Paralytic Ileus

Karen Woodfork West Virginia University, Morgantown, USA

ã 2007 Elsevier Inc. All rights reserved.

Introduction

Ileus is a failure of the intestinal contents to pass through the gastrointestinal tract.
Paralytic ileus (adynamic ileus) is caused by a failure of peristalsis rather than a mechani-
cal obstruction such as a tumor, adhesion, or foreign body Summers (1999). Paralytic ileus
generally refers to an acute condition of impaired gastrointestinal motility, in contrast to
chronic conditions such as chronic intestinal pseudo-obstruction and gastroparesis. Para-
lytic ileus is most frequently seen following abdominal surgery, but may also result from
inflammatory processes in the abdominal, thoracic, or retroperitoneal areas, intestinal
ischemia, electrolyte imbalances, systemic sepsis, and as a side effect of some drugs
Turnage and Bergen (1998). Paralytic ileus slows or halts the passage of stools and flatus,
resulting in moderate to severe abdominal distension, mild to moderate pain, nausea/
vomiting, and the potential for acid-base imbalances and organ system failure.

Definition

Paralytic ileus (adynamic ileus) is a partial or complete inhibition of the movement of the
gastrointestinal contents resulting from the failure of peristalsis rather than to mechanical
obstruction Summers (1999). This condition tends to be acute, as opposed to chronic
intestinal pseudo-obstruction and diabetic gastroparesis.

Classification

Paralytic ileus (adynamic ileus) is a motility disorder of the intestine resulting from the
acute failure of peristalsis Summers (1999). It may be classified on the basis of its etiology.
For example, postoperative ileus, which occurs following surgery, is the most common
form of paralytic ileus. Other forms, such as those result from metabolic derangements,
acid-base abnormalities, electrolyte imbalances, or drug therapy, often occur in critically
ill patients. Paralytic ileus of neuropathic origin stems from pathological processes that
impair the functioning of the intrinsic or extrinsic innervation of the gastrointestinal tract,
whereas myopathic paralytic ileus results from processes that damage the gastrointestinal
musculature.
Paralytic ileus may be classified on the basis of the site of hypomotility. Acute colonic
pseudoobstruction (Ogilvie syndrome) results from colonic hypomotility and produces a
massive but reversible dilation of the colon Summers (1999). Postoperative ileus involves
hypomotility of all segments of the gastrointestinal tract, with small intestinal hypomo-
tility occurring for several hours, gastric hypomotility for 1–2 days, and colonic hypo-
motility for 3–5 days Baig and Wexner (2004).

Consequences

Impairment of gastrointestinal motility can have significant pathological consequences.

For example, reflux of intestinal contents into the stomach can result in
1
2 Paralytic Ileus

