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Acute interstitial pneumonia (Hamman-Rich syndrome)

Acute interstitial pneumonia (Hamman-Rich syndrome)
Literature review current through: Jan 2024.
This topic last updated: Apr 12, 2023.

INTRODUCTION — Acute interstitial pneumonia (AIP) is a rare and fulminant form of diffuse lung injury originally described by Hamman and Rich in 1935 [1,2]. AIP is classified as an idiopathic interstitial pneumonia (IIP), and among the IIPs, it has the most acute onset and rapidly progressive course [1-4].

AIP is similar in presentation to the acute respiratory distress syndrome (ARDS) and probably represents a subset of cases of idiopathic ARDS [5]. (See "Acute respiratory distress syndrome: Clinical features, diagnosis, and complications in adults".)

The clinical presentation, diagnosis, treatment, and prognosis of AIP will be reviewed here. The other idiopathic interstitial pneumonias and the approach to patients with interstitial lung disease are discussed separately. (See "Idiopathic interstitial pneumonias: Classification and pathology" and "Approach to the adult with interstitial lung disease: Clinical evaluation" and "Approach to the adult with interstitial lung disease: Diagnostic testing".)

EPIDEMIOLOGY — AIP generally affects previously healthy individuals without a prior history of lung disease and occurs with roughly equal frequency in male and female individuals [6-9]. It is not associated with cigarette smoking. Most patients are over the age of 40 years, with a mean age of 50 to 55 years [3,6,7,9,10].

PATHOLOGY — AIP has the histopathologic appearance of diffuse alveolar damage (DAD) [3]. DAD is a reaction pattern that occurs in response to a number of known causes of lung injury, but in the case of AIP, it is idiopathic (table 1) [11]. DAD has characteristic temporal phases in its evolution — acute exudative, organizing proliferative, and healed (or fibrotic) phases (table 2) [3,7]. (See "Idiopathic interstitial pneumonias: Classification and pathology".)

The histopathologic changes characteristic of the acute "exudative" stage are usually not observed on lung biopsy specimens of AIP, as biopsies are frequently obtained later in the clinical course. The most characteristic features of AIP are those found during the organizing, "proliferative" stage of DAD and include [3,5]:

Marked thickening of the alveolar septa due to interstitial edema, inflammatory cell infiltration, fibroblast proliferation (within the interstitium and airspaces), and type II cell hyperplasia (picture 1A-C)

Collapse and apposition of adjacent alveolar septa

Hyaline membranes (most prominent during the acute phase) in focal areas along alveolar septa

Thrombi in small arteries

The healing phase of AIP may show no apparent residue or may reveal variable degrees of interstitial fibrosis and/or airway scarring (picture 2).

An important feature of AIP is the presence of a temporally uniform lesion, which suggests that an episode of acute lung injury occurred at a single time point [5]. This differs from usual interstitial pneumonia (UIP), in which pathologic lesions are of different ages with alternating areas of normal lung, interstitial inflammation, fibroblast foci, and honeycomb change. However, the clinical course of patients with UIP may be complicated by "acute exacerbations" or an "accelerated phase of rapid clinical decline" without an identifiable cause. When this occurs, pathologic findings of both AIP and UIP are noted. (See "Idiopathic interstitial pneumonias: Classification and pathology", section on 'Usual interstitial pneumonia' and "Acute exacerbations of idiopathic pulmonary fibrosis".)

In a small autopsy series, marked myofibroblast proliferation was seen in the lungs of all patients with AIP, but was inconsistently seen in patients with infectious causes of ARDS and was mild in patients with ARDS from drug toxicity [12]. Pathologic evidence of multiorgan failure was absent in AIP, but uniformly present in patients with infection and inconsistently present in those with drug-induced toxicity. (See "Sepsis syndromes in adults: Epidemiology, definitions, clinical presentation, diagnosis, and prognosis", section on 'Multiple organ dysfunction syndrome'.)

PATHOGENESIS — The exact mechanism of the initial injury to the pulmonary endothelium and epithelium in AIP is unknown. Based on studies of animal models and human bronchoalveolar lavage, it is believed that the following sequence of events contributes to the clinical picture of AIP [6].

