Paediatric Chest


Abnormal Lung Opacity

Focal alveolar filling usually fluid or exudate.

  • Bacterial consolidation – usually oval/round/ill-defined/fluffly, peripheral -> entire lobe (whole lung uncommon). Bacterial pneumonia is space-occupying (can have volume loss when resolving); Streptococcus pneumonia most common, Haemophilus influenzae reduced due to HiB vaccine, Mycoplasma occasionally (?compression of alveoli rather than true consolidation). G-neg bacilli in infants and immunocomprimised. TB if accompanied by LN.
  • Viral consolidation – uncommon, may may cause consolidation in severe infection, likely represents interstitial disease compressing alveoli; adenovirus, influenza, parainfluenza, RSV.
  • Fungal, infarction, contusion and haemorrhage.
  • Atelectasis common, with bronchial disase (viral, reactive airways disease, asthma); volume loss (shift of fissures/mediastinum).

Multiple patchy lung opacities in:

  • Infection esp Staph, Mycoplasma, fungal, opportunistic
  • Aspiration – usually medial bases; hydrocarbon, near drowning
  • Immune-mediated pneumonitis – milk allergy, hypersensitvity pneumonitis
  • Uremic lung disease
  • Haemorrhage (idiopathic pulmonary haemosiderosis)
  • Oedema

Parahilar peribronchial usually peribronchial inflammation and oedema from bronchitis. Bilateral ill-defined hazy hilar opacity, if extensive -> ‘shaggy’ cardiac borders (inflammatory oedema). Acute usually viral, Mycoplasma, Chalmydia trachomatis (usually postnatal), pertussis, follicular bronchitis (lymphoid follicles along airways). Chronic in asthma, CF, immunologic deficiency disease, recurrent/chronic aspiration; may -> bronchiectasis.

Hazy, reticular/reticulonodular opacities indicate interstitial process (many also cause parahilar peribronchial opacity). In the neonate this may be poor inspiration, HMD (small lung volumes), retained fluid, aspiration, pneumonia, oedema, lymphangiectasia.

  • Infection esp viral or Mycoplasma (may be confined to one lobe). Occasionally bacterial infection in neonate, Histoplasma capsulatum, Coccidioides immitis.
  • Noncardiogenic oedema – acute glomerulonephritis (Na and fluid retention -> hypervolaemia, cardiomegaly, pulmonary vascular congestion, oedema), near drowning, raised ICP, inhalation injury, drug overdose, ARDS.
  • Cardiogenic oedema due to raised PV pressure, impeded flow -> LV in PV atresia, cor triatriatum, hypoplastic left heart syndrome.
  • Pulmonary lymphangiectasia or haemangiomatosis (rare)
  • Idiopathic pulmonary haemosiderosis – recurrent haemorrhage -> fibrosis (chronic diffuse haziness/reticular).
  • Langerhans cell histiocytosis (LCH) – interstitial cysts and nodules esp UL, normal/increased volumes.
  • Interstitial lung disease – Predominat LL in tuberous sclerosis, connective tissue disease, primary interstitial pneumonitis.
  • Leukaemia, lymphoma, lymphatic mets.
  • Lymphocytic infiltrative disease (LIP)

Widespread miliary nodules (<5mm) often haematogenous dissemination of TB or histoplasmosis, occasionally viral pneumonitis, idiopathic pulmonary haemosiderosis, metastases.

Abnormal Lung Volume

Aeration evaluated with relative lung/hemithorax size, radiolucency and pulmonary vascularity. Bilateral smallness in underexpansion, diaphragmatic elevation (neuromuscular abnormatliy, abdominal mass/fluid/bowel distension), tracheal inspiratory obstruction (mass, FB, extrinsic compression). Hyperlucent small hemithorax usually pulmonary hypoplasia (congenital or acquired, [[Paediatric_Chest#Pulmonary Hypoplasia|see below]])

Hyperinflation -> hyperlucency, dome of diaphragm below 10th post rib (6th anterior rib), increased AP diameter, flattened diaphragms, thinned cardiac silhouette with less contact with diaphragm.

Bilateral overinflation usually airways obstruction (central or diffuse and peripheral):

  • Small airway obstruction – viral bronchitis, bronchiolitis (mucosal oedema, bronchospasm- > air trapping and overinflation; worse in younger children), cystic fibrosis (consider if multiple episodes of bronchiolitis), asthma.
  • Central airway obstruction – may be extrinsic (vascular anomaly, mediastinal cyst/neoplasm/adenopathy) or intrinsic (foreign body, neoplasm, granuloma, stenoses). Right-sided arch, double arch (usually more sup large post R, small ant L; reverse S configuration on Ba Sw; retrotracheal opacity, narrowing and ant tracheal bowing on lat), aberrant R SCA, ligamentum arteriosum, PDA from LSCA, pulmonary sling/aberrant L PA (rare, L PA from R PA passing betw trachea and oesophagus; R lung under- or over-aerated).

