week 5 discussion

Description

DOMAIN: HISTORY

1a) Identify two (2) additional questions that were not asked in the case study and should have been?
1b) Explain your rationale for asking these two additional questions.
1c) Describe what the two (2) additional questions might reveal about the patient’s health.

DOMAIN: PHYSICAL EXAM
For each system examined in this case;
2a) Explain the reason the provider examined each system.
2b) Describe how the exam findings would be abnormal based on the information in this case. If it is a wellness visit, based on the patient’s age, describe what exam findings could be abnormal.
2c) Describe the normal findings for each system.
2d) Identify the various diagnostic instruments you would need to use to examine this patient.

DOMAIN: ASSESSMENT (Medical Diagnosis)
Discuss the pathophysiology of the:
3a) Diagnosis and,
3b) Each Differential Diagnosis
3c) If it is a Wellness, type ‘Not Applicable’

DOMAIN: LABORATORY & DIAGNOSTIC TESTS
Discuss the following:
4a) What labs should be ordered in the case?
4b) Discuss what lab results would be abnormal.
4c) Discuss what the abnormal lab values indicate.
4d) Discuss what diagnostic procedures you might want to order based on the medical diagnosis.
4e) If this is a wellness visit, discuss what the U.S. Preventive Taskforce recommends for patients in this age group.

Unformatted Attachment Preview

Family Medicine 19: 39-year-old male with epigastric pain
User: ARIADNA ZARZUELA
Email: [email protected]
Date: December 23, 2023 9:41 PM
Learning Objectives
The student should be able to:
Differentiate among common etiologies based on the presenting symptom of abdominal pain.
Conduct a focused history and physical exam appropriate for differentiating between common etiologies of a patient presenting with abdominal
pain.
Educate a patient about an aspect of abdominal pain respectfully, using language that the patient understands.
Find and apply diagnostic criteria and surveillance strategies for dyspepsia.
Perform a focused physical exam that can identify complications of Gastroesophageal Reflex Disease.
Describe an evidence-based management plan that includes surveillance of abdominal pain including PUD, GERD, dyspepsia.
Describe an evidence-based management plan that includes pharmacologic and non-pharmacologic treatment of dyspepsia, GERD, gastritis,
PUD, and h.pylori.
Discuss the epidemiology of h. pylori infection.
Knowledge
Systems Based Differential Diagnoses Considerations for a Chief Complaint of Abdominal Pain
Appendicitis, cholecystitis/cholelithiasis, diverticulitis, functional dyspepsia (FD, formerly non-ulcer dyspepsia (NUD)),
gastroesophageal reflux disease (GERD), gastritis, gastroenteritis, acute or chronic hepatic failure with resulting complications
(e.g., ascites), acute hepatitis (e.g., viral, autoimmune, alcoholic, drug-induced), inflammatory bowel disease, intestinal ischemia,
Gastrointestinal
intestinal obstruction, irritable bowel syndrome, cholelithiasis, cholecystitis, choledocholithiasis, cholangitis, pancreatitis, peptic
ulcer disease (PUD), perforation/peritonitis (e.g., gastric, colonic, intestinal), gastric outlet obstruction, intra-abdominal or hepatic
abscess, tumor.
Cardiac/Vascular Myocardial infarction, angina pectoris, abdominal aortic aneurysm dissection or rupture, mesenteric arterial thrombosis.
Psychogenic
Anxiety, panic disorder, somatoform disorder, post-traumatic stress disorder.
Pulmonary
Pleurisy, lower lobe 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), cutaneous nerve entrapment.
Metabolic
Drug overdose, ketoacidosis, iron or lead poisoning, uremia, acute intermittent porphyria.
