Lung-nontumor
Last revised 22 January 2008
Last major update November 2003
Copyright (c) 2003-2008, PathologyOutlines.com, Inc.
See also Lung-tumor, Mediastinum, Pleura, Trachea
Bold and underlined topics are hypertext links-may open a new window
Primary references, normal anatomy, normal histology, findings of no clinical significance, biopsy, patterns of injury
Cystic disease/congenital anomalies: general, bronchial atresia, bronchopulmonary dysplasia, cystic adenomatoid malformation, cystic fibrosis, cysts, emphysema due to alpha-1-antitrypsin deficiency, hypoplasia, lobar overinflation, mesenchymal cystic hamartoma, sequestrations
Chronic obstructive pulmonary disease: general, asthma, bronchiectasis, chronic bronchitis, emphysema
Infections: general, abscess, adenovirus, AIDS, Aspergillus, atypical mycobacteria, bacillary angiomatosis, Blastomyces, Candida, CMV, Coccidiodes, Cryptococcus, Cryptosporidium, Dirofiliaria, Echinococcus, hantavirus, Herpes simplex, Histoplasma, influenza, Legionella, malakoplakia, measles, mucor, Mycobacterium avium-intracellulare, Mycoplasma, Nocardia, organizing pneumonia, Paragonimus, Pneumocystic carinii, Pseudomonas, respiratory syncytial virus, Rhodococcus, SARS, Serratia, Staph aureus, Strongyloides, syphilis, Toxoplasma, tropical eosinophilia, tuberculosis, varicella
Granulomatous (non-infectious) inflammation: general, allergic, bronchocentric, hyalinizing granuloma, sarcoidosis, Wegener’s
Other interstitial pneumonitis/fibrosis: general, acute interstitial pneumonia, amiodarone, BOOP, bronchiolocentric interstitial pneumonitis, chronic eosinophilic pneumonia, chronic pneumonitis of infancy, DIP, diffuse panbronchiolitis, drug induced, eosinophilic, giant cell, honeycomb lung, lipoid, Loeffler’s syndrome, lymphoid interstitial pneumonia, nonspecific, obliterative bronchiolitis, PVP, respiratory bronchiolitis, UIP
Pneumoconiosis: general, aluminum, anthracosis, asbestos, asbestosis, berylliosis, coal workers’ pneumoconiosis, extrinsic allergic alveolitis, organic dust, siderosis, silicosis, silo-filler’s disease
Other non-neoplastic disease: alveolar proteinosis, amyloidosis, arteriovenous fistula, atelectasis, black spots, broncholithiasis, Crohn’s disease, crystal storing histiocytosis, diffuse alveolar damage, endometriosis, eosinophilic reactions, Goodpasture’s, hematoma, hemorrhage, idiopathic pulmonary hemosiderosis, infarct / pulmonary emboli, intravenous drug abusers, kayexalate, microlithiasis, muscular hyperplasia, polyarteritis nodosa, pulmonary edema, pulmonary hypertension, radiation, rheumatoid lung disease, rounded atelectasis, transplantation, veno-occlusive disease
Go to Lung tumors (on separate page)
AJCC Cancer Staging Manual (6th Ed)
American Journal of Surgical Pathology (AJSP), Jan 2002 to Nov 2003
Archives of Pathology and Laboratory Medicine (Archives), Jan 2002 to Nov 2003
Human Pathology (Hum Path), Jan 2002 to Sep 2003
Modern Pathology (Mod Path), Jan 2002 to Oct 2003
Rosai, J: Ackerman’s Surgical Pathology (8th Ed); Mosby-Year Book, Inc., 1996
Sternberg, S: Diagnostic Surgical Pathology (3rd Ed); Lippincott Williams & Wilkins, 1999
Websites: Loyola University-Stritch School of Medicine
Please refer to these primary references for more detailed discussions and photographs
Trachea divides into right and left mainstem bronchi
Each main bronchus divides into lobar bronchi, then into segmental bronchi
Lobar bronchi are usually called secondary bronchi and segmental bronchi are called tertiary bronchi, except in Japan, where they are called first order and second order, respectively.
