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S.-A. Engelien and D. R. Bulian
Mortality
IAH is an independent predictor for mortality increasing the mortality in ICU
patients from 1–11% to 6–30% and an inverse relation between IAH and the outcome is described. Concerning the underlying condition causing IAH, the mortality
of a secondary IAH is higher than the mortality of primary IAH [6, 12].
In contrast to IAH, the overall mortality of ACS is higher than 60% with a 90-day
mortality of 39%–76% depending on patient selection and management. Without
any treatment, mortality is more than 90%, and despite treatment, conservative and
surgical, mortality still lies between 25% and 75%. In patients undergoing decompressive laparotomy, mortality is 16–49.2%, which is described as a reduction of the
mortality by decompressive laparotomy between 16% and 37% [3, 6, 13, 14].
IAH and ACS not only increase the mortality rate, but also the length of ICU stay
and severity of organ failure. The underlying pathophysiology especially leads to
impaired kidney and lung function, which in turn can lead to increased use of renal
replacement therapy and prolonged mechanical ventilation [6].
Anatomy andPhysiology
The abdominal cavity contains organs and major blood vessels supplying and draining them. Pressure can be transmitted among the intra- and retroperitoneal spaces as
well as the anterior abdominal wall. By transmitting pressure among the intraabdominal structures, arterial blood supply and venous drainage of intra- and retroperitoneal organs may be impaired. Another parameter describing the abdominal
conditions is the abdominal compliance pointing out the relationship between
intraabdominal volume changes and changes in the IAP.Normal abdominal compliance is around 250–450mL/mmHg and in male patients, a decreased abdominal
compliance may be found. This parameter is not routinely used as its assessment is
difcult. Its curvilinear relationship explains the effectiveness of abdominal drainage [5–7].
Terminology andEtiology
ACS results from a persistent IAH and can be characterized as primary and secondary. An ACS caused by a pathology located in the abdominal region, for example,
an abdominal trauma or pancreatitis, is termed a primary ACS, whereas pathologies,
anatomically not specically located in the abdominal region, but leading to a uid
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accumulation there, dene a secondary ACS.Examples for pathologies leading to a
secondary ACS are extensive uid resuscitation and sepsis. Another subdivision of
IAH can be made depicting the onset and course, which can be acute and chronic.
Usually, ACS emerges from acute elevations in IAP.A chronic elevation of IAP can
result from obesity or liver cirrhosis and lead to an increased compliance of the
abdominal wall as well as compensatory mechanisms in the aficted organ systems
[2, 7, 10, 15].
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Risk Factors
The risk factors for IAH and ACS can, on one hand, be divided into factors increasing the volume and thereby the pressure inside the abdominal cavity, putting pressure on the abdominal cavity from the outside, and factors decreasing the compliance
of the abdominal wall.
For the latter, major abdominal trauma including burns, especially of 30% total
body surface area, or abdominal surgery can be responsible, as well as an increased
head of bed angle, a bent or prone body position, and a high body mass index [6, 8,
10, 15, 16].
A rising pressure inside the abdominal cavity can be aggravated by either an
increased intraluminal content, like an ileus, or an increased intraabdominal content
like an acute pancreatitis, a massive hernia repair, edema, ascites, hemoperitoneum
or pneumoperitoneum, for example, following laparoscopy with excessive insufation pressures. The extraperitoneal space can gain volume as well, for example, by
bleedings from pelvic fractures or the rupture of an aortic aneurysm.
Volume shifts are in general known to potentially cause an elevated IAP.That
includes massive uid resuscitation, a positive uid balance, polytransfusion, as
well as sepsis, shock, and hypotension.
Mechanical ventilation, especially a PEEP >10mmHg, or the before-mentioned
obesity apply pressure on the abdominal cavity from the outside [2, 8, 10,
15, 17–19].
On the other hand, factors like age, bacteremia, transplants (renal allograft compartment syndrome, RACS), extracorporeal membrane oxygenation (ECMO), and
coagulopathy have been shown to potentially lead to IAH.
