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Biomedical subjects

B H Rumack

Publications and source records attributed to B H Rumack.

At least 55 records · Page 3Linked to original sources
PubMed1987

Intravenous epinephrine abuse.

A 19-year-old man with a history of intravenous cocaine and amphetamine abuse injected 1.1 mg of epinephrine intravenously from an over-the-counter bronchodilator inhaler. Within seconds, headache, nausea, numbness of hands and feet, precordial chest discomfort, and palpitations developed. The patient was given a sublingual nitroglycerin tablet by a bystander and promptly had a syncopal episode. Hypotension was observed in the emergency department 10 minutes later. Administration of 2 L of Ringer's lactate maintained blood pressure at 80-90 mm Hg systolic. An electrocardiogram showed ischemic changes in the precordial leads. Cardiac enzymes remained normal. Mild hypokalemia and hyperglycemia were observed. This case illustrates an unusual route of abuse of an over-the-counter epinephrine bronchodilator.

Adult↗
PubMed1987

Hydroxycobalamin/sodium thiosulfate as a cyanide antidote.

Severe, acute cyanide poisoning is uncommon and can be very difficult to diagnose if a history of exposure is unavailable. Victims of smoke inhalation may have significant cyanide poisoning as well as carbon monoxide toxicity. The Lilly Cyanide Antidote Kit currently available in America unfortunately has its own inherent toxicity. An efficacious antidote lacking toxicity is desirable, especially in cases where the diagnosis of cyanide poisoning cannot be made with certainty. Hydroxycobalamin/sodium thiosulfate has been used in France since 1970. Both components have been shown to be safe and efficacious in animal studies. Case reports of human cyanide poisoning treated with hydroxycobalamin/sodium thiosulfate have been published only in French. Animal and human data on the use of this antidotal combination are reviewed. Hydroxycobalamin/sodium thiosulfate is an efficacious cyanide antidote with little inherent toxicity.

Acute Disease↗
PubMed1987

Acute toxic blindness: unrecognized quinine poisoning.

Two cases of acute blindness due to quinine poisoning are presented. In both cases, the diagnosis was initially unsuspected. In addition, tinnitus, decreased hearing, vomiting, abdominal pain, and confusion were noted in one patient, and the other experienced decreased hearing, headache, confusion, tachycardia, later bradycardia, and first-degree atrioventricular block. The onset of blindness was delayed more than 12 hours after ingestion in both cases. Quinine levels of 13.6 micrograms/mL and 18.6 micrograms/mL were demonstrated (therapeutic = 1 to 3 micrograms/mL). One patient developed marked constriction of visual fields and some residual decreased acuity, while the other regained normal visual acuity.

Acute Disease↗
PubMed1987

Intravenous theophylline poisoning and multiple-dose charcoal in an animal model.

Large overdoses of IV theophylline (50 to 100 mg/kg) were administered to five canines on two separate occasions. On day one, with no charcoal administered, theophylline levels were serially obtained between ten minutes and 12 hours after infusion and the animals were recovered from anesthesia. Three days later the same dose of theophylline was administered, but then 50 g activated charcoal was placed through a nasogastric tube into the duodenum every hour for eight doses. In all five animals tested, activated charcoal significantly decreased the area under the serum concentration-time curve, decreased the half-life of elimination, and increased the clearance of theophylline. This effect on pharmacokinetics was not seen when the nasogastric tube was put into the stomach instead of the small bowel because the charcoal administered did not pass beyond the pylorus. In a separate experiment in which bile theophylline concentrations were measured, it was demonstrated that enhanced elimination was not from interruption of enterohepatic circulation of theophylline. This suggests that the demonstrated physiologic mechanism is that of gastrointestinal dialysis.

Animals↗
PubMed1987

Nitrite/thiosulfate treated acute cyanide poisoning: estimated kinetics after antidote.

A 34 year old, 73 kg man ingested a 1 gram potassium cyanide pellet in a suicide attempt. Within one hour, coma, apnea, metabolic acidosis, and seizures developed. Sodium nitrite and sodium thiosulfate were administered. Dramatic improvement in the clinical condition occurred by the completion of antidote infusion. Methemoglobin level was 2% immediately after nitrite administration. Serial whole blood cyanide levels were obtained, documenting a highest measured level of 15.68 mcg/mL. Estimations of toxicokinetic parameters including terminal half-life (t 1/2) (19 hours), clearance (163 mL/minute), and volume of distribution (Vd) (0.41 L/kg) were calculated. The nitrite/thiosulfate combination was clinically efficacious in this case and resulted in complete recovery.

