Implementation of French Recommendations for the Prevention and the Treatment of Hospital-acquired Pneumonia: A Cluster-randomized Trial.

BACKGROUND: We determined whether an audit on the adherence to guidelines for hospital-acquired pneumonia (HAP) can improve the outcomes of patients in intensive care units (ICUs). METHODS: This study was conducted at 35 ICUs in 30 hospitals. We included consecutive, adult patients hospitalized in ICUs for 3 days or more. After a 3-month baseline period followed by the dissemination of recommendations, an audit on the compliance to recommendations (audit period) was followed by a 3-month cluster-randomized trial. We randomly assigned ICUs to either receive audit and feedback (intervention group) or participate in a national registry (control group). The primary outcome was the duration of ICU stay. RESULTS: Among 1856 patients enrolled, 602, 669, and 585 were recruited in the baseline, audit, and intervention periods, respectively. The composite measures of compliance were 47% (interquartile range [IQR], 38-56%) in the intervention group and 42% (IQR, 25-53%) in the control group (P = .001). As compared to the baseline period, the ICU lengths of stay were reduced by 3.2 days in the intervention period (P = .07) and by 2.8 days in the control period (P = .02). The durations of ICU stay were 7 days (IQR, 5-14 days) in the control group and 9 days (IQR, 5-20 days) in the intervention group (P = .10). After adjustment for unbalanced baseline characteristics, the hazard ratio for being discharged alive from the ICU in the control group was 1.17 (95% confidence interval, .69-2.01; P = .10). CONCLUSIONS: The publication of French guidelines for HAP was associated with a reduction of the ICU length of stay. However, the realization of an audit to improve their application did not further improve outcomes. CLINICAL TRIALS REGISTRATION: NCT03348579.

Accuracy of Zero-Heat-Flux Cutaneous Temperature in Intensive Care Adults.

OBJECTIVES: To compare accuracy of a continuous noninvasive cutaneous temperature using zero-heat-flux method to esophageal temperature and arterial temperature. DESIGN: Prospective study. SETTING: ICU and NeuroICU, University Hospital. PATIENTS: Fifty-two ICU patients over a 4-month period who required continuous temperature monitoring were included in the study, after informed consent. INTERVENTIONS: All patients had esophageal temperature probe and a noninvasive cutaneous device to monitor their core temperature continuously. In seven patients who required cardiac output monitoring, continuous iliac arterial temperature was collected. Simultaneous core temperatures were recorded from 1 to 5 days. Comparison to the esophageal temperature, considered as the reference in this study, used the Bland and Altman method with adjustment for multiple measurements per patient. MEASUREMENTS AND MAIN RESULTS: The esophageal temperature ranged from 33°C to 39.7°C, 61,298 pairs of temperature using zero-heat-flux and esophageal temperature were collected and 1,850 triple of temperature using zero-heat-flux, esophageal temperature, and arterial temperature. Bias and limits of agreement for temperature using zero-heat-flux were 0.19°C ± 0.53°C compared with esophageal temperature with an absolute difference of temperature pairs equal to or lower than 0.5°C of 92.6% (95% CI, 91.9-93.4%) of cases and equal to or lower than 1°C for 99.9% (95% CI, 99.7-100.0%) of cases. Compared with arterial temperature, bias and limits of agreement were -0.00°C ± 0.36°C with an absolute difference of temperature pairs equal to or lower than 0.5°C of 99.8% (95% CI, 95.3-100%) of cases. All absolute difference of temperature pairs between temperature using zero-heat-flux and arterial temperature and between arterial temperature and esophageal temperature were equal to or lower than 1°C. No local or systemic serious complication was observed. CONCLUSIONS: These results suggest a comparable reliability of the cutaneous sensor using the zero-heat-flux method compared with esophageal or iliac arterial temperatures measurements.

Circulating immature granulocytes with T-cell killing functions predict sepsis deterioration*.

OBJECTIVES: Primary objective was to identify leukocyte subsets that could predict the early evolution of sepsis at 48 hours (i.e., deterioration or stability/improvement). Secondary objectives were to evaluate the prognostic value of leukocyte subsets on mortality and immunosuppressive properties of immature granulocytes. DESIGN: Twenty-three peripheral blood leukocyte subsets were analyzed using a new-generation 10-color flow cytometry. T-cell killing activity of immature granulocytes was explored using a sorting method specifically developed. SETTING: ICUs and emergency departments. PATIENTS: All patients admitted to emergency department and ICU for sepsis ongoing for less than 24 hours were eligible. Exclusion criteria were pregnancy, age less than 18 years, solid tumors, HIV infection, hematological or inflammatory conditions, and immunosuppressive drugs. Finally, 177 patients were included. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: The two most salient features of sepsis were decreased CD10 (CD10) and CD16 (CD16) expressions on granulocytes. With a threshold of 90% of CD10 and 15% of CD16 granulocytes, these immunophenotypic features, which are those of immature granulocytes, predicted sepsis deterioration at 48 hours with a sensitivity of 57% and 70% and a specificity of 78% and 82%, respectively. Survival rate at day 30 was 99% for patients without CD10 and CD16, 85% for patients with increased CD16 only, and 63% for patients with increased CD16 and CD10 granulocytes (p < 0.001). Among CD16 immature granulocytes, we identified a CD14/CD24 myeloid-derived suppressor cell subset with the capability of killing activated T cells. Consistently, an excess of CD16 immature granulocytes was associated with both CD3 and CD4 T-cell lymphopenia in deteriorating patients. CONCLUSIONS: Circulating immature granulocytes predicted early sepsis deterioration and were enriched in myeloid-derived suppressor cells which could be responsible for immunosuppression through the induction of T-cell lymphopenia.

Cardiac tamponade related to a coronary injury by a pericardial calcification: an unusual complication.

BACKGROUND: Cardiac tamponade is a rare but severe complication of pericardial effusion with a poor prognosis. Prompt diagnosis using transthoracic echocardiography allows guiding initial therapeutic management. Although etiologies are numerous, cardiac tamponade is more often due to a hemopericardium. Rarely, a coronary injury may result in such a hemopericardium with cardiac tamponade. Coronary artery aneurysm are the main etiologies but blunt, open chest trauma or complication of endovascular procedures have also been described. CASE PRESENTATION: A 83-year-old hypertensive man presented for dizziness and hypotension. The patient had oliguria and mottled skin. Transthoracic echocardiography disclosed a circumferential pericardial effusion with a compressed right atrium, confirmed by contrast-enhanced thoracic CT scan. A pig-tail catheter allowed to withdraw 500 mL of blood, resulting in a transient improvement of hemodynamics. Rapidly, recurrent hypotension prompted a reoperation. An active bleeding was identified at the level of the retroventricular coronary artery. The pericardium was thickened with several "sharping" calcified plaques in the vicinity of the bleeding areas. On day 2, vasopressors were stopped and the patient was successfully extubated. Final diagnosis was a spontaneous cardiac tamponade secondary to a coronary artery injury attributed to a "sharping"calcified pericardial plaque. CONCLUSION: Cardiac tamponade secondary to the development of a hemopericardium may develop as the result of a myocardial and coronary artery injury induced by a calcified pericardial plaque.