CA Pluca Nemikrocel

7/27/2019 CA Pluca Nemikrocel

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Non-small cell lung cancerHighlights

SummaryOverview

Basics

Definition

Epidemiology

Aetiology

PathophysiologyClassification

Prevention

Primary

Screening

Secondary

DiagnosisHistory & examination

Tests

Differential

Step-by-step

Criteria

GuidelinesCase history

Treatment

Details

Step-by-step
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Emerging

Guidelines

Evidence

Follow UpRecommendations

Complications

Prognosis

Resources

References

Patient leafletsCredits

Email

Print

Feedback

Share

Add to PortfolioBookmark

Add notes

History & exam

Key factors presence of risk factors cough dyspnoea haemoptysis chest pain
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weight loss

Other diagnostic factors age 65 to 70 years male sex fatigue hoarseness confusion personality changes

nausea and vomiting headache dysphagia bone pain and/or fractures weakness, paraesthesias and/or pain in C8/T1

distribution pulmonary exam abnormalities seizures cervical or supraclavicular adenopathy Horner's syndrome facial swelling dilated neck or chest/abdominal wall veins finger clubbing hypertrophic osteoarthropathy

History & exam details

Diagnostic tests
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1st tests to order chest x-ray chest CT scan

Tests to consider sputum cytology bronchoscopy biopsy pleural sampling mediastinoscopy video-assisted thoracoscopic surgery (VATS) thoracentesis MRI or CT of brain MRI of thoracic inlet PET-CT

bone scan contrast-enhanced CT liver and adrenals PFT FBC LFTs serum calcium

electrolytes and renal function EGFR mutation testing

Diagnostic tests details

Treatment details
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Ongoing

stage I and II

surgical candidateo surgery preoperative chemoradiotherapyo postoperative chemotherapyo postoperative radiotherapy non-surgical candidateo radiotherapy

o

chemotherapy

stage IIIA

surgical candidateo preoperative chemotherapy or

chemoradiationo

surgeryo postoperative chemotherapy, radiotherapy, or

chemoradiation non-surgical candidateo radiotherapyo chemotherapy

stage IIIB

resectable with no contralateral mediastinaladenopathy

o preoperative chemotherapy + preoperativeradiotherapy


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o surgeryo postoperative chemotherapy unresectable or contralateral mediastinal

adenopathyo chemoradiation

stage IV

ECOG performance 0-2 (in bed 50% of the

time)o supportive care

Treatment details

Summary The most common form of lung cancer, and

comprises 3 major subtypes: adenocarcinoma,squamous cell carcinoma, and large cell carcinoma.

Most common in older adult smokers and ex-smokers. Small tumours in the lung are often

asymptomatic, so the majority of patients either havelocally advanced or metastatic disease at diagnosis.

Most common presenting symptoms are cough,chest pain, haemoptysis, dyspnoea, and weight loss.
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A suspicious lung mass can be biopsied duringbronchoscopy or using CT guidance. Staging studies(i.e., CT, PET, mediastinal sampling) are required to

determine extent of local or regional disease and toevaluate for metastases. Treatment depends on stage of disease and

patient comorbidities. Surgery, radiotherapy andchemotherapy are the most common modalities, buttargeted biological agents are becoming increasinglyimportant.

DefinitionLung cancer comprises a group of malignant epithelial tumours arising fromcells lining the lower respiratory tract. Lung cancer is divided into 2categories: non-small cell lung cancer (NSCLC) and small cell lung cancer.NSCLC accounts for more than 85% of all lung cancers.[1] There are 3 maintypes of NSCLC (adenocarcinoma, squamous cell carcinoma and large cellcarcinoma) and these are grouped into further subtypes.

EpidemiologyWorldwide, lung cancer is the most common non-cutaneous cancer and isincreasing at a rate of 0.5% per year. Globally, lung cancer accounts for overa million deaths a year and remains the most common cause of cancermortality worldwide, with 17.6% of the world total.[7] [8]Lung cancer is thethird most common cancer type in Europe, with NSCLC accounting for 80%of all lung cancer cases.[8] [9]Incidence and mortality figures vary widely but appear to correlate withtobacco use. In 2000, worldwide smoking is estimated to have caused 85% of

lung cancer in men and 47% of lung cancer in women, with the highest ratesin Europe and North America.[7] In the US, lung cancer rates increaseddramatically during the mid-1900s, a few decades following the rapid rise intobacco use. Recent declines in the incidence rate of lung cancer may relateto reductions in tobacco use in more recent decades. The incidence of lungcancer in men began to decline in the 1980s. The incidence of lung cancer inwomen began to decline over 10 years later, in the late 1990s. The decliningincidence of lung cancer has decreased the overall mortality rate. Between
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1994 and 2002, the annual percentage decline in the age-adjusted mortalityrate in men and women in the US was 0.9%.[10]Almost half of cases arenow seen in developing countries, where mortality rates are also slightlyhigher.[7] In the US, one quarter of the population still smoke, indicating thatlung cancer will continue as an important public health issue.

Lung cancer is also the leading cause of cancer mortality in the US. Anestimated 174,470 people were diagnosed and 162,460 died from lungcancer in the US in 2006.[10] The number of deaths from lung cancer ismore than colorectal, breast, and prostate cancers combined.[10]Afteradjusting for age, the incidence of lung cancer is about 60% higher in men.

