complications of gi endoscopy(2)

784 GASTROINTESTINAL ENDOSCOPY VOLUME 55, NO. 7, 2002

This is one of a series of statements discussing theutilization of gastrointestinal endoscopy in commonclinical situations. The Standards of PracticeCommittee of the American Society for Gastro-intestinal Endoscopy prepared this text. In preparingthis guideline, a MEDLINE literature search wasperformed, and additional references were obtainedfrom the bibliographies of the identified articles andfrom recommendations of expert consultants. Whenlittle or no data exist from well-designed prospectivetrials, emphasis is given to results from large seriesand reports from recognized experts.

Guidelines for appropriate utilization of endos-copy are based on a critical review of the availabledata and expert consensus. Further controlled clini-cal studies are needed to clarify aspects of this state-ment, and revision may be necessary as new dataappear. Clinical consideration may justify a course ofaction at variance to these recommendations.

Upper GI endoscopy is a very commonly performedprocedure used as a diagnostic tool to evaluatepatients with a wide range of problems and com-plaints. Complications related to diagnostic evalua-tions are rare. Based on a 1974 survey conducted bythe American Society for Gastrointestinal Endoscopy,it was estimated that the overall complication ratebased on over 200,000 esophagogastroduodenoscopy(EGD) examinations was 0.13% and carried an asso-ciated mortality of 0.004%.1 More current data forcomplication rates, specifically looking at diagnosticendoscopic examinations, are relatively understudiedand prospective multicenter analyses have not beenconducted in a systematic fashion. With the introduc-tion of large multicenter databases, such as the CORI(Clinical Outcomes Research Initiative) project, bet-ter estimates of complications should be available inthe future. However, although more accurate datamay be obtained for immediate postprocedure com-plications, late complications may still be underesti-mated because of under-reporting. Rates of complica-tions are critically dependent on the method of datacollection (prospective/retrospective), definition ofcomplication, and duration of follow-up.

Major complications related to diagnostic proce-dures can be broken down into cardiopulmonarycomplications, complications related to sedation,infectious complications, perforation, and bleeding.

CARDIOPULMONARY COMPLICATIONS/COMPLICATIONS RELATED TO SEDATION

Cardiopulmonary complications related to sedationand analgesia are the most common type of complica-tion seen with diagnostic endoscopy, accounting for upto 46% of those reported in the above-mentionedASGE survey were related to sedation.1,2 This approx-imates a more recently reported proportion of 40% aspublished in 1991 by ASGE in collaboration with theFood and Drug Administration.3 These complicationsrange from minor changes in vital signs to myocardialinfarctions, respiratory depression, and shock/hy-potension.2 Additionally, with the introduction ofpulse oximetry, a greater number of nonclinically rel-evant events have been reported. It is estimated thatoxygen desaturation may occur in up to 70% ofpatients undergoing various endoscopic examinations;more severe desaturation occurs less commonly.4,5

Factors leading to oxygen desaturation include diffi-culty with intubation, which may be related to the sizeof the endoscope. Patient factors include age and histo-ry of cardiovascular/pulmonary disease. Complicationsmay arise related to the procedure itself, such as vaso-vagal reflex secondary to the intubation process and/orto overinsufflation of air.

Judicious use of conscious sedation with appro-priate monitoring equipment may help control therate and severity of complications. The reader isreferred to the ASGE documents regarding theappropriate use of conscious sedation and appropri-ate resuscitation equipment that should be main-tained in an endoscopy lab.6-10

Sedation-related complications are generally iden-tified during the procedure. Appropriate manage-ment includes “basic life support” if necessary. Propermanagement requires the presence of resuscitationmedications, including reversal agents and equip-ment in all areas where endoscopy is performed.

INFECTIOUS COMPLICATIONS

Infectious complications related to diagnostic endos-copy result either from the procedure itself or from theuse of contaminated equipment. Transient bacteremiamay occur during a diagnostic endoscopic procedureand is found more often for therapeutic procedures.11-13

The incidence is relatively low and the rate of bac-terial endocarditis or other complications in patients

American Society For Gastrointestinal Endoscopy

Complications of upper GI endoscopy

Title Author

VOLUME 55, NO. 7, 2002 GASTROINTESTINAL ENDOSCOPY 785

not at risk for endocarditis (e.g., normal cardiacvalves) is extremely low and estimated to be 1 in 5 to10 million.14 The reader is referred to the ASGE doc-ument regarding the use of antibiotic prophylaxis forthose patients who are at risk for endocarditis becauseof valvular abnormalities.15 Uncommon complicationsinclude retropharyngeal and retroesophageal abscess-es in patients who have had difficult intubations.16,17

This may be related to retropharyngeal trauma and/ornonclinically apparent perforations.

Issues related to contaminated equipment havebeen reviewed in the ASGE documents entitledInfection Control During Gastrointestinal Endos-copy; Guidelines for Clinical Application andTransmission.18,19 The reader is referred to thesedocuments, for a discussion of appropriate cleaningprocedures to prevent such contamination.

PERFORATION

Perforation of the upper GI tract related to diagnos-tic endoscopy is relatively low. In the above-men-tioned 1974 ASGE survey, the perforation rate was0.03% and with a mortality rate of 0.001%.1Predisposing factors to perforations include thepresence of anterior cervical osteophytes, Zenker’sdiverticulum, esophageal strictures, and malignan-cies.20-22 Although uncommon, perforations of theesophagus are associated with a relatively highmortality rate that approximates 25%.20

Pain is the most common and reproducible symp-tom related to perforation.20-23 Fever, crepitance, chestpain, pleuritic chest pain, leukocytosis, and pleuraleffusion may also be present. Perforations with asso-ciated air dissection may be diagnosed by plain radio-graph of the neck and/or chest. If a perforation is sus-pected, this may be localized by use of contrast media.Water-soluble contrast is usually used initially. If asite of perforation cannot be determined, barium orCT scan may be used in a repeat examination. A neg-ative study does not rule out a perforation, however.55

The approach to a patient with a perforationdepends on the state of health of the individual, thesite of the perforation, and the overall prognosis. Inselected patients, early recognition may allow med-ical management with nasogastric suction, intra-venous antibiotics, and parenteral hyperalimenta-tion. Perforations related to endoscopy are bestapproached in cooperation with surgical colleagues.Surgical management is required for larger perfora-tions when the pleural space is involved and for fail-ure to respond to medical management.

BLEEDING

Significant bleeding is a rare complication of diag-nostic upper endoscopy. Bleeding may be more like-

ly in individuals with thrombocytopenia and/orcoagulopathy.1 However, diagnostic upper endoscopyappears to be safe in patients with platelet counts aslow as 20,000.1 Biopsies should be performed withcaution below this level and platelet transfusionsshould be considered.1,6,7

Mallory-Weiss tears occur in <0.1% of diagnosticendoscopies and are usually not associated with sig-nificant bleeding.

COMPLICATIONS OF UPPERGASTROINTESTINAL DILATION

Determining the exact incidence of complications isdifficult due to the low frequency and a lack of largestudies comparing various methods of dilation. Themost commonly observed complications of dilation ofstrictures are perforation, pain, hemorrhage, andbacteremia/sepsis.

BENIGN PEPTIC ESOPHAGEAL STRICTURES

In the 1974 survey of members of the AmericanSociety for Gastrointestinal Endoscopy the compli-cation rate for dilation of the esophagus with mer-cury filled dilators was 0.4%. The most commoncomplication in the group using mercury-filled dila-tors was bleeding.

