Seizures in exotic pets (Proceedings)
When presented with a seizuring dog or cat, the steps to take are familiar to most veterinarians. However, with a non-traditional species, even knowing where and how to administer treatments presents a challenge, as well as what might be common etiologies. With a little additional familiarity, any practitioner can effectively treat any seizuring patient.
The most important aspect to remember, regardless of species, is to first control the seizures, and return the patient's body temperature and vital parameters to normal. As with any animal, prolonged seizures may result in permanent deficits, but the extent of these deficits cannot be assessed for several days. Supportive care may be required during that time, including fluid therapy, nutritional support, and sometimes even management of the sedated or debilitated patient, including turning the patient, lubricating eyes, and physical therapy.
In any seizuring patient, check blood glucose, and administer a dextrose bolus if necessary. If vascular access is not readily available, or if the animal is actively seizuring, proceed as you would in any other species. Administer diazepam, 0.5-1.0 mg/kg. Administer intravenously if possible, but this may be a challenge in exotic patients. As an alternative, administer rectally (or cloacally) or orally, as diazepam is readily absorbed across mucous membranes – use double the intravenous dose for this route. Diazepam can also be administered intramuscularly, but it is poorly absorbed via this route. Absorption of intramuscular medications in birds is almost as rapid as intravenous, but slower in other species. The dose may be doubled if necessary. Alternatively, administer midazolam intramuscularly at 0.5-2.0 mg/kg.
If a single dose of diazepam is not effective, repeat up to three times. Diazepam can be administered via continuous intravenous or intraosseous infusion. Start at a rate of 1.0 mg/kg/hr diazepam added to intravenous fluids. If cerebral edema is suspected, administer mannitol, 0.5-1.0 g/kg IV over 20 minutes, and consider administering a single dose of prednisolone sodium succinate or methylprednisolone sodium succinate, 10 mg/kg IV, or dexamethasone sodium phosphate 1-2 mg/kg IV. (Do not administer steroids repeatedly in most exotic species, as they are highly susceptible to the immunosuppressive effects of steroids. Exception: ferrets.) Once seizures have stopped for 12-24 hours, taper the valium infusion slowly over the next 12-24 hours. If valium does not control seizures, begin a constant rate infusion of phenobarbital, 2-10mg/kg/hr. This can be given in conjunction with the diazepam; monitor for respiratory depression. If patients are unresponsive, add dextrose to the IV drip, as many of these small patients will rapidly become hypoglycemic if not eating. Once controlled, depending on etiology, oral phenobarbital can be used for long term seizure management. Potassium bromide can also be used for seizure control. Check blood levels of phenobarbital within 2-3 weeks of starting therapy; potassium bromide levels may not reach a steady state for 60-90 days. Adjust dosages based on blood levels.
Common causes of seizures in exotic pets by species
Most common in juveniles with diarrhea or anorexia, very rare in adults even when anorexic. Treat with intravenous dextrose 50% slowly to effect, followed with a 5% IV dextrose drip until patient is eating. Address underlying causes.
Juvenile or adult. Rather than true seizures, actually causes head tilt (may be severe), rolling, torticollis, vestibular signs,. However, owners often describe their pets as seizuring. Onset may be acute or gradually progressive. Protozoal infection may occur as juvenile, but animals generally are asymptomatic; clinical signs may appear at any time. Linked to immunocompromise in other species. Avoid steroids. Treat with supportive care, pad cage, meclizine, syringe feeding and eye lubrication if necessary. Treatment with albendazole or fenbendazole may control shedding, but will not eliminate the organism, and can cause toxicity. Prognosis: varies, but is independent of severity of clinical signs.
Probably overdiagnosed as a cause of clinical signs in neurologic rabbits, but may spread to the central nervous system and cause either abscess formation or meningitis. Treat with supportive care, antimicrobials. Fluoroquinolones are beneficial in many cases and are readily available in most practices.
Rarely, a severe case of otitis or even ear mites can be so disturbing that the rabbit may fall over and become ataxic, giving the appearance of seizures. Diagnose and treat as in other species.
Toxins, toxoplasmosis, metabolic disturbances – uncommon. Treat as in any companion species. Avoid steroids whenever possible. Idiopathic epilepsy can exist. Baylisascaris procyonis infections can occur in rabbits with contact with raccoon feces, and will cause progressive neurologic signs and death. There is no antemortem test or treatment.
