Chocolate Toxicity

Ch0colate Toxicity

Chocolate contains methylxanthine (theobromine + caffeine). The concentration of theobromine is 3-10 times that of caffeine, but both contribute to the clinical signs in chocolate toxicosis.

Mechanism of action:

Methylxanthine is a competitive antagonist of cellular adenosine receptors, which causes CNS stimulation (tremors, anxiety, seizures), myocardial stimulation (tachycardia and tachyarrhythmias), diuresis, and (at very high doses) gastrointestinal ulceration. Methylxanthines also increases calcium intracellularly leading to increased muscular and cardiac contractility. Methylxanthines may also exert their effects by competing for benzodiazepine receptors within the central nervous system and by inhibiting phosphodiesterase, resulting in increased intracellular cyclic adenosine monophosphate.

The half-lives of theobromine and caffeine in dogs are 17.5 hours and 4.5 hours. Theobromine and caffeine each have an LD50 of 100 to 200 mg/kg, however, clinical signs can be seen as low as 20 mg/kg.

Clinical Sings:

Clinical signs usually occur within 6–12 hours of ingestion. The initial clinical signs include vomiting, diarrhea, polydipsia, bloating, and restlessness. Sings may progress to hyperactivity, urination, ataxia, muscle tremors, tachycardia, bradycardia, arrhythmias, hyperthermia, seizures, coma, and death. Death is generally due to cardiac arrhythmias or respiratory failure.

Secondary pancreatitis has been reported because of the high fat content of many chocolate products. Gastrointestinal obstruction may occur from ingestion of wrappers or if the chocolate congeals into a mass.

Differential diagnosis:

  • Other toxins: Pesticides, organophosphates antihistamine or decongestant toxicosis, mycotoxins.

  • Drugs: LSD, amphetamines, cocaine toxicosis

Diagnostics:

  • CBC and serum biochemistry: hypokalemia

  • ECG abnormalities: Include tachycardia, ventricular dysrhythmias and bradycardia

  • Urine specific gravity: low

  • Stomach content analysis: presence of chocolate and methylxanthine

Treatment:

There is no specific antidote for methylxanthines. The objective is to eliminate the methylxanthine toxin by decontamination and support of clinical signs. In severe cases, clinical signs may persist for up to 72 hours because of the long half-life of theobromine in dogs (17.5 hours vs. 4.5 hours for caffeine).

A) Emesis:

Induction of emesis in dogs

  • Apomorphine: Administer 0.02–0.04 mg/kg IV or IM or 1.5–6 mg dissolved and placed into the conjunctival fornix. If apomorphine was placed in the eye, after emesis, the patient’s eye should be thoroughly lavaged with sterile saline.

Note: If excessive sedation occurs from apomorphine, the sedation may be reversed by the administration of naloxone (0.01–0.04 mg/kg IV, IM, SC), but this will not reverse the emetic effects.

  • Hydrogen peroxide 3%: Administer 1–5 mL/kg PO, with a maximum dose of 3 tablespoons (45 mL). If the patient does not vomit within 10 minutes, give 3% hydrogen peroxide 0.5 mL/kg PO once.

Induction of emesis in cats

  • Xylazine: Administer 0.44–1 mg/kg IM or SC (can reverse with yohimbine 0.1 mg/kg IM, SC, or IV slowly).

  • Medetomidine: Administer 10 μg/kg IM (can reverse with atipamezole (Antisedan) 25 μg/kg IM).

B) Decontamination via emesis or gastric lavage

  • Activated charcoal with sorbitol: Administer 1–2 g/kg (3–6 mL/lb) PO once. In methylxanthine toxicosis patients, repeat the administration of activated charcoal without sorbitol q3–6h for 36 hours after ingestion. Administer a cathartic only once.

C) Intravenous fluids

Place an intravenous catheter. Administering intravenous fluids at twice the maintenance levels will support the cardiovascular system and enhance urinary excretion. Because caffeine can be reabsorbed from the bladder, place a urinary catheter in moderately to severely affected animals. Serum electrolytes should be monitored, and any imbalances corrected as needed.

D) Seizures

  • Diazepam: Dogs 0.5 to 2 mg/kg IV; Cats 0.5 to 1 mg/kg IV.

  • Pentobarbital: 2–30 mg slow IV to effect as needed.

E) Bradycardia

  • Administer atropine 0.02 mg/kg IV.

F) Tachycardia

If the patient has tachycardia, administer a beta blocker such as propranolol 0.02–0.06 mg/kg slow IV or metoprolol 0.5–1 mg/kg PO q8h in dogs, 12.5–25 mg/cat PO q8–12h.

G) Premature ventricular contractions (PVCs)

If the patient has PVCs, administer lidocaine.

  • Dogs: 1–2 mg/kg IV bolus followed by 25–75 mg/kg/min IV infusion.

  • Cats: 0.25–1 mg/kg IV bolus followed by 5–40 mg/kg/min IV infusion.

H) Muscle Tremors

  • Methocarbamol: 44 mg/kg IV; administer half slowly until relaxation and continue to effect.

I) The administration of famotidine, and aluminum hydroxide or aluminum carbonate may neutralize the gastrointestinal irritation caused by caffeine toxicosis.

  • Famotidine: 0.5- 1 mg/kg IV or PO every 12 – 24 hours.

Patient monitoring

  • Heart rate, ECG, and blood pressure every 1 to 4 hours, unless continuous monitoring is warranted.

  • Seizure watch.

  • Temperature every 4 hours for hyperthermia.

  • Renal function.

Prognosis: Complete recovery with treatment; if treatment is started within 2 to 4 hours of ingestion. Guarded with advanced neurologic and cardiovascular signs.

Theobromine and Caffeine Values

The default theobromine and caffeine values for the chocolate toxicity converter are shown in the table below. It should be noted that theobromine and caffeine default values can be changed.