Reference — Med-Surg
DKA vs HHS Quick Reference
Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) are the two major acute hyperglycemic emergencies in diabetes. While they share hyperglycemia as a common feature, their pathophysiology, severity, and management differ significantly. Early recognition and differentiation is essential.
Educational use only. Both DKA and HHS require immediate provider involvement, ICU-level monitoring, and institution-specific protocols. Treatment decisions and fluid/insulin infusion rates are provider-ordered. Never manage these independently. This material supports nursing education and exam review. It is not medical advice and is not a substitute for clinical judgment, institutional policy, or medical direction. Always follow facility protocols and current provider orders.
DKA vs HHS — Key Comparison
| Parameter | DKA | HHS |
|---|---|---|
| Typical diabetes type | Type 1 (primarily); also Type 2 | Type 2 (primarily; often older adults) |
| Plasma glucose | > 250 mg/dL (often 300–600) | > 600 mg/dL (often 800–1200+) |
| Ketones (serum/urine) | Significantly elevated — moderate to large | Absent or minimal (trace) |
| Arterial pH | < 7.30 (often 7.00–7.24) | > 7.30 (usually > 7.35) |
| Bicarbonate (HCO₃) | < 18 mEq/L (often < 10) | > 18 mEq/L (typically normal) |
| Anion gap | Elevated (> 12 mEq/L) — high anion gap metabolic acidosis | Normal or mildly elevated |
| Serum osmolality | Variable — may be normal or elevated | Markedly elevated (> 320 mOsm/kg) |
| Dehydration | Moderate — typically 3–6 L deficit | Profound — typically 8–12+ L deficit |
| Mental status | Alert to confused (varies with severity) | Severely altered — stupor to coma common |
| Onset | Hours to days (often rapid) | Days to weeks (gradual, insidious) |
| Mortality | < 1–5% with treatment | 10–20% (higher due to older age, comorbidities) |
DKA — Pathophysiology
DKA occurs in the setting of absolute or near-absolute insulin deficiency. Without insulin, cells cannot take up glucose. Glucagon secretion rises, stimulating hepatic gluconeogenesis and glycogenolysis (hyperglycemia). Simultaneously, unrestrained lipolysis releases free fatty acids, which the liver converts to ketone bodies (beta-hydroxybutyrate, acetoacetate) — producing an anion gap metabolic acidosis.
Classic clinical findings:
- Kussmaul respirations: Deep, rapid breathing — the lungs compensate for metabolic acidosis by exhaling CO₂ (respiratory compensation)
- Fruity/acetone breath: From exhaled acetone (a ketone)
- Nausea, vomiting, abdominal pain: Common in DKA (less in HHS)
- Polyuria, polydipsia, dehydration: Osmotic diuresis from hyperglycemia
- Electrolyte shifts: Potassium — serum K⁺ may be falsely elevated (acidosis shifts K⁺ out of cells) while total body K⁺ is severely depleted from urinary losses
Common triggers: missed insulin doses, infection (most common), myocardial infarction, trauma, surgery, or new diagnosis of Type 1 diabetes.
HHS — Pathophysiology
HHS occurs in Type 2 diabetics who retain enough residual insulin secretion to prevent lipolysis and ketogenesis, but not enough to prevent progressive hyperglycemia. The result is extreme hyperglycemia (often > 600–1000 mg/dL) without the ketoacidosis of DKA. The extreme hyperglycemia drives osmotic diuresis and profound fluid losses — often 8–12 liters or more — leading to hyperosmolarity and severe neurological impairment.
Classic clinical findings:
- Extreme hyperglycemia: Often > 600 mg/dL; may exceed 1000 mg/dL
- Profound dehydration: Signs include severe tachycardia, hypotension, dry mucous membranes, skin tenting
- Neurological changes: Confusion, lethargy, stupor, coma — correlate with osmolality
- No significant acidosis: pH and HCO₃ are near normal
- No Kussmaul respirations or fruity breath (no significant ketosis)
Common triggers: infection (most common), inadequate fluid intake, medications (diuretics, steroids, antipsychotics), undiagnosed diabetes.
Treatment Priorities
| Intervention | DKA | HHS |
|---|---|---|
| Fluid resuscitation | 0.9% NS 1 L/hour initially; switch to 0.45% NS after volume restored | 0.9% NS aggressive initial resuscitation; larger volumes (8–12+ L total over 24–48 hours) |
| Insulin | Regular insulin IV infusion (0.1 units/kg/hour) — hold until K⁺ ≥ 3.5 mEq/L | Lower dose insulin (fluid resuscitation is more important initially); insulin after fluid resuscitation begins |
| Potassium replacement | Critical — add KCl to fluids. Replace aggressively; hold insulin if K⁺ < 3.5 | Replace as needed; typically less severe K⁺ deficit than DKA |
| Dextrose addition | Add D5 to IV fluids when glucose reaches 200–250 mg/dL (to continue insulin safely) | Add D5 when glucose reaches 300 mg/dL (glucose lowering is more gradual) |
| Bicarbonate | Consider only if pH < 6.9 (controversy; generally not recommended above this threshold) | Not indicated (no acidosis) |
| Glucose lowering rate | 50–75 mg/dL/hour | 50–70 mg/dL/hour (gradual — rapid lowering risks cerebral edema) |
| Treat precipitant | Identify and treat trigger (infection, missed insulin, MI) | Identify and treat trigger (infection, dehydration, medication) |
Nursing Priorities (Both Conditions)
- Hourly glucose monitoring during insulin infusion; adjust per protocol
- Potassium monitoring every 1–2 hours — critical in DKA. Do not administer insulin if K⁺ < 3.5 mEq/L.
- Strict intake and output — insert urinary catheter for accurate UO measurement
- Neurological assessment — mental status, GCS in HHS; cerebral edema risk with rapid glucose correction
- Continuous cardiac monitoring — hypokalemia and hyperkalemia both cause dysrhythmias
- Assess for signs of infection (most common precipitant of both) — fever, WBC, wound, urine
- Monitor for resolution criteria: DKA resolved when glucose < 200, HCO₃ ≥ 15, pH > 7.3, anion gap normal
- Transition to subcutaneous insulin before discontinuing IV insulin (overlap by 1–2 hours)
Related Resources
Standards & sources
Fact-checked Jun 21, 2026This page is written to align with Academy of Medical-Surgical Nurses (AMSN) · Current medical-surgical nursing standards. It is an educational summary, not a citation of any single document — always verify specific doses, values, and protocols against current guidelines and your facility policy. How we source content →