A patient undergoes a split-thickness skin graft (STSG) for a large leg defect. At 5 days post-graft, the graft appears white and non-adherent with a seroma beneath. Which mechanism best explains early graft failure in this specific scenario?

• A Failure of plasmatic imbibition due to seroma separating the graft from the bed, preventing neovascularisation ✓
• B Immunological rejection of allograft tissue
• C Absence of dermal papillae in STSG preventing revascularisation
• D Lack of fibrin 'glue' because the graft was fixed with staples rather than sutures

Explanation

Skin graft survival proceeds in three phases: plasmatic imbibition (first 24-48 hours, graft absorbs plasma from wound bed nutrients), inosculation (vascular connections form between graft and bed vessels, day 2-5), and neovascularisation (new vessels grow into graft, day 4-7). Any fluid accumulation (seroma or haematoma) between the graft and the bed physically separates them, preventing plasmatic imbibition and subsequent vascular ingrowth, leading to graft failure. Infection (particularly beta-haemolytic Streptococcus group A) is another major cause. This is an autograft (not allograft), so immunological rejection does not apply. STSG does not include dermal papillae but this is not the mechanism of seroma-related failure.

Reference: Bailey & Love's Short Practice of Surgery, 27th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.