Fig. 23.1
Common causes and location of chronic abdominal pain
Table 23.1
Characteristics of abdominal pain
Epigastric pain |
Referred pain from pancreas, stomach and hepatobiliary tree |
Umbilical pain |
Small bowel and right colon |
Lower abdominal pain |
Colon |
Pathophysiology
Visceral pain is transmitted from nociceptors found on the walls of the abdominal viscera via sympathetic and parasympathetic pathways [2]. This pain is nonspecific because of the wide divergence and relatively small number of afferent fibers innervating a large area with extensive ramification. Pain is often perceived in the midline since slow conducting afferent pain fibers from the viscera have bilateral entry into the spinal cord. The symptoms of abdominal pain are described as aching, cramping, or burning that fluctuates in intensity. In addition, others may complain of diffuse mid-abdominal discomfort described as paroxysmal, deep, squeezing, and diffuse. Referred pain to a different part of the body may also occur. The intensity of the stimulus is as essential as its quality. Severe visceral pain may also generate a secondary physiologic reaction mediated by the autonomic nervous system and manifested by nausea, vomiting, sweating, lightheadedness, and salivation further confounding the diagnosis.
Certain characteristics of the pain may facilitate the origin of the abdominal pain. Pain will typically present based on embryonic origin: foregut, midgut, and hindgut. Pain from the esophagus, stomach, pancreas, and hepatobiliary tree is usually referred to the epigastrium. Periumbilical localization occurs from the small bowel and right colon (midgut); the rest of the colon and the genitourinary organs (hindgut) cause pain that presents in the lower abdomen. It is also important to note its onset, whether acute or insidious, and its temporal profile. The circumstances that intensify or alleviate the pain are significant. Relief with eating or antacids suggests ulcer disease or gastroesophageal reflux. Postprandial pain, depending on its location, character, and timing, could be biliary, ischemic, or associated with a more benign condition, such as lactose intolerance or irritable bowel syndrome. Seasonal patterns frequently are seen in ulcer disease and, occasionally, with regional enteritis. The pain of inflammatory bowel disease and irritable bowel syndrome may be relieved by defecation, whereas heat usually relieves pain of musculoskeletal origin. Posture, sudden movement, coughing, straining, and sneezing may worsen the pain from peritoneal irritation or of spinal origin. The abdomen is not exempt from psychogenic pain. This may be manifested as a component of irritable bowel syndrome. Although common, psychological pain should and does remain a diagnosis of exclusion.
Another important consideration in assessing abdominal pain is that it is an important manifestation of inflammation. Inflammatory cytokines and other inflammatory mediators sensitize primary afferent neurons in the intestinal lumen. Pain associated with pancreatitis is secondary to an inflammatory response to pancreatic parenchymal injury. Pancreatic inflammation, neural remodeling and injury, and changes in the central nervous system contribute to ongoing pain in this condition [3]. Pain management is multifactorial and may involve physiologic and psychologic factors.
Physiologic Causes of Chronic Abdominal Pain
Esophagus
Heartburn
Chronic abdominal pain related to gastroesophageal reflux disease (GERD) can be difficult to diagnose. The symptoms associated with GERD may be mimic other disease processes. Thus symptoms attributable to GERD may often go undiagnosed for long period of time. Patients with atypical GERD are often more challenging to treat than those with typical GERD because they often have unpredictable responses to antisecretory therapy. Aggressive acid reduction using proton pump inhibitors (PPIs) twice daily before meals for 3–4 months is the standard treatment for atypical GERD after other causative factors have been excluded including a normal EGD. An initial therapeutic trial of PPIs is more acceptable to most patients than pH testing, which can be uncomfortable, cumbersome, and unreliable in clinical correlation to pain. The advantage of using PPIs is that they can also demonstrate a cause-and-effect relationship. If atypical symptoms improve or resolve, expert opinion is to taper antisecretory therapy to once-daily PPIs or H2-receptor antagonists at the lowest effective dose over 3–6 months. This regimen may be the best way to demonstrate a causal relationship between GERD and extra-esophageal symptoms, with most treatment trials demonstrating a 50–70 % overall response rate [4]. To determine whether they have adequate acid control, patients who do not respond to empiric PPI therapy should undergo pH monitoring and esophageal manometry. At equivalent doses, PPIs are therapeutically equivalent for treatment of reflux symptoms.
