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The trachea is approximately 22 cm long, with a cross -sectional area of 2 cm. Pulmonary Pathology Online At the tracheal carina it divides into two major bronchi. The right bronchus diverges at a lesser angle from the trachea, which is why foreign material is more frequently aspirated on the right side. On entering the lung the bronchus divide into lobar br onchi and then into segmental bronchi, which supply the 19 segments of the lung. Because the segments are individual units with their own bronchovascular supply, they can be resected individually. The number of further ramifications of the bronchi depends on the distance from the hilum. Thus, there is a substantial number of ramifying bronchi in axial pathways that traverse the long distance to the periphery of the lung, such as the posterior basal segment, whereas there are far fewer in lateral pathways supplying the lung close to the hilum. The tracheobronchial tree has cartilage and tracheobronchial mucous glands in the wall. The glands are compound tubular glands that display both mucous (pale cells) and serous cells (granular, m ore basophilic cells). Between them, both types of cell secrete most of the mucus that is found in the tracheobronchial tree. The tracheobronchial tree is lined by a pseudostratified epithelium, which appears as layers, although all cells reach the basem ent membrane. Most of the cells are ciliated, but mucus -secreting (goblet) cells also exist, as well as basal cells that do not reach the surface. The basal cells are thought to be precursor cells that differentiate to form the more specialized cells of th e tracheobronchial epithelium. K (for Kulchitsky-like) cells which resemble the argentaffin and argyrophil cells found in the gut and elsewhere, are neuroendocrine cells that contain a variety of hormonally active polypeptides and vasoactive amines. Althou gh at one time these cells were thought to derive from the neural crest and migrate to the epithelium of the bronchus, it is now clear that they share a common stem cell with other cells of the bronchus and gut. Succeeding the bronchi are the (membranous) bronchioles, which differ from bronchi in that they contain neither cartilage nor mucus -secreting glands. As with bronchi, the number of branchings and their length depends on the pathway from the hilus to the periphery of the lung. In axial pathways ther e may be up to 25 branchings of conducting airways and a length of approximately 23 cm, whereas in lateral pathways there are only seven generations and a total length of about 8 cm. The epithelium of the bronchioles becomes thinner, until only one cell la yer is apparent.
The last purely conducting structure is the terminal bronchiole, after which the airways have alveoli in their walls. A major change then occurs as the gas -exchanging unit, the acinus, is encountered. This unit consists of, in series: 1) Respiratory bronchioles, airways with both alveolated and nonalveolated epithelium in their walls, 2) Alveolar ducts, conducting structures with only alveoli in their walls,& 3) Alveolar sacs, terminal structures lined entirely by alveoli. The acinus is the unit of gas exchange in the lung. Understanding this structure is critical to understanding the very important condition known as emphysema. Alveoli, the gas-exchanging structures of the lung, are lined by two types of epithelium. - Type I cells cover 95% of the alveolar surface, although they comprise only 40% of all the epithelial cells of the alveolus. They are thin and have a large surface area, a combination of that facilitates gas exchange. - Type II cells comprise 60% of the alveolar lining cells, but because they are more cuboidal they contribute only a small part to the total alveolar surface area. These cells secrete the surfactant material of the alveolar surface that maintains the patency of alveoli. It should be noted that bronchioles are also line by surfactant and that displacement of surfactant by inflammatory exudates leads to the bronchiolar instability and thus impairs their function. Type I cells are very vulnerable to injury, and when they die, type II cells multiply and differentiate to form type I cells, thereby reconstituting the alveolar surface area. The alveolar epithelial cells are connected by tight junctions that prevent the passage of even small molecules through the epithelial surface. The alveolar wall contains a dens e network of capillaries, each alveolus having approximately 1000 capillary segments, about 15 micrometer long and 8 micrometer in diameter. The capillaries are lined by endothelial cells that resemble type I epithelial cells in that they have abundant fla t cytoplasm but differ in that their junctions are ´leakyµ or ´semitightµ. Because the junctions are tighter on the arterial side and looser in the small venules, molecules the size of albumin can pass through the capillary endothelium. Both the endotheli um and epithelium have basal laminae, and when they are adjacent they fuse into a single basal lamina that forms the thin side of the alveolar capillary membrane where gas exchange is most efficient.
and proteoglycans are found there. connective tissue partitions that subdivide the lung into small respiratory units. A crucial concept in understanding the lung pathology is that of the interstitium of the lung. are also found on the thick side of the alveolar capillary membrane. the basal lamina e are separate. fibroblasts. There are no lymphatics in most alveolar walls. which lies along a lobular septum. the bronchovascular bundle. The veins then continue in the lobular septa.On the opposite side (the thick side). NOTE: The proximal airways are lined by pseudostratified ciliated columnar epithelium and the distal airwa ys by non-ciliated cuboidal epithelium. some of which contain muscle filaments (myofibroblasts). which resemble the smalles t arteries. join with other veins and drain into the lobular septa. Specialized cells found in the lining of the airways include Kulchitsky cells. so that the arterial wall is partly muscular and partly non-muscular where the elastic laminae fuse. which constitute s the interstitial space of the alveolar wall. In addition. This is composed of the connective tissue that surrounds the veins and bronchovascular bundle and the tissue on the thick side of the alveolar capillary membrane. and the pleura. In vessels about 100 micrometer in diameter or less. The proportion of goblet cells is lower in the distal airways than in the proximal airways. diastase -resistant granules in the apical . and the pleural lymphatics drain toward the hilus via bronchovascular lymphatics. The pulmonary arteries accompany the airways in a sheath of connective tissue known as the bronchovascular bundle. The smallest veins. is where significant fluid and molecular exchange occurs and where edema begins. This region. elastin. The smallest arteries have no muscle. They are succeeded by arteries whose walls have two elastic laminae with a layer of muscle between them. The lymphatics commence in alveoli at the periphery of the acinus. The lymphatics of the lobular septa and bronchovascular bundle accompany these structures. and there is a corresponding increase in the number of Clara cells after bronchial injury. Clara cells and goblet cell. The more proximal arteries are elastic and then become transitional (four or fewer elastic laminae in their walls). joining other veins to form a network that is separate fro m the bronchovascular bundles. muscle extends in a spiral fashion between the elastic laminae. and collagen. they are recognized by PAS -positive.
