Pleura and Chest Wall

Pleural or extrapleural lesions (cf parenchymal) make obtuse angles with pleura, well-defined pushing lung border, change from sharp to poorly marginated on orthogonal views, don’t change position with respiration, may extend across fissures.

Pleural Effusion

Normal volume is 2-5mL, with formation depending on Starling’s law (hydrostatic and oncotic forces) between parietal pleura capillaries and pleural space, normally formed by filtration from parietal capillaries and resorbed via parietal lymphatics. Echogenic fluid ± particles/debris or septation is exudate; anechoic fluid may be transudate, exudate or even empyema. Split pleura sight (thickened enhancing parietal and visceral pleura) is seen in any inflammatory cause. Types include:

  • Transudate – Formed by high plasma capillary hydrostatic or reduced oncotic pressures, with pleural/serum protein ratio <0.5, pleural/serum LDH <0.6 and pleural LDH <200IU/L. Tx is usually of underlying disorder.
    • LVF – Usually bilateral, larger on the right, isolated right 2x common than isolated left.
    • Fluid overload – From renal failure, pregnancy, constrictive pericarditis.
    • Hypoproteinaemia – From liver disease, nephrotic syndrome, severe malnutrition, protein losing enteropathy.
  • Exudative pleural effusions – Increased capillary permeability with pleural/serum protein ratio >0.5, LDH ratio >0.6 and plearal LDH >200IU/L. From pleural inflammation or invasion. Loculations may be treated with intrapleural fibrinolytics (streptokinase, urokinase, TPA) or open pleural drainage by video-assisted thoracoscopic surgery (VATS).
    • Parapneumonic effusion – Associated with pneumonia (40% have effusion esp S.aureus, G neg) via visceral pleural inflammation causing thickening, capillary permeability and lymphatic obstruction. Stage 1 is exudative; stage 2 is fibrinopurulent containing bacteria and neutrophils with fibrin deposition imparing resorption and causing loculations; stage 3 at 2-3/52 is ingrowth of fibroblasts causing pleural fibrosis entrapping the lung, may cause dystrophic calcificaiton. Tx drained if it will reduce pleural fibrosis, infection, or prolonged hospitalisation; increased risk if larger, loculated, pH <7.2, positive gram stain or culture.
    • Empyema – Associated with bacterial pneumonia, septic emboli, lung abscess; uncommon in fungal, viral or parasitic infections. Less commonly from infection in spine, mediastinum and chest wall. Most are loculated, elliptical, most common posterior and inferior space, thickening and enhancement of parietal pleura. Loculated with loculations demonstrating mass effect (convex margins), hazinesss/stranding of the adjacent extrapleural fat. DDx lung abscess where Tx is surgical drainage cf empyema chest drain; abscess tends to be round, thick, irregular, acute angles with chest wall. TB effusion/empyema from ruptured subpleural granuloma is straw coloured, has >70% lymphocytes and low glucose. Epeyma neccessitans is extention into chest wall, from TB (most common), actinomyces, aspergillus, mucormycosis.
    • Neoplasm – Lung, breast, pelvic, gastric, lymphoma. May be from pleural involvement or lymphatic obstruction anywhere from parietal pleural to mediastinal nodes. Exudative, may be bloody. Smooth/lobulated pleural thickening, mediastinal/hilar LN/mass, solitary/multiple prenchymal nodues. Tx often requires sclerosis with talc, may need indwelling catheters allowing intermittent patient-directed drainage.
    • Serositis – From SLE, RA (may persist unchanged for years), sarcoidosis (rare), Wegener granulomatosis, Dressler/postpericardiotomy syndrome (Tx NSAIDs). May be associated with pericardial effusion.
    • Pulmonary infarct – Usually small unilateral serosanguinous exudate. May be associated with elevated diaphragm and peripheral wedge (Hampton hump).
  • Haemothorax – Laceration of vessels or trauma. Blood coagulates rapidly, septations form early. Pleural motion may cause defibrination and lysis of the clot. Fluid >80HU, rib fractures, surgical emphysema. Large haemothoraces may require large bore drainage to prevent pleural fibrosis and lung entrapment.
  • Abdominal disease – Peritoneal fluid may enter via transdiaphragmatic lymphatic channels or defect in diaphragm, more common on right (larger lymphatic channels). Pancreatitis usually left exudative ± bloody effusion, rupture of pancreatic duct may cause pancreaticopleural fistula. Amylase in pleural fluid may be from pancreatitis, malignancy or oesophageal perforation. Subphrenic abscesses may cause diaphragmatic paresis, bibasal atelectasis and pleural effusion. Pelvic and abdominal tumours may cause benign pleural effusions eg ovarian fibroma (Meigs syndrome, usually transudative and resolve after removal of tumour), pancreas, ovarian, lymphoma, uterine leiomyomas.
  • Chylothorax – Triglycerides in chylomicrons (>110mg/dL), from perforated thoracic duct. Upper duct injury causes left chylothorax (crosses at T6 -> L SCA/IJV); lower duct causes right. From malignancy, iatrogenic trauma, TB. Tx is of underlying cause and/or surgical ligation of duct.
  • Drugs – May cause pleural inflammation (methysergide) or lupus-like syndrome (phenytoin, isoniazid, hydralazine, procainabmide). Nitrofurantoin may cause pleuropulmonary disease with eosinophilia.

