sodium-bicarbonate and Drug-Overdose

This review aimed to explore and summarize information from available cases of pediatric acute hydroxychloroquine overdose with confirmed hydroxychloroquine exposure to give the clinicians a helpful perspective for its better recognition and management.. Electronic searches were conducted in PubMed/MEDLINE, Web of Science, Scopus, EBSCO and Serbian Citation Index. The abstracts from 2 toxicology conferences were manually checked for additional relevant publications, as well as reference lists of the retrieved publications. Descriptive statistics, narrative summation, and tabulation of the extracted data were made.. Nine publications and a total of 9 patients were included in the review. Reported age of the patients varied from 2.5 to 16 years (median, 16 years). There were more female patients (77.8%). Estimated total ingested hydroxychloroquine dose was reported in 7 cases (77.8%), and it ranged from 4.0 to 20.0 g (median: 12.0 g). Four patients (44.4%) ingested hydroxychloroquine with a coingestant. Altered mental status (100.0%), cardiotoxicity (88.9%), hypotension (77.8%), and hypokalemia (55.6%) were the most commonly reported clinical manifestations. The majority of the patients were hospitalized (88.9%). More than half of the patients (55.6%) were reported to be treated in the intensive care unit. Most frequently reported therapeutic measures were the following: administration of intravenous fluids/infusions (77.8%), vasopressors (77.8%), bicarbonate therapy-sodium bicarbonate (66.7%), potassium replacement (55.6%), and intubation/ventilation (55.6%). Three patients (33.3%) died.. Management of acute hydroxychloroquine overdose in children should be symptomatic and tailored to observed clinical manifestations. There is a need for additional investigations to better understand the impact and effectiveness of various treatment options.

Topics: Adolescent; Child; Child, Preschool; Drug Overdose; Female; Humans; Hydroxychloroquine; Hypotension; Sodium Bicarbonate; Vasoconstrictor Agents

Sodium bicarbonate is a well-known antidote for tricyclic antidepressant (TCA) poisoning. It has been used for over half a century to treat toxin-induced sodium channel blockade as evidenced by QRS widening on the electrocardiogram (ECG). The purpose of this review is to describe the literature regarding electrophysiological mechanisms and clinical use of this antidote after poisoning by tricyclic antidepressants and other agents. This article will also address the literature supporting an increased serum sodium concentration, alkalemia, or the combination of both as the responsible mechanism(s) for sodium bicarbonate's antidotal properties. While sodium bicarbonate has been used as a treatment for cardiac sodium channel blockade for multiple other agents including citalopram, cocaine, flecainide, diphenhydramine, propoxyphene, and lamotrigine, it has uncertain efficacy with bupropion, propranolol, and taxine-containing plants.

Topics: Action Potentials; Anti-Arrhythmia Agents; Antidepressive Agents, Tricyclic; Antidotes; Antimalarials; Arrhythmias, Cardiac; Drug Overdose; Heart Conduction System; Heart Rate; Humans; Risk Factors; Sodium Bicarbonate; Sodium Channel Blockers

Calcium channel blockers (CCBs) are some of the most commonly used medications in clinical practice to treat hypertension, angina, cardiac arrhythmias, and some cases of heart failure. Recent data show that CCBs are the most common of the cardiovascular medications noted in intentional or unintentional overdoses.(1) Novel treatment approaches in the form of glucagon, high-dose insulin therapy, and intravenous lipid emulsion therapies have been tried and have been successful. However, the evidence for these are limited to case reports and case series. We take this opportunity to review the various treatment options in the management of CCB overdoses with a special focus on high-dose insulin therapy as the emerging choice for initial therapy in severe overdoses.

Topics: Airway Management; Calcium Channel Blockers; Calcium Compounds; Catecholamines; Drug Overdose; Fat Emulsions, Intravenous; Glucagon; Humans; Hyperinsulinism; Sodium Bicarbonate

Diphenhydramine toxicity commonly manifests with antimuscarinic features, including dry mucous membranes, tachycardia, urinary retention, mydriasis, tachycardia, and encephalopathy. Severe toxicity can include seizures and intraventricular conduction delay. We present here a case of a 23-year-old male presenting with recurrent seizures, hypotension and wide complex tachycardia who had worsening toxicity despite treatment with sodium bicarbonate. The patient was ultimately treated with intravenous lipid emulsion therapy that was temporally associated with improvement in the QRS duration. We also review the current literature that supports lipid use in refractory diphenhydramine toxicity.

Topics: Antidotes; Diphenhydramine; Drug Overdose; Drug Therapy, Combination; Fat Emulsions, Intravenous; Histamine H1 Antagonists; Humans; Hypertonic Solutions; Male; Sodium Bicarbonate; Tachycardia, Ventricular; Young Adult

State-of-the-art therapy for beta-adrenergic receptor blocker and calcium channel antagonist toxicity is reviewed in the light of new insights into drug-induced shock. A brief discussion of pathophysiology, including cardiac, hemodynamic, and metabolic effects of cardiac drug toxicity, provides a foundation for understanding the basis of therapy. The major focus of this review is a critical evaluation of antidotal use of calcium, glucagon, catecholamines, insulin-euglycemia, and other novel therapies based on investigational studies and cumulative clinical experience.

Topics: Adrenergic beta-Antagonists; Antidotes; Calcium Channel Blockers; Calcium Gluconate; Cardiovascular Diseases; Catecholamines; Drug Overdose; Humans; Renal Dialysis; Resuscitation; Sodium Bicarbonate

Topics: Antidepressive Agents, Tricyclic; Antidotes; Clinical Medicine; Consensus; Drug Overdose; Evidence-Based Medicine; Guidelines as Topic; Humans; Poison Control Centers; Poisoning; Sodium Bicarbonate; Toxicology; Treatment Outcome

Overdoses of tricyclic antidepressants are among the commonest causes of drug poisoning seen in accident and emergency departments. This review discusses the pharmacokinetics, clinical presentation and treatment of tricyclic overdose.

Topics: Anti-Arrhythmia Agents; Antidepressive Agents, Tricyclic; Cardiovascular Diseases; Drug Overdose; Humans; Inactivation, Metabolic; Sodium Bicarbonate; Sorption Detoxification

Sodium bicarbonate infusion is widely recommended in textbooks for patients who present with self-poisoning from tricyclic antidepressives. Cardiac conduction disorders could also be treated or prevented by means of such an infusion. The scientific basis for these recommendations was investigated by using Medline to search for publications about clinical studies that supported the use of sodium carbonate; 111 articles were scrutinized. Observational studies and case reports mention a rapid improvement in hypotension and cardiac arrhythmias following the administration of sodium bicarbonate. Results from animal experiments are contentious; it is not clear whether alkalinisation or the administration of extra sodium causes the effect. Randomized studies in patients have not been carried out. As the toxicity of sodium bicarbonate is low, and its potential benefit appears to be high, we recommend its use, despite the lack of scientific evidence. No recommendations concerning dosing, concentration and the length of the therapy can be provided on the basis of the literature.

Topics: Adult; Antidepressive Agents, Tricyclic; Arrhythmias, Cardiac; Drug Overdose; Female; Humans; Hypotension; Infusions, Intravenous; Retrospective Studies; Sodium Bicarbonate

Tricyclic antidepressant poisoning causes predictable electrocardiographic abnormalities and can be lethal. Cardiac arrhythmias, hypotension, seizures, and coma are common. Sodium bicarbonate is still considered the treatment of choice for severe toxicity, although a variety of supportive measures may be taken. Hypertonic saline appears to be a promising alternative. A QRS interval longer than 100 ms appears to be a better predictor of serious complications than is an elevated serum tricyclic antidepressant level. Cardiovascular toxicity is classically manifested as ventricular dysrhythmias, hypotension, heart block, bradyarrhythmias, or asystole. Activated charcoal binds tricyclic antidepressants. Give 30 to 50 g orally or by nasogastric tube with or without a cathartic (sorbitol 0.5 g/kg or 30 g of magnesium sulfate). Sodium bicarbonate is indicated if the QRS duration is more than 100 ms or the terminal right-axis deviation is more than 120 degrees. The suggested dosage is 1 to 2 mEq/kg, repeated as needed. Tricyclic antidepressants are used not only for depression but also for chronic pain syndromes, obsessive-compulsive disorder, panic and phobic disorders, eating disorders, migraine prophylaxis, and peripheral neuropathies.

