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210
E.M. Pauli and R.M. Juza
Fig. 20.2 Deep surgical site infection following operative debridement and several days of negative pressure
wound therapy. Note the exposed onlay biologic mesh at
the base of the wound
Seroma
Seroma formation , the accumulation of sterile
serous fl uid within the spaces created during herniorraphy, frequently complicates open ventral
hernia repair (Fig. 20.3 ). Seromas occur as a con-
sequence of the extent of tissue mobilization and
local infl ammatory reactions to mesh and suture
material [ 26 , 27 ]. Surgical dissection creates
dead space between anatomic planes which function as a space for transudative fl uid to collect.
Fluid may collect at a greater rate if the peritonealized hernia sack is left in situ within subcutaneous tissues.
Seroma formation rates vary between 0 and
36% depending on the surgical technique and
type of the mesh employed for repair [ 22 , 28 – 35 ].
For open ventral hernia repair, the incidence of
seroma formation is directly dependent on the
surgical technique employed. Placing mesh in the
sublay position is superior to onlay mesh placement based on numerous published studies
(Table 20.2 ). It has been postulated that the supe-
rior vascularity in the retrorectus plane reduces
the incidence of seroma formation over the poorly
vascularized lipocutaneous fl aps created in open
ventral hernia repairs when the mesh is placed in
the onlay position. This theory is supported by
studies evaluating the outcomes of endoscopic
component separation which avoids creating
large devascularized fl aps by endoscopically
releasing the external oblique. This signifi cantly
decreases the wound complications associated
with onlay mesh placement [ 17 , 29 , 31 ].
Seroma prevention is based on two main principles: reducing dead space volume and minimizing devascularized tissue. Preoperative patient
factors including obesity, smoking, and diabetes
have all been shown to increase the rate of seroma
formation [ 25 , 33 ]. Postoperatively, the use of
closed suction drains to prevent fl uid accumulation is widely practiced during open ventral hernia repair to reduce dead space volume, but
management of drains is by no means standardized. Our preference is to leave the drains in place
until daily output is less than 30 cc per day for
two consecutive days. A recent review of the literature was unable to demonstrate a direct benefi t
of drains versus no drains; however, this more
likely highlights the paucity of high-quality studies directly related to seroma management [ 36 ].
Abdominal binders are also a modality widely
used to decrease seroma formation by decreasing
dead space volume and therefore decreasing fl uid
accumulation. Effective duration of therapy necessary to prevent seroma formation is not well
described and is often limited by patient tolerance. Additionally, less widely practiced methods such as the use of quilting stitches and the
application of fi brin sealant to dissected planes
theoretically assist physiologic closure of the
dead space; however, the literature is mixed
regarding the effi cacy of these methods and there
is no clear evidence to support the use of either
regularly [ 37 , 38 ].
Despite the frequency of seroma formation,
this low acuity complication has limited highlevel research. Management is largely directed by
small studies, case reports, and empiricism.
Diagnosis occurs clinically or radiographically.
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Fig. 20.3 Benign, asymptomatic seromas ( arrows ) ( a ) Seroma surrounding biologic mesh in the retrorectus space.
( b ) Seroma within the subcutaneous dead space created following hernia reduction
Table 20.2 Seroma rates following open ventral hernia repair
n = Method of repair Mesh location Seroma (%)
Harth et al. [
Albright et al. [
Giurgius et al. [
Fox et al. [
Satterwhite et al. [
Paajanen et al. [
Rosen et al. [
McLanahan [
Peterson et al. [
Iqbal [
29 ] 22 Anterior component
separation
30 ] 14 Anterior component
separation
31 ] 15 Anterior component
separation
32 ] 26 Anterior component
separation
33 ] 106 Anterior component
separation
22 ] 84 Retrorectus Sublay 9
34 ] 49 Retrorectus Sublay 0
35 ] 104 Retrorectus Sublay 1
28 ] 175 Retrorectus Sublay 6
12 ] 254 Retrorectus Sublay 4
Onlay 5
Onlay 36
Onlay 33
Onlay 0
Onlay 18
211
When sterile and asymptomatic, the majority can
be observed for spontaneous, albeit potentially
protracted resolution over the course of weeks to
months. Intervention is indicated when the
ative pressure therapy are additional management
strategies for infected seromas not amendable to
or failing percutaneous drainage and targeted
antibiotic therapy.
