Diagnosis and treatment of patients with recurrent gastroduodenal hemorrhage - Shaprynskyi V.O. 2009

Conclusions

The issue of gastric and duodenal ulcer disease remains one of the most pressing challenges in abdominal surgery. Following the general clinical consensus on the Maastricht guidelines and the widespread Structure/175.html">Implementation of Helicobacter pylori eradication in clinical practice, the number of surgeries for PEPTIC ULCER DISEASE has decreased dramatically. This primarily concerns elective surgery; the number of elective Procedures performed in 2000 was 4,392, compared to 1,234 in 2008, representing a 72% decrease. The number of emergency surgeries during the same period decreased nearly 1.5-fold (17,418 operations in 2000, 13,096 in 2002, and 10,426 in 2008). However, There is a trend toward a relatively stable rate of emergency surgeries over the past 6 years, particularly regarding procedures performed at the height of profuse recurrent bleeding, while the reduction in these surgeries compared to 2000 is associated with the widespread clinical adoption of endoscopic hemostasis techniques. Despite the rapid decline in surgical activity for this pathology, the management of recurrent ulcer bleeding remains the domain of the surgeon rather than the endoscopist, let alone the gastroenterologist.

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Fig. Number of surgeries performed for peptic ulcer disease in Ukraine from 2000 to 2008.

Therefore, the management of patients with peptic ulcer disease complicated specifically by recurrent gastrointestinal bleeding of ulcer Etiology remains highly relevant today.

In this book, we have endeavored to highlight our approach to treating such patients and to present the developed Treatment algorithm for this pathology.

Analyzing a vast body of domestic and foreign literature, as well as our own clinical data, we identified several theories regarding the occurrence of recurrent bleeding: The Theory of the aggressive acid-peptic factor as a cause of clot lysis and recurrent bleeding; the theory of Helicobacter pylori infection of the mucosa; the theory of intravascular clot Fibrinolysis driven by increased Blood fibrinolytic activity and The Development of DIC syndrome in these patients; the theory of enhanced alterative processes against the Background of progressive tissue Hypoxia in the ulcer zone; the theory of a specific pathomorphological substrate developing at the ulcer base in patients with recurrent gastrointestinal bleeding of ulcer etiology; the theory of autoimmune aggression; the theory of endocrine (APUD) system dysfunction in the gastric and duodenal mucosa; the theory of GI bleeding and its recurrence as a genetically determined factor in peptic ulcer patients; the theory of hyperdynamic enhancement of local blood flow; and the mechanical theory. However, these theories do not always explain the occurrence of rebleeding in a specific patient. Many of them compete and often contradict one another. Naturally, isolating a single theory and claiming it as the sole cause of recurrent bleeding would be incorrect. The combination of all these factors genetically determines and causes deep pathological Changes in the gastric and duodenal walls, serving as the background for the development and recurrence of bleeding. Meanwhile, the mechanical theory and the theory of the so-called "hypertensive crisis" appear to act as the trigger mechanism for recurrent Hemorrhage.

Summarizing these data, it can be concluded that the only effective Prevention of recurrent bleeding in patients with peptic ulcer disease complicated by gastrointestinal bleeding is the surgical removal of the pathological focus. However, determining such a level of structural changes in the ulcer area is often possible only by studying surgical specimens, and measuring these parameters is too expensive and time-consuming for rapid screening of patients at high risk of acute recurrent GI bleeding of ulcer etiology. Therefore, our subsequent research was aimed at finding widely accessible factors for predicting recurrent bleeding. Having analyzed 616 patients with peptic ulcer disease complicated by gastrointestinal bleeding and performed a logistic regression Analysis of the obtained parameters, we identified 3 risk factors for recurrent GI bleeding. Factors that significantly (p<0.05) influenced the risk of recurrent bleeding included hemostasis (prior to endoscopic hemostatic therapy) (x2 = 42.9, p<0.0001), ulcer size (x2 = 8.0, p=0.0180), and Hemoglobin level at admission (x2 = 11.4, p=0.0034). Based on these factors, a predictive model for determining the risk of recurrent bleeding was developed. The model was based on the formula:

r = {1+exp(-(-4.8246 + 3.6319*(hemostasis F2c) + 3.9199*(hemostasis F2b) + 4.0320*(hemostasis F2a) + 5.1472*(hemostasis F1b) + 6.2921*(hemostasis F1a) + 1.9528*(ulcer size 1-2 cm) + 1.9619*(ulcer size > 2 cm) + 1.9125*(Hb 71-90 g/l) + 2.8288*(Hb < 70 g/l))}-1,

where r > 0.9 - high risk of recurrent bleeding; 0.7 > r < 0.9 - moderate risk; r < 0.7 - low risk.

The results of our studies aligned with those from both domestic and foreign clinics hosting gastrointestinal bleeding centers.

Concurrently, by analyzing the efficacy of endoscopic techniques for managing recurrent gastrointestinal bleeding, we were able to substantiate our active, individualized, and rational approach, and to define the indications for Surgical treatment in these patients.

The developed active, individualized, and rational approach allowed us to reduce postoperative mortality in patients with recurrent gastrointestinal bleeding of ulcer etiology to 14.3%, mortality among non-operated patients to 16.7%, and overall mortality to 15.8%. The overall mortality rate among patients with peptic ulcer disease complicated by gastrointestinal bleeding (all patients with and without recurrent bleeding) was 3.3%.

Once hemostasis is achieved, either endoscopically or surgically, clinicians face another crucial task: preventing late recurrent bleeding. Eradication of Helicobacter pylori can significantly reduce the likelihood of late recurrent bleeding. If patients must continue taking NSAIDs for various reasons, they should adhere to the following guidelines: use the least toxic NSAIDs to manage Arthritis symptoms; co-prescribe proton pump inhibitors alongside NSAID use; prescribe cyclo-oxygenase-2 selective anti-inflammatory drugs for patients taking NSAIDs; and all patients with GI bleeding must be tested for Helicobacter pylori, with those testing positive undergoing a course of eradication therapy.

First-line therapy: Omeprazole 20 mg twice daily; Clarithromycin 500 mg twice daily; Amoxicillin 1000 mg twice daily (Pilobact Neo). The course of treatment is 7 days.

Omeprazole 20 mg twice daily, Clarithromycin 250 mg twice daily, Tinidazole 500 mg twice daily (Pilobact, Pilomat). The course of treatment is 7 days.

Rabeprazole 20 mg twice daily, Ornidazole 500 mg twice daily, Clarithromycin 500 mg twice daily (Ornistat). The course of treatment is 7 days.

Pantoprazole 40 mg twice daily, Amoxicillin 1000 mg twice daily, Clarithromycin 500 mg twice daily (B-clatinol). The course of treatment is 7 days.

Tetracycline 250 mg twice daily, Metronidazole 200 mg twice daily, Bismuth subcitrate 300 mg twice daily (Gastrostat). The course of treatment is 7 days.

Lansoprazole 30 mg twice daily, Clarithromycin 250 mg twice daily, Tinidazole 500 mg twice daily (Clatinol). The course of treatment is 7 days.

Amoxicillin 750 mg twice daily, Metronidazole 500 mg twice daily (Helicocin). The course of treatment is 7 days.

Second-line therapy: includes first-line drugs plus bismuth subcitrate (De-Nol, Gastro-Norm), 1 tablet 4 times daily.