Ventral Hernia and Abdominal Release Procedures

Definitions

Hernia is derived from Latin meaning “rupture” or “protruding viscous” and a ventral hernia is a protrusion of viscera, usually intestine, through the layers of the anterior abdominal wall. A true hernia has a defect in the fascia of the abdominal wall and the formation of a hernia sac of peritoneum that contains visceral organs. Other bulges that may appear similarly, but are not true hernias, are diastasis recti and eventration. Diastasis recti is the thinning and broadening of the linea alba that leads to a bulge at the midline and is usually asymptomatic. An eventration is a bulge resulting from lack of muscle tone in the abdominal wall due to trauma, denervation, and surgical or congenital absence of the muscle. Neither diastasis recti nor eventration has a fascial defect and there is no hernia sac in either scenario.

Ventral hernia can be further defined by location and origin. An incisional hernia occurs at any previous surgical site of the anterior abdominal wall. Traumatic hernias occur due to injury of the fascia and musculature of the abdominal wall, and can be in any location. Lateral abdominal wall hernias, also known as flank hernias, are often caused by blunt trauma with disruption of the attachments of the lateral muscles of the abdominal wall. Subxiphoid hernias are located just inferior to the xiphoid at the midline. Epigastric hernias can be spontaneous or incisional at the midline between the xiphoid and the umbilicus. Umbilical hernias are located at the umbilicus and can be congenital or acquired spontaneously. Hypogastric hernias at the midline, inferior to the umbilicus are rare spontaneous occurrences. Suprapubic and parailiac hernias occur adjacent to the bony structures of the pelvis. Finally, spigelian hernias are spontaneous hernias that occur along the semilunar line, typically at its junction with the arcuate line of Douglas.

The European Hernia Society (EHS) has introduced a ventral and incisional hernia classification system in an attempt to create a common language for the evaluation and treatment of ventral hernias. Primary and incisional hernias are separated in this classification system ( Tables 52.1 and 52.2 ). A primary ventral hernia is divided by location between midline hernias (epigastric and umbilical) and lateral hernias (spigelian and lumbar). The size of primary ventral hernias is categorized into small (<2 cm), medium (2 to 4 cm), and large (>4 cm). Any weakness or protrusion at the site of a surgical scar defines an incisional hernia for the EHS, and because these hernias are more variable, the classification system is slightly more involved. First, incisional hernias are divided into medial or lateral, with the lateral edge of the rectus abdominis being the dividing line. Midline hernias are placed into one of five vertical zones (M1 to M5) ranging from subxiphoid to suprapubic. Lateral hernias are divided into four zones (L1 to L4) with subcostal, flank, and iliac stacked medial to the anterior axillary line and lumbar (L4) hernias arising anywhere dorsolateral to this line. Incisional hernias are divided into recurrent or not, and both length and width are taken into consideration. Hernias with multiple defects are measured at the point of greatest distance in either axis. Finally, width is divided into W1 (<4 cm), W2 (4 to 10 cm), and W3 (>10 cm). There was no consensus within the EHS on nomenclature for incisional hernias.

Irrespective of the cause and location of the ventral hernia, current trends in repair are led by the philosophy of restoring a functional and anatomic abdominal wall, including the reconstruction of the tendinous insertion of the related muscles or re-creation of the linea alba.

Anatomy

The anterior abdominal wall is a complex layering of muscle, fascia, and aponeuroses, all of which work symbiotically to fill a variety of functions ( Fig. 52.1 ). The anterior abdominal wall protects and supports the viscera and aids with respiration by pulling down the rib cage in expiration. It also participates in a multitude of bodily functions, allows for rotation, bending, and flexion of the trunk, and protects the spine from hyperextension.