The rapid onset of a widespread injury pattern suggests a single insult as an initiating factor [6]. Alveolar epithelial cell damage and death lead to elaboration and release of mediators such as tumor necrosis factor alpha, interleukin 1beta, and monocyte chemoattractant factor. Recruitment of neutrophils into the alveolar spaces and alveolar septae leads to further cellular damage, possibly via release of toxic oxygen radicals and proteases. Undoubtedly, other inflammatory cells contribute to progression of the epithelial cell injury and airspace exudation. The extent of epithelial cell injury and basement membrane damage may modulate the nature and extent of the subsequent fibroblastic response in AIP.

Following the acute phase, a stage of organization ensues that is characterized by fibroblast proliferation and connective tissue synthesis. The hyaline membranes are resorbed or incorporated into the alveolar septa and are overgrown by proliferating type II epithelial cells.

In patients with a fibrotic response, fibroblast proliferation and differentiation into myofibroblasts leads to production of collagen, widening of the alveolar septae, and organization of the alveolar exudate [13]. Alveolar wall collapse and apposition, associated with reepithelization of the fibrotic exudate within the alveolar space, contribute to the severity and extent of the fibrotic process. Resolution of the injury occurs in some patients, others develop a progressive fibrotic response. (See "Pathogenesis of idiopathic pulmonary fibrosis".)

CLINICAL FEATURES — The onset of AIP is usually rapid, with a prodromal illness that typically lasts 7 to 14 days prior to presentation [3,6,14]. The most common presenting signs and symptoms are fever, cough, and progressive, severe shortness of breath, affecting 75, 79, and 90 percent, respectively [3,9,15]. The majority will have hypoxemia at presentation and most will require intubation and mechanical ventilation within a few days. Patients may also report prodromal symptoms of myalgias, arthralgias, chills, and malaise [11].

Tachypnea and diffuse crackles are frequently present on lung examination [3]. Digital clubbing is typically not seen. The presence of clubbing suggests that the AIP is occurring as an exacerbation of underlying fibrotic disease, such as idiopathic pulmonary fibrosis [16]. (See "Idiopathic interstitial pneumonias: Classification and pathology", section on 'Usual interstitial pneumonia' and "Acute exacerbations of idiopathic pulmonary fibrosis".)

Careful cardiac, cutaneous, joint, and muscle examinations are performed to exclude heart failure and known causes of acute respiratory distress syndrome (ARDS) or interstitial pneumonia.

EVALUATION — The initial evaluation of patients with acute interstitial pneumonia is similar to that for acute lung injury/acute respiratory distress syndrome (ALI/ARDS). The possibility of cardiogenic pulmonary edema (heart failure) is excluded (eg, plasma brain natriuretic peptide level, echocardiogram). Known causes of noncardiogenic pulmonary edema and diffuse pulmonary opacities are sought (table 1 and table 3), using the studies outlined below. If this testing is negative, a lung biopsy is often obtained. (See "Acute respiratory distress syndrome: Clinical features, diagnosis, and complications in adults" and "Natriuretic peptide measurement in heart failure".)

Laboratory — Routine laboratory studies are nonspecific and more helpful in identifying alternative diagnoses than in making a diagnosis of AIP. A peripheral leukocytosis is common (mean 12,100 cells/microL, range 5600 to 21,800 cells/microL).

A plasma brain natriuretic peptide level and an echocardiogram are often obtained to help exclude cardiogenic pulmonary edema.

Tests for connective tissue diseases can help to exclude an acute exacerbation of previously undiagnosed dermatomyositis, polymyositis, rheumatoid arthritis, primary Sjögren's disease, or systemic lupus erythematosus [3,17]. We typically obtain serum muscle enzymes (eg, alanine aminotransferase (ALT), aspartate aminotransferase (AST), aldolase, creatine kinase), an antinuclear antibody test, an anti-Jo-1 antibody, and a rheumatoid factor. If these tests are negative, additional tests for antibodies to RNA synthetases (eg, anti-PR-7, anti-PR-12), signal recognition particle (anti-SRP) or helicase (anti-Mi-2) may be obtained. The laboratory evaluation of the various connective tissue diseases is discussed separately. (See "Interstitial lung disease in dermatomyositis and polymyositis: Clinical manifestations and diagnosis" and "Interstitial lung disease in rheumatoid arthritis" and "Interstitial lung disease associated with Sjögren's disease: Clinical manifestations, evaluation, and diagnosis" and "Pulmonary manifestations of systemic lupus erythematosus in adults".)

