Tintinalli's Emergency Medicine > Section 9: Gastrointestinal Emergencies > Chapter 72.
Acute Abdominal Pain >
Scope and Definitions
Acute abdominal pain is commonly defined as pain of less than 1 week's duration.1 This
chapter discusses nontraumatic acute abdominal pain in postpubescent males and
females. Abdominal pain in women in the third trimester of pregnancy or the first month
postpartum is discussed in Chaps. 102, 105.
Epidemiology
Data from the U.S. National Center for Health Statistics indicate that stomach and
abdominal pain was the principal reason offered by patients for visiting EDs in 2000
(annual incidence approximately 63/1000 ED visits).2 Admission rates for abdominal
pain vary markedly, ranging from 18 to 42 percent, with rates as high as 63 percent
reported in patients over 65 years of age.
Pathophysiology
Abdominal pain is traditionally divided into three categories: visceral, parietal, and
referred. In general, visceral (autonomic) and parietal (somatic) are considered the two
basic causes of abdominal pain. Referred pain can be considered separately as a cortical
misperception of either visceral or parietal afferent stimuli. Although each type of pain is
thought to have a different neuropathophysiology, the categories are not entirely discrete.
For example, visceral pain often blends with parietal pain as a pathologic process
evolves. Still, these distinctions are clinically useful ways of thinking about abdominal
pain.
Visceral Pain
Visceral abdominal pain is usually caused by stretching of fibers innervating the walls or
capsules of hollow or solid organs, respectively. Less commonly, it is caused by early
ischemia or inflammation. Severity ranges from a steady ache or vague discomfort to
excruciating or colicky pain. Because the visceral afferents follow a segmental
distribution, visceral pain can be localized by the sensory cortex to an approximate spinal
cord level determined by the embryologic origin of the organ involved. For example,
foregut organs (stomach, duodenum, biliary tract) produce pain in the epigastric region;
midgut organs (most small bowel, appendix, cecum) cause periumbilical pain; and
hindgut organs (most of colon, including sigmoid) as well as the intraperitoneal portions
of the genitourinary tract cause pain initially in the suprapubic or hypogastric area.
Because intraperitoneal organs are bilaterally innervated, stimuli are sent to both sides of
the spinal cord, causing intraperitoneal visceral pain to be felt in the midline, independent
of its right- or left-sided anatomic origin. For example, stimuli from visceral fibers in the
wall of the appendix enter the spinal cord at about T10. When obstruction causes
appendiceal distention in early appendicitis, pain is initially perceived as midline
periumbilical area, corresponding roughly to the location of the T10 cutaneous
dermatome.
Parietal Pain
Parietal or somatic abdominal pain is caused by irritation of fibers that innervate the
parietal peritoneum, usually the portion covering the anterior abdominal wall. Because
parietal afferent signals are sent from a specific area of peritoneum, parietal pain—in
contrast to visceral pain—can be localized to the dermatome superficial to the site of the
painful stimulus. As the underlying disease process evolves, the symptoms of visceral
pain give way to the signs of parietal pain, causing tenderness and guarding. As localized
peritonitis develops further, rigidity and rebound appear.
Referred Pain
Referred pain is felt at a location distant from the diseased organ. Similar to visceral pain,
and in contrast to parietal pain, referred pain produces symptoms, not signs. Unlike
visceral pain, referred pain is usually ipsilateral to the involved organ and is felt in the
midline only if the pathologic process is also located in the midline. This is because
referred pain, in contrast to visceral pain, is not mediated by fibers providing bilateral
innervation to the cord. Similar to visceral pain, referred pain patterns are based upon
developmental embryology. For example, the ureter and the testes were once
anatomically contiguous, and therefore share the same segmental innervation, supplying
afferent fibers to the lower thoracic and upper lumbar segments of the spinal cord. Thus
acute ureteral obstruction is often associated with ipsilateral testicular pain. Other sites of
referred pain reflect similar dermatomal sharing, providing explanations for otherwise
puzzling associations, e.g., supra- or subdiaphragmatic irritation and ipsilateral
supraclavicular or shoulder pain; gynecologic pathology and back or proximal lower
extremity pain; biliary tract disease and right infrascapular pain; and myocardial ischemia
and midepigastric, neck, jaw, or upper extremity pain.
Clinical Features
Conceptual Framework
Classification
The classification scheme divides abdominal pain into two main categories:
Intraabdominal (i.e., arising from within the abdominal cavity or retroperitoneum) and
extraabdominal. Intraabdominal causes are divided by organ system into the "3-G's": GI
(gastrointestinal), GU (genitourinary), and GYN (gynecologic), plus a fourth, less
common but often catastrophic group of VASCULAR emergencies. Each of these four is
further subdivided into specific diagnoses within that organ system. Pain of
extraabdominal origin, which is substantially less common, is similarly divided into four
broad etiologic categories of cardiopulmonary, abdominal wall, toxic-metabolic, and
neurogenic. A systematic evaluation is necessary in the assessment of acute abdominal
pain.
Finally, nonspecific abdominal pain (NSAP), which is the most common cause of
abdominal pain among ED patients, is listed as a third category. Nonspecific abdominal
pain stands alone since it is not known to what extent it may represent an underlying
intra- vs. extraabdominal problem.
Abdominal Topography
By combining the four-quadrant approach traditionally used by U.S. physicians with
selected aspects of a strategy widely employed throughout Europe and Asia, a simple
model of abdominal topography can be developed. In addition to the four standard
quadrants (RUQ, RLQ, LUQ, LLQ), this model includes four areas of the abdomen that
are not discrete, but rather constitute combinations of all or part of two or more
quadrants: (1) upper half of abdomen (UHA), which includes an area of pain as small as
the mid-epigastrium, or as large as the RUQ + LUQ combined; (2) lower half of abdomen
(LHA), which similarly includes an area of pain as small as the midhypogastrium or as
large as the RLQ + LLQ combined; (3) central (CTL), which includes an area of pain
composed of the centermost "quarters" of all four discrete quadrants, such that carving
out these areas from each quadrant defines a periumbilical or central quadrant; and (4)
generalized (GEN), which includes poorly localized pain encompassing much, perhaps
most, of the abdomen, including at least some portion of all four discrete quadrants.
This topographic configuration incorporates both the early (visceral, poorly localized)
and late (parietal, better localized) pain of an evolving intraabdominal pathological
process, as well as the more generalized pain associated with toxic-metabolic
derangements.
However, the association between the location of overlying pain or tenderness and
underlying disease is so variable that about one case of abdominal pain in every three that
comes to operation presents in a fashion that clinicians retrospectively regard as atypical.
Failure to appreciate this may represent the largest single reason that error in the clinical
diagnosis of abdominal pain is so common.
Historical Features
Historical data can be conveniently divided into attributes of pain, associated symptoms,
and past history.
Pain Attributes
The principal characteristics of abdominal pain include location, quality, severity, onset,
duration, aggravating and alleviating factors, and change in any of these features over
time.
Associated Symptoms
These can be subdivided into one of the four main organ systems associated with
intraabdominal pain.
Gastrointestinal Symptoms
Anorexia, nausea, and vomiting (unless bloody) are among the least helpful symptoms in
altering the conditional probability that a patient does or does not have a GI cause of
abdominal pain. For example, vomiting has been reported in over 40 percent of patients
with salpingitis, and in over 60 percent of patients with renal colic. Lower GI symptoms
such as nonbloody diarrhea or constipation are similarly too insensitive and nonspecific
to significantly alter the probability of a GI cause of abdominal pain.
Genitourinary Symptoms
The hallmark of abdominal pain of GU origin is the concomitant development of some,
often subtle, alteration in micturition, e.g., dysuria, frequency, urgency, hematuria,
incomplete emptying, or incontinence (usually overflow). Non-GU pathology may
develop in organs contiguous to the GU system, giving the appearance of an intrinsic GU
problem. For example, an inflamed appendix lying across the bladder may cause urinary
frequency.
Gynecologic Symptoms
Distinguishing GI from GYN causes of acute abdominal pain is one of the most
challenging clinical dilemmas in emergency practice. A thorough gynecologic history is
indicated, including menses, mode of contraception, fertility, sexual activity, sexually
transmitted diseases, vaginal discharge, recent dyspareunia, and a past gynecologic
history, to include pregnancies, deliveries, abortions, ectopics, cysts, fibroids, pelvic
inflammatory disease, and laparoscopy.
Vascular Symptoms
History of MI, other ischemic heart disease or cardiomyopathy, atrial fibrillation,
anticoagulation, congestive failure, peripheral vascular disease, or a family history of
aortic aneurysm are all pertinent historical features in older patients.
Past Medical History
This includes a history of recent and current medications (including nonsteroidal antiinflammatory drugs and antibiotics), past hospitalizations, in- or outpatient surgeries,
diabetes, other chronic diseases (including HIV status and risk factors), and any history
of recent trauma. A social history that includes habits (tobacco, alcohol, and other drug
use), occupation, possible toxic exposures, and living circumstances (homeless, dwelling
heated, running water, living alone, other family members ill with similar symptoms)
provides important background and context in which to place the presenting complaint of
acute abdominal pain.
Physical Examination
General
The patient's general appearance, including facial expression, diaphoresis, pallor, and
degree of agitation provides information about the severity of pain. Although this is
critically important in determining the need for analgesia, intensity of abdominal pain
may bear no relationship to the severity of illness. For example, the pain of early
mesenteric ischemia may be a vague discomfort, in contrast to the excruciating pain of
ureteral colic. Nevertheless, uncomplicated kidney stones have no short-term mortality,
while the majority of patients with ischemic small bowel go on to die.
Patients with colicky pain, which is characteristically visceral due to distention of a
hollow organ, are often unable to lie still, while those with peritonitis prefer to remain
immobile.
Vital Signs
A reliable means of obtaining a core temperature is important, although absence of fever,
especially in the elderly, has no predictive value. Careful counting of rate and observation
of depth of respirations for 15 s is often overlooked. However, it can provide crucial
information about tachypnea or hyperpnea, which may be subtle. Pulse and blood
pressure should include orthostatic changes if, after obtaining the history, there is any
reason to suspect intravascular volume contraction. A pulse increase of thirty points lying
to standing at 1 minute (or the development of symptoms of presyncope) has been shown
to be highly specific for the loss of a liter of blood or its equivalent (roughly 3 L of NS).
Changes in blood pressure have not been shown to be discriminatory, probably because
they are late findings representing failure of a reflex tachycardia to maintain cardiac
output. The tilt-test threshold of thirty points of pulse change may not be applicable to
patients on medications such as beta-blockers, diabetics (who may have an autonomic
neuropathy), and among the elderly, due to the effects of aging on the cardiac conducting
system.
Abdomen
Inspection
The abdomen should be inspected for distention (with air or fluid), scars, and masses.
Auscultation
Contrary to conventional teaching, absent or diminished bowel sounds provide little
clinically useful information. Patients with operative confirmation of peritonitis due to
perforation of peptic ulcer have been noted to have normal or increased bowel sounds
preoperatively. Hyperactive or obstructive bowel sounds, although of limited value, are
somewhat more helpful for the diagnosis of small bowel obstruction (SBO). However,
many with SBO can also have absent or diminished bowel sounds. It appears, therefore,
that only hyperactive or obstructive bowel sounds have clinical utility, increasing the
likelihood of SBO by about fivefold; however, normal or absent bowel sounds appear
very nearly valueless, as evidenced by their occurrence with roughly the same frequency
in both SBO and perforated peptic ulcer.
