David J. Doedens

Iodine absorption in burn patients treated topically with povidone‐iodine

Povidone‐iodine is used as a topical antimicrobial in burn patients. Although absorption of iodine has been thought to be negligible, several patients have recently.been noted with substantial elevations of serum free iodide. Unexplained abnormalities occurred in several of these patients, renal failure, metabolic acidosis, and elevation of serum glutamic oxaloacetic transaminase. It is conceivable that the large iodide loads noted were at least in part responsible for these abnormalities.

Asphyxial deaths from the recreational use of nitrous oxide

The recreational use of nitrous oxide is widespread. Nitrous oxide for recreational use is usually obtained from anesthesia tanks or whipped-cream machine chargers or cans. Twenty previously described deaths associated with recreational nitrous-oxide use describe anesthesia tanks and whipped-cream machine dispensors as a source. Five deaths associated with nitrous oxide use are presented; two involving whipped-cream cannisters as the source, two involving anesthesia tanks, and one involving a racing fuel tank as a source of nitrous oxide. Autopsy findings in our cases were subtle or negative, but usually suggestive of asphyxia. Through a laboratory simulation, we have confirmed that nitrous oxide displaces oxygen in a closed space, which probably leads to asphyxia. A review of the literature, neuropharmacology, and pathophysiology of nitrous oxide use is also presented.

Case Report Increased serum iodide concentration from iodine absorption through wounds treated topically with povidone-iodine

Increased serum iodide concentrations secondary to iodine absorption through wounds treated with povidone-iodine dressings is described. Hyperchloremic acidosis and a disparity between serum chloride concentrations determined by two different methods suggested the presence of an unidentified halide. Cardiovascular instability and renal failure occurred concurrent with systemic iodide accumulation. Measurement of serum iodide concentration should be performed when povidone-iodine is used topically in patients with impaired renal function.

Inhibition of pyruvate carboxylase by chloropyruvic acid and related compounds.

Abstract 3-Chloro-1,2-propanediol (CPD), a compound with male antifertility activity in several species, was slowly metabolized in rat liver slices. Incorporation of 14CO2 into glucose in slices incubated with lactate or pyruvate was inhibited by CPD and by chloropyruvic acid, a possible metabolite. At 0.1 mM, chloropyruvic acid (CPA) and related compounds, including beta-chlorolactic, fluoropyruvic and chloroacetic acid, inhibited incorporation into glucose of label from [U−14C]alanine without affecting production of ketone bodies or 14CO2. Inhibition was not observed in similar preparations using succinate as substrate. In mitochondria, concentrations of 1–10 mM CPA inhibited CO2 fixation by 56–95 per cent. Relative inhibition was CPA > fluoropyruvic acid > beta-chlorolactic acid > chloroacetic acid. In acetone powder extracts, CPA at 1–10 mM reduced CO2 fixation by 21–86 per cent. Relative inhibition was CPA > beta-chlorolactic acid > chloroacetic acid. Interconversion between CPA and chlorolactate was not catalyzed by lactic dehydrogenase, nor did these compounds inhibit this enzyme. The data indicate that CPA and related acids may inhibit gluconeogenesis by specific inhibition of pyruvate carboxylase. Whether or not this metabolic effect is involved in the development of sterility after administration of CPD remains to be determined

Heroin, Morphine, and Hydromorphone Determination in Postmortem Material by High Performance Liquid Chromatography

A procedure has been developed for the simultaneous determination of heroin, morphine, and hydromorphone from postmortem tissues by reversed phase high performance liquid chromatography (HPLC) using electrochemical detection. This method permits the direct determination of unmetabolized heroin from antemortem or postmortem urine as evidence of illegal drug use. Presumptive confirmation of heroin was based on the ability to hydrolyze the HPLC heroin fraction to morphine. Heroin was also confirmed in urine by gas chromatographic/mass spectroscopic (GC/MS) analysis of the HPLC fraction. Analysis of postmortem blood, gastric contents, urine, and injection site tissues have revealed the presence of morphine and hydromorphone, while heroin has only been identified in urine.

Concealment of the Body in Drug Deaths

Discovery of a concealed body often leads to the assumption that the manner of death was homicide. However, in cases where death has resulted from illicit drug use or drug abuse, the body may be concealed to protect persons involved in drug abuse or drug marketing.

Toxicity of sodium lodide in the rabbit: Effects on hydrogen ion homeostasis, hepatic and renal functions☆☆☆

Abstract The effect of parenteral sodium iodide on hepatic and renal function and acid-base balance was studied in New Zeland white rabbits. Four groups of rabbits were infused intravenously with either 0.15 m NaCl or NaI in different concentrations, 0.03–0.15 m . Renal function as measured by blood-urea-nitrogen and urine protein excretion, hepatic cellular integrity, reflected in the serum activity of glutamic oxaloacetic transaminase, and acid-base balance determined by arterial pH and pCO 2 , were the parameters chosen for study. The groups receiving the largest amount of iodide manifested severe hepatic changes, moderate renal changes, and metabolic acidosis. Histologic examination showed marked hepatic vacuolization and necrosis at the highest iodide dose. Renal tubular cells were vacuolated and occasionally necrotic. The genesis of the acidosis is obscure and may be augmented by an inadequate renal compensation for systemic acidosis. It is concluded that, in the rabbit, iodide is toxic to the liver and kidney and produces metabolic acidosis.