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APPROACH TO HYPERLUCENT LESION IN HRCT

APPROACH TO HYPERLUCENT LESION IN HRCT

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  • 1.Nodular peribronchovascular interstitial thickening in a patient with sarcoidosis. Numerous small nodules surround central bronchi and vessels.2.
  • The yellow arrows indicates the pulmonary vessels

Hrct iv Hrct iv Presentation Transcript

  • PRESENTED BY : DR SHAMIMGUIDED BY : DR A PATIL (MD)GMC BHOPAL
  • Interpretation of interstitial lung diseases isbased on the type of involvement of thesecondary lobule.
  • LINEAR AND RETICULAR OPACITIES NODULES AND INCREASED LUNG NODULAR ATTENUATION OPACITIES PARENCHYMAL Consolidation OPACIFICATION Ground glassHRCT PATTERN CYSTIC LESIONS, EMPHYSEMA, AND BRONCHIEACTASIS MOSAIC ATTENUATION AND PERFUSION DECREASED LUNG ATTENUATION AIR TRAPPING ON EXPIRATORY SCANS
  • SMOOTH • Pulmonary edema/ hemorrhage • Lymphoma / leukemia (Venous, lymphatic ) • Lymphangitic spread of carcinoma NODULAR • Sarcoidosis(lymphatic or infiltrative • Lymphangitic spread of carcinoma diseases) IRREGULAR • TB (Due to adjacent lung • Sarcoidosis, fibrosis ) • Silicosis, talcosis
  • Nodular 7
  • IS IT IN CONTACT WITH PLEURA NO YESCENTRILOBULAR PERILYMPHATIC RANDOM
  • • Random – touch pleura – scattered in lung• Centrilobular –away from pleura• Perilymphatic – around vessels, bronchi – touch pleura or fissure
  • Ground glass Consolidation •Hazy attenuation •Denser attenuation •Vessels seen •Obscuration of vessels •dark bronchus sign •air bronchogram‘.
  • Ground glass Consolidation •Hazy attenuation •Denser attenuation •Vessels seen •Obscuration of vessels •dark bronchus sign •air bronchogram‘.
  • Chronic eosinophilic pneumonia (left) versus Organizing pneumonia (right)
  • Typical UIP pattern with in a patient with idiopathic pulmonaryfibrosis
  • UIP NSIP• Honeycombing • Ground glass• Subpleural • Septal lines• Lower lungs • Lower lungs• Clinical-fibrosis, • Clinical-better poor prognosis prognosis
  • Combination of ground glass opacity andseptal thickening : Alveolar proteinosis.
  •  Alveolar proteinosis Infection (PCP, viral, Mycoplasma, bacterial) NSIP Organizing pneumonia (COP/BOOP) Neoplasm (Bronchoalveolar Ca) Pulmonary hemorrhage Edema (heart failure, ARDS, AIP) Sarcoid
  • Heterogeneous lung density having a zonal or geographic pattern of distribution with areas of “ground glass attenuation” alternating with areas of “decreased” lung density
  • MOSIAC PATTERN DEPENDENT LUNG ONLY NONDEPENDENT LUNG EXPIRATION PRONE POSITION NO AIR TRAPPING NOT AIR TRAPPING RESOLVE RESOLVE VESSEL SIZE PLATE GROUNDATELECTASIS GLASS AIRWAYS DECREASED NORMAL DISEASE GROUND VASCULAR GLASS 29
  •  It refers to mixed densities # Consolidation # Ground Glass Opacities # Normal Lung # Mosaic Perfusion• Signifies mixed infiltrative and obstructive disease
  • Common cause are : 1. Hypersensitive pneumonitis 2. Sarcoidosis 3. DIP 31
  • LINEAR AND RETICULAR OPACITIES NODULES AND INCREASED LUNG NODULAR ATTENUATION OPACITIES PARENCHYMAL Consolidation OPACIFICATION Ground glassHRCT PATTERN CYSTIC LESIONS, EMPHYSEMA, AND BRONCHIEACTASIS MOSAIC ATTENUATION AND PERFUSION DECREASED LUNG ATTENUATION AIR TRAPPING ON EXPIRATORY SCANS
  • LINEAR AND RETICULAR OPACITIES NODULES AND INCREASED LUNG NODULAR ATTENUATION OPACITIES PARENCHYMAL Consolidation OPACIFICATION Ground glassHRCT PATTERN CYSTIC LESIONS, EMPHYSE MA, AND BRONCHIEACTASIS MOSAIC ATTENUATION AND PERFUSION DECREASED LUNG ATTENUATION AIR TRAPPING ON EXPIRATORY SCANS
  • DECREASED LUNG ATTENUATION
  • •Cyst.•Bleb .?•Bulla .??•Cavity.???•Pneumatocele.????•Emphysematous bulla.???????