gastric colonization by intestinal bacteria Madl and Druml (2003) which may be
aspirated into the lungs as a result of either vomiting or migration into the esophagus
and pharynx.
Metabolic imbalances may be caused by ileus, although the origin of these disturbances
is complicated by the fact that ileus is often caused by such imbalances Summers (1999).
Impaired motility of the stomach may cause emesis of fluid high in HCl and KCl, resulting
in hypokalemia, hypochloremia, and metabolic alkalosis. Impaired motility of the distal
duodenum or proximal duodenum may cause alkaline biliary and pancreatic secretions to
be lost in the vomitus, producing metabolic acidosis.
Abdominal pain and distension can result from the accumulation of gas from swallowed
air or bacterial metabolism Summers (1999). Impairment of colonic motility can then
allow the accumulation of gas and, potentially, colonic rupture.
Bacterial overgrowth, which may result in mild mucosal injury, may occur during
paralytic ileus Summers (1999), and malabsorption and nutrient deficiencies may result
from bacterial catabolism of nutrients. Inflammation and disruption of the gastrointestinal
mucosa can cause fluid leakage into the intestinal wall and lumen Madl and Druml (2003).
Several liters of fluid may become trapped in this way, resulting in hypovolemia and
circulatory impairment.
Paralytic ileus is associated with increased luminal pressure, which may produce
intestinal wall ischemia in very severe cases Madl and Druml (2003). Sustained paralytic
ileus may produce an intra-abdominal pressure (IAP) of 30 mm Hg or higher (normal IAP
0 mm Hg). Intra-abdominal hypertension, defined as an IAP greater than 18–20 mm Hg,
results in a decrease in the perfusion of most organ systems. Abdominal compartment
syndrome is defined as an IAP > 20–25 mm Hg in the presence of organ dysfunction or
other systemic consequences.
Sustained intra-abdominal hypertension is associated with a concomitant increase in
intra-thoracic pressure, which impairs cardiac filling, ventricular compliance, and venous
return Madl and Druml (2003). This, in turn, decreases cardiac output, thereby threaten-
ing a number of organ systems. The development of acute renal failure is the most life-
threatening complication of paralytic ileus. This occurs when elevated IAP compresses
the kidneys, producing an increase in renal venous resistance and renal venous pressure,
which activates the renin-angiotensin-aldosterone system. This, combined with the
decreased cardiac output, produces acute renal failure.
Damage to other organs can occur as a consequence of the elevated IAP associated with
paralytic ileus. Elevated IAP decreases hepatic perfusion and portal venous blood flow,
potentially causing portal venous hypertension and bleeding of esophageal varices Madl
and Druml (2003). Elevated IAP also decreases splanchnic perfusion, resulting in further
intestinal dysfunction, bacterial overgrowth, and, rarely, sepsis. The elevated intra-tho-
racic pressure associated with elevated IAP decreases lung compliance, functional resid-
ual capacity, alveolar pressure, and arterial oxygenation. Because elevated intra-thoracic
pressure can produce an increase in central venous pressure and intracranial pressure,
neurological complications can develop as a consequence of paralytic ileus.

Associated Disorders

Paralytic ileus is not a primary disorder but rather an underlying cause. Surgery, particu-
larly that involving the abdominal wall (laparotomy), can cause a form of paralytic ileus
known as postoperative ileus Kehlet and Holte (2001). Women who undergo Caesarean
sections may suffer from postoperative ileus with radiographic findings that mimic colonic
obstruction Kammen et al (2000).
 Paralytic Ileus 3

A variety of potentially serious conditions are seen in association with paralytic ileus
Summers (1999), Madl and Druml (2003). These include diabetic ketoacidosis, pulmo-
nary failure, sickle cell disease, myocardial infarction, pulmonary embolism, abdominal
trauma or hemorrhage, severe burns and fractures, sepsis, and poisoning (e.g. heavy metal
poisoning, spider and other venoms). Intraperitoneal or retroperitoneal infections such as
peritonitis, appendicitis, pseudomembranous colitis, diverticulitis, and pyelonephritis
are also associated with paralytic ileus, as is pneumonia. Abdominal inflammatory con-
ditions such as inflammatory bowel disease, pancreatitis, and cholecystitis are associated
with paralytic ileus, as are abdominal ischemia, abdominal irradiation, ascites, kidney
stones, and certain malignancies. Prolonged or complicated mechanical obstruction can
lead to development of paralytic ileus, as can various primary neuropathic and myopathic
processes associated with long-term impairment of gastrointestinal motility, such as
diabetic neuropathy and myotonic dystrophy.

