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(Chest. 2004;125:1530-1535.)
© 2004 American College of Chest Physicians

"Imitators" of the ARDS*

Implications for Diagnosis and Treatment

Marvin I. Schwarz, MD, FCCP and Richard K. Albert, MD, FCCP

* From the Division of Pulmonary Sciences and Critical Care Medicine, University of Colorado Health Sciences Center, Denver Health Medical Center, Denver, CO.

Correspondence to: Marvin I. Schwarz, MD, FCCP, Division of Pulmonary Sciences and Critical Care Medicine, Campus Box C272, School of Medicine 5525, 4200 East Ninth Ave, Denver, CO 80222; e-mail: marvin.schwarz{at}uchsc.edu

Key Words: acute interstitial pneumonias • ARDS • BAL


   Introduction
TOP
 Introduction
Prevalence of Diffuse,...
 The "Imitators"
 Evaluation of the Imitators
 Role of BAL
 Treatment of the Imitators
 Summary
 References
 
Acute lung injury (ALI) and ARDS (ALI/ARDS) are defined as follows: (1) an illness having an acute onset, (2) an arterial oxygen tension/inspired oxygen fraction <= 200 mm Hg (or <= 300 mm Hg for ALI), (3) the presence of bilateral infiltrates on frontal chest radiographs, and (4) a pulmonary artery occlusion pressure <= 18 mm Hg if measured, or no clinical evidence of left atrial hypertension when not measured.12

There are a group of diffuse, noninfectious parenchymal lung diseases that often present in an acute fashion and fulfill all of the clinical, physiologic, and radiographic criteria for ALI/ARDS. Some of these have distinct BAL characteristics and/or specific histologic findings. It is important to distinguish these from ALI/ARDS because most cases seem to respond to the early initiation of systemic corticosteroid therapy. In addition, studies evaluating novel interventions for ALI/ARDS should not include these patients because their outcomes are dissimilar from ALI/ARDS.

This opinion article summarizes what is known about these diffuse noninfectious parenchymal diseases and focuses on the differences in their histologies, BAL findings, prognoses, and treatment responsiveness. We suggest that these conditions should be considered, prompting further diagnostic testing, in every patient thought to have ALI/ARDS ascribed to "pneumonia," and in those without a well-recognized predisposing factor.


   Prevalence of Diffuse, Noninfectious Parenchymal Lung Disease Mimicking ALI/ARDS
TOP
 Introduction
 Prevalence of Diffuse,...
The "Imitators"
 Evaluation of the Imitators
 Role of BAL
 Treatment of the Imitators
 Summary
 References
 
In the absence of a prospective study of consecutive patients meeting the diagnostic criteria for ALI/ARDS who undergo lung biopsy, it is not possible to know how frequently the acute diffuse, noninfectious parenchymal diseases meet the diagnostic criteria for ALI/ARDS. It is clear, however, that that many patients with these conditions fit the definition of ALI/ARDS. The most common predisposing causes of ALI/ARDS in most series are trauma, aspiration, and sepsis.34567 However, approximately one third of the 861 patients enrolled in the study3 of low tidal volume ventilation for ALI/ARDS had pneumonia identified as their precipitating problem. Specific diagnostic criteria for pneumonia were not defined. Rather, patients were assigned this predisposing factor on the basis of each investigator’s clinical judgment at each site (R. Brower, MD; personal communication; June 11, 2003). A similar prevalence of pneumonia is reported in other series of ALI/ARDS.5678

The diffuse, noninfectious parenchymal lung diseases often present with symptoms that are consistent with pneumonia.910 This may contribute to the fact that despite extensive microbiologic and serologic testing, an infectious etiology can only be found in approximately 50% of patients presenting with what is considered to be a community-acquired pneumonia.8 Accordingly, we suggest that patients thought to have ALI/ARDS on the basis of pneumonia, and those considered to have ALI/ARDS but without a defined predisposing condition, should undergo BAL and, depending on the findings, a lung biopsy, to exclude one of the acute noninfectious parenchymal lung diseases.


   The "Imitators"
TOP
 Introduction
 Prevalence of Diffuse,...
 The "Imitators"
Evaluation of the Imitators
 Role of BAL
 Treatment of the Imitators
 Summary
 References
 
Table 1 lists the histologic patterns, usual etiologies, and BAL cellular constituents of the acute noninfectious parenchymal lung diseases that often meet ALI/ARDS criteria. These noninfectious pneumonias have protean manifestations, many of which suggest an infectious process. These include fever, myalgias, nonproductive cough, and progressive dyspnea.910 The WBC counts, erythrocyte sedimentation rates, and C-reactive protein and serum lactic dehydrogenase levels are often elevated. Radiographic studies often show diffuse alveolar infiltrates reminiscent of ALI/ARDS. Although not always the case, the acute respiratory failure caused by these entities requires mechanical ventilation and the use of high levels of inspired oxygen and positive end-expiratory pressure as in ALI/ARDS.


