Hydatid disease
Round or oval opacity, clearly defined, the shape varies
with change in position.
Pericyst – external capsule of the host tissue.
The cyst – double wall: thick outer membrane (exocyst)
and a thin inner wall of germinal cells (endocyst).
The cyst may rupture into a bronchus – fluid-air level. The
collapsed cyst wall may float on the fluid surface – water-lilly
or iceberg sign.
Rupture of the pericyst or host capsule leaves air between
it and the exocyst – crescent or meniscus sign.
Chronic obstructive pulmonary disease (COPD)
Progressive obstruction to airflow. Two components:
-Chronic bronchitis is a clinical diagnosis: excessive
mucus formation and cough for more than 3 months during 2
consecutive years. Chest films add little information.
-Emphysema is a pathologic diagnosis: abnormal
enlargement of air space distal to the terminal nonrespiratory
bronchiole.
Etiology – unknown: tobacco smoke, air pollution
Emphysema
Abnormal enlargement of distal air spaces distal to the
terminal bronchioles with destruction of alveolar walls with
or without fibrosis.
Types: panacinar, centriacinar, paraseptal
Rx:
[Link] and flattening of the diaphragms with
blunting of the costophrenic angles.
[Link] radiolucency of the lung
[Link] retrosternal radiolucency
[Link]-sheath trachea
[Link] spaced ribs
Vascular abnormalities: decreased number of vessels in
areas of abnormal lung, absence of peripheral pulmonary
vessels, fewer arterial branches.
HRCT:
Centriacinar – the central portion of the pulmonary nodule
is involved
Panacinar – the whole acinus is involved and central
arteries and bronchioles can be seen
Paraseptal – emphysematous changes adjacent to septal
lines in periphery and along fissures.
Asthma
Hyperirritability of airways causes reversible airway
obstruction. Etiology-unknown.
Types: extrinsic, allergic form (childhood asthma,
immunologically mediated hypersensitivity to inhaled
antigens) + intrinsic asthma (adults, no immediate
hypersesitivity)
Rx: normal CXR in majority of patients; severe or
chronic asthma – air trapping, hyperinflation, bronchial wall
thickening
Complications: acute pulmonary infection, mucous
plugs, tracheal or bronchial obstruction, pneumothorax
Bronchiectasis
Irreversible dilatation of bronchi ( reversible bronchial
dilatation may be seen in viral and bacterial pneumonia).
Types: cylindrical, varicose, cystic.
Pathogenesis – obstruction (neoplasm, inflammatory
nodes, foreign body, aspiration) – infection and traction.
Plain film – tramline (horizontal, parallel lines
corresponding to thickened, dilated bronchi) + bronchial
wall thickening + indistinctness of central vessels due to
peribronchovascular inflammation + atelectasis.
HRCT – bronchi appear larger than accompanying
vessels.
Bronchogenic carcinoma
Risk factors – smoking, radiation, uranium miners,
asbestos exposure.
CENTRAL
Endobronchial – air trapping, atelectasis.
Exobronchial – nodule, irregular borders, high intensity,
connected to the hilum.
Rx + bronchoscopy + CT
PERIPHERIC
Opacity, high intensity, irregular borders; cavitation
Pancoast –Tobias – rib + destruction, chest wall invasion,
involvement of subclavian vessels, brachial plexus
involvement
Rx + CT + biopsy
METASTASES
- Hematogeneous
- Lymphatic
PARANEOPLASTIC SYNDROMES
Metabolic – Cushing, carcinoid, hypercalcemia,
hypoglycemia
Muskulo-skeletal – neuromyopathies, clubbing of fingers
Other – thrombophlebitis, anemia
Do not forget : Tumor staging (TNM) !!!
Idiopathic pulmonary fibrosis
Progressive inflammation, fibrosis and destruction of
lung of unknown cause.
Lung biopsy is necessary for diagnosis.
Treatment – steroids useful in 50%.
Clinical findings: clubbing, nonproductive cough,
dyspnea, weight loss.
Radiographic features:
[Link]: primarily in lower lung + peripheral
subpleural involvement
[Link] pattern: early – ground glass appearance, later
– reticular pattern in lower lobes, endstage –
honeycombing, traction bronchiectasis
[Link] lung volumes
[Link] hypertension with cardiomegaly
Sarcoidosis
Systemic granulomatous disease of unknon etiology -
lung, skin, eye, hepatosplenomegaly, CNS, salivary glands,
joints.
