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9 Contemporary Management of the Open Abdomen 225
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initial truncated laparotomy where bleeding is arrested through packing or ligation and enteric contamination stemmed through stapling off bowel ends or with
running sutures. At the end of this phase, the abdomen is left open protected by
a temporary abdominal dressing, with the aims of reducing the risk of abdominal
compartment syndrome (see below) and facilitating later definitive surgery with
restoration of anatomy. The patient is then stabilised on the critical care unit with
correction of acid–base derangements, permissive hypotension, avoidance of crystalloids and resuscitation using packed red blood cells with fresh frozen plasma
and platelets as necessary. This has been termed damage control resuscitation and
in trauma can confer both a survival advantage and a reduction in length of stay
[21]. Once back to pre-injury physiology, typically in 24 hours or less, the patient
is returned to the operating theatre for definitive surgical management and planned
fascial-fascial abdominal closure.
DCL is assumed by many to reduce mortality in trauma patients and yet survivors of this strategy are often left with long-term debilitating complications such
as intestinal fistulas and large ventral hernias as well as having prolonged stays in
critical care [57]. It remains unclear what the indications are for an open abdomen
in civilian trauma, there is considerable variation in its use between institutions
and there is a growing belief that it is overused and at times unnecessary [25]. A
multi-institutional study of 209 DCLs from six Level 1 trauma centres in the USA,
representing 24% of all emergency laparotomies, determined that 47 (22%) were
unnecessary and would have been better served by definitive laparotomy and primary closure [25]. The ideal DCL rate varied between institutions from 13–27%.
DCL patients considered safe for definitive laparotomy were similar to the DCL
group on arrival but demonstrated superior responses to resuscitation and haemorrhage control. Traditionally trauma surgeons were encouraged to make decisions
about damage control surgery as early as possible in the treatment algorithm,
but these data suggest the condition of the patient at the end of surgery should
determine whether definitive laparotomy and immediate closure are appropriate.
In 2018, the World Society for Emergency Surgery (WSES) published evidencebased guidelines on the use of the open abdomen in both trauma and non-trauma
patients [19]. Persistent hypotension, acidosis (pH < 7.2), hypothermia (temperature < 34 °C) and coagulopathy were identified as strong predictors of the need for
a decompressive laparotomy in trauma (Grade 2A-weak recommendation based on
high quality evidence).
More recently a systematic review attempted to define situations where DCL
would improve patient survival [57].
•
Hypothermia
•
Acidosis
•
Coagulopathy developing intraoperatively
•
Injury pattern that precludes expedient definitive repair
•
Combined vascular and pancreatic gunshot injury
•
> 1 major abdominal vascular injury
•
> 2 abdominal visceral injuries
226 D. A. J. Slade
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•
Patients receiving > 10 units of packed red blood cells
The abdomen may also be left open in trauma patients in situations where it is
physically impossible to close the fascia,
•
Significant abdominal tissue loss
•
Development of abdominal compartment syndrome on closing
•
Gross visceral oedema,
•
Failure to control the source of contamination
•
Planned relook surgery is necessary
(WSES Grade 2B-weak recommendation, moderate quality evidence [19]).
9.2.2 Intra-Abdominal Hypertension and Abdominal
Compartment Syndrome
Normal intra-abdominal pressure (IAP) should be between 0–5 mmHg, but in critically ill adults a baseline IAP is typically 5–7 mmHg, this can increase to between
9 and 14 mmHg in morbidly obese patients [38]. Consensus definitions for intraabdominal hypertension (IAH) and abdominal compartment syndrome (ACS) were
published in 2006, management guidelines in 2007 and both were updated in a
single clinical practice guideline in 2013 [17, 32, 38] (Table 9.2).
IAH is graded as follows:
The World Society of the Abdominal Compartment Syndrome (WSACS)
defined IAH as a sustained or pathological intra-abdominal pressure reading
greater than 12 mmHg and this has been associated with an 11-fold increase
in mortality compared to patients without IAH—although it remains uncertain
whether treating IAH improves patient outcomes [38]. However, it is often the case
that IAP is infrequently or simply not measured in at risk patients and protocols
designed to avoid IAH make good clinical sense. Clinical examination is notoriously unreliable, and diagnosis is dependent on continuous or repeated transducer
readings measured at the end of expiration with the patient supine. Kron described
ACS in patients following ruptured aortic aneurysm surgery and with it the first
description of a simple, reliable and low cost method for IAP measurement [36].
