Feasibility and safety of ultrasound-aided thoracentesis in mechanically ventilated patients.

OBJECTIVE: Thoracentesis in a ventilated patient is rarely performed because of the risk of pneumothorax. We have evaluated the safety of this procedure when aided by ultrasound. DESIGN: Prospective study. SETTING: Medical intensive care unit, university-affiliated hospital. PATIENTS: 45 procedures were performed in 40 consecutive patients with ultrasound signs of pleural effusion, all mechanically ventilated. INTERVENTIONS: Pleural effusion was defined on ultrasound as a collection of fluid between parietal and visceral pleura leading to variations in interpleural distance during breathing. When the interpleural distance was >/= 15 mm and visible over three intercostal spaces, a needle (16 or 21 G) was inserted after ultrasound localization in a patient in either dorsal or lateral decubitus. RESULTS: No complication occurred in the 45 thoracenteses. Fluid was obtained in 44 of 45 procedures, thus confirming the diagnosis of pleural effusion. The procedure was immediate (less than 10 s) in 40 of 45 cases. It was easy (i. e., keeping the patient supine) in 22 of 45 procedures. In 44 cases where fluid was obtained, only 27 bedside radiographs revealed signs of effusion, whereas 17 showed absence of a visible effusion. Ultrasound thus appeared more efficient than bedside X-ray in detecting pleural effusion. CONCLUSIONS: If basic rules are followed, ultrasound localization makes thoracentesis a safe, easy and simple procedure in patients on mechanical ventilation.

Occult alveolar haemorrhage in pulmonary veno-occlusive disease.

Pulmonary veno-occlusive disease (PVOD) is a rare cause of pulmonary arterial hypertension that affects predominantly post-capillary pulmonary vessels. A major concern with PVOD is the poor response to available therapies and the risk of pulmonary oedema with continuous intravenous epoprostenol. The present authors hypothesised that alveolar haemorrhage may be a characteristic feature of pulmonary veno-occlusive disease, as compared with other forms of pulmonary arterial hypertension that predominantly involve pre-capillary pulmonary arteries. This paper reports a series of 19 patients with either PVOD (n = 8) or idiopathic pulmonary arterial hypertension (IPAH; n = 11) who underwent bronchoalveolar lavage. Cytological analyses were performed and differential counts were made on Perls-stained preparations. The Golde score was used to assess alveolar haemorrhage. As compared with IPAH, PVOD was characterised by a higher percentage of haemosiderin-laden macrophages (40+/-37 versus 3+/-6%), resulting in elevated Golde scores (81+/-88 versus 4+/-10). It was concluded that occult alveolar haemorrhage is a common feature of pulmonary veno-occlusive disease. Detecting occult alveolar haemorrhage may be of interest in the diagnostic approach of pulmonary veno-occlusive disease.

Prevention of hepatopulmonary syndrome and hyperdynamic state by pentoxifylline in cirrhotic rats.

Inhibition of tumour necrosis factor-alpha (TNF-alpha), levels of which are increased in the blood of cirrhotic rats, prevents hyperdynamic circulatory state, mainly by decreasing the vascular overproduction of nitric oxide. Hepatopulmonary syndrome, which is characterised by intrapulmonary vascular dilatation and increased alveolar to arterial oxygen tension difference (PA-a,O2), is mainly related to pulmonary over-production of NO by macrophages accumulated in lung vessels. Since TNF-alpha is a potent activator of macrophagic inducible nitric oxide synthase (NOS), the aim of this study was to investigate whether TNF-alpha inhibition prevented hepatopulmonary syndrome and hyperdynamic circulatory state in rats with cirrhosis. TNF-alpha was inhibited by 5 weeks of pentoxifylline (10 mg x kg body weigh(-1) x day(-1)) in rats with cirrhosis induced by common bile duct ligation. Cardiac output, pulmonary and systemic vascular resistance, PA-a,O2 and cerebral uptake of intravenous technetium-99m-labelled albumin macroaggregates (which reflects intrapulmonary vascular dilatation) were similar in sham- and pentoxifylline-treated cirrhotic rats. Blood TNF-alpha concentrations and pulmonary intravascular macrophage sequestration, as assessed by morphometric analysis and radioactive colloid uptake, were decreased with pentoxifylline. Pentoxifylline also prevented increases in aorta and lung NOS activities and inducible NOS expression. Thus pentoxifylline prevents development of hyperdynamic circulatory state and hepatopulmonary syndrome, probably by inhibiting the effects of tumour necrosis factor-alpha on vascular nitric oxide synthase and intravascular macrophages. These results support an important role for tumour necrosis factor-alpha in the genesis of hepatopulmonary syndrome.