Organophosphate (OP) pesticides are the most common source of human toxicity globally, causing high mortality and morbidity despite the availability of atropine as a specific antidote and oximes to reactivate acetylcholinesterase. The primary toxicity mechanism is inhibition of acetylcholinesterase (AchE), resulting in accumulation of the neurotransmitter, acetylcholine, and abnormal stimulation of acetylcholine receptors. Thus, the symptoms (muscarinic, nicotinic, and central nervous system) result from cholinergic overactivity because of AchE inhibition. OP can also cause rhabdomyolysis, pancreatitis, parotitis, and hepatitis. OP therapy includes decontamination, supportive therapy, and the use of specific antidotes such as atropine and oximes. However, there has been a paucity of controlled trials in humans. Here we evaluated the literature for advances in therapeutic strategies for acute OP poisoning over the last 10 years.

Purpose: The hypnotic effect of zolpidem is comparable to benzodiazepines, but has less abuse and addiction potential than benzodiazepines, so is one of the most commonly prescribed hypnotics. The frequency of acute zolpidem overdose has increased, but clinical analysis and severity predictors are not known in Korea. Methods: A retrospective evaluation of histories, clinical courses, and laboratory findings of each patient treated from June, 2000, to May, 2006, in a university hospital for acute zolpidem intoxication. Results: We evaluated 30 patients, including 16 co-intoxication cases. Twenty-five patients presented mental alterations but became alert within 2 days. All patients recovered completely. The median zolpidem concentration was 0.9 mg/L (range: $0.2{\sim}7.4\;mg/L$). There was a weak correlation between the amount ingested and zolpidem concentration (r=0.25). None of them presented severe laboratory abnormalities, and these abnormalities did not relate to zolpidem concentration. Conclusion: The clinical progress of acute zolpidem intoxication is mild. We could not predict zolpidem concentration or clinical severity from the amount ingested and could not predict the clinical course from laboratory findings in the emergency department.

Purpose: Chlorine gas is a common irritant that usually causes mild respiratory symptoms. One severe symptom, RADS (Reactive Airway Dysfunction Syndrome), is not well known to physicians. We analyzed the clinical features of chlorine gas exposure. Methods: We prospectively collected 25 cases of chlorine gas exposure near our emergency center on January 10th, 2007, and analyzed demographic data, event-to-ER interval, symptoms, and laboratory results based on medical records. Results: Only 2 patients out of 25 were admitted because of severe symptoms, the rest were discharged without complications. Sixty percent of them visited the ER within 12 h of exposure. The most common symptoms were chest discomfort (60%), headache (40%), nausea (40%), throat irritation (26%), and cough (32%). Two out of eight dyspnea cases showed abnormal pulmonary function, but only one case was diagnosed as RADS. Conclusion: Most symptoms after chlorine gas exposure can be treated conservatively. However, patients with chlorine exposure should be followed up long term for delayed complications.

Purpose: Unrefined tablets prepared from Aconitum tubers are occasionally used in Korean folk medicine. This study defines the potential sources, clinical toxicology, and treatment of aconitine poisoning. Methods: A retrospective survey was conducted in 63 patients in the ED of a tertiary University Hospital with suspected toxicity from an unrefined tablet prepared from Aconitum tubers from 1999 to 2007. Results: A total of 63 cases enrolled included 26 men and 37 women, aged 30 to 86 years. Forty-eight patients ingested aconitine tablets as digestives, 26 tablets on average. After a latent period of 30 to 450 minutes, patients developed a combination of neurologic (87.3%), gastrointestinal (82.5%), cardiopulmonary (41.3%), and other (28.6%) features typical of aconitine poisoning. Initial ECG abnormalities revealed dysrhythmia (61.9%), conduction disturbance (42.9%), and abnormal waveforms (39.7%), with 28.6% of patients having normal ECGs. All patients received supportive treatment or close observation regardless of ingestion amounts. Patients with hypotension or ventricular arrhythmia were treated with inotropic agents or amiodarone. Conclusion: Toxicologic signs and symptoms can occur after the consumption of aconitine tablets, regardless of ingestion amount. The risk occurs because of inadequately processed aconitine roots. This study will provide important data for public education and distribution regulations for Aconitum sp. in Korea.

