Guillaume Hékimian

Bedside Contribution of Electrical Impedance Tomography to Set Positive End-Expiratory Pressure for ECMO-Treated Severe ARDS Patients.

Rationale: Optimal positive end‐expiratory pressure (PEEP) is unknown in patients with severe acute respiratory distress syndrome (ARDS) on extracorporeal membrane oxygenation receiving mechanical ventilation with very low tidal volume. Objectives: To evaluate the ability of electrical impedance tomography (EIT) to monitor a PEEP trial and to derive from EIT the best compromise PEEP in this setting. Methods: A decremental PEEP trial (20‐0 cm H2O) in 5 cm H2O steps was monitored by EIT, with lung images divided into four ventral‐to‐dorsal horizontal regions of interest. The EIT‐based PEEP providing the best compromise between overdistention and collapsed zones was arbitrarily defined as the lowest pressure able to limit EIT‐assessed collapse to less than or equal to 15% with the least overdistention. Driving pressure was maintained constant at 14 cm H2O in pressure controlled mode. Measurements and Main Results: Tidal volume, static compliance, tidal impedance variation, end‐expiratory lung impedance, and their respective regional distributions were visualized at each PEEP level in 15 patients on extracorporeal membrane oxygenation. Low tidal volume (2.9‐4 ml/kg ideal body weight) and poor compliance (12.1‐18.7 ml/cm H2O) were noted, with significantly higher tidal volume and compliance at PEEP10 and PEEP5 than PEEP20. EIT‐based best compromise PEEPs were 15, 10, and 5 cm H2O for seven, six, and two patients, respectively, whereas PEEP20 and PEEP0 were never selected. Conclusions: The broad variability in optimal PEEP observed in these patients with severe ARDS under extracorporeal membrane oxygenation reinforces the need for personalized titration of ventilation settings. EIT may be an interesting noninvasive bedside tool to provide real‐time monitoring of the PEEP impact in these patients.

Intra-aortic balloon pump protects against hydrostatic pulmonary oedema during peripheral venoarterial-extracorporeal membrane oxygenation

Background: Increased left ventricular afterload during peripheral venoarterial-extracorporeal membrane oxygenation (VA-ECMO) support frequently causes hydrostatic pulmonary oedema. Because physiological studies demonstrated left ventricular afterload decrease during VA-ECMO assistance combined with the intra-aortic balloon pump (IABP), we progressively changed our standard practice systematically to associate an IABP with VA-ECMO. This study aimed to evaluate IABP efficacy in preventing pulmonary oedema in VA-ECMO-assisted patients. Methods: A retrospective single-centre study. Results: Among 259 VA-ECMO patients included, 104 received IABP. Weinberg radiological score-assessed pulmonary oedema was significantly lower in IABP+ than IABP– patients at all times after ECMO implantation. This protection against pulmonary oedema persisted when death and switching to central ECMO were used as competing risks (subhazard ratio 0.49, 95% confidence interval (CI) 0.33–0.75; P<0.001). Multivariable analysis retained IABP as being independently associated with a lower risk of radiological pulmonary oedema (odds ratio (OR) 0.4, 95% CI 0.2–0.7; P=0.001) and a trend towards lower mortality (OR 0.54, 95% CI 0.29–1.01; P=0.06). Finally, the time on ECMO free from mechanical ventilation increased in IABP+ patients (2.2±4.3 vs. 0.7±2.0 days; P=0.0003). Less frequent pulmonary oedema and more days off mechanical ventilation were also confirmed in 126 highly comparable IABP+ and IABP– patients, propensity score matched for receiving an IABP. Conclusions: Associating an IABP with peripheral VA-ECMO was independently associated with a lower frequency of hydrostatic pulmonary oedema and more days off mechanical ventilation under ECMO.

Extracorporeal Membrane Oxygenation for Acute Decompensated Heart Failure.

