Abdominal Pain
Jason A. Dominitz, M.D. , MHS, John H. Sekijima, M.D., and Mary Watts, M.D
.

I. Introduction


I.A. Background

Abdominal pain is one of the most common causes of visits to a primary care provider, accounting for 2.5 million visits to office-based physicians per year.[1] It is the most frequent cause for gastroenterology consultation.[2,3,4,5] The overall economic and social impact of abdominal pain is staggering. While a specific diagnosis can be obtained in many patients, no identifiable etiology is found in approximately 35%-51% of patients with abdominal pain.[6,7] A thorough review of all causes of abdominal pain is beyond the scope of this chapter. For detailed information regarding the causes of abdominal pain, the standard gastroenterology texts serve as an excellent resource.[8,9]

In compiling this review of abdominal pain, the authors chose selected references from a PubMed literature search through February 1999. The MeSH heading "abdominal pain" was used, as were selected specific causes of abdominal pain. Special attention was devoted to controlled trials and comprehensive reviews. Key references from these articles were also reviewed and are referenced. Special emphasis was placed on articles that provide evidence or guidelines for the diagnosis and management of selected specific causes of abdominal pain.


I.B. General Approach to the Patient with Abdominal Pain

When confronted with a patient complaining of abdominal pain, the provider must first rule out catastrophic causes of pain, such as dissecting aortic aneurysm, perforated viscus, or bowel obstruction. As with all patient encounters, the provider should begin with an appropriate history and physical examination. However, the initial appearance of the patient will guide the nature and urgency of the history and physical. If the patient is hemodynamically unstable, then efforts should be made to rapidly stabilize the patient. If an abdominal aortic aneurysm is suspected, then surgical consultation should be obtained immediately, with the expectation that the patient may require emergent surgery. If an abdominal aortic aneurysm is not suspected and the abdomen is rigid, then abdominal and chest radiographs should be rapidly obtained, along with surgical consultation. The radiographs should be carefully examined for evidence of perforation or obstruction, which may require prompt exploratory surgery. If the radiographs are nonspecific, then other causes of a rigid abdomen should be considered, such as acute pancreatitis, toxins, hematologic or metabolic disorders.

In the absence of a rigid abdomen, or if the patient is hemodynamically stable, the provider becomes challenged with sorting through a long list of possible diagnoses. Unfortunately, 35% of patients admitted with abdominal pain have no identifiable etiology for their symptoms.[6] In the primary care setting, the average abdominal pain episode has been reported to require an average of 1.32 visits and cost $123.36.[7] In 51% of these cases, no specific diagnosis was reached.

We have found that it is helpful to start by determining whether the symptoms are acute (i.e. onset within days to weeks) or chronic. Although atypical presentations can occur for any condition, many causes of abdominal pain have characteristic locations which can help guide the diagnostic approach. Therefore, we suggest that the location of the pain be used next to narrow down the diagnostic possibilities. At this point, the specific historical features, physical examination findings, and routine laboratory tests can either suggest a specific diagnosis or guide the next appropriate investigation (e.g. radiographic study, consultation or endoscopy).

Acute abdominal pain in older patients often results from infectious, inflammatory, or ischemic disorders and bears special mention. Elderly patients may not have the traditional systemic and local features of an infection. In a retrospective review of 103 patients over age 65, the most common causes of hospitalization for acute abdominal pain included biliary disease in 23%, diverticulitis in 12%, intestinal obstruction in 11% and constipation in 9%.[10] Almost 14% of patients had no clear etiology of their pain. In-hospital mortality was nearly 6%.


I.C. Cost-Effective Approach

In today's managed care environment, there is increased pressure for the provider to determine the most cost-effective approach to working up a patient with abdominal pain. Clearly, patients bring to the encounter their own fears regarding the etiology of their pain, including malignancies and ulcers. While various studies have been conducted to identify the most cost-effective means of evaluating patients with abdominal complaints (e.g. dyspepsia),[11,12,13,14,15,16,17] there is no clear consensus. In addition, these studies have failed to account for the often intangible benefit derived by the patient from a negative study. Recently, Wiklund et al. studied the benefits of a negative endoscopy in patients with dyspepsia and found that quality of life improves despite persistent symptoms.[18] Therefore, we recommend that providers use an approach which is designed to first exclude acute life-threatening diagnoses such as a dissecting aneurysm, perforation, or obstruction. Once these have been reasonably excluded, the provider should employ a systematic approach to obtain a thorough history and physical with pertinent laboratory, radiologic, and endoscopic procedures. The choice of the most appropriate test is determined by a host of factors which may or may not be directly related to the patient. For example, for patients with uncomplicated dyspepsia, testing and treating for Helicobacter pylori or empiric therapy with acid suppression or promotility agents may be an appropriate first step. However, if the patient is very concerned about the possibility of a malignancy, then endoscopy would be appropriate. As it has been shown that the cost-differential between early endoscopy and empiric therapy may be negligible,[12] this approach is clearly justifiable. For patients with symptoms consistent with the irritable bowel syndrome, appropriate tests will depend upon the specific clinical situation. For example, in a young female patient with cramping lower abdominal pain relieved with defecation, alternating constipation and diarrhea, bloating, and mucus in the stool, it would be reasonable to obtain a routine blood count, pregnancy test, and consider pelvic ultrasound. However, for an older female patient, abdominal/pelvic ultrasound and either sigmoidoscopy or colonoscopy would be recommended.


II. Evaluation of the Patient with Abdominal Pain


II.A. History

The history alone can suggest a specific diagnosis for a variety of causes of abdominal pain. For example, patients with known atherosclerotic disease, weight loss, food avoidance, and post-prandial pain should be considered to have mesenteric angina until proven otherwise. The history should encompass the chronicity, onset, duration, quality, location and radiation of the pain. In addition, associated symptoms as well as alleviating and aggravating factors should be determined. (Table 1) compares the features of some common causes of acute abdominal pain.

While acute pain often appears to be more dramatic or serious than chronic pain, one should not assume that chronic pain is any less significant. Patients with gastrointestinal malignancies may present with chronic pain as their primary complaint. Pain which wakes a patient from their sleep or is acute in onset suggests possible strangulation or perforation of the bowel. Pain which is gradual in onset suggests an inflammatory process, such as appendicitis, or an infectious process, such as an abscess. Sometimes the patient can recall preceding abdominal trauma which may result in something as minor as a bruised rib to something as critical as a ruptured spleen. The duration of pain can often aid in the diagnosis as well. For example, acute pancreatitis can cause pain lasting days while biliary colic typically lasts for several minutes or hours. Cramping or squeezing pain suggests a luminal origin, such as a partial or complete obstruction of a peristaltic organ (e.g. bowel obstruction or renal colic). The visceral peritoneum is innervated by C fibers, which are slow transmitters. These fibers produce dull, crampy pain, usually of insidious onset and poorly localized. The parietal peritoneum, skin, and muscles are innervated by the fast transmitting A - neurons which result in sharp pain, often of acute onset and well localized.

Due to the relatively sparse innervation of the viscera, patients are often unable to localize their pain. In addition, through a process known as functional divergence, a small number of abdominal afferents will stimulate a large number of spinothalamic tract neurons.[19] Functional divergence also results in associated physiologic responses to abdominal pain, such as changes in pulse, blood pressure, muscle tone, and motor and secretory reflexes.[19,20,21] Since most abdominal organs originate as midline structures embryologically, they have bilaterally symmetric innervation. Digestive tract pain, therefore, is generally midline.[22] Abdominal pain which is localized to either side suggests that the pain originates from those organs with innervation which is predominantly one-sided (e.g. kidneys, ureters and ovaries), or from structures with somatic innervation.[22] For some organs with bilateral innervation (e.g. ascending and descending colon and gallbladder), there may be a lateral predominance which can help localize the etiology.[23] The embryologic origin of the abdominal structures determines the clinical pain location as shown in (Table 2). However, due to variability in innervation between patients, pain originating from a particular organ may not be clinically manifest as one might expect. Pain may also migrate over time. When appendiceal inflammation first occurs, the patient generally experiences periumbilical pain due to the bilaterally symmetric innervation of the appendix and its midgut origin. As the inflammation progresses and involves the parietal peritoneum, the pain is experienced in the right lower quadrant.[24] Radiation of pain can also help refine the differential diagnosis. For example, pancreatic pain typically radiates to the back, while cardiac ischemia may produce pain radiating to the neck, jaw, or left upper extremity.

The patient should be asked if any symptoms are associated with the pain, such as nausea, vomiting, diaphoresis, palpitations, fever, chills, gastrointestinal bleeding, weight loss, jaundice, diarrhea, constipation, steatorrhea, mucus in the stool, change in stool caliber, early satiety, bloating, dysphagia, odynophagia, heartburn, sourbrash (i.e. a sour or bitter taste in the back of the throat), or waterbrash (i.e. excessive salivation). Anorexia may suggest gastric disease, especially when accompanied by epigastric pain and/or early satiety. The relation of vomiting to meals is often helpful. Patients who vomit immediately after eating may have functional vomiting. Vomiting which occurs within 30-60 minutes of a meal suggests mucosal disease of the stomach. Vomiting which occurs hours after a meal is indicative of gastric outlet obstruction or gastroparesis.[25] Aggravated or alleviating symptoms, such as food, dairy products, antacids, physical exertion, stress, and passage of stool or flatus should be determined. Sitophobia (fear of eating due to pain) may be indicative of gastric outlet obstruction, intestinal ischemia, or a gastric malignancy. In women, one needs to obtain a menstrual and sexual history and consider gynecologic pathology. Pelvic inflammatory disease and ovarian cysts may produce pain which can mimic acute appendicitis. Ectopic pregnancy can present with acute or subacute abdominal pain.

