Intravascular haemolysis has been associated with acute kidney injury (AKI) in different clinical settings (cardiac surgery, sickle cell disease). Haemolysis occurs frequently in critically ill burn patients. The aim of this study was to assess the predictive value of haptoglobin at admission to predict major adverse kidney events (MAKE) and AKI in critically ill burn patients. We conducted a retrospective, single-centre cohort study in a burn critical care unit in a tertiary centre, including all consecutive severely burned patients (total burned body surface > 20% and/or shock and/or mechanical ventilation at admission) from January 2012 to April 2017 with a plasmatic haptoglobin dosage at admission. A total of 130 patients were included in the analysis. Their mean age was 49 (34–62) years, their median total body surface area burned was 29% (15–51%) and the intensive care unit (ICU) mortality was 25%. Early haemolysis was defined as an undetectable plasmatic haptoglobin at admission. We used logistic regression to identify MAKE and AKI risk factors. In multivariate analysis, undetectable haptoglobin was associated with MAKE and AKI (respectively, OR 6.33, 95% CI 2.34–16.45, p < 0.001; OR 8.32, 95% CI 2.86–26.40, p < 0.001). Undetectable plasmatic haptoglobin at ICU admission is an independent risk factor for MAKE and AKI in critically ill burn patients. This study provides a rationale for biomarker-guided therapy using haptoglobin in critically ill burn patients.

Deep sternal wound infection after cardiac surgery remains a serious complication associated with a poor prognosis. Deep sternal wound infection is classified by the Centers for Disease Control and Prevention as deep incisional surgical site-infection and mediastinitis. This study aims to describe the incidence, perioperative characteristics, and outcomes of deep sternal wound infection on the basis of clinical presentations. This monocentric retrospective study included all consecutive patients who underwent cardiac surgery with cardiopulmonary bypass between 2006 and 2019 in a tertiary teaching hospital. The primary outcome was 90-day mortality, and the main secondary outcome was a landmark analysis of 90-day mortality, excluding patients who died within the first 28 days. Among the 14,850 patients included in this study, deep sternal wound infection occurred in 542 (3.6%) patients: 390 (72%) presented with deep incisional surgical site-infection and 152 (28%) presented mediastinitis. Patients with deep sternal wound infection had a lower 90-day survival than patients without deep sternal wound infection; in particular, patients with mediastinitis had the lowest survival rate compared to deep incisional surgical site-infection- and deep sternal wound infection -free patients (82% vs 94% vs 95%, respectively; both comparisons P < .001), and mediastinitis was an independent risk factor for 90-day mortality. No difference in 90-day survival was observed between patients without deep sternal wound infection and patients with deep incisional surgical site-infection (P = .378). However, in the landmark analysis, both deep incisional surgical site-infection and mediastinitis were associated with lower survival compared with patients without deep sternal wound infection and were independent risk factors for mortality. Deep incisional surgical site-infection and mediastinitis exhibited distinct incidences, bacterial characteristics, and prognoses, with mediastinitis being associated with the poorest prognosis. However, when the competing risk of death was considered, deep incisional surgical-site infection diSSI also emerged as an independent risk factor for 90-day mortality.

Ketamine-associated cholestatic liver injury is reported in patients with severe burn injury, but its association with patient outcome is unclear. We investigated the relationship between ketamine exposure, cholestatic liver injury, and outcome of critically ill patients with burn injury. In a retrospective study, patients with severe burn injury were analysed across two periods: unrestricted ketamine prescription (ketamine-liberal) and capped ketamine dosage (ketamine-restricted). The primary endpoint was cholestatic liver injury, and the secondary endpoint was 3-month mortality. Binary logistic regression models and the revised electronic causality assessment method were used to measure the strength of associations and causality assessment, respectively. Of 279 patients (median age 51 [IQR 31–67] years; 63.1% men; burned surface area 28.5%, IQR 20–45%), 155 (56%) were in the ketamine-liberal group, and 124 (44%) were in the ketamine-restricted group, with comparable clinical characteristics, except for ketamine exposure (median doses 265.0 [IQR 0–8,021] mg and 20 [IQR 0–105] mg, respectively; p <0.001). A dose- and time-dependent relationship was observed between ketamine exposure and cholestatic liver injury. Ketamine restriction was associated with a reduced risk of cholestatic liver injury (adjusted odds ratio 0.16, 95% CI 0.04–0.50; p = 0.003) and with a higher probability of 3-month survival (p = 0.035). The revised electronic causality assessment method indicated that ketamine was probably and possibly the cause of cholestatic liver injury for 14 and 10 patients, respectively. Cholangitis was not observed in the ketamine-restricted group. In propensity-matched patients, the risk of 3-month mortality was higher (adjusted odds ratio 9.92, 95% CI 2.76–39.05; p = 0.001) in patients with cholestatic liver injury and ketamine exposure ≥10,000 mg. Other sedative drugs were not associated with liver and patient outcome. In this cohort, ketamine restriction was associated with less cholestatic liver injury and reduced 3-month mortality. In a cohort of 279 critically ill patients with burn injury, ketamine was associated with a risk of liver bile duct toxicity. The risk was found to be dependent on both the dosage and duration of ketamine use. A restriction policy of ketamine prescription was associated with a risk reduction of liver injury and 3-month mortality. These findings have implications for the analgesia and sedation of critically ill patients with ketamine, with higher doses raising safety concerns.

Background: Burns intensive care units (BICUs) have reduced mortality in patients with burns, but infections and sepsis remain the leading causes of death. Infections with multidrug-resistant (MDR) bacteria increase the risk of death in patients with burns, whose risk of acquiring such infections is higher due to various factors, including prolonged hospitalization and invasive procedures. Methods: A retrospective study was performed in a French BICU over 8 years to analyze the epidemiology and risk factors for bloodstream infections (BSIs). Results: In total, 1402 patients were admitted to the BICU. Thermal burns were the most common cause of injury, and the median total body surface area burned was 10%. Patients had various comorbid conditions, particularly smoking and hypertension. BSI occurred in 303 (21%) patients. When compared with patients without BSI, patients with BSI were older, had higher severity scores and a larger total body surface area burned, and were more likely to develop complications. The prevalence of monomicrobial and polymicrobial BSI remained stable during hospitalization, with gram-positive pathogens such as Staphylococcus aureus most common during the first week but with gram-negative pathogens, particularly MDR Pseudomonas aeruginosa, becoming more prevalent after 15 days. The distribution of microorganisms remained stable throughout the study, except for a significant decrease in Acinetobacter baumannii rates and an increase in MDR P aeruginosa rates after 2015. Conclusions: An understanding of the epidemiology of BSI-causing microorganisms over time is crucial for sepsis management to ensure the selection of appropriate empirical antimicrobial therapy and to highlight the need for infection prevention and antimicrobial stewardship.