Age and sex of the patient. Kulchitsky cells form part of the diffuse neuroendocrine system and so contai n cytoplasmic dense core granules. Indications and techniques: The lung biopsy is widely recognized as a valuable tool for the diagnosis and management of diverse pulmonary disorders. bronchiolitis. ii) Fibrosing lung diseases and iii) Rejection changes in heart / lung transplants. intimal thickening in pulmonary vessels and oncocytic metaplasia of submucous glands. Inflammatory changes such as active bronchitis. Other reasons for lung biopsy include: i) Assessment of inflammatory lesions such as sarcoidosis . Age-related changes in the lung include calcification and ossification of cartilage in the large airways. Pleural biopsy is usually taken: -To help in the differential diagnosis of pleural effusions and pleural tumours. and video assisted thoracoscopic surgery biopsy are the principal tools that have been developed for obtaining lung tissue for histopathological examination. iv) Rarely biopsies are taken in the investigation of asthma and its response to treatment. open lung biopsy. The trauma of biopsy or open surgery commonly causes fresh intra -alveolar hemorrhage. treatment and palliation of neoplasms. tuberculosis and fungal infections. and areas of granulation tissue can be seen in biopsy or excision specimens as a result of previous instrumentation.part of their cytoplasm. . The transbronchial lung biopsy. . INDICATIONS: Specimens from lungs are taken: -For the diagnosis. and so this feature should not be interpreted as a pathological process. Along with the lung or pleural bi opsy specimen following clinical information should be provided by the clinician to the histopathologist : Lung Biopsy Specimen: .Clinical signs and symptoms and their duration.
diabetes insipidus. Endoscopic . transbronchial.2%. 31 transbronchial biopsies.History of tuberculosis . . . small cell carcinoma in 9.History of smoking. Tissue samples.Results of other investigations :(radiological and microbiological ).51(9-10):431-5. 22 percutaneous needle pleural biopsie s and 91 combined forceps and transbronchial biopsies) in whom biopsies were performed during 1996 in the Specialized Hospital for Lung Diseases Brezovik. has significantly increased the efficacy of diagnostics of bronchopulmonary and pleural diseases.Age and sex of the patient. not bigger than 3 -4 mm.hilar lymphadenopathy. systemic malignancy or other diseases (Cushing¶s syndrome. radiological and bronchoscopic examinations. Pleural biopsy specimen: . INTRODUCTION: During the last 20 years routine application of various methods of multiple "small biopsies" of the lungs such as forceps.Occupation . Med Pregl. In 99 cases (73.History of tuberculosis or systemic malignancy.6% of patients. 1998 Sep-Oct.3%) out of 135 clinically "obvious" neoplasms. trucut percutaneous and so on. the histopathological examination confirmed existence of malignant tumor: squamous cell carcinoma in 80%. . ..History of hilar lymphadenopathy .Results of other investigation:( radiological and microbiological). MATERIAL AND METHODS: By correlation of clinic al and histological diagnoses we analyzed the diagnostic efficiency of microscopic examinations of "small biopsies" of the respiratory tract in 319 patients (175 bronchial forceps biopsies. RESULTS: Overall concordance between the clinical and histopathological diagnosis was 82.Clinical signs and symptoms and their duration.Occupation (especially history of asbestos exposure).History of previous instrumentation in the lung .History of smoking. significance and possibilities of improving clinical -pathological cooperation in this field of clinical pathology.6% and adenocarcinoma in 5. can be the basis for making a definite therapeutical decision only if a skillful surgeon has performed the biopsy by correct instruments and from the right place and sent it for histol ogical analysis with other important clinical information. In other patients it was n ot possible to perform a more precise classification.Med Pregl. . . This study is a comment on quality. Correlation between the clinical and pathohistol ogic diagnosis in "small biopsies" of the lung. hypertrophic osteoarthropathy. 1998 Sep-Oct. .51(9-10):4315. . rheumatoid arthritis & other connective tissue disease).Clinical examination . in which diagnostic pathological changes are expected on the b asis of previous clinical.
96(6):654-7 Transbronchial lung biopsy through the flexible bronchoscope is used widely for the diagnosis of diffuse lung disease. lymphoma. comparing FB with other diagnost ic techniques. is a minimally invasive technique used to diagnose mediastinal and pulmonary masses and to stage lung cancer patients with mediastinal lymphadenopathy. these patients were subjected to open lung biopsies. Since it is safe. flexible bronchoscopy (FB) with forceps biopsy and transbronchial needle aspiration (TBNA).Am J Clin Pathol. When nonspecific findings by transbronchial lung biopsy do not correlate with the clinical picture.1%) were not representative.11(4):701-21. fluoroscopy. Additionally. vii-viii In the past 2 decades. The diagnoses included bronchiolitis obliterans. 2000 May. but the increase of diagnostic efficiency requires application of more sophisticated histological diagnostic methods (immunohistochemical) and more frequent utilization of bioptic procedures which are more convenient for detection of peripheral pulmonary lesions (transbronchial and percutaneous fine needle aspiration biopsies of the lungs). but may merely indicate that t he true diagnosis has been missed. CT. however.113(5 Suppl 1):S97-108 Bronchoscopic needle aspiration biopsy. tuberculosis. Subsequently. metastatic carcinoma. open lung biopsy should be performed. alveolar proteinosis.Chest Surg Clin N Am. it is not a replacement for open lung biopsy. interstitial fibrosis or nonspecific pneumonitis. the authors propose a rating scale based on the degree of invasiveness and diagnostic yield. accurate. We retrospectively studied 38 patients with diffuse lung disease whose transbronchial lung biopsies yielded nonspecific abnormalities. . a significant number of specimens obtained by the bronchoscopic 2 -mm biopsy forceps will reveal nonspecific findings. transtracheal needle aspiration. computed tomography (CT) -guided. Although transbronchial lung biops y is useful in the diagnosis of many diffuse lung diseases. which encompasses transbronchial needle aspiration. and ways that it may be optimized. Such a report may be an accurate reflection of the presence of idiopathic pulmonary fibrosis or nonspecific pneumonitis. 2001 Nov. In this article the authors present an algorithm for the diagnosis and staging of lung cancer that addresses sampling of suspiciou s lesions and lymph nodes by means of FB. 1987 Nov Dec. transthoracic fine -needle aspiration (FNA). emphasizing tissue -based diagnosis and staging by means of image -guided technology with the highest diagnostic yield. its use may increase in the comin g years. is rather high. with particular attention to the increasing role of TBNA in this field. They discuss the approach to the diagnosis and stagin g of lung cancer by techniques guided by FB.specimens of 29 patients (9. Nineteen of the 38 patients (50%) had a specific diagnosis made by open lung biopsy. ultrasonography. its limitations. CONCLUSION: The level of diagnostic efficiency (73. Bronchoscopic needle aspiration biopsy. and endobronchial needle a spiration. It is important that pathologists who examine cytology specimens understand this procedure. and bronchioloalveolar cell carcinoma. Bronchoscopy in diffuse lung disease: evaluation by open lung biopsy in nondiagnostic transbronchial lu ng biopsy. and endoscopic ultrasonography (EUS) have revolutionized lung c ancer diagnosis and staging by facilitating precise biopsy of lung lesions and virtually all mediastinal lymph -node stations.Ann Otol Rhinol Laryngol. which have been clinically diagnosed as malignancies. Bronchoscopic diagnosis and staging of lung cancer. and EUS.3%) of definitive histopathological verification of bronchopulmonary lesions. and potentially cost -efficient. eg.
