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Svc obstruction

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svc syndrome/obstruction

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Svc obstruction

  1. 1. SUPERIOR VENA CAVA SYNDROME Dr. PRAPULLA CHANDRA
  2. 2. OBJECTIVES  DEFINITION  HISTORY  ANATOMY  PATHOGENESIS  ETIOLOGY  CLINICAL FEATURES  DIAGNOSIS  TREATMENT  PROGNOSIS
  3. 3. SVC SYNDROME  Constellation of signs and symptoms caused by obstruction of blood flow in the superior vena cava secondary to external compression, invasion, constriction or thrombosis of the SVC  Can be partial or complete obstruction
  4. 4. HISTORY  First recorded description of SVC obstruction (SVCO) - 1757 when William Hunter described the entity in a patient with a syphilitic aortic aneurysm.  For nearly two centuries- nonmalignant processes such as aortic aneurysms, syphilitic aortitis, or chronic mediastinitis due to tuberculosis were the predominant etiologic factors.  Now Rare
  5. 5.  In the preantibiotic era- ◦ syphilitic thoracic aortic aneurysms,  fibrosing mediastinitis,  untreated infection were frequent causes of the SVC syndrome.  Subsequently, malignancy became the most common cause, accounting for 90 percent of cases by the 1980s.  More recently, the incidence of SVC syndrome due to thrombosis has risen, largely because of increased use of intravascular devices such as catheters and pacemakers.  Benign causes now account for 10 to 20 percent of cases of SVC syndrome.
  6. 6. ANATOMY  SVC originates in the chest, behind the first right sternocostal articulation, from the confluence of two main collector vessels: Right and Left brachiocephalic veins which receive the ipsilateral internal jugular and subclavian veins.  Internal jugular vein drains-----head and deep sections of the neck  Subclavian vein--- upper limbs, superior chest and superficial head and neck.
  7. 7.  After the brachiocephalic convergence, the SVC follows the right lateral margin of the sternum in an inferoposterior direction.  Finally, it enters the pericardium superiorly and opens into the right atrium  The SVC’s length ranges from 6 to 8 cm.  Its diameter is usually 20-22 mm.
  8. 8.  The blood pressure ranges from -5 to 5 mmHg and the flow is discontinuous depending on the heart pulse cycle.  The SVC receives a single affluent vein: the azygos vein.  The azygos vein joins the SVC from the right side, at its mid length, above the right bronchus.
  9. 9.  No valve divides the superior vena cava from the right atrium. As a result, the right atrial and right ventricular contractions are conducted up into the internal jugular vein and, through the sternocleidomastoid muscle, can be seen as the jugular venous pressure.
  10. 10. AZYGOS VEIN  Azygos vein transports deoxygenated blood from the posterior walls of the thorax and abdomen into the superior venacava. It is formed by the union of  Ascending lumbar veins with  Right subcostal veins At the level of the 12th thoracic vertebra  Ascending in the posterior mediastinum, and arching over the right main bronchus posteriorly at the root of the right lung to join the superior vena cava.
  11. 11.  A major tributary is the hemiazygos vein, a similar structure on the opposite side of the vertebral column. Other tributaries include  Bronchial veins,  Pericardial veins, and  Posterior right intercostal veins.  It communicates with the vertebral venous plexuses.
  12. 12. HEMIAZYGOS VEIN  It runs superiorly in the lower thoracic region, just to the left side of the vertebral column.  Hemiazygos vein and the accessory hemiazygos vein, when taken together, essentially serve as the left-sided equivalent of the azygos vein.  It usually begins in the left ascending lumbar vein or renal vein, and passes upward through the left crus of the diaphragm to enter the thorax.
  13. 13.  It continues ascending on the left side of the vertebral column, and at the level of the 9th thoracic vertebra, it passes rightward across the vertebral column, behind the aorta, esophagus, and thoracic duct, to end in the azygos vein.  The hemiazygos may or may not be continuous superiorly with the accessory hemiazygos vein.  It receives the 9th, 10th, and 11th posterior intercostal veins and the subcostal vein of the left side, and some esophageal and mediastinal veins.
