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Master radiology notes chest
1. Chest radiology 1
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Normal Chest
Oblique views : retrocardiac area, post. costophernic angles & chest walls.
AP view : ribs are projected over different areas of lung from those of PA + post chest
wall is shown.
Appicogram: A.Apical view : Pt leans back, AP projection & tube angled 50-60
upward (projection of clavicles up).
B.Lordotic view : PA view, Pt leans back, (project clavicles,also done in
cases of middle lobe collapse.
Paired :Insp. & exp. film.
1. Demonstrates air trapping
2. Diaphragm movement.
3. Small pneumothorax.
4. Interstitial shadowing.
Penetrated film :
1. To show the hidden areas.
2. Demonstration of rib destruction.
3. Cavitation or calcification.
4. Air bronchogram demonstration.
Comment on plain film:
I. Posteroanterior view :
1. Criteria of good quality film:
Centralization: med ends of clavicles = distance from spine t4
Full inspiration: ant 6th rib, post 10th rib .
Penetration: bodies, discs just visible through cord shadow upper 3rd only.
2. Trachea :
Examined for (narrowing, displacement, intraluminal lesion).
Normally, it is midline in its upper part, then deviates slightly to the right around
the aortic knuckle.
NB: *Right paratracheal strip:
- On the right side, the tracheal margin can be traced down to the right main
2. Chest radiology 2
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bronchus. It is present on 60% of films. Normally, it measures less than 5 mm.
Widening occurs with (tracheal malignancy, mediastinal tumors, pleur.effusion)
Azygus vein :
-Lies in the angle between the right main bronchus and trachea.
-Enlarged in (supine position, portal hypertension, I.V.C & S.V.C obstruction,
constrictive pericarditis).
- On erect film, should be < 10mm.
Carinal angle on inspiration is 60-75 degree.
Pathologically enlarged in a. Enlarged left atrium.
b. Enlarged carinal L.N.
3. Heart and mediastinum :
comment on size, shape, and displacement.
4. Diaphragm :
-Outline, shape, position.
-The right hemidiaphragm is higher than left (due to heart pushing on the left side
and not due to liver elevating the Rt), a difference greater than 3cm is significant.
The right hemidiaphragm can be traced from anterior to posterior on the lateral film, while the
left cannot.
-Loss of outlines means that the adjacent lung contains no air.
-On inspiration, the domes are at level of : * 6th rib anteriorly
* below or at 10th rib posteriorly. .
5. Pleura :
-Position of horizontal fissure. (The horizontal fissure runs from the hilum to region
of 6th rib).
-Costophrenic and cardiophrenic angles.
On lateral film : The horizontal fissure runs anteriorly.
Both oblique fissures, start posteriorly at the level of T4 or T5, passing through hilum.
- The left fissure finishes 5cm behind the anterior costophrenic angle, the right ends
Subpulmn. pleural effusion :
1. Erect PA : elevation of diaphragm & the apex of effusion has a more lat. position
2. Supine film : - Opaque hemithorax with decrease visualization of pulm vs.
- Blunt costophrenic angle.
- Apical cap.
- Loss of diaphragm out line
3. Decubitus view with horizontal beam : fluid level along the affected side.
3. Chest radiology 3
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6. Lung fields :
Hidden areas :(apices, diaphragm, mediastinum, hilae and bones).
7. Hilum :
Shape, position, density :
-Normally the left hilum is 1/2-1cm higher than right (because left pulm.a. lies above
the left main bronchus before passing post.)
-They should be of equal density and size with concave lateral borders.
-Only the pulmonary arteries and upper lobe veins significantly contribute to hilar
* Ant junctioned line: is where the lungs meet anterior to the ascending aorta. It is only 1 mm thick
(from below suprasternal notch).
* Post junctional line : is where the lungs meet posteriorly behind the esophagus. It is 2mm thick
(from
lung apex to level of knuckle).
* Thymus : both borders may be wavy (sign of Mulvey) dt costal cartilage indentation. It is sail
shaped, right border more straight male >female.
* Main fissures : (tangential x-ray beam)
1. PA : horizontal fissure runs from hilum to 6th rib in axillary lines may be slight down curve.
2. Lat : All fissures : oblique fissures commence post from D4 or D5 passing through ! hilum, !
left is steeper & finishes 5cm behind ! ant costophrenic angle.
* Accessory fissures :
1. Azygous fissure : comma shaped, base & nearly always rt sided (failed azygous v. to
migrate). Left side hemiazygous vein.
2. Superior accessory fissure : separates !apical from basal segments of lower lobes.
3. Inferior accessory fissure : separates ! medial basal from the other basal segments (from
cardio
phrenic angle).
4. Left sided horizontal fissure : separates lingula from other upper lobe segments.
Hidden areas :
1. Apices: appicogram.
2. Mediastinum and Hila: lateral film (for central lesions).
3. Diaphragms: post.& lat. basal segments of lower lobes & ! post. sulcus are partially observed.
4. Bones: AP, expiratory film & obliques - Tomography.
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shadows.
-The maximum diameter of normal descending branch of the right pulmonary
artery is 10-16mm in males, and 9-15mm in females.
-In erect position, the lower lobe vessels are larger than the upper lobe vessels as
the perfusion and areation of the upper zones are reduced.
-The pulmonary arteries accompanying the bronchi, while the veins :
a. Have fewer branches.
b. Less defined and larger.
c. Do not follow the bronchi.( They follow (drain via) interlobular septa)
* Upper lobe bronchus may appear as a ring shadow adjacent to upper outer hilum.
Pulmonary segments & bronchi :
8. Bronchial vessels :
-Normally not visualized on film.
-The arteries arise from ventral surface of the descending aorta at the level T5-T6.
-Enlarged bronchial arteries, appear as multiple small nodules around hilum.
Cause of enlargement :
* General (congestive cyanotic heart disease).
* Local (bronchiectasis, primary carcinoma).
Lymph nodes :
* Intrapulmn lymphatics drain to bronchopulmn node (1st group involved by spread from a periph.
tumor).
* Mediastinal Lns (may be involved by tumors above or below the diaphragm).
1. Ant. mediastinal nodes: (drain thymus & Rt heart - in region of aortic arch.).
2. Intrapulmn. nodes : along main bronchi.
3. Middle mediastinal nodes (lung, bronchi, lt ht, lower trachea & visceral pleura)
a. Bronchopulmn (hilar), drain into.
b. Carinal
c. Tracheo bronchial (Rt - adjacent to azygous , Lt - near RLN).
d. Paratracheal
4. Post mediastinal nodes : drain post diaphragm & lower oesophag. lie around lower descending
aorta & lower oesoph.
5. Parietal nodes: (ant & post behind sternum) ,drain soft tissue & parietal pleura (also intercostal
region).
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9. Pulmonary segments and bronchi (see Sutton)
-Pulm. segments not separated by pleura. Normal bronchi are not visualized in periph lung zones.
10. Acinus : (functioning lung unit).
-Is that portion of lung which arises from the terminal bronchiole.
-When filled with fluid, it is seen as a 5mm shadow = acinar or alveolar shadowing.
-The pores of Koha, connect the alveoli. The canals of lambert exist between
bronchioles and alveoli.
11. Below diaphragm : (Gas shadow, calcification)
-Chialiditis syndrome : Interposition of bowel between liver and diaphragm (often
transient).
12. Soft tissue :
-Mastectomy, Poland syndrome (cong absent pectoral ms), nipple shadows.
-Companion shadows : 2-3 mm thick // to upper clavicles & inf border of ribs.
13. Bones : (Clavicles, scapula, ribs, spines).
II. Lateral Film : Comment on the following :
1. The clear spaces: (retrosternal, retrocardiac).
-Normally, the retrosternal space measures less than 3cm at its widest point.
2. Vertebral translucency :
-The vertebral bodies become progressively more translucent caudally.
Loss of this translucency (Posterior basal consolidation, Para Vertebral mass).
3. Diaphragm outlines :
-Loss of the outline (pleural effusion, consolidation).
4. Pulmonary arteries :
-The left pulmonary artery lies above& posterior to end on carina, the right lies and
in front.
5. Others :
-Fissures (displacement, thickening, loculated interlobar effusion).
6. Chest radiology 6
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Differential Diagnosis
Krley’s Lines :
1. A-lines : Thin, non branching lines radiating from the hilum (2-5cm in length,
thick deep intercommunicating lymphatics, DD: blood vessels).
2. B-lines : -Transverse, thin line of 1-3cm.
-Seen at the base of the lung lying perpendicular to ! pleura (in costo-
phrenic angle).
-Formed by thickened interlobular septa (in lat film seen behind !
sternum () = D lines.
3. C-lines : A spider’s web appearance : interlacing lymphatics.
*Causes of visualization : (Lymphatic obst).
1.Pulmonary edema.
2.Mitral valve disease.
3.Pneumoconiosis.
4.Lymphangitis carcinomatosa unilateral kerly, Blues.
5.Lymphoma.
6.Alveolar cell carcinoma.
7.Interstitial fibrosis.
8.Sarcoidosis.
Silhouette Sign :
-It permits localization of the lesion on the PA view by studying the mediastinal and
diaphragmatic outlines.
-These outlines are visualized because the adjacent alveoli are aerated.
-If air is displaced, the adjacent borders are obliterated where the lesion is located,
conversely if the border is retained and the abnormality is superimposed, the lesion
must be either anterior or posterior e.g.:
* Lesions of the middle lobe (rt) and lingula (lt) affect the right and left
cardiac border.
* Obliteration of the aortic knuckle is a feature of disease in apico-posterior
7. Chest radiology 7
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segment of upper lobe (left).
* A well defined mass seen above the clavicle is always posterior.
The Hilum Overlap sign :
Helps to distinguish a larger heart from a mediastinal mass :
A mediastinal mass hilum is seen through mass.
Cardiomegaly hilum is displaced.
Air bronchogram :
An important sign. The bronchus if air filled and not fluid filled becomes visible,
when air is displaced from the surrounding alveoli (parenchyma).
*Causes :
1. Consolidation (Pneumonia, infarction, collapse, Pulm hge, TB).
2. Pulmonary edema.
3. H.M.D = Hyaline membrane disease.
4. Lymphona.
5. Alveolar cell carcinoma.
6. Sarcoidosis.
7. Adult respiratory distress syndrome.
N.B:
* An air bronchogram does not occur within pleural fluid or solid tumor.
* It may be present in consolidation distal to a malignancy if the bronchus
remains patent.
Alveolar or acinar shadowing :
-Fluid filled acinus that forms (4-10) 7mm shadow, rapidly coalesce into fluffy, ill
defined cotton wool shadows and homogenous mostly non segmental.
NB: *Air bronchogram and silhouette signs are characteristic features.
*Pulmn. Shadowing: alveolar(acinar),or interstitial.
-A ground glass appearance or a generalized homogenous haze seen with alveolar
shadowing may have a bat’s wing distribution, when a homogenous shadow
spreads, from hilae with a periph.translucent rim.(peripheral lung field spared, butterfly),
commonly due to cardiac failure and clears quickly after treatment.
11. Chest radiology 11
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(Aspergillosis)
5-Vascular :
-Pulmonary infarction.
-Hematoma. -AVM.
6-Collagen disease
-Rh. Arthritis.
7-Sarcoidosis.
8-Congenital :
-Sequestrated segment.
-Bronchogenic cyst.
9-Non Pulmonary :
-Skin lesion (lateral film helps to distinguish extra pulm masses:* Intrapulmonary mass has
acute angles with lung edge. *Extrapulmonary & mediastinal masses form obtuse angles.
-Bone lesion
-Pleura (encysted effusion, plaque)
-Artifacts.
