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First published online on March 30, 2007
Chest, doi:10.1378/chest.07-0323
doi:10.1378/chest.07-0323
(Chest. 2007; 132:214-220)
© 2007 American College of Chest Physicians
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Acute Exacerbation of Interstitial Pneumonia Other Than Idiopathic Pulmonary Fibrosis*

I-Nae Park, MD; Dong Soon Kim, MD; Tae Sun Shim, MD; Chae-Man Lim, MD; Sang Do Lee, MD; Younsuck Koh, MD; Woo Sung Kim, MD; Won Dong Kim, MD; Se Jin Jang, MD and Thomas V. Colby, MD, FCCP

* From the Division of Pulmonary and Critical Care Medicine (Drs. Park, D.S. Kim, Shim, Lim, Lee, Koh, W.S. Kim, and W.D. Kim) and Department of Pathology (Dr. Jang), College of Medicine, University of Ulsan College of Medicine, Asan Medical Center, Seoul, Korea; and Department of Pathology (Dr. Colby), Mayo Clinic, Scottsdale, AZ.

Correspondence to: Dong Soon Kim, MD, Division of Pulmonary and Critical Care Medicine, University of Ulsan College of Medicine, Asan Medical Center, 388–1 Pungnap-2dong, Songpa-gu, Seoul 138–736, Korea; e-mail: dskim{at}amc.seoul.kr

Abstract

Backgrounds: Acute exacerbation (AE) in idiopathic pulmonary fibrosis (IPF) is increasingly recognized as a relatively common and highly morbid clinical event. However, clinical data on AE in non-IPF interstitial pneumonia are sparse. This study was performed to find the frequency, clinical features, and outcome of AE in non-IPF interstitial pneumonia.

Methods: Retrospective analysis of 10 patients who satisfied the modified Akira criteria for AE during follow-up of 74 patients with surgical lung biopsy-confirmed idiopathic nonspecific interstitial pneumonia (I-NSIP) and 93 patients with biopsy-confirmed interstitial pneumonia associated with collagen vascular disease (CVD-IP).

Results: AE occurred in six patients with I-NSIP (1-year frequency, 4.2%) and in four patients with CVD-IP (rheumatoid arthritis [RA], n = 3; scleroderma, n = 1), with 1-year frequency of 3.3%. Median age was 58 years (range, 47 to 75); six patients were female. AE occurred in two patients immediately after surgical biopsy. Median duration of acute symptom before hospital admission was 10 days (range, 1 to 30). Median ratio of PaO2 to the fraction of inspired oxygen (FIO2) was 172 (range, 107 to 273), and PaO2/FIO2 ratio was < 200 in six patients. Surgical lung biopsy performed at the time of AE in two patients revealed diffuse alveolar damage superimposed on nonspecific interstitial pneumonia pattern. Four patients with I-NSIP survived to discharge and were followed up for 24 months (range, 6 to 121).

Conclusion: AE occurred in the patients with I-NSIP with apparently better prognosis. In patients with CVD-IP, AE occurred mostly with RA-usual interstitial pneumonia in our small series with poor outcome.

Key Words: acute exacerbation • collagen vascular disease • idiopathic nonspecific interstitial pneumonia • surgical lung biopsy

