Q. What is Diabetic Ketoacidosis (DKA), and what are the steps that an ED physician should take to manage DKA in its early stages?
A. Diabetic Ketoacidosis is a potentially fatal condition that occurs in patients with Diabetes Mellitus 1 and 2. The pathophysiology of DKA involves hyperglycemia, dehydration, ketosis, and electrolyte imbalance — all effects of insulin deficiency, increased insulin counter-regulatory hormones (cortisol, glucagon, growth hormone), and peripheral insulin resistance. In simpler terms, the body thinks it is starving because the cells are not taking up enough glucose. As a result, it begins to break down fat and protein in order to produce more glucose. In the process, highly acidic ketones are produced and cause a severe chemical imbalance in the bloodstream. At the same time, the hyperglycemia causes more frequent urination, which leads to dehydration, electrolyte loss, and ultimately, a reduction of total body potassium. In the ER, a patient with DKA may present with excessive thirst, frequent urination, nausea and vomiting, abdominal pain, fatigue, shortness of breath, fruity scented breath, and confusion. To confirm DKA diagnosis specifically, the physician will also check for high blood sugar levels and high ketone levels in the urine. Following diagnosis, the doctor will 1) collect blood to get the patient’s metabolic profile; 2) infuse 1 L of 0.9% sodium chloride over 1 hour; 3) ensure potassium level of >3.3 mEq/L before initiation of insulin therapy (supplement potassium intravenously if needed); and finally, 4) initiate IV insulin therapy, during which insulin will go directly into the bloodstream to uptake glucose from the blood. Step 3 is particularly important — if a doctor does not check that the potassium levels are at an acceptable level, the institution of insulin therapy and correction of hyperglycemia can result in hypokalemia, furthering damage to the body. Resources: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4085289/