Also consider:
Medication, vitamin, and herbal supplement side effects
Dietary factors (dietary intolerances, such as lactose, gluten, fructose, or artificial sweeteners [e.g., sorbitol, xylitol, sucralose])
Potential Cultural Barriers to Seeking Medical Attention
There may be a variety of reasons for an individual’s reluctance to seek medical care, making it imperative that the clinician explore these issues with
each patient individually and not rely on assumptions.
While all patients should be directly asked the reason for their reluctance to seek medical care, the patient’s social and work situation should raise a
flag. Undocumented immigrants may fear that if they seek medical attention, the health care system may report them to the government. This fear is
not unfounded, and providers should be sensitive about disclosing patients’ immigration status.
Also, patients may view health from a holistic standpoint, where physical problems cannot be separated from nonphysical problems. Those with this
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viewpoint may be less likely to visit a clinician’s office or access preventive services, including vaccinations. A holistic approach has been shown to
improve health outcomes in some studies, and should not be dismissed.
Recent immigrants who are unfamiliar with the U.S. health care system may view it as confusing, intimidating, and unfriendly (native residents may
also feel this way). Immigrant patients may be wary of receiving lower-quality care because of discrimination and racism. Providers should actively
check biases to ensure they are providing an equal standard of care.
Dyspepsia: Definition, Symptoms, Epidemiology, and Etiology
Definition
Dyspepsia is literally “bad digestion, and may describe having “indigestion.”
Symptoms
Patients with dyspepsia experience upper abdominal pain or discomfort that is episodic or persistent. It is often associated with belching, bloating,
heartburn, early satiety, nausea, and/or vomiting.
Epidemiology
About a quarter of adults are affected by dyspepsia, but many people self-diagnose and self-treat. Even though most people don’t seek medical care
for it, dyspepsia accounts for approximately 5% of all visits to family physicians and is the most common symptom leading to GI referral in the U.S.
Etiology
Condition
% of Dyspepsia Cases
Functional dyspepsia (FD), formerly known as non-ulcer dyspepsia (NUD)
(specific etiology for dyspepsia can’t be identified, but often improves with acid
suppression)
70%
Peptic ulcer disease (PUD)
20%
GERD
20%
Gastritis/duodenitis
10%
Medication side effects
Common
Pancreatitis
Less common
Gastric, pancreatic, and esophageal cancer
Important though uncommon (< 2%) Non-GI causes Rare, but should always be included in differential diagnosis (such as angina and dissecting aortic aneurysm) Agents that Cause or Contribute to Peptic Ulcer Disease Aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) are the predominant pharmacologic agents that contribute to the development of PUD. Classically, older adults 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 older adults. 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 injury, and, in combination with NSAID use or H. pylori infection increases the risk of ulceration. 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. 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. Moderate to severe physiologic stress may lead to stress ulceration , predominantly in patients in the intensive care unit (ICU). Significant mental health disorders such as chronic depression and suicidal ideation have been associated with a higher risk of developing PUD in some observational studies. Peptic Ulcer Disease versus Gastroesophageal Reflux Disease Symptoms Some symptoms of PUD directly contrast those of GERD. © 2023 Aquifer, Inc. - ARIADNA ZARZUELA ([email protected]) - 2023-12-23 21:41 EST 2/9 PUD GERD Characterized by episodic or recurrent epigastric "aching," "gnawing," or "hunger-like" pain or discomfort Classic symptoms of retrosternal heartburn and regurgitation/ reflux Symptoms occur on an empty stomach and may be relieved by meals More likely to occur postprandially, when gastric volume is increased, or with specific food triggers However, this is not always true, and there can be some differences in symptoms based on the location of an ulcer. For example, gastric ulcer pain may occur 5 to 15 minutes after eating and remain until the stomach empties, which may be up to several hours in duration; the pain may otherwise be absent during times of fasting. Pain from duodenal ulcers is often relieved by eating, drinking milk, or taking antacids but may return anywhere from 90 minutes to four hours after eating a meal. Both