Although idiopathic pulmonary fibrosis (IPF) has typically an insidious, slowly progressive clinical course, acute exacerbation (AE) is increasingly recognized as a relatively common and highly morbid clinical event in patients with IPF.12345678 From autopsy findings, diffuse alveolar damage (DAD) superimposed on chronic fibrotic lung, a histologic pattern of AEs, was found in some patients with not only IPF but also interstitial pneumonia related to collagen vascular disease (CVD-IP), and on a histologic background of both usual interstitial pneumonia (UIP) and fibrotic nonspecific interstitial pneumonia (NSIP).9 However, detailed clinical data are not available, and DAD at autopsy findings may be complicated with preterminal acute events. Acute interstitial pneumonia with DAD pattern could occur in patients with collagen vascular disease (CVD) including polymyositis/dermatomyositis, rheumatoid arthritis (RA), scleroderma, and systemic lupus erythematosus; however, most of them were the initial presentation of CVD-IP rather than AE of preexisting interstitial pneumonia.91011121314151617 Recently Parambil et al18 reviewed nine patients with DAD pattern on surgical lung biopsy of the patients with CVD, and six of them had preexisting lung diseases. These reports suggest that AE can occur in non-IPF interstitial pneumonia; however, there is no more clinical information on this condition. Therefore, we performed this study to estimate the frequency of AE in non-IPF interstitial pneumonia, especially surgical lung biopsy-confirmed idiopathic-NSIP (I-NSIP) and surgical biopsy-proven CVD-IP in our cohorts, and to analyze clinical, radiologic, and pathologic features, and outcome.

Materials and Methods

Diagnostic Criteria
For the diagnosis of I-NSIP and the individual pattern of interstitial pneumonia, we used the American Thoracic Society/European Respiratory Society consensus classification, and individual CVDs were diagnosed according to the criteria of each society.19202122232425 For the diagnosis of AE, we used the Akira criteria7: (1) subjective worsening of dyspnea within the last 1 month; (2) new ground-glass opacities or consolidation on chest radiograph or high-resolution CT (HRCT); (3) hypoxemia with decline ≥ 10 mm Hg in PaO2 from the previous level; (4) no evidence of infection by negative respiratory culture and serologic test results for respiratory pathogens; and (5) no clinical evidence of pulmonary embolism, congestive heart failure, or pneumothorax as a cause of acute worsening. However, two of the subjects did not have PaO2 data prior to AE because they first presented at the time of AE, and their surgical lung biopsy performed at that time showed DAD superimposed on NSIP pattern. For these patients, we used the criteria of acute lung injury (PaO2/fraction of inspired oxygen ratio [FIO2] < 300) in these patients.26

Subjects
From 1993 to April 2006, I-NSIP was diagnosed in 74 patients and CVD-IP was diagnosed in 93 patients by surgical lung biopsy at Asan Medical Center, Korea, and all of them were included in the study. Most of the subjects were included in previous articles.272829 Among these patients, AE was diagnosed in six patients with I-NSIP and four patients with CVD-IP.

All clinical and laboratory data were collected retrospectively from medical records. Spirometry (Vmax22; Sensormedics; Yorba Linda, CA), lung volumes by plethysmography (6200 Plethysmograph; Sensormedics), and diffusion capacity of the lung for carbon monoxide (Vmax229D; Sensormedics) were measured, and the results are expressed as a percentage of normal predicted values.30 HRCT was performed (HiSpeed Advantage Scanner; GE Medical Systems; Milwaukee, WI; or Somatom Plus 4; Siemens Medical Systems; Erlangen, Germany). BAL was performed as previously described.31 Biopsy slides were reviewed independently by at least two pathologists and reclassified according to the American Thoracic Society/European Respiratory Society consensus classification of interstitial pneumonia as described in detail in previous report.29 Data are expressed as median (range). The frequency of AE was obtained from the Kaplan-Meier survival curve by censoring AE as the "death variable." This study was approved by the Institutional Review Board of Asan Medical Center.

Results

Frequency of AE
Among 74 patients with surgical lung biopsy-confirmed fibrotic I-NSIP, the estimated 1-year frequency of AE was 4.2%. The estimated 1-year frequency in surgical lung biopsy-confirmed CVD-IP (n = 93) was 3.3% (Fig 1 ); however, it was 5.6% among the patients with CVD-UIP (n = 36) and 11.1% in RA-UIP (n = 18).


Figure 1
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  		Figure 1.. The 1-year frequency of AE among all the patients with biopsy-proven I-NSIP (n = 74) and CVD-IP (n = 93) at Asan Medical Center.

