Alterações histopatológicas pulmonares em pacientes com insuficiência respiratória aguda: um estudo em autopsias

Soeiro, Alexandre de Matos; Parra, Edwin Roger; Canzian, Mauro; Farhat, Cecília; Capelozzi, Vera Luíza

doi:10.1590/s1806-37132008000200002

Cited by 5 publications

(21 citation statements)

References 20 publications

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“…As expected, PE was the most common pattern observed (72.9% of cases) and was also the most specific finding associated with AMI, as described previously in other studies (4,16,17). AMI has been described as the most important etiologic factor associated with the development of PE in hospitalized patients (16).…”

Section: Discussionsupporting

confidence: 89%

“…The prevalence (39.4% of cases) of more than one diagnosis demonstrates the complexity and severity of illness among the patients that presented ARF as the cause of death after AMI. These findings could indicate the necessity of a different therapeutic strategy for these patients with poor prognoses (4,13,19),. A study published in 2008 analyzed the use of continuous positive airway pressure in patients with PE secondary to AMI and reported an intrahospital mortality of 11%.…”

Section: Discussionmentioning

confidence: 93%

“…The pulmonary histopathological analysis showed PE in 72.9% (159) of patients, DAD in 17.4% (38), LPIP in 4.1% (9) and AH in 1.8% (4). …”

Section: Resultsmentioning

confidence: 99%

“…Acute respiratory failure (ARF) is a major cause of death in patients with a variety of primary underlying diseases (1-4). The clinical and radiographic findings of ARF are nonspecific (5-7).…”

Section: Introductionmentioning

confidence: 99%

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Postmortem diagnosis of acute myocardial infarction in patients with acute respiratory failure - demographics, etiologic and pulmonary histologic analysis

Soeiro¹,

Ruppert²,

Canzian³

et al. 2012

Clinics

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OBJECTIVES:Acute respiratory failure is present in 5% of patients with acute myocardial infarction and is responsible for 20% to 30% of the fatal post-acute myocardial infarction. The role of inflammation associated with pulmonary edema as a cause of acute respiratory failure post-acute myocardial infarction remains to be determined. We aimed to describe the demographics, etiologic data and histological pulmonary findings obtained through autopsies of patients who died during the period from 1990 to 2008 due to acute respiratory failure with no diagnosis of acute myocardial infarction during life.METHODS:This study considers 4,223 autopsies of patients who died of acute respiratory failure that was not preceded by any particular diagnosis while they were alive. The diagnosis of acute myocardial infarction was given in 218 (4.63%) patients. The age, sex and major associated diseases were recorded for each patient. Pulmonary histopathology was categorized as follows: diffuse alveolar damage, pulmonary edema, alveolar hemorrhage and lymphoplasmacytic interstitial pneumonia. The odds ratio of acute myocardial infarction associated with specific histopathology was determined by logistic regression.RESULTS:In total, 147 men were included in the study. The mean age at the time of death was 64 years. Pulmonary histopathology revealed pulmonary edema as well as the presence of diffuse alveolar damage in 72.9% of patients. Bacterial bronchopneumonia was present in 11.9% of patients, systemic arterial hypertension in 10.1% and dilated cardiomyopathy in 6.9%. A multivariate analysis demonstrated a significant positive association between acute myocardial infarction with diffuse alveolar damage and pulmonary edema.CONCLUSIONS:For the first time, we demonstrated that in autopsies of patients with acute respiratory failure as the cause of death, 5% were diagnosed with acute myocardial infarction. Pulmonary histology revealed a significant inflammatory response, which has not previously been reported.

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Section: Discussionsupporting

confidence: 89%

Section: Discussionmentioning

confidence: 93%

“…The pulmonary histopathological analysis showed PE in 72.9% (159) of patients, DAD in 17.4% (38), LPIP in 4.1% (9) and AH in 1.8% (4). …”

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Postmortem diagnosis of acute myocardial infarction in patients with acute respiratory failure - demographics, etiologic and pulmonary histologic analysis

Soeiro¹,

Ruppert²,

Canzian³

et al. 2012

Clinics

Self Cite

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show abstract

“…Given the restrictions when performing an open-lung biopsy in patients with acute and severe respiratory distress, a limited number of studies have examined biopsy data from this patient group [11–13]. Thus, forensic autopsies and the examination of DAD prevalence may be an alternative area of research [14, 15]. …”

