History

In the timeless treatise on abdominal pain bearing his name,

first published in 1921, Sir Zachary Cope tells us, “It can be
confidently asserted that a large number, if not the majority, of
acute abdominal conditions could be diagnosed by considering
carefully the history of onset.”15 Despite the advances made
in clinical imaging in the century since then, history taking
remains the most important component of the initial evaluation of the patient with acute abdominal pain. Characteristic
features of pain associated with various common causes of
acute abdominal pain are shown in Table 11.2. Attention to
these features can lead to a rapid clinical diagnosis or exclusion of important diseases in the differential diagnosis, thereby
enhancing the reliability and effectiveness of subsequent diagnostic testing. For example, plain abdominal films are most
efficacious when limited to patients with symptoms of intestinal obstruction.

Comparison of Common Causes of Acute Abdominal Pain

Cause Onset Location Character Descriptor Radiation Intensity
Appendicitis Gradual Periumbilical area early; RLQ late Diffuse early;
localized later
Aching None ++
Cholecystitis Acute Mid-epigastrium, RUQ, right scapula Localized Constricting Scapula ++
Pancreatitis Acute Epigastrium, T10-L2 area of the back Localized Boring Midback ++ to +++
Diverticulitis Gradual LLQ Localized Aching None ++ to +++
Perforated peptic ulcer Sudden Epigastrium Localized early,
diffuse later
Burning None +++
SBO Gradual Periumbilical area Diffuse Cramping None ++
Mesenteric ischemia, infarction Sudden Periumbilical area Diffuse Agonizing None +++
Ruptured abdominal aortic
aneurysm
Sudden Abdomen, back, flank Diffuse Tearing None +++
Gastroenteritis Gradual Periumbilical area Diffuse Spasmodic None + to ++
Pelvic inflammatory disease Gradual Either LQ, pelvis Localized Aching Upper thigh ++
Ruptured ectopic pregnancy Sudden Either LQ, pelvis Localized Sharp None ++
+, mild; ++, moderate; +++, severe; LQ, lower quadrant

