Hospital Medicine

Epigastric Abdominal Pain

Epigastric Abdominal Pain

I. Problem/Condition.

Epigastric abdominal pain is a common chief complaint that may arise from a wide spectrum of causes, and therefore treatment will likely be completely different depending on the etiology. It is therefore paramount to be methodical in characterizing the pain in order to obtain the correct diagnosis. Questions that address onset (gradual or sudden), location, duration (intermittent or constant), character (dull, achy, throbbing, stabbing, sharp, etc.), frequency, radiation, associated symptoms (presence of nausea, vomiting, fevers, chills, diarrhea, etc.), and exacerbating or relieving factors are all pivotal to narrowing the differential diagnosis.

Once a concise differential diagnosis is made, the physician can tailor the physical exam and order specific laboratory and other diagnostic studies to arrive at a final diagnosis and initiate treatment.

II. Diagnostic Approach.

A. What is the differential diagnosis for this problem?

There are several general different causes for epigastric abdominal pain. Broad categories include gastrointestinal (GI), vascular, obstructive, cardiac, pulmonary, vertebral and psychiatric. GI causes include Peptic Ulcer Disease (PUD) (see peptic ulcer disease) whether from reflux or secondary causes such as increased pressure from external source (i.e., hiatal hernia, mass), pancreatitis, gallbladder disease (see Right-upper quadrant pain) and esophagitis (infectious or other).

Vascular causes include abdominal aortic aneurysm (see AAA) and mesenteric ischemia. Obstructive processes may include Gastric Outlet Obstruction (GOO) or malignancy. Malignancy may present as esophageal, gastric, pancreatic cancer as well as cancers from more distant sites when advanced (i.e., hepatic). Cardiac causes can include myocardial infarction (MI), pericarditis, pericardial or pleural effusion (see chest pain). Pulmonary causes may be from a process such as pneumonia. Other etiology include vertebral causes (vertebral infiltration by cancer, vertebral infection (osteomyelitis, discitis), severe gout with axial involvement, herniated disc), and psychiatric causes (anxiety, depression, history of sexual abuse).

B. Describe a diagnostic approach/method to the patient with this problem.

An easy approach to creating a differential diagnosis for epigastric abdominal pain is to start at the epigastrium and then follow a large spiral inward, thereby considering organs that are anatomically near the epigastrium, then remembering psychiatric causes as well (which may include abuse). One might start with superficial causes such as Herpes Zoster or cellulitis (see Zoster or cellulitis), then move inward to consider GI causes listed above. Spiralling towards the right will bring us to cardiac causes, pulmonary causes, then spiralling downward will bring us to pancreatic causes. Continuing inward will address vascular causes (presuming central vessels), coming up again will cover gallbladder causes and then finally continuing inward will bring us to vertebral causes.

Once a differential diagnosis is created, the physician will obtain thorough historical information to help narrow the differential to a realistic, concise list to prioritize during the work-up.

1. Historical information important in the diagnosis of this problem.

When investigating GI causes of epigastric pain, such as PUD, certain factors may make it more likely to be present, such as age >60, chronic non-steroidal anti-inflammatory drugs (NSAID) exposure, concomitant glucocorticoid use and tobacco use. The quality of the pain is likely to be gnawing in uncomplicated PUD. Duodenal ulcers typically cause pain 2-5 hrs after a meal in the absence of a food buffer, may awaken the patient at night, and be more continuous. The pain may be associated with nausea, vomiting, chronic pain and weight loss (see Duodenal ulcer). Gastric ulcers may be more episodic in pain, pyloric channel ulcers, may have food-provoked symptoms due to visceral sensitization, and gastroduodenal dysmotility pain typically worsens with eating. Gastric ulcers may be associated with nausea, vomiting, chronic pain, and weight loss.

Complicated PUD may present as bleeding ulcers with melena being present 20-52% of time. To investigate presence of melanotic stools ask about black, tarry, particularly foul-smelling stools. Hematemesis (vomiting blood) is present 15-30% of time, and both melena and hematemesis are present 31-50%. There may be worsening abdominal pain in preceding days than at baseline.

Perforated ulcers will present with sudden severe upper abdominal pain, possibly radiating to shoulder and exacerbated by movement. If considering esophagitis, make sure to ask about factors that may compromise the immune system, such as risk factors for HIV (history of blood transfusion, unprotected sex especially anoreceptive, presence of another sexually transmitted infection, multiple sex partners, intravenous drug use), DM and chronic steroid use.

