A 62-year-old woman with type 2 diabetes mellitus presents with a 5-day history of progressive confusion, weakness, and polyuria. She has been unwell with a respiratory tract infection for the past week but did not seek medical care. On examination, she is lethargic, respiratory rate 16/min (not laboured), blood pressure 95/60 mmHg, and skin turgor is poor. Blood glucose is 680 mg/dL, serum osmolality 335 mOsm/kg, arterial pH 7.32, HCO₃⁻ 18 mEq/L, serum Na⁺ 148 mEq/L, and serum K⁺ 5.2 mEq/L. Urine dipstick shows 1+ ketones and 3+ glucose. What is the most likely diagnosis, and which finding best differentiates it from DKA?

Explanation

## Diagnosis: Hyperosmolar Hyperglycaemic State (HHS) **Key Point:** This patient has HHS, not DKA. The cardinal differentiating features are: - Minimal ketonuria (1+, not 3+) - Relatively preserved pH (7.32, not <7.30) - Extreme hyperglycaemia (680 mg/dL) with extreme hyperosmolality (335 mOsm/kg) - Absence of Kussmaul respiration ## Comparison Table: DKA vs HHS | Feature | DKA | HHS | |---|---|---| | **Typical patient** | Type 1 (or T2 with stress) | Type 2, elderly, poor access to care | | **Onset** | Acute (hours) | Insidious (days to weeks) | | **Blood glucose** | 250–600 mg/dL | 600–1200 mg/dL | | **Serum osmolality** | <320 mOsm/kg | >320 mOsm/kg (often >330) | | **pH** | <7.30 (severe acidosis) | >7.30 (mild/no acidosis) | | **HCO₃⁻** | <15 mEq/L | >15 mEq/L | | **Ketonuria** | 3+ (large) | 0–1+ (trace/small) | | **Respiratory pattern** | Kussmaul (deep, laboured) | Normal or mild tachypnoea | | **Mortality** | 1–5% | 5–15% | | **Precipitants** | Infection, DKA, non-compliance | Infection, stroke, MI, dehydration | **High-Yield:** HHS is characterized by **relative insulin deficiency** (enough to suppress ketogenesis but not enough to control hyperglycaemia and osmolality). DKA is characterized by **absolute insulin deficiency** (ketogenesis proceeds unchecked). ## Why This Patient Has HHS 1. **Minimal ketonuria (1+):** In DKA, ketonuria is 3+ or 4+. Here, only trace ketones are present because residual insulin suppresses lipolysis. 2. **Preserved pH (7.32):** HCO₃⁻ is 18 (mild reduction). In DKA, pH would be <7.25 and HCO₃⁻ <12. 3. **Extreme hyperosmolality (335 mOsm/kg):** Calculated osmolality = `$2(Na^+) + \frac{glucose}{18} + \frac{BUN}{2.8} = 2(148) + \frac{680}{18} + \frac{BUN}{2.8} \approx 335$`. This extreme osmolality is the hallmark of HHS. 4. **Type 2 diabetes, elderly, insidious onset over 5 days:** Classic HHS presentation. DKA typically presents acutely over 12–24 hours. 5. **Respiratory rate 16/min (normal):** No Kussmaul respiration. In DKA with pH 7.18, RR would be 28–32. **Clinical Pearl:** The respiratory tract infection triggered HHS by increasing insulin resistance and causing dehydration. Unlike DKA, HHS does NOT cause metabolic acidosis severe enough to trigger compensatory hyperventilation. ## Management Implications ```mermaid flowchart TD A[HHS Diagnosis]:::outcome --> B[Fluid Resuscitation]:::action B --> C[0.9% NS: 1 L/hr × 2-4 hrs]:::action C --> D[Monitor osmolality q2-4h]:::action D --> E{Osmolality < 320?}:::decision E -->|No| F[Continue aggressive fluids]:::action E -->|Yes| G[Switch to 0.45% NS]:::action G --> H[Start insulin 0.05 U/kg/hr]:::action H --> I[Lower glucose more slowly than DKA]:::action I --> J[Target: 50-70 mg/dL/hr reduction]:::action ``` **Mnemonic: HHS = High Osmolality, Hyperglycaemia, Subtle acidosis** — Remember the "3 H's" to distinguish from DKA's "3 K's" (Kussmaul, Ketones, Ketoacidosis).