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Media Gallery

Approximately half of the patients with idiopathic pulmonary fibrosis develop clubbing. Clubbing is commonly seen in patients with asbestosis.
Lung volume is plotted against transpulmonary pressure. Compliance is the change in volume for a given change in pressure. A patient with emphysema has a higher lung compliance compared with a patient with no lung disease, while a patient with restrictive lung disease has a reduction in compliance.
Idealized flow volume curves for normal, obstructive, and restrictive lungs.
The expiratory flow volume curves of 2 patients are depicted graphically. A is a patient with restrictive lung disease (idiopathic pulmonary fibrosis), low forced vital capacity (FVC), but an increased ratio of forced expiratory volume in 1 second (FEV1) to FVC because of increased elastic recoil. B is a patient with chronic obstructive lung disease whose FEV1/FVC ratio is low but whose lung volumes are increased.
Pulmonary function test results from a patient with restrictive lung disease.
Gross pathology of small and firm lungs due to restrictive lung disease from advanced pulmonary fibrosis.
Intrinsic lung disease may progress to extensive fibrosis, regardless of etiology. This is described as honeycomb lung.
End-stage sarcoidosis.
Usual interstitial pneumonitis (left).
Usual interstitial pneumonitis (right).
Histopathology of a case of idiopathic pulmonary fibrosis. Alveolitis with fibroblast proliferation and collagen deposition is present.
In usual interstitial pneumonitis or idiopathic pulmonary fibrosis, subpleural and paraseptal inflammation is present, with an appearance of temporal heterogeneity. Patchy scarring of the lung parenchyma and normal, or nearly normal, alveoli interspersed between fibrotic areas are the hallmarks of this disease. Additionally, the lung architecture is completely destroyed.
Characteristic features of usual interstitial pneumonitis as described in the image below.
Cryptogenic organizing pneumonia (also called proliferative bronchiolitis) is often patchy and peribronchiolar. The proliferation of granulation tissue within small airways and alveolar ducts is excessive and is associated with chronic inflammation of surrounding alveoli.
Cryptogenic organizing pneumonia, as described in the image below, showing a close-up view of fibrogranulation tissue in terminal airspaces.
Granulomatous lung diseases are marked by granulomas characterized by the accumulation of T lymphocytes, macrophages, and epithelioid cells. These may progress to pulmonary fibrosis. This low-power image shows well-formed granuloma along the airway.
Multiple well-formed noncaseating granulomas secondary to sarcoidosis.
Sarcoid granulomas.
High-power view of sarcoid granuloma shows giant cells.
A patient who developed restrictive lung disease had findings of cryptogenic organizing pneumonia on an open lung biopsy specimen.
A patient who developed restrictive lung disease had findings of cryptogenic organizing pneumonia on an open lung biopsy specimen. The biopsy sample shows intraluminal buds of granulation tissue.
Lymphocytic interstitial pneumonitis, for which the prominent finding is a lymphoid infiltrate that involves both the interstitium and alveolar spaces.
Usual interstitial pneumonitis honeycombing.
Chest radiograph of a 67-year-old man diagnosed with idiopathic pulmonary fibrosis, based on open lung biopsy findings. Extensive bilateral reticulonodular opacities are seen in both lower lobes.
High-resolution CT scan of the same patient in the image below demonstrates peripheral honeycombing and several areas of ground-glass attenuation. Ground-glass opacification may correlate with active alveolitis and a favorable response to therapy.
A CT scan image from a 59-year-old woman shows advanced pulmonary fibrosis. Extensive honeycombing and traction bronchiectasis are present.
Restrictive lung disease may occur in stage II and stage III sarcoidosis. In this image, mediastinal lymphadenopathy is shown secondary to stage II disease.
Sarcoidosis on CT scan shows nodules in midlung zones. These nodules are predominantly along the bronchovascular bundles and in a subpleural location.
Restrictive lung disease secondary to sarcoidosis.
A chest radiograph of stage III sarcoidosis. This stage refers to pulmonary infiltrates without evidence of mediastinal lymphadenopathy.
Chest radiograph from a 39-year-old woman with severe kyphoscoliosis who developed hypercapnic respiratory failure. Spirometry findings showed a severe restrictive lung disease, with a forced expiratory volume in one second of 0.4 L/s and a forced vital capacity of 0.5 L.
The flow volume curve of a patient with lung fibrosis.
Likely case of idiopathic pulmonary fibrosis, which should be treated with prednisone.
Pressure volume curve comparing lungs with emphysema, lungs with restrictive disease, and normal lungs.

