The role of the laboratory in treatment of the poisoned patient: laboratory perspective.
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Clinical Laboratory Techniques↗
Biomedical subjects
D N Bailey
Publications and source records attributed to D N Bailey.
Extraction of acidic drugs from water and plasma: study of recovery with five different solvents.
The recovery of 28 acidic drugs from water and plasma was investigated spectrophotometrically using five different solvents for extraction: hexane, diethyl ether, toluene, n-butyl chloride, and chloroform. Nine barbiturates, three sulfonamides, four diuretics, and twelve other acidic drugs were studied. As classes, the barbiturates, the sulfonamides, and the diuretics were optimally extracted with diethyl ether from both water and plasma, while considerable variation in recovery was noted among solvents for the other drugs. In general, recoveries from water were higher than those from plasma with most solvents, except for the sulfonamides for which recoveries were often better from plasma. Extraction recoveries for the individual drugs are tabulated and compared.
Barbiturates↗
Inhibition of methadone and phenobarbital percutaneous absorption by parenterally administered ethanol.
Four hours after the topical administration of either aqueous methadone hydrochloride or sodium phenobarbital to hairless (SKH, hr-1/hr-1) mice, the mean drug concentration in liver was significantly lower in ethanol-treated mice than in control animals that had received only water (methadone study, p less than 0.01; phenobarbital study, p less than 0.02). No statistically significant difference was noted between the mean concentrations for test and control mice when either methadone or phenobarbital were given by intraperitoneal injection instead of topically, suggesting that ethanol inhibits the percutaneous absorption of these drugs in vivo.
Animals↗
Propylene glycol as a cause of lactic acidosis.
Propylene glycol (PG) concentrations were measured in 35 sera and eight cerebrospinal fluids (CSF) from five patients receiving intravenous medications containing PG as a vehicle. Serum concentrations ranged from 6 to 711 mg/L, and CSF concentrations from 11 to 566 mg/L. The CSF concentrations were as high as 85% of the serum concentrations. In several instances, PG was also measured in urine and pleural fluid. Lactate concentrations ranged up to 24.1 mEq/L (217 mg/dL) and showed statistically significant correlation (r = 0.921) with the PG concentrations in serum (p less than 0.01). The PG:creatinine clearance ratios in two patients were 35.5% and 48.8%. Serum half-lives in two patients were 4.7 and 5.6 hrs. Propylene glycol administration may be an important cause of lactic acidosis in the hospitalized patient.
Acidosis↗
Inhibition of phencyclidine percutaneous absorption by parenterally administered hypertonic saline.
Four hours after topical application of phencyclidine hydrochloride to hairless (hr-1/hr-1) mice, the mean hepatic concentration of phencyclidine (512.8 ng/g) was significantly lower for mice that had received intraperitoneal injections of sodium chloride, 1.75 mol/L (3500 mOsm/kg), than for control mice that had received equal volumes of water by the same route (2108.5 ng/g) (p less than 0.05). Hypertonic saline instilled intraperitoneally seemed to inhibit percutaneous absorption of phencyclidine hydrochloride. The effect may have been mediated by production of cutaneous dehydration.
Animals↗
Ethchlorvynol ingestion: interpretation of blood concentrations and clinical findings.
Thirty-eight patients who ingested ethchlorvynol were seen at our institution over an 8.7 year period. Eleven involved ethchlorvynol alone ("pure") while the remainder included at least one other drug ("mixed"). Twenty-three of the patients were women. Six patients required hospitalization. Five patients were chronic users of the drug. Admission ethchlorvynol blood concentrations ranged from 3 to 46 mg/L ("pure") and from 3 to 75 mg/L ("mixed"). For the "pure" cases the most common physical findings were depressed level of consciousness (10 cases), dysarthria (7), mydriasis (6), nystagmus (6), areflexia (4), tachycardia (4), and hypotension, ataxia, and respiratory depression (2 cases each). Following "pure" ingestion, ethchlorvynol concentrations greater than 19 mg/L were usually associated with dysarthria, mydriasis, nystagmus, and tachycardia. When concentrations exceeded 38 mg/L, coma, areflexia, hypotension, and respiratory depression were generally noted as well. All patients recovered with supportive care alone.
Adult↗
Blood concentrations and clinical findings in nonfatal and fatal intoxications involving glutethimide and codeine.
Blood concentrations and clinical findings were evaluated in twenty-six nonfatal and twelve fatal intoxications involving the combination of glutethimide and codeine ("loads"). The mean glutethimide concentration was 10 +/- 5 mg/L for nonfatal cases (range 2-18 mg/L) and 13.9 +/- 6.6 mg/L for fatal cases (range 4.6-26.4 mg/L). The mean codeine concentration for fatal intoxications was 1.21 +/- 1.17 mg/L (range 0.13-4.32 mg/L). Codeine concentrations were not measured in cases of nonfatal intoxication. Nine nonfatal cases required hospitalization on a medical ward (mean length of stay 3 +/- 3 days). Depressed level of consciousness was the most common abnormal physical finding (24 cases); 18 patients were lethargic but arousable with nonpainful stimulation and 6 patients with serum glutethimide concentrations of 10 mg/L or greater were comatose. The level of consciousness showed statistically significant correlation with the glutethimide concentration (P less than 0.01). Twenty-four nonfatal intoxications involved at least one other drug in addition to glutethimide and codeine (salicylates in 12 and acetaminophen in 4), while only 7 fatal cases involved at least one additional drug (acetaminophen and diazepam in 3 each). The finding of glutethimide should prompt a search for codeine and vice versa, especially when the presence of either does not in and of itself explain the clinical condition of the patient.
Adult↗
Binding of antiarrhythmic drugs to human placenta in vitro.
Lidocaine, procainamide and quinidine binding to human placenta was investigated in vitro. Pooled whole human placental homogenate supplemented with either non-radiolabelled lidocaine, procainamide or quinidine over the concentration range 50-5,000 x 10(-7) mol/L was submitted to equilibrium dialysis against phosphate buffer, pH 7.4, 0.1 mol/L. Post-dialysis drug concentrations were measured by enzyme immunoassay. Data were analyzed by the method of Scatchard. No binding to placenta was noted for either lidocaine or procainamide. In contrast, up to 22 percent of quinidine was bound. Two binders were defined as follows: #1 (Ka, 7.37 x 10(5) L/mol; Bo, 1.55 x 10(-7) mol/L) and #2 (Ka, 7.11 x 10(4) L/mol; Bo, 4.05 x 10(-6) mol/L). The concentrations of quinidine binding sites in moles per gram of placenta were 1.55 x 10(-9) and 4.05 x 10(-8), respectively. These data suggest that quinidine may be accumulated in human placenta.
Anti-Arrhythmia Agents↗
Lidocaine, quinidine, and theophylline binding to human milk.
Lidocaine, quinidine, and theophylline binding to normal pooled mature human milk was determined using equilibrium dialysis at 4 degrees C. Binding to milk was compared with binding to pooled human serum. The observed binding was related to the relative lipid solubility of each drug in milk. The potential for the excretion of each drug into milk was also evaluated.
Animals↗