Biomedical subjects

J Ger

Publications and source records attributed to J Ger.

At least 19 recordsLinked to original sources

PubMed2001

Acetylcholinesterase inhibition and the extrapyramidal syndrome: a review of the neurotoxicity of organophosphate.

Organophosphate poisonings are not uncommon, and are the leading cause of death in suicide patients in Taiwan. Acute cholinergic crisis caused by the inhibition of synaptic acetylcholinesterase is the major manifestation of organophosphate poisoning and may cause death within minutes. Delayed neurotoxicities include intermediate syndrome and delayed polyneuropathy have also been described. However, these symptoms may not characterize the complete picture of organophosphate poisoning. Among the 633 patients ever admitted to our hospital with organophosphate poisoning, three patients were found exhibiting impermanent neuromuscular dysfunction, including blepharoclonus, oculogyric crisis, intermittent dystonia, rigidity, and tremor, with two of them developing mask face, dyskinesia and akathisia later, following acute cholinergic crisis. The symptoms appeared within 4 days with the duration ranging from 25 days to 2 months. Other causes of the extrapyramidal syndrome noted on these patients have been excluded, and we consider the extrapyramidal syndrome a possible neurotoxic manifestation of organophosphate poisoning, which is transient, needs no treatment, and may be missed because of the critical condition, in a minority of patients. The mechanism remains to be identified, but may be related to the impediment of the function of acetylcholinesterase to modify nigrostriatal dopaminergic system, which is independent of hydrolyzing acetylcholine. More detailed observation for organophosphate poisoned patients and more studies for the biological functions of acetylcholinesterase including the influence on the nigrostriatal dopaminergic system are needed.

Acetylcholinesterase↗

PubMed2001

Rhabdomyolysis: an unusual feature with mushroom poisoning.

Rhabdomyolysis resulting from mushroom poisoning previously has been unreported in the literature. We present an outbreak of Russula subnigricans poisoning with rhabdomyolysis. The most severely ill patient presented with rhabdomyolysis, severe electrolyte disturbance (hyperkalemia, hypocalcemia), respiratory failure, acute renal failure, pulmonary edema, ventricular tachycardia, and circulatory shock. Mycotoxin may be the cause of rhabdomyolysis. In areas where mushroom gathering is common, mushroom poisoning should be included in the differential diagnosis of rhabdomyolysis.

Female↗

PubMed2001

Food poisoning due to methamidophos-contaminated vegetables.

BACKGROUND: Organophosphate poisoning is well known for its characteristic symptoms and signs, but food poisoning caused by pesticide-contaminated food is seldom reported. CASE REPORT: We report three incidents of food poisoning that resulted from exposure to the organophosphate insecticide methamidophos in vegetables. These outbreaks caused a cholinergic syndrome in 4 patients. The cholinergic overactivity led as to suspect organophosphate food poisoning. All patients recovered well following appropriate therapy. The clinical diagnosis of organophosphate poisoning was confirmed by reduced levels of erythrocytes and plasma cholinesterase and the presence of methamidophos in the vegetable leftovers. The implicated vegetables and levels of methamidophos were: Ipomoea batatas 255 ppm, Gynura bicolor 110 ppm, and red cabbage 26.3 ppm. Since methamidophos is normally applied to vegetables during planting, improper selection and/or overuse of pesticide or improper harvest times may explain the occurrence of these high residue levels of methamidophos.

Adult↗

PubMed2001

Acute toxicities of betel nut: rare but probably overlooked events.

