[Danger of mechanical ventilation : Macklin effect during induced barotrauma]. / Danger de la ventilation mécanique : l'effet Macklin sur un barotraumatisme induit.

Intubation followed by mechanical ventilation is a classic technic for managing severe respiratory failure in hospital practice. Far from being exempted of risks, this technic can lead to serious complications. We hereby present illustrating images of a complication directly linked to the non-physiological respiratory mode on which mechanical ventilation is based, namely barotrauma linked to positive ventilatory pressures.

L'intubation suivie de ventilation mécanique est une technique classique de gestion de l'insuffisance respiratoire grave en pratique hospitalière. Loin d'être dénuée de risques, cette technique de support vital peut elle-même être source de complications graves. Nous vous présentons en images une complication directement liée au mode respiratoire non physiologique sur lequel repose la ventilation mécanique, à savoir le barotraumatisme lié aux pressions ventilatoires positives.

[Pulmonary tumour thrombotic microangiopathy associated with a gastric adenocarcinoma]. / Microangiopathie thrombotique tumorale pulmonaire associée à un adénocarcinome gastrique.

We report the case of a 67 years old patient with a history of gastric adenocarcinoma who died in a context of severe dyspnea and whose autopsy will confirm the diagnosis of a Pulmonary Tumor Thrombotic Microangiopathy (PTTM). PTTM is a fatal pulmonary complication associated to multiple cancers. It starts with an acute or subacute respiratory failure quickly evolving towards fatal thrombo-embolic pulmonary hypertension and right heart failure. Pre-mortem diagnosis is difficult and not frequent because the pathology is rare, the underlying neoplastic disease is not always known, clinical and radiological signs are not specific and progression is fast. When made soon enough, PTTM diagnosis avoids useless and sometimes harmful medication. In some cases, an improvement of patient's symptoms and comfort is observed. Some studies described several months of extended survival.

Nous rapportons le cas d'un patient de 67 ans avec un antécédent d'adénocarcinome gastrique décédé dans un contexte de dyspnée majeure et dont l'autopsie confirmera la présence d'une microangiopathie thrombotique tumorale pulmonaire (Pulmonary Tumor Thrombotic Microangiopathy - PTTM). La PTTM est une complication pulmonaire fatale associée à de multiples cancers. Elle se présente par une insuffisance respiratoire d'installation aiguë ou subaiguë, évoluant rapidement vers une hypertension thrombo-embolique pulmonaire et une insuffisance cardiaque droite fatales. Le diagnostic ante-mortem est difficile et rarement posé car la pathologie est rare. L'affection néoplasique sous-jacente n'est pas toujours connue, les signes cliniques et radiologiques sont peu spécifiques et son évolution est rapide. Réalisé à temps, le diagnostic permet, néanmoins, d'éviter une médication inefficace et parfois délétère. Dans certains cas, on observe une amélioration des symptômes et de l'inconfort du patient et, parfois, une survie prolongée de quelques mois.

[Acute respiratory distress syndrome]. / Le syndrome de détresse respiratoire aiguë.

Since its first description in 1967, a lot of progress has been made in understanding the pathophysiology, diagnosis and management of acute respiratory distress syndrome (ARDS). This nosological entity is based on the appearance of a diffuse alveolar damage associating pulmonary epithelial barrier disruption with an alveolar filling, both responsible of profound hypoxemia and important morbi-mortality. Nowadays, ARDS remains a frequent syndrome, associated with various etiologies. Diagnosis is based on the occurrence of acute hypoxic respiratory failure not explained by cardiac insufficiency or volume overload, within 7 days after a recognized risk factor, and in the presence of bilateral pulmonary opacities not fully explained by effusions, atelectasis or nodules on the chest radiography. Survivors present an increased risk of developing cognitive decline, depression, post-traumatic stress, and typical ICU related side-effects such as polyneuropathy and sarcopenia. In this context and not withstanding significant recent progress in the field of mechanical ventilation and extra-corporeal respiratory assistance, early diagnosis remains essential to identify patients with ARDS in order to offer them the most appropriate therapy.

