Best Practice & Research Clinical Gastroenterology

Vol. 17, No. 3, pp. 445 456, 2003

doi:10.1053/ybega.2003.380, www.elsevier.com/locate/jnlabr/ybega

Systemic consequences of ileus

Christian Madl* MD

Professor of Medicine
Department of Internal Medicine IV, Intensive Care Unit, University of Vienna, Waehringer Guertel 18-20,
A-1090 Vienna, Austria

Wilfred Druml MD

Professor of Medicine
Department of Internal Medicine III, Division of Nephrology, University of Vienna, Waehringer Guertel 18-20,
A-1090 Vienna, Austria

Ileus refers to the partial or complete blockage of the small and/or large intestine either by functional
(adynamic or paralytic ileus) or mechanical bowel obstruction. The diffuse gastrointestinal
dysmotility during functional and mechanical ileus may result in intestinal dilatation, increased
luminal pressure and gut wall ischaemia which may lead to increased intra-abdominal pressure (IAP).
Any type of ileus may promote abdominal fluid sequestration with severe systemic hypovolaemia,
intestinal bacterial overgrowth with the evolution of bacterial translocation and systemic invasive
infections and inflammation of the intestinal wall with concomitant release of cytokines and the
development of the systemic inflammatory response syndrome. The most serious complications of
ileus are mediated by an increase in IAP. Intra-abdominal hypertension has been found in up to 20% of
critically ill patients and may lead to a broad pattern of systemic consequences with multiple organ
dysfunction, including cardiovascular, hepatic, pulmonary, renal and neurological function. The
abdominal compartment syndrome is an emergency condition which is defined as elevation of IAP
above 20 to 25 mmHg and the presence of systemic consequences. Therapeutic considerations
include the maintenance of adequate hydration status, avoidance of drugs known to impair intestinal
perfusion, stimulation of gastric and intestinal motility and various nutritional aspects. Colonic tube
placement after decompressive colonoscopy may be effective in reducing intestinal dilatation. In the
abdominal compartment syndrome the open abdominal approach with decompressive laparotomy
by opening the peritoneal cavity and temporary abdominal closure is the therapy of choice.

Key words: bowel obstruction; ileus; intra-abdominal pressure; abdominal hypertension;

abdominal compartment syndrome; multiple organ dysfunction.

DEFINITION AND INTRODUCTION

Ileus refers to the partial or complete blockage of the small and/or large intestine either
because the regular, rhythmic squeezing motion (peristalsis) is impaired (adynamic or

* Corresponding author.
E-mail address: christian.madl@akh-wien.ac.at

1521-6918/03/$ - see front matter Q 2003 Elsevier Science Ltd. All rights reserved.
446 C. Madl and W. Druml

paralytic ileus/bowel obstruction) or because of a mechanical obstruction (mechanical

ileus/bowel obstruction). Ileus is characterized by abdominal distension, lack of bowel
sounds, accumulation of gas and fluids in the bowel and decreased gastrointestinal
passage with delayed or absent defecation.1
Both types, functional and mechanical bowel obstruction, are associated with
increased luminal pressure which might cause gut wall ischaemia and may lead to
increase in intra-abdominal pressure (IAP). Intra-abdominal hypertension has been
found in up to 20% of critically ill patients and may lead to a broad pattern of systemic
consequences with multiple organ dysfunction, including cardiovascular, hepatic,
pulmonary, renal and neurological function.2 The most serious complication is the
abdominal compartment syndrome, a life-threatening condition presenting as an
indication for decompressive laparatomy.

