Abstract Introduction Contrast-induced nephropathy (CIN) has been extensively studied in the ward but only scarcely in intensive care unit (ICU) patients, even if they may be particularly prone to ...develop or to worsen acute kidney insufficiency. We aimed to measure the incidence of CIN in a large ICU population using the Acute Kidney Injury Network (AKIN) definition and to investigate its impact on patients' outcome. Methods In this 3-year retrospective study, we included all patients undergoing, during their stay in our medical ICU, a contrast media–enhanced computed tomographic scan. Change in serum creatinine between baseline (24 hours before to 12 hours after contrast media injection) and its maximum value over the 96 hours after contrast media injection was recorded. Contrast-induced nephropathy was defined as a 44.2- μ mol/L absolute or a 25% relative minimal increase in serum creatinine over 48, 72, or 96 hours and according to the stage 1 of the AKIN classification (at least 26.4 μ mol/L or 50% increase over 48 hours). Results A total of 398 contrast-enhanced computed tomographic scans performed among 299 patients were analyzed. Incidence of CIN was 14% according to the AKIN definition and ranged from 8% (48-hour absolute definition) to 23% (96-hour relative definition). The need for renal replacement therapy and ICU mortality were significantly higher in case of CIN. After adjusting for other variables associated with ICU mortality, the occurrence of at least 1 CIN episode during the ICU stay (AKIN criteria) was independently associated with ICU mortality (odds ratio, 3.85; 95% confidence interval, 1.85-8.00). Conclusions Even if incidence varied greatly depending on the definition, CIN appeared frequent in our critically ill patients. The AKIN definition, independently associated with ICU mortality, may allow unifying diagnostic criteria to further evaluate this condition that impacts morbidity and mortality.
Background
Infectious complications are a major cause of morbidity and mortality after heart transplantation (HT). However, the epidemiology and outcomes of these infections in the recent population ...of adult heart transplant recipients have not been investigated.
Methods
We conducted a single-center retrospective study on infectious complications occurring within 180 days following HT on consecutive heart transplant recipients, from January 2011 to June 2015 at Bichat University Hospital in Paris, France. Risk factors for non-viral infections occurring within 8, 30 and 180 days after HT were investigated using competing risk analysis.
Results
Overall, 113 patients were included. Fifty-eight (51%) HTs were high-priority allocations. Twenty-eight (25%) patients had an extracorporeal membrane oxygenation (ECMO) support at the time of transplantation. Ninety-two (81%) patients developed at least one infection within 180 days after HT. Bacterial and fungal infections (
n
= 181 episodes) occurred in 80 (71%) patients. The most common bacterial and fungal infections were pneumonia (
n
= 95/181 episodes, 52%), followed by skin and soft tissue infections (
n
= 26/181, 14%). Multi-drug-resistant bacteria were responsible for infections in 21 (19%) patients. Viral infections were diagnosed in 44 (34%) patients, mostly Cytomegalovirus infection (
n
= 39, 34%). In multivariate subdistribution hazard model, prior cardiac surgery (subdistribution hazard ratio sHR = 2.7 95% CI 1.5–4.6
p
< 0.01) and epinephrine or norepinephrine at the time of HT (sHR = 2.3 95% CI 1.1–5.2
p
= 0.04) were significantly associated with non-viral infections within 8 days after HT. Prior cardiac surgery (sHR = 2.5 95% CI 1.4–4.4
p
< 0.01), recipient age over 60 years (sHR = 2.0 95% CI 1.2–3.3
p
< 0.01) and ECMO following HT (sHR = 1.7 95% CI 1.0–2.8
p
= 0.04) were significantly associated with non-viral infection within 30 days after HT, as well as within 180 days after HT.
Conclusion
This study confirmed the high rate of infections following HT. Recipient age, prior cardiac surgery and ECMO following HT were independent risk factors for early and late bacterial and fungal infections.
Background. Evidence from a recent randomized controlled trial suggests that dexamethasone as adjunct therapy in adult pneumococcal meningitis reduces mortality and neurological sequelae. However, ...adding dexamethasone has the potential to reduce penetration of vancomycin into the cerebrospinal fluid (CSF). We sought to determine concentrations of vancomycin in serum and CSF of patients with suspected or proven pneumococcal meningitis receiving dexamethasone to assess the penetration of vancomycin into the CSF during steroid therapy. Methods. In an observational open multicenter study, adult patients admitted to the intensive care unit because of suspected pneumococcal meningitis received recommended treatment for pneumococcal meningitis, comprising intravenous cefotaxime (200 mg per kg of body weight per day), vancomycin (administered as continuous infusion of 60 mg per kg of body weight per day after a loading dose of 15 mg per kg of body weight), and adjunctive therapy with dexamethasone (10 mg every 6 h). Vancomycin levels in CSF were measured on day 2 or day 3 of therapy and were correlated with protein levels in CSF and vancomycin levels in serum (determined at the same time as levels in CSF). Results. Fourteen patients were included. Thirteen had proven pneumococcal meningitis; 1 patient, initially suspected of having pneumococcal meningitis, was finally determined to have meningitis due to Neisseria meningitidis. Mean levels of vancomycin in serum and CSF were 25.2 and 7.2 mg/L, respectively, and were positively correlated (r = 0.6; P = .025). A positive correlation was also found between the ratio of vancomycin in CSF to vancomycin in serum and the level of protein in CSF (r = 0.66; P = .01). Conclusions. Appropriate concentrations of vancomycin in CSF may be obtained even when concomitant steroids are used. Dexamethasone can, therefore, be used without fear of impeding vancomycin penetration into the CSF of patients with pneumococcal meningitis, provided that vancomycin dosage is adequate. This study is registered at http://www.ClinicalTrials.gov/ (registration number NCT00162578).
