Deng Jf

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 hydrofluoric acid exposure reported to Taiwan Poison Control Center, 1991–2010:

Background: Hydrofluoric acid (HF) is a dangerous chemical that can cause severe cutaneous burns as well as possible systemic toxicity. Methods: We retrospectively analyzed all human HF exposure cases reported to the National Poison Control Center of Taiwan between 1991 and 2010. Results: In this 20-year survey, 324 calls were identified, with a majority of dermal exposure (84%). Occupational exposure accounted for 80% of all cases, with workers in semiconductor industry (61%), cleaning industry (15%), chemical or metal industry (13%), and other industries (11%). Electrolyte imbalances were uncommon, hypocalcemia, hypomagnesemia, and hypokalemia were recorded in 8.6%, 1.2%, and 1.5% of all cases, respectively. Most cases (64%) of dermal exposure received antidotal treatment. Treatment modalities of dermal exposure included calcium gluconate soaking, 49.8%; intravenous calcium, 20.6%; and topical use of calcium gluconate gel, 13.9%. Twenty patients (7%) received surgery. Following HF exposure, the majority of patients presented with mild (56.5%) or moderate (36.7%) toxic effects. However, four patients were severely intoxicated; two patients died of HF-related dysrhythmia and shock. Conclusions: Significant symptomology may occur following HF exposure, and most of the HF exposure required hospitals evaluation. Calcium gluconate soaks appear to be effective in reducing local pain and tissue damage. Hyperkalemia should not be overemphasized as a common finding in HF exposure, hypokalemia tends to occur in cases of severe HF poisoning.

Methomyl-alphamethrin poisoning presented with cholinergic crisis, cortical blindness, and delayed peripheral neuropathy.

Objective. Methomyl–alphamethrin is a mixture of carbamate and pyrethroid insecticides. Carbamate insecticides function as reversible cholinesterase inhibitors, which may produce life-threatening cholinergic syndrome. Cortical blindness and delayed neuropathy were rarely reported complications of carbamate insecticide exposures. Here we reported a case of intentional methomyl–alphamethrin ingestion. Case report. A 41-year-old woman attempted suicide by drinking 200 mL of methomyl–alphamethrin insecticide and soon presented with unconsciousness, hypothermia, and shock. She developed pulseless electrical activity and regained spontaneous circulation after resuscitation. Diagnosis of carbamate poisoning was made by her clinical features, decreased levels of cholinesterases and the presence of methomyl in her urine. She complained of blurred vision and blindness 4 days post-exposure. Visual evoked potential and brain magnetic resonance imaging study confirmed the diagnosis of cortical blindness. On day 21, she had low limbs numbness, progressive weakness, and right foot drop. Electophysiological tests performed on day 27 revealed neuropathy of bilateral peroneal nerves. Conclusion. We reported a patient who manifested severe carbamate insecticide poisoning and developed cortical blindness and delayed neuropathy. Physicians should be aware of these rare toxicities among patients with severe carbamate insecticide poisoning.

Utility of flumazenil in zopiclone overdose

DMPS (2,3-dimercapto-1-propanesulfonic acid) 250 mg IV every 8 h was prescribed, and hemodialysis was performed once to enhance the excretion of the complex of metal and chelating agent. The patient’s urine output increased progressively, and his renal function returned to normal on the second day. After 6 days of DMPS treatment, the patient’s creatinine clearance was 99.4 mL/min. The total amount of arsenic excreted in urine was 156 mg. A minimal skin rash was noted, which was controlled with antihistamine during the course of DMPS therapy. Realgar, as a traditional medicine, has been widely used orally and appears to be less toxic than arsenic trioxide. In Chinese medicine, realgar is suggested to be used clinically after a refining procedure (1). Unrefined realgar mineral contains appreciable amounts of other more toxic arsenic forms, such as arsenic trioxide and calcium or magnesium arsenite. The purity of As4S4, the principle ingredient of natural realgar mineral, might explain the possible diverse uses. In conclusion, realgar mineral can induce severe arsenic intoxication resulting from possible blending of toxic arsenics. Realgar wine should not be used as an oral medication until it is proved to be safe or free from other toxic arsenic species.