Cavitation :
-Radiologically : A cavity is a translucency within the lung parenchyma surrounded
by a complete wall (thick : 3mm or more)
*Sites of predilection for certain pathologies :
-TB mostly upper lung zone, infraclavicular.
- Aspiration abscess mostly right side, lower zone.
- Amoebic abscess always in the right lower zone.
- Pulmonary infarction commonly lower zones.
- Sequestrated segment left sided.
*Comment on wall pattern :
- Malignant tumors thick irregular wall with eccentric cavitation.
*Comment on presence of fluid level.
Intracavitary bodies :
-Aspergillesis : mycetoma.
-Hydatid : disintegrated.
-Lung gangrene bl. clot in cavity.
-cavitary sq. cell carcinoma.
-simple lung abscess.
12. Chest radiology 12
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*Comment on content of cavity :
- Irregular masses of blood clots or necrotic tumor may be seen within cavity.
*Comment on satellite lesions ? : Are common with TB.
*Comment on surrounding lung tissue.
Causes of cavitation : (P77, same reasons as solitary nodule, but cavitation occurred, +
bronchietasis, bullae
A. Infection: Staph.(commonest), Klebsiella (abscess),TB, Amoebic, Hydatid, Fungal
(aspergillosis).
B. Malignant : Primary, 2ry, Lymphoma.
C. Aspiration abscess
D. Pulm, infarction, hematoma.
E. Pneumoconiosis : Caplan’s syndrome.
F. Cystic Bronchiectasis, sequst. lung, bronchogenic carc.
G. Sarcoidosis.
H. Bullae, pneumatocele - thin wall.
NB: Cong., trauma, inflam/inf/grannuloma, Neop., Vasc, others.
Causes of multiple cavities :
1. Abscesses 2. Lymphoma 3. Metastasis 4. Rheumatd nodules
Causes of fluid levels on chest Film:
1. Intrapulmonary cavitation
2. Hydropneumothorax
3. Esophageal (pharyngeal pouch, Achalasia)
4. Mediastinal (infection, esophageal perforation).
5. Pneumopericardium (trauma, aspiration).
6. Chest wall infection, fractures.
Thick wall cavity: Thin wall cavity:
1.Acute abscess 1.Bullae
2.Most metastases 2.Pneumatoceles
3.Most neoplasma (usually sq. cell) 3.Cystic Bronchiectasis
4.Lymphomas 4.Hydatid cyst
5.Wegener’s grannuloma 5.Traumatic lung cyst
6.Rheumatoid nodule 6.Carcinoma
7.Chronic inactive TB cavity.
13. Chest radiology 13
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7. Diaphragm hernia, eventration, rupture.
Calcification : (low KVP)
A. Intrapulmonary :
1. Granuloma, infections :
a.TB (commonest, m.imp), foci are in upper zone, scattered & of variable size.
b.Histoplasmosis characterized by focal areas surrounded by small haloes.
c.Hydatid cyst rarely (fine rim of calcification in wall).
d.Actinomycosis.
e.Chronic abscess
f. Chicken pox.
2. Tumors:
a.Metastasis (osteo, chondrosarcoma). c.A.V.M.
b.hamartoma (pop corn calcification). d.Carcinoid T.
3. Chronic pulmonary venous hypertension mitral valve disease.
4. Hematoma, infarction.
5. Alveolar microlithiasis: tiny sand like densities in mid and lower zone due to
calcium phosphate deposits in the alveoli.
6 Metastatic due to hypercalcaemia: Chronic renal failure, 2ry hyperparathy.,
M.Myeloma.
7. Rare causes as: Sarcoidosis, Silicosis (egg shell calcification).
B. Pleural : TB, asbestosis, empyema, talc, old haemothorax.
C. LN : TB, histo, sarcoid, silicosis, lymphoma after irradiation.
D. Mediastinal : cardiac, vascular, tumors.
NB:
* Ruptured hydatid cysts have daughter cysts floating within!cavity = water lily sign.
* Other intracavitary lesions include inspissated pus, blood clot & cavernoliths.
* Blood clots occur with cavitating neoplasm, tuberculosis & primary infarcts.
* Common in primary tumors, & irregular masses.
* Uncommon in cavitating metastases & TB cavities.
* Meniscus sign is when intracavitary body is surrounded by crescent of air,
commonly described with fungus balls such as aspergilloma, ! ball moves as : pt,
change position.
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E. Pulm A : Aneurysm, P++, thrombus.
F. Chest wall : bone, breast, soft tiss., cartilage, parasites.
Causes of unilateral hypertransradiant hemithorax :
A. Rotation : (positional)
1. poor technique
2. scoliosis.
B. Chest wall :
1. Mastectomy.
2. Poliomyelitis (unilateral pectoral muscle affection).
3. Poland’s syndrome (Unilateral absence of pectoral muscles + rib defect with
syndactly) in 10% of patients.
C. Pleura :
Pheumothorax.
DD: Localized transradiancy : *Bullae. *Emphysema. *Cyst. *Encysted pneumothorax.
*Pneumatocele.
D. Lung :
1. Compensatory emphysema.
2. Obstructive emphysema.
3. Macloed’s syndrome (the late sequalae of childhood bronchiolitis).
4. Unilateral bullae.
5. Congenital lobar emphysema.
E. Pulmonary vessels :
Pulmonary embolism of a major pulmonary artery at least lobar in size.
Causes of bilateral hypertransradiant hemithoraces :
A. With over expansion of lungs :
1. Chronic obstructive emphysema :
a.Large central pulmonary arteries.
b.Peripheral arterial pruning.
c.Bullae.
2. Pulmonary Asthma.
3. Acute bronchiolitis.
Child (1st year of life).
15. Chest radiology 15
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*Bronchial wall thickening.
*Collapse or consolidation are common.
4. Tracheal, laryngeal or bilateral bronchial stenosis.
B. With normal or small lungs:
1. Cong heart disease oligemia e.g Right to left shunt.
2. Multiple pulmonary embolism.
3. Primary pulmonary hypertension.
4. Pulmonary artery stenosis.
5. Bilharziasis.
Increased density of a hemithorax :
A. With central mediastinum :
1. Consolidation.
2. Small or moderate pleural effusion.
3. Mesothelioma. 4. Also technical ( Rotation, scoliosis)
B. With mediastinal displacement away from dense hemithorax :
1. Large pleural effusion 2. Diaphragmatic hernia.
C. With mediastinal displacement towards dense hemithorax :
1. Collapse 2. post pneumonectomy 3. Lymphangitis carcinomatosa
4. Pulmonary agenesis and hypoplasia herniation of the other lung across
!midline.
Pneumonia with an enlarged hilum :
1. Primary pneumonia (TB, Viral, Mycoplasma, 1ry histoplasmosis IMN.),
2. 2ry pneumonias tumor
Consolidation with bulging of fissures :
1. Infection (klebsiella pn., streptococcus pn. TB)
2. Abscess (Staph, Klebsiella).
3. Bronchial carcinoma.
Causes of apical shadows :
1. Pleural caps: Unilateral or bilateral, crescent shaped, may represent old
pleural thickening, may present in 5% or population,.
2. Pancost tumor.
3. pueumothorax, bullae.
16. Chest radiology 16
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4. Infection (TB) + Apical fibrosis (TB, Radiation, Aspergillosis, silicosis, Histocytosis
&
Histioplamosis, sarcoidosis, scleroderma, ankylosing).
5. Pleural fluid.
6. Soft tissue (sternocliedomastoid, companion shadows, hair).
Causes of hilar enlargement :
A.Unilateral :
1. Apparent (rotation, scoliosis).
2. Normal in young women.
3. Lymph nodes as in bronchial carcinoma, lymphoma, infection as 1ry TB,
histoplasmosis, actinomycosis.
4. Pulmonary artery (post stenotic dilation, embolus, aneurysm).
5. Others (mediast, mass, peripheral pneumonia ?? I think central).
B. Bilateral :
1. Expiratory film.
2. Nodal (lymphoma, sarcoidosis, TB, carcinoma, histoplasmosis and fungi).
3. Pulmonary artery: pulmonary hypertension, congenital heart disease.
4. Extrinsic allergic alveolitis, pneumoceniosis.
EGG Shell calcification of lymph nodes :
1. Silicosis.
2. Coal miners pneumonia, amylodosis, histoplasmosis.
3. Sarcoidosis.
4. Lymphoma following radiotherapy.
Causes of small hilum:
Unilateral: normal, apparent, lobar collapse, Mcleod, unilat pul embolism and
hypoplastic pulmonary-artery.
Bilateral; cyanotic HD, central pulm embolus.
Neonatal respiratory distress :
A. Pulmonary causes :
1. With no mediastinal shift :
a. Hyaline memb. disease (ground glass appearance, larger opacities, patches of
consolidation + air bronchogram (well apparent).
17. Chest radiology 17
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b. Transient tachypnea (wet lung disease).
c. Meconium aspiration syndrome.
d. Pneumonia - Pulmonary hge resemble H.M.D
e. Choanal atresia.
f. Abnormal thoracic cage osteogenesis imperfecta.
2. With mediastinal shift away from abnormal side.
a. Diaphragmatic hernia.
b. Congenital. lobar emphysema.
c. Pleural effusion (rare)
3. With mediastinal shift towards the abnormal side.
a. Atelectasis (mostly misplaced endotracheal tube).
b. Agenesis.
B. Cardiac causes.
C. Cerebral causes (Hge, edema, drugs).
D. Metabolic causes (Acidosis, Hypoglycemia).
E. Abdominal causes (Massive organomegaly e.g. polycystic kidney).
Cysts : has an epithelial wall and completely closed.
Bleb : Air encysted related to pleura & completely closed → pneumothorax.
Bulla : destruction of alveoli resulting in parenchymal air encystment.
Cavity : Its wall is compressed tissues or fibrous tissue.
Pneumatocele : Thin, hair line walled air cavity.
Airway obstruction :
1. Partial hyperinflation.
2. Complete collapse.
3. Bronchocele.
4. Bronchiectasis.
5. Pneumonitis abscess.
Value of tomography :
1. To improve visualization of a lesion.
2. To localize & confirm an intrapulmonary lesion.
3. To evaluate hilum & proximal airways.
18. Chest radiology 18
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4. To search for a suspected lesion e.g. metastases.
5. To evaluate : mediastinum & chest wall.
Chest Wall
Comment on :
A. Sternum :
1. Developmental abnormality (depressed "pectus excavatum" sternum in cong.H.D.:
ant. ribs are vertical & post ribs are horizontal, heart is displaced to the left &
appears enlarged with straight left border, prominent lung markings (Rt paracardiac)
misdiagnosed as consolidation).
2. Erosion (adjacent mediastianal mass anteriorly, infection).
3. Tumours (chondroma, chontrosarcoma, secondaries).
4. Fractures.
B. Clavical :
1. Absence outer end : (Cleidocranial dysostosis).
2. Erosion : Outer or medial end :
- Rheumatoid arthritis.
- Hyperparathyroidism.
- Infection.
3. Tumour (aneurysmal bone cyst, Ewing).
4. Fracture.
C. Ribs:
Superior or inferior unilateral or bilateral.
Rib notching (superior surface) :
A. Connective tissue disease (Rh arthritis, S.L.E, Sceleroderma).
B. Metabolic Hyperparathyroidism
C. Miscellaneous :
- Neurofibromatosis.
- Marfans’ syndrome.
- Osteogenesis impertecta.
19. Chest radiology 19
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- Poliomyelitis
- Old age.
Rib notching (inferior surface):
Occurs due to hypertrophy of the intevesselsor with neutumours.
