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Causes and Prognosis of Diffuse Alveolar Damage Diagnosed on Surgical
Lung Biopsy.Chest.
2007 May 2;
Background
Diffuse alveolar damage (DAD) is a relatively common histopathologic
finding at autopsy, particularly in patients dying with acute
respiratory distress syndrome, and can result from a variety of
causes. The spectrum of causes and associated prognostic implications
for DAD diagnosed by surgical lung biopsy are unclear. Methods We
identified 58 consecutive patients with DAD diagnosed by surgical lung
biopsy over a 7-year period, January 1996 through December 2002. The
presenting clinico-radiologic features, causes, and clinical course of
these patients were studied. Results The median age was 61 years, 48%
were women, and 60% were immunocompromised. Ninety percent of patients
fulfilled the criteria for acute respiratory distress syndrome at the
time of surgical lung biopsy. Chest radiography demonstrated bilateral
parenchymal infiltrates while computed tomography revealed
predominantly ground-glass and consolidative opacities. Infections
were the most common cause of DAD (22%). Other causes were
non-infectious pulmonary complications of hematopoietic stem cell or
solid-organ transplantation (17%), connective-tissue diseases (16%),
acute exacerbation of idiopathic pulmonary fibrosis (12%), drugs
(10%), and radiation therapy (2%). Twelve patients (21%) had acute
interstitial pneumonia, i.e., no identifiable cause or predisposing
condition for DAD. Overall hospital mortality was 53% with highest
mortality (86%) occurring among patients for whom DAD represented
acute exacerbation of idiopathic pulmonary fibrosis. Conclusion Our
study showed that infections and acute interstitial pneumonia are the
most common causes of DAD diagnosed by surgical lung biopsy. Hospital
mortality rate associated with DAD may vary depending on the
underlying cause.
An
immunohistochemical study in a fatal case of acute interstitial
pneumonitis (Hamman-Rich syndrome) in a 15-year-old boy presenting as
sudden death.Forensic
Sci Int. 2007 Jan 5;
Acute
interstitial pneumonitis (AIP), also known as Hamman-Rich syndrome, is
a distinct type of idiopathic interstitial pneumonia affecting
patients of both genders without pre-existing lung diseases. We
describe the case of a fulminant form of AIP and discuss the
pathophysiological mechanisms of AIP with reference to the
histological pattern. A 15-year-previously-healthy male boy presented
to the Hospital with a 6-day history of malaise, fever and cough. The
clinical prodromes were followed by the acute onset of increasing
shortness of breath rapidly progressing in acute respiratory failure.
Chest X-ray demonstrated bilateral diffuse airspace opacification; the
high resolution CT confirmed the presence of bilateral, symmetric
diffuse ground-glass attenuation. The patient was admitted to the
intensive care unit, but died after few hours. An autopsy was
performed within 24h. The histological examination of lung specimens
showed a pattern of diffuse alveolar damage. immunohistochemical,
microbiological and toxicological tests were also carried out. The
clinical presentation, the histological findings and the exclusion of
infective, traumatic, toxic and metabolic causes of acute respiratory
distress syndrome (ARDS) allowed us to conclude that the boy was
affected by AIP. In conclusion, AIP is a diagnosis of exclusion. It
has a mortality rate ranging about 50%, despite mechanical
ventilation. In fatal cases of AIP diagnosis can be based on clinical
presentation, radiological, histological and microbiological findings
and can be further confirmed by immunohistochemical analysis.
Acute
exacerbation (acute lung injury of unknown cause) in UIP and other
forms of fibrotic interstitial pneumonias.Am
J Surg Pathol. 2007 Feb;31(2):277-84.
