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Biomedical subjects

J F Deng

Publications and source records attributed to J F Deng.

90 records · Page 5Linked to original sources

Amphetamine poisoning in infant: report of two cases.

Amphetamine poisoning is rare in children. Here we report two male infants with acute poisoning due to accidental amphetamine ingestion. One infant had a family history of drug abuse and the other was due to poor supervision of the parents. Although typical clinical symptoms and signs (including restlessness, hyperactivity, hypertension, tachycardia and tachypnea....etc.) were found, both were completely recovered after treatment. The principle of management of amphetamine poisoning are presented.

Akathisia, Drug-Induced↗

[The urinary screening and identification of amphetamines in clinical toxicology laboratory--VGH].

Amphetamines abuse has recently become a problem in this country. Four case identification, we used Emit-d.a.u. amphetamine assay to screen the amphetamines in human urine, and then confirmed them by gas chromatography-ion trap detector (GC-ITD). From January 1989 to August 1990, 267 urinary samples were requested by the physicians for amphetamine identification. Six samples were accompanied with drug powders used by the patients. Among the 267 samples, 79 were confirmed for the presence for both of methamphetamine and amphetamine. Neither the presence of amphetamine nor methamphetamine itself was detected. Among the six packs of drug powder tested, methamphetamine but not amphetamine was detected in four. We found that fenfluramine and diethylpropion would have false positive amphetamine reactions in Emit-d.a.u. assay. All the samples originated from 34 hospitals were widely distributed in the country. Other drugs concomitantly used included ethanol, morphine, flunitrazepam and ephedrine. Since methamphetamine can be metabolized to amphetamine but not vers versa, our study confirmed the abuse of methamphetamine not amphetamine in this country.

Amphetamines↗

[Ethanol intoxication treated with flumazenil: a case report].

Ethanol possesses anxiolytic and anticonflict effect in low dose, but exhibits consciousness depression in higher serum level. It also has addictive effects on benzodiazepines (BZD) and its mechanism has been thought to be closely related to GABA-BZD receptor complex. Flumazenil is a well-known potent antagonist in benzodiazepine intoxication. It can restore the patients' consciousness in case of BZD overdose in comatose condition. In the treatment of ethanol intoxication, flumazenil has not been well-accepted as an antidote. We report a case of severe ethanol intoxication (serum level: 512 mg/dl) with deep coma. Flumazenil 0.5 mg restored her consciousness 90 mins after antidote had been administrated. According to the literature, improvement of conscious level was not due to decay of serum ethanol level but flumazenil itself, which has potential benefit to the condition of ethanol intoxication. This effect is delayed as compared with its using in BZD overdose.

Adult↗

[Clinical experience in benzodiazepine antagonist].

Flumazenil, a potent benzodiazepine antagonist, is a newly synthetic imidazo-benzodiazepine, which blocks the neurological effects of benzodiazepines. The purpose of this study was to evaluate the effects of this agent in reversal of benzodiazepine overdose and differentiation of comatous patients with drug overdose. Fifteen comatous patients with suspected sedatives/hypnotics overdose were included in this study and flumazenil 0.25 mg per dose was administrated intravenously. The average score of Glasgow Coma Scale increased from 7.13 +/- 2.92 to 10.93 +/- 3.67 after one dose of flumazenil. Clear consciousness was restored after multiple doses of flumazenil administration. Three cases with different drug history and variant response after flumazenil treatment were also illustrated and discussed. The dosage of flumazenil used in this study ranged from 0.25 mg to 3 mg (average 0.87 +/- 0.74 mg). We concluded that flumazenil is an excellent antidote for benzodiazepine overdose and valuable for differentiating the patients in comatose.

Adolescent↗

New therapy for hydrocarbon pneumonitis--nasal prongs continuous positive airway pressure (NPCPAP).

Respiratory failure and conscious disturbance developed in a 18-month-old girl following ingestion of an unknown quantity of spot remover solution, a petroleum distillate product. Rapid deterioration was noted within 2 hours after ingestion. The patient became stable in condition and dramatically improved through intensive care with respiratory support by using nasal prongs continuous positive airway pressure (NPCPAP). To our knowledge, this may be the first case being successfully managed with this technique.

