الإفراز المعدي Gastric Secretion

WoW

مبين متعوب عليها

الله يعطيك العافية

الله يعطيكي العافية
جهد متعوب عليه

هاد شغل أكتر من رائع ، الله لا يضيعلك تعب يارب

يعتقد أن هذه الزيادة في الإفراز خلال فترة وجود المحرضات العاطفية هي أحد العوامل المتهمة في تطور القرحة الهضمية

من العوامل المؤدية لحدوث القرحة الهضمية
والتعرض للضغط النفسي

DO they still teach you this ancient unproven theory ?
Stress DOES NOT CAUSE ulcers, though it could lead to dyspepsia and pain but NOT ULCER

The stress that could lead to ulceration is major head trauma, burns, mecahnical ventilation for > 3 days..
BUT NOT EMOTIONAL STRESS.

Popel whom are at risk for bleeding in the hospital are those described above +
1- Older patients >60
2- Patients with history or previous bleeding
30 Patients on NSAIDs
4- Patients with multiple medical problems and coagulopathy

SO for those patients you may chose to use prophylactic treatment with H2 RB (receptro blockers)or even better PPI (proton pump inhibitors)

مشكورة بيرلاية
ومشكور دكتور ABIM

والطاهر هي نهايتي باخر السنة السادسة

طيب...
شكراً لكم جميعاً...

بس أنا وجدت الآتي في:

2- Guyton & Hall
يمكن أن يساهم الإفراز الزائد من الببسين في إحداث التقرح الهضمي:
في أغلب الناس المصابين بقرحه في الجزء الأول من العفج يكون الإفراز الحمضي المعدي أكثر من الطبيعي وفي بعض الإحيان يكون ضعف الطبيعي...
مع أن هذا الإفراز الزائد يمكن أن يتحرض من خلال الإنتان (مثلاً جرثومي من قبل الملوية البوابية),فإن التجارب المجراة على الحيوان مع وجود دليل لتحريض عصبي زائد للإفرازات الهضمية بينت أن زيادة العصارة المعدية لأي سبب (مثلاً اضطرابات نفسية) هو سبب أساسي للتقرح الهضمي ...
بالإضافة للإنتان الجرثومي والتحريض العصبي المسؤولان عن زياده في عصارة المعده فإنه يوجد عوامل مهيئة للقرحات:
التدخين
الكحول
الأسبرين

,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,

بدي حواب نهائي مين الصح ؟؟؟

مشان عدّل ما يجب تعديله في الصفحة لأن هذه مسؤولية....

طيب ممكن تعطوني مصادر جيب منها أحدث الدراسات عن ذلك ..؟؟

مشكورين...

Uptodate 2007

بتوقع بيقصد الأسباب الكبيرة متل الحروق والstress والعمليات الكبيرة وبالتالي مافي اختلاف

رائع

جد أنا عم احفظ الصفحات عندي مشان لما خلص الامتحان اعد اقرأهن على رواق

وجد شكراً كمان على الفلاشات اللي عم تنزلوها

كتير حلوة ومفيدة

و إن شاء الله بعد الامتحانات رح نعلن عن مفاجأة القسم العلمي الجديدة ( سر بيرلاتي لا تقولوها لحدا ) و نرجع نكمل شغل بإذن الله

كل التوفيق

يعطيكي الف عافيةpearls-2

والله شي حلو

وروان

ان شاء الله بتم على خير

موفقين

شكراً روان ...
قصدي عفواً
ونحنا بانتظار المفاجأة

i still think ALL hospitalized patients should take it... there should be something true about this... right

the quick answer is; wrong . you have to way the risks and the benefit of any treatment before giving it. supressing acid production on every in patient can be harmful ;
1- unjustified cost [in the cost-effective analysis ]
2- some studies r linking acid suppresion with aspiration pneumonia ,diarrhea and c. diff colitis. in addition to the side effects of these medications [although rare but if you give it to everybody then you will see it more]
I will look for a good article about the subject and post it here

sorry for the typo ;weigh not way

so we shouldn't give AntiH2 to every patient..great advice thanx alot doc

thanks dr.Omar
very helpful info.

waiting for the article.

