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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_1498_Библиотеки_им_академика_М_И_Перельмана.pdf
314
G.L. Adrales and E. Honigsberg
Trade name Manufacturer Source Processing Terminal sterilization Cross-linked Handling
XenMatrix Davol, C.R. Bard
(Cranston, RI)
Porcine dermis E beam radiation No No need for
rehydration
TutoPatch Tutogen medical.
RTI biologics
(Alachua, FL)
Bovine
pericardium
Osmotic contrast
bathing, hydrogen
peroxide, sodium
oxide
Gamma radiation No No need for
rehydration
Veritas Synovis surgical
(St. Paul, MN)
Bovine
pericardium
Hydrogen peroxide,
ethanol, propylene
oxide
No No need for
rehydration
Permacol Covidien
(Norwalk, CT)
Porcine dermis Hexamethylene
diisocyanate
Gamma radiation Yes No need for
rehydration
CollaMend Davol, C.R. Bard
(Cranston, RI)
Porcine dermis Sodium sul fi de,
sodium
hypochlorite,
hydrocholoric
acid, hydrogen
peroxide
Yes 3-min rehydration
PeriGuard Synovis surgical Bovine
pericardium
Glutaraldehyde Yes 2-min rehydration
SurgiMend TEI bioscience
(Boston, MA)
Bovine fetal
dermis
Ethylene oxide Yes 1-min rehydration
Table 26.1. (continued)
315
26. Biologic Prosthetics: What Are They and How Do They
goal of creating a more durable biomaterial [ 3 ] . Whereas un-cross-linked
biologic mesh may degrade within months, highly cross-linked mesh
may persist for years [ 4– 6 ] . In a rodent model of ventral hernias, Gaertner
demonstrated the durability of cross-linked biologics compared to non-
cross-linked bioprosthetics [ 7 ] . At 6 months, the cross-linked meshes
were grossly intact, whereas the non-cross-linked mesh was absent. This
correlated with signi fi cantly decreased tensile strength of the non-cross-
linked meshes.
Intentional cross-linking may decrease mesh degradation and
fi broblast encapsulation but could also adversely alter the extracellular
matrix structure to limit cell in fi ltration and negatively impact the
remodeling process and reduce ingrowth [ 3, 8 ] . Liang et al. demonstrated
that a higher degree of cross-linking in bovine pericardium was associated
with persistence at 1 year after implantation but also limited cell
in fi ltration with tissue regeneration restricted to the periphery of the
mesh [ 9 ] . Decreased cell in fi ltration may have negative consequences
such as reducing angiogenesis, mesh incorporation, and resistance to
infection [ 9 ] . It is important to note that these effects will vary between
various patient clusters and cannot yet be predicted for each individual
patient.
The Biology of Biologic Mesh
The structure of biologic mesh is meant to favor prosthetic
incorporation. Biologic meshes demonstrate superior biocompatibility
as compared to synthetic meshes [ 10 ] . Native tissue growth into the
bioprosthesis theoretically contributes to the strength of the biomaterial.
Unlike synthetic mesh, the acellular scaffold of collagen, elastin, and
extracellular matrix contains residual growth factors that ideally will
attract host endothelial cells and fi broblasts. The porosity of the biologic
graft permits migration of host cells and adherence, promotes
angiogenesis, and allows collagen deposition and remodeling to replace
the graft with host tissue. As described by Melman et al., remodeling is
characterized by six factors: cellular in fi ltrate, individual cell types,
neovascularization, extracellular matrix deposition, scaffold degradation,
and fi brous encapsulation [ 10 ] . Graft degeneration must be balanced
with native tissue ingrowth as the host response to the biologic graft can
either result in integration of the mesh or a disproportionate in fl ammatory
response leading to excessive fi brosis and scarring, mesh encapsulation,
316
G.L. Adrales and E. Honigsberg
and excessive mesh degradation, all of which ultimately leads to mesh
failure [ 11 ] .