Initially subpulmonic (elevated diaphragm, lateral peaking of diaphragm accentuated on expiration, lung base close to minor fisure, increased separation to stomach bubble; layers on lateral decubitus) then -> posterior and lateral costophrenic sulci. Pleural meniscus requires moderate amount (>175mL). Lateral decubitus with affected side down is most sensitive with as little as 5mL seen. Supine hazy opacity with obscuration of diaphragm and blunted costophrenic angle, apical cap, apparent mediastinal widening. Pleural fluid displaces crura lat, peritoneal fluid displaces them medially; peritoneal fluid does not extend posteromedial to the liver (bare area). Pseudodiaphragm – band of atelectasis. Locules of fluid (lenticular against chest wall) may be multiple and simulate pleural masses. Pseudotumours – loculated fluid in minor/incomplete major fissure, can disappear rapidly with diuresis (‘vanishing lung tumour’).


Tramatic pneumothorax (most common) is introduction of air from the atmosphere or laceration of visceral pleura. From penetrating trauma or iatrogenic injury. Blunt trauma may acutely increase intrathoracic pressure -> alveolar rupture with gas tracking peripherally rupturing into pleural space, laceration of tracheobronchial tree causing large bronchopleural fistula, oesophageal rupture, or rib fracture with free edge lacerating lung.

Primary spontaneous pneumothrax mostly young/middle-aged men, familial, tall, often have blebs or bullae at apices that subside spontaneously as air is resporbed. Tx closed tube drainage, thoracoscopic bullectomy if recurrent.

Secondary spontaneous pneumothorax usually associated with blebs, bullae, cysts or cavities. Causes include:

  • Sudden increased intrathoracic pressure in otherwise normal lungs – Acute obstruction to expiration from bronchoconstriction/asthma, Valsalva maneuver (crack cocaine, marijuana smoking, vaginal childbirth).
  • COPD – Asthma or emphysema.
  • Cystic lung disease – Sarcoidosis, LCH, LAM, CF, TS.
  • Infection – Necrotising pneumonia or lung abscess (G neg or anaerobic bacteria, TB, PCP).
  • Pulmonary infarction (rare)
  • Neoplasm – Bronchogenic carcinoma, ruptured necrotising subpleural metastasis (uncommon, sarcomas esp osteogenic, lymphoma, germ cell tumours).
  • Connective tissue disorders – Eg Marfan syndrome, Ehlers-Danlos, cutis laxa; from ruptured apical bullae.
  • Mechanical ventilation
  • ARDS with rupture of small peripheral cystic airspaces
  • Catamenial pneumothorax (rare) – Women in 30s, ?cyclical necrosis of pleural endometrial implants causing air leak, rarely peritoneal air during menstruation via diaphragmatic defect. Tends to be small, resolves spontaneously. Tx oral contraceptives.

Curvilinear line (DDx skin, bullae, vessels), reduced comparitive density and absent lung markings peripherally, possible air-fluid level inferiorly. May be better seen on lateral/decubitis or expiratory view. 30% not seen on supine, most nondependent is anterior/anteromedial; hyperlucent hemithorax, sharp mediastinal borders, deep sulcus sign (costophrenic deep and hyperlucent), double diaphragm sign (air in anterior costophrenic sulcus enhancing difference between dome and inferior diaphragm). Subpulmonic pneumothorax is rare, localised hyperlucency with pleural line parallel to diaphragm. Loculated pneumothoraces from adhesions between visceral and parietal pleura. On ultrasound there is a highly echogenic shadowing line that lacks the gliding sign (no respiratory movement).

