pulmo viewboxes block 8

BLOCK 8 brings you

The Viewbox

ofPulmonary Radiology

Normal Chest

April C. Tagayona

Outline

Projection

PositionLateral PositionIndications• Assess mediastinal structures:

heart, sternum, retrocardiac space, lung

• Confirmation of findings in PA/AP views

• used to evaluate blunting of posterior gutter in pleural effusion

Image criteriaa) Ribs posterior to vertebrae should

be superimposedb) CP angles and lung apices includedc) Hilar region should be at centerd) Circular structures on this view may

represent blood vessels

Position

Oblique ViewIndications• Assess tracheal

bifurcation• Study heart, hilum

and ribs

Tracheal lumen should normally be about 1.5cm.

Adequacy

Must show all structures present in the chest X-ray template

No cut-offsoApices should be visualized especially when suspecting pneumothorax and TBoCostophrenic angles should be visualized especially with pleural effusion

Exposure

PA VIEWGood exposure if the spines of T1 – T4 are exposed.

ExposurePA VIEW

Underexposure if <T4 are exposed Overexposure if >T4 are exposed

Exposure

LATERALGood exposure if sternum is visible and right and left ribs overlap

Inspiratory Effort

Adequate if the diaphragm is along the 5th to 6th anterior rib or the 9th to 10th posterior rib

Inspiratory Effort

Inadequate effort• Crowding• Increased lung markings• Wide mediastinum

Obliquity

Spinous process and clavicular heads used as reference = equidistant

Structures should be symmetrical on right and left.

Outline

Lungs

Symmetrical radiolucency Bronchovascular ratio R hilum lower

Lungs• Fissures slightly visible

• Right Lung: 3 lobes and 2 fissures• Left Lung: 2 two lobes and 1 fissure

Lungs Vasculature

• Tapering from central to periphery

• Outer 1/3 usually has no markings

Trachea

Midline, within the boundaries of the vertebral body

Location: C6 – T5

Bifurcates at T5

Trachea

Tracheal lumen: 1.5 cm

Subcarinal angle must be <900

Heart

• Right border:SVC, RA, IVC

• Left border:Aortic arch, left pulmonary a.,left atrial appendage,left ventricle

Heart

• Cardiothoracic ratio– Adults:

<0.50 – 0.52– Children:

<0.56

Mediastinum• the space between the

two pleural sacs which contains all the structures in the thorax except the lungs and the pleura

• Mediastinal width– Upright: 8 cm– Supine: 10 cm

Diaphragm

R hemidiaphragm is higher than the L, lies at 5th ICS on moderately deep inspiration

Pneumonia

MG Villafuerte

Pneumonia• Infection of the lung parenchyma• Airspaces are filled with:

– bacteria or other microorganisms– pus – Fibrin

• Entry through 3 routes– Tracheobronchial tree– Pulmonary vasculature– Direct spread

Pneumonia• Clinical manifestation:

– Fever– Cough– Dyspnea, pleuritic chest pain

On PE:– Rales– Diminished breath sounds (localized)– Percussion dullness– Egophony on auscultation

Radiographic FindingsAirspace opacities Intersitital opacities ConsolidationAir bronchograms• Possible complications:

– Pleural effusions– Empyema– Atelectasis– Pneumothorax

• usually in basal segments

Lobar pneumonia

• homogenous lung opacification or consolidation

• starts as a localized infection of the terminal air spaces

• inflammatory edema spreads to adjacent lung via the terminal airways and pores of Kohn

homogenous opacification at the left lower lung

Pores of Khon• interalveolar connections (pores b/w adjacent alveoli)• for collateral ventillation•allows passage of other materials such as fluid or bacteria

Pores of Khon• interalveolar connections (pores b/w adjacent alveoli)• for collateral ventillation•allows passage of other materials such as fluid or bacteria

Lobar pneumonia

• Increased opacity/ consolidation of the left lower lobe

• increased density behind the left heart shadow

• Where is the pnemonia?• What lobe?

We want to know which lobe of the lung is affected. Thus, we usually request for both a

PA/AP and a lateral view.