In fl ammation and wound healing are critical to the integration of
biologic prostheses with host tissue [ 12 ] . Monocytes and macrophages
are the key cells in this process. Various cytokines are involved including
IL-1 b that stimulates fi broblast proliferation, IL-8 that stimulate both
neutrophils and endothelial proliferation, and VEGF that promotes
angiogenesis. Cytokine expression varies depending on the implanted
bioprosthesis. Biologic mesh is designed to elicit a minimal chronic
in fl ammatory response. Animal studies have shown, however, that the
in fl ammatory in fi ltrate and subsequent adhesion formation to the
biomaterial vary from mesh to mesh [ 13 ] . Orenstein et al. demonstrated
that AlloMax (CR Bard) induced the greatest expression of VEGF, IL-8,
and IL-6 compared to AlloDerm (LifeCell), FlexHD (MTF), and Gore
BioA (W.L. Gore) in an in vitro study. Interestingly, AlloDerm was the
lowest inducer of cytokines [ 12 ] . The difference in immunologic response
is most likely related to differences in the processing and/or sterilization
of the different biologic grafts. The inconsistent host in fl ammatory
response to individual bioprostheses has clinical implications, as other
authors have demonstrated variable levels of mesh degradation in animal
models, with durability of some materials at 9 months postimplantation,
while others undergo signi fi cant degradation [ 14 ] . Mesh degradation
ultimately correlates with mesh strength, critical in the setting of
abdominal wall defect repair.
As previously noted, cross-linking also affects the remodeling
process. Animal models of abdominal wall hernias have demonstrated
that in the short-term, non-cross-linked biologic grafts stimulate more
favorable remodeling factors with signi fi cantly increased earlier cellular
in fi ltration, extracellular matrix deposition, and neovascularization [ 3,
15 ] . However, over time, cross-linked biologic meshes showed similar
histological results as compared to the non-cross-linked materials.
Additionally, these early histologic differences did not correlate with
signi fi cant differences in the tensile strength of the mesh repair, regardless
of cross-linking.
Biologic prostheses are thought to be resistant to infection due to
neovascularization during the remodeling process. However, the ability
to clear bacteria is variable among biologic prostheses. In a rodent model
of infected hernia repair, non-cross-linked biomeshes demonstrated
signi fi cantly higher rates of bacterial clearance than cross-linked meshes
[ 16 ] . Cross-linking may prevent fi broblast in fi ltration and tissue ingrowth,
thus retarding the host’s ability to clear bacteria. This fi nding was
317
26. Biologic Prosthetics: What Are They and How Do They
supported in a retrospective review of patients undergoing complex
ventral hernia repair: cross-linked porcine biomeshes showed relatively
higher rates of infection and subsequent explantation compared to non-
cross-linked meshes [ 17 ] . This contradicts the widely held belief that all
biologic grafts do not need to be removed if infected.
Current Indications
The theoretical advantage of biologic mesh over synthetic mesh in
certain clinical situations has appealed to surgeons, mostly in the United
States. These meshes are not yet widely favored in Europe and elsewhere
in part due to the high cost of the biologic mesh over its cheaper and
more widely applicable synthetic mesh counterpart. Biologic prostheses
have been utilized as biologic dressings, maxillofacial reconstruction,
breast reconstruction, and in various challenging surgical scenarios,
including complex abdominal wall reconstruction and management of
enterocutaneous fi stulas [ 1 ] .
The use of biologic mesh in primary or recurrent ventral or inguinal
hernia repair in the uncontaminated and previously uninfected fi eld is
dif fi cult to justify due to the high material cost without obvious added
bene fi t. There is very little data regarding the performance of biologic
mesh in these settings. The poor performance of the mesh in terms of
laxity in a bridging repair makes this an unacceptable repair in the
uncontaminated setting. Blatnik et al. documented a recurrence rate of
80% for bridging repair with acellular dermal matrix at an average cost
of $5,100 per patient, comparing the repair to an “expensive hernia sac.”
[ 18 ] The laxity associated with biologic mesh has been documented in
other series [ 19 ] .
The use of allograft or xenograft as reinforcement of a primary ventral
hernia repair is felt to be a more sound approach. This fi ts with what we
know of the science of biologic meshes in that placement in well-
vascularized tissue is favorable for the ingrowth and remodeling process.
Rosen’s group at Case Western investigated this and found a reduction in
ventral hernia recurrence rate with a components separation midline
repair reinforced with acellular dermal matrix (20%) compared to the
80% recurrence after bridging allograft repair [ 20 ] .
The presence of contamination may limit the applicability of
permanent synthetic mesh in some hernia repairs. Biologic mesh may be
acceptable for this purpose or for placement in open wounds as a staged
closure in complex abdominal wall reconstruction. There is limited data
318
G.L. Adrales and E. Honigsberg
in both of these areas, with some noting a high risk of hernia recurrence
and associated infection. The data is mostly limited to animal models
and case series [ 21, 22 ] . However, the lack of suitable alternatives has
made biologic mesh attractive for contaminated fi eld hernia repair.
