12 Abdominal wall reconstruction

Navin K. Singh, Marwan R. Khalifeh, Jonathan Bank

Synopsis

Abdominal wall reconstruction techniques are indicated for hernia repair, reconstruction of tumor defects, congenital defects, and correction of traumatic defects (e.g., from damage control laparotomies).

Patients may be complicated by fistulae, adhesions, infections, scarring from previous injury or surgery, and presence of dehisced prior mesh.

Preoperative optimization of patients is requisite – smoking cessation, weight loss if indicated, and nutritional restitution.

Autologous techniques are ideal in reconstruction, utilizing muscle and fascia – utilizing separation of components and fascia lata grafts.

Prosthetic meshes and bioprosthetics may be utilized in addition to, or in lieu of, flaps for recalcitrant cases.

Advanced techniques may include tissue expanders, laparoscopic methods, free flaps, and even abdominal wall transplantation.

Postoperative management begins in the intensive care unit (ICU) and continues into postoperative rehabilitation.

Introduction

The history of abdominal wall reconstruction is ensconced in the surgery-in-general literature. Abdominal wall hernias, which occur either congenitally (e.g., umbilical) or in an acquired fashion (e.g., postpartum, posttrauma, and postsurgery or iatrogenically), are routinely treated by general surgeons. Plastic surgery involvement in abdominal wall reconstruction came to the fore in complex cases where routine techniques exploiting local tissues and mesh would not suffice. Plastic surgery consultation became indicated for flap mobilization, regional tissue transfers, free flaps, and tissue expansion techniques. A seminal paper by Ramirez et al.¹ revisited and popularized components separation as a useful technique in abdominal wall reconstruction. What has followed is an understanding of abdominal wall muscular dynamics, the role of component separation and muscle realignment as a central tenet of any reconstruction, and advances such as endoscopic or minimally invasive methods to perform component separation. Recent advances include perforator-sparing techniques, and evolution in biologic as well as synthetic meshes.

Closure of routine laparotomies itself causes many postoperative hernias. Easy to recall are the fulminant complications such as eviscerations, septic dehiscences, often despite retention sutures placed initially or at “take-back” surgery. Yet approximately 20% of laparotomies become incisional hernias in the US. Given that more than 4 million laparotomies are performed annually, this is a staggering number. Only about 90 000 are repaired annually, leaving both a huge backlog of cases that must be addressed as well as a future opportunity to deliver care to those who have limitations in activity, chronic pain, and functional issues such as chronic constipation or urinary retention from these hernias which are the sequelae of so many laparotomies.

Most surgeries are performed in the rich world – the world’s wealthiest 2 billion people get 75% of all the surgery done each year while the poorest 2 billion only get 4%.² With increasing access to care, parts of the developing world will face similar challenges of abdominal wall reconstruction.

The ascendancy of the evidence-based medicine paradigm over the last two decades has focused attention on both the short-term failure rates of techniques as well as the long-term data. A landmark paper by Luijendijk et al.³ showed that, if followed for 10 years, the failure rates with primary suture techniques are 2 in 3, and with synthetic meshes 1 in 3. This is unacceptably high. Consequently, there has been an escalation in interest and an introduction of novel techniques in addressing these problems, as long-term data highlight the inadequacy of previous methods. The influence of evidence-based medicine has driven a resurgence of investigations into abdominal wall reconstruction techniques, as well as multispecialty collaboration between general surgeons, colorectal surgeons, trauma surgeons, minimally invasive surgeons, and plastic surgeons.

Patients and surgeons are seeking a decrease in herniation rates in the long term, not just a delay until reherniation. Quality measures, cost containment, and cost-effectiveness are paramount in the minds of institutions, payors, and credentialing committees, as we operate in a changing healthcare paradigm.

Historical perspective

Phases in abdominal wall reconstruction

• Primary suture techniques (hernia repair)

• Development of synthetic mesh

• Component separation ^1,³^–⁹

• Use of biologic meshes and acellular dermal matrices.