These risk factors can inuence and aggravate each other. Like massive volume
resuscitation not only leads to intraabdominal uid excess, but it may also facilitate
a reduced compliance of the abdominal wall by causing abdominal wall edema. IAP
rises even more, the blood circulation wanes, and ischemia occurs affecting organs
and the abdominal wall, which leads to a reduced compliance of the latter. This is
just one partial aspect of the vicious circle induced [8, 10, 15, 20, 21] (Table23.1).
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Table 23.1
Primary ACS Secondary ACS
Abdominal trauma Positive uid balance
Pancreatitis Sepsis, shock, hypotension
Bleeding, i.e. rupture of an aneurysm, or pelvic fracture Severe burn
Tumor Polytransfusion
Surgery, e.g. massive hernia replacement ECMO
Pneumoperitoneum Bacteriemia
Ileus Coagulopathy
Transplant
Edema of intra−/retroperitoneal organs
Ascites
Peritonitis
Postoperative complication, e.g. anastomosis leakage
Causes of IAH and ACS
Pathophysiology
IAH may lead to compromises in several organ systems. Its pathophysiological
impact on them resembles a state like sepsis. The vasomotor tone is lost, the glycocalyx is damaged, and intercellular junctions of the endothelium collapse.
Consequently, the vascular permeability increases. In this scenario, uid resuscitation is required to stabilize hemodynamics. That results in a vicious circle as uid
resuscitation leads to IAH and ACS and as IAH stimulates anti-diuretic hormone
(ADH) release, the situation aggravates. In the critically ill, a correlation between
IAP and extracellular water content is reported. Moreover, an elevated IAP may
result in prodromal, sub-clinical organ dysfunction and can lead to multiple organ
dysfunction syndrome (MODS). In the following, the effects of IAH and ACS on
different organ systems are depicted [7, 12, 22].
Cardiovascular System
An elevation of IAP leads to a reduced cardiac preload by diminishing the venous
return to the heart. This may be due to an absolute loss of volume or compression of
the inferior vena cava (IVC). Furthermore, an increased IAP can inuence the intrathoracic pressure. Pulmonary vascular resistance rises compromising the right ventricular ejection fraction (RVEF). This expedites a loss of left ventricular
end-diastolic volume and a disturbed myocardial contractility while the cardiac
afterload increases due to a mounting vascular resistance. These effects come along
with a decreased cardiac output and arterial hypotension leading to tachycardia,
which shortens the diastolic coronary blood ow [7, 12, 23].
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Gastrointestinal System
Abdominal perfusion pressure (APP) is the difference between the mean arterial
pressure (MAP) and the IAP (APP=MAP−IAP). In other words, an increase in
IAP leads to capillary compression, a lowered APP, and thereby, intestinal hypoxia.
Mesenteric vein compression makes matters worse. The decreased venous drainage
facilitates intestinal edema and bacterial translocation [7, 8, 12].
Renal System
The impact of IAH on the renal system is also multifactual. The diminished cardiac
output and therewith a reduced intravascular pressure come up against the raised
pressure in the abdominal cavity. Not only a sufcient splanchnic, but also renal
perfusion may not be retained. The microcirculatory ow and the glomerular ltration rate are reduced as the renal cortex and veins are compressed. The latter can be
described as an increased renal venous pressure, which seems to play the most
important role in renal failure in IAH.
The renin–angiotensin–aldosterone system (RAAS) is activated as renin is
secreted when the renal blood ow is lowered. Blood pressure regulation, vascular
resistance, as well as uid and electrolyte balance are deranged. As IAH often
affects the kidneys rst, oliguria may be one of the earliest signs of ACS [7, 12, 23].
Respiratory
A raised pressure in the abdominal cavity elevates the diaphragm and the intrathoracic pressure increases. This causes both a decreased compliance and functional
residual capacity.
