Resp Spotters p.singh

7/31/2019 Resp Spotters p.singh

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Sarcoid granulomas are the hall mark of this disease .

Distributed primarily along the lymphatics in (most helpful in making apathologic diagnosis)

-peri bronchovascular interstitial space (both in perihilar region and lobularcore)

-interlobular septa Subpleural interstitial space

CXR-

Symmetric,bilateral hilar and paratracheal lymphadenopathy with or withoutconcomitant parenchymal abnormalities(60-70%)

HRCT-1) Small nodules in perilymphatic distribution,visible in relation to:

peribronchovascular regions adjacent to perihilar vessels and bronchi,fissures, subpleural regions, interlobular septa, centrilobular regions.


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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 ofinterstitial nodules or fibrosis

8) regular or nodular bronchial wall thickening and bronchial luminalabnormalities

9) Few patients-mosaic perfusion on inspiratory HRCT notedAir trapping on expiratory HRCT due to endoluminal or submucosal sarcoidgranulomas or fibrotic obstruction of airways is more common.

10) Lymph node calcification not uncommon


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Chronic changes-

1) Fibrosis becomes prominent

2) Irregular reticular opacities (along the perihilar bronchovascular bundles) and

irregular septal thickening3) 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 tractionbronchiectasis

Honeycombing and lung cysts-less common


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D/D-

1)Pulmonary lymphangitic carcinomatosis

2)Silicosis

3)Coal workers pneumoconiosis

4)Berryliosis


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Unknown etiologyFamilial occurrence (50%)

Symptoms-progressive shortness of breath

Characterized by widespread intra-alveolar calcifications, representing microliths orcalcospheres

CXR-1) Fine micronodulation diffusely involving both lungs (sharply defined nodules


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HRCT-

1) Calcific nodules(< 1mm) , sometimes confluent seen predominantly along thecardiac borders and dorsal (posterior) portions of lower lung zones (insubpleural 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 reticulationmay be predominant finding (calcification inconspicuous)


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D/D of diffuse pulmonary calcification-

1)metastatic pulmonary calcification

2)renal failure

3)previous infection-varicella,histoplasmosis

4)pulmonary ossification in lung fibrosis

5)amyloidosis

6)sarcoidosis

7)pneumoconiosis


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Neuroendocrine tumors (< 5% of all pulmonary tumors)

TYPICAL CARCINOIDS ATYPICAL CARCINOIDS

- 85-90% 10-15%

- pneumonia, hemoptysis common rare

- arise centrally in main,lobar arise peripherally in the lungor segmental bronchi

-Predominantly intraluminal with a polypoid worse outcome

configuration, may grow within the lumen

of bronchus in a tooth-pastelike fashion

-Predom.extraluminal (ice-berg lesions)


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may secrete ACTH in sufficient quantities to cause cushings syndrome

CXR and CT-

- Majority arise in larger bronchi and cause partial or complete bronchialobstruction resulting in atelectasis

Tumor visible as a hilar mass in about 25% patients

- small tumors in lobar, segmental and sub segmental bronchi- cause mucusdistension 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 andlarger tumors

multiple nodular type or curvilinear

-marked Contrast enhancement


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**bronchial lumen can be seen to widen as it approaches the tumor(not seen inbronchial carcinoma)

MRI ( T2 wt or STIR seq) - helpful in small tumors which are difficult todistinguish from larger vessels


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Form of obliterative bronchiolitis commonly resulting from viral injury to thedeveloping 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 obliterativebronchiolitis

CXR-1) 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


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CT-

More commonly shows bilateral abnormalities

1) Confirms unilateral transradiancy - transradiant regions are ofteninhomogenous, containing a patchwork of local decreased attenuation andhypovascular areas interspersed with lung of normal density

2) air-trapping

3) bronchiectasis- frequent finding

4) areas of collapse and scarring


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D/D-

1)Congenital hypoplastic lung

2)Congenital lobar emphysema

3)Pulmonary artery hypoplasia

4)Proximal interruption of pulmonary artery


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Common in potential blood- forming organs like liver, spleen and lymph nodes inpatients with anemia