PATHOPHYSIOLOGY

Recent pathophysiological concepts of "paralytic ileus" describe a chaotic activity of

individual cells with loss of synchronization and impaired peristalsis instead of the
conventional view of paralysis and cessation of motor activity of gut muscularis. The
diffuse gastrointestinal dysmotility during functional and mechanical bowel obstruction
may result in increased luminal pressure with intestinal dilatation (Figure 1). Nitric
oxide, a known inhibitor of smooth-muscle tone, may be involved in the pathogenesis of
intestinal dilatation. During intestinal dilatation or inflammation, neutrophils may invade
the muscle layer and damage muscle cells directly by release of proteolytic enzymes and
cytokines.3 This inflammatory response leads to the release of nitric oxide in the
intestinal muscle layer which paralyses muscle cells, leading to aggravation of intestinal
dilatation. The amount and activity of nitric oxide synthase correlates significantly with
the severity of intestinal dilatation.4 In animal studies, the diameter of intestinal
dilatation, intestinal contractility and gut luminal pressure has improved after
pharmacological therapy with nitric oxide synthase inhibitors.3 Gut wall ischaemia,

Organ dysfunction
Ileus
Heart
Lung
Intra-abdominal pressure
Kidney
Distension Liver
Circulation
Impaired microcirculation Brain Multiple
Organ Failure

Stasis Peritonitis
Fluid sequestration
Hypovolaemia Shock
Injured intestinal wall Hypoalbuminaemia

Bacterial translocation
Endotoxins
Bacterial overgrowth
Cytokines

Figure 1. Pathophysiology of systemic consequences of ileus.

 Systemic consequences of ileus 447

a consequence of intestinal dilatation and increased intraluminal pressure, leads to a

systemic uptake of cytokines and other inflammatory mediators (Figure 1). This
inflammatory response contributes to the systemic symptoms of ileus and correlates
with the severity of ileus.

AETIOLOGY

Aetiological considerations of ileus include blockage of the small and large intestine as
well as mechanical and adynamic or paralytic bowel obstruction. Disorders associated
with mechanical bowel obstruction may be located outside the gut wall (tumour mass,
large haematoma, post-operative adhesions, volvulus), within the gut wall (gastroin-
testinal tumours, inflammatory bowel diseases, diverticulitis, post-infectious stricture)
or intraluminal (invagination, foreign body, gallstones, cophrolithiasis).
Adynamic or paralytic ileus may affect all parts of the gastrointestinal tract and is one
of the most common complications in critically ill patients. A number of mechanisms
contribute to the development of paralytic ileus. As an adverse consequence of surgical
procedures, post-operative ileus occurs as a result of inhibitory neural reflexes and
inflammatory processes.1 In critically ill patients the use of opioids and catecholamines
is one of the major reasons contributing to paralytic ileus. Paralytic ileus is also often
associated with intraperitoneal or retroperitoneal infection, oedema or ascites
secondary to massive fluid resuscitation during septic or toxic shock with capillary
leakage. Diffuse inflammation of the intestinal wall during inflammatory bowel diseases,
acute bacterial or parasitic intestinal infections or antibiotic-induced pseudomem-
branous colitis with the most serious form of toxic megacolon, may lead to severe
paralytic ileus. Ileus may also be produced by mesenteric ischaemia, by abdominal
arterial or venous injury, by retroperitoneal or intra-abdominal haematomas, or by
metabolic disturbances (e.g. hypokalaemia).
In the critically ill, the degree of impairment of intestinal motility is tightly correlated
to the severity of illness and mortality. A strong predictor of impairment of intestinal
motility is renal function; there is a tight correlation of serum creatinine and intestinal
motility.5

SYSTEMIC CONSEQUENCES

Both functional and mechanical bowel obstruction are associated with a broad
spectrum of systemic consequences (Table 1, Figure 1). The most serious complications
are mediated by increased IAP resulting in sustained intra-abdominal hypertension with
a relatively constant systemic clinical picture and multiple organ dysfunction syndrome.

Gastroduodenal reflux/aspiration

Impairment of motility and compromised propulsion of intestinal contents promotes

reflux of intestinal juice of the small intestine back into the stomach and increases
gastric residuals. A consequence is gastric colonization with intestinal bacteria,
ascension of microorganisms into the oesophagus and into the pharynx and silent
aspiration into the tracheobronchial tree.6 This, together with overt vomiting and
aspiration, increases the risk of evolution of pneumonia.
448 C. Madl and W. Druml

Table 1. Spectrum of systemic complications in patients with ileus and intra-abdominal hypertension.