Bronchioles lack cartilage and submucosal glands
Right lung has 3 lobes, left lung has 2 lobes plus lingula
Right bronchus more vertical than left, thus aspirated material tends to enter right lung
Lung has double arterial supply - pulmonary and bronchial
Lungs are surrounded by visceral pleural membrane; inner chest cavity is lined by parietal pleural membrane; these membranes define the pleural space, which normally has minimal volume
Regional lymph nodes: paratracheal, pre- and retrotracheal, aortic, subcarinal, periesophageal, inferior pulmonary ligament, hilar, peribronchial, intrapulmonary
Gross images: cross section #1, #2, lungs and bronchi
Lung parenchyma consists of airways (bronchi / bronchioles) and alveoli
Alveolar capillary basement membrane fuses with alveolar epithelium to form a single membrane for oxygen and carbon dioxide diffusion
Acinus / terminal respiratory unit contains 3-5 terminal bronchioles, alveolar ducts and alveoli
Alveoli are lined by respiratory epithelium (pseudostratified, columnar, ciliated)
Alveoli contain type I and II pneumocytes
Type I pneumocytes: 95%, flattened
Type II pneumocytes: 5%, produce surfactant (lamellar bodies on EM), involved in repair if type I destroyed
Bronchial-bronchiolaar epithelium contains goblet cells, neuroendocrine (Kultschitsky’s) cells, serous cells, basal cells, Clara cells and ciliated cells
Neuroendocrine cells: numerous in neonatal bronchial and bronchiolar epithelium; rare in adults except as clusters within epithelium of bronchi and bronchioles
Clara cells: increase towards terminal bronchiole; have secretory function; main progenitor cell after bronchiolar injury; have apical PAS+ diastase resistant secretory granules
Submucosal glands: contain serous and mucus cells with myoepithelial lining; may have oncocytic changes
Lymphatics: not present in alveolar walls
Pulmonary arteries: have internal and external elastic membrane, compared to a single elastic layer in pulmonary veins
Normal findings in alveoli: alveolar macrophages, corpora amylacea, blue bodies (calcium carbonate), megakaryocytes
Normal findings in interstitium: anthracotic pigment, scattered silica crystals
Pores of Kohn: perforations in alveolar walls; permit passage of bacteria and exudate between alveoli
Micro images: bronchus #1, #2, bronchiole
Virtual slides: fetal lung, lung-baby, normal lung
Histologic findings of no clinical significance
Apical caps: zones of fibrosis with chronic inflammatory infiltrate in lung apices
Ectopic tissue: skeletal muscle, pancreas, adrenal cortex, neuroglia
Intrapulmonary lymph nodes
Metaplastic bone: age related finding in bronchial cartilage; associated with bone marrow elements; also rarely associated with alveolar exudate
For non-neoplastic lesions, clinical correlation is essential
Evaluating biopsies: alveolar space, alveolar septal membrane, conducting airways, pulmonary arteries, other vessels and lymphatics
Tips of lingula and right middle lobe typically show more fibrosis than elsewhere
Frozen section is recommended for open biopsies so (a) tissue arrives fresh, not in preservative, (b) pathologist can tell surgeon if specimen is adequate and representative
Elastic and trichrome stains are often helpful for non-neoplastic tissue
Patterns of injury for non-neoplastic disease
Source: Sternberg, S: Diagnostic Surgical Pathology (3rd Ed); Lippincott Williams & Wilkins, 1999
Interstitial inflammation/fibrosis: DIP, UIP, diffuse alveolar damage, Langerhans cell histiocytosis, asbestosis, amyloidosis, sarcoidosis, extrinsic allergic alveolitis
Intraalveolar reaction: DIP, pulmonary alveolar proteinosis, infection, extrinsic allergic alveolitis, chronic eosinophilic pneumonia
Small-airway disease: bronchiolitis obliterans, respiratory bronchiolitis, mycoplasma infection, viral infection, extrinsic allergic alveolitis, eosinophilic pneumonia
Large-airway disease: allergic bronchopulmonary aspergillosis, bronchocentric granulomatosis, TB, fungi, Wegener’s
Granulomatous vasculitis: Wegener’s, sarcoidosis, Churg-Strauss, bronchocentric granulomatosis, fungi, TB
Small vessel disease: primary pulmonary hypertension, thromboembolism, polyarteritis nodosa, veno-occlusive disease, Churg-Strauss syndrome
Hemorrhage: Goodpasture’s, SLE, immune complex glomerulonephritis, idiopathic pulmonary hemosiderosis, Wegener’s