Vasculature. Pneumoconiosis .Diagnosis in Asbestos-related diseases. Interstitial fibrosis. . Pneumocystis infection. Argyrophil stains such as Grimelius for neuroendocrine granules of carcinoid tumours.5 (Acid mucin): Mesothelioma (Mesothelioma-Online) Combined Alcian blue/diastase PAS. Organizing pneumonia. . Tuberculosis Elastic/van Gieson stain for: (collagen) . Ziel-Neelsen stain: For mycobacterial organisms. (elastin) .(basement membrane / neutral mucin): Adenoid cystic Ca. Eg.HISTOCHEMICAL STAIN: Periodic acid schiff (PAS): PAS. IMMUNOHISTOCHEMICAL / FLUORESCENCE: Pneumocystis antibodies : Pneumocystis carinii Cytomegalovirus antibody : Cytomegalovirus infection OTHER ANALYSIS: Polarising microscopy for birefringent material: Talc . HISTOCHEMICAL STAIN: Periodic acid Schiff (PAS): Clear cell tumours PAS with diastase pretreatment (Neutral mucin): Adenocarcinoma (Alcian blue pH 2. Mineral analysis: (light or electron microscope) .Fibrosis . Pulmonary Hypertension . chronic lung rejection Congo red : for amyloid (primary / secondary). Perls¶ prussian stain: for ferric iron. ferruginous bodies.Glycogen : Fungi PAS with diastase pretreatment (Neutral mucin): Pulmonary Alveolar Proteinosis Grocott : For Fungi . Eg. Pulmonary Hemorrhage von Kossa stain phosphate. Mica . Vasculitis.
Cytokeratin 5 / 6 .2 and other cytokeratins give paranuclear dot positivity in small cell carcinoma and can be used as part of a panel. More specific markers. N -CAM. synaptophysin. S100. (Thyroid and pulmonary origin) Mesothelioma Adenocarcinoma An approach to histopathological reporting of the pulmonary parenchymal biopsies: I) In the bronchioles: . Granulomatous . as in bronchiolitis obliterans: . desmin.IMMUNOHISTOCHEMICAL STAIN: Immunohistochemical stains for NSE and PGP 9. Synaptophysin . Immunostains can be usefully applied in typing of neoplasms .Obliterative changes in bronchioles with fibrous scarring. are not easily identified in poorly differentiated tumours and small cell carcinoma. Thrombomodulin . chromogranin.Peribronchial or peribronchiolar inflammation: Non-specific: Reactive lymphoid follicles as in follicular bronchiectasis or follicular bronchiolitis .CAM 5. leucocyte common antigen. surfactant.5 have limited value in distinguishing small cell carcinoma from other types of carcinoma in small biopsies as they are often non-specific and unreliable. CD56 : Neuroendocrine Tumours. light chains.2. Lymphocyte markers . CAM 5. such as chromogranin and N-CAM. SUMMARY OF IMMUNOSTAINS USEFUL IN THE DIAGNOSIS OF PULMONARY TUMOURS: Histochemistry and Immunohistochemistry in the diagnosis of Mesothelioma: click here Carcinoembryonic antigen Leu-M1 Ber-EP4 Surfactant apoprotein A Thyroid transcription Factor 1 Calretinin . Chromogranin A . .B and T cell markers.
.Hemosiderin deposition in areas of hemorrhage.Lymphatic infiltration by tumour cells as in extra -pulmonary primary adenocarcinoma (lymphangitis carcinomatosa).Amyloid. . . epithelioid hemangioendothelioma . .Asbestos bodies. as in malignant lymphoma.Calcification.Heavy lymphocytic infiltrate. -Destruction of alveolar walls with interstitial and intra -alveolar fibrosis.Hyaline membranes in diffuse acute alveolar damage. .Palisaded granulomas in Wegener¶s granulomatosis and rheumatoid nodules .Smooth muscle cells in lymphangioleiomyomatosis .Organizing granulation tissue in bronchiolar lumina. . .Calcified bodies (Schaumann bodies) in areas of hyaline fibrosis in sarcoidosis. extrinsic allergic alveolitis. lymphoma. -Alveolar walls: . . dystrophic in areas of long standing fibrosis.Architecture: -Destruction of alveolar walls without fibrosis in emphysema .Focal acute inflammation with central necrosis and scattered giant cells in fungal pneumonias. . . as in lymphoid interstitial pneumonia (LIP).Non-necrotizing well formed granulomas in sarcoidosis .Non-necrotizing poorly formed granulomas in extrinsic allergic alveolitis. . . . .Necrotizing granulomas in mycobacterial and fungal infection . monomorphic and atypical lymphoid infiltrate.metastatic in the elastic of alveolar walls. alveolar collapse. . Kaposi's sarcoma . as in cryptogenic organizing pneumonia (also known as bronchiolitis obliterans organizing pneumonia or BOOP). .Alveolar lining cells: .Interstitial inflammatory infiltration .Interstitial fibrosis. and bronchiolization in advanced interstitial lung disease. II) In the alveoli and interstitium: ..
-viral inclusions. -giant cell pneumonia ( measles infection in childr en.Hemorrhage or accumulation of haemosiderin . idiopathic pulmonary hemosiderosis. -atypical cells: seen with some cytotoxic drugs such as busulfan or bleomycin.. in obstructive pneumonitis or pulmonary alveolar proteinosis . . III) In the blood vessels: . -squamous metaplasia as a result of chronic inflammation . . oft en with cholesterol crystals. -bronchiolisation of distal air spaces in advanced diffuse pulmonary fibrosis. . such as cytomegalovirus or measles. occasionally respiratory syncytial virus infection or parainfluenza B). often associated with cholesterol crystal clefts. . which may be mucus secreting or non-mucus secreting.foamy in obstructive pneumonitis or lipid pneumonia .laden macrophages in hemorrhagic diathesis. . pulmonary venous hypertension. -multinucleate foreign body giant cells.Organizing exudates (Masson bodies -Masson's Tumour) in organizing pneumonia. -Granular eosinophilic debris.Intra-alveolar irregular laminated calcospherites in pulmonary microlithiasia. .Alveolar lumina: -Inflammatory cells: -polymorphs in bacterial pneumonias . µblue bodies¶ associated with lysosomal accumulation in such conditions as DIP . pulmonary capillaritis. -histiocytes/macrophages . -tumour cells lining alveoli in bronchioloalveolar ca rcinoma. containing fine lipofuscin pigment in desquamated interstitial pneumonia. . -eosinophils in eosinophilic pneumonia . first identified in asbestosis but also seen in other conditions.Proliferation of type II pneumocytes in the r eparative phase of hyaline membrane disease.Granular and foamy lightly eosinophilic material in pneumocystis pneumonia .cytoplasmic hyaline in type II pneumocytes.Multinucleate giant cells: -giant cell interstitial pneumonia (hard metal disease). in pulmonary alveolar proteinosis.