Synthetic mesh-based reconstruction – a subject of fevered debate

Many abdominal hernias can, should be, and are repaired using synthetic mesh. The development of mesh was a major accomplishment and part of the long march forward in the repair of recalcitrant hernias.

The long-term failure of mesh can be ascribed to many causes, including cyclical fatigue and biofilm contamination. The repair breakdown is most often at the junction of the native tissues and the mesh, rather than through a fracture of the mesh itself. This occurs independently of suturing technique (interrupted or running) or suture material (absorbable or nonabsorbable).

The ultimate cause is posited as a failure of true biologic tissue ingrowth into the mesh. Tissue grows around the mesh (in the case of a porous mesh, the growth is around the interstices) and relies on scar strength to mitigate risk of recurrence. Biofilm contamination can lead to infection, which causes separation of the mesh from surrounding tissue, and thus failure of the repair and the need for removal of the device. Encapsulation, the body’s normal response to a foreign body by multinucleated giant cell reaction, can also lead to contraction of the mesh leading to failure at the margins where it is mechanically pulled away from native fascial edges. Encapsulation can then lead to extrusion and failure of the repair.

Currently, there is a shift towards biologic meshes and away from synthetic meshes, particularly in infected or contaminated patients, although each method of repair retains its own niche.

The following are broadly accepted contraindications to implantation of synthetic mesh: removal of previous infected mesh, enterotomies during adhesiolysis, peritonitis, repair of peristomal hernia, open abdominal wall wound, enterocutaneous or enteroatmospheric fistula, and colostomy reversal. A relative contraindication is a previous history of infection. Those with prior history of infection are at higher risk for repeat infection from indolent biofilm reactivation, hence the concern for bacterial implantation of a prosthetic device.

Discussion of biofilm pathophysiology is beyond the purview of this chapter. In brief, free-floating planktonic bacteria may become sessile, enabling adherence to various surfaces in the body, including implanted prosthetics. Numerous bacterial adaptive mechanisms have been revealed, including quorum sensing, reduced growth rate in the presence of antibiotics to decrease bactericidal vulnerability, and plasmid exchange to increase resistance to antibiotics. Approximately 95% of the biomass of a biofilm is bacteria – the remainder is a network of scaffolding that aggregates these bacteria. Scientific inquiry has accelerated on this subject but it remains a poorly elucidated topic at present, and its role in failure of abdominal wall reconstruction is only slowly being understood. Whether it is flagrant infection or insidious biofilm formation in the setting of fistulae, enterotomies, peritonitis, colostomy reversal, or open abdominal wall wounds, the odds of failure with a prosthetic in these scenarios are increased over autologous or biologic techniques which avoid synthetic mesh.

The components separation method

The technique most credited for the advancement in approach to abdominal wall reconstruction using autologous methods is the components separation method, as popularized in the modern plastic surgery literature by Ramirez et al. in 1990.¹ Demonstrating clinical vignettes and elegant cadaver dissections, this manuscript advanced the technique of using bipedicled, neurotized, musculofascial advancement of the rectus abdominis muscles and internal oblique with transversus abdominis muscles. Historically, however, this technique had been mooted as early as 1916 by Gibson,⁸ then again in 1929 by Dixon,⁹ and finally in 1961 by Donald Young.⁴ Young described separating the transversus/internal oblique/rectus unit from the external oblique, similar in principle to components separation.

Components separation is a more nuanced way of performing the classic trauma teaching of lateral relaxing incisions. By laying bare the anatomy of the abdominal wall, Ramirez et al. showed that releasing the rectus abdominis muscle at the linea semilunaris from the external oblique muscles creates an avascular plane between the external oblique and the rectus–internal oblique–transversus complex.¹ Since the segmental intercostal innervation to the rectus abdominis muscle arises deep to the internal oblique musculature, this technique preserves not only the vascularity but also the innervation to the muscle, which is principal in a stable reconstruction. Blood supply to the rectus abdominis muscle arises from segmental intercostals, as well as from the superior epigastric artery as it becomes the terminus of the internal mammary artery. The dominant blood supply is from the deep inferior epigastric artery (DIEA) as it arises from the external iliac artery.

