Help
Subscribe


GastroHep.com - the global online resource for all aspects of gastroenterology, hepatology and endoscopy

 20 November 2017

Advanced search
GastroHep.com - the global online resource for all aspects of gastroenterology, hepatology and endoscopy Profile of Roy Pounder

Home

News
Journals
Review Articles
Slide Atlas
Video Clips
Online Books  
Advanced Digestive Endoscopy
Classical Cases
Conference Diary
PubMed
International GH Links
USA GH Links
National GH Links
National GI Societies
Other Useful Links




Emails on Gastroenterology and Hepatology
the National AIDS Treatment Advocacy Project
Visit the gastroenterology section of the EUMS

Online books

View all the figures for this chapter.

Upper Endoscopy

Editor: Joseph Sung


4. Upper GI bleeding (non-variceal)

John Lee

Top of page Synopsis  Next section

The incidence of acute bleeding from the upper digestive tract has lessened somewhat in recent years, owing mainly to the reduction in ulcer disease. However, ulcers still account for approximately half of all cases of upper gastrointestinal bleeding requiring hospital treatment. Varices are the second commonest cause of serious bleeding. Bleeding can occur also from erosions, tears, tumors and vascular malformations. This contribution concentrates on ulcer bleeding; varices are addressed in another chapter.

Fortunately, ulcer bleeding stops spontaneously in 75–80% of patients, with a relatively benign outcome. However, despite the numerous advances in endoscopic and medical therapy, intensive care and surgery, the mortality rate can be high as 8–10%. Mortality occurs in patients with massive and recurrent bleeding, especially in elderly patients with major comorbidities. Bleeding which commences in hospitalized patients is especially serious. Approximately a third of the patients with significant ulcer bleeding will develop recurrent bleeding on long-term follow-up, in the absence of active intervention.

Much progress has been made in methods for endoscopic diagnosis and treatment of patients with acute bleeding over recent years. This contribution reviews methods for hemostasis, the care of patients after treatment, and the prediction and prevention of rebleeding. It concludes with some hopes for future progress in this field.

Diagnostic methods  Previous section Next section

Although the clinical history and physical examination may provide some clues about the cause of bleeding (e.g. aspirin-induced peptic ulcer), they are too non-specific to be useful clinically, as is the result of nasogastric lavage.

Endoscopy  Previous section Next section

Skillful modern endoscopy is > 95% accurate in determining the cause of bleeding in patients presenting with upper gastrointestinal hemorrhage, especially when performed within 48 h of the onset. Barium study should be avoided in acute bleeding, since it interferes with endoscopic visualization necessary for hemostasis. Angiography is only helpful in patients with active bleeding. Routine early endoscopy was avoided in the past, because one of the first randomized studies comparing it to routine endoscopy did not show any improvement in morbidity or mortality [1]—unsurprisingly, since endoscopy was used only to diagnose rather than to treat the cause of the bleeding. In addition, mortality is not always the best end point to use in clinical bleeding studies, because its low occurrence requires a large sample size. However meta-analyses have shown that endoscopic hemostasis reduces mortality [2,3]. Finally over-emphasis on mortality tends to ignore other important outcomes such as rebleeding, transfusion, hospital stay, cost, and need for surgery, all of which are significantly improved by endoscopic therapy.

Early endoscopy is helpful in a different way for the 50–60% of patients with peptic ulcer bleeding who don't need hemostasis, because it can precisely predict the clinical outcome. This information can then be used to triage patients with good outcome to less intensive and thus expensive care as outpatients [4].

Endoscopy, when and where?  Previous section Next section

Patients who continue in hemodynamic unstability require urgent endoscopy, preferably in the intensive care unit. All others can undergo endoscopy as soon as is practical, hopefully within 24–48 h. Patients with clean-based ulcers who have negligible risk of rebleeding could then be discharged after the procedure (Fig. 1). One practical approach is to perform the endoscopy before admitting the patient from the emergency department, provided that the endoscopy unit is open. Patients presenting after hours could be held in the emergency department to undergo the procedure during the next available session. Otherwise, admission to the intensive care unit should be reserved for patients with continued hemodynamic instability after fluid resuscitation (~ 2 L) or with a comorbid condition requiring the intensive care unit, such as myocardial ischemia.

Lavage before endoscopy?  Previous section Next section

Lavage is usually unnecessary before endoscopy, because placing the patient in the left lateral position pools the blood in the fundus and the greater curve of the stomach, and usually exposes most of the bleeding lesions, which tend to be in the oesophagus, the lesser curve, the antrum, or the duodenal bulb. If the bleeding lesion is not seen then the patient can be turned, the head of the bed elevated, blood suctioned (connect the suction tubing directly to the biopsy channel of the endoscope), or endoscopy repeated 1–2 hours after administering erythromycin or metoclopramide. The chance of missing a second bleeding lesion under a blood pool is low for patients with non-variceal bleeding, but is not obviously zero, and thus all such patients should undergo repeat endoscopy in 24–48 hours [5].