When evaluating pancreatitis, it is essential to obtain a history of alcohol intake, both amount and frequency, and dietary choices (focusing on fatty and processed food consumption), since alcoholic and gallstone pancreatitis are the most common causes. Ask if pain radiates to the back. The risk of developing pancreatitis from alcohol consumption is dose-dependent once >48 drinks/week are consumed (3.3 times higher with >48 drinks/week as compared to fewer drinks). Smoking is also a dose-dependent risk factor: people who smoke roughly half a pack of cigarettes per day have 1.5 times more risk of developing pancreatitis than those who don't smoke regularly, and people who smoke >25 cigarettes per day have a 3.3-fold risk of developing pancreatitis as compared to non-smokers.

Obtain history of dyslipidemia, medication use, and recent procedures (such as ERCP) and pregnancy; high triglycerides, medications (sulfa drugs, metronidazole, estrogen, mesalamine, isoniazid, enalapril, codeine, etc.) can also induce pancreatitis, although less often. Medications that cause pancreatitis much less often are ACE-Inhibitors, Calcium-channel blockers, Depakote and NSAIDs. For further information, see acute pancreatitis.

Cardiovascular causes as an etiology for epigastric pain are likely to be found in people with co-morbid conditions placing the patient at risk for cardiovascular disease such as Diabetes Mellitus (DM), Hypertension, known coronary artery disease (CAD), dyslipidemia, sedentary lifestyle, and smoking history, but also in patients with renal failure and auto-immune diseases. For more details, see chest pain.

Pulmonary causes for epigastric pain such as pneumonia, may be found in people with immune compromise (elderly, co-morbid conditions such as DM, chronic steroid use, HIV co-infection) and are likely to present with sudden onset of fevers, chills, cough productive of yellow-green-brown sputum, and general malaise. For further details, see pneumonia. AAA is more likely to present in a patient with a smoking history (smoking history increases likelihood five-fold), and typically affects men more than women. Most common symptoms are abdominal or back pain. For more details, see AAA. For details of intestinal ischemia, see generalized abdominal pain.

Malignancy, such as esophageal, gastric or pancreatic cancer, usually presents with ongoing epigastric pain and is likely to be associated with weight loss, other constitutional symptoms such as fatigue and decreased appetite, and presence of risk factors such as tobacco and alcohol consumption. When considering gastric outlet obstruction (GOO) ask questions screening for malignancy (weight loss, fevers, night sweats, early satiety, nausea, vomiting), since the vast majority of cases are related to underlying malignancy (pancreatic, lymphoma, biliary), and history of prior ulcers (chronic ulcers may lead to strictures). It is useful to ask about abdominal distention and malnutrition.

If considering cholecystitis, see RUQ pain.

For psychiatric causes, investigate a history of anxiety problems, recent stressors or increase in stress level, and history of sexual abuse; see anxiety or sexual abuse.

2. Physical Examination maneuvers that are likely to be useful in diagnosing the cause of this problem.

Uncomplicated PUD usually presents with localized gnawing or burning pain that is reproducible upon palpation of the epigastrium. However, if considering complicated PUD, compare blood pressure to the patient's baseline to evaluate if he/she is hypotensive, check for evidence of involuntary guarding or rebound to evaluate for perforation, and always perform rectal exam to evaluate for gross blood or maroon stools.

If considering presence of HIV infection, pay attention to overall appearance suggesting chronic infection such as bitemporal wasting, as well as thrush on the tongue. When considering pancreatitis look for Cullen's sign on abdomen (peri-umbilical bruise) or Grey Turner signs (ecchymosis on flank). Note that these signs are uncommon, present later in course of acute pancreatitis (several days into hospital stay) and are non-specific (can present in ovarian cyst hemorrhage, strangulated umbilical hernia, hemoperitoneum, or hemorrhagic ascites, cirrhosis with portal hypertension, among others). If either of these signs are present, they portend a poorer prognosis.

Presence of jaundice is likely to indicate biliary obstruction. If considering malignancy as the etiology of epigastric pain, pay special attention to the lymphatic system (supraclavicular, peri-umbilical, etc.). For atypical presentation of cholecystitis perform Murphy's sign (see cholecystitis).

Refer to other chapters for non-GI causes for epigastric pain, but in summary pay attention to cardiac exam for murmurs as possible evidence of new ischemic disease. Listen for egophony, increased dullness to percussion, or decreased fremitus for pneumonia.

3. Laboratory, radiographic and other tests that are likely to be useful in diagnosing the cause of this problem.

If considering complicated PUD as the etiology behind the epigastric pain, obtain serum IgG H. pylori antibodies, stool H. pylori antigen, CBC, coagulation studies, abdominal radiograph to look for perforation, and an EGD once perforation is ruled out to assess presence of bleeding or ulcer, and extent of either, if present. EGD will also be able to determine if esophagitis is present. Obtain an HIV test if considering opportunistic infections.