Most centers currently use either wire-guided,polyvinyl dilators (e.g., Savary-Gilliard) or balloondilators. In comparative trials, there is no evidencethat push dilators result in a higher rate of perfo-rations when dilating benign esophageal stric-tures.26-30 In a recent article comparing variousdilating systems, all perforations occurred withblind passage of Maloney dilators through complexstrictures.30 There were no perforations when usingballoon dilators or wire-guided Savary-type dila-tors. Blind passage of mercury-filled dilators or theuse of metal olives may be associated with higherrates of perforation.

Severe pain, bleeding, and bacteremia (includingendocarditis or CNS infection) are other complica-tions associated with esophageal dilation.

Caustic strictures may be at greater risk of perfo-ration due to the greater length and luminal com-promise that are characteristic for these lesions.32

In a 25-year review of dilating caustic esophagealstrictures, perforation was noted to occur in 17% ofpatients.33

ACHALASIA

Pneumatic dilation of achalasia may be associatedwith a lower risk of complications when a gradeddilation technique with low-compliance balloons isused. It is suggested to start dilation with a 30-mmballoon. Nonresponders should then undergo dila-

tion with a 35-mm balloon and subsequently a 40-mm balloon if needed.46 Avoiding inflation pres-sures greater than 11 psi may be associated withfewer complications.45

Prevention of dilation-related perforation may bepossible by limiting dilation to less than 15-mmdiameter. Two studies describing perforation ratesof 4 and 6.7% were associated with dilation togreater than 15 mm.48,49

MALIGNANT ESOPHAGEAL STRICTURES

The rate of perforation for dilating malignantesophageal strictures is higher than for benign stric-tures. The literature defines a rate of approximately10% based on several studies.38-41

Two studies evaluating the treatment of esopha-geal strictures occurring after radiation treatment ofesophageal cancer demonstrated a perforation rateof 2% to 6.5% per person.42,43 Dilation of a radiationstricture was not associated with a higher rate ofperforation when compared with dilation of a malig-nant stricture that did not receive radiation.43

GASTRIC OUTLET OBSTRUCTION

Studies report success with balloon dilation with alow complication rate. The rate of perforation variesfrom 0% to 6.7%.48-53 It appears as though perfora-tions occur with attempts to dilate the gastric outletto greater than 15-mm diameter.

There is no evidence at present that the use ofdilating balloons is associated with a lower rate ofcomplications as compared with wire-guided, push-type dilators.54

PEG COMPLICATIONS

Minor complications associated with PEG place-ment occur in 13% to 43% of patients59-61 andinclude tube occlusion, maceration from leakage ofgastric contents around the tube, and peristomalpain. Major complications, reported in 0.4% to 8.4%of procedures58,59,61-63 include infection, bleeding,perforation, ileus, injury of internal organs, tumorseeding, and death. Procedure-related mortality hasbeen reported to range from 0% to 2%,59,61,64,65 with30-day mortality in the range of 6.7% to 26%, oftenrelated to patient comorbidities.59-61,64-67

Infectious complications of PEG include woundinfections, abscess, peritonitis, necrotizing fasciitis,and aspiration pneumonia. Peristomal wound infec-tions occur at the site of PEG insertion through theabdominal wall in up to 41% of patients.60,62,68,69

However, use of antibiotic prophylaxis has beendemonstrated to significantly reduce the risk ofperistomal infections60,69-72 and is cost-effective.73

Several authors have reported cases of necrotizing

fasciitis,74-77 which has been theorized to be relatedto failure to make the abdominal incision largeenough to allow for appropriate wound drainage.75

Risk factors for necrotizing fasciitis include diabetesmellitus, atherosclerosis, alcoholism, malnutrition,immunosuppression, and older age.74 Signs of necro-tizing fasciitis include high fevers, cellulitis, skinedema, and subcutaneous emphysema, though ahigh index of suspicion is often required for makingthe diagnosis.76 Treatment includes surgicaldebridement and antibiotics. Despite these mea-sures, mortality ranges from 30% to 70%.74-76

Patients may develop aspiration pneumonia at thetime of PEG placement because neurologic sequelaeof stroke and dysphagia are common indications fora PEG.59,66 Whether these patients aspirate duringthe procedure itself, or aspirate their own secretionsor feeds, is difficult to ascertain. Pneumoperitoneumis typically a benign occurrence, which has beenreported in up to 38% of patients undergoinguncomplicated PEG.78-80

Bleeding can result from injury to gastric orabdominal wall vessels.59 Gastric tears may occurduring PEG placement.59,66 Because PEG placementinvolves the essentially blind placement of a needlethrough the abdominal wall and into the stomach,injury to internal organs, such as the liver andcolon,81-83 can occur. Numerous authors have report-ed cologastrocutaneous fistulae.81-83,85-92 These fistu-lae can remain silent until the original PEG tube isexchanged for a replacement tube. In the chronic set-ting, prompt removal of the tube has been recom-mended as the fistula is reported to heal withinhours.93 Optimal management of colonic perforationin the acute setting is poorly studied, though surgeryshould be considered in patients with clinical evi-dence of perforation or severely malnourishedpatients who are at risk for poor wound healing.81

Feeding tubes may also migrate and becomeimpacted in the abdominal wall.94-96 This “buriedbumper syndrome” is believed to result from exces-sive traction on the internal PEG bolster. Ischemicnecrosis of the gastric epithelium occurs, with resul-tant erosion of the internal bolster through the gas-tric wall.94 Signs include resistance to flow throughthe tube and immobility of the tube. Endoscopically,the PEG may not be visible. Treatment involvesremoval of the tube and placement of a new tube.61

Some have advocated avoiding direct contactbetween the internal bolster and the gastricmucosa.97 Although it is important to maintainapposition of the gastric wall to the abdominal walluntil the fistula tract is mature, the externalbumper can be subsequently loosened in an attemptto avoid this complication.

Author Title


Many PEGs are placed for dysphagia secondaryto head and neck cancers. Several reports raise con-cern of potential facilitation of metastases as somepatients have metastases develop at the PEG inser-tion site.98-101 It is unclear whether this results fromhematogenous spread or through transport of exfoli-ated tumor cells by the feeding tube. One final com-plication to note is accidental tube dislodgement.Use of an abdominal binder after placement mayprevent accidental PEG removal.59 With early dis-lodgement, peritonitis may develop because there isnot a mature fistulous tract. If a mature tract is pre-sent (greater than 1 month), then a suitable replace-ment tube should be inserted as soon as possible.Foley catheters are readily available and effective.However, care must be taken to prevent duodenalobstruction by the balloon. Therefore, an externalbolster should be improvised.102 In patients inwhom it is unclear whether or not the track ismature, confirmation of correct replacement tubelocation should be confirmed with contrast injectionand fluoroscopy.

Although placement of a PEG/JET has the samecomplications as PEG, these tubes may be moreprone to clogging (4%-18%), unintentional removal(11%-18%), and tube migration (6%).103,104 Wolfsonet al.105 have reported tube dysfunction in 53% of 75patients during 275 days of follow-up. Nevertheless,the reduced risk of aspiration (estimated relativerisk reduction of 91% in a single observationalstudy)61 appears to justify use in carefully selectedpatients.