Chronology
The time courses of several common causes of acute abdominal pain
are diagrammed in Fig. 11.5. The rapidity of onset of pain is often a
measure of the severity of the underlying disorder. Pain that is sudden
in onset, severe, and generalized is likely to be the result of an intraabdominal catastrophe such as a perforated viscus, mesenteric
infarction, or ruptured aneurysm. Affected patients usually recall the exact
moment of onset of their pain. Progression is an important temporal factor in abdominal pain. In some disorders (e.g.,
gastroenteritis),
pain is self-limited, whereas in others (e.g., appendicitis), pain is progressive. Pain associated with obstruction has a repeating
crescendodecrescendo pattern that may be diagnostic particularly when it occurs
in association with nausea and vomiting. The duration of abdominal
pain is also important. Patients who seek evaluation of abdominal
pain that has been present for an extended period (e.g., weeks) are less
likely to have an acute life-threatening illness than patients who present within hours to days of the onset of their symptoms.
Location
The location of abdominal pain provides a clue to interpreting
the cause. As noted earlier, a given noxious stimulus may result
in a combination of visceral, somatic-parietal, and referred pain,
thereby creating confusion in interpretation unless the neuroanatomic pathways are considered. For example, the pain of
diaphragmatic irritation from a left-sided subphrenic abscess may be
referred to the shoulder and misinterpreted as pain from ischemic
heart disease (see Fig. 11.4). Pain radiating to the back from pancreatic or biliary pathology may be conflated with
musculoskeletal processes, thereby delaying treatment. Changes in location
may represent progression from visceral to localized parietal peritoneal irritation, as with appendicitis, or represent development
of diffuse peritoneal irritation, as with a perforated ulcer.
Intensity and Character
Acute abdominal pain usually follows one of three patterns.
Pain that is prostrating and physically incapacitates the sufferer
is usually due to a severe life-threatening disease like a perforated viscus, ruptured aneurysm, or severe pancreatitis. By contrast,
patients with obstruction of a hollow viscus, as in intestinal
obstruction, renal colic, or biliary pain, present with gradual
onset of cramping pain that follows a sinusoidal pattern of intense
pain alternating with a period of relief. Nausea and vomiting are
characteristic symptoms associated with this group of disorders.
The obstructed viscus need not be the intestine for nausea or
vomiting to occur, as in the case of a kidney stone. The third
pattern is of gradually increasing discomfort, usually vague and
poorly localized at the start but becoming more localized as the
pain intensifies. This picture is usually due to inflammation, as
with acute appendicitis or diverticulitis. Some disorders, such as
acute cholecystitis, may start out as colicky pain but evolve into
a constant pain as cystic duct obstruction leads to gallbladder
inflammation. The clinician should be cautious in assigning too
much importance to a patient’s description of the pain; exceptions are common, and a given descriptor may be attributable to
a number of conditions. Symptoms in the elderly can be subtle
despite the presence of life-threatening pathology, making this
group particularly challenging.
Aggravating and Alleviating Factors
The relationship of pain to positional changes, meals, bowel
movements, and stress may yield important diagnostic clues.
Patients with peritonitis lie motionless, whereas those with renal
colic may writhe in an attempt to find a comfortable position.
Sometimes, certain foods exacerbate pain. A classic example is the
relationship between the intake of fatty foods and development of
biliary pain. Pain associated with duodenal ulcer is often alleviated by meals. By contrast, patients with gastric ulcer or chronic
mesenteric ischemia may report exacerbation of pain with eating. Patients often self-medicate to alleviate symptoms. A history
of chronic antacid or NSAID use, for example, may suggest the
presence of PUD. This is a growing consideration as patients
and physicians increasingly rely on NSAIDs as alternatives to
opioids for chronic pain.
Associated Symptoms
Information regarding changes in constitutional symptoms (e.g.,
fever, chills, night sweats, weight loss, myalgias, arthralgias),
digestive function (e.g., anorexia, nausea, vomiting, flatulence,
diarrhea, constipation), jaundice, dysuria, changes in menstruation, and pregnancy should be solicited from the patient. A careful
review of these symptoms may reveal important diagnostic
information. Clear vomitus suggests gastric outlet obstruction,
whereas feculent vomitus suggests more distal small bowel or
colonic obstruction. A constellation of findings may indicate a
particular disease entity.
Past Medical History
A careful review of the patient’s other medical problems often
sheds light on the presentation of acute abdominal pain. Previous
experience with similar symptoms suggests a recurrent problem.
Patients with a history of partial SBO, renal calculi, or pelvic
inflammatory disease are likely to have recurrences. A patient
whose presentation suggests intestinal obstruction, and who
has no prior surgical history, deserves special attention because
of the likelihood of surgical pathology such as a hernia or neoplasm. Patients with a systemic illness, such as scleroderma, SLE,
nephrotic syndrome, porphyria, or sickle cell disease, often have
abdominal pain as a manifestation of the underlying disorder.
Abdominal pain may also arise as a side effect of a medication
taken for another disease.
Severity
B
CA
Time
D
Fig. 11.5 Patterns of acute abdominal pain. A, Many causes of
abdominal pain subside spontaneously with time (e.g., gastroenteritis). B, Some pain is colicky (i.e., the pain progresses and remits over
time); examples include intestinal, renal, and biliary pain (colic). The
time course may vary widely from minutes in intestinal and renal pain
to days, weeks, or even months in biliary pain. C, Commonly, acute
abdominal pain is progressive, as in acute appendicitis or diverticulitis.
D, Certain conditions have a catastrophic onset, such as a ruptured
abdominal aortic aneurysm.
150 PART III Symptoms, Signs, and Biopsychosocial Issues
Physical Examination
The physical examination of the patient with acute abdominal
pain begins with an assessment of the patient’s appearance and
assessment for signs of sepsis or shock, as described earlier. The
patient’s ability to converse, breathing pattern, position in bed,
posture, degree of discomfort, and facial expression should be
noted. A patient lying still in bed in the fetal position and reluctant to move or speak, with a distressed facial expression, is likely
to have peritonitis. A patient who writhes and frequently changes
position has purely visceral pain, as in intestinal obstruction or
gastroenteritis. Tachypnea may be a sign of metabolic acidosis
caused by shock. Atrial fibrillation noted on physical examination or an electrocardiogram may suggest mesenteric arterial
embolus. All patients should undergo a careful systematic examination regardless of the differential diagnosis suggested by the
history.
Abdominal Examination
Examination of the abdomen is central to evaluating a patient with
acute abdominal pain and should begin with careful inspection.
The entire abdomen, from the nipple line to the thighs, should
be exposed. Obese patients should be asked whether the degree of
protrusion of the abdominal wall is greater than usual. Asthenic
patients may feel themselves to be distended but have relatively
little apparent abdominal protrusion. Assessment for the presence of bowel sounds and their character should precede any
maneuvers that will disturb the abdominal contents. Before concluding that an abdomen is silent, the examiner should listen for
at least 2 minutes and in more than one quadrant of the abdomen.
Experienced listeners may distinguish the high-pitched churning
of a mechanical SBO from the more hollow sounds of toxic megacolon (like dripping in a cavern). Nevertheless, some studies
have
cast doubt on the reliability of bowel sound assessment in patients
with SBO and other conditions,17 and clinicians should avoid basing clinical decisions too heavily on assessment of bowel
sounds.
Auscultation may, however, be a good way to assess tenderness.
When listening with the stethoscope, the astute clinician may
begin to palpate the abdomen with the head of the stethoscope
while carefully watching the patient’s facial expression. If tenderness is detected, an assessment for rebound tenderness should be
carried out next to look for evidence of peritonitis. Rebound tenderness may be elicited by jarring the patient’s bed or stretcher or
by finger percussion. Palpation is performed next. If pain is emanating from one particular region, that area should be palpated
last to detect involuntary guarding and muscular rigidity. Patients
with a rigid abdomen rarely reveal any additional findings (e.g.,
a mass) on physical examination. Because these patients usually
have a surgical emergency, abdominal examination can be done
more completely once the patient is under anesthesia, just before
laparotomy.
Genital, Rectal, and Pelvic Examinations
The pelvic organs and external genitalia should be examined in
every patient with acute abdominal pain. The rectum and vagina
provide additional avenues for gentle palpation of pelvic viscera.
Gynecologic pathology should be excluded in all women with
acute abdominal pain.
Laboratory Data
The history and physical examination findings generally are
not sufficient to establish a firm diagnosis in a patient with
acute abdominal pain. All patients with acute abdominal pain
should have a CBC, with a differential count, and urinalysis. Determination of serum electrolyte, blood urea nitrogen,
creatinine, and glucose levels is useful for assessing the patient’s
fluid and acid-base status, renal function, and metabolic state and
should be done for every patient with acute abdominal pain who
presents to an emergency department. Urine or serum pregnancy
testing must be performed in all women of reproductive age with
abdominal pain. Liver biochemical tests and serum amylase or
lipase levels should be ordered for patients with upper abdominal
pain or with jaundice.
Leukocytosis, particularly when associated with band forms,
is an important finding. Metabolic acidosis, an elevated serum
lactate level, or depressed bicarbonate levels are associated with
tissue hypoperfusion and shock. Patients who manifest these findings are likely to require urgent surgical intervention or
intensive
care.
Imaging Studies
CT
The development of high-speed helical CT has revolutionized
the evaluation of acute abdominal pain. In many conditions,
such as appendicitis, CT can almost eliminate diagnostic uncertainty. In the pre-CT era, history taking and physical examination
alone had a specificity of approximately 80%; by contrast,
the sensitivity and specificity of CT for acute appendicitis are
94% and 95%, respectively. A negative CT in the setting of
acute abdominal pain has considerable value in excluding common disorders.
The question arises as to whether CT should be a standard
part of the evaluation in all patients with acute abdominal pain.
Several arguments against routine CT have been raised.18 First,
CT can be performed in a number of ways, and the most efficacious method must be chosen in any given clinical setting.
For example, a patient with suspected renal colic should have
a limited, non–contrast-enhanced, renal calculus protocol CT;
obtaining a standard oral and IV contrast CT in this case may
obfuscate rather than illuminate the pathology. Alternatively, a
patient in whom arterial occlusive disease is suspected should
undergo CT arteriography using a bolus IV contrast technique.
A radiologist should be consulted regarding selection of the
most appropriate CT study in a given patient. Second, some
diseases, such as acute cholecystitis and cholangitis, are not
optimally imaged by CT. A patient with RUQ pain who is suspected of having either of these diagnoses should undergo a US
of the RUQ as the primary diagnostic test. Third, as noted earlier, a patient who is unstable or exhibits signs of shock should
be evaluated by a surgeon before any imaging study is considered. In a patient with suspected trauma or hemoperitoneum,
the focused abdominal sonogram for trauma (FAST; see later),
which can be done at the bedside in the emergency department,
is a preferable approach. The presence of shock and fluid in
the abdomen is an indication for immediate laparotomy, and
further diagnostic maneuvers, including CT, add little value to
the patient’s care.
A final consideration regarding the role of CT in evaluating acute abdominal pain is radiation exposure. Particularly
for patients younger than 35 years of age and those who have
required multiple examinations, abdominal CT may increase the
lifetime risk of cancer.18 Additionally, unless a life-threatening
condition is suspected, CT is best avoided in a pregnant patient,
in whom MRI is a suitable alternative.19

