Clostridium Difficile Infections
The American College of Gastroenterology published updated guidelines on Clostridium Difficile infection.
Clostridium difficile infection (CDI) is a leading cause of hospital-associated illness and is becoming a more difficult infection to control and treat. Fecal stool transfer is now being discussed and patients are becoming more aware of the difficult issues related to this intestinal infection. The current guidelines are therefore posted to provide our readers with a basis for further discussions with their physicians. It is suggested that patients are treated depending on severity of disease (mild-to-moderate, severe, or complicated disease). Therapy with metronidazole remains the choice for mild to moderate disease but may not be adequate for patients with severe or complicated disease.
Diagnostic tests
- Only stools from patients with diarrhea should be tested for Clostridium difficile.
- Repeat testing should be discouraged.
- Testing for cure should not be done.
Management of mild, moderate, and severe CDI
- If a patient has strong a pre-test suspicion for CDI, empiric therapy for CDI should be considered regardless of the laboratory testing result.
- Any inciting antibiotics should be discontinued, if possible.
- Patients with mild-to-moderate CDI should be treated with metronidazole 500 mg orally three times per day for 10 days.
- Patients with severe CDI should be treated with vancomycin 125 mg four times daily for 10 days.
- Failure to respond to metronidazole therapy within 5 – 7 days should prompt consideration of a change in therapy to vancomycin at standard dosing.
- For mild-to-moderate CDI in patients who are intolerant / allergic to metronidazole and for pregnant / breastfeeding women, vancomycin should be used at standard dosing.
- In patients in whom oral antibiotics cannot reach a segment of the colon, such as with Hartman’s pouch, ileostomy, or colon diversion, vancomycin therapy delivered via enema should be added to treatments above until the patient improves.
- The use of anti-peristaltic agents to control diarrhea should be avoided, as they may obscure symptoms and precipitate complicated disease. If used, anti-peristaltic agents must be accompanied by medical therapy for CDI.
- For complicated disease, supportive care should be offered i.e. iv fluids and electrolyte replacement. In the absence of ileus or significant abdominal distention, oral or enteral feeding should be continued.
- CT scanning of the abdomen and pelvis is recommended in complicated CDI.
- Oral vancomycin (125 mg four times per day) plus iv metronidazole (500 mg three times a day) is the treatment of choice in severe and complicated CDI.
- Vancomycin delivered orally (500 mg four times per day) and per rectum (500 mg in a volume of 500 ml four times a day) plus intravenous metronidazole (500 mg three times a day) is the treatment of choice for patients with complicated CDI with ileus or toxic colon and / or significant abdominal distention.
- Surgical consultation should be obtained in all patients with complicated disease and considered in patients with any one of the following:
- hypotension requiring vasopressor therapy
- clinical signs of sepsis and organ dysfunction (renal and pulmonary)
- mental status changes
- white blood cell count ≥ 50,000 cells / μ l, lactate ≥ 5 mmol / l
- failure to improve on medical therapy after 5 days.
Management of recurrent CDI (RCDI)
Patient face a 30% recurrence risk with the first infection and a 60% recurrence risk if a second infection has occurred.
- The first recurrence of CDI can be treated with the same regimen as used for the initial episode. If severe, however vancomycin should be used.
- The second recurrence should be treated with a pulsed vancomycin regimen.
- If there is a third recurrence after a pulsed vancomycin regimen, fecal microbiota transplant (FMT) should be considered.
- There is limited evidence for the use of adjunct probiotics to decrease recurrences in patients with RCDI.
- No effective immunotherapy is currently available.
Management of patients with CDI and co-morbid conditions
- All IBD patients hospitalized with a disease flare should undergo testing for CDI.
- IBD patients with diarrhea in the setting of prior quiescent disease, or in the presence of risk factors (i.e. recent hospitalization, antibiotic use) should be tested.
- Patients with IBD and severe colitis may benefit from empiric therapy against CDI and treatment of an IBD flare while awaiting results of C. difficile testing.
Diagnosis And Management Of Gastroesophageal Reflux Disease
The current GERD diagnosis and treatment guidelines as published by the American College of Gastroenterology provide an overview of GERD, its presentation, and recommendations for the diagnosis and management of this important disease.
Diagnosis:
- Typical symptoms (i.e. heartburn, regurgitation) establish a diagnosis of GERD. Therefore empiric PPI therapy is reasonable.
- The diagnosis of non-cardiac chest pain (due to reflux) requires the exclusion of cardiac causes.
- Routine EGDs are not needed in classic GERD patients to establish a diagnosis of reflux, but are advised if alarm symptoms are reported (i.e. hematemesis, dysphagia, weight-loss, anemia etc.).
- Routine follow-up EGDs are not needed in patients without Barrett’s or new symptoms.
- pH- and/or impedance-monitoring are indicated before endoscopic or surgical therapy in NERD (non-erosive reflux) patients and those patients who fail conventional therapy.
Medical Treatment:
To help reduce reflux symptoms and treat the acid injury, several treatment strategies can be used:
- Weight loss, elevation of the head of bed, and avoidance of meals before bedtime are recommended.
- The routine recommendations of avoidance of trigger foods (i.e. chocolate, caffeine, alcohol, acidic or spicy foods) are no longer strongly supported.