Unilateral hyperlucent hyperexpanded lung may be obstructive emphysema (reduced vessels from compression and hypoxia-induced spasm) or compensatory overinflation (normal or increased vessels), confirmed with insp/exp views. Needs to be differentiated from pneumothorax (compression of thymus), air-filled lung cyst/pneumatocele, markedly distended stomach in diaphragmatic hernia. Causes of unilateral obstructive emphysema include:

  • Endobronchial lesion – foreign body, mucous plug (asthma, viral LRTI), tuberculous granuloma
  • Congenital lobar emphysema
  • Bronchial stenosis/atresia – hyperexpanded lobe. Perihilar oval opacity (mucocoele in obstructed bronchus).
  • Aquired lobar emphysema – bronchial damage from inflammation or bronchopulmonary dysplasia (BPD).
  • Extrinsic compression – vascular anomaly, mediastinal mass/cyst.

Pulmonary cavities usually inflammatory or post-inflammatory:

  • Lung abscess from bacterial pneumonia solitary or multiple, thick irregular wall with air-fluid levels. May be distal to a bronchial obstruction/foreign body. Cavitary TB rare.
  • Pneumatocoeles – thin walled, common with infection (esp staph, Tb), from bronchiolar obstruction -> air trapping and rupture. Or blunt chest trauma, hydrocarbon pneumonitis, LCH. Usually small and resolve, but can be large. Occasionally rupture -> pneumothraox or pneumomediastinum.
  • Congenital lung cysts – uncommon. Thin-walled, usually LL. Asymptomatic unless infected or rapidly expand.
  • CCAM
  • Congenital diaphragmatic hernia (bowel loops resembling cavities)

Pleural Effusion

Lateral and apical pleural thickening, subpulmonic collection (flattening and lateral peaking of raised lung base edge), opaque hemithorax of normal/increased volume.

  • Unilateral pleural effusion may be from parapneumonic transudate (esp Mycoplasma), empyema (staph, Haemophilus, pneumococcus) if large or loculated, subdiaphragmatic inflammatory transudate (abscess, pancreatitis), complication of thoracic catheter, rarely intrathoracic tumour involving pleura.
  • Bilateral serous pleural effusions in acute glomerulonophritis, nephrotic syndrome, lymphoma (esp NHL), neuroblastoma, congestive heart failure, collagen vascular disease, fluid overload.
  • Haemothorax from trauma (direct chest wall ± rib fractures, or aortic rupture from deceleration), bleeding disorder, rarely aneurysm of ductus arteriosus rupture.
  • Chylothorax most common cause of massive neonatal effusion, usually unilateral, R>L. Cause uncertain, ?traumatic tear/congenital defect of thoracic duct. Occasionally from SVC thrombosis (difficult to treat), rarely pulmonary lymphangiectasia. Usually resolves with thoracentesis, may requrire chest tube drainage or pleuroperitoneal shunt.

Pneumothorax and Pneumomediastinum

Pneumothorax in neonate causes spinnaker sail sign (elevated thymus off cardiac sillhouette, may -> sup mediastinal pseudomass).

Neonatal and Congenital Lung Disease

Apex of dome of diaphragm at 10th post rib.

Generally high lung volume, streaky perihilar opacity in term baby is meconium aspiration, TTN or neonatal pneumonia. Low volumes, granular opacities is surfactant deficiency or beta-haemolytic strep.

Acute diffuse pulmonary consolidation may be oedema (PDA), haemorrhage (surfactant therapy), worsening SDD, neonatal pneumonia, diffuse microatelectasis (underexpansion).

Lines and Tubes

Umbilical arterial catheters -> pelvis to iliac aa -> aorta. High lines @T8-10, low lines below L3, to prevent major arterial thrombosis.

Umbilical venous catheter -> left portal vein -> ductus venosis -> hepatic vein -> IVC. Ideally @ RA/IVC junction. Deflection into portal veins may -> hepatic haematoma, abscess.

PICCs (as small as 2-3F) via arm or scalp ideally at mid SVC. Intracardiac may -> atrial laceration -> pericardial tamponade, haemorrhage, death; too proximal may flip into contralateral brachiocephalic/jugular v.

NICU usually use high-frequency oscillator ventilation (supraphysiologic rate ~ 1000/min with very low tidal volumes), not moving diaphragm; causes less air-block complications. Conventional ventilation larger tidal volume ~22/min.

Extracorporeal Membranous Oxygenation (ECMO)

Bypass of pulmonary blood flow through semipermeable silicon membrane via large-calibre catheters (hence premature infants often too small). Interupts PAH and persistent fetal circulation, reduces damaging barotrauma/high O2. Used in congenital diaphragmatic hernia, meconium aspiration, neonatal sepsis, pneumonia. Lungs invariably become opaque due to reduced ventilator settings, often have pleural effusions (obscured). Arteriovenous or venovenous ECMO. AV ECMO – RCCA catheter with tip at arch, IJV catheter tip at RA. Some catheters have radiolucent end with small marker at tip. Patients are anticoagulated.