Here is the article

Review
Nature Clinical Practice Gastroenterology & Hepatology (2007) 4, 562-570
doi:10.1038/ncpgasthep0953
Received 8 May 2007 | Accepted 6 August 2007

Therapy Insight: prophylaxis of stress-induced gastrointestinal bleeding in critically ill patients
Frank H Klebl* and Jürgen Schölmerich About the authors

Correspondence *Department of Internal Medicine I, University of Regensburg, D-93042 Regensburg, Germany

Email frank.klebl@klinik.uni-regensburg.de

Summary
Stress-induced gastrointestinal bleeding is associated with increased morbidity and mortality in critically ill patients. Within the past few decades, the incidence of stress-induced gastrointestinal bleeding has decreased. Prophylaxis of stress-induced gastrointestinal bleeding, which is aimed at preventing morbidity and mortality, has to be achieved with as few adverse effects as possible. Data indicate that not all critically ill patients need prophylaxis for stress-induced gastrointestinal bleeding. The main risk factors associated with clinically important hemorrhage are mechanical ventilation for >48 h, and coagulopathy (thrombocyte count <50/nl, partial thromboplastin time (PTT) >2 times the upper limit of the normal range, international normalized ratio (INR) >1.5). Ranitidine is more effective than sucralfate for the prevention of clinically important bleeding. Immediate-release omeprazole is as effective as cimetidine, and is more efficient at increasing the intragastric pH. As yet, however, there is no firm evidence that any of the drugs used for prophylaxis of stress-induced gastrointestinal bleeding in critically ill patients decrease mortality or the length of hospital stay. When to stop prophylaxis is decided on clinical grounds rather than on the basis of data from clinical studies.

Review criteria
Personal files containing manuscripts dealing with stress-induced gastrointestinal bleeding and its prophylaxis were updated with a PubMed search that used combinations of the terms "intensive care", "critical care", "gastrointestinal bleeding", "stress ulcer", "proton pump inhibitors", "H2-receptor antagonists", "antacids", "pirenzepine", and "sucralfate".

Keywords: bleeding prophylaxis, stress-induced gastrointestinal bleeding, stress ulcer

Top of pageIntroduction
Stress-induced lesions in the gastrointestinal tract can cause overt bleeding and hemodynamic instability in critically ill patients. Endoscopy studies have demonstrated that these lesions develop in many patients within the first few days of a critical illness (many lesions develop within 24 h).1, 2, 3, 4 Concepts that explain the pathophysiology of these lesions have been developed.5 Critical illness leads to splanchnic hypoperfusion via several routes, such as vasoconstriction caused by increased endogenous or exogenous catecholamines, hypovolemia, reduced cardiac output, and an increase in the levels of proinflammatory cytokines.5, 6 Consequently, there is reduced mucosal blood flow, decreased gastrointestinal motility, enhanced acid back-diffusion within the stomach, and reduced bicarbonate secretion, all of which contribute to the development of stress lesions. Experimental data suggest that bile reflux also contributes to erosion and ulcer formation in the stomach or esophagus.7, 8

Occult bleeding is frequently encountered in critically ill patients, and overt bleeding has been reported to occur in 4–25% of critically ill patients.1, 2, 9 The prevalence of clinically important bleeding is much lower (0.6–2.6%).2, 9, 10 Clinically important bleeding is defined as overt hemorrhage complicated within 24 h by a drop in blood pressure of more than 20 mmHg, an increase in pulse rate of more than 20 beats per min or a drop in systolic blood pressure of more than 10 mmHg measured on sitting up, or a decrease in the hemoglobin level of more than 20 g/l with no increase in hemoglobin levels after subsequent transfusion by the number of units transfused minus 20 g/l.11

Clinically important bleeding is associated with increased morbidity and mortality in critically ill patients,5, 11 although most patients do not die from gastrointestinal bleeding itself.12, 13, 14 In a post-hoc analysis of patients at risk of developing clinically important stress-induced gastrointestinal bleeding, it was calculated that clinically important bleeding increased the time of hospital stay by approximately 4–8 days, and was associated with up to a fourfold increase in mortality (range of relative risk: 1–4),11, 15 which ranges from 37% to 77%.12, 13, 14, 16, 17, 18, 19 Not surprisingly, therefore, many attempts have been made to find prophylactic measures to prevent upper gastrointestinal bleeding in this group of patients. As yet, however, there is no consensus on either patient selection or the choice of method for prophylaxis of stress-induced gastrointestinal bleeding (Table 1).20, 21, 22, 23, 24 Many intensivists use drugs to prevent stress-related gastrointestinal bleeding despite the perceived low frequency of this complication.23, 24

Table 1 Preferred choice of stress-related bleeding prophylaxis in surveys.