Aside from historical features directly related to the abdominal pain, it is important to obtain a thorough history concerning past medical problems (e.g. prior gastrointestinal disease and atherosclerotic disease), past surgical history (e.g. prior cholecystectomy), and family and social history (e.g. Armenian or Sephardic Jewish patients at risk for familial Mediterranean fever).


II.B. Physical Examination

The physical examination of the abdomen should be carefully and thoroughly conducted on all patients. The exam is often unremarkable in patients with uncomplicated diseases. Though fever is often present in patients with infectious or inflammatory processes, elderly patients may not become febrile even with a significant infection. The facial expression may reflect the degree of pain that the patient is experiencing. Bowel sounds may be absent in the presence of perforation or ileus. The presence of a succussion splash more than 2 hours postprandially suggests gastric outlet obstruction. Signs of peritonitis include fever, tenderness and guarding. Patients with peritoneal inflammation will have tenderness elicited by gently jostling the exam table or jarring the patients heal when the leg is extended.[22] Guarding can often be voluntary. By using the stethoscope to apply pressure to the abdomen, the examiner may assess for voluntary guarding. Patients who are apprehensive when the examiners hand is pressed against the abdomen will often relax their abdomen when they believe that the examiner is listening with the stethoscope. In a study of hospitalized patients with acute abdominal pain, the presence of rebound was found to have no predictive value for the presence of peritonitis.[26] The physical exam should also include assessment of the sclera for jaundice, cardiovascular and pulmonary examination for congestive heart failure or pneumonia, pelvic examination for gynecologic causes of abdominal pain, and a careful rectal exam.


II.C. Laboratory Tests

The initial laboratory evaluation will depend to a large extent upon the setting in which the patient presents. Laboratory tests should not be ordered frivolously, as unexpected abnormalities can often result from random laboratory error and result in unnecessary additional testing and patient concern. However, these tests are clearly a vital part of the work-up for abdominal pain. For patients presenting to the emergency department with acute abdominal pain, initial labs should include a CBC with differential, electrolytes (i.e. sodium, potassium, chloride, calcium, magnesium and phosphorous), serum chemistries (e.g. bicarbonate, blood urea nitrogen, creatinine, serum glucose, amylase and lipase), liver function tests (ALT, AST, alkaline phosphatase and bilirubin), urinalysis, and possibly coagulation labs and a pregnancy test. Blood may also be necessary for typing and crossmatching, depending upon the clinical situation. Blood cultures should be obtained from febrile patients. In addition, an electrocardiogram should be strongly considered as myocardial ischemia can present as isolated abdominal pain. Although this "shotgun" approach may seem wasteful, it may be necessary to maintain the efficiency of the emergency department setting, especially as these tests can aid in making a more rapid diagnosis and in preparing the patient for possible surgery. For non-acute patients, the laboratory tests should be tailored to the clinical situation and a more stepwise approach may be utilized.


II.D. Radiographs


II.D.1. Non-Contrast Studies

An abdominal series of plain radiographs can be vital to the diagnosis of abdominal pain. These films should include a flat plate of the abdomen, and upright view of the abdomen, and an upright chest radiograph. These films can identify evidence of perforation (often best seen on the chest film as free intraperitoneal air under the diaphragm or retroperitoneal air), bowel obstruction, air in the portal venous system or biliary tree, calcium deposits (e.g. gallstones, renal or ureteral stones, appendicoliths, chronic pancreatitis, aortic aneurysm), foreign bodies, and pneumatosis (i.e. air in the bowel wall suggesting possible ischemia). It should be noted that when looking for free air, the patient should remain in an upright position for at least 5 minutes to allow the air to percolate up to the diaphragm. For those patients unable to assume an upright position, a left lateral decubitus film may suffice. The patient should remain with the left side down for at least 10 minutes. It has been estimated that the plain film is diagnostic of gastrointestinal obstruction in 50%-60% of cases, equivocal in 20%-30%, and normal, non-diagnostic, or misleading in 10%-20% of cases.[27] The plain radiograph can also show evidence of an intraabdominal inflammatory or infectious process (e.g. when a normal psoas shadow is obscured by a pelvic abscess).


II.D.2. Contrast Studies

Radiologic contrast studies are often over utilized in the evaluation of abdominal pain. The standard barium upper gastrointestinal series (UGI) can provide information regarding esophageal motility, esophageal stenoses and peptic ulceration. However, the UGI is neither as sensitive nor as specific as endoscopy for mucosal abnormalities, such as erosive esophagitis and peptic ulcer.[28,29,30,31] A barium enema (BE) will demonstrate the colonic anatomy and may also fill the terminal ileum. A BE may show evidence of diverticulosis, strictures, fistulas and mucosal masses (e.g. polyps and cancer). Barium contrast studies should not be utilized for the evaluation of an acute abdomen. Intravenous urography is often used to demonstrate a calculus in the urinary tract.[32]


II.E. Imaging Tests


II.E.1. Ultrasound

Abdominal ultrasound is often a useful, non-invasive test to help identify the etiology of abdominal pain. Ideally, patients should have nothing by mouth for several hours prior to their examination.

Ultrasound is commonly used to evaluate right upper quadrant pain to identify biliary abnormalities such as bile duct dilatation, gallbladder wall thickening, pericholecystic fluid, gallstones, and sludge.[33] Ultrasound can also identify pancreatic abnormalities, such as duct dilation and fluid collections, though overlying bowel gas often limits the quality of the examination. Other information elicited by ultrasound includes the presence of ascites or other signs of chronic liver disease (e.g. fatty liver or cirrhotic appearing liver), gynecologic abnormalities (e.g. ovarian cysts, ectopic pregnancy, or uterine fibroids), renal abnormalities (e.g. hydronephrosis, renal cysts) and acute appendicitis.[34]


II.E.2. Computed Tomography

Computed tomography (CT) is a powerful tool in the evaluation of abdominal pathology. However, as its use is associated with significant cost, CT should be reserved for those patients in whom the diagnosis cannot be safely established with less expensive means. Computed tomography is useful for establishing many causes of abdominal pain, such as abdominal aortic aneurysms, intro-abdominal fluid collections, diverticulitis, bowel obstruction, intestinal ischemia, perforated viscus, appendicitis and pancreatitis.[34] It can also identify lesions suggestive of primary cancers or metastatic disease. Unenhanced helical CT has been shown to be quite accurate in the diagnosis of ureteral stone disease.[35]


II.E.3. Magnetic Resonance Imaging

There are few indications for magnetic resonance imaging (MRI) in the evaluation of abdominal pain. The utility of MRI in the performance of cholangiopancreatography (MRCP) is under study. This procedure may replace diagnostic endoscopic retrograde cholangiopancreatography (ERCP) in many settings, and allows for imaging the pancreaticobiliary system in patients whose anatomy prohibits ERCP (e.g. Roux-en-Y surgical anastomosis).


II.F. Endoscopy

Gastrointestinal endoscopy is another useful test in the evaluation of abdominal pain. Like CT, the cost associated with endoscopy needs to be considered in the management of the patient. Endoscopic procedures commonly utilized include: esophagogastroduodenoscopy (EGD), flexible sigmoidoscopy, colonoscopy, and endoscopic retrograde cholangiopancreatography (ERCP). For many patients, such as those with dyspepsia, EGD can serve several purposes. In addition to establishing the specific etiology for the symptom (e.g. peptic ulcer disease, erosive esophagitis, gastric cancer), tissue can be obtained at the time of endoscopy for histopathology or assessment for Helicobacter pylori. Even if no organic pathology is identified, a negative endoscopy can serve to reassure the patient.[18] Endoscopy is more accurate than contrast radiography[28,29,30,31] and is preferred by patients.[36] Likewise, sigmoidoscopy and colonoscopy can identify a specific cause of the patients symptoms (e.g. sigmoid volvulus, colitis, malignancy and ischemia), exclude the presence of organic pathology (e.g. as in the patient with irritable bowel syndrome) and treat colonic abnormalities (e.g. sigmoid volvulus and colonic polyps). For patients with suspected pancreaticobiliary disorders, ERCP can establish a specific etiology (e.g. chronic pancreatitis, pancreatic cancer and choledocholithiasis) and is often used to treat these conditions (e.g. sphincterotomy and stone extraction for choledocholithiasis or stenting for biliary obstruction). Other endoscopic procedures which are beyond the scope of this chapter include biliary manometry and endoscopic ultrasound. Endoscopic procedures are generally safe and very well tolerated.

