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BLOCK 8

brings you

The Viewbox
of Pulmonary Radiology

Normal Chest

April C. Tagayona

Outline
 Assessment of technical factors
Projection Position Adequacy Exposure Inspiratory Effort Obliquity

 Examine
Lungs Heart Mediastinum Trachea Diaphragm Osseous structures Soft tissues

Projection
Criteria Direction of Beam PA AP X-ray beam from behind, X-ray beam from the front to plate in front of the patient posterior, plate behind the patient Upright Supine

Patient Position

Projection
Criteria Mongolian Hat Sign Present PA AP Absent; vertebral bodies are rectangular

Projection
Criteria Ribs Clavicle Angulated V-shaped PA AP Straighter More horizontal

Projection
Criteria PA Scapula Winging Heart magnification Heart not magnified AP No winging Heart and other structures more magnified

Position
Lateral Position
Indications 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 criteria a) Ribs posterior to vertebrae should be superimposed b) CP angles and lung apices included c) Hilar region should be at center d) Circular structures on this view may represent blood vessels

Position
Oblique View
Indications 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-offs
o Apices should be visualized especially when suspecting pneumothorax and TB o Costophrenic angles should be visualized especially with pleural effusion

Exposure

PA VIEW Good exposure if the spines of T1 T4 are exposed.

Exposure
PA VIEW

Underexposure if <T4 are exposed

Overexposure if >T4 are exposed

Exposure

LATERAL Good 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
 Assessment of technical factors
Projection Position Adequacy Exposure Inspiratory Effort Obliquity

 Systematic Approach
Lungs Heart Mediastinum Trachea Diaphragm Osseous structures Soft tissues

Lungs

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

Lungs

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 Findings
 Airspace opacities  Intersitital opacities  Consolidation  Air 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 Pores edema inflammatory of Khonspreads interalveolar connections to adjacent lung via the (pores airways and alveoli) terminalb/w adjacentpores of for collateral ventillation Kohn allows passage of other materials such as fluid or homogenous opacification at bacteria
the left lower lung

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

Interstitial pneumonia

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 Inflammation and enlargement of hilar and mediastinal lymph nodes Granuloma w/ central caseation necrosis
Macrophages epitheloid cells Delayed hypersensitivity

Inflammatory focus

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

Atelectatic Changes
Right upper lobe infiltrates with possible 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 Populations  Iatrogenic

Clinical Findings
 Weakness, 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 plugging Lobar atelectasis Segmental 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 atelectasis Cicatrization atelectasis

Atelectasis
KB Tagomata
Complete right lung atelectasis

Atelectasis
KB Tagomata
Complete right lung atelectasis

Radiography
Direct signs
- displacement of fissures - opacification of the collapsed lobe - crowding of vessels

Indirect signs
- 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 Abscess
Necrosis of the pulmonary tissue Formation 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
Duration
Acute: <4-6 weeks Chronic: >6 weeks

Etiology
Primary: infectious in origin Secondary: caused by a preexisting condition, spread from an extrapulmonary site, bronchiectasis and/or an immunocompromised state

Signs and Symptoms


Productive cough Fever Sweats Weight Loss Decreased breath sounds Crackles Egophony Dullness 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 lesion Presence of pleural effusion Presence of consolidation Presence 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

FUNGUS BALL
Roughly spherical mass-like collection of fungal hyphae, mixed with mucus and cellular debris
Most commonly caused by Aspergillus fumigatus Aspergillus grows on dead leaves, stored grain, compost piles, and other decaying vegetation

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:
 Cough  Fever  Chest Pain  Difficulty of breathing  Hemoptysis

Diagnostic tests:
 Chest x-ray  Chest CT scan  Sputum culture

RADIOGRAPHIC FINDINGS
Seen in x-ray and CT as a round or ovoid intracavitary mass
Can 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 Emphysema
Gk. 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 & Symptoms


 Difficulty breathing  Productive cough  Wheezing  Weight loss  Prolonged expiration  Breathes to pursed lips  Barrel 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
Pink puffers Uniform distension of Tachypnea airspaces throughout Normal pO2 lobule Findings: Predilection for lower Hyperinflated lungs lobes Peripheral vascular attenuation Associated with alpha Normal size heart & 1-antitrypsin deficiency.
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

