INTENSIVE CARE
Gastrointestinal problems
in intensive care
Mark Kubicki
Stephen J Warrillow
Abstract
Gastrointestinal issues are common in ICU and include both surgical
and non-surgical problems. A high index of suspicion and regular clin-
ical assessment are necessary due to inherent difficulties evaluating
critically ill and ventilated patients. Gastrointestinal failure may compli-
cate or even precipitate multi-organ failure with systemic inflammatory
response due to bacterial translocation. Intra-abdominal hypertension
can be under-recognized and causes renal failure and other complica-
tions. Although colonic pseudo-obstruction is often conservatively
managed, early recognition and treatment can prevent perforation.
Stress-related mucosal bleeding is common in ICU, but serious
gastrointestinal haemorrhage is rare. Early enteral nutrition and H2-re-
ceptor antagonists reduce the incidence of upper gastrointestinal
bleeding in high-risk ICU patients. Although delayed bowel motions
are the norm, lack of defecation may also occur. This does not neces-
sarily equate to constipation and should only be treated if problems
occur.
Keywords Constipation; gastrointestinal failure; haemorrhage;
intensive care; intra-abdominal compartment syndrome; obstruction
Royal College of Anaesthetists CPD Matrix: 2C00
Gastrointestinal (GI) problems are often overlooked in the
intensive care unit (ICU) or deferred to the attention and skills of
nursing staff. However, GI dysfunction is a marker of systemic
unwellness. Complete assessment and treatment of the critically
ill patient should involve assessment of the GI system. Common
GI problems are classified into surgical or non-surgical (Table 1).
GI symptoms and signs
GI symptoms and signs are common in ICU patients, with 60% of
patients having at least one GI problem during their stay (Table
2). Significant increases in mortality and length of ICU stay
occur with abnormal or absent bowel sounds, bowel distension
or haemorrhage.1 Assessment may be difficult as many GI
symptoms are subjective and patients are often unable to reliably
report them.
Although care of the GI tract plays a significant role in ICU
care, there are limited investigations or specific biochemical
Mark Kubicki MBBS FCICM is an Intensive Care Specialist at the Austin
Hospital, Heidelberg, Melbourne, Australia. Conflicts of interest: none
declared.
Stephen J Warrillow MBBS FCICM FRACP is a Senior Intensive Care
Consultant at the Austin Hospital, Heidelberg, Melbourne, Australia.
Conflicts of interest: none declared.
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Please cite this article in press as: Kubicki M, Warrillow Stephen J, Gastrointestinal problems in intensive care, Anaesthesia and intensive care
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Learning objectives
After reading this article, you should be able to:
C describe the common and serious gastrointestinal problems
that present in the ICU
C detail the complications and treatment of abdominal compart-
ment syndrome and colonic pseudo-obstruction
C outline the treatment and prevention of GI haemorrhage and
assessment of motility problems including constipation
markers of function. The most easily quantifiable measurements
are haemorrhage, nasogastric (NG) aspirates and serum lactate.
However, there is a lack of uniform definitions (for example, the
expected normal daily NG aspirate volumes range from 150 ml to
500 ml). Because of this, regular thorough clinical examination
and high index of suspicion are needed for potential GI problems.
Gastrointestinal failure
Gastrointestinal failure (GIF) variously defined as ‘gastroparesis
and intestinal ileus’, or ‘gastrointestinal haemorrhage’, is com-
mon, with an incidence of 18%.2 However, GIF is not included in
illness severity scores such as MOFS, SOFA or APACHE III due to
problems in the reliability of data and lack of consensus
definition.
GIF may be one of the driving forces for multi-organ failure
(MOF), secondary to bacterial translocation and entry of endo-
toxin into the circulation. The GI tract is colonized by w100
trillion organisms and it has become increasingly recognized that
alterations in the intestinal microbiome plays a role in the
development in numerous diseases, including sepsis.3 Further-
more, because the GI tract is also involved in endocrine, meta-
bolic, immunological, nutrition and barrier functions,
development of GIF is associated with an increase a range of
adverse outcomes. These including prolonged ICU stay, addi-
tional ventilation days and a nine fold increase in mortality (44%
vs 5%).2 It is noteworthy that while the risk of serious gastro-
intestinal complications in elective cardiac-surgical patients is
low (2.5%), when they do occur, the associated mortality is up to
33%.4 GIF resulting from non-occlusive ischaemia is not un-
common in severe burns and is associated with a high mortality.
Abdominal compartment syndrome (ACS)
Normal intra-abdominal pressure (IAP) is 5e7 mmHg although
this may be mildly elevated in obese patients and can increase to
15 mmHg postoperatively. Intra-abdominal hypertension (IAH)
is defined as an IAP
12 mmHg, and is graded I to IV according
to severity (Table 3). Abdominal compartment syndrome (ACS)
is grade III or IV IAH, plus new organ failure or dysfunction.5 IAH
occurs in 50% of ICU patients, but is often unrecognized. How-
ever, ACS is rare, and the recorded incidence of 5e12% may
reflect reporting bias.
Causes and consequences of ACS
ACS is caused by increased intra-abdominal volume, decreased
abdominal wall compliance or a combination of both (Table 4). It
may be primary (due to an intra-abdominal cause), secondary
1 Ó 2017 Published by Elsevier Ltd.
 INTENSIVE CARE

