A skin graft is a procedure where healthy skin is transplanted from one part of the body to cover an area of damaged or missing skin, such as from severe burns or trauma. For the graft to be successful, it must establish a new blood supply at the recipient site, a process called “graft take.” When transplanted tissue comes from a source other than the patient’s own body, the immune system recognizes it as foreign. This natural defense mechanism, intended to destroy invading pathogens, can turn against the new tissue, leading to skin graft rejection.
Understanding Different Graft Types
The source of the transplanted tissue determines the risk of rejection, classifying grafts into three main categories. The safest and most common type is the autograft, which uses skin taken from the patient’s own body. Since the tissue is genetically identical, the immune system fully accepts it, and the risk of rejection is essentially zero. Autografts are the preferred method due to their high success rate.
Allografts involve tissue transferred from one human donor to a genetically different recipient, typically sourced from cadavers or living donors. Because the tissue carries different genetic markers, the recipient’s immune system strongly recognizes it as foreign. Allografts are often used as a temporary biological dressing for large burn wounds until the patient’s own skin can be harvested. Rejection is expected within one to two weeks in an immunocompetent patient without intervention.
The third category is the xenograft, where tissue is transplanted from an animal species, often a pig, into a human. These grafts are the most immunogenic, meaning they elicit the strongest immune response. Xenografts are used only as temporary biological covers to prevent fluid loss and infection. Due to the extreme genetic disparity, the body will reject a xenograft within days to a few weeks, necessitating its eventual removal.
How the Immune System Attacks Foreign Tissue
The biological mechanism behind rejection centers on the body’s method for identifying “self” versus “non-self” using specific identification tags. These tags are proteins known as Major Histocompatibility Complex (MHC) molecules, or Human Leukocyte Antigens (HLA) in humans. Every person has a unique combination of these surface proteins on nearly all their cells, and the immune system is trained to recognize only its own set.
When an allograft or xenograft is placed, specialized immune cells called antigen-presenting cells (APCs) within the graft migrate to the recipient’s lymph nodes. These APCs display the foreign HLA tags to T-lymphocytes (T-cells), which are the primary drivers of rejection. The T-cells become activated and proliferate, differentiating into effector cells that travel back to the graft site. These activated T-cells then directly attack and destroy the donor tissue cells, leading to inflammation and graft destruction.
The timing of this immune attack varies, leading to different types of rejection. Hyperacute rejection happens within minutes to hours after transplantation, caused by pre-existing antibodies that immediately recognize donor antigens. Acute rejection is the most common form in skin grafts, occurring days to weeks after the procedure, driven primarily by T-cell activation. Chronic rejection is a slow, ongoing process that can take months or years, often involving repeated cycles of damage and repair that compromise the graft’s function.
Identifying the Signs of Rejection
Recognizing the signs of rejection early allows for clinical intervention to save the graft. One of the most telling visual signs is a change in the graft’s color. A healthy graft appears pink as blood flow is re-established, but a failing graft often darkens or becomes black, indicating tissue death. The grafted skin may also fail to blanch (whiten) when pressed gently, which signals poor blood circulation.
Physical symptoms at the graft site often include increasing redness and swelling around the edges of the transplanted tissue. Patients may report persistent pain and a feeling of warmth, indicating a strong inflammatory response. Fluid buildup underneath the graft (such as a hematoma or seroma) can physically lift the graft and prevent blood vessel ingrowth, leading to failure.
Systemic signs of a severe immune reaction or infection often accompany the local symptoms. A fever or chills may signal a body-wide response to the failing tissue. To definitively diagnose rejection and differentiate it from other causes of graft failure (such as infection or poor blood flow), a biopsy is performed. This allows clinicians to view the tissue under a microscope for signs of inflammation and immune cells attacking the donor tissue.
Preventing and Treating Rejection
Managing and preventing skin graft rejection, particularly for allografts, begins with pre-operative planning and tissue compatibility testing. Clinicians perform HLA matching and donor screening to ensure the closest possible compatibility. Better HLA compatibility significantly reduces the strength of the immune response, though a perfect match is rarely feasible outside of identical twins.
Post-operative care is equally important, focusing on meticulous wound management to ensure the graft adheres and establishes its blood supply. Avoiding excessive movement or pressure on the site is necessary, as mechanical stress can disrupt blood vessel ingrowth. Patient compliance with wound care protocols and prescribed medications is a significant factor in preventing complications like infection, which can lead to graft loss.
The primary medical treatment for existing or anticipated rejection is immunosuppressive therapy. These medications suppress the overactive immune system, making it more tolerant of the foreign tissue. Treatment must be carefully balanced because a suppressed immune system increases the patient’s susceptibility to infections. If rejection is severe and the graft is failing, the non-viable tissue must be surgically removed.