. pulmonary venous hypertension and plexogenic pulmonary arteriopathy. dilatation lesions.Replacement of the vein wall by a network of capillaries with abnormal capillaries in alveolar walls in pulmonary capillary hemangiomatosis. .Obliteration by connective tissue in pulmonary veno -occlusive disease. .Thickening of the media with arteriolization in pulmonary venous hypertension. Histopathological reporting of pulmonary biopsy in cases of idiopathic lung fibrosis ..Intimal thickening-eccentric in thromboembolic pulmonary hypertension. . .Pulmonary hypertension and thromboembolic disease: .Infiltration of vessel walls by atypical lymphoid cells in angiocentric lymphoma (lymphomatoid granulomatos is).Vasculitis: -Eosinophil infiltration with granuloma formation in Churg -Strauss syndrome. necrotizing sarcoidal granulomatosis.These biopsies are not useful for the diagnosis or staging of the various histopathological subsets of Idiopathic Pulmonary Fibrosis .Trans-bronchial lung biopsy (TBLB) is the initial procedure of choice in those patients likely to have diffuse parenchymal lung disease in which small samples may be diagnostic.These biopsies should be at least 4 cm in maximum diameter when inflated and include a depth of at least 1. associated with organizing thrombus or other embolic material.Muscularization of arterioles in hypoxic pulmonary hypertension . . plexiform lesions and fibri noid necrosis in plexogenic pulmonary arteriopathy. .Veins: .5 cm.medial hypertrophy in hypoxic pulmonary hypertension.Muscular arteries . .By open/video assisted thoracoscopic (VATS) l ung biopsies it is possible to adequately examine the secondary lobules and the distribution of the disease process. . microscopic polyarteritis and hypersensitivity vasculitis. and reaction to talc particles in drug addicts. -Granulomas in vessel walls in sarcoidosis . -Extravascular granulomas and areas of necrosis in Wegener¶s granulomatosis. . .Capillaritis with alveolar hemorrhage in Wegener¶s granuloma tosis. concentric in plexogenic pulmonary arteriopathy . subintimal longitudinal muscle fibres in hypoxic p ulmonary hypertension. .
Specimens taken for examination of diffuse . 4. Transbronchial biopsy interpretation in the patient with diffuse parenchymal lung disease. Arch Pathol Lab Med. giant cells.g. or predominantly sub -pleural (Eg. CONTEXT: The most common lung tissue samples seen by pathologists worldwide a re obtained with the flexible bronchoscope.The distribution.g. 9. metaplastic or neoplastic changes? Any viral inclusions?) 6. Epithelial lining (any hyperplastic. UIP )? 3. in collagen vascular disease and asbestosis?). contain deep alveolar tissue and are from a site involved by active disease. Alveolar lumina (any abnormality. Is there any smooth muscle proliferation? Are the smooth muscle fibers mature? 12.a brief practical guide: 1. Blood vessels (any evidence of veno-occlusive disease which may produce parenchymal changes similar to IPF? Any vasculitis? Or thrombi?). . hemorrhage. 7. such as organizing exudates. NSIP ). intensity. Low power magnification: . Pleura (is there any fibr osis/chronic inflammation e. Any other abnormality (e. 2. 8. accumulation of macrophages. Usual Interstitial Pneumonia (UIP)? . Bronchi or bronchioles (any abnormality such as bronchiolitis obliterans?).Is the disease process temporally uniform Eg. Are there any granulomata.131(3):407-23.g. Histological interpretation of lung biopsies and what to look for . Non-specific interstitial pneumonia (NSIP) or temporally and spatially heterogeneous Eg. or scattered individual giant cells? Any foreign material? 11. Detailed clinical history and radiological findings should always be obtained and taken into consideration in the interpretation of lung biopsies. amyloid).Are the changes predominantly centri -lobular Eg. lymphatics (any abnormality?)..Biopsy samples from the middle lobe or lingula may be taken provided they are of adequate size. hyaline membrane?) 5. and nature of fibrosis and inflammation. 2007 Mar. hemosiderin)? Asbestosis 10. Interlobular septa (any abnormality?). Any ferruginous bodies (particularly asbestos)/ Any pigment (e. Respiratory bronchiolitis interstitial lung disease (RBILD) . diffuse throughout the secondary lobule (Eg.
