B. Zane Horowitz

Intermediate syndrome after malathion ingestion despite continuous infusion of pralidoxime.

Case Report: A 33-year-old female ingested an unknown quantity of malathion in a suicide attempt. Cholinergic signs consistent with severe organophosphate intoxication developed and were treated within 6 hours of ingestion. Intravenous atropine and a continuous infusion of pralidoxime (400 mg/h) were administered. Prolonged depression of plasma and red blood cell cholinesterases were documented. Despite an initial clinical improvement and the presence of plasma pralidoxime concentrations exceeding 4 μg/mL, the patient developed profound motor paralysis consistent with the diagnosis of Intermediate Syndrome. In addition to the dose and frequency of pralidoxime administration, other factors including persistence of organophosphate in the body, the chemical structure of the ingested organophosphate, and the time elapsed between ingestion and treatment may limit the effectiveness of pralidoxime as an antidote in organophosphate ingestions. This case study suggests that these factors should be taken into account in assessing the risk of Intermediate Syndrome after intentional organophosphate ingestions.

Fatal Cardiovascular Collapse Following Acute Colchicine Ingestion

Background: A previously published prognostic rule predicts 100% survival after ingestion of cochicine doses less than 0.5 mg/kg and 100% mortality after ingestion of more than 0.8 mg/kg. This rule inaccurately predicted survival in a recent case. Case Report: We present a case of fatal colchicine poisoning in an adult who ingested a maximum of 39.6 mg of colchicine (0.40 mg/kg). He subsequently developed hypotension which was refractory to fluid resuscitation and infusion of vasopressors. He died of cardiovascular collapse approximately 35 hours after ingestion. Discussion: Fatal outcomes are possible even with colchicine doses less than 0.5 mg/kg. Physicians caring for colchicine-poisoned patients must be prepared for the possibility of acute cardiovascular collapse and ventricular dysrhythmias regardless of the reported dose of colchicine.

Amanita smithiana mushroom ingestion: A case of delayed renal failure and literature review

IntroductionIn the Pacific Northwest a new pattern of mushroom ingestion has emerged, attributed toAmanita smithiana, in which renal failure has been the predominant manifestation.Case ReportA 55-year-old male ate 3 raw wild mushrooms in a salad and had onset of severe nausea and vomiting within 6 hours. His vital signs were unremarkable. His labs were significant for a BUN of 14mg/dL (5.0 mmol/L), and a creatinine of 1.0 mg/dL (88umol/L), transaminases were elevated with an AST of 56 U/L (nl 9–40) and an ALT of 131 U/L (nl 14–72). Treatment was initiated with N-acetyl cysteine, penicillin, and milk thistle extract on the presumption that this was an amanitin-toxin containing mushroom. He developed acute renal failure that was not responsive to our treatment. Dialysis started on day 4 with a creatinine of 6.5 mg/dL, which peaked on day 7 at 10.2 mg/dL. We were able to obtain a positive mushroom identification by a mycologist asAmanita smithiana. The patient was discharged from the hospital for outpatient dialysis on day 10 and dialysis catheter was removed 39 days after ingestion with a creatinine of 1.4 mg/dL (123.8 umol/L).DiscussionAmanita smithiana mushroom poisoning presents within 6 hours of ingestion with GI toxicity, and develops delayed onset of renal insufficiency over the first 1 to 4 days. The early hospitalization of this case allowed a profile of the onset of liver and renal injury. Mild elevation of hepatic transaminases occurred on presentation and peaked 24 hours after the ingestion. Renal injury was detected 1 day after presentation, and progressed to require hemodialysis by 4 days postingestion. This pattern of delayed-onset renal toxic mushroom ingestion is emerging among mushroom ingestions in Western North America.