  •  Nonspecific term  Destruction of airspaces Well defined >1cm  Low attenuation areas Smooth walled <3mm  Wall-less <1mm Epithelial or fibrous wall  Area of emphysema Necrosis or defoliation >1cm Epithelial or fibrous wall Irregular Wall >3mm  Cyst/ Bulla + acute pnemonia  Small bulla touching the pleura
  •  Lung cysts well defined , circumscribed air containing lesions with a wall thickness of less than 4mm. They are lined by usually fibrous or cellular epithelium. Cavities are defined as radiolucent areas with a wall thickness of more than 4mm and are seen in infection (TB, Staph, fungal, hydatid), septic emboli, squamous cell carcinoma and Wegeners disease.
  •  Hyperlucent ring formed through necrosis or defoliation is called a cavity. Ring expanded through pressure or fusion of alveolar spaces is called cyst When the wall is distinct call it a cyst When its not distinct call it emphysematous cyst or bullae.
  • 1. Langerhan Histiocytosis2. Lymphangiomyomatosis3. Lymphoid interstitial pneumonia
  • Multiple bizarre shaped cysts. There was an upper lobe predominance. Thepatient had a long history of smoking.
  • Multiple bizarre shaped cysts. There was an upper lobe predominance. Thepatient had a long history of smoking.
  •  Aka., Pulmonary Histiocytosis X / Eosinophilic Granuloma. Probably an allergic reaction to cigarette smoke since >90% are active smokers. Upper and mid lobe predominance. Early stages : Granulomatous nodules containing Langerhans histiocytes and eosinophils. Later stages : Granulomas are replaced by fibrosis and the formation of cysts.
  •  Early nodular stage:  Centrilobular granulomatous reaction by Langerhans histiocytes.  Proliferation of Langerhan’s cells around the small airways; cellular nodules develop and become increasingly fibrotic as the disease progresses. Cystic stage:  Bronchiolar obliteration causes alveolar wall fibrosis and cyst formation often at different times.
  • The early phaseis characterisedby a nodularinfiltrate.
  • The late phase ischaracterised bymultiple cysts, thelargest of which has abizarre shapecharacteristic of latestage disease.
  •  Depend on the stage of the disease. In early disease,  Small irregular or stellate nodules in centrilobular location. As some nodules begin to cavitate there is temporal heterogeneity.
  •  Late stage (more commonly seen)  The cysts tend to be small (typically <1cm) and may initially be round and thick-walled.  They may coalesce , become larger and have bizarre shapes (bilobed or clover-leaf shaped) Up to 20% present with pneumothorax
  • NODULAR EARLY CYSTIC LATE CYSTIC STAGE
  • It started as small noduli, which progressed over time to cavitating nodules.In the end this will progress to bizarre shaped cysts, that replace normal lungtissue.
  • Early stage Langerhans cell histiocytosis with small nodules.There are no cysts visible
  • Multiple thin-walled cysts of variable size and some with bizarre outlines.
