Algorithm for rational use of Film Array Pneumonia Panel in bacterial coinfections of critically ill ventilated COVID-19 patients.

The FilmArray Pneumonia Panel has proven to be an effective tool for rapid detection of main respiratory pathogens. However, its rational use needs appropriate knowledge and formation regarding its indication and interpretation. Herein, we provide some advices to help with success of its daily routine use, particularly in critically ill ventilated COVID-19 patients. Clinical Trial registration number: NCT04453540.

[Complications and prognosis of infective endocarditis]. / Complications et pronostic de l'endocardite infectieuse.

Clinical manifestations of infective endocarditis may involve almost all body organs. They are usually classified as either cardiac or extra-cardiac complications. The first stage of infection is the development of intra-cardiac vegetation, which may further spread with an increase in size and number of vegetations, destructive valve lesions, and perivalvular extension of the infection. These anatomical lesions are responsible for hemodynamic disorders, mostly valvular regurgitation, and often lead to heart failure, which is the most frequent complication of IE. Embolic events may affect various vascular territories, the most frequent sites being brain, spleen and kidney for left-sided IE, and lung for right-sided IE. Cerebral complications may be of ischemic, hemorrhagic and/or infectious origin, are often the revealing symptoms of IE, and are well-recognized factors of poor prognosis. IE remains a dreadful disease with an in hospital mortality of 20%, a 5 year mortality of 40% and a significant morbidity.

Possible relationship between antiphospholipid antibodies and embolic events in infective endocarditis.

OBJECTIVE: Antiphospholipid (aPL) antibodies may activate platelets and contribute to vegetation growth and embolisation in infective endocarditis (IE). We aimed to determine the value of aPL as predictors of embolic events (EE) in IE. METHODS: We studied 186 patients with definite IE (Duke-Li criteria, all types of IE) from the Nanc-IE prospective registry (2007-2012) who all had a frozen blood sample and at least one imaging procedure to detect asymptomatic or confirm symptomatic EE. Anticardiolipin (aCL) and anti-ß2-glycoprotein I (ß2GPI) antibodies (IgG and IgM) were assessed after the end of patients' inclusion. The relationship between antibodies and the detection of EE after IE diagnosis were studied with Kaplan-Meier and Cox multivariate analyses. RESULTS: At least one EE was detected in 118 (63%) patients (52 cerebral, 95 other locations) after IE diagnosis in 80 (time interval between IE and EE diagnosis: 5.9±11.3 days). At least one aPL antibody was found in 31 patients (17%).Detection of EE over time after IE diagnosis was more frequent among patients with anti-ß2GPI IgM (log-rank P=0.0036) and that of cerebral embolisms, among patients with aCL IgM and anti-ß2GPI IgM (log-rank P=0.002 and P<0.0001, respectively).Factors predictive of EE were anti-ß2GPI IgM (HR=3.45 (1.47-8.08), P=0.0045), creatinine (2.74 (1.55-4.84), P=0.0005) and vegetation size (2.41 (1.41-4.12), P=0.0014). Those of cerebral embolism were aCL IgM (2.84 (1.22-6.62), P=0.016) and anti-ß2GPI IgM (4.77 (1.79-12.74), P=0.0018). CONCLUSION: The presence of aCL and anti-ß2GPI IgM was associated with EE, particularly cerebral ones, and could contribute to assess the embolic risk of IE.

Critical Illness-Related Corticosteroid Insufficiency in Cardiogenic Shock Patients: Prevalence and Prognostic Role.

BACKGROUND: Cardiogenic shock shares with septic shock common hemodynamic features, inflammatory patterns, and most likely similar complications such as critical illness-related corticosteroid insufficiency. The aim of this study was to evaluate the prevalence of critical illness-related corticosteroid insufficiency in cardiogenic shock patients and to secondarily assess its prognostic value on 90-day mortality. METHODS: A single-center prospective observational study conducted over a 3-year period and including all patients with cardiogenic shock. Main exclusion criteria were patients with prior cardiac arrest, sepsis, ongoing corticosteroid therapy, and etomidate administration. A short corticotropin test was performed in the first 24 h following admission. Serum cortisol levels were measured before (T0) and 60 min (T60) after administration of 250 µg of cosyntropin. Critical illness-related corticosteroid insufficiency was defined according to the 2017 consensus definition (basal total cortisol<10 µg·dL or a delta cortisol T60-T0<9 µg·dL) as well as the thresholds published in 2016 in cardiogenic shock patients associated with worst prognosis (basal total cortisol>29 µg·dL and delta cortisol T60-T0<17 µg·dL). RESULTS: Seventy-nine consecutive patients hospitalized in intensive care for cardiogenic shock met the inclusion criteria. Overall mortality was 43% at day 90. Forty-two percent had critical illness-related corticosteroid insufficiency using the 2017 consensus definition and 32% using the 2016 cardiogenic shock thresholds. Presence of critical illness-related corticosteroid insufficiency was not an independent factor associated with 90-day mortality irrespective of the thresholds used. CONCLUSION: Critical illness-related corticosteroid insufficiency is a frequent occurrence in medical cardiogenic shock. However, in this study, such insufficiency was not associated with prognosis.

