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The high incidence of AKI in trauma patients should lead to early identification of those at risk of AKI to establish a resuscitation strategy that aims at preventing AKI.

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O ver the past years, particular attention has been given to herpes virus reactivations among immunocompetent critically ill patients. Although the true pathogenicity of these reactivations is still debated, some authors have hypothesized that it could be related to specific immune failure caused by sepsis or multi-organ failure. Others have argued that it is only a marker of severity. There is increasing evidence that reactivation of cytomegalovirus (CMV) and herpes simplex virus (HSV) is associated with mortality or morbidity, mainly for ventilator-acquired pneumonia. [1,2] CMV seroprevalence ranges from 40% to 95% depending on several factors, including age and geographic area. HSV1 seroprevalence is around 65% among the French population. Epstein-Barr virus (EBV) reactivation has been well docu- Original Article Epstein-Barr Virus Reactivation in Critically IllImmunocompetent Patients Background: Herpes viruses can be reactivated among immunocompetent patients in intensive care unit (ICU). Cytomegalovirus (CMV) and herpes simplex virus (HSV) have been the most studied. We hypothesized that Epstein-Barr virus (EBV) could also be reactivated in immunocompetent patients during their stay in ICU and that this would be associated with morbidity and mortality. Methods:This prospective observational study included 90 patients with an ICU stay of ≥ 5 days. CMV and HSV were considered when clinically suspected and DNA was researched in blood or bronchoalveolar lavage (BAL). EBV DNA viral quantification was performed in the blood samples. Results:EBV DNA was detected in blood of 61 patients (median length for positivity of 7.5 days). CMV DNA was detected in blood of 16 patients (median length for positivity of 13.5 days) and BAL of 6 patients. HSV1 DNA was detected in the BAL of 28 patients (median length for positivity of 7.5 days). Nineteen patients had no viral reactivation, 1 experienced only CMV, 32 had only EBV, 5 had only HSV, 6 had EBV and CMV, 14 had EBV and HSV, and 9 patients reactivated three viruses. Mortality was higher among patients with EBV reactivation (33/61 vs. 7/25, p = 0.02). Length of stay (21 vs. 10 days, p < 0.001) and length of mechanical ventilation (15 vs. 7 days, p < 0.001) were higher among patients with EBV reactivation. Conclusions: This study shows that EBV DNA is detected in blood of diverse ICU patients with ≥ ≥ 5 days of stay and that it is associated with morbidity and mortality. Larger dynamic prospective studies are needed to correlate viral reactivation with immune system evolution during ICU stay and to determine the role of polyviral reactivations. (Biomed J 2015;38:70-76)