seroma becomes infected or symptomatic
20.4 ). Although some advocate needle aspi-
(Fig.
rating these collections, this risks inoculating an
otherwise sterile collection [
39 ]. Evidence of an
infected seroma includes localized and/or systemic reactions. When treatment is required, percutaneous closed suction drainage is the preferred
method of management. Open drainage and neg-
Hematoma
Hematomas following open ventral hernia repair
are uncommonly reported, but can occur from
several sources. Bleeding from named vessels
(typically the epigastric vessels) generally occurs
as a direct injury not recognized during retrorectus dissection or during transfascial suture place-
212
E.M. Pauli and R.M. Juza
Fig. 20.4 Infected subcutaneous seroma ( arrow ) with
loculation, septation, and an air fl uid level
ment. Component separation hernia repairs
involve transection of myofascial barriers, and
bleeding from cut edges of muscles can occur
(Fig. 20.5a ). Subcutaneous bleeding can also
occur into the space created by raising large lipocutaneous fl aps during anterior component separation (Fig. 20.5b ). Patients with bleeding
diathesis, thrombocytopenia, or the need for early
post-operative anticoagulation (e.g. mechanical
valve patients) are at a higher risk for postherniorraphy hematoma.
Hematomas are managed conservatively
unless bleeding is ongoing or there is hemodynamic instability. Correction of coagulopathy,
withholding prophylactic anticoagulation, and
pressure dressings may all have benefi t.
Transfusion may be required for large hematomas. Like seromas, the majority of hematomas
can be observed for spontaneous resolution and
should only be drained for clinically relevant
symptoms or infection.
Wound Dehiscence
Wound dehiscence involves separation of the skin
edges in the absence of surgical site infection.
Contributing factors include poor blood supply to
the skin edges, poor suturing technique or damage
to suture material, and radial tension on the wound
edges due to tissue loss or body habitus. As with
many other post-operative complications, wound
dehiscence is poorly reported in the literature
(Table 20.1 ). There is a clear spectrum of compli-
cation that can be classifi ed as wound dehiscence
ranging from minor separation requiring no dedicated therapy to complete wound disruption and
mesh exposure (Fig. 20.6 ). Wound dehiscence is
generally managed with local wound therapy
including dressing changes. Mesh exposure from
wound dehiscence may warrant mesh removal.
Enterocutaneous Fistulae Formation
Enterocutaneous fi stula (ECF) formation has been
reported in cases of intraperitoneally placed prosthesis as a consequence of mesh eroding into bowel
(Fig. 20.7 ) [ 40 , 41 ]. By moving the mesh into the
more protected onlay or sublay positions, enterocutaneous fi stula formation is a rare complication.
Other causative factors in ECF formation include
delayed leak from an enteroenterostomy performed
during the course of the herniorraphy and underlying patient disease (e.g. Crohn’s Disease). Many
cases of fi stula formation reported in the literature
have occurred in contaminated fi elds where fi stula
or perforation was already present prior to repair
[ 33 , 41 – 43 ]. When an ECF develops, management
is similar to other ECF in other post-operative settings; sepsis must be controlled, nutrition augmented parenterally (depending on fi stula output),
and skin cared for aggressively. Extirpation of the
mesh is essential to gain control of and excise the
involved segment of bowel [ 41 – 43 ].