- PPIs (proton-pump inhibitors) should be used for 8 weeks. PPIs (i.e. omeprazole (Prilosec or Zegerid), pantoprazole (Protonix), lanzoprazole (Prevacid), esomeprazole (Nexium), dexlansoprazole (Kapidex), rabeprazole (Aciphex) are all similar in effect. PPIs should be given 30-60 min before a meal, staring at a once a day morning dose; dose and timing adjustment are reasonable (i.e. increasing the dose, switching to another PPI) if poor response to daily dosing is noted.
- Long-term therapy is warranted in patients with recurrent symptoms after PPIs were discontinued, and with complicated disease i.e. erosive esophagitis, Barrett’s. Long-term therapy should be offered at the lowest possible dose.
- Nighttime H2 blockers can be used in patients with break through symptoms. H2 blockers may offer an effective alternative to PPIs in patients without erosive disease. But are usually not as effective.
- Therapy for GERD other than acid suppression, including prokinetic therapy and/or baclofen, should not be used without prior diagnostic evaluation.
- There is no role for sucralfate (Carafate) in the non-pregnant GERD patient. PPIs are safe in pregnant patients if clinically indicated (UGs personal comment: omeprazole is a category C drug and should be avoided).
Surgical Options:
For those who fail medical therapy and life style modifications, surgery (a Nissen fundoplication) may be a viable option but should be discussed with the treating physician.
- Surgical therapy is generally not recommended in patients who do not respond to PPI therapy (UGs personal comment: possible exceptions to this rule must be carefully reviewed with the treating physician).
- Preoperative ambulatory pH monitoring is mandatory in patients without evidence of erosive esophagitis.
- All patients should undergo preoperative manometry to rule out achalasia or scleroderma-like esophagus.
- Surgical therapy equally effective when compared to medical therapy in patients with chronic GERD when performed by an experienced surgeon.
- Obese patients contemplating surgical therapy for GERD should be considered for bariatric surgery. Gastric bypass would be the preferred operation in these patients.
- Currently the usage of current endoscopic therapy or transoral incisionless fundoplication cannot be recommended as an alternative to medical or traditional surgical therapy.
Potential Risks of PPIs:
- Patients with known osteoporosis can remain on PPI therapy. Concern for hip fractures and osteoporosis should not affect the decision to use PPI long-term except in patients with other risk factors for hip fracture.
- PPI therapy can be a risk factor for Clostridium difficile infection; use with care in patients at risk.
- Short-term PPI usage may increase the risk of community-acquired pneumonia. The risk does not appear elevated in long-term users.
- PPI therapy does not need stopped in clopidogrel (Plavx) users as there does not appear to be an increased risk for adverse cardiovascular events.
Atypical Reflux Presentations:
While GERD can be a potential factor in patients with asthma, chronic cough, or laryngitis, careful evaluation for non-GERD causes should be undertaken.
A diagnosis of reflux laryngitis should not be made based upon laryngoscopy findings. (… as often suggested by ENT physicians – UG personal comment).
- A PPI trial is recommended to treat extraesophageal symptoms in patients who also have typical symptoms of GERD.
- Upper endoscopy is not recommended as a means to establish a diagnosis of GERD-related asthma, chronic cough, or laryngitis. (UG personal comment: … unless other reasons warrant an EGD or a BRAVO pH monitoring system is placed).
- Reflux monitoring should be considered before a PPI trial in patients with extraesophageal symptoms who do not have typical symptoms of GERD.
- Non-responders to a PPI trial should be considered for further diagnostic testing and are addressed in the refractory GERD section below.
- Surgery should generally not be performed to treat extraesophageal symptoms of GERD in patients who do not respond to acid suppression with a PPI.
Refractory GERD:
The first step in management of refractory GERD is optimization of PPI therapy. Upper endoscopy should be performed in refractory patients with typical or dyspeptic symptoms .
- In patients in whom extraesophageal symptoms of GERD persist despite PPI optimization, assessment for other etiologies should be pursued through concomitant evaluation by ENT, pulmonary, and allergy specialists.
- Patients with refractory GERD and negative evaluation by endoscopy (typical symptoms) or evaluation by ENT, pulmonary, and allergy specialists (extraesophageal symptoms), should undergo ambulatory reflux monitoring.
- Reflux monitoring off medication can be performed by any available modality (pH or impedance-pH). Testing on medication should be performed with impedance-pH monitoring in order to enable measurement of nonacid reflux.
- Refractory patients with objective evidence of ongoing reflux as the cause of symptoms should be considered for additional antireflux therapies, which may include surgery. Patients with negative testing are unlikely to have GERD and PPI therapy should be discontinued.
Complications Associated with GERD:
Complications of GERD include esophageal strictures, Barrett’s metaplasia, or bleeding. The Los Angeles (LA) classification system should be used when describing the endoscopic appearance of erosive esophagitis.
- Grade A: One (or more) mucosal break no longer than 5 mm, that does not extend between the tops of two mucosal folds (a mucosal break being defined as an area of slough or erythema with discrete demarcation from the adjacent mucosa).
- Grade B: One (or more) mucosal break more than 5 mm long that does not extend between the tops of two mucosal folds.
- Grade C: One (or more) mucosal break that is continuous between the tops of two or more mucosal folds but which involves less than 75% of the circumference.
