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Tiêu đề Infections and Other Noninflammatory-Bowel-Disease Colitides
Trường học University of Medical Sciences
Chuyên ngành Gastroenterology
Thể loại lecture notes
Năm xuất bản 2023
Thành phố City
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Số trang 63
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Chapter 51: Radiation Proctopathy 607Results of laser treatment The largest series of 47 patients reported a decrease of daily rectal bleeding from 87% of patients to 11% P< 0.001 [8]..

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Chapter 49: Infections and Other Noninflammatory-Bowel-Disease Colitides 593

large Therapy is dependent on prevention of impaction

(Fig 49.19)

Preparation artifacts

The preparation for colonoscopy can induce mucosal

changes in the rectum which could be mistaken for IBD

They are not friable, and regress within days of the

pro-cedure (Fig 49.20)

References

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Fig 49.18 Angioectasias of radiation proctopathy over the

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Fig 49.20 Typical red-ring signs of a phospho-soda prep as

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Fig 49.19 Stercoral ulcer due to fecal impaction.

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26 DuPont HL, Formal SB, Hornick RB et al Pathogenesis of

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28 Snyder JD, Wells JG, Yashuk J, Puhr N, Blake PA Outbreak

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30 Griffin PM, Olmstead LC, Petras RE Escherichia coli O157.

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33 Ryan CA, Tauxe RV, Hosek GW et al Escherichia coli O157:

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34 Bentley G, Webster JH Gastro-intestinal tuberculosis: a

10-year review Br J Surg 1967; 54: 90–6.

35 Goldberg J Colonoscopic diagnosis of colonic tuberculosis.

Gastrointest Endosc 1984; 30: 216.

36 Gomez-Rubio M, de Cuenca B, Opio V, Ulloa J, Garcia J.

Colonic tuberculosis An unusual endoscopic diagnosis.

Endoscopy 1993; 25: 377.

37 Tabrisky J, Lindstrom RR, Peters R, Lachman RS

Tuber-culosis enteritis: review of a protean disease Am J enterol 1975; 63: 49–57.

Gastro-38 Ferentzi CV, Sieck JO, Ali MA Colonoscopic diagnosis and medical treatment of ten patients with colonic tuberculosis.

Endoscopy 1988; 20: 62–5.

39 Shah S, Thomas V, Mathan M et al Colonoscopic study

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40 Eboda MA, Akande B Massive lower gastrointestinal

hem-orrhage from abdominal tuberculosis Trop Geogr Med 1991;

43: 307–9.

41 Chutkan RK, Balba NH Infectious Diseases of the Colon In:

DiMarino AJ, Benjamin SB, eds Gastrointestinal Disease: an Endoscopic Approach, 2nd edn Thorofare, NJ: Slack, 2002:

43 Bhargava DK, Tandon HD, Chawla TC, Shriniwas Tandon

BN, Kapur BM Diagnosis of ileocecal and colonic

tubercu-losis by colonoscopy Gastrointest Endosc 1985; 31: 68–70.

44 Pettengell KE, Pirie D, Simjee AE Colonoscopic features of

early intestinal tuberculosis Report of 11 cases S Afr Med J

1991; 79: 279–80.

45 Breiter JR, Hajjar JJ Segmental tuberculosis of the colon

diagnosed by colonoscopy Am J Gastroenterol 1981; 76:

369–73.

46 Zyngier FR, Liberal MH, Dechoum A Tuberculous colitis

manifested by skip-lesions of the colon Gastrointest Endosc

1986; 32: 375.

47 Franklin GO, Mohapatra M, Perrillo RP Colonic

tubercu-losis diagnosed by colonoscopic biopsy Gastroenterology

1979; 76: 362–4.

48 Bhargava DK, Shriniwas Chawla TC, Tandon BN, Kapur

BM Intestinal tuberculosis: bacteriological study of tissue

obtained by colonoscopy and during surgery J Trop Med Hyg 1985; 88: 249–52.

49 Bartlett JG Pseudomembranous enterocolitis and biotic-associated diarrhea In: Feldman M, Friedman LS,

anti-Sleisenger MH, eds anti-Sleisenger and Fordtran’s Gastrointestinal and Liver Disease: Pathophysiology/Diagnosis/Management, 7th edn Philadelphia: WB Saunders, 2002: 1914–31.

50 Tedesco FJ, Corless JK, Brownstein RE Rectal sparing in antibiotic-associated pseudomembranous colitis: a prospect-

ive study Gastroenterology 1982; 83: 1259–60.

51 Burbige EJ, Radigan JJ Antibiotic-associated colitis with

normal-appearing rectum Dis Colon Rectum 1981; 24: 198–

53 Bartlett JG Treatment of antibiotic-associated

pseudomem-branous colitis Rev Infect Dis 1984; 6: S235–41.

54 Wenisch C, Parschalk B, Hasenhundl M, Hirschl AM, Graninger W Comparison of vancomycin, teicoplanin, metronidazole, and fusidic acid for the treatment of

Clostridium difficile-associated diarrhea Clin Infect Dis 1996;

22: 813–18.

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Chapter 49: Infections and Other Noninflammatory-Bowel-Disease Colitides 595

and comparison to collagenous colitis Dig Dis Sci 1989; 34:

71 Berman LG, Burdick D, Heitzman ER, Prior JT A critical

reappraisal of sigmoid peridiverticulitis Surg Gynecol Obstet 1968; 127: 481–91.

72 Stollman NS, Raskin JB Diverticular disease In: DiMarino

AJ, Benjamin SB, eds Gastrointestinal Disease: An Endoscopic Approach, 2nd edn Thorofare, NJ: Slack, 2002: 859–79.

73 Imperiali G, Meucci G, Alvisi C et al Segmental colitis ciated with diverticula: a prospective study Am J Gastro- enterol 2000; 95: 1014–16.

asso-74 McFarland LV, Elmer GW, Surawicz CM Breaking the cycle:

treatment strategies for 163 cases of recurrent Clostridium difficile disease Am J Gastroenterol 2002; 97: 1769–75.

75 Baert F, Schmit A, D’Haens G et al Budesonide in

colla-genous colitis: a double-blind placebo-controlled trial with

histologic follow-up Gastroenterology 2002; 122: 20–5.

76 Harig JM, Soergel KH, Komorowski RA, Wood CM Treatment of diversion colitis with short chain fatty acid

irrigation N Engl J Med 1989; 320: 23–8.

77 Gibson GR, Whitacre EB, Ricotti CA Colitis induced by

nonsteroidal anti-inflammatory drugs Arch Intern Med

1992; 152: 625–32.

78 Clarkston W, Bonacini M, Peterson I Colitis due to

Histoplasma capsulatum in the acquired immune deficiency syndrome Am J Gastroenterol 1991; 86: 913.

79 Blaser, MJ, Smith, PD, Ravdin, JI Viral infections In: Blaser

MJ, Smith PD, Ravdin JI et al., eds Infections of the GI Tract.

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81 Horsburgh CR Epidemiology of Mycobacterium avium plex disease Am J Med 1997; 102: 11–15.

com-55 Blumencranz H, Kasen L, Romeu J, Waye JD, LeLeiko NS.

The role of endoscopy in suspected amebiasis Am J

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56 Luterman L, Alsumait AR, Daly DS, Goresky CA

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1985; 31: 204–6.

57 Nebel OT, el-Masry NA, Castell DO, Farid Z, Fornes MF,

Sparks HA Schistosomal colonic polyposis: endoscopic and

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65 Levine JS, Smith PD, Brugge WR Chronic proctitis in male

homosexuals due to lymphogranuloma venereum

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66 Giardiello FM, Hansen FC III, Lazenby AJ et al Collagenous

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(microscopic) colitis: clinicopathologic study of 18 patients

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Introduction

Sir William Heneage Ogilvie first described acute colonic

pseudo-obstruction (ACPO) in 1948 in two patients with

far-advanced intraabdominal malignancies [1] He was

the first to postulate an underlying imbalance between

the sympathetic and parasympathic innervation of the

colon as the cause of this disorder Ogilvie’s patients,

however, developed subacute symptoms over the course

of 2 months and thus represent an atypical

presenta-tion of what we now recognize as ACPO The hallmark

features of ACPO consist of acute colonic dilation in

the absence of a mechanical etiology This condition is

increasingly recognized and is associated with

substan-tial morbidity and mortality

Epidemiology and predisposing factors

The exact incidence of ACPO in hospitalized patients

is unknown Vanek and Al-Salti [2] analyzed 400 cases

of ACPO and found that it occurred most commonly

in the sixth decade and was more common in men

than women More than 90% of patients had

signific-ant comorbid disease, thought to be contributing to the

syndrome About 50% of cases occurred in the

post-operative state The diverse underlying medical and

surgical problems associated with ACPO are listed in

Table 50.1

Pathophysiology

The pathophysiology of ACPO is still not entirely

under-stood but there is evidence of an imbalance between the

sympathetic and parasympathic nervous system, which

leads to a functional obstruction caused by atony of the

distal colon followed by progressive dilation of the

cecum and ascending colon [1,3]

Ogilvie favored the sympathetic deprivation theory,

leading to unopposed parasympathic stimulation and

thereby resulting in “excessive and probably

incoor-dinated contraction” of the distal colon [1] mimicking

obstruction More recent theories postulate either an

impairment of the sacral parasympathetic outflow [3–5]

or excessive sympathetic stimulation [6,7] The clinical

presentation of ACPO resembles Hirschsprung’s disease,supporting the hypothesis of impaired parasympatheticfunction [5], which is also supported by the commonlyobserved transition point at the level of the splenicflexure The parasympathetic innervation of the colondistal to the splenic flexure is via the pelvic splanchnicnerves whereas the more proximal colon is innervated

by the vagus (Fig 50.1)

The proponents of the sympathetic stimulation theory[6,7] argue that right-sided colonic motility is impaired

Chapter 50 Acute Colonic Pseudo-obstruction

Hubert Nietsch and Michael B Kimmey

Table 50.1 Causes of acute colonic pseudo-obstruction

[2,11,17,18,33,45–50].

Neurologic

Parkinson’s disease Alzheimer’s disease Cerebrovascular accident Multiple sclerosis Spinal cord disease Craniotomy

Cardiovascular

Myocardial infarction Congestive heart failure Post cardiac arrest

Respiratory

Pneumonia Mechanical ventilation Acute respiratory distress syndrome

Metabolic

Hyponatremia Hypocalcemia Hypomagnesemia Liver failure Renal failure Hypothyroidism

Infective/inflammatory

Acute cholecystitis Pelvic abscess Spontaneous bacterial peritonitis Acute pancreatitis

Sepsis Herpes zoster Appendicitis

Neoplasia

Retroperitoneal Metastatic cancer

Post surgical

Cardiac surgery Cesarian section Gynecologic surgery Pelvic surgery Organ transplantation Orthopedic surgery

Post traumatic

Pelvic trauma Spinal cord injury Femoral fracture

Drugs

Narcotics Tricyclic antidepressants Phenothiazines Antiparkinson agents Calcium channel blockers Benzodiazepines Clonidine Vincristine

Edited by Jerome D Waye, Douglas K Rex, Christopher B Williams

Copyright © 2003 Blackwell Publishing Ltd

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Chapter 50: Acute Colonic Pseudo-obstruction 597

by excessive sympathetic inhibition This theory is

sup-ported by animal experiments performed in the 1920s

and 1930s [8] showing increased colonic peristalsis after

spinal anesthesia, which leads to a temporary paralysis

of sympathetic input This was the rationale for the

induction of spinal anesthesia as a successful treatment

of adynamic ileus in Europe in the 1920s

Clinical presentation

ACPO is usually seen in middle-aged to elderly critically

ill patients in the intensive care unit or postoperatively

and is exacerbated by immobility and narcotic pain

medications Symptoms usually develop gradually over

3–7 days Significant abdominal distension is seen in

all patients, associated with pain (83%), vomiting (57%),

constipation (51%), and fever (37%) The bowel sounds

are variable and can be normal or hyperactive (40%),

hypoactive (31%), high-pitched (17%), or absent (12%)

[2] If peritoneal signs are present, transmural ischemia

or perforation should be suspected

Diagnosis

Abdominal examination shows significant distension

in all patients, with variable degrees of tenderness Thepresence or quality of bowel sounds is also variable.Peritoneal signs are suggestive of transmural ischemia

or perforation and mandate surgical consultation.The diagnosis is confirmed by plain abdominal radio-graphs, which typically show significant distension ofthe colon with predominance of the right side in theabsence of mechanical obstruction (Fig 50.2) A cut-offsign at the splenic flexure is frequently observed [5].Initial studies suggested that a cecal diameter ofgreater than 12 cm increases the risk of perforation sub-stantially [9] The case series by Vanek and Al-Salti [2] reported no cecal perforation with a cecal diameter

< 12 cm, 7% perforation risk with cecal diameters of12–14 cm, and 23% perforation risk with a cecal dia-meter> 14 cm However, more recent reports suggestthat the duration of significant cecal dilation is more

predictive of ischemia than the cecal diameter per se

Inferior mesenteric ganglion

Pudendal nerves

S2 3 4

Fig 50.1 Schematic diagram illustrating colonic innervation.