Surfactant Deficiency Diseae (SDD)

(Respiratory distress syndrome RDS, hyaline membrane disease HMD). Almost all are preterm; increased risk with males, maternal diabetes, C-section. Occurs in 60% of those <28/40, 30% 28-34/40, <5% >34/40. Sufactant consists of mostly dipalmitoyl phosphatidylcholine (lecithin), hydrophilic glycoproteins and hydrophobic proteins. Surfactant synthesis is increased with glucocorticoids and labour, suppressed with insulin (in infants to diabetic mothers). Lung immaturity with lack of surfactant (type II alveolar cells, reduces surface tension of acini) -> poorly distensible, collapsed alveoli, microatelectasis. Progressive atelectasis -> hypoperfusion -> endothelial damage and leak of plasma -> protein and fibrin rich alveolar exudate -> hyaline membranes, impairing gas exchange -> hypoxia, further imparing surfactant synthesis. Hypoxia, acidosis, reduced perfusion; respiratory distress within fist few hours. Small volume lungs, fine granular pattern (1-2mm bubbles of distended alveolar ducts and terminal bronchioles superimposed over general alveolar collapse) with air bronchograms extending to periphery. At expiration lungs are completely opaque. Pleural effusion suggests pneumonia (esp strep) rather than HMD. Normal CXR at 6hrs excludes HMD. DDx neonatal pneumonia, pulmonary lymphagiectasis, TTN, congenital heart disease with severe PV obstruction (but normal-increased lung volumes). Hypoxaemia may cause PDA – large increasingly opaque lungs (oedema) with loss of granular pattern, cardiomegaly, pulmonary vascular congestion.

Treated with endotracheal surfactant therapy via nebulised or aerosol via tracheal catehter or adapted ETT, reducing oxygen/ventilator demands, air-block Cx, intracranial haemorrhage, BPD, death; but increased PDA, pulmonary haemorrhage, acute desaturation. Complete, central or asymmetric clearing. Positive pressure-assisted ventilation may improve oxygenation or cause pulmonary interstitial emphysema, pneumomediastinum, pneumothorax, pneumopericardium, pneumoperitoneum, rarely air embolism.

Pulmonary Haemorrhage

Premature. In 1st 3 hours, resolving within 2-3 days. May be a complication of surfactant therapy.

Transient Tachypnoea of the Newborn (TTN)

(Retained foetal lung fluid, wet lung disease, transient respiratory distress of the newborn). Delayed clearance of foetal lung fluid. Grunting and tachypnoea in otherwise healthy term infant (esp C-section with absent thoracic squeeze), maternal diabetes or sedation. CXR findings minimal, diffuse haziness/reticulation, streaky parahilar opacity, granular pattern, N/large volumes, cardiomegaly, ± pleural effusion. Peribronchial cuffing may cause air-trapping. Sx at 6hrs, peaks 1/7, resolves 2-3/7. DDx pneumonia, HMD.

Meconium Aspiration

More common in term/postmature infants. Often assymptomatic. Intrauterine foetal distress -> passage of meconium which may be aspirated -> obstructed peripheral bronchioles, uneven subsegmental atelectasis with alternating overdistension. Hyperexpansion. Also -> chemical pneumonitis. Coarse reticulonodular/nodular opacities. Rope-like perihilar densities. Pleural effusions. If severe, progressive air-trapping -> airblock complications with pneumothorax (in 20-40%), pneumomediastinum. Hypoxia may -> persistent foetal circulation (R>L shunt). Tx endotracheal suction, hymidified O2, ECMO (if severe).

Neonatal Pneumonia

Aquired intrauterine, at birth or postnatal. Patchy asymmetric perihilar opacities, hyperinflation, ± pleural effusion. DDx meconium aspiration.

Beta-haemolytic strep pneumonia most common in neonates, acquired during birth (25% women colonised). Prem > term. Bilat granular opacities, low lung volumes, effusion (in 25-67%, cf SSD).

Pulmonary Interstitial Emphysema (PIE)

Air-block complication from marked increase alveolar pressure -> leakage from distended terminal airways -> dissection through interstitium and lymphatics. Focal or diffuse serpiginous bubblelike or linear branching lucencies extending to periphery. Involved lung is hyperinflated with static volume (stiff lungs). Usually transient. Warning sign for other air-block complications. May -> expansive multicystic mass with interstitial air cysts. DDx BPD, partially treated SSD; but PIE usually in 1st 1-2/52 with abrupt onset.

Bronchopulmonary Dysplasia (BPD)

(Chronic lung disease of prematurity, CLD). From prolonged positive pressure-assisted ventilation and oxygen toxicity (high O2 arrests septation of lungs, increases ROS). Risk factors include O2 dependence at 36/40, sepsis, very low birth weight (in 50% of <1000g), prematurity. Chronic high oxygen also increases risk of retinopathy of prematurity (retrolental fibroplasia). There is reduction in alveolar septation with large simplified alveoli, dysmorphic capillaries, potentially reversible. Impossible to tell if there is superinfection. Apperances can change rapidly. Can occur without surfactant deficiency.

  • Oedematous phase/’leaky lung syndrome’ – damage to basement membrane of capillaries -> interstitial oedema (hazy/reticular pattern), may persist for weeks/months. Treated with fluid restriction and diuretics, vitamin A, low-dose dexamethasone.
  • Bubbly phase – usually later but can be simultaneous. Overdistended alveolar groups (others atelectatic). Dilated acini, alveolar septal injury with inflammation/scarring, may -> necrotising bronchiolitis, lobar emphysema. Over-aerated lungs with bubbles/cysts of varying sizes, scattered atelectasis, air-trapping, architectural distortion.

Often returns to normal at 2-5yo. Long-term there may be hyperinflation, normal/minor abnormal pulmonary function, exercise intolerance, recurrent infections, asthma.

