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Gastroenterol Clin N Am

32 (2003) 12291247

Bowel obstruction and pseudo-obstruction

Charles J. Kahi, MD, Douglas K. Rex, MD*
Division of Gastroenterology and Hepatology, Indiana University Medical Center,
550 North University Boulevard, UH 4100, Indianapolis, IN 462025121, USA

Bowel obstruction results from mechanical interruption of the ow of

intestinal contents, whereas pseudo-obstruction is characterized by dilation
of the bowel in the absence of a causative anatomic lesion. The clinician
evaluating the patient with one of these syndromes is faced with several
challenges. First, bowel obstruction has to be dierentiated from pseudoobstruction, because the two entities have completely dierent etiologies
and pathophysiologic mechanisms, with resultant diverging approaches to
management. When true obstruction is present, the next step is to determine
the site and nature of the causative lesion; small bowel obstruction (SBO) is
in general caused by benign lesions, in distinction to colonic obstruction,
which is frequently caused by neoplasms. More importantly, the clinician
needs to determine whether the obstruction is partial or complete, and
whether or not intestinal ischemia has occurred. This is of major therapeutic
relevance because it helps determine which patients should be managed
surgically. When pseudo-obstruction is present, the chronicity of the process
has to be determined: acute colonic pseudo-obstruction (ACPO) can result
in substantial morbidity and mortality if unrecognized, and treatment is
primarily nonsurgical. Chronic intestinal pseudo-obstruction and congenital
or acquired megacolon are completely separate disorders and are not further
This article is divided into two sections: in the rst, the diagnosis and
therapy of SBO and large bowel obstruction (LBO) are discussed, with
emphasis on specic situations where the gastroenterologist plays a major
role in management. In the second, ACPO is reviewed, with an update on
medical and endoscopic therapeutic options.

* Corresponding author.
E-mail address: drex@iupui.edu (D.K. Rex).
0889-8553/03/$ - see front matter 2003 Elsevier Inc. All rights reserved.


C.J. Kahi, D.K. Rex / Gastroenterol Clin N Am 32 (2003) 12291247

Peritoneal adhesions following laparotomy account for up to 75% of
cases of SBO [1,2]. Lower abdominal and pelvic surgeries, particularly
colectomy and appendectomy, are frequently complicated by the development of adhesive bands, which may lead to SBO [35]. Any abdominal
surgery, including cholecystectomy [5] and gynecologic procedures [6],
however, may predispose to the formation of adhesions. Hernias are the
underlying etiology in about 25% of cases of SBO [7], the inguinal type
being most frequently implicated [2]. Other less common causes of SBO
include Crohns disease, ischemia, radiation, intussusception, volvulus,
neoplasms, gallstones, and bezoars.
The site and severity of obstruction determine the clinical presentation and
course of patients with SBO. The unifying feature is intravascular volume
depletion with its attendant systemic consequences, including electrolyte
imbalances, oliguria, renal insuciency, and hemodynamic instability.
Fluids and swallowed air accumulate proximal to the obstruction, predisposing to bacterial overgrowth. When this occurs, there is increased gas
production, which worsens the distention [8], and increased susceptibility for
systemic complications caused by bacterial translocation outside the gut [9].
If the obstruction is unresolved, the process perpetuates itself; the intestine
loses its absorptive capability and uid moves into the intestinal lumen,
further worsening the distention [10,11]. Ultimately, this compromises blood
supply to the aected segment of intestine, rst leading to strangulation, then
necrosis, then perforation. Strangulation is much more common when
a hernia is the underlying cause of SBO, compared with adhesions [7].
Clinical features
The classic symptoms of SBO are abdominal distention, vomiting,
obstipation, and crampy abdominal pain with paroxysms that occur every 4
or 5 minutes [12]. Symptom severity varies with the degree and site of
obstruction; patients with proximal obstruction tend to have more nausea
and vomiting compared with those with distal SBO. Feculent emesis may
occur because of bacterial overgrowth. Strangulation should be suspected
when pain becomes continuous and focal, particularly if the patient is
known to have a hernia [12]. Passage of stool and atus may still occur in
partial SBO and early complete SBO as the intestine distal to the obstruction
evacuates its contents; however, the presence of obstipation is a reliable
indicator of complete obstruction [12].
Abdominal distention and tenderness are the most common ndings on
physical examination; the presence of peritoneal signs should suggest

C.J. Kahi, D.K. Rex / Gastroenterol Clin N Am 32 (2003) 12291247


strangulation, mandating urgent laparotomy. Strangulation should also be

suspected when signs of systemic toxicity are present. Bowel sounds may be
hyperactive and high-pitched initially but may become hypoactive as
intestinal motility decreases with unresolved obstruction [12].
Laboratory ndings in SBO are nonspecic and include leukocytosis with
a left shift, electrolyte abnormalities, elevated urea nitrogen and hematocrit,
and a metabolic alkalosis caused by vomiting and dehydration [12]. Lactic
acidosis, hyperkalemia, and elevated amylase and lipase levels may occur in
the setting of bowel ischemia; however, no laboratory parameter has
sucient specicity to distinguish simple from strangulated obstruction [13].
Plain supine and upright abdominal radiographs should be obtained in all
patients with suspected SBO. Supine lms can help estimate the degree of
distention; upright lms can show multiple air-uid levels with distended
loops of small bowel, and determine whether air is present in the colon
(absence of air makes complete obstruction more likely) [12]. Free air and
pneumatosis intestinalis are ominous ndings and should lead to prompt
surgical intervention [12]. Most cases of SBO can be diagnosed with the
combination of clinical features and radiographic ndings. About 20%
to 30% of patients present with atypical symptoms or nondiagnostic
abdominal lms [7,1416] and are best evaluated with abdominal CT. CT
scanning can delineate the level and severity of SBO, and provide insight on
the underlying etiology (except adhesions) and associated intra-abdominal
pathology. The sensitivity and specicity of abdominal CT in the diagnosis
of SBO are about 90% [14,1719]. Contrast studies, such as small bowel
follow-through and enteroclysis, are very useful in dierentiating complete
from partial SBO; however, they are not accurate in determining the nature
of the obstructing lesion and are usually used as a second-line diagnostic
modality when clinical, plain radiographic, and CT scan ndings are
equivocal [18].
Management: general principles
All patients with SBO should be resuscitated with isotonic intravenous
uids, their electrolyte derangements corrected, and undergo placement of
a nasogastric tube to help prevent further bowel distention [12]. Long
decompression tubes do not decrease the need for surgery and tend to form
kinks in the small bowel, and have largely been abandoned as a therapeutic
modality [2022].
The central dilemma for clinicians managing patients with SBO is to
determine if and when surgical intervention is indicated. Patients with
complete SBO have a low likelihood of spontaneous resolution and a high
risk for strangulation, arguing for early surgical intervention [12].
The presence of signs of peritoneal irritation and systemic toxicity


