Traumatic brain injury is a common concern in the small animal emergency patient. Appropriate, effective management of these patients can have a dramatic impact on outcome. Traumatic brain injury causes primary structural damage as a result of contusion, laceration, compression and/or haemorrhage of the parenchyma. Patients that survive the initial injury are at risk of deterioration and possibly death due to progressive derangements in blood flow and cellular function, a process known as secondary brain injury. The clinician cannot alter the extent of the primary injury and instead must focus on preventing or minimising the occurrence of secondary brain injuries.

Intracranial Pressure

The cranial vault is an enclosed space which contains three essential components: brain parenchyma, blood and cerebral spinal fluid (CSF). Brain trauma patients can have increases in intracranial volume and hence pressure as a consequence of cerebral oedema, haemorrhage, vasodilation and venous outflow obstruction. Intracranial hypertension will reduce cerebral blood flow (see below), alters neuronal function and if severe can lead to herniation of the cerebrum or cerebellum. This can cause brainstem compression and is often a terminal event.

If cerebral ischemia occurs there is a 'cerebral ischemic response'. This stimulates systemic hypertension in an attempt to improve cerebral blood flow. This hypertensive response is called the Cushing's reflex and is accompanied by a bradycardia.

Hypertension in the brain trauma patient requires immediate intervention

When autoregulation is intact, cerebral vessels will vasodilate in response to hypercapnia or hypoxemia. The PCO₂ is one of the most important determinants of cerebral blood flow. If vasodilation occurs it can effectively increase the blood volume within the cranium and contribute to intracranial hypertension.

Assessment of the Head Trauma Patient

As with all emergency patients the primary survey of airway, breathing and circulation should be assessed first. The patient should be fully resuscitated before neurologic injuries are evaluated. Patients with head trauma may also sustain spinal trauma and should be handled cautiously until these injuries have been evaluated.

A brief evaluation of abrasions and/or lacerations over the head is performed for evidence of decompressed or open skull fractures. The external ear canals are examined for the presence of blood or CSF which may indicate the presence of basilar skull fractures. Clear fluid from the external ear canal can be collected and a blood glucose measured. CSF has a blood glucose of ~60% of serum glucose, true nasal/aural discharges do not contain glucose. The sensitivity and specificity of this method for detecting CSF in veterinary patients has not been evaluated.

Neurological assessment should include evaluation of the level of consciousness, cranial nerve reflexes and skeletal motor responses. The aim of assessment is to determine the location and severity of the injury. Serial neurologic examinations need to be performed in the first 24 hours as rapid changes in status can occur and will require immediate intervention if therapy is to be successful.

Important cranial nerve reflexes to evaluate include:

 Menace reflex

 Eye position

 Pupil size

 Pupillary light reflex

 Palpebral reflex

 Oculocephalic reflex

 Gag reflex

Examining the pupils helps determine the nature and severity of the brain injury (Table 1). In addition serial pupil examinations are one of the most useful methods for detecting changes in patient status.

Table 1. Interpretation of pupil size and reactivity.

*Anisocoria in the absence of orbital trauma

Abnormalities in a cranial nerve reflex indicate injury to the brainstem or the neural pathway connecting to the brainstem. Multiple cranial nerve deficits is highly suggestive of brainstem injury. The two most useful cranial nerve reflexes for rapid assessment of brainstem function are the gag reflex and the presence of physiologic nystagmus, otherwise known as the oculocephalic reflex. If these two reflexes are absent it strongly indicates significant brainstem injury and a guarded prognosis.

The segmental spinal reflexes should be evaluated when possible, without excessive manipulation of the patient. Abnormalities in thoracic and/or pelvic limb reflexes will help identify spinal trauma. Cases of brain injury without spinal injury tend to have normal or possibly exaggerated spinal reflexes.

Decerebrate posture: patient has opisthotonos and extensor rigidity of all four limbs. The animal is unresponsive and does not detect deep pain sensation. This is associated with rostral brainstem lesions and is generally associated with a grave prognosis.

Decerebellate posture: patient has opisthotonos and extensor rigidity of the thoracic limbs and variable extension/flexion of the pelvic limbs. The animal is conscious and aware with normal pupil responses. This is associated with acute cerebellar lesions and has a far better prognosis than decerebrate rigidity.

Indications of cerebral injury: circling, ataxia, blindness, altered mentation, loss of consciousness, seizures, Cheyne-Stokes respirations

Indications of brainstem injury: coma, loss of gag, lack of physiologic nystagmus (oculocephalic reflex), strabismus, non-responsive pupils, apneustic or ataxic respiratory pattern, decerebrate posture

Indications of cerebellum / vestibular injury: head tilt, rolling, nystagmus, ataxia, decerebellate posture

Prognosis

Brainstem injuries have a poor prognosis and these patients can develop acute cardiorespiratory abnormalities. Patients with cerebral injuries tend to be more stable and although prognosis for recovery may be difficult to predict, animals can survive significant cerebral trauma if given sufficient time. This is probably aided by the reality that pets do not need to regain the level of function that a human patient requires. Cerebellar injuries can usually be managed and many of these animals will recover sufficient function to go home and lead a good quality of life. They may however have permanent gait and co-ordination abnormalities. Recovery from brain injury and accurate assessment of function requires time; it may take months (even years) for maximal recovery to occur.