 
Demographic and Clinical Features
Demographic and clinical characteristics are shown in Table 1 . Median age at the time of AE was 58 years (range, 47 to 75); six patients (60%) were female. Two patients (I-NSIP, n = 1;CVD-NSIP, n = 1) had AE after surgical lung biopsy (1 day and 11 days, respectively). In the remaining eight patients, the time between the diagnosis of interstitial pneumonia and the onset of the AE ranged from 2 to 54 months (Fig 1).


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  		Table 1.. Clinical Data of 10 Patients With I-NSIP and CVD-IP*

 
Surgical lung biopsy was performed at the time of AE in two patients with I-NSIP. One patient had been followed up for 4 years due to abnormal chest imaging results (interstitial pneumonia pattern) without respiratory symptom or lung function abnormality, and sudden dyspnea developed 3 days prior to hospital admission. The other patient had dyspnea and diffuse parenchymal infiltration on chest radiography 7 months prior to hospital admission, and corticosteroid therapy was administered at other hospital from 6 weeks before the admission for 1 month. However, 10 days after the discontinuation of steroid treatment, the dyspnea worsened acutely and the patient was transferred to our hospital.

All subjects presented with rapid worsening of respiratory symptoms including dyspnea (Medical Research Council grade 4–5), cough, and whitish sputum for median duration of 10 days (range, 1 to 30). Five patients had fever. Inspiratory crackles were present in all cases. None of the patients had clinical evidence of heart disease, pneumothorax, or pulmonary embolism.

Among 10 patients with AE, AE developed in 6 patients during a course of corticosteroid with or without immunosuppressive therapy (cyclophosphamide, n = 3; azathioprine, n = 1). The median dose of prednisolone was 35 mg/d (range, 20 to 40), and four of the patients (CVD-IP, n = 3; and I-NSIP, n = 1) were undergoing tapering from an initial high dose of prednisolone. One patient was receiving home oxygen therapy.

Laboratory and BAL Findings
At the time of AE, all subjects were hypoxemic. The median ratio of PaO2/FIO2 was 172 (range, 107 to 273). Six of 10 patients met the criteria for ARDS including PaO2/FIO2 ratio < 200. Six patients presented an increased WBC count, and elevated values of erythrocyte sedimentation rate or C-reactive protein were found in nine patients. BAL was performed in seven patients at time of AE (Table 2 ). Microbiological studies including stains for acid-fast bacilli and Pneumocystis carinii; cultures for bacteria, mycobacteria, fungus, and virus; and serologic tests to identify infectious pathogen were performed on BAL fluid (n = 7) as well as blood (n = 10), sputum (n = 10), urine (n = 9), bronchial washing (n = 7), and tracheal secretions (n = 4); and the results were all negative. The lung tissues (n = 4) obtained by surgical lung biopsy were also cultured, and nothing was found.


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  		Table 2.. Laboratory Findings at the Time of AE*

 
Radiologic Features
On chest radiography, all patients displayed newly developed diffuse bilateral ground-glass opacity with/without consolidation at time of AE, superimposed on underlying chronic fibrotic changes. The HRCT films at time of AE were available in eight patients because two patients were rapidly deteriorating and intubated before undergoing HRCT. The distribution pattern of new ground-glass opacity was peripheral in three patients, multifocal in three patients, and diffuse in two patients (Fig 2 ).


Figure 2
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  		Figure 2.. HRCT findings before and at the time of AE in a 63-year-old woman with I-NSIP and AE showing multifocal patchy type. An initial HRCT (top left, A, and top right, B) shows the minimal reticular opacity in the subpleural area of the lung. In follow-up HRCT after 16 months (bottom left, C, and bottom right, D), ground-glass opacities of multifocal patchy distribution have developed in both lungs.

