Head Trauma

• 50% of trauma deaths involve head injury.
• There are 2 million cases of traumatic brain injury (TBI) per year in the US, many of which require in-hospital treatment including either surgical intervention or close observation.
• TBI is classified as mild, moderate or severe based on the Glasgow Coma Score (GCS).
• Severe TBI, accounts for 10% of all TBI, is defined as a GCS of less than 9 and has a mortality rate of close to 40%. Moderate TBI accounts for approximately 10% of all TBI, and is defined as a GCS from 9 to 13.
• Mild TBI is defined as a patient with a GCS equal to or >14.

Pathophysiology

• Acceleration/deceleration injuries
• Serious intracranial hemorrhage may occur without any direct blows or penetrating injuries to the head.
• In these injuries the brain moves within the cranial vault causing a shearing and/or stretching effect on intracranial vessels which can possibly lead to hemorrhage.
• The brain may also strike against the inner wall of the skull causing further brain injury (a contra coup injury).
• The initial traumatic injury to brain tissue is defined as the primary brain injury.
• Secondary brain injury occurs at a time after the initial mechanical trauma.
• Common causes of secondary brain injury may include hypoxia, hypotension, increased intracranial pressure (ICP) or severe anemia from exsanguinations.
• ICP
• The intracranial space is essentially a nonexpendable space, and if there is expansion of one or more of the components of this space, such as occurs with intracerebral hemorrhage or cerebral edema, the ICP will rise above the normal of 15 mm Hg.
• Limited compensatory mechanisms exist to help control this rise in ICP.
• The most common mechanism is displacement of cerebral spinal fluid (CSF) from the brain to the spinal canal.
• If the ICP becomes equal to or greater than the systemic arterial blood pressure, cerebral perfusion will stop and death of brain tissue will occur secondary to ischemia.
• The elevated ICP may also lead to brain herniation.
• Brain herniation occurs when brain tissue is displaced through the opening in the tentorium. This herniating brain tissue eventually causes compression of the brain stem leading to death.
• A dilated and fixed pupil usually occurs on the ipsilateral side of the herniation due to compression of the oculomotor nerve.

Skull Fractures

• Occur when the applied trauma causes disruption of the normal anatomy of the skull.
• Categorized as linear or depressed, open (scalp violated) or closed.
• Comminuted fractures may also occur and usually indicate an extremely forceful impact to the cranium.
• Because a significant amount of traumatic force is required to produce any kind of skull fracture, mandibular fracture, a high index of suspicion for additional associated head injuries such as traumatic brain injury should be maintained.
• Noncontrast CT scan of the head with bone windows is the diagnostic modality of choice.
• Basilar skull fractures are a special type of linear skull fracture where the fractures extend through the base of the skull.
• The most common location is the temporal bone.
• Clinical findings in basilar skull fracture may include:
• Hemotympanum caused by hemorrhage into the middle ear.
• Battle’s sign described as ecchymosis occurring behind the patient’s ear Raccoon eyes (periorbital ecchymosis)
• CSF rhinorrhea or otorrhea also occur frequently with basilar skull fracture.

Epidural Hematoma

• An epidural hematoma is a collection of blood between the dura and the inner table of the skull.
• In approximately 80% of cases there is associated skull fracture.
• Commonly occurs across the location of the middle meningeal artery.
• Arterial hemorrhage ensues causing the dura to be separated from the inner table of the skull as the hematoma expands.
• Tears of the dural sinuses also may lead to epidural hematoma formation.
• The rapidly expanding hematoma compresses underlying brain tissue which may lead to herniation.
• The classic presentation of the patient with an epidural hematoma often includes a transient loss or decrease in the patient’s level of consciousness followed by an interval of normal or improvement in mental status (lucid interval). The patient may also present with nonspecific complaints commonly seen with head injuries such as headache, vertigo, nausea and vomiting.
• Subsequent to this lucid interval the patient develops a second episode of decrease in mental status.
• The time frames of these various phases of change in mental status are variable depending on the size, location and rapidity of development of the epidural hematoma.
• Only 30% of patients with the diagnosis of an epidural hematoma will present classically.
• Statistically epidural hematomas are diagnosed in only 0.5% of head injury patients with a mortality rate of 15-25%.
• The diagnostic test of choice is a noncontrast CT scan of the head.
• The CT scan will reveal a hyperdensity that is lenticular in appearance on the surface of the brain.
• Immediate neurosurgical consultation is necessary with many cases needing operative intervention.
• If an increase in ICP is suspected interval treatment aimed at decreasing ICP is indicated pending neurosurgical intervention to prevent herniation.

