Figure A1 Aging changes in arteries. Abnormalities in the pulmonary arteries can be observed in many surgical lung biopsy specimens, unrelated to clinical evidence of pulmonary hypertension. This phenomenon is seen most commonly in aging smokers and in the vicinity of localized scars. Vessel tortuosity is the common denominator, and if medial thickening is present, it tends to be patchy and somewhat eccentric (possibly representing tangent sectioning).
Figure A2 Amyloid, nodular. A specific manifestation of amyloid, nodular amyloid, produces one or more mass lesions, but most often has no relation to systemic amyloidosis. Multinucleated giant cells are often present at the periphery of larger amyloid deposits within the lesions. Some examples of nodular amyloid in the lung are related to forms of low-grade B cell lymphoma.
Figure A3 Amyloid in the wall of a pulmonary artery (Congo red stain for amyloid). The arrow points to a focus of dense, waxy, homogeneous amyloid, stained red with this method. Note this same focus in Fig. A4 under plane-polarized light, where the diagnostic apple-green birefringence can be seen.
Figure A4 Amyloid in the wall of a pulmonary artery (Congo red stain, plane-polarized light). The red "Congophilic” focus of amyloid (arrow; also shown in Fig. A3) turns apple-green in color under polarization.
Figure A5 Amyloid, alveolar septal, hematoxylin and eosin stain. Note the uniform deposition of amorphous eosinophilic amyloid in alveolar walls. In contrast to collagen, amyloid deposits lack a fibrillar appearance when examined by light microscopy with the substage condenser lowered or removed.
Figure A6 Amyloid, tracheobronchial, hematoxylin and eosin stain. (Arrows show deposits in tracheal wall.)
Figure A7 Anthracosis (focal) parenchymal. Anthracotic pigment is a common incidental finding in surgical lung biopsy specimens and transbronchial biopsy specimens. A characteristic distribution is often discernible, with dust deposited along lymphatic routes in the pleura and bronchovascular sheaths. It is always prudent to seek clinical and radiologic correlation before ascribing such changes to pneumoconiosis.
Figure A8 Anthracosis (focal) in pleura. Small foci of dust accumulation along pleural lymphatic routes are an expected finding in smokers and city dwellers.
Figure A9 Subpleural zones of pale elastotic fibrosis. Subpleural zones of elastotic fibrous scar occur as an incidental finding in the upper lung zones. The phenomenon is easy to recognize and is important because such incidental scars may be mistaken surgically for a tumor. If an apical cap is identified by frozen section analysis, the pathologist can encourage additional biopsies in search of more specific findings.
Figure A10 Arterial medial hyaline sclerosis. Hyaline sclerosis of the pulmonary arterial media can occur as a consequence of fibrosis and other lung injury (here in a case of sarcoidosis, a multinucleated giant cell is seen in the upper right).
Figure A11 Arterial medial calcification. Calcification may occur in the media of pulmonary arteries as an incidental finding. This small artery has dramatic medial calcification in the setting of chronic mitral stenosis.
Figure A12 Artifactual lymphatic dilation can occur from injection fixation and is not always a sign of true pathology. The optimal (and easiest) form of surgical biopsy fixation is agitation (see Chapter 2). Overzealous injection of fixative using a syringe can produce distinctive artifacts.
Figure A13 Artifactual hemorrhage. Fresh blood in alveolar spaces may occur as a consequence of operative manipulation. To distinguish such artifactual hemorrhage from pathologic alveolar hemorrhage, a search for hemosiderin-laden macrophages and abnormal cellularity of the alveolar interstitium is often helpful. (See Chapter 11 for a discussion of diffuse alveolar hemorrhage.)
Figure A14 Asteroid body in a multinucleated giant cell. Asteroid bodies are distinctive eosinophilic inclusions composed of cytoskeletal components and collagen. They are not specific for sarcoidosis and are seen in a minority of patients with this disease.
Figure A15 Atelectasis. The lung is typically collapsed as part of the video-assisted thoracoscopic surgical procedure. For this reason, biopsy specimens that are allowed to fix by immersion, without removal of staples, may be difficult to interpret given the dense approximation of alveolar walls. Agitation fixation is a preferable technique. (See Chapter 2 for a discussion of fixation methods.)
Figure A16 Biopsy site. On rare occasions, a previous biopsy procedure may result in a reparative reaction that can be seen in subsequent wedge biopsy or lobectomy specimens.