Ulcer stigmata  Previous section Next section

Endoscopy will show one of three possible findings in patients with ulcer bleeding. Approximately 40–45% have a clean-based ulcer; 40% have stigmata of recent hemorrhage, and 15–20% have either oozing or spurting [6].

Removing clots?  Previous section Next section

An adherent clot (i.e. one resistant to washing) is found in up to 15% of cases (Fig. 2). An adherent clot should be removed to expose any underlying stigmata for treatment, as the risk of rebleeding is almost as high for clots as for stigmata of recent hemorrhage [7]. Probably the safest way to remove an adherent clot is to inject liberally 1 : 10 000 epinephrine through the clot into the ulcer base then transect it using a cold snare.

Top of page Endoscopic hemostasis  Previous section Next section

Available techniques  Previous section Next section

Many endoscopic methods for treatment have been developed and evaluated. Injection, 10 Fr heat probe, 10 Fr multipolar electrocoagulation (MPEC), and laser have been shown in randomized controlled studies to be effective at stopping active bleeding and preventing rebleeding in patients with stigmata of recent hemorrhage, significantly reducing transfusion, hospital stay, cost of care, and urgent surgery. Although no single study has been or will be likely to have the power needed to demonstrate significant reduction in mortality, meta-analysis has shown mortality reduction in the range of 45% [3]. The results of endoscopic hemostasis appear comparable regardless of the method used for patients with non-bleeding stigmata of recent hemorrhage and oozing ulcers, but combination therapy using epinephrine injection and thermocoagulation is significantly more effective compared to injection alone for spurting ulcer bleeding (hemostasis of 93% vs. 70%) [8]. On the basis of these data, a large-channel therapeutic endoscope should be used in every patient with upper gastrointestinal bleeding, since it cannot be determined in advance which patient will have spurting hemorrhage and require combination therapy using a 10 Fr thermal probe. Finally, clipping appears to be as effective if not better than thermocoagulation (rebleeding rate of 2% vs. 21%) for ulcer bleeding, and can be deployed using a diagnostic endoscope [9].

Injection hemostasis  Previous section Next section

Effective agents for injection therapy include epinephrine, saline, glucose, alcohol, and sclerosant for active bleeding and alcohol and sclerosant for non-bleeding stigmata of recent haemorrhage. Epinephrine is injected in 1 mL aliquots around and into the bleeding point until bleeding stops and mucosal blanching occurs; typically this requires 10–20 mL. Epinephrine injection is safe and can be repeated with minimal risk. Alcohol is injected in 0.1–0.2 mL aliquots for a total dose of 0.5–1.0 mL. Repeat therapy using alcohol or a sclerosant increases the risk of perforation.

Thermal methods  Previous section Next section

Thermocoagulation using a 10 Fr probe, but not a 7 Fr probe has been shown to improve significantly the outcome of patients with peptic ulcer bleeding, partly because only the larger probe provides enough rigidity to tamponade the vessel effectively. Thermal devices can coagulate an artery up to 2 mm in diameter under experimental conditions, which fortunately is larger than the average diameter of a bleeding ulcer artery (0.7 mm range). The heat probe should be set at 30 J and applied for 4–6 pulses before changing position, and the MPEC probe set at 15 watts and applied for 15–20 s before changing position (Fig. 3). Thermocoagulation is usually performed at four quadrants surrounding the lesion, followed by application to the bleeding point. The end-point of hemostasis is cessation of bleeding and obliteration of the previously raised stigmata, i.e. the scorched earth appearance. Although thermocoagulation is very safe, repeat therapy increases the risk of perforation.

Combination methods  Previous section Next section

Combination therapy using injection of 1 : 10 : 000 epinephrine (1 mL aliquots for total of ~10 mL) followed by thermocoagulation should be used in patients with spurting ulcers [8]. In addition to providing superior hemostasis, injection slows the bleeding and facilitates the accurate placement of the thermal probe.

Top of page Care after bleeding  Previous section Next section

Diet  Previous section Next section

Resuming a regular diet after endoscopy does not harm the patient. Alternatively a clear liquid diet could be considered in patients with questionable hemostasis or if repeat endoscopy is needed to clear the stomach.

Acid suppression  Previous section Next section

All patients should receive high-dose intravenous proton pump inhibitor therapy (e.g. omeprazole or pantoprazole 80 mg bolus followed by 8 mg/ h continuous infusion) for three days, followed by full-dose oral therapy for ulcer healing [10]

H.Pylori  Previous section Next section

All patients should be tested for H. pylori, preferably using at least two tests and with eradication confirmed in infected patients.

Aspirin and NSAIDs  Previous section Next section

All patients should be screened for NSAID and/or aspirin use and their use discontinued whenever possible.

Discharge  Previous section Next section

Patients with stigmata of recent hemorrhage could be discharged 24–48 hours after resuscitation and hemostasis and patients with spurting hemorrhage 48–72 hours later, as the risk of rebleeding decreases rapidly over the initial 72 hours.

