Ackee Fruit Toxicity Medication

The mainstay of treatment in ackee fruit poisoning is to maintain a normal blood glucose level. Antiemetics are usually indicated to control the vomiting. Administer activated charcoal as soon as possible after ingestion. Treat convulsions with benzodiazepines.

Class Summary

Consider activated charcoal decontamination in any patient who presents within 4 hours of ingestion. Activated charcoal is used for drug absorption and may be all that is required in mild-to-moderate toxicity. Activated charcoal is not absorbed and is excreted entirely through the GI tract.

Activated charcoal (Actidose-Aqua, Liqui-Char)

Emergency treatment in poisoning caused by drugs and chemicals. Network of pores present in activated charcoal absorbs 100-1000 mg of drug per g of charcoal. Prevents absorption by adsorbing drug in the intestine. Multidose charcoal may interrupt enterohepatic recirculation and enhance elimination by enterocapillary exsorption. Theoretically, by constantly bathing the GI tract with charcoal, the intestinal lumen serves as a dialysis membrane for reverse absorption of drug from intestinal villous capillary blood into intestine. Does not dissolve in water.

Class Summary

Prompt gluconeogenesis is achieved with glucagon. Emergent blood glucose elevation requires the intravenous administration of dextrose.

Dextrose (D-glucose)

Used to promptly increase serum glucose level. Monosaccharide absorbed from intestine and distributed, stored, and used by tissues. Patients may recover if IV dextrose is administered before permanent damage due to low blood glucose levels occurs.

Glucagon

Polypeptide hormone identical to human glucagon; acts only on liver glycogen, converting it to glucose; do not use as empiric therapy because patients tend to be glycogen-depleted and may not improve; may be used temporarily until IV access obtained.

Class Summary

These agents are used to control vomiting associated with ackee fruit poisoning.

Prochlorperazine (Compazine)

A phenothiazine derivative. May relieve nausea and vomiting by blocking postsynaptic mesolimbic dopamine receptors with its anticholinergic effects and by depressing reticular activating system.

Promethazine (Phenergan)

Phenothiazine derivative. Has antihistaminic, sedative, anti–motion sickness, antiemetic, and anticholinergic effects.

Metoclopramide (Reglan)

Stimulates motility of upper GI tract. Dopamine antagonist that stimulates acetylcholine release in myenteric plexus. Acts centrally on chemoreceptor triggers in floor of fourth ventricle, providing important antiemetic activity.

Class Summary

These act in the GABA-benzodiazepine receptor complex and are used to control seizures.

Lorazepam (Ativan)

Sedative hypnotic with short onset of effects and relatively long half-life. May depress all levels of CNS, including limbic and reticular formation, by increasing action of GABA (major inhibitory neurotransmitter in brain).

Diazepam (Valium)

Depresses all levels of CNS (eg, limbic and reticular formation), possibly by increasing activity of GABA.

Class Summary

Insulin secretion may be altered by various mechanisms.^[6] Diazoxide inhibits pancreatic secretion of insulin, stimulates glucose release from the liver, and stimulates catecholamine release, which elevates blood glucose levels. Octreotide is a peptide with pharmacologic action similar to that of somatostatin, which inhibits insulin secretion.

Diazoxide (Hyperstat IV)

Reserved for severe persistent hypoglycemia. Increases blood glucose by inhibiting pancreatic insulin release, possibly through an extrapancreatic effect.

Octreotide (Sandostatin)

Acts primarily on somatostatin receptor subtypes II and V. Inhibits GH secretion and has multiple endocrine and nonendocrine effects, including inhibition of glucagon, VIP, and GI peptides. Highly effective in treatment of hypoglycemia caused by sulfonylurea overdose. Despite lack of published descriptions of its use in Jamaican vomiting sickness, may be useful in this setting.