Figure A17 Blue bodies. These distinctive laminated and calcified hematoxyphilic bodies are a nonspecific finding. They may be seen in the alveolar spaces focally in a number of interstitial lung diseases where alveolar macrophages accumulate.
Figure A18 Bone marrow embolus. Embolized fragments of bone marrow are incidental findings in resected lung tissue.
Figure A19 Bronchial mucosa basement membrane thickening. This finding can be seen in patients with chronic airway diseases.
Figure A20 Bronchial mucosa subepithelial elastosis. This change is a nonspecific finding seen on occasion in lung biopsy specimens from older patients.
Figure A21 Bronchial mucosa subepithelial elastosis. Elastic tissue stains, such as this Verhoeff stain, highlight in black the abnormal accumulation of elastic fibers.
Figure A22 Bronchiolar tortuosity. This clearly abnormal finding is commonly observed in the lungs of chronic smokers with degrees of chronic obstructive pulmonary disease and in the vicinity of parenchymal scars or bulla. When this process is widespread in the biopsy material, consideration of small airways disease with constrictive bronchiolitis is worthwhile (see Chapter 9).
Figure A23 Calcified granuloma in pleura. The occurrence of fibrotic and focally calcified (blue fractured area at the center) granulomas in the lung varies in accordance with the distribution of regional endemic infections, such as histoplasmosis (Mississippi and Ohio River valleys) and coccidioidomycosis (desert Southwest and California; see Chapter 7).
Figure A24 Carcinoid tumorlet (now simply tumorlet). These benign neuroendocrine cellular proliferations resemble their carcinoid tumor counterparts in peripheral lung, both lesions having a tendency toward spindled cell morphology. They always occur within and around the bronchovascular sheaths. By definition, tumorlets do not exceed 4 mm in maximal radial dimension. They may be longer than this on occasion because they follow the terminal airways in the longitudinal plane of the airway. They may occur with or without associated clinical lung disease, but most often they are seen in association with chronic airway injury (see Chapter 13). Tumorlets can also be reliably distinguished from carcinoid tumors based on strict morphology because the endocrine cell nests of the tumorlet are separated into small packets by sclerotic collagen (as illustrated in this image). Carcinoid tumors are more solid in growth pattern.
Figure A25 Cartilage ossification. This phenomenon is a consequence of aging and has no clinical relevance.
Figure A26 Corpora amylacea. These eosinophilic spherical structures are found sporadically within the airspaces. They are nonspecific findings, and they rotate plane-polarized light weakly. The concentric rings and radial striations of corpora amylacea are best seen with the microscope substage condenser lowered. Some special stains enhance these features (see Fig. A27).
Figure A27 Corpora amylacea stain readily with the Grocott methenamine silver histochemical method.
Figure A28 Cholesterol cleft in a giant cell. A common finding seen in association with granulomatous inflammation, cholesterol clefts in giant cells are more a manifestation of chronic airway obstruction than hypersensitivity pneumonitis (which is typically the first response from clinicians when they see these in biopsy specimens).
Figure A29 Crush artifact. Acquisition and processing of lung samples may result in irrevocable tissue damage by crushing, especially when the involved tissue is composed of fragile cells (typically lymphocytes or undifferentiated tumor cells). This example shows small cell carcinoma.
Figure A30 Desquamative interstitial pneumonia-like reaction (DIP-like reaction). Accumulation of macrophages in the alveolar spaces is the hallmark of the smoking-related diffuse lung disease known as desquamative interstitial pneumonia. Unfortunately, a wide spectrum of diseases with increased alveolar macrophages occurs, and the simple presence of dense alveolar macrophages in a biopsy specimen or microscopic field is insufficient for a diagnosis of idiopathic DIP (see Chapter 8). The term DIP-like reaction may be useful in situations in which this finding is focal in the biopsy specimen.
Figure A31 Eosinophilic pleuritis after pneumothorax. Some cases of spontaneous pneumothorax may result in surgical intervention for repair of a persistent air leak. When this occurs, a portion of lung in the vicinity of the perforation may be sent for pathologic evaluation. Dramatic inflammatory changes and peculiar parenchymal fibrosis may be seen, often accompanied by tissue eosinophilia.
Figure A32 Eosinophils in a smoker. As a general rule, extravascular eosinophils are a significant finding in lung biopsy specimens. Smokers typically have increased tissue eosinophils, but these are never accompanied by evidence of acute lung injury, unless it is significant.
Figure A33 Emphysema centriacinar, mild. As a general rule, mild emphysema is not graded microscopically, although it is clearly evident.
