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Therapeutic Monitoring of Adverse Drug Reactions (ADRs)
Published in Frank A. Barile, Barile’s Clinical Toxicology, 2019
where glucose and blood urea nitrogen (BUN) concentrations are in milligrams per deciliter. The osmolar gap is determined by subtracting the calculated value from the measured osmolarity. The normal osmolar gap is less than 10 mOsm. An increase in the gap above 10 suggests poisoning with ethanol, ethylene glycol, isopropanol, or methanol. It is important to note that depending on the method used to determine the osmolar gap, a normal value does not rule out poisoning with ethylene glycol or methanol.
Acid–base disturbances
Published in Sherif Gonem, Ian Pavord, Diagnosis in Acute Medicine, 2017
The normal range for the osmolal gap is 10–15 mOsm/kg. A value higher than this implies the presence of a significant quantity of unmeasured osmotically active solutes. Therefore the osmolal gap is a useful diagnostic tool for the investigation of unexplained high anion gap metabolic acidosis. The commonest cause of an elevated osmolal gap in clinical practice is poisoning by volatile alcohols.
Death by hand sanitizer: syndemic methanol poisoning in the age of COVID-19
Published in Clinical Toxicology, 2021
Sarah Denise Holzman, Jaiva Larsen, Ramandeep Kaur, Geoffrey Smelski, Steven Dudley, Farshad Mazda Shirazi
In all four patients with a measured osmolality, both the osmolal gap and anion gap were extremely high. An elevated osmolal gap, which indicates the presence of an osmotically active substance, can be useful in establishing the presence of a toxic alcohol. An osmolal gap range of (-)10 to 20 mOsm/kg H2O has been suggested as “normal” [15]. Clinicians vary in their threshold for concern with osmolal gap elevations, but an osmolal gap >25 mOsm/kg H2O is generally considered clinically significant [10,16,17]. Limitations of the osmolal gap include the variability in the formula used to calculate the gap, the wide variability for baseline “normal” gap among individuals, and the elevation in gap due to other medical conditions [18–22]. Additionally, as toxic alcohols are metabolized, the osmolal gap is expected to decline rendering it insensitive to a late-presenting methanol intoxication [18–22]. Since timely methanol concentrations are usually unavailable, clinicians must assess the poisoning based upon clinical history, physical findings, the anion gap, and the osmolal gap [16–22].
Distinguishing between toxic alcohol ingestion vs alcoholic ketoacidosis: how can we tell the difference?
Published in Clinical Toxicology, 2021
Emily T. Cohen, Mark K. Su, Rana Biary, Robert S. Hoffman
In many hospitals, TA concentrations are not available in a clinically relevant timeframe [3]. Clinicians must therefore rely on other criteria to determine whether to initiate costly treatment (fomepizole and hemodialysis) for TA ingestion. Surrogates perform poorly. The presence of calcium oxalate crystals in urine is neither sensitive nor specific for ethylene glycol ingestion [4,5]. Sodium fluorescein is sometimes added to ethylene glycol antifreeze formulations to better visualize engine coolant leaks. This additive, when ingested, causes urine to fluoresce. However, urine samples sometimes fluoresce regardless of the presence of ethylene glycol, and inter-rater reliability is poor [6,7]. An elevated osmol gap is often used to help diagnose TA ingestion, because methanol and ethylene glycol contribute osmols that are not accounted for by commonly used osmol gap mathematical formulas. However, baseline osmol gaps vary in the population from −14 to +10 mOsm/L, and a person’s baseline osmol gap is rarely known before they present for emergency care [8]. A seemingly “normal” osmol gap is sometimes elevated for the individual in question. Additionally, the osmol gap decreases as the TA is metabolized. For these reasons, while an elevated osmol gap may be suggestive of a diagnosis of TA ingestion (presuming that the clinician has accounted for osmols contributed by ethanol, which are occasionally forgotten), a normal osmol gap cannot be used to exclude this diagnosis.
The role of the clinical laboratory in diagnosing acid–base disorders
Published in Critical Reviews in Clinical Laboratory Sciences, 2019
In any patient with an unexplained high AG acidosis, coma, suspicion of ingestion of a (toxic) non-ethanolic alcohol and in hospitalized patients with an increased risk of iatrogenic propylene glycol intoxication (e.g. high dose lorazepam in sedated patients in an intensive care unit), one should exclude the possibility of a toxic alcohol intoxication [130–132]. Laboratory confirmation of a toxic alcohol ingestion is often not rapidly available, but the osmolal gap can be a vital clue to this diagnosis