Head injury in dogs and cats

Patients that have had a head injury can develop lesions or impairment of intracranial and extracranial functions. The extracranial alterations which are most often detected and that must be looked for and treated if present are: traumatic shock, impaired ventilation or oxygenation, airway obstruction, head fractures, chest trauma and its complications, spinal injuries, fractures of the ribs and anterior limbs, haemorrhages and hyperglycaemia. The therapeutic priorities are aimed at controlling intracranial pressure and oxygenation of the brain tissue. Neurological function should be monitored continuously throughout the entire duration of the treatment.

PATHOPHYSIOLOGY

In cases of head injury, primary and secondary lesions can be distinguished; the former is immediate and is the direct consequence of the central nervous system (CNS) injury (e.g. laceration of brain tissue), while the latter can develop in the following hours or days, and is a result of the alterations induced by the trauma. The secondary lesion is caused by a cascade of physiological and biochemical events, such as the release of mediators of inflammation, excitatory neurotransmitters and alterations in the permeability of the blood-brain barrier. The complications resulting from the secondary lesion can compromise vital functions and cause the death of the patient. The primary lesion, which can produce cerebral concussion responsible for a temporary loss of consciousness, does not cause histologically detectable cerebral alterations. After regaining consciousness, some patients exhibit a state of confusion and appear disoriented. When the head injury is followed by a violent displacement of the brain, cerebral contusion may occur at the site of the  impact, in the opposite hemisphere (deceleration or whiplash injury)_¹ or in both areas. This type of injury causes intracranial haemorrhage; when the bleeding is severe the blood can occupy the subarachnoid space (between the arachnoid and pia mater), subdural space (between the dura mater and subarachnoid membrane) and epidural space (between the skull and dura mater) or parenchyma (accumulation of blood in the cerebral parenchyma)._² Cerebral haemorrhage causes impairment of cerebral functions and widespread neurological dysfunction. Cerebral laceration is characterized by the loss of brain tissue.

The alterations induced by the secondary lesion can lead to neuronal death. The causes may be of intracranial or extracranial origin. The latter are:

• hypotension;
• hypoxia;
• hyperglycaemia;_³
• hypoglycaemia;
• hypercapnia;
• hypocapnia;
• hyperthermia;
• electrolyte imbalances;
• acid-base imbalances.

The intracranial causes of the secondary lesion are:

• increase in intracranial pressure;
• impairment of the blood-brain barrier;
• cerebral oedema;
• vasoconstriction;
• infections.

Head injury causes a massive release of excitatory neurotransmitters, mediators of inflammation, glutamate and other reactive chemical species that promote the entry of Na+ and Ca++ into the neurone, depolarising it and promoting the release of the excitatory neurotransmitters. When the increase in intracellular calcium exceeds and overwhelms its own removal system, there is severe cell injury or death. The release of vasoactive substances can cause oedema and deficits of cerebral perfusion. The excessive metabolic activity resulting from the excitatory neurotransmitters causes depletion of the adenosine triphosphate (ATP) stores, facilitates the production of free radicals (highly reactive compounds that can damage the neurone) and results in hypoperfusion and tissue acidosis. The primary and secondary lesions are responsible for cerebral damage due to cerebral perfusion pressure deficit, also because the damaged brain tissue loses its self-regulating capacity.

Sudden increases in the volume of the intracranial contents caused by an increase in cerebrospinal fluid, blood volume or the lesion can cause a dramatic increase in intracranial pressure, which can make the cerebral oedema worse. Cerebral oedema (which can be cytotoxic, interstitial or vasogenic) alters cerebral perfusion, increasing the risk of ischaemia. Hypoxia, by inducing an increase in cerebral blood flow in the attempt to improve brain tissue oxygenation, can cause an increase in intracranial pressure._¹

MANAGEMENT OF PATIENTS WITH HEAD INJURIES

Patients with head injuries must be monitored closely, and the following vital parameters measured and recorded:

• heart rate;
• respiratory frequency;
• colour of the mucous membranes;•capillary refill time;
• temperature;•systemic arterial pressure;
• oximetry.

