Dr.

Priyanka singh

Sarcoid granulomas are the hall mark of this disease . Distributed primarily along the lymphatics in (most helpful in making a pathologic diagnosis) -peri bronchovascular interstitial space (both in perihilar region and lobular core) -interlobular septa Subpleural interstitial space

CXRSymmetric,bilateral hilar and paratracheal lymphadenopathy with or without concomitant parenchymal abnormalities(60-70%)

HRCT1) Small nodules in perilymphatic distribution,visible in relation to: peribronchovascular regions adjacent to perihilar vessels and bronchi, fissures, subpleural regions, interlobular septa, centrilobular regions.

upper lobe predominance is common. 2) nodular thickening of perihilar and PBV interstitium 3) subpleural nodules-typical of sarcoidosis 4) irregular or nodular interlobular septal thickening-apparent in majority 5) Centrilobular nodules 6) Confluence of granulomas large opacities suggestive of frank consolidation 7) patchy areas of ground glass opacities superimposed on a background of interstitial nodules or fibrosis 8) regular or nodular bronchial wall thickening and bronchial luminal abnormalities 9) Few patients-mosaic perfusion on inspiratory HRCT noted Air trapping on expiratory HRCT due to endoluminal or submucosal sarcoid granulomas or fibrotic obstruction of airways is more common. 10) Lymph node calcification not uncommon

Chronic changes1) Fibrosis becomes prominent 2) Irregular reticular opacities (along the perihilar bronchovascular bundles) and irregular septal thickening 3) Most common early HRCT finding of fibrosis with lung destruction-posterior displacement of main and upper lobe bronchi Progressive fibrosis-masses of fibrous tissue ,more in upper lobes with traction bronchiectasis Honeycombing and lung cysts-less common

D/D1)Pulmonary lymphangitic carcinomatosis 2)Silicosis 3)Coal workers pneumoconiosis 4)Berryliosis

Unknown etiology Familial occurrence (50%) Symptoms-progressive shortness of breath Characterized by widespread intra-alveolar calcifications, representing microliths or calcospheres

CXR1) Fine micronodulation diffusely involving both lungs (sharply defined nodules <1mm in diameter) -Lower lobe predominance -the opacities may be confluent, which gives lungs a uniformly white appearance ,with total obliteration of mediastinal and diaphragmatic contours 2) occasionally, reticular pattern or septal lines supeimposed on characterstic sandstorm appearance noted 3) Other findings-bullae in lung apices zone of increased lucency between the lung parenchyma and ribs (black pleural line) pleural calcification

HRCT1) Calcific nodules(< 1mm) , sometimes confluent seen predominantly along the cardiac borders and dorsal (posterior) portions of lower lung zones (in subpleural parenchyma and in association with bronchi and vessels) Perilobular and centrilobular distribution of calcification seen 2) calcific interlobular septal thickening commonly noted

3) Intraparenchymal cysts and paraseptal emphysema

-in children and patients with early disease-ground glass opacity or reticulation may be predominant finding (calcification inconspicuous)

D/D of diffuse pulmonary calcification1)metastatic pulmonary calcification

2)renal failure 3)previous infection-varicella,histoplasmosis 4)pulmonary ossification in lung fibrosis

5)amyloidosis
6)sarcoidosis 7)pneumoconiosis

Neuroendocrine tumors (< 5% of all pulmonary tumors)

TYPICAL CARCINOIDS
- 85-90% - pneumonia, hemoptysis common - arise centrally in main,lobar or segmental bronchi -Predominantly intraluminal with a polypoid configuration, may grow within the lumen of bronchus in a tooth-pastelike fashion -Predom.extraluminal (ice-berg lesions)

ATYPICAL CARCINOIDS
10-15% rare arise peripherally in the lung worse outcome

may secrete ACTH in sufficient quantities to cause cushings syndrome

CXR and CT- Majority arise in larger bronchi and cause partial or complete bronchial obstruction resulting in atelectasis Tumor visible as a hilar mass in about 25% patients - small tumors in lobar, segmental and sub segmental bronchi- cause mucus distension of bronchi beyond obstruction (bronchocele) - dominant feature -10-20% present as solitary pulmonary nodule - nodule is well defined, round, oval , lobulated or notched usually with smooth edge - calcification or ossification CT helpful , more common in centrally located and larger tumors multiple nodular type or curvilinear -marked Contrast enhancement

