An elderly woman from a nursing home was transferred to hospital because of profound weakness and areflexia. Her oral intake had been poor for a few days. Current medication was a sleeping tablet which was administered by nursing staff as needed.
Admission biochemistry (in mmol/l): Na+ 145, K+ 1.9, Cl- 86, bicarbonate 45, anion gap 14 and a spot urine chloride 74 mmols/l.
Arterial Blood Gases
pCO2 49 mmHg
pO2 - not given
HCO3 44.4 mmol/l
The history does not indicate any particular acid-base disorder. There is no respiratory distress. There is suggestion of a drug-related disorder. The areflexia could indicate a hypokalaemia. There is no evidence of diarrhoea, vomiting or polyuria. The poor oral intake suggests the possibility of dehydration and maybe lactic acidosis due to poor perfusion but there is no indication of increased respiratory effort (as expected ie Kussmaul respirations). Simply put, the history is not indicative of a particular acid-base disorder.
The biochemistry results tell a more interesting acid-base story. The high bicarbonate, hypochloraemia & severe hypokalaemia suggests a significant metabolic alkalosis.
Severe metabolic alkalosis with life-threatening hypokalaemia. The cause is not yet determined. The high urinary chloride suggests a cause in the volume-resistant group (ie the 'chloride' resistant group).
The severe hypokalaemia is the cause for the weakness and requires urgent therapy. Intravenous K+ replacement is urgently indicated. Hypokalaemia can cause serious arrhythmias. It can also cause rhabdomyolysis which can result in hyperkalaemia (& malignant arrhythmias) and renal failure.
These two causes are not present in this case so other causes must be considered.
Consider the 2 major groups of causes of metabolic alkalosis: these groups are differentiated by measurement of the urinary chloride level.
The 2 major divisions of Metabolic Alkalosis
Chloride responsive’ group (urine chloride < 10 mmol/l)
Key Feature: Chloride Deficiency
Typical causes in the low urine chloride group are:
‘Chloride resistant’ group (urine chloride > 20 mmol/l)
Key Feature: Excess Steroids or Current Diuretic Use
The urine chloride at 74 mmol/l is very high in this patient and this suggests a diagnosis in the second group.
Biphasic action of diuretics: Diuretics cause a high urine chloride while they are causing a diuresis, but a low urine chloride when measured after their pharmacological action has passed. As diuretic use is common, this relationship to the timing of a dose should be known to assist in interpretation of the urine chloride result. The basic problem is that recent diuretic use by increasing urinary chloride is interfering with the usefulness of spot urine chloride measurement when attempting to sort out the cause of a metabolic alkalosis.
This patient recovered with correction of the potassium deficit. Further investigation failed to find a cause for the metabolic alkalosis. Hyperfunctioning of the adrenal cortex was not present. So excluding diuretic therapy, loss of gastric juice and excess adrenocortical activity leaves a diagnosis in the ‘idiopathic’ group.
The major aetiologic factor in this group seems to be the presence of severe potassium deficiency with plasma [K+] < 2 mmol/l (as in this case). Saline solutions (ie chloride replacement) alone do not correct the alkalosis but adding potassium replacement invariably does in these patients. Potassium depletion usually does not cause a severe alkalosis unless chloride depletion is also present.
Studies have reported high mortality rates associated with severe alkalosis but it has not been established that the relationship is directly causal.