Head Trauma in the Cat: 2. Assessment and Management of Traumatic Brain Injury

Abstract

Practical relevance Feline trauma patients are commonly seen in general practice and frequently have sustained some degree of brain injury.

Clinical challenges Cats with traumatic brain injuries may have a variety of clinical signs, ranging from minor neurological deficits to life-threatening neurological impairment. Appropriate management depends on prompt and accurate patient assessment, and an understanding of the pathophysiology of brain injury. The most important consideration in managing these patients is maintenance of cerebral perfusion and oxygenation. For cats with severe head injury requiring decompressive surgery, early intervention is critical.

Evidence base There is a limited clinical evidence base to support the treatment of traumatic brain injury in cats, despite its relative frequency in general practice. Appropriate therapy is, therefore, controversial in veterinary medicine and mostly based on experimental studies or human head trauma studies. This review, which sets out to describe the specific approach to diagnosis and management of traumatic brain injury in cats, draws on the current evidence, as far as it exists, as well as the authors' clinical experience.

CRANIOFACIAL INJURY

The first part of this two-part article, addressing the diagnosis and management of craniofacial injury, appears on pages 806–814 of this issue of J Feline Med Surg and at: doi:10.1016/j.jfms.2011.09.002

Primary assessment

It is all too tempting when faced with a cat presenting with severe neurological signs to rush into evaluation of its neurological status. Human studies have shown, however, that up to 60% of head trauma patients have concurrent systemic injuries involving the thorax (lung contusion, pneumothorax, neurogenic pulmonary oedema), abdomen (splenic torsion, bladder/urethral rupture), spine and/or long bones (fracture/luxation). ¹ Initial physical assessment of these feline emergency cases should, therefore, focus on any immediately life-threatening abnormalities and evaluation of vital functions, all of which can influence not only the interpretation of the neurological examination but also the prognosis for the patient.

Upon arrival, the cat should be carefully triaged, with immediate assessment of the ABCs (airway, breathing, circulation) to determine whether it is stable. There may be concurrent conditions that, even if not critical, will require appropriate monitoring so that potential problems can be anticipated and prevented.

Initial neurological evaluation

Once the primary survey is complete, and any conditions that are life-threatening have been identified and addressed, the cat can then undergo specific neurological assessment. The aims at this stage are to:

• Determine whether the nervous system is indeed affected.

• Obtain an anatomic diagnosis (forebrain, brainstem, cerebellar, ± spinal cord involvement, or multifocal).

• Gain information about the prognosis.

In human patients, traumatic brain injury (TBI) is graded as mild, moderate or severe on the basis of the level of consciousness as described on the Glasgow coma scale (GCS). This is a tool that provides a quantitative measure that can be used to assess initial neurological status, progression of signs and prognosis. A modified version of the GCS has been proposed in veterinary medicine for dogs and provides an objective way for the clinician to grade the patient on admission and to monitor any response to treatment. ⁸ Although an almost linear correlation between the GCS score on admission and probability of survival over a 48-h period has been shown in dogs, there is as yet no information in the literature showing a correlation with long-term outcome and functional outcome in dogs or cats with TBI.

Pathophysiology of brain injury

Intracranial Pressure and Cerebral Perfusion

Intracranial pressure (ICP) is defined as the pressure exerted between the skull and the intracranial tissues. ² The cerebral perfusion pressure is calculated by subtracting ICP from mean arterial pressure (MAP) and gives an indication of the pressure gradient driving blood flow across the brain (ie, cerebral blood flow [CBF]). ² As ICP increases towards MAP, cerebral perfusion becomes impaired. Systemic blood pressure must increase to prevent a decrease in cerebral perfusion pressure and a resultant decrease in CBF.

Primary and secondary injuries

Head trauma can produce primary and secondary brain injury. ^3,4 Primary injuries, which are not treatable or reversible, describe the direct tissue damage that occurs at the time of initial impact. When the head is struck, neurons and intracranial blood vessels are subjected to direct impact as well as flexion, extension and shearing forces as the brain moves inside the cranium.