Pulmonary Lymphangiectasia

Rare. May be isolated or associated with congenital heart disease or generalised lymphangiectasia. Isolated from abnormal lymphatic development, dilated and obstructed lymphatic channels. Associated with CHD usually from severe pulmonary venous obstruction (hypoplastic left heart syndrome, total anomalous pulmonary venous return type III, pulmonary vein atresia). Diffuse coarse reticular/reticulonodular pattern, hyperinflation, pleural effusions. Pulmonary haemangiomatosis is similar, also rare.

Congenital Diaphragmatic Hernia (CDH)

Large hernias -> severe respiratory distress after birth. Up to 50% associated with congenital heart disease, most have malrotation. Compression of lung in utero -> hypoplasia. Hypoxia, persistent fetal circulation from hypoxia-induced PAH. High mortality despite early diagnosis and surgery, improved with ECMO. Poor prognosis indicated by lack of aerated ipsilateral lung, low percentage of aerated contralateral lung, severe mediastinal shift. Small hernias may be asymptomatic. Absence/paucity of gas-filled loops in abdomen. NG may be lodged at oesophagogastric junction due to acute turn in herniated stomach.

  • Bochdalek (post-med diaphragm). L:R 5:1.
  • Morgagni (ant). Usually less severe.

Pulmonary Hypoplasia

Usually from PA deficiency or compression of developing lung. Small lung with reduced number and size of aiways, alveoli and vessels. Congenital causes include:

  • Hypoplasia/absent ipsilateral PA (reduced lung markings)
  • Congenital heart disease (TOF – left lung, PDA, ASD, VSD)
  • Congenital pulmonary scimitar/venolobar syndrome (hypogenetic lung syndrome) – 40% asymptomatic, some recurrent infection or L>R shunt. Almost all R-sided. Partial anomalous venous return (IVC with L>R shunt), hypoplasic/absent PA, ± bilateral L-sided bronchial branching, sequestration, systemic arterialisation, accessory diaphragm, eventration, horseshoe lung (pos-inf fusion of lungs), cardiac anomalies (ASD, coarctation of aorta, PDA, TOF), absent IVC. Vertical curvilinear/scimitar shaped draining vein at medial right lower lung seen in 1/3. Small R hemithorax with diaphragmatic elevation/eventration, dextroposition of heart, herniation of L lung.
  • Pulmonary agenesis (rare) – insult during 4/40, R=L. R associated with congenital heart/skeletal/GIT/GU anomolies. Severe volume loss with opacity, rib crowding, absent bronchus and PA.
  • Developmental thoracic compression of the lungs – short ribs and small thoracic cage. Asphyxiating thoracic dystrophy, thanatophoric dwarfism, Ellis-van Creveld syndrome; usually severe -> demise. Also in chromosomal abnormalities (trisomies).
  • Intrathoracic compression. Congenital diaphragmatic hernia – increased volume on one side compresses other lung -> bilat hypoplasia; earlier in gestation the hernia the more severe. Chylothorax, large intrathoracic cysts/tumours (neuroblastoma, teratoma, cystic adenomatoid malformation), marked cardiomegaly.
  • Extrathoracic compression – Potter/oligohydramnios syndrome/sequence from oligohydramnios -> compression; in bilateral renal agenesis, congenital renal cystic disease, obstructive uropathy (post urethral valves, prune belly syndrome). Persistent diaphragmatic elevation, prolonged distended abdo (mass or ascites).
  • Primary hypoplasia (unexplained)
  • Hemivertebrae and scoliosis
  • Horseshoe lung uncommon variant where RLL crosses betw oesophagus and heart to join left lung.

Swyer-James syndrome is acquired after severe obliterative bronchiolitis -> obstruction, bronchiectasis (not always) and distal airspace destruction. Collateral drift -> air-trapping (cf congenital causes). V/Q can verify exp airway obstruction and reduced perfusion. Typically small hyperlucent lung with reduced vascularity. May have fibrotic reticular pattern in lung.

Congenital Pulmonary Airway Malformation (CPAM)

(previously congenital cystic adenomatoid malformation CCAM). Dysplastic usually adenomatous tissue within variable sized cysts communicating with bronchial tree, replacing normal alveoli. Abnormal proliferation of bronchioles and suppression of alveoli. Most detected prenatally or have respiratory distress at birth. M>F. Most one lobe, no lobar predilection. Type 1 (60-75%) large 20-100cm cysts, good prognosis; type 2 (15-40%) numerous uniform small cysts 5-50mm, poor prognosis (associated with other anomalies); type 3 (rare) microscopic cysts (grossly solid), very poor prognosis. 1st few days fluid filled before air replacement. Typically increases in size until 25/40 before regressing. Cysts may gradually enlarge -> respiratory distress. No systemic arterial supply (cf sequestration). Tx of symptomatic CPAM is resection, asymptomatic controversial. Increased risk of infection, rarely Ca. May scar down and resolve after infection.

