The open abdomen, indications, management and definitive closure
Coccolini et al. World Journal of Emergency Surgery
The open abdomen, indications, management and definitive closure
Federico Coccolini 0
Walter Biffl 2
Fausto Catena 1
Marco Ceresoli 0
Osvaldo Chiara 6
Stefania Cimbanassi 6
Luca Fattori 5
Ari Leppaniemi 4
Roberto Manfredi 0
Giulia Montori 0
Giovanni Pesenti 5
Michael Sugrue 3 7
Luca Ansaloni 0
0 General Surgery Department, Papa Giovanni XXIII Hospital , Piazza OMS 1, 24127 Bergamo , Italy
1 General surgery Department, Ospedale Maggiore , Parma , Italy
2 Denver Health Medical Center , Denver, CO , USA
3 Letterkenny Hospital and the Donegal Clinical Research Academy , Donegal , Ireland
4 Department of Abdominal Surgery, University of Helsinki , Helsinki , Finland
5 Unità Operativa di Chirurgia d'Urgenza, Azienda Ospedaliera “San Gerardo” , Monza , Italy
6 Niguarda Trauma Center, Ospedale Niguarda Ca'Granda , Milan , Italy
7 University College Hospital , Galway , Ireland
The indications for Open Abdomen (OA) are generally all those situations in which is ongoing the development an intra-abdominal hypertension condition (IAH), in order to prevent the development of abdominal compartmental syndrome (ACS). In fact all those involved in care of a critically ill patient should in the first instance think how to prevent IAH and ACS. In case of ACS goal directed therapy to achieve early opening and early closure is the key: paradigm of closure shifts to combination of therapies including negative pressure wound therapy and dynamic closure, in order to reduce complications and avoid incisional hernia. There have been huge studies and progress in survival of critically ill trauma and septic surgical patients: this in part has been through the great work of pioneers, scientific societies and their guidelines; however future studies and continued innovation are needed to better understand optimal treatment strategies and to define more clearly the indications, because OA by itself is still a morbid procedure.
Open abdomen; Peritonitis; Pancreatitis; Trauma; Management; Closure
The first to describe the use of the open abdomen (OA)
technique, in a generalized peritonitis was probably
Andrew J. McCosh in 1897 . However this clinical
approach to a critically ill patient at that time was unusual
and while again referred to by Ogilvie in the mid 1940’s
 and only recently became popular in patients
undergoing damage control surgery (DCS). The indications for
Open Abdomen are generally trauma, abdominal sepsis,
severe acute pancreatitis and in general situations in
which is ongoing the development an intra-abdominal
hypertension condition (IAH), in order to prevent the
development of abdominal compartmental syndrome
(ACS). The concept of abdominal damage control
surgery has two basic components; controlling bleeding and
contamination in the abdominal cavity, and leaving the
abdomen open, to decompress or facilitate return at
planned re-laparotomy. Maintaining the abdomen
domain requires a temporary abdominal closure (TAC).
Unlike in trauma patients with massive bleeding, the
main aims of the OA approach both in severe secondary
peritonitis and severe acute pancreatitis (SAP) are sepsis
control and expedite subsequent surgical interventions.
Mortality rates are high, usually over >30 % 
depending on the patient cohort. The challenging situation
to manage requires a multidisciplinary approach by the
surgeon and the ICU team in a specific staged process
Pathophysiology of abdominal compartment syndrome
While recognized for over a century ACS was returned
to clinical care in the 1980’s, when Kron and colleagues
 described the course of its development following
repair of a ruptured abdominal aortic aneurysm. The term
was coined by Fietsam in 1989 in patients undergoing
abdominal aortic surgery. Since that time, much
progress has been made in its management, including the
detection, treatment, and prevention .
The World Society of the Abdominal Compartment
Syndrome convened in 2004 to create a consensus
statement on the definition, diagnosis, and treatment of ACS
Fig. 1 Schematic flow-chart for the treatment of the open abdomen
. Table 1 contains a partial list of the definitions. The
abdomen and pelvis, while anatomically distinct,
represent a single space and thus should be considered as one
in discussion of intra-abdominal pressure (IAP) and
ACS. The abdominopelvic cavity is a closed space, and
the elasticity of its walls and the character of its contents
determine the IAP. The IAP is fairly uniform throughout
and therefore measurement anywhere within the cavity
reflects the entire cavity. The IAP varies with
diaphragmatic excursion: it increases with diaphragmatic
contraction (inspiration) and decreases with expiration. The
abdominal perfusion pressure (APP), analogous to the
cerebral perfusion pressure, has been proposed as a
more accurate predictor of visceral perfusion and
consequently a target for intervention. A target APP of
≥60 mmHg is associated with improved survival in the
setting of IAH and ACS [6, 7].
Normal IAP is actually below 0 mmHg. In the setting
of conditions such as morbid obesity, pregnancy, liver
disease with ascites, IAP may be chronically elevated to
10–15 mmHg without evidence of altered physiology
. During illness or following surgery, IAP is higher, on
Table 1 Consensus definitions related to intra-abdominal hypertension and abdominal compartment syndrome
Sustained or repeated pathological elevation of IAP ≥12 mmHg
Sustained IAP >20 mmHg (with or without APP <60 mmHg) that is associated with a new organ dysfunction or failure
ACS associated with injury or disease in abdomino-pelvic cavity
ACS in absence of conditions originating in the abdomino-pelvic cavity
IAP intra-abdominal pressure, APP abdominal perfusion pressure, MAP mean arterial pressure, IAH intra-abdominal hypertension, ACS abdominal compartment
syndrome. Adapted from Malbrain et al. 
the order of 5–7 mmHg, due to factors such as tissue
edema or ileus. The point at which IAP becomes IAH
has been a matter of debate; the consensus definition
settled on 12 mmHg as this is the lowest point at which
pathologic effects are noted . A grading system was
proposed by the Denver General Hospital group in 1996,
in the interest of guiding interventions . The WSACS
consensus definition varies slightly and is as follows:
Grade I (12–15 mmHg); Grade II (16–20 mmHg); Grade
III (21–25 mmHg); Grade IV (>25 mmHg) (Table 1) .