- Grade D: One (or more) mucosal break which involves at least 75% of the esophageal circumference.
Patients with LA Grade A esophagitis should undergo further testing to confirm the presence of GERD. If severe reflux injury is encountered during an EGD, a repeat endoscopy should be performed e after a course of therapy to exclude underlying Barrett’s esophagus. Continuous PPI therapy is recommended following peptic stricture dilation to improve dysphagia and reduce the need for repeated dilations. Injection of intra-lesional corticosteroids can be used in refractory, complex strictures due to GERD. Treatment with a PPI is suggested following dilation in patients with lower esophageal (Schatzki) rings. Screening for Barrett’s esophagus should be considered in patients with GERD at high risk based on epidemiologic profile (See the UG Barrett’s article).
Guidelines for the Diagnosis and Management of Gastroesophageal Reflux Disease. Am J Gastroenterol 2013; 108:308–328
Colon Cancer – A Few Facts To Remember
- One in four people in the US will die from cancer.
- Colon Cancer is a treatable and preventable disease.
- Colon cancer is the leading GI cancer and second leading cause of cancer death for both men and women, the third leading cancer for men (after lung and prostate) and third leading cancer for women (after lung and breast cancer)
- Colon cancer has no early symptoms.
- Colon Cancer rates and deaths have dropped by 20% due to better screening implementations.
- An estimated 150,000 people will be diagnosed with colorectal cancer in the US in 2013 and an estimated 50,000 people will die from it in 2013.
- One out of twenty people will get colon cancer (~5.1% chance), yet colon cancer is a preventable disease.
- Any screening is better than none; screening starts typically at age 50 unless an individual is at high risk (family history of colon cancer or inherited genes)
- A colonoscopy is the most effective screening tool.
- It is a treatable disease if found early and a preventable disease if polyps are noted and removed.
- The life saving screening colonoscopy procedure is safe and easy, although time consuming. It is private and not embarrassing.
- Other less defined risk factors for colon cancer may be:Smoking
Diabetes
Sedentary life style
High meat- and processed meat-diet
African American race
Obesity
Heavy alcohol consumption - Signs and symptoms of colon cancer:
- Pain
- Anemia
- Rectal bleeding
- Change in bowel habits
- Urgency
- Weight loss
Colon Cancer Screening
Although screening for colon cancer is recommended starting at age 50, as of 2008, only about 63% of Americans between the ages of 50-75 years of age underwent this recommended screening. This article will address some commonly asked questions regarding colon cancer and the screening guidelines in place to prevent deaths from this serious disease.
1. Why do I need to be screened? Colon cancer is the second leading cause of cancer deaths in America (lung cancer is still number one). In 2009, colon cancer killed almost 52,000 Americans. It affects both genders and all races. Screening for colorectal cancer helps prevent this disease and greatly lessens the likelihood of dying from colon cancer. The goal of screening is to find precancerous polyps (abnormal growths) so they can be removed before they turn into cancer. Screening can also identify colon cancer in its early stages when it can be more effectively treated and potentially cured.
2. Do I really need a colonoscopy if I feel fine and have no symptoms? Colon cancer is generally slow growing. It can take many years for a precancerous polyp to progress into a malignant tumor. Unfortunately, once a person exhibits actual symptoms of colon cancer, the disease is often too advanced to be cured. Symptoms associated with colon cancer include blood in the stool, change in size of stool, abdominal pain, unintentional weight loss, and worsening constipation or diarrhea. More often, however, patients with early stage colon cancer have no symptoms and feel like their normal selves.
3. What are my screening options and which option is best for me? This decision should ultimately be made between you and your primary care physician. Screening options available include simple stool tests looking for blood, flexible sigmoidoscopy (looking just at the left side of the large colon), standard colonoscopy (looking at the entire large colon), and virtual colonoscopy (done with a CT scanner). Virtual colonoscopy often seems appealing because it does not require the bowel preparation that traditional colonoscopy does, and it appears to be as good as standard colonoscopy for detecting cancers and large precancerous polyps. Unfortunately, it is expensive, not covered by insurances, and associated with radiation exposure. In addition, if any polyps or tumors are identified, the patient must also undergo a standard colonoscopy as a virtual colonoscopy cannot biopsy or remove any detected polyps or tumors.
4. I have a family member with colon cancer or polyps. When should I start my screening? While we do not fully understand all of the factors that can contribute to the development of colon cancer, it is clear that genetics play a role. The guidelines recommend that anyone with a single first degree relative or two second degree relatives with a history of colon cancer or colon polyps should start their screening at age 40, or ten years prior to the relative’s earliest diagnosed polyp or tumor, whichever comes first. For example, if your mother was diagnosed with colon cancer at age 65, you should start your screening at age 40. If, however, your mother’s tumor was found at age 45, then your screening should start at age 35.
5. How often do I need to be screened? If no polyps are found during your initial screening, then you do not need a colonoscopy more frequently than every 10 years. That means that most patients only require a total of four screening colonoscopies in their lives. If, however, you have a family history of colon cancer or polyps, or if polyps are found on your initial colonoscopy, then you will need to be screened more regularly.