BACKGROUND: Betel nut chewing has long been a social habit in Taiwan and other Asian and tropical countries. It produces various autonomic and psychoneurologic effects including tachycardia, flushing, warmth, cholinergic activation, alertness, and euphoria. Although the oral carcinogenic effects are well known, data concerning its acute toxicity are few. To better understand the toxicity of betel nut, cases reported to the Taiwan Poison Control Center as probable or possible betel nut-related toxicity (January 1988-June 1998) were reviewed. In the 17 cases suitable for review (14 males, 3 females, age 21 to 60 years), the most common manifestations were tachycardia/palpitations (7); tachypnea/dyspnea (6); hypotension and sweating (5); vomiting, dizziness, and chest discomfort (4); abdominal colic, nausea, numbness, and coma (3); and acute myocardial infarction and related manifestations (2). The reported quantity of betel nut used was low (1 to 6 nuts), except an extract of 100 betel nuts was used in 1 case and 66 chewed in another. Most cases recovered within 24 hours after the exposure. One patient developed probable acute myocardial infarction and ventricular fibrillation and died despite repeated cardiac defibrillation. Although betel nut chewing is widespread, significant toxicity as reported to a poison center is rare. Because most betel nut-related effects are transient and mild in nature, the incidence of such events is likely to be underreported. Nevertheless, betel nut chewing can produce significant cholinergic, neurological, cardiovascular, and gastrointestinal manifestations. It is possible that it may aggravate cardiac diseases in susceptible patients but this hypothesis must be further investigated. Treatment is symptomatic. With timely support, rapid and complete recovery is anticipated but a small risk of major complications cannot yet be discounted.

Adult↗

PubMed2001

Acute ethylene chlorohydrin poisoning: experience of a poison control center.

BACKGROUND: Ethylene chlorohydrin (CAS 107-07-3), a chemical once used in hastening grape vine sprouting in Taiwan, has caused severe toxicity upon acute exposure. Although such use of ethylene chlorohydrin is now prohibited in Taiwan, poisoning still occurs following its illegal use. Since data concerning human ethylene chlorohydrin poisoning remain rare, we report our experience in treating acute ethylene chlorohydrin-poisoned patients. METHODS: A retrospective analysis was conducted to evaluate patients with ethylene chlorohydrin poisoning reported to Taiwan Poison Control Center during 1985-1998. RESULTS: Seventeen patients with ethylene chlorohydrin poisoning were identified. There were 11 male and 6 female patients, ranging in age from 2 to 70 years (median 53 years). The intent of exposure was suicide in 5, accident in 9, and occupational exposure in 3 patients. Oral ingestion was the most common route of exposure (14 patients). Seven out of the 17 patients died within 24 hours due to metabolic acidosis and respiratory failure. Ethanol therapy, used in 2 patients, had no apparent benefit. Moderate or mild poisoning was characterized by gastrointestinal effects only and an uneventful recovery. CONCLUSIONS: Ethylene chlorohydrin can result in severe metabolic acidosis, respiratory failure, coma, and death after acute exposure.

Accidents↗

PubMed2001

Cholestatic hepatitis caused by acute gold potassium cyanide poisoning.

INTRODUCTION: Poisoning after oral ingestion of gold potassium cyanide is rarely reported. A case of suicidal ingestion of gold potassium cyanide (potassium dicyanoaurate; CAS# 13967-50-5) is described. CASE REPORT: A 27-year-old man attempted suicide by ingesting 5 mL gold potassium cyanide solution. He developed vomiting, hyperamylasemia, and hepatic dysfunction. Cyanide poisoning was not detected but acute gold toxicity was noted. Pathologic findings of the liver showed centrilobular cholestasis with eosinophilic degeneration. The whole blood and serum gold were 4361 and 6011 microg/L, respectively, and the 24-hour urine gold was 429 microg/d in samples obtained on day 4. CONCLUSION: Gold-induced hepatotoxicity has been seen infrequently in patients receiving gold therapy. Reported agents include sodium aurothiomalate, sodium aurothiopropranol sulfonate, aurothioglucose, aurothiopolypeptide (Auro-detoxin), auric sulfide, and gold thiosulfate, our report adds gold potassium cyanide.

Acute Disease↗

PubMed1999

Diverse manifestations of oral methylene chloride poisoning: report of 6 cases.