- 1st and 2nd I.C. ant. & Post. costo-cervical trunk (2nd part of subclavian artery).
- 3-12 anterior inter. mammary artery 1st part of subclavian.
- 3-12 posteriorly aorta.
Causes :
-Aorta: coarctation, occlusion
-Subclavian : Takayasu disease.
-Reduced pulm flow (oligemia): Pulmonary atresia or stenosis - Fallot’s tetralogy.
-Venous : (S.V.C., I.V.C. obstruction)
-Shunts : Pulmonary or intercostal AV fistula. (Blalock operation = pulm systmic shunt)
-Others : Hyperparathyroidism, neurogenic tumour and idiopathic.
N.B. : When aorta is obstructed reversed blood flow :
- Coarctation notching of 1st and 2nd ribs : not develop because of its origin from subclavian.
- Lower ribs not affected unless : lower abd aorta is affected.
- Preductal coarctation no rib notching.
Cervical ribs : Rib anomalies (hypoplasia , bridging, bifid).
1-2%, arises from C7 with the transverse process pointing caudally.
DD: Hypoplastic 1st rib (arise from D1).
Fracture :
- Cough fracture (6-9) ribs at axillary line.
- Stress fracture 1st rib.
- Pathological fracture: senile osteoporosis, myleoma, cushing disease.
Selerosis :
A. Generalized (osteo-petrosis, metastasis, myelofibrosis).
B. Localized (Paget disease).
N.B: Looser’s zone : areas of uncalcified osteoid tissue (osteomalacia): rib deformity creates
20. Chest radiology 20
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a bell shaped thorax.
Expansion :
a. Localised
- Paget.
- Fibrous dysplasia.
- Haemangioma.
- Aneurysmal cyst, chondroma.
- Eosinophillic granuloma.
b. Generalized :
- Thalassaemia (expansion more marked proximally + abnormal trabeculae)
- Hurlur’s syndrome (generalized expansion sparing the proximal end).
- Rickets (widening of rib ends).
D. Thoracic spine :
Comment on:
1- Alignment, disc spaces (calcification = post-traumatic, ankyloses, ochronosis,
destruction in infective process). 2-Sclerosis (single dense vertebra (ivory)=
lymphoma, paget's and metastasis. 3-Destruction (pedicle = metastases).
4- Paraspinal lines.
Straight back syndrome :
- Loss of normal thoracic kyphosis strenum parallel to spine compression of mediastinum.
- In PA view : - heart appears to be enlarged
- prominent atrial appendage
- prominent aortic knuckle.
Causes of anterior erosion of vertebral bodies :
1. Aneurysm of descending aorta.
2. Gross enlargement of left atrium.
3. Vascular tumours.
4. Neurofibromatosis.
21. Chest radiology 21
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Soft tissue of chest wall :
A. Skin lesion: lipoma may appear as pulmonary lesion, lateral film confirms the
diagnosis, artefacts: hair plaits, buttons...
B. Surgical etmphysema.
C. Breast, axillary folds and masses + Thyroid.
Diaphragm
Appearance ; (normal variants)
1. Scalloping (short curves of diaphragm, convex upward).
2. Muscle slips (small curved lines, concave upward).
3. Diaphragmatic hump or dromedary diaphragm (severe form may appear as double
contour in PA view N.B.: These is no diaphragmatic defect).
Eventration :
- Mainly left sided (thin, weak diaphragm).
- Left hemidiaphragm is elevated with mediastinal shift to the right, a feature rarely
seen with paralysis.
- May be associated with partial gastric volvulus.
- Reduced movement (seen under fluoroscopy) paradoxical movement or abscent.
Diaphragmatic movement :
On screen, normally the left hemidiaphragm move more than right by 3-6cm
Paradoxical movement : (Moves up with inspiration)
- Diaphragmatic paralysis.
- Subdiaphragmatic infection.
- Eventration.
Thickness of diaphragm :
- On left side between fundus gas and left lung (normal average of 8mm) normal
diaphragm 2-3 mm.
- If more than 8mm pathological (may be due to)
- Tumour of diaphragm : Lipomas - neurofibrimas, fibromas & cysts.
- Gastric tumour.
- Pleural effusion.
- Subphremic lesion.
Hernia of diaphragm :
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- Morgagni Rt side & anterior in cardiophrenic angle.
- Hiatus hernia superimposed on cardiac shadow in PA.
- Bochdalek → Postero lat. from pleuro periteneal canal - Usually congential→lt side→
respiratory distress - Contain spleen, fat, kid, omentum or bowel.
Rupture of diaphragm :
- Trauma, surgical, may be idiopathic.
- Mainly on the left side herniation of stomach, colon strangulation.
DD : 1. Eventration (intact diaphragm)
2. Pneumothorax.
Subphrenic abscess :
- More on Rt side easy diagnosed.
- US & CT.
- Plain film :
1. Ipsilateral basal atelectasis & pleural effusion.
2. Elevated diaphragm with paradoxical or movement.
3. Gas beneath diaphragm dt. infection by gas forming org (Horizontal beam film).
4. Depression of liver edge or gastric fundus.
Causes of unilateral elevated hemidiaphragm :
A. Causes above the diaphragm :
1. Phrenic nerve palsy (bronchogenic carcinoma, surgery, trauma, idiopathic,
radiotherapy, DM, TB glands, HZ virus) ccc by:
- Smooth hemidiaphragm.
- No movement.
- Central mediastinum.
2. Pulmonary collapse.
3. Pulmonary infarction.
4. Pleural disease (old haemothorax, empyema or thoracotomy).
5. Upper motor neuron lesion hemiplegia.
B. Diaphragmatic causes of bilateral elevated hemidiaphragm :
- Eventration.
C. Causes below diaphragm :
23. Chest radiology 23
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- Gaseous distension of stomach or splenic flexure.
- Subphrenic abscess, hepatic abscess, pancreatitis.
DD: 1. Subpulmonary effusion.
2. Ruptured diaphragm.
Causes of bilateral elevated diaphragm :
1. Poor inspiratory effort.
2. Causes above diaphragm :
- Bilateral basal pulmonary collapse.
- Small lungs e.g. fibrosing alveolitis.
3. Causes below diaphragm :
a. Ascitis.
b. Pregnancy.
c. Obesity.
d. HSM.
e. Iatraobdominal mass.
f. Subphenic abscess (bilateral).
g. Pneumoperitoneum.
Superior medistinum mass :
- Thryoid, thymus, teratodermoid, lymphangiona, L.N., aneurysm, spinal Pott’s,
neurogenic tumours, enteric cyst, pouches.
Rib diseases :
- Notching →Sup → NF, collagen, HPT.
→Inf. → coarctation, SVC obstruction, operation, NF.
- Sclerosis → Myelosclerosis, osteopetrosis, Paget, metastasis.
- Expansion → Dysplasia fibrous
Tumours ABC, haemangisms.
Blood. dis thalassemia
Nutritional Rickets.
- Destruction → MM, metastasis, lymphona.
- Fracture.
- Cervical rib & bifid.
Linear & band shadows :
1. Pulmonary infarcts
2. Plate atalectasis often post operatively.
3. Mucus filled bronchi : gloved finger branching pattern (bronchoceles).
4. Kerley's B lines.
DD : hump in PA film
appears as a shadow in Rt
cardiophrenic angle:
1. Fat pad.
2. Lipoma.
3. Pericordial cyst.
4. Morgagni hernia.
25. Chest 24
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OCCUPATIONAL LUNG DISORDERS
PNEUMOCONIOSIS
Def.: Disease due to inhalation of particular matters.
A. Organic :
1. Damage to the tracheobronchial tree:-
Occupational asthma :
-History of exposure to animal and fungal spores and in chemical industry
e.g. Byssinosis, cotton dust inhalation.
-Has the same radiological picture of asthma during attack.
2. Damage to lung parenchyma :
Extrinsic allergic alveolitis or hypersensitivity pneumonitis:
A large variety of organic dust particles & microorganisms are small
enough (1-2m, < 10m) to reach the alveoli (act as allergens) to provoke
Ag-Ab reaction within 4-6 hours after exposure. Most of allergens are
fungal spores and proteins. eg: Farmers lung, Air condition: fungal spores and drugs
Clinically :
-6 hours after exposure fever, chills, dyspnea, cough.
-No wheezes or eosinophillia.
Radiologically :
A. During acute attack :
-May be normal.
-Mainly shows ground glass appearance with loss of definition of pulmon.vessels.
-In severe cases, extensive air space filling acinar shadowing with coalescence,
picture resemble pulmonary edema.
B. Between attacks (normal) :
-In subacute phase: reticulonodular pattern (fine lines together with small nodules
(1-3 mm).
C. With repeated attacks : pulmonary fibrosis :
Characterized by coarse lines particularly in mid and upper zones, together with
ring shadows 5-8mm causing honey comb appearance which is predominant in
upper zones (DD fibrosing alveolitis).
26. Chest 25
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B. Inorganic :
Damage to lung parenchyma and pleura:
1. Coal worker’s pneumoconiosis :
-Disorders due to inhalation of coal dust particles.
-It exists in 2 forms:
A. Simple pneumoconiosis :
*Causes no respiratory disability.
*Multiple discrete nodular opacities (1-4mm) more condensed in upper zones
which is mainly associated with reticular pattern Reticulonodular
appearance.
B. Complicated pneumoconiosis :
*Causes respiratory disability : progressive dyspnea, Haemoptysis.
*Gives picture of progressive massive fibrosis:
a.Large irregular opacities (1-10 cm).
b.Usually bilateral, upper zonal and asymmetrical.
c. A linear strands from opacity to periphery of lung.
d. Picture of complication (emphysema, ischemic necrosis
Cavitation).
??TB- Bronchogenic carcinoma.
NB: Miners with rheumatoid disease may develop crops of nodules varying in size 1-
10 cm know as (Caplan’s nodules or syndrome).
2. Silicosis :
Due to exposure to silica particles e.g. sand blasting and pottery, ceramic industries.
Radiologically :
Very similar to cool workers pneumoconiosis which mainly differentiated by egg-
shell calcification of enlarged hilar lymph nodes.
Simple forms : As cool workers pn. with or without hilar lymphadenopathy.
Complicated: As cool workers pn.
NB: Two important diseases may occur in association with silicosis and coal workers
pn. (TB and Bronchial carcinoma).
27. Chest 26
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3. Asbestosis :
The asbestos fibers, when inhaled, pass to the respiratory bronchioles and acini,
where they are engulfed by Macrophages and evoke a fibrotic response. Also, they
may penetrate visceral pleura, causing pleural reaction.
A. Pulmonary changes :
-Predominantly in lower lung zones (DD silicosis upper)
-Earliest changes are seen in costophrenic angles.
-At first the vessels have indistinct margins & are associat. with fine irregular lines.
-When fibrosis progress lines become more profuse reticular network pattern.
-With more progression give honey comb pattern, which is best seen in lateral
and oblique views
-Complications : Bronchial carcinoma, which is strongly related to cigarette
smoking.
NB: Fine irregular line Reticular network honey comb.
B. Pleural changes:
1. Pleural plaques :
-They are not seen for at least 10 years following exposure.
-They usually do not calcify until a latent period of 20 years.
-They are of variable size and have a characteristic distribution on parietal pleura.
a. Adjacent to ribs more prevalent in the axillary part of midchest and tend
to spare to upper zones and costophrenic angles.
b. Over central tendon of diaphragm which produce characteristic curvilinear
opacities on diaphragmatic pleura. Best seen in oblique views.
-CT is very sensitive for early detection.
2. Malignant Mesothelioma :
-The majority of such tumor is related to asbestos exposure and it does not arise
from pleural plaques.
