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P. Cowled and R. Fitridge
Further Reading
Cowled PA, Khanna A, Laws PE, Field JB, Varelias A, Fitridge RA. Statins inhibit neutrophil
inltration in skeletal muscle reperfusion injury. J Surg Res. 2007;141:267–76. https://doi.
org/10.1016/j.jss.2006.11.021.
Granger DN, Kvietys PR.Reperfusion therapy—What’s with the obstructed, leaky and broken cap-
illaries? Pathophysiology. 2017;24:213–28.
Khanna A, Cowled PA, Fitridge RA.Nitric oxide and skeletal muscle reperfusion injury: cur-
rent controversies (research review). J Surg Res. 2005;128:98–107. https://doi.org/10.1016/j.
jss.2005.04.020.
Lutz J, Thurmel K, Heemann U.Anti-inammatory treatment strategies for ischemia/reperfusion
injury in transplantation. J Inamm (Lond). 2010;7:27. https://doi.org/10.1186/1476-9255-7-27.
Stoksz K, Ledakowicz-Polak A, Zagorski M, Zielinska M.Ischaemic preconditioning—Current
knowledge and potential future applications after 30 years of experience. Adv Med Sci.
2017;62:307–16.
https://doi.org/10.1016/j.advms.2016.11.006.
https://doi.org/10.1016/j.pathophys.2017.09.003.
Chapter 19
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Abdominal Compartment Syndrome
andOpen Abdomen Treatment
MartinBjörck
Key Learning Points
Intra-abdominal hypertension (IAH) is the sustained or repeated pathological
•
elevation of intra-abdominal pressure (IAP)>12mmHg.
• Abdominal perfusion pressure (APP) is the mean arterial pressure (MAP)
minus IAP.
• Abdominal compartment syndrome (ACS) is the sustained IAP > 20 mmHg
(with or without an APP <60mmHg) which is associated with new organ dys-
function or failure.
• Intra-abdominal pressure is most commonly measured using the Foley manom-
eter method, which can be performed in and out of the ITU environment.
• ACS occurs in up to 20% of cases of open and endovascular repair of ruptured
AAA.A further cohort of patients managed with emergency ruptured AAA open
repair will require prophylactic open abdomen treatment.
• Major risk factors for the development of ACS include uid overload/generalised
oedema, post-operative bleeding and bowel ischaemia.
•
The duration of IAH before decompression laparotomy (DL) is associated with
the frequency of development of acute renal failure and need for dialysis.
• Non-surgical management of IAH includes drainage of gastric contents, early
enteral feeding, adequate pain relief, use of neuromuscular blockade, reducing
uid overload and the early use of a massive transfusion protocol in patients
suspected to require 10 or more units of blood.
• A major problem associated with DL is lateralisation of the abdominal wall,
which occurs when the musculature and fascia of the abdominal wall move later-
ally away from the midline with time. Vacuum-assisted wound closure and mesh-
mediated fascial traction is widely used to manage ACS and is associated with
high rates of primary delayed fascial closure.
M. Björck (*)
Department of Surgical Sciences, Vascular Surgery, Uppsala University, Uppsala, Sweden
e-mail: martin.bjorck@surgsci.uu.se
R. Fitridge (ed.), Mechanisms of Vascular Disease,
https://doi.org/10.1007/978-3-030-43683-4_19
441© Springer Nature Switzerland AG 2020
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M. Björck
19.1 Introduction
The appreciation that a tense abdomen is life-threatening was rst described in ancient
Greece. In 1984, the vascular surgeon Irving Kron named the condition abdominal
compartment syndrome (ACS). He described ACS following surgery for ruptured
abdominal aortic aneurysm (RAAA) [1]. ACS is often a consequence of aggressive
resuscitation after major bleeding, and thus it is partly an iatrogenic condition. The rst
international conference on Intra-Abdominal Hypertension (IAH) and the Abdominal
Compartment Syndrome was held in 2004. The conference resulted in the publication
of two important consensus documents describing the denitions [2], risk factors [2]
and treatment guidelines [3]. These were later revised using the GRADE Methodology.
The Updated Consensus Denitions and Clinical Practice Guidelines from the World
Society of the Abdominal Compartment Syndrome were published in 2013 [4].