Impaired organ
function Symptoms

Gastrointestinal reflux " , fluid sequestration, bacterial overgrowth,

tract bacterial translocation, bowel distension, mesenteric
blood flow #
Cardiovascular cardiac output # , contractility # , systemic vascular resistance " ,
system central venous pressure " , pulmonary capillary wedge pressure "
Liver hepatic perfusion # , portal venous blood flow # , hepatic function #
Lung intrathoracic pressure " , alveolar pressure " , lung compliance # ,
paO2/FiO2 ratio # , work of breathing "
Kidney renal blood flow # , glomerular filtration rate # , urinary output #
Cerebrum intracranial pressure " , cerebral perfusion # ,
cerebral venous outflow # , cerebral function #

Fluid sequestration/hypovolaemia

Any type of ileus is associated with profound effects on body fluid balance. At least the
conventional view of obstructive ileus states that increasing distension and concomitant
rise of intraluminal and/or IAP compromise intestinal perfusion, impair microcirculation
(especially the post-capillary venous system) and ultimately result in fluid sequestration
into the intestinal wall and into the intestinal lumen. Moreover, in obstructive ileus
there is also the development of a profound inflammation of the intestinal wall which
promotes fluid loss into the luminal space. In paralytic ileus mucosal perfusion is
increasedat least in the early stages and in the absence of an elevation in IAPby the
inflammatory reaction of the intestinal wall.7,8
This fluid sequestration into the third space can account for several litres, can result
in hypovolaemia and circulatory impairment, and can cause or aggravate various
systemic consequences of ileus. Fluid and circulatory management is crucial for the
prevention of these complications and thus presents a cornerstone in the therapy of
patients with ileus (see below).

Bacterial overgrowth

Both obstructive and paralytic ileus are associated with alterations of intestinal flora,
with overgrowth of bacteria, especially Escherichia coli.9,10 With impairment of
protective effects of gastrointestinal mucus layer, micro-organisms and/or endotox-
ins/exotoxins may adhere to or invade the mucosa, cause mucosal inflammation, and
increase mucosal perfusion and hypersecretion.
Concomitant and/or inadequate antibiotic medication can promote bacterial
selection and overgrowth. This will result in antibiotic-induced diarrhoea or colitis
but also presents an important factor in promoting bacterial translocation. In this
context the gastrointestinal tract has also been designated an undrained abscess.11 A
tight relationship between gastrointestinal colonization and the evolution of invasive
infections has been demonstrated. This also forms the rationale for intestinal lavage
procedures to reduce bacterial overgrowth.
 Systemic consequences of ileus 449

Bacterial translocation

The term translocation denotes the permeation of viable microorganisms (bacteria,

viruses, fungi), fragments of microorganisms (endotoxin) or macromolecules through
an intact or injured intestinal wall into the lymphatic system and/or the intestinal venous
circulation. Translocation presents an important physiological mechanism for the
presentation of antigens to the immune system; this promotes maturation of the
immune system and evolution of immune tolerance, which are necessary for eliciting an
adequate inflammatory response to an infection. Translocation, however, can become a
pathological phenomenon when either the type or the number of intestinal bacteria is
abnormal and/or the barrier function of the intestinal wall is impaired and/or the
systemic immunocompetence of the organism is compromised. This will result in spill-
over of microorganisms into the lymphatic system (and via the vena cava superior into
the circulation and the lung) and/or into the portal circulation and the liver and finally
promote the evolution of systemic infections and septicaemia, respectively (gut
hypothesis of sepsis).12,13
In patients with ileus all three determinants of translocation are involved: bacterial
overgrowth, inflammation and impairment of barrier function of the intestinal wall and,
in most critically ill patients, an impairment of systemic immuncompentence as well.14
With increasing IAP mesenteric blood flow is progressively reduced and mucosal
defence functions are further compromised.15
Affecting intestinal circulation, this scenario is further aggravated by the use of
vasoactive drugsespecially adrenaline (epinephrine), dopamine and potentially also
vasopressin.