ACS develops as a result of alterations in perfusion
related to IAH. Early literature on the syndrome variably
defined the ACS; generally speaking, it was felt that ACS
represented a pathologic elevation of IAP that was
associated with organ dysfunction. The consensus definition
selected a sustained IAP >20 mmHg, recognizing that
lower levels of IAH may be associated with organ
dysfunction. The final common pathway of organ
dysfunction is hypoperfusion. The effects and manifestations of
IAH on various organ systems are listed in Table 2 .
ACS is classified as primary if it is the result of a
pathophysiologic process within the abdominopelvic cavity.
It may be a result of bleeding, acute accumulation of
ascites fluid, rapidly growing tumor or other mass,
retroperitoneal edema, packing of visceral injuries, etc.
Secondary ACS refers to development of ACS in the
absence of a primary abdominopelvic process. In early
descriptions, the secondary ACS was identified in patients
who had massive resuscitation from hemorrhage or
sepsis . Ischemia/reperfusion injury may leads to
massive accumulation of ascites, and bowel and
retroperitoneal edema from accumulation of extracellular/
extravascular fluid . Increasingly it is recognized that
secondary ACS is partly iatrogenic secondary to
excessive fluid resuscitation.
Diagnosis and treatment
The role of elevated IAP is fundamental in
understanding the evolution from IAH to ACS. Basing on the
different patients and the setting into which they are
admitted the measurement of IAP can be less or more
helpful but in any case it remains a cornerstone.
Recently Starkopf et al. found that the risk of IAH in
mechanically ventilated patients is very low especially if
they have a positive end expiratory pressure (PEEP) <
10 cm H2O, PaO2/FiO2 > 300 and BMI < 30 kg/m2 and
without pancreatitis, hepatic failure/cirrhosis with
ascites, gastrointestinal bleeding or laparotomy and the use
of vasopressor/inotropes at admission . In all those
patients with the aforementioned characteristics the
measurement of IAP might be considered.
According to the World Society of the Abdominal
Compartment Syndrome 2013 consensus guidelines, IAP
should be measured when there are at least 2 known risk
factor for IAH/ACS in critically ill or injured patients
. Serial measurements should be performed during
the patient’s critical illness, preferably every 4–6 h. To
measure the IAP the bladder pressure is considered the
gold standard and should be taken at end-expiration
with the patient supine and the transducer zeroed at the
midaxillary line after an instillation of saline into the
bladder. Another option available, if the bladder pressure
is contraindicated (due to a constitutive augmented
bladder pressure, e.g. in pelvic hematoma), is the
measurement with the stomach technique . Moreover
exist the possibility to measure the intra-abdominal
pressure via rectal, vaginal, inferior vena cava and direct
In treating patients with IAH, key principles include:
optimization of systemic perfusion and organ function,
institution of specific medical procedures to reduce
IAP, and prompt surgical decompressive laparotomy for
refractory IAH. Great emphasis has been placed on
prevention, with early, prompt haemostatic control,
aggressive balancing of resuscitation to include abundant
coagulation factors. Tailoring the response for
individual patients is essential to ensure that optimal
outcomes are achieved. Further measures to alleviate IAH
include sedation, analgesia, and neuromuscular
blockade can be used to decrease IAP. Is it has been shown
that persistent IAH of >18 mmHg is an independent
cause of renal failure in general surgical patients
admitted to ICU .
When employing early goal-directed fluid resuscitation
is crucial to remember that correction of hypovolemia
must be balanced carefully to avoid an iatrogenic
secondary abdominal compartment syndrome. The keys in the
end are prompt return to status quo, hemorrhage control,
Table 2 The effects of IAH on various organ systems, and clinical manifestations of ACS
Elevated Intra Cranial Pressure
Metabolic acidosis, bowel ischemia
Cardiovascular Decreased venous return, increased afterload
Increased intrathoracic pressure with decreased cerebral venous outflow
Decreased perfusion of liver and intestine
Upward pressure on diaphragm, decreased compliance and functional residual
capacity, increased air way resistance
Hypoxia, hypercarbia, elevated airway pressure,
decreased tidal volume
eradication of sepsis, removal of fluid either by
percutaneous catheter drainage and finally decompression.
day one, percutaneous drainage of fluid collections and
sedation and muscle relaxation.
Open abdomen in trauma
The management of complex problems in major trauma
patients using OA and TAC techniques has gained
popularity and become a valuable tool for the emergency
surgeon. Notwithstanding the evolution of supportive
care and the development of new and sophisticated
commercial devices for TAC have significantly
simplified clinical management, OA is still associated with
serious complications such as nutritional problems
with fluid and protein loss, loss of abdominal domain
secondary to fascial retraction, frozen abdomen and
entero-atmospheric fistulas (EAF). For these reasons,
OA should be reserved for selected cases only and with
the aim of obtaining early abdominal closure, possibly
with primary fascial repair . In trauma patients
frequent indications for OA after injury are the
prevention or treatment of ACS, the need for a “second look”
operation in abdominal injuries, post-injury septic
abdomen and injury with partial or entire loss of the
Prevention and treatment of IAH/ACS
The prevalence of ACS in trauma patients has fallen in
centers with advanced medical care, some reporting falls
from 30 to almost 0 % . Where trauma and
emergency surgery systems are not so advanced IAH and
ACS can be expected to occur in up to 40 % of ICU
admission respectively. Risk factors for IAH/ACS in
trauma patients are: (i) increased intra-retroperitoneal
contents consequent to hemorrhage from organ or
pelvic injury, or emergency surgery with packing
procedures, (ii) increased intraluminal contents occurring in
post-injury bowel paresis, (iii) decreased abdominal wall
compliance when abdominal injury occurs in patients
with high body mass index or for an associated third
degree burn of the abdominal wall and (iv) increased
visceral edema following massive fluid/blood resuscitation.
