CASE #5

A 68-year-old woman, admitted to the hospital after having profuse diarrhea for one week, was found to have acute salmonella enteritis. Weight was 60 kg. Blood pressure was 100/60 mm Hg supine and 70/40 mm Hg on standing. Tissue turgor was markedly reduced.

 

Between days 1 and 2, the patient was treated with large amounts of intravenous fluids containing sodium, potassium, chloride and bicarbonate.

 

 

LABORATORY DATA:

 

SERUM:

Hospital Day 1

Hospital Day 2

Creatinine

3.5 mg/dl

1.2 mg/dl

Sodium

133 mEq/L

137 mEq/L

Potassium

2.5 mEq/L

4.2 mEq/L

Chloride

118 mEq/L

114 mEq/L

Bicarbonate

5 mEq/L

16 mEq/L

 

 

ARTERIAL BLOOD:

 

PaCO2

16 mm Hg

20 mm Hg

pH

7.11

7.52

 

 

URINE:

 

Na

10 meq/L

K

15 meq/L

Cl

45 meq/L

 

 

 

  1. Characterize the acid-base disturbance present on day 1. What is its cause?

    2. Non anion gap (hyperchloremic) metabolic acidosis

    · respiratory compensation is appropriate (review nomogram/compensation chart)

    · diarrhea is cause

     

  2. Calculate and interpret the serum anion gap on Day 1.

    3. AG = 10; Non gap met acidosis: RTA vs. loss of alkali in lower GI tract

     

     

  3. Calculate and interpret the urine anion gap on Day 1. How is it used?

    4. Urine AG = 10 +15 - 45 = -20; negative gap in face of acidemia suggests that ammonium is present in urine, and that a. ammoniagenesis is intact and b. proton secretion is intact; this would be consistent with diarrhea or possibly Type II (proximal) RTA

     

  4. How does a low serum potassium concentration help one establish a correct diagnosis in a patient such as this?

    5. ¯ K: diarrhea, (often) Type 1 and 2 RTA

    ­ K: Type IV RTA

     

    REVIEW: RTA terminology confusion; emphasize mechanism, not terminology

     

    Classical Terminology: Type I = distal

    Type II = proximal

    Type IV =hyperkalemic

     

     

     

  5. Characterize the acid-base disturbance present on day 2. How did it develop?

 

Metabolic acidosis with respiratory alkalosis. Treatment of the patient with bicarbonate has raised the serum HCO3, but pCO2 has remained low because of slow diffusion of bicarbonate into the CNS, thus causing the CNS to continue to sense a persistent acidosis and maintain the hyperventilation. This ALKALEMIA is a common and potentially lethal side effect of bicarbonate therapy in metabolic acidosis and is a reason for caution in bicarbonate therapy.