Tab le 9.2 World Society of the Abdominal Compartment Syndrome (WSACS) definitions [32]
Intra-abdominal hypertension Intra-abdominal pressure (mmHg)
Grade I 12–15
Grade II 16–20
Grade III 21–25
Grade IV >25
Abdominal compartment syndrome >20 with new organ dysfunction/failure
9 Contemporary Management of the Open Abdomen 227
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The method uses a pressure transducer attached to a urinary bladder catheter with
a maximal instillation volume of 25mls of sterile saline and zeroed at the level of
the mid-axillary line, as this is the easiest anatomical landmark to identify even in
the obese [17].
Abdominal compartment syndrome (ACS) is a persisting IAP > 20 mmHg with
new organ dysfunction. The consequence of raised intra-abdominal pressure is a
reduction in venous return affecting intra-abdominal organ perfusion and upward
pressure on the diaphragm impeding lung function. The negative effects of IAH
occur long before the development of ACS. Changes in IAP affect the perfusion of
most intra-abdominal organs but one of the earliest and most visible signs of IAH
is oliguria as a consequence of pressure differences across the renal glomerulus
and a reduction in renal filtration [41].
The incidence of ACS in the critically ill is dependent on case-mix (medical,
surgical or trauma), is inconsistently measured and reported despite the WSACS
guidelines, but is somewhere between 1 and 6% [31, 71].
Recent studies show that the incidence of ACS is falling, possibly due to better
perioperative care, restricted fluid resuscitation, earlier recognition and management but that the most at risk patients are the obese and those with acute severe
pancreatitis [40, 71, 20].
It is clear that elevated IAP is widely prevalent in critically ill patients and IAH
and ACS are causes of significant mortality and morbidity in this population [6,
39, 40]. However, in clinical practice what constitutes a pathological IAP is not an
absolute value but a trend which becomes significant when there is associated end
organ dysfunction.
Decompressive laparotomy and abdominal compartment syndrome
Peritonitis, trauma, severe burns, ruptured abdominal aortic aneurysm and vascular
emergencies, severe acute pancreatitis and mechanical bowel obstruction often in
combination with aggressive fluid resuscitation are all potential causes of ACS [4,
35, 39, 40, 70, 74, 77]. Patients should be treated with a high index of suspicion
for developing ACS, and should have IAP measurements taken every 4–6 h [32].
Rising or persistently raised IAP should be treated immediately by medical management strategies as below. Patients whose IAP fails to respond to these measures
should undergo either interventional radiological or surgical decompression within
24 h [32, 71].
The presence of IAH with s
should trigger treatment and management strategies based on the following 4
general principles [17]:
erial monitoring of IAP, at least 4 hourly
1. S
ptimisation of systemic perfusion and organ function through
2. O
nstitution of specific measures to reduce IAP including:
3. I
•
implementing optimal sedation, analgesia, neuromuscular blockade, and
g or goal-directed fluid resuscitation to avoid a positive cumulative
limitin
fluid balance
ustained, reliable IAP readings of > 12 mmHg
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•
changes to body positioning and removal of restrictive dressings or release
of eschars (burns)
•
gut decompression with nasogastric intubation, neostigmine for colonic
pseudo-obstruction, cessation of enteral feed, enemas or endoscopy
•
reduction of excess fluid with renal replacement therapies or hemofiltration
•
reducing abdominal distension with percutaneous catheter decompression or
failing that
4. Radiologically guided percutaneous catheter drainage of obvious intra-
peritoneal fluid which may avoid decompressive laparotomy.
However, if an IAP > 20 mmHg is present with new organ dysfunction and refractory to steps 1–4 then surgical d
considered (WSES guidelines Grade 2B-weak recommendation, moderate quality
evidence [19]).
