Post-cardiac surgery fungal mediastinitis: clinical features, pathogens and outcome.

OBJECTIVES: The occurrence of mediastinitis after cardiac surgery remains a rare and severe complication associated with poor outcomes. Whereas bacterial mediastinitis have been largely described, little is known about their fungal etiologies. We report incidence, characteristics and outcome of post-cardiac surgery fungal mediastinitis. METHODS: Multicenter retrospective study among 10 intensive care units (ICU) in France and Belgium of proven cases of fungal mediastinitis after cardiac surgery (2009-2019). RESULTS: Among 73,688 cardiac surgery procedures, 40 patients developed fungal mediastinitis. Five were supported with left ventricular assist device and five with veno-arterial extracorporeal membrane oxygenation before initial surgery. Twelve patients received prior heart transplantation. Interval between initial surgery and mediastinitis was 38 [17-61] days. Only half of the patients showed local signs of infection. Septic shock was uncommon at diagnosis (12.5%). Forty-three fungal strains were identified: Candida spp. (34 patients), Trichosporon spp. (5 patients) and Aspergillus spp. (4 patients). Hospital mortality was 58%. Survivors were younger (59 [43-65] vs. 65 [61-73] yo; p = 0.013), had lower body mass index (24 [20-26] vs. 30 [24-32] kg/m2; p = 0.028) and lower Simplified Acute Physiology Score II score at ICU admission (37 [28-40] vs. 54 [34-61]; p = 0.012). CONCLUSION: Fungal mediastinitis is a very rare complication after cardiac surgery, associated with a high mortality rate. This entity should be suspected in patients with a smoldering infectious postoperative course, especially those supported with short- or long-term invasive cardiac support devices, or following heart transplantation.

Ability of procalcitonin to distinguish between bacterial and nonbacterial infection in severe acute exacerbation of chronic obstructive pulmonary syndrome in the ICU.

BACKGROUND: To assess the ability of procalcitonin (PCT) to distinguish between bacterial and nonbacterial causes of patients with severe acute exacerbation of COPD (AECOPD) admitted to the ICU, we conducted a retrospective analysis of two prospective studies including 375 patients with severe AECOPD with suspected lower respiratory tract infections. PCT levels were sequentially assessed at the time of inclusion, 6 h after and at day 1, using a sensitive immunoassay. The patients were classified according to the presence of a documented bacterial infection (including bacterial and viral coinfection) (BAC + group), or the absence of a documented bacterial infection (i.e., a documented viral infection alone or absence of a documented pathogen) (BAC- group). The accuracy of PCT levels in predicting bacterial infection (BAC + group) vs no bacterial infection (BAC- group) at different time points was evaluated by receiver operating characteristic (ROC) analysis. RESULTS: Regarding the entire cohort (n = 375), at any time, the PCT levels significantly differed between groups (Kruskal-Wallis test, p < 0.001). A pairwise comparison showed that PCT levels were significantly higher in patients with bacterial infection (n = 94) than in patients without documented pathogens (n = 218) (p < 0.001). No significant difference was observed between patients with bacterial and viral infection (n = 63). For example, the median PCT-H0 levels were 0.64 ng/ml [0.22-0.87] in the bacterial group vs 0.24 ng/ml [0.15-0.37] in the viral group and 0.16 ng/mL [0.11-0.22] in the group without documented pathogens. With a c-index of 0.64 (95% CI; 0.58-0.71) at H0, 0.64 [95% CI 0.57-0.70] at H6 and 0.63 (95% CI; 0.56-0.69) at H24, PCT had a low accuracy for predicting bacterial infection (BAC + group). CONCLUSION: Despite higher PCT levels in severe AECOPD caused by bacterial infection, PCT had a poor accuracy to distinguish between bacterial and nonbacterial infection. Procalcitonin might not be sufficient as a standalone marker for initiating antibiotic treatment in this setting.

Hemodynamic efficiency of hemodialysis treatment with high cut-off membrane during the early period of post-resuscitation shock: The HYPERDIA trial.