Topics: Antidepressive Agents, Tricyclic; Charcoal; Drug Overdose; Electrocardiography; Emergency Treatment; Female; Half-Life; Heart Conduction System; Humans; Middle Aged; Risk; Sodium Bicarbonate; Suicide, Attempted; United States

Topics: Adult; Antidepressive Agents, Tricyclic; Arrhythmias, Cardiac; Clinical Trials as Topic; Drug Overdose; Emergency Medicine; Evidence-Based Medicine; Female; Humans; Injections, Intravenous; MEDLINE; Sodium Bicarbonate; Treatment Outcome; United Kingdom; United States

Topics: Animals; Antidepressive Agents, Tricyclic; Arrhythmias, Cardiac; Cardiovascular Diseases; Child, Preschool; Drug Overdose; Female; Humans; Hypertonic Solutions; Hypotension; Infant, Newborn; Sodium Bicarbonate

Topics: Adult; Antidotes; Buffers; Charcoal; Doxylamine; Drug Overdose; Drug Therapy, Combination; Female; Fluid Therapy; Gastric Lavage; Histamine H1 Antagonists; Humans; Infusions, Intravenous; Injections, Intravenous; Length of Stay; Male; Rhabdomyolysis; Saline Solution; Sodium Bicarbonate; Treatment Outcome

Bupropion cardiotoxicity widens QRS complexes by inhibiting cardiac gap junctions. Sodium bicarbonate is the standard treatment for QRS widening from sodium channel blockade, but its effect on QRS widening in bupropion cardiotoxicity is not well-studied.. This is a retrospective cohort study of bupropion overdoses from 10 hospitals between January 2010 and June 2022. Patients with documented administration of sodium bicarbonate and QRS duration > 100 milliseconds on pre-bicarbonate electrocardiogram were included. Patients with no electrocardiogram within four hours of treatment or with baseline pre-overdose wide QRS and < 10 milliseconds widening from baseline were excluded. The primary outcome was a change in QRS duration between the pre-bicarbonate electrocardiogram and the first electrocardiogram after initial bicarbonate administration. Secondary outcomes included prevalence of post-bicarbonate QRS < 100 milliseconds, change in electrocardiogram intervals after total bicarbonate administration, and change in metabolic parameters and hemodynamics. Wilcoxon signed-rank testing was performed on the primary outcome. Linear regression modeling was performed to test for an association between change in QRS and bicarbonate dosing.. Thirteen patients were included for final analysis. The median age was 32 years, and 54% were male. Six patients developed seizures; one developed ventricular tachycardia, and four received vasopressors. The median QRS and QTc pre-bicarbonate were 116 and 495 milliseconds, respectively. The median change in QRS duration was -2.0 milliseconds, which was not statistically significant (. Sodium bicarbonate did not significantly decrease QRS duration in this small retrospective cohort of bupropion overdoses.

Topics: Adult; Bicarbonates; Bupropion; Cardiotoxicity; Drug Overdose; Electrocardiography; Female; Humans; Male; Retrospective Studies; Sodium Bicarbonate

Management of patients with salicylate toxicity frequently requires urine alkalinization to enhance excretion of salicylate. One strategy for determining when to stop urine alkalinization is to wait for two consecutive serum salicylate concentrations to be less than 300 mg/L (2.17 mmol/L) and declining. When alkalinization of the urine ceases, a rebound in serum salicylate concentration can occur from tissue redistribution or delayed gastrointestinal absorption. Whether this can lead to rebound toxicity is not well understood.. This was a single-center, retrospective review of cases with a primary ingestion of acetylsalicylic acid reported to the local poison center over a five-year period. Cases were excluded if the product was not listed as the primary ingestion or if there was no serum salicylate concentration documented after discontinuation of intravenous sodium bicarbonate infusion. The primary outcome was the incidence of serum salicylate rebound to a concentration greater than 300 mg/L (2.17 mmol/L) after discontinuation of intravenous sodium bicarbonate infusion.. A total of 377 cases were included. Of these, eight (2.1%) had a serum salicylate concentration increase (rebound) after stopping the sodium bicarbonate infusion. All these cases were acute ingestions. Five of the eight cases had rebound serum salicylate concentrations that were greater than 300 mg/L (2.17 mmol/L). Of these five patients, only one reported recurrent symptoms (tinnitus). Prior to stopping urinary alkalinization, the last or the last two serum salicylate concentrations were less than 300 mg/L (2.17 mmol/L) in three and two cases, respectively.. In patients with salicylate toxicity, the incidence of rebound in serum salicylate concentration after cessation of urine alkalinization, is low. Even if serum salicylate rebounds to supratherapeutic concentrations, symptoms are often absent or mild. Routine repeat serum salicylate concentrations after urine alkalinization is stopped may be unnecessary unless symptoms recrudesce.

Topics: Aspirin; Drug Overdose; Humans; Incidence; Salicylates; Sodium Bicarbonate

Flecainide is a 1C antidysrhythmic that is primarily used for ventricular tachycardia or premature ventricular contractions when other treatment is ineffective. It has a very narrow therapeutic window which may cause death in a double dose and requires inpatient initiation for cardiac monitoring. Despite established pharmacokinetic data from flecainide in therapeutic dosing, there is negligible data on flecainide toxicokinetics after an intentional overdose. Due to the inherent differences in pharmacokinetic and toxicokinetic principles, rarely can the peak effect or elimination half-life accurately be applied to the poisoned patient after an overdose. In overdose, flecainide can cause a variety of fatal dysrhythmias which may require sodium bicarbonate for stabilization but also may reduce the renal elimination of flecainide, meaning the life-saving treatment may prolong the time of toxicity.. We present a case of an acute ingestion of flecainide with a known time of ingestion and known amount of ingestion who experienced subsequent life-threatening effects which required endotracheal intubation, sodium bicarbonate, aggressive electrolyte repletion, and multiple days in an intensive care unit.. Serial serum and urine samples revealed a prolonged toxic serum concentration of flecainide.. These results demonstrate the change in elimination kinetics of flecainide in the setting of urinary alkalization which is evident through prolonged morphologic changes present on serial electrocardiograms.

Topics: Anti-Arrhythmia Agents; Arrhythmias, Cardiac; Drug Overdose; Electrocardiography; Flecainide; Humans; Sodium Bicarbonate

Sodium bicarbonate therapy (SBT) is currently indicated for the management of a variety of acute drug poisonings. However, SBT effects on serum potassium concentrations may lead to delayed QTc prolongation (DQTP), and subsequent risk of adverse cardiovascular events (ACVE), including death. Emergency department (ED)-based studies evaluating associations between SBT and ACVE are limited; thus, we aimed to investigate the association between antidotal SBT, ECG changes, and ACVE.. This was a secondary data analysis of a consecutive cohort of ED patients with acute drug overdose over 3 years. Demographic and clinical data as well as SBT bolus dosage and infusion duration were collected, and outcomes were compared with an unmatched consecutive cohort of patients with potential indications for SBT but who did not receive SBT. The primary outcome was the occurrence of ACVE, and secondary outcomes were delayed QTc (Bazett) prolongation (DQTP), and death. Propensity score and multivariable adjusted analyses were conducted to evaluate associations between adverse outcomes and SBT administration. Planned subgroup analysis was performed for salicylates, wide QRS (> 100 ms), and acidosis (pH < 7.2).. Out of 2365 patients screened, 369 patients had potential indications for SBT, of whom 31 (8.4%) actually received SBT. In adjusted analyses, SBT was found to be a significant predictor of ACVE (aOR 9.35, CI 3.6-24.1), DQTP (aOR 126.7, CI 9.8-1646.2), and death (aOR 11.9, CI 2.4-58.9). Using a propensity score model, SBT administration was associated with ACVE (OR 5.07, CI 1.8-14.0). Associations between SBT and ACVE were maintained in subgroup analyses of specific indications for sodium channel blockade (OR 21.03, CI 7.16-61.77) and metabolic acidosis (OR: 6.42, 95% CI: 1.20, 34.19).. In ED patients with acute drug overdose and potential indications for SBT, administration of SBT as part of routine clinical care was an independent, dose-dependent, predictor of ACVE, DQTP, and death. This study was not designed to determine whether the SBT or acute overdose itself was causative of ACVE; however, these data suggest that poisoned patients receiving antidotal SBT require close cardiovascular monitoring.

Topics: Action Potentials; Adolescent; Adult; Aged; Aged, 80 and over; Antidotes; Dose-Response Relationship, Drug; Drug Overdose; Emergency Service, Hospital; Female; Heart Conduction System; Heart Rate; Humans; Long QT Syndrome; Male; Middle Aged; Risk Assessment; Risk Factors; Sodium Bicarbonate; Time Factors; Treatment Outcome; Young Adult

Diphenhydramine, a first generation H. A 22-year-old woman presented with altered mental status secondary to intentional ingestion of 240 combination caplets of naproxen sodium 220 mg and diphenhydramine hydrochloride 25 mg. While in the emergency department, she manifested a wide-complex tachycardia in the setting of hypotension that required repeated administration of sodium bicarbonate to overcome the sodium channel blockade caused by diphenhydramine. Aggressive potassium repletion was performed simultaneously. Her clinical course was complicated by status-epilepticus that required intubation. Orogastric lavage was performed, which returned blue pill slurry consistent with the ingested caplets. The patient was extubated on hospital day 2 and transferred to psychiatry thereafter. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: In light of recent social media trends, such as the "Benadryl challenge" and its widespread availability, emergency providers should be familiar with diphenhydramine toxicity, especially the life-threatening neurologic consequences and risk of cardiovascular collapse. NSAIDs, such as naproxen, and other nonprescription analgesics are becoming more and more important in light of the current opioid crisis. There should be an emphasis on understanding these medications and their potential implications when taken in overdose.

