Air Space

Alvoelar walls consist of capillary endothelium, basement membrane and surrounding pulmonary interstitium, alveolar epithelium (flat type I pneumocytes covering 95%; type II pneumocytes synthesizing surfactant, aid in repair, and can give rise to type I cells), and alveolar macrophages (free or loosely attached to epithelial cells, belong to the mononuclear phagocyte system).


Incomplete expansion, usually with increased density.


  • Obstructive/resorptive atelectasis – Secondary to complete endobronchial obstruction (might not cause atelectasis due to collateral flow). Incomplete obstruction causes airtrapping (check-valve effect). Trapped pure oxygen is absorbed more rapidly (within minutes) than air. From bronchogenic carcinoma, foreign bodies, mucous plugs, malpositioned tubes, inflammatory/post-traumatic bronchostenosis, broncholith, extrinsic compression (LN, aortic aneurysm, LA).
  • Passive/relaxation/compressive – Mass effect from pleural thickening (effusion, pneumothorax), pleural/chest wall mass, intrapulmonary mass (bullae, abscess, tumour), elevated diaphragm. Lung collapses with dissociation from chest wall.
  • Cicatricial/contraction – Parenchymal fibrosis causes lung destruction and loss of compliance reducing volume. Localised in chronic upper lobe fibronodular TB. Diffuse in interstitial fibrosis.
  • Adhesive – Surfactant deficiency. Type 2 pneumocytes (produces surfactant to reduce surface tension) damaged by GA, ischaemia, radiation.
  • Discoid/plate-like/linear/subsegmental (Fleischner lines) – Single or multiple, perpendicular to pleura. Hypoventilation -> alveolar collapse, most commonly bases and posteriorly. Common in hypoventilation (chest pain, postop, distended abdo). Deep to invaginations of visceral pleura formed by incomplete fissures or scars.
  • Segmental atelectasis – Thin linear to wedge-shaped opacity which does not abut a fissure, best seen on CT.
  • Rounded atelectasis (folded lung, Blesovsky syndrome, atelectatic pseudotumour) – Uncommon, chronic atelectasis forms lower lobe mass (20-70mm, usually peripheral), in any condition associated with exudative/proteinaceous pleural effusion (esp asbestos-related). Pleural adhesions form in resolving phase of effusion causing lung to roll in a ball as it re-expands, or pleural fibrosis maturation retracts and causes infolding of underlying lung. Curvilinear bronchovascular bundle/comet tail entering from hilar aspect is characteristic. Acute angle with pleura, adjacent to area of pleural thickening. Enhances.

Lobar atelectasis/collapse – Direct (fissures, vessels) and indirect signs (shift of other structures). Displaced fissure with concave shape, increased density, bronchovascular crowding, tracheal/cardiac/mediastinal shift, hilar elevation (upper lobe) or depression (lower lobe), diaphragmatic elevation, ‘shifting granuloma’ (of preexisting granuloma), reduced hemithorax volume with rib crowding/approximation (chronic), absent air bronchograms, triangular configuration with apex at hilum. Chronic -> compensatory hyperinflation of other lobes with possible herniation of contralateral upper lobe (bowing of the anterior junction line). Golden/reverse S sign – S shaped fissure with lobar collapse from obstructing central carcinoma. Mucoid/fluid bronchogram – trapped secretions in bronchus distal to obstruction in atelectasis.

  • Right upper lobe – Collapses superomedially. Minor fissure -> superomedially; superior major fissure -> anteromedially. Paramediastinal density obscures paratracheal stripe, azygos vein. Juxtraphrenic tenting/peaking of diaphragm from stretching of inferior accessory fissure or inferior pulmonary ligament. Usually from TB scarring, endobronchial tumour, mucous plugging. Peripheral atelectasis – rare, lobe collapses against lateral chest wall; more common in children.
  • Left upper lobe/lingular – Collapses anteriorly with density along anterior chest wall. Major fissure -> anterior. PA veiling haze fading laterally and inferiorly oblitering aortic knob, AP window, heart; apex lucent from hyperinflated superior LLL. Luftsichel sign – crescent of air along mediastinum/aortic arch = expanded superior LLL between arch and collapsed LUL laterally. Ascending aorta may be clearly visible due to herniated right lung anteriorly. Juxtraphrenic peak and peripheral atelectasis as per RUL collapse. Usually from scarring or endobronchial tumour.
  • Right middle lobe – Minor fissure -> inferiorly, major -> superiorly. PA vague density obscuring heart border with triangular density. Mild indirect signs. Usually cicatrization from infection with fibrosis and bronchiectasis.
    • Middle lobe syndrome – Chronic obstructive collapse from chronic inflammation with slow clearance due to collateral shift. Bronchiectasis, chronic bronchitis, pleural thickening.
  • Lower lobes – Collapses to mediastinum. Upper major fissure -> inferomedially, lower -> posteromedially. PA triangular opacity/sail sign (lat margin = major fissure), obscures diaphragm. If inferior pulmonary ligmant is not attached to diaphragm the lobe may form a rounded opacity against mediastinum. Obscured interlobar artery. Upper triangle sign – shadow from upper mediastinal shift displacing anterior junctional tissues. Flat waist sign – severe LLL collapse with displacement and rotation of heart flattening countour between aortic knob and MPA. RLL collapse usually from mucous plugs, foreign body, endobronchial tumour; LLL from cardiomegaly, postop esp CABG.
  • Combined RML and RLL – PA triangular opacity (superior border = depressed minor fissure) obscuring heart border and diaphragm extends to costophrenic angle. Obstructed bronchus intermedius from mucous plug or tumour.
  • Combined RUL and RML – Unusual, usually in neoplasm obstructing both bronchi.