C.J. Kahi, D.K. Rex / Gastroenterol Clin N Am 32 (2003) 12291247

mandate for early laparotomy; however, their absence cannot reliably

exclude strangulation [13]. In contrast, the risk of strangulation is very low
in patients with partial SBO [13] and most can be managed safely
nonsurgically [21].
Management: specic situations
Obturation of the small bowel lumen
Rarely, obstruction of the small bowel can result from the impaction of
food bezoars, foreign bodies, and gallstones. Treatment is usually enterotomy with segmental resection if needed. Small bezoars can be removed
eectively endoscopically, especially those located proximally. Larger, more
distal concretions require surgical intervention. Gallstone ileus is a particular
example of SBO where endoscopy may be eective. The term ileus is
actually a misnomer, because most cases result from a true obstruction of
the small intestinal lumen by a gallstone; most commonly, the stone has
eroded into the bowel through a cholecystoduodenal stula [23]. Endoscopic
removal, with or without lithotripsy, initially can be attempted if the point
of obstruction is reachable with a colonoscope or push enteroscope [24,25];
surgical enterolithotomy with subsequent cholecystectomy and stulectomy
are the next steps in management [26].
In contrast to pediatric cases, which are usually caused by hypertrophied
ileal lymphoid tissue, adult intussusception is associated with a small bowel
malignancy in up to 75% of patients [27]. Surgical resection is the treatment
of choice [12].
Small bowel malignancies
These include adenocarcinoma, lymphoma, and carcinoid. Laparotomy
with segmental resection is indicated for diagnosis and relief of obstruction
in most cases [28].

Malignancy, usually adenocarcinoma, accounts for about 60% of cases
of LBO, whereas volvulus and diverticular strictures constitute most of the
rest [12]. The same principles guiding the management of SBO, including
attention to signs of strangulation, intravenous hydration, and nasogastric
suctioning, also apply to the management of LBO. In the case of malignant
obstruction, the placement of endoluminal stents is an alternative for
patients with nonresectable tumors and those who are not candidates for
palliative diversion [2935]. Colonic volvulus represents a special situation
in which the gastroenterologist might be called on to provide emergent
therapy and is discussed next.

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Colonic volvulus
Volvulus, or torsion, can occur in any portion of the gastrointestinal tract,
but most commonly involves the cecum, followed by the sigmoid colon [36].
Patients with cecal volvulus are usually in the sixth decade of life [37] and
many have underlying congenital or acquired abnormalities that lead to
increased cecal mobility. The presentation is similar to that of SBO; the
cecum either can twist axially or fold on itself in an anterior-cephalad
direction, which is referred to as cecal bascule [38]. Abdominal radiographs classically show a massively dilated, kidney-shaped cecum extending
into the left upper quadrant or epigastrium (Fig. 1) [39]. Treatment is
primarily surgical, because cecopexy often needs to be performed to prevent
recurrence. There are reports of successful reduction of cecal volvulus by
colonoscopy; however, the risk of perforation is high [40,41]. In contrast,
sigmoid volvulus tends to aect older, more debilitated patients, particularly
the institutionalized and those with concomitant psychiatric disorders
[42,43]. Symptoms are similar to SBO, although vomiting is a less prominent
feature. Diagnosis is established with plain abdominal radiography, which
reveals an ahaustral sigmoid with a tapered end pointing toward the right
upper quadrant (bent inner tube, Fig. 2A) [44]. In equivocal cases, a watersoluble or barium enema may be performed to ascertain the diagnosis; this
may actually resolve the volvulus in about 5% of adult patients [45]. In
distinction with other causes of bowel obstruction, initial treatment of
sigmoid volvulus is nonsurgical with proctosigmoidoscopic reduction. A
exible or rigid sigmoidoscope is inserted into the rectum and advanced until
a spiral-shaped lumen is visualized, indicating the area of volvulus. As the
scope is gently advanced, the sigmoid colon gradually straightens until the
torsion is completely reduced; this is often accompanied by passage of stool
and atus. There is some controversy as to whether this procedure can be
used safely if mucosal ischemia is visualized; one factor to take into account
is that the endoscopic assessment of ischemia is an inaccurate predictor of the
depth of ischemic injury to the colonic wall. Some endoscopists leave a rectal
tube behind to decrease the risk of recurrence; however, the usefulness of this
practice is not rmly established (Fig. 2B). Overall, in the acute setting,
endoscopic reduction is successful in 60% to 95% of cases [43,4649]. The
risk of recurrence is 40% to 60% [4143,47,49], which mandates subsequent
sigmoid resection for denitive therapy. Mortality rates in the presence of
gangrene are 25% to 80% in dierent series [41,47,49], necessitating
expeditious evaluation and therapy of patients with colonic volvulus.