Subdural Hematoma

• A subdural hematoma is described as bleeding that occurs between the brain and dura.
• This type of intracranial hemorrhage occurs more commonly than the previously discussed epidural hematoma. (approximately 30% of patients presenting with a serious head injury) Subdural hematomas have a venous source for their hemorrhage and therefore accumulate at a much slower rate than epidural hematomas.
• The most common mechanism is a tearing of bridging veins secondary to shearing force (e.g., acceleration/deceleration)
• The presence of brain atrophy places an individual at increased risk for this type of injury.
• e.g., the elderly patient or chronic alcoholics.
• An acute subdural hematoma is defined as one that causes symptoms within the first 24 h.
• A sub acute subdural hematoma becomes symptomatic in the time frame of 24 h to 2 wk after a traumatic event.
• A chronic subdural hematoma is seen in those patients who become symptomatic beyond the 2 wk time period.
• A lucid interval, although classically associated with epidural hematomas, may occur with any intracranial hemorrhage including subdural hematomas.
• Patient complaints on presentation to the emergency department may include headache, vertigo, altered mental status, focal neurological deficits, nausea and vomiting.
• CT scan makes the diagnosis and neurosurgical consultation should be obtained.

Traumatic Subarachnoid Hemorrhage

• Describes a condition of blood in the subarachnoid space secondary to injury to subarachnoid vessels.
• Commonly seen in patients with severe head injury (40% of patients).
• The patient who is not altered typically complains of photophobia and cephalgia.
• The CT scan demonstrates blood in the sulci and basal cisterns.
• In a small number of patients the amount of blood present is not sufficient to be detected by CT.
• One of the major complications of any type of subarachnoid hemorrhage is the development of secondary vasospasm which may result in secondary injury.
• Normally occurs in a time frame ranging from 2 days to 2 wk after the initial injury.
• The use of the calcium channel blocker nimodipine may be helpful in reducing the occurrence of this vasospasm.
• Neurosurgical consultation and admission to a monitored bed are required.

Cerebral Contusion/Intracerebral Hemorrhage

• A cerebral contusion is a traumatic brain injury that demonstrates areas of edema and hemorrhage.
• Usually secondary to rapid deceleration/acceleration.
• Other common mechanisms include direct blunt trauma to the head, motor vehicle accidents and falls from significant height.
• The most common locations for contusions to occur are the frontal and temporal lobes.
• The majority of patients present with some degree of alteration in mental status.
• CT scan of the head demonstrates small punctuate areas of intraparenchymal hemorrhage.
• Hospital admission and neurosurgical admission are warranted.
• Contusions to the brain can occur at the direct site of trauma or may occur on the opposite side of the patient’s brain (a countercoup injury).
• In patients with a history of previous injury, larger intracerebral hemorrhages may occur.

Concussion

• Blunt head injury with associated transient loss of consciousness.
• The patient will usually have a nonfocal neurologic examination.
• Amnesia and occasional cognitive impairment are classic findings.
• Most patients make a complete recovery; however some may develop a post concussion syndrome.
• Post-concussion syndrome consists of headache, vertigo, insomnia, anxiety and memory.
• impairment that may last for many weeks to months after the initial injury.
• This syndrome is considered to be a mild form of diffuse axonal injury.
• CT scan of the head in these cases is normal.

