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.

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.