Head injury is a dynamic process in which the outcome depends not only on the severity of the initial injury, but also on the resulting secondary effects. In most cases the initial injury is not amenable to treatment, and therapy must be directed towards the management of secondary effects and the provision of an optimal physiologic environment for recovery of neural function. Animals with head injury frequently have serious injuries elsewhere. Problems such as shock, hemorrhage, airway obstruction, pneumothorax, and traumatic cardiac arrhythmias should be detected and treated.

A clear airway must be established and maintained and the patient placed in an oxygen rich environment with its head elevated. An oxygen cage or mask provides sufficient oxygen to prevent hypoxemia, but will not prevent hypercarbia in a hypoventilating animal. Tracheal intubation and mechanical ventilation is indicated in animals that are apneic or hypoventilating. Monitoring of tidal volume and blood gases facilitates the identification of animals requiring ventilatory support. If measurement of tidal volume and blood gases is unavailable, ventilatory assistance should be assumed to be necessary in semicomatose and comatose animals. Mental status, temperature, pulse, and respiration should be recorded as points of reference for future evaluation of response to treatment or for signs of later deterioration. Laboratory tests of special value are hematocrit, plasma protein, blood gases, and electrolyte determination. Collection of CSF usually is contraindicated due to the risk of brain herniation.

Cerebral blood flow usually is reduced in the first 24 hours following traumatic brain injury. The longer the duration of reduced cerebral blood flow, the worse will be the patient outcome.

Unfortunately after severe head injury, the relationship between cerebral blood flow and cerebral metabolic rate may be altered, resulting in either cerebral ischemia or cerebrovascular engorgement, both of which are associated with a very poor outcome in human head injury patients. Head-injured patients require maintenance of normal systemic and cerebral hemodynamics. Hypotension and hypoxia have been found to be strong predictors of outcome in people with head injury. Two important goals in this type of patient are preservation of cerebral perfusion pressure (cerebral perfusion pressure [CPP] = mean arterial pressure [MAP] minus intracranial pressure [ICP]) and maintenance of systemic oxygen availability. Ideally MAP (preferably measured via arterial catheterization) and ICP should be constantly monitored in these patients. Hemodynamic goals include a MAP greater than 80-90 mm Hg and less than 115-120 mm Hg. Hypertension should be treated if MAP exceeds 130-140 mm Hg.

Intravenous Fluid Therapy

Although restricting the volume of intravenous fluid administered once was advocated to protect the blood-brain barrier and prevent cerebral edema, fluid restriction only minimally affects cerebral edema. Attempts to control ICP through dehydration are likely to fail, and may result in further cerebral injury. Lactated Ringers solution and 0.9% saline are the most commonly recommended crystalloid isotonic solutions used to correct shock, hypovolemia and dehydration in traumatic brain injury patients (so-called resuscitative fluids). Hypertonic saline also may be used to treat shock, and its administration usually is associated with a decrease in ICP. Regardless of the fluid chosen, it must be given in sufficient volume to prevent or treat hypotension and shock and maintain an acceptable MAP.

Increased Intracranial Pressure

ICP monitoring is primarily a means for guiding therapy. Just as it is impossible to achieve optimal control of blood pressure or blood glucose without appropriate monitoring, it is not possible to treat ICP without direct pressure measurements. It has been known for several decades that one cannot ascertain ICP simply by observing clinical signs such as pupillary size and reactivity, or motor responses, prior to brain herniation. ICP data allow a clinician to manage a head-injured patient based on objective data. There is good evidence that virtually all therapies used to control ICP are "double-edged swords" and that these therapies should therefore not be used without the knowledge that ICP is, in fact, elevated.

ICP data also are strong predictors of outcome. Patients with normal ICP have the best prognosis, whereas those with increased but controllable ICP do less well and those with uncontrollable ICP do the worst. ICP may be measured by intraventricular, subarachnoid, subdural and epidural catheters. Each of the monitoring systems has advantages and disadvantages. ICP monitoring complications include infection, hemorrhage, malfunction, obstruction, or malposition. Calibration, monitoring for infection, and checking fluid-coupled devices for obstruction are necessary tasks in maintaining an optimal ICP monitoring system.

Although normal ICP in humans is reported to be between 0-10 mm Hg, normal values in dogs appear to be higher with a range of 15-25 mmHg recently reported in awake dogs. Most human centers use 20 mm Hg as the arbitrary upper limit, beyond which treatment is initiated. In a large prospective study in people reported in 1993, outcome was adversely affected when ICP was over 25 mm Hg, mean arterial BP under 80 mm Hg, and cerebral perfusion pressure under 60 mm Hg. An arbitrary upper limit for ICP in dogs has yet to be established. The role of cerebral perfusion pressure in the development of brain ischemia and the importance of monitoring ICP trends should not be overlooked.

Although CSF drainage may be used to reduce ICP elevations, this may have limited benefits as with brain swelling the ventricles and basal cisterns usually become obliterated and only small amounts of CSF can be drained from the intracranial compartment.

