Diabetic Ketoacidosis (DKA)
and
Hyperosmolar Hyperglycemic State in Adults (HHS)
· Definitions
HHS: extreme hyperglycemia w/o ketoacidosis, but with hyperosmolar state and altered mental status in type 2 diabetics. Usually hyperglycemia àosmotic diuresis àdehydration àmore hyperglycemia.
DKA: a triad of hyperglycemia, anion gap metabolic acidosis, and ketonemia. Occurs mostly in type 1 Diabetics. Hyperglycemia develops from decreased glucose uptake into the cells, increased gluconeogenesis. Ketosis develops because of inability to use glucose àmobilization and oxidation of fatty acids and increased ketogenic state of the liver with decreased ketone clearance.
· Precipitating events (VERY similar for both)
HHS: Inadequate insulin intake (under treated OR noncompliant), DEHYDRATION, infection (pneumonia, UTI, sepsis), acute illness (myocardial infarction, stroke, acute pancreatitis, acute renal failure, mesenteric ischemia, cholecystitis, etc), mediations (steroids)
DKA: Inadequate insulin intake (under treated OR noncompliant OR newly diagnosed diabetes [20-25%]), infection (pneumonia, UTI, sepsis), acute illness (myocardial infarction, stroke, acute pancreatitis, acute renal failure mesenteric ischemia, cholecystitis, etc), medications, steroids
· Clinical Presentation
HHS: Usually insidious (subacute) presentation of polyuria, polydipsia, and weight loss a few days before hospital admission. Present with dehydration and altered mental status. Usually sugar > 600 but even > 1000!
DKA: Usually acute presentation over 24 hours. Present with h/o polyuria, polydipsia, nausea, vomiting, abdominal pain, hyperventilation (2/2 metabolic acidosis) called Kussmaul’s respirations (with odor of acetone), eventually altered mental status, somnolence as academia progresses. Usually sugar >500 but < 800
· Physical Exam
HHS: Signs of volume depletion (low skin turgor, hypotensive, tachycardic, dry mucous membranes), altered mental status
DKA: Signs of volume depletion (low skin turgor, hypotensive, tachycardic, dry mucous membranes), +/- altered mental status, Kussmaul’s respirations (deep and fast) to compensate for metabolic acidosis, fruity odor of breat from acetone
· Laboratory investigations:
Hyperglycemia and hyperosmolality are the two primary laboratory findings in patients with DKA or HHS; patients with DKA also have a high anion gap metabolic acidosis (Na – [Cl +HCO3] )Most patients: acute increase BUN and creatinine ( reduction in glomerular filtration rate induced by hypovolemia).
All pts: Electrolytes (correct sodium for glucose = Measured sodium + 0.016 * (Serum glucose - 100), anion gap, urine ketones, serum ketones if urine ketones +, CBC, urinalysis, ABG (if available and anion gap elevated or ketones +)
· Treatment: FREQUENT REASSESSMENT (vitals, urine output ….place a foley, RBG, ph if available, FREQUENT electrolytes)
o DKA: rule out possible precipitants, AGGRESSIVE hydration (at least 10 cc/kg/hr of isontonic solution….for the first few hours until euvolemia reached), frequently requires 3-6 liters, insulin bolus of 10 units followed by 0.1 units/gk/hr until anion gap closes, RBG every hour, when glucose < 14…add dextrose to the IVF and continue insulin drip to metabolize ketones àSC insulin (then 2-3 h later turn off insulin drip), Add potassium (20 meq) to IVF if serum K < 4.5
o HHS:rule out possible precipitants, AGGRESSIVE hydration (at least 10-15 cc/gk/hr of isotonic fluid for the first few hours), frequently requires 8-10 liters, insulin bolus of 10 units followed by 0.1 units/gk/hr, RBG every hour, when glucose < 14…add dextrose to the IVF à until mentally alert and the plasma osmolality is below 315 mosmol/kg and pt can eat à SC insulin (then 2-3 h later turn off insulin drip), Add potassium (20 meq) to IVF if serum K < 4.5.
DKA CASE
A 23 yo F is brought to the hospital after being found unconscious by her family in the house. She is known to have insulin-dependent diabetes mellitus.
1. What are your immediate concerns about this patient?
2. What are possible mechanisms of coma in a diabetic patient?
3. What is at the top of your differential diagnosis?
You are concerned about DKA, hypoglycemia and hyperosmolar-hyperglycemic state. You first ensure that the patient’s vital signs are stable, that IV access is obtained, and that a RPG is obtained. Then you obtain additional history from the family. They state that the patient had been complaining of pain and burning with urination for the past several days. She had some nausea yesterday and did not take her evening or morning insulin as she did not eat dinner or breakfast. She seemed sleepy this morning and later this afternoon was found in bed, breathing deeply and unresponsive.
4. What risk factors does the patient have for developing DKA?
5. What physical findings are you looking for?
On exam the patient is unresponsive with dry skin and mucous membranes and rapid, deep respirations. BP is 100/60 supine, falling to 80/50 when head of bed is raised. HR is 110, RR 24, temperature is 37.5. Abd is soft but the patient groans when moderate pressure is applied. Blood glucose returns at 16.
6. What labs and studies do you want at this point?
7. What treatment do you want to begin?
You order a urine dipstick and culture, blood cultures, FBP with diff, creat, sodium and potassium, CXR. You start her on IVF at a rate of 1000ml/hr and give her 10U regular insulin followed by an insulin drip at .1U/kg/hr. Empiric antibiotics are also started for a presumptive UTI. A foley is placed to monitor UOP. After 12 hours of treatment the patient is awake, breathing comfortably at a rate of 18 and able to respond to questions. The RPG is now 12.
8. How long should you keep the patient on an insulin drip for? Do you want to change anything about the fluid management in the patient? If you decide to stop the insulin drip when would you give the patient the first dose of SC insulin?
- Immediate concerns: vital signs. Always check for evidence of hemodynamic or respiratory compromise.
2 & 3. Ddx for comatose patient is broad due to the limited information at this point. Diabetic ketoacidosis is #1 due to the patient’s known hx of IDDM. Other possibilities include: drug ingestion, hypoglycemia (or any other toxic-metabolic encephalopathy), infection (cerebral malaria, meningitis, etc), stroke (less likely due to pt’s age)
4. #1 risk factor is a hx of insulin-dependent DM. Missing several doses of insulin & recent infection are other risk factors.
5. On exam, look for evidence of metabolic acidosis (deep & fast respirations) and evidence of hypovolemia (hypotension, tachycardia, dry mucous membranes, poor skin turgor, poor capillary refill, low urine output). Also assess for altered mental status.
6. Check serum electrolytes, BUN & creatinine. Check a bicarbonate level & ABG if available. Check urine for ketones. Also due infection workup (FBP, urinanalysis, +/- CXR).
7. Treatment: FLUIDS, FLUIDS, FLUIDS! Start with several liters of normal saline (+ 20mEq KCL if serum K+ <4.5) + 10 units IV regular insulin bolus followed by 0.1 units/kg/hr until evidence that anion-gap acidosis has closed (improvement in respiratory status). Check glucose every hour & add 5% dextrose to IVF when glucose < 14. Be sure to give a dose of subcutaneous insulin 2-3 hours prior to stopping insulin drip to prevent rebound hyperglycemia.
