Hypokalaemia and refractory asystole complicating diabetic ketoacidosis, lessons for prevention Salman Abdulaziz, 1 Ousama Dabbagh, 2 Mohamed Ousama Al Daker, 3 Imad Hassan 1 1 Department of Internal Medicine, King Abdulaziz Medical City, King Fahad National Guard Hospital, Riyadh, Saudi Arabia 2 Division of Pulmonary, Critical Care and Environmental Medicine, University of Missouri, Columbia, Missouri, USA 3 Division of Endocrinology, Department of Internal Medicine, King Abdulaziz Medical City, King Fahad National Guard Hospital, Riyadh, Saudi Arabia Correspondence to Dr Salman Abdulaziz, dr-salman@hotmail.com To cite: Abdulaziz S, Dabbagh O, Al Daker MO, et al. BMJ Case Reports Published online: 5 December 2012 doi:10.1136/bcr-2012- 007312 SUMMARY Summary We report a unique case of diabetic ketoacidosis in which a relatively low potassium level on admission was associated with consequent life- threatening and refractory arrhythmia secondary to inappropriate use of intravenous insulin and bicarbonate therapy. The latter was reversed by rapid bolus potassium injection. Although we do not advocate this approach in every case, we emphasise that a bolus injection of potassium may be life saving in such cases. The lessons from this case have led to multidisciplinary meetings and modification of the institute’s diabetic ketoacidosis clinical pathway. BACKGROUND Severe hypokalaemia may precipitate profound and life-threatening cardiac complications including arrhythmia and asystole. It has also been cited in the literature as an important cause to consider in resuscitation-refractory cardiac arrest. 1 Slow potas- sium infusion over an extended period of time is the recommended therapeutic modality for paren- teral potassium replacement, yet more rapid potas- sium injections may be warranted in special circumstances. 23 In this report, we describe the case of a 23-year-old woman, who had a cardiac arrest sec- ondary to severe hypokalaemia complicating dia- betic ketoacidosis because of the aggressive use of bicarbonate therapy. Full recovery after successful resuscitation followed bolus replacement of potas- sium via central venous injections. We additionally report on mandatory changes and amendments to the hospital’s diabetic ketoacidosis clinical pathway that were introduced in the wake of the compli- cated clinical course this patient had. CASE PRESENTATION A 23-year-old woman presented to the emergency room with a history of generalised fatigue and decreased level of consciousness. She had 2 weeks history of polyuria, polydipsia, weight loss and a cough productive of yellow sputum. Medical history was negative. On examination, the patient looked ill, drowsy (Glasgow Coma Score, GCS = 10/15), in respira- tory distress and was dehydrated. Vital signs exam- ination revealed an oral temperature of 36.5°C, a regular pulse of 110/min, blood pressure of 135/ 85 mm Hg with significant postural drop and a respiratory rate of 24/min oxygen saturation (SaO 2 ) was 85% on room air. The jugular venous waves were not visible and heart sounds were normal. Respiratory system examination was normal apart from right-sided lower zone coarse crackles. There were no meningeal signs, focal or other neurological abnormalities. Abdominal and gynaecological exam- inations were similarly normal. INVESTIGATIONS Her laboratory investigations on admission are shown in table 1. The patient was in severe metabolic acidosis with pH 6.90, PaCO 2 21.1 mm Hg, PaO 2 50.0 mm Hg and HCO3 - 4.1 mmol/l. Her electrocardiogram showed sinus tachycardia with no QT-interval prolongation. TREATMENT The patient was initially given 1 l bolus of isotonic saline followed by an average of 1 litre of isotonic saline per hour; however, potassium chloride was added soon to the intravenous fluid. Four units intravenous bolus of regular insulin was given fol- lowed by a 4 units/h regular insulin infusion. She was electively intubated owing to low oxygen saturation and low GCS. Potassium chlor- ide 40 mEq/1 of normal saline was started at a rate of 100 cc/h. Hundred millilitres of 8.4% sodium bicarbonate intravenous bolus was given to correct the acidosis. OUTCOME AND FOLLOW-UP Around 2 h after bicarbonate administration, the patient developed pulseless wide QRS complex ventricular tachycardia and cardiopulmonary resus- citation (CPR) was commenced. Ventricular fibrilla- tion (VF) ensued for which a biphasic 150 J nonsynchronised DC shock was delivered. A 4 min asystole followed, for which a transcutaneous pace- maker was attached. Cardiopulmonary resuscitation was continued and magnesium sulphate, as well as calcium chloride, was infused. The patient briefly regained normal pulse before reverting back to VF followed by asystole. The latter was refractory to repeated epinephrine doses. Intravenous insulin infusion was discontinued immediately after hypo- kalaemia was suspected and stat potassium level was reported to be 1.7 mmol/l. A 40 mmol of KCl intravenous bolus was given immediately through the central line and this led to immediate reversal of asystole and a return to sinus rhythm. The patient was then transferred to the intensive care unit. Insulin infusion was held till the potas- sium level reached 3.3 mmol/l, while the potassium infusion was running to correct hypokalaemia. (table 2) No more doses of bicarbonate were given. Intravenous Tazocin was started to treat possible aspiration pneumonia. Echocardiogram was normal and she did not have any further arrhythmias. Enteral nutrition was started after closure of the Abdulaziz S, et al. BMJ Case Reports 2012. doi:10.1136/bcr-2012-007312 1 Reminder of important clinical lesson