Top of page Rebleeding  Previous section Next section

Recurrent bleeding may occur early, within hours to days of the index bleed, or late, after months to years. While there is no formal definition as to what constitutes early rebleeding, it seems reasonable to define it as occurring during the hospitalization or within 5–7 days of the onset of bleeding. Late rebleeding is usually defined as recurrent hemorrhage requiring hospitalization and endoscopy.

Early rebleeding  Previous section Next section

It can be difficult at times to diagnose early rebleeding, since many patients with presumed rebleeding do not undergo repeat endoscopy. The diagnosis can be ambiguous even in patients undergoing repeat endoscopy, since the ulcer may have already stopped bleeding by the time the procedure is performed. For these reasons, most studies do not require endoscopic confirmation of active bleeding, but rely on some combination of hemodynamic parameter, hematemesis, ongoing melena, blood transfusion requirement, and falling blood count to diagnose rebleeding.

Predictors of rebleeding  Previous section Next section

Early rebleeding after hemostasis has been often (but not always) associated older age, comorbid illness, posterior interior duodenal bulb ulcer, large ulcer size, active bleeding, and hypotension. The best characterized predictor of early rebleeding is the endoscopic appearance of the ulcer.

Ulcer stigmata  Previous section Next section

A clean-based ulcer means that the bleeding point has already healed. Stigmata of a recent hemorrhage (also called a pigmented protuberance or a visible vessel) usually take the form of a clot overlying a ruptured artery or a pseudoaneurysm, and are associated with recent bleeding [11]. Finally, active bleeding can be seen as oozing or spurting. Untreated patients with clean-based ulcers will rebleed at a rate of 0–5%, those with flat spots at 5–10%, and those with pigmented protuberances at 40–45%. A patient with arterial spurting will continue to bleed or rebleed in > 75% of cases (Fig. 4). If we accept that a clean-based ulcer does not have a bleeding lesion, then the rare patient who rebleeds with a clean-based ulcer must have had stigmata of recent hemorrhage that were missed. The high interobserver variability for diagnosing stigmata of recent hemorrhage supports this concept (Fig. 5) [12,13].

Endoscopic hemostasis is effective at stopping the bleeding in 85–98% of patients initially, but treated patients may rebleed in up to 20% of cases—unsurprisingly, since the endoscopist cannot determine the path of the bleeding vessel or whether the therapy obliterated the bleeding point. Even the 'objective' method of checking Doppler is prone to both false positive (from other vessels) and negative (from missing the bleeding artery) results [14].

Prevention of rebleeding  Previous section Next section

Raising the intragastric pH improves coagulation by enhancing platelet aggregation and plasma coagulation factors, inhibiting pepsin, and starting ulcer healing. While conceptually simple, raising and maintaining the intragastric pH > 4 is difficult clinically, short of using high-dose continuous intravenous proton pump inhibitor therapy. For example 80 mg of intravenous omeprazole bolus followed by continuous infusion at 8 mg/ h for 3 days significantly reduced the risk of rebleeding after endoscopic hemostasis from 22.5% to 6.7% in one study [10]. The end-point of the study was rebleeding within 30 days; but most reduction in rebleeding occurred during the initial three days of therapy. Although intravenous omeprazole is not available in the United States, intravenous pantoprazole, which has a similar pharmacokinetic profile, could be substituted in the same doses. No convincing evidence supports the use of other medical therapies such as somatostatin analogue, vasopressin, or tranexamic acid to reduce rebleeding after hemostasis. Similarly, repeating endoscopy in 24 h and re-treating the bleeding lesion does not seem to reduce the rebleeding risk significantly [15].

Treatment of rebleeding  Previous section Next section

Three choices for patients with rebleeding are [1] medical management (i.e. blood transfusion and waiting) [2], repeat endoscopic therapy, and [3] surgery. Although medical management is a reasonable alternative initially, most patients with ongoing bleeding require some sort of treatment or risk dying. A randomized comparative trial showed that repeat endoscopic therapy was comparable to surgery, but resulted in significantly fewer complications (15% vs. 36%) [16]. Repeat epinephrine injection and heat probe therapy achieved permanent hemostasis in 73%, resulted in perforation in 4% and failed in 23% of cases. Six out of seven patients in the repeat endoscopy group who developed a complication had salvage surgery. These data clearly support repeating endoscopic hemostasis before operating in patients with rebleeding.

Late rebleeding  Previous section Next section

Approximately a third of the patients with major ulcer hemorrhage will experience recurrent ulcer bleeding within 3 years. Three issues are key to this problem- H. Pylori, acid suppression [17,18], and NSAIDs.

H.pylori  Previous section Next section

It is now well established that eradication of H. pylori will virtually eliminate the risk of recurrent ulcer disease and bleeding in a patient with a 'pure'H. pylori ulcer [19]. Therefore patients with H. pylori-caused bleeding peptic ulcers who are confirmed to have had the infection eradicated and are not using aspirin (including low dose) or NSAIDs do not require maintenance acid suppression for prevention of delayed rebleeding.

