Secondary pulmonary lobule (SPL) is the elemental unit of lung function.

• Each SPL is b/n 1 -2.5 cm in diameter and contains a centrilobular artery and a central bronchus, each branching many times to ultimately produce acinar arteries and respiratory bronchioles.

  • CT: centrilobular artery is often visible as a faint dot, bronchus is NOT visible

  • Acinus is basic unit of gas exchange containing several generations of branching respiratory bronchioles, alveolar ducts, and alveoli.

  • Generally 12 or fewer acini per secondary lobule.

• Pulmonary veins and lymphatics collect in the periphery of each SPL.

• Connective tissue (interlobular septa) encases each SPL.

  • Thickening of the interlobular septa can be seen on CT and suggests pathologic enlargement of either the venous or lymphatic spaces.

Incomplete expansion of all (complete) or part of the lung w/ corresponding diminution in lung volume.

Causes:

• Bronchial obstruction

• Mucus plugging

• External compression (small lung volumes, pleural effusions)

Air bronchograms are NOT seen in atelectasis when the cause is central bronchial obstruction. Can be seen w when cause is external compression.

Consolidation  can be described on radiograph or CT; ground glass (GG) is reserved for CT. 

Although consolidation implies PNA, both consolidation and GG are nonspecific findings w a broad differential depending:

• Chronicity: acute vs chronic

• Distribution: focal vs patchy or diffuse

Alveolar filling process that produces increased pulmonary density or attenuation 2/2 blood, pus, water or cells (neoplastic or inflammatory).

• Pulmonary vessels are NOT visible 

• +/- Air bronchograms represent a lucent air-filled bronchus/bronchiole w/n a consolidation and are often present if airway is patent.

• +/- intrinsic cavitation

• Consolidation causes silhouetting of adjacent structures on xray.

• Consolidations in adults should be followed to complete imaging resolution to exclude underlying malignancy.

Distribution

• Lobar

• Multilobar

• Diffuse

• Multifocal

Mechanisms

• Partial alveolar filling w/ blood, puss, water, cells &/or collapse (atelectasis)

• Interstitial/ alveolar wall thickening

• Increased blood volume

• Combo of the above 

CT shows hazy gauze-like opacity through which pulmonary vessels are still visible.

Acute GGO ddx is similar to consolidation since many of these entities can cause partial airspace filling which progresses to completely fill the airspaces later in dz. Chronic GGO has similar but broader ddx compared to chronic consolidation. 

Opacities located w/n 1-2 cm of pleural surfaces; AKA subpleural. Associated findings can help narrow DDX. 

• UIP and NSIP: peripheral and basilar reticular opacities +/- honeycombing, traction bronchiectasis/bronchiolectasis.

• Chronic eosinophilic PNA: upper-lobe predominance, can be migratory

• Organizing PNA: can be associated w/ infection, medications, and inflammatory conditions, or may be cryptogenic.

• Pulmonary infarction: consolidation w intrinsic lucencies and pleural embolism; often associated w chest pain

• Pulmonary contusion: other trauma related abnormalities; FX, PTX

• Alveolar sarcoidosis: mediastinal/hilar LAD

Intralobular lines: fine linear opacities identified w/n confines of SPL.

• There are no intralobular septa!

• Parenchymal (intralobular) interstitium: interstitial network of thin CT fibers in alveolar walls; supports SPL. 

• Combine IST and intralobular lines = reticular opacities.

IST w/ superimposed GGO thought to resemble the appearance of a stone path.

Nonspecific but first described for alveolar proteinosis, where GGO is caused by filling of alveoli by proteinaceous material and the IST is caused by lymphatics taking up the same material.

DDX

• Pulmonary edema (MCC)

• Hemorrhage

• ARDS

• Pulmonary alveolar proteinosis: idiopathic dz characterized by alveolar filling by proteinacous substance.

• Pneumocystic jiroveci PNA

• Adenocarcinoma (uncommon cause)

• Lipoid PNA: inflammatory PNA caused by rxn to aspirated lipids.

• Micronodules (<3 mm) have a 0.2 % chance of being CA, 4-7 mm nodule is malignant in 2.7% of cases.

• Oblong, polygonal, triangular,  flat, or geometric in shape, typically intrapulmonary LNs

• Subpleural location

• Clustering nodules suggests an infectious process

• Large size (most important RF) regardless of morphology: 

  • 0.8-3 cm nodules have 18% risk of being lung CA

  • Masses >3 cm have a high chance of being malignant

• Irregular edge of spiculated margins

• Ground glass nodules (mixed attenuation nodules containing both solid and GG) are more likely to be malignant than a solid nodule.

