Severe hypokalemia – an instructive case history report

In health serum potassium concentration is maintained within the approximate reference range of 3.5-5.2 mmol/L (or 3.5-5.2 mEq/L). Hypokalemia (reduced serum potassium) is therefore defined as serum potassium <3.5 mmol/L (or <3.5 mEq/L). Severe hypokalemia (<3.0 mmol/L) is associated with muscular weakness progressing to paralysis if particularly severe; and potentially fatal cardiac arrhythmia. 

Severe hypokalemia is thus a serious condition requiring urgent medical intervention (correction). The case history of a patient who suddenly developed particularly severe hypokalemia (serum potassium 1.6 mmol/L) following neurosurgical treatment is recently published. In discussion of the case history the authors provide a valuable overview of potassium metabolism and the causes/mechanisms of hypokalemia.

The case concerns a previously well 45-year-old man who was emergently admitted to hospital with reduced consciousness (GCS 9), following sudden collapse and seizure at home. CT scan revealed that he was suffering extensive subarachnoid and intraventricular hemorrhage following rupture of an aneurysm of the left anterior communicating artery, a major blood vessel in the brain. 

Emergency treatment, conducted under general anesthesia, comprised placing of an external ventricular drain to relieve increased intracranial pressure, and coil embolization of the aneurysm to halt blood loss. Serum potassium at the time of anesthesia induction was 3.5 mmol/L.

Postoperative therapy included two doses of mannitol (75 g), an osmotic diuretic to help reduce intracranial pressure. Serum potassium was 4.2 mmol/L at this time but over the following 24 hours it reduced rapidly to a nadir of 1.6 mmol/L, despite administration of potassium. 

During this crucial 24-hour period as serum potassium was falling there were other concerns: the patient’s intracranial pressure remained high and his cerebral perfusion pressure remained low. It was decided to induce coma by pentobarbital infusion, and also induce hypothermia. With continued administration of potassium, serum potassium began to rise and was within normal limits a day later. 

Sadly, it became clear that the prognosis for this patient was not good; despite all interventions intracranial pressure remained high and blood perfusion of the brain remained inadequate. Eventually, 4 days after admission, by which time the patient’s kidneys were failing, life support was removed with family agreement.

In a carefully argued discussion, the authors of this case history conclude that hypokalemia in this case was largely treatment-related (iatrogenic) and multifactorial. They suggest that the initial decrease in plasma potassium was due to excessive loss in urine due to the osmotic diuresis induced by mannitol administration. This was followed by massive intracellular shift of potassium (from serum into cells). 

Several factors likely contributed to this potassium shift, including administered pentobarbital, administered alkali, induced hypothermia and an endogenous adrenergic surge that is known to accompany subarachnoid hemorrhage.