Right Upper Pneumonia

Right Middle Lobe Pneumonia

Right Lower Lobe Pneumonia

Bronchopneumonia

Multifocal

Patchy

Management

PULMONARY TUBERCULOSIS

JC Tayag

Pulmonary Tuberculosis

• Lung infection caused by Mycobacterium• Transmission: Inhalation of droplet nuclei• Clinical manifestations

– Fever– Night sweats– Fatigue– Loss of appetite– Weight loss– Cough– Hemoptysis

pathophysiology

Air droplets w/ M.

tuberculosis

inhaled

implanted

Subpleural location

Phagocytized by alveolar

macrophages

Bacilli overcome

immune response

Inflammatory focus

Macrophages epitheloid

cells

Granuloma w/ central

caseation

necrosis

Delayed hypersensitivit

y

Inflammation and

enlargement of

hilar and mediastinal lymph

nodes

Primary tuberculosis

• In children and immunocompromised• Most patients are asymptomatic and have

no radiographic sequelae of infection• Ghon complex: Parenchymal lesion + associated lymph node

• Ranke complex: Ghon complex heals fibrosis + calcification

• Unilateral lymph node enlargement• Hematogenous dissemination to regions

with high partial pressure of oxygen

Postprimary disease

• Contained by granulomatous response/ microscopic foci clinically silent

• Recurs years later, weakened host defenses• Chills, night sweats, weight loss• Cavitation: active and transmissible disease• Rassmussen aneurysm hemoptysis• Parenchymal healing: fibrosis + bronchiectasis + volume loss

Radiological Findings

• Tuberculoma• Focal nodular

opacities• Cavitation• Bronchiectasis• Endobronchial spread• Atelectatic changes• Secondary

emphysema

• Consolidation• Pleural effusion• Miliary TB

Tuberculoma

• Solitary

• Well-defined

• Up to 4 cm in diameter

Focal Nodular Opacities

• 2-10 mm in diameter

• Localized to one or two regions of the lungs

• Common in upper lung segments

Cavitation

• Thick-walled cystic structure

• Irregular inner lining

• Wall thickness at least 1 mm

Bronchiectatic Changes

• Abnormal permanent dilatation of the bronchi

• Thickened bronchi

• Reticular pattern

Endobronchial Spread

• Multiple nodule• 2-10 mm in

diameter• Seen in two or

more lobes or in a lobe other than the one containing a cavity or area of consolidation

Endobronchial Spread

• Tree-in-bud pattern

Right upper lobe infiltrates with

possible atelectatic

changes

Atelectatic Changes

•Cavity formation

•Bullae

•Possible endobronchial spread

•Atelectasis = tracheal and mediaistinal deviation

•Compensatory hyperaeration of left lung

Diaphragmatic tenting

Miliary TB

TALAN, Ceri Jane Homillano

Miliary Tuberculosis

• Hematogenoues dissemination of Mycobacterium Tuberculosis

• 1-3% of all cases of TB• Manifestation of primary TB• Clearing is frequently rapid• Calcification is rare

Primary vs. Reactivation

• Progressive primary disease local focus in the lung lymphatic and hematogenous

dissemination of bacilli granulomatous encapsulation (weeks to months)

Progressive tuberculosis : distant foci fail to heal (within first 6 mos.)

Predilection for spread to the most vascular organs (liver, spleen, bone marrow and brain)

• Reactivation of a latent focus reactivation of a latent focus of infection with subsequent

erosion into adjoining lymphatics or blood vessels years to decades after primary infection

Why the Name?

• Miliary-Like millet seeds, John Jacobus Manget, 1700

• Each one is a granuloma with central caseation necrosis surrounded by epitheliod cells and fibrous tissue.

Risk Factors & Signs and Symptoms• Risk Factors

Immunocompromised PopulationsIatrogenic

• Clinical FindingsWeakness, fatigue (90%)Weight loss (80%)Fever (80%)Cough (60%)Generalized lymphadenopathy (40%)Hepatomegaly (40%)Multi-organ dysfunction

Radiographic Imaging

• Millet seed sized nodules (1-3 mm) spread uniformly on diseased organ.

• The lesions can grow to as big as 5 mm if left untreated but more often than not, the disease produces innumerable, non-calcified nodules

• Can be clearly delineated or have hazy outlines• May take time before they appear radiographically• It can sometimes be associated with intra- and

interlobular septal thickening

Uniformly spread fine granular or nodular lesions, about 2-3 mm in size, in the lung parenchyma.

Some nodules are clearly delineated whereas some have hazy outlines.

Diffuse, randomly distributed nodular lesions (1-2 mm in

size) in the lung parenchyma.

Multiple nodular lesions seen in the lung parenchyma

and the neck region.

Abdominal miliary TB. Multiple, randomly distributed nodules, about 3-4 mm, on the liver. Ascites might also

be present in these x-rays.