Those patients with a known anatomic defect are best treated by surgical repair. Patients with intrathoracic stomachs require surgical intervention via reduction of their anatomic defect and Nissen fundoplication. These patients typically do not respond well to aggressive antisecretory therapy. There are several studies which demonstrate the efficacy and safety of surgical therapy for refractory GERD. One study found that 96.5 % of patients were satisfied with results of the procedure after 6.4 years, although 14 % were still taking continuous PPI therapy, and 27 % had GERD-related symptoms (e.g., regurgitation, dysphagia, bloating, noncardiac chest pain) [5]. Another study found that antireflux surgery was more effective than PPI therapy for long-term control of symptoms; however, obstructive symptoms (e.g., dysphagia, rectal flatulence, inability to belch or vomit) were more common in patients who underwent surgery. A total of 91.3 % of patients surveyed following surgery were satisfied with their operation, and 96 % commented they would have surgery again for their symptoms [6]. As such, patients with intrac GERD and an anatomic defect should be referred for surgical intervention.
Pain in Pancreatic Disease
Natural History of Chronic Pancreatitis
The most common cause of long-term abdominal pain due to pancreatic disease is chronic pancreatitis. Chronic pancreatitis is characterized by irreversible morphological and functional abnormalities due to longstanding inflammation and fibrosis of the pancreatic parenchyma. This is associated with intractable pain, malabsorption, and in some cases diabetes mellitus. Chronic abdominal pain is arguably the most important component of chronic pancreatitis and often leads to significant morbidity and disability. It places a tremendous burden on the medical care system as the cost of treating patients with chronic pancreatitis averages $17,000 per year. The most common cause of chronic pancreatitis is long-term alcohol use but other frequently observed causes include hereditary, autoimmune, and environmental factors. A large proportion of patients have no discernable cause for chronic pancreatic and are thus considered idiopathic. It commonly affects men more often than women with the onset of symptoms typically occurring in middle age, with the mean age of 48.9 (±15.4) years reported in one large North American survey [7].
The pathophysiology of pain from chronic pancreatitis remains poorly understood. Strictures in the main pancreatic duct, along with peri-pancreatic fibrosis, have been thought to result in increased pancreatic tissue pressure (ductal hypertension) and ischemia (compartment syndrome). Changes in neural density, hypertrophy, and both perineural and endoneural inflammatory infiltration (neuritis) have been described in patients with debilitating pancreatitis which have correlated with the intensity of the abdominal pain.
Most patients considered for surgical intervention for disabling abdominal pain should have a morphologic change in the pancreas. In those patients with no known discernable morphologic abnormality and chronic disabling pain, a total pancreatectomy with auto islet transfusion is one option. In a minority of patients, there are potentially treatable lesions such as pseudocysts or pancreatic ductal disruption. In other patients, strictures in the main pancreatic duct, along with peri-pancreatic fibrosis, have been thought to result in increased pancreatic tissue pressure (ductal hypertension) and ischemia (compartment syndrome). However, measurements of pancreatic ductal pressure in patients have not always correlated with pain or reliably predicted the success of ductal decompression procedures (e.g., lateral pancreaticojejunostomy or endoscopic intraductal stenting). In addition, the morphological changes are as common in patients with painless pancreatitis as in those with pain.
