STOWE, VT. — Uncertain triggers, therapeutic controversies, and potentially fatal complications can compromise emergency management of diabetic ketoacidosis, according to Steven M. Hulsey, M.D.
Diabetic ketoacidosis (DKA) is a major, acute metabolic complication of diabetes that requires immediate and intensive care.
Although DKA is not a difficult diagnosis per se—particularly in the context of known type 1 diabetes—evaluation and treatment can be challenging, Dr. Hulsey said at an emergency medicine update sponsored by the University of Vermont.
Diagnosis and management of the severe insulin deficiency that sets the ketoacidotic chain in motion are only half the battle. The other half is identifying the event or condition that precipitated the metabolic disorder and addressing it appropriately to restore normal balance and prevent recurrences.
“Initially, you want to make sure that what is causing the ketoacidosis isn't itself a life-threatening condition, such as myocardial infarction or sepsis,” said Dr. Hulsey, noting that in some cases, the “trigger” could pose at least as great a threat as the DKA.
Excessive urination, severe thirst, fruity-smelling breath, abdominal pain, nausea, vomiting, fatigue, breathing difficulties, and mental confusion are among the telltale symptoms of DKA.
Blood glucose levels higher than 250 mg/dL, large quantities of ketones in the urine and plasma, low serum bicarbonate (less than 15 mmol/L), elevated anion gap (more than 16 mmol/L), and a blood pH of less than 7.3 confirm a diagnosis of DKA.
Because there is no clinically significant difference between arterial and venous pH estimates in patients with DKA, “go ahead and get the venous sample upon insertion of the IV for fluid resuscitation,” Dr. Hulsey recommended. “This spares the patient a painful arterial stick later.”
Severe electrolyte disturbances are also characteristic of DKA. The most dangerous of these, total body potassium loss, is difficult to assess, because it is typically not mirrored in serum potassium levels—a factor that must be considered before treatment.
Initial blood potassium levels usually are normal to high, despite substantial total body potassium deficits. This is because the acidosis encourages leakage of intracellular potassium.
Treatment with insulin—a cornerstone of DKA therapy—drives potassium back into the cells, and levels may drop very quickly.
For this reason, frequent blood potassium checks are critical during therapy.
“If serum potassium levels are even just slightly low on the first test, that means that total body potassium is probably critically low and must be replenished before giving the patient insulin,” Dr. Hulsey said. “If potassium levels are normal, total body potassium is probably low and should be replenished [along with insulin infusion].”
The pillars of DKA treatment include efforts to correct life-threatening dehydration, hyperglycemia, ketonemia and acidemia, and electrolyte disturbances. Toward this end, aggressive fluid resuscitation is warranted unless the patient has signs of any condition, such as congestive heart failure, that might be exacerbated by large volumes of intravenous fluids.
A less aggressive approach is also recommended when treating children and adolescents, who are at greater risk for cerebral edema.
It has been suggested, though not proven, that over-aggressive fluid replacement is linked to this rare, often fatal complication. “But most physicians choose to err on the side of underreplacement in kids,” Dr. Hulsey said.
Intravenous insulin is also indicated, although there is ongoing debate about dosing and infusion rates.
In the past, large doses of insulin were recommended early in DKA therapy. Current thinking is that hyperglycemia should be corrected gradually to avoid hypoglycemia, hypokalemia, and cerebral or pulmonary edema, he said. Blood glucose levels should be monitored hourly, and insulin dose should be adjusted accordingly.
There currently is no consensus on the practice of administering an intravenous bolus of regular insulin as a way to jump-start recovery efforts before low-dose infusion.
“In reality, a bolus dose is not needed [before low-dose infusion] to obtain optimal plasma levels, because the time needed to reach normal glycemic levels is the same,” Dr. Hulsey said. “And there is the possibility that a bolus dose may increase the risk for hypokalemia.”
A bolus dose should be considered, however, when a substantial delay in treatment is anticipated, he said.
In such circumstances, it is not unreasonable to administer successive small bolus doses, as long as potassium levels are being monitored.
The use of intravenous bicarbonate to reduce the immediate risks of extremely low pH is also a contentious topic.
The theoretical advantages include a reduction in cardiac irritability, respiratory discomfort, and intravenous chloride load, while the theoretical disadvantages include the possibility of hypokalemia and arrhythmia and exacerbated intracellular and intracerebral acidosis.