High-Resolution CT Chest

High resolution CT (HRCT) of the chest is a thin slice technique (0.5 to 1.25 mm) reconstructed with a sharp (high spatial frequency) lung algorithm to show the secondary pulmonary lobule, the smallest unit of lung structure visible on CT. It is done without contrast in full inspiration, with additional expiratory images and prone images when needed.

Modern volumetric scanners acquire the whole chest continuously with contiguous thin slices, and reconstruct in axial, coronal and sagittal planes and with minimum and maximum intensity projections. Effective dose is about 1 to 4 mSv with low dose settings and iterative reconstruction.

HRCT is the key test for diffuse lung disease. Interstitial lung diseases affect about 60 to 80 in every 100 000 people, and idiopathic pulmonary fibrosis occurs in 10 to 20 in every 100 000 with a median survival of 3 to 5 years after diagnosis.

HRCT can diagnose a usual interstitial pattern with a specificity of over 90%, avoiding surgical lung biopsy in many patients, and narrows the differential diagnosis of ground glass, nodular and cystic diseases, bronchiectasis and small airway disease.

Indications. Unexplained dyspnoea, dry cough or crackles with a normal or non-specific radiograph. Suspected interstitial lung disease (fibrosis, sarcoidosis, hypersensitivity pneumonitis, connective tissue disease lung involvement, drug induced and radiation lung disease). Restrictive lung function with a reduced transfer factor.

Suspected bronchiectasis and its causes. Small airway disease (obliterative bronchiolitis, mosaic attenuation). Emphysema assessment and cystic lung disease (lymphangioleiomyomatosis, Langerhans cell histiocytosis).

Occupational lung disease (silicosis, asbestosis, coal worker pneumoconiosis). Suspected opportunistic infection. Follow up of fibrosis and response to treatment.

Pre-transplant evaluation. Not for focal disease (use the routine CT chest with contrast as needed).

Contraindications and precautions. Pregnancy: avoid unless essential. Children: use low dose, age adjusted techniques. Patients must hold their breath well, because motion degrades the study: practice breathing instructions before the scan.

Contrast is not given for the HRCT itself. Acute illness (acute pulmonary oedema, active infection) alters the pattern; scan when stable if possible, unless the clinical situation is urgent.

Preparation and technique. No preparation. The patient lies supine with arms raised over the head, breath held at full inspiration. Slice thickness is 1.0 to 1.25 mm or less, with a sharp lung kernel, window level -600 HU and width 1500 HU, and the field of view limited to the chest.

Expiratory images at end expiration (full breath out) show air trapping and tracheal collapse, and prone images (full inspiration) separate dependent density from early subpleural fibrosis. Radiation dose is reduced by lower tube current, and ultra-low-dose scans are used for young patients and follow up.

Normal appearances. The secondary pulmonary lobule is a polygonal unit 1 to 2.5 cm across, bounded by thin connective tissue septa, with a central bronchiole and artery, and lymphatics and veins in the septa and subpleural area.

A normal HRCT shows thin or invisible septa, clear fissures, smooth bronchial walls with airways similar in diameter to the neighbouring artery, uniform lung density in inspiration (with a mild gravity dependent gradient), and no cysts or nodules.

In expiration the lung density increases by 100 HU or more, and the trachea narrows by under 50% in the sagittal plane. Mild subpleural dependent opacity resolves in prone positioning.

Interpretation.