The role of biologic mesh has been explored in prevention of
parastomal hernias with promising results [ 23 ] . Biologic mesh has also
been used in the treatment of parastomal hernias where infection is a
concern [ 24 ] . With increasing reports of prophylactic synthetic mesh
placement at the time of ostomy construction, the use of biologic mesh
in this preventative setting may decline [ 25, 26 ] .
Biologic mesh has been utilized in the reinforcement of paraesophageal
hernia repair. The randomized controlled trial of mesh repair for
paraesophageal hernia lead by Oelschlager is one of the only level I
human studies of biologic mesh [ 27 ] . This study showed a decreased risk
of hernia recurrence with mesh repair, from 24 to 9%. The recommendation
for mesh reinforced hiatal repair is made with some caution; signi fi cant
mesh complications, ranging from mesh erosion to esophageal stenosis
and fi brosis as well as a recurrence rate closer to that of the non-mesh
group, were documented in a follow-up study [ 28 ] .
Limitations
Biologic mesh materials have not escaped the complications often
associated with synthetic mesh, such as infection and hernia recurrence
[ 2, 28– 30 ] . There are also additional limitations unique to this group of
prosthetics. Concern exists over the potential for disease transmission with
the use of biologic mesh [ 1 ] . Although these materials are processed and
often sterilized, there are reported cases of transmission of prion-related
disease from allografts. There are no reported cases of HIV transmission,
although the risk of HIV transmission is estimated at one in 1.67 million
[ 1, 31 ] . Despite processing to decellularize biologic mesh, DNA fragments
have been shown to remain in tested samples [ 32 ] . This could have other
implications regarding heterografts and the host immune response.
Another disadvantage is the signi fi cant cost of biologic mesh materials.
In general, these grafts cost ten times more than the synthetic equivalent,
although heterografts on average cost 20% less than allografts [ 1, 2 ] .
Finally, an often overlooked consideration is the impact of cultural or
religious beliefs on patients’ acceptance of biologic grafts. The source
and processing of the biologic mesh should be considered and discussed
with the patient in the process of informed consent [ 33 ] .
319
26. Biologic Prosthetics: What Are They and How Do They
Conclusion
In summary, biologic grafts represent a major advancement in
complex hernia repair. Further investigation regarding the appropriate
indications and performance of the grafts based on individual properties
such as cross-linking is needed. Given the high cost of most of these
materials and the limited available data, biologic mesh should be used
judiciously and only when permanent synthetic mesh is deemed
complications of these materials, such as visceral erosion, warrant
caution, and sound surgical judgment [ 2, 29, 30 ] .
References
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abdominal wall defects, and reconstruction and treatment of pelvic organ prolapse: a
review of the clinical evidence. Am Surg. 2010;76(11):1290–9.
2. Rosen MJ. Biologic mesh for abdominal wall reconstruction: a critical appraisal. Am
Surg. 2010;76(1):1–6.
3. Butler CE, Burns NK, Campbell KT, Mathur AB, Jaffari MV, Rios CN. Comparison of
cross-linked and non-cross-linked porcine acellular dermal matrices for ventral hernia
repair. J Am Coll Surg. 2010;211(3):368–76.
4. Bachman S, Ramshaw B. Prosthetic material in ventral hernia repair: how do I choose?
Surg Clin North Am. 2008;88(1):101–12. ix.
5. Courtman DW, Errett BF, Wilson GJ. The role of crosslinking in modi fi cation of the
immune response elicited against xenogenic vascular acellular matrices. J Biomed
Mater Res. 2001;55(4):576–86.
6. Abolhoda A, Yu S, Oyarzun JR, McCormick JR, Bogden JD, Gabbay S. Calci fi cation
of bovine pericardium: glutaraldehyde versus no-react biomodi fi cation. Ann Thorac
Surg. 1996;62(1):169–74.
7. Gaertner WB, Bonsack ME, Delaney JP. Experimental evaluation of four biologic
prostheses for ventral hernia repair. J Gastrointest Surg. 2007;11(10):1275–85.
8. Jarman-Smith ML, Bodamyali T, Stevens C, Howell JA, Horrocks M, Chaudhuri JB.
Porcine collagen crosslinking, degradation and its capability for fi broblast adhesion
and proliferation. J Mater Sci Mater Med. 2004;15(8):925–32.
9. Liang HC, Chang Y, Hsu CK, Lee MH, Sung HW. Effects of crosslinking degree of an
acellular biological tissue on its tissue regeneration pattern. Biomaterials.
2004;25(17):3541–52.