Secondary injury is the additional insult imposed on the neural tissue following the primary impact. Cerebral ischaemia is an important factor in secondary brain injury. The deleterious effects of ischaemia involve several different processes including generation of free radicals, lipid peroxidation, breakdown of arachidonic acids, and accumulation of glutamate and aspartate, excitatory amino acids which interact with NMDA (N-methyl-D-aspartate) receptors and lead to intracellular accumulation of calcium ions. ⁴ The main contributors to secondary ischaemia in head-injured patients are hypoxaemia, hypercapnia, systemic hypotension and intracranial hypertension. ^{3 –5} In these patients, normal cerebral autoregulation is disrupted, with uncoupling of CBF and metabolism. CBF decreases early after trauma, the magnitude of the decrease being related to the severity of the injury. ^2,6 Later in the clinical course, the low-flow state may persist; alternatively, metabolic uncoupling may lead to hyperaemia whereby CBF is increased beyond the metabolic requirements of the brain.

Changes in ICP after head trauma

The normal intracranial contents can be divided into four compartments: brain tissue, interstitial water, cerebrospinal fluid (CSF) and cerebral blood volume (CBV). With trauma involving the head, cerebral oedema, CSF accumulation, vascular congestion or the presence of an intracranial mass, such as a blood clot or depressed skull fracture, lead to an abnormal volume increase inside the skull, which acts as a rigid box. At first, ICP shows little tendency to increase as long as compensation for the space occupation is available. Compensatory mechanisms include increased CSF absorption and displacement to the spinal subarachnoid space, increased venous return and decreased CBF (Fig 1). ^2,4 At a later stage, the same increase in volume produces a distinct rise in pressure, and the immediate onset of clinical signs. As illustrated in Fig 2, the steepest part of the curve is at the point where the compensatory mechanisms are virtually exhausted — the so-called decompensatory phase. At this critical point, any further abnormal volume added to the tightly compressed intracranial state will produce a massive rise in ICP and clinically this may be associated with herniation of the brain through the tentorium cerebelli or into the foramen magnum. ²

FIG 1.

The total volume of the contents of the cranial cavity (brain tissue, interstitial water, blood and CSF) is fixed. After head trauma, the volume of the intracranial contents may increase due to haemorrhage, oedema or CSF accumulation. The brain has the capacity to tolerate small increases in volume by adjusting the size of one of the components. Shunting CSF to the spinal subarachnoid space, decreasing CSF production, and increasing CSF absorption can rapidly decrease the CSF compartment. Additionally, venous blood can be redirected out of the cranial cavity and CBF will decrease to compensate for ICP elevation. Once these compensatory mechanisms have been exhausted, small increases in volume will result in dramatic elevations in ICP, which will be accompanied by a rapid decline in the cat's neurological status. Ultimately, increases in ICP lead to brain herniation and death

FIG 2.

Relationship between ICP and intracranial volume. During the compensatory phase, increases in intracranial volume produce minimal changes in ICP. Once the compensatory mechanisms have been exhausted, small increases in intracranial volume result in a dramatic increase in ICP (decompensatory phase)

Unfortunately, the neurological signs associated with significantly increased ICP often become evident too late for any therapy to be effective. With the exception of oedema reduction by mannitol, the only intracranial constituent that can be readily modified in volume by physiological or pharmacological interventions is the CBV. Although the CBV represents only a small part of the intracranial volume, even small increases in CBV can result in steep rises in ICP when compensatory mechanisms to control ICP have been exhausted. ⁷ As cerebral perfusion pressure is determined by the difference between MAP and ICP, a high ICP will lead to cerebral ischaemia (see inset box above).

