Bronchogenic carcinoma DR MAGDI SASI

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Bronchogenic carcinoma DR MAGDI SASI

  1. 1. 1 1 BRONCHOGENIC CARCINOMA BY DR MAGDI AWAD SASI 2014 BRONCHOGENIC CARCINOMA ESSENTIAL FOR DIAGNOSIS: New cough or change in chronic cough Dyspnea , 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 , scleroderma Environmental risk factors:  Asbestosis (( pipe lagging ;electrical wire insulation ))  Chromium  Arsenic  Iron oxides  Radon gas
  2. 2. 2 2 BRONCHOGENIC CARCINOMA BY DR MAGDI AWAD SASI 2014 HISTOLOGY: 1. SCLC==small cell lung cancer 25% Prone to early haematogenous spread ;rarely amenable to surgery 2. NSCLC==non—small 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%
  3. 3. 3 3 BRONCHOGENIC CARCINOMA BY DR MAGDI AWAD SASI 2014 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
  4. 4. 4 4 BRONCHOGENIC CARCINOMA BY DR MAGDI AWAD SASI 2014 TREATMENT OF SVC: 1) Surgery 2) Chemotherapy 3) External beam radiation 4) Endovascular stenting 5) Venous angioplasty or bypass Horners syndrome-----pancoasts tumour: Pancoast tumors are 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 )) , C8—T2 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
  5. 5. 5 5 BRONCHOGENIC CARCINOMA BY DR MAGDI AWAD SASI 2014 Brain – severe 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 a disease or symptom that is the consequence of cancer in the body but, unlike mass effect, is not due to the local presence of cancer cells. These phenomena are mediated by humoral factors (by hormones or cytokines) excreted by tumor cells or by an immune response against the tumor. Paraneoplastic syndromes are typical among middle aged to older patients, and they most commonly present with cancers of the lung, breast, ovaries or lympSMALL CELL CARCINOMAhatic system (a lymphoma). Sometimes the symptoms of paraneoplastic syndromes show before the diagnosis of a malignancy, 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---biochemical –low K 2.SIADH 3.Hyperaldosteronism Squamous carcinoma 1.Hypercalcemia 2.Hyperparathyrodism--Parathyroid hormone-related protein), TGF-α, TNF, IL-1[7] Bronchial adenoma -- Carcinoid syndrome B. NEUROLOGICAL- 1. Peripheral neuropathy 2. Subacute sensory neuropathy 3. Guillain-Barré 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 a distal 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.
  6. 6. 6 6 BRONCHOGENIC CARCINOMA BY DR MAGDI AWAD SASI 2014 3.Guillain-Barré 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 most commonly 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
  7. 7. 7 7 BRONCHOGENIC CARCINOMA BY DR MAGDI AWAD SASI 2014 rule out epidural compression from metastatic tumor—a 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 as painful swelling of the joints (knees, ankles, wrists, elbows, metacarpophalangeal joints) with effusion and sometimes fingertip clubbing. SIGNS: Cachexia , Anemia ,Lymphadenopathy – suparclavicular 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.
  8. 8. 8 8 BRONCHOGENIC CARCINOMA BY DR MAGDI AWAD SASI 2014 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
  9. 9. 9 9 BRONCHOGENIC CARCINOMA BY DR MAGDI AWAD SASI 2014 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 the tumour. 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
  10. 10. 10 10 BRONCHOGENIC CARCINOMA BY DR MAGDI AWAD SASI 2014 2. MRI brain /CT brain with contrast CNS symptoms Abnormal clinically 3. Radionuclide bone scan Increase ALP Increase calcium Bony 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 lesions and 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 radiotherapy—for 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 tumour Tx----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.
  11. 11. 11 11 BRONCHOGENIC CARCINOMA BY DR MAGDI AWAD SASI 2014 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 LYMPH NODE METASTASIS survival I. Tis, T1 or T2 Limited local disease NO MO 74% II. T1 // T2 T3 Limited local diseae w ipsilateral hilar/ locally invasive N1 N0 MO 55% MO 39% III a T3 T1---T3 Limited local disease w perbronchial /locally with invasive subcarinal N1 N2 MO 22% MO III b T1-----T4 T4 Contralateral LN ,supraclavicular ,malignant effusion N3 N0--- N2 MO MO IV T1-----T4 Distant metastases No-N3 M1
  12. 12. 12 12 BRONCHOGENIC CARCINOMA BY DR MAGDI AWAD SASI 2014
  13. 13. 13 13 BRONCHOGENIC CARCINOMA BY DR MAGDI AWAD SASI 2014 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 can’t be treated surgically c) Multidrug platinum based therapy shows a trend toward improved survival in I and IIe
  14. 14. 14 14 BRONCHOGENIC CARCINOMA BY DR MAGDI AWAD SASI 2014 STAGE IIA STAGE IIB
  15. 15. 15 15 BRONCHOGENIC CARCINOMA BY DR MAGDI AWAD SASI 2014 STAGE III A
  16. 16. 16 16 BRONCHOGENIC CARCINOMA BY DR MAGDI AWAD SASI 2014 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
  17. 17. 17 17 BRONCHOGENIC CARCINOMA BY DR MAGDI AWAD SASI 2014 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 +Etopside b) Cisplatin + radiotherapy PROGNOSIS: NSCLC 50% 2yr with out spread 10% 2yr with spread SCLC 3 months if untreated 1 ½ year if treated DRUGS MAY BE USED: Codeine Bronchodilator analgesics steroids antidepresent
  18. 18. 18 18 BRONCHOGENIC CARCINOMA BY DR MAGDI AWAD SASI 2014
  19. 19. 19 19 BRONCHOGENIC CARCINOMA BY DR MAGDI AWAD SASI 2014 OTHER OPTIONS OF TREATMENT: 1.Laser therapy 2.Cryosurgery 3.Photodynamic therapy 4.Electrotherapy 5.Biological therapy---targeted therapy They include erlotinib (Tarceva),gefitinib (Iressa), crizotinib (Xalkori) and afatinib (Giotrif).
  20. 20. 20 20 BRONCHOGENIC CARCINOMA BY DR MAGDI AWAD SASI 2014

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