pulmo viewboxes block 8
DESCRIPTION
Pulmo viewboxes BLOCK 8TRANSCRIPT
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BLOCK 8 brings you
The Viewbox
ofPulmonary Radiology
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Normal Chest
April C. Tagayona
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Outline
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Projection
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Projection
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Projection
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Projection
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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
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Position
Oblique ViewIndications• Assess tracheal
bifurcation• Study heart, hilum
and ribs
Tracheal lumen should normally be about 1.5cm.
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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
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Exposure
PA VIEWGood exposure if the spines of T1 – T4 are exposed.
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ExposurePA VIEW
Underexposure if <T4 are exposed Overexposure if >T4 are exposed
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Exposure
LATERALGood exposure if sternum is visible and right and left ribs overlap
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Inspiratory Effort
Adequate if the diaphragm is along the 5th to 6th anterior rib or the 9th to 10th posterior rib
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Inspiratory Effort
Inadequate effort• Crowding• Increased lung markings• Wide mediastinum
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Obliquity
Spinous process and clavicular heads used as reference = equidistant
Structures should be symmetrical on right and left.
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Outline
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Lungs
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Lungs
Symmetrical radiolucency Bronchovascular ratio R hilum lower
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Lungs• Fissures slightly visible
• Right Lung: 3 lobes and 2 fissures• Left Lung: 2 two lobes and 1 fissure
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Lungs
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Lungs
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Lungs Vasculature
• Tapering from central to periphery
• Outer 1/3 usually has no markings
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Trachea
Midline, within the boundaries of the vertebral body
Location: C6 – T5
Bifurcates at T5
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Trachea
Tracheal lumen: 1.5 cm
Subcarinal angle must be <900
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Heart
• Right border:SVC, RA, IVC
• Left border:Aortic arch, left pulmonary a.,left atrial appendage,left ventricle
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Heart
• Cardiothoracic ratio– Adults:
<0.50 – 0.52– Children:
<0.56
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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
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Diaphragm
R hemidiaphragm is higher than the L, lies at 5th ICS on moderately deep inspiration
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Pneumonia
MG Villafuerte
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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
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Pneumonia• Clinical manifestation:
– Fever– Cough– Dyspnea, pleuritic chest pain
On PE:– Rales– Diminished breath sounds (localized)– Percussion dullness– Egophony on auscultation
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Radiographic FindingsAirspace opacities Intersitital opacities ConsolidationAir bronchograms• Possible complications:
– Pleural effusions– Empyema– Atelectasis– Pneumothorax
• usually in basal segments
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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
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Lobar pneumonia
• Increased opacity/ consolidation of the left lower lobe
• increased density behind the left heart shadow
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• 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.
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Right Upper Pneumonia
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Right Middle Lobe Pneumonia
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Right Lower Lobe Pneumonia
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Bronchopneumonia
Multifocal
Patchy
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Management
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PULMONARY TUBERCULOSIS
JC Tayag
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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
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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
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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
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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
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Radiological Findings
• Tuberculoma• Focal nodular
opacities• Cavitation• Bronchiectasis• Endobronchial spread• Atelectatic changes• Secondary
emphysema
• Consolidation• Pleural effusion• Miliary TB
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Tuberculoma
• Solitary
• Well-defined
• Up to 4 cm in diameter
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Focal Nodular Opacities
• 2-10 mm in diameter
• Localized to one or two regions of the lungs
• Common in upper lung segments
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Cavitation
• Thick-walled cystic structure
• Irregular inner lining
• Wall thickness at least 1 mm
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Bronchiectatic Changes
• Abnormal permanent dilatation of the bronchi
• Thickened bronchi
• Reticular pattern
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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
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Endobronchial Spread
• Tree-in-bud pattern
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Right upper lobe infiltrates with
possible atelectatic
changes
Atelectatic Changes
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•Cavity formation
•Bullae
•Possible endobronchial spread
•Atelectasis = tracheal and mediaistinal deviation
•Compensatory hyperaeration of left lung
Diaphragmatic tenting
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Miliary TB
TALAN, Ceri Jane Homillano
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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
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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
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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.
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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
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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
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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.
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Diffuse, randomly distributed nodular lesions (1-2 mm in
size) in the lung parenchyma.
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Multiple nodular lesions seen in the lung parenchyma
and the neck region.
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Abdominal miliary TB. Multiple, randomly distributed nodules, about 3-4 mm, on the liver. Ascites might also
be present in these x-rays.