OBJECTIVE: Methylene chloride is a solvent used in domestic and industrial preparations, such as paint removers and degreasing agents. Although it is considered of low toxicity, acute toxic manifestations have been reported following inhalation of methylene chloride, mainly from working in an enclosed environment. Oral ingestion of methylene chloride, however, remains rare and its consequences are less clearly understood. CASE REPORTS: The various clinical manifestations of 6 patients with oral ingestion of methylene chloride are reported. Central nervous system depression, tachypnea, and corrosive gastrointestinal injury were the most common presentations following ingestion. An elevated carboxyhemoglobin level was documented in only 2 patients (35% and 8.4% carboxyhemoglobin, respectively). Due to a frequent misleading history of "chloroform" ingestion and unawareness of probable carboxyhemoglobin production in these patients, carboxyhemoglobin was not routinely measured. Renal failure, hepatic failure, and acute pancreatitis occurred in the 2 most severe cases of methylene chloride ingestion. CONCLUSIONS: Ingestion of methylene chloride can result in diverse manifestations, including a high carboxyhemoglobin level. Corrosive gastrointestinal injury is common in oral poisoning and needs further therapeutic consideration. A high index of suspicion and appropriate laboratory studies are needed in those patients who allegedly ingest "chloroform" but do not present the incriminating solvent to their treating physicians. The presence of an elevated carboxyhemoglobin level suggests the diagnosis of methylene chloride poisoning. Symptomatic and supportive measures remain the mainstay in the treatment of patients with oral methylene chloride poisoning.

Administration, Oral↗

PubMed1999

Characteristics and risk factors of acetaminophen-induced hepatitis in Taiwan.

BACKGROUND: Overdose of acetaminophen may cause hepatic injury and fatal fulminant hepatic failure. Acetaminophen is the most common form of drug-induced hepatic injury in Western countries. However, there is no formal report of this important issue in Taiwan. To assess the clinical characteristics and risk factors of acetaminophen-induced hepatitis in Taiwan, we conducted this study. METHODS: A total of 71 patients who were intoxicated or overdosed with acetaminophen at Veterans General Hospital-Taipei between February, 1991 and June, 1997 were enrolled in this study. Acetaminophen-induced hepatitis was defined according to the Paris international consensus criteria. RESULTS: Suicide attempt was the major cause (67/71) of acetaminophen overdose. Sixty-two of the patients were female. The mean patient age was 24.5 +/- 9.7 years (+/- standard deviation, SD). Nineteen of 71 patients had acetaminophen-induced hepatitis. The peak serum alanine aminotransferase, aspartate aminotransferase and total bilirubin concentrations were 4,181.0 +/- 931.4 IU/l (mean +/- SD), 4,148.0 +/- 1,147.5 IU/l and 2.6 +/- 0.4 mg/dl, respectively. The hepatitis group had higher ingested acetaminophen doses and serum peak acetaminophen levels than did those of the nonhepatitis group (24.9 g vs 12.9 g, p = 0.004; 132.0 mg/l vs 61.7 mg/l, p = 0.013). A higher percentage of alcohol consumption was also noted in the hepatitis group than in the nonhepatitis group (32% vs 12%, p = 0.05). After logistic regression for multivariate analysis, alcohol consumption was the most important risk factor for acetaminophen-induced hepatitis (odds ratio = 8.14, p = 0.018), followed by ingested acetaminophen dose (odds ratio = 1.21, p = 0.001). Most patients received acetylcysteine treatment in time. Two of the 19 patients with hepatitis died. CONCLUSIONS: The majority of acetaminophen-induced hepatitis in Taiwan occurs in young females who attempt suicide. Alcohol consumption and the dose of acetaminophen ingested were the significant risk factors for acetaminophen-induced hepatitis. Alcohol should not be concomitantly used with acetaminophen. Early diagnosis and administration of the antidote are crucial to decrease mortality.

Acetaminophen↗

PubMed1998

Prolonged severe withdrawal symptoms after acute-on-chronic baclofen overdose.

INTRODUCTION: Baclofen is frequently used to treat muscle spasticity due to spinal cord injury and multiple sclerosis. Baclofen overdose can lead to coma, respiratory depression, hyporeflexia, and flaccidity. An abrupt decrease in the dose of baclofen due to surgery or a rapid tapering program may result in severe baclofen withdrawal syndrome manifesting hallucinations, delirium, seizures, and high fever. Severe baclofen withdrawal syndrome secondary to intentional overdose, however, has not received mention. CASE REPORT: A 42-year-old male receiving chronic baclofen therapy, 20 mg/d, attempted suicide by ingesting at least 800 mg of baclofen. He was found in coma 2 hours postingestion with depressed respirations, areflexia, hypotonia, bradycardia, and hypotension. Treatment with intravenous fluids, atropine, dopamine, and hemodialysis was associated with restoration of consciousness within 2 days but disorientation, hallucinations, fever, delirium, hypotension, bradycardia, and coma developed during the following week. Baclofen withdrawal syndrome was not diagnosed until hospital day 9, when reinstitution of baclofen rapidly stabilized his condition. Oral overdosage of baclofen causes severe neurological and cardiovascular manifestations due to its GABA and dominant cholinergic effects. Severe baclofen withdrawal syndrome is manifest by neuropsychiatric manifestations and hemodynamic instability. Caution should be exercised after a baclofen overdose in patients receiving chronic baclofen therapy.

