Evaluation of Abdominal Pain

James M. Richter

One of primary care’s most daunting challenges is the outpatient assessment of abdominal pain. When the pain is acute in onset, triage decisions have to be made regarding the need for hospital admission and surgical intervention. If the pain is chronic or recurrent, the challenge is to design a safe, efficient plan for workup that will distinguish among many possible etiologies. In instances in which the exact cause of pain is not immediately evident, an empiric trial of therapy or a thoughtful test selection may help to suggest the underlying pathophysiology, narrow the differential diagnosis, and guide further assessment and treatment. Also important are the need to decide on the proper speed and extent of evaluation and to keep in mind nondigestive etiologies, such as ovarian carcinoma (see Chapter 116) and myocardial ischemia (see Chapter 20), that may present as abdominal discomfort.

PATHOPHYSIOLOGY AND CLINICAL PRESENTATION (1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11 and 12)

The major mechanisms of abdominal pain include distension of a hollow viscus from obstruction, peritoneal irritation, vascular insufficiency, mucosal ulceration, altered bowel motility, capsular distention, metabolic disorder, nerve injury, abdominal wall injury, and referral from an extra-abdominal site.

Obstruction

Pain receptors in the bowel, biliary tree, and ureters respond to distention and increased wall tension. The severity of the pain is a function of the speed of onset as well as the degree of distention. Obstruction that develops slowly during weeks to months may be relatively subtle in presentation in comparison with acute obstruction, which produces a more dramatic picture. In acute obstruction, the pain is severe and “colicky” or wavelike in nature; it makes the patient restless.

Small Bowel

The pain of acute small-bowel obstruction is characteristically colicky at the beginning. The patient is often comfortable between bouts of pain. Severity decreases with time as bowel
motility diminishes. Complete strangulation of the small bowel is associated with steady pain from secondary vascular insufficiency or peritoneal irritation. Vomiting is common, particularly in proximal obstruction; when the problem is distal, vomiting is less frequent. Flatus and passage of small amounts of stool may occur at the outset, but they soon cease if the obstruction is complete. Diarrhea is noted in some cases of partial obstruction. On examination, the patient appears restless during bouts of pain. The temperature is typically normal or only mildly elevated. The abdomen may be distended, especially when the obstruction is distal. High-pitched, hyperactive bowel sounds are characteristic but not always present. Tenderness to palpation is not impressive unless ischemia or leakage of bowel contents has occurred and caused peritonitis. The stool is usually negative for occult blood.

Large Bowel

Obstruction of the large bowel is, in most instances, less painful and associated with less vomiting than is obstruction of the small intestine. Constipation or a change in bowel habits often precedes complete obstruction. Diarrhea may occur with partial obstruction. Distention is greater than that seen in small-bowel obstruction. Stools are frequently positive for occult blood.

In cases of bowel obstruction, the white blood cell count may be normal, even in association with a strangulating obstruction (i.e., with compromise of the intestinal blood supply in addition to blockage of the lumen). A plain radiograph of the abdomen (supine and upright) in patients with small-bowel obstruction often shows distention of loops of small bowel with high air-fluid levels. This, together with an absence of gas in the large bowel (distal to the obstruction), is characteristic of small-bowel obstruction. The radiographic appearance of colonic obstruction varies with the competency (or incompetency) of the ileocecal valve. If the valve is competent, less small-bowel dilation ensues.

Cystic Duct

Sudden obstruction of the cystic duct by a stone produces acute pain, sometimes referred to as biliary “colic.” Unlike the cramping pain of acute intestinal obstruction, the pain of acute cystic duct obstruction is mostly steady, lasting more than 1 hour after sudden onset. Acute cholecystitis is associated with localized peritonitis in addition to obstruction. Pain is typically maximal in the right upper quadrant or epigastrium, radiates to the scapular region, and is accompanied by nausea, vomiting, and fever without jaundice; at times only mild epigastric discomfort is present (see Chapter 69). Murphy sign (inspiratory arrest in response to right upper quadrant palpation) may be seen, and right upper quadrant tenderness to percussion or pressure over the gallbladder is also a suggestive finding. Laboratory investigation usually reveals a leukocytosis and sometimes a modest alkaline phosphatase elevation; bilirubin levels are usually not elevated. Gallstones in the absence of ductal obstruction or gallbladder wall inflammation are often asymptomatic (see Chapter 69).