According to the US National Cancer Institute's Surveillance Epidemiologyand End Results (SEER) registry, lung cancer incidence rates are highest inblack people and non-Hispanic white people and lowest in Native Americans,Hispanics and Asian/Pacific Islanders.[11]

EpidemiologyWorldwide, lung cancer is the most common non-cutaneous cancer and isincreasing at a rate of 0.5% per year. Globally, lung cancer accounts for overa million deaths a year and remains the most common cause of cancermortality worldwide, with 17.6% of the world total.[7] [8]Lung cancer is thethird most common cancer type in Europe, with NSCLC accounting for 80%of all lung cancer cases.[8] [9]Incidence and mortality figures vary widely but appear to correlate withtobacco use. In 2000, worldwide smoking is estimated to have caused 85% oflung cancer in men and 47% of lung cancer in women, with the highest ratesin Europe and North America.[7] In the US, lung cancer rates increaseddramatically during the mid-1900s, a few decades following the rapid rise intobacco use. Recent declines in the incidence rate of lung cancer may relateto reductions in tobacco use in more recent decades. The incidence of lungcancer in men began to decline in the 1980s. The incidence of lung cancer inwomen began to decline over 10 years later, in the late 1990s. The decliningincidence of lung cancer has decreased the overall mortality rate. Between1994 and 2002, the annual percentage decline in the age-adjusted mortalityrate in men and women in the US was 0.9%.[10]Almost half of cases arenow seen in developing countries, where mortality rates are also slightlyhigher.[7] In the US, one quarter of the population still smoke, indicating thatlung cancer will continue as an important public health issue.Lung cancer is also the leading cause of cancer mortality in the US. Anestimated 174,470 people were diagnosed and 162,460 died from lungcancer in the US in 2006.[10] The number of deaths from lung cancer is
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more than colorectal, breast, and prostate cancers combined.[10]Afteradjusting for age, the incidence of lung cancer is about 60% higher in men.

According to the US National Cancer Institute's Surveillance Epidemiologyand End Results (SEER) registry, lung cancer incidence rates are highest inblack people and non-Hispanic white people and lowest in Native Americans,

Hispanics and Asian/Pacific Islanders.[11]

PathophysiologyThe 3 major subtypes of NSCLC are squamous cell carcinoma,adenocarcinoma and large cell carcinoma. Approximately 32% of NSCLC areadenocarcinomas, which tend to be located more peripherally in thelung.[17] The relative frequency of adenocarcinoma is rising and is currentlythe most common histology in women and non-smokers.[18]Adenocarcinomas are thought to metastasise early.

Approximately 30% of lung cancers are squamous cell carcinomas, whichtend to involve the central airways. As compared with adenocarcinomas,squamous cell carcinomas are thought to metastasise later in the diseasecourse. Large cell carcinomas, accounting for about 10% of lung cancers, areundifferentiated tumours without histological features typical of a squamouscell or adenocarcinoma and tend to arise centrally.[17]A rare subset ofpoorly differentiated NSCLC is sarcomatoid carcinoma.[19]Bronchioloalveolar carcinoma (BAC) is a rare lesion, characterised by thegrowth of tumour cells along the surface of alveolar walls - so-called lepidic

growth - with no evidence of tissue destruction or invasion.[20]As such it isbest considered adenocarcinoma-in-situ (AIS), since lesions fulfilling theWHO definition of BAC show no evidence of invasion and patients withcomplete surgical resection have 100% 5-year survival.[21] [22] Lesions thatshow tissue invasion but also a component of lepidic spread should not becalled BAC but instead are considered to be adenocarcinomas (with a lepidiccomponent). Multi-focal lesions showing a lepidic growth pattern may occur.Some of these patients will have multiple synchronous AIS and, usually, atleast one associated adenocarcinoma.[23] Other cases probably representlepidic spread of otherwise invasive adenocarcinoma. Most of these casesshow mucinous adenocarcinoma (also known as mucinous BAC) and maymimic pneumonic consolidation rather than present as a typical solitarypulmonary nodule.[23]
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ClassificationThe 1999 World Health Organization/International Association for the

Study of Lung Cancer histological classification of lung and

pleural tumors[2]NSCLC:

1.3.1. Squamous cell carcinoma

1.3.1.1. Papillary

1.3.1.2. Clear cell

1.3.1.3. Small cell

1.3.1.4. Basaloid

1.3.3. Adenocarcinoma

1.3.3.1. Acinar

1.3.3.2. Papillary

1.3.3.3. Bronchioloalveolar carcinoma

o 1.3.3.3.1. Non-mucinous (Clara/pneumocytetype II)

o 1.3.3.3.2. Mucinous
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o 1.3.3.3.3. Mixed mucinous and non-mucinousor intermediate cell type

1.3.3.4. Solid adenocarcinoma with mucin

1.3.3.5. Adenocarcinoma with mixed subtypes

1.3.3.6. Variants

o

1.3.3.6.1. Well-differentiated fetaladenocarcinoma

o 1.3.3.6.2. Mucinous ('colloid')adenocarcinoma

o 1.3.3.6.3. Mucinous cystadenocarcinoma

o 1.3.3.6.4. Signet ring adenocarcinoma

o 1.3.3.6.5. Clear cell adenocarcinoma

1.3.4. Large cell carcinoma

1.3.4.1. Large cell neuroendocrine carcinoma

o 1.3.4.1.1. Combined large cellneuroendocrine carcinoma


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1.3.4.2. Basaloid carcinoma

1.3.4.3. Lymphoepithelioma-like carcinoma

1.3.4.4. Clear cell carcinoma

1.3.4.5. Large cell carcinoma with rhabdoidphenotype

1.3.5. Adenosquamous carcinoma

1.3.6. Carcinomas with pleomorphic, sarcomatoid or sarcomatous elements

1.3.6.1. Carcinomas with spindle and/or giantcells

o

1.3.6.1.1. Pleomorphic carcinoma

o 1.3.6.1.2. Spindle cell carcinoma

o 1.3.6.1.3. Giant cell carcinoma

1.3.6.2. Carcinosarcoma

1.3.6.3. Pulmonary blastoma

1.3.6.4. Others


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Small cell lung cancer:

1.3.2. Small cell carcinoma

o 1.3.2.1. Combined small cell carcinoma

Primary preventionPatients should be asked about current smoking status on each presentationto medical care. Smokers should be educated about the health risks ofsmoking and advised to quit. Multiple options (non-pharmacological andpharmacological) are available to assist patients with smoking cessation.