Untreated post-injury ACS is an independent predictor
of organ failure  that is often difficult to reverse, and
should be prevented using different strategies. delayed
decompression may not reverse the sequalae of IAH and
ACS . At the end of a damage control operation, it
would be ideal to measure IAP to decide for fascial
closure: however this is technically difficult unless a
continuous IAP technique is used . Some authors prefer to
left open the abdomen for 24–48 h if the value is greater
than 12 mmHg Moreover, in trauma patients with
elevated IAP (with or without previous surgery) every
medical strategy to reduce IAP should be applied: ng tube,
colonic decompression, prokinetic medications, supine
position, negative fluid balance starting from post-injury
Need for a “second look” operation
A second look procedure is planned when the initial
operation has been stopped in a damage control setting for
physiologic exhaustion of the patient, bleeding from
remote areas not amenable to surgical correction, vascular
injuries of visceral vessels with risk of bowel ischemia,
resected and closed bowel with subsequent need for
anastomosis or stoma, complex liver injury treated with
packing, and the need for transfer to a higher level
facility. All these cases require TAC that allows for a simple
re-operation for definitive abdominal care.
Post-injury septic abdomen
Septic abdomen may develop following hollow viscus
injuries for penetrating or blunt trauma, particularly in
cases of delayed diagnosis or leakage after primary repair
of colonic wounds. Unusual conditions are septic
evolutions of complex duodeno-pancreatic injuries. Recent
clinical series suggest that OA associated with negative
pressure therapy (NPT) improves observed survival
compared with P-POSSUM expected survival in severe
peritonitis . In a porcine model of peritoneal fecal
contamination, NPT reduced systemic inflammation
thereby improving organ function .
Loss of abdominal wall
This is an unusual condition following penetrating
injuries caused by high velocity military weapons or blast
injuries. It is sometimes a consequence of extensive
surgical debridement after soft tissue infection by
necrotizing germs that have spread to the abdominal wall. The
abdomen is of necessity open and requires TAC until it
is possible to reconstruct the wall.
Open abdomen in abdominal sepsis and pancreatitis
The main aims of the open abdomen approach in severe
secondary peritonitis and severe acute pancreatitis (SAP)
are to facilitate the clearance of the infectious material,
expedite subsequent surgical interventions and prevent
the development of abdominal compartment syndrome
In severe secondary peritonitis, a staged approach may
be required for three different reasons, although they are
often used in combinations.
Firstly, the inability to control the source of
contamination in a single operation: Instead of the traditional
model of one definitive operation and possible reoperation
only performed as needed (relaparotomy on-demand
strategy), there are two other options to manage a
severely contaminated peritoneal cavity. One, termed
planned relaparotomy refers to a technique where the
need for a second operation is recognized and decided
at the initial operation. Another option, the open
abdomen technique, is leaving the abdomen open and
treating the infected peritoneal cavity like an “open abscess”
with frequent irrigations and TAC techniques .
Secondly, if the surgeon feels the patient wont
tolerate a definitive repair and/or abdominal wall closure,
the operation is deliberately abbreviated due to the
severe physiological derangement and suboptimal local
conditions for healing, and restoration of intestinal
continuity is deferred to the second operation
(deferred anastomosis technique) This is particularly
important in hypotensive patients who are already received
Thirdly, the presence of extensive visceral edema may
increase the risk of ACS development, if primary fascial
closure is attempted . To prevent ACS, the
abdominal incision is left open and the viscera are covered with
one of the TAC methods. ACS can develop from a
number of complications related to intra-abdominal sepsis
including but not limited to large volume fluid
resuscitation resulting in visceral edema and intra-abdominal free
fluid collection, retroperitoneal, intra-abdominal and
abdominal wall bleeding and ileus, pseudo-obstruction and
mechanical obstruction of the bowel.
Severe acute pancreatitis
Since the late 1970s a treatment option for SAP was an
open management with frequent dressing changes in
order to facilitate the clearance of infection and an
adequate drainage analogously to the open management of
an incised abscess.
Patients underwent surgical interventions to achieve
control of the infection source, the infected peripancreatic
necrosis. If the source control at the initial operation was
incomplete and if repeated measures to achieve it were
needed, the abdomen was left open between procedures.
Gradually the cavity decreased in size and often healed by
secondary intention after formation of granulation tissue.
Even in the case of an enteric fistula secondary to the
open abdomen treatment, expectant management often
resulted in acceptable results, although the open
management was associated with poorer results than the closed
drainage methods [24–27].
It was suggested that a significant proportion of patients
with SAP dying of early multiple organ dysfunction
syndrome in effect died of unrecognized and untreated ACS
caused by massive fluid resuscitation, capillary leak and
visceral edema [28, 29].
Although percutaneous drainage of pancreatic ascites
can, in some cases, decrease IAP at least temporarily,
surgical decompression is the most reliable method to
relieve IAH and restore vital organ functions, especially
in the pulmonary, cardiovascular and renal systems.
There are three options for surgical decompression in
patients with no recent abdominal incision (that often is
the case in SAP). A long vertical midline incision is most
commonly used and it has been showed to decrease IAP
effectively: it is rapid and easy to perform, but it is
associated with a risk of intestinal fistulas and in many cases
failure to close the fascia requiring complex
reconstructive surgery at a later stage . Transverse laparostomy
is a promising alternative and isolated reports have
shown its effectiveness in reducing IAP . Although it
takes slightly longer to perform than midline
laparostomy, same principles of managing the open abdomen
can be applied without additional equipment.