Topics: Diphenhydramine; Drug Overdose; Female; Humans; Naproxen; Sodium Bicarbonate; Tachycardia; Young Adult

Here, we review the case of a 26 1/7 weeks' gestation premature female infant born to a mother who intentionally ingested a large quantity of Tylenol, aspirin, quetiapine, and prenatal vitamins. The neonate subsequently had markedly elevated levels of both Tylenol and aspirin when checked on the first day of life. While overall clinically stable, the neonate did demonstrate coagulopathy as evidenced by abnormal coagulation studies. Both poison control and a pediatric gastroenterologist/hepatologist were consulted. She successfully tolerated a course of N-acetylcysteine; her subsequent Tylenol level was markedly decreased and the neonate exhibited no further effects of toxicity. The salicylate level decreased on its own accord. To our knowledge, this is the first report of a neonate at 26 weeks' gestation that has been successfully managed for supratherapeutic concentrations of acetaminophen and acetylsalicylic acid secondary to maternal ingestion. While rare, this case may serve as a reference for the effectiveness of N-acetylcysteine in premature infants in such instances.

Topics: Acetaminophen; Antidepressive Agents; Antidotes; Aspirin; Cystine; Drug Overdose; Female; Humans; Infant, Newborn; Infant, Premature; Infant, Premature, Diseases; Maternal Exposure; Poisoning; Pregnancy; Quetiapine Fumarate; Sodium Bicarbonate; Suicide, Attempted

Topics: Amitriptyline; Antidepressive Agents, Tricyclic; Cardiotoxicity; Drug Overdose; Electrocardiography; Heart Rate; Humans; Infusions, Intravenous; Male; Middle Aged; Predictive Value of Tests; Sodium Bicarbonate; Tachycardia, Ventricular

Lacosamide is a third-generation antiepileptic drug. Its likely mechanism of action is via neuronal sodium channel blockade, via a unique manner compared with other antiepileptic drugs that block sodium channels. A paucity of information exists regarding lacosamide overdosage. Lacosamide overdosage is thought to cause QRS prolongation and seizures, due to its effect of sodium channel blockade. The potential efficacy of sodium bicarbonate to reverse the effects of lacosamide has not been well studied. Furthermore, prior reports of lacosamide toxicity have occurred in the setting of concomitant polypharmacy. Thus, the isolated toxic effects of the drug have not been well elucidated.. We report a case of a suspected, single-ingestion overdose on lacosamide. The patient developed signs of cardiotoxicity and seizure. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: After lacosamide overdosage, the emergency physician must be capable of acute management of subsequent lacosamide toxicity. Understanding the mechanisms of action causing toxicity due to this drug can help the clinician to anticipate the interventions that may be needed or useful to treat this potentially toxic ingestion.

Topics: Arrhythmias, Cardiac; Cardiotoxicity; Drug Overdose; Electrocardiography; Epilepsy; Female; Humans; Lacosamide; Middle Aged; Seizures; Sodium Bicarbonate

A woman in her fifties was admitted to hospital with decreased awareness and circulatory failure. She had been treated with left atrial cryoablation a few weeks before admission and had been cardioverted a few days after the procedure because of relapse of atrial fibrillation.. On admission, the patient had systolic blood pressure of 80 mm Hg and an ECG with broad QRS-complexes at 380 ms. We suspected intoxication and she was intubated to administer activated charcoal after gastric lavage. She was cardiovascularly unstable and in need of intravenous infusion of noradrenaline and adrenaline. Further investigations at her home suggested that she had poisoned herself with 4-5 g flecainide, 0.3 g oxazepam and 0.5 g meclizine. After administration of 500 mmol sodium bicarbonate and 5 mmol calcium chloride, the QRS complexes narrowed temporarily. On day 2, due to sustained bradycardia and hypotension despite receiving adrenergic medications, a temporary pacemaker was implanted, leading to improved heart rate and blood pressure. She experienced several complications including hypertensive pulmonary oedema, atrial fibrillation, extensively prolonged QT interval because of polypharmacy and Takotsubo cardiomyopathy. She was discharged from the hospital in good health on day 17. At a follow-up visit at the outpatient clinic 12 weeks later, cardiac function had normalised. The QT interval was now normal; however, there were persistent T-wave inversions in leads I, aVL and V4-6.. Flecainide blocks sodium channels in cardiomyocytes. Intoxication with flecainide is rare, with mortality rates of about 10 %. Sodium bicarbonate in larger doses has been reported to stabilise patients with flecainide intoxication due to modification of the binding of flecainide to sodium receptors in cardiomyocytes, and due to alkalisation which makes flecainide detach from sodium receptors. Our patient had a temporary effect with narrowing of QRS complexes after receiving sodium bicarbonate. She also showed a beneficial effect from implantation of a temporary pacemaker, although earlier case reports have described problems with high thresholds and capture failure.

Topics: Anti-Arrhythmia Agents; Charcoal; Drug Overdose; Electrocardiography; Female; Flecainide; Humans; Middle Aged; Pacemaker, Artificial; Shock; Sleepiness; Sodium Bicarbonate

Topics: Buffers; Dermatologic Agents; Drug Overdose; Fluid Therapy; Humans; Leucovorin; Male; Methotrexate; Middle Aged; Psoriasis; Skin Ulcer; Sodium Bicarbonate; Treatment Outcome

We describe a 27-year-old female with repeated episodes of pulseless electrical activity due to intoxication with a substance that was unidentified at presentation. Severe QRS widening was observed and empiric treatment with sodium bicarbonate and intravenous lipid emulsion was administered. In this case, intraosseous administration of lipid emulsion failed to improve haemodynamic parameters, suggesting that this dose remained in the bone marrow compartment. We recommend that physicians become aware of this possibility and to avoid intraosseous administration of lipid emulsion.

Topics: Adult; Antimalarials; Buffers; Calcium Gluconate; Cardiovascular Agents; Chloroquine; Critical Care; Drug Overdose; Electrocardiography; Fat Emulsions, Intravenous; Female; Heart Arrest; Humans; Infusions, Intraosseous; Sodium Bicarbonate; Suicide, Attempted; Treatment Outcome

Flecainide intoxication is a severe intoxication that can lead to cardiogenic shock. We report on a 68-year-old female patient, who presented with a flecainide intoxication in the setting of renal failure. She was managed with invasive supportive therapy at the ICU and infusion of sodium bicarbonate and intravenous lipid emulsion (ILE, intralipid 20%), after which she made a complete recovery.

Topics: Aged; Anti-Arrhythmia Agents; Bradycardia; Buffers; Cardiotonic Agents; Drug Overdose; Electrocardiography; Fat Emulsions, Intravenous; Female; Flecainide; Humans; Kidney Failure, Chronic; Renal Elimination; Shock, Cardiogenic; Sick Sinus Syndrome; Sodium Bicarbonate; Treatment Outcome

We report a case of a 74-year-old lady admitted to the emergency department with a very broad QRS complex caused by flecainide intoxication due to acute renal failure. Appropriate recognition of the ECG changes and symptoms provoked by flecainide intoxication permitted quick directed treatment with intravenous administration of high dose sodium bicarbonate, which resolved the QRS elongation.

Topics: Accidental Falls; Aged; Anti-Arrhythmia Agents; Drug Overdose; Electrocardiography; Fatigue; Female; Flecainide; Humans; Sodium Bicarbonate; Tachycardia, Ventricular; Treatment Outcome

Topics: Adult; Antidepressive Agents, Tricyclic; Antidotes; Bradycardia; Diagnosis, Differential; Drug Overdose; Electric Countershock; Electrocardiography; Female; Heart Arrest; Humans; Sodium Bicarbonate; Substance-Related Disorders; Suicide, Attempted

Topics: Acidosis; Adolescent; Antidepressive Agents, Tricyclic; Drug Overdose; Female; Humans; Hypokalemia; Hypotension; Pneumonia; Respiration, Artificial; Respiratory Distress Syndrome; Sodium Acetate; Sodium Bicarbonate; Suicide, Attempted; Vasoconstrictor Agents

We report a rare fatal case of acute metformin overdose in a 19-year-old woman.

Topics: Acidosis; Blood Gas Analysis; Cardiotonic Agents; Drug Overdose; Fatal Outcome; Female; Heart Arrest; Humans; Hypoglycemia; Hypoglycemic Agents; Hypotension; Long QT Syndrome; Metformin; Sodium Bicarbonate; Young Adult