1 2 1 4 2 5 3 6 3

10

11

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 Cessation Supplemental Oxygen Bronchodilators Steroids Lung volume reduction surgery Lung 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
Escape of air into the pulmonary interstitium, lymphatics, and venous circulation

Ventilation

Rupture of alveolar ducts

May remain or be taken up by the pulmonary lymphatic system

Gas dissects into the interstitium

Air leak persists with the pressure of ventilation and motion of respiration

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

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

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)

Pulmonary Arterial Hypertension (PAH)


Complications RV hypertrophy RV dilatation and failure Pathophysiology

Increase 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)

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)

Case (Plate 1 of 2)
Findings
Enlarged PA knob (white) Enlarged central arteries (green) Pruning (sharp falloff 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/destruction

3.Injury
of capillaries (e.g. ARDS)

Signs Heart size Blood flow Kerley lines Edema

Cardiac Enlarged Inverted Common Basilar

Renal Normal Balanced Common Central butterfly

Lung Injury Normal Normal Absent Diffuse Very common Not common

Air Not common Not common bronchograms Pleural Very common Common effusions

Pulmonary Edema
Early stages: fluid in lower lobes Advanced stages: all lobes may be involved

Radiographic Findings
Perihilar haziness Peribronchial cuffing Cephalization Monocle sign - vessel:bronchiole ratio Kerley lines Bats wing/Pulmonary opacities

Radiographic Findingss
Perihilar haziness (1) Cephalization (2) Monocle sign (3)
3 2

Kerley A

Kerley B

Radiographic Findings
Bat s wings

Pulmonary Edema
Stages 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 Edema
Grade 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 Edema
Grade 3 Pulmonary Edema (aka Alveolar Filling)
-PCWP > 25 mmHg Expected radiographic findings: a.Perihilar opacity b.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 enlargement If without heart enlargement: 1. Acute MI or Acute MR 2. AS w/o LV failure (yet) 3. Obstruction of central pulmonary veins (fibrosing mediastinitis, PV thromosis) 4. Renal 5. 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 Findings


Structural or physiological mechanisms Thickening of interlobular septa due to excess pressure Recruitment of apical vessels to accommodate excess blood (back)flow Possible left sided heart failure Back flow of blood from right ventricle to right atrium to pulmonary vein Kerley A Long and oblique, from hila; present only with Kerley B lines Kerley B Most common, 1-2 cm, horizontal, perpendicular to pleural surface Radiographic correlate Kerley lines Cephalization Cardiomegaly Predominantly perihilar haziness

Kerley C 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 Cardiomegaly more often Kerley lines Cephalization Butterfly appearance greater density of vessels in perihilar region Pleural effusion more common

Non-cardiogenic Usually no cardiomegaly Alveolar edema Lack of cephalization

Plates
Kerley lines Perihilar haziness Cephalization Cardiomegaly

Plates
Kerley lines Perihilar haziness Cephalization Cardiomegaly

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 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:
y Collagen vascular diseases y Paragonimiasis y Uremia y Drug reactions y Asbestos-related pleural disease

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

True Absence of pneumothorax vascular marking beyond the

Inner margin of bullae/ cysts usually are concave rather than convex and do not conform exactly to the contours of the costophrenic sulcus Pleural line Pleural line is usually parallels usually bowed at the shape of the the center toward chest wall the lateral chest

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

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: 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: 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 STATS


Most 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

ANTERIOR MEDIASTINU M Hilum overlay sign

ANTERIOR MEDIASTINU M Hilum overlay sign Silhouette sign

MIDDLE MEDIASTINUM 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 invasion b) 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, strandlike network of interstitial-type density extending outward from the hila well into the parenchyma

Lymphangitic Carcinomatosis
peribronchial cuffing linear opacities (Kerley B lines)

Lymphangitic Carcinomatosis
peribronchial cuffing linear opacities (Kerley B lines)

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 exposure o 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
Inhalation of fine asbestos fibers Deposition at airway bifurcations, bronchioles, alveoli Direct injury to epithelial cells and macrophages Release if reactive oxygen species, cytokines Alveolitis (INFLAMMATOY PHASE) Local proliferation of fibroblasts (FIBROSIS PHASE) Fibers migrate to distal sites (cetrifugal pattern; from bronchi then outward) Progressing Alveolitis and interstitial fibrosis

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

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.

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

Asbestosis
Coarse interstitial pattern Pleural plaques Shaggy heart sign

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Pulmonary Radiology