Hyperglycemic crises resident survival guide

For more information about DKA, click here.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Syed Hassan A. Kazmi BSc, MD [2], Husnain Shaukat, M.D [3]

Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) are life threatening complications of untreated or inadequately treated diabetes mellitus. HHS is characterized by hyperglycemia, hyperosmolarity and dehydration; whereas DKA is characterized by hyperglycemia, acidosis, and ketosis.^[1]

Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated. Hyperosmolar hyperglycemic state is a life-threatening condition and must be treated as such irrespective of the causes.

Common causes of hyperosmolar hyperglycemic state (HHS) include:

• Infections:
  • Pneumonia^[2]
  • Sepsis^[3][4][5]
  • Genitourinary tract infections^[6]
• Drugs:^[7][8]
  • Antipsychotic agents (clozapine, olanzapine, risperidone)
  • Illicit drugs (cocaine and alcohol)
  • Corticosteroids^[9]
  • Glucagon^[10]
  • Interferon^[11]
  • Pentamidine^[12][13]
  • Sympathomimetic agents (albuterol, dopamine, dobutamine, terbutaline, ritodrine, thiazide diuretics)^[14][15]
• Myocardial infarction^[16]
• Pancreatitis^[17]
• Shock/hypovolemia^[18]
• Trauma^[19]
• Undiagnosed diabetes mellitus^[20]
• Noncompliance to insulin treatment:^[21][22]
  • Body image issues
  • Financial problems
  • Lack of insulin^[5]
  • Psychological factors
  • Self-neglect
  • Accidental
  • Neglect by caregivers

The diagnostic approach and management management of HHS and DKA are based on the ADA guidelines published in 2009.^[1]

• The diagnosis of diabetic ketoacidosis is made in the presence of:
  • Hyperglycemia– Plasma glucose > 250 mg/dL
  • Anion gap metabolic acidosis– pH < 7.3; Serum bicarbonate < 15 mEq/L
  • Ketonemia/ Ketonuria
• Shown below is a table summarizing the diagnosis of Diabetic ketoacidosis according the the American Diabetes Association (ADA) guidelines. ^{[23] [24]}

• Check labs initially and every 2-4 hours.
• Immediately check urine for ketones with dipstick and send urine to the lab for analysis.
• Initiate IV insulin as soon as the patient arrives and satisfies the diagnostic criteria of DKA.
• Assess the trigger that precipitated DKA and treat the cause.
• In patients with potassium(K) < 3.3 mEq/L, fluids and potassium replacement must be done before initiating insulin therapy, to prevent further hypokalemia.
• Admit the patient to the floor; however, if the pH < 7.0 or the patient is unconscious then admit to ICU.
• Make sure to calculate the corrected sodium level when evaluating the sodium level. Sodium can be falsely low due to the elevated glucose level; in order to correct for this, add 1.6 mmol/L of Na+ for every 100 mg/dL of glucose > 100 mg/dL.
• Monitor for complications of DKA itself or of the therapy.
• In case the patient has cardiac or renal compromise, monitor serum osmolality and frequently assess the cardiac, renal and mental status.

• Do not stop IV insulin until DKA has resolved.
• Do not stop IV insulin, even if subcutaneous insulin is administered because it needs time to kick in.
• Do not give insulin if K+ levels are below 3.3 mEq/l because it may further exacerbate the hypokalemia.
• Do not use 0.9% NaCl if corrected Na+ levels > 145 mEq/l, use 0.45% instead.
• Avoid rapid correction of plasma osmolality and serum sodium, to prevent fatal cerebral edema.
• Maximum reduction in plasma osmolality should be 3 mOsmol/kg per hour.
• Do not supplement phosphate excessively, clinical trials have not shown any benefits. Supplement phosphate only if there is an actual deficit.
• DO not use subcutaneous sliding scale insulin in management of hyperglycemia due to diabetes type 1.^[25]

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