Depuis sa première description en 1967, des progrès majeurs ont été réalisés dans la compréhension de la physiopathologie, le diagnostic et la prise en charge du syndrome de détresse respiratoire aiguë (SDRA). Cette entité nosologique repose sur l'apparition d'un dommage alvéolaire diffus associant une rupture de la barrière épithéliale pulmonaire avec un comblement alvéolaire à l'origine d'une hypoxémie profonde. De nos jours, le SDRA reste un syndrome fréquent, grevé d'une mortalité élevée, et prenant source dans de multiples situations pathologiques. Le diagnostic du SDRA repose sur l'apparition d'une insuffisance respiratoire aiguë hypoxique non expliquée par une insuffisance cardiaque ou une surcharge volémique, dans un délai de 7 jours suivant l'apparition d'un facteur de risque reconnu, en présence d'opacités pulmonaires bilatérales non complètement expliquées par des épanchements, des atélectasies ou des nodules. Les survivants sont à haut risque de développer un déclin cognitif, une dépression, ou un stress post-traumatique en plus des effets secondaires classiques d'une longue hospitalisation en unité de soins intensifs que sont la polyneuropathie ou la sarcopénie. Dans ce contexte, et en dépit de progrès importants dans le domaine de la ventilation mécanique et de l'assistance respiratoire par circulation extra-corporelle, il reste primordial d'identifier précocement les patients souffrant de SDRA afin de leur proposer la thérapeutique la plus appropriée dès les premiers signes cliniques.

Effect of a fluid challenge on the Surgical Pleth Index during stable propofol-remifentanil anaesthesia.

BACKGROUND: The Surgical Pleth Index (SPI), derived from pulse amplitude and heartbeat interval, is proposed to monitor anti-nociception during anaesthesia. Its response to noxious stimulation can be affected by the intravascular volume status. This study investigated the effect of a fluid challenge (FC) on SPI during steady-state conditions. METHODS: After Institutional Review Board approval, 33 consenting patients undergoing neurosurgery received a 4 ml/kg starch FC over less than 5 min under stable surgical stimulation conditions and stable propofol (Ce(PPF) ) and remifentanil (Ce(REMI) ) effect-site concentrations as estimated by target-controlled infusion systems. Intravascular volume status was assessed using the Delta Down (DD). We looked at the SPI response to FC according to DD, Ce(PPF) , and Ce(REMI) . RESULTS: Following FC, SPI did not change in 16, increased in 12, and decreased in 3 patients. Ce(REMI) poorly affected the SPI response to FC. In normovolaemic patients, the probability of an SPI change after FC was low under common Ce(PPF) (0.9 to 3.9 µg/ml). A decrease in SPI was more probable with worsening hypovolaemia and lowering Ce(PPF) , while an increase in SPI was more probable with increasing Ce(PPF) . SPI changes were only attributable to modifications in pulse wave amplitude and not in heart rate. CONCLUSIONS: During stable anaesthesia and surgery, SPI may change in response to FC. The effect of FC on SPI is influenced by volaemia and Ce(PPF) through pulse wave amplitude modifications. These situations may confound the interpretation of SPI as a surrogate measure of the nociception-anti-nociception balance.

Measurement of pleural pressure swings with a fluid-filled esophageal catheter vs pulmonary artery occlusion pressure.

PURPOSE: Pleural pressure measured with esophageal balloon catheters (Peso) can guide ventilator management and help with the interpretation of hemodynamic measurements, but these catheters are not readily available or easy to use. We tested the utility of an inexpensive, fluid-filled esophageal catheter (Peso) by comparing respiratory-induced changes in pulmonary artery occlusion (Ppao), central venous (CVP), and Peso pressures. METHODS: We studied 30 patients undergoing elective cardiac surgery who had pulmonary artery and esophageal catheters in place. Proper placement was confirmed by chest compression with airway occlusion. Measurements were made during pressure-regulated volume control (VC) and pressure support (PS) ventilation. RESULTS: The fluid-filled esophageal catheter provided a high-quality signal. During VC and PS, change in Ppao (∆Ppao) was greater than ∆Peso (bias = -2 mm Hg) indicating an inspiratory increase in cardiac filling. During VC, ∆CVP bias was 0 indicating no change in right heart filling, but during PS, CVP fell less than Peso indicating an inspiratory increase in filling. Peso measurements detected activation of expiratory muscles, development of non-west zone 3 lung conditions during inspiration, and ventilator-triggered inspiratory efforts. CONCLUSIONS: A fluid-filled esophageal catheter provides a high-quality, easily accessible, and inexpensive measure of change in pleural pressure and provided insights into patient-ventilator interactions.