Diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar state (HHS) are acute complications of diabetes mellitus (DM). DKA is seen primarily in individuals with type 1 DM and HHS in individuals with type 2 DM. Both disorders are associated with absolute or relative insulin deficiency, volume depletion, and altered mental status. The metabolic similarities and differences in DKA and HHS are summarized in Table 23-1.
TABLE 23-1LABORATORY VALUES IN DKA AND HHS (REPRESENTATIVE RANGES AT PRESENTATION) ||Download (.pdf) TABLE 23-1LABORATORY VALUES IN DKA AND 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)c |
|Sodium, meq/L ||125–135 ||135–145 |
|Potassium,a meq/L ||Normal to ↑b ||Normal |
|Magnesiuma ||Normalb ||Normal |
|Chloridea ||Normal ||Normal |
|Phosphatea ||Normal to ↓b ||Normal |
|Creatinine, μmol/L (mg/dL) ||Slightly ↑ ||Moderately ↑ |
|Osmolality (mosmol/mL) ||300–320 ||330–380 |
|Plasma ketonesa ||++++ ||± |
|Serum bicarbonate,a meq/L ||<15 meq/L ||Normal to slightly ↓ |
|Arterial pH ||6.8–7.3 ||>7.3 |
|Arterial PCO2,a mmHg ||20–30 ||Normal |
|Anion gapa [Na – (Cl + HCO3)], meq/L ||↑ ||Normal to slightly ↑ |
DKA results from insulin deficiency with a relative or absolute increase in glucagon and may be caused by inadequate insulin administration, infection (pneumonia, urinary tract infection, gastroenteritis, sepsis), infarction (cerebral, coronary, mesenteric, peripheral), surgery, trauma, drugs (cocaine), or pregnancy. A common precipitating scenario is the pt with type 1 DM who erroneously stops administering insulin because of anorexia/lack of food intake caused by a minor illness, followed by lipolysis and progressive ketosis leading to DKA.
The initial symptoms of DKA include anorexia, nausea, vomiting, polyuria, and thirst. Abdominal pain, altered mental function, or frank coma may ensue. Classic signs of DKA include Kussmaul respirations and an acetone odor on the pt’s breath. Volume depletion can lead to dry mucous membranes, tachycardia, and hypotension. Fever and abdominal tenderness may also be present. Laboratory evaluation reveals hyperglycemia, ketosis (β-hydroxybutyrate > acetoacetate), and metabolic acidosis (arterial pH 6.8–7.3) with an increased anion gap (Table 23-1). The fluid deficit is often 3–5 L and can be greater. Despite a total-body potassium deficit, the serum potassium at presentation may be normal or mildly high as a result of acidosis. Similarly, phosphate may be normal at presentation despite total-body phosphate depletion. Leukocytosis, hypertriglyceridemia, and hyperlipoproteinemia are common. Hyperamylasemia is usually of salivary origin but may suggest a diagnosis of pancreatitis. The measured serum sodium is reduced as a consequence of osmotic fluid shifts due to hyperglycemia (1.6-meq reduction ...