US
FAST is a rapid, reliable, bedside test to detect fluid in the
abdominal cavity. Although its main usefulness is for the evaluation of injured persons, this examination also aids in the
diagnosis of any condition that results in free intraperitoneal fluid;

imaging of the aorta can be added, allowing a rapid assessment

for aortic aneurysm. Point-of-care abdominal US has become
a routine and highly reliable part of the evaluation of acute
abdominal pain.20
Other Diagnostic Tests
Other diagnostic imaging modalities like MRI and radionuclide
scanning (e.g., 99mTc-labeled hydroxyl iminodiacetic acid [HIDA]
scan) and endoscopy usually take a secondary role in the evaluation of the patient with acute abdominal pain. Use of these tests
is generally guided by the results of CT or US. Angiography may
be useful not only for establishing a diagnosis of visceral ischemia
but also for delivering therapy aimed at improving or re-establishing blood flow. Diagnostic peritoneal lavage, although seldom
used now, is useful when a patient is too unstable from a cardiopulmonary standpoint to tolerate imaging studies. The finding
of leukocytes in the lavage effluent in an unstable patient may,
in extreme circumstances, constitute sufficient grounds for laparotomy. In a patient who is unstable and deteriorating and has
signs of an acute abdomen, laparotomy as a diagnostic maneuver
should be considered if imaging is considered prohibitively risky.
An overall approach to the patient with acute abdominal pain is
illustrated in Fig. 11.6.
CAUSES
Acute abdominal pain is usually defined as pain of less than 1 week
in duration. Patients usually seek attention within the first 24 to
48 hours, although some may endure longer periods of abdominal discomfort. The most common reason for a patient to seek
emergency department evaluation of abdominal pain is so-called
nonspecific abdominal pain; between 25% and 50% of all patients
who visit an emergency department for abdominal pain will have
no specific disease identified. The distribution of the causes of
abdominal pain in patients who present to an emergency department is shown in Table 11.3.
Acute Appendicitis
Acute appendicitis is a ubiquitous problem, accounting for approximately 5% of all emergency department visits for patients
under
65 years of age21 and 30% of acute surgical abdominal emergencies in patients under 50 years of age worldwide.22 Appendicitis
accounted for 318,000 hospital admissions in the USA in 2006,23
and has an overall incidence of approximately 82 to 110/100,000
population in North America.24 The lifetime risk of appendicitis
is 8.6% for males and 6.7% for females in Western countries,25
and may be twice this risk in Asia.26