Other SSOs: Erythema, Ischemia,
Granulation Tissue
There are a variety of other minor wound-related
issues that fall under the SSO umbrella including
wound erythema, wound ischemia , and granulation tissue formation . Erythema may signal an
early SSI or may be related to reactions to tape,
suture material, or tension from an abdominal
binder. No treatment strategies exist, but those
potentially related to infection are generally
treated with empiric antibiotics . Wound ischemia
is not widely reported in the literature, and can
take a variety of forms including wound edge
ischemia leading to dehiscence (Table 20.1 ,
Fig. 20.6a ) or severe full thickness ischemia of a
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Fig. 20.5 Acute post-operative hematomas ( arrows ) ( a ) retroperitoneal hematoma following posterior component
separation with transversus abdominis release. ( b ) Subcutaneous hematoma following retrorectus hernia repair
213
Fig. 20.6 Various degrees of wound dehiscence ( a )
Multiple areas of minor wound dehiscence following
component separation hernia repair in a patient with complex intersecting incisions. ( b ) Large area of wound dehis-
lipocutaneous fl ap (Fig. 20.1 ). Management
depends on the degree of ischemia and any concerns for an underlying SSI, but wound debridement and dressing changes are typical management
cence following primary (suture) hernia repair performed
under tension. ( c ) Complete wound dehiscence and bio-
logic mesh exposure following a bridged repair in a patient
with signifi cant wound tension due to morbid obesity
with suture sinuses is best treated with local
exploration and suture removal. La rge areas of
granulation tissue associated with mesh exposure
are best managed by mesh excision.
strategies . Granulation tissue can take a variety of
forms from minor wound edge areas of non-healing, to suture sinus tracts (Fig.
wounds with chronic mesh infections (Fig.
20.8 ), to large open
20.9 ).
Granulation at wound edges can be managed with
chemical cautery ablation. Granulation associated
Pulmonary Complication
Pulmonary complications following abdominal
wall reconstruction are a common and morbid
214
E.M. Pauli and R.M. Juza
Fig. 20.7 ( a ) Enterocutaneous fi stula that developed 5
years following a multiply recurrent incisional hernia
repair. At exploration, the fi stula was associated with
Fig. 20.8 Granulation tissue associated with permanent
suture sinuses
complication. Pneumonia, respiratory distress
requiring upgrade in care, or intubation and prolonged ventilator dependence are considered
serious complications of hernia repair. Such complications are reported in as many as 15–20% of
patients undergoing component separation hernia
repairs [ 44 – 47 ]. Contributing factors to pulmo-
nary complications include chronic obstructive
pulmonary disease, baseline dyspnea, prolonged
operative time, and elevated intra- operative airway pres sures [ 44 – 47 ].
Patients experiencing postoperative respira-
tory failure have longer hospital admissions
underlay mesh erosion into the jejunum that was noted on
pre-operative CT scan ( b )
(21.0 ± 18.5 vs. 5.9 ± 5.5 days, p < 0.001), a higher
mortality rate (14.7% vs. 0.1%, p < 0.001), and an
added cost of $60,933 per patient [ 45 , 47 ].
Pulmonary complications are managed with
aggressive pulmonary toilet, non-invasive ventilation, and endotracheal ventilator assistance as
necessary. Rarely, tracheostomy is necessary
after open hernia repair for prolonged ventilatordependent respiratory failure.
Predictive models and preven tative strategies
for pulmonary complications have been described
[ 44 , 45 ]. The greater the change in plateau airway
pressure, the greater the risk of developing a
respiratory complication with an odds ratio of
8.67 for a change in plateau pressure ≥6 cm H 2 O
and an odds ratio of 11.5 for a change in plateau
pressure ≥9 cm H
O [ 44 ]. As such, the fi nding of
2
an elevation in plateau pressure of >6 mmHg following open ventral hernia repair should prompt
overnight ventilator support to permit normalization of plateau pressure.
