An unnatural death by propan-1-ol and propan-2-ol.

A fatality of an inpatient ingesting a disinfectant containing ethanol, propan-1-ol, and propan-2-ol is reported. The alleged survival time was about 1 h. Major findings at autopsy were an extended hemorrhagic lung edema, an edematous brain, and shock kidneys. Concentrations of alcohols and acetone, a major metabolite of propan-2-ol, were determined from body fluids (blood from the heart and the femoral vein, urine, gastric contents) and tissues (brain, muscle, liver, kidneys, lungs) by headspace/gas chromatography using 2-methylpropan-2-ol as the internal standard. All samples investigated were positive for propan-1-ol, propan-2-ol, ethanol, and acetone except stomach contents, where acetone was not detectable. The low concentration of acetone compared to propan-2-ol likely supports the short survival time. The concentration ratios estimated from the results are in accordance with the physico-chemical properties of the particular alcohols, their different affinities towards alcohol dehydrogenase as well as their interdependence during biotransformation. Autopsy did not reveal the cause of death. According to the few published data, blood concentrations of 1.44 and 1.70 mg/g of propan-2-ol and propan-1-ol, respectively, are considered sufficient to have caused the death. This case also points to the need to restrict access to antiseptic solutions containing alcohols in wards with patients at risk.

[Atypical poisoning with mixture of toxic alcohols--a case report]. / Nietypowe zatrucie mieszanina alkoholi niespozywczych--opis przypadku.

UNLABELLED: We presented the male who was addicted to ethanol, and who drank the mixture of different toxic alcohols. Toxicological screening of ingested fluid found 42% vol propan-1-OL, and 17% vol propan-2-OL (isopropanol). After regaining consciousness, the patient stated that substance is becoming more and more popular as a new type of cheap alcohol, and because of its "low price and high power". CONCLUSIONS: 1. It is advisable to consult all cases of poisoning with inedible alcohols with Regional Centers of Toxicology. 2. There is an urgent need to create a reference toxicological laboratories, which would have the ability to diagnose poisoning with different xenobiotics. 3. Further training for students and doctors, about diagnosis and therapy of acute poisonings, should be done. 4. The endemic foci of intoxication with inedible alcohols should be checked and discovered.

[Comparative morphological characteristics of changes in the liver in case of poisoning with alcohol-containing liquids in human and following subacute treatment of animals with ethyl and propyl alcohols, ethylene glycol and their mixtures].

The authors present results of comparative morphological studies of changes in the liver after intoxication with alcohol-containing liquids in human and following subacute treatment of animals with ethyl and propyl alcohols, ethylene glycol and their mixtures. It was shown that poisoning caused by individual chemical substances and their mixtures induced significantly different changes in the liver of animals. The mixtures produced much more serious toxic lesions in the parenchymal tissue than individual spirits (including development of necrotization foci) and contributed to enhanced mortality of experimental animals. The morphological picture of the liver in human subjects poisoned by a mixture of alcohols resembled that after intoxication with carbon tetrachloride and was consistent with the changes in people who had died during episodes of mass poisoning with surrogate alcoholic beverages and alcohol-containing liquids.

A case of mixed intoxication with isopropyl alcohol and propanol-1 after ingestion of a topical antiseptic solution.

We report a mixed intoxication with isopropyl alcohol and propanol-1 in a hospitalized patient who ingested, on two separate days, two 100 ml bottles of a topical antiseptic solution containing isopropyl alcohol and propanol-1. Eight hours after the second ingestion, plasma concentrations of isopropanol, propanol-1 and acetone were 37 mg/dL, <10 mg/dL, and 227 mg/dl, respectively. Despite a lack of severe toxicity, 4-methylpyrazole (fomepizole) was initiated. This case points out the need to limit access to alcohol-containing antiseptic solutions on wards where alcoholic and psychotic patients are hospitalized.

Poisoning with 1-propanol and 2-propanol.

