Acute intestinal failure

Gordon L. Carlsona,b and Paul Darkb

a

National Intestinal Rehabilitation Centre, Department

of Surgery and bInfection, Injury and Inflammation
Research Group, Salford Royal Hospital NHS
Foundation Trust, Manchester Academic Health
Sciences Centre, Salford, UK
Correspondence to Professor Gordon L. Carlson,
Department of Surgery, Salford Royal Hospital NHS
Foundation Trust, Eccles Old Road, Salford M6 8HD,
UK
Tel: +44 161 206 5655;
e-mail: [email protected]
Current Opinion in Critical Care 2010,
16:347352

Purpose of review
The review aims to highlight the importance of acute gastrointestinal failure in the
postoperative patient, to clarify the clinical circumstances in which acute intestinal
failure complicates postoperative management, and to discuss recent advances and
controversy in our understanding of the cause and pathogenesis.
Recent findings
Acute postoperative intestinal failure ranges from a self-limiting condition of disordered
intestinal peristaltic activity, through to a complex critical illness state associated with
abdominal sepsis and intestinal fistulation. Recent developments have focused on
the mechanisms of paralytic ileus and preventive strategies, usually as part of programmes
of fast-track or enhanced recovery care, and on the optimum management of patients
with severe abdominal sepsis, including planned versus on-demand relaparotomy, open
abdominal management of severe sepsis and negative pressure wound therapy.
Summary
Many cases of acute intestinal failure are preventable. Improvements in understanding
and preventing paralytic ileus through changes in postoperative care may facilitate
recovery of gastrointestinal function after abdominal surgery. Further and betterorganized studies are needed to define the optimum strategies for treating patients with
severe abdominal sepsis, managing the patient with the open abdomen and defining the
role of enteral, as opposed to parenteral nutritional support in such patients.
Keywords
enhanced recovery, fistula, ileus, parenteral nutrition, sepsis
Curr Opin Crit Care 16:347352
2010 Wolters Kluwer Health | Lippincott Williams & Wilkins
1070-5295

Introduction
Whereas failure of organ systems has long been recognized
as a key feature of critical illness, the potential for failure of
the gastrointestinal system as both a consequence and a
potential driver of the critical illness state has been of more
recent interest. The current review addresses the cause,
pathogenesis and epidemiology of acute postoperative
intestinal failure, and highlights current advances and
controversies in the management of the postoperative
patient with acute intestinal failure.
Definition of intestinal failure

Intestinal failure is defined as a reduction in functioning

gut mass below the minimum amount required for adequate digestion and absorption of nutrients [1]. Although
this definition was subsequently modified to include
failure of the intestinal tract to maintain adequate
hydration and electrolyte balance in the absence of
artificial fluid and electrolyte support [2], an arguably
more important development relates to the classification
of intestinal failure into several distinct patterns of illness,
all characterized by defective intestinal function as outlined above, but with considerable differences in cause,
time course, management and prognosis.
1070-5295 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

North American clinicians generally regard intestinal

failure chiefly as a chronic condition, synonymous with
short bowel syndrome, to be treated either by long-term
home parenteral nutrition or, increasingly, intestinal
transplantation. In contrast, European authors refer to
this condition as type III intestinal failure, but also
recognize acute syndromes in which intestinal failure
can be said to exist. In this context, type I intestinal
failure describes a very short-lived, and self-limiting
state, commonly seen in the postoperative period,
whereas type II intestinal failure principally relates to
the development of surgical complications associated
with abdominal sepsis and, in particular, intestinal fistulation. Although type II intestinal failure may also be selflimiting (e.g. when an intestinal fistula heals spontaneously), it tends to follow a course of several weeks
or months and is likely to require surgical treatment, as
opposed to simply supportive care.
Type I intestinal failure

Type I intestinal failure is exceedingly common; so

common in fact that we know very little of its epidemiology. There are few reliable data available pertaining to
the frequency with which artificial nutritional support is
required, even in otherwise routine postoperative care.
DOI:10.1097/MCC.0b013e328339fabe

