Core Topics in General & Emergency Surgery: Companion to Specialist Surgical Practice (16 page)

Andrew C. de Beaux

A hernia is defined as an abnormal protrusion of a cavity's contents, through a weakness in the wall of the cavity, taking with it all the linings of the cavity, although these may be markedly attenuated. The anterior abdominal wall can be divided into two structural/functional zones: the upper ‘parachute area’ aiding respiratory movement and a lower ‘belly support’ area. Functional failure in the abdomen may lead to epigastric and umbilical hernia in the upper zone and to inguinal and femoral hernia in the lower zone. The external abdominal hernia is the commonest form of hernia, the most frequent varieties being the inguinal (75%), umbilical (15%) and femoral (8.5%).

Hernias can be described as reducible, incarcerated or strangulated. A reducible hernia is one in which the contents of the hernial sac can be manually introduced back into the abdomen while, conversely, an irreducible or incarcerated hernia cannot be manipulated back into the abdomen. A strangulated hernia occurs when the vascular supply to the contents contained within the hernia is compromised, resulting in ischaemic and gangrenous tissue.

Multiple factors contribute to the development of hernias. Hernias are associated with a number of medical conditions, including connective tissue disorders such as Ehlers–Danlos syndrome, as well as a number of abnormal collagen-related disorders such as varicose veins and arterial aneurysm. In essence, hernias can be considered design faults, either anatomical or through inherited collagen disorders, although these two aetiological factors probably work together in the majority of patients. Anatomical design faults can be considered at any site where structures within the cavity exit through an opening in the wall of the cavity, such as blood vessels, bowel or the spermatic cord. This is typical, for example, around the oesophagus and in the groin. However, not everyone develops a groin hernia so other factors must be important. The fascia and surrounding tissues that cover muscle, acting to hold the muscle bundles together, may appear relatively avascular, but it remains a complex and living structure. The genetic code for fascia is coded on DNA, and within fibroblasts the sequence is messenger RNA, transfer RNA, peptide formation, with fusion of peptides into approximately 1000-amino-acid polypeptides called alpha chains. The endoplasmic reticulum converts these to procollagen. Procollagen is the large building block of collagen, comprising triple-helix strands, stabilised by hydroxylation of proline and lysine, which is vitamin C dependent. These triple-helix strands form microfibrils, then fibrils, then fibres and finally bundles. These collagen bundles surrounded by extracellular matrix comprise fascia. The control of this process is mediated through matrix metalloproteinases, which in turn are controlled by tissue inhibitory metalloproteinases. If this is not complex enough, there is also control by collagen-interacting proteins and receptors such as fibronectin, tenasin and collagen receptor discoidin domain receptor 2. Fascia and tendon are made up of type I and type III collagen (type II is found in cartilage and type IV in the basement membrane of cells). In cross-section, there is a bimodal distribution of bundle size. The larger bundles are type I collagen, imparting the strength to the fascia or tendon. The type III collagen bundles are smaller and are thought to provide elastic recoil following stretch when the tissues have been loaded. The type I to III collagen ratio varies between individuals but is constant in all the fascia of a particular individual.

A clinical observation was made by surgeons in the late 1960s that the anterior rectus sheath some distance from the hernial defect was thinner than normal, especially in those patients with direct hernias.
¹
Since then, research has demonstrated a variety of defects in collagen synthesis in such patients.
^2,
3
The current notion is that the majority of hernias are a disease of collagen metabolism. One of the key factors in this is the type I to III collagen ratio. The lower this ratio, from an average of around 5, the more likely the individual is to develop a hernia. Currently, collagen typing is not used in clinical practice to help decide perhaps which patients merit a mesh as opposed to a suture repair, but this may well be a development in the near future.

Much will be mentioned about mesh repairs of hernias in the remainder of this chapter, but this section gives a brief overview of mesh and its science.

Many companies produce a variety of mesh for hernia repair. These are either synthetic (man made) or biological (preparations from animal or human tissue). The majority of synthetic meshes are woven from either polypropylene or polyester. Biological meshes are typically animal collagen, either from skin or bowel, but there are also human preparations. Biological meshes tend to be much more expensive and are thus reserved for specialist use.