Loperamide, a non-prescription anti-diarrheal agent, is a peripheral mu-opioid receptor agonist that is excluded from the blood-brain barrier by p-glycoprotein at therapeutic doses. Overdoses of loperamide penetrate the central nervous system (CNS), leading to abuse. We report cardiac conduction abnormalities and dysrhythmias after ingestion of a recreational supra-therapeutic dose of loperamide confirmed with an elevated blood loperamide concentration.. A 48-year-old woman with a history of alcohol and benzodiazepine abuse presented to the emergency department (ED) with somnolence, weakness and slurred speech. She was taking 20 to 40 tablets of 2 mg loperamide 1-2 times/day for weeks along with clonazepam and whiskey. Vital signs were: blood pressure (BP), 124/90 mmHg; heart rate (HR), 88/min; respiratory rate(RR), 20/min; T, 36.9 °C; O2 saturation 100% on room air (RA). Glucose was 6.4 mmol/L. Electrocardiogram (ECG) had a ventricular rate of 58/min, QRS 164 ms, QT 582 ms with no discernable p-waves. Lactate was 3.5 mmol/L and potassium was 6.2 mEq/L. Labs were notable for an anion gap of 20 mEq/L, ethanol of 3.9 mmol/L, creatinine of 2.3 mg/dL and loperamide concentration of 210 ng/mL (average therapeutic plasma concentration 1.2 ng/mL). She became hypotensive, but responded to fluids. Following treatment for hyperkalemia with calcium, insulin, dextrose, and hypertonic sodium bicarbonate a repeat ECG had a ventricular rate of 66/min, QRS 156 ms, and QT 576 ms. Magnesium was given and pacer pads were placed. During the infusion of magnesium, her BP fell to 92/58 mmHg with a HR of 54/min, RR 14/min, O2 saturation of 97% on RA so the infusion was stopped. The ECG after the magnesium infusion had a ventricular rate of 51/min, QRS of 134 ms, and QT 614 ms. In the ICU she had multiple runs of non-sustained ventricular tachycardia that did not require therapy. Over the next 48 h she improved and was transferred to a floor bed. On day four of hospitalization the patient left against medical advice. At that time, her ECG showed sinus tachycardia with a heart rate 114/min, QRS 82 ms, QT 334 ms.. Loperamide produces both QRS and QT prolongation at supra-therapeutic dosing. A blood loperamide concentration of 210 ng/mL is among the highest concentrations reported. Supra-therapeutic dosing of loperamide is promoted on multiple drug-use websites and online forums as a treatment for opioid withdrawal, as well as for euphoric effects. With the current epidemic of prescription opioid abuse, toxicity related to loperamide, an opioid agonist that is readily available without a prescription is occurring more frequently. It is important for clinicians to be aware of the potentially life-threatening toxicity related to loperamide abuse in order to provide proper diagnosis, management and patient education.

Topics: Alcoholism; Arrhythmias, Cardiac; Benzodiazepines; Blood Pressure; Calcium; Central Nervous System; Clonazepam; Dose-Response Relationship, Drug; Drug Overdose; Electrocardiography; Emergency Service, Hospital; Female; Glucose; Heart Rate; Humans; Hyperkalemia; Insulin; Loperamide; Magnesium; Middle Aged; Respiratory Rate; Sodium Bicarbonate; Substance-Related Disorders

A 28-year-old woman was admitted in a comatose state following ingestion of 5 g of amitriptyline. On arrival, there was intermittent seizure activity and a broad complex tachycardia on the ECG. Immediate resuscitation included 8 mg lorazepam, 2 L crystalloid fluid, 100 mL 8.4% sodium bicarbonate, 2 g of magnesium sulphate and lipid emulsion infusion. Despite this, the broad complex tachycardia persisted with haemodynamic instability. The case was discussed with the National Poisons Information Service, which advised further 8.4% sodium bicarbonate to achieve serum alkalinisation. Following this, the QRS duration reduced and haemodynamic stability was achieved. Serum alkalinisation continued in the intensive treatment unit before the patient was successfully extubated on day 5 and discharged on day 7 with no neurological sequelae. To our knowledge, this case is the largest recorded overdose of amitriptyline to have survived to discharge. The importance of serum alkalinisation in the management of tricyclic antidepressant poisoning is highlighted.

Topics: Adult; Amitriptyline; Antacids; Antidepressive Agents, Tricyclic; Drug Overdose; Female; Humans; Sodium Bicarbonate; Tachycardia

This case report describes the possible benefit of intravenous lipid emulsion in two patients surviving a severe intoxication with hydroxychloroquine in a dose that was previously considered to be lethal. The first case involves a 25-year-old female who ingested 17.5 grams of hydroxychloroquine, approximately one hour before presentation. An ECG showed QRS widening and the lab results showed hypokalaemia. She became unconscious, and developed hypotension and eventually apnoea. After intubation, supportive care consisted of norepinephrine and supplementation of potassium. Moreover, sodium bicarbonate and intravenous lipid emulsion were started to prevent cardiac toxicity. After these interventions, haemodynamic stability was established within a few hours. Although cardiomyopathy was confirmed, the patient recovered after two weeks. The second case concerns a 25-year-old male who took 5 grams of hydroxychloroquine. At presentation, two hours after intake, he showed QTc prolongation and hypokalaemia. The patient was treated with the usual supportive care and, although presentation to hospital was later, with intravenous lipid emulsion. Also this patient recovered. In conclusion, these cases show the benefit of supplemental intravenous lipid emulsion to prevent cardiac toxicity after a severe intoxication with hydroxychloroquine.

Topics: Adult; Arrhythmias, Cardiac; Chromatography, Liquid; Drug Overdose; Electrocardiography; Fat Emulsions, Intravenous; Female; Humans; Hydroxychloroquine; Hypokalemia; Hypotension; Male; Norepinephrine; Potassium Chloride; Sodium Bicarbonate; Suicide, Attempted; Tandem Mass Spectrometry; Vasoconstrictor Agents

Flecainide is a Class Ic antiarrythmic agent associated with adverse events due to its pro-arrythmic effects. We report the case of a 33-year-old female presenting in cardiac arrest after a flecainide overdose treated with intravenous fat emulsion (IFE), sodium bicarbonate (NaHCO₃), and extracorporeal membrane oxygenation (ECMO). This case reviews the pathophysiology and management of flecainide toxicity including novel strategies of IFE and ECMO.

Topics: Adult; Anti-Arrhythmia Agents; Drug Overdose; Electrocardiography; Extracorporeal Membrane Oxygenation; Fat Emulsions, Intravenous; Female; Flecainide; Heart Arrest; Humans; Sodium Bicarbonate

Lacosamide treats partial seizures by enhancing slow inactivation of voltage-gated sodium channels. The described cardiac toxicity of lacosamide in the literature to date includes atrioventricular blockade (PR prolongation), atrial flutter, atrial fibrillation, sinus pauses, ventricular tachycardia and a single cardiac arrest. We report a second case of cardiac arrest following an intentional lacosamide overdose.. A 16 year-old female with a seizure disorder was found unresponsive in pulseless ventricular tachycardia after intentionally ingesting 4.5 g (76 mg/kg) lacosamide, 120 mg (2 mg/kg) cyclobenzaprine and an unknown amount of levetiracetam. Exact time of ingestion was unknown. Her initial electrocardiogram (ECG) demonstrated sinus tachycardia at 139 beats per minute, QRS duration 112 ms, and terminal R-wave in lead aVR > 3 mm. Despite treatment with 150 mEq of sodium bicarbonate, she had persistent EKG findings eight hours after presentation. Her serum lacosamide concentration nine hours after presentation was elevated at 22.8 μg/mL, while serum cyclobenzaprine concentration was 16 ng/mL (therapeutic: 10-30 ng/mL), and serum levetiracetam concentration was 22.7 μg/mL (therapeutic: 12-46 μg/mL). On hospital day three, ECG demonstrated resolution of the terminal R-wave with QRS of 78 ms. The patient recovered without physical or neurologic sequelae.. The patient's lacosamide, cyclobenzaprine and levetiracetam overdose was associated with QRS prolongation and terminal right axis deviation--suggesting sodium channel blockade as a likely etiology for her cardiac arrest. Cyclobenzaprine has potential for sodium channel blockade and ventricular dysrhythmias although cardiac toxicity due to cyclobenzaprine alone is rare. The combination of cyclobenzaprine with lacosamide may have resulted in cardiovascular collapse. In conclusion, overdose of lacosamide combined with therapeutic concentrations of sodium channel blocking xenobiotics may cause cardiac conduction delays and cardiac arrest.

Topics: Acetamides; Adolescent; Amitriptyline; Anticonvulsants; Drug Interactions; Drug Overdose; Electrocardiography; Epilepsy; Female; Heart Arrest; Humans; Lacosamide; Levetiracetam; Piracetam; Risk Factors; Sodium Bicarbonate; Sodium Channel Blockers; Sodium Channels; Suicide, Attempted; Tachycardia, Ventricular; Treatment Outcome

We present an 18-month boy with imipramine poisoning to illustrate the neuro-cardiac toxic effects of this potentially deadly poison in children. The toddler ingested an unknown amount of imipramine from a non-childproof bottle which clearly labelled that the drug must be kept out of reach from children. He developed neurologic and cardiac symptoms. Electrocardiography (ECG) showed tachycardia and widened QRS. He was immediately treated with bicarbonate infusion and made an uneventful recovery. This is the youngest and only reported case of symptomatic imipramine ingestion in our locality. Imipramine has been surpassed by newer antidepressants for the treatment of depression in the past decade. Literature is searched to review the mortality rate in young children. Intensive care neuro-cardiac support contributes to the favorable outcome. Despite clear labelling of the bottle, carelessness on the part of the adult and the use of non-childproof bottle are definite preventable factor to such potentially fatal ingestion.

Topics: Accidents, Home; Adrenergic Uptake Inhibitors; Antidepressive Agents, Tricyclic; Arrhythmias, Cardiac; Drug Overdose; Electrocardiography; Heart Conduction System; Heart Rate; Humans; Imipramine; Infant; Infusions, Intravenous; Male; Neurotoxicity Syndromes; Sodium Bicarbonate; Tachycardia; Time Factors; Treatment Outcome

Metformin-associated lactic acidosis or lacticemia has been widely reported as an adverse drug effect in diabetic patients with other significant comorbidities and in acute overdose in adults. Lacticemia has been reported twice in a previously healthy pediatric population, both of which were suicide attempts and required hemodialysis. We report a case of a 17-year-old, nondiabetic, healthy adolescent girl with metformin-associated lacticemia who intentionally overdosed on metformin, had no coingestants, and was treated only with crystalloids. Furthermore, she did not require intravenous bicarbonate administration or extracorporeal removal.