Middle-aged and older ferrets, often due to insulinoma. Will present hypothermic, moribund, or actively seizuring. Check blood glucose. If <60mg/dL, administer IV 50% dextrose to effect, and begin a 5% dextrose drip. Prednisone is beneficial for its gluconeogenic effects and can be used long term with minimal side effects. Manage any adverse effects of seizures.
Canine distemper virus
Although seizures are a rare manifestation in ferrets, this disease is usually evidenced by dermatitis around the muzzle, eyes, and sometimes feet and mucocutaneous junctions, as well as fever, ocular or nasal discharge. Euthanasia is recommended.
Toxins, metabolic disturbances, CNS lymphoma – uncommon. Treat as in any companion species. Avoid steroids whenever possible. Idiopathic epilepsy can exist.
For unknown reasons, guinea pigs with fur lice sometimes will demonstrate true seizure activity. Intense pruritus has been one proposed cause. Treat with ivermectin, subcutaneously. Studies have shown that in guinea pigs, therapeutic efficacy is diminished with oral administration as compared to injectable.
Although probably not true seizures, urinary obstruction or cystic calculi may cause enough discomfort that a guinea pig may collapse, pass out, or paw as he tries to right himself. Diagnose radiographically. Treat as in other species.
In these animals, hypoglycemia is linked to anorexia from dental disease. Administer 50% dextrose, begin a dextrose drip, and begin feeding liquid formula such as ensure, 2-cal, or similar to maintain and stabilize patient. Sedation and tooth trim can be performed once stable.
Limiting ridge at junction of stomach prevents vomiting or eructation. Pain may promote aerophagia. Severe distention of the stomach may occur. Similar to bloat in dogs, vascular compromise and arrhythmias may occur. Alleviate distention by passing a large-bore red-rubber tube, or trocharize with a large-bore needle. Address underlying cause.
Uncommon in general.
From anorexia due to dental disease. Treat with IV or oral dextrose, supplemental feeding.
Treat as in other species. Administer steroids (short-acting) as single dose intramuscularly if IV access cannot be obtained.
Small rodents (hamster, gerbil, mouse, rat)
Seizures are perhaps most commonly caused from fluid, glucose, and electrolyte losses associated with diarrhea. Administer fluids subcutaneously or intraosseously, and dextrose orally or intraosseously.
Can have idiopathic epilepsy. No treatment usually indicated.
Usually attributed to poor diet of only fruits and vegetables. More common in juveniles due to higher calcium requirements. Confine to a small cage or area. Administer calcium orally, (may give a single dose IM), and Vitamin D if available. Treatment must continue for several weeks.
These species are marsupials, and blood glucose normally may be about 50mg/dL. Treating for hypoglycemia is controversial.
There is a poorly understood demyelinating disease which affects ability to ambulate and sometimes affects CNS, causing vestibular signs. No treatment is known.
Acute or chronic. Metal particles may be radiographically evident, but their absence does not rule out lead toxicity. (Do not confuse mineral densities in ventriculus with metal density. Compare density to bone for mineral and a radiopaque marker for metal.) May present with clenched feet, neurologic signs, or fulminant seizure activity. Some species may have bloody urine (Amazon parrots, conures). Treatment: Fluids, Supportive care, anticonvulsants, chelation with CaEdta (injectable- can give IM or SQ) DMSA (dimercaptosuccinic acid – oral) or D-penicillamine (oral, available at many human pharmacies). Gavage with bulk feeding, peanut butter, Metamucil to help eliminate metal from GI tract. Use extreme caution if patient is vomiting.
May be due to prerenal or true renal causes, or infectious agents; measured by elevation in uric acid. Urinary obstruction is extremely rare. Treat as in other patients, with IV or IO fluids, H2 blockers, supportive care, reassess.
It is controversial whether or not hepatic encephalopathy truly occurs in birds. Nitrogenous waste is not the end-product of hepatic metabolism in birds, yet with severe hepatic disease, neurologic signs may be present. Treat underlying cause. Manage with supportive care, antimicrobials if infectious agents are suspected, B-vitamin, lactulose. May consider milk thistle (liquid alcohol-free formulation) and/or S-adenosylmethionine.
Chlamydophila psittaci (psittacosis)
Infectious disease that affects liver, respiratory, and/or CNS. Any or all body systems may be involved including CNS. Classic description is a bird with ocular and or nasal discharge, green urates, leukocytosis, and hepatic enzyme elevations. However, neurologic signs can occur alone. Treat seizures as in other patients, with supportive care, nutritional support, and anticonvulsants. Treat Chlamydophila with doxycycline or vibramycin for 6 weeks.