Acute
exacerbation of usual interstitial pneumonia (UIP) is a condition in
which patients with UIP, and occasionally other forms of fibrotic
interstitial lung disease, develop rapid respiratory failure,
accompanied by extensive radiologic infiltrates. The pathologic
features of this condition are ill-defined in the literature and the
outcome is unclear. We report 12 such patients, 9 with underlying UIP,
2 with underlying fibrotic nonspecific interstitial pneumonia, and 1
with underlying chronic hypersensitivity pneumonitis, who underwent
surgical lung biopsy for diagnosis. High-resolution computed
tomography data were available in 11 cases and showed the presence of
extensive bilateral ground-glass opacities, sometimes accompanied by
focal consolidation, superimposed on underlying fibrosis. Three
microscopic patterns of acute lung injury were seen: diffuse alveolar
damage (DAD), organizing pneumonia (OP), and a pattern of numerous
very large fibroblast foci superimposed on underlying fibrosis. After
the biopsy, all patients were treated with steroids, in some instances
accompanied by cyclophosphamide or azathioprine. Ten patients survived
the acute episode and were discharged with survival times of 1 to 11
months; of these cases, 6 showed a pattern of OP or OP plus extensive
fibroblast foci; 2 a pattern of extensive fibroblast foci only; and 2
a pattern of DAD. Both patients who died had histologic DAD. We
conclude that acute exacerbation of UIP and other fibrotic lung
diseases produces a variety of pathologic patterns on biopsy, and that
patients with OP or extensive fibroblast foci as the acute pattern
seem to do better than those with DAD. Our data also imply that
survival (of the acute episode) may be better than the literature
suggests.
Acute
interstitial pneumonia and acute exacerbations of idiopathic pulmonary
fibrosis.
Semin Respir Crit Care Med. 2006
Dec;27(6):659-67.
Acute
interstitial pneumonia (AIP) and acute exacerbations of idiopathic
pulmonary fibrosis (AEIPF) are similar respiratory disorders
characterized by the rapid development of progressive dyspnea and
cough. Both frequently lead to respiratory failure and death.
Pathologically, each is characterized by the presence of a diffuse
alveolar damage (DAD) pattern; in AIP, DAD is the sole pattern,
whereas in AEIPF DAD is superimposed upon a background usual
interstitial pneumonia. They differ in that patients with AEIPF have
preexisting idiopathic pulmonary fibrosis, whereas patients with AIP
have no predisposing disorders to account for their disease. Because
both presentations overlap with multiple other causes of acute lung
injury, a comprehensive evaluation is necessary to rule out disorders
such as overwhelming infection or congestive heart failure. Although a
confident diagnosis can be achieved without it, a surgical lung biopsy
is necessary to provide a definitive diagnosis. Despite minimal
evidence, glucocorticoids are frequently begun once microbiological
evaluation confirms the absence of infection. Despite therapy, the
case fatality rate ranges up to 70% for both, with most patients dying
in the first 2 weeks. Survivors of the acute event can recover to
their previous baseline; however, most AIP survivors will stabilize
with some functional impairment, whereas in those with AEIPF,
progressive fibrosis with functional deterioration is the rule.
Acute
interstitial pneumonia following surgery for primary lung cancer.Eur
J Cardiothorac Surg. 2006
Oct;30(4):657-62. Epub 2006 Aug 8.
OBJECTIVE:
Although acute interstitial pneumonia is a life-threatening
complication following surgery for lung cancer, the cause and risk
factors for acute interstitial pneumonia remain unknown. We conducted
this study to determine the characteristics of acute interstitial
pneumonia after pulmonary resection and to identify the risk factors
for this disease. METHODS: We experienced 16 (2.0%) cases of acute
interstitial pneumonia among 822 patients who underwent pulmonary
resection for primary lung cancer over a period of 12 years. We
performed a retrospective analysis of these patients, comprising the
patients' background, the operative procedure, the radiographic
characteristics and the prognosis. RESULTS: In all patients, the
shadow appeared within 1 week after the operation. Twelve patients
required mechanical ventilatory support due to the development of
respiratory failure. The site of the tumor (right side), preoperative
radiation or chemotherapy, pneumonectomy, blood transfusion, and
intraoperative complication were independent risk factors for the
incidence of acute interstitial pneumonia (P=0.001, 0.0484, 0.0012,
0.0002, 0.0003, respectively) in the multivariate analysis. Nine of
the 16 patients died due to respiratory failure, resulting in a
mortality rate of 56.3%. The maximum amount of lactate dehydrogenase (LDH)
in the operative death patients was significantly higher than that in
the survivors (472+/-138IU/l vs 257+/-79IU/l, respectively, P=0.0031).
CONCLUSIONS: We concluded that in order to reduce the incidence of
acute interstitial pneumonia, it is necessary to perform careful
postoperative management for patients who are male, have right lung
disease, have undergone preoperative chemo or radiation therapy, or
have undergone pneumonectomy.
Histopathologic features and outcome of patients with acute
exacerbation of idiopathic pulmonary fibrosis undergoing surgical lung
biopsy.Chest.