COMPLICATIONS OF ENDOSCOPIC FOREIGNBODY RETRIEVAL

Complications directly attributable to the endo-scopic removal of foreign bodies are very rare, andwhen complications occur it is difficult to determinewhether the cause was the endoscopy or the foreignobject itself.113 Nonetheless, endoscopic foreign bodyretrieval and meat disimpaction have been associat-ed with complications in up to 8% of cases.114,115

Additional techniques may decrease the risks asso-ciated with foreign body removal. The risk of aspira-tion or mucosal injury may be reduced by the use ofan esophageal overtube.112,116 Esophageal overtubeshave been associated with bleeding and perforation,and these risks should be weighed against the bene-fits of overtube use in each case.117 Mucosal injuryfrom the removal of sharp objects can be limited byremoving the object such that the point is trailing andby using an overtube.116,117 A latex hood fitted overthe end of the endoscope may also be beneficial inprotecting the mucosa from laceration.168 Blind pas-sage of bougies or use of papain (meat tenderizer) to

dislodge meat impaction should be avoided due to thesignificant risk of perforation.1 Endoscopically, it maybe possible to gently push an esophageal food bolusinto the stomach, particularly if the endoscope can bemaneuvered around the bolus under direct vision.117

To assess for mucosal lacerations, bleeding, andthe presence of underlying pathology (present inmost esophageal food impactions), reinsertion of theendoscope after foreign body clearance should beperformed.116 Most mucosal injuries can be treatedconservatively and bleeding that is not self-limitedcan be treated with standard endoscopic techniques.Failure of endoscopic removal occurs in less than 5%of cases and surgery should be considered.114

COMPLICATIONS IN THE TREATMENT OFESOPHAGEAL MALIGNANCIES

Injection of sclerosants such as ethanol directly intothe tumor to achieve tumor necrosis may damagenormal tissues because of tracking of the sclerosantalong tissue planes leading to perforation and thedevelopment of fistulae.122

Thermal methods to apply heat energy directly tothe tumor include bipolar cautery, laser, and argonplasma coagulation.123-125 Major complicationsinclude perforation and the development of fistulaein up to 10%.122,124,125 Minor complications includepain, edema, and treatment-induced strictures.123

Photodynamic therapy (PDT) complications aresimilar to the other ablative techniques (bleeding,perforation, fistulae, strictures) but also include sunphotosensitivity.124,126,127 Dysphagia may initiallyworsen after PDT requiring hospital admission forintravenous fluids, and PDT has been associatedwith atrial fibrillation and the development ofpleural effusions.124,126

Esophageal endoprostheses made of plastic or aself-expanding metal material have been used to re-establish luminal patency. The plastic stents havebeen replaced by the self-expanding metal stentsdue to the significantly lower complication rates.128

Postdeployment complications occur in 20% to 40%and include stent migration, hemorrhage, foodimpaction, and tumor ingrowth or overgrowth.121,129

Death is seen in 3% because of exsanguinating hem-orrhage, aspiration, and perforation.130 Chest painafter insertion occurs in approximately 20%.131,132

Pretreatment with chemoradiotherapy has beenreported to increase the incidence of complicationsby some authors133 but not others.134 An antirefluxstent is now available that may decrease refluxsymptoms, but whether it will decrease the risk ofaspiration is unknown.135

Endoscopic techniques and patient educationmay be useful in avoiding or managing complica-

Title Author


tions. Blind bougienage of malignant stricturesshould be avoided.120 Expandable stents are prefer-able to nonexpandable plastic stents.128 Stent occlu-sion caused by tumor ingrowth can be avoided byuse of a covered stent, and overgrowth treated withthermal ablative techniques or insertion of anotherstent.130,136 Laser, APC, or PDT-induced stricturescan be treated with dilation or placement of astent.123,125,126 Patients with stents that cross theGE junction should keep the head of the bed raisedto 30 degrees and avoid eating for several hoursbefore retiring. Patients undergoing PDT are at riskfor phototoxicity and need to use sunscreen andavoid direct sunlight exposure for up to 6 weeks.121

COMPLICATIONS OF ENDOSCOPICHEMOSTASIS: ENDOSCOPIC VARICEAL

SCLEROTHERAPY

Treatment of esophageal varices by sclerotherapy(EVS) is acknowledged to have several potentialcomplications. These may be local (esophageal)and/or systemic. The overall rate of complications isdifficult to ascertain because endoscopic series havevaried by technique, sclerosant, and follow-up.137

The overall complication rate has been estimated tobe between 35% to 78%, with a mortality rate of 1%to 5%.138,139

It has been estimated that ulcerations secondaryto EVS occur in 50% to 78%.140,141 Significant bleed-ing can occur in 6% of these patients.141 Most ofthese ulcers are asymptomatic but can be diagnosedby endoscopy 4 to 7 days after an EVS session. Ulcerformation does not appear to correlate with thechoice of sclerosant or injection technique. They mayoccur more often if sclerotherapy sessions are con-ducted in closely timed (<1 week) sessions.142,143

Therefore elective EVS sessions for variceal eradi-cation should be planned on a weekly or greaterinterval. Unfortunately, it does not appear that anti-secretory therapy (H2RAs, PPIs) or sucralfate pre-vent ulcer formation.144-147 Omeprazole may beeffective in healing these ulcerations.148,149

Esophageal perforation may occur acutely in 2%to 5% of patients shortly after EVS.150 Delayed per-foration is known to occur, but the incidence isunknown. Early diagnosis may be difficult because25% to 50% of patients undergoing EVS have chestpain develop. However, this symptom usually abateswithin 24 to 48 hours.151

Esophageal stricture formation can occur weeksto months after EVS sessions in 2% to 20% ofpatients.152,153 This can be diagnosed by upper gas-trointestinal series and/or endoscopy. When EVS isperformed with paravariceal injection with polido-canol, stricture formation appears to correlate with

the number of EVS sessions and the amount of scle-rosant used.154 There are no data on other scle-rosant use and technique affecting stricture forma-tion. Treatment is similar to that of benign pepticstrictures, with endoscopic dilation.

Up to 5% of patients may experience aspirationpneumonia after EVS.153-156 This complication usu-ally occurs during emergent sessions for varicealbleeding. The endoscopist should have a low thresh-old for airway protection (endotracheal intubation)in patients with altered mental status and/or signif-icant hemetemesis. Other commonly reported com-plications related to EVS include pleural effusionand bacterial peritonitis.

ENDOSCOPIC BAND LIGATION

Endoscopic band ligation (EBL) has emerged as thepreferred endoscopic intervention for the treatmentof esophageal varices. This is in part because of itsfavorable side effect profile as compared with EVS.Esophageal ulcer formation is seen in 5% to 15% andthere is a lower tendency for ulcer-related bleedingthan EVS.153,155-158 Perforation has been reported in0.7% of 284 patients in 5 randomized trials.153,155-157

These perforations were associated with use of anovertube for facilitating multiple endoscope passes.Overtube use for this purpose is now discouragedand with multibanding devices, generally unneces-sary. However, passing the overtube over anesophageal bougie may decrease the rate of perfora-tion. Esophageal stricture formation as a conse-quence of EBL is rare. No strictures were reported in8 randomized trials.153,155-158 Only single cases havebeen presented in the literature.159,160 The true inci-dence of this complication is unknown.

Aspiration pneumonia was seen in 1% of patientsamong 7 randomized trials.153,155-158 These 7 trialsshowed a bacterial peritonitis rate of 4%. The over-all mortality attributable to the acute complicationsof ligation in prospective trials is 1%.

