Plasma lactate and 3-hydroxybutyrate levels in patients with acute ethanol intoxication

Fulop, Milford; Bock, Jay L.; Ben‐Ezra, Jonathan; Antony, Michael A.; Danzig, Jeffrey B.; Gage, Joseph S.

doi:10.1016/0002-9343(86)90008-2

Cited by 46 publications

(23 citation statements)

References 12 publications

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“…The syndrome of alcoholic ketoacidosis (AKA) is uncommon in patients with acute ethanol intoxication, being found in Ͻ10% of patients (112)(113)(114). It is most frequent in patients who have long-term ethanol intake and liver disease and develop the syndrome after a period of binge drinking (39,112) and is associated with reduced food intake and episodes of vomiting; the latter might explain the concurrence of metabolic alkalosis noted in some patients (39,112,115,116).…”

Section: Epidemiologymentioning

confidence: 99%

“…Excess production of acetoacetic acid and ␤-hydroxybutyric acid underlies the metabolic acidosis, with increased NADH favoring production of ␤-hydroxybutyrate compared with acetoacetate (115), the ratio of these ketones rising from the normal value of 3:1 to more than 9:1 (112)(113)(114)(115). The increased NADH also favors increased lactic acid production; therefore, concomitant lactic acidosis even in the absence of impaired tissue perfusion is not uncommon (39,112,115).…”

Section: Pathophysiologymentioning

confidence: 99%

“…The increased NADH also favors increased lactic acid production; therefore, concomitant lactic acidosis even in the absence of impaired tissue perfusion is not uncommon (39,112,115). However, the increase in lactic acid production is small, and severe lactic acidosis in the absence of sepsis or hypotension is rare (39,112,114,115).…”

Section: Pathophysiologymentioning

confidence: 99%

“…This test detects acetoacetate but not ␤-hydroxybutyrate. Therefore, the nitroprusside test of urine of blood may revealed a trace positive reading (112,114,115,119,120). Negative readings, although they can occur, are uncommon: Only 10 of 74 patients with AKA had a negative test for ketones.…”

Section: Laboratory Findingsmentioning

confidence: 99%

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Toxic Alcohol Ingestions

Kraut¹,

Kurtz²

2008

Clinical Journal of the American Society of Nephrology

355

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: Epidemiologymentioning

confidence: 99%

Section: Pathophysiologymentioning

confidence: 99%

Section: Pathophysiologymentioning

confidence: 99%

Section: Laboratory Findingsmentioning

confidence: 99%

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Toxic Alcohol Ingestions

Kraut¹,

Kurtz²

2008

Clinical Journal of the American Society of Nephrology

355

326

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“…Mais l'influence du métabolisme de l'éthanol sur les concentrations sanguines des lactates est encore discutée. Dans certaines études ou cas cliniques, la concentration est augmentée [10,11,[14][15][16][17], ou se maintenait [65][66][67] ou encore baissait [58,59]. Pour ces derniers auteurs, l'augmentation de la lactatémie après absorption d'éthanol pourrait être la consé-quence de pathologies associées, d'un jeûne ou de la présence d'un autre toxique [65,67].…”

Section: Discussionunclassified

Influence du site de prélèvement sur l’étude cinétique et métabolique de l’éthanol

et al. 2012

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Résumé -Objectif : L'analyste n'obtenant pas toujours les mêmes prélèvements sanguins, nous proposons d'étudier l'influence du site de prélèvement sanguin sur l'étude cinétique et métabolique de l'éthanol. Méthode : Sur un modèle animal, le rat mâle Sprague-Dawley âgé de 7 à 9 semaines, les cinétiques sanguines de l'éthanol, sériques de l'acétate et du lactate, artérielles et veineuses, sont déterminées respectivement par analyse de l'espace de tête en chromatographie en phase gazeuse et électrophorèse capillaire de zone. L'animal est cathétérisé soit au niveau d'une artère fémorale, soit au niveau d'une veine caudale. Résultats : Lors de la phase d'absorption, l'éthanolémie artérielle croît plus rapidement et plus intensément que l'éthanolémie veineuse ; après la phase de distribution, elles tendent à se confondre. Contemporainement, les acétates, métabolites de l'éthanol, apparaissent plus concentrés dans le compartiment artériel que veineux périphérique ; les lactates, produits indirects du métabolisme de l'éthanol, présentent une cinétique artérielle similaire à celle de l'acétate, les concentrations veineuses restant anormalement élevées pendant l'étude. Conclusion : Le sang veineux prélevé lors de cette étude n'a pas donné accès à la réalité cinétique et métabolique de l'éthanol. Ainsi, en comparaison avec le compartiment artériel, l'éthanol et l'acétate sont présents en quantité moindre dans le sang veineux, l'éthanol y apparaissant plus lentement. Le sang veineux prélevé s'est même avéré inadapté à l'étude cinétique des lactates. Cette étude confirme, si nécessaire, que les résultats et l'interprétation d'une analyse sont préconditionnés par le prélèvement lui-même, ce dernier n'étant pas toujours réalisé sous les indications d'un analyste. Mots clés :Recueil de prélèvements sanguins/méthode, éthanol/sang, éthanol/métabolisme, acétates/sang, lactates/sang Abstract -Objective: Because the analyst does not always obtain the same sampling of blood, we suggest studying the influence of the site of blood sampling on kinetic and metabolic studies of ethanol. Method: On an animal model, 7-to-9-week-old Sprague-Dawley male rats, arterial and venous blood kinetics of ethanol and serum kinetics of acetate and lactate were, respectively, determined by head-space chromatography analysis and capillary zone electrophoresis. The animal is catheterized either at the femoral artery, or at the caudal vein. Results: During the absorption phase, the arterial blood ethanol grew more quickly and more intensely than the venous; after the distribution phase, they tended to merge. At the same time, acetates, produced during ethanol metabolism, were more concentrated in the arterial compartment than the venous; lactates, indirect products of ethanol metabolism, presented an arterial kinetics similar to acetate, and venous concentrations remained abnormally high throughout the study. Conclusion: The venous blood samples taken during this study did not give access to the kinetic and metabolic reality of ethanol. So, compared with t...

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Alcoholism, ketoacidosis, and lactic acidosis

Fulop¹

1989

Diabetes Metab. Rev.

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Plasma lactate and 3-hydroxybutyrate levels in patients with acute ethanol intoxication

Cited by 46 publications

References 12 publications

Toxic Alcohol Ingestions

Toxic Alcohol Ingestions

Influence du site de prélèvement sur l’étude cinétique et métabolique de l’éthanol

Alcoholism, ketoacidosis, and lactic acidosis

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