Abdomen agudo

Med Clin N Am 90 (2006) 481–503

Acute Abdominal Pain
Mark H. Flasar, MD*, Eric Goldberg, MD
Division of Gastroenterology and Hepatology, Department of Medicine, University of Maryland Medical Center, Baltimore, MD, USA

Abdominal pain is a common complaint in all settings of medical practice. In the United States in 2002, abdominal pain was the chief complaint of over 7 million patientspresenting to an emergency department (ED), accounting for 6.5% of all patient visits [1]. In primary care practices in 2002, abdominal pain was a complaint of more than 13.5 million patient visits, accounting for 1.5% of patient encounters [2]. In certain situations, abdominal pain may be a symptom of a severe, life-threatening disease process, whereas in other situations, it may be a symptom of amore benign underlying condition. This review provides a framework for understanding abdominal pain, so that practitioners may determine those patients who need a more expedited evaluation, and reviews the pathophysiologic mechanisms underlying abdominal pain. A general approach to the patient is outlined, and several causes of abdominal pain are considered in detail, focusing on the most severeand commonly encountered. A general understanding of abdominal anatomy, physiology, and pathophysiology is vital when formulating a differential diagnosis for abdominal pain. In addition, it is important to understand how abdominal pain is generated and perceived by the patient. The abdominal viscera are innervated with nociceptive afferents within the mesentery, on peritoneal surfaces, and withinthe mucosa and muscularis of hollow organs. These afferents respond to both mechanical and chemical stimuli, producing sensations of dull, crampy, insidious pain. The principal mechanical stimulus is stretching, whereas a variety of chemical stimuli, including substance P, serotonin, prostaglandins, and Hþ ions, are perceived as noxious by visceral chemoreceptors [3]. Abdominal pain occurs in threebroad patterns, visceral, parietal, and referred. Visceral nociception typically involves stretching and
* Corresponding author. Division of Gastroenterology and Hepatology, Department of Medicine, University of Maryland Medical Center, 22 South Greene Street, Baltimore, MD 21201. E-mail address: mflasar@medicine.umaryland.edu (M.H. Flasar). 0025-7125/06/$ - see front matter Ó 2006 Elsevier Inc.All rights reserved. doi:10.1016/j.mcna.2005.11.005 medical.theclinics.com

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distension of the abdominal organs, but torsion and contraction also contribute. The pain is carried on slow-conducting C-fibers. Patients often describe pain of visceral origin as a dull ache. Visceral pain is often located at the midline because visceral innervation of abdominal organs istypically bilateral. Pain location corresponds to those dermatomes that match the innervation of the injured organ [3]. Generally, visceral pain from organs proximal to the ligament of Treitz (embryonic foregut), including the hepatobiliary organs and spleen, is felt in the epigastrum. Visceral pain from abdominal organs between the ligament of Treitz and the hepatic flexure of the colon (embryonicmidgut) is felt in the periumbilical region. Visceral pain generated from organs distal to the hepatic flexure (embryonic hindgut) is perceived in the midline lower abdomen. Parietal pain is typically sharp and well localized, resulting from the direct irritation of the peritoneal lining. Parietal peritoneal afferents are A delta fibers with a rapid conduction velocity, which results in a sharp painsensation similar to skin and muscle pain. Because parietal innervation is unilateral, lateralization of pain occurs [3]. Referred pain occurs when visceral afferents carrying stimuli from a diseased organ enter the spinal cord at the same level as somatic afferents from a remote anatomic location; it is typically well localized. A single diseased organ may produce all three types of pain. For...