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% 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 singlecontrast 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



Elevated liver blood tests
Ultrasound evidence of biliary obstruction

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 1015% 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 radioopaque. 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 salpingooophorectomy.
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 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. 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.