Ming-Ling Wu

Agricultural Avermectins: An Uncommon But Potentially Fatal Cause of Pesticide Poisoning

STUDY OBJECTIVE Avermectins have been used in the control of parasites and insects; however, human data concerning poisoning are lacking. This study investigated the clinical spectrum of avermectin poisoning. METHODS A retrospective study was conducted to evaluate patients with avermectin poisoning reported to a poison center from September 1993 through December 1997. RESULTS Eighteen patients with abamectin (Agri-Mek; 2% wt/wt abamectin) exposure and 1 with ivermectin (Ivomec; 1% wt/vol ivermectin) ingestion were identified. There were 14 male and 5 female patients, ranging in age from 15 to 83 years. Most patients were exposed as a result of attempted suicide (14). Oral ingestion (15) was the most common route of exposure. Four patients were asymptomatic, and 8 had minor symptoms after a mean ingestion of 23 mg/kg abamectin (4.2 to 67 mg/kg), or after dermal and inhalation contact. Seven patients manifested severe symptoms, such as coma (7), aspiration with respiratory failure (4), and hypotension (3), after a mean ingestion of 100.7 mg/kg avermectin (15.4 mg/kg for ivermectin and 114.9 mg/kg for abamectin). All 7 patients received intensive supportive care; 1 patient died 18 days later as a result of multiple organ failure. CONCLUSION Ingestion of a large dose of avermectin may be associated with life-threatening coma, hypotension, and subsequent aspiration.

Russell's viper snakebite in Taiwan: differences from other Asian countries

Formosan Russells viper (Daboia russelli siamensis) is the sixth most frequent cause of snakebite in Taiwan. Its venom has been thought to have both neurotoxic and hematoxic properties. This vipers snakebite is rare and thus scarcely subjected to systemic studies. In this paper, we retrospectively analyzed and described 18 cases of viper snakebite from 1987 to 1999. Like that of the Russells viper snakebite in other South East Asian areas, varied degrees of acute renal failure, incoagulable blood with bleeding diathesis and hemolysis were the major symptoms found in the systemic envenoming patients. Systemic thrombosis seems to be the distinguishing feature in Formosan Russells viper snakebite. Neither symptoms nor signs of neuromuscular junction blocking effects were observed, which is another difference from symptoms observed after bites of some other Russells viper subspecies, suggesting a significant geographic variation. These findings confirmed the clinical importance of Russells viper snakebite in Taiwan.

The Clinical Significance of Hyperamylasemia in Organophosphate Poisoning

OBJECTIVE Hyperamylasemia with a presumptive diagnosis of acute pancreatitis has been reported following organophosphate poisoning but there are no large-scale studies incorporating more specific diagnostic criteria. METHODS Retrospective review of the medical records of 159 patients with a diagnosis of organophosphate poisoning over 3 years. Serum amylase, pancreatic amylase, salivary amylase, lipase and cholinesterase levels, and the clinical manifestations were analyzed. RESULTS Serum amylase data was available for 121 of the 159 study patients. Hyperamylasemia (amylase > or = 360 U/L) was found in 44 patients (36%). Lipase was measured in 28 patients with hyperamylasemia; 9 of 28 had hyperlipasemia (lipase > or = 380 U/L). The finding of hyperamylasemia was closely related to clinical severity and presence of shock. A presumptive diagnosis of painless acute pancreatitis was diagnosed by hyperlipasemia associated with hyperamylasemia, clinical severity, serum LDH, and leukocyte counts. Two patients with presumptive pancreatitis died. Shock, coma, and hypoalbuminemia were the factors predicting fatality. CONCLUSIONS Hyperamylasemia is frequent in severe organophosphate poisoning. However, hyperamylasemia is not synonymous with acute pancreatitis and pancreatic amylase is not a reliable parameter in the diagnosis of organophosphate-induced pancreatitis due to its low sensitivity and specificity. Lipase assay is indicated in patients with hyperamylasemia for early diagnosis of pancreatitis. Proper image studies and even pathological examination are also needed to confirm the extent of pancreatic injury. With prompt diagnosis and appropriate treatment, a complete recovery can be anticipated unless the patient has otherwise unrelated complications.