Common Bile Duct

Acute common bile duct obstruction produces epigastric pain, often accompanied by marked nausea and vomiting; jaundice ensues. Chronic obstruction that develops gradually leads to ductal dilation that is often painless. Physical examination may reveal a tender right upper quadrant, but in comparison with that of acute cholecystitis, tenderness may be less focal and deeper. A palpable gallbladder suggests gradual progressive development of ductal obstruction, typically caused by malignancy. Alkaline phosphatase is markedly elevated, as is serum bilirubin.

Pancreatitis

Typically, acute pancreatitis produces constant epigastric, periumbilical, or left or right upper abdominal pain radiating to the back, often increased by food and decreased by upright posture. Vomiting can be persistent. Examination reveals abdominal tenderness and may include decreased bowel sounds, distention, and fever. Chronic pancreatitis characteristically presents as bouts of epigastric pain, often occurring in alcoholic patients after years of excessive drinking. Sometimes chronic pancreatitis is heralded by a severe attack of acute pancreatitis. The pain of chronic pancreatitis is not entirely constant and often varies in intensity over days to weeks. There may be exacerbations of pain, nausea, and vomiting after eating or drinking alcohol.

Urinary Tract

Obstruction within the urinary tract can present as abdominal pain. Acute ureteral blockade by a stone is extremely uncomfortable. Onset is sudden, and the pain is cramping, beginning in the back and flank and radiating into the lower abdomen and groin. If acute pyelonephritis develops, upper abdominal pain, fever, and chills may ensue. Acute bladder outflow obstruction presents as lower abdominal distention and suprapubic pain. Symptoms of prostatism (see Chapter 134) may precede the episode.

Peritoneal Irritation

Peritoneal irritation causes a severe continuous pain because of the rich innervation of the parietal peritoneum. Focal injury results in well-localized discomfort that is described as sharp, aching, or burning. Spread of the irritant process leads to moregeneralized abdominal pain. Severity is related to the nature of the irritant and the speed with which the noxious exposure occurs. Reflex spasm of the overlying abdominal wall musculature can produce involuntary guarding. Rebound tenderness is prominent on physical examination. Most important, the pain is accentuated by pressure changes in the peritoneum; thus, palpation, coughing, or movement may increase the pain, leading the patient to lie still, in contrast to the restlessness of patients with “colicky” pain.

Focal Peritonitis

Focal peritonitis of the retroperitoneum, which is characteristic of early appendicitis, may be tested by having the patient lie on the left side and extend the right hip (psoas sign). Bowel sounds are often reduced or absent, especially when the irritation is generalized. The origin of the peritoneal irritant need not be digestive; it can originate from other systems (e.g., from ovarian carcinoma).

Familial Mediterranean Fever

Familial Mediterranean fever, an infrequent autosomal recessive disorder most prevalent among Sephardic Jews, Turks, Arabs, and Armenians, causes recurrent attacks of serositis and fever. Any serosal surface may be involved, accounting for its protean manifestations, including fever, peritoneal irritation, pleuritis, and arthritis. Self-limited attacks lasting days to weeks typically begin during childhood or early adulthood. Presentations may mimic peritonitis, juvenile rheumatoid arthritis (monoarticular or oligoarticular joint involvement), or pleurisy. The brief but severe attacks are accompanied by marked elevations in sedimentation rate and acute-phase reactants. A serious consequence is amyloidosis, sometimes resulting in renal impairment. Colchicine provides dramatic relief from the pain of an acute attack and also prevents amyloid deposition and renal impairment.

Vascular Disease

Vascular disease of the abdomen can result in a host of abdominal pain presentations, many of which simulate those of other etiologies.

Acute Arterial Insufficiency

Acute arterial insufficiency (resulting from atherosclerosis, embolus, or sickle cell crisis) may present with severe abdominal pain, but sometimes the early presentation is subtler, with mild constant pain the only symptom for several days in the absence of tenderness or rigidity. The diagnosis may not become apparent until ischemic necrosis, bowel perforation, and peritoneal soilage set in, leading to peritonitis, lactic acidosis, and shock.