10. Melman L, Jenkins ED, Hamilton NA, et al. Early biocompatibility of crosslinked and
non-crosslinked biologic meshes in a porcine model of ventral hernia repair. Hernia.
2011;15(2):157–64.
320
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11. Mulier KE, Nguyen AH, Delaney JP, Marquez S. Comparison of Permacol and
Strattice for the repair of abdominal wall defects. Hernia. 2011;15(3):315–9.
12. Orenstein SB, Qiao Y, Kaur M, Klueh U, Kreutzer DL, Novitsky YW. Human
monocyte activation by biologic and biodegradable meshes in vitro. Surg Endosc.
2010;24(4):805–11.
13. Stanwix MG, Nam AJ, Hui-Chou HG, et al. Abdominal ventral hernia repair with
current biological prostheses: an experimental large animal model. Ann Plast Surg.
2011;66(4):403–9.
14. Pierce LM, Grunlan MA, Hou Y, Baumann SS, Kuehl TJ, Muir TW. Biomechanical
properties of synthetic and biologic graft materials following long-term implantation
in the rabbit abdomen and vagina. Am J Obstet Gynecol. 2009;200(5):549 e541–48.
15. Deeken CR, Melman L, Jenkins ED, Greco SC, Frisella MM, Matthews BD. Histologic
and biomechanical evaluation of crosslinked and non-crosslinked biologic meshes in a
porcine model of ventral incisional hernia repair. J Am Coll Surg. 2011;212(5):
880–8.
16. Harth KC, Broome AM, Jacobs MR, et al. Bacterial clearance of biologic grafts used
in hernia repair: an experimental study. Surg Endosc. 2011;25(7):2224–9.
17. Shah BC, Tiwari MM, Goede MR, et al. Not all biologics are equal! Hernia.
2011;15(2):165–71.
18. Blatnik J, Jin J, Rosen M. Abdominal hernia repair with bridging acellular dermal
matrix–an expensive hernia sac. Am J Surg. 2008;196(1):47–50.
19. Bluebond-Langner R, Keifa ES, Mithani S, Bochicchio GV, Scalea T, Rodriguez ED.
Recurrent abdominal laxity following interpositional human acellular dermal matrix.
Ann Plast Surg. 2008;60(1):76–80.
20. Jin J, Rosen MJ, Blatnik J, et al. Use of acellular dermal matrix for complicated ventral
hernia repair: does technique affect outcomes? J Am Coll Surg. 2007;205(5):654–60.
21. Saettele TM, Bachman SL, Costello CR, et al. Use of porcine dermal collagen as a
prosthetic mesh in a contaminated fi eld for ventral hernia repair: a case report. Hernia.
2007;11(3):279–85.
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 709–711.
23. Wijeyekoon SP, Gurusamy K, El-Gendy K, Chan CL. Prevention of parastomal
herniation with biologic/composite prosthetic mesh: a systematic review and meta-
analysis of randomized controlled trials. J Am Coll Surg. 2010;211(5):637–45.
24. Lo Menzo E, Martinez JM, Spector SA, Iglesias A, Degennaro V, Cappellani A. Use
of biologic mesh for a complicated paracolostomy hernia. Am J Surg. 2008;196(5):
715–9.
25. Janson AR, Janes A, Israelsson LA. Laparoscopic stoma formation with a prophylactic
prosthetic mesh. Hernia. 2010;14(5):495–8.
26. Janes A, Cengiz Y, Israelsson LA. Experiences with a prophylactic mesh in 93
consecutive ostomies. World J Surg. 2010;34(7):1637–40.
27. Oelschlager BK, Pellegrini CA, Hunter J, et al. Biologic prosthesis reduces recurrence
after laparoscopic paraesophageal hernia repair: a multicenter, prospective, randomized
trial. Ann Surg. 2006;244(4):481–90.
321
26. Biologic Prosthetics: What Are They and How Do They
28. Stadlhuber RJ, Sherif AE, Mittal SK, et al. Mesh complications after prosthetic
reinforcement of hiatal closure: a 28-case series. Surg Endosc. 2009;23(6):1219–26.
29. Robinson TN, Clarke JH, Schoen J, Walsh MD. Major mesh-related complications
following hernia repair: events reported to the Food and Drug Administration. Surg
Endosc. 2005;19(12):1556–60.
30. Harth KC, Rosen MJ. Major complications associated with xenograft biologic mesh
implantation in abdominal wall reconstruction. Surg Innov. 2009;16(4):324–9.
