The biology of hernia formation

Abstract

Abdominal wall hernias occur when tissue structure and function are lost at the load-bearing muscle, tendon, and fascial layer. The fundamental biologic mechanisms are primary fascial pathology or surgical wound failure. In both cases, cellular and extracellular molecular matrix defects occur. Primary abdominal wall hernias have been associated with extracellular matrix diseases. Incisional hernias and recurrent inguinal hernias more often involve a combination of technical and biologic limitations. Defects in wound healing and extracellular matrix synthesis contribute to the high incidence of incisional hernia formation following laparotomy.

Figures

Fig. 1

A normal wound healing cascade. In otherwise normal tissue, without impediments to wound healing, sequential cellular and molecular elements of tissue repair are activated.

Fig. 2

During the initial “lag-phase” of healing, the laparotomy wound is mechanically weakest. As surgical patients recover, increasing abdominal wall loads can cause acute wound failure.

Fig. 3

Incisional hernias occur when suture fails, suture lines are too loose, or suture pulls through the tissue adjacent to the wound. This develops before the laparotomy wound scar is mechanically capable of withstanding the distractive forces. The provisional matrix (PM) is comprised of immature and weak matrix glycoproteins and collagen isoforms. In addition, the scar to wound interface is not developed.

Fig. 4

The peritoneal view of a rodent model of incisional hernias. The hernias develop well-defined hernia rings, hernia sacs and visceral adhesions, all characteristic of the incisional hernias that develop in humans. Modeling like this confirms biological limits of laparotomy wound repair and suggests that pathological changes occur in the wound and musculature of the abdominal wall following wound failure in otherwise normal tissue.