Thoracic manifestations rare

usually consist ofparavertebral soft tissue

masses(caused by extrusion of marrow through the thinned cortex of theposterior ribs)

Pt. may be asymptomatic or paraplegia from cord compression

Common anemias resulting in EMH congenital hemolytic anemias-thalassemia,hereditary spherocytosis,sickle celldisease


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CXR-1) 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 boneusually 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

MRI-

1) masses are usually heterogenous

show increased signal intensity on T1 wt images


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Tuberculosis is one of the important causes of miliary nodulation of lung andprompt 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 bepresent in patients with normal chest radiograph

More readily detected with HRCT and have a random distribution in relation tosecondary pulmonary lobule

Miliary TB does not leave residual calcification


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D/D OF MILIARY MOTTLING

1)Silicosis

2)Histoplasmosis

3)Metastases

4)Hemochromatosis


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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


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CXR-1) 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)HRCT-

1) Areas of consolidation and ground glass opacity - 30% cases upper lungpredominance of parenchymal abnormalities

2) Thickened interlobular septa and bronchovascular bundles

3) pleural effusion - large or small

Survival with appropriate management is 100%


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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 nasalpolyps

symptoms similar to TB

Blood eosinophilia-common(90%) but not universal

Sputum eosinophilia


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CXR-Peripheral, 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 oneor 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

CT-

Shows strikingly peripheral , multifocal consolidation or ground glass opacity

Pts scanned within 1 month of onset of symptoms: bilateral subpleuraldistribution

Pts scanned > 1 month after onset of symptoms: patchy consolidation withperipheral opacities (* but the subpleural zone is clear )

Dense bandlike structures parallel and about 1-2 cms deep to chest wall,whichmay traverse the fissures ( in more chronic cases and also in resolving phase )


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CHARACTERSTIC FEATURES- Blood eosinophilia

Absent or mild signs and symptoms

One or more fairly homogenous non-segmental pulmonary consolidations thatare transitory and/or migratory-tendency to be peripherally located

Spontaneous clearing of consolidations


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

CXR-

1) Esophageal dilation is best appreciated on lateral chest x-ray, fluid - filled dilatedesophagus is seen to displace the trachea and carina forward

-When esophagus is dilated , it displaces the displaces the lung behind the right halfof trachea (forming posterior tracheal stripe), so the posterior tracheal stripeappears thickened on lateral chest radiograph

* if thickened post.tracheal stripe is seen in association with anterior bowing oftrachea and anterior displacement of carina (esophageal dilation can beconfidentally diagnosed )

2) Frontal radiograph - absence of air in in the expected location of stomachbubble

-Air-fluid level within the dilated esophagus is noted


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D/D OF ESOPHAGEAL DILATION-1) Motility disorders

2) Destruction of the myenteric plexus by the tumor at esophago gastricjunction- carcinoma esophagus , submucosal esophageal neoplasms like GIST,chest wall leiomyomas and leiomyosarcomas

3) Distal obstruction stricture , extrinsic compression


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Most common oppurtunistic infection in HIV infected patientsCXR-

1) 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 involvingupper 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)


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Central , perihilar or upper lobe distribution

Pneumothorax related to cysts

Bronchiectasis or bronchilolectasis

Acute phase of PCP- scattered foci of ground glass opacities with septalthickening

Resolving disease or subacute infection- reticular opacities representingthickened interlobular septa and intralobular lines seen in association withground glass opacity (crazy-paving)

Chronic PCP- interstial fibrosis and honey-combing

* spontaneous pneumothorax in in AIDS pt is virtually diagnostic of pcp (may bethe first radiographic manifestation

* calcification is more typical of disseminated PCP


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Also k/a extrinsic allergic alveolitis - is a pulmonary syndrome caused byrepeated exposure and sensitization to a variety of organic and chemicalantigens

Etiology - asspergillus,thermophilic actinomyces, trichosporum,mycobacterium avium complex , isocyanates

CXR-1) 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


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HRCT-1) Poorly defined centrilobular nodules - < 5 mm in diameter , profuse throughout

the lung ,but a mid to lower lung zone predominance noted (*ground glassattenuation)

