75-Year-Old Man With Abdominal Pain andReux

Luis D. Lomeli, MD, MPH, and Thomas F. Mangan, MD

A 75-year-old man presented to theoutpatient clinic with a 5-day historyof new-onset gastroesophageal reuxand sharp postprandial left upper quadrantabdominal pain without radiation. He describednausea and early satietyminutes after starting hismeal, followed by pyrosis and regurgitation ofhis recently ingested food. His abdominal painwould start within an hour and would oftenbe associated with an episode of emesis. Hissymptoms were not relieved by over-the-counter antacids. On review of systems, the pa-tient denied any dysphagia, odynophagia, fe-vers, chills, weight loss, alcohol use, or historyof smoking. He had a history of chronic dailyheadaches with a recent exacerbation, for whichhe was taking aspirin and several differenttypes of nonsteroidal anti-inammatory drugs(NSAIDs).

At presentation, vital signs included a tem-perature of 36.8C, heart rate of 67 beats/min,respiratory rate of 18 breaths/min, and bloodpressure of 140/54 mm Hg. On examination,the patient appeared very uncomfortable.Physical examination revealed a distendedand tender abdomen without organomegalyor peritoneal signs. Findings on the remainderof a complete physical examination wereunremarkable.

1. Which one of the following is the mostlikely cause of this patients abdominalpain?a. Gastric outlet obstructionb. Gastroparesisc. Splenic infarctiond. Acute pancreatitise. Myocardial infarction

The differential diagnosis of abdominal painis broad but can be narrowed on the basis of thelocation, associated symptoms, and physical ex-amination ndings. Although many disorderscan cause left upper quadrant abdominal pain,the constellationof symptomsandphysical exam-ination ndings in our patient most likely suggest

a gastric outlet obstruction. Patients typicallypresent with epigastric abdominal pain, vomit-ing, early satiety, and abdominal distention.Onphysical examination, a succussion splash maybe elicited by listening over the upper abdomenwhile gently moving the patient from side toside. Gastroparesis can cause a very similar clin-ical picture but would be associated with agradual and prolonged clinical course. Splenicinfarction should be considered in patientswith atrialbrillation, a rapidly enlarging spleen,and a history of a hypercoagulable state.1 Acutepancreatitis typically presents as epigastric painwith a bandlike radiation to the back associatedwith nausea and vomiting.Most commonly, it issecondary to gallstone disease and alcoholintake.2 A myocardial infarction should alwaysbe included in the differential diagnosis of pa-tients presenting with lower chest or upperabdominal pain.

The patient underwent abdominal radiog-raphy, which showed a markedly dilated stom-ach and no intra-abdominal free air. At thispoint, the patient was directly admitted to thehospital for further work-up and treatment.Initial laboratory evaluation at the hospitalrevealed the following (reference ranges pro-vided parenthetically): hemoglobin, 10.6 g/dL(13.5-17.5 g/dL); mean corpuscular volume,93.2 fL (81.2-95.1 fL); platelet count, 237 109/L (150-450 109/L); leukocytes, 11.0 109/L (3.5-10.5 109/L); creatinine, 1.3 mg/dL (0.8-1.3 mg/dL); and serum urea nitrogen,26 mg/dL (8-24 mg/dL).

2. For symptomatic management in thispatient, which one of the followingwould be the best next step?a. Intravenous pain medicationb. Antibiotic therapyc. Nasogastric (NG) decompressiond. Rehydration with normal salinee. Intravenous pantoprazole

Administration of intravenous pain medi-cation could be considered to alleviate the

See end of article forcorrect answers toquestions.

Resident in Internal Medicine,Mayo School of GraduateMedical Education, Rochester,MN (L.D.L.); Advisor to resi-dent and Consultant inGastroenterology and Hepa-tology, Mayo Clinic, Roches-ter, MN (T.F.M.).

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patients acute pain. However, it may maskworsening symptoms and does not address theetiology of the patients pain. The patient hasan elevated leukocyte count but is afebrile andhas no signs of peritonitis on physical examina-tion or free air on abdominal radiography. There-fore, antibiotics are not immediately indicated.Placement of an NG tube is the best step at thistime. The patients pain and reux symptomsare likely secondary to his distended abdomen.The NG tube would provide relief by decreasingthe pressure and distention in his stomach. Itwould be appropriate to start intravenous hydra-tion after an NG tube has been placed. The pa-tient presented with an elevated creatinine leveland is most likely dehydrated from poor intakeand repeated emesis. Initiation of an empiric pro-ton pump inhibitor is also indicated because thepatient is at increased risk for gastrointestinal(GI) damage from his NSAID use; however,this would not be the best next step.

An NG tube was placed, and 1.5 L of uidwas removed over the course of 2 hours. Thisprovided the patient substantial relief. He wasrehydrated with normal saline, and an intrave-nous proton pump inhibitor was administeredempirically. Clinically, his symptoms continuedto suggest a high-grade gastric outlet obstruction.