Treatment

• 50% of cases are undiagnosed antemortem• 2HRZE, 4HR• Duration: 6-9 months, 9-12 if there is meningeal

involvement

• Miliary TB, if left untreated, is almost 100% fatal

Atelectasis

KB Tagomata

Atelectasis

• Partial or complete loss of volume of a lung• Diminished volume of air in the lung with

associated reduction of lung volume• divided into two

– obstructive– non-obstructive

Atelectasis

• Obstructive– most common type– reabsorption of gas from the alveoli when

communication between the alveoli and the trachea is obstructed

– from foreign body, tumor, and mucous pluggingLobar atelectasisSegmental ateclectasis

Atelectasis

• Non-Obstructive– from loss of contact between the parietal and

visceral pleurae, compression, loss of surfactant, and replacement of parenchymal tissue by scarring or infiltrative disease

Relaxation/passive atelectasis Compression atelectasis Adhesive atelectasisCicatrization atelectasis

Atelectasis

KB Tagomata

Complete right lung atelectasis

RadiographyDirect signs Indirect signs

- displacement of fissures - opacification of the collapsed lobe- crowding of vessels

- displacement of the hilum- mediastinal shift toward the side of collapse-elevation of ipsilateral diaphragm- loss of volume on ipsilateral hemithorax- crowding of the ribs- compensatory hyperlucency of the remaining lobes- silhouetting of the diaphragm or the heart border

Pulmonary Abscess

Mithi Kalayaan S. Zamora

Pulmonary AbscessNecrosis of the pulmonary tissueFormation of cavities containing necrotic

debris or fluid Caused by microbial infection

Most common pathogens are anaerobic bacteria, but about half of all cases involve both anaerobic and aerobic organisms such as streptococci and staphylococci

Usually caused by bacterial infection from lung aspiration of oral secretions/ food (aspiration pneumonia)

Pulmonary Abscess

DurationAcute: <4-6 weeksChronic: >6 weeks

EtiologyPrimary: infectious in originSecondary: caused by a preexisting condition,

spread from an extrapulmonary site, bronchiectasis and/or an immunocompromised state

Signs and SymptomsProductive coughFeverSweatsWeight LossDecreased breath soundsCracklesEgophonyDullness to percussion

Pathophysiology

Inflammation

Tissue necrosis

Abscess formation

Rupture into a bronchus

Air- and fluid-filled cavity

Radiographic Findings

Findings include:Presence of thick-walled cavitary lesionPresence of pleural effusionPresence of consolidationPresence of air-fluid level

Right lower lobe most common site of infection

Cavitary lesion, thick-walled, with air-fluid level

Cavity

Pleural effusion

FUNGUS BALL

Marian Clare U. Toledo

• Most commonly caused by Aspergillus fumigatus

• Aspergillus grows on dead leaves, stored grain, compost piles, and other decaying vegetation

• Roughly spherical mass-like collection of fungal hyphae, mixed with mucus and cellular debris

FUNGUS BALL

PULMONARY ASPERGILLOSIS• Saprophytic aspergillosis, or aspergilloma: most

common form, colonization of preexisting cavities

• Allergic bronchopulmonary aspergillosis (ABPA): hypersensitivity reaction to the fungus

• Chronic necrotizing aspergillosis: cavitary pneumonic illness that often affects patients with preexisting chronic lung disease

• Angioinvasive aspergillosis:affects immunocompromised patients

ASPERGILLOMA

• Usually asymptomatic, but may also present with:CoughFeverChest PainDifficulty of breathingHemoptysis

• Diagnostic tests:Chest x-rayChest CT scanSputum culture

RADIOGRAPHIC FINDINGS• Seen in x-ray and CT as a round or ovoid

intracavitary massCan be outlined by a lucency of air

• Monod Sign • Air Crescent Sign –indicates recovery phase

Can fill the whole cavity• Small area of consolidation around cavity is

typical• Usually Mobile• Adjacent pleura may be thickened

Monod Sign Air-crescent

THANK YOU!