**bronchial lumen can be seen to widen as it approaches the tumor(not seen in bronchial carcinoma) MRI ( T2 wt or STIR seq) - helpful in small tumors which are difficult to distinguish from larger vessels

 Form of obliterative bronchiolitis commonly resulting from viral injury to the

developing lung (before the age of 8yrs) Virus- adenovirus , measles virus Nonviral causes- mycoplasma pneumoniae , pertusis Non-infectious hydrocarbon ingestion Reflects a combination of hypoplasia of pulmonary vasculature and obliterative bronchiolitis

CXR1) Unilateral transradiancy (due to reduced lung perfusion) Size and no. of mid lung and peripheral vessels are reduced on affected side 2) Contralateral plethoric lung (due to increased blood flow) 3) Small hilum on involved side (but lung volume is normal or only slightly decreased) 4) mediastinum- may show some shift to affected side 5) Ipsilateral air trapping- key finding

CTMore commonly shows bilateral abnormalities 1) Confirms unilateral transradiancy - transradiant regions are often inhomogenous, containing a patchwork of local decreased attenuation and hypovascular areas interspersed with lung of normal density 2) air-trapping

3) bronchiectasis- frequent finding

4) areas of collapse and scarring

D/D1)Congenital hypoplastic lung 2)Congenital lobar emphysema 3)Pulmonary artery hypoplasia 4)Proximal interruption of pulmonary artery

Common in potential blood- forming organs like liver, spleen and lymph nodes in patients with anemia Thoracic manifestations rare usually consist of paravertebral soft tissue masses(caused by extrusion of marrow through the thinned cortex of the posterior ribs) Pt. may be asymptomatic or paraplegia from cord compression Common anemias resulting in EMH

congenital hemolytic anemias-thalassemia,hereditary spherocytosis,sickle cell disease

CXR1) Focal paravertebral masses (usu. in lower of thorax) - masses are well marginated, bilateral, contain no calcification, show no rib destruction 2) Foci of EMH can also be seen as subpleural masses adjacent to ribs - adjacent bone usually normal or shows findings of marrow expansion CT 1) helpful in demonstrating lace-like marrow expansion in adjacent bones 2) heterogenous or homogenous soft tissue attenuation masses some fat may be present within the mass calcification uncommon MRI1) masses are usually heterogenous show increased signal intensity on T1 wt images

 Tuberculosis is one of the important causes of miliary nodulation of lung and

prompt diagnoses and treatment are vital

Results from hematogenous dissemination of disease

RADIOGRAPHIC FINDINGS Widespread fine nodules , unifomly distributed and equal in size

As there is a threshold below which nodules are invisible , miliary TB can be present in patients with normal chest radiograph
More readily detected with HRCT and have a random distribution in relation to secondary pulmonary lobule Miliary TB does not leave residual calcification

D/D OF MILIARY MOTTLING 1)Silicosis 2)Histoplasmosis 3)Metastases 4)Hemochromatosis

Diagnostic criteria Acute febrile illness of < 5 days duration Hypoxemic respiratory failure alveolar or alveolar / interstitial chest radiographic opacity BAL eosinophil level of > 25% (key to diagnosis , greatly raised 30-80%) Prompt or complete response to steroids without relapse on withdrawl Absence of parasitic , fungal and other infections Av age at presentation-30 yrs No gender predilection

h/o asthma or atopy may or may not be present

CXR1) Shows mixed alveolar / interstitial pattern - bilateral 2) Septal thickening 3) Pleural effusion - 70% cases-bilateral more common than unilateral (above findings seen in absence of clinical cardiac failure or overhydration)

HRCT1) Areas of consolidation and ground glass opacity - 30% cases upper lung predominance of parenchymal abnormalities 2) Thickened interlobular septa and bronchovascular bundles 3) pleural effusion - large or small Survival with appropriate management is 100%