ScreeningScreening for lung cancer is not recommended. To date there is no class Ievidence (randomised trials) demonstrating a survival benefit with screening,with either chest x-ray or spiral CT.[61] [62] [63] The US National LungScreening Trial, sponsored by the National Cancer Institute, randomlyassigned 50,000 smokers or former smokers to annual screening with chest

x-ray or spiral CT. The study opened in 2002 and closed in 2004.[64]Apreliminary report (November 2010) demonstrated a 20% reduction in lungcancer mortality,[65] which was confirmed in the final paper.[66]

Secondary preventionSmoking cessation should be encouraged, even in patients with establishedlung cancer. There is evidence that there is a survival benefit in all lungcancer patient groups in those who stop smoking, and (especially wherelong-term survival is the aim of treatment, as in surgical resection) this shouldbe considered an essential element of the management.[120]

MonitoringAfter potentially curative treatment for lung cancer, patients should befollowed regularly to assess for disease recurrence and treatment-relatedtoxicity. For example, following radiotherapy patients may developinflammation of the lung, termed pneumonitis. This is rarely lethal but mayrequire treatment. Chemotherapy can depress blood counts, leading to
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anaemia with fatigue and dyspnoea, thrombocytopenia (bleeding) and/orneutropenia (infection). Blood counts need to be monitored until they recover.

A history and physical examination should be performed every 4 to 6 monthsfor the first 2 years and annually thereafter. Imaging of the chest (chest x-rayor CT) should be performed on a similar schedule.

For patients with metastatic disease who have completed palliativechemotherapy and/or radiotherapy, similar follow-up is recommended.Routine imaging in the absence of symptoms is generally discouraged.

Complications

Complicationhide all

post-obstructive pneumonia/hypoxia

see our comprehensive coverage of Overview of pne

Pneumonia is common in lung cancer patients and icentral, obstructing tumour. Patients may not presenpneumonia such as fever, dyspnoea, and productive

sometimes be difficult to interpret secondary to tumo

Antibiotics should be initiated. Relieving the obstructmodalities can be used such as external beam radio(temporary insertion of a radioactive source at the siplacement, laser debulking of obstructing tumour, ph

surgical resection. Photodynamic therapy is a miniminvolves the interaction of light, a photosensitising agphotosensitising agent is administered intravenouslythroughout the body. Via a flexible fibre bronchoscoppredetermined wavelength is focused on the endobr
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photosensitising agent absorbs photons of the approreactive oxygen species that are toxic to cancer cells

Treatment should be instituted relatively quickly for pcompromise.

superior vena cava syndrome (SVCS)

The most common cause of SVCS is lung cancer. B

medial extension of a right upper lobe tumour can co(SVC), impeding the return of blood from the face ancollateral pathways develop when the SVC is comprof symptoms depend on the speed of obstruction. Thfacial and upper extremity oedema, dyspnoea, cougexamination demonstrates facial plethora and distenoccasionally abdominal wall veins.[5]SVCS is rarely a medical emergency and every effodiagnosis before initiating therapy. Supplemental oxoften helpful. Treatment depends on the clinical scepatients will improve with radiotherapy and/or chemotake several days. Patients with marked symptoms srelatively quickly. Endovascular stents may be effect

relief. Surgical intervention is rarely required.[5]

paraneoplastic syndromes

Treatment of the underlying tumour often alleviates s
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syndromes. Other supportive measures depend on t

Last updated: Mar 08Prognosis

SurvivalSurvival after definitive treatment of NSCLC depends principally on stage ofdisease and ability to undergo standard treatment. Patients with adverseprognostic factors, including poor performance status and pretreatmentweight loss, have a worse prognosis irrespective of treatment.

Patients whose tumours are resected, usually with sampling of draininglymph nodes, are assigned a pathological stage. Pathological stage is moreaccurate than clinical stage, as clinical stage relies on radiographic imagingthat has a finite sensitivity and specificity. Comparing outcomes (survival) ofpatients who are staged surgically with patients who are staged clinically isdifficult for multiple reasons. Many of the medical contraindications thatprohibit surgery, such as older age, poor performance status, severe

concurrent medical illness and poor pulmonary function, are independentprognostic factors for survival. Furthermore, surgical upstaging (e.g., findingcancer in lymph nodes that appeared uninvolved by preoperative imaging) isknown to occur in more than 20% to 25% of patients with clinical stage Idisease.[115]With these caveats, the 5-year survival rates for patients undergoing surgical(pathological) staging are as follows: stage IA: 67%; stage IB: 57%; stage IIA:55%; stage IIB: 39%; and stage IIIA: 23% to 25%.[119] Survival for clinicallystaged patients is as follows: stage IA: 61%; stage IB: 38%; stage IIA: 34%;

stage IIB: 22% to 24%; stage IIIA: 9% to 13%; stage IIIB: 3% to 7%; andstage IV: 1%.

