Kenneth D. Katz

Case series of synthetic cannabinoid intoxication from one toxicology center

Synthetic cannabinoid use has risen at alarming rates. This case series describes 11 patients exposed to the synthetic cannabinoid, MAB-CHMINACA who presented to an emergency department with life-threatening toxicity including obtundation, severe agitation, seizures and death. All patients required sedatives for agitation, nine required endotracheal intubation, three experienced seizures, and one developed hyperthermia. One developed anoxic brain injury, rhabdomyolysis and died. A significant number were pediatric patients. The mainstay of treatment was aggressive sedation and respiratory support. Synthetic cannabinoids pose a major public health risk. Emergency physicians must be aware of their clinical presentation, diagnosis and treatment.

SAFETY AND EFFECTIVENESS OF ACETADOTE FOR ACETAMINOPHEN TOXICITY

BACKGROUND Acetaminophen (APAP) toxicity is commonly encountered in the Emergency Department. Until 2004, treatment consisted of either oral N-acetylcysteine (NAC) or filtered oral NAC administered intravenously (i.v.). Intravenous acetylcysteine (Acetadote) is a new Food and Drug Administration-approved i.v. formulation of acetylcysteine manufactured by Cumberland Pharmaceuticals in Nashville, Tennessee. Little post-marketing data exists on the effectiveness and safety of i.v. acetylcysteine. OBJECTIVES We evaluated the clinical presentations and outcomes of patients treated with i.v. acetylcysteine for APAP toxicity. METHODS We performed a retrospective chart review of patients treated with i.v. acetylcysteine for APAP ingestion. The primary outcome measures were: adverse reactions to and effectiveness of i.v. acetylcysteine, as defined by elevation of transaminases, liver failure, renal failure, death, and hospital length of stay (LOS). Data collected included: comorbidities, allergies, intentionality, timing and dosing of i.v. acetylcysteine, hospital LOS, transaminases > 1000 IU/L, development of liver failure requiring transplant, development of renal failure requiring hemodialysis, death, and anaphylactoid reactions. RESULTS Sixty-four patients met our study criteria. Overall, 16 (25%) patients developed transaminases > 1000 IU/L, 4 (6%) of them died and 2 (3%) received liver transplants. Of the 15 patients (23%) treated within 8 h, none died or developed liver or renal failure, and only 1 developed transient transaminase elevation > 1000 IU/L. In the patients treated outside of 8 h, the median LOS was 3 days, whereas the group treated within 8 h had a median LOS of only 1 day. Six (9%) patients developed anaphylactoid reactions, 2 of whom received the i.v. acetylcysteine bolus over 15 min. Five of these patients were treated pharmacologically and completed treatment, and one had treatment discontinued for undocumented reasons. CONCLUSION Intravenous acetylcysteine seemed to be a safe and effective formulation of N-acetylcysteine.

Seizure During Hyperbaric Oxygen Therapy for Carbon Monoxide Toxicity: A Case Series and Five-year Experience

BACKGROUND Hyperbaric oxygen (HBO) therapy is recommended to reduce the delayed neurologic sequelae resulting from carbon monoxide (CO) toxicity. Although HBO is generally well tolerated, there exists a risk of seizure in all patients that may be increased in patients with predisposing factors including: fever, hypothermia, prior seizure, or brain injury. CASE REPORT We present two cases of patients without known risk factors who experienced seizures associated with HBO therapy during treatment for CO toxicity. CONCLUSION This facilitys 5-year experience and a review of the germane literature are also presented to elucidate the risk factors and incidence of seizures in patients treated with HBO for CO toxicity.

Four-Year Experience with Methotrexate Exposures

IntroductionUnintentional methotrexate (MTX) acute oral overdose is rarely reported.MethodsWe conducted a retrospective chart review of all human exposure calls (> 150,000 charts) for MTX ingestions reported to our Poison Center during 2000–2003.ResultsThirteen patients met the criteria. The average amount of MTX ingested was 13.03 mg (data from 7 cases), and the average patient age was 43 years (20 months to 80 years). No significant toxicities occurred.DiscussionAlthough intravenous MTX toxicity can be severe, this does not appear to be a phenomenon associated with either acute unintentional or suicidal oral ingestion.

Prolonged toxicity in a 2-year-old after accidental ingestion of aripiprazole.