Topics: Acidosis, Lactic; Adolescent; Drug Overdose; Female; Humans; Hypoglycemic Agents; Metformin; Renal Dialysis; Sodium Bicarbonate; Suicide, Attempted

Topics: Alkalosis; Antacids; Diagnosis, Differential; Drug Overdose; Gastritis; Gastrointestinal Agents; Heartburn; Humans; Male; Medicine, Traditional; Middle Aged; Self Medication; Severity of Illness Index; Sodium Bicarbonate; Tachycardia, Ventricular; Treatment Outcome

Topics: Anti-Inflammatory Agents, Non-Steroidal; Antidepressive Agents, Tricyclic; Aspirin; Charcoal; Cholinergic Antagonists; Drug Overdose; Female; Half-Life; Humans; Middle Aged; Peristalsis; Sodium Bicarbonate; Time Factors

Flecainide is a class IC antidysrhythmic primarily indicated for ventricular dysrhythmias and supraventricular tachycardia (SVT). Class IC antidysrhythmic overdose has a reported mortality of 22%, and death results from dysrhythmias and cardiovascular collapse. We report a near-fatal flecainide overdose in an 18-day-old treated successfully with sodium bicarbonate.. An 18-day-old, 2 weeks premature, 4-kg boy developed persistently high heart rates (220-240 beats/min) and electrocardiographic changes consistent with SVT. There was minimal response to vagal maneuvers, adenosine, and esmolol, and a transthoracic echocardiogram showed no underlying structural abnormality. The patient was then started on flecainide 4 mg orally every 8 h (Q8h). After the fourth dose he developed lethargy, cold clammy skin, and a heart rate of 40 beats/min with no palpable pulse. The patient was given 0.1 mg of atropine intravenously, with an increase of the heart rate to 160 beats/min. The child's cardiac monitor revealed a wide-complex tachycardia with left bundle branch morphology, with associated pallor and poor capillary refill. Sodium bicarbonate was administered intravenously due to suspected flecainide toxicity. Approximately 5 min after intravenous administration of 10 mEq of 8.4% sodium bicarbonate twice, his rhythm converted to a narrow-complex tachycardia. A serum flecainide concentration was 1360 μg/L (therapeutic, 200-1000 μg/L) drawn 1 h before the cardiac arrest. It was later discovered that a twofold dosing error occurred: the patient received 8 mg Q8h instead of 4 mg Q8h for four doses.. Flecainide toxicity in children is rare, especially in neonates. It is important for clinicians to be able to identify and treat this uncommon poisoning.

Topics: Anti-Arrhythmia Agents; Arrhythmias, Cardiac; Drug Overdose; Flecainide; Humans; Infant, Newborn; Male; Medication Errors; Sodium Bicarbonate; Treatment Outcome

Amitriptyline, a tricyclic antidepressant, has a well-described toxicity profile, and acute ingestions are common in the pediatric toxicology world. However, little can be found in the literature regarding chronic overdose. We describe a case of a 6-year-old girl who was prescribed amitriptyline 30 mg nightly for sleep problems, but was mistakenly given 300 mg (15 mg/kg) nightly for over a month. She was noted to have mental status changes and difficulty reading several days after starting the medication. She presented to the local children's hospital in status epilepticus with significant cardiac conduction abnormalities on ECG. Her total amitriptyline/nortriptyline level was found to be 1676 ng/mL (normal therapeutic level 50-300 ng/mL). She was treated for several days with sodium bicarbonate. Within 24 h, her neurologic status improved and had returned to baseline within several days. Her ECG normalized, and she was discharged home, without apparent sequelae. A brief discussion of possible protective mechanisms (including pharmacogenomic) is presented.

Topics: Amitriptyline; Antidepressive Agents, Tricyclic; Child; Drug Overdose; Electrocardiography; Female; Humans; Nortriptyline; Sleep Wake Disorders; Sodium Bicarbonate; Status Epilepticus; Treatment Outcome

Diphenhydramine is an antihistamine commonly implicated in overdose. It has many pharmacologic effects, including sodium channel blockade. Overdoses in toddlers causing QRS prolongation are only rarely reported and never with effective use of sodium bicarbonate. We report a diphenhydramine overdose in a toddler with multiple markers of sodium channel blockade effectively treated with sodium bicarbonate.. A 13-month-old infant girl was brought in by the emergency medical service for a witnessed tonic-clonic seizure. Two hours previously, the child had been found with an open bottle of 25-mg diphenhydramine tablets, 24 of which were missing. Midazolam was administered with seizure resolution. Examination revealed 4-mm reactive pupils; nystagmus; warm, dry, flushed skin; and altered mental status. Initial electrocardiograms revealed sinus tachycardia at a rate of 180 beats per minute, a prolonged QRS of 130 milliseconds (from a baseline of 65 milliseconds), and a positive terminal R wave in aVR, which later resolved after sodium bicarbonate treatment. The patient was discharged home the following day with no sequelae.. Diphenhydramine toxicity is a common poisoning in children. Toxicity typically presents with signs and symptoms of the anticholinergic toxidrome. Diphenhydramine also has sodium channel-blocking properties, and this can be shown in the form of prolonged QRS and a terminal R wave in aVR. QRS prolongation and aVR abnormalities from diphenhydramine ingestion in a toddler have been reported, but effective use of sodium bicarbonate has not.. Electrocardiographic finding consistent with sodium channel blockade should be recognized as a complication of pediatric diphenhydramine overdose, and they seem responsive to hypertonic sodium bicarbonate.

Topics: Anticonvulsants; Cholinergic Antagonists; Diphenhydramine; Drug Overdose; Electrocardiography; Emergencies; Female; Heart Conduction System; Humans; Hypertonic Solutions; Infant; Midazolam; Seizures; Sodium Bicarbonate; Sodium Channel Blockers; Sodium Channels; Tachycardia, Sinus

Salicylates are common exposures. We report an unusual case of salicylate ingestion, as salsalate, with resolution of symptoms and return of salicylate levels to non-toxic values, with a subsequent, unexpected recrudescence to toxic levels requiring reinstitution of therapy. A 31-year-old man ingested unknown amounts of salsalate, hydroxyzine, and a benzodiazepine. He was intubated and treated with IV sodium bicarbonate and two doses of oral activated charcoal. Eight hours after presentation, his serum salicylate concentration peaked at 55 mg/dL, and then decreased to a nadir of 5.6 mg/dL 38 h after presentation, coinciding with return of GI motility. Several hours later salicylate concentrations began to rise, peaking 67 h after presentation at 61.7 mg/dL. He was treated with sodium bicarbonate and charcoal, which resulted in decreased serum salicylate to therapeutic levels. Salicylate ingestions are known to exhibit unusual toxicokinetics and absorption in overdose; however, this is the first case we are aware of that shows a return to toxic concentrations after apparent resolution of toxicity. Recrudescence of salicylate concentrations to a degree that would dictate reinstitution of therapy for overdose is unusual and may warrant prolonged monitoring of serum salicylate concentrations in salsalate ingestions.

Topics: Adult; Antacids; Anti-Inflammatory Agents, Non-Steroidal; Antidotes; Benzodiazepines; Charcoal; Depressive Disorder; Drug Overdose; Humans; Hydroxyzine; Hypnotics and Sedatives; Male; Recurrence; Salicylates; Sodium Bicarbonate; Stress Disorders, Post-Traumatic; Suicide, Attempted

Acute intoxication with acetylsalicylic acid is a severe event commonly seen in children resulting from wide availability of this drug without prescription. Cases of self-poisoning resulting from overdose continue to occur and, although far less common, they are often severe and life-threatening. We report a 14-year-old girl who presented to the emergency department with tachypnea and altered mental status as a result of acetylsalicylic acid overdose in a suicide attempt. We discuss her presentation and the pathophysiological considerations leading to the management decisions taken during her emergency department stay, highlighting the role of the clinician and therapeutic drug monitoring consultant. The use of rapid decontamination with multiple doses of charcoal, even when more than 4 hours have passed since ingestion, and the use of urinary alkalinization are stressed. Timely management can obviate the need for dialysis. Published cases of acetylsalicylic acid intoxication are reviewed.

Topics: Adolescent; Anti-Inflammatory Agents, Non-Steroidal; Antidotes; Aspirin; Charcoal; Confusion; Drug Overdose; Female; Humans; Hydrogen-Ion Concentration; Respiratory Rate; Sodium Bicarbonate; Suicide, Attempted; Urine

Topics: Acidosis, Lactic; Adrenergic alpha-Agonists; Anti-Inflammatory Agents; Antidiuretic Agents; Drug Overdose; Epinephrine; Glucose; Humans; Hydrocortisone; Hypoglycemic Agents; Insulin; Male; Metformin; Middle Aged; Norepinephrine; Sodium Bicarbonate; Suicide, Attempted; Treatment Outcome; Vasopressins

Metformin, widely used in the treatment of diabetes mellitus, is known to cause lactic acidosis in both therapeutic use and after an overdose. We report the case of a 40-year-old woman who claimed to have ingested between 75 and 100 grams of metformin and subsequently developed severe lactic acidosis. She eventually developed a peak serum lactate level of 40.0 mmol/L and a serum pH nadir of 6.59 and became obtunded, hypotensive, and hypothermic. After aggressive supportive therapy with mechanical ventilation, vasopressor agents, sodium bicarbonate, and hemodialysis, her metabolic derangements steadily improved and she made a complete recovery without any residual sequelae. Her admission serum metformin concentration was later determined to be 160 microg/mL (therapeutic range is 1-2 microg/mL). There are several case reports and case series describing lactic acidosis secondary to metformin ingestion, although the exact mechanism remains unclear. The overall management of metformin overdose is reviewed. This case represents the largest reported amount of ingested metformin, the lowest serum pH, and the highest serum lactate concentration in any intentional metformin overdose survivor in the literature. Despite potentially lethal metabolic derangements, such patients can survive with aggressive supportive care.