2005 Nov;128(5):3310-5.
STUDY
OBJECTIVES: To define the clinicopathologic features and outcome of
acute exacerbation in patients with idiopathic pulmonary fibrosis (IPF)
undergoing surgical lung biopsy. DESIGN: Retrospective, single-center
study. SETTING: Tertiary care, referral medical center. PATIENTS:
Seven patients with acute exacerbation of IPF who underwent surgical
lung biopsy. RESULTS: The median age of these seven patients was 70
years (range, 59 to 74 years); two were women. Five patients had a
smoking history and included two current smokers. All patients were
experiencing an exacerbation of dyspnea for a median duration of 14
days (range, 7 to 28 days) prior to presentation. In three of these
patients, the acute deterioration was the presenting feature of IPF,
while in the remaining four patients the diagnosis of IPF had
previously been established. Chest radiography demonstrated bilateral
mixed alveolar-interstitial infiltrates in all of them. CT revealed
ground-glass opacities and consolidation bilaterally in all patients
with associated peripheral honeycombing in six of them.
Echocardiography was performed in six patients and demonstrated
pulmonary hypertension in all. BAL fluid was obtained in five patients
and revealed neutrophilia in all. Surgical lung biopsy showed diffuse
alveolar damage (DAD) in five patients with associated collagen
fibrosis and honeycomb changes typical of usual interstitial pneumonia
(UIP). One biopsy showed a combination of UIP and organizing
pneumonia, while one biopsy showed only DAD. Despite treatment with
lung-protective ventilation strategies and high-dose systemic
corticosteroids, six patients (86%) died during their hospitalization.
CONCLUSIONS: Although IPF is typically associated with an insidious,
slowly progressive clinical course, acute exacerbations occur and may
be the presenting manifestation in some patients. In either situation,
current management strategies including high-dose corticosteroid
therapy appear to be relatively ineffective for these patients with
acute exacerbation undergoing surgical lung biopsy.
Nonhomogeneous immunostaining of hyaline membranes in different
manifestations of diffuse alveolar damage.
Clinics.
2006 Dec;61(6):497-502.
PURPOSE: To
determine the nature of hyaline membranes in different manifestations
of diffuse alveolar damage, [pulmonary and extrapulmonary acute
respiratory distress syndrome], and idiopathic [acute interstitial
pneumonia]. MATERIALS AND METHODS: Pulmonary specimens were obtained
from 17 patients with acute respiratory distress syndrome and 9
patients with acute interstitial pneumonia. They were separated into 3
different groups: (a) pulmonary diffuse alveolar damage (pDAD) (n =
8), consisting only of pneumonia cases; (b) extrapulmonary diffuse
alveolar damage (expDAI) (n = 9), consisting of sepsis and septic
shock cases; and (c) idiopathic diffuse alveolar damage (iDAD) (n =
9), consisting of idiopathic cases (acute interstitial pneumonia).
Hyaline membranes, the hallmark of the diffuse alveolar damage
histological pattern, were examined using various kinds of antibodies.
The antibodies used were against surfactant apoprotein-A (SP-A),
cytokeratin 7 (CK7), cytokeratin 8 (CK8), alpha smooth muscle actin
(alpha-SMA), cytokeratin AE1/AE3 (AE1/AE3), and factor VIII-related
antigen (factor VIII). RESULTS: Pulmonary diffuse alveolar damage
showed the largest quantity of hyaline membranes (12.65% +/- 3.24%),
while extrapulmonary diffuse alveolar damage (9.52% +/- 3.64%) and
idiopathic diffuse alveolar damage (7.34% +/- 2.11%) showed
intermediate and lower amounts, respectively, with the difference
being statistically significant between pulmonary and idiopathic
diffuse alveolar damage (P < 0.05). No significant difference was
found for hyaline membranes Sp-A immunostaining among pulmonary
(15.36% +/- 3.12%), extrapulmonary (16.12% +/- 4.58%), and idiopathic
(13.74 +/- 4.20%) diffuse alveolar damage groups. Regarding factor
VIII, we found that idiopathic diffuse alveolar damage presented
larger amounts of immunostained hyaline membranes (14.12% +/- 6.25%)
than extrapulmonary diffuse alveolar damage (3.93% +/- 2.86%), with
this difference being statistically significant (P < 0.001). Equally
significant was the difference for progressive decrease of cytokeratin
AE1/AE3 immunostaining in hyaline membranes present in the
extrapulmonary diffuse alveolar damage (5.42% +/- 2.80%) and
idiopathic diffuse alveolar damage (0.47% +/- 0.81%) groups (P <
0.001). None of the groups stained for cytokeratin CK-7, CK-8,
vimentin, or a anti-smooth muscle actin. CONCLUSIONS: This study
showed that only the epithelial/endothelial components (SP-A, factor
VIII, and AE1/AE3) of the alveolar/capillary barrier are present in
hyaline membranes formation in the 3 groups of patients with diffuse
alveolar damage. The significant difference in the expression of
factor VIII-related antigen and cytokeratin AE1/AE3 in the expDA
versus iDAD groups as well as the significant difference in the amount
of hyaline membranes present in the pDAD versus iDAD groups are
suggestive of a local and specific lesion with different pathways
(direct, indirect, or idiopathic), depending on the type of diffuse
alveolar damage.