Congenital Lobar Emphysema (CLE)

(Neonatal/congenital lobar hyperinflation CLH). Check/ball valve obstruction causing air trapping and emphysema to a lobe (LUL > RML > RUL; rare in lower lobes). From extrinsic compression (bronchogenic cyst, anomalous L PA), cangenital deficiency of bronchial cartilage, congenital/acquired bronchial stenosis. 50% present in 1st 1/12, 75% in 6/12. Minority have associated anomalies esp cardiac. Hyperlucent, hyperexpanded lobe, may fill entire hemithorax, attenuated blood vessels, diaphragmatic depression, mediastinal shift, accentuated on expiration or ipsilateral decubitus. Bronchovascular bundle at periphery of lucency. Newborn may be opaque due to delayed clearance of fluid. Tx lobectomy if Sx, may spontaneously resolve.

Bronchial Atresia

Developmental stenosis/atresia of lobar/segmental bronchi, causing obstruction and distal bronchiectasis. Most asymptomatic. Round/oval/branching central opacity (mucous-filled dilated bronchus mucocoele) with distal hyperlucency and air-trapping of supplied lung. Most common LUL (esp apicoposterior segment), RUL, RML. Tx conservative.

Bronchopulmonary Sequestration

Mass of abnormal pulmonary tissue lacking connection to bronchial tree, persisting systemic arterial supply, variable systemic/pulmonary venous drainage, cystic and bronciectatic. May be mixed lesion with CCAM (esp type 2). May have air from collateral drift. After infection, air may be introduced -> multiloculated cystic mass. Best modality CECT for systemic arterial supply and characterisation if not sequestration

  • Intralobar (95%) – covered by visceral pleura of adjacent lung; 2/3 medial basal segment LLL, 1/3 RLL. Oval or triangular opacity. Present as recurrent pneumonia (usually late childhood). Supplied by single artery from infradiaphragmatic aorta (entering via pulmonary ligament) with drainage via pulmonary veins.
  • Extralobar (5%) – covered by own pleura (may be adjacent to lung, within or below diaphragm), 90% L-sided. Associated with other anomalies in 65% (diaphragmatic eventration, hernia). Most asymptomatic. Supplied by several systemic and occasionally pulmonary with systemic venous drainage (azygos, hemiazygos, IVC).

Persistent Pulmonary Hypertension

(Persistent fetal circulation). Persistent high neonatal pulmonary vascular resistence. Primary, or secondary to hypoxia. CXR variable, more reflective of underlying pathology.

Pulmonary Ateriovenous Malformation (AVM)

Congenitally weakened capillaries causing dilatation and tortuosity, fed by single PA and PV. Most assymptomatic until young adult, haemoptysis, R>L shunt (SOB, paradoxical emboli/stroke). 80% associated with hereditary haemorrhagic telangiectasia. Commonly subpleural lower lobes, 1/3 multiple, often lobulated with vessels extending to hilum. Tx embolisation.

Bronchogenic Cyst

Abnormal budding of tracheobronchial tree. Lined with respiratory epithelium, smooth mussle ± cartilage. Filled with mucoid liquid. In lung parenchyma (usually central/perihilar) or middle mediastinum (65-90%, commonly subcarinal or right paratracheal). Most are solitary. May cause compression of distal trachea/bronchi, airtrapping in distal lung. Do not contain air until infected. Well-defined fluid or cystic air-fluid lesion.

Neuroenteric Cyst

(Split notochord syndrome). Failure to obliterate neuroenteric canal, with connection from GIT (endoderm) to skin (ectoderm). Lined by intestinal, pancreatic or leptomeningeal tissue. Associated with vertebral anomalies and cyst.

Other Lung Masses

Most commonly a pseudomass from spherical pneumonia (early stage), abscess (usually cavitation with air-fluid levels), postinflammatory pseudotumour/plasma cell granuloma (reactive healing pneumonia, calc uncommon, resolves over years). Most common true lung mass is postinflammatory granulomas (TB of fungs), usually small, calcified.

  • Mucocoele in bronchial atresia – central oval nodule with overaeration of involved lobe.
  • Primary lung tumours – rare, majority benign. Include sarcomas, primitive neuroectodermal tumours, squamous cell carcinoma, pleuropulmonary blastoma (rare, epithelial and mesenchymal elements, often from congenital lung cyst; solid or cystic). Most common malignant neoplasm (single or multiple) is metastases including Wilms tumour, Ewing sarcoma, osteosarcoma, rhabdomyosarcoma.
  • Pulmonary hamartoma – benign congenital with flocculent calc.
  • Laryngeal papilloma spreading to trachea and lungs (rare)

Upper Airways


(Acute larngotracheobronchitis). Most common upper airway obstruction. 6/12-3yo. Viral (parainfluenza 1/2, influenza A), self-limited, usually associated with LRTI. Barking/coupy cough, intermittent inspiratory stridor. Glottic and subglottic mucosal inflammation/oedema -> narrowing. Loss of normal shoulders/lateral convexities of subglottic trachea -> inverted V/steeple sign, obliteralted ventricles and true cords. Tx inhaled corticosteroids.


(Epiglottitis). Most H.influenzae, incidince reduced with vaccine. Acute stridor, dysphagia, fever, respiratory distress when recumbent. 2-4yo. Single lat XR to reduce maneuvers performed, manipulation may cause diffuse laryngeal oedema with acute respiratory compromise. Markedly enlarged epiglottis like a thumb, thickened aryepiglottic folds convex sup. May have soft palate and prevertebral swelling. Dilated airways above the epiglottis. Subglottic oedema.

