Disturbances of electrolytes and blood chemistry in acute alcohol intoxication

Abstract

Prevalence of electrolyte disturbances and biochemical changes were determined in patients admitted to the emergency room of the Department of Internal Medicine in Innsbruck, Austria during a six-month period. The value of biochemical parameters for the detection of chronic alcohol abuse was also investigated. The most frequent electrolyte disturbances found were hypernatremia (41%), hyperchloremia (21%), hypermagnesemia (17%) and hypocalcemia (15%), whereas hypokalemia and hypophosphatemia were observed quite rarely (5% and 3.4%, respectively). The most frequent biochemical changes observed were consistent with signs of cellular toxicity i.e. increased liver enzymes (elevated gamma-glutamyltransferase (GGT), aspartate aminotransferase, alanine aminotransferase and lactic dehydrogenase) as well as signs of pancreatitis (elevated serum lipase and amylase) and muscle damage (elevated creatine kinase). The most frequent changes in blood counts were leucocytosis (23%), thrombocytopenia (14%), and anemia (12%). C-reactive protein showed only minimal elevation. Male sex and level of blood alcohol were detected as major risk factors for the diagnosis of chronic alcohol abuse in the patient sample investigated. When testing the value of routinely measured parameters for predicting the presence of chronic alcohol abuse, GGT and mean corpuscular volume of red blood cells (MCV) appeared to be of equal value. A combination of elevated blood alcohol with an increase in either of these markers may be interpreted as high risk for chronic alcohol abuse in this particular group of patients.

Metabolic Abnormalities in Alcoholic Patients: Focus on Acid Base and Electrolyte Disorders

“…In particular, the mean (SD) total magnesium levels was 0.7 ± 0.2 mmol/L, which was significantly lower than that observed in the 203 normal controls (0.9 ± 0.3 mmol/L, p<0.001) [13]. The underlying pathogenic mechanisms of hypomagnesaemia in alcoholic patients include: a)Increased renal losses of Mg 2+ caused by coexistent metabolic acidosis [8], hypophosphatemia [14,15] as well as by a direct magnesiuric effect of acute alcohol consumption [13][14][15][16][17]. Furthermore, magnesiuria could be the result of transient hypoparathyroidism reported during alcohol intoxication.…”

“…Hypocalcaemia is also a frequent electrolyte abnormality in alcoholic patients with a prevalence ranged between 5-15% [17,26]. As previously mentioned hypocalcaemia is believed to be the result of hypomagnesaemia, as reversible hypocalcaemia is frequently found in association with magnesium depletion [11,27] (Table 2).…”

“…In this regard, magnesium is required for the normal activity of the Na + -K + -ATPase pump, responsible for the active transport of potassium into the cells. The correlation between serum potassium and magnesium levels as well as between serum magnesium levels and potassium excretion in alcoholic patients with hypokalemia strengthen the importance of hypomagnesaemia in the development of hypokalemia [11][12][13][14][15][16][17][18][19][20][21][22][23]24].…”

Another 'soberade' on the market: does Outox keep its promise?

“…Alcohol consumption, especially chronic alcohol abuse, not only causes severe physical damage directly and indirectly [25,26] but can also cause secondary injuries, especially in connection with road traffic. Consequently, many products are currently offered as soberades, such as 'Bangout' in Hungary, 'Break-Down' in the USA and 'alcokill' in Austria and Germany, all containing fructose as the main ingredient.…”

Phosphorus in Sudanese Alcoholism in Khartoum State

“…Also increased gastrointestinal magnesium losses due to diarrhea or steatorrhea may play a role in the development of hypomagnesaemia in some patients. (12) Hypophosphatemia is the second common electrolyte abnormality observed in alcoholism, they commonly consume a phosphate-deficient diet which may play a role in the pathogenesis of hypophosphatemia. (13) In addition, ethanol per induce proximal tubular dysfunction associated with decreased phosphate reabsorption and inappropriate phosphaturia .…”