To demonstrate the feasibility and safety of weekly high-dose liposomal amphotericin B (L-AmB) (as a pre-emptive antifungal treatment) for 2 weeks in patients with septic shock and Candida ...colonization.
Pilot, multicentre, open-label, prospective study conducted in seven French ICUs. Non-immunocompromised patients, receiving mechanical ventilation were eligible if they presented ICU-acquired severe sepsis requiring newly administered antibacterial agents and Candida colonization in at least two sites. Exclusion criteria included the need for antifungal therapy and creatinine > 220 μmol/L. All patients were to receive a high-dose L-AmB (10 mg/kg/week) for two weeks. A follow-up period of 21 days following the second administration of L-AmB was conducted. Treated patients were compared to 69 matched untreated controls admitted in the same ICUs before the study period.
Twenty-one patients were included in the study, of which 20 received at least one infusion of high-dose L-AmB. A total of 24 adverse events were identified in 13(61%) patients. Fourteen adverse events were categorized as serious in 8(38%) patients. In four cases the adverse events were considered as potentially related to study drug administration and resulted in L-AmB discontinuation in one patient. Few patients experienced severe renal toxicity since no patient presented with severe hypokalemia. No patients required renal replacement therapy. Compared to matched controls, no significant increase in serum creatinine levels in patients receiving high-dose L-AmB was reported.
Weekly administration of high-dose L-AmB has a manageable safety profile and is feasible in patients with ICU-acquired sepsis and multiple Candida colonization. Trials of L-AmB versus other antifungal agents used as pre-emptive antifungal therapy are warranted.
ClinicalTrials.gov NCT00697944.
Background
β-lactams are the main antibiotics used against wild-type AmpC-producing Enterobacterales (wtAE). However, they may fail or select AmpC-overproducing mutants. Our aim was to assess factors ...associated with clinical failure of β-lactams in the treatment of wtAE infection.
Methods
From September 2017 to December 2020, we prospectively included all consecutive patients treated by definitive β-lactams therapy for wtAE infection in four university ICUs. Clinical failure was defined as inadequate response to antimicrobial therapy leading to death or to the switch for a broader-spectrum antibiotic.
Results
177 patients were included and 29.4% progressed to clinical failure.
E. cloacae
was the most prevalent species (42.4%) and ventilator-associated pneumonia (VAP) was the most frequent wtAE infection (69.5%). Cefepime and cefotaxime were used as definitive antibiotic treatment in 42.9% and 27.7% of patients, respectively. Occurrence of AmpC-overproduction was documented in 5.6% of patients and was associated with clinical failure (
p
= 0.004). In multivariate analysis, VAP (
p
< 0.001, OR 11.58 95% CI 3.11–43.02 and
K. aerogenes
(
p
= 0.030, OR 3.76 95% CI 1.13–12.46) were independently associated with clinical failure. Conversely, cefotaxime as definitive treatment was found inversely associated with the risk of clinical failure (
p
= 0.022, OR 0.25 95% CI 0.08–0.82). After inverse probability weighting, cefotaxime showed a 20% risk reduction of clinical failure (95% CI 5–35%,
p
= 0.007) whatever the location of infection, the SOFA score on the day of wtAE infection, or the bacterial species.
Conclusions
Clinical failure in the treatment of wtAE infections is associated with the infection site and the causal microorganism. Additionally, cefotaxime use is probably protective against clinical failure in wtAE infection.
Background
In France, the incidence of severe imported malaria cases increased since early 2000. Artesunate was available (temporarily use authorization) since mid-2011 in France and commonly used ...for severe malaria since early 2013. Thus, the study objectives were to describe the patients with severe imported malaria admitted in intensive care unit (ICU) and assess the changes in clinical presentation and outcomes before and after this date.
Methods
Retrospective observational single-center study in the infectious diseases ICU of a referral university hospital, conducted on patients admitted for severe imported malaria from 2004 to 2017. Demographic variables, severity scores, WHO’s severity criteria on admission, treatment, and ICU and hospital lengths of stay were collected. Patients’ characteristics and outcomes were compared between both periods. A poor outcome was defined as the composite endpoint of death, or requirement for vasopressors, invasive mechanical ventilation and/or renal replacement therapy.