Tension pneumothorax is an emergency, often from iatrogenic trauma in mechanically ventilated patients. Check-valve pleural defect with pleural gas pressure exceeding atmospheric pressure, complete collapse of lung, impaired venous return. Expanded hyperlucent hemithorax with medially retracted lung, ipsilateral diaphragmatic depression/inversion, contralateral mediastinal shift (not specific, hence mostly clinical diagnosis).

Bronchopleural fistula – Communication between pleural space and peripheral airway, results in empyema (cf intractable pneumothrax communicating with peripheral airspace). From dehiscence of bronchial stump (after lobectomy, pneumonectomy), necrotising infection. Loculated intrapleural gas and fluid, air-fluid level in postpneumonectomy space, drop in air-fluid level in early postop period with shift of mediastinum back to midline (normal postpneumonectomy space should normally gradually fill with fluid with ipsilateteral mediastinal shift). CT may demonstrate actual fistula.

DDx pleural lipoma – Smooth fatty mass.


Localised fibrosis usually end-result of peirpheral pleuropulmonary inflammation; flat, smooth over 1-2 intercostal spaces, usually hidden en face; from pneumonia, infarct, asbestos (bilateral), trauma, previous chemical pleurodesis or drug-related pleural disease. DDx apical cap – <5mm, nonspecific fibrosis of apical lung and adjacent visceral pleura; slight asymmetry is common but significant asymmetry, growth, inferior convexity, rib desctruction or Sx warrants CT/MR/biopsy. Companion shadows of 1st and 2nd ribs are pleural layers and subpleural fat, most prominent in obese patients.

Pleural calcification en face is geographic with round/lobulated borders. Visceral pleural calcification usually unilateral, from previous haemothorax, empyema (eg TB), or any form of pleural thickening. Parietal pleural thickening usually bilateral, from asbestos exposure.

Focal pleural masses are usually benign tumours eg lipoma (from chest wall or subpleural fat changing shape with respiration/position), fibroma, neurofibroma, may be loculated effusion/empyema/haematoma. Smooth diffuse pleural thickening includes pleural fibrosis, haemothorax, previous empyema/exudative effusion (incl asbestos), interstitial fibrosis, pleural effusion. Lobulated thickeing includes mesothelioma, metastases, multiloculated effusion/empyema.

Localised Fibrous Tumour of Pleura (LFTP)

(Solitary fibrous tumour, previously benign mesothelioma). Uncommon, from subpleural mesenchymal cells. 80% benign, but 15% locally recur after resection. Well-defined, spherical or oblong, occasionally attached to pleura by narow pedicle (pathognomonic), may be homogeneous or heterogeneous with areas of necrosis. Associated with HPOA and hypoglycaemia. No association with asbestos exposure.

Asbestos-Realted Pleural Disease

Prolonged asbestos exposure may cause:

  • Pleural effusions – After 10-20yrs, dose related. Usually small, uni/bi-lateral, exudative ± blood. Diagnosis of exclusion. Latency >20yrs prompts evaluation for mesothelioma. 1/3 develop diffuse pleural fibrosis.
  • Pleural plaques – Develops 20-30yrs after asbestos exposure, proportional to length and severity of exposure. Pearly white, dense bands of collagen, do not contain asbestos bodies/fibres. Plaques on parietal pleural (visceral plaques associated with interstitial fibrosis), most diaphragm and lower posterolateral; sparing of costophrenic sulci and mediastinal pleura. Discrete, bilateral 2-10mm thick, punctate or linear calcification common. En face lesions are geographic opacities like holly leaf. Invariably bilateral on gross inspection, may be radiographically unilateral (most on L).
  • Diffuse pleural fibrosis
  • Malignant mesothelioma


(Diffuse pleural fibrosis). Diffuse thickening >1/4 of costal pleural surface. From resolution of exudative effusion (including asbestos), confluence of asbestos plaques, empyema or haemothorax, subpleural extension of interstitital fibrosis. May encompass entire lung causing entrapment, restrictive lung disease; Tx pleurectomy/decortication. Thin smooth band with sharp internal margin usually unilateral on dependent pleural space (posterior and inferior). Blunting of lateral but not posterior costophrenic sulcus (cf fluid). Usually spares interlobar fissures and mediastinal pleura.

Pleural Metastases

Lobulated, irregular, usually associated with effusion. Includes adenocarcinomas from lung, breast, ovary, kidney, GIT; lymphoma with subpleural deposits; or direct invasion from invasive thymoma, thymic carcinoma, rarely NHL. Contrast distinguishes solid from loculated fluid. Indistinguishable from mesothelioma. May have chest wall invasion ± rib destruction.

