Managing massive bleeding from a peptic ulcer remains a challenge, and it should involve a multidisciplinary team. Endoscopy is the first-line treatment. Even with larger ulcers, endoscopic hemostasis can be achieved in the majority of cases. Surgery is clearly indicated in patients in whom arterial bleeding cannot be controlled at endoscopy. Angiographic embolization is an alternate option, particularly in those unfit for surgery. In selected patients judged to belong to the high-risk group, a more aggressive postendoscopy management is warranted. The role of early elective surgery or angiographic embolization in selected high-risk patients to forestall recurrent bleeding remains controversial.
In an old surgical series, massive bleeding from a peptic ulcer has been defined as blood loss of such a magnitude that the patient is either in shock or bleeding actively and being treated for shock. Blood transfusion would be required not simply to correct anemia but to restore or maintain vital signs. There are also signs of active bleeding from the upper gastrointestinal tract as indicated by hematemesis and melena or passage of blood per rectum, associated with continuing bloody aspirate after gastric lavage. In another study of massive bleeding in duodenal ulcer, Gardner and Baronofsky defined massive bleeding as a recent episode of melena or hematemesis and hemoglobin of 8 g/dL or less or a fall in blood pressure.
Mortality in patients with massive bleeding is unacceptably high. They merit intensive monitoring and aggressive treatment. The National United Kingdom Audit conducted in 1993 was a population-based, multicenter, prospective observational study in 4185 patients presenting with acute upper gastrointestinal bleeding. The Audit reported a crude mortality of 14%. In the cohort, there were 2071 patients with peptic ulcer presenting with acute hemorrhage. In the 251 patients (12%) that came to surgery, mortality was 24%.
Clinical assessment and preparation of patients
Patients with upper gastrointestinal bleeding require prompt assessment and volume resuscitation. Hematemesis, passage of fresh melena, shock, and a low hemoglobin level signify significant ongoing bleed or a recent significant bleed. Endotracheal intubation should be considered in patients with active hematemesis, unstable vital signs, or altered mental state to minimize the risk of aspiration pneumonia. Coagulopathy exacerbates bleeding and should be corrected with blood products. Massive bleeding mandates emergency endoscopy. Emergency endoscopy is performed as soon as the patient is stabilized after initial resuscitation. In patients with exigent bleeding, endoscopy can be performed during resuscitation. A more liberal policy in emergency endoscopy should be offered to elderly patients and patients with comorbid illnesses, because they tolerate blood loss poorly and are more likely to suffer from organ dysfunctions consequent to hypotension.
Endoscopic treatment
Endoscopic therapy remains the first treatment modality in the management of bleeding peptic ulcers, even in those presenting with massive bleeding. Endoscopy allows the bleeding source to be localized and excludes varices as the cause of upper gastrointestinal bleeding, as the management is different from that of ulcer bleeding. As endoscopic signs or stigmata of bleeding are prognostic, an early endoscopy enables clinicians to risk-stratify patients. More importantly, endoscopic therapy improves outcomes in patients with actively bleeding ulcers and ulcers with a visible vessel. Sacks and colleagues performed a meta-analysis of 25 randomized controlled trials that compared endoscopic hemostasis to standard treatment. The systematic review showed that endoscopic therapy reduced the risk of recurrent and continued bleeding (69% relative reduction), emergency surgery (62% relative reduction), and mortality (30% relative reduction). Cook and colleagues analyzed data from 30 trials and concluded that endoscopic therapy significantly reduced the rate of rebleeding, surgery, and mortality. The effects were greatest in patients with active bleeding ulcers or nonbleeding, visible vessels. There is also recent evidence to suggest that endoscopic treatment of adherent clots is beneficial. Kahi and colleagues performed a meta-analysis pooling results of six clinical trials with 240 randomized patients (two in abstract form only) and concluded that endoscopic therapy would be more effective in preventing recurrent bleeding when compared with medical therapy alone (rate of recurrent bleeding, 8.2% vs 24.7%).
We now have evidence that the addition of a second modality to injection therapy further improves patients’ outcomes. A Cochrane systematic review pooled data from 17 trials that compared epinephrine injection to epinephrine injection and a second treatment method in 1763 high-risk patients. The addition of a second treatment conferred a reduction in rate of recurrent bleeding from 18.8% to 10.4%, emergency surgery from 10.8% to 7.1%, and mortality from 5% to 2.5%, regardless of which second procedure was applied. We favor the use of hemoclips or a 3.2-mm heater probe. We believe that firm tamponade of the bleeding artery and its coaptive coagulation with a contact thermal probe produce secure hemostasis. The use of hemoclips is closer to surgical ligature in hemostasis. We performed a pooled analysis of 15 randomized trials that compared hemoclips to the use of a heater probe in nonvariceal bleeding. The rate of definitive hemostasis was high with either treatment modalities (81.5% vs 81.2%, respectively). There was no difference in the rate of recurrent bleeding, surgery, and death. In clinical practice, successful placement of clips is particularly difficult in fibrotic ulcer with a tangential position, where many difficult ulcers occur. In a randomized trial, 10% of patients randomized to a hemoclip group did not receive hemoclip placement due to technical failure. The use of either modality should not be mutually exclusive.