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Table 1. Causes of Restrictive Lung Disease

Causes	Examples	Diagnosis	PFT Findings
Pleural	Trapped lung, pleural scarring, large pleural effusions, chronic empyema, asbestosis	Radiography, CT scanning, pleural manometry, pleural biopsy	Low RV^a, low TLC, low FVC
Alveolar	Edema, hemorrhage	Radiography, CT scanning, physical examination	Increased DLCO^b in hemorrhage (Intrapulmonary hemoglobin absorbs the carbon monoxide, thus increasing the DLCO reading.)
Interstitial	Interstitial lung disease including IPF^c, NSIP^d, COP^e	Radiography, CT scanning, physical examination, echo often shows pulmonary hypertension	Low RV, low FVC, low TLC, decreased DLCO, poor lung compliance
Neuromuscular	Myasthenia gravis, ALS^f, myopathy	Physical examination, EMGs^g, serology	Low RV, low TLC, low NIF^h, low MMVⁱ
Thoracic/extrathoracic	Obesity, kyphoscoliosis, ascites	Physical examination	Low ERV^j and FRC in obesity, low VC^k, TLC, FRC^l in kyphoscoliosis
^aResidual volume. ^bDiffusion capacity of the lungs for carbon monoxide. ^cIdiopathic pulmonary fibrosis. ^dNonspecific interstitial pneumonitis. ^eCryptogenic organizing pneumonia. ^fAmyotrophic lateral sclerosis. ^gElectromyography. ^hNegative inspiratory force. ⁱMaximal voluntary ventilation. ^jExpiratory reserve volume. ^kVital capacity. ^lFunctional residual capacity.

Table 2. Contrasting Clinical, Radiologic, and Histologic Features of Acute Interstitial Pneumonia (AIP), Usual Interstitial Pneumonia (UIP), Nonspecific Interstitial Pneumonia (NSIP), ^[43]and COP ^[44]

Features	AIP	UIP	NSIP	COP
Pathologic
Temporal appearance	Uniform	Heterogeneous	Uniform	Uniform
Interstitial inflammation	Scant	Scant	Usually prominent	Variable
Collagen fibrosis	No	Patchy	Variable, diffuse	No
Fibroblast proliferation	Diffuse, interstitial	Patchy (fibroblast foci)	Occasional	Patchy, airspace
COP areas	Rare	No	Rare	--
Honeycomb changes	Rare	Yes	Rare	No
Hyaline membranes	Yes, often focal	No	No	No

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Author

Jonathan Robert Caronia, DO Fellow, Department of Pulmonary and Critical Care Medicine, Lenox Hill Hospital, North Shore LIJ Health System

Disclosure: Nothing to disclose.

Coauthor(s)

Chuan Jiang, MD Physician, Lenox Hill Hospital, Northwell Health

Chuan Jiang, MD is a member of the following medical societies: American College of Physicians, Society of Hospital Medicine

Disclosure: Nothing to disclose.

Klaus-Dieter Lessnau, MD, FCCP Former Clinical Associate Professor of Medicine, New York University School of Medicine; Medical Director, Pulmonary Physiology Laboratory, Director of Research in Pulmonary Medicine, Department of Medicine, Section of Pulmonary Medicine, Lenox Hill Hospital

Klaus-Dieter Lessnau, MD, FCCP is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Medical Association, American Thoracic Society, Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Daniel R Ouellette, MD, FCCP Associate Professor of Medicine, Wayne State University School of Medicine; Medical Director, Pulmonary Medicine General Practice Unit (F2), Senior Staff and Attending Physician, Division of Pulmonary and Critical Care Medicine, Henry Ford Hospital

Daniel R Ouellette, MD, FCCP is a member of the following medical societies: American College of Chest Physicians, American Thoracic Society, Society of Critical Care Medicine

Disclosure: Received research grant from: Sanofi Pharmaceutical.

Chief Editor

John J Oppenheimer, MD Clinical Professor, Department of Medicine, Rutgers New Jersey Medical School; Director of Clinical Research, Pulmonary and Allergy Associates, PA

John J Oppenheimer, MD is a member of the following medical societies: American Academy of Allergy Asthma and Immunology, American College of Allergy, Asthma and Immunology, New Jersey Allergy, Asthma and Immunology society

Disclosure: Received research grant from: quintiles, PRA, ICON, Novartis: Adjudication<br/>Received consulting fee from AZ for consulting; Received consulting fee from Glaxo, Myelin, Meda for consulting; Received grant/research funds from Glaxo for independent contractor; Received consulting fee from Merck for consulting; Received honoraria from Annals of Allergy Asthma Immunology for none; Partner received honoraria from ABAI for none. for: Atlantic Health System.

Additional Contributors

Laurie Robin Grier, MD Medical Director of MICU, Professor of Medicine, Emergency Medicine, Anesthesiology and Obstetrics/Gynecology, Fellowship Director for Critical Care Medicine, Section of Pulmonary and Critical Care Medicine, Louisiana State University Health Science Center at Shreveport

Laurie Robin Grier, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Society for Parenteral and Enteral Nutrition, Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Lalit K Kanaparthi, MD Attending Physician, North Florida Lung Associates

Lalit K Kanaparthi, MD is a member of the following medical societies: American College of Chest Physicians, American Medical Association, American Thoracic Society

Disclosure: Nothing to disclose.

Acknowledgements

Sat Sharma, MD, FRCPC Professor and Head, Division of Pulmonary Medicine, Department of Internal Medicine, University of Manitoba; Site Director, Respiratory Medicine, St Boniface General Hospital

Sat Sharma, MD, FRCPC is a member of the following medical societies: American Academy of Sleep Medicine, American College of Chest Physicians, American College of Physicians-American Society of Internal Medicine, American Thoracic Society, Canadian Medical Association, Royal College of Physicians and Surgeons of Canada, Royal Society of Medicine, Society of Critical Care Medicine, and World Medical Association

Disclosure: Nothing to disclose.