Case Report
A 27-year-old previously healthy male was referred with a two week history of vomiting, high grade fever and abdominal pain, which was diagnosed as appendicitis. On admission to the referral facility he was diagnosed with a new presentation of type 1 diabetes mellitus. Post appendectomy he was referred to our facility for further management. On arrival, he was semi-conscious, barely responsive to pain and had laboured breathing. He also had electrolyte imbalance with severe hypokalaemia of 1.6 mmol/L and an elevated random blood glucose level.
Physical examination revealed a well-nourished albeit severely dehydrated male weighing about 53kg. He was febrile and had Kussmaul breathing. His vitals were: BP = 151/69 mmHg; HR = 132 beats per minute, RR = 32 breaths per minute, SPO2 = 96% on room air, Temperature = 38.9°C, random blood glucose = 16.6 mmol/L. A bedside ultrasound revealed a collapsed inferior vena cava (IVC). His initial point-of-care venous blood gas showed metabolic acidosis (pH = 7.20, PCO2 = 21.5 mmHg, HCO3 = 10.1 mmol/L) with severe hypokalaemia of 2.2 mmol/L (3.5-5.0 mmol/L), hypernatremia of 167 mmol/L (135-145 mmol/L) and hyperchloremia of 125 mmol/L (98-109 mmol/L).  Serial venous blood gases and electrolytes were performed every 3 to 6 hours (Table 1). Urine analysis was unremarkable including the absence of urinary ketones.
Central venous access was obtained in the right subclavian vein and a 4 L bolus of Ringers lactate was administered followed by a free water deficit maintenance using 5% Dextrose water admixed with potassium chloride (KCl) 40 - 80 mmol which ran at 125 ml/h (KCl rate of 10 – 20 mmol/h). Simultaneously, a fast-acting insulin infusion at 0.05 U/kg/h (2.5 U/h) was also administered. Post-operative broad-spectrum parenteral antibiotics were initiated, and the patient was admitted to the ICU.
After 24 hours of admission, we noted the patient had a urinary output of 9 L of dilute urine with a negative fluid balance of 3 L. His serum potassium was persistently low despite receiving a continuous KCl infusion for over 24 hours. At this point, his serum potassium level was 1.94 mmol/L. Serum magnesium levels were ordered to rule out probable cause of refractory hypokalaemia, which revealed hypomagnesemia of 0.50 mmol/L (0.66 -1.25 mmol/L). All other blood investigations including brain and abdominal CT scan were unremarkable except for the ECG which showed diffuse U-wave morphology (Fig.1) correlating with hypokalaemia and/or hypomagnesemia. Urinary specific gravity was found to be low with a value of 1.005. Plasma levels of antidiuretic hormone (ADH) and urine osmolality were not available at our centre.