The scale incorporates three domains (see box below) — (1) level of consciousness, (2) posture and limb motor function, (3) brainstem reflexes — with a score of 1–6 being assigned to each domain. Thus, the total score ranges from 3–18, with lower scores indicating more severe neurological deficits. ⁸

The authors recommend using the modified GCS in all feline TBI cases. It is important that the initial neurological examination is interpreted in the light of the cardiovascular and respiratory systems, as shock can have a significant effect on neurological status. Neurological assessment should be repeated every 30–60 mins in cats with severe head injury to assess for deterioration and to monitor the efficacy of any therapies administered. ⁹

Level of consciousness

The level of consciousness is the first element that should be evaluated and represents an important criterion for grading head injury as mild, moderate or severe. ^10,11 The level of consciousness is classified as normal, depressed, obtunded, stuporous or comatose depending on the cat's response to external stimuli. Stupor and coma both represent a state of unconsciousness. While a stuporous cat can be aroused by a painful stimulus, a comatose cat will fail to respond to any environmental stimuli, including pain.

As a rule, altered states of consciousness relate either to a diffuse lesion or widespread multifocal lesions of both cerebral hemispheres, or to a focal lesion affecting the ascending reticular activating system (ARAS) of the brainstem. ^8,10 The ARAS functions to arouse the cerebral cortex and maintains the state of wakefulness. Coma typically indicates severe bilateral or global cerebral injury or severe brainstem damage, and carries a guarded prognosis. ¹⁰ It is important to be aware that extensive blood loss, moderate or severe hypothermia or hypoxaemia can also severely alter the level of consciousness. These abnormalities should, therefore, be addressed before drawing any conclusions about a patient's level of consciousness.

Modified Glasgow coma scale ⁸

Extensive blood loss, moderate or severe hypothermia and hypoxaemia should be addressed before drawing any conclusions about a patient's level of consciousness.

Posture and limb motor function

Spontaneous and evoked limb movements are assessed as part of the initial neurological evaluation. The cat's posture after head trauma can also provide information about the location and degree of brain injury.

• Decerebrate posture is observed as a result of a rostral brainstem lesion (between the colliculi of the midbrain) and carries a guarded to poor prognosis. It is characterised by rigid extension of all limbs and opisthotonus (dorsoflexion of the head and neck), and is associated with a stuporous or comatose mental status.

• Decerebellate posture is often caused by an acute cerebellar lesion and can sometimes be episodic. The rostral part of the cerebellum is inhibitory to the stretch reflex mechanism of antigravity muscles (extensor muscle tone). Lesions at this level can result in opisthotonus, with the forelimbs extended. Compared with the decerebrate posture, the hips may be flexed as a result of increased tone in the iliopsoas muscle and mentation remains normal.

Brainstem reflexes

Evaluation of pupil size/response and eye movements is the basis for assessing the brainstem category on the modified GCS. ^8,10

Pupillary abnormalities are common following head injury. However, primary ocular injuries must be considered in the assessment of the pupils as they may alter the pupillary size and light reflexes. The size of the pupils represents a balance between the parasympathetic system, which is responsive to the amount of light entering the eye, and the sympathetic system, which is responsive to the emotional state of the animal. The parasympathetic component of the oculomotor nerve (CN III) is involved in the control of pupillary constriction. The tone of the iris dilator muscle is maintained by the sympathetic system, which keeps the pupil partially dilated under normal conditions and dilates it more notably during periods of stress or fear, and in response to painful stimuli.

Assessment of pupil shape and size should be determined in ambient light as well as in darkness. Normally, the two pupils should be symmetrical in shape and equal to each other in size. Miotic pupils indicate diffuse forebrain injury. ⁸ 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 (Fig 3). Fixed, unresponsive and mid-range pupils are usually seen with cerebellar herniation. ⁸

FIG 3.

