Seminars in respiratory and critical care medicine
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Pneumothoraces are classified as spontaneous, traumatic, and iatrogenic. Spontaneous pneumothoraces (SP) occur without recognized lung disease (primary, PSP) or due to an underlying lung disease (secondary, SSP). Treatment of PSP and SSP has been quite heterogeneous in the United States; adoption of the recently published American College of Chest Physicians guidelines will hopefully improve care. ⋯ Iatrogenic pneumothoraces appear most commonly due to transthoracic needle aspiration and may be treated in carefully selected patients with observation. The presence of underlying emphysema in the setting of an iatrogenic pneumothorax usually mandates placement of a drainage catheter. Newer mechanical ventilation modes and strategies may limit the development of positive pressure ventilation- related iatrogenic pneumothoraces.
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Semin Respir Crit Care Med · Aug 2001
Lymphocytic interstitial pneumonia and other lymphoproliferative disorders in the lung.
Lymphocytic interstitial pneumonia (LIP) is a clinicopathologic term that relates histologically to a dense interstitial infiltrate of mainly T cells, plasma cells, and histiocytes, with germinal centers often identified. Its precise etiology is unknown, but there are strong clinical associations with several autoimmune disorders, as well as both congenital and acquired immunodeficiency syndromes. ⋯ LIP may also be histologically indistinguishable from nodular lymphoid hyperplasia and lymphomas arising from mucosa-associated lymphoid tissue (MALT) but can usually be differentiated via analysis of clinical and imaging data plus assessment of immunohistochemistry and gene rearrangement studies. Other entities include lymphomatoid granulomatosis, intravascular lymphomatosis, Castleman's disease, primary pleural lymphomas, primary effusion lymphomas, plasmacytomas, and secondary involvement by lymphoma, but these should all be readily distinguishable from lymphocytic interstitial pneumonia if all clinical, imaging, and histological data are apparent.
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Usual interstitial pneumonia (UIP) is a distinct histological lesion observed in idiopathic pulmonary fibrosis (IPF), but can be found in other etiologies. The diagnosis of UIP can be established by surgical lung biopsy or by high resolution thin section computed tomographic scans (provided the radiographic features are classical). Historically, patients labeled as "IPF'' encompassed a group of disorders including UIP as well as other idiopathic interstitial pneumonias, which differ from UIP in prognosis and responsiveness to therapy. ⋯ Single-lung transplantation is a viable option for patients failing medical therapy. Novel therapeutic strategies based upon inhibiting fibroproliferation or enhancing alveolar reepithelialization are desperately needed. In this article, we discuss diagnostic criteria for UIP (both histopathological and radiographic), natural history and clinical course, and therapeutic approaches (both current and future).
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Early reports of late outcomes among survivors of ARDS indicated that most patients improved dramatically after their intensive care unit stay, and few lived with residua of their once-severe pulmonary injury. Over the last decade, a collection of new studies with improved methodology and novel questions has improved our understanding of life after ARDS. After reviewing these newer investigations in the context of previously published literature, we have drawn several preliminary conclusions: (1) Long-term survival after hospital discharge is unaffected by ARDS, but is strongly affected by ARDS risk factor and comorbidities. (2) Respiratory symptoms after ARDS are more prevalent than previously indicated, but improve over the first 12 months of recovery. (3) Pulmonary function testing reveals marked impairment soon after ARDS. ⋯ A small group of patients have severe impairment without improvement. (4) Quality of life, functional independence, and cognitive function are severely affected by ARDS, with dramatic improvement over the first year. Quality of life is lower than in matched critically ill controls. (5) Significant numbers of ARDS survivors suffer from posttraumatic stress syndrome. This is an exciting time for research in long-term outcomes of ARDS, with potential for future studies that validate these single-center hypotheses, explore their ramifications, and investigate the impacts of changing practices in the intensive care unit in the acute phase of ARDS.
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The acute respiratory distress syndrome (ARDS) is a life-threatening syndrome that may occur in any patient without any predisposition and that is mostly triggered by underlying processes such as sepsis, pneumonia, trauma, multiple transfusions, and pancreatitis. ARDS is defined by (1) acute onset, (2) bilateral infiltrates in chest x-rays, (3) absence of left ventricular failure, and (4) severe arterial hypoxemia with a PaO2/FiO2 ratio less than 200 mmHg. Still, ARDS is feared (mortality 30-40%) and relatively frequent (incidence between 13.5 per 100,000 to 75 per 100,000). ⋯ Despite ongoing and intensive scientific research in this area, the mechanisms underlying ALI/ARDS are still not completely understood, and until recently, there were no studies demonstrating any beneficial effect of a single treatment modality in ARDS. The recent report that a specific approach to ventilatory support can significantly reduce mortality in ARDS underscores the need for better understanding of the pathophysiological events occurring in this syndrome. This review therefore summarizes the current pathophysiological concepts underlying the evolution of acute hypoxemic respiratory failure and focuses on: (1) possible reasons for the development of ALI/ARDS; (2) cellular and humoral mediator responses leading to a sustained and self-perpetuating inflammation of the lung; (3) consequences with regard to fluid balance, pulmonary perfusion, ventilation, and efficiency of gas exchange; and (4) mechanisms underlying the aggravating complications commonly seen in ARDS, especially ventilator-associated lung injury, ventilator-associated pneumonia, and lung fibrosis.