Malignant Mesothelioma

Rare, 80% have history of asbestos exposure with latency 30-40yrs, may occur with minimal exposure but risk increaes with dose, esp crocidolite (but chysotile more common as was more prevalent). No cummulative effect with smoking (cf lung cancer). May also occur in the peritoneum, pericardium, tunica vaginalis, genital tract. Types include epithelial (more common, better prognosis), sarcomatous or mixed. May require immunohistochemical or electron microscope analysis to destinguish from adenocarcinoma (esp epithelial). Lobulated, irregular, thick >10mm, calcification/ossification in 20%, usually associated with effusion. Contiguous spread into lung, chest wall, mediastinum, diaphragm. Involvement of mediastinal pleura may prevent mediastinal shift (cf mets). Diaphragmatic invasion best seen on coronal, important to determine for resection. Ipsilateral adenopathy in 50%. Tx pleurectomy in selected patients with limited disease. Prognosis 6-12 months.

Chest Wall Soft Tissue

  • Poland syndrome – Autosomal recessive unilateral abscence of sternocostal head of pectoralis major, ipsilateral syndactyly, rib anomalies. May have associated aplasia of the ipsilateral breast. Hyperlucency of hemithorax.
  • Benign skin lesions – Moles, naevi, warts, neurofibromas, accessory nipples.
  • Abscesses – Mostly staph and TB, cause poorly defined opacity, enhancing wall, usually obvious clinically.
  • Benign neoplasms – Lipomas (intra/extra-thoracic or dumbell lipoma), haemangioma (uncommon, phleboliths, hypertrophy of involved bones), desmoid (rare fibroblastic, histologically benign but locally invasive, most commonly abdominal wall after local trauma).
  • Malignant tumours – Fibrosarcoma and liposarcoma (esp post-radiation), mets, melanoma, bronchogenic carcinoma, Askin tumour (PNET/Ewings from rests in chest wall, children and young adults, very aggressive with high mortality).

Bony Thorax

Congenital rib anomalies include:

  • Bony fusion and bifid ribs
  • Intrathoracic ribs (very rare) – Accessory rib from vertebral body or posterior rib extending inferolaterally into thorax, R>L.
  • Ribbon ribs – Thin, wavy, associated with osteogenesis imperfecta, neurofibromatosis.
  • Cervical rib from C7 – May cause thoracic outlet syndrome ± fibrous band.
  • 11 of fewer pairs of ribs – Associated with Down syndrome, atrioventricular canal.

First 3 ribs are protected by scapula and clavicles, hence fracture suggests severe trauma. 10th-12th ribs may be associated with splenic/liver injury. Flail chest – >/=3 contiguous ribs fractured in more than one place with free segment moving paradoxically on respiration, requires surgery. Multiple old fractures suggests chronic alcoholism or previous MVA. Exuberant callus in patients receiving corticosteroids. Sternal body fracture and sternomanubrial dislocation 25-45% mortality, from injury to aorta, diaphragm, heart, tracheobronchial tree, lung.

Primary malignancy is uncommon, includes chondrosarcoma, osteogenic sarcoma, fibrosarcoma. Metastases from multiple myeloma (permeative, may be indistinuishable from severe osteoporosis), breast, bronchogenic (lytic), RCC or thyroid (expansile), prostate. Benign tumours include fibrous dysplasia (most common monoostotic lesion), EG, Brown tumour, osteochondroma, enchondroma, osteoblastoma.

Infection usually spread from lungs, pleural space or vertebrae; esp TB, actinomycosis, nocardia.

Costal cartilage ossification (in 70% of patients) in females usually centrally extending to sternum (‘solitary finger’) whereas males usually peripheral (two finger ‘peace’ sign).

Sprengel deformity – Congenital hypoplastic elevated scapula; Klippel-Feil syndrome if associated with omovertebral bone, fused cervical vertebrae, hemivertebrae, kyphoscoliosis, rib anomalies.

Winged scapula – Superiorly displaced with inferior portion posterior, foreshortening it; from denervated serratus anterior.


  • Pectus excavatum (funnel chest) – Inwardly depressed sternum with ribs protruding anteriorly. Autosomal dominant or sporadic. May be associated with Marfan syndrome, Poland syndrome, osteogenesis imperfecta, congenital scoliosis, mitral valve prolapse. Heart displaced to left, loss of R heart border (depressed soft tissues) and vertically orientated anterior ribs.
  • Pectus carinatum (pigeon breast) – Outward bowing of sternum. Congenital form M>F, may have FHx of chest wall deformities, scoliosis. Acquired from congenital ASD/VSD, complete atrioventricular canal, severe childhood asthma. Deepening of retrosternal space.
  • Sternotomies may not develop bony union. Retrosternal haematoma usually resolves within several weeks. Bony destruction or gas days-weeks later suggest osteomyelitis.

