no benefit for
induced hypothermia when added to other standard-of-care measures in patients with intracranial hypertension refractory to initial
treatment within 10 days of TBI; deaths and unfavorable outcomes were somewhat more common in patients receiving therapeutic
hypothermia [208].
Two trials of hypothermia therapy in children with TBI have shown no improvement in neurologic or other outcomes; one showed a
nonsignificant increase in mortality [209,210]. (See "Elevated intracranial pressure (ICP) in children: Management", section on
'Temperature control'.)
ADVANCED NEUROMONITORING
In order to supplement intracranial pressure (ICP) monitoring, several technologies have 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 (CBF), and metabolism, with the goal of improving the detection and management of secondary brain injury.
While observational data suggest that these monitoring tools provide unique information that may help to individualize the management
of patients with severe head injury, clinical trial data demonstrating improved outcomes with use of these multimodality advanced

neuromonitoring approaches are awaited.
Such techniques include:
● Jugular venous oximetry – Retrograde cannulation of the internal jugular vein that allows measurement of oxygen saturation in the
blood exiting the brain [211]. Normal jugular venous oxygen saturation (SjVO2) is approximately 60 percent. SjVO2 <50 percent for
10 minutes is considered a "cerebral desaturation" and implies a mismatch between oxygen delivery and demand in the brain.
These desaturation episodes are associated with unfavorable neurologic outcomes in this setting [11,212,213]. Jugular venous
oximetry protocols that specify stepwise escalation of therapy to improve cerebral perfusion when desaturations occur have been
used at several institutions; however, randomized clinical trials have not been performed.
● Brain tissue oxygen tension (PbtO2) monitoring – Intraparenchymal oxygen electrode placed in a manner similar to a fiberoptic ICP
probe that measures PbtO2 in the white matter [214]. Normal PbtO2 is >20 mmHg; duration and depth of PbtO2 below 15 mmHg
are associated with worsened outcome [215]. Some studies have shown improved outcomes in patients managed with treatment
protocols directed at optimization of PbtO2 as compared with historical controls [216,217]. A phase 2 randomized clinical trial
(BOOST-2) demonstrated the feasibility of a goal-directed management protocol for the optimization of PbtO2 following TBI [218]; a
phase 3 trial (BOOST-3) is underway.
● Cerebral microdialysis – Intraparenchymal probe placed in a manner similar to a PbtO2 probe that allows measurement of
extracellular glucose, lactate, pyruvate, and glutamate [219,220]. A lactate:pyruvate ratio >40 is suggestive of anaerobic
metabolism, which is believed to exacerbate secondary brain injury.
● Thermal diffusion flowmetry – Intraparenchymal probe placed in a manner similar 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.
● Pressure reactivity index (PRx) – The continuously monitored moving correlation coefficient between mean ICP and mean arterial
pressure (MAP), used as a measure of cerebral autoregulation. A direct correlation of ICP with MAP, with a PRx close to +1.0,
suggests the absence of cerebral autoregulation and may be seen with refractory intracranial hypertension. PRx thresholds of 0.25
and 0.05, suggesting the presence of robust cerebral autoregulation, predicted survival and favorable outcome, respectively, in one

study [144]. The PRx has also been used to identify optimal cerebral perfusion pressure (CPP) [221] and ICP [222] goals in
individual TBI patients based on quantification of cerebral autoregulation.
INTERVENTIONS WITH UNCERTAIN OR NO BENEFIT
Hemostatic treatments — There is no evidence that hemostatic therapy benefits noncoagulopathic patients with severe TBI, and such
treatments (tranexamic acid, recombinant human factor VIIa) should not be used outside of a clinical trial [223,224].
While the use of tranexamic acid did not result in improved outcomes in two randomized clinical trials in TBI [225,226], a subsequent
systematic review that pooled the findings of two trials found a statistically significant decrease in hemorrhage expansion following TBI
with the use of tranexamic acid, along with a trend toward improved outcomes [227]. The results of the CRASH-3 trial of this agent in
TBI are awaited [228].
Recombinant human factor VIIa has not been shown to be of overall benefit in patients with nontraumatic intracerebral hemorrhage
(ICH) and is not used in the setting of traumatic ICH. (See "Spontaneous intracerebral hemorrhage: Treatment and prognosis", section
on 'Hemostatic therapy'.)
Neuroprotective treatment — A wide range of agents targeting various aspects of the brain 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
[229]. No benefit was found for intravenous (IV) progesterone administration in two randomized trials in acute severe TBI [230,231].
Citicoline was not found to be effective at improving outcomes in a randomized trial of 1213 patients with TBI [232].
Erythropoietin has been postulated to have neuroprotective effects. However, two randomized clinical trials have not demonstrated a
benefit in patients with TBI [233,234]. In the larger study of 606 patients with TBI, neurologic outcome at six months was not improved,
while mortality was nonsignificantly lower (11 versus 16 percent) in patients who received erythropoietin [234]. A hemoglobin
transfusion of 10 g/dL did not result in improved functional outcomes at six months as compared with the usual threshold of 7 g/dL in
one trial [233].
Other agents being investigated include magnesium [235], hyperbaric oxygen [236], and cyclosporine [237], among others [238].