Host defences at the pharynx, trachea and central bronchi. At small diatal bronchi and pulmonary parenchyma cellular and humoral immune system response -> pneumonia -> eradication or suppresion. Infection can occur via:

  • Trachebronchial tree with inhalation or aspiration:
    • Lobar/alveolar pneumonia – Typical of pneumococcus. Distal airspaces -> spread via pores of Kohn and canals of Lambert -> nonsegmental consolidation -> entire lobe. Larger bronchi usually spared forming air bronchograms, with volume loss unusual. Stages include:
      • Congestion – Red, heavy, boggy lungs from vascular engorgement, intra-alveolar fluid.
      • Red hepatization – Massive confluent exudate with neutrophils, red cells, fibrin filling alveolar spaces.
      • Grey hepatization – Resorption of red cells and persistence of fibrinosuppurative exudate.
      • Resolution – Enzymatic digestion of exudate leaving semi-fluid debris which is resporbed, ingested by macrophages, expectorated or organised by fibroblasts. Usually heals without sequalae. 90% in younger immunocompetent resolves by 2/52, delayed with advancing age. Hence generally follow-up (if required) in 6-8/52. 95% of pneumonia that hasn’t resolved in 1/12 has an underlying disease (esp emphysema, chronic bronchitis, bronchogenic carcinoma).
    • Lobular bronchopneumonia – Typical of staphylococcus. Lobular bronchi -> peripherally along bronchus -> other lobules causing ‘patchwork quilt’. Filling of airways, hence absence of air bronchograms, common segmental atelectasis. Tissue destruction with healing by scarring is common.
    • Interstitial pnuemonia (infectious bronchiolitis) – Typically viral (RSV, adenovirus), Mycoplasma, PCP; but may be from bacteria (TB, MAC, S.aureus, H.influenzae, bardatella) or fungi (aspergillus). Inflammatory thickening of bronchial and bronchiolar walls and pulmonary interstitium causing bronchial wall thickening and reticulonodular opacity, tree-in-bud (peribronchiolar inflammation). Alveolar spaces usually aerated, but atelectasis may occur from small airways obstruction. May progress to bronchopneumonia.
  • Pulmonary vasculature – From sepsis causing patchy and bilateral involvement worse at bases (dependent blood flow).
  • Direct spread from mediastinum, chest wall or upper abdomen.

In imunocompromised if:

  • Lobar/segmental consolidation – G-neg, G-pos, legionella
  • Nodules ± cavitation – staph, fungi, nocardia, legionella, neoplasm
  • Diffuse – PCP, viral, fungi, toxoplasmosis, strongyloides stercoralis, drug reaction, haemorrhage, radiation pneumonitis, NSIP, lymphangitic carcinomatosis.
  • Large nodules – fungi, nocardia

Pneumonia syndromes (clinical settings) include:

  • Community-acquired peumonia (CAP) – Often follows viral URTI. S.pneumoniae, H.infuenzae, M.catarrhalis, S.aureus, Legionella, Enterobacteriaceae, Pseudomonas.
  • Community-acquired atypical pneumonia – Moderate sputum but minimal consolidation, only moderate neutrophilia. Mycoplasma, viruses (RSV, parainfluenza, influenza A/B, adenovirus, SARS), chlamydia, Coxiella burnetii (Q fever).
  • Hospital-acquired (nosocomial) – G-neg rods, enterobacteriaceae, pseudomonas, S.aureus (MRSA).
  • Aspiration pneumonia – Anaerobic oral flora mixed with aerobic bacteria.
  • Chronic pneumonia – Mostly immunocompetent patients. Nocardia, actinomyces, granulomatous (TB, atypical mycobacteria, histoplasma, coccidiodes, blastomyces).
  • Necrotizing pneumonia and abscess – Anaerobic bacteria (very common), S.aureus, Klebsiella, Strep.pyogenes, type 3 pneumococcus
  • Pneumonia in immunocompromised – Humoral and innate immunodeficiency typically results in increased pyogenic bacterial infections. Cell-mediated immunodeficiency generally leads to increased infections of intracellular microbes (mycobacteria, herpesvirus) and low virulence organisms (PCP). 25% of lung disease is noninfectious. Most common diffuse disease from CMV, PCP, drug reaction. Focal disease from G-neg rods, S.aureus, aspergillus, candida, malignancy/NHL.
    • HIV risk of infection 6x normal, >/= 2 bacterial pneumonias/yr is an AIDS-defining illness. Highly active antiretrovial therapy (HAART) and prophylaxis has reduced opportunistic infections in HIV/AIDS, most are now bacterial. Most commonly H influenzae, S aureus, E coli, P aeruginosa; uncommonly Nocardia asteroides, Rhodococcus equi, Bartonella henselae, B.quintana (Bacillary angiomatosis). Cavitation more common than normal, may have multiple microabscesses. Generally TB and bacterial infections occur when CD4 counts are >200cells/mL, PCP may develop when CD4<200, CMV and MAI <50.
    • Immunodeficiency from renal transplants, corticosteroids commonly Legionella pneumophila and L micdadei.


  • Abscess – Tissue destruction and necrosis, esp type 3 pneumococci, Klebsiella, S.aureus, anaerobic organisms. May occur after aspiration (most common), complication of primary lung infection, septic embolism, neoplasia (10-15%, esp older patients) or direct spread. Primary cryptogenic lung abscesses has no known cause. May contain air if communicates with bronchial tree. Develops into gangrene of the lung with large multi-locular cavities. May extend into pleural caivty, bleed, spread with septic emboli elsewhere in body or rarely secondary amyloidosis. HPOA may develop within a few weeks.
  • Empyema
  • Bacteraemia with dissemination to heart valves, pericardium, brain, kidneys, spleen, joints.

