Purpose: In many Korean hospitals, serum acetaminophen concentrations in cases of overdose cannot be measured initially because of inadequate laboratory facilities. Under these circumstances, physicians base the administration of the antidote, N-acetylcysteine, on ingestion amounts as determined by initial history taking. We therefore examined the correlated between ingested amounts and serum acetaminophen concentrations. Methods: Medical records were reviewed retrospectively for patients who presented to the ED with acetaminophen overdose between January 2002 and March 2006. Fifty-nine patients were recruited and sixteen patients were excluded. The forty-three remaining patients were placed into either the high-risk or low-risk group based on their ingested amount (140 mg/kg), and were separately categorized into the toxic or non-toxic group based on their serum acetaminophen concentrations, according to the Rurnack-Matthew nomogram. Results: Ten patients (83.3%) among twelve in the high-risk group were found to have non-toxic serum concentrations, and just one patient (3.2%) among thirty-one in the low-risk group fell into the toxic group based on their serum concentrations. The sensitivity and specificity of risk stratification of the ingested amount as a predictor of intoxication requiring antidote therapy were 66.7% and 75.0%, respectively. Conclusion: This study suggests that the therapeutic decision for acetaminophen overdose should not be based solely on ingested amount only, but requires assessment of acetaminophen concentration.

Purpose: Previous studies have reported that plasma cholinesterase (AchE) concentration can serve as a useful prognostic parameter in cases of acute organophosphate (OP) poisoning. However, there has been considerable disagreement regarding the degree of its prognostic value. Earlier cross-sectional and one- time point studies were plagued with methodologic flaws, making it difficult to interpret their results. The purpose of this study was to clarify the prognostic value of time-variable cholinesterase levels and their relationship with clinical outcomes in OP poisoning. Methods: We reviewed medical and intensive care records of patients with acute OP poisoning admitted to our emergency department between March 1998 and Sep 2006. We collected patient information regarding poisoning, clinical, and demographic features. Patients were assessed for clinical outcomes and AchE concentrations on days 1, 2, 3, 5, and 7 and on the final day. Results: During the study period, 58 patients were enrolled in this study. There was a statistically significant difference in the AchE differentials on 1-3 days for patients requiring mechanical ventilation and for patients with mild poisoning (p<0.05). Also, the decrease in the log AchE concentration correlated with longer durations of mechanical ventilation (r=-0.411, p=0.002). Conclusion: In severe OP poising, measurements of time-variable AchE concentrations can be helpful in the prediction of mortality, the development of intermediate syndrome, and duration of mechanical ventilation.

Purpose: It is not easy to detect carbon monoxide (CO) leakage, and CO-intoxicated patients do not show a specific set of symptoms. The aims of this study are to clinically evaluate patients with CO gas intoxication from a CO leak at an underground shopping center, and to discuss the establishment of a disaster prevention plan. Methods: A total of 51 patients intoxicated by CO gas exposure in a gas disaster at a underground shopping center in Seoul on September 8, 2006 were enrolled in this study, and the patients' medical records were retrospectively reviewed. Results: The mean patient age was $29.4{\pm}6.3$. The initial mean COHb level was $14.98{\pm}6.97%$. The number of patients with COHb greater than 25% was three, and six patients experienced a syncopal attack. Only one patient-was treated with hyperbaric oxygen therapy. However, none of the patients complained of severe neurologic or cardiovascular symptoms. Conclusion: The symptoms of CO intoxication are non-specific and difficult to define, and the detection of CO leak-age is difficult. Thus, workplaces should be equipped with leakage sensors and automatic alarm systems and should have develop disaster prevention plans.

Phenytoin has been used globally as an effective anticonvulsant. Among its adverse effects, peripheral neuropathy including polyneuropathy has sometimes been reported. We report a case of sensorimotor polyneuropathy associated with high serum level and long-term phenytoin therapy. A 29-year-old male presented with motor weakness in all extremities. He was treated with phenytoin (400 mg/day) for about eight years because of generalized tonic clonic seizure. During none conduction assessment, sensorimotor polyneuropathy was discovered.

Metronidazole is an antimicrobial drug widely used against various types of infectious agents, including protozoa, amoeba, Helicobacter pylori, and anaerobes. Metronidazole may produce some adverse effects on hematologic, immunologic, neurologic and other systems. We report a case of reversible metronidazole-induced encephalopathy. The toxic dose of metronidazole and the onset of encephalopathy were variable. Two patients showed abnormally high signal intensity in the bilateral dentate nucleus of cerebellum, and characteristic abnormalities were detected by brain magnetic resonance imaging (MRI) and T2-weighted images, fluid-attenuated inversion recovery images and/or diffusion weighted imaging (DWI). Discontinuation of metronidazole resulted in the improvement of the neurologic symptoms over a period of two to three weeks. We followed up the brain MRI with DWI in one case following obvious clinical improvement, and the previously detected lesion had disappeared.