Furthermore, compressive atelectasis occurs, as well as an increased alveolar dead
space followed by a ventilation-perfusion mismatch and hypoxic bronchial artery vasoconstriction. Accessory breathing muscles come into use, while the chest wall compliance is reduced and breathwork increases. Consequently, in mechanically ventilated
patients, this necessitates an elevated inspiratory peak pressure and end expiratory pressure. Hypercapnia as well as a decline in PaO2/FiO2 ratio may be observed [7, 12, 23].
Central Nervous System
The high intrapleural pressure caused by ACS raises a functional compression of the
jugular veins. Venous drainage of the cranium is affected, intracranial pressure rises,
and the cerebral perfusion pressure is decreased. The result is cerebral hypoxia,
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which leads to encephalopathy impairing among others the vital regulatory centers
in the brain and homeostatic mechanisms are compromised [7, 12].
S.-A. Engelien and D. R. Bulian
Poly-Compartment Syndrome
Poly-compartment syndrome describes a simultaneously increased pressure in two
or more body compartments. It is a rare but life-threatening condition. By a pressure
relief of one of the affected compartments, the outcome can be improved [12].
Symptoms
As ACS is mostly seen in critically ill and not always addressable patients, the determination of clinical symptoms is limited. Some patients report abdominal pain,
dyspnea, or other non-specic symptoms like fatigue and headache. Clinical hints
for ACS may be progressive oliguria and respiratory distress. Hypotension and
tachycardia can be observed as well as high jugular venous pressure, jugular venous
distension, and peripheral oedema. In the clinical examination, signs of peritonism
or hypoperfusion may be found, and some patients show a restlessness. In the blood
gas analysis, inferences from metabolic acidosis about ACS can be drawn [10].
Diagnostics
Clinical Examination
Physical examination of the abdomen may give hints but fails to assuredly reveal an
ACS.The palpatory ndings may show a tense abdomen, but the sensitivity of
abdominal palpation in this issue is only 40% [10, 24–26].
Imaging Techniques
In radiological examinations of the abdomen or thorax, especially a CT scan, hints
of an ACS can be found like compression of the IVC, inltration of the retroperitoneum, and an increased ratio of anteroposterior-to-transverse abdominal diameter
(positive round belly sign). Furthermore, bowel wall thickening with enhancement
and bilateral inguinal herniation may be pictured [7, 27, 28].
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An adjuvant usage of ultrasound may give more information on possible dysfunctions: a smaller IVC section area and an increased resistive index of the renal
arteries may be hints for an early hemodynamic impairment. Via echocardiography
a reduced preload or ventricular dysfunctions can possibly be detected. Furthermore,
ultrasound can be used to show the bowel activity qualitatively and quantitatively,
large bowel contents or free intrabdominal uid.
Even if imaging techniques can reveal pathologies associated with IAH, they are
insufcient for an early and accurate diagnosis, and IAP measurements are recommended [8, 29–31].
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IAP Measurement
There are many techniques described to measure IAP.In general, it can be measured
directly and indirectly. Direct measurement via an intraabdominal catheter is the
most sensitive but also most invasive method and thereby potentially complicative.
It is, for example, used during laparoscopy when the abdomen is insufated with
gas. Indirect measurements use hollow organs in the abdominal cavity and include
intragastric, intraintestinal (colon, rectum), intravaginal, and intravesical. Moreover,
intravenous measurements (IVC) can be helpful.
But despite these numerous options, the standard method for IAP measurement
is via the bladder using an instillation volume of maximal 25mL of sterile saline
after zeroing the transducer at the level of the midaxillary line. The wall of the bladder is considered to function as a membranous pressure transducer, but only when
containing 25mL of liquid. Compared to the simple catheterization of the bladder,
intravesical pressure monitoring does not increase the risk of urinary tract infection.
An IAP measurement is recommended in critical patients with (the abovementioned) risk factors for IAH. Measurements are recommended every 4–6h and
the development of protocols for IAP measurement is endorsed.