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  		Table 1. Acute Noninfectious Diffuse Parenchymal Lung Diseases and Their Underlying Histology, Etiology, and BAL Cellular Content

 
Acute interstitial pneumonia (AIP) corresponds to the idiopathic clinicopathologic entity originally described by Hamman and Rich.1112 A similar presentation and histology (ie, organizing diffuse alveolar damage) representing one form of an acute immunologic pneumonia occurs with the collagen vascular diseases (CVDs) or as the result of an idiosyncratic reaction to a pneumotoxic drug.1314 AIP may appear in patients with preexisting idiopathic pulmonary fibrosis, and in this setting it has a particularly dismal prognosis.15 Idiopathic AIP (Hamman-Rich syndrome) is an acute, usually fulminant pneumonitis. Patients have symptoms that have lasted from a few days to several weeks. The age range is wide, the mean being 50 years.16 Of the conditions listed in Table 1, AIP has the poorest outcome. Persistence and progression of fibrosis in surviving patients, as well as episodes of recurrence have been documented.17 In one series17 of 13 patients, only 1 patient had full radiographic and physiologic recovery, although 67% survived the initial hospitalization. One report indicates that seven of eight patients with AIP, requiring mechanical ventilation and confirmed by surgical biopsies, survived following treatment with methylprednisolone (280 ± 143 mg/d). This was compared to a 50% mortality in ARDS in the same study.18 AIP is the one acute noninfectious parenchymal disorder that is indistinguishable from ALI/ARDS by BAL or surgical biopsy, and has been referred to as ARDS without a precipitating cause. Clinical clues that suggest AIP as opposed to an undefined pneumonia causing ARDS include the lack of accompanying multiorgan failure and the presence of cystic structures and traction bronchiectasis on the high-resolution CT scan, in addition to the patchy ground-glass density and areas of consolidation that are expected in both AIP and ALI/ARDS.1920

Acute eosinophilic pneumonia (AEP) first described in 1989 usually occurs in healthy young adults who present with a duration of illness that is usually less than a week and without a discernable precipitating event.2122 Some cases, however, have occurred following environmental dust exposure, the initiation of cigarette smoking, or as a noninfectious complication of AIDS.22232425 A number of medications can also result in acute eosinophilic lung disease. Peripheral eosinophilia, which is expected in other pulmonary eosinophilic syndromes is unusual and, if present, is not striking.2122 Some patients have high fevers, pleuritic chest pain, and eosinophilic pleural effusions, the latter being a useful distinguishing feature in patients with diffuse infiltrates.22 All patients present with some degree of acute respiratory failure and up to 50% require mechanical ventilation.26 Since AEP is a onetime event, and is very sensitive to treatment, full recovery can be expected.27 There is a report of one patient in whom AEP redeveloped after reinstitution of tetracycline therapy.28

Bronchiolitis obliterans organizing pneumonia (BOOP) is best recognized as a subacute syndrome process producing symptoms over several months, often following an antecedent upper respiratory tract infection.29 Less commonly, BOOP may be an acute, fulminant process resulting in respiratory failure requiring mechanical ventilation.3031323334 The acute form is either idiopathic or associated with a CVD or a drug toxicity.35363738 Imaging studies indicate patchy nonspecific areas of consolidation. Although the existing literature only describes approximately 20 cases, the results of treatment for idiopathic acute BOOP seem to be inferior to that of subacute BOOP. It is less likely to return with corticosteroid withdrawal as is the case in the subacute form of BOOP.

Diffuse alveolar hemorrhage (DAH) has many causes and several possible underlying histologies.394041424344454647 A confounding problem is that hemoptysis, the expected symptom, is absent in up to 33% of cases.3940 It is important to establish the cause of DAH since virtually all cases, except those associated with overwhelming diffuse alveolar damage, are potentially reversible. Recurrences are to be expected particularly if the underlying histology indicates pulmonary capillaritis (ie, a small vessel vasculitis of the lung), the pathology that underlies some systemic vasculitidies; CVD; the antiphospholipid antibody syndrome; or anti-basement membrane antibody (ABMA) disease.394041424344454647 Bland pulmonary hemorrhage, defined as alveolar filling with RBCs, but without septal inflammation, can result from anticoagulant overuse, thrombolytic therapy, and conditions that result in thrombocytopenia.

