Thread: A 52-year-old Man With a Low Bicarbonate Level

Case Presentation

JB is a 52-year-old cachectic white male with a history of peripheral vascular disease and hepatitis C; he was recently hospitalized for an infected sacral decubitus ulcer. During that hospitalization, his examination revealed diffuse lymphadenopathy suggestive of malignancy. He then presented to the emergency department (ED) after a 2-week history of decreased oral intake, altered mental status, and syncope. In the ED, the patient was hypotensive, with an initial systolic blood pressure of 60 mm Hg, and had tachycardia, with a heart rate of 100 beats per minute. He had leukocytosis (white blood cell count 27.4), lactic acidosis, and was in acute renal failure with a creatinine level of 2.1 mg/dL (previous admission creatinine was 0.9). At that time, 2 sets of blood cultures were drawn, and antibiotic therapy was initiated with vancomycin, ciprofloxacin, and a piperacillin and tazobactum injection (Zosyn). He received a 2-L normal saline bolus, and his systolic blood pressure improved to 90 mm Hg.

The patient was admitted to the intensive care unit (ICU) with the following vital signs, laboratory values, and measurements:Temperature 95.2°F; pulse 82 beats per minute; respirations 18 breaths per minute; blood pressure 95/63 mm Hg;

Electrolyte panel: Sodium 133 mEq/L, potassium 4.8 mEq/L, chloride 92 mEq/L, bicarbonate 24 mEq/L, blood urea nitrogen (BUN) 57, creatinine 2.1 mg/dL, glucose 168 mg/dL;

Arterial blood gas: pH 7.34, pCO2 39, pO2 179;

Anion gap 17, lactic acid elevated at 7.6; and

Height 68 inches, weight 98.9 pounds.


The patient remained in the ICU for 2 days and was treated for hypovolemia and sepsis with IV fluid hydration and broad-spectrum antibiotics. He had aggressive volume expansion with a 1-L 0.9% normal saline bolus, followed by normal saline at 250 cc/hour. His blood pressure improved appropriately, with the systolic blood pressure increasing to 120 mm Hg. His laboratory values also showed improvement, with his lactic acidosis and acute renal failure resolving. On the second hospital day, his IV fluid rate was decreased to150 cc/hour.

Once he was hemodynamically stable, the patient was transferred to the medicine floor on the third day of his hospitalization. He was treated with maintenance IV fluids (0.9% normal saline at 125 cc/hour) and kept for continued monitoring.

As the patient awaited a lymph node biopsy (for further evaluation of his lymphadenopathy), he continued to receive 0.9% normal saline at 125 cc/hour for 3 days, which was then decreased to 100 cc/hour. On the seventh hospital day, the patient complained of some mild shortness of breath at rest and had increasing oxygen requirements. At that time, the following laboratory values were recorded: sodium ,145 mEq/L; potassium, 3.1 mEq/L; chloride, 117 mEq/L; bicarbonate, 15 mEq/L; BUN, 35; creatinine, 1.0 mg/dL; and glucose, 168 mg/dL

The Problem

Identify the acid-base disturbance and formulate a differential diagnosis.

What other laboratory tests would you order?

__________________________________________________ ______________________

Discussion to follow....!!

Chest X Ray and then Thorax CT
This is SIRS / CARS / MARS and ARDS With Respiratory and Metabolic Acidosis

Solution and Discussion

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