Palpation
The vast majority of clinical information obtained from examination of the abdomen is
acquired through gentle palpation, using the middle three fingers, and beginning at a
distance from the area of maximum pain. Voluntary guarding (contraction of the
abdominal musculature in anticipation of or in response to palpation) can be diminished
by asking patients to flex their knees. Those who remain guarded following this
maneuver will often relax if the clinician's hand is placed over the patient's, and the
patient is then asked to use their own hand to palpate their abdomen. In contrast to the
symptom of pain, tenderness is a sign in which pain is produced by palpation. Optimally,
the patient's tenderness will be confined to one of the four discrete quadrants. However,
this is often not the case, and one finds more diffuse tenderness encompassing one or
more of the four combined areas noted above. Peritoneal irritation is suggested by rigidity
(involuntary guarding or reflex spasm of abdominal muscles), as is pain referred to the
point of maximum tenderness when palpating an adjacent quadrant.
Rebound tenderness, often regarded as the clinical criterion standard for peritonitis, has
several important limitations. In patients with peritonitis, the combination of rigidity,
referred tenderness, and especially pain with coughing usually provides sufficient
diagnostic confirmation that little additional information is gained by eliciting the
unnecessary pain of rebound. False positives occur in about one patient in four without
peritonitis, perhaps due to a nonspecific startle response. Based on this, one might
reasonably question whether rebound has sufficient predictive value to justify the
discomfort it causes patients.
Enlargement of the liver or spleen, and other masses, including a distended bladder,
should be sought. One should also examine for hernias in both men and women,
particularly those that are tender, suggesting incarceration or strangulation.
In women, the pelvic examination—like the pregnancy test—may provide the clinician
with relevant information that would not have been expected on the basis of the history.
For this reason, it is wise to perform a pelvic examination in the evaluation of abdominal
pain, particularly in women of reproductive age.
Although the rectal examination is widely regarded as an essential component in the
assessment of abdominal pain, particularly in suspected appendicitis, there is little
evidence that rectal tenderness in patients with RLQ pain provides useful incremental
information beyond what has already been obtained by other components of the physical
examination. Grossly melanotic, maroon, or bloody stool indicates GI bleeding. The test
for occult blood, although routinely done, loses sensitivity if not performed serially over
several days. Conversely, repeated rectal examinations performed over several hours by
multiple examiners tends to reduce the specificity of the test for occult blood, presumably
due to local trauma. Among patients with a final diagnosis on follow-up of NSAP, 10
percent had a positive stool test for occult blood.
Basic Laboratory and Radiographic Tests
The complete blood count and plain abdominal film are among the most overutilized tests
in emergency practice. Neither test offers sufficiently powerful likelihood ratios (see
below) to revise disease probability. One approach to the use of both these tests is to take
note only of high threshold abnormalities, e.g., a very elevated WBC (>20,000/mm3), but
to resist the temptation to draw any reassurance from a "normal" WBC or a "nonspecific
bowel gas pattern."
Complete Blood Count
The limited clinical utility of the CBC can be demonstrated most readily by examining its
performance characteristics in the three most common causes of abdominal pain:
Appendicitis, biliary tract disease (principally cholecystitis), and NSAP. Based upon a
metaanalysis of three studies containing a total of over 1800 patients, a WBC exceeding
the threshold value of 10,000/L only doubled the odds of appendicitis, while a WBC
below this cutoff point reduced the odds by only about half. As noted below in the
discussion of likelihood ratios (LRs), an LR (+) = 2 and an LR (–) = 0.4 are of marginal
clinical value.
For acute cholecystitis, the LRs of the WBC count are virtually identical to those seen in
appendicitis, and of equally limited clinical utility.
In one large, well-conducted series of patients with NSAP, 28 percent (95% CI; 22 to
34%) of patients were reported to have WBC counts >10,500/L. In the development of a
decision rule for identification of NSAP, investigators did not find the CBC to be of value
in distinguishing patients with NSAP from other, more serious diagnoses. Because of the
design of studies on NSAP, it is not possible to calculate a specificity or likelihood ratios
for the performance of the WBC count in this setting. However, using 28 percent as the
approximate sensitivity of the test, it is possible to estimate that, in order for leukocytosis
to be of any value in NSAP (defined as producing LRs that deviate significantly from 1),
the WBC count would have to demonstrate substantially better specificity than was seen
in either appendicitis or cholecystitis.
All of the above refers only to individual WBC counts. There is some evidence that serial
counts may assist in the identification of appendicitis. However, in this setting, it would
seem wiser to obtain a CT rather than risk a perforation or other complication while
obtaining serial WBCs and waiting for development of leukocytosis.
Plain Abdominal Radiograph
The plain abdominal radiograph (PAR) is often ordered as an "abdominal series," the
meaning of which is variously defined. In some institutions, this includes an upright
abdomen, in others an upright chest; in still others, only a single supine film is obtained.
The utility of the erect abdominal film, when added to the combination of the supine
abdominal and erect chest film, is generally low and does not impact management.
Abdominal films in suspected appendicitis, NSAP, or urinary tract infection are also
unlikely to be helpful, and can be misleading.
An additional limitation of the plain abdominal radiograph is poor interrater reliability for
commonly used radiographic signs.
Restriction of PARs to patients with suspected obstruction or perforation would reduce
utilization by over 80 percent with no adverse impact on management. Ultrasound may
be a more sensitive test for detection of free air than the combination of upright chest and
left lateral decubitus plain films (93 vs. 79 percent), which is one of the principal uses for
plain radiography in abdominal pain.3 Ultrasound can be extremely helpful, particularly
as a rapid bedside screening test, but it is highly operator-dependent and limited by
overlying gas and obesity. Computed tomography (CT) is markedly superior for
identifying virtually any abnormality that could be seen on plain films, particularly SBO
and renal colic (Tables 72-1 and 72-2). Bedside sonography, combined with computed
tomography would seem to be the key to obviating the need for continued use of the PAR
in the future.
Table 72-1 Diagnostic Tests for Small Bowel Obstruction
Target Diagnosis Test Sensitivity (Range) Specificity (Range) LR (+) LR (–)
Small bowel obstruction (SBO) Plain abdominal films 63% (44–71%) 54% (38–65%) 1
0.7
SBO high-grade CT with IV +/– PO contrast 90% (81–97%) 96% (85–98%) 22 0.1
SBO low- & high-grade CT with IV +/– PO contrast 64% (55–85%) 79% (68–88%) 3 0.5
SBO with ischemia CT with IV +/– PO contrast 83% (32–100%) 88% (61–100%) 7 0.2
Table 72-2 Diagnostic Tests for Renal Colic
Test Sensitivity [95% CI] (Range) Specificity [95% CI] (Range) LR (+) LR (–)
Microscopic Urinalysis 84% [81–87%]* 48% [43–53%] 2 0.3
Plain abdominal film 58% (39–68%) 74% [47–88%] 2 0.6
Unenhanced helical CT (criterion standard) — — — —
Intravenous pyelogram (IVP) 78% [67–88%] 95% [91–99%] 16 0.2
Ultrasonography (without Doppler) 74% (19–100%) 95% (90–100%) 15 0.3
Doppler ultrasound (resistive index) 90% [79–97%] 100% [94–100%] 30 0.1
* Brackets indicate 95% CI; parentheses indicate range.
Diagnosis and Testing
Diagnosis is now more closely linked to appropriate disposition and treatment than was
the case when the only interventions in abdominal pain were laparotomy or observation
with medical management.
Accurate diagnosis is extremely difficult using only clinical information and basic
laboratory tests. When initial and final diagnoses are compared, diagnostic accuracy falls
somewhere between 50 and 65 percent overall. Diagnostic error in adults with abdominal
pain increases in proportion to age, ranging from a low of 20 percent if only young adults
are considered, to a high of 70 percent in the very elderly.
Although some improvement in clinical diagnostic accuracy occurs with experience,
most is due to diagnostic imaging.
Performance Characteristics of Diagnostic Tests
Tables 72-1, 72-2, 72-4, 72-5, 72-6, 72-7, 72-8, 72-9, 72-10, and 72-11 provide a
summary of the performance of diagnostic tests used in the ED work-up of acute
abdominal pain. These test properties are displayed as sensitivity, specificity, and
likelihood ratios. When derived from a metaanalysis of several studies, sensitivity and
specificity, bounded by 95 percent confidence intervals (CIs), are calculated using the
Summary Receiver Operating Characteristics (SROC) methodology, which adjusts for
interstudy variation in diagnostic threshold.4 Under conditions where merged studies are
too clinically or statistically heterogenous for valid metaanalysis, aggregate sensitivity
and specificity are calculated as weighted means, bounded by ranges.
