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Diabetic Ketoacidosis

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Diabetic Ketoacidosis, DKA

  • Epidemiology
  1. Age distribution of DKA Cases
    1. Age over 70 years: 14%
    2. Age 51 to 70 years: 23%
    3. Age 30-50 years: 27%
    4. Age under 30 years: 36%
    5. Henricksen (2007) Diabetes Res Clin Pract 76(1): 51-6 [PubMed]
  2. Prevalence of DKA
    1. Age under 20 years: 6% will have at least one case of DKA
    2. Fritsch (2011) Pediatr Diabetes 12(4 pt 1): 307-12 [PubMed]
  • Pathophysiology
  1. Insulin deficiency
    1. Diabetes Mellitus
      1. Type I Diabetes Mellitus
      2. Type II Diabetes Mellitus with Ketosis-prone diabetes (accounts for 20-50% of DKA cases)
        1. Black or latino
        2. Male
        3. Overweight
        4. Middle-aged
        5. Diabetes MellitusFamily History
    2. Uncontrolled Blood Sugars (see precipitating factors below)
      1. See Medication Causes of Hyperglycemia
      2. New onset Diabetes Mellitus
      3. Insulin non-compliance
      4. Acute Infection (e.g. Pneumonia, Urinary Tract Infection)
      5. Insulin Pump failure
      6. Diabulimia (Eating Disorder variant of skipping Insulin to lose weight)
      7. Physiologic stressors (Myocardial Infarction, Cerebrovascular Accident)
  2. Compensatory response to lack of usable fuel sources (in the absence of Insulin)
    1. Paradoxical exacerbation of Hyperglycemia
      1. Release of Glucagon, Catecholamines, cortisol, and Growth Hormone
      2. Catabolism to Glucose of proteins and glycogen
      3. Results in osmotic diuresis, dehydration and hyperosmolar state
    2. Lipase secretion
      1. Free Fatty Acid metabolism
      2. Results in increased Ketone production (acetone, acetoacetone, Beta hydroxybutyrate)
      3. Results in acidosis
  • Precipitating Factors
  • Symptoms
  1. Timing
    1. Rapid onset of symptoms
    2. Follows febrile illness (40%)
  2. Hyperglycemia symptoms
    1. Polyuria and polydipsia (98%)
    2. Polyphagia (23%)
  3. Gastrointestinal symptoms
    1. Nausea and Vomiting (50-80% of cases)
    2. Abdominal Pain (30% of patients)
      1. May present as a vague Abdominal Pain with minimal tenderness on exam
      2. Consider Pancreatitis or Pyelonephritis (both are common in DKA)
  4. Miscellaneous symptoms
    1. Weight loss (81%)
    2. Fatigue (62%)
    3. Dyspnea (57%)
    4. Weakness
    5. Lethargy
  • Signs
  1. Mental clouding (lethargy to coma)
  2. Metabolic Acidosis findings
    1. Kussmaul Breathing
    2. Acetone on breath
  3. Dehydration (often >10% dehydrated)
    1. Dry Skin with loss of Skin Turgor
    2. Eyes sunken
    3. Tachycardia and possibly Hypotension
    4. Temperature below normal
  • Labs
  1. Bedside Glucose
    1. Glucose >250 mg/dl
  2. Urinalysis
    1. Glucosuria
    2. Urinary Tract Infection
    3. Ketonuria
      1. See Urine Ketones
      2. Highly sensitive for Diabetic Ketoacidosis
        1. High Negative Predictive Value
        2. Negative Urine Ketone excludes DKA diagnosis
        3. Schwab (1999) Ann Emerg Med 34:342-6 [PubMed]
      3. Poor Specificity
        1. Confirm with Serum Beta Hydroxybutyrate
          1. Beta hydroxybutyrate is converted to Acetoacetate which is then detected on the Urine Dipstick as Ketones
        2. Normal serum bicarbonate and Anion Gap suggests resolving DKA or false positive ketonuria
  3. Chemistry Panel (Chem8)
    1. Serum Glucose increased (Hyperglycemia)
    2. Serum Sodium decreased (Hyponatremia)
      1. Requires correction for Glucose (Pseudohyponatremia secondary to Hyperglycemia)
      2. Serum Sodium correction calculation: sNa + 0.016 * (Glu - 100)
    3. Serum Potassium
      1. Metabolic Acidosis results in initial underestimation of Serum Potassium
      2. As acidosis corrects, Potassium enters cells in exchange for Hydrogen Ion and Serum Potassium falls
      3. Low Serum Potassium on presentation suggests severe Hypokalemia
    4. Serum Chloride depressed (Hypochloremia)
    5. Serum Bicarbonate depressed (<18 mEq/L)
    6. Anion Gap elevated
      1. Typically >10-12 and often >16 in DKA