Acute
interstitial pneumonitis during chemotherapy for haematological
malignancy.Eur
J Cancer Care (Engl). 2005
Sep;14(4):336-41.
Fourteen adult
patients with haematological malignancies (eight non-Hodgkin's
lymphoma, one multiple myeloma, one chronic lymphocytic leukaemia, two
acute lymphoblastic leukaemia and two acute myeloid leukaemia)
developed acute interstitial pneumonitis (IP) during the course of
chemotherapy. All patients manifested high fever over 38 degrees C,
bilateral diffuse pulmonary interstitial infiltrates in the chest
radiograph and severe hypoxia without hypercapnia in the arterial
blood gas analysis. Pathogenic microorganisms were not detected in
repeated examinations in any patient. Chemotherapy given included
various anti-neoplastic drugs. Five patients had received granulocyte
colony-stimulating factor (G-CSF) for chemotherapy-induced leucopenia.
The onset was associated with an increase of leucocytes in 10
patients. All patients were treated with high dose steroid hormone and
broad spectrum antibiotics with or without anti-fungal agents, and
three required mechanical ventilation. Eleven patients quickly
recovered from these situations, whereas three died. Autopsies were
done in two patients and disclosed pneumocystis carinii (PC)
pneumonitis in one and non-specific pulmonary congestive oedema and
fibrosis in the other. In conclusion, IP of unknown cause could
develop in patients with various haematological malignancies
especially at the recovery phase of chemotherapy-induced leucopenia
irrespective of the previous G-CSF administration. High dose steroid
hormone should be used as therapy for such patients as soon as
possible after exclusion of an infective aetiology.
Acute
interstitial pneumonia.Clin
Chest Med. 2004 Dec;25(4):739-47, vii
The idiopathic
interstitial pneumonias have unknown etiology and are characterized by
diffuse parenchymal lung involvement and the potential to develop
pulmonary fibrosis. Most portend a reduction in life expectancy due,
in part, to the absence of effective therapies. The symptoms of
idiopathic interstitial pneumonia develop insidiously. In
contradistinction, acute interstitial pneumonia (AIP, also known as
acute interstitial pneumonitis) is unique in that it has a very rapid
to fulminant onset, leading to early hospitalization and a high
initial case fatality ratio but, potentially, a more favorable
long-term prognosis for survivors. Despite its contemporary
description nearly 20 years ago, knowledge of this disease has
increased little. This review focuses on AIP and its current place
among the idiopathic interstitial pneumonias.
Video-assisted
thoracoscopic lung biopsy as a possible cause of acute interstitial
pneumonia in a patient with nonspecific interstitial pneumonia.
Can Respir J. 2004 Sep;11(6):437-40.
The present
case report describes a 44-year-old woman who presented with dyspnea
due to diffuse interstitial lung disease. High-resolution computed
tomography showed features of usual interstitial pneumonia, but the
lung biopsy obtained by video-assisted thoracoscopy was consistent
with a histological pattern of nonspecific interstitial pneumonia.
Following the procedure, the patient developed progressive respiratory
distress and died on postoperative day 13 with a clinical picture of
acute interstitial pneumonia. The autopsy showed evidence of diffuse
alveolar damage superimposed on the background pattern of nonspecific
interstitial pneumonia. The present case report supports the notion
that patients with a variety of subtypes of idiopathic interstitial
pneumonias may be at risk of exacerbation of their underlying disease
following thoracic procedures, including video-assisted thoracoscopic
lung biopsy.
