History

Fact Explanation
Abdominal pain Episodic gnawing or burning epigastric, postprandial and nocturnal pain due to GI mucosal injury caused by the evasion of H.pylori and/or aspirin/NSAIDS[3]. Pain usually occurs 2-5 hours after meals or on an empty stomach. Pain is relieved by intake of food, antacids, or anti-secretory agents. Children present with poorly localized abdominal pain. In 30% of old patients with peptic ulcers, abdominal pain is usually absent. Postprandial epigastric pain is more likely to be relieved on ingestion of food or antacids in patients with duodenal ulcers than in those with gastric ulcers. [1]
Persisting upper abdominal pain radiating to the back Suggests penetration. [2]
Sudden, rapidly spreading, severe upper abdominal pain Pain is worsened on movement and it suggests peptic ulcer perforation. [2]
Vomiting Large amounts of vomit containing undigested food [2] is usually associated with an obstruction due to pyloric stenosis or a gastric ulcer. [2]
Anemia, hematemesis, melena, hematochezia or heme-positive stool Suggests bleeding from a possible gastric ulcer. [4]
Weight loss / Loss of appetite Due to reduced appetite caused by fear of abdominal pain. Characteristic of gastric ulcers. [1] Also suggests cancer. [2] and gastric outlet obstruction. [2]
Cardiovascular disease therapy Patients taking medications such as low-dose aspirin (for the prevention of a cardiovascular event, such as myocardial infarction or thrombotic stroke), NSAIDS or any other antithrombotics for cardiovascular diseases are at an increased risk of developing GI injury and complications (peptic or bleeding ulcers). [3]
History of GI bleeding Patients who have had bleeding in the past from ulcers, experience recurrent bleeding within one year. [2]
Family history Risk factor for PUD. [1]
Medications Use of nonsteroidal anti-inflammatory drugs (NSAIDs) including aspirin, oral bisphosphonates, potassium chloride and immunosuppressive medications have been known to contribute to PUD. [3]
Personal history Question the patient of any personal history of peptic ulcers [6], cigarette smoking, excessive alcohol consumption, drug use, and emotional stress. These increase the risk of peptic ulcers. [2]
Syncope Indicates a possible duodenal perforation. [5]
References
  1. RAMAKRISHNAN K, SALINAS RC. Peptic ulcer disease. Am Fam Physician [online] 2007 Oct 1, 76(7):1005-12 [viewed 29 May 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/17956071
  2. CRYER B, MAHAFFEY KW. Gastrointestinal ulcers, role of aspirin, and clinical outcomes: pathobiology, diagnosis, and treatment J Multidiscip Healthc [online] :137-146 [viewed 29 May 2014] Available from: doi:10.2147/JMDH.S54324
  3. YUAN YUHONG, PADOL IRENEUSZ T, HUNT RICHARD H. Peptic ulcer disease today. Nat Clin Pract Gastroenterol Hepatol [online] 2006 February, 3(2):80-89 [viewed 29 May 2014] Available from: doi:10.1038/ncpgasthep0393
  4. LEE CW, SAROSI GA JR. Emergency Ulcer Surgery Surg Clin North Am [online] 2011 Oct, 91(5):10.1016/j.suc.2011.06.008 [viewed 29 May 2014] Available from: doi:10.1016/j.suc.2011.06.008
  5. THORSEN K, GLOMSAKER TB, VON MEER A, SøREIDE K, SøREIDE JA. Trends in Diagnosis and Surgical Management of Patients with Perforated Peptic Ulcer J Gastrointest Surg [online] 2011 Aug, 15(8):1329-1335 [viewed 29 May 2014] Available from: doi:10.1007/s11605-011-1482-1
  6. BAZALDUA OV, SCHNEIDER FD. Evaluation and management of dyspepsia. Am Fam Physician [online] 1999 Oct 15, 60(6):1773-84, 1787-8 [viewed 31 May 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/10537391