Lymphoid infiltrates: lymphocytic interstitial pneumonia, lymphoma, lymphoid aggregates, extrinsic allergic alveolitis
Eosinophils: chronic eosinophilic pneumonia, Churg-Strauss syndrome, bronchocentric granulomatosis, Langerhans cell histiocytosis
Cystic disease/congenital anomalies
Congenital or acquired:
Congenital: cysts, cystic adenomatoid malformation, lobar hyperinflation, sequestrations
Acquired: emphysema, healed abscess, honeycombing
Mixed: cystic fibrosis
Portion of bronchial tree with normal branching pattern, but without any demonstrable connection to the central bronchial tree
Complication of prematurity
Respiratory distress continues for months
Patients have limited pulmonary reserve, develop repeated infections, often have pulmonary hypertension and develop cor pulmonale
Micro: bronchiolar and interstitial fibrosis, compensatory emphysema of less damaged acini, inadequate alveolar development causes fewer but larger alveoli
Micro images: severe fibrosis, large alveoli
Virtual slides: respiratory distress syndrome & bronchopulmonary dysplasia
Cystic adenomatoid malformation
Rare hamartomatous disorder, 1 per 25,000 births
Variably sized cysts lined by “adenomatoid” columnar-type epithelium
Associated with stillbirth, neonatal distress and bronchial atresia; type I found in older children and adults
May develop with and be related to other congenital or acquired lung conditions (Archives 2002;126:934)
May regress spontaneously
Classification:
Type 0: 1-3%, small/firm lungs; formerly called acinar dysplasia; associated with other malformations, incompatible with life
Type I: 60-70%: large cysts up to 10 cm, lined by pseudostratified ciliated cells interspersed with mucus cells; may appear late; good prognosis since can resect; shows lepidic growth within cysts and adjacent lung, resembles bronchioalveolar carcinoma
Type II: 10-15%: small cysts up to 2 cm, resemble dilated bronchioles separated by normal alveoli; associated with other malformations; poor prognosis
Type III: 5%, solid gross appearance, excess bronchiolar structures separated by small air spaces with cuboidal epithelium resembling fetal lung; poor prognosis
Type IV: 15%, large cysts up to 10 cm, lined by flattened epithelium; good prognosis; similar to grade 1 pleuropulmonary blastoma although less cellular; sample generously to rule out blastoma
Case reports: Case of the Week #58
Treatment: close followup for asymptomatic infants, with elective surgery for persistent lesions within the first year of life (Arch Dis Child Fetal Neonatal Ed 2006;91:F26, Int J Gynaecol Obstet 2005;89:99)
Gross images: type I, type II, type II cut surface
Micro images: various examples, type I
type II: image #1; #2; #3; #4; #5; #6
Molecular: no karyotypic abnormalities, no p53 mutations (Pediatr Dev Pathol 2006;9:190)
References: AJSP 2003;27:1139
1 in 20 in US are carriers; most common mutation is #708 (seen in 70% with disease)
Mutations cause reduced chloride ion in secretions, thicker respiratory secretions, upper respiratory infections, late pancreatic insufficiency
Mutations also cause defective cilia and infertility
Meconium ileus seen in 5-10% of patients; also intussusception
Gross: emphysema, bronchiectasis, abscess, fibrosis
Gross images: image1
DD: Kartegeners (defective cilia syndrome)
Cystic fibrosis associated infections
Burkholderia cepacia: unique to cystic fibrosis, seen in 20% of patients; causes rapid deterioration of pulmonary status and death; transmitted person to person, has marked social impact as those infected are excluded from social functions (camps) and ineligible for transplant; treat with Chloramphenicol, trimethoprim-sulfamethoxazole
Pseudomonas aeruginosa: bacteria produces alginate, a capsular protein that mediates adherence; mucoid phenotype is unique to cystic fibrosis; bacteria is never eradicated from lung; treat with ceftazidime
Staphylococcus aureus: infection persists despite treatment
Stenotrophomonus maltophilia: aerobic gram negative rod, multidrug resistant, smells like onions; treat with trimethoprim-sulfamethoxazole, resistant to imipenim
Abnormal detachment of a fragment of primitive foregut
Usually are bronchogenic cysts, adjacent to bronchi, may not connect with airways, filled with air/mucin; may become infected
Emphysema due to alpha-1-antitrypsin deficiency
Genetic deficiency