Adult↗

PubMed1998

The clinical significance of hyperamylasemia in organophosphate poisoning.

OBJECTIVE: Hyperamylasemia with a presumptive diagnosis of acute pancreatitis has been reported following organophosphate poisoning but there are no large-scale studies incorporating more specific diagnostic criteria. METHODS: Retrospective review of the medical records of 159 patients with a diagnosis of organophosphate poisoning over 3 years. Serum amylase, pancreatic amylase, salivary amylase, lipase and cholinesterase levels, and the clinical manifestations were analyzed. RESULTS: Serum amylase data was available for 121 of the 159 study patients. Hyperamylasemia (amylase > or = 360 U/L) was found in 44 patients (36%). Lipase was measured in 28 patients with hyperamylasemia; 9 of 28 had hyperlipasemia (lipase > or = 380 U/L). The finding of hyperamylasemia was closely related to clinical severity and presence of shock. A presumptive diagnosis of painless acute pancreatitis was diagnosed by hyperlipasemia associated with hyperamylasemia, clinical severity, serum LDH, and leukocyte counts. Two patients with presumptive pancreatitis died. Shock, coma, and hypoalbuminemia were the factors predicting fatality. CONCLUSIONS: Hyperamylasemia is frequent in severe organophosphate poisoning. However, hyperamylasemia is not synonymous with acute pancreatitis and pancreatic amylase is not a reliable parameter in the diagnosis of organophosphate-induced pancreatitis due to its low sensitivity and specificity. Lipase assay is indicated in patients with hyperamylasemia for early diagnosis of pancreatitis. Proper image studies and even pathological examination are also needed to confirm the extent of pancreatic injury. With prompt diagnosis and appropriate treatment, a complete recovery can be anticipated unless the patient has otherwise unrelated complications.

Acute Disease↗

PubMed1998

A fatal case of acute ferric chloride poisoning.

Death from ferric chloride poisoning has never been reported in Taiwan. We report a fatality from the suicidal ingestion of ferric chloride solution used as an etching agent for printed circuitry. A 25-y-old woman presented with vomiting after ingestion of 200 ml ferric chloride solution (pH 1.0). She had hypoxemia and severe metabolic acidosis with respiratory alkalosis initially. Three hours after her ingestion she presented with drowsy consciousness, tachycardia, tachypnea and protracted vomiting. Laboratory studies showed leukocytosis, elevated glucose, aspartate aminotransferase, amylase, lactate dehydrogenase, and total bilirubin, coagulation defect and hemolysis. Aspiration pneumonia and vision loss were also noted. Four hours after ingestion cardiopulmonary arrest suddenly occurred after severe vomiting and she expired. Toxicological studies showed marked elevation of serum iron (2440 micrograms/dl); the estimated oral dose of ferric chloride was equivalent to 11.52 g (230 mg/kg) of elemental iron. This patient did not receive deferoxamine due to rapid deterioration and a late diagnosis. Deferoxamine should be given in any symptomatic patient or in the presence of anion gap metabolic acidosis with a history of ferric chloride ingestion.

Acidosis↗

PubMed1997

Scombroid fish poisoning: an overlooked marine food poisoning.