Lead, Mercury, and Arsenic Poisoning Due to Topical Use of Traditional Chinese Medicines

BACKGROUND Metal poisonings through a mucocutaneous route are reported rarely in the literature. METHODS We report 2 cases of heavy metal intoxication from inappropriate use of Chinese mineral medicines confirmed by toxicologic investigations. RESULTS A 51-year-old man developed perianal gangrene and a high fever after a 2-week anal use of hong-dan herbal mixtures for anal fistula. He presented gastrointestinal and constitutional symptoms, followed by skin rash, anemia, hair loss, peripheral neuropathy, and muscle atrophy. Elevated urine arsenic and mercury confirmed the heavy metal poisonings. The hong-dan mixture contained lead tetraoxide, arsenic, and mercury. He was treated with 2,3-dimercapto-1-propanesulfonic acid, with partial improvement, but peripheral neuropathy persists 4 years later. A 75-year-old man developed anorexia, weight loss, headache, dizziness, nausea, vomiting, constipation, weakness, and anemia after a 3-month use of an herbal patch for chronic leg ulcer. His blood lead concentration was 226 μg/dL, and the lead content of the herbal patch was 517 mg/g. Chelation with ethylene diamine tetraacetic acid and dimercaptosuccinic acid was followed by clinical recovery. CONCLUSION These cases documented serious systemic poisoning after the short-term use of traditional Chinese medicines containing heavy metals in damaged or infected tissue.

Food Poisoning Due to Methamidophos-Contaminated Vegetables

Background: Organophosphate poisoning is well known for its characteristic symptoms and signs, but food poisoning caused by pesticide-contaminated food is seldom reported. Case Report: We report three incidents of food poisoning that resulted from exposure to the organophosphate insecticide methamidophos in vegetables. These outbreaks caused a cholinergic syndrome in 4 patients. The cholinergic overactivity led us to suspect organophosphate food poisoning. All patients recovered well following appropriate therapy. The clinical diagnosis of organophosphate poisoning was confirmed by reduced levels of erythrocytes and plasma cholinesterase and the presence of methamidophos in the vegetable leftovers. The implicated vegetables and levels of methamidophos were: Ipomoea batatas 255 ppm, Gynura bicolor 110 ppm, and red cabbage 26.3 ppm. Since methamidophos is normally applied to vegetables during planting, improper selection and/or overuse of pesticide or improper harvest times may explain the occurrence of these high residue levels of methamidophos.

Neonicotinoid insecticides: an emerging cause of acute pesticide poisoning

Introduction. Neonicotinoids are a relatively new class of insecticides. They exhibit agonistic effects at postsynaptic nicotinic receptors in insects and are believed to have low toxicity in humans. Methods. We conducted a retrospective analysis of all neonicotinoid exposures reported to the Taiwan National Poison Center to better understand the toxicity profile of neonicotinoid insecticides. Results. A total of 70 patients were analyzed. Most exposures involved suicidal ingestions of imidacloprid alone. Clinical manifestations of neonicotinoid insecticide toxicity bear some resemblance to those of acute nicotine poisoning. Although most exposures were of mild-to-moderate severity, eight patients developed major effects and two died. Aspiration pneumonia and respiratory failure were the main cause of severe toxicity. Conclusion. Significant toxicity of neonicotinoids can occur following large amount of oral ingestion. Poisoned patients may present with cholinergic syndrome, and judicious use of atropine seems justified. Symptomatic treatment, especially ventilator support, remains most important in clinical management.