Case historyA 65-year-old man presents with a 2-month history of a dry persistent coughand 4.5 kg unintentional weight loss. He denies fevers, dyspnoea, sorethroat, rhinorrhoea, chest pain or haemoptysis. Medical history is significantfor COPD and hypertension. Family history is non-contributory. He smoked 1
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pack of cigarettes daily for 40 years but quit 5 years ago. No adenopathy ispalpable on examination and breath sounds are diminished globally withoutfocal wheezes or crackles.

Other presentationsLung cancer can present without symptoms. This is possibly due to the largefunctional reserve of the lungs and lack of pain fibres within the lungparenchyma. Consequently, lung cancer can present as an incidental masson chest x-ray or CT. Eventually, patients develop symptoms from localtumour growth within the lung, including cough, dyspnoea, chest pain and/orhaemoptysis.[3] [4] Haemoptysis typically consists of blood-tinged sputum.Massive haemoptysis is rare. Invasion of the pleura or chest wall can causechest pain. Obstruction of major airways can cause dyspnoea, wheezing or

post-obstructive pneumonia. A pneumonia that does not rapidly clear withantibiotics is cause for concern for lung cancer, especially in patients with atobacco history.Lung cancer often spreads to mediastinal lymph nodes. Symptoms frommediastinal adenopathy are relatively rare. However, bulky adenopathy cancause hoarseness (impingement of the recurrent laryngeal nerve), paralysisof the diaphragm (impingement of the phrenic nerve), difficulty swallowing(impingement of the oesophagus) or superior vena cava syndrome, typicallycharacterised by upper extremity and facial oedema, orthopnoea, cough and

venous distension of the neck and chest wall.[5]Lung cancer can also present as a superior sulcus tumour (sometimes calleda Pancoast tumour), most commonly presenting with shoulder pain.[6] Thesetumours may also compress and invade the brachial plexus (causingweakness and/or atrophy of the intrinsic muscles of the hand, paraesthesiasand/or pain in a C8/T1 distribution) or sympathetic chain (causing Horner'ssyndrome characterised by ptosis, meiosis and ipsilateral anhidrosis). Otherpresentations include clubbing, hypertrophic osteoarthropathy andhypercalcaemia of malignancy.

Differential diagnosisCondition Differentiating signs/symptoms
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Small cell lung cancer Typical features include co

haemoptysis, chest pain, dhoarseness (if recurrent la

paralysis). Frequently unwshort of breath, with signs weight loss.

Finger clubbing and hyperosteoarthropathy may be p

less common in small cell compared with NSCLC.

Usually wheezing from undor bronchial obstruction, crpost-obstructive pneumon

or diminished breath sounbronchial obstruction are pearly disease.

Facial and upper extremitydistended neck veins, andcollateral vessels may indicompression of the superio

Features related to distant(e.g., bone pain and/or pat


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fractures from bony metasconfusion, personality chaweakness, focal neurologi

nausea and vomiting, and from brain metastases).

Brachial plexus involvemeweakness and/or atrophy omuscles of the hand and p

and/or pain in a C8/T1 distimpact the sympathetic chHorner's syndrome (ptosisipsilateral anhidrosis).

Metastatic cancer

Symptoms will relate to theprimary tumour and there symptoms of pain, weight cough, dyspnoea, clubbingwheezing. Physical findingnot be present depending stage of tumour.


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Pneumonia/bronchitis Clinical and radiological fe

bronchitis or pneumonia shwith appropriate treatment

Recurrent pneumonia or bsmoker or former smoker ssuspicion of lung cancer.

Organising pneumonia

(cryptogenic organising

pneumonia orbronchiolitis obliterans

organising pneumonia)

Normally presents as an inillness followed by a secon

lasting 1 to 4 months, withfever, non-productive cougdyspnoea, and weight lossfeatures pleuritic chest pai


22/101

haemoptysis.

In most patients, auscultat

fine, dry lung crepitations. is unusual.


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Pulmonary tuberculosis Cough longer than 2 to 3 wdiscoloured or bloody sputsweats and weight loss, lopleuritic chest pain.


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Sarcoidosis Cough, dyspnoea, fatigue,

fever, night sweats, rash, ephotophobia, blurred visionPulmonary examination is unrevealing. Can affect anphysical findings depend o


25/101

organs affected. Skin lesiomaculopapular eruptions, snodular lesions and red-pu

lesions.

Infectious granuloma History may include travel areas, pet/animal exposurleisure activities (e.g., cavi


26/101

May feature cough, dyspnhaemoptysis, weight loss, aches, skin lesions and nig

Many possible causes: Hiscapsulatum, Mycobacteriutuberculosis,Coccidioidesimmitis, Cryptococcusneoformans,Aspergillus, Pa boydii, Fusarium spp, zy

and others. Non-specific skin findings

atypical mycobacteria andcryptococcosis. Lymphadeactive disease.


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Amyloidosis Weight loss, paraesthesias

and fatigue are the most csymptoms associated withand are common to all sysweight loss of >9 kg is com

vessel involvement can caclaudication, calf and limb and, rarely, angina. Amylopresent in around 1 in 6 paperiorbital. Eyelid petechiaHepatomegaly >5 cm belocostal margin is seen in 10

and splenomegaly is usuadegree.


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Rheumatoid arthritis Arthralgias, pain, skin nod

effusions, pleuritis, joint padeformity.