Chronic Mesenteric Insufficiency

Chronic mesenteric insufficiency characteristically produces dull or aching postprandial pain (“abdominal angina”) localized to the epigastrium or midabdomen when the increased oxygen demand of digesting a meal outpaces the available blood supply. Onset is usually within an hour of eating, peaking at the time of maximal oxygen demand; severity is proportional to the size and fat composition of the meal as well as the degree of obstruction to blood flow. Symptoms can persist for 2 to 3 hours.

Symptoms vary with the vascular territory involved and may herald acute infarction in cases of critical stenosis. Nausea, vomiting, and bloating characterize celiac artery ischemia. In midgut ischemia due to superior mesenteric artery disease, the predominant complaints are pain and weight loss. Constipation accompanied by occult blood loss characterizes chronic inferior mesenteric artery insufficiency. Some patients lose considerable amounts of weight because of the fear that eating will induce pain. Abdominal bruits are reported in 20% to 60% of cases; extra-abdominal signs of atherosclerotic vascular disease (e.g., carotid or femoral bruits) are often detectable.

Aortic Dissection

Aortic dissection or rupture of an abdominal aortic aneurysm produces severe acute abdominal pain that often radiates to the back or genitalia. Before dissection, aneurysms are usually silent, but physical examination may reveal an increase in aortic diameter (>3.0 cm). The greater the increase in aortic diameter on examination, the more likely it is that an aneurysm is present. Clinically silent abdominal aneurysms are often discovered serendipitously during workup for other causes of abdominal pain. Risk of catastrophic rupture is minimal as long as aneurysm diameter remains less than 5.0 cm. However, the probability over time of continued growth in diameter is substantial, necessitating careful follow-up (see later discussion). Aneurysms may also compromise arterial flow to the gut and result in ischemia.

Mesenteric Venous Thrombosis

Mesenteric venous thrombosis is a less common cause of intestinal ischemia than is arterial occlusion. It may present similarly, although it often has a more slowly progressive course. Both aortic dissection and mesenteric thrombosis typically result in pain complaints that are in excess of those elicited by physical examination.

Mucosal Injury

Ulceration or inflammation of the gastrointestinal tract is often accompanied by pain.

Peptic Ulcer Disease

Although the exact mechanism of pain in peptic ulcer disease is incompletely understood, it is believed that acid inflaming submucosal tissue and nerves plays a major role. This hypothesis is supported by the observation that neutralization of acid often provides immediate relief. The pain pattern of duodenal ulcer disease usually parallels the acid-peptic cycle (see Chapter 68). Unless perforation or penetration into the pancreas is present, the pain is mostly confined to the epigastrium. Patients use such terms as gnawing, aching, and burning to describe their discomfort. Radiation of pain into the back in patients with duodenal ulcer suggests perforation into the pancreas.

Inflammation

Inflammation of the middle or lower intestine, as seen with acute gastroenteritis and acute flares of inflammatory bowel disease (see Chapter 73), can disturb motility and absorption. In most instances, the pain is diffuse and cramping from altered motility, but occasionally it is focal and can simulate appendicitis or other surgical conditions. Fever, nausea, and vomiting are often prominent in the early stages of gastroenteritis; bowel sounds are usually hyperactive.

Immune-Mediated Injury (Adult Celiac Disease [Sprue]; see also Chapter 64)

A genetically predisposed inappropriate T cell response to ingested gluten causes immune-mediated damage to the smallbowel mucosa. Presenting symptoms can be subtle and nonspecific, including episodic or nocturnal diarrhea, flatulence, and weight loss along with iron deficiency. Steatorrhea may be absent if disease is limited to the proximal small bowel. Bloating, fatigue, and vague abdominal discomfort are common and may be mistaken for symptoms of irritable bowel syndrome. Iron deficiency anemia may be the only manifestation.

Altered Bowel Motility

This mechanism predominates in functional bowel disturbances, of which irritable bowel syndrome and psychophysiologic disturbances are the best examples.

Irritable Bowel Syndrome

Spasmodic, nonpropulsive, segmental contractions of large bowel result in high intraluminal pressures, manifested by cramping lower abdominal pain and bloating. In addition, there is a component of perceptive (nociceptive) dysfunction contributing to feelings of abdominal discomfort (see Chapter 74). Constipation alternating with diarrhea and mucous stools is a typical finding, as are pain relieved by defecation, more frequent and loose stools with the onset of pain, and a feeling of incomplete evacuation. Altered motility and chronically increased intraluminal pressures may lead to diverticular disease (see Chapter 75).

