dr magdi sasi

8/11/2019 DR MAGDI SASI

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1 BRONCHOGENIC CARCINOMA BY DR MAGDI AWAD SASI 2014

BRONCHOGENIC CARCINOMA

ESSENTIAL FOR DIAGNOSIS:

New cough or change in chronic coughDyspnea , haemoptysis ,anorexia

New or enlarging mass , persistant infiltration , atelectasis or pleural effusion on

CXR

Male ; smoker ;age 40 years

Cytological finding on sputum ,pleural fluid ,biopsy

RISK FACTORS

Cigarette smoking 90% male ; 80% female---critical in the history

A familial predisposition is recognized

Increased risk in COPD ,sarcoidosis , pulmonary fibrosis , sclerodermaEnvironmental risk factors:

Asbestosis (( pipe lagging ;electrical wire insulation ))

Chromium

Arsenic

Iron oxides

Radon gas


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HISTOLOGY:

1. SCLC==small cell lung cancer 25%

Prone to early haematogenous spread ;rarely amenable to surgery

2. NSCLC==nonsmall cell lung cancer

Early disease may be cured resection; spread slowly

Squamous cell ca.--- 25%--- centrally located and spread slowly

Adenocarcinoma ----40%---peripheral nodule or mass

Small cell ca. ------20%--- begins centrally and infiltrate submucosa

Large cell ca.-------10%---peripheral or central

Brocchoalveolar cell ca.----spreads intraalveolar

DIFFERENTIAL DIAGNOSIS:

1. Pneumonia

2. Tuberculosis

3. Lymphoma

4. Metastatic carcinoma

5. Sarcoidosis

6. Foreign body aspiration

7. Benign carcinoid tumour

SIGNS AND SYMPTOMS:

75%--90% are symptomatic at the time of diagnosis.

The presentation depends on:

1. Type of tumour

2. Location of tumour

3. Extent of spread

4. Presence of paraneoplastic syndrome

A. Chest symptoms:

Cough --- new onset or change of the quality and severity of cough in s

smoker who used to have a chronic cough.

Haemoptysis---30%

Dyspnea --------60%


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Chest pain------ 40% from bony metastasis or pleural involvement .

LOCAL SPREAD----preesure by the mass over the surrounding structures or

spread to them----from the lymph node 2ry or the mass causing

endobronchial obstruction and postobstructive pneumonia (( unresolving

or recurrent )) .Lung cancer is one of the causes of unresolving pneumonia

or persistent lung opacity in smoker male 50yr.

B. Pressure symptoms:

Esophagus ---dysphagia

Trachea ---- stridor , change of the voice , hoarsness

Recurrent laryngeal nerve----- hoarsness of voice

C. Superior vena cava obstruction:

Caused by partial or complete obstruction of SVC.

C/F

Swelling of the face and neck

Headache ,dizziness ,syncope

Visual disturbance

Facial flushing

Dilated anterior chest wall veins or collateral veins

Brawny eodema

Cyanosis of the face and arms Bending over or laying down accentuates symptoms.

D/D OF SVC OBSTRUCTION:

1. Superior mediastinal tumors:

Lung ca. , thyroid ca. ,thymoma ,lymphoma ,teratoma , angiosarcoma

2. Aneurysm of the aortic arch

3. Chronic fibrotic mediastinitis---TB ,histoplasmosis ,pyogenic ,methysergide.

4. Constrictive pericarditis

5. Thrombophlebitis 2ry to CVL or pacemaker wire.

For diagnosis:

HISTORY / EXAMINATION

CT SCAN / MRA

CONTRAST VENOGRAPHY


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TREATMENT OF SVC:

1) Surgery

2) Chemotherapy

3) External beam radiation

4) Endovascular stenting

5) Venous angioplasty or bypassHorners syndrome-----pancoasts tumour:

Pancoasttumorsare lung cancers that begin at the top of the right or left lung and

invade the chest wall. They are also called superior sulcustumors . Apical lung

cancer with invasion of cervical sympathetic chain plexus resulting in:

1. Miosis (( constricted pupil ))

2. Enophthalmos (( sunken eye ))

3. Partial ptosis

4. Ipsilateral loss of sweating (( anhidrosis))

Pancoast tumor causes shoulder ,arm pain (( brachial plexus )) , C8T2 invasion.

Pain in the shoulder, radiating down the upper inner arm, can be the first sign of a

Pancoast tumor. The patient may have Hoarse of voice or bovine cough with

unilateral recurrent laryngeal nerve palsy and vocal cord paralysis.

D. The patient may present with evidence of metastasis to other systems


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Brainsevere headache of recent onset in elder smoker male, convulsion

in a patient above age of 40y with lung opacity in smoker , coma ,gradual

onset of limb weakness of month duration in elder male smoker.