NSAIDs and aspirin  Previous section Next section

The risk of delayed rebleeding of an ulcer from aspirin or NSAID treatment can be similarly lowered by stopping the offending drug, whenever possible. Discontinuation or alternative therapy is especially important in patients with increased risk of bleeding, such as previous bleeding of a complicated ulcer, older age, and use of multiple and higher doses of NSAIDs. Alternatively, the dosage of the NSAID used can be reduced and/or prophylaxis administered in patients who cannot discontinue it. Newer agents appear to be safer in this regard.

Two large trials comparing celecoxib or rofecoxib to conventional NSAID therapy showed reduced ulcer complications, including bleeding, only for patients not taking concomitant aspirin cardioprophylaxis [23,24]. What is unclear from these studies of primary prevention is whether proton pump inhibitor prophylaxis or COX-2 inhibitor therapy will be similarly effective in reducing the risk of clinically significant rebleeding in patients with a previous history of NSAID-induced ulcer bleeding, i.e. secondary prevention.

One of the few studies to address specifically the risk of delayed rebleeding in patients continuing to use NSAIDs randomized patients with H. pylori infection and aspirin or naproxen use to antibiotic therapy or omeprazole 20 mg QD maintenance [25]. H. pylori eradication before starting 80 mg of aspirin daily reduced the risk of delayed rebleeding similarly to omeprazole (probability of rebleeding of 1.9% vs. 0.9%, respectively), but was significantly less effective than omeprazole for patients taking naproxen 500 mg BID (probability of rebleeding of 18.8% vs. 4.4%). Thus long-term proton pump inhibitor prophylaxis appears to be indicated only in patients infected with H. pylori who are taking full-dose NSAID therapy.

Acid suppression  Previous section Next section

Two large studies showed that maintenance therapy using misoprostol 200 µg QID or omeprazole 20 mg QD was significantly better than placebo in reducing the risk of recurrent gastric ulceration (recurrence of 10% vs. 13% vs. 32%, respectively), but only omeprazole was superior to placebo in reducing the recurrence of duodenal ulcers (recurrence of 3% for omeprazole, 12% for control, and 10% for misoprostol) [20]. Another study showed that omeprazole 20 mg QD was superior to ranitidine 150 mg QD for preventing gastric and duodenal ulcers (5.2% vs. 16.3%% and 0.5% vs. 5.7%, respectively) [21]. Although it might be tempting to assume that a reduction in endoscopically diagnosed ulcers as shown in these studies would also reduce clinical symptoms such as bleeding, no data exist to corroborate this notion. Thus at this time it remains unproven whether long-term proton pump inhibitor therapy actually reduces the risk of delayed ulcer rebleeding.

Misoprostol 200 µg QID has been shown to reduce significantly ulcer complications, including bleeding [22]. Unfortunately, 25% of the patients dropped out because of side-effects of the misoprostol. Moreover, the clinical relevance of the 'statistically significant' (odds ratio, 0.598; p = 0.049) result remains to be determined, as misoprostol prophylaxis only prevented 17 more complications (out of 4404 randomized patients) compared to placebo.

Top of page Non-ulcer bleeding  Previous section Next section

Variceal bleeding is discussed elsewhere. Bleeding from erosions is rarely a serious problem, except in the case of Dieulafoy lesions. These essentially are small erosions with an exposed vessel. These lesions are sometimes missed by inexperienced endoscopists, because they are small, and often high in the stomach. They are often best seen and treated in retroversion. Whilst all types of endoscopic hemostasis can be used, clipping seems to be particularly effective in these cases.

Patients with Mallory–Weiss tears often give a history of repeated retching or vomiting. Although the original description was of massive hemorrhage, this is very unusual. When treatment is necessary, endoscopists should be mindful of the risk of perforating the damaged esophagus. Clipping is now favored over injection or thermal methods.

Top of page Issues and future trends  Previous section Next section

There are several areas where further developments and study would be beneficial.

New suturing devices, clips, and bands  Previous section Next section

Two different suturing devices have been approved by the FDA for use in anti-reflux therapy. Their use for bleeding therapy is limited by the inaccuracy of suture placement, superficial depth of suture, poor visibility and high costs. Banding is ineffective against most ulcer bleeding, because the fibrotic base cannot be sucked up for banding. Two commercially available clipping devices are better at stopping ulcer bleeding but still cumbersome to use, and have variable depth of penetration. Several devices which could be used to perform full-thickness suturing should be available in the near future.

Visualization (scope size)  Previous section Next section

Which endoscope to use in this context remains a dilemma. Large channels facilitate lavage, but the necessary increased scope size may be problematic. Scopes with greater than the standard channel size (10 FG) have been proposed.

