Initial Potassium Replacement in Diabetic Ketoacidosis: The Unnoticed Area of Gap.

Diabetic ketoacidosis is an acute complication of diabetes mellitus (DM). It affects all the types of DM and hence is a continuous threat for all the diabetes patients (1). DKA is a well-studied disease. Among the precipitating causes, mostly reported factors are non-compliance of patients with the antidiabetic treatment, and infection; others, however, may not have any precipitating cause (1, 2). The progress of disease is very simple; lack of insulin causes hyperglycemia and inability of glucose to enter the cell. In-turn, triglycerides are broken down to free fatty acids which are used as a source of energy (1, 3, 4). In due process, the end-product of this metabolic derangement, i.e., ketones, cause acidification of blood causing major disruption in homeostasis. Similar to pathophysiology, the treatment of DKA is also simple and encompasses administration of insulin to achieve euglycaemia, and administration of crystalloid or colloidal solution to attain euvolaemia and euelectrolytaemia (1-3). Nevertheless, by the time patient reports for medical attention, these simple derangements and the rectification pathway have had gone significant derailment with potassium being the most affected ion throughout the event and resolution of DKA (5, 6). In similar context, potassium adds on to further exacerbation of already compensating, due to acidosis and respiratory distress observed in DKA, cardiovascular system (CVS). [ABSTRACT FROM AUTHOR]