gastric and duodenal ulcers may be associated with nausea and vomiting occurring anytime shortly after eating to several hours later. Given the population prevalence of obesity and hiatal hernia, conditions that predispose a patient to acid reflux, it is not uncommon for a patient with PUD or functional dyspepsia to also have GERD. Gastroesophageal Reflux Disease: Pathophysiology, Symptoms, Complications, and Quality of Life Pathophysiology GERD is a chronic relapsing condition in which gastric contents reflux through the lower esophageal sphincter (LES) into the esophagus and oropharynx. Transient LES relaxations are believed to be the primary etiologic factor. Ineffective esophageal clearance (as seen with scleroderma, for example) and delayed gastric emptying (as seen with gastroparesis, for example) may also be contributing factors in some patients. Increased intra-abdominal pressure is also a predisposing factor (obesity/central adiposity, pregnancy, constricting garments), especially in the presence of a hiatal hernia. Symptoms 1. Gastroesophageal reflux: epigastric or retrosternal burning that sometimes radiates to the throat and tends to worsen when: Gastric volume is increased (after large meals) Gastric contents are located near the gastroesophageal junction (reclining or bending) Intra-abdominal pressure is increased (such as with obesity, pregnancy, abdominal binders, or girdles). 2. Esophageal spasm: sharp, stabbing, substernal chest pain that may be triggered by temperature extremes (e.g., hot coffee, ice water). Heartburn, esophageal reflux, and esophageal spasm commonly occur at night or after the consumption of trigger foods or a large meal. Symptoms of GERD may also be precipitated by: Spicy, acidic, and fatty foods Chocolate Mint Smoking Alcohol and caffeine Eating large portions Lying supine after a meal Wearing tight clothing around the waist Some medications (calcium channel blockers, beta-agonists, alpha-adrenergic agonists, theophylline, nitrates, and some sedatives) When severe reflux reaches the pharynx and mouth or is aspirated, it can cause atypical signs and symptoms of GERD or laryngopharyngeal reflux (LPR). Atypical symptoms may point to (but alone does not sufficiently support) a diagnosis of GERD. Atypical signs and symptoms of GERD: Asthma, especially new onset in an adult with no history of atopy Chronic cough Dental enamel loss Globus sensation Hoarseness Noncardiac chest pain Recurrent laryngitis Recurrent pharyngitis Subglottic stenosis Complications © 2023 Aquifer, Inc. - ARIADNA ZARZUELA ([email protected]) - 2023-12-23 21:41 EST 3/9 About 60% of cases of GERD can be classified as non-erosive reflux disease (NERD). Unfortunately, symptom frequency, duration, and severity do not help to differentiate the endoscopic/histologic grade of esophagitis and cannot be used to reliably diagnose complications of GERD. Quality of life Patients who have GERD generally report decreased quality of life, reduced productivity, and decreased well-being. In many patients, reported health-related quality of life is lower than age-matched patients who have untreated angina pectoris, diabetes mellitus, or chronic heart failure. 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 erosive esophagitis. Replacement of the squamous epithelium of the esophagus by columnar epithelium (Barrett's Esophagus) may result from chronic erosive esophagitis. Two to five percent of cases of Barrett's esophagus may be further complicated by esophageal adenocarcinoma. PUD Hemorrhage or perforation into the peritoneal cavity may occur, causing GI bleeding or severe, persistent abdominal pain with peritoneal signs. Duodenal ulcer, inflammation, and fibrotic scarring can impair gastric emptying due to gastric outlet obstruction. Alarm Symptoms Warranting Referral to Gastroenterology for Endoscopy Dysphagia Difficulty in swallowing. Dysphagia to solids suggests possible peptic stricture. Progressive dysphagia potentially indicates carcinoma. Dysphagia to liquids suggests a motility disorder. Dysphagia to both solids and liquids suggests obstruction—for example, achalasia (closed LES) or tumor. Initial onset of upper Increased risk of cancer. GI symptoms after Older age at onset increases the likelihood of organic disease (PUD, cancer) rather than functional dyspepsia (FD) or nonage 50 erosive reflux disease (NERD). NERD meets the same diagnostic criteria as GERD but shows no erosions on endoscopy. Early satiety May be associated with gastroparesis or gastric outlet obstruction (stricture or cancer). Hematemesis Suggests bleeding ulcer, mucosal erosions (erosive gastritis/esophagitis), esophageal tear (Mallory-Weiss), or esophageal varices. Hematochezia Indicates a rapidly bleeding ulcer, mucosal