Diagnosis: biopsy – bronchial, open lung biopsy, lymph
node, parotid gland or nasal mucosa biopsy; Kweim test.
Stage 0 – initial normal film.
Stage 1 – adenopathy – symmetric hilar adenopathy;
paratracheal, tracheobronchial and azygos adenopathy is
commonly associated with hilar adenopathy (Garland’s triad).
Stage 2 – adenopathy with pulmonary opacities ( reticulo-
nodular pattern, large nodules).
Stage 3 - pulmonary opacities without hilar adenopathy.
Stage 4 – pulmonary fibrosis, upper lobes with bullae.
Silicosis
- Causative agent is silicone dioxide
- Pathology: silica is phagocytosed by pulmonary
macrophages, cytotoxic reaction causes formation of
noncaseating granuloma, granuloma develop into
silicotic nodules, pulmonary fibrosis develop as
nodules unite.
- Radiographic features:
[Link] pattern
[Link] pattern – may precede or be associated with
nodular pattern
[Link] adenopathy
[Link] massive fibrosis
Asbestos exposure – thoracic manifestations:
Pleura:
Pleural plaques – have no functional significance; preferred location
– bilateral, posterolateral mid and lower chest.
Diffuse pleural thickening – may cause respiratory symptoms;
thickening of interlobar fissures.
Pleural calcifications – in absence of other histories (hemothorax,
empyema, TB, previous surgery) is pathognomonic of asbestos
exposure.
Benign pleural effusions – sterile, serous exudate.
Lung:
Interstitial fibrosis – reticular pattern, initial subpleural location,
progression from bases to apices, no hilar adenopathy.
Malignancy:
Malignant mesothelioma
Bronchogenic carcinoma
GI malignancies
PULMONARY EDEMA
Abnormal accumulation of fluid in the extravascular
pulmonary tissues.
Causes:
- cardiogenic - LV failure, mitral regurgitation,
ruptured chordae, endocarditis
- renal - renal failure, volume overload
- lung injury - septic shock, fat embolism, inhalation,
aspiration
Interstitial edema:
- Perivascular blurring – margins of the vessels become
indistinct and widened in the parahilar area
- Peribronchial blurring
- Hilar haze – a loss of definition of large central
pulmonary vessels with increase in opacity
- Kerley lines : Kerley B lines are dense, horizontal lines
that measure about 2cm in length, they are seen in lower lung
and represent secondary interlobular septathickened by fluid.
Kerley A lines are longer (5-10cm) and extend from the hila
toward the periphery; they are seen in upper lobes.
- Pleural effusion
Alveolar edema:
- Air-space disease: patchy consolidation, air
bronchograms ( bilateral opacities that extend outward from
the hilum)
PULMONARY EMBOLISM
Types:
- Incomplete infarct – hemorrhagic pulmonary edema
without tissue necrosis, resolution within days
- Complete infarct – tissue necrosis, healing by scar
formation
Risk factors – immobilization, recent hip surgery,
cardiac disease, malignancy, estrogen use
Clinical findings – chest pain, tachypnea, dyspnea,
rales, hemoptysis, fever
Imaging algorithm – CXR + scintigraphy + angiography
+ helical CT
Plain film
- Westermark sign – localized pulmonary oligemia
- Hampton sign – triangular peripheral cone of infarct (
blood in secondary pulmonary lobules)
- Fleischner sign – increased diameter of pulmonary
artery
- Cor pulmonale – sudden increase in size of RV, RA
- Pulmonary edema, atelectasis, pleural effusion
Scintigraphy - ventilation – perfusion mismatch
Angiography
- Constant intraluminal filling defects in PA
- Complete cut off of PA or its branches
- Delayed filling and emptying of venous phase
PULMONARY VASCULATURE
Precapillary ( arterial ) hypertension :
- Increased resistance – obstructive ( embolism ) +
obliterative ( emphysema, interstitial disease) +
constrictive ( anoxia )
- Increased flow – large left-to-right shunts
RX – marked enlargement of PA + constriction of
segmental and peripheral arteries + normal or small pulmonary
veins + the heart may show alteration consistent with the
initial defect.
