Toxic transdermal absorption of isopropyl alcohol with falsely elevated creatinine.

Transdermal absorption of isopropyl alcohol (IPA) can cause toxicity at high doses, but case reports of this phenomenon are limited. This is a single patient encounter and chart review describing a 33-year-old previously healthy female who presented obtunded, wrapped in IPA soaked round cotton pads with overlying shrink wrap, her family's home remedy for a mild persistent rash. This case highlights several interesting aspects of IPA toxicity, including evidence that toxic doses of IPA are possible through transdermal absorption and creatinine may be falsely elevated due to acetone's interference with the measurement of creatinine on some assays.

Putatively lethal ingestion of isopropyl alcohol-related case: interpretation of post mortem isopropyl alcohol and acetone concentrations remains challenging.

Isopropyl alcohol, or propan-2-ol (IPA), is found in numerous chemicals including alcohol-based hand rubs whose use has been recently widely extended to the general population since the onset of the COVID-19 pandemic. This widespread of IPA use could potentially, but not necessarily, be responsible for an increase in IPA poisoning cases (e.g., in alcoholics and/or for suicide attempt, even more in a lockdown situation). Forensic identification of IPA-related fatalities remains challenging as IPA post mortem detection can also result from antemortem or post mortem production, or post mortem contamination. In order to illustrate this issue, we report the case of a 33-year-old man found dead with a bottle of pure IPA liquid close to him. Toxicological positive results only consisted in IPA (464, 260, 465 and 991 mg/L) and acetone (1560, 2340, 3040 and 1360 mg/L) in blood, vitreous humour, urine and bile, respectively (determinations using headspace gas chromatography with flame ionization detection). These IPA absolute concentrations and IPA-to-acetone ratios appear inferior to those usually reported in the literature (higher than 1000 mg/L and 1.1, respectively) in IPA poisoning cases. In conclusion, this death can be cautiously regarded as an IPA ingestion-related fatality in the hypothesis of a survival time which have promoted IPA metabolism to acetone: this hypothesis is supported by the putative limited IPA-ingested dose. This report emphasizes the fact that post mortem IPA and acetone concentration interpretation involves to take account of (i) results in multiple biological specimens, (ii) complete case history, and (iii) a search of possible IPA presence at the scene of death.

Postmortem diagnosis of ketoacidosis: Levels of beta-hydroxybutyrate, acetone and isopropanol in different causes of death.

Data from 496 autopsy cases with positive beta hydroxybutyrate (BHB), acetone or isopropanol in blood were investigated. The cases were divided into different groups according to cause of death. Cases with cause of death due to diabetic ketoacidosis (DKA, n=54) had the highest levels of BHB (median 1085mg/L) and acetone (median 330mg/L). Cases with cause of death due to alcoholic ketoacidosis (AKA, n=57) had high levels of BHB (median 500mg/L) and acetone (median 110mg/L). Cases with cause of death due to hypothermia (n=12) had similar BHB and acetone levels as the AKA group (median BHB 520mg/L and acetone 80mg/L). Cases with cause of death due to isopropanol intoxication (n=17) had high levels of isopropanol (median 430mg/L) and acetone (330mg/L), but undetected or low levels of BHB. Cases with cause of death due to other than the above mentioned (n=349) had median BHB levels of 100mg/L and median acetone levels of 20mg/L. BHB analysis is crucial for the diagnosis of postmortem ketoacidosis, since it is the main marker of ketoacidosis and helps distinguish between different causes of death. Acetone levels correlate with BHB levels in endogenous ketoacidosis, so acetone can be used as an initial screening marker to identify cases where BHB analysis should be performed, but positive acetone threshold should be maximum 20mg/L. Positive BHB is proof of endogenous ketoacidosis, whereas negative BHB indicates isopropanol intoxication or postmortem acetone/isopropanol formation by microorganisms in cases of decomposition. There is no correlation between BHB and the postmortem interval, and no sign of postmortem formation, so BHB analysis is useful even in cases of severe decomposition.

Sustained low-efficiency dialysis (SLED) therapy following ingestion of isopropanol in a pediatric patient.

