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At a glance
- To develop diabetic ketoacidosis (DKA) the patient must experience a relative insulin deficiency in the setting of increased counter-regulatory hormone concentrations.
- Appropriate treatment of the presenting stressor can minimize the impact of DKA on the patient.
- The first step in DKA therapy is fluid resuscitation.
- During therapy, closely monitor patients to assure steady progress and avoid adverse events.
Diabetic ketoacidosis (DKA) is a serious acute diabetes complication, manifested by a life-threatening hyperglycemic crisis. DKA is defined by the presence of the triad of hyperglycemia, anion gap metabolic acidosis and ketonemia.1 Although the condition is a medical emergency, it can be effectively treated. Nevertheless, the hospitalization burden is high, and the total cost of care is estimated to be in the billions.
The keys to successful treatment are timely diagnosis, appropriate initial intervention, recognition of concomitant illness, appropriate electrolyte management, and attentive transition to oral feeding and subcutaneous insulin upon pH normalization.
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The most recent CDC reporting data show 123,000 discharges for DKA in 2007. Of those, 89% were older than age 15 years, and males outnumbered females by a few percentage points.2 These hospitalizations came at a steep price, with direct and indirect costs of $2.4 billion. This amount accounted for one quarter of the total direct costs of caring for these patients. For patients requiring more than one DKA admission, it represented a full half of their total direct costs.3
Normal glucose management
To fully understand the various facets of effective DKA treatment, it is necessary to be familiar with the roles of select hormones in managing glucose loads.
A nondiabetic adult holds only about 5 g of glucose in circulation at any given time. This is roughly the same amount of glucose contained in a bite-sized candy bar and about one-eighth of the amount found in a 12-oz can of cola. To prevent a doubling or tripling of the serum glucose concentration with the ingestion of common sugar loads, hormonal regulation of glucose concentration must be brisk and effective. On the other hand, to prevent hypoglycemia during periods of fasting, counter-regulation must be equally robust.
The liver is the primary glucose-regulating organ. It responds to insulin and glucagon, which are the main hormones responsible for glucose homeostasis. Both are produced and released by the pancreas. Their actions generally oppose each other in a regulatory/counter-regulatory balance.
Insulin. When the glucose load is absorbed into the blood, insulin is released from the beta cells of the pancreatic islets. The insulin serves a number of functions important to glucose regulation and utilization (Table 1). Overall, it stimulates glucose uptake and utilization as fuel. Insulin also allows for storage of excess glucose for later use. In this way, the presence of insulin provides a mechanism for removing excess glucose from circulation and preventing hyperglycemia, and is thus considered a regulatory hormone.
Glucagon. Glucagon is active primarily in the liver (Table 2), and its effect is essentially the opposite of that of insulin. Glucagon is released from the alpha cells of the pancreatic islets. Its release is inhibited by the presence of insulin and glucose and stimulated by the presence of catecholamines and glucocorticoids. For this reason, glucagon levels tend to increase during times of low blood-glucose concentrations and stress. It acts in a number of ways to increase serum glucose concentration and inhibit its storage. In this way, the presence of glucagon prevents hypoglycemia, and is thus considered a counter-regulatory hormone.
Table 3 lists the other major counter-regulatory hormones and their primary actions.