Exudative Tracheitis

(Bacterial tracheitis, membranous croup, membranous laryngotracheobrinchitis). Uncommon. Purulent infection (Staph.aureus, multimicrobial) of trachea with exudative plaques. Unwell, 6-10yo. Linear soft tissue filling defect (membrane) in airway (nonadherent mucous clears with cough), plaquelike irregularity of tracheal wall, asymmetric or symmetric subglottic narrowing. Cx exudative membrane sloughing -> occlusion. Tx endoscopic membrane stripping, intubation.

Obstructive Sleep Apnoea (OSA)

Enlarged adenoid/palatine or lingual tonsils. Lat XR for adenoids with convex tissue post nasopharynx >12mm. Thickened tissue post soft palate, ‘kissing’ palatine tonsils, massively enlarged. Oedematous soft palate if significant OSA from repetitive trauma/snoring. Adenoid tonsils can grow back after tonsillectomy, palatine cannot.
MR sleep study for complicated cases.

Glossoptosis – posterior motion of tongue during sleep with maintained lat diameter. Associated with macroglossia, micrognathia, reduced muscular tone. Down syndrome, Pierre-Robin sequence, neuromuscular disorders (cerebral palsy).

Hypopharyngeal/retroglossal collapse – primary (reduced muscle tone) or secondary (neg pressure from superior obstruction). Cylindrical collapse of retroglossal airway.

Lower Airways

In infants, buckling of the trachea in expiration is normal.

Extrinsinc lower airway compression from:

  • Double aortic arch – Sx soon after birth, surround and compress lower/mid trachea and oesophagus, usually R arch dominant and more sup. Tx non-dominant arch ligation.
  • Pulmonary sling – LPA from RPA coursing betw trachea and oesophagus. Flattened (AP)/pancake trachea, asymemetric lung inflation. Associated with CHD, complete trachea rings, anomalous origin R bronchus.
  • R arch with aberrant LSCA (RAA-ALSCA). Tracheal compression if ring with persistent ductus ligament (not seen on imaging), Kommerell diverticulum or midline descending aorta (stacking of vasc structures).
  • Innominate artery compression syndrome – normally cross anterior to trachea. Compression if arising more to the left, mediastinum crowded by large thymus.

Tracheal masses

  • Haemangioma, usually subglottic, associated with facial haemangiomas, asymmetrical subglotting narrowing
  • Tracheal papilloma
  • Tracheal granuloma


Tracheal wall softening from abnormal cartilage. Intermittent expiratory collapse with >50% reduction in cross-sectional areas (cf stenosis fixed narrowing). Diffuse or focal (from vascular compression).

Foreign Body

Usually bronchus. Asymmetric aeration, hyperinflation, oligaemia, atelectasis, consolidation, pneumothorax, pneumomediastinum. 97% radiolucent. Inspiratory CXR normal in 1/3, air trapping seen on expiratory view.

Laryngeal/tracheal FB stridor, resp distress. Density within airway, loss of airway wall silhouette.

DDx Swyer-James syndrome, pulmonary hypoplasia.

Congenital High Airway Obstruction Syndrome (CHAOS)

Obstruction from in-utero laryngeal atreasia, subglottic stenosis, extrinsic mass (esp lymphatic malformations, teratomas). Massively increased lung volumes, flattened/everted diaphragms, fetal hydrops, polyhydramnios. Tx ex utero intrapartum treatment (EXIT) wih head delivered via C-section, tracheotomy or intubation prior to complete delivery and termination of placental circulation.


See Airways

Cystic Fibrosis (CF)

(Mucoviscidosis). AR with carrier 1:20 in Caucasians, incidence 1:2500. Defect in cystic fibrosis transmembrane conductance regulator (CFTR) gene on chromosome 7, usually encodes the epithelial chloride channel protein. Disorder of ion transport in epithelial cells, reducing fluid secretion in exocrine glands, respiratory GI and reproductive tracts. Diagnosed by persistently elevated sweat electrolyte concentrations. Abnormally viscus/mucous secretions causing:

  • Lungs – airway obstruction, infection, bronchitis, bronchiectasis, recurrent infections. Mucous plugging in distended bronchioles with hyperplasia and hypertrophy of the mucous-secreting cells. CXR normal or hyperinflation, peribronchial opacity, mucous plugging, bronchiectasis, lymphadenopathy, enlarged PAs (PAH). Cx focal pneumonia (S.aureus, H.influenze, Psudomonas, mycobacteria, ABPA), pneumothorax, haemorrhage.
  • Pancreas – Affectected in 85-90% with pancreatic insuficiency, steatorrhea, malnutrition, avitaminosis A (causing squamous metaplasia of epithelia). Plugging of pancreatic ducts causes atrophy of exocrine glands, progressive fibrosis leaving the islets within a fibrofatty stroma. Mucous plugs may cause meconium ileus.
  • Liver – Plugged bile canaliculi with hepatic steatosis, focal biliary cirrhosis (in 1/3).
  • Salivary glands – Progressive duct dilatation, glandular atrophy then fibrosis.
  • Chronic sinusitis.
  • Intestinal obstruction
  • Male infertility in 95% with congenital bilateral absence of the vas deferens, azoospermia.

Heterozygotes of the gene have higher risk of respiratory and pancreatic disesases, including idiopathic chronic pancreatitis, late-onset chronic pulmonary disease, idiopathic bronchiectasis, obstructive azoospermia (bilateral absence of vas deference).



