Urgent considerations

See Differentials for more details

The goal in assessing patients with TBI is to rapidly identify intracerebral injury and to prevent secondary brain injury by maintaining oxygenation and perfusion of the brain.[45][46]​

Management of patients with TBI requires rapid and thorough assessment, and frequently requires initiation of treatment prior to definitive diagnosis.

Polytrauma is common: about 40% to 50% of patients with severe TBI have other coexisting serious traumatic injuries, and up to 10% have coexisting spinal cord injury.[47][48]

The need for neurosurgical intervention (craniotomy, elevation of skull fracture, increased intracranial pressure monitor, or ventriculostomy) doubles when the Glasgow Coma Scale (GCS) drops from 15 to 14.[9]

Initial approach: airway, breathing, circulation, disability

The initial approach to a patient with TBI includes the rapid assessment of airway, breathing, circulation, and disability (ABCD), with appropriate interventions as indicated.

Airway and breathing

The initial assessment of airway and breathing must coincide with determination of need for cervical spine immobilization due to the increased risk of cervical spine injury in patients with TBI.[18][45]

Cervical collars should be instituted until cervical spine injury has been ruled out.

Hypoxia and hypercapnia are both known to worsen outcomes in TBI. A single episode of hypoxia is significantly associated with a worse outcome, and periods of hyper- or hypocapnia are both associated with poorer outcomes.[49]

In the prehospital setting, airway adjuncts are indicated if the patient is not spontaneously breathing, not able to maintain an open airway or not able to maintain >90% oxygen saturation with supplementary oxygen.[50]

Upon arrival in the emergency department, US and UK guidelines recommend inserting a tracheal tube in the patient with TBI and a GCS score of <9.[18][45]​​​ These patients are at risk of aspiration and respiratory depression. Other indications for intubation and ventilation include:[18]

  • Loss of protective laryngeal reflexes

  • Ventilatory insufficiency, as judged by blood gases: hypoxemia (PaO₂ less than 13 kPa on oxygen) or hypercarbia (PaCO₂ more than 6 kPa)

  • Irregular respirations.

Oxygenation should be closely monitored using pulse oximetry.[51]​ Ventilation should be monitored using continuous capnography with an end-tidal CO₂ target of 35 to 40 mmHg.[50][52][53]

For most patients, maintenance of normal ventilation is the goal. Hyperventilation is only indicated as a temporizing measure when a patient with TBI has clinical evidence of cerebral herniation, such as asymmetric pupils, dilated and nonreactive pupils, extension motor posturing, progressive neurologic deterioration, or flaccidity.[50]

Circulation

Even one episode of prehospital or in hospital hypotension negatively impacts outcome after brain injury.[46]​[54][55][56][57]​​​​ In most cases, hypotension is caused by extracranial bleeding, although autonomic dysfunction due to the TBI can contribute to hypotension.

One retrospective review suggested that patient outcomes improved when systolic blood pressure (BP) was maintained at ≥110 mmHg for patients 15 to 49 years old, ≥100 mmHg for patients 50 to 69 years old, and ≥110 mmHg for patients ≥70 years old.[58] These systolic BP targets have been adopted by the Brain Trauma Foundation guidelines for the management of of severe traumatic TBI (level III recommendation based on low-quality body of evidence).[6] In children with severe TBI, both hypotension and severe hypertension are associated with increased 24-hour mortality.[59]

The concern that fluid resuscitation may worsen cerebral edema and/or bleeding is theoretical, and studies have repeatedly demonstrated that patients who remain normotensive have improved outcomes.[60][61]​​ The resuscitative fluid of choice for patients with TBI and hypotension is 0.9% sodium chloride, with blood products used as appropriate in the polytrauma patient. In the adult patient, 0.9% sodium chloride should be given in 2-liter boluses.[62][63]​ In the pediatric patient, 0.9% sodium chloride should be given as 20 ± 10 mL/kg bolus to maintain an age and weight appropriate blood pressure, with consideration of blood products if repeated boluses are indicated.[64]​​[65][66]​​

Disability: initial neurologic examination

Perform a brief, focused neurologic examination with attention to the GCS, pupillary examination, and motor function.

The GCS is widely used to assess the level of consciousness in patients with TBI, and provides prognostic information that allows the physician to plan for expected diagnostic and monitoring requirements.[45] [ Glasgow Coma Scale Opens in new window ]

The following scoring system is applied:[44]

  • GCS of 13-15 is associated with mild brain injury

  • GCS of 9-12 is associated with moderate brain injury

  • GCS of <9 is associated with severe brain injury.