• Usual interstitial pattern: subpleural and basal predominant reticulation, honeycombing (clustered subpleural cysts in several layers with shared walls) and traction bronchiectasis, with little ground glass; diagnostic of idiopathic pulmonary fibrosis in the right clinical setting. A probable pattern lacks honeycombing; an alternative pattern shows features such as upper zone predominance, extensive ground glass, consolidation, micronodules, cysts or mosaic attenuation.
• Non-specific interstitial pneumonia: bilateral basal ground glass and fine reticulation with subpleural sparing, traction bronchiectasis, and little honeycombing, common in connective tissue disease (systemic sclerosis, myositis, rheumatoid arthritis).
• Hypersensitivity pneumonitis: ill defined centrilobular ground glass nodules, mosaic attenuation with air trapping on expiratory scans, and the "three density" sign; fibrotic forms show upper zone fibrosis with bronchiolectasis.
• Sarcoidosis: perilymphatic nodules along bronchovascular bundles, fissures and subpleural region with upper zone predominance, symmetrical hilar and mediastinal lymphadenopathy, and fibrotic distortion with conglomerate masses in advanced disease.
• Organising pneumonia: peripheral or peribronchial consolidation, reversed halo sign, and migratory opacities.
• Respiratory bronchiolitis and desquamative interstitial pneumonia: centrilobular nodules and diffuse ground glass in smokers, with emphysema.
• Pulmonary alveolar proteinosis: crazy paving (ground glass with smooth septal thickening) with sharply demarcated geographic borders.
• Pulmonary oedema: smooth septal thickening, ground glass in a gravity dependent gradient, effusions and cardiomegaly.
• Lymphangitic carcinomatosis: nodular or beaded septal thickening, usually unilateral or asymmetric, with lymphadenopathy.
• Infection: tree-in-bud (infectious bronchiolitis: tuberculosis, atypical mycobacteria, bacterial), miliary nodules (random distribution), Pneumocystis (diffuse ground glass with cysts and sparing of the periphery), and viral pneumonitis (patchy ground glass).
• Bronchiectasis: signet ring sign, lack of tapering, visible airways within 1 cm of the pleura, cylindrical, varicose or cystic forms; causes include previous infection, cystic fibrosis (upper zone), primary ciliary dyskinesia (middle lobe and lingula, with situs inversus), allergic bronchopulmonary aspergillosis (central, with high attenuation mucus), and traction.
• Small airway disease: mosaic attenuation with vessel size differences, air trapping on expiration, and constrictive bronchiolitis after transplant or infection.
• Emphysema: centrilobular (upper zones, centrilobular lucencies without walls), panlobular (basal, uniform), paraseptal (subpleural), and bullae.
• Cystic lung disease: lymphangioleiomyomatosis (diffuse thin walled round cysts in women, chylous effusion), Langerhans cell histiocytosis (upper zone, irregular bizarre cysts with nodules, sparing the costophrenic angles), Birt-Hogg-Dube syndrome (basal lower zone cysts near the mediastinum), and lymphoid interstitial pneumonia (perivascular cysts).
• Pneumoconiosis: silicosis (small centrilobular and perilymphatic nodules in upper zones, eggshell calcification of nodes, progressive massive fibrosis), asbestosis (basal subpleural fibrosis with pleural plaques), and coal worker disease.
• Drug and radiation lung: amiodarone (high attenuation consolidation), methotrexate and bleomycin (non-specific interstitial pattern or hypersensitivity pattern), and radiation fibrosis conforming to the field.
• Pulmonary vascular disease: enlarged central arteries, mosaic perfusion (chronic thromboembolic disease), and veno occlusive disease (smooth septal thickening, centrilobular ground glass, nodes).

Critical values and findings needing immediate action.

• Acute exacerbation of fibrosis (new bilateral ground glass on a fibrotic background): urgent respiratory review, high dose steroids and supportive care.
• Diffuse alveolar damage, extensive bilateral ground glass in a ventilated patient: critical care review and search for infection.
• Pneumocystis or other opportunistic infection pattern: start treatment while awaiting confirmation.
• Pneumothorax in cystic lung disease or fibrosis: drainage.
• Miliary nodules: tuberculosis workup and early treatment.
• Lymphangitic spread or tumour pattern: urgent oncological assessment.
• Fibrosis with progression on treatment: specialist review for antifibrotic therapy and transplant assessment.

Limitations and artefacts.

• Motion and poor inspiration create ground glass and blur small structures; repeat if the breath hold fails.
• Dependent atelectasis simulates early fibrosis at the bases; prone images resolve it.
• Expiratory scanning is needed to diagnose air trapping; a scan in inspiration only can miss small airway disease.
• Inspiratory level differences change lung density and texture between visits: compare like with like.
• Sharp kernels exaggerate noise, and low dose settings reduce the visibility of subtle ground glass.
• Many patterns overlap (usual interstitial pneumonia versus fibrotic hypersensitivity pneumonitis versus connective tissue disease), so discussion at a multidisciplinary meeting with clinical and serological data is needed.
• Normal HRCT does not exclude early interstitial disease or all small airway disease; lung function and biopsy may be needed.
• Smoking related changes (emphysema, respiratory bronchiolitis, mild basal reticulation) are common in healthy older people, and age related subpleural change is not disease.
• Heart motion and cardiac pulsation blur adjacent lung (lingula, left lower lobe).

Special groups.

• Patients with connective tissue disease (systemic sclerosis, rheumatoid arthritis, myositis, Sjogren syndrome): regular HRCT, since lung disease is a leading cause of death.
• Patients on drugs known to cause lung toxicity: baseline and follow up scans when symptoms arise.
• Children: low dose techniques; HRCT is used for bronchiolitis obliterans, cystic fibrosis and neonatal lung disease.
• Smokers: emphysema, interstitial abnormalities and lung cancer screening overlap.
• Pregnancy: avoid unless essential.
• Regions: silicosis and other pneumoconioses from mining and quarrying, tuberculosis sequelae, HIV-related lymphoid interstitial pneumonia and Pneumocystis, hypersensitivity pneumonitis from farming and birds, and post-infective bronchiectasis are all frequent; HRCT is limited to referral centres, and diagnosis often rests on the radiograph and clinical findings.

Follow up tests. Full lung function tests with transfer factor, six minute walk test with oxygen saturation, autoimmune serology (antinuclear antibody, rheumatoid factor, anti-cyclic citrullinated peptide, myositis and scleroderma antibodies), precipitin tests for hypersensitivity pneumonitis, serum angiotensin converting enzyme (limited value) and calcium,

bronchoalveolar lavage and transbronchial or cryobiopsy, surgical lung biopsy for selected unclear cases, echocardiography for pulmonary hypertension, sputum and microbiology, immunoglobulins, sweat chloride and ciliary function tests for bronchiectasis, repeat HRCT at 6 to 12 months for fibrosis, and referral to a multidisciplinary interstitial lung disease team.