Introduction

Head trauma (HT) or traumatic brain injury (TBI) have been used as synonymous terms, but they are two different entities. HT is defined as a head injury that is clinically evident due to the presence of external injuries (ecchymosis, lacerations, deformities) produced by an external force. TBI refers specifically to an injury of the brain itself, caused also by an external force but is not always clinically evident. Management of cats and dogs suffering from HT or TBI can be challenging. HT is a complex disease and most patients suffer from additional injuries due to the initial trauma. In dogs, HT is mostly due to blunt vehicular trauma, and in cats due to high-rise syndrome. Severe TBI is associated with a high mortality in both humans and small animals. Treatment of the brain injured patient is focused on reestablishment of global perfusion and on maintaining adequate cerebral perfusion.

Pathophysiology

Cerebral perfusion pressure (CPP) is determined by intracranial pressure (ICP) minus the mean arterial pressure (MAP) and gives an indication of the pressure gradient driving blood flow across the brain (the cerebral blood flow [CBF]). As ICP increases towards MAP, cerebral perfusion becomes impaired. Systemic blood pressure must increase to prevent a decrease in cerebral perfusion pressure and subsequent decrease in CBF.

Brain injury after HT can be separated in two categories: primary and secondary injury:

Primary injury is not treatable or reversible and is due to the initial trauma. It is a result of the direct mechanical damage to brain parenchyma such as contusions, haematomas, lacerations, and diffuse axonal injury. Secondary injury is a result of the combination of systemic extracranial insults and intracranial physical and biochemical changes, which occur within minutes to hours after trauma. This stage of intracranial injury is largely mediated through increased activity and accumulation of excitatory neurotransmitters (i.e., glutamate, asparate), generation of reactive oxygen species (ROS), lipid peroxidation, and production of proinflammatory cytokines. These substrates can contribute to neuronal cell damage and possibly cell death, with resultant cerebral oedema formation, followed by increased intracranial pressure (ICP), a compromised blood-brain barrier (BBB) and alterations in cerebrovascular reactivity. Further factors contributing to secondary brain injury are hypoxaemia and ischaemia, hypercapnia, systemic hypotension, intracranial hypertension which lead to ATP depletion, accumulation of intracellular sodium and calcium, nitric oxide accumulation, and cerebral lactic acidosis. Acute increases in ICP often trigger the “Cushing’s reflex,” a characteristic combination of systemic hypertension and sinus bradycardia. Decrease in CPP due to high ICP leads to a dramatic increase in sympathetic tone. This results in vasoconstriction, increase in cardiac output and significant increase in systolic and mean blood pressure. This increased blood pressure (systolic blood pressure values up to >200 mm Hg) induces a reflex bradycardia. The presence of a Cushing’s reflex in a HT patient is a sign of life-threatening intracranial hypertension and has to be treated immediately and aggressively with hyperosmolar therapy.

Initial Patient Assessment

Patients must be assessed and treated for abnormalities in their respiratory, cardiovascular, and neurological systems first. Assessment and stabilization of the respiratory tract is mandatory during initial management of the traumatized patient. In addition, head and facial trauma is frequently associated with injuries to the upper airways and can significantly impair respiratory function. Cats and dogs with pleural space disease (pneumothorax, diaphragmatic herniation) can be identified by an asynchronous or inverse breathing pattern in combination with decreased lung sounds on auscultation. Pulmonary contusion and pneumothorax are the most common abnormalities after chest trauma. For assessment of the cardiovascular status, mentation, mucous membrane colour, capillary refill time, heart rate, pulse quality, and body temperature are determined.