Endoscopic treatment
Endoscopic therapy remains the first treatment modality in the management of bleeding peptic ulcers, even in those presenting with massive bleeding. Endoscopy allows the bleeding source to be localized and excludes varices as the cause of upper gastrointestinal bleeding, as the management is different from that of ulcer bleeding. As endoscopic signs or stigmata of bleeding are prognostic, an early endoscopy enables clinicians to risk-stratify patients. More importantly, endoscopic therapy improves outcomes in patients with actively bleeding ulcers and ulcers with a visible vessel. Sacks and colleagues performed a meta-analysis of 25 randomized controlled trials that compared endoscopic hemostasis to standard treatment. The systematic review showed that endoscopic therapy reduced the risk of recurrent and continued bleeding (69% relative reduction), emergency surgery (62% relative reduction), and mortality (30% relative reduction). Cook and colleagues analyzed data from 30 trials and concluded that endoscopic therapy significantly reduced the rate of rebleeding, surgery, and mortality. The effects were greatest in patients with active bleeding ulcers or nonbleeding, visible vessels. There is also recent evidence to suggest that endoscopic treatment of adherent clots is beneficial. Kahi and colleagues performed a meta-analysis pooling results of six clinical trials with 240 randomized patients (two in abstract form only) and concluded that endoscopic therapy would be more effective in preventing recurrent bleeding when compared with medical therapy alone (rate of recurrent bleeding, 8.2% vs 24.7%).
We now have evidence that the addition of a second modality to injection therapy further improves patients’ outcomes. A Cochrane systematic review pooled data from 17 trials that compared epinephrine injection to epinephrine injection and a second treatment method in 1763 high-risk patients. The addition of a second treatment conferred a reduction in rate of recurrent bleeding from 18.8% to 10.4%, emergency surgery from 10.8% to 7.1%, and mortality from 5% to 2.5%, regardless of which second procedure was applied. We favor the use of hemoclips or a 3.2-mm heater probe. We believe that firm tamponade of the bleeding artery and its coaptive coagulation with a contact thermal probe produce secure hemostasis. The use of hemoclips is closer to surgical ligature in hemostasis. We performed a pooled analysis of 15 randomized trials that compared hemoclips to the use of a heater probe in nonvariceal bleeding. The rate of definitive hemostasis was high with either treatment modalities (81.5% vs 81.2%, respectively). There was no difference in the rate of recurrent bleeding, surgery, and death. In clinical practice, successful placement of clips is particularly difficult in fibrotic ulcer with a tangential position, where many difficult ulcers occur. In a randomized trial, 10% of patients randomized to a hemoclip group did not receive hemoclip placement due to technical failure. The use of either modality should not be mutually exclusive.
What is the limit to endoscopic therapy?
A big bleed is often consequent to a big eroded artery. Blood flow is proportional to the fourth power of the vessel diameter; a small increase in diameter would greatly increase flow. Swain and colleagues studied 27 gastrectomy specimens in patients who underwent urgent surgery for bleeding gastric ulcers. He used thin-barium angiography to study the bleeding artery underneath these ulcers. The study predated the widespread use of endoscopic therapy. It was not entirely clear if the ulcers studied had been treated by endoscopic means. The bleeding artery had a mean external diameter of 0.7 mm (0.1–1.8 mm). In 13 ulcers, the arteries were subserosal and were technically outside the stomach wall. The other bleeding arteries were smaller than 1 mm in size and were submucosal in disposition. In about half of the arteries, there were aneurysmal dilations at the bleeding point. Larger penetrating ulcers are more likely to erode into larger subserosal arteries. Swain and colleagues published only in an abstract the size of arteries in patients who died after a major bleed from their peptic ulcers. The mean diameter of the bleeding artery was 3.75 mm.
In a canine mesenteric artery model, Johnston and colleagues studied the limits of endoscopic thermocoagulation in securing hemostasis. The authors emphasized the need for firm compression onto the artery by a contact probe. Due to the limit in the size of the endoscope channel, a 3.2-mm contact thermal probe is arguably the best available hemostatic device. The use of a 3.2-mm contact thermocoagulation device was shown to consistently seal arteries up to 2 mm in size. Findings of an in vitro model in a real clinical situation may not be as applicable as conditions are often less ideal.
