The latest medical research on Intensive Care Medicine

The research magnet gathers the latest research from around the web, based on your specialty area. Below you will find a sample of some of the most recent articles from reputable medical journals about intensive care medicine gathered by our medical AI research bot.

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Diaphragm thickening in cardiac surgery: a perioperative prospective ultrasound study.

Annals of Intensive Care

Diaphragm paresis is common after cardiac surgery and may delay the weaning from the ventilator. Our objective was to evaluate diaphragm thickening during weaning and secondly the muscle thickness as a marker of myotrauma.

Patients undergoing elective cardiac surgery were prospectively included. Ultrasonic index of right hemidiaphragm thickening fraction (TF) was measured as a surrogate criterion of work of breathing. A TF < 20% was defined as a low diaphragm thickening. Measurements of TF were performed during three periods to study diaphragm thickening evolution defined by the difference between two consecutive time line point: preoperative (D - 1), during a spontaneous breathing trial (SBT) in the intensive care unit and postoperative (D + 1). We studied three patterns of diaphragm thickness at end expiration evolution from D - 1 to D + 1: > 10% decrease, stability and > 10% increase. Demographical data, length of surgery, type of surgery, ICU length of stay (LOS) and extubation failure were collected.

Of the 100 consecutively included patients, 75 patients had a low diaphragm thickening during SBT. Compared to TF values at D - 1 (36% ± 18), TF was reduced during SBT (17% ± 14) and D + 1 (12% ± 11) (P < 0.0001). Thickness and TF did not change according to the type of surgery or cooling method. TF at SBT was correlated to the length of surgery (both r = - 0.4; P < 0.0001). Diaphragm thickness as continuous variable did not change over time. Twenty-eight patients (42%) had a > 10% decrease thickness, 19 patients (29%) stability and 19 patients (28%) in > 10% increase, and this thickness evolution pattern was associated with: a longer LOS 3 days [2-5] versus 2 days [2-4] and 2 days [2], respectively (ANOVA P = 0.046), and diaphragm thickening evolution (ANOVA P = 0.02). Two patients experience extubation failure.

These findings indicate that diaphragm thickening is frequently decreased after elective cardiac surgery without impact on respiratory outcome, whereas an altered thickness pattern was associated with a longer length of stay in the ICU. Contractile activity influenced thickness evolution. Trial registry number ID NCT02208479.

Quantitative Lipidomics in Pulmonary Alveolar Proteinosis.

American Journal of

Pulmonary alveolar proteinosis is characterized by filling of the alveolar spaces by lipoprotein rich material of ill-defined composition, and which is caused by molecularly different and often rare diseases occurring from birth to old age.

Quantitative lipidomic analysis of lipids and surfactant proteins A, B and C from lavage fluids of patients with different causes of proteinosis in comparison to healthy contols.

During the last decades we collected alveolar lavage samples from patients with PAP due to autoantibodies against GMCSF, genetic mutations in CSF2RA, MARS, FARSB, NPC2 and secondary to myeloid leukemia. Their lipid composition was quantified.

Free cholesterol was largely increased by 60-fold and cholesterol esters by 24-fold. There was an excessive more than 130-fold increase in ceramide and other sphingolipids. Particularly long chain ceramide d18:1/20:0 or d18:1/24:0 were elevated, likely contributing to the pro-apoptotic environment observed in pulmonary alveolar proteinosis. Cellular debris lipids like phosphatidylethanolamine or phosphatidylserine were only moderately increased by 4 to 7-fold. The surfactant lipid class phosphatidylcholine expanded 17-fold, lyso- phosphatidylcholine 54-fold, and the surfactant proteins A, B, C 144-, 4- and 17-fold. All these changes did not differ between the various diseases causing pulmonary alveolar proteinosis.

This insight into the alveolar lipidome may provide monitoring tools and may open new therapeutic strategies for pulmonary alveolar proteinosis.

A clinical evaluation of two central venous catheter stabilization systems.

Annals of Intensive Care

ISRCTN, ISRCTN13939744. Registered 9 July 2015, .

