Lighter fluid poisoning [keywords]
- Quantitative determination of n-propane, iso-butane, and n-butane by headspace GC-MS in intoxications by inhalation of lighter fluid. [Journal Article, Research Support, Non-U.S. Gov't]
- J Anal Toxicol 2002 Jan-Feb; 26(1):35-42.
This report describes a fully elaborated and validated method for quantitation of the hydrocarbons n-propane, iso-butane, and n-butane in blood samples. The newly developed analytical procedure is suitable for both emergency cases and forensic medicine investigations. Its practical applicability is illustrated with a forensic blood sample after acute inhalative intoxication with lighter fluid; case history and toxicological findings are included. Identification and quantitation of the analytes were performed using static headspace extraction combined with gas chromatography-mass spectrometry. In order to reconcile the large gas volumes injected (0.5 mL) with the narrowbore capillary column and thus achieve preconcentration, cold trapping on a Tenax sorbent followed by flash desorption was applied. Adequate retention and separation were achieved isothermally at 35 degrees C on a thick-film capillary column. Sample preparation was kept to a strict minimum and involved simply adding 2.5 microL of a liquid solution of 1,1,2-trichlorotrifluoroethane in t-butyl-methylether as an internal standard to aliquots of blood in a capped vial. Standards were created by volumetric dilution departing from a gravimetrically prepared calibration gas mixture composed of 0.3% of n-propane, 0.7% of iso-butane, and 0.8% of n-butane in nitrogen. In the forensic blood sample, the following concentrations were measured: 90.0 microg/L for n-propane, 246 microg/L for iso-butane, and 846 microg/L for n-butane.
- [Fatal lighter fluid snuffing]. [Letter]
- Ugeskr Laeger 1988 Apr 25; 150(17):1060-1.
- Toxicity with intravenous injection of naphtha in man. [Case Reports, Journal Article]
- Clin Toxicol 1980 May; 16(3):335-43.
Intravenous injection of charcoal lighter fluid (naphtha) in a suicidal attempt led to development of severe hemorrhagic pneumonitis in a 40-year-old individual. Presenting symptoms consisted of pleuritic chest pain, epigastric discomfort, and dyspnea; they appeared within 2 hours after injection. Development of roentgenographic changes lagged behind the clinical symptoms by several hours. Fever and leukocytosis were present despite the absence of demonstrable superimposed bacterial infection. The pathology seemed exclusively confined to the pulmonary system with no clinical or laboratory evidence of extrapulmonary involvement. Repeated clinical, radiographic, and pulmonary function evaluations over an 18-month follow-up period have shown complete resolution of pulmonary lesions without residual abnormalities.
- Hemorrhagic pneumonitis after intravenous injection of charcoal lighter fluid. [Case Reports, Journal Article]
- Ann Intern Med 1979 May; 90(5):794-5.
- Pneumatoceles as a complication of chemical pneumonia after hydrocarbon ingestion. [Journal Article]
- Am J Roentgenol Radium Ther Nucl Med 1975 Nov; 125(3):531-7.
Of 338 children with hydrocarbon ingestion, 134 (40 percent) had pneumonia. Pneumonia was most common after kerosene, furniture polish and lighter fluid ingestion. The pneumonia was most severe, however, with furniture polish. Pneumatoceles occurred in 14 children, most commonly with charcoal lighter fluid ingestion. Pneumatoceles generally appeared late, after the consolidation had cleared. Pneumatoceles were often large, septate and irregular, and sometimes contained fluid levels.
- Ingestion of charcoal lighter fluid. [Journal Article]
- J Pediatr 1975 Oct; 87(4):633-6.
- The role of "leakage" of tubular fluid in anuria due to mercury poisoning. [Journal Article]
- J Clin Invest 1967 May; 46(5):695-704.
The role of "leakage" of tubular fluid in anuria produced by mercury poisoning was studied in rats by micropuncture techniques. After an initial brisk diuresis, almost all animals were completely anuric 24 hours after HgCl(2) injection. Lissamine green injected intravenously in the early stage of anuria appeared in the beginning of the proximal tubule, but the color became progressively lighter as the dye traversed the proximal convolutions. The dye was barely visible in the terminal segments of the proximal tubule; it did not appear at all in the distal tubules. These observations suggest that the proximal epithelium had become abnormally permeable to Lissamine green. Tubular fluid to plasma inulin (TF/P(In)) ratios and inulin clearance were measured in individual nephrons at three sites: early proximal tubule, late proximal tubule, and distal tubule. It was found that TF/P(In) ratios were abnormally low in the late proximal and distal tubules. Inulin clearance was normal at the beginning of the proximal tubule but fell by more than 60% by the late proximal convolutions. Thus, the proximal tubule had also become permeable to inulin. We conclude from these observations that anuria in mercury poisoning can occur in the presence of a normal glomerular filtration rate. The absence of urine flow appears to be due to complete absorption of the filtrate through an excessively permeable tubular epithelium. The driving force affecting this fluid absorption is probably the colloid oncotic pressure of the peritubular capillary blood.