Most LRTIs are viral (95% of 5/12-5y). Streptococcus pneumoniae and esp Mycoplasma pneumoniae (30%) increases with school-aged children. Followup CXR only if persistent/recurrent Sx, or underlying immunodeficiency. Findings can take 2-4/52 to resolve. CECT can help in nonresponsive pneumonia for detecting suppurative complications.

Viruses affect airways causing inflammation of small airways and peribronchial oedema. Peribronchial opacity, symmetric coarse markings radiating from hila, ‘dirty’/’budy’ central lungs, bronchial wall thickening, airway narrowing. Necrotic debris and mucous plugging -> occlusion with hyperinflation and subsegmental atelectasis (may mimic bacterial consolidation). Air trapping and collapse more common than adults due to smaller airways, poorly developed collateral air flow, more abundant mucous.

Bacterial inhalation -> airspaces -> inflammatory exudate and oedema in acini. Lobar or segmental consolidation with air bronchograms. ‘Round’ pneumonia more common <8yo, usually S.pneumoniae, in post and lower lobes; ?poorly developed collateral air drift. Pleural effusions common. CXR 92% negative predictive value for bacterial pneumonia.

Primary TB may cause lobar consolidation, highly associated with hilar lymphadenopathy, pleural effusion. Suspect when not acutely unwell.

Suppurative complications:

  • Parapneumonic effusions – In children very commonly empyema. Ultrasound may show high grade/complex (fibrinopurulent with fronds, septations, loculations) or low grade/simple (anechoic) effusion. Loculations may not be seen on CT. Comples effusions benefit from aggressive drainage. Pleural thickening/enhancement, extrapleural fat stranding not helpful.
  • Ischaemia/infarction – reduced/absent enhancement of parenchyma.
  • Lung abscess – dominant suppuration surrounded by fibrous wall, uncommon in healthy children. Fluid or air-filled cavities with enhancing walls, typically no evidence of surrounding necrosis.
  • Pneumatocoele – thin-walled cysts occuring later.
  • Cavitatary necrosis (necrotising pneumonia) – usually from intense/prolonged illness. Dominant area of necrosis with variable thin-walled cysts. Loss of normal architecture, reduced enhancement, loss of lung-pleural margin, air/fluid cavities lacking enhancing border. More common in strep or multi-drug resistent S.aureus. Good prognosis with medical management alone. Long term minimal or no scarring.
  • Bronchopleural fistula
  • Pulmonary gangrene

Long term sequalae include bronchiectasis and Swyer-James syndrome. Swyer-James – unilateral lung hyperlucency ?virus-induced necortising bronchiolitis -> obliterative bronchiolitis. Hyperlucent enlarged lung with static volume, reduced vessels. Obliterative bronchiolitis may affect only portion of lung.


See Airways

Chronic Aspiration

In neurologic abnormal (cerebral palsy), chronic tracheotomy. HRCT bronchiectasis, tree-in-bud, interstitial opacity, more in lower lobes.

Hydrocarbon Aspiration

Gasoline, furniture polish, kerosene, lighter fluid. Chemical pneumonitis and atelectasis from surfactant destruction, mostly in bases. CXR may be normal <12h; if normal at 24h excludes significant aspiration. Opacities may persist for weeks, may -> pneumatocoeles.

Acute Chest Syndrome in Sickle Cell Anaemia

Fever, chest pain, hypoxia, pulmonary opacities. More common in children 2-4yo. Most common cause of death in sickle cell. ?Rib infarction -> splinting -> atelectasis -> infection. Segmental/lobar opacities, cardiomegaly, rib infarcts on bone scan. Tx O2, ABs, analgesia.

Mediastinum, Hila and Chest Wall

Anterior Mediastinum

  • Normal thymus
  • Lymphoma – most common in teenagers. Hodgin lymphoma and lymphoblastic NHL. Associated with cervical lymphadenopathy. Calcification in untreated lymphoma is rare.
  • Benign germ cell tumours – dermoids only contain ectodermal elements, teratomas contain elements from all dermal layers. Mature teratomas have calcification, fluid and fat.
  • Malignant germ cell tumours.
  • Thymoma
  • Multilocular thymic cysts – associated with AIDS.
  • Thyroid – enlarged and heterogeneous with calcifications in LCH.
  • Haemangiomas – solid, echogenic, small cystic areas (vascular lakes), blood flow seen on Doppler.
  • Cystic hygroma (large macrocystic lymphangioma) – congenital malformation of lymphatics, commonly from neck. Locally invasive, often -> mediastinum. Multiloculated, cystic.


Prominent at birth, easily visible up to ~2yo, seen up to ~5-10yo. Normal thymus superior mediastinum retrosternal space, homogeneous, smooth bilatateral widening of mediastinum, silhouettes cardiac borders, smooth notch with it and heart, wavy undulating contour (compression from overlying ribs), triangular ‘sail’ sign of promenent lobe (R>L). Quadrilateral in children, triangular in teenagers. May have extensions into neck, extending posterior between innominate and L brachicephalic aa. On US multiple linear connective tissue septa, or dot-like echogenicities. Bulging or convexity of borders, heterogeneity, displaced/compressed trachea/vessels, calcification suggests pathology. Spinnaker sail sign – uplifted from pneumomediastinum. MR best test for normality.