Acute pancreatitis can be evaluated by obtaining a lipase level (more specific than amylase), BMP to evaluate renal function and possibly electrolyte imbalances (sodium, potassium), and CBC to evaluate WBC, hemoglobin, and hematocrit level. Obtain a chest x-ray if there is any indication that respiration is compromised, or a computed tomography (CT) of the abdomen to evaluate for necrosis, phlegmon, pseudocyst, or abscess. Consideration of malignancy should also be evaluated with CT abdomen with intravenous and oral contrast.

Gastric outlet obstruction should be evaluated with a barium swallow. CXR can evaluate presence of pneumonia or suggest vertebral causes of epigastric pain. Abdominal ultrasound can evaluate both abdominal aneurysm and gallbladder disease.

C. Criteria for Diagnosing Each Diagnosis in the Method Above.

Diagnosis of complicated PUD is determined by the findings on endoscopy, serology for H. pylori in ulcerative disease and HIV test if considering other infectious etiology.

Diagnosing pancreatitis is made with two of the following three features: elevated lipase or amylase greater than 3 times upper limit of normal, characteristic pain and findings consistent with pancreatitis on abdominal CT with contrast (to distinguish between interstitial edematous pancreatitis and necrosis). Age >55, obesity (BMI >30), organ failure at admission or pleural effusions are risk factors for severity that should be considered upon admission. Admission labs that help distinguish between mild and severe pancreatitis are hematocrit and Ranson's criteria (relying on age, WBC, blood glucose, LDH and AST).

Malignancy and gastric outlet obstruction are determined by findings on abdominal CT.

D. Over-utilized or “wasted” diagnostic tests associated with the evaluation of this problem.

For any source of acute GI bleed, including complicated PUD, there is no role for guaiac testing in the inpatient setting - it offers no information on acute bleeds (acute bleeds will be faster, and therefore manifest as melena, maroon stools or frank blood) and needs preparation in order to be accurate, a preparation that is rarely done prior to the patient coming to the hospital. Conversely, a rectal examination is always warranted.

III. Management while the Diagnostic Process is Proceeding.

A. Management of Clinical Problem Epigastric Abdominal Pain.

For complicated PUD if bleeding is suspected, stabilize the patient with volume resuscitation through two large-bore IVs, type and screen red blood cells (RBCs) and consult GI specialist to evaluate for endoscopy. Intravenous proton-pump inhibitors (PPI) may be initiated in the interim. Oral dosing of PPIs is less expensive than IV dosing, and some studies suggest it may be an option for the treatment of patients with peptic ulcer bleeding. However, where available, IV dosing is currently considered standard of care. If oral dosing is being considered, a high dose of an oral PPI should probably be used (e.g., omeprazole, pantoprazole, or esomeprazole 40 mg twice per day). In one randomized trial with 244 patients who received endoscopic therapy for bleeding peptic ulcers, patients were randomly assigned to IV esomeprazole (80 mg bolus followed by 8 mg/hour infusion) or oral esomeprazole (40 mg orally every 12 hours). Outcomes were similar between those who received IV esomeprazole and those who received oral esomeprazole with regard to recurrent bleeding within 30 days (8 vs. 6 %), blood transfusions (2 vs. 1 units), need for repeat endoscopic therapy (1.7 vs. 2.4 %), and length of hospital stay (median 4 days for both patient-groups).

Risk factors for re-bleeding are age >65, poor health status, co-morbidities, and low initial hemoglobin (lower than the patient's baseline). Prior to discharge, the patient should be counseled to avoid inciting factors (NSAIDs, tobacco, alcohol), and treat H. pylori if identified during endoscopy. If perforation is suspected, urgent surgical consultation is indicated. A NG tube should be placed to decrease amount of gastric contents emptying into peritoneum.

If pancreatitis is present, first determine if it's mild or severe, looking in particular at the presence of organ failure and pancreatic necrosis, but also at the Hematocrit and Ranson's criteria. Sustained organ failure is considered present if there is hypotension refractory to fluid bolus, sustained hypoxemia and renal insufficiency despite fluid bolus and warrants prompt transfer of the patient to the MICU. If there is also presence of necrosis in addition to multi-organ system failure, there is a greater than one third chance for mortality.

Other signs that may warrant transfer to the MICU are tachypnea, development of oliguria, obesity (BMI >30), tachycardia (HR >120 bpm), encephalopathy and increasing narcotic requirements. Presence of pancreatic necrosis requires surgical consultation. Monitor for decompensation in the first 48 hours, with repeated vital signs including respiration, saturations, labs (specifically renal function, haematocrit, serum calcium), and signs of bleeding, either through GI tract or superficially.

If suspicion of gallstone as etiology of pancreatitis is present, consult GI to evaluate for an endoscopic retrograde cholangiopancreatography (ERCP) to remove the stone. Bowel rest (NPO - nil per os), fluid resuscitation, and analgesia are the mainstay of supportive care for pancreatitis. Feeding is always preferable enterally, the earlier the better once patient is stabilized. If the patient does not improve clinically with the above interventions, consider repeating abdominal CT to see if patient has developed any complications (abscess, necrosis, phlegmon, or worsening if already present).

