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Tricyclic Antidepressant Toxicity in Pediatrics Treatment & Management

  • Author: Derrick Lung, MD, MPH; Chief Editor: Timothy E Corden, MD  more...
Updated: Apr 22, 2016

Medical Care

During initial evaluation and stabilization, clinicians should bear in mind that symptoms of cyclic antidepressant (CA) toxicity generally appear within 2 hours of ingestion. Severe signs of toxicity, such as seizures and dysrhythmias, usually occur within the first 6 hours after ingestion.

As with any overdose, good supportive care is the mainstay of treatment in patients with cyclic antidepressant poisoning, and the first priority is to assess and treat any abnormalities in airway, breathing, and circulation (the ABCs). Early intubation for patients with significant signs of toxicity, including seizures and central nervous system (CNS) depression, is prudent. Patients who are obtunded and those with impending respiratory failure should clearly be intubated for airway protection and ventilatory support. Intravenous fluids should be started for patients who are hypotensive.

Cardiac monitoring should be instituted as soon as possible because of the risk of dysrhythmias. An electrocardiogram (ECG) should be performed early to look for a large terminal R wave in aVR, and for prolongation of the QRS and QT intervals, which confirm significant cyclic antidepressant exposure and consequent risk for seizures and dysrhythmias. If seizures do occur, they should be initially treated with benzodiazepines.

The patient should be examined for signs and symptoms of cyclic antidepressant toxicity, and ECG should be performed early to look for a terminal R wave in lead aVR, which is a sign of cyclic antidepressant drug effect that is not necessarily indicative of toxicity, and for prolongation of the QRS and QT intervals, which is more ominous and is possibly indicative of toxin-induced sodium channel blockade.

Symptoms of cyclic antidepressant toxicity generally present within 2 hours of ingestion. Seizures and arrhythmias are most likely to occur in the first 6 hours after ingestion. All patients with suspected cyclic antidepressant ingestion should undergo cardiac monitoring for a minimum of 6-8 hours. Monitoring should continue in symptomatic patients until the ECG findings have been normal for 24 hours.

Asymptomatic patients should be screened for suicidal intent and admitted to a psychiatric facility as appropriate after an observation period of at least 6 hours.



Decontamination measures include activated charcoal administration and possibly gastric lavage.[48]

Activated charcoal

If the patient's airway protective reflexes are intact, 1 g/kg of activated charcoal should be administered as soon as possible. Multidose charcoal may enhance elimination and should be considered. Charcoal should be withheld in patients who are obtunded or seizing because the risk of aspiration may outweigh the benefits of charcoal.[47]

Gastric lavage

Consider gastric lavage if the patient has a known or suspected significant ingestion that occurred within 1 hour of presentation.[11] However, a 2013 position paper by the American Academy of Clinical Toxicology and the European Association of Poisons Centres and Clinical Toxicologists notes that only weak evidence supports gastric lavage as a beneficial treatment, even in special situations.[12]

In addition, the potential benefit of gastric lavage needs to be weighed against its potential adverse events, such as vomiting, aspiration, and esophageal perforation. Also, the position paper advises that in the rare instances in which lavage is indicated, it should be performed only by personnel with proper training and expertise[12] —and as the use of gastric lavage has precipitously decreased over the last two decades, there are likely very few health care personnel with experience and comfort performing the procedure.


Management of Seizures

Seizures secondary to cyclic antidepressant toxicity are generally self-limiting but should be treated because the acidosis produced by vigorous muscle contraction and impaired ventilation during seizure activity may increase the concentration of free drug and increase toxicity.

Benzodiazepines are the agents of choice. Phenobarbital may be used as a long-acting anticonvulsant. Phenytoin and other electrolyte-channel modulating antiepileptics have traditionally been considered third-line for drug-induced seizures.


Management of Cardiovascular Toxicity

Hypotension should be initially treated with intravenous fluid boluses. Vasopressors should be started for refractory hypotension. Agents with alpha-adrenergic effects should be chosen.

Dopamine is not usually effective in these patients because its mechanism of action partially depends on the release of endogenous norepinephrine. Cyclic antidepressants block reuptake of norepinephrine, and stores may be depleted in overdose. Animal studies have suggested that epinephrine may cause fewer dysrhythmias than norepinephrine in this setting.

Sodium bicarbonate, given in boluses of 1-2 mEq/kg, is the first-line treatment for severe cardiotoxicity (eg dysrhythmia, conduction disturbance), in order to overcome cardiac sodium channel blockade. Sodium bicarbonate should also be given when the QRS duration is >120 msec, since a prolonged QRS is a portent of severe cardiotoxicity. An adequate dose will result in rapid shortening of the QRS duration. There is no absolute maximum dose threshold.

