Sudden onset of collapse is a common presenting sign in small animal practice but not all such animals are afflicted with neurological disease. Physical examination, haematology and biochemistry are invaluable in distinguishing neurological lesions from other causes of weakness such as fever, sepsis or hypovolaemia. Always try to ascertain the level of mental awareness of the animal during and after the collapse. Systemically unwell animals are depressed (obtunded), which mimics cerebral disease. Syncopal animals lose consciousness but return to normal mentation almost immediately, unlike seizure activity, which usually leaves the animal more lethargic than normal for a variable period of time lasting minutes to hours. A severely depressed mentation (stupor) or a persistent lack of response to stimuli (coma) signal dysfunction of the brainstem or cerebrum. Stupor and coma occur in metabolic or structural encephalopathies. Signs of vestibular disease causing a loss of balance and subsequent collapse are usually strikingly obvious on examination. An animal that has acutely lost balance is mentally alert but usually pays less attention to the owner, as it struggles to regain its footing.
Collapse may be sustained (recumbency), or may occur episodically, with spontaneous resolution.
Causes of collapse
|Associated activity||May or may not be associated with exercise, feeding, Valsalva manoeuvre||Often at rest|
|Duration of collapse||<1 minute||>1 minute|
|Return of mental alertness||Within seconds||Usually quiet, lethargic for minutes to hours|
|Mucous membranes||Pale||Cyanosis or normal|
The history and physical examination localized the cause of collapse in the following dogs of identical age and breed.
The dog had been diagnosed with pituitary-dependent hyperadrenocorticism (PDH) 3 months prior to referral when the collapsing episodes had also been reported. The collapsing episodes all appeared to be the same and consist of the dog sinking down to the floor into sternal recumbency, where it stayed motionless for a few minutes in a mentally unresponsive state. The dog then lifted its head and rose to a standing position. He was described as being a bit lethargic after the event and the dog rested for several hours before returning to normal. The events occur at any time of the day but had not occurred when out exercising. There was no history of exercise intolerance although the dog did collapse on two occasions when let into the garden to urinate and defecate. Treatment was trilostane for hyperadrenocorticism.
Examination was made difficult by the dog biting the neurologist. Once muzzled, the dog persisted in trying to bite which was apparently out of character. The dog was otherwise neurologically normal but was pot-bellied, had patchy alopecia and panted a lot.
The events may be either syncope or seizure activity. Raised intracranial pressure can result in collapse. Seizures are often followed by a period of slightly altered mentation. The intermittent nature of the collapse with an altered mentation, along with a return to normal, was suggestive of cerebral involvement. It is common for animals to be fearful in a consulting room so the act of biting the vet should not immediately be ascribed to intracranial disease.