The evidence supporting decompressive laparotomy remains limited, and whilst
it clearly lowers IAP, improving haemodynamic, respiratory, and renal function,
its application must be balanced with the associated mortality of it in combination
with ACS and its morbidity [20]. In patients who have undergone decompressive
laparotomy and are left with an open abdomen, IAH may still persist and the effect
on organ function is not uniform with some studies showing no effect at all [79,
24]. Therefore, its use should be carefully considered and restricted to when all
other medical options fail.
There are three described surgical techniques for decompressing the abdomen:
ecompressive laparotomy should be strongly
•
midline laparotomy
•
bilateral transverse subcostal laparotomy which has the disadvantage of being
destructive
•
and the less invasive subcutaneous linea alba fasciotomy where three short mid-
line skin incisions are made to divide the linea alba only, avoiding opening the
peritoneal cavity [71].
Of these three, only midline laparotomy has any substantial data to support its use.
A systematic review of 15 studies (3 of which included children under 18 years
of age only) on the effect of decompressive laparotomy in ACS in 286 patients
found the following [20]:
•
it reduced IAP by an average of 13.5 (range 11–17) mmHg
•
it improved urine output by a mean of 95.3 + 105.3 ml/hr
•
it was associated with a 49.7% mortality (range 22.2–71.4%)
•
in children there were similar findings including reductions in IAP, improved
haemodynamics and a mortality of 60.8% (range 16.7–100%).
9 Contemporary Management of the Open Abdomen 229
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9.2.3 Peritonitis and Intra-Abdominal Sepsis
Whilst DCL is credited with popularising the use of the open abdomen in critically
ill patients, what is often not appreciated is that it was already an established
technique in the management of severe and intractable peritonitis [12, 42, 63]. It
was first described by McCosh in 1897 in the treatment of “septic peritonitis” and
the first series of 14 patients with diffuse peritonitis was published by Steinberg in
1979 [1]. Intra-abdominal sepsis is by far the commonest indication for an open
abdomen outside of North America, comprising 68.9% in the UK and 46% from
European audits [15, 61]. It should also be recognised that septic patients who are
managed with an open abdomen in the UK and Europe are generally older and
more co-morbid than those reported in trauma series, suggesting their outcomes
may be quite different.
Peritonitis and intra-abdominal sepsis are separate entities but often confused.
Intra-abdominal infection causes peritonitis usually through bacterial inflammation
[87]. Peritonitis and intra-abdominal infection have been classified according to
their causation into primary, secondary, and tertiary (Table 9.3).
Primary peritonitis is typically monomicrobial whereas anaerobic or polymicrobial infection suggests secondary peritonitis derived from the gastrointestinal
tract. Primary peritonitis requires a medium such as ascites or peritoneal dialysis
fluid which is then seeded spontaneously by bacteria. The mainstay of treatment
is therefore antibiotic therapy.
Tab le 9.3 Simplified classification of peritonitis after Wittmann [87]
Peritonitis type Description Subclassification Description
Primary Diffuse bacterial peritonitis
+ intact viscera
Secondary Originating from defect in
viscus
Ter t iary Peritonitis-like (disturbed
host immune response)
CAPD = continuous ambulatory peritoneal dialysis
A Spontaneous peritonitis
in children
B Spontaneous peritonitis
in adults
C Peritonitis + CAPD
D Tuberculous/
granulomatous
peritonitis
A Acute perforation eg
diverticulitis
B Postoperative eg
anastomotic leak
C Post-traumatic
A Peritonitis without
evidence of pathogens
B Fungal peritonitis
C Low grade pathogenic
bacterial peritonitis
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Secondary peritonitis, however, can be thought of as a surgical disease, generated through a breach in the physical or functional integrity of the gastrointestinal
tract, often generating intra-abdominal sepsis (IAS) and where timely surgical
intervention is critical both in achieving source control and removal of contamination. It is the second commonest cause of sepsis after pulmonary infection and
carries a mortality of between 20–60% [11, 87]. Secondary peritonitis may also
be caused by mesenteric ischaemia, volvulus, or trauma [18].