Table 72-4 Diagnostic Tests for Appendicitis
Test Sensitivity [95% CI] (Range) Specificity [95% CI] (Range) LR (+) LR (–)
Plain abdominal radiograph 48% [41–54%] 58% [54–62%] 1 0.9
Abdominopelvic ultrasound (real-time, graded compression, gray-scale) 55% [48–62%]
95% [93–97%] 11 0.5
Abdominopelvic ultrasound (color Doppler added to gray-scale) 84% [77–91%] 96%
[88–100%] 21 0.2
Abdominopelvic unenhanced helical CT (no PO, IV, or colonic contrast) 88% [82–94%]
97% [94–99%] 29 0.1
Abdominopelvic helical CT (double [PO + IV] contrast; no colonic contrast) 91% [81–
98%] 95% [90–98%] 18 0.1
Focused appendiceal (RLQ) unenhanced helical CT (no PO, IV, or colonic contrast) 87%
[78–93%] 97% [92–99%] 29 0.1
Focused appendiceal (RLQ) helical CT (PO contrast only; no IV or colonic contrast) 76%
[62–87%] 95% [90–98%] 15 0.3
Focused appendiceal (RLQ) helical CT (PO + colonic contrast; no IV contrast) 100%
[94–100%] 95% [84–99%] 21 0.03
Focused appendiceal (RLQ) helical CT colonic contrast only; no PO or IV contrast) 98%
[90–100%] 98% [89–100%] 49 0.02
MRI (gadolinium-enhanced) 97% [85–100%] 92% [75–99%] 12 0.03
Table 72-5 Diagnostic Tests for Biliary Tract Disease
Target Diagnosis Test Sensitivity [95% CI] (Range) Specificity [95% CI] (Range) LR (+)
LR (–)
Cholelithiasis Plain abdominal radiograph 64% [59–68%] 68% [52–83%] 2 0.5
Cholelithiasis Ultrasound (US) 91% [84–97%] 97% [95–99%] 30 0.1
Cholelithiasis CT 85% (77–96%) 97% (86–99%) 28 0.2
Acute cholecystitis US 86% (65–97%) 97% (87–100%) 29 0.1
Acute cholecystitis Color velocity imaging & power Doppler US 93% (77–100%) 97%
(88–100%) 31 0.1
Acute cholecystitis Radionuclide scanning 95% [91–98%] 90% [86–94%] 10 .05
Common duct obstruction US 90% (38–95%) 92% (48–97%) 11 0.1
Common duct obstruction CT 83% (51–90%) 87% (44–94%) 6 0.2
Common duct obstruction Radionuclide scanning 93% (81–99%) 92% (84–100%) 12 0.1
Common duct obstruction MR cholangiography 95% (85–96%) 97% (85–99%) 32 0.05
Common duct stone US 85% (19–76%) 89% (52–98%) 8 0.2
Common duct stone CT 71% (29–82%) 86% (55–92%) 5 0.3
Common duct stone MR cholangiography 95% (86–100%) 96% (87–100%) 24 0.05
Table 72-6 Diagnostic Tests for Acute Pancreatitis
Target Diagnosis Test Sensitivity (Range) Specificity (Range) LR (+) LR (–)
Inflammation Serum amylase 82% (72–93%) 85% (78–94%) 5 0.2
Inflammation Serum lipase >2x normal 90% (79–99%) 92% (85–98%) 11 0.1
Pancreatic necrosis CT with PO & bolus IV contrast 92% (75–100%) 95% (92–100%)
18 0.1
Drainable collections Transabdominal ultrasound (US) 54% (23–83%) 88% (47–100%) 4
0.5
Drainable collections CT with PO & bolus IV contrast 90% (72–100%) 48% (32–85%) 2
0.2
Drainable collections MRI (unenhanced) 92% (66–100%) 88% (79–100%) 8 0.1
Acute hemorrhagic pancreatitis Unenhanced CT (criterion standard) — — — —
Biliary pancreatitis Serum alanine aminotransferase (ALT) >3x normal 54% (38–73%)
92% (77–96%) 7 0.5
Common bile duct obstruction US 90% (38–95%) 92% (48–97%) 11 0.1
Common bile duct obstruction CT 83% (51–90%) 87% (44–94%) 6 0.2
Common bile duct obstruction Radionuclide scanning 93% (81–99%) 92% (84–100%) 12
0.1
Common bile duct obstruction MR cholangiography 95% (85–96%) 97% (85–99%) 32
0.05
Table 72-7 Diagnostic Tests for Acute Diverticulitis
Target Diagnosis Test Sensitivity (Range) Specificity (Range) LR (+) LR (–)
Inflammation or abscess Ultrasonography (high resolution, graded compression) 83%
(77–91%) 95% (86–99%) 17 0.2
Inflammation or abscess Helical CT with colonic contrast only (no IV or PO contrast)
98% (88–99%) 99% (96–100%) 98 0.02
Table 72-8 Diagnostic Tests for Acute Pelvic Inflammatory Disease
Target Diagnosis Test Sensitivity [95% CI] (Range) Specificity [95% CI] (Range) LR (+)
LR (–)
Salpingitis (macroscopic laparoscopy) Erythrocyte sedimentation rate >15 mm per h 78%
(45–81%) 44% (25–57%) 1 0.5
Salpingitis (macroscopic laparoscopy) C-reactive protein 70% (54–93%) 59% (48–90%)
2 0.5
Salpingitis (macroscopic laparoscopy) Endometrial biopsy 80% (70–89%) 76% (67–
89%) 3 0.3
Salpingitis (macroscopic laparoscopy) Gonococcus or Chlamydia cultured from upper
genital tract 65% [41–85%] 100% [75–100%] 5 0.4
Salpingitis (macroscopic laparoscopy) Transvaginal power Doppler 100% [83–100%]
80% (56–94%) 5 0.1
Endometritis (endometrial biopsy) Conventional transvaginal sonography 85% [54–98%]
100% [91–100%] 18 0.2
Salpingitis (fimbrial minibiopsy) Laparoscopy (macroscopic) 50% [29–71%] 80% [66–
90%] 2 0.6
Endometritis (endometrial biopsy) Laparoscopy (macroscopic) 93% [68–100%] 67%
[41–87%] 3 0.1
Salpingitis/endometritis (fimbrial minibiopsy or endometrial biopsy) Laparoscopy
(macroscopic) 48% [30–67%] 79% [66–88%] 2 0.7
Chlamydia cultured from upper genital tract Laparoscopy (macroscopic) 53% [28–77%]
67% [22–96%] 2 0.7
Table 72-9 Diagnostic Tests for Ectopic Pregnancy
Target Diagnosis Test Specificity [95% CI] (Range) Specificity [95% CI] (Range) LR (+)
LR (–)
Pregnancy Serum hCG [10 mIU/mL = (+)] 99% [92–100%] 98% [94–100%] 50 .01
Pregnancy Serum hCG [25 mIU/mL = (+)] 98% [91–100%] 99% [94–100%] 98 .02
Pregnancy Urine hCG [>20 mIU/mL = (+)] 98% [96–100%] 98% [96–99%] 49 .02
Pregnancy Urine hCG [>50 mIU/mL = (+]] 95% [90–98%] 99% [97–99%] 95 .05
IUP TVS on all patients w/ (+) hCG 94% [90–97%] 93% [88–97%] 13 .06
IUP TVS on patients w/ hCG <1500 mIU/mL 33% [10–65%] 98% [90–100%] 16 0.7
IUP TVS on patients w/ hCG1500 mIU/mL 98% [95–99%] 90% [81–96%] 10 0.2
Ectopic TVS on all patients w/ (+) hCG 56% [35–76%] 99% [97–100%] 56 0.4
Ectopic TVS on patients w/ hCG <1500 mIU/mL 25% [5–57%] 96% [87–99%] 6 0.8
Ectopic TVS on patients w/ hCG >1500 mIU/mL 80% [52–96%] 99% [97–100%] 80 0.2
Ectopic Progesterone <22 ng/mL 98% [96–100%] 29% [27–31%] 1 .07
Ectopic Culdocentesis 56% (38–81%) 70% (20–86%) 2 0.6
Ruptured ectopic Culdocentesis 68% (52–84%) 76% (39–93%) 3 0.4
Table 72-10 Diagnostic Tests for Abdominal Aortic Aneurysm
Target Diagnosis Test Sensitivity (Range) Specificity (Range) LR (+) LR (–)
Uncomplicated abdominal aortic aneurysm (AAA) Sonography 92% (81–100%) 89%
(85–100%) 9 0.1
Leaking/ ruptured AAA (intra- or retro-peritoneal) Sonography 12% (4–52%) 84% (34–
100%) 1 1
Uncomplicated or leaking/ruptured AAA (intra- or retro-peritoneal) CT 97% (82–100%)
95% (86–100%) 19 .03
Detailed preoperative anatomy Conventional angiography No longer a preferred
emergency procedure
Detailed preoperative anatomy MRI/MRA Not a preferred emergency procedure at this
time
Table 72-11 Diagnostic Tests for Ischemia of the Small and Large Bowel
Target Diagnosis Test Sensitivity [95% CI] (Range) Specificity [95% CI] (Range) LR (+)
LR (–)
Small bowel ischemia Conventional angiography 88% (62–98%) 95% (93–100%) 18 0.1
Small bowel ischemia CT & CT angiography (including multi-detector row image
acquisition with 3D reformatting) 77% (57–92%) 85% (71–100%) 5 0.3
Small bowel ischemia Gadolinium-enhanced MRA (including 3D reformatting) 83%
(78–100%) 89% (71–99%) 8 0.2
Small bowel ischemia/infarction Serum lactate (persistent elevation without alternative
explanation) 90% (66–100%) 62% (42–77%) 2 0.2
Ischemic colitis Colonoscopy 93% (82–100%) 90% (85–100%) 9 0.1
Large bowel infarction Color Doppler sonography 82% [48–98%] 92% [64–100%] 10
0.2
Definition of Likelihood Ratios (LR's)
(See also ref. 5.) In the far right-hand columns of Tables 72-1, 72-2, 72-4, 72-5, 72-6, 727, 72-8, 72-9, 72-10, and 72-11, test performance is expressed using positive and negative
likelihood ratios (LRs).
LRs are often divided into positive and negative LRs, expressed as follows: LR of a
positive test = (TPR/FPR) = [(true positive rate)/(false positive rate)] = [sensitivity/(1 –
specificity)]. LR of a negative test = (FNR/TNR) = [(false negative rate)/(true negative
rate)] = [(1 – sensitivity)/specificity]. LR calculations derived from sensitivities or
specificities of 100 percent are calculated conservatively by using the midpoint of the
95% CI surrounding the estimate of sensitivity or specificity in order to avoid obtaining a
clinically meaningless LR (+) of ∞ or an LR (–) of 0.
The formal definition of an LR (+) is simply a special case of the general definition of
LRs: An LR (+) is the likelihood that a positive test result would be found in a patient
with the target disorder, compared to the likelihood of a positive test result occurring in a
patient without the target disorder. The definition of an LR (–) is the likelihood that a
negative test result would be found in a patient with the target disorder, compared to the
likelihood of a negative test result occurring in a patient without the target disorder.
Interpretation of LR's
In general, an LR (+) of 1 to 2, or an LR (–) of 0.5 to 1, alters disease probability by a
small and clinically insignificant degree. In contrast, LR (+)s >10, or LR (–)s <0.1 may
have a very substantial impact on clinical decision-making through meaningful revision
of disease probability. LR (+)s of 2 to 10, or LR (–)s of 0.5 to 0.1 may still make some
small contribution to management, depending on their magnitude and the clinical context
in which they are applied. Because LRs are odds, a diagnostic test with an LR (–) = 0.1 is
as powerful as a diagnostic test with an LR (+) = 10.
Clinical Application of LR's
Likelihood ratios (LRs) combine the stability of sensitivity and specificity with the utility
of predictive values, resulting in an index of test performance that can be applied directly
to a particular patient at the bedside. This is done by multiplying an LR (+) or LR (–)
times the pretest odds of disease, resulting, respectively, in an increase or decrease in
posttest odds of disease. The larger the LR (+) or the smaller the LR (–), the more
powerful the test is to revise the posttest probability of a given target disorder.
Although odds (O) and probabilities (p) are mathematically different, they are
conceptually similar and easily interconverted according to the following formulas: O =
p/(1 –p), and p = O/(O + 1). Thus, if O = 1:1, p = 1/(1 + 1) = ½= .5 or 50 percent
probability; conversely, if p = 0.5 or 50 percent , O = .5/(1 – .5) = .5/.5 = 1:1.
Once determined, an LR can be incorporated directly into the calculation of posttest
probability by employing Bayes' theorem: (LR) x (clinically estimated pretest odds of
disease) = (posttest odds of disease). This simple equation illustrates a convergence
between the central strategy underlying diagnostic testing, i.e., the revision of disease
probability, and the fundamental nature of likelihood ratios.
The performance characteristics of the various tests shown in Tables 72-1, 72-2, 72-4, 725, 72-6, 72-7, 72-8, 72-9, 72-10, and 72-11 are incorporated into the discussion of
specific diagnoses below.
Specific Diagnoses
The data in Table 72-3 were drawn from a combined series of over 8500 cases of acute
abdominal pain (<1 week duration) presenting to over 200 EDs in 17 countries during a
10-year period. The data were collected on a highly standardized instrument.
In virtually all large series of acute abdominal pain in adults, the substantial majority of
final diagnoses include nonspecific abdominal pain (NSAP), appendicitis, and biliary
tract disease (usually cholecystitis), in that order, accounting for nearly 75 percent of all
acute abdominal pain. However, as shown in Table 72-3, as patients age, the triad
remains, but the order changes to: biliary tract disease (again, usually cholecystitis),
followed by NSAP and appendicitis.