Full table
Figures & Tables index
Download Power Point slide (74K)

Several questions arise when trying to define the optimal method for the prevention of stress-induced bleeding. Do all patients need medication aimed at preventing stress-induced bleeding? Which patients should receive treatment to prevent bleeding? Are there drugs that are effective at reducing stress-induced bleeding? For how long should bleeding prophylaxis be employed? In 2000, Messori et al., who performed a meta-analysis on the effect of ranitidine and sucralfate for the prevention of stress-induced bleeding, stated that "Our main conclusion is that there are insufficient data on effectiveness to be able to conclude anything one way or the other."25 Although little has changed since then, in this Review we address some of the questions listed above and present hints to help intensivists decide whether to use prophylaxis for stress-induced bleeding and, if so, which prophylactic agent to use.

Top of pagePatient selection
Do all critically ill patients need medication aimed at preventing stress-induced bleeding? If prophylaxis of bleeding is perceived as maintaining adequate perfusion of gastrointestinal organs and ensuring an adequate oxygen and nutrient supply, then the answer to this question obviously must be yes. It is, however, common sense that these are goals for critically ill patients and, therefore, they need not be discussed further here. We, therefore, need to ask instead whether all critically ill patients need drugs aimed at preventing or alleviating stress-induced lesions.

In a cohort study, Faisy et al. compared two phases in which different strategies had been employed for the prevention of stress-induced lesions.26 In the first phase, stress-ulcer prophylaxis was prescribed to all critically ill patients: 736 patients received either sucralfate (n = 700) or ranitidine (n = 36). In the second phase, which included 737 patients, no prophylaxis was used. When the two phases were compared, there was no difference in the incidence of overt bleeding, clinically important bleeding, or mortality in the intensive care unit (ICU). These findings might suggest that there is no need for bleeding prophylaxis; however, it is also possible that the drugs used in the first cohort were simply ineffective.

Several studies have been performed to elucidate the risk factors for stress-induced bleeding in the critically ill. The largest study included 2,252 patients.16 In this study, univariate analysis indicated that there were several risk factors for stress-induced bleeding, but after multivariate analysis only two risk factors remained significant: mechanical ventilation for more than 48 h, and coagulopathy (thrombocyte count <50/nl, partial thromboplastin time (PTT) >2 times the upper limit of the normal range, international normalized ratio (INR) >1.5; Table 2). Of the patients who had at least one of these two risk factors, 3.7% (95% CI 2.5–5.2%) developed clinically important bleeding. Only 0.1% (95% CI 0.02–0.5%) of the 1,405 patients who did not have these risk factors suffered from this complication. The number needed to treat to avoid one episode of stress-induced gastrointestinal bleeding was calculated to be more than 900 in the latter group of patients, with the assumption that twice the number of patients would have developed clinically important bleeding if no prophylaxis had been used. This number is too high to consider the prophylaxis for stress-induced bleeding prevention useful.

Table 2 Risk factors for clinically important bleeding among 2,252 patients admitted to an intensive care unit according to Cook et al.16

Full table
Figures & Tables index
Download Power Point slide (82K)

Prolonged mechanical ventilation and coagulopathy have been confirmed as relevant risk factors by the findings of other, smaller studies.19, 27 Ventilated patients who have renal insufficiency are at a particularly high risk of developing clinically important bleeding.17 Patients with hepatic disorders have an increased risk of death if they develop bleeding.13 In addition, previous prophylaxis of stress-related bleeding has been found not to be associated with survival once bleeding has occurred.13