Parasympathetic pathways (stimulatory/prokinetic):

prevertebral ganglia and sacral nerves (red) and vagus

(yellow) Sympathetic pathways (inhibitory): thoracic spinal

cord to inferior mesenteric plexus and pelvic plexus (green).

Fig 50.2 Abdominal radiograph of patient with acute colonic

pseudo-obstruction following internal fixation of a fractured femur.

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complicate surgery if perforation is present and

endo-scopic decompression if this is required

Complications

The dreaded complication of progressive colonic

dilation is transmural ischemia followed by perforation

However, the frequency of this complication, which

requires emergency colonic resection, has significantly

decreased in recent case series The risk of perforation

was initially reported to be as high as 13% with a

mortal-ity of 43% [11] A summary of more recent studies shows

a perforation risk of 3% [12] The surgical mortality may

be as high as 40–50%, if perforation occurs [13]

Management

Supportive medical care

Initial management for the first 24–48 h is conservative,

with close attention to correcting any fluid and

elec-trolyte imbalances that may be present The

medica-tion list should be carefully scrutinized and drugs that

might delay intestinal transit, such as anticholinergics

or opiates, should be discontinued if possible [14] The

abdominal examination needs to be followed carefully

and daily abdominal radiographs obtained to monitor

for progressive dilation and evidence of perforation The

introduction of a nasogastric tube for decompression is

advisable for most patients, and in selected cases a rectal

tube might also be of help Mobilization of the patient

with frequent turning might facilitate the passage of

flatus Success rates of supportive management are

vari-able but can be as high as 96%, as reported in a cohort

of cancer patients from Sloan-Kettering Cancer Center

[15]

Pharmacotherapy

When colonic dilation persists or progresses despite servative therapy, specific pharmacotherapy to stimul-ate the parasympathic innervation of the colon should beattempted (Table 50.2) Catchpole [16] first proposed thecombined use of a sympathetic blocker (guanethidine)followed by a cholinesterase inhibitor (neostigmine) tocorrect the sympathetic/parasympathic imbalance Sub-sequent small case series suggested that a majority ofpatients with ACPO could be effectively treated usingneostigmine [17–19]

con-A double-blind, randomized, placebo-controlled ical trial reported by Ponec and colleagues [20] con-clusively showed a dramatic improvement of clinicalstatus and colonic distension in the majority of patientstreated with intravenous neostigmine, making endo-scopic intervention unnecessary in most cases In thisstudy, patients were treated with 2 mg of neostigmineadministered over a few minutes by slow intravenouspush Patients were monitored continuously by electro-cardiography with atropine available at the bedside, assymptomatic bradycardia is the most significant adverseeffect of this treatment Of 11 patients who receivedneostigmine, 10 (91%) had prompt colonic decompres-sion with a median time to response of only 4 min,whereas none of the patients receiving placebo (saline)had a clinical response Seven patients in the placebogroup and the one patient in the neostigmine group whofailed initial response received open-label neostigmine

clin-3 h after the initial infusion, with prompt colonic compression noted in all patients Only two patientsdeveloped recurrent symptoms requiring colonoscopicdecompression [20]

de-Several studies have since confirmed the safety

of neostigmine for the treatment of ACPO, reporting

Number of Initial decompression Recurrence

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Chapter 50: Acute Colonic Pseudo-obstruction 599successful colonic decompression in 79–93% of cases.

Several different neostigmine infusion protocols have

been used, including 2-mg and 2.5-mg intravenous

boluses and 2.5 mg administered over 60 min [21–24], all

with similar success rates

Recurrence of colonic distension following successful

decompression using neostigmine occurs in up to 16% of

patients In these situations, neostigmine can be safely

readministered, leading to colonic decompression in

approximately two-thirds of cases [21,23]

The observed adverse effects of neostigmine, like

other cholinesterase inhibitors, include excessive

saliva-tion (38%), vomiting (9%), abdominal pain (62%),

brady-cardia (9%), and bronchospasm Patients must therefore

be closely monitored during drug administration with

continuous electrocardiography and atropine available

at the bedside [20] Symptomatic bradycardia responds

to administration of atropine, but this also leads to a

re-versal of any benefit of neostigmine in relieving colonic

dilation The coadministration of glycopyrrolate, an

antimuscarinic anticholinergic agent, seems to decrease

the incidence of bradycardia without reducing

neostig-mine’s efficacy [25,26]

Suitable candidates for neostigmine administration

are hence patients with ACPO who have no evidence

of mechanical bowel obstruction, a resting heart rate

greater than 60 beats per minute with a systolic blood

pressure greater than 90 mmHg, and no active

bron-chospasm [14,20] Neostigmine is contraindicated in

patients on β-blockers and those who have significant

acidosis or recent myocardial ischemia, because of the

risk of inducing cardiac arrhythmias [18]

Anecdotal case reports with other prokinetic agents

show variable success rates in the treatment of ACPO

Intravenous erythromycin, which acts as a motilin

re-ceptor agonist, showed some success in a total of five

reported cases [27–29] The efficacy of intravenous

cisap-ride, no longer available in the USA, was highly variable

in case reports of five patients [7,30,31]

The new 5-hydroxytryptamine 5-HT4receptor ists (tegaserod, prucalopride) might be theoretically useful for stimulating colonic motility in the setting ofACPO, but no data are yet available with the use of thesemedications in ACPO [14]

agon-Colonoscopic decompression

Pharmacologic treatment of ACPO has markedly duced the need for urgent colonoscopic decompression.While previously considered to be the treatment ofchoice for progressive colonic dilation, it is now usuallyreserved for patients who have failed treatment withneostigmine (Fig 50.3) No randomized comparativestudies of colonoscopic decompression with neostigmine

re-or other treatment modalities are available A mary of 11 retrospective studies involving 264 patientsshows a high initial success rate for colonoscopic decom-pression (64–100%), with an average recurrence rate of23% (range 13–65%) (Table 50.3) Complications werereported in 3% [32,33] The largest single-center seriesfrom the Mayo Clinic shows a similar experience in 50patients, with an overall success rate of 88% complicated

sum-Conservative measures (NG, rectal tube, stop narcotics, mobilize patient)

Success Stop

Fail Bradycardia, active bronchospasm, renal failure?

Yes

No

Colonoscopic decompression

Fail

Neostigmine 2.0 mg IV

Fig 50.3 Algorithm for management of acute colonic

pseudo-obstruction.

Table 50.3 Reports of colonoscopic

decompression of acute colonic

pseudo-obstruction.

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by one procedure-related perforation The overall

hos-pital mortality is 30% [34]

Colonoscopic decompression is technically more

chal-lenging compared with routine colonoscopy since the

colon is unprepared and the patients are often critically

ill, necessitating performance of the procedure in an

intensive care unit Enemas are not very helpful in

pre-paration for colonoscopy and should be done gently, if

at all, due to the risk of perforation Liquid stool must

be suctioned and irrigated at the time of colonoscopy in

most cases Air insufflation should be kept to a minimum

to prevent further cecal dilation, which could potentially

precipitate perforation It is important to reach the hepatic

flexure in order to achieve significant decompression,

although cecal intubation is not required [35] Jetmore

and colleagues [33] reported that colonic decompression

was almost twice as successful if the ascending colon

was reached (initial success 71% vs 37%) If mucosal

changes suggestive of acute ischemia are encountered,

the procedure should be terminated and the patient

referred for emergency colectomy The overall decrease

in cecal diameter following colonoscopic decompression

is generally quite modest, with an average reduction ofonly 2 cm [36]

Up to 40% of patients develop recurrence of colonicdistension after initial successful colonoscopic decom-pression This led to the introduction of decompressiontubes, which are inserted at the time of the initial proced-ure Harig and colleagues [37] performed a randomizedtrial in 20 patients comparing endoscopic decompres-sion alone vs additional insertion of a modified enter-oclysis catheter and demonstrated a reduction in therecurrence of colonic dilation from 44% to 0% Decom-pression tubes remained in place for an average of 3–4days without any reported complications

The two most commonly used decompression tubesare a modified enteroclysis catheter, with additional side holes at the tip or a 14F colon decompression kit(Wilson-Cook Medical, Winston-Salem, NC) A flexibleguidewire is placed through the endoscope channel andthe tip is directed into the cecum under fluoroscopy Theendoscope is then slowly withdrawn leaving the wire inplace Fluoroscopy is helpful in keeping the wire straightduring complete withdrawal of the colonoscope Thedecompression tube is then advanced under fluoro-scopic guidance, using traction on the wire to keep itstraight while the tube is advanced The decompressiontube is than taped to the patient’s buttock and connected

to low intermittent suction It is advisable to flush thetube with water every 4 h to prevent clogging with stool

Fig 50.4 (a) Abdominal radiograph of patient with acute

colonic pseudo-obstruction following bone marrow

transplantation for leukemia (b) Abdominal radiograph of

same patient immediately following colonoscopy at which

time a 14F decompression tube was placed.

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Chapter 50: Acute Colonic Pseudo-obstruction 601The patient’s clinical status should be followed care-

fully with daily abdominal radiographs (Fig 50.4) The

catheters are usually left in situ for 2–4 days, until colon

decompression is complete and underlying reversible

contributors to ACPO are reversed Use of larger tubes

up to 40F in diameter (Levacuator, Mallinckrodt Medical,

St Louis, MO) has been described in case reports, with

more rapid decompression and less tube clogging [38] A

minority of patients may not respond to these measures

and if there is suspicion of acute ischemia or perforation

the patient should be referred for immediate surgery

Percutaneous cecostomy

In the absence of ischemia or perforation, percutaneous

cecostomy (PCC) should be considered as a minimally

invasive alternative to surgery in those critically ill

patients where induction of general anesthesia poses a

significant risk Both transperitoneal and retroperitoneal

approaches for PCC have been described [39–41] The

early work by VanSonnenberg and colleagues [42]

showed the technical feasibility and safety of PCC tubes

The theoretically safer retroperitoneal approach did not

lead to a lower risk of peritonitis than the anterior

trans-peritoneal approach [42] The technique was recently

refined by using additional T-fasteners, which allow for

better colonic apposition to the abdominal wall, thereby

potentially reducing the risk of fecal soilage of the

abdominal cavity [43] No studies comparing the efficacy

and safety of pharmacotherapy, endoscopic intervention,

radiographically guided PCC, and surgery are available

Surgery

Peritoneal signs or free air on abdominal radiography

are clear indications for laparotomy and colectomy [2]

The definitive surgical management depends on the

viability of the cecum and ascending colon at the time

of exploration Partial colectomy is indicated for

trans-mural ischemia and perforation but carries a high

mortality in these critically ill patients Surgical

decom-pression in the absence of perforation, through an open

or laparoscopic cecostomy, is an alternative to colectomy

if the local expertise is not available to perform

com-puted tomography-guided PCC [44]

Prognosis

The overall mortality of ACPO remains approximately

30%, despite the recent advances in its management

[2,34] This reflects the severity of the underlying disease

process leading to ACPO and is not directly related to

the colonic complications The impact of pharmacologic

therapy on the outcome of patients with ACPO has not

yet been fully assessed

References

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depriva-tion: a new clinical syndrome Br Med J 1948; 2: 671–3.

