Ackee Fruit Toxicity Medication
- Author: Dave A Holson, MD, MBBS, MPH; Chief Editor: Timothy E Corden, MD more...
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.
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.
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.
Dextrose and glucose stimulators
Prompt gluconeogenesis is achieved with glucagon. Emergent blood glucose elevation requires the intravenous administration of dextrose.
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.
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.
These agents are used to control vomiting associated with ackee fruit poisoning.
A phenothiazine derivative. May relieve nausea and vomiting by blocking postsynaptic mesolimbic dopamine receptors with its anticholinergic effects and by depressing reticular activating system.
Phenothiazine derivative. Has antihistaminic, sedative, anti–motion sickness, antiemetic, and anticholinergic effects.
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.
These act in the GABA-benzodiazepine receptor complex and are used to control seizures.
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).
Depresses all levels of CNS (eg, limbic and reticular formation), possibly by increasing activity of GABA.
Insulin secretion may be altered by various mechanisms. 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.
Reserved for severe persistent hypoglycemia. Increases blood glucose by inhibiting pancreatic insulin release, possibly through an extrapancreatic effect.
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.
Sharma S, Yacavone MM, Cao X, Samuda PM, Cade J, Cruickshank K. Nutritional composition of commonly consumed composite dishes for Afro-Caribbeans (mainly Jamaicans) in the United Kingdom. Int J Food Sci Nutr. 2009 Apr 1. 1-11. [Medline].
Emanuel MA, Gutierrez-Orozco F, Yahia EM, Benkeblia N. Assessment and profiling of the fatty acids in two ackee fruit (Blighia sapida Köenig) varieties during different ripening stages. J Sci Food Agric. 2013 Mar 15. 93(4):722-6. [Medline].
Schwartzbord JR, Emmanuel E, Brown DL. Haiti's food and drinking water: a review of toxicological health risks. Clin Toxicol (Phila). 2013 Nov. 51(9):828-33. [Medline].
Joskow R, Belson M, Vesper H, et al. Ackee fruit poisoning: an outbreak investigation in Haiti 2000-2001 and review of the literature. Clin Toxicol (Phila). 2006. 44 (3):267-73.
Moya J. Ackee (Blighia sapida) poisoning in the Nothern Province, Haiti, 2001. Epidemiol Bull. June 2006. 22 (2):8-9.
Gaillard Y, Carlier J, Berscht M, et al. Fatal intoxication due to ackee (Blighia sapida) in Suriname and French Guyana. GC-MS detection and quantification of hypoglycin-A. Forensic Sci Int. 2011 Mar 20. 206(1-3):e103-7. [Medline].
American Medical Association; American Nurses Association-American Nurses Foundation; Centers for Disease Control and Prevention; Center for Food Safety and Applied Nutrition, Food and Drug Administration; Food Safety and Inspection Service, US Departm... Diagnosis and management of foodborne illnesses: a primer for physicians and other health care professionals. MMWR Recomm Rep. 2004 Apr 16. 53:1-33. [Medline].
Vlasselaers D, Milants I, Desmet L, et al. Intensive insulin therapy for patients in paediatric intensive care: a prospective, randomised controlled study. Lancet. 2009 Feb 14. 373(9663):547-56. [Medline].
Addae JI, Melville GN. A re-examination of the mechanism of ackee-induced vomiting sickness. West Indian Med J. 1988 Mar. 37(1):6-8. [Medline].
[Guideline] Barceloux DG. Akee fruit and Jamaican vomiting sickness (Blighia sapida Koenig). Dis Mon. Jun 2001. 55 (6):318-26.
Barennes, H, Valea, I, Boudat AM, et al. Early glucose and methylene blue are effective against unripe ackee apple poisoning in mice. Food and Chemical Toxicology. 2004. 42(5):809-815. [Medline].
Bressler R, Corredor C, Brendel K. Hypoglycin and hypoglycin-like compounds. Pharmacol Rev. 1969 Jun. 21(2):105-30. [Medline].
CDC. Toxic hypoglycemic syndrome--Jamaica, 1989-1991. MMWR Morb Mortal Wkly Rep. 1992 Jan 31. 41(4):53-5. [Medline].
Eddleston M, Persson H. Acute plant poisoning and antitoxin antibodies. J Toxicol Clin Toxicol. 2003. 41(3):309-15. [Medline].
Kean EA. Commentary on a review on the mechanism of ackee-induced vomiting sickness. West Indian Med J. 1988 Sep. 37(3):139-42. [Medline].
Larson J, Vender R, Camuto P. Cholestatic jaundice due to ackee fruit poisoning. Am J Gastroenterol. 1994 Sep. 89(9):1577-8. [Medline].
McTague JA, Forney R Jr. Jamaican vomiting sickness in Toledo, Ohio. Ann Emerg Med. 1994 May. 23(5):1116-8. [Medline].
Mills J, Melville GN, Bennett C, et al. Effect of hypoglycin A on insulin release. Biochem Pharmacol. 1987 Feb 15. 36(4):495-7. [Medline].
Tanaka K, Kean EA, Johnson B. Jamaican vomiting sickness. Biochemical investigation of two cases. N Engl J Med. 1976 Aug 26. 295(9):461-7. [Medline].