Increased Osmolal Gap in Alcoholic Ketoacidosis and Lactic Acidosis

Schelling, Jeffrey R.; Howard, Randy L.; Winter, Sara; Linas, Stuart L.

doi:10.7326/0003-4819-113-8-580

Cited by 118 publications

(47 citation statements)

References 17 publications

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“…An osmolal gap can also be found in some other disorders that might be considered in the differential diagnosis of alcohol-related intoxications, such as ketoacidosis, lactic acidosis, and renal failure and in critically ill patients with hyponatremia, but this osmolal gap is Յ15 to 20 mOsm/L (21,22,27). Thus, an osmolal gap Ͼ20 mOsm/L indicates accumulation in the blood of one of the alcohols; however, the absence of an osmolal gap does not exclude an alcohol-related intoxication, because alcohol concentrations that are sufficient to produce clinical and laboratory abnormalities might not raise serum osmolality appreciably (12,13,(23)(24)(25).…”

Section: Effect Of Alcohols On Serum Osmolality and The Osmolal Gapmentioning

confidence: 99%

Toxic Alcohol Ingestions

Kraut¹,

Kurtz²

2008

Clinical Journal of the American Society of Nephrology

369

326

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Alcohol-related intoxications, including methanol, ethylene glycol, diethylene glycol, and propylene glycol, and alcoholic ketoacidosis can present with a high anion gap metabolic acidosis and increased serum osmolal gap, whereas isopropanol intoxication presents with hyperosmolality alone. The effects of these substances, except for isopropanol and possibly alcoholic ketoacidosis, are due to their metabolites, which can cause metabolic acidosis and cellular dysfunction. Accumulation of the alcohols in the blood can cause an increment in the osmolality, and accumulation of their metabolites can cause an increase in the anion gap and a decrease in serum bicarbonate concentration. The presence of both laboratory abnormalities concurrently is an important diagnostic clue, although either can be absent, depending on the time after exposure when blood is sampled. In addition to metabolic acidosis, acute renal failure and neurologic disease can occur in some of the intoxications. Dialysis to remove the unmetabolized alcohol and possibly the organic acid anion can be helpful in treatment of several of the alcohol-related intoxications. Administration of fomepizole or ethanol to inhibit alcohol dehydrogenase, a critical enzyme in metabolism of the alcohols, is beneficial in treatment of ethylene glycol and methanol intoxication and possibly diethylene glycol and propylene glycol intoxication. Given the potentially high morbidity and mortality of these intoxications, it is important for the clinician to have a high degree of suspicion for these disorders in cases of high anion gap metabolic acidosis, acute renal failure, or unexplained neurologic disease so that treatment can be initiated early. Table 1. Methanol, ethylene glycol, diethylene glycol, and propylene glycol intoxication and alcoholic ketoacidosis can produce hyperosmolality and metabolic acidosis (3-9). Isopropanol intoxication is usually associated with hyperosmolality alone (4,5). Importantly, several of these disorders can be fatal or produce irreversible tissue damage if they are not quickly recognized and treated appropriately (4 -15). Effect of Alcohols on Serum Osmolality and the Osmolal GapThe normal serum osmolality of 285 to 290 mOsm/L is due to sodium and its counterbalancing ions, bicarbonate and chloride, and glucose and urea. It can be calculated using the following equation:Serum osmolality (mOsm/L) ϭ 2 ϫ Na ϩ ϩ blood urea nitrogen (mg/dl)/2.8 ϩ glucose (mg/dl)/18. The serum osmolality measured by freezing point depression is usually within 10 mOsm/L of the calculated serum osmolality (16). Accumulation of low molecular weight substances in the serum (such as each of the alcohols) will raise the measured serum osmolality above that of the calculated serum osmolality, producing an osmolal gap (4,5,16 -18). The effect of each of the alcohols on serum osmolality is shown in Table 2. Methanol gives rise to the greatest increment in serum osmolality, followed by ethanol, isopropanol, ethylene glycol, propylene glycol, and diethylene glycol in that...