Table 72-3 Causes of Acute Abdominal Pain Stratified by Age
Final Diagnosis 50 Years (N = 2406) <50 Years (N = 6317)
Biliary tract disease 21% 6%
Nonspecific abdominal pain (NSAP) 16% 40%
Appendicitis 15% 32%
Bowel obstruction 12% 2%
Pancreatitis 7% 2%
Diverticular disease 6% <.1%
Cancer 4% <.1%
Hernia 3% <.1%
Vascular 2% <.1%
Gynecologic <.1% 4%
Other 13% 13%
Intraabdominal Diagnoses by Organ System
Gastrointestinal
Appendicitis
In spite of a large number of algorithms and decision rules incorporating many different
clinical and laboratory features, an accurate preoperative diagnosis of appendicitis has
remained elusive for more than a century. In at least 20 percent of patients with
appendicitis, the diagnosis is missed; conversely, normal appendices are found in 15 to
40 percent of all operations performed for suspected appendicitis. Thus the diagnosis of
appendicitis turns out to be either a false positive or false negative just about as often as it
turns out to be correct.6
Among patients presenting to an ED with acute abdominal pain, the pretest probability,
or prevalence, of appendicitis is roughly 10 to 25 percent. Converting this to odds to
facilitate multiplication by LRs, the pretest odds of appendicitis in patients with
undifferentiated acute abdominal pain is roughly between 0.1 and 0.3. Five clinical
features appear to have sufficiently powerful LR (+)s that the presence of any one should
drive up the clinical odds to the point that an imaging procedure is indicated. Those
clinical features with some predictive value include: Pain located in the RLQ [LR (+) =
8]; pain migration from the periumbilical area to the RLQ [LR (+) = 3]; rigidity [LR (+) =
4]; pain before vomiting [LR (+) = 2 to 3]; and a positive psoas sign [LR (+) = 2].
Anorexia is not a useful symptom. In fact, about one patient in three with surgically
documented appendicitis is not anorectic preoperatively.
In excluding the diagnosis of appendicitis, the absence of RLQ pain [LR (–) = 0.2],
presence of similar previous pain [LR (–) = 0.3], and absence of typical pain migration to
the RLQ [LR (–) = 0.5] are only somewhat helpful. This is because no single historical or
physical finding is sufficiently powerful to exclude the diagnosis. Therefore, to clinically
rule out appendicitis, one relies upon the absence of several key features, or the presence
of a strong competing alternative diagnosis. Lacking either of these conditions, an
imaging procedure, usually a CT, should be obtained.
Although sonography is an option in suspected appendicitis, the CT is generally preferred
in adults and nonpregnant women with a working diagnosis of appendicitis because
ultrasound of the appendix is technically challenging, highly operator-dependent, and
often unavailable after hours. Additionally, although ultrasound has a sufficiently
powerful LR (+) that a positive finding usually results in surgery, its poor LR (–)
precludes its use as a screening (rule-out) test. Color-flow Doppler added to the standard
graded compression gray-scale sonography improves test performance by detecting
appendiceal and periappendiceal inflammation. However, the increment in LRs is
insufficient to change the clinical implications of the test results, i.e., a positive finding
still favors surgical intervention, and a negative result fails to exclude the diagnosis.
As shown in Table 72-4, CT of suspected appendicitis can be targeted at the RLQ or
include the entire abdomen and pelvis. It can be performed as an unenhanced
(noncontrast) study, or may be done with various combinations of PO, IV, or colonic
contrast. Although the focused appendiceal CT obtained with colonic contrast appears to
have excellent test properties and has been shown to alter management in the majority
(59 percent) of cases,7 these targeted examinations are not commonly performed because
they are so narrowly focused on the RLQ that a negative result often requires a repeat
abdominopelvic CT. Evidence of appendicitis on any type of abdominal CT has such a
high LR (+) that it almost invariably drives surgical intervention. Although the LR (–) is
sufficiently strong to reduce the odds of appendicitis by about tenfold, it is not as strong
as the LR (+). Absence of evidence of appendicitis on CT, or even visualization of an
apparently normal appendix therefore does not exclude the diagnosis with the same
degree of certainty that a positive CT confirms it.
For example, if the clinician is working with a 50 percent pretest probability of
appendicitis (not an unreasonable estimate, given the prevalence of the disease in the
population), a negative CT reduces that posttest probability to just under 10 percent.
While this finding, depending upon the clinical picture, might be sufficient to stay the
surgeon's hand, logical application of Bayes' theorem does not support use of a negative
CT as grounds for discharging the patient from the ED. In order to make such a
disposition, the prior probability of appendicitis would have to be substantially lower
than 50 percent. This example also assumes the optimal conditions under which the
studies used to generate the contents of Table 72-4 were conducted, i.e., complete filling
of the entire appendiceal lumen in order to exclude distal appendicitis, a helical machine
with narrowly collimated beams (optimally 5-mm cuts), and an experienced radiologist
trained in body CT available to read the images. The relative rarity of such conditions
may help to explain the observation that, in spite of several well-conducted clinical trials
demonstrating the salutary impact of advances in abdominal imaging on diagnostic
accuracy in appendicitis, the population-based incidence of misdiagnosis and perforation
have not changed over the past decade.8
Biliary Tract Disease
This is the most common diagnosis in ED patients 50 years old. Among those found to
have pathologically-confirmed acute cholecystitis, the majority lack fever and about 40
percent lack a leukocytosis. Recognition that the diagnoses of cholecystitis, "biliary
colic," and symptomatic common duct obstruction may represent pathologically distinct
entities that cannot be reliably distinguished from one another on clinical grounds, has led
some authors to redefine the clinical target disorder as simply "biliary tract disease."
Although there is an association between symptomatic biliary tract disease and steady
postprandial upper abdominal pain that radiates to the upper back, the likelihood ratios of
individual signs, symptoms, and combinations of signs and symptoms are relatively weak
discriminators. Just over one-third of patients have pain isolated to the RUQ, although
about two-thirds have tenderness in that location. Most of the remainder complain of
diffuse pain in the upper half of the abdomen, and among those with pain in the lower
abdomen, it is almost invariably in the RLQ. Among the one-third who do not have RUQ
tenderness, the distribution is about equally divided among the upper half, the right side,
and generalized tenderness throughout the belly.
As shown in Table 72-5, sonography is the initial test of choice for patients with
suspected biliary tract disease. In many institutions, this can be performed rapidly at the
bedside by the ED physician as an extension of the clinical assessment. Ultrasound is
better in the identification of cholecystitis than in the detection of common duct
obstruction. Cholescintigraphy (radionuclide scanning) of the biliary tree is a more
sensitive test than sonography for the diagnosis of both these conditions.9 At present, CT
does not have a major role in the initial work-up of biliary tract disease, although it will
often identify unexpected abnormalities of the gallbladder on an abdominopelvic double
contrast CT obtained for other reasons, particularly if thinly collimated cuts are obtained.
MR cholangiography has shown extremely good sensitivity and specificity in identifying
stones and other obstructions of the common duct.10
Small Bowel Obstruction
The central issues in small bowel obstruction (SBO) are diagnosis of the primary disorder
and early detection of secondary strangulation or ischemia, when present. Only two
historical features (previous abdominal surgery and intermittent/colicky pain) and two
physical findings (abdominal distention and abnormal bowel sounds) appear to have
predictive value. Although about two-thirds of SBO presents with generalized or central
abdominal pain, and about half have generalized tenderness, the LRs of these findings
alone or in combination are such that SBO is another diagnosis that requires imaging
confirmation. The general limitations of bowel sounds have been noted previously. As
shown in Table 72-1, and also discussed above, the plain abdominal film is hampered by
a large number of indeterminate readings, leaving it with LRs that are of marginal utility.
The CT is far superior to the plain film in detection of high-grade SBO, but is limited in
its ability to identify low-grade obstruction, which may require small-bowel followthrough.11
Those patients with ischemic bowel secondary to strangulation are extremely difficult to
detect clinically or with plain radiography. Here the CT is useful in altering the likelihood
of ischemia, and has been shown to have a substantial impact on treatment.
Acute Pancreatitis
About 80 percent of acute pancreatitis in the United States is caused by alcohol or
gallstones, with one etiology predominating over the other depending on the population
studied. The pain and tenderness of acute pancreatitis are limited to the anatomic area of
the pancreas in the upper half of the abdomen in only a minority of instances. Most
patients' pain and tenderness include this area, but in about half the pain extends well
beyond the upper abdomen to cause generalized tenderness. This may be related to the
absence of a capsule that might otherwise contain the inflammation, and to the difficulty
of localizing pathology that—much like that of an abdominal aortic aneurysm—resides
deep in the belly and extends into the retroperitoneum. Other features of the history and
physical exam, such as quality of pain—which is steady and severe in the majority of
patients—or vomiting, have not been shown to have sufficient discriminatory power to
make them clinically useful. Thus most patients with upper, central, or generalized
abdominal pain and tenderness, who lack an alternative explanation for their presentation
will require further testing.
As lipase assays have improved in accuracy and speed over the last several years, serum
lipase has begun to replace amylase as the preferred ED screening test for suspected acute
pancreatitis. By setting the threshold for a positive test at twice the upper limit of normal
serum lipase, the likelihood ratios for lipase are better than twice as powerful as those of
serum amylase in confirming or excluding the diagnosis of acute pancreatitis (Table 726).12 Preliminary reports that ratios of urine to serum amylase or of lipase to amylase
improve diagnostic accuracy have not been validated. Like amylase, the accuracy of
serum lipase in the diagnosis of acute pancreatitis is inversely related to the time elapsed
between symptom onset and presentation.
Depending upon institutional custom, a diagnosis of acute pancreatitis may be sufficient
to determine the appropriate admitting service. However, in settings where not all
pancreatitis is admitted to a single service, or where it is expected that the ED will make a
monitored vs. unmonitored bed admitting decision, it may be necessary for the ED to
assess the patient for biliary pancreatitis and for the likelihood of peripancreatic
complications, such as necrosis, hemorrhage, or drainable fluid collections. Although the
height of pancreatic enzyme elevations do not have prognostic value, a double contrast
helical CT stages severity and predicts mortality earlier than the Ranson criteria.
Because timely identification of biliary pancreatitis is important, early assessment for
common bile duct obstruction is necessary, particularly among patients over 50 years old.
All patients with an ALT >150 U/L (about 3x normal), including alcoholics, are at
increased risk of biliary pancreatitis (see Table 72-6). Because elevations in transaminase
due to alcoholic hepatitis may mask an increased ALT secondary to obstruction, this
subset of alcoholic patients warrants evaluation for common duct obstruction.
Unfortunately, there are no blood tests or imaging modalities short of MR
cholangiography that possess a sufficiently powerful LR (–) to exclude common duct
obstruction in all patients (see Table 72-6). Depending on availability, a double contrast
helical CT is usually performed first to examine the pancreas and identify peripancreatic
complications. Contingent upon the CT protocol used—principally the thinness of the
collimated beam—the common bile duct may be adequately visualized. Usually,
however, it is necessary to follow the CT with a sonogram of the biliary tree because the
LR (–) of ultrasound is superior to CT in this setting (see Table 72-6).13 If sonography is
unavailable, a radionuclide scan is a reasonable alternative test for the detection of
complete obstruction. In the future, the problem of distinguishing primary inflammatory
(usually alcoholic) pancreatitis from secondary obstructive (usually biliary) pancreatitis
may be resolved through wider availability of MR cholangiopancreatography (MRCP).
This test simultaneously and noninvasively images the pancreas and common bile duct,
and may ultimately obviate the need for purely diagnostic ERCP.
