Hyperglycemic crises resident survival guide

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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