2 Vanek VW, Al-Salti M Acute pseudo-obstruction of the

colon (Ogilvie syndrome): an analysis of 400 cases Dis Colon Rectum 1986; 29: 203–10.

3 Spira I, Rodrigues R, Wolff W Pseudo-obstruction of the

colon Am J Gastroenterol 1976; 65: 397–408.

4 Bachulis BL, Smith PE Pseudo-obstruction of the colon Am

J Surg 1978; 136: 66–72.

5 Nivatvongs S, Vermeulen F, Fang D Colonoscopic

decom-pression of acute pseudo-obstruction of the colon Am J Surg

1982; 196: 598–600.

6 Lee JT, Taylor BM, Singleton BC Epidural anesthesia for acute pseudo-obstruction of the colon (Ogilvie’s syndrome).

Dis Colon Rectum 1988; 31: 686–91.

7 MacColl C, MacCannell KL, Baylis B, Lee SS Treatment of acute colonic pseudo-obstruction (Ogilvie’s syndrome)

with cisapride Gastroenterology 1990; 98: 773–6.

8 Burstein CL Effect of spinal anesthesia on intestinal

activ-ity Proc Soc Exp Biol Med 1939; 42: 291–3.

9 Gierson ED, Storm FK, Shaw W, Coyne SK Caecal rupture

due to colonic ileus Br J Surg 1975; 62: 393–6.

10 Johnson CD, Rice RP, Kelvin FM et al The radiologic ation of gross cecal distension: emphasis on cecal ileus AJR

evalu-Am J Roentgenol 1985; 145: 1211–17.

11 Soreide O, Bjerkeset T, Fossdol J Pseudo-obstruction of the colon (Ogilvie syndrome): a genuine clinical condition? Review of the literature (1948–75) and a report of 5 cases.

Dis Colon Rectum 1977; 20: 487–91.

12 Rex DK Colonoscopy and acute colonic

pseudo-obstruc-tion Gastrointest Endosc Clin North Am 1997; 7: 499–508.

13 Wojtalik RS, Lindenauer SM, Kahn SS Perforation of the

colon associated with adynamic ileus Am J Surg 1973; 125:

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14 De Giorgio R, Barbara G, Stanghellin V et al Review article:

the pharmacologic treatment of acute colonic

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15 Sloyer AF, Panella VS, Demas BE et al Ogilvie’s syndrome: successful management without colonoscopy Dig Dis Sci

1988; 33: 1391–6.

16 Catchpole BN Ileus: use of sympathetic blocking agents in

its treatment Surgery 1969; 66: 811–20.

17 Hutchinson R, Griffiths C Acute colonic

pseudo-obstruc-tion: a pharmacologic approach Ann R Coll Surg Engl 1992;

74: 364–7.

18 Stephenson BM, Morgan AR, Salaman JR, Wheeler MH.

Ogilvie’s syndrome: a new approach to an old problem Dis Colon Rectum 1995; 38: 424–7.

19 Turegano-Fuentes F, Munoz-Jimenez F, Del Valle-Hernandez

E et al Early resolution of Ogilvie’s syndrome with venous neostigmine Dis Colon Rectum 1997; 40: 1353–7.

intra-20 Ponec RJ, Saunders MD, Kimmey MB Neostigmine for the

treatment of acute colonic pseudo-obstruction N Engl J Med

1999; 341: 137–41.

21 Paran H, Silverberg D, Mayo A, Shwartz I, Neufeld D, Freund U Treatment of acute colonic pseudo-obstruction

with neostigmine J Am Coll Surg 2000; 190: 315–18.

22 Trevisani GT, Hyman NH, Church JM Neostigmine: safe and effective treatment for acute colonic pseudo-obstruction.

Dis Colon Rectum 2000; 43: 599–603.

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39 Crass JE, Simmons RL, Mathis PF, Charles WM cutaneous decompression of the colon using CT guidance in

Per-Ogilvie syndrome AJR Am J Roentgenol 1985; 144: 475–6.

40 Casola G, Withers C, vanSonnenberg E, Herba MJ, Saba RM, Brown RA Percutaneous cecostomy for decompression of

the massively distended cecum Radiology 1986; 158: 793–4.

41 Haaga JR, Bick JR, Zollinger RM CT-guided percutaneous

catheter cecostomy Gastrointest Radiol 1987; 12: 166–8.

42 VanSonnenberg E, Varney RR, Casola G et al Percutaneous

cecostomy for Ogilvie syndrome: laboratory observations

and clinical experience Radiology 1990; 175: 679–82.

43 Chevallier P, Marcy PY, Francois E et al Controlled

transperitoneal percutaneous cecostomy as a therapeutic alternative to endoscopic decompression of Ogilvie’s syn-

drome Am J Gastroenterol 2002; 97: 471–4.

44 Groff W Colonoscopic decompression and intubation of

the cecum for Ogilvie’s syndrome Dis Colon Rectum 1983;

48 Romeo DP, Solomon GD, Hover AR Acute colonic

pseudo-obstruction: a possible role for colocolonic reflex J Clin Gastroenterol 1985; 7: 256–60.

49 Wanebo H, Mathewson C, Conolly B Pseudo-obstruction of

the colon Surg Gynecol Obstet 1971; 133: 44–8.

50 Wegener M, Boersch G Acute colonic pseudo-obstruction (Ogilvie’s syndrome): presentation of 14 of our own cases

and analysis of 1027 cases reported in the literature Surg Endosc 1987; 1: 169–74.

51 Kukora JS, Dent TL Colonoscopic decompression of massive

non-obstructive cecal dilation Arch Surg 1977; 112: 512–17.

52 Starling JR Treatment of nontoxic megacolon by

colono-scopy Surgery 1983; 94: 243–5.

53 Nakhgevany KB Colonoscopic decompression of the colon

in patients with Ogilvie’s syndrome Am J Surg 1984; 148:

22 cases and review of the literature Am J Surg 1984; 147:

243–5.

23 Abeyta BJ, Albrecht RM, Schermer CR Retrospective study

of neostigmine for the treatment of acute colonic

pseudo-obstruction Am Surg 2001; 67: 265–8.

24 Van der Spoel JI, Oudemans-van Straaten HM, Stoutenbeck

CP, Bosman RJ, Zandstra DF Neostigmine resolves

crit-ical illness-related colonic ileus in intensive care patients

with multiple organ failure: a prospective, double-blind,

placebo-controlled trial Intensive Care Med 2001; 27: 822–7.

25 Ostheimer GW A comparison of glycopyrrolate and

atrop-ine during reversal of nondepolarizing neuromuscular

block with neostigmine Anesth Analg 1977; 56: 182–6.

26 Mirakur RK, Briggs LP, Clarke RS, Dundee JW, Johnston

HM Comparison of atropine and glycopyrrolate in a

mix-ture with pyridostigmine for the antagonism of

neuromus-cular block Br J Anaesth 1981; 53: 1315–20.

27 Armstrong DN, Ballantyne GH, Modlin IM Erythromycin

for reflex ileus in Ogilvie’s syndrome (letter) Lancet 1991;

337: 378.

28 Bonacini M, Smith OJ, Pritchard T Erythromycin as therapy

for acute colonic pseudo-obstruction (Ogilvie’s syndrome).

J Clin Gastroenterol 1991; 13: 475–6.

29 Rovira A, Lopez A, Cambray C, Gimeno C Acute colonic

pseudo-obstruction (Ogilvie’s syndrome) treated with

ery-thromycin Intensive Care Med 1997; 23: 798.

30 Pelkmans PA, Michielsen PP, Jorens PG, Van Maercke YM.

Cisapride in Ogilvie’s syndrome Gastroenterology 1990; 99:

1194–5.

31 Mazloum BW, Barnes JB, Lee M Cisapride as a successful

treatment for acute intestinal pseudo-obstruction South

Med J 1996; 89: 828–30.

32 Gosche JR, Sharpe JN, Larson GM Colonic decompression

for pseudo-obstruction of the colon Am Surg 1989; 55:

111–15.

33 Jetmore AB, Timmcke AE, Gathright JB Jr, Hicks TC, Ray JE,

Baker JW Ogilvie’s syndrome: colonoscopic

decompres-sion and analysis of predisposing factors Dis Colon Rectum

1992; 35: 1135–42.

34 Geller A, Petersen BT, Gostout CJ Endoscopic

decompres-sion for acute colonic pseudo-obstruction Gastrointest

Endosc 1996; 44: 144–50.

35 Strodel WE, Nostrant TT, Eckhauser FE, Dent TL.

Therapeutic and diagnostic colonoscopy in nonobstructive

colonic dilation Ann Surg 1983; 197: 416–21.

36 Pham TN, Cosman BC, Chu P, Savides TJ Radiographic

changes after colonoscopic decompression for acute

pseudo-obstruction Dis Colon Rectum 1999; 42: 1586–91.

37 Harig JM, Fumo DE, Loo FD et al Treatment of acute

non-toxic megacolon during colonoscopy: tube placement versus

simple decompression Gastrointest Endosc 1988; 34: 23–7.

38 Yarze JC, Winchell EC A novel device for colonic tube

decompression Am J Gastroenterol 2000; 95: 2136.

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Introduction

Radiation proctopathy can be a disabling delayed

out-come of radiation therapy directed at pelvic

malig-nancies Rectal outlet bleeding can be severe enough to

result in anemia and transfusion dependency Bleeding

typically develops from 6 months to 1 year after

com-pletion of radiation therapy and is due to friable mucosal

angiectasias Although many approaches to controlling

bleeding from chronic radiation proctopathy have been

attempted, ranging from topical enema formulations

to surgical diversion of the rectum, endoscopic

coagula-tion therapy is effective and the easiest to use successful

therapy This chapter discusses the issues surrounding

the development of chronic bleeding due to radiation

proctopathy and focuses on endoscopic methods of

treatment

Radiation proctopathy (a better term than “radiation

proctitis”) is a frustrating problem for patients and

man-aging physicians Radiation therapy (external beam and

intracavitary) is a common modality of treatment for

pelvic malignancies, especially with supervoltage

tech-niques and computerization for modeling dosimetry

Malignancies of the uterus, prostate, cervix, bladder, and

rectum as well as lymphomas are treated with pelvic

radiation The rapidly dividing mucosa of the

gastroin-testinal tract is vulnerable to radiation, with the entire

colon, rectum, and pelvic small bowel susceptible to

injury Although the rectal mucosa is more resistant to

the damaging effects of radiation compared with the rest

of the colon and small bowel, because of its proximity to

the uterine cervix and prostate, the rectum is the most

common gastrointestinal organ to be affected by pelvic

radiation (> 90%) [1] In addition to the close anatomic

relation of the rectum to the pelvic organs, the rectum is

in a fixed position within the pelvic field of radiation

Fixed organs are generally more likely to be damaged

by radiation compared with mobile organs such as the

small bowel, where peristalsis causes different portions

of the intestine to move in and out of the field of

radiation

Acute radiation injury is common and typically occurs

during radiation [2] The findings within the rectum are

consistent, with a proctitis with mucosal edema,

ulcera-tion, erythema, and spontaneous bleeding Histologicfindings include mucosal cell loss, acute inflammation,eosinophilic crypt abscesses, and endothelial swelling ofarterioles Most patients recover but some progress to achronic stage Radiation proctopathy is diagnosed whenthere are rectal mucosal changes and clinical symptomsthat develop 3–6 months after completion of therapy[3,4] The frequency of this late complication varies from

5 to 20% in different series [4,5]

The clinical features of radiation proctopathy includediarrhea, tenesmus, rectal pain, rectal bleeding (lowgrade or severe), stricture, and fistulae into adjacentorgans [6] Rectal bleeding can be daily or episodic, withmultiple passages of blood and clot Incontinence ofblood is a common complaint