Liver --- vague abdominal pain ,abdominal mass , jaundice.

Adrenal ---lose of weight and apetite with hypoglycemia .

E. Paraneoplastic syndrome:A paraneoplastic syndrome is adisease orsymptom that is the consequence ofcancer in

the body but, unlikemass effect,is not due to the local presence of cancer cells. These

phenomena are mediated byhumoral factors (byhormones orcytokines)excreted by

tumor cells or by animmune response against thetumor.Paraneoplastic syndromes are

typical among middle aged to older patients, and they most commonly present with

cancers of thelung,breast,ovaries or lympSMALL CELL CARCINOMAhatic system

(alymphoma).Sometimes the symptoms of paraneoplastic syndromes show before the

diagnosis of amalignancy,which has been hypothesized to relate to the disease

pathogenesis.

Commonly seen in small cell lung carcinoma. The patient will show dysfunction of the

central nervous system and endocrine system with out metastasis.

A. ENDOCRINE---

Small cell carcinoma 1.Cushing syndrome---biochemicallow K

2.SIADH

3.Hyperaldosteronism

Squamous carcinoma 1.Hypercalcemia

2.Hyperparathyrodism--Parathyroid hormone-related protein),TGF-,TNF,IL-1[7]

Bronchial adenoma --

Carcinoid syndrome

B. NEUROLOGICAL-1. Peripheral neuropathy

2. Subacute sensory neuropathy

3. Guillain-Barr syndrome

4. Eaton-Lambert syndrome

5. Subacute cerebellar degeneration

6. Encephalitis

7. Subacute necrotizing myelopathy

8. Dermatomyositis

9. Subacute motor neuronopathy

1.Peripheral neuropathy is the most common neurologic paraneoplastic syndrome. It is usually adistal sensorimotor polyneuropathy that causes mild motor weakness, sensory loss, and absent

distal reflexes.

2.Subacute sensory neuropathy is a more specific but rare peripheral neuropathy. Dorsal root

ganglia degeneration and progressive sensory loss with ataxia but little motor weakness develop;

the disorder may be disabling. Anti-Hu, an autoantibody, is found in the serum of some patients

with lung cancer. There is no treatment .
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3.Guillain-Barr syndrome, another ascending peripheral neuropathy, is a rare finding in the

general population and probably more common in patients with Hodgkin lymphoma.

4.Eaton-Lambert syndrome is an immune-mediated, myasthenia-like syndrome with weakness

usually affecting the limbs and sparing ocular and bulbar muscles. It is presynaptic, resulting

from impaired release of acetylcholine from nerve terminals. An IgG antibody is involved. The

syndrome can precede, occur with, or develop after the diagnosis of cancer. It occurs mostcommonly in men with intrathoracic tumors (70% have small or oat cell lung carcinoma).

Symptoms and signs include fatigability, weakness, pain in proximal limb muscles, peripheral

paresthesias, dry mouth, erectile dysfunction, and ptosis. Deep tendon reflexes are reduced or

lost. The diagnosis is confirmed by finding an incremental response to repetitive nerve

stimulation: Amplitude of the compound muscle action potential increases > 200% at rates > 10

Hz. Treatment is first directed at the underlying cancer and sometimes induces

remission. Guanidine (initially 125 mg po qid, gradually increased to a maximum of 35 mg/kg),

which facilitates acetylcholine release, often lessens symptoms but may depress bone marrow

and liver function. Corticosteroids and plasma exchange benefit some patients .

5.Subacute cerebellar degeneration causes progressive bilateral leg and arm ataxia, dysarthria,and sometimes vertigo and diplopia. Neurologic signs may include dementia with or without brain

stem signs, ophthalmoplegia, nystagmus, and extensor plantar signs, with prominent dysarthria

and arm involvement. Cerebellar degeneration usually progresses over weeks to months, often

causing profound disability. Cerebellar degeneration may precede the discovery of the cancer by

weeks to years. Anti-Yo, a circulating autoantibody, is found in the serum or CSF of some

patients, especially women with breast or ovarian cancer. MRI or CT may show cerebellar atrophy,

especially late in the disease. Characteristic pathologic changes include widespread loss of

Purkinje cells and lymphocytic cuffing of deep blood vessels. CSF occasionally has mild

lymphocytic pleocytosis. Treatment is nonspecific, but some improvement may follow successful

cancer therapy.

6.Encephalitis may occur as a paraneoplastic syndrome, taking several different forms,

depending on the area of the brain involved.

1. Global encephalitis has been proposed to explain the encephalopathy that occurs most

commonly in small cell lung cancer.

2. Limbic encephalitis is characterized by anxiety and depression, leading to memory loss,

agitation, confusion, hallucinations, and behavioral abnormalities.