III. Specific Causes of Abdominal Pain


III.A. Abdominal Wall Pain

Abdominal pain originating from structures other than the visceral organs should always be considered as part of a complete evaluation. Skin, subcutaneous fat, muscle, and bone are all possible sources of pain.[37] Some examples of causes of abdominal wall pain are shown in (Table 4).


III.A.1. Features of Abdominal Wall Pain[38]

1 Often discretely localized by examining fingertips
2 Constant site of tenderness
3 Superficial tenderness
4 Positive Carnett’s sign

Carnett’s sign:[39]

The examiner palpates the abdomen to elicit a localized area of tenderness. The patient is then asked to contract the abdominal musculature by raising the head or straightened legs off the table. With the patient holding this position, palpating pressure is reapplied to the site of discomfort and the patient is asked if the pain decreases or increases in severity. If the pain is truly intra-abdominal, then the contracted abdominal wall should diminish the tenderness by protecting the underlying viscera. In contrast, if the cause of the pain resides in the abdominal wall the elicited pain should at least be as severe and often enhanced.


III.A.2. Treatment

For pain that is well localized, superficial and positive on Carnett’s testing, a local 2 cc injection of 0.25% bupivacaine hydrochloride or 1% lidocaine can be beneficial. 40 mg of triamcinolone acetate may be mixed with the anesthetic to prolong the effect.[38]


III.B. Peptic Ulcer Disease


III.C. Dyspepsia


III.D. Bowel Obstruction


III.D.1. Etiology


In adults, bowel obstruction most commonly results from external hernias or postoperative adhesions.[6] Other causes include malignancy, colonic diverticular disease, volvulus, gallstone ileus, and intussusception. In children, obstruction is most commonly associated with intussusception, atresia, or meconium ileus.



III.D.2. Clinical Presentation

Patients with bowel obstruction typically present with fairly sudden onset of crampy abdominal pain, abdominal distention and failure to pass flatus. If the obstruction is partial, the patient may have the same symptoms, though will continue to pass flatus. When the obstruction involves the proximal small bowel, the pain tends to be more sharp, is epigastric in location, and is accompanied by frequent bilious vomiting. When the obstruction involves the distal bowel, the pain tends to be periumbilical in location and is accompanied by less frequent, though often feculent, vomiting. The patient is typically restless and ill appearing. Fever, tachycardia, and orthostatic hypotension may be present, as life-threatening dehydration can occur.[40] Hyperactive bowel sounds with rushes and/or high pitched tinkling sounds are classically found. The abdomen is tender to palpation with involuntary guarding.


III.D.3. Diagnosis

In addition to an appropriate clinical presentation, radiographic imaging is a critical component in the diagnosis of intestinal obstruction. Abdominal radiographs reveal dilated loops of bowel, often with air-fluid levels, proximal to the obstruction, with normal caliber or collapsed bowel distally. When the diagnosis is not evident, an abdominal CT scan is frequently regarded as the test of choice in identifying obstruction. A single-contrast water soluble contrast enema may help rule out a large bowel obstruction.

III.D.4. Treatment

When bowel obstruction is suspected, surgical consultation should be immediately obtained as surgical treatment may be required. Delay in treatment may result in ischemia and infarction of bowel. A nasogastric tube should be inserted and intermittent suction applied to remove gastrointestinal secretions and minimize nausea and vomiting. Intussusception may be reduced with a diagnostic and therapeutic barium enema. Sigmoid volvulus may be initially diagnosed with a contrast enema study and treated with the placement of a rectal tube (e.g. a red rubber catheter) above the level of the volvulus. Alternatively, a sigmoidoscopy may be performed to reduce the volvulus. Surgery is often necessary to remove the involved bowel in order to prevent recurrent volvulus.


III.E. Irritable Bowel Syndrome (IBS)


III.E.1. Epidemiology and Pathogenesis

IBS is a common functional gastrointestinal disorder without identifiable laboratory, structural or histological abnormalities. It has been estimated that at least 8 billion dollars of direct charges are spent annually in the U.S. on physician, laboratory and radiology examinations in patients with this condition.[41] According to one U.S. household survey, IBS individuals were noted to have a 2-3 fold increase in work absenteeism over those without symptoms.[42]

Women are both more commonly affected and more likely to visit a physician with this condition than their male counterparts. Psychosocial factors such as stress, anxiety and depression may significantly modify the expression of IBS but are not diagnostic features.

A variety of motor abnormalities of both the small and large bowel have been observed in IBS patients. However no specific motility disturbance distinguishes the IBS patient from normal subjects in the resting state, and many of the abnormal motor findings do not correlate well with clinical symptoms.

Balloon distention and air insufflation studies of the ileum and colorectum have revealed that patients with IBS report pain at lower volumes and/or pressures than asymptomatic controls. This lower pain threshold has also been referred to as visceral hyperalgesia or hypersensitivity.[43] These findings may help to explain such complaints as urgency, incomplete evacuation, bloating and discomfort.


III.E.2. Diagnosis

The diagnosis of IBS is generally made on the basis of clinical manifestations and symptom criteria. (Table 3). Typically, a patient with IBS will present to the office with variable complaints of abdominal pain, altered bowel habits and bloating. The abdominal discomfort may be quite heterogeneous in quality, intensity and location. The pain is characteristically relieved by the passage of stool or flatus and may be exacerbated by eating or emotional stress. Moreover, there appears to be considerable overlap with functional esophageal, gastroduodenal, bowel and anorectal symptoms.[41] In one study of patients presenting with typical IBS symptoms, dyspepsia was found to be the predominant symptom one year later.[44] Extraintestinal complaints such as fatigue, headache, urological symptoms and fibromyalgia are often present as well.[41,45]

Approximately half of the patients with functional bowel disease suffer from depression and anxiety.[46] Previous physical and sexual abuse is also more frequently found and is associated with increased IBS severity and physician visits.[47,48]


III.E.3. Evaluation

Choosing which, if any, laboratory, endoscopic or radiological tests to order will depend on a detailed history and physical examination. New onset complaints in an older patient, nocturnal symptoms, weight loss, fever or a steadily deteriorating course should prompt a diligent search for more ominous diseases such as malignancy or inflammatory bowel disease. A CBC is appropriate and many physicians will also add a chemistry panel, thyroid tests and a sedimentation rate.[49] However, these tests are rarely abnormal in the young patient presenting with symptoms typical of IBS.[50]

For diarrhea predominant patients, stool evaluation for ova and parasites, Giardia antigen, occult blood and qualitative fat are important considerations. Measurement of serum carotene can aid in the evaluation of malabsorption. Moreover, a 48-72 hour stool collection for weight and fat can be crucial in distinguishing IBS from a more serious condition. Absence of steatorrhea (< 7 gms of stool fat/24h ) and total stool output (< 200-250 gms/24h ) in patients consuming a diet containing 100 gms of fat per day are consistent with functional disease.

Flexible sigmoidoscopy is appropriate in patients with chronic diarrhea to rule out significant mucosal disease. Colonoscopy should strongly be considered for any individual over the age of 50 with new symptoms or a family history of colorectal neoplasms. Furthermore, in the female patient with predominantly lower abdominal pain, a careful pelvic examination is mandatory and a gynecologic referral or pelvic ultrasonography may be indicated as well.


III.E.4. Treatment

A strong physician-patient relationship is critical and allows for effective education and reassurance. Dietary modification is appropriate when gas-forming vegetables and fruits, excessive caffeine, fructose or sorbitol containing products exacerbate the symptoms. Similarly, a 2 week trial of a lactose free diet is a practical consideration.

Although the efficacy of fiber supplementation in IBS has never been definitively proven, a therapeutic trial is recommended. Natural fiber such as wheat bran or supplements like psyllium, polycarbophil, and methylcellulose may all cause bloating and discomfort, but these symptoms usually resolve within a few weeks. Tailoring the medications to particular symptoms should be the rule. For patients with predominant pain, antispasmodics or anticholinergic agents may be of benefit. In addition, low dose tricyclic antidepressants may be useful by directly modulating sensory nerve pathways, via antidepressant effects or by anticholinergic side effects. For diarrhea prone patients judicious usage of loperamide is often helpful. Further information regarding the diagnosis and management of IBS are available in recent reviews.[51,52]


III.E.5. Indications for Referral

1 Severe or refractory symptoms

2 Diagnosis is unclear

3 Evidence of rectal bleeding


III.F. Ischemic Bowel Disease


III.F.1. Acute Mesenteric Ischemia


III.F.1.a. Clinical Features

Acute mesenteric ischemia (AMI) is increasingly common, accounting for 0.1% of hospital admissions. It is a highly morbid condition, with a mortality rate exceeding 60%.[53,54] Risk factors for AMI include cardiac arrhythmias, advanced age, low cardiac output, atherosclerosis, congestive heart failure, severe valvular cardiac disease, recent myocardial infarction, and intra-abdominal malignancy.[55] Causes of AMI include mesenteric arterial occlusion (either embolus or thrombosis), mesenteric venous occlusion, and nonocclusive events (e.g. vasospasm). While approximately 50% of cases of AMI are attributable to embolization of the superior mesenteric artery, 25% of AMI cases result from thrombosis of a pre-existing arthrosclerotic lesion, and approximately 25% of AMI cases result from nonocclusive mesenteric ischemia (NOMI).[56]

