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Biomedical subjects

B R Ekins

Publications and source records attributed to B R Ekins.

12 recordsLinked to original sources
PubMed1994

Wound botulism.

Wound botulism is a rare infectious and toxicologic complication of trauma and i.v. drug abuse. Only 39 cases have been reported in detail in the English literature. This case report describes a patient with wound botulism who presented to four medical facilities before receiving definitive diagnosis and treatment. Although his history and physical examination were consistent with wound botulism, diagnosis and therapy were delayed because this rare disease was not considered initially in the differential diagnosis. Wound botulism should be considered in trauma patients and i.v. drug abusers who present with cranial nerve palsies and descending paresis.

Abscess↗
PubMed1993

Amelioration of nifedipine poisoning associated with glucagon therapy.

Glucagon relieves calcium channel blocker-induced hypotension in animal studies. There are no published case reports of glucagon relieving hypotension in patients with calcium channel blocker poisoning. We describe a patient who developed hypotension after ingestion of 900 mg nifedipine. Therapy with IV lactated Ringer's solution and calcium chloride alone did not relieve his hypotension. However, hypotension rapidly resolved after the addition of IV glucagon therapy. This is the first case report of glucagon therapy at least temporally associated with relief of hypotension in a patient with calcium channel blocker poisoning. More research is needed to determine the appropriate role for glucagon in treating patients with calcium channel blocker poisoning.

Adult↗
PubMed1991

Cyanide toxicity from acetonitrile-containing false nail remover.

A patient presented without symptoms 30 minutes after ingesting acetonitrile, also known as methylacyanide. He had prompt gastric lavage and activated charcoal administration. Hours later, the onset of clinical toxicity was heralded by mental status abnormalities and vomiting prior to a generalized seizure. Following administration of sodium thiosulfate, the patient made an uneventful recovery. A blood cyanide level drawn shortly after presentation, but reported after the patient had been discharged, documented significant exposure. During hospitalization, cyanide toxicity was inferred from the history of ingestion of acetonitrile, plus a significant absence of venous blood hemoglobin desaturation. Because even small amounts can be harmful and toxicity is delayed, all acetonitrile ingestions should be presumed dangerous. Patients should be observed and repeatedly evaluated for at least 24 hours. In the absence of cyanide level determinations, lethargy, vomiting, seizures, and the lack of normal venous blood hemoglobin desaturation are clues to cyanide toxicity.

Acetonitriles↗
PubMed1987

The effect of activated charcoal on N-acetylcysteine absorption in normal subjects.

The discovery of the effectiveness of oral antidotes such as N-acetylcysteine (NAC) for acetaminophen poisonings has raised questions about the appropriateness of concomitant administration with activated charcoal. A number of studies have attempted to clarify this question without complete success. This study was designed to evaluate the difference in serum levels of NAC when given with activated charcoal. Nineteen patients completed a two-phase cross-over study in which they served as their own controls. Each subject in phase 1 received 140 mg/kg of diluted, chilled NAC orally, and venous blood samples were drawn for analysis. Phase 2 consisted of a 100-g dose of activated charcoal followed by NAC. Samples were transported immediately and assayed using spectrophotometry. A reduction in peak NAC level of 29% (P less than .02) and a reduction of total area under the curve (AUC) of 39% (P less than .001) was noted. Although it may be preferable to avoid completely the use of activated charcoal when using NAC to treat overdoses of acetaminophen, we recommend that if these agents are used together, doses of NAC be increased by 40% to compensate for the decreased oral absorption of NAC.

Absorption↗
PubMed1985

Standardized treatment of severe methanol poisoning with ethanol and hemodialysis.

Seven patients with methanol poisoning were treated with ethanol, hemodialysis and supportive measures. The interval between ingestion and initiation of ethanol therapy varied from 3 to 67 hours and from ingestion to dialysis from 9 to 93 hours. All patients survived, but one had permanent visual impairment. A 10% ethanol solution administered intravenously is a safe and effective antidote for severe methanol poisoning. Ethanol therapy is recommended when plasma methanol concentrations are higher than 20 mg per dl, when ingested doses are greater than 30 ml and when there is evidence of acidosis or visual abnormalities in cases of suspected methanol poisoning.

Adolescent↗
PubMed1978

Acute digoxin poisonings: review of therapy.

Acute digoxin poisoning, its recognition and management, are reviewed. The uses of syrup of ipecac, gastric lavage, activated charcoal, cholestyramine, colestipol, edetate sodium and cathartics as measures to terminate the drug exposure are discussed. Measures to hasten digoxin elimination, such as the use of furosemide, hemodialysis and digoxin-specific antibodies are reviewed. Supportive management may include treatment with atropine, phenytoin, lidocaine, propranolol, glucose, insulin and sodium polystyrene sulfonate. Proper management of digoxin poisoning involves the use of standard decontamination procedures (emesis or gastric lavage). Activated charcoal is strongly recommended, followed by rapidly acting cathartics. Antiarrhythmic therapy usually involves atropine sulfate and phenytoin sodium.

Acute Disease↗
PubMedDate not supplied

Trends in childhood poisoning: a collaborative study 1970, 1975, 1980.

A collaborative study of 273 treated poisonings at three regional poison control centers showed a significant decrease in salicylism from 19% of all cases in 1970 to 9% in 1975 and 11% in 1980. A temporal correlation with safety packaging was also seen in the decrease in poisonings by household products from 36% and 42% of all treated poisonings in 1970 and 1975 to 21% in 1980. Poisonings by non-salicylate medications increased from 45% to 68% of treated ingestions. Therapeutic mishaps were relatively constant at 27%, 20% and 20% of all poisonings by medications. In children under one year of age 59% of medicinal poisonings were therapeutic mishaps, significantly higher than the 27% incidence for ages 1 to 5 years. Therapeutic mishaps and ingestions of household products resulted in significantly longer hospitalizations than accidental ingestion of medications. Additional data from two other regional centers permitted analysis of a total of 47 cases of treated salicylism. Therapeutic mishaps showed a possible upward trend from 27% of salicylate poisonings in 1970 to 36% in 1980. Almost all of the therapeutic mishaps with salicylates involved repeated overdose; 18 of the 19 mishaps due to other medications were allergic reactions.

Accidents↗