6. What can I do to prevent colon cancer? While there is no foolproof method to preventing colon cancer, colon cancer has been associated with smoking, excessive alcohol (more than one drink a day), lack of exercise, obesity, and a high fat, low fiber diet. Ultimately though, the best prevention against colon cancer is catching and removing precancerous polyps early, before they have the chance to progress to malignancy. Please be sure to talk to your primary care physician about colon cancer screening to determine when and how this is right for you.
Treatment And Prevention Of NSAID-Associated GI-Complications
By Dr. EJ Frech
Adapted from the original publication in Therapeutics and Clinical Risk Management 2009:5 65–73
This article reviews the medical therapy and prophylaxis of NSAID-associated gastrointestinal complications including peptic ulcer disease and non-ulcer dyspepsia.
Introduction
Over one hundred million prescriptions for non-steroidal anti-inflammatory drugs (NSAIDs) were written in the US in 2000, mostly for chronic pain syndromes and rheumatologic conditions. This likely represents only a fraction of NSAID used in the US due to readily available over the counter (OTC) forms of these drugs, including aspirin. Due to the aging population the use of aspirin for the chemoprevention of cardiovascular, cerebrovascular, peripheral vascular disease and metabolic syndrome is likely to continue to increase. The recent widely publicized concerns regarding increased cardiovascular risks associated with cyclo-oxygenase-2 (COX-2) selective inhibitors [i.e. Vioxx – Rofecoxib] has also contributed to increased use of non-selective NSAIDs. In spite of being among the most widely prescribed pharmaceuticals, NSAIDs have long been recognized as a major cause of gastrointestinal morbidity. NSAID-associated gastrointestinal complications range from dyspepsia without endoscopic findings to severe complications such as ulcer-related perforation, obstruction, or hemorrhage. The use of chronic NSAIDs increases the risk of peptic ulcer disease complications by 3- to 5-fold. Overall, 15%–35% of all peptic ulcer complications are reportedly related to chronic NSAID use. Major adverse gastrointestinal events attributed to NSAIDs are responsible for over 100,000 hospitalizations, US $2 billion in healthcare costs, and 17,000 deaths in the US each year.
Despite available medications to aid treatment of NSAID-associated complications, the number of hospitalizations and deaths has remained unchanged in the US. While clinically significant complications such as perforation, obstruction, or hemorrhage are relatively uncommon (1%–2% of all NSAID users, overall incidence of 2%–4% per year), gastrointestinal symptoms such as nausea, heartburn, dyspepsia, and abdominal pain are common and may occur in up to 40% patients taking chronic NSAIDs. Certain groups of persons are at increased risk for developing NSAID-related complications, including patients with a prior history of peptic ulcer disease, the elderly, patients taking high dose NSAIDs, and patients taking concurrent anticoagulation or corticosteroids. Therapeutic strategies to reduce NSAID-associated gastrointestinal complications have focused on treatment of acute events such as peptic ulcer disease and prevention of future events. Historically, the most widely employed prevention strategies involved either cyclo-oxygenase 2 (COX-2) selective inhibitors [i.e. Celebrex – Celecoxib] or administration of a nonselective NSAID with a proton pump inhibitor.
Pathogenesis of NSAID-associated peptic ulcer disease
NSAIDs and Helicobacter pylori are known to independently increase the risk for gastroduodenal ulcers and ulcer bleeding. This has important diagnostic and treatment implications as both ulcerogenic factors are highly prevalent. The relationship between H. pylori infection and NSAID use has important treatment implications. While it is generally thought that H. pylori infection and NSAIDs induce mucosal damage by different mechanisms, there is ongoing debate whether their coincidence is independent, additive, synergistic, or antagonistic. Whether eradication of H. pylori modifies the ulcer risk in patients on chronic NSAIDs remains a topic of debate. Mucosal injury caused by NSAIDs likely occurs by several different mechanisms and can be broadly divided into topical and systemic effects. Most NSAIDs including aspirin are readily absorbed across the gastric mucosa and temporarily trapped within the epithelial cells and cause damage to the gastrointestinal mucosa. The systemic effects play a more central role in the pathogenesis of NSAID-induced ulcers. NSAIDs exert their effects by interfering with prostaglandin production through the direct inhibition of cyclooxygenase activity. Most NSAIDs, including aspirin inhibit COX-1 and COX-2 equally. The ideal NSAID would inhibit COX-2, thereby reducing inflammation, without acting on COX-1 and its cytoprotective effects. The inhibition of COX-1 and loss of protective gastrointestinal prostaglandins may cause a local ischemic injury by reduction in mucosal blood flow. While associated with less gastrointestinal toxicity, selective COX-2 inhibitors [Celebrex – celecoxib] are still associated with some risk for gastrointestinal toxicity particularly at higher doses and in high risk patients. Recently publicized concerns regarding the increased cardiovascular and thromboembolic risk in patients taking selective COX-2 inhibitors [i.e. Vioxx – Rofecoxib] and high doses of some nonselective NSAIDs has led to a global re-evaluation of the use of these drugs in clinical practice.
Medical therapy for NSAID-associated peptic ulcer disease
The treatment of peptic ulcer disease in H. pylori negative patients relies on prompt discontinuation of NSAIDs and the initiation of medical therapy to promote ulcer healing. Options for medical treatment include cytoprotective agents such as sucralafate [Carafate] and the prostaglandin analogue misoprostol [Cytotec]. The latter aims to restore the prostaglandins which become depleted by COX-1 inhibition. Acid-suppressive agents including histamine-2 antagonists (H2RAs) and proton pump inhibitors (PPIs) have also been employed as medical therapy.