Ileus
Delay in the resumption of intestinal function, or
ileus , is a normal physiologic response to open
abdominal surgery. For hernia surgery, where
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Fig. 20.9 ( a ) Chronic non-healing midline wound resulting from exposure and infection of PTFE mesh that was
removed in clinic ( b ) and in the operating room ( c )
215
there may be signifi cant bowel manipulation as
well as a need for higher dose post-operative narcotics, paralytic ileus is an anticipated part of the
normal post-operative recovery that resolves
spontaneously. Prolonged ileus may be clinically
signifi cant, leading to abdominal pain, vomiting,
a need for imaging studies (to differentiate from
mechanical bowel obstruction or other post-operative complication such as a missed bowel
injury), and results in patient dissatisfaction and a
prolonged hospital stay. Ileus is more likely following open ventral hernia surgery than laparoscopic hernia repair and may relate to more
signifi cant shifts in fl uids and electrolytes, greater
degrees of bowel manipulation, and higher postoperative narcotic use.
Ileus is managed conservatively with electrolyte
replacement, nasogastric decompression, and
patience. Imaging studies help differentiate ileus
from small bowel obstruction (Fig. 20.10 ). Prolonged
ileus may necessitate the institution of parenteral
nutrition until full bowel recovery is made.
Acute Kidney Injury
Acute kidney injury (AKI), diagnosed as an
increase in serum creatinine of ≥0.3 within
48 hours or increase in serum creatinine to ≥1.5
times baseline within 7 days, is an uncommon, but
likely under-reported, complication of abdominal
wall reconstruction [
48 ]. Contributing factors to
AKI include baseline chronic kidney disease, myoglobinuria (from prolonged operative times and
muscle trauma during hernia repair), dehydration
and volume shifts associated with open surgery,
nephrotoxic drugs administered in the peri-operative period. Despite this, complex abdominal wall
reconstruction can be safely conducted even in
patients at high risk for AKI [ 49 ]. AKI should be
managed with supportive therapy including volume resuscitation, withdrawal of nephrotoxic
drugs, and renal replacement therapy if indicated.
Intra- Abdominal Hypertension
Heightened awareness of intra-abdominal hypertension (intra-abdominal pressure ≥12 mmHg)
and abdominal compartment syndrome (intraabdominal pressure ≥20 mmHg) has led to growing attention to the severity of this clinical entity
in the context of an acute abdomen from abdominal trauma, pancreatitis, or perforated viscus
50 – 53 ]. This entity is increasingly recognized as
[
a common but transient occurrence following
216
E.M. Pauli and R.M. Juza
Fig. 20.10 Ileus following parastomal hernia repair with
posterior component separation and transversus abdominis release. Contrast administered via the catheter in the
stoma (RUQ) traverses the length of the GI tract, fi lling
multiple, dilated loops with no clear transition zone. This
resolved spontaneously
complex open ventral hernia repair and its
contribution to the post-operative renal and pulmonary complications noted above has been
questioned [ 54 ]. Intra-abdominal hypertension
should likely be viewed as a “permissive” consequence of the procedure that resolves with conservative measures.
Mesh Complications
Mesh Infection
Mesh infection complicates as many as 8% of
open ventral hernia repairs, a rate almost ten
times higher than laparoscopic repairs [ 55 – 57 ].
There are clear differences between the rates of
mesh infections between different methods of
herniorraphy and between different locations for
mesh placement (underlay vs. sublay vs. onlay).
Albino et al. evaluated cases requiring mesh
explantation when surgical site infection complicated hernia repair and found signifi cant differences between onlay mesh position (5%) and
sublay (retrorectus) position (0.5%) [ 19 ]. This is
attributable to the large lipocutaneous fl aps created for onlay repairs which complicate bacterial
clearance when mesh contacts the poorly
vascularized anterior fat layer (Fig. 20.2 ).