Stabilization of the Head Trauma Patient - Extracranial Therapy

Adequate oxygenation, ventilation, and volume replacement are the cornerstones of initial stabilization of any trauma patient, and especially of the HT patient. Patient stabilization is based on the A (Airway) B (Breathing) C (circulation) scheme. Airway patency should be assessed as soon as possible. Oxygen supplementation can be provided by flow by oxygen, via a loose-fitting face mask, or in an oxygen cage. Target values for oxygenation are SpO₂ >95%, and PaO₂ >80 mm Hg, respectively. Nasal oxygen tubes are contraindicated in animals with HT, due to sneezing which can occur after nasal irritation, which results in increased ICP. Hypoventilation has to be avoided because even mild hypercapnia leads to increase in ICP. In addition, hyperventilation and hypocapnia should be avoided, because it leads to vasoconstriction with resultant decrease in cerebral blood flow leading to cerebral ischaemia. The venous PCO₂ should be maintained between 35–45 mm Hg. Animals with pneumothorax need thoracocentesis and may need a chest tube to evacuate the chest and allow adequate ventilation. The primary goal of fluid therapy in trauma is rapid restoration of the effective circulating volume. Major concerns in patients with TBI are that aggressive fluid therapy may exacerbate brain oedema. In the injured brain the blood brain barrier may be disrupted which leads to increased permeability to both ions and colloids. However, hypotension has to be avoided. Suitable types of fluids are isotonic crystalloids, artificial colloids, hypertonic crystalloids (NaCl 7%), or blood products. Boluses of isotonic crystalloids (20 mL/kg in the dog and 5–10 mL/kg in the cat) are administered over 10–15 minutes, until improved tissue perfusion is archived. Hypertonic saline (NaCl 7%) is another option for fluid resuscitation of trauma patients, which is explained later in this text. Synthetic colloids (6% HES 130/0.4 or 0.42) are indicated if fluid therapy with isotonic crystalloids is insufficient and are administered in a dose of 5–10 mL/kg in dogs and 3–5 mL/kg in cats over 10 minutes (maximum 30 mL/kg/24h). Mean arterial pressure (MAP) should be maintained at 80–100 mm Hg and systolic arterial pressure at 100–120 mm Hg to preserve normal cerebral perfusion pressure. If the animal is euvolemic and not in shock, isotonic crystalloids should be administered at a maintenance rate (2–3 mL/kg/h) and the patient should be monitored for ongoing blood loss. Red blood cell transfusions are indicated to restore oxygen-carrying capacity and should be started at PCV not lower than 20% in animals with acute haemorrhage.

Neurologic Assessment

A thorough neurological examination in a traumatized patient has to be delayed until the patients’ respiratory and cardiovascular status is stable! Initial neurologic assessment is, therefore, focused on the mental status and if possible, brain stem reflexes (size and symmetry of the pupils, pupillary light reflex). Once the primary survey is complete and conditions that are life threatening have been addressed, the patient can undergo neurologic evaluation. Primary goals are to determine whether the nervous system is indeed affected, to localize the problem and obtain an anatomical diagnosis, and to gain information about the prognosis. The modified Glasgow coma scale (GCS) has been proposed in veterinary patients and provides an objective way for the clinician to grade the patient with TBI at the time of admission and to monitor the patient’s response to treatment. The scale incorporates three domains: (1) level of consciousness, (2) posture and limb motor function, and (3) brain stem reflexes. Neurological assessment should be repeated every 30–60 minutes.

Level of Consciousness

The level of consciousness is classified as normal, depressed, obtunded, stuporous, or comatose, depending on response to external stimuli. Stuporous patients are unconscious, but can be aroused with painful stimuli; comatose patients fail to respond to any environmental stimulus. Coma typically indicates severe bilateral or global cerebral injury or severe brainstem damage, and carries a guarded prognosis. However, extensive blood loss, moderate or severe hypothermia or hypoxaemia can also severely alter the level of consciousness.

Posture and Limb Motor Function

Decerebrate posture (rigid extension of all limbs and opisthotonus + stupor or coma) is observed as a result of a rostral brainstem lesion and carries a guarded to poor prognosis. Decerebellate posture (opisthotonus, with the forelimbs extended, mentation normal) is often caused by an acute cerebellar lesion and can sometimes be episodic.

Brain Stem Reflexes

Normally, the two pupils should be symmetrical in shape and equal to each other in size. In the absence of concurrent ocular trauma, miotic pupils indicate diffuse forebrain injury. Progression to mydriasis may indicate brain herniation and a progressive brainstem lesion and is an indication for immediate, aggressive therapy. Bilateral mydriasis with no response to light is usually indicative of an irreversible midbrain lesion or brain herniation and carries a poor prognosis. Fixed, unresponsive and mid-range pupils are usually seen with cerebellar herniation. The oculocephalic reflex (physiological nystagmus) can be induced by rotating the head in the vertical and horizontal planes. This reflex can be impaired in an animal with a brainstem lesion as a result of involvement of central vestibular nuclei, medial longitudinal fasciculus or cranial nerve nuclei that innervate the extra-ocular muscles.

Intracranial Therapy

Simple therapies may be instituted to help minimize increases in ICP. Positioning of the head in an elevated fashion (15–30°) and avoidance of compression of both jugular veins are important.