IAS may progress to life-threatening organ dysfunction and a dysregulated host
response ending in multiorgan failure and death.
The causative infection in tertiary peritonitis is more usually nosocomial, such
as Enterobacter, Enterococcus, Acinetobacter, Citrobacter, Pseudomonas or fungal
[18]. Tertiary peritonitis is frequently the result of persistence or failed management of secondary peritonitis characterised by multiple trips to theatre for
attempted source control and with a mortality greater than that of secondary
peritonitis (64 vs 33%, respectively) [43].
Diagnosis of IAS is primarily clinical; a typical history being rapid-onset
abdominal pain with tenderness, fever, tachycardia and/or tachypnoea along with
a raised white cell count and raised acute phase proteins (C-reactive protein,
procalcitonin). Indicators of organ dysfunction such as oliguria, altered mentation, an elevated lactate and hypotension should raise additional concern around
the development of septic shock [60]. Ultrasound and Computed Tomography
(CT) scanning are both useful in achieving a diagnosis with CT having a higher
sensitivity and specificity for detecting IAS and its causes [60].
Source control in intra-abdominal sepsis
Management of IAS is centred around rapidly achieving a diagnosis followed by
timely source control, with mortality directly related to the speed and effectiveness
of intervention [2]. Source control is the institution of measures to control a focus
of infection and in IAS is achieved predominantly by laparotomy involving not just
drainage but often resection of perforated or necrotic tissue. It should be supported
by the immediate institution of appropriate empirical antibiotics, modified later by
culture and sensitivity of the infectious agent where available. Hypotension and
oliguria require prompt treatment with judicious intravenous fluid therapy to correct the disturbed physiology and improve end organ perfusion. Mortality rates and
the establishment of tertiary peritonitis are directly related to failure in achieving
rapid source control at the earliest opportunity [55, 60].
Relaparotomy-planned or on demand
Koperna and Schulz carried out a retrospective review of 523 consecutive patients
treated for secondary peritonitis over a decade; 105 of whom failed initial source
control [33]. They suggested that there was no difference between planned or on
demand return to theatre with equivalent mortality (54.5% and 50.6% respectively)
but those patients who underwent on demand laparotomy within 48 h of the failed
source-control laparotomy had the lowest mortality at 9%.
9 Contemporary Management of the Open Abdomen 231
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In 2007, the Dutch peritonitis study group published a multicentre study comparing two strategies for the surgical management of secondary peritonitis [78].
232 patients were randomly allocated to either a planned relaparotomy every
36–48 h after the index laparotomy until the peritoneal cavity was macroscopically clean or to an on-demand pathway where patients returned to theatre only
where there was clinical deterioration or lack of improvement with a likely
intra-abdominal cause. The was no difference in mortality or peritonitis-related
morbidity between the two strategies but the on-demand group had a substantial
reduction in relaparotomies, healthcare costs and use of resources.
The main conclusion of this trial is important as it decided a long-running
debate, but it is also interesting that in the on-demand group, 42% of patients
underwent a relaparotomy of which 31% were negative. It highlights the difficulty
in discerning the difference in critically ill patients between failed source control mandating further surgery and successful source control with lack of clinical
improvement that does not mandate surgical treatment. The authors commented
that a more rigorous use of CT scanning may have prevented unnecessary returns
to theatre and reduced the negative laparotomy rate. This could never be truer than
today, where many clinicians have rapid access to round the clock, high quality,
multi-slice CT imaging which guides most treatment decisions in post-operative
patients. CT also identifies those suitable for minimally invasive, percutaneous
drainage thereby avoiding the “second hit” of a repeat laparotomy.
Rapid source control laparotomy in intra-abdominal sepsis
It is important to note that whilst damage control laparotomy has been extended to
emergency general surgery (also termed rapid source control laparotomy -RSCL),
very little evidence exists to support the creation of an open abdomen in IAS [32].
Over twenty years ago, Bosscha and colleagues questioned the safety of an open
abdomen in 67 consecutive patients with severe secondary peritonitis, recording
an in-hospital mortality of 42%, prolonged mean hospital stay of 60 days (5–167),
a fistulation rate of 24%, and a reoperation rate for mesenteric bleeding of 24%.
