Metabolic Alkalosis in the Patient With Uremia

Abstract

A 55-year-old man was admitted with the chief complaints of nausea, vomiting, abdominal pain, and weakness. He experienced intermittent nausea and vomiting that became progressively more severe for several weeks. During the last week he could not retain food in his stomach, and developed moderately severe epigastric pain. He became progessively weaker, which the patient attributed to lack of food. He also admitted moderate to heavy alcohol intake. He had a past history of peptic ulcer disease, gout, and 15 years of hypertension for which he took medications sporadically. About a year prior to the current admission, a physician told him that the high blood pressure had caused kidney damage. He had had nocturia (once or twice) for many years, which became more pronounced (two or three times per night) during the last 6 months. During the last week he noticed a reduced volume of urine, with a sharp decline over the last 24 hours. Physical examination showed a well-developed, thin, anxious, pale, and somewhat confused white man. Vital signs included pulse rate, 96/min and regular; respirations, 18/min; blood pressure, 156/110 mm Hg supine and 140/100 mm Hg sitting; and a normal temperature. The skin was pale, with poor turgor in the upper part of the body, although mild pitting edema was present in his legs. Conjunctivae and oral mucosae were pale. A systolic ejection murmur was heard at the base of his heart. Scattered inspiratory rales were present at both pulmonary bases. The abdomen was soft, without distention, and moderately tender to palpation in the epigastric and umbilical areas. The prostate was slightly enlarged, but the bladder was not distended. No occult blood was present in the stool. The chest x-ray showed an enlarged heart and possibly a small amount of fluid in the costophrenic pleural space. The electrocardiogram changed consistently with left ventricular hypertrophy. Laboratory tests disclosed anemia, advanced renal in sufficiency, electrolyte disturbances, and a mixed acidbase disturbance (metabolic acidosis and metabolic alkalosis) (Table 1). An increased anion gap, common in severe renal failure and not uncommon in alkalemia, was also observed. The 8 mmollL increment in the anion gap approximately reflects the 8 mmol/L of retained acid that, in turn, consumed 8 mmollL of bicarbonate. Thus, had the renal failure acidosis not been present, the serum bicarbonate concentration would have increased from 38 mmol/L to perhaps as high as 46 mmollL. The clinical picture was initially interpreted as a vicious circle of uremia, vomiting, and worsening of the uremic syndrome by volume contraction. Persistent hypertension despite volume contraction was almost certainly related to his long history of essential hypertension and perhaps to an exaggerated release of renin that was triggered by the hypovolemia. Administration of 0.9% NaCl solution corrected the dehydration but failed to increase the urine output. The patient was dialyzed (standard acetate bath) through a subclavian catheter, with marked improvement of his blood chemical profile. However, attempts to remove the nasogastric tube were unsuccessful because of the recurrrence and persistence of vomiting. On the third day after admission, following endoscopy and x-ray examination of the stomach, a diagnosis of pyloric stenosis secondary to chronic peptic ulcer disease was determined. Treatment began with intravenous ranitidine and fluid replacement with 0.9% NaCl solution, later changed to 5% dextrose in 0.3% NaCl and 20 mmoles KCI. The dialysis bath had the standard acetate concentration and 4.0 mmollL KCI. Packed red-cell transfusions were given before surgical correction of the pyloric stenosis.