It goes without saying that any mesh should have the usual properties of any implant, including being non-allergenic, non-carcinogenic, have good incorporation into tissue and mimic the tissue it is replacing or reinforcing. The abdominal wall is not a rigid structure, but regularly copes with increases in abdominal pressure on coughing and sneezing, etc. of up to 200 mmHg. The abdominal wall elasticity is greater in women than in men and is greater in the craniocaudal direction than transversely or obliquely. The traditional standard weight polypropylene mesh, of around 100 g/m
²
, is significantly over-engineered, with a burst strength at least an order of magnitude greater than the anterior abdominal wall and an elasticity of much less.
⁴
As a result there are now many polypropylene meshes on the market of lighter weight. There are no strict definitions of light weight and heavy weight but a reasonable guideline is that mesh of 40–80 g/m
²
is medium weight and < 40 g/m
²
is light weight. However, it is not just the weight of the mesh that imparts elasticity and flexibility. The weave of the strands in the mesh may impart varying flexibility or elasticity to the mesh in different directions of pull, so-called anisotropy. Pore size or the size of the large holes in the mesh is also important. Mesh has a volume with length, breadth and thickness. The amount of empty space within the ‘volume’ of the mesh is the porosity and the effective porosity is the amount of empty space within the volume of the mesh made up of holes that are bigger than 1 mm diameter. It has recently been proposed that an effective porosity of a mesh for hernia repair should be at least 60%.
⁵
Fibrosis will occur around each strand of the mesh. If the strands are close together, the fibrosis around each strand will coalesce together, forming a solid scar plate. As the scar plate matures it will shrink, reducing the overall size of the mesh. The minimum pore size should be about 1 mm
²
but many meshes have pore sizes around 3–5 mm. Increasing the macroporosity of the mesh produces a scar net, rather than a scar plate, with normal tissue in between the fibre/scar complex, reducing mesh/scar shrinkage and improving flexibility (
Fig. 4.1
). In addition to the macropore size, mesh also has micropores within the mesh material itself. These should be at least 10 μm in size. If the micropore size is smaller, bacteria can harbour in the pores out of reach of the larger inflammatory cells.

The majority of synthetic meshes in the UK are polypropylene. Gore-tex and other polytetrafluoroethylene (PTFE)-based meshes also have some popularity. PTFE has no macropores so will be encapsulated by fibrous tissue with minimal tissue ingrowth. Polyester-based meshes are gaining popularity and have some advantages over polyproplyene but are multifilament rather than monofilament. The multifilament arrangement increases the developed surface of the mesh (around 2000 mm
²
per cm
²
mesh as compared to 200 mm
²
per cm
²
for polypropylene) and thus improves tissue incorporation. As a result, the peel strength (the effort required to separate the mesh from the tissues once it is incorporated) is greater, in the region of 190 N as compared to 160 N for a polypropylene mesh (
Fig. 4.2
).

There is increasing evidence that lightweight, large pore mesh is of benefit to the patient.
⁶
Although there are some reports that suggest the recurrence rate may be higher
⁷
when such mesh is used, it is likely that this is due to technical reasons. Fixation sutures on such mesh should be placed at least 1 cm in from the edge of the mesh and slightly larger meshes may need to be used.

Traditional meshes placed within the abdominal cavity have a high rate of adhesions of the omentum and bowel to the mesh. This can result in bowel fistulation or make subsequent laparotomy more difficult, with increased risk of bowel perforation and thus the need for bowel resection during the process of re-entering the abdominal cavity.
⁸
A number of tissue-separating meshes are available, where the intra-abdominal side of the mesh is coated with a product to minimise adhesion formation. It would be fair to say that while such coatings do reduce adhesion formation, in the majority of patients significant adhesion to such coatings still occurs. The main points of adhesion appear to be the edge of the mesh and to the points of fixation, either sutures, tacks or staples. Nevertheless, it is likely that these products will improve in the future, as meshes become more physiological, perhaps impregnated with growth hormones and other biologically active molecules to improve the mesh/tissue integration.

Biological mesh (a slight misnomer as most biological meshes are really sheets of collagen) has gained popularity in hernia repair. It is, however, disappointing that, from the thousands of biological meshes that have been implanted worldwide (often at great expense as biological mesh is 10–100 times more expensive than polypropylene mesh), follow-up data on only just a few hundred patients have been published. What is becoming evident, though, is that biological meshes are not all the same. The major difference, in addition to the animal and anatomical source of the mesh, is the degree of chemical processing, or crosslinking, of the biological product. The more the collagen is crosslinked, the more resistant it is to bacterial collagenase breakdown in the presence of infection. The downside to crosslinking is that the more the collagen is crosslinked, the less tissue ingrowth and integration occurs, with reduction in potential strength to the repair. It is becoming evident that most biological meshes have no role in dirty wounds, acting as little more than a very expensive dressing. They are too expensive for use in clean wounds as any benefit is not worth the huge price difference, and using them for bridging (mesh spanning the fascial gap as opposed to augmentation, where the mesh reinforces or augments the fascial closure) also results in a high percentage of failure. The author's opinion is that there is no good evidence available to suggest that biological mesh is superior or even as good as polypropylene in clean/contaminated operations. Similarly, there is a lack of comparative evidence in contaminated operations, although fortunately this is a very small part of hernia surgery.