-Appear as (see pleural diseases) nodular pleural thickening / hemorrhagic effusion/ central
mid diaphragm dt collapse / Rib involvement may occur.
3. Benign pleural effusion + pleural thickening. (not common to occur)
29. Chest 28
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DIFFUSE PULMONARY FIBROSIS
INTERSTITIAL LUNG FIBROSIS (I.L.F)
Causes :
1. Inorganic dusts: (Silica, Asbestos inhalation).
2. Organic dusts: (Extrinsic Allergic Alveolitis).
3. Drugs, poisons and toxic fumes.
4. Fibrosing alveolitis (Interstitial Pneumonia): Cryptogenic & Secondary lower
zone.
5. Histocystosis X.
6. Sarcoidosis.
7. Neurofibromatosis.
8. Tuberous sclerosis.
9. Adult respiratory distress syndrome.
10. Lymphangiomyomatosis.
11. Chronic pulmonary edema.
12. Collagen dis. (Rhtoid basal/ SLE/ AS upper/scleroderma/ PAN /Wegner
granuloma/Loffler’s. ).
NB: *Key (clinically, defin, ground glassreticulonodular honey combing
*5C : Cough/ cyanosis/ clubbing/ crepitation/ Cor pulmonale.
1. Fibrosing Alveolitis Or diffuse interstitial pneumonia :
-A group of disorders characterized by an inflammatory reaction in alveolar walls
with alveolar exudate and a tendency to progressive fibrosis. Eventually, there is
complete destruction of alveolar architecture.
-Hamman-Rich syndrome: Idiopathic pulmonary fibrosis & muscular cirrhosis of
the lung all are conditions all are included in the causes of such illness.
-Types :
1ry: Cryptogenic.
2ry: In association to a variety of systemic conditions e.g. Rh. arthritis,
S.L.E., Ank. Spond., Ulcerative colitis.
30. Chest 29
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Cryptogenic fibrosing alveolitis :
A clinical syndrome of unknown cause (autoimmune).
Clinically :
-Middle age patients presented with presented with dyspnoea, dry cough, clubbing
of fingers, basal crepitations.
-Lung functions studies restrictive defect.
Pathologically : (Five distinct histological entities are described)
1. Usual interstitial pneumonia (most common).
2. Desquamative interstitial pneumonia.
3. Diffuse alveolar damage with Bronchiolitis obliterans.
4. Lymphocytic interstitial pneumonia.
5. Giant cell interstitial pneumonia.
Radiological features :
1. In earliest stage :
-Lungs may look normal.
-The earliest minimal changes appear :
1. Ground glass (Haze) in bases …. more easily seen in both cardiophrenic
angles (mainly unequal with more on right) which extend upward and
outward to costophrenic angles forming:
2. Generalized ground glass haziness of lungs.
2. With progression :
The pulmonary vessels lose their normal clarity and a fine reticulo nodular
pattern develops in the lower zones.
3. With more progression :
-Give (honeycomb appearance) coarse reticular pattern (at base) and ring
shadows (5-10mm).
-Best seen in post-costophrenic angle in lateral view.
-CT is very sensitive in early detection.
31. Chest 30
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2. Histocystosis X :
A disease of unknown etiology, usually affects multiple organs including the lungs.
Abn. proliferation of RE cells in (Bm - lung - HSM - LN).
3 varieties :
1. Eosinophillic Granuloma (mainly affect lungs).
2. Hand-Schullar Christian disease.
3. Laterer-Siwe disease.
Eosinophillic Granuloma :
Young adults (male : female = 4.1)
Pathology :
There is histocytic infiltration of the alveolar walls leading to its fibrosis
causing disorganization of the pulmonary architecture with formation of air cysts.
Radiological features :
-Wide spread, bilateral and symmetrical.
-In earliest stage normal.
-Reticulonodular pattern diffuse nodular shadowing in mid and upper zones (1-
10mm) associated with fine lines.
-With progression give honey comb appearance.
-Spontaneous pneumothorax in 20% (dt air cysts).
-Pleural reaction and hilar lymphadenopathy (rare).
-Open lung biopsy is best method to confirm diagnosis.
III. Sarcoidosis :
Multisystemic, granulomatous disorder of unknown etiology, characterized by
presence of non caseating epithelioid cell granolumas with predilection to involve
lungs, skin, L.N., adrenal, uveal tracts, C.N.S and bone.
Incidence :
(30-50ys), more common in black races, female: male =2:1).
Diagnosis :
1. Clinical data.
2. Radiological findings.
3. Histopathology. Broncho alveolar lavage.
4. Kveim test: intradermal injection of extract of sarcoid tissue reaction = +ve.
5. Gallium 67 scanning (taken by nodes and parenchymal lesions).
32. Chest 31
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Radiological findings :
The radiographic abnormalities progress through 3 stages :
1. Lymphadenopathy only.
2. Lymphadenopathy + pulmonary lesions.
3. Pulmonary lesions only.
Sarcoid lymphadenopathy : has the following features :
-Nodal enlargement does not develop after parenchymal shadowing.
-Appears as bilateral symmetrical lobulated hilar enlargement not common to be
asymmetrical (rarely unilateral).
-Hilar enlargement involves both tracheo bronchial and more distal bronchopulm.
lymph nodes involvement of the later is a feature of sarcoidosis where it
causes easily visualization of inferomedial border of hilum by adjacent air
containing lung.
-Hilar adenopathy is an isolated finding in about 1/3 of cases, it is associated with
right paratracheal adenopathy in another 1/3 and with bilateral paratracheal in the
remainder 1/3.
-Even with massive adenopathy, the clinically significant compression of adjacent
air ways is extremely unusual = No compression on airway.
-In 90% of cases nodal enlargement is maximal in the first radiograph and usually
disappears within 6-12 months. It may persist in 5% of cases. Recurrence of
adenopathy is very rare.
-In 5% of cases, calcification giving a characteristic egg shell fashion.
Causes of Bilateral hilar enlargement :
1. Sarcoidosis 2. Lymphoma 3. Metastasis
4. Lymphatic leukemia 5. TB (1ry) 6.Coccidioidomycosis
7. Others (silicosis, histoplasmosis, amyloidosis).
Causes of Egg shell calcification:
1. Sarcoidosis 2. Histoplasmosis.
3. Silicosis 4. Amyloidosis.
5. Lymphoma (post. irrad). 6. SIS but not TB
33. Chest 32
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Sarcoid parenchymal changes :
-In 20-50% with or without nodes.
-Characteristically, they appear as nodal enlargement is subsiding (DD lymphoma).
-Mainly it is bilateral, wide spread many patterns.
1. Small nodules :
2-3mm rounded or irregular nodules, slightly well defined (miliary) and
symmetrical, bilateral mainly uniform in distribution from apex to base.
2. Reticulation :
-A network of fine lines radiating from hilae.
-Kerley’s B lines may be seen from lymphatic seedlings.
3. Reticulonodular: more common, + pleural effusion & thickening.
4. Large nodules:
Multiple bilateral 1-4cm in diameter, rounded or oval in shape, usually with ill
defined border.
5. Homogenous cloudy opacities :
-Commonly contains air bronchogram giving features of consolidation.
-May be single or multiple, range from 1 cm to a segment.
-2/3 of parenchymal shadowing clear completely and 1/3 progress to :
6. Fibrosis :
-Coarse linear shadows with evidence of volume loss+ ring shadows+honey comb.
-Condensation and contraction of the fibrous tissue produces:-
1.Distortion of pulmonary architecture.
2.Elevation of hilae i.e displacement of landmarks.
X-ray staging :
0 normal
1 bilat hilar LN
2 adenopathy + pulm infiltrate
3. pulm infiltrate alone.
NB: LN + fibrosis (widespread)
34. Chest 33
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Complications of massive fibrosis :
-Bullae formation.
-Cor pulmonale.
-Bronchiectasis.
-pueumothorax.
IV-Tuberous Sclerosis and Lymphangiomyomatosis:
In both diseases, there is smooth muscle proliferation in bronchi, lung, vessels, ‘
lymphatics, lymph nodes and alveolar wall.
a. More common in females.
b. Mainly in lower lobe.
c. Pleural effusion (chylous) characteristic for lymphangiomata.
V. Neurofibromatosis :
The same as in Histocystosis X.
Collagen vascular diseases :
1. S.L.E.
Characterized by widespread inflammatory changes in CT, B1vs and serosal surface.
Radiological features :
1. Pleural effusion - Mostly bilateral, small, associated with pleuritic pain.
2. Segmental basal collapse : Thick horizontal band shadows at lung bases,
which occurs due to restricted diaphragmatic movement by pleurisy.
3. Pulmonary consolidation either due to (2ry infection or lupus pneumonitis).
4. Pulmonary edema : secondary to heart failure.
5. Diffuse interstitial shadowing : as in fibrosing alveolitis (rare).
6. Diminished diaphragmatic excursion: may be due to myopathy of the
diaphragmatic muscles.
35. Chest 34
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II. Rheumatoid Disease :
Radiographic features of intrathoracic manifestation of Rh. disease:
1. Pleural effusion: (unilateral or bilateral).
2. Necrobiotic nodules: Vary in size (few mm to few cm) single or multiple.
3. Caplan’s syndrome : In patient with rh. exposed to silica.
Identical nodules, characteristically appear rapidly in crops which contain silica
dust on histological examination.(crops of nodules = Caplan nodulo)
4. Fibrosing Alveolitis :
Appears as basal reticulonodular shadowing which may progress into honey
comb lung with loss of lung volume end stage lung.
5. Pulmonary hypertension and cor pulmonale (rare) = complication of fibrosis
III. Systemic Sclerosis (scleroderma):
-Picture of fibrosing Alveolitis (ground glass appearance/ fine reticulonodular/ honey
comb
appearance).
-Air oesophagogram may be evident in lateral film due to absence or diminished
peristalsis.
-Basal patchy consolidation due to aspiration pneumonia.
-High incidence of bronchogenic carcinoma.
IV. AnkvlS:
-Unilateral or bilateral.
-Upper lobar fibrosis with upward retraction of hilae + bullae formation.
-Apical pleural thickening.
*Causes of upper lobe fibrosis:
1. TB 5. Eosinophillic granuloma.
2. Post irradiation. 6. Sarcoidosis.
3. Histoplasmosis. 7. Ankylosing spondylitis.
4. Aspergillosis. 8. Progressive massive fibrosis.
*Causes of lower lobe fibrosis:
1. Asbestosis
2. Cryptogenic
3. Rheumatoid.
36. Chest 35
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V. Polyarteritis Nodosa :
-Vasculitis of medium sized arteries.
-Kidneys most commonly affected.
Radiologically :
-Transient areas of consolidation which may appear rapidly then disappear
(Loeffler’s syndrome).
- Accentuation of vascular lung markings.
- Large nodules (few cm) may cavitate.
VI. Wegener’s Granulomatosis :
-More common in females.
-Vasculitis affecting mainly small arteries and associated with segmental ‘
glomerulonephritis in 85% necrotising granulomas affecting lung. Vasculitis
“necrotising”→ skin-face, lung, kid.
Radiologically :
-Single or multiple well defined pulmonary masses varying in size from few mm
to few cm which frequently cavitate.
-Air space shadowing, may occur mainly due to pulmonary hge.
-Pleural effusion.
-Hilar and mediastinal lymphadenopathy.
VII. Pulmonary eosinphilia (Eosinophillic Pneumonia): (??Loeffler’s $.)
Eosinophillic pulmonary infiltrate + increased eosinophills in peripheral blood.
Causes :
-Bilhariziasis, ascaris, arkylostoma.