Examination

Fact Explanation
Hypotension, tachycardia, weak pulse, tachypenia, decreased pulse pressure, cool clammy skin, delayed capillary refill, slight anxiety Signs of shock indicating complicated PUD, which suggests hypovolemia/ anaemia due to significant upper GI blood loss and also a possible perforated duodenal ulcer. [1]
Fever, hypotension, oliguria Suggest sepsis and circulatory compromise caused by a perforated peptic ulcer. [2]
Generalized abdominal tenderness, rebound tenderness, board-like abdominal wall rigidity, hypoactive bowel sounds Clinical signs of peritonitis suggesting a perforated peptic ulcer. These may be masked during the physical examination in older patients with a perforated peptic ulcer and also in those taking steroids, immunosuppressants, or narcotic analgesics. [2]
Dehydration; a tympanitic epigastric mass with visible gastric peristalsis In addition to symptoms suggesting obstruction, these signs maybe witnessed in a patient presenting with gastric outlet obstruction (pyloric stenosis) whose underlying cause is peptic ulcer disease in 5-8% of patients. [2]
References
  1. CRYER B, MAHAFFEY KW. Gastrointestinal ulcers, role of aspirin, and clinical outcomes: pathobiology, diagnosis, and treatment J Multidiscip Healthc [online] :137-146 [viewed 29 May 2014] Available from: doi:10.2147/JMDH.S54324
  2. RAMAKRISHNAN K, SALINAS RC. Peptic ulcer disease. Am Fam Physician [online] 2007 Oct 1, 76(7):1005-12 [viewed 3 June 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/17956071

Differential Diagnoses

Fact Explanation
Nonulcer dyspepsia (NUD) or functional dyspepsia Patient comes in with dyspepsia but no specific etiological cause can be identified. [1]
Gastroesophageal Reflux Disease Patient would complain of heartburn and regurgitation; and that the epigastric pain radiates to the throat worsening while eating, bending or on lying down. Esophageal spasm from GER is characterized by sharp, stabbing substernal pain which commonly occurs at night or on consumption of a large meal. The patient may also have a chronic cough or hoarseness. [1]
Gastritis Gastric infection by H.pylori has recently been found to initially present as a superficial gastritis. Endoscopic examination followed by a biopsy would confirm a diagnosis. [6]
Eosinophilic esophagitis Clinical presentation varies with age. Patients of any age may complain of heart burn. Infants and toddlers present with non-specific symptoms such as failure-to-thrive, fussiness, poor growth, feeding intolerance or food aversion, abdominal pain, nausea, vomiting, and regurgitation. In contrast, dysphagia is the most characteristic symptom in adolescents and adults. Determine presence of any atopic diseases because EoE has a strong association with asthma, allergic rhinitis and sinusitis, atopic dermatitis, and food allergies. [2]
Cancer Malignancies are rare but is to be suspected if the patient is over 50 years of age and presents with 'alarm symptoms'. [1]
Biliary tract disease Severe episodic pain may occur which lasts for hours unlike the pain caused by peptic ulcers which tends to occur after a meal and especially occurs on consumption of a large fatty meal; and also on belching. Patient may report of a history of jaundice, dark urine and acholic stools. [1]
Acute pancreatitis Patient complains of abrupt severe stabbing pain which radiates to the back and does not relieve for many hours. Patient may also have a history of heavy alcohol consumption. [1]
Medications Ask the patient for a drug history to determine if any agent is being taken which is associated with dyspepsia such as: Acarbose(Precose), Alcohol, Alendronate(Fosamax), Cisapride(Propulsid), Codeine, Iron, Metformin(Glucophage), NSAIDs, Oral antibiotics(e.g., erythromycin), Orlistat(Xenical) Potassium, Corticosteroids(e.g., prednisone), Theophylline. [1]
Ischemic heart disease It is important to rule out a cardiac etiology because patients with IHD relate their symptoms to the stomach rather than the heart and differentiating between GI and cardiac pain is clinically challenging. Burning pain usually indicates a GI etiology, whereas pressure radiating to the left arm typically suggests a cardiac origin. Chronic and positional pain is more likely indicative of a GI origin, such as pain on lying down is more typical of GERD than of cardiac disease. [1]
Irritable bowel syndrome This syndrome is generally associated with abnormal bowel habits and the patient would report of more looser and frequent stools with pain on set and that the pain relieves on defecating. Patient would have abdominal distension. [1] [3]
Metabolic disorders Usually the patient may have a medical history of diabetes mellitus, hypothyroidism or hyperthyroidism, or hyperparathyroidism. [1]
Crohn disease Crohn's ulceration may involve any region of the entire GI tract and involvement of the gastroduodenal region is rare but may present with abdominal pain, anorexia, weight loss, nausea, vomiting. Other symptoms on involvement of other regions of the GI tract are diarrhea, fever, weight loss, abdominal masses, and anemia with extraintestinal manifestations including osteoporosis, inflammatory arthropathies, scleritis, nephrolithiasis, cholelithiasis, and erythema nodosum. [4]
Zollinger-Ellison syndrome (ZES) It is a rare disorder that can cause gastric or duodenal ulcers (usually multiple) from excessive acid secretion. Consider ZES if a patient has severe peptic ulceration, kidney stones, watery diarrhea, or malabsorption. ZES can also be associated with multiple endocrine neoplasia type I, which occurs earlier than isolated ZES. Patients would usually have fasting serum gastrin levels of more than 200 pg/mL and basal gastric acid hypersecretion of more than 15 mEq/h. Proton pump inhibitor (PPI) therapy should be discontinued at least 2 weeks before the gastrin level is measured. [5]
References
  1. BAZALDUA OV, SCHNEIDER FD. Evaluation and management of dyspepsia. Am Fam Physician [online] 1999 Oct 15, 60(6):1773-84, 1787-8 [viewed 31 May 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/10537391
  2. DELLON ES. Eosinophilic esophagitis Gastroenterol Clin North Am [online] 2013 Mar, 42(1):133-153 [viewed 31 May 2014] Available from: doi:10.1016/j.gtc.2012.11.008
  3. THOMPSON WG. Gastrointestinal symptoms in the irritable bowel compared with peptic ulcer and inflammatory bowel disease. Gut [online] 1984 Oct, 25(10):1089-1092 [viewed 31 May 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1432538
  4. WILKINS T, JARVIS K, PATEL J. Diagnosis and management of Crohn's disease. Am Fam Physician [online] 2011 Dec 15, 84(12):1365-75 [viewed 31 May 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/22230271
  5. ITO T, CADIOT G, JENSEN RT. Diagnosis of Zollinger-Ellison syndrome: Increasingly difficult World J Gastroenterol [online] 2012 Oct 21, 18(39):5495-5503 [viewed 31 May 2014] Available from: doi:10.3748/wjg.v18.i39.5495
  6. OWEN DA. Gastritis and carditis. Mod Pathol [online] 2003 Apr, 16(4):325-41 [viewed 31 May 2014] Available from: doi:10.1097/01.MP.0000062995.72390.14

