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251
21. Evolution of Incisional and Ventral Hernia Repair
References
1. Flum DR, Horvath K, Koepsell T. Have outcomes of incisional hernia repair improved
with time? A population-based analysis. Ann Surg. 2003;237(1):129–35.
2. Harth K, Rosen MJ. Repair of ventral abdominal wall hernias. In: Souba WW, Fink
MP, Jurkovich GJ, Kaiser KR, Pearce WH, Pemberton JH, Soper NJ, editors. ACS
surgery: principles and practice. New York: WebMD Professional Publishing; 2007.
3. Diener MK, Voss S, Jensen K, Büchler MW, Seiler CM. Elective midline laparotomy
closure: the INLINE systematic review and meta-analysis. Ann Surg.
2010;251(5):843–56.
4. Brown SR, Tiernan J. Transverse versus midline incisions for abdominal surgery.
Cochrane Database of Syst Rev. 2005;(4):CD005199. DOI: 10.1002/14651858.
CD005199.pub2 .
5. Bevis PM, Windhaber RA, Lear PA, Poskitt KR, Earnshaw JJ, Mitchell DC.
Randomized clinical trial of mesh versus sutured wound closure after open abdominal
aortic aneurysm surgery. Br J Surg. 2010;97(10):1497–502.
6. Harissis HV, Douitsis E, Fatouros M. Incarcerated hernia: to reduce or not to reduce?
Hernia. 2009;13(3):263–6.
7. Nuttall HCW. Rectus transplantation in the treatment of ventral herniae. Br Med J.
1926;1(3395):138–39.
8. Ramirez OM, Ruas E, Dellon AL. “Components separation” method for closure of
abdominal-wall defects: an anatomic and clinical study. Plast Reconstr Surg.
1990;86(3):519–26.
9. Usher FC, Fries JG, Ochsner JL, Tuttle Jr LL. Marlex mesh, a new plastic mesh for
replacing tissue defects. II. Clinical studies. AMA Arch Surg. 1959;78:138–45.
10. Shankaran V, Weber DJ, Reed 2nd RL, Luchette FA. A review of available prosthetics
for ventral hernia repair. Ann Surg. 2011;253(1):16–26.
11. Read RC. Milestones in the history of hernia surgery: prosthetic repair. Hernia.
2004;8:8–14.
12. Luijendijk RW, Hop WC, van den Tol MP, de Lange DC, Braaksma MM, IJzermans
JN, Boelhouwer RU, de Vries BC, Salu MK, Wereldsma JC, Bruijninckx CM, Jeekel J.
A comparison of suture repair with mesh repair for incisional hernia. N Engl J Med.
2000;343(6):392–8.
13. Burger JW, Luijendijk RW, Hop WC, Halm JA, Verdaasdonk EG, Jeekel J. Long-term
follow-up of a randomized controlled trial of suture versus mesh repair of incisional
hernia. Ann Surg. 2004;240(4):578–83. discussion 583–5.
14. Hawn MT, Snyder CW, Graham LA, Gray SH, Finan KR, Vick CC. Long-term
follow-up of technical outcomes for incisional hernia repair. J Am Coll Surg.
2010;210(5):648–55. 655–7.
15. Gray SH, Vick CC, Graham LA, Finan KR, Neumayer LA, Hawn MT. Variation in
mesh placement for ventral hernia repair: an opportunity for process improvement?
Am J Surg. 2008;196(2):201–6. Epub 2008 May 29.
16. Hawn MT, Snyder CW, Graham LA, Gray SH, Finan KR, Vick CC. Hospital-level
variability in incisional hernia repair technique affects patient outcomes. Surgery.
2011;149(2):185–91.
252
M.D. Sur and L.B. Katz
17. Itani KMF, Hur K, Kim LT, Anthony T, Berger DH, Reda D, Neumayer L, for the
Veterans Affairs Ventral Incisional Hernia Investigators. Comparison of laparoscopic
and open repair with mesh for the treatment of ventral incisional hernia: a randomized
trial. Arch Surg. 2010;145(4):322–8.
18. Bansal VK, Misra MC, Kumar S, Rao YK, Singhal P, Goswami A, Guleria S, Arora
MK, Chabra A. A prospective randomized study comparing suture mesh fi xation
versus tacker mesh fi xation for laparoscopic repair of incisional and ventral hernias.
Surg Endosc. 2011;25(5):1431–8.
19. Greenstein AJ, Nguyen SQ, Buch KE, Chin EH, Weber KJ, Divino CM. Recurrence
after laparoscopic ventral hernia repair: a prospective pilot study of suture versus tack
fi xation. Am Surg. 2008;74(3):227–31.
20. LeBlanc KA, Whitaker JM, Bellanger DE, Rhynes VK. Laparoscopic incisional and
ventral hernioplasty: lessons learned from 200 patients. Hernia. 2003;7(3):118–24.