Proventricular dilatation disease
An inflammatory viral disease that affects the neuromuscular junctions, with a predilection for the GI tract and more specifically the proventriculus. "Classic" disease form is intestinal, with whole seeds passing in droppings, weight loss, sometimes regurgitation, and radiographically enlarged proventriculus. However, "Atypical" form of disease can have CNS manifestations as the only form. Proventriculus may or may not be radiographically enlarged. Diagnosis is made at necropsy. Treatment is as in other species, supportive care, but is generally unrewarding.
As in humans, complete cause of this is unknown, but predisposing factors include obesity and high-fat (all-seed) diets. Most common in Amazon parrots, occasionally macaws and African grey parrots, but may exist in any species. Cholesterol and triglyceride elevations may or may not be present. Clinical signs are often cyclical, waxing/waning focal or grand mal seizures, which may seem to respond to therapy but continue to recur. Mental dullness may persist. Diagnosis is almost always post-mortem. Treatment is unrewarding.
Hyperlipemic syndrome/lipid emboli
This syndrome is linked to hyperestrogenism in reproductively active females. Excessive lipid circulates in the bloodstream, causing vascular sludging and lipid emboli. Layperson terminology is "yolk stroke", although it is not truly a yolk embolus. This syndrome can often be recognized at the time of blood collection – the blood is so saturated with lipid that the appearance has been describes as "strawberry milkshake" or "creamy tomato soup", which is readily apparent. (Use caution when collecting blood, as these birds may have clotting disorders as well.) Cholesterol and/or triglycerides are consistently elevated in this disease. Treatment consists of dilution/diuresis with fluids, and cholesterol-lowering statin drugs (human products such as lopid, zocor, cholestipol may be compounded for avian use). Niacin may be added as well. Treatment may be rewarding, but some manifestations such as head tilt may persist. Treatment should be continued for life and diet modification should be concurrent.
Most commonly identified in African grey parrots (genetic), or egg-laying females of any species. Also present in pigeons/doves on poor diets. In addition to seizures, clinical signs include muscle fasciculation, pathologic fractures, ataxia, and posterior paresis. In reproductively active females, total body calcium may be normal. Ionized calcium levels are most useful. Treat with injectable and oral calcium, vitamin D, and supportive care, including nutritional support. Prognosis is good if seizures can be controlled.
Most common in juveniles who are weaning or any debilitated, anorexic bird. Lack of food for 24 hours in any pet bird can be life-threatening. Treat with IV dextrose. Can gavage 50% dextrose diluted 1:1 with LRS or 0.9% NaCl. Treat underlying cause, control seizures, begin regular gavage feeding of a highly digestible product.
And metabolic bone disease (nutritional secondary hyperparathyroidism): Occurs commonly in juvenile animals receiving inadequate dietary calcium and/or ultraviolet light. Most common in lizards, almost nonexistent in snakes. Soft bones, soft jaw, poorly visible bones radiographically, sometimes pathologic fractures of long bones or spine. This is not an acute problem but may have acute manifestations. Administer calcium orally whenever possible; if injectable calcium is used, only one dose should be given IM followed by oral. Ascertain calcium and phosphorous levels prior to administering. Total calcium levels may be normal. One dose of vitamin D is appropriate. Treat the underlying disease. Calcitonin may be administered following several days of calcium administration.
Renal Secondary hyperparathyroidism
More common in adult animals, often on vitamin supplementation or protein-based diet. Bones are strong; there may be a decline in body condition. Tremors or seizures can be elicited with movement. This is believed to be a sign of renal failure. Blood calcium levels are low but phosphorous levels are elevated. Uric acid may or may not be abnormal. The high levels of phosphorous are believed to bind calcium and make it unavailable for use by the body. Administration of calcium in this situation may lead to metastatic mineralization of the great vessels as the calcium and phosphorous complex in the bloodstream. In these patients, treat with fluids and phosphorous binders until the calcium/phosphorous ration approaches 1:1, then supplemental calcium may be added. In the author's experience, there is no correlation between the severity of the hypocalemia and hyperphosphatemia and the prognosis for recovery.
Should always be considered. If suspected or identified, treat as in other species.
References Available Upon Request