Diverticulitis
Clinical diagnostic accuracy in one large study of colonic diverticulitis was only 34
percent [95% CI; 26 to 42%]. When the "possible/equivocal" clinical diagnoses were
removed from analysis, and only those patients with a pretest diagnosis of either "highly
suspected" or "very unlikely" were included as clinical positives and negatives
respectively, the LR (+) was 2 to 3, and the LR (–) was 0.4, neither of which offers much
help in the revision of disease probability. Of those patients with diverticular abscesses,
diagnostic performance was somewhat better, with 70 percent categorized as "highly
suspected" and the remainder as "possible/equivocal." No documented abscesses were
categorized clinically as "very unlikely."
Pain in diverticulitis was confined to the LLQ in less than one-fourth of documented
cases, and to the lower half of the abdomen in only an additional one-third of patients.
With respect to tenderness, it was as likely to be generalized as it was to be limited to the
lower half of the abdomen or to the LLQ. About 10 percent of patients with operatively
confirmed diverticulitis lacked abdominal pain and 20 percent had no abdominal
tenderness whatsoever, most of whom were elderly. Older patients are also at risk for a
severe and often fatal complication of diverticulitis only rarely seen in younger age
groups: free perforation of the colon.
As shown in Table 72-7, CT with colonic contrast is the test of choice for diverticulitis,
demonstrating excellent performance characteristics that are superior to ultrasound.
Sonography relies on identification of an inflamed diverticulum to make the diagnosis,
which is often obscured in patients with complicated diverticulitis.14 In contrast, CT
accurately identifies abscesses and other complications, informing surgical management
strategies.15
Genitourinary
Renal Colic
As in appendicitis, a number of clinical decision rules have been developed to identify
patients with the preimaging diagnosis of ureterolithiasis. Most algorithms include
features of the pain, e.g., location (unilateral flank), onset (abrupt), quality (colicky), and
radiation (groin/testicle/labia). Although hematuria and plain abdominal films still appear
in many clinical algorithms, the weak LRs of both tests, as shown in Table 72-2, do not
provide strong support for their continued inclusion in the diagnostic evaluation of
suspected renal colic.16
Although the IVP has a specificity comparable to unenhanced helical CT, because of the
IVP's poor sensitivity, demonstrated in head-to-head comparison, noncontrast helical CT
has become the criterion standard for the diagnosis of renal colic. Traditional sonography
has performance characteristics that are similar to those of the IVP (see Table 72-2).
However, with the addition of Doppler ultrasound, elevation of the "renal resistive index"
in one kidney relative to the other may identify the presence of a stone in the ipsilateral
ureter. Based on preliminary data, this test appears to have a strong LR (+), but its LR (–
), though good, is not as powerful as that of unenhanced helical CT (see Table 72-2).
Because this test requires specialized equipment and a skilled operator, its availability to
the ED is not comparable to CT.
In older patients, any presentation that resembles renal colic, with or without hematuria,
mandates the exclusion of an abdominal aortic aneurysm (AAA). This is yet another
reason to obtain a noncontrast helical CT, since it performs extremely well in the
detection of both ureteral stones and AAAs.
Because the GU tract is mostly retroperitoneal, it only uncommonly causes significant
anterior abdominal tenderness. A notable exception to this is an impacted stone at the
ureterovesical (U-V) junction where the ureter enters the bladder, producing ipsilateral
lower quadrant pain and tenderness. Because stones at the U-V junction (like those at the
uretero-pelvic [U-P] junction) are less likely to produce colicky pain than are stones
located between the top and bottom of the ureter, impaction of a stone at the U-V
junction on the right may easily mimic appendicitis, and will require a noncontrast CT to
identify stone disease. If this shows neither a stone nor evidence of other intraabdominal
pathology, a double contrast abdominopelvic CT should be obtained, searching for
evidence of appendicitis.
Acute Urinary Retention
Another common GU cause of abdominal pain is acute urethral obstruction, producing a
distended bladder. When the obstruction is truly acute, the tense bladder often feels like a
solid mass rather than a fluid-filled hollow viscus. However, if one always considers this
common entity when confronted with a midline mass of variable tenderness arising from
the lower half of the abdomen, insertion of a urethral catheter easily makes the diagnosis
and treats the immediate problem.
Gynecologic Pain
Acute Pelvic Inflammatory Disease
Absence of a criterion standard has further confounded the already clinically difficult
diagnosis of acute pelvic inflammatory disease (PID). Laparoscopic and histopathologic
findings, both of which have been proposed as diagnostic standards, are discordant.
Because gross laparoscopic findings have historically been used as the standard in most
well-designed studies, the LRs of clinical features, laboratory results, and sonographic
findings that follow have been measured against direct macroscopic inspection of the
adnexa, unless otherwise noted.
Symptoms such as lower abdominal pain, which would be expected to have a high LR (–)
for PID, have not been studied because they typically represent inclusion criteria for
study enrollment. To date, there have been no historical features associated with
laparoscopic PID that demonstrate clinically useful LRs in more than one study
population. Similar to lower abdominal pain, signs such as adnexal and cervical motion
tenderness have not been well-studied because they have also been used as inclusion
criteria in most investigations. The only physical finding associated with laparoscopic
PID across more than one study population is an abnormal vaginal discharge. In spite of
this statistical association, the LRs of vaginal discharge range from 0.5 to 2.5,
representing very limited power to alter disease probability. Elevated temperature and a
palpable mass have been inconsistently associated with PID. The white blood cell count
has not been found to be helpful in any of the studies that examined it. For the
performance characteristics of other laboratory tests that have been associated with PID
(e.g., the erythrocyte sedimentation rate [ESR] and C-reactive protein [CRP]), see Table
72-8. An examination of this table suggests that the best noninvasive test presently
available for suspected PID is transvaginal sonography, in which a positive test result,
such as a thickened tubal wall, increases the likelihood of PID about 18 times. If this is
supplemented by transvaginal power Doppler, a negative test result, such as absence of
the hyperemia associated with tubal inflammation, will decrease the likelihood of PID by
about tenfold.17
As in the evaluation of ectopic pregnancy (see below), the role of culdocentesis in the
diagnosis of PID is not well-supported by evidence.
Ectopic Pregnancy
In ruptured ectopic pregnancy, abdominal pain is almost universally present. However, as
emphasis in ectopic pregnancy has shifted to identification of patients prior to rupture—
with the goal of preserving fertility—pain may be absent at this earlier stage, with a
sentinel complaint of only vaginal bleeding. Therefore, any woman of childbearing age
who presents to the ED with abdominal pain or abnormal vaginal bleeding should receive
a qualitative pregnancy test (either urine or serum) as a screening measure.
The poor predictive performance of historical features, such as "risk factors," and of the
physical examination (sensitivity 19 percent, LR [–]= 0.8 for ectopic pregnancy among
women with high hCG levels), argue persuasively that this diagnosis cannot be excluded
on clinical grounds.
For this reason, the results of a urine or serum pregnancy test, independent of other data,
will determine if further testing is indicated to exclude an ectopic. All commercial
pregnancy tests are highly accurate, with excellent LRs (Table 72-9). If the qualitative
hCG is positive, the preferred test is bedside transvaginal sonography (TVS), targeted
solely at answering the question: Is this pregnancy in the uterus? In patients not
undergoing treatment for infertility, clear visualization of an intrauterine pregnancy (IUP)
in two perpendicular views essentially excludes an ectopic pregnancy. If an IUP is not
seen, this must be interpreted in the context of the discriminatory zone (DZ) of the
quantitative hCG. The DZ is the threshold level of serum HCG, above which a normal
IUP should be seen on sonography. The accuracy of TVS permits reduction of the DZ to
an operator-dependent level of 1500 mIU/mL. The performance of the TVS in the
identification or exclusion of intrauterine and ectopic pregnancy is shown as a function of
hCG levels in Table 72-9.18 Although there is a broad range of normal variation in hCG
kinetics, failure of levels to increase by about 66 percent within 48 h in first-trimester
pregnancy suggests an abnormal gestation. This will not distinguish a threatened
miscarriage or blighted pregnancy from an ectopic. However, it does signal a potential
problem that requires tracking of serial hCGs over time and subsequent investigation with
TVS. If a diagnosis cannot be firmly established, laparoscopy is indicated.
Progesterone levels may be helpful if >22 ng/mL, since this markedly reduces the
likelihood of an ectopic. A serum progesterone below this threshold, however, is not
helpful (LR [+] = 1), since most pregnant women with levels <22 ng/mL will not be
harboring an ectopic.19
As shown in Table 72-9, culdocentesis compares poorly to TVS performed by an
experienced sonographer above the DZ, both in the identification of ectopic pregnancy
and in distinguishing ruptured from unruptured ectopics. Indeed, LRs associated with
culdocentesis, analyzed under conditions that optimize test performance by excluding
nondiagnostic (dry) taps, range between 0.4 and 3, indicating poor discrimination. These
data suggest that, with the widespread availability of quantitative hCG measurement and
experienced TVS, there is little justification for performing this invasive and painful
procedure.
Vascular
Abdominal Aortic Aneurysm
Although abdominal aortic aneurysms (AAAs) have little in common with aortic
dissections, these two major forms of catastrophic disease of the aorta are often lumped
together. Dissections are uncommon causes of abdominal pain and, because they almost
invariably originate in the thoracic aorta, usually produce chest or upper back pain before
migrating into the abdomen as the dissection moves distally.
AAAs on the other hand tend to enlarge, become aneurysmal over years, and rather than
dissect, leak and rupture. Fewer than half of AAAs present with the triad of hypotension,
abdominal or back pain, and a pulsatile abdominal mass; over three-quarters are
normotensive. Spontaneous containment of bleeding is the principal determinant of
prehospital survival and degree of hypotension, if any, on arrival. Absence of abdominal
pain or tenderness is entirely compatible with a contained leak extending into the
retroperitoneum. Neither the presence or absence of femoral pulses or an abdominal bruit
have LRs that deviate very far from 1, and therefore are not helpful clinically. In fact,
palpation is the only feature of the physical exam that has been shown to have some
clinical utility. As might be expected, the LR (–) for palpation is poor, ranging from 0.5
to 0.7 in a recent pooled analysis. The LR (+), however, ranges from 12 to 16 as the size
of the aneurysm increases from >3 cm to >4 cm.20 Thus, inability to palpate an enlarged
aorta in a patient with suspected AAA should not deter one from obtaining an imaging
procedure in a stable patient or moving directly to the OR if the patient is unstable.
Conversely, palpation of an enlarged aorta in the same patient should only serve to
increase the urgency with which imaging or surgical intervention occurs as the next step,
again contingent upon hemodynamic instability.
In emergency practice, this means that any stable patient, particularly one over 50 years
old, presenting with recent onset of abdominal/flank/low back pain is likely to require
either a normal aortic sonogram (performed by an experienced operator) or a noncontrast
helical CT (criterion standard) before an AAA can be excluded from the differential
diagnosis. Although sonography has the advantage of ready availability at the bedside in
many EDs, in contrast to the CT it can only identify an AAA, and cannot provide
additional information about leakage or rupture (Table 72-10). In unstable patients, if a
bedside sonogram can be obtained during resuscitation, visualization of an enlarged aorta
in the setting of a suggestive clinical picture is taken as de facto evidence of leakage or
rupture, requiring immediate surgery.
Because MRI is limited in its ability to identify fresh bleeding, MR technology, including
MR angiography, is not an appropriate emergency procedure.
