Chocolate Toxicity In Pets

Dr.Amandeep Department Of Veterinary MedicineL2013V40M GADVASU

INTRODUCTION

• Theobromine poisoning

• Overdose reaction to the alkaloid theobromine, found

in chocolate , beverages & some other foods

• LD50 of caffeine and theobromine are 100-200 mg/kg

• It may result in potentially life-threatening cardiac

arrhythmias and CNS dysfunction.

INTRODUCTION

• Cocoa beans contain about 1.2% theobromine by

weight

• Processed chocolate, in general has smaller amounts

• Contributing factors include indiscriminate eating

habits & readily available sources of chocolate

• Deaths have also been reported in livestock fed cocoa

by-products

Dogs v/s Cats v/s Humans

• Serious poisoning happens more frequently in

domestic animals, which metabolize theobromine

much more slowly than humans

• If large numbers of filled chocolate candies are

consumed, another serious danger is posed by the fat

and sugar in the fillings, which can sometimes trigger

life-threatening PANCREATITIS several days later

Dogs v/s Cats v/s Humans

• Toxic dose for cats is even lower than for dogs

• But cats are less prone to eating chocolate since they

are unable to taste sweetness

• Half-lives of theobromine and caffeine in dogs are 17.5

hr and 4.5 hr respectively.

In Dogs

• Mild signs like vomition, diarrhea, polydipsia at 20

mg/kg

• Cardiotoxic effects at 40-50 mg/kg

• Seizures at >=60mg/kg

• One ounce of milk chocolate per pound of body weight

is a potentially lethal dose

Pathogenesis

Theobromine and caffeine are readily absorbedfrom GIT & widely distributed throughout body

Metabolized in liver and undergo enterohepaticrecycling

Methylxanthines are excreted in urine as bothmetabolites and unchanged parent compounds

Theobromine and caffeine competitively inhibit cellular adenosine receptors

Resulting in CNS stimulation, diuresis, and tachycardia

Pathogenesis (EFFECT ON MUSCLES)

• Methylxanthines also increase intracellular calcium

levels by increasing cellular calcium entry

• And inhibiting intracellular sequestration of calcium by

the sarcoplasmic reticulum of striated muscle

• Net effect is increased strength and contractility of

skeletal and cardiac muscle

Pathogenesis

• Methylxanthines may also compete for benzodiazepine

receptors within CNS and inhibit phosphodiesterase,

resulting in increased cyclic AMP levels

• Methylxanthines may also increase circulating levels of

epinephrine and norepinephrine

Methylxanthines have following modes of action

• Antagonism of Adenosine Receptors: this antagonism results

in stimulation of the central nervous system and an increase in

heart rate and also diureses

• Inhibition of Cyclic Nucleotide phosphodiesterase:

consequently there is an increase in cyclic AMP, which in turn

leads to greater catecholamine release and their effect

• Modulation of Intracellular Calcium Concentrations:Ventricular

fibrillation, and other cardiac dysrhythmias are most frequently

the ultimate cause of death

Clinical Signs• Within 6-12 hours

• Initially

Nausea & Polydipsia

Vomiting & Diarrhea

Abdominal distension

Restlessness & increased Urination

• Progress to hyperactivity, polyuria, ataxia, tremors &

seizures

Clinical Signs

• Tachycardia, premature ventricular contractions,

tachypnea, cyanosis, hypertension, hyperthermia,

bradycardia, hypotension or coma

• In later course hypokalemia, due to cardiac dysfunction

• Eventually death due to cardiac arrhythmias,

hyperthermia or respiratory failure

Lesions

• No specific lesions

• May be found in animals succumbing to chocolatetoxicosis

• Hyperemia, hemorrhages or congestion of multipleorgans

• Severe arrhythmias may result in pulmonary edema orcongestion

• Chocolate or cocoa bean hulls be present in the GI tract

Diagnosis Diagnosis

• Amphetamine toxicosis

• Cocaine toxicosis

• Ingestion of antihistamines and antidepressants

• Other CNS stimulants

Treatment

• Dogs presenting with clinical signs

• Inital stabilisation of Cardiorespiratory System:

– Tachycardia: beta-blockers, eg orally administered metoprolol @ 0.2-0.4 mg per kg slow I/V every 8 hours

– Premature Ventricluar Contractions: lidocaine; iv bolus of 1-2mg/kg I/V followed by 25-80 mg/kg/min infusion administered slowly,

– Bradycardia: Atropine at dose of 0.01mg to 0.02mg per kg

Treatment

• Treatment of seizures and hyperactivity

– IV Diazepam at a dose of 0.5 to 2 mg/kg

– Alternative to diazepam is barbiturates

– Treating the seizures and hyperactivity should help

restore normal body temperature

– If animal still hyperthermic then this should be

treated directly

Treatment

• Correction of acid/base and electrolyte inbalances

• Insertion of urinary catheter

– Helps prevent further absorption of theobromine

and caffeine across bladder wall as methyxanthines

can be reabsorbed across urinary bladder wall

Treatment

Dogs with a known history of recent chocolate ingestion but who have not yet developed clinical signs

• Administration of apomorphine (0.03mg/kg IV) or

hydrogen peroxide (1-5 ml/kg po) - to induce emesis

• Activated charcoal (1-4g/kg,po) in order to minimise

further absorption of methylxanthines

Prognosis

• Clinical signs can persist upto 72 hours

• If treated correctly and early enough with in 5min

consult the prognosis is good and a complete recovery

can be expected

• For animals presenting with seizures and arrhythmias

the prognosis is guarded.

Thanks