Richard A. LeCouteur, BVSc, PhD, Diplomate ACVIM (Neurology), DECVN
Head injury in dogs and cats results most frequently from direct physical trauma. Head injury is a dynamic process. The outcome depends not only on the severity of the initial injury, but also on the resulting so-called secondary effects. Animals with head injury frequently have serious injuries elsewhere and shock, hemorrhage, airway obstruction, pneumothorax, and traumatic cardiac arrhythmias should be detected and treated.
Cerebral blood flow is usually reduced in the first 24 hours following traumatic brain injury. Systemic hypotension can result in inadequate cerebral perfusion pressure leading to cerebral ischemia. In addition, normal autoregulation of cerebral blood flow may also be impaired, making blood flow to damaged brain regions dependent on systemic blood pressure. While optimal cerebral perfusion pressure level is not yet entirely clear, several clinical studies in people suggest that cerebral perfusion pressure of 70-80 mm Hg, (mean arterial pressure [MAP] 80-90 mm Hg), may be a critical threshold.
Normally cerebral blood flow is closely regulated by cerebral metabolic rate. 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 head injury patients.
Intracranial Pressure Changes
The correlation between high ICP and poorer outcome in head injured people has been well demonstrated. Lowering elevated ICP reduces the risk of herniation and ensures adequate cerebral perfusion. ICP data are also strong predictors of outcome. Patients with normal ICP have the best prognosis, whereas those with uncontrollable pressure do the worst.
Intracranial pressure can be measured by intraventricular, subarachnoid, subdural and epidural catheters. Each monitoring systems has advantages and disadvantages and complications include infection, hemorrhage, malfunction, obstruction, or malposition.
Although there is no single best fluid for every patient with traumatic brain injury, isotonic crystalloids are widely used and seem the most appropriate. The use of hypertonic saline for short-term cardiovascular stabilization following trauma may be beneficial for patients at risk for elevated intracranial pressure. Glucose containing fluids are not recommended following sever head injury. Hyperglycemia develops within minutes of experimental brain injury and in head-injured people the more severe the hyperglycemia the poorer the neurological outcome.
Hyperosmolar therapy is one of the most effective 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 has become a cornerstone in the management of increased ICP. It is probable that mannitol has two distinct effects in the brain: 1) an immediate plasma expanding effect which reduces the hematocrit, reduces blood viscosity, increases cerebral blood flow, and increases cerebral O2 delivery; 2) a delayed osmotic effect that occurs 15-30 minutes after administration when gradients are established between plasma and cells. Its effects persist for a variable period ranging from 1 to 3 hours depending on clinical conditions. Mannitol should be administered as repeated boluses, rather than continuous infusion.
Hypertonic (e.g., 10% saline) solutions are hyperosmolar fluids that also appear to be a promising therapy for the treatment of intracranial hypertension and cerebral edema.
Clinical and Research Drug Therapies
Despite the wealth of research efforts directed toward the discovery of neuroprotective drugs, many potential candidates that appeared promising in experimental studies (e.g., Tirilazad mesylate), have not proven to be efficacious in clinical trials, or have been limited by unacceptable side 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.
High dose barbiturate therapy may be considered as a last resort to reduce ICP (via a reduction in cerebral metabolic rate) in hemodynamically stable sever head injury patients with intracranial hypertension refractory to maximal medical and surgical ICP lowering therapy.
A recent study of the therapeutic use of hypothermia (32 to 33°C for 24 hours) in people with traumatic brain injury found that hypothermia was associated with a significant improvement in outcome 3 and 6 months after the injury..
Aggressive hyperventilation (PaCO2<25 mm Hg) was once strongly advocated in the management of brain edema, because it can 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.
Management of the Head Trauma Patient
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 may correct 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. 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 is usually contraindicated due to the risk of brain herniation.
Head-injured patients require maintenance of systemic and cerebral hemodynamics. The two most important goals are preservation of cerebral perfusion pressure (cerebral perfusion pressure = mean arterial pressure - ICP) and maintenance of systemic oxygen availability. Ideally mean arterial blood pressure (preferably measure via arterial catheterization) and ICP should be constantly monitored in these patients. Hemodynamic goals include a MAP>80-90 mm Hg and <115-120 mm Hg. Hypertension should be treated if MAP exceeds 130-140 mm Hg.
Intravenous Fluid Therapy
Fluid restriction only minimally affects cerebral edema and attempts to control ICP through dehydration are likely to fail, and may result in further 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. Hypertonic saline may also be used to treat shock and its administration is usually 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 mean arterial blood pressure.
Increased Intracranial Pressure
Although normal ICP in man 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. 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.
Mannitol is best suited for use in reducing brain edema, particularly in comatose patients or those with deteriorating neurologic 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 patients 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 observed. 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 evacuation of intracranial mass lesions should be taken 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 should always 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. While sophisticated power-driven instruments are useful in performing a craniectomy, this procedure can be accomplished with a trephine and bone rongeurs.
Complications include CSF leakage, meningitis, and aspiration pneumonia. If a CSF leak persists beyond 7 days, surgical closure should be considered. 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. Most animals with brain trauma have depressed swallowing reflexes, so oral feeding may result in aspiration pneumonia. The most important chronic complication of head injury is the occurrence of epilepsy, usually within 2 years of injury. 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.