  14. 14. ACCESSORY HEMIAZYGOS VEIN  Receives the posterior intercostal veins from the 4th, 5th, 6th, and 7th ICS.  It either crosses the body of 8th thoracic vertebra to join the azygous vein or ends in the hemiazygos.  When this vein is small, or altogether absent, the left superior intercostal vein may extend as low as the 5th or 6th ICS.
  15. 15. Posterior intercostal veins There are eleven posterior intercostal veins on each side.  The 1st posterior intercostal vein, drains into the brachiocephalic vein or the vertebral vein.  The 2nd and 3rd (and often 4th) posterior intercostal veins drain into the superior intercostal vein.  The remaining posterior intercostal veins drain into the azygos vein on the right, or the hemiazygos vein and accessory hemiazygous on the left.
  16. 16. SVC OBSTRUCTION  In SVC obstruction, the azygos vein is responsible for the most important collateral circulation. According to the expected collateral pathways, the SVC can be divided into two segments:  Supra-azygos or preazygos and  Infra-azygos or postazygos SVC.
  17. 17.  There are four possible collateral systems which were first described in 1949 by McIntire and Sykes. They are represented by 1. Azygos venous system, 2. Internal thoracic venous system, 3. Vertebral venous system and 4. External thoracic venous system.
  18. 18. 1. Azygos venous system is the only direct path into the SVC. 2. Internal thoracic vein is the collector between SVC and inferior vena cava (IVC) via epigastric and iliac veins. 3. Vertebral veins with intercostals, lumbar and sacral veins, represent the posterior network between SVC and IVC. 4. External thoracic vein system is the most superficial and it is represented by axillary, lateral thoracic and superficial epigastric veins.
  19. 19. ETIOLOGY Malignant  Lung cancer  Lymphomas  Thymoma  Mediastinal germ cell tumors  Mediastinal metastases  Mesothelioma  Leiomyosarcoma and angiosarcoma  Neoplastic thrombi  Anaplastic thyroid cancer
  20. 20. Benign  Fibrosing mediastinitis (idiopathic or radiation- induced)  Infectious diseases – 1. Tuberculosis, 2. Histoplasmosis, 3. Echinococcosis, 4. Syphilis, 5. Aspergillosis, 6. Blastomycosis, 7. Filariasis, 8. Nocardiosis.  Thrombosis (non- neoplastic)  Lymphadenopathies 1. sarcoidosis, 2. Behçet’s syndrome, 3. Castleman’s disease  Aortic aneurysm  Substernal goiter  Pericardial, thymic, bronchogenic cysts  Iatrogenic 1. Pacemaker and defibrillator placement 2. Central venous catheters
  21. 21. PATHOPHYSIOLOGY  Pathogenetic basis of SVCS is obstruction to the blood flow.  It can be intrinsic or extrinsic obstruction.  Intrinsic—uncommon, caused by thrombosis or invading tissue.  Extrinsic factors develop from compression or stricture of the vein.  In physiologic conditions, blood return to the right atrium is facilitated by the pressure gradient between the right atrium and venae cavae.
  22. 22.  When obstruction of the SVC occurs, the vascular resistances rise and the venous return decreases.  When SVC shows a significant stenosis (3/5 of the lumen or more), blood flow is redirected through the collateral circulation in order to bypass the obstruction and restore the venous return.
  23. 23.  In acute impairments, the blood flow is not rapidly distributed through the collateral network so symptoms arise markedly.  In the case of slow-growing diseases, the collateral venous network has enough time to expand in order to receive the circulating volume.  For this reason, long-lasting, severe SVC obstruction can sometimes be found without significant symptoms
  24. 24. The clinical seriousness is related to several factors: 1. Level of obstruction and rapidity of development, determining the effectiveness of collateral circulation 2. Impairment of lymphatic drainage (pulmonary interstitial edema or pleural effusion) 3. Involvement of other mediastinal structures (compression or invasion of heart, pulmonary artery and central airways, phrenic nerve paralysis)
  25. 25.  Superficial dilated vascular routes are the main sign of collateral circulation and appear swollen and non- pulsating.  In case of marked obesity, superficial veins can be missing at inspection.  Variety of collateral circulation and the differences in the venous rearrangement are expression of the SVC obstruction site. Anatomic classification includes three levels of obstruction: 1. Obstruction of the upper SVC, proximal to (above the level of) azygos entry point. 2. Obstruction with azygos involvement. 3. Obstruction of the lower SVC, distal to (below the level of) azygos entry point.