In 2000, Shestak et al.⁵ further described the components separation method and detailed its limitations. The surgical goal is to recreate the midline tendon (linea alba) where the paired rectus muscles are held to length, and the relentless unopposed lateral traction of the external oblique, internal oblique, and transversus complex is paired to the contralateral complex. The authors describe incising the fascia 1 cm lateral to the linea semilunaris, identifying the plane between the external oblique and internal oblique fascia (Fig. 12.1). They underscore the importance of dissecting superior to the internal oblique fascia, thus protecting the underlying nerves to the rectus abdominis muscle, and avoiding injury to the spigelian fascia (reducing the likelihood of a spigelian hernia). Extent of lateral dissection is determined by the amount of laxity present, with maximal advancement of each ipsilateral complex toward the midline of 4 cm in the upper abdomen, 8 cm at the waist, and 3 cm in the lower abdomen. An additional 2 cm can be advanced with elevation of the rectus muscle off the posterior rectus sheath (see Fig. 12.9, below).

Fig. 12.1 (A) Normal anatomy above and below the arcuate line. (B) Steps in component separation method: the transition point where the external oblique muscle becomes tendinous and attaches on to the anterior rectus sheath aponeurosis is identified as the linea semilunaris. On either side (1, 4), 10–20 mm lateral to the linea semilunaris, a fasciotomy is made, separating the external oblique from the rectus abdominis. Cautery stimulation can also be used to check the orientation of muscular fibers. An avascular plane is entered (between the external oblique and the internal oblique muscles). Orthogonal orientation of the fibers can confirm the correct plane. The segmental neurovascular bundles are protected, coursing deep to the internal oblique muscle. The plane between the rectus abdominis and the posterior rectus sheath may be developed by incising just lateral to the linea alba (2) to gain additional length (3). Flap edges are sutured together. (C) Cross-sectional illustration showing external oblique muscle release.

As previously mentioned, the dominant perfusion of the soft tissues and skin of the anterior abdomen is the territory of the DIEA as well as contributions from the superficial inferior epigastric artery and from the intercostals. A notorious complication of components separation is marginal or incisional necrosis of the soft-tissue pannus, a result of devascularization of the anterior abdominal soft tissues by dividing the perforators that course through and perforate the rectus abdominis muscles. Several techniques have been advanced to minimize the risk of ischemic complications.¹⁰

Restoring abdominal wall integrity in contaminated tissue-deficient wounds using autologous fascia grafts)

The tensor fascia latae (TFL) technique has been described and utilized as a pedicled or free flap, as well as a nonvascularized graft, and has been shown to revascularize, incorporate, and restore peritoneal continuity (of substantial importance in patients with Crohn’s disease and extensive adhesive disease). In addition, in the event of a repeat laparotomy, it can be reincised and subsequently reapproximated, and expected to heal, similar to native fascia.¹¹

As a pedicled flap, the TFL musculocutaneous unit is vascularized based on the transverse branch of the lateral femoral circumflex artery. A type I muscle by the Mathes–Nahai classification, its arc of rotation can treat composite defects of the infraumbilical abdominal wall. A free TFL muscle or musculocutaneous flap is more versatile and can replace large defects (up to half of the anterior abdominal wall) anywhere in the abdomen. The free flap is typically anastomosed to intraperitoneal vessels such as the right or left gastroepiploic artery on the greater curvature of the stomach, omental vessels, or regional vessels in the musculature such as the superior epigastric or DIEA.¹²

Consistent with established principles, autologous tissue-based repairs have been shown to expedite wound healing and outperform traditional synthetic mesh-based techniques in contaminated, tissue-deficient abdominal hernias.¹³

Rise of the biologics – seeking the holy grail of ideal repair material

The ideal repair material should be biocompatible or inert, nonallergenic, nonresorbable/permanent, cost-effective, resilient (since no material can be resistant) to infection or contamination, kinematic and having mechanical characteristics with high tensile strength, radiolucent, accessible for repeat operative access for intra-abdominal process.

