Electrolyte Imbalance During Cirrhotic Ascites, March 13, 1998

Electrolyte Imbalance During Cirrhotic Ascites, March 13, 1998

During cirrhotic ascites, water and sodium retention lead to intracellular hypokalemia. Furthermore, the use of diuretics exacerbates potassium deficiency. Therefore, patients with cirrhosis should routinely supplement potassium; low potassium levels can also result in low calcium, low magnesium, low chloride, and low sodium. In short, patients with cirrhosis in the ascitic stage are essentially "low in everything." A small proportion of cirrhosis patients may develop hepatorenal syndrome, in which urea nitrogen rises, CO2-P falls, creatinine, creatine, urea, and uric acid all increase, and the electrolytes in the blood undergo major changes—first, potassium decreases, then potassium increases. Due to the blockage of phosphate excretion, hyperphosphatemia and hypocalcemia occur: some patients develop hyperparathyroidism, in which blood calcium rises, blood phosphorus falls, CO2-P declines, and acidosis sets in. Acid can bind sodium ions and calcium ions, so low sodium and low calcium become even more pronounced. At this point, the body's resistance decreases, putting it in a state of infection, urine output decreases, and hepatic encephalopathy is more likely to occur.