The modern management of patients with upper gastrointestinal bleeding includes, in selected patients, the performance of timely multimodal endoscopic hemostasis followed by profound acid suppression. This article discusses the available data on the use of antisecretory regimens in the management of patients with bleeding peptic ulcers, which are a major cause of non-variceal upper gastrointestinal bleeding, and briefly addresses other medications used in this acute setting. The most important clinically relevant data are presented, favoring fully published articles.
The modern management of patients with upper gastrointestinal bleeding includes, in selected patients, the performance of timely multimodal endoscopic hemostasis followed by profound acid suppression. This article discusses the available data on the use of antisecretory regimens in the management of patients with bleeding peptic ulcers, which are a major cause of non-variceal upper gastrointestinal bleeding, and briefly addresses other medications used in this acute setting. The most important clinically relevant data are presented, favoring fully published articles.
The biologic rationale for acid suppression in patients with upper gastrointestinal bleeding
Acid has been shown to inhibit platelet aggregation and even favors platelet disaggregation. Based on in vitro and animal experiments, the pH target required to avert these deleterious effects and favor hemostasis is thought to approximate 6.0 to 6.5. Acid is also known to facilitate clot lysis through the activation of pepsin, which occurs at pH levels below 2. Acid suppression, leading to pH levels more than 4, may prevent fibrinolysis. The rationale for acid suppression in upper gastrointestinal bleeding is based on the following deleterious effects of gastric acid on clot stability:
Decreased platelet aggregation, and even platelet disaggregation
Increased clot lysis from pepsin activation by acid
Increased fibrinolytic activity that is impaired by acid
A pH of 6.0 to 6.5 is targeted to reverse these effects based on in vitro and animal data.
After endoscopic therapy is performed for a high-risk ulcer lesion (eg, a visible vessel or pigmented protuberance), approximately 72 hours are required for most lesions to evolve and begin to display low-risk ulcer stigmata. This finding is corroborated by most clinical trials, including a recent large international study, that have shown that peptic ulcer rebleeding occurs predominantly during the first 72 hours after endoscopic treatment and the initiation of high-dose intravenous proton pump inhibitor (PPI) infusion.
Therefore, experts have hypothesized that acid suppression may stabilize intraluminal clots during this high-risk period, and result in a subsequent improvement of outcomes in patients with peptic ulcer bleeding. PPIs also exhibit anti-inflammatory properties of unclear clinical relevance discussed later.
Box 1 lists the relevant clinical recommendations for proton pump inhibitor–related use in the acute management of patients with non-variceal upper gastrointestinal bleeding.
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