The Biology of Complex Abdominal Wall Defects: Definitions and Causes

Fig. 5.1

Extensive fasciitis by Streptococcus pyogenes of urethral source involving the abdominal and thoracic walls and the extremities and creating a superficial complex abdominal wall defect

Causes of Complex Abdominal Wall Defects

Full-thickness open abdominal (OA ) wounds primarily are encountered in patients after acute trauma, infectious processes, or after abdominal catastrophes. In some instances, such defects represent life-threatening conditions with loss of domain, persistent infections, exposed abdominal viscera, bowel fistulas, and lateral retraction of the abdominal wall (Fig. 5.2). Furthermore, some patients are gravely ill, in poor general health, with several significant medical problems, including sepsis, compromised nutritional status, immunosuppression, and cardiopulmonary problems. Such patients will need to be managed aggressively and in a timely fashion to avoid further complications and deterioration that could affect the outcome of any future reconstructive procedure or endanger their lives.

Fig. 5.2

Postoperative full-thickness complex abdominal wall defect with large enteroatmospheric fistula

In other patients, there is no tissue loss but simply a loss of domain with chronic and long-standing recurrent incisional hernia s (Fig. 5.3) [6]. Long-standing neglected primary abdominal wall hernias with loss of domain, which can create a complex clinical problem, are less frequent (Fig. 5.4).

Fig. 5.3

Loss of domain after recurrent incisional herni a

Fig. 5.4

Loss of domain after long-standing neglected right inguinoscrotal hernia

In a practical and specific sense, acquired CAWDs are mainly caused by abdominal wall infections complicating surgical procedures, with resulting recurrent incisional hernias, the OA approach after damage control (DC) procedures in acute care surgical problems, or less frequently, ablative resection of primary or recurrent tumors, among other less-common conditions [6].

Abdominal Wall Infections and Recurrent Incisional Hernias

An acute wound infection is the main etiologic factor, although not the only one, behind the development of recurrent incisional hernia s. These ventral hernias represent the main etiologic group within most series of CAWDs. Ghazi et al. from Emory University in Atlanta described a series of 165 patients with CAWDs treated over a 7-year period; of these individuals, 101 (61%) were recurrent ventral hernias [7].

To a lesser extent, severe and extensive abdominal wall necrotizing infections requiring surgical resection can also occasionally result in CAWDs. They occur most frequently after gastrointestinal operations, especially in the immune-compromised host with multiple comorbidities, and might be associated with fistulas of the gastrointestinal tract. Clostridial myonecrosis, although rare, is the most severe form of abdominal wall infection (Figs. 5.5 and 5.6).

Fig. 5.5

Postoperative fulminant necrotizing fasciitis of the abdominal wall after creation of a colostomy for diverticulitis

Fig. 5.6

Same patient as in Fig. 5.5 undergoing extensive debridement and resection of the infected abdominal wall tissues

Failure of biomaterials represents a significant setback in patient care. Patients might present with an array of problems ranging from wound dehiscence and infection to suture line disruptions with subsequent formation or recurrence of abdominal wall hernias, mesh extrusion, or even intra-abdominal complications such as bowel damage and fistulas. The incidence of fistula formation with various alloplastic materials has been reported to be as high as 33%. It has also been well recognized that the incidence of fistulas is increased with the use of some type of synthetic prostheses, and that fistula formation can occur even when absorbable meshes are used.

Damage Control and the Open Abdomen Approach

CAWDs in this setting are the result of emergency laparotomies performed for a number of severe conditions and can pose a formidable challenge to the clinical surgeon. A damage control (DC) laparotomy in trauma and emergency surgery, with repeated reentries in the abdominal cavity, is a harbinger of a potential CAWD.

An OA is defined as an abdominal wound requiring temporary abdominal closure due to the skin and fascia not being closed after laparotomy. It is classified in four grades according to severity [8, 9]. The DC surgery and the OA approach have led to an increase in survival of the patient with severe trauma, and this has created an increased need to reconstruct complex defects thereafter (Fig. 5.7). The incidence of chronic ventral hernias is very common in this setting, with a wide range (13–80%) that depends on patient-specific factors and institutional patterns of practice (i.e., aggressive fascial repair vs. a “planned ventral hernia” approach) [10]. Because of the potentially devastating consequences of prosthetic infections, biologic meshes, both crosslinked and non-crosslinked, are currently being recommended when native tissue component repair is not possible [11–14]. These meshes, together with the vacuum-pack technique, are diminishing the rate of planned ventral hernia approaches, in favor of early primary fascial closure [15, 16], with a likely decrease in the overall morbidity and the percentage of CAWDs resulting from this DC/OA surgery [17]. Nevertheless, the data to date suggests that the majority of patients repaired with biological mesh may develop laxity of the repair resulting in a hernia 6–12 months later [18].