In the absence of concurrent ocular trauma, miotic pupils may indicate loss of cortical input or direct damage to sympathetic centres in the diencephalon, allowing unopposed oculomotor pupillary constriction. Pupils that are initially miotic and then become mydriatic and unresponsive to light are indicative of a progressive severe brainstem lesion (mostly seen with raised ICP and caudal subtentorial herniation)

Spinal injury (in particular, cervical injuries) should be ruled out prior to evaluating the oculocephalic reflex.

Evaluation of spontaneous ocular movement and the oculocephalic reflex (physiological nystagmus) represents an important part of brainstem assessment in the unconscious patient. The oculocephalic reflex 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 extraocular muscles (CN III, IV and VI). Spinal injury (in particular, cervical injuries) should be ruled out prior to evaluating this reflex as it involves moving the head and neck.

Is the head injury mild, moderate or severe?

At the completion of the neurological assessment, the clinician should be able to classify the cat's head injury on admission as mild, moderate or severe. The level of consciousness offers a first screening — with head injury being classified as mild in a normal or depressed/obtunded/ delirious animal, moderate in a stuporous animal, and severe in a comatose animal. Evaluation of pupil size/response and eye movement, as well as the presence of abnormal postures, helps to further subdivide patients within the moderate to severe categories according to the modified GCS scoring scheme. This process will guide treatment planning and monitoring.

Additional diagnostics

Emergency database

Because of the likelihood of multisystemic injury associated with head trauma, the initial emergency database should focus on packed cell volume and refractometric total protein to assess the degree of blood loss; blood glucose; blood pressure; electrocardiography; and arterial blood gas analysis to assess perfusion, ventilation, oxygenation and acid-base status. ^11,12 Specific consideration should be given to serum glucose concentration since cats with head trauma may have hyperglycaemia and the degree of hyperglycemia is associated with the severity of head trauma. However, the degree of hyperglycaemia does not appear to be associated with outcome. ¹³ The development of hyperglycaemia following head trauma is considered a component of the stress response to injury, which results in many metabolic alterations. ^14,15

Monitoring of blood pressure is essential to ensure adequate arterial and cerebral perfusion pressures are maintained.

Brain imaging

Brain imaging is recommended in cats with moderate-to-severe neurological deficits that are refractory to aggressive extracranial and intracranial stabilisation (see treatment section), and those with progressive neurological signs. ^4,9,12 Skull radiographs are usually of limited value, but can sometimes identify fractures of the calvarium. The two modalities of choice are magnetic resonance imaging (MRI) and computed tomography (CT) (Figs 4 and 5). Both have their advantages, although CT seems to be the most suitable for cats with head trauma (being faster, less expensive, and providing better resolution of bone details and acute haemorrhage).

FIG 4.

CT scan (bone window) of a cat involved in a road traffic accident, showing a comminuted depressed fracture of the temporal bone on the left side (arrow). Courtesy of J Fraser McConnell, University of Liverpool

FIG 5.

Transverse T2-weighted (a), T2* (b) and dorsal T2-weighted (c) magnetic resonance images of the head of a domestic shorthair cat with a penetrating injury to the brain (suspected bite wound). Although the damage to the calvarium can be difficult to appreciate on MRI, the associated parenchymal damage can be identified (star). These scans reveal swelling of the left temporalis muscle (arrow-head), a small defect within the skull (arrow) and a mass lesion within the right parietal lobe associated with vasogenic oedema and a mass effect (midline shift). T2* sequences are particularly useful for identifying intracranial bleed, which is visible as an area of hypointensity when compared with the signal intensity of brain parenchyma. Courtesy of the Animal Health Trust, Newmarket, UK

Cats with head trauma may have hyperglycaemia as a stress response to injury.

Cervical spinal and thoracic radiographs or CT scans are also advised at the time of any skull imaging to rule out concurrent lesions.

Brain imaging is an important step in the decision-making process when dealing with a head trauma patient, as it will help to determine whether to pursue medical treatment, and/or surgical treatment if there is evidence of a depressed skull fracture, intra- or extra-axial haemorrhage or CSF leakage.

