Tertiary peritonitis: considerations for complex team-based care

Abstract

Peritonitis, as a major consequence of hollow visceral perforation, anastomotic disruption, ischemic necrosis, or other injuries of the gastrointestinal tract, often drives acute care in the emergency department, operating room, and the ICU. Chronic critical illness (CCI) represents a devastating challenge in modern surgical critical care where successful interventions have fostered a growing cohort of patients with prolonged dependence on mechanical ventilation and other organ supportive therapies who would previously have succumbed much earlier in the acute phase of critical illness. An important subset of CCI patients are those who have survived an emergency abdominal operation, but who subsequently require prolonged open abdomen management complicated by persistent peritoneal space infection or colonization, fistula formation, and gastrointestinal (GI) tract dysfunction; these patients are described as having tertiary peritonitis (TP).The organ dysfunction cascade in TP terminates in death in between 30 and 64% of patients. This narrative review describes key-but not all-elements in a framework for the coordinate multiprofessional team-based management of a patient with tertiary peritonitis to mitigate this risk of death and promote recovery. Given the prolonged critical illness course of this unique patient population, early and recurrent Palliative Care Medicine consultation helps establish goals of care, support adjustment to changes in life circumstance, and enable patient and family centered care.

Keywords: Critical care; Infection; Morbidity; Mortality; Surgery; Tertiary peritonitis.

Fig. 1

Tertiary peritonitis is severe recurrent or persistent intra-abdominal inflammation after escape from or primary failure to achieve source control in a compromised host. This subset of chronic critical illness is characterized by prolonged systemic inflammation associated with acute respiratory distress syndrome (ARDS) ventilatory failure, renal failure, hypercatabolism, and severe protein–calorie malnutrition

Fig. 2

Frozen open abdomen in tertiary peritonitis, with multiple enteroatmospheric fistulae, demonstrating a patient without options for definitive source control. Clinical image courtesy of Dr. Kaplan. Patient permission obtained for photograph

Fig. 3

Triphasic approach to anesthesia considerations in tertiary peritonitis. 1 Focused evalution of cardiopulmonary stability, airway access history, and vascular access. 2 Planned plasma volume expansion, or pre-emptive administration of vasopressor agents, agile and vigilant cardiovascular monitoring and intervention. 3 Structured hand-offs so that all team members are present at the same time has been evaluated and serves as a best practice to ensure information fidelity. (HATRICC Trial) [65, 66]

Fig. 4

Pharmacologic dosing recommendations in critically ill patients, extrapolated from studies in healthy volunteers and other non-critically ill patient populations, may lead to unintended toxicities or therapeutic failures resulting from alterations in bioavailability, volume of distribution, and clearance. Diminished enterohepatic blood flow, decreased protein concentration, and acute kidney injury will each increase the risk of toxicities unless standard doses are adjusted. Additionally, since gastrointestinal absorption can be appreciably compromised in the critically ill, the intravenous route of drug administration is often preferred to ensure rapid onset of action and complete antimicrobial bioavailability

Fig. 5

Pathogens associated with tertiary peritonitis include Gram-negative aerobes (e.g., Pseudomonas, Enterobacter, Acinetobacter), enteric anaerobes, Gram-positive bacteria (e.g., coagulase-negative species, methicillin-resistant Staphylococcus aureus, and Enterococcus), and Candida species. Bacterial antimicrobial resistance is common and of particular concern in patients that have been acutely hospitalized for greater than 48 h (especially in an ICU), recently completed a course of therapeutic antibiotics, or completed an inpatient acute care stay or received home wound care or dialysis within the preceding 90 days

Fig. 6

Failure or inability to utilize enteral nutrition, in combination with inflammation and interstitial edema, results in bacterial translocation. Prolonged fasting also depletes the luminal secretions containing brush-border enzymes that are necessary for efficient absorption of nutrients