Acid-Base Physiology

Case 21 : A vague historian with weakness and diarrhoea

Clinical Deatils

History: A 39 year old woman was admitted with a history of generalised weakness, dyspnoea, continuous nausea and diarrhoea. Bowel motions were frequent and watery.

The patient was a vague historian but previous contact with the patient and letters in the chart from other hospitals revealed that the patient had a very long history of laxative abuse. Past history included an admission to another hospital 10 months previously where the discharge diagnosis was 'Sjogren’s syndrome' (based on one antinuclear antibody test result) 'complicated by renal tubular acidosis and mild chronic renal failure'. This hospital had difficulty following up the patient because she had given an incorrect address and phone number. There had also been two recent admissions to another hospital with renal failure (creatinine about 0.30 mmol/l). Renal function rapidly improved to normal with intravenous fluid administration on both occasions.

The patient had admitted to abuse of diuretics on one of these previous admissions.

Examination: On admission this time, she was listless and vague, weight 42 kgs, BP 85/55, temp 37°C, pulse 75/min. Examination of heart, chest and abdomen was unremarkable.

Investigations: Na+ 125, K+ 2.8, Cl 101-, HCO3- 14, glucose 5.2, urea 21.5, creatinine 0.29 mmol/l. Anion gap was 10 mmol/l.

On ultrasound, kidneys were normal in size and the collecting system was not dilated. A psychiatric opinion was obtained during the admission regarding an eating disorder.

Arterial Blood Gases

pH   7.29

pCO2  25.6 mmHg

pO2  111 mmHg

HCO3  12.0 mmol/l


1. Initial clinical assessment

Possibilities suggested by the history are:

This may not seem to have narrowed down the possibilities much but all of these suggestions are supported by one or more aspects of the clinical details and should be considered. The weakness may be due to dehydration or hypokalaemia. A set of electrolytes and a blood gas result should sort out the diagnosis in this case. Based on past experience the patient is considered an unreliable historian so the clinician should proceed with this in mind.

Acid-base disorders due to renal failure typically don't develop until the creatinine is > 0.30 to 0.35 mmol/l so at 0.29, no significant metabolic acidosis due to renal failure would be anticipated.

2. Acid-base diagnosis

Proceeding systematically:

  1. pH: The acidaemia indicates an acidosis is present.
  2. Pattern: A low HCO3 & a low pCO2 indicate a metabolic acidosis. The HCO3 is beyond the lower limit (of 18mmol/l) for a simple respiratory alkalosis with metabolic compensation.
  3. Clues: The anion gap is normal. The chloride level is normal but this is in association with hyponatraemia (ie a 'relative hyperchloraemia' could be considered to be present). The urea & creatinine are elevated but only just to the level after which a renal acidosis may start to develop. Hypokalaemia is present. The plasma glucose is normal.
  4. Compensation: By rule 5, the expected pCO2 is 1.5 x 12 + 8 = 26mmHg. This matches the actual pCO2 of 25.6mmHg so there is no indication of a co-existent respiratory acid-base disorder
  5. Formulation: A normal anion gap metabolic acidosis with maximal respiratory compensation. No evidence of metabolic alkalosis. 
  6. Confirmation: Calculation of the urinary anion gap will assist in differentiating between the gut & the kidney as the cause of the acidosis. Measurement of urinary pH will assist with diagnosis of renal tubular acidosis. A repeat set of electrolytes would be useful also. 

3. Clinical Diagnosis

A normal anion gap metabolic acidosis is present. The chloride level is within the normal range because of the presence of significant hyponatraemia. This is an example of a normal anion gap acidosis without hyperchloraemia. (See Section 8.4).


This patient has a history of abuse of laxatives and diuretics in the setting of an eating disorder. The electrolyte results show hyponatraemia, hypokalaemia, hypobicarbonataemia and renal failure. Past history suggests renal function and electrolyte results will improve rapidly with appropriate fluid and electrolyte therapy.

Normal anion gap acidosis in most cases has either a renal or a gut cause. In this case the significant diarrhoea is sufficient to account for the disorder in this patient but this may not be correct. Chronic laxative abuse is typically associated with a metabolic alkalosis but there was no evidence of this acid-base disorder here. There is some evidence that laxative abuse may result in interstitial renal damage that could cause a renal tubular acidosis. The diagnosis ‘Sjogren’s syndrome’ has in the past been used for this patient but this diagnosis is considered not confirmed - this syndrome can be associated with a distal renal tubular acidosis so this diagnosis cannot be entirely discounted. It is possible the patient may be abusing other drugs (eg acetazolamide) which might be responsible for the acidosis.

Patients who are vague or unreliable historians can be easily dismissed and not investigated thoroughly. Such patients with eating disorders warrant careful investigation and cooperation between the various hospitals and clinicians caring for them and such management will need to include psychiatric assessment. The complex psychopathology in patients with eating disorders make long-term success difficult.

Patients with volume depletion and hypokalaemia may develop rhabdomyolysis and the outcome of this can be fatal (eg hyperkalaemia, renal failure, arrhythmias). Such outcomes have been reported in patients with laxative abuse.

Related Material

Other on-line cases related to this case and with useful discussion:

1. Case Report: A 27-Year-Old Woman With Numbness and Weakness of the Extremities

2. Case Report: Chronic, diagnosis-resistant hypokalaemia