The major clinical features of chronic pancreatitis include functional failure (exocrine and endocrine) and pain. The glandular failure can usually be managed satisfactorily by replacement strategies (enzymes or insulin) to restore nutritional and metabolic stability. Pain though has remained a major clinical challenge; it is present in up to 90 % of cases and is the primary cause of hospitalization in most patients [8]. Unfortunately, pain in chronic pancreatitis remains difficult to treat. A lack of understanding about the underlying biology has led to various empirical approaches that are often highly invasive and based purely on anatomical grounds [9].
The workup for a patient with chronic pancreatitis requires computed axial tomography scan with a 2 mm slices through the pancreas. Endoscopic retrograde cholangiopancreatography (ERCP) with endoscopic ultrasound have proven to be extremely useful in defining the pancreatic anatomy. It not only provides fine anatomic details of the anatomy but also allows therapeutic interventions to be performed. Magnetic resonance cholangiopancreatography (MRCP) has also proven to be invaluable as an additional imaging modality and has replaced ERCP for studying of the ductal system. Finer details of ductal anatomy can be delineated with MRI that is not often demonstrated in other imaging modalities.
The use of ultrasound has become an increasingly common modality for diagnosis chronic pancreatitis at our institution. EUS detects structural abnormalities of the pancreatic duct and parenchyma indicative of fibrosis. To summarize the Rosemont criteria, the presence or absence of nine ductal and parenchymal criteria was routinely assessed in a prospective manner: hyperechoic foci, hyperechoic strands, cysts, lobularity, calcifications, hyperechoic duct margins, visible side branches, main pancreatic duct dilation, and main pancreatic duct irregularity (score 0–9) [10]. The presence of four or more features was considered abnormal. An adjunctive test is the use of secretin to stimulate pancreatic function. Pancreatic function testing is an independent, complementary marker for fibrosis, as they assess the degree of pancreatic exocrine insufficiency.
Selection of Surgical Procedure
General consensus exists that the initial therapy for chronic pancreatitis should be nonoperative management with an emphasis on eliminating etiologic factors, antioxidants and exocrine suppression with oral pancreatic enzymes. Surgery is considered in patients who fail conservative measures. In general, surgical intervention should only be performed in those patients with an expected low morbidity and mortality. An optimal surgical procedure should resolve intractable pain and concomitant complications of the chronic pancreatitis which may include duodenal and biliary obstruction. Part of the goal of the operation is to maximize of endocrine and exocrine function with sparing of the pancreatic parenchyma and improve quality of life.
The choice of surgical procedure to be undertaken depends upon the morphologic abnormality. In general, surgical procedures for chronic pancreatitis can be divided into operations that require resection, those that involve drainage of the pancreatic duct or a combination of both. In patients with a dilated pancreatic duct, decompression of the pancreatic duct is probably the best choice since pancreatic function can be preserved. Various decompressive techniques have been developed over the years which include the traditional lateral pancreaticojejunostomy (Partington–Rochelle or one of its variations) [11]. Those with an inflammatory head mass would most likely benefit from a Whipple, Beger, or Frey procedure. Patients with small-duct disease can be a challenging surgical dilemma. In these patients with no clear anatomic abnormality, a V-shaped excision or Izbicki procedure has been described with some success. Otherwise, a total pancreatectomy with or without auto islet transfusion may be considered. Unfortunately, no approach guarantees absolute success, although the data would suggest that surgical approaches have the most durable pain relief.
Related posts:
Gastroparesis: Pathophysiology of Chronic Abdominal Pain and Current Treatment
Chronic Abdominal Pain of Gynecologic Causes: Diagnosis and Treatment
Gastric and Other Visceral Stimulation for Chronic Painful Gastrointestinal Motility Disorders
Establishing Diagnosis of Chronic Abdominal Pain: Gastroenterologist View
The Epidemiology of Chronic Abdominal Pain
Lessons Learned from Visceral Sensory Stimulation: Implications for Treatment of Chronic Abdominal Pain
Full access? Get Clinical Tree
