Download Abdominal Pain Referral Guidelines

Abdominal Pain
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%
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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
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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]
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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
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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 workup 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
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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, nondiagnostic, 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
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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
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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
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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
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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
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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
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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)
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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.
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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.
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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-midabdominal 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.
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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.
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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
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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.
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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).
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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
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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
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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
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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
●
●
Elevated liver blood tests
Ultrasound evidence of biliary obstruction
3 Suspected cholangitis
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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.
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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
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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
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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
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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.
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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.
2.
3.
4.
5.
6.
Fever (suggesting proximal infection)
Evidence of complete ureteral obstruction with a nonfunctioning kidney
Solitary kidney
Evidence of extravasation of urine
Stone over 7mm
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
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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
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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]
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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
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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.
2.
3.
4.
5.
6.
7.
Surgical emergencies such as appendicitis cannot be excluded;
The patient is pregnant;
The patient does not respond clinically to oral antimicrobial therapy;
The patient is unable to follow or tolerate an outpatient oral regimen;
The patient has severe illness, nausea and vomiting, or high fever;
The patient has a tubo-ovarian abscess; or
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
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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
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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
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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 5aminosalicylyc acid derivatives such as for the management of ulcerative colitis. Some patients
need to be managed with immunosuppresants. This usually begins with oral prednisone. Longterm 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.
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