eMedicine Specialties > Pediatrics: Cardiac Disease and Critical Care Medicine > Toxicology

Toxicity, Monoamine Oxidase Inhibitor: Treatment & Medication

Author: Soumya Ganapathy, MD, Consulting Staff, Department of Emergency Medicine, Union Memorial Hospital
Coauthor(s): Frank A Maffei, MD, FAAP, Associate Professor of Pediatrics, Temple University School of Medicine; Director of Medical Student Affairs, Geisinger Health System; Pediatric Critical Care Attending Physician, Janet Weis Children's Hospital at Geisinger Medical Center
Contributor Information and Disclosures

Updated: Jan 23, 2008

Treatment

Medical Care

As with most toxic ingestions, the cornerstone of management is continuous monitoring, decontamination when clinically indicated, and meticulous supportive care.

  • Give careful attention to airway management.
  • Maintain euvolemia because patients with monoamine oxidase inhibitor (MAOI) poisoning can become dehydrated secondary to their hypermetabolic state.
  • Maintain euthermia, especially in patients with suspected serotonin syndrome. Water mist sprays with fanning are effective. The removal of clothing and the use of cooling blankets may also be effective.
  • Treat seizures and agitation with intravenous benzodiazepines.
  • Decontamination with activated charcoal should be performed with caution and with attention to the possibility of airway compromise.
  • Treat hypertension only if it is sustained and clinically significant.

Consultations

  • Close consultation with a medical toxicologist or personnel from a regional poison center is recommended.
  • Consult a pediatric intensivist.
  • Consult a psychiatrist in cases of suspected intentional ingestion.

Medication

Decontamination agents

Consider activated charcoal decontamination in any patient who presents within one hour of the ingestion. Activated charcoal is used for drug adsorption and may be sufficient in mild-to-moderate toxicity. It is not absorbed and is excreted entirely through the GI tract.


Activated charcoal (Actidose-Aqua, Liqui-Char)

Emergency treatment in drug or chemical poisoning. Network of pores adsorbs 100-1000 mg of drug per gram of charcoal, decreasing GI absorption of the poison. Does not dissolve in water. In an acute overdose, most effective if given within 1 h of ingestion.

Adult

50-100 g PO (1 g/kg) or 10 times amount of ingested poison; administer as susp in 4-8 oz of water

Pediatric

1 g/kg PO administered with water as a slurry

May inactivate ipecac syrup if used concomitantly; decreases effectiveness of coadministered medications; do not mix with sherbet, milk, or ice cream (decreases adsorptive properties)

Documented hypersensitivity; poisoning or mineral acid or alkali overdose

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

Not effective in ethanol, methanol, or iron salt poisoning; monitor airway reflexes, neurologic parameters, and bowel sounds

Vasopressors

Sympathomimetics produce direct or indirect stimulation of adrenergic receptors and have various actions depending on the specific receptors involved. Stimulation of alpha1-receptors produces smooth muscle contraction. In the cardiovascular system, this effect leads to vasoconstriction and increased blood pressure; in the eye, this effect leads to mydriasis. Other affected organs include the urinary sphincter and uterus. Stimulation of beta1-receptors has an inotropic effect and also increases the heart rate. Stimulation of beta2-receptors leads to smooth muscle relaxation and produces vasodilatation.

Hypotension is initially treated with isotonic fluids. Vasoactive agents are used if hypotension remains refractory despite the administration of intravenous fluids. Norepinephrine is preferred to dopamine because dopamine is an indirect sympathomimetic and can cause an uncontrollable and erratic release of norepinephrine.


Norepinephrine (Levophed)

Used to treat protracted hypotension after adequate fluid-volume replacement. Stimulates beta1- and alpha-adrenergic receptors, which in turn increase cardiac muscle contractility, heart rate, and vasoconstriction. As a result, systemic blood pressure and coronary blood-flow increase.

Adult

0.5-30 mcg/min IV infusion; titrate to effect

Pediatric

0.05-1 mcg/kg/min IV infusion; titrate to effect

In MAOI poisoning, effects can be potentiated; start at low doses; effects increase with concurrent tricyclic antidepressants, MAOIs, antihistamines, guanethidine, methyldopa, or ergot alkaloids; atropine may block reflex tachycardia caused by norepinephrine and enhances pressor response

Documented hypersensitivity; peripheral or mesenteric vascular thrombosis because ischemia may be increased and area of infarct extended

Pregnancy

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

Precautions

If possible, correct blood-volume depletion before administration; administer into large vein because extravasation can cause severe tissue necrosis; caution in occlusive vascular disease

Antihypertensives

Do not use these drugs routinely. Often, the hypertension is transient and clinically insignificant. Avoid administering pure beta-blockers because they can produce an unopposed alpha effect.


Sodium nitroprusside (Nitropress)

Allows control of hypertensive emergency with rapid onset and short duration. Used as continuous infusion in closely monitored setting (ie, arterial access in pediatric ICU). Produces vasodilation and increases inotropic activity of the heart. At higher doses. May exacerbate myocardial ischemia by increasing heart rate.

