DKA and HHS
Define and recognize DKA and HHS
Diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar syndrome (HHS) - insulin deficiency causing less glucose uptake and more counterregulatory hormones resulting in the release of fatty acids and oxidation leading to ketonemia and metabolic acidosis.
DKA Diagnosis - absolute or relative insulin deficiency, hyperglycemia, positive for ketones, metabolic acidosis
increases gluconeogenesis, glycogenolysis, less glucose used
develops over a hours to days driven by acidosis, thus more common in young people with T1DM, usually alert, N/V and abdominal pain, Kussmaul breathing (deep/labored), low blood gas
HHS Diagnosis - enough insulin to avoid ketosis, severe hyperglycemia 600+ mg/dL, hyperosmolality 320+ mOsm/kg, severe dehydration
develops over days to weeks, thus more common in old people with T2DM, change in cognitive state, co-presenting with other acute illness
Complications - hypoglycemia, hypokalemia, thrombosis, kidney injury, osmotion. Osmotic demyelination syndrome and cerebral edema more common in children potentially fatal.
Monitoring - labs and clinical endpoints differs slightly with a focus on correcting acidosis in DKA and dehydration/volume status in HHS.
Feature | DKA (Diabetic Ketoacidosis) | Same | HHS (Hyperosmolar Hyperglycemic Syndrome) |
|---|---|---|---|
Population | Younger, mostly T1DM | Older, mostly T2DM | |
Risk Factors | New onset DM, missed insulin, SGLT2 inhibitors, pancreatitis, trauma, | infection, MI, stroke,stress, social determinants, meds: antipsychotics, steroids | Older age, T2DM, |
Onset | Rapid (hours to days) | Gradual (days to weeks) | |
Signs/Symptoms | weight loss, vomiting, dehydration, weakness, mental status change (normal → coma), | Polyuria, polydipsia, polyphagia, dehydration, weakness, dyspnea, poor skin turgor, hypotension, tachycardia, abdominal pain, Kussmaul breathing (deep/labored), fruity breath odor, increased WBC | mental status change, severe confusion, coma, dyspnea, poor skin turgor, hypotension, tachycardia, |
Diagnosis | Absolute or relative insulin deficiency; high glucose; positive ketones; acidosis (low HCO₃, low pH <7.4, high anion gap) | Enough insulin to limit ketosis; very high glucose (>600 mg/dL); severe hyperosmolality (>320 mOsm/kg); dehydration; | |
Fluid Replacement | Initial: 15-20 mL/kg or 1-3L LR bolus; then LR/0.45% NS at 250-500 mL/hr; potassium supplemented as needed; Bag 1 (no dextrose) and Bag 2 (dextrose); titrate to BG | ||
Insulin Therapy | reduce rate as BG falls <250,<150,<100. lower 50-100 mg/dL over 4-8H | Regular insulin IV infusion: 0.1 units/kg/hr +/- bolus | reduce rate as BG falls <300,<150,<100. lower 50-100 mg/dL over 8-10H |
Potassium Therapy | Hold insulin if K<3.5; supplement potassium before insulin with bolus if low (e.g. 40 mEq), maintain K 4–5 mEq/L; monitor and adjust based on labs | ||
Resolution Steps | Acidosis resolves first (normalize anion gap + HCO₃), glucose <200 mg/dL, dehydration improved, may need to add more insulin and dextrose if acidosis worsens | Hyperglycemia resolves first (BG <200) followed by improved osmolality and dehydration acidosis minor or absent | |
Transition to SQ Insulin | After acidosis resolves, | overlap IV with SQ 1–2 hr, transition to home regimen or initiate SQ 0.5–0.8 unit/kg/day | After volume and glucose improvement |
Lab Values
Lab Test | Normal Range | DKA Criteria | HHS Criteria |
|---|---|---|---|
Glucose | 80–180 mg/dL | >250 mg/dL | >600 mg/dL |
Serum Osmolality | 277–297 mOsm/kg | Mild elevation | >320 mOsm/kg |
Anion Gap | 7–16 | High (>16) | Typically normal/mildly high |
Serum Bicarb (CO₂) | 23–33 mmol/L | Low (<15–18) | Normal (>18) |
Beta-Hydroxybutyrate | 0–0.4 mM/L | >3.0 mM/L | Negative/trace |
Urine/Blood Ketones | Negative | Positive | Negative/trace |
pH | 7.32–7.43 | <7.3 | >7.3 |
Potassium (K) | 3.5–5 mEq/L | Variable | Variable |
Sodium correction | 134–147 mEq/L | Calculate if high glucose Na + 0.016(glucose – 100) | Calculate if high glucose |
Mg | 0.8-1.5 mmol/L | <0.07 mmol/L | <0.07 mmol/L |
Phos | 0.7-1.1 mmol/L | <0.08 mmol/L | <0.08 mmol/ |
Summarize the PKPD, dosing, mechanism of action, side effects, and administration of each medication discussed
Insulin: Acts by facilitating glucose uptake and utilization, inhibiting gluconeogenesis, glycogenolysis, and lipolysis. Regular insulin is used IV in DKA/HHS for rapid action. Side effects include hypoglycemia, hypokalemia, and allergic reactions rarely. Administered as continuous IV infusion with monitoring.
Potassium: Replaced based on serum levels, usually as potassium chloride in IV fluids or orally. Hypokalemia is a major risk during insulin therapy as insulin drives potassium into cells.
Fluids: Lactated Ringer’s preferred due to physiologic buffering and reduced chloride load compared to normal saline.
Other adjunctive treatments in comorbid conditions, infections, or precipitating factors.
Develop a treatment plan for a given patient integrating clinical pearls, guidelines, labs, and literature presented
Initial assessment includes identifying DKA vs HHS by clinical and lab criteria like serum glucose, ketones, pH, bicarbonate, and osmolality.
Start fluid resuscitation promptly with lactated Ringer's or balanced crystalloids, bolus 15-20 mL/kg initially.
Initiate insulin infusion at 0.1 units/kg/hr after initial fluid bolus and once potassium is >3.5 mEq/L.
Monitor electrolytes, glucose, ketones, fluid status hourly or as needed.
Adjust insulin and fluids as glucose levels decline aiming for gradual normalization while preventing hypoglycemia or hypokalemia.
Supplement potassium as needed to maintain levels at 4-5 mEq/L.
Transition to subcutaneous insulin only after resolution of acidosis (DKA) or improvement in clinical status (HHS).
Anticipate complications including hypoglycemia, hypokalemia, thrombosis, and cerebral edema especially in children.
Use clinical cases from the lecture to highlight key points, e.g., emphasizing not to transition insulin too early if acidosis persists.