erosions, varices, OR a lower intestinal source of bleeding. Iron deficiency anemia May indicate bleeding from a peptic ulcer, mucosal erosions, or cancer. In patients over age 50, the most likely cause is GI blood loss. Odynophagia Painful swallowing is associated with infections (e.g., candida, CMV, HSV), inflammation, erosions, or cancer. Recurrent vomiting Suggestive of gastric outlet obstruction. Weight loss When unintentional or unexplained, it is more likely to be associated with malignancy and needs to be treated as such until proven otherwise. GERD and PUD Physical Exam: Signs of Complications or Other Associated Diseases Hemodynamic Hypotension or tachycardia may indicate significant blood loss from a gastrointestinal bleed. status Signs of anemia Brittle nails and cheilosis (cracks and sores on the lips), pallor of palpebral (eyelid) mucosa or nail beds, and tachycardia or heart murmur are suggestive of anemia. Signs of malignancy Weight loss, palpable mass, presence of signal lymph nodes ("Virchow node”, L. supraclavicular node), and acanthosis nigricans (velvety, hyperpigmented skin, usually on the neck, under the arms, or in the groin) are signs of possible malignancy. © 2023 Aquifer, Inc. - ARIADNA ZARZUELA ([email protected]) - 2023-12-23 21:41 EST 4/9 Signs of gallbladder disease Right upper quadrant pain. 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 while the examiner palpates deeply. If the patient abruptly stops inhaling (as the tender gallbladder comes in contact with the examiner's fingers) the test is considered positive. Epidemiology of H. pylori Infection An estimated 30% to 40% of the U.S. 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 though worldwide prevalence is decreasing, antibiotic resistance is increasing. H. pylori is uniquely adapted to life in the stomach. Its location in the gastric mucosa, where it does not invade the gastric epithelium, 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. Serological studies in developing nations, including Latin and Central America, have demonstrated prevalence rates of 80% to 90% for H. pylori infection in all adults, regardless of age. A population-based study examining the prevalence of H. pylori infection across several generations of Latinos in the San Francisco Bay Area found prevalence rates in immigrants, first-generation, and second-generation U.S.-born Latinos to be 31%, 9%, and 3%, respectively. Compared with second-generation U.S.-born Latinos, the age-adjusted odds ratios for H. pylori were 9.70 for immigrants and 4.32 for first-generation U.S.-born Latinos (95% CI). Both household and birth-country environments have probably contributed to declining H. pylori prevalence among successive generations of Latinos. Clinical Skills How to Interview a Patient Via an Interpreter Speak as you would normally, directly to the patient and not to the interpreter. The interpreter should interpret in the first person, without editing it in any way. Often, the interpreter will sit just behind the patient and in their ear, or off to the side where the interpreter won't obstruct your ability to face the patient, make direct eye contact, and feel like you're talking with the patient directly. Ideally, it should feel like the interpreter is just a conduit for the conversation between you and the patient. Management Empiric Treatment for GERD, Gastritis, and PUD An empiric treatment strategy for GERD, gastritis, FD, and PUD is the most widely accepted initial therapeutic intervention in patients without red-flag symptoms. Empiric treatment begins with a trial of over-the-counter anti-secretory therapy, either a histamine-2 receptor antagonist (H2RA) 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. Several randomized trials have demonstrated that the "PPI test," defined as a short-term trial of prescription-strength PPI, is both sensitive and specific for diagnosing GERD in patients with classic symptoms and can significantly reduce the need for upper endoscopy/EGD and 24-hour pH monitoring. This test has been shown to save over $350 per patient evaluated, reduce upper endoscopies by 64%, and reduce the number of esophageal monitoring tests by 53%. The natural history of both GERD and functional dyspepsia are variable, and antisecretory therapy should be stopped after a successful eight-week course, or used in a pulse dose manner (daily for short periods of time when symptoms recur) in patients without red-flag signs/symptoms. Addressing lifestyle modifications with patients who report symptoms of GERD and FD is a reasonable approach to therapy. There is reported benefit in some patients and expert opinion suggests that dietary/lifestyle changes be encouraged in patients with GERD, although