Glucocorticoids — The use of glucocorticoid therapy following head trauma was found to be harmful in a large trial of patients with
moderate to severe TBI [239]. More than 10,000 patients were randomly assigned to treatment with methylprednisolone or to placebo
within eight hours of presentation. Patients treated with glucocorticoids had increased mortality at two weeks (21 versus 18 percent;
relative risk [RR] 1.18) and at six months (26 versus 22 percent; RR 1.15) [240].
PROGNOSIS
Outcomes — Cohort studies have suggested that patients with severe head injury (Glasgow Coma Scale [GCS] score ≤8) have
approximately a 30 percent risk of death. At least one cohort study found that survivors of TBI continue to have a substantially
increased risk of mortality for at least 13 years after the trauma [241].
Multiple studies indicate, however, that significant proportions (30 to 65 percent) of patients with severe TBI will regain an
independence, and that functional recovery following severe TBI can occur very slowly, extending beyond even 6 to 12 months [242-
250]. In one Australian study, one-quarter of patients who were severely disabled or vegetative at six months following decompressive
craniectomy for TBI improved to a state of moderate disability or better by 18 months [251].
Approximately 5 to 15 percent of patients with severe TBI are discharged from acute care in a vegetative state [252-254]. Only half of
these patients regain consciousness over the next year, and virtually all of these patients remain severely disabled. Outcomes are
somewhat better for those in minimally conscious state. The persistent vegetative and minimally conscious states are described
separately. The use of prognostic indicators for these outcomes is better defined for hypoxic-ischemic brain injury than for TBI [255].
(See "Hypoxic-ischemic brain injury in adults: Evaluation and prognosis", section on 'Persistent vegetative state' and "Hypoxic-ischemic
brain injury in adults: Evaluation and prognosis", section on 'Minimally conscious state'.)
A randomized trial of amantadine (starting at 100 mg twice daily) in 184 patients admitted to inpatient rehabilitation in a vegetative or
minimally conscious state after severe TBI found that amantadine treatment was associated with accelerated recovery during the four-
week active treatment phase [256]. Rates of improvement subsequently slowed after treatment withdrawal in the amantadine group,
and at week 6, disability scores in the two groups were similar. Further study is needed to determine a benefit for amantadine on long-
term prognosis and its role in the treatment of patients with severe TBI. The mechanism of action for putative beneficial effect of
amantadine is unclear; it is speculated that antagonism of N-methyl-D-aspartate and/or indirect agonism of dopamine may be involved.

Among patients with more moderate TBI pre-trauma, educational attainment is associated with increased odds of disability-free
recovery [257].
Individual risk factors — 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. While many individual
negative outcome predictors have been identified, each is associated with a significantly high false-positive rate and must not be used
in isolation to estimate a prognosis.
Identified risk factors include [21,24,25,27,109,135,229,253,258-266]:
● GCS score at presentation (especially the GCS motor score) (table 1)

● Full Outline of UnResponsiveness (FOUR) score (table 2)
● Presence of severe computed tomography (CT) abnormalities (high-grade subarachnoid hemorrhage, cisternal effacement, midline
shift, leukoaraiosis)
● Pupillary function
● Age
● Associated extracranial injuries and complications
● Hypotension
● Hypoxemia
● Pyrexia
● Elevated intracranial pressure (ICP)
● Reduced cerebral perfusion pressure (CPP)
● Bleeding diathesis (low platelet count, abnormal coagulation parameters)
Magnetic resonance imaging (MRI) has also been studied as a prognostic tool following TBI [267-270]; diffuse axonal injury (DAI) and
brainstem injury on MRI may predict poor long-term functional outcomes [271,272]. However, favorable outcomes may occur despite
the presence of lesions on MRI traditionally thought to portend a poor prognosis [273], and MRI should not be used in isolation to guide
prognostication following severe TBI.