Objective: Long-term outcomes of patients treated with venoarterial-extracorporeal membrane oxygenation for acute decompensated heart failure (i.e., cardiogenic shock complicating chronic cardiomyopathy) have not yet been reported. This study was undertaken to describe their outcomes and determine mortality-associated factors. Design: Retrospective analysis of data prospectively collected. Setting: Twenty-six–bed tertiary hospital ICU. Patients: One hundred five patients implanted with venoarterial-extracorporeal membrane oxygenation for acute decompensated heart failure. Intervention: None. Measurements and Main Results: From March 2007 to January 2015, 105 patients were implanted with venoarterial-extracorporeal membrane oxygenation for acute decompensated heart failure in our ICU (67% of them had an intraaortic balloon pump to unload the left ventricle). Their 1-year survival rate was 42%; most of the survivors were transplanted either directly or after switching to central bilateral centrifugal pump, ventricular-assist device, or total artificial heart. Most deaths occurred early after multiple organ failure. Multivariable analyses retained (odds ratio [95% CI]) pre–extracorporeal membrane oxygenation Sequential Organ Failure Assessment score of more than 11 (3.3 [1.3–8.3]), idiopathic cardiomyopathy (0.4 [0.2–1]), cardiac disease duration greater than 2 years pre–extracorporeal membrane oxygenation (2.8 [1.2–6.9]), and pre–extracorporeal membrane oxygenation blood lactate greater than 4 mmol/L (2.6 [1.03–6.4]) as independent predictors of 1-year mortality. Only 17% of patients with pre–extracorporeal membrane oxygenation Sequential Organ Failure Assessment scores of 14 or more survived, whereas 52% of those with scores less than 7 and 60% of those with scores 7 or more and less than 11 were alive 1 year later. Conclusions: Among this selected cohort of 105 patients implanted with venoarterial-extracorporeal membrane oxygenation for acute decompensated heart failure, 1-year survival was 42%, but better for patients with pre–extracorporeal membrane oxygenation Sequential Organ Failure Assessment scores of less than 11. Venoarterial-extracorporeal membrane oxygenation should be considered for patients with acute decompensated heart failure, but timing of implantation is crucial.

Three-dimensional transoesophageal echocardiography for cardiac output in critically ill patients: A pilot study of ultrasound versus the thermodilution method

BACKGROUND Three-dimensional transoesophageal echocardiography (3D-TOE) is a new noninvasive tool for quantitative assessment of left ventricular (LV) volumes and ejection fraction. AIM The objective of this pilot study was to evaluate the feasibility and accuracy of 3D-TOE for the estimation of cardiac output (CO), using transpulmonary thermodilution with the Pulse index Contour Continuous Cardiac Output (PiCCO) system as the reference method, in intensive care unit (ICU) patients. METHODS Fifteen ICU patients on mechanical ventilation prospectively underwent PiCCO catheter implantation and 3D-TOE. 3D-TOE LV end-diastolic and end-systolic volumes were determined using semi-automated software. CO was calculated as the product of LV stroke volume (end-diastolic volume-end-systolic volume) multiplied by heart rate. CO was also determined invasively by transpulmonary thermodilution as the reference method. RESULTS Among 30 haemodynamic evaluations, 29 (97%) LV 3D-TOE datasets were suitable for CO calculation. The mean 3D-TOE image acquisition and post-processing times were 46 and 155seconds, respectively. There was a correlation (r=0.78; P<0.0001) between PiCCO and 3D-TOE CO. Compared with PiCCO, the 3D-TOE CO mean bias was 0.38L/min, with limits of agreement of -1.97 to 2.74L/min. CONCLUSIONS Noninvasive estimation of CO by 3D-TOE is feasible in ICU patients. This new semi-automated modality is an additional promising tool for noninvasive haemodynamic assessment of ICU patients. However, the wide limits of agreement with thermodilution observed in this pilot study require further investigation in larger cohorts of patients.

Retrieval of severe acute respiratory failure patients on extracorporeal membrane oxygenation: Any impact on their outcomes?

