eMedicine Specialties > Emergency Medicine > Toxicology

Plant Poisoning, Hypoglycemics

Jennifer Coles Schecter, MD, Staff Physician, Department of Emergency Medicine, Lahey Clinic, Burlington, MA
Sage W Wiener, MD, Assistant Professor, Department of Emergency Medicine, State University of New York Downstate, Director of Medical Toxicology, Department of Emergency Medicine, Kings County Hospital Center

Updated: Nov 10, 2009

Introduction

Background

More than 270 plant species have been identified as having hypoglycemic potential. Many of these plants are used in developing countries in the treatment of diabetes. The most well known of these plants are listed below:

• Herb fenugreek (Trigonella foenum-graecum)
• Bitter melon gourd (Momordica charantia)
• Climbing ivy gourd (Coccinia indica)
• Mamijava (Enicostemma littorale)
• Asian ginseng (Panax ginseng)
• American ginseng (Panax quinquefolius)
• Siberian ginseng (Eleutherococcus senticosus)
• Ackee tree (Blighia sapida)
• Prickly pear (Opuntia robusta)
• Yellow bells (Tecoma stans [family Bignoniaceae])

Most of the plants studied have shown minimal-to-moderate effects on glucose regulation, with the exception of ackee fruit and bitter melon. Bitter melon produces hypoglycemia via steroidal saponins (charantin, insulinlike peptides, and alkaloids), but it has never been reported to result in fatality. This article focuses on the potentially fatal effects produced by ackee fruit ingestions. Ackee fruit causes profound hypoglycemia due to hypoglycin A, a toxic compound contained in the fruit. In addition, several references regarding other plants with hypoglycemic effects have been included.

Ackee fruit is produced biannually by the tropical evergreen tree, Blighia sapida. Although indigenous to West Africa, it is commonly found in the Caribbean islands, Central America, South America, and southern Florida. In South America, the fruit has been used to treat colds, fever, and diseases as varied as edema and epilepsy, though no clinical trials support these uses. In Jamaica, ackee fruit is a food staple, commonly prepared like scrambled eggs or boiled with fish. The fruit itself is 10 cm wide and weighs 100 g. It houses 3 glossy, black seeds contained within a straw- to red-colored husk and covered by a thick, oily appearing yellow aril. The outer aril is closed in unripe ackee fruit. Upon ripening, the aril spontaneously opens. Unripe fruit and the water used to cook it are toxic and cause Jamaican vomiting sickness when ingested.

Fatal epidemics of this illness have been well studied in Haiti, West Africa, and Jamaica. These epidemics tend to coincide with food shortages. The disease is characterized by profound hypoglycemia and intractable vomiting. Before widespread recognition of the hypoglycemia produced by this illness, the mortality rate approached 80%.

Pathophysiology

Two water-soluble toxins are present in unripe ackee fruit, hypoglycin A and hypoglycin B. Hypoglycin A is L-alpha-amino-beta-[methylene cyclopropyl]propionic acid. Hypoglycin A is found in both the aril and the seeds of the unripe fruit. Hypoglycin B is a gamma-L-glutamyl derivative of hypoglycin A and is found only in the seeds of the fruit.

Hypoglycin A is metabolized by transamination and oxidative decarboxylation to form methylenecyclopropylacetic acid (MCPA). MCPA then forms nonmetabolizable carnitine and coenzyme A (CoA) esters, rendering them unavailable for other metabolic reactions. Hypoglycemia results because CoA and carnitine are required for long-chain fatty acid oxidation, and oxidation is required for gluconeogenesis. Thus, hypoglycemia results from an inability to perform gluconeogenesis. This inhibition of fatty acid metabolism also results in the accumulation of unusual dicarboxylic acids that are subsequently excreted in the urine such as 2-ethyl malonate, 2-methyl succinate, glutarate, and adipate.

Additionally, MCPA inhibits acyl-CoA dehydrogenases. Inhibition of butyryl CoA dehydrogenase stops the oxidation of long-chain fatty acids at the level of hexanoyl CoA and butyryl CoA, causing decreased production of nicotinamide adenine dinucleotide (NADH) and acetyl CoA. Their lowered concentration further inhibits gluconeogenesis. Hypoglycin A does not affect insulin release or serum insulin levels in animal models.