Given the numerous underlying etiologies, the clinical presentation can be quite variable. Abdominal pain is classically out of proportion to the physical exam findings of tenderness. The pain may initially be colicky in nature, it generally progresses to a continuous, less severe pain. Associated symptoms include vomiting and diarrhea, with or without hematochezia. Patients may be asymptomatic or have only mild symptoms (e.g. ischemic colitis or traumatic disruption); some may have abdominal distention and bloody stool (e.g. venous thrombosis or arterial embolism); and others may have severe symptoms, with sudden onset of crampy, continuous pain (e.g. arterial thrombosis).[57] Physical exam may initially be benign, though abdominal distention, hyperactive bowel sounds, peritoneal signs, and sepsis may develop.(Table 12)


III.F.1.b. Diagnosis

Diagnosis of acute mesenteric ischemia requires a high index of suspicion in many cases, as the clinical presentation and laboratory findings are often nonspecific. Laboratory abnormalities may include leukocytosis, acidosis, and elevations of amylase, alkaline phosphatase, or creatine phosphokinase. Abdominal radiographs may reveal a nonspecific bowel gas pattern or, in late cases, pneumatosis intestinalis. Angiography is often diagnostic, especially in cases of thrombosis and embolism. Other radiologic tests of use include CT,[58] MRI,[59] and duplex ultrasound of the aorta and splanchnic vessels.[60] Laparotomy may be required for definitive diagnosis as well as treatment.

III.F.1.c. Treatment

Patients with intestinal ischemia require aggressive supportive care, including treatment of cardiovascular collapse and sepsis. Careful monitoring of volume status and urine output, as well as broad spectrum antibiotics are warranted. Surgical consultation should be emergently obtained for consideration of laparotomy.

III.F.2. Chronic Mesenteric Vascular Occlusive Disease


III.F.2.a. Epidemiology

Nonacute occlusive intestinal ischemia or intestinal angina is a relatively uncommon disorder most often caused by severe atherosclerotic disease of at least two of the three major splanchnic vessels (celiac, superior and inferior mesenteric arteries). Typically there are plaque stenoses located at the ostia of the aorta or involving the proximal first few centimeters of the vessel.

Despite the relatively high prevalence of atherosclerotic disease of mesenteric vessels on autopsy, angiographic studies or duplex ultrasound scanning, clinical evidence of chronic ischemia is quite uncommon.[61,62,63] Splanchnic collateral blood flow is generally well preserved and many individuals will remain without complaints despite the presence of significant occlusive disease.


III.F.2.b. Diagnosis

Symptomatic patients typically suffer from recurrent mid-abdominal pain generally occurring within 10-30 minutes of eating. The pain may be described as dull or cramping in nature and will often persist for 2-4 hours before gradually dissipating. In the more advanced setting, marked weight loss results from a fear of eating and the consumption of smaller meals. Not surprisingly, coronary or peripheral vascular disease may also be evident.

After ruling out more common causes of abdominal pain, workup begins with noninvasive doppler flow studies of the mesenteric vessels. Angiography is generally necessary to confirm diagnosis.


III.F.2.c. Treatment


Percutaneous balloon angioplasty, endarterectomy and surgical bypass procedures have all been employed with variable success.[64,65]

III.F.3. Colonic Ischemia

III.F.3.a. Epidemiology

Colonic ischemia is the most common form of gastrointestinal ischemia. The majority of patients are elderly with concomitant atherosclerotic disease. Major risk factors include elective aortic surgery and ruptured aortic aneurysm repair. Other factors include acute cardiac failure, shock or hypovolemia. Classic watershed areas such as the splenic flexure and sigmoid colon are particularly susceptible to ischemic injury. Younger individuals may also develop colon ischemia secondary to systemic vasculitis, medication reactions (estrogens, vasopressin, gold compounds), drug abuse (methamphetamines and cocaine) and long distance running. Colon ischemia has been recently reviewed.[66]


III.F.3.b. Clinical features

Acute onset of lower abdominal cramping discomfort, followed by rectal bleeding is typical. Hemodynamically significant bleeding is uncommon. Examination usually reveals mild to moderate tenderness over the affected colonic segment. Marked tenderness or rebound suggests bowel necrosis, demanding an urgent surgical consultation.

Differential diagnosis includes infection, inflammatory bowel disease, diverticulitis and malignancy. Diagnosis is generally made by flexible sigmoidoscopy or colonoscopy. Submucosal hemorrhage, edema and ulceration are classically noted. Biopsies confirm ischemia when there is mucosal infarction.

III.F.3.c. Management

 

Initial management involves optimizing the patient’s fluid and cardiovascular status. Some physicians advocate the use of broad spectrum antibiotics although this has never been proven to be of benefit in humans.

The majority of patients do quite well and go on to complete clinical and endoscopic resolution. Others develop strictures or a chronic ulcerating process that may be confused with inflammatory bowel disease. A minority present with a rapidly progressive process and develop signs and symptoms of gangrenous bowel. These patients require urgent surgery.




III.F. 4. Abdominal Aortic Aneurysm

III. F. 4. a. Etiology and Pathophysiology

Most intra-abdominal aneurysms occur in the aorta below the origin of the renal arteries. Their cause is multi-factorial and related to weakening in the collagenous wall of the aorta. When aneurysms leak they cause stretching of sensory nerves in the retroperitoneum around the aorta and result in lower-back pain and sometimes symptoms of renal colic.

III. F. 4. b. Clinical Features

Most abdominal aortic aneurysms are asymptomatic until they rupture. Sometimes lower-mid-abdominal pain is present prior to rupture although this is unusual. Most commonly, pain is the main feature of a ruptured aneurysm. The patient typically describes a very severe, sudden, tearing pain in the mid-abdomen and back, often with radiation to the left flank. With rapid blood loss, there are symptoms and signs of shock including syncope and orthostatic dizziness.

III. F. 4. c. Management

Initial management is directed at correcting hypovolemia with large caliber intravascular access, and infusion of crystalloid and blood. This is a medical and surgical emergency that requires prompt operative intervention.


III.G. Appendicitis

III.G.1. Epidemiology

The annual incidence of acute appendicitis is 1:1,000. The risk for a child less than 5 years of age of having an appendectomy for appendicitis is about 8.6% for boys and 6.7% for girls.[67] Approximately 80% of cases occur in people less than 40 years of age, with a peak incidence in those aged 10-30.

III.G.2. Clinical Features

The clinical features of patients with appendicitis are shown in (Table 6). Abdominal pain was universally present in this study. Diarrhea may be present in some patients. The features of appendicitis with and without perforation are shown in (Table 7). The risk of perforation is increased in preschool children and elderly patients. The differential diagnosis of acute appendicitis includes pyelonephritis, gastroenteritis, pelvic inflammatory disease, ovarian cyst, ruptured ectopic pregnancy, Crohn's disease, cecal diverticulitis, mesenteric adenitis, and infectious ileocolitis.

III.G.3. Diagnosis

The diagnosis of acute appendicitis is often difficult. Rasmussen and Hoffmann have reviewed the reliability of the signs and symptoms of acute appendicitis.[68] Migration of pain to the right iliac fossa and/or guarding/rigidity supports the diagnosis of appendicitis. However, the diagnosis should be doubted in the absence of anorexia, nausea and vomiting, or when the symptoms have persisted for more than 72 hours without perforation, or when tenderness is absent from the right iliac fossa. One study suggests the following indicators favoring appendicitis over pelvic inflammatory disease in young women with right lower quadrant pain: anorexia and onset of pain later than day 14 of the menstrual cycle.[69] Indicators favoring pelvic inflammatory disease included a history of vaginal discharge, urinary symptoms, prior pelvic inflammatory disease, tenderness outside the right lower quadrant, cervical motion tenderness, vaginal discharge, and positive urinalysis.


Ultrasonography is often very useful in the diagnosis of appendicitis, with a positive and negative predictive value of approximately 90%. However, in a meta-analysis of studies of ultrasound for appendicitis, Orr et al. concluded that ultrasound should not be used in the setting of a classic presentation for appendicitis due to a high false-negative rate.[70] The normal appendix is compressible with a diameter of <6 mm. When appendicitis is present, the appendix is typically fluid-filled, noncompressible, distended beyond 6 mm, and tender with focal compression.[34] The positive and negative predictive values of CT also exceed 90% (Table 8).[34] Although ultrasound is less expensive and more available that CT, ultrasound is also more operator dependent than CT.

III.G.4. Treatment

Surgical consultation should be immediately obtained when patients are suspected of having acute appendicitis.

