Hepatitis E Virus Infection after Platelet Transfusion in an Immunocompetent Trauma Patient.

Hepatitis E virus (HEV) infection causes acute liver disease, but severe infections are rare in immunocompetent patients. We describe a case of HEV infection in a previously healthy male trauma patient in France who received massive transfusions. Genotyping confirmed HEV in a transfused platelet pool and the donor.

Changes in brain tissue oxygenation after treatment of diffuse traumatic brain injury by erythropoietin.

OBJECTIVES: To investigate the effects of recombinant human erythropoietin on brain oxygenation in a model of diffuse traumatic brain injury. DESIGN: Adult male Wistar rats. SETTING: Neurosciences and physiology laboratories. INTERVENTIONS: Thirty minutes after diffuse traumatic brain injury (impact-acceleration model), rats were intravenously administered with either a saline solution or a recombinant human erythropoietin (5000 IU/kg). A third group received no traumatic brain injury insult (sham-operated). MEASUREMENTS AND MAIN RESULTS: Three series of experiments were conducted 2 hours after traumatic brain injury to investigate: 1) the effect of recombinant human erythropoietin on brain edema using diffusion-weighted magnetic resonance imaging and measurements of apparent diffusion coefficient (n = 11 rats per group); local brain oxygen saturation, mean transit time, and blood volume fraction were subsequently measured using a multiparametric magnetic resonance-based approach to estimate brain oxygenation and brain perfusion in the neocortex and caudoputamen; 2) the effect of recombinant human erythropoietin on brain tissue PO2 in similar experiments (n = 5 rats per group); and 3) the cortical ultrastructural changes after treatment (n = 1 rat per group). Compared with the sham-operated group, traumatic brain injury saline rats showed a significant decrease in local brain oxygen saturation and in brain tissue PO2 alongside brain edema formation and microvascular lumen collapse at H2. Treatment with recombinant human erythropoietin reversed all of these traumatic brain injury-induced changes. Brain perfusion (mean transit time and blood volume fraction) was comparable between the three groups of animals. CONCLUSION: Our findings indicate that brain hypoxia can be related to microcirculatory derangements and cell edema without evidence of brain ischemia. These changes were reversed with post-traumatic administration of recombinant human erythropoietin, thus offering new perspectives in the use of this drug in brain injury.

Anaesthesiological support in a cardiac electrophysiology laboratory: a single-centre prospective observational study.

BACKGROUND: Implantation of cardiovascular implantable electronic devices (CIEDs) has greatly increased during the last decade and anaesthetic management of these patients remains an open question. OBJECTIVE: This study describes anaesthetic management and risk factors associated with complications occurring during these procedures. DESIGN: A single-centre prospective observational study. SETTING: Grenoble University Hospital, France, from May 2010 to October 2010. PATIENTS: All patients admitted to the cardiac electrophysiology laboratory were included. INTERVENTION: None. MAIN OUTCOME MEASURES: Clinical data, anaesthetic and medical characteristics as well as complications (respiratory or cardiovascular) and treatment were recorded by the anaesthetic nurse at the end of each procedure. RESULTS: Two hundred and sixty-nine patients were included, 229 (85%) with an American Society of Anaesthesiologists (ASA) status of 3 or 4, 103 (38%) with a New York Heart Association (NYHA) functional class of 3 or 4 and 136 (51%) with a left ventricular ejection fraction of less than 40%. Two hundred and forty-seven (92%) of the patients underwent deep sedation and 12 (8%) general anaesthesia. Seventy-eight (29%) patients had at least one complication, among whom 21 (27%) had at least one considered as severe. Fifty (19%) of the patients had a respiratory complication and 46 (17%) a cardiovascular complication; the latter was more frequently severe (41 vs. 12%; P=0.001). Lead extraction [odds ratio (OR) 13.7, 95% confidence interval (CI) 3.5 to 53.3; P<0.001], NYHA status of 4 (OR 11.8, 95% CI 1.8 to 74.8; P<0.001), implantable cardioverter-defibrillator (ICD) testing by T-wave shock (OR 3.9, 95% CI 1.53 to 10.2; P=0.005) and length of procedure (OR 1.01, 95% CI 1.004 to 1.031; P=0.013) were identified as independent risk factors for cardiovascular complications. CONCLUSION: Patients requiring cardiovascular implantable electronic device (CIED) implantation were fragile with a high complication rate and a high rate of severe complications even with anaesthesiological support. These complications, as well as the need for deep sedation or general anaesthesia, clearly justify the involvement of a qualified anaesthesiologist.