-Fungi: (Aspergillus fumigatus).
-Drugs : sulfonamides.
-Unknown : Cryptogenic pulm eosinophillia.
-Polyarteritis Nodosa.
Radiologically :
A. Loeffler’s syndrome : diagnostic vertical (short & thick) band // to chest wall
separated from pleura :
-Transient pulmonary eosinophillia which produces, ill defined non segmental
areas of consolidations in periphery of lungs.
-These changes are characteristically short lived (few days) and self limited.
37. Chest 36
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B. Chronic pulmonary eosinophillia :
-The same radiological picture of Loeffler’s syndrome but much more persistent.
-Classically occur in atopic middle aged females.
VIII. Pulmonary Hemorrhage & Haemosiderosis :
Multifocal bleeding at acinar level distal to terminal bronchioles with exclusion
of bleeding states as leukemia and anticoagulant.
Clinical Picture:
Haemoptysis and anemia :
Causes of Pulmonary Haemosiderosis :
1. Idiopathic : Children.
Repeated episodes of hge and the lung return to normal between attacks.
2. Associated with renal disease :
Good pasture syndrome = Antiglomerular basement membrane antibody.
3. Drugs : Penicillamine.
4. Part of widespread Vasculitis e.g. Wegener’s granuloma.
5. Miscellaneous: As in heart disease (M.S). Pulmn V. congestion.
Radiological features :
1. Of Pulmonary hge :
a. Fleeting, migrating opacities with ill defined margins like pulmonary edema ± ill
defined nodules (6mm) may be seen.
b. Airbronchogram.
c. Repeated attacks fibrosis.
NB: In severe cases, both lungs can be almost totally opacified but may be normal in
acute attack.
2. Of Haemosiderosis:
-may be normal.
- ill defined micronodular opacities (miliary) with air bronchogram.
NB: Pulmonary hge : Acinar shadow
Haemosiderosis: Miliary
38. Chest 37
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DISEASES OF THE PLEURA
I. Pleural fluid (effusion): types and causes :
a. Transudate :
-Clear, thin and watery fluid.
-Protein < 3gm/dl.
-caused by :
1. Cardiac failure.
2. Hypoproteinaemia (nephrotic$., hepatic C., Anemia).
3. Meig’s $.
b. Exudate :
-Cloudy amber yellow thick and sticky fluid.
-Protein > 3 gm/dl.
-Caused by :
1. Bacterial pneumonia, pulmonary TB.
2. Pulmonary malignancy (1ry or metastatic).
3. Pulmonary infarction.
4. Subphrenic infection.
5. Pancreatitis.
c. Haemothorax:
-Caused by :
1. Frank blood in pl. sac (trauma, blood dis.)
2. Blood stained effusion (pulm, infarction, bronchial carcinoma).
d. Chylothoras :
-Milky fluid high in fatty acids and neutral fat.
-Caused by obstruction or destruction of the thoracic lymphatics. The
commonest cause is :
1. Chest-trauma.
2. Filariasis, lymphoma.
3. Malignant invasion.
Radiological appearance :
A. Free effusion (in the absence of pleural adhesions).
1. Small effusion:
-< 100 cc; can not be detected by PA and lateral films but detected by decubitus
view, U/S and CT.
-100-200 cc: Can fill the posterior costophrenic recess and appear in lateral film,
39. Chest 38
____________________________________________________________________________
while not detected in PA view.
-> 200 cc: Effusion can be detected in PA view blunting of costophrenic angle.
2. Moderate effusion :
-A homogenous opacity in the lower lung zone, devoid of all lung markings,
spreading upwards, obliterating the costophrenic recess and obscuring the
diaphragmatic shadow, with well defined concave upper edge, rising laterally
more than medially (rising to the axilla).
-Tracking of the fluid in the pulmonary fissures (best seen in the lateral views).
3. Massive effusion :
-Complete or partial radio opacity of the hemithorax.
-Retraction of the underlying lung toward the hilum.
-Shift of the mediastinum toward the opposite side.
NB: Massive effusion + lack of mediastinal shift, suggesting underlying lung collapse
mostly due to bronchial carcinoma.
Atypical distribution of pleural fluid:
1. Lamellar effusion :
-Common in children and patient with heart dis.
-A shallow collection between the chest wall and lung surface, which sometimes
spares the costophrenic recess.
2. Sub-pulmonary effusion:
-An effusion accumulate between the diaphragm and under surface of the lung
false impression of elevated hemi-diaphragm.
-± Blunted costophrenic recess or tracking of fluid into fissures.
-With change in posture, in decubitus and supine films, the fluid will move in free
pleural space (diagnostic).
-On the left side increased distance between gastric air bubble and lung base.
-On the right side, a large effusion may collect in the azygo-esophageal recess and
mimic a retro-cardiac mass.
B. Loculated or Encysted effusion :
It is due to partial obliteration of the pleural space between visceral and parietal
pleura due to pleural disease or between visceral pleural at lung fissures.
Radiological appearance :
A. Costal encysted pleural effusion :
-Site : Along the chest wall (usually posterior and laterally).
40. Chest 39
____________________________________________________________________________
-R.A: Their radiological appearance depends on whether they are viewed en face,
in profile or obliquely.
-Best determined by fluoroscopy:
*Profile: well circumscribed, biconvex opacity with the peripheral border
adjacent to the chest wall and the inner border is convex and well defined.
*En-face: Radio-opacity of relatively low density.
*If air fluid level is seen it will be either due to therapeutic aspiration, or
development of bronchopleural fistula.
B. Interlobar encysted pleural effusion :
Common to occur in patients with heart failure.
1. Encysted effusion within horizontal fissure :
-Appears as lenticular; oval or rounded shadow with well demarcated edge. In
both frontal and lateral views.
-The remaining part of the fissure to be thickened due to extension of fluid
in the fissure.
2. Encysted effusion within the oblique fissure:
-PA view : Appears as rounded or oval shadow mainly well defined lower border
and ill defined upper margin.
-Lateral : Appears as a typical lenticular well defined shadow along fissure
(diagnostic).
* Interlobar effusion disappears rapidly after ttt, and may recur in subsequent episodes
of heart failure so known as pseudo or vanishing tumors, phantom tumor
Encysted effusion Middle lobe consolidation
* lenticular shape with extension into
the fissure in lateral film.
* Obliteration of right cardiac border is
not common.
* Air bronchogram.
* distorted bronchovasc. markings.
* compensatory emphysema.
* Obscuration of right cardiac order is
common.
DD. of encysted effusion :
-Extrapleural opacity from costal type.
-Parenchymal lung dis from interlobar type.
-mediastinal mass from mediastinal type.
-Free effusion DD by gravitational method.
41. Chest 40
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* Subpulmn encysted effusion : same as free effusion but the fluid doesn’t move into
pleural space with changing posture.
* Encysted mediastinal pleural effusion : mimic a mediastinal mass, diagnosis by
CT.
Effusion :
Free/ atypically ( lamellar, / subpulmonary).
Encysted (costal encysted, interlobar, mediastinal, subpulmonary
42. Chest 41
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II. PNEUMOTHORAX
Definition : Air within the pleural cavity due to defect in parietal or visceral pleura.
Etiology :
1. Spontaneous pneumothorax :
-Is the commonest type.
-In young adults cong. pleural bleb (usually in lung apex).
-Children staph. pneumonia.
-Old age Emphysema or chronic bronchitis.
-Other causes :
*Rupture of subpleural TB focus.
*Rupture of subpleural cyst in bronchial carcinoma or rupture of cavitating
metastasis.
*Conditions associated with interstitial pulmonary fibrosis, cystic fibrosis
Sarcoidosis.
2. Traumatic pneumothorax :
-Chest trauma due to : penetrating wound, closed chest trauma, fracture rib.
-Pleural or lung biopsy.
-Bronchoscopy and oesophagoscopy.
-C.V.P catheters introduction.
Radiological appearance :
A. A small pneumothorax :
-In the erect position, small pneumothorax collects at the apex and appears as a
small radiolucency in the pleural space which is devoid of lung markings. The
apex of lung retracts towards the hilum. The sharp white line of visceral pleura
will be visible.
-Expiratory films diagnostic, since on full expiration, the lung volume is at its
smallest while volume of pleural air is unchanged.
B. Large pneumothorax :
-A large radiolucency, which is devoid of lung markings.
-Lung retraction.
-Mediastinal shift toward the normal side which increase with expiration.
43. Chest 42
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C. Tension pneumothorax (valvular type):
-Mechanism : Air moves in but not out during respiration.
-N.B.:
*Open pneumothorax: air moves freely during respiration.
*Closed pneumothorax: No movement of air occurs.
-Radiological appearance :
*The ipsilateral lung may be squashed against the mediastinum.
*Depressed ipsilateral diaphragm.
*Mediastinal shift, especially during inspiration.
-D.D.:
*From large pneumothorax with mediastinal shift on fluoroscopy more
mediastinal shift to contralateral side in inspiration with tension
pneumothorax (?? encystment,, adhesion, thickening,, fluid collection,
collapse/consolidation) .
Complications of pneumothorax :
1. Encystment pneumothorax: due to pleural adhesion.
R.A.: Ovoid, radiolucency adjacent to the chest wall.
D.D.: Subpleural cyst and bulla.
2. Pleural adhesion:
R.A:. Appears as a line shadow between the two pleural layers preventing
relaxation of the underlying lung.
Rupture of this adhesion may produce hydropneumothorax.
3. Lobar collapse or consolidation:
4. Pleural fluid collection :
-Small amount fluid level at costophrenic angle.
-Large amount hydropneumothorax “ horizontal air fluid level”.
5. Pleural thickening :
-In chronic cases, thickening of visceral or parietal pleura may occur.
-Thickening of the visceral pleura may prevent re-expansion of the lung
which needs decortication.
* Cardiac Tamponade
NB:
1. open air in pleura communicate with atmosphere.
2. closedeg: ruptured bleb(So not open). increase pleural pr. but still -ve
3. Tension valve like tear air in not out !! increased pleural pr.
44. Chest 43
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III. PLEURAL THICKENING
Causes :
1. Pleurisy : primary, secondary to lung infection or infarction.
2. Previous low grade TB infection apical.
3. End result of empyema, haemothorax.
4. Following radiotherapy of the chest.
5. After asbestosis exposure diffuse pleural plaques.
6. Old age.
7. Malignancy
Common sites :
1. End of pleural fissures.
2. Apices of the lung.
3. Whole pleura (diffuse pleural thickening).
Radiological appearance :
Bilateral apical thickening or symmetrical :
- Elderly patients.
- Uncertain etiology.
- Not due to TB.
- Ischaemia is a probable factor.
Unilateral apical thickening or asymmetrical :
- Pancost tumor.
- TB + Ank. spondylitis.
- Always of pathological significance.
Extensive pleural thickening :
- (unilateral or bilateral) Fibrothorax.
- Common with asbestosis.
Diffuse pleural thickening :
- Usually, the end result of previous thoracotomy, empyema, or haemothorax.
- This may cause reduced ventilation of the surrounding lung decrease in the
volume of that hemithorax.
- Decortication of the visceral pleura is needed.
45. Chest 44
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IV. PLEURAL CALCIFICATION
Causes : The same as pleural thickening :
Radiological appearance :
-Continuous sheet or discrete plaques - usually producing dense, coarse, irregular
shadows.
-When viewed tangentially - characteristically parallel to the chest wall.
-When viewed en face bizarre form of calcification, which may cast an ill
defined shadow mimic to pulmonary infiltrate.