 Cryptogenic form of eosinophilic lung disease 3rd to 7th decade F:M=2:1 50% pts are atopic, 40% asthmatics, 5-10% have allergic rhinitis and nasal

polyps
symptoms similar to TB
Blood eosinophilia-common(90%) but not universal Sputum eosinophilia<50% Total WBCcount and ESR-raised

Serum IgE-normal or minimally elevated

CXRPeripheral, non-segmental homogenous consolidation sometimes with an air bronchogram (classic pattern seen in 2/3rd pts) Opacities lie against the chest wall and may surround the lung or just occupy one or two zones particularly the apices If they resolve they usually recur in the same place (i.e rarely truly migratory) Mixed peripheral and central consolidation-common pattern

CTShows strikingly peripheral , multifocal consolidation or ground glass opacity Pts scanned within 1 month of onset of symptoms: bilateral subpleural distribution Pts scanned > 1 month after onset of symptoms: patchy consolidation with peripheral opacities (* but the subpleural zone is clear ) Dense bandlike structures parallel and about 1-2 cms deep to chest wall,which may traverse the fissures ( in more chronic cases and also in resolving phase )

CHARACTERSTIC FEATURES Blood eosinophilia Absent or mild signs and symptoms One or more fairly homogenous non-segmental pulmonary consolidations that

are transitory and/or migratory-tendency to be peripherally located

Spontaneous clearing of consolidations

 caused by failure of relaxation of lower esophageal sphincter resulting in esophageal

dilatation

CXR1) Esophageal dilation is best appreciated on lateral chest x-ray , fluid - filled dilated esophagus is seen to displace the trachea and carina forward -When esophagus is dilated , it displaces the displaces the lung behind the right half of trachea (forming posterior tracheal stripe), so the posterior tracheal stripe appears thickened on lateral chest radiograph * if thickened post.tracheal stripe is seen in association with anterior bowing of trachea and anterior displacement of carina (esophageal dilation can be confidentally diagnosed )

2) Frontal radiograph - absence of air in in the expected location of stomach bubble -Air-fluid level within the dilated esophagus is noted

D/D OF ESOPHAGEAL DILATION1) Motility disorders 2) Destruction of the myenteric plexus by the tumor at esophago gastric junction- carcinoma esophagus , submucosal esophageal neoplasms like GIST, chest wall leiomyomas and leiomyosarcomas 3) Distal obstruction stricture , extrinsic compression

Most common oppurtunistic infection in HIV infected patients

CXR1) diffuse bilateral or alveolar infiltrates or both (85% cases) 2) Fine to medium reticular or nodular opacities or ill-defined hazy consolidation (most characterstic appearance) 3) About 10% patients show air-filled cysts or pneumatoceles , typically involving upper lobe

HRCT* patchy or diffuse bilateral ground glass opacity * consolidation * thick-walled , irregular or septated cysts or cavities centrilobular opacities interlobular septal thickening Small (centrilobular or diffuse) or large nodules (rare)

Central , perihilar or upper lobe distribution Pneumothorax related to cysts Bronchiectasis or bronchilolectasis

Acute phase of PCP- scattered foci of ground glass opacities with septal thickening
Resolving disease or subacute infection- reticular opacities representing thickened interlobular septa and intralobular lines seen in association with ground glass opacity (crazy-paving)

Chronic PCP- interstial fibrosis and honey-combing

* spontaneous pneumothorax in in AIDS pt is virtually diagnostic of pcp (may be the first radiographic manifestation * calcification is more typical of disseminated PCP

 Also k/a extrinsic allergic alveolitis - is a pulmonary syndrome caused by

repeated exposure and sensitization to a variety of organic and chemical antigens

Etiology - asspergillus,thermophilic actinomyces, trichosporum,

mycobacterium avium complex , isocyanates

CXR1) Ground glass opacification 2) Fine nodular or reticulonodular pattern (more prominent in sub acute phase) [ Lower lung predominance ] 3) Chronic cases - fibrosis with upper lobe retraction, reticular opacity, volume loss and honeycombing may be seen