Those characteristics are potentially obtainable in many biologic meshes, which are sourced from acellular dermal matrices (human, porcine, bovine), or other large sheeted xenogeneic sources such as acellular bovine pericardium. Processing involves making these materials acellular to decrease the risk of rejection, as well as enzymatically cleaving the xenogeneic epitopes that could cause a cross-species reaction in biologic meshes derived from nonhuman sources (Fig. 12.2). Discussion of the available types of mesh is beyond the scope of this chapter.

Fig. 12.2 (A, B) Different types of dermal matrices from human, porcine, or bovine source are enzymatically processed, rendering these materials de-epithelialized and acellular. This decreases the risk of rejection while retaining the collagenous matrix, allowing for vascular ingrowth. Enzymatic cleavage of the xenogeneic epitopes reduces a cross-species reaction in biologic meshes derived from nonhuman sources.

Processing can further involve cross-linking to increase strength, although this may decrease the ability of macrophages and monocytic lineage cells to migrate into the biologic sheet. Cross-linking can make biologic tissues inaccessible to migration by cells that use metalloproteases to grow into tissues and facilitate inosculation of blood vessels into existing channels.

Biologics may be better able to tolerate exposure – and may granulate through if kept moist and not allowed to desiccate. Case studies and prospective trials have demonstrated that exposed biologic mesh may be managed by wet dressings, silver sulfadiazine dressings, or vacuum-assisted closure (VAC) utilizing negative-pressure wound therapy (NPWT).

Histological studies in both animal models as well as incidental biopsies of biologics from human surgery have demonstrated revascularization and recanalization of blood vessels and the presence of macrophages, elastin, and organized collagen in the explanted biologic biopsy.

In the setting of contamination, colonization, or infection, prosthetic repairs are at higher risk for failure and thus autologous reconstruction via flaps or biologic meshes is preferred.

Primary closure versus synthetic mesh repair

Factors such as body mass index (BMI), smoking status, nutritional status, and the presence of comorbidities (e.g., diabetes mellitus, chronic obstructive pulmonary disease (COPD)) have been investigated to see which predispose to postoperative herniation.¹⁴ The patients at highest risk of recurrence have an infected mesh or dehiscence from a septic cause. Potentially contaminated wounds (stoma, prior infection, enterotomy) are inherently higher-risk (Fig. 12.3). The problem remains multifactorial. Whether running or interrupted sutures are used, whether permanent or slow-resorbing sutures are employed, whether figure-of-eight knots or simple knots are put down, none has been conclusively shown to have a significant outcome difference.

Fig. 12.3 Hernia grading system: assessment of risk for surgical site occurrences. Wound infection defined as being contained within the skin or subcutaneous tissue (superficial), or involving the muscle and/or fascia (deep). COPD, chronic obstructive pulmonary disease.

(Reproduced from Breuing K, Breuing K, Butler CE, et al. Incisional ventral hernias: review of the literature and recommendations regarding the grading and technique of repair. Surgery. 2010;148:544–558.)

When hernias are repaired, the long-term success of these techniques is surprisingly low. The authoritative papers by Luijendijk et al. in 2000 ³ and by Burger et al. in 2004¹⁵ indicate that, while mesh is superior to primary suture technique, even mesh repair over a 10-year follow-up period has a 32% failure rate. Numerous causes are thought to contribute to these findings – cyclical fatigue of the synthetic mesh device by constant respiratory excursion of the abdomen, lack of true bioincorporation into the mesh, or biofilm seeding leading to capsular contraction, encapsulation, and eventual extrusion.

