Prevacid

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

James L. Gutmann DDS, Cert Endo, PhD, FICD, FACD, FADI

  • Professor Emeritus, Baylor College of Dentistry, Texas A & M
  • University System, Dallas, Texas, USA

Vitamin A accumulates and should not be supplemented beyond the recommended dietary allowance gastritis symptoms treatment mayo clinic order prevacid. The preferred route has been the subject of considerable controversy during the past 40 years gastritis diet cheese buy prevacid online now. Both routes have advantages and disadvantages gastritis y sintomas discount prevacid uk, and nitrogen balance can be achieved by either route gastritis diet order generic prevacid online. Disadvantages of parenteral nutrition include cost gastritis diet buy prevacid 30 mg low price, procedure (central venous catheter)-related complications gastritis diet 2 buy generic prevacid 15mg on line, an increased likelihood of metabolic complications, including hyperglycemia, and an increased risk of infectious complications. Enteral nutrition is much less expensive, is more physiologic, is associated with fewer metabolic complications such as electrolyte abnormalities and hyperglycemia, and stimulates gut function and preserves mucosal integrity and barrier function better than parenteral nutrition does. Disadvantages of enteral nutrition include the requirement for an intact and functioning gastrointestinal tract, procedure (feeding tube placement)-related complications, pulmonary aspiration, malabsorption, feeding intolerance (pain, vomiting, bloating, diarrhea), and as a result, an inability to deliver the entire nutrient prescription. The gastrointestinal tract is a major interface between the host and the environment and not only regulates the ingestion and absorption of nutrients but is also responsible for defending the host against noxious microorganisms and toxins. Typical daily electrolyte requirements include sodium 60 to 100 mEq/day, potassium 60 to 100 mEq/day, magnesium 10 to 20 mEq/day, calcium 10 to 15 mEq/day, chloride 80 to 120 mEq/day, and phosphorus 20 to 30 mmol/day. Particular attention should be paid to the intracellular electrolytes (potassium, phosphorus, and magnesium), which are required for attainment of nitrogen balance58 and serum levels of which can fall precipitously when nutrition support is initiated. These IgA-producing lymphocytes then migrate to distant organs such as lungs, liver, and kidneys, where they form mucosal-associated lymphoid tissue and produce secretory IgA. Several meta-analyses comparing enteral and parenteral nutrition have shown significant reductions in infectious complications with the use of enteral nutrition. Whether this is the primary reason for the increased infection risk associated with parenteral nutrition is less clear. In several of the studies mentioned in previous paragraphs, many of the patients managed with parenteral nutrition received significantly more calories and had a higher incidence of hyperglycemia80 than did their enterally fed counterparts. In a study in which parenterally fed patients had a higher incidence of sepsis, twice as many patients receiving parenteral nutrition had hyperglycemia as enterally fed patients. There was no difference in 30-day mortality, and secondary endpoints were largely similar with the exception of more vomiting in the enterally fed patients. The incidence of infection was lower in the enterally fed group, but this difference was explained by the subset of trials in which the parenterally fed group received more calories and presumably had poor glucose control. Autophagy is an important housekeeping process that is normally activated by cellular stress to remove cellular damage. All patients received early enteral nutrition by protocol and had insulin infused to maintain normoglycemia. Further, patients in the late initiation group had significantly fewer infections, a significant reduction in the proportion of patients requiring more than 2 days of mechanical ventilation, a significant median reduction of 3 days in the duration of renal replacement therapy, and a mean reduction in health care costs of approximately $1600. There was no difference in ventilator-free days between the groups and the fully fed group had more gastrointestinal intolerance. None has been consistently shown to improve outcomes when compared with conventional formulas. Pulmonary failure formulas are designed for patients with acute respiratory failure associated with chronic lung disease. They contain at least 50% of calories as fat and thus reduce carbon dioxide production and decrease the work of breathing relative to highcarbohydrate formulas. Few data suggest a benefit with specific pulmonary formulas, and avoidance of overfeeding is more important in reducing ventilatory demand. They contain high concentrations of branched-chain amino acids and reduced concentrations of aromatic amino acids. Although these solutions have been shown to correct the abnormal amino acid profile characteristic of patients with liver failure,111,112 it is less clear that they actually treat hepatic encephalopathy. Patients with acute renal failure frequently have associated catabolic illness and as a result need more protein rather than less. Current recommendations for critically ill patients with acute renal failure are that standard recommendations for protein and calories should be followed, and that specialty formulas only be used for management of significant electrolyte abnormalities. Electrolytes can usually be added in standard stock concentrations or individually. Vitamins and trace elements are generally added in standard quantities but can be supplemented. Histamine 2 (H2) blockers for stress ulcer prophylaxis and regular insulin can also be added. Enteral formulas are usually premixed with a fixed nonprotein calorie-to-nitrogen ratio, and the needs of a specific patient are generally met by changing the formula. Protein and carbohydrate supplements can be added at the bedside to alter premixed formulas. Enteral formulas can be classified in numerous ways, including the form in which protein is provided. Such solutions contain 45% to 60% of calories as carbohydrate (oligosaccharides), 20% to 35% of calories as longchain fats. Hydrolyzed formulas provide protein as peptides or amino acids, are generally low in fat, and are designed for patients with gut dysfunction or malabsorption. Controlled studies comparing hydrolyzed or elemental formulas with intact formulas have not demonstrated improved tolerance or outcomes. High-protein formulas contain more than 45 g protein per 1000 kcal and are designed for patients with increased protein needs, such as patients with catabolic illness. Calorie-dense formulas are designed for patients in whom fluid restriction is required. They are generally relatively low in protein and not ideal for a stressed patient. Immunomodulating Enteral Formulas Immunomodulating enteral formulas are supplemented with various combinations of specific nutrients, arginine, -3 polyunsaturated fatty acids, nucleotides, glutamine, and antioxidants aimed at improving immune function and reducing inflammation in critically ill patients. Arginine is a nonessential amino acid that has both beneficial and deleterious effects. It is a secretagogue for anabolic hormones, supports T-cell function, detoxifies ammonia, and supports wound healing via metabolism to polyamine and proline. Considered a nonessential amino acid, glutamine may become conditionally essential when skeletal muscle stores and plasma levels become depleted