ACPO, also synonymous with acute colonic ileus and Ogilvies
syndrome, was rst described in 1948 by Sir Heneage Ogilvie [50]. In his
seminal paper, he presented two patients with tumors of the lumbar spine

Fig. 1. (A) Cecal volvulus. Note massively enlarged, kidney-shaped cecum (arrows), which has
been displaced into the left upper quadrant. The arrowheads point to the appendix, now in the
right upper quadrant. (Courtesy of John C. Lappas, MD, Indianapolis, IN.) (B) Upright
abdominal radiograph of patient in A. Note very prominent air-uid level. (Courtesy of John C.
Lappas, MD, Indianapolis, IN.) (C) Barium enema of patient in A and B. The arrow points to
the area of the volvulus, with a dilated cecum in the cephalad direction. (Courtesy of John C.
Lappas, MD, Indianapolis, IN.)

C.J. Kahi, D.K. Rex / Gastroenterol Clin N Am 32 (2003) 12291247


Fig. 2. (A) Sigmoid volvulus. Note U-shaped, massively dilated, and ahaustral sigmoid.
(Courtesy of John C. Lappas, MD, Indianapolis, IN.) (B) Radiograph of patient in A after
successful endoscopic detorsion and placement of a tube into the sigmoid colon. (Courtesy of
John C. Lappas, MD, Indianapolis, IN.)

and progressive colonic dilation over 2 months. His patients did not have
ACPO senso stricto, because their course was subacute. As currently
understood, Ogilvies syndrome occurs within days, mostly in severely ill
hospitalized patients.
A variety of conditions have been cited in association with ACPO; these
are summarized in Table 1.
Ogilvie originally suggested that autonomic imbalance was the cause of
ACPO, and this remains the most widely accepted explanation. Although the
exact pathophysiologic mechanism is still unclear, it is thought that excessive
sympathetic stimulation, combined with suppressed parasympathetic activity, leads to a state of adynamic colonic ileus. This theory forms the basis of
the newer pharmacologic approaches to therapy, as discussed later.
Clinical features
Most patients with ACPO are already hospitalized for a severe illness
[5053] and frequently identied during consultation on surgical services
[54]. Symptoms usually develop over 3 to 7 days, although the onset can
occur over 24 to 48 hours [54]. The disease is more common in those older


C.J. Kahi, D.K. Rex / Gastroenterol Clin N Am 32 (2003) 12291247

Table 1
Etiologies and associations underlying ACPO
Laxative abuse
Calcium channel blockers
Amphetamine overdose
Cytotoxic drugs
Anti-parkinsonian agents
Metabolic and endocrine
Myocardial infarction
Congestive heart failure
Heart transplantation
Aortic aneurysms
Other surgeries
Chroni obstructive pulmonary
Mechanical ventilation
Lung transplantation
Renal failure
Ethanol ablation of renal cancer
Renal transplantation

Gastrointestinal bleeding
Retroperitoneal hematoma
Mesenteric thrombosis
Liver failure
Liver transplantation

Herpes zoster
Physical exertion

Small cell lung cancer
Generalized cancer
Multiple myeloma
Acute myeloid leukemia
Invasion of lumbar sympathetics
Pelvic trauma
Pelvic, hip fracture
Pelvic, hip surgery
Joint arthroplasty
Disk surgery
Obstetric and gynecologic
Normal pregnancy
Normal delivery
Cesarean section
Placenta previa
Pelvic irradiation
Multiple sclerosis
Parkinsons disease
Spinal cord disease
Lumbar surgery

Data from References [47,5052,57,59,62,63,67,7579,8285,8789,94123].

Modied from Rex DK. Colonoscopy and acute colonic pseudo-obstruction. Gastrointest
Endosc Clin N Am 1997;7:499508; with permission.

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than 60 and 60% are men [52]. Symptoms of ACPO are similar to those
of true obstruction, and include abdominal distention, pain, nausea, and
vomiting. The frequency of passage of bowel movements and atus is
quite variable and ranges from obstipation to paradoxical diarrhea [54].
Physical examination almost universally shows abdominal distention and
tympany. Bowel sounds are frequently present [52] and have a highpitched quality when the distention is signicant. Abdominal tenderness is
not a prominent feature and when present with peritoneal signs, fever, or
leukocytosis, should trigger an immediate evaluation to rule out
The diagnosis of ACPO is conrmed by plain abdominal radiographs
that show massive colonic dilation [55]. The right colon and cecum are
most commonly involved, although the dilation may extend distally into
the transverse colon, splenic exure, and distal colon (Fig. 3). The greatest
fears in ACPO are ischemia and perforation; the risk of spontaneous
perforation is 3% to 15%, with a mortality rate of 50% [54]. There is no
consensus on the cecal diameter that should be used as a cuto to
diagnose ACPO. Some reports have suggested a diameter of 12 cm [52,56];
however, there is no linear relationship between cecal size and risk of
perforation. Some patients have recovered after reaching a cecal diameter
of 25 cm [57], whereas others have perforated with diameters of 10 cm or
less [54]. The duration of dilation may be more important than its
magnitude; in one report, the risk of perforation increased markedly after
6 days of distention [58]. In general, patients have to be assessed
individually and a combination of cecal size, duration of dilation, and
presence of signs of systemic toxicity used to estimate the risk of perforation. It is of paramount importance to exclude mechanical obstruction in
the evaluation of patients with suspected ACPO, because cutos (absence
of air in the distal colon) can be seen in both conditions. In equivocal
cases, a water-soluble enema or colonoscopy should be performed to rule
out true obstruction [54]. Small bowel air-uid levels are typically seen
with mechanical obstruction and are usually absent in ACPO [54]. Other
diagnostic considerations include toxic megacolon and Clostridium dicile
colitis. Patients with the former condition tend to have more signs of
systemic toxicity than their counterparts with ACPO (fever, abdominal
tenderness, marked leukocytosis) and usually have a history of inammatory bowel disease.
The gastroenterologist consulted for a patient with ACPO is challenged
to decide on the appropriate management strategy. The risk of spontaneous
perforation is dicult to estimate based on clinical or radiographic grounds,


C.J. Kahi, D.K. Rex / Gastroenterol Clin N Am 32 (2003) 12291247

Fig. 3. ACPO. The cecum is dilated to 12 cm, with gradual tapering into the transverse colon.
Air is seen in the descending colon. (Courtesy of John C. Lappas, MD, Indianapolis, IN.)