Type E botulism

There are seven known serotypes of botulism, designated A through G; almost all human cases of botulism are caused by types A, B, and E. Botulism type E is the predominant serotype causing disease associated with native Arctic foods. In the circumpolar regions of the world, the coastal soils are rich in botulism type E, and consumption of fish and marine animals in these areas are the sources of clusters of botulism. Unlike spores of type A and B, botulism type E can withstand freezing down to 3.5°C. Alaskan native fermentation of fish heads, fish eggs, and beaver tail allow proper anaerobic conditions for botulinum toxin to be elaborated from Clostridium botulinum. The consumption of whale meat, “muktuk” has also been associated with outbreaks of botulism in Alaska and the Canadian Arctic. Elsewhere in the Arctic regions, type E botulism has been associated with Norwegian “rakfisk” prepared by a process similar to fermented Alaskan foods. Outbreaks in Egypt with the salted gray mullet “faseikh”, in Israel and New York linked to salted uneviscerated whitefish “kapchunka”, in Iran from eating “ashbal” an uncooked salmon, and in Japan with “izushi” a traditional fermented fish preserved in rice have occurred. Importation of vacuum-packed whitefish from Alaska and Canada has also been associated with sporadic cases of botulism type E in Europe. In March 2010, the Center for Disease Control and Prevention released the heptavalent antitoxin (H-BAT) for use in the USA, under an Investigational New Drug program, as the preferred treatment for food-borne botulism, including type E, which had not been covered by the bivalent antitoxin, the prior approved antitoxin product in the USA.

Treatment of toxicity from amphetamines, related derivatives, and analogues: A systematic clinical review

BACKGROUND Overdose of amphetamine, related derivatives, and analogues (ARDA) continues to be a serious worldwide health problem. Patients frequently present to the hospital and require treatment for agitation, psychosis, and hyperadrenegic symptoms leading to pathologic sequelae and mortality. OBJECTIVE To review the pharmacologic treatment of agitation, psychosis, and the hyperadrenergic state resulting from ARDA toxicity. METHODS MEDLINE, PsycINFO, and the Cochrane Library were searched from inception to September 2014. Articles on pharmacologic treatment of ARDA-induced agitation, psychosis, and hyperadrenergic symptoms were selected. Evidence was graded using Oxford CEBM. Treatment recommendations were compared to current ACCF/AHA guidelines. RESULTS The search resulted in 6082 articles with 81 eligible treatment involving 835 human subjects. There were 6 high-quality studies supporting the use of antipsychotics and benzodiazepines for control of agitation and psychosis. There were several case reports detailing the successful use of dexmedetomidine for this indication. There were 9 high-quality studies reporting the overall safety and efficacy of β-blockers for control of hypertension and tachycardia associated with ARDA. There were 3 high-quality studies of calcium channel blockers. There were 2 level I studies of α-blockers and a small number of case reports for nitric oxide-mediated vasodilators. CONCLUSIONS High-quality evidence for pharmacologic treatment of overdose from ARDA is limited but can help guide management of acute agitation, psychosis, tachycardia, and hypertension. The use of butyrophenone and later-generation antipsychotics, benzodiazepines, and β-blockers is recommended based on existing evidence. Future randomized prospective trials are needed to evaluate new agents and further define treatment of these patients.

“Parachuting” Meth: A Novel Delivery Method for Methamphetamine and Delayed-Onset Toxicity From “Body Stuffing”

Background. Methamphetamine is an illicit stimulant that is typically smoked, insufflated, or injected. We report an unusual method of ingesting methamphetamine called “parachuting” and its implications for the treatment of “body stuffers.” Case Report. A 25-year-old man wrapped methamphetamine into a plastic baggie and ingested it in an attempt to “parachute.” He presented to an Emergency Department 10 hours after his ingestion because he realized that he forgot to puncture the baggie. He had no complaints and had a transient tachycardia. He was treated with activated charcoal and whole bowel irrigation, observed for 24 hours, and discharged. He returned 42 hours after his ingestion with tachycardia (220 bpm), agitation, hypertension (179/74 mmHg), and rhabdomyolysis (CPK 7771 U/L), requiring mechanical ventilation and a midazolam drip (10 mg/hr). Conclusion. “Parachuting” is a novel method of ingesting methamphetamine. We report a case of a single-packet “body stuffer” with severe symptom onset that was delayed over 36 hours. Treatment protocols for “body stuffers” using this technique may require more prolonged observation and/or imaging studies to determine the absence of gastrointestinal packets.