Primary treatment of NSAID-associated peptic ulcer disease
Whenever possible, the primary treatment for NSAID-associated peptic ulcer disease should include discontinuing potential causative agents. In some instances this may not be possible due to concerns of the underlying chronic disease. This commonly occurs in patients with vascular diseases, especially coronary artery disease, which may pose high risk if antiplatelet therapy such as aspirin is discontinued. Numerous studies have evaluated endoscopic ulcer healing rates in the context of continued NSAID use. The extent of gastroduodenal mucosal damage caused by NSAIDs is highly dependent on the intraluminal gastric pH. Low intragastric pH enhances the diffusion of NSAIDs into the gastric mucosa and may facilitate local mucosal injury. While H2RAs have been associated with variations in 24-hour acid suppression, the profound and sustained acid suppressive effects exhibited by proton pump inhibitors have revolutionized the treatment of acid-related gastrointestinal diseases. Multiple clinical trials have evaluated ulcer healing rates using proton pump inhibitors in chronic NSAID users. PPIs were in general superior to H2RAs, misoprostol, or sulcrafate; for study details, please refer to a detailed discussion in the original paper.
Secondary prophylaxis of NSAID-induced peptic ulcer disease
Once resolution of NSAID-associated peptic ulcer disease has been demonstrated, a careful assessment of risks and benefits of continued NSAID therapy should be undertaken before continuation of NSAID therapy. A number of risk factors have been identified that may be helpful in predicting an increased risk for NSAID-related complications. A history of complicated peptic ulcer disease and the use of multiple NSAIDs are major risk factors for recurrent complications. Therefore, prevention is recommended in high risk patients who are unable to discontinue NSAIDs or who have high risk medical comorbidities that favor continued NSAID therapy, i.e. patients with cardiovascular or cerebrovascular disease. It was concluded that for high risk patients, esomeprazole was well-tolerated and most effective in preventing peptic ulcer disease in those taking chronic NSAIDs – for details, please refer to a detailed discussion in the original paper. Combination treatment of a proton pump inhibitor and a selective COX-2 inhibitor has been suggested for optimal gastrointestinal protection in the highest risk patients, particularly those who have had complicated peptic ulcer disease.
Primary prophylaxis of NSAID-induced peptic ulcer disease
It is widely accepted that particularly proton pump inhibitors are effective in the treatment and prevention of recurrent NSAID-associated peptic ulcer disease. Primary prophylaxis against gastrointestinal complications in chronic NSAID users has been more controversial – for a more detailed discussion, please refer to the original paper. PPIs, H2RAs, misoprostol, or sulcrafate have all been studied and proven to be effective compared to no intervention. While most COX-2 inhibitors are no longer widely available, these drugs provided an alternative strategy in primary and secondary prophylaxis. Several large outcomes studies have demonstrated significantly fewer upper gastrointestinal events in patients treated with selective COX-2 inhibitors compared to non-selective NSAIDs. Whether aspirin negates the potentially protective benefits of selective COX-2 inhibitors remains controversial and patients receiving both aspirin and a selective COX-2 inhibitor may require prophylactic anti-ulcer therapy if they are at risk for gastroduodenal toxicity.
Secondary prophylaxis of NSAID-induced peptic ulcer disease using other antiplatelet agents
Aspirin has a known dose-related risk of gastrointestinal adverse events, particularly in elderly patients. Newer antiplatelet drugs, such as Plavix – clopidogrel have been proposed as an alternative in the prevention and treatment of vascular diseases. The 2000 American College of Cardiology – American Heart Association Guidelines recommended the use of clopidogrel for hospitalized patients with coronary syndromes who are unable to take aspirin because of major gastrointestinal intolerance. This has prompted investigators to evaluate the risk of recurrent ulcer bleeding using other antiplatelet medications. It was concluded that the risk of gastrointestinal bleeding in the aspirin plus esomeprazole group was significantly lower than the clopidogrel group and therefore superior in the prevention of recurrent ulcer bleeding. While the mechanism remains unknown, studies showed that clopidogrel poses a significant risk of peptic ulcer disease. This does not support the proposed 2000 ACC/AHA guidelines for use of clopidogrel in patients with previous gastrointestinal intolerance.
Potential protective effects of nitrovasodilators are of particular interest considering that concurrent use of aspirin and nitrates is common in patients with cardiovascular disease. Nitrates and nitric-oxide releasing drugs are believed to exert their protective effects by maintaining mucosal blood flow at the level of the gastroduodenal microcirculation, thereby counteracting one of the principal deleterious effects of COX-1 inhibition. Recent studies concluded that there was a benefit from co-administration of antisecretory drugs and nitrates in the prevention of upper GI peptic ulcer bleeding associated with NSAIDs, including aspirin.
Treatment of NSAID-associated gastrointestinal symptoms
As many as 40% patients treated with chronic NSAIDs experience upper gastrointestinal symptoms such as dyspepsia, abdominal pain, and heartburn. As many patients require NSAIDs to control their primary underlying chronic disease and cannot tolerate a dose reduction, interruption, or discontinuation of the drugs, studies have been conducted to address whether antisecretory agents are effective in controlling gastrointestinal symptoms related to NSAIDs despite the absence of endoscopic findings. It was concluded that esomeprazole improves upper gastrointestinal symptoms associated with chronic NSAID use, including selective COX-2 inhibitors.