but portends a poor prognosis if it does occur. In addition, a colonoscopy

for decompression is frequently requested, but dicult to justify in patients
who have easily correctable underlying causes or likely to respond to
pharmacologic therapy, and itself carries a risk of perforation. Finally, the
advent of neostigmine has shifted the ACPO treatment paradigm toward
noninvasive modalities.
The approach to patients with ACPO should follow the guidelines
detailed next, and is summarized in algorithm form in Fig. 4.
Conservative management
The rst step in the treatment of patients with ACPO is similar to those
with SBO: adequate intravenous hydration, nasogastric tube suctioning, and
vigilance for signs of systemic toxicity. Most importantly, underlying
precipitant factors have to be identied and addressed: electrolyte abnormalities should be corrected and any oending medications (especially
narcotics and anticholinergics) discontinued. In addition, the patient should
be mobilized out of bed; however, many patients are nonambulatory. In this

C.J. Kahi, D.K. Rex / Gastroenterol Clin N Am 32 (2003) 12291247

Fig. 4. ACPO management algorithm.



C.J. Kahi, D.K. Rex / Gastroenterol Clin N Am 32 (2003) 12291247

situation, regular turning side-to-side and if possible the prone position or

the knee-chest position should be encouraged [54]. A rectal examination
should be performed every 6 hours because this facilitates passage of atus;
a rectal tube can be placed, although the eectiveness of this technique has
not been proved [54]. Collectively, conservative measures are eective in
33% to 100% of cases [57,5967]. In one study [57], the mean response time
was 3 days. Patients should be followed with serial abdominal examinations
and radiographs to monitor for response or evidence of ischemia or
Pharmacologic treatment
If conservative measures fail after 24 to 48 hours, pharmacologic
modalities can be attempted. There are anecdotal reports of success with
prokinetic agents, such as intravenous erythromycin [68], cisapride [69], and
metoclopramide [54]; however, cisapride is not available in the United States
and may not be eective in all cases [70]. Metoclopramide primarily aects
upper gastrointestinal tract motility and could theoretically worsen ACPO
by moving more upper gastrointestinal contents into an adynamic colon
[54]. Neostigmine has now emerged as the only therapy for ACPO that has
been assessed in a randomized controlled trial [71]. Neostigmine is a potent
parasympathomimetic and can correct the autonomic imbalance thought to
cause ACPO. Initial uncontrolled trials of neostigmine showed rapid
resolution of ACPO in more than 80% of patients [72,73]. The most
compelling evidence comes from a randomized, double-blind, placebocontrolled trial conducted by Ponec et al [71]: 21 patients with ACPO who
had failed conservative therapy were randomized to receive 2 mg of
intravenous neostigmine versus saline placebo. Ten of 11 patients receiving
neostigmine responded promptly (median time of 4 minutes) with
evacuation of stool and atus, whereas none of the 10 patients randomized
to placebo improved. Eight of these 10 subsequently responded to
neostigmine in the open-label phase of the study. The rate of recurrence
of ACPO was low (11%). Symptomatic bradycardia necessitating atropine
occurred in two patients; other side-eects were mild and self-limited and
included excessive salivation, abdominal pain, and vomiting. Neostigmine is
contraindicated in the presence of bradyarrhythmias, mechanical obstruction, colonic ischemia or perforation, and pregnancy. It should be used with
caution in patients with active bronchospasm or renal insuciency. A recent
report revealed that female gender and advanced age are associated with
a response to neostigmine in patients who failed conservative therapy, and
highlighted the fact that the medication tends to be underused, even in the
absence of contraindications [74].
Colonoscopic decompression
No trials comparing pharmacologic interventions with colonoscopy
for ACPO have been performed, and the eectiveness of neostigmine is

C.J. Kahi, D.K. Rex / Gastroenterol Clin N Am 32 (2003) 12291247


likely to decrease the use of colonoscopic decompression. Still, this

remains the procedure of choice in the subset of patients who do not
respond to conservative and pharmacologic modalities. Many series have
been reported [52,5963,65,7591]; overall, colonoscopy is eective in 70%
of cases, with a recurrence rate of 40%, complication rate of 3%, and
mortality of 1%. Colonoscopy for ACPO should only be performed by
experts. Bowel preparation is not possible and there is no consensus on
the use of enemas before the procedure [54]. Minimal air insuation is
used and as little as possible sedation administered. The colonoscope is
guided through the dilated sections, which should be deated enough to
relieve tension but not to a degree that hinders further lumen visualization
and advancement. Cecal intubation in ACPO is technically dicult because of elongation of the dilated colon; prolonged attempts at cecal
intubation are inadvisable [54]. Passage of the hepatic exure is more
likely to result in successful decompression than when it is not passed
[86,87]; the scope should be advanced beyond the hepatic exure when
practical [54]. The visualization of mucosal ischemia during colonoscopy
does not automatically mandate proceeding to surgery, because the endoscopic appearance of ischemia correlates poorly with transmural necrosis
and may be reversible; some patients have been managed successfully
with colonoscopic decompression in the face of ischemia [90]. A tube
should be placed for decompression to decrease the risk of recurrence,
although this has not been studied in a controlled fashion [54]. Several
tube placement methods have been described; uoroscopy should be used
in most cases because it results in successful tube placement in the proximal
colon nearly 100% of the time [54]. One technique entails attaching sutures
to a nasogastric tube; the sutures are then grasped with a biopsy forceps and
the tube is dragged alongside the colonoscope and released in the proximal colon [81]. This method is cumbersome and carries the risk of displacing the tube distally as the colonoscope is withdrawn [54]. At Indiana
University, the authors use the following technique: after the colonoscope
is advanced as far as possible, a sti Savary wire (or another wire that
resists coiling) is pushed through the biopsy channel and the scope
withdrawn. Next, the tip is cut o a well-lubricated 18F catheter Levin
tube and it is passed over the guidewire into the proximal colon; the
guidewire is then withdrawn under uoroscopy and the tube connected to
gravity [54]. Over-the-wire colon decompression sets are commercially
available; all use exible guidewires (0.035 in) with 480-cm catheters sized
7F, 8.5F, 10F, or 14F catheter. The disadvantages of these kits are that the
wires tend to loop easily, whereas the small catheter size makes them prone
to clogging [54], thus the authors preference for their homemade
Percutaneous endoscopic cecostomy [92] and transperitoneal cutaneous cecostomy [93] have been used in ACPO but neither have gained widespread use.


