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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
Exposure
PA VIEW
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
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
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
We want to know which lobe of the lung is affected. Thus, we usually request for both a PA/AP and a lateral view.
Bronchopneumonia
Multifocal Patchy
Interstitial pneumonia
Management
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
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
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
Miliary-Like millet seeds, John Jacobus Manget, 1700 Each one is a granuloma with central caseation necrosis surrounded by epitheliod cells and fibrous tissue.
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
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
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
Cavity
Pleural effusion
FUNGUS BALL
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
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
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
Grazielle S. Verzosa
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
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
Roger Velasco
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)
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
11 Pulmonary Edema
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)
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
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
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
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
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
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
Thoraxic displacement
Narrowed ICS
Mediastinal shift
Management
Pleurectomy (Decortication)
Peeling or stripping of a constricting membrane from the pleural surface
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
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
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
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
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
Skin fold
Artifactual densities
False positive
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 Pleural line Pleural line is usually parallels usually bowed at the shape of the the center toward chest wall the lateral chest
PNEUMOHYDROTHORAX
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: MANAGEMENT
Chest tube drainage If loculated, CT guidance
MEDIASTINAL MASS
Angeli Waga
Normal Mediastinum
ANTERIOR MEDIASTINUM PA: Widening at the superior mediastinum L: Obliterated retrosternal clear space
Jeremiah R. Vallente
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
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
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
Asbestosis
Coarse interstitial pattern Pleural plaques Shaggy heart sign
BLOCK 8
View Box
Pulmonary Radiology