there is little evidence to support improvement in symptomatic outcomes in the absence of pharmacotherapy. Patients should be referred for upper endoscopy/EGD in the setting of alarm or extraesophageal symptoms to rule out significant disease, or in cases that do not respond to empiric treatment strategy after eight weeks. The upper GI series can be useful in determining complications of GERD (e.g., esophageal stricture) but has poor utility in diagnosing GERD and should not be used for this purpose. In some cases, the upper GI series may reveal a gastric or duodenal ulcer, but it is not the gold standard test to make this diagnosis, and EGD is still required for confirmation and biopsy. The 24-hour pH probe is most appropriately utilized when the diagnosis of GERD cannot easily be determined, when patients desire referral for surgical treatment of their GERD/hiatal hernia, or when patients with classic symptoms of GERD (heartburn, regurgitation) do not improve after appropriate trials of two different PPIs. © 2023 Aquifer, Inc. - ARIADNA ZARZUELA ([email protected]) - 2023-12-23 21:41 EST 5/9 Management of Dyspepsia Unresponsive to Short-Term PPI Trial Check for contributing agents Inquire about NSAID and/or aspirin use at each visit, as this may play a role in the symptoms. Antisecretory therapy There are several therapies for functional dyspepsia that are similar to those for PUD. PPI therapy has been shown to be superior to placebo treatment with regard to relative risk reduction of functional dyspepsia (Number needed to treat [NNT] = 9). Evidence exists to support an empiric trial of histamine-2 receptor antagonists, although some data suggests these medications are no more beneficial than prokinetics (e.g. metoclopramide) or antacids. A subset of patients with functional dyspepsia will not respond favorably to any form of antisecretory therapy and will continue to experience symptoms. Updated guidelines recommend a trial of pro-kinetic therapy. Test for H. pylori Testing for H. pylori is NOT indicated in patients with classic GERD symptoms and should be performed only in patients with functional dyspepsia or non-reflux upper GI symptoms (e.g. nausea, vomiting, epigastric pain, early satiety) if the clinician plans to offer treatment for positive results. Deciding which test to use in which situation relies upon an understanding of the benefits, limitations, and costs of the individual tests, as well as the suspected prevalence of H. pylori infection in the patient population. The H. pylori IgG serologic test confirms evidence of past infection and an immunologic response to H. pylori. In a population with a high prevalence of active H. pylori infection (e.g. patients born in endemic areas), it is an inexpensive and useful first-time test. However, if the population prevalence of active infection is low (e.g. patients born in the U.S.), then the test may yield a high number of false-positive results. It should not be used to confirm the eradication of H. pylori after treatment as it can remain positive for years. The urea breath test accurately detects active infection but is more expensive than serologic testing. It is less accurate during PPI therapy, and patients would need to stop the PPI for at least two weeks before a urea breath test (bismuth and antibiotics should also be stopped for at least two weeks before a urea breath test). However, urea breath testing may be appropriate depending on the characteristics of the population being tested. The stool antigen test for H. pylori is also accurate and widely available, but it is also more expensive and less convenient than serologic testing. The stool antigen and urease breath tests may also be used as confirmatory tests after a positive serologic test. If an endoscopy is indicated (i.e., due to the presence of alarm symptoms), or in patients who have been taking a PPI, antibiotics, or bismuth, endoscopic testing for H. pylori, (tissue biopsies from the gastric body and antrum for rapid tissue urease testing or histology) should be performed in lieu of other H. pylori tests. After H. pylori infection is ruled out, the following therapies have been proposed for functional dyspepsia: Tricyclic antidepressants have been found to improve symptoms in patients with functional dyspepsia without affecting the sensation of gastric distention. Prokinetics have been found to improve symptoms of functional dyspepsia, specifically early satiety, and bloating, though the evidence supporting this is of low quality. A systematic review determined that there is insufficient evidence to support the efficacy of psychological therapies—including cognitive behavioral therapy, hypnotherapy, relaxation training, and interpersonal therapy—for the