ENDOSCOPIC NONVARICEAL HEMOSTASIS

Endoscopic hemostasis of nonvariceal bleeding ismost often achieved by injection and/or thermalelectrocoagulation. Injection of sclerosants (tradi-tionally used for sclerotherapy) may lead to tissuenecrosis and rarely perforation.161 The most com-monly used injection agent is epinephrine. No perfo-rations have been reported in patients treated withepinephrine injection for bleeding ulcers in random-ized trials. However, tissue necrosis and ulcerationmay occur with decreased arterial blood flow to theinjected site.162,163

Endoscopic thermal hemostasis may be achievedby bipolar or multipolar electrocoagulation (MPEC),

Author Title


heater probes, or laser. Randomized controlled trialsusing MPEC have reported rates of perforationbetween 0% and 2%.164,165

Induction of bleeding is a relatively common com-plication of electrocoagulation, occurring in up to 5%of cases.164,165 Usually this can be controlled duringthe endoscopic procedure.

Hemostasis using a heater probe has similarrates of perforation as MPEC. However, repeattreatment when performed within 24 to 48 hours ofthe initial session is associated with up to 4% risk ofperforation.166 Recurrent bleeding rates are similarto that of MPEC.

SUMMARY

Endoscopic complications will inevitably occur if anendoscopist does many procedures. Knowledge ofpotential complications and their expected frequen-cy can lead to improved risk-benefit analysis byphysicians and patients as well as true informedconsent by patients. Early recognition of complica-tions and prompt intervention may minimizepatient morbidity.

REFERENCES

1. Silvis SE, Nebel O, Rogers G, Sugawa C, Mandelstam P.Endoscopic complications. Results of the 1974 AmericanSociety for Gastrointestinal Endoscopy Survey. JAMA1976;235:928.

2. Benjamin SB. Complications of conscious sedation. Gastro-intest Endosc Clin N Amer 1996;6:2.

3. Arrowsmith JB, Gerstman BB, Fleischer DE, Benjamin SB.Results from the American Society for GastrointestinalEndoscopy/U.S. Food and Drug Administration collaborativestudy on complication rates and drug use during gastroin-testinal endoscopy. Gastrointest Endosc 1991;37:421.

4. Barkin JS, Krieger B, Blinder M, Bosch-Blinder L, GoldbergRI, Phillips RS. Oxygen desaturation and changes inbreathing pattern in patients undergoing colonoscopy andgastroscopy. Gastrointest Endosc 1989;35:526.

5. Dark DS, Campbell DR, Wesselius LJ. Arterial oxygendesaturation during gastrointestinal endoscopy. Am JGastroenterol 1990;85:1317.

6. ASGE. Modifications in endoscopic practice for the elderly.Gastrointest Endosc 2000;52:849-51.

7. Brown, RD, Goldstein JL. Quality assurance in the endos-copy unit: an emphasis on outcomes. Gastrointest EndoscClin North Am 1999;9:4.

8. ASGE. Sedation and monitoring of patients undergoing gas-trointestinal endoscopic procedures. Gastrointest Endosc1995;42:626-9.

9. ASGE. Establishment of gastrointestinal endoscopy areas.Gastrointest Endosc 1999;50:910-12.

10. ASGE. Monitoring equipment for endoscopy. GastrointestEndosc 1995;42:615-7.

11. Baltch AL, Buhac I, Agrawal A, O’Connor P, Bram M,Malatino E. Bacteremia after upper gastrointestinal endos-copy. Arch Intern Med 1977;137:594.

12. Botoman VA, Surawicz CM. Bacteremia with gastrointesti-nal endoscopic procedures. Gastrointest Endosc 1986;32:342.

13. Norfleet RG, Mitchell PD, Nulholland DD, Philo J. Does bac-teremia follow upper gastrointestinal endoscopy? Am JGastroenterol 1981;76:420.

14. Mogadam M, Malhotra SK, Jackson RA. Pre-endoscopicantibiotics for the prevention of bacterial endocarditis: do weuse them appropriately? Am J Gastroenterol 1994;89:832.

15. ASGE. Antibiotic prophylaxis for gastrointestinal endos-copy. Gastrointest Endosc 1995;42:630-5.

16. Carmody TJ, Wergowske GL. Retropharyngeal abscess andhematoma in an elderly woman following esophagoscopyand endotracheal intubation. J Am Geriatr Soc 1983;31:499.

17. Enat R, Levitan R. Retroesophageal abscess twenty-fivedays after esophagoscopy. An unusual complication ofendoscopy. Gastrointest Endosc 1972;18:167.

18. ASGE. Infection control during gastrointestinal endoscopy.Gastrointest Endosc 1999;49:836-41.

19. ASGE. Transmission of infection by gastrointestinal endos-copy. Gastrointest Endosc 2001;54:824-8.

20. Pettersson G, Larsson S, Gatzinsky P, Sudow G.Differentiated treatment of intrathoracic oesophageal per-forations. Scand J Thorac Cardiovasc Surg 1981;15:321.

21. Schulze S, Pedersen VM, Hoier-Madsen K. Iatrogenic perfo-ration of the esophagus. Acta Chirurgica Scandinavia1982;148:679.

22. Wychulis AR, Fontana RS, Payne WAS. Instrumental perfo-ration of the esophagus. Dis Chest 1969;55:184.

23. Larsen K, Jensen BS, Axelsen F. Perforation and rupture ofthe esophagus. Scand J Thorac Cardiovasc Surg 1983;17:311.

24. Lanza FL, Graham DY. Bougienage is effective therapy formost benign esophageal strictures. JAMA 1978;240:844-7.

25. Patterson DJ, Graham DY, Smith L, Schwartz JT, Alpert E,Lanza FL, et al. Natural history of benign esophageal stric-ture treated by dilation. Gastroenterology 1983;85:346-50.

26. Cox JG, Winter RK, Maslin SC, Jones R, Buckton GK, HoareRC, et al. Balloon or bougie for dilatation of benignoesophageal stricture? An interim report of a randomizedcontrolled trial. Gut 1988;29:1741-7.

27. Shemesh E, Czerniak A. Comparison between Savary-Gilliard and balloon dilatation of benign esophageal stric-tures. World J Surg 1990;14:518-22.

28. Cox JGC, Winter RK, Maslin SC, Dakkak M, Jones R,Buckton GK, et al. Balloon or bougie for dilatation of benignesophageal stricture. Dig Dis Sci 1994;39:776-81.

29. Saeed ZA, Winchester CB, Ferro PS, Michaletz PA, SchwartzJT, Graham DY. Prospective randomized comparison ofpolyvinyl bougies and through-the-scope balloon for dilationof peptic strictures of the esophagus. Gastrointest Endosc1995;41:189-95.

30. Hernandez LJ, Jacobson JW, Harris MS. Comparison amongthe perforation rates of Maloney, balloon and Savary dila-tion of esophageal strictures. Gastrointest Endosc 2000;51:460-2.

31. Yamamoto H, Hughes RW, Schroeder KW, Viggiano TR,DiMagno EP. Treatment of benign esophageal stricture byEder-Puestow or balloon dilators: a comparison betweenrandomized and prospective nonrandomized trials. MayoClin Proc 1992;67:228-36.

32. Clouse RE. Complications of endoscopic gastrointestinaldilation techniques. Gastrointest Endosc Clin NA 1996;6:323-41.

33. Karnak I, Tanyel FC, Buyukpamukcu N, Hicsonmez A.Esophageal perforations encountered during the dilation ofcaustic esophageal strictures. J Cardiovasc Surg 1998;39:373-7.