In suspected malignancy, ensure no obstruction is present, however if present, consult surgery. Ensure adequate pain management and nutritional intake.

With GOO, stenting is useful for patients with shorter life expectancies while gastrojejunostomy tubes may be preferable for patients with longer life expectancies.

B. Common Pitfalls and Side-Effects of Management of this Clinical Problem.

It is not uncommon in pancreatitis to withhold oral intake unnecessarily long and not start enteral feedings soon enough once the patient stabilized. Begin oral feeds as soon as the patient has an appetite.

For cases of malignancy or other narcotic-requiring conditions, always remember to provide sufficient bowel care with laxatives in conjunction with narcotics to avoid the common side effects of nausea, vomiting, constipation and small bowel obstruction.


To Edward Pankey, MD and John Wysocki, MD for their thorough research.

IV. What's the evidence?

Gururatsakul, M, Holloway, RH, Talley, NJ, Holtmann, GJ. "Association between clinical manifestations of complicated and uncomplicated peptic ulcer and visceral sensory dysfunction". J Gastroenterol Hepatol. vol. 25. 2010. pp. 1162.

Spiegel, BM, Dulai, GS, Lim, BS. "The cost-effectiveness and budget impact of intravenous versus oral proton pump inhibitors in peptic ulcer hemorrhage". Clin Gastroenterol Hepatol. vol. 4. 2006. pp. 988.

Tsoi, KK, Hirai, HW, Sung, JJ. "Meta-analysis: comparison of oral vs. intravenous proton pump inhibitors in patients with peptic ulcer bleeding". Aliment Pharmacol Ther. vol. 38. 2013. pp. 721.

Sung, JJ, Suen, BY, Wu, JC. "Effects of intravenous and oral esomeprazole in the prevention of recurrent bleeding from peptic ulcers after endoscopic therapy". Am J Gastroenterol. vol. 109. 2014. pp. 1005.

Svanes, C. "Trends in perforated peptic ulcer: incidence, etiology, treatment, and prognosis". World J Surg. vol. 24. 2000. pp. 277-283.

Kurata, JH, Nogawa, AN. "Meta-analysis of risk factors for peptic ulcer. Nonsteroidal antiinflammatory drugs, Helicobacter pylori, and smoking". J Clin Gastroenterol. vol. 24. 1997. pp. 2-17.

Hernández-Díaz, S, Rodríguez, LA. "Steroids and risk of upper gastrointestinal complications". Am J Epidemiol. vol. 153. 2001. pp. 1089-1093.

Wara, P, Stodkilde, H. "Bleeding pattern before admission as guideline for emergency endoscopy". Scand J Gastroenterol. vol. 20. 1985. pp. 72-78.

Laszlo, A, Kelly, JP, Kaufman, DE, Sheehan, JE, Retsagi, G, Wiholm, BE, Koff, RS, Sundstrom, A, Shapiro, S. "Clinical aspects of upper gastrointestinal bleeding associated with the use of nonsteroidal antiinflammatory drugs". Am J Gastroenterol. vol. 93. 1998. pp. 721-725.

Barkun, A, Bardou, M, Marshall, JK. "Consensus recommendations for managing patients with nonvariceal upper gastrointestinal bleeding". Ann Intern Med. vol. 139. 2003. pp. 843-857.

Kristiansen, L, Gronbaek, M, Becker, U, Tolstrup, JS. "Risk of pancreatitis according to alcohol drinking habits: a population-based cohort study". Am J Epidemiol. vol. 168. 2008. pp. 932-937.

Tolstrup, JS, Kristiansen, L, Becker, U, Gronbaek, M. "Smoking and risk of acute and chronic pancreatitis among women and men: a population-based cohort study". Arch Intern Med. vol. 169. 2009. pp. 603-609.

Badalov, N, Baradarian, R, Iswara, K, Li, J, Steinberg, W, Tenner, S. "Drug-induced acute pancreatitis: an evidence-based review". Clin Gastroenterol Hepatol. vol. 5. 2007. pp. 648-661.

Gibson, J, Behrman, S, Fabian, T, Britt, L. "Gastric outlet obstruction resulting from peptic ulcer disease requiring surgical intervention is infrequently associated with Helicobacter pylori infection". J Am Coll Surg. vol. 191. 2000. pp. 32-37.

Behrman, SW. "Management of complicated peptic ulcer disease". Arch Surg. vol. 140. 2005. pp. 201-208.

Jeurnink, S. "Gastrojejunostomy versus stent placement in patients with malignant gastric outlet obstruction: a comparison in 95 patients". J Surg Onc. vol. 96. 2007. pp. 389-396.

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