Pseudohyperkalemia is a spuriously high serum potassium measurement in a patient with no clinical evidence of hyperkalemia. It has been reported to occur in patients with leukocytosis and thrombocytosis. Only a few cases of pseudohyperkalemia have been reported in patients after splenectomy. Two cases of pseudohyperkalemia occurring after emergency splenectomy for abdominal trauma are presented to highlight their clinical presentation and sequalae. Consecutive patients who underwent emergency splenectomy for trauma and subsequently developed pseudohyperkalemia were monitored in Universiti Kebangsaan Malaysia Medical Centre for their clinical sequalae. Both the patients developed leukocytosis, thrombocytosis and high serum potassium level within 2-weeks of their splenectomies. They did not demonstrate any symptoms and signs of hyperkalemia. Their conditions resolved spontaneously without any specific treatment. Pseudohyperkalemia should be suspected in a similar clinical scenario to avoid unnecessary treatment that could lead to severe hypokalemia.
Barbiturate coma therapy (BCT) is a treatment option that is used for refractory intracranial hypertension after all other options have been exhausted. Although BCT is a brain protection treatment, it also has several side effects such as hypotension, hepatic dysfunction, renal dysfunction, respiratory complications and electrolyte imbalances. One less concerning but potentially life-threatening complication of BCT is dyskalaemia. This complication could present as severe refractory hypokalaemia during the therapy with subsequent rebound hyperkalaemia after cessation of the therapy. Judicious potassium replacement during severe refractory hypokalaemia and gradual cessation of the therapy to prevent rebound hyperkalaemia are recommended strategies to deal with this complication, based on previous case series and reports. In this case report, we show that these strategies were applicable in improving severe hypokalaemia and preventing sudden, life-threatening rebound hyperkalaemia. However, even with use of these strategies, BCT patients could still present with mild, asymptomatic hyperkalaemia.
High anion gap metabolic acidosis (HAGMA) is a hallmark of Diabetic Ketoacidosis (DKA). Occasionally, a Normal Anion Gap Metabolic Acidosis (NAGMA) can be seen, especially during the treatment phase. In this case report, a 55-year-old lady with diabetes mellitus who presented with a 2-day history of fever, lethargy and multiple episodes of vomiting and diarrhoea. Initial laboratory investigations revealed: capillary blood glucose as 27 mmol/L, urine ketone as 3+, blood ketone as 3.5 mmol/L, serum bicarbonate as 14 mmol/L, and serum chloride as 95 mmol/L. She was treated with intravenous normal saline fluid resuscitation and constant rate insulin infusion which was fortunately accompanied by stabilization of blood glucose and normalization of blood ketone to 0.2 mmol/L. However, despite normalization of her anion gap (25 to 14), she remained unwell with acidotic breathing due to refractory hyperchloraemic NAGMA with bicarbonate at 11 mol/L and chloride of 112 mmol/L. It was then decided to administer 100 mL of 8.4% Sodium Bicarbonate solution. The next day, she was no longer tachypneic as her bicarbonate and carbon dioxide improved to 21 mmol/L and 32 mmHg respectively. The presence of NAGMA in DKA should prompt clinicians to conduct a thorough search for possible underlying causes, such as gastrointestinal fluid loss, sepsis and chloride load from aggressive fluid resuscitation with normal saline. Sodium bicarbonate should only be considered in intractable cases to correct a NAGMA and not routinely used in the treatment of DKA.