Bacterial Pneumonia

Gram-positive bacteria:

  • Streptococcus pneumoniae/pneumococcus – Most common CAP, more common in elderly, alcoholics, compromised hosts (esp splenectomy). Usually lobar pneumonia with air bronchograms esp lower lobes or posterior segment upper lobes, rapid exudate formation. Cavitation rare (except serotype 3). Pleural effusions in 10%. Occasionally patchy lobular opacities (similar to bronchopneumonia), rarely reticulonodular pattern; may relate to preexisting lung disease, partial tratment or impaired immune response. In children may be spherical opacity = round pneumonia. Positive blood culture in 20-30%. Complete clearing with treatment in 2/52, in elderly/comorbidities 8-10/52.
  • Staphylococcus aureus – Most common in hospitalised/debilitated patients, haematogenous spread from endocarditis/IDC/IVDU/pacemaker wires, CAP complicating viral infection. Usually bronchopneumonia with confluent lobar opacification in severe disease. Bilateral in 40%. Abscess formation in 30%. Haematogenous seeding (septic emboli) -> multiple small poorly defined nodular opacities with peripheral and lower zone predominance (increased blood flow) -> sharply defined -> cavitate. Pleural effusions in 50%, half of these empyemas. Pneumatocoele (thin walls, rapid change in size in late phase of infection cf abscess) common in children -> pneumothorax.
  • Streptococcus pyogenes – Rare, viral infection or strep pharyngitis. Lobular or segmental lower lobe. Abscess, cavitation, empyema common.
  • Anthrax (Bacillus anthracis) – Sporulating bacillus. Naturally occuring inhalational anthrax rare. Haemorrhagic lymphadenitis (hilar enlargement), mediastinitis (mediastinal widening), haemorrhagic pleural effusions. Peribronchial opacity, dense (unenhanced) lymphadenopathy and effusions. Frank consolidation uncommon.

Gram-negative bacteria – 50% of nosocomial infections. Small ill-defined nodules to confluent/lobar, usually bilateral, multifocal, lower lobes. Abscess, cavitation, effusion common.

  • Klebsiella pneumoniae – Older alcoholic men, debilitated hospitalised patients, thick gelatinous sputum. Homogeneous lobar with bronchograms, increased volume of lobe (exuberate exudate, bulging fissure). Pulmonary gangrene (arteritis and vascular thrombosis) uncommon.
  • Other enterobacteriaceae (Escherichia coli, Proteus)
  • Haemophilus influenzae – Common CAP, increased risk with COPD (most common exacerbation), alcoholism, diabetes, splenectomy. Normal colonizer of pharynx. Bronchitis, may -> bilateral lower lobe bronchopneumonia. Paediatric pneumonia has high mortality.
  • Pseudomonas aeruginosa – Most common hostpital-acquired infection, debilatated, mechanical ventilation, CF. High mortality. Inhalation -> patchy consolidation, abscess common. Haematogenous -> diffuse, bilateral ill-defined nodules. Small effusion common.
  • Legionnaires disease (Legionella pneumophila) – G-neg bacillus in air conditioning/humidifiers, older men, COPD or malignancy, nosocomial in immunocompromised/renal failure/malignancy. Peripheral -> sublobar -> lobar/multilobar consolidation, occasionally round pneumonia. Effusion in 30%. Cavitation only in immunocompromised. Radiogaphic resolution is prolonged and lags clinical resolution.
  • Pittsburgh pneumonia (Legionella micdadei) – Immunocompromised. Multiple well-circumscribed centrally cavitating nodules.

Anaerobic bacteria usually from aspiration, G-neg bacilli (Bacteroides and Fusobacterium), majority polymicrobial. Dependent distribution (supine posterior ULs and superior LL; erect basal segments of LLs). Peripheral lobular and segmental shadowing. Cavitation common. Abscess and empyema in up to 50%.

Atypical bacterial infections:

  • Mycoplasma – Bacterial and viral characterstics. 10-30% of CAP. 2-3/52 subacute illness. Occasional otitis media and rash. May cause local epidemics in closed communities. Interstitial inflammation -> patchy segmental opacity -> lobar consolidation. Tree-in-bud. Often unilateral, lower lobes. Radiographic resolution 4-6/52.
  • Actinomycosis israelii – Anaerobic G-pos in oropharynx flora, causes infection in devitalised/infected tissue. Commonly after dental extractions (mandibular osteomyelitis, soft tissue abscess). Aspiration of infected debris or direct extension. Peripheral LL opacity, occasionally mass-like. Disregards anatomical barriers with extension to pleura (empyema), chest wall (abscess, rib osteomyelitis). Chronic -> extensive fibrosis. Rarely miliary dissemination.
  • Nocardia (usually N asteroides) – Branching filamentous bacillus, opportunistic in immunosuppresed and alveolar proteinosis. Homogeneous nonsegmental opacity/mass. Cavitation and LN frequent. May -> empyema, osteomyelitis.
  • Mycobacterium Tuberculosis (TB) – Aerobic acid-fast bacillus. Cell-mediated/delayed hypersensitivity immunity. In immunocompromised tests are less sensitive. In TB findings depend on immune dysfunction estimated by CD4 count (>200 postprimary; 50-200 consolidation, rim enhancing lymphadenopathy, effusion; <50 diffuse reticular or nodular/miliary). Tree-in-bud suggests active endobronchial spread, seen in 70% of active TB with caseous material in and around bronchioles. Other signs of active disease include consolidation, miliary disease or cavities. Inactive disease if unchanged over 6/12, calcified nodules, linear opacities, bronchiectasis.
    • Primary TB – Classically disaese of childhood, increasing incidence with HIV epidemic. Droplet nuclei inhaled -> implant subpleurally (usually midzone) -> initial unchecked replication (<3/52, may dissemiate to multiple sites) -> T-cell response after 3/52 -> macrophages transform to bacteriocidal epithelioid cells (may fuse to form giant cells) -> aggregate into granulomas with central caseous necrosis -> may drain to regional nodes with caseation. Contained by granulomatous response, with most asymptomatic and completely resolve. Gohn focus is the parenchymal lesion, Gohn complex combined with the regional LN, Ranke complex when these undergo fibrosis and calcify (95%). 90-95% of children, and 10-30% of adults (esp if immunocompromised) have lymphadenopathy (may be only sign), usually unilateral hilar R>L, may have low density centre and peripheral enhancement. The initial haematogenous dissemination -> microscopic foci to high partial pressure O2 regions (apices, renal medullae, bone marrow), only when they coalesce to they become macroscopically visible with calcifications; clinically silent serving as reactivation source.
    • Progressive primary TB (most infants) – Local parenchymal progression with lower/middle lobe consolidation, hilar adenopathy (usually unilateral), pleural effusion (may be seen without lung disease). Cavitation is uncommon. Endobronchial spread with tree-in bud, multifocal in 25%, bilateral in 10-15%. Unilateral effusion in 25%. Empyema may spread to extrapleural collection (empyema necessitans). Slow radiographic resolution, heals with calcification. Lymphohaematogenous dissemination may lead to meningitis, miliary TB. Tuberculoma – Discrete 5-40mm well-defined nodule more common in postprimary TB than primary, usually upper lobes, satellite nodules common (galaxy sign).
    • Postprimary/secondary TB – Weakened host defences (aging, EtOH, diabetes, cancer, HIV) with reactivation of latent infection or exogenous reinfection. Cough and constitutional Sx, may be asymptomatic or insidious. Reactivation in areas of high oxygen tension (Assmann focus) including apical and posterior segment UL, superior LL with prompt and marked tissue response (pre-existing hypersensitivity). Ill-defined patchy/nodular opacities. In immunocompetent there is progressive fibrosis leaving a fibrocalcific scar. In elderly and immunsuppressed, may become progressive. Tissue destruction and cavitation is common (indicates active transmisible disease), may -> transbronchial spread -> tree-in-bud with multifocal bronchopneumonia. Lymphadenopathy uncommon unless immunocompromised. Pleura is almost always eventually involved after parenchymal disease (rare without cf primary TB) with serous pleural effusions, tuberculous empyema or obliterative fibrous pleuritis. Erosion into PA -> Rasmussen aneurysm -> haemoptysis. Usually ABs -> granulomatous control -> fibrosis, bronchiectasis, volume loss/cicatrizing atelectasis. Late complications include interstitial fibrosis, haemoptysis/bronchiectasis, mycetoma in TB cavity, erosion of broncholith (calcified peribronchial LN) into bronchus, bronchostenosis (healed endobronchial TB). In those with advanced immunosuppression it resembles progressive primary TB.
    • Isolated tuberculosis – Secondary infection in any organ that the disease was initially spread to. Commonly tuberculous meningitis, renal TB, adrenals (Addison disease), osteomyelitis, vertebrae (Pott disease with paraspinal ‘cold’ abscesses tracking along tissue planes), fallopian tubes (salpingitis).
    • Miliary TB – Haematogenous dissemination of primary or reactivation, diffuse bilateral randomly distributed 2-3mm nodules. Involves any organ, but commonly involves lung, liver, bone marrow, spleen, adrenals, meninges, kidneys, fallopian tubes, epididymis. Patient will be unwell with high mortality. DDx metastases (thyroid, melanoma), silicosis (upper zone predominance), chickenpox/varicella (dense calcifications).
  • Nontuberculous mycobacteria – M avium-intracellulare (MAI), M Kansasii, M.gordonae. No/rare pleural effusion. 3 forms of disease including:
    • Fibrocavitary (classic) – Esp elderly males with underlying lung disease (COPD, fibrosis), AIDS, chronically ill. Upper lobes with apical and posterior segment consolidation, cavities, scars, linear/nodular opacity ± calcification. Similar to secondary TB, but slower progression.
    • Airways disease (non-classic, Lady Windermere) – Elderly Caucasian women with no underlying lung disease. Bronchiectasis, centrilobular nodules, tree-in-bud. All lobes but esp RML and lingula.
    • Resembling HP with GGOs, centrilobular nodules, air trapping.

Viral Pneumonia

Common URTI, uncommon pneumonia (also uncommon in AIDS). Diagnosis of exclusion, CXR nonspecific with bronchopneumonia or interstitial pneumonia, patchy opacities, bronchial wall thickening, tree-in-bud. Usually complete resolution, occasionally bronchiectasis, bronchilitis obliterans (may -> unilateral hyperlucent lung/Swyer-James syndrome), interstitial fibrosis.

  • Influenza – Severe haemorrhagic pneumonia may occur in elderly, cardiopulmonary disease, immunocompromise, pregnancy. Patchy LL opacity. Children often interstitial reticulonodular. Lobar consolidation, effusion or cavitation suggests superinfection with Strep or Staph.
  • Respiratory syncytial virus (RSV) and parainfluenza virus – Common in children, in adults usually debilitated/immunocompromised.
  • Varicella-zoster (chicken-pox, shingles) – Can be severe in adults (esp immunocompromised, lymphoma). Diffuse bilateral ill-defined 5-10mm nodules. Usually completely resolves, occasionally involutes and calcifies (innumerable 2-3mm foci).
  • Adenovirus – Usually causes overinflation, bronchopneumonia, lobar atelectasis. In children lobar/segmental consolidation.
  • Severe acute respiratory syndrome associated coronavirus (SARS-CoV) – Nonspecific findings, causes SARS. Uni/bi-lateral peripheral/lower zone opacity -> central lungs. LN and effusions uncommon.
  • Cytomegalovirus (CMV) – Common with cell-mediated immunodeficiency (renal transplant, lymphoma), uncommon in AIDS. Diffuse reticular/nodular LL opacities.

Fungal Pneumonia

Fungi elicit necrotising granulomatous reactions. High mortality with untreated invasive infection. Confirmation made with serological assays (complement fixation, immunodiffusion), histology.

