Pierre Bouzat

Diagnostic Accuracy of Ultrasonography in the Acute Assessment of Common Thoracic Lesions After Trauma

BACKGROUND The accuracy of combined clinical examination (CE) and chest radiography (CXR) (CE + CXR) vs thoracic ultrasonography in the acute assessment of pneumothorax, hemothorax, and lung contusion in chest trauma patients is unknown. METHODS We conducted a prospective, observational cohort study involving 119 adult patients admitted to the ED with thoracic trauma. Each patient, secured onto a vacuum mattress, underwent a subsequent thoracic CT scan after first receiving CE, CXR, and thoracic ultrasonography. The diagnostic performance of each method was also evaluated in a subgroup of 35 patients with hemodynamic and/or respiratory instability. RESULTS Of the 237 lung fields included in the study, we observed 53 pneumothoraces, 35 hemothoraces, and 147 lung contusions, according to either thoracic CT scan or thoracic decompression if placed before the CT scan. The diagnostic performance of ultrasonography was higher than that of CE + CXR, as shown by their respective areas under the receiver operating characteristic curves (AUC-ROC): mean 0.75 (95% CI, 0.67-0.83) vs 0.62 (0.54-0.70) in pneumothorax cases and 0.73 (0.67-0.80) vs 0.66 (0.61-0.72) for lung contusions, respectively (all P < .05). In addition, the diagnostic performance of ultrasonography to detect pneumothorax was enhanced in the most severely injured patients: 0.86 (0.73-0.98) vs 0.70 (0.61-0.80) with CE + CXR. No difference between modalities was found for hemothorax. CONCLUSIONS Thoracic ultrasonography as a bedside diagnostic modality is a better diagnostic test than CE and CXR in comparison with CT scanning when evaluating supine chest trauma patients in the emergency setting, particularly for diagnosing pneumothoraces and lung contusions.

Cerebral Extracellular Lactate Increase is Predominantly Nonischemic in Patients with Severe Traumatic Brain Injury

Growing evidence suggests that endogenous lactate is an important substrate for neurons. This study aimed to examine cerebral lactate metabolism and its relationship with brain perfusion in patients with severe traumatic brain injury (TBI). A prospective cohort of 24 patients with severe TBI monitored with cerebral microdialysis (CMD) and brain tissue oxygen tension (PbtO2) was studied. Brain lactate metabolism was assessed by quantification of elevated CMD lactate samples (>4 mmol/L); these were matched to CMD pyruvate and PbtO2 values and dichotomized as glycolytic (CMD pyruvate > 119 μmol/L vs. low pyruvate) and hypoxic (PbtO2 < 20 mm Hg vs. nonhypoxic). Using perfusion computed tomography (CT), brain perfusion was categorized as oligemic, normal, or hyperemic, and was compared with CMD and PbtO2 data. Samples with elevated CMD lactate were frequently observed (41 ±8%), and we found that brain lactate elevations were predominantly associated with glycolysis and normal PbtO2 (73 ± 8%) rather than brain hypoxia (14 ±6%). Furthermore, glycolytic lactate was always associated with normal or hyperemic brain perfusion, whereas all episodes with hypoxic lactate were associated with diffuse oligemia. Our findings suggest predominant nonischemic cerebral extracellular lactate release after TBI and support the concept that lactate may be used as an energy substrate by the injured human brain.

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 11&bgr;-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.

Transcranial Doppler to screen on admission patients with mild to moderate traumatic brain injury.