Pulmonary EmphysemaGk. Emphysan “inflate”; en “in”; physan “inflate”

Angelique Bea C. Uy

Block 8

Pulmonary Emphysema

• permanent enlargement of airspaces distal to the terminal bronchioles and the destruction of the alveolar walls without obvious fibrosis

• bronchioles loose their elasticity and collapse, trapping air in the air sacs leading to hyperinflation

Signs & SymptomsDifficulty breathingProductive coughWheezing Weight lossProlonged expirationBreathes to pursed lipsBarrel chested

Risk Factor

SMOKING

Pathogenesis

Centrolobular PE• Most common• Airspace distension in central portion of lobule, with

sparing of distal parts• Affects upper more than lower lobes• Strongly associated with smoking• “Blue bloaters”

– Chronic hypoxemia with secondary polycythemia• Findings:

– Mild hyperinflation– Increased linear parenchymal markings– Bullae uncommon– “increased markings emphysema”

Panlobular PE

• Uniform distension of airspaces throughout lobule

• Predilection for lower lobes

• Associated with alpha-1-antitrypsin deficiency.

• Pink puffers”– Tachypnea– Normal pO2

• Findings:– Hyperinflated lungs– Peripheral vascular

attenuation– Normal size heart &

pulmonary vessels– Bullae common– “Arterial deficiency

emphysema”

Paraseptal PE• Selective distension of peripheral airspaces

adjacent to septa• Sparing of centrilobular region• Seen in immediate subpleural region of upper

lobes• May coalace to form apical bullae, which may

rupture to spontaneous pneumothorax

Paracicatricial/Irregular• Lung tissue associated with fibrosis that bears

no consistent relationship to a given portion of the lobule• Associated with old granulomatous

inflammation

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• Hyperaerated lungs- inc lucency with dec vascular markings on both sides

• Intercostal spaces enlarged• Narrowing of the diameter of the

heart- vertical heart- may be because of the dropping of diaphragm position and some degree of hypertrophy of RV

• Flattening and descent of diaphragm below ant 7th rib

• Blunting of costophrenic angle

• Hyperaerated lungs- inc lucency with dec vascular markings on L side

• Intercostal spaces mildly enlarged• Diaphragmatic domes flattened

below 7th rib• Blunting of costophrenic angle

Management

Smoking CessationSupplemental OxygenBronchodilatorsSteroidsLung volume reduction surgeryLung transplantation

Pulmonary Interstitial Emphysema

Grazielle S. Verzosa

Pulmonary Interstitial Emphysema

• Collection of gases outside of the normal air passages and inside the connective tissue of the peribronchovascular sheaths, interlobular septa, and visceral pleura secondary to alveolar and terminal bronchiolar rupture

• A Type of “Air Leak Syndrome”– Air in the lungs → extra-alveolar spaces

Pulmonary Air Leak Syndrome Types

• Pulmonary Interstitial Emphysema

• Pneumothorax• Pneumomediastinum• Pneumopericardium• Pneumoperitoneum• Subcutaneous

Emphysema

Pathophysiology

• Leakage of air into the pulmonary interstitial space, lymphatic and perivascular space– Poor lung compliance and Positive Pressure

Ventilation (respiratory distress) – Air trapping which leads to alveolar overdistention

• meconium aspiration syndrome• amniotic fluid aspiration

Pathophysiology

Pathophysiology

• PIE leads to compression of adjacent functional lung tissue and vascular structures and hinders both ventilation and pulmonary blood flow, resulting in impedance of oxygenation, ventilation, and blood pressure.

• PIE is a vicious cycle. PIE in one lung causes compression atelectasis of the adjacent lung, leading to the need for more ventilation which leads to more chances of air leak.

Risk Factors• Very Low birth weight• Premature• Low APGAR• Respiratory Distress Syndrome• Amniotic fluid aspiration• Infection• Neonatal sepsis• Pneumonia• Hypoplastic lung


• Linear lucencies: coarse, non-branching, 3-8 mm, vary in width, rarely exceed 2 mm

• Can be confused with air-bronchogram • Cyst-like radiolucencies: diameter from 1-4

mm, generally round but may appear oval or slightly lobulated

• Hyperaerated lungs• Displacement of adjacent organs to the

contralateral side

AP View•Right lung occupies the entire right side of the thoracic cavity, heart is pushed to the left side

•Low right HD compared to the left

•Multiple areas of disorganized, non-branching, linear to cyst-like lucencies with non-uniform sizes

Lateral View

Pulmonary Arterial Hypertension

Roger Velasco

Pulmonary Arterial Hypertension (PAH)

Definition–Abnormal elevation in pulmonary artery pressure–> 25 mmHg at rest (systolic)–> 30 mmHg during exercise (systolic)

Causes–Left heart failure–Pulmonary parenchyma or vascular disease–Thromboembolism–Combination–L to R shunts in ASD, VSD, PDA–PAH is the most common cause of Cor Pulmonale (RV enlargement)