As noted earlier, the appearance of "renal colic" in older patients should be regarded as
representing an AAA until the CT proves otherwise. Fortunately, the important
distinction between a kidney stone and an AAA can be readily made by obtaining a
helical unenhanced abdominopelvic CT.
Mesenteric Ischemia
Mesenteric ischemia can be divided into arterial and venous disease (mesenteric venous
thrombosis [MVT]). Arterial disease can be subdivided into occlusive and nonocclusive
(NOMI or low-flow state). Finally, occlusive arterial disease (generally understood to
mean superior mesenteric artery occlusion) may be further categorized into thrombotic or
embolic. Several features combine to produce a very high mortality associated with
mesenteric ischemia: (1) Unless young patients have an arrhythmia (usually atrial
fibrillation causing embolization) or a hypercoagulable state (causing MVT), individuals
with mesenteric ischemia tend to be older with substantial age-related comorbidity; (2)
the small bowel, which is supplied by the superior mesenteric artery, has a warm
ischemia time of only 2 to 3 h; (3) the clinical picture is characterized initially by poorly
localized visceral-type abdominal pain, without tenderness; (4) patients may become
transiently better after a few hours of ischemia at the time of onset of mucosal infarction,
only to develop peritoneal findings as full-thickness necrosis of the bowel wall becomes
clinically apparent over several more hours; and (5) timely diagnosis requires that
conventional angiography, an invasive procedure, be obtained early in older, often fragile
patients who may not appear initially to be as ill as they are.
There are some distinctions that can be made among the four major forms of mesenteric
ischemia: (1) embolic disease is the most abrupt in onset, and MVT the most indolent,
with the temporal profile of arterial thrombosis somewhere in between; (2) NOMI is
usually accompanied by clinical evidence of a low-flow state, typically due to cardiac
disease, which responds to improvement in cardiac output; (3) MVT may be more
amenable to noninvasive diagnosis with CT, occurs in younger patients, has a lower
mortality, and can be treated with immediate anticoagulation; (4) following diagnosis,
arteriography with papaverine infusion may be an important component of treatment in
patients with splanchnic vasoconstriction.
Elevation of serum phosphate was initially thought to be a sensitive marker for
mesenteric ischemia, but this has not been supported by subsequent work. As shown in
Table 72-11, serial serum lactates that remain persistently normal reduce the likelihood of
mesenteric ischemia by more than tenfold. Unfortunately the test has a weak LR (+)
because lactate is elevated in many other conditions, and therefore lacks adequate power
to increase the probability of mesenteric ischemia in any clinically important way.
Conventional invasive angiography is the diagnostic and initial therapeutic procedure of
choice at the present time (see Table 72-11).21
Ischemic Colitis
As is characteristic of all vascular diseases, ischemic colitis is predominantly a disease of
older patients. About 80 percent of individuals have diffuse or lower abdominal visceral
pain, accompanied by diarrhea in about 60 percent, often mixed with blood. In contrast to
mesenteric ischemia, ischemic colitis is not generally due to large-vessel occlusive
disease, angiography is not usually indicated, and if performed is often normal. The
diagnosis is typically made by colonoscopy, which is preferred to sigmoidoscopy. Color
Doppler sonography can also be used for diagnosis. Rectal sparing, in contrast to
ulcerative colitis, is a typical finding in ischemic colitis. Not surprisingly, the severity of
the presentation is related to the extent of occlusion and ischemia. In the majority of
cases, only segmental portions of the mucosa and submucosa slough. These then go on to
heal uneventfully with conservative management. At the opposite end of the spectrum is
full-thickness infarction of the colon, occurring in about 20 percent of cases. Bowel
necrosis, whether segmental or pancolitic, causes peritonitis, requiring partial or complete
colectomy.
In between mucosal/submucosal ischemia and full-thickness infarction of the large bowel
is an intermediate form of ischemic colitis involving portions of the muscular layer of the
large bowel. These areas of deep but incomplete ischemia may later heal with stricture
formation, placing the patient at risk for subsequent large bowel obstruction or chronic
segmental colitis. In many instances, the attack of ischemic colitis that led to stricture
formation may have been so mild that medical care was not sought at the time, and the
episode forgotten entirely by the patient.
Extraabdominal Diagnoses
Cardiopulmonary
If the patient is complaining of pain in the upper half of the abdomen (with or without
tenderness), the chest should be examined for basilar involvement of lung parenchyma or
pleura. Because the stethoscope exam is neither sensitive nor specific for the diagnosis of
pneumonia, pulmonary infarction, small pleural effusions, or small pneumothoraces, a
chest film should be obtained. Whether a decubitus or expiratory film is requested
depends on clinical suspicion of effusion or pneumothorax, respectively. A negative film,
especially if the pain is pleuritic in quality, introduces pulmonary embolism into the
differential diagnosis.
If the pain is epigastric, and the patient is in an age/gender group in whom coronary
artery disease is prevalent, a further cardiac history and ECG should be obtained.
Ischemic cardiac pain referred to the epigastrium is not associated with significant
tenderness, although cutaneous dysesthesia may be present, similar to that found in the
upper extremity in other ischemic cardiac pain patterns.
Abdominal Wall
Pain originating from the abdominal wall may be confused with visceral pain because
superficial innervation from the lower thoracic roots enter the spinal cord via the same
dorsal horn as the deeper visceral afferents. A useful and underutilized test is the sit-up
test, also known as Carnett's sign. Following identification of the site of maximum
abdominal tenderness, patients are asked to fold their arms across their chest and sit up
halfway. The examiner maintains a finger on the tender area, and if palpation in the semisit-up position produces the same or increased tenderness, the test is said to be positive
for an abdominal wall syndrome. The logic of this is that tensing of the abdominal
muscles would be likely to protect the underlying peritoneum and intraabdominal organs,
thus reducing tenderness if the cause of pain were deep. In patients unable to perform a
sit-up, simply asking them to raise their head and shoulders off the bed is usually
sufficient to tense the abdominal muscles.
Abdominal wall syndromes overlap with hernias, neuropathic causes of abdominal pain,
and NSAP.
Hernias
Hernias represent a special type of abdominal wall syndrome, characterized by a defect
through which intraabdominal contents protrude, often intermittently, during transient
increases in intraabdominal pressure. Uncomplicated hernias are ordinarily asymptomatic
or at worst, aching and uncomfortable, but do not generally cause significant pain unless
they have become incarcerated or strangulated. Although the vast majority of hernias are
inguinal, there are many other types that must be considered, including incisional,
periumbilical, and particularly in women, femoral hernias. Sonography of the abdominal
wall is helpful in identifying hernias and other causes of abdominal wall pain.
Other Abdominal Wall Syndromes
Other causes of abdominal wall pain include rectus sheath hematomas and trauma to
other portions of the abdominal wall. In older patients or in those on anticoagulants, the
trauma may be minor and forgotten. In circumstances in which the injury is due to
stretching, causing tearing of muscle fibers, the overlying skin will not show any
evidence of bruising that might otherwise provide a clue to the presence of bleeding into
the abdominal wall.
Toxic-Metabolic
Toxic
A large number of infectious agents irritate the GI tract, producing pain that is usually
crampy. Concomitant vomiting or diarrhea suggests a gastroenteritis or enterocolitis.
Although many agents cause both upper and lower GI tract symptoms, in adults usually
one symptom complex predominates over the other. Because most of these infections are
confined to the mucosa of the GI tract, there is an absence of significant tenderness. This
is because the parietal peritoneum is not irritated by mucosal disease. If infarction,
penetration, or perforation of the bowel wall occurs, as may happen with some of the
invasive dysenteries (e.g., Salmonella), peritoneal tenderness follows. This is the reason
that abdominal tenderness of any significance should never be attributed to
uncomplicated "gastroenteritis." Furthermore, because the overall incidence of
symptomatic mucosal GI infections declines markedly with age (with the exception of
antibiotic-associated diarrhea), the probability of "gastroenteritis" as the basis for
abdominal complaints, particularly pain, in the elderly is very low indeed.
Other infections are associated with abdominal pain, although their pathophysiology is
less clear. These include group A beta-hemolytic streptococcal pharyngitis, with or
without associated scarlet fever, Rocky Mountain spotted fever, and early toxic shock
syndrome.
The other major category of toxic causes of abdominal pain are those secondary to
poisoning and overdose. These are numerous and tend to be nonspecific/nondiagnostic in
most instances. An exception to this is envenomation by the female black widow spider,
which is said to mimic peritonitis. This might represent a diagnostic dilemma if no
history was taken and only the abdomen was examined. However, because the rigid
abdomen following envenomation is due to muscular spasm, which begins at the site of
the bite and gradually spreads to involve other large muscle groups of the back and
proximal extremities, the prominence of extraabdominal signs and symptoms, as well as
their historical evolution, should point the clinician away from a primary intraabdominal
process. Isopropanol-induced hemorrhagic gastritis may be associated with cramping
pain. Cocaine-induced intestinal ischemia progressing to infarction and perforation has
been reported. Iron poisoning produces abdominal pain, and may cause hematemesis due
to its direct corrosive effects on the GI tract. Large amounts of iron left in the stomach
may also cause perforation. Mercury salts cause severe corrosion of the GI tract,
associated with shock. Acute inorganic lead toxicity is typically associated with severe,
crampy, abdominal pain. This is in contrast to chronic lead toxicity in which abdominal
pain, if present, is usually less severe and often associated with constipation. The
development of abdominal pain following electrical injury suggests a potentially serious
complication and the need for admission. Opioid withdrawal produces abdominal pain,
usually crampy in character, associated with diaphoresis and piloerection. In some
individuals, the abdominal skin is dysesthetic, but significant tenderness should not be
present. Mushroom toxicity, though rarely fatal, is commonly accompanied by a chemical
gastroenteritis and severe abdominal pain out of proportion to tenderness.
Metabolic
Anion-gap metabolic acidoses, particularly those seen in diabetic (DKA) and alcoholic
(AKA) ketoacidosis, are common causes of abdominal pain. Although the discomfort
associated with DKA and AKA has been attributed to gastric distention and paralytic
ileus, this has not been clearly substantiated. In DKA or AKA, it is critical to consider the
possibility that an underlying abdominal problem may have triggered the ketoacidosis,
rather than the reverse. This is a particularly challenging clinical problem when amylase
or lipase levels are elevated, since both AKA and DKA can be a consequence or a cause
of acute pancreatitis. If the acidosis is resistant to standard treatment, or the pain persists
after normalization of the pH, intraabdominal disease should be suspected.
Of the endocrinopathies associated with abdominal pain, adrenal crisis is the most
striking. Patients are often shocky and diffusely peritoneal. The syndrome appears to be
related to hypocortisolism rather than hypoaldosteronism. Without a history of similar
prior episodes following reduced intake or absorption of adrenal steroids, these patients
may be indistinguishable from those with an intraabdominal catastrophe. Other
endocrinopathies and electrolyte abnormalities associated with abdominal pain include
thyroid storm and hypo- and hypercalcemia. This pain is generally crampy, and
tenderness is absent unless the hyperthyroid state has caused acute hepatomegaly and
distention of the liver capsule. Hypoglycemia has been reportedly associated with
abdominal pain, but the evidence supporting this is unconvincing.
A painful sickle cell crisis is a common cause of abdominal pain, second only to
musculoskeletal pain as the most common manifestation of a vasoocclusive crisis in
homozygous (SS) disease. Occasionally, patients with SC disease and other symptomatic
heterozygous forms may present with abdominal pain due to splenomegaly or splenic
infarct. Those with heterozygous sickle trait (SA) are almost invariably asymptomatic.