Laterally, the abdominal wall is constructed of three layered flat muscles. From superficial to deep these are the external oblique (EO), internal oblique (IO), and transversus abdominis muscles. The transversalis fascia is the deepest layer of fascia in the abdominal wall and separates the transversus abdominis muscle from the peritoneum. The EO muscle runs inferior-medially, originating at the lower costal margin and inserting at the linea alba, iliac crest, and pubic tubercle to form the inguinal ligament. The IO muscle runs perpendicular to the EO with its origination at the lateral half of the inguinal ligament, anterior iliac spine, and thoracolumbar fascia and inserting into the lower ribs and linea alba. Finally, the transversus abdominis muscle runs horizontally from the iliac crest, lateral inguinal ligament, and costal cartilage to insert into the linea alba and joins the IO to form the conjoint tendon.

Each muscle body is surrounded by its relevant fascia and these laminal layers join to form aponeurotic connections for each flat muscle. Medially the three aponeuroses form the linea semilunaris, which lies at the lateral edge of the rectus abdominis muscle. The rectus abdominis is a vertically oriented muscle originating at the pubic symphysis and inserting into the fifth to seventh costal cartilages. In the upper third of the abdomen, the EO aponeurosis and anterior lamina of the IO aponeurosis fuse to form the anterior rectus sheath, while the posterior lamina of the IO overlies the transversus abdominis muscle body. The transversus abdominis muscle extends medially in the upper abdomen, just deep to the rectus muscle, and the posterior lamina eventually joins the transversus abdominis aponeurosis to form the posterior rectus sheath. In the middle third of the abdomen, the transversus abdominis muscle ends more laterally and the posterior rectus sheath is formed by the aponeurosis of the transversus abdominis and the posterior lamina of the IO aponeurosis. In the lower third of the abdomen, below the arcuate line, the IO and transversus abdominis aponeurosis fuse with the EO aponeurosis as part of the anterior rectus fascia, leaving only peritoneum deep to the rectus abdominis.

Medial to the body of the rectus abdominis muscle, all of the flat muscle aponeuroses fuse to create the linea alba and the midline of the anterior abdominal wall. The linea alba is widest at the xiphoid, where the rectus muscles diverge to insert into the costal cartilages and narrows to a thin line of fascia below the umbilicus until it reaches the pubic symphysis. The linea alba is weakest at the umbilicus, which lies at the midpoint between xiphoid and pubis and is a cicatricial remnant of the umbilical cord.

The spigelian fascia is a fusion of the IO and transversus abdominis aponeurosis that lies between the semilunar line and the lateral edge of the rectus abdominis muscle body. The spigelian fascia is weak inferior to the umbilicus as the aponeuroses of IO and TAMs run parallel in this location, so there is minimal crosslinking for strength. This weakness is worsened where the inferior epigastric arteries traverse the rectus abdominus muscle.

The vascular supply of the rectus abdominis enters the muscles laterally via branches of the inferior and superior epigastric arteries. The rectus abdominis is innervated segmentally via the thoracoabdominal (T7 to T11) nerves that also enter the muscle body at the lateral edge, just medial to the linea semilunaris. The vascular supply for the flat muscles of the abdomen are branches of intercostal arteries that run with thoracoabdominal nerves in the neurovascular space between the IO and transversus abdominis muscles. The skin and subcutaneous tissue of the anterior abdominal wall gets its blood supply from deep perforators that branch from the deep inferior and superior epigastric vessels.

Etiology and Epidemiology

Ventral hernia formation is complex and multifactorial, and hernias may be congenital or acquired. Congenital hernias are present from birth and include complex entities such as omphalocele and gastroschisis, or more straightforward defects such as primary umbilical or epigastric hernias. More than 80% of primary congenital umbilical hernias will close spontaneously before the age of 5 and will not require repair. However, congenital epigastric hernias may be symptomatic with incarcerated preperitoneal fat and require surgical intervention. Acquired ventral hernias are of the spontaneous or incisional variety. Spontaneous hernias most often occur at weaknesses of the abdominal wall, along the midline, or at the arcuate line or spigelian fascia. However, trauma to the abdominal wall may also lead to herniation in other locations. Incisional hernias are defined as any ventral herniation that is located at a previous surgical site or incision, including trocar sites. Spontaneous ventral hernias are diagnosed in adulthood and are usually the effect of increased abdominal pressure related to obesity, pregnancy, ascites, or other factors. Increased abdominal pressure leads to enlargement of the hernia defect as well as increased likelihood of incarceration. Fig. 52.2 shows the anatomic location of acquired and congenital hernias.