- 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


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5) mosaic attenuation pattern - common6) air- trapping on expiratory imaging may be predominant or only feature

D/D-

1) Smoking related respiratory bronchiolitis

2) When only ground glass opacification present - viral infection , organizingpneumonia , 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 differentialdiagnosis of NSIP and UIP


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Abnormal direct communication between pulmonary artery and vein Most congenital

50-70% located in lower lobes

70% unilateral

36% multiple lesions

Simple and complex AVMCXR-

- 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


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D/D-Pulmonary varix

Systemic artery to pulmonary vein shunt

Retroperitoneal varices

Pulmonary metastasis

Granuloma

Pulmonary pseudotumor


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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 onCT even before blood cultures become positive

CXR and CT appearance-

1) Multiple pulmonary opacities - may occur in any portion of lung (but usuallymaximal in lower zones)

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

-Frequently cavitate


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

2) feeding vessel sign-

Common 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 emboliand sterile thrombo-embolic infarctions than in other conditions

3) Pleural effusion and empyema - common features


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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 conglomerateto form a circumferential lobular sheet of soft tissue density encasing the lung

- Often runs into fissures accompanied with varying amounts of pleural f luid

* neoplastic encasement of lung fixes the mediastinum ,so mediastinal shiftaway 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 adjacentpleural effusion ; but when nodules are tiny the only CT feature may be pleuraleffusion

4) Calcification -rare


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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 benigndisease and other neoplasms from MM


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D/D-1) Pleural involvement by other malignant tumors - bronchial adenocarcinoma,

breast carcinoma, malignant thymoma and lymphoma

2) Benign conditions eg asbestos related benign pleural effusion, tuberculouspleural thickening,past or present empyema, asbestos related pleural plaques

*circumferential pleural thickening and thickening extending over themediastinal pleura seen in MM (but rare in benign pleural disease)

Uptake of FDG with PET imaging correlates with prognosis


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Due to inhalation of free silica (silicon dioxide)Simple silicosis-

CXR-

1) 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

CT-

1) Centrilobular micronodules

-Upper zone preponderance (spreads anteriorly and inferiorly as the diseaseprogresses

-Subpleurally the nodules may cluster to form pseudoplaques

-Larger nodules may calcify


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CT-Confirms 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 avascularnecrosis and cavitation may occur

-Irregular punctate calcification maybe seen within the lesions

Assymetry between lungs may occur in early PMF


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D/D OF LYMPH NODE CALCIFICATION-1) 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 neoplasmsMetastases from primary tumor osteosarcoma,chondrosarcoma,mucinousadenocarcinoma

[**egg-shell cacification ]


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Complications of silicosis-1) 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


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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 ossifiednodules develop after years of pulm. venous congestion

Sec. pulm. arterial hypertension-pulmonary valve regurgitation , rightventricular dilatation and functional tricuspid regurgitation

CXR-

1) 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


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CXR-1) pulmonary plethora

2) Figure of 8/snowmans/cottage loafof bread heart-altered cardiacsilhouette by enlarged supracardiac

veins - result in enlarged superiormediastinal shadow with convexlateral borders

3) Later,pulmonary vascular occlusivedisease develops resulting inpulmonary hypertension


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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 septalwall - result in tricuspid regurgitation

- Proximal portion of RV cavity is atrialized but it contracts synchronously withthe ventricle

- RV performance markedly reduced

patent fortamen ovale or atrial septal defect frequently seen - results inRt-to-lt shunt inducing central cyanosis


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CXR-1) Enlarged globular or square cardiac silhouette

-RA is characterstically markedly enlarged causing a prominent , smoothlyconvex right lateral heart border (with increasing contact with the sternumanteriorly and a bulging posterior border on lateral view )

-Left border of cardia is also smoothly convex , superiorly it approaches themidline 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


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D/D-ENLARGED GLOBULAR CARDIA WITH REDUCEDPULSATION WITH PULMONARY OLIGEMIA

1) Endomyocardial fibrosis

2)Uhls anomaly

3) Critical pulmonary stenosis

4) Pericardial effusion


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Self limited viral inflammation of the airways resulting in symmetric subglotticedema and croupy cough