The presence of hypotension, hypoxia and a perfusion deficit must be recognized promptly and treated aggressively. Oxygen therapy can be performed using nasal probes or an oxygen tent (especially for cats and small patients). When hypoxia is suspected, or when it is not possible to perform oximetry or measure the partial pressure of oxygen, it is a good rule to administer oxygen to all patients with head injury. In these patients the mean arterial pressure should be kept between 50 and 150 mmHg to maintain cerebral perfusion; if the mean arterial pressure cannot be measured, the systolic arterial pressure should be kept above 100 mmHg. When hypotension is detected, resuscitating  fluid therapy should be given with crystalloids or colloids. If crystalloids are used, they should be administered at shock doses (60-90 ml/kg/hour i.v. in dogs and 40-55 ml/kg/hour i.v. in cats). Colloids should be administered at a dose of 10-20 ml/kg/day i.v. in dogs and as slow bolus injections of 5 ml/kg i.v. every 15 minutes in cats. A 7% hypertonic saline solution can be used at a dose of 2-4 ml/kg/day. There are no documented contraindications in veterinary medicine proscribing the use of colloids or hypertonic saline solution in patients with head injury because of an increased risk of cerebral haemorrhage.

The neurological examination is an important additional element of the emergency visit, the purpose of which is to establish the existence, size, neuroanatomical location and prognosis of the lesion. In an emergency, the neurological examination must evaluate the mental state, posture, gait nd cranial and spinal nerves, at the very least. Some signs and symptoms of the neurological examination can be affected by pain, by therapy for the pain and by the state of agitation resulting from the release of catecholamines during the traumatic shock; it is, therefore, a good rule to repeat the neurological evaluation several times during hospitalisation and treatment.

Mental state. The animal’s state of consciousness can be differentiated into alert, depressed, stuporous or comatose. Depression and confusion are characteristic of a brain problem affecting both hemispheres; stupor and coma indicate brainstem damage, while hyperarousal or delirium can indicate a limbic lesion.

Posture and gait are evaluated by stimulating the patient to move. Gait analysis, following a head injury, may show rotation of the head, an altered position of the trunk and legs and increased or decreased muscle tone. An upper motor neuron lesion causes stiffness of the extensor muscles; opisthotonus with stiffness of the four legs is associated with decerebration (mesencephalic lesions), while opisthotonus with hyperextension of the front legs and flexion of the hind legs is associated with cerebellar lesions (decortication)._¹

Cranial nerves. In head trauma it is essential to examine the cranial nerves, evaluating pupil diameter (uni- or bilateral miosis, uni- or bilateral mydriasis), pupillary reflexes (direct and consensual response), the visual positioning reflex and the presence of physiological or pathological nystagmus). Pupils responding normally to light stimulus indicate proper functioning of the brainstem with a not particularly serious lesion; fixed, miotic pupils indicate cerebral hemisphere injuries, unilateral mydriasis indicates worsening or a hernia; mydriatic pupils suggest very severe midbrain injuries. After examining the pupils, the trigeminal nerve (sensory nerve of the face) and the facial nerve (motor nerve of the muscles of facial expression, sensory nerve of part of the oral cavity) are evaluated, ascertaining the perception of facial, palpebral and corneal pain. Vestibulocochlear nerve lesions can produce ataxia, rotation of the head, walking in circles, pathological nystagmus and hearing loss. The swallowing reflex depends on the glossopharyngeal and vagus nerves; tongue retraction depends on the hypoglossal nerve._² Through the neurological examination it is possible to locate the area of the brain affected by the head injury and determine whether the lesion involves the cerebral cortex, thalamus, hypothalamus, brainstem, vestibular system or cerebellum.