Elmunzer and colleagues systematically reviewed 10 prospective series that evaluated predictive factors for endoscopic failure ( Table 1 ). Two of them employed epinephrine injection as a single modality of therapy. Most commonly identified preendoscopic factors were hemodynamic instability and the presence of comorbid illnesses. During endoscopy, active bleeding, large ulcer size, location of ulcer at posterior bulbar duodenum, and lesser curve were identified as predictors for endoscopic failure. The author remarked that on the basis of consistency and statistical strength, hemodynamic instability, active bleeding, large ulcer size, and posterior duodenal location appear to be the most important predictors of recurrent bleeding. Larger ulcers located at the posterior bulbar duodenum and lesser curve are likely to erode into large arterial complexes—the gastroduodenal artery complex and the left gastric artery proper or its branches. The arteries are often sizable. Bleeding from these arteries exceeds the limit of what endoscopic devices can secure.
| Predictor | Study | % Rebleeding in Entire Study Population | % Rebleeding in Patients With Predictor | % Rebleeding in Patients Without Predictor | Odds Ratio (95% CI) |
|---|---|---|---|---|---|
| Hemodynamic instability | Guglielmi | 20 (86/429) | 41.1 (30/73) | 14.8 (54/366) | 3.68 (1.99–6.81) |
| Wong a | 8.3 (94/1,128) | 19.2 (35/182) | 6 (56/946) | 2.21 (1.40–3.48) | |
| Thomopolous a | 22 (86/390) | 47.1 (24/51) | 16(54/339) | 2.31 91.33–6.97) | |
| Brullet (DU) a | 16.7 (17/102) | 32.0 (8.25) | 12.3(10/81) | 3.53 (1.27–4.1) | |
| Park | 20 (25/127) | NR | NR | NR | |
| Comorbid illness | Villanueva | 24.5 (57/233) | 36.5 (42/115) | 12.7 (15/118) | NR |
| Saeed | 12 (8/69) | NR | NR | Likelihood ratio 7.63, P = 0.005 | |
| Active bleeding | Guglielmi | 20 (86/829) | 20.3 (39/192) | 18 (45/247) | 14.47 oozing, 13.38 spurting |
| Wong a | 8.3 (94/1,128) | 12.1 (71/587) | 4.2 (23/541) | 1.65 (1.07–2.56) | |
| Chung | 25.2 (35/139) | NR | NR | 6.48 (1.88–22.49) | |
| Thomopolous a | 22 (86/390) | 48.9 (46/94) | 10.8 (32/296) | 2.45 (1.51–3.93) | |
| Brullet (GU) a | 13.1 (23/175) | 26 (13/50) | 8 (10/125) | 2.98 (1.12–7.91) | |
| Large ulcer size (≥ 2 cm) | Guglielmi | 20 (86/429) | 31.3 (40/128) | 14.1 (44/311) | 4.61 (2.20–9.64) |
| Wong a | 8.3 (94/1,128) | 14.8 (36/244) | 6.6 (58/884) | 1.80 (1.16–2.83) | |
| Brullet a (GU) | 13.1 (23/175) | 23.9 (16/67) | 6.5 (7/108) | 3.64 (1.34–9.89) | |
| Brullet a (DU) | 16.7 (17/102) | 36.3 (8/22) | 12 (10/84) | 2.29 (1.13–10.9) | |
| Large ulcer size (>1 cm) | Villanueva | 24.5 (57/233) | 42.0 (34/81) | 15.1 (23/152) | NR |
| Posterior duodenal ulcer | Thomopolous a | 22 (86/390) | 43.2 (16/37) | 17.6 (62/353) | 2.48 (1.37–7.01) |
| Park | 20 (25/127) | 44 (11/25) | 13.7 (14/102) | NR | |
| Villanueva | 24.5 (57/233) | 57.1 (20/35) | 18.7 (37/198) | NR | |
| Lesser gastric curve ulcer | Brullet a (GU) | 13.1 (23/175) | 22.9 (16/70) | 6.7 (7/105) | 2.79 (1.01–7.69) |
| Park | 20 (25/127) | 35 (7/20) | 16.8 (18/107) | NR |
Related posts:
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Predicting Poor Outcome from Acute Upper Gastrointestinal Hemorrhage
Stress-Induced Ulcer Bleed ing in Critically Ill Patients
Helicobacter pylori -Negative Nonsteroidal Anti-Inflammatory Drug-Negative Ulcer
Differences in Peptic Ulcer Between the East and the West
Balancing Risks and Benefits of Cyclooxygenase-2 Selective Nonsteroidal Anti-Inflammatory Drugs
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