Complications–RV hypertrophy–RV dilatation and failure

PathophysiologyIncrease in resistance within the pulmonary circulation

Increasing in RV systolic pressure to preserve cardiac output

Progressive remodeling of the vasculature (sustains pulmonary HPN even if the initiating factor is removed)


Radiologic findings–Enlarged central pulmonary arteries–Abrupt tapering of pulmonary arteries (pruning)–RV hypertrophy in later stages–Obliterated retrosternal space–Calcifications on elastic arteries due to atherosclerosis (specific for PAH)–Increased vascular calibre 1:2 (UL to LL)

Case (Plate 1 of 2)Findings

•Enlarged PA knob (white)•Enlarged central arteries (green)•Pruning (sharp fall-off in size from central to peripheral arteries) (blue)•Calcifications (red?)

Case(Plate 2 of 2)

Findings•MPA enlargement and its central branches •Pruning•Expected associated cardiac findings:

• Enlarged LA• Enlarged LV• Enlarged RV

•Calcification occasionally observed in central pulmonary vessels

Pulmonary arterial hypertension

11 Pulmonary Edema

Godfrey Josef R. Torres

Pulmonary Edema

• accumulation of fluid in the interstitial or alveolar compartment

Causes:1.Alterations in Starling forces

– hydrostatic (cardiogenic), oncotic (e.g. renal, hepatic)2.Lymphatic changes

– overwhelmed lymphatics, tumor compression/destruction3.Injury

– of capillaries (e.g. ARDS)

Signs Cardiac Renal Lung InjuryHeart size Enlarged Normal NormalBlood flow Inverted Balanced NormalKerley lines Common Common Absent

Edema Basilar Central butterfly Diffuse

Air bronchograms

Not common Not common Very common

Pleural effusions Very common Common Not common

Pulmonary Edema

Early stages: fluid in lower lobes

Advanced stages: all lobes may be involved


• Perihilar haziness

• Peribronchial cuffing

• Cephalization

• Monocle sign - ↑ vessel:bronchiole ratio

• Kerley lines

• Bat’s wing/Pulmonary opacities

Radiographic Findingss

• Perihilar haziness (1)

• Cephalization (2)

• Monocle sign (3) 1

2

3

Kerley A

Kerley B


• Bat’s wings

Pulmonary EdemaStages according to Pulmonary Capillary Wedge Pressure (studied on patients with Acute cardiac decompensation)

Grade 0-Pulmonary Capillary Wedge Pressure probably a bout 8 to 12 mm Hg (NORMAL)

Grade 1 Pulmonary Edema- PCWP 12 to 18 mmHg

-Expected radiographic findings:a.Cephalization (due to constriction of lower lobe vessels)

Pulmonary EdemaGrade 2 Pulmonary Edema (aka Interstitial Edema)

-PCWP ~ 19 to 25 mmHg

-Expected radiographic findings:

a.Loss of vascular definition

b.Peribronchial cuffing

c.Kerley B lines

Grade 2 Pulmonary Edema (aka Interstitial Edema)

Radiographic Findings :

(-) Heart size enlargement (CT ratio: 0.5)(+) Blood flow inversion (cephalization)(+) Kerley B lines(+) Peribronchial cuffing(+) Increased vascular pedicle width (0.8 cm, normal: 0.5)(-) Basilar edema(-) Airbronchograms(-) Pleural effusion

Pulmonary EdemaGrade 3 Pulmonary Edema (aka Alveolar Filling)

-PCWP > 25 mmHg

Expected radiographic findings:a.Perihilar opacityb.Lower opacity

Radiographic Findings(+) Heart size enlargement (CT ratio: 0.65)(+) Blood flow inversion (cephalization)(+) Peribronchial cuffing(+) Increased vascular pedicle width (0.85 cm, normal: 0.5)(+) Basilar edema(-) Airbronchograms

*Pleural effusion possible due to blunting of CPA

Pulmonary Edema• Slides shown are probably stages of Pulmonary Edema secondary to a cardiac

cause• Differentials:If with heart enlargement:1. Outflow obstruction with LV failure (e.g. Aortic stenosis)2. Chronic LV failure (post-MI)3. Obstruction or incompetent mitral valve (MS, MR, left atrial myxoma); with LA

enlargementIf without heart enlargement:1. Acute MI or Acute MR2. AS w/o LV failure (yet)3. Obstruction of central pulmonary veins (fibrosing mediastinitis, PV thromosis)4. Renal5. Lung injury (e.g. Shock, severe burns, sepsis, narcotic overdose, pancreatitis,

drowning)

Pulmonary Congestion

Constantine L. Yu Chua

Pulmonary Congestion

• Some sources use “pulmonary congestion” and “pulmonary edema” similarly.

