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Biomedical subjects

Jean Claude Raphael

Publications and source records attributed to Jean Claude Raphael.

7 recordsLinked to original sources

Prognosis and risk factors of early onset pneumonia in ventilated patients with Guillain-Barré syndrome.

OBJECTIVE: Invasive mechanical ventilation is required in 30% of patients with Guillain-Barré syndrome (GBS) and is associated with pneumonia and increased mortality. Our objective was to determine the incidence, characteristics, outcomes, and risk factors of pneumonia in GBS patients receiving mechanical ventilation. DESIGN AND SETTING: Study of a prospective database in an intensive care unit of a university hospital. PATIENTS: The study included 81 patients who required intubation for GBS. Neurological findings, vital capacity, and signs of respiratory distress were recorded at admission and at intubation. A score predicting the risk of intubation (0-4) was calculated for each patient. Pneumonia was diagnosed based on predefined criteria and retrospectively confirmed by two observers. Early-onset pneumonia was defined as pneumonia diagnosed within 5 days after intubation. MEASUREMENTS AND RESULTS: Mean vital capacity was 57 +/- 22% of predicted at admission and 33 +/- 11% at intubation. Pneumonia developed in 63 patients (78%), including 48 with early-onset pneumonia. Bacteria were consistent with aspiration. Of the 63 patients with pneumonia 11 (18%) had septic shock, 6 (10%) had acute respiratory distress syndrome, and 9 (14%) died. In the univariate analysis milder weakness, a lower risk of intubation (score < 2), and time from admission to intubation longer than 2 days were associated with early-onset pneumonia. Time from admission to intubation was the only independent predictor in the multivariate logistic regression model. CONCLUSIONS: Early-onset pneumonia is a common and severe complication that is related to aspiration in patients with GBS. Delaying intubation may increase the risk of early-onset pneumonia.

APACHE↗

Respiratory dysfunction in Guillain-Barré Syndrome.

Guillain-Barré Syndrome is the leading cause of nontraumatic acute paralysis in industrialized countries. About 30% of patients have respiratory failure requiring intensive care unit (ICU) admission and invasive mechanical ventilation. Progressive weakness of both the inspiratory and the expiratory muscles is the mechanism leading to respiratory failure. Aspiration pneumonia and atelectasis are common consequences of the bulbar muscle weakness and ineffective cough. The classical signs of respiratory distress occur too late to serve as guidelines for management, and measurements of vital capacity and static respiratory pressures are useful to determine the best times for starting and stopping mechanical ventilation. Several factors present at admission and during the ICU stay are known to predict a need for invasive mechanical ventilation. They include rapidly progressive motor weakness, involvement of both the peripheral limb and the axial muscles, ineffective cough, bulbar muscle weakness, and a rapid decrease in vital capacity. Specific treatments (plasma exchange and intravenous immunoglobulins) have decreased both the number of patients requiring ventilation and the duration of ventilation. The need for mechanical ventilation is associated with residual functional impairments, although all patients eventually recover normal respiratory muscle function.

Guillain-Barre Syndrome↗

Pressure support versus assisted controlled noninvasive ventilation in neuromuscular disease.

INTRODUCTION: Noninvasive ventilation (NIV) is being increasingly used in patients with chronic neuromuscular disorders, but the optimal ventilation mode remains unknown. We compared physiological short-term effects of assist/controlled ventilation (ACV) and two pressure-limited modes (pressure-support ventilation [PSV] and assist pressure-controlled ventilation [ACPV]) in patients with neuromuscular disease who needed NIV. METHODS: Tidal volume was 10 to 12 mL/kg. The ACPV mode used the same respiratory cycle timing as the volume-limited mode. The level of inspiratory support was set to achieve the same tidal volume during the other ventilatory modes. RESULTS: Thirteen patients with neuromuscular disease who met international criteria for NIV were included. The three ventilatory modes increased alveolar ventilation and decreased respiratory effort indices. However, no difference in breathing or respiratory effort was found among the three modes, with the exception that inspiratory peak flow and percentage of triggered cycles were higher during PSV than volume-limited ventilation. Interestingly, no relationship was observed between subjective patient preference and inspiratory effort indices or percentage of triggered cycles. CONCLUSION: In chronic, stable patients with neuromuscular disease, both noninvasive ACV, ACPV, and PSV had similar effects on alveolar ventilation and respiratory muscle unloading, despite some differences in the pattern of breathing and percentage of triggered cycles.