Acute hypersensitivity pneumonitis (HP) is characterized by fever, cough, dyspnea, and an increased WBC count appearing 4 to 6 h following the inhalation of an organic antigen.48 In most cases, it is a recurrent, self-limited episode of pneumonitis that is often initially treated as a community-acquired pneumonia until the nature of the disease is discovered and the antigen can be eliminated or avoided. On occasion, acute HP can present with fulminant acute respiratory failure, which is clinically and radiographically indistinguishable from ALI/ARDS or its other imitators.49505152 If unrecognized, cases of fulminant acute HP can be fatal.


   Evaluation of the Imitators
TOP
 Introduction
 Prevalence of Diffuse,...
 The "Imitators"
 Evaluation of the Imitators
Role of BAL
 Treatment of the Imitators
 Summary
 References
 
In patients who present with an acute, noninfectious, parenchymal lung disease without a recognized ALI/ARDS risk factor, the possibility of an illicit or prescribed drug, a systemic immunologic disease, or an environmental exposure being the cause must be considered along with infection. Various classes of drugs, particularly chemotherapeutic agents, can manifest as any of the histologic categories in Table 1.53545556575859 An acute immunologic pneumonia complicating a CVD can present with organizing diffuse alveolar damage, as in AIP, acute BOOP, or DAH secondary to either pulmonary capillaritis or bland hemorrhage.131435363940424446 This can occur in a patient with a previously diagnosed CVD, or the pneumonitis may represent the initial manifestation. Although the lung may be the only apparent organ involvement, a careful search for systemic involvement should be undertaken. It is critical to carefully seek evidence suggesting renal involvement in the form of a focal, segmental, necrotizing glomerulonephritis that is characterized by proteinura, hematuria, and RBC casts.394041 This rapidly progressive glomerulonephritis is common to the CVD, the systemic vasculitidies, and ABMA disease and requires prompt treatment if chronic renal insufficiency is to be avoided.

Serologic testing directed at the aforementioned systemic diseases should be undertaken. In addition, serum creatinine phosphokinase and ferritin should be measured as increased levels may suggest polymyositis and adult-onset Still disease, respectively.6061 A reduced hematocrit in the face of diffuse pulmonary infiltrates may be the first indication of DAH.62


   Role of BAL
TOP
 Introduction
 Prevalence of Diffuse,...
 The "Imitators"
 Evaluation of the Imitators
 Role of BAL
Treatment of the Imitators
 Summary
 References
 
BAL should be performed early on and preferably after tracheal intubation. The samples should be sent for identification of selected infectious agents and a differential WBC count (Table 1). In addition to excluding the possibility of the occasional diffuse fulminant viral or atypical pneumonia due to Mycoplasma pneumoniae, Legionella pneumophiliaor Chlamydia pneumoniae in the immunocompetent host, the results of the differential WBC count may obviate the need for further intervention. BAL eosinophilia in this setting establishes the diagnosis of AEP again (peripheral eosinophilia is unusual).2122 Lymphocytosis without a marked elevation of neutrophils strongly suggests acute HP, although acute BOOP may also demonstrate BAL lymphocytosis exceeding 30%.3148 The finding of bloody aliquots on sequential BAL samples indicates DAH.41 This finding will require further evaluation as outlined in the previous section. Similar to ALI/ARDS and the infectious pneumonias, the BAL in AIP and acute BOOP can have a predominance of neutrophils and minor increases in the percentages of lymphocytes and eosinophils.1116

Timing and Indication for Surgical Biopsy
If the BAL results are nonspecific and the clinical condition of the patient permits, we recommend consideration for surgical biopsy. Most can be performed via the video-assisted transthorascopic approach. In patients with abnormal coagulation study findings or thrombocytopenia, an open thoracotomy may be preferable. The open approach may also be appropriate if the degree of respiratory failure is severe. For each patient, the benefit vs risk of surgical biopsy must be taken into consideration.

Lung biopsy is recommended in patients with DAH unless the etiology is obvious (eg, a previously diagnosed CVD, clinical features of a vasculitis such as Wegeners granulomatosis, microscopic polyangiitis, or Henoch-Schoenlein purpura that presents with systemic manifestations in addition to DAH and pulmonary capillaritis).39404142 Moreover, pulmonary capillaritis causing DAH may represent an isolated small-vessel vasculitis of the lung without serologic or systemic manifestations pointing to a CVD or vasculitis.62 DAH complicating a CVD may have several underlying histologies, each with different treatment recommendations and prognoses. Regardless of the underlying histologies, it is important to obtain immunofluorescent staining of lung tissue in this acute setting, since the presence of immune complexes is suggestive of a CVD, and the presence of linear basement membrane staining indicates ABMA disease.434445


   Treatment of the Imitators
TOP
 Introduction
 Prevalence of Diffuse,...
 The "Imitators"
 Evaluation of the Imitators
 Role of BAL
 Treatment of the Imitators
Summary
 References
 