during catabolic illness, thereby resulting in adverse effects on gut barrier and immune function. A meta-analysis of 14 randomized trials in which glutamine-supplemented nutrition was compared with standard nutrition demonstrated reduced infectious morbidity and mortality rates with glutamine supplementation, particularly in parenterally nourished surgical patients. In a 2001 meta-analysis of 22 studies (2419 patients) in which enteral nutrition supplemented with various combinations of arginine, -3 fatty acids, glutamine, and nucleotides was compared with conventional enteral nutrition, the supplemented patients had decreased infectious morbidity but no difference in mortality rates when compared with patients receiving the control diet. In the subsequently published and largest (597 patients) randomized trial to date, immunonutrition had no benefit in terms of infectious morbidity, length of hospital stay, number of ventilator days, or mortality rate. Second, the immunomodulating enteral formulas studied contained varying combinations of arginine, -3 polyunsaturated fatty acids (fish oil), glutamine, and antioxidants. Overall, the immunomodulating diets had no effect on mortality rate but did demonstrate significant reductions in secondary infections. The physical examination might, on occasion, demonstrate abnormal end-organ function that reflects malnutrition, but more commonly it is useful for the assessment of body mass and detection of specific nutrient deficiencies. Signs and symptoms of selected vitamin and mineral deficiencies are presented in Tables 78. They are affected by a number of variables other than nutritional status, such as hydration state and gastrointestinal and urinary losses, and must therefore be used cautiously in a critically ill patient. Serum albumin levels are decreased in nephrotic syndrome, enteropathies, hepatic failure, and dialysis (particularly peritoneal dialysis), as well as in the setting of acute volume expansion. Levels may be increased in the presence of dehydration, hypercortisolemia, and anabolic hormones, such as insulin, growth hormone, and estrogen. Although serum albumin levels are useful in predicting surgical mortality rate and monitoring nutritional status over the long term, they are much less useful in monitoring a critically ill patient. It is subject to the same influences as mentioned for albumin and, in addition, is affected inversely by serum iron levels. Levels rise in patients with renal disease175 and with excess vitamin A administration and are reduced in patients with liver disease, cystic fibrosis, hyperthyroidism, and vitamin A deficiency. Transthyretin (thyroxine-binding prealbumin) is involved in the transport of thyroid hormone and is a carrier for retinol-binding protein. Levels are low in patients with hyperthyroidism, cystic fibrosis, chronic illness, and acute stress. Because of its short half-life and ease of measurement, transthyretin is the visceral protein of choice for nutritional assessment and monitoring, although its use in a critically ill patient is controversial. During catabolic illness, hepatic protein synthesis is reprioritized, under the influence of cytokines, with increased synthesis of acute-phase reactant proteins and decreased synthesis of visceral proteins. Whether transthyretin levels are reflective of appropriate nutrition support or simply a reflection of the course and severity of the inflammatory response is unclear. An initial transthyretin level lower than 50 mg/L or failure to increase by 40 mg/L per week has been associated with a poor prognosis. Ideally, positive nitrogen balance is the goal, but minimizing the nitrogen deficit in a critically ill patient is probably more realistic when one considers the fact that proteolysis in the skeletal muscle compartment, which constitutes 70% of body protein stores, is likely to exceed protein synthesis related to the inflammatory response and wound healing, simply because of the size of the compartments involved. Nitrogen balance is calculated as follows: Nitrogen balance (g) = Nitrogen intake (g) - Nitrogen output (g) Nitrogen intake (g) = Protein or amino acid intake (g) 6. In health, urea constitutes 90% of urinary nitrogen, whereas in catabolic states, urea may represent as little as 70% of urinary nitrogen. Numerous techniques for assessment and monitoring of energy balance have been studied, including continuous whole-body calorimetry,191 the doubly labeled water technique,191 and nuclear magnetic resonance spectroscopy using phosphorus 31,192 but no method is ideal. Although they are potentially useful, these methods are either cumbersome, expensive, or impractical for use in critically ill patients. Intracellular electrolyte levels should be measured before starting nutrition support, 1 or 2 days after starting support, and at least weekly thereafter. Liver function and coagulation parameters should be evaluated weekly and as needed. Glucose should be measured every 6 hours initially and then as needed; it can be measured as often as every 2 hours when continuous insulin infusions are being used. Complications of Nutrition Support Complications of nutrition support include those related to the route of nutrition support and those related to nutrition support in general and are discussed in the following paragraphs. Perhaps the most important problem with nutrition support is failure to achieve therapeutic goals. Recommendations for appropriate doses of protein and calories, electrolytes, vitamins, and trace elements are discussed in previous text. Complications of Enteral Nutrition Support Complications specific to enteral nutrition support include mechanical or technical complications, gastrointestinal complications, and aspiration pneumonia. Mechanical and technical complications of enteral nutrition include feeding tube misplacement, gastrointestinal perforation, sinusitis, otitis media, ulceration of the nasal septum, and obstruction of the feeding tube. Proper placement of feeding tubes in the gastrointestinal tract should be confirmed radiographically or with pH testing before feeding is initiated. Soft, small-caliber tubes such as Miller-Frederick or Dobhoff tubes seem to cause sinusitis less frequently. In mechanically ventilated patients, feeding tubes may be placed orally to minimize the incidence of sinusitis. In these situations, tube placement under fluoroscopic guidance or endoscopic tube placement should be considered. Dislodgment of the feeding tube is a frequent and frustrating problem and can be disastrous when the tube dislodged is a recent, surgically placed tube such as a gastrostomy or jejunostomy tube. When a surgically placed tube has been present for longer than 1 to 2 weeks, the stomach or intestine should be adherent to the abdominal wall and the tube can usually be replaced through the existing tract, as long as the tube is replaced within a few hours before the tract begins to close. A radiograph with contrast enhancement should be used to verify replacement of the tube in the appropriate location. Dislodgment of a surgically placed tube within a week of placement can result in peritonitis from spillage of enteral formula or gastrointestinal contents into the abdominal cavity. Care should be taken to properly secure all feeding tubes either with sutures and tape or with commercially available fixation systems, and tubes should be protected with appropriate patient restraints and caregiver attention when the patient is being moved. Feeding tube obstruction occurs most frequently when tubes are not routinely flushed or when