Pediatric Monoamine Oxidase Inhibitor Toxicity Medication
- Author: Soumya Ganapathy, MD; Chief Editor: Timothy E Corden, MD more...
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.
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.
For maximum effect, administer within 30 min after ingesting poison. Sorbitol may be added to activated charcoal to improve its palatability. Sorbitol should never be used with multiple doses of charcoal, and never in children younger than 1 y.
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.
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.
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.
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). Higher doses produce vasodilation and increases inotropic activity of the heart. May exacerbate myocardial ischemia by increasing heart rate.
Blocks beta1-, alpha-, and beta2-adrenergic receptor sites, decreasing blood pressure.
Alpha1- and alpha2-adrenergic blocker that blocks circulating epinephrine and norepinephrine action, reducing hypertension that results from catecholamine effects on the alpha-receptors.
Woytowish MR, Maynor LM. Clinical relevance of linezolid-associated serotonin toxicity. Ann Pharmacother. 2013 Mar. 47(3):388-97. [Medline].
Dawson JK, Earnshaw SM, Graham CS. Dangerous monoamine oxidase inhibitor interactions are still occurring in the 1990s. J Accid Emerg Med. 1995 Mar. 12(1):49-51. [Medline].
Hazell P. Depression in children and adolescents. Clin Evid (Online). 2009 Jan 7. 2009:[Medline].
Shulman KI, Herrmann N, Walker SE. Current place of monoamine oxidase inhibitors in the treatment of depression. CNS Drugs. 2013 Oct. 27(10):789-97. [Medline].
Jarrott B, Vajda FJ. The current status of monoamine oxidase and its inhibitors. Med J Aust. 1987 Jun 15. 146(12):634-8. [Medline].
Larsen JK. MAO inhibitors: pharmacodynamic aspects and clinical implications. Acta Psychiatr Scand Suppl. 1988. 345:74-80. [Medline].
Mowry JB, Spyker DA, Cantilena LR Jr, Bailey JE, Ford M. 2012 Annual Report of the American Association of Poison Control Centers' National Poison Data System (NPDS): 30th Annual Report. Clin Toxicol (Phila). 2013 Dec. 51(10):949-1229. [Medline]. [Full Text].
Stewart JW, Thase ME. Treating DSM-IV depression with atypical features. J Clin Psychiatry. 2007 Apr. 68(4):e10. [Medline].
Bosse GM, Matyunas NJ. Delayed toxidromes. J Emerg Med. 1999 Jul-Aug. 17(4):679-90. [Medline].
Dilsaver SC. Monoamine oxidase inhibitor withdrawal phenomena: symptoms and pathophysiology. Acta Psychiatr Scand. 1988 Jul. 78(1):1-7. [Medline].
Engorn B, Flerlage J, eds. The Harriet Lane Handbook. A Manual for Pediatric House Officers. 20th ed. Philadelphia: Saunders; 2015.
Feinberg SS. Combining stimulants with monoamine oxidase inhibitors: a review of uses and one possible additional indication. J Clin Psychiatry. 2004 Nov. 65(11):1520-4. [Medline].
Frazer A, Conway P. Pharmacologic mechanisms of action of antidepressants. Psychiatr Clin North Am. 1984 Sep. 7(3):575-86. [Medline].
Gillman PK. Monoamine oxidase inhibitors, opioid analgesics and serotonin toxicity. Br J Anaesth. 2005 Oct. 95(4):434-41. [Medline].
Hyman Rapaport M. Translating the evidence on atypical depression into clinical practice. J Clin Psychiatry. 2007. 68 Suppl 3:31-6. [Medline].
Krishnan KR. Revisiting monoamine oxidase inhibitors. J Clin Psychiatry. 2007. 68 Suppl 8:35-41. [Medline].
Linden CH, Rumack BH, Strehlke C. Monoamine oxidase inhibitor overdose. Ann Emerg Med. 1984 Dec. 13(12):1137-44. [Medline].
Lucena MI, Carvajal A, Andrade RJ, Velasco A. Antidepressant-induced hepatotoxicity. Expert Opin Drug Saf. 2003 May. 2(3):249-62. [Medline].
Rapaport MH. Dietary restrictions and drug interactions with monoamine oxidase inhibitors: the state of the art. J Clin Psychiatry. 2007. 68 Suppl 8:42-6. [Medline].
Sarko J. Antidepressants, old and new. A review of their adverse effects and toxicity in overdose. Emerg Med Clin North Am. 2000 Nov. 18(4):637-54. [Medline].
Siderowf A, Kurlan R. Monoamine oxidase and catechol-O-methyltransferase inhibitors. Med Clin North Am. 1999 Mar. 83(2):445-67. [Medline].