BACKGROUND: After resuscitation of cardiac arrest (CA), an acute circulatory failure occurs in about 50% of cases, which shares many characteristics with septic shock. Most frequently, supportive treatments are poorly efficient to prevent multiple organ failure and death. We evaluated whether an early plasma removal of inflammatory mediators using high cut-off continuous veno-venous hemodialysis (HCO-CVVHD) could improve hemodynamic status and outcome of these patients. PATIENTS AND METHODS: We performed a randomized open-label trial. Patients with post-cardiac arrest shock (defined as requirement of norepinephrine or epinephrine infusion > 1 mg/h) were included. The experimental group received 2 distinct sessions of HCO-CVVHD during the first 48 h following ICU admission. The control group received continuous veno-venous hemofiltration (CVVH) with standard membranes if needed. The primary endpoint was the delay to shock resolution asssessed by the length of catecholamine infusion. Number of vasopressors-free days at day 28, arterial blood pressure measures every 6-hours, daily fluid balance and mortality (ICU and day-28) were evaluated as secondary endpoints. RESULTS: 35 patients were included: 17 (median age 68.4, 59% male) in the HCO-CVVHD group and 18 (median age 66.3, 83% male) in the control group. Baseline characteristics did not differ between the two groups. Day-28 mortality rate was 64.7% and 72.2% in the HCO-CVVHD and control group, respectively (p = 0.72). Probability of vasopressors discontinuation over time was similar in the two groups (p for logrank test = 0.67). Number of day-28 catecholamine-free days was 25.1 [0, 26.5] and 24.5 [0, 26.2] in the HCO-CVVHD and control group, respectively (p = 0.65). No difference was observed regarding the daily-dose of vasopressors, arterial pressure profile and fluid balance. CONCLUSION: In cardiac arrest patients, HCO-CVVHD did not decrease the lenght of post-resuscitation shock and had no significant effect on hemodynamic profile. REGISTRATION: NCT00780299.

Usefulness of early plasma S-100B protein and Neuron-Specific Enolase measurements to identify cerebrovascular etiology of out-of-hospital cardiac arrest.

BACKGROUND: While S-100B protein and Neuron-Specific Enolase (NSE) dosages have been extensively investigated for neurological prognostication after cardiac arrest (CA), there is no data about their ability to detect a cerebrovascular cause of CA. We assessed the utility of plasma S-100B protein and NSE measurements for early diagnosis of primary neurological cause in resuscitated CA patients. PATIENTS AND METHODS: Case control study based on two prospectively acquired CA databases. Patients with a primary cerebrovascular etiology were compared with randomly selected CA of non-neurological cause. S-100B protein and NSE were measured at ICU admission in all patients. RESULTS: CA was due to a cerebrovascular etiology in 18 patients (subarachnoid hemorrhage, n = 15; ischemic stroke, n = 3), with an ICU mortality of 100%. Comparative group was constituted with 66 patients (cardiac etiology n = 45, respiratory etiology n = 21), with an ICU mortality of 71%. Admission S-100B protein concentration was 2.0 [0.63-7.15] µg/L in the cerebrovascular group and 0.45 [0.24-1.95] in the non-cerebrovascular group (p < 0.001). In contrast, NSE concentration was similar in cerebrovascular and non-cerebrovascular etiologies (35 [25-103] µg/L vs. 27 [19-47] respectively, p = 0.16). Area under ROC curves for S-100B protein and NSE to predict cerebrovascular cause of CA was 0.75 [95% CI: 0.64-0.87] and 0.61 [95% CI: 0.45-0.76], respectively. CONCLUSIONS: Even if S-100B protein dosage performs slightly better than NSE, early dosages of these biomarkers are poorly predictive of a cerebrovascular etiology of CA. Our results suggest that early measurement of brain biomarkers should not be recommended to tailor the imaging strategy employed to investigate the CA cause.

Time Course of Septic Shock in Immunocompromised and Nonimmunocompromised Patients.