Diffuse Axonal Injury (DAI)

• DAI is a common cause of prolonged coma after head blunt head injury.
• Mortality rate is approximately 30%.
• The injury itself is a shearing type injury causing microscopic neuronal injury diffusely throughout the brain.
• The patient is found to be comatose with an otherwise nonlocal neurologic examination.
• CT scan of the head will reveal nonspecific findings such as evidence of edema, indistinct gray/white matter interface and loss of cortical sulci. The ventricles may also be compressed.
• All of these findings are secondary to the diffuse axonal tissue injury and edema formation.
• Autonomic dysfunction is commonly seen in these patients.

Clinical Evaluation of the Traumatic Head Injury Patient

• Primary survey and secondary surveys as previously discussed.
• It is of paramount importance that patients with a head injury not become hypoxic or hypotensive both of which can lead to secondary brain injury.
• All patients with a GCS of 8 or less should be endotracheally intubated using rapid sequence technique.
• Patients who have higher GCS scores should be intubated if there is any potential risk of aspiration or airway compromise.
• Intravenous access should be obtained immediately and volume resuscitation initiated with crystalloid (NS or LR) as clinically indicated.
• If the patient is not volume depleted, avoid the administration of excess intravenous fluid which can exacerbate the development of cerebral edema.
• In the patient who is volume depleted, after initial volume administration has stabilized the patient, be judicious with additional fluid administration.
• Hypotonic fluid should be avoided for volume resuscitation.
• Laboratory studies should include:
• CBC, basic metabolic panel and coagulation studies should be obtained.
• Bedside glucose determination (Accucheck) and hemoglobin (Hemacue) should be obtained.
• Other laboratory tests may be indicated based on physical findings, history and the possibility of additional traumatic injuries being present.
• Radiographic evaluation should include:
• A CT scan of the head should be obtained as soon as possible.
• Additional radiographic studies are indicated as dictated by the clinical situation.
• Have a low threshold for obtaining cervical spine radiographs in the head-injured patient.

Treatment of the Head-Injured Patient

• If any evidence of an increased ICP is present aggressive management to lower the ICP should be initiated.
• The head of the patient’s bed should be elevated 30 degrees assuming that there is no contraindication such as hypotension or spinal injury.
• In the intubated patient it was previously thought that hyperventilation was useful to decrease the ICP. Recent studies however show that routine hyperventilation can actually lead to worsening of neurological outcome. Although hyperventilation does cause a decrease in cerebral blood flow, in many cases it does so to the point of causing cerebral ischemia. Current guidelines only recommend hyperventilation in the setting of impending herniation.
• Osmotically active agents such as mannitol can be helpful in lowering ICP. The dosage for mannitol is 0.25-1.0 g/kg intravenously. The loop diuretic furosemide can be given along with mannitol to potentiate its effects in lowering ICP.
• The administration of hypertonic saline has shown some promise in lowering of ICP, but at this time further clinical studies are needed to clearly delineate its potential usefulness.
• Blood transfusion should be given in the setting of severe anemia to maximize cerebral oxygen delivery.
• There are no clinical benefits obtained by the administration of steroids to the patient with traumatic brain injury.
• Appropriate intravenous sedation and analgesia is extremely important in the endotracheally intubated patient.
• The restless and agitated patient will develop increased ICP and by carefully sedating the patient ICP increases can be limited.
• It is important not to use neuromuscular blocking drugs for paralysis in patients who are not adequately sedated, or significant increases in ICP will occur.
• The patient who is not adequately sedated and is pharmacologically paralyzed will be noted to have an increased heart rate, blood pressure and ICP.
• Prophylactic anticonvulsant medication is recommended for high risk patients with severe traumatic brain injury.
• The most commonly used medication for this is phenytoin (Dilantin).
• Acute seizure activity should be treated immediately with lorezepam or diazepam both of which are benzodiazepines.
• Seizure activity itself can cause a transient rise in intracranial pressure.
• Neurosurgical consultation should be arranged as soon as possible. This may require transfer to specialized facilities.
• For the patients with mild traumatic brain injury if their GCS is 15, normal neurologic exam and their CT scan is normal they may be discharged home with appropriate head injury instructions and follow-up.