CT seems to be the most suitable imaging modality for cats with head trauma — being faster, less expensive, and providing better resolution of bone details and acute haemorrhage than MRI.

Treatment priorities

The most important consideration in the head-injured patient is maintenance of cerebral perfusion and oxygenation. Hypovolaemia and hypoxaemia must be recognised and treated immediately as, certainly in human TBI patients, they are strongly correlated with elevated ICP and increased mortality. ^{7,16 –19} The initial approach to treatment of head trauma should, therefore, focus on extracranial stabilisation, closely followed, where indicated, by therapies directed towards intracranial stabilisation.

Careful monitoring is essential during the initial period and should include assessment of vital parameters as well as neurological status (Table 1).

Table 1.

Vital parameters in the cat

Parameter monitored	Intended goal
Blood pressure	MAP 80–100 mmHg SBP 120 mmHg
Oxygen saturation of haemoglobin (pulse oximetry)	SpO2 ≥95%
Heart rate and rhythm	80–150 bpm Avoid tachy/bradycardias Avoid arrhythmias
Respiratory rate and rhythm	10–20/min
Body temperature	37–38°C
Blood gases	PaO2 ≥80 mmHg PaCO2 35–40 mmHg
Central venous pressure	5–12 cmH2O

Tier 1 Therapy: extracranial stabilisation

Extracranial stabilisation primarily involves oxygen therapy, management of ventilation, fluid resuscitation and support of MAP. In the recumbent cat, the head should be kept slightly elevated above the horizontal to assist in lowering ICP by increasing venous return from the brain. ⁴

Oxygen therapy and management of ventilation

CBF is tightly controlled by alterations in vasomotor tone regulated according to changes in arterial oxygen (PaO₂) and carbon dioxide (PaCO₂) partial pressures, and systemic blood pressure. Arterial carbon dioxide tension is one of the most potent regulators of CBF while arterial oxygen tension has little effect on CBF in the physiological range. Capnography provides breath-by-breath assessment of the adequacy of ventilation assuming normal cardiovascular function. This technique measures CO₂ in the expired patient gases (PETCO₂), which approximates the CO₂ tension in the alveoli (PaCO₂). As alveolar gases should be in equilibrium with arterial blood, PETCO₂ can be used to approximate PaCO₂ (Fig 6).

FIG 6.

Capnography provides breath-by-breath assessment of ventilation assuming normal cardiovascular function. Adequate ventilation is required to maintain cerebral oxygen delivery and prevent increases in ICP

Elevated PaCO₂ levels cause vasodilation of cerebral vasculature and a subsequent increase in CBV and ICP, while decreased PaCO₂ levels cause vasoconstriction. ²⁰ Adequate oxygenation [PaO₂ ≥80 mmHg; SpO₂ ≥95%] and ventilation [PaCO₂ 35–40 mmHg; PETCO₂ 30–35 mmHg] is required to maintain cerebral oxygen delivery and prevent increases in ICP. ²¹

Hypovolaemia and hypoxaemia are strongly correlated with elevated ICP and increased mortality in humans with traumatic brain injury.

Mechanical ventilation is required if PaCO₂ is >45 mmHg.

Supplemental oxygen is indicated in most cats with TBI and can be provided by flow-by at 100 ml/kg/min. ^9,11 Mechanical ventilation is indicated in patients with respiratory failure, whether the result of inadequate alveolar ventilation (hypercapnic respiratory failure) or inadequate oxygen exchange (hypoxaemic respiratory failure). ²¹ Hypercapnic ventilatory failure may be seen where there is concurrent cervical spinal cord injury or involvement of the brainstem respiratory centre. It is generally considered to be present when PaCO₂ >50 mmHg. However, any increase in CO₂ may have detrimental effects on ICP in the context of TBI. Therefore, mechanical ventilation is required if PaCO₂ >45 mmHg. Hypoxaemic respiratory failure can be the result of hypoventilation, pulmonary contusion or neurogenic pulmonary oedema. ²¹