OBJECTIVES: To address the impact of underlying immune conditions on the course of septic shock with respect to both mortality and the development of acute infectious and noninfectious complications. DESIGN: An 8-year (2008-2015) monocenter retrospective study. SETTING: A medical ICU in a tertiary care center. PATIENTS: Patients diagnosed for septic shock within the first 48 hours of ICU admission were included. Patients were classified in four subgroups with respect to their immune status: nonimmunocompromised and immunocompromised distributed into hematologic or solid malignancies and nonmalignant immunosuppression. Outcomes were in-hospital death and the development of ischemic and hemorrhagic complications and ICU-acquired infections. The determinants of death and complications were addressed by multivariate competing risk analysis. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Eight hundred one patients were included. Among them, 305 (38%) were immunocompromised, distributed into solid tumors (122), hematologic malignancies (106), and nonmalignant immunosuppression (77). The overall 3-day, in-ICU, and in-hospital mortality rates were 14.1%, 37.3%, and 41.3%, respectively. Patients with solid tumors displayed increased in-hospital mortality (cause-specific hazard, 2.20 [95% CI, 1.64-2.96]; p < 0.001). ICU-acquired infections occurred in 211 of the 3-day survivors (33%). In addition, 95 (11.8%) and 70 (8.7%) patients exhibited severe ischemic or hemorrhagic complications during the ICU stay. There was no association between the immune status and the occurrence of ICU-acquired infections. Nonmalignant immunosuppression and hematologic malignancies were independently associated with increased risks of severe ischemic events (cause-specific hazard, 2.12 [1.14-3.96]; p = 0.02) and hemorrhage (cause-specific hazard, 3.17 [1.41-7.13]; p = 0.005), respectively. CONCLUSIONS: The underlying immune status impacts on the course of septic shock and on the susceptibility to ICU-acquired complications. This emphasizes the complexity of sepsis syndromes in relation with comorbid conditions and raises the question of the relevant endpoints in clinical studies.

A Multicenter Randomized Trial Assessing the Efficacy of Helium/Oxygen in Severe Exacerbations of Chronic Obstructive Pulmonary Disease.

RATIONALE: During noninvasive ventilation (NIV) for chronic obstructive pulmonary disease (COPD) exacerbations, helium/oxygen (heliox) reduces the work of breathing and hypercapnia more than air/O2, but its impact on clinical outcomes remains unknown. OBJECTIVES: To determine whether continuous administration of heliox for 72 hours, during and in-between NIV sessions, was superior to air/O2 in reducing NIV failure (25-15%) in severe hypercapnic COPD exacerbations. METHODS: This was a prospective, randomized, open-label trial in 16 intensive care units (ICUs) and 6 countries. Inclusion criteria were COPD exacerbations with PaCO2 ≥ 45 mm Hg, pH ≤ 7.35, and at least one of the following: respiratory rate ≥ 25/min, PaO2 ≤ 50 mm Hg, and oxygen saturation (arterial [SaO2] or measured by pulse oximetry [SpO2]) ≤ 90%. A 6-month follow-up was performed. MEASUREMENTS AND MAIN RESULTS: The primary endpoint was NIV failure (intubation or death without intubation in the ICU). The secondary endpoints were physiological parameters, duration of ventilation, duration of ICU and hospital stay, 6-month recurrence, and rehospitalization rates. The trial was stopped prematurely (445 randomized patients) because of a low global failure rate (NIV failure: air/O2 14.5% [n = 32]; heliox 14.7% [n = 33]; P = 0.97, and time to NIV failure: heliox group 93 hours [n = 33], air/O2 group 52 hours [n = 32]; P = 0.12). Respiratory rate, pH, PaCO2, and encephalopathy score improved significantly faster with heliox. ICU stay was comparable between the groups. In patients intubated after NIV failed, patients on heliox had a shorter ventilation duration (7.4 ± 7.6 d vs. 13.6 ± 12.6 d; P = 0.02) and a shorter ICU stay (15.8 ± 10.9 d vs. 26.7 ± 21.0 d; P = 0.01). No difference was observed in ICU and 6-month mortality. CONCLUSIONS: Heliox improves respiratory acidosis, encephalopathy, and the respiratory rate more quickly than air/O2 but does not prevent NIV failure. Overall, the rate of NIV failure was low. Clinical trial registered with www.clinicaltrials.gov (NCT 01155310).

