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
| Save Table
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 further, rigidity
and rebound appear. Patients with peritonitis generally prefer to
Referred pain is felt at a location distant from the diseased
organ. Referred pain patterns are also based upon developmental embryology.
For example, the ureter and the testes were once anatomically contiguous,
and therefore share the same segmental innervations. Thus, acute
ureteral obstruction is often associated with ipsilateral testicular
pain. Referred pain is usually perceived on the same side as the
involved organ, because it is not mediated by fibers that provide
bilateral innervation to the cord. Referred pain is felt in the
midline only if the pathologic process is also located in the midline.
The goal of this chapter is to present a pragmatic scheme based on
patient acuity and the presence or absence of modifying factors
that identify special populations of patients with abdominal pain.
The clinical answers to the questions below can be used to determine
the urgency and method of the diagnostic approach.
- Is this patient critically ill?
- Does the patient have a constellation of symptoms that fit
a known disease pattern?
- Are there special conditions (risk factors) that would make
it difficult to identify the critical illness or known disease process?
Patients with abdominal pain who present with critical illness require
simultaneous resuscitation and rapid evaluation. Stable patients
undergo standard assessments, using the history and the physical
examination to guide the evaluation. If during the assessment special
modifying factors are noted (such as immunocompromise), alternative
testing or diagnostic evaluation may be needed.
Is This Patient
Critically ill patients need stabilization before diagnosis.
Although the patient’s general appearance provides important
information about the severity of pain and the need for analgesia,
the intensity of abdominal pain may bear no relationship to the
severity of illness. Red flags include extremes of age, severe pain
of rapid onset, abnormal vital signs, dehydration, and evidence
of visceral involvement (e.g., pallor, diaphoresis, vomiting).
Vital signs are frequently abnormal in critically ill patients,
but normal vital signs do not preclude serious
illness, particularly in high-risk groups like the elderly and the
immunocompromised. Shock that develops rapidly after the onset of
acute abdominal pain is usually the consequence of intra-abdominal
hemorrhage. Systolic pressure does not drop until blood loss reaches
30% to 40% of normal blood volume. Tachycardia
is a useful parameter for the assessment of volume depletion, but
its absence does not exclude blood/fluid loss. Pulse and
blood pressure assessment should include orthostatic changes if,
after obtaining the history, there is any reason to suspect intravascular
volume depletion. An increase in pulse rate of 30 beats/min
after standing for 1 minute (or near-syncope that develops with
a lesser increase) represents the loss of a liter of blood or its
equivalent (a 20% blood loss for an average adult; roughly
3 L of normal saline). The presence of ...