crushed medications are delivered through the tubes. Numerous techniques have been used to clear obstructed tubes, including flushing with cola, pancreatic enzymes, cranberry juice, and streptokinase, although none is universally successful. Clearing a nasoenteric tube with a stylet or wire carries the risk of perforating the gastrointestinal tract and should be avoided unless done under fluoroscopic guidance to ensure that the stylet remains within the tube lumen. Gastrointestinal complications such as abdominal distention, nausea, vomiting, diarrhea, and constipation occur in approximately 60% of critically ill patients receiving nutrition support. Prokinetic agents such as metoclopramide may restore gastric motility and allow gastric feeding. Advancement of the feeding tube into the proximal jejunum facilitates enteral nutrition in patients with pancreatitis. Clostridium difficile overgrowth is perhaps the most serious cause of antibiotic-associated diarrhea, and stool should be assayed for C. Antibiotics may also cause diarrhea by eliminating the bacteria that ferment dietary fiber into short-chain fatty acids. Short-chain fatty acids are important for maintaining colonic mucosal integrity and enhance water and electrolyte absorption. A change in formula or more gradual institution of nutrition support can be used to overcome problems caused by nutrient intolerance, disuse atrophy, and short-gut syndrome. Semi-elemental or peptide formulas may reduce diarrhea in patients with mucosal atrophy. H2 blockers can be used to decrease the contribution of gastric secretions to diarrhea in patients with short-gut syndrome.

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In patients presenting with dysphagia gastritis diet order prevacid 30mg amex, eosinophilic esophagitis should by excluded by multiple mucosal biopsies obtained at different levels of the esophagus gastritis symptoms hunger generic prevacid 15 mg mastercard. Scleroderma esophagus may sometimes be confused with achalasia gastritis diet 6 days prevacid 30mg lowest price, particularly in patients with a dilated esophagus on barium swallow and poor peristaltic contractions in the thoracic esophagus on barium swallow or esophageal manometry gastritis gluten buy prevacid 15mg free shipping. Physiologic changes in the esophagus contribute to poor esophageal clearance and marked gastroesophageal reflux gastritis diet xtreme proven prevacid 30 mg. Pulmonary interstitial fibrosis can result from either direct involvement of the disease gastritis diet breakfast discount prevacid online american express, or from aspiration of refluxate. Generally, antireflux surgery should be avoided because of the risk of severe postoperative dysphagia. Otherwise, a partial fundoplication, generally with a Collis procedure and esophageal lengthening, is performed. However, symptoms can be relatively mild despite severe mucosal disease, and esophageal disease correlates better with degree of pulmonary involvement rather than disease in the stomach or intestine. In addition, in the older literature, symptom duration prior to diagnosis averaged 4. The incidence appears to be increasing and this is not only due to increased recognition of the disorder as a consequence of increased endoscopic volume, but perhaps due to other factors as well. This is evidenced by a population-based study that documented incidence of eosinophilic esophagitis in Olmsted County, Minnesota, where the incidence was 9. Similar population-based studies in Switzerland have also concluded that the incidence of eosinophilic esophagitis is increasing and may actually be approaching that of inflammatory bowel disease. Full diagnostic criteria are (1) clinical symptoms of esophageal dysfunction; (2) increased eosinophils in esophageal mucosal biopsies; (3) secondary causes of esophageal eosinophilia have been excluded; (4) lack of sustained response to high-dose proton pump inhibition treatment or normal pH monitoring of the distal esophagus; (5) response to treatment (elimination diet, topical glucocorticoids) supports the diagnosis. The disorder is being diagnosed with much greater frequency, and increased recognition, by virtue of increased endoscopic volume, alone may not be responsible for this trend. More than 80% of patients diagnosed with eosinophilic esophagitis complain of dysphagia, and between 5% and 16% of patients undergoing endoscopic evaluation for dysphagia are found to have eosinophilic esophagitis. Further, more than 50% of patients presenting with frank food impaction are diagnosed with eosinophilic esophagitis. However, considerable evidence suggests that eosinophilic esophagitis is an allergic disorder induced by antigen sensitization either through foods and/or aeroallergens. A majority of patients have evidence of food allergies and a concurrent history of respiratory allergies. A seasonal variation has been documented in the diagnosis of eosinophilic esophagitis that correlated with pollen counts. By contrast, food anaphylaxis is uncommon, occurring in less than 15% of pediatric patients with eosinophilic esophagitis. The recruitment of eosinophils occurs in several inflammatory or infectious conditions and after exposure to inhaled or ingested allergens. Eosinophils also release chemoattractants, such as interleukins, which can perpetuate an inflammatory response. Diagnostic Criteria the usual criteria for the diagnosis of eosinophilic esophagitis include the following: 1. Clinical symptoms of esophageal dysfunction, especially dysphagia and a history of meat impaction. In addition, patients may have also demonstrated normal pH monitoring of the distal esophagus. As noted below under treatment considerations, responses to treatment such as dietary elimination, topical corticosteroids, etc support but are not required for diagnosis. With regards to esophageal biopsies, two to four biopsies should be obtained from both the proximal and distal esophagus to maximize the likelihood of detecting esophageal eosinophilia in all patients. Further, at the time of diagnosis, biopsies should be obtained from the antrum and/or duodenum to rule out other causes of esophageal eosinophilia. Symptoms and Signs the leading symptom in adults is recurrent attacks of dysphagia. Mean duration of symptoms before diagnosis and initiation of treatment in one large series was 4. Recurrent dysphagia is present in the majority of patients, as is the history of food impaction. A personal history of allergic diseases (ie, airway, food, or skin allergies) is frequently present. Serum immunoglobulin E (IgE) elevations have been documented in one series in two-thirds of the patients. However, it should be emphasized that there is no difference in symptoms, endoscopic findings, or histology in patients with increased serum IgE levels versus those with normal IgE levels. Symptoms appear to be more pronounced in patients with peripheral blood eosinophilia. Endoscopy Endoscopic features associated with eosinophilic esophagitis are highly variable. Other more frequent findings include trachea-like circular rings that can be transient or fixed, white exudates, white nodules with granularity, linear furrowing, and vertical lines on the esophageal mucosa. Finally, strictures in the proximal, middle, or distal esophagitis are sometimes encountered. Examples of typical endoscopic findings in eosinophilic eosinophils are shown in Plates 18 and 19. Other disorders also may be associated with increased eosinophilic infiltration of the esophagus (see later). Accordingly, biopsies should be taken in both the distal and mid-esophagus