Investigations - for Diagnosis

Fact Explanation
Full Blood Count Insignificant but done to exclude any other abnormalities and is also reassuring. [5]
Helicobacter pylori testing Regardless of whether a patient is taking aspirin and all those with an ulcer should be tested for H. pylori infection to determine the best treatment. [2] *Serologic ELISA: Useful only for initial H.pylori testing (sensitivity 85%; specificity 79%) and cannot be used for the confirmation of eradication. *Urea breath test: Best test that can detect an active H.pylori infection [3] (sensitivity 95%-100% , specificity 94%-99% ). This is also the test of choice to confirm eradication but PPI therapy should be stopped for 2 weeks before the test. *Stool antigen test: An inconvenient but an accurate H.pylori test that can be done (sensitivity 91%-98%; specificity 94%-99%) and can also be used to confirm eradication. [1]
Esophagogastroduodenoscopy (EGD) Prompt EGD is indicated for patients with 'alarm symptoms' (anemia, hematemesis, melena, or heme-positive stool; vomiting, anorexia or weight loss; persisting upper abdominal pain radiating to the back or severe, spreading upper abdominal pain) those whose symptoms do not respond to medications; and those older than 55 years. [2] EGD helps in the accurate diagnosis and differential diagnosis of PUD and ulcer complications (e.g. biopsy of gastric lesions can be done to exclude malignancy or to obtain tissue for an H. pylori diagnostic test). [1] An EGD is the most important step of management in a patient with an acute upper GI bleeding to establish the cause of bleeding (60% is due to peptic ulcer disease) and also to hemostasis during the endoscopy to control the source of bleeding. [4] Biopsies should ideally be taken in a systematic fashion, taking samples of antrum, corpus and going distally down the upper GI tract. [6]
Barium or Gastrografin contrast radiography (double-contrast hypotonic duodenography) Indicated when endoscopy is unsuitable or not feasible, or if complications such as gastric outlet obstruction is suspected. [1]
References
  1. RAMAKRISHNAN K, SALINAS RC. Peptic ulcer disease. Am Fam Physician [online] 2007 Oct 1, 76(7):1005-12 [viewed 29 May 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/17956071
  2. CRYER B, MAHAFFEY KW. Gastrointestinal ulcers, role of aspirin, and clinical outcomes: pathobiology, diagnosis, and treatment J Multidiscip Healthc [online] :137-146 [viewed 29 May 2014] Available from: doi:10.2147/JMDH.S54324
  3. YUAN YUHONG, PADOL IRENEUSZ T, HUNT RICHARD H. Peptic ulcer disease today. Nat Clin Pract Gastroenterol Hepatol [online] 2006 February, 3(2):80-89 [viewed 29 May 2014] Available from: doi:10.1038/ncpgasthep0393
  4. LEE CW, SAROSI GA JR. Emergency Ulcer Surgery Surg Clin North Am [online] 2011 Oct, 91(5):10.1016/j.suc.2011.06.008 [viewed 29 May 2014] Available from: doi:10.1016/j.suc.2011.06.008
  5. THORSEN K, GLOMSAKER TB, VON MEER A, SøREIDE K, SøREIDE JA. Trends in Diagnosis and Surgical Management of Patients with Perforated Peptic Ulcer J Gastrointest Surg [online] 2011 Aug, 15(8):1329-1335 [viewed 29 May 2014] Available from: doi:10.1007/s11605-011-1482-1
  6. OWEN DA. Gastritis and carditis. Mod Pathol [online] 2003 Apr, 16(4):325-41 [viewed 31 May 2014] Available from: doi:10.1097/01.MP.0000062995.72390.14

