Commentary Bleeding from stress-related gastrointestnal mucosa disease in critcal patents remains a major clinical management problem in the intensive care unit in both adults and pediatrics. Although the incidence is low (1%-6%), a substantal proporton presents clinical risk factors (such as mechanical ventlaton greater than 48 hours and coagulopathies) that predict an increased risk of bleeding. In additon, we can fnd lesions of the gastrointestnal mucosa in up to 75 to 100% of patents in the ICU. Although rare, stress ulcer bleeding is a serious complicaton with an estmated high mortality of 40 to 50%, mainly due to decompensaton of an underlying conditon or mult-organ failure. Although the majority of ICU patents receive stress ulcer prophylaxis, mainly with IBP, there is some controversy surrounding its efcacy and safety. Indeed, no individual trial has shown that stress ulcer prophylaxis reduces mortality. Some reports suggest that the use of IBP increases the risk of nosocomial infectons. However, several meta-analyzes and cost- efectveness studies suggest that IBP are clinically more efectve and cost-efectve than histamine-2 receptor antagonists (H2RA), without considerable increases in nosocomial pneumonia [1]. In pediatrics gastrointestnal hemorrhages are described in up to 10% of the complicatons in patents with critcal illness of these 1.6% are signifcant hemorrhages, of these are associated with risk factors such as respiratory failure, coagulopathy or PRISM score>10, with incidences probably even older in neonatal ICUs [2]. The pathophysiology is complex and begins with vasoconstricton, mucosal ischemia eventually leads Bleeding that results from stress ulceratons is called stress ulcer related bleeding (SURB). Upper Gastrointestnal Bleeding (UGIB) can also originate in other places, for example, refux esophagits, which has a diferent approach. Recently, it has become clear that acid suppression does not prevent UGIB or SURB. It is believed that stress ulcers are caused by decreased mucosal blood fow, ischemia and reperfusion injury, and therefore are less related to acid secreton than peptc ulcers. However, the pathophysiology has not been fully clarifed [3]. Patents in critcal conditon may have an alteraton in gastric mucosa from the frst 24 hours of admission resultng from erosion, ulcers and even signifcant bleeding causing hemodynamic instability. To prevent mucosal damage caused by acid produced by gastric cells several pharmacological optons as sucralfate whose main functon is used is to inhibit acid secreton, this adheres to epithelial cells to cover the gastric mucosa and create a thin protectve layer between the mucosa and the gastric acid in the stomach lumen; receptor antagonists Histamine-2 are also used being an antagonist of H2 receptors and proton-pump inhibitor which inhibits this the adenosine resultng฀ in reducing the producton of acid by the parietal cells [4]. The normal gastric mucosa is designed and highly adapted to resist acid fuids in gastric light. The integrity of the gastric mucosa is normally formed by the mucus layer, a phospholipid barrier, the tght junctons between the epithelial cells, the ability to regenerate the mucosa, the producton of prostaglandins and the blood fow of the mucosa. Loss of one or more of these barriers leads to decreased integrity of the gastric mucosa. In critcal patents, infammatory status and altered circulaton of the splanchnic region may result in a reducton of one or more of these defense mechanisms. When alteratons in the integrity of the gastric mucosa occur, gastric acid is allowed to reach the deeper layers of the mucosa, which can lead to the formaton of a gastric ulcer. Mucosal damage occurs in 75% to 100% of patents admited to the ICU in shock. Probably, the main reason for a disrupton of the mucosal barrier functon in any critcal patent is a reducton in mucosal circulaton. A perfused mucosa normally recovers from the lesion in a mater of hours, but a damaged splanchnic perfusion during an infammatory state makes recovery difcult (Figure 1) [4]. DOI:10.36648/2471-805X.5.3.100037 What's New in Preventng Pediatric Gastrointestnal Bleeding in Critcally Ill Patents? Andrea Carolina Zarate Vergara 1 , María Alexandra Pérez Sotelo 2 and Irina Suley Tirado Pérez 3* 1 Pediatric Intensive Care, University of Santander, Santander, Colombia 2 Department of Pediatric Oncology Hematology, Internatonal Hospital of Colombia, Colombia 3 Palliatve Master Pediatric Care, University of Santander, Santander, Colombia * Corresponding author: Irina Suley Tirado Pérez, Master Pediatric Palliatve Care, Graduate Student o f Pediatric Intensive Care, University of Santander, Colombia, E-mail: irinasuley@gmail.com Received date: December 08, 2019; Accepted date: December 21, 2019; Published date: December 29, 2019 Citation: Vergara ACZ, Sotelo MAP, Pérez IST (2019) What's New in Preventing Pediatric Gastrointestinal Bleeding in Critically Ill Patients? Journal of Pediatric Care Vol.5 No.3:1. 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