Section: Introductionmentioning

confidence: 99%

Diffuse Alveolar Damage of the Lungs in Forensic Autopsies: Assessment of Histopathological Stages and Causes of Death

Ürer

Ersoy

Yilmazbayhan

2012

The Scientific World Journal

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Introduction. Diffuse alveolar damage (DAD) is a morphological prototype of acute interstitial pneumonia. Hospital autopsies or open-lung biopsies are used to monitor common alveolar damage and hyaline membrane (HM) development histopathologically. The aim of this study was to detect histopathological profiles and frequency of DAD and HM in adult forensic autopsies. Materials and Methods. In total, 6813 reports with histopathological samples in 12,504 cases on which an autopsy was performed between 2006 and 2008 were investigated. Sixty-six individuals >18 years of age who were diagnosed with DAD were included. Hematoxylin- and eosin-stained lung preparations were reexamined in line with the 2002 American Thoracic Society/European Respiratory Society idiopathic interstitial pneumonia consensus criteria. Results. Histopathological examination revealed that 50 cases (75.7%) were in the exudative phase and 16 (24.2%) were in the proliferative phase. Only the rate of alveolar exudate/oedema in exudative phase cases (P = 0.003); those of alveolar histiocytic desquamation (P = 0.037), alveolar fibrosis (P = 0.017), chronic inflammation (P = 0.02), and alveolar fibrin (P = 0.001) in proliferative cases were significantly higher. The presence of alveolar fibrin was the only independent variable in favour of proliferative cases (P = 0.016). Conclusion. The detection of all DAD morphological criteria with the same intensity is not always possible in each case. Forensic autopsies may provide a favourable means for expanding our knowledge about acute lung damage, DAD, and interstitial lung disease.

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Analysis of pulmonary vascular injury and repair during Pseudomonas aeruginosa infection‐induced pneumonia and acute respiratory distress syndrome

et al. 2019

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Herein we describe lung vascular injury and repair using a rodent model of Pseudomonas aeruginosa pneumonia-induced acute respiratory distress syndrome (ARDS) during: 1) the exudative phase (48-hour survivors) and 2) the reparative/fibro-proliferative phase (1-week survivors). Pneumonia was induced by intratracheal instillation of P. aeruginosa strain PA103, and lung morphology and pulmonary vascular function were determined subsequently. Pulmonary vascular function was assessed in mechanically ventilated animals in vivo (air dead space, P a O 2 , and lung mechanics) and lung permeability was determined in isolated perfused lungs ex vivo (vascular filtration coefficient and extravascular lung water). At 48 hours post infection, histological analyses demonstrated capillary endothelial disruption, diffuse alveolar damage, perivascular cuffs, and neutrophil influx into lung parenchyma. Infected animals displayed clinical hallmarks of ARDS, including increased vascular permeability, increased dead space, impaired gas exchange, and decreased lung compliance. Overall, the animal infection model recapitulated the morphological and functional changes typically observed in lungs from patients during the exudative phase of ARDS. At 1 week post infection, there was lung histological and pulmonary vascular functional evidence of repair when compared with 48 hours post infection; however, some parameters were still impaired when compared with uninfected controls. Importantly, lungs displayed increased fibrosis and cellular hyperplasia reminiscent of lungs from patients during the fibro-proliferative phase of ARDS. Control, sham inoculated animals showed normal lung histology and function. These data represent the first comprehensive assessment of lung pathophysiology during the exudative and reparative/fibro-proliferative phases of P. aeruginosa pneumonia-induced ARDS, and position this pre-clinical model for use in interventional studies aimed at advancing clinical care.

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Alterações histopatológicas pulmonares em pacientes com insuficiência respiratória aguda: um estudo em autopsias

Cited by 5 publications

References 20 publications

Postmortem diagnosis of acute myocardial infarction in patients with acute respiratory failure - demographics, etiologic and pulmonary histologic analysis

Postmortem diagnosis of acute myocardial infarction in patients with acute respiratory failure - demographics, etiologic and pulmonary histologic analysis

Diffuse Alveolar Damage of the Lungs in Forensic Autopsies: Assessment of Histopathological Stages and Causes of Death

Analysis of pulmonary vascular injury and repair during Pseudomonas aeruginosa infection‐induced pneumonia and acute respiratory distress syndrome

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