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DKA Vs HHS

Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) are two medical emergencies seen in diabetes that differ based on the presence of ketoacidosis and degree of hyperglycemia. DKA is more common in type 1 diabetes and involves ketonemia, acidosis, and glucose levels usually between 500-800. HHS is more common in type 2 diabetes and involves very high glucose over 1000 without ketones but with high osmolality and neurological abnormalities. Treatment involves monitoring glucose and electrolytes closely, aggressive fluid resuscitation, and intravenous insulin to restore glucose levels and mental status.

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367 views2 pages

DKA Vs HHS

Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) are two medical emergencies seen in diabetes that differ based on the presence of ketoacidosis and degree of hyperglycemia. DKA is more common in type 1 diabetes and involves ketonemia, acidosis, and glucose levels usually between 500-800. HHS is more common in type 2 diabetes and involves very high glucose over 1000 without ketones but with high osmolality and neurological abnormalities. Treatment involves monitoring glucose and electrolytes closely, aggressive fluid resuscitation, and intravenous insulin to restore glucose levels and mental status.

Uploaded by

deckerjake
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© Attribution Non-Commercial (BY-NC)
We take content rights seriously. If you suspect this is your content, claim it here.
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Diabetic ketoacidosis (DKA) vs Hyperosmolar hyperglycemic state (HHS) Differ clinically according to the presence of ketoacidosis and the

degree of hyperglycemia. - DKA (more common in type 1 DM, mortality 5-10%) o Hyperglycemia (usually 500-800) o Ketonemia o Anion gap metabolic acidosis (usually >20)  Bicab is mildly to severely reduced. - HHS (more common in type 2 DM, mortality 10-20%) o Very high serum glucose (frequently >1000) o No ketones in serum or urine (can have mild ketonemia)  Small amount of insulin prevents ketogenesis. o pH usually >7.30  Bicarb usually >20 o High plasma osmolality (may reach 380 mosmol/kg) o Neurological abnormalities often present **Significant overlap occurs, perhaps in as many as 1/3 of patients** DKA usually develops rapidly, over a 24 hour period HHS is more insidious, developing over several days with polydipsia, polyuria, and weight loss. Neurologic deterioration occurs with effective plasma osmolarity above 320 to 330 mosmol/kg. (Normal = 285-295) o Effective Posm = (2xNa) + (Glucose/18) Signs of volume depletion are common in both DKA and HHS: o Decreased skin turgor o Dry axilla and oral mucosa o Low JVP o Hypotension Neurological impairment is common in HHS. Fruity flavored breath (acetone) and deep respirations (Kussmaul) in DKA. Three ketone bodies are produced in DKA: o Two ketoacids  beta-hydroxybutyric acid  acetoacetic acid o One neutral ketone  acetone At presentation, Patients with DKA and HHS have a potassium deficit that averages 3 to 5 mg/kg. o Measured concentration is usually normal (or even elevated) however, probably due to insulin deficiency. -

o Insulin therapy can cause hypokalemia, and thus careful monitoring and administration of K is essential. Treatment Monitor glucose levels every 1 hour until stable. Monitor BMP, osmolality, and venous pH every 2-4 hours. o ABGs are not necessary as pH can be accurately estimated from VBG for this purpose. o Serum bicarb is usually sufficient for monitoring degree of acidosis. Average fluid loss is 3-6 liters in DKA and 8-10 liters in HHS. o Initiate fluid replacement with normal saline.  10-15mL/kg infusion rate. o Give regular insulin IV, continuous, at least 0.14U/kg/hr.  *Do not give if K is <3.3 o When serum glucose falls to 200 (for DKA) or 250-300 (for HHS), switch fluid to D5/NS or D10/NS. Goals: o Close anion gap o Restore mental status o Restore patient ability/desire to eat

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