Classification of gastrointestinal problems in ICU Causes and pathology of abdominal compartment

syndrome3
Non-surgical Surgical
Primary cause Pathological process
Motility problems Bowel obstruction
Diarrheoa Ischaemia Increased Gastrointestinal dilatation
C Infectious Perforation intra-abdominal Intra-abdominal or retro-peritoneal mass
C Non-infectious Haemorrhage or Stress Related Mucosal Bleeding volume Intra-abdominal fluid (ascites/blood)
Constipation Intra-abdominal Compartment Syndrome Pneumoperitoneum
Malabsorption Pancreatitis Decreased abdominal Abdominal surgery (tight closure)
Hepatitis Cholecystitis (calculous and acalculous) wall compliance Abdominal wall haematoma
Liver Failure Surgical correction of large hernias
Both Obesity
Table 1
Trauma
Sepsis and shock
Pancreatitis
Approximate prevalence of bowel symptoms and signs in Massive fluid resuscitation
ICU patients (after Reintam et al.)1 Burns
Colonic ischaemia
Bowel symptom or sign Prevalence (%)
Intra-abdominal infection
Absent or abnormal bowel sounds 41
Table 4
Vomiting 38
High (>500 ml/day) NGa aspirate 23
Diarrheoa 14
Bowel distension 11 mechanical effects. The kidneys are the main extra-peritoneal
Haemorrhage 7 organs affected and renal impairment appears to be indepen-
a
dent of cardiac output. Impaired renal vascular flow results in an
NG, nasogastric.
increase in renin, angiotensin and aldosterone production, and a
Table 2
reduction in glomerular filtration rate.
IAH also increases central venous, pulmonary artery occlu-
sion and intracranial pressures. Increased intrathoracic pressure
results in decreased end-diastolic volume, reduced preload and
Grading of IAH according to IAP (adapted from de Waele increased afterload, the latter is due to direct vascular bed
et al.).3 ACS is grade III or IV plus new organ dysfunction compression and sympathetic activation. Finally, ventilation is
(shaded area) compromised due to decreased thoracic wall and diaphragm
IAHa grade Normal I II III IV compliance.

IAPb (mmHg) 5e7 12e15 16e20 21e25 >25 Measurement and treatment of ACS
a
Clinical examination is unreliable in estimating IAP, so it must be
IAH, intra-abdominal hypertension.
b
IAP, intra-abdominal pressure.
measured using an indwelling urinary catheter (Box 1). Renal
and mesenteric vascular ultrasound is an alternative means of
Table 3 assessing IAP.

(due to an extra-abdominal cause, especially massive fluid

resuscitation) or recurrent (which persists or recurs despite Measurement of IAPa
treatment). The incidence is higher in patients with septic shock,
acute pancreatitis, liver transplant, major trauma (including
burns) and following major abdominal surgery.
As a result of reduced abdominal perfusion pressure (APP),
IAH results in decreased perfusion and eventual ischaemia of
intra-abdominal organs. An APP less than 60 mmHg is associated
with a worse outcome. This causes splanchnic hypoperfusion,
increased mucosal permeability and bacterial translocation. IAH
is an independent predictor of poor outcome and, if ACS de-
velops, has a reported mortality of up to 50%.
Physiological consequences occur also to organs outside the
peritoneal cavity due to the systemic effects of ischaemia and Box 1
Step 1: Fill an empty bladder to 50e100 ml with sterile saline.
Step 2: Allow fluid to flow back to the clamp and occlude the
IDCb.
Step 3: Attach a manometer via a Y-connector to the IDC.
Step 4: Measure IAP with the patient supine, using the symphysis
pubis or mid-axillary line as the zero, at end of expiration.
From www.wsacs.org, accessed September 2011.
a
IAP ¼ intraabdominal pressure.
b
IDC ¼ indwelling catheter.

