Reliability of Intragastric pH probe catheter equipped with temperature sensor for minute to minute monitoring in critically ill patients

Pantoprazole is a gastric acid pump inhibitor similar to omeprazole used as the sodium salt in the treatment of erosive esophagitis associated with gastroesophageal reflux disease and pathological hypersecretion associated with Zollinger-Ellison syndrome. Pantoprazole works as a restrictor of H/K ATPase. Thus it leads to a reduction of hydrochloric acid production in the stomach and the pH value of the gastric juice come rise, which leads to a reduction of aggressiveness of the gastric juice and thus to accelerate healing of gastric wall injuries.(as for example:SRMD) Changes in inflammatory cytokines and inhibition of prostaglandin synthesis lead to reduced resistance of gastric mucosa to damaging factors. Some studies performed on the role of cytokines in gastric pH and peptic ulcer disease are as following: Increase of Helicobacter.Pylori in endoscopic studies was due to low mucosal concentrations of IL-8, IL-1a and high concentration of IL-13 and in another study increased concentration of TNF-a and IL-6 was associated with H.Pylori gastritis. No relationship between IL-1B gene polymorphism and gastric secretion in younger healthy volunteers is seen. Inhibitory potency of twice-a-day omeprazole on gastric acidity is enhanced by eradication of H.Pylori and is correlated to fall in gastric juice NH3. Gastoesophageal reflux disease-associated esophagitis induces endogenous cytokine production (IL-6). IL-8/STREM is an independent factor for the generation of peptic ulcer disease and might behave as an anti-inflammatory mediator in chronic gastritis. The effect of HBD-2 in pathogenesis of gastritis may be through its function as immune and inflammatory mediator. These results indicate that classic cytokines are important mediators associated with esophagitis and gastritis. Experimental section: Upon admission to the ICU all the patients who did need nasogastric tube and met the following inclusion criteria would be enrolled to intragastric pH – temp monitoring trial. - Inclusion criteria: 1. Age>18 2. Base line intra gastric pH<3.5 3. High risk patients a. patients with Coagulopathy disorders. b. Ventilator dependant patients, shock, respiratory failure, trauma, sepsis. - exclusion criteria 1. History of peptic ulcer disease, active G.I bleeding 2. Patients with zollinger Ellison 3. Recipient of H2 blockers & NSAIDs 4. Tube feeding 5. Creatinin>2 or Creatinine>25%increase in baseline 6. abnormal LFT (3 times > base line) 21 patients would be randomized in 3 groups. Group A: receive pantoprazole 40 mg/BD Group B: receive a bolous dose of pantoprazole 25mg stat and then 3 mg/hr Group C( Control group): receive standard treatment The study would last 64 hrs (two 24 hrs and a 16 hrs wash-out period between them, which patients intra gastric temp and pH monitored every 3hrs, with our intra gastric probe catheter simultaneously 5cc of gastric Juice is going to be obtained every 6hrs and pH shall be detected via pH meter. The level of inflammatory interleukins IL1, TNF? and anti inflammatory interleukins IL10, EGF of patient’s gastric juice with enzyme-link immunoassay in 2, 12, 24, 48, 64 hrs after admission of the patient two the ICU. To find out that is there any relation between intra gastric pH and temp and the levels of this inflammatory and anti inflammatory factors. Endoscopy will be perform pre and post intervention for the patients to compare the degree of mucosal damage due to Stress between group (RMD)