Etiology

Paralytic ileus occurs in conjunction with many conditions involving physical injury or
critical illness. Postoperative ileus is seen to some extent after any type of abdominal
surgery (post laparotomy), and may develop after non-abdominal surgery as well Baig and
Wexner (2004). In the absence of an underlying pathology, intestinal motility returns
within three to five days. Abdominal surgery activates inhibitory reflex pathways in the
intestine and inflammatory cascades that inhibit intestinal motility. Inhalational general
anesthetics, such as enflurane and halothane, decrease gastric emptying. However, the
colon motility is most susceptible to inhibition by these anesthetics. Other drugs used
during surgery, such as opiates and anticholinergics, can decrease gastrointestinal motility
Summers (1999), Turnage and Bergen (1998). The use of thoracic epidural anesthesia
during abdominal surgery results in less ileus than does the use of systemic opioids. Other
drugs known to impair intestinal motility including certain antipsychotics (phenothia-
zines, clozapine), calcium channel blockers (verapamil, diltiazem, and nifedipine),
tricyclic antidepressants (amitriptyline and doxepin), cancer chemotherapeutic agents
(vinca alkaloids, cytarabine, and irinotecan), immunosuppressive drugs (sirolimus and
tacrolimus), colchicine, and ganglionic blockers Summers (1999), Turnage and Bergen
(1998), Harada et al (2002), Tjon et al (1990). Botulism poisoning can also produce
paralytic ileus Critchley and Mitchell (1990).
A large number of conditions that accompany or produce critical illness can cause
paralytic ileus. Burns covering a large percentage of the body can cause gastrointestinal
complications, including paralytic ileus Kowal-Vern et al (1997). Abdominal trauma,
penetrating wounds, and retroperitoneal or intraperitoneal hemorrhage can initiate
ileus Summers (1999), Turnage and Bergen (1998). Gastrointestinal motility can also be
compromised by electrolyte derangements and metabolic imbalances such as hypokale-
mia, hyponatremia, hypomagnesemia, hypermagnesemia, ketoacidosis, uremia, porphyria,
heavy metal poisoning, and thyroid or parathyroid disorders. Paralytic ileus may develop
in the wake of inflammatory or infectious conditions such as sepsis, peritonitis, pancrea-
titis, cholecystitis, appendicitis, diverticulitis, inflammatory bowel disease, celiac disease,
toxic megacolon, and pyelonephritis. Conditions resulting in intestinal ischemia, such as
arterial insufficiency or thrombosis, may impair gastrointestinal motility, as may condi-
tions affecting the thoracic cavity, such as myocardial infarction, lower lobe pneumonias,
and lower rib fractures. Venoms from black widow spiders and jellyfish have also been
implicated in certain cases of paralytic ileus Ponompalam (2002).
4 Paralytic Ileus

Epidemiology

The National Center for Health Statistics reported 5,558 deaths from ‘‘paralytic ileus and
intestinal obstruction without hernia,’’ 78 deaths from ‘‘paralytic ileus’’ and 370 deaths
from ‘‘ileus, unspecified’’ National Center for Health Statistics (2005) in the United States
for 2002. In the 2003–2004 financial year, approximately 0.2% of the over 13 million
diagnoses reported to England’s Department of Health were cases of ‘‘paralytic ileus and
intestinal obstruction without hernia’’ Department of Health (2005).
Certain populations are at higher risk for paralytic ileus than others. Decreased
gastrointestinal motility occurs, to some extent, following any abdominal surgery (lapa-
rotomy), but may also appear after non-abdominal surgery Baig and Wexner (2004).
Recovery from postoperative ileus generally occurs within 3–5 days. Patients undergoing
high-risk surgeries are at increased risk of postoperative ileus that progresses to a more
severe paralytic ileus. For example, 36% those undergoing cardiopulmonary bypass
develop paralytic ileus Simic et al (1999). In contrast, less than 1% of women having a
Caesarean section develop symptoms of paralytic ileus severe enough to warrant investi-
gation Kammen et al (2000).
Individuals suffering from non-surgical physiological insults are at increased risk of
paralytic ileus. A study of 2114 burn patients showed 9% having severe gastrointestinal
complications, with up to 69% of these experiencing paralytic ileus Kowal-Vern et al
(1997).
Certain medications increase the risk of paralytic ileus. For example, over 8% of 211
patients receiving chemotherapy with cytarabine (cytosine arabinoside, Ara-C) may
develop paralytic ileus Vlasveld et al (1991). A study of 48 cases of Ogilvie’s syndrome
showed that, at the time of diagnosis, 56% of these patients were taking opioids, 42%
phenothiazines, 27% calcium channel blockers, and 15% tricyclic antidepressants
Jetmore et al (1992).