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Please cite this article in press as: Kubicki M, Warrillow Stephen J, Gastrointestinal problems in intensive care, Anaesthesia and intensive care
medicine (2017), https://doi.org/10.1016/j.mpaic.2017.12.011
 INTENSIVE CARE

First-line treatment options for ACS include avoidance of

prone positioning, titration of PEEP, gastric and colonic decom-
pression, neostigmine or other prokinetic agents and neuro-
muscular blockade to prevent splinting. Diuresis, renal
replacement therapy or peritoneal fluid drainage may also be
useful. Decompressive laparotomy is rarely needed.

GI ischaemia
GI ischaemia can present as peritonism, abdominal distension,
ileus or pseudo-obstruction, lower GI bleeding, abnormal
biochemical markers (e.g. lactic acidosis) or worsening general
clinical status (e.g. shock with increasing vasopressor require-
ment). It can also cause ischaemic hepatitis, pancreatitis or
acalculous cholecystitis.

Causes and investigations

Acute GI ischaemia is usually due to thrombosis (60%) or em-
bolism (30%). It is rarely due to reduced cardiac output or IAH.
Triggers include vascular or cardiac surgery, burns, hypo-
volaemia, acute renal failure (ARF), prolonged ventilation, atrial
fibrillation or catecholamines. It is worsened by oxygen shunting
and reduced autoregulation of GI blood-flow in critical illness.
Clinical signs and abnormal test results are often late and non-
specific. The investigation of choice is contrast enhanced CT,
although if the diagnosis is clinically obvious, an urgent lapa-
rotomy is indicated. A CXR may reveal sub-diaphragmatic free
gas and colonoscopy often shows mucosal ischaemia. Blood test
abnormalities are non-specific, but include elevation in serum
lactate, CRP and WCC or anaemia and lactatic acidosis. Serum
lactate >2.5 mmol/L is associated with increased mortality in
patients with ischaemic colitis.6
Consequences
Untreated GI ischaemia results in increased gut permeability,
translocation of bacteria and endotoxin release, leading to GIF
and MOF. Mortality rates associated with GI ischaemia are very
high (60e80%), particularly with non-occlusive ischaemia. Fifty
percent of patients require haemofiltration and additional com-
plications such as pneumonia and urinary tract infection are
common. Ischaemic colitis also accounts for 20% of lower GI
bleeding. Treatment of clinically significant GI ischaemia in-
volves an urgent laparotomy and bowel resection or less-
commonly revascularization.
GI obstruction and pseudo-obstruction
Mechanical GI obstruction presents with nausea, regurgitation or
vomiting, increased gastric residual volume (GRV), abdominal
pain and the absence of flatus or bowel movements. This re-
quires surgical referral and treatment.
Acute colonic pseudo-obstruction (Ogilvie’s syndrome) is a
diagnosis of exclusion, based on massive colonic distension (>10
cm) and absence of mechanical obstruction (Figure 1). Predis-
posing conditions include trauma, surgery, cardiac disease,
infection, renal failure, electrolyte disturbances, narcotic use and
parasympathetic dysfunction.
Abdominal X-ray (AXR) shows a massively dilated colon,
particularly caecum and right colon. Water-soluble contrast en-
emas can both rule out mechanical obstruction and help
Figure 1 X-ray of pseudo-obstruction.
decompress the bowel. If unrecognized, continued distension,
ischaemia and perforation occurs in 1e3% of patients, with a
mortality of 50e71%.7 Perforation is rare if the caecal diameter is
less than 12 cm. If there are peritoneal signs, evidence of perfo-
ration or deterioration in clinical condition, urgent surgical
consultation is required.
In the absence of peritonism or ischaemia, 90% of patients
respond to conservative treatment within 6 days. Regular clinical
assessment is required and serial AXRs are sufficient to assess
caecal diameter. Conservative treatment involves bowel rest, NG
and rectal tube decompression, as well as treatment of underly-
ing medical issues such as correction of electrolyte imbalances,
avoidance of opiates and treatment of sepsis.
Neostigmine is an effective treatment (2.0e2.5 mg IV over
3e5 minutes). This can be repeated in 3 h6 although infusion at
0.4e0.8 mg/h may be safer with fewer side effects. Side effects
including sweating and bradycardia which respond to atropine.
Endoscopic decompression and caecal tubes can also be tried.
GI bleeding
Major bleeding occurs in 1.5% of ICU patients. It can be divided
into upper (oesophagus, stomach and duodenum) or lower
(jejunum to large bowel) GI tract bleeding.
Upper GI bleeding
Upper GI bleeding (UGIB) is usually due to peptic ulcer disease
(PUD), varices or stress related mucosal bleeding (SRMB). It
presents with haematemesis, malaena, anaemia, shock or
hypovolaemia. Investigation and treatment includes endoscopy,
CT angiography, angiographic embolization or laparotomy. The
preferred strategy will depend on the clinical condition, available
resources and the therapeutic intent.7