V. BRONCHOPlEURAL FISTULA
Communication between the air way and pleural space :
Causes :
1. Complication of pneumonectomy.
2. Rupture of lung abscess or empyema.
3. Carcinoma of nearby bronchus.
4. Penetrating chest trauma.
Radiological appearance :
Plain :
Picture similar to hydro or pyopneumothorax (if persists or enlarges after surgery,
BP fistula should be considered).
Contrast study :
-Injection of lipidol or hydrast into pleural space (sinography or passes into the
bronchial tree.
-Injection into bronchial tree passes to pleural space.
46. Chest 45
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VI. PLEURAL TUMOURS
-Benign (Lipoma) and (fibroma) = Benign mesothelioma.
-Malignant Primary = Malignant mesothelioma.
-Malignant secondary = commonest sites is breast, bronchogenic...
Pleural fibroma :
Usually associated with hypertrophic osteoarthropathy joint pain and clubbing.
Radiological appearance :
Well defined lobulated mass :
- Site : Costal, diaphragmatic, mediastinal or at pleural fissures.
- Size : Small or occupy most of hemithorax.
Subpleural lipoma :
- Well defined rounded masses.
- May change their shape with respiration (fluoroscopy).
Malignant mesothelioma :
Usually due to prolonged exposure to asbestdust.
Radiological Appearance :
- Nodular pleural thickening around all or part of a lung.
- Hemorrhagic pleural effusion may be present, which may obscure ! mass.
- Mediastinum is mainly central despite of the presence of a large effusion due to
underlying collapse of the lung by:
*Ventilation restriction by the tumor.
*Bronchial ??/ stasis by tumor compression.
- Rib involvement may occur not common as in metastasis.
- Other asbestosis changes (pleural thickening, pl. calcification)
- CT is the best method for assessing the extent of malignant mesothelioma.
- Percutaneous or U/S needle biopsy is diagnostic.
47. Chest 46
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CHRONIC OBSTRUCTIVE
AIRWAY DISEASE
I-Bronchial asthma :
Definition : Widespread narrowing of the bronchi, which is paroxysmal and
reversible.
Pathogenesis : Hyper-reactivity of the larger air ways to a variety of stimuli
narrowing of bronchi, wheezing, dyspnea.
Types :
1. Extrinsic or atopic asthma : Associated with history of allergy eg.
Aspergillosis (↑ IgE).
2. Intrinsic or non atopic: Precipitated by a variety of factors as exercise,
infections.
Radiological appearance :
*In between acute attacks: Normal chest.
*During acute attacks :
1. Evidences of hyper inflation “see later”.
2. Prominent bronchovascular markings.
3. Hilar vessels enlargement (enlarged central pulmonary artery) with
normal pulmonary vessels distal to hilae, mainly due to reversible
pulmonary hypertension.
*Radiographic picture of associated conditions:
1. Recurrent infections especially in children, causing bronchial wall thickening
“peri-bronchial cuffing”. Appear *End-on ring shadows.
*Profile tubular tram-line shadows.
2. Flitting, patchy infiltrates of Aspergillosis.
*Radiographic picture of complications :
1. Manifestations of lower respiratory tract infection.
2. Lobar atalectasis: dt: obstruction of a lobar bronchus by plugs of sticky mucus
or mycelia of Aspergillus. Most common in Rt middle lobe.
3. Pneumothorax and pneumomediastinum: due to rupture of the alveoli by high
expiratory pressure.
48. Chest 47
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II-Chronic bronchitis :
Definition : Production of cough on most of day, during at least 3 consecutive
months for more than 2 years, without apparent cause.
(> in smokers, ♂, Pollution)
Pathology :Hypertrophy of mucous secreting glands interference with mucociliary
function dt: viscous sputum production with plugging of distal air ways.
Radiographic picture :
- 50% of patients normal chest.
- Signs of over inflation.
- An appearance which is characteristic for chronic bronchitis: Dirty chest:-
- Accentuated bronchovascular marking with small, ill defined opacities which
may represent small focal areas of atalectasis, fibrosis, perivascular and peri-
bronchial edema. DD: IPF & bronchiectasis
- Bronchial wall thickening “As before”. Peribronchial cuffing : rounded, tram like.
*Picture of complications :
- Emphysema.
- Cor-pulmonale.
- T.B.
- Bronchogenic carcinoma.
- Pneumothorax.
Bronchography :
- Unnecessary but pathogneumonic for diagnosis of chronic bronchitis.
- Shows, evidence of hypertrophy of mucous secreting glands in larger air ways.
- Irregular wall of proximal bronchi.
- Abrupt termination of bronchial division after 5-8 generations = Prune tree.
Emphysema :
Definition : Enlargement of airways beyond (distal) to the terminal bronchioles with
dilation and destruction of their walls.
NB:- *Trachea, bronchi & bronchioles are strictly conducting airways.
*Resp. bronchioles, alveolar ducts & alveolar sacs-conducting & respiratory structures.
*Alveoli are purely respiratory function.
*Bulla : emphysematous space with diameter > 1 cm in the distended state & its walls are
made up of compressed surrounding lung or pleura.
49. Chest 48
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Secondary pulmonary lobule : Areas supplied by 3-5 terminal conducting
bronchioles, separated by septa = 3-5 acini
Respiratory acinus = lung distal to a terminal bronchiole.
Composed of all respiratory structures distal to a terminal bronchiole = primary
lobule (Respiratory bronchiole, alveolar duct and sac.)
Types of emphysema :
A. Air trapping present at the respiratory bronchiole “symptomatic”:
1.Panacinar : Panlobular :
- Non selective process, characterized by destruction of all the lung distal to the
terminal bronchiole. ??Alpha-1-anti-trypsin deficiency.
- It may be localized or generalized.
2. Obstructive emphysema : misnomer : obstructive hyperinflation (bec. distal airway
is not necessarily destroyed).
- It occurs, when a larger bronchus is partially occluded by an intra-luminal mass
ball valve effect of this mass, in such a way that air enters the lung on
inspiration but is trapped on expiration.(FB or peribronchial tumor).
3. Para-cicatricial emphysema:
-Distention & destruction of terminal air spaces adjacent to fibrotic lesions eg TB.
4. Congenital lobar emphysema :
- Refers to an overinflated lobe which compresses adjacent normal lung producing
respiratory distress mainly in the neonatal period.
- Causes :
1. Deficiency of a bronchial wall cartilage.
2. Obstruction to a lobar bronchus by an extrinsic mass or anomalous vessels.
3. Alveolar abnormality
*Polyalveolar lobe increased number of alveoli in a lobe
*Rigid alveoli with surrounding stroma.
5. Unilateral or lobar emphysema (Macleod’s syndrome):
- It is probably the result of a childhood viral infection causing bronchiolitis and
obliteration of the small airways, the involved distal air ways are ventilated by
collateral air drift air trapping of pan-acinar type.( hypertransradiant hemithorax
dt decrease perfusion.)
Causes of unilateral lung transradiancy :
50. Chest 49
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1. Technical radiographic factors.
2. Thoracic cage abnormalities.
3. Pulmonary embolism.
4. Compensatory or obstructive emphysema.
B. No air trapping “asymptomatic”:
1. Centri-acinar : centrilobular.
- Selective process, characterized by destruction and dilatation of respiratory
bronchioles, where the alveolar ducts, sacs and alveoli are spared.
- It is frequently found in chronic bronchitis.
2. Focal dust emphysema :
- Similar to centri-acinar emphysema, but in association with cool dust exposure.
3. Para-septal emphysema:
- Usually involves the periphery of the secondary lobules at the lung periphery
occasionally causes bullae formation.
4. Senile emphysema :
- Dilatation of the alveolar ducts due to the aging process.
- Non significant.
5. Compensatory emphysema (hyperinflation):
- Hyperinflation of the unaffected or remaining lung due to collapse of a part or all
of the lung.
Causes of lobar emphysema :
I-Bronchial obstruction:
- Abnormal bronchial wall (cartilage deficiency, bronchial stenosis)}Panacinar
- Extensive bronchial compression.}Panacinar
1.Vascular anomalies vascular ring or sling.
2.Mediastinal mass e.g. bronchogenic cyst.
- Intra-bronchial obstruction: (All obstructive except 4 is paracicatricial)
1. Mucous plugs. 3. Tumors.
2. F.B. “Peanut”. 4. Endo-bronchial TB.
II. Parenchymal abnormalities: (congenital)
1. Polyalveolar lobe.
2. Rigid alveoli.
NB: *Type I resp failure: diffusion defect (hypoxic, normo or hypocapnic eg pul. edema, pure
51. Chest 50
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emphysema, ARDS. (Oxygen as much as you want)
*Type II : ventilation defect (hypoxic, hypercapneic) GOAD, restrictive lung dis (differentiated
by FEV1). ( Care with oxygen therapy)
Radiological appearance :
The classical radiographic appearance of advanced emphysema consists of a triad
of findings (overinflation, vascular damage, bullae).
I. Panacinar :
1. Over inflation : manifested by low flat diaphragm
- Normally at end of deep inspiration the diaphragm is at the level of 6th-7th
anterior rib in frontal view, and 10-11 posterior rib. Best seen in lateral view.
- In emphysema, there is low position of the diaphragm below these levels at end
of inspiration, associated with flattening of the diaphragmatic dome.
- The low flat diaphragm results in an apparently small heart, “elongated” and
decreased cardio-thoracic ratio < 40%, & transverse ribs.
- Limited diaphragmatic movement with emphysema by fluoroscopy and
inspiratory, expiratory films, Where diaphragmatic excursion is about 5-10cm,
in emphysema it is < 3cm.
- Enlargement of retrosternal translucent zone on the lateral radiograph measured
from the back of the sternum to the anterior aspect of lower ascending aorta ..
should be 4cm or greater to be considered abnormal.
- Increased AP diameter of chest (barrel chest) due to bowing of the sternum
and increase thoracic kyphosis.
2. Vascular changes :
A. In widespread, generalized emphysema:
- The midfield and peripheral pulmonary vessels are attenuated in both size and
number, where the normal smooth gradation in size of vessels from the hilum
outwards is lost.
- The hilar vessels being larger than normal with abrupt tapering.
B. Localized emphysema :
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There is uneven distribution of pulmonary vessels where :
- Vessels of occasionally increased caliber are present in unaffected areas of lung
... termed marker vessels which is used as a touchstone for normality and allow
one to identify emphysematous area.
- The vessels are smaller and more deficient in the emphysematous areas.
- When, emphysema is predominantly basal (lower lobe emphysema) which is
common in panacinar type, it is mainly associated with “upper lobe blood
diversion”, as the perfusion of emphysematous lung is less than normal and the
pulmonary blood flow is diverted to less affected areas of lung.
- With development of cor pulmonale or left heart failure, the radio graphic
picture of emphysema will alter where :
a. The signs of hyperinflation may be decreased.
b. The level of diaphragm will rise, this is due to pulmonary edema
decrease of the hung volume.
c. The heart may appear normal or enlarged.
DD of upper lobe blood diversion :
1. High pulmonary venous pressure as in left heart failure.
2. Severe lower lobe disease.
- Emphysema.
- Fibrosing Alveolitis.
- Bronchiectasis.
- Pulmonary embolism.
3. Bullae :
Can be identified in about 1/3 of patients of emphysema, also may be seen
independently of emphysema.
Radiological appearance:
a. Rounded or oval translucency, more than > 1cm in size.
b. Smooth, curved, hair line wall (compressed lung parenchyma.)
c. Causing distortion or displacement of pulmonary vessels.
d. May be single or multiple.
e. Usually peripheral.
Giant bullae :
53. Chest 52
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- It occupies most of the hemithorax.
- Compression of adjacent lung.
- Displacement of fissure and depression of hemi-diaphragm.