ILEUS AND INFLAMMATORY RESPONSE

Both obstructive and adynamic ileus finally will lead to inflammation of the intestinal
wall. Together with the augmentation of bacterial translocation, the intestine will evolve
as a focus of inflammation, with concomitant secondary events such as the activation of
populations of immunocompetent cells, release of cytokines and increased formation of
reactive oxygen intermediates which, together, will mediate extraintestinal manifes-
tations. Thus, ileus per se can promote a systemic inflammatory response syndrome
and can also progress to multiple organ dysfunction syndrome even in the absence of
major elevations in IAP.16

Increase in abdominal pressureabdominal hypertensionthe abdominal

compartment syndrome

The most serious complications of ileus are mediated by an increase in IAP. It is still a
matter of debate which pressure threshold is pathological.17 Normal IAP is equal to
0 mmHg or is even slightly negative in spontaneously breathing individuals (Table 2). In
ventilated patients IAP can increase up to 10 mmHg. While an IAP below 10 mmHg
certainly has no major consequences, relevant elevations start at 13 15 mmHg and
higher. An IAP above 18 20 mmHg is usually referred to as intra-abdominal
hypertension (Table 2). Abdominal compartment syndrome is an emergency condition
which can develop at IAP elevations above 20 25 mmHg. Abdominal compartment
syndrome is defined as elevation of IAP and the presence of systemic consequences,
especially impaired organ functions. Direct measurements of IAP by connecting
450 C. Madl and W. Druml

Table 2. Intra-abdominal pressure (IAP) in different

situations.

IAP (mmHg)

Normal equal to zero

Ventilated patient up to 10 mmHg
Increased IAP .12 mmHg
Intra-abdominal hypertension .1820 mmHg
Abdominal compartment syndrome .2025 mmHg

an intraperitoneal catheter to a pressure transducer can give an accurate measurement

of IAP but this is impractical in the intensive care unit. The most widely accepted
method in critically ill patients is the transurethral measurement of urinary bladder
pressure via a Foley catheter.18 A standard procedure, with a pressure transducer using
the same volume infused into the urinary bladder, and with the patient in the same
position, resulted in highly reproducible and comparable data.18,19
Causes of elevations of IAP are manifold and are not restricted to ileus. For example,
abdominal trauma, traumatic retroperitoneal haematoma, abdominal surgery, pancrea-
titis, massive ascites, diagnostic laparatomy and even haemorrhagic shock may increase
IAP.20
Major consequences of elevated IAP are certainly caused by cardiovascular and
pulmonary manifestations and an impairment of organ perfusion of most organ systems
of the body. However, inflammatory reactions, fluid sequestration, translocation and
evolution of permeation peritonitis are also aggravated by intra-abdominal hyperten-
sion.15 In fact, the spectrum of associated complications of elevated IAP is so broad that
(at least abdominal compartment syndrome) presents an important cause of multiple
organ dysfunction syndrome (MODS).
The clinical manifestations of elevated IAP depend on the duration of the elevation.
Organ dysfunction has been observed within 4 6 hours after development of IAP. As
an example, a continuous IAP of 30 mmHg resulted in renal failure with anuria after
20 hours. Thus, decompression manoeuvres should certainly be initiated within
24 hours.

Cardiovascular

An increase in IAP and concomitant increase in intrathoracic pressure results in a

progressive impairment of cardiac output.21 In patients with increased IAP, venous
return, cardiac filling, ventricular compliance and contractility are all affected.22 In an
animal model an increasing IAP from 15 to 20 and to 25 mmHg produced graded
decreases in cardiac output of 14, 21 and 35%, respectively.23 In medical ICU patients,
non-surgical abdominal decompression resulted in a significant decrease in central
venous pressure, pulmonary capillary wedge pressure and pulmonary artery
pressure.24 At the same time, cardiac output and mean arterial pressure increased
significantly. At least in milder stages of abdominal hypertension, mean arterial pressure
is not affected because of compensatory rises in systemic vascular resistance. The
volume status of the patient is of the utmost importance in modulating the effects
which are more pronounced in hypovolaemia.25 Volume loading and circulatory
 Systemic consequences of ileus 451

support is a central therapeutic manoeuvre to mitigate systemic consequences. Many,

but not all, of the organ involvements listed below are consequences of decreased
cardiac output.

Intestinal

The gut (but also the liver) presents the organs most sensitive to increases in IAP. The
reduction in mesenteric blood flow further compromises intestinal defence functions
and promotes bacterial translocation (see above). Measurement of intramucosal pH by
gastric tonometry in patients with abdominal hypertension showed a decreased pH
with an increased IAP.26 In patients with abdominal trauma and increased IAP
intramucosal pH improved in 75% after abdominal decompression.27 When IAP is
raised above 15 mmHg splanchnic perfusion is decreased, resulting in visceral
hypoperfusion and aggravation of intestinal dilatation. Pre-existing hypovolaemia, low
cardiac output and catecholamine therapy with negative effects on splanchnic blood
flow may exacerbate intestinal dysfunction in patients with intra-abdominal hyperten-
sion. Therapeutic manoeuvres must be aimed particularly at preserving intestinal
functions in intensive care patients.

Hepatic

Elevation of IAP impairs both hepatic perfusion and portal venous blood flow.28 In an
animal model, an increase in IAP to 10 mmHg led to an acute decrease in hepatic
arterial blood flow by 39%.28 The impairment of hepatic blood flow during increased
IAP may be aggravated by hypovolaemia. In a recent study, intra-abdominal
hypertension with an IAP . 25 mmHg was found in 32% of 108 patients following
orthotopic liver transplantation and was associated with renal failure, delayed post-
surgical weaning from ventilation and higher mortality.29 After abdominal decompres-
sion, for example by paracentesis in cirrhotic patients, hepatic blood flow increases.
Therefore, recurrent paracentesis may be beneficial in patients with liver failure and
may prevent organ dysfunction. Furthermore, IAP may promote venous portal
hypertension in cirrhotic patients and may be responsible for bleeding episodes from
oesophageal varices.

Pulmonary

A rise in IAP also results in a progressive increase in intrathoracic pressure and has
consequences for a broad pattern of respiratory functions. Increased IAP led to an
elevation of the diaphragm with a concomitant compression of the pulmonary
parenchyma and a consecutive drop in the functional residual capacity.30 IAP may also
affect lung mechanics and the chest wall with decreased lung compliancewhich
promotes development of atelectasis and increased intrapulmonary shunt.31 Even a
moderate increase in IAP results in a significant increase in peak and plateau alveolar
pressures and negatively influences gas exchangeand last, but not least, the work of
breathing.32 Richardson and Trinkle demonstrated significantly elevated peak airway
pressures once IAP had reached 20 mmHg.21
In mechanically ventilated patients, abdominal decompression leads to a sudden
improvement in alveolar pressure, lung compliance and arterial oxygenation. For
example, in trauma patients, decompressive laparotomy led to an increased lung
452 C. Madl and W. Druml

compliance from 26 to 36 ml/cm/H2O with a significant drop in peak airway pressure

from 49 to 20 cm H2O. This resulted in a significant improvement of the paO2/FiO2
ratio.33 Mechanically ventilated patients with abdominal hypertension require higher
airway pressure levels for alveolar recruitment. The best PEEP for these patients to
keep the lung open seems to be higher than for patients without intra-abdominal
hypertension. It is suggested that PEEP in patients with abdominal hypertension be
maintained at least 2 cm H2O higher than the measured IAP.2 Especially in obese
patients with higher baseline values of IAP, the negative effects of abdominal
hypertension are more pronounced.34 In spontaneously breathing patients with
intra-abdominal hypertension, lung volume and oxygenation are also reduced and the
work of breathing is increased. Therefore, spontaneously breathing patients with
increased IAP following extubation should be maintained in a semi-supine position to
unload the diaphragm and to decrease compression of the pulmonary parenchyma,
thereby improving arterial oxygenation and facilitating spontaneous breathing.

Renal

For many years it has been known that increases in IAP cause an impairment of renal
function.2,18,35 Increases from above 10 mmHg result in a progressive decrease in renal
blood flow, of glomerular filtration and urinary output. Also, proteinuria correlates
with renal venous pressure and IAP, respectively. Several factors could contribute: renal
venous pressure, which causes an increase in the reninangiotensin aldosterone
system, direct compression of the kidneys, with increase in vascular resistance,
reduction in cardiac output and potentially also compression of the ureters.36 38
Endocrine factors, such as increased sympathetic output and augmented non-osmotic
antidiuretic hormone secretion, may also be involved. Evolving acute renal failure is the
most serious complication. It has been frequently shown that the development of acute
renal failure in critically ill patients is the main determinant of survival.39

Neurological

Intra-abdominal hypertension may lead to increased intracranial pressure by decreased

cerebral blood outflow with a functional obstruction of the jugular venous system.40
IAP increases the intrathoracic pressure, resulting in an increased central venous
pressure with venous stasis. Because the intracranial volume is limited by the skull
bone, intra-abdominal hypertension results in an acute and immediate increased
intracranial pressure and diminished cerebral perfusion pressure. Studies in a porcine
model have shown that an increased IAP up to 25 mmHg resulted in an increase in
intracranial pressure from 7 to 21 mmHg with a concomitant decrease in cerebral
perfusion pressure from 82 to 62 mmHg.40 In particular, this phenomenon has also
been observed in patients with multiple abdominal and head trauma. Furthermore,
intra-abdominal hypertension induced by diagnostic laparoscopic surgery resulted in an
acute increase in intracranial pressure in patients with head trauma.41 Acute intra-
abdominal hypertension may also be responsible for the neurological deterioration in
trauma patients without obvious signs of head trauma. Decreasing the abdominal
pressure by decompressive laparotomy showed an amelioration of increased
intracranial pressure in severe head trauma.42 Furthermore, experimental median
sternotomy and pleuropericardiotomy prevented the increase in intracranial pressure
in a porcine model with increased IAP.40
 Systemic consequences of ileus 453

Table 3. Therapeutic considerations in patients with ileus and intra-abdominal hypertension.

Fluid management Maintain adequate hydration, volume loading

Circulatory support Avoid drugs known to impair intestinal

Stimulation of intestinal motility
Nutritional considerations
Abdominal decompression
perfusion (adrenaline, dopamine, vasopressin)
Metoclopramide, cisapride, erythromycin, cholinergics,
opioid antagonists, enemas, laxatives, early start of enteral
nutrition
Minimal enteral nutrition with dietary fibre,
immunonutrition, probiotics, glutamine in parenteral nutrition
Surgical decompression, colonoscopic decompression

THERAPEUTIC CONSIDERATIONS (TABLE 3)

Fluid management and circulatory support

Because of the pronounced consequences of ileus on volume status and circulatory

functions, it is of the utmost importance to support cardiovascular functions and to
maintain an adequate hydration status of the patient. Volume loading and circulatory
support using catecholamines must be followed vigorously in these patients. Drugs
known to impair intestinal perfusion, such as adrenalin, dopamine and potentially also
vasopressin or analogues, should be cautiously used.