That bleeding prophylaxis can be safely withheld in critically ill patients who don't have the two major risk factors detailed has been demonstrated in studies conducted to examine the effect of introducing a standard protocol for the prevention of stress-induced bleeding. Restricting the use of prophylaxis to patients who have risk factors does not lead to increased morbidity or mortality and is cost-effective.28, 29, 30 Of note, patients who have major burns, a previous short-term history of peptic ulcers or gastrointestinal bleeding, or head injuries, have not been studied sufficiently to conclude that they can have prophylaxis safely withheld—in the study by Cook et al. examiners were not encouraged to omit prophylaxis in these cases.16

Top of pagePotentially prophylactic agents
PPIs, histamine-2-receptor antagonists (H2RAs), sucralfate, pirenzepine, prostaglandin analogs and antacids have all been studied as potentially active drugs for the prevention of stress-induced bleeding. The theoretical advantage of PPIs—related to their ability to elevate intragastric pH more effectively than the other drugs—has yet to be translated into a practical advantage with respect to clinically important end points (rates of clinically important bleeding and mortality) as determined from clinical trials conducted with sufficient numbers of patients. The other drugs listed above are also far from ideal. It is, therefore, not surprising that there has been wide ranging disagreement about which drug should be preferred.20, 21, 22, 23, 24

Several meta-analyses have been performed to try to clarify the effect of different drugs on the rate of clinically important bleeding. Antacids are effective at reducing the rate of overt bleeding;9 however, their use is inconvenient, reduces the time frame for enteral feeding, interferes with the absorption of other oral drugs, and their efficacy for this indication is inferior to H2RAs.31 Antacids have, therefore, been largely abandoned for this indication. Prostaglandin analogs have not proved effective.32

The selective antimuscarinic drug pirenzepine has been tested in small European studies (as cited in Tryba and Cook32). Pirenzepine reduces the risk of stress-induced bleeding, and might be particularly effective in neurosurgical patients and patients with head trauma;32 however, probably because of its anticholinergic side effects, this drug has not achieved broad acceptance as a prophylactic agent and has not been examined further in studies in the past 10 years or so.

In the meta-analysis by Cook et al. H2RAs were associated with a reduction in the rate of clinically important gastrointestinal bleeding, with a relative risk of 0.4 (95% CI 0.2–0.9) when compared with placebo.31 Mortality, however, was not reduced significantly by H2RAs. The meta-analysis by Messori et al. considered the H2RA ranitidine alone, which resulted in a low number of patients being included in the analysis. No significant association was found between use of the agent and decreased incidence of clinically important bleeding.25

In the one study on sucralfate that could be analyzed in the meta-analyses by Messori et al. and Cook et al., the drug had no effect on the incidence of clinically important bleeding.25, 31 Compared with H2RAs, sucralfate was associated with a similar rate of clinically important bleeding and a trend towards reduced rates of ventilator-associated pneumonia or mortality. As a consequence of the findings of the meta-analysis by Cook et al.,31 a large study was performed to compare ranitidine with sucralfate in critically ill patients who had risk factors for stress-induced gastrointestinal bleeding.33 Ranitidine (50 mg intravenously three times a day) was significantly better than sucralfate (1 g via a gastric tube four times a day) at preventing clinically important bleeding, with a relative risk of 0.4 (95% CI 0.2–0.9). The absolute rates of clinically important bleeding were 3.8% in the sucralfate group and 1.7% in the ranitidine group. In contrast to the trend found in the meta-analysis,31 there was no significant difference between the drugs in the rates of ventilator-associated pneumonia or death.

In summary, the findings of the meta-analyses performed suggest that H2RAs decrease the risk of clinically important bleeding, because of old studies that were performed with cimetidine. Ranitidine is significantly better than sucralfate (at least in the mode of application used in the study by Cook et al.33). As yet, there is no proof that H2RAs reduce mortality or the duration of hospital stay. It is also debated whether the effect of H2RAs that was demonstrated decades ago is still relevant in a situation in which there is a decreased rate of clinically important bleeding.34

There are drawbacks to the use of H2RAs. Tachyphylaxis occurs within the first 2 days of use.18, 35 In a post-hoc analysis, Cook et al. found that the benefit of ranitidine decreases during the course of treatment given when the patient is in the ICU.17 Patients who bleed early during their stay in the ICU, on the other hand, have a lower risk of dying than patients who bleed later.11 Adverse effects occur infrequently but can be severe and relevant in critically ill patients (e.g. arrhythmias, negative inotropy, bronchoconstriction, hepatitis, interstitial nephritis, or thrombocytopenia).32 For cimetidine in particular, drug interactions have to be considered. Moreover, the optimal dosage and mode of application, as well as the optimal choice of H2RA, have not been defined. It is not surprising, therefore, that there has been an awakening of interest in PPIs as potential drugs for bleeding prevention in critically ill patients.