34. Fregonese D, Di Faco G, Di Toma F. Balloon dilatation of

Title Author


anastomotic intestinal stenoses: long term results. Endos-copy 1990;22:249-53.

35. Ikeya T, Ohwada S, Ogawa T, Tanahashi Y, Takeyoshi I,Koyama T, et al. Endoscopic balloon dilation for benignesophageal anastomotic stricture: factors influencing itseffectiveness. Hepatogastroenterology 1999;46:959-66.

36. Honkoop P, Siersema PD, Tilanus HW, Stassen LPS, HopWCJ, van Blankenstein M. Benign anastomotic stricturesafter transhiatal esophagectomy and cervical esophagogas-trostomy: risk factors and management. J ThoracCardiovasc Surg 1996;111:1141-8.

37. Pereira-Lima JC, Ramires RP, Zamin I, Cassal AP, MarroniCA, Mattos AA. Endoscopic dilation of benign esophagealstrictures: report on 1043 procedures. Am J Gastroenterol1999;94:1497-501.

38. Anderson PE, Cook A, Amery AH. A review of the practice offiberoptic endoscopic dilatation of oesophageal stricture.Ann R Coll Surg Engl 1989;71:124-7.

39. Neuhaus H, Hoffman W, Dittler HJ, Niedermeyer HP,Classen M. Implantation of self-expanding esophagealmetal stents for palliation of malignant dysphagia.Endoscopy 1992;24:405-10.

40. Newcomer MK, Brazer SR. Complications of upper gas-trointestinal endoscopy and their management. Gastro-intest Endosc Clin N Am 1994;4:551-70.

41. Van Dam J, Rice TW, Catalano MF, Kirby T, Sivak MV Jr.High-grade malignant stricture is predictive of esophagealtumor stage. Risks of endosonographic evaluation. Cancer1993;71:2910-17.

42. Swaroop VS, Desai DC, Mohandas KM, Dhir V, Dave UR,Gulla RI, et al. Dilation of esophageal strictures induced byradiation therapy for cancer of the esophagus. GastrointestEndosc 1994;40:311-5.

43. Ng TM, Spencer GM, Sargeant IR, Thorpe SM, Brown SG.Management of strictures after radiotherapy for esophagealcancer. Gastrointest Endosc 1996;43:584-90.

44. Eckardt VF, Kanzler G, Westermeier T. Complications andtheir impact after pneumatic dilation for achalasia: prospec-tive long-term follow-up study. Gastrointest Endosc 1997;45:349-53.

45. Nair LA, Reynolds JC, Parkman HP, Ouyang Q, Strom BL,Rosato EF, et al. Complications during pneumatic dilationfor achalasia or diffuse esophageal spasm: analysis of riskfactors, early clinical characteristics, and outcome. Dig DisSci 1993;38:1893-904.

46. Kadakia SC, Wong RKH. Graded pneumatic dilation usingRigiflex achalasia dilators in patients with primaryesophageal achalasia. Am J Gastroenterol 1993;88:34-8.

47. Molina EG, Stollman N, Grauer L, Reiner DK, Barkin JS.Conservative management of esophageal nontransmuraltears after pneumatic dilation for achalasia. Am J Gastro-enterol 1995;91:15-8.

48. Kozarek RA, Botoman VA, Patterson DJ. Long-term follow-up in patients who have undergone balloon dilation for gas-tric outlet obstruction. Gastrointest Endosc 1990;36:558-61.

49. DiSario JA, Fennerty MB, Tietze CC, Hutson WR, Burt RW.Endoscopic balloon dilation for ulcer-induced gastric outletobstruction. Am J Gastroenterol 1994;89:868-71.

50. Kuwada SK, Alexander GL. Long-term outcome of endo-scopic dilation of nonmalignant pyloric stenosis. Gastro-intest Endosc 1995;41:15-7.

51. Misra SP, Dwivedi M. Long-term follow-up of patientsundergoing balloon dilation for benign pyloric stenosis.Endoscopy 1996;28:552-4.

52. Hewitt PM, Krige JEJ, Funnell IC, Wilson C, Bornman PC.

Endoscopic balloon dilatation of peptic pyloroduodenalstrictures. J Clin Gastroenterol 1999;28:33-5.

53. Boylan JJ, Gradzka MI. Long-term results of endoscopicballoon dilatation for gastric outlet obstruction. Dig Dis Sci1999;44:1883-6.

54. Scolapio JS, Pasha TM, Gostout CJ, Mahoney DW,Zinsmeister AR, Ott BJ, et al. A randomized prospectivestudy comparing rigid to balloon dilators for benignesophageal strictures and rings. Gastrointest Endosc 1999;50:13-7.

55. Sawyer R, Phillips C, Vakil N. Short- and long-term outcomeof esophageal perforation. Gastrointest Endosc 1995;41:130-4.

56. Miller RE, Bossart PW, Tiszdnkel HI. Surgical managementof complications of upper gastrointestinal endoscopy andesophageal dilation including laser therapy. Am Surg1987;53:667-71.

57. Gauderer MW, Ponsky JL, Izant RJ Jr. Gastrostomy withoutlaparotomy: a percutaneous endoscopic technique. J PediatrSurg 1980;15:872-5.

58. Amann W, Mischinger HJ, Berger A, Rosanelli G, SchweigerW, Werkgartner G. Percutaneous endoscopic gastrostomy(PEG). 8 years of clinical experience in 232 patients. SurgEndosc 1997;11:741-4.

59. Larson DE, Burton DD, Schroeder KW, DiMagno EP.Percutaneous endoscopic gastrostomy. Indications, success,complications, and mortality in 314 consecutive patients.Gastroenterology 1987;93:48-52.

60. Akkersdijk WL, van Bergeijk JD, van Egmond T, Mulder CJ,van Berge Henegouwen GP, van der Werken C.Percutaneous endoscopic gastrostomy (PEG): comparison ofpush and pull methods and evaluation of antibiotic prophy-laxis. Endoscopy 1995;27:313-6.

61. Mathus-Vliegen LM, Koning H. Percutaneous endoscopicgastrostomy and gastrojejunostomy: a critical reappraisal ofpatient selection, tube function and the feasibility of nutri-tional support during extended follow-up. GastrointestEndosc 1999;50:746-54.

62. Foutch PG, Haynes WC, Bellapravalu S, Sanowski RA.Percutaneous endoscopic gastrostomy (PEG). A new proce-dure comes of age. J Clin Gastroenterol 1986;8:10-5.

63. Rabeneck L, Wray NP, Petersen NJ. Long-term outcomes ofpatients receiving percutaneous endoscopic gastrostomytubes. J Gen Int Med 1996;11:287-93.

64. Wolfsen HC, Kozarek RA, Ball TJ, Patterson DJ, BotomanVA, Ryan JA. Long-term survival in patients undergoingpercutaneous endoscopic gastrostomy and jejunostomy. AmJ Gastroenterol 1990;85:1120-2.

65. Hull MA, Rawlings J, Murray FE, Field J, McIntyre AS,Mahida YR, et al. Audit of outcome of long-term enteralnutrition by percutaneous endoscopic gastrostomy. Lancet1993;341:869-72.

66. Panos MZ, Reilly H, Moran A, Reilly T, Wallis PJ, Wears R,et al. Percutaneous endoscopic gastrostomy in a generalhospital: prospective evaluation of indications, outcome, andrandomised comparison of two tube designs. Gut 1994;35:1551-6.

