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
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
Last full review/revision May 2013 by Sharon M. Gwaltney-Brant, DVM, PhD, DABVT, DABT