Diabetes mellitus is one of the most prevalent metabolic conditions in India, to the extent that we’re now known as the diabetes capital of the world. It is estimated that the number of people suffering from diabetes in the country is close to hitting the distressing mark of 69.9 million in the next 3 years and 80 million by 2030.
Hospital ERs are rife with cases of diabetic ketoacidosis which are difficult to manage at a lower peripheral centre. Timely detection, comprehensive evaluation, and effective management are essential in managing this life-threatening condition.
Diabetic Ketoacidosis is a condition in which there is a drastic decrease in the circulating insulin levels in the body; the hormone responsible for glucose uptake by the cell, which triggers the increase in the secretion of counterregulatory hormones. It is characterised by a triad of hyperglycemia, ketonemia and high anion gap metabolic acidosis caused by the body being pushed into a catabolic state. The patient presents with vague symptoms such as nausea, vomiting, abdominal pain, increased thirst, and urination. Kussmaul breathing and fruity odour are specific signs present on examination along with severe dehydration.
The American Diabetes Association (ADA) admission guidelines are a plasma glucose concentration greater than 250 mg per dL (13.9 mmol per L) with an arterial pH level below 7.30, a serum bicarbonate level of less than 15 mEq per L, and a moderate or greater level of ketones in the serum or urine. They also proposed a grading system to assess the severity of DKA, which classifies DKA into mild, moderate, or severe based on the degree of metabolic acidosis (levels of blood pH and bicarbonate) and the presence of altered mental status.
These patients should be monitored closely and frequently with hourly blood glucose and urine ketone monitoring until the patient is stable and the blood urea nitrogen, serum creatinine, and electrolyte levels should be monitored every 2 to 6 hours depending on the severity of DKA. It is essential to find the precipitating factor or underlying cause which triggered the DKA. Urinary catheterization is done to monitor the urine output and the adequacy of the hydration.
The mainstay of treatment includes administering fluids and insulin.
Fluid replacement by itself will also lower blood glucose! This effect is seen when intravenous (IV) fluid therapy expands the intravascular volume, improves renal perfusion, and reduces peripheral insulin resistance by reducing levels of counterregulatory hormones. Initial IV fluid replacement starts with 0.9% sodium chloride (normal saline) at a rate of about 1-2L per hour over the 1st hour. Following this, further fluid therapy is decided on the basis of the electrolyte levels, urine output, and hydration of the patient. If the patient is in shock, continue with the previous rate of fluid administration but in the presence of mild to moderate hypovolemia, the rate of administration is reduced to 500mL/ hour for 4 hours followed by 250-500mL/hour thereafter.
Once hypovolemia is corrected, the type of IV fluids is determined by the level of corrected serum sodium; if the level is low (<135 mmol/L), 0.9% sodium chloride is continued and if the level is normal or high (≥135 mmol/L), IV fluids should be changed to 0.45% sodium chloride. When the blood glucose level has dropped below 200 mg per dL, 5% dextrose should be added along with 0.45% sodium chloride, to maintain blood glucose concentration at 150–200 mg/dL. If dextrose is not given, further ketosis may occur.
Intravenous insulin is used due to its rapid onset of action. A bolus of regular insulin at 0.1kg/hour is given followed by an insulin infusion at a rate of 0.1 unit/kg/hour. If blood glucose does not fall by at least 10% in 1 hour, increase the IV infusion rate by 1 unit/hour. When the blood glucose level falls to less than 200 mg per dL, 5% dextrose should be added so as to maintain the blood glucose levels at 150-200mg/dL.
Acidosis increases potassium levels and glucose administered with insulin lowers them. Before treatment of DKA, the level of potassium usually is normal or elevated. Target serum potassium level should be between 4-5 mmol/L. If the potassium level is less than 3.3 mEq per L, 20 – 30mEq/L potassium chloride should be given every hour as a replacement immediately and insulin should be started only after the potassium level is above this level.
The proposed American Diabetes Association (ADA) criteria for DKA resolution include serum glucose level less than 200 mg/dL and two of the following: serum bicarbonate level greater than 15 mEq/L, pH above 7.3, and anion gap less than 12 mEq/L. Therefore, the treatment goal of DKA is to improve hyperglycemia and to stop ketosis with subsequent resolution of acidosis. The patient should be able to tolerate oral feeding. If the patient is not able to eat, it is recommended to continue the IV fluids and insulin infusion.
So, when you venture out into the world of emergencies as a doctor, remember that even something as simple as hydration can be essential to saving lives.