Initial studies have demonstrated that the use of PPIs can elevate intragastral pH in critically ill patients to such an extent that, in theory, the elevation should enable adequate thrombocyte function and prohibit clot digestion by intraluminal proteases.36, 37, 38 Not all studies, however, have congruent findings.39 The first comparison of a PPI with another drug for the prevention of bleeding in critically ill was published by Levy et al.,40 who found a significantly lower rate of stress-induced gastrointestinal bleeding when using omeprazole compared with ranitidine (6% vs 31%). The number of patients in this study (n = 67) was, however, far too low to yield conclusive results with sufficient power. In addition, the ranitidine group had a higher rate of 'pretend' risk factors, and the bleeding rate in this group was unexplainably high and much higher than in other trials; therefore, the validity of the results is questionable.

A parallel group comparison of omeprazole, famotidine, sucralfate and placebo was performed by Kantorova et al. in approximately 70 patients in each group (mainly trauma and surgical patients) who needed mechanical ventilation for at least 48 h.34 These authors found that there was no significant difference in the rate of clinically important bleeding, ventilator-associated pneumonia, mortality, time on mechanical ventilation, or duration of ICU stay among the different treatment groups.34 It is worth noting, however, that many exclusion criteria (e.g. thrombocytopenia, and renal insufficiency requiring hemodialysis) had been applied.

Conrad et al. demonstrated the noninferiority of omeprazole compared with cimetidine for the prevention of stress-induced gastrointestinal bleeding in a randomized, double-blind, multicenter study.41 In their trial, 359 patients who needed mechanical ventilation for 48 h or more, who had an Acute Physiology and Chronic Health Evaluation II (APACHE II) score of 11 or more and who had at least one additional risk factor for upper gastrointestinal bleeding were randomized to receive immediate-release omeprazole (40 mg twice a day [6–8 h apart] on day 1 and 40 mg once a day on days 2–14 via a gastric tube) or cimetidine (300 mg bolus given intravenously followed by 50 mg per hour up to day 14). Dose adjustment was possible to maintain intragastric pH above 4. Of note, clinically important bleeding was defined differently in the study by Conrad et al.41 than in the study by Cook et al.33 and had less stringent criteria. Clinically important bleeding was defined by Conrad et al. as persisting bright red blood that did not clear after adjustment of the gastric tube despite a 5–10 min lavage, or 8 h of persistent coffee-grounds material positive for Gastroccult® (Beckman Coulter, Fullerton, CA) with aspirates not clearing with 100 ml or more of saline lavage on days 1–2, or persistent Gastroccult®-positive coffee-grounds material over 2–4 h on days 3–14 in three consecutive aspirates not clearing with 100 ml or more of saline lavage. This definition was adopted from the study by Martin et al., which led to the approval of cimetidine for the prophylaxis of stress-induced gastrointestinal bleeding in the US.42

Conrad et al. found that there was no significant difference in the rate of clinically important bleeding (intention to treat: 3.9% in the omeprazole group, 5.5% in the cimetidine group; Table 3), the rate of nosocomial pneumonia, or mortality between the groups.41 Overt bleeding was more frequent in the cimetidine group, and data on adequate intragastric pH control, as well as data on maintenance of a higher median gastric pH on each of the trial days, were in favor of the omeprazole group. An advantage of omeprazole with regard to clinically important bleeding, mortality, duration of hospital stay, or relevant morbidity has yet to be demonstrated.