A third alternative used in SAP is the subcutaneous
linea alba fasciotomy, where the fascia is incised through
three small skin incisions leaving the rest of the skin and
the peritoneum intact . Although it eliminates the
OA, it might not be always effective enough . In
addition, the subcutaneous fasciotomy always results in
a ventral hernia requiring repair later on.
Infected pancreatic necrosis is an established indication
for surgical necrosectomy, ideally postponed until 4 weeks
after the onset of symptoms and performed most
commonly through a midline incision . Because ACS
usually commences during the first few days of the disease
and the (usually) sterile necrosis is unripe, there are no
indications to explore the pancreas or the peripancreatic
spaces further. In addition to causing significant bleeding,
it could also introduce an infection to the peri-pancreatic
space . Although both midline and transverse incisions
could later be utilized for necrosectomy, transverse
subcostal incision could be justified for decompression when
concomitant necrosectomy is planned or anticipated in
patients with late onset ACS.
Management of OA and its definitive closure
The management of patients with OA is a particularly
challenging issue that requires compulsorily a
multidisciplinary approach with a strength interaction among
the surgeon and the intensive care unit (ICU) team in
order to offer the best treatment to these critical
A management plan to reduce risk of ACS developing,
both primary and secondary, should ideally begin before
the patient gets to the emergency room e from there get
to the operatory room where the surgeon decide to leave
open the abdomen.
In the ICU a patient with OA requires a specific
management. Coagulopathy should be treated with balanced
transfusion  with a restrictive fluid management
strategy in order to prevent acute lung injury (ALI) and
acute respiratory distress syndrome (ARDS) [36–39]; in
trauma the application of a Exsanguination Protocol with
massive transfusion showed a decreased mortality with
lower incidence of severe sepsis/septic shock and multi
organ failure (MOF) and lower ventilator associated
pneumonitis (VAP), ventilatory failure, and ACS [35, 40].
pH should be maintained > 7.2 and checked with a
frequent measurement of arterial lactate level. The heat
loss in a patient with OA is a problem that should be
constantly kept in mind. Hypothermia should be treated
reaching an ideal temperature > 37 °C with passive
rewarming, air warmers and Bair Hugger Therapy .
These patients should receive a tailored ventilatory
support with a low tidal volume in order to prevent ALI
and ARDS that can be exacerbated by VAP and
transfusion-related ALI . Infectious complications,
not only in the abdomen, are associated with failed
abdominal closure [42, 43]: an adequate antibiotic therapy
should be directed toward the underlying disease that
culminated in the OA with an empirical anti-enterococcal
coverage in patients with prior antibiotic exposure .
Another important issue in the ICU is the pain control
with a consequent reduction in agitation, stress and fear.
Adequate sedation levels should be maintained and
strictly monitored in order to reduce the recall of unpleasant
experiences and the awareness.
Fluid balance and nutrition
Other fundamental issues in critically ill patient with OA
are fluid and electrolytes balance and nutrition support.
Patients with OA have an increased insensible fluid loss.
In addition, these wounds are open into the peritoneal
cavity, adding significantly to the amount of fluid loss
across the wound surface. Hydration and volume status
should be meticulously monitored, ideally the patients
weight should be documented daily. The negative pressure
wound therapy contributes to a decrease in fluid losses
across the open wound surfaces by significantly reducing
evaporation  and draining into a dedicated canister as
V.A.C pack or Ab-thera (KCI, San Antonio, TX), facilitates
fluid collection and allows a more accurate estimation of
fluid losses from the wound and peritoneal cavity. The
measured fluid losses can then be more precisely replaced,
and hypovolemia can be minimized or potentially avoided.
Generally a critically ill patient is in a hypercatabolic
state that’s associated with muscle proteolysis, acute
protein malnutrition, impairment in immune function, and
subclinical development of MOF. Moreover OA is a
significative source of nitrogen loss in the critically ill patient
with an estimate loss of 2 g of nitrogen per liter of
abdominal fluid output  requiring an adjusted integration. A
patient with OA represents one of the sickest, most
inflamed, and subsequently most hypermetabolic among
surgical patients. A particular attention must be given to
this critical aspect: once the resuscitation is near complete
and the GI tract allows it enteral nutrition should be
initiated as soon as possible, with a clear benefit for the patient
in a lower time to fascia closure and a lower pneumonia
and fistula rate [47–49].
Temporary abdominal closure techniques
Several different TAC techniques to left open the
abdomen exist. The ideal one should be easy to apply and
remove, should allow rapid access to a surgical second-look,
should drain secretions, should ease primary closure and
should has morbidity and mortality acceptable, should
allow easy nursing, and last but not least should be readily
available and cheap. During years, different methods for
TAC have been proposed. From late ‘70s and during ‘80s,
abdominal dressings for OA were quite simple, and the
attention during treatment was focused only on protection
and control of the bowel outside the abdomen. Through
years, the attention of surgeons moved from protection of
the ileus to preservation of the peritoneal space and
prevention of lateral retraction of the fascia, which are the
most important obstacles against the reconstruction of the
abdominal wall at the end of the treatment.
One of the simplest and most inexpensive way to cover
the viscera is approximating only the skin with a simple
running suture or using towel clips. Another easy method
is the plastic silo, also known as Bogotà bag, with a
nonadherent plastic sheet, usually from sterile 3 lt. urology
irrigation bag, sutured between the fascial edges or the skin.
