Acid-Base Physiology: Examples for 9.6

Case History 7: A man with diarrhoea and dehydration

Clinical Details

A 44 year old moderately dehydrated man was admitted with a two day history of acute severe diarrhoea. Electrolyte results (in mmol/l): Na+ 134, K+ 2.9, Cl- 113, HCO3- 16, urea 12.3, creatinine 0.30 mmol/l. Anion gap 8.

Arterial Blood Gases

pH 7.31

pCO2 33 mmHg

pO2  - not given

HCO3 16 mmol/l

K+ 2.1 mmol/l


Firstly, the initial clinical assessment

The possibilities suggested by the history of severe diarrhoea with hypovolaemia are:

Secondly, the acid-base diagnosis

Looking at the results systematically:-

  1. pH: A net acidaemia is present so an acidosis must be present to have caused this.
  2. Pattern: Both the pCO2 & HCO3 are low - this pattern is found in respiratory alkalosis and in metabolic acidosis. Now we know that an acidosis must be present (because of the acidaemia), so therefore the diagnosis is metabolic acidosis
  3. Clues:
    • The normal anion gap with an elevated chloride suggests a normal anion gap acidosis.
    • The elevated urea & creatinine is noted but this has not been sufficient to elevate the anion gap so there has not been significant retention of acid anions.
    • There is no evidence to support the co-existence of a high AG acidosis and a normal AG acidosis. The delta ratio is slightly negative and certainly not in the range which would suggest a combined acidosis.
  4. Compensation: Here we ask is the respiratory compensation appropriate? The maximal amount of respiratory compensation takes 12-24 hours to occur so sufficient time has elapsed. The expected pCO2 (by Rule 5) is (1.5 x 16 + 8) which is 32 mmHg. This is close to the actual measured value of 33mmHg, so no primary respiratory disorder is present. This is consistent with the history as there was no evidence of a respiratory disorder.
  5. Formulation: The acid-base diagnosis is a normal anion gap metabolic acidosis with appropriate respiratory compensation.
  6. Confirmation: This is no investigation which can assist here. A lactate level would have been useful to totally exclude any lactic acidosis.

Finally, the clinical diagnosis

This patient has acute diarrhoea causing a mild normal anion gap metabolic acidosis. The volume loss is probably responsible for pre-renal azotaemia.


Pertinent points were the acidaemia, elevated chloride, normal anion gap and the elevation of urea and creatinine. Note that this laboratory has calculated the anion gap as (Na + K) - (Cl + HCO3).

Some pre-renal renal failure is present but there is no evidence of a high anion gap acidosis due to renal failure. As a general guideline, acidosis usually does not occur in renal failure until GFR is less than 20 mls/min (or a creatinine level of about 0.30-0.35 mmol/l). Similarly tissue perfusion is still adequate enough to prevent development of a lactic acidosis. Hypovolaemia results in secondary hyperaldosteronism which increases sodium reabsorption but increases excretion of K+ resulting in hypokalaemia.

This example is Case 8 reported by Walmsley & White (1985)