The ECG should be monitored for the desired effect of QRS narrowing during and immediately after bolus therapy, and then subsequent QRS widening for ongoing or recrudescent cardiotoxicity. The serum pH should be closely monitored and should not be allowed to exceed 7.55. Serum potassium should also be closely monitored for the development of hypokalemia.

Serum alkalinization with sodium bicarbonate is adjunctive therapy in cyclic antidepressant overdose. Alkalinization of the serum to a pH level of 7.45-7.55 increases protein binding and has been shown to decrease the QRS interval, stabilize dysrhythmias, and increase blood pressure in patients with cyclic antidepressant poisoning. Caution is advised, as some patients may not be able to tolerate the fluid load.

Hypertonic saline may be carefully considered as an alternative to sodium bicarbonate. Animal studies and some human case reports of treatment with hypertonic saline (without serum alkalinization) have shown similar effects on myocardial conduction parameters.[13] Therapy with hypertonic saline should be strongly considered in patients who are already alkalemic and in those who cannot tolerate the large volume load associated with intravenous bicarbonate administration.

Adjunctive treatment of cardiac dysrhythmias

Cardiac dysrhythmias should be treated according to the hemodynamic stability of the patient. Correction of hypoxia, hypotension, and acidosis should be attempted in conjunction with other pharmacologic interventions. Sodium bicarbonate therapy should be initiated in such patients (see above).

Lidocaine is the only recommended antiarrhythmic.[14] As a class Ib antiarrhythmic, it exhibits fast on-off sodium channel binding, in contrast to class Ia and Ic antiarrhythmics. Cardiac sodium channel recovery time for class Ib antiarrhythmics is rapid (< 1 second), compared to class Ia (1-10 seconds) and class Ic (>10 seconds) antiarrhythmics. Competitive binding at cardiac sodium channels by lidocaine against cyclic antidepressants (believed to exhibit class Ia effects) is thought to mitigate cardiac toxicity and dysrhythmias.

Magnesium has also been suggested as an adjunct for refractory ventricular dysrhythmias.[37, 15]

Other antiarrhythmic medications are less ideal. Like cyclic antidepressants, class Ia and Ic drugs block sodium channels and prolong depolarization and, therefore, may exacerbate the effects of cyclic antidepressants on the myocardium. Beta-blockers and calcium-channel blockers (class II and IV) are likely to further depress myocardial contractility and cause worsening hypotension. Class III drugs prolong the QT interval and may increase the risk of a malignant ventricular dysrhythmia.

All patients should be monitored for dysrhythmias for at least 12 hours. Patients with signs of severe toxicity (eg altered mental status, hypotension, prolonged QRS duration, seizures, etc) should be admitted to an intensive care unit setting.


Enhanced Elimination

Dialysis has no known role for dialysis except for patients with renal failure. Cyclic antidepressants are lipophilic and exhibit high protein-binding, thus are generally poor candidates for extracoporal removal. However, successful use of charcoal hemoperfusion for life-threatening amitriptyline poisoning has been reported.[16]


Lipid Emulsion Therapy

There is increasing enthusiasm for use of lipid emulsion therapy (LET) as a potential nonspecific antidote for poisonings due to lipophilic toxicants. Originally established as an antidote for local anesthetic toxicity, LET has been reportedly used with variable success in some published cases of CA toxicity.[17] In particular, there are two published pediatric cases (an intentional, self-harm ingestion of amitriptyline by a 13-year-old, and a large exploratory ingestion of dothiepin by a 20-month-old) in which ventricular tachycardia was converted to sinus tachycardia within minutes of instituting LET.[18, 19]

Current dosing recommendations have been provided by the American College of Medical Toxicologists.[20] A 20% lipid emulsion is administered as a 1.5 ml/kg bolus over 2-3 minutes. This is followed by a continuous infusion at 0.25 ml/kg/min, which should be discontinued when the patient’s condition has stabilized.

Published experience indicates that if LET is going to be effective, then rapid and noticeable clinical improvement (eg, return of spontaneous circulation, termination of malignant dysrhythmia) should follow the initial bolus. If no effect is noted, an immediate second bolus may be considered. If there is still no observable response, further doses should not be considered unless the patient is in extremis.