Alpha-1-antitrypsin (AAT) inhibits proteases, particularly elastase (which digests lung tissue), which is secreted by neutrophils during inflammation
PiMM: normal phenotype; 90% of population
PiZZ: associated with AAT deficiency; 80% develop symptomatic emphysema; occurs earlier and is more severe in smokers
Neutrophils are normally present in lung and alveolar space; when stimulated, neutrophils and macrophages increase in number and release elastase and oxygen free radicals, which causes emphysema unless counteracted by antiproteases such as AAT
Smokers have more neutrophils and macrophages in alveoli, tobacco use enhances release of elastase from neutrophils, enhances elastase activity, oxidants in tobacco smoke inhibit AAT
Lung weighs less than normal with fewer alveoli than expected for gestational age
Bilateral disease is fatal
Causes: oligohydramnios (renal agenesis, fetal membrane rupture), decreased intrathoracic space (renal cystic disease, diaphragmatic hernia), reduced breathing (anencephaly, musculoskeletal disorders)
Gross images: image1
Also called congenital lobar emphysema
Infants or young children
Perhaps due to hypoplasia of bronchial cartilage; associated with other cardiopulmonary anomalies
Affects left or right upper lobe or right middle lobe
May cause severe compression of other pulmonary lobes
Not emphysema since no tissue destruction
Micro: massive distention of alveolar spaces but no tissue destruction
Multifocal, bilateral cysts < 1 cm lined by normal or metaplastic respiratory epithelium resting on a cambium layer of mesenchymal cells
Sequestrations (intralobar and extrapulmonary lobar)
Lobes or segments of lung without a normal connection to the airway system
Extrapulmonary sequestrations: external to lung, covered with separate pleural lining, may be anywhere in thorax or mediastinum; usually infants, abnormal masses, 90% on left side, 20% have other congenital anomalies; associated with polyhydramnios and edema
Intralobar sequestrations: within the lung, usually lower lobe, segment is supplied by a large artery from aorta, not invested with its own pleura, associated with infections, bronchiectasis, chronic inflammation, fibrosis
Blood supply is from aortic branches, NOT pulmonary arteries
Chronic obstructive pulmonary disease (COPD)
Also called chronic obstructive lung disease (COLD)
Major cause of bed defining disability in US
Major symptom is dyspnea (shortness of breath)
Usually due to cigarette smoking
Site of disease: bronchi-chronic bronchitis, bronchiectasis, asthma; bronchioles-bronchiolitis, acini-emphysema
Obstructive airway disease: increase in resistance to airflow due to obstruction at any level; includes emphysema, chronic bronchitis, bronchiectasis, asthma, tumor, foreign body; reduced maximal airflow rates (FEV1)
Restrictive airway disease: reduced expansion of lung parenchyma with decrease in total lung capacity; normal FEV1; due to chest wall disorders (polio, obesity, pleural disease, kyphoscoliosis), interstitial / infiltrative diseases (ARDS, dust diseases, interstitial fibrosis)
Chronic relapsing inflammatory disorder characterized by hyperreactive airways, causing episodic, reversible bronchoconstriction
Usually associated with atopy, mediated by IgE
Has increased in Western hemisphere over past 30 years
Extrinsic: Type I hypersensitivity; either atopic (due to allergens), occupational or due to allergic bronchopulmonary aspergillosis
Intrinsic: nonimmune; due to aspirin ingestion, pneumonia, cold, stress, exercise
Status asthmaticus: unremitting attacks due to exposure to previously sensitized antigen; may be fatal
Gross: overdistended lungs, small areas of atelectasis, thick mucus plugs in proximal bronchi containing whorls of shed epithelium
Gross images: mucus plugs #1, #2, #3, thickened bronchial walls, status asthmaticus #1, #2, #3
Micro: Curschmann spirals, eosinophils contain Charcot-Leyden crystals (eosinophil membrane protein); increased mucosal goblet cells and submucosal glands, thickened basement membrane, bronchial smooth muscle hypertrophy, airway wall edema
Micro images: smooth muscle hypertrophy and inflammatory cells #1, #2, #3, goblet cells and inflammatory cells, Curschmann spiral, eosinophils and Charcot-Leyden crystals
DD: allergic bronchopulmonary aspergillosis, bronchocentric granulomatosis without the granulomatous inflammation