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Section: Effect Of Alcohols On Serum Osmolality and The Osmolal Gapmentioning

confidence: 99%

Toxic Alcohol Ingestions

Kraut¹,

Kurtz²

2008

Clinical Journal of the American Society of Nephrology

369

326

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“…3,9,10 The laboratory technique chosen to define osmolarity and the formula used for measuring osmolality for establishing the osmol gap are neither sensitive nor specific for these toxic alcohols. [9][10][11][12][13][14] The earlier appropriate therapy is initiated for methanol or ethylene glycol ingestions, the better the outcome in preventing the serious consequences of blindness, renal dysfunction, neurotoxicity, acidemia, metabolic acidosis, pancreatitis, and death. [15][16][17] Therapies include altering the toxic alcohol's metabolism with antidotal treatment using ethanol, 8,15,18 fomepizole, 19,20 removal of the alcohols by hemodialysis, 13,18,21,22 supportive care with sodium bicarbonate, 13 and fluid resuscitation, 13 and the administration of adjuvant therapies (thiamine, pyridoxine, and leucovorin 2 ) appropriate to the toxin ingested.…”

mentioning

confidence: 99%

The Utility of an Alcohol Oxidase Reaction Test to Expedite the Detection of Toxic Alcohol Exposures

Hack

Chiang

Howland

et al. 2000

Academic Emergency Medicine

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“…Also, the OG will decrease over time as an alcohol is metabolized [2], resulting in cases of EG poisoning with normal OG [4]. Likewise, we are concerned that reflexive testing will be unnecessary in cases where osmolarity is elevated and there is a clear etiology for the metabolic acidosis, such as alcoholic ketoacidosis and diabetic ketoacidosis [5]. Therefore, we suggest considering limiting the toxic alcohol ordering to cases in which there is either a clinical suspicion of poisoning or an unexplained acidosis.…”

Section: Dear Editormentioning

confidence: 99%

Letter in Response to: “Use of a Rapid Ethylene Glycol Assay: a 4-Year Retrospective Study at an Academic Medical Center”

2016

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Dear editor,In their 2015 JMT article, Rooney and colleagues discussed the utility of a rapid ethylene glycol (EG) assay in the management of patients with suspected EG poisoning [1]. Although we enjoyed the study, we would like to clarify a few points with the authors and readers.First, it is not clear why the institution's algorithm used an osmolal gap (OG) >15 as the threshold to reflexively test for EG. We caution readers about the limitations of using OG as a screening tool for toxic alcohols, as the normal limits of OG can range from −14 to +10 [2,3]. The normal OG also varies depending on the formula used to calculate osmolality and the type of instruments used by the laboratory to measure the serum osmolality. Also, the OG will decrease over time as an alcohol is metabolized [2], resulting in cases of EG poisoning with normal OG [4]. Likewise, we are concerned that reflexive testing will be unnecessary in cases where osmolarity is elevated and there is a clear etiology for the metabolic acidosis, such as alcoholic ketoacidosis and diabetic ketoacidosis [5]. Therefore, we suggest considering limiting the toxic alcohol ordering to cases in which there is either a clinical suspicion of poisoning or an unexplained acidosis.Additionally, the present study did not clarify how 222 rapid EG assays were performed in 106 patient encounters. This information would be useful to further grasp the utility and limitations of rapid EG assays. Were tests repeated as a result of laboratory error or as part of a laboratory protocol? Is the assay difficult to run correctly on a single attempt? Finally, the study's methods cannot exclude false negatives of the rapid EG assay because the gold standard of gas chromatography (GC) was used in only a small portion of negative results.We agree with the authors that decreasing reliance on GC is important, highlighting the fact that rapid EG assays carry a similar financial burden to GC but are potentially faster and more convenient to use. However, because propylene glycol (PG) interference continues to occur, GC capability of the laboratory is still a necessary component of the algorithm to exclude ethylene glycol toxicity. We also agree with the authors that further studies are needed to improve techniques to minimize PG interference and to develop technology for rapid methanol testing and commend them on their efforts to date.

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Increased Osmolal Gap in Alcoholic Ketoacidosis and Lactic Acidosis

Cited by 118 publications

References 17 publications

Toxic Alcohol Ingestions

Toxic Alcohol Ingestions

The Utility of an Alcohol Oxidase Reaction Test to Expedite the Detection of Toxic Alcohol Exposures

Letter in Response to: “Use of a Rapid Ethylene Glycol Assay: a 4-Year Retrospective Study at an Academic Medical Center”

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