Hypothermia for Neuroprotection in Convulsive Status Epilepticus.

BACKGROUND: Convulsive status epilepticus often results in permanent neurologic impairment. We evaluated the effect of induced hypothermia on neurologic outcomes in patients with convulsive status epilepticus. METHODS: In a multicenter trial, we randomly assigned 270 critically ill patients with convulsive status epilepticus who were receiving mechanical ventilation to hypothermia (32 to 34°C for 24 hours) in addition to standard care or to standard care alone; 268 patients were included in the analysis. The primary outcome was a good functional outcome at 90 days, defined as a Glasgow Outcome Scale (GOS) score of 5 (range, 1 to 5, with 1 representing death and 5 representing no or minimal neurologic deficit). The main secondary outcomes were mortality at 90 days, progression to electroencephalographically (EEG) confirmed status epilepticus, refractory status epilepticus on day 1, "super-refractory" status epilepticus (resistant to general anesthesia), and functional sequelae on day 90. RESULTS: A GOS score of 5 occurred in 67 of 138 patients (49%) in the hypothermia group and in 56 of 130 (43%) in the control group (adjusted common odds ratio, 1.22; 95% confidence interval [CI], 0.75 to 1.99; P=0.43). The rate of progression to EEG-confirmed status epilepticus on the first day was lower in the hypothermia group than in the control group (11% vs. 22%; odds ratio, 0.40; 95% CI, 0.20 to 0.79; P=0.009), but there were no significant differences between groups in the other secondary outcomes. Adverse events were more frequent in the hypothermia group than in the control group. CONCLUSIONS: In this trial, induced hypothermia added to standard care was not associated with significantly better 90-day outcomes than standard care alone in patients with convulsive status epilepticus. (Funded by the French Ministry of Health; HYBERNATUS ClinicalTrials.gov number, NCT01359332 .).

Determinants and significance of cerebral oximetry after cardiac arrest: A prospective cohort study.

AIM OF THE STUDY: To study the determinants and the evolution of cerebral oximetry determined by near-infrared spectroscopy after out-of-hospital cardiac arrest of cardiac origin during therapeutic hypothermia and rewarming, and to compare cerebral oximetry values between patients with good and bad prognosis. METHODS: In this prospective, non-interventional, single center study, all consecutive patients between 18 and 80 years admitted for out-of-hospital cardiac arrest (OHCA) with a no flow less than 10min, a low flow of less than 50min and a persistent coma after ROSC with Glasgow score equal or less than seven at baseline were included. RESULTS: Between February 2012 and January 2013, 43 patients were admitted for OHCA in our ICU. Twenty-two patients (51%) were discharged with no or minimal neurologic complications (CPC 1-2). Mortality rate in the ICU was 46.5%. Cerebral oximetry (rSO2) was correlated with temperature, heart rhythm, PaO2, hemoglobin, and mean arterial pressure. Mean rSO2 during the 48 first hours was not different between patients with good and bad neurologic outcomes, respectively, 61.8 (5.9) vs. 58.1 (8.8), P=0.13, as during the period of hypothermia. The minimal value of rSO2 during the first 48h was significantly different between patients with good prognosis and those with bad prognosis, respectively, 45.0 (6.8) vs. 31.7 (15.0), P=0.0009. CONCLUSIONS: In this prospective cohort of OHCA patients, main determinants of rSO2 were systemic variables. Monitoring of rSO2 does not allow discriminating patients with good or bad outcome, but could be useful for identifying vulnerable periods for the development of neurologic injury.

Platelet transfusions in cancer patients with hypoproliferative thrombocytopenia in the intensive care unit.