Typically, acute appendicitis begins with prodromal symptoms

of anorexia, nausea, and vague periumbilical pain. Within 6 to 8
hours, the pain migrates to the right lower quadrant and peritoneal
signs develop. In uncomplicated appendicitis, a low-grade fever to
38°C and mild leukocytosis are usually present. A higher temperature and WBC count are associated with perforation and
abscess
formation. Common features of the history, physical examination,
and WBC count in patients with appendicitis have been combined
into a predictive tool known as the Alvarado score (Table 11.4).27
For men, a score of 4 or less accurately excludes appendicitis; the
score is less useful in women and children.28 Atypical presentations of acute appendicitis, however, are common, and a diagnosis
of acute appendicitis should not be rejected simply on the basis of
the patient’s history and physical examination alone. An Appendicitis Inflammatory Response score has also been proposed. 29
In children, mesenteric adenitis (or lymphadenitis) is frequently
mistaken for acute appendicitis but is often preceded by a sore
throat and is self-limited. Mesenteric adenitis may also be caused
by Yersinia enterocolitica (see Chapter 110).
Whereas plain abdominal films are not diagnostic and have little role in the diagnosis of acute appendicitis, CT has dramatically
improved the accuracy of diagnosis in patients with acute appendicitis. An appendix diameter greater than 10 mm is generally
considered diagnostic of appendicitis, although the normal range
for the diameter of the appendix may extend to nearly 13 mm.30
Other CT signs of acute appendicitis include periappendiceal fat
inflammation, presence of fluid in the RLQ, and failure of contrast
dye to fill the appendix.31 The addition of CT has reduced the
negative appendectomy rate to about 5%.32 Because CT entails
radiation exposure,18 some authorities advocate avoiding CT in
children and adolescents,33 in whom a higher degree of diagnostic
uncertainty is tolerated in favor of lower radiation exposure (see
Chapter 120). In this setting, US of the appendix has a sensitivity
of 0.86 and specificity of 0.81 for detecting acute appendicitis.34 In
a pregnant patient in whom radiation exposure is also a significant
concern, MRI has become the imaging method of choice, with a
sensitivity and specificity approaching those of CT.35
Acute Biliary Disease
Biliary disease accounts for approximately 7% of visits to an
emergency department for abdominal pain and 14% to 21% of
admissions for patients over 65 years of age.21, 22 Affected patients
generally present at some point on the spectrum between biliary
pain (“biliary colic”) and acute cholecystitis. Biliary pain is a syndrome of RUQ or epigastric pain, usually postprandial, caused
by
transient obstruction of the cystic duct by a gallstone; it is selflimited, generally lasting less than 6 hours. Acute cholecystitis is,
in most cases, caused by persistent obstruction of the cystic duct
by a gallstone. The pain of acute cholecystitis is almost indistinguishable from that of biliary pain, except that it is persistent.
The pain usually is a dull ache that is localized to the RUQ or
epigastrium with radiation around the back to the right scapula.
Nausea, vomiting, and low-grade fever are common. On examination, RUQ tenderness, guarding, and Murphy sign (inspiratory
arrest on palpation of the RUQ) are typical. The WBC count
is usually mildly elevated but may be normal. Mild elevations in
serum total bilirubin and alkaline phosphatase levels are common.
The role of gallstones in the etiology of biliary pain and acute
cholecystitis makes US of the RUQ the key diagnostic test. Demonstration of gallstones may suggest biliary pain, whereas the
finding of stones with gallbladder wall thickening, pericholecystic
fluid, and pain on compression of the gallbladder with the ultrasound probe (sonographic Murphy sign) is essentially diagnostic
of acute cholecystitis and has replaced hepatobiliary scintigraphy
(e.g., HIDA scan) in the diagnosis of acute cholecystitis.36 US,
while sensitive for the presence of stones, has been found to have
poorer sensitivity (73.4%) and specificity (85.5%) for the detection of acute cholecystitis.37 Consideration of imaging findings in
the context of the physical examination and laboratory findings
is essential for accurate diagnosis. The Tokyo consensus criteria
for the diagnosis of acute cholecystitis are shown in Table 11.5.
Patients with acute cholecystitis are best managed with cholecystectomy within 48 hours.38,39 Patients who are older and
tachycardic and have ultrasonographic evidence of gallbladder wall
thickening, particularly those with a WBC count greater than
13,000/mm3, are at higher risk for gangrenous cholecystitis and
generally require emergent open cholecystectomy.40,41
Patients who present with RUQ pain, jaundice, and signs of
sepsis should be suspected of having obstruction of the bile duct
by a gallstone. RUQ pain, fever and chills, and jaundice (Charcot
triad) are suggestive of ascending cholangitis.42 These patients
require IV fluids, antibiotics, and bile duct drainage, usually by
endoscopy (see Chapters 65, 66, 67, and 70).
SBO
Intestinal obstruction is a common cause of abdominal pain in
both the developed and developing world22 and occurs in patients
of all ages. In pediatric patients, intussusception, congenital malformations such as malrotation and Meckel diverticulum are the
most common causes.43 In adults, about 70% of cases are cause