It is postulated that increased concentrations of glutaric acid may have an inhibitory effect on glutamic acid decarboxylase, causing a decrease in GABA production and an increase in concentration of glutamate. This mechanism can explain the proconvulsive effect of hypoglycin A.

Frequency

United States

The true incidence of ackee poisoning is unknown. Ackee fruit sales are illegal in the United States, likely leading to underreporting. Cases have been reported after consumption of fruit illegally shipped or transported by travelers. Several isolated, nonfatal cases have been reported in Ohio, Connecticut, and New York.

Though shipment of ackee fruit into the United States is still banned, the Food and Drug Administration (FDA) is considering modifying this ban. Research by Whitaker et al has led to evaluation of sampling plans to detect hypoglycin A in ackee fruit. This research will help the FDA to develop a cost-effective monitoring program to reduce lots of misclassified product and to increase consumer safety.^1,2

International

• Jamaica: Although endemic to Jamaica, the epidemiology of ackee poisoning is not well characterized. The true incidence is likely underreported. Incidence has been estimated at 2 cases per 100,000 annually for persons younger than 15 years and 0.4 case per 100,000 persons annually for those older than 15 years.³
• West Africa: Based on recent epidemics, the incidence in children aged 2-6 years is estimated to be about 40 cases per 100,000 population.
• Other: Most cases occur in developing nations in Africa and the Caribbean. Incidence rates in other areas have not been well studied.

Mortality/Morbidity

Ackee poisoning has killed an estimated 5,000 people since 1886. Children are more likely than adults to experience fatal complications of ackee poisoning. The most well-studied epidemics have been in Haiti, Jamaica, and West Africa.

• Jamaica: Large-scale poisonings reach epidemic proportions typically during the winter months. Between January 1989 and July 1991, 28 patients reported symptoms of ackee poisoning. Six of 28 patients died. The most common symptoms were vomiting, coma, and seizures. Seven of the patients had confirmed hypoglycemia. Most of the cases occurred between January and March.³
• West Africa: In 1998, in Burkina Faso, an epidemic of fatal encephalopathy was linked to ackee poisoning. Between January and May of 1998, 29 children aged 2-6 years died. The clinical presentation was similar to that of Jamaican vomiting sickness and toxic hypoglycemic syndrome; the most common symptoms included hypotonia, convulsions, and coma.⁴
• Haiti: From November 2000 to March 2001, 60 cases with symptoms consistent of ackee poisoning (ie, continuous vomiting, abdominal pain, loss of consciousness, convulsions within 24 h) were recorded in 2 districts of Haiti's Northern Province. Retrospective analysis confirmed 31 of the 80 cases were related to consumption of ackee fruit. The mean age of the victims ranged from 6 months to 88 years, with a median of 7 and an average of 16. The case-fatality rate was 52%.⁵

Race

Reported cases in Africa, Jamaica, and Haiti occurred in blacks.

Sex

In reported cases, no difference in sex distribution was noted.

Age

Poisoning is more common in persons younger than 15 years, and severe poisoning is more common in the pediatric population.

Clinical

History

• Typically, ackee fruit poisoning causes epidemics, with multiple children becoming ill.
• The patient may provide a history of ingesting unripe ackee fruit or water in which unripe ackee had been cooked. More than one family member may be ill.
• Sudden onset of vomiting begins 2-6 hours after ingestion with generalized epigastric discomfort. However, symptoms may appear within minutes.
• After a period of prostration lasting up to 18 hours, a second bout of vomiting may occur. 
• Unless treatment is given, this episode can progress to seizures, coma, and death.
• In severe poisoning, death usually occurs within 12 hours after ingestion.

Physical

• Nausea and vomiting occur in 75% of patients; severe vomiting may be followed by a quiescent phase, followed by recurrent vomiting.
• Diaphoresis and pallor may be observed.
• Tachypnea, tachycardia, and hypotension due to dehydration may be noted.
• Weakness and paresthesias may be present.
• Seizures, generalized tonic clonic, occur in 24% of patients.
• Drowsiness and coma occurs in 25% of patients.
• Death in severe, untreated cases can reach 80%.

Causes

• Causes include ingestion of unripe ackee fruit, canned ackee fruit, ackee fruit that has been forcibly opened or water in which unripe ackee fruit has been cooked.