1-Propanol and 2-propanol are isomers of an alcohol with three carbons. They are colorless liquids with a sweet odor. 1-Propanol is metabolized by alcohol dehydrogenase to propionic acid and presents with metabolic acidosis and elevated anion gap, whereas 2-propanol is metabolized by alcohol dehydrogenase to acetone and presents with rapidly developing (within 3-4 h after exposure) ketosis and ketonuria but without metabolic acidosis. We report a patient who simultaneously ingested a lethal dose of 1-propanol and 2-propanol as a hand disinfectant in hospital. The patient lost consciousness and stopped breathing within half an hour after ingestion. He was intubated and artificially ventilated. Initial laboratory results showed mixed acidosis with elevated anion gap, but ketonuria appeared only 12 h after admission and 6 h following the regaining of consciousness. Therefore, laboratory results in simultaneous poisoning with two isomers of alcohol are not just a sum of laboratory results obtained in isolated poisoning with each isomer because they influence each other's metabolism: 1-propanol retards the metabolism of 2-propanol to acetone. In conclusion, 1-propanol and 2-propanol poisoning presents early with mixed acidosis and elevated anion gap and only later with ketonuria.

[Acute oral poisoning with isopropyl alcohol in alcoholics]. / Ostre doustne zatrucie alkoholem izopropylowym u osoby uzaleznionej od alkoholu etylowego.

The symptoms and clinical course of repeated poisonings with isopropyl alcohol in ethanol addicted 43-years old man is presented in the study. The blood and urine concentrations of isopropanol and acetone and also the blood ethanol concentration are given. The biological half-life of isopropanol calculated for the first 12 hours from admission to the Clinic was 6.9 hours. The biological half-life of acetone in the first 6 hours of hospitalisation was 5 hours, and then a considerable slowing down up to 29 hours was noted. The clinical symptoms, similar to ethanol poisoning, including strongly manifested catatonia and ketonuria without metabolic acidosis indicate the isopropanol intoxication. Hypokalemia should to be taken into consideration in treatment of isopropanol poisoning. An intravenous bicarbonates should be administered carefully e.g. when rhabdomyolysis occur.

Discrepancies in osmolal gaps and calculated alcohol concentrations.

OBJECTIVES: To estimate unexplained osmolal gaps (UEOG) during ethanol ingestions after accounting for measured ethanol concentrations and to explore the causes of observed discrepancies. DESIGN AND SPECIMENS: A random convenience sample of serum specimens with a request to perform osmometry for the detection of alcohols was studied. MAIN OUTCOME MEASURES: Serum concentrations of sodium, glucose, urea nitrogen, ethanol, osmolality, and ethanol were measured by two analytic methods to determine calculated osmolalities and osmolal gaps using two commonly used formulas. RESULTS: In 79 serum specimens submitted for osmometry, mean ethanol concentrations were 199 +/- 154 (SD) mg/dL; 15 specimens had no detectable ethanol. After regression of the calculated ethanol concentrations and the measured ethanol concentrations, the Dorwart and Chalmers formula showed a large constant bias of 45.217 +/- 6.414 (SE) mOsm/kg in predicting measured ethanol concentrations. The Smithline and Gardner formula was similarly as precise (r = .9786), but had a much smaller bias of -3.929 +/- 6.623 (SE) mOsm/kg. Actual mean differences between measured and calculated osmolalities (including ethanol osmols) gave an estimate of UEOG seen during ethanol ingestions. Using the less biased formula, the mean UEOG was 1.4 +/- 8.5 mOsm/kg, giving a 95% upper limit of the reference range of 18 mOsm/kg in this population with ethanol ingestions. Three significant outliers were identified and their UEOG could be explained by the presence of mannitol, isopropanol, or possibly a change in the assumed value for fractional water, normally a constant in these formulas for calculated osmolality. Other specific causes of osmolal gap and UEOG are discussed. CONCLUSION: The potential range of osmolal gaps seen during ethanol ingestions after accounting for ethanol is demonstrated to be greater than in previous studies, which have included a lower proportion of ethanol-intoxicated subjects in their study sample.

Measurement of serum isopropanol and the acetone metabolite by proton nuclear magnetic resonance: application to pharmacokinetic evaluation in a simulated overdose model.