• Some would say that pulmonary congestion would precede pulmonary edema.

• Pulmonary congestion is engorgement with blood in the vessels of the lungs.

• Pulmonary edema accumulation of fluid inside the air spaces of the lungs.

Non-cardiogenic

• “Pulmonary edema”• Altered alveolar-capillary membrane

permeability• Decreased plasma oncotic pressure• Increased negativity of interstitial pressure• Lymphatic insufficiency• Neurogenic• Narcotic overdose

Cardiogenic

• “Congestive heart failure”• Pulmonary congestion pulmonary edema• Left sided failure due to any of the following:

– Myocardial infarction– Tachyarrhythmias– Myocarditis– Myocardiopathy– Aortic/mitral stenosis or regurgitation– B blocker/CCB overdose

Pulmonary Congestion FindingsStructural or physiological mechanisms Radiographic correlate

Thickening of interlobular septa due to excess pressure

Kerley lines

Recruitment of apical vessels to accommodate excess blood (back)flow

Cephalization

Possible left sided heart failure Cardiomegaly

Back flow of blood from right ventricle to right atrium to pulmonary vein

Predominantly perihilar haziness

Kerley A Kerley B Kerley C

Long and oblique, from hila; present only with Kerley B lines

Most common, 1-2 cm, horizontal, perpendicular to pleural surface

Reticular network of lines, not usually seen

Herring, W. (2002). Congestive Heart Failure. Retrieved August 15, 2011 from Learning Radiology website: http://www.learningradiology.com/lectures/cardiaclectures/chfppt.pdf

Cardiogenic Non-cardiogenic

• Cardiomegaly more often• Kerley lines• Cephalization• “Butterfly appearance” – greater

density of vessels in perihilar region• Pleural effusion more common

• Usually no cardiomegaly• Alveolar edema• Lack of cephalization

Plates• Kerley lines• Perihilar haziness• Cephalization• Cardiomegaly

Cystic Bronchiectasis

R. Soyangco

• Irreversible dilatation of the bronchi resulting from infection.– Insult chronic inflammation cartilage damage and

abnormal permanent dilatation of bronchi

• Maybe focal (previous PTB) or diffused (cystic fibrosis)

• 3 morphologic forms: cylindric, varicose, saccular or cystic

• Clinical Presentations:– Productive cough– Hemoptysis– Dyspnea– Wheezing– Pleuritic chest pain– Fever– Weakness– Weight loss

• Radiographic findings (often non-specific):– Scarring– Volume loss– Loss of sharp definition of the bronchovascular markings• For the given plates:– Cystic bronchiectasis: multiple peripheral thin-walled cysts,

with or without air fluid levels, that tend to cluster together in the distribution of a bronchovascular bundle (“honeycomb”)

Fibrothorax

Angelli Tolibas

Fibrothorax

• defined as pleural thickening extending over more than ¼ of the costal pleural surface

• dense fibrous layer of approximately 2 cm thickness; almost always on visceral pleura

• The thickness of pleura in fibrothorax should not exceed 5cm. – If >5cm, suspect mesothelioma (malignancy of

pleura)

Etiology

• 3 main causes:– Hemothorax– Tuberculosis– Bacterial lung infection

• Other causes:Collagen vascular diseasesParagonimiasisUremiaDrug reactionsAsbestos-related pleural disease

Pathophysiology

When pleural inflammation is intense, its resolution may be associated with the deposition of a thick layer of dense fibrous tissue on the visceral pleura.

As a result of the marked pleural thickening, the hemithorax becomes contracted, and its mobility is reduced.

As the fibrothorax progresses, the intercostal spaces may narrow, the size of the involved hemithorax may diminish, and the mediastinum may be displaced ipsilaterally.

Pathophysiology:

• Radiologically, a peel of uniform thickness surrounds the lung.

• Calcification occurs frequently on the inner aspect of the peel and provides an indicator by which the thickness of the peel may be accurately measured .