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348 Postoperative problems

Uncorroborated surveys of the use of prolonged total

parenteral nutrition (TPN) in hospitals in England have
recently suggested, however, that the annual incidence
of type II intestinal failure may be as high as 18 per
million population per year, based upon a patient
requiring TPN for at least 14 days [3], and the incidence
of type I intestinal failure is thus likely to be considerably
in excess of that, even if the criterion for diagnosis
of postoperative intestinal failure is a requirement
only for the prolonged use of postoperative parenteral
nutrition.
Common causes of type I intestinal failure include mechanical intestinal obstruction and nonmechanical (i.e.
paralytic) ileus, the latter arising most commonly as a
consequence of abdominal surgery, but also occasionally
as a consequence of intra-abdominal or retroperitoneal
infection or inflammation, other critical illness states
including spinal and head injury, pneumonia, hip fracture
and multiple organ failure. Less commonly, type I intestinal failure may develop as a consequence of severe
enteric infection, inflammatory bowel disease, radiotherapy or chemotherapy [4].
Type I intestinal failure developing in the early postoperative period is most commonly associated with mechanical intestinal obstruction or paralytic ileus. The frequency of early postoperative small bowel obstruction
varies according to how it is defined, but, assuming a
conventional definition of obstruction developing within
30 days of surgery, after resumption of gastrointestinal
function, and with radiological or surgical evidence of
mechanical obstruction [5], as many as 10% of patients
undergoing abdominal surgery will develop significant
early postoperative mechanical bowel obstruction and
present with abdominal distension, vomiting, constipation and radiological findings of dilated small intestine.
Postoperative small bowel obstruction is most likely to
occur in patients who undergo open abdominal surgery in
the infracolic compartment, especially colectomy or
ileoanal pouch surgery, or emergency surgery, particularly appendicectomy when there has been appendicular perforation [6]. In contrast, postoperative small
bowel obstruction is much less common after laparoscopic surgery, and occurs after less than 0.5% of procedures [7]. In the majority of cases in which early small
bowel obstruction develops after open surgery, the
obstruction is the result of adhesions and can be managed
conservatively, using nasogastric drainage and intravenous feeding. The obstruction settles spontaneously
in at least 70% of cases within 14 days, with a negligible
risk of intestinal strangulation [6]. Most of the cases that
settle spontaneously do so within the first 7 days, however, and the frequency of spontaneous resolution falls
off markedly at that point, leading some to suggest that
consideration for laparotomy should be given to those

patients who continue to show signs of intestinal obstruction after 7 days [5]. In contrast, obstruction developing
after laparoscopic surgery is much more commonly the
result of port-site herniation [7] and early laparotomy
should be considered in order to avoid strangulated
obstruction. It is especially important to distinguish
mechanical obstruction from paralytic ileus in patients
with early postoperative small bowel obstruction and
prompt radiological assessment, preferably by a contrast-enhanced CT scan, seems to be the most appropriate imaging modality [8]. Those patients who require
relaparotomy can be extremely challenging to manage.
The abdominal cavity can be hostile in the early postoperative period and inadvertent intestinal injury, even if
recognized and treated immediately, is associated with a
high incidence of abdominal sepsis, intestinal fistulation
and type II intestinal failure [9] (see below).
Postoperative ileus is also a frequent cause of type I
intestinal failure and indeed, frequently needs to be
distinguished from mechanical intestinal obstruction.
The clinical importance of postoperative ileus is underlined by the fact that it is currently the most common
reason for delayed discharge following abdominal surgery
[10], leading to a mean increase in length of hospital stay
of approximately 5 days and a 10-fold increase in readmission rates. Postoperative ileus occurs as a result of
transient impairment of coordinated intestinal motility
[11]. Whereas it may affect all segments of bowel, the
pattern of recovery differs according to the portion of the
intestinal tract affected, with recovery occurring notably
quicker in the small intestine than in the stomach or
the colon [12]. The return of colonic motility appears to
be the key factor responsible for the clinical resolution
of postoperative ileus [13]. The mechanisms of ileus
are probably complex and multifactorial. Whereas ileus
usually complicates abdominal surgery, it may also complicate critical illness states and nonabdominal surgical
procedures, including hip surgery, retroperitoneal and
spinal procedures, lower limb orthopaedic and neurosurgery [14]. Whereas disordered intestinal electrical
activity may be the immediate cause of the clinical
syndrome of abdominal distension, constipation, nausea
and vomiting [13], the pathogenesis of the abnormal
electrical and contractile activity may relate to release
of inflammatory mediators, including cytokines, prostaglandins and nitric oxide [12,13], as well as inhibitory
sympathetic nervous activity induced by handling of the
intestines. These effects may be augmented by the
effects of gut hormones and neurotransmitters, including
vasoactive intestinal polypeptide, substance P and calcitonin gene-related peptide [15]. In particular, opioids,
both endogenous and exogenously administered, seem to
play a central role in the development of postoperative
ileus, probably via m-receptor mediated reduction of
transit [16].

