Jou-Fang Deng

Bromadiolone, a potent, long-acting anticoagulant rodenticide is frequently tinted to a red or pink color and mixed with cereals as rat bait. Six peoples working in a small factory suffered from a severe bleeding tendency several weeks after consuming a rice meal that was tainted with bromadiolone mistaken to be healthy food. High serum levels of bromadiolone and excessive bleeding were found in these individuals, and they needed vitamin K1 therapy for weeks. These cases indicated that long-acting anticoagulant rodenticide might induce cumulative toxicity in repeated, low-dose exposure, and the blood levels of bromadiolone might be an indicator for antidote therapy if available.

Background: Tetramethylammonium hydroxide (TMAH) is a quaternary ammonium compound that is both a base corrosive and a cholinergic agonist, and it is widely used in the photoelectric and semiconductor industries. It causes corrosive skin injuries and systemic cholinergic toxicity with death primarily resulting from respiratory failure without efficacious early decontamination. Methods: A retrospective observational study was performed of all cases of TMAH exposure reported to the Taiwan Poison Control Center between July 2010 and October 2017. Retrieved medical records were independently reviewed by two trained clinical toxicologists. Results: Despite immediate (< 5 min) skin decontamination with copious amounts of tap water, one patient exposed to 25% TMAH involving ≥5% of total body surface area (TBSA) developed significant systemic toxicity. Patients exposed to 25% TMAH involving ≤1% TBSA developed first-degree chemical skin injuries but no systemic toxicity. Among patients exposed to lower concentrations (≤2.38%) of TMAH, the majority only experienced first-degree chemical skin injuries without systemic signs. Patients exposed to 0.5% TMAH involving nearly their entire TBSA developed no chemical skin injuries or systemic toxicity. All patients who had only first-degree chemical skin injuries did not develop systemic toxicity after exposure to either 2.38% or 25% TMAH. Conclusions: TMAH acts as an alkaline corrosive and cholinergic agonist. Systemic signs attributable to TMA⁺ can rapidly lead to respiratory failure and death after dermal exposure. We have demonstrated that an amphoteric solution may be efficacious for skin decontamination on-site immediately to prevent or ameliorate such toxicity. This practice especially carries a valuable potential in managing victims (patients) who have been exposed to those chemicals with immediate life-threatening toxicity (e.g. TMAH), suggesting that its early utilization deserves further study.

Background. Realgar (arsenic sulfide) is thought to be safe with few reports on toxicities or adverse effects and has been used in Traditional Chinese Medicine for many centuries. Serious realgar poisoning is rare, and we report a fatal case resulted from short-term use of realgar-containing herbal medicine through dermal route. Case details. A 24-year-old man with atopic dermatitis had received 18 days of oral herbal medicine and realgar-containing herbal ointments over whole body from a Traditional Chinese Medicine (TCM) practitioner. Seven days after the herbal use, he had diminished appetite, dizziness, abdomen discomfort, itching rash, and skin scaling. He later developed generalized edema, nausea, vomiting, decreased urine amount, diarrhea, vesico-edematous exanthems, malodorous perspiration, fever, and shortness of breath. He was taken to the hospital on Day 19 when the dyspnea became worse. Toxic epidermal necrolysis complicated with soft tissue infection and sepsis was noted, and he later died of septic shock and multiple organ failure. The post-mortem blood arsenic level was 1225 μg/L. Herbal analysis yielded a very high concentration of arsenic in three unlabeled realgar-containing ointments (45427, 5512, and 4229 ppm). Conclusion. Realgar-containing herbal remedy may cause severe cutaneous adverse reactions. The arsenic in realgar can be absorbed systemically from repeated application to non-intact skin and thus should not be extensively used on compromised skin.

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.

Both moclobemide and fluoxetine are used in the treatment of depression, and have been shown to produce fewer side effects than conventional tricyclic antidepressants. A combination of moclobemide and fluoxetine has been used in refractory depression, however there is potential for severe serotonin toxicity. We describe a lethal case of serotonin toxicity in a 36 year-old woman after she ingested multiple drugs, including moclobemide 4500 mg, fluoxetine 200 mg, propranolol 300 mg and several benzodiazepines. The clinical features included coma, mydriasis, hyperthermia, tremor, hyperreflexia, rhabdomyolysis, renal failure and respiratory insufficiency. Eventually, the patient died of disseminated intravascular coagulation and circulatory collapse at 22.5 h postingestion. Toxicological analysis of the patient's blood confirmed high levels of moclobemide 150 μg/mL (therapeutic 1-3 μg/mL), fluoxetine 3750 ng/mL (therapeutic 47-469 ng/mL) and several benzodiazepines. In conclusion, a combination of moclobemide and fluoxetine should be avoided in depressed patients with high suicidal tendencies. Moreover, early recognition and aggressive intervention are the mainstays in the management of potentially life-threatening serotonin toxicity.

Acute pancreatitis is a potentially fatal disease with no known cure. The initial events in acute pancreatitis may occur within the acinar cells. We examined the effect of sesamol on (i) a cerulein-induced pancreatic acinar cancer cell line, AR42J, and (ii) cerulein-induced experimental acute pancreatitis in rats. Sesamol inhibited amylase activity and increased cell survival. It also inhibited medium lipid peroxidation and 8-hydroxydeoxyguanosine in AR42J cells compared with the cerulein-alone groups. In addition, in cerulein-treated rats, sesamol inhibited serum amylase and lipase levels, pancreatic edema, and lipid peroxidation, but it increased pancreatic glutathione and nitric oxide levels. Thus, we hypothesize that sesamol attenuates cerulein-induced experimental acute pancreatitis by inhibiting the pancreatic acinar cell death associated with oxidative stress in rats.

Objective. To describe the toxidromes associated with plant poisonings in Taiwan. Methods. Retrospective review of acute single-plant exposures with clinical signs and symptoms reported between January 1987 and December 2006 by hospitals to the network of Taiwan Poison Control Centers. Recorded data included demographic data, intent of exposures, exposure routes, clinical findings, and therapeutic strategies. Results. There were 389 cases that met the criteria. Each case was placed into one of the expected toxidromes: anticholinergic, mucosal inflammation, gastroenteritis, acute multisystem organ failure, delayed multisystem organ failure, cholinergic, cardiac dysrhythmia, hepatotoxicity, dermatitis, seizures, and dyspnea. Anticholinergic poisoning was the most common toxidrome. Conclusion. Plant poisonings can be classified into recognizable toxicologic syndromes. These toxidromes may guide a clinician's evaluation and management before a botanist can confirm the actual plant identity.