Gastroenterol Clin N Am

32 (2003) 1229–1247

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 46202–5121, USA

Bowel obstruction results from mechanical interruption of the flow 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 differentiated from pseudo-
obstruction, because the two entities have completely different 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
discussed.
This article is divided into two sections: in the first, the diagnosis and
therapy of SBO and large bowel obstruction (LBO) are discussed, with
emphasis on specific 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 Ó 2003 Elsevier Inc. All rights reserved.
doi:10.1016/S0889-8553(03)00091-8
1230 C.J. Kahi, D.K. Rex / Gastroenterol Clin N Am 32 (2003) 1229–1247

SBO
Etiology
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 de-
velopment of adhesive bands, which may lead to SBO [3–5]. 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 Crohn’s disease, ischemia, radiation, intussusception, volvulus,
neoplasms, gallstones, and bezoars.

Pathophysiology
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 insufficiency, and hemodynamic instability.
Fluids and swallowed air accumulate proximal to the obstruction, predis-
posing 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 fluid moves into the intestinal lumen,
further worsening the distention [10,11]. Ultimately, this compromises blood
supply to the affected segment of intestine, first 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 flatus 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 findings on
physical examination; the presence of peritoneal signs should suggest
 C.J. Kahi, D.K. Rex / Gastroenterol Clin N Am 32 (2003) 1229–1247 1231

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].

Diagnosis
Laboratory findings in SBO are nonspecific 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
sufficient specificity to distinguish simple from strangulated obstruction [13].
Plain supine and upright abdominal radiographs should be obtained in all
patients with suspected SBO. Supine films can help estimate the degree of
distention; upright films can show multiple air-fluid 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 findings and should lead to prompt
surgical intervention [12]. Most cases of SBO can be diagnosed with the
combination of clinical features and radiographic findings. About 20%
to 30% of patients present with atypical symptoms or nondiagnostic
abdominal films [7,14–16] 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 specificity of abdominal CT in the diagnosis
of SBO are about 90% [14,17–19]. Contrast studies, such as small bowel
follow-through and enteroclysis, are very useful in differentiating 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 findings are
equivocal [18].

Management: general principles

All patients with SBO should be resuscitated with isotonic intravenous
fluids, 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 [20–22].
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
1232 C.J. Kahi, D.K. Rex / Gastroenterol Clin N Am 32 (2003) 1229–1247

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: specific 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 enter-
otomy with segmental resection if needed. Small bezoars can be removed
effectively endoscopically, especially those located proximally. Larger, more
distal concretions require surgical intervention. Gallstone ileus is a particular
example of SBO where endoscopy may be effective. 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 fistula [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 fistulectomy
are the next steps in management [26].

Intussusception
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].

LBO
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 [29–35]. 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 radio-
graphs 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 affect 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 water-
soluble 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
flexible 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 flatus. 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 firmly established (Fig. 2B). Overall, in the acute setting,
endoscopic reduction is successful in 60% to 95% of cases [43,46–49]. The
risk of recurrence is 40% to 60% [41–43,47,49], which mandates subsequent
sigmoid resection for definitive therapy. Mortality rates in the presence of
gangrene are 25% to 80% in different series [41,47,49], necessitating
expeditious evaluation and therapy of patients with colonic volvulus.

ACPO
ACPO, also synonymous with acute colonic ileus and Ogilvie’s
syndrome, was first 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-fluid 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) 1229–1247 1235

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, Ogilvie’s syndrome occurs within days, mostly in severely ill
hospitalized patients.

Etiology
A variety of conditions have been cited in association with ACPO; these
are summarized in Table 1.

Pathogenesis
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 activ-
ity, 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
[50–53] and frequently identified 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
1236 C.J. Kahi, D.K. Rex / Gastroenterol Clin N Am 32 (2003) 1229–1247

Table 1
Etiologies and associations underlying ACPO
Medications Abdominal Infectious
Narcotics Appendicitis Herpes zoster
Anticholinergics Cholecystitis Cytomegalovirus
Phenothiazines Pancreatitis
Laxative abuse Gastritis Miscellaneous
Benzodiazepines Gastrointestinal bleeding Amyloidosis
Calcium channel blockers Surgery Physical exertion
Clonidine Retroperitoneal hematoma Sepsis
Vincristine Abscess Burns
Interleukin Mesenteric thrombosis Idiopathic
Amphetamine overdose Liver failure
Cytotoxic drugs Liver transplantation
Anti-parkinsonian agents
Oncologic
Metabolic and endocrine Small cell lung cancer
Alcoholism Generalized cancer
Hypokalemia Multiple myeloma
Hyponatremia Acute myeloid leukemia
Hypocalcemia Retroperitoneal
Hypercalcemia Invasion of lumbar sympathetics
Diabetes
Hypothyroidism Orthopedic
Pelvic trauma
Cardiovascular Pelvic, hip fracture
Myocardial infarction Pelvic, hip surgery
Congestive heart failure Joint arthroplasty
Heart transplantation Disk surgery
Aortic aneurysms
Other surgeries Obstetric and gynecologic
Normal pregnancy
Pulmonary Normal delivery
Chroni obstructive pulmonary Cesarean section
disease Hysterectomy
Pneumonia Placenta previa
Mechanical ventilation Pelvic irradiation
Thoracotomy
Lung transplantation Neurologic
Dementia
Renal Multiple sclerosis
Renal failure Parkinson’s disease
Nephrolithiasis Spinal cord disease
Surgery Lumbar surgery
Ethanol ablation of renal cancer Craniotomy
Renal transplantation
Data from References [47,50–52,57,59,62,63,67,75–79,82–85,87–89,94–123].
Modified from Rex DK. Colonoscopy and acute colonic pseudo-obstruction. Gastrointest
Endosc Clin N Am 1997;7:499–508; with permission.
 C.J. Kahi, D.K. Rex / Gastroenterol Clin N Am 32 (2003) 1229–1247 1237