Continuous and real-time IAP monitoring is viable, but it is not standard practice. Therefore, a three-way vesical catheter is needed to provide a steady ow of
25mL saline solution [3, 6, 8, 24, 32–34].
Advice onIntravesical Measurement ofIAP
IAP should be measured at end-expiration in the supine position. As described previously, an increased head of bed angle is known to be a risk factor for IAP and
ACS.For a head of the bed angle of 30°, the average increase of IAP is 4mmHg and
for 45°, it is 9mmHg. The absence of abdominal muscle contractions should be
checked in advance [5, 6, 8, 35].
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S.-A. Engelien and D. R. Bulian
Prevention
To prevent IAH and ACS, some aspects can be taken care of in patients at risk,
such as the before-mentioned patient’s body position with a recommended low
head of the bed angle. A positive uid balance can increase IAP, so after the acute
resuscitation of the critically ill, further uid overload should be avoided and a
protocol can help to do so. Moreover, the use of enhanced ratios of plasma to red
blood cells is recommended. In general, an optimal pain and anxiety relief should
be aimed, and to prevent malperfusion, an APP of a minimum of 50mmHg should
be aimed in critically ill patients [7, 8, 36].
Therapy ofIAH andACS
Conservative Treatment
In general, the soonest possible initiation of an adequate therapy is of major concern. A stepwise application of interventions is recommended to maintain an IAP
below 15mmHg considering the etiology of IAH or ACS in the patient as well as
the clinical situation [8].
Evacuate Intraluminal Content
Gastroenteral decompression with nasogastric or rectal tubes can contribute to pressure relief in a dilated stomach or colon. To evacuate intraluminal contents, the use
of prokinetic agents is also recommended. If these actions are not sufcient, enteral
nutrition should be minimized and enemas should come to use. A further escalation
is a discontinuation of enteral feeding, and a colonoscopic decompression should be
considered [6, 8].
Evacuate Intraabdominal Space Occupying Lesions/Fluid
In suspicion of intraabdominal space occupying lesions, ultrasound should be used
for the detection in the rst place. If ultrasound is not informative, a computed
tomography is recommended. To evacuate uid, percutaneous catheter drainage
should be performed rstly, if technically possible, before considering surgical
treatment. That drainage of intraabdominal uid is a safe as well as effective therapy. The efciency of draining a few hundred milliliters in signicantly lowering
IAP as well as partially avoiding EDL has been demonstrated, especially in severely
burned patients [8, 37–40].
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Improve Abdominal Wall Compliance
The rst step to improve abdominal wall compliance is to ensure an adequate analgesia and sedation and remove constrictive dressings. The head of the bed angle
should be lowered. If these actions are not sufcient, a reverse Trendelenburg position may be supportive. Brief trials of neuromuscular blockade as further, temporary interventions are suggested [5, 6, 8, 35].
Optimize Fluid Administration
In the case of an elevated IAP, excessive uid resuscitation must be avoided and
after initial stabilization of the patient, a zero to negative uid balance by day three
should be targeted. The use of hypertonic uids and colloids as an escalation of
therapy can be considered. Moreover, diuretics may be used. If these therapies are
depleted, hemodialysis and ultraltration come into question [6, 8].
Optimize Systemic/Regional Perfusion
For an optimized systemic or regional perfusion, a goal-directed uid resuscitation
guided by hemodynamic monitoring is endorsed [8].
However, if there is insufcient success by the conservative therapy with development of organ dysfunction or failure and progressive IAH or an existing intraabdominal focus as a trigger for IAH, EDL is necessary. In the latter case, the
combination of pressure relief and simultaneous focal treatment is crucial.
Surgical Treatment
The correct and, above all, timely indication of EDL is a decisive factor for patient
outcome. An unnecessary EDL can worsen the patient’s outcome just as much as a
delayed EDL. EDL should be performed immediately at the onset of ACS and after
the failure of the above-mentioned interventions. This should be at least within the
rst 24h but can then reduce mortality by almost 10% [41].