  • The bizarre outline of and distribution (mid and upper zonal with relative sparing of the lungbases and the tip of the middle lobe/lingula) of cysts is a useful diagnostic feature
  •  Nodular LCH:  Sarcoidosis: perilymphatic distribution.  Metastases: random distribution. Cystic LCH:  LAM: round cysts, evenly distribution in women in the child-bearing age  Cystic bronchiectasis: signet ring sign.  Centrilobular emphysema: no walls, central dot.  LIP
  •  The most challenging differential diagnosis in this patient is centrilobular emphysema. The upper lobe predominance is not helpful in the differential as we can appreciate this in many inhalational diseases. Emphysema however is defined as airspaces without definable walls. Usually we can identify the central dot sign.
  •  Emphysema:  when it is severe, can mimic Langerhans cell histiocytosis.  When it extends beyond the centrilobular area to the edge of the secondary lobule, it may look as if it is cystic with walls.  In patients with LCH, the pathologist may find LCH, but also areas of emphysema, respiratory bronchiolitis and even fibrosis. So these smoking-related diseases do not represent discrete entities.
  • 40 year old female with no history of smoking . Multiple cysts that are evenlydistributed througout the lung ( in contrast to LCH).Notice the pneumothorax.
  • Lymphangioleiomyomatosis (LAM) is a rare, idiopathic disorder occurring exclusively in females of child-bearing age. Clinical findings:  Majority of patients present with dyspnea.  Chylous pleural effusions (40%), Pneumothorax (40%), hemoptysis (40%).  Patients die within 10 years of the onset of symptoms.  Pregnancy may exacerbate disease.
  •  Characterized by progressive proliferation of spindle cells, resembling smooth muscle. Proliferation of these cells along the bronchioles leads to air trapping and the development of thin- walled lung cysts. Rupture of these cysts can result in pneumothorax.
  •  The cardinal histopathologic finding is the abnormal proliferation of ‘immature’ smooth muscle cells around the small airways, pulmonary vessels, lymphatics and alveolar septa. Interestingly, the pulmonary abnormalities of LAM are similar to those seen in patients with tuberous sclerosis.
  • LMG characterised byareas of smooth muscleproliferation (LAM cells)which contribute to thewall of a typical cyst.
  •  Multiple thin-walled cysts of roughly uniform size. Unlike LCH, the cysts in LAM tend to be rounded and uniformly distributed throughout the parenchyma with no regional sparing. There is a conspicuous absence of nodules.
  •  Numerous thin-walled cysts, surrounded by normal parenchyma.  Round in shape and more or less uniform.  Cysts range from 2mm to 5cm in diameter,  Wall thickness ranges from barely perceptible to 4 mm.  Cysts are distributed diffusely throughout the lungs and upper and lower lobes are involved to a similar degree. Mediastinal or hilar adenopathy . Chylous Pleural effusions (40%). Recurrent pneumothorax (40%)
  •  Langerhans cell histiocytosis:  > 90% are smokers, cysts have irregular shapes and the basal costophrenic angles are spared. Centrilobular emphysema:  characterized by airspaces that have no perceptible wall, centrilobular artery seen as dot in the centre. Lymphoid interstitial pneumonitis:  seen in patients with HIV and Sjogren syndrome.
  •  LIP is uncommon, being seen mainly in patients with autoimmune disease, particularly Sjogrens syndrome, and in patients with AIDS. Symptoms are nonspecific and often those of the patients underlying disease HRCT findings are usually nonspecific.
  •  LIP is a clinicopathological term for a pulmonary lymphoproliferative abnormality associated with several disease entities including connective tissue disorders HIV infection and Dysproteinaemic states, Idiopathic LIP is exceedingly rare. On histologic examination there is a interstitial cellular infiltrate comprising small, mature lymphocytes and plasma cells.
  • there is a diffuse interstitialinfiltrate of lymphocytes,most marked around thebronchovascular bundlesand thickening of alveolarwalls.
  •  Admittedly, HRCT may be wholly non-specific: Variable combinations of  ground-glass opacification,  nodules (ill-defined centrilobular or subpleural) and  thickening of the interlobular septa,. However, in some patients with LIP, the above features may be associated with thin-walled cysts.
  • A patient with Sjogrens syndrome with LIP
  • Lymphocytic interstitial pneumonia in Sjögren’s syndrome.In addition to the diffuse ground-glass opacification there are multiple thin-walled cystsin both lungs. At least two irregular nodules (arrows), representing amyloid deposition,are noted in the right lower lobe
  • Lymphangiomyomatosis, LIP Langerhans cell histiocytosis.