by postoperative adhesions; incarcerated hernias, IBD, and

malignancies make up most of the remainder.44,45 SBO is characterized by sudden, cramping, periumbilical abdominal pain.
Nausea and vomiting occur soon after the onset of pain and provide temporary relief of discomfort. Physical examination reveals
an acutely ill, restless patient. Fever, tachycardia, and signs of
volume contraction, including orthostatic hypotension, are common. Abdominal distention is common but may be difficult to
discern in the setting of obesity. Although auscultation in patients
with SBO is frequently thought to be characterized by hyperactive bowel sounds and audible rushes, these signs are unreliable. 17
The patient’s abdomen may be diffusely tender to percussion and
palpation, although the physical examination may be unremarkable even in the presence of visceral distress. Peritoneal signs
should be considered a sign of intestinal ischemia or perforation.
Leukocytosis and lactic acidosis suggest intestinal ischemia or
infarction.
Plain films of the abdomen are diagnostic when they reveal
dilated loops of small intestine with air-fluid levels and decompressed distal small bowel and colon. 46 Plain abdominal films
can be misleading in a patient with proximal jejunal obstruction, because dilated bowel loops and “air-fluid levels” may be
absent. CT is superior for establishing the diagnosis and location
of intestinal obstruction. The presence of reduced bowel wall
enhancement in the setting of other findings of SBO significantly
increases the probability of strangulation; a lack of free abdominal fluid significantly decreases the probability of strangulation. 47
Other findings, such as a transition point, are not reliable predictors of ischemia or the need for intervention. 47
In patients with SBO who have reassuring physical examinations and laboratory findings, initial treatment is with bowel rest,
IV fluids, nasogastric decompression, and close observation.48,49
For patients with SBO who are admitted for a trial of nonoperative management, many centers administer 120 mL of dilute
imaging contrast material by mouth or nasogastric tube. The
appearance of the contrast in the cecum within 12 hours predicts resolution of obstruction.50 Surgery is required for patients
who fail conservative management or have evidence of complete
obstruction, especially if ischemia is suspected, but patients with
adhesive SBO require surgery in fewer than 20% of cases (see
Chapter 123).48,50
Acute Diverticulitis
Acute diverticulitis is a common disease. Approximately 80% of
affected patients are older than 50 years of age.51 The overall
incidence of the disease has increased by as much as 50%, with
an even greater increase in younger persons.52,53 Patients with
diverticulitis usually present with constant, dull LLQ pain and
fever. They may complain of constipation or obstipation and
are usually found to have a leukocytosis. Physical examination
demonstrates LLQ tenderness and, in some cases, a LLQ mass.
Localized peritoneal signs are frequent. In severe cases, generalized peritonitis may be present, making differentiation from
other causes of a perforated viscus difficult. CT is reliable in confirming the diagnosis, with a sensitivity of 97%, 54 and should be
performed routinely in the emergency evaluation of patients with
diverticulitis.
Acute diverticulitis presents as a spectrum of disease from
mild abdominal discomfort to gross fecal peritonitis, which is
an acute surgical emergency. The severity of diverticulitis, as
determined by CT, is best described using the Hinchey grading
system (see Table 121.2 in Chapter 121). Patients with mild disease and no CT findings of perforation, in the absence of limiting
comorbid disease, can generally be treated as outpatients.
Those with Hinchey grade I diverticulitis (localized pericolic
abscess or inflammation) frequently require hospitalization for
IV antibiotics. Patients with Hinchey grade II diverticulitis (pelvic, intra-abdominal, or retroperitoneal abscess) should undergo
CT-guided drainage of the abscess and receive a course of broadspectrum IV antibiotics. Patients with Hinchey III (generalized
purulent peritonitis) and IV (generalized fecal peritonitis) diverticulitis frequently require emergency surgery (see Chapter 121).
Despite the descriptive utility of grading systems for diverticulitis, there is little evidence to support their predictive value in
deciding between surgical and medical management.55 Patients
presenting with significant abdominal pain or tenderness benefit
from early surgical consultation.
Acute Pancreatitis
Hospital admissions for acute pancreatitis in the USA seem to
be increasing.56 Acute pancreatitis typically begins as acute pain
in the epigastrium that is constant, unrelenting, and frequently
described as boring through to the back or left scapular region.
Fever, anorexia, nausea, and vomiting are typical. Patients with
pancreatitis are usually more comfortable sitting upright, leaning forward slightly. Physical examination reveals an acutely ill
patient in considerable distress. Patients are usually tachycardic
and tachypneic. Abdominal examination reveals hypoactive
bowel sounds and marked tenderness to percussion and palpation in the epigastrium. Abdominal rigidity is a variable finding.
In rare patients, flank or periumbilical ecchymoses (Grey-Turner
or Cullen sign, respectively) develop in the setting of pancreatic necrosis with hemorrhage. Extremities are often cool and
cyanotic, reflecting underperfusion. WBC counts of 12,000 to
20,000/mm3 are common. Elevated serum and urine amylase levels are usually present within the first few hours of pain; serum
lipase is also elevated. Depending on the cause and severity of
pancreatitis, serum electrolyte, calcium, and blood glucose levels
and liver biochemical test and arterial blood gas results may be
abnormal. US is useful for identifying gallstones as a potential
cause of pancreatitis. CT is reserved for patients with severe or
complicated pancreatitis.57
Although most cases of acute pancreatitis are self-limited, as
many as 20% of patients have severe disease with local or systemic
complications, including hypovolemia and shock, renal failure,
liver failure, and hypocalcemia. A number of prognostic physiologic scales (e.g., the SOFA and APACHE II scores) have been
advocated as measures of the severity of acute pancreatitis.58 The
Ranson score, first published in 1974, remains a useful and widely
used checklist for the early assessment of patients with acute pancreatitis.59 The Ranson score consists of 5 early and 6 late
factors
that indicate severe pancreatitis (see Table 58.2). A simpler bedside index of the severity of acute pancreatitis (BISAP),
consisting