Pathophysiology

Paralytic ileus results from alterations in the neuronal activity and signaling that control
gastrointestinal motility. While gastrointestinal motility is stimulated by the parasympa-
thetic nervous system, it is inhibited by the sympathetic and coordinated by the enteric
(intrinsic) nervous system. The pathophysiology of paralytic ileus is determined by its
cause. Myogenic forms result from muscular dysfunction such as that associated with
myotonic dystrophy. Neurogenic forms of ileus involve dysfunction of the autonomic
nervous system and/or the enteric nervous system. These types of ileus result from
excessive inhibition of gut motility, deficient excitation of motility, or both. Metabolic
abnormalities, including hypokalemia and ketoacidosis, some drugs, and trauma in the
spine or retroperitoneal region can produce alterations in neuronal function that lead to
paralytic ileus Summers (1999).
Postoperative ileus is the best-studied type of paralytic ileus, with an alteration in
neuronal activity being a major component of the pathophysiology of this condition Baig
and Wexner (2004), Kehlet and Holte (2001), Turnage and Bergen (1998). Surgical stress
initiates a reflex that enhances sympathetic activity at the myenteric plexus, thus decreas-
ing intestinal motility. Blockade of the efferent limb of this reflex by epidural administra-
tion of local anesthetics decreases the duration of post-operative ileus. Blockade of the
afferent limb of this reflex with kappa-opioid agonists or cyclooxygenase (COX) inhibitors
may also lessen post-operative ileus De Winter, (2003). In addition to sympathetic
reflexes, surgical manipulation of the intestines activates inhibitory non-adrenergic,
 Paralytic Ileus 5

non-cholinergic (NANC) neurons in the gastrointestinal tract, resulting in the release of

nitric oxide (NO), an inflammatory mediator, and vasoactive intestinal peptide (VIP), a
neurotransmitter that promotes gastric muscle relaxation. Postoperative ileus is also
associated with an increase in the local release of substance P and calcitonin gene-
related peptide Baig and Wexner (2004).
Inflammation is another component in the pathophysiology of postoperative ileus.
Surgical trauma elicits a migration of leukocytes into the intestinal tissues that correlates
temporally with gut paralysis Kehlet and Holte (2001). Induction of cyclooxygenase-
2 (COX-2) and the consequent increase in prostaglandin synthesis appears to contribute
to the development of postoperative ileus. Bowel manipulation may open a pathway
between the intestinal lumen and the muscularis, allowing bacterial products such as
lipopolysaccharide (LPS or endotoxin) to enter and produce inflammation Schwarz et al
(2002).
The physiology of sepsis-induced paralytic ileus is believed to involve a decrease in
gastric and small intestinal motility produced by LPS Schwarz et al (2002). LPS activates
inducible nitric oxide synthase (iNOS) in resident intestinal macrophages. The resul-
tant increase in NO release stimulates the production of inflammatory mediators that
decrease smooth muscle contractility. Include in this group are cyclic guanylate mono-
phosphate (cGMP) and, potentially, oxidants such as peroxynitrite.
The paralytic ileus induced experimentally in mice by the intraperitoneal administra-
tion of acetic acid is accompanied by an increase in the endocannabinoid anandamide.
Development of this condition is blocked by the CB1 cannabinoid receptor antagonist
SR141716A, and is worsened by an anandamide reuptake inhibitor Mascolo et al (2002).