 
Pulmonary Function Data
Pulmonary function data prior to AE were available in nine patients. Eight patients had a restrictive ventilatory defect with a median FVC of 52% of predicted (range, 34 to 69%), diffusion capacity of the lung for carbon monoxide of 47% (range, 19 to 59%), and total lung capacity of 61% (range, 39 to 101%). The remaining one patient had normal pulmonary function test results in spite of abnormal HRCT findings. At the time of AE, only four patients were able to perform spirometry with a median decline of FVC of 23% of predicted (range, 15 to 59%).

Pathology Findings
Eight patients had undergone surgical lung biopsy prior to AE, and AE developed in two of them immediately after biopsy. The pathologic consensus diagnosis for these eight patients was NSIP in five patients (I-NSIP, n = 4; CVD, n = 1) and UIP in all three patients with CVD-RA without acute lung injury features. The remaining two patients (all with I-NSIP) underwent surgical lung biopsy at the time of AE, and both patients showed DAD pattern (hyaline membrane and organizing DAD without hyaline membrane, respectively) superimposed on NSIP pattern (Fig 3 ).


Figure 3
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  		Figure 3.. Pathology findings at the time of AE in a 63-year-old woman undergoing surgical lung biopsy at the time of AE. Top, A: Typical background pattern of fibrotic NSIP (hematoxylin-eosin, original x 200). Bottom, B: The other area of the same patient shows acute lung injury features manifesting as DAD pattern with fibrinous exudates (arrows) and inflammatory cell infiltration in the airspaces (hematoxylin-eosin, original x 400).

 
Treatment and Outcome
Nine patients were treated with broad-spectrum antibiotics and high-dose systemic corticosteroid therapy: six patients received IV pulse therapy (methylprednisolone, 250 mg to 1 g/d for 3 days), and three patients received 1 mg/kg/d of prednisolone. One patient was treated with broad-spectrum antibiotics with a maintenance dose of methylprednisolone (15 mg/d). Six patients received mechanical ventilation, and all six died from progressive disease combined with (n = 2) or without (n = 4) ventilator-associated pneumonia after a median of 26 days (range, 11 to 41). Four patients survived to discharge from the hospital, and the median duration of follow-up was 24 months (range, 6 to 121). All of survivors had idiopathic NSIP, whereas all of patients with CVD-IP died.

Discussion

Our experience showed that AE occurred in the patients with I-NSIP and CVD-IP. The estimated 1-year frequency of AE in our series was 4.2% in surgical lung biopsy-confirmed I-NSIP, 3.3% in CVD-IP, 5.6% in surgical biopsy-proven CVD-UIP, and 11.1% in RA-UIP. The clinical, radiologic, and pathologic features of our patients were similar to that of IPF. The exact frequency of AE in IPF is not known, and the reported numbers vary widely because of the difference in study design, and also due to the different case definitions.13233 In our previous report3 on a large cohort of patients with surgical lung biopsy-confirmed IPF/UIP during the same period of this study using Akira criteria, the 1-year frequency of AE was 15.4%. The frequency in our patients with surgical lung biopsy-confirmed I-NSIP seems to be lower than that of IPF/UIP. However, the frequency of AE in our patients with surgical lung biopsy-confirmed CVD-UIP, especially in RA-UIP, may not be lower than that of IPF/UIP.

The etiology of AE in most of the patients in this study was unknown as in IPF, except for two patients with AE immediately after surgical lung biopsy. In IPF, occurrence of AE after the surgical lung biopsy has been reported before3; Kondoh et al34 observed that postbiopsy exacerbation occurred in 2.1% of 236 consecutive patients undergoing surgical biopsy for diffuse lung disease. The finding of our study34 shows that the surgical lung biopsy can induce or aggravate the rapid worsening of respiratory conditions in patients with idiopathic NSIP as well as IPF/UIP. RA was the most common underlying disease among patients with CVD-UIP in our study, and three of four patients with AE in CVD-IP had RA. At the time of presentation, they were receiving oral prednisone with or without a cytotoxic agent; however, none of these patients was being treated with lefunomide or methotrexate, which has been associated with drug-induced lung disease.353637 Concerning the relationship of activity of CVD with AE, at the time of surgical biopsy our patients had active RA. However, at the time of AE, the activity of RA was stable, suggesting that the activity of CVD may not be related to the occurrence of AE in our patients.