Topics: Acidosis, Lactic; Adult; Drug Overdose; Female; Humans; Hypoglycemic Agents; Hypotension; Metformin; Poisoning; Sodium Bicarbonate

To describe a case of life-threatening flecainide intoxication in a toddler, secondary to accidental reversal of syringes used for oral administration.. A 2-year-old male with a history of a persistent junctional reciprocating tachycardia had been receiving flecainide 4.8 mg/kg/day (1 mL 3 times daily) and nadolol 2 mg/kg/day (5 mL once daily) for 10 months. One morning, 3 hours after the drugs were administered, he became bradycardic (heart rate 50 beats/min) and then presented to the emergency department with vital signs absent. After initial cardiopulmonary resuscitation and epinephrine, he was bradycardic; this was followed by wide-complex tachycardia that converted rapidly to narrow-complex tachycardia after bolus administration of intravenous sodium bicarbonate for suspected flecainide intoxication. Following resuscitation, he remained hemodynamically stable and was discharged in normal sinus rhythm without neurologic sequelae. Drug concentrations obtained at the time of presentation showed a serum concentration of flecainide of 0.668 microg/mL. Drug formulations were also analyzed and found to contain the expected concentration of flecainide.. Literature regarding adverse drug events in the pediatric outpatient population is reviewed, as well as how these risks apply to flecainide, a medication with a low margin of safety. Pediatric experience with flecainide intoxication and sodium bicarbonate administration as an antidote is reviewed. Analysis of the serum drug concentrations demonstrated blood concentrations consistent with syringe reversal, which would have produced a 5-fold flecainide overdose. The Naranjo probability scale indicated a highly probable relationship between flecainide ingestion and the life-threatening event in this case.. This case of life-threatening flecainide intoxication in a young child, secondary to accidental reversal of medication syringes, underscores the importance of providing parents with accurate dispensing information and labeling medication bottles and syringes in an unambiguous manner.

Topics: Administration, Oral; Anti-Arrhythmia Agents; Bradycardia; Cardiopulmonary Resuscitation; Child, Preschool; Drug Overdose; Flecainide; Humans; Male; Medication Errors; Sodium Bicarbonate; Syringes; Tachycardia

Tricyclic antidepressant (TCA) morbitity is primarily due to cardiac arrhythmias and hypotension, which become more refractory to treatment as acidosis progresses (Ann Emerg Med. 1985;14:1-9; Clin Toxicol. 2007;45:203-233; Flomenbaum N, Goldfrank L, Hoffman R, et al. Goldfrank's toxicologic emergencies. 8th ed. McGraw-Hill Companies, Inc, 2006). Early recognition and aggressive treatment are necessary for patient survival.

Topics: Antidepressive Agents, Tricyclic; Arrhythmias, Cardiac; Cyclohexanols; Desipramine; Drug Overdose; Electrocardiography; Female; Humans; Middle Aged; Sodium Bicarbonate; Venlafaxine Hydrochloride

Tako-tsubo syndrome (TTS) refers to the apical ballooning of the left ventricle observed when angiographic ventriculography is performed in patients presenting with electrocardiographic changes suggestive of acute coronary syndrome (new transient ST-segment deviation (>0.05 mV) or T-wave inversion (>0.2 mV)), mild elevation of cardiac markers, but normal coronary arteries at the angiogram.. A 54-year-old woman developed the characteristic features of TTS 44 hours following nortriptyline overdose. The admission ECG showed increased QRS duration rapidly reversible after sodium bicarbonate infusion. There was a minimal increase in troponin I level. The ECG performed at the time of chest pain revealed deeply negative T waves in leads I, II, III, aVF, V1 to V6 and remained abnormal at 5 weeks follow-up. In contrast, a complete recovery of left ventricular function was observed within one week.. The pathophysiology of TTS, a variant of myocardial stunning, is still incompletely understood but could be related to sympathetic overstimulation. The possibility of TTS following toxic exposure is discussed.

Topics: Antidepressive Agents, Tricyclic; Drug Overdose; Electrocardiography; Female; Follow-Up Studies; Humans; Middle Aged; Nortriptyline; Sodium Bicarbonate; Takotsubo Cardiomyopathy; Troponin I; Ventricular Dysfunction, Left

Topics: Antidepressive Agents, Tricyclic; Clinical Trials as Topic; Drug Overdose; Humans; Saline Solution, Hypertonic; Sodium Bicarbonate; Treatment Outcome

A Brugada electrocardiographic pattern (BEP) associated with tricyclic antidepressant (TCA) overdose has been reported rarely, but its reversal by sodium bicarbonate has not been described previously. We reported a case of amitriptyline overdose induced Type 1 BEP which was reversed by 150 mEq of intravenous sodium bicarbonate.

Topics: Adult; Amitriptyline; Antidepressive Agents, Tricyclic; Brugada Syndrome; Drug Overdose; Electrocardiography; Humans; Male; Sodium Bicarbonate; Suicide

Topics: Antiemetics; Arrhythmias, Cardiac; Drug Overdose; Electrocardiography; Humans; Indoles; Quinolizines; Sodium Bicarbonate; Sodium Channels

Topics: Antidepressive Agents, Tricyclic; Drug Overdose; Electrocardiography; Emergency Medicine; Female; Humans; Internship and Residency; Intubation, Intratracheal; Middle Aged; Nortriptyline; Sodium Bicarbonate; Suicide, Attempted

This report describes a Brugada electrocardiographic pattern after tricyclic antidepressant intoxication that fails to resolve following sodium bicarbonate treatment. A 50-year-old male ingested 13.6 grams of amitriptyline and presented in cardiopulmonary arrest. After initial resuscitation, the patient developed a Brugada electrocardiographic pattern. The pattern persisted despite intravenous administration of 700 mEq of sodium bicarbonate. Five hours after the last dose of sodium bicarbonate and 18 hours after initial presentation, the Brugada pattern resolved. No co-ingestants were ingested and an ischemic pattern was not seen on electrocardiogram. The serum amitriptyline level was >1000 ng/ml. Response of the tricyclic-induced Brugada pattern to sodium bicarbonate has not been previously reported.

Topics: Amitriptyline; Antidepressive Agents, Tricyclic; Brugada Syndrome; Drug Overdose; Electrocardiography; Humans; Male; Middle Aged; Sodium Bicarbonate; Sodium Channels; Treatment Failure

Topics: Aged; Antidepressive Agents, Tricyclic; Antihypertensive Agents; Drug Interactions; Drug Overdose; Female; Humans; Lypressin; Sodium Bicarbonate; Terlipressin

We describe a case of a 2-year-old boy who ingested 35 mg.kg(-1) of amitriptyline. He developed central nervous system toxicity, as demonstrated by coma and seizures and cardiac toxicity (cardiac arrest) within 1 h of ingestion. The cardiac toxicity was refractory to standard therapy. His cardiac rhythm alternated between ventricular tachycardia and pulseless ventricular tachycardia/ventricular fibrillation for a period of 17 h. Following prolonged cardiopulmonary resuscitation and aggressive supportive management, the patient recovered both cardiovascularly and neurologically. An echocardiogram and MRI brain were subsequently performed and were normal. The patient was discharged 2 weeks later with normal cognitive, behavioral and motor function. We discuss the benefit of prolonged and effective cardiopulmonary resuscitation in the management of this potentially fatal poisoning.

Topics: Adrenergic beta-Agonists; Amitriptyline; Analgesics, Non-Narcotic; Anticonvulsants; Blood Gas Analysis; Cardiopulmonary Resuscitation; Child, Preschool; Coma; Drug Overdose; Heart Arrest; Humans; Hypnotics and Sedatives; Kidney; Magnesium Sulfate; Male; Seizures; Sodium Bicarbonate; Time Factors; Treatment Outcome; Vasodilator Agents

A 25-year-old man was brought to the emergency room after being found unconscious. Electrocardiography (ECG) showed changes classical of tricyclic antidepressant (TCA) poisoning. These included sinus tachycardia, QTc prolongation, QRS complex widening, right axis deviation and positive R waves in lead aVR. This unique ECG highlights the importance of lead aVR, which often tends to be ignored. Treatment is started based on ECG findings.

