Traumatic head injury (Proceedings)


Traumatic head injury (Proceedings)

Aug 01, 2009

Trauma is a common presenting complaint in the small animal veterinary emergency room and traumatic brain injury (TBI) occurs in a high proportion of these patients. Common causes of TBI in dogs and cats include motor vehicle accidents, animal interactions, falls, blunt trauma, gunshot wounds and other malicious human behaviors. A global view of the patient is critical when treating TBI. Both extracranial and intracranial priorities must be addressed. Life-threatening extracranial issues, such as penetrating thoracic and abdominal wounds or airway obstruction, as well as compromise of oxygenation, ventilation, or volume status must be identified and treated appropriately. Once extracranial factors have been addressed, the focus shifts to intracranial priorities, such as maintenance of adequate cerebral perfusion pressure (CPP), oxygen delivery to the brain, and treatment of acute intracranial hypertension.


The pathophysiology of head trauma can be separated into two categories: primary injury and secondary injury. Primary injury is a direct and immediate result of the traumatic event itself and may include concussion, cerebral contusion, hematoma, and skull fracture. Secondary injury occurs in the subsequent hours to days and results from a series of physiologic and biochemical events that perpetuate neuronal tissue damage. Both systemic and intracranial insults contribute to this phenomenon and can occur independently or in combination. Systemic derangements that contribute to secondary brain injury include hypotension, hypoxemia, and disorders of ventilation. Hypoventilation leads to increased cerebral blood volume and hypoxemia while hyperventilation results in cerebral vasoconstriction and reduced perfusion. Metabolic abnormalities, such as hyperglycemia, hypoglycemia, electrolyte imbalances and acid-base disturbances further perpetuate this phenomenon. Intracranial insults that further exacerbate neuronal tissue damage include increased intracranial pressure (ICP), compromise of the blood-brain barrier, mass lesion, cerebral edema, infection, vasospasm and seizure.

Intracranial pressure and cerebral perfusion

Because the skull is a rigid structure, the volumes of the 3 normal components of the intracranial space (the brain, cerebrospinal fluid and blood) must exist in a dynamic equilibrium. This relationship is summarized by [Vintracranial = Vbrain + VCSF + Vblood]. A sudden increase in any of these volumes without a compensatory decrease in one of the others, or the presence of an additional volume due to intracranial hemorrhage can lead to dramatic increases in ICP.

Cerebral perfusion pressure (CPP) is the net driving pressure leading to blood flow to the brain. It is defined as the difference between systemic mean arterial blood pressure (MAP) and intracranial pressure (ICP) [CPP = MAP – ICP]. Both primary and secondary brain injuries result in increased ICP. This combined with hypotension (a common sequela of trauma) lead to decreased CPP and worsening of cerebral injury.

In the normal brain, autoregulatory mechanisms maintain constant cerebral blood flow (CBF) over a wide range of MAP (50 mmHg – 150 mmHg). These autoregulatory mechanisms are commonly compromised in patients with TBI making them more susceptible to ischemic injury with decreases in MAP. Acute increases in ICP will often trigger the Cushing's Reflex, a characteristic combination of systemic hypertension and sinus bradycardia. The initial drop in CPP resulting from increased ICP leads to a dramatic increase of sympathetic tone, causing systemic vasoconstriction and increased cardiac output, ultimately leading to significant increases in MAP. Stimulation of baroreceptors in the aorta and carotid sinus by the increase in MAP triggers a reflex sinus bradycardia. The presence of the Cushing's Reflex in a patient with head trauma is a sign of a potentially life-threatening increase in ICP and should be treated promptly.


Because of the likelihood of multi-systemic injury associated with head trauma, initial diagnostics and patient monitoring should focus upon a global assessment of patient stability. An initial emergency database should consist of a packed cell volume and total solids to assess for hemorrhage, blood glucose to assess severity of injury, and a blood gas (venous or arterial) to assess perfusion, ventilation, oxygenation, and acid-base status. If possible, samples for a complete blood count and blood chemistry should be obtained prior to therapy to assess renal and hepatic function, as well as to screen for other systemic disease. In general, occlusion of the jugular vein is contraindicated in patients with TBI, as this can lead to increased ICP due to decreased venous outflow from the brain; therefore, samples should be obtained peripherally, or via peripherally inserted central catheters.

Imaging of the head is indicated in patients with localizing signs of brain dysfunction, moderate to severe neurologic deficits that do not respond to aggressive extracranial and intracranial stabilization, and patients with deteriorating neurologic status. These studies can yield information about targets of potential surgical intervention, such as intracranial hemorrhage, skull fractures, or cerebrospinal fluid leaks. Skull radiographs have low sensitivity in the assessment of patients with TBI and rarely yield useful diagnostic information. Computed tomography (CT) is a sensitive imaging modality that yields excellent detail for assessment of skull fracture, acute hemorrhage, and brain edema.