Clinical Manifestations

• Symptoms– Chest tightness and pain– Non-productive cough– Fatigue/Malaise– Difficulty breathing

• Signs– unequal chest expansion– reduced excursion of ipsilateral hemi-diaphragm– dullness on percussion– impaired transmission of breath sounds

What to look for

• “pleural peel” surrounds the lungnarrowing of the ipsilateral intercostal spaces

• Pleural calcifications (usually on inner side of peel)

• Ipsilateral shift of mediastinum to area of decreased lung volume

• Deviation of the thorax, trachea, and spine

• Blunting of the lateral costophrenic sulcus may be seen

Thoraxic displacement

Narrowed ICS

Pleural peel/ veil-like opacity

Mediastinal shift

Obliterated costophrenic angle

Management

• Pleurectomy (Decortication)– Peeling or stripping of a constricting

membrane from the pleural surface

Pleural Effusion

VERGARA, Nicho Angelo

Pleural Effusion

• Excess fluid (>5 mL) that accumulates in the pleural cavity

• Mismatch between the rates of inflow and outflow of fluid in the pleural space

• Two types:– transudative– exudative

Blunting or Meniscus sign

• Lateral decubitus– at least 5-10mL

• Lateral upright – at least 50 mL

• PA upright– at least 200mL

Remember that:

• radiographic appearance depends on – the patient's position – the mobility of the pleural fluid

• Sensitivity to detect pleural effusion– lateral decubitus > lateral (upright) > PA (upright)

• Supine radiographs– Increased opacity with or without obscuration of

the vascular markings– Apical cap

Subpulmonic Effusion

Subpulmonic effusion

• usually less than 300-350cc• accumulates at base of lung between visceral

and parietal pleura• follows the contour of the hemidiaphragm• more often right-sided, transudative, and due

to cardiac failure

Radiographic signs

• apparent lateral displacement of the dome of hemidiaphragm

• increased distance between stomach bubble and base of lung

• “Flat-edge sign” on lateral view

lateral displacement of the dome of hemidiaphragm

increased distance between stomach bubble and base of lung

Summary

• Blunting or Meniscus Sign• Opacification of the Hemithorax in supine• Subpulmonic Effusion

– displacement of the dome of hemidiaphragm– Increased distance in between gastric bubble and

hemidiapragm

Pneumothorax

Ann Camille Q. Yuga

Pneumothorax

• Accumulation of gas in the pleural space

• Hydropneumothorax = air + water• Hemopneumothorax = air + blood• Pyopneumothorax = air + pus• Chylopneumothorax = air + chyle

• Classification of pneumothorax:A. Spontaneous : without antecedent trauma to the

thorax(1) Primary spontaneous: occurs in the absence

of underlying lung disease(2) Secondary spontaneous: accompanies an

underlying lung disease

B. Traumatic pneumothorax : can result from both penetrating and blunt chest trauma

*Iatrogenic pneumothorax: results from a complication of a diagnostic or therapeutic intervention

C. Tension pneumothorax: occurrence of positive pleural pressure, which is transmitted to the mediastinum resulting in decreased venous return to the heart and reduced cardiac output

• Radiographic manifestations:

Pleural line (PA and lateral view)Pleural gas findings notable in the apex and in the

space between the lung and chest wall (upright) or juxtacardiac area, lateral chest wall and subpulmonic region (supine)

“deep sulcus sign” - deep costophrenic angle

• Radiographic manifestations of tension pneumothorax:

Mediastinal shift – displacement of the mediastinal organs from the midline position on maximum inspiration

Diaphragmatic depressionRib cage expansion

Skin fold Artifactual densities

Avascular bullae/ thin-walled cysts

False positive Vascular markings are still visible beyond the skin fold

Artifactual densities usually do not parallel the course of the chest wall over their entire length

Inner margin of bullae/ cysts usually are concave rather than convex and do not conform exactly to the contours of the costophrenic sulcus

True pneumothorax

Absence of vascular marking beyond the pleural line

Pleural line usually parallels the shape of the chest wall

Pleural line is usually bowed at the center toward the lateral chest wall.

