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

Toxicity, Monoamine Oxidase Inhibitor

Soumya Ganapathy, MD, Consulting Staff, Department of Emergency Medicine, Union Memorial Hospital
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

Updated: Jan 23, 2008

Introduction

Background

The increased use of antidepressants with safer toxicologic profiles has made monoamine oxidase inhibitor (MAOI) poisoning uncommon among children. MAOIs are still used in patients with Parkinson disease and refractory and atypical depression. Antibiotics, such as the anti– methicillin-resistant Staphylococcus aureus drug linezolid, are MAOIs. Although MAOI ingestion is rare, MAOI overdoses can potentially cause significant morbidity and mortality.¹

Pathophysiology

Monoamine oxidase is a mitochondrial enzyme that functions to deaminate primary and secondary aromatic amines. The deamination of aromatic amines (eg, norepinephrine) leads to the compounds deactivation. MAOIs prevent the breakdown of aromatic amines in the neuronal cytosol, resulting in the storage of larger concentrations of active aromatic amines in neuronal vesicles and, therefore, an increased release of these neurotransmitters into the synaptic cleft with each action potential.

Two types of monoamine oxidases are recognized: monoamine oxidase A (MAO-A) and monoamine oxidase B (MAO-B). MAO-A preferentially deaminates norepinephrine and serotonin, whereas MAO-B mainly deaminates phenylethylamine and dopamine. MAO-A inhibitors increase the levels of norepinephrine and serotonin and are used in the treatment of clinical depression. MAO-B inhibitors increase the dopaminergic concentrations in the brain and have been successfully used in the treatment of Parkinson disease.²

Many drugs and foods can potentiate the adrenergic and serotonergic effects of MAOIs. This characteristic is particularly important because many adverse affects involving MAOIs are due to drug-drug and drug-food interactions.³  

Frequency

United States

MAOIs overdoses are relatively uncommon. According to the American Association of Poison Control Centers' Toxic Exposures Surveillance System (AAPCC-TESS), 285 MAOI exposures were reported in 2003. Of those exposures, 35 were in patients aged 19 years or younger, and 32 were in patients younger than 6 years.

Mortality/Morbidity

• In 2005, the AAPCC-TESS reported 107 exposures that resulted in moderate or major morbidity
• In 2005, the AAPCC-TESS reported 2 exposures that resulted in death.

Age

Most unintentional ingestions occur in toddlers, and most pediatric intentional ingestions occur in adolescents.

Clinical

History

Monoamine oxidase inhibitors (MAOIs) are not typically prescribed to children; they are prescribed to adults in a household. Therefore, as in all suspected pediatric ingestions, inquiring about all drugs in the home and evaluating each as a possible cause of the child’s presentation is essential.

MAOIs may not produce symptoms for as long as 24 hours after an acute overdose. Symptoms can be attributed to various physiologic derangements, as follows:

• Symptoms related to a hyperadrenergic state
  • Dizziness
  • Headache
  • Agitation
  • Blurry vision
  • Shortness of breath
  • Chest pain
• Symptoms related to serotonin excess
  • Altered mentation (confusion, anxiety, agitation)
  • Fever
  • Muscle cramps or rigidity
  • Hallucinations
  • Anxiety
  • Agitation
  • Diaphoresis
  • Diarrhea
• Symptoms related to cardiovascular compromise (usually delayed)
  • Pallor
  • Syncope or presyncope
• Weakness

Physical

Signs of MAOI overdoses depend on the quantity ingested, the time elapsed since the ingestion, and the presence of co-ingestions.

• Cardiac system
  • Hypertension due to a hyperadrenergic state may be observed early. It may be transient and should not be aggressively treated unless the patient is symptomatic.
  • Orthostatic hypotension and frank hypotension can occur later.
  • Tachycardia is usually present. Arrhythmias are relatively uncommon unless a co-ingestion is involved.
• Pulmonary system - Pulmonary edema (late finding)
• Autonomic findings
  • Hyperpyrexia
  • Mydriasis
  • Diaphoresis
  • Flushing
• CNS
  • Agitation
  • Hyperreflexia
  • Muscular rigidity
  • Tremors/muscle spasms
  • Seizures
  • Coma

Causes

Signs and symptoms depend on the time of presentation and whether a co-ingestion occurred. The mechanisms for MAOI-related toxicity can be divided into those related to MAOI overdose alone and those related to MAOI interactions with other substances.