The endoscopic findings of radiation proctopathyinclude mucosal pallor, friability, spontaneous oozing,angiectasia, and rarely ulceration (Fig 51.1) [7] The angiectasias are the hallmark findings distinctive for thisdisorder These endoscopic features begin at the dentateline and typically occupy the distal rectum (Fig 51.2)

An occasional patient may have sigmoid involvement,typically women whose radiation has been directedhigher in the pelvis, which has implications regard-ing treatment strategy and outcomes (Fig 51.3) [8] Thehistology of this late sequela includes fibrosis within the lamina propria and endarteritis of the arterioles[2]

Treatment approaches for radiation proctopathy

Rectal bleeding is the most vexing problem for whichendoscopic treatment is sought A variety of treatmentregimens have been attempted without objective data

to support efficacy Steroids (oral and by retention enema), sulfasalazine, 5-aminosalicylic acid preparations (oral and enema), sucralfate enemas, sodium pentosan-polysulfate PPS (synthetic sulfated polysaccharides),hyperbaric oxygen, short-chain fatty acids, nutritionaltherapy, and even angiographic embolization (despitethe ischemic origins postulated and even observed) are among the various treatments attempted for radi-ation proctopathy [3,9–13] Sucralfate enemas have been

Chapter 51 Radiation Proctopathy

Christopher J Gostout

Colonoscopy Principles and Practice

Edited by Jerome D Waye, Douglas K Rex, Christopher B Williams

Copyright © 2003 Blackwell Publishing Ltd

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lation or panmucosal injury (e.g topical formalin) Bothgeneral methods are intended to eventually inducescarification of the mucosa to prohibit the reformation

of angiectasias The Nd:YAG and argon laser have beenthe most commonly used early reported methods fol-lowed by bipolar electrocoagulation and argon plasmacoagulation [8,17–29] Dilute formalin can be instilledinto the rectum via an enema or directly applied dur-ing proctoscopy or flexible sigmoidoscopy [30–36] On follow-up after endoscopic therapy, the number of angi-

Fig 51.1 Angiectasias of radiation proctopathy can vary in

presentation within the distal rectum: (a) dense vascular

lesions with coalescence; (b) scattered infrequent lesions.

Fig 51.2 Angiectasias typically extend down to the dentate

line and can be approached from (a) retroflexed or (b,c) straight viewing positions.

shown to offer benefit in a small randomized and short

follow-up trial compared with oral sulfasalazine and

steroid enemas [9]

Surgery is reserved for intractable cases as a last resort

and also for obstruction, perforations, and fistulae [6]

Surgical treatment is approached individually and has

consisted of diverting colostomy and resection with

potential coloanal pull-through anastomosis [14] The

morbidity of surgery is significant and complications as

high as 79% have been reported [15]

Endoscopic therapy has become the favored

inter-vention for control of bleeding Laser phototherapy was

first described by Leuchter and colleagues in 1982 [16]

and since then confirmed by different experiences to be

a useful method to treat the friable angiectasias The

rationale of endoscopic therapy has been to eradicate

the many angiectatic lesions using either direct

coagu-(a)

(b)

(c) (b)

(a)

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Chapter 51: Radiation Proctopathy 605

ectatic lesions are noticeably diminished or completely

eradicated and mucosal friability may also disappear

Criteria for selection of ideal patients for

endos-copic coagulation have been described and are shown

in Table 51.1 Assessment of the efficacy of endoscopic

therapy can be based on the criteria listed in Table 51.2

However, “patient satisfaction” has not been directly

assessed by quality-of-life measures

Endoscopic therapy

Endoscopic therapy can be carried out in the outpatient

setting It is important to perform an initial complete

colonoscopy to assess the extent of involvement (rectumand/or sigmoid) and to seek other causes of bleeding Aformal bowel preparation is needed when electrocoagu-lation (bipolar or argon plasma coagulation) is to be used

in order to eliminate the risk of gaseous explosion

In the patient with bleeding from radiation pathy, the angiectasias within the distal rectum areextremely friable, with bleeding induced by the slightestcontact of any instrument or device This degree of friability generated the interest in noncontact therapywith laser photocoagulation as an alternative to the traditional thermal contact methods of endoscopic treat-ment Because of its portability, safety, and excellentresults, the argon plasma coagulator has become analternative noncontact method to the laser

procto-There are three critical aspects of endoscopic therapythat are applicable to all the treatment methods and worthy of emphasis prior to the discussion of each treat-ment approach Consideration of these key points willimprove the outcome of the experience for both theendoscopist and the patient

1 Endoscope selection has not been formally studied The

use of a gastroscope has intuitive advantages, chiefly the small caliber of the insertion tube This minimizesunwanted contact-induced bleeding due to straight andretroflexed tip positions, permitting greater atraumaticmaneuverability within the rectum The narrow radius

of the retroflexed tip also enhances access to the lesions

at and immediately above the dentate line

2 During thermal therapy, use the least amount of ing energy (Fig 51.4) This will avoid creating deep,

coagulat-slowly resolving, and invariably problematic thermalulcers (Fig 51.5) Such ulceration can cause bleeding thatmay exceed the bleeding experienced prior to endo-scopic therapy Bleeding is from the margins of theseulcers and is not amenable to any endoscopic interven-tion The ulcers are usually associated with troublesomerectal and perineal pain There is no treatment for thesymptomatic thermal ulcer other than time to allowhealing Overtreatment should be avoided when coagu-lated areas bleed lest deep thermal injury result Oftenbleeding will stop by washing and waiting for reactiveedema to appear Nothing further should be done if thetreated site appears to be adequately coagulated with

a uniform white coagulum Minimization of excessivethermal energy will eliminate the development of stric-tures as well

3 The goal is to treat all the angiectasias in each session.

Changing the patient’s position from the more mon left lateral decubitus may allow access to lesionsobscured by pooled materials Cleansing accumulatingblood and clot continuously will avoid obscuring thetreatment site and also prevent inadvertent coagulation

com-of adherent blood mistaken for vascular lesions, as onlyvascular lesions should be coagulated More widespread

Table 51.1 Criteria for selection of ideal patients for

endoscopic coagulation.

Chronic hematochezia

Transfusion-dependent anemia for 6 months or longer

Bleeding refractory to medical management

No active nonrectal bleeding source

No tumor recurrence

No postradiation fistulae, ulceration, or strictures

Fig 51.3 Segmental involvment of the distal sigmoid above

and separate from the distal rectal lesions.

Table 51.2 Assessment of the efficacy of treatment for chronic

radiation proctopathy.

Decrease in rectal bleeding

Patient satisfaction (quality-of-life improvement)

Increase in hemoglobin level

Reduction in transfusion requirements

Reduction in hospital admissions

Improvement in endoscopic appearance

Trang 14

coagulation of surrounding mucosa will increase the risk

for stricture and ulceration Angiectasias must be treated

down to the dentate line Failure to do so is a common

reason for “refractory bleeding.”

Once bleeding has been controlled, patients may

direct their attention to nonbleeding symptoms, which

include frequent stooling, tenesmus and, particularly,

urgency

Laser therapy

The Nd:YAG laser with a wavelength of 1.06 nm has a

depth of penetration of up to 5 mm compared with 2 mm

for the argon and KTP (potassium titanyl phosphate)

532 nm lasers The monochromatic light energy from

these lasers is absorbed more efficiently by the darker

ectatic blood vessels as opposed to the surrounding

non-vascular mucosa [8] Argon laser energy is preferentially

absorbed by red-colored or pigmented tissues as is thelight energy of the KTP device [37]

With the Nd:YAG laser, the lowest power settingshould be used with a maximum pulse duration of 0.5 s

A starting power of 40 W per pulse can be used, with ther reductions by 5 W if there is cavitation or charring

fur-at any trefur-atment site The tip is maintained fur-at a distance

of 1 cm or less from the mucosal surface All visiblelesions are coagulated in a proximal to distal sequence.Dependent portions are treated first to avoid pooling

of blood and suboptimal access to the vascular lesions.Tangential distal lesions, if difficult to approach by the noncontact method, can be conveniently treated by contact coagulation using a heater probe (OlympusAmerica, Mellville, NY) or bipolar electrocautery probe.Angiectasias clustered at and just above the dentate line present the greatest challenge to noncontact laserphotocoagulation They are best approached from aretroflexed position Frequent decompression of thecolon to prevent gaseous distension is necessary forpatient comfort As mentioned above, all visible lesionsshould be treated in each treatment session The argonlaser can be used at a power setting of 3–8 W with similarshort pulse durations

After the initial endoscopic coagulation session, thepatient should be given a sufficient amount of time toallow the coagulated areas to heal The treatment siteswill ulcerate and can bleed This usually occurs severaldays to a week following the treatment and after an ini-tial period of absent bleeding It is important to informpatients of this sequence and encourage patience Apractical interval for follow-up that will allow healing

of treatment sites, cessation of treatment-induced ing, and an accurate assessment of residual lesions is

bleed-3 months If at any point the patient notices resolution ofbleeding or a marked reduction of bleeding to trivial andepisodic amounts, with cessation of transfusion needsand anemia, then supplemental treatment can be avoided

Fig 51.4 (a) Before and (b) after

argon plasma coagulation Note that

a white coagulum ablates the angiectasia Charring and cavitating the mucosa should be avoided.

Fig 51.5 Thermal ulceration complicating argon plasma

coagulation This ulceration is typically deep, accompanied by

anal pain, and gives rise to refractory bleeding Some may heal

in time.

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Chapter 51: Radiation Proctopathy 607

Results of laser treatment

The largest series of 47 patients reported a decrease

of daily rectal bleeding from 87% of patients to 11%

(P< 0.001) [8] The median duration of rectal

bleed-ing before treatment was 11 months despite previous

medical treatment (98%) or bypass colostomy (6%)

The median hemoglobin level increased from 9.7 to

11.7 g/dL (P< 0.001) Transfusion dependence decreased

from 57% of patients to 9% after laser treatment (P<

0.01) In another series of eight patients using Nd:YAG

laser therapy, there was a decrease in the average

trans-fusion requirements and hospital admissions

through-out the entire follow-up period subsequent to the first

laser treatment [17] In a series of 14 patients treated by

argon laser photocoagulation, no recurrence of

bleed-ing was reported in 50% of patients and only minor

infrequent bleeding in the remaining patient group

dur-ing follow-up [18]

Transmural necrosis and fibrosis with perforation

or stricture formation are more common with Nd:YAG

laser due to its inherently deeper penetration

Complica-tion rates of 5–15% have been reported with the more

widely used Nd:YAG laser for a variety of indications in

the rectum, colon, and small bowel [18] The Mayo laser

group [8] experienced a 6% complication rate with no

deaths; 4% of patients ultimately required surgery for

control of bleeding Nonfatal complications involved

hypotension with subendocardial infarction, a seizure,

and a rectovaginal fistula Fistula was the only

com-plication directly attributed to the laser treatment and

was managed with rectosigmoid resection and an

end-sigmoid colostomy Of 47 patients, 39 (83%) were

fol-lowed for longer than 6 months and of these 36 who

responded to treatment continued to be in remission

Long-term remission is the usual outcome, although

female gender and sigmoid involvement were

associ-ated with poor outcome in the Mayo series Gynecologic

cancers requiring expanded radiation along with female

pelvic anatomy may cause more proximal lesions in the

sigmoid The multiple bends of the sigmoid colon and

the usually extensive number of vascular lesions

over-whelm attempts at any coagulation modality In patients

with known sigmoid involvement, it is feasible to first

concentrate therapy exclusively within the rectum since

continued clinically significant bleeding from the

sig-moid colon can then be managed by surgical resection

No immediate or later complications have been reported

after argon laser therapy

Preliminary results with photodynamic therapy

performed by the Mayo laser group on patients with

refractory bleeding limited to the rectum have been

very encouraging In theory, presensitizing the vascular

lesions with a parenteral injection of a photosensitizing

agent, such as hematoporphyrin derivative, before

inducing selective autodestruction after exposure to apreselected wavelength of laser light has great appeal It

is possible that this alternative form of laser therapy,although costly, may offer a less invasive and even betteroutcome in the more difficult patients, including thosewith involvement proximal to the rectum