Specifically. Clinical and radiologic context is provided for the more specific diagnostic entities. Conclusion: Our data suggested that the presence of acute exacerbation at the time of biopsy and lower DL(CO) were predictors of higher mortality after the surgical lung biopsy. 95% CI: 1. (3) The patients with low DL(CO) (<50% predicted) had higher mortality and complication rate than high DL(CO) group. However. OBJECTIVE: To present and discuss the most common histopathologic patterns and diagnostic entities seen in transbronchial biopsy specimens in the setting of diffuse or multifocal lung disease. slice thickness 10 mm. were enrolled.3%. Mortality and risk factors for surgical lung biopsy in patients with idiopathic interstitial pneumonia. intravenous drug abuse -related microangiopathy. DATA SOURCES: The published literature and experience from a consultation practice. A low -dose protocol with acquisition of single slices was used on a 16 -row CT scanner: 80 kVp.334. Results: (1) The mortality rate 30 days aft er the surgical lung biopsy was 4.or multifocal parenchymal lung abnormalities pose special challenges for the general surgical pathologist. radiologic distribution of abnormalities. Biopsy specimens were processed by standard histopathological and immunohistochemical techniques and effective doses were individually calculated. Pneumologie.6%) compared to non -AE (3.31(6):1115 -9. Epub 2007 Apr 5. from April 1990 to August 2003. p=0. 2007 Jun.05). METHODS: Twelve childre n (7-males. Low-Dose CT-Guided Transthoracic Lung Biopsy for Evaluation of Non -Infectious Chronic Interstitial Lung Disease in Children. Background: The overall safety of sur gical lung biopsy in patients with idiopathic interstitial pneumonia (IIP) remains controversial. and these challenges are often compounded by high clinical expectations for accurate and specific diagnosis. lower DL(CO). AE was followed by biopsy it self in three cases. sarcoidosis. and histopathologic patterns is essential. Korea.011) was an independent risk factor. the surgical pathologist can substantially influence the diagnostic workup and help guide the clinician to an ac curate clinical/radiologic/pathologic diagnosis. and presence of AE were significant risk factors for 30 -day mortality (p<0.365. acute lung injury. Wegener granulomatosis. Biopsy performed at the time of acute exacerbation (AE) resulted in higher 30 -day mortality (28. age range: 7 months -15 years) with non-infectious IP of unknown origin and inconclusive clinical tests underwent CT guided TLB with a 20-gauge biopsy instrument. This study was performed to investigate the mortality and complication rate and identify the risk factors for surgical lung biopsy in patients with IIP. With this information. 2007 May 25. eosinophilic pneumonia. diffuse alveolar hemorrhage. alveolar proteinosis. organizing pneumonia. BACKGROUND: Children with interstitial pneumonitis (IP) of unknown origin often have to undergo open lung biopsy to establish a final diagnosis. Knowledge of the clinical context. Langerhans cell histiocytos is. Metho ds: A total of 200 patients with IIP who underwent surgical lung biopsy at the Asan Medical Center. which was significantly higher than the control group. OBJECTIVE: The aim of this study was to retrospectively evaluate the efficacy and radiation exposure of low -dose CT-guided TLB in children with non -infectious IP of unknown origin. Open lung biopsy is an invasive procedure with major potential complications. and lymphangioleiomyomatosis are presented.0%.727 -74.05). Complications and mortality were analyzed retrospectively. chronic cellular infiltrates. CONCLUSIONS: The transbronchial biops y specimen can provide valuable information for clinical management in the setting of diffuse or multifocal lung disease. CT -guided transthoracic lung biopsy (TLB) has become a common diagnostic procedure in adults.Eur J Cardiothorac Surg. p<0. . multivariate analysis revealed that only AE (OR: 11. Computed tomographic scans are useful for selecting appropriate patients to undergo biopsy and in limiting the differential diagnosis. 20 mAs. In the meantime. (2) Univariate analysis indicated that lower FVC.
Lung fibrosis is the most important complication of both the "limited" and "diffuse cutaneous form" of systemic sclerosis.1 mSv).78 mSv (0. The risk of postoperative complications appears to be greatest in those dependent on oxygen and those who have pulmonary hyperte nsion. prolonged air leaks.1. The histological pattern is that of "Usual Interstitial Pneumonia" (UIP) or "Non -specific Interstitial Pneumonia" (NSIP). sarcoidosis and a group of inherited or other rare miscellaneous disorders. however. based on the combination of clinical observations. these include connective tissue disorders. Diffuse parenchymal lung disorders (DPLD) can develop in a variety of systemic disorders. neoplastic disorders. The cause of sarcoidosis remains unknown. Incidence of postoperative mortality. pneumonias.65(6):350-65. RESULTS: Three deaths occurred within 60 days after biopsy for a mortality rate of 4. Biopsy rarely may trigger an acute exacerbation of usual interstitial pneumonitis. 2003. Pulmonary involvement occurs in more than 90% of all patients with sarcodosis. Forms characterised by an acute clinical onset or a low grade lung inv olvement have the highest spontaneous remission rate. The pathogenesis of the disorder is thought to consist of an abnormal. which demonstrated idiopathic pulmonary fibrosis. To shed light on the risk -benefit ratio for this recommendation. Diffuse interstitial lung disorders in systemic diseases. we examined the morbidity and mortality associated with video-assisted thoracoscopic surgical (VATS) lung biopsy in a group of outpatients. CONCLUSION: Low-dose CTguided TLB can be a helpful method for investigating children with non -infectious IP of unknown origin thus making open lung biopsy unnecessary. This information may be used in weighing the risk -benefit ratio of biopsy in individual patients. Application of a low -dose protocol leads to a significant reduction of radiation exposure in CT -guided TLB. 1% to 12%). Risk factors for complications of surgery were examined. Risk factors for morbidity included preoperative dependence on oxygen therapy and pulmonary hypertension.5%. 11% to 31%) experienced one or more complications of surgery.4% (95% confidence interval [CI]. and 19.83(3):1140-4. 2007 Mar. Grading into 4 stages is based on the chest radiograph. The diagnosis therefore is descriptive. systemic sclerosis and Churg Strauss vasculitis. the effective dose of CT-guided TLB was 0.Ann Thorac Surg. vasculitis. Complications of video-assisted thoracoscopic lung biopsy in patients with interstitial lung disease.RESULTS: All biopsies were performed without major complications. excessive regenerative response to . Schematically grouped. and the histological documentation of non -caseating epit heloid granulomas in tissue biopsies.Verh K Acad Geneeskd Belg. the clinical suspicion could be disproved. even in ambulatory pa tients. chest X ray. This overview focuses on sarcoidosis . On average. and re -admissions were calculated. In 2 patients (17 %) the results of TLB were inconclusive. is not an entirely benign procedure. CONCLUSIONS: VATS lung biopsy for diagnosis of ILD. Aggregation of articles published over the past 10 years reporting on surgical lung biopsy for the diagnosis of ILD yielded a postoperative mortality rate of 2% to 4.1% (95% CI. A final diagnosis could be established in 9/12 patients (75 %) by CT guided TLB. The three patients who died had usual interstitial pneumonia on their biopsy specimen and were reintubated postoperatively for acute lung injury. involving 90% of all patients. Two children (17 %) developed a small pneumothorax/pulmonary haemorrhage that resolved spontaneously. Treatment with steroids is only indicated if organ involvement leads to functional impairment.4 . METHODS: A retrospective cohort study was conduc ted of 68 consecutive ambulatory patients with radiographically apparent interstitial lung disease (ILD) referred for VATS biopsy during a 6 -year period. BACKGROUND: Current guidelines recommend surgical lung biopsy for diagnosis of interstitial lung diseases (ILDs) in selected patient s. Open lung biopsy was performed in 1 patient (8 %).