19.2 Denition ofIntra-abdominal Hypertension
(IAH)/ Abdominal Compartment Syndrome (ACS)
“IAH is dened by a sustained or repeated pathological elevation in intra- abdominal
pressure (IAP) >12mmHg.” This is the denition of IAH, as rst stated in the 2006
consensus document [2], and was unaltered in the updated guidelines in 2013 [4]. It
has been shown in both animal research and in clinical studies that an IAP above
12mmHg negatively affects organ function, in particular renal function [5]. It is
important to note that a single elevated value may be the result of the patient being
in pain, or passing stools. This threshold for negative effects on organ function is
important to consider in patients operated on for RAAA, since multiple prospective
clinical studies have shown that it is uncommon that the IAP is <12mmHg in the
early postoperative period after open surgical repair (OSR) [6–8]. If hemodynamically unstable patients are treated with EVAR, the situation is quite similar [9].
Although the evidence based approach used in the revision of the Guidelines [4]
did not nd support for a sub-denition of low abdominal perfusion pressure
(APP = MAP − IAP < 60 mmHg), it is a clinical observation that hypotensive
patients are more sensitive to IAH. (APP = Abdominal Perfusion Pressure,
MAP=Mean Arterial Pressure).
ACS is dened as a sustained IAP >20 mmHg (with or without an APP
<60mmHg) that is associated with new organ dysfunction/failure [4]”. Again, the
exact wording is important: “a sustained IAP >20mmHg” means that the measurement has to be repeated at least once, and it needs to be associated with “new organ
dysfunction/failure”, with a temporally-associated deterioration of vital organ function. ACS is dened as the combination of this high IAP and its effect on vital organ
function, never as a mere measurement of the pressure!
There are many ways to measure IAP. Most commonly IAP is measured in the
bladder, intermittently or continuously. Our preferred method is the FoleyManometer
method (Holtech Medical, Charlottenlund, Denmark) with the advantage that it can
easily be applied outside of the ICU, a great advantage especially after EVAR for
RAAA, since those patients seldom need to stay in the ICU after surgery (Fig.19.1a,b).
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a
b
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Fig. 19.1 (a) The Foley Manometer device is placed between the urinary catheter and the urine
collecting bag. If the patient is anuric the system is lled with saline, otherwise the urine from the
patient serves as measuring medium. (b) When the IAP is measured the “0mmHg” mark of the
manometer tube is placed at the mid-axillary line or at the level of the iliac crest (mark for future
reference). The lter is elevated vertically above the patient, and the bio-lter clamp is opened.
Read the pressure in end-expiration, the tube is graded in mmHg (13.6mm between each mark).
Finally the clamp is closed, and the system is replaced in its drainage position
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M. Björck
19.3 How Common Is IAH/ACS After AAA Repair?
Although IAH and ACS occur in other clinical scenarios such as trauma, intestinal
ischaemia and aortic dissection, the situation that the vascular surgeon most often
has to consider the possibility of IAH/ACS is after AAA repair, in particular after
rupture. The incidence of ACS will depend on several factors. The approach to
resuscitation is of paramount importance. Balogh etal. showed that the administration of crystalloids is an independent risk factor for the development of ACS in
abdominal trauma patients [10], and this is true in any bleeding patient. A policy of
preoperative permissive hypotension in RAAA is likely to decrease the risk of
developing post-operative IAH/ACS.
Mell etal. showed that patients who received less than one unit of plasma for
every two units of red blood cells during RAAA repair, had a four times higher
mortality than those given more plasma [11], highlighting the importance of “massive transfusion” protocols. These protocols were introduced in most modern hospitals during the last decade, reducing both mortality and uid overload, thereby
decreasing the risk of ACS.
The introduction of endovascular aneurysm repair (EVAR) [12, 13] by Volodos
in 1985 transformed aortic surgery. The application of EVAR in patients with
RAAA was rst reported by Ohki and Veith in 2000 [14], and has become more
frequently used over time worldwide [15]. In a contemporary nationwide study
from the Swedish vascular registry (Swedvasc), ACS occurred as often after EVAR
as after OSR (6.9% versus 6.8%), although 10.7% of those operated on with OSR
had been primarily left with an open abdomen (OA), thus preventing ACS [16, 17].
If measured consistently, IAP >20mmHg occurs in about half the patients after
OSR of a RAAA, and 20% develop ACS [5, 6]. In many older series, patients operated on for RAAA with EVAR were more haemodynamically stable, resulting in a
lower incidence of IAH/ACS after EVAR [7]. The Zürich group who treated virtually all ruptured AAA patients with EVAR and who monitored IAP, reported a high
incidence (20%, 20/102) of ACS [
spective cohort study in four Swedish hospitals, the risk of requiring treatment with
open abdomen (OA) after aortic repair was higher after rupture, but similar after
EVAR and OR; in all, 28 of 1041 operations or 2.9% of cases [18].