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Acute intestinal failure Carlson and Dark 349

Recent years have seen an increasing recognition that ileus

is not an automatic consequence of abdominal surgery and
that it may be, at least in part, an avoidable consequence of
perioperative care [17]. This has led to the development of
enhanced recovery, or fast track programmes, designed to
promote rapid return of normal physiological (including
intestinal) function after surgery. The establishment of
multimodal care pathways, including the avoidance of
mechanical bowel preparation and perioperative fluid
overload, the use of epidural analgesia and individually
optimized perioperative fluid regimens, together with
preoperative carbohydrate loading, early mobilization
and reintroduction of oral fluids and diet, may be associated
with a significant reduction in the incidence of postoperative ileus [18] in the absence of complications such as
intra-abdominal infection and anastomotic leakage. Evidence from randomized controlled trials of individual
components of enhanced recovery programmes suggest
that the key elements of the enhanced recovery programme that hasten the postoperative recovery of gastrointestinal function are the use of epidural analgesia [19]
and avoidance of excessive perioperative fluid, sodium and
chloride administration [20]. Interestingly, the evidence
that laparoscopic surgery per se reduces ileus, when undertaken within a conventional postoperative management
pathway, is inconclusive [21]. Other techniques which
have been recently studied with a view to promoting
the rapid return of postoperative intestinal activity include
the use of chewing gum [22], and m opioid receptor
anatagonists [23,24], whereas other agents that may show
future promise in prevention or treatment of paralytic ileus
include motilin analogues [25].
Type II intestinal failure

In contrast to type I intestinal failure, which generally

requires little more than careful conservative management with high-quality nutritional support and exclusion
of correctable underlying causes, type II intestinal failure
is a serious condition with a considerable associated
mortality and a predominantly surgical cause [4]. Type
II failure may not be self-limiting, with the exception of
those patients with simple intestinal fistulation, in whom
spontaneous healing may occur with effective nutritional
and metabolic support. Patients generally develop type II
intestinal failure as a result of complications of abdominal
surgery, leaving them with severe abdominal sepsis and
intestinal fistulation [4,26]. Sepsis and fistulation are the
primary factors associated with the development of intestinal failure in more than 70% of patients, although
approximately 10% will also have a significant reduction
in absolute bowel length even at diagnosis (i.e. they will
go on to develop type III intestinal failure, irrespective of
treatment) [27].
The most important single aspect of any therapeutic
strategy in the management of patients with type II

intestinal failure is thus prompt diagnosis and treatment

of abdominal sepsis. Inadequately treated abdominal
sepsis was recognized as the most common cause of death
in patients with intestinal fistulas almost 30 years ago [28],
and a recent review of more than 400 patients with type II
intestinal failure associated with intestinal fistulation has
shown that little has changed, with patients with type II
intestinal failure who present with sepsis being almost
30 times as likely to die as patients who present without
sepsis [29]. Management of sepsis associated with type II
intestinal failure involves adequate radiological localization, usually by contrast-enhanced computed tomography (which, in experienced hands, has a diagnostic
accuracy of more than 97% [30]) and percutaneous drainage whenever possible, thus avoiding the second hit
associated with a difficult further laparotomy in a patient
who is usually already critically ill. Percutaneous drainage
may be impractical, impossible, or ineffective in certain
circumstances, notably in patients with multiple abscess
between intestinal loops, or when abdominal sepsis is
associated with complete anastomotic discontinuity, and
in those patients early laparotomy should be considered.
Surgical treatment early in the management of type II
intestinal failure will usually involve prompt exteriorization of fistulating intestine or at the very least, a proximal
defunctioning stoma and effective drainage of a focus of
sepsis. In such patients, age, severity of acute illness and
therapeutic delay beyond 48 h have significant negative prognostic implications [31]. Whereas failure to
improve after apparent source control is also a significant
negative prognostic factor [32], and has previously led
some to suggest that patients with severe abdominal
sepsis should be repeatedly taken back to theatre for
planned relaparotomy until no focus of sepsis can be
shown to remain within the abdomen, this strategy has
proved controversial [33] and a recent randomized controlled trial has shown that careful monitoring and further
laparotomy when required (laparotomy on demand) is
equally effective in terms of morbidity and mortality and
results in a significantly lower rate of negative laparotomy, duration of hospital treatment and time spent
requiring ventilatory support [34].
In cases of recurrent severe abdominal sepsis, adequate
source control may necessitate management of the
patient with an open abdomen (laparostomy) [35]. Indications for open abdominal management of patients
with severe sepsis include extensive abdominal contamination, combined with an inability to defunction fistulating intestine with a proximal stoma because of the
severity of abdominal adhesions. In such cases, attempts
to resect fistulating intestine may lead to injury to otherwise normal intestine, resulting in extensive enterectomy
and type III intestinal failure. Loss of normal intestine
following management of abdominal septic complications in this manner has, in fact, been shown to be the