HRCT1) Poorly defined centrilobular nodules - < 5 mm in diameter , profuse throughout the lung ,but a mid to lower lung zone predominance noted (*ground glass attenuation) - Usually regress with removal of exposure 2) Ground glass attenuation - most common in AHP - may be patchy or diffuse - middle lung zone predominance - may resolve with removal of exposure 3) Lung cysts - 10% of subacute hypersensitivity pneumonitis 4) CHP - fibrosis signified by irregular linear opacities , traction bronchiectasis, lobar volume loss , honey combing - mid zone predominance( but may be seen in upper or lower lobes ) -emphysema

5) mosaic attenuation pattern - common 6) air- trapping on expiratory imaging may be predominant or only feature

D/D1) Smoking related respiratory bronchiolitis 2) When only ground glass opacification present - viral infection , organizing pneumonia , DIP or NSIP

3) when mixed ground glass opacification and air trapping sarcoidosis

Pts with CHP-may exhibit pattern of NSIP *hypersensitivity pneumonitis should always be considered in the differential diagnosis of NSIP and UIP

 Abnormal direct communication between pulmonary artery and vein Most congenital 50-70% located in lower lobes 70% unilateral 36% multiple lesions Simple and complex AVM

CXR- sharply defined pulmonary nodule , may have lobulated borders - Uniform density - Curvilinear opacities medial to nodule

CECT- best imaging modality

- Enhancement of nodule similar to enhancement of other vascular structures - Large feeding artery and draining vein

D/DPulmonary varix Systemic artery to pulmonary vein shunt Retroperitoneal varices Pulmonary metastasis Granuloma Pulmonary pseudotumor

Common sources
Infected venous catheters Tricuspid valve endocarditis Septic thrombophlebitis Indwelling prosthetic devices

*diagnosis may be first suggested at chest CT as abnormalities may be seen on CT even before blood cultures become positive

CXR and CT appearance1) Multiple pulmonary opacities - may occur in any portion of lung (but usually maximal in lower zones)

-Either round (nodular) in shape or wedge shaped densities based on pleura and pointing towards hilum (like an infarct)
-Frequently cavitate

Air bronchograms frequently seen in all types of opacity including nodular lesions on CT

2) feeding vessel signCommon CT finding of both sterile and infected infarcts It is a distinct vessel leading to apex of a peripheral area of consolidation Not specific for embolic sequelae but seen more frequently with septic emboli and sterile thrombo-embolic infarctions than in other conditions 3) Pleural effusion and empyema - common features

 Asbestos exposure noted in almost half the patients Peak age at presentation-40-70yrs

IMAGING FINDINGS-

1) Extensive nodular or lobular thickening of the pleura which may conglomerate to form a circumferential lobular sheet of soft tissue density encasing the lung - Often runs into fissures accompanied with varying amounts of pleural fluid

* neoplastic encasement of lung fixes the mediastinum ,so mediastinal shift away from the site of effusion is not seen in MM
2) Ipsilateral volume loss 3) On CT- soft tissue density of tumor tissue is easily distinguished from adjacent pleural effusion ; but when nodules are tiny the only CT feature may be pleural effusion 4) Calcification -rare

On MRI-T1 wt images - signal intensity slightly greater than muscle -T2 wt images - moderately greater than muscle Enhances significantly with gadolinium Contrast enhanced T1 wt sequences with fat saturation-help distinguish benign disease and other neoplasms from MM

D/D1) Pleural involvement by other malignant tumors - bronchial adenocarcinoma, breast carcinoma, malignant thymoma and lymphoma 2) Benign conditions eg asbestos related benign pleural effusion, tuberculous pleural thickening,past or present empyema, asbestos related pleural plaques

*circumferential pleural thickening and thickening extending over the mediastinal pleura seen in MM (but rare in benign pleural disease)
Uptake of FDG with PET imaging correlates with prognosis

Due to inhalation of free silica (silicon dioxide)

Simple silicosisCXR1) 1-3 mm round well-defined nodules in the posterior portion of upper 2/3 rd of lungs , symmetric -Sometimes calcified -With time the nodules increase in size and number and may involve all zones 2) Reticular pattern may also be noted

