Signs and Symptoms
Over a period of 24 hours, symptoms such as nausea, vomiting, increased thirst, and polyuria develop due to dehydration caused by osmotic diuresis and glucosuria.5 Patients may also present with hypotension and tachycardia. Confusion, deep gasping breaths or Kussmaul respirations, and metabolic acidosis result from hyperventilation and failure to compensate for the increased serum concentration of ketone bodies. Ketone production leads to a fruit-like odor in the patient’s breath and ketonuria in the urinalysis. In DKA, laboratory values will indicate metabolic acidosis and abnormal serum electrolytes. In both DM and DKA, increased urea and creatinine due to dehydration, increased ketones, and the presence of diabetic nephropathy are useful indicators of impaired kidney function.12
Management and Treatment
Diabetic ketoacidosis can be managed and reversed, especially when recognized and treated early.6,13 Dehydration in DKA can be corrected with IV fluid replacement. Normal saline (0.9%) can be started at 15 to 20 mL/kg/h or 1 L/h. As the patient’s vital signs stabilize, IV fluids can be titrated to a lower dose of 250 to 500 mL/h. Monitoring BP and electrolytes are key at this point as alterations in sodium levels and glucose levels may require switching to half-normal saline and/or dextrose.
The hyperglycemic state of patients with DKA is managed by IV insulin. An initial bolus of 0.1 U/kg/h can be given, but should only be administered when potassium levels are greater than 3.3 mmol/L.14 If adequate perfusion can be maintained, then 0.14 U/kg/h can be used instead of a bolus. Glucose levels must be monitored; once the levels decrease to approximately 200 mg/dL, the infusion rate of insulin should be titrated down to 0.05 to 0.1 U/kg/h. Dextrose is then added to maintain glucose levels at approximately 150 to 200 mg/dL.
Electrolytes, especially potassium, must be monitored closely in patients with DKA. Insulin leads to the shift of potassium into cells. The lack of insulin keeps potassium in the extracellular space. Due to osmotic diuresis, potassium is lost in the urine, leading to hypokalemia. Potassium levels in patients with DKA should be maintained at a level between 4 to 5 mmol/L. Patients with potassium levels between 3.3 to 5.2 mmol/L can be started on IV potassium between 20 to 30 mmol/h. If the patient is severely hypokalemic (<3.3 mmol/L), insulin should be withheld, and only IV potassium should be given at a rate of 20 to 30 mmol/h.
Bicarbonate levels can also be managed as acidosis can lead to both neurological and cardiac complications. If the patient’s pH is less than 6.9, the American Diabetes Association recommends starting 100 mmol of sodium bicarbonate in 400 mL sterile water (in addition to potassium chloride at 200 mL/h) for 2 hours. Dosing should be repeated every 2 hours until the patient’s pH is greater than 6.9.
In uncomplicated cases of DKA, the condition is resolved when a patient’s pH is greater than 7.3; glucose level is less than 200 mg/dL; and bicarbonate level is greater than or equal to 18 mmol/L. After patients become hemodynamically stable, they can be discharged and managed at home with a combination of intermediate- or long-acting insulin as well as short- or rapid-acting insulin.
Complications and Mortality
Diabetic ketoacidosis can cause sudden and fluctuating changes in the body. Therefore, it is very important to monitor a patient’s laboratory values very carefully and frequently to avoid any pitfalls. Since patients can present with hyponatremia due to the osmotic draw of glucose in the blood,13 sodium levels may have to be corrected. The corrected serum sodium can be calculated by adding 1.6 mmol/L for every 100 mg/dL of glucose (when finger-stick readings are above 200 mg/dL).15 Patients with DKA can also present with leukocytosis (even in the absence of infection) and hypertriglyceridemia (due to impaired lipoprotein lipase).15 Serum creatine may be elevated due to blood acetoacetate levels.15
Interestingly, there are other acute conditions that can mimic DKA.15 For example, chronic ethanol abuse can lead to ketoacidosis. Unlike DKA, however, alcoholic ketoacidosis does not have profound hyperglycemia, which can help differentiate the two during initial assessment.
Complications due to DKA can arise comprising the patient’s health, including hypoglycemia, hypokalemia, rhabdomyolysis, acute renal failure, pulmonary edema, and shock.16 Cerebral edema is seen in up to 1% of DKA patients,15 the cause of which may be due to the severity of the acidosis, high glucose levels, and rapid hydration. Even when cerebral edema is reduced, patients are often neurologically impaired. Mortality rates from DKA deaths due to cerebral edema can be as high as 24%.13 In the United States, over 100,000 patients with DM per year are admitted to the hospital for DKA, and 9% of patients with DM suffer from DKA-related complications postdischarge.15 With current treatment protocols, mortality rates for DKA-associated deaths are now down to 1%.6,15