  • Ehler Danlos Tuberous Sclerosis Pneumocystis
  • black holes with no walls
  •  Permanent dilatation of the air spaces distal to terminal bronchiole, accompanied by destruction of their alveolar walls without obvious fibrosis Emphysema typically presents as areas of low attenuation without visible walls as a result of parenchymal destruction.
  •  Most common type Strongly associated with smoking. Often the centrilobular artery is visible in the centre of these lucencies (central DOT) Most commonly in the upper lobes 83
  • Histologic specimen shows areas of lung destruction surrounding a smallcentrilobular artery (arrow)
  • Centrilobular emphysema due to smoking.The periphery of the lung is spared (blue arrows).Centrilobular artery (yellow arrows) is seen in the center ofthe hypodense area
  • Centrilobular artery (arrows) in many of the low-attenuating areas.
  •  Affects the peripheral parts of the secondary pulmonary lobule adjacent to the pleura and interlobar fissures Produces subpleural lucencies. Can be isolated phenomenon in young adults, or in older patients with centrilobular emphysema 87
  •  Paraseptal emphysema is localized near fissures and pleura and is frequently associated with bullae formation (area of emphysema larger than 1 cm in diameter). Apical bullae may lead to spontaneous pneumothorax
  • Paraseptal emphysema with small bullae
  • Paraseptal emphysema Honeycomb cystsOccur in a single layer at the pleural May occur in several layers in thesurface subpleural lungPredominate in the upper lobes Predominate at the lung basesUnassociated with significant fibrosis Asso with other findings of fibrosis.Associated with other findings of -emphysema 92
  •  Complete destruction of the entire secondary pulmonary lobule. An overall decrease in lung attenuation Reduction in size of pulmonary vessels Lower lobe predominance In alpha-1-antitrypsin deficiency, but also seen in smokers with advanced emphysema 93
  • Alpha-1-antitrypsin deficiency
  • • Does not represent a specific histological abnormality• Emphysema characterized by large bullae• Often associated with centrilobular and paraseptal emphysema
  • Previously known as irregular or cicatricial emphysema  can be seen in association with fibrosis  with silicosis and progressive massive fibrosis or  sarcoidosis 98
  • Centrilobular Panlobular Paraseptal emphysema emphysema emphysema• Most common type • Affects the whole • Adjacent to the• Irreversible secondary lobule pleura and destruction of • Lower lobe interlobar fissures alveolar walls in the predominance • Can be isolated centrilobular • In alpha-1- phenomenon in portion of the antitrypsin young adults, or in lobule deficiency, but also older patients with• Upper lobe seen in smokers centrilobular predominance and with advanced emphysema uneven distribution emphysema • In young adults• Strongly associated often associated with smoking. with spontaneous pneumothorax
  • Centrilobular E Panlobular E Paraseptal E Paracicatricial ESynonyms: Centriacinar emphysema. Panacinar emphysema. Distal acinar emphysema. Irregular emphysema. Dilatation of the Dilatation of the entire Dilatation of the alveolar No consistent respiratory bronchioles acinus from respiratory ducts & alveolar sacs. relationship to any (in the central portion of bronchioles to alveolar portion of 2ry lobule. the acini). sacs.Pathology: Normal & Uniform enlargement of Focal areas of Emphysematous changes emphysematous alveolar all acini through both emphysematous changes adjacent to areas of spaces adjacent to each lungs. adjacent to normal lung. pulmonary scarring. otherSite: Lung apex. Involves whole lung but Subpleural lung. Adjacent to areas of Central areas with more sever at the lung pulmonary scarring. sparing of the peripheral base. areas.Aetiology: Smoking. α1 anti-trypsin deficiency Smoking Pulmonary scarringChest x- Signs of hyperinflation.ray: Signs of pulmonary hypertension. Emphysematous bullae.High Emphysematous spaces: Diffuse decrease in lung Peripheral (subpleural Areas of decreasedresolution Focal areas of decreased attenuation. and peribronchovascular) attenuation adjacent toCT: attenuation, Pulmonary vascular areas of decreased pulmonary fibrosis. More than 1 cm, pruning. attenuation less than Associated with traction Without definable wall. Difficult to detect early, 1cm. bronchiectasis. Surrounded by a normal because of lack of (if more than 1 cm it is lung, adjacent normal lung. considered subpleural Contains a central dot bullae). representing pulmonary arteriole.