Investigations - Followup

Fact Explanation
Post-treatment urea breath test or endoscopy Follow-up testing is very important because of the risk of ulcer recurrence and the potential for malignancy caused by H. pylori infection. These follow-up tests are indicated in collaboration with a gastroenterologist for patients having a history of ulcer complications, gastric mucosa-associated lymphoid tissue (MALT), or early gastric cancer to ensure successful H.pylori eradication. [1]
Stool antigen test This testing is routinely indicated for patients with persistent symptoms following eradication therapy. [1]
References
  1. MEURER LN, BOWER DJ. Management of Helicobacter pylori infection. Am Fam Physician [online] 2002 Apr 1, 65(7):1327-36 [viewed 31 May 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/11996414

Management - General Measures

Fact Explanation
Patient education Counsel patients about the importance of completing the drug regimen needed for effective eradication. [2] Also make them aware about the risks of dyspepsia leading to recurrence and slow healing. Advice them to discontinue the use of NSAIDs, cigarette smoking, alcohol, and illicit drug use. NSAIDs delay ulcer healing [1]and hence regardless of the underlying etiology of the ulcer NSAID therapy should be discontinued. Smoking has also found to have a synergistic relationship with H. pylori and hence it should be stopped. [2]
References
  1. RAMAKRISHNAN K, SALINAS RC. Peptic ulcer disease. Am Fam Physician [online] 2007 Oct 1, 76(7):1005-12 [viewed 31 May 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/17956071
  2. MEURER LN, BOWER DJ. Management of Helicobacter pylori infection. Am Fam Physician [online] 2002 Apr 1, 65(7):1327-36 [viewed 31 May 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/11996414