Scombroid fish poisoning is a food-borne chemical intoxication caused by certain spoiled fish that contain a large amount of histamine and some biogenic diamines. It has gradually become a world-wide medical problem and probably is the most common cause of fish poisoning. As the data on the incidents of scombroid fish poisoning in Taiwan remains scarce, we report 2 incidents of scombroid fish poisoning in Northern Taiwan. We collected data of the 2 outbreaks of suspected fish poisoning which were reported to us in 1996. An epidemiological investigation was undertaken. Questionnaire interviews were given to persons who ate lunch in the same cafeteria in outbreak 2. The leftover fish were sent for species identification and toxin analysis. The first incident involving 4 women occurred in March 1996. All cases experienced flush, dizziness, blurred vision and skin rashes after eating lunch. A non-scombroid fish of Makaira with histamine levels as high as 84.13 mg/100 g flesh was implicated in this incident. In August 1996, another incident involving some cases who ate lunch at the same cafeteria were investigated. A total of 146 questionnaires were distributed with a return of 132 questionnaires (90.4%). Fifty-five employees reported positive signs or symptoms; 48 persons who ate fish and 7 women who did not eat fish were ill. Fish was the only food associated with the illness with an attack rate of 73.8% (p < 0.001). The incriminated fish was later identified as a scombroid fish of Euthynnus with a histamine content of 271.9 mg/100 g flesh in 1 leftover piece and 118.5 mg/100 g flesh in another piece. Most cases in these 2 outbreaks received treatment with antihistamines and had rapid and complete recovery. The diagnosis of scombroid fish poisoning could be misdiagnosed as food allergy or bacterial food poisoning if physicians are not aware of such poisoning. The nonspecific but characteristic symptomatology of histamine food poisoning and previous consumption of fish should alert physicians to the possibility of scombroid fish poisoning. Unless complicated with shock or respiratory distress, supportive treatment with antihistamines usually concludes with a good prognosis. Toxin analysis of the fish flesh remains the most important step in approaching a confirmed diagnosis.

Adolescent↗

PubMed1996

Acute isoniazid intoxication: a case report.

Since its introduction in 1952, isoniazid has remained one of the drugs of choice in the treatment and prophylaxis of tuberculosis. In populations with a high prevalence rate of tuberculosis or suicide rate, acute ingestion of isoniazid has occasionally been reported. Acute intoxication by isoniazid is known to cause symptoms of seizures, metabolic acidosis, coma, and even death. These clinical symptoms, however, are not well recognized by physicians in Taiwan, even though the prevalence rate of tuberculosis is relatively high here. This report concerns the case of a 25-year-old female with a past history of tuberculosis who presented with the symptoms of refractory seizures, metabolic acidosis and deep coma after intentional ingestion of some unknown drug. Although implicating agents were not recognized initially, she was successfully revived with basic resuscitation, anticonvulsants and correction of metabolic acidosis. A review of her history revealed that her ingestion of five grams of isoniazid in this case was responsible for the entire clinical spectrum. Given easy access to isoniazid in Taiwan, a diagnosis of isoniazid poisoning should always be considered in patients who present with the classical symptoms of refractory seizures, metabolic acidosis and coma.

Acidosis↗

PubMed1995

Back pain among workers in the United States: national estimates and workers at high risk.

Back pain accounts for about one fourth of workers' compensation claims in the United States. The Occupational Health Supplement to the 1988 National Health Interview Survey provided an opportunity to assess the scope of this problem. The 30,074 respondents who worked in the 12 months before the interview were defined as "workers", and those with back pain every day for a week or more during that period were defined as "cases." A weighting factor was applied to the answers to derive national estimates. In 1988, about 22.4 million back pain cases (prevalence 17.6%) were responsible for 149.1 million lost workdays; 65% of cases were attributable to occupational activities. For back pain attributed to activities at work, the risk was highest for construction laborers among males (prevalence 22.6%) and nursing aides among females (18.8%). Our analyses show that back pain is a major cause of morbidity and lost production for U.S. workers and identifies previously unrecognized high risk occupations, such as carpenters, automobile mechanics, maids, janitors, and hairdressers, for future research and prevention.

Adult↗

PubMed1995

Severe rhabdomyolysis mimicking transverse myelitis in a heroin addict.

