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401
34. Chronic Mesh Infections
different immune response, causing fi broblast ingrowth, fi brin deposition,
and mesh contraction at different rates depending on the layer. As the
two layers of mesh contract at different rates, the layers tend to delaminate
despite sutures securing them together. The mesh delamination creates a
dead space between the mesh layers that may be prone to infection.
Furthermore, the delamination may expose adhesiogenic polypropylene
mesh to the bowel, that could lead to fi stula formation.
Mesh coatings such as carboxymethylcellulose-sodium hyaluronate
are highly hydrophilic and have been demonstrated in vitro to separate
from the less hydrophilic polypropylene mesh. This leads to an increase
in bacterial adherence compared to uncoated mesh [ 8 ] .
Microbiology
Infection of a bioprosthesis by bacteria is dependent upon the ability
of bacteria to adhere to mesh. While surface characteristics of the
prosthetic play a role, adhesion is partly a function of the hydrophobicity
and hydrophilicity of the microorganism itself [ 8 ] . For example, a
hydrophobic organism such as Staphylococci binds with dif fi culty to a
hydrophilic surface [ 9 ] . Gram-negative bacteria such as Escherichia coli
and Pseudomonas aeruginosa bind with dif fi culty to hydrophobic mesh
such as PTFE [ 10 ] .
The source of the bacterial inoculation is frequently skin fl ora, either
from contamination during the time of mesh placement or from
postoperative wound complications. Staphylococcus species, including
methicillin-sensitive Staphylococcus aureus (MSSA), methicillin-
resistant Staphylococcus aureus (MRSA), Staphylococcus epidermidis ,
and Streptococcus species including group B organisms are common
isolates. Skin fl ora that produce bio fi lms on the prosthetics, such as S.
epidermidis , are particularly dif fi cult to eradicate, and are often the
reason for the chronic nature of the mesh infection. Antibiotic therapy
with a fi rst-generation cephalosporin or vancomycin may be useful in
conjunction with surgical drainage or mesh explantation.
Gram-negative bacteria, including Enterobacteriaceae and anaerobic
bacteria are less common isolates. Potential sources of contamination
include direct contamination from wound infections, intra-abdominal
infections or fi stulae, or rarely hematogenous seeding. Rarely, fungal or
atypical organisms can cause chronic mesh infections.
402
A. Churyla and A.B. Lederman
Management
Chronic mesh infections have an indolent presentation without signs
of systemic infection. This allows for careful planning to control
infection, remove unsalvageable mesh, resect gastrointestinal fi stulae,
and repair any resulting hernia. The standard for chronic mesh infection
is mesh explantation and reconstruction. Prior to surgery, any cellulitis or
acute abscess is controlled with antibiotics and drainage as necessary.
Suspected fi stulae may be studied with CT or sinogram to demonstrate
the anatomy. The operative approach generally involves resection of
sinus tracts, removing the infected mesh, and reconstructing the
abdominal wall. Chronic gastrointestinal fi stulae are resected, and an
anastomosis can usually be safely created as long as the patient has fully
recovered from previous abdominal surgery and has a good nutrition
status. Reconstruction of the abdominal wall is often the most dif fi cult
task and may be accomplished with primary closure or component
separation techniques. Biologic mesh may be useful as an adjunct to
reinforce the tissue repair. Implantation of a prosthetic is not recommended
due to the high risk of recurrent infection. Delayed closure after mesh
explantation is also reported, utilizing negative pressure wound therapy
(NPWT) or other wound care techniques as an interim.
Mesh salvage has also been reported but has limited success. This
approach uses long-term antibiotic therapy, minimal debridement of
visibly infected tissue or mesh, and often NPWT. Mesh salvage is only
possible when infection is limited and the majority of mesh is incorporated
into the abdominal wall. Although there are case reports of successful
mesh salvage of PTFE, since PTFE is microporous and tends to have
limited incorporation, it is much less likely to be successfully treated
nonoperatively when compared to macroporous mesh.
Percutaneous drainage, open drainage, or serial debridements are
usually necessary in order to achieve success with mesh salvage. These
patients can usually be managed as an outpatient and rarely require
inpatient care or procedures. There are several reports that describe good
outcomes with long-term antibiotic irrigation of infected sinus tracts or
cavities with mesh involvement [ 11 ] . The local or topical application of
high-concentration antibiotics may help with mesh salvage.
The salvage of chronically infected mesh is only possible in certain
circumstances [ 12 ] . The infection needs to be isolated to a small portion
of the mesh, not involving the entire mesh. Macroporous mesh that
allows for greater encapsulation with scar has a higher rate of mesh
403
34. Chronic Mesh Infections
salvage than microporous mesh. While there are case reports of PTFE
salvage, the lack of incorporation of PTFE into tissue generally precludes
mesh salvage.
