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Hypoglycemic Plant Poisoning Medication

  • Author: Nathan Reisman, MD; Chief Editor: Asim Tarabar, MD  more...
 
Updated: Apr 28, 2015
 

Medication Summary

Supportive treatment with glucose, fluid, and electrolyte replacement is the mainstay of therapy. Antiemetics are used to control vomiting, and benzodiazepines are used to control seizures. Supplemental carnitine may be considered, although it has not been studied in this context.

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GI decontaminant

Class Summary

These agents are used to adsorb toxin in the GI tract, limiting systemic adsorption.

Activated charcoal (Liqui-Char)

 

Emergency treatment in poisoning caused by drugs and chemicals. Network of pores present in activated charcoal adsorbs 100-1000 mg of drug per gram of charcoal. Does not dissolve in water.

For maximum effect, administer as soon as possible after ingesting poison.

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Nutrients

Class Summary

Dextrose is used to reverse hypoglycemia. Carnitine, an amino acid derivative, is synthesized from methionine and lysine and is required in energy metabolism. It can promote excretion of excess fatty acids in patients with defects in fatty acid metabolism or specific organic acidopathies that bioaccumulate acyl CoA esters.

Dextrose (D-glucose)

 

Monosaccharide absorbed from the intestine and then distributed, stored, and used by the tissues.

Parenterally injected dextrose is used in patients unable to sustain adequate oral intake. Direct oral absorption results in a rapid increase in blood glucose concentrations.

Dextrose is effective in small doses, and no evidence exists that it may cause toxicity. Concentrated dextrose infusions provide higher amounts of glucose and increased caloric intake in a small volume of fluid.

Levocarnitine (Carnitor)

 

May facilitate transport of fatty acids into mitochondria. Carnitine has been used successfully in treatment of chronic valproate toxicity associated with hyperammonemia. Chronic valproate toxicity is thought to inhibit carnitine-dependent transfer of fatty acids from cytosol into mitochondria for beta-oxidation.

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Somatostatin analogs

Class Summary

These agents are used to reduce blood levels of GH glucagon and VIP peptides.

Octreotide (Sandostatin)

 

Acts primarily on somatostatin receptor subtypes II and V. Inhibits GH secretion and has a multitude of other endocrine and nonendocrine effects, including inhibition of glucagon, VIP, and GI peptides. Inhibits insulin release.

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Antianxiety Agent

Class Summary

Benzodiazepines may be used to treat seizures.

Lorazepam (Ativan)

 

Sedative hypnotic with short onset of effects and relatively long half-life.

By increasing the action of gamma-aminobutyric acid (GABA), which is a major inhibitory neurotransmitter in the brain, may depress all levels of CNS, including limbic and reticular formation.

Important to monitor patient's blood pressure after administering dose. Adjust as necessary.

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Antiemetics

Class Summary

Antiemetics may be used to control severe and persistent vomiting. Agents in this class may also prevent nausea and vomiting associated with emetogenic cancer chemotherapy

Ondansetron (Zofran)

 

Selective 5-HT3-receptor antagonist that blocks serotonin both peripherally and centrally. Prevents nausea and vomiting associated with emetogenic cancer chemotherapy (eg, high-dose cisplatin) and complete body radiotherapy.

Metoclopramide (Reglan)

 

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

Granisetron (Kytril)

 

At chemoreceptor trigger zone, blocks serotonin peripherally on vagal nerve terminals and centrally.

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Contributor Information and Disclosures
Author

Nathan Reisman, MD Clinical Assistant Instructor, Department of Emergency Medicine, Kings County Hospital Center, SUNY Downstate Medical Center

Nathan Reisman, MD is a member of the following medical societies: Emergency Medicine Residents' Association, Society for Simulation in Healthcare

Disclosure: Nothing to disclose.

Coauthor(s)

Sage W Wiener, MD Assistant Professor, Department of Emergency Medicine, State University of New York Downstate Medical Center; Director of Medical Toxicology, Department of Emergency Medicine, Kings County Hospital Center

Sage W Wiener, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American College of Medical Toxicology, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

John T VanDeVoort, PharmD Regional Director of Pharmacy, Sacred Heart and St Joseph's Hospitals

John T VanDeVoort, PharmD is a member of the following medical societies: American Society of Health-System Pharmacists

Disclosure: Nothing to disclose.

Chief Editor

Asim Tarabar, MD Assistant Professor, Director, Medical Toxicology, Department of Emergency Medicine, Yale University School of Medicine; Consulting Staff, Department of Emergency Medicine, Yale-New Haven Hospital

Disclosure: Nothing to disclose.

Additional Contributors

B Zane Horowitz, MD, FACMT Professor, Department of Emergency Medicine, Oregon Health and Sciences University School of Medicine; Medical Director, Oregon Poison Center; Medical Director, Alaska Poison Control System

B Zane Horowitz, MD, FACMT is a member of the following medical societies: American College of Medical Toxicology

Disclosure: Nothing to disclose.

Acknowledgements

Michael Hodgman, MD Assistant Clinical Professor of Medicine, Department of Emergency Medicine, Bassett Healthcare

Michael Hodgman, MD is a member of the following medical societies: American College of Medical Toxicology, American College of Physicians, Medical Society of the State of New York, and Wilderness Medical Society

Disclosure: Nothing to disclose.

Jennifer Coles Schecter, MD Resident Physician, Department of Emergency Medicine, Lahey Clinic, Burlington, MA

Disclosure: Nothing to disclose.

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