Alterations of the Gas Exchange Apparatus in Adult Respiratory Insufficiency Associated with Septicemia^1,2

Abstract

Lung tissue from 9 patients dying in different stages of an acute respiratory distress syndrome due to septicemia was fixed by a postmortem transthoracic injection method for an ultrastructural and morphometric analysis. At the initial stage of septic lung disease a widespread interstitial and alveolar edema was the essential finding. The capillary endothelium was relatively well preserved; in particular, no large endothelial gaps could be detected. In contrast, local destruction of the squamous epithelium, often covered by hyaline membranes, and a rapid proliferation of Type II epithelial cells were noted. In the subacute stage, cuboidal transformation of the epithelium and fibrotic alterations of the interstitium were the predominant findings. The extent of fibrotic alterations of lung architecture was not clearly related to the time course of the disease; on the other hand, the thickening of the air-blood barrier estimated by morphometry mirrored the disturbances of gas exchange and lung mechanics. The nonspecificity of the lesions observed in the subacute as well as in the acute stage of the disease provided further evidence of a uniform and characteristic reaction pattern of the lung that does not reflect the type and route (via blood or inspired air) of the damaging agents. Hence, it appears questionable whether lung biopsy specimens obtained from patients with acute respiratory distress syndrome can contribute to the diagnosis of the underlying disease.

Adult Respiratory Distress Syndrome with Increased Serum and Bronchoalveolar Lavage Fluid Levels of Squamous Cell Carcinoma-Related Antigen.

“…While peripheral blood neutropenia may occur in ARDSdue to the accumulation of neutrophils in large numbers within the lung in the early stage of acute lung injury (8,9), the pancytopenia observed in the present patient was suspected as a complication of ibuprofen therapy. However, the etiology of ARDS in this patient could not be identified as ibuprofen because pancytopenia also mayappear in viral infection and DLSTwas not strongly positive.…”

Pathophysiology of Acute Lung Injury and the Acute Respiratory Distress Syndrome

“…7 The alveolar epithelium is disrupted and the denuded basement membrane may be lined by fibrin-rich hyaline membranes. 8,9 Microthrombi may be visualized in the pulmonary capillaries. Injury to the capillary endothelium may be visualized by electron microscopy.…”

“…Injury to the capillary endothelium may be visualized by electron microscopy. 8,9 Although most histopathological studies have focused on the lung, ALI/ARDS is rarely a single-organ disease. Rather, these syndromes are almost allows systemic with multiorgan involvement.…”

“…14 In ALI/ARDS, alveolar epithelial injury leads to a decrease in the capacity for alveolar epithelial fluid transport that may contribute to the severity and duration of pulmonary edema. 8,15 Because of the increase in microvascular permeability in ALI, concomitant increases in lung microvascular hydrostatic pressure (as might occur with aggressive volume resuscitation) will lead to even greater formation of pulmonary edema. 16 …”

Contribution of proliferation and DNA damage repair to alveolar epithelial type 2 cell recovery from hyperoxia

“…Regenerating rat AEC2 exhibit elevated cyclin and cyclin-dependent kinase (cdk) expression and activity during recovery following injury, indicating the regain of proliferative function (10,39). During this period, the number of proliferating AEC2 has been reported to increase severalfold in rats (10,36), mice (2), and humans (4). In human patients, this phase of recovery from lung injury has been associated with an elevated risk of morbidity and mortality (33).…”