Overview

Carcinoma of the lung is the leading cause of cancer-related death worldwide. The thoracic surgeon's role spans the entire pathway — from workup and mediastinal staging through resection of early and locally advanced disease, management of complications, and selected oligometastatic disease.

This chapter covers the surgical perspective. Systemic therapy, immunotherapy, and screening protocols evolve rapidly — current guidelines are signposted throughout.

Risk factors

  • Smoking: single most important risk factor — accounts for ~90% of cases; cigarette > pipe/cigar/bidi; second-hand smoke confers risk; risk falls progressively after 15 years of cessation
  • Occupational: asbestos, radon, uranium mining, foundry work, polycyclic aromatic hydrocarbons
  • Genetic: Li-Fraumeni syndrome (p53 mutation); first-degree relative with lung cancer
  • Pre-existing lung pathology: IPF, COPD, prior lung cancer or head and neck cancer
  • Environmental: air pollution, biomass fuel burning (cooking in enclosed spaces)
Lung cancer screening

Low-dose CT (LDCT) screening reduces lung cancer mortality in high-risk individuals. Eligibility criteria and nodule management protocols are updated regularly. Refer to NCCN or USPSTF current guidelines for specific age and pack-year thresholds.

Histological classification

Lung malignancies are classified as NSCLC (non-small cell lung carcinoma) or SCLC (small cell lung carcinoma). NSCLC accounts for ~85% of primary lung cancers.

Table 24 · IHC markers in the three main subtypes of NSCLC
FeatureAdenocarcinomaSquamous cell carcinomaCarcinoid
MorphologyGlandular differentiationIntercellular bridges, keratin pearlsSmall blue round cells
IHC markersTTF1, Napsin, Mucin, CK7, EGFR, KRAS, EML-ALKCK5/6, p40, p63, 34βE12Chromogranin, histamine, 5-HIAA, NSE
LocationPeripheral (usually)Central (usually)Central
Mutation profileEGFR, ALK, KRAS (non-smokers and Asians more common)KRAS, PIK3CA (smokers)
Molecular profiling

All advanced NSCLC should undergo molecular profiling for EGFR, ALK, ROS1, KRAS G12C, PD-L1, and other targetable mutations. Results guide systemic therapy selection. For current targeted therapy recommendations, refer to ESMO or NCCN guidelines.

Clinical features

Symptoms — by mechanism
Primary tumourCough · haemoptysis · dyspnoea · wheeze · chest pain · stridor (tracheal involvement)
Local invasionHorner's syndrome (T1 root + cervical sympathetic) · SVC obstruction · dysphagia (oesophageal) · hoarseness (RLN palsy) · phrenic nerve palsy
MediastinalPericardial effusion · SVC syndrome · tracheo-oesophageal fistula
ParaneoplasticSIADH (SCLC) · hypercalcaemia (SCC) · ACTH secretion · Lambert-Eaton (SCLC) · clubbing · hypertrophic osteoarthropathy (adenoCa)

Investigations and workup

  • Chest X-ray
  • CECT thorax and upper abdomen
  • PET-CT — staging, identifies occult distant disease, guides biopsy of metabolically active lesions
  • MRI brain — for stage III and adenocarcinoma
  • Pulmonary function tests — essential before resection
  • Cardiac evaluation as indicated
  • Tissue diagnosis — bronchoscopy ± EBUS, CT-guided biopsy, VATS or mediastinoscopy

TNM staging — 8th edition (AJCC/IASLC)

T — Primary tumour
T stageDescription
T1a≤1 cm
T1b1–2 cm
T1c2–3 cm
T2a3–4 cm OR involves main bronchus ≥2 cm from carina OR visceral pleura OR partial atelectasis
T2b4–5 cm
T35–7 cm OR chest wall / phrenic nerve / parietal pericardium OR satellite nodule in same lobe
T4>7 cm OR carina / great vessels / oesophagus / vertebra / heart / trachea OR satellite in different ipsilateral lobe
N — Nodal status
N stageDescription
N0No regional lymph node metastasis
N1Ipsilateral peribronchial or hilar nodes
N2Ipsilateral mediastinal or subcarinal nodes
N3Contralateral mediastinal / hilar or scalene / supraclavicular nodes

Mediastinal nodal staging

Mediastinal staging is required in all cases — it can be omitted only for peripheral tumours <3 cm with no CT/PET-positive nodes. The aim is the highest possible certainty of nodal status before curative resection.

Table 22 · Indications for invasive mediastinal staging
CT/PET findingsAction
No mediastinal nodes, peripheral tumour <3 cmProceed to resection (omit mediastinal staging)
CT enlarged nodes ± PET positiveInvasive staging mandatory
Central tumour or N1 nodesInvasive staging recommended
PET negative mediastinum in high-risk tumourInvasive staging still recommended
Table 23 · Nodal stations accessed by staging procedures
ProcedureNodal stations accessed
Cervical mediastinoscopy2R, 2L, 4R, 4L, 7
VAMLA1, 2, 4, 7, 8
TEMLAAll mediastinal stations except station 9
Anterior mediastinotomy (Chamberlain)5, 6 — aortopulmonary window (left-sided tumours)
EBUS-TBNA2, 4, 7, 10, 11, 12 — real-time ultrasound-guided
EUS-FNA7, 8, 9 — complementary to EBUS for posterior/inferior stations

Treatment — early stage NSCLC (Stage I and II)

Surgical resection is the standard of care for resectable stage I and II NSCLC with confirmed N0 or N1 disease and adequate cardiopulmonary reserve.