67. Llaneza PP, Menendez AM, Roberts R, Dunn GD.Percutaneous endoscopic gastrostomy: clinical experienceand follow-up. South Med J 1988;81:321-4.

68. Jonas SK, Neimark S, Panwalker AP. Effect of antibioticprophylaxis in percutaneous endoscopic gastrostomy. Am JGastroenterol 1985;80:438-41.

69. Jain NK, Larson DE, Schroeder KW, Burton DD, CannonKP, Thompson RL, et al. Antibiotic prophylaxis for percuta-

Author Title


neous endoscopic gastrostomy. A prospective, randomized,double-blind clinical trial. Ann Int Med 1987;107:824-8.

70. Gossner L, Keymling J, Hahn EG, Ell C. Antibiotic prophy-laxis in percutaneous endoscopic gastrostomy (PEG): aprospective randomized clinical trial. Endoscopy 1999;31:119-24.

71. Preclik G, Grune S, Leser HG, Lebherz J, Heldwein W,Machka K, et al. Prospective, randomised, double blind trialof prophylaxis with single dose of co-amoxiclav before per-cutaneous endoscopic gastrostomy. BMJ 1999;319:881-4.

72. Dormann AJ, Wigginghaus B, Risius H, Kleimann F,Kloppenborg A, Grunewald T, et al. A single dose of ceftri-axone administered 30 minutes before percutaneous endo-scopic gastrostomy significantly reduces local and systemicinfective complications. Am J Gastroenterol 1999;94:3220-4.

73. Kulling D, Sonnenberg A, Fried M, Bauerfeind P. Costanalysis of antibiotic prophylaxis for PEG. GastrointestEndosc 2000;51:152-6.

74. Haas DW, Dharmaraja P, Morrison JG, Potts JR.Necrotizing fasciitis following percutaneous endoscopic gas-trostomy. Gastrointest Endosc 1988;34:487-8.

75. Greif JM, Ragland JJ, Ochsner MG, Riding R. Fatal necro-tizing fasciitis complicating percutaneous endoscopic gas-trostomy. Gastrointest Endosc 1986;32:292-4.

76. Cave DR, Robinson WR, Brotschi EA. Necrotizing fasciitisfollowing percutaneous endoscopic gastrostomy. Gastro-intest Endosc 1986;32:294-6.

77. Person JL, Brower RA. Necrotizing fasciitis/myositis follow-ing percutaneous endoscopic gastrostomy. GastrointestEndosc 1986;32:309.

78. Plumser AB, Gottfried EB, Clair MR. Pneumoperitoneumafter percutaneous endoscopic gastrostomy. Am J Gastro-enterol 1984;79:440-1.

79. Stassen WN, McCullough AJ, Marshall JB, Eckhauser ML.Percutaneous endoscopic gastrostomy: another cause of“benign” pneumoperitoneum. Gastrointest Endosc 1984;30:296-8.

80. Gottfried EB, Plumser AB, Clair MR. Pneumoperitoneumfollowing percutaneous endoscopic gastrostomy. A prospec-tive study. Gastrointest Endosc 1986;32:397-9.

81. Maccabee DL, Dominitz JA, Lee SW, Billingsley KG. Acutepresentation of transverse colon injury following percuta-neous endoscopic gastrostomy tube placement: case reportand review of current management. Surg Endosc 2000;14:296.

82. van Gossum A, DesMarez B, Cremer M. A colo-cutaneous-gastric fistula: a silent and unusual complication of percu-taneous endoscopic gastrostomy. Endoscopy 1988;20:161.

83. Minocha A, Rupp TH, Jaggers TL, Rahal PS. Silent colo-gas-trocutaneous fistula as a complication of percutaneous endo-scopic gastrostomy. Am J Gastroenterol 1994;89:2243-4.

84. Foutch PG, Talbert GA, Waring JP, Sanowski RA.Percutaneous endoscopic gastrostomy in patients with priorabdominal surgery: virtues of the safe tract. Am JGastroenterol 1988;83:147-50.

85. Bui HD, Dang CV, Schlater T, Nghiem CH. A new complica-tion of percutaneous endoscopic gastrostomy. Am JGastroenterol 1988;83:448-51.

86. Miller RE, Castlemain B, Lacqua FJ, Kotler DP.Percutaneous endoscopic gastrostomy. Results in 316patients and review of literature. Surg Endosc 1989;3:186-90.

87. Ponsky JL, Gauderer MW, Stellato TA, Aszodi A.Percutaneous approaches to enteral alimentation. Am JSurg 1985;149:102-5.

88. Stefan MM, Holcomb GWd, Ross AJ. Cologastric fistula as a

complication of percutaneous endoscopic gastrostomy. Jpn:J Parenteral Enteral Nutr 1989;13:554-6.

89. Marion MT, Zweng TN, Strodel WE. One-stage gastrostomybutton: an assessment. Endoscopy 1994;26:666-70.

90. Saltzberg DM, Anand K, Juvan P, Joffe I. Colocutaneous fis-tula: an unusual complication of percutaneous endoscopicgastrostomy. Jpn: J Parenteral Enteral Nutr 1987;11:86-7.

91. Murphy S, Pulliam TJ, Lindsay J. Delayed gastrocolic fistu-la following percutaneous endoscopic gastrostomy (PEG). JAm Geriatr Soc 1991;39:532-3.

92. Fernandes ET, Hollabaugh R, Hixon SD, Whitington G. Latepresentation of gastrocolic fistula after percutaneous gas-trostomy. Gastrointest Endosc 1988;34:368-9.

93. Gauderer MW, Stellato TA. Gastrostomies: evolution, tech-niques, indications, and complications. Curr Problems Surg1986;23:657-719.

94. Klein S, Heare BR, Soloway RD. The “buried bumper syn-drome”: a complication of percutaneous endoscopic gastros-tomy. Am J Gastroenterol 1990;85:448-51.

95. Behrle KM, Dekovich AA, Ammon HV. Spontaneous tubeextrusion following percutaneous endoscopic gastrostomy.Gastrointest Endosc 1989;35:56-8.

96. Shallman RW, NorFleet RG, Hardache JM. Percutaneousendoscopic gastrostomy feeding tube migration andimpaction in the abdominal wall. Gastrointest Endosc1988;34:367-8.

97. Foutch PG, Woods CA, Talbert GA, Sanowski RA. A criticalanalysis of the Sacks-Vine gastrostomy tube: a review of 120consecutive procedures. Am J Gastroenterol 1988;83:812-5.

98. Meurer MF, Kenady DE. Metastatic head and neck carcino-ma in a percutaneous gastrostomy site. Head Neck 1993;15:70-3.

99. Preyer S, Thul P. Gastric metastasis of squamous cell carci-noma of the head and neck after percutaneous endoscopicgastrostomy—report of a case. Endoscopy 1989;21:295.

100. Huang DT, Thomas G, Wilson WR. Stomal seeding by per-cutaneous endoscopic gastrostomy in patients with headand neck cancer. Arch Otolaryngol—Head Neck Surg 1992;118:658-9.

101. Bushnell L, White TW, Hunter JG. Metastatic implantationof laryngeal carcinoma at a PEG exit site. GastrointestEndosc 1991;37:480-2.

102. Kirtley DW, Willis MJ, Thomas E. Reducing PEG woundproblems. Gastrointest Endosc 1987;33:51-2.

103. DeLegge MH, Duckworth PF Jr, McHenry L Jr, Foxx-Orenstein A, Craig RM, Kirby DF. Percutaneous endoscopicgastrojejunostomy: a dual center safety and efficacy trial[published erratum appears in Jpn J Parenter Enteral Nutr1995 Jul-Aug;19:329]. Jpn: J Parenteral Enteral Nutr 1995;19:239-43.

