Biomedical subjects
Publications and source records attributed to B H Rumack.
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Methaemoglobin is haemoglobin with the iron oxidised to the ferric (Fe ) state from the normal (or reduced) ferrous (Fe++) state. Methaemoglobinaemia refers to the presence of greater than the normal physiological concentration of 1 to 2% methaemoglobin in erythrocytes. Methaemoglobin is incapable of transporting oxygen. It has an intense dark blue colour; thus, clinical cyanosis becomes apparent at a concentration of about 15%. The symptoms are manifestations of hypoxaemia with increasing concentrations of methaemoglobin. Concentrations in excess of 70% are rare, but are associated with a high incidence of mortality. Methaemoglobinaemia may be congenital but is most often acquired. Congenital methaemoglobinaemia is of two types. The first is haemoglobin M disease (several variants) which is due to the presence of amino acid substitutions in either the alpha or beta chains. The second type is due to a deficiency of the NADH-dependent methaemoglobin reductase enzyme. This deficiency has an autosomal dominant transmission, and both homozygous and heterozygous forms have been reported. The heterozygous form is not normally associated with clinical cyanosis, but such individuals are more susceptible to form methaemoglobin when exposed to inducing agents. A wide variety of chemicals including several drugs, e.g. the antimalarials chloroquine and primaquine, local anaesthetics such as lignocaine, benzocaine and prilocaine, glyceryl trinitrate, sulphonamides and phenacetin, have been reported to induce methaemoglobinaemia. An intense 'chocolate brown' coloured blood and central cyanosis unresponsive to the administration of 100% oxygen suggests the diagnosis. A simple bedside test using a drop of the patient's blood on filter paper helps to confirm the clinical suspicion. Methaemoglobin can be quantitated rapidly by a spectrophotometric method.(ABSTRACT TRUNCATED AT 250 WORDS)
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Patients frequently come to the emergency department or contact a poison center following exposure to plants. These cases are often challenging owing to difficulty in correct identification of the involved plant. A case of two patients who demonstrated anticholinergic syndromes after ingesting an unknown, wild plant is described. Chemical analysis of two suspect plants collected in the same location allowed a probable diagnosis of poisoning from ingestion of henbane (Hyoscyamus niger).
A 33-year-old man ingested 14 g of diflunisal (Dolobid, a NSAID), 3 propoxyphene-acetaminophen tablets, and ethanol. Although salicylate ingestion was specifically denied, toxicology screening revealed markedly elevated salicylate levels (176 mg/dL, 100 mg/dL, 41 mg/dL at 4 1/2, 10 and 24 hours postingestion). Blood ethanol level was 450 mg/dL. There was no respiratory alkalosis, metabolic acidosis, or increased anion gap to suggest salicylate toxicity. The patient recovered fully. Comparison testing of the salicylate assay technique used in the case (TDx fluorescence polarization immunoassay) and another commonly used technique (Trinder colorimetric assay) revealed marked cross-reactivity between salicylate and diflunisal. Samples of known diflunisal concentration were tested using the TDx salicylate assay. Percent cross-reactivity [(reported salicylate concentration/actual diflunisal concentration) x 100] was found to be 130 to 152.8% over the concentration range tested. Cross-reactivity between diflunisal and salicylate using the Trinder colorimetric assay was 20 to 52.5% over the concentration range tested. Diflunisal is not metabolized to salicylate and thus this cross-reactivity represents a significant drug-laboratory interaction. Salicylate levels measured by these methods appear to be unreliable when diflunisal is present.
A 22-month-old, 10 kg child ingested 32 mg of chlorambucil and developed irritability, myoclonic-like muscle jerks, an exaggerated startle reflex, vomiting, and EEG changes within a few hours. The neurologic symptoms improved overnight, and the patient was discharged at about 28 hours postingestion. During the three weeks of follow-up, mild bone marrow suppression occurred and resolved. A normal EEG was reported at 33 weeks postingestion.
Carbon tetrachloride (CCl4) undergoes hepatic reductive metabolism to trichloromethyl (.CCl3) and peroxytrichloromethyl (CCl3OO.) free radicals, toxic intermediates which may initiate hepatocellular damage. Recent investigations have demonstrated a potential role for hyperoxia and hyperbaric oxygen as therapeutic interventions for CCl4 poisoning. Elevated oxygen concentrations in vitro and in vivo reduce lipid peroxidation and hepatotoxicity. In vivo studies of hyperbaric oxygen following administration of CCl4 in a rat model have shown improved survival and decreased hepatotoxicity. Case reports of human poisoning, with potentially lethal ingested doses of CCl4, also suggest a potential role for treatment with hyperbaric oxygen. Hyperoxia may act by altering the metabolism of CCl4. These studies and case reports support the recommendation that 100% normobaric and hyperbaric oxygen should be treatment considerations for CCl4 poisoning.