Acute
interstitial pneumonia. A clinicopathologic, ultrastructural, and cell
kinetic study.Am
J Surg Pathol. 1986 Apr;10(4):256-67.
Eight cases of
acute interstitial pneumonia were studied to define the clinical and
pathologic features and to determine the relationship to chronic
interstitial pneumonia. Clinically, this disease differs from the
chronic interstitial pneumonias by a sudden onset and a rapid course.
Five patients died of respiratory failure after 23 days to 2 months,
and two died of other complications after 3 1/2-6 months. An etiologic
agent could not be identified in any case. The histologic hallmark was
interstitial fibrosis and edema associated with type II pneumocyte
hyperplasia. The fibrosis differed from that seen in the chronic
interstitial pneumonias by extensive fibroblast proliferation and
relatively little collagen deposition. Autoradiographic studies of
tritiated thymidine (3H-TdR) uptake showed high labeling indices in
interstitial cells and type II pneumocytes. Evidence of acute lung
injury, including both endothelial and epithelial cell damage, was a
prominent ultrastructural feature. These findings emphasize that acute
interstitial pneumonia is a clinically and pathologically distinct
form of interstitial pneumonia that should be separated from the group
of chronic interstitial pneumonias.
Acute
fibrinous and organizing pneumonia: a histological pattern of lung
injury and possible variant of diffuse alveolar damage.Arch
Pathol Lab Med. 2002 Sep;126(9):1064-70.
CONTEXT: The
histologic patterns of diffuse alveolar damage (DAD), bronchiolitis
obliterans with organizing pneumonia (BOOP), and eosinophilic
pneumonia (EP) are well-recognized histologic patterns of lung injury
associated with an acute or subacute clinical presentation. We have
recognized acute fibrinous and organizing pneumonia (AFOP) as a
histologic pattern, which also occurs in this clinical setting but
does not meet the classic histologic criteria for DAD, BOOP, or EP and
may represent an underreported variant. OBJECTIVE: To investigate the
clinical significance of the AFOP histologic pattern and to explore
its possible relationship to other disorders, including DAD and BOOP.
DESIGN: Open lung biopsy specimens and autopsy specimens were selected
from the consultation files of the Armed Forces Institute of
Pathology, which showed a dominant histologic pattern of
intra-alveolar fibrin and organizing pneumonia. Varying amounts of
organizing pneumonia, type 2 pneumocyte hyperplasia, edema, acute and
chronic inflammation, and interstitial widening were seen. Cases with
histologic patterns of classic DAD, BOOP, abscess formation, or
eosinophilic pneumonia were excluded. To determine the clinical
behavior of patients with this histologic finding, clinical and
radiographic information and follow-up information were obtained.
Statistical analysis was performed using Kaplan-Meier and chi(2)
analysis. RESULTS: Seventeen patients (10 men, 7 women) with a mean
age of 62 years (range, 33-78 years) had acute-onset symptoms of
dyspnea (11), fever (6), cough (3), and hemoptysis (2). Associations
believed to be clinically related to the lung disease included
definitive or probable collagen vascular disease (3), amiodarone (1),
sputum culture positive for Haemophilus influenza (1), lung culture
positive for Acinetobacter sp. (1), lymphoma (1), hairspray (1),
construction work (1), coal mining (1), and zoological work (1). Six
patients had no identifiable origin or association. Follow-up revealed
2 clinical patterns of disease progression: a fulminate illness with
rapid progression to death (n = 9; mean survival, 0.1 year) and a more
subacute illness, with recovery (n = 8). Histologic analysis and
initial symptoms did not correlate with eventual outcome, but 5 of the
5 patients who required mechanical ventilation died (P =.007).
CONCLUSIONS: Acute fibrinous and organizing pneumonia is a histologic
pattern associated with a clinical picture of acute lung injury that
differs from the classic histologic patterns of DAD, BOOP, or EP.
Similar to these patterns of acute lung injury, the AFOP pattern can
occur in an idiopathic setting or with a spectrum of clinical
associations. The overall mortality rate is similar to DAD and
therefore may represent a histologic variant; however, AFOP appears to
have 2 distinct patterns of disease progression and outcome. The need
for mechanical ventilation was the only parameter that correlated with
prognosis. None of the patients with a subacute clinical course
required mechanical ventilation.