Introduction: Cardiovascular collapse due to large ingestions of isopropanol is rare. We report a case of a pediatric patient who had severe CNS and respiratory depression and cardiovascular collapse and was not hemodynamically stable enough to undergo hemodialysis.Case report: A 14-year-old 50 kg male was initially reported to have ingested an unknown amount of HEET® gas line antifreeze about 1 h prior to emergency department (ED) arrival. Despite severe CNS and respiratory depression and cardiovascular collapse, the patient was not initially acidotic. The patient did have an elevated osmolar gap. Approximately 6 h post-ingestion relatives updated the history to reflect that the product was in fact called ISO-HEET® which contains 99% isopropanol. Based on these concerns, a serum isopropanol and acetone levels were obtained that resulted at 475 and 75 mg/dL, respectively. Nephrology was consulted and it was decided to start the patient on sustained low-efficiency dialysis (SLED) which commenced 11 h post-ingestion. Serum and ultrafiltrate concentrations for isopropanol and acetone decreased to normal range over the course of SLED therapy.Discussion: SLED was instituted in this patient primarily for the treatment of elevated serum lactate, isopropanol, and acetone concentrations. The patient's systemic clearance was calculated as 26.9 mL/min. During SLED therapy, the patient was able to clear isopropanol and acetone at 41.21 mL/min and 29.74 mL/min, respectively. SLED therapy is a viable treatment option when a patient is hemodynamically unstable and hemodialysis is not an option.

Riding (High) into the danger zone: a review of potential differences in chemical exposures in fighter pilots resulting from high altitude and G-forces.

INTRODUCTION: When in flight, pilots of high performance aircraft experience conditions unique to their profession. Training flights, performed as often as several times a week, can expose these pilots to altitudes in excess of 15 km (~50,000 ft, with a cabin pressurized to an altitude of ~20,000 ft), and the maneuvers performed in flight can exacerbate the G-forces felt by the pilot. While the pilots specifically train to withstand these extreme conditions, the physiologic stress could very likely lead to differences in the disposition of chemicals in the body, and consequently, dangerously high exposures. Unfortunately, very little is known about how the conditions experienced by fighter pilots affects chemical disposition. Areas covered: The purpose of this review is to present information about the effects of high altitude, G-forces, and other conditions experienced by fighter pilots on chemical disposition. Using this information, the expected changes in chemical exposure will be discussed, using isopropyl alcohol as an example. Expert opinion: There is a severe lack of information concerning the effects of the fighter pilot environment on the pharmacokinetics and pharmacodynamics of chemicals. Given the possibility of exposure prior to or during flight, it is important that these potential effects be investigated further.

Mixed isopropanol-methanol intoxication following ingestion of alcohol-based hand rub solution
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Traditionally, ingestion of alcohol-based hand rub solution results in isopropanol poisoning, which has a low toxicity. We describe a case of combined methanol and isopropanol intoxication by ingestion of alcohol-based hand rub solution. Metabolic acidosis was absent in our patient, presumably because formic acid production is blocked by isopropanol, which inhibits alcohol dehydrogenase. Our case highlights the importance of considering methanol intoxication in patients who ingested alcohol-based hand rub solution, even when there is no metabolic acidosis, and timely removal of the toxic alcohols by dialysis in these patients would prevent permanent retinal damage.
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Toxicity from automotive screenwashes reported to the United Kingdom National Poisons Information Service (NPIS) from 2012 to 2015.

BACKGROUND: Automotive screenwashes commonly contain ethylene glycol, methanol, and/or isopropanol; ethanol is also included in many formulations. The concentrations and combinations of each constituent vary considerably between the products. This study was undertaken to investigate the toxicity of automotive screenwashes as reported by telephone to the United Kingdom National Poisons Information Service (NPIS). METHODS: Enquiries to the NPIS relating to automotive screenwashes were analyzed retrospectively for the period January 2012 to December 2015. RESULTS: There were 295 enquiries involving 255 individual exposures. The majority (n = 241, 94.5%) of exposures involved ingestion and 14 of these also involved other routes. Six cases were due to skin contact alone, three to inhalation alone, three to eye contact alone, one to ear exposure alone and another occurred from inhalation and skin contact. Children below 5 years of age accounted for 26% of all ingestions. The identity (and therefore composition) of the screenwash was known with certainty in 124 of 241 ingestions and included methanol in 106 formulations, isopropanol in 72, ethylene glycol in 38, and ethanol in 104. The World Health Organisation/International Programme on Chemical Safety/European Commission/European Association of Poison Centres and Clinical Toxicologists Poisoning Severity Score was known in 235 of 241 cases of ingestion: most patients were asymptomatic (n = 169, 71.9%), but 59 (25.1%) developed minor (PSS 1), six (2.6%) moderate (PSS 2), and one patient severe (PSS 3) features; this patient later died. Nausea (n = 10), vomiting (n = 11), abdominal pain (n = 10), metabolic acidosis (n = 8) and raised anion gap (n = 8) were reported most commonly after ingestion. CONCLUSIONS: Most patients (71.9%) ingesting automotive screenwash did not develop features. The implication is that the amount of screenwash ingested was very small. Skin and eye exposure produced either no features or only minor toxicity.