  • Histoplasmosis (Histoplasma capsulatum) – Usually asymptomatic or flu-like Sx. Ohio and Mississippi rivers, Caribbean. Inhalation of spore contaminated dust with bird/bat droppings. Intracellular parasite of macrophages. Nonspecific subsegmental opacities ± LN, if large inoculum > 3-4mm nodules with adenopathy; or solitary <30mm nodule (histoplasmoma, common LL, frequently calcifies). Old = multiple <10mm calcified nodules ± LN calcification (concentric with tree-bark appearance). Spread is similar to TB. In emphysema -> uni/bi-lat UL cicatrising atelectasis, fibrocavitary disease, fibrosing mediastinitis, bronchostenosis. Asymptomatic haematological spread common (-> calcifying granulomas). Fulminant disseminated histoplasmosis in immunosuppressed without granuloma formations.
  • Coccydioidomycosis (Coccidioides immitis) – Aucte (40%), self-limiting; ‘valley fever’ if with erythema nodosum/multiforme and arthralgia. Soutwest/west USA and Mexico. Almost all who inhale the spores become infected and develop a delayed-type hypersensitivity reaction (organism blocks fusion of phagosome with lysosome). CXR normal or segmental opacities resolving over several months. Occasional lymphadenopathy and effusion. Persistent coccidoidomycosis if symptomatic/radiographic >6-8/52 with nodules/masses (coccidioidomas, round pneumonia esp subpleural UL, may -> thin-walled cavities), consolidation, miliary nodules. Chronic progressive -> UL fibrocavitary disease. Disseminated/miliary type rare, but typical in immunocompromised with miliary nodules, diffuse nodules or reticulonodular opacities.
  • Blastomycosis (Blastomyces dermatitidis) – Central/southeast USA, Canada, Mexico, Middle East, Africa, India. Chronic systemic esp lungs and skin. Lungs often assymptomatic or pneumonia-like. Nonspecific homogeneous nonsegmental opacity esp UL, mass(es) (esp if Sx >1/12) cavitating in 15%, or diffuse reticulonodular opacity. Effusions and LN uncommon. Disseminated miliary in immunocompromised.
  • Aspergillus (A. flavus, A. niger)
    • Allergic bronchopulmonary aspergillosis (ABPA) – Hypersensitivity to aspergillus in airway. Usually young adults with asthma/atopy. Central varicose or cylindrical bronchiectasis in upper zones, occasionally air-fluid levels in airways, mucoid impaction (finger-in-glove, tree-in-bud), plugs may be high density (calcium oxalate concentrates in fungus), surrounding GGO/inflammation, fleeting peripheral/parahilar consolidation, atelectasis (from mucous plugs).
    • Aspergilloma (mycetoma, fungus ball) – Ball of hyphae, mucus and debris in preexisting cavity (TB, sarcoid; less commonly bullae, bronchiectasis, abscess). Colonisation with no invasion, but may progress to invasive in immunocompromise. Usually asymptomatic, or haemoptysis (may be massive). Usually upper lobes. Air cresent separates from cavity wall, can roll dependently, may not see if fungal ball completely fills the cavity. Pleural thickening may be the earliest sign. Suspect invasion if there is thickening of the cavity wall.
    • Semi-invasive (chronic necrotising) aspergillosis – Mildly impaired immunity. Invasion into previously diseased tissue -> slowly progressive opacity or chronic cavitation.
    • Invasive pulmonary aspergillosis – Neutropenic lymphoma/leukaemia, chemotherapy or corticosteroids, terminal AIDS; uncommonly milder compromise (COPD, ILD). Large nodular opacities to diffuse consolidation (most opacity is haemorrhage and oedema). Effusion usually empyema. Cavitation/air crescent indicates neutrophils returning to normal. Angioinvasive aspergillus invades vessels causing thrombosis, haemorrhage, infarction; causing peribronchial consolidation/GGO, occasionally pleural wedge-shaped consolidation, may cavitate. CT halo sign with density (necrotic lung from septic infarction) surrounded by GGO reduced attenuation (oedema and haemorrhage); very suggestive in the setting of immunocompromise. DDx other angioinvasive fungal infection (mucormycosis, candidiasis, coccidiodomycosis), haemorrhagic mets, Wegeners. May see air cresent sign from retracted infarcted lung within a cavity.
  • Cryptococcosis (Cryptococcus neoformans) – May affect any immunocompromised patient. Budding yeast common in soil and bird droppings. Disseminates from lungs to CNS, bones, mucocutaneous tissues. Single/multiple nodules/masses (mimics carcinoma), single/multiple patchy airspace opacities, or multiple small/miliary nodules. Cavitation, lymphadenopathy and pleural effusions more common in AIDS.
  • Candidiasis (Candida albicans) – Unusual, in immunocompromised with severe neutropenia. Common coloniser in immunocompromised. Diffuse bilateral nonsegmental airspace/interstitial opacities.
  • Mucormycosis – Rare, in immunocompromised patients with lymphoma, leukaemia, diabetes. Usually assciated with paranasal sinus infection. Solitary nodule/mass or focal airspace opacity.
  • Pneumocystis jiroveci pneumonia (PCP, previously P carinii) – Common in lungs, but pneumonia only in immunocompromised esp late AIDS with CD4<200, reduced with HAART and trimethprim prophylaxis. CXR normal early in disease, interstitial pneumonia with fine reticular/linear perihilar opacities, GGO (perihilar or diffuse), interlobular septal thickening, crazy paving. If untreated -> confluent symmetric airspace opacification. Thin-walled cysts/pneumatocoeles in 10-30%, usually upper lobes, may -> pneumothorax or bronchopleural fistula. Atypical features (in 10%) include upper lobe predominance, focal/asymmetric consolidation, nodules ± cavitation, miliary pattern, pleural effusions, lymphadenopathy. Systemic pneumocystis involves liver, spleen, kidney, LN with microabscesses or punctate calcifications.

Parasitic Infection

Uncommon. May elicit eosinophilic pneumonia.

