Canine and Feline Epilepsy. Luisa De Risio
IV every 4 h for five treatments, then every 6 h for four additional treatments; or 22 ml/kg IV of a 5% solution every 4 h for six treatments, then every 6 h for four treatments; or a constant rate IV infusion of 5% solution at 5.5 ml/kg/h
Detergents and Disinfectants
Hexachlorophene
Overview
Hexachlorophene is used as a germicide in soaps, shampoos and disinfectant solutions. Exposure may result from both topical contact and ingestion (Bath, 1978; Thompson et al., 1987). Nursing puppies have been poisoned following hexachlorophene application to the mammary glands of the bitch (Ward et al., 1973).
Clinical presentation
Clinical signs in dogs are usually characterized by acute onset of tremors, especially of the head, which may increase with excitement and disappear during rest or sleep. Opisthotonus, severe seizures and death have also been reported. Clinical signs in cats include mydriasis, vomiting, weakness, ataxia, spastic or flaccid paralysis and hypovolaemic shock (Thompson et al., 1987).
Management
Treatment involves decontamination, supportive care, skeletal muscle relaxants and AEMs (see Table 4.1 and Chapters 12 and 24).
Prognosis
Clinical recovery may take 4 to 6 weeks.
Heavy Metals
Lead
Overview
Lead is the most common heavy metal causing toxicosis in animals. Sources of lead intoxication include lead-based paints, linoleum, putty, roofing felt, golf balls, bullets or pellets, fishing weights, old car batteries, wheel weights, improperly glazed ceramic water bowls and toys (Morgan, 1994). The most commonly identified source of exposure in dogs and cats is lead-based paint chips or dust, usually from home renovation. Cats can ingest old paint dust and chips contaminating the coat while grooming (Knight and Kumar, 2003). High-fat low-calcium diets may facilitate absorption of lead from the alimentary tract.
Mechanism of action
The toxic mechanism of lead is caused predominantly by its ability to substitute for other polyvalent cations (particularly divalent cations, such as calcium (Ca2+) and zinc (Zn2+)) in multiple molecular processes, and subsequently affect metal transport, energy metabolism, membrane ionic channel conduction, inter- and intracellular signalling, diverse enzymatic processes (including sulfhydryl-containing enzymes involved in haem synthesis), protein maturation, cell adhesion and regulation of gene transcription. The effects of lead neurotoxicity include decreased cellular energy metabolism, impaired haem biosynthesis (resulting in increased erythrocytes fragility, basophilic stippling and circulating nucleated erythrocytes), oxidative stress, lipid peroxidation, altered activity of second messenger systems, altered neurotransmitter release (e.g. decreased GABA neurotransmission) and neurotransmitter receptor density, excitotoxicity, apoptosis impaired development and function of oligodendrocytes, abnormal myelin formation, abnormal neurotrophic factor expression, abnormal dendritic branching patterns and disruption of the blood-brain barrier (Lidsky and Scneider, 2003; Garza et al., 2006).
Clinical presentation
Clinical presentation is variable depending on duration and degree of exposure. Gastrointestinal signs (including vomiting, anorexia, diarrhoea and sometimes also abdominal pain) precede or accompany neurological signs (including seizures, blindness, obtundation, hyperexcitability, behavioural changes, head pressing, ataxia and tremors) (Zook et al., 1967; Knecht et al., 1979; Morgan, 1994). Clinical signs in cats may be more vague than in dogs and most commonly include anorexia, vomiting and seizures. Central vestibular abnormalities, including vertical nystagmus and ataxia, have also been reported in cats with lead poisoning (Knight et al., 2001). Clinical signs can be acute or chronic. In cases of chronic exposure, the seizures are intermittent (Bratton and Kowalczyk, 1989).
Diagnosis
Haematology and serum biochemistry may reveal one or more of the following abnormalities: nucleated erythrocytes and basophilic stippling in red blood cells with no or mild anaemia, increased packed cell volume, leukocytosis, elevated hepatic enzymes, hyper-glycaemia and hypercholesterolaemia. Radiography may allow identification of metallic material in the gastrointestinal tract (e.g. golf balls or toys) or subcutaneously (e.g. pellets). Blood lead levels of 40 μg/dl or higher are considered diagnostic of lead poisoning (Morgan, 1994). However, blood lead concentration fluctuates and due to sequestration in other organs does not necessarily correlate with total body burden of lead or with clinical signs (Bratton and Kowalczyk, 1989; Knight and Kumar, 2003). If the blood lead values are in the high normal range and lead poisoning is suspected clinically, treatment followed by measurement of urine lead levels can be diagnostic. Electroencephalographic changes in non-sedated dogs are characterized by intermittent high-amplitude slow wave activity (Knecht et al., 1979). A post-mortem diagnosis can be made by analysing lead concentration in kidneys, liver, brain and bones (Knight and Kumar, 2003). Levels of 3.6 to 10 μg/g by wet weight of liver tissue are considered diagnostic of lead toxicosis (Bratton and Kowalczyk, 1989).
Management
Treatment of lead toxicosis involves prevention of further exposure, decontamination of the individual (e.g. bathing in case of lead-laden dust coat exposure, administration of cathartics and/or enemas, endoscopic or surgical removal of lead-containing foreign bodies), decontamination of the environment, supportive care and chelation therapy to remove lead from the blood and soft tissues. The cathartic magnesium sulfate (250–500 mg/kg PO in dogs and 200 mg/kg PO in cats) can help to decrease lead absorption by forming insoluble lead sulfate. Treatment with the chelating agent, calcium disodium ethylene diamine tetraacetate (CaNa2EDTA), using a dose of 25 mg/kg intravenously or orally, four times a day for 2 to 5 days, has resulted in recovery within 36 to 48 h. However, in some animals, CaNa2EDTA has initially worsened neurologic signs. The most recently available chelator, succimer (meso-2,3-dimercaptosuccinic acid), administered at 10 mg/kg of body weight, orally, every 8 h, for 10 days, has been reported to be safe and effective in the treatment of lead poisoning in dogs and cats (Ramsey et al., 1996; Knight et al., 2001). Succimer may also be administered rectally as a solution in patients that are vomiting or that are unable to take oral medications. Chelation therapy with calcium EDTA (27 mg/kg SC for 5 days) alone or in association with D-penicillamine (33–55 mg/kg/day divided every 6–8 h) has also been reported. Seizures should be treated promptly with diazepam and/or other AEMs (see Table 4.1, and Chapters 12 and 24). Thiamine supplementation (1–2 mg/kg IM or 2 mg/kg PO every 24 h) can contribute to neurological improvement.
Prognosis
Clinical response to therapy is the best prognostic indicator. Prognosis is favourable in the majority of lead-poisoning cases treated with chelating agents (Morgan, 1994). Continuous or uncontrolled seizures may be associated with a less favourable prognosis.