Epigastric hernias occur at the midline above the umbilicus where perforating neurovascular bundles travel through the fascial layers that interlace to create the linea alba. These defects are usually quite small but often have an incarcerated mushroom of preperitoneal fat that can be quite symptomatic for the patient.

Umbilical hernias occur through the base of the umbilicus or in the surrounding tissue. The umbilical ring is formed as the flat discus of fetal cells begins its three-dimensional fold and is surrounded by the amniotic cavity. It eventually fuses with the linea alba and rectus complexes, and the umbilical cord is created. Here the linea alba is penetrated by the umbilical veins and arteries and after birth a cicatrix is formed as these vessels degenerate into the falciform and umbilical ligaments. It is thought that this is the weakest part of the abdominal wall; either the cicatrix itself or the tissues surrounding it are weak, allowing for vulnerability and the formation of umbilical or periumbilical hernias. Other patient factors may add to the stress of the abdominal wall and contribute to the formation of ventral hernias, such as disorders of collagen formation, sleep apnea, steroid use, and smoking or chronic lung diseases. Whatever the etiology, umbilical hernias are a common problem and approximately 200,000 repairs are done in the United States every year.

Incisional hernias occur in up to 40% of patients after midline laparotomy. An innate problem with suture closure of laparotomy is that tension is required to approximate the rectus abdominis muscles and counter tension of the lateral abdominal wall musculature. Such tension may contribute to overtightening of sutures and ischemia to the midline tissues.

There are three types of incisional hernias: acute wound dehiscence and evisceration due to sutures tearing through tissue, subacute with early gapping of the tissues approximated under tension, and chronic remodeling of the scar tissue causing “Swiss-cheese” or “cheese-cutting” hernias, formed as sutures cut through the weakened scar tissue. Thus, technical factors such as slipped knots, tension, and overtightened sutures can predispose to hernia development. Surgical site infection (SSI) has also been found to increase the risk of hernia by 50%.

Laparotomy closure should be done in a continuous fashion with a slowly absorbable monofilament suture with all midline layers en bloc. Two recent randomized controlled trials have found that small stitches, incorporating about 5 mm of midline tissue and taken about 5 mm apart reduces the risk of infection, wound dehiscence, and incisional hernia development. This is a change from historical surgical dogma where 1 cm was felt to be the proper amount of tissue and distance between stitches. Proper “small bite” technique should be confirmed at the time of closure by measuring the suture-to-wound-length ratio to be at least 4 to 1. Although small bites may take longer to complete than the traditional larger bites, the added operating room time accounts only for a small increased cost and the cost savings with the reduced incidence of ventral hernia and complications is much greater. There has also been some recent interest in exploring the use of prophylactic mesh at closure of primary laparotomy for incisional hernia prevention. A randomized controlled trial of mesh versus suture closure after abdominal aortic aneurysm repair found a fourfold reduction in hernia development with the use of prophylactic mesh. This study also showed a longer time to hernia development for those with mesh placement, and no increase in complications or mesh infections. A meta-analysis of prophylactic mesh placement during laparotomy in high-risk patients also found a significant decrease in incisional hernia development with prophylactic mesh placement, longer operating room (OR) times, and shorter hospital stays. Therefore, prophylactic use of mesh during closure of laparotomy in high-risk patients can be considered to reduce the risk of incisional hernia, but no strong recommendations can be made for the general population.