Rib Notching

Inferior rib notching (more common) from enlarged subcostal groove (intercostal n, a or v), esp posterior bilateral, may be narrow or wide, deep or shallow. Gradual development, rare <7yo, 1st 2 ribs uninvolved (these aa arise from costocervical trunk). May be only on left if aortic narrowing is proximal to an aberrant R SCA, only on R if proximal to L SCA. Causes include:

  • Aortic stenosis/obstruction distal to L SCA – From coarctation, aortic thrombosis, Takayasu aortitis. Dilatation and tortuosity of intercostal aa eroding bone.
  • Congenital heart disease – Esp TOF with reduced pulmonary blood flow, enlarged collateral supply to oligaemic lungs.
  • SVC or subclavian vein obstruction.
  • Blalock-Taussig procedure – Anastomosis of proximal SCA to ipsilateral PA.
  • Multiple intercostal neurofibromas in NF1, associated with ribbon ribs, kyphoscoliosis, scalloped posterior vertebral bodies.

Superior rib notching is of unknown pathogenesis ?disturbance of osteoblastic and osteoclastic activity and stress of intercostal mm. From paralysis, collagen vascular disease (RA, SLE), marked tortuosity of intercostal aa from severe long-standing aortic obstruction.


Unilateral diaphragmatic elevation from:

  • Eventration – Congenital absence/underdeveloped diaphragmatic muscle, causes localised anteromedial elevation in older patients. Complete diaphragmatic eventration L>R, indistinguishable from paralysis.
  • Reduced lung volume – Hypoplastic lung, atelectasis/collapse, resection.
  • Paralysis – Idiopathic (viral neuritis, M>F, usually R), iatrogenic phrenic nerve injury, phrenectomy (treatment for TB), malignant involvement of phrenic nerve (bronchogenic carcinoma), diaphragmatic muscle inflammation (pleuritis, LL pneumonia, subphrenic abscess). Sniff test (US or fluoroscopic) shows paradoxical superior movement of diaphragm with sniffing.
  • Upper abdominal mass – Hepatomegaly, splenomegaly, gastric/colonic distention, ascites (usually bilateral).
  • Apparent diaphragmatic elevation – Diaphragmatic hernia, subpulmonic effusion.

Bilateral diaphragmatic elevation may be from underexpansion, neuromuscular disturbance, intrathoracic (interstitial fibrosis, pleural fibrosis, chest wall disease eg obesity) or intra-abdominal disease (ascites, hepatosplenomegaly, pregnancy). Bilateral diaphragmatic paralysis in cervical cord injury, MS, or myopathy in SLE.

Unilateral diaphragmatic depression/flattening seen with compensatory hyperinflation (contralateral small lung) or ipsilateral pneumothorax (inverted diaphragm if tension). Bilateral depression may be permanent in emphysema or transient in asthma/air trapping.

Diaphragmatic hernias include:

  • Oesophageal hiatal hernia – Density behind heart ± air-fluid level. May include stomach, omental fat, rarely ascites. May cause GOR, rarely strangulation.
  • Bochdalek hernia – Embryonic pleuroperitoneal canal. Hypoplasia of ipsilateral lung if large. L>R (?protective effect of liver). Posterolateral supradiaphragmatic mass, but may be anywhere along posterior surface. May contain retroperitoneal fat, omentum, spleen or kidney.
  • Morgagni hernia (least common) – Parasternal defect, invariably on R. Cardiophrenic angle mass containing omental fat, liver or transverse colon. High transverse colon, blood vessels in fatty paracardiac mass.
  • Tramatic hernia – Tear/rupture of central or posterior diaphragm, 90% on L (liver dissipates force). Indistinct/elevated lung base edge, thickening/retraction of diaphragm, collar/waist sign (of herniated viscus), dependent vicera sign (contact with posterior ribs of herniated organ). May contain stomach, small bowel, colon, omentum, spleen, kidney, L liver.

Primary diaphragmatic tumours are rare. Benign lesions include lipoma, fibroma, schwannoma, neurofibroma, leiomyoma, echinococcal cysts, extralobar sequestrations. Malignant lesions include fibrosarcomas. Focal extrapulmonary mass obscuring the hemidiaphragm. Direct invasion from lower lobe bronchogenic carcinoma, mesothelioma or subphrenic neoplasm is more likely.