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Wegener's

granulomatosis Cough, chest pain, dyspno

haemoptysis, rhinorrhoea,ear/sinus pain, hoarsenessanorexia, weight loss, palp

painful ulcers, uveitis, uppinflammation, and sinus pa


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Non-Hodgkin's

lymphoma Aggressive NHL lymphom

with fever, drenching nightmalaise, weight loss, coug

breath, abdominal discomfchange in mental status, dataxia, pleural effusion,lymphadenopathy, pallor, pjaundice, hepatomegaly, sskin nodules, and abnormaexam. Low-grade NHL patminimally symptomatic or
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Hodgkin's lymphoma Predominantly a disease o

Most patients present withmonth history of persistent

most commonly of the cerv

Carcinoid tumour Often asymptomatic with n

examination. May cause cdyspnoea, haemoptysis, uwheezing, or post-obstructif tumour is endobronchial.


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Tracheal tumours Common symptoms includ

cough, haemoptysis, wheeLess commonly, hoarsenedysphagia may be present


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Thyroid mass Symptoms and signs depe

mass. May be visible/palpa

anterior aspect of neck. Madysphagia, hoarseness, dibreathing and pain in neckalso be signs and symptomhypothyroidism dependingof the mass.


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Hamartoma Usually asymptomatic with

findings. About 1% to 20%be endobronchial and can dyspnoea, wheezing or rec

infections, secondary to aiobstruction.

Arteriovenousmalformation (AVM)

Dyspnoea is uncommon. Mhaemoptysis, pulmonary barteriovenous communicathaemorrhagic telangiectas


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mucous membranes and oCyanosis and finger clubbNeurological symptoms fro

aneurysms, cerebral embo

Bronchogenic cyst Usually diagnosed in infan

childhood, although 50% d15 years of age. Approximpatients are asymptomaticchest pain (often pleuritic) (due to oesophageal comp


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the most common symptomfeature recurrent cough aninfection/pneumonia, supe

syndrome, tracheal comprpneumothorax.

Thymoma/thymic

carcinoma Approximately 30% of pati

thymoma are asymptomatdiagnosis. May also presechest pain, signs of upper congestion, superior vena syndrome, dysphagia or hohave features of paraneop


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syndromes associated withincluding myasthenia gravlupus erythematosus, rheu

arthritis, thyroiditis and Sjosyndrome. Around 30% ofsymptoms suggestive of mgravis (e.g., ptosis, double

Germ cell tumour Occur mostly in men aged

About one third of patientsasymptomatic. Symptoms the size of the lesion. Maypain, breathing problems, fever, headache and fatigu


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History & examinationKey diagnostic factorshide allpresence of risk factors (common)

Includes cigarette smoking; exposure to tobacco

smoke, radon gas, or asbestos; and the presenceof COPD.

cough (common)


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A new or persistent cough, especially in a currentor former smoker, is suspicious and requiresimaging of the chest.

Cough is present at diagnosis in over 50% ofpatients with lung cancer and may be secondaryto post-obstructive pneumonia, endobronchialtumour or pleural effusion.[4]

dyspnoea (common) Present at diagnosis in the majority of

patients.[3] Possible causes include tumour obstruction of the

airway, underlying COPD, pneumonia, phrenicnerve paralysis or a pleural effusion.

haemoptysis (common) Occurs in approximately 25% of patients.[4] Although massive haemoptysis is rare, patients

with lung cancer often cough up blood-tingedsputum. Haemoptysis in a smoker is suspiciousfor lung cancer.

chest pain (common) Chest pain or discomfort is present in

approximately 33% of patients.[4]

The lung is devoid of pain fibres. Therefore, mostpatients with chest pain have tumours invadingthe pleura or chest wall. However, even patientswith early disease can present with chestdiscomfort. Shoulder pain is the most common
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symptom in patients with superior sulcustumours.[6]

weight loss (common)

Independent negative prognostic factor andshould be specifically addressed. It is morecommon in patients with locally advanced ormetastatic disease. Most clinical trials defineclinically relevant weight loss as >5%.[41] [42]

Other diagnostic factorshide all

age 65 to 70 years (common) The median age of patients with lung cancer is 65

to 70 years. Less than 10% of cases arediagnosed before 50 years of age.[39]

male sex (common) More common in men, but the age-standardised

male-to-female incidence ratio for white patients

is decreasing and is currently approximately 1.6(60% higher in men).[39]

fatigue (common) Non-specific symptom of lung cancer, and is

often multi-factorial.pulmonary exam abnormalities (common)

Auscultation of the lungs may demonstratewheeze, crackles, decreased breath sounds, anddullness to percussion.

hoarseness (uncommon)
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2% to 18% can present with hoarseness,secondary to recurrent laryngeal nerveparalysis.[4]

confusion (uncommon) A common symptom of brain metastases and

electrolyte disturbances such as hypercalcaemiaand hyponatraemia. Up to 25% of patients withlung cancer develop brain metastases.[40]

personality changes (uncommon) Strongly suspicious of brain metastases in those

affected with lung cancer.nausea and vomiting (uncommon)

May indicate brain metastases.headache (uncommon)

May indicate brain metastases.dysphagia (uncommon)

May occur if the tumour itself or enlargedmediastinal lymph nodes have significantlyimpinged on the oesophagus.

bone pain and/or fractures (uncommon) Pain or pathological fractures can result from

bone metastases. The axial skeleton and

proximal long bones are most frequentlyinvolved.[4]weakness, paraesthesias and/or pain in C8/T1distribution(uncommon)
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Superior sulcus tumours can invade the brachialplexus causing weakness and/or atrophy of theintrinsic muscles of the hand, and paraesthesias

and/or pain in a C8/T1 distribution.seizures (uncommon) A symptom of brain metastases.