21. Shah RH, Sharma A, Khullar R, Soni V, Baijal M, Chowbey PK. Laparoscopic repair
of incarcerated ventral abdominal wall hernias. Hernia. 2008;12(5):457–63.
22. Candage R, Jones K, Luchette FA, Sinacore JM, Vandevender D, Reed 2nd RL. Use of
human acellular dermal matrix for hernia repair: friend or foe? Surgery. 2008;144(4):
703–9. discussion 709–11.
253
B.P. Jacob and B. Ramshaw (eds.), The SAGES Manual of Hernia Repair,
DOI 10.1007/978-1-4614-4824-2_22,
© Springer Science+Business Media New York 2013
22. Tissue Ingrowth: The Mesh–Tissue
Interface: What Do We Know So Far?
Gregory J. Mancini and A. Mariah Alexander
For any given hernia patient, the primary challenge is for the surgeon
to utilize a technique and a prosthetic choice (given the anatomy,
intraoperative fi ndings, and defect size) that combined will provide the
best overlap and optimize the surface area of the mesh/tissue interface.
Due to the importance of tissue ingrowth at this mesh/tissue interface
(MTI) in preventing recurrence, the MTI may very well be the most
important aspect involved with a hernia repair. Examining the
prosthetics used in hernia surgery has only recently garnered attention in
the literature. The title itself infers a challenge to a long-held axiom that
the mesh materials are inert in the human body. Any general surgeon
who has had the opportunity to operate in a mesh-occupied surgical fi eld
can validate that the material explanted often has little in common with
the original material implanted. Questions persist about what is happening
at the mesh–tissue interface after the material is surgically placed. This
chapter will focus in the interactions of prosthetic mesh material with the
host tissues in the dynamics of hernia surgery.
Background: History of Mesh Implants
Early modern records of hernia repair show Witzel and Geopel utilizing
gold and silver wires interwoven in a fi ligree pattern and implanted as a
prosthetic mesh. Gold and silver fi ligree materials gave way to stainless
steel mesh in the 1940s. The plastics revolution of the 1950s and 1960s
provided the early building block for mesh materials still widely used
today: polypropylene, polyester, and polytetra fl uoroethylene (PTFE)
mesh. Polyester was knitted into braided mesh fabric in the 1950s and
become the fi rst multi fi lament, macroporous, nonmetallic mesh to be
254
G.J. Mancini and A.M. Alexander
widely adopted in hernia repair. Dr. Francis Usher is widely credited with
the development of surgical polypropylene. He published his fi ndings in
JAMA in 1962 regarding a new synthetic, nonabsorbable, mono fi lament
mesh used to close contaminated wounds [
1 ] . This polypropylene
mono fi lament was later woven for mesh production. W.L. Gore developed
the process of expanding PTFE (ePTFE) to create a soft, fl exible, and
durable microporous sheet mesh that gained broad application in
laparoscopic ventral hernia repair in the 1990s. These three mesh materials
account for over 90% of the mesh market worldwide.
The Ideal Situation
Hernias occur because of a mismatch between the regional strength of
the abdominal wall fascia and the tensile forces generated during active
living. Ideally, any material or technique used in hernia repair would shift the
balance in favor of abdominal wall integrity. The high recurrence rates
observed in primary suture repair techniques motivated surgeons to look into
permanent implantable material. The material would have optimal tensile
strength to bolster the integrity of the abdominal wall and withstand the
stressors of vigorous physical activities. Yet it would remain as soft, fl exible,
compliant, and as dynamic as the muscles and fascia that the material
supports. Additionally the material would be inexpensive, easily sterilized,
chemically inert, noncarcinogenic, and hypoallergenic. Creating the ideal
hernia material poses a tremendous challenge to our biomedical engineers
and industry partners. Options include synthetic nonabsorbable materials,
synthetic absorbable materials, and nonsynthetic or biologic materials.
Current State of the Art
Realistically, the ideal mesh has yet to be created. Many of the
synthetic mesh materials available today ful fi ll much of the requirements
outlined, so much so that prosthetic mesh is used in the vast majority
hernia repairs worldwide. The widespread utilization of mesh combined
with the prevalence of hernia disease has allowed surgeons to observe
the shortcomings of these materials. Hernia recurrence became an
accepted consequence of primary suture repair herniorrhaphy. The mesh
era introduced lower hernia recurrence rates along with unforeseen and
255
22. Tissue Ingrowth: The Mesh–Tissue Interface
unexpected new problems. Mesh infections, erosions, migration, and
loss of biocompliance, though rare occurrences, have been seen with
nearly every type of prosthetic material used in hernia surgery (Figs. 22.1 ,
22.2 , 22.3 , and 22.4 ). Recent mesh explant studies by Ramshaw et al.
have begun to characterize the chemical and mechanical alterations that
Fig. 22.1. Explanted ePTFE/polypropylene composite mesh after failed hernia
repair shows mesh contraction.