in patients with suspected eosinophilic esophagitis. Characteristic histologic findings in eosinophilic esophagitis are shown in Plate 20. Variability in diagnostic criteria for eosinophilic esophagitis: a systematic review. Eosinophilic esophagitis in children and adults: a systematic review and consensus recommendations for diagnosis and treatment. Features that independently predicted eosinophilic esophagitis included younger age; symptoms of dysphagia; documented food allergies; observation of esophageal rings, linear furrows, white plaques, or exudates by upper endoscopy; absence of a hiatal hernia; and a higher maximum eosinophil count. Although increased eosinophilic infiltration in the esophagus is characteristic of eosinophilic esophagitis, it is not exclusively found in that disorder. Increased eosinophils can be found in the distal esophagus in reflux esophagitis but not in the mid-esophagus. Clinical, endoscopic, and histologic findings distinguish eosinophilic esophagitis from gastroesophageal reflux disease. High intraepithelial eosinophil counts in esophageal squamous epithelium are not specific for eosinophilic esophagitis in adults. This preparation was well tolerated in 20 children and led to histologic improvement in 80% of these patients. Systemic Corticosteroids Systemic corticosteroids are effective in eosinophilic esophagitis, but side effects limit their use, especially for periods longer than 4 weeks. They may be indicated when urgent symptom relief is required as with patients experiencing severe dysphagia, dehydration, and significant weight loss or esophageal strictures. Esophageal Dilation Esophageal dilation may be necessary in patients with strictures, but it must be done carefully as it has been associated with deep mucosal tears, esophageal perforation, increased postendoscopic analgesia, and difficulty in inserting the endoscope. Approximately half of the patients treated with esophageal dilation will become asymptomatic. However, once the medication was discontinued, six of the eight patients had a recurrence of their symptoms. Data are insufficient to recommend leukotriene receptor antagonists for the treatment of eosinophilic esophagitis. Topical Corticosteroids Several studies that have employed topical fluticasone in doses ranging from 220 to 440 g two to four times daily have demonstrated symptom improvement and complete resolution of symptoms in up to 75% of cases. Patients are generally instructed to swallow rather than inhale the fluticasone and not use a spacer. Patients receiving the higher dose of fluticasone are more likely to develop esophageal candidiasis. Furthermore, higher doses of fluticasone (ie, >440 g/day) have been associated with systemic side effects, including cataracts and adrenal suppression. Although the use of swallowed corticosteroids is effective in relieving symptoms for a short period of time (4 months or less), long-term efficacy remains controversial. Although data are limited, this preparation may well be a viable alternative to using E. Cromolyn Sodium Cromolyn sodium, a mast cell stabilizer, has not shown any apparent benefit for patients with eosinophilic esophagitis although it has no significant adverse effects. Dietary Therapy Dietary therapy is an important emerging form of therapy for eosinophilic esophagitis. Elemental (amino-based formula diets)-Peterson et al assessed the efficacy of an elemental diet in adults with eosinophilic esophagitis. Eighteen adults with eosinophilic esophagitis were given an elemental diet for 4 weeks or just 2 weeks if their response was complete. It should be noted that while elemental diets are effective in alleviating symptoms and affecting objective evidence of improvement, these diets are not well tolerated in some patients. Elimination diets-This can be difficult because patients are typically sensitive to multiple food groups that include common and uncommon foods. Several studies have demonstrated a poor correlation of diagnostic skin testing, radioallergosorbent testing, and IgE skin prick tests with improvement in either symptoms or tissue inflammation. Empiric elimination diet with removal of common food allergies-One center did report a significant improvement in patients on a specific food elimination diet. Kagalwalla and colleagues demonstrated that eliminating the six most common allergenic foods (dairy, eggs, wheat, soy, peanuts, and fish/shellfish) resulted in significant improvement in 74% of the 35 patients who received the six-food elimination diet. Randomized, doubleblind, placebo-controlled trial of fluticasone propionate for pediatric eosinophilic esophagitis. Budesonide is effective in adolescent and adult patients with active eosinophilic esophagitis. Recurrent episodes of dysphagia were documented in 29 of 30 patients, and the symptoms were more pronounced in patients with peripheral eosinophilia. Eosinophilic esophagitis does not seem to be associated with esophageal metaplasia (ie, Barrett esophagus or cardiac metaplasia or esophageal neoplasms). Natural history of primary eosinophilic esophagitis: a follow-up of 30 adult patients for 11. Oral viscous budesonide: a potential new therapy for eosinophilic esophagitis in children. Treatment of eosinophilic esophagitis: overview, current limitations, and future directions. Effects of six-food elimination diet on clinical and histologic outcomes in eosinophilic esophagitis. Treatment end points and maintenance medical management remain incompletely defined. Treatment initiatives are aimed at relieving symptoms, which may or may not be accompanied by histologic response and resolution of eosinophilic esophagitis. In this regard, after treatment, esophageal eosinophilia can persist, and such patients may be asymptomatic or only have minimal symptoms. There is no consensus on how to define histologic remission in response to treatment. It may well be necessary to continue treatment in patients with documented eosinophilic esophagitis and persistent esophageal symptoms in the absence of esophageal abnormalities. The disease frequently recurs when therapy is discontinued (ie, glucocorticosteroids) or dietary modifications are discontinued. This paradigm changed dramatically in 1984 when Marshall and Warren reported that a curved bacillus, initially named Campylobacter pyloridis and subsequently classified as H pylori, was linked to ulcers. Multiple studies have since shown that eradication of H pylori significantly reduces the rate of ulcer recurrence. Only a small fraction of ulcers are associated with neoplasia or caused by acid hypersecretory states such as Zollinger-Ellison syndrome and other rare disorders. The incidence of both gastric and duodenal ulcers in developed countries rapidly increased throughout the 19th century and peaked during the first half of the 20th century. Since the 1950s, however, the incidence and prevalence of both ulcers have steadily declined. There has also been a decrease in the prevalence of H pylori over recent decades, attributed to improved hygiene and widespread use of antibiotics in developed countries. These trends are thought to reflect an underlying birth cohort effect with a decrease in H pylori incidence among younger generations. A systematic review of the literature on the epidemiology of peptic ulcer disease estimated an annual incidence ranging from 0. In the United States, over 4 million individuals are affected by peptic ulcers, and approximately 15,000 die from ulcer complications each year. Over twothirds of ulcer patients develop the disease between the ages of 25 and 64 years.