Our records include two cases of DIC in snakebite patients. One patient, who was 48-years old, was bitten in his left ankle 3 days before admission to our hospital. Initial symptoms were painful swelling, extensive ecchymosis, and persistent bleeding at the bite site. He visited and was admitted to a local hospital, but his condition did not improve with supportive care that included a single dose of antivenin. He was transferred to our hospital. His condition was compatible with DIC. We tried multi-dose antivenin therapy and blood product transfusion. At the seventh hospital day, the patient's symptoms were completely resolved. The other patient, who was 75 years old, was bitten in his right thumb. Initial symptoms were painful swelling of the right arm and persistent bleeding at the bite site, and within minutes of hospital admission, the patient experienced massive hematochezia. We peformed laboratory tests, the results of which were compatible with DIC, and the next day a sigmoidscopic examination showed ischemic colitis. We administered multi-dose antivenin therapy and blood product tranfusion. At the third hospital day mild anemia still existed, but the patient's clinical condition was improved. No signs or symptoms of gastrointestinal bleeding were observed. In these two cases, multi-dose antivenin therapy and transfusion effectively resolved symptoms of DIC. Platelet concentrate transfusion was required only for acute thrombocytopenia. After resolution of DIC, platelet counts were returned to normal ranges within a few days. The authors propose that multidose antivenin therapy and coagulation factor transfusion might be useful for improving coagulopathy in snakebite patients.

Historically, the common folk have made use of various wild herbs for both food and medicinal purposes. However, the misuse of these wild herbs can lead to adverse consequences, including severe poisoning in some cases. In cases of poisoning from wild herbs, patients can exhibit a variety of symptoms depending on the herbs involved, which in addition to gastrointestinal symptoms may include hemodynamic alteration and abnormal neurologic signs. In the present case, two patients were admitted to the emergency room with symptoms of toxicity after consuming Rhododendron brachycarpum liquor. Rhododendron brachycarpum and other wild herbs contain the toxic material grayanotoxin. Because of its serious toxic symptoms, great caution must be exercised in using rhododendrons for food and medicinal purposes.

Neurotoxic shellfish poisoning (NSP) can result from eating filter-feeding shellfish carrying brevetoxins produced by the marine dinoflagellate Krenia brevis (formally Gymnodinium breve). Brevetoxins enhance sodium entry into cells via voltage-sensitive sodium channels and have an excitatory effect. The incubation period is three hours (range 15 minutes-18 hours). NSP is characterized by gastroenteritis combined with neurologic symptoms. Gastrointestinal (GI) symptoms include abdominal pain, nausea, diarrhea and burning pain in the rectum. Neurologic symptoms are paresthesia, reversal of hot and cold temperature sensation, myalgia, headache, vertigo, and ataxia. Other symptoms may include malaise, tremor, dysphagia, bradycardia, decreased reflexes, dilated pupils, seizure, and coma. The health problem caused by K. breviscan be associated with a red tide bloom. We encountered 3 cases of neurotoxic shellfish poisoning. They all presented with GI and neurologic symptoms andrecovered after conservative treatment.

Acute toxic methemoglobinemia is an infrequent complication of the use of various drugs. Severe methemoglobinemia is very often fatal. Methylene blue is an effective drug in the treatment of methemoglobinemia patients. However, failure to respond to methylene blue has been described in patients with sulfhemoglobinemia, chlorate poisoning, and glucose-6-phosphate dehydrogenase deficiency. It is even possible that hemolysis may occur due to methylene blue treatment itself. We encountered a case of a 71-year-old woman who developed methemoglobinemia caused by alprazolam intoxication. She presented with hemolytic anemia and did not respond to methylene blue. In spite of concerted N-acetylcysteine therapy, the hemolytic anemia became aggravated and the patient died eleven days after intoxication.

Myoclonus is manifested in a variety of situations including metabolic derangements, brain lesions, epilepsy, and drugs toxicity. We reported a rare case of amitriptyline-induced myoclonus. A 64-year-old man with a tension-type headache was administered amitriptyline at 15 mg/day. Eight days after initiation of amitriptyline, multifocal myoclonus developed, involving the face and upper extremities. Two hours after the administration of clonazepam at 1 mg, myoclonus resolved completely.

Acute methemoglobinemia is induced by various causes, especially ingestion of oxidizing agents such as phenazopyridine, dapsone, and nitrite. Indoxacarb is an oxadiazine insecticide with high insecticidal activity and low mammalian toxicity. It is known to block voltage-gated Na+ channels in insects and mammals, but the mechanism is not yet well understood. We describe a case of a 41-year-old woman with methemoglobinemia that developed following Indoxacarb ingestion, which improved after intravenous injection of methylene blue. This is the first known such case. If signs and symptoms of methemoglobinemia occur after Indoxacarb ingestion, antidotal therapy with methylene blue should be considered as a necessary treatment.