Signs and Symptoms

Patients with paralytic ileus exhibit a failure to pass flatus or stools along with moderate to
severe abdominal distension Summers (1999), Turnage and Bergen (1998). Pain is mild to
moderate, poorly localized, and steady in nature, in contrast to the severe cramping pain
associated with mechanical obstruction. Vomiting, if present, is infrequent, with small
amounts of sour or bilious vomitus. Examination will reveal a nearly silent abdomen with
infrequent and hypoactive bowel sounds. Low-pitched gurgles or weak tinkling sounds
may be heard rarely. This is in sharp contrast to the loud, hyperactive, high-pitched
sounds associated with mechanical obstruction. A resonant sound elicited by percussion of
the abdomen (tympany) can be heard in association with paralytic ileus and indicates gas
trapped in the intestine. Although not characteristic of ileus, a succussion splash may be
detected when the abdomen is shaken if there are large volumes of fluid or gas in dilated
loops of bowel.
Because paralytic ileus is not a primary disorder, the patient may present with
additional signs and symptoms of the underlying condition responsible for the ileus (e.g.
sepsis, hypokalemia, drug side effects).
A plain radiograph differentiates ileus from mechanical obstruction Summers (1999).
In ileus, the film shows gas present throughout the stomach, small intestine, and colon,
with more in the colon than the small bowel. Loops of distended bowel may be seen near
the site of an inflammatory process, such as that associated with appendicitis or pancrea-
titis. Ogilvies syndrome, which is a paralytic ileus affecting the colon, produces a dilation
of the colon, with the greater dilation generally seen at the cecum. Mechanical obstruc-
tion, in contrast, produces a greater degree of gas and fluid accumulation than does ileus.
Gas and fluid accumulate proximal to the site of obstruction, causing dilation of the
intestinal lumen, but fluid, gas, and feces initially persist distal to the point of obstruction.
After 12–24 hours the bowel empties. In complete obstruction, the bowel distal to the
6 Paralytic Ileus

point of obstruction collapses, but in incomplete obstruction, a small amount of air

persists in the distal bowel although its diameter is generally smaller than normal. Orally
administered barium contrast medium rapidly passes through to the colon with ileus but
not with mechanical obstruction.

Standard Therapies

Treatment of paralytic ileus must first address the underlying cause, such as a metabolic
abnormality, sepsis or an adverse response to a drug therapy Summers (1999). Supportive
measures involve correcting dehydration and acid-base or electrolyte imbalances. Drugs
that decrease intestinal motility should be withdrawn or their doses reduced. Nothing is
taken orally, with temporary total parenteral nutrition required in protracted cases.
Surgical consultation should be obtained when mechanical obstruction or peritoneal
signs, such as pain, rebound tenderness, and rigidity of the abdominal musculature
(guarding) elicited by the movement of the abdominal wall, are present. These indicate
inflammatory processes such as appendicitis, ischemic bowel changes, or perforation.
Nasogastric decompression is a classic supportive treatment that prevents swallowed
air from passing distally and removes upper gastrointestinal secretions Summers (1999). It
is typically used, on an intermittent basis, to relieve severe pain and bloating caused by
ileus. A meta-analysis of 26 trials found that nasogastric decompression is effective in
decreasing abdominal distension and vomiting, although it is associated with an increased
risk of pulmonary complications, such as atelectasis and pneumonia, and an increased
time to first oral intake Cheatham et al (1995). The use of nasogastric decompression does
not decrease the length of hospitalization.
There are conflicting data regarding the effectiveness of early postoperative feeding in
decreasing the duration of postoperative ileus Baig and Wexner (2004). Although some
studies indicate an increase in nausea in the early feeding groups, none demonstrated an
increase in paralytic ileus or postoperative complications in the early feeding groups.
A small study of sham feeding showed that patients given gum to chew three times during
the first postoperative day experienced a shorter duration of postoperative ileus Asao et al
(2002).
Gentle enemas may be useful in evacuating the distal bowel in cases of acute colonic
pseudoobstruction (Ogilvie syndrome) Summers (1999). Frequent radiographs should be
taken to monitor the colonic diameter. Most commonly this condition resolves spontane-
ously with supportive, non-invasive treatment. It is often stated that non-invasive man-
agement of acute colonic pseudoobstruction may be continued until the colonic diameter
reaches 12 cm, at which point there is a high risk of colonic perforation leading to fatal
sepsis. However, a rapidly expanding diameter may provide a better correlation with the
risk of impending perforation, as may the duration of colonic dilation. Under these
conditions, surgical intervention may be indicated. Most commonly, colonoscopic defla-
tion is used. While this procedure has a 75–100% success rate it is not without risk of
causing perforation of the colon, especially in a poorly prepared colon. Surgical cecost-
omy was more commonly used in the past to treat this condition and may still be indicated
for some patients.
There is little in the way of definitive pharmacotherapy for paralytic ileus. Many agents
used to stimulate intestinal motility in conditions such as gastroparesis are ineffective or
minimally effective in those with paralytic ileus Bungard and Kale-Pradham (1999), Baig
and Wexner (2004). Numerous studies have shown that metoclopramide, a dopamine D2
and serotonin 5-HT3 receptor antagonist and a 5-HT4 receptor agonist, is ineffective in
shortening the duration of postoperative ileus. Erythromycin, a motilin receptor agonist
that stimulates contractile activity of the upper gastrointestinal tract appears to be
 Paralytic Ileus 7

