NPWT with instillation is particularly indi­cated to manage patients with infected orthope­dic wounds (open fractures, osteomyelitis). Debridement of the infected and devitalized tis­sue and bone is important prior to the initiation of the NPWTi, especially for chronic infections where the presence of a biolm may make pene­tration of antibiotics into tissues and bones and treatment of chronic infection more difcult.

Godina [10] found that early ap cover in pri­mary trauma with a soft tissue defect was associ­ated with a lower rate of failure of the ap, a lower rate of postoperative infection, a shorter time to bone healing, and a shorter mean length of hospital stay.

Skin grafts can include either a portion of der­mis (split-thickness graft) or the entire dermis (full-thickness graft). Split-thickness grafts can tolerate less vascularization of the recipient site but have a greater amount of contraction. The donor site generally heals spontaneously, through epithelialization from cells of hair follicles and sweat glands. Large areas of split-thickness grafts can be taken to cover big defects such as in large­surface- area burns. Full-thickness grafts require a better vascular bed for survival but undergo less contracture. Thus, if the recipient site is not well vascularized, full-thickness grafts have a greater

The phenomena occurring during the revascu- larization phase have been a matter of research for more than one century. In 1874, Thiersch pro­posed the theory of inosculation. This theory states that the cut vessels from the host bed line up with the cut ends of the vessels of the graft and form anastomoses. The process begins immedi­ately, and vascular connections have been dem­onstrated as early as 22 h after grafting. At the beginning of the twentieth century, some authors proposed another theory. These works indicated that the original vasculature in the skin graft degenerates. Endothelial cells and capillary buds from the host invade the graft, restoring blood ow. Again, the process begins immediately, and as early as 9h after grafting, inammatory cells can be seen invading the graft. By the fourth post­operative day, ow through the graft has been reestablished. More recently, a third theory, rst proposed by Henry, has evolved to describe skin graft revascularization. This theory states that the original vasculature of the graft does indeed degenerate. However, the acellular basal lamina persists, providing a conduit for the ingrowth of the new vascular tree from the host bed. Histologic studies have identied acellular patent vascular channels in the skin graft 48 h after grafting, which later become endothelialized from the invading host capillary buds.

imbibition. Concomitantly, the capillary buds and vascular endothelium developing in the bed invade the graft in both a random pattern and through patent vascular channels.

In larger grafts, the dressing should apply gen­tle pressure on the graft to promote graft adher-

To prevent infection, apart from systemic anti­biotics, local antiseptics should be used in the dressing. Nitrofurazone cream or povidone­iodine gel can be used on top of the graft before the compression dressing is placed.