Critical Care Aspects of Alcohol Abuse

Ibrahim Al-Sanouri MD; Matthew Dikin MD; Ayman O. Soubani MD

Disclosures

South Med J. 2005;98(3):372-381. 

In This Article

Metabolic and Renal Complications

Metabolic derangements in chronic alcoholics are frequent in the MICU setting. These occur in patients with acute intoxication, withdrawal, or even with chronic ethanol exposure. The most common and potentially life-threatening abnormalities include hypokalemia, hypomagnesemia, hypophosphatemia, hypoglycemia, ketoacidosis, and lactic acidosis.

The pathophysiology of hypophosphatemia in heavy drinkers is multifactorial. Poor intake, ethanol-enhanced urinary excretion, emesis, and antacid use are some of the most common causes of low serum phosphorus. In addition, if there is alcoholic ketoacidosis or vitamin D deficiency, there may be phosphaturia and subsequent hypophosphatemia. Severe hypophosphatemia (<1 mEq/dL) may lead to seizures, hypoventilation, or even coma. In addition, it may result in rhabdomyolysis and subsequent acute renal failure. Moreover, tissue hypoxia may ensue because of a decrease in 2,3 DPG level. Low levels of ATP secondary to hypophosphatemia increase the incidence of bacterial or fungal infections because of poor phagocytosis or opsonization.

Hypomagnesemia in alcoholics commonly develops because of a decrease in renal reabsorption of magnesium, poor nutritional status, and nasogastric suctioning. Furthermore, during an acute alcoholic withdrawal, there is a shift of magnesium, phosphorus, and potassium into the cells and ensuing hypomagnesemia. Manifestations of severe hypomagnesemia (<1 mEq/dL) include muscle weakness, increased deep tendon reflexes, and cardiac dysrhythmias triggered by prolonged PR or QT intervals.

Hypokalemia occurs because of emesis, skin or gastrointestinal losses, or concomitant hypomagnesemia. Patients with severe hypokalemia (level <2.5 mEq/L) display weakness, hypoventilation, paralytic ileus, and ventricular dysrhythmias.

Hypoglycemia is common and is due to a decrease in endogenous glucose production and a decrease in glycogenolysis.

Alcoholic ketoacidosis is an important syndrome to recognize because it is potentially fatal but easily reversed. Ethanol is metabolized by alcohol dehydrogenase to acetaldehyde, which in turn is metabolized to acetyl-CoA. This process generates hydrogen ions and reduces nicotinamide adenine dinucleotide (NADH):

CH3CH2OH + NAD → CH3CHO + NADH + H

Ethanol → Acetaldehyde

The accumulation of reduced NADH leads to a reduction in oxidized NAD+. Since gluconeogenesis depends on the availability of NAD+, ethanol intoxication impairs the generation of glucose. When glycogen stores are depleted, hypoglycemia ensues. The resultant low insulin state promotes the breakdown of fatty acids, which are then metabolized to ketone bodies.[98]

Lactate dehydrogenase catalyzes the synthesis of lactate from pyruvate, using NADH as a cofactor and generating NAD+:

CH3COCOO + NADH + H → CH3CHOHCOO + NAD+

Pyruvate → Lactate

Accumulating NADH by ethanol favors the generation of lactate and causes lactic acidosis.[98] Patients with alcoholic ketoacidosis are usually hypoglycemic, stuporous, and prone to have nausea, vomiting, and aspiration. At this stage, ethanol may be completely metabolized and no longer detectable. These patients are usually acidotic, with the presence of ketones as well as lactic acid. Treatment consists of hydration with intravenous fluids and glucose.

Alcohol-induced acute renal failure may be due to prerenal azotemia, rhabdomyolysis, or hepatorenal syndrome. In addition, Newell et al[99] reported that 50 to 100% of patients with hepatic cirrhosis caused by alcohol have an associated glomerulonephropathy, histologically identical with immunoglobulin A nephropathy.

The treatment of these common metabolic derangements is supportive and includes prompt electrolyte and glucose replacement, dehydration, and maintaining adequate nutritional status.

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