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Diabetic Ketoacidosis (DKA)


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Author: Leigh Vaughn

 

DKA definition:

Elevated glucose, presence of ketones, metabolic acidosis (triad) + dehydration, with absolute or relative insulin deficiency à increase counter regulator hormones à breakdown of fat and muscle.  Not a hyperosmolar state like Hyperglycemic Hyperosmolar State (HHS).

Epidemiology:

  • Most common at onset Type 1 DM, recurrent episodes common
  • Can occur in Type 2 DM.  More often affects young
  • Death can be related to cerebral edema or the precipitating trigger/illness for the DKA.
  • Mortality < 1%, significantly lower than mortality of HHS

 Triggers (The “I’s”):

  • Initial (new onset) disease
  • Insulin omission (adherence, access, absorption)
  • Infection
  • Ischemia (ACS, stroke)
  • Intra-abdominal (pancreatitis, cholecystitis, ischemic bowel, pregnancy)
  • Ingestions (ETOH, substance abuse, meds-steroids, antipsychotics, thiazides, pentamidine)

 Pathophysiology:

  • 3 causes of increased glucose: Gluconeogenesis, Glycogenolysis, Impaired glucose utilization
  • Increase glucose + deficiency of insulin  + stress (trigger) à increases the secretion of glucagon, catecholamines, cortisol, and growth hormone (counter-regulatory hormones) à promotion of lipolysis à increases FFA delivery to the liver à FFA converted by free fatty acyl CoA into ketones

Clinical presentation:

  • Develops over hours to days; not days to weeks, like HHS.   
  • Polyuria, Polydipsia, Polyphagia, Fatigue, Muscle cramps (from Acidosis), Flushed facial appearance, Kussmaul’s respirations and dyspnea (from acidosis) à Nausea and vomiting à Abdominal pain, Dehydration à Hypotension, Shock, Altered consciousness/Coma

Workup:

  • Basic metabolic panel (Mg, phos, calcium), urinary glucose, serum & urine ketones, ABG. 
  • Consider: Infectious workup, CBC, cultures, CXR, urine culture, telemetry, UDS, amylase (can be increased even without pancreatitis), lipase, troponin, EKG, pregnancy test, CT head

Results:

  • Elevated anion gap > 12+ moderate, severe; pH< 7.3
  • Sodium can be low or high depending on degree of water loss
  • Correction of initial low à Sodium 1.6 increase in Na for every 100 increments of glucose over initial 200 mg/dL
  • Presence of urinary ketones (Beta-hydroxybutyrate may not be detected on urine dipsticks)
  • Glucose elevated but usually much lower than HHS
  • Potassium can be high or low. If presenting K is high, patients are usually still total body K depleted and K rapidly falls as acidosis is corrected.

Treatment:

  • Volume resuscitation: initially IV NS, rate depends on clinical scenario;  change fluids to D5 1/2 NS, when glucose less than 200mg/dL (Fluid deficits usually 5-7 L in DKA compared to HHS 8-10 L)
  • Monitor:  glucose hourly, basic chemistry profile (anion gap), plasma osmolality, and venous pH every two to four hours.  Monitor BP, urine output.
  • Replace electrolytes: Potassium replacement when Potassium < 5.3
    • No routine phosphate replace, unless Phos < 1.0
    • No clear role for HCO3 replace (unless pH<6.9, potassium life threateningly high)
    • Insulin
      • Insulin lowers blood glucose by decreasing hepatic gluconeogenesis and lowers ketones by reducing lipolysis and glucagon release.
      • IV regular insulin: 0.14 units/kg/hour without bolus after fluid resuscitation (or 0.1 units/kg/hour with bolus of 0.1 units/kg), only use SQ if mild DKA.
      • Do not start insulin unless K+ > 3.3- concerns for arrhythmia.  When glucose reaches 200 mg/dL, consider decreasing the insulin infusion rate to 0.02 to 0.05 U/kg per hour
      • When starting SQ insulin, make sure there is clinical improvement and the ability to tolerate oral intake. There should be a 2 hour overlap of IV drip and SQ insulin.

 End point of treatment:

  • Closed gap < 12, BS <200, and subcutaneous insulin already begun
  • Most patients will develop a non-gap acidosis (unless CKD V, ESRD) due to resolving ketoacidosis after gap is closed.
  • Ketonuria may persist for more than 36 hours due to the slower removal of acetone.

DKA in atypical patients (AKA: DM 1.5, atypical DM)

  • DKA presenting in patients who are not completely insulin deficient
  • Features similar to Type 2: more common in obese, Hispanic or African-American, Native-American, associated with + Fam Hx, low prevalence of auto-antibodies, possible to eventually be treated without insulin
  • Features similar to Type 1: often with short onset, ketosis formation,
  • Quick correction, initially insulin is required but may not be needed long-term.
  • May be helpful to obtain C-peptide

Clinical Pearls:

  • DKA and Hyperosmolar state (HHS) are disease on the same spectrum, but their clinical presentation and pathophysiology, and thus, their treatment differ. 
  • DKA is an acidosis from a deficiency or relative deficiency of insulin which leads to a metabolic acidosis. The fluid deficits are not as severe as those seen in hyperosmolar state and DKA can occur at much lower glucose levels than seen in HHS.
  • The initial evaluation of DKA must include a careful search for an underlying trigger (infection, cardiac disease) and timely replacement of intravascular volume, correction of electrolytes and administration insulin.

References:

Kitabchi AE, Umpierrez GE, et al. Hyperglycemic Crises in Adult Patients With Diabetes. A consensus statement from the American Diabetes Association,Diabetes Care July 2009 vol. 32 no. 7 1335-1343