Although a GCS of 13 is classically considered as mild, many experts believe that it should be considered within the moderate category.[10][11][12]​​​​​​ Clinical guidelines in Australia recognize the increased morbidity associated with a GCS of 13, and limit the classification of mild TBI to those patients with a GCS of 14 or 15.[13]​The Mayo classification system for TBI classifies patients with TBI into definite, probable, and possible, based on the patient’s clinical and CT findings.[14]

GCS severity is inversely correlated to numerical magnitude. GCS can be serially performed by different members of the healthcare team in order to monitor neurologic status; inter-rater reliability is generally considered to be good, although this has been questioned.[67][68][69][70][71]

A score of 13 to 15 is associated with good outcomes, although a GCS of 15 cannot be used to rule out intracranial injury.

A score <9 is associated with clinical deterioration and poor outcomes. Serial GCS monitoring provides clinical warning of deterioration.

If there is asymmetry between the right and left side or the upper and lower limbs, use the best motor response to calculate the GCS: this is the most reliable predictor of outcome.[45]

[Figure caption and citation for the preceding image starts]: Adult and pediatric GCSFrom Dr Micelle J. Haydel; used with permission [Citation ends].com.bmj.content.model.assessment.Caption@4d28a1b7

The Simplified Motor Score (obeys commands = 2, localizes pain = 1, and withdraws to pain or worse = 0) has been shown to have predictive power similar to the GCS.[72]

Similarly, the use of a binary assessment of the GCS-motor (GCS-m) score to determine if the patient obeys commands or not (i.e., GCS-m score <6 if patient does not obey commands; GCS-m score=6 if patient obeys commands) has been proposed as a triage tool for out-of-hospital care. One retrospective analysis found a GCS-m score of <6 is similarly predictive of serious injury as the total GCS score.[73]

The FOUR scale, which adds brainstem reflexes and respiratory patterns to motor and eye findings, has also been shown to have similar predictive power to the GCS.[74][75]

Pupillary reflexes function as an indication of both underlying pathology and severity of injury, and should be monitored serially.[76]​ The pupillary examination can be assessed in an unconscious patient or in a patient receiving neuromuscular blocking agents or sedation.[16][76]

Pupils should be examined for size, symmetry, direct/consensual light reflexes, and duration of dilation/fixation. Abnormal pupillary reflexes can suggest herniation or brainstem injury. Orbital trauma, pharmacologic agents, or direct cranial nerve III trauma may result in pupillary changes in the absence of increased intracranial pressure (ICP), brainstem pathology, or herniation.

  • Pupil size:

    • The normal diameter of the pupil is between 2 and 5 mm, and although both pupils should be equal in size, a 1-mm difference is considered a normal variant.

    • Abnormal size is noted by >1 mm difference between pupils.

  • Pupil symmetry:

    • Normal pupils are round, but can be irregular due to ophthalmological surgeries.

    • Abnormal symmetry may result from compression of CNIII, which can cause a pupil to initially become oval before becoming dilated and fixed.

  • Direct light reflex:

    • Normal pupils constrict briskly in response to light, but may be poorly responsive due to ophthalmological medications.

    • Abnormal light reflex may be seen in sluggish pupillary responses associated with increased ICP. A nonreactive, fixed pupil has <1 mm response to bright light and is associated with severely increased ICP.

Tranexamic acid

Tranexamic acid is an antifibrinolytic medication that has been demonstrated to reduce mortality in severely injured trauma patients.[77][78][79]​​​​[80]​ 

Meta-analyses of placebo-controlled clinical trials have failed to demonstrate that tranexamic acid consistently reduces mortality in patients with TBI.[81][82][83][84]​​​​​​​ Although there is no compelling evidence for the routine use of tranexamic acid in patients with TBI (unless there is associated extracranial trauma), it appears to be safe in these patients and local guidance regarding its use may vary.

Sedation and analgesia

Patients with TBI often have considerable agitation, and may have other painful injuries. In addition to increased metabolic demand, pain and agitation can lead to difficulties in obtaining: imaging studies; mental status monitoring; and evaluating the physiological responses to resuscitative measures.

Analgesic and anxiolytic medications should be given after a full neurologic examination has been performed, and then in consideration of the overall hemodynamic status of the patient. Short-acting agents are preferable until the patient has been stabilized and has a definitive diagnosis.[45]

Disadvantages to using analgesics or sedatives include the potential for depression in cardiorespiratory function and compromised assessment of neurologic status.

Approach to elevated intracranial pressure (ICP)

Patients with elevated ICP may exhibit vomiting, altered mental status, oculomotor deficits, and pupillary deficits. Late signs of elevated ICP and herniation include bilateral fixed and dilated pupils, Kussmaul respirations, and Cushing Triad (widened pulse pressure, bradycardia, and irregular respiration).