BACKGROUND: Thrombocytopenia is a frequent finding in critically ill cancer patients for whom indications of platelet transfusions are unclear. We herein addressed the current practices in platelet transfusion and the risk of bleeding in cancer patients with hypoproliferative thrombocytopenia in the intensive care unit (ICU). METHODS: A retrospective monocenter study over a 7-year period was conducted in a medical ICU. Adult patients with malignancies and hypoproliferative thrombocytopenia, and who received at least one platelet concentrate during their ICU stay, were included. RESULTS: 296 patients were included and received a total of 904 platelet transfusions, for prophylactic indications in 300 (33.2 %) episodes, for securing an invasive procedure in 257 (28.4 %), and for treatment of minor to major bleeding manifestations in 347 (38.4 %). Most prophylactic transfusions (80 %) were performed at platelet count thresholds below 10-20 × 10(9)/L. Platelet increments were generally low in all three indications, 10 (interquartile range 2-25), 11 (2-25), and 8 (0-21) × 10(9)/L, respectively. A total of 97 major ICU-acquired bleeding events occurred in 40 patients. About half of those bleeding episodes (54.7 %) occurred at platelet counts below 20 × 10(9)/L. However, neither low admission platelet count nor low nadir platelet counts were predictive of ICU-acquired bleeding. The in-ICU mortality rate tended to be higher in patients with severe ICU-acquired bleeding events (50 vs. 36 %). CONCLUSIONS: Most prophylactic platelet transfusions were given using thresholds of 10-20 × 10(9)/L in critically ill thrombocytopenic cancer patients. The individual risk of ICU-acquired severe bleeding appears hardly predictable with the depth of thrombocytopenia.

Immediate Percutaneous Coronary Intervention Is Associated With Improved Short- and Long-Term Survival After Out-of-Hospital Cardiac Arrest.

BACKGROUND: Whether to perform or not an immediate percutaneous coronary intervention (PCI) after out-of-hospital cardiac arrest is still debated. We aimed to evaluate the impact of PCI on short- and long-term survival in out-of-hospital cardiac arrest patients admitted after successful resuscitation. METHODS AND RESULTS: Between 2000 and 2013, all nontrauma out-of-hospital cardiac arrest patients admitted in a Parisian cardiac arrest center after return of spontaneous circulation were prospectively included. The association between immediate PCI and short- and long-term mortality was analyzed using logistic regression and Cox multivariate analysis, respectively. Propensity score-matching method was used to assess the influence of PCI on short- and long-term survival. During the study period, 1722 patients (71.5% male, median age 60 [49.6, 72.2] years) were analyzed: 628 (35.6%) without coronary angiography, 615 (35.7%) with coronary angiography without PCI, and 479 (27.8%) with both. Among these groups, day 30 and year-10 survival rates were 21% and 11.9%, 35% and 29%, 43% and 38%, respectively (P<0.01 for each). PCI as compared with no coronary angiography was associated with a lower day-30 and long-term mortality (adjORcoro with PCI versus no coro 0.71, 95% confidence interval [0.54, 0.92]; P=0.02 and adjHRcoro with PCI versus no coro 0.44, 95% confidence interval [0.27, 0.71]; P<0.01, respectively). PCI remained associated with a lower risk of long-term mortality (adjHR 0.29; 95% confidence interval [0.14, 0.61]; P<0.01) in propensity score-matching analysis. CONCLUSIONS: Immediate PCI after out-of-hospital cardiac arrest was associated with significant reduced risk of short- and long-term mortality. These findings should suggest physicians to consider immediate coronary angiography and PCI if indicated in these patients.

Timing and causes of death in septic shock.