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A study of itopride in healthy subjects found that it reduces total postprandial volume without significantly accelerating gastric emptying or altering gastric motor or sensory function gastritis gerd diet buy 15 mg prevacid overnight delivery. This suggests that itopride nervous gastritis diet buy prevacid with paypal, if efficacious in functional dyspepsia prepyloric gastritis definition discount prevacid 15 mg online, is likely therapeutic in ways other than altering gastrointestinal motility gastritis diet virus cheap prevacid 30mg fast delivery. Safety was comparable to placebo in these studies gastritis diet purchase prevacid online, with the rare occurrence of prolactin elevation in the patients receiving itopride (3 gastritis zittern 30mg prevacid fast delivery. Systematic reviews on H2-blockers versus placebo have shown improvement in epigastric pain, but not global symptoms. Proton pump inhibitors: effective first-line treatment for management of dyspepsia. Among the prokinetic agents available in the United States are metoclopramide and macrolide antibiotics, most commonly, erythromycin. The use of these drugs has shown no clear relationship between pharmacologic enhancement of motility and improvement in symptoms of functional dyspepsia. Therefore, the benefit of prokinetics cannot be attributed solely to accelerated peristalsis. An example is the negative influence that many drugs (eg, erythromycin and metoclopramide) have on postprandial fundic relaxation, or accommodation. A systematic review of 14 randomized controlled trials reported prokinetics to be more effective than placebo in functional dyspepsia. Another systematic review of 17 studies looked at cisapride and domperidone (also not available in the United States, again due to cardiac arrhythmia risk) and found both agents to be superior to placebo, but only by a global assessment of improvement by the investigator. A double-blind, randomized, placebo-controlled trial of itopride (100 and 200 mg three times daily) on gastric motor and sensory function in healthy volunteers. Meta-analysis of the effects of prokinetic agents in patients with functional dyspepsia. Tegaserod treatment for dysmotility-like functional dyspepsia: results of two randomized, controlled trials. Efficacy of cisapride and domperidone in functional (nonulcer) dyspepsia: a meta-analysis. Antidepressants and anxiolytic agents-The efficacy of antidepressants and anxiolytics is based largely on clinical observation and anecdotal data. However, 28% of patients dropped out because of adverse reactions, with the most commonly reported adverse effects being dry mouth, sleep disturbance, constipation, and confusion. Use of selective serotonin reuptake inhibitors in functional dyspepsia has been studied in one randomized controlled trial and was not found to be superior to placebo. These drugs may be helpful in patients with concurrent depression, but further studies are needed to demonstrate clinical efficacy. Treatment of functional dyspepsia with sertraline: a double-blind randomized placebo-controlled pilot study. Other drugs-Antacids and bismuth have each been evaluated in a few trials for functional dyspepsia and have been consistently found to be no better than placebo. Sucralfate has been studied in several limited trials and found to be no more effective than placebo. Consequently, all of these agents play no major role in the treatment of functional dyspepsia. Buspirone, a 5-hydroxytryptamine 1A receptor agonist, has been demonstrated to relax the proximal stomach in healthy individuals. In a recent randomized, double-blind, placebo-controlled trial of patients with functional dyspepsia, treatment with buspirone for 4 weeks led to significant improvement in gastric accommodation and reduction in symptoms compared to placebo. It represents another potential treatment option for functional dyspepsia, especially those caused by altered gastric accommodation. Antinociceptive agents such as gabapentin or pregabalin have been suggested as potential agents for management of discomfort or distress related to functional gastrointestinal disorder. These drugs have been found to modulate the central processing of pain and may impact autonomic functions. In a post hoc analysis of six randomized controlled trial of patients with general anxiety disorder and gastrointestinal symptoms, pregabalin led to significant improvement in the anxiety and gastrointestinal symptoms over placebo. Impact of gastrointestinal symptoms on response to pregabalin in generalized anxiety disorder: results of a six-study combined analysis. Efficacy of buspirone, a fundusrelaxing drug, in patients with functional dyspepsia. Recommendations for pharmacotherapy-To summarize, if, after providing reassurance and basic dietary and lifestyle interventions, symptoms persist, the clinician can consider a trial of pharmacologic agents. If H pylori testing yields a positive result, treatment is recommended with the understanding that eradication may or may not improve symptoms. A systematic review of herbal remedies was published examining 17 studies that evaluated agents such as Angelica, artichoke, boldo, gentian, ginger, lemon balm, milk thistle, peppermint, and turmeric. Although the definitions of functional dyspepsia and study methodologies had significant heterogeneity, the symptom improvement scores ranged from 60% to 90% favoring treatment over placebo. Few adverse reactions were associated with the remedies, but formal safety reporting was not routinely available. Psychological Therapy Psychological therapy addresses the cognitive aspects of the pathophysiology of functional dyspepsia. Several modalities have been used, including cognitive-behavioral therapy, biofeedback, hypnotherapy, relaxation therapy, and insightoriented psychotherapy. A systematic review of randomized controlled trials of psychological therapies found four eligible trials on applied relaxation therapy, psychodynamic psychotherapy, cognitive therapy, and hypnotherapy that all reported symptomatic improvement at 1 year. However, the studies were of small sample size and had other technical limitations to provide adequate evidence for efficacy. In general, a significant number of patients with functional dyspepsia became asymptomatic or improved overall after 1 to several years. One study in Taiwan reported that patients with H pylori infection and functional dyspepsia were less likely to be symptom free at 2 years