Table 3 Prevention of stress-related bleeding and inadequate pH by omeprazole and cimetidine: results in the intention-to-treat population reported by Conrad et al.41

Full table
Figures & Tables index
Download Power Point slide (92K)

PPIs are frequently used in patients perceived to be at high risk of stress-related gastrointestinal bleeding.24 As omeprazole possibly affects neutrophil function,43, 44 the drug's theoretical advantage of providing a more potent elevation of intragastric pH than other possible prophylactic agents has to be translated into a proven clinical advantage by the findings of future trials before it is routinely used for this patient group. The stomach has been discussed as a possible source for the colonization of the respiratory tract and development of ventilator-associated pneumonia, and gastric colonization is associated with drugs that elevate intragastric pH.45 Whether pH-elevating drugs are associated with an increased risk of ventilator-associated pneumonia as compared with sucralfate or placebo is still being debated.9, 25, 31, 33, 46, 47

In conclusion, there are data that support the use of H2RAs as prophylactic drugs aimed at preventing stress-induced bleeding in critically ill at-risk patients. Immediate-release omeprazole is not inferior to cimetidine. Conclusive studies on other PPIs or formulations have not been published in full. The widespread use of PPIs to prevent stress-related bleeding has not yet been substantiated by a proven advantage in hard clinical end points in clinical studies.

Top of pageStopping Prophylaxis
To our knowledge, no prospective study has attempted to define the optimal time at which to discontinue prophylaxis for stress-induced bleeding. In an as yet unpublished survey, two out of every three Bavarian intensivists reported that they discontinue bleeding prophylaxis when risk factors are no longer present.48 This figure is much higher than the figure of 2% reported in the survey by Lam et al., which was performed in North America around 10 years ago.20 This survey also found that approximately every fifth intensivist (21%) would stop prophylaxis when the patient was discharged from the ICU, and as many (23%) noted that they would end prophylaxis when starting a patient's enteral feeding—a figure similar to that reported in another US study (29%),23 but much lower than the 84% of intensivists reported to stop prophylaxis when starting enteral feeding as reported in a UK study (Table 4).24 It is also of interest that many other conditions were perceived as risk factors for stress-induced bleeding in addition to mechanical ventilation for more than 48 h, and coagulopathy.20, 48

Table 4 Reasons for discontinuation of stress-related bleeding prophylaxis in surveys.

Full table
Figures & Tables index
Download Power Point slide (64K)

In a post-hoc analysis, enteral feeding was associated with a reduced risk of clinically important bleeding in critically ill patients on prolonged mechanical ventilation (relative risk 0.3; 95% CI 0.13–0.67).17 Enteral feeding and the use of ranitidine were, however, independently associated with this reduced risk. In a retrospective cohort study in patients with major burns, the change of the prophylactic strategy to beginning enteral feeding as early as possible, compared with the use of cimetidine and antacids to maintain intragastric pH more than 4 in the preceding period, was associated with a reduced rate of overt bleeding and a nonsignificant reduction in the rate of serious bleeding.49 Not all studies, however, have found enteral feeding to be associated with a risk reduction.16 It is also unclear whether enteral feeding was only a surrogate marker for less morbidity in the post-hoc analysis mentioned above (i.e. enteral feeding was only used in patients who could tolerate it as compared with sicker patients who had paralysis of the gastrointestinal tract). Consequently, whether enteral nutrition is efficacious as a prophylaxis for stress lesions is controversial.5, 50 Although it seems to be possible to withhold prophylaxis for stress-induced bleeding in enterally fed patients,32 more research needs to be done to decide whether this really is the case.

Some published data indicate that inadequate prophylaxis for stress-induced lesions is frequently encountered in hospitals and that this has consequences for expenditure and care after discharge.51, 52 The indication for drug prophylaxis in an individual patient should, therefore, be reconsidered regularly. At present, it seems advisable to consider stopping bleeding prophylaxis when risk factors resolve. This strategy was adopted in the clinical trial by Conrad and colleagues.41

Top of pageACID suppression as THE sole approach TO prophylaxis
Thrombocyte function and the digestion of fibrin clots by gastric proteases is pH-dependent. In theory, elevating the intragastric pH should, therefore, promote styptic reactions.6, 18, 53, 54 Moreover, PPIs, which increase intraluminal pH in the stomach most effectively, are potent drugs for the prevention of NSAID-induced gastroduodenal ulcers and the treatment of peptic ulcer bleeding, and are superior to other drugs used to heal Helicobacter pylori-negative peptic ulcers.55, 56 Is pH, therefore, most relevant to the development of stress-induced bleeding as well?