Figure A34 Emphysema centriacinar, severe. When this degree of emphysema is observed throughout the biopsy specimen, the patient typically has well-recognized chronic obstructive pulmonary disease clinically.
Figure A35 Emphysema, paraseptal. This form of airspace dilation presumably occurs as a result of traction accentuated at the periphery of the lobule. This phenomenon occurs more commonly in the upper lobes and probably plays a role in the formation of apical bulla and the occurrence of pneumothorax.
Figure A36 Focal parenchymal scar. Focal scars, such as that seen here, are nonspecific, especially when they occur singly.
Figure A37 Formalin (artifactual) pigmentation. Inadequately buffered formalin interacts with blood to produce a brown crystalline precipitate.
Figure A38 Formalin pigmentation under polarized light. A simple method to verify the presence of formalin pigment is the use of plane-polarized light. Formalin pigment is birefringent.
Figure A39 Goblet cell hyperplasia in a smoker. Chronic irritation caused by cigare The smoke induces hyperplasia of mucus-secreting goblet cells in the bronchial epithelium.
Figure A40 Hamartoma. These distinctive benign lung lesions are so well circumscribed that they tend to "shell out” of the lung parenchyma on gross examination. They are composed of an admixture of mesenchymal cells, mature cartilage, fat, and epithelium. Calcification may be present.
Figure A41 Iatrogenic foreign material in a giant cell. Patients who undergo extensive surgical procedures or require recurrent venous access for therapy may have isolated giant cells containing foreign material.
Figure A42 Interstitial air, chronic. Chronic positive end-expiratory pressure during ventilation can result in air dissection into the lung interstitium with the formation of peculiar pseudocysts lined by giant cells (see inset for a higher magnification of these lining cells) and surrounded by a fibrous wall. This phenomenon is referred to as persistent interstitial pulmonary emphysema.
Figure A43 Interstitial extramedullary hematopoiesis. This phenomenon can be mistaken for a form of inflammatory interstitial lung disease. An important clue is the presence of aggregations of erythrocyte precursors (arrows) and megakaryocytes (arrowhead).
Figure A44 Intravenous drug abuse. Individuals who crush medication tablets and inject them intravenously can have peculiar foreign body reactions with inclusions of either pill-binding material (today, microcrystalline cellulose) or tablet coatings, as seen in this example of blue ribbons of the pill material crospovidone.
Figure A45 Iron in vascular elastic tissue (endogenous pneumoconiosis). Elastic fibers of pulmonary veins may become encrusted with iron in situations where chronic passive congestion or other forms of chronic hemorrhage supervene. The encrusted fibers may appear brown, gray, or black, and stain with the Prussian blue histochemical method for iron. A giant cell reaction, with engulfed fiber fragments, often occurs in the immediate vicinity of the affected vessel.
Figure A46 Kuhn hyaline. Eosinophilic material resembling Mallory hyaline may be observed in type II epithelial cells as a nonspecific finding in a number of lung diseases and disorders. The material is composed of condensed intermediate filaments.
Figure A47 Lambertosis (peribronchiolar metaplasia). Bronchiolar epithelial metaplasia may occur as a consequence of chronic irritation and other injury to the terminal airways. Because the canals of Lambert (direct communication channels that exist between terminal airways and laterally adjacent alveoli) are often involved, the term lambertosis has been coined. A better term is bronchiolar or peribronchiolar metaplasia.
Figure A48 Megakaryocyte in alveolar septum. Megakaryocytes may be seen frequently as an incidental finding in surgical lung biopsy specimens.
Figure A49 Meningothelial-like nodule. Previously referred to as minute pulmonary chemodectomas, these perivenular lesions seem to be associated with chronic hypoxia, although no specific etiology or normal cellular progenitor has yet been identified. They occur along pulmonary veins, away from the small airways. This feature is helpful in distinguishing them from carcinoid tumorlets that grow along the airways.
Figure A50 Metastatic alveolar calcification. Chronic hemodialysis and disorders that result in hypercalcemia may lead to extensive pulmonary calcification, sometimes referred to as pulmonary calcinosis. The finding is often asymptomatic clinically and differs from dystrophic calcification by the lack of osseous metaplasia (see the discussion of dendriform calcification in Chapter 7).
Figure A51 Mucostasis, early. The early manifestation of goblet cell hyperplasia and excess mucus production may be seen as extrusion of mucus into the alveolar ducts from terminal airways.
