Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) are similar but distinct diabetic emergencies that are frequently encountered in the ED. Patients with DKA or HHS present with hyperglycemia and dehydration and frequently appear quite ill physically. In both syndromes, there is insufficient insulin levels to transport glucose into cells.
As previously noted, although DKA and HHS share similar characteristic signs and symptoms, they are two distinct conditions that must be differentiated in the clinical work-up. One characteristic that helps the emergency physician (EP) to distinguish between the two conditions is the patient age at symptom onset. Although both conditions can occur at any age, diabetic ketoacidosis typically develops in younger patients, less than 45 years, who have little or no endogenous insulin production, whereas HHS usually occurs in much older non-insulin-dependent patients (who are often greater than 60 years old). 1-3 This review discusses the similarities and differences in the etiology, diagnosis, and treatment of DKA and HHS to guide evaluation and simplify management, highlighting practical tips and clinical pearls. When applicable, information has been organized into groups of five to facilitate retention and recall.
The Etiology of DKA Vs HHS
The fundamental underlying issue in both DKA and HHS is an absolute or relative lack of insulin that results in an increase in counter-regulatory hormones, including glucagon, cortisol, and catecholamines.
Insulin has five main actions: (1) to drive glucose into cells; (2) to drive potassium into cells; (3) to create an anabolic environment; (4) to inhibit breakdown of fat; and (5) to block the breakdown of proteins. (Table 1).
Table 1.
Diabetic ketoacidosis typically develops in patients who lack significant endogenous insulin; this insufficiency of circulating insulin causes hyperglycemia and hyperkalemia, the creation of a catabolic state with high levels of both ketone bodies and free-fatty acids due to the breakdown of proteins and fats.
In contrast, HHS occurs in patients who produce a sufficient amount of insulin to drive potassium into cells and to inhibit the breakdown of proteins and fats; as such these patients are not ketoacidotic. However, patients with HHS do not produce enough insulin to drive glucose intracellularly. As the glucose levels increase, patients with HHS become increasingly hyperosmolar and dehydrated, resulting in further elevation of glucose levels, causing a perpetual cycle of increasing glucose and resultant hyperosmolarity and dehydration.1-3 It is important to appreciate that both hyperglycemic crises result in an osmotic diuresis leading to severe dehydration and urinary wasting of electrolytes.