Adult

0.1-8 mcg/kg/min IV infusion; titrate to effect

Pediatric

Administer as in adults

Effects additive when administered with other hypotensive agents

Documented hypersensitivity; idiopathic hypertrophic subaortic stenosis and atrial fibrillation or flutter

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

Use only after euvolemia established; caution in increased intracranial pressure, hepatic failure, severe renal impairment, or hypothyroidism; caution in cerebrovascular disease or coronary artery disease; in renal or hepatic insufficiency, levels may increase and can cause cyanide toxicity; can lower blood pressure and thus should be used only if mean arterial pressure >70 mm Hg


Labetalol (Normodyne, Trandate)

Blocks beta1-, alpha-, and beta2-adrenergic receptor sites, decreasing blood pressure.

Adult

20-30 mg IV over 2 min, followed by 40-80 mg q10min; alternately, start continuous infusion at 2 mg/min until blood pressure controlled; not to exceed 300 mg/dose

Pediatric

0.2-0.5 mg/kg/dose IV; not to exceed 20 mg/dose or continuous infusion of 0.25-1.5 mg/kg/h

Decreases effect of diuretics and increases toxicity of methotrexate, lithium, and salicylates; cimetidine may increase blood levels; glutethimide may decrease effects by inducing microsomal enzymes

Documented hypersensitivity; cardiogenic shock, pulmonary edema, bradycardia, atrioventricular block, uncompensated congestive heart failure, reactive airway disease, and severe bradycardia

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

Caution in impaired hepatic function; discontinue if signs of liver dysfunction present


Phentolamine (Regitine)

Alpha1- and alpha2-adrenergic blocker that blocks circulating epinephrine and norepinephrine action, reducing hypertension that results from catecholamine effects on the alpha-receptors.

Adult

1-5 mg IV bolus, repeat q10-15min prn

Pediatric

0.02-0.1 mg/kg IV bolus, may repeat q10-15min prn; not to exceed 5 mg/dose

Concurrent epinephrine or ephedrine may decrease effects; ethanol increases toxicity

Documented hypersensitivity; coronary or cerebral arteriosclerosis and renal impairment

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

Caution in tachycardia, peptic ulcer, and gastritis; cerebrovascular occlusions and myocardial infarctions can occur

Anticonvulsants

These agents are used to prevent seizures and terminate clinical and electrical seizure activity.


Lorazepam (Ativan)

Benzodiazepines can be used to treat agitation, seizures, or muscle rigidity.

Adult

2 mg IV, slowly over 2 min

Pediatric

0.1 mg/kg IV; not to exceed 2 mg/dose; may be repeated

Probenecid and valproic acid increase concentration (may need to reduce dose); theophylline can reverse sedative effects

Pregnancy

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

Precautions

May need to adjust dose in hepatic and renal insufficiency

More on Toxicity, Monoamine Oxidase Inhibitor

Overview: Toxicity, Monoamine Oxidase Inhibitor
Differential Diagnoses & Workup: Toxicity, Monoamine Oxidase Inhibitor
Treatment & Medication: Toxicity, Monoamine Oxidase Inhibitor
Follow-up: Toxicity, Monoamine Oxidase Inhibitor
References

References

  1. Dawson JK, Earnshaw SM, Graham CS. Dangerous monoamine oxidase inhibitor interactions are still occurring in the 1990s. J Accid Emerg Med. Mar 1995;12(1):49-51. [Medline].

  2. Jarrott B, Vajda FJ. The current status of monoamine oxidase and its inhibitors. Med J Aust. Jun 15 1987;146(12):634-8. [Medline].

  3. Larsen JK. MAO inhibitors: pharmacodynamic aspects and clinical implications. Acta Psychiatr Scand Suppl. 1988;345:74-80. [Medline].

  4. Stewart JW, Thase ME. Treating DSM-IV depression with atypical features. J Clin Psychiatry. Apr 2007;68(4):e10. [Medline].

  5. Bosse GM, Matyunas NJ. Delayed toxidromes. J Emerg Med. Jul-Aug 1999;17(4):679-90. [Medline].

  6. Dilsaver SC. Monoamine oxidase inhibitor withdrawal phenomena: symptoms and pathophysiology. Acta Psychiatr Scand. Jul 1988;78(1):1-7. [Medline].

  7. Feinberg SS. Combining stimulants with monoamine oxidase inhibitors: a review of uses and one possible additional indication. J Clin Psychiatry. Nov 2004;65(11):1520-4. [Medline].

  8. Frazer A, Conway P. Pharmacologic mechanisms of action of antidepressants. Psychiatr Clin North Am. Sep 1984;7(3):575-86. [Medline].

  9. Gillman PK. Monoamine oxidase inhibitors, opioid analgesics and serotonin toxicity. Br J Anaesth. Oct 2005;95(4):434-41. [Medline].