Arterial blood gases — Most patients develop moderate to severe hypoxemia, often with a PaO2/FiO2 (arterial oxygen tension/fraction of inspired oxygen) ratio 200 mmHg or less, which is in the range of the acute respiratory distress syndrome (ARDS). (See "Acute respiratory distress syndrome: Clinical features, diagnosis, and complications in adults", section on 'Diagnosis'.)

Imaging — The chest imaging findings are similar to those seen in acute respiratory distress syndrome (ARDS). The chest radiograph reveals diffuse, bilateral, air-space opacification (image 1) [3,7,10]. High resolution computed tomographic (HRCT) scans typically show bilateral, patchy, symmetric areas of ground glass attenuation, often accompanied by airspace consolidation, septal thickening, and traction bronchiectasis (image 2) [18-20].

Other findings that may be seen include a predominantly subpleural distribution of disease, and sparse honeycombing (less than 5 percent of the lung) [21]. (See "Acute respiratory distress syndrome: Epidemiology, pathophysiology, pathology, and etiology in adults".)

Microbiologic tests — A key component of the evaluation of patients with suspected AIP is the exclusion of underlying infection, beginning with a careful history regarding potential exposures. Microbiologic investigation typically includes nasopharyngeal aspirates for influenza testing, induced sputum for Pneumocystis jirovecii immunofluorescence, serologic tests for atypical and viral pneumonias (eg, Coccidioides, Chlamydia, coronavirus), and urinary antigen tests (eg, Streptococcus pneumoniae and Legionella), as indicated by the history and physical examination.

Most patients with AIP have a nonproductive cough, so sputum cultures are usually not available. Bronchoalveolar lavage and bronchial brushing are generally performed to obtain respiratory tract samples for immunofluorescence and culture. (See 'Bronchoscopy and BAL' below.)

Polymerase chain reaction (PCR)-based diagnostic panels that assess multiple respiratory viruses simultaneously on serologic or bronchoalveolar lavage samples can be performed in two to three hours in some hospital laboratories. (See "Clinical evaluation and diagnostic testing for community-acquired pneumonia in adults", section on 'Differential diagnosis' and "Seasonal influenza in adults: Clinical manifestations and diagnosis".)

Bronchoscopy and BAL — The main role of bronchoscopy and bronchoalveolar lavage (BAL) is to exclude other diseases in the differential of AIP, such as alveolar hemorrhage, eosinophilia, infection, and diffuse infiltration by cancer or lymphoma. The majority of patients will undergo bronchoscopy with bronchoalveolar lavage. Depending on whether the oxygen saturation can be adequately maintained with supplemental oxygen by nasal cannula, this may require intubation and supportive ventilation.

Samples from the BAL are sent for cell counts, cultures (eg, bacterial, mycobacterial, fungal, viral), enzyme immunoassay, direct immunofluorescence, and cytologic analysis (eg, viral inclusion bodies, malignant cells). Samples from bronchial brushings are also sent for cytologic evaluation for viral inclusion bodies. (See "Role of bronchoalveolar lavage in diagnosis of interstitial lung disease" and "The diffuse alveolar hemorrhage syndromes", section on 'Bronchoalveolar lavage'.)

The BAL cellular profile in acute interstitial pneumonia may show a marked increase in neutrophils and atypical epithelial cells, although these findings are nonspecific [22].

Lung biopsy — If the initial minimally invasive tests do not yield an alternate diagnosis, a clinical decision must be made regarding whether to perform transbronchial, video-assisted (VATS), or open lung biopsy [23]. We favor obtaining a video-assisted lung biopsy early in the course, in the hopes of identifying a treatable process.

Some clinicians may choose to perform a transbronchial biopsy first to assess for sarcoidosis, lymphangitic carcinomatosis, acute eosinophilic pneumonia, and alveolar proteinosis, prior to proceeding to VATS or open biopsy. For patients with early, milder disease this may allow a less invasive evaluation. On the other hand, when respiratory impairment is progressing rapidly, VATS or open lung biopsy will lead to a diagnosis more expeditiously. (See "Role of lung biopsy in the diagnosis of interstitial lung disease".)

Lung biopsy specimens are also examined for evidence of other specific causes of ARDS. As an example, areas of necrosis are typically not seen in AIP and suggest possible infection, infarct, or vasculitis. Well-formed granulomas, viral inclusions, and neutrophilic abscesses may suggest infection, while poorly formed granulomas suggest hypersensitivity pneumonitis.