Corticosteroid after etomidate in critically ill patients: a randomized controlled trial.

OBJECTIVE: To investigate the effects of moderate-dose hydrocortisone on hemodynamic status in critically ill patients throughout the period of etomidate-related adrenal insufficiency. DESIGN: : Randomized, controlled, double-blind trial (NCT00862381). SETTING: University hospital emergency department and three intensive care units. INTERVENTIONS: After single-dose etomidate (H0) for facilitating endotracheal intubation, patients without septic shock were randomly allocated at H6 to receive a 42-hr continuous infusion of either hydrocortisone at 200 mg/day (HC group; n = 49) or saline serum (control group; n = 50). MEASUREMENTS AND MAIN RESULTS: After completion of a corticotrophin stimulation test, serum cortisol and 11ß-deoxycortisol concentrations were subsequently assayed at H6, H12, H24, and H48. Forty-eight patients were analyzed in the HC group and 49 patients in the control group. Before treatment, the diagnostic criteria for etomidate-related adrenal insufficiency were fulfilled in 41 of 45 (91%) and 38 of 45 (84%) patients in the HC and control groups, respectively. The proportion of patients with a cardiovascular Sequential Organ Failure Assessment score of 3 or 4 declined comparably over time in both HC and control groups: 65% vs. 67% at H6, 65% vs. 69% at H12, 44% vs. 54% at H24, and 34% vs. 45% at H48, respectively. Required doses of norepinephrine decreased at a significantly higher rate in the HC group compared with the control group in patients treated with norepinephrine at H6. No intergroup differences were found regarding the duration of mechanical ventilation, intensive care unit length of stay, or 28-day mortality. CONCLUSION: These findings suggest that critically ill patients without septic shock do not benefit from moderate-dose hydrocortisone administered to overcome etomidate-related adrenal insufficiency.

Dynamic SOFA score assessments to predict outcomes after acute admission of octogenarians to the intensive care unit.

BACKGROUND: Identifying which octogenarians could benefit most from continuing critical care is challenging. We aimed to see if responses to therapies using the sequential organ failure assessment (SOFA) score on day 4 after unplanned admission to the intensive care unit (ICU) could be associated with short-term mortality. METHODS: In this prospective observational cohort study, data from 4 ICUs in a University Hospital included SOFA scores on admission and day 4, along with preadmission measurements of frailty, comorbidities, nutritional status and number of medications. Outcome measures included mortality and loss of autonomy on day 90 after admission. RESULTS: Eighty-seven critically ill patients aged 80 years or older with preadmission functional independence and no missing SOFA score data on day 4 were studied (primary analyses). The mortality rate on day 90 was 30%. In a univariate Cox model, the SOFA score on day 4 was significantly associated with mortality rate: hazard ratio = 1.18 per one-point increase, 95% confidence interval (CI), 1.08 to 1.28 (p<0.001). A SOFA score of 6 or more on day 4 could correctly classify 75% of patients who died on day 90, with a sensitivity of 54% and a specificity of 84%. After adjustment, the SOFA score on day 4, neurological failure on admission and the number of preadmission medications were significantly associated with mortality on day 90, with an area under the receiver operating characteristic curve of 0.81 (95% CI, 0.71 to 0.91). These findings were confirmed in a sensitivity analysis with 109 patients. Preadmission frailty was the only variable independently associated with loss of autonomy in the 49 surviving patients. CONCLUSION: Measuring SOFA score on day 4 and preadmission frailty could help predict mortality and loss of autonomy on day 90 in octogenarians after their acute admission to the ICU.