The clinical features of our patients were similar to that of AE in IPF, except slightly younger age and nonsmoking female predominance in our series, which may be related to the female and nonsmoker predominance of the whole group of I-NSIP and CVD-IP compared to IPF. Because some of the subjects did not have arterial blood gas analysis before the AE, in those patients we used the criteria of acute lung injury: PaO2/FIO2 ratio < 300.26 However, PaO2/FIO2 ratio was < 200 in most of the patients. All of our patients had newly developed ground-glass opacities/consolidations in both lungs on chest radiography and on HRCT, except two patients who could not tolerate HRCT. The distribution pattern of newly developed ground-glass opacity or consolidation on HRCT was the same as AE of IPF: peripheral, multifocal, and diffuse pattern.37 Several studies346 have showed that neutrophils were predominant in BAL fluid of the patients with AE in IPF. Our patients with CVD-UIP had similar findings. However, in our AE patients with I-NSIP, lymphocytes were predominant cell type in BAL fluid. The reason for this discrepancy is not known. One possibility is that AE may be just an exaggerated response of underlying disease process because many patients with stable NSIP have an increased number of lymphocytes in BAL fluid.3839 However, the number of patients in our study is too small to draw any conclusion.

Because 60% of the patients were receiving steroid therapy at the time of AE, infection, particularly opportunistic infection, was the most important differential diagnosis; and an extensive workup including BAL studies with exhaustive microbiological tests was performed with negative results. The pathologic features of two of our patients were almost identical with that of IPF, except the underlying chronic disease was NSIP pattern. The outcome of AE in idiopathic NSIP in this small series seems to be better than that of IPF, whereas all four of our patients with AE in CVD-IP died. Actually, the survival rate of our patients with AE in CVD-IP was worse than that of AE in IPF,2 or that of acute interstitial pneumonia.404142 Furthermore, Parambil et al18 reported that in patients with DAD and CVD, the outcome appears to be worse for those with preexisting chronic CVD-IP compared to those without. Similar to AE of IPF, steroid and/or immunosuppressant agents had little benefit for our patients.

The limitation of our study is that the number of the subjects was too small for proper evaluation of the risk factors, prognosis, treatment effect, or prognostic factors. Another limitation is our study was restricted to surgical lung biopsy-proven cases. However, the confirmation of NSIP requires surgical biopsy; therefore, it is an inevitable limitation. The other limitation is that the pathologic confirmation of AE was done in only two patients with NSIP; however, AE is a clinically defined entity rather than pathologic phenomenon.

In summary, in spite of small number of the patients, we demonstrated that AE occurred in the patients with surgical lung biopsy-confirmed I-NSIP with apparently better prognosis than that of IPF/UIP. AE occurred also in patients with CVD-IP, mostly in RA-UIP in our small series with poor outcome. Further study is required to identify etiology, risk factors, prognostic markers, and effective treatments.

Footnotes

Abbreviations: AE = acute exacerbation; CVD = collagen vascular disease; CVD-IP = interstitial pneumonia related to collagen vascular disease; DAD = diffuse alveolar damage; FIO2 = fraction of inspired oxygen; HRCT = high-resolution CT; I-NSIP = idiopathic nonspecific interstitial pneumonia; IPF = idiopathic pulmonary fibrosis; NSIP = nonspecific interstitial pneumonia; RA = rheumatoid arthritis; UIP = usual interstitial pneumonia

This work was performed in the Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Ulsan College of Medicine, Asan Medical Center.

All of the authors contributed substantially to this work and are all responsible for the content of the article. The authors have no conflicts of interest in association with this article to disclose.

Received for publication February 7, 2007. Accepted for publication March 9, 2007.

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