Airway protection/anesthesia  Previous section Next section

Propofol and MAC (monitored anesthesia care) will gain wider acceptance for endoscopy in the near future, which should make procedures easier for patients and physicians. Airway protection will continue to be needed for patients at risk for aspiration; the development of better methods for clearing the stomach could decrease the need for intubation.

Training  Previous section Next section

Increasing use of models and computers for training should improve endoscopic expertise. Implementation of a feedback system (for example Doppler after hemostasis) could be an effective training aid.

Top of page References  Previous section

 1 Peterson, WL, Barnett, CC & Smith, HJ et al. Routine early endoscopy in upper-gastrointestinal-tract bleeding: a randomized, controlled trial. N Engl J Med 1981; 304: 925–9. PubMed

 2 Sacks, HS, Chalmers, TC & Blum, AL et al. Endoscopic hemostasis. An effective therapy for bleeding peptic ulcers. JAMA 1990; 264: 494–9. PubMed

 3 Cook, DJ, Guyatt, GH & Salena, BJ et al. Endoscopic therapy for acute non variceal upper gastrointestinal hemorrhage: a meta-analysis. Gastroenterology 1992; 102: 139–48. PubMed

 4 Lee, JG, Turnipseed, S & Romano, PS et al. Endoscopy-based triage significantly reduces hospitalization rates and costs of treating upper GI bleeding: a randomized controlled trial. Gastrointest Endosc 1999; 50: 755–61. PubMed

 5 Stollman, NH, Putcha, RV & Neustater, BR et al. The uncleared fundal pool in acute upper gastrointestinal bleeding: implications and outcomes. Gastrointest Endosc 1997; 46: 324–7. PubMed

 6 Laine, L & Peterson, WL. Bleeding peptic ulcer. N Engl J Med 1994; 331: 717–27. PubMed

 7 Jensen, DM. Spots and clots – leave them or treat them? Why and how to treat. Can J Gastroenterol 1999; 13: 413–5. PubMed

 8 Chung, SC, Lau, JY & Sung, JJ et al. Randomised comparison between adrenaline injection alone and adrenaline injection plus heat probe treatment for actively bleeding ulcers. BMJ 1997; 314: 1307–11. PubMed

 9 Cipolletta, L, Bianco, MA & Marmo, R et al. Endoclips versus heater probe in preventing early recurrent bleeding from peptic ulcer: a prospective and randomized trial. Gastrointest Endosc 2001; 53: 147–51. PubMed

10 Lau, JY, Sung, JJ & Lee, KK et al. Effect of intravenous omeprazole on recurrent bleeding after endoscopic treatment of bleeding peptic ulcers. N Engl J Med 2000; 343: 310–6. PubMed

11 Swain, CP, Storey, DW & Bown, SG et al. Nature of the bleeding vessel in recurrently bleeding gastric ulcers. Gastroenterology 1986; 90: 595–608. PubMed

12 Lau, JY, Sung, JJ & Chan, AC et al. Stigmata of hemorrhage in bleeding peptic ulcers: an interobserver agreement study among international experts. Gastrointest Endosc 1997; 46: 33–6. PubMed

13 Laine, L, Freeman, M & Cohen, H. Lack of uniformity in evaluation of endoscopic prognostic features of bleeding ulcers. Gastrointest Endosc 1994; 40: 411–7. PubMed

14 Wong, RC, Chak, A & Kobayashi, K et al. Role of Doppler US in acute peptic ulcer hemorrhage: can it predict failure of endoscopic therapy? Gastrointest Endosc 2000; 52: 315–21. PubMed

15 Messmann, H, Schaller, P & Andus, T et al. Effect of programmed endoscopic follow-up examinations on the rebleeding rate of gastric or duodenal peptic ulcers treated by injection therapy: a prospective, randomized controlled trial. Endoscopy 1998; 30: 583–9. PubMed

16 Lau, JY, Sung, JJ & Lam, YH et al. Endoscopic retreatment compared with surgery in patients with recurrent bleeding after initial endoscopic control of bleeding ulcers. N Engl J Med 1999; 340: 751–6. PubMed

17 Jensen, DM, Cheng, S & Kovacs, TO et al. A controlled study of ranitidine for the prevention of recurrent hemorrhage from duodenal ulcer. N Engl J Med 1994; 330: 382–6. PubMed

18 Garcia Rodriguez, LA & Ruigomez, A. Secondary prevention of upper gastrointestinal bleeding associated with maintenance acid-suppressing treatment in patients with peptic ulcer bleed. Epidemiology 1999; 10: 228–32. PubMed

19 Macri, G, Milani, S & Surrenti, E et al. Eradication of Helicobacter pylori reduces the rate of duodenal ulcer rebleeding: a long-term follow-up study. Am J Gastroenterol 1998; 93: 925–7. PubMed

20 Hawkey, CJ, Karrasch, JA & Szczepanski, L et al. Omeprazole compared with misoprostol for ulcers associated with nonsteroidal antiinflammatory drugs. Omeprazole versus Misoprostol for NSAID-induced Ulcer Management (OMNIUM) Study Group. N Engl J Med 1998; 338: 727–34. PubMed