this has not been substantiated. . punch biopsies or material obtained by thoracoscopy. Concern has risen that CysLT1 receptor antagonists might induce production of pANCA. Specimens: These are either needle biopsies (e. To date. Histopathological reporting of pleural biopsy Closed pleural biopsy for neoplasm or inflammatory lesions: Indication: Closed pleural biopsy is done to determine causes of pleural effusion after fluid analysis has been nondiagnostic. nerves and lung parenchyma. Closed pleural biopsy has fairly low sensitivity for diagnosis of cancer but it can be increased by adding cytologic evaluation. .In areas of pleural fibrosis and adhesions blood vessels can appear thick walled and sclerosed.g. Distinction can be difficult in the following conditions: 1) A florid reactive mesothelial proliferation and a mesothelial neoplasm 2) A tubuloglandular mesothelioma and metastatic adenocarcinoma. It is necessary to do further investigations and follow-up in patients that have inflammation in pleural bi opsy.Indicators towards mesothelioma as opposed to a reactive proliferation are a single population of frankly malignant cells arranged in papillary. skeletal muscle. Churg Strauss vasculitis is characterised by asthma. Trucut). adipose tissue. Tissues present include : Pleura.Invasion of underlying tissue with transition to spindle cell forms ( a biphasic pattern) is also a useful feature. An approach to histopathological reporting of pleural biopsy: Comments should be made on the following features: .Pleural thickening: -Hyaline fibrous tissue with a basket weave pattern in pleural plaques: . . or may take on a pseudoangiomatous appearance. It is an efficient method in diagnosis of Tuberculosis and malignant pleural effusions. tubulopapillary or microcystic pattern. . The affected vessels wall shows signs of fibrinoid necrosis and are infiltrated by eosinophils. blood eosinophilia and vasculitis of the small vessels. distinct from mesothelial cells. pANCA (anti myeloperoxidase) is considered to play a role in the pathogenesis of the disease.Involvement of the pleura by metastatic adeno carcinoma is suggested by a separate population of malignant cells.an auto-immune mediated lung injury.
Value of closed pleural biopsy in diagnosis of pleural effusion. with fibrinoid necrosis in rheumatoid disease : .Reactive proliferation of mesothelial cells .Eosinophils often seen in pneumothorax (eosinophilic pleuritis). pneumothoraces are often spontaneous but malignancy becomes more likely with increasing age. .Metastatic carcinoma. Open pleural biopsy .Palisaded histiocytes.-Cellular fibrous tissue in an inflammatory process or neoplasia: .The type and severity of inflammatory infiltrate. -The presence of specific features such as granulomas -The presence of neoplasia. . Specimens taken for treatment of recurrent pneumothorax: Pneumonectomy or pleural stripping may be performed for recurrent pneumothoraces.Necrotizing granulomas in tuberculous pleurisy : . .Asbestos bodies are present.Features of inflammatory lesions: . fibrous (sarcomatoid) or desmoplastic : .There is fibrosis .non-specific. the report should comment on the following features: .Mesothelioma : epithelial. benign or malignant : . 2005. In young patients. .It is involved by spread of tumor . The microscopical report should comment on: .Localized fibrous tumor of pleura. . When underlying lung is included.Presence of neoplasm: . which can be multinucleate. mixed (biphasic).pleural strip: Open pleural biopsy is often necessary for the diagnosis of mesothelioma as a confident diagnosis can usually be made only when adequate tissue is available.Przegl Lek.62(12):1325-7.
Kyobu Geka. and only 1 (9%) lived longer than 2 years after diagnosis. In all 62 patients CPB enabled to diagnose 13 cases with neoplasmatic effusions (majority being adenocarcinomas) and 16 cases of tuberculosis in histological and/or microbiological examination.6%) . In 4 cases. 9 patients died and 2 survived. 0 to 51) months. proceeded by ultrasound examination. 2007 Jan. malignancy and tuberculosis were undiagnosed. 7 (64%) died within 6 months after the first presentation. Median period between symptom onset and presentation was 1 (range. 0 to 22) month. biphasic) are difficult. extrapleural pneumonectomy in 3. In 6 cases (28. The diagnosis of malignant pleural mesothelioma (MPM) is challenging although MPM is highly aggressive tumor. Symptoms included dyspnea in 4 patients. The incidence of the disease is increasing and is estimated to reach its peak in 2025. International Mesothelioma Interest Group (IMIG) staging included stage II in 6 patients. The current diagnostic gold standard i s principally based on light microscopic examination of hematoxylin -eosin and immunohistochemical stains of large tissue sections. and by video -assisted thoracoscopic surgery (VATS) [5 ] . and stage IV in 2. Closed pleural biopsy proves to be an efficient method in diagnosis of Tuberculosis and malignant pleural effusions. Diffuse malignant pleural mesothelioma. In 7 patients we confirmed neoplastic pleural infiltrates in cytological examination of pleural effusion. stage III i n 3. sarc omatoid. p leural fluid cytology in 2. pleural drainage in 2. A definitive diagnosis was made by closed pleural biopsy in 8 patients. Th ere were 33 cases with non -specific inflammatory changes. 0 to 6) month. by open biopsy via thoracotomy (2). Histological subtypes included epithelioid in 6 patients. 55 to 90) years.The aim of the study was to assess closed pleural biopsy (CPB) as a diagnostic method of pleural effusion. Median period between presentation and diagnosis was 1 (range. During the follow-up period. by biopsy under thoracoscopy with local anesthesia (9). A history of asbestos exposure was identified in 3 patients and suspected in 5. chest pain in 3. However. initial diagnosis of MPM were not confirmed because of missing malignant tissue (1 case) . It helped to obtain specimen for histological and microbiolo gical examination even with cases of small amount of fluid. dyspnea plus chest pain i n 2. in 23% of cases with post -inflammatory changes. and best supportive care in 2. The diagnosis of MPM was confirmed by histopathological examination of pleura l tissue samples obtained by closed biopsy under computed tomography (CT) or ultrasonography -guided (5 cases). We studied correlation between initial and final histological diagnosis retrospectively from the records of 21 cases with MPM from 1989 to 2005. However. In 26 patients videothoracoscopy (VTS) was carried out and 20 of those had post -inflammatory changes.60(1):35-9 Malignant pleural mesothelioma is an uncommon neoplasm that caused 647 deaths in Japan in 2004. Pleural biopsy under those diagnostic methods led to initial diagnosis of MPM in 15 of 21 cases (71. Current problems in the diagnosis of malignant pleural mesothelioma. and unknown in 2. This in turn implicates the necessity for further diagnostic procedures including VTS. Of the 11 patients. Treatment included intrapleural chemotherapy in 4 patients. biphasic in 1. We reviewed the clinical features in 11 consecutive patients with pathologically confirmed diffuse malignant pleural mesothelioma in our institution from January 1997 to December 2002. pathological diagnosis of MPM and classification of histological findings into 1 of the 3 subtypes (epithelial.60(1):14-8. Of the 11 patients. CPB using Cope needle was performed in 62 patients. 2007 . and cough in 2. Kyobu Geka. and autopsy in 1. 9 were male and 2 were female with a mean age of 66 (range. however we confirmed neoplasmatic effusions and in next 2 cases --tuberculosis. Median survival time after diagnosis was 3 (range. sarcomatoid in 2.4%) .