Argon plasma coagulation

Argon plasma coagulation (APC) has replaced lasercoagulation therapy for radiation proctopathy for manypractices The device is portable and therefore availablefor use in any procedure room, provided that measuresare taken to eliminate or dramatically reduce the electricalinterference the device can produce in the endoscopicvideo imaging system The advantages of this modalityinclude noncontact coagulation and shallow depth ofinjury As a result, treated areas of radiation proctopathyheal more quickly compared with the Nd:YAG laser and the endpoint of therapy can be reached sooner Therecommended settings include a power range within30–45 W and a gas flow rate of 0.9 L/min Care should betaken to avoid unnecessary contact between the APCprobe and the rectal mucosal surface in order to main-tain a shallow coagulation injury from the monopolarcoagulating energy Higher power or, more import-antly, prolonged coagulation of a focal area will result

in deep injury and a subsequent thermal ulcer Ulcers

in radiated mucosa are slow to heal and will frustrate care The end-firing probe is more desirable than theside-firing probe, which often results in contact therapy.Those lesions at and just above the dentate line can betreated with the endoscope in a retroverted position,unlike laser therapy This is possible because of the ad-vantageous electrical plasma arcing toward the mucosawith the probe tip in any position relative to the intendedarea of treatment As with laser therapy, treatment isinterrupted regularly to decompress the colon

Results of argon plasma coagulation

There are a number of experiences in the literature, most retrospective, that have reported on the number

of treatment sessions observed until clinical ment, as measured by direct endoscopic observation and use of bleeding scores, units of blood transfused,hemoglobin change, and complications One of the earli-est and largest experiences with APC reported dramaticimprovement in bleeding scores and an increase inhemoglobin of 1.9 g/dL in anemic patients with no seri-ous complications [20] Overall success in controllingbleeding has ranged from 70 to 95%, with complete cessation of bleeding ranging from 47 to 80% [23–29].Power settings in these reports have ranged from 40 to

improve-50 W Success in control of bleeding has occurred with

Trang 16

one to four treatment sessions, with control of bleeding

reported as long as 36 months after completed therapy

[27] Complications have included pneumoperitoneum,

refractory ulceration, and rectal stenosis Recurrence

of lesions have been infrequently reported after long

periods of remission

Bipolar and heater probe coagulation

Although less preferable because of contact-induced

bleeding and tissue adherence to the tip of the

coagu-lating probe, bipolar and heater probe coagulation

can be performed with successful results [21,22] The

Gold probe (Boston Scientific Corporation, Microvasive

Endoscopy, MA) is advantageous compared with the

original multipolar probe because of the larger

coagulat-ing surface and less tissue adherence These probes work

well in coagulating vascular lesions in the very distal

rectum, at and just above the dentate line, with the

endo-scope in a retroflexed position Treating these extremely

distal lesions adequately often makes a major difference

to long-term outcome The power settings are 12–16 W

with a continuous pulse mode for the bipolar probe, and

10–15 J for the heater probe There have been no

com-plications other than anal pain during coagulation near

the dentate line [22] Of note, patients treated by these

contact thermal modalities appeared to require more

fre-quent treatment sessions compared with the laser and

argon plasma devices

Topical formalin

Initially used to control bleeding from the bladder in

radiation-induced hemorrhagic cystitis, formalin

treat-ment for radiation proctopathy was first reported by

Rubinstein and colleagues in 1986 [30] A dilute (4%)

formaldehyde solution is used, which has been

demon-strated in animal models to be free of toxic adverse

effects [38] Reported experiences have directly instilled

formalin in up to 50-mL aliquots, exposing the rectal

mucosa for a limited time, from 30 s to 15 min, followed

by rinsing [30,31,33–36] Alternative methods have

involved painting the mucosa with a formalin-soakedswab via an anoscope or rigid proctoscope or applyingguaze-soaked pads for up to 45 min [32] Comparisonstudies are underway (Mayo Clinic DevelopmentalEndoscopy Unit) to prospectively compare formalinwith argon plasma coagulation

Unlike coagulation therapy, the endoscopic servations during and immediately after treatment areminimal There is usually a diminution in the amount

ob-of friability and bleeding during the treatment andsometimes a blanching of the vascular lesions Formalin can bind to proteins and, by doing so, causes cellularnecrosis Eventually, considerable edema develops thatcan reduce the rectal lumen by greater than 50%, al-though it is asymptomatic Animal studies have shown

no change in rectal compliance [38] Over a span of days,superficial mucosal ulceration develops that resembles aproctitis Formalin should not be used in patients whohave any preexisting ulceration, since the superimposedchemical injury involving the ulcers induces consider-able pain

Results of formalin therapy

Success in the control of bleeding has ranged from 71 to100%, with the majority of patients experiencing controlafter one treatment session [30–36] Follow-up has beenreported after 4–64 months [34] Most surgical experi-ences have involved treatment under general anesthesia,although in our experience the procedure can be performed readily with or without conscious seda-tion Described complications include lower abdominalcramps during treatment, anal and perineal pain aftertreatment, self-limited fissures, severe chemical colitis,and a rectovaginal fistula [30–36] Anal pain after treat-ment has been reported in up to 25% of patients [30–36]

Summary(Table 51.3)

At present, there is little evidence to support the benefits

of medical therapy The scant but encouraging ence with sucralfate enemas suggests that an initial trial

Minimal bleeding (infrequent, scant), no anemia Sucralfate enemas (topical formalin)

Refractory bleeding (daily), clots and incontinence, Endoscopic coagulation (topical

Refractory bleeding, failed coagulation (formalin), Photodynamic therapy

sigmoid involvement, anemia

Refractory bleeding, failed photodynamic therapy, Surgery

sigmoid involvement, complications, anemia

Table 51.3 Treatment

recommendations for radiation proctopathy.

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Chapter 51: Radiation Proctopathy 609should be considered for those patients who experi-

ence nuisance rectal outlet bleeding, unassociated with

anemia [39] For patients who are anemic due to

bleed-ing, endoscopic coagulation therapy is the first line of

treatment Argon plasma coagulation has performed so

well that it can be endorsed as the preferred coagulation

treatment method Since the argon plasma coagulator

and the laser are not universally available, meticulous

contact coagulation with shallow injury devices such as

the heater probe or any of the bipolar electrocautery

probes can be used Careful use of these devices may

require a few extra treatment sessions compared with

the noncontact therapies Patients who remain refractory

to endoscopic therapy, especially those with segmental

involvement of the colon proximal to the rectum, are

candidates for surgical extirpation of the involved

seg-ment or bypass surgery to facilitate manageseg-ment of

the frequent loss of blood Photodynamic therapy may

offer an excellent alternative to surgery for the

refract-ory patient when there is more extensive

involve-ment Additional prospective experience with topical

formalin, including the identification of an ideal

endo-scopic method of application, may bring this modality

into the mainstream and has the potential to change this

treatment schema

References

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831 patients with squamous cell carcinoma of the intact

uterine cervix treated with 3000 rads or more whole pelvic

irradiation Am J Roentgenol 1970; 108: 293–304.

2 Haboubi NY, Schofield PF, Rowland PL The light and

electron microscopic features of early and late phase

radiation-induced proctitis Am J Gastroenterol 1988; 83:

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3 Babb RR Radiation proctitis: a review Am J Gastroenterol

1996; 91: 1309–11.

4 Kinsella TJ, Bloomer WD Tolerance of the intestine to

radi-ation therapy Surg Gynecol Obstet 1980; 151: 273–84.

5 Buchi K Radiation proctitis: therapy and prognosis JAMA

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6 Jao SW, Beart RW, Gunderson LL Surgical treatment of

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7 Reichelderfer M, Morrissey JF Colonoscopy in radiation

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8 Viggiano TR, Zighelboim J, Ahlquist DA et al Endoscopic

Nd: YAG laser coagulation of bleeding from radiation

proc-topathy Gastrointest Endosc 1993; 39: 513–17.

9 Kochhar R, Sharma SC, Gupta BB et al Rectal sucralfate in

radiation proctitis Lancet 1988; ii: 400.

10 Grigsby PW, Pilepich MV, Pearson CL Preliminary results

of a phase I/II study of sodium pentosanpolysulfate in the

treatment of chronic radiation-induced proctitis Am J Clin

Oncol 1990; 13: 28–31.

11 Charneau J, Bouachour G, Person B et al Severe

hemor-rhagic radiation proctitis advancing to gradual cessation

with hyperbaric oxygen Dig Dis Sci 1991; 36: 373–5.

12 Al-Sabbagh R, Sinicrope FA, Sellin JH et al Evaluation of

short chain fatty acid enemas: treatment of radiation

proc-titis Am J Gastroenterol 1996; 91: 1814–16.

13 Athanasoulis CA, Walkman AC, Barnes AB, Herbst AL Angiographic control of pelvic bleeding from treated carci-

noma of the cervix Gynecol Oncol 1976; 4: 144–50.

14 Gazet JC Parks coloanal pull-through anastomosis for

severe, complicated radiation proctitis Dis Colon Rectum

1993; 36: 135–8.

15 Gilinsky NH, Burns DG, Barbezat GO et al The natural

his-tory of radiation-induced proctosigmoiditis: an analysis of

88 patients Q J Med 1983; 205: 40–53.

16 Leuchter RS, Petrilli ES, Dwyer RM et al Nd:YAG laser apy of rectosigmoid bleeding due to radiation injury Obstet Gynecol 1982; 59: 655–75.

ther-17 Alexander TJ, Dwyer RM Endoscopic Nd:YAG laser ment of severe radiation injury of the lower gastrointestinal

treat-tract: long-term follow-up Gastrointest Endosc 1988; 34:

407–11.

18 Taylor JG, DiSario JA, Buchi KN Argon laser therapy for

hemorrhagic radiation proctitis: long-term results intest Endosc 1993; 39: 641–4.

Gastro-19 O’Connor JJ Argon laser treatment of radiation

procto-pathy Arch Surg 1989; 124: 749.

20 Silva RA, Correia AJ, Dias LM, Viana HL, Viana RL Argon plasma coagulation therapy for hemorrhagic radiation

proctosigmoiditis Gastrointest Endosc 1999; 50: 221–4.

21 Maunowry V, Brunetaud JM, Cortot A Bipolar agulation treatment for hemorrhagic radiation injury of the

electroco-lower digestive tract Gastrointest Endosc 1991; 37: 493–4.

22 Jensen DM, Machicado GA, Cheng S, Jensen ME, Jutabha R.

A randomized prospective study of endoscopic bipolar electrocoagulation and heater probe treatment of chronic

rectal bleeding from radiation telangiectasia Gastrointest Endossc 1997; 45: 20–5.

23 Smith S, Wallner K, Dominitz JA et al Argon plasma lation for rectal bleeding after prostate brachytherapy Int J Radiat Oncol Biol Phys 2001; 51: 636–42.

coagu-24 Villavicencio RT, Rex DK, Rahmani E Efficacy and plications of argon plasma coagulation for hematochezia re-

com-lated to radiation therapy Gastrointest Endosc 2002; 55: 70–4.

25 Taieb S, Rolachon A, Cenni JC et al Effective use of argon

plasma coagulation in the treatment of server radiation

proctitis Dis Colon Rectum 2001; 44: 1766–71.

26 Tjandra JJ, Sengupta S Argon plasma coagulation is an effective treatment for refractory hemorrhagic radiation

proctitis Dis Colon Rectum 2001; 44: 1759–65.

27 Kaassis M, Oberti E, Burtin P, Boyer J Argon plasma lation for the treatment of hemorrhagic radiation proctitis.

coagu-Endoscopy 2000; 32: 673–6.

28 Tam W, Moore J, Schoeman M Treatment of radiation

proc-titis with argon plasma coagulation Endoscopy 2000; 32:

667–72.

29 Fantin AC, Binek J, Suter WR, Meyenberger C Argon beam coagulation for treatment of symptomatic radiation-

induced proctitis Gastrointest Endosc 1999; 49: 515–18.