Heroin addiction is known to cause various medical and neurological complications. We report here a case of rhabdomyolysis following heroin abuse, in which a neurological lesion mimicking transverse myelitis was also noted. A 29-year-old man was found comatose in a kneeling position one day after a heroin overdose. On admission, he was awake, yet with total paralysis of his lower legs. Physical examination revealed marked swelling and tenderness of the four limbs, especially the lower extremities. Deep tendon reflexes and positional sense were absent in both legs; however, pin-prick sense was preserved. Transverse myelitis or spinal cord vasculitis was the initial working diagnosis. Laboratory tests disclosed significantly elevated creatinine kinase of 146289 U/L. Though suffering transient acute renal failure, his neurological abnormalities gradually improved over four weeks and a left foot drop was the only residual lesion at discharge. Rhabdomyolysis, a well defined complication following heroin use, may also cause concomitant neurological symptoms, for which careful differential diagnosis is warranted. With the increasing number of heroin addicts in Taiwan, more cases with rhabdomyolysis-induced neurological symptoms may be observed in the future.

Adult↗

PubMed1995

Features of centipede bites in Taiwan.

In order to define characteristics that would help differentiate a centipede bite from a viper bite, we designed a prospective study using the data collection system of a Poison Control Center. The clinical goal is to rapidly distinguish envenomations for which antitoxin may be indicated (viper) from those for which palliative care only is appropriate (centipede). During a year period, 31 cases, including two cases receiving double bites in each event, were reported. Centipede lengths were estimated to range from 3 to 20 cm. Ninety-two per cent of the bite marks were pointed in shape. A local reaction developed at the bitten site, but usually remaining localized to a 10 x 10 cm area of involvement. The length of the biting animal, the bite mark characteristics, the presence of haemorrhagic vesicles, the wound size and the progression of local reactions are useful in the rapid clinical differentiation between centipede bites and viper bites.

Adolescent↗

PubMed1994

Survival of paraquat intoxication complicated with mediastinal emphysema: a case report.

Paraquat intoxication is a common medical problem in this country. The mortality is high, particularly in the cases of high dose ingestion. Mediastinal emphysema observed in paraquat intoxication always means mortality, however, we experienced a survivor. A 29 y/o female ingested about 10-15 c.c. of 24% (2.4-3.6 gm) paraquat to attempt suicide. Nausea and protracted vomiting occurred shortly after. During hospitalization, mediastinal emphysema developed on the 7th day and subsided 10 days later. Serum paraquat level determination revealed 185 ng/ml in 20 hours after ingestion and 34 ng/ml on the 6th day. She received general supportive treatments with the augmentation of sodium thiosulfate. Hypokalemia had been observed for 11 days and was intractable until hypomagnesemia was identified and corrected. So far, she had returned back to her work for more than 1 year, although the chest x-ray revealed slight pulmonary fibrosis. The high ingested dose, oral ulcers, high serum level and mediastinal emphysema of this patient all implicate a poor prognosis of paraquat intoxication; however, these contradict the observed survival of our patient. In conclusion, mediastinal emphysema observed in paraquat intoxication is not related to the serum level of paraquat. It does not absolutely lead to death and may simply come from the esophageal rupture after vigorous vomiting in paraquat intoxication.

Adult↗

PubMed1994

Adult respiratory distress syndrome and late death following imipramine overdose: a case report.

Adult respiratory distress syndrome (ARDS) after tricyclic antidepressant (TCA) overdose has been reported, but has not received as much attention in the literature as hemodynamic instability, cardiac arrhythmias or seizures. This report concerns a 33-year-old female who ingested a large amount of imipramine in an attempted suicide. She developed deep coma, hypotension, cardiac dysrhythmias and seizures. Although she survived initially, ARDS developed and she died of severe hypoxia nine days later. Her lung injury may have been the result of a variety of factors including prolonged hypotension, aspiration pneumonia, sepsis or a direct action on the lung parenchyma by imipramine. The literature pertaining to etiology, epidemiology, pathophysiology and management of TCA-induced lung injury has been reviewed. In one series of severe TCA overdose, an ARDS rate of 9% was reported. The risk of developing pulmonary edema and ARDS should be considered in severe TCA-poisoned patients. To try to prevent this complication, early intubation should be considered to avoid aspiration, and cautious volume loading, plus judicious use of alpha-adrenergic agonists, is indicated to prevent protracted hypotension.

Adult↗