Other studies are evaluating the potential of biomarkers, such as the levels of S-100β protein, neuron-specific enolase, and α-synuclein
in the blood and/or cerebrospinal fluid (CSF), to predict neurologic outcome [274-276].
Outcome prediction models — Outcome prediction models derived from large datasets, incorporating multiple predictors, have been
developed and have undergone external validation [262,277-279]. However, it is important to recognize that all outcome prediction
models in neurologic injury are prone to confounding by self-fulfilling prophecies (where the presence of variables widely considered to
be predictors of poor outcome lead to the delivery of an unfavorable prognosis to the family with consequent withdrawal of life support)
within the datasets of patients used to develop and validate the model. A group of investigators in Sweden has described an
overestimation of both mortality and poor outcomes in patients managed aggressively with an ICP-targeted treatment protocol
[280,281].
Therefore, 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 in patients with severe TBI.
The two most widely used publicly available prediction models are the International Mission for Prognosis and Analysis of Clinical Trials
in TBI (IMPACT) and Corticosteroid Randomisation After Significant Head Injury (CRASH) models:
● The CRASH prediction model was derived from the large international clinical trial of glucocorticoids in TBI with 10,008 subjects
from high-, middle-, and low-income countries [282]. Variables in this model include country, age, GCS, pupillary reactivity, the
presence of significant extracranial injury, and specific findings on CT.
● The IMPACT model was developed using data from 8509 patients in 11 studies [283]. The variables in this model include age, GCS
motor score, and pupillary reactivity as core clinical variables, as well as the occurrence of hypoxia and hypotension, the Marshall
CT grade (table 5) plus other CT findings, and glucose and hemoglobin levels.
These models have been validated in large cohorts of patients, and may have more limited applicability to individual prognostication.
SOCIETY GUIDELINE LINKS

Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately.
(See "Society guideline links: Traumatic brain injury and concussion".)
INFORMATION FOR PATIENTS
UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces
are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have
about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials.
Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to
12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients.
(You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
● Basics topic (see "Patient education: Closed head injury (The Basics)")
SUMMARY AND RECOMMENDATIONS
Patients with severe traumatic brain injury (TBI), defined by a Glasgow Coma Scale (GCS) score <9, 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 <60 mmHg) and hypotension (systolic blood pressure [BP] <100 mmHg) are priorities in the
management of patients with severe TBI beginning during their prehospital care. (See 'Initial evaluation and treatment' above.)
● Patients with TBI and GCS score <9 should undergo endotracheal intubation in the emergency department (ED), if not before.
Specific considerations exist when performing endotracheal intubation in patients with suspected elevation in intracranial pressure
(ICP). Multiple factors must be considered when making decisions about prehospital intubation of patients with severe TBI. (See
'Prehospital' above and 'Emergency department' above.)