III.H. Diverticular Disease

III.H.1. Clinical Features

Diverticulosis of the colon is quite common and is associated with aging and with decreased fiber intake. As most patients with diverticulosis are asymptomatic, one must use caution before attributing symptoms to diverticulosis. Patients with diverticulosis may complain of crampy discomfort, typically in the left lower quadrant, which is often associated with constipation or diarrhea. Physical exam often reveals tenderness over the left lower abdomen. When fever, leukocytosis, or rebound tenderness are present, diverticulitis should be suspected. A palpable inflammatory mass may be present and there is often a change in bowel habits (either constipation or diarrhea). In elderly patients, a high index of suspicion for diverticulitis is necessary as they may not have classic symptoms of diverticulitis. Diverticulitis is reported to occur in about 10-25% of persons with diverticulosis who are followed for more than 10 years. Most of these patients can be managed as an outpatient with oral antibiotics. Complications of diverticulitis include abscess formation, fibrosis, bowel obstruction, fistulization (e.g. to the bladder, vagina, or bowel), and peritonitis. Brisk, painless bleeding may be present.

III.H.2. Diagnosis

The diagnosis of diverticulitis can be facilitated with the use of ultrasound or CT. Barium enema should not be performed in the setting of acute symptoms in order to allow for resolution of some of the inflammatory process and to minimize the risk of perforation. Colonoscopy should likewise be avoided upon initial presentation. All patients should have colonic imaging with either barium enema or colonoscopy after an initial attack of diverticulitis has subsided in order to exclude tumors and other significant pathology.

III.H.3. Treatment

The medical treatment of diverticular disease is outlined in (Table 9). Surgery may be necessary for patients who fail medical therapy within 72 hours, patients with two or more episodes of diverticulitis, and immunocompromised patients. Some have recommended surgical treatment for those patients who have diverticulitis prior to age 40.[71,72] However, this recommendation has recently be challenged.[73] Surgical consultation should be obtained for patients with signs or symptoms of peritonitis or obstruction, or when an abscess is present.

III.I. Gallstone Disease

III.I.1. Biliary Colic

Classic biliary colic is characterized by a discrete episode of steady, severe pain, typically located in the epigastrium or right upper quadrant. It may radiate into the back or right scapular region but usually does not fluctuate, as implied by the term colic. In general, the pain comes on rapidly, lasts from 30 minutes to 3 hours, and then gradually subsides. Biliary colic is not associated with fever, leukocytosis, or acute peritoneal signs. The presence of these findings, or biliary pain that lasts for more than 4 to 6 hours, should raise suspicion for acute cholecystitis. On occasion, it is difficult to differentiate biliary colic from cardiac pain or other intraabdominal processes. Taking a careful history is absolutely critical because an accurate description of the quality and character of the pain often is the only criterion on which the decision to operate is based. Moreover, an ill-advised cholecystectomy for atypical or vague symptomatology often results in the postoperative recurrence of identical complaints.

True attacks of biliary pain should be distinguished from dyspeptic symptoms such as belching, epigastric burning, bloating, heartburn, flatulence and fatty food intolerance. These are nonspecific complaints and suggest other diagnoses, such as gastroesophageal reflux, peptic ulcer disease, or irritable bowel syndrome. Similarly, abdominal discomfort that is present day after day or is fleeting in nature (less than 10 to 15 minutes) should not be attributed to the presence of gallstones. Ultrasonographic findings of gallstones are shown in (figure 3A).

III.I.2. Acute Cholecystitis

Acute obstruction of the cystic duct by a stone leads to gallbladder distention and a host of potential injury-inducing mechanisms. Histologically, the findings range from edema, erythema, and mild mucosal inflammation to gross infiltration of the wall with polymorphonuclear neutrophils and evidence of frank necrosis and perforation.

On clinical presentation, patients with acute cholecystitis often complain of continuous upper abdominal pain and a history of similar, but self-limited, attacks in the past (i.e. biliary colic). They may be nauseated, but usually do not obtain pain relief by vomiting or changing positions. On examination, these patients typically have temperatures of 99 degrees to 100 degrees Fahrenheit and exhibit right subcostal tenderness and localized parietal pain because of progressive gallbladder inflammation. A classic Murphy’s sign may be elicited when the patient’s inspiration is abruptly halted as a result of contact of an inflamed gallbladder and the parietal peritoneum. Generalized rebound tenderness and an acute, rigid abdomen should raise suspicion for a perforation. Ultrasonic findings of acute cholecystitis are shown in figure 4.



III.I.3. Choledocholithiasis

III.I.3.a. Clinical Features

Choledocholithiasis, or stones in the common bile duct, are found in about 10-15 percent of patients with symptomatic gallstones. Most of these stones originate in the gallbladder and pass through the cystic duct into the common bile duct. Although some stones pass uneventfully into the duodenum, or reside in the duct without causing apparent symptoms, the natural history of common duct stones is much less benign than that of incidental stones found in the gallbladder. Obstruction in the distal duct or ampulla may give rise to serious complications of jaundice, cholangitis, or gallstone pancreatitis.

The term cholangitis refers to the presence of a bacterial infection behind an obstructed bile duct. Patients with cholangitis may have biliary pain, fever or chills, and jaundice (Charcot’s triad). Findings on examination often are less dramatic than the parietal pain and local tenderness of acute cholecystitis.

III.I.3.b. Diagnosis

The clinical diagnosis of choledocholithiasis can be quite difficult. Common laboratory features include elevated bilirubin, alkaline phosphatase, and AST. The common bile duct diameter may also be increased, though may be normal. Ultrasound may demonstrate choledocholithiasis, though the majority of stones are missed.[74] In a review of 1264 consecutive patients undergoing cholecystectomy, the presence or absence of choledocholithiasis was confirmed in 465 patients.[75] Important independent predictors of choledocholithiasis included bilirubin, common bile duct diameter, AST, alkaline phosphatase, and age. Blood cultures are commonly positive and the organisms found include E coli, Klebsiella, Enterobacter, Pseudomonas, Enterococci, and gut anaerobe species (15 percent).

III.I.3.c. Treatment

Some patients respond clinically to aggressive broad-spectrum antibiotic coverage and intravenous fluids. However, true cholangitis should be viewed as a medical emergency and the presence of hypotension, mental status changes or severe sepsis should prompt the immediate drainage of the biliary system by endoscopic sphincterotomy, percutaneous transhepatic drainage, or surgery.

III.I.4. Indications for Referral

III.I.4.a. Surgery

1.Patient with typical episode/s of biliary colic.
2.Evidence of acute cholecystitis

III.I.4.b. Gastroenterology

1. Diagnosis of biliary colic uncertain or equivocal.
2. Evidence of biliary obstruction
3. Clinical suspicion of cholangitis




III.J. Acute Pancreatitis

III.J.1. Diagnosis

Steady upper abdominal pain is the hallmark feature of acute pancreatitis. The pain often radiates to the back and may be associated with variable degrees of nausea and vomiting. On examination, the tenderness is localized to the epigastrium in mild cases and may be generalized with rigidity and guarding in severe cases.

The diagnosis of acute pancreatitis depends on the history and physical exam as well as confirmatory elevations in either amylase or lipase levels. If either enzyme is greater than 3 times the normal range, the diagnosis is virtually secure.[76] Levels below this are nonspecific and other intra-abdominal conditions as well as renal insufficiency may be the cause. Lipase levels are probably more specific than amylase levels and remain elevated for a longer period of time.[77] Absolute levels do not correlate with severity. Serum alanine aminotransferase (ALT) is the most useful liver blood test for the diagnosis of gallstone pancreatitis. ALT levels greater than three times normal are 95% specific for biliary pancreatitis but only 50% sensitive.[78] A combination of abdominal ultrasonography (US) and abnormal liver blood tests (ALT, bilirubin) offers the best accuracy.[79] An ultrasound to detect gallstones, sludge or dilation of the common bile duct should be a routine examination in all patients with an initial episode of acute pancreatitis.[80] The evaluation and management of acute pancreatitis has been recently reviewed.[81]

III.J.2. Etiology

III.J.2.a. Obstructive Causes of Acute Pancreatitis

1. Gallstones
Biliary sludge
Hemobilia

2. Ampullary obstruction
Carcinoma
Adenoma
Periampullary diverticulum
Sphincter of Oddi dysfunction

3. Other duodenal abnormalities
Stricture
Crohn's disease
Afferent loop obstruction
Pancreas divisum
Pancreatic duct stricture
Parasites (Ascaris, Clinorchis)

III.J.2.b. Toxic or Metabolic Causes of Acute Pancreatitis

1. Ethanol
2. Hypertriglyceridemia (>2000 mg/dl)
3. Hypercalcemia
4. Uremia
5. Drugs (see Table 12 Drugs associated w/ pancreatitis)

III.J.2.c. Miscellaneous Causes of Acute Pancreatitis

1. Trauma
2. Viral (mumps, coxsackie, CMV, hepatitis A, B, C)
3. Ischemia (hypoperfusion, vasculitis, emboli)
4. Penetrating ulcer
5. Post-procedural (ERCP, sphincterotomy)
6. Hypothermia
7. Choledochal cyst

III.J.3. Management

Several prognostic scoring systems have been developed to help identify the patient with severe pancreatitis (Ranson’s criteria (Table 5), Apache II , (Table 13) ). Ranson’s criteria (Table 5) are probably the most widely recognized signs. Severe pancreatitis is defined by having three or more criteria. Moreover, mortality has been shown to be approximately 10-20% in those individuals with 3-5 Ranson’s signs present and > 50% with 6 or more. Patients identified with severe pancreatitis should be aggressively supported in an intensive care setting with intravenous fluid support and monitoring of serum calcium. Prophylactic antibiotics such as imipenem or a fluoroquinolone should be administered.[80,82] If there is evidence of severe biliary pancreatitis of suspected gallstone origin or cholangitis then urgent ERCP should be performed.[80,82]

Dynamic CT imaging may be used to distinguish between interstitial and necrotizing pancreatitis. It is especially helpful in the patient who is not improving or when there is evidence of infectious complications. In this situation a CT guided fine needle aspiration directed at areas of fluid collection or necrosis should be performed to rule out pancreatic infection.

