19: 39-year-old man with epigastric pain Flashcards
Systems Approach to Abdominal Pain
Gastrointestinal
Appendicitis, cholecystitis/cholelithiasis, diverticulitis/diverticulosis, dyspepsia, gastroesophageal reflux disease, gastritis, acute or chronic hepatic failure with resultant complications (e.g., ascites), acute hepatitis (e.g., viral, autoimmune, alcoholic, drug-induced), inflammatory bowel disease, intestinal ischemia, intestinal obstruction, irritable bowel syndrome, pancreatitis, peptic ulcer, perforation/peritonitis (e.g., gastric, colonic, intestinal), gastric outlet obstruction, tumor (e.g., gastric, hepatic, pancreatic, intestinal, colonic).
Cardiac
Myocardial infarction, angina pectoris, abdominal aortic aneurysm dissection or rupture.
Psychogenic
Anxiety, panic disorder, somatiform disorder, post-traumatic stress disorder.
Pulmonary
Pleurisy, pneumonia, pulmonary infarction, tumor.
Renal
Nephrolithiasis, pyelonephritis, cystitis, tumor.
Musculoskeletal
Abdominal wall muscle strain, hernia (e.g., ventral, inguinal, incarcerated), abscess (e.g., psoas, subphrenic), trauma (e.g., contusion, hematoma).
Metabolic
Drug overdose, ketoacidosis, iron or lead poisoning, uremia.
Agents that Cause or Contribute to Peptic Ulcer Disease
Aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs) are the predominant pharmacologic agents that contribute to the development of PUD. Classically, the elderly are at the highest attributable risk of ulceration and perforation due to chronic NSAID use. Chronic NSAID use is a leading cause of morbidity in the elderly.
Moderate to severe physiologic stress may lead to stress ulceration , predominantly in patients in the intensive care unit (ICU).
Colonization of the stomach by H. pylori renders the underlying mucosa more vulnerable to peptic acid damage by disrupting the mucous layer, liberating enzymes and toxins, and adhering to the gastric epithelium. In addition, the body’s immune response to H. pylori incites an inflammatory reaction that contributes to tissue injury and leads to chronic gastritis. In most individuals the chronic gastritis is asymptomatic and does not progress. In some cases, however, altered gastric secretion coupled with tissue injury leads to peptic ulcer disease. In other cases, gastritis progresses to mucosal atrophy, intestinal metaplasia, and eventually gastric carcinoma. Rarely, persistent immune stimulation of gastric lymphoid tissue can lead to gastric lymphoma.
There is no evidence to support a cause-and-effect association between cigarette smoking and PUD. However, cigarette smoking does decrease vascularity to gastric mucosal cells, resulting in decreased rates of mucosal healing after insult, and in combination with NSAID use or H. pylori infection, increases the risk of ulceration.
Complications of GERD and PUD
GERD
Esophagitis develops when the mucosal defenses that normally counteract the effect of injurious agents are overwhelmed by refluxed acid, pepsin, or bile.
Peptic strictures from fibrosis and constriction occur in about 10 percent of patients with reflux esophagitis.
Replacement of the squamous epithelium of the esophagus by columnar epithelium (Barrett’s esophagus) may result from reflux esophagitis. Two to five percent of cases of Barrett’s esophagus may be further complicated by adenocarcinoma.
PUD
Hemorrhage or perforation into the peritoneal cavity or adjacent organs (causing severe, persistent abdominal pain).
Ulcer scar healing or inflammation can impair gastric emptying leading to gastric outlet obstruction syndrome.
Alarm Symptoms Warranting Referral to Gastroenterology for Endoscopy
Dysphagia
Difficulty in swallowing. Dysphagia to solids suggests possible development of peptic stricture. Rapidly progressive dysphagia potentially indicates adenocarcinoma. Dysphagia to liquids suggests development of a motility disorder.
Initial onset of upper GI symptoms after age 50
Increased chance of cancer.
Early satiety
May be associated with gastroparesis or gastric outlet obstruction (stricture or cancer).