ineffective as well. Bethanechol, a muscarinic cholinergic receptor agonist, has minimal

prokinetic activity in ileus and produces significant cholinergic side effects.

Agent Name Discussion

Neostigmine Neostigmine, an acetylcholinesterase inhibitor, enhances parasympathetic

nerve activity. By inhibiting the breakdown of acetylcholine, neostigmine
facilitates cholinergic neurotransmission in the gastrointestinal tract,
stimulating gastrointestinal motility. A study of patients with Ogilvie
syndrome revealed that intravenously administered neostigmine (2 mg)
produces a rapid evacuation of flatus or stool in 91% of patients, with a
median time to passage of 4 minutes Ponec et al (1999).

Experimental Therapies

Agent Name Discussion

Cisapride Cisapride is a serotonin 5-HT4 receptor agonist and a weak 5-HT3 receptor
antagonist. It promotes the release of acetylcholine from postganglionic
nerves in the myenteric plexus, producing a prokinetic effect on the stomach
and small intestine. Three out of four studies of intravenous cisapride
demonstrated a significant decrease in the duration of postoperative ileus
Baig and Wexner (2004). Other routes of administration were less effective.
Cisapride was withdrawn from the United States market in 2000 because
prolongs the Q-T interval and causes cardiac arrhythmias. It is available only
to eligible patients in the United States who are enrolled in limited-access
investigational programs.
Alvimopan (ADL Alvimopan is a mu opioid receptor antagonist. Because of its minimal systemic
8-2698) bioavailability, its action is limited to the gastrointestinal tract. It does not
interfere with the centrally-mediated pain relieving effects of opioid
analgesics. Clinical studies have revealed that alvimopan decreases
significantly the duration of postoperative ileus and the length of hospital stay
for those who had undergone abdominal surgery Taguchi et al (2001). In July
2005, the FDA issued an approvable letter for alvimopan.
SR141716A The endocannabinoid system is involved in the control of intestinal motility,
with cannabinoid CB1 receptors found within the enteric nervous system.
Animal studies suggest that hyperactivity of this system may be involved in
the pathogenesis of paralytic ileus. Mascolo and colleagues Mascolo et al
(2002) found that the CB1 receptor antagonist SR141716A significantly
increases intestinal motility in a mouse model of paralytic ileus.
Ethyl pyruvate Ethyl pyruvate inhibits the development of ileus in a mouse model of
postoperative ileus Harada et al (2005). Its effects may be due to a decrease
in the expression of pro-inflammatory cytokines that are released in
response to bowel manipulation.
Ghrelin analogs RC-1139, an analog of the prokinetic peptide ghrelin, counteracts
postoperative ileus in rats in the presence or absence of morphine Poitras
et al (2005).