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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
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Atelectasis
KB Tagomata
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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
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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
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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
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Atelectasis
KB Tagomata
Complete right lung atelectasis
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Atelectasis
KB Tagomata
Complete right lung atelectasis
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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
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Pulmonary Abscess
Mithi Kalayaan S. Zamora
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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)
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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
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Signs and SymptomsProductive coughFeverSweatsWeight LossDecreased breath soundsCracklesEgophonyDullness to percussion
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Pathophysiology
Inflammation
Tissue necrosis
Abscess formation
Rupture into a bronchus
Air- and fluid-filled cavity
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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
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Cavitary lesion, thick-walled, with air-fluid level
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Cavity
Pleural effusion
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FUNGUS BALL
Marian Clare U. Toledo
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• 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
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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
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ASPERGILLOMA
• Usually asymptomatic, but may also present with:CoughFeverChest PainDifficulty of breathingHemoptysis
• Diagnostic tests:Chest x-rayChest CT scanSputum culture
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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
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Monod Sign Air-crescent
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THANK YOU!
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Pulmonary EmphysemaGk. Emphysan “inflate”; en “in”; physan “inflate”
Angelique Bea C. Uy
Block 8
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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
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Signs & SymptomsDifficulty breathingProductive coughWheezing Weight lossProlonged expirationBreathes to pursed lipsBarrel chested
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Risk Factor
SMOKING
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Pathogenesis
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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”
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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”
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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
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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
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• 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
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Management
Smoking CessationSupplemental OxygenBronchodilatorsSteroidsLung volume reduction surgeryLung transplantation
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Pulmonary Interstitial Emphysema
Grazielle S. Verzosa
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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
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Pulmonary Air Leak Syndrome Types
• Pulmonary Interstitial Emphysema
• Pneumothorax• Pneumomediastinum• Pneumopericardium• Pneumoperitoneum• Subcutaneous
Emphysema
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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
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Pathophysiology
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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.
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Risk Factors• Very Low birth weight• Premature• Low APGAR• Respiratory Distress Syndrome• Amniotic fluid aspiration• Infection• Neonatal sepsis• Pneumonia• Hypoplastic lung
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Radiographic Findings
• 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
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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
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Lateral View
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Pulmonary Arterial Hypertension
Roger Velasco
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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)
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Pulmonary Arterial Hypertension (PAH)
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)
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Pulmonary Arterial Hypertension (PAH)
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)
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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?)
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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
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Pulmonary arterial hypertension
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11 Pulmonary Edema
Godfrey Josef R. Torres
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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)
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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
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Pulmonary Edema
Early stages: fluid in lower lobes
Advanced stages: all lobes may be involved
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Radiographic Findings
• Perihilar haziness
• Peribronchial cuffing
• Cephalization
• Monocle sign - ↑ vessel:bronchiole ratio
• Kerley lines
• Bat’s wing/Pulmonary opacities
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Radiographic Findingss
• Perihilar haziness (1)
• Cephalization (2)
• Monocle sign (3) 1
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Kerley A
Kerley B
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Radiographic Findings
• Bat’s wings
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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)
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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
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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
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Pulmonary EdemaGrade 3 Pulmonary Edema (aka Alveolar Filling)
-PCWP > 25 mmHg
Expected radiographic findings:a.Perihilar opacityb.Lower opacity
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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
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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)
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Pulmonary Congestion
Constantine L. Yu Chua
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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.
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Non-cardiogenic
• “Pulmonary edema”• Altered alveolar-capillary membrane
permeability• Decreased plasma oncotic pressure• Increased negativity of interstitial pressure• Lymphatic insufficiency• Neurogenic• Narcotic overdose
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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
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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
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Herring, W. (2002). Congestive Heart Failure. Retrieved August 15, 2011 from Learning Radiology website: http://www.learningradiology.com/lectures/cardiaclectures/chfppt.pdf
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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
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Plates• Kerley lines• Perihilar haziness• Cephalization• Cardiomegaly
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Plates• Kerley lines• Perihilar haziness• Cephalization• Cardiomegaly
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Plates• Kerley lines• Perihilar haziness• Cephalization• Cardiomegaly
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Cystic Bronchiectasis
R. Soyangco
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• 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
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• Clinical Presentations:– Productive cough– Hemoptysis– Dyspnea– Wheezing– Pleuritic chest pain– Fever– Weakness– Weight loss
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• 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”)
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Fibrothorax
Angelli Tolibas
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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)
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Etiology
• 3 main causes:– Hemothorax– Tuberculosis– Bacterial lung infection
• Other causes:Collagen vascular diseasesParagonimiasisUremiaDrug reactionsAsbestos-related pleural disease
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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.