Differential Diagnoses

Other Problems to Be Considered

Fatty liver of pregnancy
Chronic valproic acid use
Chronic nucleoside analog (eg, didanosine [DDL], zidovudine [AZT]) use
Ingestion of outdated tetracycline
Ingestion of oral hypoglycemics (sulfonylureas) (eg, metformin, phenformin, chlorpropamide)
Quinine ingestion
Disopyramide ingestion
Pentamidine ingestion
Streptozotocin exposure
Vacor exposure
Herbal product and tea consumption (eg, pennyroyal oil, margosa oil, comfrey, chaparral, germander, groundsel or senecio, Jin Bu Huan, and Syo-saiko-to)

Workup

Laboratory Studies

• Fingerstick glucose/rapid glucose determination to evaluate for hypoglycemia (Glucose levels as low as 3 mg/dL have been reported.)
• Chemistry panel (sodium, potassium, chloride, carbon dioxide, blood urea nitrogen, and creatinine levels) to evaluate for acidosis, hypokalemia, and electrolyte disturbance as a cause for vomiting
• Serum ketone levels (if present, suggest other cause of hypoglycemia)
• Urinalysis in ackee poisoning shows acidosis and no ketosis.
• Serum ammonia level (Hyperammonemia is characteristic.)
• Liver transaminase level and prothrombin time (PT)/activated partial thromboplastin time (aPTT) to assess extent of liver toxicity
• Arterial pH to evaluate acid/base status
• Serum lactate levels (may be elevated)
• Cerebrospinal fluid (generally reveals low glucose level)

Imaging Studies

• Nonenhanced head CT may be performed to exclude intracranial pathology as a cause for altered mental status, seizures, or focal neurologic deficits.

Other Tests

• Gas chromatography of urine: Excess excretion of medium-chain dicarboxylic acids, such as 2-ethylmalonic, 2-methylsuccinic, and glutaric acid, is a distinctive finding in this illness.
• Presence of positive serum or urine level of hypoglycin A or its metabolite methylenecyclopropyl acetic acid (MCPA) indicates exposure to ackee fruit.
• Autopsy findings include massive steatosis of the liver (comparable with Reye syndrome).

Procedures

• Endotracheal intubation: A secure airway may be necessary for patients presenting with seizures or coma.
• Intravenous access: Intravenous access may be needed to administer glucose-containing solutions, intravenous antiemetics and anticonvulsants, and volume resuscitation.

Treatment

Prehospital Care

• Hypoglycemia and airway compromise should be identified.
• Intravenous access and administration of dextrose, benzodiazepines (if needed to control seizures), and dextrose-containing intravenous fluid, as necessary, should be provided.

Emergency Department Care

• ED management of ackee poisoning is mainly supportive.
• Obtain a rapid fingerstick glucose and initiate glucose replacement with D50W boluses (D25W boluses in young children and D10W in neonates) and continuous infusions of 10% dextrose, as needed.
• Airway assessment and endotracheal intubation, if necessary, should be performed.
• Activated charcoal may be administered once the airway is secured.
• Electrolyte status should be assessed.
• Antiemetics such as metoclopramide, odansetron, or granisetron may be administered for profuse vomiting.
• Seizure precautions should be followed; treat seizures with benzodiazepines and dextrose.
• Theoretically, L-carnitine could be beneficial similar to its effect in valproic acid toxicity.

Consultations

• Consultation with a poison center and toxicologist may be helpful.
• Contact public health authorities for suspected outbreaks.

Medication

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.

GI decontaminant

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.

Dosing

Adult

1 g/kg PO (generally 50-100 g)

Pediatric

<1 year: Not recommended
>1 year: 1-2 g/kg PO (generally 15-30 g)

Interactions

Effectiveness of other medications decreases with coadministration; do not mix charcoal with sherbet, milk, or ice cream (decreases adsorptive properties)

Contraindications

Documented hypersensitivity; co-ingestion of caustic substances; unprotected airway, high aspiration risk

Precautions

Pregnancy

A - Fetal risk not revealed in controlled studies in humans

Precautions

Nutrients

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.