21 Yeomans, ND, Tulassay, Z & Juhasz, L et al. A comparison of omeprazole with ranitidine for ulcers associated with nonsteroidal antiinflammatory drugs. Acid Suppression Trial: Ranitidine versus Omeprazole for NSAID-associated Ulcer Treatment (ASTRONAUT) Study Group. N Engl J Med 1998; 338: 719–26. PubMed

22 Silverstein, FE, Graham, DY & Senior, JR et al. Misoprostol reduces serious gastrointestinal complications in patients with rheumatoid arthritis receiving nonsteroidal anti-inflammatory drugs. Ann Intern Med 1995; 123: 241–9. PubMed

23 Bombardier, C, Laine, L & Reicin, A et al. Comparison of upper gastrointestinal toxicity of rofecoxib and naproxen in patients with rheumatoid arthritis. VIGOR Study Group. N Engl J Med 2000; 343: 1520–8. PubMed

24 Silverstein, FE, Faich, G & Goldstein, JL et al. Gastrointestinal toxicity with celecoxib vs nonsteroidal anti-inflammatory drugs for osteoarthritis and rheumatoid arthritis: the CLASS study: a randomized controlled trial. Celecoxib Long-Term Arthritis Safety Study JAMA 2000; 284: 1247–55. PubMed

25 Chan, FK, Chung, SC & Suen, BY et al. Preventing recurrent upper gastrointestinal bleeding in patients with Helicobacter pylori infection who are taking low-dose aspirin or naproxen. N Engl J Med 2001; 344: 967–73. PubMed