Furthermore, each successive attempt at repair of a recurrent hernia is likely to be more complex and complicated than the previous, and, all other factors remaining constant, is less likely to be successful, since scarring is increased and local flap options may already have been exhausted.

Evidence-based medicine is now de rigueur when addressing almost any clinical concern. No longer satisfied with anecdotes, the savvy clinician demands the data – and it is this critical scrutiny that has highlighted the deficiencies of time-honored techniques and opened the surgical community to challenge the status quo. Collaboration and cross-pollination of techniques between the general surgery and plastic surgery disciplines have led to greater insights than each could have individually. The type of material used – acellular cadaveric dermis (from human or animal source) or different types of mesh (polypropylene, soft polypropylene) – remains a topic of debate in the literature, with studies revealing favorable results with either material.^16,¹⁷

Basic science/disease process

Hernias and abdominal wall defects may be asymptomatic or symptomatic, and range from the minor cosmetic inconvenience to major destructive processes of the abdominal wall. Congenital umbilical hernias are usually repaired in infancy or childhood. Inguinal herniorrhaphy is similarly undertaken in childhood or in adulthood when they become symptomatic. Major defects such as gastroschisis or omphalocele are not addressed in this chapter – they require multiteam approaches and staged operations.

Acquired defects resulting from straining during heavy labor, load-bearing exercises, and childbirth are defects in the fascia that tend to enlarge, if unsupported by a truss or unrepaired. Narrow-neck hernias are at greater risk for incarceration and strangulation of bowel, whereas large-neck hernias, although more dramatic, are less likely to cause bowel trauma. Success rates with smaller defects in healthy patients are high. Some recur, and may require multiple surgeries.

Analysis of the National Safety and Quality Improvement Program (NSQIP database) highlights the surgeon’s intuition: comorbidities of smoking, diabetes mellitus, COPD, coronary artery disease, poor nutritional status/low serum albumin, immunosuppression, chronic corticosteroid use, obesity, and advanced age increase the risk for postoperative infection and failure. Infection, in turn, creates a higher risk of repair failure. Once the cascade is established, serial failures can turn a small, reparable defect into a challenge.

Other hernias begin as multiple small “Swiss cheese” defects, and when one defect is repaired, the other unrepaired defect(s) can enlarge. These defects may be dormant and arise as a consequence of old retention suture puncture points, prior stoma sites, or drain sites. Thus, some recurrences may not be true failures of hernia repair so much as failure of diagnosis of multiple defects. Ideally, there should be a preoperative computed tomography (CT) scan confirming the location and number of fascial defects, and at the time of repair there should be a wider dissection to identify occult hernias in proximity to the index hernia. Laparoscopic evaluation can provide a broader view of the abdominal wall and potentially identify previously occult defects as well.

Rarely, other failures may arise as a consequence of collagen vascular disorders. The patient with multiple failed attempts and signs consistent with Ehlers–Danlos syndrome, including hypermobility of skin and hyperextensibility of joints, should be referred to a rheumatologist for workup of collagen vascular disorders. This is relatively uncommon and incidence may be approximately 1 in 5000 live births worldwide.

Rectus diastases are not true abdominal wall fascial defects but are pathological stretching to the linea alba either congenitally or, most frequently, postpartum. Functionally, a diastasis is analogous to an aneurysm – wherein the adventitia (fascia) and intima (peritoneum) are intact but the muscular layer is absent (Fig. 12.4). In techniques for abdominal wall reconstruction that do not centralize muscle, or cases in which the abdominal muscles have retracted beyond the possibility to be reapproximated, a functional diastasis remains, in lieu of the tendinous fusion of the paired rectus abdominis muscles. This diastasis can enlarge over time from intra-abdominal pressure, even to the point of requiring repair. Repair is achieved without intraperitoneal entry, by plicating or imbricating the defect so that the rectus abdominis muscles are returned to the midline (Fig. 12.5).