Dosing

Adult

D50W (0.5-1 g/kg or 1-2 mL/kg) IV, followed by a D10W drip to maintain serum glucose level above 100 mg/dL

Pediatric

Neonates: D10W bolus
Young children: D25W bolus (0.5-1 g/kg or 2-4 mL/kg)
D10W in 0.2% NS at 7 mg dextrose/kg/min can be initiated as infusion, with frequent adjustments based on serum glucose evaluations and consultation with a pediatrician

Interactions

Caution when administering parenteral fluids to patients receiving corticosteroids or corticotropin, especially if solution contains sodium ions

Contraindications

Diabetic coma if blood sugar levels are extremely high; do not administer concentrated solution if intraspinal or intracranial hemorrhage is present; avoid in patients who are dehydrated and diagnosed with delirium tremens, hepatic coma, or glucose-galactose malabsorption syndrome

Precautions

Pregnancy

A - Fetal risk not revealed in controlled studies in humans

Precautions

Continuous infusions of >10% dextrose, not for infusion through peripheral line (may cause thrombosis; administer instead through central venous catheter)
May cause nausea when infused; IV dextrose solutions may result in dilution of serum electrolyte concentrations or overhydration when fluid overload occurs; caution in patients with congested states or pulmonary edema; caution in subclinical diabetes mellitus or carbohydrate intolerance; increased risk exists of inducing significant hyperglycemia or hyperosmolar syndrome if solution is administered rapidly, especially in patients with chronic uremia or carbohydrate intolerance; concentrated solutions should not be administered IM/SC; rates of dextrose infusion higher than 0.5 g/kg/h may produce glycosuria; at infusion rates of 0.8 g/kg/h, the incidence of glycosuria is 5%; monitor fluid balance, electrolyte concentrations, and acid-base balance closely; dextrose administration may produce vitamin B-complex deficiency

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.

Dosing

Adult

1-3 g/d PO divided in 3 or 4 doses; typical replacement dose is three 330-mg tabs tid; 50-100 mg/kg IV over 30 min bolus, followed by 15 mg/kg q4h over 10-30 min

Pediatric

50-100 mg/kg/d PO divided in 4 doses; 50 mg/kg IV over 30 min

Interactions

None reported

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Monitor blood chemistries, vital signs, and overall clinical condition of the patient; nausea, vomiting, abdominal cramps, and diarrhea may occur

Somatostatin analogs

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.

Dosing

Adult

Initial: 50 mcg SC tid; may increase dose to 500 mcg tid
Doses of 300-6000 mcg/d or higher seldom result in additional biochemical benefit

Pediatric

Not established

Interactions

May reduce effects of cyclosporine; patients on insulin, oral hypoglycemic agents, beta-blockers, or calcium channel blockers may need dosage adjustment

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Side effects primarily related to altered GI motility and include nausea, abdominal pain, diarrhea, and increased incidence of gallstones and biliary sludge; because of alteration in counter-regulatory hormones (ie, insulin, glucagon, GH), hypoglycemia or hyperglycemia may be seen; bradycardia, cardiac conduction abnormalities, and arrhythmias have been reported; because of inhibition of TSH secretion, hypothyroidism may also occur; exercise caution in patients with renal impairment; cholelithiasis may occur

Antianxiety Agent

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.

Dosing

Adult

Dose is 0.05-0.1 mg/kg; usually, given at 4 mg/dose IV slowly over 2-5 min and repeat in 10-15 min prn; cumulative dose of 8 mg/d typically considered maximum
1-10 mg/d PO/IV/IM divided bid/tid

Pediatric

Infants and children: 0.05-0.1 mg/kg IV slowly over 2-5 min; repeat prn in 10-15 min at 0.05 mg/kg; not to exceed 4 mg/dose
Adolescents: 0.07 mg/kg IV slowly over 2-5 min and repeat in 10-15 min prn; not to exceed 4 mg/dose

Interactions

Toxicity of benzodiazepines in CNS increases when used concurrently with alcohol, phenothiazines, barbiturates, and MAO inhibitors

Contraindications

Documented hypersensitivity; preexisting CNS depression, hypotension, and narrow-angle glaucoma; reversal agents (eg, flumazenil) contraindicated when lorazepam used for life-threatening conditions (eg, control of intracranial pressure or status epilepticus)

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in renal or hepatic impairment, myasthenia gravis, organic brain syndrome, or Parkinson disease; use caution when sedating patients with profuse vomiting because aspiration may result

Antiemetics

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.

