Chapter 71 Allograft Complications and Risk Factors
Introduction
Allograft use has been increasing because donor site morbidity is avoided. Although this benefit is well understood, the drawbacks are more complicated and less well understood. The purpose of this chapter is to collect information on potential allograft risk and allograft complications to help surgeons in their risk-benefit analyses. Some of the information contained in this chapter can be found elsewhere in the chapters on stability results (see Chapter 69) and infections (see Chapter 70). Potential allograft complications/risks can be divided into three categories: (1) graft failure or increased laxity and late graft laxity; (2) infection; and (3) disease transmission. The first two also occur with autografts; the third is allograft specific. Potential causes for increased allograft laxity are: (1) radiation sterilization; (2) nonradiation sterilization; (3) freezing; (4) increased donor age; and (5) increased allograft shelf life. Potential causes for increased allograft infection and disease transmission risk are: (1) failure to follow tissue-handling guidelines; (2) fraudulent procurement practices; (3) lack of sterilization; (4) foreign body effects; and (5) harvest/preparation contamination.These are summarized in Box 71-1. It is of interest to note that two of these factors involve human error by individuals not within the surgeon’s control. This highlights the inherently increased risk in allografts versus autografts attendant to the fact that so many delicate and exacting tasks must be properly performed before the graft gets to the operatingroom. Most tissue banks are run meticulously and with great care. However, human error, or intentional human misbehavior, can occur with the surgeon unaware.
Areas of Morbidity
Graft Failure and Laxity
The meta-analytic data presented in Chapter 69 showed allografts to have a failure rate two to three times that of autografts, even when radiated grafts were removed from consideration. It also showed the allograft normal stability rate to be significantly lower. This effect occurred in both bone–patellar tendon–bone (BPTB) and soft tissue grafts. This material is covered in more detail in that chapter. Despite these overall worse stability results, it should be pointed out that some reports show excellent allograft stability rates.1
Delayed Graft Failure
There is some evidence that allografts have a tendency toward late failure,2–4 whereas autografts have shown very little tendency to late failure.5 This perhaps mirrors the experience with bone allografts, which can fracture years after clinical implantation. This late failure has been accompanied by biopsy evidence of late or absent recellularization,2,3,6 which may be causally related. It may be that allograft-implanted patients should be counseled that late failure can occur. A longer period of follow-up for allograft patients may be indicated than is necessary with autografts.
Infection
It is not clear whether the overall infection rate is higher for allografts than for autografts, but there is evidence that it may be so. The Centers for Disease Control and Prevention (CDC), in a well-known analysis of one surgicenter’s experience, showed no infections in autografts and sterilized allografts but a 3% infection rate7 in unsterilized allografts. In our clinical experience the only infected anterior cruciate ligament reconstruction (ACLR) failures we have seen have been in allografts. We have seen one patient with two infected allografts from two different tissue banks operated at two different hospitals by different surgeons for each procedure. This patient went on to autograft revision without incident.
Disease Transmission
The rate of disease transmission risk is difficult to evaluate because routine viral testing of post-allograft patients is not carried out, although it is certainly very low. A recent report, however, included a patient who had hepatitis B transmitted from a donor who initially tested negative for hepatitis B and whose allograft was radiated. After the recipient contracted hepatitis, repeated, more sophisticated testing showed that that the donor was indeed the source of the hepatitis virus.8 Studies would indicate that the current sub–3Mrad levels of radiation now most often employed would be expected to kill neither the hepatitis nor human immunodeficiency viruses.9,10 Higher levels in the 5Mrad range are probably necessary. Newer protocols using such higher doses with radioprotectant may provide the answer.11