Head trauma (Proceedings)
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 lesion.
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 or edema.
After the cardiovascular and respiratory systems have been stabilized, attention should focus on treatment of neurologic injuries.
The two factors known to contribute to secondary brain injury are hypotension (leading to cerebral hypoperfusion and hypoxemia. Cerebral perfusion pressure (CPP) is calculated as the patient's MAP minus ICP, and represents the primary determinant for cerebral blood flow and cerebral oxygen and nutrient delivery.
For head trauma patients the goal of fluid resuscitation is a MAP >80 mm Hg. The fear that initial volume resuscitation may exacerbate cerebral edema is unfounded, and volume restriction is contraindicated in head-injured patients. Hypertonic saline (7.5% NaCl) combined with an artificial colloid (i.e., hydroxyethylstarch) is considered the fluid of choice for resuscitation of hypovolemic head trauma patients. This combination has experimentally been shown to rapidly expand volume and decrease ICP (by decreasing cerebral edema), thereby restoring cerebral perfusion pressure (CPP). Oxygen supplementation is indicated in all cases of head trauma. If the animal has compromised ventilation, then mechanical ventilation should be considered to provide adequate oxygenation and prevent hypercarbia, which can lead to increased ICP.
General therapeutic measures in animals with head trauma should be directed at minimizing increases in ICP. A simple approach is to elevate the head and neck 15–30 degrees above the rest of the body to maximize venous drainage from the head and subsequently lower ICP. Avoid positions that cause jugular vein compression because this elevates ICP. Elevating the head more than 30 degrees may be detrimental because it can decrease cerebral blood flow, increase ICP, and decrease CPP.
Specific therapy directed at lowering ICP is restricted to those patients with either clinical signs of increased ICP or measured elevation in ICP. Mannitol, 0.5–1.0 g/kg IV over 20 minutes is the first line of therapy. It acts as an osmotic diuretic to lower ICP, as a rheologic agent to improve microvascular blood flow within the brain and to scavenge free radicals. A clinical response to mannitol therapy may be seen within 5-10 minutes, with maximal effects noted within 20-40 minutes of administration. An improvement in mentation, posture, and pupillary signs indicate a positive response to mannitol therapy. If there is an insufficient response to the first dose of mannitol, an additional bolus can be given 40-60 minutes later. Lack of improvement with this therapy indicates that the brain damage will not be responsive to mannitol therapy and further therapy may not be warranted. The benefits that mannitol have on lowering ICP in the rest of the brain outweigh the concern that mannitol may result in worsening of intracranial hemorrhage. The side effects associated with repeated mannitol administration include hyperosmolarity, hypovolemia, and electrolyte disturbances (elevated sodium most commonly), therefore, adequate fluid therapy and monitoring are necessary.
In acutely deteriorating patients, hyperventilation aimed at lowering the PaCO2, to 30–35 mm Hg can be considered. Reduction of PaCO2 decreases cerebral blood flow and thus decreases ICP. Excessive or long-term hyperventilation, however, can lead to cerebral vasospasm and secondary brain injury. Failure to respond to medical management may be an indication for an emergency craniotomy.
Moderate hypothermia (32°C–33°C) has been found to hasten recovery and improve the degree of recovery in human head trauma victims compared to those treated with conventional therapy. Hypothermia has many purported effects on brain injury, including reducing metabolic demands of the brain, limiting inflammatory mediator release, and improving regional blood flow to damaged tissues. There is no information about the practicality, side effects or efficacy in veterinary patients.
Induction of a barbiturate coma was previously recommended to decrease cerebral metabolic rate and ICP. However, this therapy has come under question in light of harmful effects noted in human head trauma patients. If barbiturates are used in veterinary head trauma patients, then extensive monitoring of BP and ability to ventilate (PaCO2) is required to minimize adverse effects.
Dewey, C.W. Emergency management of the head trauma patient. Vet Clin North Am Small Anim Pract 30:207–225, 2000.
Syring, R.S., Otto, C.M., Drobatz, K.J. Hyperglycemia in dogs and cats with head trauma: 122 cases (1997-1999). J Am Vet Med Assoc 218:1124-1129, 2001.
Fletcher, D.J. and R. S. Syring. 2009. "Traumatic Brain Injury". In Small Animal Critical Care Medicine. edited by D.C. Silverstein, and K. Hopper, 658-662. St. Louis: Saunders Elsevier.