Pharmacotherapy of Acute Non-Variceal Bleeding (1998)

Jenkins et al. [1] review the action and application of unassociated with an ulcerating process. All of these vessels will characteristically have a start-and-stop bleeding somatostatin and its analogue, octreotide. The authors of this review all have experience using somatostatin for pattern depending upon the integrity of the thrombus plugging the rent in the exposed vessel. The rationale the control of acute non-variceal bleeding. Passing thought is sometimes given these two drugs regarding for acute interventional pharmacotherapy has therefore reflected an effort to stabilize this clot or fibrin plug. their use in selected patients with refractory bleeding from any non-variceal cause and location. Their use is typically Limited anatomic data published over a decade ago demonstrated that the critical plug we speak of may become deferred for want of any convincing data to support their use and perhaps an element of uncertainty as to the disrupted (with rebleeding) via a process involving recannulization which is in contradistinction to the more comexpected physiologic effects of these drugs on a bleeding lesion within the upper or lower gut. We are all well mon notion that disruption is due to effects of the gastric juices immediately surrounding and bathing the nefarious versed in the standard percentages of patients with nonvariceal upper GI bleeding who spontaneously stop arterial plug [2]. This may be the reason why control of gastric acid secretion with H2-receptor antagonists and bleeding (80%), who continue to bleed (20%), and who will die as a result of a bleeding event (10%). The authors pH control only with antacids has failed to demonstrate benefit. However, use of proton pump inhibitors in doses contend that somatostatin plays a role in the management of the high-risk patient with acute non-variceal upper GI capable of inducing anacidity have been demonstrated to reduce rebleeding in patients with peptic ulcers and bleeding. They have also identified the insufficient data supporting the use of octreotide for the same patient nonbleeding visible vessels [3]. Antifibrinolytic therapy with tranexamic acid makes considerable sense in applygroup. Let us examine the evidence for the urgent use of somatostatin. ing the rationale for thrombus stabilization to control rebleeding, but has unfortunately failed. Non-variceal upper GI bleeders at high risk for rebleeding share a common problem, an exposed or visible Where does somatostatin fit in with regard to thrombus stabilization? Somatostatin demonstrates an inhibitory vessel which is typically located within a mucosal defect such as an ulcer. The ulcer may be peptic, due to prior effect on pepsin secretion. Jenkins et al. [1] have identified some of the potentially critical observations reported and thermal injury (e.g., post-polypectomy or sphincterotomy), traumatic (e.g., Mallory-Weiss tear), or neoplastic, applied these to patients with peptic ulcers: pepsin, especially pepsin 1, tends to have higher activity than in noreither benign (e.g., leiomyoma), or malignant. In patients with a Dieulafoy lesion the exposed vessel is typically mals; the proteolytic activity of pepsin 1 persists despite