Fig. 22.2. Explanted intra-abdominal mesh material with erosion into the small
bowel visceral.
256
G.J. Mancini and A.M. Alexander
Fig. 22.3. CT scan of the abdomen shows retraction of the mesh implant from
the left rectus muscle of abdominal wall allowing hernia recurrence.
Fig. 22.4. Explanted polypropylene mesh material that shows dense fi brosis
within the surrounding soft tissue.
257
22. Tissue Ingrowth: The Mesh–Tissue Interface
the mesh undergoes in vivo [ 2 ] . There is a puzzling disconnect between
the millions of well-healed mesh hernia repairs and the poorly tolerated
but well-documented mesh repair complications.
Host Response to Foreign Material
A fundamental principle of prosthetic implant use in hernia surgery
is that the host response to the material has a common in fl ammatory
pathway. The phases of normal wound healing, hemostasis, in fl ammation,
proliferation, and remodeling, are well understood. What is less well
understood is how wound healing is affected by the presence of a
prosthetic mesh implant. Assertions that synthetic materials have inert
characteristics have been shown to be less than true [ 3– 5 ] . The implant
undergoes an assault by the host immune response, fi rst, as a bystander
in the acute phase and then chronically as it is recognized as nonself.
Incorporation begins at the time of implantation. Tissue trauma
occurs during the process of hernia repair, such that acute phase reactants
are recruited to the injury site. The implant is subjected to the neutrophil
and macrophage oxidative stress that can begin the chemical alteration of
the implant. It is unlikely, due to the short duration, that the mesh
experiences signi fi cant chemical or mechanical alterations occurring in
this phase of wound healing.
As the tissues begin to heal, the normal transition to fi broblast recruitment
and collagen deposition is disrupted by a chronic foreign body response. A
cell-mediated chronic in fl ammatory reaction to the implant chemo-attracts
T cells and more macrophages. At this phase, the macrophages assume an
activated morphology producing abundant amounts of hydrolytic enzymes
that further chemically alter the mesh material [ 6– 8 ] .
The chronic immune response to the mesh is focused at the implant–
host interface. This is only part of the healing process underway in at the
surgical site. Around the implant, normal revascularization occurs with
development of granulation tissue and collagen remodeling. The amount
of chemical alteration of the mesh and the degree of collagen disruption
seen at the implant–host interface depends both on the properties of the
mesh implant and the individual host immune system. The variety of
mesh products combined with wide variance in the host immune response
may account for the broad spectrum of observations seen in clinical
practice [ 9– 11 ] .
258
G.J. Mancini and A.M. Alexander
In summary, at the host–implant interface, two major processes are
taking place. The host reaction to the prosthetic causes a chemical change
in the material that can lead to mechanical changes such as mesh
shrinkage, stiffening, and fracture. Likewise, the prosthetic causes a
chronic host response that disrupts collagen deposition and remodeling
process that may lead to tissue scari fi cation, contracture, or encapsulation.
The subsequent sections of this chapter will look at how different
prosthetic materials, different surgical techniques, and different patient
characteristics may alter this common in fl ammatory pathway.
Material Basics
Polypropylene mesh begins as mono fi lament that synthesized through
a controlled polymerization of propylene chains. The mono fi lament is
then woven in to a mesh implant. Different proprietary weave techniques
account for the wide variety of commercial products in the marketplace.
Inspection of the macrostructure of the mesh reveals polypropylene
implants with different material weight, pore size, tensile strength,
and fl exibility. At a molecular level, all polypropylene meshes share a
common morphology. The propylene chains are carbon backbone with
hydrogen and methyl side chains. Degradation occurs when free radicals
and oxygen attack the methyl groups creating chain fractures and cross-
links [ 12 ] . Additionally, aldehydes and carboxylic acid are produced as
chemical by-products. Evidence of this happening in vivo comes from
Cozad et al. explant study. The materials were harvested and then tested
utilizing spectral and thermal analysis [ 2 ] .
Polyethylene terephthalate (PET) is a synthetic polyester polymer
created by combining ethylglycol and terephthalic acid. Like
polypropylene, polyester is a created by polymerization of a base
monomer into long chains. Similarly, polyester has a carbon backbone.
The ester side chains of polyester con fi rm differently the surface
interactions as compared to polypropylene materials. Polyester has
hydrophilic properties that attract water molecules to its surface. In
biologic systems, polyester’s hydrophilic properties may insulate the
implant from the oxidative stresses generated in the host immune
response. Cozar’s synthetic mesh explant study showed that polyester
mesh experiences both chemical and mechanical degradation in vivo.