31. Simonds RJ, Holmberg SD, Hurwitz RL, et al. Transmission of human
immunode fi ciency virus type 1 from a seronegative organ and tissue donor. N Engl J
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32. Gilbert TW, Freund JM, Badylak SF. Quanti fi cation of DNA in biologic scaffold
materials. J Surg Res. 2009;152(1):135–9.
33. Jenkins ED, Yip M, Melman L, Frisella MM, Matthews BD. Informed consent:
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323
B.P. Jacob and B. Ramshaw (eds.), The SAGES Manual of Hernia Repair,
DOI 10.1007/978-1-4614-4824-2_27,
© Springer Science+Business Media New York 2013
27. Open Component Separation
for Abdominal Wall Reconstruction
David Earle
The occurrence of ventral hernia as a sequence of abdominal section
is so common that it should command our thoughtful consideration.
B. Brindley Eads, M.D. 1901
Reconstructive surgery has been de fi ned as trying to make something
abnormal normal. This is in contrast to cosmetic surgery, the goal of
which is to make something normal, better—at least in the eyes of the
beholder. It is important to note that there is no consensus on a single
de fi nition of abdominal wall reconstruction, although many use this term
to refer to complex abdominal wall hernia repairs that involve some sort
of component separation technique as part of the procedure. Complex
ventral hernia repair has been an underestimated disease by surgeons and
patients alike for years, unless you happen to be the patient or surgeon
facing such a daunting task. This sentiment was speci fi cally noted in the
closing remarks of the discussion of an article about incisional hernia
repair in 1978 by Dr. Harold Harrower from Providence, Rhode Island,
who stated, “Junior house of fi cers tend to underestimate the complexity
of incisional hernia repairs. Supervision by senior surgeons improves
their understanding of the problem and the results” [ 1 ] . Local abdominal
wall musculoaponeurotic fl aps have been utilized as far back as 1894
when Gerseny of Vienna described splitting the rectus fascia [ 2 ] . Charles
Gibson suggested that these local fl aps are only intended for dif fi cult
cases that “would have been denied operative relief or subjected to some
procedure of doubtful value, such as the implantation of a fi ligree” [ 3 ] .
Ramirez described “separation of components” in 1990 as a potential
solution to repairing large ventral hernias [ 4 ] . His primary goal was to be
able to mobilize fl aps of the musculoaponeurotic abdominal wall such
that they could possibly be reapproximated, or reconstructed. What he
did not take in to account in his manuscript were the short and long term
324
D. Earle
physiologic issues associated with this. The anterior fi bers of the external
oblique muscles, acting bilaterally, are responsible for trunk fl exion. This
action pulls the midline from both sides, in essence pulling the linea alba
“apart.” After an external oblique “release,” at least in the short term, the
absence of the force of the external oblique muscles creating tension on
the midline closure may serve as one mechanism for successful healing
of the midline repair.
In addition, there is no mutually agreed upon de fi nition of “component
separation” save for the fact that some of the aponeuroses, muscles, or
overlying sheathes of the abdominal wall are in some way divided and/
or mobilized to enable closure of the defect. All muscles and aponeurosis
have been mobilized in some way, and many series do not even have a
single method of reconstruction, variably utilizing a variety of prosthetics
in a variety of locations within the abdominal wall, making comparisons
of outcomes nearly impossible [
5, 6 ] .
Additionally, it appears that the external oblique is the least important
of the fl ank muscles in terms of respiratory assistance based on
electromyography studies [ 7, 8 ] and lumbar spine support [ 9 ] , making
this a logical choice for division and separation as part of an abdominal
wall reconstruction.
This chapter will focus on separation of the external oblique muscle
with detachment of its medial insertion just lateral to the rectus muscle,
combined with posterior rectus sheath mobilization. This is currently the
most widely practiced method for component separation utilized for the
purpose of a midline abdominal wall reconstruction. For the remaining part
of this chapter, the term component separation (CS) will refer to release of
the external oblique and posterior rectus sheath as described above.
Additionally, prosthetic-related issues such as type and placement are
beyond the scope of this chapter and are discussed elsewhere in this book.
Indications and Relative Contraindications
It is important to note that a component separation technique is only one
technical part of an abdominal wall reconstruction. Other technical
components of an abdominal wall reconstruction include suturing technique,
prosthetic use and placement, management of the excess skin and
subcutaneous tissue, and management of concomitant procedures such as
gastrointestinal and gynecological procedures to name a few. In general, the
indications for utilizing a component separation technique should be based
on the aligned goals of the patient and surgeon, anatomic details of the