A skin graft is a surgical procedure that moves healthy skin to an area where skin is damaged or missing. This technique is used for extensive wounds, burns, or areas of tissue loss too large to close with stitches. A potential complication is graft rejection, where the recipient’s immune system identifies the new skin as foreign and attacks it, which can lead to graft failure.
The Immune System’s Role in Rejection
The human immune system distinguishes between the body’s own cells (“self”) and foreign cells (“non-self”). This identification is mediated by proteins on the cell surface called Human Leukocyte Antigens (HLAs), which function as unique markers for each individual. When a skin graft uses tissue from another person (an allograft), the recipient’s immune system inspects the donor tissue’s HLAs.
If the donor’s HLAs are not a close match to the recipient’s, the immune system perceives the graft as a threat. This mismatch triggers an immune response, where immune cells are mobilized to attack and destroy the foreign tissue. The degree of HLA mismatch can influence the speed and intensity of the rejection.
Conversely, rejection does not occur when a graft is taken from the patient’s own body (an autograft). Because the HLAs on the donated skin are identical to the patient’s own cells, the immune system recognizes the tissue as “self.” This allows the graft to integrate and heal without an immune attack.
Classifications of Rejection
Skin graft rejection is categorized into three types based on timing and the immune mechanisms involved. Hyperacute rejection is the most rapid, occurring within minutes to hours after surgery. This response is caused by pre-existing antibodies in the recipient’s blood that match the donor’s tissue antigens. These antibodies bind to the new tissue, leading to blood clot formation that cuts off blood supply and causes the graft to fail.
Acute rejection is more common, happening within the first few days to weeks, though it can occur up to a few months post-transplant. This rejection is driven by the recipient’s T-cells, a type of white blood cell, recognizing the donor’s HLAs as foreign. The T-cells then attack the graft tissue, leading to inflammation and damage. A biopsy during an acute rejection episode will show infiltration by immune cells.
Chronic rejection develops over several months to years after surgery. It is characterized by a slower, progressive loss of graft function and is often the result of repeated, low-grade acute rejection episodes. The process involves immune responses that cause gradual damage to the blood vessels supplying the graft, leading to tissue death. In these cases, removal of the graft is often the only solution.
Recognizing the Signs of Rejection
Early identification of graft rejection is important for successful intervention. Patients should monitor the graft site for specific changes, as one of the most common signs is a change in the color of the grafted skin. The tissue may turn dark red, purple, or black, indicating the blood supply is compromised and the tissue may be dying.
Another indicator is the condition of the area surrounding the graft. Increased redness and swelling around the graft site are common signs of an inflammatory immune response. The site may also become more painful or tender than expected after surgery. Fluid buildup under the graft, known as a seroma or hematoma, can also prevent it from properly adhering.
Any discharge or drainage from the wound is a warning sign. Pus or foul-smelling drainage often points to an infection, which can be both a cause of graft failure and a sign of rejection. Systemic symptoms, such as a fever or chills, can also accompany local signs, suggesting a widespread reaction that requires immediate medical attention.
Medical Interventions for Rejection
Preventing rejection begins before surgery with a process called tissue typing. This procedure analyzes and compares the HLAs of the potential donor and recipient to find the closest possible match, reducing the risk of a strong immune response. Patients are also started on immunosuppressive medications before the transplant and must continue them long-term. These drugs dampen the immune system to prevent it from attacking the new graft.
If signs of rejection appear after surgery, the first line of treatment is often to adjust the patient’s immunosuppressive regimen. This may involve increasing the dosage of current medications or introducing new, more potent drugs to control the immune attack. For localized inflammation, topical treatments such as steroid creams may be applied to the graft site to reduce the immune response in that area. These interventions are most effective when rejection is caught early.
If these treatments fail and the graft continues to deteriorate, more decisive action is required. The non-viable tissue may need to be surgically removed in a process called debridement to prevent infection and prepare the wound bed for a future graft. If rejection is severe or chronic, complete removal of the failed graft may be necessary. Following a failed graft, medical teams will reassess the patient’s case to determine the cause and plan for a subsequent graft if it is a viable option.