5 Head trauma
Being hit by a car, human, large animal, falling tree or furniture, being shot at or in a dog fight are all reported causes of head trauma in small animals. The dog that knocks its head against a door frame and carries on walking will not have sustained clinically significant head trauma.
A sudden onset of stupor or coma (Table 5.1) should not automatically be blamed on external trauma, unless, of course, the event is witnessed or has produced other physical evidence. The owner must always be questioned, however briefly, on the animal’s recent health status.
|Hyperosmolar (DKA; hypernatraemia)|
|Hypo-osmolar (water intoxication)|
|Hydrocephalus||Herniation with secondary compression of brainstem|
In this case, the dog had been exercising off the lead and out of view. A train was heard to pass nearby. The dog was called but failed to return. The animal was found soon after, in lateral recumbancy in an unresponsive mental state. The owners presented the dog, saying it had been hit by a train.
Initial assessment of a traumatized animal is done quickly and is repeated at frequent intervals. Mental state, pupil size and pupil light reflex (PLR), eye movement (resting position, spontaneous movement, and vestibulo-ocular reflex, VOR) should be noted. Approximately 10% of traumatic brain-injured humans also have a cervical spine injury. Avoid rotating or hyperextending the neck.
The Glasgow Coma Scale was modified by Dr Andy Shores for use in small animals and this helps monitor progression of signs (Table 5.2). One study found that there was a 50% probability of survival during the first 48 hours after head trauma in dogs with a score of 8. Contrary to humans, the age of the animal did not predict survival. The study was not able to suggest a long-term prognosis based on either survival or functional capacity.
|Small animal coma scale||Score|
|Normal gait, normal spinal reflexes||6|
|Hemiparesis, tetraparesis, or decerebrate activity||5|
|Recumbent, intermittent extensor rigidity||4|
|Recumbent, constant extensor rigidity||3|
|Recumbent, constant extensor rigidity with opisthotonus||2|
|Recumbent, hypotonia of muscles, depressed or absent spinal reflexes||1|
|Normal pupillary light reflexes and oculocephalic reflexes||6|
|Slow pupillary light reflexes and normal to reduced oculocephalic reflexes||5|
|Bilateral unresponsive miosis with normal to reduced oculocephalic reflexes||4|
|Pinpoint pupils with reduced to absent oculocephalic reflexes||3|
|Unilateral, unresponsive mydriasis with reduced to absent oculocephalic reflexes||2|
|Bilateral unresponsive mydriasis with reduced to absent oculocephalic reflexes||1|
|Level of consciousness|
|Occasional periods of alertness and responsive to environment||6|
|Depression or delirium, capable of responding but response may be inappropriate||5|
|Semicomatose, responsive to visual stimuli||4|
|Semicomatose, responsive to auditory stimuli||3|
|Semicomatose, responsive only to repeated noxious stimuli||2|
|Comatose, unresponsive to repeated noxious stimuli||1|
Note: Asymmetrical abnormalities (e.g. pupil size) are assigned the lower score of the two possible. Score before medication and supportive care administered. Oculocephalic reflex, VOR; Semicomatose-stuporous.
Examination in this case revealed:
The lesion was localized to the cerebrum or brainstem ARAS based on the coma.
It seemed highly unlikely that a dog could be hit by a train and not be visibly damaged by the experience. Head trauma from a blunt projectile may have occurred. Increased intracranial pressure from neoplasia, cerebral haemorrhage, or inflammation would be expected to have shown some earlier signs of mentation or behaviour change or have a less-acute onset but this is not always the case. Metabolic encephalopathy can alter mentation acutely and for extended periods of time (hours).