III.J.4. Complications

Pancreatitis may result in local and systemic complications. Local complications may include pancreatic necrosis (with or without infection) (figure 6), fluid collections and pseudocysts (figure 7), fistulas and pancreatic ascites. Systemic complications include shock, hypocalcemia, gastrointestinal hemorrhage, renal dysfunction, respiratory failure, and vascular thrombosis.

III.J.5. Reasons for GI referral:

1 Severe pancreatitis
2 Evidence of biliary pancreatitis

3 Suspected cholangitis






III.K. Chronic pancreatitis

III.K.1. Diagnosis

A deep, boring, upper abdominal pain often radiating to the back is the most typical feature of chronic pancreatitis. The pain may be partially relieved by sitting upright and leaning forward and is frequently exacerbated by eating meals. The pattern is quite variable with some individuals experiencing discrete episodes followed by pain free intervals, while others complain of nearly constant pain. Weight loss from anorexia and decreased caloric intake is often observed and may be profound in the advanced cases. Pancreatic exocrine insufficiency and steatorrhea or endocrine insufficiency leading to poorly controlled diabetes are also important factors. Alcohol use is the most common cause of chronic pancreatitis in the United States. Other causes of chronic pancreatitis include hereditary pancreatitis, obstructive chronic pancreatitis, tropical pancreatitis, and idiopathic pancreatitis.

Amylase and lipase levels may be elevated, particularly early in the clinical course or during discrete episodes or attacks. As the disease progresses, the magnitude of the enzyme levels diminish and often become normal in individuals complaining of constant unremitting pain. Distal bile duct obstruction from disease in the head of the pancreas may be reflected in a rise of serum bilirubin, alkaline phosphatase or transaminases.

Diabetes results when more than 80% of the gland is destroyed. Stool collections for 48 or 72 hours may demonstrate steatorrhea. Normal fecal fat is < 7g of fat excreted/24 hours on a 100 gm fat/day diet. Physiologic or pancreatic function studies such as the secretin stimulation or bentiromide tests are reliable only in those patients with advanced disease. Since these patients can usually be diagnosed by other means, functional studies are rarely used in routine clinical practice.

Plain films demonstrating calcifications in the region of the pancreas are virtually pathognomonic for chronic pancreatitis.(figure 8) These calcifications are intraductal in location and are most often observed in alcoholic or hereditary pancreatitis. Computed tomography, particularly helical CT, is superior to ultrasonography in imaging the pancreas. Mass lesions, fluid collections and pseudocysts, subtle calcifications, ductal dilatation may be seen. Complications such as splenic or portal vein thrombosis may also be demonstrated. ERCP is quite sensitive in assessing for pancreatic ductal abnormalities such as focal strictures, dilation or ectatic changes of the main duct and blunting of the side branches. Endoscopic ultrasound or EUS has been shown to have excellent sensitivity and specificity for chronic pancreatitis. Heterogeneity of pancreatic parenchymal echogenicity, along with dilatation of the ductal system are the key features and appear to be quite specific for chronic pancreatitis.

III.K.2. Treatment

III.K.2.a. Steatorrhea

Steatorrhea occurs when the pancreas is unable to produce sufficient lipase to digest dietary fat. This does not occur until pancreatic lipase is reduced to <10% of normal. Pancreatic enzyme supplementation with approximately 30,000 U of lipase per meal is an effective means of controlling steatorrhea. Either enteric-coated enzyme preparations should be used, or gastric acid should be suppressed with H2 blockers or proton pump inhibitors to prevent intragastric enzyme degradation.[83,84,85] If steatorrhea persists, a low fat diet with medium chain triglyceride supplementation may improve the symptoms.

III.K.2.b. Pain

The pain of chronic pancreatitis can be very difficult to manage. Abstention from alcohol use is critical, especially in patients with alcoholic chronic pancreatitis. Analgesics are often required to control pain due to chronic pancreatitis. A single provider should take responsibility for prescribing analgesia in order to minimize abuse. The use of a chronic pain clinic is often useful. The role of pancreatic enzyme supplementation for pain control is controversial and requires further study.[86,87] The use of octreotide to reduce pain is under study and cannot be recommended at this time. Endoscopic and surgical treatment may be appropriate for select patients.[88] The treatment of pain in chronic pancreatitis has been recently reviewed.[89]

III.K.3. Indications for GI referral

1. Etiology of chronic pancreatitis is unclear
2. Pain is severe or difficult to manage
3. Progressive weight loss
4. Complications including pseudocysts, biliary obstruction, splenic vein thrombosis, pancreatic ascites or fistula
5. Abdominal imaging showing either a dilated pancreatic duct or suggestion of a mass lesion.



III.L. Pancreatic Carcinoma

III.L.1. Epidemiology

In the U.S. approximately 29,000 new cases of pancreatic carcinoma are diagnosed each year.[90] It remains a lethal disease with only 3% of patients alive at 5 years.[91] Cigarette smoking, chronic pancreatitis and in particular hereditary pancreatitis appear to be associated with an increased frequency of pancreatic cancer.[92,93] Most patients are over age 60.

III.L.2. Clinical features

Symptomatic patients often complain of anorexia, weight loss, or abdominal pain. Jaundice and biliary obstruction may be present if the mass involves the head of the pancreas. Recently, a group of investigators showed that the presence of abdominal pain was a negative predictor of resectability and survival.[94]

III.L.3. Diagnosis and Staging

Helical CT imaging is gaining widespread acceptance for diagnosis and staging of pancreatic carcinoma (figure 9). It has a reported accuracy of 77%, 58%, and 79% for determination of the T(tumor), N(node), and M(metastasis) stage.[95] Moreover, a grading system to determine unresectability demonstrated sensitivities and specificities of 84% and 98% when greater than half the circumference of a major visceral vessel (SMA, SMV, portal vein, celiac or hepatic arteries) was involved with tumor.[96] There is some debate regarding the necessity of a CT guided fine needle aspiration (FNA) for preoperative diagnosis of carcinoma. Some pancreatic surgeons believe that if the history and blood test abnormalities suggest carcinoma and the helical CT demonstrates a resectable mass in the head of the pancreas, then the patient should be prepared for an operation.[97]

The role of endoscopic ultrasound (EUS) continues to be defined. It appears to offer more accurate detection of smaller than 3cm lesions, better lymph node staging, and determination of major venous involvement that precludes complete surgical resection.[98] In addition it offers the potential for diagnostic fine needle aspiration.[99] EUS is operator dependent and has not been widely available.

Endoscopic retrograde cholangiopancreatography (ERCP) should be performed particularly if the bile or pancreatic ducts are dilated and no discrete mass is seen by CT imaging (figure 10). Periampullary lesions may be endoscopically identified and biopsied. Alternatively a focal irregular pancreatic duct stricture or cutoff consistent with a small pancreatic mass may be demonstrated. Ductal brushings for cytology and/or molecular marker studies may enhance the diagnostic accuracy.

Palliative therapy is available for relief of jaundice, duodenal obstruction, and pain control. In jaundiced patients who are unresectable, ERCP and biliary stent decompression offers the least invasive form of palliation. For duodenal obstruction, laparoscopic surgical bypass or endoscopic duodenal stent placement should be considered. Pain due to pancreatic carcinoma can often be controlled with narcotic analgesia. However, a celiac plexus block can be performed for refractory pain.

III.L.4. Treatment

Surgical resection offers the only chance for longterm survival. Unfortunately, only 10-15% are truly resectable at the time of the diagnosis. Moreover, the best results suggest that no more than 20% of those who are resected for cure will be alive at 5 years.[100,101]

To date only one randomized trial of adjuvant chemoradiation following potential resection for cure has been published. A modest increase in survival was documented.[102] Gemcitabine, a novel nucleoside analogue, appears to offer a small improvement in survival as well as quality of life for those with unresectable cancer.[103]

III.L.5. Indications for GI Referral

1 Evaluation of obstructive jaundice
2 Dilated bile and/or pancreatic ducts without a discrete mass lesion
3 CT evidence of a potentially resectable pancreatic mass lesion





III.M. Renal Stones (Nephrolithiasis)

III.M.1. Clinical Presentation

Urinary tract obstruction causes pain as a result of distention of the collecting system or renal capsule. The rate at which distention occurs, rather than the degree of distention, determines the degree of pain, which can often be quite severe. Patients with nephrolithiasis usually present with flank pain. This pain is typically constant and steady, in contrast to intestinal pain, though it can be cramping or colicky. The pain often radiates to the lower abdomen initially, then includes the testes or labia as the stone moves distally. Nausea and vomiting are commonly present. The patient is typically uncomfortable appearing and restless, with costovertebral angle tenderness and abdominal tenderness. Signs of peritonitis should be absent.