Conclusion
High healing rates of peptic ulcers related to chronic NSAID use are achieved with medical therapy, particularly if the causative agent can be discontinued. The American Gastroenterological Association (AGA) recently released a consensus statement following a panel discussion of physicians in gastroenterology, rheumatology, cardiology, and internal medicine. The panel emphasized a careful review of treatment indications and risk factors, taking into consideration risks for both gastrointestinal and cardiovascular complications. If the causative agent cannot be discontinued, a reduced dose or switch to a more COX-2 selective NSAID in conjunction with co-administration of PPIs was suggested. Misoprostol was effective in reducing the risk of gastric ulcers in high risk patients such as the elderly and patients with previous history of peptic ulcer disease. Yet misoprostol has not been demonstrated to reduce the risk of duodenal ulcerations nor reduction in symptoms related to chronic NSAIDs. Moreover, misoprostol is often poorly tolerated due to gastrointestinal side effects. H2-receptor antagonist therapy is inadequate for patients receiving NSAIDs with risk factors for GI complications; moreover, they have been supplanted by the highly efficacious and well tolerated proton pump inhibitors. Lansoprazole has been shown to be effective in the primary treatment and secondary prophylaxis of NSAID-associated peptic ulcer disease, including maintenance therapy following resolution of duodenal ulcers. Esomeprazole is the only proton pump inhibitor effective in both primary and secondary prophylaxis of NSAID-associated peptic ulcer disease. Esomeprazole is highly effective in reducing non-ulcer related symptoms associated with chronic NSAID use and may help reduce the risk of bleeding from non-NSAID antiplatelet drugs. Clinical studies provide supportive evidence for the use of antisecretory medicine, especially PPIs, in the primary treatment of NSAID-associated peptic ulcer disease. Peptic ulcer disease and related complications may be prevented in chronic NSAID users with primary prophylactic use of adequate doses of misoprostol and anti-secretory medicines, especially PPIs. Aggressive prevention strategies should be undertaken in high-risk patients especially those with a history of peptic ulcer disease to prevent against recurrent peptic ulcer disease and its associated complications.
Diverticular Disease – A Common Problem
Diverticulosis is a common colonic finding. Diverticulosis refers to the presence of diverticula, while the term Diverticulitis implies inflammation of these diverticula. Unrecognized or untreated diverticulitis can cause abscesses or fistula formation, bowel obstruction, or even perforation. A diverticulum is a protrusion of colonic mucosa and submucosa, herniating through the colonic muscle layer, thereby only covered by serosa. Such herniation/protrusion occurs at weak points in the bowel wall where blood vessels penetrate.
The prevalence of diverticular disease increases with age (< 20% at age 40, >60% by age 60), and diverticular disease shows equal sex distribution or a slight female predominance. Most patients have sigmoid involvement, while a third also have more proximal disease. An overall observed increase in diverticulosis suggests an environmental or lifestyle effect, as a decreasing dietary fiber intake due to a westernized diet and sedentary lifestyle, both seemingly predisposing patients to the development of diverticular disease. As such, diverticulosis is less common in vegetarians and more likely in obese patients with a diet high in fat and red meat intake. It is unclear why physical activity might prevent diverticulosis. A clear correlation between constipation and diverticulosis has not been shown, although abnormal colonic motility may predispose to the development of diverticulosis due to increased intraluminal colonic pressures.
Diverticulitis causes a variety of symptoms such as left lower quadrant pain, nausea, vomiting, fevers, even urinary symptoms all the way to walled of perforations, fistulizing disease, colonic obstruction, free perforation and peritonitis. While some patients may only complain of cramping, bloating, flatulence, and irregular defecation, the presentation depends on the severity of inflammation and related complications (abscess, fistula, obstruction, perforation). A physical exam may show abdominal tenderness with or without a tender abdominal mass, abdominal distention, or even severe generalized tenderness suggesting peritonitis due to a perforation. A CT scan is the preferred test in patients suspected of having acute diverticulitis, as it allows for a diagnosis as well as assessment of severity od disease (allowing for identification of major complications i.e. peritonitis, perforation, fistulas, obstruction). Treatment of acute diverticulitis usually requires in- or outpatient antibiotics but may also require CT-guided percutaneous abscesses drainage or even surgery.
Once the acute episode of diverticular disease has resolved, semi-elective follow-up to establish the extent of disease and to rule out coexistent lesions (i.e. carcinoma) is advised. A colonoscopy is likely the test of choice although a CT colography may be an acceptable alternative. Once diverticular disease has resolved, initiation of a high-fiber diet and addition of fiber supplements appear to reduce the risk of subsequent occurrences and complications. Avoidance of small food particles (i.e. nuts/seeds) as often suggested is probably of little proven benefit.
Diverticular bleeding, another complication of diverticulosis is caused by injury to an adjacent arterial vessel and typically occurs in the absence of diverticulitis. Diverticular bleeding is usually painless and often self-limited with intermittent passage of maroon or bright blood. Yet about 5% of patients with diverticulosis may present with significant bleeding; many are over 60 years old and have multiple comorbid conditions. Bleeding is usually managed in the inpatient setting with a colonoscopy being the treatment modality of choice; Interventional Radiology and Surgery may be needed if bleeding can’t be managed with a scope.