The most reliable means of determining whether the abdominal pain is part of a crisis or
secondary to an underlying intraabdominal problem is to ask the patient whether or not
this is the pain of a typical crisis or whether it represents a pattern break. If the latter, the
problem is usually localized to the RUQ, either secondary to biliary tract disease (about
75 percent of those with SS have bilirubin stones due to chronic hemolysis) or
hepatomegaly due to sinusoidal sludging of sickled cells. Additional considerations for
SS patients include pancreatitis, Salmonella infection, and mesenteric venous thrombosis.
Less common "metabolic" entities associated with abdominal pain include virtually all
forms of vasculitis, especially systemic lupus and Henoch-Schönlein purpura, porphyria,
and familial Mediterranean fever. Each of these may produce peritonitis.
Neurogenic
The hallmark of neurogenic abdominal pain is a dysesthetic sensation, particularly in
response to light touch in the area of discomfort. This has been characterized by one
author as the "hover" sign, in which the patient shows signs of discomfort when the
examining hand is hovering just above or is passed very lightly over the area of
dysesthesia. A positive hover sign may be mistakenly interpreted as indicating a
generally hyperreactive patient, rather than a normal physiologic response to a
dysesthetic or anticipated dysesthetic stimulus.
Because deep and superficial nerve fibers from the same area of the abdomen may enter
the cord together, dysesthesias have also been reported with other, more serious,
intraabdominal disease, such as appendicitis. In the latter, however, the problem is
usually more acute, and either upon presentation or subsequently, is accompanied by
tenderness (in contrast to dysesthesia alone). This category includes neural entrapment
syndromes such as rectus nerve entrapment and iliohypogastric entrapment following a
Pfannelstiel incision. A number of other incisional entrapment syndromes have been
described. Many of these patients will have a positive Carnett's test, but the hover sign is
probably more indicative of neurogenic abdominal pain.
Radicular problems causing abdominal pain include diabetic or zosteriform
radiculopathy, the latter characterized by dysesthesias outlining a dermatome, usually
with some "spillover" into contiguous dermatomes on either side of the involved root.
The dysesthesias may present as lancinating, ticlike bouts of shooting pain or continuous
burning. Accompanying vesicles confirm the diagnosis, although the pain may precede
the cutaneous eruption by several days. Diabetic neuropathic involvement of a root,
plexus, or nerve can be confirmed by electromyography.
There is evidence that greater attention to the examination of the abdominal wall reduces
the frequency with which the diagnosis of NSAP is made. In one report, about 25 percent
of patients with the diagnosis of NSAP were found to have abdominal wall syndromes.
Nonspecific Abdominal Pain (NSAP)
Despite a thorough work-up, the largest single group of patients seen in the ED will have
no definite diagnosis, and will receive the designation of nonspecific abdominal pain
(NSAP). It is essential that diagnostic terms with specific meanings, such as
gastroenteritis or gastritis, not be used as catch-all phrases to describe patients with
NSAP.
Although NSAP is a diagnosis of exclusion, there are some clinical features
characteristically associated with it. Nausea, present in nearly half the patients, is the
most common symptom after abdominal pain. Pain location is usually mid-epigastric or
in the lower half of the abdomen. Tenderness is not usually severe, is absent in about onethird of the patients, and localized to the RLQ or mid-epigastrium in another one-third.
Laboratory tests are usually normal, although a mild leukocytosis is entirely compatible
with NSAP. Abdominal radiographs are virtually always normal or nonspecific. The key
to confirming NSAP is reexamination over time (see below).
Special Considerations
Diagnostic accuracy of acute abdominal pain in those 50 years old is less than 50 percent,
reaching a low of about 30 percent in octogenarians. For a detailed discussion of
diagnosing abdominal pain in the elderly, see Chap. 73.
The causes of abdominal pain in elderly patients differ substantially from those seen in
younger patients. For example, as shown in Table 72-12, the most common cause of
abdominal pain in virtually all consecutive series of adults presenting to the ED is NSAP.
However, when ED patients are dichotomized by age at 50 years old, NSAP remains at
the top of the list of diagnoses in the younger cohort, but among older patients is
markedly diminished in prevalence to <20 percent (see Table 72-3).
Table 72-12 Most Common Causes of Acute Abdominal Pain
Final Diagnosis Proportion of >10,000 Patients
Nonspecific abdominal pain (NSAP) 34%
Appendicitis 28%
Biliary tract disease 10%
Small bowel obstruction 4%
Acute gynecologic disease 4%
Salpingitis 68%
Ovarian cyst 21%
Ectopic 6%
Incomplete abortion 5%
Pancreatitis 3%
Renal colic 3%
Perforated peptic ulcer 3%
Cancer 2%
Diverticular disease 2%
Other (<1% each) 6%
There are a number of serious vascular causes of abdominal pain seen almost exclusively
among patients 50 years old, such as mesenteric ischemia, ischemic colitis, and AAA.
Among common causes of abdominal pain in both young and old, the nature of the
presentation and evolution of the same illness is often very different. Using appendicitis
as the most common example, those 50 years old are much more likely to have
generalized pain and tenderness (about 14 percent) than are younger patients (about 2
percent). The absence of localization to an area of maximum pain or tenderness may help
to account for the nearly tenfold difference in perforation rate (4 percent vs. 37 percent)
in those >60 years old when compared to their younger counterparts. Later presentation
in the course of their illness may also contribute to the increased perforation rate (75
percent of the elderly with appendicitis have >24 h of symptoms before seeking care), as
may the higher frequency of distention in older patients, making the physical examination
more difficult.
An additional contributor to the high incidence of perforation in appendicitis in the
elderly is an understandable but unfortunate reluctance to operate on frail elderly patients
without clear-cut signs of peritoneal irritation. This is reflected in the well-established
inverse association between negative laparotomies and perforated appendices. At about
the age of 45 years, the negative laparotomy rate begins to decrease in parallel with the
increase in perforations until each plateaus at about 80 years of age. Thus, the negative
laparotomy rate for appendicitis is lowest in the oldest, who are the group most likely to
perforate, and therefore most in need of early, expedient surgery.
Therefore, one must assume that the elderly patient with abdominal pain has surgical
disease. In support of this is the observation that about 40 percent of all patients >65
years old presenting to the ED with abdominal pain ultimately require surgery.
HIV/AIDS
There are several features of HIV/AIDS patients presenting to the ED with abdominal
pain that merit special attention. Abdominal pain is rarely the index event that identifies a
patient with HIV. Rather, most patients presenting with HIV-associated acute abdominal
pain will have previously met criteria for AIDS and be aware of their diagnosis.
Distinguishing acuity of pain from an extensive background of severe, chronic illness
represents the principal challenge in the evaluation of abdominal pain in HIV-positive
patients. Identifying a precise infectious etiology for the pain at the time of presentation
is well beyond the purview of emergency medicine.
Enterocolitis is the most common cause of abdominal pain in AIDS patients. It is
typically accompanied by profuse diarrhea and dehydration. If associated with fecal
leukocytes, it is more often accompanied by bacteremia than in immunocompetent
patients. Perforation, when it occurs, tends to be large bowel perforation, often caused by
cytomegalovirus (CMV). Obstruction presents in a typical fashion, but may be due to an
unusual cause such as Kaposi sarcoma, lymphoma, or atypical mycobacteria.
Biliary tract disease is very common in AIDS patients, presenting in one of two unique
forms: (1) AIDS-related cholangiopathy, caused principally by CMV or Cryptosporidium
spp. (this can be treated with sphincterotomy), and (2) AIDS-associated cholecystitis,
which is usually acalculous and has a propensity for early perforation.
Treatment
General Strategies
Hypotension
Clinically important decreases in cardiac output are commonly underdiagnosed in the
elderly. This is because many older patients have chronic systolic hypertension, making
the traditional threshold value of 100 mm Hg systolic an insensitive marker for shock in
the elderly. Conversely, healthy young women with abdominal pain, particularly if
pregnant, may run systolic BPs that rarely reach 100 mm Hg. Thus in abdominal pain, as
in all other clinical circumstances, hypotension is relative; the BP must be interpreted in
context if it is to provide meaningful information.
In abdominal pain with relative hypotension, management depends on the presumed
etiology. In the absence of heavy GI bleeding, which is not usually accompanied by
abdominal pain, younger patients are most likely to be volume-contracted from vomiting,
diarrhea, decreased oral intake, or third-spacing into the GI tract or peritoneum.
Treatment is isotonic crystalloid.
In a smaller number of young patients, hypotension may be the result of abdominal
sepsis. In this setting, in addition to appropriate antibiotics (see below) and isotonic
crystalloid, pressors may be necessary to sustain BP until more definitive intervention
can be undertaken. Vasoconstrictors are indicated in septic (vasodilatory) shock, with
norepinephrine bitartrate (Levophed) or high-dose dopamine as the usual choice of
agents.
In older patients, in addition to volume contraction and a higher incidence of abdominal
sepsis, associated cardiovascular disease represents a third possible cause of decreased
cardiac output. Indeed, in nonocclusive mesenteric ischemia, diminished cardiac output is
the cause, rather than the consequence, of the presenting abdominal pain. In this
circumstance, if the problem is acute myocardial ischemia, an aortic balloon pump may
be necessary to buy time until the underlying problem can be corrected with angioplasty
or bypass. If the decreased cardiac output is secondary to congestive failure, appropriate
treatment for CHF is indicated with the caveat that digoxin is thought to be
contraindicated in mesenteric ischemia because of a theoretical concern about worsening
vasoconstriction. If pump failure appears to be the problem, dolbutamine may be used
while slowly administering isotonic crystalloid. Arterial or venous pH and lactate levels
are a more accurate means of monitoring end-organ perfusion and shock than is the BP.
Analgesics
In the U.S., analgesia is usually withheld from patients with acute abdominal pain until a
firm treatment plan is formulated. There is no evidence to support this longstanding
practice, which has been attributed to Sir Zachary Cope. More than 75 years ago, Dr.
Cope wrote that provision of analgesia to patients with abdominal pain might obscure the
diagnosis, with dire consequences. There are many reasons why this may have been sage
advice in 1921, not the least of them being the likely outcome of perforation and sepsis in
the preantibiotic era. However, much has changed since that time in both the diagnosis
and treatment of abdominal pain: (1) There have been major advances in diagnostic
technology, the accuracy of which—in contrast to the serial clinical examination—is
largely independent of the patient's degree of evolving pain and tenderness; (2) There
have been parallel advances in therapeutic technology, including the universal
availability of antibiotics and sophisticated intra- and perioperative monitoring.
There are at least five published randomized clinical trials, too heterogeneous for
metaanalysis, but each consistent with the hypothesis that administration of opioids to
patients with abdominal pain is at least safe. Although none of these trials answers the
question definitively, at least one of them suggests that diagnosis and management of
abdominal pain may, if anything, be facilitated by opioids. The plausibility of this is
supported by an improved ability to obtain a history from a patient relieved of severe
pain, and the enhanced localization of tenderness through reduction of guarding. In spite
of these data, about 75 percent of emergency physicians recently surveyed indicated that
they did not administer opioids until after a surgeon had seen the patient.22
The information on the safety of opioids cannot be extrapolated to nonsteroidal antiinflammatories (NSAIDs) such as parenteral ketorolac, because NSAIDs are not pure
analgesics and have the potential to mask evidence of early peritoneal inflammation. At
the present time all available evidence, and the recent recommendation of the Agency for
Healthcare Research and Quality (AHRQ),23 favors judicious use of opioid analgesia in
the ED management of acute abdominal pain.