treatment of functional dyspepsia. However, individual trials have reported some modest clinical benefits in symptomatic improvement. Alternative therapies are gaining popularity in patients with gastrointestinal conditions, and studies of varying quality suggest that slippery elm, capsaicin, peppermint oil, caraway oil, and artichoke leaf may improve symptoms. However, there is as yet no compelling evidence on which to base a recommendation for these alternative therapies. Note: Peppermint oil decreases lower esophageal sphincter pressure and may worsen GERD symptoms. Patients should be educated that herbal remedies are not regulated by the U.S. Food and Drug Administration (FDA), may not have been studied for safety, and can have adverse side effects, which often include GI side effects. Rule out GI bleeding If symptoms have not improved, it is reasonable to assess for occult GI bleeding as an alarm sign to guide further assessment. Occult GI bleeding will eventually lead to iron deficiency anemia, which can be diagnosed through a complete blood count (microcytosis and low hemoglobin with prolonged iron deficiency), ferritin (if low a sign of iron depletion before microcytosis and anemia), iron studies (low iron saturation occurs with more iron deficiency). The CBC and iron tests can assess the degree of blood loss and determine the urgency of GI referral. Testing for blood in stool can be useful in confirming the need for further gastrointestinal workup for occult blood loss. Fecal occult blood testing (FOBT) should be included to rule out occult GI bleeding. Fecal immunochemical testing (FIT) is not suitable for detecting gastric/upper GI bleeding, and it should not be used if the suspected source of bleeding is proximal to the ligament of Treitz. Guaiac-based fecal occult blood tests (FOBT), such as Hemoccult II SENSA, are indicated to check for occult upper GI bleeding. Multiple negative FOBTs do not exclude the presence of either upper or lower GI blood loss. Diets high in red meat, iron, and vitamin C may cause false-positive results with guaiac-based tests. Endoscopy It might seem reasonable to refer the patient to gastroenterology for endoscopy to determine if the patient has endoscopically confirmed PUD versus functional dyspepsia (in which case an upper endoscopy would appear unremarkable). But in the absence of alarm symptoms, the cost and risk of endoscopy do not outweigh the benefits of testing and treating at this point. First-Line Treatment for H. pylori "Triple therapy" for 14 days: PPI standard dose twice daily © 2023 Aquifer, Inc. - ARIADNA ZARZUELA ([email protected]) - 2023-12-23 21:41 EST 6/9 Amoxicillin 1 g twice daily Clarithromycin 500 mg twice daily "Quadruple therapy" for 10 to 14 days: PPI standard dose twice daily Metronidazole 250 mg four times daily Tetracycline 500 mg four times daily Bismuth subsalicylate or subcitrate 300 mg four times daily One alternative 10-day to 14-day triple regimen to consider in patients who are allergic to penicillin, in areas with low clarithromycin resistance, is: PPI standard dose twice daily Clarithromycin 500 mg twice daily Metronidazole 500 mg twice daily Other combination regimens have been used successfully, though none are currently FDA-approved for this indication (Saleem, Howden 2020). Management of Epigastric Pain Resistant to Salvage Therapy—Endoscopy If symptoms persist despite salvage therapy, upper endoscopy/EGD is required for evaluation to rule out PUD or malignancy and to undergo mucosal biopsy for evaluation of persistent H. pylori infection. Abdominal ultrasound may also be considered to evaluate for biliary/pancreatic 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 a documented 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 There is evidence to suggest that a small but significant subgroup of patients with functional dyspepsia will experience clinical benefit following H. pylori eradication. There is no clear evidence to support the idea that eradicating H. pylori consistently worsens or improves GERD symptoms, however, eradication of this alkalinizing infection has been purported to induce acid-related symptoms in some patients. Studies Evaluation of Persistent Symptoms of Dyspepsia—Investigating H. pylori Eradication The fecal antigen test and urea breath test are reasonable next steps to evaluate the eradication of H. pylori. 1. The fecal antigen test involves the collection of a small stool sample by the patient; the sample is then analyzed in a laboratory by trained personnel. 2. 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 may be more
readily available in some areas 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. 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.