Early prediction of norepinephrine dependency and refractory septic shock with a multimodal approach of vascular failure.

PURPOSE: The purpose of the study is to improve our ability to detect catecholamine dependency and refractory septic shock. METHODS: Fifty-one patients with septic shock were studied within the first 4 hours of norepinephrine administration. Patients were divided into 2 groups according to their evolution in the intensive care unit, namely, group A, shock reversal, and group B, no shock reversal. Reversal of shock was defined as the maintenance of a systolic blood pressure greater than or equal to 90 mm Hg without vasopressor support for 24 hours or more. Vascular reactivity was tested using incremental doses of phenylephrine. Muscle tissue oxygen saturation and its changes during a vascular occlusion test were measured. RESULTS: Group B patients had a higher Sequential Organ Failure Assessment (SOFA) score and lactate level and more frequently received norepinephrine and renal replacement. Overall mortality was 100% in group B (16/16) and 20% (7/35) in group A. Phenylephrine increased mean arterial pressure in a dose-dependent manner more significantly in group A patients than in group B (P = .0004). Basal tissue oxygen saturation and the recovery slope after vascular occlusion test were lower in group B. In multivariate analysis, 4 parameters remained independently associated with mortality: the increase in mean arterial pressure at phenylephrine 6 µg/kg per minute, the recovery slope, SOFA score, and norepinephrine doses at H0. CONCLUSIONS: The intensity of septic shock-induced vascular hyporesponsiveness to vasopressor is tightly linked to septic shock severity and evolution and may potentially be identified early with simple to obtain parameters such as near-infrared spectroscopy value, SOFA score, or norepinephrine dose.

Death of an alcohol-dependent patient following intentional drug intoxication: implication of baclofen?

Used in the treatment of spasticity at low doses, baclofen is also prescribed off-label at high doses for the treatment of alcohol dependence. Several cases of baclofen intoxication have been reported, but only 1 case deals with the treatment of alcohol dependence. Thus, we report the first death in the context of baclofen off-label use of an alcohol-dependent patient with a high blood baclofen concentration after intentional drug intoxication. The safety profile of baclofen in the treatment of alcohol dependence is reviewed and discussed, underlining the obligatory caution that may support any prescription of high doses of baclofen in this off-label indication and especially in patients with concomitant psychiatric disorders.

Comparison of norepinephrine-dobutamine to epinephrine for hemodynamics, lactate metabolism, and organ function variables in cardiogenic shock. A prospective, randomized pilot study.

OBJECTIVE: There is no study that has compared, in a randomized manner, which vasopressor is most suitable in optimizing both systemic and regional hemodynamics in cardiogenic shock patients. Hence, the present study was designed to compare epinephrine and norepinephrine-dobutamine in dopamine-resistant cardiogenic shock. DESIGN: Open, randomized interventional human study. SETTING: Medical intensive care unit in a university hospital. PATIENTS: Thirty patients with a cardiac index of <2.2 L/min/m and a mean arterial pressure of <60 mm Hg resistant to combined dopamine-dobutamine treatment and signs of shock. Patients were not included in cases of cardiogenic shock secondary to acute ischemic events such as myocardial infarction. Noninclusion criteria also included immediate indication of mechanical assistance. INTERVENTIONS: Patients were randomized to receive an infusion of either norepinephrine-dobutamine or epinephrine titrated to obtain a mean arterial pressure of between 65 and 70 mm Hg with a stable or increased cardiac index. MAIN RESULTS: Both regimens increased cardiac index and oxygen-derived parameters in a similar manner. Patients in the norepinephrine-dobutamine group demonstrated heart rates lower (p<.05) than those in the epinephrine group. Epinephrine infusion was associated with new arrhythmias in three patients. When compared to baseline values, after 6 hrs, epinephrine infusion was associated with an increase in lactate level (p<.01), whereas this level decreased in the norepinephrine-dobutamine group. Tonometered PCO2 gap, a surrogate for splanchnic perfusion adequacy, increased in the epinephrine-treated group (p<.01) while decreasing in the norepinephrine group (p<.01). Diuresis increased in both groups but significantly more so in the norepinephrine-dobutamine group, whereas plasma creatinine decreased in both groups. CONCLUSIONS: When considering global hemodynamic effects, epinephrine is as effective as norepinephrine-dobutamine. Nevertheless, epinephrine is associated with a transient lactic acidosis, higher heart rate and arrhythmia, and inadequate gastric mucosa perfusion. Thus, the combination norepinephrine-dobutamine appears to be a more reliable and safer strategy.