Purpose: Acute toxic hepatitis is a common cause of acute liver failure (ALF). We investigated the causes, clinical manifestation, and outcomes of ALF patients who underwent liver transplantation due to acute toxic hepatitis caused by herbal medicines and preparations. Methods: Between January 1992 and May 2008, we retrospectively reviewed the medical records of 24 patients who were transplanted due to acute toxic hepatitis caused by herbal medicines and preparations. We applied the RUCAM score to patients with acute toxic hepatitis and assessed the relationship between herbal preparations and liver injury. We studied the patients' medication history, liver function tests, and clinical outcomes. Results: The type of liver injury was divided into three groups: hepatocellular type, 14 patients (58.3%); cholestatic type, 4 patients (16.7%); and mixed type, 6 patients (25%). Polygonum multiflorum Thunberg (3 cases) was the most common cause of acute toxic hepatitis, followed by Acanthopanax senticosus (2 cases), pumpkin juice (2 cases), Dictamnus dasycarpus Turcz (2 cases), Hovenia dulcis (1 case), Phellinus linteus (1 case), and Artemisia capillaries (1 case). One year survival after liver transplantation was 76%. Conclusion: We identified the herbal preparations leading to acute liver failure. Many patients consider herbal remedies to be completely free of unwanted side effects. However, we found that many herbal products have biological activities that can lead to severe hepatotoxicity.

Purpose: Surveys on poisoning usually involves intoxication rather than inhalation, skin contact, etc. Therefore, we examined the characteristics of patients who visited the emergency department in an industrial complex after acute industrial exposure to toxic materials. Methods: Medical records of patients exposed to toxic materials in the work places from April, 2006, to March, 2008, were analyzed retrospectively. Inhalation patients due to fire were excluded. Results: Subjects included 66 patients, with a mean age of $35.4{\pm}10.9$ years, mostly men (91%). Toxicity occurred in 51 patients (77%) by contact, 15 patients (23%) by inhalation, and none by oral ingestion. For toxic materials, 10 patients were exposed to hydrofluoric acid, 8 to hydrochloric acid, 7 to sodium hydroxide, 7 to metals, and others. The face and hands were the most frequent exposure site by contact. Most exposures were caused by accidents, with 29 cases (42%) exposed because of carelessness or not wearing protective equipment. Most complaints were pain on exposure site, but 7 of the inhalation patients complained of dyspnea. The majority of patients with contact exposure were discharged after wound care or observation. After inhalation exposure, 1 patient died and 5 patients were admitted to the intensive care unit. Conclusion: Major causes of workplace exposure were not wearing protective equipment or carelessness. Although contact exposures are usually benign, cautious observation and management are required in patients with inhalation exposure.

A 36-year-old female was transferred to our emergency medical center with decreased mental status after a 6.0 g propafenone overdose because of domestic disturbance. She had no previous history of epilepsy, diabetes mellitus, hypertension or psychiatric illness. Before presenting to our center, gastrointestinal decontamination, charcoal administration, and endotracheal intubation due to bradycardia and generalized seizure had been performed. Soon after hospital arrival, at 5 h after ingestion, she collapsed into shock and fatal arrhythmia. We successfully resuscitated the patient with amiodarone, sodium bicarbonate, a large volume of normal saline, calcium, and ventilator care. At 23 h after ingestion, she was fully recovered and had no subjective signs or symptoms. To our knowledge, this is the first case report of intentional propafenone overdose in Korea, which we report with reviews of the previous literature.