Jakob et al. studied 40 patients who had acute cardio-circulatory or respiratory failure and gave them ranitidine (50 mg three times a day intravenously) or placebo.57 Intraluminal pH, mucosal pCO2, and the mucosa-arterial pCO2 gradient did not differ between the groups. Mortality, however, was associated with increased intraluminal pH in the placebo as well as the ranitidine group. These findings confirm those of other studies that suggest that there is a lack of acid secretion into the stomach early in the course of a severe critical illness.32, 41

Some studies had already demonstrated that gastric intramucosal pH is more relevant than intraluminal pH for the development of stress-induced lesion.2, 58 Zandstra and Stoutenbeek tried to prevent stress-induced bleeding without conventional stress-ulcer prophylaxis in long-term ventilated patients by maintaining adequate tissue perfusion (and oxygenation) in combination with infection prevention and suppression of inflammatory reactions.59 They found a very low stress-ulcer-related bleeding rate of 0.6%. Although this does not substitute for proper head-to-head comparisons, it seems likely that the effect of pH-modifying drugs is not the only determinant of the development of stress-induced lesions. pH-modifying drugs do not target many of the factors that are considered relevant to the pathophysiology of these lesions in the early stages of critical illness. On the other hand, there are data to suggest that acid contributes to stress-related lesions.18 It therefore seems that suppression of acid production is one, but not the only, target for the prevention of these complications in critically ill patients.

Top of pageConclusions
At present, we know more about the circumstances that allow prophylaxis for stress-induced gastrointestinal bleeding to be withheld safely in critically ill patients than we do about the circumstances that render prophylaxis obligatory (see Box 1 for guidelines for the prescription of drugs for the prevention of stress-induced bleeding).

Box 1 Guidelines for the prescription of drugs for the prevention of stress-induced bleeding.
Consider prophylaxis when one of the following risk factors is present:

Mechanical ventilation for >48 h expected
Coagulopathy (thrombocyte count <50/nl, partial thromboplastin time >2 times the upper limit of the normal range, or international normalized ratio >1.5)
Previous short-term history of peptic ulcer or gastrointestinal bleeding, major burns, or severe head injuries

Possible choice of drugs:

Histamine-2-receptor antagonists
Immediate-release omeprazole

Discontinuation of prophylaxis should be considered when risk factors are no longer present.

General measures to prevent stress-induced lesions (e.g. avoiding arterial hypotension, maintaining adequate oxygen supply, correction of acid–base balance, early enteral nutrition) seem to be prudent.32 In patients who require mechanical ventilation for more than 48 h or who have coagulopathy, H2RAs and PPIs can decrease the rate of clinically important bleeding. A previous short-term history of peptic ulcer or gastrointestinal bleeding, major burns, or severe head injuries are regarded as indications for prophylaxis, and it is not clear whether prophylaxis can be safely withheld in patients with these conditions. When to discontinue prophylaxis should be decided on clinical grounds and should be discussed when risk factors are no longer present.

Key points

Not all critically ill patients are in need of bleeding prophylaxis
Withholding bleeding prophylaxis in suitable candidates is cost-effective
Mechanical ventilation for >48 h and coagulopathy (thrombocyte count <50/nl, partial thromboplastin time more than two times the upper limit of the normal range, international normalized ratio >1.5) are the main risk factors for stress-induced upper gastrointestinal bleeding
Histamine-2-receptor antagonists decrease the risk of clinically important upper gastrointestinal bleeding in patients at risk
Immediate-release omeprazole is as effective as cimetidine for the prevention of clinically important gastrointestinal bleeding, but its superiority has yet to be proven

شكرا كتير دكتور ويجزيك الخير لأنك ما بس مخلص بعلمك وعملك وإنما مخلص بنشرك للمعلومة ومساعدة من يأتي بعدك
أمثالك يا أستاذنا فعلا قلائل

طبعا قريت الSummry وحأطبع بقية المقال لأقراه كله لأنو بحب أتعامل مع الورق أكتر من شاشة اللابتوب

وكل عام وأنت بخير

i just read it, thanks.