Skin graft take: thickness, phases and failure

Split versus full thickness

A skin graft has no blood supply of its own, so it lives or dies by the recipient bed — and how much dermis it carries decides almost everything else about its behaviour. A split-thickness graft (SSG) takes epidermis and part of the dermis; a full-thickness graft (FTSG) takes the whole dermis.

Thickness bands and donor sites

Split grafts are graded by dermatome setting, conventionally quoted in thousandths of an inch. The thinner the graft, the better it takes and the faster its donor heals — and the more it contracts and the worse it looks.

Thin (Thiersch–Ollier)

About 0.008–0.012 inch (0.2–0.3 mm).

Intermediate (Blair–Brown)

About 0.012–0.018 inch (0.3–0.45 mm).

Thick (Padgett)

About 0.018–0.030 inch (0.45–0.75 mm).

Full thickness

The entire dermis; real depth varies with site, age and sex.

Common SSG donor sites are the thigh, buttock, back and upper arm, and in children the scalp, which hides the scar and heals quickly. FTSG donors are chosen to match colour and texture: post-auricular, pre-auricular, supraclavicular and upper eyelid skin for the face, where skin from above the clavicles matches best; groin, inner arm or hypothenar skin for the hand. Dermis is thin in young children and the elderly, so the same dermatome setting takes a relatively deeper graft and risks a slow-healing donor site.

Primary and secondary contraction

Primary contraction is the immediate recoil of a graft after harvest, caused by elastin in the dermis, so it is greatest in full-thickness grafts. Secondary contraction is the later shrinkage of the healed graft and its bed, driven by myofibroblasts, and it is greatest in thin split grafts.

The rule that ties them together: the more dermis a graft carries, the more it recoils at harvest and the less it contracts afterwards, because dermis appears to curb myofibroblast activity in the bed. That is why an FTSG goes on a digit, an eyelid or a flexion crease, where late contraction would cause a contracture or ectropion, and why a dermal substitute under a thin SSG reduces contraction.

The three phases of take

Take proceeds through plasmatic imbibition, inosculation and revascularisation; a graft that is not adherent and revascularising by the end of the first week will not survive.

1. Plasmatic imbibition (first 24–48 h). A fibrin layer glues graft to bed and the graft absorbs nutrient-rich exudate by passive diffusion. It swells and survives on largely anaerobic metabolism — the phase most vulnerable to fluid and shear.
2. Inosculation (48–72 h). Capillary ends in the graft and bed align and connect, and flow begins through the graft's original vessels.
3. Revascularisation (about day 4–7). New vessels grow from the bed into the graft and fibroblasts replace the fibrin bond with collagen. Lymphatic drainage returns in parallel, so the oedema of imbibition settles.

Later events matter when counselling patients. Sensation returns from the bed and edges over months and recovers better in thicker grafts. Sweating follows sympathetic reinnervation, so thin grafts stay dry and need emollient. Grafts darken with sun exposure, so protection is advised while the graft matures.

The recipient bed

A graft needs a vascular bed: granulation tissue, muscle, fascia, periosteum, perichondrium and paratenon all accept a graft. Bare cortical bone, tendon stripped of paratenon, cartilage without perichondrium, exposed metalwork and heavily irradiated tissue do not.

• Bone: burr the outer cortex to bleeding bone, or wait for granulation to cover it.
• Tendon: preserve paratenon. Without it a flap is usually the better answer — a dermal regeneration template can bridge only small exposed areas, and a graft stuck to tendon tethers its glide.
• Uncertain bed: NPWT can build granulation, and a staged dermal template (such as Integra) creates a neodermis to graft later.
• Structures needing gliding, padding or bone cover: use a flap — see Flap classification.

Why grafts fail

Grafts fail because something lifts them off the bed, something moves them on it, bacteria dissolve the bond, or the bed cannot support them. Haematoma and seroma are classically cited as the leading cause, because even a thin layer of fluid blocks imbibition and inosculation.

Meshing, bolsters and NPWT

Meshing lets fluid escape, lets a graft drape over an irregular bed and expands its coverage; the price is a permanent mesh pattern and more secondary contraction. The interstices heal by epithelialisation from the graft strands, more slowly as the ratio widens, and the real expansion is less than the nominal ratio.

Fixation prevents shear. A tie-over bolster suits small grafts on contoured sites such as the face and scalp; NPWT holds larger or awkward grafts against the bed and removes exudate, which suits irregular or mobile areas. Splint across joints. First inspection is usually at around day 5, and sooner for pain, odour, fever or strike-through.