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INTRODUCTION AND EPIDEMIOLOGY
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More adult patients visit the ED for “stomach and abdominal pain, cramps, or spasms” than for any other chief complaint.1 Demographics (age, gender, ethnicity, family history, sexual orientation, cultural practices, geography) influence both the incidence and the clinical expression of abdominal disease.1 History, physical examination, and laboratory studies can be helpful, but imaging is often required to make a specific diagnosis. Clinical suspicion for serious disease is especially important for patients in high-risk groups.
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Abdominal pain is divided into three neuroanatomic categories: visceral, parietal, and referred.
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Obstruction, ischemia, or inflammation can cause stretching of unmyelinated fibers that innervate the walls or capsules of organs, resulting in visceral pain. Visceral pain is often described as “crampy, dull, or achy,” and it can be either steady or intermittent (colicky). Because the visceral afferent nerves 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 71-1).
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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.
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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 remain immobile.
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Referred pain is felt at a location distant from the diseased organ. Referred pain patterns are also based on developmental embryology. For example, the ureter and the testes were once anatomically ...