  26. 26. Obstruction of the upper SVC proximal to the azygos entry point.  In this situation, there is no impediment to normal blood flow through the azygos vein which opens into the patent tract of the SVC.  Venous drainage coming from the head neck, shoulders and arms cannot directly reach the right atrium.  From the superior tract of the SVC, blood flow is reversed and directed to the azygos, mainly through the right superior intercostal vein.
  27. 27. Obstruction with azygos involvement  In this case, the azygos vein cannot be used as collateral pathway and the only viable blood return is carried by minor vessels to IVC (cava-cava or anazygotic circulation).  From the internal thoracic veins, blood is forced to the intercostal veins, then to azygos and hemiazygos veins.  The flow is thus reversed into the ascending lumbar veins to the iliac veins.
  28. 28.  Direct anastomosis between the azygos’ origin and the IVC and between hemiazygos and left renal vein are also active.  In addition, the internal thoracic veins can flow into the superior epigastric veins.  From the superior epigastric veins, blood is carried to the inferior epigastric veins across the superficial system of the cutaneous abdominal veins and finally to the iliac veins.  Another course is between the thoraco-epigastric vein (collateral of the axillary vein) and the external iliac vein.
  29. 29.  In these conditions, the collateral circulation is partly deep and partly superficial.  Physical examination often reveals SVC obstruction.  The reversed circulation through the described pathways, remains less efficient than the azygos system and venous hypertension is usually more severe.  For this reason, this kind of SVC obstruction is often related to important symptoms, dyspnea and pleural effusion.  The ensuing slow blood flow may be responsible for superimposed thrombosis.
  30. 30. Obstruction of the lower SVC distal to the azygos entry point  In this condition, the obstruction is just below the azygos arch.  The blood flow is distributed from the superior body into the azygos and hemiazygos veins, in which the flow is inverted, to the IVC tributaries.
  31. 31.  In this type of obstruction, the superficial collateral system is not always evident but the azygos and hemiazygos congestion and dilatation are usually important.  The hemodynamic changes lead to edema and cyanosis of the upper chest and pleural effusion. Pleural effusion is often slowly-growing and rightsided, probably due to anatomical reasons:  There is a wider anastomosis between hemiazygos and IVC than between azygos and IVC.
  32. 32. Classification of SVCS  There are three main classification proposals which follow different methods of categorization. Doty and Standford’s classification (anatomical) 1. Type I: stenosis of up to 90% of the supra- azygos SVC 2. Type II: stenosis of more than 90% of the supra- azygos SVC 3. Type III: complete occlusion of SVC with azygos reverse blood flow 4. Type IV: complete occlusion of SVC with the involvement of the major tributaries and azygos vein
  33. 33. Yu’s classification (clinical) 1. Grade 0: asymptomatic (imaging evidence of SVC obstruction) 2. Grade 1: mild (plethora, cyanosis, head and neck edema) 3. Grade 2: moderate (grade 1 evidence + functional impairment) 4. Grade 3: severe (mild/moderate cerebral or laryngeal edema, limited cardiac reserve) 5. Grade 4: life-threatening (significant cerebral or laryngeal edema, cardiac failure) 6. Grade 5: fatal
  34. 34. Bigsby’s classification (operative risk)  Low risk  High risk The low risk patients present with  No dyspnea at rest,  No facial cyanosis in the upright position,  No change of dyspnea, No worsening of facial edema and Cyanosis during the supine position.  The high risk patients present with facial cyanosis or dyspnea at rest in the sitting position.
