Ségolène Mrozek

Soluble form of the receptor for advanced glycation end products is a marker of acute lung injury but not of severe sepsis in critically ill patients

Objectives:Levels of the soluble form of the receptor for advanced glycation end products (sRAGE) are elevated during acute lung injury. However, it is not known whether this increase is linked to its involvement in alveolar epithelium injury or in systemic inflammation. Whether sRAGE is a marker of acute lung injury and acute respiratory distress syndrome, regardless of associated severe sepsis or septic shock, remains unknown in the intensive care unit setting. Design:Prospective, observational, clinical study. Setting:Intensive care unit of an academic medical center. Patients:A total of 64 consecutive subjects, divided into four groups: acute lung injury/acute respiratory distress syndrome (n = 15); acute lung injury/acute respiratory distress syndrome plus severe sepsis/septic shock (n = 18); severe sepsis/septic shock (n = 16); and mechanically ventilated controls (n = 15). Interventions:None. Measurements and Main Results:Plasma sRAGE levels were measured at baseline and on days 3, 6, and 28 (or at intensive care unit discharge, whichever occurred first). Baseline plasma levels of sRAGE were significantly higher in patients with acute lung injury/acute respiratory distress syndrome, with (median, 2951 pg/mL) or without (median, 3761 pg/mL) severe sepsis, than in patients with severe sepsis (median, 488 pg/mL) only and in mechanically ventilated controls (median, 525 pg/mL). Levels of sRAGE were correlated with acute lung injury/acute respiratory distress syndrome severity and decreased over time but were not associated with outcome. Lower baseline plasma sRAGE was associated with focal loss of aeration based on computed tomography lung morphology. Conclusions:sRAGE levels were elevated during acute lung injury/acute respiratory distress syndrome, regardless of the presence or absence of severe sepsis. The plasma level of sRAGE was correlated with clinical and radiographic severity in acute respiratory distress syndrome patients and decreased over time, suggesting resolution of the injury to the alveolar epithelium. Further study is warranted to test the clinical utility of this biomarker in managing such patients and to better understand its relationship with lung morphology during acute lung injury/acute respiratory distress syndrome.

Brain temperature: physiology and pathophysiology after brain injury.

The regulation of brain temperature is largely dependent on the metabolic activity of brain tissue and remains complex. In intensive care clinical practice, the continuous monitoring of core temperature in patients with brain injury is currently highly recommended. After major brain injury, brain temperature is often higher than and can vary independently of systemic temperature. It has been shown that in cases of brain injury, the brain is extremely sensitive and vulnerable to small variations in temperature. The prevention of fever has been proposed as a therapeutic tool to limit neuronal injury. However, temperature control after traumatic brain injury, subarachnoid hemorrhage, or stroke can be challenging. Furthermore, fever may also have beneficial effects, especially in cases involving infections. While therapeutic hypothermia has shown beneficial effects in animal models, its use is still debated in clinical practice. This paper aims to describe the physiology and pathophysiology of changes in brain temperature after brain injury and to study the effects of controlling brain temperature after such injury.

Biomarkers and acute brain injuries: interest and limits

For patients presenting with acute brain injury (such as traumatic brain injury, subarachnoid haemorrhage and stroke), the diagnosis and identification of intracerebral lesions and evaluation of the severity, prognosis and treatment efficacy can be challenging. The complexity and heterogeneity of lesions after brain injury are most probably responsible for this difficulty. Patients with apparently comparable brain lesions on imaging may have different neurological outcomes or responses to therapy. In recent years, plasmatic and cerebrospinal fluid biomarkers have emerged as possible tools to distinguish between the different pathophysiological processes. This review aims to summarise the plasmatic and cerebrospinal fluid biomarkers evaluated in subarachnoid haemorrhage, traumatic brain injury and stroke, and to clarify their related interests and limits for diagnosis and prognosis. For subarachnoid haemorrhage, particular interest has been focused on the biomarkers used to predict vasospasm and cerebral ischaemia. The efficacy of biomarkers in predicting the severity and outcome of traumatic brain injury has been stressed. The very early diagnostic performance of biomarkers and their ability to discriminate ischaemic from haemorrhagic stroke were studied.

Successful treatment of inverted Takotsubo cardiomyopathy after severe traumatic brain injury with milrinone after dobutamine failure

BACKGROUND Takotsubo cardiomyopathy can occur at the early phase of severe acute brain injuries. In the case of cardiac output decrease or shock, the optimal treatment is still a matter of debate. Due to massive stress hormone release, the infusion of catecholamines may have limited effects and may even aggravate cardiac failure. Other inotropic agents may be an option. Levosimendan has been shown to have potential beneficial effects in this setting, although milrinone has not been studied. METHODS We report a case of a young female presenting with inverted Takotsubo cardiomyopathy syndrome after severe traumatic brain injury. RESULTS Due to hemodynamic instability and increasing levels of infused norepinephrine, dobutamine infusion was begun but rapidly stopped due to tachyarrhythmia. Milrinone infusion stabilized the patients hemodynamic status and improved cardiac output without deleterious effects. CONCLUSION Milrinone could be a good alternative when inotropes are required in Takotsubo cardiomyopathy and when dobutamine infusion is associated with tachyarrhythmia.

