Solution to "A 52-Year-Old Man With a Low Bicarbonate Level"

Robert M. Centor, MD; Rashmi K. Murthy; Sarah L. Prophet


January 18, 2008

This is the solution to a case we presented recently. You may review the case here.

The patient had complained of dyspnea, and an abnormal electrolyte panel revealed a decreased bicarbonate level of 15 and an elevated chloride level of 117. His anion gap was calculated as follows:

Anion gap = Na+ - (HCO3 - + Cl-)

Anion gap = 145 - (15 + 117) = 13 (borderline normal)

With only this information, one would be quick to suspect that his acid-base disturbance was a normal gap metabolic acidosis and that his dyspnea represented compensatory hyperventilation.

The differential diagnosis of a normal gap (hyperchloremic) metabolic acidosis includes diarrhea, saline-induced metabolic acidosis, and renal tubular acidosis.

1. Diarrhea results in gastrointestinal loss of bicarbonate via stool; this lowers the plasma bicarbonate level and causes a normal anion gap metabolic acidosis.

2. When a patient is given normal saline, the hyperchloremic intravenous fluid increases the patient's chloride anion levels, causing a metabolic acidosis. Normal saline (NaCl) combines with water to create a strong acid (HCl) and a strong base (NaOH), as shown here:

NaCl + H2O HCl + NaOH

The normal concentrations in plasma are sodium 140 mEq and chloride 100 mEq. Normal saline contains 154 mEq sodium and 154 mEq chloride. The addition of this sodium and chloride causes a greater increase in chloride than sodium, moving the acid-base equilibrium toward HCl and causing a metabolic acidosis.

3. There are 3 types of renal tubular acidosis (RTA). A positive urine anion gap is suggestive of RTA as the cause of nongap metabolic acidosis, as opposed to diarrhea or normal saline. The urine anion gap is also important to distinguish from the different RTAs and is calculated as follows:

Urine anion gap = UNa + UK - UCl

A positive urine anion gap (Cl- is less than K+ and Na+) suggests a distal acidification defect, whereas a negative urine anion gap (Cl- is greater than K+ and Na+) suggests renal or extrarenal loss of bicarbonate. The urine anion gap is negative in patients without RTA because they can appropriately increase the ammonium in their urine to excrete the excess acid as NH4Cl, leading to a rise in the urine chloride concentration and a negative urine anion gap. Patients with RTA are unable to properly buffer and excrete the excess acid and do not appropriately increase the urinary ammonium levels, resulting in a positive urine anion gap.

Type 1 (distal) RTA is the inability of the renal tubule to eliminate hydrogen ions properly. These patients have metabolic acidosis, hypokalemia (renal potassium loss), an inappropriately alkaline urine pH (> 5.3) in the presence of acidemia (inability to acidify urine), and a positive urine anion gap. There is a decrease in net hydrogen ion excretion and ammonium production, so the dietary acid load is not properly excreted.Type 2 (proximal) RTA is the result of renal bicarbonate wasting as a result of a defect in the proximal tubular reabsorption of filtered bicarbonate. In this condition, bicarbonate wasting occurs only when the plasma bicarbonate is above the bicarbonate reabsorption threshold. These patients can have hypokalemia or normokalemia and have a negative urine anion gap. Secretion of hydrogen ions is not a problem in these patients and therefore their urine is acidified appropriately. When the defect in proximal tubular reabsorption is generalized and includes other solutes such as amino acids, glucose, phosphorous, and urate, it is called Fanconi syndrome.

Type 4 RTA occurs as a result of aldosterone deficiency or tubular unresponsiveness to aldosterone. Patients have a normal anion gap metabolic acidosis, hyperkalemia, and a positive urine anion gap. There is abnormal distal K+ secretion, H+ secretion, and Na+ reabsorption. The most common cause of type 4 RTA is secondary to diabetes. It can also occur with the use of potassium-sparing diuretics, hyporeninemic hypoaldosteronism, or collecting duct dysfunction secondary to renal insufficiency.

An important teaching point of this case is that whenever you see an abnormal electrolyte panel suggestive of an acid-base disturbance, you should first order an arterial blood gas. Also, if nonanion gap metabolic acidosis is a possibility, you should check urine electrolytes and calculate the urine anion gap.

Our patient's laboratory tests showed the following values:

Electrolyte panel: sodium 145 mEq/L; potassium 3.1 mEq/L; chloride 117 mEq/L; bicarbonate 15 mEq/L; blood urea nitrogen (BUN) 35; creatinine 1.0 mg/dL; glucose 120 mg/dL

Arterial blood gas: pH 7.43; pCO2 20; pO2 59

Urine electrolytes: UNa 65; UK 70; UCl 116

In evaluating these laboratory values, we note that the patient is slightly alkalemic (pH from arterial blood
gas = 7.43), not acidemic. Also, his low PCO2 indicates a primary respiratory alkalosis.

Hyperventilation causes respiratory alkalosis. The common differential diagnosis includes hypoxia, sepsis/fever, hepatic failure, pulmonary edema, pulmonary embolism, anxiety, central nervous system (CNS) disease (central hyperventilation), drugs (salicylates), pregnancy, and hyperthyroidism.

Because our patient was complaining of shortness of breath and his oxygen requirement had increased over the past few days, we also ordered a chest x-ray. This provided evidence of pulmonary edema, which was causing his hyperventilation, hypoxia, and respiratory alkalosis. The edema was a result of overestimating his maintenance intravenous fluid requirements. The patient weighed 98.9 pounds, which is much less than the average patient weight. His maintenance intravenous fluids should have been about 85 mL/hour. Instead, he remained on the floor for several days with his maintenance intravenous fluids running at 125 mL/hour, which caused volume overload and resulted in the development of pulmonary edema.

As soon as the cause of the problem was identified, we discontinued his maintenance intravenous fluids and the patient underwent diuresis with furosemide. Subsequently, his oxygen saturation improved, his oxygen requirements decreased, and his plasma bicarbonate increased to normal levels.

Thus, this case demonstrates that one cannot diagnose an acid-base disorder solely on the basis of an electrolyte panel. A full evaluation will always include an arterial blood gas. In this patient, the arterial blood gas pointed to the diagnosis and directed the proper treatment.

Read and participate in the discussion of this case here, and watch for another new case soon.


Comments on Medscape are moderated and should be professional in tone and on topic. You must declare any conflicts of interest related to your comments and responses. Please see our Commenting Guide for further information. We reserve the right to remove posts at our sole discretion.
Post as: