Gastrointestinal Failure in The ICU COCC 2016

CE: Swati; MCC/220208; Total nos of Pages: 14;
MCC 220208
REVIEW
URRENT
C
OPINION
Gastrointestinal failure in the ICU

Annika Reintam Blaser a,b, Stephan M. Jakob c, and Joel Starkopf b,d
Purpose of review
The current review summarizes different aspects of assessment of gastrointestinal function and provides a
practical approach to management of adult patients with gastrointestinal dysfunction in the ICU.
Recent findings
Different ways to define gastrointestinal failure have been used in the past. Recently, the term acute
gastrointestinal injury (AGI) has been proposed to specifically describe gastrointestinal dysfunction as a
part of multiple organ dysfunction syndrome. Possible pathophysiological mechanisms and different aspects
in assessment of gastrointestinal function in adult ICU patients are presented. Currently, there is no single
marker that could reliably describe gastrointestinal dysfunction. Therefore, monitoring and management is
still based on complex assessment of different gastrointestinal symptoms and feeding intolerance, even
though this approach includes a large amount of subjectivity. The possible role of biomarkers (citrulline,
enterohormones, etc.) and additional parameters like intra-abdominal pressure remains to be clarified.
Summary
Defining gastrointestinal failure remains challenging but broad consensus needs to be reached and
disseminated soon to allow conduct of interventional studies. A systematic approach to management of
gastrointestinal problems is recommended.
Keywords
acute gastrointestinal injury, dysfunction, failure, gastrointestinal, intensive care
INTRODUCTION
Gastrointestinal function in ICU patients is difficult
to evaluate and there is no unique and easily
applicable practical definition of gastrointestinal
failure. Various functions of the gastrointestinal
system (digestive, endocrinologic, immunologic,
and barrier) make its normal function fairly
indefinable in ICU patients. As a result, none of
the available scoring systems for multiple organ
dysfunction syndrome (MODS) does appraise the
gastrointestinal system, even though the importance of gastrointestinal failure in MODS has been
recognized for years [13].
The current review aims to summarize different
aspects of assessment of gastrointestinal function
and provides a practical approach to the management of adult patients with gastrointestinal
dysfunction in the ICU.
TERMINOLOGY, DEFINITIONS, AND

SCORING SYSTEMS
Large inconsistency exists in terminology describing
gastrointestinal disorders in ICU patients [4]. The
approach of researchers and experts is very different,
depending to some extent on the primary area of

interest (Table 1) [518]. In the critically ill, gastric
and intestinal problems are not always distinguishable, whereas severity may vary from mild to
life-threatening. Gastrointestinal dysfunction could
be a better term to describe the changes in severity in
continuum, whereas gastrointestinal failure is a yesor-no phenomenon, describing only the most severe
form of dysfunction [1,19]. However, the term
gastrointestinal dysfunction in broader perspective
describes all gastrointestinal symptoms frequently
occurring in humans, also in those not needing
hospital admission. All these aspects have been well
considered by the Working Group on Abdominal
a
Department of Intensive Care Medicine, Lucerne Cantonal Hospital,
Lucerne, Switzerland, bDepartment of Anaesthesiology and Intensive
Care, University of Tartu, Tartu, Estonia, cDepartment of Intensive Care
Medicine, University Hospital of Bern, University of Bern, Bern,
Switzerland and dDepartment of Anaesthesiology and Intensive Care,
Tartu University Hospital, Tartu, Estonia
Correspondence to Annika Reintam Blaser, Department of Intensive

Care Medicine, Lucerne Cantonal Hospital, Spitalstrasse, 6000 Lucerne,
Switzerland. Tel: +41795142121; e-mail: annika.reintam.blaser@ut.ee
Curr Opin Crit Care 2016, 22:000000
DOI:10.1097/MCC.0000000000000286
1070-5295 Copyright 2016 Wolters Kluwer Health, Inc. All rights reserved.
www.co-criticalcare.com
Copyright 2016 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
MCC 220208
Gastrointestinal system
KEY POINTS
AGI could be used to describe gastrointestinal
dysfunction as a part of MODS.
Single symptoms describing different gastrointestinal
motility disorders cannot be equalized with
gastrointestinal organ failure.
A scoring system/grading of severity is needed to
allow conduct of interventional studies.
Diagnosis of feeding intolerance should not be based
only on gastric residual volumes but rather comprise an
algorithmic stepwise approach, possibly also including
defined management/treatment options.
Assessment of gastrointestinal function is still limited
today to clinical and radiological assessment; a few
promising biomarkers need to be further studied.
perfusion, where increased intestinal bacteriagenerated compound trimethylamine-N-oxide was

predictive of the 5-year mortality risk [24].
One mechanism for decreasing gastrointestinal
barrier function is reduction of transepithelial
electrical resistance [25]. In principle, this effect
can be attenuated by muscarinic stimulation which
may offer a treatment option in the future [25].
Traumatic brain injury is another example where
secondary gastrointestinal failure with increased
intestinal permeability may occur, being at least
partially induced by increased sympathetic tone:
intraperitoneal administration of labetalol in mice
subjected to traumatic brain injury decreased intestinal TNF-a concentrations and intestinal permeability and maintained intestinal architecture
[26].
EPIDEMIOLOGY
Problems of the European Society of Intensive Care
Medicine, and resulted in definitions for acute
gastrointestinal injury (AGI) with four grades of
severity (Table 2) [16]. However, none of the existing
definitions is well validated providing grading with
readily applicable clinical severity scores. Moreover,
it needs to be underlined that none of these
approaches considers other than digestive function
(like endocrine, immunological, and barrier) of the
gastrointestinal system.
PATHOPHYSIOLOGICAL MECHANISMS
Gastrointestinal failure develops as a direct consequence of organ injury or secondary to hypoperfusion. In both situations, depending on the type
and severity of the insult, an inflammatory response
may amplify the vicious circle of hypoperfusion and
gastrointestinal injury (Fig. 1) [15,20,21]. Hormonal
mediators of gastrointestinal motility may be
relevant in pathophysiology of gastrointestinal dysfunction, clinically often expressed as delayed gastric emptying [22]. However, the gastrointestinal
failure associated with MODS is most likely caused
by hypoperfusion and ischaemia/reperfusion injury
leading to altered mucosal barrier and immunoinflammatory reaction via release of biologically
active factors into the blood as well as mesenteric
lymphatics [21] (Fig. 1). Some recent studies have
tried to address these pathophysiological events. In
acute aortic dissection, serum levels of diamine
oxidase, an enzyme mostly located in intestinal
mucosa, are increased and correlated with inflammatory markers [23]. Translocation of bacterial
products has also been shown in patients with heart
failure and chronically impaired gastrointestinal
2
The incidence of gastrointestinal failure depends

heavily on the definitions applied. Acalculous cholecystitis and stress ulcer bleeding demanding transfusions are infrequent, which explains the low
incidence of gastrointestinal dysfunction/failure
in earlier studies [6,7]. A recent multicenter study
reported clinically important gastrointestinal bleeding (not present at ICU admission) in 2.6% of ICU
patients [27 ]. Different gastrointestinal signs, in
contrary, are common and may be observed in up to
60% of mechanically ventilated patients [11,28,29].
Three or more gastrointestinal symptoms may occur
in about 20% of patients during their ICU stay and
in 6% if concomitant occurrence on one day is
considered [11,30].
&&
DIAGNOSIS AND MANAGEMENT

Diagnosis of gastrointestinal failure in ICU patients
is complex, relying much on clinical assessment of
abdominal symptoms. Lack of validated markers
for monitoring explains why assessment of the
gastrointestinal system is poorly integrated in the
management of ICU patients and gastrointestinal
failure is often misdiagnosed [15]. We suggest that a
systematic approach taking into account different
aspects including course of illness should be applied,
whereas specific management relies on different
symptoms. Possible ways to detect gastrointestinal
dysfunction with respective management are summarized in Table 3 [3144,45 ,4648], whereas a
systematic approach is presented in Fig. 2 [16]. Even
though gastrointestinal motility disorders are central in clinical management today, one should not
automatically consider each single motility disorder
as gastrointestinal failure. However, a careful
&
Volume 22 Number 00 Month 2016
Ileus >7 days or bleeding requiring six blood

products per 24 h
GI dysfunction [6]
Presence of cholecystitis, stress ulcer, GI bleeding,

necrotizing enterocolitis, and/or pancreatitis
Presence of food intolerance, gastrointestinal

haemorrhage, and/or ileus documented in the
patient data at any period of their ICU stay
Concomitant presence of FI and IAH
Presence of three or more coincident GI symptoms
GI failure [7]
GI failure [9]
GI failure (GIF score) [10]
GI failure [11]
Gastrointestinal failure
Presence of feeding intolerance defined as vomiting,

gastric residual volume approximating amount of
previously given enteral nutrition, abdominal
distension or diarrhoea in patients with no ileus and
no previous bowel surgery
Definition
GI dysfunction [5]
Gastrointestinal dysfunction
Term
None
0 normal GI function;
1 enteral feeding <50% of
calculated needs or no feeding
3 days after abdominal
surgery; 2 FI (enteral feeding
not applicable because of high
gastric aspirate volume,
vomiting, bowel distension, or
severe diarrhoea) or IAH;
3 FI and IAH; 4 abdominal
compartment syndrome
None
0 normal functioning;
1 (moderate) acalculous
cholecystitis or stress ulcer;
2 (severe) bleeding from
stress ulcer necessitating
transfusion of more than 2 units
RBC per 24 h, necrotizing
enterocolitis and/or
pancreatitis, and/or
spontaneous perforation of
gallbladder
GI failure (defined as massive

bleeding requiring>six blood
products per 24 h) 2nd
grade of severity
GI dysfunction 1st grade of

severity in MODS score
None
Grading
Table 1. Different approaches to define gastrointestinal dysfunction/failure in ICU patients
Multicentre prospective study, 377 pt. GI failure was

associated with higher 28-day mortality
Single centre prospective study, 264 pt. GI failure

associated with higher ICU and 90-day mortality
Retrospective analysis, 2588 pt. Development of GIF

was independent predictor for death
Historical first attempt to quantify the severity of

multiple organ failure, including GI failure. 15 years
later GIF excluded from score due to problems in
reliability [8]
Included in multiple organ dysfunction score (MODS),

modified from Goris et al. 3700 pt, GI failure (in
2.6% pt.) was not an independent predictor of
mortality
Single-centre, 208 pt. Significantly higher mortality in

FI patients (P < 0.0005)
Comment
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Gastrointestinal failure in the ICU Reintam Blaser et al.
Rapid reduction of small-bowel enterocytic function
because of acute reduction of enterocyte mass and/
or acute dysfunction of enterocytes responsible for
decreased absorptive capacity and reduced
citrulline synthesis
Acute intestinal failure [14]
Four grades of severity: AGI I

(self-limiting condition), AGI II
(GI dysfunction), AGI III (GI
failure), AGI IV (manifesting GI
failure, life-threatening). See
also Table 2
None
None
Type I acute, short-term and

usually self-limiting condition;
Type II prolonged acute
condition, often in metabolically
unstable patients; Type III
chronic condition, in
metabolically stable patients,
requiring intravenous
supplementation over months or
years
5 grades of severity, evaluation of

IAP, lactic acidosis, gastric
residuals, progression of enteral
feeding, constipation, diarrhoea
and bowel sounds
Grading
AGI, acute GI injury; FI, feeding intolerance; GI, gastrointestinal; IAH, intra-abdominal hypertension; MODS, multiple organ dysfunction syndrome.
AGI [16]
Gut failure [15]
Alterations of the guts physiology that ultimately end

in intestinal barrier breakdown, bacterial
translocation, and development of sepsis, MODS
and death
Malfunctioning of the GI tract in critically ill patients
because of their acute illness
Reduction of gut function below the minimum

necessary for the absorption of macronutrients and/
or water and electrolytes, such that intravenous
supplementation is required to maintain health and/
or growth
Intestinal failure [13]
Other
No clear-cut definition of intestinal failure, but 5-grade

score based on seven symptoms and signs
Definition
Lausanne intestinal failure

estimation (LIFE score) [12]
Intestinal failure
Term
Table 1 (Continued)
Poorly validated (one single-centre prospective study

with 133 pt [17] and one retrospective study with
874 pt [18])
No specific markers proposed
No cut off value(s) proposed
The European Society for Clinical Nutrition and

Metabolism (ESPEN) recommendations developed
not specifically for ICU patients; no grading of
severity for daily assessment, but time needed for
diagnosis
Not validated in published trials
Comment
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Table 2. Definitions and description of grades of acute gastrointestinal injury [16]
Clinical definition/examples, all irrespective to previous
abdominal pathology or intervention if not stated otherwise
Grade
Definition
No AGI
No malfunctioning of GI system
No GI symptoms, starting and increasing enteral feeding >50% of

needs is possible
AGI grade I
Risk to develop GI failure. GI symptoms

after an insult, self-limiting
Postoperative nausea and/or vomiting after abdominal surgery,

trauma or interventions (endoscopic etc.)
Absence of bowel sounds, especially
During the first days after abdominal surgery
With postoperative opioid analgesia
During deep sedation
On the first days in ICU in a patient with shock
Mild diarrhoea (does not require correction of fluid and electrolyte
balance)
Abdominal distension
AGI grade II
GI dysfunction, which requires

interventions, several or severe
symptoms, not leading to deterioration
of general condition
GI symptoms that require intervention

Gastroparesis with large GRV/reflux
Paralysis of the lower GI tract
Severe diarrhoea (requires correction of fluid and electrolyte
balance)
IAH grade I (IAP 1215 mmHg)
Visible blood in gastric content or stool
AGI grade III
GI failure, symptoms persist or progress

despite interventions, worsening
MODS
Despite treatment, symptoms are persisting

Large GRV
Vomiting
Persisting GI paralysis
Occurrence or worsening of abdominal distension (subjectively)
and/or bowel dilatation (objectively)
Progression of IAH
Severe diarrhoea
Mechanical ileus
Persisting abdominal sepsis by complicated peritonitis, pancreatitis
etc.
AGI grade IV
Dramatically manifested GI failure,

immediately life-threatening
Bowel ischaemia with necrosis

GI bleeding leading to haemorrhagic shock
Ogilvies syndrome
Abdominal compartment syndrome requiring decompression
AGI, acute GI injury; GI, gastrointestinal; GRV, gastric residual volume; IAH, intra-abdominal hypertension; IAP, intra-abdominal pressure; MODS, multiple organ
dysfunction syndrome.
assessment of gastrointestinal symptoms is important in detecting the tip of the iceberg in the complex
mechanism of gastrointestinal failure.
Clinical assessment
Evaluation of the gastrointestinal tract is greatly
interfered by therapies applied in critically ill
patients. There is no consensus whether dysphagy
should be seen as a part of gastrointestinal dysfunction or not. We feel that this serious problem in
critically ill patients leading to aspiration of gastric
contents needs special attention, but should be
addressed separately from gastrointestinal dysfunction. Therefore, this issue is not further addressed in
the current review. Abdominal signs and symptoms
(pain, distension, and discoloration) are not always

related only to the gastrointestinal tract. Moreover,
pain is difficult to assess in unconscious or sedated,
mechanically ventilated patients. Besides the fact
that assessment of gastrointestinal symptoms stays
subjective, additional confusion has been caused by
lack of definitions suitable for ICU patients. Therefore, consensus definitions of gastrointestinal symptoms for ICU patients have been recently proposed
[16]. These definitions and management suggestions are summarized in Table 3.
Assessment of feeding intolerance

From a physiological point of view feeding intolerance is a natural reflection of gastrointestinal
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Primary injury in GI system
Abdominal pathology
(e.g. trauma, surgery)
Inflammatory response 1
Recovery
distension, emesis, diarrhoea, or subjective discomfort) [51 ]. Using this definition, feeding intolerance
was observed in 30.5% of mechanically ventilated
patients staying in ICU for at least 72 h and its
development was associated with impaired outcomes [51 ]. However, the likelihood of resulting
in discontinuation of enteral nutrition is probably
very different between vomiting, diarrhoea, and
discomfort.
In the future, a consensus on definition of
feeding intolerance should be reached. The issue
is complicated as completely different approaches
are needed to address intolerance to feeding in
upper and lower parts of the gastrointestinal tract.
Therefore, we suggest to base this future definition
on the algorithm, possibly including stepwise application of theraputic measures (e.g. prokinetics and
postpyloric feeding).
Of note, feeding intolerance cannot be considered as the only equivalent of gastrointestinal
failure as its diagnosis requires a challenge of enteral
feeding, whereas gastrointestinal failure should
be possible to be diagnosed also independent of
feeding.
&
&
Severe illness
Non-abdominal
pathology
Hypoperfusion
Resuscitation
Vasopressors
Fluids
Secondary injury to
GI system
Loss of barrier
Bacterial and endotoxin

transloction to portal blood and
lymhatics
Sepsis
Ischaemia/reperfusion
edema
Recovery
Translocation of proinflammatory factors

to lymphatics
MODS
FIGURE 1. Pathophysiological mechanisms of acute

gastrointestinal injury as a part of multiple organ dysfunction
syndrome. MODS, multiple organ dysfunction syndrome.
dysfunction or failure. This has led to attempts

to incorporate it in scoring systems for gastrointestinal failure/dysfunction [5,10,11,49]. Unfortunately, as occurrence of feeding intolerance highly
depends on feeding practices and a universally
accepted definition for feeding intolerance is lacking, the strength of relationship between feeding
intolerance and mortality is highly variable
between the studies [39]. A large gastric residual
volume (GRV) during enteral feeding is the most
commonly used sign of feeding intolerance,
although the usefulness as well as the clinically
relevant threshold of GRV remains under debate.
However, a GRV of at least 250 ml was highly
predictive for delayed gastric emptying measured
by scintigraphy [50].
Recently, it has been suggested that complex
assessment of gastrointestinal symptoms, including
vomiting, diarrhoea, and bowel distension rather
than GRV alone, is more strongly associated with
ICU mortality and therefore could provide a better
definition of feeding intolerance as a sign of gastrointestinal dysfunction [16,32]. In a large retrospective study, feeding intolerance was defined as
interruption of enteral nutrition because of a gastrointestinal reason (large gastric residuals, abdominal
6
Intra-abdominal pressure
Intra-abdominal pressure (IAP) is not a direct reflection of gastrointestinal function. On the other hand,
increased IAP may reduce blood flow to intraabdominal organs, including the gastrointestinal
tract, with consequent functional impairment
[52]. Simplicity and relatively well validated
measurement technique of IAP via the bladder fosters its application [40]. Gastrointestinal symptoms
occur more frequently in patients with increased
IAP, whereas the direction of this relationship is
unclear [53]. Few attempts have been made to
incorporate IAP values in scoring systems for gastrointestinal dysfunction/failure [10,54]. The role of
IAP in routine assessment/monitoring of gastrointestinal failure remains to be clarified in large-scale
prospective studies.
Radiological imaging
Static radiological imaging (ultrasound, abdominal x-ray, computed tomography, or magnetic
resonance imaging) allows detecting structural
changes, which could be linked with functional
disturbances. Dynamic studies require specific
complex investigations, but may give valuable
information on motility. There are no clear recommendations when which specific imaging technique should be used, but some suggestions are
provided in Table 3.
Occurrence of any visible
regurgitation of gastric content
irrespective of the amount [16]
Absence of stool for three or more
consecutive days without
mechanical obstruction [16].
No consensus
Colonic diameter >6 cm (>9 cm

for caecum) or small bowel
diameter >3 cm [16,36]
Lower GI paralysis
Bowel dilatation
2083%; different terms used for

diagnosis (constipation or
impaired GI transit) [34,35]
848% [31,32]
Assessment requires radiological imaging

Not known
(ultrasound, plain x-ray or CT-scan) and is
therefore limited to severe cases. Cave:
Bowel distension may lead to bacteraemia
Possibly associated with longer length of

stay and prolonged weaning from
mechanical ventilation
Assess in all patients. Start laxatives early.

Check for bowel dilatation and distension
Assess in all patients. Take measures to

prevent aspiration of gastric contents
Not known
22% in pt with EN [32]
Vomiting/regurgitation
Not clear. It can be present during bowel

obstruction occurring in parts of the bowel
as attempts to overcome obstruction
Excessive bowel sounds are heard

on auscultation [16]. Observerdependent
Hyperperistalis
Not known
3841% [11,30]
Not clear. Complete lack of bowel sounds is

abnormal, but presence of bowel sounds
does not confirm normal motility or
improvement of paralysis
All patients. May be important sign of

abdominal wall infection. Grey-Turners or
Cullens sign in pancreatitis
Not known
5963% [29,30]
Discoloration of abdominal wall.

Observer-dependent
Abdominal discoloration
All patients. May be a sign of bowel

dilatation. Check other abdominal signs
and GI symptoms. Nonspecific
521% [11,2931]
No bowel sounds are heard at

cautious auscultation [16].
Observer-dependent
Tympany on percussion
suggesting increased content of
air in the abdomen. Observerdependent
Tympany on percussion
All patients. Nonspecific
Not known
Prevalence in ICU
Absent bowel sounds
Outward expansion beyond the

usual girth. Observer-dependent
Abdominal distension
Assess in all patients. Differentiate diffuse or

localized, document progression in time.
Nonspecific
Application/importance
Gastrointestinal symptoms
Subjective feeling of pain
Abdominal pain
General abdominal signs
Clinical assessment
Definition/s
Table 3. Recommendations for assessment of gastrointestinal function in clinical practice and management suggestions in ICU patients
Rule out bowel obstruction.

Consider: neostigmine;
endoscopic decompression;
and surgery. Measure IAP
(management see below). Cave
toxic megacolon
Consider: reducing opiates/

sedation; laxatives;
mobilization; and neostigmine
Guidelines for management of

postoperative vomiting and
nausea [33]
Rule out bowel obstruction
None. As a single GI symptom,

absent bowel sounds should not
cause delay of EN
Consider infection, discuss with

surgeon. Document progression
If concomitant abdominal
distension and pain >
consider imaging and measure
IAP
Measure IAP. Consider bowel

management (laxatives etc).
Exclude or treat gastric
distension
Differential diagnosis; analgesia
Management
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IAP >20 mmHg together with new
or worsening organ failure [40]
Abdominal compartment
syndrome
Free air/fluid
Radiological assessment, static
Sustained IAP 12 mmHg [40]
Intolerance of enteral feeding for

whatever clinical reason
(vomiting, large GRV,
diarrhoea etc.) [16]. No
consensus
Relevant for outcome: three or
more GI symptoms, incl. large
GRV [32]
Intra-abdominal hypertension
IAP
Feeding intolerance
Assessment of feeding intolerance
Large GRV
>200 ml defined as large GRV

(NB. not equal to feeding
intolerance) [16]. No consensus
3 loose or liquid stools per day

with a stool weight >250 g/
day [37]
Diarrhoea
Measurement of GRV
Any bleeding into the GI tract

lumen, confirmed by
macroscopic presence of blood
in vomited fluids, gastric
aspirate or stool [16]
Definition/s
GI bleeding
Table 3 (Continued)
Warrants immediate caution
Potentially life-threatening condition.

Requires management
Measure in patients at risk [41] and in case

of abdominal/bowel distension. Probably
associated with adverse outcome [43]
Assess in all patients. Take measures to

prevent aspiration of gastric contents
No consensus. The authors support GRV

measurements in initial phase of enteral
feeding. Gastroparesis is common in ICU
patients
Assess in all patients
Assess in all patients. Substantial proportion

of ICU patients exhibit clinical risk factors
for increased risk of bleeding (3 coexisting diseases, coagulopathy, liver
disease, use of acid suppressants, renal
replacement therapy and higher organ
&&
failure score) [27 ]
14% [4244]
2040% [4144]
275% [39]
9% with proposed definition [32]
867%, depending on the

definition used (150500 ml)
[39]
1421% [37,38]
2.6% (clinically important new GI

&&
bleeding) [27 ]
Prevalence in ICU
Discuss with surgeon
Consult surgeon. WSACS

management algorithms [40]
Continue IAP measurements until

IAP < 12 mmHg. If increasing,
consider/use WSACS
management algorithms [40]
Management according to
specific GI symptom
Gastroparesis: prokinetics
(metoclopramid and
erythromycin) and postpyloric
feeding
Lower GI paralysis bowel
dilatation: see above
200500 ml at single
measurement -> continue
regular measurements
>500 ml -> reduce/stop EN [16]
Differential diagnosis [37];

exclude or treat Clostridium
difficile colitis, consider specific
reasons (e.g. pancreatic
exocrine insufficiency and bile
acid diarrhoea) and treat
respectively, consider other EN
formula, supportive therapy
(wound and skin care), and
reduce EN (last measure!)
Optimize coagulation, start PPI.

Consider: endoscopy;
interventional radiology; and
surgery
Management
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None unless bowel distension
See Feeding intolerance
None. Discuss with surgeon
ACS, abdominal compartment syndrome; EN, enteral nutrition; GI, gastrointestinal; GRV, gastric residual volume; IAP, intra-abdominal pressure; PPI, proton pump inhibitor; WSACS, the Abdominal Compartment
Society.
Individual interpretation. Exclusion of

mechanical obstruction
Increased GI transit time
Normal gastrointestinal transit

time is around 48 h [47].
Normal orocecal transit time for
liquids is 40170 min [48]
Individual interpretation
Delayed gastric emptying
Radiological assessment, dynamic
Possible sign of irreversible damage. Cave:

pneumatosis on CT does not always
indicate transmural necrosis of the bowel.
Higher probability of the latter, if
concomitant portomesenteric venous gas
is detected [46]
None. Discuss with surgeon.

Consider negative fluid balance
to reduce venous pressure
Individual interpretation
No clear-cut values, visual

evaluation. Some comparisons
of heart failure patients show
2535% increase in thickness
&
vs. controls [45 ]
Thickness of bowel wall
Intestinal pneumatosis
See bowel dilatation
Interpret in context with clinical assessment
Discuss with surgeon
Management
Colonic diameter >6 cm (>9 cm

for caecum) or small bowel
diameter >3 cm
Prevalence in ICU
Increased bowel diameter
Warrants immediate caution
Definition/s
Decreased/interrupted
mesenteric blood flow
Table 3 (Continued)
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Yes
GI symptoms ?
No
AGI I
Symptoms mild, expectedly self-limiting (e.g.postop)

General condition improving
Yes
Ensure normal fluid and electrolyte status

Start/increase EN if no reason to delay
Reduce medications that impair motility
Consider early use of laxatives
Re-evaluate first 6-hourly, later 12-hourly
Gastroparesis
AGI II
No
Define the problem

Consider IAP measurements
Consider trophic EN
Diarrhoea
GI symptoms ?
Metoclopramid
Erythromycin
No
No AGI
Set caloric target

Increase EN slowly
Use feeding protocol
Cave refeeding syndr.
Reduce the risk of
aspiration
Aim 50-80% of needs
during the acute phase
Aim 80-100% of
needs by day 3
Check prescribed vs.
delivered calories
Re-evaluate daily
Persisting feeding
intolerance
Consider postpyloric EN
EN tolerated ?
Condition improving?
No
AGI III
Intervention is needed
Consult surgeons, gastroenterologist, radiologists
Stop EN, insert/open nasogastric tube
Consider
Endoscopy (to stop bleeding or decompress)
Interventional radiology to stop bleeding or
drain fluid collections
Laparotomy
Stop laxatives
and prokinetics
Find trigger37
Exclude or treat
C. difficlle
Check
anamnesis
medications
Consider
malassimilation
Lower GI paralysis
Consider laxatives
Measure IAP
Bowel distension
Consider
Neostigmine
Supportive therapy
Specific after diagnosis
Continue EN
Search for undiagnosed abdominal

pathology
Continue therapy according to the
symptom (limit prokinetics to max 5 days)
Treat IAH 44
Consider trying again minimal EN
Consider supplemental PN after day 4-7
Re-evaluate every 12 hours
Critical decompensation through AGI?
AGI IV
Yes
FIGURE 2. Assessment and management of different grades of acute gastrointestinal injury (AGI). AGI I, increased risk
of developing gastrointestinal dysfunction or failure; AGI II, gastrointestinal dysfunction; AGI III, gastrointestinal failure; AGI IV,
manifesting gastrointestinal failure, life-threatening. ACS, abdominal compartment syndrome; CT, computed tomography; EN,
enteral nutrition; FI, feeding intolerance; GRV, gastric residual volume; IAP, intra-abdominal pressure; PPI, proton pump
inhibitor; WSACS, The Abdominal Compartment Society.
Methods to assess gastric emptying

Several methods to measure gastric emptying have
been studied, but none of them has found its way
into clinical routine.
Measurement of gastric emptying in the critically ill involves the marker infused via nasogastric
tube and monitored via imaging, or indirectly via
blood or breath analysis [55 ]. Scintigraphy, where
the disappearance of a radioactive labelled nutrient
is directly visualized, is considered a gold standard
&
10
of gastric emptying measurements, but has several

limitations (radioactive, commonly solid isotopelabelled food, and transportation) for using it in
ICU patients. Recently, it has been proposed to
use nutrient properties as the source of visual information using magnetic resonance imaging instead
of radioactive tracers [56].
Indirect tests of gastric emptying include drug
absorption (paracetamol), carbohydrate absorption
(3-O-methylglycose), and isotope breath tests
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(e.g. 13C). Some studies have assessed gastric volume

and character of contents with refractometry [57] or
ultrasound [58,59 ].
&
Assessment of assimilation of nutrients

There is no reliable test in routine clinical use that
would allow assessment of assimilation of nutrients
in critically ill patients. However, recent studies
suggested carbohydrate malabsorption in ICU
patients, possibly related to reduced intestinal
expression of glucose transporters [60 ]. In this
study by Deane et al., glucose and 3-O-methylglucose were infused intraduodenally and duodenal
mucosal biopsies were performed before and after
infusion [60 ]. Faecal weight and energy content
measured by bomb calorimetry have been suggested
as markers of malabsorption [61]. Low faecal elastase
levels occur in ICU patients, possibly related to fat
malassimilation because of pancreatic exocrine
insufficiency [62]. Malassimilation as a cause of
diarrhoea should always be considered and a systematic approach to differential diagnosis and management applied [37].
&
&
Assessment of barrier function

Barrier function has been assessed by the permeation
of large, poorly absorbed probe molecules [63]. There
is some evidence of increased intestinal permeability
in critically ill patients, but multiple confounding
factors including gastrointestinal dysmotility make
the results difficult to interpret [63,64].
Laboratory markers
Diamine oxidase has been proposed as a specific
marker for gut mucosal damage because the enzyme
seems to be preferentially located in intestinal
mucosa. However, values in patients with and without suspected damage overlap widely [23].
Similarly, intestinal fatty acid-binding protein
(I-FABP) is supposed to be expressed exclusively in
the epithelium of the gastrointestinal tract. Recent
studies demonstrated significantly higher I-FABP
concentrations in patients with mesenteric ischaemia compared to patients with acute abdomen and
preserved gut perfusion [65,66]. Although specificity was 100% and sensitivity 90% for the proposed
cut-off value, both D-dimer and leukocyte reached
the same percentages as I-FABP. In patients with
acute abdomen without mesenteric ischaemia, both
specificity and sensitivity for I-FABP were below 80%
when compared with control study participants and
worse than the percentages for D-dimer and leukocyte counts [65].
D-lactate is produced by intestinal bacteria and

its concentration in human blood is very low under
normal conditions. If intestinal mucosal and capillary permeability increase, for example, during mesenteric ischaemia, blood D-lactate concentrations
increase. In pigs with abdominal compartment
syndrome, D-lactate in the jugular vein blood is
increased, but the changes over time were essentially the same as for L-lactate [67]. Increased
D-lactate concentrations have been demonstrated
also in patients with acute abdomen with and without mesenteric ischaemia [66].
The amino acid citrulline, produced by enterocytes from glutamine, has been suggested as a
specific gastrointestinal marker. A recent study
found lower values in rats subjected to LPS compared with a control group [68]. In patients with
evolving septic shock, plasma citrulline concentrations were decreased with lowest values when
bacterial translocation occurred [69]. Whether or
not this reflects early acute intestinal dysfunction
has to be elucidated in further studies.
Plasma levels of certain enterohormones (cholecystokinin, ghrelin, glucagon-like peptide-2, and
peptide YY) are altered in critical illness [70], but
their role in diagnostics and management of gastrointestinal failure remains to be clarified.
As a conclusion, the current data do not provide
enough evidence that any of these markers can help
in early detection of gastrointestinal dysfunction.
Methods to assess splanchnic perfusion