Assessment of brain midline shift using sonography in neurosurgical ICU patients

IntroductionBrain midline shift (MLS) is a life-threatening condition that requires urgent diagnosis and treatment. We aimed to validate bedside assessment of MLS with Transcranial Sonography (TCS) in neurosurgical ICU patients by comparing it to CT.MethodsIn this prospective single centre study, patients who underwent a head CT were included and a concomitant TCS performed. TCS MLS was determined by measuring the difference between the distance from skull to the third ventricle on both sides, using a 2 to 4 MHz probe through the temporal window. CT MLS was measured as the difference between the ideal midline and the septum pellucidum. A significant MLS was defined on head CT as >0.5 cm.ResultsA total of 52 neurosurgical ICU patients were included. The MLS (mean ± SD) was 0.32 ± 0.36 cm using TCS and 0.47 ± 0.67 cm using CT. The Pearson’s correlation coefficient (r2) between TCS and CT scan was 0.65 (P <0.001). The bias was 0.09 cm and the limits of agreements were 1.10 and -0.92 cm. The area under the ROC curve for detecting a significant MLS with TCS was 0.86 (95% CI =0.74 to 0.94), and, using 0.35 cm as a cut-off, the sensitivity was 84.2%, the specificity 84.8% and the positive likelihood ratio was 5.56.ConclusionsThis study suggests that TCS could detect MLS with reasonable accuracy in neurosurgical ICU patients and that it could serve as a bedside tool to facilitate early diagnosis and treatment for patients with a significant intracranial mass effect.

Accidental hypothermia in severe trauma

Hypothermia, along with acidosis and coagulopathy, is part of the lethal triad that worsen the prognosis of severe trauma patients. While accidental hypothermia is easy to identify by a simple measurement, it is no less pernicious if it is not detected or treated in the initial phase of patient care. It is a multifactorial process and is a factor of mortality in severe trauma cases. The consequences of hypothermia are many: it modifies myocardial contractions and may induce arrhythmias; it contributes to trauma-induced coagulopathy; from an immunological point of view, it diminishes inflammatory response and increases the chance of pneumonia in the patient; it inhibits the elimination of anaesthetic drugs and can complicate the calculation of dosing requirements; and it leads to an over-estimation of coagulation factor activities. This review will detail the pathophysiological consequences of hypothermia, as well as the most recent principle recommendations in dealing with it.

Plasma sRAGE is independently associated with increased mortality in ARDS: a meta-analysis of individual patient data

PurposeThe soluble receptor for advanced glycation end-products (sRAGE) is a marker of lung epithelial injury and alveolar fluid clearance (AFC), with promising values for assessing prognosis and lung injury severity in acute respiratory distress syndrome (ARDS). Because AFC is impaired in most patients with ARDS and is associated with higher mortality, we hypothesized that baseline plasma sRAGE would predict mortality, independently of two key mediators of ventilator-induced lung injury.MethodsWe conducted a meta-analysis of individual data from 746 patients enrolled in eight prospective randomized and observational studies in which plasma sRAGE was measured in ARDS articles published through March 2016. The primary outcome was 90-day mortality. Using multivariate and mediation analyses, we tested the association between baseline plasma sRAGE and mortality, independently of driving pressure and tidal volume.ResultsHigher baseline plasma sRAGE [odds ratio (OR) for each one-log increment, 1.18; 95% confidence interval (CI) 1.01–1.38; P = 0.04], driving pressure (OR for each one-point increment, 1.04; 95% CI 1.02–1.07; P = 0.002), and tidal volume (OR for each one-log increment, 1.98; 95% CI 1.07–3.64; P = 0.03) were independently associated with higher 90-day mortality in multivariate analysis. Baseline plasma sRAGE mediated a small fraction of the effect of higher ΔP on mortality but not that of higher VT.ConclusionsHigher baseline plasma sRAGE was associated with higher 90-day mortality in patients with ARDS, independently of driving pressure and tidal volume, thus reinforcing the likely contribution of alveolar epithelial injury as an important prognostic factor in ARDS. Registration: PROSPERO (ID: CRD42018100241).

Reversible Cerebral Vasoconstriction Syndrome with Intracranial Hypertension: Should Decompressive Craniectomy Be Considered

Background: Reversible cerebral vasoconstriction syndrome (RCVS) is a rare cause of intracerebral hemorrhage (ICH) causing intracranial hypertension. Methods: Case report. Results: We report a case of RCVS-related ICH leading to refractory intracranial hypertension. A decompressive craniectomy was performed to control intracranial pressure. We discuss here the management of RCVS with intracranial hypertension. Decompressive craniectomy was preformed to avoid the risky option of high cerebral perfusion pressure management with the risk of bleeding, hemorrhagic complications, and high doses of norepinephrine. Neurological outcome was good. Conclusion: RCVS has a complex pathophysiology and can be very difficult to manage in cases of intracranial hypertension. Decompressive craniectomy should probably be considered.