Samy Figueiredo

Background: Community-acquired intra-abdominal infections (CA-IAIs) exhibit significant clinical heterogeneity. However, most studies focusing on CA-IAIs do not stratify comparisons by infection site. Methods: This post hoc analysis of the prospective multicenter PERICOM cohort (13 French university hospitals, April 2018 to February 2019) included adult patients with CA-IAIs requiring surgical management. We compared clinical characteristics, microbiology, and outcomes between appendicular and non-appendicular sites. Secondary analyses assessed the impact of Enterococcus spp., Pseudomonas aeruginosa, or fungal documentation, and the theoretical coverage of empirical antibiotic regimens. Results: Of the 205 patients, 86 (42%) had appendicular and 119 (58%) had non-appendicular CA-IAIs. Appendicular CA-IAIs involved younger patients with fewer comorbidities and were followed by fewer major postoperative complications (Clavien-Dindo score ≥ 3: 10% versus 43%, p < 0.001) and no deaths (0% versus 12%, p < 0.001). Among 118 culture-positive patients, appendicular CA-IAIs showed higher rates of non-fermenting Gram-negative bacilli (25% versus 10%, p = 0.046) and anaerobes (53% versus 28%, p = 0.008) and were more often polymicrobial (76% versus 55%, p = 0.020). Conversely, Staphylococcus spp. (0% versus 9%, p = 0.036) and fungal co-infection (0% versus 12%, p = 0.010) were confined to non-appendicular CA-IAIs. Furthermore, Enterococcus spp. documentation (24/118, 20%) identified patients with greater admission severity and higher 28-day mortality (33% versus 2%, p < 0.001). Amoxicillin-clavulanic acid plus gentamicin covered the isolates of 92% of patients versus 61% for third-generation cephalosporin plus metronidazole (p < 0.001), a difference identical in both appendicular and non-appendicular sites. Conclusions: Appendicular and non-appendicular CA-IAIs appear to be distinct entities, supporting stratified management. Future guidelines should consider site-specific strategies, therapeutic individualization, and the integration of CA-IAI ecology.

Infections caused by extended-spectrum β-lactamase-producing Klebsiella pneumoniae (ESBL-KP) are constantly rising worldwide and are often reported as causative agent of outbreaks in intensive care units (ICUs). During the first wave of the COVID-19 pandemic, bacterial cross-transmission was thought unlikely to occur due to the reinforcement of hygiene measures and prevention control. However, we report here an ESBL-producing K. pneumoniae (ST394) isolate responsible for a nosocomial outbreak in an ICU dedicated to COVID-19 patients.

Renal perfusion status remains poorly studied at the bedside during septic shock. We sought to measure cortical renal perfusion in patients with septic shock during their first 3 days of care using renal contrast enhanced ultrasound (CEUS). We prospectively included 20 ICU patients with septic shock and 10 control patients (CL) without septic shock admitted to a surgical ICU. Cortical renal perfusion was evaluated with CEUS during continuous infusion of Sonovue (Milan, Italy) within the first 24 h (day 0), between 24 and 48 h (day 1) and after 72 h (day 3) of care. Each measurement consisted of three destruction replenishment sequences that were recorded for delayed analysis with dedicated software (Vuebox). Renal perfusion was quantified by measuring the mean transit time (mTT) and the perfusion index (PI), which is the ratio of renal blood volume (rBV) to mTT. Cortical renal perfusion was decreased in septic shock as attested by a lower PI and a higher mTT in patients with septic shock than in patients of the CL group (p = 0.005 and p = 0.03). PI values had wider range in patients with septic shock (median (min-max) of 74 arbitrary units (a.u.) (3–736)) than in patients of the CL group 228 a.u. (67–440)). Renal perfusion improved over the first 3 days with a PI at day 3 higher than the PI at day 0 (74 (22–120) versus 160 (88–245) p = 0.02). mTT was significantly higher in patients with severe acute kidney injury (AKI) (n = 13) compared with patients with no AKI (n = 7) over time (p = 0.005). The PI was not different between patients with septic shock with severe AKI and those with no AKI (p = 0.29). Although hemodynamic macrovascular parameters were restored, the cortical renal perfusion can be decreased, normal or even increased during septic shock. We observed an average decrease in cortical renal perfusion during septic shock compared to patients without septic shock. The decrease in cortical renal perfusion was associated with severe AKI occurrence. The use of renal CEUS to guide renal perfusion resuscitation needs further investigation.

The optimal control of blood volume without fluid overload is a main challenge in the daily care of intensive care unit (ICU) patients. Accordingly this study focused on the identification of biomarkers to help characterize fluid overload status. Sixty-seven patients were studied from ICU admission to day 7 (D7). Blood and urine samples were taken daily and sodium and water balance strictly calculated resulting in a total cumulative assessment of ∆Na+ and ∆H2O. Furthermore, plasmatic biomarkers (cortisol, epinephrine, norepinephrine, renin, angiotensin II, aldosterone, pro-endothelin, copeptine, atrial natriuretic peptide, erythropoietin, mid-regional pro-adrenomedullin (MR-proADM)) and Sequential Organ Failure Assessment (SOFA) scores were measured at D2, D5 and D7. Blood volumes were measured with 51Cr fixed on red blood cells at D2 and D7. The ∆Na+ or ∆H2O were increased in all patients but never related to blood volumes at D2 nor D7. Total blood volumes were at normal values with constantly low red blood cell volumes and normal or decreased plasmatic volume. Weight, plasmatic proteins, and hemoglobin were weakly related to ∆Na+ or ∆H2O. Amongst all tested biomarkers, only MR-proADM was related to sodium and fluid overload. This biomarker was also a predictor of SOFA scores. Plasmatic concentration in MR-proADM seems to be a good surrogate for evaluation of ∆Na+ or ∆H2O and predicts sodium and extracellular fluid overload. ClinicalTrials.gov: NCT01858675 in May 13, 2013.