Topics: Adult; Antidepressive Agents, Tricyclic; Drug Overdose; Electrocardiography; Humans; Male; Sodium Bicarbonate; Tachycardia, Sinus; Unconsciousness

Topics: Acidosis; Adolescent; Anti-Infective Agents; Anticonvulsants; Cognition Disorders; Diazepam; Drug Overdose; Humans; Male; Nalidixic Acid; Seizures; Sodium Bicarbonate; Suicide, Attempted

The cardiotoxicity of tricyclic antidepressants is a well-described phenomenon requiring serious consideration in patients who have taken an overdose. In patients who are at high risk for suicide attempts, selective serotonin reuptake inhibitors (SSRIs) were thought to constitute a safe alternative. However, evidence is accumulating that they, too, possess proarrhythmic properties, which must be reconciled in the setting of an overdose. An 82-year-old woman intentionally ingested citalopram 1.6 g. Several hours after presentation, she developed sinus arrest and junctional bradycardia that resolved after infusion of intravenous sodium bicarbonate solution. Thereafter, she demonstrated no further electrocardiographic abnormalities and was safely transferred to the psychiatry service without the need for a temporary transvenous pacemaker. The dramatic effect of the sodium bicarbonate on the arrhythmia represents a probable event according to the Naranjo probability scale. Intravenous sodium bicarbonate may serve as an effective antidote to SSRI-induced bradyarrhythmias.

Topics: Aged; Aged, 80 and over; Arrhythmia, Sinus; Bradycardia; Citalopram; Depression; Drug Overdose; Electrocardiography; Female; Humans; Injections, Intravenous; Sodium Bicarbonate; Suicide, Attempted; Treatment Outcome

In this report of a near-fatal metformin ingestion successfully treated with alkalinization and high-volume hemofiltration, we discuss the management of severe lactic acidosis and demonstrate that early aggressive intervention resulted in a positive outcome.. Case report.. A tertiary pediatric intensive care unit.. The patient was a healthy 14-yr-old female found by a sibling following a seizure of unknown duration, thought to be secondary to hypoglycemia as a consequence of a self-ingestion of metformin, atenolol, and diclofenac. She responded well to advanced resuscitation but progressively developed severe lactic acidosis, bradycardia, and hypotension in addition to persistent hypoglycemia. The peak lactate level was 37.5 mmol/L with an albumin corrected anion gap of 65 mmol/L.. She was treated with high-volume venovenous hemofiltration and aggressive alkalinization therapy. The latter facilitated control of severe acidosis, whereas the hemofiltration removed the ingested drugs in addition to endogenously produced lactate precipitated by metformin.. In this case, early and aggressive treatment of the acidosis and cardiovascular compromise with inotropes, venovenous hemofiltration, and large doses of sodium bicarbonate in metformin overdose resulted in a successful outcome even in the presence of severe acidosis and very high lactate levels.

Topics: Acidosis, Lactic; Adolescent; Drug Overdose; Female; Fluid Therapy; Hemofiltration; Humans; Hypoglycemic Agents; Metformin; Sodium Bicarbonate

Topics: Adult; Antidotes; Carisoprodol; Charcoal; Chlordiazepoxide; Clindamycin; Drug Overdose; Drug Therapy, Combination; Flumazenil; Gastric Lavage; Humans; Male; Muscle Relaxants, Central; Naloxone; Sodium Bicarbonate; Sorbitol; Temazepam; Treatment Outcome

Topics: Animals; Antidepressive Agents, Tricyclic; Cardiovascular Diseases; Disease Models, Animal; Drug Overdose; Humans; Hyperventilation; Saline Solution, Hypertonic; Sodium Bicarbonate

Topics: 1-Propanol; Adrenergic beta-Antagonists; Adult; Drug Overdose; Female; Humans; Sodium Bicarbonate

Topics: Antidepressive Agents, Tricyclic; Attitude of Health Personnel; Drug Overdose; Humans; Hydrogen-Ion Concentration; Poison Control Centers; Sodium Bicarbonate; Surveys and Questionnaires; United States

A 31-year-old man ingested 400 mg of citalopram (Celexa) after an argument with his parents and girlfriend 13 h before presentation. Paramedics witnessed the patient having a generalized clonic seizure. The electrocardiogram (EKG) revealed a wide QRS complex, prolongation of the QTc interval, and left bundle branch pattern. He was treated with sodium bicarbonate with resolution of these changes. The patient was continued on a sodium bicarbonate infusion and demonstrated no further EKG abnormalities. Sodium bicarbonate should be considered as a treatment modality in patients with EKG abnormalities of prolongation of QRS or QTc interval after citalopram overdose.

Topics: Adult; Citalopram; Drug Overdose; Electrocardiography; Humans; Male; Seizures; Selective Serotonin Reuptake Inhibitors; Sodium Bicarbonate

To describe the clinical presentation of patients with cyclic antidepressant (CA) and use of sodium bicarbonate (NaHCO(3)) in the treatment of this overdose in the prehospital setting.. A three year retrospective observational review of records was performed using the San Diego County Quality Assurance Network database for prehospital providers. All adult patients who were treated with NaHCO(3) by paramedics for a CA overdose were included. Demographic data, presenting cardiovascular and neurological symptoms, paramedic treatments, and any changes in status were reviewed.. Twenty one patients were treated by paramedics with NaHCO(3) for CA overdose. Seventeen patients (80%) presented with mental status changes, including 11 presenting with a GCS<8. Seven of the 21 (33%) presented with a cardiac arrhythmia expected to possibly respond to NaHCO(3) treatment. Seven of the 21 (33%) were hypotensive, and five (24%) patients had reported seizure activity. Only 2 of the 21 patients (10%) treated with NaHCO(3) had recorded improvements after administration of the drug, while the other 19 remained stable without any deterioration. Sixteen of 21 patients (76%) were given NaHCO(3) for indications on standing order, while five patients were treated outside the standing order indications by base physician order with none of the five patients having any change in status ater treatment.. After prehospital NaHCO(3) use in patients with CA overdose, there were no complications reported, two patients improved in status and the others remained unchanged. Base hospital physician orders of NaHCO(3) for indications beyond the standing orders were not associated with changes in patient status.

Topics: Adult; Aged; Allied Health Personnel; Antidepressive Agents; Antidotes; Arrhythmias, Cardiac; California; Coma; Drug Overdose; Emergency Medical Services; Female; Humans; Male; Middle Aged; Retrospective Studies; Sodium Bicarbonate; Time Factors

To show the effectiveness of emergency extracorporeal membrane oxygenation (ECMO) in treating severe, life-threatening flecainide intoxication.. Case report.. Intensive care unit in a quaternary care center.. A patient with electromechanical dissociation after severe flecainide acetate overdose.. ECMO.. A 30-yr-old male with a history of depression presented after a severe flecainide overdose with plasma concentrations exceeding 20 times the upper boundary of the therapeutic range. At presentation, the patient was in refractory cardiocirculatory collapse and was successfully resuscitated with ECMO. Twenty-six hours later, extracorporeal support could be discontinued and the patient made a full recovery.. In patients with severe but potentially reversible cardiac dysfunction attributable to flecainide intoxication, ECMO can maintain cardiac output and vital organ perfusion while allowing time for drug redistribution, metabolism, and clearance.

Topics: Acidosis; Adult; Anti-Arrhythmia Agents; Drug Overdose; Electrocardiography; Epinephrine; Extracorporeal Membrane Oxygenation; Flecainide; Humans; Male; Respiration, Artificial; Sodium Bicarbonate; Suicide, Attempted; Treatment Outcome

Topics: Antidepressive Agents, Tricyclic; Buffers; Cardiopulmonary Resuscitation; Drug Overdose; Humans; Research Design; Respiration, Artificial; Saline Solution, Hypertonic; Sodium Bicarbonate

The tricyclic antidepressant (TCA) agents are recognized for their potentially lethal cardiovascular and neurological effects in poisoned patients. The 12-lead electrocardiogram (ECG) has emerged as a popular bedside tool in the evaluation of TCA toxicity. Although the history and physical examination play a key role in the assessment of the patient with potential TCA poisoning, the presence or absence of features of the TCA toxidrome are not sufficient to detect or exclude toxicity from this class of drugs. A variety of ECG findings occur with TCA toxicity. Aside from the sinus tachycardia due principally to anticholinergic effects, TCA-toxic changes seen on the ECG are attributable primarily to the sodium channel blockade caused by these agents. The majority of patients at significant risk for developing cardiac or neurological toxicity will have a QRS complex greater than 0.10 seconds or a rightward shift of the terminal 40 ms of the frontal plane QRS complex vector. The majority of these patients will also display these changes early in their emergency department stay. However, the appearance of these findings, either alone or in combination, does not mean the patient will develop significant cardiac or neurological toxicity. The ECG can neither unequivocally rule in nor rule out impending toxicity; recognizing these limitations, the emergency physician can use this bedside tool in combination with other clinical data during the assessment of the poisoned patient.

Topics: Adolescent; Adrenergic Uptake Inhibitors; Adult; Amitriptyline; Antidepressive Agents, Tricyclic; Antidotes; Arrhythmia, Sinus; Charcoal; Cholinergic Antagonists; Doxepin; Drug Overdose; Electrocardiography; Female; Humans; Point-of-Care Systems; Sodium Bicarbonate; Sodium Channel Blockers; Sorption Detoxification; Tachycardia

Reports of acute toxicity following sulfasalazine ingestion are rare. A case of an acute ingestion of sulfasalazine 50 g and paracetamol 50 g resulting in severe lactic acidosis, seizures, coagulopathy, hyperglycemia, ketosis, and methemoglobinemia is reported. Despite the ingestion of a large amount of paracetamol with serum paracetamol 5486 nmol/L (844 mg/L), significant hepatotoxicity did not occur. The patient recovered fully following administration of intravenous N-acetylcysteine, methylene blue, sodium bicarbonate, and supportive therapy.

