A 48-year-old male with a history of chronic corticosteroid use for COPD undergoes an open cholecystectomy. On postoperative day 5, the surgical wound shows delayed epithelialization and poor granulation tissue formation. Which of the following mechanisms best explains the impaired wound healing in this patient?

Explanation

## Corticosteroids and Wound Healing Impairment Chronic corticosteroid use significantly impairs wound healing through multiple mechanisms: ### Primary Mechanism (Correct Answer): **Decreased collagen synthesis and reduced angiogenesis** are the hallmark effects of corticosteroids on wound healing. - Corticosteroids inhibit **fibroblast proliferation and function**, reducing type I and III collagen deposition - They suppress **angiogenesis** by inhibiting endothelial cell proliferation and reducing vascular endothelial growth factor (VEGF) expression - This leads to weak granulation tissue, poor epithelialization, and delayed wound closure - The effect is particularly pronounced during the proliferative phase (days 3–21) ### Why This Matters Clinically: **High-Yield:** Corticosteroids affect the **proliferative phase** of wound healing most severely, not the inflammatory phase. ### Key Point: The impaired wound healing with corticosteroids is dose- and duration-dependent. Chronic use (as in this COPD patient) causes significant compromise. ## Comparison Table: | Phase | Effect of Corticosteroids | |-------|---------------------------| | Inflammatory (0–3 days) | Mildly reduced; some neutrophil inhibition | | Proliferative (3–21 days) | **Severely impaired** — ↓ fibroblasts, ↓ collagen, ↓ angiogenesis | | Remodeling (>21 days) | Prolonged; weak scar formation | **Mnemonic:** **CAST** = Corticosteroids impair: **C**ollagen synthesis, **A**ngiogenesis, **S**trength, **T**issue formation.