● ED evaluation should include frequent clinical neurologic assessments and a computed tomography (CT) scan of the head. (See
'Emergency department' above.)
Impending cerebral herniation is an emergency and should be suspected in a patient with significant pupillary asymmetry, unilateral
or bilateral fixed and dilated pupils, decorticate or decerebrate posturing, respiratory depression, and the "Cushing triad" of
hypertension, bradycardia, and irregular respiration.
When impending herniation due to elevated ICP is suspected in a patient with severe TBI, we recommend empiric interventions
including endotracheal intubation, head of bed (HOB) elevation, hyperventilation, and a bolus dose of 23.4 percent sodium chloride
or mannitol pending the results of the CT and measurement of ICP (Grade 1C). (See 'Impending cerebral herniation' above.)
● Hyperventilation should be avoided in the first 24 to 48 hours and should not exceed PaCO2 <30 mmHg except as a temporizing
measure in a patient with impending cerebral herniation. Positive end-expiratory pressure (PEEP) up to 15 to 20 cm H2O may be
utilized to manage acute respiratory distress syndrome (ARDS) following TBI while ICP is monitored. (See 'Ventilation' above.)
● Surgical evacuation of epidural, subdural, and intracerebral hematomas should be decided based upon hematoma volume and
associated mass effect, in conjunction with the patient's neurologic status. (See 'Surgical treatment' above.)
● For patients with severe TBI and an abnormal CT scan showing evidence of mass effect from lesions such as hematomas,
contusions, or swelling, we suggest ventriculostomy and ICP monitoring along with treatment of elevated ICP to target pressures
below 22 mmHg (Grade 2C). (See 'ICP and CPP monitoring' above.)
Appropriate first measures include removal of cerebrospinal fluid (CSF) through the ventriculostomy, HOB elevation, and
appropriate analgesia and sedation, followed by osmotic therapy with either hypertonic saline or mannitol. (See 'Initial treatment'
above and 'Cerebrospinal fluid drainage' above and 'Sedation and analgesia' above and 'Osmotic therapy' above.)
For patients with elevated ICP refractory to initial therapy, treatment options include decompressive craniectomy, barbiturate coma,
and induced hypothermia. Patients with refractory ICP elevation have a generally poor prognosis, and further interventions should
be based on a risk-benefit discussion with family. (See 'Refractory ICP elevation' above.)
● We suggest using normal saline rather than colloid solutions to maintain euvolemia (Grade 2B). (See 'Hemodynamic management'
above.)
● We recommend short-term (one-week) use of antiseizure drugs for the prevention of early seizures (Grade 1B). Patients with
seizures should be treated to prevent recurrence. We suggest levetiracetam for prevention and treatment of seizures (Grade 2C);
other antiseizure drugs (eg, fosphenytoin) that can be provided parenterally are reasonable alternatives. (See 'Antiseizure drugs
and electroencephalography monitoring' above and "Post-traumatic seizures and epilepsy".)
● Fever and hyperglycemia should be avoided for their potential to exacerbate secondary neurologic injury. Nutritional support to
caloric goals should be achieved by day 5 from injury using enteral nutrition. Coagulopathy should be corrected to maintain an
international normalized ratio (INR) <1.4 and a platelet count >75,000/mm3. (See 'Temperature management' above and 'Glucose
management' above and 'Nutritional support' above and 'Management of coagulopathy' above.)
● Paroxysmal sympathetic hyperactivity (PSH) may occur following TBI and correlates with severity of injury. (See 'Paroxysmal
sympathetic hyperactivity' above.)
● We recommend mechanical thromboprophylaxis with intermittent pneumatic compression for the prevention of venous
thromboembolism (VTE) (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. (See 'Hemodynamic management' above.)
● While outcome prediction models have been developed, they are imperfect, and a trial of early aggressive neurosurgical and
neurocritical care management, including surgical removal of evacuable lesions and ICP monitoring, should be undertaken in most
patients with severe TBI. (See 'Prognosis' above.)
ACKNOWLEDGMENT
The editorial staff at UpToDate would like to acknowledge Nicholas Phan, MD, FRCSC, FACS, and J Claude Hemphill, III, MD, MAS,
who contributed to an earlier version of this topic review.
Use of UpToDate is subject to the Subscription and License Agreement.
Topic 4826 Version 21.0


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10/9/2019 Management of acute severe traumatic brain injury - UpToDate

Official reprint from UpToDate®

INTRODUCTION AND DEFINITION

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INITIAL EVALUATION AND TREATMENT

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- SpO2 <90 to 93 percent despite the use of supplemental oxygen

- Clinical signs of cerebral herniation (see 'Impending cerebral herniation' below)

- Long transport time

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INTENSIVE CARE MANAGEMENT

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INTRACRANIAL PRESSURE MANAGEMENT

Initial treatment — Simple techniques should be instituted as soon as possible:

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• Mannitol: 1 to 1.5 g/kg [137]

• 23.4 percent sodium chloride (NaCl): 30 to 60 mL administered over 10 minutes [138]

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consequent rebound cerebral edema.

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neuromonitoring approaches are awaited.

Such techniques include:

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INTERVENTIONS WITH UNCERTAIN OR NO BENEFIT

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Identified risk factors include [21,24,25,27,109,135,229,253,258-266]:

● GCS score at presentation (especially the GCS motor score) (table 1)

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SOCIETY GUIDELINE LINKS

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INFORMATION FOR PATIENTS

SUMMARY AND RECOMMENDATIONS

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