An 80-year-old woman with hypertension presents to the emergency department with the sudden onset of severe abdominal pain. The pain began abruptly 1 hour prior to her arrival, without any apparent antecedent events. She complains of excruciating, diffuse, sharp abdominal pain that is constant, does not radiate, and exacerbates with movement, especially during the ambulance ride to the hospital. She had a single episode of emesis, but otherwise denies any associated symptoms.
The patient is afebrile, but tachycardic and tachypneic, and has relative hypotension with systolic blood pressure in the 90s. She appears anxious, diaphoretic, and uncomfortable. Her abdomen is distended, tympanitic, and diffusely tender, with rebound and guarding in all quadrants. Her laboratory tests reveal a leukocytosis of 16,000 with a bandemia, glucose of 240, and lactate of 3.
Abdominal pain is a leading reason for emergency department visits.1 Acute abdominal pain accounts for 40% of emergency surgical hospital admissions, and a large proportion of these patients have perforated hollow viscus or impending gastrointestinal perforation.2 In Western countries, the incidence of gastrointestinal perforation for patients not taking nonsteroidal anti-inflammatory drugs is 0.1 per 1000 person-years.3 Early diagnosis and intervention are key, as mortality for patients with hollow viscus perforation and secondary peritonitis exceeds 20%.2,4,5
Perforated hollow viscus is characterized by loss of gastrointestinal wall integrity with subsequent leakage of enteric contents. Direct trauma or tissue ischemia and necrosis lead to full-thickness disruption of the gastrointestinal wall and perforation. Perforation may occur at any site within the alimentary tract, from mouth to anus, and the site of the perforation largely determines the patient’s presentation and clinical course.
Exposure of the normally sterile peritoneal cavity to intraluminal contents causes either a chemical peritonitis or secondary bacterial peritonitis. Proximal perforations can leak acidic gastric or caustic biliary or pancreatic secretions, and the resultant chemical peritonitis triggers a robust systemic inflammatory response syndrome (SIRS) with the potential for rapid clinical deterioration.2,6 In contrast, distal perforations leak intraluminal contents that are more chemically inert, but that carry a high bacterial load. Their clinical course may be more insidious, with development of purulent or fecal peritonitis and intra-abdominal abscess or phlegmon.2
Perforated hollow viscus should be considered in the differential diagnosis for any patient presenting with an acute abdomen. Often, patients describe initially localized, visceral pain that becomes diffuse, dramatic, and severe, and progresses to peritonitis. Alternatively, patients with advanced age, obesity, immunosuppression, or contained perforation may present with minimal findings. Associated symptoms are nonspecific and may include fever, chills, nausea, vomiting, anorexia, change in bowel habits, weight loss (for contained perforation), syncope, dizziness, and dysuria.
Because patients with perforated hollow viscus may present in a moribund state and have ...