Besides angiography and computed tomography,
MRI has been used for many years to evaluate
tissue perfusion, especially in the brain. In abdominal organs, the application of MRI perfusion
techniques has been more difficult, especially
because of interference with respiration. Recently,
free breathing gadolinium-enhanced MRI of the
liver has been proposed [71]. The technique can
be applied within 56 min, and high temporal
resolution reconstructed afterwards [71]. Nevertheless, at least for regional perfusion assessment,
ultrasound-based technologies are still the most
convenient, cheapest, and quickest methods
in the gastrointestinal tract, albeit not for continuous use and difficult to perform in very obese
individuals.
Management
Management of gastrointestinal failure is based on a
complex clinical assessment, optimizing organ perfusion, and treatment of specific gastrointestinal
symptoms.
11
MCC 220208
Preventive measures have been insufficiently

studied but may include minimized use of opioids
and sedatives, epidural analgesia, early mobilization, early enteral nutrition, and early use of laxatives [72], most of which are difficult to apply in
severely ill patients.
Management of specific conditions is summarized in Table 3 and complex management algorithm
presented in Fig. 2.
The role of nutrition in the early stage of critical
illness is not clear, but there is increasing evidence
and broadening consensus that aggressive early feeding as well as prolonged underfeeding both should
be avoided [7375]. Therefore, the therapeutic window of nutrition is probably narrower than
previously thought. Whether and how the timing,
formula and administration strategy of enteral nutrition influences the course of gastrointestinal failure
is not clear. Some recent evidence suggests that
concentrated enteral nutrition formula may be
associated with slowed gastric emptying [76].
Critically ill patients with gastrointestinal dysfunction need a multidisciplinary approach for
optimal coordination of diagnostics and management through gastroenterologists, surgeons, radiologists, specialists for infectious diseases, nurses,
physiotherapists as well as wound and stoma
care specialists.
Avoidance of complications like malnutrition,
respiratory complications through aspiration of gastric contents, wound infections, and skin lesions
through diarrhoea etc. is an important part of management of patients with gastrointestinal failure.
FUTURE RESEARCH
Missing description of normal gastrointestinal function in ICU patients and subjectivity in clinical
assessment results in difficulties to define study
endpoints and outcome measures. International
collaboration is warranted to reach consensus on
how to plan the future research in this field.
CONCLUSION
Defining gastrointestinal failure in ICU patients
remains challenging. A validated scoring system
describing a continuum of this organ dysfunction
still needs to be developed to allow proper conduction of interventional studies. Until then, daily
clinical assessment of gastrointestinal symptoms
and syndromes should be applied. For this, we
recommend using terminology, definitions and
grading of acute gastrointestinal injury. The care
of these patients should be based on a systematic
management approach.
12
Acknowledgements
None.
Financial support and sponsorship
This work was supported by the Ministry of Education
and Research of Estonia (IUT3424).
Conflicts of interest
A.R.B. has received honoraria for advisory board
participation from Fresenius Kabi, Nestle and Nutricia.
S.M.J.: The Department of Intensive Care Medicine,
Inselspital Bern, has, or has had in the past, research
contracts with Abbott Nutrition International, B. Braun
Medical AG, CSEM SA, Edwards Lifesciences Services
GmbH, Kenta Biotech Ltd, Maquet Critical Care AB, and
Omnicare Clinical Research AG; and research & development/consulting contracts with Edwards Lifesciences SA,
Maquet Critical Care AB, Nestle and Orion Pharma. The
money is/was paid into a departmental fund; S.M.J. does
not/did not receive any personal financial gain. The
department has received unrestricted educational grants
from the following organizations for organizing a quarterly postgraduate educational symposium, the Berner
Forum for Intensive Care: Fresenius Kabi; GSK; MSD;
Lilly; Baxter; Astellas; AstraZeneca; BjBraun; CSL Behring; Maquet; Novartis; Covidien; Mycomed; RobaPharma; Orion Pharma. J.S. has received honoraria for
advisory board participation from B. Braun Melsungen
AG.
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