Adult↗
PubMed1987

A case of MAO inhibitor/MDMA interaction: agony after ecstasy.

After ingesting 3,4-methylene-dioxy-methamphetamine (MDMA) and the monoamine oxidase (MAO) inhibitor phenelzine, a 50 year old male developed marked hypertension, diaphoresis, altered mental status, and hypertonicity lasting 5-6 hours. This clinical course is typical of interaction between MAO inhibitors and some sympathomimetics including amphetamines. Such interaction has not previously been described involving MDMA. Sympathomimetic-MAO inhibitor interactions can cause excessive release of endogenous bioactive amines (e.g. norepinephrine, serotonin). Hypertensive crisis, intracranial hemorrhage, hypertonicity, and severe hyperthermia have occurred due to sympathomimetic-MAO inhibitor interactions. MDMA shares structural and pharmacologic features with other agents capable of causing this interaction, and this case suggests that MDMA can cause significant toxicity in patients taking MAO inhibitors.

3,4-Methylenedioxyamphetamine↗
PubMed1987

Toxicity of Cyclamen persium (Mill).

Cyclamen spp contain toxic saponins, although the number of serious exposures is very low. The plant was investigated for toxic and pharmacologic properties in the 1950's and 1960's, but there is little current investigation. Cyclamens have been found both as woodland plants and houseplants in Europe for years, and the plant is becoming increasingly popular in the US. Poison centers should be aware of the potential toxicity of this plant, especially that of the rhizomatous tubers. Additional data on exposures reported to poison centers may be helpful in further defining the toxicity of this plant.

Humans↗
PubMed1986

Human overdose with the veterinary tranquilizer xylazine.

Three patients self-injected the veterinary tranquilizing agent xylazine (Rompun). The first patient developed mild bradycardia and hypotension, miosis, and a feeling of disorientation. The other two patients became apneic and required intubation and mechanical ventilation. Initial mild hypertension followed by mild hypotension and a mildly elevated blood glucose was seen in the second patient, whereas both the second and third patients developed mild bradycardia. Xylazine has structural similarity to the phenothiazines and pharmacological activity similar to clonidine. With increasing veterinary use, the availability and potential for human exposures may also increase.

Adult↗
PubMed1986

Acetaminophen overdose in children and adolescents.

Ingestion of acetaminophen by young children and adolescents is common. Most children under the age of 6 who have ingested pediatric products can be safely managed at home. Children under the age of 6 who have taken a significant ingestion should be evaluated with a plasma level 4 or more hours after ingestion and, if toxic, treated with the antidote NAC prior to 16 hours postingestion. Less than 5 per cent of children under the age of 6 with toxic plasma levels will develop transient hepatic abnormalities. Adolescents who use acetaminophen in a suicidal or manipulative attempt should be seen and evaluated with a plasma acetaminophen level 4 or more hours postingestion. If the level is in the potentially toxic range on the nomogram, they should be treated prior to 16 hours postingestion with the antidote NAC. All patients should be evaluated for the possibility of other drugs or ingestants, especially if there is a change in the sensorium early in the course. The expected course of events in a patient with a toxic level of acetaminophen in the plasma is to have nausea, vomiting, and diaphoresis the first 24 hours. Following this, the patient should feel better but may begin to develop abnormalities of SGOT, SGPT, bilirubin, and prothrombin. Toxic patients will have peak enzyme levels at 72 to 96 hours. Over 99 per cent of patients will recover to normal values by 7 to 8 days postingestion. Long-term sequelae are not known.

Acetaminophen↗
PubMed1986

Clinical toxicology of cyanide.

Cyanide poisoning causes a high incidence of severe symptomatology and fatality. There are numerous sources of potential cyanide exposure. Without the history of cyanide exposure, diagnosis is often difficult. Treatment with supportive measures and available specific and efficacious antidotes frequently allows survival. The toxicology of cyanide, including sources, clinical features, diagnosis, and treatment, is reviewed.

Amygdalin↗
PubMed1986

Hydrogen sulfide poisoning from toxic inhalations of roofing asphalt fumes.

Hydrogen sulfide poisoning from inhalation of roofing asphalt fumes is a rare but devastating injury. Two cases of toxic inhalation involving exposure to several gases, including hydrogen sulfide, evolved from cooling asphalt, are presented. Both victims were treated with supportive measures, including 100% normobaric oxygen, and one also received sodium nitrite. In one patient rapid, complete recovery was temporally associated with nitrite administration. The patient not treated with sodium nitrite survived with apparently permanent severe neurological sequelae.

Adult↗