Strengthening this argument, Petersen et al.
evaluated the effect of placing mesh in a well
vascularized space by comparing complete versus incomplete rectus sheath closure when the
mesh was placed in the retrorectus plane.
Incomplete closure resulted in direct mesh contact with the lipocutaneous layer directly beneath
the midline wound. They found a ninefold
decrease (2% vs. 18%) in mesh infection when
the anterior fascia could be closed over mesh
placed in the retrorectus plane [ 28 ].
Mesh type also contributes to the rate of
infection with multifi lament, microporous, and
heavy- weight meshes having higher associated
rates of infection [ 58 , 59 ]. Light-weight, macro-
porous, monofi lament meshes elicit a decreased
foreign body reaction, permit improved bacterial clearance and better integrate into tissue
[ 60 – 67 ].
Mesh infections present in a variety of ways:
they can be acute or delayed following the repair;
they may present with typical signs of systemic
infection or with more subtle signs such as chronic
pain or skin changes; they may be associated with
a superfi cial or deep SSI; or they can occur independent of these (Fig. 20.11 ) [ 68 ]. When a mesh-
related infection occurs, a synergistic medical and
surgical approach of targeted antibiotic therapy
and removal of the mesh is the traditional management strategy [ 39 ]. This strategy has been modi-
fi ed in recent years, as monofi lament, macroporous
mesh (polyester, polypropylene) may respond to
antibiotics and drainage alone, whereas PTFE
infection generally requires complete mesh
removal (Figs. 20.9 and 20.12 ).
Mesh Erosion
Mesh erosion into the GI tract is a welldocumented and likely underreported late complication of mesh placement (Fig. 20.7 ).
Intra-peritoneal mesh (especially uncoated mesh)
has been associated with erosion and the development of late entero- or colo-cutaneous fi stulae
(Fig. 20.13 ) [ 35 , 40 , 69 – 71 ]. Such fi stulae gener-
ally do not resolve with conservative measures as
the mesh acts as a foreign body responsible for
keeping the fi stulae open. Partial mesh resection
is necessary when managing these fi stulae, but
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217
Fig. 20.11 Skin changes resulting from underlying mesh
infections. ( a ) Cellulitis, skin ischemia from an acute deep
surgical site, and polypropylene mesh infection. ( b )
Fig. 20.12 Three-month healing process ( left to right ) of
exposed, infected light-weight polyprolyene mesh following parastomal hernia repair with component separation.
complete excision of well incorporated mesh is
not mandatory.
Mesh Fracture
The recognition that light-weight, macroporous,
monofi lament meshes generate improved tissue
integration, improved bacterial clearance,
decreased foreign body reaction, and cause less
chronic pain has resulted in a migration away
from the use of their heavy-weight counterparts.
This migration, however, has led to an increasing
recognition of central mesh failure (CMF) as a
mechanism of hernia recurrence (Fig. 20.14 ).
Erythematous petechial, pruritic rash associated with
smoldering PTFE infection
Following initial washout, the mesh was permitted to
granulate without the need for systemic antibiotics or
mesh removal
Initial reports of CMF occurred in cases of
light- weight polypropylene use with incomplete
closure of the anterior fascial layers [ 72 ].
Subsequently, Petro et al. reported a 19% recurrence rate due to CMF when mid-weight monofi lament polyester mesh was placed in a sublay
position with complete anterior fascial closure
[ 73 ]. They emphasized cautious use of light-
weight meshes, particularly when there is inadequate fascial closure to support the mesh.
Mesh fracture has also been well documented
with other devices, most notably the Kugel ventral hernia mesh device which contained a periph-
218
E.M. Pauli and R.M. Juza
Fig. 20.13 Endoscopic view of polypropylene mesh eroded
into the colon following an open parastomal hernia repair
0.1–0.6%, but this data refl ects minor abdominal
wall procedures [ 74 ]. Complex open abdominal
wall reconstructions likely have a higher VTE rate
of 0.8–1.7% associated with major general surgery
[ 75 ]. With higher BMI being a major risk factor
for hernia development and recurrence, one must
also consider the higher risk classifi cation for VTE
that is associated with obesity [ 76 ]. VTE preven-
tion, diagnosis, and treatment follow standard protocols and little special consideration needs to be
given to the nature of the herniorraphy itself.