References
1. Grant AM. Open mesh versus non-mesh repair of groin hernia: meta-analysis of
randomized trials based on individual patient data [corrected]. Hernia. 2002;6:130–6.
2. Birolini C, Utiyama EM, Rodrigues Jr AJ, Birolini D. Elective colonic operation and
prosthetic repair of incisional hernia: does contamination contraindicate abdominal
wall prosthesis use? J Am Coll Surg. 2000;191:366–72.
3. Leber GE, Garb JL, Alexander AI, Reed WP. Long-term complications associated
with prosthetic repair of incisional hernias. Arch Surg. 1998;133:378–82.
4. Mann DV, Prout J, Havranek E, et al. Late-onset deep prosthetic infection following
mesh repair of inguinal hernia. Am J Surg. 1998;176:12–4.
5. Taylor SG, O’Dwyer PJ. Chronic groin sepsis following tension-free inguinal
hernioplasty. Br J Surg. 1999;86:562–5.
6. Amid PK, Shulman AG, Lichtenstein IL, et al. Biomaterials for abdominal wall hernia
surgery and principles of their applications. Langenbecks Arch Surg. 1994;379:168–71.
7. Demiter S, Gecim IE, Aydinuraz K, et al. Af fi nity of Staphylococcus epidermidis to
various prosthetic graft materials. J Surg Res. 2001;99:70–4.
8. Aydinuraz K, Agalar C, Agalar F, et al. In vitro S. epidermidis and S. aureus adherence
to composite and lightweight polypropylene grafts. J Surg Res. 2009;157:e79–86.
9. Reifsteck F, Wee S, Wilkinson BJ. Hydrophobicity—hydrophilicity of staphylococci.
J Med Microbiol. 1987;24:65–73.
10. Engelsman AF, Gooitzen MD, van der Mei HC, et al. In vivo evaluation of bacterial
infection involving morphologically different surgical meshes. Ann Surg.
2010;251(1):133–7.
11. Trunzo JA, Ponsky JL, et al. A novel approach for salvaging infected prosthetic mesh
after ventral hernia repair. Hernia. 2009;13:545–9.
12. http://sageswiki.org/index.php?title=Use_of_synthetic_mesh_in_the_infected_ fi eld .
Accessed 5 July 2011.
405
B.P. Jacob and B. Ramshaw (eds.), The SAGES Manual of Hernia Repair,
DOI 10.1007/978-1-4614-4824-2_35,
© Springer Science+Business Media New York 2013
35. Adhesions After Lap Ventral:
Do They Matter?
Dennis L. Fowler
The Incidence and Consequences
of Intra-abdominal Adhesions
Intra-abdominal adhesions are the cause of signi fi cant morbidity and
mortality. Beyond the technical challenge posed by adhesions, they cause
enormous human suffering and cost to society. In 1994, a comprehensive
report based on the National Hospital Discharge Survey indicated that
303,836 patients underwent adhesiolysis [ 1 ] . These procedures were
associated with 846,415 inpatient days and incurred $1.3 billion in
hospital and surgeon costs. Ten years later, those numbers had increased
slightly. In 2004, more than 342,000 patients underwent adhesiolysis [ 2 ] .
Many other patients who did not require adhesiolysis were admitted to
the hospital with either a bowel obstruction or complaints of pain caused
by adhesions. Many other patients are af fl icted with infertility caused by
adhesions [ 3– 5 ] .
In addition to the human and fi nancial cost of treating conditions that are
caused by adhesions, they are commonly the cause of adverse consequences
during surgery for conditions unrelated to the adhesions themselves. The
presence of adhesions increases the chance of converting a laparoscopic
operation to an open operation, increases the time required to enter the
abdomen, and is the primary cause of bowel injury at the time of trocar
insertion during laparoscopic surgery [ 6 ] . In short, adhesions are frequently
the cause of a signi fi cant technical complication during an operation.
Although any condition inciting an in fl ammatory response may cause
intra-abdominal adhesions, by far, the most common cause of adhesions is
previous surgery. Until the late twentieth century, surgeons performed
essentially all abdominal surgery with an open laparotomy, and up to 95%
of patients who undergo a laparotomy develop adhesions [ 7, 8 ] . Depending
406
D.L. Fowler
on the underlying disease and the nature of the procedure at the time of the
primary surgical procedure, up to 30% of patients will develop a bowel
obstruction secondary to adhesions after a laparotomy. [
9 ] After any colon
resection, patients have a 5–10% chance of an adhesion-related admission
within 5 years, and the incidence of adhesion-related admission within
5 years after proctocolectomy is 15.4% [
10, 11 ] .