Female↗

The essential role of a poison center in handling an outbreak of barium carbonate poisoning.

Acute barium salt poisoning may cause acute hypokalemia and result in respiratory paralysis and ventricular tachyarrhythmias. The early nonspecific gastrointestinal symptoms of barium poisoning due to food contamination could be confused with other benign food poisonings. Early diagnosis and initiation of intensive supportive care is essential. We report an outbreak of acute barium carbonate poisoning, occurring at a family reunion party, which resulted in 9 hospital admissions. All of the victims initially developed nausea, vomiting, abdominal colic, dizziness and watery diarrhea followed by numbness of the face and distal extremities 1-2 h after ingesting fried flour-coated sweet potatoes. The flour was later confirmed to be contaminated with barium carbonate. One person died in the emergency room with a serum potassium level of 0.8 mEq/L. Two other victims developed ventricular tachycardia and respiratory paralysis but completely recovered with the treatment advice provided by the poison center. The poison center was successful in helping to make the correct diagnosis in a timely manner, immediately distribute the treatment protocol, and coordinate the laboratory confirmation of barium carbonate poisoning.

Adult↗

An outbreak of chromium ulcer in a manufacturing plant.

On May 23, 1989, managers of a manufacturing plant requested an investigation of an outbreak of hand ulceration and skin discoloration among workers. The plant has manufactured kitchen ranges for 30 years and employs approximately 633 hourly workers. The affected employees worked in the enamel department, where metallic range tops are coated with a "ground coat" or sprayed with an enamel coloring, and then baked in ovens at 1200F. Our evaluation included physical examinations, environmental sampling, and a questionnaire eliciting information concerning skin ulceration job history, demographics, and use of protective practices. We identified 10 enamel department workers (13.5%) who developed chromium ulcers between January 1st and June 30th, 1988. Ulcers were found on hands, forearms, periumbilical area and/or axillae. Within the enamel department, workers who handled conveyer hooks used to suspend range tops as they passed through the oven were at greatest risk (rate ratio (RR) = 12.44, 95% confidence interval (CI) = 2.90-53.35). Workers who wore gloves were protected from developing ulcers (RR = 0.08, 95% CI = 0.01-0.60). Normally, trivalent chromium (Cr+3) does not cause skin ulcers unless it is oxidized to hezavalent chromium Cr+6). The enamel used contained only Cr+3, not Cr+6, but analysis of hooks that had passed through the oven revealed Cr+6 on their surface. A mechanical failure of the oven resulted in the formation of sharp edges of the parts and consequently causing the abrasion of exposed skin. We believe Cr+3 was converted to Cr+6 during the baking process which associated with the mechanical failure of the oven causing this outbreak.

Age Factors↗

Effects of calcium-channel blockers on picrotoxin-induced centrogenic arrhythmias in cats.

Intravenous picrotoxin injection has been established as a model of producing arrhythmias, mainly through enhanced central sympathetic outflow. The effects of calcium-channel blockers, and a beta-blocker on these arrhythmias were tested in chloralose-anesthetized cats. Picrotoxin (10 mg/kg, i.v.) produced mostly ventricular, sometimes supraventricular tachycardias and ectopic beats, as well as a marked elevation of arterial blood pressure. Nifedipine at the doses of 2 micrograms/kg (i.v. or i.c.) and 5 micrograms/kg (i.v.) transiently suppressed the arrhythmias in some of the cats tested. With the dose of 10 micrograms/kg (i.v.), it promptly and consistently abolished the arrhythmias without recurrence and significantly reduced the blood pressure (-62 +/- 8/-59 +/- 8 mmHg, delta systolic pressure/delta diastolic pressure, p less than 0.001, n = 9). A similar degree of blood pressure reduction (-69 +/- 8/-67 +/- 7 mmHg, n = 6) after sodium nitroprusside (4-5 mg/kg, i.v.) injection abolished the arrhythmias in 4 of 6 cats; however, there was marked ECG evidence of myocardial ischemia in 3 cats. Verapamil (50 micrograms/kg, i.v.) transiently abolished the arrhythmias and significantly decreased the blood pressure (7/7 cats), whereas a larger dose (150 micrograms/kg) had a persistent effect (2/4 cats). Propranolol at a dose of 240 micrograms/kg also consistently abolished the arrhythmias without recurrence in all 4 cats. We conclude that nifedipine, verapamil and propranolol are effective in the treatment of picrotoxin-induced arrhythmias. This result indicates that calcium-channel blockers or beta-blockers may be clinically effective in the treatment or prevention of arrhythmias caused by intracranial lesions with enhanced sympathetic outflow.