compared to those without H pylori (49% vs 58%). Complementary and Alternative Medical Therapy Nonprescription therapies have been tried in functional dyspepsia, often being self-prescribed. Nevertheless, studies have been conducted with several of 227 Disorders of Gastric & Small Bowel Motility Walter W. The standardized 4-hour gastric emptying scintigraphy scan using a low-fat, egg-white meal is the recommended test for gastroparesis. Accelerated gastric emptying and dumping syndrome are often related to postgastric surgery and may have symptoms that mimic delayed emptying. Important events that occur during gastric filling and emptying include fundic relaxation (accommodation) in response to food ingestion, antral contractions and churning (trituration) of large food particles, and finally pyloric relaxation. Sympathetic fibers arise from the thoracic spinal nerves, extending to postganglionic nerves that run along the celiac plexus and the vascular supply to the stomach. The sympathetic innervation includes afferent pain fibers that arise from the stomach, as well as motor fibers that innervate the pyloric sphincter. The submucosal plexus receives only parasympathetic input and innervates the cells of epithelial layer and muscular externa. The myenteric plexus, on the other hand, is situated between the middle circular and the outer longitudinal muscle layers, receiving both sympathetic and parasympathetic input. It mediates the motor function of both muscle layers and the secretory functions of the mucosa. Treatment of these conditions includes dietary, medical, and, rarely, surgical therapies. Research in gastroparesis is ongoing with a focus on improving diagnostics and newer therapeutic agents. Dumping syndrome is a postsurgical iatrogenic problem that is occurring less often in relation to gastric ulcer surgery, but may be increasing among bariatric surgery patients in tandem with the increase in surgical treatment of obesity. They are located in the myenteric plexus and are responsible for basal slow-wave activity, which occurs at 3 cycles per minute. This slow-wave activity is also called the electronic control activity or the pacesetter potential. Gastric accommodation occurs with distention of the fundus to make room for the incoming ingested contents. This response is mediated by the parasympathetic activity from the vagal nerve through cholinergic neurotransmitters, and inhibitory input by neurotransmitters such as nitric oxide, vasointestinal peptide, and serotonin. The ingested contents upon entering the stomach are distributed, triturated, and then emptied into the duodenum. The rate of liquid emptying is slowed by increased osmolarity, nutrient content, and carbonation. Solids, on the other hand, are stored in the fundus, churned in the antrum, and emptied in two phases: a lag period and a linear emptying period. During the lag period, food particles move proximally to distally and undergo trituration and redistribution. Trituration occurs in the antrum with high-amplitude contraction waves that propagate proximally to distally. The pylorus ultimately regulates how much content is emptied into the duodenal bulb by coordinated contractions and maintenance of the lumen with fixed tone. Besides mechanical factors, neurohormonal factors also control the rate of emptying. Glucagon and incretins (eg, amylin and glucagon-like peptide 1) slow gastric emptying. The presence of chyme in the duodenum provides negative feedback on the rate of emptying as mediated by duodenal distention, acidification, or perfusion with fats and protein. The regulation of duodenal intake controls the level of postprandial hyperglycemia from nutrient absorption. A tertiary referral series of 146 patients showed the causes of gastroparesis to be 36% idiopathic, 29% diabetic, 14% postgastric surgery, 7. Gastroesophageal diseases Gastroesophageal reflux Gastritis (chronic or acute) Acute gastroenteritis (cytomegalovirus) Atrophic gastritis Peptic ulcer disease Neuromuscular disorders Muscular dystrophy Parkinson disease Systemic disorders Diabetes mellitus Hypothyroidism Uremia Chronic liver disease Anorexia nervosa Rheumatologic disorders Scleroderma Surgical procedures Gastrectomy Roux-en-Y syndrome Vagotomy Pyloromyotomy Pancreatectomy Antireflux operations Combined heart-lung transplantation Trauma Head injuries Spinal cord injuries Other etiologies Idiopathic Medications Idiopathic pseudo-obstruction Amyloidosis Camilleri M. It is a severe form of dysmotility that is considered a failure or insufficiency of the "intestinal pump. These can generally be separated into congenital versus acquired causes, and myopathic versus neuropathic processes. The true prevalence of gastroparesis has been difficult to study due to underdiagnosis and the lack of inexpensive diagnostic testing that is also widely available. A large population-based study in Olmsted County, Minnesota, estimated the age-adjusted prevalence of definite gastroparesis, defined as delayed gastric emptying on scintigraphy and typical symptoms for more than 3 months, to be 24. The mean age of gastroparetic patients in one study was 45 years, with a mean age of onset of 33. Prevalence of gastrointestinal symptoms associated with diabetes mellitus: a population-based survey of 15000 adults. The incidence, prevalence, and outcomes of patients with gastroparesis in Olmsted County, Minnesota, from 1996 to 2006. Gastrointestinal tract symptoms among persons with diabetes mellitus in the community. Symptoms and Signs Typical complaints of gastroparesis include postprandial nausea, vomiting, belching, early satiety, bloating, discomfort, or pain. Oral contrast should be water soluble to prevent formation of barium concretions in the gastrointestinal tract with dysmotility. Gastroparesis may be demonstrated by retained contrast in the stomach or its slow gastric transit into the small bowel. However, its use in the evaluation for gastroparesis is still limited to the research setting. Retained food despite overnight fast may also be seen in the stomach during upper endoscopy in patients with gastroparesis. Diarrhea and malabsorption may be a consequence of bacterial overgrowth caused by altered peristalsis. Symptoms to look for include dry mouth, eyes, or vagina; difficulties with visual accommodation in bright light; anhidrosis (absence of sweating); impotence; dizziness on standing; scleroderma symptoms such as Raynaud phenomenon, skin tightening, and peripheral paresthesia; and numbness or focal weaknesses.