DIAGNOSIS — The diagnosis of acute interstitial pneumonia (AIP) is based upon two findings:

The presence of a clinical syndrome of idiopathic acute respiratory distress syndrome (ARDS)

AND

Pathologic confirmation of diffuse alveolar damage (DAD).

Thus, after an initial clinical, laboratory, and microbiologic evaluation, an open or thoracoscopic lung biopsy is necessary to confirm the diagnosis. (See 'Evaluation' above.)

For those patients whose lung function is not adequate to safely allow a lung biopsy, a presumptive diagnosis of AIP may be based on the presence of a compatible clinical syndrome and the absence of clinical, serologic, or bronchoalveolar lavage evidence of an alternative diagnosis.

DIFFERENTIAL DIAGNOSIS — The differential diagnosis of AIP includes a number of pulmonary diseases [16]. Many of the disorders with a similar presentation to AIP are identified on the basis of laboratory, microbiologic, and bronchoalveolar lavage testing, including heart failure, the diffuse alveolar hemorrhage syndromes, acute eosinophilic pneumonia, cryptogenic organizing pneumonia (also known as idiopathic bronchiolitis obliterans organizing pneumonia), and hypersensitivity pneumonitis. Others may become apparent after examination of the lung biopsy. (See 'Lung biopsy' above.)

Once the diagnosis of diffuse alveolar damage (DAD) is confirmed by lung biopsy, we ensure that known causes of DAD have been excluded (eg, connective tissue disease, drug-induced toxicity, radiation pneumonitis, toxin-exposure, or viral infection) (table 1 and table 3). (See 'Laboratory' above.)

As DAD can be the initial presentation of connective tissue disease, most often rheumatoid arthritis, amyopathic dermatomyositis, or polymyositis, these disorders are evaluated by careful examination for cutaneous and joint manifestations and by laboratory testing [24,25]. (See 'Laboratory' above and "Diagnosis and differential diagnosis of rheumatoid arthritis" and "Clinical manifestations of dermatomyositis and polymyositis in adults", section on 'Clinical manifestations'.)

AIP should be distinguished from two other forms of idiopathic interstitial pneumonia: usual interstitial pneumonia (UIP) (image 3A-C) and desquamative interstitial pneumonia (DIP). Distinguishing features among these clinicopathologic entities include the types of prodromal illness, radiographic and histopathologic findings, the clinical course, and the response to therapy (table 4). The major clinical difference at presentation is disease duration: AIP is an acute disease of abrupt onset, whereas DIP has a subacute course over weeks to months, and UIP has a chronic course over more than one year [9]. (See "Idiopathic interstitial pneumonias: Classification and pathology".)

Also in the differential diagnosis of AIP is an "acute exacerbation" or an "accelerated phase of rapid clinical decline" complicating the clinical course of another interstitial pneumonia, whether idiopathic (eg, idiopathic pulmonary fibrosis [IPF], nonspecific interstitial pneumonia [NSIP]), or due to a connective tissue disease (eg, rheumatoid arthritis, scleroderma) [25]. Histological examination of the lung in these cases reveals a pattern of DAD on the background of usual interstitial pneumonia or NSIP. The evaluation and management of acute exacerbations of IPF are discussed separately. (See "Acute exacerbations of idiopathic pulmonary fibrosis".)

TREATMENT — The main treatment for acute interstitial pneumonia (AIP) is supportive care. The benefit of glucocorticoids remains unclear, although these are widely used, as described below.

Supportive care — General supportive care for patients with acute respiratory failure includes supplemental oxygen, ventilatory support, and prevention of complications (eg, venous thromboembolism, gastrointestinal bleeding, nosocomial pneumonia). Noninvasive or invasive mechanical ventilation is usually required, since most patients develop respiratory failure. Supportive care and ventilator strategies are discussed separately. (See "Acute respiratory distress syndrome: Ventilator management strategies for adults" and "Acute respiratory distress syndrome: Fluid management, pharmacotherapy, and supportive care in adults" and "Noninvasive ventilation in adults with acute respiratory failure: Benefits and contraindications", section on 'Hypoxemic nonhypercapnic respiratory failure not due to ACPE'.)