Clinical Reasoning
Differential for Chronic Progressively Worsening Upper Abdominal Pain
Most likely/Most important diagnoses
Functional
Dyspepsia
A diagnosis of exclusion, FD is defined by specific Rome IV criteria: “one to three days per week of symptoms of postprandial
fullness, early satiety, epigastric pain, or epigastric burning without evidence of structural disease”
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Inflammation or irritation of the stomach lining often causes sharp epigastric pain. This pain may be variably worsened or
improved with eating food.
Gastritis
Inflammatory forms of gastritis may be caused by chronic infections, such as H. pylori, or acute infections, such as
enterovirus.
Noninflammatory forms of “gastritis” are histologically termed gastropathy. These may be caused by chemical irritants to the
stomach, including alcohol and medications.
May present with mild epigastric pain and symptoms commonly worsen after meals, although the pain is classically
described as “burning” and is typically located in the substernal rather than epigastric area.
May be associated with regurgitation and, rarely, dysphagia.
GERD
Hematemesis in the setting of GERD-like symptoms is unusual and represents an alarming symptom warranting prompt GI
referral for evaluation.
Nausea, vomiting, hematochezia, and melena are not typically associated with GERD.
Epigastric pain that improves with meals is the hallmark of PUD of the duodenum (DU). In PUD of the stomach (GU),
symptoms characteristically worsen with meals.
Peptic ulcer
disease
(PUD)
NSAID use and H. pylori infections are associated with the development of PUD.
Hematemesis, if present, suggests a more complicated disease and warrants urgent GI referral.
Melena commonly occurs in the setting of an upper GI bleed secondary to PUD or hemorrhagic gastritis (e.g., NSAID-gastritis).
Hematochezia occurs in the setting of an upper GI bleed only when massive (e.g., variceal rupture).
Less Likely Diagnoses
Abdominal wall
muscle strain
Unlikely in the absence of an inciting event or a positional component to the pain.
More likely to present as an acute abdomen, with severe abdominal pain, nausea and vomiting, ill appearance on exam,
and clinical signs of dehydration.
Acute
pancreatitis
Pain is typically located in the epigastric area with radiation to the back, improves with leaning forward , and worsens
with eating. Symptoms often last for hours without relief.
Characterized by elevations in serum lipase and amylase.
Acute and chronic pancreatitis are most commonly caused by alcohol use and gallstones. Some patients may not be
forthcoming about alcohol use, especially if they perceive judgment or are in denial about problem use.
Angina pectoris
Classically presents with substernal chest pain or pressure , but may present with epigastric pain and nausea or
vomiting.
GERD is the most common cause of noncardiac chest pain (NCCP).
A possible etiology for abdominal pain, but other diagnoses should always be considered first.
Anxiety
May be associated with additional ty