104. DeLegge MH, Patrick P, Gibbs R. Percutaneous endoscopicgastrojejunostomy with a tapered tip, nonweighted jejunalfeeding tube: improved placement success. Am J Gastro-enterol 1996;91:1130-4.

105. Wolfsen HC, Kozarek RA, Ball TJ, Patterson DJ, BotomanVA. Tube dysfunction following percutaneous endoscopicgastrostomy and jejunostomy. Gastrointest Endosc 1990;36:261-3.

106. Henderson JM, Strodel WE, Gilinsky NH. Limitations ofpercutaneous endoscopic jejunostomy. Jpn: J ParenteralEnteral Nutr 1993;17:546-50.

107. Shike M, Schroy P, Ritchie MA, Lightdale CJ, Morse R.Percutaneous endoscopic jejunostomy in cancer patientswith previous gastric resection. Gastrointest Endosc 1987;33:372-4.

Title Author


108. Shike M, Berner YN, Gerdes H, Gerold FP, Bloch A, SessionsR, et al. Percutaneous endoscopic gastrostomy and jejunosto-my for long-term feeding in patients with cancer of the headand neck. Otolaryngol—Head Neck Surg 1989;101:549-54.

109. Shike M, Wallach C, Likier H. Direct percutaneous endo-scopic jejunostomies. Gastrointest Endosc 1991;37:62-5.

110. Shike M, Latkany L, Gerdes H, Bloch AS. Direct percuta-neous endoscopic jejunostomies for enteral feeding.Gastrointest Endosc 1996;44:536-40.

111. Rumalla A, Baron TH. Results of direct percutaneous endo-scopic jejunostomy, an alternative method for providingjejunal feeding. Mayo Clinic Proceedings 2000;75:807-10.

112. ASGE. ASGE Guideline for the management of ingested for-eign bodies. Gastrointest Endosc 1995;42:622-5.

113. Webb WA. Management of foreign bodies of the upper gas-trointestinal tract: update. Gastrointest Endosc 1995;41:39-51.

114. Vizcarrondo FJ, Brady PG, Nord HJ. Foreign bodies of theupper gastrointestinal tract. Gastrointest Endosc 1983;29:208-10.

115. Berggreen PJ, Harrison ME, Sanowski RA, Ingebo K,Noland B, Zierer S. Techniques and complications ofesophageal foreign body extraction in children and adults.Gastrointest Endosc 1993;39:626-30.

116. Ginsberg GG. Management of ingested foreign objects andfood bolus impactions. Gastrointest Endosc 1995;41:33-8.

117. Carr-Locke DL, Al-Kawas FH, Branch MS, Byrne WJ,Edmundowicz SA, Jamidar PA, et al. Overtube use in gas-trointestinal endoscopy. Gastrointest Endosc 1996;44:767-70.

118. Faigel DO, Fennerty MB. Miscellaneous diseases of theesophagus. In: Yamada T, editor. Textbook of gastroenterolo-gy. Philadelphia: Lippincott Williams & Wilkins; 1999. p.1304-25.

119. Cooper GS, Blades EW. Indications, contraindications andcomplications of upper gastrointestinal endoscopy. In: SivakMV Jr, editor. Gastroenterologic endoscopy. Philadelphia:WB Saunders; 2000. p. 438-54.

120. Hernandez LJ, Jacobson JW, Harris MS. Comparison amongthe perforation rates of Maloney, balloon and Savary dila-tion of esophageal strictures. Gastrointest Endosc 2000;51:460-1.

121. Lightdale CJ. Esophageal cancer. Am J Gastroenterol 1999;94:20-9.

122. Carazzone A, Bonavina L, Segalin A, Ceriani C, Peracchia A.Endoscopic palliation of oesophageal cancer: results of aprospective comparison of Nd:YAG laser and ethanol injec-tion. Eur J Surg 1999;165:351-6.

123. Jensen DM, Machicado G, Randall G, Tung LA, English-Zych S. Comparison of low-power YAG laser and BICAPtumor probe for palliation of esophageal cancer strictures.Gastroenterol 1988;94:1263-70.

124. Carr-Locke DL, Conn MI, Faigel DO, Laing K, Leung JW,Mills M, et al. Developments in laser technology. Gastro-intest Endosc. In press.

125. Heindorff H, Wojdemann M, Svendsen LB. Endoscopic pallia-tion of inoperable cancer of the oesophagus or cardia by argonelectrocoagulation. Scan J Gastroenterol 1998;33:21-3.

126. Overholt BF, Panjehpour M, Haydek JM. Photodynamictherapy for Barrett’s esophagus: follow-up in 100 patients.Gastrointest Endosc 1999;49:1-7.

127. Maier A, Tomaselli F, Gebhard F, Rehak P, Smolle J, Smolle-Juttner FM. Palliation of advanced esophageal carcinomaby photodynamic therapy and irradiation. Ann Thorac Surg2000;69:1006-9.

128. Knyrim K, Wagner HJ, Bethge N, Keymling M, Vakil N. A

controlled trial of an expansile metal stent for palliation ofesophageal obstruction due to inoperable cancer. N Engl JMed 1993;329:1302-7.

129. Carr-Locke DL, Branch MS, Byrne WJ, Conn MI, Laing K,Nelson DB, et al. Stents for gastrointestinal strictures.Gastrointest Endosc 1998;47:588-93.

130. Faigel DO. Endoscopy for the diagnosis and management ofesophageal cancer. ASGE Clinical Update 2000;8:1-4.

131. Bartelsman JFW, Bruno MJ, Jensema AJ, Haringsma J,Reeders JWAJ, Tytgat GNJ. Palliation of patients withesophagogastric neoplasms by insertion of a coveredexpandable modified Gianturco-Z endoprosthesis: exper-inces in 153 patients. Gastrointest Endosc 2000;51:134-8.

132. Siersema PD, Hop WCJ, van Blankenstein M, Dees J. A newmetal stent (Flamingo stent) for palliation of malignantdysphagia: a prospective study. Gastrointest Endosc2000;51:139-45.

133. Kinsman KJ, DeGregorio BT, Katon RM, Morrison K, SaxonRR, Keller FS, Rösch J. Prior radiation and chemotherapyincrease the risk of life-threatening complications afterinsertion of metallic stents for esophagogastric malignancy.Gastrointest Endosc 1996;43:196-203.

134. Raijman I, Siddique I, Lynch P. Does chemoradiation thera-py increase the incidence of complications with self-expand-ing coated stents in the management of malignantesophageal strictures. Am J Gastroenterol 1997;92:2192-6.

135. Dua KS, Kozarek RA, Kim JP, Evans J, Hogan WJ, ShakerR. Anti-reflux self-expanding metal esophageal stent: clini-cal evaluation in patients. Gastrointest Endosc 2000;51:AB118.

136. Raijman I, Siddique I, Ajani J, Lynch P. Palliation of malig-nant dysphagia and fistulae with coated expandable metalstents: experience in 101 patients. Gastrointest Endosc1998;48:172-9.

137. Sanowski RA, Waring JP. Endoscopic techniques and com-plications in variceal sclerotherapy. J Clin Gastroenterol1987;9:504-13.

