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A 56-year-old with diarrhea and weakness

Cleveland Clinic Journal of Medicine. 2015 October;82(10):671-676 | 10.3949/ccjm.82a.14124
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CASE CONTINUED: EXAMINATION AND LABORATORY VALUES

The patient’s primary care physician had recently referred him to a gastroenterologist, and 4 days before presenting to the emergency department he had undergone abdominal and pelvic computed tomography (CT) with iodinated contrast, which had showed hepatic steatosis and pancreatic atrophy.

On examination now, the patient’s temperature is 97.5°F (36.4°C), heart rate 90 beats per minute, respirations 18 breaths per minute, oxygen saturation 99% on room air, and blood pressure 85/55 mm Hg. His body mass index is 32.5 kg/m2. His oral mucosa is dry. The rest of the examination is normal. No rash or ulcers are noted.

His laboratory values (Table 2) are notable for sodium 130 mmol/L, potassium 2.2 mmol/L, bicarbonate 9 mmol/L, blood urea nitrogen 32 mg/dL, creatinine 4.18 mg/dL, and international normalized ratio 5.4. Arterial blood gases drawn on admission reveal pH 7.32 and pCO2 19 mm Hg.

ACID-BASE DISTURBANCES

3. The patient’s acidosis is most likely related to which of the following?

  • Sepsis
  • Diarrhea
  • Metformin
  • Acute kidney injury

It is most likely related to diarrhea. The patient has a non-anion-gap metabolic acidosis. (The anion gap can be calculated by subtracting the sum of the serum bicarbonate and chloride values from the sodium—here, 130 – [112 + 9] = 9—and most textbooks list the reference range as 10–12 mmol/L.) Non-anion-gap metabolic acidosis results from excessive loss of bicarbonate or impaired ability of the kidney to excrete acid. Bicarbonate losses can occur in diarrhea or in ureteral diversion to the colon. Impairment in urinary acidification can occur in renal tubular acidosis.

To determine the cause of non-anion-gap acidosis, calculating the urine anion gap can be useful (Table 3), as it reflects the ability of the kidneys to excrete acid and is an indirect measure of ammonium excretion. Our patient’s urine anion gap is –45 mmol/L ([62 + 8] – 115), which supports diarrhea as the cause of his non-anion-gap acidosis. Sepsis, metformin use, or acute kidney injury would result in an anion-gap acidosis.

To manage acid-base disturbances, it is important to first determine whether there is a single primary disturbance with compensation or a mixed disorder. In the case of metabolic acidosis, for every 1-mmol/L decrease in bicarbonate, there should be a corresponding 1.3-mm Hg decrease in pCO2. Our patient’s laboratory data show that he had a pure non-anion-gap metabolic acidosis.8 His sensation of dyspnea was likely related to respiratory compensation as evidenced by an appropriately low pCO2.

CASE CONTINUED: HIS LABORATORY VALUES IMPROVE

The patient is admitted to the hospital for fluid resuscitation with normal saline and potassium and magnesium replacement.

Renal ultrasonography reveals normal-appearing kidneys without obstruction. The calculated fractional excretion of sodium is 3.4%. Urine microscopy reveals two to five hyaline casts per low-power field. His urine output remains adequate, and 3 days after hospitalization, his renal function starts to improve, as reflected in falling serum creatinine and blood urea nitrogen levels: his creatinine level has declined to 1.91 mg/dL and his blood urea nitrogen level has declined to 24 mg/dL. His acute kidney injury is attributed to intravenous contrast given for computed tomography, as well as to volume depletion and hypotension.

Stool studies for ova, parasites, and Clostridium difficile are negative. Fecal calprotectin and lactoferrin are useful noninvasive markers of intestinal inflammation but were not checked in this case.

Loperamide, taken as needed, is started for his diarrhea, along with empiric pancreatic enzyme replacement. After 3 days of treatment with oral vitamin K 10 mg, his international normalized ratio comes down to 1.4, from his admission value of 5.4. Given the clinical concern for fat malabsorption, vitamin D levels are also checked: his 25-hydroxyvitamin D level is less than 10 ng/mL (lower limit of normal 20). His fecal neutral fats are reported as normal, but split fats are increased.