Adult↗

Assessing inspiratory muscle strength by sniff nasal inspiratory pressure.

The sniff nasal inspiratory pressure (SNIP) consists in the measurement of pressure through an occluded nostril during sniffs performed through the controlateral nostril. It is an accurate and noninvasive approximation of esophageal pressure swing during sniff maneuvers. However SNIP can underestimate esophageal pressure swing in subjects with nasal obstruction, patients with chronic obstructive pulmonary disease and severe neuromuscular patients. Nevertheless, since SNIP maneuver has predicted normal values, is noninvasive and is easier to perform than maximal inspiratory pressure (MIP) maneuver, it could be considered as the first simple test to use in order to assess inspiratory muscle weakness. In addition, because it is as reproducible as MIP, it can be suitable to follow inspiratory muscle function in chronic neuromuscular patients. Because, of the important limit of agreement between SNIP and MIP, these two methods are not interchangeable but complementary.

Forced Expiratory Volume↗

Circulating vasopressin levels in septic shock.

OBJECTIVE: To assess the frequency of vasopressin deficiency in septic shock. DESIGN: Prospective cohort study. SETTING: Intensive care unit at Raymond Poincaré University Hospital. PATIENTS: A cohort of 44 patients who met the usual criteria for septic shock for < 7 days. A second cohort of 18 septic shock patients were enrolled within the first 8 hrs of disease onset. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: General demographics, severity scores, vital signs, standard biochemical data, and circulating vasopressin levels were systematically obtained at baseline in the two cohorts. Vasopressin deficiency was defined by a normal plasma vasopressin level in the presence of a systolic blood pressure of <100 mm Hg or in the presence of hypernatremia. Baroreflex sensitivity was systematically evaluated in patients of the first cohort when vasopressin deficiency was noted. In the second cohort of patients, plasma levels of vasopressin were obtained at baseline, 6, 24, 48, and 96 hrs after shock onset. In the first population, plasma vasopressin levels were inversely correlated to the delay from shock onset. Fourteen patients had relative vasopressin deficiency: 12 patients had systolic blood pressure <100 mm Hg, with impaired baroreflex sensitivity in four, and three patients had hypernatremia. In the second population, only two patients had relative vasopressin deficiency. The plasma levels of vasopressin significantly decreased over time (p < 10-3). CONCLUSIONS: Plasma vasopressin levels are almost always increased at the initial phase of septic shock and decrease afterward. Relative vasopressin deficiency is seen in approximately one-third of late septic shock patients.

Analysis of Variance↗

Multifocal necrotizing leukoencephalopathy in septic shock.

OBJECTIVE: Multifocal necrotizing leukoencephalopathy, characterized by multiple microscopic foci of necrosis involving the white matter of the pons, has been described mainly after chemotherapy or radiotherapy for brain cancer and in HIV infection. The role of circulating cytokines has been suggested but remains to be assessed. DESIGN: Prospective case series. SETTING: A 26-bed general medical intensive care unit at a university hospital. PATIENTS: Septic shock patients. MEASUREMENTS AND PATIENTS: In three patients who died from septic shock, careful postmortem examination of the brain was performed, including studies of neuronal apoptosis and cytokine expression. MAIN RESULTS: In one patient, typical lesions of multifocal necrotizing leukoencephalopathy were seen. As compared with control 1 and control 2 who did not have multifocal necrotizing leukoencephalopathy, marked lesions of the pons, including vacuolization, apoptosis, microglial activation, and expression of tumor necrosis factor-alpha and interleukin-1beta, were observed in the case. Simultaneously, case 1 had markedly increased circulating levels for tumor necrosis factor-alpha, interleukin-1beta, interleukin-6, interleukin-8, interleukin-10, soluble tumor necrosis factor receptor II, and for interleukin-1 receptor antagonist. CONCLUSION: Septic shock is a newly described cause of multifocal necrotizing leukoencephalopathy, probably mediated by an excessive systemic inflammatory response.

Adult↗