The size and orientation of the laparotomy incision may be factors in
the development of adhesions, but there is no reliable method to prevent
adhesions during surgery [ 12 ] . Anecdotal experience and some initial
observational studies suggested that laparoscopic surgery resulted in
fewer and less severe adhesions than those caused by laparotomy [ 13 ] ;
however, other studies regarding adhesions after colorectal surgery
suggest that the incidence of adhesions is not signi fi cantly different
between open and laparoscopic colectomy [ 14 ] .
Some of the important factors that increase the likelihood of extensive
adhesion formation include ischemia, surgical trauma, in fl ammation,
hemorrhage, thermal injury, and reactions to foreign bodies [ 15 ] . Although
foreign bodies such as gloves, powders, sutures, sponges, and irrigating
solutions all incite a response that can lead to adhesion formation, the
foreign body of most concern in this discussion is hernia mesh.
Prosthetic Mesh as a Cause of Adhesions
Most surgeons have seen extensive, dense adhesions between
polypropylene mesh and viscera at the time of re-exploration in patients
with previously placed intraperitoneal mesh. Because these fi ndings
often led to dif fi cult operations and sometimes caused complications,
surgeons became reluctant to place mesh intraperitoneally. The occasional
occurrence of these extremely dif fi cult situations has led to attempts to
develop mesh that would incite fewer adhesions. The main concern on
reoperation after previous intra-abdominal mesh placement is the
ingrowth that can occur between the viscera and a macroporous mesh.
Adherence (adhesions) without ingrowth results in minimal to moderate
effort to lyse the adhesions. But, with ingrowth, the mesh may need to be
cut off of the abdominal wall, or a bowel resection may need to be
performed to complete an operation. In rare cases, ingrowth may also
lead to fi stula or abscess formation.
There is no widely accepted method for determining the extent and
density of adhesions in the peritoneal cavity short of abdominal
407
35. Adhesions After Lap Ventral: Do They Matter?
exploration. Because it is unethical to subject patients to repeat laparotomy
or laparoscopy simply to explore for the presence of adhesions,
investigators cannot conclusively determine the extent and density of
adhesions formed after mesh placement. We really only know the extent
of adhesion formation in the small, but signi fi cant, percent of patients
who require a repeat operation after mesh placement. For this reason, to
evaluate meshes that were designed to prevent adhesions, investigators
have documented for several types of new meshes the extent and density
of adhesion formation at either laparoscopy or necropsy in several animal
studies [ 16– 27 ] .
These studies typically compare the extent and severity of adhesion
formation after placement of a composite mesh (two layers) or coated
mesh (single layer) with the extent and severity of adhesion formation
after placement of a single-layer uncoated mesh, usually polypropylene.
The composite mesh is designed to enable excellent tissue ingrowth into
one layer while preventing adhesion formation and/or ingrowth into the
other layer. The layer designed to lie against the abdominal wall is called
the parietal layer, and the layer designed to lie against the omentum or
viscera is called the visceral layer.
The parietal layer is usually a porous synthetic mesh with interstices
into which the body can grow. The porous layer should enable fi rm
incorporation of the mesh into the parietes. The visceral layer is
microporous, usually either expanded polytetra fl uoroethylene (ePTFE)
or an anti-adhesive material such as a hydrophilic anti-adhesive
collagen layer, a hyaluronate/carboxymethylcellulose combination, or
polyvinylidene fl uoride although other materials have also been tested.
A coated mesh is a single-layer mesh that is coated with a material to
prevent adhesions, such as a hydrogel.
Most studies in the animals documented tissue ingrowth into the
parietal layer of the composite or coated mesh that was equivalent to
ingrowth into plain polypropylene but with fewer and less dense adhesions
to the visceral layer than to plain polypropylene. Based on the results of
animal studies, surgeons often choose a composite mesh hoping that fewer
serious adhesions will form. However, there are no human studies
con fi rming this. Despite the belief that the composite meshes cause fewer
intraperitoneal adhesions, there continues to be occasional anecdotal
reports of serious adhesions caused by composite meshes [ 28 ] (Fig. 35.1 ).
Some investigators have reported successful identi fi cation and
documentation of the location and density of intraperitoneal adhesions
with the use of abdominal ultrasound [ 29 ] ; however, not all investigators
have found the use of ultrasound to accurately identify adhesions.