Glucocorticoids — Once the diagnosis of AIP is made, we typically initiate high dose systemic glucocorticoids, although data are limited. Evidence in support of high dose glucocorticoid therapy is limited to small case series that used a variety of glucocorticoid regimens and reported widely varying results [3,6,9,14,15,26,27]:

In the largest series of 29 patients, survival was 45 percent among patients treated with glucocorticoids and 33 percent among those not treated with glucocorticoids [3]. The dose of glucocorticoids was not provided.

In a series of 10 patients, early administration of pulse dose glucocorticoids was associated with survival in eight [15].

Seven of eight patients survived in another series in which a mean dose of 240 mg per day of methylprednisolone was used [26].

Six of eight patients treated with an unknown dose of glucocorticoids survived the initial hospitalization [9].

Mortality was 100 percent in a series of 12 patients treated with methylprednisolone 8 mg/kg per day [14].

We usually initiate empiric broad-spectrum antibiotics at the same time as glucocorticoids, given the difficulty of completely excluding infection. The choice of antibiotics is discussed separately. (See "Treatment of community-acquired pneumonia in adults who require hospitalization", section on 'Intensive care unit'.)

High-dose glucocorticoid therapy is continued for several days and then tapered slowly over several weeks to months, as tolerated.

Surveillance for glucocorticoid-induced side effects (eg, hyperglycemia, increased susceptibility to infection, gastritis, and critical illness myopathy) is appropriate. In patients receiving high-dose, systemic glucocorticoids, the use of neuromuscular blockade during mechanical ventilation increases the risk of post-paralytic critical illness myopathy and is avoided whenever possible. (See "Neuromuscular blocking agents in critically ill patients: Use, agent selection, administration, and adverse effects", section on 'Administration'.)

Other immunosuppressive therapy — Alternative immunosuppressive therapies (eg, vincristine, cyclophosphamide, cyclosporine, and azathioprine) have been reported in case reports of AIP, although success was limited [8,9,28,29]. In a patient who underwent single lung transplantation for AIP, the combination of cyclosporine, azathioprine, and prednisolone to suppress rejection led to partial improvement in the native lung [28].

Lung transplantation — Lung transplantation has been reported in patients with progressive interstitial lung disease thought to be due to AIP [9,28,30,31].

PROGNOSIS — The in-hospital mortality from AIP is high (greater than 50 percent), and the majority of those who survive the initial hospitalization die within six months of presentation [3,7,10,14]. Those who recover may have substantial or complete recovery of lung function [5,9]. However, recurrence of AIP and the development of chronic interstitial lung disease have been reported among a substantial fraction of those who survive the initial hospitalization [9,16]. No known factors predict the course of disease among AIP survivors.

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Interstitial lung disease".)

SUMMARY AND RECOMMENDATIONS

Definition – Acute interstitial pneumonia (AIP) is a rare and fulminant form of diffuse lung injury that generally occurs in previously healthy individuals. (See 'Introduction' above.)

Clinical features – The onset of AIP is usually rapid, with a prodromal illness of 7 to 14 days. The most common clinical signs and symptoms are fever, cough, and shortness of breath. (See 'Clinical features' above.)

Diagnosis – The diagnosis of AIP is based upon the presence of a clinical syndrome of idiopathic acute respiratory distress syndrome (ARDS) AND histologic confirmation of diffuse alveolar damage. (See 'Diagnosis' above.)

Differential diagnosis – The differential diagnosis of AIP includes heart failure, the diffuse alveolar hemorrhage syndromes, acute eosinophilic pneumonia, cryptogenic organizing pneumonia (also known as idiopathic bronchiolitis obliterans organizing pneumonia), hypersensitivity pneumonitis, and diffuse alveolar damage of known cause (table 1). (See 'Differential diagnosis' above.)

Treatment

Supportive care – The main treatment of AIP is supportive care. Noninvasive or invasive mechanical ventilation is often required, as most patients develop respiratory failure. (See 'Supportive care' above.)

Systemic glucocorticoids – For patients with a diagnosis of AIP, we suggest initiating high dose systemic glucocorticoids, although supportive data are limited (Grade 2C). We typically administer empiric broad-spectrum antibiotics simultaneously. (See 'Glucocorticoids' above.)

Prognosis – The in-hospital mortality from AIP is high (greater than 50 percent). Those who survive the initial illness may have substantial or complete recovery of lung function or may experience recurrence of AIP or the progression of chronic interstitial lung disease. (See 'Prognosis' above.)

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References

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