Diabetic ketoacidosis and hyperglycemic hyperosmolar state

Sepsis

Urinary tract infection

Pneumonia

Myocardial infarction

Stroke

Gastrointestinal bleeding

Medication noncompliance

Newly diagnosed diabetes

Presentation

Classic presentation

Classic symptoms of hyperglycemia including polyuria, polydipsia, polyphagia, dizziness, and weakness.
Abdominal pain, nausea, and vomiting.
Altered mental status.
Deep breathing (Kussmaul respiration) with fruity odor.
Table 59.2 lists the differential diagnoses of patients in DKA.

Table 59.2. Differential diagnosis of DKA

Ketoacidosis
• Alcoholic ketoacidosis

Anion-gap acidosis
• Salicylate toxicity
• Toxic alcohols (methanol, ethylene glycol, propylene glycol)
• Uremia
• Lactic acidosis (sepsis, shock)

Hypoglycemia

Trauma

Critical presentation

Profound hypotension due to severe dehydration.
Coma, requiring airway protection.

Diagnosis and evaluation

Signs of dehydration
- Dry mucous membranes
- Altered mental status
- Orthostatic hypotension
- Tachycardia.
Signs of hyperglycemia
- Kussmaul respirations
- Fruity odor of ketones (some people cannot smell this).
Diagnostic tests
- Glucometry – point of care glucose level is typically greater than 250mg/dL (13.89 mmol/L) (may read “high”).
- Treatment of presumed DKA should begin with rehydration and evaluation for precipitating cause in the setting of a “high” glucometer reading. Further treatment often awaits laboratory results.
- Chemistry is critical for obtaining glucose and electrolyte levels and calculating anion gap (anion gap = sodium – [chloride + bicarbonate]).
  - Serum potassium is often elevated and will correct with insulin therapy, fluid replacement, and correction of acidosis. Remember: DKA patients are often depleted in total body potassium.
  - Other electrolytes such as magnesium, phosphate, and calcium may also be depleted during DKA and monitoring them is important.
  - Consider checking serum lipase to exclude pancreatitis as a precipitating factor for the hyperglycemia. But keep in mind that hyperglycemia can cause pancreatitis as well.
  - Serial chemistry monitoring every 1–2 hours is recommended during treatment because of rapid fluid and electrolyte shifting.
  - Sodium should be adjusted for elevated glucose. Na⁺ artificially decreases approximately 1.6 mEq/L for every 5.55 mmol/L (100 mg/dL) the glucose is above normal. For example, if the sodium is measured at 120 mEq/L, blood glucose is 400 mg/dL, the glucose is 300 units above normal (3 × 1.6 = 4.8). Therefore the corrected sodium is 120 + 4.8 >124.8 mEq/L. Above glucose levels of 400 mg/dL, the correction is less reliable and a correction factor of 2.4 mEq/L appears to be more accurate.
- Serum acetone measurement indicates presence of ketonemia and may correlate with the degree of dehydration and breakdown of fatty acids that occur in DKA.
- Blood gas measurement is important for determining the degree of acidosis. Venous blood gas has been demonstrated to be as reliable as arterial blood gas for pH monitoring.
- Chest radiography to exclude pneumonia as a precipitating cause of DKA.
- Urinalysis evaluates the presence of ketonuria (commonly acetoacetate) and/or presence of urinary tract infection.
- Critical pitfall: Negative urine ketone testing does not exclude the presence of DKA.
- ECG evaluates the presence of ischemia or STEMI (ST-segment elevation myocardial infarction) and provides important morphological features of electrolyte abnormalities before starting insulin and potassium therapy.