cervical or supraclavicularadenopathy (uncommon)

The most common sites of regional spread arethe hilum and mediastinum. The next echelon of

lymph node spread is the supraclavicular fossaeand cervical chains. In a proportion of cases thesupraclavicular lymphadenopathy is impalpable,but detectable by ultrasound examination of theneck.[43]

Horner's syndrome (uncommon) Triad of ptosis, meiosis and ipsilateral anhidrosis

occurs most frequently in patients with superiorsulcus tumours, which can invade thesympathetic plexus.

facial swelling (uncommon) May indicate compression of the superior vena

cava, either from mediastinal adenopathy or aright upper lobe tumour extending centrally intothe mediastinum.

dilated neck or chest/abdominal wallveins (uncommon)


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Distended neck veins or venous collaterals on thechest or abdominal wall may indicatecompression of the superior vena cava.

finger clubbing (uncommon) More common in NSCLC than in small cell lung

cancer.[44]hypertrophic osteoarthropathy (uncommon)

Painful arthropathy of the wrists, ankles, andknees with periosteal new bone formation. Morecommon in cases of adenocarcinoma.

Risk factorshide all

Strong

cigarette smoking There are numerous epidemiological studies

linking lung cancer and cigarettesmoking.[12] [13] [14]

Tobacco smoke contains multiple carcinogensincluding polynuclear aromatic hydrocarbons,aromatic amines, N-nitrosamines, and otherorganic and inorganic compounds.[16]

environmental tobacco exposure Environmental tobacco smoke (second-hand

smoke) is an important cause of lung cancer andapproximately 2% to 3% of lung cancer casesmay be attributed to it. In an analysis of 37published epidemiological studies, the relative
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risk of a non-smoking woman who has a smokinghusband being diagnosed with lung cancer was24% higher (relative risk 1.24) than a non-

smoking woman with a non-smokinghusband.[24]chronic obstructive pulmonary disease

There are numerous studies showing an excessrisk of lung cancer in patients with chronicobstructive pulmonary disease even when thesmoking history is corrected for. This excess risk

is variously estimated as between 2- and 6-foldand is higher the more severe the impairment ofthe FEV1.[25]

family history A history of lung cancer in a first degree relative

is associated with an approximate doubling of the

risk, independent of the smoking history.[26] Thisrelative risk is as high as 5-fold where thecancers develop in first degree relatives underthe age of 60 years.

radon gas exposure Uranium is normally found in the earth's crust.

Upon decay, radon gas is produced, which canpercolate into homes. Radon gas is inert butdecays with a half-life of 3.8 days into polonium214 and polonium 218. Both substances emitalpha-particles that damage DNA and can lead tomalignant transformation.
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Numerous case-control studies have associatedboth occupational (mining) and residential radonexposure to lung cancer. Radon may contribute

up to an estimated 10% of all lung cancercases.[27] [28]

Weak

asbestos exposure Asbestos fibres are carcinogens that lodge in the

lung and are a risk factor for lung cancer,especially in smokers and for heavily exposedpeople.[29]Epidemiological data have linkedasbestos with lung cancer, with or withoutasbestosis, a diffuse interstitial lung fibrosissecondary to asbestos exposure.[30]

Diagnostic tests1st tests to orderhide allTest

chest x-ray

A standard PA chest x-ray is an inexpensive and sim

pain and/or haemoptysis. In some centres a lateral c

In patients with diagnosed lung cancer, chest x-raysand evaluate for re-expansion of a collapsed lung af


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radiotherapy).

A chest x-ray is recommended on a routine basis (ev

thereafter) after definitive treatment of lung cancer.

chest CT scan

A new abnormality on chest x-ray needs to be furthescan including the upper abdomen.[45]A chest CT

especially smokers, with problematic symptoms raislung cancer, even if there is a normal chest x-ray. Indistinguish lymph nodes from vessels, especially in tTreatment recommendations often hinge on whetheoccurred. CT is non-invasive but has limitations. For60%, specificity is approximately 80%, positive predand negative predictive value is about 85%.[46] [47

After treatment, follow-up CT scans are occasionallytrials or where there is a genuine concern that there disease not easily evaluated on a simple chest x-ray

Tests to considerhide all

Test

sputum cytology

A non-invasive and relatively simple diagnostic methcentres. The specificity is high but the sensitivity is lo
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usefulness in terms of patient management.[32] Mowhich cannot be achieved with sputum cytology, canchemotherapy.

More likely to be positive with central lesions than w

bronchoscopy

Bronchoscopy, typically performed with a flexible broprocedure in which the proximal bronchial tree can b

areas biopsied.[48]Endobronchial masses can be biopsied with forcepsand alveolar lavage increase the diagnostic yield. Traccessible parenchymal lesions and mediastinal lymultrasound guidance can be done.[33] [36] [35] [34]Overall, the sensitivity for centrally located lesions isfor peripheral lesions is lower and depends on numb

proximity to the bronchial tree. In general, endobronbrushings or washings.Detection of small peripheral lesions (


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Transthoracic needle aspiration biopsy, typically usinsuspicious peripheral pulmonary lesions that are not

Transbronchial needle aspiration biopsy of accessiblymph nodes is also now widely practiced and can bendobronchial ultrasound guidance. The use of endonumber and levels of mediastinal nodes than can bealso be used to access other mediastinal nodes plus

Alternatively, lymph node biopsy can provide informof disease. Sampling is either of nodes in the supracaccessed via endobronchial ultrasound,[33] [34] [35(EUS)[51] or surgically via mediastinoscopy, video-aopen surgical procedure.

pleural sampling

Many patients present with a pleural effusion, and cygive sufficient material to obtain a cytological diagnobiopsy using Abram's or Cope's needles is of very limthoracoscopy (which can be either 'medical' or 'surg

mediastinoscopy

Treatment recommendations often hinge upon presenodes. Mediastinoscopy is considered the most senprocedure, and endobronchial ultrasound is often us
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involves a small horizontal incision in the low neck, tlymph nodes along the trachea and below the carinaperformed under general anaesthesia.