Iatrogenic Hernia Formation
As component separation herniorraphy has
become increasingly utilized to address complex
ventral hernias, there has been greater recognition
of the risk of creating iatrogenic hernias with these
types of repairs. While uncommon, such iatrogenic
hernias can be diffi cult to address and require mastery of a variety of hernia repair techniques.
Injury to the Linea Semilunaris
Full thickness injury to the semilunar line can
occur during anterior component separation with
Fig. 20.14 Laparoscopic view of a recurrent incisional
hernia as a consequence of central mesh failure (Photo
courtesy of Dr. Yuri W. Novitsky, Case Western Reserve
University)
eral memory ring composed of polyester held
between layers of polypropylene. This device
was recalled by the Food and Drug Administration
in 2005, due to reports of ring fracture leading to
bowel perforation and obstruction. The exact
mechanism of polyester ring fracture has not
been elucidated.
Mesh fracture typically presents as a hernia
recurrence or a complication thereof (such as bowel
obstruction) and should be managed as such.
Thromboembolic Complications
There are few studies directly addressing the risk
of venous thromboembolism (VTE) following
open ventral hernia repair. The risk of VTE following an abdominal wall procedure is quoted at
Fig. 20.15 Lateral hernia resulting from a full thickness
injury to the linea semilunaris during an anterior component separation with external oblique release. The lateral
musculature (Transversus Abdominis (T), Internal
Oblique (I) and External Oblique (E)) have been disconnected from the rectus abdominis muscle (R)
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Fig. 20.16 Iatrogenic lateral
hernias ( arrowheads ) resulting
from full thickness injury to
the linea semilunaris during
robotic posterior component
separation. The lateral
musculature (L) has been
disconnected from the rectus
muscles (R) bilaterally (Photo
courtesy of Dr. Yuri
W. Novitsky, Case Western
Reserve University)
219
Fig. 20.17 Laparoscopic view of acutely incarcerated
small bowel ( a ) within an intra-parietal hernia defect ( b )
following posterior component separation with transversus abdominis release. Note the location of the hernia is
external oblique release (Fig. 20.15 ) or during
posterior component separation (Fig.
20.16 ) if
care is not taken to respect correct myofascial
boundaries. Such defects can span the entire
length of the rectus muscle, from costal margin to
inguinal ligament. Recent reports suggest that
posterior component separation utilizing transversus abdominis release can successfully
address this type of iatrogenic hernia [ 77 ].
Posterior Layer Defects
Failure to adequately recreate a closed visceral
sac during any of the posterior component separation herniorraphies can result in defects that
permit bowel to herniate between this layer and
the mesh layer (Fig. 20.17 ). Such intra-parietal
hernias can present acutely as an early small
between the posterior rectus sheath and the sublaypositioned polypropylene mesh (Photo courtesy of Dr.
Yuri W. Novitsky, Case Western Reserve University)
bowel obstruction requiring surgical reintervention. A high index of suspicion must be
maintained to correctly diagnose this complication. Fortunately, laparoscopy can often be used
to reduce the bowel and to reinforce the posterior
layer defect with mesh. This avoids midline
wound re-exploration, anterior fascial opening,
and mesh transection or removal.
R e f e r e n c e s
1. Henriksen NA, et al. Risk factors for incisional hernia
repair after aortic reconstructive surgery in a nationwide study. J Vasc Surg. 2013;57(6):1524–30. 1530
e1–3.
2. Hoer J, et al. Factors infl uencing the development of
incisional hernia. A retrospective study of 2,983 lapa-
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