Functional Dyspepsia

This condition is characterized by chronic or recurrent upper abdominal discomfort or pain, often in conjunction with foodrelated dysmotility symptoms (e.g., bloating, fullness, nausea, early satiety). Many patients have concurrent esophageal reflux and irritable bowel syndrome, supporting the concept of “irritable gut syndrome” (see Chapter 74).

Psychiatric Disturbances

Psychiatric disturbances, especially anxiety and mood disorders, are common in persons with irritable bowel syndrome who seek medical attention. Symptoms may arise from any area of the intestinal tract—esophagus, stomach, small intestine, and biliary tree, as well as the colon. The result is a broad spectrum of presentations, which includes nausea, vomiting, dyspepsia, and flatulence in addition to cramping abdominal pain.

Acute Ileus

Causes include peritonitis (resulting from a variety of causes), systemic infections, bowel ischemia, abdominal surgery (a common etiology), abdominal trauma, pharmacologic agents (especially anticholinergics and narcotics), and metabolic disturbances (particularly hypokalemia).

Intestinal Pseudoobstruction

Clinical features mimic those of intestinal obstruction. Symptoms may be chronic (recurrent or persistent) or occur acutely (socalled acute ileus). Symptoms can include vomiting and abdominal distention; diarrhea or constipation may also be seen. Plain films of the abdomen demonstrate intestinal dilation, suggestive of partial obstruction. It is noteworthy that the syndrome of chronic pseudoobstruction may precede the recognition of associated systemic diseases by many years (see later discussion). Chronic intestinal pseudoobstruction is often idiopathic, although it may occur in the setting of scleroderma, Parkinson disease, drug use (opiates, phenothiazines, tricyclic antidepressants, or antiparkinsonian medications), hypercalcemia, diabetes, myxedema, amyloidosis, radiation enteritis, and chronic laxative abuse.

Capsular Distention

Distention of the well-innervated capsule surrounding digestive organs is a potential source of constant, aching abdominal pain. Hepatic capsular distention leading to right upper quadrant pain occurs in hepatitis, congestive heart failure, fatty infiltration (hepatic steatosis), and subcapsular hematoma. The pain of splenic capsular distention, as may occur secondary to blunt trauma (e.g., in a motor vehicle accident), localizes to the left upper quadrant. With subdiaphragmatic peritoneal irritation, the patient may experience pain radiating to the ipsilateral shoulder. With splenic trauma, a deceptive period of many hours may pass before peritoneal signs develop if a subcapsular hematoma temporarily retards the spilling of blood into the peritoneum.

Metabolic Disturbances

Metabolic disturbances may mimic intra-abdominal etiologies or sometimes result from them and exacerbate the clinical presentation.

Ketoacidosis

Ketoacidosis presents with severe abdominal pain in 8% of instances and may be accompanied by emesis and an elevated white blood cell count. Symptoms are caused, at least in part, by accompanying gastroparesis. An acute intra-abdominal event such as cholecystitis in a diabetic may be the precipitant.

Porphyria

Porphyria sometimes simulates bowel obstruction because of the cramping abdominal pain and hyperperistalsis that may occur. Acute intermittent porphyria presents with moderate to severe colicky abdominal pain, which may be localized or generalized. Abdominal symptoms may be the result of intestinal dysmotility; vomiting and diarrhea are also common complaints. Fever and leukocytosis may be present, but on examination, the abdomen is found to be soft. Proximal muscle pain and a range of neuropsychiatric symptoms accompany the abdominal pain. The clinical features of hereditary coproporphyria and variegate porphyria are similar to those described for acute intermittent porphyria; skin lesions may be prominent.

Lead Poisoning

Lead poisoning may also present with abdominal pain. Such pain is typically wandering, poorly localized, colicky, and accompanied by a rigid abdomen. Encephalopathy, peripheral neuropathy, and anemia are associated features. The urine coproporphyrin test is a more reliable indicator of this entity than is a serum lead level, which can be normal.