9], similar to the incidence after OSR.In a pro-
19.4 Pathophysiology andRisk Factors forACS After
AAA Repair
Most risk factors for the development of ACS are associated with bleeding, shock
and resuscitation, and they are well described in the guidelines [4]. In the largest
study published so far on ACS after AAA repair, 120 out of 8765 patients (1.4%)
developed the complication [17]. In these 120 patients, all the case records, including all the data from the ICU and reoperations, were scrutinized and three main
pathophysiological mechanisms were identied.
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1. The most common cause was uid overload/general oedema, which was the
main cause in 55 patients (47%).
2. Postoperative bleeding was the cause of IAH/ACS in 34 (29%). As expected,
those patients developed ASC most rapidly after the rst operation of AAA repair.
3. Finally, in 27 patients (23%) bowel ischaemia was identied as the main cause of
IAH/ACS, although a vicious circle is established when in most cases a gangrenous
colon dilates, resulting in further increase of IAP, and more pronounced ischaemia.
This mechanism had previously been studied in a prospective study after RAAA,
when a direct association between IAH and colonic ischaemia was veried [8].
This paper [17] also reported that ACS developed early in most cases (and in particular after EVAR). Decompression laparotomy (DL) was performed within 24 h
after completion of AAA repair in 56 (49%), between 24 and 48h in 30 (26%) and
after 48h in 29 (25%). The duration of IAH before DL was associated with with the
likelihood of development of renal failure and need of renal replacement therapy
(RRT). This association had previously been shown in a prospective multicentre study
of patients treated with open abdomen (OA) for ACS, in a mixed ICU patient population which was dominated by trauma, but also included patients with RAAA [19].
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19.5 Prevention ofACS andMedical Management
It is also possible to treat IAH in a proactive way, preventing further deterioration of
the patient and development of ACS.This treatment is sometimes referred to as
“medical management”, or “conservative management”, which is not an appropriate label since it can be quite aggressive. The aim is to prevent further increase of
the IAP, as well as to support organ function.
There are two mechanisms through which the IAP can be reduced. One is volume reduction of the intra-abdominal cavity. Evacuation of the retroperitoneal
hematoma after EVAR for RAAA has been attempted with lumpectomy (surgical
approach through the lateral/dorsal part of the abdominal wall). Another alternative
was described by Hörer et al., who inserted tissue plasminogen activator (tPA)
through a 20F catheter placed in the hematoma with CT guidance in 13 patients
[20]. None of these techniques are truly minimally invasive, and major (even fatal)
bleeding complications, were reported. Decompression midline laparotomy seems
both safer and more effective than these approaches.
Drainage of gastric content is important, but early enteral nutrition should not be
halted [21], since bowel movements are of strategic importance. Enteral feeding can
be initiated on the rst postoperative day, even in the presence of IAH, but the gastric contents should be drained twice daily to avoid accumulation. However, enemas
and other activities to stimulate the faecal ow are seldom effective after aortic
repair. Early enteral nutrition and avoiding opioids are more effective and epidural
anaesthesia is preferred (see below). It is common that the IAP increases hours
before the rst bowel action, after which the IAP drops substantially. Free drainable
uid in the abdominal cavity after AAA repair is uncommon.
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M. Björck
Abdominal compliance (AC) measures the ease of abdominal expansion,
expressed as a change (delta=Δ) in intra-abdominal volume (IAV) per change in
intra-abdominal pressure (IAP): AC = ΔIAV/ΔIAP. This is a dynamic variable
which is dependent on baseline IAV and IAP, as well as on reshaping and stretching
capacity of the abdominal wall. The rst phenomenon is that the abdomen transforms from an oval into a circular shape (reshaping), followed by stretching, and
nally by a rapid increase in IAP.In a review of AC, the most important conclusion
was that patients with high IAP have a reduced AC, making the IAP very sensitive
to small changes in IAV [22]. This phenomenon explains the often dramatically fast
increase of IAP before the ACS develops, and why proactive early and frequent
monitoring of IAP, and preventive actions, are so important.
One of the most effective ways of decreasing the IAP is pain relief, but it is also
strategically important to avoid opioids, to prevent obstipation. During RAAA
repair there is seldom time to insert an epidural catheter prior to surgery, and after
surgery the patient often has coagulopathy. We routinely discuss this with the anaesthesiologists, postpone the use of low molecular weight heparin (LMWH) medication, give platelets if necessary, and then use epidural analgesia whenever possible.
This is quite effective in reducing IAP, can often increase urinary output, and
become the turning point in the critical postoperative period.
