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* Corresponding author.
E-mail address: drex@iupui.edu (D.K. Rex).
0889-8553/03/$ - see front matter 2003 Elsevier Inc. All rights reserved.
doi:10.1016/S0889-8553(03)00091-8
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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 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.
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 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
1231
1232
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 [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
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.)
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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.
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 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
1236
Table 1
Etiologies and associations underlying ACPO
Medications
Narcotics
Anticholinergics
Phenothiazines
Laxative abuse
Benzodiazepines
Calcium channel blockers
Clonidine
Vincristine
Interleukin
Amphetamine overdose
Cytotoxic drugs
Anti-parkinsonian agents
Metabolic and endocrine
Alcoholism
Hypokalemia
Hyponatremia
Hypocalcemia
Hypercalcemia
Diabetes
Hypothyroidism
Cardiovascular
Myocardial infarction
Congestive heart failure
Heart transplantation
Aortic aneurysms
Other surgeries
Pulmonary
Chroni obstructive pulmonary
disease
Pneumonia
Mechanical ventilation
Thoracotomy
Lung transplantation
Renal
Renal failure
Nephrolithiasis
Surgery
Ethanol ablation of renal cancer
Renal transplantation
Abdominal
Appendicitis
Cholecystitis
Pancreatitis
Gastritis
Gastrointestinal bleeding
Surgery
Retroperitoneal hematoma
Abscess
Mesenteric thrombosis
Liver failure
Liver transplantation
Infectious
Herpes zoster
Cytomegalovirus
Miscellaneous
Amyloidosis
Physical exertion
Sepsis
Burns
Idiopathic
Oncologic
Small cell lung cancer
Generalized cancer
Multiple myeloma
Acute myeloid leukemia
Retroperitoneal
Invasion of lumbar sympathetics
Orthopedic
Pelvic trauma
Pelvic, hip fracture
Pelvic, hip surgery
Joint arthroplasty
Disk surgery
Obstetric and gynecologic
Normal pregnancy
Normal delivery
Cesarean section
Hysterectomy
Placenta previa
Pelvic irradiation
Neurologic
Dementia
Multiple sclerosis
Parkinsons disease
Spinal cord disease
Lumbar surgery
Craniotomy
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 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
perforation.
Diagnosis
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.
Management
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,
1238
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.)
1239
1240
1241
1242
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 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.
Acknowledgement
The authors thank John C. Lappas, MD, (Indiana University Medical
Center, Department of Radiology), for providing the radiographs used to
illustrate this manuscript.
References
[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
1969;118:5415.
[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:
12425.
[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
1989;124:699701.
[10] Shields R. The absorption and secretion of uid and electrolytes by the obstructed bowel.
Br J Surg 1965;52:7749.
1243
[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;
177:3758.
[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:
11720.
[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.
1244
[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
1992;40:657.
[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
1987;206:14.
[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:
5104.
[45] Madiba TE, Thomson SR. The management of sigmoid volvulus. J R Coll Surg Edinb
2000;45:7480.
[46] Anderson JR, Lee D. The management of acute sigmoid volvulus. Br J Surg 1981;68:
11720.
[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;
145:12117.
[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.
1245
[62] Koneru B, Selby R, OHair DP, Tzakis AG, Hakala TR, Starzl TE. Nonobstructing
colonic dilatation and colon perforations following renal transplantation. Arch Surg
1990;125:6103.
[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
1985;36:4014.
[65] Bullock PR, Thomas WE. Acute pseudo-obstruction of the colon. Ann R Coll Surg Engl
1984;66:32730.
[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:
25865.
[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;
34:237.
[86] Starling JR. Treatment of nontoxic megacolon by colonoscopy. Surgery 1983;94:
67782.
1246
[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;
86:14726.
[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
2000;29:23946.
[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:
3958.
[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.
1247
[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
1982;77:2312.
[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.