CT1) Centrilobular micronodules -Upper zone preponderance (spreads anteriorly and inferiorly as the disease progresses -Subpleurally the nodules may cluster to form pseudoplaques -Larger nodules may calcify

2) Interlobular septal thickening 3) Hilar and mediastinal lymph node enlargement- egg-shell calcification maybe seen on CXR or CT

Progressive massive fibrosisAlso k/a complicated/conglomerate silicosis

CXR1) nodules >1 cms in diameter 2)Round or oval mass near the periphery of lung , with a well-defined lateral border that parallels the lateral chest wall Lateral view-confirms posterior location lens shaped appearance of conglomerate mass Coalesced nodules lead to contraction of upper lobes-retraction of hilacompensatory emphysema in lower lobes 3) Apical pleural thickening

CTConfirms the CXR findings 1) Shows a peripheral zone of paracicatricial emphysema 2) Fibrous bands may be noted extending to pleural surface 3) Round or ovoid masses , outer margin // the chest wall -Large lesions(5cms or >)show irregular attenuation areas s/o avascular necrosis and cavitation may occur -Irregular punctate calcification maybe seen within the lesions Assymetry between lungs may occur in early PMF

D/D OF LYMPH NODE CALCIFICATION1) Benign ds : ** Tuberculous and fungal ds.(histoplasmosis) ** Sarcoidosis ** Silicosis and coal workers pneumoconiosis ** amyloidosis Pneumocystis jinoveci infection in patients with AIDS Castleman disease 2) Malignant ds : ** Treated lymphomas and other neoplasms

Metastases from primary tumor osteosarcoma,chondrosarcoma,mucinous adenocarcinoma

[**egg-shell cacification ]

Complications of silicosis1) Chronic bronchitis 2) Emphysema-mostly centrilobular (but cicatricial emphysema in PMF) 3) predisposition to mycobacterial infection - pulmonary or extra-pulmonary 4) Increased risk of UIP , scleroderma , rheumatoid arthritis 5) Pleural thickening and round atelectases

Most frequently the result of rheumatic fever

mitral valve disease increases left atrial pressure - transmitted to pulm. veins

-when severe leads to interstitial and alveolar edema.

Parenchymal lung changes - haemosiderosis and intrapulmonary ossified

nodules develop after years of pulm. venous congestion

Sec. pulm. arterial hypertension-pulmonary valve regurgitation , right

ventricular dilatation and functional tricuspid regurgitation

CXR1) cardinal radiologic feature-selective left atrial enlargement aneurysmal enlargement of left atrium-is when left atrium reaches to within an inch or so of chest wall on either side of chest 2) Left atrial appendage is prominent 3) Straightening of left heart border

4) Calcification - in the wall of left atrium curvilinear , lies high in cardiac shadow (on lateral x-ray-seen in upper posterior aspect of the heart at the top of left atrium) Mitral valve calcification-on lateral view seen in the postero-inferior aspect of the heart 5) Right ventricle appears enlarged in lateral view as it is pushed against the sternum by enlarged left atrium In pulmonary arterial hypertension right ventricle is truly enlarged 6) Upper lobe blood diversion 7) Interstitial edema Pulmonary alveolar edema 8) Pulmonary arterial hypertension 9) Pulmonary haemosiderosis 10) Pulmonary ossified nodules - lung bases

 None of the pulmonary veins is connected to left atrium In supracardiac pattern-the drainage is into the veins above the heart (usually

into the left innominate vein)

Most frequent pattern of TAPVD

-Rt and Lt pulmonary veins meet behind LA in a venous confluence - from which a large vertical vein passes upwards in front of Lt hilum to meet the Lt innominate vein - which recieves total pulmonary venous return -The dilated Lt innominate vein transmits blood to the SVC (which also becomes dilated ) and enters the enlarged Rt atrium - From RA blood passes to enlarged RV and then to pulmonary arteries (plethora) - Minority of RA blood passes through an invariable ASD into small LA