Hematemesis
Vomiting blood, which suggests bleeding ulcer, mucosal erosions (erosive gastritis/esophagitis), esophageal tear (Mallory-Weiss), or esophageal varices.
Hematochezia
Passing red blood with stool, which may indicate a rapidly bleeding ulcer or mucosal erosions.
Iron deficiency anemia
The presence of hematemesis, hematochezia, and/or iron deficiency anemia may indicate possible bleeding from a peptic ulcer, mucosal erosions, or cancer.
Odynophagia
Painful swallowing, which is associated with infections (e.g. candida), erosions, or cancer.
Recurrent vomiting
Suggestive of gastric outlet obstruction.
Weight loss
Associated with malignancy.
GERD/PUD Physical Exam: Signs of Complications or Other Associated Diseases
Hemodynamic status
Hypotension or tachycardia may indicate significant blood loss from a gastrointestinal bleed.
Signs of anemia
Brittle nails and cheilosis (cracks and sores on the lips) are signs of anemia. Pallor of palpebral (eyelid) mucosa or nail beds may also be present with anemia.
Signs of malignancy
Weight loss, palpable mass, presence of signal lymph nodes (Virchow’s nodes) and acanthosis malignancy nigricans (velvety, light-brown-to-black skin, usually on the neck, under the arms or in the groin)
are signs of possible malignancy.
Signs of gall bladder disease
Jaundice or a positive Murphy’s sign. (A test for Murphy’s sign is performed by asking the patient to breathe out and then gently placing the hand in the approximate location of the gallbladder. The patient is then instructed to inspire. If the patient stops inhaling (as the tender gallbladder comes in contact with the examiner’s fingers) the test is considered positive.)
Signs of hypo or hyperthyroidism
Constipation, cool or pale skin, coarse hair, or non-pitting edema (myxedema) or delayed relaxation phase of deep tendon reflexes (DTRs) may be present in hypothyroidism. Diarrhea, warm skin, thinning hair, eyelid lag, brisk DTRs, or tachycardia may be present in hyperthyroidism. Though a very rare cause of dyspepsia, thyroid disease should be considered.
Epidemiology of H. pylori Infection
An estimated 30% to 40% of the US population is infected with H. pylori.
The prevalence of H. pylori infection varies across different geographic regions, ethnic groups, and household conditions.
H. pylori infection is thought to occur via fecal-oral transmission during childhood in underdeveloped nations.
Ninety percent of patients worldwide with duodenal ulcers are infected with H. pylori.
It is rare in developed countries, and the worldwide prevalence is decreasing.
H. pylori is uniquely adapted to life in the stomach. Its location in the gastric mucosa, where it does not invade the gastric epithelium, which provides the organism with protection from the host immune mechanisms and results in challenges in the delivery of antimicrobial agents to eradicate infection.
The strongest evidence to support the role of H. pylori as an etiology of PUD is the elimination of ulcer recurrence after eradication.
An empiric treatment strategy for GERD, gastritis, and PUD is the most widely accepted initial therapeutic intervention in patients without red flag symptoms.
The empiric treatment strategy for a patient who exhibits the classic symptomatology of GERD with heartburn and regurgitation begins with a self-directed trial of over-the-counter anti-secretory therapy, either a histamine-2 receptor antagonist or a proton-pump inhibitor (PPI). Many patients consult their primary care physicians because their symptoms have persisted, or because they would like a prescription, which may reduce their out-of-pocket cost for anti-secretory therapy.
Management of Dyspepsia Unresponsive to Short-Term PPI Trial
Check for contributing agents
Inquire about NSAID and/or aspirin use
There are several therapies for functional dyspepsia that are similar to those for PUD.