C.J. Kahi, D.K. Rex / Gastroenterol Clin N Am 32 (2003) 12291247

Surgical therapy, including cecostomy and colectomy, should be
considered in the rare patients who fail conservative, pharmacologic, and
endoscopic therapies for ACPO. Surgery is also indicated in patients who
develop evidence of ischemia or perforation at any point in the course of
their illness.

The gastroenterologist is frequently involved in the care of patients with
bowel obstruction and pseudo-obstruction. In the case of obstruction, the
central problem is determining which patients should be managed surgically.
In both SBO and LBO, evidence of vascular compromise to the gut mandates surgical intervention. Most patients with pseudo-obstruction respond
to conservative therapy or neostigmine. Endoscopic decompression is indicated in recalcitrant cases, with surgery reserved as a last resort.
The authors thank John C. Lappas, MD, (Indiana University Medical
Center, Department of Radiology), for providing the radiographs used to
illustrate this manuscript.
[1] Bizer LS, Liebling RW, Delany HM, Gliedman ML. Small bowel obstruction: the role of
nonoperative treatment in simple intestinal obstruction and predictive criteria for
strangulation obstruction. Surgery 1981;89:40713.
[2] Greene WW. Bowel obstruction in the aged patient: a review of 300 cases. Am J Surg
[3] Nieuwenhuijzen M, Reijnen MM, Kuijpers JH, van Goor H. Small bowel obstruction
after total or subtotal colectomy: a 10-year retrospective review. Br J Surg 1998;85:
[4] Edna TH, Bjerkeset T. Small bowel obstruction in patients previously operated on for
colorectal cancer. Eur J Surg 1998;164:58792.
[5] Zbar RI, Crede WB, McKhann CF, Jekel JF. The postoperative incidence of small bowel
obstruction following standard, open appendectomy and cholecystectomy: a six-year
retrospective cohort study at Yale-New Haven Hospital. Conn Med 1993;57:1237.
[6] Al-Took S, Platt R, Tulandi T. Adhesion-related small-bowel obstruction after
gynecologic operations. Am J Obstet Gynecol 1999;180(2 pt 1):3135.
[7] Mucha P Jr. Small intestinal obstruction. Surg Clin North Am 1987;67:597620.
[8] Levitt MD. Volume and composition of human intestinal gas determined by means of an
intestinal washout technique. N Engl J Med 1971;284:13948.
[9] Deitch EA. Simple intestinal obstruction causes bacterial translocation in man. Arch Surg
[10] Shields R. The absorption and secretion of uid and electrolytes by the obstructed bowel.
Br J Surg 1965;52:7749.

C.J. Kahi, D.K. Rex / Gastroenterol Clin N Am 32 (2003) 12291247


[11] Wright HK, OBrien JJ, Tilson MD. Water absorption in experimental closed segment
obstruction of the ileum in man. Am J Surg 1971;121:969.
[12] Turnage RT, Bergen P. Intestinal obstruction and ileus. In: Feldman M, Friedman LS,
Sleisenger MH, editors. Gastrointestinal and Liver Disease, 7th edition, vol. 2.
Philadelphia: WB Saunders; 2002. p. 211328.
[13] Sarr MG, Bulkley GB, Zuidema GD. Preoperative recognition of intestinal strangulation
obstruction: prospective evaluation of diagnostic capability. Am J Surg 1983;145:17682.
[14] Megibow AJ, Balthazar EJ, Cho KC, Medwid SW, Birnbaum BA, Noz ME. Bowel
obstruction: evaluation with CT. Radiology 1991;180:3138.
[15] Balthazar EJ, George W. Holmes Lecture. CT of small-bowel obstruction. AJR Am J
Roentgenol 1994;162:25561.
[16] Dunn JT, Halls JM, Berne TV. Roentgenographic contrast studies in acute small-bowel
obstruction. Arch Surg 1984;119:13058.
[17] Daneshmand S, Hedley CG, Stain SC. The utility and reliability of computed tomography
scan in the diagnosis of small bowel obstruction. Am Surg 1999;65:9226.
[18] Peck JJ, Milleson T, Phelan J. The role of computed tomography with contrast and small
bowel follow-through in management of small bowel obstruction. Am J Surg 1999;
[19] Suri S, Gupta S, Sudhakar PJ, Venkataramu NK, Sood B, Wig JD. Comparative
evaluation of plain lms, ultrasound and CT in the diagnosis of intestinal obstruction.
Acta Radiol 1999;40:4228.
[20] Fleshner PR, Siegman MG, Slater GI, Brolin RE, Chandler JC, Aufses AH Jr. A
prospective, randomized trial of short versus long tubes in adhesive small-bowel
obstruction. Am J Surg 1995;170:36670.
[21] Brolin RE, Krasna MJ, Mast BA. Use of tubes and radiographs in the management of
small bowel obstruction. Ann Surg 1987;206:12633.
[22] Brolin RE. Long tubes vs nasogastric tubes in the treatment of intestinal obstruction.
Arch Surg 1987;122:118.
[23] Lobo DN, Jobling JC, Balfour TW. Gallstone ileus: diagnostic pitfalls and therapeutic
successes. J Clin Gastroenterol 2000;30:726.
[24] Lubbers H, Mahlke R, Lankisch PG. Gallstone ileus: endoscopic removal of a gallstone
obstructing the upper jejunum. J Intern Med 1999;246:5937.
[25] Bourke MJ, Schneider DM, Haber GB. Electrohydraulic lithotripsy of a gallstone causing
gallstone ileus. Gastrointest Endosc 1997;45:5213.
[26] Abou-Saif A, Al-Kawas FH. Complications of gallstone disease: Mirizzi syndrome,
cholecystocholedochal stula, and gallstone ileus. Am J Gastroenterol 2002;97:24954.
[27] Nagorney DM, Sarr MG, McIlrath DC. Surgical management of intussusception in the
adult. Ann Surg 1981;193:2306.
[28] Zollinger RM Jr. Primary neoplasms of the small intestine. Am J Surg 1986;151:6548.
[29] de Gregorio MA, Mainar A, Tejero E, et al. Acute colorectal obstruction: stent
placement for palliative treatmentresults of a multicenter study. Radiology 1998;209:
[30] Aquise M, Tejero E, Mainar A. A new option in the treatment of complete and acute
obstruction due to colorectal cancer. Endoscopy 1997;29:229.
[31] Mainar A, Tejero E, Maynar M, Ferral H, Castaneda-Zuniga W. Colorectal obstruction:
treatment with metallic stents. Radiology 1996;198:7614.
[32] Cwikiel W, Andren-Sandberg A. Malignant stricture with colovesical stula: stent
insertion in the colon. Radiology 1993;186:5634.
[33] Keen RR, Orsay CP. Rectosigmoid stent for obstructing colonic neoplasms. Dis Colon
Rectum 1992;35:9123.
[34] Mainar A, De Gregorio Ariza MA, Tejero E, et al. Acute colorectal obstruction:
treatment with self-expandable metallic stents before scheduled surgery: results of
a multicenter study. Radiology 1999;210:659.