Anti-Hu antibodies, directed against RNA binding proteins, may be present in the serum

and spinal fluid. MRI may disclose areas of increased contrast uptake and edema .

7.Subacute necrotizing myelopathy is a rare syndrome in which rapid ascending sensory and

motor loss occurs in gray and white matter of the spinal cord, leading to paraplegia. MRI helps


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rule out epidural compression from metastatic tumora much more common cause of rapidly

progressive spinal cord dysfunction in patients with cancer. MRI may show necrosis in the spinal

cord.

C. Hypertrophic osteoarthropathy is prominent with certain lung cancers and manifests aspainful swelling of the joints (knees, ankles, wrists, elbows, metacarpophalangeal joints) with

effusion and sometimes fingertip clubbing.

SIGNS:

Cachexia , Anemia ,Lymphadenopathysuparclavicular and axillary ,clubbing .

Ptosis with atrophy of small muscles of hand on the same side , enophthalmos if apical

Chest ---- may be normal , or signs of consolidation ,or pleural effusion or collapse

Situation in which lung cancer should be a high suspicion:

1. Unexplained unilateral pleural effusion of 2 month in elder smoker

2. Unresolving signs of lung consolidation of 1 month duration

INVESTIGATION:

Routine --- CBC ,RFT ,LFT, BLOOD SUGER ,S. CALCIUM , LDH ,ALP

CBC--- complete blood count

RFT ----renal function test

LFT----liver function test

LDH---lactic dehydrogenase

ALP----alkaline phosphokinase

1. Sputum cytology---highly specific but insensitive

2. Serum tumor markers ----are neither sensitive nor specific

3. Tissue or cytology specimen is needed for diagnosis.

Tissue diagnosis may not necessary prior to surgery in some cases where the

lesion is enlarging or the patient will undergo Surgical resection regardless of the

outcome of biopsy

4. Pulmonary function tests are required in all NSLC patients prior to surgery.

Preoperative FEV1 2 L is adequate to undergo surgery.

Estimate of postresection FEV1 is needed if 2L preoperative.


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5. Imaging studies

Nearly all patients have abnormal findings on CXR or CT SCAN

Pleural effusion

Peripheral circular opacity

Hilar adenopathy and mediastinal thickening (( squamous))Infiltrates single or multiple nodules (( alveolar))

Central or peripheral masses ((large cell))

Consolidation

Lung collapse

Bony secondaries


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CT scan of chest through the adrenal glands :

May not be necessary if patient has obvious M1 disease

IV iodine contrast enhancement is not essential but is recommended in probable

mediastinal invasion.

Is the most important modality in staging to determine the resectibility of thetumour.

For staging ,Brain MRI , Abdominal CT or radionuclide bone scanning should be

targeted to symptoms and signs.

Recommended tests for selected patients:

1. Ultra sound liver/CT liver with contrast

Abnormal clinical evaluation

Increased LFT

Abnormal non contrast CT


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2. MRI brain /CT brain with contrast

CNS symptoms

Abnormal clinically

3. Radionuclide bone scan

Increase ALP

Increase calciumBony pain

4. Pulmonary function test

Lung resection

Thoracic radiotherapy

5. Quantative radionuclide perfusion

Lung scan or exercise testing to evaluate maximum o2 consumption.

DIAGNOSTIC PROCEDURES:

1. Bronchoscopy---tissue diagnosis(10%90%) and operability

2. Percutaneous fine needle aspiration---sensitivity 50%--90% for peripheral lesionsand superficial lymph nodes.

3. Thoracocentesis can be diagnostic in malignant effusion ((65%))

4. Thoracoscopy ---is preferred to pleural biopsy if pleural fluid cytology non

diagnostic after two thoracocentensis

5. Mediastinoscopy

Treatment SUMMARY:NSCLC

Excision is the treatment of choice for peripheral tumors with no metastatic

spread stage I / II 25%Curative radiotherapy is an alternative if respiratory reserve poor

Chemotherapy and radiotherapyfor more advanced disease.

It is staged with TNM international staging system.

SCLC

Are nearly always disseminated at presentation

They may respond to chemotherapy

SATGING OF THE LUNG CANCER:

T---PRIMARY TUMOUR

T0----no evidence of primary tumourTx----malignant cells in the bronchial secretion but not visualized

Tis--- carcinoma in situ

T1---- 3cm , surrounded by lung or visceral pleura ,in lobar or more distal airway

T2 --- 3cm , or any size either involves a main bronchus 2 cm distal to the

carina , OR any size invades the visceral pleura , OR has associated atelectasis ,

obstructive pneumonitis extending to the hilum but not all the lung.