Acute human Glufosinate-containing herbicide poisoning

Abstract Background. Glufosinate-containing herbicides are commonly used worldwide. Data on acute human glufosinate poisoning however remain scarce. Methods. We retrospectively reviewed the medical records of all glufosinate poisoned cases reported to the Taiwan National Poison Control Center and two medical centers in Taiwan from August 1993 through February 2010. Their demographic and clinical data were then analyzed to identify potential predictors of severe effects following acute glufosinate poisoning. Results. One hundred and thirty-one patients, including 115 oral and 16 non-oral exposures, were eligible for final analysis. Among patients with oral exposure, 25 were asymptomatic, while the others developed gastrointestinal, neurological, cardiovascular, and/or respiratory manifestations. Seven patients (6.1%) died following deliberate glufosinate ingestion. The median dose of glufosinate ingestion was 30.4 grams (interquartile range 18.5–45.6 grams) in the severe/fatal group compared to 6.8 grams (interquartile range 3.7–16.2 grams) in the non-severe group (p <0.001). Older age (≥61 years; adjusted OR 4.9, 95% CI 1.3–17.9) and larger amount of glufosinate ingestion (≥13.9 grams; adjusted OR 25.2, 95% CI 4.8–132.5) were positively associated with the development of severe toxicity, whereas ethanol consumption (adjusted OR 0.1, 95% CI <0.1–0.5) was inversely associated with the risk of severe toxicity. Conclusion. Although glufosinate is generally thought to be of low toxicity to humans, severe effects can occur and may be associated with older age, larger amount of ingestion and absence of concomitant ethanol consumption.

Acute Severe Chromium Poisoning After Dermal Exposure to Hexavalent Chromium

Severe acute chromium poisoning related to dermal involvement has rarely been reported in the literature. We report a case of acute severe chromium poisoning through skin exposure as a result of a chemical burn of 15% of the body surface area and multiple organ failure after short-term exposure. Medical interventions, including mechanical ventilation, continuous venovenous hemofiltration, and plasmapheresis were performed. In addition, a chelating agent, dimercaptopropane sulfonic acid, was infused intravenously, combined with intravenous N-acetylcysteine and ascorbic acid as adjuvant therapy. The patient was discharged on day 33 without long-term sequelae. The consequence of transdermal exposure of hexavalent chromium should not be overlooked.

Survival after hypocalcemia, hypomagnesemia, hypokalemia and cardiac arrest following mild hydrofluoric acid burn

Background. Although hydrofluoric (HF) acid burns may cause extensive tissue damage, severe systemic toxicity is not common after mild dermal exposure. Case. A 36-year-old worker suffered a first-degree burn of 3% of his total body surface area as a result of being splashed on the right thigh with 20% HF acid. Immediate irrigation and topical use of calcium gluconate gel prevented local injury. However, the patient developed hypocalcemia and hypomagnesemia, hypokalemia, bradycardia, and eventually had asystole at 16 h post-exposure, which were unusual findings. He was successfully resuscitated by administration of calcium, magnesium, and potassium. Conclusion. This report highlights a late risk of HF acid dermal exposure.

Acute Cycas Seed Poisoning in Taiwan

Objective: The seeds of cycads contain cycasin and neocycasin, which belong to the family of cyanogenic glycosides. These glycosides of cycads are considered pseudocyanogenic with little potential to liberate hydrogen cyanide as other cyanogenic glycosides do. This study investigated the clinical spectrum of Cycas seed poisoning and its cyanogenic potential. Methods: This was a retrospective chart review conducted at the Poison Control Center in Taiwan (PCC‐Taiwan) from 1990 to 2001. Results: Twenty‐one cases of Cycas seed poisoning were identified. The reasons for seed ingestion were misuse as an edible food (70%), health promotion (10%), cancer prevention (10%), cosmetic use (5%), and gastrointestinal discomfort (5%). All patients had eaten the seeds after washing and cooking them. The time from ingestion to the onset of symptoms ranged from 30 min to 7h (mean 2.8h); patients had ingested between 1 to 30 seeds. Respiratory depression did not occur. Severe vomiting was the most striking symptom. All patients except one presented with gastrointestinal disturbance, and 90% sought medical care at the emergency department. Within 24h, all patients had recovered. Six patients had blood cya nide or thiocyanate levels measured. Although the levels were higher than normal, they did not reach the toxic range. Conclusions: The cyanogenic potential of Cycas seeds is documented in our cases. The gastrointestinal symptoms were severe enough that most patients sought medical attention but recovery was quick and complete.