• The adverse effects related to an MAOI overdose alone can be divided into 4 phases.
  • Phase 1 is a period of latency that lasts approximately 6-12 hours. The delayed appearance of signs and symptoms is thought to be related to the gradual accumulation of norepinephrine and serotonin.
  • Phase 2 is characterized by a catecholamine surge that causes sympathetic and CNS excitation.
  • In phase 3, hypotension and CNS depression occur.
  • Phase 4 involves secondary complications such as rhabdomyolysis, renal failure, pulmonary edema, myocardial infarction, and disseminated intravascular coagulopathy.
• Reactions caused by the interactions of MAOIs with other drugs and foods can also cause toxicity.
  • Drug and food interactions related to MAOIs can occur at therapeutic or toxic doses.
  • The effects of indirect-acting adrenergic drugs are markedly potentiated when combined with MAOIs. These agents include methylphenidate (Ritalin), phenylephrine, ephedrine, cocaine, and amphetamines.
  • Direct-acting sympathomimetics such as epinephrine, norepinephrine, isoproterenol, carbidopa, and L-methyldopa directly act on the postsynaptic receptors rather than the releasing presynaptic vesicles, and they do not cause such a marked adrenergic response.
  • Tricyclic antidepressants (TCAs) block the inactivation of norepinephrine and serotonin;⁴ TCAs taken in combination with MAOIs can lead to excessive catecholamine and serotonin activity, a potentially life-threatening situation. Because of the prolonged action of MAOIs, a 2-4 week washout period must be observed before treatment with TCAs is started.
  • In conjunction with selective serotonin reuptake inhibitors (SSRIs), MAOIs can produce a hyperserotoninergic state known as serotonin syndrome. An altered mental status, autonomic instability, and neuromuscular dysfunction characterize the syndrome.
  • Similar toxicity can occur when MAOIs are combined with drugs that have serotonin reuptake inhibitory properties, such as tramadol, linezolid, meperidine, or dextromethorphan.
  • Foods containing tyramine, such as aged cheese, red wine, overripe foods, aged meat, fava beans, beer, avocado, and yeast extracts, can cause a similar hyperadrenergic state, leading to hypertension or stroke, in individuals taking MAOIs.

Differential Diagnoses

Other Problems to Be Considered

Ethanol withdrawal
Malignant hyperthermia
Sedative/hypnotic withdrawal
Serotonin syndrome
Heat stroke/heat exhaustion

Workup

Laboratory Studies

• Rapid bedside glucose determination
• ABG determination - Indicated if a compromise in oxygenation or ventilation is suspected
• Lactate level - May be useful in phases 2 and 3 of an acute overdose to help determine end-organ perfusion
• Determination of serum electrolyte, calcium, and magnesium levels - Calculation of the anion gap possibly helpful in screening for co-ingestions
• Evaluation of serum acetaminophen and salicylate levels - Indicated in intentional overdoses
• Screening for serum levels of alcohol (ethanol, methanol, isopropyl alcohol) - Indicated if alcohol ingestion is clinically suspected
• Urine pregnancy test - Indicated in all women of childbearing age
• Urinalysis and urine pH determination - May be useful in the setting of rhabdomyolysis
• Urine drug screening - Comprehensive drug screening and screening for commonly abused drugs possibly helpful in assessing co-ingestions
• Evaluation of levels of specific monoamine oxidase inhibitor (MAOI) drugs - Not readily available and, therefore, not clinically useful

Imaging Studies

• Chest radiography is indicated if aspiration is a concern.
• Perform postintubation chest radiography to evaluate the position of the endotracheal tube in relation to the carina if respiratory support is needed.

Other Tests

• Sinus tachycardia is the most common ECG abnormality.
• Nonspecific T-wave changes are also reported.