Neuro-muscular blockade (NMB) is an effective way of immediately reducing IAP
when the patient is on the ventilator, which is often the case, especially after OSR of
RAAA.It reduces IAP by 30–50%, which is often sufcient to improve renal function,
reduce uid overload, and reverse the situation of increasing IAP before ACS develops.
In a study on 191 trauma patients undergoing damage control laparotomy, 92 who were
on NMB during the rst 24 h had higher primary fascial closure rate [23]. A large
French RCT showed that NMB used for 48h in 340 mixed ICU patients was safe and
improved survival in patients with acute respiratory failure [24]. There are no published
specic data on the effect of NMB in RAAA patients, but in our experience it works well.
Reducing uid overload acts through both mechanisms: reducing intra- abdominal
volume and also making the abdominal wall more compliant, as the oedema
decreases. Intensivists have different opinions how uid overload can be prevented,
and this issue is highly controversial. Many argue that colloids are benecial in this
situation, others that they only leak into the extra-cellular space, adding further to
the uid overload and affecting renal function negatively. In our practice, plasma
tends to be used in the early post-operative phase, when the patient is often coagulopathic, and hypertonic 20% albumin combined with furosemide or renal replacement therapy is used later in the postoperative phase [
25]. If the patient is on a
ventilator, an increased PEEP may help to recruit uid from the lungs.
Fluid overload is often more iatrogenic than is recognized. The Uppsala protocol
is very restrictive with regard to the administration of crystalloids from early resuscitation. Not all are aware of the fact that when fractionated blood products (erythrocytes, plasma and thrombocytes, 1:1:1) are given to compensate for 1L of blood
loss, 4–500mL of saline solution is also added. Thus, even if only blood products
are given, the transfusion to compensate for 10L of blood loss will automatically
result in a uid overload of 4–5L of saline, making further administration of crystalloids dangerous [4, 11, 25].
19 Abdominal Compartment Syndrome andOpen Abdomen Treatment
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19.6 Decompression Laparotomy (DL)
When ACS is developing or present, the only effective treatment is DL.It should
preferably be performed in the midline, from the costal arch to the symphysis pubis.
To not open the entire abdomen is a classical mistake. It is not only less effective,
but also more difcult to close.
The timing of DL is important but a complex issue in clinical practice. Ideally the
two strategies of early or delayed DL should be compared in a randomised trial. It
does not make sense to wait until severe organ dysfunction/failure has developed
before performing DL, but OA treatment itself is a morbid procedure associated
with both morbidity and mortality. In the large Swedish cohort of 120 patients
treated for ACS after AAA repair, timing of DL, i.e. the duration of IAP >15mmHg,
or >20mmHg, was not associated with mortality, but was associated with need of
RRT (dialysis) [17]. This lack of association with increased mortality is probably a
result of confounding factors, since it makes sense to perform DL as soon as possible, once the decision has been made. This is another advantage of starting to
monitor IAP and treat IAH early: if the patient fails to improve on intensive medical
therapy the decision to perform DL can be taken without further delay, since we
already know that the patient has not responded to non-surgical treatment.
When a decision to perform DL has been taken, often in the middle of the night,
there may be a waiting list for the operating theatre. Other patients may have high
priorities, in which case NMB can reduce the ischaemic injury to the abdominal
organs whilst waiting. It is important to inform the anaesthesiologist that the patient
needs to have an extra bolus of uid prior to DL, to avoid hypotension, which is
common when you open or reopen the abdomen during DL.
The effect of DL is often dramatic, reducing IAP, improving oxygenation and
urinary output. Effects on multiple organ failure scores (SOFA, APACHE) are not
as immediate, however, since multiple organ failure is not reversed quickly. In a
multicentre study on 33 patients undergoing DL for overt ACS with different pathologies including RAAA, the IAP decreased from 23 mmHg (range 21–27) to
12mmHg [
9–15, 26] after 2h [19].
19.7 Prophylactic Open Abdomen Treatment
Is it better to leave all patients open as a routine after OSR of a RAAA, or is it better
to close most patients (who do not have an obvious tense abdomen), and follow
them closely in the postoperative period? In their experience, the Mayo Clinic
reported having left 19% open after RAAA repair (43/223) [27]. A similar experience was reported from Zürich [9], and in a Swedish national cohort study this
proportion was 10.7% after OSR [16]. It is obvious from all reports that a proportion
needs to be left open primarily, but what proportion remains controversial.
Based on a systematic EBM review of the literature, the Updated Consensus
document favour primary closure and IAP measurement [4]. They recommend
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