Acute interstitial
pneumonitis. Case series and review of the literature.
Medicine (Baltimore). 2000 Nov;79(6):369-78.
Acute
interstitial pneumonitis (AIP) is an acute, idiopathic interstitial
lung disease characterized by rapidly progressive diffuse pulmonary
infiltrates and hypoxemia requiring hospitalization. The case-fatality
ratio is high. Previous reports suggested that survivors of the acute
event have a favorable outcome. We undertook this study to examine the
natural history of survivors. We had observed several patients who
experienced recurrent episodes of AIP and chronic progressive
interstitial lung disease. We sought to determine longitudinal
survival in these patients and to compare our experience with that in
the medical literature. Overall, we identified 13 biopsy-proven cases
of AIP. The mean patient age was 54 years in our review, which is
identical to previous reports. Twelve patients were hospitalized and
all 12 required mechanical ventilation. Overall hospital survival was
67%. All patients demonstrated abnormalities in gas exchange at
presentation. Radiographs typically demonstrated bilateral patchy
densities that progressed to a diffuse alveolar filling pattern in
nearly all cases. All biopsy specimens showed organizing diffuse
alveolar damage. Longitudinal data were available for 7 patients. Two
died of AIP recurrences. A third died of complications of heart
failure shortly after hospital discharge. One patient progressed to
end-stage lung disease and required lung transplantation. Two patients
experienced persistent pulmonary symptoms, accompanied in 1 by
progressive lung fibrosis. One patient had nearly complete recovery of
lung function 2 years following AIP. (Follow-up information was
unavailable for 2 survivors.) In our literature review, 5 of 7
patients reported experienced some recovery of lung function. One case
of progressive interstitial lung disease requiring lung
transplantation was reported. The reported mortality was much higher
than in our experience (74% versus 33%). The mean time from symptom
onset to death was 26 days, compared with 34 days in our experience.
The use of corticosteroids did not appear to influence survival,
although this has not been tested in a rigorous manner. The better
survival in our series may be related in part to a survivor selection
bias. In contrast to previous reports, we found that survivors of AIP
may experience recurrences and chronic, progressive interstitial lung
disease. We did not identify any clinical or pathologic features that
predict mortality in these patients. Likewise, there were no features
that predicted the longitudinal course in survivors. Further study to
identify causal factors is required in the hope of preventing
morbidity and mortality related to this disease.
Pathological
examination of 11 autopsy cases of acute onset interstitial pneumonia
of unknown etiology.Nihon
Kyobu Shikkan Gakkai Zasshi. 1992
Jul;30(7):1234-41.
In 11 autopsy
cases of acute onset interstitial pneumonia of unknown etiology, all
cases had thickening of alveolar septa with various degrees of
lymphocytic infiltration and fibroblast proliferation. Only a few
cases had edematous alveolar septa, which were weakly positive in
alcian-blue staining. Intra-alveolar, intra-alveolar duct and
intra-bronchiolar organization was a characteristic finding. These
findings may represent the repair phase rather than the exudative
phase of diffuse alveolar damage. Localized bacterial pneumonia was
superimposed in 3 cases, and neither Pneumocystis carinii nor viral
inclusion bodies were identified in any case. The severity of fibrosis
was not obviously correlated with the period of artificial
ventilation. From these findings, terminal infection and oxygen
therapy did not seem to significantly modify the course of acute-onset
interstitial pneumonia. Further examination of autopsy cases as well
as open-lung biopsy is important to elucidate the time course of
acute-onset interstitial pneumonia.
Hamman-Rich
syndrome revisited.
Mayo Clin Proc. 1990 Dec;65(12):1538-48.
In this
article, we retrospectively review 29 cases of Hamman-Rich syndrome.
As in some other recent reports, we have used the term "acute
interstitial pneumonia" to emphasize the clinical and pathologic
features of these cases and to distinguishm the more common
chronic interstitial pneumonias, particularly idiopathic pulmonary
fibrosis. Of the 29 patients, 12 survived, some after a long and
complicated hospitalization. The histologic features were those of
organizing diffuse alveolar damage, and some patients, including
survivors, had extensive fibroblastic distortion of lung parenchyma.
The overall survival among these patients was not appreciably
different from the survival of patients with the adult respiratory
distress syndrome in general.
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