3. Which one of the following should beperformed next in this patient?a. Barium upper GI seriesb. Water-soluble contrast upper GI seriesc. Computed tomography of the

abdomend. Esophagogastroduodenoscopy (EGD)e. Gastric emptying study

Barium or water-soluble contrast upper GIseries are useful studies for visualizing theesophagus, stomach, and duodenum. Thesestudies may reveal the failure of contrast toempty into the duodenum, supporting the diag-nosis of a gastric outlet obstruction. Computedtomography may show a distended stomachwith an air-uid level. It may also help distin-guish the specic cause of the obstruction. Thesetests can be very useful when the diagnosis is un-clear or there is concern about a perforation.However, in this case, there is already strong ev-idence in support of a gastric outlet obstruction.These extra tests may put the patient at risk foraspiration and radiation exposure and would

not alter management. Esophagogastroduode-noscopy is the best test at this time because itwould establish the diagnosis of a gastric outletobstruction, identify a cause, and allow for po-tential endoscopic treatment. A gastric emptyingstudy is performed by measuring the amount oftime radioactively labeled food takes to emptyfrom the stomach. This test is indicated whenthere is suspicion for a gastric motility diseaseand would not be appropriate at this time.

After NG decompression, the patient un-derwent EGD, which revealed a 20-mm pre-pyloric ulcer consistent with NSAID use and anearly obstructing (>90% obstructed) circum-ferential duodenal ulcer. Because of the degreeof obstruction, balloon dilation was performed.

4. Besides peptic ulcer disease, whichone of the following would be the mostcommon cause of gastric outletobstruction in this patient?a. Malignant neoplasmb. Gastric polypc. Crohn diseased. Gallbladder stonee. Caustic injury

After peptic ulcer disease, a malignancyneoplasm is the most common cause of gastricoutlet obstruction in patients presenting withepigastric abdominal pain and weight loss.With the advent of proton pump inhibitor ther-apy and its increased use, the incidence of pepticulcer disease has decreased, andmore malignanttumors have been found to cause gastric outletobstructions.3 These tumors include primarygastroduodenal adenocarcinoma, GI stromal tu-mors, lymphomas (eg, mucosa-associatedlymphoid tissue lymphoma), pancreatic neo-plasms, gallbladder tumors, bile duct cancer,andmetastasis from other primary sites.4 Gastricpolyps are mostly benign and asymptomatic.Rarely, gastric polyps may lead to an obstructionof the pylorus if they are large enough. Crohndisease can involve the GI tract from theoropharynx to the anus but mainly affects theterminal ileum. This possibility could be consid-ered if the patient has a history of Crohn disease,specically with stricturing. On rare occasions, agallbladder stone can create a stulous tract sec-ondary to inammation and cause an obstruc-tion of the pylorus or duodenum. Patients whoingest a caustic material (either high or low

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pH) may present with gastric outlet obstruction.Most commonly, these materials will cause stric-turing of the esophagus, but they may also affectthe pylorus.

After EGD, the patients NG outputdecreased considerably and was no longerrequired. He began to tolerate oral intakeand was transitioned to an oral proton pumpinhibitor. Plans were started for dismissalfrom the hospital.

5. Which one of the following is the mostimportant hospital dischargerecommendation for this patient?a. Avoidance of NSAIDSb. Repeated EGDc. Testing for Helicobacter pylori infectiond. Initiation of misoprostole. Change to a cyclooxygenase 2

inhibitor

Patients are at high risk of having anotherNSAID-related complication if they have a his-tory of a complicated ulcer, especially if recent,or have 2 or more of the following risk factors:age greater than 65 years, high-dose NSAIDtherapy, previous history of uncomplicated ul-cer, and concurrent use of aspirin, corticoste-roids, or anticoagulants.5 Our patient had arecent NSAID-related complication, is olderthan 65 years, and was taking aspirin concur-rently. Therefore, this patient would be at veryhigh risk and should be strongly advised toavoid all NSAIDS. Although routinely per-formed, surveillance endoscopy after gastric ul-ceration remains controversial.6 In theory, thisprocedure could detect poorly healing ulcersthat may in fact be secondary to malignancy.However, screening all patients with a gastriculcer would produce low yield and be costly;thus, this decision should be individualized.Surveillance endoscopy should be consideredin patients with gastric ulcers that are suspiciousfor malignancy at the time of rst endoscopy,in patients who remain symptomatic despiteappropriate therapy, or if there was no clear eti-ology at the time of discovery. Our patient wastaking a large amount of NSAIDs, and the endo-scopic appearance of his gastric ulcer wasconsistent with NSAID use; therefore, surveil-lance endoscopy may be unnecessary. Thepatient should also be tested for H pylori

infection because it increases the risk of pepticulcer disease, and eradication may preventrecurrence in NSAID users.5 However, avoidingNSAIDs is the most important recommendationto resolve the patients peptic ulcer disease.Misoprostol, 200 mg 4 times a day, has beenfound to be as effective as proton pump inhibi-tors to reduce the risk of ulcer disease and itscomplications in patients taking NSAIDS.5

