The Acute Abdomen

Abstract

The acute abdomen is considered by many to be the sudden onset of abdominal pain requiring surgical intervention. In reality, not all causes of acute abdominal pain require surgery, and likewise not all “surgical” abdomens are necessarily of acute onset. The assessment of the acute abdomen pain is an art form that all surgeons must master. Understanding the nature of the abdominal pain, as well as the ability to obtain a thorough history and physical, may be the only tools necessary to determine the diagnosis and whether urgent surgical intervention is required. If a patient is stable, carefully chosen diagnostic studies may help to pinpoint or confirm the diagnosis and guide intervention. Abdominal pain can be divided into two components that correlate with the innervation of the visceral and parietal peritoneum. The visceral peritoneum is innervated by C fibers that course with the autonomic ganglia. Visceral pain is a response to injury of the organ and its adherent visceral peritoneum. Distension, stretch, traction, compression, torsion, ischemia, and inflammation of the visceral peritoneum trigger visceral pain fibers. Contrarily, abdominal organs are insensate to heat, cutting, or electrical stimulation. C fibers are unmyelinated, polymodal nociceptors that conduct slowly (0.5–5 m/s) producing a dull, crampy pain. C fibers travel bilaterally with the sympathetic and parasympathetic chains, and will often be interpreted as vague, central abdominal pain. Organs proximal to the ligament of Treitz, embryologically derived from the foregut (stomach, duodenum, pancreas), will refer to the celiac chain. This is perceived as epigastric pain. Likewise, the midgut (small bowel and right colon) presents as periumbilical pain and the hindgut (transverse, left, sigmoid colon, and rectum) as hypogastric pain. Somatic pain travels via Aδ somatic fibers coursing with the spinal nerves T7 through L2. Aδ fibers are thinly myelinated, fast conductors that, when fired, are perceived as sharp, pricking pain. When an abdominal process inflames the parietal peritoneum, or peritonitis, the pain becomes severe and localizes to the source of inflammation. Movement or aggravation of the parietal peritoneum will exacerbate the pain. Clinicians often describe pain as referred or associated with rebound or rigidity. The perception of pain removed from the location of its source, or referred pain, can be predicted by the nerves with which the pain fibers travel. For example, appendiceal obstruction leading to its distension will present as vague, dull, referred visceral pain to the umbilicus. An inflamed gallbladder causing parietal irritation of the diaphragm will refer via the phrenic nerve as shoulder pain. The retroperitoneal genitourinary organs and pancreas share innervation with the abdominal viscera and can also present as abdominal pain. The pain may be vague from referral via the autonomic ganglia of the abdomen and pelvis, or more severe from direct irritation of the abutting parietal peritoneum. While pain is described by the patient, this should be distinguished from the tenderness invoked on exam. Rebound tenderness occurs after deep palpation of the abdomen is released and indicates peritoneal inflammation. Similarly, muscular rigidity is an involuntary spasm of the abdominal muscles in response to parietal inflammation. When the rigidity is voluntarily overcome by the patient, this is referred to as voluntary guarding. Involuntary guarding cannot be overcome and suggests a more ominous, diffuse peritonitis.