III.M.2. Diagnosis

In patient with nephrolithiasis, urinalysis usually reveals microscopic or gross hematuria, though it may be absent in up to 10% of patients. Pyuria is variably present. An abdominal radiograph may show the location of the stone, as 90% of stones are radio-opaque. According to a study of 288 patients with intractable flank pain, the combination of a plain film of the abdomen with an ultrasound to identify the presence of a calculus in the renal-urinary tract has a positive predictive value of 100% and a negative predictive value of 81%.[32] See (Table 10) for the test characteristics of plain film, ultrasound, and the combination compared to the gold standard of an intravenous urogram. Unenhanced helical CT has also been shown to be an excellent test for the identification of ureteral stone disease. In a study of 417 patients with acute flank pain, CT had a 95% sensitivity, 98% specificity and 97% accuracy.[35] These authors recommend unenhanced CT for patients with flank pain and either no history of stone disease, or a history of stone disease with no visible stone on abdominal radiograph. The differential diagnosis of renal colic includes dissection of the aorta, musculoskeletal pain and malingering.

III.M.3. Treatment

Patients with nausea and vomiting may be unable to maintain adequate hydration and require admission to the hospital for management. Urologic consultation should be obtained when fever is present (suggesting proximal infection); when there is evidence of complete ureteral obstruction with a nonfunctioning kidney; when the patient has a solitary kidney; when there is evidence of extravasation of urine; or for stones larger than 7 mm, as spontaneous passage is unlikely.[104] Other patients may be managed conservatively with oral hydration. The urine should be screened in an attempt to recover the stone. Narcotic analgesics and antiemetics are usually required. If the stone has not passed within 6 weeks, urologic consultation should be obtained.

III.M.4. Indications for Urologic Consultation

  1. Fever (suggesting proximal infection)
  2. Evidence of complete ureteral obstruction with a nonfunctioning kidney
  3. Solitary kidney
  4. Evidence of extravasation of urine
  5. Stone over 7mm
  6. Failure of stone to pass within 6 weeks
III.N. Pyelonephritis

III.N.1. Clinical Features

Patients with pyelonephritis typically present with flank pain, fever, abdominal pain, and symptoms of bladder irritation (urgency, dysuria, and frequency). Fever and chills are often present. Physical examination will usually reveal costovertebral angle tenderness.

III.N.2. Diagnosis

Urinalysis reveals bacteria, white blood cells, nitrite and leukocyte oxidase. The presence of white cell casts is diagnostic of pyelonephritis. A urine culture should also be obtained.

III.N.3. Treatment

The presence of pyelonephritis in men suggests a structural abnormality and should prompt an immediate investigation, including ultrasound and urologic consultation. Hospitalization is usually indicated. If an abscess is suspected, a CT scan should be obtained. For otherwise healthy women, pyelonephritis can be managed as an outpatient with a 10-14 day course of oral antibiotics. Close follow-up is mandatory. The antibiotic should be adjusted according to the culture results. Inpatient management is required for acutely ill patients, unreliable patients, pregnant patients, or patients with significant comorbidity.[105]

III.O. Gynecological Problems

III.O.1. Adnexal Torsion

III.O.1.a. Clinical Presentation

Abdominal pain may result from pathology of the ovaries and fallopian tubes. When a pathologic disease results in abnormal enlargement of the adnexa, there is increased risk of twisting of the adnexa along the axis of the infundibulopelvic ligament.[106] Common causes of torsion include an enlarged functional ovarian cyst or neoplasm, though some patients have grossly normal adnexa. Although torsion can occur at any age, it is most common in women of reproductive age.

Patients with adnexal torsion typically present with abrupt onset of severe, unilateral, lower quadrant pain with associated nausea and vomiting.[106] The character of the pain is usually sharp, though it can be colicky in nature. The pain may wax and wane as the torsion is intermittently relieved or in the case of partial torsion, causing decreased vascular flow but not thrombosis.[107] Fever is not a typical feature, and may suggest an alternate diagnosis. Also, the white blood cell count is not predictive of adnexal torsion. However, fever and leukocytosis may develop when necrosis or infection of the adnexa occurs.

III.O.1.b. Diagnosis

Unfortunately, there is no diagnostic test or study that can make a definitive diagnosis, short of surgical exploration. Ectopic pregnancy should be ruled out with a pregnancy test. Pelvic examination typically reveals a tender, unilateral mass. However, when the patient has torsion in the setting of a grossly normal adnexa, the mass will not be present until edema has set in. Therefore, serial examinations may be required.[106] Color Doppler sonography and CT have been shown to be useful in making the diagnosis of adnexal torsion.[108,109]

III.O.1.c. Treatment

Due to the risk of adnexal infarction, torsion is a surgical emergency. Surgical exploration, typically laparoscopically, is diagnostic and allows for definitive therapy. Many cases can be conservatively managed with unwinding of the adnexa. Viability is then assessed and only gangrenous adnexa are resected. The risk of retorsion is very low when the cause is found and treated.[110] Therefore, ovariopexy is not routinely needed.

III.O.2. Ectopic Pregnancy

III.O.2.a. Epidemiology

For unclear reasons, the number of ectopic pregnancies increased four-fold from 17,800 in 1970 to 88,000 in 1989.[111] This corresponds to approximately 1 in 200 pregnancies. Fortunately, the mortality has decreased, possibly due to early detection and intervention.[106] Risk factors for ectopic pregnancy include previous laparoscopically proven pelvic inflammatory disease (PID), previous tubal pregnancy, current intrauterine device use, and previous tubal surgery.[112] When pregnancy occurs in a patient who has undergone a tubal ligation, 10% to 50% are ectopic.[113]

III.O.2.b. Clinical features

When a ruptured tubal pregnancy occurs, the clinical presentation can be quite subtle or may be dramatic, including an acute abdomen or hemorrhagic shock.[106] Patients will often complain of abrupt onset of lateralized pelvic pain. The pain may initially be dull and cramping in nature. Hemoperitoneum may develop, with resultant shoulder pain from diaphragmatic irritation, an urge to defecate, and syncope. Most patients will have a history of menstrual abnormality. Other symptoms of pregnancy may be present as well, such as breast tenderness.

III.O.2.c. Diagnosis

The diagnosis of ectopic pregnancy is based upon a positive beta-hCG test and ultrasonography. More than 95% of patients with ectopic pregnancies will have a positive urine hCG test.[114] Endovaginal ultrasonography is more sensitive for the diagnosis of ectopic pregnancy than transabdominal scanning. Ultrasound can also identify other conditions in the differential diagnosis, such as blighted ovum or threatened abortion.[106] Other diagnostic aids include suction curettage, culdocentesis, and laparoscopy. Although laparoscopy is the gold standard, 3% of ectopic pregnancies will be missed with this approach.[106]

III.O.2.d. Treatment

Patients with suspected ectopic pregnancy should be managed with the assistance of an obstetrician/gynecologist. A laparoscopic approach is appropriate for hemodynamically stable patients, as this is both diagnostic and therapeutic. Hemodynamically unstable patients may require emergency laparotomy. There is no role for medical therapy for the treatment of a ruptured ectopic pregnancy.[106] Conservative tube-sparing surgery may be possible for women desiring to retain fertility.[112] Medical therapy with the antineoplastic agent methotrexate is an option for the treatment of early, unruptured ectopic pregnancy.[115]

III.O.3. Pelvic Inflammatory Disease, Salpingitis and Tubo-Ovarian Abscess


Detailed information from the Centers for Disease Control regarding the management of sexually transmitted diseases, including pelvic inflammatory disease (PID) is available on the world wide web at www.cdc.gov/epo/mmwr/preview/mmwrhtml/00050909.htm.