And yes: Diverticulosis appears to be hereditary. Patients with diverticular disease often ask whether diverticulosis runs in families. There appears to be good evidence that it does in fact run in families. A recently published study showed a much stronger relative risk in monozygotic compared with dizygotic twins suggesting that there is a real genetic risk. (Strate LL et al. Heritability and familial aggregation of diverticular disease: A population-based study of twins and siblings. Gastroenterology 2013 Apr; 144:736)
Gastro-Esophageal Reflux Disease (GERD)
GERD, more commonly referred to as heartburn, occurs when acidic contents in the stomach flow back into the food pipe (esophagus). This phenomenon occurs because the valve between the stomach and the esophagus (the lower esophageal sphincter) inappropriately relaxes, allowing acid to travel back into the esophagus.
What are symptoms of GERD?
Heartburn and acid indigestion are the most common symptoms. However, when acid bathes the esophagus, the problem can manifest as other less-classic symptoms. These can include a sour or bitter taste in the mouth, involuntary regurgitation of food or fluid into the mouth, hoarseness, sore throat or the need to clear the throat, dental erosions, wheezing, dental erosions, or unexplained cough.
What causes GERD?
Temporary relaxation of the lower esophageal sphincter, which allows the backflow of stomach acid into the esophagus, is influenced by a variety of conditions. Large meals as well as certain foods contribute to these episodic relaxations. Obesity, tight clothing around the waist and pregnancy can also contribute by increasing pressure in the abdomen, which can allow acid to overcome the barrier between the stomach and the esophagus. Smoking, excessive alcohol use, and hiatal hernias can also induce GERD.
What harm can occur?
The stomach has a tough lining that is made to resist acid, but the esophagus does not. Thus, the most common complication of heartburn is esophagitis, or inflammation of the esophagus, which can cause ulcers or bleeding. Sometimes the inflammation can lead to scarring or narrowing of the esophagus. Pre-malignant changes, which can progress to cancer, can occur due to changes in the cells that line the esophagus. This is commonly referred to as Barrett’s esophagus and should be followed closely to ensure cancer does not develop.
How do you treat GERD?
The first step in treating GERD is dietary and lifestyle modification. Avoid fatty or spicy foods, tomato-based products, citrus drinks, chocolate, coffee, and peppermint. It is also recommended to eat smaller meals, lose weight, stop smoking, and abstain from alcohol. Nighttime symptoms can be improved by not eating within three hours of sleeping, or propping up the head of the bed. If symptoms persist, then over-the-counter antacids can help for a short period of time. More potent prescription medications can also be used under the direction of your doctor. Surgery is an option for patients who don’t respond fully to medical therapy or for those with severe GERD.
When should I see a doctor about GERD?
See a doctor if your classic symptoms are not controlled with dietary and lifestyle modifications or if you are using over-the-counter medications more than twice a week. You should seek immediate medical attention if you have chest pain, unexplained weight loss, food that sticks in your chest after swallowing, bloody vomit, or black, tarry bowel movements.
Irritable Bowel Syndrome
What is Irritable Bowel Syndrome?
Irritable bowel syndrome, or IBS, is a common condition and affects up to 15% of people over a lifetime. IBS is more common in women and tends to be more active during the reproductive years (after menstruation begins and before menopause). Although IBS is more commonly seen in women, many men also suffer from IBS.
IBS is a disturbance of gut function. The bowel looks normal when visualized during a colonoscopy, CT scan or x-ray. The problem arises from the way the bowel “works” and in the way the bowel processes sensory input.
Symptoms of IBS include abdominal pain, bloating, diarrhea and/or constipation. Many with IBS will experience alternating diarrhea and constipation. Having a bowel movement or passing gas often relieves pain and bloating. Bowel movements may be urgent, making it difficult to make it to the toilet in time. Others with IBS feel like the bowels do not empty completely. Symptoms often get worse with stress, with overeating, or with the ingestion of certain foods. Blood in the stool and unexplained weight loss are not typically seen with IBS alone, and should prompt additional evaluation.
What tests are appropriate in the evaluation of IBS?
The evaluation of IBS symptoms may vary, depending on one’s age and presenting symptoms. A health professional should perform a complete history and physical exam. Further testing may include labs, stool studies or imaging (ultrasound, x-ray, etc.). You may need a colonoscopy, especially if you are over 50 years old or having worrisome symptoms like blood in the stool.
What does “Irritable” mean?
Irritable means that the nerve endings in the lining of the bowel are extremely sensitive, and that the nerves that control the muscles of the bowel are unusually active. The result is that the bowel is too sensitive to “normal” events such as the passage of gas, fluid or stool. This leads to inappropriate muscular activity that can cause cramping, diarrhea or constipation.
What is the effect of diet on IBS?
Diet is almost always a contributing factor in IBS. Keeping a food and symptom diary may help identify certain foods that aggravate your IBS. Common offending foods are those that contain high fat, dairy/lactose, fructose (like that in high fructose corn syrup or many fruits), gluten, monosodium glutamate, artificial sweeteners or “gassy” vegetables such as beans, broccoli and cauliflower. But, just about every food has been implicated in the production of IBS symptoms, so it is important to identify which particular foods increase your symptoms.
