## HHS vs DKA: Acid–Base Status as Discriminator **Key Point:** In HHS, **serum pH and bicarbonate remain relatively normal** (pH > 7.30, HCO~3~^−^ > 18 mEq/L) despite extreme hyperglycemia and hyperosmolality. This preserved acid–base status is the defining biochemical distinction between HHS and DKA. ### Pathophysiologic Explanation **Why HHS preserves acid–base balance:** - In HHS, **residual insulin secretion** (though insufficient to lower glucose) is **sufficient to suppress lipolysis** - Without lipolysis, ketone body production is minimal - Without ketones, no metabolic acidosis develops - The hyperosmolality and hyperglycemia cause neurologic dysfunction via osmotic stress, not acidosis **Why DKA develops acidosis:** - Severe insulin deficiency → unopposed lipolysis → massive ketone production - Ketones (β-hydroxybutyrate, acetoacetate) consume bicarbonate - Metabolic acidosis develops (pH < 7.3, HCO~3~^−^ < 18 mEq/L) ### Diagnostic Acid–Base Criteria | Parameter | DKA | HHS | | --- | --- | --- | | **pH** | < 7.30 | > 7.30 | | **HCO~3~^−^** | < 18 mEq/L | > 18 mEq/L | | **Anion gap** | Elevated (> 12) | Normal or slightly elevated | | **Serum ketones** | Marked (> 3 mmol/L) | Absent or trace | | **β-hydroxybutyrate** | High | Low | **Clinical Pearl:** A patient with severe hyperglycemia (> 600 mg/dL) and **normal pH + normal HCO~3~^−^** should immediately raise suspicion for HHS. The absence of acidosis despite extreme glucose elevation is the hallmark. **High-Yield:** The **preserved acid–base status in HHS** is so characteristic that it is used in diagnostic criteria. DKA is defined by the **presence of metabolic acidosis**; HHS is defined by its **absence**. **Mnemonic:** **"HHS = High glucose, High osmolality, Healthy pH"** — the pH is preserved because ketosis is absent. [cite:Harrison 21e Ch 397]
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