Hydrogen peroxide ingestion associated with portal venous gas and treatment with hyperbaric oxygen: a case series and review of the literature

Introduction. Ingestion of concentrated hydrogen peroxide (H2O2) has been associated with venous and arterial gas embolic events, hemorrhagic gastritis, gastrointestinal bleeding, shock, and death. Although H2O2 is generally considered a benign ingestion in low concentrations, case reports have described serious toxicity following high concentration exposures. Hyperbaric oxygen (HBO) has been used with success in managing patients suffering from gas embolism with and without manifestations of ischemia. Methods. Poison center records were searched from July 1999 to January 2010 for patients with H2O2 exposure and HBO treatment. Cases were reviewed for the concentration of H2O2, symptoms, CT scan findings of portal gas embolism, HBO treatment, and outcome. Results. Eleven cases of portal gas embolism were found. Ages ranged from 4 to 89 years. All but one ingestion was accidental in nature. In 10 cases 35% H2O2 was ingested and in 1 case 12% H2O2 was ingested. All abdominal CT scans demonstrated portal venous gas embolism in all cases. Hyperbaric treatment was successful in completely resolving all portal venous gas bubbles in nine patients (80%) and nearly resolving them in two others. Ten patients were able to be discharged home within 1 day, and one patient had a 3.5-day length of stay. Conclusions. HBO was successful in resolving portal venous gas embolism from accidental concentrated H2O2 ingestions.

The Impact of Bittering Agents on Pediatric Ingestions of Antifreeze

Background. Legislation requiring bittering of antifreeze enables assessment of the impact on frequency, volume, and severity of pediatric antifreeze ingestions. Methods. US poison control data for antifreeze ingestions in children younger than 5 years were analyzed comparing 232 ingestions occurring in states after enactment of bittering requirements with 6218 cases occurring in states (or at times) where bittering was not required. Results. The frequency of pediatric antifreeze ingestions was unchanged after implementation of bittering in Oregon and California. The medical outcome distribution, median volume ingested, and observed clinical effects were no different in bittered compared with nonbittered groups. Likewise, the rates of hospital admission, critical care treatment, and use of alkalinization, hemodialysis, or intubation showed no differences with bittering. Conclusion. Despite the appealing logic of limiting the ingested volume and thereby the severity of poisonings by adding aversive agents, and despite promising results in volunteer studies, bittering agents do not decrease the frequency or severity of pediatric antifreeze poisonings. The addition of bittering agents to household products cannot be justified based on actual poisoning data.

Iatrogenic neonatal mercury poisoning from mercurochrome®treatment of a large omphalocele

A 3,498 gram newborn with a large omphalocele detected by prenatal ultrasound was delivered at 3811⁄2 weeks by cesarean section in a metropolitan university teaching hospital. From the 1st through 4th days of life, she received topical povidone-iodine (BetadineO) applied twice daily over the omphalocele. From the 5th through 10th days of life, she underwent twice daily dressing changes with 2% merbromin (Mercurochrome®), until the hospital pharmacy exhausted its supply of merbromin (60 mL) and could obtain no more from any other hospitals in the region. Once merbromin was no longer available, the pediatric surgical service began using silver sulfadiazine (Silvadene®) from the 11th day of life onward. Blood mercury concentration obtained on the 9th day of life

Amanita phalloides poisoning

A Vietnamese family living in the Pacific Northwest harvested several wild mushrooms grown in their front lawn. All three in the family suffered from delayed GI symptoms starting approximately 12 h after ingestion. One patient died and two developed hepatic injury. We provide photography and describe common characteristics of Amanita phalloides mushroom.