of blood urea nitrogen greater than 25 mg/dL, impaired mental status, systemic inflammatory response syndrome, age older
than 60 years, and pleural effusion, has also proved useful.60 The
Atlanta classification system for acute pancreatitis has great utility for bedside decision making. 61 Patients without organ failure
or local or systemic complications are classified as mild and may
be treated expectantly. Moderately severe acute pancreatitis is typified by organ failure of less than 48 hours’ duration. When
organ
failure persists for more than this time, or affects multiple organ
systems, severe acute pancreatitis is present. Patients in this last
group usually require multidisciplinary care in an intensive care
unit. A minority of patients with severe acute pancreatitis present
with a profound intra-abdominal catastrophe, usually caused by
thrombosis of the middle colic artery or right colic artery, which
travel in proximity to the head of the pancreas, with resulting
colonic infarction. This process may not be seen clearly on CT
obtained early in the course of disease and should be suspected in
any case marked by rapid hemodynamic collapse. Such patients
require immediate laparotomy (see Chapter 58).
Perforated Peptic Ulcer
As many as 4 million people worldwide are affected by PUD. Of
these, as many as 5% present with perforation.62 The epidemiology of PUD is changing (see Chapter 53). The incidence of Hp
infection has decreased dramatically since the late 1990s.63 The
overall incidence of PUD has declined by as much as half, and the
number of patients requiring hospital admission for severe and
complicated PUD has also decreased.22 Improved therapeutic
modalities, including PPIs, eradication of Hp (see Chapter 52),
and endoscopic methods for control of hemorrhage (see Chapter
20), have reduced the number of patients with PUD who require
surgical intervention,64 although the frequency of complicated
disease has increased in older adults, in whom morbidity and
mortality related to surgery are also increased.65 The author’s
anecdotal experience suggests that the switch from opioids to
NSAIDs in response to the epidemic of substance use disorder
has resulted in an increasing frequency of perforated PUD in
younger patients.
Patients with a perforated peptic ulcer typically present with
the sudden onset of severe diffuse abdominal pain. These patients
may be able to specify the precise moment of the onset of symptoms. In the usual case, the afflicted patient presents acutely with
excruciating abdominal pain, often without prodromal symptoms. Abdominal examination reveals peritonitis, with rebound
tenderness, guarding, and abdominal muscular rigidity. In such
cases, distinguishing perforated ulcer from other causes of a perforated viscus (e.g., perforated colonic diverticulum, perforated
appendicitis) may not be possible. Older or debilitated patients
may present with less dramatic symptoms, with perforation identified by the presence of free intraperitoneal air on an upright
abdominal film or CT.
A perforated peptic ulcer should be suspected in any patient
with the sudden onset of severe abdominal pain who presents
with abdominal rigidity and free intraperitoneal air. Pneumoperitoneum is detected on an abdominal film in 75% of patients (Fig.
11.7). In equivocal cases, CT of the abdomen usually suggests the
diagnosis by demonstrating edema in the region of the gastric
antrum and duodenum, associated with extraluminal air. CT may
not be diagnostic, however, and patients with diffuse peritonitis
or hemodynamic collapse should be explored surgically. Laparotomy is acceptable as the primary diagnostic maneuver in such
patients. Endoscopy is not advisable when the diagnosis of a perforated peptic ulcer is suspected; insufflation of the stomach can
convert a sealed perforation into a free perforation. Survival following emergency surgery for complications of PUD is
surprisingly poor. Implementation of evidence-based practice modeled
on the Surviving Sepsis Guidelines in Denmark reduced the 30-day
mortality rate from 30% to 25% in patients with a perforated
peptic ulcer.66 The 2-year mortality rate in these patients was
over 40% (see also Chapter 53).
Acute Mesenteric Ischemia
Acute mesenteric ischemia can result from occlusion of a mesenteric vessel as a result of an embolus, which may emanate from
an atheroma of the aorta or cardiac mural thrombus, or primary
thrombosis of a mesenteric vessel, usually at a site of atherosclerotic stenosis. Embolic occlusion had accounted for up to
50% of cases of mesenteric ischemia in the 1980s but, because
of advances in the management of risk factors for embolization,
accounts for no more than one third of cases in the 2010s. It most
commonly affects the superior mesenteric, presumably because
of the less acute angle of the superior mesenteric artery origin
from the abdominal aorta.67 Atherosclerotic stenosis of the mesenteric vessels can result in primary arterial thrombosis. Patients
usually have a history of atherosclerotic disease, particularly in
the coronary or cerebrovascular circulation. Primary thrombosis
now accounts for up to 68% of cases of mesenteric ischemia.67
Nonocclusive mesenteric ischemia results from inadequate visceral perfusion and can also lead to intestinal ischemia and
infarction; such cases are usually consequent to critical illnesses like
cardiogenic or septic shock. Nonocclusive mesenteric ischemia,
also referred to as “low-flow” mesenteric ischemia, accounts for
10% of cases. The remaining 10% of cases of mesenteric ischemia
result from venous thrombosis, usually associated with a thrombophilia, and focal segmental ischemia of the small intestine (see
Chapter 118). Because most cases of mesenteric ischemia occur in
patients with significant cardiovascular comorbidities, outcomes
are poor. Perioperative mortality ranges from 50% to nearly
100%.67,68
The hallmark of the diagnosis of acute mesenteric ischemia is
the abrupt onset of intense cramping epigastric and periumbilical
pain out of proportion to the findings on abdominal examination.
Other symptoms may include diarrhea, vomiting, bloating, and
melena. On physical examination, most patients appear acutely
ill, but the presentation may be subtle. Shock is present in about
25% of cases.
CT angiography is the best initial diagnostic test for suspected
acute mesenteric ischemia. Mesenteric angiography may be useful for determining the cause of intestinal ischemia and defining
Fig. 11.7 Upright chest film of an 80-year-old man with the acute
onset of severe epigastric pain demonstrating free intra-abdominal air
under the right hemidiaphragm. The patient has pneumoperitoneum
as a result of a perforated viscus. At surgery, perforation of an anterior
duodenal ulcer was found.
CHAPTER 11 Acute Abdominal Pain 155
11
the extent of vascular disease; however, CT has largely replaced