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Health care is transforming rapidly in the face of new technology gastritis symptoms diarrhoea purchase prevacid 30mg on line, health care consumerism gastritis diet natural purchase prevacid mastercard, and heightened attention to costs gastritis diet ? cheap prevacid 15 mg line. Hospital operating margins are continually shrinking while inefficient or unsafe care is increasingly being denied payment in the United States gastritis diet uric acid cheap prevacid amex. This pattern will continue to grow as new pay-for-performance gastritis symptoms sweating purchase prevacid 30 mg line, pay-for-value gastritis wiki discount 30 mg prevacid mastercard, and pay-for-quality programs emerge. It is a truism that what we learned as students, what we practice as clinicians, and what we teach the next generation as instructors must all be different if the field is to progress. Those who administer and those who educate must not only anticipate change, they must also catalyze those changes. Transformation always comes with costs, and it is the responsibility of leaders to manage both. The introduction or conversion of an electronic health record system is a familiar example of coevolution and the need for leadership to manage people, technology, and the processes of care to ensure that patients are made safer. We emphasize that the most important word in the phrase "intensive care unit" is "unit. Energy is consumed not only in the tasks but also in the constant struggle to create order in the face of chaos. Stocking the clean utility room or the electronic medication dispenser serves as a convenient example: items that are outmoded, expired, or have fallen into disuse must be identified, evaluated and, where appropriate, superseded. Ensuring that those decisions are made regularly is an administrative responsibility. This variation makes it difficult for hospital leaders to measure the value of any unit and attempts at comparing units often create tension among unit leaders, compounding and concealing inefficiencies. What, then, are the coordinating characteristics that predict system-level success of critical care The financial stability of health care organizations will hinge on how well they can manage population health. Hostility manifested as silence, pejorative remarks, backbiting, and so on are profoundly destructive. Conflict is inevitable in the chief administrative suite and at the bedside; promoting expeditious, honorable, and reasonable resolutions through collective adherence to a code of conduct is, in our view, essential to maintaining integrity. Rather, it is a commitment that there should be a plan and an accounting of financial, physical, and human investment to achieve a desired goal. If the new personnel are assigned tasks currently absorbed by others, what new activities and what improved outcomes can be expected of those shedding tasks Health care system administrators demand strategy, and strategy nearly always involves sacrifice. This is true in business, in games, and in the allocation of health care resources. For example, delaying replacement of a piece of equipment may free up funds to perform a study to show that there is a reason to make a different investment that results in better equipment. The sacrifice here will likely be investment of time and effort to conduct the study, write the report, and make the presentation. We hasten to add that whereas strategy is important, logistics and execution are more important. That execution nearly always requires engagement of and communication with key stakeholders. It is difficult to imagine a controlled trial because the process of horizontal integration takes time and before-and-after studies are subject to legitimate critique about the confounding effect of that time. Nevertheless, there are abundant data to suggest that horizontal integration provides for meaningful interunit comparative data as well as mechanisms to drive improvement (such as competitive incentive plans). Regarding the weakness of vertical integration, the challenge is that vertical integration can never be complete unless there is a parent accountable care organization. A more limited vertical integration (perhaps from the emergency department through palliative care, but excluding preventative health and primary care) could be duplicative and wasteful in the setting of an accountable care organization. This is true, but ignores the reality that accountable care organizations are rarely complete. The number of beds and volume of patients served generally leads to economies of scale, with the understanding that the economies are punctuated with the need to increment resources when thresholds are reached (step fixed costs). Professional "coverage" can often be aggregated during off-hours to provide essential services. It should be remembered that size can also create inefficiencies; the usual problem relates to communication barriers as the unit increases in size. Regarding economies of scale, most health care organizations have supply chains that operate on the principles of bulk purchasing, local warehousing, and just-in-time delivery. The cost models are complex, including not just the purchase prices but the logistical cost of maintaining local and warehouse inventory. Thus the decision (for example) to use a particular brand of mattress pad different from the health system standard can result in many thousands of dollars of hidden costs. Imagine having a single type of ventilator; it means one type of spare parts, one type of accessories, one reservoir of clean machines on standby for use, and one type of training cost. This should not suggest slavish dependence on a single source for essentials, but it does suggest that purchasing in bulk consistently provides unique leverage at many points in the care continuum, which is only partially reflected in the purchase contract price. The third imperative-fiscal responsibility-requires skills that are typically neither taught nor learned until ascent to a leadership position. Nonclinical administrators typically introduce that third imperative into the conversation with allusions of "building value" and "improving performance. Understanding Standardization Standardization-better thought of as removing unnecessary variation-can apply to people, processes, equipment, and supplies. Critical care professionals are trained more to competencies and less to standards. There are neither expectations nor restrictions on specific sequences provided that the key findings are gleaned and reported. Although most practitioners develop a consistent routine, there is no agreed-upon "one best way. The range of processes available to standardize is vast and far exceeds the time and effort available. If the outcome is not critical, will standardization reduce costs or improve satisfaction None of this is easy- witness the difficulty in standardizing a process that should be easy and has great impact on safety-namely, handwashing. Although cash incentives are effective, even small tokens like coffee cards and candy bars are powerful tools to change behaviors. If there are several types of ventilators, spares and repairs and skills must be maintained for all types. Similar to all durable equipment, from beds, to defibrillators, to monitors, to ultrasound machines, the consumables add up as well. A tour through the "clean utility room" often reveals near-identical kits and, worse, items that expire through lack of regular use. Equipment and supplies often represent the first and easiest targets for standardization. Some tasks have "sunsetted" owing to technological advancements, such as the filing of laboratory data and imaging reports into physical charts. Others are candidates for simplification and