However, the use of misoprostol has beenlimited because of its adverse effects, includingcramping and diarrhea. Cyclooxygenase 2 in-hibitors are a reasonable alternative in patientsrequiring long-term NSAID use because theyconfer a lower risk of ulcer disease. The useful-ness of this medication would be limited in ourpatient because its benecial effects are negatedby aspirin use and have been associated withcardiovascular adverse effects.5

DISCUSSIONWith the identication and treatment of H py-lori infection and the introduction of protonpump inhibitors and histamine 2 receptor an-tagonists, the epidemiology of gastric outletobstructions has decreased.3 It is estimatedthat less than 2% of patients with peptic ulcerdisease experience the complication of gastricoutlet obstruction, and malignancy has be-come the predominant etiology.7

Depending on the etiology, patients maypresent acutely or with a gradually progres-sive course. Initial symptoms may includeearly satiety and abdominal discomfort orheaviness. As the obstruction progresses, pa-tients may experience nausea, pyrosis, regur-gitation, and vomiting associated with meals.In addition, patients may have weight loss,abdominal bloating, and epigastric or left up-per quadrant abdominal pain.7 Physical ex-amination may reveal abdominal distention,tenderness, and a succussion splash.6 Withprogression of the obstruction, patients mayexperience chronic malnutrition, dehydra-tion, and electrolyte abnormalities such asmetabolic alkalosis and hypokalemia second-ary to repeated vomiting. As with our patient,who presented with normocytic anemia, thepresentation of a gastric outlet obstructionmay also be complicated by GI bleeding.

In our case, the patient presented acutelywith all of the previously mentioned symptoms.

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His history included a recent exacerbation of hisheadache disorder and concomitant use of highdoses of multiple NSAIDs, which underscoresthe importance of obtaining a thorough medica-tion use history including identifying specicover-the-counter NSAIDs by name. Our pa-tients history and physical examination ndingswere suggestive of a peptic ulcereinducedgastric outlet obstruction.

Despite the high suspicion for an NSAID-induced complication in our patient, it wasimportant to perform upper endoscopy toconrm our diagnosis, assess the extent andlocation of the obstruction, and offer potentialtherapeutic interventions. The mechanismbehind an ulcer-mediated obstruction includesedema, inammation, and subsequent brosisand scaring. The latter is what often necessi-tates endoscopic balloon dilation. Once dila-tion is achieved and all other risk factors areaccounted for, patients have a favorable long-term response to treatment.4,8

Correspondence: Address to Thomas F. Mangan, MD, Di-vision of Gastroenterology and Hepatology, Mayo Clinic,200 First St SW, Rochester, MN 55905 (mangan.thomas@mayo.edu).

REFERENCES1. Antopolsky M, Hiller N, Salameh S, Goldshtein B, Stalnikowicz R.

Splenic infarction: 10 years of experience. Am J Emerg Med.2009;27(3):262-265.

2. Swaroop VS, Chari ST, Clain JE. Severe acute pancreatitis. JAMA.2004;291(23):2865-2868.

3. Shone DN, Nikoomanesh P, Smith-Meek MM, Bender JS. Ma-lignancy is the most common cause of gastric outlet obstructionin the era of H2 blockers. Am J Gastroenterol. 1995;90(10):1769-1770.

4. ASGE Standards of Practice Committee, Fukami N,Anderson MA, Khan K, et al. The role of endoscopy in gastro-duodenal obstruction and gastroparesis. Gastrointest Endosc.2011;74(1):13-21.

5. Lanza FL, Chan FK, Quigley EM, Practice Parameters Committeeof the American College of Gastroenterology. Guidelines forprevention of NSAID-related ulcer complications. Am J Gastro-enterol. 2009;104(3):728-738.

6. ASGE Standards of Practice Committee, Banerjee S, Cash BD,Dominitz JA, et al. The role of endoscopy in the management ofpatients with peptic ulcer disease. Gastrointest Endosc. 2010;71(4):663-668.

7. McQuaid KR. Chapter 15. Gastrointestinal disorders. In:Papadakis MA, McPhee SJ, Rabow MW, eds. CURRENT MedicalDiagnosis & Treatment 2013. 52nd ed. New York, NY:McGraw-Hill; 2013. http://www.accessmedicine.com/content.aspx?aID6395. Accessed March 22, 2013.

8. Cherian PT, Cherian S, Singh P. Long-term follow-up of patientswith gastric outlet obstruction related to peptic ulcer diseasetreated with endoscopic balloon dilatation and drug therapy.Gastrointest Endosc. 2007;66(3):491-497.

CORRECT ANSWERS: 1 a. 2. c. 3. d. 4. a. 5. a

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