Organophosphate insecticides, commonly used in agriculture, are a gradually increasing cause of accidental and suicidal poisoning. Intoxication can occur by ingestion, inhalation or dermal contact. Exposure to organophosphorus agents causes a sequentially triphasic illness consisting of the cholinergic phase, the intermediate syndrome, and organophosphate-induced delayed polyneuropathy. Acute pancreatitis as a rare complication of organophosphate intoxication has also been infrequently observed. We report a case of intoxication with organophosphate (phos-phamidon) by parenteral exposure (inhalation and/or dermal contact). A 34-year-old male patient was transferred to our Emergency Medical Center and was intubated due to a progressive respiratory failure. He presented with meiotic pupils, cranial nerve palsies, weak respiration, and proximal limb motor weaknesses without sensory changes. He had been employed in filling syringes with phosphamidon during the previous month. Because the patient's history and symptoms suggested organophosphate intoxication with intermediate syndrome, he was mechanically ventilated for 18 days with continuous infusion of atropine and pralidoxime (total amounts of 159 mg and 216 g, respectively). During his admission, hyperamylasemia and hyperli-pasemia were detected, and his abdominal CT scan showed a finding compatible with acute pancreatitis. He was administered a conservative treatment with NPO and nasogastric drainage. The patient was discharged and showed neither gastrointestinal nor neurologic sequelae upon follow up at one week and three months.

Poisonings caused by 'mad honey' are known to occur in response to grayanotoxins, which bind to sodium channels in the cell membrane, increasing membrane sodium permeability and preventing inactivation. Mild symptoms of mad honey intoxication are dizziness, weakness, hypersalivation, nausea, vomiting, and paresthesia. Severe intoxication, however, leads to serious cardiac manifestations such as atrioventricular block, dose-dependent hypotension, bradycardia, and respiratory depression. Atropine and vasoactive drugs improve symptoms of both bradycardia and respiratory rate depression. We report an unusual case of saliva-type hyperamylasemia in a mad honey poisoning patient who developed clinically significant bradycardia. She recovered fully within 3 days following atropine administration and medical treatment.

Methylene blue is a basic thiazine dye frequently used for histologic staining. In clinical toxicology settings, it is also used to treat clinically significant methemoglobinemia. It has dose-dependent oxidation or reduction properties, acting as a reducing agent at lower doses and as an oxidizing agent at higher doses. Hemolytic anemia and hyperbilirubinemia are known toxic effects of methylene blue treatment that have been reported clinically. A 42-year-old woman developed significant methemoglobinemia after acute dapsone overdose; she was treated appropriately with intravenous methylene blue in the therapeutic range. The patient's methemoglobin levels returned to normal. However, 2-4 days later she was noted to have rebound methemoglobinemia, hemolytic anemia, and hyperbilirubinemia. A repeat of Coomb's test and other anemia workups were negative. For management of methylene blue-induced hemolytic anemia, she was administered steroid therapy, N-acetylcysteine, and a blood transfusion. She ultimately recovered, and there were no long-term sequelae from the methylene blue poisoning.

Welders are exposed to a number of hazards including metal fumes, toxic gases, electricity, heat, noise, and radiation such as ultraviolet and infrared light. We encountered a patient who developed non-cardiogenic pulmonary edema within a day after cutting copper pipe with an oxyethylene torch. The patient was a 26-year-old welder. He complained of dyspnea, generalized myalgia, and febrile sensation the following morning. The patient's chest X-ray and chest CT scan showed extensively distributed and ill-defined centrilobular nodules. Both his symptoms and chest X-ray abnormalities improved spontaneously. We attributed the patient's symptoms to non-cardiogenic pulmonary edema due to nitrogen dioxide, reasoning that: 1) the pipe consisted only of copper, according to material safety data sheet (MSDS); 2) a previous report in the literature demonstrated increased nitrogen dioxide levels under similar conditions; 3) the patient's clinical course and radiologic findings were very reminiscent of non-cardiogenic pulmonary edema following accidental exposure to nitrogen dioxide.

The various species of aconitum contain diterpene (C-20) and norditerpene (C-19) forms of the natural alkaloid aconitine that cause neurologic, gastrointestinal, cardiovascular symptoms. In chinese medicine, these plants has been used as drugs to treat pain, dyspepsia, cerebrovascular disease, and so on. Because the therapeutic window is narrow, poisoning may occur from unintentional exposure, with a variety of toxic effects such as arrhythmia, hypotension, paresthesia, paralysis, nausea, vomiting, and abdominal pain. Aconitine-containing folk remedies are widely used in Korea. We encountered two cases of ventricular arrhythmia in patients who ingested tablets, known as 'Wha-Pung-Dan' made with aconitine extracts and were subsequently admitted to the ED. A 42 year-old man who took 35 tablets presented with ventricualr tarchycardia, and 40 year-old woman who took 40 tablets showed premature ventricular contractions. Both patients were discharged normally without any complications after three days.