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Clinical presentations of lung cancer. By: Khaled Zamzam MD, FCCP Head of chest dept. Air Force Hospital.

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clinical presentations of lung cancer

Clinical presentations of lung cancer


KhaledZamzam MD, FCCP

Head of chest dept.

Air Force Hospital


The history and physical examination is an important initial step in evaluating patients with suspected lung cancer as it usually will uncover important informationregarding a patient’s stage of disease and prognosis and associated medical complications of the underlying cancer.


The clinical presentation of lung cancer usually relates to the development of a new, or worsening of a preexisting clinical symptom or sign and, less frequently, to an abnormal CXR shadow in an asymptomatic patient.

  • More than 90% of patients with lung cancer are symptomatic at presentation.

Patients who present with symptoms at the time of diagnosis have a far worse outcome than those who do not.


Resectable lung cancer will seldom be diagnosed based on the medical history.

  • Approximately 50% of patients will have demonstrable metastatic lesions or evidence of unresectabilityat the time of the first diagnosis.

Further testing will reveal that another 15% are unresectable.

  • Finally, another 5 to 10% of patients will be found to be unresectable at surgery.
  • Thus, only 25 to 30% of cases are potentially curable by surgery.

Physical examination findings usually parallel the symptoms.

  • The physical examination will become positive only late in the course of the disease.
  • If the first clue to the diagnosis comes from the physical examination, it is probably too late to expect any chance for a cure.
  • Is by far the most common presenting symptom in patients with lung cancer (75%).
  • Is usually mildly productive or even dry.
  • In some patients it may present as paroxysmal, while in a minority, those affected by a secretory bronchoalveolar carcinoma may be associated with bronchorrhea, and shortness of breath out of proportion to the radiographic findings.

Most patients also present with a chronic productive cough due to chronic bronchitis, and in these patients the initial manifestation of lung cancer development is a change in the character of cough or the appearance of blood tinged sputum.

  • In 60% of cases.
  • A recent appearance of dyspnea on exertion or even at rest may be related to the central (trachea or main bronchus) development of lung cancer and in this case is commonly associated with wheeze.
  • However, dyspnea may be due to a variety of factors, including:


  • Atelectasis,
  • Postobstructivepneumonia,
  • Pleural effusion,
  • Pulmonary embolus,
  • Lymphangiticspread.
  • Arrhythmia or
  • Tamponaderesulting from pericardial effusion.
  • In 35% of cases.
  • Is rarely severe.
  • Is an important sign in smokers.
  • If related to the development of lung cancer, is usually associated with abnormal CXR.
  • However, in the case of normal CXR, further diagnostic examinations are mandatory in the high risk patient including, CT, bronchoscopy and repetitive sputum cytology.

It may also be due to:

    • Invasion of a large mediastinal vessel including, the pulmonary artery itself or one of its branches.
    • Obstructive pneumonia.
    • Pulmonary embolism and infarction.
  • The tumouritself causes low grade fever, due to release of pyrogenic cytokines such as: IL-6, TNF-α.
  • Obstructive pneumonia: many cases are sterile and the inflammatory reaction that leads to parenchymal consolidation is presumably due to retained secretions. However, the occurrence of fever is usually due to secondary infection. If pneumonia reoccurs in the same side in a high risk patient is very suspicious of occult lung cancer.
chest pain
Chest pain:
  • Pleural involvement: stitching.
  • Chest wall involvement: dull aching.
  • In 18% of cases.
  • May result from vocal cord paralysis in patients with mediastinal disease affecting the recurrent laryngeal nerve.
  • occasionally, patients with massive mediastinal disease may develop bilateral vocal cord paralysis, resulting in stridor due to upper airway obstruction.

According to Pancost’s classic description, a lung cancer at a definitve location at the thoracic inlet produces constant & characteristic phenomena of pain in the 8th & 1st & 2nd thoracic trunk distribution, & Horner’s syndrome.


Pancosttumour is quite consistantly a lung cancer, however other malignancies as well as inflammatory &infectious diseases (are rare etiologic conditions) that develop peripherally at the apex of the upper lobes, at or near the superior pulmonary sulcus.

common rare conditions causing pancost s syndrome
Common & rare conditions causing Pancost’s syndrome:
  • Neoplasms:
    • Lung cancer.
    • Adenoid cystic carcinoma.
    • Haemangiopericytoma.
    • Mesothlioma.
    • Plasmacytoma.
    • Lymphomatoidgranulomatosis.
    • Lymphoma – non-Hodgkin.
    • Thyroid carcinoma.
    • Metastatic neoplasms.


    • Staphylococcus aureus, Pseudomonas aeruginosa.
    • Tuberculosis.
    • Nocardiosis, Actinomycosis.
    • Hydatid cyst.
    • Pasteurellamultocida.
    • Mucoromycosis, asegilloma. Cryptococcus neformans.
    • Mycotic aneurysm.


    • Cervical rib syndrome.
    • Thyroid cyst.
    • Amyloidoma.
    • Smpathetic dystrophy.