- May cause mediastinal shift or extends across the midline or retro-sternal space.
NB:*Many bullae may be invisible on chest radiograph and can be demonstrated by :
- Expiratory films, (air trapping within the bullae).
- CT scanning.
Complications of bullae formation :
1. Infection :
- Where a fluid may partially fill it forming fluid level or completely filling it
and appears as a well-defined homogenous opacity.
- The surrounding lung shows inflammatory changes.
2. Hemorrhage : Forming fluid level.
3. Pneumothorax : Rare if rupture.
DD: of localized transradiancy :
1. Bullae.
2. Encysted pneumothorax.
- The bullae shows - Curvilinear margin, outer aspect of which makes an
acute angle with the chest wall.
- Has lung tissue peripherally.
3. Cyst.
4. Pneumatocele tomography may be needed.
5. Localized emphysema.
II. Obstructive emphysema :
1. Vascular changes as before.
2. Air trapping picture by fluoroscopy and expiratory films.
*Transradiancy of affected lobe or segment.
*Deviation of mediastinum to normal side.
*Low flat ipsilateral diaphragm with restricted movement.
3. When lobar :
*Displacement of fissures.
*Compressed lung tissue around.
III. Macloed’s syndrome :
54. Chest 53
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1. Plain :
-Hyperlucency of the affected lung due to attenuation of vessels within it.
-Air trapping effect of the affected lung, but no over inflation as above.
2. Bronchography :
Not usually indicated, but shows a characteristic app.:
- Main and segmental bronchi are normal.
- Irregular dilatation of peripheral bronchi till, 6th order division.
- Lack of bronchial filling distal to the 6th order division (bronchiolitis obliterans)
giving pruned tree appearance.
3. Pulmonary angio:
- Not commonly used, reveals: attenuation of pulmonary vasculature of the
affected side.
4. Isotope :
- perfusion scan shows decrease flow.
- Ventilation scan air trapping
DD. of unilateral emphysema : =Other causes of hypertransradiant hemithorax :
A. Rotation :
- Technical.
- Scoliosis :hypertansradiant hemithorax is the side to which the patient is turned.
B. Chest wall deficiency :
- Mastectomy.
- Poland’s syndrome (congenital absence of pectoral muscles).
C. Pleural :
- Contra-lateral pleural effusion with patient supine.
- Pneumothorax.
D. Parenchymal :
- Lobar collapse compensatory emphysema.
- Bronchial.
1. Obstructive emphysema. 3. Macloed’s syndrome.
2. Unilateral bollus emphysema.
- Arterial :
1. Congenital absence of one of pulm. a.
2. Pulm. A. (occlusion embolism, nearby carcinoma)
IV- Congenital Lobar Emphysema:
55. Chest 54
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- Variable degree of overinflation of one lobe mostly the upper & middle lobes →
show hyperlucency with few visible lung markings.
- The over expanded lobe leads to
1. Compresses remaining lung
2. Flattens or inverts ipsilateral lung
3. Mediastinal shift towards opposite side.
4. May herniate across the midline to opposite side.
DD of Cong. Lobar Emphysema:
1. Tension pneumothorax : - Entire ipsilateral lung is collapsed.
- No vascular markings within it.
2. Congenital cyst : evidence of other cysts.
3. Compensatory hyperinflation (no evidence of expiratory air trapping).
4. Obstructive hyperinflation ...... mainly due to mucous inspissation and plugging
of a bronchus which may give identical picture of C.L.E…..so bronchoscopy is
essential before surgical resection of lobe in C.I.E.
V. Emphysema with chronic bronchitis : (centriacinar/ no air trapping)
Clinically emphysema of two type (Pink Buffer, Blue Blotter)
Pink Buffer :( Pt. by major effort ventilates sufficient to maintain normal bl. Gases).
More common with pan acinar emphysema.
- Manifestation of hyperinflation.
- Peripheral vascular attenuation.
“Where we call arterial deficiency pattern of emphysema”
Blue Bloater : (Chronically retains Co2 dt poor alveolar ventilation).
More common with centri-acinar emphysema :
- Increased bronchovascular marking ... dirty chest.
- Enlarged central pulmonary arteries ....... possibly with cardiac enlargement.
(+ Cor pulmonale → edema)
- Signs of hyperinflation is not severe.
This is called ..... increased markings pattern of emphysema.
- Patient with chronic bronchitis shows features between these two extremes
(panacinar + centri-lobular).
Complications of emphysema :
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1. Pneumonia : produces, ill defined, patchy, nodular shadowing.
2. Pulmonary edema: of left heart failure with upper lobar in distribution.
3. High incidence of bronchial carcinoma.
4. Cor-pulmonal.
5. Pneumothorax.
6. Respiratory failure.
DD of Emphysema:
1. Asthma: during acute attacks.
2. Primary pulmonary arterial hypertension .... there is no evidence of hyper
inflation.
57. Chest 56
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LARGE AIR WAY OBSTRUCTION
Causes of bronchial obstruction:
A. In the lumen:
1. Foreign body.
- Air trapping > atalectasis.
- Lower lobe is most frequently affected.
2. Mucus plug.
- Post operative, asthma.
3. Misplaced endo-tracheal tube.
4. Broncho -pulmonary aspergillosis.
B. In the wall (mural):
1. Carcinoma of bronchus Tapered narrowing ± irregularity.
2. Bronchial adenoma Smooth, rounded filling defect.
3. Inflammatory stricture (TB).
4. Bronchial atresia.
5. Sarcoid granuloma.
6. Fracture bronchus.
C. Outside the wall:
1. Adenopathy.
2. Mediastinal tumor.
3. Enlarged left atrium.
4. Aortic aneurysm, vascular ring.
5. Cong., vascular anomalies.
Manifestations of partial or complete major air way obstruction:
1. Collapse or atalectasis. (if complete ob.)
2. Obstructive hyperinflation if partial ob (valve).
3. Obstructive pneumonitis abscess.
4. Bronchocele.
5. Bronchiectasis.
58. Chest 57
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COLLAPSE (ATELECTASIS)
Collapse means partial or complete loss of volume of a lung.
Mechanisms of collapse (types):
1. Relaxation or passive collapse.
Air or fluid in the pleural sac passively causes the lung to retract towards its
hilum.
2. Cicatrization collapse :
The lung can not normally expand (decrease lung compliance) decrease it
volume. Occur in pulmonary fibrosis.
3. Adhesive collapse :
Normally the surface tension of the alveoli is decreased by surfactant
disturbance of such mechanism leads to alveolar collapse with patent major
airway. e.g. respiratory distress syndrome in premature.
4. Resorption collapse (obstructive): (causes : outside - inside - lumen)
Acute bronchial obstruction leads to absorption of gases within the alveoli by the
blood of pulmonary capillaries leads to alveolar collapse no air bronchogram.
Radiological appearance of collapse: (direct - indirect).
A. Direct signs (Lobar signs) of collapse :
- Displacement of the interlobar fissures. The most reliable sign.
The degree of displacement depend on extent of collapse.
- Loss of aeration or increased density of the collapsed area.
The collapsed area adjacent to mediastinum or the diaphragm will obscure
their defined border “silhouette sign”.
- Vascular and bronchial signs:
Crowding of vessels in the collapsed area.
Crowding of bronchi if there is air bronchogram.
B. Indirect signs (extra-labor):
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1. Elevation of the hemidiaphragm: especially in lower lobes collapse.
2. Mediastinal shift:
- Tracheal shift to the same side in upper lobe collapse.
- Shift of the heart to the same side in lower lobe collapse.
3. Hilar displacement:
- Elevated in upper lobe collapse.
- Depressed in lower lobe collapse.
4. Compensatory hyperinflation of the normal parts of the lung:
- In total lung collapse compensatory hyperinflation of the contralateral
lung ? explain.
5. Rib approximation.
PATTERNS OF COLLAPSE
A. Entire lung collapse “complete collapse”:
Acute obstruction to one of the main bronchi lung collapse and causes
1. Opacification of the hemithorax.
2. Displacement of the mediastinum to the affected side.
3. Elevation of the diaphragm.
4. Rib approximation.
5. Compensatory hyperinflation of contralateral lung.
a. Hyperlucency with accentuation of its vascular marking.
b. Widening of rib spaces.
c. Herniation across mediastinum, mainly occur in the retrosternal space or in
azygo-ocsophageal recess posteriorly or across the midline.
B. Lobar collapse:
1. Right upper lobe collapse :
PA view : -The outer aspect of minor fissure moves upward with concavity inferior.
- Tracheal shift to the right.
- Loss of definition of shape of right border of superior mediastinum
(Silhouette sign),
60. Chest 59
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- Elevation of right hilum with more horizontal course.
- Compensatory hyperinflation of the lower lobes.
N.B: In marked collapse, the collapsed area comes to lie against the apex
and mediastinum simulating (apical pleural thickening, or superior
mediastinal widening.
Lateral view :
- The minor fissure and upper part of the oblique fissure move towards
each other.
- Effacement of the anterior margin of the aorta.
- Wedge like opacity with its base towards apex of the lung and its apex
towards the hilum.
2. Right middle lobe collapse:
PA view : - Lateral part of minor fissure moves downward.
- The area of opacity, mainly not seen but usually sufficient to blur the
sharp right heart border (Silhouette sign) best sign.
Lat. view :
- The minor fissure and lower half of oblique fissure move towards each
other with bowing of one of them or both.
- Increased density of middle lobe.
- In severe collapse band shadow extends downward and forward from
hilum.
Lordotic view:
- The collapsed middle lobe appears as triangular shadow with its apex
pointing laterally from which, the fissure line usually extend to chest
wall.
DD.: Encysted interlobar effusion of lower part of major fissure (no air bronchogram,
lat view → lenticular, no oblit. of cardiac silhouette.
3. Lingular collapse :
Mainly involved in left upper lobe collapse :
PA view : Loss of definition of the left cardiac border.
Lat. view : Ant. displacement of lower part of oblique fissure and increased opacity anterior to it.
61. Chest 60
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4. Collapse of the right or left lower lobe :
PA view :
- With minor volume loss no increase in radio-opacity.
- As collapse progress, there is increase in radio-opacity forming a triangular
shadow with its apex in hilar region and its base on diaphragm. On the left side it
lies behind the heart and penetrated film may be needed ... In this situation,
indirect signs are important such as:
a. Silhouette sign: on left side (obscuration of the margin of hemidiaphragm
and descending aorta). On right side : The border mainly remains sharp.
b. Hilar depression with medial shift of its inferior component.
c. Hyperinflation of the ipsilateral upper lobe.
d. Diaphragmatic and mediastinal shift.
Lateral view :
- The lower part of oblique fissure mainly bowed convex backwards & sometimes
its upper posterior aspect is depressed by compensatory hyperinflation of upper
lobe.
- With marked volume loss increased radio opacity in the posterior
costophrenic angle and loss of lucency of the lower dorsal spines.
5. Left upper lobe collapse :
PA view :
- Ill defined hazy opacity present in upper, mid and sometimes lower zones. More
dense at hilum.
- III defined border of aortic knuckle, hilum and the left cardiac border it lingula is
involved (Silhouette sign +ve.)
- Shift of trachea to the left.
- Hyperinflation of the left lower lobe.
- Elevated hilum.
Lat. view :
- Anterior displacement of the oblique fissure.
- With increased collapse, the upper lobe retracts posteriorly, forming an
elongated opacity extending from the apex, anterior to ! hilum and lined
posterior by oblique fissure.
62. Chest 61
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C. Multilobar collapse :
Right middle and lower lobe collapse dt to obstruction of bronchus intermedius.