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 flatus 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 high-
pitched quality when the distention is significant. Abdominal tenderness is
not a prominent feature and when present with peritoneal signs, fever, or
leukocytosis, should trigger an immediate evaluation to rule out
perforation.

Diagnosis
The diagnosis of ACPO is confirmed 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 flexure, 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 cutoff 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 perfora-
tion. It is of paramount importance to exclude mechanical obstruction in
the evaluation of patients with suspected ACPO, because cutoffs (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-fluid levels are typically seen
with mechanical obstruction and are usually absent in ACPO [54]. Other
diagnostic considerations include toxic megacolon and Clostridium difficile
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 in-
flammatory bowel disease.

Management
The gastroenterologist consulted for a patient with ACPO is challenged
to decide on the appropriate management strategy. The risk of spontaneous
perforation is difficult to estimate based on clinical or radiographic grounds,
1238 C.J. Kahi, D.K. Rex / Gastroenterol Clin N Am 32 (2003) 1229–1247

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 difficult 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 first 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 identified and addressed: electrolyte ab-
normalities should be corrected and any offending 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) 1229–1247 1239

Fig. 4. ACPO management algorithm.

1240 C.J. Kahi, D.K. Rex / Gastroenterol Clin N Am 32 (2003) 1229–1247

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 flatus;
a rectal tube can be placed, although the effectiveness of this technique has
not been proved [54]. Collectively, conservative measures are effective in
33% to 100% of cases [57,59–67]. 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
perforation.

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 effective in all cases [70]. Metoclopramide primarily affects
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, placebo-
controlled 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 flatus, 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-effects were mild and self-limited and
included excessive salivation, abdominal pain, and vomiting. Neostigmine is
contraindicated in the presence of bradyarrhythmias, mechanical obstruc-
tion, colonic ischemia or perforation, and pregnancy. It should be used with
caution in patients with active bronchospasm or renal insufficiency. 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 effectiveness of neostigmine is
 C.J. Kahi, D.K. Rex / Gastroenterol Clin N Am 32 (2003) 1229–1247 1241

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 [52,59–63,65,75–91]; overall, colonoscopy is effective 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 insufflation is
used and as little as possible sedation administered. The colonoscope is
guided through the dilated sections, which should be deflated enough to
relieve tension but not to a degree that hinders further lumen visualization
and advancement. Cecal intubation in ACPO is technically difficult be-
cause of elongation of the dilated colon; prolonged attempts at cecal
intubation are inadvisable [54]. Passage of the hepatic flexure is more
likely to result in successful decompression than when it is not passed
[86,87]; the scope should be advanced beyond the hepatic flexure when
practical [54]. The visualization of mucosal ischemia during colonoscopy
does not automatically mandate proceeding to surgery, because the endo-
scopic 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; fluoroscopy 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 prox-
imal colon [81]. This method is cumbersome and carries the risk of dis-
placing 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 stiff Savary wire (or another wire that
resists coiling) is pushed through the biopsy channel and the scope
withdrawn. Next, the tip is cut off a well-lubricated 18F catheter Levin
tube and it is passed over the guidewire into the proximal colon; the
guidewire is then withdrawn under fluoroscopy and the tube connected to
gravity [54]. Over-the-wire colon decompression sets are commercially
available; all use flexible 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
alternative.
Percutaneous endoscopic cecostomy [92] and transperitoneal cutane-
ous cecostomy [93] have been used in ACPO but neither have gained wide-
spread use.
1242 C.J. Kahi, D.K. Rex / Gastroenterol Clin N Am 32 (2003) 1229–1247

Surgery
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.

Summary
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 man-
dates surgical intervention. Most patients with pseudo-obstruction respond
to conservative therapy or neostigmine. Endoscopic decompression is indi-
cated in recalcitrant cases, with surgery reserved as a last resort.

Acknowledgement
The authors thank John C. Lappas, MD, (Indiana University Medical
Center, Department of Radiology), for providing the radiographs used to
illustrate this manuscript.

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