LET does have several major drawbacks. For one, its mechanism of action is unclear. The most popular explanation is the “lipid sink” theory, which proposes that by introducing a new intravascular lipid “compartment,” lipophilic drugs will be attracted to the intravascular space and pulled away from target sites (eg, brain, heart).

Early reports that demonstrate rather marked increases in blood levels of drugs after receiving LET supported this theory.[21] However, animals models show that LET is more accurately a “conduit for redistribution.” Animal models demonstrate that toxicants are redistributed among body sites.[22]

Thus, the logical, unanswered question is, Can LET cause harmful, rather than therapeutic, drug redistribution? The potential effects of redistribution of a toxicant into a more problematic end-organ site ought to be considered. Also, providers must weigh the potential effects of redistribution of therapeutic medications that critical patients are actively receiving. Fortunately, vasopressors have little lipophilicity and so should be minimally affected by LET. However, other common resuscitative medications (eg, amiodarone) are very lipophilic, and the possibility of reversing their therapeutic effects must be considered.[23]

Secondly, a number of case series and registries have suggested a range of possible adverse reactions.[24, 25] Clearly, LET causes a hypertriglyceridemia that can sometimes render laboratory blood/serum measurements uninterpretable for up to 12 hours. Some patients sustain a pancreatitis (by elevated lipase and amylase measurements) of unclear clinical significance. Other reported possible adverse effects (eg, acute respiratory distress syndrome [ARDS]) are not clearly distinct from patients’ critical illness.

Finally, optimal (for therapy and safety) dosing is unknown. The original dosing strategy for local anesthetic toxicity continues to be used universally. It is unknown whether (and if so, how) age, body weight, toxicant, or other factors should modify dosing.



Recommended consultations are as follows:

  • The regional poison control center or a clinical toxicologist should be consulted in all cases of suspected poisoning
  • A pediatric psychiatrist should be consulted if intentional ingestion is suspected
  • Child protective services should be notified if inadequate supervision or Münchhausen syndrome by proxy is suspected
Contributor Information and Disclosures

Derrick Lung, MD, MPH Assistant Clinical Professor, Department of Emergency Medicine, San Francisco General Hospital; Assistant Medical Director, California Poison Control System, San Francisco Division

Derrick Lung, MD, MPH is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Emergency Physicians, American College of Medical Toxicology, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Jeffrey R Tucker, MD Assistant Professor, Department of Pediatrics, Division of Emergency Medicine, University of Connecticut School of Medicine, Connecticut Children's Medical Center

Disclosure: Received salary from Merck for employment.

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, Wisconsin Medical Society

Disclosure: Nothing to disclose.

Additional Contributors

Michael E Mullins, MD Assistant Professor, Division of Emergency Medicine, Washington University in St Louis School of Medicine; Attending Physician, Emergency Department, Barnes-Jewish Hospital

Michael E Mullins, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Emergency Physicians

Disclosure: Received stock ownership from Johnson & Johnson for none; Received stock ownership from Savient Pharmaceuticals for none.


Heidi Connolly, MD Associate Professor of Pediatrics and Psychiatry, University of Rochester School of Medicine and Dentistry; Director, Pediatric Sleep Medicine Services, Strong Sleep Disorders Center

Heidi Connolly, MD is a member of the following medical societies: American Academy of Pediatrics, American Thoracic Society, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Christopher I Doty, MD, FACEP, FAAEM Assistant Professor of Emergency Medicine, Residency Program Director, Department of Emergency Medicine, Kings County Hospital Center, State University of New York Downstate Medical Center

Christopher I Doty, MD, FACEP, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, Council of Emergency Medicine Residency Directors, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Frank A Maffei, MD, FAAP Associate Professor of Pediatrics, Temple University School of Medicine; Medical Director, Pediatric Intensive Care Unit, Janet Weis Children's Hospital at Geisinger Health System

Frank A Maffei, MD, FAAP is a member of the following medical societies: American Academy of Pediatrics

Disclosure: Nothing to disclose.

Samara Soghoian, MD, MA Clinical Assistant Professor of Emergency Medicine, New York University School of Medicine, Bellevue Hospital Center

Samara Soghoian, MD, MA is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Medical Toxicology, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Rashida Y White-McCrimmon, MD Resident Physician, Department of Emergency Medicine, Kings County Hospital Center, State University of New York Downstate Medical Center

Rashida Y White-McCrimmon, MD is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, and Emergency Medicine Residents Association

Disclosure: Nothing to disclose.

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Toxicity, antidepressant. ECG shows the terminal R wave in aVR and the widened QRS complex associated with tricyclic antidepressant (TCA) toxicity.
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