Prior to intubation, 2% lidocaine can be given at 0.5–1.0 mg/kg IV to prevent elevations in ICP. Propofol 0.5–2.0 mg/kg can be given slowly intravenously to effect should sedation be required for intubation. If long-term sedation/intubation is required, the cat can be administered propofol by constant rate infusion at 0.1–0.6 mg/kg/min. Note that consecutive day administration of propofol can be associated with Heinz body formation in cats; although this rarely causes significant anaemia, cats on long-term propofol infusion should be monitored for this complication. ²²

MAP should be maintained at 80–100 mmHg and SBP at 120 mmHg to preserve normal cerebral perfusion pressure.

Fluid therapy

Circulatory shock as a result of hypovolaemia causes a significant reduction in organ perfusion. During the compensatory phase of the shock syndrome, blood pressure is maintained by the body's responses to reduced tissue perfusion, which include increases in heart rate, peripheral vasoconstriction, shifts in fluid from the interstitial space to the intravascular space and reduced urine production. Once the fluid deficit exceeds the ability of the body to compensate (decompensatory shock), decreases in blood pressure occur. There is a substantial body of evidence in human medicine to suggest that systemic hypotension independently increases the morbidity and mortality associated with TBI. ⁵

Hypovolaemia should initially be corrected by rapid fluid replacement. The choice of fluid used for resuscitation is less important than the amount given. However, dextrose solutions should be avoided as hyperglycaemia has been shown to have deleterious effects in patients with head injury. ¹³

• If the cat is hypotensive (MAP 40–50 mmHg or SBP <90 mmHg), isotonic crystalloid boluses of 10–20 ml/kg should be given to effect until normal blood pressure is restored. ¹¹ MAP should be maintained at 80–100 mmHg and SBP at 120 mmHg to preserve normal cerebral perfusion pressure. If isotonic crystalloid administration alone is ineffective, colloid fluids such as hetastarch or tetrastarch can be added at 2.5–5 ml/kg over at least 15 mins to a maximum of 20 ml/kg.

• If the cat is euvolaemic and not in shock (capillary refill time <1.5 s, mucous membrane colour pink, peripheral pulse strong and regular, MAP 80–100 mmHg or SBP 120 mmHg, heart rate 80–150 bpm), isotonic crystalloids such as Hartmann's should be administered initially at a maintenance fluid rate (2–3 ml/kg/h) and the cat monitored for potential ongoing blood loss with an associated drop in blood pressure. ¹¹

Blood products are indicated to restore oxygen-carrying capacity and colloid osmotic pressure if there are signs of hypoperfusion with a PCV <18–20% or total protein <50 g/l. If blood products are not available, oxyglobin can be used for oxygen-carrying support; it can be administered as a bolus of 2.5 ml/kg in hypovolaemic patients, ¹¹ or as a constant rate infusion in euvolaemic anaemia. ²³

Intracranial stabilisation is indicated in cats with moderate-to-severe head injury, which are refractory to aggressive extracranial stabilisation or have progressive neurological signs.

Resuscitation end-point

Once normovolaemia and adequate oxygenation and ventilation have been achieved, a complete neurological examination can be performed and the cat evaluated for other traumatic injuries.

Tier 2 therapy: Intracranial stabilisation

Once initial assessment and extracranial stabilisation have been carried out, medical intervention to address intracranial issues should be considered, with the main focus being to decrease ICP. In practical terms, following adequate volume resuscitation, the use of hyperosmolar therapy (in particular mannitol) is the next most useful therapeutic modality to reduce ICP in severe brain injury. ¹¹

Intracranial stabilisation is indicated in cats with moderate-to-severe head injury that are refractory to aggressive extracranial stabilisation, and those with progressive neurological signs.