C.J. Kahi, D.K. Rex / Gastroenterol Clin N Am 32 (2003) 12291247

[35] Tejero E, Mainar A, Fernandez L, Tobio R, De Gregorio MA. New procedure for the
treatment of colorectal neoplastic obstructions. Dis Colon Rectum 1994;37:11589.
[36] Ballantyne GH, Brandner MD, Beart RW Jr, Ilstrup DM. Volvulus of the colon:
incidence and mortality. Ann Surg 1985;202:8392.
[37] Rabinovici R, Simansky DA, Kaplan O, Mavor E, Manny J. Cecal volvulus. Dis Colon
Rectum 1990;33:7659.
[38] Pousada L. Cecal bascule: an overlooked diagnosis in the elderly. J Am Geriatr Soc
[39] Haskin PH, Teplick SK, Teplick JG, Haskin ME. Volvulus of the cecum and right colon.
JAMA 1981;245:24335.
[40] Friedman JD, Odland MD, Bubrick MP. Experience with colonic volvulus. Dis Colon
Rectum 1989;32:40916.
[41] Brothers TE, Strodel WE, Eckhauser FE. Endoscopy in colonic volvulus. Ann Surg
[42] Baker DM, Wardrop PJ, Burrell H, Hardcastle JD. The management of acute sigmoid
volvulus in Nottingham. J R Coll Surg Edinb 1994;39:3046.
[43] Arnold GJ, Nance FC. Volvulus of the sigmoid colon. Ann Surg 1973;177:52737.
[44] Agrez M, Cameron D. Radiology of sigmoid volvulus. Dis Colon Rectum 1981;24:
[45] Madiba TE, Thomson SR. The management of sigmoid volvulus. J R Coll Surg Edinb
[46] Anderson JR, Lee D. The management of acute sigmoid volvulus. Br J Surg 1981;68:
[47] Grossmann EM, Longo WE, Stratton MD, Virgo KS, Johnson FE. Sigmoid volvulus in
Department of Veterans Aairs Medical Centers. Dis Colon Rectum 2000;43:4148.
[48] Mangiante EC, Croce MA, Fabian TC, Moore OF III, Britt LG. Sigmoid volvulus:
a four-decade experience. Am Surg 1989;55:414.
[49] Ballantyne GH. Review of sigmoid volvulus: history and results of treatment. Dis Colon
Rectum 1982;25:494501.
[50] Ogilvie S. Large-intestine colic due to sympathetic deprivation: a new clinical syndrome.
BMJ 1948;2:6713.
[51] Nanni G, Garbini A, Luchetti P, Ronconi P, Castagneto M. Ogilvies syndrome (acute
colonic pseudo-obstruction): review of the literature (October 1948 to March 1980) and
report of four additional cases. Dis Colon Rectum 1982;25:15766.
[52] Vanek VW, Al-Salti M. Acute pseudo-obstruction of the colon (Ogilvies syndrome): an
analysis of 400 cases. Dis Colon Rectum 1986;29:20310.
[53] Addison NV. Pseudo-obstruction of the large bowel. J R Soc Med 1983;76:2525.
[54] Rex DK. Colonoscopy and acute colonic pseudo-obstruction. Gastrointest Endosc Clin
N Am 1997;7:499508.
[55] Bryk D, Soong KY. Colonic ileus and its dierential roentgen diagnosis. AJR Am J
Roentgenol 1967;101:32937.
[56] Vantrappen G. Acute colonic pseudo-obstruction. Lancet 1993;341:1523.
[57] Sloyer AF, Panella VS, Demas BE, et al. Ogilvies syndrome: successful management
without colonoscopy. Dig Dis Sci 1988;33:13916.
[58] Johnson CD, Rice RP, Kelvin FM, Foster WL, Williford ME. The radiologic
evaluation of gross cecal distension: emphasis on cecal ileus. AJR Am J Roentgenol 1985;
[59] Watson CJ, Jamieson NV, Johnston PS, et al. Early abdominal complications following
heart and heart-lung transplantation. Br J Surg 1991;78:699704.
[60] Stratta RJ, Starling JR, DAlessandro AM, et al. Acute colonic ileus (pseudo-obstruction)
in renal transplant recipients. Surgery 1988;104:61623.
[61] Moses Y, Weissberg D, Kaufman M, Weizbard E. Acute pseudo-obstruction of the colon.
S Afr J Surg 1991;29:1820.