A Brief Review on Toxic Alcohols: Management Strategies.

The information on burden of alcohol abuse in Iran is scarce. However, the available data show that mortality rates and frequency of its use have increased in the Iranian community. In particular, Iran occupies the 1st rank in the number of outbreak incidents and victims of toxic alcohols such as methanol in the Middle East. Mortality and morbidity of toxic alcohols are high if prompt diagnosis and treatment are not initiated rapidly. On-time diagnosis, proper case finding, and standard treatment have an essential role to reduce mortality and morbidity of toxic alcohols particularly blindness and other physical and psychological disabilities. This review focuses on intoxication with methanol, ethylene glycol, and isopropanol, and their treatment.

Toxic Alcohol Ingestion: Prompt Recognition And Management In The Emergency Department.

Identifying patients with potential toxic alcohol exposure and initiating appropriate management is critical to avoid significant patient morbidity. Sources of toxic alcohol exposure include ethylene glycol, methanol, diethylene glycol, propylene glycol, and isopropanol. Treatment considerations include the antidotes fomepizole and ethanol, and hemodialysis for removal of the parent compound and its toxic metabolites. Additional interventions include adjunctive therapies that may improve acidosis and enhance clearance of the toxic alcohol or metabolites. This issue reviews common sources of alcohol exposure, basic mechanisms of toxicity, physical examination and laboratory findings that may guide rapid assessment and management, and indications for treatment.

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.

Toxic alcohol ingestion: prompt recognition and management in the emergency department [digest].

Identifying patients with potential toxic alcohol exposure and initiating appropriate management is critical to avoid significant patient morbidity. Sources of toxic alcohol exposure include ethylene glycol, methanol, diethylene glycol, propylene glycol, and isopropanol. Treatment considerations include the antidotes fomepizole and ethanol, and hemodialysis for removal of the parent compound and its toxic metabolites. Additional interventions include adjunctive therapies that may improve acidosis and enhance clearance of the toxic alcohol or metabolites. This issue reviews common sources of alcohol exposure, basic mechanisms of toxicity, physical examination and laboratory findings that may guide rapid assessment and management, and indications for treatment. [Points & Pearls is a digest of Emergency Medicine Practice].

Isopropanol poisoning.