The purpose of this investigation was to 1) compare the performance of proton nuclear magnetic resonance spectroscopy to gas chromatography head-space analysis in the measurement of serum isopropanol and its metabolite, acetone, obtained during a simulated overdose, and 2) compare pharmacokinetic parameters obtained using the two analytical techniques. Three healthy volunteers ingested 0.6 mL/kg of 70% isopropanol and blood samples were obtained at baseline, 0.16, 0.33, 0.66, 1.0, 1.5, 2.0, 3.0, 4.0, 6.0, 8.0, 12.0, and 24.0 hours post-ingestion. Resulting sera were analyzed by gas chromatography head-space analysis and proton nuclear magnetic resonance spectroscopy for determination of isopropanol and acetone concentrations. A correlation between concentrations quantitated by gas chromatography head-space analysis versus proton nuclear magnetic resonance spectroscopy was determined using linear regression. Pharmacokinetic disposition parameters were determined from serum concentration-time data and compared using analysis of variance. For isopropanol, the linear regression equation which describes the relationship between gas chromatography head-space analysis and proton nuclear magnetic resonance spectroscopy was y = 1.041x - 2.180 (r2 = 0.995, p < 0.0001); for acetone, y = 1.022x - 0.946 (r2 = 0.984, p < 0.0001). Pharmacokinetic disposition parameters derived from the two analytical methods were comparable. Proton nuclear magnetic resonance spectroscopy can be used to rapidly quantitate serum isopropanol and acetone concentrations in the same sample when gas chromatography head-space analysis is unavailable. Also, proton nuclear magnetic resonance spectroscopy can be used to follow serial serum concentrations during an ingestion for the purpose of pharmacokinetic analysis.

Isopropyl alcohol intoxication in a neonate through chronic dermal exposure: a complication of a culturally-based umbilical care practice.

A 21-day-old boy presented to our emergency department hypotonic, lethargic, and intermittently unresponsive to pain. A workup for ketoacidosis, sepsis, and central nervous system hemorrhage was negative. A urine drug screen collected eight hours after hospitalization showed 39 mg/dl of isopropyl alcohol and 76 mg/dl of acetone. The first serum drug analysis was not performed until 18 hours after admission, at a time when there had been clinical improvement. The isopropyl alcohol concentration was 8 mg/dl, and the acetone concentration was 203 mg/dl. Management was supportive, and the patient stabilized. He was discharged from the hospital in good health in three days. A further review of the history showed no evidence for an oral exposure to isopropyl alcohol. However, since leaving the maternity hospital the mother had been applying gauze pads or cotton balls soaked with isopropyl alcohol to the umbilicus with every diaper change. We conclude that the child suffered from an isopropyl alcohol intoxication that occurred by absorption through the umbilical area.

Severe isopropanolemia without acetonemia or clinical manifestations of isopropanol intoxication.

This is the first reported case of severe isopropanolemia in a patient who did not experience associated clinical manifestations and acetonemia. The patient was found lying face down in a hotel lobby but at admission was alert and oriented to place and person. Toxicological analysis of the patient's serum revealed the presence of isopropanol at a concentration of 72 mmol/L. An increased serum osmolal gap (81 mOsm/kg) was also observed. The serum concentration of isopropanol decreased to 9.5 mmol/L 15.5 h after admission with an estimated half-life of elimination of 5-7 h. No serum acetone was detected throughout the patient's hospitalization. The identity of isopropanol was confirmed by gas chromatography/mass spectrometry. The patient remained awake and alert while in the hospital and was discharged 5 days after admission. These unusual findings raise some fundamental questions about the role of isopropanol conversion to acetone in the manifestation of symptoms usually associated with isopropanol intoxication.

Two-week-old infant with isopropanol intoxication.