Imaging

Survey radiographs of the skull and spine are recommended in all brain trauma patients to rule out vertebral fractures and to identify depressed skull fractures. Unfortunately routine radiographs do not allow evaluation of parenchymal changes. Thoracic radiographs are always indicated in the trauma patient, especially if there are signs of respiratory distress or emergency surgery is contemplated. Computed tomography (CT) is far more accurate at identifying skull fractures and bone fragments in the parenchyma. It can also identify intraparenchymal changes such as haemorrhage and oedema but in general magnetic resonance imaging (MRI) is far more sensitive at imaging intraparenchymal disease.

Supportive Care

All head trauma patients should receive oxygen therapy in the initial stabilization period and it should be continued in those patients with moderate to severe injury in an effort to minimize the ischemic insult to the brain. Oxygen therapy by oxygen hood or cage is ideal. Nasal oxygen catheters should be avoided as the restraint needed for placement may cause jugular vein occlusion and subsequent elevations in ICP. Head trauma patients often have nasal turbinate fractures and in severe cases there can be fractures of the cribriform plate. These abnormalities can be further aggravated by the passage of a nasal oxygen catheter.

As cerebral perfusion pressure is highly dependent on mean arterial pressure (MAP) it is essential to aggressively resuscitate and support the cardiovascular system of the brain trauma patient. In an effort to maintain a high serum osmolality and hence reduce cerebral oedema, 0.9% NaCl is the isotonic fluid of choice for the management of these animals. Hypotonic solutions such as half strength saline or 5% dextrose are contraindicated. Hypertonic saline may be preferable for resuscitation of the hypovolemic patient. Monitoring of arterial blood pressure should be performed whenever possible. The aim is to maintain MAP > 90 mm Hg. Episodes of hypertension (MAP>140 mm Hg, Systolic pressure>160 mm Hg) are strongly suggestive of intracranial hypertension.

Appropriate analgesia is essential for the trauma patient; opioids are used for their strong analgesic properties, minimal adverse effects and can be reversed. Care to titrate the opioid dose such that it does not cause significant increases in PCO₂ is important.

Initial blood work should include a venous blood gas measurement in order to assess the PvCO₂. Because elevations in PCO₂ cause cerebral vasodilation and consequently increase ICP it is very important to prevent hypercapnia. PaCO₂ is ideally maintained at 35-40 mm Hg (PvCO₂ ~ 40-45 mm Hg).

Intracranial Hypertension

Any patient with brain injury is at risk of intracranial hypertension and should be handled carefully. What may seem to be quite benign manipulations of the animal can have dramatic consequences. Occlusion of a jugular vein can impair cerebral venous drainage and increase ICP. For this reason jugular blood samples and jugular catheters should be avoided in head trauma victims. Patients in lateral recumbency are best kept with their heads elevated at a 30° angle to aid venous return while minimally impairing cerebral perfusion. Intubation can cause increases in ICP and for this reason lidocaine should be applied to the larynx of dogs and cats with brain injury prior to the procedure.

Evidence of elevated ICP includes vomiting, deteriorating neurological state, Cushing's reflex (systemic hypertension and bradycardia) and papilledema on fundic examination. Imaging with CT or MRI can show changes associated with intracranial hypertension and direct intracranial pressure measurement can be performed using specialized equipment.

Patients with evidence of intracranial hypertension are treated with hypertonic fluid therapy:

 Hypertonic saline: slow IV injection (over 3-5 minutes)--a suggested dose is 3-4 ml/kg of 7.5% NaCl, or

 Mannitol: given as a 15-20 minute IV infusion--0.5-1.0 g/kg

These doses can be repeated, hypertonic saline can be given to keep serum sodium ~ 160-165 mEq/L. Mannitol is used to elevate serum osmolality ~ 20mosm greater than normal.

Anaesthesia

If it is necessary to anaesthetise a patient with intracranial disease it is important to avoid agents which can exacerbate intracranial hypertension. Inhalant anaesthetics, especially halothane cause cerebral vasodilation and are generally considered contraindicated in these patients. Ketamine may also cause elevations in ICP. Other injectable agents such as propofol and barbiturates are recommended, consideration of the animal's cardiovascular status is important when using these drugs. Ideally any patient with intracranial disease should receive positive pressure ventilation during anaesthesia to prevent fluctuations in PCO₂.

Corticosteroids

There is no clinical evidence showing benefits of steroids in patients with head trauma. Experimentally, high dose corticosteroids are beneficial when given within minutes of the traumatic insult while late administration of steroids can have negative effects on neurological outcome. Corticosteroids can result in hyperglycemia and this is considered detrimental in patients with neurological injury. Given the significant side effects of high dose corticosteroid administration and the lack of evidence of associated improvement in neurological recovery or outcome they are not currently recommended for head trauma patients.

References

1.  Guidelines for management of traumatic brain injury. Brain Trauma Foundation, New York. 2000

2.  Bagley RS. Intracranial pressure in dogs and cats. Comp Vet Cont Educ 1996;18(6):605-620

3.  Fletcher DJ, Syring RS. Traumatic brain injury. In: Silverstein DC, Hopper K (eds). Textbook of small animal critical care medicine, Saunders, St Louis, 2009, p658

4.  Sturges BK, LeCouteur RA. Intracranial hypertension. In: Silverstein DC, Hopper K (eds). Textbook of small animal critical care medicine, Saunders, St Louis, 2009, p423