Data regarding the effectiveness of treatment of the acute, noninfectious parenchymal lung diseases come from individual reports and small case series. The literature also suffers from considerable variability in the timing, dosing, and duration of treatment. In general, corticosteroids are recommended. In addition, depending on the specific disorder, immunosuppressive drugs are added. Plasmapheresis is recommended for patients with ABMA disease.63

There are > 90 cases of AIP recorded in the literature, but the response to corticosteroid treatment can only be assessed in 26.1617 For these, the average mortality exceeded 70%. In a small treated group, 70% survived the acute event. In a recent series64 of 13 patients, the mortality was 50%; even allowing for the fact that 2 of these patients died after a recurrence of their AIP, and 2 others acquired progressive fibrotic lung disease, the mortality in AIP exceeds that currently attributed to ARDS.64 Information regarding timing of therapy was unavailable. In general, 250 mg of methylprednisolone was administered as a single daily dose or repeated for a total of 1g/d IV for 3 days followed by a gradual taper. Given the high mortality and possibly an improved outcome, corticosteroid therapy, as outlined above, should be initiated in a suspected case prior to tissue conformation. No information is available concerning additional therapies for the treatment of AIP.

Corticosteroids are very effective for AEP. The literature reports > 50 treated patients. Complete resolution occurs within 7 days, and without residual physiologic impairment. AEP in the vast majority of cases does not recur.303233

In acute BOOP, because of the paucity of reported cases, the results of treatment are less clear. The mortality may be as high as 70%, particularly if it accompanies a CVD.313536 In one report, three of five patients with acute idiopathic BOOP survived after receiving corticosteroids within the first week after biopsy. Corticosteroid treatment was delayed up to 2 weeks in the nonsurvivors.35 Other studies303334 support improved survival with early diagnosis and initiation of corticosteroid therapy.

DAH secondary to a systemic vasculitis, or a CVD, should be immediately treated with corticosteroids and a second immunosuppressive agent such as cyclophosphamide. Active glomerulonephritis is an additional mandate for immediate therapy. Although recurrences are possible as the medications are tapered, survival after the initial event approximates 70% in patients with CVD, and 80% in those with a systemic vasculitis or isolated pauci-immune pulmonary capillaritis.394041

It is difficult to draw any conclusion regarding the efficacy of treatment for patients with acute fulminant HP, as only a few fatal cases appear in the literature.53545556 Interestingly, all of these were attributed to avian antigens.


   Summary
TOP
 Introduction
 Prevalence of Diffuse,...
 The "Imitators"
 Evaluation of the Imitators
 Role of BAL
 Treatment of the Imitators
 Summary
References
 
When confronted with a case of acute respiratory failure severe enough to meet the diagnostic criteria of ALI/ARDS but without a predisposing cause, it is important to consider the alternate diagnoses reviewed above, and to attempt to establish a diagnosis as expediently as possible utilizing BAL with differential counts and, if necessary, the consideration for surgical biopsy. The most common error is that the episode of respiratory failure is incorrectly attributed to an infectious pneumonia and appropriate therapy is either not administered or delayed.

Because the literature suggests that a delay of specific therapy for some of these conditions worsens outcome, it seems prudent to administer systemic corticosteroids between 250 mg and 100 mg of IV methylprednisolone for a minimum of 3 days prior to the return of BAL, the microbiologic studies, and/or the surgical biopsy. If the microbiologic studies reveal a potential causative agent, corticosteroids would obviously be discontinued.

Some would argue that any diffuse pneumonitis that fulfills the ALI/ARDS criteria is ALI/ARDS and should be treated accordingly. A similar debate involved John Murray and Tom Petty in 1975.6566 Petty was the "lumper" and Murray was the "splitter," citing a difference in survivals for the various predisposing causes of ARDS. Neither author mentioned any of the conditions listed in Table 1, however. We submit that it is appropriate to call these conditions the "imitators" of ALI/ARDS since they may meet the diagnostic criteria of ALI/ARDS but have different therapeutic implications and outcomes.


   Footnotes
 
Abbreviations: ABMA = anti-basement membrane antibody; AEP = acute eosinophilic pneumonia; AIP = acute interstitial pnuemonia; ALI = acute lung injury; BOOP = bronchiolitis obliterans organizing pneumonia; CVD = collagen vascular disease; DAH = diffuse alveolar hemorrhage; HP = hypersensitivity pneumonitis

Supported by NHLBI SCOR HL-27353.

Received for publication July 11, 2003. Accepted for publication October 14, 2003.


   References
TOP
 Introduction
 Prevalence of Diffuse,...
 The "Imitators"
 Evaluation of the Imitators
 Role of BAL
 Treatment of the Imitators
 Summary
 References
 

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