Management - Specific Treatments

Fact Explanation
Initial resuscitation Initial management of a perforated duodenal/gastric ulcer includes of giving the patient large-volume crystalloids; nasogastric suction; and administration of intravenous broad-spectrum antibiotics against gram-negative rods, anaerobes, and oral flora. Followed by a laparotomy and the placement of an omental patch whereas for a perforated gastric ulcer an omental patch, wedge resection of the ulcer, or a partial gastrectomy and reanastomosis may be performed. Any coexisting H.pylori infection must be eradicated to prevent any future recurrences and complications needing further medical/surgical treatment. [2]
Eradication of Helicobacter pylori Standard treatment for H.pylori positive ulcers: H.pylori eradication + PPI (has the most potent acid inhibition plus cures the infection). [1] Treatment duration is 10 to 14 days and following are the course options: 'Triple therapy' : *Omeprazole (Prilosec) (20 mg twice daily) OR lansoprazole (Prevacid) (30 mg twice daily), plus amoxicillin (1 g twice daily) OR metronidazole (Flagyl) (500 mg twice daily) (if allergic to penicillin) plus clarithromycin (Biaxin) (500 mg twice daily). *Ranitidine bismuth citrate (Tritec) (400 mg twice daily) plus clarithromycin (500 mg twice daily) OR metronidazole (500 mg twice daily) plus tetracycline (500 mg twice daily) OR amoxicillin (1 g twice daily). *Levofloxacin (Levaquin) (500 mg daily) plus amoxicillin (1 g twice daily) plus pantoprazole (Protonix) (40 mg twice daily). (Eradication rates have been reported to be 80%-90% or higher). 'Quadruple therapy': Indicated for patients who did not respond to triple therapy. [4] *Bismuth subsalicylate (Pepto-Bismol) (525 mg (two tablets) four times daily) plus metronidazole (250 mg four times daily) plus tetracycline (500 mg four times daily) plus H2 blocker (for 28 days) OR proton pump inhibitor (for 14 days). [2] Patients should be referred to a gastroenterologist if treatment fails to respond for a second time. [4]
Proton pump inhibitors (PPI) Standard treatment for H.pylori -positive and -negative ulcers; prevention of NSAID/aspirin-induced ulcers and intravenous administration for bleeding ulcers. PPIs have the most potent acid inhibition. [1] Treatment duration for duodenal ulcer is 4 weeks and 8 weeks for gastric ulcer with 80%-100% healing. *Omeprazole (20 mg daily) *Lansoprazole (15 mg daily) *Rabeprazole (Aciphex) (20 mg daily) *Pantoprazole (40 mg daily) [2]
Histamine H2 blockers Used for the treatment of H.pylori -negative ulcers. [1] Healing of duodenal ulcers has been seen 70%-80% after four weeks and 87%-94% after eight weeks. *Ranitidine (Zantac) 150 mg two times daily OR 300 mg at night. *Famotidine (Pepcid) 20 mg two times daily OR 40 mg at night. *Cimetidine (Tagamet) 400 mg two times daily OR 800 mg at night. [2]
Sucralfate (Carafate) (1 g four times daily) Treatment duration is 4 weeks and its effectiveness is similar to H2 blockers. [2]
Prostaglandin analogs (Misoprostol) Used for the treatment of H.pylori -negative ulcers and for the prevention of NSAID/aspirin-induced ulcers. [1]
Phosphatidylcholine-aspirin (PL2200) Used for the treatment of H.pylori -negative ulcers and for the prevention of aspirin-induced ulcers. [1]
Surgery Rarely needed. [2] But surgery is highly indicated when there is development of complications from PUD (commonly GI bleeding), failure of initial endoscopic hemostasis attempts [3], poor response to medical therapy or a need for multiple rounds of medical therapy for ulcers, and high-risk factors (eg, history of PUD, dependence upon steroid or NSAID therapy). [2] *Duodenal ulcer: truncal vagotomy, selective vagotomy, highly selective vagotomy, partial gastrectomy. *Gastric ulcer: partial gastrectomy with gastroduodenal or gastrojejunal anastomosis (in bleeding gastric ulcers). [1]
References
  1. CRYER B, MAHAFFEY KW. Gastrointestinal ulcers, role of aspirin, and clinical outcomes: pathobiology, diagnosis, and treatment J Multidiscip Healthc [online] :137-146 [viewed 29 May 2014] Available from: doi:10.2147/JMDH.S54324
  2. RAMAKRISHNAN K, SALINAS RC. Peptic ulcer disease. Am Fam Physician [online] 2007 Oct 1, 76(7):1005-12 [viewed 29 May 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/17956071
  3. LEE CW, SAROSI GA JR. Emergency Ulcer Surgery Surg Clin North Am [online] 2011 Oct, 91(5):10.1016/j.suc.2011.06.008 [viewed 29 May 2014] Available from: doi:10.1016/j.suc.2011.06.008
  4. MEURER LN, BOWER DJ. Management of Helicobacter pylori infection. Am Fam Physician [online] 2002 Apr 1, 65(7):1327-36 [viewed 31 May 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/11996414