Concerns that the braided and woven pattern of polyester mesh may
provide a greater surface area for bacterial colonization have been
259
22. Tissue Ingrowth: The Mesh–Tissue Interface
disproven. An animal study in which polyester mesh was intentionally
inoculated with bioluminescent staphylococcus at the time of implantation
showed signi fi cant clearance by postoperative day one [ 13 ] .
PTFE is essentially a long-carbon chain backbone with fl uoride
atoms as side groups. The carbon–carbon and carbon– fl uoride covalent
bonds of this compound provide chemical and mechanical stability.
Expanded polytetra fl uoroethylene (ePTFE) used in implants is made in a
proprietary process by combining PTFE nodes that are interconnected by
PTFE fi brils. ePTFE’s synthetic manufacturing process yields a
microporous sheet of material that has air spaces between the PTFE
nodes allowing for air fl ow but hydrophobic making it waterproof.
Though chemically stable, in vivo studies have shown mechanical
changes in ePTFE. Schoenmaeckers et al. looked at ePTFE shrinkage
after laparoscopic ventral hernia repair in 40 patients. Surface area
shrinkage rates observed ranged from 0 to 24%, with a mean of 7.5%
after an average 17.9 months after implantation [ 14 ] .
Mesh Weight (Density)
The concept of mesh weight or density has mainly pertained to
discussions about polypropylene mesh. Hernia recurrence with this
material appeared to be related to mesh contraction or shrinkage allowing
separation from the fascial edge. The early heavyweight polypropylene
mesh contains 80 g/m
2
of polypropylene and provided tensile strengths
of 90 N/cm. Tensiometry studies showed that this mesh product had
tensile strengths logarithmically greater than that of healthy fascia (12–
16 N/cm). Conversely, newly designed lightweight mesh contains 30 g/
m
2
of polypropylene and provides 30–40 N/cm of tensile strength. As
data emerged about chronic host response causing mechanical changes
in the mesh, a new concept evolved. Less synthetic material would elicit
less host in fl ammation, a thereby reduced mesh contraction [ 15, 16 ] .
This concept of the impact of mesh weight on mesh contraction has not
been applied to PET of ePTFE.
Mesh Pore Size
Good integration into the host tissue is a desired quality of a hernia
material. The pores within the mesh allow for host collagen deposition,
thereby strengthening the integration of the mesh to the abdominal wall.
260
G.J. Mancini and A.M. Alexander
This concept is why most all hernia implants utilize a woven mesh
design. Early polypropylene and polyester mesh materials were often
constructed by large fi bers interlocked by tight weaves, making small
pore sizes of less than 1 mm (1,000 microns). Despite this small pore
size, early polypropylene and polyester meshes are still considered
macroporous. Newer polyester and polypropylene materials are woven
with smaller fi bers or mono fi laments and use a looser weave patterns that
provide larger pore sizes [ 17, 18 ] .
This contrasts with ePTFE that has an average pore size of 3 microns,
making it microporous. In comparison, the average size of a platelet is 3
microns, a water droplet is 10 microns, a macrophage is 21 microns, and
a fi broblast is 30 microns. The microporous structure of ePTFE limits
the depth of cellular in fi ltration within the material and thereby limits the
degree of tissue incorporation. This attribute can be favorable when
the mesh is implanted near anatomic structures, like intestinal serosa,
where tissue ingrowth is not desired. The chronic foreign body response
is limited to the ePTFE surface which produces a dense, collagen-rich
fi brous capsule. Studies on larger pore (30–90 micron) ePTFE implants
are in progress to assess if mesh encapsulation can be converted to mesh
integration [ 19 ] .
Animal Experimentation of Mesh–Tissue Interface
While there may not be one “best” product, animal experiments at the
very least have proven that the products indeed are NOT created equal.
Animal studies have helped show that the tissue ingrowth begins early
and increases in strength over time. In a porcine laparoscopic ventral
hernia model, Majercik et al. [ 20 ] demonstrated that the bulk of tissue
ingrowth occurs during the fi rst 2 weeks after inserting a polypropylene
mesh, and by 4 weeks, the strength of the ingrowth had already reached
a strength equivalent to 95% of the peak strength seen at 12 weeks. By
fi xing sheets of polypropylene and ePTFE composite mesh to the
abdominal walls and then harvesting them at different time intervals (2,
4, 6, and 12 weeks), the authors were able to demonstrate a peel strength
of 0.83 pounds at 2 weeks, of 1.06 pounds at 4 weeks, and 1.13 pounds
at 12 weeks (5 N). Histologic examination of specimens showed complete
cellular in fi ltration into and through the entire layer of the polypropylene
up to the ePTFE layer. This study, which looked at the peel strength of
the polypropylene layer used in a heavyweight polypropylene/ePTFE