BACKGROUND: Most studies about septic shock report a crude mortality rate that neither distinguishes between early and late deaths nor addresses the direct causes of death. We herein aimed to determine the modalities of death in septic shock. METHODS: This was a 6-year (2008-2013) monocenter retrospective study. All consecutive patients diagnosed for septic shock within the first 48 h of intensive care unit (ICU) admission were included. Early and late deaths were defined as occurring within or after 3 days following ICU admission, respectively. The main cause of death in the ICU was determined from medical files. A multinomial logistic regression analysis using the status alive as the reference category was performed to identify the prognostic factors associated with early and late deaths. RESULTS: Five hundred forty-three patients were included, with a mean age of 66 ± 15 years and a high proportion (67 %) of comorbidities. The in-ICU and in-hospital mortality rates were 37.2 and 45 %, respectively. Deaths occurred early for 78 (32 %) and later on for 166 (68 %) patients in the ICU (n = 124) or in the hospital (n = 42). Early deaths were mainly attributable to intractable multiple organ failure related to the primary infection (82 %) and to mesenteric ischemia (6.4 %). In-ICU late deaths were directly related to end-of-life decisions in 29 % of patients and otherwise mostly related to ICU-acquired complications, including nosocomial infections (20.4 %) and mesenteric ischemia (16.6 %). Independent determinants of early death were age, malignancy, diabetes mellitus, no pathogen identification, and initial severity. Among 3-day survivors, independent risk factors for late death were age, cirrhosis, no pathogen identification, and previous corticosteroid treatment. CONCLUSIONS: Our study provides a comprehensive assessment of septic shock-related deaths. Identification of risk factors of early and late deaths may determine differential prognostic patterns.

Is copeptin level associated with 1-year mortality after out-of-hospital cardiac arrest? Insights from the Paris registry*.

OBJECTIVES: The availability of circulating biomarkers that helps to identify early out-of-hospital cardiac arrest survivors who are at increased risk of long-term mortality remains challenging. Our aim was to prospectively study the association between copeptin and 1-year mortality in patients with out-of-hospital cardiac arrest admitted in a tertiary cardiac arrest center. DESIGN: Retrospective monocenter study. SETTING: Tertiary cardiac arrest center in Paris, France. PATIENTS: Copeptin was assessed at admission and day 3. Pre- and intrahospital factors associated with 1-year mortality were analyzed by multivariate Cox proportional analysis. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Two hundred ninety-eight consecutive out-of-hospital cardiac arrest patients (70.3% male; median age, 60.2 yr [49.9-71.4]) were admitted in a tertiary cardiac arrest center in Paris (France). After multivariate analysis, higher admission copeptin was associated with 1-year mortality with a threshold effect (hazard ratio(5th vs 1st quintile) = 1.64; 95% CI, 1.05-2.58; p = 0.03). Day 3 copeptin was associated with 1-year mortality in a dose-dependent manner (hazard ratio(2nd vs 1st quintile) = 1.87; 95% CI, 1.00-3.49; p = 0.05; hazard ratio(3rd vs 1st quintile) = 1.92; 95% CI, 1.02-3.64; p = 0.04; hazard ratio(4th vs 1st quintile) = 2.12; 95% CI, 1.14-3.93; p = 0.02; and hazard ratio(5th vs 1st quintile) = 2.75; 95% CI, 1.47-5.15; p < 0.01; p for trend < 0.01). For both admission and day 3 copeptin, association with 1-year mortality existed for out-of-hospital cardiac arrest of cardiac origin only (p for interaction = 0.05 and < 0.01, respectively). When admission and day 3 copeptin were mutually adjusted, only day 3 copeptin remained associated with 1-year mortality in a dose-dependent manner (p for trend = 0.01). CONCLUSION: High levels of copeptin were associated with 1-year mortality independently from prehospital and intrahospital risk factors, especially in out-of-hospital cardiac arrest of cardiac origin. Day 3 copeptin was superior to admission copeptin: this could permit identification of out-of-hospital cardiac arrest survivors at increased risk of mortality and allow for close observation of such patients.

Is epinephrine during cardiac arrest associated with worse outcomes in resuscitated patients?