CXR1) pulmonary plethora 2) Figure of 8/snowmans/cottage loaf of bread heart-altered cardiac silhouette by enlarged supracardiac veins - result in enlarged superior mediastinal shadow with convex lateral borders 3) Later,pulmonary vascular occlusive disease develops resulting in pulmonary hypertension

 Uncommon congenital anomaly

- Septal and posterior leaflets of the tricuspid valve are long and redundant -and there proximal portion is plastered to the wall of RV particularly along septal wall - result in tricuspid regurgitation - Proximal portion of RV cavity is atrialized but it contracts synchronously with the ventricle - RV performance markedly reduced
patent fortamen ovale or atrial septal defect frequently seen - results in

Rt-to-lt shunt inducing central cyanosis

CXR1) Enlarged globular or square cardiac silhouette -RA is characterstically markedly enlarged causing a prominent , smoothly convex right lateral heart border (with increasing contact with the sternum anteriorly and a bulging posterior border on lateral view )

-Left border of cardia is also smoothly convex , superiorly it approaches the midline so that the vascular pedicle of the heart is narrow
2) Outline of the heart is sharply defined due to poor pulsation 3) Lungs -oligemic

D/D-ENLARGED GLOBULAR CARDIA WITH REDUCED PULSATION WITH PULMONARY OLIGEMIA

1) Endomyocardial fibrosis 2)Uhls anomaly 3) Critical pulmonary stenosis

4) Pericardial effusion

 Self limited viral inflammation of the airways resulting in symmetric subglottic

edema and croupy cough

CXRAP view - loss of normal shoulders (lateral convexities) of the subglottic trachea secondary to subglottic edema : steeple sign, pencil tip or inverted V sign -Symmetric ,subglottic narrowing with narrow portion of the airway extending more inferiorly than the level of pyriform sinuses Lateral radiographNarrowing of subglottic trachea Loss of definition of subglottic trachea Hypo pharyngeal overdistension Normal epiglottis and aryepiglottic fold Hypopharynx may be collapsed with distension of the lower cervical trachea - if expiratory image

RADIOGRAPHS TAKEN TO EXCLUDEAspirated foreign body Epiglottitis Exudative tracheitis Subglottic hemangioma

 Congenital absence of the left pectoralis major and minor muscle

CXRPectoralis major produces a broad band-like opacity extending downwards and medially from axilla Unilateral absence or hypoplasia of pectoralis major unilateral transradiancy and an abnormal anterior axillary fold as seen with mastectomy

Accompanied with ipsilateral hand and arm anomalies (particularly syndactyly) with or without pectoralis muscle , rib anomalies , hypoplasia of breast and nipple ( Polands syndrome present in approx. 10% of pts. with syndactyly )

Ct scanThin-walled fluid- filled cysts useful for identifying pathognomic features in ruptured or complicated cysts, like detached or collapsed endocyst membranes and intact daughter cysts

MR allows reliable differentiation of fluid filled cysts from solid tumors Cysts-low signal intensity on T1 WT images

high signal intensity on T2 WT images

 Aspergillus fumigatus most common causative agent Occurs in pts who are atopic and long standing asthmatics, can occur in non-

asthmatics too
10% prevalence in pts with cystic fibrosis Slight female preponderance 20-40yrs of age

10% pts of ABPM may have allergic fungal sinusitis

symptoms Acute stage-wheeze,dyspnea,cough(often productive &ass. With minor

hemoptysis)
50% pts-pleuritic pain,h/o coughing up mucus plugs Fever,malaise.wt loss Eosinophilia-mild to moderate

Radiographic findings-major findings Acute stage(transient) consolidation(80%)-can be massive and homogenous to subsegmental and smaller opacities little zonal predilection cavitation in areas of consolidation :due to bronchiectasis, cavitatory bacterial infection or mycetoma formation Consolidation is transient, and when clears leaves residual bronchiectasis 20-30%pts with consolidation are asymptomatic mucoid impaction(30%)- due to retained secretions within the airways basic opacity:linear sharply demarcated,branched or unbranched band like shadowthat points to the hilum(tooth-paste shadow),in clusters(bunch of grapes) usu.proximal airways involved,if distal bronchiectatic airways are involved(gloved finger shadow) On ct-appear as band like abnormalities in expected position of bronchi

