More adult patients visit EDs annually in the U.S. for “stomach and
abdominal pain, cramps, or spasms” than for any other chief complaint.
In 2006, 6.7% of ED visits—8.04 million patient encounters—were
for abdominal pain.1 Demographics (age, gender,
ethnicity, family history, sexual orientation, cultural practices,
geography) influence both the incidence and the clinical expression
of abdominal disease. The history, vital signs, and physical findings
may not point to a specific diagnosis, and laboratory testing is
often not helpful. Although we cannot always identify the exact
cause of the patient’s pain, we do seek to exclude life-threatening
disease and to narrow the list of diagnostic possibilities for further
workup. On the whole, clinical suspicion for serious disease is
paramount, especially for patients in high-risk groups.
Traditionally, abdominal pain has been divided into three neuroanatomic
categories: visceral, parietal, and referred.
Visceral pain is usually caused by the stretching of unmyelinated
fibers that innervate the walls or capsules of organs.
Less commonly, it is caused by early ischemia or inflammation. Visceral
pain is often described as “crampy, dull, or achy,” and
it can be either steady or intermittent in nature. Patients with
colicky visceral pain are often unable to lie still. Because the
visceral afferents follow a segmental distribution, visceral pain
is localized by the sensory cortex to an approximate spinal cord
level determined by the embryologic origin of the organ involved
Table 74-1 Visceral Pain
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Table 74-1 Visceral Pain
|Embryologic Origin||Involved Organs||Location of Visceral Pain|
|Foregut||Stomach, first/second parts of duodenum, liver,
gall bladder, pancreas||Epigastric area|
|Midgut||Third/fourth parts of duodenum, jejunum, ileum,
cecum, appendix, ascending colon, first two thirds of transverse
|Hindgut||Last one third of transverse colon, descending colon, sigmoid,
rectum, intraperitoneal GU organs||Suprapubic 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 in the midline periumbilical area, corresponding roughly
to the location of the T10 cutaneous dermatome.
Parietal (somatic) abdominal pain is caused by irritation of myelinated
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 ...