CXR-

AP view - loss of normal shoulders (lateral convexities) of the subglottic tracheasecondary to subglottic edema : steeple sign, pencil tip or inverted V sign

-Symmetric ,subglottic narrowing with narrow portion of the airway extendingmore inferiorly than the level of pyriform sinuses

Lateral radiograph-

Narrowing 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 - ifexpiratory image


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RADIOGRAPHS TAKEN TO EXCLUDE-Aspirated foreign body

Epiglottitis

Exudative tracheitis

Subglottic hemangioma


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Congenital absence of the left pectoralis major and minor muscleCXR-

Pectoralis major produces a broad band-like opacity extending downwards andmedially 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 )


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Ct scan-

Thin-walled fluid- filled cysts

useful for identifying pathognomic features in ruptured or complicated cysts,

like detached or collapsed endocyst membranes and intact daughter cysts

MRallows reliable differentiation of f luid filled cysts from solid tumors

Cysts-low signal intensity on T1 WT images

high signal intensity on T2 WT images


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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 minorhemoptysis)

50% pts-pleuritic pain,h/o coughing up mucus plugs

Fever,malaise.wt loss

Eosinophilia-mild to moderate


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Radiographic findings-major findingsAcute stage(transient)-

consolidation(80%)-can be massive and homogenous to subsegmental andsmaller opacities

little zonal predilection

cavitation in areas of consolidation :due to bronchiectasis, cavitatory bacterial

infection or mycetoma formationConsolidation 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 likeshadowthat points to the hilum(tooth-paste shadow),in clusters(bunch of grapes)

usu.proximal airways involved,if distal bronchiectatic airways are involved(glovedfinger shadow)

On ct-appear as band like abnormalities in expected position of bronchi


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Atelectasis(20%)subsegmental,segmental,lobar or may affect whole lung

chronic stage(permanent)-

Bronchiectasis-proximal bronchiectasis (characterstic finding and highlyspecific 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


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minor findings- Airway wall thickening

Small nodules

Pleural effusions

Pleural thickening

Mycetoma

Small nodules

Linear scars


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Hamartomatous mass of fibrous tissue and smooth muscles containing cysticspaces lined by columnar or cuboidal respiratory epithelium.cystscommunicate 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 periodRecurrent lung infections

3types:

1)type1- single/multiple cysts2-10 cms in diameter(ciliated respiratory epithelium)

2)type2-multiple cysts


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Radiographic findings-Variable appearance ,depending on the size of cysts

Solid to multicystic mass with variable amounts of air and fluid

May cause mass effect

On ct-

Used 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 chestradiograph

No evidence of systemic arterial blood supply


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On MRI-usually 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

USG-

For 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


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

Involved lung is dysplastic

Arterial supply-systemic source ,arising from descending aorta

Symptoms-recurrent pneumonia like symptoms

cyanosisIntralobar extralobar

within normal lung separate with own pleural covering

Venous drainage-pulmonary systemic

Left side(60-70%) left(90%)

Uncommon ass. congenital anomalies frequentAge at diagnosis-50%by 20 yrs 60% in 1st year

M=F M:F=4:1

Infections-common rare


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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 descendingaorta

May have other systemic sources as well


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Autosomal recessive multisy stem disorder of exocrine gland function characterized inrespiratory tract byrecurrent infection,chronic obstruction and chronic sinusitis

with nasal polyps

Radiographic findings-

Early:hyperinf lation and/or lobar atelectasis

Increased perihilar markings

Later:upper lobe predominant bronchiectasis

Multiple small ill defined opacities in lung periphery from small airway mucoidimpaction

Persistent atelectasis-subsegmental,segmental or lobar

Recurrent pneumonia

Pulmonary arterial enlargement

Hilar adenopathy

Cor pulmonale

Apical cystic bronchiectasis,bullae

Predisposed to pneumothorax


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On ct- More sensitive for detecting mild disease

Bronchial wall thickening and dilatation

Cylindrical,varicose and saccular bronchiectasis

signet ring sign:dilated bronchus in associationwithadjacent artery on axial

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

small centrilobular bronchioles

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Resp Spotters p.singh