Three patients with extensive necrotizing pneumonia due to Panton-Valentine leukocidin-positive Staphylococcus aureus strains and with aggravating factors (leukopenia count of less than 3 ؋ 10 9 /liter in all three cases and hemoptysis in two cases) were successfully treated with toxin-suppressing agents introduced rapidly after hospital admission. CASE REPORT Patient 1. In December 2007, a 6-month-old boy presented to the emergency department with a 5-day history of a virallike syndrome, including rhinorrhea, fever, and diarrhea. On admission, he had dry cough, moderate dyspnea, altered general status, and sepsis (39.4°C, heart rate of 198 beats per minute [bpm], tachypnea, and marbling). The initial laboratory tests showed a C-reactive protein level of 73.4 mg/liter and a total leukocyte count of 7.3 ϫ 10 9 /liter. Chest radiography revealed a basal left-sided infiltrate without pleural effusion ( Fig. 1). Treatment with ceftriaxone and supportive measures was started, but his respiratory status worsened. Severe hypoxemia was present, with partial pressure of oxygen in arterial blood (PaO2) of 3.9 kPa under 3 liters/min of nasal oxygenotherapy. Eight hours after admission, a second chest radiograph revealed extensive bilateral infiltrate and pleural effusion (Fig. 1). He was admitted to the pediatric intensive care unit (PICU) with signs of septic shock (oliguria and altered mental status) which improved with fluid resuscitation. Laboratory tests showed lactic acidosis (pH 7.27 and lactic acid at 5.50 mmol/liter), hypoxemia, and leukopenia (1.83 ϫ 10 9 /liter) (Fig. 2). Pleural puncture yielded purulent fluid (40 ml) that tested negative by Gram staining and pneumococcal antigen detection. Staphylococcal necrotizing pneumonia was suspected in view of the rapid clinical deterioration, leukopenia, and negative tests for pneumococci. Vancomycin and clindamycin were added to ceftriaxone 15 h after admission. Staphylococcus aureus was detected in pleural fluid 24 h after admission, and culture yielded a Panton-Valentine leukocidin (PVL)-positive community-acquired methicillin-resistant S. aureus (MRSA) strain belonging to European clone sequence type 80 (ST80). The strain was susceptible to clindamycin, and the MIC to vancomycin was 1.5 mg/liter. The patient's status gradually improved, despite the need for pleural drainage because of recurrent pleural effusion. He was discharged from the PICU on day 7. Eight days after PICU admission, he remained febrile (39.3°C) and still had respiratory disorders (dyspnea and diminished left vesicular murmur), but the leukocyte count had risen to 32 ϫ 10 9 /liter (Fig. 2). Computed tomography (CT) revealed significant pleural effusion, multiple lung lesions, and pleural abscesses. Pleural decortication was performed. Intraoperative pleural samples were positive for the same strain of PVL-positive MRSA, and antibiotic treatment was switched to rifampin plus clindamycin. The boy was discharged from the hospital on day 28, on a 3-week course of oral antibiotics. Serologic tests and...

BackgroundClosed-loop resuscitation can improve personalization of care, decrease workload and bring expert knowledge in isolated areas. We have developed a new device to control the administration of fluid or simultaneous co-administration of fluid and norepinephrine using arterial pressure.MethodWe evaluated the performance of our prototype in a rodent model of haemorrhagic shock. After haemorrhagic shock, rats were randomized to five experimental groups: three were resuscitated with fluid and two with co-administration of fluid and norepinephrine. Among groups resuscitated with fluid, one was resuscitated by a physician and two were resuscitated according to two different closed-loop algorithms. Among groups resuscitated with fluid and norepinephrine, one was resuscitated by a physician and the other one by the closed-loop device. The precision of arterial pressure during the resuscitation period was assessed using rising time, time passed in the target area and performance error calculations.ResultsGroups resuscitated with fluid had similar performances and passed as much time in the target area of 80–90 mmHg as the manual group [manual: 76.8% (67.9–78.2), closed-loop: 64.6% (45.7–72.9) and 80.9% (59.1–85.3)]. Rats resuscitated with fluid and norepinephrine using closed-loop passed similar time in target area than manual group [closed-loop: 74.4% (58.4–84.5) vs. manual: 60.1% (46.1–72.4)] but had shorter rising time to reach target area [160 s (106–187) vs. 434 s (254–1081)] than those resuscitated by a physician. Rats resuscitated with co-administration of fluid and norepinephrine required less fluid and had less hemodilution than rats resuscitated with fluid alone. Lactate decrease was similar between groups resuscitated with fluid alone and fluid with norepinephrine. ConclusionsThis study assessed extensively the performances of several algorithms for closed-loop resuscitation of haemorrhagic shock with fluid alone and with co-administration of fluid and norepinephrine. The performance of the closed-loop algorithms tested was similar to physician-guided treatment with considerable saving of work for the caregiver. Arterial pressure closed-loop guided algorithms can be extended to combined administration of fluid and norepinephrine. Electronic supplementary materialThe online version of this article (10.1186/s13613-018-0436-0) contains supplementary material, which is available to authorized users.

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