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 INTENSIVE CARE

PUD accounts for 36% of UGIB in ICU patients with risk factors
including infection with Helicobacter pylori and medications such Risk factors for stress-related mucosal bleeding (SRMB)
as NSAIDs, SSRIs and corticosteroids. Endoscopic therapies are Major risk factors Minor risk factors
now the mainstay of care and include options such as direct
adrenaline injections, sclerosing agents, cauterization, clipping or Mechanical Hypotension, sepsis,
banding. Administration of proton-pump inhibitors (PPIs) in- ventilation >48 hrs liver failure, renal failure,
creases stomach pH >6, which stabilizes clots. Therapeutic ad- coagulopathy glucocorticoids, anticoagulant therapy,
juncts include somatostatin, octreotide and tranexamic acid. major surgery or trauma,
Variceal bleeding occurs in the distal oesophagus and prox- severe burns, head trauma,
imal stomach and can be difficult to control. Portal hypertension multi-organ failure
from underlying cirrhosis is the most important predisposing history of GI bleeding
factor. Endoscopic treatment involves rubber band ligation helicobacter pylori
(RBL), sclerotherapy, cyanoacrylate glue or thrombin injections.
SRMB prophylaxis should be given for those with major risk factors and consid-
Both octreotide or terlipressin (a vasopressin analogue) reduce ered for those with minor.
the risk of further bleeding7 and are useful adjuncts to endo-
scopic interventions. Balloon tamponade with a Sengstaken- Table 5
Blakemore tube may be utilized as a temporizing measure for
refractory variceal haemorrhage, but patient outcomes are often enteric fistula or faecal containment devices. Upper GI sources
poor in this situation. Prophylactic antibiotics, such as cephalo- of brisk bleeding account for 15% of haematochezia. High-risk
sporins or quinolones, reduce mortality.8 patients include age >60 years, shock, significant comorbidities,
Fresh haematemesis can result in life-threatening catastrophic and aspirin or other NSAID use. Initial resuscitation and treat-
blood loss and requires concomitant resuscitation, investigation ment is as per UGIB, with investigations including colonoscopy,
and specific treatment.9 Age, shock, comorbidities and re- CT angiography or red call scans (nuclear scintigraphy).
bleeding predict mortality. Treatment principles for cata- Mesenteric angiography, embolization or surgery are indicated
strophic bleeding include resuscitative measures, with particular if the bleeding does not resolve.8 Angiography has a high yield
attention to protecting the airway, replacement of red cells, in older patients and those who have recently received several
clotting factors and platelets, and vitamin K. Recent evidence units of blood.
suggests that maintaining haemoglobin above 7.0 g/dl reduces
re-bleeding and other complications.10 Endoscopic intervention Constipation and diarrhoea
allows both specific causes to be identified and therapy to be Delayed bowel motions is common in ICU patients, with up to
applied. 80% of patients passing no motions in the first 72 hours of
admission. The most likely reason for non-defecation in ICU is an
Stress-related mucosal bleed (SRMB)
empty bowel (Table 6).14 Gastric motility may also be reduced by
Approximately 60e90% of critically ill patients have some evi-
sepsis and shock, elevated levels of endotoxin, inflammatory
dence of SRMB at endoscopy, but this causes problems a small
mediators, and nitric oxide production. Sedatives, opiates and
number (0.6e9%) of patients. It is thought to result from gut
vasoactive drugs directly reduce motility.
ischaemia due to hypotension, vasoconstriction or inflammatory
mediators and increased intraluminal acidity in acute illness.
Because major SRMB increases ICU stay and mortality, stress
ulcer prophylaxis should be used in all patients with major risk
Delayed bowel motions and constipation9
factors, and considered in those with minor risk factors (Table 5).
Although prophylaxis does reduce the risk of bleeding for the low Reasons for lack ofReduced nutritional and fibre intake
risk group, there is no mortality benefit10 and the evidence to bowel motion Reduced mobility and exercise
support routine use in this population is lacking. Sedative agents reducing urge to defecate
Prophylaxis regimes include histamine receptor antagonists Anti-kinetic effect of medications (opiates and
(e.g. ranitidine) or PPIs (e.g. pantoprazole) as the second line. A vasopressors)
PPI may be used as a first line agent if the patient usually takes Gastrointestinal failure
them, but there is no observed difference in efficacy. Acid sup- Constipation
pression has no effect on the rate of nosocomial pneumonia, but Signs and symptoms Desire to evacuate the bowel
may increase the rate of clostridium difficile infection.11 Early of constipation Sense of fullness and inability to defecate
enteral nutrition (EN) decreases the risk of UGIB, especially despite effort
SRMB by improving gastric blood flow, buffering intraluminal Passage of small and hard stools
acid and promoting secretion of cytoprotective prostaglandins. If Abdominal distension
EN is fully established, medical prophylaxis is not be required. Abdominal discomfort
A rectum full of stools on PR examination
Lower GI bleeding Palpation of stools on abdominal
Lower GI bleeding, particularly haematochezia (acute bright examination
blood PR), can be life threatening and results from GI
ischaemia, tumour, diverticulae, varices or rarely from aorto- Table 6