and should be carried out prior to invasive proced ures such as thoracoscopy or open pleural biopsy. 2002 Nov. Twelve cases were excluded due t o transudative effusion (N=6) and obtaining no pleural tissue (N=6). CONCLUSION: Pleural biopsy by thoracoscopy under local anaesthesia should be actively carried out in patients with pleurisy. METHODS: We retrospectively reviewed the diagnostic utility of all closed pleural biopsies performed from January 1988 to December 1997 at the King Fahad National Guard Hospital. RESULTS: One hundred and twenty -two pleural biopsies were performed in 116 patients using cope needle in 39. OBJECTIVE: Closed pleural biopsy is known to be diagnostic in approximately 75% of pleural effusion undiagnosed by thoracocentesis or pleural fluid evaluation. Specific diagnoses were obtained in 54 cases giving a diagnostic yield of 49.6% (25/27). because the technique has a high diagnostic rate and can be easily and safely carried out. Closed pleural needle biopsy: predicting diagnostic yield by examining pleural fluid parameters. SETTING: The Institute of Pulmonology. obtaining large tissue samples in the initial examination by les s invasive thoracoscopy is recommended. initial diagnosis of MPM were not confirmed. However. Lung cancer with pleural dissemination was diagnosed in 27. Diagnostic value of thoracoscopic pleural biopsy for pleurisy under local anaesthesia. The operations took 11 -145 min. Abram's needle in 82. tuberculous pleurisy in 32. Kingdom of Saudi Arabia.1% (134/138). Hadassah University Hospital.8% (30/32). This shows that closed pleural biopsy is still of value as a diagnostic procedure. The diagnostic efficacy in the cases of carcinoma was 92. Diagnostic yield of closed pleura l biopsy in exudative pleural effusion.Saudi Med J. CONCLUSION: By closed pleural biopsy 49. with a mean of 46 min.76(8):722-4 BACKGROUND: We find pleural effusion in clinical practice frequently. PATIENTS AND METHODS: Forty -four patients who underwent closed pleural needle biopsies were included in this study. with a mean of 59 years.1%. 2006 Aug. other tumour in 2 and pyothorax in 9 patients. DESIGN: A retrospective analysis.1% of undiagnosed exudative pleural effusions could be diagnosed. The overall diagnostic efficacy was 97. In 2 cases examined by closed biopsy and in 3 examined by thoracoscopy under local anesthesia. METHOD: A retrospective study of 138 patients who had been diagnosed by thoracoscopy in our hospital was carried out between January 1995 and January 2005. The purpose of this st udy was to determine the efficacy of closed pleural biopsy in a Saudi tertiary care teaching hospital.96(11):890-4 OBJECTIVE: Pleural fluid parameters that predict a diagnostic closed pleura l needle biopsy were investigated. We directly examine the thoracic cavity by thoracoscopy under local anaesthesia. Thoracoscopy directly without thoracocente ses was carried out in 28 of 138 patients. A non specific diagnosis was obtained in 5 6 (50.Respir Med.24(3):282-6. Of these 10 revealed neoplasia. To get the accurate diagnosis of MPM. 2003 Mar. RESULTS: The patients were 114 men and 24 women.9%) cases.and relatively small and sarcomatous element (5). ANZ J Surg. malignant pleural mesothelioma in 10. . ranging in age from 21 to 85 years. and 9 empyema. The right side was involved in 83 patients and the left side in 55. 35 tuberculosis. it is difficult to make a diagnosis definitively by thoracocentesis or closed pleural biopsy. carry out pleural biopsy and make a definitive pathological diagnosis in pleurisy. No major complications occurred during the examin ation. non -specific pleurisy in 58. and Trucut needle in one patient. in malignant pleural mesothelioma it was 100% (10/10) and in tuberculosis it was 93. Riyadh.
glucose. In 66 cases of nonspecific inflammation diagnosed by CPB. lactate dehydrogenase.1 years). Determining the optimal number of specimens to obtain with needle biopsy of the pleura.4 +/ . and pleural tuberculosis in 3 cases. Pleural adhesions can lower its diagnostic value. 1989. Diagnostic value of medical thoracoscopy in pleural disease: a 6-year retrospective study. cholesterol. triglycerides. and six cases of empyema.05). Prior to thoracoscopy. CONCLUSIONS: Medical thoracoscopy appears to be efficient and relatively safe in the management of pleural disease. In those case s in which the diagnosis was uncertain or effusion persisted.The study of the pleural fluid included: pH.6%). with a total of five biopsies for each patient: four for pathological examination (taken numerically in the order in which they were performed: D1. thoraco scopy specified the histologic type in 7 cases. Follow up revealed malignancy including mesothelioma and lymphoma. of which 149 were diagnostic and 19 were indicated for therapeutic assessment in malignant mesothelioma (MM). mean age +/ . glucose. Malignancy was identified in 10 patients (23%). P < 0. D2. D3 and D4) and one for microbiological testing. 775 +/. albumin and adenosine deaminase). lactate dehydrogenase (LDH). LDH may serve as a useful guide in deciding whether to perform closed pleural biopsy or to proceed to thoracoscopically guided biopsy. pH. from patients with diagnostic and non diagnostic pleural biopsies were compared. 1994. thoracoscopy. of whom 70% had adenocarcinoma.96(1):14-7 The aim of this study was to define the number of pleural biopsy samples necessary for optimum diagnostic performance and determine to wh at extent they are complementary. Thus. biochemical testing of pleura/serum (proteins. In 18 cases in which the CPB diagnosis was MM. LDH levels less than 510 U l( -1) were highly predictive of a negative biopsy (negative predictive value of 86. while the pleural effusion either resolved. In a 6 -year retrospective study of patients having undergone at least one medical thoracoscopy. cytology and microbiological testing (Gram -staining. to December 31. There was one thoracoscopy-related death. SETTING/PATIENTS: From January 1. LDH levels in pleural fluid from patients with diagnostic pleural biopsy were higher than in patients with non-diagnostic pleural biopsies (1436 +/ .121(5):1677-83. one case of sepsis . CONCLUSIONS: Low levels of LDH (< 510 U l( -1)) were highly predictive of a negative pleural needle biopsy. remained stable or an alternative benign process was identified in 19 patients (63%). 168 medical thoracoscopies were performed on 154 patients (123 men. RESULTS: Thirteen patients (29%) had diagnostic biopsies. haemogram.109 U l(-1). Three other patients had non -malignant specific diagnosis. The bi opsies were performed using a Cope needle. In 12 cases of carcinoma diagnosed by CPB. at least one CPB had been performed in 120 of 149 cases. and white blood cell count with differential cell counts. anaerobes and mycobacteriae cultures). RESULTS: Thoracoscopy challenged the CPB -based diagnosis in 43 of 96 cases. thoracoscopy revealed MM in 16 cases. 61 +/.333 U l(-1) vs. STUDY OBJECTIVES: Unlike thoracocentesis and closed pleural biopsy (CPB). mainly owing to pleural adhesions that limited access to the pleural cavity.Pleural fluid values of protein. 2002 Jan. in 10 of 30 (33%) patients with non -diagnostic biopsies. medical thoracoscopy permits biopsy with direct visualization.Respir Med.There were no significant differences in . 2002 May.SE.7 years.Chest. and one patient died of unrelated cause. adenocarcinoma in 10 ca ses. performed for precise staging. yielding a diagnosis in 96 cases. aerobes. undetermined carcinoma in 3 cases. a thoracoscopy or thoracotomy was performed. Eighty -four closed pleural biopsies were performed in our department between June 1996 and January 1998 on 55 males and 29 females with an average age of 64. challenged the diagnosis in 4 cases. Thoracoscopic diagnoses were found to be erroneous in 10 of 149 cases. we analyzed the diagnostic yield of thoracoscopy and its value in the management of pleural disease.16.