Animals↗

Hydrogen sulfide poisonings in hot-spring reservoir cleaning: two case reports.

The potential hazards to maintenance personnel cleaning hot-spring reservoirs are reported following two severe and unusual episodes of acute hydrogen sulfide poisoning involving seven workers. In the first episode, five victims lost consciousness immediately after climbing down a manhole to the bottom of a reservoir disregarding a strong odor of rotten eggs. One of them died immediately. Of the four who lived, three developed hemorrhagic keratoconjunctivitis and aspiration pneumonia, but no sequelae were observed 2 years later. In the second episode, two workers had been cleaning the reservoir for about 2 hours when one collapsed and his companion went to seek help. Both died of acute respiratory distress syndrome due to pulmonary edema within 12 hours. Since hot-spring bathing is a popular recreation in Taiwan, other accidents of hydrogen sulfide poisoning may have occurred but have not been reported. Such clinical information is helpful to enable regulators to initiate proper precautions to safeguard those workers involved.

Acute Disease↗

Outbreak of carbon tetrachloride poisoning in a color printing factory related to the use of isopropyl alcohol and an air conditioning system in Taiwan.

Three workers from a color printing factory were admitted to community hospitals in 1985 with manifestations of acute hepatitis. One of the three had superimposed acute renal failure and pulmonary edema. An investigation was subsequently conducted at the plant to determine the etiology of the outbreak and the prevalence of liver disease among the remaining workers. Comprehensive medical evaluations were conducted, which included physical examinations, liver function tests, and serological screening for hepatitis. Seventeen of 25 workers from the plant had abnormal liver function tests 10 days after the outbreak, and a significant association was found between the presence of abnormal liver function tests and a history of recently having worked inside any of three rooms in which an interconnecting air conditioning system had been installed to cool the printing machines. After further investigation, it was determined that the incident occurred following inadvertent use of carbon tetrachloride to clean a pump in the printing machine. A simulation of the pump cleaning operation revealed ambient air levels of carbon tetrachloride of 300-500 ppm. Ultimately, it was concluded that the outbreak was in all likelihood due to the combined use of carbon tetrachloride and isopropyl alcohol in the cleaning operation. This outbreak underscores the importance of adopting appropriate industrial hygiene measures in a rapidly industrializing nation such as Taiwan.

1-Propanol↗

Carbamazepine toxicity: comparison of measurement of drug levels by HPLC and EMIT and model of carbamazepine kinetics.

A 23-month-old boy accidently ingested 2000 mg (148 mg/kg) of carbamazepine. The delayed onset of convulsions coincided with the peak serum level of total parent drug and an active metabolite (carbamazepine 10,11-epoxide). Comparisons of homogeneous enzyme multiplied immunoassay technique (EMIT) and high pressure liquid chromatography (HPLC) revealed that the EMIT slightly over-estimated plasma carbamazepine levels due to immunochemical cross reactivity with the epoxide metabolite. The peak plasma levels of the parent drug plus the active metabolite were more accurately determined by HPLC. These results emphasize the need to understand both the presence of active metabolites and characteristics of the assay being used in managing clinical intoxication with carbamazepine.

Carbamazepine↗

Strychnine poisoning. Recovery from profound lactic acidosis, hyperthermia, and rhabdomyolysis.

