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Review
. 2018 Jun 18:361:k1407.
doi: 10.1136/bmj.k1407.

Secondary peritonitis: principles of diagnosis and intervention

Affiliations
Review

Secondary peritonitis: principles of diagnosis and intervention

James T Ross et al. BMJ. .

Abstract

Secondary peritonitis accounts for 1% of urgent or emergent hospital admissions and is the second leading cause of sepsis in patients in intensive care units globally. Overall mortality is 6%, but mortality rises to 35% in patients who develop severe sepsis. Despite the dramatic growth in the availability and use of imaging and laboratory tests, the rapid diagnosis and early management of peritonitis remains a challenge for physicians in emergency medicine, surgery, and critical care. In this article, we review the pathophysiology of peritonitis and its potential progression to sepsis, discuss the utility and limitations of the physical examination and laboratory and radiographic tests, and present a paradigm for the management of secondary peritonitis.

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Conflict of interest statement

Competing interests: We have read and understood BMJ policy on declaration of interests and declare the following interests: none.

Figures

Fig 1
Fig 1
Common etiologies of secondary peritonitis in adults
Fig 2
Fig 2
Peritoneum and diaphragmatic lymphatic drainage. The abdominal cavity is divided by the mesentery into two major compartments, the greater and lesser sacs. The lesser sac is bound by the retroperitoneum posteriorly, the stomach and greater omentum anteriorly, and the transverse colon and transverse colon mesentery inferiorly. The remainder of the abdominal cavity is the greater sac, and the two are connected via the foramen of Winslow. This is relevant to the clinical diagnosis of secondary peritonitis as perforation into the lesser sac, such as a perforated ulcer in the posterior gastric wall, may be temporarily contained in the lesser sac, preventing the patient from developing peritonitis. The peritoneum forms a semipermeable barrier through which water and solutes are passively exchanged. Regular circulation of peritoneal fluid is driven in part by the movement of the diaphragm. Bacteria and larger debris are cleared via stomata, lymphatic portals between mesothelial cells, which are concentrated on the diaphragmatic surface. The embryology, histology, and physiology of the peritoneum were reviewed recently by van Baal et al
Fig 3
Fig 3
Management algorithm. Patients with localized peritonitis who are hemodynamically stable should receive broad spectrum antibiotics and cross sectional imaging. Those with evidence of bowel compromise, feculent, or four quadrant contamination should have laparotomy. Patients with acute appendicitis, acute cholecystitis, or perforated peptic ulcer may undergo laparoscopic resection or repair. Select patients with purulent peritonitis or in whom the diagnosis is unclear may undergo laparoscopy with lavage or conversion to laparotomy as necessary. Those with contained perforation should be managed with a trial of conservative management or percutaneous drainage depending on the accessibility and size of the abscess. Failure to improve clinically with conservative management or after intervention should prompt repeat imaging with percutaneous drainage or exploration as needed. Patients with generalized peritonitis or localized peritonitis with hemodynamic instability should receive fluid resuscitation and broad spectrum antibiotics, with vasopressors if necessary. Once patients have been resuscitated, they should be taken for urgent laparotomy. We advise that the rare patient with abdominal sepsis who cannot be stabilized with appropriate fluids, antibiotics, and vasopressors should not be taken for surgery because of the negligible chance of survival. In some cases, these patients may be candidates for bedside procedures. Patients without peritonitis should be evaluated for clinical risk of bowel compromise. Patients over 65 years, or with significant cardiovascular disease or bowel obstruction, should be considered to be at high risk of bowel compromise and should receive cross sectional imaging (see “Identification of patients at high risk of bowel compromise”). Patients without peritonitis or high risk of bowel compromise should undergo focused investigation guided by the clinical presentation (see “Imaging to clarify diagnosis”). The management of these patients is beyond the scope of this review. This algorithm deliberately excludes hemodynamically unstable patients with abdominal pain but without peritonitis. This combination of symptoms covers a broad range of diagnoses that are beyond the scope of this review
Fig 4
Fig 4
Utility of radiographic studies in diagnosis of acute abdominal pain. *When used in addition to physical examination and laboratory tests; if used in addition to computed tomography, improves specificity (87% v 41%) but not sensitivity (88% in both groups). †Organ dose ranges from 0.01 mSv to lung in anterior-posterior chest film to 0.25 mSv to stomach in anterior-posterior film of abdomen. ‡When used in addition to physical examination and laboratory tests. §Assuming induction of cancer is proportional to radiation dose even for very small doses of radiation, so-called linear non-threshold model, risk of death from cancer attributable to single computed tomography scan is approximately 0.02% in 50 year old patient and 0.06% in 25 year old patient

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