INTRODUCTION: Isopropanol is a clear, colorless liquid with a fruity odor and a mild bitter taste. Most commonly found domestically as rubbing alcohol, isopropanol is also found in numerous household and commercial products including cleaners, disinfectants, antifreezes, cosmetics, solvents, inks, and pharmaceuticals. AIM: The aim of this review is to critically review the epidemiology, toxicokinetics, mechanisms of toxicity, clinical features, diagnosis, and management of isopropanol poisoning. METHODS: OVID MEDLINE and ISI Web of Science were searched to November 2013 using the words "isopropanol", "isopropyl alcohol", "2-propanol", "propan-2-ol", and "rubbing alcohol" combined with the keywords "poisoning", "poison", "toxicity", "ingestion", "adverse effects", "overdose", or "intoxication". These searches identified 232 citations, which were then screened via their abstract to identify relevant articles referring specifically to the epidemiology, toxicokinetics, mechanisms of toxicity, clinical features, diagnosis, and management of isopropanol poisoning; 102 were relevant. Further information was obtained from book chapters, relevant news reports, and internet resources. These additional searches produced eight non-duplicate relevant citations. EPIDEMIOLOGY: The majority of isopropanol exposures are unintentional and occur in children less than 6 years of age. Although isopropanol poisoning appears to be a reasonably common occurrence, deaths are rare. TOXICOKINETICS: Isopropanol is rapidly absorbed following ingestion with peak plasma concentrations occurring within 30 min. It can also be absorbed following inhalation or dermal exposure. Isopropanol is widely distributed with a volume of distribution of 0.45-0.55 L/kg. Isopropanol is metabolized by alcohol dehydrogenase to acetone, acetol and methylglyoxal, propylene glycol, acetate, and formate with conversion of these metabolites to glucose and other products of intermediary metabolism. The elimination of isopropanol is predominantly renal, though some pulmonary excretion of isopropanol and acetone occurs. In one case 20% of the absorbed dose was eliminated unchanged in urine, with the remainder excreted as acetone and metabolites of acetone. The elimination half-life of isopropanol is between 2.5 and 8.0 h, whereas elimination of acetone is slower with a half-life following isopropanol ingestion of between 7.7 and 27 h. MECHANISMS OF TOXICITY: While the exact mechanism of action of isopropanol has not been fully elucidated, brain stem depression is thought to be the predominant mechanism. While the clinical effects are thought to be mostly due to isopropanol, acetone may also contribute. CLINICAL FEATURES: The major features of severe poisoning are due to CNS and respiratory depression, shock, and circulatory collapse. The most common metabolic effects are an increased osmol (osmolal) gap, ketonemia, and ketonuria. Diagnosis. Poisoning can be diagnosed using the measurement of isopropanol serum concentrations, though these may not be readily available. Diagnosis is therefore more typically made on the basis of the patient's history and clinical presentation. An osmol gap, ketonemia, and/or ketonuria without metabolic acidosis, along with a fruity or sweet odor on the breath and CNS depression support the diagnosis. Management. Supportive care is the mainstay of management with primary emphasis on respiratory and cardiovascular support. Hemodialysis enhances elimination of isopropanol and acetone and should be considered in very severe poisoning. CONCLUSIONS: Severe isopropanol poisoning results in CNS and respiratory depression and circulatory collapse. Treatment primarily consists of symptom-directed supportive care. Although hemodialysis increases the elimination of isopropanol and acetone substantially, it should only be considered in severe life-threatening poisonings. Patients usually make a full recovery provided they receive prompt supportive care.

[Acute alcohol poisonings among patients in Toxicology Unit, Nofer Institute of Occupational Medicine in the period of time 2007-2012]. / Zatrucia alkoholami wsród pacjentów Oddzialu Toksykologii Instytutu Medycyny Pracy im. J. Nofera w Lodzi, hospitalizowanych w latach 2007-2012.

UNLABELLED: The purpose of the research was to present the analysis of acute alcohol poisonings (ethanol, methanol, ethylene glycol, isopropanol) in Toxicology Unit (TU), Nofer Institute of Occupational Medicine (NIOM), Lódz, Poland. MATERIALS AND METHODS: To further analysis were chosen all cases, whose were coded according to the International Statistical Classification of Diseases and Related Health Problems 10th Revision. RESULTS: There were 10,936 acute poisonings in the analyzed period of time 2007-2012 years, 3,088 of them referred to alcohol poisonings (28%). The largest group of patients included cases with ethanol intoxication (2,883 subjects), the second and third one-cases with methanol and ethylene glycol poisonings (99 and 98 respectively), 8 cases were poisoned with isopropanol. The largest group of patients includes cases at age less than 30 years. Patients at age above 60 years formed the lowest group among the total number of poisonings. Most of the admitted cases were men (2,417 patients) and cases hospitalized due to ethanol abuseladdiction (93%). Ethylene glycol poisonings constituted the leading cause of deaths (10 subjects). CONCLUSIONS: The study shows, that intoxications with alcohols are a big problem in NIOM and the number of alcohol poisonings markedly increased in the years 2007-2012.

Short-term immunological effects of non-ethanolic short-chain alcohols.

Short-chain alcohols are embedded into several aspects of modern life. The societal costs emanating from the long history of use and abuse of the prototypical example of these molecules, ethanol, have stimulated considerable interest in its general toxicology. A much more modest picture exists for other short-chain alcohols, notably as regards their immunotoxicity. A large segment of the general population is potentially exposed to two of these alcohols, methanol and isopropanol. Their ubiquitous nature and their eventual use as ethanol surrogates are predictably associated to accidental or deliberate poisoning. This review addresses the immunological consequences of acute exposure to methanol and isopropanol. It first examines the general mechanisms of short-chain alcohol-induced biological dysregulation and then provides a tentative model to explain the molecular events that underlie the immunological dysfunction produced by methanol and isopropanol. The time-related context of serum alcohol concentrations in acute poisoning, as well as the clinical implications of their short-term immunotoxicity, is also discussed.