The correct interpretation of acute abdominal pain is challenging. Few other clinical situations demand greater judgment, because the most catastrophic of events may be forecast by the subtlest of symptoms and signs. A meticulously executed, detailed history and physical examination are of the greatest importance. The etiologic classification in Table 13-1, although not complete, forms a useful basis for the evaluation of patients with abdominal pain.
Table 13-1 Some Important Causes of Abdominal Pain
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Table 13-1 Some Important Causes of Abdominal Pain
|Pain Originating in the Abdomen|
Parietal peritoneal inflammation
Perforated appendix or other perforated viscus
Pelvic inflammatory disease
Mechanical obstruction of hollow viscera
Obstruction of the small or large intestine
Obstruction of the biliary tree
Obstruction of the ureter
Embolism or thrombosis
Pressure or torsional occlusion
Sickle cell anemia
Distortion or traction of mesentery
Trauma or infection of muscles
Distention of visceral surfaces, e.g., by hemorrhage
Hepatic or renal capsules
Inflammation of a viscus
|Pain Referred from Extraabdominal Source|
Acute myocardial infarction
Myocarditis, endocarditis, pericarditis
Congestive heart failure
Esophageal disease, spasm, rupture, inflammation
Torsion of the testis
Acute adrenal insufficiency
Familial Mediterranean fever
C′1 esterase inhibitor deficiency (angioneurotic edema)
Radiculitis from infection or arthritis
Spinal cord or nerve root compression
Insect or animal envenomations
Black widow spiders
The diagnosis of “acute or surgical abdomen” is not an acceptable one because of its often misleading and erroneous connotation. The most obvious of “acute abdomens” may not require operative intervention, and the mildest of abdominal pains may herald an urgently correctable lesion. Any patient with abdominal pain of recent onset requires early and thorough evaluation and accurate diagnosis.
Some Mechanisms of Pain Originating in the Abdomen
Inflammation of the Parietal Peritoneum
The pain of parietal peritoneal inflammation is steady and aching in character and is located directly over the inflamed area, its exact reference being possible because it is transmitted by somatic nerves supplying the parietal peritoneum. The intensity of the pain is dependent on the type and amount of material to which the peritoneal surfaces are exposed in a given time period. For example, the sudden release into the peritoneal cavity of a small quantity of sterile acid gastric juice causes much more pain than the same amount of grossly contaminated neutral feces. Enzymatically active pancreatic juice incites more pain and inflammation than does the same amount of sterile bile containing no potent enzymes. Blood and urine are often so bland as to go undetected if their contact with the peritoneum has not been sudden and massive. In the case of bacterial contamination, such as in pelvic inflammatory disease, the pain is frequently of low intensity early in the illness until bacterial multiplication has caused the elaboration of irritating substances.
The rate at which the irritating material is applied to the peritoneum is important. Perforated peptic ulcer may be associated with entirely different clinical pictures dependent only on the rapidity with which the gastric juice enters the peritoneal cavity.
The pain of peritoneal inflammation is invariably accentuated by pressure or changes in tension of the peritoneum, whether produced by palpation or by movement, as in coughing or sneezing. The patient with peritonitis lies quietly in bed, preferring to avoid motion, in contrast to the patient with colic, who may writhe incessantly.
Another characteristic feature of peritoneal irritation is tonic reflex spasm of the abdominal musculature, localized to the involved body segment. The intensity of the tonic muscle spasm accompanying peritoneal inflammation is dependent on the location of the inflammatory process, the rate at which it develops, and the integrity of the nervous system. Spasm over a perforated retrocecal appendix or perforated ulcer into the lesser peritoneal sac may be minimal or absent because of the protective effect of overlying viscera. A slowly developing process often greatly attenuates the degree of muscle spasm. Catastrophic abdominal emergencies such as a perforated ulcer may be associated with minimal or no detectable pain or muscle spasm in obtunded, seriously ill, debilitated elderly patients or in psychotic patients.
Obstruction of Hollow Viscera
The pain of obstruction of hollow abdominal viscera is classically described as intermittent, or colicky. Yet the lack of a truly cramping character should not be misleading, because distention of a hollow viscus may produce steady pain with only very occasional exacerbations. It is not nearly as well localized as the pain of parietal peritoneal inflammation.
The colicky pain of obstruction of the small intestine is usually periumbilical or supraumbilical and is poorly localized. As the intestine becomes progressively dilated with loss of muscular tone, the colicky nature of the pain may diminish. With superimposed strangulating obstruction, pain may spread to the lower lumbar region if there is traction on the root of the mesentery. The colicky pain of colonic obstruction is of lesser intensity than that of the small intestine and is often located in the infraumbilical area. Lumbar radiation of pain is common in colonic obstruction.
Sudden distention of the biliary tree produces a steady rather than colicky type of pain; hence, the term biliary colic is misleading. Acute distention of the gallbladder usually causes pain in the right upper quadrant with radiation to the right posterior region of the thorax or to the tip of the right scapula, but is not uncommonly midline. Distention of the common bile duct is often associated with pain in the epigastrium radiating to ...