Angioneurotic Edema

Angioneurotic edema, caused by C′ esterase inhibitor deficiency, may result in episodic and severe abdominal pain. If this diagnosis is suspected, it is useful to check the serum level of C4, which is low in cases of C′ esterase inhibitor deficiency.

Nerve Injury

Nerve injury from encroachment or irritation is an important mechanism of abdominal pain. The source of pain may be intraabdominal, as occurs when a pancreatic cancer or pancreatitis damages or inflames adjacent splanchnic nerves, or it may be extra-abdominal, as occurs when a nerve root supplying an abdominal wall dermatome becomes irritated in herpes zoster. Abdominal pain occurs in about 75% of patients with cancer of the pancreas; it is usually epigastric and most common in patients with tumor involving the body or tail of the pancreas. Sometimes, the pain radiates to the back or is confined to it. Nerve root irritation from herpes zoster may be mistaken for an intra-abdominal process, especially before the rash appears. Often, the patient complains of a severe, lancinating pain resembling that from an intra-abdominal source. An associated rectus muscle spasm may simulate peritonitis, but there is no effect on bowel function, as there is with peritoneal irritation, and palpation may actually alleviate the rectus muscle spasm. The pain of herpes infection often precedes the rash by several days and may persist after the skin clears, particularly in the elderly (see Chapter 193).

Abdominal Wall Pathology

Abdominal wall pathology can also be mistaken for disease inside the abdominal cavity. Traumatic injury to the musculature of the wall produces pain that is constant, aching, and exacerbated by movement or pressure on the abdomen. The muscles may be in spasm, simulating the involuntary guarding of peritonitis. When a generalized myositis is responsible for the muscle pain, discomfort occurs in the limbs as well as in the abdomen. Occasionally, a tender mass in the wall, such as a rectus sheath hematoma, is found to be the source of difficulty.

Referred Pain

Chest Sources

Referred pain from a process originating in the chest is sometimes an etiology of abdominal complaints. Pulmonary infarction and pneumonia of the lower lobes are among the chest problems that may present as pain in the upper abdomen; at times, reflex
muscle spasm accompanies the pain. Upper abdominal pain, nausea, and vomiting may be the principal manifestations of an acute inferior myocardial infarction. However, symptoms and signs of cardiac or pulmonary disease accompany most intrathoracic sources of abdominal pain.

Ovarian Cancer and Other Pelvic Sources

Both benign and malignant ovarian masses, even those still confined to the pelvis, are frequent sources of abdominal complaints. In addition to causing pelvic pain and urinary urgency, such pelvic pathology is significantly associated with increasing abdominal girth and bloating. Even though such symptoms are nonspecific and common in primary care practice, they take on added meaning when new in onset or more frequent (20 to 30 times per month vs. 2 to 3 times per month) or more severe than usual. Almost half of women with ovarian cancer experience the combination of bloating, increased abdominal size, and urinary symptoms, compared with 8% of those without such cancer presenting to primary care clinics.

DIFFERENTIAL DIAGNOSIS (10,12)

Because the number of possible causes of abdominal pain is large, it is helpful to consider the differential diagnosis in terms of pathophysiologic mechanisms (Table 58-1). The nature of the pain can sometimes be more discriminating than location and suggest a pathophysiology that can narrow the differential. Etiologies causing obstruction, peritoneal irritation, and vascular insufficiency are among the most dangerous. In about 70% of cases, adhesions or external hernias cause mechanical smallbowel obstruction; 90% of cases of large-bowel obstruction are attributable to diverticular disease and carcinoma. Acute arterial insufficiency results most often from systemic embolization secondary to atrial fibrillation, severe atherosclerotic occlusive disease, and hypoperfusional states. Pelvic pathology is a common extra-abdominal source of peritoneal irritation.

Other pathophysiologic mechanisms, such as nerve injury, metabolic imbalance, abdominal wall disease, and disordered motility, may produce symptoms that superficially mimic those of a more worrisome etiology; however, conditions associated with these mechanisms are usually more annoying than dangerous (an important exception is diabetic ketoacidosis). Pain referred from an extra-abdominal site is more of a problem; significant cardiac disease (e.g., inferior myocardial infarction) or pulmonary pathology (e.g., lower lobe pneumonia) may present as abdominal pain.