Antiemetics
Metoclopramide (Reglan) appears to be a more effective antiemetic than
prochlorperazine (Compazine). Most patients will respond within 10 min to 10 to 20 mg
of intravenous metoclopramide given slowly to minimize extrapyramidal side effects. In
many institutions, 25 to 50 mg of intravenous diphenhydramine (Benadryl) is
administered as prophylaxis against dystonias. Liberal use of antiemetics may obviate the
need for insertion of a nasogastric tube, whose therapeutic value in abdominal pain has
never been convincingly demonstrated.
Antibiotics
Antibiotics are indicated in suspected abdominal sepsis and in most patients with
localized, and all patients with diffuse, peritonitis. Endogenous gut flora cause abdominal
infections in the GI or GU tract. Primary gynecologic infections, of which PID is the
prototype, behave differently and will be discussed separately under the treatment of
suspected PID, below. In all intraabdominal nongynecologic infections, minimal
coverage should be targeted at anaerobes and facultative aerobic gram-negatives. An
exception to this generalization is the need to provide additional coverage for grampositive aerobes (e.g., Pneumococcus) in spontaneous bacterial peritonitis (SBP). SBP,
also known as primary peritonitis, occurs in patients with cirrhosis and ascites, probably
due to spontaneous bacteremic seeding of ascitic fluid. The modifier "primary" is used to
distinguish SBP from the more common peritonitis secondary to intraabdominal organ
inflammation, ischemia, leakage, or perforation.
Historically, a two-drug regimen, attacking gram-negative aerobes with an
aminoglycoside (gentamicin or tobramycin, 1.5 mg/kg IV q8h, or amikacin 5 mg/kg IV
q8h) and anaerobes with metronidazole (1 g intravenous loading dose, followed by 500
mg IV q6h, given slowly) or clindamycin (900 mg IV q8h) has been used to obtain the
requisite coverage for intraabdominal infections. While dual therapy may still be
necessary for sicker, older, immunocompromised, or hypotensive patients, monotherapy
with a second-generation cephalosporin, such as cefoxitin (2 g IV q6h) or cefotetan (2 g
IV q6h) is often adequate for those who are less ill. Alternative "combined" monotherapy
includes ampicillin-sulbactam (3 g IV q6h) or ticarcillin-clavulanate (3.1 g IV q6h). For
patients requiring a more potent regimen, but in whom one is reluctant to use an
aminoglycoside, the combination of piperacillin-tazobactam (3.3 g IV q6h) appears to be
at least as effective as imipenem-cilastatin (1 g IV q6h, maximum dose), particularly in
treatment of suspected biliary sepsis, and is less likely to cause seizures.
For patients with a history of severe allergy to penicillins or cephalosporins, aztreonam (2
g IV q6h, maximum dose) and clindamycin or metronidazole is a safe alternative. In
SBP, monotherapy with a third-generation cephalosporin such as ceftriaxone (2 g IV
q12h, maximum dose) or cefotaxime (2 g IV q4h, maximum dose) broadens the spectrum
sufficiently to cover for Pneumococcus in addition to the gram-negative enteric bacteria,
such as E. coli.
Gynecologic infections differ from those of the GI and GU tract in several important
respects: (1) They do not generally cause a septic syndrome; (2) elderly patients, who are
most likely to suffer mortality from delay in the treatment of abdominal infections or
sepsis, do not generally present with primary gynecologic infections as the cause of their
abdominal pain; and (3) treatment of PID requires different antibiotic combinations than
do GI and GU infections.
For outpatient treatment of PID, the combination of a single dose of ceftriaxone 250 mg
IM plus azithromycin 1 g PO given under direct observation, has become standard in
many EDs. However, the CDC still recommends ceftriaxone 250 mg IM plus
doxycycline 100 mg PO bid for 14 days rather than azithromycin for outpatient PID. For
inpatient treatment, the recommendation remains cefoxitin 2 g IV q6h plus doxycycline
100 mg q12h IV until improvement, then 100 mg PO bid to complete 14 days. However,
many inpatient physicians are also using azithromycin in preference to doxycycline. If
there is evidence of a tubo-ovarian abscess, the cure rate may be increased with use of
triple antibiotic coverage: clindamycin 900 mg IV q8h plus gentamicin 1.5 mg/kg IV q8h
plus ampicillin 1 g IV q6h. Doses of all aminoglycosides recommended assume normal
renal function, and must be adjusted for decreased glomerular filtration rate.
Disposition
General Indications for Admission
In addition to those with a specific diagnosis requiring admission, the following patients
should be seriously considered as candidates for hospitalization: those who appear ill; any
elderly or immunocompromised (including HIV-positive) patient (with or without
comorbidity) in whom the diagnosis is unclear; young, apparently healthy patients in
whom the diagnosis is unclear and all potentially serious causes of abdominal pain have
not been reasonably excluded; intractable pain or vomiting; acute or chronically altered
mental status; inability to follow discharge or follow-up instructions; undomiciled, living
in a shelter, or otherwise lacking social supports; and alcohol or other drug use.
Nonspecific Abdominal Pain
A substantial number of patients who are discharged with the diagnosis of NSAP are
initially admitted as suspected appendicitis. This may be the reason that there appears to
be an unexplained predominance of RLQ pain among patients discharged with the
diagnosis of NSAP.
Although this entity is poorly understood pathophysiologically, follow-up among patients
discharged from the ED with this diagnosis has found that nearly 90 percent are better or
asymptomatic at 2 to 3 weeks. Similarly, follow-up of patients discharged from inpatient
services with the diagnosis of NSAP has shown that about 80 percent have no further
problems and are asymptomatic at 5 years. Of the remainder, about one-third are
rehospitalized, of whom one-third of these have appendicitis. Some of these individuals
probably had early appendicitis on their prior admission, with spontaneous resolution due
to disimpaction of the appendiceal lumen. Of this group, it is plausible that some later
developed recurrent appendicitis and required appendectomy. The remaining two-thirds
of patients who were neither rehospitalized nor asymptomatic, turned out to have benign
gynecologic and colonic problems, most commonly irritable bowel.
The key to confirming NSAP as a working diagnosis is reexamination in 24 h, repeated
as necessary over time if patients remain symptomatic. Whether this occurs on the
inpatient service, in an ED observation unit, or follow-up in the ED depends on the
culture of the institution, the clinician's degree of uncertainty about the diagnosis, and the
presence of facilities for reliable outpatient follow-up.
References
1. American College of Emergency Physicians: Clinical policy: Critical issues for the
initial evaluation and management of patients presenting with a chief complaint of
nontraumatic acute abdominal pain. Ann Emerg Med 36:406, 2000.
2. McCaig LF, Nghi L: National Hospital Ambulatory Medical Care Survey: 2000
Emergency Department Summary. Advance data from vital and health statistics, no. 326.
Hyattsville, MD: National Center for Health Statistics, 2002, p. 14.
3. Chen SC, Wang HP, Chen WJ, et al: Selective use of ultrasonography for the detection
of pneumoperitoneum. Acad Emerg Med 9:643, 2002. [PMID: 12045083]
4. Irwig LI, Tosteson ANA, Gatsonis C, et al: Guidelines for meta-analyses evaluating
diagnostic tests. Ann Intern Med 120:667, 1994. [PMID: 8135452]
5. Gallagher EJ: Clinical utility of likelihood ratios. Ann Emerg Med 31:391, 1998.
[PMID: 9506499]
6. McColl I: More precision in diagnosing appendicitis. New Engl J Med 338:190, 1998.
[PMID: 9428821]
7. Rao PM, Rhea JT, Novelline RA, et al: Effect of computed tomography of the
appendix on treatment of patients and use of hospital resources. New Engl J Med
338:141, 1998. [PMID: 9428814]
8. Flum DR, Morris A, Koepsell T, et al: Has misdiagnosis of appendicitis decreased over
time? A population-based analysis. JAMA 286:1748, 2001. [PMID: 11594900]
9. Kalimi R, Gecelter GR, Caplin D, et al: Diagnosis of acute cholecystitis: Sensitivity of
sonography, cholescintigraphy, and combined sonography-cholescintigraphy. J Am Coll
Surg 193:609, 2001. [PMID: 11768676]
10. Magnuson TH, Bender JS, Duncan MD, et al: Utility of magnetic resonance
cholangiography in the evaluation of biliary obstruction. J Am Coll Surg 189:63, 1999.
[PMID: 10401742]
11. Burkill GJ, Bell JR, Healy JC: The utility of computed tomography in acute small
bowel obstruction. Clin Radiol 56:350, 2001. [PMID: 11384132]
12. Vissers RJ, Abu-Laban RB, McHugh DF: Amylase and lipase in the emergency
department evaluation of acute pancreatitis. J Emerg Med 17:1027, 1999. [PMID:
10595892]
13. Harvey RT, Miller WT: Acute biliary disease: Initial CT and follow-up US versus
initial US and follow-up CT. Radiology 213:831, 1999. [PMID: 10580962]
14. Hollerweger A, Macheiner P, Rettenbacher T, et al: Colonic diverticulitis: diagnostic
value and appearance of inflamed diverticula-sonographic evaluation. Eur Radiol
11:1956, 2001. [PMID: 11702128]
15. Kircher MF, Rhea JT, Kihiczak D, et al: Frequency, sensitivity, and specificity of
individual signs of diverticulitis on thin-section helical CT with colonic contrast material:
Experience with 312 cases. AJR 178:1313, 2002. [PMID: 12034590]
16. Luchs JS, Katz DS, Lane MJ, et al: Utility of hematuria testing in patients with
suspected renal colic: Correlation with unenhanced helical CT results. Urology 59:839,
2002. [PMID: 12031364]
17. Molander P, Sjoberg J, Paavonen J, et al: Transvaginal power Doppler findings in
laparoscopically proven acute pelvic inflammatory disease. Ultrasound Obstet Gynecol
17:233, 2001. [PMID: 11309174]
18. Barnhart KT, Simhan H, Kamelle SA: Diagnostic accuracy of ultrasound above and
below the beta-hCG discriminatory zone. Obstet Gynecol 94:583, 1999. [PMID:
10511363]
19. Buckley RG, King KJ, Disney JD, et al: Serum progesterone testing to predict ectopic
pregnancy in symptomatic first-trimester patients. Ann Emerg Med 36:95, 2000. [PMID:
10918099]
20. Lederle FA, Simel DL: The rational clinical examination. Does this patient have
abdominal aortic aneurysm? JAMA 281:77, 1999. [PMID: 9892455]
21. Horton KM, Fishman EK: Volume-rendered 3D CT of the mesenteric vasculature:
Normal anatomy, anatomic variants, and pathologic conditions. Radiographics 22:161,
2002. [PMID: 11796905]
22. Wolfe JM, Lein DY, Lenkoski K, et al: Analgesic administration to patients with an
acute abdomen: A survey of emergency physicians. Am J Emerg Med 18:250, 2000.
[PMID: 10830676]
23. Brownfield E: Pain management: Use of analgesics in the acute abdomen. Agency for
Healthcare Research and Quality (AHRQ).
http://www.ahrq.gov/clinic/ptsafety/chap37a.htm Accessed June 11, 2002.
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