  •  A sharply demarcated area of emphysema ≥ 1 cm A thin epithelialized wall ≤ 1 mm. Usually associated with evidence of extensive centrilobular or paraseptal emphysema Uncommon as isolated finding, except in the apices When emphysema is associated with predominant bullae, it may be termed bullous emphysema 101
  •  A thin-walled, gas-filled space within the lung, Associated with acute pneumonia or hydrocarbon aspiration.• Often transient.• Believed to arise from lung necrosis and bronchiolar obstruction.• Mimics a lung cyst or bulla on HRCT and cannot be distinguished on the basis of HRCT findings. 102
  •  Thicker and more irregular walls than lung cysts• In diffuse lung diseases - LCH, TB, fungal infections, . and sarcoidosis. Also seen in rheumatoid lung disease, septic embolism, pneumonia, metastatic tumor, tracheobronchial papillomatosis, and Wegener granulomatosis 104
  • Cavitary nodules or cysts in tracheobronchialpapillomatosis
  • Fungal Pneumonia
  • Is the abnormal dilatation of the medium-sized bronchi(>2 mm in diameter) caused by destruction of themuscular and elastic components of bronchial walls.The proximal bronchi are less affected because they havemore cartilage and are more resistant to dilation. 108
  •  Bronchial dilatation # The broncho-arterial ratio (internal diameter of the bronchus /pulmonary artery) exceeds 1. # In cross section it appears as “signet ring appearance” Lack of bronchial tapering # the earliest sign of cylindrical bronchiectasis # One indication is lack of change in the size of an airway over 2 cm after branching. Visualization of peripheral airways # Visualization of an airway within 1 cm of the costal pleura is abnormal and indicates potential bronchiectasis 109
  • A signet-ring sign represents an axial cut of a dilated bronchus (ring) withits accompanying small artery (signet).
  • Bronchial dilation with lack of tapering .
  • # Bronchial wall thickening : Normally wall of bronchus should be less than half the width of the accompanying pulmonary artery branch.# Mucoid impaction# Air trapping and mosaic perfusion 114
  • Bronchiectasis (curved arrows) with mild to moderate bronchial wall thickening.In addition, CT scan shows mucous plugging (straight arrows) and mosaic perfusion (∗)
  • Extensive, bilateral mucoid impaction. Mosaic perfusion caused by large andsmall airway obstruction
  • Cylindrical Bronchiectasis Varicose Bronchiectasis Cystic Bronchiectasis Traction Bronchiectasis
  • # mildest form of this disease,# thick-walled bronchi that extend into the lung periphery and fail to show normal tapering 118
  • # beaded appearance of bronchial walls - dilated bronchi with areas of relative narrowing# string of pearls.# Traction bronchiectasis often appears varicose.
  • # Group or cluster of air- filled cysts,# cysts can also be fluid filled, giving the appearance of a cluster of grapes.
  • # Dilatation of intralobular bronchioles because of surrounding fibrosis# Due to fibrotic lung diseases 122
  • 1. Infective : childhood pneumonia, pertusis, measles, tuberculosis2. Non- infective causes : Bronchopulmonary aspergillosis, inhalation of toxic fumes3. Connective tissue disorder : Ehlers-Danlos Synd, Marfan synd , tracheobronchomeglay4. Ciliary diskinesia : Cystic fibrosis, Kartangener synd, agammaglobulinemia .5. Tractional bronchiectasis in interstitial fibrosis.6. Bronchial obstruction: with endobronchial tumors, broncholithiasis, and foreign body aspiration. 124
  • DECREASED LUNG ATTENUATION