30 Rubinstein E, Ibsen T, Rasmussen RB et al Formalin ment of radiation-induced hemorrhagic proctitis Am J Gastroenterol 1986; 81: 44–5.

treat-31 Saclarides TJ, King DG, Franklin JL, Doolas A Formalin instillation for refractory radiation-induced hemorrhagic

proctitis Report of 16 patients Dis Colon Rectum 1996; 39:

196–9.

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32 Biswal BM, Lal P, Rath GK et al Intrarectal formalin

applica-tion: an effective treatment for grade III hemorrhagic

radi-ation proctopathy Radiother Oncol 1995; 35: 212–15.

33 Seow-Chen F, Goh H-S, Eu K-W et al A simple and effective

treatment for hemorrhagic radiation proctopathy using

for-malin Dis Colon Rectum 1993; 36: 135–8.

34 Counter SF, Froese DP, Hart MJ Prospective evaluation of

formalin therapy for radiation proctopathy Am J Surg 1999;

177: 396–8.

35 Luna-Perez P, Rodriguez-Ramirez SE Formalin installation

for refractory radiation-induced hemorrhagic proctitis J

Surg Oncol 2002; 80 (Suppl.): 41–4.

36 Pikarsky AJ, Belin B, Efron J et al Complications following

formalin installation in the treatment of radiation induced

proctitis Int J Colorectal Dis 2000; 15: 96–9.

37 Taylor JG, Disario JA, Bjorkman DJ KTP laser therapy for

bleeding from chronic radiation proctopathy Gastrointest Endosc 2000; 52: 353–7.

38 Myers JA, Hollinger EF, Mall JW et al Mechanical,

histo-logic and biochemical effects of canine rectal formalin

instil-lation Dis Colon Rectum 1998; 41: 153–8.

39 Swaroop VS, Gostout CJ Endoscopic treatment of chronic

proctopathy J Clin Gastroenterol 1998; 27: 36–40.

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Introduction

A variety of conditions may lead to the formation of

benign and malignant strictures of the colon and rectum

(Table 52.1) Colonoscopy facilitates the clinical and

histologic study of stenotic areas in the large bowel

Therapeutic interventions through the colonoscope may

be performed as an adjunct or alternative to surgery in

selected patients with symptoms related to colorectal

strictures This chapter reviews the use of colonoscopy in

the management of benign and malignant strictures of

the colon and rectum

Colonoscopy in the diagnosis of

colorectal strictures

Colonoscopy allows direct visualization and

inspec-tion of colorectal strictures The endoscopic appearance

of the stricture may, in most instances, provide the

cor-rect diagnosis For example, endoscopic features of a

malignant stricture include an obvious mass, ulceration,

and bleeding, whereas benign strictures usually appearsmooth and symmetrical, although the visual appear-ance is not always accurate The combination of endo-scopic, clinical (prior cancer or surgery), and radiologicfeatures on computed tomography (CT) (presence orabsence of mass or inflammatory changes) allows a fairlyaccurate diagnosis of benign or malignant disease to bemade

During endoscopic evaluation or treatment of anobstructive colonic stricture the endoscopist must becareful not to overinsufflate air, since the segment be-tween the stricture and a competent ileocecal valve canbecome overdistended resulting in a proximal pneu-matic colon rupture, even though the instrument did not pass beyond the stricture This is the “closed loopphenomenon,” which must be considered whenever anarrow colon stricture is inspected [1] Tissue samplingduring colonoscopy allows for a positive diagnosis ofmalignancy to be made in a high percentage of patients.Direct forceps biopsy is the standard method of tissueacquisition Sampling of the entire portion of the stric-ture may produce a higher yield than sampling of onlythe distal portion, but can be technically difficult be-cause a severely narrowed lumen may prevent passage

of the endoscope It may be necessary to dilate a pected malignant stricture to allow passage of the endo-scope through the stricture so that complete endoscopicevaluation with tissue sampling is possible (Fig 52.1).Even if the endoscope can be insinuated into the stric-ture, it is unusual to be able to angulate the scope tipwithin the narrowed segment to permit adequate tissue sampling of the walls Another alternative to stric-ture dilation is the use of smaller-diameter endoscopes such as a pediatric or upper endoscope Although notroutinely used, brush cytology sampling may increase the diagnostic yield of malignancy over biopsy alone [2]

sus-Colorectal strictures occurring in the setting of tablished chronic ulcerative colitis should be assumed

es-to be malignant in nature Predices-tors of a malignant stricture in the setting of ulcerative colitis include longduration of disease (> 10 years), proximal location, and symptomatic large-bowel obstruction [3] Colorectalstrictures in documented Crohn’s colitis may also be

Chapter 52 Benign and Malignant Colorectal Strictures

Todd H Baron

Table 52.1 Etiology of colorectal strictures.

Benign

Diverticular disease

Anastomosis (including ileocolonic)

Inflammatory bowel disease

Primary colorectal cancer

Recurrent colorectal cancer

Colonoscopy Principles and Practice

Edited by Jerome D Waye, Douglas K Rex, Christopher B Williams

Copyright © 2003 Blackwell Publishing Ltd

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malignant; duration of disease more than 10 years, short

strictures, and involvement of more than one-third of

the large bowel appear to be associated with

malig-nancy [4]

Most symptomatic benign colorectal strictures are

fibrotic in nature However, patients with inflammatory

bowel disease or diverticular disease may have a

com-ponent of luminal compromise as a result of chronic

fibrotic changes that become symptomatically

obstruct-ive when acute inflammatory changes are superimposed

on the underlying pathology Once the acute

inflammat-ory component resolves, usually with medical therapy,

obstructive symptoms tend to resolve Balloon dilation

of a stricture in the setting of acute inflammatory changes

is likely not to be as effective as when the obstruction is

fibrotic

In the setting of immunosuppression, infections such

as cytomegalovirus may produce colonic strictures,

some of which resemble primary colorectal malignancy

[5] Therefore, in immunosuppressed patients, biopsies

should be obtained and processed appropriately for the

detection of infectious agents

Severe acute pancreatitis may result in acute and/or

chronic inflammatory changes of the colon, with fixation

and obstruction [6] It is important for the endoscopist

to recognize this well-described but underappreciated

entity, since dilation is not appropriate for the treatment

Anastomotic strictures

Colonic anastomotic strictures occur in up to 22% ofpatients following bowel resection and anastomosis [7].Factors promoting development of anastomotic stric-tures include ischemia, anastomotic dehiscence, pre-operative or postoperative radiation therapy, or cancerrecurrence (when resection is for malignant disease).The success rate of endoscopic dilation depends on sev-eral factors Pucciarelli and colleagues [8] analyzed theoutcome following dilation of anastomotic strictures.Factors associated with a successful response to dilationwere high anastomosis (> 8 cm from the anal verge), noadjuvant radiation therapy, minimal or no dehiscence,

no neoplastic recurrence, simple stricture morphology,and short stenosis (< 1 cm) These authors found whenradiation therapy, local neoplastic recurrence, and largedehiscence were present, there was nearly a 100% prob-ability of dilation failure When these three factors wereabsent, the probability of dilation failure was 5% An

Fig 52.1 Submucosal recurrence of colorectal cancer: (a) on

initial inspection the stricture appears benign; (b) after stricture

dilation and further passage of the endoscope, obvious

features of malignancy are seen.

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Chapter 52: Benign and Malignant Colorectal Strictures 613important anatomic concept is that some anastomotic

strictures are membranous and more responsive to

endo-scopic therapy, while others are transmural and

concen-tric and less responsive to endoscopic therapy

The first endoscopic therapy in which balloon dilation

was performed for a postoperative colonic stricture was

described in 1984 Since then, there have been

numer-ous reports using through-the-scope (TTS) hydrostatic

balloon dilators for dilation of anastomotic strictures

Kozarek [9] published the results of a survey of 3000

endoscopists who were queried about their use of

hydrostatic dilation of benign strictures Of 64 patients

who underwent colonic stricture dilation, 44 had

anasto-motic strictures Immediate objective and symptomatic

relief was reported in 83% and 73% of patients

respect-ively, while objective and symptomatic relief at more

than 3 months were persistent in 73% and 86%

Addi-tionally, the size of the balloon is an important

para-meter for success Of all patients undergoing colonic

stricture dilation, immediate symptomatic improvement

following balloon dilation was less than 50% when

bal-loons with a diameter under 40 French (13 mm) were

used, while a success rate of greater than 90% was

achieved with balloon dilators having a diameter of at

least 51 French (17 mm) Achalasia-dilating balloons

with a diameter of 30–40 mm have been used to dilate

rectal anastomotic colonic strictures [10], with good

long-term results in 16 of 18 (94%) patients Overall, the

success rates following balloon dilation of anastomoticstrictures range from 70 to 90% [7]

Over-the-wire plastic dilators (Savary–Gilliard) arealso used to treat anastomotic strictures in the left colon,particularly those close to the anus Werre and col-leagues [11] described this technique in 15 patients Afterendoscopic placement of a guidewire across the stric-ture, 10–19 mm dilators were passed through the narrowsegment under fluoroscopic guidance Ten patients had

a complete response after three or less sessions, whereasfive patients underwent four or more procedures with-out a complete response, suggesting that if patients donot respond to dilation within a few sessions, they arenot likely to respond There are no prospective trialscomparing balloon dilation to Savary dilators In a retro-spective comparative study, balloon dilation was found

to produce a better response after a single session thanbougie dilation (77% vs 52% respectively) [12] Bothmethods of dilation may lead to complications of per-foration and bleeding There are no specific guidelines

on diameters of dilators and number of dilations per session, as there are for esophageal dilation Althoughthere are no supportive data, it is assumed that moreaggressive dilation may be performed in the rectum asopposed to more proximal disease Additionally, thereare no data to support injection of corticosteroids intoanastomotic strictures to improve the long-term out-come following dilation

In summary, the response rate following dilation ofanastomotic strictures is variable and dependent uponseveral factors With proper patient selection, balloon orrigid dilation is the initial nonoperative treatment ofchoice (Fig 52.2)

Fig 52.2 Anastomotic stricture: (a) smooth membranous-type

anastomotic rectal stricture; (b) hydrostatic through-the-scope

balloon dilation using a 20-mm balloon (the membranous

nature is more obvious during dilation).

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The use of an endoscopic electroincision technique has

been described as a method to treat benign anastomotic

colorectal stenoses Brandimarte and Tursi [13] described

39 patients with central membranous anastomotic

“stric-tures” defined by barium enema and endoscopy A

needle-knife electrocautery device, as used for

endo-scopic retrograde cholangiopancreatography (ERCP)

precutting techniques, was used to incise the stricture

radially in six directions No other therapy (such as

bal-loon dilation) was performed Patients were followed

clinically and endoscopically for a mean of 25 months

without recurrence of stricture or symptoms The use of

this electroincision technique to augment balloon

dila-tion therapy has also been proposed as a treatment for

refractory strictures In a series of 35 patients, Truong

and colleagues [14] performed electroincision, cutting

radially in four directions followed by balloon dilation

Two-thirds of the patients required one treatment A

good response was obtained in all patients following

one to three sessions Recently, the incision technique

has been described using Nd:YAG laser with excellent

results in 9 of 10 patients [15]

Because of the potential complications, electroincision

should be performed only by experienced endoscopists

in selected patients with membranous-type strictures

Inflammatory bowel disease

Most of the data regarding endoscopic dilation of colonic

strictures occurring in the setting of inflammatory bowel

disease is derived from the treatment of recurrent

Crohn’s disease with stricturing at the site of colocolonic

or ileocolonic anastomoses Nearly all of these reports

have used TTS balloons [16] Couckuyt and colleagues

[17] prospectively evaluated the outcome of 55 patients

with clinically symptomatic ileocolonic strictures

fol-lowing endoscopic TTS balloon dilation with balloons

ranging in diameter from 18 to 25 mm Long-term

suc-cess was achieved in 62% of patients, although

perfora-tion occurred in six patients (11%) In another study

where the maximum balloon diameter was 18 mm,

sim-ilar results were achieved with no perforations [18] The

addition of corticosteroid injections may improve the

outcome following endoscopic therapy [19,20] One case

of successful wire-guided bougienage dilation of an

ileocolonic anastomotic stricture after failed TTS balloon

dilation has been reported [21]