III.O.3.a. Epidemiology

Pelvic inflammatory disease (PID) and acute salpingitis result in substantial morbidity in America, including more that 350,000 annual hospital admissions and 150,000 annual surgical procedures.[116] Complications of PID include pelvic abscess, ectopic pregnancy, salpingitis isthmica nodosa, tubal infertility, chronic pelvic pain, and pelvic adhesions.[106] The term pelvic inflammatory disease encompasses many conditions, including endometritis, salpingitis, tubo-ovarian abscess, and pelvic peritonitis.[117] Most cases result from sexually transmitted organisms, especially N. gonorrhoeae and C. trachomatis, though upwards of 50% of cases of clinically diagnosed PID are culture negative. A single episode of acute salpingitis can result in infertility in 13% of patients.[118] Tubo-ovarian abscess (TOA) is the most serious condition associated with salpingitis, with a mortality rate of 8.6% if rupture occurs.[119] PID and TOA result from bacteria in the upper female genital tract, usually associated with sexually transmitted disease or instrumentation of the uterus. The rate of PID progressing to TOA has been reported to be between 1% and 4%.[120] Pelvic inflammatory disease is usually polymicrobial, including both anaerobic and aerobic bacteria.[121]

III.O.3.b. Clinical Features

The typical symptoms of PID begin soon after menstruation and include fever, nausea, and abdominal pain.[122] Physical exam is notable for cervical motion tenderness and, in some cases, adnexal enlargement. Although most women with TOA will have fever and leukocytosis, 20-30% of women are afebrile and a significant proportion have a normal white blood cell count.[123] If rupture of a TOA occurs, signs and symptoms of peritonitis will result and may progress to shock and death if not appropriately managed.[106]

III.O.3.c. Diagnosis

The diagnosis of PID is inexact. A clinical diagnosis of symptomatic PID has a positive predictive value for salpingitis of 65%-90% in comparison with laparoscopy.[117] Some authors feel that PID should not be diagnosed in the absence of objective evidence of infection (e.g. leukocytosis or a positive cervical culture) as the diagnosis of PID may prejudice the patient's future care.[124] However, in order to decrease the rate of untreated PID, the Center for Disease Control and Prevention has published minimum criteria necessary to institute antibiotic therapy for suspected PID.[125] The four minimum criteria (all of which need to be present) for the diagnosis of PID are shown in (Table 11).[117] Women presenting with PID and a palpable pelvic mass may have a TOA or other adnexal process, such as an hydrosalpinx. Ultrasonography is very useful in establishing the diagnosis of TOA, although the "gold standard" remains laparoscopy.[126]

III.O.3.d. Treatment

Hospitalization is recommended for patients with the following criteria:[117]
  1. Surgical emergencies such as appendicitis cannot be excluded;
  2. The patient is pregnant;
  3. The patient does not respond clinically to oral antimicrobial therapy;
  4. The patient is unable to follow or tolerate an outpatient oral regimen;
  5. The patient has severe illness, nausea and vomiting, or high fever;
  6. The patient has a tubo-ovarian abscess; or
  7. The patient is immunodeficient (i.e., has HIV infection with low CD4 counts, is taking immunosuppressive therapy, or has another disease).

Commonly used treatments for PID in the ambulatory setting include:[117]

1. Ceftriaxone 250 mg IM, one dose, or Cefoxitin (Mefoxin), 2gm IM, one dose with Probenecid 1 gm orally,
plus Doxycycline, 100 mg orally twice a day for 14 days,

2. Ofloxacin, 400 mg orally two times a day for 14 days, plus Metronidazole 500 mg orally, two times a day for 14 days.

3. Trovafloxacin, 200mg daily for 14 days
[127].

Inpatient treatment regimens include the following:[117]

1. Cefoxitin 2 g IV every 6 hours or cefotetan 2 g IV every 12 hours, and Doxycycline 100 mg IV or orally every 12 hours,

2. Gentamicin 2 mg/kg IV or IM as an initial dose followed by 1.5 mg/kg every 8 hours, and Clindamycin 900 mg IV every 8 hours.

Patients with TOA may be managed with medical therapy in many cases. Inpatient management is appropriate to insure an adequate response to therapy. Some cases will require a drainage procedure (e.g. CT directed drainage). However, surgical intervention is appropriate to prevent septic shock and potential death in the following situations:[106]

1. Questionable diagnoses, when another surgical emergency may exist (e.g. appendicitis)
2. Rupture of an abscess
3. Failure of medical therapy

III.O.4. Endometriosis

III.O.4.a. Epidemiology

Endometriosis is the presence of ectopic foci of endometrial tissue. The pathophysiologic process by which endometriosis causes pain is not well understood. Many patients with endometriosis are asymptomatic.[128] In fact, during laparoscopic tubal ligation, between 15%-43% of asymptomatic women are found to have endometriosis.[128,129] Nevertheless, endometriosis is one of the most common indications for hysterectomy in the United States.[130]

III.O.4.b. Clinical features

The clinical features of endometriosis may include pelvic pain, tenderness, or dyspareunia. The pain classically is described as dysmenorrhea with pelvic pain and dyspareunia.[130] The cyclic nature with exacerbation before and during menses suggests an hormonal influence. Although some patients may experience pain throughout the cycle, constant or non-cyclic pain suggests another etiology.

III.O.4.c. Diagnosis

Endometriosis may be suspected on the basis of clinical presentation and response to therapy. However, surgical exploration remains the standard diagnostic approach, as other conditions (e.g. dysmenorrhea) may respond similarly to therapy directed at presumed endometriosis. The diagnosis of endometriosis may be reliably established based upon the visual characteristics seen during laparoscopy, without the need for histologic confirmation.[131] In a clinical commentary on endometriosis, Hurd proposed three criteria necessary for the attribution of chronic pelvic pain to endometriosis.[130]

  1. Cyclic pain
  2. Endometriosis must be diagnosed surgically
  3. Appropriate treatment of endometriosis results in prolonged pain relief
III.O.4.d. Treatment

Endometriosis may be treated with medical therapy, surgical therapy, or a combination. Medical therapy generally consists of hormonal therapy in order to induce either pseudopregnancy (e.g. progesterone or continuous oral contraceptive drugs) or pseudomenopause (e.g. danazol). Surgical management may range from laser vaporization of endometriosis to total abdominal hysterectomy with bilateral salpingo-oophorectomy.

III.P. Inflammatory Bowel Disease

III.P.1. Ulcerative Colitis

III.P.1.a. Etiology and Pathophysiology

Ulcerative colitis is caused by an immune process causing inflammation in the large intestine. Inflammation involves only the mucosal lining, typically begins at the anus, and extends for a variable distance proximally. It does not involve the small intestine.

III.P.1.b. Clinical Presentation

Patients with ulcerative colitis present with some combination of diarrhea, bloody stools, and abdominal pain. They may also have the symptom of tenesmus which is a feeling of urgency often not accompanied by a significant bowel movement. This is a sign of rectal inflammation. Pain is typically cramping and in the lower abdominal midline. It is usually relieved by a bowel movement. Uncommonly patients without pre-existing colitis or those with a history of ulcerative colitis may present with a dilated colon and severe illness. This condition has been called toxic megacolon and is an indication for hospitalization and intensive management.

III.P.1.c. Diagnosis

The diagnosis of ulcerative colitis is usually confirmed with sigmoidoscopy that shows confluent inflamed tissue to the level of the anus. Biopsies of the involved mucosa show distortion of the crypt architecture. Biopsies can distinguish ulcerative colitis from infectious colitis.

III.P.1.d. Treatment

Most patients are managed with 5-aminosalicylic acid derivatives. More severe cases require immunosuppressive therapy with prednisone or azathioprine. Patients with active disease uncontrolled by medications benefit from total proctocolectomy. Bowel continuity can be restored through creation of an ileal J-pouch, with an anastamosis to the anus.

III.P.2. Crohn's Disease

III.P.2.a. Etiology and Pathophysiology

Crohn's Disease is another type of idiopathic inflammatory bowel disease that can involve the small and large bowel. Unlike ulcerative colitis, the inflammation goes through the entire wall of the bowel. The rectum may be spared and in fact there may be patchy or skipped areas of involvement throughout the intestinal tract. The etiology is unknown although inflammatory mediators are likely involved.

III.P.2.b. Clinical Presentation

Patients with Crohn's Disease may have symptoms of intestinal inflammation or obstruction. Inflammation typically leads to diarrhea which may be watery or bloody. The active inflammatory component may also lead to cramping, periumbilical or infraumbilical pain. With ongoing inflammation, there may be malabsorption with weight loss. Thick and inflammed bowel may obstruct and present with signs of intestinal obstruction. Patients may also have intra-abdominal abscesses or present with extraintestinal manifestations such as arthritis, uveitis, and erythema nodosum.

III.P.2.c. Treatment

Patients with predominantly large intestinal involvement may be managed with 5-aminosalicylyc acid derivatives such as for the management of ulcerative colitis. Some patients need to be managed with immunosuppresants. This usually begins with oral prednisone. Long-term prednisone is associated with significant side effects and can be avoided with other immunosuppresant medications such as azathioprine. A recently approved biologic therapy, Infliximab, has been shown to be an effective treatment for fistulas. The monocronal antibody against TNF Alpha may also have a role in the longterm treatment of refractory Crohn's disease. Many patients with Crohn's disease require surgery for treatment of obstruction or focal strictures. In general, surgery should be avoided as much as possible to prevent the development of short bowel syndrome.

IV. Conclusion/Principles on When to Refer

In this review, we have attempted to outline a general approach to the patient with abdominal pain. Our algorithms are based upon a strategy of first ruling out catastrophic causes of abdominal pain. Thereafter, we have stratified the causes of pain according to the chronicity of symptoms, followed by the pain location. This approach is based upon expert opinion and has not been formally assessed. The reader should exercise clinical judgment in all cases, especially as atypical presentations are not uncommon.

Our recommendations for referral to specialists are also based upon expert opinion. While some primary care providers may be trained and qualified to manage more complicated cases, others are not. All providers should understand their own limitations and utilize consultants in the best interest of their patients.