In the 1993 Wittmann described a new technique
(Witmann patch, Star Surgical, Burlington, Vt)
consisting in two opposite Velcro sheets sutured to the fascia
and connected on the middle allowing an easy and fast
access to the abdominal cavity, with a simple traction,
and a stepwise reapproximation preventing the fascia
Barker and colleagues in 1995 described another
technique, the vacuum pack, where a perforated plastic sheet
covers the viscera, sterile surgical towels are placed in the
wound, a surgical drain connected with a continue
negative pressure is placed on the towels and all is covered by
an airtight seal; the dressing should be changed every 2–3
days in operative room but also in the ICU. The negative
pressure allows a collection of excess fluid and keeps
constant tension on the fascia with a limited cost (50$) 
with a reported primary fascia closure rate of 68,1 % with
a total complication rate of 15 %. . The vacuum pack
was then developed with the use of a polyurethane sponge
and an adjustable pump to set the negative pressure (KCI
V.A.C. Pack, San Antonio, TX) with some advantages as
reduced need for frequent dressing changes, increased
vascularity of the wound, decreased bacterial counts and
extended opportunity for definitive fascial closure (Fig. 2).
Fig. 2 Synthetic mesh sutured to the fascial edges to maintain the traction and prevent the fascial retraction with a plastic sheet posed under in
direct contact with the intrabdominal content to protect the bowel
Another implementation of the system was introduced
by the AB-Thera (KCI, San Antonio, TX) with the use of
spider-like sponge that allow a better fluid drainage and
a better wound contraction and with a reported primary
fascia closure rate of 89 % [53, 54]. When OA is
prolonged for more than two days, the AB-Thera system
obtains better results . In a prospective observational
open-label study involving 20 trauma centers across the
USA, was demonstrated that AB-Thera was associated
with higher primary fascial closure rate and lower 30 day
all-cause mortality, possibly because of the improved
peritoneal cytokine removal with this system .
A recent modification of the Wittmann patch was
described by Dennis et al. in the 2013: the burr like sheet are
sutured not directly on the medial fascia but to the
underside of the abdominal wall, lateral to the rectus sheath,
using external blosters; on the wound is applied a vacuum
pack dressing. With this technique they showed a primary
fascia closure in 100 % of the patients .
Burlew et al. described similar results using the VAC
system (KCI, San Antonio, TX) with a polydioxanone
(PDS) suture keeping the fascia in a moderate tension
and a sequential closure of the abdomen during the
following change of dressing, every 2 days .
Acosta described a combined technique using VAC
system (KCI, San Antonio, TX) with a polypropylene
mesh applied on the fascia edge to keep it in traction
and reported a fascia closure rate of 76.6 %  (Fig. 3).
Another combined technique consist in the use of the
ABRA system (Canica Design Inc, Almonte, Ontario,
Canada), which consist in a dynamic fascial tension
device with elastomers anchored to the abdominal wall
with plastic “button anchors” with the VAC system
(KCI, San Antonio, TX) with interesting results and a
reported fascial apposition rate of 83 % [59, 60].
Which is the best and the correct management of a
patient with OA nowadays is still unclear: the technique
is relatively new and in the literature the data and the
casuistic reported are too various and too heterogeneous
to assess. With these criticisms the techniques seamed
to be associated with the best rate of primary closure
and minor complication rate are the Negative Pressure
Wound therapy and the Wittmann patch but grounded
data are needed [61, 62].
Fig. 3 Aspiration system could be placed over the eventual continuous traction system
In the management of OA with TAC the primary goal is
to close the wound within 8 days: indeed Miller reported
in a large case series, a progressive complication rate
increase after the 8th day of OA and increased morbidity
and mortality were also reported if the fascia was closed
under undue tension . If the primary closure is still
impossible to reach the surgeon has different chance.
Before the introduction of the temporary closure technique
the wounds were closed with, component separation, with
granulation tissue with split-thickness skin grafting or with
the use of synthetic mesh: in the first case it’s been created
a planned ventral hernia that requires a later surgical
correction; in the second case the use of a synthetic mesh
required a sufficient skin to cover it and exposed the patient
to the risk of fistula, adhesion formation and the risk of
infection, especially in contaminated fields . A very
interesting alternative is the use of Biological Prosthesis
(BP) [65, 66]: BP are collagen mesh derived from
allogenic or xenogenic sources and they work as a scaffold
where the host tissue can growth, covering the wall
defect activating a remodelling process in which the host
remodels the prosthesis with new healthy tissue. The
use of BP gives some advantages: the lowest
adhesiogenic potential among the prosthetic material ,
allows blood, growth and pro/anti-inflammatory factors
and drugs to reach the surgical field during the healing
process enhancing the effect against contamination or
infections. They could be divided in cross-linked and
non-cross-linked [68, 69]. The crosslinked biological
meshes are treated, after the decellularization, in order
to obtain crosslinks between and inside the collagen
chains: the presence of these bridges prolongs the
lengthening of resorption of the mesh ensuring better
tensile strength; however, this process slows the
fibroblast invasion and angiogenesis, making more difficult
the integration with the host tissue and increasing the
foreign body response by the prosthesis. The
noncrosslinked meshes have a better profile of tissue
integration and local inflammatory response, but are
subject to a faster resorption process . The Italian
Biological Prosthesis Work Group (IBPWG) proposed a
decisional model to choose which BP use, cross-linked
or not-cross-linked, creating a score on the basis of the
presence of infection and the dimension of wall defect.
 in order to facilitate the decisional process and to
obtain the better outcome for the patients.
All those involved in care of a critically ill patient should
in the first instance think how to prevent IAH and ACS.
In case of ACS goal directed therapy to achieve early
opening and early closure is the key: paradigm of closure
shifts to combination of therapies including NPWT and
dynamic closure, in order to reduce complications and
avoid incisional hernia.
There have been huge studies and progress in survival
of critically ill trauma and septic surgical patients: this in
part has been through the great work of pioneer and
scientific societies, as the WSACS and their guidelines;
however future studies and continued innovation are
needed to better understand optimal treatment strategies
and to define more clearly the indications, because OA
by itself is still a morbid procedure.