  35. 35. Clinical Presentation • Diagnosis is made by history, physical examination, and lab studies • findings will depend on 1. The degree of occlusion 2. The rapidity of development 3. Presence or absence of collateral circulation
  36. 36. PRESENTING SYMPTOMS OF SVCO These symptoms may be worsened by positional changes such as bending forward, stooping, or lying down. Common symptoms Less common •Facial puffiness(80%) •Dyspnea (63%) •Persistent cough (24%-55%) • Erythema , Swelling of the neck and/or arms(50%) •Chest pain(20%) •Dysphagia (12%) •Syncope(7%) •Visible dilatation of the veins in the upper extremity. •Orthopnea (2%) •Hoarseness (Vagus), •Periorbital edema, •Deaffness, Somnolence, •Nasal stuffiness, Pleural effusions •Lethargy(1%) •Stridor (1%) •Dizziness, •Epistaxis •Hemoptysis •Confusion
  37. 37. Physical examination  Venous distension of neck-66%  Venous distension of Chest-54%  Edema upper half of the body-50%  Paleness of lower half of the body-18%  Engorged abdomen veins-12%  Papilledema, stupor, and even coma.  Cyanosis and edema are aggravated by horizontal position and relived by upright position
  38. 38. Superior vena cava syndrome in a person with brochogenic carcinoma. Note the swelling of his face first thing in the morning (left) and its resolution after being upright all day (right).
  39. 39. DIFFERENTIAL DIAGNOSIS  Heart failure and pericardial tamponade  Nephrotic syndrome
  40. 40. Diagnosis  Diagnosis of SVCS can be made simply on physical examination.  When the extent of disease is minimal, the physical findings may not be prominent then it is difficult to diagnose.  Establishing the underlying etiology is more important because certain disorders that cause SVCS may be more amenable to specific treatment regimens. SCLC and lymphoma -Chemotherapy/irradiation, thrombosis does not respond to this treatment.
  41. 41.  Laboratory studies: Exercise test Lower chest torniquet test  Radiologic Chest x ray Ultrasonography CT MRI Contrast venography Radionucleide venography
  42. 42.  Histologic Sputum/pleural fluid cytology Bone marrow biopsy Lymph node biopsy  Procedures Bronchoscopy Thoracotomy Thoracocentesis
  43. 43. Laboratory Studies Localizing Obstruction  Pressure readings are taken from the ante-cubital vein with a 3-way stopcock spinal mannometer using 2.5 % citrate solution Exercise test (Hussay et al)  Patient opens and closes his fist forcefully for one minute while venous pressure readings are being noted.  In normal individuals, it remains constant  In SVCO pressure will rise 10 cm. or more and then gradually recedes to normal.
  44. 44. Lower chest tourniquet test  in which a tourniquet constricts the superficial thoracic collaterals and raises the venous pressure if obstruction is below the azygos. Other Test  Circulatory time is prolonged in SVCO  Infra –red photography demonstrates superficial collaterals  Phlebography
  45. 45. RADIOLOGICAL STUDIES a) CHEST RADIOGRAPHY  The initial diagnostic test for suspected SVCS.  Is not specific for SVCS.  helpful in identifying the cause of the disorder.  Parish and colleagues in 1981 –(16%) of the patients With SVCS had normal Chest radiography.  Right sided findings are common.
  46. 46. Chest radiography….. X-Ray findings suggestive of underlying malignancy, Mediastinal widening Pleural effusion(s) Right hilar mass Cardiomegaly Calcified paratracheal lymph nodes- Granulomatous disease  Anterior mediastinal mass  Normal(16%)  In the absence of previous catheterization or surgery, a normal result on chest radiography in a patient with SVCS is almost pathognomonic of chronic fibrous mediastinitis.
  47. 47. Aortic Nipple  Seen as a small soft-tissue density adjacent to the lateral border of the aortic knob on a frontal radiograph.  an aortic nipple is a radiological sign that represents the left superior intercostal vein as it runs around the aortic arch before joining the left brachiocephalic vein.  In certain conditions the aortic nipple can become enlarged and mimic lymphadenopathy or aortic aneurysm.  No treatment is needed other than treatment of the underlying condition.