Strychnine poisoning results in a predictable and treatable sequence of events involving blockade of the inhibitory neurotransmitter, extensor muscle spasms, seizures, and respiratory paralysis. These spasms may lead to hyperthermia, profound lactic acidosis, and rhabdomyolysis. Acidosis is primarily attributable to lactate, as indicated by the correlation between arterial pH and log of lactic acid concentration (r = -0.878). Interruption of the strychnine blockade is the primary therapy for strychnine poisoning. Phenobarbital in moderate doses should be the first intervention and anesthetic doses should be used if necessary. Suppression of convulsions will permit successful management of the complications of strychnine poisoning. Our patient survived, even though at one point he had a pH of 6.55, a lactate level of 32 mM/liter, a temperature of 43 degrees C, and rhabdomyolysis with an increased creatine phosphokinase level of 359,000 mU/ml (5,983 mumol/s/liter).

Acidosis↗

Reduction in caffeine toxicity by acetaminophen.

A patient who allegedly consumed 100 tablets of an over-the-counter analgesic containing sodium acetylsalicylate, caffeine, and acetaminophen displayed no significant CNS stimulation despite the presence of 175 micrograms of caffeine per mL of serum. Because salicylates have been reported to augment the stimulatory effects of caffeine on the CNS, attention was focused on the possibility that the presence of acetaminophen (52 micrograms/mL) reduced the CNS toxicity of caffeine. Studies in DBA/2J mice showed that: 1) pretreatment with acetaminophen (100 mg/kg) increased the interval between the administration of caffeine (300 to 450 mg/kg IP) and the onset of fatal convulsions by a factor of about two; and 2) pretreatment with acetaminophen (75 mg/kg) reduced the incidence of audiogenic seizures produced in the presence of caffeine (12.5 to 75 mg/kg IP). The frequency of sound-induced seizures after 12.5 or 25 mg/kg caffeine was reduced from 50 to 5% by acetaminophen. In the absence of caffeine, acetaminophen (up to 300 mg/kg) did not modify the seizures induced by maximal electroshock and did not alter the convulsant dose of pentylenetetrezol in mice (tests performed by the Anticonvulsant Screening Project of NINCDS). Acetaminophen (up to 150 micrograms/mL) did not retard the incorporation of radioactive adenosine into ATP in slices of rat cerebral cortex. Thus the mechanism by which acetaminophen antagonizes the actions of caffeine in the CNS remains unknown.

2',3'-Cyclic-Nucleotide Phosphodiesterases↗

Children poisoning in Taiwan.

Poisoning is a well known cause of morbidity and mortality in children. In Taiwan, little information has been published regarding the status of pediatric poisoning exposures. To provide more information on pediatric poisoning exposures for the purpose of poison prevention, a retrospective study was designed and conducted to analyse the data of National Poison Centre (NPC), Taiwan. All telephone inquiries concerning poisoning exposures in those under 19 years of age, received by NPC-Taiwan from July 1985 through December 1993, were included in this study. The age, sex, reason for exposure, route of exposure, substances involved and clinical outcome of those telephone calls were then analyzed. A total of 5,812 inquiries concerning poisoning exposures in children were recorded. Male exposures were more prevalent than females (59%) Vs. 41%) Accidental exposures accounted for 77.7% of the cases and most were exposed by the oral route. Substances most frequently ingested were household products, benzodiazepines and pesticides. The data revealed a mortality rate of 1.4%. Accidental poisoning exposures from household products and drugs remain a significant problem for those younger than 6 years of age. Further education of parents and care takers and the employment of child-resistant containers are needed to prevent cases of pediatric poisoning. Reduction of amphetamine abuse in adolescents is also of major concern and deserves more attention.

Adolescent↗

Identification of cyprinol and cyprinol sulfate from grass carp bile and their toxic effects in rats.

To elucidate the responsible toxic components of grass carp bile, the bile salt 5 alpha-cyprinol sulfate and its desalted form 5 alpha-cyprinol from grass carp bile were purified and identified by analyses of infrared spectrum, (1)H-, (13)C-nuclear magnetic resonance spectra and mass spectrum. The toxicity of grass carp bile powder, butanol extract of grass carp bile powder, 5 alpha-cyprinol and 5 alpha-cyprinol sulfate in rats were further determined. The kidney and liver functions were significantly affected by grass carp bile powder, butanol extract and 5 alpha-cyprinol sulfate. However, 5 alpha-cyprinol also significantly affected the kidney function, but the toxic effect was less.

Administration, Oral↗