  • Amebiasis (Entamoeba histolytica) – Usually confined to GIT and liver ± inflammatory R pleural effusion, atelectasis. May directly extend from hepatic abscess -> empyema or RLL amebic pneumonia/lung abscess.
  • Hydatid/Echinococcosis disease of the lung (Echinococcus granulosus most common) – Usually dogs definitive hosts -> sheep intermediate. Humans are accidental intermediate hosts with ingestion of eggs -> hatch in duodenum forming larvae -> liver and lungs -> encyst and enlarge. Pericyst (fibrotic lung), exocyst (chitinous layer) and inner endocyst (produces daughter cysts). Well-circumscribed, 10-200mm, spherical, no wall calcification (cf liver). Usually asymptomatic. Pericyst rupture -> meniscus/cresent sign of peripheral air, air-fluid level. Occasional crumpled floating wall in uncollapsed pericyst (sign of the camalote or water lily sign). Rarely ruptures into pleural space -> large effusion.
  • Schistosomiasis (Schistosoma mansoni, S. japonicum, S. haematobium) – Blood flukes, aquired via contact with infected water. Larvae -> skin/oropharyngeal mucosa -> veins -> pulmonary capillaries (-> allergic response -> transient opacities/eosinophilic pneumonia) -> systemic circulation. S. japonicum and S.mansoni -> mesenteric venules; S haematobium -> bladder venules. Mature flukes -> ova which may embolise to lungs, implanting at small arterioles -> granulomatous inflammation and fibrosis (miliary nodules) -> obliterative arteriolitis -> PAH and cor pulmonale (diffuse reticular with enlarged PAs).
  • Toxoplasmosis (Toxoplasma gondii) – Obligate intracellular, from cats, infection via ingestion of contaminated oocyst-containing stool. ?Chronic asymptomatic form in 50% of population. Pulmonary disease in immunocompromised with diffuse reticular opacities, less commonly airspace filling. Lymphadenopathy common, pleural effusion rare.
  • Paragonimiasis (Paragonimus westermani) – Predominately east Asia, acquired by eating raw crabs or snails. Asymptomatic or haemoptysis, fever/SOB. CXR normal in 20%, or multiple cysts of variable thickenss may become confluent associated with atelectasis/consolidation. Dense linear opacity represent burrows of the organism. Flukes may penetrate pleura -> effusion (common), may be massive.

Pulmonary Oedema

Fluid accumulation exceeds lymphatic drainage of the interstitium (axial and peripheral), first in interstitium, corners of alveolar spaces then flooding of alveoli (impairing gas exchange). From change in Starling forces (increased capillary hydrostatic pressure in LVF, reduced plasma oncotic pressure in hypoalbuminaemia, or reduced interstitial hydrostatic pressure), absence or obstruction of lymphatics, or damage to capillary/alveolar endothelium increasing permeability to protein-rich fluid.

  • Interstitial oedema – Indistinct vascular shadows, peribronchial cuffing and tram-tracking (axial interstitium), perihilar and lower zone ground glass (alveoli walls), Kerley A (central), B (peripheral), and C (network) lines (interlobular septal thickening), thickening of fissures (subpleural oedema in innermost/interstitial layer of visceral pleural).
  • Airspace oedema – Typically symmetrical coalescing nodules in mid and lower zones, Bat’s wing/butterfly/perihilar shadowing (uncommon, unknown reason), centrilobular airspace nodules -> dense opacification. May be assymetrical depending on positioning, reduced flow to one lung (PA hypoplasia, PE, extrinsic compression; this lung is ‘protected’), obstruction to lymphatic or venous drainage. RUZ in severe MR due to preferential regurgitant flow from posterosuperiorly orientated mitral valve. In COPD blood flow is obliterated (thus spared) around bullae (usually apices; simulating necrotizing pneumonia of pneumatocoele with surrounding alveolar shadowing).
  • Cardiomegaly, pulmonary venous distension and pleural effusions in cardiogenic or fluid overload oedema.
  • Re-expansion pulmonary oedema from rapid evacuation of pleural effusion/pneumothorax.

Causes: Haemodynamic oedema includes hydrostatic oedema and reduced oncotic pressure.