Animal Models

Most studies of paralytic ileus focus on postoperative ileus. In these cases the animal
models involve performing abdominal surgery (laparotomy) on a mouse, rat, or other
laboratory subject De Winter (2003) Harada et al (2005). An incision may be made
8 Paralytic Ileus

through the abdominal skin, muscle, and peritoneum, and manipulation of the intestines
may further simulate surgical procedures on humans. Surgical trauma may also be
simulated by inducing ischemia in the bowel Udassin et al (1994).
In studies of paralytic ileus produced by sepsis, bacterial endotoxin (lipopolysacchar-
ide or LPS) is injected and the effect on gastrointestinal motility measured De Winter
(2003).
Studies of the effects of drugs on gastrointestinal motility are performed by adminis-
tering the causative agent, such as an opioid, and measuring intestinal transit times Poitras
et al (2005).
Ileus resulting from the nociceptive stimulation of the peritoneum is studied by
intraperitoneally administering 120 mM acetic acid to rodents and measuring gastroin-
testinal motility 30 minutes later Mascolo et al (2002).

Other Information – Web Sites

Medline Plus. This web site, produced by the United States National Library of Medicine,
provides an overview of paralytic ileus symptoms, causes, and treatments and is aimed at
the general public: http://www.nlm.nih.gov/medlineplus/ency/article/000260.htm
Health A to Z. This web site provides basic information on paralytic ileus from the Gale
Encyclopedia of Medicine and is written for the general public: http://www.healthatoz.
com/healthatoz/Atoz/ency/ileus.jsp
AllRefer Health. This web site provides the user with access to the A.D.A. M. educational
material on intestinal obstruction and paralytic ileus. It is written for the general public:
http://health.allrefer.com/health/intestinal-obstruction-info.html
Family Practice Notebook. This web site provides a brief outline of causes, diagnosis, and
management of paralytic ileus. It is designed for physicians and other health professionals:
http://fpnotebook.com/SUR61.htm
National Center for Health Statistics. Deaths from each cause, by 5-year age groups,
Hispanic origin, race for Non-Hispanic population, and sex: United States, 2002: http://
www.cdc.gov/nchs/data/dvs/mortfinal2002_workorigi.pdf
Hospital Episode Statistics from 2003–2004 financial year from the UK Department of
Health: http://www.hesonline.nhs.uk/Ease/servlet/AttachmentRetriever?site_id=1937
&file_name=d:\efmfiles\1937\Accessing\DataTables\Diagnosis\3 character\Diagno-
sis3_0203.pdf&short_name=Diagnosis3_0203.pdf&u_id=5664

Journal Citations

Asao, T., Kuwano, H., Nakamura, J., Moringa, N., Hirayam, I., Ide, M., 2002. Gum chewing enhances
recovery from postoperative ileus after laparoscopic colectomy. J. Am. Coll. Surg., 195, 30–32.
Baig, M.K., Wexner, S.D., 2004. Postoperative ileus: a review. Dis. Colon Rectum, 47, 516–526.
Bungard, T.J., Kale-Pradhan, P.B., 1999. Prokinetic agents for the treatment of postoperative ileus in
adults: a review of the literature. Pharmacotherapy, 19(4), 416–423.
Cheatham, M.L., Chapman, W.C., Key, S.P., Sawyers, J.L., 1995. A meta-analysis of selective versus
routine nasogastric decompression after elective laparotomy. Ann Surg., 221(5), 469–476.
Critchley, E.M., Mitchell, J.D., 1990. Human botulism. Br. J. Hosp. Med., 43(4), 290–292.
De Winter, B., 2003. Study of the pathogenesis of paralytic ileus in animal models of experimentally induced
postoperative and septic ileus. Verh. K. Acad. Geneeskd. Belg., 65(5), 293–324.
Harada, T., Moore, B.A., Yang, R., Cruz, R.J. Jr, Delude, R.L., Fink, M.P., 2005. Ethyl pyruvate ameliorates
ileus induced by bowel manipulation in mice. Surgery, 138(3), 530–537.
Harada, T., Ohtaki, E., Sumiyoshi, T., Hosoda, S., 2002. Paralytic ileus induced by the combined use of
nifedipine and diltiazem in the treatment of vasospastic angina. Cardiology, 97, 113–114.
Jetmore, A.B., Timmcke, A.E., Gathright, J.B. Jr, Hicks, T.C., Ray, J.E., Baker, J.W., 1992. Ogilvie’s
syndrome: colonoscopic decompression and analysis of predisposing factors. Dis. Colon Rectum, 35
(12), 1135–1142.
 Paralytic Ileus 9