BACKGROUND:Detecting patients at risk for secondary neurological deterioration (SND) after mild to moderate traumatic brain injury is challenging. OBJECTIVE:To assess the diagnostic accuracy of transcranial Doppler (TCD) on admission in screening these patients. METHODS:This prospective, observational cohort study enrolled 98 traumatic brain injury patients with an initial Glasgow Coma Scale score of 9 to 15 whose initial computed tomography (CT) scan showed either absent or mild lesions according to the Trauma Coma Data Bank (TCDB) classification, ie, TCDB I and TCDB II, respectively. TCD measurements of the 2 middle cerebral arteries were obtained on admission under stable conditions in all patients. Neurological outcome was reassessed on day 7. RESULTS:Of the 98 patients, 21 showed SND, ie, a decrease of ≥ 2 points from the initial Glasgow Coma Scale or requiring any treatment for neurological deterioration. Diastolic cerebral blood flow velocities and pulsatility index measurements were different between patients with SND and patients with no SND. Using receiver-operating characteristic analysis, we found the best threshold limits to be 25 cm/s (sensitivity, 92%; specificity, 76%; area under curve, 0.93) for diastolic cerebral blood flow velocity and 1.25 (sensitivity, 90%; specificity, 91%; area under curve, 0.95) for pulsatility index. According to a recursive-partitioning analysis, TCDB classification and TCD measurements were the most discriminative among variables to detect patients at risk for SND. CONCLUSION:In patients with no severe brain lesions on CT after mild to moderate traumatic brain injury, TCD on admission, in complement with brain CT scan, could accurately screen patients at risk for SND.

Beyond intracranial pressure: optimization of cerebral blood flow, oxygen, and substrate delivery after traumatic brain injury

Monitoring and management of intracranial pressure (ICP) and cerebral perfusion pressure (CPP) is a standard of care after traumatic brain injury (TBI). However, the pathophysiology of so-called secondary brain injury, i.e., the cascade of potentially deleterious events that occur in the early phase following initial cerebral insult—after TBI, is complex, involving a subtle interplay between cerebral blood flow (CBF), oxygen delivery and utilization, and supply of main cerebral energy substrates (glucose) to the injured brain. Regulation of this interplay depends on the type of injury and may vary individually and over time. In this setting, patient management can be a challenging task, where standard ICP/CPP monitoring may become insufficient to prevent secondary brain injury. Growing clinical evidence demonstrates that so-called multimodal brain monitoring, including brain tissue oxygen (PbtO2), cerebral microdialysis and transcranial Doppler among others, might help to optimize CBF and the delivery of oxygen/energy substrate at the bedside, thereby improving the management of secondary brain injury. Looking beyond ICP and CPP, and applying a multimodal therapeutic approach for the optimization of CBF, oxygen delivery, and brain energy supply may eventually improve overall care of patients with head injury. This review summarizes some of the important pathophysiological determinants of secondary cerebral damage after TBI and discusses novel approaches to optimize CBF and provide adequate oxygen and energy supply to the injured brain using multimodal brain monitoring.

Prognostic factors for extracorporeal cardiopulmonary resuscitation recipients following out-of-hospital refractory cardiac arrest. A systematic review and meta-analysis

PURPOSE Association estimates between baseline characteristics and outcomes are imprecise and inconsistent among extracorporeal cardiopulmonary resuscitation (ECPR) recipients following refractory out-of-hospital cardiac arrest (OHCA). This systematic review and meta-analysis aimed to investigate the prognostic significance of pre-specified characteristics for OHCA treated with ECPR. METHODS The Medline electronic database was searched via PubMed for articles published from January 2000 to September 2016. The electronic search was supplemented by scanning the reference lists of retrieved articles and contacting field experts. Eligible studies were historical and prospective cohort studies of adult patients undergoing ECPR following OHCA. RESULTS Fifteen primary studies were included, totaling 841 participants. The median prevalence of the primary outcome (i.e., short- or long-term survival for five studies and cerebral performance for ten studies) was 15% (range, 0-50%). The primary outcome was associated with an increased odds ratio of initial shockable cardiac rhythm (2.20; 95% confidence interval [CI], 1.30-3.72; P=0.003), shorter low-flow duration (geometric mean ratio, 0.90; 95% CI, 0.81-0.99; P=0.04), higher arterial pH value (difference, 0.12; 95% CI, 0.03-0.22; P=0.01) and lower serum lactate concentration (difference, -3.52mmol/L; 95% CI, -5.05 to -1.99; P<0.001). No significant association was found between the primary outcome and patient age (the odds of female gender and bystander CPR attempt. CONCLUSION Observational evidence from published primary studies indicates that shorter low-flow duration, shockable cardiac rhythm, higher arterial pH value and lower serum lactate concentration on hospital admission are associated with better outcomes for ECPR recipients after OHCA.