• A cavitary nodule or nodule containing small cystic spaces is suspicious for malignancy.

Follow up is NOT recommended for low risk patients w solitary or multiple pulmonary nodules < 6 mm.

An interval nodule growth is suspicious; 26% increase in diameter (from 1.0 mm to 1.26 mm) is a doubling in volume.

• Doubling time for lung CA ranges from 42 days in very aggressive tumors to very 4 years in indolent lesions. 

Solid nodule w well-defined benign morphology that has not changed in size over 2 years is very likely but not definitiely benign. Longer F/U is recommended for subsolid nodules as these often represent indolent adenocarcinomas.

A decrease in size of a suspicious nodule on a single F/U study is not sufficient to establish a benign etiology.

• Transient decrease in size of a malignant lesion can occur with collapse of aerated alveoli or fibrosis.

Represents opacification of and around the centrilobular bronchiole or artery (less commonly) at the center of each SPL. On CT, multiple small nodules are seen in the centers of SPL. CNs NEVER extend to the pleural surface. CNs may be solid or GG and range in size from tiny up to a centimeter.

Caused by infectious or inflammatory conditions.

• MC inflammatory cause of CNs is HP, an exposure related lung dz.

• Infectious causes include viral PNAs

Usually occur via hematogenous spread. Can abut interlobar fissures. No specific pattern of involvement w respect to SPL and lung architecture.

• Uniform distribution of nodules; bilateral, diffuse and symmetrical

• May be upper or lower lobe predominant.

• Nodules may be related but have no consistent relationship to pleural surfaces, interlobular septa, small vessels

A miliary pattern is innumerable tiny random nodules the size of millet seeds.

DDX:

• Hematogenous mets

• Disseminated mycobacteria

• Disseminated fungal infection

• Langerhans cell histiocytosis: occasionally early nodular stage

• Sarcoidosis occasionally.

TIBOs are multiple small nodules connected to linear branching structures which resemble a budding tree branch in springtime. TIBOs are 2/2 mucus, pus or fluid impacting bronchioles and terminal bronchioles.

• Linear branching structures represent mucus-impacted bronchioles which are normally invisible on CT

• Nodules represent impacted terminal bronchioles.

• Almost always associated w small airways infection or inflammation such as endobronchial spread of TB

DDX

• Small airways disease

  • Infectious bronchiolitis:

    • Acute: viral, bacterial (mycoplasma), fungal

    • Chronic: TB, nontuberculous mycobacterial infection

  • Aspiration bronchiolitis

    • Esophageal dysmotility, hiatal hernia, esophageal/gastric interventions, H&N CA

    • Lentil (leguminous vegetables) aspiration PNA

  • Follicular bronchiolitis

    • Immunodeficiency, CT dz (RA)

• Vascular disease

  • Excipient lung dz: IV injection of crushed oral tablets

  • Tumor embolism or thrombotic microangiopathy

Cyst: circumscribed spherical space lined by thin fibrous or epithelial wall, usually <2 mm thick

Lung cyst: pulmonary thin-walled space that contains air but may contain fluid, air/fluid level or solid material.

Congenital cyst: intrapulmonary bronchogenic cyst

Mediastinal cyst: congenital anomaly of foregut budding, thymic or pericardial origin

• Acquired cyst vs cystic neoplasm

• Unilocular or multilocular

• Congenital cysts rarely affect lung or pleura

Bulla: subpleural air-filled emphysematous space >1 cm w/ thin wall <1 mm thick 

• Giant bulla occupies at least 30% of thorax volume.

• Associated w emphysema; typically paraseptal but also centrilobular

Bleb: air-filled cystic structure contiguous w/ pleura measuring <1 cm. 

• Rupture of bleb is the MCC of spontaneous PTX. 

Pneumatocele: thin-walled gas filled space surrounded by lung parenchyma; 2/2 prior lung trauma (contusion, laceration, PTX, mechanical ventilation, endobronchialvalves) or infection (PJP, staph, COVID19). Size my increases days to weeks, complete resolution is typical in months to years.

Cystic lung disease: diffuse &/or multifocal pulmonary cysts

Honeycomb cyst: lung fibrosis, layers of subpleural cysts

Age-related changes in asx elderly subjects w basilar subpleural reticulation, bronchial dilatation, perifissural nodules, and scattered thin-walled cysts.