Fig. 5.7

Open abdomen with overlying synthetic mesh and lateral retraction of the abdominal wall

Surgical site infections and intra-abdominal abscesses associated with DC/OA occur in as many as 83% of cases and might also contribute to postoperative fascial dehiscence (reported in up to 25% of DC/OA patients) [19].

Resection of Abdominal Wall Tumors

Primary malignancies of the abdominal wall are uncommon. Desmoid tumors are benign fibrous tumors that arise from the musculoaponeurotic structures of the abdominal wall. They are frequently locally invasive (aggressive fibromatosis) (Figs. 5.8 and 5.9) and local recurrence rates of 25–65% after local excision have been reported. Treatment requires wide excision followed by complex abdominal wall reconstruction in up to one-third of patients [20]. This reconstruction is usually performed immediately with synthetic materials (meshes) or myocutaneous flaps when the defect is extensive [21], and usually in collaboration with plastic and reconstructive surgeons.

Fig. 5.8

Recurrent fatal aggressive fibromatosis of the abdominal wall in a 19-year-old woman

Fig. 5.9

Lateral view of the same patient in Fig. 5.8

Complex Recurrent Incisional Hernias and the Pathophysiology of Wound Healing of the Abdominal Wall

The abdominal cavity represents one of the most active areas of surgical activity, and surgical procedures involving the gastrointestinal tract are among the most common procedures performed. Full understanding of the pathophysiology of the healing responses after the surgical procedure remains elusive. Nevertheless, progress in this area is of great interest because complications of abdominal healing represent a significant clinical and economic burden as well as decrease in quality of life [22].

The abdominal wall is a complex region of the body; all of its components are organized in delicate balance to provide maximal protection while preserving physiologic and locomotive function. It is a laminated cylinder of muscle and fascia with an overlying, well-vascularized skin envelope. It serves as a core unit for musculoskeletal posturing, a protective barrier for the viscera, and a base for respiratory mechanics. The maintenance of a constant intra-abdominal pressure allows for support in respiration, locomotion of the trunk, as well as micturition and defecation, among other physiologic functions [22].

When the abdominal wall is in a weakened state, intra-abdominal pressure follows fluid patterns and tends to exert the greatest pressure at the weakest point as opposed to the natural state of diffuse and equal distribution [7]. Although true strangulation of hernia contents is uncommon, many patients with a recurrent incisional hernia have lifestyle limiting symptoms that necessitate operative intervention. Patients may present with chronic dull abdominal pain. They might have postural alterations, leading to lumbar lordosis and chronic back pain. A massive CAWD can also lead to paradoxical respiratory motions, which inhibit respiratory mechanics.

Biological and Mechanical Factors Involved

Modern surgical practice suggests that biologic and mechanical pathways overlap during normal acute wound healing. The cellular and molecular processes activated to repair tissue from the moment of injury are under the control of biologic and mechanical signals. Successful acute wound healing occurs when a dynamic balance is met between the loads placed across a provisional matrix and the feedback and feed-forward responses of repair cells [23].

When a midline incisional hernia develops, the normal force across the composite myofascial structure is lost, functionally resulting in passive unloading of the lateral abdominal wall. Although the adjacent rectus muscles maintain their origin and insertion, the insertion of lateral oblique muscles is lost following midline laparotomy and incisional hernia formation. The linea alba of the abdominal wall is anatomically a tendon that, when severed, should induce pathologic abdominal wall muscle changes similar to those observed in the soleus and gastrocnemius muscles when the Achilles tendon is divided [24]. In a rat model of chronic incisional hernia formation, these authors showed that internal oblique muscles in herniated abdominal walls developed pathologic fibrosis, disuse atrophy, and changes in muscle fiber-type composition. Myopathic disuse atrophic changes significantly altered the phenotype of the herniated anterior abdominal wall. Hernia defects do not enlarge simply by repetitive evisceration of peritoneal contents dilating a fascial defect. Rather, the lateral muscular components of the abdominal wall retract away from the midline fascial defect, and this has therapeutic implications.

Laparotomy wound healing is a complex process involving interplay between many different types of cells; failure with progression to hernia formation is multifactorial. This failure of healing of laparotomy wounds is promoting a considerable body of research focusing on the modulation of the major effectors of wound healing; its emphasis is to improve outcome in tissue remodeling and mesh integration [25].

Biologic factors that contribute to simple and complex abdominal wall defects are multiple [26, 27]:

1.

