Traumatic Brain Injury

Initial primary brain injury following trauma occurs immediately at the time of head impact and is largely irreversible. Public health measures such as airbags, seat belts, bike helmets, and fall prevention measures are therefore essential to limit traumatic brain injury (TBI). Pathology at this initial stage includes diffuse axonal injury, intraparenchymal hemorrhage and contusion, and extraaxial hemorrhages including epidural and subdural hematoma, subarachnoid hemorrhage, and intraventricular hemorrhage. Secondary insults, including a variety of ischemic, metabolic, and inflammatory disturbances, develop over hours to days after injury and exacerbate the now injured, vulnerable brain tissue. Monitoring for secondary brain injury is the focus of hospital-based care following TBI. Main targets for intervention include limiting cerebral edema and brain compression, optimizing tissue perfusion, and minimizing metabolic distress.

A.

Neurologic status on hospital arrival, commonly measured with the Glasgow Coma Scale (GCS), is an important predictor of prognosis. Other factors indicative of the degree of brain injury include duration of loss of consciousness (LOC) and duration of posttraumatic amnesia. These factors are most helpful in predicting outcomes in severe injuries but are less reliable for mild injuries. Severity of TBI is often classified as mild (GCS 13–15, LOC < 30 minutes, posttraumatic amnesia < 24 hours), moderate (GCS 9–12, LOC 30 minutes–24 hours, posttraumatic amnesia 24 hours–7 days), and severe (GCS < 8, LOC > 24 hours, posttraumatic amnesia > 7 days).
B.

Patients with TBI frequently have additional traumatic injuries; a complete trauma survey must be conducted. Securing the airway, stabilization of the spine, and treatment of immediately life-threatening issues such as pneumothoraces, cardiac tamponade, or shock should be undertaken. Serial examinations and assessments should be performed to avoid missed injuries.
C.

Coagulopathy may be present in TBI and lead to additional secondary injury from ongoing bleeding. Prior antiplatelet and anticoagulant use should be identified, and prothrombin and partial thromboplastic times as well as platelet count measured. When present, coagulopathy should be corrected as appropriate.
D.

Urgent surgical intervention is usually required for epidural hematoma, large or acute subdural hematomas, or any hemorrhage leading to mass effect with midline shift and impending herniation.
E.

Following TBI, intracranial pressure (ICP) may be increased due to diffuse cerebral injury, focal intracranial hemorrhage, or contusions. Seizure activity may exacerbate elevations in ICP. Simple bedside measures to increase venous drainage should be implemented to lower ICP; more aggressive measures are often necessary, particularly in severe TBI. These are outlined in Chapter 59 .
F.

Monitoring of cerebral metabolism is available in some neurointensive care units and may include measurements of cerebral perfusion pressure, brain oxygen, cerebral blood flow, and cerebral microdialysis. In general, cerebral perfusion pressure (CPP) should be kept > 60 mmHg and brain oxygen should be maintained > 20 mmHg, but treatment must be individualized with the goal of matching glucose and oxygen delivery to meet cerebral metabolic demands based on the available monitoring data. In the absence of advanced neuromonitoring devices, the focus should be on minimizing systemic metabolic derangements through optimizing hemodynamics and pulmonary mechanics. A reasonable target for PaCO ₂is 35–40 mmHg; targeting lower values with prolonged hyperventilation is not advised. Oxygen saturation should be kept > 88%, and hemoglobin > 7 g/dL.
G.

TBI patients are at high risk of both clinical and subclinical seizures, which if present should be treated with antiepileptic drug therapy. Continuous electroencephalogram (EEG) monitoring may detect subclinical seizures. Prophylactic antiepileptic drug therapy is for the first 7 days after injury is reasonable, but longer treatment has not been shown to prevent posttraumatic epilepsy.
H.

Fever is common after severe TBI and is associated with poor neurological outcomes. Temperature > 38°C should be aggressively treated with acetaminophen and/or induced normothermia using surface or intravascular cooling devices. Hypothermia has been shown to have no benefit, and may even cause harm, so should be avoided. Nonsteroidal antiinflammatory drugs should be avoided in most patients given the concomitant presence or risk of intracranial hemorrhage.
I.

Hyperglycemia is associated with worse neurologic outcomes in TBI, and it is thus reasonable to treat with insulin to maintain glucose < 200mg/dL. Overly stringent glycemic control (glucose levels maintained at 70–140mg/dL) does not improve mortality and results in more hypoglycemic episodes.