The examination of the spinal nerves is mainly aimed at evaluating the nerves in the legs and makes it possible to discover whether there are spinal cord injuries as well as intracranial injuries. The non-functioning of spinal nerves leads to segmental atrophy of the involved muscles and to a decrease or absence of superficial and deep sensitivity. The reflexes that should be evaluated in the front legs are the flexor, radial extensor of the carpus, triceps and biceps reflexes, while those that should be evaluated in the rear legs are the flexor, patellar, cranial tibial and gastrocnemius reflexes. Finally, the perineal reflex and superficial and deep sensitivity should be evaluated._²

PROGNOSIS

The patient’s neurological status can be evaluated through a scoring method initially used only in human medicine but later adapted to veterinary medicine (small animal coma score, Table 1). A scale is used to evaluate motor activity, the cranial nerves and mental state. Each condition is given a score, which is an indicator of a favourable or unfavourable prognosis: the lower the score, the more serious the impairment.
                                                                                                                                                                                              

Table 1.  Small animal coma scale

TREATMENT

Treatment begins with the stabilisation of the patient by controlling airway patency, oxygenation, ventilation and restoring effective circulation of the blood. In patients with partial or complete obstruction of the airways, it should be considered whether orotracheal intubation or an emergency tracheotomy is necessary. Oxygenation should be monitored in all head injured patients by oximetry (it should exceed 95%) or by blood-gas analysis. Hypercapnia can reduce cerebral perfusion; in fact, the hyperventilation that the body uses to reduce CO₂ can produce cerebral vasoconstriction. When ventilation is inadequate, manual or mechanical positive pressure ventilation should be used. CO₂ is monitored with the aid of capnography or blood-gas analysis; this should be done when ventilation is altered. The arterial partial pressure of carbon dioxide (paCO₂) should be maintained in the range of 35-45 mmHg. In patients with severe cerebral hypertension, the ventilatory rate can be increased for brief periods until a paCO₂ of 25-35 mmHg is reached (obtaining hypocapnia-induced vasoconstriction); it is not advisable to prolong hyperventilation for long periods in order to avoid excessive vasoconstriction, which would increase the risk of cerebral ischaemia.

Patients with head injury are often affected by hypovolaemic shock, which must be promptly recognized and treated (fluidtherapy [7]); by restoring the circulation of blood and maintaining the blood pressure within range, cerebral perfusion and metabolism are restored._⁴

Following a head injury, mannitol (18%) can be administered intravenously which, given its hyperosmolarity, is capable of reducing the cerebral oedema, improving cerebral perfusion. The recommended dose is 0.5-1.5 g/kg i.v. in boluses of 15-20 minutes in both dogs and cats. Mannitol should be administered in repeated boluses in order to minimise the increase in permeability of the blood-brain barrier that it can produce. When severe cerebral oedema is suspected, it is possible to combine furosemide with the mannitol (2 mg/kg i.v. before the mannitol bolus). Since mannitol is an osmotic diuretic, it should only be administered when effective circulation has been restored and electrolytes (at least sodium and potassium) and the state of hydration must be monitored carefully.

To reduce cerebral oedema while at the same time administering a hyperosmotic solution with the capacity to expand the circulatory volume, a 7% hypertonic saline solution can be administered at a dose of 2-4 ml/kg i.v. Hypertonic saline solutions must not be administered to patients with hyponatraemia because of the high risk of pontine myelinolysis and permanent brain damage; this lesion can appear even after a few days. Because of the disappointing results obtained, the use of corticosteroids in patients with head injury is not recommended._⁴