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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 .
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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
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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
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Thoraxic displacement
Narrowed ICS
Pleural peel/ veil-like opacity
Mediastinal shift
Obliterated costophrenic angle
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Management
• Pleurectomy (Decortication)– Peeling or stripping of a constricting
membrane from the pleural surface
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Pleural Effusion
VERGARA, Nicho Angelo
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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
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Blunting or Meniscus sign
• Lateral decubitus– at least 5-10mL
• Lateral upright – at least 50 mL
• PA upright– at least 200mL
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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
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Subpulmonic Effusion
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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
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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
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lateral displacement of the dome of hemidiaphragm
increased distance between stomach bubble and base of lung
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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
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Pneumothorax
Ann Camille Q. Yuga
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Pneumothorax
• Accumulation of gas in the pleural space
• Hydropneumothorax = air + water• Hemopneumothorax = air + blood• Pyopneumothorax = air + pus• Chylopneumothorax = air + chyle
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• 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
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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
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• 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
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• Radiographic manifestations of tension pneumothorax:
Mediastinal shift – displacement of the mediastinal organs from the midline position on maximum inspiration
Diaphragmatic depressionRib cage expansion
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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.
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PNEUMOHYDROTHORAX
Ralph Rommualdo A. Zuniega
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PNEUMOHYDROTHORAX
• Accumulation of fluid and air in the pleural cavity
• Combination of pneumothorax and hydrothorax
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PNEUMOHYDROTHORAX: CAUSES
• Trauma
• Spontaneous pneumothorax
• Bronchopleural fistula
• Infection
• Diffuse lung disease
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PNEUMOHYDROTHORAX: RADIOLOGIC FEATURES
• Blunting of the Costophrenic angle
• Separation of the visceral and parietal pleura
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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
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• 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: RADIOLOGIC FEATURES
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• 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: RADIOLOGIC FEATURES
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PNEUMOHYDROTHORAX: MANAGEMENT
• Chest tube drainage
• If loculated, CT guidance
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MEDIASTINAL MASS
Angeli Waga
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Normal Mediastinum
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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
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Step 1: Mediastinal mass vs Lung mass
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Step 2: Localize in the Mediastinum
ANTERIOR MEDIASTINUM• PA: Widening at the superior mediastinum• L: Obliterated retrosternal clear space
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ANTERIORMEDIASTINU
M
• Hilum overlay sign
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ANTERIORMEDIASTINU
M
• Hilum overlay sign
• Silhouette sign
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MIDDLEMEDIASTINUM
• Mass located anterior to the spine
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MIDDLE MEDIASTINUM
• Mass surrounding right bronchus – “Donut Sign
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POSTERIOR MEDIASTINUM• Cervicothoracic sign
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Hematogenous and Lymphangitic Metastasis
Jeremiah R. Vallente
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Lung Metastasis
a) direct invasionb) hematogenous
spread
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Hematogenous Metastasis
a) pulmonary nodules
b) lymphangitic carcinomatosis
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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
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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
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Primary lesion– usually lobulated or spiculated
Metastatic lesion– usually smooth in contour
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Lymphangitic Carcinomatosis
• tumor cells invade the lymphatics within the peribronchovascular and peripheral interstitium, resulting in lymphatic dilatation, interstitial edema, and fibrosis
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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
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Lymphangitic Carcinomatosis• peribronchial
cuffing• linear opacities
(Kerley B lines)
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Lymphangitic Carcinomatosis• peribronchial
cuffing• linear opacities
(Kerley B lines)
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Lymphangitic Carcinomatosis• peribronchial
cuffing• linear opacities
(Kerley B lines)
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Asbestosis
April C. Tagayona
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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
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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
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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
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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
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Pathophysiology
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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
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Stages of asbestosis progression
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.
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Stages of asbestosis progression
Stage III progression of the coarse
interstitial pattern and honeycombing to the upper lung zones occurs
the heart and diaphragm are further obscured
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Asbestosis
• Coarse interstitial pattern
• Pleural plaques• Shaggy heart
sign
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BLOCK 8
Pulmonary Radiology
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