FCo, FCa, LA designed research; FCo, WB, FCa, MC, OC, SC, LF, AL, RM, GM,
GP, MS analyzed data; FCo, WB, OC, SC, LF, AL, GP wrote the paper. All
authors read and approved the final manuscript.
1. McCosh II AJ . The treatment of general septic peritonitis . Ann Surg . 1897 ; 25 : 687 - 97 .
2. Ogilvie WH . The late complications of abdominal war wounds . Lancet . 1940 ; 2 : 253 - 6 .
3. Perez D , Wildi S , Demartines N , Bramkamp M , Koehler C , Clavien PA . Prospective evaluation of vacuum-assisted closure in abdominal compartment syndrome and severe abdominal sepsis . J Am Coll Surg . 2007 ; 205 ( 4 ): 586 - 92 .
4. Kron IL , Harman PK , Nolan SP . The measurement of intra-abdominal pressure as a criterion for abdominal re-exploration . Ann Surg . 1984 ; 199 : 28 - 30 .
5. Balogh ZJ , Lumsdaine W , Moore E , Moore FA . Postinjury abdominal compartment syndrome: from recognition to prevention . The Lancet. 2014 ; 384 ( 9952 ): 1466 - 75 .
6. Malbrain ML , Cheatham ML , Kirkpatrick A , Sugrue M , Parr M , De Waele J , et al. Results from the international consensus of experts on intraabdominal hypertension and abdominal compartment syndrome . I. Definitions . Intensive Care Med . 2006 ; 32 : 1722 - 32 .
7. Cheatham ML , White MW , Sagraves SG , Johnson JL , Block EF . Abdominal perfusion pressure: A superior parameter in the assessment of intraabdominal hypertension . J Trauma . 2000 ; 49 : 621 - 6 .
8. Burch JM , Moore EE , Moore FA , Franciose R. The abdominal compartment syndrome . Surg Clin North Am . 1996 ; 76 : 833 - 42 .
9. Carr JA . Abdominal compartment syndrome: A decade of progress . J Am CollSurg . 2013 ; 216 : 135 - 46 .
10. Burrows R , Edington J , Robbs JV. A wolf in wolf's clothing-the abdominal compartment syndrome . S Afr Med J . 1995 ; 85 ( 1 ): 46 - 8 .
11. Biffl WL , Moore EE , Burch JM , Offner PJ , Franciose RJ , Johnson JL . Secondary abdominal compartment syndrome is a highy lethal event . Am J Surg . 2001 ; 182 : 645 - 8 .
12. Starkopf J , Tamme K , Blaser AR . Should we measure intra-abdominal pressure in every intensive care patient ? Ann Intensive Care . 2012 ; 2 Suppl 1:S9 . doi:10.1186/ 2110 - 5820 - 2 - S1 -S9.
13. Kirkpatrick AW , Roberts DJ , De Waele J , Jaeschke R , Malbrain MLNG , De Keulenaer B , et al. Intra-abdominal hypertension and the abdominal compartment syndrome: updated consensus definitions and clinical practice guidelines from the World Society of the Abdominal Compartment Syndrome . Intensive Care Med . 2013 ; 39 : 1190 - 206 .
14. Malbrain MLNG . Different techniques to measure intra-abdominal pressure (IAP): time for a critical re-appraisal . In: Applied Physiology in Intensive Care Medicine . Berlin Heidelberg: Springer ; 2009 . p. 143 - 57 .
15. Sugrue M , Jones F , Deane SA , Bishop G , Bauman A , Hillman K. Intra-abdominal hypertension is an independent cause of post-operative renal impairment . Arch Surg . 1999 ; 134 : 1082 - 805 .
16. Cothren Burlew C. The open abdomen: practical implications for the practicing surgeon . Am J Surg . 2012 ; 204 : 826 - 35 .
17. Balogh ZJ , van Wessem K , Yoshino O , Moore FA . Post injury abdominal compartment syndrome: are we winning the battle ? World J Surg . 2009 ; 33 : 1134 - 41 .
18. Sugrue M , Jones F , Janjua KJ , Deane SA , Bristow P , Hillman K. Temporary abdominal closure: a prospective evaluation of its effects on renal and respiratory physiology . J Trauma . 1998 ; 45 : 914 - 21 .
19. Horwood J , Akbar F , Maw A. Initial experience of laparostomy with immediate vacuum therapy in patients with severe peritonitis . Ann R Coll Surg Eng . 2009 ; 91 : 681 - 7 .
20. Kubiak BD , Albert SP , Gatto LA , Snyder KP , Maier KG , Vieau CJ , et al. Peritoneal negative pressure therapy prevents multiple organ injury in a chronic porcine sepsis and ischemia/reperfusion model . Shock . 2010 ; 34 : 525 - 34 .
21. Schein M. Surgical management of intra-abdominal infection: is there any evidence? Langenbeck's Arch Surg . 2002 ; 387 : 1 - 7 .
22. Ordonez CA , Sanchez AI , Pineda JA , Badiel M , Mesa R , Cardona U , et al. Deferred primary anastomosis versus diversion in patients with severe secondary peritonitis managed with staged laparotomies . World J Surg . 2010 ; 34 : 169 - 76 .
23. Plantefeve G , Hellmann R , Pajot O , Thirion M , Bleichner G , Mentec H. Abdominal compartment syndrome and intra-abdominal sepsis: two of the same kind? Acta Clin Belg . 2007 ; 62 Suppl 1 : 162 - 7 .
24. Bradley III EL . Management of infected pancreatic necrosis by open drainage . Ann Surg . 1987 ; 206 : 542 - 8 .
25. Fugger R , Schultz F , Rogy M , Herbst F , Mirza D , Fritsch A. Open approach in pancreatic and infected pancreatic necrosis: laparostomies and preplanned revisions . World J Surg . 1991 ; 15 : 516 - 21 .