Inflammation : When injuries occur, dead or dying structural cells (e.g., epithelial and endothelial cells) release inflammatory mediators that initiate an antifibrinolytic coagulation cascade, which triggers platelet aggregation, clot formation, and development of a provisional extracellular matrix (ECM). Platelet degranulation also promotes vasodilation, increased blood vessel permeability, and production of enzymes known as matrix metalloproteinases (MMPs), which temporarily disrupt the basement membrane, allowing the efficient recruitment of inflammatory cells to the site of injury. Epithelial and endothelial cells also secrete growth factors (GFs), cytokines, and chemokines, which promote the recruitment and activation of leukocytes that participate in wound repair. During this initial inflammatory phase, macrophages and neutrophils debride the wound. They also produce soluble mediators that amplify the wound-healing response by recruiting T cells and other inflammatory cells [28]. Wound strength is low during this phase and depends only on the sutures; a prolonged inflammatory response as seen with incisional foreign bodies or infections predispose to wound failure; besides, microorganism can degrade GFs and synthesize proteinases that remove ECM [26, 29]. Steroids can reduce inflammation but inhibit collagen synthesis.
2.

Fibroblasts and myofibroblasts : Fibroblasts are one of the most abundant cell types in connective tissues, responsible for tissue homeostasis under normal physiologic conditions. Myofibroblasts are derived primarily from an extensive network of mesenchymal cells, which include fibroblasts and those cells known as pericytes due to their close relationship with the capillary wall. When tissues are injured, fibroblasts become activated and differentiate into myofibroblasts; these promote wound contraction, a process in which the edges of the wound are physically pulled toward the center. They also secrete factors that are mitogenic and chemotactic for epithelial and endothelial cells, which grow inward, forming new ECM and blood vessels as they migrate toward the center of the wound [28]. Myofibroblasts are responsible for collagen synthesis and the recovery of wound-breaking strength, and is the dominant cell type during the proliferative and remodeling phases. Little is known about defective myofibroblast function in wound failure. Some authors have suggested that the loss of abdominal wall load forces signaling as a result of fascial healing failure would select an abnormal population of repair myofibroblast (mechano-transduction pathways) similar to widely described in tendons, ligaments, and bone repair [26, 30, 31]. Recent in vitro studies suggested that early fascial separation and diminished wound tension might lead to loss of a key stimulatory mechanical signal for myofibroblast proliferation, alignment, and contraction function, resulting in the inability to heal the initial wound failure with subsequent progression to hernia formation [32].
3.

Collagen: Collagen is the main structural protein in abdominal wall fascial layers (at least 80% of tissue dry weight). Defects are described either in its synthesis, with an increase of type III collagen and decrease of collagen I/III ratio and with thinner and less resistant fibers, or in its degradation, with an increase of MMP activity [26, 33]. Numerous studies have now associated incisional hernias with impaired collagen and tissue protease metabolism, and there is a strong correlation between MMP-1 and MMP-13 overexpression and recurrent hernia [33–35].
4.

Growth Factors : It is not known whether delays in the appearance of GFs contribute to the development of incisional hernias. Experimental models have demonstrated that wound treatment with transforming GF beta 2 or basic fibroblast GF stimulates angiogenesis, fibroblast chemotaxis, and collagen production, increasing wound resistance and reducing the incidence of incisional hernia [29, 36, 37].

Local and General Factors Affecting Wound Healing

Local Factors

Closure Under Tension and Blood Supply

It now appears that, in load-bearing systems like the abdominal wall, a tension equilibrium point exists that maximizes repair signals to wound repair fibroblasts (mechano-transduction pathways) [34]. Nevertheless, closure under excessive tension is probably the most common reason for several complications, ranging from superficial wound dehiscence, infection, tissue necrosis and loss, to abdominal compartment syndrome (ACS) [6]. The site of an incision may disturb the blood supply to a wound. Vertical parallel incisions on the same side of the midline impair healing of the wound placed more medially and risk necrosis of the intervening skin bridge. Suturing might adversely affect the blood supply of a healing wound, especially if there is infection and edema.

Hematoma

Postoperative seromas and hematomas , if not recognized early on and appropriately managed, also might result in wound dehiscence, infection, and tissue loss [6]. A mass of blood apparently exerts a toxic effect independent of the level of bacterial contamination and of the amount of internal pressure they produce, theoretically obstructing the dermal circulation and causing necrosis [38].

Infection

It is the most common complication of wound healing. The principal biochemical abnormality in infected wounds seems to be a disturbance of fibroblast proliferation and subsequent collagen metabolism. In DC surgery, the incidence of dehiscence and abdominal wall infections is approximately 9% and 25%, respectively, and their development is multifactorial [19]. The intra-abdominal hypertension (IAH) that commonly develops in this population reduces abdominal blood flow even in the face of maintained arterial perfusion pressures, contributing to local edema and ischemia. This impairs wound healing, and the ischemic tissue provides a site for bacterial infection.

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