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 INTENSIVE CARE
Abdominal distension worsens ventilation and delays wean-
ing, through upward diaphragmatic displacement. It also in-
creases vomiting, patient restlessness and predisposes to GI
perforation. There is also the theoretical risk of overgrowth of
Gram-negative bacteria (with an associated reduction of Gram-
positive and anaerobic flora) that results in an increase in
endotoxin load. However, promoting bowel motions through
routine laxative use does not improve clinical outcome. Pro-
biotics have a physiologically plausible benefit and are generally
regarded as safe; however, have not shown a survival benefit and
routine use is not currently recommended.
Constipation
It is difficult to define constipation in ICU (Table 6). Constipation
occurs with a bowel full of stool that cannot be evacuated despite
effort. It can also be referred to as infrequent or difficult defe-
cation caused by decreased motility of the intestine.15 Lack of
patient effort in critically ill ICU patients makes these definitions
less useful. Thus, it is unclear how common constipation is in
ICU patients and the diagnosis should not be made simply by a
delay in bowel motions.
Thorough clinical examination is needed to evaluate any
suspected motility disorder. Abdominal and rectal examinations
are necessary to rule out bowel obstruction, stricture, blood or
hard impacted stool. AXR can confirm the presence of excessive
bowel stool.
Critical illness related colonic ileus refers to non-passage of
stools without gastric retention and with normal findings on
physical and radiological examination. This should be differen-
tiated from adynamic ileus (abdominal distension, vomiting) or
Ogilvie’s syndrome (dilated colon).
Constipation should only be treated if the patient has a grossly
distended abdomen, increasing pain or there is a prolonged delay
in bowel motions. Initial agents include stimulant (bisacodyl or
senna) or osmotic (lactulose, polyethylene glycol) laxatives.
Osmotic laxatives are gas forming causing distension, discomfort
and fluid shifts. Glycerol suppositories or microlax enemas can
be used to treat faecal impaction.
Diarrhoea
Diarrhoea, defined as loose watery bowel motions, occurs in
15e50% of patients. It is a common side effect of EN, but may
indicate a serious disorder such as infection or pseudomem-
branous colitis from clostridium difficile. Diarrhoea affects fluid
and electrolyte balance and causes perineal excoriation. Treat-
ment involves addressing the underlying cause. Commercially
available devices are effective in preventing excoriation and
cross-infection. A Singer P, Anbar R, Cohen J, et al. The tight calorie control study
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medicine (2017), https://doi.org/10.1016/j.mpaic.2017.12.011
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5 Ó 2017 Published by Elsevier Ltd.