Head trauma can result from a variety of different types of injury in dogs and cats. The aim of treatment for head trauma
is the prevention of secondary brain injury. Secondary brain injury refers to pathologic processes that occur after the initial
injury, such as cerebral edema or ischemia, which potentiate the severity of original injury.
Emergency management of an animal with head trauma necessitates stabilization of the cardiovascular and respiratory systems
and maintenance of blood pressure (BP) and oxygenation. In animals with clinical evidence of increased intracranial pressure
(ICP), therapy directed at decreasing intracranial pressure (ICP) is instituted.
Physical examination findings
As with all trauma patients, the initial physical examination involves first assessment of the patient's cardiovascular and
respiratory systems. After all necessary stabilization, a neurological examination should be performed. The critical components
of the neurologic examination in patients with head trauma are those factors, which provide evidence of increased intracranial
pressure. The examination should thoroughly evaluate on level of consciousness, posture, pupil size/symmetry, and pupillary
light responses. A complete neurological examination should also include evaluation of motor activity and posture.
Altered level of consciousness indicates a lesion in the cerebral cortex or brainstem. The four levels of consciousness are
1) responsive, which can range from bright to quiet 2) depressed progressing to obtunded; the patient will appear dull or
lethargic, but is still able to respond when stimulated 3) stuporous or semicomatose; vigorous stimulation is required for
arousal and 4) comatose or unconscious; the patient does not respond to any degree of stimulation.
Evaluation of pupil size and position can be extremely valuable in the head trauma patient. Anisocoria may indicate a lesion
affecting one side of the brain either independently or worse than the opposite side. Ventrolateral strabismus occurs in patients
with oculomotor nerve damage. Absence of the pupillary light reflex, unilaterally or bilaterally, can indicate disruption
or compression of the oculomotor nerve tracts ipsilateral to the injury. Historical blindness and retinal damage must be ruled
out when interpreting changes in the pupillary light reflex. Physiologic nystagmus (oculocephalic reflexes) is the normal
tracking movements of the eye in response to turning of the head from side to side. The absence of physiologic nystagmus indicates
injury in the central region of the brainstem and can be observed with brainstem hemorrhage or compression caused by herniation.
Midrange or mydriatic pupils without a pupillary light response represents severe brainstem dysfunction. If these signs are
present on initial examination and no progression is noted, brainstem hemorrhage should be suspected. These signs, in conjunction
with a comatose state and loss of oculocephalic reflexes, are associated with a grave prognosis. Progression of pupils toward
mydriasis or loss of pupillary light response may indicate gradual elevation of ICP and potential herniation. This is an indication
to initiate therapy directed at lowering ICP.
Abnormal postures that are associated with head injury include decerebrate (decorticate) rigidity and decerebellate rigidity.
Decerebrate rigidity results from a rostral brain stem lesion and leads to extension of all four limbs and opisthotonus. Decerebellate
rigidity looks similar to Schiff Scherington posture but in addition to extension of the front legs, the hindlimbs are flexed.
Unlike the Schiff Scherington posture resulting from a thoracic spinal cord injury, decerebellate posture indicates a cerebellar
There are no unique laboratory findings associated with head trauma. The laboratory values may reflect multi-system trauma,
shock or hemorrhage. Therefore trauma patients should be evaluated thoroughly. Of particular interest in head trauma is the
presence of hyperglycemia. Recently, we observed in both dogs and cats that the degree of hyperglycemia is associated with
the severity of head injury. In humans, the degree of hyperglycemia has also been associated with prognosis; however, this
relationship has not been established in animals.
Another special concern in head trauma patients is that jugular venipuncture should be avoided, as compression of the jugular
veins raises ICP.
Other diagnostic findings
Blood pressure is a valuable tool to evaluate all trauma patients, however it is even more critical in patients with head
trauma. If a head trauma patient has hypotension (MAP <80 mm Hg), this will compromise cerebral perfusion, because mean arterial
pressure (MAP) is an important determinant of cerebral blood flow. Hypotension may predispose to secondary brain injury from
cerebral hypoperfusion. On the other hand, hypertension (MAP >100 mm Hg) may indicate elevated ICP, particularly if it is
associated with a normal to low heart rate (<100 BPM). However, tachycardia and hypertension are nonspecific and may be a
response to pain.
Routine diagnostic imaging is of limited value in most head trauma patients. Radiographs of the are an insensitive diagnostic
tool and, with the exception of depressed skull fractures, rarely provide valuable information. Radiographs may be more difficult
to interpret in young animals in which osteogenesis in not complete. If more advanced imaging is available and the animal
is stable enough to obtain images, CT scanning is the preferred for imaging bone and identifying areas of acute hemorrhage