Intentional overdosage of copper salts is seen infrequently in the U.S., but is fairly common in other countries (1). Toxic blood levels can be seen after oral ingestion of as little as one gram of copper sulfate in an adult (2). We report a case of a patient who ingested 250 grams of copper sulfate, developed transient hepatic dysfunction, and recovered after the prompt administration of chelation therapy.
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A 78 year old man was found comatose, apneic, and asystolic after closed-space smoke inhalation. He was successfully resuscitated to pulse and blood pressure at the scene. A cyanide component to the poisoning was suspected and two 300 mg doses of sodium nitrite were administered, resulting in significant hypotension. Although high methemoglobin levels were not induced, when added to simultaneously obtained carboxyhemoglobin levels, the total amount of non-oxygen transporting hemoglobin remained nearly constant for about 4-1/2 hours before hyperbaric oxygen (HBO) therapy could be administered. The patient later died in multi-organ system failure. Admission whole blood cyanide level was only 0.34 mcg/mL. These sodium nitrite adverse effects can be avoided by slow intravenous infusion and by administering only recommended doses. In smoke inhalation victims with suspected cyanide poisoning, sodium thiosulfate should be administered first, and sodium nitrite withheld until after the patient is receiving HBO therapy. When available, hydroxocobalamin (which neither induces methemoglobinemia nor causes hypotension) may be the specific cyanide antidote of choice for victims of smoke inhalation.
Excipient reactions have resulted from the use of clearly toxic substances (e.g. diethyleneglycol), the use of certain excipients in a susceptible group (e.g. very low birthweight neonates, patients with large surface area burns, patients with a history of asthma or contact dermatitis), the alteration of an excipient mixture resulting in altered bioavailability (e.g. phenytoin), and the deliberate or inadvertent extradural administration of preserved medications intended for intravenous use. Inadvertent excipient overdose has also occurred when unusually large doses of a drug containing a preservative were used [chlorbutol in morphine, ethanol in glyceryl trinitrate (nitroglycerin)]. Most excipient problems are preventable with knowledge of the currently available formulation. Government drug regulatory agencies have largely prevented introduction of a new toxic excipient; however, the new use of previously approved (but not adequately studied) excipients continues to result in unfortunate tragedies (e.g. the E-ferol incident). Populations at risk should be monitored carefully. Very low birthweight infants (less than 100g) have a well-demonstrated intolerance to many excipients, particularly during the first 2 weeks of life. Research should be directed toward development of non-preserved medications and safer diluents for this population. Drugs and excipients which have previously been demonstrated to be safer in other populations (e.g. doxapram) should be meticulously studied in this age group before widespread use is recommended. Asthmatic patients comprise another population that are frequently sensitive to excipient toxicity. In some cases, as in sulphiting agents, which are ubiquitous in foods as well as in medications, total avoidance may not be possible and prophylactic therapy may be beneficial. Inactive ingredients are clearly not consistently inert in their biological activity and therefore should not be listed as such. A more useful and concise term is excipient. It is highly recommended that all pharmaceutical manufacturers list all their excipients and make this available to practitioners and drug information centres. Alternatively or additionally, the package insert should list these excipients in accordance with good manufacturing procedures. This disclosure will help to determine the relative frequency and magnitude of problems (bioequivalence, toxicity, etc.) that excipients may have in the population, as well as enabling susceptible patients to avoid inadvertent exposure.
The symptomatology and management of toxicity caused by nonprescription stimulants is reviewed. Nonprescription stimulants contain (singly or in combination) the same basic active ingredients: caffeine 100-200 mg, phenylpropanolamine 25-50 mg, and ephedrine 25 mg. Generally, toxic reactions involve excessive CNS stimulation (e.g., increased motor activity, anxiety, and agitation) and mildly elevated pulse rate and blood pressure that resolve in six to eight hours without specific treatment. However, reactions following the ingestion of these stimulants have included severe hypertension, possible renal failure, cerebral hemorrhage, and cardiac arrhythmias. Neither ephedrine nor caffeine ingested as single entities have been reported to produce increases in blood pressure associated with end-organ damage; however, severe hypertension has followed therapeutic doses of phenylpropanolamine. General management in the overdosed patient involves establishing respiration, initiating emesis, administering activated charcoal and a cathartic, and monitoring the patient's blood pressure, ECG, fluid intake, and urinary output. The increased availability of tablets and capsules containing substantial quantities of phenylpropanolamine, caffeine, and ephedrine creates a potential for drug-induced morbidity and mortality.