Atopic asthma
Begins in childhood, triggered by environmental allergens (dander, dust, pollen, food), often positive family history
Skin test causes wheel and flare reaction
Classic example of Type I IgE mediated hypersensitivity reaction
Initial sensitization affects T helper 2 cells, which release IL-4/5, which promote IgE release by B cells, mast cells and eosinophils
Reexposure to allergen leads to mediator release from mucosal mast cells
Acute/intermediate response is bronchoconstriction, edema, mucus secretion, hypotension
Late phase reaction, due to influx of other inflammatory cells, is release of major basic protein from eosinophils, which causes epithelial damage and airway constriction
Putative mediators: leukotrienes C4, D4, E4 and acetylcholine; minor mediators: histamine, prostaglandin D2
Associated with serum eosinophilia, sputum eosinophils
Occupational asthma
Due to repeated exposure to fumes, dusts, gases, chemicals, often in minute quantities
Drug induced asthma
Associated with aspirin use
Rare, associated with recurrent rhinitis and nasal polyps
Patients are sensitive to small doses of aspirin, get urticaria and asthma
May be due to direct effects of aspirin on cyclooxygenase pathway
Nonatopic asthma
Due to respiratory infection (rhinovirus, parainfluenza virus); usually not familial
Normal serum IgE, negative skin tests
Viral induced inflammation may lower threshold of subepithelial vagal receptors to irritants
Chronic necrotizing infection of bronchi and bronchioles associated with permanent dilation of these airways
Diagnosis is based on presence of infection (stasis occurs in dilated bronchi) and obstruction
Symptoms: cough, fever, copious amounts of foul-smelling, purulent sputum
Causes: bronchial obstruction (localized bronchiectasis), congenital bronchiectasis, cystic fibrosis, intralobar sequestration of lung, immunodeficiency states, immotile cilia / Kartegeners syndrome, Young’s syndrome, necrotizing pneumonia (staphylococcus, tuberculosis)
Obstruction (due to tumor, foreign body, inspissated mucus) causes resorption of air distal to obstruction, atelectasis, intraluminal secretions
Nonobstructive bronchiectasis is due to pneumonia and atelectasis, which increase negative intrapleural pressure, which exerts an external force on bronchial walls, causing them to dilate; usually left sided affecting lower lobes
Cystic fibrosis: obstruction due to mucus plugs, infection is due to decreased ciliary clearance of bacteria
Kartegeners syndrome: autosomal recessive condition with variable penetrance, due to absent or irregular dynein arms of cilia, which causes defective bacterial clearance (bronchiectasis, sinusitis), defective cell motility during embryogenesis (situs inversus), immotile sperm (infertility)
Young’s syndrome: infertility caused by azoospermia, but without ultrastructural ciliary abnormalities
Gross: markedly distended peripheral bronchi, usually in lower lobes, can trace to pleural surface; bronchial walls irregularly thickened
Gross images: image1, image2, image3, image4
Micro: chronic inflammation, ossification and ulceration of bronchial cartilage; variable inflammation and fibrosis of alveoli; thickened pleura
Micro images: image1
Virtual slides: bronchiectasis
Diagnosis: persistent cough with sputum for 3 months in 2 consecutive years
More infections, purulent sputum, hypercapnia, hypoxia than emphysema; clinically called “blue bloaters”
May cause secondary pulmonary vascular hypertension, cor pulmonale, congestive heart failure; death due to respiratory acidosis and coma, congestive heart failure, pneumothorax
Simple chronic bronchitis: cough but no physiologic evidence of airway obstruction
Chronic asthmatic bronchitis: hyperreactive airways with intermittent bronchospasm and wheezing
Obstructive bronchitis: often have associated emphysema
Causes: 4-10x more common in smokers, also chronic irritation, infections
Tobacco interferes with ciliary action, directly damages airway epithelium, inhibits ability of white blood cells to clear bacteria; infections maintain but do not initiate chronic bronchitis
Reid index: ratio of thickness of mucus gland layer to thickness of wall between epithelium and cartilage; normal is 0.4, increased in chronic bronchitis
Gross: boggy mucosa with excessive mucinous secretions, pus