A regional trauma system to optimize the pre-hospital triage of trauma patients

IntroductionPre-hospital triage is a key element in a trauma system that aims to admit patients to the most suitable trauma center, and may decrease intra-hospital mortality. We evaluated the performance of a pre-hospital procedure in a regional trauma system through measurements of the quality of pre-hospital medical assessment and the efficacy of a triage protocol.MethodsOur regional trauma system included 13 hospitals categorized as Level I, II or III trauma centers according to their technical facilities. Each patient was graded A, B or C by an emergency physician, according to the seriousness of their injuries at presentation on scene. The triage was performed according to this grading and the categorization of centers. This study is a registry analysis of a three-year period (2009 to 2011).ResultsOf the 3,428 studied patients, 2,572 were graded using the pre-hospital grading system (Graded group). The pre-hospital gradation was closely related with injury severity score (ISS) and intra-hospital mortality rate. The triage protocol had a sensitivity of 92% (95% confidence interval (CI) 90% to 93%) and a specificity of 41% (95% CI 39% to 44%) to predict adequate admission of patients with ISS more than 15. A total of 856 patients were not graded at the scene (Non-graded group). Undertriage rate was significantly reduced in the Graded group compared with the Non-graded group, with a relative risk of 0.47 (95% CI 0.40 to 0.56) according to the definition of the American College of Surgeons Committee on Trauma (P <0.001). Where adjusted for trauma severity, the expected mortality rate at discharge from hospital was higher than observed mortality, with a difference of +2.0% (95% CI 1.4 to 2.6%; P <0.01).ConclusionsImplementation of a regional trauma system with a pre-hospital triage procedure was effective in detecting severe trauma patients and in lowering the rate of pre-hospital undertriage. A beneficial effect on outcome of such an organization is suggested.

Accuracy of Brain Multimodal Monitoring to Detect Cerebral Hypoperfusion After Traumatic Brain Injury

Objective:To examine the accuracy of brain multimodal monitoring—consisting of intracranial pressure, brain tissue PO2, and cerebral microdialysis—in detecting cerebral hypoperfusion in patients with severe traumatic brain injury. Design:Prospective single-center study. Patients:Patients with severe traumatic brain injury. Setting:Medico-surgical ICU, university hospital. Intervention:Intracranial pressure, brain tissue PO2, and cerebral microdialysis monitoring (right frontal lobe, apparently normal tissue) combined with cerebral blood flow measurements using perfusion CT. Measurements and Main Results:Cerebral blood flow was measured using perfusion CT in tissue area around intracranial monitoring (regional cerebral blood flow) and in bilateral supra-ventricular brain areas (global cerebral blood flow) and was matched to cerebral physiologic variables. The accuracy of intracranial monitoring to predict cerebral hypoperfusion (defined as an oligemic regional cerebral blood flow < 35 mL/100 g/min) was examined using area under the receiver-operating characteristic curves. Thirty perfusion CT scans (median, 27 hr [interquartile range, 20–45] after traumatic brain injury) were performed on 27 patients (age, 39 yr [24–54 yr]; Glasgow Coma Scale, 7 [6–8]; 24/27 [89%] with diffuse injury). Regional cerebral blood flow correlated significantly with global cerebral blood flow (Pearson r = 0.70, p < 0.01). Compared with normal regional cerebral blood flow (n = 16), low regional cerebral blood flow (n = 14) measurements had a higher proportion of samples with intracranial pressure more than 20 mm Hg (13% vs 30%), brain tissue PO2 less than 20 mm Hg (9% vs 20%), cerebral microdialysis glucose less than 1 mmol/L (22% vs 57%), and lactate/pyruvate ratio more than 40 (4% vs 14%; all p < 0.05). Compared with intracranial pressure monitoring alone (area under the receiver-operating characteristic curve, 0.74 [95% CI, 0.61–0.87]), monitoring intracranial pressure + brain tissue PO2 (area under the receiver-operating characteristic curve, 0.84 [0.74–0.93]) or intracranial pressure + brain tissue PO2+ cerebral microdialysis (area under the receiver-operating characteristic curve, 0.88 [0.79–0.96]) was significantly more accurate in predicting low regional cerebral blood flow (both p < 0.05). Conclusion:Brain multimodal monitoring—including intracranial pressure, brain tissue PO2, and cerebral microdialysis—is more accurate than intracranial pressure monitoring alone in detecting cerebral hypoperfusion at the bedside in patients with severe traumatic brain injury and predominantly diffuse injury.