Hypertonic therapy is the treatment of choice for increased IPC after HT/TBI and hypertonic saline (HTS) and mannitol are currently used hypertonic agents. For mannitol 20% the recommended bolus dose is 0.5–1 g/kg IV over 20 minutes. It has beneficial effects on ICP, CPP, and CBF as well as on brain metabolism. The mechanism of action is a transient plasma expansion with a decrease in blood viscosity. This results in cerebral vascular vasoconstriction and leads to a decreased cerebral blood volume (CBV) and ICP with maintained CBF. Further, mannitol promotes the shift of water from the intracellular and interstitial cerebral spaces into the vasculature, inducing an osmotic diuresis, thereby reducing cerebral oedema. This effect peaks 1 hour after administration and may persist for 6–8 hours. In addition, free radical scavenging and limitation of secondary oxidative injury in the brain has been reported. Mannitol administration is contraindicated in hypovolaemic patients. If multiple doses of mannitol or a constant rate infusion of mannitol is administered, a reverse osmotic shift can occur (accumulation of mannitol in the extravascular space and cerebral oedema). The benefits of HTS 7% were discovered from studies on “small volume resuscitation.” The dose for 7% HTS is 2–4 mL/kg over 2–5 minutes and results in an immediate restoration of intravascular volume. HTS improves the microvasculatory flow, controls intracranial pressure, improves cardiac performance, and stabilizes arterial blood pressure. An osmotic force, shifting water from the interstitial and intracellular spaces into the intravascular space is created, with resultant reduction in brain water content and ICP. In addition, regional CBF and oxygen delivery are improved due to dehydration of cerebrovascular endothelial cells and reduction of endothelial oedema. HTS solutions have also been shown to decrease brain excitoxicity and modulate the inflammatory response. Combining HTS with an artificial colloid can prolong the volume expanding effect. Because of their rapid volume expanding effect, HTS and mannitol both carry the risk of aggravating pulmonary oedema in patients with cardiac or respiratory pathology. If an individual patient is not responding to one of the two fluids, the other may yield a beneficial response. In several studies HTS resulted in a greater absolute ICP decrease and a more sustained effect than mannitol.

Additional Therapeutic Options

Glycaemic Control

Hyperglycaemia has been shown to have detrimental effects in patients with TBI and so iatrogenic hyperglycaemia, such as may occur with corticosteroid administration, must be prevented. Hyperglycaemia increases free radical production, excitatory amino acid release, cerebral oedema, and cerebral acidosis, and alters the cerebral vasculature.

Pain Control

Adequate analgesia is critical in prevention of further increase in ICP. Opioids are commonly used due to their relative lack of adverse cardiovascular effects and ease of reversal. Methadone (0.1–0.2 mg/kg) or fentanyl (0.005–0.01 mg/kg) are fast acting µ-agonists. Due to its short action, fentanyl has to be administered as a constant rate infusion (5 µg/kg/h). A disadvantage of opioids is that assessment of the neurogenic status is impaired. However, if needed, fentanyl or methadone can be antagonized with naloxone, in contrast to buprenorphine which cannot be antagonized.

Anticonvulsive Therapy

Risk factors for post-traumatic seizures include severity of injury, skull fractures, epidural, subdural, and intracerebral haematomas, penetrating head wounds, and a seizure within the first 24 hours following injury. Adverse effects of seizure activity include hyperthermia, hypoxaemia, and cerebral oedema, with resultant intracranial hypertension. Diazepam is the anticonvulsant of choice for stopping an ongoing seizure due to its rapid onset of action and reliable efficacy. For prevention of further seizures phenobarbital is recommended. Barbiturates have the ability to decrease the energy requirements of cerebral tissue, which may decrease oxygen demand by neuronal tissue resulting in vasoconstriction and decreased blood flow. This may, in turn, lead to decreased ICP. In case of ongoing seizures despite loading with phenobarbital, intravenous administration of pentobarbital or propofol can be used for induction of coma. Propofol is given at a rate of 0.1 mg/kg/m via syringe pump, but can be titrated to effect. Anaesthesia is often maintained with 0.4 mg/kg/m.

Corticosteroids

Because of the lack of evidence of any beneficial effect after TBI and strong evidence from human literature showing a detrimental effect on neurologic outcome, corticosteroids should not be administered to dogs and cats with TBI.

Furosemide

Furosemide should be reserved for patients with pulmonary oedema or oliguric renal failure. Due to its volume depleting effect, it can lead to systemic hypotension and to decreased CPP.

References

References are available upon request.