Some authors contend that all patients with colonic perforation should get prompt surgical laparotomy, and these advocates defend the traditional premise that early aggressive management decreases morbidity and mortality. Armed with the knowledge that barium sulfate can cause a progressive and lethal peritonitis, the prompt and thorough removal of all intraperitoneal barium is seen as an essential measure to avoid peritonitis or even subsequent adhesion formation. Irrigation and a gentle debriding of peritoneal surfaces is performed. Colostomy, resection, or even a Hartmann's pouch are reserved for more severe cases, including those with an obstruction distal to the perforation.2
More recently, conservative management has been heralded for asymptomatic perforations, perforations without extravasation, and for mild or localized symptoms diagnosed within 4 to 8 hours of injury. These patients are admitted to the hospital to receive bowel rest, fluids, and intravenous (IV) antibiotics. Single therapy cefoxitin will suffice in an immunocompetent patient.3 They are closely followed for 5 to 7 days and monitored for resolution of abdominal pain; reduction in pulse, temperature, or white blood cells; and return of bowel function. If peritonitis or clinical deterioration ensues, then the patient receives a laparotomy.4
While the patient in this specific case was successfully managed conservatively and discharged uneventfully with close follow-up, the question remains as to why the perforation resulted in such an extensive pattern of massive retroperitoneal air, pneumomediastinum, and subcutaneous emphysema. The pattern can be explained by a knowledge of the various fascial compartments interconnecting one anatomic structure to another. Specifically, the visceral space is a fascial compartment that extends from the neck, through the mediastinum, and eventually to the retroperitoneum, forming an anatomic connection between all three areas. Gas in any one of these areas may spread to the other via a pressure gradient from the lumen of the bowel to the adjacent soft tissues.5 Gas from pneumatosis cystoides coli can dissect along the mesentery and into the retroperitoneum. Gas extending down into the scrotal region suggests a retroperitoneal mechanism that will likely be treated conservatively. Finally, subcutaneous emphysema occurs from dissection of air from the confounds of the visceral space to the periphery, such as is the case with a pneumomediastinum tracking cephalad around the great vessels of the neck (Figure 4). Gas can also escape into the soft tissues of the abdominal wall via the anatomic connection between the posterolateral retroperitoneum and the preperitoneal flank fat.6 Ultimately, this understanding of the close anatomic fascial connections allows one to avoid becoming prematurely alarmed about the impressive imaging appearance of retroperitoneal air, pneumomediastinum, and subcutaneous emphysema without first evaluating the patient clinically.
Plain radiography is a useful initial imaging modality to make the diagnosis of bowel perforation following barium enema examination, and CT is a useful tool to differentiate retroperitoneal air from air in other compartments. An understanding of anatomic fascial compartments explains how bowel perforations can result in such a profound imaging appearance as massive retroperitoneal air, pneumomediastinum, and subcutaneous emphysema. Nonetheless, the patient's clinical examination should be followed in the postperforation period and used as a guideline for when to incorporate conservative or surgical management. Patients without intraperitoneal extravasation of barium (such as the patient in this case) who remain stable or continue to improve clinically without signs of peritonitis can be successfully managed with a conservative course of bowel rest, fluids, and IV antibiotics.
Massive retroperitoneal air, pneumomediastinum, and subcutaneous air secondary to bowel perforation after barium enema. Appl Radiol.