What is the relationship of stress to IBS?
Emotional distress can significantly influence IBS. That is why IBS may flare during times of emotional upset such as family or job problems. That does not mean that IBS is “all in your head”. It does not mean that all IBS patients are crazy or anxious. As stated previously, IBS results from a complex interaction between the mind and the gut. In many IBS patients the mind is much too aware of what is going on in the gut and the gut is much too aware of what is going on in the mind. So, if you are under increased stress, some of that stress may be transmitted to your gut. When this happens, the gut may become under-active (constipation), over-active (diarrhea) or ultra-sensitive (pain, bloating).
If you have been diagnosed with depression or anxiety, IBS may become worse when these conditions are not under good control.
How is IBS treated?
There is no “magic pill” that can make IBS symptoms go away. IBS treatment is challenging and often frustrating, as it nearly always involves lifestyle change.
The first step in the treatment of IBS is a personal evaluation of your overall well-being. Do you eat a healthy diet? Do you eat a lot of processed food or fast food? Are there certain foods that tend to aggravate your IBS? Do you exercise regularly? How do you deal with the stress in your life? Do you have untreated depression, anxiety or posttraumatic stress disorder? You cannot expect to recover from IBS if any of these issues are neglected.
Proper rest and exercise can help to reduce stress levels. Your doctor may recommend that you speak to a therapist about coping mechanisms and stress reduction techniques.
Of course, foods that make your symptoms worse should be avoided. A high fiber diet and/or fiber supplements are often helpful. Not only is fiber used in the treatment of constipation, but also is useful in the treatment in IBS marked by pain or diarrhea. Laxatives such as Miralax or Milk of Magnesia are commonly recommended for constipation.
When these measures fail, medications can be prescribed that target specific symptoms of IBS. Some of these include a class of medications called “antispasmodics” to treat pain or cramping. Other medications treat discomfort by interfering with the overly sensitive connections between brain and gut. Low dose antidepressants are commonly used to reduce the pain associated with IBS. Other medications specifically treat constipation or diarrhea.
The key to achieving relief from IBS is for patients to realize that IBS is a complex disorder with physical and stress-related dimensions. A strong partnership between an empathetic health professional and a motivated patient can produce significant improvement.
5 TIPS to help you deal with Irritable Bowel Syndrome:
1. Remember that your digestive tract is a “barometer of your overall well-being”. That is, you won’t have a happy & healthy digestive system without a healthy mind & body.
2. Avoid foods that you know will make your symptoms worse.
3. Use medications wisely. For instance, if diarrhea is the issue then take an anti-diarrheal medication before leaving home if you are worried about having diarrhea in a situation where a toilet is not readily available, like an airplane.
4. Looks for sources of stress in your life and do something about them.
5. Above all, decide who is running your life… YOU or your GUT. Life is easier if you’ve made up your mind that you are in charge!
Constipation – What You Need To Know
Constipation refers to a change in bowel habits with bowel movements being either too hard in consistency, too difficult to pass, or too infrequent (less than three times per week). Often patients with constipation need to strain or sense that bowels do not empty completely. Constipation is a very common problem with 14% of people affected and over 2.5 million healthcare provider visits per year. Factors such as a low fiber intake, dehydration, thyroid disease, hypercalcemia, medications (i.e. narcotics, diuretics), lack of timely access to bathroom facilities and many others can contribute to constipation. A clear cause is often not found. Constipation may occur more frequently in older age. Constipation can usually be diagnosed based on symptoms and a physical examination including a rectal exam. Further testing such as blood tests, x-rays, sigmoidoscopy, colonoscopy, ano-rectal motility studies may be indicated.
Treatment of constipation includes a high fiber diet (20 to 35 grams of fiber per day), fiber supplementation, staying hydrated and being physically active. OTC laxatives or enemas may be needed, especially if behavioral changes and increased fiber intake do not improve constipation.
In general, laxatives can be categorized into the following groups:
Bulk forming laxatives: These include natural fiber and commercial fiber preparations such as: Psyllium (Konsyl®; Metamucil®; Perdiem®), Methylcellulose (Citrucel®), Calcium polycarbophil (FiberCon®; Fiber-Lax®; Mitrolan®), Wheat dextrin (Benefiber®)
Hyperosmolar laxatives: Polyethylene glycol (MiraLax®, Glycolax®), Lactulose, Sorbitol
Saline laxatives: i.e. magnesium hydroxide (Milk of Magnesia®) and magnesium citrate (Evac-Q-Mag®)
Stimulant laxatives: i.e. senna (Black Draught, ex-lax®, Fletcher’s®, Castoria®, Senokot®) and bisacodyl (Correctol®, Doxidan®, Dulcolax®)
Prescription medications such as Lubiprostone (Amitiza®) or Linaclotide (Linzess®) as well as treatment options such as biofeedback, pelvic floor physical therapy and even surgery should be reviewed with the treating provider. Diseases such as Colon Cancer, Colonic Inertia, Hirschsprung Disease, Pelvic Floor Dysfunction, and an Enterocele or Rectocele must be considered and can be addressed in that setting.
Utah Gastroenterology Blog 