Dosing

Adult

Three 0.15 mg/kg (maximum 4 mg) IV doses over 2-5 min; usually administered at 4-mg increments that can be repeated; not to exceed maximum cumulative dose of 32 mg

Pediatric

<40 kg: 0.1 mg/kg IV over 2-5 min
>40 kg: 4 mg IV over 2-5 min

Interactions

Although potential for cytochrome P-450 inducers (barbiturates, rifampin, carbamazepine, and phenytoin) to change half-life and clearance of ondansetron, dosage adjustment is not usually required

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

May cause headache

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.

Dosing

Adult

10 mg IV/IM q2-3h prn

Pediatric

0.5-2 mg/kg IV q2-4h prn; not to exceed adult dose

Interactions

Anticholinergic agents may antagonize effects of metoclopramide; opiate analgesics may increase metoclopramide toxicity in CNS

Contraindications

Documented hypersensitivity; pheochromocytoma or GI hemorrhage, obstruction, or perforation; history of seizure disorders

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in history of mental illness and Parkinson disease

Granisetron (Kytril)

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

Dosing

Adult

10 mcg/kg IV over 5 min

Pediatric

Administer as in adults

Interactions

CYP-450 3A substrate, inducers (eg, phenobarbital) may decrease granisetron effect, while inhibitors (eg, erythromycin, clarithromycin) may increase granisetron toxicity

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in liver disease

Follow-up

Further Inpatient Care

Patients with the following conditions after ackee fruit poisoning should be admitted to the hospital:

• Severe, persistent hypoglycemia
• Intractable vomiting
• Seizures
• Altered mental status
• Hypotension
• Elevated liver enzyme levels or other evidence of liver damage

Deterrence/Prevention

• Patients and their families should be educated about the risks of unripe ackee fruit ingestion.

Prognosis

• Prognosis is good if unripe ackee fruit ingestion is promptly recognized and appropriately managed; however, deaths do occur.

Patient Education

• For patient education resources, visit eMedicine's Poisoning Center and Poisoning - First Aid and Emergency Center. Also, see eMedicine's patient education articles Food Poisoning, Wilderness: Poisons, and Activated Charcoal.

Miscellaneous

Medicolegal Pitfalls

• Failure to observe seizure precautions (eg, adequately control seizures and secure airway of seizing or obtunded patients)
• Failure to aggressively monitor and treat hypoglycemia
• Failure to consider other causes of hypoglycemia and liver failure
• Failure to adequately assess and manage fluid and electrolyte status
• Failure to consider diagnosis of ackee fruit ingestion
• Failure to consider potential exposure of family members or community of exposed patient

Special Concerns

• Pregnancy: In Jamaica, concern exists that ackee fruit ingestion may be associated with anencephaly, spina bifida, and hydrocephalus; however, teratogenic effects are not well established.
• Pediatric: Most cases occur in children. Generally, full recovery can be expected if hypoglycemia is identified and treated early and if liver failure and metabolic acidosis do not ensue.

References

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2. US Department of Agriculture. Improve the Detection of Quality Attributes and Chemical Agents in Agricultural Commodities. Last updated November 9, 2009. Available at http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=215290. Accessed November 10, 2009.

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Keywords

ackee fruit poisoning, hypoglycemia, ackee fruit, Jamaican vomiting sickness, hypoglycin, hypoglycin A, vomiting, Blighia sapida, B sapida, gourd bitter melon, herb fenugreek, pomegranate fruit, climbing ivy gourd, mamijava, Asian ginseng, American ginseng, Siberian ginseng, ginseng, Momordica charantia, M charantia, Trigonella foenum-graecum, T foenum-graecum, Coccinia indica, C indica, Enicostemma littorale, E littorale, Panax ginseng, P ginseng, Panax quinquefolius, P quinquefolius, Eleutherococcus senticosus, E senticosus

Contributor Information and Disclosures

Author

Jennifer Coles Schecter, MD, Staff Physician, Department of Emergency Medicine, Lahey Clinic, Burlington, MA
Disclosure: Nothing to disclose.

Coauthor(s)

Sage W Wiener, MD, Assistant Professor, Department of Emergency Medicine, State University of New York Downstate, 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, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Medical Editor

B Zane Horowitz, MD, FACMT, Professor, Department of Emergency Medicine, Oregon Health and Sciences University; 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 Academy of Clinical Toxicology and American College of Medical Toxicology
Disclosure: Nothing to disclose.

Pharmacy Editor

John T VanDeVoort, PharmD, Regional Director of Pharmacy, Sacred Heart & 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.

Managing Editor

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.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
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.

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