Articles: respiratory-distress-syndrome.
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Support Care Cancer · Nov 1993
Randomized Controlled Trial Clinical TrialRespiratory distress syndrome in patients with advanced cancer treated with pentoxifylline: a randomized study.
The inappropriate endogenous secretion of tumour necrosis factor (TNF) could play a role in the pathogenesis of acute respiratory distress syndrome (ARDS), one of the most frequent causes of death in cancer patients. Because of its capacity to inhibit TNF secretion in vitro, pentoxifylline (PTX) could be extremely useful in ARDS therapy. In this study 30 advanced cancer patients with ARDS were randomized to receive either the conventional care or conventional care plus PTX (100 mg i.v. twice a day for 7 days followed by an oral administration of 400 mg three times a day) to evaluate the efficacy of PTX in reducing TNF serum levels and in improving the symptoms of this syndrome. ⋯ TNF mean levels significantly decrease in the PTX-treated group. These data confirm in vivo the capacity of PTX to inhibit TNF secretion in patients with ARDS. Moreover PTX therapy may improve the symptoms related to ARDS without particular toxic effects.
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The traditional practice of using high inflation pressures to maintain normal tidal volumes and arterial blood gases has been encouraged by the perception of uniformly distributed damage in acute lung injury. Although the frontal chest radiograph often suggests uniformity, recent work highlights the heterogeneous pathoanatomy and lung mechanics that actually characterize the adult (acute) respiratory distress syndrome. This heterogeneity is important to consider when applying mechanical ventilation, because impressive experimental evidence strongly indicates the potential for traditional selections for volume and pressure to impede lung healing or extend damage to previously unaffected areas. ⋯ Pathologic, physiologic, and theoretical arguments favor a strategy that attempts to avoid tidal alveolar collapse and to keep transalveolar pressure (not PaCO2) within normal physiologic limits. CO2 retention may be an unavoidable consequence of such a lung-protection strategy. Although the traditional paradigm for ventilation appears in need of revision, it must be recognized that few prospective, controlled trials of alternative ventilation modes have been undertaken to prove their superiority.
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Long-term extracorporeal support for acute lung failure was introduced in 1972. In the 1970s, much effort was concentrated on technical improvements. However, a multicenter study comparing continuous positive-pressure ventilation and continuous positive-pressure ventilation plus extracorporeal circulation failed to show improvement in survival rates. ⋯ The main complication of the technique was bleeding due to systemic heparinization. However, the technology used in that period was the same as in the 1970s. Recently, technological improvement--such as percutaneous cannulation and surface-heparinized artificial lungs--has allowed clinical performances to improve substantially. "Lung rest" philosophy, coupled with safe technology, may provide a rational basis to test this technique in a randomized fashion for widespread use.
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In 1987, nitric oxide was reported to be an endothelium-dependent relaxing factor. When inhaled as a gas at low levels, nitric oxide selectively dilates the pulmonary circulation. Significant systemic vasodilation does not occur because nitric oxide is inactivated by rapidly binding to hemoglobin. ⋯ Tachyphylaxis to nitric oxide inhalation has not been observed. While additional chronic toxicology studies need to be performed, significant pulmonary toxicity has not been observed at low inhaled concentrations (< 80 parts per million by volume). Potentially, inhaled nitric oxide may be a valuable therapy in patients with adult respiratory distress syndrome.
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Oxygen therapy is administered to decrease tissue hypoxia and to relieve arterial hypoxemia. High concentrations of oxygen are often used in patients with adult respiratory distress syndrome. Supplying oxygen to animals has been known to produce tissue damage, with toxicity increasing with the increase of oxygen concentrations and exposure pressures. ⋯ Lung damage may occur as a result of normobaric hyperoxia. A severe retinopathy (retrolental fibroplasia) occurs in neonates during oxygen exposures. For all of these reasons, the lowest possible concentration of oxygen that relieves tissue hypoxia is recommended in patients with adult respiratory distress syndrome.