Objective: Mobile extracorporeal membrane oxygenation (ECMO) retrieval teams (MERTs) assure ECMO implantation and under‐ECMO retrieval of patients with most severe acute respiratory failure (ARF) to experienced ECMO centers. Although described as feasible, mobile ECMO has only been poorly evaluated in comparison with on‐site implantation. This study was undertaken to compare the indications, characteristics, and outcomes of MERT‐implanted patients with venovenous (VV)‐ECMO versus those implanted on site in our intensive care unit (ICU). Methods: Retrospective, single‐center study. Results: Among 157 VV‐ECMO implantations from 2008 to 2012, the MERT hooked up 118 (75%) patients with refractory ARF, as reflected by their median partial pressure of O2 in arterial blood/fraction of inspired oxygen of 58 (interquartile range, 50–73). ARF was accompanied by severe multiorgan failure, with a median Simplified Acute Physiology Score‐II of 71 (61‐81), median Sequential Organ Failure Assessment score of 14 (10‐16), and with 82% of the patients receiving inotropes. All patients were transported by ground ambulance: median distance was 15 (6‐25) km, and median transport time was 35 (25‐35) minutes, during which no major ECMO system–related event occurred. For the MERT‐ and on‐site–implanted groups, ICU mortality was comparable (46.6% vs 53.8%, respectively, P = .5), as were ECMO‐related complication rates (53.4% of MERT vs 53.8% of on‐site–implanted groups, P = 1.0). According to multivariable analysis, MERT ECMO implantation was not associated with ICU mortality (odds ratio, 1.1; 95% confidence interval, 0.4‐2.7; P = .85). Conclusions: ICU mortality and ECMO‐related complications of patients with MERT‐implanted VV‐ECMO who were transferred to our ECMO referral center were comparable with those implanted on site by the same team, thereby supporting this strategy to manage patients with severe ARF.

What’s new in myocarditis?

Myocarditis is an illness characterized by myocardial infiltration with inflammatory cells and non-ischemic myocyte necrosis. Typical histological finding is lymphocytic infiltration, but other forms involving eosinophilic or giant-cell inflammation exist. Coronary vasculitis is another pathogenic mechanism in some instances. The leading causes are infectious diseases, most commonly viral; immune-mediated injury (triggered by viral infection, allogenic agents such as drugs or associated with autoimmune disease); and toxins.[...]

When the heart gets the flu: Fulminant influenza B myocarditis: A case-series report and review of the literature

Purpose: To describe patients with refractory cardiogenic shock related to influenza B virus myocarditis rescued by venoarterial Extracorporeal Membrane Oxygenation (VA‐ECMO). Material and methods: Consecutive patients hospitalized in our unit for influenza‐associated myocarditis were prospectively included. We also conducted a systematic MEDLINE database literature review through the PubMed search engine, between 1946 and 2017. Results: We report the cases of 4 young patients with fulminant myocarditis requiring VA‐ECMO for 6 [5–8] days. Influenza B virus was detected in all patients, either in nasopharyngeal sampling or bronchoalveolar lavage fluid. The 4 patients received oseltamivir. Heart function recovery allowed ECMO device removal without cardiac sequelae in all 4 patients. Systematic review retrieved 184 cases of influenza‐associated myocarditis, most cases associated with H1N1 type‐A infection during the 2009 pandemic. Forty eight cases of influenza myocarditis‐associated cardiogenic shock requiring mechanical circulatory support including 3 cases due to influenza B virus were described. Mean duration of mechanical circulatory support was 8.5 ± 6 days and mortality rate was 33%. Conclusions: Influenza myocarditis is a rare but reversible cause of cardiogenic shock amenable to VA‐ECMO rescue. Early antiviral therapy and ECMO support should be considered for patients with fulminant myocarditis during an influenza epidemic.

Euglycemic ketoacidosis, a common and underecognized complication of continuous renal replacement therapy using glucose-free solutions