Figure A52 Mucostasis, advanced. Alveolar spaces may become filled with mucin in settings of advanced mucus obstruction of the airways. When more than a few airspaces are involved, a careful search for neoplastic epithelium is in order because mucinous infiltrates may be a manifestation of mucinous bronchioloalveolar carcinoma.
Figure A53 Muscular hyperplasia in a pleural vein. This incidental finding can be dramatic. Such focal nonspecific muscular hyperplasia in veins traversing the pleura is probably an age-related phenomenon.
Figure A54 Osseous metaplasia in fibrosis. Small nodules of bone may be seen in lung processes that produce fibrosis.
Figure A55 Pleural bleb. In contrast to bulla, blebs are entirely intrapleural.
Figure A56 "Pseudo”-lipid. Distinctive artifactual gas vacuoles may occur in areas of hemorrhage or inflammation.
Figure A57 Pseudomycosis. Aspirated oral bacteria can produce microabscesses and florid aspiration pneumonia. Such occurrences have been referred to as botryomycosis when colonies of bacteria show characteristic central granular bodies surrounded by a corona of Splendori-Hoppli phenomenon.
Figure A58 Respiratory bronchiolitis. This common smoking-related airway injury is often not the principal pathologic finding of the biopsy sample. Rarely, respiratory bronchiolitis may occur as the primary pathologic process in a relatively specific clinical and radiologic context, and absent findings to suggest another disease (see Chapters 8 and 9 for further discussion of respiratory bronchiolitis).
Figure A59 Scar at the tip of a lobe. Nonspecific scarring may occur in peripheral lung, often in characteristic locations (such as the tip of the middle lobe or lingula). Note the overlying dense fibrovascular adhesion, a sign of an earlier localized inflammatory event.
Figure A60 Schaumann bodies in fibrosis. These irregular calcified lamellar bodies (also known as conchoidal bodies) are an indicator of granulomatous inflammation, whether current or resolved. They are commonly seen in the granulomas of patients with sarcoidosis, but are not specific for this disease.
Figure A61 Schaumann bodies in a giant cell. Schaumann bodies in giant cells are a nonspecific finding in granulomatous inflammation and alone do not constitute evidence of sarcoidosis.
Figure A62 Silicate nodule in the pleura. Rare small silicate nodules may be seen in patients after inhalational exposure. The mere presence of a silicate nodule is not sufficient evidence of pneumoconiosis (see Chapter 10).
Figure A63 Smooth muscle hyperplasia of the alveolar ducts in a smoker. The prominence of the smooth muscle bundles, present at the tips of alveoli opening onto alveolar ducts, may be seen as a consequence of smoking and other airway irritation.
Figure A64 Smooth muscle nodule. Peculiar nodules of smooth muscle fascicles arranged in a stellate shape (sometimes with admixed fibrosis) are frequently seen in the lungs of smokers. They differ from the stellate scars of resolved (inactive) pulmonary Langerhans cell histiocytosis by the presence of excess smooth muscle. They probably represent obliterated terminal airways with associated smooth muscle proliferation.
Figure A65 Subendothelial fibrosis in pulmonary arteries. This finding is often more evident in larger pulmonary arteries. The significance is unknown in the absence of other vasculopathic changes to suggest hypertension, or thrombosis and embolization with recanalization.
Figure A66 Tortuous arteries near a scar. Scar tissue in the lung may produce peculiar vascular tortuosity. If such change causes concern, a search for other vessels away from the scar may be helpful in excluding true vasculopathic disease.
Figure A67 Tracheobronchopathia osteochondroplastica. This rare condition is characterized by submucosal nodules of metaplastic bone and cartilage typically identified endoscopically in the trachea and major bronchi. In this photomicrograph, nodules of mature bone can be seen between the tracheal cartilage rings on the mucosal side.
Figure A68 Transmogrification. Bullous placental transmogrification (also known as localized giant bullous emphysema) is a rare but distinctive localized cystic lesion that occurs in young to middle-aged adults. This lesion traditionally has been regarded as a form of emphysema, although an abnormality of interstitial cells with secondary formation of cysts has been suggested as an alternative hypothesis. (Cavazza A, Lantuejoul S, Sartori G, et al. Placental transmogrification of the lung: clinicopathologic, immunohistochemical and molecular study of two cases, with particular emphasis on the interstitial clear cells. Hum Pathol. 2004;35[4]:517-521.) the etiology is unknown and local resection is curative.
Figure A69 Vascular sclerosis in scar tissue. Arteries entrapped in dense scar may develop medial fibroelastosis.