Topics: Acetaminophen; Acetylcysteine; Acidosis, Lactic; Acute Disease; Adult; Anti-Inflammatory Agents; Blood Coagulation Disorders; Blood Platelets; Drug Combinations; Drug Overdose; Humans; Hyperglycemia; Infusions, Intravenous; Male; Methemoglobinemia; Methylene Blue; Partial Thromboplastin Time; Sodium Bicarbonate; Suicide, Attempted; Sulfasalazine

Topics: Adult; Aged; Anti-Arrhythmia Agents; Buffers; Drug Overdose; Electrocardiography; Emergency Treatment; Female; Flecainide; Humans; Hypertonic Solutions; Male; Sodium Bicarbonate; Suicide, Attempted

Topics: Acidosis, Lactic; Adult; Bicarbonates; Buffers; Drug Overdose; Humans; Hypoglycemic Agents; Lactic Acid; Male; Metformin; Renal Dialysis; Sodium Bicarbonate

Serious complications from tricyclic antidepressant (TCA) overdose are uncommon. We present a case of massive imipramine overdose complicated by ventricular fibrillation and a prolonged period of cardiovascular collapse. A total of 400 mmol of sodium bicarbonate, 5 mg of adrenaline and 80 mg of sotalol were given during 50 minutes of cardiac arrest. The patient made a full recovery with no apparent neurological sequelae. The highest TCA plasma level we could find in the published literature was 4873 ng/ml4; our patient's peak TCA level was 6000 ng/ml. Tricyclic antidepressant overdose is a common cause of intensive care unit admission. It has a low mortality rate.

Topics: Adrenergic Agonists; Adult; Anti-Arrhythmia Agents; Antidepressive Agents, Tricyclic; Critical Care; Depression; Drug Overdose; Electric Countershock; Epilepsy, Tonic-Clonic; Epinephrine; Female; Heart Arrest; Humans; Imipramine; Puerperal Disorders; Shock; Sodium Bicarbonate; Sotalol; Ventricular Fibrillation

Cyclic antidepressant (CA) overdose can produce life-threatening seizures, hypotension, and dysrhythmias. It accounts for up to half of all overdose-related adult intensive care unit admissions and is the leading cause of death from drug overdose in patients arriving at the emergency department alive. Several factors contribute to the significant morbidity and mortality associated with CA overdose. First, CAs are widely prescribed and are dispensed to patients at increased risk for attempting suicide. Second, drugs of this class generally have a low therapeutic toxic ratio. Third, in the majority of fatal cases, the patient dies before reaching a hospital. Finally, and of greatest significance for the clinician, the presenting signs and symptoms of CA overdose may be missed by the physician, even in cases of severe toxicity. Therefore, CAs must be considered early in any case of suspected overdose, and all such cases should be managed as potentially fatal ones. The following case demonstrates the current approach to the patient with significant CA toxicity.

Topics: Animals; Antidepressive Agents, Tricyclic; Drug Overdose; Electrocardiography; Emergencies; Humans; Hydrogen-Ion Concentration; Male; Middle Aged; Phenobarbital; Prognosis; Seizures; Sodium Bicarbonate

Clinicians should be aware of the complications of rhabdomyolysis in patients who ingest doxylamine succinate and other over-the-counter antihistamines. The easy availability of these substances increases the potential not only for intentional overdose by adults but also for inadvertent ingestion by children. Prompt intervention and careful assessment of renal function, urinary output, and serum creatine kinase levels may represent the difference between an uncomplicated course and acute renal failure.

Topics: Adult; Bicarbonates; Creatine Kinase; Doxylamine; Drug Overdose; Epilepsy, Tonic-Clonic; Histamine H1 Antagonists; Humans; Intubation, Intratracheal; Male; Rhabdomyolysis; Schizophrenia, Paranoid; Sodium; Sodium Bicarbonate; Suicide, Attempted

The objective of this study was to characterize the effect of intravenous hypertonic sodium bicarbonate (NaHCO3) administration in patients with moderate-to-severe cyclic antidepressant (CA) overdose. We reviewed charts of all 91 patients given the diagnosis of CA overdose in the University of California Los Angeles (UCLA) Emergency Medicine Center (EMC), who either died in the EMC or were admitted to the medical intensive care unit (MICU), and who received NaHCO3 in the EMC between 1980 and 1988. Twenty-four other patients with the same EMC diagnosis were admitted to the MICU during this period but did not receive NaHCO3. The response of blood pressure, electrocardiographic parameters, and mental status to serum alkalinization with NaHCO3 were evaluated. Major morbidity and mortality were recorded for all patients. Hypotension was corrected within 1 hour in 20 of 21 (96%) patients, QRS prolongation corrected in 39 of 49 (80%), and mental status improved in 40 of 85 (47%). There was one death, in a patient who was moribund on arrival to the EMC. No complications were attributable to the administration of NaHCO3. NaHCO3 seems to improve hypotension and normalize QRS duration rapidly in most patients treated, and improve mental status changes in almost one half. Serum alkalinization with NaHCO3, in conjunction with appropriate supportive care, seems to limit major morbidity and mortality effectively in patients with serious CA overdose.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Antidepressive Agents, Tricyclic; Child; Child, Preschool; Drug Overdose; Electrocardiography; Female; Humans; Hypertonic Solutions; Hypotension; Infant; Male; Middle Aged; Retrospective Studies; Sodium Bicarbonate

Topics: Adolescent; Bicarbonates; Desipramine; Drug Overdose; Electrocardiography; Emergency Service, Hospital; Female; Gastric Lavage; Humans; Intensive Care Units, Pediatric; Poisoning; Sensitivity and Specificity; Sodium; Sodium Bicarbonate; Substance Abuse Detection

The patient with theophylline overdose commonly presents with gastrointestinal, cardiovascular, neurologic, and electrolyte abnormalities. Respiratory alkalosis is the most common acid-base alteration, but mild metabolic acidosis has been reported. Two cases of severe lactic acidosis (pH 6.67 and 6.63) in patients without hypoxemia, shock, or prolonged seizure activity are reported. Possible causative mechanisms and aspects of therapy are discussed. Theophylline toxicity should be considered when an unconscious patient with concurrent severe metabolic acidosis presents to the emergency department.

Topics: Acidosis, Lactic; Adult; Bicarbonates; Charcoal; Coma; Drug Overdose; Emergencies; Female; Glasgow Coma Scale; Humans; Sodium; Sodium Bicarbonate; Theophylline

This is a report of an intentionally administered overdose of dimenhydrinate to a 4 month-old infant who subsequently presented with status epilepticus, coma, and life threatening ventricular dysrhythmias. Initial toxicologic analysis of the serum by fluorescence polarization immunoassay was positive for tricyclic antidepressants. Repeat analysis of the serum at 6 hours post ingestion by gas chromatography mass spectrometry analysis defined diphenhydramine 4.8 micrograms/mL. The infant was managed with IV sodium bicarbonate as utilized in tricyclic antidepressant intoxication. The dysrhythmias resolved and the infant recovered without sequelae.

Topics: Arrhythmias, Cardiac; Bicarbonates; Child Abuse; Dimenhydrinate; Drug Overdose; Gas Chromatography-Mass Spectrometry; Heart; Humans; Infant; Male; Sodium; Sodium Bicarbonate; Status Epilepticus

120 cases of class IC antiarrhythmic overdose, including propafenone, flecainide, ajmaline and prajmaline overdose, were evaluated with respect to clinical course, therapy and outcome. Whereas drug overdose in general has an overall mortality of less than 1%, intoxication with antiarrhythmic drugs of class IC was associated with a mean mortality of 22.5%. Nausea, which occurred within the first 30 minutes after ingestion, was the earliest symptom. Spontaneous vomiting probably led to self-detoxication in about half the patients. Cardiac symptoms including bradycardia and, less frequently, tachyrhythmia occurred after about 30 minutes to 2 hours. Therapeutic measures included administration of activated charcoal, gastric lavage and a saline laxative, catecholamines, and in some patients, hypertonic sodium bicarbonate, insertion of a transvenous pacemaker and hemoperfusion. Fatal outcome was mainly due to cardiac conduction disturbances progressing to electromechanical dissociation or asystolia. Resuscitation, which had to be performed in 29 patients, was successful in only two of them. No correlation was found between fatal outcome, the type of antiarrhythmic, and ingested dose. Since a specific treatment is not available and resuscitive procedures including sodium bicarbonate and insertion of a pacemaker are of limited therapeutic value, early diagnosis and primary detoxification are most important for prevention of fatal outcome.

Topics: Ajmaline; Anti-Arrhythmia Agents; Bicarbonates; Bradycardia; Drug Overdose; Flecainide; Hemoperfusion; Humans; Hypertonic Solutions; Nausea; Prajmaline; Propafenone; Resuscitation; Retrospective Studies; Sodium; Sodium Bicarbonate; Tachycardia; Vomiting