PNEUMOHYDROTHORAX

Ralph Rommualdo A. Zuniega

PNEUMOHYDROTHORAX

• Accumulation of fluid and air in the pleural cavity

• Combination of pneumothorax and hydrothorax

PNEUMOHYDROTHORAX: CAUSES

• Trauma

• Spontaneous pneumothorax

• Bronchopleural fistula

• Infection

• Diffuse lung disease

PNEUMOHYDROTHORAX: RADIOLOGIC FEATURES

• Blunting of the Costophrenic angle

• Separation of the visceral and parietal pleura




• Displacement of the mediastinum from the midline created by the presence of air

PNEUMOHYDROTHORAX: MANAGEMENT

• Chest tube drainage

• If loculated, CT guidance

MEDIASTINAL MASS

Angeli Waga

Normal Mediastinum

MEDIASTINAL MASS STATSMost masses (> 60%) are: Thymomas Neurogenic Tumors Benign Cysts Lymphadenopathy(LAD)I

In children the most common (> 80%) are: Neurogenic tumors Germ cell tumors Foregut cysts

In adults the most common are: Lymphomas Lympadenopathies Thymomas Thyroid masses

Step 1: Mediastinal mass vs Lung mass

Step 2: Localize in the Mediastinum

ANTERIOR MEDIASTINUM• PA: Widening at the superior mediastinum• L: Obliterated retrosternal clear space

ANTERIORMEDIASTINU

M

• Hilum overlay sign

ANTERIORMEDIASTINU

M

• Hilum overlay sign

• Silhouette sign

MIDDLEMEDIASTINUM

• Mass located anterior to the spine

MIDDLE MEDIASTINUM

• Mass surrounding right bronchus – “Donut Sign

POSTERIOR MEDIASTINUM• Cervicothoracic sign

Hematogenous and Lymphangitic Metastasis

Jeremiah R. Vallente

Lung Metastasis

a) direct invasionb) hematogenous

spread

Hematogenous Metastasis

a) pulmonary nodules

b) lymphangitic carcinomatosis

Pulmonary Nodules

• usually multiple, sometimes solitary

• usually bilateral• well defined, discrete,

nodular opacities of different sizes

• “cannonball” appearance• in greater numbers in the

peripheral portions of the lower lobes

Pulmonary Nodules

• usually multiple, sometimes solitary

• usually bilateral• well defined, discrete,

nodular opacities of different sizes

• “cannonball” appearance• in greater numbers in

the peripheral portions of the lower lobes

Primary lesion– usually lobulated or spiculated

Metastatic lesion– usually smooth in contour

Lymphangitic Carcinomatosis

• tumor cells invade the lymphatics within the peribronchovascular and peripheral interstitium, resulting in lymphatic dilatation, interstitial edema, and fibrosis

Lymphangitic Carcinomatosis• peripherally

radiating, coarse reticular parahilar opacities

• irregular, strand-like network of interstitial-type density

• extending outward from the hila well into the parenchyma

Lymphangitic Carcinomatosis• peribronchial

cuffing• linear opacities

(Kerley B lines)

Asbestosis

April C. Tagayona

Asbestos

• a group of minerals characterized by their fibrous crystalline structure that is composed mainly of silicate.

• found in materials used in heat and acoustic insulation, fireproofing, and roofing and flooring

Asbestosis• The Lung Center of the Philippines’ Asbestos

Screening Program (1993 to 1996) examined former workers from the Subic Naval Base in Zambales for the presence of asbestos-related disease.

• A total of 1,441 workers were screened for asbestos-related lung diseases by CXR.

• 502 workers were noted to have asbestosis

Asbestosis• Inflammation of the lungs due to chronic

inhalation of asbestos particles.• Men over age 40 with asbestos exposure are

more likely to be affected. • Risk increases with

– „ Work that involves asbestos – „ Smoking – „ Excess alcohol use

Clinical manifestations

o Clinically manifests 15-20 years after initial exposureo Most common

Shortness of breath, restrictive pattern on PFTs End-expiratory bibasal crackles

*non-specific: resembles signs and symptoms of other restrictive interstitial lung diseases

Pathophysiology

Stages of asbestosis progression

Stage I a fine, reticular

pattern, associated with ground-glass appearance: which may indicate a combination of alveolitis and interstitial fibrosis

usually at the lung bases


Stage II characterized by

progression of the small, irregular opacities into a prominent interstitial pattern

a combination of parenchymal and pleural abnormalities may partially obscure the heart border (shaggy heart sign) and diaphragm.


Stage III progression of the coarse

interstitial pattern and honeycombing to the upper lung zones occurs

the heart and diaphragm are further obscured

Asbestosis

• Coarse interstitial pattern

• Pleural plaques• Shaggy heart

sign

BLOCK 8

Pulmonary Radiology

View Box

pulmo viewboxes block 8

Documents

heart enlargement

pulmonary edema secondary

pulmonary vein kerley

yu chua pulmonary congestion

cpa pulmonary edemaslides

structures present

left ribs

kerley b lines kerley