      2. Anion Gap calculation: Na - (Cl + HCO3)
    7. Serum Osmolality (calculate and measure if available)
      1. Should be >320 mOsm/kg if DKA present
      2. Serum Osmolality calculation: 2*(Na + K) + (glu/18) + (BUN/2.8)
  4. Other electrolytes (Phosphorus and Magnesium)
    1. Serum Phosphorus decreased (Hypophosphatemia)
    2. Serum Magnesium decreased (Hypomagnesemia)
  5. Arterial Blood Gas (ABG) or Venous Blood Gas (VBG)
    1. Metabolic Acidosis (serum pH <7.30)
    2. Venous Blood Gas is equivalent to monitoring Arterial Blood Gas for pH and bicarbonate
  6. Beta hydroxybutyrate (or Serum Ketones if not available)
    1. Beta hydroxybutyrate is the most important Ketone in Diabetic Ketoacidosis
  7. Precipitating factor evaluation
    1. Complete Blood Count with differential
      1. Leukocytosis is often present regardless of underling infection
      2. Bandemia (Neutrophil band forms or Left Shifts) is highly predictive of infection
    2. Blood Culture
    3. Urine Culture
    4. Chest XRay
    5. Electrocardiogram (EKG)
      1. Detects Hypokalemia related changes
      2. Also indicated for ischemia evaluation over age 40 or over 10 years of Diabetes Mellitus
  8. Evaluation of Diabetes and Endocrine Status
    1. Hemoglobin A1C
    2. Anti-GAD65 Antibody (identifies Type I diabetics)
    3. Thyroid Stimulating Hormone (TSH)
  9. Complications (obtain as needed)
    1. Serum Lipase
      1. Frequently increased regardless of Pancreatitis
      2. Pancreatitis is present in 10-15% of DKA patients
    2. Hepatic Transaminases (AST and ALT)
      1. Typically increased in non-Alcoholic Fatty Liver disease (NASH)
    3. Troponin I
      1. Troponin I is increased in absence of myocardial injury in more than 25% of DKA patients
  1. Blood Glucose exceeds 250 mg/dl
  2. Metabolic Acidosis
    1. Serum pH < 7.30
    2. Serum Bicarbonate < 18 meq/L
  3. Serum Ketones or Beta hydroxybutyrate
    1. Increased Serum Ketones (>7-10 mmol/L or >1:2 dilution)
  4. Anion Gap (using uncorrected Serum Sodium)
    1. Anion Gap without Potassium in calculation: >12 mEq/L
    2. Anion Gap with Potassium in calculation (or lab calculated): >17 mEq/L
  • Evaluation
  • Severity
  1. Arterial pH
    1. Mild: 7.25 to 7.30
    2. Moderate: 7.00 to 7.24
    3. Severe: < 7.00
  2. Serum bicarbonate
    1. Mild: 15-18
    2. Moderate: 10 to 14
    3. Severe: < 10
  3. Mental status
    1. Mild: Alert
    2. Moderate: Drowsy
    3. Severe: Stupor
  • Management
  1. See Diabetic Ketoacidosis Management in Adults
  2. See Diabetic Ketoacidosis Management in Children
  3. Evaluate and manage underlying causes
    1. Underlying infection (e.g. urosepsis, Pneumonia, Cellulitis)
  4. Consider noncompliance due to financial concerns
    1. Facilitate lower cost options for medications
    2. See Diabetes Cost Reduction
  • Complications
  1. See Diabetic Ketoacidosis Related Cerebral Edema
  2. Metabolic Complications
    1. Severe Metabolic Acidosis
    2. Hypokalemia
    3. Hypoglycemia
    4. Hypocalcemia
  3. Non-metabolic Complications
    1. Septic Shock
    2. Hypovolemic Shock
    3. Vascular Thrombosis
    4. Pulmonary edema (aggressive rehydration)
    5. Acute Renal Failure
    6. Rhabdomyolysis
    7. Prolonged QT Interval
    8. Cerebral Edema (See Diabetic Ketoacidosis Related Cerebral Edema)
  • Prevention
  1. See Diabetes Sick Day Management
  2. Diabetic action plan based on Blood Glucose Monitoring
    1. Home monitoring of beta hydroxybutyrate or Ketones when Serum Glucose >240 mg/dl
    2. Plan for adjusting short acting Insulin
      1. Sick day Insulin coverage (reduced dose but not eliminated)
      2. Liquid diets when sick
    3. Back-up plan for Insulin Pump failure
    4. Early contact with medical provider when Glucose control acutely changes
  3. Case management
    1. Diabetic educator
    2. Frequent phone contact
  4. Consider Insulin Pump
  • Prognosis
  1. Case fatality rate: 1-5%
    1. Mortality typically due to cerebral edema
    2. Leading cause of death in diabetes under age 24 years
    3. Wang (2006) Diabetes Care 29(9): 2018-22 [PubMed]