  • Hydrostatic pulmonary oedema – Pulmonary venous hypertension -> increased capillary pressure. From LVF (N or enlarged heart), mitral stenosis/insufficiency (LA enlargment), obstructed LV outflow (coarctation or AS with normal or enlarged heart; hypoplastic LV), LA myxoma (big LA), cor triatriatum, central obstruction (mediastinitis, pulm v. stenosis/thrombosis; normal size heart) or obstructed intrapulmonary veins (pulm veoocclusive disease; normal size heart and central vv, PAH). Pleural effusions larger on the right. Widened vascular pedicle from increased blood volume (width at SVC/L subclavian a >53mm on PA). Reduced lung volumes due to reduced compliance from oedema. Clears in <3/7 with resolution peripheral -> central. Normal pulmonary capillary wedge pressure (PCWP) with flow-directed balloon occlusion (Swan-Ganz) catheters is 8-12mmHg.
    • Stage 1 – Mild elevation in PCWP (10-20mmHg) -> enlarged pulm v, constricted lower lobe vessels -> cephalization/redistribution to upper zones (debatable, also seen in L>R shunts, basal lung disease).
    • Stage 2 – Moderate (20-25mmHg) -> interstitial oedema, septal lines.
    • Stage 3 – Severe (>25mmHg) -> alveolar oedema. Evenly distributed oedema central -> peripheral in lower zones (cf capillary permeability typically more peripheral).
    • Stage 4 – Chronic or severe (>30-35mmHg) -> extravasation of red cells in the oedema causes haemosiderosis (in macrophages = heart failure cells), pulmonary ossification, chronic interstitial disease.
  • Increased capillary permeability (lung injury oedema, acute lung injury ALI) – Interstitial protein leak from damaged endothelium and/or epithelium with lung stiffness/non-compliance. Acute respiratory distress syndrome (ARDS) is severe ALI; diffuse alveolar damage (DAD) is the histological manifestation. ?Activated neutrophils in lungs -> enzymes and oxygen radicals -> endothelial damage -> DAD. From shock, major trauma/surgery, burns, sepsis (esp G neg), narcotic overdose, pancreatitis, DIC, inhalational injury (NO2 = silo-filler’s disease, hydrocarbons, smoke, chlorine, oxygen), aspiration (near drowning, gastric fluid = Mendelson syndrome), fat emboli, amniotic fluid emboli. Distinguished from hydrostatic oedema due to normal PCP and protein-rich transbronchial sampling, more peripheral oedema. Pneumonia should be suspected if focal area or effusion develops. Pneumomediastinum and pneumothorax may develop after +ve ventilation to stiff lungs. Acute interstitial pneumonia (AIP, idiopathic ALI-DAD) is widespread ALI with a rapidly progressive course and high mortality of unkown aetiology, uncommon M=F peak 50yo.
    • Stage 1 ARDS (12-24hrs) – Engorged capillaries, proteinaceous interstitial oedema, patchy peripheral opacities.
    • Stage 2 (1st week) – Injury to type I pneumocytes -> flooding of alveoli with coalescing opacity and air bronchograms -> hyaline membranes line distal airways and alveoli.
    • Stage 3 (after positive ventilation or >7 days) – Type II pneumocytes proliferate to reline surfaces (give rise to type I cells), alveolar infiltrates improve. Fibroblastic/collagenous tissue proliferates leaving minimal to extensive interstitial fibrosis. Reticulonodular pattern may resolve over several months, or remain unchanged leaving irreversible fibrosis.
  • Neurogenic oedema – Mixed hydrostatic and increased permeability oedema. From head trauma, seizure. Raised intracranial pressure -> systemic vasoconstriction and increased venous return -> increased LV diastolic pressure and hydrostatic oedema; but protein rich oedema with normal PCWP.
  • High-altitude oedema – Rapid ascent >3,500m, developing <48-72h. Hypoxaemia -> scattered PA spasm -> transient PAH -> overflow of blood to uninvolved areas -> endothelial injury -> leak. Rapid resolution (24-48h) with O2 or return to sea level.
  • Re-expansion oedema – Prolonged lung collapse >48hrs -> hypoxaemia -> anaerobic metabolism -> free radicals. Reperfusion on re-expansion -> injury and permeability oedema. Reduced with slow (24-48h) expansion, O2.
  • Acute upper airway obstruction – Marked negative intrathoracic pressure -> transudation of fluid into lungs.
  • Amniotic fluid embolism – Obstruction by mucin and fetal squames in amniotic fluid -> sudden PAH and cor pulmonale -> reduced cardiac output -> oedema. Anaphylactoid reaction and DIC contributes to shock. Bilateral confluent opacity, enlarged PAs and R heart (if severe). Confirmed by faetal squames and mucin in PA catheter samples.
  • Fat embolism – Marrow fat embolised 24-72 hrs after long bone fracture. In lung fat is hydrolysed -> fatty acids -> injury with capillary leak and haemorrhagic pulmonary oedema. Confluent GGO and airsapce opacity. Systemic fat embolism syndrome – petechial rash, CNS depression, pulmonary change. Most mild, only a minority -> death.
  • Reduced capillary oncotic pressure (hypoalbuminaemia) – Not considered an independent risk factor (but is cofactor in other conditions).

Pulmonary Haemorrhage

Massive haemoptysis is >600mL/24h. Usually intermittent (rapid development and improvement), anaemia, haemoptysis not always present, haemosiderin-laden macrophages in sputum or BAL. Normal or elevated DLCO (carbon monoxide-diffusing capacity) when cf pneumonia/oedema, due to extravascular gas-exchanging RBC. PAs rarely source of haemoptysis (except aneurysms and PAVMs), usually from enlarged/abnormal bronchial aa. Hypervascularity, systemic to PA/PV shunts.

Focal pulmonary haemorrhage from bronchiectasis, vascular malformation, bronchitis, carcinoma, PE, fat embolism, infection (invasive aspergillosis, mucormycosis, Pseudomonas, influenza, TB), trauma/contusion.

Diffuse pulmonary haemorrhage causes acute assymetric bilateral diffuse GGO/consolidation with basal predominance. Characteristic sparing of peripheries and costophrenic angles. After a few days interlobular septal thickening from accumulation of haemosiderin-laded macrophages, causing crazy-paving. Resolution in 7-14 days; slower than oedema but faster than infection. Recurrent haemorrhage -> persistent reticulation, hypertrophy of type II pneumocytes -> fibrosis. Causes include:

  • Goodpasture syndrome – Autoimmune against renal glomerular basement membrane with cross-reaction to alveolar basement membrane causing rapidly progressive glomerulonephritis and necrotizing haemorrhagic interstitial pneumonitis. 10s-20s, M>F, 90% are active smokers. Cough, haemoptysis, dyspnoea, fatigue; pulmonary Sx prior to renal failure. Poor prognosis, Tx immunosuppressants and plasmapheresis (removing anti-GBM antibodies and chemical mediators).
  • Vasculidities – Small vessel arteritis and capillaritis -> spontaneous haemorrhage. Wegener granulomatosis, PAN, Churg Strauss.
  • Other causes – SLE, RA, drug reactions (penicillamine), bleeding diathesis.
  • Idiopathic pulmonary haemosiderosis – Rare intermittent diffuse alveolar haemorrhage in children of unknown aetiology. Clinically and radiologically similar to Goodpasture syndrome. Common in children. Diagnosis of exclusion with normal renal function and absent anti-GBM antibodies. Tx immunosuppression.