There are only a few reports of successful balloon

dilation of colonic Crohn’s strictures in the absence of

previous surgery [20,22,23], with the goal being an 18-mm

dilator, achieved over several sessions In one series

of 10 Crohn’s patients under-going endoscopic therapy,

six had colonic strictures not involving the ileum, five

of which were not postoperative [20] Endoscopic tion” was performed using needle-knife electroincisionfollowed by injection of triamcinolone Unfortunately,the details of follow-up are unavailable and thisapproach cannot be recommended

“dila-In summary, endoscopic dilation for the treatment

of ileocolonic and colonic strictures in the setting ofinflammatory bowel disease is a reasonable nonsurgicalalternative, although up to one-third of patients willeventually require surgery The ideal dilation strategyand the need for adjuvant corticosteroid injection areunknown

Nonsteroidal antiinflammatory drug-induced strictures

One of the adverse effects of nonsteroidal matory drugs (NSAIDs) is the development of colonicstrictures These strictures are usually symmetrical, 2–

antiinflam-4 mm thick, may be multiple, and may occur in the rightcolon There have been only a few reports of endoscopictherapy, but it appears that large-diameter TTS balloondilation (15–20 mm) is safe and effective for treatingNSAID-induced strictures [24–26]

Miscellaneous strictures

There are few or no data on the use of endoscopic dilation for the other benign strictures outlined in Table 52.1 In the report by Kozarek [9], 5 of 44 patientsundergoing colonic dilation had diverticular strictures.All five patients had objective relief at more than

3 months following balloon dilation

Self-expandable metal stents

Self-expandable metal stents (SEMS) are approved bythe Food and Drug Administration (FDA) only for thetreatment of malignant colorectal obstruction How-ever, there are reports of their use in benign obstructive colorectal diseases The main safety concern with the use of metal stents for benign disease is the long-termconsequences of implantation When a stent is used

as a bridge to surgery to relieve acute colonic tion and allow a one-stage operation (see preoperativedecompression of malignant strictures later in this chap-ter), long-term safety is not a concern since the device isremoved at the time of operation However for the long-term nonoperative management of benign strictures,there are few data on their safety and they should beused only as the last option for patients with poor oper-ative risk There is a high rate of spontaneous migration

obstruc-of SEMS from benign strictures, which usually occurs inthe first month after insertion Although not designedfor endoscopic removal, SEMS are potentially remov-able and it is strongly recommended that in benign

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Chapter 52: Benign and Malignant Colorectal Strictures 615disease a cautious attempt should be made to remove

them within 4–8 weeks of implantation before they are

completely imbedded in the tissue Whether SEMS

spon-taneously migrate or are removed, a lasting benefit from

stent dilation may be seen

Anastomotic strictures

In patients with anastomotic strictures unresponsive to

endoscopic dilation, there are case reports of temporary

expandable metal stent placement to dilate the stricture

In one case the stent migrated distally 6 days after

inser-tion [27] Endoscopically, the colonic lumen remained

widely patent at last follow-up 12 months later In

another case, the stent was endoscopically removed 3

months after insertion and no further treatment was

required over an 18-month follow-up [28]

Inflammatory bowel disease

There is one report where SEMS were placed in two

patients for the treatment of refractory Crohn’s strictures

as an alternative to surgical strictureplasty [29] One

patient had a symptomatic descending colonic stricture

and one patient had small-bowel obstruction due to an

ileocolonic stricture The SEMS spontaneously migrated

in less than 1 month and 5 months respectively In a

sub-sequent report on the follow-up of these patients, both

remained without stricture recurrence at 3 years and

4.5 years respectively [30]

Diverticular disease

In a series of patients who underwent endoscopic SEMS

placement for treatment of colonic obstruction [31], three

patients had diverticular disease as the cause of acute

obstruction SEMS were placed successfully in all three

patients, with resolution of obstruction and subsequent

one-stage operative resection with primary anastomosis

Another group has described this scenario as well [32]

The use of SEMS for long-term nonoperative

manage-ment of fibrous diverticular strictures has not been

reported

Radiation-induced strictures

There are two case reports of SEMS placement for

treat-ment of colonic obstruction from chronic

radiation-induced colonic strictures In the initial report [33], a

stent was placed in a patient with complete rectosigmoid

obstruction The stent spontaneously migrated distally

from the stricture 19 days after placement There was

clinical and radiographic resolution of the stricture at

follow-up of 43 weeks In the other case, the stent

remained in place for 4 months until the patient died

from underlying medical illness unrelated to the stent[34]

Malignant disease

Colonic obstruction secondary to malignancy is thenumber one cause for emergency large-bowel surgery,accounting for as much as 85% of such procedures Thereare two clinical scenarios for endoscopic treatment ofmalignant colorectal strictures: preoperative decompres-sion and palliation Additionally, there are two majorendoscopic modalities for decompressing the obstructedcolon: laser therapy and SEMS Each of the two endo-scopic treatment options and clinical scenarios are dis-cussed separately

General comments

Laser

Laser therapy of primary colorectal neoplasms has beenperformed for over 15 years Laser therapy is most usefulfor treating patients who have intrinsic lesions in the distal colon that are bulky, polypoid, and exophytic (Fig 52.3) One drawback is the inability to treat intrinsicscirrhous lesions and extrinsically compressive lesions.Laser therapy, however, has an advantage over SEMS inthe ability to control bleeding from primary colorectalcancer Since laser therapy has become largely sup-planted by other modalities, its overall use is declining.Whether newer endoscopic tumor-ablative modalities,such as argon beam plasma coagulation (delivered at

Fig 52.3 Polypoid primary rectal cancer is an ideal lesion for

laser therapy.

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high settings), can produce results similar to laser

ther-apy remains to be seen

Self-expandable metal stents

SEMS are composed of a variety of metal alloys

with varying shapes and sizes depending on the

indi-vidual manufacturer and organ of placement The radial

expansile forces and degree of shortening differ between

stent types [35] Tissue reactions to SEMS in vivo are

known based on animal data as well as autopsy and

surgical findings in humans [36] Once deployed, the

tissue response to SEMS seems to be consistent

through-out the gastrointestinal tract The stent material becomes

incorporated into both the tumor and surrounding

tissue by pressure necrosis In the areas uninvolved by

tumor above and below the stenosis, the stent imbeds

deep into the wall of the organ This reaction anchors the

stent and helps to prevent stent migration With the use

of fully covered stents this integration does not always

occur and there is a higher rate of stent migration At

the present time, SEMS specifically designed for use

within the colon are uncovered Covered esophageal

stents have been used in the colon to combat problems

with tumor ingrowth and to close fistulae [37]

SEMS may produce imaging artifacts on both CT

and magnetic resonance imaging (MRI) localized to the

area around the stent that may prevent accurate

inter-pretation Most SEMS materials appear safe for MRI,

although factors such as stent shape, orientation to the

magnetic field, and type of alloy composition influence

signal intensity in vitro Therefore, information

concern-ing magnetic reactivity should be obtained before MRI is

performed in a patient who has undergone colorectal

stent placement [38,39]

Preoperative decompression

The traditional management of patients with either

subtotal or complete malignant colonic obstruction of

the left colon involves creation of a diverting colostomy

In some series, 30% of patients with primary colorectal

carcinoma presented with large-bowel obstruction [40]

These patients cannot undergo a one-stage operative

re-section of the lesion and primary colonic reanastomosis

because stool in the uncleansed colon proximal to the

ob-struction leads to breakdown of the colonic anastomosis

The standard two-stage operative procedure consists of

the initial surgery with diverting colostomy and

resec-tion of the primary tumor; reanastomosis of the colon

is performed as a second-stage operation Patients

pre-senting with complete colonic obstruction tend to be

acutely ill with more advanced disease compared with

patients without obstruction The goal of preoperative

endoscopic decompression is to allow clinical

stabiliza-tion of the patient and subsequent colonic preparastabiliza-tion

so that a one-stage operation can be performed and acolostomy avoided After successful endoscopic colonicdecompression, the patient’s comorbid medical illnessesand extent of malignancy can be addressed Addi-tionally, preoperative decompression allows preoperat-ive chemoradiation therapy to be administered If thepatient is a poor candidate for surgical resection because

of underlying illnesses, such as severe coronary arterydisease, or has unresectable or widely metastatic diseasediscovered by imaging studies, laser therapy and/orSEMS can serve as the palliative approach

Laser therapy

Although most series have described laser therapy as

a palliative modality, it has the potential to serve as

a bridge to surgery Arrigoni and colleagues [41] used endoscopic modalities to recanalize the lumen ofpatients with acute large-bowel obstruction due to colorectal cancer Using a combination of TTS balloon(18 mm) or Savary dilation (12–18 mm), snare debulk-ing, and Nd:YAG laser therapy, emergency colostomywas avoided in 16 of 17 patients by successful restoration

of the colonic lumen and relief of bowel obstruction

No complications occurred as a result of endoscopictherapy Although no patients in this series ultimatelyunderwent surgical resection, the data demonstrate theability to decompress the acutely obstructed colon withthis approach

Self-expandable metal stents

The use of SEMS as a bridge to surgery is becoming morewidely accepted Metal stents have luminal diameters

of 20–30 mm and remain in place until surgery whenthey are removed en bloc with the tumor [31] Segmentalcolonic resection after successful stent placement anddecompression has until recently been performed byopen surgery but a recent series of laparoscopic stentand tumor resection [42] has been reported

There are several small series describing successfulpreoperative placement of colonic SEMS with subsequentone-stage resections [31] A recent large multicenter series

of patients with primary colon carcinoma evaluated the effectiveness of preoperative placement of 20- and 22-mm diameter SEMS [43] Successful stent placement,with clinical resolution of large-bowel obstructionwithin 96 h, was achieved in 66 of 71 (93%) patients;

65 patients underwent elective single-stage surgery with

a primary colonic anastomosis at a mean of 8.6 days following stent placement One severe complication,intestinal perforation, occurred Although the stentswere inserted by interventional radiologists, the datacan be extrapolated to endoscopic placement

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Chapter 52: Benign and Malignant Colorectal Strictures 617Two studies have compared the outcome of patients

undergoing endoscopic placement of SEMS for relief

of acute large-bowel obstruction followed by elective

resection to those patients undergoing surgical

interven-tion without stent placement [44,45] A retrospective

study [44] reported 13 consecutive patients with

colorec-tal carcinoma who received SEMS compared with a

similar group that had traditional surgical management

at the same institution Stent placement and subsequent

clinical resolution of large-bowel obstruction was

achieved in 12 of 13 patients; in three the stents remained

for palliation A single-stage operation was performed in

eight of the nine remaining patients in the stent group

Only 2 of 13 patients treated with colonic SEMS required

colostomy compared with 10 of 13 patients in the

tra-ditional surgical group When cost data were analyzed,

a cost saving of 28.8% was seen in the SEMS group

because of a decrease in total hospital days, days spent in

the intensive care unit, and fewer surgical procedures A

more recent prospective study demonstrated similar

findings [45] in 72 patients with primary colorectal

can-cer and obstruction; SEMS were used when personnel

were available to place them If not available, traditional

surgery was performed A primary anastomosis with

avoidance of colostomy was achieved significantly more

often (85% vs 41%) in the SEMS group Despite these

promising results, there are no prospective randomized

studies of SEMS vs surgery for preoperative

decom-pression It remains to be seen whether long-term results

such as tumor recurrence rates are altered by the use of

preoperative colonic stent placement

Preoperative radiation therapy prolongs survival

after rectal cancer [46] Stent placement for obstructing

primary rectal cancer can allow the necessary time to

provide this treatment In one reported case, a full course

of chemoradiation therapy was completed following

which the tumor and stent were resected No adverse

pathologic effects were seen in the resected specimen

[47]