  • Stress atrophy secondary to any illness or steroids and may be severe (narrow mediastinum), returns in size or rebound hypertrophy with recovery.
  • DiGeorge syndrome – thymic aplasia, absent parathyroid glands and cardiovascular anomalies; from faulty development of 3rd and 4th pharyngeal pouches.
  • Large thymus almost always normal in infant (more common in boys); may also be leukaemia, lymphoma, cysts, spontaneous haemorrhage.

Middle Mediastinum


  • Lymphadenopathy – inflammatory/reactive (esp granulomatous disease) or neoplasm. Massive in lymphoma and leukaemia. Bilat hilar in viral LRTI, mycoplasma, fungi, TB, LCH, mets, sarcoid, Wegener granulomatosis, neoplasm. Unilateral in primary TB (associated with Ghon complex), mycoplasma, fungi, bacterial pneumonia, uncommon with viruses, neoplasm.
  • Bronchogenic duplication cyst – sharpy marginated, may be lobulated, common around carina, may appear solid on CT (cystic nature confirmed on MR).
  • Enteric duplication cyst – abnormal development of post division primitive foregut, from oesophagus, stomach, duodenum. Don’t communicate with oesophagus, but displace and compresses it. May have gastric mucosa causing ulceration and haemorrhage.
  • Neurenteric duplication cyst – associated with vertebral anomalies.
  • Oesophagus – Chronic foreign body erosion -> mediastinal mass (esp level of thoracic inlet). Achalasia. Hiatus hernia.
  • Aortic aneurysms rare, except for trauma, connective tissue disorders (marfan, Ehlers-Danlos syndrome).
  • Ductus bump – newborn, dilated infundibulum of ductus arteriosis, disapperas within weeks; enlargement or persistence suggests aneurysm.
  • Enlarged aorta and MPA in congenital heart disease.
  • Mass at upper L cardiac border may be herniated left atrial appendage via partial pericardial defect or coronary artery aneurysm (periarteritis nodosa, Kawasaki/mucocutaneous LN syndrome)
  • Enlarged azygos vein in total anomalous pulmonary venous return -> azygos or absent IVC with azygos continuation.

Posterior Mediastinum

  • Neurogenic tumours. Neuroblastoma (malignant), ganglioneuroblastoma or gangioneuromas (benign). Congenital, from paraspinal sympathetics. Pedicle erosion, interpedicular or rib space widening, bony erosion indicating extension from spinal canal. Calcification in 25%. Difficult to be distinguished apart. MR to assess extent, esp intraspinal. Thoracic neuroblastoma better prognosis than abdominal.
  • Neurofibromas – part of NF or solitary. Widening of intervertebral foramina.
  • Lateral thoracic meningocoeles – similar appearances to neurofibromas, also occuring in NF.
  • Neurenteric cysts – enteric duplication cysts communicating with spinal canal, almost always associated with vertebral ± spinal cord anomalies.
  • Discitis
  • Haematoma
  • Extramedullary haematopoiesis
  • Lymphangioma, teratoma, lymphoma, sarcoma (rare)
  • Bochdalek hernia
  • Pulmonary sequestration.

Chest Wall

Up to 1/3 of children have variations of ant chest wall incl tilted sternum, prominent convexity of ant rib/costal cartilage, parachondral nodules, mild pectus excavatum/carinatum. Most true lesions are from cartilage or bone, many malignant, often large at presentation.


  • Ewing sarcoma – large extrapleural soft tissue mass with rib destruction, pleural effusion.
  • Primitive neuroectodermal tumour (Askin tumour) – essentially the same as Ewing sarcoma, now part of the colelctive term Ewing sarcoma family of tumours (ESFT).
  • Metastatic rib lesions common in neuroblastoma
  • Leukaemia and lymphoma chest wall involvement common.
  • Rhabdomyosarcoma
  • Chondrosarcoma rare


  • Osteochondromas common
  • Mesenchymal hamartoma – rare, benign, usually <1yo. Solid cartilage, bone and fibroblasts ± cystic areas and haemorrhage. Noninvasive, but erode ribs and compress structures
  • Empyema necessitatis – empyema -> chest wall (Staph, Fusubacterium, TB)
  • Aneurysmal bone cyst
  • Langerhans cell histiocytosis
  • Haemangioma
  • Lymphangioma
  • Teratoma
  • Calcifying fibrous pseudotumour
  • Osteoid osteoma

Pectus excavatum mostly cosmetic. May cause chest pain, fatigue, SOBOE, palpitations, restrictive lung disease. Haller index – low mA through greatest deformity; transverse (L>R) diameter / AP diameter of inner chest wall. When severe (>3.2) > minimally invasive surgery by Nuss procedure, where curved bar slipped post to ant ribs and sternum.


  • Ribs more catilage and compliant, hence less rib fractures and more lung injury.
  • Rib fractures more likely to be posterior. Absence of trauma highly suspicious for child abuse, squeezing -> costotransvere process fracture (pathognomonic).
  • Lung contusion – nonsegmental, posterior, crescent shape, mixed confluent and nodular opacity with subpleural sparing. Lung laceration – fluid or air-filled pneumoatocoeles/cysts.
  • Aortic injury much less common than adults.