  • Aspiration pneumonitis – ‘Pure’ form without infection. Gastric fluid is highly irritating, stimulates explosive coughing, damage to bronchiolar and alveolar walls. More severe if pH <2.5, large volume, particulate matter (may elicit granulomatous reaction), young. Mendelson syndrome – massive aspiration of gastric contents. May cause extensive bilateral consolidation, diffuse discrete nodules, or irregular opacity not obviously in airspaces. Most basal, posterior and perihilar. Atelectasis from airway obstruction. May worsen over a few days before rapid improvement; if continues to worsen suggests infection/ARDS/PE.
  • Aspiration pneumonia – Mixed anaerobic infection from infected oropharyngeal contents.
  • Chronic aspiration pneumonitis – Repeated over months-years. Irregular reticular interstitial opacities (peribronchial scarring), reticulonodular pattern (granulomas around food particles) seen between episodes of acute aspiration.
  • Exogenous lipid pneumonia – Aspiration of lipid material (esp older patients with swallowing disorder or GOR ingesting mineral oil laxative or inhaled oily nose drops). Multifocal consolidation/masses of fat attenuation.


  • Pulmonary contusion – From blunt trauma adjacent to impact. Blood and oedema fill alveoli within 12hrs causing scattered consolidation, may rapidly coalesce (DDx aspiration). Stabilisation by 24hrs, improvement within 2-7 days.
  • Laceration – Shearing injury to parenchyma with elastic properties of lung transforming linear defect into rounded air cyst/pneumatocoele. May fill with blood creating air-fluid level or fill completely (pulmonary haematoma). Tends to shrink over weeks-months.

Eosinophilic Lung Disease

(Pulmonary eosinophilia, eosinophilic pneumonia).

Idiopathic eosinophillic lung disese: Allergy with excessive eosinophils ± blood in pulmonary interstitium and air spaces.

  • Acute eosonophilia – Abrupt onset respiratory failure of unknown cause, <40yo, no association with asthma. Diffuse pulmonary infiltrates. Prompt response to corticosteroids and doesn’t recur.
  • Simple pulmonary eosinophilia (Loffler syndrome) – Transient eosinophilic exudate, most patients have Hx of allergy esp asthma. Dry cough, SOB, eosinophilia. Peripheral, homogeneous, illdefined consolidation parallel to chest wall, septal thickening, fleeting/migratory (rapid clearing with new involvement in other areas). No vasculitis, fibrosis or necrosis. Most self-limiting in 4/52.
  • Chronic eosinophilic pneumonia – Sx/findings similar to Loffler syndrome, but last for >1/12. F>M. Reverse batswing pattern with peripheral consolidation/GGO, usually upper zone predominance. Improve within 4-7/7 with corticosteroids (with linear/band-like opacities), but relapse on discontinuation is common. Diagnosis of exclusion.
  • Hypereosinophilic syndrome – M>F, multiple organ damage from eosinophilic infiltration. Eosinophilia is prolonged and marked. Cardiac involvement with CHF, cardiomegaly, oedema, pleural effusions. Interstitial or airspace opacities.

Secondary eosonophilia:

  • Drugs include ABs (penicillins, nitrofurantoin), sulfasalazine, NSAIDS, aspirin, chemotherapy (bleomycin, methotrexate).
  • Tropical eosinophilia – Exaggerated response to parasites, with pulmonary eosinophilia as they migrate through alveolar capillaries into alveoli, indistinguishable from Loffler syndrome. Includes filaria, Ascaris lumbricoides, Strongyloides stercoralis, hookworm. May also occur in TB.
  • Associated with autoimmune diseases – Wegener granulomatosis, sarcoidosis, rhematoid lung disease, polyarteritis nodosa (haemorrhage from bronchial vasculitis). Allergic angiitis and granulomatosis (Churg-Strauss syndrome) is asthma, blood eosinophilia, necrotising vasculitis, extravascular granulomas and pulmonary involvement; indistinguishable from chronic eosinophilic pneumonia.

Pulmonary Alveolar Proteinosis (PAP)

Rare, lipoproteinaceous surfactant deposits within airspaces and bronchiolar spaces that stains deep pink with periodic acid-Schiff. M:F 4:1. Insidious onset, may be over years. Bilateral symmetric geographic perihilar consolidation/ground-glass with thickened interlobular and intralobular septa (crazy paving, DDx pulmonary oedema esp permeability, atypical pneumonia, haemorrhage, rarely AIS), airspace nodules at periphery of the opacity. Absent cardiomegaly, pleural effusions. Prone to superinfection with Nocardia, Aspergillus, Cryptococcus, atypical mycobacteria. Tx whole lung bronchoalveolar lavage (BAL) reducing mortality (from 1/3 untreated).

  • Acquired/idiopathic PAP (>90%) – ?Anti-granulocyte-macrophage colony-stimulating factor (GM-CSF) antibody, impairing surfactant clearance by alveolar macrophages. Typically males 20-50yo.
  • Congenital PAP – Rare neonatal respiratory distress. Genetic defect causing accumulation of intra-alveolar surfactant. Death in 3-5/12 without lung transplant.
  • Secondary PAP – Uncommon, associated with acute exposure to large amounts of silica dust (acute silicoproteinosis) and other inhalational diseases, immunocompromise (lymphoma, leukaemia, AIDS), malignancy, haematopoietic disorders.

Alveolar Microlithiasis

Rare, deposition of minute <1mm calcium phosphate calculi (calcospherites) in alveolar spaces. Strong FHx. Most develop progressive respiratory insufficiency. Alveoli otherwise normal, but interstitial fibrosis may develop if long-standing. Black pleura sign at interface with chest wall due to high density. Apical bullae common. No effective Tx.

Pulmonary Complications with Bone Marrow Transplant (BMT)

40-60% of patients receiving BMT have pulmonary complications, disease depending on phase:

  • Neutropenic phase (0-30 days) – Pulmonary oedema, alveolar haemorrhage, fungal infection, drug reaction.
  • Early phase (30-100 days) – Fungal infection, drug reaction, CMV, viral URTI, idiopathic pneumonia, acute graft-versus-host disease.
  • Late phase (>100 days) – Bronchiolitis obliterans, COP, chronic graft-versus-host disease, viral URTI (up to 6/12), idiopathic pneumonia (up to 6/12).