Chocolate toxicosis may result in potentially life-threatening cardiac arrhythmias and CNS dysfunction in animals. 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 byproducts 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. In general, however, 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 ounce (10.4 mg/g). White chocolate is a negligible source of methylxanthines. Cocoa bean hulls contain ~255 mg/oz (9.1 mg/g) methylxanthines, although some cocoa bean hull mulches have had methylxanthines removed during manufacturing for consumption.
Methylxanthine Content of Various Types of Chocolate a
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. See our chocolate toxicity calculator to determine toxicity based on an animal's weight and the amount and type of chocolate ingested.
Theobromine and caffeine, the toxic principles in chocolate toxicosis, are readily absorbed from the gastrointestinal tract and widely distributed throughout the body. They are metabolized in the liver and undergo enterohepatic recycling. Methylxanthines are excreted in the urine as metabolites and unchanged parent compounds. The half-lives of theobromine and caffeine in dogs are 17.5 hours and 4.5 hours, 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 levels of cyclic adenosine monophosphate (cyclic AMP). Methylxanthines may also increase circulating levels of epinephrine and norepinephrine.
Clinical signs of chocolate toxicosis usually occur within 6–12 hours 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.
Diagnosis of chocolate toxicosis is based on history of exposure and 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 as differential diagnoses.
Stabilization of symptomatic patients is a priority in treating chocolate toxicosis. Methocarbamol (50–220 mg/kg, slow IV; no more than 330 mg/kg per day) or diazepam (0.5–2 mg/kg, slow IV) may be used for tremors and/or mild seizures; barbiturates or other general anesthetics may be required for severe seizures. Arrhythmias should be treated as needed: administration of 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/minute infusion) for refractory ventricular tachyarrhythmias. Fluid diuresis may help stabilize cardiovascular function and hasten urinary excretion of methylxanthines.
Once a patient is stable, or when presented before clinical signs have developed (eg, within 1 hour of ingestion), decontamination should be performed. Induction of emesis via administration of apomorphine or hydrogen peroxide should be initiated; in animals that have been sedated because 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 hours in symptomatic patients for as long as signs are present (vomiting may be controlled with administration of metoclopramide, 0.2–0.4 mg/kg, SC or IM, every 6 hours as needed).
Other treatments for symptomatic patients include cardiac status monitoring via electrocardiography, correction of acid-base and electrolyte abnormalities, management of body temperature and urinary catheter placement (methylxanthines and their metabolites can be reabsorbed via the bladder). Clinical signs may persist for up to 72 hours in severe cases.