Interestingly they used an early form of mesh-mediated fascial traction (see later
section) to achieve delayed fascial closure over a mean of 9 reoperations. They
concluded that the value of employing an open abdomen relied on the lack of
other therapeutic strategies rather than the success of the technique itself.
More recently, Berg et al. investigated the use of RSCL in severe acute
diverticulitis using the American College of Surgeons National Surgical Quality Improvement Program (NSQIP) database [8]. They identified a retrospective
cohort of 460 patients with Hinchey Grade IV diverticulitis (faecal peritonitis)
of which 101 (21.9%) had RSCL and the remainder had primary fascial closure.
They were matched by propensity scoring for treatment modality following which
there was no difference between the groups for age, sex, septic shock, comorbidities, and American Society of Anaesthesia (ASA) class. The two groups
were assessed for 30-day outcomes. There was no difference in mortality, but
patients who underwent primary fascial closure had shorter hospital stays (13 versus 17 days, p = 0.02) and were twice as likely to return to their own home rather
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than intermediate care facilities. The authors commented that the percentage of
patients treated with an open abdomen was excessive and should be rationalised to
the original indications of acidosis, coagulopathy, and hypothermia in the setting
of septic shock.
Leaving the abdomen open does of course facilitate multiple returns to theatre
but it should be noted that the Dutch trial, one of the few, high quality randomised
controlled trials in the surgical management of secondary peritonitis, closed all
abdomens in both arms of the study. However, leaving the abdomen open in secondary peritonitis had been championed as the best management in life-threatening
intra-abdominal sepsis.
It is for this reason that Robledo and colleagues attempted to study open
versus closed management of the abdomen in secondary peritonitis with a singlecentre, randomised controlled trial [58]. 40 patients with peritonitis and similar
disease severity were randomly allocated following source-control laparotomy to
either definitive closure or open abdomen management. The open group had a
non-absorbable polypropylene mesh sutured to the fascial defect which was then
packed with iodine povidone-soaked gauze. The study was terminated at the first
interim analysis due to a raised relative risk (1.84) and odds ratio of death (2.85)
in the open group.
Given the lack of consensus and management guidelines concerning closing or
leaving the abdomen open in sepsis, Kao et al. retrospectively reviewed 544 nontrauma patients who underwent emergency laparotomy for secondary peritonitis
[29]. 203 patients were managed with an open abdomen, the remainder were closed
primarily. 136 (67%) of the open abdomen cases were closed at the first laparotomy, whilst 67 (33%) had multiple planned reoperations (mean 1.6 ± 1.5). The
likelihood of being left with an open abdomen was increased if surgery occurred
at night (52.7% vs 43.7% p = 0.044) and doubled if performed by an acute care
surgeon as opposed to a subspecialist (43.3% vs 21.3%). After propensity matching of 111 closely matched pairs, open abdomen patients had increased rates of
postoperative problems (71.2% vs 41.4%, p < 0.0001) including gastrointestinal
and infectious complications. Open abdomen patients had a longer length of stay
(median 13 vs 9 days, p = 0.0001) and were more likely to be discharged to intermediate care rather than home (58.6% vs 45.9%, p = 0.006). In hospital mortality
was higher with an open abdomen at 22.5% than with primary closure at 11.7%
(p = 0.006).
Whilst peritonitis and trauma may share similarities in terms of risk of IAH,
progression to ACS, inflammatory mediator cascades, and progression to multiorgan failure, they are quite different when it comes to aims of therapy, timeframe,
and outcomes (Table 9.4).
Most importantly, patients with peritonitis treated with an open abdomen spend
longer with their abdomen open, have a higher risk of fistulation, and a lower
chance of definitive fascial closure than trauma patients.