Dexmedetomidine to facilitate non-invasive ventilation after blunt chest trauma: A randomised, double-blind, crossover, placebo-controlled pilot study.

BACKGROUND: Although non-invasive ventilation (NIV) is recommended in patients with chest trauma, this procedure may expose to discomfort and even failure due to agitation or excessive pain. We tested the impact of dexmedetomidine on the duration of the first session of NIV. METHODS: This randomised, crossover study enrolled 19 patients with blunt chest trauma who needed NIV. During one cycle comprising two NIV sessions, patients received in a random order an intravenous infusion of dexmedetomidine (0.7mcg/kg/h) and placebo (saline solution) that was initiated 60min prior to NIV. Dexmedetomidine (or placebo) was titrated to maintain a Richmond Agitation Sedation Scale (RASS) score between 0 and -3. A 6-h washout period was observed between NIV sessions. The reproducibility of the drug-related effects was tested during a second cycle of two NIV sessions. RESULTS: During the first cycle, dexmedetomidine prolonged the duration of NIV compared to placebo: 280min (118-450) (median, 25-75th quartiles) versus 120min (68-287) respectively, corresponding to a median increased duration of 96min (12-180) (P=0.03). Dexmedetomidine was associated with a lower score for RASS: -0.8 (-1.0;0.0) versus 0.0 (-0.5;0.0) (P<0.01), and reduced respiratory discomfort according to the 10cm visual similar scale: 0.6cm (0.0-3.0) versus 2.2cm (0.0-5.3) (P=0.05). Pain scores, morphine consumption, and blood gas measurements were comparable between groups. No difference in the duration of non-invasive ventilation was found during the second cycle. CONCLUSIONS: In this pilot trial, dexmedetomidine could facilitate the acceptance of the first session of non-invasive ventilation for patients with chest trauma.

Erythropoietin and Its Derivates Modulate Mitochondrial Dysfunction after Diffuse Traumatic Brain Injury.

Inhibiting the opening of mitochondrial permeability transition pore (mPTP), thereby maintaining the mitochondrial membrane potential and calcium homeostasis, could reduce the induction of cell death. Although recombinant human erythropoietin (rhEpo) and carbamylated erythropoietin (Cepo) were shown to prevent apoptosis after traumatic brain injury (TBI), their impact on mPTP is yet unknown. Thirty minutes after diffuse TBI (impact-acceleration model), rats were intravenously administered a saline solution (TBI-saline), 5000 UI/kg rhEpo (TBI-rhEpo) or 50 µg/kg Cepo (TBI-Cepo). A fourth group received no TBI insult (sham-operated) (n = 11 rats per group). Post-traumatic brain edema was measured using magnetic resonance imaging. A first series of experiments was conducted 2 h after TBI (or equivalent) to investigate the mitochondrial function with the determination of thresholds for mPTP opening and ultrastructural mitochondrial changes. In addition, the intramitochondrial calcium content [Caim] was measured. In a second series of experiments, brain cell apoptosis was assessed at 24 h post-injury. TBI-rhEpo and TBI-Cepo groups had a reduced brain edema compared with TBI-saline. They had higher threshold for mPTP opening with succinate as substrate: 120 (120-150) (median, interquartiles) and 100 (100-120) versus 80 (60-90) nmol calcium/mg protein in TBI-saline, respectively (p < 0.05). Similar findings were shown with glutamate-malate as substrate. TBI-rhEpo and Cepo groups had less morphological mitochondrial disruption in astrocytes. The elevation in [Caim] after TBI was not changed by rhEpo and Cepo treatment. Finally, rhEpo and Cepo reduced caspase-3 expression at 24 h post-injury. These results indicate that rhEpo and Cepo could modulate mitochondrial dysfunction after TBI. The mechanisms involved are discussed.