Treatment of increased ICP must focus on volume reduction of one or more of the following: brain parenchyma, cerebrospinal fluid, intravascular blood volume, or an intracranial mass lesion.

Primary interventions

  • Raising the head of the bed to 30°: thought to improve venous outflow and cerebral perfusion pressure, although a Cochrane review found insufficient evidence to either support or refute this practice.[85][86]

  • Analgesics and sedation to ease pain and agitation, thought to reduce metabolic demands.

  • Inducing hypocapnia by hyperventilation reduces pCO₂, which provokes cerebral vasoconstriction, and lowers ICP. Hyperventilation should be limited to brief periods of up to 30 minutes to treat acute cerebral herniation, and it should be closely monitored using advanced brain-tissue oxygen monitoring.[85] Hyperventilation should not be used for long-term prophylaxis and, if possible, should be avoided during the first 24 hours after injury.[6]

Secondary interventions

  • Osmosis: mannitol and hypertonic saline cause a strong osmotic gradient, thereby reducing intracerebral volume. They may be used to rapidly lower elevated ICP. Although there have been numerous studies, there is insufficient clinical evidence to recommend one osmotic agent over another.[6][87][88]​ Mannitol causes significant diuresis and hypovolemia, which if untreated can result in systemic hypotension and decreased cerebral perfusion pressure.[6]​ Hypertonic saline does not cause diuresis; it can increase systemic blood pressure, thereby improving cerebral perfusion pressure. Patients must be monitored for hypernatremia.​​

  • High-dose barbiturate administration: recommended to control elevated ICP refractory to maximum standard treatment.[6] High-dose barbiturate therapy commonly lowers systemic blood pressure and may require volume replacement or vasoactive agents to prevent or ameliorate systemic hypotension.[89]

  • ICP monitoring: indicated in TBI patients with a GCS <9 and evidence of an injury on CT. ICP monitoring is also recommended in patients with severe TBI who have a normal CT and at least two of the following: motor posturing, age over 40 years, or a systolic BP less than 90 mmHg.[90] Improvement in mortality has been demonstrated in centers where ICP monitoring is routinely implemented in patients with severe TBI.[91]

  • Decompressive hemicraniectomy: indications vary and medical management should be optimized first.[92][93]

  • Hypothermia and corticosteroids have no role in the treatment of TBI.[28][94][95] [ Cochrane Clinical Answers logo ]

Coagulopathy: pre-existing

Patients with pre-existing coagulopathy have a poorer outcome than the general population. Reversal agents are prothrombotic and many patients have a poor outcome despite rapid reversal.[96]

  • All antiplatelet or anticoagulant agents should be stopped and/or reversed in the setting of traumatic intracranial hemorrhage.

  • Serial prothrombin time (PT), partial prothrombin time, international normalized ratio (INR), and platelet and fibrinogen levels should be followed in patients with severe TBI.

Correction of coagulopathy can be achieved using vitamin K (useful in patients with warfarin-related prolongation of INR), fresh frozen plasma (FFP), platelets (goal platelet count is >100,000/microliter), cryoprecipitate (used in patients with low fibrinogen levels), protamine (used for patients on heparin), activated factor VIIa, prothrombin complex concentrate (PCC), and activated prothrombin concentration (APCC).[96][97]

If a patient taking direct oral anticoagulants (DOACs) has traumatic bleeding or requires an urgent invasive procedure, reversal of the DOAC may be warranted, depending on the severity of the bleed or the nature of the planned procedure. The direct thrombin inhibitor dabigatran can be reversed with idarucizumab or APCC, and the factor Xa inhibitors apixaban and rivaroxaban can be reversed with andexanet alfa or PCC. Routine use of reversal agents in patients who have sustained head trauma, but do not have bleeding, is not recommended.[98]

Several guidelines recommend, or suggest consideration of, CT head imaging for anticoagulated patients after minor head injury, regardless of symptoms.​[18][99][100]​​ UK guidelines recommend that a CT head scan within 8 hours of the injury should be considered for all patients taking anticoagulants.[18] However, the supporting evidence base is limited.​​[99]​​[100][101]

Coagulopathy: TBI-induced

TBI has a strong association with abnormalities throughout the coagulation cascade, and prolongation of PT has been shown to be an independent risk factor of poor outcome after TBI.[102] While FFP has been a standard part of the treatment in trauma-induced coagulopathy, the use of prothrombin complex concentrate is also advocated due to its more concentrated volume.[103] Recombinant activated factor VIIa decreases the need for transfusion of packed red cells and plasma in patients with TBI-induced coagulopathy, but this has not been shown to translate into consistent improved outcomes.[97][104][105]​​

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