## Key Distinction Between DKA and HHS **Key Point:** HHS is characterized by residual insulin secretion (10–15% of normal), whereas DKA involves near-total insulin deficiency (<5%). ### Pathophysiology In HHS: - Small amounts of circulating insulin remain - This residual insulin is **sufficient to suppress lipolysis** and prevent ketone body formation - However, it is **insufficient to suppress hepatic glucose output** or enhance peripheral glucose uptake - Result: severe hyperglycemia (often >600 mg/dL) WITHOUT significant ketosis In DKA: - Absolute insulin deficiency leads to: - Unopposed lipolysis → free fatty acids → ketone bodies - Uncontrolled hepatic gluconeogenesis - Both hyperglycemia AND metabolic acidosis **High-Yield:** The presence or absence of significant ketosis is the biochemical hallmark distinguishing HHS from DKA. HHS = hyperglycemia without ketosis; DKA = hyperglycemia with ketosis. ### Comparison Table | Feature | DKA | HHS | | --- | --- | --- | | Insulin level | <5% of normal (absent) | 10–15% of normal (residual) | | Lipolysis | Unopposed → ketosis | Suppressed → no ketosis | | Glucose (mg/dL) | 250–600 | 600–1200 | | Arterial pH | <7.30 | >7.30 | | Osmolality | <320 mOsm/kg | >320 mOsm/kg | | Mortality | 1–5% | 5–15% | [cite:Harrison 21e Ch 397]
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