Chocolate toxicosis may result in potentially life-threatening cardiac arrhythmias and CNS dysfunction. Chocolate poisoning occurs most commonly in dogs, although many species are susceptible. Contributing factors include indiscriminate eating habits and readily available sources of chocolate. Deaths have also been reported in livestock fed cocoa by-products and in animals consuming mulch from cocoa-bean hulls.
Chocolate is derived from the roasted seeds of Theobroma cacao. The primary toxic principles in chocolate are the methylxanthines theobromine (3,7-dimethylxanthine) and caffeine (1,3,7-trimethylxanthine). Although the concentration of theobromine in chocolate is 3–10 times that of caffeine, both constituents contribute to the clinical syndrome seen in chocolate toxicosis. The exact amount of methylxanthines in chocolate varies because of the natural variation of cocoa beans and variation within brands of chocolate products. However, in general, the total methylxanthine concentration of dry cocoa powder is ~800 mg/oz (28.5 mg/g), unsweetened (baker's) chocolate is ~450 mg/oz (16 mg/g), semisweet chocolate and sweet dark chocolate is ~150–160 mg/oz (5.4–5.7 mg/g), and milk chocolate is~64 mg/oz (2.3 mg/g). Chocolate bars labeled as a percentage of cocoa/cacao are based on unsweetened chocolate, ie, a 65% cacao bar would contain ~293 mg (450 mg × 0.65) of methylxanthines per oz (10.4 mg/g). White chocolate is an insignificant source of methylxanthines. Cocoa bean hulls contain ~255 mg/oz (9.1 mg/g) methylxanthines.
The LD50 of both caffeine and theobromine is reportedly 100–200 mg/kg, but severe signs and deaths may occur at much lower dosages, and individual sensitivity to methylxanthines varies. In general, mild signs (vomiting, diarrhea, polydipsia) may be seen in dogs ingesting 20 mg/kg, cardiotoxic effects may be seen at 40–50 mg/kg, and seizures may occur at dosages ≥60 mg/kg. One ounce of milk chocolate per pound of body weight is a potentially lethal dose in dogs.
Theobromine and caffeine are readily absorbed from the GI tract and widely distributed throughout the body. They are metabolized in the liver and undergo enterohepatic recycling. Methylxanthines are excreted in the urine as both metabolites and unchanged parent compounds. The half-lives of theobromine and caffeine in dogs are 17.5 hr and 4.5 hr, respectively.
Theobromine and caffeine competitively inhibit cellular adenosine receptors, resulting in CNS stimulation, diuresis, and tachycardia. Methylxanthines also increase intracellular calcium levels by increasing cellular calcium entry and inhibiting intracellular sequestration of calcium by the sarcoplasmic reticulum of striated muscle. The net effect is increased strength and contractility of skeletal and cardiac muscle. Methylxanthines may also compete for benzodiazepine receptors within the CNS and inhibit phosphodiesterase, resulting in increased cyclic AMP levels. Methylxanthines may also increase circulating levels of epinephrine and norepinephrine.
Clinical signs of chocolate toxicosis usually occur within 6–12 hr of ingestion. Initial signs may include polydipsia, vomiting, diarrhea, abdominal distention, and restlessness. Signs may progress to hyperactivity, polyuria, ataxia, rigidity, tremors, and seizures. Tachycardia, premature ventricular contractions, tachypnea, cyanosis, hypertension, hyperthermia, bradycardia, hypotension, or coma may occur. Hypokalemia may occur late in the course of the toxicosis, contributing to cardiac dysfunction. Death is generally due to cardiac arrhythmias, hyperthermia, or respiratory failure. The high fat content of chocolate products may trigger pancreatitis in susceptible animals.
No specific lesions may be found in animals succumbing to chocolate toxicosis. Hyperemia, hemorrhages, or congestion of multiple organs may occur as agonal changes. Severe arrhythmias may result in pulmonary edema or congestion. Chocolate or cocoa bean hulls may be present in the GI tract at necropsy.
Diagnosis is based on history of exposure, along with clinical signs. Amphetamine toxicosis, ma huang/guarana (ephedra/caffeine) toxicosis, pseudoephedrine toxicosis, cocaine toxicosis, and ingestion of antihistamines, antidepressants, or other CNS stimulants should be considered in the differential diagnosis.
Stabilization of symptomatic animals is a priority in treating chocolate toxicosis. Methocarbamol (50–220 mg/kg, slow IV; no more than 330 mg/kg/day) or diazepam (0.5–2.0 mg/kg, slow IV) may be used for tremors and/or mild seizures; barbiturates may be required for severe seizures. Arrhythmias should be treated as needed: propranolol (0.02–0.06 mg/kg, slow IV) or metoprolol (0.2–0.4 mg/kg, slow IV) for tachyarrhythmias, atropine (0.01–0.02 mg/kg) for bradyarrhythmias, and lidocaine (1–2 mg/kg, IV, followed by 25–80 mg/kg/min infusion) for refractory ventricular tachyarrhythmias. Fluid diuresis may assist in stabilizing cardiovascular function and hastening urinary excretion of methylxanthines.
Once animals have stabilized, or in animals presenting before clinical signs have developed (eg, within 1 hr of ingestion), decontamination should be performed. Induction of emesis using apomorphine or hydrogen peroxide should be initiated; in animals that have been sedated ebecause of seizure activity, gastric lavage may be considered. Activated charcoal (1–4 g/kg, PO) should be administered; because of the enterohepatic recirculation of methylxanthines, repeated doses should be administered every 12 hr in symptomatic animals for as long as signs are present (control vomiting with metoclopramide, 0.2–0.4 mg/kg, SC or IM, qid as needed).
Other treatment for symptomatic animals includes maintaining thermoregulation, correcting acid-base and electrolyte abnormalities, monitoring cardiac status via electrocardiography, and placing a urinary catheter (methylxanthines and their metabolites can be reabsorbed across the bladder wall). Clinical signs may persist up to 72 hr in severe cases.
Last full review/revision May 2013 by Sharon M. Gwaltney-Brant, DVM, PhD, DABVT, DABT