408
D.L. Fowler
Conclusions
There is no experimental evidence from human studies that one mesh
is better than another, despite evidence in animal studies that some
meshes incite fewer and less dense adhesions. However, the severity of
the adhesion problem is clear, and the role of mesh in the formation of
adhesions is clear. Based on the evidence from animal studies and solid
theoretical reasons, the use of a composite mesh with an anti-adhesive
layer seems appropriate when hernia repair requires intraperitoneal mesh
[ 30 ] .
Summary
Adhesions are a serious and very signi fi cant cause of morbidity and
mortality in the USA. Many synthetic mesh products incite extensive and
dense adhesion formation in the abdominal cavity if placed
intraperitoneally. Because it is necessary to use mesh in many patients
who require hernia repair, it is theoretically and experimentally desirable
to use a mesh designed to reduce adhesion formation if intraperitoneal
placement of mesh is necessary.
Fig. 35.1. Intraoperative photograph showing dense adhesions between a composite
mesh and the small intestine.
409
35. Adhesions After Lap Ventral: Do They Matter?
References
1. Ray NF, Denton WG, Thamer M, et al. Abdominal adhesiolysis: inpatient care and
experience in the Unites States in 1994. JACS. 1998;186:1–9.
2. DeFrances CJ, Podgornik MN. 2004 National hospital discharge survey. Advance data
from vital and healthc statistics; no 371. Hyattwsville, MD: National Center for Health
Statistics. 2006.
3. Latenser B. Commentary (A novel hydrogel-coated polyester mesh prevents post-
surgical adhesions in a rat model). J Surg Res. 2011;166:73–4.
4. Judge TW, Parker DM, Dinsmore RC. Abdominal wall hernia repair: a comparison of
Sepramesh and Parietex composite mesh in a rabbit hernia model. J Am Coll Surg.
2007;204:76.
5. Emans PJ, Schreinemacher MH, Gijbels MJ, et al. Polypropylene meshes to prevent
abdominal herniation. Can stable coatings prevent adhesions in the long term? Ann
Biomed Eng. 2009;37:410.
6. van Goor H. Consequences and complications of peritoneal adhesions. Colorectal Dis.
2007;2:25–34.
7. Lower AM, Hawthorn RJ, Ellis H, O’Brien F, Buchan S, Crowe AM. The impact of
adhesions on hospital readmissions over ten years after 8849 open gynaecological
operations: an assessment from the Surgical and Clinical Adhesions Research Study.
BJOG. 2000;107(7):855–62.
8. Fukuhira Y, Ito M, Kakenko H, et al. Prevention of postoperative adhesions by a novel
honeycomb-patterned poly(lactide) fi lm in a rat experimental model. J Biomed Mater
Res B Appl Biomater. 2008;86B:353.
9. Ellis H, Moran BJ, Thompson JN, et al. Adhesion-related hospital readmissions after
abdominal and pelvic surgery: a retrospective cohort study. Lancet. 1999;353(9163):
1476–80.
10. Parker MC, Wilson MS, Menzies D, et al. The SCAR-3 study: 5-year adhesion-related
readmission risk following lower abdominal surgical procedures. Colorectal Dis.
2005;7(6):551–8.
11. Parikh JA, Ko CY, Magard MA, et al. What is the rate of small bowel obstruction after
colectomy? Am Surg. 2008;74:1001–5.
12. van der Wal JBC, Lordens GIT, Vrijland WW, et al. Adhesion prevention during
laparotomy. Ann Surg. 2011;253(6):1118–21.
13. Barmparas G, Branco BC, Schnuriger B, et al. The incidence and risk factors of post-
laparotomy adhesive small bowel obstruction. J Gastrointest Surg. 2010;14:1619–28.
14. Khury E, Schwenk W, Gaupset R, et al. Long-term outcome of laparoscopic surgery
for colorectal cancer: a Cochrane systematic review of randomized controlled trials.
Cancer Treat Rev. 2008;34:498–504.
15. Liakakos T, Thomakos N, Fine P, et al. Peritoneal adhesions: etiology, pathophysiology,
and clinical signi fi cance. Dig Surg. 2001;18:260–73.
16. Goldberg JM, Toledo AA, Mitchell DE. An evaluation of the Gore-Tex surgical
membrane for the prevention of postoperative peritoneal adhesions. Obstet Gynecol.
1987;70(6):846–8.
410
D.L. Fowler
17. Duffy AJ, Hogle NJ, LaPerle KM, et al. Comparison of two composite meshes using
two fi xation devices in a porcine laparoscopic ventral hernia repair model. Hernia.
2004;8:358–64.