• Perifissural nodules increase w age; typically intrapulmonary LNs; lower lung below level of carina, subpleural. <1 cm; can exhibit growth on serial imaging.

MULTIPLE LUNG CYSTS DDX

• Cystic lung disease:

  • Lymphangioleimyomatosis (LAM): diffuse cystic lung dz 2/2 smooth mm proliferation of the distal airways. LAM causes uniformly distributed thin walled spherical cysts in a diffuse distribution. It may be associated w chylous effusion and tuberous sclerosis complex. 

  • Langerhans cell histiocytosis: irregular cysts and nodules predominantly in the upper lungs.

  • Lymphoid interstitial PNA (LIP): rare dz usually associated w Sjogren syndrome and characterized by lymphocytic infiltrate, multiple cysts GGO and centrilobular nodules.

  • Birt-Hogg-Dube syndrome: AD genetic dz characterized by renal tumors (chromophobe RCC and renal oncocytoma), simple renal/pulmonary cysts, multiseptate subpleural cysts, facial papules (fibrofolliculomas). Spontaneous PTX can occur as a sequela of pulmonary cysts. 

  • Amyloid

  • Light chain deposition disease: similar to LIP; lymphoproliferative or autoimmune disorder w systemic immunoglobulin light-chain deposition; diffuse lung cysts and pulmonary nodules.

  • PJP: late stage dz; acquired immune deficiency syndrome; GGO and upper lung zone cysts.

  • Cystic mets: secondary epithelial, mesenchymal or hematopoietic malignancy.

• Congenital lung cyst:

  • Intrapulmonary bronchogenic cyst

  • Pulmonary airway malformation

• Indeterminate lung cyst: solitary, thin walled, air filled

• Mediastinal congenital cysts: 

  • Bronchogenic cyst

  • Enteric/neurenteric cyst

  • Pericardial cyst

  • Thymic cyst

• Mediastinal cystic lesions: 

  • Mature teratoma

  • Lymphangioma

  • Cystic thymic neoplasm

Reticular opacities: multiple irregular lines w net-like appearance.

• Fine < 3 mm thick

• Medium: 3-10 mm thick

• Coarse: >10 mm thick

Reticulonodular opacities: perceived combination of lines and dots; often artifactual. 

Reticular pattern:

• Multiple interlacing irregular linear opacities indicative of interstitial fibrosis

• Fine, medium, coarse reticulation.

• Does NOT indicate honeycombing.

Traction bronchiectasis: nonuniform bronchial dilatation caused by fibrosis

Traction bronchiolectasis: nonuniform bronchiolar dilatation 2/2 fibrosis

Architectural distortion: abnormal displacement of bronchi, vessels, fissures, or septa 2/2 diffuse or localized retractile fibrosis; related to interstitial fibrosis

Honeyombing: destoyed lung w fibrosis and cysts w fibrous walls. Clustered lung cysts that share their walls; subpleural and multilayered/stacked cysts. avg size 3-10 mm and can be as large as 25 mm

BASAL PREDOMINANT FIBROTIC CHANGES DDX

• Usual interstitial PNA (UIP) pattern: idiopathic pulmonary fibrosis (IPF) is a clinical syndrome or progressive pulmonary fibrosis of unknown etiology and is the MCC of basilar fibrosis. It almost always features basilar honeycombing.

• Other causes of UIP pattern: RA and asbestosis

• Nonspecific interstitial PNA: lung response to injury commonly associated w collagen vascular disease and drug reaction. NSIP typically produces peribronchial reticulation and traction bronchiectasis. GG may be present.

UPPER LOBE PREDOMINANT FIBROTIC CHANGES DDX

• Although IPF is the MCC of pulmonary fibrosis, fibrosis primarily affecting the upper lobes is typically caused by an alt dx.

  • End-stage sarcoidosis: primarily affects the upper lobes. Late stage of sarcoidosis leads to upper-lobe predominant fibrosis.

  • Chronic hypersensitivity pneumonitis

  • End-stage silicosis: late stage of silicosis may lead to fibrosis with an upper lobe predominance.

TRACTION BRONCHIECTASIS DDX

• IPF, NSIP, End-stage silicosis

• Chronic (fibrotic) HSP

• Radiation fibrosis (>12 months post tx w abnormalities that conform to radiation ports)

• Late sequela of ARDS