Procedures

• Endotracheal intubation may be required.
  • Maintaining a stable airway is the most important step in the management of any toxic ingestion.
  • Intubation is required in any patient with a decreasing level of consciousness or signs of impending respiratory failure.
  • Secure the airway before administering activated charcoal or performing gastric lavage in patients with compromised mental status.
• Venous access should be obtained.
  • Two large-bore peripheral intravenous lines should be placed in symptomatic patients.
  • Central access may be necessary for the infusion of vasoactive agents.
• Gastric lavage is reserved for patients with life-threatening overdoses (2-3 mg/kg) who present within 1 hour of the ingestion.
  • A large-bore orogastric tube should be used.
  • Isotonic sodium chloride solution is preferred to water in young children because of the risk of an electrolyte imbalance and water intoxication.
  • Before proceeding with any decontamination, secure the patient's airway.
• Foley catheterization of the bladder is indicated to assess urine output, especially in the setting of hemodynamic compromise or rhabdomyolysis.
• Arterial line placement is indicated for continuous blood pressure monitoring and frequent blood sampling in patients with a severe ingestion and cardiovascular instability.

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.

Dosing

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

Interactions

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

Contraindications

Documented hypersensitivity; poisoning or mineral acid or alkali overdose

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

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.

Dosing

Adult

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

Pediatric

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

Interactions

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

Contraindications

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

Precautions

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.

Dosing

Adult

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

Pediatric

Administer as in adults

Interactions

Effects additive when administered with other hypotensive agents

Contraindications

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

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

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.

Dosing

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

Interactions

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

Contraindications

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

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

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.

Dosing

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

Interactions

Concurrent epinephrine or ephedrine may decrease effects; ethanol increases toxicity

Contraindications

Documented hypersensitivity; coronary or cerebral arteriosclerosis and renal impairment

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

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.

Dosing

Adult

2 mg IV, slowly over 2 min

Pediatric

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

Interactions

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

Contraindications

Documented hypersensitivity

Precautions

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

Follow-up

Further Inpatient Care

• Patients with monoamine oxidase inhibitor (MAOI) overdoses should be admitted to the hospital primarily because of the prolonged latent stage.
• All patients with suspected MAOI ingestion require 24 hours of ICU care or frequent monitoring in an inpatient facility.

Inpatient & Outpatient Medications

• Avoid indirect sympathomimetics and foods that contain tyramine.
• Avoid drugs such as meperidine, dextromethorphan, and SSRIs (eg, fluoxetine, sertraline) because they can lead to a hyperserotonergic state.
• Avoid ketamine.

Transfer

• Any child with evidence of MAOI toxicity should be stabilized and transferred to a tertiary pediatric center.

Deterrence/Prevention

• Keep medications and other ingestible substances locked or safely stored where children cannot reach them.

Complications

• Pulmonary edema
• Coma
• Myocardial ischemia
• Intracerebral hemorrhage
• Rhabdomyolysis
• Acute renal failure
• Disseminated intravascular coagulation
• Hemolysis
• Subarachnoid hemorrhage
• Serotonin syndrome

Prognosis

• Mortality and morbidity are dependent on the time of presentation, the occurrence of co-ingestions, and the status of the patient upon his or her arrival in the emergency department.
• Most patients recover without sequelae when given careful supportive care.

Patient Education

• Families must be made aware of the dangers of prescription drugs, over-the-counter medications, and other potential toxins in the home.
• Patients who are taking MAOIs should be educated about the potential for drug and food interactions.
• For excellent patient education resources, visit eMedicine's Poisoning - First Aid and Emergency Center, Substance Abuse Center, and Mental Health and Behavior Center. Also, see eMedicine's patient education articles Poisoning, Drug Overdose, Activated Charcoal, and Poison Proofing Your Home.

Miscellaneous

Medicolegal Pitfalls

• Failure to properly manage the airway during decontamination is a pitfall.
• Failure to monitor patients is a pitfall, even if they are initially asymptomatic. Signs of MAOI toxicity may be delayed as long as 24 hours after the ingestion.⁵
• Failure to avoid the use of indirect sympathomimetics and serotonergic drugs is a pitfall.

References

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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. 15^th 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. 3^rd ed. 1992:2624-2628.

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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