Micro: early-hypersecretion of mucus in large airways with hypertrophy of submucosal glands in tracheobronchial tree
later-increase in goblet cells in small airways causes excessive mucus production and airway obstruction; increased Reid index; variable dysplasia, squamous metaplasia, bronchiolitis obliterans
Micro images: increased mucus glands
Diagram: Reid index
Abnormal permanent enlargement of air spaces distal to terminal bronchiole with wall destruction but without fibrosis
Differs from overinflation, which is not due to wall destruction (example: due to loss of opposite lung)
Acinar and airspace enlargement is usually due to tobacco related wall destruction
Centroacinar emphysema: 95% of emphysema cases, causes significant airflow obstruction, affects central part of acini, sparing distal alveoli; worse in upper lobes, particularly apices; walls are anthracotic with parabronchial inflammation; seen in heavy smokers, coal worker pneumoconiosis; clinically significant at age 40+ in smokers, although ventilatory deficits seen earlier
Gross images: entire lung, cut section #1, #2, bullae#1, #2, #3, smoking pattern
Micro images: dilated air spaces and loss of alveolar walls
Virtual slides: image1
Panacinar (panlobular) emphysema: 5% of cases, causes significant airflow obstruction; acini uniformly enlarged from respiratory bronchiole to terminal alveoli; usually lower lungs; associated with alpha-1-antitrypsin deficiency; lungs usually voluminous
Paraseptal (distal acinar) emphysema: minor clinically; distal acini only affected, emphysema is next to pleura, near areas of fibrosis, scarring or atelectasis; multiple continuous airspaces are affected; may be source of spontaneous pneumothorax in young adults
Irregular emphysema: minor clinically; invariably associated with scarring, irregular involvement of acini
Compensatory emphysema: response to loss of lung elsewhere, such as post-lobectomy
Senile emphysema: due to age-related alterations in internal geometry of alveoli leading to larger alveolar ducts, smaller alveoli, but no loss of elastic tissue or destruction of lung substance
Obstructive emphysema: due to tumor, foreign body or congenital lobar overinflation (infants, perhaps due to hypoplasia of bronchial cartilage; associated with other cardiopulmonary anomalies); due to ball-valve effect with inhalation via collaterals (pores of Kohn, canals of Lambert); may compress normal lung, may be life-threatening
Bullous emphysema: any form that produces blebs > 1 cm; often subpleural, near apex, associated with tuberculosis scarring; may rupture and cause pneumothorax, hemorrhage; called placental transmogrification if it resembles chorionic villi
Interstitial emphysema: air into connective tissue stroma of lung, mediastinum or subcutaneous tissue; due to alveolar tears, chest wounds, coughing, whooping cough
Pathogenesis: alteration in balance between proteases and antiproteases
Clinical: no symptoms until 1/3 of functional capacity is lost; get shortness of breath, coughing, wheezing, weight loss; barrel chest; breath through pursed lips (pink-puffer), which causes slowing of forced expiration
May cause secondary pulmonary vascular hypertension, cor pulmonale, congestive heart failure, death due to respiratory acidosis and coma, pneumothorax
Best to assess based on morphometry, not lung function data, Mod Path 2003;16:1
Infections
Lung is #1 site for infections that cause lost workdays
Pneumonia is due to impairment of normal defense mechanisms or lowered host resistance
Normal defense mechanisms: nasal clearance (sneezing, blowing, swallowing), tracheobronchial clearance (mucociliary action), alveolar clearance (alveolar macrophages)
Impairment due to suppression of cough reflex (drugs, virus), injury to mucociliary apparatus (smoking, virus, Kartegeners syndrome), injury to macrophages (tobacco, alcohol, anoxia), pulmonary congestion/edema, accumulation of secretions (cystic fibrosis)
Note: viral pneumonia predisposes to bacterial pneumonia
Common agents: Staphylococcus aureus, Streptococcus pneumoniae, Haemophilus influenza, Pseudomonas aeruginosa, coliforms
Complications: abscess, empyema, organization, sepsis, meningitis
Consolidation: exudative solidification of lung
Symptoms of pneumonia: shortness of breath, fever, productive cough, malaise, friction rub (if fibrinous pleuritis)