BACKGROUND: Although epinephrine is essential for successful return of spontaneous circulation (ROSC), the influence of this drug on recovery during the post-cardiac arrest phase is debatable. OBJECTIVES: This study sought to investigate the relationship between pre-hospital use of epinephrine and functional survival among patients with out-of-hospital cardiac arrest (OHCA) who achieved successful ROSC. METHODS: We included all patients with OHCA who achieved successful ROSC admitted to a cardiac arrest center from January 2000 to August 2012. Use of epinephrine was coded as yes/no and by dose (none, 1 mg, 2 to 5 mg, >5 mg). A favorable discharge outcome was coded using a Cerebral Performance Category 1 or 2. Analyses incorporated multivariable logistic regression, propensity scoring, and matching methods. RESULTS: Of the 1,556 eligible patients, 1,134 (73%) received epinephrine; 194 (17%) of these patients had a good outcome versus 255 of 422 patients (63%) in the nontreated group (p < 0.001). This adverse association of epinephrine was observed regardless of length of resuscitation or in-hospital interventions performed. Compared with patients who did not receive epinephrine, the adjusted odds ratio of intact survival was 0.48 (95% confidence interval [CI]: 0.27 to 0.84) for 1 mg of epinephrine, 0.30 (95% CI: 0.20 to 0.47) for 2 to 5 mg of epinephrine, and 0.23 (95% CI: 0.14 to 0.37) for >5 mg of epinephrine. Delayed administration of epinephrine was associated with worse outcome. CONCLUSIONS: In this large cohort of patients who achieved ROSC, pre-hospital use of epinephrine was consistently associated with a lower chance of survival, an association that showed a dose effect and persisted despite post-resuscitation interventions. These findings suggest that additional studies to determine if and how epinephrine may provide long-term functional survival benefit are needed.

Blood glucose level and outcome after cardiac arrest: insights from a large registry in the hypothermia era.

INTRODUCTION: The influence of blood glucose (BG) level during the post-resuscitation period after out-of-hospital cardiac arrest (OHCA) is still debated. To evaluate the relationship between blood glucose level and outcome, we included the median glycemia and its maximal amplitude over the first 48 h following ICU admission in an analysis of outcome predictors. METHODS: We conducted a database study in a cardiac arrest center in Paris, France. Between 2006 and 2010, we included 381 patients who were all resuscitated from an OHCA. A moderate glycemic control was applied in all patients. The median glycemia and the largest change over the first 48 h were included in a multivariate analysis that was performed to determine parameters associated with a favorable outcome. RESULTS: Of the 381 patients, 136 (36 %) had a favorable outcome (CPC 1-2). Median BG level was 7.6 mmol/L (6.3-9.8) in patients with a favorable outcome compared to 9.0 mmol/L (IQR 7.1-10.6) for patients with an unfavorable outcome (p < 0.01). Median BG level variation was 7.1 (4.2-11) and 9.6 (5.9-13.6) mmol/L in patients with and without a favorable outcome, respectively (p < 0.01). In multivariate analysis, an increased median BG level over the first 48 h was found to be an independent predictor of poor issue [OR = 0.43; 95 % CI (0.24-0.78), p = 0.006]. Finally a progressive increase in median BG level was associated with a progressive increase in the proportion of patients with a poor outcome. CONCLUSION: We observed a relationship between high blood glucose level and outcome after cardiac arrest. These results suggest the need to test a strategy combining both control of glycemia and minimization of glycemic variations for its ability to improve post-resuscitation care.

Disulfiram ethanol reaction mimicking anaphylactic, cardiogenic, and septic shock.

Shock is a common reason for medical intensive care unit admission, with septic and cardiogenic accounting for most of the etiologies. However, the potential severity of adverse side effects of drugs indicates that any medication should be carefully scrutinized for potential pharmacokinetic and pharmacodynamic interactions that may result. We herein report the case of a life-threatening shock mimicking successively anaphylactic, cardiogenic, and septic shock, which was finally related to disulfiram ethanol reaction. Indeed, disulfiram ethanol reaction is known to provoke unpleasant symptoms through vasodilatation in various organs. However, extreme manifestations of vasodilatory shock may lead to circulatory failure and lactic acidosis. Because of large prevalence of alcoholism and disulfiram medication, emergency physicians and medical specialists should be aware of this life-threatening condition, with its misleading presentation.