## Distinguishing DKA from HHS: Respiratory Pattern **Key Point:** Kussmaul respirations (deep, regular, labored breathing) are the hallmark respiratory sign of DKA and result from metabolic acidosis-driven respiratory compensation. They are **absent or minimal** in HHS because HHS lacks significant ketoacidosis. ### Pathophysiologic Basis DKA involves: - Lipolysis → free fatty acid mobilization → ketone body production (acetoacetate, β-hydroxybutyrate) - Metabolic acidosis (pH typically < 7.3, often < 7.1) - Respiratory compensation via medullary chemoreceptor stimulation → Kussmaul respirations HHS involves: - Severe hyperglycemia and hyperosmolality - **Minimal or absent ketosis** (insulin present in sufficient quantity to suppress lipolysis) - No significant metabolic acidosis → no respiratory drive - Mental status changes driven by hyperosmolality, not acidosis ### Comparison Table | Feature | DKA | HHS | | --- | --- | --- | | **Kussmaul respirations** | **Present (hallmark)** | Absent or minimal | | Serum pH | < 7.3 | > 7.30 | | Serum bicarbonate | < 18 mEq/L | > 18 mEq/L | | Serum ketones | Marked (> 3 mmol/L) | Absent or trace | | Osmolality | 300–320 mOsm/kg | > 320 mOsm/kg | | Blood glucose | 250–800 mg/dL | 600–1200 mg/dL | | Mortality | 1–5% | 5–15% (higher) | **Clinical Pearl:** Kussmaul respirations are so characteristic of DKA that their **presence strongly favors DKA over HHS**, even when hyperglycemia is severe in both conditions. **High-Yield:** The **absence of Kussmaul respirations in HHS** is a key discriminator — it reflects the lack of metabolic acidosis, which is the defining pathophysiologic difference between the two emergencies. [cite:Harrison 21e Ch 397]
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