Key Clinical Questions
How are diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic syndrome (HHS) diagnosed and treated?
How is hypoglycemia treated?
What are the causes of hypoglycemia in nondiabetic patients?
How is hypoglycemia avoided in the hospital?
Admissions with diabetic ketoacidosis as the primary diagnosis have increased over the past 30 years, with 140,000 recorded in the United States in 2009. However, mortality has been reduced to less than 5%. Hyperosmolar hyperglycemic syndrome is less common, but it is associated with a mortality of up to 11%, because of the greater age and comorbid conditions of the at-risk patient population.
Diabetic ketoacidosis arises in patients with absolute or severe insulin deficiency. The resulting hyperglycemia combined with an increase in counter-regulatory hormones, including glucagon, catecholamines, cortisol, and growth hormone, precipitate proteolysis and lipolysis. Lipolysis causes the accumulation of acidic ketones, and hyperglycemia leads to osmotic diuresis and electrolyte loss, precipitating the characteristic metabolic acidosis and severe dehydration.
Symptoms of DKA generally develop over a short period of time and include polyuria, polydipsia, and weight loss. Abdominal pain and vomiting are common with acidosis, and must be distinguished from an acute abdomen. Decreased mentation and deep labored Kussmaul respirations are advanced findings. Additional features of an intercurrent illness should be sought. Leukocytosis and hyperamylasemia are often detectable at presentation and normalize with treatment.
The diagnostic criteria for DKA include five laboratory conditions: plasma glucose greater than 250 mg/dL (13.9 mmol/L), anion gap of greater than 10 mEq/L, the presence of ketonuria or ketonemia, serum bicarbonate below 18 mEq/L, and arterial pH less than 7.30. Diabetic ketoacidosis is graded as mild, moderate, or severe, with increasing severity associated with lower pH and deterioration in mental status. Arterial blood gas measurement should be obtained at the outset; measurements of venous blood pH can be used to track the resolution of the acidosis thereafter. Typical laboratory findings at presentation of DKA are shown in Table 150-1.
TABLE 150-1Laboratory Values in Diabetic Ketoacidosis (DKA) and Hyperglycemic Hyperosmolar State (HHS) (Representative Ranges at Presentation) ||Download (.pdf) TABLE 150-1 Laboratory Values in Diabetic Ketoacidosis (DKA) and Hyperglycemic Hyperosmolar State (HHS) (Representative Ranges at Presentation)
| ||DKA ||HHS |
|Glucose,a mmol/L (mg/dL) ||13.9-33.3 (250-600) ||33.3-66.6 (600-1200) |
|Sodium, meq/L ||125-135 ||135-145 |
|Potassiuma,b ||Normal to ↑ ||Normal |
|Magnesiuma ||Normal ||Normal |
|Chloridea ||Normal ||Normal |
|Phosphatea,b ||Normal ||Normal |
|Creatinine ||Slightly ↑ ||Moderately ↑ |
|Osmolality (mOsm/mL) ||300-320 ||330-380 |
|Plasma ketonesa ||++++ ||+/− |
|Serum bicarbonate,a meq/L ||<15 ||Normal to slightly ↓ |
|Arterial pH ||6.8-7.3 ||>7.3 |
|Arterial Pco2'a mm Hg ||20-30 ||Normal |
|Anion gapa(Na – [Cl + HCO3]) ||↑ ||Normal to slightly ↑ |