Summary
Highlights
Other causes include vascular lesions (angiodysplasias, vascular anomalies, Dieulafoy's lesions, GAVE syndrome), neoplastic lesions (hemorrhagic polyps, adenomas, leiomyomas, carcinomas of the stomach/duodenum), and traumatic causes (Mallory-Weiss tear from forceful vomiting, direct trauma from foreign body ingestion). A rare but important cause is aorto-enteric fistula, particularly in patients with a history of abdominal aortic aneurysm repair.
The speaker reviews specific conditions with corresponding endoscopic findings. Mallory-Weiss tears are characterized by linear tears at the gastroesophageal junction following forceful vomiting. Erosive or hemorrhagic gastritis shows inflammation and erosion not deep enough to be an ulcer. Esophagitis presents with linear inflammation in the distal esophagus, sometimes leading to esophageal ulcers, and is associated with GERD symptoms. Malignancies, such as stomach carcinoma, display irregular mucosa and can cause bleeding. Peptic ulcers (gastric or duodenal) are presented as the main culprit and most common cause of non-variceal UGIB, accounting for up to 70% of cases. The video concludes by stating that Forrest classification will be discussed in part two.
A general surgeon from UITM introduces the topic of non-variceal upper gastrointestinal bleeding (UGIB), defining UGIB as bleeding proximal to the ligament of Treitz. The presentation will be divided into three parts: causes, Forrest classification, and management. This first part focuses on the causes of non-variceal bleeding, distinguishing it from variceal bleeding which originates from esophageal or gastric varices due to portal hypertension.
Non-variceal bleeding causes are broadly categorized into four types based on pathophysiology. Peptic ulcer disease is highlighted as the most common cause, with risk factors including Helicobacter pylori infection, NSAID use (e.g., diclofenac sodium, ibuprofen), physiological stress leading to stress ulcers, and hypergastrinemia (e.g., Zollinger-Ellison syndrome).
H. pylori infection disrupts the mucosal barrier and causes direct inflammation; its production of urease neutralizes gastric acid, allowing it to survive. NSAIDs inhibit cyclooxygenase, decreasing mucosal prostaglandin synthesis and impairing mucosal defense. Stress ulcers are common in ICU patients or those experiencing shock and sepsis, leading to alterations in mucosoprotective barriers.