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.

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.

Critical management

Related posts:

Burns Chronic obstructive pulmonary disease Post–cardiac arrest care Monitoring Acute respiratory distress syndrome Severe pelvic trauma