There are numerous diseases to consider when evaluating patients with upper abdominal pain and gastroparesis (Table 7.2). In this section, the causes of pain will be discussed by specific organs: (1) stomach, (2) pylorus, (3) non-gastric GI organs, and (4) non-GI causes. There are three major stomach diseases to consider when evaluating a patient with abdominal pain and gastroparesis. These include GERD, peptic ulcer disease (PUD), and gastroparesis itself.

GERD is extremely common in the general population with an incidence of 42 % [32]. The basic cause of GERD symptoms is exposure of the esophageal mucosa to gastric acid. The lower esophageal sphincter (LES) creates a pressure zone that prevents acid and gastric contents from refluxing into the esophagus during digestion. Barriers to prevent acid injury also include secretion of saliva and secondary esophageal peristalsis. The diagnosis of GERD requires a clinical history of heartburn symptoms. Empiric trials of acid suppression medications such as proton-pump inhibitors (PPI) or histamine₂ receptor antagonists (H₂ blockers) that eliminate heartburn symptoms confirm the diagnosis. Diagnostic tests for GERD include upper endoscopy and 24-h esophageal pH monitoring. Endoscopic evaluation reveals normal or inflamed esophageal mucosa, structures, or masses. During esophageal pH monitoring, a decrease in esophageal pH to less than four is considered a positive reflux event [33]. Approximately 25 % of GERD patients also have gastroparesis, so abdominal pain symptoms can overlap in these patients [34].

PUD is defined as a break in the mucosal barrier within the stomach and duodenum that evolves into erosions and ulcers. Gastric acid remains the primary cause of these erosions, but non-steroidal anti-inflammatory drugs (NSAIDs), aspirin, alcohol, and Helicobacter pylori all increase the risk for PUD. Patients with PUD have burning epigastric pain that does not typically radiate into the chest. Hematemesis or melena is more consistent with PUD compared with GERD. The diagnosis of PUD involves taking a thorough history coupled with endoscopic or radiographic evaluation of the stomach and duodenum.

Gastroparesis itself may have an abdominal pain component. In contrast to the burning pain associated with GERD and PUD, these patients may experience a vague discomfort or pain in the epigastric region that is highly variable in severity. Some patients classify their symptoms of nausea, vomiting, and bloating as “pain.” Patients with gastroparesis also may have PUD and/or GERD. One study found that 25 % of patients with GERD had delayed gastric emptying, while 70 % of these patients also had gastric dysrhythmias [34]. These overlap syndromes of GERD and gastroparesis may be differentiated to some degree with empiric treatment with PPIs. Adequate suppression of acid eliminates the symptoms related to GERD/PUD but do not improve symptoms related to gastroparesis.

Spasm of the pyloric sphincter can also cause abdominal pain and is a cause of functional obstructive gastroparesis. Patients with pylorospasm and gastroparesis typically have normal 3 cpm EGG signals because the neuromuscular apparatus in the gastric body and antrum is intact. The pyloric spasm creates an obstruction to emptying of chyme from the stomach. Therefore, these patients have the symptoms of gastroparesis including nausea, bloating, and gastric distention. However, these patients often also report post-prandial pain in the RUQ due to pylorospasm. This symptom complex may also mimic chronic cholecystitis.

There are numerous non-gastric causes of abdominal pain in patients with gastroparesis; however, only a few of these causes will be discussed here. One of the common diseases seen in patients with gastroparesis is irritable bowel syndrome (IBS). Patients with IBS experience abdominal pain or discomfort associated with constipation, diarrhea, or both [35]. These symptoms are usually increased after a meal. IBS patients must, by definition, have altered bowel habits. Though patients with gastroparesis and IBS may have abdominal distention and bloating, patients affected by gastroparesis alone do not have altered bowel habits. Patients with IBS may experience pain in the epigastrium but are more likely to report lower abdominal discomfort compared to patients with gastroparesis. Furthermore, IBS patients typically have a decrease in abdominal pain following defecation, which is not the case with gastroparesis symptoms. Similar to those gastroparesis patients experiencing pain, IBS patients often have a higher sensitivity to visceral stimuli than control patients [36].

Biliary and pancreas diseases must be ruled out in gastroparesis patients with upper abdominal pain. Gallstone disease is one of the most prevalent illnesses in the western world involving almost 20 million Americans in 2004 [37]. The RUQ pain results from intermittent obstruction of the cystic or common bile ducts. Similar to patients with gastroparesis, patients with gallstone disease exhibit post-prandial nausea and epigastric pain. However, patients with gallbladder disease also report radiation of this pain to the RUQ, back, and scapulas which is not typical in patients with gastroparesis. If gallstone disease progresses to cholecystitis, choledocholithiasis, or cholangitis, then fevers and leukocytosis develop, and these features are not present in patients experiencing pain from gastroparesis. Pancreatitis presents with post-prandial epigastric pain that radiates to the back, nausea, and vomiting. Acute pancreatitis can be differentiated from gastroparesis given its acute onset and elevated serologic tests including lipase and amylase. Patients with chronic pancreatitis may also have crampy epigastric pain and bloating, symptoms of pancreatic exocrine dysfunction including weight loss and diarrhea, and radiologic evidence of pancreatic calcifications, all of which will differentiate pancreatitis from gastroparesis.

Finally, epigastric pain may be related to causes outside the GI tract. The most common causes of non-GI tract pain in patients with gastroparesis are the abdominal wall pain syndromes. Careful history reveals these pains increase with physical movement and not ingestion of meals or defecation. Typically, a very localized “trigger point” is identified on physical examination by performing Carnett’s test [38]. During Carnett’s test, the localized tender area is compressed with a single finger and the patient raises his head or both feet off the exam table. Contraction of the abdominal wall muscles during this maneuver results in an immediate increase of abdominal pain if the pain source is within the abdominal wall [38]. These focal abdominal wall pains most often occur at sites of abdominal incisions where scar tissue or underlying adhesions have developed following abdominal surgery [39]. These focal trigger points are treated with subcutaneous injections of local anesthetics and/or steroids.

The treatment of patients with gastroparesis and abdominal pain requires a thorough understanding of specific characteristics of the pain: timing, radiation, and factors that exacerbate and relieve pain. The first step is to determine the true cause of the abdominal pain because the patient’s pain/discomfort symptoms may not be related to gastroparesis. The pain characteristics should help to identify the cause of pain and guide treatment. If doubt remains after review of the clinical history and physical examination, then further testing should be performed. An abdominal wall syndrome should be considered and evaluated in all patients with gastroparesis and abdominal pain. Treatments for gastroparesis are outlined below and summarized in Table 7.3, and focus on reducing the discomfort and pain related to neuromuscular dysfunction of the stomach [1].