Bacterial Pericarditis Caused by Penetration of a Migrated Biliary Stent from the Lateral Segment of the Liver: A Case Report

Endoscopic biliary stent insertion is a well-established procedure that is indispensable in the management of various benign and malignant biliary disorders, and one that helps prevent mortality related to invasive surgical procedures. We report a rare case of the distal migration of a biliary stent outside the abdomen to the pericardium, inducing constrictive pericarditis and septic shock. This case alerts clinicians to be aware of potential adverse events that can lead to unfavorable patient outcomes. Such adverse events can be effectively avoided through early detection and intervention.

Purulent Pericarditis: Is It Really a Disease of the Past?

The authors present a case of purulent pericarditis probably secondary to respiratory infection, a rare entity in the antibiotic era. Pericardial fluid analysis identified streptococci and oral anaerobes as the causative agents. A prolonged and complicated diagnostic and therapeutic course, which included a long stay in the intensive care unit, is described, and a review of purulent pericarditis provided. Pericardial effusion, particularly in the setting of concomitant respiratory infection and immunocompromise or other risk factors, should raise the suspicion of bacterial pericarditis and prompt its timely diagnosis and treatment. Purulent pericarditis can be lethal and has potentially severe complications, so adequate antimicrobial therapy and source control are key.

A case report of fulminant primary streptococcal pericarditis

Background Bacterial pericarditis is a rare, rapidly progressive, and highly fatal infection, even with drainage and antibiotics. Gram-positive cocci, specifically Streptococcus pneumoniae, have been the most common cause of bacterial pericarditis from either haematogenous dissemination, or spread from another adjacent site of infection. Following the introduction of antibiotics in the 1940s and more recently the pneumococcal conjugate vaccine, the incidence has drastically decreased. Case summary A previously healthy young male was diagnosed with acute pericarditis with no signs of haemodynamic compromise on initial presentation. Several hours later, he became unstable suffering from cardiac tamponade and septic shock. Despite urgent pericardiocentesis and drainage of purulent fluid, culture positive for streptococcus pneumoniae, multi-organ failure was eventually fatal. Discussion We describe a rare case of primary S. pneumoniae purulent pericarditis leading to tamponade, septic shock, and death. Due to the high mortality rate of purulent pericarditis, a high index of suspicion is needed in order to initiate appropriate therapy with antibiotics and drainage.

Constrictive pericarditis

Constrictive pericarditis is a pericardial syndrome where the pericardium becomes relatively rigid and inelastic, may be thickened and calcified or not, and impairs mid to late diastolic filling. Constrictive pericarditis is the final pathway of several different diseases or causes, usually starting from pericarditis and pericardial effusion, and progressing towards pericardial fibrosis and calcification. Constrictive pericarditis is commonly the final evolution of any type of pericarditis and pericardial effusion. The risk of developing such evolution is especially related to the aetiology. The risk of progression is especially related to the aetiology: low (<1%) in viral and idiopathic pericarditis, intermediate (2–5%) in immune-mediated pericarditis and neoplastic pericardial diseases, and high (20–30%) in bacterial pericarditis, especially purulent pericarditis. It is important to recognize transient (subacute) constrictive pericarditis early on in the process versus calcific chronic constrictive pericarditis.

Competence Mining of Vancomycin (VAN) in the Management of Infections Due to Bacterial Strains With High VAN Minimum Inhibitory Concentrations (MICs): A Novel Dosing Strategy Based on Pharmacokinetic/Pharmacodynamic Modeling

The increasing emergence of bacterial strains with high VAN MICs (BSH–VAN–M), such as Enterococcus faecalis, Enterococcus faecium, Staphylococcus aureus, Staphylococcus epidermidis, and Streptococcus bovis, results in growing concern that VAN is not effective against these isolates. Due to the limited data on VAN against BSH–VAN–M and the application limits of drugs currently considered to be effective for BSH–VAN–M, exploration of “new usages for old drugs” is reasonable to improve and maximize the efficacy of existing antibiotics. This study aimed to construct a novel dosing strategy to mine the competence of VAN in the management of BSH–VAN–M infections. Herein, we optimized the traditional intermittent i.v. infusion (TIII) method to create an optimal two-step infusion (OTSI). With pharmacokinetic (PK)/pharmacodynamic (PD) modeling at the targeted ratio of the daily area under the concentration-time curve (AUC0–24) to the minimum inhibitory concentration (MIC) (AUC0–24/MIC) of 400, we used Monte Carlo simulations to evaluate the efficacy of 25 VAN regimens (including 15 OTSI regimens and 10 TIII regimens with daily doses of up to 6 g) to treat pneumonia, meningitis, sternal osteomyelitis, mastitis, pleuritis, bacteremia, and bacterial pericarditis resulting from isolates with MICs of ≤64 mg/L and to the current E. faecalis, E. faecium, S. aureus, S. epidermidis, and S. bovis populations with a pooled MIC distribution. Our data indicated that 4 g/day VAN, with an OTSI but not a TIII, for mastitis, pleuritis, bacteremia, and bacterial pericarditis due to isolates with MICs of ≤4 mg/L or to the current E. faecalis, S. aureus, S. epidermidis, and S. bovis populations achieved the desired PK/PD exposure at the AUC0–24/MIC target of 400. This study suggests the superiority and feasibility of OTSI relative to TIII for the competence mining of VAN against BSH–VAN–M from the perspective of PK/PD and provides a new resource for understanding how PK/PD modeling shapes the performance of VAN to meet the growing challenges of BSH–VAN–M infections.