Hyperosmolar Therapy

Hyperosmolar therapy is one of the main treatments for cerebral edema following acute head injury. The osmotic gradient created by hypertonic solutions moves water from the cerebral intracellular and interstitial spaces into the capillaries, thereby reducing cerebral water content and ICP. Mannitol is best suited for use in reducing brain edema, particularly in comatose patients or those with deteriorating neurological status. Mannitol should be administered at a dosage of 0.5 to 1.0 Gm/kg IV over a period of 10 minutes. It may be repeated every 3-6 hours or more frequently depending on the patient's neurological status. Dangers of repeated dosage are related to effects on blood volume and electrolytes rather than specific toxicity, and the patient's blood volume status should be closely monitored. Mannitol administration may be repeated, except when there is concomitant shock or an electrolyte imbalance. A secondary increase in ICP after the initial reduction, so-called "rebound" effect appears to be rare. For a favorable prognosis, a response to medical therapy should be seen within 4 to 6 hours following commencement of treatment. An animal should be assessed every 30 minutes until stabilized.

At all times during treatment of elevated ICP the possibility that a surgical mass, or an unexpected intracranial lesion may have developed should be considered, and CT or MRI imaging obtained. Rapid removal of intracranial mass lesions should be considered without delay. Other indications for surgical decompression include the presence of open skull fractures, fractures that encroach on brain parenchyma, or fractures involving a venous sinus or middle meningeal artery. Regardless of the underlying indications for surgical decompression, craniectomy always should be considered in animals. Burr holes used in human patients to evacuate extradural hematomas have little application in dogs and cats, given the rarity of this form of hemorrhage in these species.

Clinical and Research Drug Therapies

Despite the wealth of research efforts directed toward the discovery of neuroprotective drugs, many potential therapies that appeared promising in experimental studies, have not proven to be efficacious in clinical trials, or have unacceptable adverse effects. The majority of available evidence indicates that glucocorticoids do not lower ICP, or improve outcome in severely head-injured patients. The complications associated with high dose and/or long term glucocorticoid administration are significant, and the routine use of glucocorticoids is not recommended for head trauma patients.

Other Therapies

Findings in research animals and people indicate that moderate hypothermia (32 to 33°C for 24 hours) may reduce secondary brain injury and improves the behavioral outcome. In people, hypothermia was associated with a significant improvement in outcome 3 and 6 months after brain injury.

Aggressive hyperventilation (PaCO₂ < 25 mm Hg) once was strongly advocated in the management of brain edema, because it may cause a rapid reduction of ICP. Hyperventilation reduces ICP by causing cerebral vasoconstriction and a reduction in cerebral blood flow. It now appears that the negative effect of the reduced cerebral blood flow outweighs the small increase gained in cerebral perfusion pressure and there is a risk of causing cerebral ischemia with aggressive hyperventilation. An improvement in outcome in neurological patients with severe head injury using hyperventilation therapeutically has not been demonstrated. Hyperventilation should be reserved as a last resort for the control of increased ICP refractory to all other forms of medical therapy, but is no longer recommended as a first-line therapy for intracranial hypertension or as a prophylactic therapy following severe traumatic brain injury.

Complications

Acute or chronic complications may follow head injury. These include CSF leakage, meningitis, and aspiration pneumonia. If a CSF leak persists beyond 7 days, surgical closure of the defect in the meninges should be contemplated. The use of prophylactic antibiotics in open skull fractures, or CSF leakage, is controversial. If used, they should be broad-spectrum and capable of crossing the blood-brain barrier. It should be assumed that animals with brain trauma have depressed/ineffective swallowing reflexes. It is not uncommon for oral feeding to result in aspiration pneumonia. Oral feeding should be delayed until normal mental status and effective swallowing is restored. The most important chronic complication of head injury is the occurrence of epilepsy, usually within 2 years of injury. Prophylactic treatment with anticonvulsants has not been effective in preventing these seizures. However, appropriate anticonvulsant regimens should result in control.

Throughout the management of an animal with brain trauma, intensive supportive care is essential. Factors such as frequent turning, management of nutrition, prevention of pressure sores, and attention to bladder and bowel function are of paramount importance in preventing complications commonly encountered in recumbent animals.

References

1.  Guidelines for the management of severe head injury. Brain Trauma Foundation, July 1995, Washington, DC.

2.  Zornow MH, Prough DS: Fluid management in patients with traumatic brain injury. New Horizons 3:453-455, 1995.

3.  Marshall LF, Maas AIR, Bowers Marshall S, et al: A multicenter trial on the efficacy of using tirilazad mesylate in cases of head injury. J Neurosurg 89:519-525, 1998.

4.  Marion DW, Penrod LE, Kelsey SF, et al: Treatment of traumatic brain injury with moderate hypothermia. NEJM 336: 540-546, 1997.

5.  Sturges BK, LeCouteur RA, Tripp LD: Intracranial pressure monitoring in clinically normal dogs using the Codman® ICP Express and Codman® Microsensor ICP Transducer. Proceedings American College of Veterinary Internal Medicine, Seattle, May 25-28, 2000.