Seizures occur in approximately half of patients with head injury and can arise immediately after the trauma, in the 7 days after the trauma or later on (even years later). The following anticonvulsant drugs can be used after the head injury: diazepam 0.5-1 mg/kg i.v. or, when the seizures occur repeatedly, as a continuous infusion at a rate of 0.5-2 mg/kg/hour in dogs and in cats as boluses of 0.5 mg/kg administered every 5-10 minutes up to a maximum of three administrations. When the seizures are severe and do not respond to benzodiazepines, barbiturates are administered, for example pentobarbital 2-15 mg/kg i.v. until effective or as a continuous infusion at the rate of 0.5-4 mg/kg/hour, or phenobarbital 2-5 mg/kg i.m. or as a continuous infusion at the rate of 2-6 mg/dog/hour. In dogs resistant to benzodiazepines, medetomidine can be used at a dose of 1-6 mg/kg i.v. or i.m. or potassium bromide orally, nasally or rectally at a dose of 100 mg/kg administered every 4 hours up to a maximum of six times._² Polyethylene glycol (PEG), a non-toxic inorganic hydrophilic polymer, has shown antioxidant and neuroprotective properties;_⁵ there are no studies so far that document its efficacy in small animals. PEG reduces free radical production, cell damage and impairment of the blood-brain barrier and it appears capable of repairing the neuronal cell membranes damaged by the trauma. It has been observed that the interruptionofnerve impulseconduction andaxonal transportin the damaged areas of brain tissue is a result of the accumulation of beta-amyloid protein precursors produced with the head trauma; this protein is removed by PEG and the neurological outcome is improved._⁶ There are numerous studies_^7,8,9 in which the use of hypothermia to treat head injury has been described. The body temperature is reduced to 35-35.5°C (in humans). Hypothermia prevents the oxidative damage caused by the increase in brain metabolism and is useful for controlling intracranial pressure; it has also been used in veterinary medicine to treat seizures and to control intracranial pressure and cerebral metabolism._¹⁰ Maintaining a patient’s body temperature at 35°C gives sufficient cerebral perfusion without causing cardiac dysfunction or a deficiency in oxygenation._⁷

Patients that are resistant to pharmacological therapy must undergo a careful neurological examination since surgery, such as decompression craniotomy, has to be considered as an option. Surgery is usually performed to reduce intracranial pressure by removing a mass (e.g. haematoma) or fractured bones that are compressing the brain. Surgical treatment is only possible after careful localisation of the space-occupying mass through diagnostic imaging (nuclear magnetic resonance or computed axial tomography).

References

1. Bernardini M. Traumi, In: Neurologia del cane e del gatto. Milano: Poletto editore; 2002, pp.176-181.
2. Fossum T.W., Hedlund C.S., Johnson A.L., et al. Fondamenti di neurochirurgia, In: Chirurgia dei piccoli animali. 3th edn: Elsevier 2008, pp.1397-1406.
3. Syring R.S., Otto C.M., Drobatz K.J. Hyperglycemia in dogs and cats with head trauma: 122 cases (1997-1999). J Am vet Med Assoc. 2001; 218(7): 1124-1129.
4. Dewey C.W. Emergency management of the head trauma patient. Principles and practice. Vet Clin North Am Small Anim Pract . 2000; 30(1) 207-225, vii-viii.
5. Koob A.O., Duerstock B.S., Babbs C.F., Sun Y., Borgens R.B. Intravenous polyethylene glycol inhibits the loss the cerebral cells after brain injury. J Neurotrauma. 2005; 22(10): 1092-1111.
6. Koob A.O., Borgens R.B. Polyethylene glycol treatment after traumatic brain injury reduces beta-amyloid precursor protein accumulation in degenerating axons. J Neurosci Res. 2006; 83(8): 1558-1563.
7. Tokytomi T., Morimoto K., Miyagi T., Yamaguchi S., Ishikawa K., Schigemori M. Optimal temperature for the management of severe traumatic brain injury: effect of hypothermia on intracranial pressure, systemic and intracranial hemodynamics, and metabolism. Neurosurgery. 2007;61(1 suppl.):256-265; discussion 265-266.
8. Tokutomi T., Miyagi T., Takeuchi Y., Karukaya T., Katsuki H., Shigemori M. Effect of 35 degrees C hypothermia on intracranial pressure and clinical outcome in patient with severe traumatic brain injury. J Trauma. 2009; 66(1): 166-173.
9. Wright J.E. Therapeutic hypothermia in traumatic brain injury. Crit Care Nurs Q. 2005;28(2):150-161.
10. Hayes G.M. Severe seizures associated with traumatic brain injury managed by controlled hypothermia, pharmacologic coma, and mechanical ventilation in a dog. J Vet Emerg Crit Care, San Antonio. 2009;19(6):629-634.