138. Schuman BM, Beckman JW, Tedesco FJ, Griffin JW Jr,Assad RT. Complications of endoscopic injection sclerother-apy. A review. Am J Gastroenterol 1987;82:823-30.

139. Zambelli A, Arcidiacano PG, Arcidiacano R et al.Complications of endoscopic variceal sclerotherapy (EVS): amulticenter study of 1192 patients. Gastroenterology 1993;104:1023.

140. Sarin S, Nanda R, Scahdev G, Chari S, Anand BS, Broor SL.Intravariceal versus paravariceal slcerotherapy: a prospec-tive, controlled, randomized trial. Gut 1986;28:657-62.

141. Piai G, Cipolletta L, Claar M, Marone G, Bianco MA, ForteG, et al. Prophylactic sclerotherapy of high risk esophagealvarices: results of a multicentric prospective controlledtrial. Hepatology 1988;8:1495-507.

142. Sarin S, Sachdev G, Nanda R, Batra SK, Anand BS.Comparison of two time schedules for endoscopic scle-rotherapy: a prospective randomized controlled study. Gut1986;27:710-6.

143. Westaby D, Melia W, McDougall B, Hegarty JE, Williams R.Injection sclerotherapy for oesophageal varices: a prospec-tive randomised trial of different schedules. Gut 1984;25:129-35.

144. Tabibian N, Smith J, Graham D. Sclerotherapy–associatedesophageal ulcers: lessons from a double-blind, randomisedcomparison of sucralfate suspension versus placebo.Gastrointest Endosc 1989;35:312-7.

145. Poison RJ, Westaby D, Gimson, AE Hayes PC, Stellon AJ,Hayllar K, et al. Sucralfate for the prevention of early

Author Title


rebleeding following injection sclerotherapy for esophagealvarices. Hepatology 1989;10:279-87.

146. Tamura S, Shiozaki H, Kabayashi K, Yano H, Tahara H,Miyata M, et al. Prospective randomized study on the effectof ranitidine against injection ulcer after endoscopic injec-tion sclerotherapy for esophageal varices. Am J Gastro-enterol 1991;86:477.

147. Garg PK, Sidhu SS, Bhargava DK. Role of omeprazole inprevention and treatment of postendoscopic variceal scle-rotherapy esophageal complications. Double-blind random-ized study. Dig Dis Sci 1995;40:1569.

148. Gimson A, Poison R, Westaby D, Williams R. Omeprazole inthe management of intractable esophageal ulceration fol-lowing injection sclerotherapy. Gastroenterology 1990;99:1829.

149. Johlin FC, Labrecque DR, Neil GA. Omeprazole healsmucosal ulcers associated with endoscopic injection scle-rotherapy. Dig Dis Sci 1992;37:1373.

150. Copenhagen Esophageal Varices Sclerotherapy Project.Sclerotherapy after first variceal hemorrhage in cirrhosis. NEngl J Med 1984;311:1594.

151. Heaton ND, Howard ER. Complications and limitations ofinjection sclerotherapy in portal hypertension. Gut 1993;34:7-10.

152. Koch H, Henning H, Grimm H, Soehendra N. Prophylacticsclerosing of esophageal varices-results of a prospective con-trolled study. Endoscopy 1986;18:40.

153. Steigmann GV, Goff JS, Michaletz-Onody PA, Korula J,Lieberman D, Saeed ZA, et al. Endoscopic sclerotherapy ascompared with endoscopic ligation for bleeding esophagealvarices. N Engl J Med 1992;326:1527.

154. Sorenson T, Burcharth F, Pedersen ML, Findahl F.Esophageal stricture and dysphagia after endoscopic scle-rotherapy for bleeding varices. Gut 1984;25:473.

155. Jensen DM, Kovacs TOG, Randall GM, et al. Initial resultsof a randomized prospective study of emergency banding vssclerotherapy for bleeding gastric or esophageal varices.Gastrointest Endosc 1993;88:1493.

156. Laine L, El-Newihi HM, Migikovsky B, Sloane R, Garcia F.Endoscopic ligation compared with sclerotherapy for thetreatment of bleeding esophageal varices. Ann Int Med1993;119:1.

157. Lo GH, Lai KH, Cheng JS, Hwu JH, Chang CF, Chen SM, etal. A prospective randomized trial of sclerotherapy versusligation in the management of bleeding esophageal varices.Hepatology 1995;22:466.

158. Young MF, Sanowski RA, Rasche R. Comparison and char-acterization of ulcerations induced by endoscopic ligation ofesophageal varices versus endoscopic sclerotherapy.Gastrointest Endosc 1993;39:119.

159. Chen WC, Hou MC, Lin HC, Chang FY, Lee SD, et al.Symptomatic esophageal stricture after endoscopic varicealligation-success of endoscopic balloon dilation. Chung Hua IHseuh Tsa Chih 2000;63:144-7.

160. Rai RR, Nijhawan S, Singh G. Post-ligation stricture: a rarecomplication. Endoscopy 1996;28:406.

161. Fleischer DE. Therapy for gastrointestinal bleeding. In:Geenen JE, Fleischer DE, Waye JD, editors. Techniques intherapeutic endoscopy. 2nd ed. New York: Gower MedicalPubl. 1.1-1.27.

162. Chung SS, Lau JY, Sung JJ, Chan AC, Lai CW, Ng EK, et al.Randomised comparison between adrenaline injection aloneplus heat probe treatment for actively bleeding ulcers.BMJ1997;314:1307-11.

163. Lin HJ, Tseng GY, Perng CL, Lee FY, Chang FY, Lee SD.Comparison of adrenaline injection and bipolar electrocoag-ulation for the arrest of peptic ulcer bleeding. Gut 1999;44:715-9.

164. Rutgeerts P, Vantrappen G, Van Hootegem P, Broeckaert L,Janssens J, Coremans G, et al. Neodymium-YAG laser pho-tocoagulation versus electrocoagulation for the treatment ofseverely bleeding ulcers: a randomised comparison. Gastro-intest Endosc 1987;33:199-202.

165. Jensen DM. Endoscopic control of nonvariceal upper gas-trointestinal hemorrhage. In Yamada T, Alpers DH, Laine L,Owyang C, Powell DW, editors. Textbook of gastroenterolo-gy. Phildelphia: Lippincott Williams and Wilkins; 1999. p.2857-79.

166. Lau JY, Sung JJ, Lam YH, Chan AC, Ng EK, Lee DW, et al.Endoscopic retreatment compared with surgery in patientswith recurrent bleeding after initial endoscopic control ofbleeding ulcers. N Engl J Med 1999;34:751-6.

167. VanOsEC, Kamath PS, Gostout CJ, Heit JA. Gastro-enterological procedures among patients with disorders ofhemostasis: evaluation and management recommendations.Gastrointest Endosc 1999;50:536-43.

168. Kao LS, Nguyen T, Dominitz J, Teicher HL, Kearney DJ.Modification of a latex glove for the safe endoscopic removalof a sharp gastric foreign body. Gastrointest Endosc 2000;52:127-9.

Prepared by:Standards of Practice Committee

Glenn M. Eisen, MD, ChairTodd H. Baron, MDJason A. Dominitz, MDDouglas O. Faigel, MDJay L. Goldstein, MDJohn F. Johanson, MDJ. Shawn Mallery, MDHareth M. Raddawi, MDJohn J. Vargo II, MDJ. Patrick Waring, MDRobert D. Fanelli, SAGES RepJo Wheeler-Harbough, SGNA Rep

Title Author


complications of gi endoscopy(2)

Documents