Resection principles

  • Anatomical resection (lobectomy or segmentectomy) is superior to wedge excision — higher local control, better survival
  • Systematic mediastinal lymph node dissection (SMLND) — minimum 6 stations (3 N2 + 3 N1)
  • VATS is the preferred approach — equivalent oncological outcomes with reduced morbidity, shorter length of stay
  • R0 resection (clear margins) is the primary surgical goal — R1 or R2 resections carry significantly worse prognosis
  • 5-year survival after R0 resection: approximately 60–80% for stage I, 40–50% for stage II
Cardiopulmonary fitness for resection

Predicted post-operative FEV1 (ppoFEV1) and DLCO are the primary functional parameters. ppoFEV1 >40% predicted and ppoDLCO >40% predicted are generally safe thresholds for lobectomy. For borderline patients, cardiopulmonary exercise testing (VO2 max) provides additional risk stratification.

Adjuvant therapy after resection

Indications for adjuvant chemotherapy and targeted therapy after R0 resection depend on stage, molecular profile, and comorbidities. Refer to current ESMO or NCCN guidelines.

Treatment — locally advanced NSCLC (Stage III)

Stage III NSCLC is a heterogeneous group — from resectable N2 disease (IIIA) to unresectable bulky mediastinal or contralateral nodal disease (IIIB/IIIC). Multidisciplinary team discussion is essential for every stage III patient before any treatment is initiated.

Resectable N2 disease (Stage IIIA)

For selected patients with single-station, non-bulky N2 disease identified pre-operatively:

  1. Induction concurrent chemoradiotherapy (CRT) — platinum-based doublet chemotherapy with concurrent thoracic radiotherapy, typically 45–50 Gy over 5–6 weeks
  2. Reassessment at 4–6 weeks — re-staging CT and PET-CT; mediastinoscopy if initial staging was by CT/PET only
  3. Surgery if R0 resection feasible — lobectomy preferred over pneumonectomy; pneumonectomy after induction CRT carries prohibitive mortality (>20%) and should be avoided where possible
  4. Adjuvant therapy — continuation of systemic therapy per multidisciplinary decision
Surgical note — post-induction resection

Surgery after induction CRT carries increased risk: obliterated tissue planes, friable vessels, bronchial stump healing compromise, and impaired respiratory reserve. Sleeve resections should be approached with extreme caution after radiotherapy. Bronchial stump reinforcement with vascularised tissue is mandatory. These operations should be performed only in high-volume centres.

Unresectable Stage III (IIIB / IIIC)

Standard of care is definitive concurrent chemoradiotherapy followed by consolidation immunotherapy. Surgery does not have a role. Refer to current ESMO/NCCN guidelines for systemic therapy protocols.

Current guidelines — locally advanced NSCLC

Treatment protocols for stage III NSCLC are evolving rapidly with immunotherapy consolidation agents. For current recommendations, refer to ESMO Locally Advanced NSCLC guidelines and NCCN guidelines.

Pancoast tumour (superior sulcus tumour)

A primary lung tumour located in the apex of the lung involving the chest wall at the superior sulcus, typically invading the first rib, lower brachial plexus (C8–T2), and often the subclavian vessels and sympathetic chain. Accounts for <5% of all lung cancers.

Pancoast syndrome

The classic triad: shoulder and arm pain radiating along the ulnar nerve distribution (C8–T1); ipsilateral Horner's syndrome (ptosis, miosis, anhidrosis — sympathetic chain involvement); wasting of small muscles of the hand (T1 involvement). Not all Pancoast tumours produce the full syndrome.

Treatment

Resectable Pancoast tumours are treated with induction concurrent CRT (as per locally advanced protocol above) followed by en-bloc resection — the apex of the chest wall, involved rib(s), vertebral body if involved, and the involved portion of the lower trunk of the brachial plexus. The standard resection is a posterior approach (Shaw-Paulson) or anterior transcervical approach (Dartevelle) depending on the extent of vascular involvement.

  • Absolute contraindications: N2/N3 nodal disease, distant metastases, >50% vertebral body involvement, involvement of brachial plexus above C8
  • 5-year survival after complete (R0) resection: approximately 30–45%
Further reading

All clinical content should be verified against current guidelines before clinical application. This resource is intended for revision and educational purposes only.

Standard textbooks

  • Shields TW, LoCicero J, Reed CE, Feins RH. General Thoracic Surgery. 7th ed. Lippincott Williams & Wilkins.
  • Sellke FW, del Nido PJ, Swanson SJ. Sabiston & Spencer Surgery of the Chest. 9th ed. Elsevier.
  • Pearson FG, et al. Thoracic Surgery. 3rd ed. Churchill Livingstone.

Current guidelines & resources