Laparoscopic port site hernias are a growing problem within the incisional hernia category given the increasing use of laparoscopy and robotics, and the exploration of single-site minimally invasive approaches. The incidence of port site hernias has been shown to be between 0% and 5.2%. Ninety-six percent of port site hernias occur at 10-mm and larger port sites, and 86% occur at the umbilicus. However, more recent studies have shown rates reaching 22% to 39% after ventral hernia repair with large mesh and bariatric surgeries. It is generally believed that any port larger than 5 mm in diameter should be closed to prevent port site hernias. However, it remains controversial, and we believe that dilating, noncutting trocars less than 12 mm do not require closure. Single-incision laparoscopic and robotic surgeries have been found to have slightly higher incidence of port site hernias of 3%, although this has improved over time and more recent studies have shown no difference. Port site hernias may be difficult to diagnose because they may occur early, late, intrafascially, or as Richter-type hernias. Wound- and patient-related factors may also play a role in the formation of port site hernias: infection, delayed healing, steroids, collagen disorders, obesity, and increased abdominal pressure are all known to predispose to herniation.

Presentation and Indications for Surgery

Most patients with ventral hernias present to the office with complaints of a bulge in their abdominal wall. The bulge may be more noticeable after physical activity, Valsalva maneuvers, coughing, or any other activities that increase intraabdominal pressure. Some patients will present with complaints of pain or discomfort along with the bulge, although about 25% of patients will be asymptomatic. Pain associated with ventral hernias may be related to incarceration and at times relieved with rest, lying down, or reduction of the hernia contents. The most concerning presentations are incarcerated ventral hernias with signs of bowel obstruction or strangulation, which is more common with small defects. Other complaints that may accompany a ventral hernia are cosmetic, gastrointestinal or urinary symptoms, generalized pain, back pain, and respiratory difficulties.

The mere presence of a ventral hernia is often considered a de facto indication for a surgical intervention. Other than incarceration and strangulation, generalized pain is the most common reasons surgeons choose to intervene on ventral hernias. However, many ventral hernia patients have complex medical histories and the repairs are fraught with potential complications. Morbidity rates after ventral hernia repair can reach 60% and mortality rates can be as high as 5.3%. Despite high complication and morbidity rates, surgery is often felt to be the primary treatment option for ventral hernias, largely because the natural history of ventral/incisional hernias is unstudied. A recent series of watchful waiting for ventral hernias showed no change in pain, functionality, or quality of life after 2 years of watchful waiting for minimally symptomatic ventral hernias larger than 9 cm. The risk of incarceration or strangulation was less than 5% and another 8% of patients requested repair for symptoms within the 2 years. This study is limited by a small sample size, but the low rates of complications and progression of disease mirrors the results of a randomized controlled trial for minimally symptomatic inguinal hernias that has shown that watchful waiting can be safe. Also, although patients with symptomatic ventral hernias report improvement in pain and quality of life, patients with limited symptomatology report similar pain levels before and after repair. However, follow-up data have shown a high rate of disease progression and although watchful waiting may be relatively safe, we believe most patients should be optimized and undergo repair in the earlier stages of the disease.

Principles of Ventral Hernia Repair

Tissue-based repairs of ventral hernias have been developed in an attempt to decrease recurrence rates; the Mayo repair used a “vest-over-pants” technique and mattress sutures to imbricate fascial edges and approximate healthy tissue. However, long-term follow-up found similar recurrence rates to fascial suture approximation. In the 1990s, a randomized controlled trial showed a 50% decrease in ventral hernia recurrence with the use of mesh compared to suture repair. The decreased rate of recurrence was even more significant in smaller hernias, although with an associated increase in complications. Surgical site infections and the presence of abdominal aortic aneurysms increased the risk of hernia development. Patients randomized to mesh repair suffered more complications, but had lower levels of postoperative pain.

The introduction of prosthetics has been a game changer in the repair of ventral hernias, and today the use of mesh reinforcement is recommended in the majority of ventral hernia repairs. Prosthetics used in hernia repair are in constant evolution and no “ideal” mesh has been discovered. The qualities of the ideal mesh include good tissue incorporation, limited foreign body reaction, and sufficient strength to withstand the forces of the abdominal wall along with good flexibility and compliance.