18. McGinty JJ, Hogle NJ, McCarthy H, et al. A comparative study of adhesion formation
and abdominal wall ingrowth after laparoscopic ventral hernia repair in a porcine
model using multiple types of mesh. Surg Endosc. 2005;19(6):786–90.
19. Gonzalez R, Rodeheaver GT, Moody DL, et al. Resistance to adhesion formation: a
comparative study of treated and untreated mesh products placed in the abdominal
cavity. Hernia. 2004;8:213–9.
20. Harrell AG, Novitsky YW, Peindl RD, et al. Prospective evaluation of adhesion
formation and shrinkage of intra-abdominal prosthetics in a rabbit model. Am Surg.
2006;72(9):808–13.
21. Novitsky YW, Harrell AG, Cristiano JA, et al. Comparative evaluation of adhesion
formation, strength of ingrowth, and textile properties of prosthetic meshes after long-
term intra-abdominal implantation in a rabbit. J Surg Res. 2007;140(1):6–11.
22. Jacob B, Hogle NJ, Durak E, et al. Tissue ingrowth and bowel adhesion formation in
an animal comparative study: polypropylene vs. Proceed
®
vs. Parietex Composite
®
.
Surg Endosc. 2007;21(4):629–33.
23. Novitsky YW, Harrell AG, Hope WW, et al. Meshes in hernia repair. Surg Technol Int.
2007;16:123–7.
24. Gruber-Blum S, Petter-Puchner AH, Brand J, et al. Comparison of three separate
antiadhesive barriers for intraperitoneal onlay mesh hernia repair in an experimental
model. Br J Surg. 2010;98:442–9.
25. Fortelny RH, Petter-Puchner AH, Glaser KS, et al. Adverse effects of polyvinylidene
fl uoride-coated polypropylene mesh used for laparoscopic intraperitoneal onlay repair
of Incisional hernia. Br J Surg. 2010;97:1140–5.
26. Letter 1 and Letter 2 re: Fortelny, et al. in BJS;97:1140–5. Br J Surg.
2011;98:156–60.
27. Bringman S, Conze J, Cuccurulla D, et al. Hernia repair: the search for ideal meshes.
Hernia. 2010;14:81–7.
28. Jenkins ED, Yom V, Melman L, et al. Prospective evaluation of adhesion characteristics
to intraperitoneal mesh and adhesiolysis-related complications during laparoscopic
re-exploration after prior ventral hernia repair. Surg Endosc. 2010;24:3002–7.
29. Arnaud JP, Hennekinee-Mucci S, Pessaux P, et al. Ultrasound detection of visceral
adhesion after intraperitoneal ventral hernia treatment: a comparative study of protected
versus unprotected meshes. Hernia. 2003;7:85–8.
30. Eriksen JR, Gogenur I, Rosenberg J. Choice of mesh for laparoscopic ventral hernia
repair. Hernia. 2007;11:481–92.
411
B.P. Jacob and B. Ramshaw (eds.), The SAGES Manual of Hernia Repair,
DOI 10.1007/978-1-4614-4824-2_36,
© Springer Science+Business Media New York 2013
36. Chronic Pain After Ventral Hernia
Repair
Victor B. Tsirline , David A. Klima , Igor Belyansky ,
and Kent W. Kercher
Prior to the widespread use of synthetic mesh for ventral hernia repair
(VHR), recurrence after primary fascial repair was an accepted yet
disappointing complication in up to 67% of repairs [ 1 ] . Mesh reinforcement
has now helped to drastically reduce recurrence rates to <10% in a
majority of studies [ 1– 6 ] with only the most complicated repairs having
higher recurrence rates of up to 29% [ 7– 10 ] . With an ever increasing
number of VHR performed in the United States (now reaching an
estimated 250,000 annually) [ 11 ] and advancements in hernia repair
techniques and materials, attention has become increasingly focused on
functional outcomes, quality-of-life measures, and aesthetics. Chronic
pain, speci fi cally, has dominated the literature with regard to inguinal
hernia repair for years and more recently has become a major focus in
VHR [ 12, 13 ] . While the incidence of chronic pain after VHR is variable,
surgeons may choose not to operate on an asymptomatic patient for fear
of the chronic consequences patients may face. In the subsequent text, we
seek to de fi ne chronic pain and help identify the etiologies, treatments,
and plausible efforts to avoid pain in this relatively common procedure.
De fi nitions
The International Association for the Study of Pain (IASP) de fi nes
chronic pain as pain lasting more than 3 months after insult. In de fi ning
post-herniorrhaphy pain, it is important to distinguish between surgical
and neuropathic pain. Surgical pain is inevitable, generally uniform, and
resolves over time. It arises from a combination of sharp skin incision,