Metabolic acidosis in the alcoholic: A pathophysiologic approach

Ml, Halperin; Hammeke, Michael D.; Josse, R G; Jungas, Robert L.

doi:10.1016/0026-0495(83)90197-x

Cited by 110 publications

(66 citation statements)

References 27 publications

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“…Resolution of AKA occurs after administration of dextrose and/or saline; however, the metabolic acidosis resolves more quickly and ␤-hydroxybutyrate levels fall more rapidly when both are administered together (121,122). Saline administration alone, although effective in restoring volume deficits, could also theoretically convert the metabolic acidosis to a hyperchloremic form, as described for DKA (70).…”

Section: Treatmentmentioning

confidence: 99%

See 1 more Smart Citation

Toxic Alcohol Ingestions

Kraut¹,

Kurtz²

2008

Clinical Journal of the American Society of Nephrology

348

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: Treatmentmentioning

confidence: 99%

“…Insulin is not routinely recommended. However, if significant hyperglycemia or life-threatening acidemia is present, then insulin may be indicated (122). Base administration is not usually required given the rapid resolution of acid-base abnormalities once appropriate therapy is initiated.…”

Section: Treatmentmentioning

confidence: 99%

Toxic Alcohol Ingestions

Kraut¹,

Kurtz²

2008

Clinical Journal of the American Society of Nephrology

348

326

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“…Furthermore, there are opinions that insulin should be contraindicated because of the risk of hypoglycemia (8,14,19,20). It has been reported that most patients with AKA do not have concomitant DM (6,9) and it has been considered that the co-existence of AKA and DKA is exceptional (14). As in Case 2, however, the co-existence of both conditions could happen.…”

Section: Discussionmentioning

confidence: 99%

Alcoholic Ketoacidosis Associated with Multiple Complications: Report of 3 Cases

et al. 2004

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We report 3 patients with alcoholic ketoacidosis (AKA). All had a history of excessive intake and abrupt termination of alcohol. They showed tachypnea, tachycardia, abdominal tenderness, and epigastralgia. Metabolic acidosis with an increased anion gap, decreased PaCO2 and ketonemia were present. One patient whose ratio of 3-hydroxybutyric acid to acetoacetic acid was 4.0 was associated with diabetic ketoacidosis. All patients were successfully hydrated with electrolyte, glucose and thiamine. Complications such as liver dysfunction, lactic acidosis, acute pancreatitis, Wernicke's encephalopathy, rhabdomyolysis and heart failure were present.

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“…Major hypothermia has also been described as a marker for severe acidosis. 2,3 In spite of some features that are not usual in AKA, the diagnosis of an inherited fatty acid disorder was unlikely because of her age and the history of chronic alcoholism.…”

Section: Discussionmentioning

confidence: 99%

“…Acetoacetate was 15 mmol/ L (RR 50 ¢2) and b-hydroxybutyrate 30¢4 mmol/ L (RR 50 ¢3). The b-hydroxybutyrate/acetoacetate ratio was normal (2). Following treatment with glucose infusion, alkali and vitamin supplements, the patient quickly showed a marked improvement, and her metabolic and neurological disorders were alleviated completely.…”

Section: Case Studymentioning

confidence: 95%

Major ketogenesis and the absence of an osmolar gap in an atypical case of alcoholic ketoacidosis

Renom

Maisonneuve²,

Kim

et al. 2003

Ann Clin Biochem

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A new case of alcoholic ketoacidosis (AKA) is presented because of unusual clinical and biochemical features. Although it shares some similarities with typical cases of AKA, it appears as unique because of predominantly neurological, rather than abdominal symptoms, major ketogenesis with normal ketone body ratio, the presence of large amounts of propanediol and the absence of an osmolar gap. Ann Clin Biochem 2003; 40: 424-426

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Metabolic acidosis in the alcoholic: A pathophysiologic approach

Cited by 110 publications

References 27 publications

Toxic Alcohol Ingestions

Toxic Alcohol Ingestions

Alcoholic Ketoacidosis Associated with Multiple Complications: Report of 3 Cases

Major ketogenesis and the absence of an osmolar gap in an atypical case of alcoholic ketoacidosis

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