A. Gacouin

Procalcitonin: a valuable indicator of infection in a medical ICU?

Abstract Objective: To assess the use of procalcitonin (PCT) for the diagnosis of infection in a medical ICU. Design: Prospective, observational study. Patients: Seventy-seven infected patients and 24 patients with systemic inflammatory response syndrome (SIRS) due to other causes. Seventy-five patients could be classified into sepsis (n=24), severe sepsis (n=27) and septic shock (n=24), and 20 SIRS patients remained free from infection during the study. Plasma PCT and C-reactive protein (CRP) levels were evaluated within 48 h of admission (day 0), at day 2 and day 4. Results: As compared with SIRS, PCT and CRP levels at day 0 were higher in infected patients, regardless of the severity of sepsis (25.2±54.2 ng/ml vs 4.8±8.7 ng/ml; 159±92 mg/l vs 71±58 mg/l, respectively). At cut-off values of 2 ng/ml (PCT) and 100 mg/l (CRP), sensitivity and specificity were 65% and 70% (PCT), 74% and 74% (CRP). PCT and CRP levels were significantly more elevated in septic shock (38.5±59.1 ng/ml and 173±98 mg/l) than in SIRS (3.8±6.9 ng/ml and 70±48 mg/l), sepsis (1.3±2.7 ng/ml and 98±76 mg/l) and severe sepsis (9.1±18. 2 ng/ml and 145±70 mg/l) (all p=0.005). CRP, but not PCT, levels were more elevated in severe sepsis than in SIRS (p<0.0001). Higher PCT levels in the patients with four dysfunctional organs and higher PCT and CRP levels in non-survivors may only reflect the marked inflammatory response to septic shock. Conclusion: In this study, PCT and CRP had poor sensitivity and specificity for the diagnosis of infection. PCT did not clearly discriminate SIRS from sepsis or severe sepsis.

Effects of epinephrine on right ventricular function in patients with severe septic shock and right ventricular failure: a preliminary descriptive study.

Objective: To recognize patients with unresponsive septic shock and right ventricular (RV) failure and to evaluate the effects of epinephrine on RV performance in these patients. Design: Prospective descriptive study. Setting: Medical intensive care unit. Subjects: 14 consecutive patients in septic shock unresponsive to fluid loading, dopamine, and dobutamine. Interventions: Evaluation of RV function by thermodilution with a pulmonary artery catheter equipped with a rapid-response thermistor. Measurements were obtained before and during epinephrine infusion to achieve a systolic arterial pressure ≥ 90 mmHg or a mean arterial pressure (MAP) ≥ 70 mmHg. Results: At the time of inclusion in the study the hemodynamic pattern in the 14 patients was as follows: (MAP) 58 ± 14 mmHg, systemic vascular resistance (SVR) 1046 ± 437 dyne · s · cm–5· m–2, pulmonary artery occlusion pressure (PAOP) 14 ± 4 mmHg, mean pulmonary artery pressure (MPAP) 24 ± 4 mmHg, right arterial pressure (RAP) 11 ± 4 mmHg, cardiac index (CI) 4 ± 1.7 l/min per m2. During epinephrine infusion, MAP, CI and stroke volume index (SVI) were increased (27 %, p < 0.01; 20 %, p < 0.01; 15 %, p < 0.05, respectively). There was no change in PAOP, SVR or heart rate. Seven patients (group A) had marked RV failure defined by both RV dilation [RV end-diastolic volume index (RVEDVI) > 92 ml/m2] and low RV ejection factor (RVEF) (< 52 %) and 7 did not (group B). Group A had a lower baseline RVEF than group B (24 ± 7 vs 45 ± 9 %, p < 0.05), a higher RVEDVI (134 ± 28 vs 79 ± 17 ml/m2, p < 0.01), and a higher RVES (systolic) VI (103 ± 30 vs 43 ± 11 ml/m2, p < 0.01). The other hemodynamics, especially RAP and RV stroke work index (RVSWI) were no different in the two groups and did not predict RV dysfunction. In group A, epinephrine infusion improved RVEF (25 %, p < 0.05) by a reduction in RVESVI (− 8 %, p < 0.05) without any change in RVEDVI or in RAP, in spite of a rise in MPAP (11 %, p < 0.05). A rise in RVSWI (76 %, p < 0.05), SVI (23 %, p < 0.05), and CI (24 %, p < 0.05) was also achieved. An upward vertical shift of the Frank-Starling relationship RVSWI/RVEDVI and an upward shift to the left of the pressure volume relationship pulmonary artery peak pressure/RVESVI was observed only in the group with RV failure following treatment with epinephrine. In group B (without RV failure), RV parameters were not modified by epinephrine. Conclusion: In patients with severe septic shock, RV dysfunction was identified by the use of an RVEF pulmonary artery catheter and was improved by epinephrine by means of an improvement in RV contractility.

Human rabies despite postexposure vaccination.

In December 1996, a previously healthy 50-year-old Caucasian female traveler was admitted to a local hospital in the state of Goa, India, after she had been bitten by a stray dog. The animal was not available for quarantine or testing. The patient was in India for 10 days and had no previous rabies exposure or preor post-exposure treatment. She received chloroquine and proguanil as antimalarial prophylaxis.