The per cent of unplanned CVC removal in the two study groups was 2% (suture group 2 out of 86 patients) and 6% (suture-free group 5 out of 85 patients). Both securement methods were well tolerated in terms of skin irritation. The time and ease of application and removal of either securement systems were not rated significantly different. There was also no significant difference in CVC migration between the two securement systems in exploratory univariate and multivariate analyses. Overall, 42% (36 out of 86) of the CVC secured with sutures and 56% (48 out of 85) of the CVC secured with the suture-free securement system had CVC migration of ≥ 2 mm.

The two securement systems performed similarly in terms of CVC migration and unplanned removal of CVC; however, the feasibility study was not powered to detect statistically significant differences in these two parameters.

The Diagnosis of Bronchopulmonary Dysplasia in Very Preterm Infants: An Evidence-Based Approach.

American Journal of

Current diagnostic criteria for bronchopulmonary dysplasia rely heavily on the level and duration of oxygen therapy, do not reflect contemporary neonatal care, nor adequately predict childhood morbidity.

To determine which of 18 pre-specified, revised definitions of bronchopulmonary dysplasia, that variably define disease presence and severity according to the level of respiratory support and supplemental oxygen administered at 36 weeks postmenstrual age, best predicts death or serious respiratory morbidity through 18-26 months corrected age.

We assessed infants born <32 weeks' gestation between 2011-2015 at 18 centers of the National Institute of Child Health and Human Development Neonatal Research Network.

Of 2677 infants, 683 (26%) died or developed serious respiratory morbidity. The criteria that best predicted this outcome defined bronchopulmonary dysplasia according to treatment with the following support at 36 weeks postmenstrual age, irrespective of prior or current oxygen therapy: no bronchopulmonary dysplasia, no support (n=773); grade 1, nasal cannula ≤2L/min (n=1038); grade 2, nasal cannula >2L/min or non-invasive positive airway pressure (n=617); and grade 3, invasive mechanical ventilation (n=249). These criteria correctly predicted death or serious respiratory morbidity in 81% of study infants. Rates of this outcome increased stepwise from 10% among infants without bronchopulmonary dysplasia to 77% among those with grade 3 disease. A similar gradient (33%-79%) was observed for death or neurodevelopmental impairment.

The definition of bronchopulmonary dysplasia that best predicted early childhood morbidity categorized disease severity according to the mode of respiratory support at 36 weeks postmenstrual age, irrespective of supplemental oxygen use. This article is open access and distributed under the terms of the Creative Commons Attribution Non-Commercial License 4.0 (

Determinants of left ventricular ejection fraction and a novel method to improve its assessment of myocardial contractility.

Annals of Intensive Care

The aim of this study was to quantify the impact of different cardiovascular factors on left ventricular ejection fraction (LVEF) and test a novel LVEF calculation considering these factors.

10 pigs were studied. The experimental protocol consisted of sequentially changing afterload, preload and contractility. LV pressure-volume (PV) loops and peripheral arterial pressure were obtained before and after each intervention. LVEF was calculated as stroke volume (SV)/end-diastolic volume (EDV). We studied global cardiac function variables: LV end-systolic elastance (Ees), effective arterial elastance (Ea), end-diastolic volume and heart rate. Diastolic function was evaluated by means of the ventricular relaxation time (τ) and ventricular stiffness constant (β) obtained from the end-diastolic PV relationship. Ventriculo-arterial coupling (VAC), an index of cardiovascular performance, was calculated as Ea/Ees. LV mechanical efficiency (LVeff) was calculated as the ratio of stroke work to LV pressure-volume area. A linear mixed model was used to determine the impact of cardiac factors (Ees, Ea, EDV and heart rate), VAC and LVeff on LVEF during all experimental conditions. LVEF was mainly related to Ees and Ea. There was a strong relationship between LVEF and both VAC and LVeff (r2 = 0.69 and r2 = 0.94, respectively). The relationship between LVEF and Ees was good (r2 = 0.43). Adjusting LVEF to afterload ([Formula: see text]) performed better for estimating Ees (r2 = 0.75) and improved the tracking of LV contractility changes, even when a peripheral Ea was used as surrogate (Ea = radial MAP/SV; r2 = 0.73).

LVEF was mainly affected by contractility and afterload changes and was strongly related to VAC and LVeff. An adjustment to LVEF that considers the impact of afterload provided a better assessment of LV contractility.

Update in Neurocritical Care: a summary of the 2018 Paris international conference of the French Society of Intensive Care.

