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.

Venous thromboembolism (VTE) is one of the most common preventable causes of in-hospital death in trauma patients surviving their injuries. We assessed the prevalence, incidence and risk factors for deep venous thrombosis (DVT) and pulmonary embolism (PE) in critically ill trauma patients, in the setting of a mature and early mechanical and pharmacological thromboprophylaxis protocol. This was a prospective observational study on a cohort of patients from a surgical intensive care unit of a university level 1 trauma centre. We enrolled consecutive primary trauma patients expected to be in intensive care for ≥48 h. Thromboprophylaxis was protocol driven. DVT screening was performed by duplex ultrasound of upper and lower extremities within the first 48 h, between 5 and 7 days and then weekly until discharge. We recorded VTE risk factors at baseline and on each examination day. Independent risk factors were analysed using a multivariate logistic regression. In 153 patients with a mean Injury Severity Score of 23 ± 12, the prevalence of VTE was 30.7%, 95 CI [23.7–38.8] (29.4% DVT and 4.6% PE). The incidence was 18%, 95 CI [14–24] patients-week. The median time of apparition of DVT was 6 days [1; 4]. The global protocol compliance was 77.8% with a median time of introduction of the pharmacological prophylaxis of 1 day [1; 2]. We identified four independent risk factors for VTE: central venous catheter (OR 4.39, 95 CI [1.1–29]), medullar injury (OR 5.59, 95 CI [1.7–12.9]), initial systolic arterial pressure <80 mmHg (OR 3.64, 95 CI [1.3–10.8]), and pelvic fracture (OR 3.04, 95 CI [1.2–7.9]). Despite a rigorous, protocol-driven thromboprophylaxis, critically ill trauma patients showed a high incidence of VTE. Further research is needed to tailor pharmacological prophylaxis and balance the risks and benefits.

The diagnostic value of hemoglobin (Hb) for detecting a significant hemorrhage (SH) in the early phase of trauma remains controversial. The present study aimed to assess the abilities of Hb measurements taken at different times throughout trauma management to identify patients with SH. All consecutive adult trauma patients directly admitted to six French level-1 trauma centers with at least one prehospital Hb measurement were analyzed. The abilities of the following variables to identify SH (≥ 4 units of red blood cells in the first 6 h and/or death related to uncontrolled bleeding within 24 h) were determined and compared to that of shock index (SI): Hb as measured with a point-of-care (POC) device by the prehospital team on scene (POC-Hbprehosp) and upon patient’s admission to the hospital (POC-Hbhosp), the difference between POC-Hbhosp and POC-Hbprehosp (DeltaPOC-Hb) and Hb as measured by the hospital laboratory on admission (Hb-Labhosp). A total of 6402 patients were included, 755 with SH and 5647 controls (CL). POC-Hbprehosp significantly predicted SH with an area under ROC curve (AUC) of 0.72 and best cutoff values of 12 g/dl for women and 13 g/dl for men. POC-Hbprehosp < 12 g/dl had 90% specificity to predict of SH. POC-Hbhosp and Hb-Labhosp (AUCs of 0.92 and 0.89, respectively) predicted SH better than SI (AUC = 0.77, p < 0.001); best cutoff values of POC-Hbhosp were 10 g/dl for women and 12 g/dl for men. DeltaPOC-Hb also predicted SH with an AUC of 0.77, a best cutoff value of − 2 g/dl irrespective of the gender. For a same prehospital fluid volume infused, DeltaPOC-Hb was significantly larger in patients with significant hemorrhage than in controls. Challenging the classical idea that early Hb measurement is not meaningful in predicting SH, POC-Hbprehosp was able, albeit modestly, to predict significant hemorrhage. POC-Hbhosp had a greater ability to predict SH when compared to shock index. For a given prehospital fluid volume infused, the magnitude of the Hb drop was significantly higher in patients with significant hemorrhage than in controls.

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.

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.