26. Fugger R , Götzinger P , Sautner T , Mittlböck M , Rogy M , Adamer K , et al. Necrosectomy and laparostomy - a combined therapeutic concept in acute necrotizing pancreatitis . Eur J Surg . 1995 ; 161 : 103 - 7 .
27. Bosscha K , Hulstaert PF , Hennipman A , Visser MR , Gooszen HG , van Vroonhoven TJMV , et al. Fulminant acute pancreatitis and infected necrosis: results of open management of the abdomen and “planned” reoperations . J Am Coll Surg . 1998 ; 187 : 255 - 62 .
28. De Waele J , Hoste E , Blot S , Decruyenaere J , Colardyn F. Intraabdominal hypertension in patients with severe acute pancreatitis . Crit Care . 2005 ; 9 : R452 - 7 .
29. Keskinen P , Leppäniemi A , Pettilä V , Piilonen A , Kemppainen E , Hynninen M. Intra-abdominal pressure in severe acute pancreatitis . World J Emerg Surg . 2007 ; 2 : 2 .
30. De Waele JJ , Hoste EAJ , Malbrain MLNG . Decompressive laparotomy for abdominal compartment syndrome - a critical analysis . Crit Care . 2006 ; 10 :R51.
31. Leppäniemi A , Mentula P , Hienonen P , Kemppainen E. Transverse laparostomy is feasible and effective in the treatment of abdominal compartment syndrome in severe acute pancreatitis . In press.
32. Leppäniemi AK , Hienonen PA , Siren JE , Kuitunen AH , Lindström OK , Kemppainen EA . Treatment of abdominal compartment syndrome with subcutaneous anterior abdominal fasciotomy in severe acute pancreatitis . World J Surg . 2006 ; 30 : 1922 - 4 .
33. Leppäniemi A , Hienonen P , Mentula P , Kemppainen E. Subcutaneous linea alba fasciotomy, does it really work ? Am Surg . 2011 ; 77 : 99 - 102 .
34. Werner J , Hartwig W , Hackert T , Buchler MW . Surgery in the treatment of acute pancreatitis - open pancreatic necrosectomy . Scand J Surg . 2005 ; 94 : 1130 - 4 .
35. Gunter Jr OL , Au BK , Isbell JM , Mowery NT , Young PP , Cotton BA . Optimazing outcomes in damage control resuscitation: identifying blood product ratiosassociated with Improved survival . J Trauma . 2008 ; 65 ( 3 ): 527 - 34 .
36. Borgman MA , Spinella PC , Perkins JG , Grathwohl KW , Repine T , Beekley AC , et al. The ratio of blood products transfused affects mortality in patients receiving massive transfusions at a combat support hospital . J Trauma . 2007 ; 63 ( 4 ): 805 - 13 .
37. Kauvar DS , Lefering R , Wade CE . Impact of hemorrhage on trauma outcome: an overview of epidemiology, clinical presentations, and therapeutic considerations . J Trauma . 2006 ; 60 ( 6 Suppl): S3 - 11 .
38. Dutton WD , Diaz Jr JJ , Miller RS . Critical care issues in managing complex open abdominal wound . J Intensive Care Med . 2012 ; 27 ( 3 ): 161 - 71 .
39. Stewart RM , Park PK, Hunt JP , McIntyre Jr RC , McCarthy J , Zarzabal LA , et al. Less is more: improved outcomes in surgical patients with conservative fluid administration and central venous catheter monitoring . J Am Coll Surg . 2009 ; 208 ( 5 ): 725 - 35 . discussion 735-7.
40. Cotton BA , Au BK , Nunez TC , Gunter OL , Robertson AM , Young PP. Predefined massive transfusion protocols are associated with a reduction in organ failure and postinjury complications . J Trauma . 2009 ; 66 ( 1 ): 41 - 8 .
41. Rosenberg AL , Dechert RE , Park PK , Bartlett RH , NIH NHLBI ARDS Network. Review of a large clinical series: association of cumulative fluid balance on outcome in acute lung injury: a retrospective review of the ARDSnet tidal volume study cohort . J Intensive Care Med . 2009 ; 24 ( 1 ): 35 - 46 .
42. Teixeira PG , Salim A , Inaba K , Brown C , Browder T , Margulies D , et al. A prospective look at the current state of open abdomens . Am Surg . 2008 ; 74 ( 10 ): 891 - 7 .
43. Vogel TR , Diaz JJ , Miller RS , May AK , Guillamondegui OD , Guy JS , et al. The open abdomen in trauma: do infectious complications affect primary abdominal closure? Surg Infect (Larchmt) . 2006 ; 7 ( 5 ): 433 - 41 .
44. Harbarth S , Uckay I. Are there patients with peritonitis who require empiric therapy for enterococcus ? Eur J Clin Microbiol Infect Dis . 2004 ; 23 ( 2 ): 73 - 7 .
45. Caro A , Olona C , Jimenez A , Vadillo J , Feliu F , Vicente V. Treatment of the open abdomen with topical negative pressure therapy: a retrospective study of 46 cases . Int Wound J . 2011 ; 8 : 274 - 9 .
46. Cheatham ML , Safcsak K , Brzezinski SJ , Lube MW . Nitrogen balance, protein loss, and the open abdomen . Crit Care Med . 2007 ; 35 ( 1 ): 127 - 31 .
47. Collier B , Guillamondegui O , Cotton B , Donahue R , Conrad A , Groh K , et al. Feeding the open abdomen . J Parenter Enter Nutr . 2007 ; 31 ( 5 ): 410 - 5 .
48. Dissanaike S , Pham T , Shalhub S , Warner K , Hennessy L , Moore EE , et al. Effect of immediate enteral feeding on trauma patients with an open abdomen: protection from nosocomial infections . J Am Coll Surg . 2008 ; 207 ( 5 ): 690 - 7 .