Annals of Intensive Care

The 2018 Paris Intensive Care symposium entitled "Update in Neurocritical Care" was organized in Paris, June 21-22, 2018, under the auspices of the...

Alveolar Macrophage Transcriptional Programs are Associated with Outcomes in Acute Respiratory Distress Syndrome.

American Journal of

Serial measurements of alveolar macrophage (AM) transcriptional changes in patients with acute respiratory distress syndrome (ARDS) could identify cell-specific biologic programs that are associated with clinical outcomes.

Determine whether AM transcriptional programs are associated with prolonged mechanical ventilation and 28-day mortality in subjects with ARDS.

We performed genome-wide transcriptional profiling of AMs purified from bronchoalveolar lavage fluid collected from 35 patients with ARDS. Cells were obtained at baseline (Day 1), Day 4, and Day 8 after ARDS onset (n = 68 total samples). We identified biologic pathways that were enriched at each timepoint in subjects alive and extubated within 28 days after ARDS onset (Alive/ExtubatedDay28) versus those dead or persistently supported on mechanical ventilation at day 28 (Dead/IntubatedDay28).

"M1-like" and pro-inflammatory gene sets such as IL-6-JAK-STAT5 signaling were significantly enriched in AMs isolated on Day 1 in Alive/ExtubatedDay28 versus Dead/IntubatedDay28 subjects. In contrast, by Day 8 many of these same pro-inflammatory gene sets were enriched in AMs collected from Dead/IntubatedDay28 compared with Alive/ExtubatedDay28 subjects. Serially-sampled Alive/ExtubatedDay28 patients were characterized by an AM temporal expression pattern of Day 1 enrichment of innate immune programs followed by prompt downregulation on Days 4 and 8. Dead/IntubatedDay28 subjects exhibited an opposite pattern, characterized by progressive upregulation of pro-inflammatory programs over the course of ARDS. The relationship between AM expression profiles and 28-day clinical status was distinct in subjects with Direct (pulmonary) versus Indirect (extrapulmonary) ARDS.

Clinical outcomes in ARDS are associated with highly distinct AM transcriptional programs.

Understanding Lactatemia in Human Sepsis: Potential Impact for Early Management.

American Journal of

Hyperlactatemia in sepsis may derive from a prevalent impairment of oxygen supply/demand and/or oxygen utilization. Discriminating between these two mechanisms may be relevant for the early fluid resuscitation strategy.

Understanding the relationship between central venous oxygen saturation (ScvO2), lactate and base excess to better determine the origin of lactate.

Organ dysfunction severity scores, physiological variables of hepatic, metabolic, cardiac and renal function and 90-day mortality.

ScvO2 was lower than 70% only in 35% of patients. Mortality, organ dysfunction scores, lactate were highest in the first and sixth sextiles of ScvO2. Although lactate level related strongly to mortality, it was associated with acidemia only when kidney function was impaired (creatinine >2 mg/dL), as rapidly detected by a negative alactic base excess. In contrast, positive values of alactic base excess were associated with a relative reduction of fluid balance.

Hyperlactatemia is powerfully correlated with severity of sepsis and it is caused more frequently by impaired tissue oxygen utilization, rather than by impaired oxygen transport. Concomitant acidemia was only observed in the presence of renal dysfunction, as rapidly detected by alactic base excess. The current strategy of fluid resuscitation could be modified according to the origin of excess lactate.

Design of IPF Clinical Trials in the Era of Approved Therapies.

American Journal of

The approval of nintedanib and pirfenidone for treatment of idiopathic pulmonary fibrosis has introduced complexity into the design of clinical tri...

In the ICU - delirium post cardiac arrest.

Current Opinion in Cell Biology

The present review aims to describe the clinical impact and assessment tools capable of identifying delirium in cardiac arrest survivors and providing strategies aimed at preventing and treating delirium.

Patient factors leading to a cardiac arrest, initial resuscitation efforts, and postresuscitation management all influence the potential for recovery and the risk for development of delirium. Data suggest that delirium in cardiac arrest survivors is an independent risk factor for morbidity and mortality. Recognizing delirium in postcardiac arrest patients can be challenging; however, detection is not only achievable, but important as it may aid in predicting adverse outcomes. Serial neurologic examinations and delirium assessments, targeting light sedation when possible, limiting psychoactive medications, and initiating patient care bundles are important care aspects for not only allowing early identification of primary and secondary brain injury, but in improving patient morbidity and mortality.