Constrained by the narrow confines of the thoracic inlet, the developing carcinoma invades the lymphatics of the endothoracic fascia and involves by direct extension one or more of the following structures:

    • The lower roots of the brachial plexus.
    • The intercostal nerves.
    • The stellate ganglion.
    • The sympathetic chain.
    • Adjacent ribs & vertebrae.

It’s initial clinical picture is pain localized to the shoulder & the vertebral border of the scapula.

  • Later the pain extends down the arm towards the elbow, along the distribution of the ulnar nerve (T1 nerve root involvement) and subsequently to the ulnar surface of the forearm and the small ring finger of the hand.

Weakness & atrophy of the muscles of the hand supervenes, as well as the loss of the triceps reflex.

  • When the lung cancer invades the sympathetic chain and the stellate ganglion, Horner’s syndrome (enophthalmos, meiosis, ptosis, & anhidrosis) develops on the ipsilateral side of the face.

Adjacent bone involvement increases the severity of the pain.

  • Invasion of the spinal canal & spinal cord leads to spinal cord compression syndrome.

The vast majority of superior sulcus tumours are due to NSCLC & can be staged as T3N0M0 ( stage IIB) or higher.

  • T3 refers to the direct invasion of the chest wall.
  • T4 refers to the direct invasion of the mediastinum, great vessels, the eosophagus, the trachea, vertebral body, or the heart.

CXR: homogenous opacty in left lung apex.

  • CT: osteolysis of the adjacent rib.
  • MRI: infiltration of the lower scalene muscle & brachial plexus.

The SVC is a 6–8cm long, thin-walled, low-pressure vessel that drains venous blood from the head, neck, upper extremities, and upper thorax to the heart.

  • It extends from the junction of the right & left innominate veins to the right atrium.

It is located in the middle mediastinum and is surrounded by:

    • The sternum.
    • Trachea.
    • Right bronchus.
    • Aorta.
    • Pulmonary artery.
    • Perihilar & paratracheal L.N.

Several space-occupying lesions in the middle mediastinum may compress or invade the vessel, leading to blood flow reduction or complete obstruction.

  • In such conditions, intravascular thrombosis quite constantly coexists.

SVC syndrome is the clinical syndrome that results from the homonymous vessel obstruction or the severe reduction of venous return from the head, neck, & upper ext.remities.

common rare conditions causing svc syndrome
Common & rare conditions causing SVC syndrome:
  • Neoplasms:
    • Lung cancer (70%).
    • Lymphomas, non-Hodgkin or Hodgkin.
    • Metastatic cancers.
    • Teratoma, Hamartoma, cystic hygroma, thymoma.
    • Thyroid carcinoma.
    • Choriocarcinoma,
    • Aparaganglioma, neurogenic tumour, Schwannoma.
    • Melanoma, lymphocytic leukemia


    • Tuberculosis.
    • Histoplasmosis.
    • Syphilis.
    • Aspergillosis.
    • HIV infection.
    • Actinomycosis & Nocardiosis.
    • Klebsiellapneumoniae.
    • Hydatid cyst.

Vascular conditions:

    • Thromboembolism.
    • Catheter related: e.g., pacemakers, defibrillators.
    • Pericarditis.
    • Aortic aneurysm, right sunclavian aneurysm, innominate artey aneurysm.
    • Budd – Chiarisyndrome..
    • Behcet’s disease.
    • Vasculitis.
    • A-V fistulas.
    • Leucocytoclasticvasculitis.
    • Heparin induced thrombosis.
    • Thoracic outlet syndrome.


    • Fibrosingmediastinitis.
    • Encapsulated pleural effusion.
    • Sarcoidosis.
    • Cystic fibrosis.
    • Retrosternal goitre.
    • Postsurgery.

Clinically, it presents with head, facial, neck, upper thorax, and upper extremity edema and venous distension.

  • Headache, cyanosis, and the formation of an extensive collateral circulation.
  • Bending forward or lying down aggravates symptoms & signs.
  • Laryngeal edema and in severe cases, stuper and coma may ensue.

Because of the localization of the causative process in the mediastinum, SVC syndrome may coexist with other mediastinal syndromes such as, dysphagia, vocal horseness, & dyspnea due to large airway obstruction.

  • the obstruction develops slowly, allowing the development of a collateral venous system that is evident at the time of the physical examination.

The severity of the SVC syndrome depends upon the therapidity of occlusion and collateral vessel development.

  • Collateral venous return to the heart, in the case of obstruction, occurs through 4 principal pathways:

The azygos venous system: Azygos vein, Hemiazygos vein, & the connecting intercostal veins.

  • The internal mammary venous system: plus the tributaries and the secondary communications to the superior & inferior epigastric veins.
  • & 4)The long thoracic venous system and its connections to the femoral & vertebral veins, respectively.

In the absence of tracheal compression and airway compromise, it is rarely an oncologic emergency.

  • In the majority of cases there is enough time to obtain an etiological diagnosis and decide upon adequate & specific management.
  • Chemotherapy & radiotherapy are effective in relieving symptoms in lung cancer-related SVC syndromes.
  • The insertion of stents may provide a more rapid relief.

CXR: Opacity in the right upper lobe with extensive basis in mediastinum

  • CT( contrast enhanced): Mass compressess & circumscribes the SVC, also evident the azygos dilatation.