Paratracheal and subcarinal lymph nodes can be as

The overall sensitivity of cervical mediastinoscopy ispredictive value of about 90%.[47]

video-assisted thoracoscopic surgery (VATS)VATS can be used to evaluate aorticopulmonary winaccess to paraoesophageal and pulmonary ligamen

thoracentesis

Thoracentesis involves placing a needle between ththat has accumulated in the pleural space. Ultrasounsmall pleural effusions.

MRI or CT of brain

Patients with locally advanced NSCLC, especially ad

harbouring brain metastases and should be staged wcurative treatment is proposed.


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MRI of thoracic inlet

For patients with superior sulcus tumours, MRI of theassessing resectability.

PET-CT

PET-CT is complementary to CT, facilitating accuratregional, and distant disease.[52]

PET is considered a standard staging study for patieconfirmation of abnormal findings is often necessaryknown metastatic disease, PET is unnecessary.

The PET accuracy for mediastinal staging is as follo85%, specificity about 90%, positive predictive valuepredictive value approximately 93%.[46] [53]

bone scan

Should be ordered when patients have new bone pa

Not necessary if staging with PET is performed, whicscan.[54]Test sensitivity is between 60% and 100%. Specifici

contrast-enhanced CT liver and adrenals


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Chemotherapy, and to a lesser degree radiotherapynecessitating baseline and periodic analysis of blood

LFTs

May be elevated if hepatic metastases.

Lone elevation of alkaline phosphatase level may ind

serum calcium

Elevated in hypercalcaemia of malignancy, more co

electrolytes and renal function

Recommended as baseline before treatment is initia

Hyponatraemia may be related to the syndrome of inalthough this is more commonly seen in small cell lu

EGFR mutation testing

Testing for mutations of the tyrosine kinase gene thareceptor (EGFR) in tumour cells enables targeted thpatients.


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Step-by-step diagnostic approachPersistent cough with or without haemoptysis and weight loss in a smokerover the age of 50 are key features that should alert the clinician to thepossibility of lung cancer. However, lung cancer can present without

symptoms as an incidental mass on chest x-ray or CT.

HistorySymptoms of a primary tumour include cough, haemoptysis, chest painand/or dyspnoea. Some patients may present with hoarseness, secondary torecurrent laryngeal nerve paralysis. Patients may also present with non-specific symptoms such as weight loss or fatigue.

Smoking history, nutritional status and performance status (an objectiveassessment of the patient's ability to perform activities of daily living) shouldbe specifically addressed.

Most patients develop distant metastasis during the course of their disease.The most frequent sites of distant metastasis are the lungs, liver, brain, boneand adrenal glands. Symptoms depend on the sites and extent ofinvolvement. Pain or fractures can develop as a result of bone metastasis.

Lung cancer is the most common cause of brain metastasis.[31] Commonsymptoms include confusion, personality change, seizures, weakness, focalneurological deficits, nausea and vomiting, and headaches.

Physical examinationThe general appearance of the patient is important. The patient may appearunwell and short of breath, and have evidence of recent weight loss. Theneck and supraclavicular fossae should be carefully examined for

adenopathy. Finger clubbing and hypertrophic osteoarthropathy may bepresent.

Though the pulmonary examination is normal in some patients with early lungcancer, most present with 1 or more findings during auscultation. Thefollowing symptoms are common: wheezing from underlying COPD orbronchial obstruction; crackles due to post-obstructive pneumonia or


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atelectasis; and diminished breath sounds from bronchial obstruction, pleuraleffusion and/or COPD. Pleural effusions can be assessed with percussion ofthe lung fields, showing a characteristic dullness.

Facial and upper extremity swelling, distended neck veins and dilatedcollateral vessels on the chest or abdominal wall may indicate compression ofthe superior vena cava.

Superior sulcus tumours can invade the brachial plexus causing weaknessand/or atrophy of the intrinsic muscles of the hand, and paraesthesias and/orpain in a C8/T1 distribution. Additionally, these tumours can impact thesympathetic chain causing Horner's syndrome (ptosis, meiosis and ipsilateralanhidrosis).

InvestigationsSelecting the appropriate diagnostic and staging studies for an individualpatient is complex, and a multi-disciplinary team approach is recommended.This should include a thoracic surgeon, medical oncologist, radiationoncologist, respiratory physician, pathologist and diagnostic radiologist.Numerous imaging modalities are used to stage lung cancer, but not allstudies need be obtained on all patients.

A chest x-ray and contrast-enhanced CT of the chest and upper abdomen arestandard and help define the primary tumour and evaluate for regionalspread.

A standard PA chest x-ray is an inexpensive andsimple initial step to evaluate cough, chest pain

and/or haemoptysis. In some centres a lateral chestx-ray may be performed as well.

A new abnormality on chest x-ray needs to befurther assessed with contrast-enhanced CT. A chest


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CT should also be obtained in patients, especiallysmokers, with problematic symptoms and a normalchest x-ray.