Effect of moderate hyperventilation and induced hypertension on cerebral tissue oxygenation after cardiac arrest and therapeutic hypothermia.

AIM Improving cerebral perfusion is an essential component of post-resuscitation care after cardiac arrest (CA), however precise recommendations in this setting are limited. We aimed to examine the effect of moderate hyperventilation (HV) and induced hypertension (IH) on non-invasive cerebral tissue oxygenation (SctO2) in patients with coma after CA monitored with near-infrared spectroscopy (NIRS) during therapeutic hypothermia (TH). METHODS Prospective pilot study including comatose patients successfully resuscitated from out-of-hospital CA treated with TH, monitored with NIRS. Dynamic changes of SctO2 upon HV and IH were analyzed during the stable TH maintenance phase. HV was induced by decreasing PaCO2 from ∼40 to ∼30 mmHg, at stable mean arterial blood pressure (MAP∼70 mmHg). IH was obtained by increasing MAP from ∼70 to ∼90 mmHg with noradrenaline. RESULTS Ten patients (mean age 69 years; mean time to ROSC 19 min) were studied. Following HV, a significant reduction of SctO2 was observed (baseline 74.7±4.3% vs. 69.0±4.2% at the end of HV test, p<0.001, paired t-test). In contrast, IH was not associated with changes in SctO2 (baseline 73.6±3.5% vs. 74.1±3.8% at the end of IH test, p=0.24). CONCLUSIONS Moderate hyperventilation was associated with a significant reduction in SctO2, while increasing MAP to supra-normal levels with vasopressors had no effect on cerebral tissue oxygenation. Our study suggests that maintenance of strictly normal PaCO2 levels and MAP targets of 70mmHg may provide optimal cerebral perfusion during TH in comatose CA patients.

The impact of erythropoietin on short-term changes in phosphorylation of brain protein kinases in a rat model of traumatic brain injury

We found that recombinant human erythropoietin (rhEPO) reduced significantly the development of brain edema in a rat model of diffuse traumatic brain injury (TBI) (impact-acceleration model). In this study, we investigated the molecular and intracellular changes potentially involved in these immediate effects. Brain tissue nitric oxide (NO) synthesis, phosphorylation level of two protein kinases (extracellular-regulated kinase (ERK)-1/-2 and Akt), and brain water content were measured 1 (H1) and 2 h (H2) after insult. Posttraumatic administration of rhEPO (5,000 IU/kg body weight, intravenously, 30 mins after injury) reduced TBI-induced upregulation of ERK phosphorylation, although it increased Akt phosphorylation at H1. These early molecular changes were associated with a reduction in brain NO synthesis at H1 and with an attenuation of brain edema at H2. Intraventricular administration of the ERK-1/-2 inhibitor, U0126, or the Akt inhibitor, LY294002, before injury showed that ERK was required for brain edema formation, and that rhEPO-induced reduction of edema could involve the ERK pathway. These results were obtained in the absence of any evidence of blood–brain barrier damage on contrast-enhanced magnetic resonance images. The findings of our study indicate that the anti edematous effect of rhEPO could be mediated through an early inhibition of ERK phosphorylation after diffuse TBI.