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Tab le 9.4 Comparisons between trauma and non-trauma patients treated with open abdomen [3,
27]
Criteria Trauma Peritonitis
Pathophysiology Coagulopathy Inflammation
Aims of surgery Haemostasis
Aims of therapy Correct coagulopathy
Mean duration of open abdomen Short-2–3 days 3–9 days (depending on cause)
Fistulation rate % (95% CI) 2–5%* 12.1% (10.1–14.4)§
Fascial closure rate % (95% CI) 64–96%* 50.2% (43.4–57)§
*
Weighted proportions, range between different open abdomen temporary abdominal closure tech-
niques (skin-only, patch, vacuum closure, static and dynamic therapy)
§
Weighted mean for all temporary abdominal closure techniques
Control contamination
Normothermia
Correct pH
Drainage of infection
Control infective source
Sterilise peritoneum
Correct vasoplegia
Reduce inflammatory mediators
9.2.4 Acute Mesenteric Ischaemia, Pancreatitis, and Burns
Without Abdominal Trauma
Acute mesenteric ischaemia is an infrequent diagnosis affecting just 0.09–0.2%
hospital admissions but a frequent cause of emergency intestinal resection with
a mean in-hospital mortality rate, even after surgical intervention, of 64% (range
24–85%) [5, 66]. The mainstay of surgical management before CT angiography
and endovascular techniques became readily available was resection of ischaemic
bowel.
The index laparotomy was frequently conducted along DCL principles and following bowel resection, many patients were left with an open abdomen.
second-look laparotomy followed in 24–48 h, at which gut viability could be
re-assessed, and bowel which had demarcated could be resected [5].
With better access to CT and endovascular therapy, the management and prognosis of mesenteric ischaemia has improved, and treatment has moved away from
DCL techniques. High-resolution CT angiography can allow an earlier diagnosis,
with treatment started before the gut becomes irreversibly ischaemic. Laparotomy
is still indicated if there is CT evidence of ischaemic bowel or if peritonitis is
present.
Approximately 30% of patients with severe acute pancreatitis develop ACS
and when this occurs it is associated with a high mortality of up 75% even with
early surgical management [68]. ACS in pancreatitis may be predicted by a number of factors which are present on admission including an elevated APACHE II
or Glasgow-Imrie score, tachypnoea (respiratory rate > 20/min), or acute kidney
injury [68].
In burns patients without abdominal trauma, who undergo high-volume crystalloid resuscitation, there is now recognition that IAH and ACS are commonly
A later,
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under-recognised and under-treated with an incidence of 36–70% and 1–20%
respectively [4].
The indications for decompressive laparotomy in pancreatitis, burns or any
other pathology that generates ACS are exactly the same and the treatment
algorithm outlined by WSES above should be followed.
Finally, it should be noted that all the techniques for management of the open
abdomen have also been advocated for patients with a burst abdomen where it is
impossible to directly suture the fascia closed, on the basis that they share similar
features.
9.3 Management of the Open Abdomen
9.3.1 Temporary Abdominal Closure Dressings
Temporary abdominal closure (TAC) refers to any method of dressing for an open
abdomen. It is a misnomer as the majority of dressings do nothing to close the
abdomen; they simply attempt to protect it.
Features of an ideal temporary abdominal closure dressing should include:
•
Protection of abdominal organs
•
Management or prevention of fluid losses
•
Prevention of bowel injury and fistulation
•
Protection from adhesions to the anterior abdominal wall,
•
Prevention of fascial retraction
•
Cost-effectiveness and ease of use
Many dressings have been used in open abdomen management and they can be
categorised into static, dynamic, or mixed techniques.
When assessing the merits of various TAC techniques, it is helpful to consider the amended Bjorck classification of the open abdomen (Table 9.5), from
which it can be appreciated that the most effective dressing will minimise side
wall adhesions and fixation whilst keeping the peritoneal cavity clean. It should be
recognised that adhesions and fibrin deposition start forming within just 24 h, and
it is the formation of these that determines abdominal wall fixation. What is clear
is that initial management determines both the duration and subsequent complexity
of the open abdomen, and that the likelihood of early fascial closure exists with
Grades 1 & 2 without enteric leak whereas Grades3&4preclude it. In addition,
poor management leads to fixation, the risk of fistulation and progression from a
rapidly salvageable position to an unsalvageable one.
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