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350 Postoperative problems

most common cause of type III intestinal failure in

Crohns disease [36]. Although a small randomized controlled trial has shown that leaving the abdomen open
does not reduce morbidity or mortality from abdominal
sepsis [37], there may be instances in which marked
visceral oedema resulting from fluid retention and intestinal inflammation, combined with a rigid abdominal
wall, may make it technically impossible to close the
abdomen, or may lead to concerns about the development of abdominal hypertension even if it should prove
possible to do so [38,39]. When the severity or complexity of abdominal sepsis makes open abdominal management mandatory, great care should be taken to avoid
secondary bowel injury within the open abdominal
wound. Whereas the prognosis for patients with type II
intestinal failure associated with intestinal fistulation
improved markedly between the 1970s and 1980s with
the introduction of parenteral nutrition and improvements in antibiotic therapy, with mortality rates falling
from over 50% to less then 20%, the prognosis for those
patients with fistulation into an open abdominal wound
has remained consistently high [40,41], probably as a
consequence of the difficulty of treating sepsis and providing wound care and nutritional support. Injury to
exposed bowel within the open abdomen may therefore
have catastrophic consequences and should consequently
be avoided at all costs.
The patient with an open abdominal wound may be
especially demanding to nurse and the objectives of
providing comfortable and secure abdominal wound care,
without causing bowel injury may be difficult to attain.
The management of patients with severe abdominal
sepsis and multiple organ failure who may require periods
of ventilatory support in the prone position can be
particularly challenging, because of the conflicting
demands of managing the respiratory failure and providing secure and effective wound care. In general, such
patients can be safely ventilated in the prone position
provided great care is taken not to disturb abdominal
dressings when repositioning the patient. It is advisable
to involve expert nursing staff with specialist training in
enterostomal or wound care whenever such patients are
being repositioned.
The techniques used for the management of the open
abdominal wound are the source of significant current
controversy. The use of negative pressure wound therapy
has proved popular in the management of the abdomen
temporarily left open after damage control laparotomy
when undertaken for trauma, and large cohort studies
appear to suggest that it is well tolerated and results in a
low rate of secondary intestinal fistulation [42]. These
results have not been entirely supported by the only
currently available randomized controlled trial of this
therapy [43], however, which showed a much higher

(albeit not statistically significant) incidence of fistulation

in patients in the negative pressure treatment arm. The
use of negative pressure wound therapy in the management of the septic open abdomen is consequently the
source of particularly significant current controversy, with
some authors suggesting that it is well tolerated and
effective under these circumstances [44,45], whereas
others have raised concerns regarding the incidence
of secondary enteric injury and associated mortality
[46,47,48].
Current practice in managing patients with type II intestinal failure thus focuses on the early diagnosis and
management of abdominal sepsis (in order to avoid
the need for open abdominal management), and the
provision of effective nutritional support, usually in
the form of parenteral nutrition. Developments in techniques for combining stoma care and enteral feeding
have, however, recently allowed effective enteral feeding (fistuloclysis) in selected patients with high-output
intestinal fistulation [49,50], by combining drainage of
intestinal effluent and infusion of enteral feed, with or
without reinfusion of chyme, in selected patients with
type II intestinal failure, and either proximal stomas or in
whom there is enterocutaneous continuity at the site of
fistulation. Whereas these techniques are certainly better tolerated and less costly than parenteral nutrition,
they are not simple to undertake, may not be applicable
to patients with a very high fistula or stoma output and
long-term comparative data on clinical efficacy are currently unavailable.

Conclusion
Acute inability of the gastrointestinal tract to support
nutritional, fluid and electrolyte requirements is a common postoperative problem, but ranges in scope and
severity from the stable postoperative patient with
abdominal distension and vomiting who will settle spontaneously with nasogastric drainage and intravenous fluid
therapy for a few days, through to the critically ill patient
on the intensive care unit with severe sepsis, an open
abdomen and multiple intestinal defects. Recent developments in the field of acute postoperative intestinal
failure range from attempts to gain an understanding
and prevent (or at least minimize) the former and to
provide effective critical care for the latter. In the context
of the most severe cases of type II intestinal failure, the
ultimate aim of treatment, which includes not only
patient survival but also avoidance of permanent intestinal failure, may be difficult to achieve. Centralization
of care for these patients in units with large multidisciplinary teams, composed of physicians, nurses, dieticians, pharmacists, enterostomatherapists and clinical
psychologists, may represent the most appropriate and
cost-effective means by which to achieve this. Future

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Acute intestinal failure Carlson and Dark 351

directions of research for acute intestinal failure seem

likely to not only focus on those elements of enhanced
recovery pathways most likely to minimize the postoperative disruption of intestinal function, but to also
expand the strikingly deficient evidence base on which
the principles of management of type II intestinal failure
are currently established.

References and recommended reading

Papers of particular interest, published within the annual period of review, have
been highlighted as:

of special interest
 of outstanding interest
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World Literature section in this issue (pp. 395396).
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