This tumour originates from the basal cell layer of the bronchial wall. What is it all about?
The disease is much more common in the western world and the highest prevalence has been reported from Scotland. In Asia also the number of cases reported is steadily increasing and bronchogenic carcinoma accounts for 0.12-0.13% of all medical admissions in the major general hospitals.
The role of external factors such as carcinogens derived from cigarette smoke, and from atmospheric pollution in the pathogenesis has been established by several epidemiological studies. In addition to cigarette smoke, exposure to several substances such as 3, 4 benzpyrene from automobile smokes, asbestos, nickel chromate, arsenic, vinyl chloride, Uranium and radioactive materials increase the risk of developing pulmonary cancer. Among these the most widely investigated factor is cigarette smoking. Cigarettes and to a less extent beedies, considerably increase the risk of developing bronchogenic carcinoma. especially the squamous and large cell types. Adenocarcinoma and small cell carcinomas do not show this relationship. Smoking more than 20 cigarettes dialy for 20 years or more, increases the risk of developing bronchogenic carcinoma 8-10 times above that of non-smokers. Cigar and pipe-smoking is less and the components of the paper have been found to increase the risk cumulatively. Both inhalation of smoke exhaled by others in a closed environment, are found to be harmful. Incidence in males is 10-15 times more than that in females. The disease is most frequent in the fifth and sixth decades.
The lesion may be epidermoid carcinoma (50-60%), undifferentiated carcinomas (small and large cell types 30-40%) and adenocarcinoma (5-10%). One variety of adenocarcinoma is bronchiolo-alveolar cell carcinoma. In some tumours both epidermoid and adenocarcinomatous patterns are seen. Around 50% of tumors are situated centrally proximal to a segmental bronchus, and the rest upper lobe. In some cases adenocarcinoma may supervene on areas of infarction or scars of tuberculosis. Lung tumours have been staged, taking into account the size, location, local effects, local lymphadenopathy and distant metastases.
In many cases a long latent period may elapse before the tumour produces symptoms. Sometimes the radiological abnormality may be the finding that draws attention. In some cases metastases are the first to produce symptoms. Clinical features may be described as;
1. intrathoracic manifestations
2. symptoms due to metastases, and
3. paraneoplastic syndromes.
General symptomatology includes nonspecific manifestations such as tiredness, anorexia, weight loss, clubbing of fingers and toes, fever and pulmonary osteoarthropathy.
Cough due to irritation of the bronchus may be troublesome, interfering with sleep. In the chronic smoker, this is likely to be mistaken for cough due to excessive smoking. Hemoptysis occurs in many cases. Bleeding may be from the tumour or from other pulmonary complications. The tumour may block the bronchus and lead to obstructive symptoms like unilateral or localized wheezing, atelectasis, recurrent Pneumonia or Lung abscess. Further complications like Pleurisy or empyema may be evident. At times the obstruction to the bronchus becomes valvular and the affected segment undergoes localized emphysema. In some cases, a peripheral tumour undergoes central liquefaction and abscess formation.
Tumour of the apical region or the lung may invade the pleura, the brachial plexus and the cervical sympathetic chain. In most cases the tumour is a squamous cell carcinoma and this is called “Pancoast’s tumours” or superior sulcus tumour. Involvement of the brachial plexus leads to intense neuralgic pain along the arm. Paralysis of the sympathetic chain gives rise to ipsilateral Horner’s syndrome.
Malignant pleural effusion may develop due to spread to the pleura. At times, the tumour may grown along the pleural surface resulting in pleural thickening. The hilar lymph nodes are enlarged. Mediastinal glands may be affected and enlargement of these structures gives rise to mediastinal syndrome. Compression of the phrenic nerve gives rise to diaphragmatic paralysis. Malignant pericardial effusion may develop. Direct spread to the ribs may lead to their destruction.
Physical examination of the chest may reveal signs of consolidation, cavitation, atelectasis, or pleural effusion. Enlargement of pretracheal and scalene lymph nodes and recent onset of finger should suggest the possibility of malignancy.
Widespread secondaries may occur in the liver, bone, adrenal glands, brain, kidney, spleen, peritoneum, skin, and other organs manifestations caused by metastases may be presenting features in many. For example, late onset seizures of a pathological fracture may be the first evidence of bronchogenic neoplasm.
Bronchogenic carcinoma may lead to paraneoplastic syndromes since the tumour may elaborate several hormones or allied substances. Well- known endocrine presentations include hypercalcemia, syndrome of inappropriate ADH secretion, Cushing’s syndrome, carcinoid syndrome, and feminization in makes. Neuro-muscular manifestations like proximal myopathy, myasthenic syndrome (Eaton- Lambert), peripheral neuropathy, and cortical cerebella myositis, Polyarthritis, thrombocytopenic purpura, myelophthisic anemia, leukemoid reaction, red cell aplasia, and secondary polycythemia may develop in rare cases.