Isopropyl alcohol continues to be a frequent toxicologic exposure. However, no cases involving the newborn period have been described. A 14-day-old male infant presented to the emergency department (ED) with the mother's chief complaint that "He is not himself." Physical examination observed the infant to be lethargic and hypotonic. Laboratory evaluation revealed a positive urine drug screen for isopropanol and acetone. Elevated serum levels (in mg/dl) of isopropanol/acetone at 2:45, 4:15, 11:10, and 29:53 hours postpresentation were 101/136, 81/149, 20/155, and 5/72, respectively. Overall, this patient did remarkably well with minimal supportive care and was noted to have a normal neurologic examination within 10 hours of presentation despite rising serum acetone levels. This case brings into question the hypothesis that acetone, a metabolite of isopropanol, prolongs central nervous system depression in acute isopropyl alcohol intoxication. The importance of urine drug screens in children who present to the ED with unusual neurologic examinations is appreciated.

The use of delta osmolality to predict serum isopropanol and acetone concentrations.

We investigated whether serum delta osmolality will predict the total serum concentration of isopropanol and acetone metabolite. Three isopropanol ingestions were monitored by delta osmolality determinations followed by quantification of serum isopropanol and acetone concentrations. The delta osmolality was established by routine chemical analysis and standard freezing point depression osmometry. Serum isopropanol and acetone levels were quantified by gas chromatography-head space analysis (GC-HS). Patients were initially suspected of having isopropanol intoxication secondary to an elevated delta osmolality discrepancy (measured - calculated > 10 mOsm). Serum concentrations versus delta osmolality were analyzed by linear regression (correlation coefficient r = 0.713; p < 0.05). The delta osmolality paralleled and decreased relative to the total low molecular weight of volatile concentration in each case. In emergencies, delta osmolality may be a screening test to identify rapidly patients at risk for complications associated with isopropanol ingestion when GC-HS is not available.

Fatal inhalational isopropyl alcohol poisoning in a neonate.

A 37 weeks gestation, 1500 gram male infant with multiple dysmorphic features underwent surgery for gastroschisis several hours after birth. During post-operative mechanical ventilation, 70% isopropyl alcohol was accidentally placed in the humidifier of the ventilator, resulting in an estimated 2 h exposure. While the baby seemed clinically stable, initial neurological examination was confounded by recent sedation and pancuronium paralysis. Initial post-operative hypotension was corrected with fluid administration and remained stable for the remainder of the clinical course. By 2 h post-exposure, he was moving, breathing spontaneously and opening his eyes. Isopropyl alcohol and acetone levels at 1, 6, 10 h post exposure were 31/10, 22/15, 15/20 mmol/L respectively. Isopropyl alcohol elimination t1/2 was 9.6 h. Dialysis or exchange transfusion were considered but due to their high risk and the stable infant condition, it was elected to continue with supportive care only. 12.5 h post-exposure, he suddenly became cyanotic, bradycardic, then asystolic. Resuscitation efforts were unsuccessful. To our knowledge, this is the youngest patient reported to have toxic inhalational exposure to isopropyl alcohol and the first report on isopropyl alcohol pharmacokinetics at this age.

Acute isopropanol ingestion: pharmacokinetic parameters in the infant.

We describe a case of isopropanol intoxication in a 2-month-old infant. The source of isopropanol and both the route and time of ingestion could be clearly identified. Serial measurements of isopropanol and acetone provided data for calculating their respective elimination half-lives. Isopropanol (half-life = 5.8 hr) clearance was similar to values reported for adults; acetone (half-life = 10.8 hr) was eliminated twice as rapidly as in adults.

Serum determinations in toxic isopropanol ingestion.

A toxic dose of isopropyl alcohol was ingested by six male mongrel dogs to evaluate the relationship between acetone production and isopropyl degradation. Maximal serum isopropyl levels were achieved approximately 2 to 3 hours after ingestion of 60 mL of 70% isopropyl alcohol. Acetonemia occurred rapidly in the serum (within 15 minutes of ingestion) and continued to rise after isopropanol levels plateaued. The levels of acetone and isopropanol correlated positively throughout the study model with an r of .54 (P less than .001). It is concluded that there is a positive relationship between acetone production and isopropyl metabolism in the setting of a toxic ingestion of isopropanol. Acetone's persistence as a serum marker may be beneficial in identifying isopropyl hours after a suspected ingestion.