Sequential venous angiograms, before (left), during (middle, PRESTENT), and , after placement of the stent (right, POSTSTENT)


Compression, entrapment, or invasion of the recurrent laryngeal nerve by the primary cancer or its nodal metastases around the aortic arch, leads to horseness.

  • Horseness is an uncommon sign at presentation & appears late in the natural history of the disease.

Recurrent laryngeal nerve palsy predisposes to lung aspiration and is associated with ineffective ability to cough and expectorate.

  • Rarely, recurrent laryngeal nerve palsy manifests with dysphagia both for solids & liquid foods, since this nerve contributes to the innervation of the cricoid muscles & the proximal esophagus.

Neoplastic involvement can also affect the phrenic nerve.

  • Clinically, phrenic nerve palsy may be asymptomatic in patients with good respiratory reserve, or may manifest with dyspnea on exertion or even at rest in the respiratory compromized patient.

Lung cancer is the leading cause of malignant pleural effusion. A pleural effusion is observed in 15% of patients at their first evaluation.

  • However, during the course of the disease at least 50% of patients with diseminated disease will develop a pleural effusion.
direct mechanisms
Direct mechanisms:
  • Pleural metastatic involvement, inducing increased pleural permeability.
  • Pleural lymphatic obstruction by metastases, decreasing pleural fluid drainage.
  • The mediastinal LN involvement that also leads to decrease pleural lymphatic drainage.
  • The thoracic duct interruption that leads to chylothorax.
  • Large bronchial obstruction leads to atelectasis, decreasing intrapleural pressure, thus increasing fluid formation.
indirect mechanisms
Indirect mechanisms:
  • Hypoproteinemia.
  • Postobstructive pneumonitis.
  • Pulmonary embolism.
  • Postradiation therapy.

The most common sites of metastasis of lung cancer are:

    • The adrenal glands,
    • Liver,
    • Central nervous system (CNS), and
    • Bone.

Adrenal metastases are quite common in patients with (NSCLC) but rather uncommon in patients with (SCLC).

  • Adrenal metastases are rarely symptomatic, are not typically associated with any findings on physical examination, and are usually only discovered on routine radiographic studies (chest radiography and CT of the chest).

Occasionally, however, massive adrenal metastases can cause flank pain. In addition, patients with advanced bilateral adrenal metastases may develop symptoms of adrenal insufficiency.


Liver metastases occur frequently in patients with lung cancer, more commonly with SCLC than with NSCLC.

  • The symptoms of hepatic metastases may include jaundice and right upper quadrant pain associated with the findings of hepatomegaly and liver tenderness on examination.

However, these findings usually occur only in patients with very advanced liver disease.

  • More commonly, hepatic metastases present with less specific symptoms, such as anorexia, malaise, and weight loss.

Metastases to the CNS are commonly seen in both SCLC and NSCLC (particularly adenocarcinoma).

  • While CNS metastases are often asymptomatic and discovered only incidentally during radiographic evaluation, there are certainly many symptoms and physical findings related to CNS involvement that the clinician should be attuned to when doing the baseline history and physical examination.

Symptoms of brain metastases may include:

    • headache,
    • Altered mental status,
    • Seizure,
    • Nausea and vomiting,
    • Focal motor or sensory deficits,
    • Cranial nerve palsies, and
    • Cerebellar symptoms, such as ataxia.

Another form of CNS metastasis from lung cancer is involvement of the spinal cord.

  • This may occur in the form of spinal cord compression (usually due to direct extension of vertebral body metastases into the spinal canal), intramedullary metastases (relatively uncommon), or leptomeningeal seeding of the spinal canal.

Spinal cord compression and intramedullary metastases are rarely asymptomatic and should be identified rapidly as they constitute neurological emergencies necessitating immediate treatment.


About 90% of patients complain of back pain—either localized or radicular—as their first symptom.

  • At diagnosis, about 75% of patients will note muscle weakness, and 50% will have associated sensory loss below the level of the metastasis.

Bowel or bladder incontinence is another less common symptom of cord compression.

  • On physical examination, patients with spinal cord compression typically have back tenderness at the site of metastasis.

Other associated findings on physical examination may include:

    • Sensory loss or paresis below the level of the metastasis,
    • Decrease in anal sphincter tone,
    • Muscle spasticity, and
    • Abnormal deep tendon reflexes.

Leptomeningeal metastases are most commonly seen with adenocarcinoma of the lung.

  • Symptoms and physical findings associated with this relatively uncommon complication may include:
    • Headache, seizure, altered mental status, cranial nerve deficits (typically involving multiple nerves bilaterally), radicular pain, and incontinence.

Skeletal metastases occur in about one third of patients with lung cancer.

  • Patients with bone metastases often complain of pain and are found to have bone tenderness on physical examination.

Many patients, however, may be asymptomatic, with this finding discovered incidentally on a routine bone scan or because of elevated alkaline phosphatase levels or hypercalcemia.

  • Bone marrow involvement, which may occur with SCLC but is uncommon with NSCLC, may result in nonspecific symptoms of fatigue.