D3 and D4). )amyloid . In conclusion. no specific diagnosis could be made. the diagnostic yield did not increase with more biopsy samples. The increase in diagnostic yield with the number of biopsies was more remarkable in the carcino ma cases. One high quality sample should be enough to obtain a diagnosis. fungal.Singapore Med J. depending on the number of biopsies performed.39(5):196-9 BACKGROUND: Pleural biopsy is invaluable for the etiological diagnosis of pleur al diseases in the presence of an exudative pleural effusion. CONCLUSION: Closed pleural biopsy using a Tru -cut needle is effective for the specific diagnosis of exudative pleural effusion. Conventionally. The use of a perpendicular approach to biopsy the pleura does not seem to increase the complication in moderate to large pleural effusion. D2. lymphocytic and obliterative bronchiolitis (Transplant rejection. but not for the group with tuberculosis.Non-granulomatous: Bronchopneumonia . We report our experience in performing closed pleural biopsy using a Tru cut needle without ultrasound guidance in moderate to large exudative pleural effusion. METHODS: Closed Tru -cut biopsy was performed in 27 consecutive patients with exudative pleural effusion who volunteered to undergo the procedure. The best diagnostic performance for malignant pathology was obtained with four samples. The biopsy specimen was sent for histopathology. Anatomical distribution of pulmonary diseases Conducting airways: Bronchial / Bronchiolar Disorders: 1.This was true for total group and the group with carcinomas. connective tissue disease) 2. mucoid impaction. where it increased by 35% when four biopsies were performed (54% with one biopsy versus 89% with four biopsies. foreign body. bronchocentric granulomatosis (allergic. RESULTS: A specific diagnosis of tuberculosis was obtained on histopathology of pleural tissue in 12 out of 16 patients (diagnostic yield 75%) and in 5 out of 7 patients with malignancy (diagnostic yield 71%).Extracellular deposits: Bone/cartilage (tracheobronchopathia osteoplastica). pleural biopsy is either performed with the Cope's or the Abrams pleural biopsy needles. Pleural fluid analysis and other relevant in vestigations required to obtain a specific diagnosis were carried out. Among the other 4 patients. A few investigators have used the Tru -cut biopsy needle with or without ultrasound guidance. viral. We used a perpendicular approach to biopsy the pleura instead of the tangential approach de scribed earlier.002). but there were differences in the sum of the samples. the diagnostic yield increased with the number of biopsy samples in the total group and the group with mali gnancy but not in the group with tuberculous effusions. P < 0. Blind pleural biopsy using a Tru -cut needle in moderate to large pleural effusion --an experience. other causes of exudative pleural effusion were detected in 3 and in 1 patient. fungal (Fungal Infections ).Granulomatous : Mycobacterial (Tuberculosis). 3.the diagnostic yield of each individual sample (D1. despite extensive investigation. connective tissue disease). In pleural tuberculosis. 1998 May. toxin.
Goodpasture·s syndrome. Giant cells: Foreign body . Hypoxic arteriopathy . Hypertensive: Pulmonary Hypertension Plexigenic arteriopathy . Angiocentric Disorders: 1. Churg . allergy. Lymphangitis carcinomatosa / malignant lymphoma . Pulmonary Alveolar Proteinosis . pulmonary venous occlusion. Non-granulomatous: Acute interstitial pneumonia . Lymphangioleiomyomatosis . 2. pulmonary hypertension .Strauss syndrome . Sarcoidosis. Lipid Pneumonia . (Lobar Pneumonia . Granulomatous disease . Lymphangiocentric Disorders: Pneumoconioses. Vaso -occlusive disease. Alveolar Disorders : 1. Acellular : Edema . parasites. Vasculitides: Wegener·s granulomatosis . 3. Thrombotic arteriopathy . Cellular : Erythrocytes: Hemorrhagic . 2. Tuberculosi s . Lymphomatoid Granulomatosis . Legionella . pneumocystis. Fibrosis: Organizing pneumonia Interstitial Disorders : 1. Congestive vasculopathy . smoking.(tracheobronchial). systemic lupus erythematosus . Macrophages: Desquamative interstitial pneumonia . drugs . Hard metal dis ease. usual interstitial . non -specific interstitial pneumonia . Necrotizing sarcoid granulomatosis . chronic mitral stenosis. pulmonary hemosiderosis. Neutrophils: Bacterial pneumonia. Broncho-pneumonia ) Eosinophils: Eosinophilic pneumonia.
viral pneumonitis. 2. diffuse . aluminium ). Extracellular Deposits: Calcium (calcinosis. Langerhans cell histiocytosis. Amyloid (nodular amyloidoma. 3. Eosinophilic Pneumonia. neoplasia .alveolar septal) Mixed intraalveolar and interstitial disorders: Diffuse alveolar damage. blue bodies). asbestosis . psammoma b odies. dystrophic. pneumoconiosis ( talc . Mesothelium: Reactive / Neoplastic . sarcoid .pneumonia (+/ -). extrinsic allergic alveolitis . infection . Granulomatous: Tuberculosi s . Pulmonary Alveolar Microlithiasis. fungi. secondary) 2. Pleural Disorders: Mesothelioma -Online 1.hard metal beryllium.(primary . Submesothelial connective tissue: Connective tissue disease .
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