49. Cothren CC , Moore EE , Ciesla DJ , Johnson JL , Moore JB , Haenel JB , et al. Postinjury abdominal compartment syndrome does not preclude early enteral feeding after definitive closure . Am J Surg . 2004 ; 188 ( 6 ): 653 - 8 .
50. Wittmann DH , Aprahamian C , Bergstein JM , Edmiston CE , Frantzides CT , Quebbeman EJ , et al. A burr-like device to facilitate temporary abdominal closure in planned multiple laparotomies . Eur J Surg . 1993 ; 159 ( 2 ): 75 - 9 .
51. Brock WB , Barker DE . Burns RPTemporary closure of open abdominal wounds: the vacuum pack . Am Surg . 1995 ; 61 ( 1 ): 30 - 5 .
52. Barker DE , Green JM , Maxwell RA , Smith PW , Mejia VA , Dart BW , et al. Experience with vacuum-pack temporary abdominal wound closure in 258 trauma and general and vascular surgical patients . J Am Coll Surg . 2007 ; 204 ( 5 ): 784 - 92 .
53. Lindstedt S , Malmsjö M , Hlebowicz J , Ingemansson R. Comparative study of the microvascular blood flow in the intestinal wall, wound contraction and fluid evacuation during negative pressure wound therapy in laparostomy using the V .A.C. abdominal dressing and the ABTheraopen abdomen negative pressure therapy system . Int Wound J . 2013 . doi:10.1111/iwj.12056. [Epub ahead of print].
54. Frazee RC , Abernathy SW , Jupiter DC , Hendricks JC , Davis M , Regner JL , et al. Are commercial negative pressure systems worth the cost in open abdomen management ? J Am Coll Surg . 2013 ; 216 ( 4 ): 730 - 3 .
55. Cheatham ML , Demetrides D , Fabian TC , Kaplan MJ , Miles WS , Schreiber MA , et al. Prospective study examining clinical outcomes associated with negative pressure wound therapy system and Barker's vacuum packing technique . World J Surg . 2013 ; 37 : 2018 - 30 .
56. Dennis A , Vizinas TA , Joseph K , Kingsley S , Bokhari F , Starr F , et al. Not so fast to skin graft: transabdominal wall traction closes most “domain loss” abdomens in the acute setting . J Trauma Acute Care Surg . 2013 ; 74 ( 6 ): 1486 - 92 .
57. Burlew CC , Moore EE , Biffl WL , Bensard DD , Johnson JL , Barnett CC . One hundred percent fascial approximation can be achieved in the postinjury open abdomen with a sequential closure protocol . J Trauma Acute Care Surg . 2012 ; 72 ( 1 ): 235 - 41 .
58. Petersson U , Acosta S , Björck M. Vacuum-assisted wound closure and mesh-mediated fascial traction-a novel technique for late closure of the open abdomen . World J Surg . 2007 ; 31 ( 11 ): 2133 - 7 .
59. Salman AE , Yetişir F , Aksoy M , Tokaç M , Yildirim MB , Kiliç M. Use of dynamic wound closure system in conjunction with vacuum-assisted closure therapy in delayed closure of open abdomen . Hernia . 2014 ; 18 ( 1 ): 99 - 104 .
60. Haddock C , Konkin DE , Blair NP . Management of the open abdomen with the Abdominal Reapproximation Anchor dynamic fascial closure system . Am J Surg . 2013 ; 205 ( 5 ): 528 - 33 .
61. Boele van Hensbroek P , Wind J , Dijkgraaf MG , Busch OR , Goslings JC . Temporary closure of the open abdomen: a systematic review on delayed primary fascial closure in patients with an open abdomen . World J Surg . 2009 ; 33 ( 2 ): 199 - 207 .
62. Roberts DJ , Zygun DA , Grendar J , Ball CG , Robertson HL , Ouellet JF , et al. Negative-pressure wound therapy for critically ill adults with open abdominal wounds: a systematic review . J Trauma Acute Care Surg . 2012 ; 73 ( 3 ): 629 - 39 .
63. Miller RS , Morris Jr JA , Diaz Jr JJ , Herring MB , May AK . Complications after 344 damage-control open celiotomies . J Trauma . 2005 ; 59 ( 6 ): 1365 - 71 .
64. Dinsmore RC , Calton Jr WC , Harvey SB , Blaney MW . Prevention of adhesions to polypropylene mesh in a traumatized bowel model . J Am Coll Surg . 2000 ; 191 ( 2 ): 131 - 6 .
65. Rosen MJ , Krpata DM , Ermlich B , Blatnik JA . A 5-year clinical experience with single-staged repairs of infected and contaminated abdominal wall defects utilizing biologic mesh . Ann Surg . 2013 ; 257 ( 6 ): 991 - 6 .
66. Campanelli G , Catena F , Ansaloni L . World Journal of Emergency Surgery . World J Emerg Surg . 2008 ; 3 : 33 .
67. Catena F , Ansaloni L , D'Alessandro L , Pinna A. Adverse effects of porcine small intestine submucosa (SIS) implants in experimental ventral hernia repair . Surg Endosc . 2006 ; 21 ( 4 ): 690 .
68. 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 .
69. Melman L , Jenkins ED , Hamilton NA , Bender LC , Brodt MD , Deeken CR , 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 .
70. Orenstein SB , Qiao Y , Klueh U , Kreutzer DL , Novitsky YW . Activation of human mononuclear cells by porcine biologic meshes in vitro . Hernia . 2010 ; 14 ( 4 ): 401 - 7 .
71. Coccolini F , Agresta F , Bassi A , Catena F , Crovella F , Ferrara R , et al. Italian Biological Prosthesis Work-Group (IBPWG): proposal for a decisional model in using biological prosthesis . World J Emerg Surg . 2012 ; 7 ( 1 ): 34 .