Micro images: aspiration pneumonia
Virtual slides: early pneumonia, aspiration pneumonia-adult, aspiration pneumonia-infant, organizing pneumonia
Bronchopneumonia
Patchy consolidation of the lung centered on bronchi
Gross images: whole lung, cut surface, cut surface-close up #1, #2, patchy consolidation #1, #2
Micro: neutrophils in bronchi, bronchioles and adjacent alveolar spaces; lipid pneumonia if marked lipid laden macrophages
Micro images: bronchopneumonia with adjacent normal lung, patchy involvement, neutrophils in alveoli, destruction of lung tissue
Virtual slides: bronchopneumonia, with abscess #1, #2
Lobar pneumonia
Affects entire lung but now rare due to antibiotics; associated with increased virulence of organism or increased host vulnerability (infants, elderly); may be due to extension of existing bronchiolitis or bronchitis
Gross images: whole lung, cut surface #1, #2, red hepatization, gray hepatization #1, #2
Micro: initially congestion with bacteria and few neutrophils; then red hepatization (grossly resembles liver) with massive congestion, neutrophils, fibrin; then gray hepatization with fibrinopurulent exudate and organization; then resolution with resorption of exudate
Virtual slides: lobar pneumonia
Due to sinobronchial infections, dental sepsis, aspiration (due to alcoholism, coma, debilitation), primary bacterial infection (Staphylococcus aureus, Klebsiella pneumonia, Streptococcus pneumonia), fungi, bronchiectasis, post-transplant, septic emboli, neoplasia induced obstruction, idiopathic
Aspiration induced abscesses more common on right side (right sided bronchus is more vertical), usually single
Air fluid level present if there is communication with air passages
Symptoms: cough, fever, copious foul-smelling sputum, fever, chest pain, weight loss, clubbing of digits
10% of cases are associated with underlying carcinoma
May extend into pleural cavity, create septic emboli causing meningitis or brain abscess, serve as nidus for fungal overgrowth (Mucor, Aspergillus), spread elsewhere in lung
Treatment: lobectomy
Gross: thick fibrotic walls and surrounding pneumonia in chronic abscesses
Gross images: cut surface, abscess cavities #1, #2, abscess and bronchopneumonia
Micro images: early abscess #1, #2, with bacteria, chronic abscess
Cold agglutinins present in 20%
Micro: epithelial cells contain smudged nuclei with bricklike intranuclear inclusions; also necrosis of bronchial and alveolar epithelium and acute inflammation
Micro: interstitial inflammation (no inclusions identifiable)
Neonatal adenovirus infection of lung
More typical findings in liver and adrenal glands than in lung
Micro: glassy nuclei; severe necrotizing bronchiolitis extending into ducts and airways
Diagnose with bronchoalveolar lavage, transbronchial biopsy or open lung biopsy
Nonspecific features resemble DIP or lymphocytic interstitial pneumonia
Patients often have multiple infections
Open lung biopsies should routinely be stained for Pneumocystis, fungi, mycobacteria
Cavitary lesions: Staphylococcus, fungi (Candida, Aspergillus, Cryptococcus, Histoplasma, Blastomyces), Mycobacterium tuberculosis, Mycobacterium avium intracellulare, Rhodococcus equi
Patients also have infections from CMV, Pneumocystis carinii, toxoplasma, microsporidia
Associated with Kaposi’s sarcoma
Occurs as secondary colonization of lung abscess, aspergilloma, allergic bronchopulmonary aspergillosis or invasive aspergillosis in immunocompromised
Associated with renal transplant recipients
Gross images: abscess
Micro: dichotomous (into two nearly equal branches) branching, septate hyphae, often invade vessels
Micro images: fungus ball, hyphae, PAS, Diff-Quik stain
Virtual slides: aspergilloma (fungal ball)
Allergic bronchopulmonary aspergillosis
Bronchocentric granulomas in asthmatics that contain numerous eosinophils, and noninvasive Aspergillus organisms or other fungi
Also thick mucus plugs
Over time, bronchi become dilated, causing bronchiectasis
Associated with immunosuppression, chronic obstructive lung disease, prior TB, pneumoconiosis, bronchiectasis, lung carcinoma
Culture required for diagnosis
Positive stains: acid fast (bacilli are longer [20 microns], more coarsely beaded and more bent than M. tuberculosis bacilli)
Pseudoneoplastic vascular proliferation affecting lungs, bronchi, other site