Copyright © Blackwell Publishing, 2003

Go to top of page Email this page Email this page to a colleague

Synopsis
Introduction
Diagnostic upper endoscopy
  Normal esophagus
   Hiatus and Z-line
   Glycogenic acanthosis
   Erythema
   GEJ variants
  Abnormal esophagus
   Erythematous areas and erosions
   Ulcers
   Strictures
   Hiatal hernia
Endoscopy in esophagitis
  Endoscopic staging of esophagitis
   Savary–Miller classification
   Hetzel–Dent classification
   MUSE classification
   Los Angeles classification
  Other lesions associated with GERD
   Schatzki's ring
   Mallory–Weiss tear
   Scleroderma
  Postoperative changes after fundoplication
  Endoscopic biopsy
  Chromoendoscopy in GERD
Endoscopic management of esophageal strictures
  Esophageal dilation
   Principles of esophageal dilation
   Mechanical dilation
   Pneumatic (balloon) dilation
   Techniques of dilation
   Dilation of distal esophageal (Schatzki's) rings
  Concomitant medical therapy for strictures
  Refractory strictures
   Intralesional injection of corticosteroids
   Other endoscopic methods for strictures
  Complications of esophageal stricture dilation
Endoscopic therapies for GERD
  Radiofrequency energy delivery (Stretta®)
   Stretta® technique
   Mechanisms of action
   Complications
  Endoscopic implantation of bulking agents
   Inert polymer microspheres
   Enteryx™
   Expandable hydrogel prosthesis (Gatekeeper™)
  Endoscopic plication systems
   Endoluminal gastric plication (ELGP)
   NDO
   Boston Scientific device
Outstanding issues and future trends
  Disclosure
References
Synopsis
  Barrett's esophagus
  Esophageal cancer
Barrett's esophagus
  Introduction
  Definition of Barrett's esophagus
   Long-segment Barrett's esophagus (LSBE)
   Short-segment BE (SSBE)
   Ultra-short BE (SSBE)
  Risk factors for Barrett's esophagus
   Gastroesophageal reflux disease (GERD)
   H.pylori and GERD
   Age, sex, and race
   Other risk factors
  Epidemiology of Barrett's esophagus
  Natural history of Barrett's esophagus
  Pathogenesis of Barrett's esophagus
   Acid
   Bile
   Helicobacter pylori
  Novel diagnostic techniques for Barrett's esophagus
   Introduction
   Chromoendoscopy
   Magnification/high-resolution endoscopy
   Other investigational techniques
   Endoscopic ultrasonography (EUS)
   Light induced fluorescence (LIF)
   Optical coherence tomography (OCT)
   Reflectance and elastic light scattering spectroscopy
   Confocal microscopy
   Raman spectroscopy (RS)
  Screening for Barrett's esophagus
   Rationale
   Esophagogastroduodenoscopy (EGD)
  Diagnosis of Barrett's esophagus
  Management of Barrett's esophagus
   Surveillance
   Rationale
   Procedure/techniques
   Utility of surveillance
   Chemoprevention of Barrett's esopahgus
   Medical reduction of acid load
   Endoscopic therapy for Barrett's esophagus
   Thermal ablation: Monopolar/bipolar/heater probe electrocoagulation
   Photodynamic therapy (PDT)
   Endoscopic mucosal resection (EMR)
   Surgery for Barrett's esophagus
  Barrett's esophagus conclusion
Esophageal cancer
  Introduction
  Risk factors for esophageal cancer
  Epidemiology of esophageal cancer
  Natural history of esophageal cancer
  Diagnosis of esophageal cancer
   Clinical features
   Laboratory data
   Radiology
   Endoscopy
   Staging
  Management of esophageal cancer
   Endoscopy
   Ablative techniques
   Endoscopic mucosal resection (EMR)
   Endoscopic dilation
   Injection therapy (EIT)
   Esophageal endoprosthesis (EE)
   Surgery for esophageal cancer
   Radiation therapy for esphageal cancer
   Chemotherapy for esophageal cancer
  Esophageal cancer conclusion
  Outstanding issue and future trends
References
Synopsis
  Diagnostic methods
   Endoscopy
   Endoscopy, when and where?
   Lavage before endoscopy?
   Ulcer stigmata
   Removing clots?
Endoscopic hemostasis
  Available techniques
  Injection hemostasis
  Thermal methods
  Combination methods
Care after bleeding
  Diet
  Acid suppression
  H.Pylori
  Aspirin and NSAIDs
  Discharge
Rebleeding
  Early rebleeding
  Predictors of rebleeding
   Ulcer stigmata
  Prevention of rebleeding
  Treatment of rebleeding
  Late rebleeding
   H.pylori
   NSAIDs and aspirin
   Acid suppression
Non-ulcer bleeding
Issues and future trends
  New suturing devices, clips, and bands
  Visualization (scope size)
  Airway protection/anesthesia
  Training
References
Synopsis
Background
National history of variceal bleeding
  Mechanism of bleeding
   Variceal stigmata
  Risk of bleeding
  Prognostic indices
  Rebleeding
Endoscopy: general
Endoscopic treatments
  Endoscopic injection sclerotherapy (EST)
  EST technique
   Sclerosants
   Accessory devices
   Post-EST care
   EST—proof of value?
  Endoscopic variceal ligation (EVL)
   Multi-fire devices
   Recurrence
  Comparing EST and EVL
   Cyanoacrylate (Histoacryl®) injection
  Complications of EST and EVL
  Detachable mini-snare
   Technique
   Results
Treatment of ACUTE variceal hemorrhage
  Pharmacological treatments
  Combined endoscopic and pharmacological therapy
  Surgery
  Tipss
   Comparing TIPSS with endoscopic treatments
  Consensus approach to acute bleeding
  Combined endoscopic therapies vs. single therapy
   Synchronous combinations
   Metachronous combinations
Prophylactic treatment of esophageal varices
  Detection and surveillance
  Endoscopic prophylaxis
Gastric varices
Endoscopic ultrasonography in variceal hemorrhage
  EUS and gastric varices
Outstanding issues and future trends
References
Synopsis
Introduction
Gastritis
  H.pylori-associated gastritis
  Gastritis: clinical manifestations and symptoms
Ulcer disease
  H.pylori and ulcers
  H.pylori: the pathogenetic pathway
   Pattern and phenotype of gastritis in association with H. pylori
   Alterations in the homeostasis of gastric hormones and acid secretion related to H. pylori
   Gastric metaplasia in the duodenum is a prerequisite for H. pylori colonization
   Interaction of H. pylori with the mucosal barrier
   Ulcerogenic strains of H. pylori
   Genetic factors and H. pylori
   The therapeutic proof of causality: H. pylori and ulcers