Results
189 patients were included, 98 in 2004–2012 and 91 in 2013–2017, most often from West and Central African countries (96%). The number of WHO criteria for severe malaria was comparable in both groups, but SAPS II, SOFA and ICU length of stay were significantly higher in 2004–2012, while patients of African origin living in France were less frequent (
p
< 0.01). The outcome was poor for 41/98 cases in 2004–2012 and 12/91 cases in 2013–2017 (
p
< 0.01). The risk factors of poor outcome on the multivariate logistic regression were a neurological failure (adjusted odds ratio (adjOR = 3.23; 95% CI (1.03–10.08),
p
= 0.004), cardio-circulatory failure (adjOR = 9.92; 95% CI (2.34–42),
p
= <0.01) and creatinine blood levels > 265 µmol/L (adjOR = 10.76; 95% CI (3.17–36.53),
p
< 0.01). In the multivariate analysis, IV artesunate was not associated with a better outcome. Patients of African origin did not seem to have a better outcome than Caucasian patients or those from other origins (adjOR = 0.59; 95% CI (0.21–1.65),
p
= 0.31).
Conclusion
Patients with imported malaria admitted in ICU in 2013–2017 were less severely ill than those in 2004–2012. These trends could be partially explained by the increasing proportion of African patients visiting friends or relatives or living in endemic areas.
Patients with infective endocarditis (IE) are generally referred to the intensive care unit (ICU) for one or more organ dysfunctions caused by complications of IE. Neurologic events are frequent ...causes of ICU admission in patients with IE. They can arise through various mechanisms consisting of stroke or transient ischemic attack, cerebral hemorrhage, mycotic aneurysm, meningitis, cerebral abscess, or encephalopathy. Most complications occur early during the course of IE and are a hallmark of left-sided abnormalities of native or prosthetic valves. Occlusion of cerebral arteries, with stroke or transient ischemic attack, accounts for 40% to 50% of the central nervous system complications of IE. CT scan is the most easily feasible neuroimaging in critically unstable patients. However, magnetic resonance imaging is more sensitive and when performed should follow a standardized protocol. In patients with ischemic stroke who are already receiving oral anticoagulant therapy, this treatment should be replaced by unfractionated heparin for at least 2 weeks with a close monitoring of coagulation tests. Mounting evidence shows that, for both complicated left-sided native valve endocarditis and
Staphylococcus aureus
prosthetic valve endocarditis, valve replacement combined with medical therapy is associated with a better outcome than medical treatment alone. In a recent series, approximately 50% of patients underwent valve replacement during the acute phase of IE before completion of antibiotic treatment. After a neurological event, most patients have at least one indication for cardiac surgery. Recent data from literature suggest that after a stroke, surgery indicated for heart failure, uncontrolled infection, abscess, or persisting high emboli risk should not be delayed, provided that the patient is not comatose or has no severe deficit. Neurologic complications of IE contribute to a severe prognosis in ICU patients. However, patients with only silent or transient stroke had a better prognosis than patients with symptomatic events. In addition, more than neurologic event
per se
, a better predictor of mortality is neurologic dysfunction, which is associated with location and extension of brain damage. Patients with severe neurological impairment and those with brain hemorrhage have the worse outcome.
Management of herpes simplex encephalitis (HSE) has been considerably improved by the availability of acyclovir therapy and rapid polymerase chain reaction (PCR)—based diagnostic assays. Prognostic ...factors for this rare affliction are, however, misestimated. We conducted a large retrospective multicenter study that included 93 adult patients in whom HSE was diagnosed by PCR from 1991 through 1998 and who were treated with intravenous acyclovir. Among the 85 patients assessed at 6 months, 30 (35%) had a poor outcome, which led to death in 13 patients (15%) and severe disability in 17 (20%). The outcome was favorable for 55 patients (65%). A multivariate analysis identified 2 factors that were found to be independently associated with poor outcome: a Simplified Acute Physiology Score II ⩾27 at admission and a delay of >2 days between admission to the hospital and initiation of acyclovir therapy. Early administration of antiviral therapy is the only parameter that can be modified to improve the prognosis of patients with HSE.
Summary Objectives Our objective was to compare the virulence of 5 strains of Acinetobacter baumannii by using a mouse model of pneumonia. Methods Six-week old female C3H/HeN mice were used. The ...pneumonia was inducted by intra-tracheal inoculation of 5. 106 bacteria. Spontaneous outcome was evaluated by mortality, mice weight variations, and a clinical score. Bacterial counts in lungs, spleen and blood, and inflammatory response in lungs (dosages of tumor necrosis factor-alpha and macrophage inflammatory protein-2) were also measured. Lastly, a histological examination of lungs was performed for 3 strains, giving a histological score. Results Global mortality varied from 13% to 79% ( P < 10−4 ). Bacterial counts in lungs within the 4 days following inoculation varied significantly according to different strains. The evolution curves of bacterial counts were also different. There was a significant correlation between the clinical score and mortality ( P < 0.05) but not between bacterial counts in lungs and mortality. The increase of pro-inflammatory mediator production in lungs and the histological score also varied according to strains. Conclusions These results demonstrate the variability of the virulence between strains, and suggest that bacterial proliferation is not the only virulence factor responsible for the pathogenesis in A. baumannii pneumonia.
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