Discrepancy between clinical criteria for diagnosing acute respiratory distress syndrome secondary to community acquired pneumonia with autopsy findings of diffuse alveolar damage

Abstract

Diffuse alveolar damage (DAD) is the underlying pathological finding in most cases of acute respiratory distress syndrome (ARDS). The objective of this study was to compare clinical criteria for ARDS secondary to community acquired pneumonia with autopsy findings of DAD and to determine the discrepancy rate between the two. We compared prospectively obtained clinical diagnosis of ARDS secondary to community acquired pneumonia with autopsy findings of DAD and pneumonia. Forty nine patients dead with a clinical diagnosis of ARDS secondary to pneumonia who underwent autopsy between 1986 and 2004 in our ICU were included with systematic histopathological analysis of all lung lobes. The discrepancy rate between the premortem clinical diagnosis of ARDS secondary to pneumonia and DAD at autopsy was determined. Seven patients were found to have neither infection nor DAD at autopsy. Six patients showed pathologic signs of DAD without evidence of infection. Out of 38 patients meeting clinical criteria for ARDS secondary to pneumonia and proven pneumonia at autopsy, 25 met criteria for DAD at autopsy. Therefore, 18 out of 49 patients who were clinically diagnosed with ARDS did not actually show pathological signs of DAD, resulting in a discrepancy rate of 37%. Despite an acceptable correspondence between clinical criteria for ARDS secondary to pneumonia and autopsy findings of DAD a significant number of patients had neither signs of DAD nor infection.

Acute pulmonary injury: high-resolution CT and histopathological spectrum

“…The acute phase (Figure 1) occurs during the first week after the initial insult. The main histological findings seen during this phase are capillary congestion, interstitial and intraalveolar oedema associated with fibrin and formation of hyaline membranes, which are most prominent at 3-7 days [3,4]. Thrombi may develop as a result of localised alterations in the coagulation pathway.…”

“…Thrombi may develop as a result of localised alterations in the coagulation pathway. The organising phase ( Figure 2) occurs after 1-2 weeks and is characterised by fibroblast proliferation admixed with scattered mononuclear inflammatory cells, resulting in the formation of organised granulation tissue [4,5]. Type-2 pneumocyte hyperplasia also occurs and may show considerable cytological atypia [4].…”

“…The organising phase ( Figure 2) occurs after 1-2 weeks and is characterised by fibroblast proliferation admixed with scattered mononuclear inflammatory cells, resulting in the formation of organised granulation tissue [4,5]. Type-2 pneumocyte hyperplasia also occurs and may show considerable cytological atypia [4]. Oedema and hyaline membranes are not prominent during this phase [4].…”

Application of extracorporeal membrane oxygenation in severe ARDS secondary to pneumonia: a case report

“…ARDS is a type of acute diffuse, inflammatory lung injury, leading to increased pulmonary vascular permeability, increased lung weight, and loss of aerated lung tissues [10]. The clinical features are hypoxemia and bilateral radiographic opacities, associated with increased venous admixture, increased physiological dead space, and decreased lung compliance [10].…”

“…The clinical features are hypoxemia and bilateral radiographic opacities, associated with increased venous admixture, increased physiological dead space, and decreased lung compliance [10]. The morphological hallmark of the acute phase is diffuse alveolar damage (ie, edema, inflammation, hyaline membrane, or hemorrhage) [11].…”