formal angiography in these cases. Patients with acute embolic or

thrombotic intestinal ischemia should be referred for immediate
revascularization and bowel resection.69 Patients with nonocclusive
mesenteric ischemia are best managed by treatment of the underlying shock state. For patients with persistent symptoms,
laparotomy
for resection of infarcted intestine may be necessary. Transcatheter
vasodilator therapy may be helpful for patients who are found to
have vasospasm on visceral arteriography (see Chapter 118).
Abdominal Aortic Aneurysm
Rupture of an abdominal aortic aneurysm (AAA) is heralded by
the sudden onset of acute, severe abdominal pain localized to the
midabdomen or paravertebral or flank areas. The pain is tearing in
nature and associated with prostration, lightheadedness, and diaphoresis. If the patient survives transit to the hospital, shock is the
most common presentation. Physical examination reveals a pulsatile, tender abdominal mass in about 90% of cases. The classic
triad
of hypotension, a pulsatile mass, and abdominal pain is present in
75% of cases and mandates immediate surgical intervention.69 In
patients with a suggestive history, emergency department US is a
reliable method for the diagnosis of AAA in patients in shock and
is sufficient evidence for emergency intervention. Endovascular
methods for repair of an AAA have resulted in improved outcomes,
although the short-term mortality rate is 40%.70 Patients with suspected rupture of an AAA require urgent vascular surgery
consultation to maximize the probability of survival.
Abdominal Compartment Syndrome
Although not usually presenting as acute abdominal pain, abdominal compartment syndrome (ACS) warrants consideration in
any
patient with an abdominal emergency. First reported in the setting of massive intra-abdominal trauma, ACS, defined as
pathologic elevation of intra-abdominal pressure, is now recognized as
a frequent complication of many severe disease processes.71 The
peritoneal cavity normally has a pressure of 5 to 7 mm Hg; it
may be higher in obese persons.72 An elevated intra-abdominal
pressure may develop in a patient who survives massive volume
resuscitation with resulting visceral edema or who has a disease
like severe pancreatitis that can cause visceral or retroperitoneal
edema. Intra-abdominal hypertension (IAH) is defined as abdominal pressure of 12 mm Hg or higher.71 Elevation of intra-
abdominal pressure that compromises visceral perfusion defines ACS.
The kidney is particularly prone to underperfusion in this setting,
and renal failure may be the first sign of ACS.73
Primary ACS is defined as ACS that arises from pathology
within the peritoneal cavity, such as gastric distention or edema
from acute pancreatitis.71 More common is secondary ACS, in
which massive bowel wall edema secondary to shock is responsible for IAH. A third form, tertiary ACS, or recurrent ACS,
results from overzealous attempts at abdominal wound closure
after management of primary or secondary ACS.72 Risk factors
for ACS are listed in Box 11.1.
Intra-abdominal pressure can be measured simply by connecting a transducer to a urinary catheter, with the zero-reference
point at the midaxillary line in a supine patient. An international
consensus conference has established a grading scheme for ACS,
shown in Table 11.6, based on the measured bladder pressure.74
A normal value for bladder pressure is less than 7 mm Hg. Grade
I ACS is defined as a pressure of 12 to 15 mm Hg, grade II as
16 to 20 mm Hg, grade III as 21 to 25 mm Hg, and grade IV as
greater than 25 mm Hg. Nonsurgical options for treating lowgrade ACS include gastric decompression, sedation, neuromuscular
blockade, placing the patient in a reverse Trendelenburg
position while allowing the hips to remain in a neutral position,
and diuretics. In a patient with high-grade ACS, particularly when

enal or respiratory function is compromised, laparotomy with

creation of an open abdomen is most effective.75 Management
of the open abdomen requires specific surgical expertise usually
found in referral medical centers. Fortunately, the frequency of
ACS has declined substantially in the 2000s, owing to increased
awareness of the syndrome and advances in resuscitation.72,76
Other Intra-abdominal Causes
Other intra-abdominal causes of acute abdominal pain include
gynecologic conditions (e.g., endometritis, acute salpingitis with