Dear Editor, Acute kidney injury (AKI) is a frequent and severe condition in intensive care unit patients that may require renal replacement therapy; most frequently continuous renal replacement therapy (CRRT). Phosphatecontaining replacement fluids are glucose-free solutions commonly used to prevent hypophosphatemia [1]. If hypoglycemia is a well-known complication of their use in CRRT, euglycemic ketoacidosis (EKA) has never been described in this setting. We prospectively screened all anuric patients receiving CRRT with glucose-free replacement solution, and included patients who had induced EKA between February and May 2017. Ketoacidosis was deemed possible when non-lactic metabolic acidosis did not improve in patients on CRRT. Because all patients were anuric, we measured ketonemia and used urinary test strips in the effluent fluid. EKA diagnosis was retained when arterial serum bicarbonate was < 20 mEq/l and decreased despite ongoing CRRT, in the absence of lactic acidosis and in the presence of ketones in the serum or CRRT effluent fluid. Eighteen patients (15% of our patients on CRRT in this period) developed EKA during CRRT using phosphatecontaining solution (Phoxilium®). Median (interquartile range) time between CVVHDF initiation and ketonemia detection was 43 (26–75) h. Patient characteristics are listed in ESM 1. Half of them had a medical history of diabetes mellitus (5 insulin-dependent). Ten patients were on ECMO, and all had multi-organ failure with subsequent food intolerance, resulting in low enteral calories intake despite normocaloric goal. The day of ketonemia detection, metabolic acidosis had worsened despite efficient continuous renal replacement therapy (with decrease of serum creatinine) and the absence of hyperlactatemia (Table 1). Only three patients were receiving insulin and most of them had low glucose or food intake. Increasing glucose intake and insulin infusion resolved ketoacidosis in all cases (Table 1). To our knowledge, this is the first description of euglycemic ketoacidosis in critically ill patients on CRRT using phosphate-containing glucose-free replacement solution. Euglycemic ketoacidosis, first described by Munro in 1973 [2], is a very rare presentation of diabetic ketoacidosis, mainly reported in diabetic patients with decreased caloric intake, alcohol consumption, chronic liver disease or in pregnant women [3]. This condition typically occurs in the setting of insulin resistance and starvation [4], two common findings in critically ill patients. By removing substantial amounts of glucose from the blood (from 30 to 160 g per day depending on glycemia and hemofiltration rate) [6], CRRT with glucose-free solution could contribute in as little as 2–3 days to the depletion of the glycogen stores, elevation of glucagon, and activation of lipolysis-releasing ketogenesis substrates, and shift the carbohydrate metabolism towards gluconeogenesis and ketogenesis, then inducing euglycemic ketoacidosis.

Co-infection with influenza-associated acute respiratory distress syndrome requiring extracorporeal membrane oxygenation

The co-infection frequency and impact among influenza-associated acute respiratory distress syndrome (ARDS) patients requiring extracorporeal membrane oxygenation (ECMO) are not known. This retrospective observational analysis concerned data prospectively collected from patients admitted to our medical intensive care unit (ICU) who received ECMO support for influenza-associated ARDS between 2009-2016. Co-infection was defined as occurring within 48 h following ICU admission. Among the 77 ARDS patients requiring ECMO support, 39 (51%) developed co-infections, with Staphylococcus aureus [18 (46%) of the co-infected patients] being the most prevalent pathogen. Panton-Valentin leukocidin (PVL)-producing S. aureus was isolated from 10 patients (56% of S. aureus co-infections and 26% of all co-infections). Co-infected patients were comparable with those without co-infection, except for BMI, initial disease severity and antibiotic treatment prior to admission. Co-infection was associated with higher in-ICU mortality (62% vs. 29%; P = 0.006) and with fewer ECMO-free days [median (IQR) 0 (0-19) vs. 23 (0-46); P = 0.004] and fewer mechanical ventilation-free days [0 (0-0) vs. 6 (0-35); P = 0.003] on Day 60. Multivariable analysis retained age >49 years, pre-ECMO Simplified Acute Physiology Score (SAPS) II score >70 and co-infection as independent predictors of hospital mortality. In conclusion, co-infection is frequent in ECMO-treated patients with influenza-associated ARDS, affecting ca. 50%, and is independently associated with poor outcome. Staphylococcus aureus was the most frequently identified pathogen, with a high rate of PVL-positive S. aureus. Whether specific therapy targeting PVL-producing S. aureus should be given remains to be determined.

Correction to: Venoarterial extracorporeal membrane oxygenation for refractory cardiogenic shock post-cardiac arrest

The second element of the first author’s name was misinterpreted as a given name, whereas in fact it is part of his family name. The correct version of his name for indexing purposes is therefore M. Pineton de Chambrun (not M. P. de Chambrun).