C.J. Kahi, D.K. Rex / Gastroenterol Clin N Am 32 (2003) 12291247


[62] Koneru B, Selby R, OHair DP, Tzakis AG, Hakala TR, Starzl TE. Nonobstructing
colonic dilatation and colon perforations following renal transplantation. Arch Surg
[63] Hart MB, Rosemurgy AS. Cecal pseudo-obstruction: early therapy should be nonoperative. Am Surg 1990;56:436.
[64] Gilchrist AM, Mills JO, Russell CG. Acute large-bowel pseudo-obstruction. Clin Radiol
[65] Bullock PR, Thomas WE. Acute pseudo-obstruction of the colon. Ann R Coll Surg Engl
[66] Bachulis BL, Smith PE. Pseudo-obstruction of the colon. Am J Surg 1978;136:6672.
[67] Baker DA, Morin ME, Tan A, Sue HK. Colonic ileus. Indication for prompt
decompression. JAMA 1979;241:26334.
[68] Bonacini M, Smith OJ, Pritchard T. Erythromycin as therapy for acute colonic pseudoobstruction (Ogilvies syndrome). J Clin Gastroenterol 1991;13:4756.
[69] MacColl C, MacCannell KL, Baylis B, Lee SS. Treatment of acute colonic pseudoobstruction (Ogilvies syndrome) with cisapride. Gastroenterology 1990;98:7736.
[70] Pelckmans PA, Michielsen PP, Jorens PG, Van Maercke YM. Cisapride in Ogilvies
syndrome. Gastroenterology 1990;99:11945.
[71] Ponec RJ, Saunders MD, Kimmey MB. Neostigmine for the treatment of acute colonic
pseudo-obstruction. N Engl J Med 1999;341:13741.
[72] Stephenson BM, Morgan AR, Salaman JR, Wheeler MH. Ogilvies syndrome: a new
approach to an old problem. Dis Colon Rectum 1995;38:4247.
[73] Hutchinson R, Griths C. Acute colonic pseudo-obstruction: a pharmacological
approach. Ann R Coll Surg Engl 1992;74:3647.
[74] Loftus CG, Harewood GC, Baron TH. Assessment of predictors of response to neostigmine for acute colonic pseudo-obstruction. Am J Gastroenterol 2002;97:311822.
[75] Geelhoed GW. Colonic pseudo-obstruction in surgical patients. Am J Surg 1985;149:
[76] Kukora JS, Dent TL. Colonoscopic decompression of massive nonobstructive cecal
dilation. Arch Surg 1977;112:5127.
[77] Martin FM, Robinson AM Jr, Thompson WR. Therapeutic colonoscopy in the treatment
of colonic pseudo-obstruction. Am Surg 1988;54:51922.
[78] Nakhgevany KB. Colonoscopic decompression of the colon in patients with Ogilvies
syndrome. Am J Surg 1984;148:31720.
[79] Strodel WE, Nostrant TT, Eckhauser FE, Dent TL. Therapeutic and diagnostic
colonoscopy in nonobstructive colonic dilatation. Ann Surg 1983;197:41621.
[80] Nivatvongs S, Vermeulen FD, Fang DT. Colonoscopic decompression of acute pseudoobstruction of the colon. Ann Surg 1982;196:598600.
[81] Nano D, Prindiville T, Pauly M, Chow H, Ross K, Trudeau W. Colonoscopic therapy of
acute pseudo-obstruction of the colon. Am J Gastroenterol 1987;82:1458.
[82] Bode WE, Beart RW Jr, Spencer RJ, Culp CE, Wol BG, Taylor BM. Colonoscopic
decompression for acute pseudo-obstruction of the colon (Ogilvies syndrome): report of
22 cases and review of the literature. Am J Surg 1984;147:2435.
[83] Wegener M, Borsch G. Acute colonic pseudo-obstruction (Ogilvies syndrome):
presentation of 14 of our own cases and analysis of 1027 cases reported in the literature.
Surg Endosc 1987;1:16974.
[84] Gosche JR, Sharpe JN, Larson GM. Colonoscopic decompression for pseudo-obstruction
of the colon. Am Surg 1989;55:1115.
[85] Harig JM, Fumo DE, Loo FD, et al. Treatment of acute nontoxic megacolon during
colonoscopy: tube placement versus simple decompression. Gastrointest Endosc 1988;
[86] Starling JR. Treatment of nontoxic megacolon by colonoscopy. Surgery 1983;94:


C.J. Kahi, D.K. Rex / Gastroenterol Clin N Am 32 (2003) 12291247

[87] Jetmore AB, Timmcke AE, Gathright JB Jr, Hicks TC, Ray JE, Baker JW. Ogilvies
syndrome: colonoscopic decompression and analysis of predisposing factors. Dis Colon
Rectum 1992;35:113542.
[88] Feldman RA, Karl RC. Diagnosis and treatment of Ogilvies syndrome after lumbar
spinal surgery: report of three cases. J Neurosurg 1992;76:10126.
[89] Krige JE, Hudson DA, Kottler RE. Acute colonic pseudo-obstruction: current diagnosis
and management. S Afr Med J 1989;75:2714.
[90] Fiorito JJ, Schoen RE, Brandt LJ. Pseudo-obstruction associated with colonic ischemia:
successful management with colonoscopic decompression. Am J Gastroenterol 1991;
[91] Lee JT, Taylor BM, Singleton BC. Epidural anesthesia for acute pseudo-obstruction of
the colon (Ogilvies syndrome). Dis Colon Rectum 1988;31:68691.
[92] Ponsky JL, Aszodi A, Perse D. Percutaneous endoscopic cecostomy: a new approach to
nonobstructive colonic dilation. Gastrointest Endosc 1986;32:10811.
[93] Chevallier P, Marcy PY, Francois E, et al. Controlled transperitoneal percutaneous
cecostomy as a therapeutic alternative to the endoscopic decompression for Ogilvies
syndrome. Am J Gastroenterol 2002;97:4714.
[94] Bruno MJ, van Dorp WT, Ferwerda J, Dekker W, Schut NH. Colonic pseudoobstruction due to beta2-microglobulin amyloidosis after long-term haemodialysis. Eur J
Gastroenterol Hepatol 1998;10:71720.
[95] Cakir E, Baykal S, Usul H, Kuzeyli K, Cinel A. Ogilvies syndrome after cervical
discectomy. Clin Neurol Neurosurg 2001;103:2323.
[96] Goral V, Uyar A, Muftuoglu E. Ogilvies syndrome in patient with multiple myeloma.
Dig Liver Dis 2002;34:85.
[97] Breccia M, Girmenia C, Mecarocci S, et al. Ogilvies syndrome in acute myeloid leukemia:
pharmacological approach with neostigmine. Ann Hematol 2001;80:6146.
[98] Huber FX, Eckstein HH, Mohring K, Allenberg JR. Ogilvies syndrome following renal
transplantation. Nephrol Dial Transplant 1998;13:12857.
[99] McMahon JM, Underwood ES, Kirby WE. Colonic spasm and pseudo-obstruction in an
elongated colon secondary to physical exertion: diagnosis by stress barium enema. Am J
Gastroenterol 1999;94:33624.
[100] Petrisor BA, Petruccelli DT, Winemaker MJ, de Beer JV. Acute colonic pseudoobstruction after elective total joint arthroplasty. J Arthroplasty 2001;16:10437.
[101] Rodrigues G, Kannaiyan L, Gopasetty M, Rao S, Shenoy R. Colonic pseudo-obstruction
due to herpes zoster. Indian J Gastroenterol 2002;21:2034.
[102] Roberts CA. Ogilvies syndrome after cesarean delivery. J Obstet Gynecol Neonatal Nurs
[103] Shapiro AM, Bain VG, Preiksaitis JK, Ma MM, Issa S, Kneteman NM. Ogilvies
syndrome associated with acute cytomegaloviral infection after liver transplantation.
Transpl Int 2000;13:415.
[104] Teh SH, ORiordain DS, OConnell PR. Colonic pseudo-obstruction following acute
pancreatitis. Ir J Med Sci 1998;167:412.
[105] Golden GT CJ. Colonic ileus and perforation in patients requiring mechanical ventilation
support. Chest 1975;68:6614.
[106] Bender GN, Do-Dai DD, Briggs LM. Colonic pseudo-obstruction: decompression
with a tricomponent coaxial system under uoroscopic guidance. Radiology 1993;188:
[107] Caccese WJ, Bronzo RL, Wadler G, McKinley MJ. Ogilvies syndrome associated with
herpes zoster infection. J Clin Gastroenterol 1985;7:30913.
[108] Caraceni P, Fagiuoli S, Wright HI, Nadir A, Van Thiel DH. Gastrointestinal
complications of liver transplantation. Ital J Gastroenterol 1995;27:2939.
[109] Imai A, Mikamo H, Kawabata I, Kondoh H, Tamaya T. Acute pseudo-obstruction of the
colon (Ogilvies syndrome) during pregnancy. J Med 1990;21:3316.

C.J. Kahi, D.K. Rex / Gastroenterol Clin N Am 32 (2003) 12291247


[110] Kadesky K, Purdue GF, Hunt JL. Acute pseudo-obstruction in critically ill patients with
burns. J Burn Care Rehabil 1995;16(2 pt 1):1325.
[111] Lopez MJ, Memula N, Doss LL, Johnston WD. Pseudo-obstruction of the colon during
pelvic radiotherapy. Dis Colon Rectum 1981;24:2014.
[112] Melamed M, Rabushka SE, Melamed JL. Colon ileus associated with low spine disease.
Clin Radiol 1969;20:4751.
[113] Nomdedeu JF, Nomdedeu J, Martino R, et al. Ogilvies syndrome from disseminated
varicella-zoster infection and infarcted celiac ganglia. J Clin Gastroenterol 1995;20:1579.
[114] Ohri SK, Patel T, Desa L, Spencer J. Drug-induced colonic pseudo-obstruction: report of
a case. Dis Colon Rectum 1991;34:34751.
[115] Post AB, Falk GW, Bukowski RM. Acute colonic pseudo-obstruction associated with
interleukin-2 therapy. Am J Gastroenterol 1991;86:153941.
[116] Robbins RD, Schoen R, Sohn N, Weinstein MA. Colonic decompression of massive cecal
dilatation (Ogilvies syndrome) secondary to cesarian section. Am J Gastroenterol
[117] Roman RJ, Loeb PM. Massive colonic dilatation as initial presentation of mesenteric vein
thrombosis. Dig Dis Sci 1987;32:3236.
[118] Romeo DP, Solomon GD, Hover AR. Acute colonic pseudo-obstruction: a possible role
for the colocolonic reex. J Clin Gastroenterol 1985;7:25660.
[119] Schuer MD, Baird HW, Fleming CR, et al. Intestinal pseudo-obstruction as the
presenting manifestation of small-cell carcinoma of the lung: a paraneoplastic neuropathy
of the gastrointestinal tract. Ann Intern Med 1983;98:12934.
[120] Shaxted EJ, Jukes R. Pseudo-obstruction of the bowel in pregnancy: case reports. Br J
Obstet Gynaecol 1979;86:4113.
[121] Soreide O, Bjerkeset T, Fossdal JE. Pseudo-obstruction of the colon (Ogilvies syndrome),
a genuine clinical conditions? Review of the literature (19481975) and report of ve
cases. Dis Colon Rectum 1977;20:48791.
[122] Terhune DW, Petrochko N Jr, Jordan GH, Kovalcik PJ, Lynch DF Jr. Ogilvies syndrome
developing after ethanol ablation of renal cell carcinoma. J Urol 1985;133:8389.
[123] Wanebo H, Mathewson C, Conolly B. Pseudo-obstruction of the colon. Surg Gynecol
Obstet 1971;133:448.