Hyperosmolar therapy

Hyperosmolar agents currently in clinical use for TBI are mannitol and hypertonic saline.

• Mannitol The main effect of mannitol is to enhance CBF. This occurs as a result of the drug's immediate plasma-expanding effect, which reduces the haematocrit, increases the deformability of erythrocytes and thereby reduces blood viscosity. It has been shown to reduce cerebral oedema, increase cerebral perfusion pressure and CBF, and improve neurological outcome in head-injured patients. There is insubstantial evidence to suggest that mannitol exacerbates intracranial haemorrhage. Although there is controversy with regard to their effectiveness, osmotic diuretics are still routinely used in the control of ICP in human patients with known intracranial haemorrhage, as the benefits far outweigh the theoretical risks. ^4,9 Mannitol therapy (0.25–1.0 g/kg IV over 10–20 mins up to q8h) may be initiated to treat suspected elevated ICP secondary to head trauma. Mannitol should, however, be avoided in hypovolaemic patients.

• Hypertonic saline Hypertonic saline (7%) 3–5 ml/kg over 15 mins may be used as an alternative in the face of hypovolaemia. ⁹ Because sodium does not cross the blood—brain barrier, hypertonic saline has osmotic effects similar to those of mannitol. Other benefits of hypertonic saline include volume expansion and positive inotropic effects. Unlike mannitol, rebound hypotension is uncommon as sodium is actively reabsorbed by the kidneys, especially in hypovolaemic patients.

• Frusemide The use of frusemide has been called into question because of the potential for intravascular volume depletion and systemic hypotension, ultimately leading to decreased cerebral perfusion pressure. It should be reserved for cats with pulmonary oedema or oligoanuric renal failure.

Temporary hyperventilation

Given that CBV is another intracranial component that contributes to ICP (see page 816), hyperventilation (to PaCO₂ <35 mm Hg) can be used temporarily in a rapidly deteriorating animal to reduce ICP. ¹² In effect, this induces hypocapnic cerebral vasoconstriction. However, excessive or chronic hyperventilation can be accompanied by a reduction in global CBF, which may drop below ischaemic thresholds. Therefore, this is not a recommended therapy unless the PaCO₂ can be closely monitored with capnography or arterial blood gas analysis.

Tier 3 therapy: Surgery

Elimination of any space-occupying mass within the cranial vault is the third method by which ICP reductions can be obtained (Fig 7). Decompressive craniectomy is indicated within 12 h in patients with severe head injury that are refractory to extracranial and intracranial stabilisation, or that have extra-axial haematomata or severely depressed calvarial fractures on advanced imaging. ^2,4,12

FIG 7.

Domestic shorthair cat recovering from a rostrotentorial craniectomy to evacuate an extra-axial parietal haematoma following a road traffic accident

Surgery is indicated in cats with severe head injury that are refractory to extracranial and intracranial stabilisation, or have extra-axial haematomata or severely depressed calvarial fractures.

Ancillary treatment

Corticosteroids

Given the lack of evidence for any beneficial effect of corticosteroids after TBI, and strong evidence in the human literature showing a detrimental effect on neurological outcome, 24 corticosteroids should not be administered to cats with TBI.

Analgesics and sedatives

Adequate analgesia is essential to prevent further elevations in ICP. ²⁰ Many analgesic and sedative drugs have effects on intracranial physiology that, under certain circumstances, may result in further neuronal insult. Analgesic drugs should be selected that have minimal impact on regulation of CBF. ²⁰ Minimal depression of the cardiovascular and respiratory systems is important for maintaining adequate cerebral perfusion and oxygenation while minimising secondary neuronal injury. The potential complications of opioid administration that are particularly important in animals with head injury include bradycardia (and associated hypotension) and respiratory depression (and associated hypercapnia). Opioids can also cause pupillary dilation, which can potentially interfere with neurological assessment. However, when carefully titrated to effect, with monitoring of pulmonary function, opioids are safe to use in cases of intracranial hypertension. ²⁰