PA view :
- A triangular shadow, with its apex at hilum and its base on diaphragm extending
laterally to costophrenic angle.This distinguish it from isolated lower lobe
collapse.
- Obliteration of diaphragm and right cardiac border.. DD: subpulmonary effusion
or elevated right diaphragm.
Lat view :
Radio opacity of a well defined upper border extending downward and forward
from back to front which obliterates the whole hemidiaphragm.
D. Atypical forms of collapse :
1. Rounded atalectasis or folded lung:
- A homogenous opacity, with ill defined edges, always pleural based and
associated with chronic pleural thickening DD: pulmonary mass.
- A vascular shadow may be seen to radiate from part of opacity mimicking a
comet’s tail comet sign.
- This type of collapse occurs, when pleural effusion causes fold of the adjacent
lung mainly lower lobe and the folding failed to resolve when effusions subsides
(with asbestosis).
2. Fleischner’s plate atalectasis :
- Linear densities appear in the lower lung fields soon after abdominal surgery.
63. Chest 62
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CONSOLIDATION
Definition: Means replacement of air in one or more acini by fluid or solid
material. The smallest unit of consolidation is a single acinus which
casts a shadow approximately 7mm in diameter.
Causes of consolidation:
- The most common cause is acute inflammatory exudation associate with
pneumonia.(TB, infarction, collapse), (same as causes of alveolar and acinar shadows)
- Other causes:
- Pulmonary edema.
- Hemorrhage, aspiration.
- Alveolar carcinoma, lymphoma.
Consolidation is either : patchy, segmental, or lobar
Consolidation :
- When associated with patent air way air bronchogram is seen with to change
in volume .
- When it occurs secondary to bronchial obstruction no air bronchogram seen
and there is decrease in lung volume = consolidation collapse.
Air in alveoli is displaced by:
Fluid
Pneumonia, TB, IPF, bronciectasis
Pulmn. edema
Pulmn. hge
Pulmn infection
Soft tissue
Alveolar cell carcinoma
lymphoma
64. Chest 63
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OBSTRUCTIVE PNEUMONITIS
Pneumonic consolidation distal to an obstructive lesion :
The presence of underlying airway obstruction with consolid. can be suspected from :
1. Segmental or lobar distribution.
2. Atalectasis : Marked volume loss, which does not occur with simple
pneumonia. Tomography and bronchoscopy can exclude br.
obstruction.
3. Drowned lung: When fluid and exudate fill the lung distal to an obstruction
appears as dense homogenous consolidation with absent air
bronchogram.
4. Slow resolution : Generally if pneumonic consolidation persists more than > 8
weeks after appropriate therapy in a patient who does not
have any systemic disease→ suspect underlying obstruction
5. Recurrence : Repeated pneumonia to same segment or lobe is highly
suggestive of obstructing bronch. lesion, or local parenchymal
abnormality as bronchiectasis.
OBSTRUCTIVE HYPERINFLATION
See emphysema
BRONCHOCELE (MUCOID IMPACTION)
Definition: Accumulation of mucus, pus or caseous materials within distended
bronchi distal to a segmental bronchus but without collapse.
Radiological features :
- Oval or finger like branding homogenous opacities along the axis of bronchial
tree usually upper lobe.
- Tomography (this low density is clearly seen)>
- Bronchography shows obstruction as sharp cut off in the contrast column.
- With increasing distension, bronchocele assumes a round shape DD from
bronchogenic cyst.
- Infection bronchiectatic changes.
DD: Arteriovenous malformation by:
*Multiplicity in AVM with presence of feeding and draining vessels.
*Absence of obstructive hyperinflation in AVM.
65. Chest 64
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BRONCHIECTASIS
Irreversible dilatation of a bronchus (persistant dilataion of ! bronchi ass. with suppurative
infla.
Etiology :
Commonly due to a severe, recurrent or persistent infection which leads to
dilation of large airways and obstruction with destructive process of smaller ones
bronchiolitis obliterans.
NB: Inflammation & destruction: large bronchi dilated (yield under pr.)
* Small obstructed (bronchiolitis obliterans).
Predisposing factors (infection) :
1. TB
2. Severe childhood pneumonia especially (pertussis, measles).
3. Those associated with bronchial obstruction.(luminal, extraluminal, intraluminal ).
4. Those associated with either inborn immunological defect or with inborn
structural abnormalities of bronchial wall e.g. Kartagner’s syndrome.
*Non infective bronchial wall damage : occurs following inhalation of toxic gases and
allergic damage of aspergillosis.
Site :
- May be localized, multifocal or generalized.
- It is commonly basal but it may be confined to upper zone e.g. TB.
CP: See internal medicine (Chest: cough,expectoration, positional- toxemia,clubbing, complict)
Types of bronchiectasis : (features of bronchography)
1. Cylindrical bronchiectasis : = tubular.
- Bronchial dilation is generally mild with more or less parallel walls, “squared
of” ends and some preservation of the side branches.
- DD :
a. Chronic bronchitis mild and more widespread.
b. Collapsed lobe mechanical dilation of collapsed lobe.
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2. Varicose and cystic or saccular type :
- Much more dilatation and irregularity with a beaded or saccular outline to
airway which end in a bulbous fashion.
- The side branches are permanently occluded and only a handful of bronchial
generations distal to the lobar bronchi remain patent.
3. Fusiform bronchiectasis :
- Varicose bronchiectasis with preserved side branches.
- This appearance, typically at segmental or subsegmental level is highly
suggestive of allergic aspergillosis.
Radiological features :
1. It may be normal in 7%
2. Peribronchial thickening and retained secretions.
3. Cystic spaces = air fluid levels.
4. Crowded vessels i.e loss of volume.
5. Coarse honeycomb pattern in very severe disease.
Bronchography : as types of bronchiectasis.
CT : Can identify the degree of bronchiectatic changes and underlying disease
(before surgery.)
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PULMONARY NEOPLASM
Benign : Intrabronchial tumors (adenoma), pulmonary tumors (hamartoma, angioma)
Malignant : Bronchial, carcinoma., others, metastasis, malig, lymphoma, (carcinoid,
cylindroma).
BRONCHIAL OR BRONCHOGENIC CARCINOMA
Incidence: Male:female 5:1, Age : peak at 6th decade.
Predisposing factors : Cigarette smoking and asbestosis (pneumocon).
Pathological types :
1. Squamous cell carcinoma 50%. (central, large cavitates).
2. Adenocarcinoma, including alveolar c. carc. 20% (bronchioloalveolar cell/
periph., pancost.
3. Undifferentiated carcinoma.
- Small cells (Oat cell type) 20%. (APUD, never cavitates, small , massive hilar LN)
- Large cell type 10%. ( periph. or central.)
Types :
- Central: tumor arising at bronchus - early complain 66%
- Peripheral: tumor arise from lung tissue late complain 33%
Diagnosis of bronchogenic carcinoma depends on :
1. Clinical picture.
2. Radiological pictures.
a. Plain.
b. Tomography : Better definition of lesion but does not differentiate benign
from malignant.
c. Computed tomography (the best) + MRI.
d. Biopsy (U/S, CT guided, or at bronchoscopy).
NB: Central : WHO I: sq-cell car central, large, cavitates.
WHO II: oat small all anaplastic central, never cavitates, small, hilaer LN.
Peripheral: WHO III: Adenocarcinoma pancost, apical, peripheral, horner.
WHO IV: Large cell carcinoma.
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Radiological features :
A. Peripheral tumors: A mass in lung having the following features :
1. Shape : Mainly spherical, may be oval or dumbbell shaped.
2. Border (edge):
- Lobulated, notched (umblicated) or irregular ill-defined.
- Corona radiata: Numerous fine strands may be seen radiating into lung from
mass with more transradiant lung parenchyma than normal between these
strands which is highly suggestive for carcinoma.
3. Size : variability is unusual to identify a nodule, until it is 1cm in size or more.
4. Calcification : Lack of calcification is the basis and when it is present it is mainly
due to engulfment of the tumor to pre-existing calcified granulomata (TB,
fungal)
5. Cavitation : (better seen by CT or tomography).
- The peripheral lung mass may cavitate, revealing central air lucency.
- An air fluid level (when communicates with air way).
*The cavity : a. Frequently eccentric.
b. Thick, irregular wall, rarely smooth.
c. Tumor nodules may be visible, which may break off and lie within
the cavity simulating to a mycetoma.
*NB:-Squamous cell carcinoma cavitates more frequently than the other types while
Oat cell carcinoma never cavitates. -DD : from other cavitary lung lesions.
6. Mass effect:
- Bronchocele, due to obstruction to the segmental or subsegmental bronchus.
- Appear as peripheral tubular density which may branch &occur distal to the
mass.
7. A peripheral line shadow (Tail):
- May be seen between a peripherally located mass lesion and pleura.
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- This phenomenon can occur in both benign and malignant lesion.
- It is mainly due to plate like atalectasis, secondary to bronchial obstruction or
septal edema due to lymphatic obstruction.
B. Central tumors : Identified by (mass, signs of air way obstruction).
1. Signs of central carcinoma :
1. Unilateral hilar enlargement which is either due to:
a. Central bronchial mass.
b. Enlargement of lymph nodes (hilar).
Differentiated by shape & extent of lesion.
* The more lobular ! shape, the more ! wide spread more suggestive for
adenopathy.
* Increased density of hilum at one side without significant enlargement may
occur to super imposition of the mass on hilum.
2. Signs of air-way obstruction (+ SVC)
- Encroachment of ! tumor on bronchial lumen causes irregular narrowing or even
complete obstruction of a major bronchus leading to :
a. Atalectasis (+ its signs).
b. Consolidation due to :
- Inability to evacuate secretion.
- 2ry infection (pneumonia).
c. Consolidation-collapse.
NB: Features suggestive of pneumonia secondary to a bronchial
carcinoma :
1. Pneumonia confined to one lobe with loss of volume.
- (No) air bronchogram mainly absent.
- Bronchoscopy should be done.
2. An associated hilar mass is rare to occur with simple pneumonia.
3. Pneumonia that remains confined to one segment for more than 2 weeks
without clearing or spreading into other segments as in simple pneumonia.
4. Persistence of localized pneumonia on appropriate antibiotic therapy for
more than 8 weeks.
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C. Spread of tumor :
1. Hilar and mediastinal lymph node metastasis :
- May be present at the time of initial diagnosis particularly with adenocarcinoma
and Oat cell carcinoma.
- Central adenopathy may be difficult to be recognized by plain film and can be
only recognized by CT or tomography.
- CT is the most sensitive method for detecting mediastinal adenopathy.
- The size of ! L.N. detected is of great importance in suggestion of metastasis.
* < 1 cm in diameter much suggestive to normal.
* 1-2 cm in diameter considered abnormal but not necessarily neoplastic.
* > 2cm more suggestive of metastatic neoplasm.
2. Mediastinal invasion :
- Can not be evident on plain film, unless phrenic nerve is invaded.
- CT can provide evidence of mediastinal invasion.
- Phrenic nerve paralysis high hemidiaphragm on chest X-ray.
*Cause of high hemidiaphragm in Br. carc.
- Phrenic nerve paralysis.
- Lower lobe collapse.
- Subpulmonary effusion.
- Liver enlargement (2ry to metastasis).
3.Pleural invasion:…….. pleural effusion
*Causes of pleural effusion in bronchial carcinoma :
a. Invasion of the pleura by tumor.
b. 2ry to lymphatic obstruction.
c. 2ry to associated pneumonia.
4. Chest wall invasion :
- The peripheral lung carcinoma may cross the pleura and invade the chest wall
causing rib or spinal destruction (+ Horners syndrome.)