Prosthetics are first divided by material type and can be synthetic, biologic, or biosynthetic. Synthetic meshes are usually made of polypropylene, polyester, or polytetrafluoroethylene (PTFE). Biologic meshes are either cadaveric allograft or xenograft tissue grafts that are processed to reduce host reaction and improve tissue integration. Finally, the newest category of biosynthetic meshes are made of slowly absorbable biodegradable synthetic polymers. Synthetic and biosynthetic meshes can be further divided into monofilament or multifilament construction, micro- or macroporous, and heavy, midweight, or lightweight types. Finally, to reduce visceral adhesion and fistula formation, there are covered meshes made for intraabdominal placement. It is important for the surgeon to be educated on the types of meshes available for hernia repair, the benefits and limitations of each mesh type, and to have an algorithm for choosing mesh in individual hernia repairs. We prefer to use a macroporous, midweight monofilament polypropylene mesh for most extraperitoneal repairs. However, heavyweight polypropylene meshes are used in cases where more significant support of the repair is needed. Our use of biologic meshes is limited to actively infected fields and in cases of staged repair with a planned hernia. The role of slowly absorbable biosynthetics is currently evolving.

The most appropriate positioning of mesh within the abdominal wall is as big a question as which type of mesh to use. Neither of these questions has been answered in the literature, although 75% to 80% of hernia repairs involve mesh to reduce the risk of recurrence. Mesh can be placed as an onlay, sublay, underlay, or interposition ( Fig. 52.3 ). Onlay mesh is placed above the anterior rectus sheath, whereas sublay mesh is positioned within the layers of the abdominal wall, typically retromuscular or in the preperitoneal plane. An underlay mesh is placed within the abdominal cavity underneath the peritoneum. Recurrence rates are lowest with sublay or retromuscular mesh placement, followed by underlay mesh placement. Interposition mesh placement has the highest recurrence rate, reported to be as high as 80%. Interposition mesh placement is fraught with complications and also holds the highest SSI rate, whereas sublay mesh placement has the lowest SSI rate and lowest rate of mesh excision. However, there is significant discrepancy in the literature regarding outcomes related to mesh location, which accentuates the need for clinical decision making during ventral hernia repair. Mesh location, like mesh type, should be decided based upon patient characteristics, anticipated technique, and the characteristics of the hernia in question.

To help with clinical decision making in the repair of ventral hernias, as well as the ability to study and compare outcomes, the Ventral Hernia Working Group (VHWG) proposed a ventral hernia grading scale and recommendations for repair. In 2010, the VHWG developed a four-grade scale of ventral hernias: Grade 1 includes healthy patients with no comorbidities or history of wound infections or contamination; grade 2 captures comorbid patients without infection or contamination; grade 3 includes higher-risk patients with potential for contamination with the presence of a stoma, history of wound infection, or opening of the intestinal tract; and grade 4 captures patients with active infections, fistulas, or contamination. This grading scale was evaluated and modified 2 years later by Kanters et al., who found that increased grade correlated with increased risk of recurrence as well as surgical site occurrence (SSO). However, they found significant difference between grades 2 and 3 with regard to SSO and proposed a modification of the grading scale to include only three grades. grade 1 remains the same low-risk group, grade 2 is mostly the same class of comorbid patients, with the added inclusion of a history of wound infection, and grade 3 is the contaminated group. One of two major limitations of the modified grading system by Kanters et al. is that it segregated the groups based on often clinically irrelevant SSOs and not SSIs. Furthermore, there were not a sufficient number of patients with dirty (CDC wound class 4) wounds resulting in those patients being grouped together with patients with contamination and active infection in the grade 3 category.

The VHWG also provided guidance in the repair of ventral hernias with the first step including the evaluation of the hernia grade. The choice of repair technique and type of prosthetic used is then decided. For grade 3 and 4 hernias, the VHWG does not recommend the use of synthetic mesh and states that biologics can be considered. However, Carbonell and colleagues have found that synthetic mesh can be used in clean-contaminated and contaminated cases with favorable outcomes. More recently Majumder and colleagues showed that the use of biologic mesh in clean-contaminated and contaminated ventral hernia repairs was associated with a markedly increased risk of surgical site events (SSEs), SSIs, and recurrence. Therefore, the touted advantages of biologic grafts appear to have been exaggerated and their utilization continues to decline.