Acute human glufosinate-containing herbicide poisoning.

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 hemolysis following iodine tincture ingestion.

Iodine tincture poisoning is uncommon regardless of its widespread use as an antiseptic in daily practice. Previously reported effects of iodine-containing antiseptic poisoning included topical irritation, corrosive effects, allergic response, and hepatic or renal injury, which mainly resulted from complications of topical use during surgical procedures. We herein reported an unusual case of severe hemolysis and acute renal failure following intentional ingestion of iodine tincture containing 60 mg/ml iodine and 40 mg/ml potassium iodide in 70% v/v ethanol. The patient completely recovered 8 weeks later after receiving supportive treatment, plasma exchange, and temporary hemodialysis.

Tetramethylammonium hydroxide poisoning.

INTRODUCTION: Tetramethylammonium hydroxide (TMAH) is widely used as a developer or etchant in semiconductor and photoelectric industries. In addition to alkalinity-related chemical burn, dermal exposure to TMAH may also result in respiratory failure and/or sudden death. The latter toxic effect has been of great concern in Taiwan after the occurrence of three fatalities in recent years. To better understand the toxicity following dermal exposure to TMAH, we analyzed all cases with TMAH exposure reported to the Taiwan Poison Control Center (PCC-Taiwan). CASE REPORTS: In total, there were 13 cases of such exposure, including three patients who died after being exposed to 25% TMAH. A worker also developed severe effects manifesting muscle weakness, dyspnea, hyperglycemia, and chemical burn (28% of total body surface area) shortly after an accidental exposure to 2.38% TMAH. He received endotracheal intubation with assisted ventilation for 2 days and survived. CONCLUSION: Skin corrosive injury related to the alkalinity of TMAH and the ganglionic toxicity of tetramethylammonium ion might contribute to the clinical manifestations that occurred after dermal TMAH exposure. Thorough skin decontamination followed by prompt respiratory support should be the mainstay in the management of dermal TMAH exposure. Preventive strategies are warranted as well to decrease future occupational TMAH exposures.

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.

Why can Taiwan utilize criminal law to discipline physicians?

Modern medicine was first introduced into Taiwan by missionary hospitals in 1865. However, Japanese governors following Japan's medical reform applied modern medicine as the standard of practice in the year 1896. They also imported 150 doctors from Japan to promote public hygiene and control infectious diseases, such as malaria, plague, cholera, dysentery, etc. The reasons that the Courts started to use criminal law to deal with medical malpractice during 1950-1960s may be attributed to the following: costly and ineffective civil actions, chaotic medical licensing, a period of upheaval during the 1947 massacre (228 incident), Chinese Civil War (1947-1949), political unrest, "White Terror" and "Espionage Act" during the period of martial law (1949-1987), social injustice and economic depression. The general environment for medical practice in Taiwan has changed greatly in the past 60years. It is time for us to look around the world to set up standards of negligence for both clinical and criminal cases as soon as possible. In the mean time, the Department of Health should consider adopting the Good Medical Practice guidelines from the United Kingdom to strengthen the administrative power to regulate physicians' behaviors.

Human Melia azedarach poisoning.

INTRODUCTION: In traditional Chinese medicine, Melia azedarach (Ku-lian) is used orally and topically as an antiparasitic and antifungal agent. Although toxicity of this plant has been widely described in veterinary literature, human poisoning is rarely reported. We describe five patients with M. azedarach poisoning who recovered with supportive care. CASE SERIES: Five patients were identified retrospectively from the database of the Taiwan National Poison Center at the Taipei Veterans General Hospital. Three cases were on-site patients, and two were telephone consultations from outside hospitals. Neurological symptoms were the major manifestation in four cases: weakness, myalgia, numbness, and ptosis. Treatment was symptomatic and supportive; all patients recovered without sequelae. DISCUSSION: It is not known which limonoids are responsible for human toxicity. In the Chinese medical literature, human M. azedarach poisoning is said to occur if six to nine fruits, 30 to 40 seeds, or 400 g of the bark is consumed. Onset of symptoms typically occurs within 4-6 h, but as short as 0.5 h had been documented. In our patients, the onset of M. azedarach poisoning was variable, ranging from a few hours to up to 3 weeks after consumption of the herb. CONCLUSIONS: M. azedarach poisoning may result in gastrointestinal, cardiovascular, respiratory, or neurological effects, and death in severe cases.

Formic acid: a rare but deadly source of carbon monoxide poisoning.

INTRODUCTION: Formic acid decomposes upon contact with strong acids producing carbon monoxide. Carbon monoxide poisoning from such a source, however, is extremely rare. CASE REPORT: A 26-year-old man committed suicide by mixing 2.5 L of formic acid and 2.5 L of sulfuric acid in three beakers and staying in a closed room. The 53-year-old father performed cardiopulmonary resuscitation on his son but soon lost consciousness. In hospital, he initially manifested coma, hypoxemia, metabolic acidosis, and a carboxyhemoglobin level of 45.8%. He was treated with hyperbaric oxygen but developed acute respiratory distress syndrome on day four despite an early improvement. He was successfully weaned from the ventilator on day 8. The 53-year-old mother felt dizziness, headache and had a carboxyhemoglobin level of 23.0%. Her symptoms improved after oxygen therapy. DISCUSSION AND CONCLUSIONS: Formic acid is a highly fatal source of carbon monoxide poisoning when mixed with sulfuric acid. In addition to the toxicities of carbon monoxide, concomitant inhalation of formic acid fumes can cause severe lung injury, which may complicate the management of carbon monoxide poisoning.

Acute hepatic injury and renal failure after ingestion of snake gallbladder.

Ingestion of snake gallbladder has been practiced in ancient Chinese civilizations to improve vision and relieve arthritic pain. Although little is known about the composition of snake gallbladder, ingestion is still practiced in some Chinese cultures. Adverse effects of ingesting snake gallbladder have not yet been reported. Here, we present a case of acute hepatic injury and delayed-onset renal failure after ingestion of snake gallbladders. The patient subsequently recovered after supportive care, combined with plasma exchange and hemodialysis. He was the only survivor of the four victims suffering from intoxication of snake gallbladder in the last three years in our hospital.

Clinical experience of acute ferric chloride poisoning.

Ferric chloride is both a corrosive acid and iron compound; reports of poisoning in humans are rare. A retrospective study was conducted to evaluate patients with ferric chloride exposure reported to Poison Control Center-Taipei Veterans General Hospital during 1990-2001. After exclusion of incomplete records, 16 patients with ferric chloride exposure were analyzed (9 male, 7 female aged 12 to 70 y). The exposures were occupational inhalation (18.7%), suicidal ingestion (56.3%), and accidental ingestion (25.0%). Major symptoms and signs were nausea/vomiting (68.8%), sore throat (68.8%), abdominal pain (37.5%), oral ulcers (37.5%), metabolic acidosis (25.0%), aspiration pneumonia (18.8%), respiratory failure (12.5%), diarrhea (12.5%), and hypotension (12.5%). The severity of poisonings were fatal 6.3%, severe 18.8%, moderate 31.2%, mild 37.5%, and asymptomatic 6.3%. Deferoxamine therapy was given in 9 hospitalized patients with good recovery; however the fatal case did not receive deferoxamine due to rapid deterioration and a late diagnosis. The serum iron level known in 7 cases ranged from 40 to 2440 microg/dL. Ingestion of ferric chloride may result in serious morbidity and mortality. Inappropriate labeling and storage lead to accidental swallowing or misdiagnosis. Early diagnosis is important, especially in seriously poisoned patients.