Kammen, B.F., Levine, M.S., Rubesin, S.E., Laufer, I., 2000. Adynamic ileus after Caesarean section
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Poitras, P., Polvino, W.J., Rocheleau, B., 2005. Gastrokinetic effect of ghrelin analog RC-1139 in the rat.
Effect on post-operative and on morphine induced ileus. Peptides, 26(9), 1598–1601.
Ponec, R.J., Saunders, M.D., Kimmey, M.B., 1999. Neostigmine for the treatment of acute colonic pseudo-
obstruction. N. Engl. J. Med., 341(3), 137–141.
Ponompalam, R., 2002. An unusual case of paralytic ileus after jellyfish envenomation. Emerg. Med. J., 19,
357–358.
Schwarz, N.T., Beer-Stolz, D., Simmons, R.L., Bauer, A.J., 2002. Pathogenesis of paralytic ileus: intestinal
manipulation opens a transient pathway between the intestinal lumen and the leukocytic infiltrate of the
jejunal muscularis. Ann. Surg., 235(1), 31–40.
Simic, O., Strathausen, S., Hess, W., Ostermeyer, J., 1999. Incidence and prognosis of abdominal
complications after cardiopulmonary bypass. Cardiovasc. Surg., 7(4), 419–424.
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935–940.
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Udassin, R., Eimerl, D., Schiffman, J., Haskel, Y., 1994. Epidural anesthesia accelerates the recovery of
postischemic bowel motility in the rat. Anesthesiology, 80(4), 832–836.
Vlasveld, L.T., Zwaan, F.E., Fibbe, W.E., Tjon, R.T., Tham, T.A., Kluin, P.M., Willemze, R., 1991.
Neutropenic enterocolitis following treatment with cytosine arabinoside-containing regimens for
hematological malignancies: a potentiating role for amsacrine. Ann. Hematol., 62(4), 129–134.

Book Citations

Turnage, R.H., Bergen, P.C., 1998. Intestinal Obstruction and Ileus. Weisiger, R.A., Bilhartz, L.E., Zorab, R.
(Ed.), Sleisenger and Fordtran’s Gastrointestinal and Liver Disease, pp. 1799–1809, 1799–1809.
Summers, R.W., 1999. Approach to the Patient with Ileus and Obstruction. Yamada, T. (Ed.), Textbook of
Gastroenterology. .
National Center for Health Statistics, 2005. Deaths from each cause, by 5-year age groups, Hispanic origin,
race for Non-Hispanic population, and sex: United States, 2002. .
Department of Health 2005 Hospital Episode Statistics from 2003–2004. .

Further Reading

Holte, Kehlet, Postoperative ileus: progress towards effective management, Drugs, 62(18) (2002)
2603–2615.
Galligan, Vanner, Basic and clinical pharmacology of new motility promoting agents, Neurogastroenterol.
Motil., 17(5) (2005) 643–653.
Fazel, Verne, New solutions to an old problem: acute colonic pseudo-obstruction, J. Clin. Gastroenterol. 39
(1) (2005) 17–20.