Acute respiratory failure caused by secondary alveolar proteinosis in a patient with acute myeloid leukemia : a case report

Pulmonary alveolar proteinosis (PAP) is a rare cause of chronic respiratory failure due to progressive alveolar accumulation of a periodic acid-schiff (PAS) positive proteinaceous material. In some cases, the rapid accumulation of intra-alveolar material leads to acute respiratory failure (ARF). We report the causative role of secondary PAP in the case of a 26-year-old man with acute myeloid leukemia who developed fever, increased serum lactate deshydrogenase level and ARF, and required mechanical ventilation. The diagnosis of PAP was established by the examination of material obtained by bronchoalveolar lavage (BAL). Respiratory improvement occurred several days after the patient had recovered from neutropenia. This report underlines the importance of the early diagnosis of PAP as a potential cause of ARF in leukemic patients. Adequate stain on BAL fluid provides the diagnosis and avoids repeated invasive procedures and inappropriate treatments.

Légionelloses graves en réanimation

Resume Depuis vingt ans, Legionella pneumophila a ete identifiee dans plusieurs series comme etant l’un des principaux agents infectieux impliques dans la survenue de pneumonies graves, tant communautaires que nosocomiales. De facon surprenante, tres peu d’etudes se sont interessees specifiquement aux patients pris en charge en reanimation. Selon les series, la mortalite des legionelloses pulmonaires graves prises en charge en reanimation est de 15 a 33 %. La precocite du traitement antibiotique approprie conditionne probablement le pronostic des legionelloses pulmonaires graves ; ce qui incite a inclure un traitement empirique contre L. pneumophila dans le traitement des pneumonies graves. Depuis 1977, l’erythromycine est le traitement de choix des legionelloses pulmonaires. Les fluoroquinolones et les nouveaux macrolides ont in vitro une activite superieure a celle de l’erythromycine et une meilleure penetration intracellulaire. Ces donnees experimentales suggerent qu’il y aurait un interet a traiter les legionelloses pulmonaires graves avec une fluoroquinolone ou un nouveau macrolide plutot qu’avec de l’erythromycine. Cependant, ces donnes experimentales ne sont confirmees par aucune etude clinique controlee.

Survie à long terme des bronchopathes chroniques obstructifs après la réanimation

OBJECTIVE To compare the one year survival after discharge from ICU of patients with chronic obstructive pulmonary disease (COPD) admitted for acute hypercapnic respiratory failure and who required mechanical ventilation. METHODS Retrospective cohort study on 130 patients, 52 patients were treated with non-invasive ventilation (NIV) and 78 patients with conventional mechanical ventilation (CMV). RESULTS In 73 patients the cause for respiratory failure could not be identified. Long-term survival was significantly better following NIV than with CMV (p=0.02 by log-rank testing), but the better prognosis associated with use of NIV was not found in patients with no documented cause for the respiratory failure. After adjusting for male gender, age>65 years, simplified acute physiology score II>35, prior long-term home oxygen therapy, treatment with steroids, FEV1<30% of predicted value, body-mass index<21 kg/m2, albumin level<30 g/L, right ventricular failure, ventilator-associated pneumonia and cause of respiratory failure, NIV remained independently associated with better outcomes (adjusted hazard ratio 0.55; 95% CI 0.31-0.97; p=0.04). CONCLUSIONS Our results suggest that in COPD patients requiring mechanical ventilation and who survived after an ICU stay, the use of NIV is an independent factor associated with a better long-term survival, especially in those with a documented cause of respiratory failure.

Syndrome de détresse respiratoire aiguë sur hémorragie intra-alvéolaire révélant une vascularite

Intra-alveolar hemorrhage (IAH) could be revealed by acute respiratory failure. The classic association of hemoptysis - anemia - radiological infiltrates is suggestive and has to be confirmed by broncho-alveolar lavage with Golde score. Etiologies included immune and non-immune diseases, with specific treatment for each. We report a case of IAH revealed by acute respiratory distress syndrome and anemia (3 g/dL), related to pulmonary and cerebral vasculitis without renal involvement. The patient was efficiently treated with corticosteroids and cyclophosphamide. This case highlights the critical role of BAL cytological analysis with Golde score, and the need for a rapid and accurate diagnosis in order to guide specific treatment. If histology is needed, renal biopsy even without renal involvement, or surgical lung biopsy is possible.

COPD is independently associated with 6-month survival in patients who have life support withheld in intensive care

In‐hospital outcomes following decisions of withholding or withdrawing in Intensive Care Unit (ICU) patients have been previously assessed, little is known about outcomes after ICU and hospital discharge. Our objective was to report the 6‐month outcomes of discharged patients who had treatment limitations in a general ICU and to identify prognostic factors of survival.

Dysfonction immunitaire induite par la ventilation mécanique

RésuméLa ventilation mécanique (VM), même si elle fait partie de l’arsenal thérapeutique indispensable en réanimation, va induire ou aggraver des lésions pulmonaires. Les cellules du parenchyme pulmonaire ainsi que les cellules immunitaires du poumon vont être capables de convertir les forces mécaniques générées par la VM en un signal biologique qui va entraîner une réaction inflammatoire. Cette inflammation « stérile » locale puis systémique va entraîner une dysfonction du système immunitaire, source de morbidité et de mortalité pour le patient de réanimation.AbstractAlthough mechanical ventilation is an essential support in patients admitted to the intensive care unit, clinical and experimental studies have shown that it could be harmful and could induce lung injury. Pulmonary and immune cells can convert mechanical stimuli into biological signals that will lead to inflammation. This sterile inflammation both locally and systemically will cause immunosuppression.