Aripiprazole (Abilify), or 7-{4-[4-(2,3-dichlorophenyl)-1-piperazinyl]butyloxy}-3,4-dihydro-2(1H)-quinolone, is a novel atypical antipsychotic possessing a long half-life. Although not a Food and Drug Administration-approved indication, low-dose aripiprazole is used to treat pediatric psychiatric conditions. Data regarding toxicity of low-dose aripiprazole ingestions in children are limited. We report the case of an accidental ingestion of two 5-mg aripiprazole tablets by a 2-year-old girl with a measured drug level of 160 ng/mL approximately 34 hours after ingestion. She exhibited marked lethargy, tremor, and tachycardia persisting over 72 hours. Emergency physicians, pediatricians, and psychiatrists should be aware of the potential for significant and prolonged toxicity in children even with relatively small-dose aripiprazole exposures.

Birth Outcomes Following Self‐Inflicted Poisoning During Pregnancy, California, 2000 to 2004

OBJECTIVE To describe birth outcomes following intentional acute poisoning during pregnancy. SETTING California Linked Vital Statistics-Patient Discharge Database, 2000 to 2004. PARTICIPANTS Pregnant women age 15 to 44, who had a singleton live birth or fetal death that occurred between gestational ages 20 and 42 weeks who were discharged from the hospital for an intentional poisoning were compared to pregnant women discharged from the hospital for any nonpoisoning diagnosis. Intentional acute poisoning hospital discharges were identifed by the presence of an ICD-9-CM E-Codes E950-E952 (suicide, attempted suicide and self-inflicted injuries specified as intentional.) METHODS Through a retrospective cohort design, birth outcomes including low birth weight; preterm birth; fetal, neonatal, and infant death; and congenital anomalies were identified by the presence of ICD-9-CM diagnosis codes or by notation in the dataset. RESULTS There were 430 hospital discharges for an intentional poisoning during pregnancy documented in the dataset (rate=25.87/100,000 person years). The rate of intentional poisoning was greatest in the first weeks of gestation and declined with increasing gestational age. Analgesics, antipyretics, and antirheumatics were most commonly implicated. Adverse birth outcomes associated with intentional poisoning included preterm birth (odds ratio [OR]=1.34; 95% Confidence Interval [CI] [1.01, 1.77]), low birth weight (OR=1.49; 95% CI [1.04, 2.12]), and circulatory system congenital anomalies (OR=2.17; 95% CI [1.02, 4.59]). CONCLUSION Intentional acute poisoning during pregnancy was associated with several adverse birth outcomes; however, these relationships may be confounded by concomitant maternal substance abuse.

Hypothermia: An Unusual Indication for Gastric Lavage

BACKGROUND Previous reports suggest that gastric lavage holds many risks and is not routinely indicated for decontamination of the overdose patient. OBJECTIVE To present a case of overdose with concurrent accidental hypothermia where gastric decontamination was utilized. CASE REPORT A 50-year-old hypothermic, comatose patient was transported to the Emergency Department with a concurrent, massive medication ingestion diagnosed incidentally on a routine abdominal computed tomography scan. Both active and passive rewarming measures, in conjunction with gastric lavage and retrieval of multiple pill fragments, were performed, and the patient survived to hospital discharge without sequelae. Interestingly, the patient admitted to an intentional ingestion of both labetalol and lorazepam. CONCLUSION Due to hypothermia-mediated changes in metabolism, including gastric atony and decreased hepatic metabolism, gastric lavage may provide additional benefit in the management of severely hypothermic patients with potentially lethal, massive pill ingestions.

Successful treatment of metoprolol-induced cardiac arrest with high-dose insulin, lipid emulsion, and ECMO.