• For cats with severe pain, the use of short-acting reversible opioids such as fentanyl or remifentanil is preferred. These drugs have a relatively fast onset and short duration of action, giving them a pharmacokinetic profile suitable for infusion. ²⁰ Fentanyl is best started as a low constant rate infusion at 1 μg/kg/h IV and increased gradually to achieve the desired level of pain management and avoid the risk of exacerbating any mentation deficits. Remifentanil can be given as a constant rate infusion at 0.2–0.5 μg/kg/min. These drugs may be reversed using an opioid antagonist such as naloxone if significant respiratory or cardiovascular depression is observed.

• For cats with mild to moderate pain, buprenorphine, at 0.01–0.02 mg/kg IV/IM/buccal, or pethidine, at 2–5 mg/kg IM/SC, can be administered q2–4h.

• For cats showing severe agitation, sedation can be achieved using an intravenous infusion of dexmedetomidine at 0.1–1.0 μg/kg/h; this will also provide some analgesia.

Antiseizure treatment

Seizures should be initially treated with a benzodiazepine such as diazepam (0.5–2.0 mg/kg) or midazolam (0.2–0.5 mg/kg) given intravenously. If the bolus is successful in ceasing seizure activity, but additional seizures subsequently occur, additional boluses or a constant rate infusion may be administered (diazepam 0.5–2.0 mg/kg/h or midazolam 0.2 mg/kg/h in 0.9% saline). Refractory seizures may require additional therapy such as a continuous infusion of propofol (4–8 mg/kg bolus to effect followed by a constant rate infusion of 1–5 mg/kg/h). ² All the above drugs, although useful emergency agents, cause varying degrees of sedation, which is undesirable in cases of TBI. Intravenous levetiracetam can provide a viable alternative and can be administered as a 20 mg/kg intravenous bolus. The anticonvulsant effect is rapid and is maintained for several hours, longer than a single diazepam intravenous dose.

Prophylactic anticonvulsants — what role?

The role of prophylactic anticonvulsant therapy in cats with TBI remains unclear. Antiseizure treatment is indicated in human patients with TBI who develop immediate or early seizures (24 h to 7 days). The majority of studies done in humans with TBI do not support the use of the prophylactic anticonvulsants evaluated thus far for the prevention of late (>7 days) post-traumatic seizures. ²⁵ Routine seizure prophylaxis later than 1 week following TBI is, therefore, not recommended. If late post-traumatic seizures occur in a cat, the patient should be managed using a standard approach for new-onset seizures. As phenobarbitone may cause sedation and ataxia, the authors prefer the use of oral levetiracetam, at 20 mg/kg q8h, as antiseizure medication.

KEY POINTS

• Initial physical assessment of a head trauma patient should focus on any imminently life-threatening abnormalities and evaluation of vital functions, all of which can influence not only the interpretation of the neurological examination but also the prognosis for the cat.

• The aims of the neurological examination are to determine if the nervous system is affected, obtain an anatomic diagnosis (forebrain, brainstem, cerebellar, ± spinal cord involvement, or multifocal), and gain information about the prognosis.

• The initial approach to treatment of head trauma should focus on extracranial stabilisation (oxygen therapy, management of ventilation, fluid resuscitation and support of mean arterial blood pressure), closely followed, where indicated, by therapies directed towards intracranial stabilisation (hyperosmolar therapy, hyperventilation) and, where indicated, surgical decompression.

• The most important consideration in head injury is maintenance of cerebral perfusion and oxygenation. Hypovolaemia and hypoxaemia must be recognised and treated immediately.

• Brain imaging is recommended in patients with moderate-to-severe neurological deficits that are refractory to aggressive extracranial and intracranial stabilisation.

Biography