automation, such as the recording of intravenous fluid administration that can be automated via device integration. We do not mean to suggest a wholesale revision of workflows, but rather a critical examination of the value stream and the assignment of each team member to the specific tasks. Quite the opposite-there should be a leadership team that visibly embodies the behaviors expected of the workforce. At a minimum, this demands a partnership between the nurse unit director and the physician unit director. Set standards high and goals higher; demand the former and incentivize the latter. For example, there should be standards of family visitation, hand hygiene, use of universal precautions, and timely administration of antibiotics when sepsis is suspected. Such general standards do not preclude local additions that are necessarily focused in particular units-for example, adherence to practices regarding extraventricular drains in neurology units and intraaortic balloon pumps in cardiac units. Rather, the mechanisms by which those general standards are communicated, compliance evaluated, and corrected provide a foundation for unit-specific behaviors. Albumin utilization was also decreased over a 2-year intervention with an estimated savings of $2. Interestingly, although the physicians were ineligible for this incentive, their billable time increased from 4. The tasks can be further divided into those that must be performed at the bedside. An alternate division of tasks relates to the profession(s) qualified to complete the task. The aforementioned bladder catheter could be inserted by a physician, an advanced practice provider, a nurse, or a specialized catheter insertion "team. Insertion of peripherally inserted central venous catheter line teams is one example of a task where constant repetition seems to improve outcomes. The process of charting, for example, can be accelerated with voice recognition transcription or use of a scribe. Monitoring of vital signs, laboratory data, and medication interactions can be performed remotely. A list of domains that have formed the bases for recent incentives is included in Table 70. We will neither review nor dwell on "burnout," a construct that is increasingly applied to critical care among the many medical professions. Although most critical care professionals find their work deeply satisfying, they are no different than the general population in being susceptible to depression, fatigue, isolation, and other common threats to mental health. One area in which critical care professionals may differ from the general population is their chronic and repeated professional exposure to emotionally stressful situations. We hasten to add that critical care professionals knowingly choose such exposures when they join the professions, yet only a fraction experience burnout syndrome. Although compensation is important, a sense of teamness and of a "work family" sharing the joys and burdens may play heavily into decisions by an employee to remain or depart. Those who report burnout emphasize isolation, depersonalization, and emotional exhaustion. Thus attention to well-being cannot be a response to crises but rather must be engineered into the fabric of daily work. By 2030, nursing shortage ratios will be largest in the Western portion of the United States, followed by the South, Midwest, and Northeast regions. Ninety-eight percent of nurses believed that the shortage would increase stress on nurses, 93% indicated it would lower quality of care, 93% reported it would cause nurses to leave the profession, and only one-fifth believed that their working conditions would improve or that respect for nurses would increase. We have deployed tele-critical care to leverage our scarce experienced physicians and critical care nurses, thereby enabling guidance on demand. The patient may be enrolled in a protocol related to the primary illness for which critical care is incidental. For example, patients with sepsis might be randomly assigned to receive a placebo or a study drug in addition to standard care. Failure to do so may result in protocol violation, patient injury, and study interruption. This section briefly reviews the convergent training pathways and the role of the administrator in facilitating effective learning toward practice. This section omits consideration of formal training in critical care research, except where such training is needed to prepare bedside professionals to participate in clinical research trials. Pathways to Degrees, Licensure, Certification, and Credentialing Although the professions of critical care are diverse, there are homologies among the paths to competency. For this largest cohort of learners, administrators must ensure that learners are constantly accompanied by teacher/supervisors; that appropriate confidentiality agreements are in place; and that the role of the learner is appropriately restricted (often to observation and unofficial "student" entries into the medical record). In general, licensure is sufficient to qualify for some care privileges, although there are nuances. For example, a newly graduated physician may qualify for limited licensure as a trainee provided he or she is supervised in an accredited postgraduate training program. A newly graduated physician assistant will have one or more supervising physicians. The administrator has three typical tasks associated with mentorship of the newly licensed professional: (1) verifying the existence of a training plan; (2) verifying the assignment of one or more supervising mentors, including clarification of the roles and responsibilities of trainee and mentor; and (3) monitoring completion, including an objective determination from the responsible individuals that training is satisfactory and complete and further an attestation that the trainee can practice independently. Whereas licensing is a regulatory and legal matter, certification by a board representing that profession validates not only that the individual has completed a prescribed course of training but also that certain advanced competencies have been evaluated and found satisfactory, typically by an examination that may be written, oral, simulated, or a combination thereof. Of note, certification by a board occurs not only at different stages across professions but also can occur at different experience levels within a profession. For example, boardcertified internal medicine physicians require 2 to 3 years of postgraduate training to complete critical care medicine training and enter the examination process, whereas board-certified surgeons and anesthesiologists require a single additional year of critical care medicine training. The administrator must understand the pipeline, including how trainees in all the professions are actually funded for their training. Credentialing to one or more hospitals is required before independent practice of critical care medicine within a profession. Privileges are granted to the professional permitting services within a scope of practice. Specific Education Issues the previous section outlined educational processes and milestones with homologies among the critical care professions. The administrator is often called on to offer solutions to three related challenges. The number of learners exceeds the capacity of the trainers and/or training sites. Although this may be perceived as a challenge confined to academic health science centers, it affects every hospital and critical care site because critical care staffs predictably have turnover. All of this takes professional time and it is rarely (if ever) accounted for in the budget. The administrator is therefore required to verify training assignments while ensuring that patient care needs are met.

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