Postcapillary ( venous ) hypertension
RX – constriction of the pulmonary arteries and veins in
the lower zones and dilatation of the arteries and veins in the
upper lobes caused by redistribution of blood.
PLEURA
- Visceral pleura – covers lung
- Parietal pleura – covers rib ( costal pleura), diaphragm
(diaphragmatic pleura), mediastinum ( mediastinal pleura )
Pleural effusions - excess fluid in the pleural space. Two types:
transudates and exudates.
Causes – tumor, inflammation, cardiovascular, metabolic, trauma
Rx: lateral decubitus films – most sensitive (may detect as little as
25ml)
Rx: Pa, lateral films – blunting of costophrenic angles
Posterior costophrenic angle: 75 ml required for detection
Lateral costophrenic angle : 175 ml required for detection
Large effusions – all cardiophrenic angles obliterated, mediastinal
shift, elevated diaphragm.
Loculated pleural effusions are accumulations of pleural fluid within
the fissures and cannot shift freely within the pleural space.
Empyema – purulent fluid in the pleural space
- Pleural effussion with lenticular shape and obtuse angle
with the chest wall
- Differential diagnosis – abscess (acute angle)
Pneumothorax – air into the pleural space
Malignant mesothelioma
- Irregular, nodular, peripheral pleural opacities with
associated ipsilateral effusion; extension into interlobar
fissures is frequent; rib destruction
- CT method of choice.
THE MEDIASTINUM
Approach to mediastinal masses
- Location – anterior, middle, posterior
- Invasive or noninvasive mass
- Content – fat, cystic, solid, enhancement
Normal variants causing a wide mediastinum
- Antero-posterior projection
- Mediastinal fat: obesity, steroid therapy
- Vascular tortuosity – elderly patients
- Low inspiration, supine position
ANTERIOR MEDIASTINAL TUMORS
Thymic Hyperplasia – most common anterior mediastinal mass in
the pediatric age group;enlarged thymus without focal masses; no
increase in size over time; CT
Thymoma:
Asymmetric location on one side; homogeneous density; contrast
enhancement; calcifications
Thymolipoma – contains fat
Thyroid masses:
Goiters :
- Thoracic inlet masses
- Mass is contigous with cervical thyroid and is well defined
- Heterogeneous density by CT and prolonged contrast enhancement
- Tracheal displacement
Other:
- Thyroid carcinoma has irregular borders
- Thyroid lymphomas generally show little enhancement
Hodgkin’s lymphoma
-The pathologic diagnosis is based on the presence of Reed-
Sternberg cells
- 90% originate in the lymph nodes, 10% originate in extranodal
lymphoid tissues of parenchymal organs
- bimodal age distribution with peaks at 30 and 70 years
Radiographic features:
- superior mediastinal nodal involvement; contigous progression
from one lymph node group to the next; lung involvement: mass or
direct extension from involved nodes; pleural effusions
Non-Hodgkin’s lymphoma
- 60% originate in lymph nodes, 40% in extranodal sites
- increased incidence in patients with altered immune status
Radiographic features:
- hilar adenopathy – may be noncontigous
- lung involvement – mass, may occur without adenopathy
extrathoracic spread – nasooropharynx, GI tract
MIDDLE MEDIASTINAL TUMORS
Bronchopulmonary foregut malformations
- bronchogenic cysts – ventral defects containing
respiratory epithelium
- enteric cysts – posterior defects containing
gastrointestinal epithelium ( gastric mucosa, esophageal
mucosa, small bowel mucosa, pancreatic tissue)
Radiographic features:
- round mass of water density
Castleman’s disease ( giant benign lymph node
hyperplasia)
Rx: bulky mediastinal mass (3-12cm), dense homogeneous
contrast enhancement, calcification, slow growth
POSTERIOR MEDIASTINAL TUMORS
Neural tumors
Peripheral nerves, 45%, benign
- schwanoma (arise from nerve sheath)
- neurofibroma (contain all elements of nerve)
Rx – arise posteriorly in neural foramina, may cause
erosion or widening, usually is round or oval and 2 vertebral
bodies long, enhancement with contrast
Sympathetic ganglia
- Ganglioneurinoma (benign)
- Neuroblastoma (malignant)
Rx – arise anterolateral, usually elongated and fusiform
and 2 vertebral bodies long