or without tubo-ovarian abscess, ovarian cysts or torsion, ectopic pregnancy); SBP (Chapter 93); functional dyspepsia (Chapter
14); infectious gastroenteritis (Chapters 110 to 112); viral hepatitis and other liver infections (Chapters 78 to 84); pyelonephritis;
cystitis; mesenteric lymphadenitis; IBD (Chapters 115 and 116);
and other bowel disorders such as IBS (Chapter 122) and intestinal pseudo-obstruction (Chapter 124). Vascular compromise
of an epiploic appendage due to axial torsion can result in epiploic appendigitis.77,78 This syndrome can imitate appendicitis,
diverticulitis, or other pathologies but has a self-limited natural
history and usually requires only symptomatic management with
NSAIDs.78 The diagnosis is best confirmed by demonstration of
an inflamed ovoid fatty mass adjacent to a noninflamed segment
of the colon on CT.79
Extra-abdominal and Systemic Causes
Acute abdominal pain may arise from disorders involving extraabdominal organs and systemic illnesses. Examples are listed in
Box 11.2. Surgical intervention for patients with acute abdominal
pain arising from an extra-abdominal or systemic illness is seldom
required except in cases of pneumothorax, empyema, and esophageal perforation. Esophageal perforation may be iatrogenic,
result from blunt or penetrating trauma, or occur spontaneously
(Boerhaave syndrome; see Chapter 45).
Angioedema is characterized by acute, self-limited edema of
the dermis, subcutaneous tissue, mucosa, and submucosa. The
edema may affect the skin of the face, usually around the mouth,
tongue, throat, extremities, and genitalia. Involvement of the GI
tract may cause acute episodes of colicky pain, sometimes accompanied by nausea, vomiting, and diarrhea. Mast-cell mediated
angioedema, often caused by allergic reactions to foods, drugs,
or insect stings, is characterized by urticaria, flushing, pruritus,
throat tightness, bronchospasm, and hypotension. Bradykinininduced angioedema is not associated with these symptoms, has
a more prolonged course, and is less clearly associated with an
identifiable trigger, although angiotensin-converting enzyme
inhibitor therapy is a known cause. Bowel wall angioedema can
be seen in patients on angiotensin-converting enzyme inhibitors
and in those with hereditary or acquired deficiency or dysfunction of C1 inhibitor and can be visualized on abdominal US or
CT. Treatment of an attack depends on the acuity and severity
and may include airway and hemodynamic support, discontinuation of potential triggers, antihistamines, glucocorticoids, and,
in cases of hereditary angioedema, use of purified C1 inhibitor
concentrate, a kallikrein inhibitor, and a bradykinin B2 receptor
antagonist.
Special Circumstances
Extremes of Age
Evaluation of acute abdominal pain in patients at the extremes
of age is a challenge. Historical information and physical examination findings are often difficult to elicit or are unreliable.
Similarly, laboratory data may be misleadingly normal in the
face of serious intra-abdominal pathology. For these reasons,
patients at the extremes of age are often diagnosed late in the
course of the disease, thereby resulting in increased morbidity.
For example, the perforation rate for appendicitis in the general
population averages 10% but exceeds 50% in infants. The presentation of acute abdominal conditions is highly variable in these
populations, and a high index of suspicion is required. A carefully
obtained history, thorough physical examination, and high index
of suspicion are the most useful diagnostic aids.
In the pediatric population, the causes of acute abdominal pain
vary with age. In infancy, intussusception, pyelonephritis, gastroesophageal reflux, Meckel diverticulitis, and bacterial or viral
enteritis are common. In children, Meckel diverticulitis, cystitis,
pneumonitis, enteritis, mesenteric lymphadenitis, and IBD are
prevalent. In adolescents, pelvic inflammatory disease, IBD, and
the common adult causes of acute abdominal pain predominate.
In children of all ages, two of the most common causes of pain
are acute appendicitis and abdominal trauma secondary to child
abuse.
In the older adult population, biliary tract disease accounts for
almost 25% of cases of acute abdominal pain and is followed in
frequency by nonspecific abdominal pain, malignancy, intestinal
obstruction, complicated PUD, and incarcerated hernia. Appendicitis, although rare in older patients, usually manifests late in its
course and is associated with high morbidity and mortality rates.

PREGNANCY

he gravid woman with acute abdominal pain presents a difficult

diagnostic dilemma. Acute appendicitis and cholecystitis develop
in pregnant women at the same rates as in their nonpregnant
counterparts. A number of additional diagnoses, such as placental abruption and pain related to tension on the broad ligament,
must be distinguished from nonobstetric diagnoses. The risk of
radiation injury to the developing fetus must be considered when
imaging studies are planned.
Surgery in pregnancy is not rare; approximately 1 in 500
pregnancies will be associated with a nonobstetrical general
surgical intervention.80 Primary consideration is given to the
health of the mother. Emergency interventions during pregnancy carry a risk of fetal loss that varies with gestational age
and the type of intervention. The middle 3 months of gestation
are preferable for abdominal surgical intervention; this period
presents the lowest risk for teratogenicity and spontaneous
labor.
Appendicitis occurs in about 1 in 2000 pregnancies and is
equally distributed among the three trimesters. In later stages of
pregnancy, the appendix may be displaced cephalad, with consequent displacement of the signs of peritoneal irritation away from
McBurney point. US or, in challenging cases, MRI may be useful
for establishing a diagnosis in this setting. Biliary tract disease is
also common during pregnancy. Open or laparoscopic management of these diseases is safe but is associated with adverse
obstetrical outcomes in approximately 5% of cases.81
Immunocompromised Hosts
In addition to diseases like appendicitis and cholecystitis that
occur in the general population, a number of diseases unique to
immunocompromised hosts may manifest with acute abdominal pain: neutropenic enterocolitis, drug-induced pancreatitis,
graft-versus-host disease, pneumatosis intestinalis, and CMV
and fungal infections (see Chapter 36). Patients infected with
HIV can present a particular challenge (see Chapter 35). When