Stimulation of gastric and intestinal motility

Maintenance of gastric/intestinal motility must present a primary therapeutic goal in the

management of any intensive care patient. Impairment of motility is a crucial element in
the development of ileus and associated complications. Structured early interventions
and prophylactic measures can maintain motility and enable enteral nutrition.43
Potential interventions include stimulation of gastric motility with metoclopramide,
cisapride or erythromycin and stimulation of intestinal motility using cholinergics,
cisapride, opiate-antagonists, enemas, salinic laxatives etc. In adynamic ileus, an early
start of enteral nutrition also promotes intestinal motility.

Nutritional considerations

Enteral nutrition has evolved as a crucial element in the management of the critically ill,
for restoration and maintenance of intestinal functions, perfusion, motility and barrier
functions. It has been convincingly shown that even in patients in whom a quantitatively
sufficient enteral nutrition is impossible, low amounts of enteral nutrients can help to
support intestinal functions (minimal enteral nutrition).44
Several modifications of the enteral diet can enhance the beneficial effects of enteral
nutrition. Enteral diets should contain dietary fibre which can exert a broad spectrum
of effects such as promoting motility, formation of short-chain fatty acids through
fermentation by bacteria ( prebiotics supporting colonic function), and reduction of
translocation.
Furthermore, nutrients known to enhance the immunocompetence of the organism
have been added to enteral diets (immunonutrition). These diets have been shown to
454 C. Madl and W. Druml

decrease infectious complications and to reduce the length of stay in the intensive care
unit and the hospital, respectively, in several groups of patients.45 If enteral nutrition is
impossible, and parenteral nutrition becomes necessary, the composition of the
nutrition can be modified specifically to support intestinal functions. The most
important nutrientwhich also acts on the intestine after intravenous infusionis
glutamine, a conditionally-essential amino acid in catabolic disease states. Addition of
glutamine to the parenteral nutrition has been shown to improve intestinal barrier
function, to stimulate the gastrointestinal immune system, to reduce evolution of
infectious complications and also to improve survival rates in various groups of
patients.46 This concept has, however, been questioned.
Finally, the addition of probiotics to enteral nutrition has been shown to support
intestinal barrier functions, to reduce mucosal inflammation by inhibiting the adherence
of pathological microorganisms to the mucosal surface, and to prevent or reduce
antibiotic-induced intestinal complications.47

Abdominal decompression

In cirrhotic patients with ascites, abdominal decompression by paracentesis increases

hepatic blood flow and may prevent organ dysfunction. In patients with functional bowel
obstruction decompressive colonoscopy led to a marked reduction of intestinal
dilatation in more than 80% of cases.48 However, colonic dilatation relapses within a few
days in up to 44% of all patients.49 Colonic tube placement for 2 3 days after
decompressive colonoscopy is more effective than decompressive colonoscopy alone.50
In the abdominal compartment syndrome temporary decompressive laparotomy is
the therapy of choice and involves either re-opening a prior laparotomy incision orin
patients who have not recently undergone laparotomyopening the peritoneal cavity
via a midline incision.51 This open abdomen approach with temporary abdominal
closure leads to an immediate drop in airway pressure, acute increase in urinary output
and improvement in haemodynamic parameters.20

Practice points
ileus might cause gut wall ischaemia and may lead to an increase in IAP
intra-abdominal hypertension has been found in up to 20% of critically ill
patients
intra-abdominal hypertension presents an important cause of multiple organ
dysfunction syndrome
ileus may promote abdominal fluid sequestration, intestinal bacterial over-
growth and bacterial translocation
volume loading and circulatory support is of the utmost importance in ileus
in the abdominal compartment syndrome decompressive laparotomy is the
therapy of choice

Research agenda
detailed clinical studies on the impact of nitric oxide inhibition in patients with
ileus are necessary
 Systemic consequences of ileus 455

pathological thresholds of IAP for different clinical conditions remain to be

defined
controlled studies are necessary to define the efficacy of medical treatment
options in patients with ileus and impaired organ function
in critically ill patients controlled studies are necessary to define the influence
of abdominal decompression on organ function and mortality

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