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T3---- any size with direct extension into the chest wall ,diaphragm ,mediastinal

pleura ,parietal pericardium , OR tumor in the main bronchus 2cm distal to

carina with out involving the carina , OR atelectasis or obstructive pneumonitis

involving the entire lung

T4---- any size , with invasion of mediastinum ,heart ,great vessels ,trachea

,oesophagus , vertebral body , carina or malignant effusion ((pleura&pericardium))Or satellite tumor nodules within the ipsilateral lobe of the lung.

N----REGINAL NODES

Nx---------------------------cant be assessed

No---------------------------none involved mediastinoscopy

N1--------------------------- peribrochial / ipsilateral hilum / both

N2---------------------------I-mediastinal /subcarinal

N3-------------------------- contralateral mediastinal/ hilum /supraclavicular (ips/contra)

M----DISTANT METASTASIS

Mo--------------none

M1--------------present

STAGE TUMOUR LYMPHNODE

METASTASISsurvival

I.Tis, T1 or T2

Limited local disease NO MO 74%

II.

T1 // T2

T3Limited local diseae w ipsilateral hilar/locally invasive

N1

N0

MO 55%

MO 39%

III aT3T1---T3

Limited local disease w perbronchial/locally with invasive subcarinal

N1N2

MO 22%MO

III bT1-----T4

T4Contralateral LN ,supraclavicular,malignant effusion

N3N0---N2

MOMO

IV

T1-----T4

Distant metastases No-N3 M1


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TREATMENT:

NON SMALL CELL LUNG CANCER (( NSCLC))

A. Stage I / II ------------------------ cured surgically

B. Stage III A ------------------------ may benefit from surgery( multimodal protocols)

C. Stage III B ------------------------ resection surgery after multimodal protocols

D. Stage IV ------------------------- palliative

Neo adjuvant chemotherapy

1. Administration in advance of surgery / radiation therapy

2. Widely used in stage III A and III B

Adjuvant chemotherapy

a) Administration of drugs following surgery / radiotherapy

b) Stage III A // III B who cantbe treated surgically

c) Multidrug platinum based therapy shows a trend toward improved survival in I and IIe


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STAGE IIA STAGE IIB


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STAGE III A


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STAGE III B

STAGE IV

Performance status & symptom control in stage III B & IV may be improved by chemotherapy.

Pleural drainage and pleurodesis

For symptomatic pleural effusion


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Palliative--- radiotherapy=== external beam : used for

a) Bronchial obstruction

b) SVC obstruction

c) Haemoptysis

d) Bony pain

e) Brain metastasis

SVC OBSTRUCTION------- Dexamethazone , Radiotherapy , SVC stent

Endobronchial therapy-------

a) Tracheal stenting

b) Cryotherapy

c) Laser

d) Brachytherapy (( radioactive source ))

Chemotherapy in SCLC:

Limited stage disease ------------------ cisplatin/ etoposide 50%--70%complete response

Extensive disease ------------------ cisplatin / etoposide 15%--40% complete response

Remissions last 6---8 months

Median survival 4 months after recurrence to

a) Cyclophosphamde + Doxorubicin + Vincristin +Etopsideb) Cisplatin + radiotherapy

PROGNOSIS:

NSCLC 50% 2yr with out spread

10% 2yr with spread

SCLC 3 months if untreated

1 year if treated

DRUGS MAY BE USED:

Codeine Bronchodilator analgesics steroids antidepresent


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OTHER OPTIONS OF TREATMENT:

1.Laser therapy

2.Cryosurgery

3.Photodynamic therapy

4.Electrotherapy

5.Biological therapy---targeted therapy

They includeerlotinib (Tarceva),gefitinib (Iressa),crizotinib (Xalkori) andafatinib (Giotrif).
http://www.cancerresearchuk.org/cancer-help/type/lung-cancer/treatment/biological-therapy-for-lung-cancer#erlotinibhttp://www.cancerresearchuk.org/cancer-help/type/lung-cancer/treatment/biological-therapy-for-lung-cancer#gefitinibhttp://www.cancerresearchuk.org/cancer-help/type/lung-cancer/treatment/biological-therapy-for-lung-cancer#crizotinibhttp://www.cancerresearchuk.org/cancer-help/type/lung-cancer/treatment/ssLINK/afatinibhttp://www.cancerresearchuk.org/cancer-help/type/lung-cancer/treatment/ssLINK/afatinibhttp://www.cancerresearchuk.org/cancer-help/type/lung-cancer/treatment/biological-therapy-for-lung-cancer#crizotinibhttp://www.cancerresearchuk.org/cancer-help/type/lung-cancer/treatment/biological-therapy-for-lung-cancer#gefitinibhttp://www.cancerresearchuk.org/cancer-help/type/lung-cancer/treatment/biological-therapy-for-lung-cancer#erlotinib


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