  Ulcers: clinical features and diagnosis
   Test and treat
   Endoscopic diagnosis
Treatment of peptic ulcers
  Acid suppression
  H.pylori eradication
NSAIDs and gastrointestinal pathology
  Introduction
  Clinical and histological characteristics of NSAID-related injury
  Epidemiology of NSAIDs and gastric injury
  Risk modifiers of injury with NSAIDs
   Dosage and type of NSAID
   Age
   Prior ulcer
   Anticoagulants
   Corticosteroids
   H.pylori infection and NSAIDs combined
  Management of NSAID-associated gastrointestinal toxicity
   Selective COX-2 inhibitors
   Prophylaxis against NSAID injury
Conclusion
  H.pylori
  NSAIDs
  Prophylaxis
Outstanding issues and future trends
References
Synopsis
Definitions
  Gastric carcinoma
  Premalignant gastric lesions
  Gastric polyps as premalignant lesions
   Adenomatous polyps
   Cystic fundic polyps
   Hyperplastic or hyperplasiogenic polyps
   Fibro-inflammatory polyps
   Hamartomas and juvenile polyps
   Other polyps
  Premalignant conditions in the gastric mucosa
   Carditis
   Chronic atrophic gastritis
Histopathological classification of gastric neoplasia
  TNM classification
  Vienna classification
Epidemiology
  Geographical variations of risk
  Proximal and distal gastric cancer
  Causal factors
   Cancer at the EG junction
   Cancer in the distal or non-cardia stomach
  Time trends in incidence and mortality from gastric cancer
   A generalized decline of the disease
   Time trends in Japan
Gastric carcinogenesis
  From inflammation to cancer
  The APC mutation in gastric carcinogenesis
  Mutagenesis in the Lauren classification
  Hereditary gastric cancer
Symptoms of gastric cancer
Endoscopy in the diagnosis of gastric cancer
  Methods
   At the EG junction
   In the non-cardia stomach
  Technological advances in equipment
   Magnification
   Digitization of the image
   Spectroscopic techniques
  Macroscopic appearance of digestive neoplastic lesions
  Endoscopic classification of superficial neoplastic gastric lesions
   At the EG junction
   In the non-cardia stomach
Non-endoscopic procedures in the diagnosis of gastric cancer
  Radiological imaging and ultrasound
  Molecular biology
   Proliferative indices
   P53 protein and TP53 mutations
   Cytokeratins
   Mucins
  Staging of gastric cancer
Clinical relevance of early diagnosis of gastric cancer
Treatment decisions for gastric cancer
  The role of tumor staging
  Treatment with curative intent
  Other therapeutic options
Endoscopic treatment with curative intent
  Technique of endoscopic mucosal resection (EMR)
   EMR with a cap [97]: EMR-C (aspiration method)
   EMR with a ligating cap [102]: EMR-L (aspiration method)
   EMR with tissue incision [103,105,107,108]
   EMR grasp-method [100,103]
  Indications for EMR
  Results and complications of EMR
Surgery for gastric cancer
  Lymphadenectomy
  Extent of the resection
  Palliative gastrectomy
Chemoradiation in advanced gastric cancer
  Chemoradiation protocols (palliation)
  Adjuvant chemoradiation protocols
Endoscopic palliation with Nd:YAG laser
Endoscopic palliation with stents
  Types of stents
  Placement of the stent and indications
  Results and complications of stenting
   Results at the EG junction
   Results at the gastric outlet
   Complications
Guidelines in surveillance
Prevention of gastric cancer
  Prevention and H. pylori infection
  Prevention through dietary intervention
  Unplanned prevention
Secondary prevention of gastric cancer
  Gastroscopy and opportunistic screening
  Mass screening
   In Japan
   In other countries
   Strategy of detection worldwide
References
Synopsis
Introduction
  Benefits of nutrition support
  Enteral access
Gastric or enteric feeding?
Nasogastric (NG) feeding
  NG tube placement
  NG tube management
  NG tube complications
Nasojejunal (NJ) feeding
  Technique
   Different tubes
   Prokinetics
   Fluoroscopy or endoscopic assistance
   The drag technique
   Through the scope passage
  NJ tube management
  NJ tube feeding complications
   Bronchial misplacement
Percutaneous endoscopic gastrostomy (PEG)
  Indications
   Cancer patients
   Stroke
   Dementia
  Contraindications
  PEG technique
  PEG tube management
   Feeding
   Diarrhea
  Complications of PEG
   Tube dislodgement
Percutaneous endoscopy gastrostomy/jejunostomy (PEG/J)
  Indications/contraindications
  J tube placement through a PEG (PEG/J)
  PEG/J tube management
  Complications of PEG/J tubes
Direct percutaneous endoscopic jejunostomy (DPEJ)
  Indications/contraindications
  DPEJ technique
  DPEJ tube management
  DPEJ tube complications
Enteral formulations
  Blenderized formulations
  Lactose-containing formulations
  Lactose-free formulations
  Elemental formulations
  Specialty formulations
  Modular feedings
  Supplemental regimes
  Immune enhancing diets (IED)
Conclusions
Outstanding issues and future trends
References
Introduction
Techniques
  Sonde enteroscopy
  Push enteroscopy
   Depth of insertion
   Routine biopsy?
  Intraoperative enteroscopy
   Laparoscopic-assisted enteroscopy [32]
   Combined techniques
  Capsule enteroscopy
Clinical applications of enteroscopy and capsule endoscopy
  Obscure gastrointestinal bleeding
   Definitions and prevalence
   Alternative diagnostic procedures in obscure bleeding
   When to use enteroscopy in obscure bleeding
   Pathology of obscure bleeding
   Medical therapy for angiodysplasia
   Diagnostic yield and outcomes of enteroscopic techniques in bleeding
   Comparing capsule and push enteroscopy
   Repeat standard endoscopies before enteroscopy?
   Unusual causes of obscure bleeding
   Enteroscopic therapy for bleeding
   Intraoperative enteroscopy for obscure bleeding
   Push enteroscopy or capsule endoscopy for bleeding?
  Small intestinal mucosal diseases
   Celiac disease
   Crohn's disease
  Small bowel tumors
  Novel indications
Conclusion
Outstanding issues and future trends
References

Blackwell Publishing


GastroHep.com is a Blackwell Publishing registered trademark
© 2017 Wiley-Blackwell and GastroHep.com and contributors
Privacy Statement
Disclaimer
About Us