Persistent hypotension, acidosis, hypothermia, and coagulopathy associated with
IAH indicate the need for EDL. If correctly indicated, an improvement in oxygenation and a reduction in ventilatory pressures occur immediately. Furthermore, a
resumption of urine output or an increase in diuresis usually arises within a few
hours [42]. This is also a positive predictive value for patient survival.
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In the case of an unstable patient, we prefer a damage control approach. A primary resection of the ischemic, perforated, or severely injured bowel segments with
respective blind closure using a stapler and secondary anastomotic creation in a
second procedure after intensive care stabilization of the patient would be exemplary. In the case of mesenteric ischemia, the indication for damage control is very
generous, even if indocyanine green perfusion control of the bowel is used [43, 44]
since secondary resection is more frequently necessary.
S.-A. Engelien and D. R. Bulian
Surgical Technique
Incision Pattern
Even though transverse incisions, also with leaving the peritoneum intact, are
described, we prefer the median laparotomy. In our opinion, the cranial extent
should be limited as much as possible, especially in the case of an acute costal arch
angle, since here a later, secondary fascial closure may become impossible even
with minor fascial dehiscence due to the xation of the abdominal wall fascia at the
costal arch.
After the abdomen has been opened, the entire intraabdominal content should
always be explored rst. Surprising ndings, especially perfusion disturbances of
the intestine or previously unknown hernias, can possibly be detected and must be
treated properly. As a next step, the underlying disease of the ACS, for example, an
acute, necrotizing, and infected pancreatitis, must be addressed according to the
ndings. An infectious focus underlying the ACS should be treated following general standards of care, if possible.
Technique ofTemporary Abdominal Wall Closure
After completion of the focus control and thorough irrigation of the abdomen, the
rst question is whether the abdominal wall can be denitively and completely
closed again. This is usually not possible without risking a recurrence of IAH or
persistent ACS.Multiple procedures with varying degrees of complexity and cost
have been described. For example, we would like to mention the skin only or silo
closure [45], the inexpensive Bogota bag [46], the use of a so-called Wittman patch
[47], and the use of a commercial abdominal Negative Pressure Wound Therapy
(NPWT) set, which we prefer (Fig.23.1). The NPWT seems to improve the survival
rate of the patients undergoing open abdomen therapy, even if the mechanism is still
unclear [48].
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Fig. 23.1 Commercial abdominal Negative Pressure Wound Therapy (NPWT) set
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Open Abdomen
In our opinion, the second question is whether an open abdomen is necessary in the
longer term or whether a denitive abdominal closure already seems realistic a few
days later, after one or if need be two revisions. The fascial edges of the laparotomy
wound retract if laparostomy is necessary in the longer term, making denitive secondary abdominal wall closure more difcult or impossible. This is why we take a
different approach here to counteract fascial retraction in this case.
In the case of an open abdomen expected only for a short time or in a damage
control procedure, we recommend repositioning the intestine and the omentum
majus, if present, and completely covering the intraabdominal organ volume with a
large visceral protective layer (VPL). The omentum majus should be stretched as far
as possible to cover the small intestine, as it provides protection and is easy to
detach during revision. The VPL must always be placed far laterally into the paracolic gutters as well as cranially and caudally so that the bowel is not in contact with
the anterior and lateral abdominal wall.
To place the foil far cranially, the ligamentum teres et falciforme hepatis must be
cut. If a stoma is present, the foil must be slit and placed far laterally around the
stoma on both sides. Then a polyurethane sponge, cut according to the size of the
remaining abdominal wall defect, is placed on the VPL in the defect and the defect
is taped with a foil, which is overlapping several inches. Any contact between the
sponge and the intestine must be absolutely avoided. A small hole is cut in the adhesive foil, the suction foot is attached and, after the connection to a pump, a negative
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