Test for H. pylori
Rule out GI bleeding
Endoscopy
First-line Treatment for H. pylori
“Triple therapy” for 10 to 14 days (70% to 85% eradication rate) :
- -PPI standard dose twice daily (esomeprazole is dosed once daily)
- -Amoxicillin 1 g twice daily
- -Clarithromycin 500 mg twice daily
“Quadruple therapy” for 10 to 14 days (75% to 90% eradication rate):
- -PPI standard dose once or twice daily (OR ranitidine 150 mg twice daily)
- -Metronidazole 250 mg four times daily
- -Tetracycline 500 mg four times daily
- -Bismuth subsalicylate 525 mg four times daily
An alternative 10- to 14-day triple regimen to consider in patients who are allergic to penicillin (70% to 85% eradication rate):
- -PPI standard dose twice daily
- -Clarithromycin 500 mg twice daily
- -Metronidazole 500 mg twice daily
Management of Epigastric Pain Resistant to Salvage Therapy - Endoscopy
If symptoms persist despite salvage therapy, upper endoscopy/EGD is requiredfor evaluation to rule out PUD or malignancy and to undergo mucosal biopsy for evaluation of persistent H. pylori infection. Abdominal ultrasound should also be considered to evaluate for biliary disease as the cause of his persistent epigastric pain.
Universal post-treatment testing for H. pylori eradication is ideal but is neither practical nor cost-effective. Accepted indications for testing to prove eradication after antibiotic therapy, based upon expert consensus, include:
- -any patient with an H. pylori-associated ulcer
- -individuals with persistent dyspeptic symptoms despite the test-and-treat strategy –those with H. pylori-associated MALT (mucosa-associated lymphoid tissue) lymphoma individuals who have undergone resection of early gastric cancer
- -patients planning to resume chronic NSAID therapy
The 24-hour pH probe is considered the gold standard for confirming the diagnosis of GERD, but is not commonly required to make this diagnosis. While upper endoscopy/EGD is neither sensitive nor specific for diagnosing GERD, it is the most useful test for evaluation of complications of GERD including erosive esophagitis, esophageal stricture, Barrett’s esophagus, and adenocarcinoma of the esophagus.
Evaluation of Persistant Symptoms of Dyspepsia - Investigating H. pylori Eradication
The fecal antigen test and urea breath test are reasonable next steps to evaluate eradication of H. pylori.
- The fecal antigen test involves collection of a stool sample the size of an acorn by either the clinician or the patient; the sample is then analyzed in a laboratory by trained personnel.
- The urea breath test requires specialized equipment and patient preparation.
Both tests have been reported to have a sensitivity and specificity for active H. pylori infection of > 90%. The H. pylori fecal antigen test is less expensive and may be more cost-effective than the urease breath test.
- -If the fecal antigen test or the urea breath test is positive, the patient will require re-treatment for a resistant infection, but this should not be given prior to testing for the presence of active H. pylori infection.
- -If the fecal antigen test or urea breath test is negative, and the patient continues to have symptoms, he should be referred to a gastroenterologist for an upper endoscopy/EGD and mucosal biopsy.
GERD
May present with mild epigastric pain, and symptoms commonly worsen after meals, although the pain is classically described as “burning” and may be located in the substernal rather than epigastric area.
Hematemesis in the setting of GERD-like symptoms is unusual and represents an alarm symptom indicative of an upper GI bleed or tumor and warrants prompt GI referral for evaluation and upper endoscopy.
Hematochezia and melena are not typically associated with GERD.
Peptic ulcer disease
PUD
Epigastric abdominal pain that improves with meals is the hallmark of PUD. However, in some cases, symptoms of PUD may worsen with meals.
NSAID use is associated with the development of PUD.
Hematemesis, if present, suggests more complicated disease including bleeding ulcer and warrants urgent GI referral and endoscopy.
Melena commonly occurs in the setting of an upper GI bleed secondary to PUD or hemorrhagic gastritis (e.g. NSAID-gastritits). Hematochezia only occurs in the setting of an upper GI bleed when massive (e.g. variceal rupture).
Gastritis
Inflammation or irritation of the stomach lining often causing sharp epigastric pain. This pain may be variably worsened or improved with eating food .
Inflammatory forms of gastritis may be caused by chronic infections such as H. pylori or acute infections such as viruses.
Non-inflammatory forms of ‘gastritis’ are more properly histologically termed gastropathy. These may be caused by chemical irritants to the stomach, including alcohol and NSAIDs.
Differential for Chronic Progressively Worsening Upper Abdominal Pain: Most Likely / Most Important Diagnoses
- GERD
- PUD
- Gastritis