β-Adrenergic antagonist toxicity causes cardiovascular collapse often refractory to standard therapy. Alternative therapies include high-dose insulin, lipid emulsion, and venoarterial extracorporeal membrane oxygenation (VA-ECMO). A 47-year-old man ingested 10 g of metoprolol tartrate in a suicide attempt. Upon emergency department presentation, he was comatose, bradycardic, and hypotensive. Glucagon (14 mg IV) and vasopressor/inotropic support (epinephrine 0.1 μg/[kg min], dobutamine 10 μg/[kg min]) were administered. Despite these therapies, he developed cardiac arrest for 55 minutes, requiring epinephrine (5 mg IV) and vasopressin (40 U IV) with multiple episodes of return of spontaneous circulation. Additional vasopressor administration (vasopressin 0.04 U/min, norepinephrine 0.5 μg/[kg min]) did not improve his hemodynamics. High-dose insulin (250 U IV) and 20% lipid emulsion (100 mL bolus with 200 mL/30 min infusion) were administered, and VA-ECMO was initiated with hemodynamic improvement. His postarrest neurologic examination demonstrated lack of brainstem reflexes and cortical motor response. He awoke 11.5 hours after time of ingestion. Venoarterial extracorporeal membrane oxygenation was discontinued at hospital day 3, and the patient was discharged on hospital day 10 with excellent neurologic recovery. A serum metoprolol level measured 25,000 ng/mL (therapeutic 20-340 ng/mL). High-dose insulin has been shown to be beneficial in β-adrenergic antagonist cardiotoxicity. Lipid emulsion is thought to act as a lipid extractor, lowering serum and tissue levels. Venoarterial extracorporeal membrane oxygenation was used with the above therapies, restoring organ perfusion and allowing intrinsic drug metabolism and elimination. High-dose insulin, lipid emulsion, and VA-ECMO should be considered for refractory cardiac arrest secondary to β-adrenergic antagonist toxicity such as metoprolol.

Neurologic recovery following cardiac arrest due to carbon monoxide poisoning

Sir, We present an interesting case of a patient who received therapeutic hypothermia (TH) following cardiac arrest due to carbon monoxide (CO) poisoning and achieved good neurologic recovery. A 93-year-old man was exposed to CO at home after attempting to repair his furnace. His carboxyhemoglobin level at presentation to the outlying hospital was 35%. Following intubation for airway protection, 100% inspired oxygen therapy was initiated, and the patient was transferred to this facility. Upon arrival, the patient had a Glasgow Coma Score of six (Eyes-one, Verbal-one, Motor-four). Corneal, gag, cough, and pupillary responses were preserved. He suffered a witnessed pulseless electrical activity (PEA) arrest in this facility’s emergency department. He received cardiopulmonary resuscitation as well as one ampule each of intravenous adrenaline (epinephrine), atropine, calcium chloride and sodium bicarbonate. Return of spontaneous circulation was achieved after five minutes. Protocolized post-cardiac arrest care utilizing intravenous cold saline and external cooling was initiated to lower the patient’s core temperature to 34°C.1 Goal temperature (34 °C) was achieved at hour seven post-arrest. After thirteen hours at this temperature, he was re-warmed gradually (0.25–0.5 °C/hour). He showed neurologic improvement on hospital day two, and “excellent” neurologic recovery was noted on hospital day six. At that time, he was oriented to person and recalled the events that led to his illness; his mini-mental status exam score was 24. His course was later complicated by large bowel obstruction. He understood the risks, benefits, and alternatives of surgical management of this condition, and he himself refused surgical intervention. He was discharged on hospital day 19 to hospice care. Review of the literature shows that cardiac arrest following CO exposure has a very poor prognosis.2 While a handful of patients appear to have survived cardiac arrest following CO exposure, there are no reported cases of patient survival with good neurological recovery. Mild TH improves neurologic outcome following cardiac arrest.1, 3 The American Heart Association recommends this therapy in unresponsive patients with return of spontaneous circulation following out-of-hospital ventricular fibrillation or ventricular tachycardia arrests.4 However, it does not address the use of TH following PEA arrests or CO-mediated arrests. This patient with CO-related PEA cardiac arrest improved neurologically, suggesting TH may benefit certain patients who arrest due to CO poisoning.

A 17-Year-Old Girl With Cough--Pulseless After Drug Overdose. Sodium benzonatate overdose.

A17-year-old girl with a history of depression, but no prescribed antidepressants, arrives to the emergency department (ED) in cardiac arrest. After an argument with her father, the girl admitted to swallowing 12 tablets of a medication. Her father had found her within 10 minutes of the ingestion; she seemed drowsy and complained of nausea and dizziness. During transport to the ED, approximately 30 minutes after drug ingestion, she rapidly developed generalized convulsions and then became apneic. An initial assessment in the ED finds the girl to be unresponsive and pulseless. Chest compressions are started, and a bagvalve-mask is applied for assisted ventilation. Naloxone, 2 mg intravenously (IV), is administered without response. A bedside blood glucose measurement is 228 mg/dL. The defibrillators cardiac monitor reveals ventricular fibrillation. Advanced cardiac life support protocol is initiated, and 2