Pathological confirmation of disease is of great importance before treatmentcan commence, although in some cases this is only finally established whenthe lesion is surgically resected. The choice of which test is used to gain atissue sample depends on the location of the lesion.

The simplest method is sputum cytology.However, although the specificity is high, the

sensitivity low, and the cost may outweigh theusefulness in terms of patient management.[32] Moreover, accurate histological analysis, whichcannot be achieved with sputum cytology, can nowaid in the selection of appropriate chemotherapy.Cytology is more likely to confirm the diagnosis in

central lesions than in peripheral lesions. More invasive but safe procedures include

flexible bronchoscopy and transthoracic needleaspiration biopsy.

Transbronchial needle aspiration biopsy of

accessible parenchymal lesions and mediastinallymph nodes is now widely practised and can becarried out with or without endobronchial ultrasoundguidance. The use of endobronchial ultrasoundexpands the number and levels of mediastinal nodes
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that can be sampled. Endoscopic ultrasound can alsobe used to access other mediastinal glands plus theleft adrenal gland.

Bronchoscopy is performed when CTabnormalities (e.g., a mass or adenopathy) areaccessible to the bronchoscope. Also used to assessnew and/or unexplained pulmonary symptoms (e.g.,haemoptysis, wheezing, cough). Flexiblebronchoscopy requires conscious sedation. During

the procedure, the tracheobronchial tree is carefullyexamined. Endobronchial tumours can be biopsied.Washings, brushings, and bronchoalveolar lavageare performed. Suspicious parenchymal lesions andmediastinal lymph nodes that are accessible can alsobe biopsied. Endobronchial ultrasound can also be

used to biopsy mediastinal lymph nodes and somesubmucosal tumours,[33] [34] which can provideinformation regarding tissue diagnosis and stage in asingle procedure.[35] [36]

Transthoracic needle aspiration biopsy is oftennecessary for peripheral lesions that are inaccessible

to bronchoscopy. If a pleural effusion exists,thoracentesis collects cells for cellular evaluation ofmalignancy, and CT-guided biopsy of the pleura ispossible in some patients. Ultrasound guidance isrecommended except in very large effusions.
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In some special situations, a patient can be treated for presumed cancer ifthe history, physical examination and radiological imaging (ideally PET-CT)are most consistent with cancer, and when a biopsy is not possible. However,this is a rare situation.

After a pathologic diagnosis is obtained, further staging studies are obtainedto guide appropriate treatment.

PET-CT is a valuable staging tool and helpsidentify occult regional and distant disease.

Although PET-CT is an effective modality tostage the mediastinum, tissue sampling of themediastinum via mediastinoscopy or endobronchialultrasound remains the most accurate method and isoften indicated.

Video-assisted thoracoscopic surgery (VATS)can be used to evaluate aorticopulmonary windowlymph nodes. VATS also allows access toparaoesophageal and pulmonary ligament lymphnodes.

A bone scan should be obtained if the patient has

new bone pain or the alkaline phosphatase iselevated, to determine presence of bone metastasis.However, if staging with PET is performed, the bonescan is unnecessary, as PET is more accurate.


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A head CT or MRI is indicated in patients withearly-stage NSCLC if brain metastases aresuspected based on symptoms. Patients with locally

advanced NSCLC, especially adenocarcinoma, are athigher risk of harbouring brain metastases andshould be staged with a head CT or MRI ifaggressive local therapy is recommended.

For patients with superior sulcus tumours, MRI ofthe thoracic inlet may be helpful in assessing

resectability, though high-quality multi-slice CTimaging is probably as good in most circumstances.

Pleural effusions are relatively common in lungcancer patients and portend a poor prognosis,approaching that of metastatic disease. Therefore,

pleural effusions need to be evaluated bythoracentesis if there is no other evidence ofmetastatic disease.

Ancillary studiesAn FBC, chemistry panel, and LFTs including alkaline phosphatase should beperformed in all patients as baseline tests before initiation of treatment and todetect paraneoplastic syndromes such as hypercalcaemia of malignancy,cancer-related anaemia and, rarely, ectopic ACTH secretion (Cushing'ssyndrome, resulting in hyperglycaemia and hypokalaemia). In metastaticdisease, alkaline phosphatase levels can be elevated, indicating potentialbone or liver metastases.


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All lung cancer patients anticipated to receive chest radiotherapy or surgeryshould have PFTs performed, including FEV1 and diffusing capacity of thelung for carbon monoxide.[37] [38]

Testing for mutations of the tyrosine kinase gene that encodes the epidermalgrowth factor receptor (EGFR) in tumour cells enables targeted therapy to be

considered in a subset of patients, particularly never-smokers and those withnon-squamous histology (i.e., adenocarcinoma and large cell carcinoma).

Click to view diagnostic guideline references.Diagnostic criteria

Non-small cell lung cancer UICC/IASLC staging (7th

edition, 2007)[58]The 6th edition[59] of the staging classification produced by the InternationalUnion Against Cancer (UICC) and adopted by the American Joint Committeeon Cancer (AJCC) has now been superseded by the staging classificationproduced by the UICC and the International Association for the Study of LungCancer (IASLC), 7th edition.[58]

The Eastern Cooperative Oncology Group (ECOG)

performance status[60]These scales and criteria are used by doctors and researchers to assess howa patient's disease is progressing and how the disease affects the daily livingabilities of the patient, and to determine appropriate treatment and prognosis:

Grade 0: fully active, able to carry on all pre-disease performance without restriction

Grade 1: restricted in physically strenuous activitybut ambulatory and able to carry out work of a light orsedentar

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