  10. Hyman Rapaport M. Translating the evidence on atypical depression into clinical practice. J Clin Psychiatry. 2007;68 Suppl 3:31-6. [Medline].

  11. Krishnan KR. Revisiting monoamine oxidase inhibitors. J Clin Psychiatry. 2007;68 Suppl 8:35-41. [Medline].

  12. Linden CH, Rumack BH, Strehlke C. Monoamine oxidase inhibitor overdose. Ann Emerg Med. Dec 1984;13(12):1137-44. [Medline].

  13. Lucena MI, Carvajal A, Andrade RJ, Velasco A. Antidepressant-induced hepatotoxicity. Expert Opin Drug Saf. May 2003;2(3):249-62. [Medline].

  14. Sarko J. Antidepressants, old and new. A review of their adverse effects and toxicity in overdose. Emerg Med Clin North Am. Nov 2000;18(4):637-54. [Medline].

  15. Siberry GK, Iannone R, eds. The Harriet Lane Handbook. In: A Manual for Pediatric House Officers. 15th ed. Mosby-Year Book: 2000.

  16. Siderowf A, Kurlan R. Monoamine oxidase and catechol-O-methyltransferase inhibitors. Med Clin North Am. Mar 1999;83(2):445-67. [Medline].

  17. Tollefson GD. Monoamine oxidase inhibitors: a review. J Clin Psychiatry. Aug 1983;44(8):280-8. [Medline].

  18. Wax P, Hoffman J, Keyes CD. Neuroleptics, lithium, and monoamine oxidase inhibitors. In: Rosen P, Barkin R, eds. Emergency Medicine. 3rd ed. 1992:2624-2628.

Further Reading

Keywords

monoamine oxidase inhibitor, antidepressant overdose, antidepressant poisoning, antidepressant overdoses, antidepressant poisonings, antidepressant-induced hepatotoxicity, childhood ingestions, MAO antidepressant, MAO antidepressant overdose, MAO antidepressant toxicity, MAO antidepressant poisoning, MAOI, MAOIs, MAOI overdose, MAOI toxicity, MAOI poisoning, monoamine oxidase A, MAO-A, monoamine oxidase B, MAO-B, phenelzine, tranylcypromine, isocarboxazid, Parkinson disease, methicillin-resistant Staphylococcus aureus, hypertension, tachycardia, hyperpexia, mydriasis, diaphoresis, rhabdomyolysis, renal failure, pulmonary edema, myocardial infarction, disseminated intravascular coagulopathy, serotonin syndrome

Contributor Information and Disclosures

Author

Soumya Ganapathy, MD, Consulting Staff, Department of Emergency Medicine, Union Memorial Hospital
Soumya Ganapathy, MD is a member of the following medical societies: American College of Emergency Physicians
Disclosure: Nothing to disclose.

Coauthor(s)

Frank A Maffei, MD, FAAP, Associate Professor of Pediatrics, Temple University School of Medicine; Director of Medical Student Affairs, Geisinger Health System; Pediatric Critical Care Attending Physician, Janet Weis Children's Hospital at Geisinger Medical Center
Frank A Maffei, MD, FAAP is a member of the following medical societies: American Academy of Pediatrics
Disclosure: Nothing to disclose.

Medical Editor

Michael E Mullins, MD, Assistant Professor, Department of Emergency Medicine, Washington University School of Medicine
Michael E Mullins, MD is a member of the following medical societies: American Academy of Clinical Toxicology and American College of Emergency Physicians
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine.com, Inc
Disclosure: Pfizer Inc Stock Investment from broker recommendation; Avanir Pharma Stock Investment from broker recommendation

Managing Editor

Jeffrey R Tucker, MD, Assistant Professor, Department of Pediatrics, Division of Emergency Medicine, University of Connecticut and Connecticut Children's Medical Center
Jeffrey R Tucker, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Pediatrics, and Massachusetts Medical Society
Disclosure: Nothing to disclose.

CME Editor

Paul D Petry, DO, FACOP, FAAP, Clinical Assistant Professor of Pediatrics, University of North Dakota, School of Medicine and Health Sciences; Consulting Staff, Altru Health System
Paul D Petry, DO, FACOP, FAAP is a member of the following medical societies: American Academy of Osteopathy, American Academy of Pediatrics, American College of Osteopathic Pediatricians, and American Osteopathic Association
Disclosure: Nothing to disclose.

Chief Editor

Timothy E Corden, MD, Associate Professor of Pediatrics, Co-Director, Policy Core, Injury Research Center, Medical College of Wisconsin; Associate Director, PICU, Children's Hospital of Wisconsin
Timothy E Corden, MD is a member of the following medical societies: American Academy of Pediatrics, Phi Beta Kappa, Society of Critical Care Medicine, and Wisconsin Medical Society
Disclosure: Nothing to disclose.

 
 
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