Palliation of malignant colonic obstruction

Laser therapy

Laser therapy is useful for palliation of both colonic

obstruction and bleeding from primary colorectal

can-cer In patients with obstruction, it appears that laser

therapy is most effective in treating small tumors With

tumors smaller than 3 cm in diameter there can be a high

probability of symptomatic improvement from

obstruct-ive symptoms [48] Patients with large tumors require

several sessions to maintain an adequate lumen The

response rate in large tumors is not 100% and patients

with extensive disease may not be improved with laser

therapy

Two large series of laser therapy for palliation of colorectal cancer have been published The largest study[49] included 272 patients undergoing palliative therapyfor rectosigmoid cancers, with a high immediate successrate (85%) and low major complication rate (2%) for palliation of obstructive symptoms Another study [50]evaluated the long-term outcome of laser palliation

of rectal cancer in 219 patients Long-term follow-up was obtained until death (mean 6.7 months) Resultswere analyzed based upon the predominant symptom

of obstruction, bleeding or other symptoms (soiling,tenesmus, and diarrhea) Significantly more patients inthe obstruction group (25%) eventually required palliat-ive colostomy Patients with obstruction required signi-ficantly more treatment sessions compared with theother groups Palliation of bleeding was achieved in 83%

of patients Major complications of perforation (4.1%),fistula (3.2%), bleeding (4.1%), and abscess formation(1.7%) were seen This study demonstrates that the out-come of laser therapy depends on whether the modality

is used to treat obstruction or bleeding

Overall, successful palliation is achieved in 80–90% ofpatients using laser An average of approximately threeprocedures is required to achieve sufficient and lastingrelief of obstructive symptoms Serious complications(bleeding, perforation, severe pain) occur in up to 10–15% of patients [51–53]

Self-expandable metal stents

Patients with colorectal carcinoma and colonic tion who have extensive local or metastatic disease are poor operative candidates for surgical resection, asare patients with obstruction secondary to noncolonic pelvic malignancies (e.g bladder or ovarian carcinoma)

obstruc-or metastatic diseases (e.g breast carcinoma) Thesepatients are candidates for colonic SEMS placement forpalliation [54–56] Several other series have demon-strated successful palliation of obstruction with avoid-ance of colostomy in 85–100% of patients In some series,the stents effectively palliated obstruction for more than

1 year [57–59]

The largest series of endoscopic stent placement forpalliation of obstructive primary rectal and rectosig-moid obstruction was published by Spinelli and Mancini[60] Stents were successfully placed in 36 of 37 patients.Three early migrations occurred Of the remaining 33patients, 28 had good long-term resolution of obstruc-tion without need for further treatment

Nearly all the published series have used uncoveredstents One study found an unacceptably high rate

of migration using fully covered stents [61] ever, in a recent study using partially covered stents for palliation of malignant left-sided obstruction, onlytwo stent migrations occurred in 16 patients [62] At

Trang 26

How-a meHow-an follow-up of 21 weeks, no stent occlusion wHow-as

seen

Although randomized comparative trials of stent

placement vs colostomy are lacking, SEMS is an option

for avoiding permanent colostomy in terminally ill

patients with colonic obstruction Following

uncomplic-ated colorectal stent placement, patients may resume

oral food intake after clinical decompression After

pal-liative colorectal stent placement, patients are advised to

consume a low-residue diet and use stool softeners or

laxatives to avoid stent occlusion from stool impaction

Complications of colon SEMS placement may occur

during the procedure, early after placement (early

com-plications), or late after insertion Early complications

include perforation, migration, bleeding, stent

mal-position, and stent occlusion by stool impaction Free

perforation during SEMS insertion may be a

devastat-ing complication, since fecal material is spilled into

the abdominal cavity This may be more difficult to

manage surgically compared with proceeding directly

to a diverting colostomy Additionally, the patient will

become more acutely ill, producing a potentially worse

surgical outcome Improper deployment of the stent or

proximal stent migration after successful placement

results in a stent floating freely within the lumen above

the stricture This is usually of no consequence,

assum-ing an additional stent(s) is properly placed to relieve the

obstruction (personal experience) Stents placed very

distally in the rectum may produce tenesmus, rectal

pain, and fecal incontinence; patients should be advised

of this possibility prior to stent placement In general,

stent placement more than 2 cm proximal to the anal

canal does not interfere with anal function Late

com-plications include distal stent migration, bleeding, and

perforation [63] Stent migration may be completely

asymptomatic or result in rectal bleeding or tenesmus

Removal of distally migrated stents from the rectum is

not technically difficult and is best performed using a

rat-toothed forceps Stent occlusion from tumor

over-growth, inover-growth, or stool impaction requires

endo-scopic intervention Obstruction by tumor ingrowth or

overgrowth can be managed with placement of

addi-tional stents through the original stent(s) It is unknown

whether previous radiation increases the risk of

stent-related complications

Some patients with widely advanced malignancies

and colonic obstruction may not improve following

suc-cessful stent placement because of other unidentified

sites of malignant gastrointestinal obstruction or diffuse

peritoneal carcinomatosis with small-bowel encasement

Palliation of malignant fistulae

Patients with malignancy within the pelvis may suffer

from fistulae to surrounding structures such as the

vagina or bladder In this setting, covered esophagealstents have been used to close such fistulae and produceexcellent palliation [37,64]

Materials for and techniques of endoscopic insertion of colonic SEMS

The duration of the procedure is highly variable anddepends on the degree of difficulty encountered travers-ing or accessing the stricture At least one full hour oftime should be allotted once sedation is administered.The stent chosen should be at least 3–4 cm longer thanthe obstruction to allow an adequate margin of stent oneither side of the obstruction

Stent types

Although any type of SEMS may be used within thecolon, including esophageal, tracheobronchial, and bili-ary stents, dedicated colonic SEMS are commerciallyavailable Three different self-expandable colonic stentsare approved by the FDA in the USA for treatment ofmalignant obstruction [65] One of these stents has alonger and smaller predeployment delivery system (10French) that allows passage of stents directly throughthe working channel of a therapeutic colonoscope, andthese stents can be placed as proximal as the ascendingcolon

Distal lesions producing colonic obstruction arewithin the reach of a standard flexible sigmoidoscope orupper endoscope For lesions proximal to the descend-ing colon, it is usually necessary to use a colonoscope If

a stent is chosen that will pass through the workingchannel of the endoscope, a therapeutic channel (≥ 4.2

mm diameter) is required

Other materials that should be readily availableinclude biliary catheters and guidewires Hydrophilicbiliary guidewires (Terumo, Tokyo, Japan) are especiallyuseful in order to “cannulate” or traverse obstructivelesions A stiff 0.035 inch guidewire is needed for stabil-ity during stent placement once the lesion has been traversed Water-soluble radiographic contrast may also

be needed to define stricture length as well as to strate the lumen for correct passage of catheters If mark-ing of the tumor margins is desired, injection needles forplacement of radiopaque contrast are needed

demon-Patient preparation and positioning

Patients with complete obstruction have usually ated any stool below the lesion and bowel preparation

evacu-is not necessary In those patients who have subtotalobstruction in the distal colon, one or two cleansing ene-mas are usually adequate; with a more proximal lesionand subtotal obstruction, a cautious colonoscopy bowel

Trang 27

Chapter 52: Benign and Malignant Colorectal Strictures 619preparation should be given Prophylactic antibiotics

should be considered in patients with complete

obstruc-tion and a markedly dilated colon because insufflaobstruc-tion of

air during the procedure may promote microperforation

and bacteremia

The patient should initially be placed in the left

lateral decubitus position Rotating the patient into the

supine position allows for a better anatomic view under

fluoroscopy, if used Standard intravenous conscious

sedation is usually administered, but is not absolutely

necessary for distal lesions

Description of procedure

Placement of SEMS in the rectum and distal sigmoid

without the use of TTS stents uses similar techniques

as for esophageal stent placement Deployment of TTS

stents, which are usually necessary for treating more

proximal obstruction, is more analogous to ERCP with

placement of a metal biliary stent These two approaches

to SEMS placement are discussed separately It is

imper-ative to have nursing assistants competent in complex

therapeutic endoscopic procedures and SEMS

place-ment to assist with these procedures

Nonfluoroscopic-guided stent placement

Non-TTS stent placement

For distal left-sided lesions, the area may be accessed

entirely under endoscopic guidance [60] If the

endo-scope cannot be passed through the lesion, the stricture

is cautiously dilated with a 15-mm TTS balloon A 10-mmendoscope is then passed through the stricture to allowplacement of a Savary guidewire as high as possibleabove the lesion As the endoscope is withdrawn, thestenosis is measured and the position/orientation of thelumen assessed After the undeployed stent is passedacross the stricture, the endoscope is reinserted to verifyand monitor the exact position of the distal end of thestent Alternatively, in patients with intrinsic lesions,laser therapy may be used to recanalize the lumen toallow passage of the endoscope and guidewire [65] Both

of these methods permit stent placement without the use

of fluoroscopy

TTS stent placement

If the endoscope passes easily through the lesion, a stiff0.035 inch guidewire with a floppy tip is placed throughthe endoscope channel and passed proximally at least

20 cm beyond the point of obstruction (Fig 52.4a) Oncethe stent passes through the endoscope channel, theendoscope is withdrawn below the distal margin of thestricture and the stent is deployed under direct endo-scopic guidance (Fig 52.4b)

Endoscopic/fluoroscopic stent placement

If the endoscope cannot be passed easily through the lesion, a hydrophilic biliary guidewire preloadedthrough a standard biliary catheter is used to “cannul-ate” or traverse the stricture, as is done during ERCP(Fig 52.5a) Once the wire has passed through the stric-ture, recognized fluoroscopically by the anatomicallycorrect position of the wire passing into an air-filleddilated proximal bowel, the catheter is advanced overthe guidewire through the lesion After removal of theguidewire, water-soluble radiographic contrast is injected

Fig 52.4 Endoscopic view of through-the-scope placement of

self-expandable metal stent for palliation of malignant colonic

obstruction: (a) a guidewire has been advanced across the

lesion; (b) immediately after deployment of stent.

Trang 28

Once the stent is fully deployed, the ends of the stentshould be carefully inspected fluoroscopically If eitherend is not flared or fully expanded, the endoscopistshould be suspicious that the stent chosen may have

Fig 52.5 Endoscopic placement of a through-the-scope stent

using fluoroscopic guidance: (a) endoscope is advanced to the

site of the lesion and a guidewire and catheter are advanced

through the area of obstruction; (b) guidewire is replaced by

a stiff guidewire and the delivery system is introduced;

(c) stent is initially deployed at the proximal portion of the lesion under both endoscopic and fluoroscopic guidance; (d) stent is fully expanded and symmetric in diameter throughout its length.

to confirm both proper position and luminal patency

At this point, the stiff 0.035 inch guidewire is placed

through the catheter and the procedure proceeds as

described above (Fig 52.5b–d)

Trang 29

Chapter 52: Benign and Malignant Colorectal Strictures 621been too short to cover the entire length of the stricture.

At this point contrast can be injected into the stent to

assess complete patency If needed, a second (rarely

third) overlapping stent may be required to adequately

treat the stricture

Limitations and success rate

The technical success rate for placement of colonic SEMS

in experienced centers is close to 100% Using

endo-scopic techniques stents may be placed into the right

colon [66], whereas with radiologic guidance alone stent

placement is limited to the left colon Limitations of

suc-cessful placement include inability to pass a guidewire

through the stricture and anatomic difficulties such as a

severely angulated and “fixed” sigmoid, which prevents

advancing the endoscope to the site of the lesion

Avoidance of complications

Two important tips are helpful in avoiding

intra-procedural perforation The first is limiting the amount

of air insufflation during the examination, especially in

patients with a dilated cecum The second is avoiding

aggressive dilation before or after stent insertion [65]

Summary

Colonoscopy plays a major role in the evaluation and

treatment of patients with benign and malignant

colo-rectal strictures Tissue sampling allows the diagnosis

of malignancy Successful treatment of benign strictures

is achieved using colonoscopically directed dilation

Endoscopic placement of expandable metal stents into

the colon is useful for both preoperative and palliative

relief of malignant colonic obstruction

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