Developing delirium after cardiac arrest is associated with increased morbidity and mortality. The importance of addressing modifiable risk factors, recognizing symptoms early, and initiating coordinated treatment strategies can help to improve outcomes within this high risk population.

Particle Depletion Does Not Remediate Acute Effects of Traffic-Related Air Pollution and Allergen: A Randomized, Double-Blinded Crossover Study.

American Journal of

Diesel exhaust (DE), an established model of traffic-related air pollution, contributes significantly to the global burden of asthma and may augment the effects of allergen inhalation. Newer diesel particulate-filtering technologies may increase NO2 emissions, raising questions regarding their effectiveness in reducing harm from associated engine output.

To assess the effects of diesel exhaust and allergen co-exposure on lung function, airway responsiveness, and circulating leukocytes, and determine whether diesel exhaust particle-depletion remediates these effects.

In this randomized double-blinded crossover study, 14 allergen-sensitized participants (9 with airway hyper-responsiveness) underwent an inhaled allergen challenge after 2h exposures to DE, particle-depleted DE (PDDE) or filtered air. The control condition was inhaled saline after filtered air. Blood sampling and spirometry were performed before and up to 48h after exposures. Airway responsiveness was evaluated at 24h.

PDDE-allergen co-exposure impaired lung function more than DE-allergen, particularly in those genetically at risk. DE-allergen and PDDE-allergen each increased airway-responsiveness in normally-responsive participants. DE-allergen increased blood neutrophils, and was associated with persistent eosinophilia at 48h. DE and PDDE each increased total peripheral leukocyte counts in a manner affected by participant genotypes. Changes in peripheral leukocytes correlated with lung function decline.

Co-exposure to diesel exhaust and allergen impaired lung function, which was worse after particle-depletion (which increased NO2). Thus, particulates are not necessarily the sole or main culprit responsible for all harmful effects of diesel exhaust. Policies and technologies aimed at protecting public health should be scrutinized in that regard.

Unique Effect of Aspirin Therapy on Biomarkers in Aspirin-Exacerbated Respiratory Disease: A Prospective Trial.

American Journal of

Daily high-dose aspirin therapy benefits many patients with aspirin-exacerbated respiratory disease but provides no benefit for aspirin-tolerant asthmatics. Type 2 inflammation characterizes aspirin-exacerbated respiratory disease.

We sought to determine whether high-dose aspirin therapy changes biomarkers of type 2 inflammation in aspirin-exacerbated respiratory disease.

Forty-two subjects with aspirin-exacerbated respiratory disease underwent an aspirin desensitization and were placed on high-dose aspirin (1300 mg daily). Fifteen aspirin-tolerant asthmatics were also placed on high-dose aspirin. Biologic specimens and clinical parameters were collected at baseline and after 8 weeks on aspirin. Urinary eicosanoids, plasma tryptase and cytokine levels, platelet-leukocyte aggregates, and granulocyte transcripts were assessed.

Eight weeks of high-dose aspirin decreased nasal symptoms and urinary prostaglandin E metabolite (P<.05) and increased urinary leukotriene E4 (P<.01) levels in subjects with aspirin-exacerbated respiratory disease, but not in those with aspirin-tolerant asthma. Urinary prostaglandin D2 and thromboxane metabolites decreased in both groups. In aspirin-exacerbated respiratory disease subjects only, exhaled nitric oxide (P<.05), plasma tryptase (P<.01), and blood eosinophil (P<.01) and basophil (P<.01) counts increased and plasma tryptase correlated with eosinophil counts (Pearson's r= 0.514, P<.01) on aspirin. After correction for eosinophil counts, aspirin-induced changes in blood granulocyte transcripts did not differ between groups. Aspirin had no effect on platelet-leukocyte aggregates, platelet activation markers, or plasma cytokines in either group.

High-dose aspirin therapy for 8 weeks paradoxically increases markers of type 2 inflammation in subjects with aspirin-exacerbated respiratory disease, despite reducing nasal symptoms. This effect of aspirin is unique to aspirin-exacerbated respiratory disease and not observed in aspirin-tolerant asthmatics. Clinical trial registration available at, ID NCT01597375.