In South Korea, attempted suicide by paraquat (PQ) intoxication is fairly common, and is lethal by pulmonary fibrosis and hypoxemia. However, the treatment of PQ poisoning is primarily supportive management. To increase the survival rate associated with PQ intoxication, many treatments have been developed. Here, we treated a case of PQ intoxication with steroid pulse therapy. A 23-year-old man was admitted to the hospital because of PQ intoxication. He drank two mouthfuls of Gramoxon (24% commercial paraquat). His vital signs were stable, but he had a throat infection, and navy blue urine in the sodium dithionite test. Standard treatment, including gastric lavage with activated charcoal was performed, and emergent hemoperfusion with a charcoal filter was initiated 11 h after PQ ingestion. Pharmacotherapy was initiated 18 h after PQ ingestion with the administration of 5 mg dexamethasone. On day 10, chest PA showed pulmonary fibrosis. Therefore, we initiated steroid pulse therapy, with 1g methylprednisolone in 100 mL of D5W administered over 1 h repeated daily for 3 days, and 1 g cyclophosphamide in 100 mL of D5W administered over 1 h daily for 2 days. On day 15, dexamethasone therapy was initiated. On day 30, pulmonary fibrosis was improved. Thus, if pulmonary fibrosis becomes exacerbated after dexamethasone therapy during the subacute stage, pulse therapy with methylprednisolone and cyclophosphamide could be helpful.

Methylene blue is the first choice for treating methemoglobinemia, any increase in normal methemoglobin levels. Methemoglobin is an abnormal hemoglobin in which the iron has been oxidized to the ferric(+3) state, making it incapable of oxygen transport. Methemoglobinemia most commonly results from exposure to oxidizing chemicals, but may also arise form genetic, dietary, or even idiopathic etiologies. Patients with low methemoglobin levels are asymptomatic, but high methemoglobin levels can lead to headaches or even death. Methylene blue, the first-line treatment for methemoglobinemia, can also produce hemolytic anemia. Jaundice or dark urine during methylene blue treatment may indicate hemolytic anemia. A 47-year-old female patient with a history of depressive mood disorder developed significant methemoglobinemia after ingesting a Propanil overdose. Twenty-two hours after ingestion, methemoglobin levels in the blood were 73.2%. She was treated with intravenous methylene blue in the therapeutic range (1 mg/kg every 4 h for 3days). The 2nd day after methylene blue use, methemoglobin levels in the blood were 33%, and the 5th day decreased to 10% with better general condition. The patient had hyperbilirubinemia after hemolytic anemia, but she recovered completely.

A 47-year-old woman ingested about 12 mg of colchicine with suicidal intent. Colchicine, a highly poisonous alkaloid, is a commonly used treatment for gout, Bechet's disease, and familial Mediterranean fever. Despite the knowledge of its side effects, the risk of a significant overdose is under-appreciated. She suffered from acute multisystem toxicity, including gastrointestinal disorders, bone marrow suppression, alopecia, and probable pancreatitis, but she ultimately recovered with supportive therapy. We report a case of acute colchicine toxicity from a single overdose with a review of the literature.

Lamotrigine is a newer anti-epileptic drug for adjunctive treatment of refractory epilepsy, partial seizures, generalized tonic-clonic seizures, and bipolar disorder. Lamotrigine overdose causes serious central nervous and cardiovascular problems, but reports are uncommon. Few lamotrigine overdoses have been described because anti-epileptic drug use is limited and usually used with combination of other anti-epileptic drugs. In addition, most patients visit emergency departments with multi-drug overdoses, so few cases of lamotrigine poisoning alone exist. We had a female patient visit our emergency department a couple of hours after a lamotrigine overdose treated with intravenous hydration and urine alkalization by NaHCO3. She recovered successfully without any evidence of renal injury. However, she developed profound rhabdomyolysis, a previously unreported complication of this medication. We suggest that serial creatine kinase levels should be measured after lamotrigine poisoning.

Phytolacca americana poisoning is a benign plant intoxication that causes gastrointestinal symptoms, including abdominal cramps, vomiting, diarrhea, and gastrointestinal bleeding. Other signs and symptoms include diaphoresis, salivation, visual disturbance, and seizures or mental changes. We report two cases of patients who experienced confusion and abdominal pain, vomiting, and hematemesis after oral ingestion of pokeweed. A 60-year-old female with confusion and a 67-year-old female with abdominal pain, vomiting, and diarrhea were admitted to the emergency department after pokeweed poisoning. After supportive treatment of hydration and gastrointestinal medication, the two patients showed full recovery within 24 h and were discharged from the hospital.