 Atelectasis(20%)

subsegmental,segmental,lobar or may affect whole lung chronic stage(permanent) Bronchiectasis-proximal bronchiectasis (characterstic finding and highly

specific for ABPA)

Distal airways remain normal and patent

Ct features of bronchiectasis: segmental or subsegmental bronchi Cystic or varicose pattern

Thin walled bronchiectatic airways

Associated mucoid impaction(may be hyperattenuating) Ass.centrilobular nodularity/tree-in-bud pattern
Mid/upper zone volume loss and scarring

minor findings Airway wall thickening Small nodules Pleural effusions Pleural thickening Mycetoma Small nodules Linear scars

Hamartomatous mass of fibrous tissue and smooth muscles containing cystic spaces lined by columnar or cuboidal respiratory epithelium.cysts communicate with bronchial tree and fill with air early in life most commonly presents during infancy or detected prenatally M>F Symptoms-respiratory distress in newborn period

Recurrent lung infections

3types: 1)type1- single/multiple cysts2-10 cms in diameter(ciliated respiratory epithelium) 2)type2-multiple cysts <2 cms in diameter(cuboidal to columnar epithelium) 3)type3-essentially solid lesions with microcysts and gland like (adenomatoid)structure

Radiographic findingsVariable appearance ,depending on the size of cysts Solid to multicystic mass with variable amounts of air and fluid May cause mass effect On ctUsed for characterization of lesion for pre surgical planning To identify lesions diagnosed prenatally but not evident on chest x-ray Cyst walls and solid components demonstrate variable enhancement mass effect demonstrated as mediastinal shift or adjacent lung compression Will demonstrate cystic spaces even in solid appearing masses on chest radiograph No evidence of systemic arterial blood supply

On MRIusually used only in prenatal diagnosis T1 WT Images-Isointense lesion T2 WT Images-hyperintense mass demonstrates mediastinal shift and compression of adjacent lung may be ass. with fetal hydrops USGFor prenatal diagnosis gray scale-echogenic mass with mass effect on adjacent lung

Fetal hydrops and poly hydramnios may be present

color doppler-no evidence of systemic arterial blood supply

Congenital area of abnormal lung that does not connect to bronchial tree or pulmonary arteries

Involved lung is dysplastic

Arterial supply-systemic source ,arising from descending aorta Symptoms-recurrent pneumonia like symptoms cyanosis

Intralobar
within normal lung Venous drainage-pulmonary Left side(60-70%) Uncommon Age at diagnosis-50%by 20 yrs M=F Infections-common systemic left(90%)

extralobar
separate with own pleural covering

ass. congenital anomalies frequent 60% in 1st year M:F=4:1 rare

 Radiographic findings-

Persistent lower lobe opacity(unchanged over multiple radiographs)-left lower lobe If infected-appears as multicystic air containing mass Extralobar sequestration presents as paraspinal mass On ct-

Opacification of lower lobe lung parenchyma

If infected-cystic air filled components noted On contrast:systemic arterial supply demonstrated-usually arisesfrom descending aorta May have other systemic sources as well

Autosomal recessive multisy stem disorder of exocrine gland function characterized in respiratory tract byrecurrent infection,chronic obstruction and chronic sinusitis with nasal polyps Radiographic findingsEarly:hyperinflation and/or lobar atelectasis Increased perihilar markings Later:upper lobe predominant bronchiectasis Multiple small ill defined opacities in lung periphery from small airway mucoid impaction Persistent atelectasis-subsegmental,segmental or lobar Recurrent pneumonia Pulmonary arterial enlargement Hilar adenopathy Cor pulmonale Apical cystic bronchiectasis,bullae Predisposed to pneumothorax

 On ct More sensitive for detecting mild disease Bronchial wall thickening and dilatation Cylindrical,varicose and saccular bronchiectasis signet ring sign:dilated bronchus in association withadjacent artery on axial

images
Tree-in-bud pattern-v or y shaped opacities due to secretions within peripheral

small centrilobular bronchioles