  48. 48. Aortic Nipple
  49. 49. Aortic Nipple… Conditions that can cause an aortic nipple are a) Normal variant is usually found in normal healthy patients in anywhere from 1.4-9.5% of people. b) Increase in venous flow such as  Recumbant position, or during expiration  Portal venous hypertension secondary to hepatofugal shunting from the liver,  congenital anomalies of the caval, azygos or hemiazygos circulation results in enlargement of the left superior intercostal vein.  partial or total anomalous pulmonary venous drainage
  50. 50. Aortic Nipple… c) Caused by increased venous resistance as in  Congestive heart failure,  Budd Chiari sydrome  absence or obstruction of the inferior vena cava The left superior intercostal vein may act as a collateral pathway, and therefore become distended, in patients with impending or actual superior vena caval obstruction
  51. 51. Impending Superior Vena Cava Syndrome  Detection of ‘aortic nipple’ on chest roentgenogram predates the clinical syndrome by 7 to10 weeks  Development of SVCS requires severe venous compromise, whereas the left SICV (superior intercostal vein) may be more sensitive indicator because of Its small caliber, Rapid distensibility, Clearly defined and highly visible location Capacity to greatly enlarge with increased resistance
  52. 52. ULTRASONOGRAPHY  SVC cannot be imaged because of poor acoustic window  Patency can be indirectly determined with normal wave forms in brachiocephalic and subclavian veins.  Exclusion of thrombus in upper extremity, subclavian, brachiocephalic and axillary veins.
  53. 53. Computed tomography scanning  CT-Provides an effective, noninvasive evaluation of the superior vena cava and its collateral circulation.  CT scanning provides 1) Anatomic details of the mediastinal and thoracic organs 2) Allows identification of the cause and extent of the obstruction, 3) Documents collateral circulation, 4) Provides guidance for Percutaneous biopsies 5) Guides the formulation for radiotherapy.
  54. 54.  Recently,, MDCT(multidetector CT) is gaining importance, with its multiplanar and 3D images combining cross-sectional imaging for diagnosis of the cause of the superior vena cava obstruction with multiplanar reformation that best delineates the level and extent of venous obstruction
  55. 55.  Surgery
  56. 56. Magnetic resonance imaging (MRI)  MRI is often important in determining the cause of SVCS.  MRI, by virtue of its multidimensional capabilities, shows the relationships of vessels, lymph nodes, and other mediastinal structures.  It is an acceptable alternative for patients with renal failure or those with contrast allergies.
  57. 57. Contrast venography  An x-ray test that provides an image of the veins after a contrast dye is injected into a vein. Advantages:-  The extent and site of obstruction.  The nature and degree of obstruction.  Patency of the superior vena cava.  Differentiation between intrinsic and extrinsic obstruction.  Assessment of collateral vessels  the degree of venous distension of the neck and arms
  58. 58. Contrast venography…..  Measurement of actual venous pressure  The presence of the internal jugular vein reflux.  Is essential prior to planning any surgical bypass operation.  Surgical bypass operations are easier to accomplish when the brachiocephalic veins are not involved.  However, if all the intrathoracic veins are obstructed, extrathoracic bypass operations can be undertaken,  Very helpful in documenting obstructions caused by thrombus formation. When thrombosis is present, treatment with fibrinolytic agents (eg, urokinase, streptokinase) is pursued and  Repeat venography can be used to evaluate treatment efficacy.
  59. 59. Venographic classification 1. Type I: stenosis of up to 90% of the supra-azygos SVC 2. Type II: stenosis of more than 90% of the supra-azygos SVC 3. Type III: complete occlusion of SVC with azygos reverse blood flow 4. Type IV: complete occlusion of SVC with the involvement of the major tributaries and azygos vein
  60. 60. Extrinsic compression of svc
  61. 61. Radionuclide venography.  This test is less invasive than contrast venography  is less specific in defining Patency and flow.  Radionuclide venography may be of value in long-term follow-up studies.
  62. 62. Diagnostic surgery.  When all other diagnostic procedures fail to provide information about the cause of SVCS, Exploratory thoracotomy be the last alternative.  Advantages—surgery allows direct visualization of the underlying disease process, assessment of the extent of disease involvement, and accessibility for tissue biopsy  However, this procedure is the most invasive and is associated with increased risks.
  63. 63.  Current guidelines stress the importance of accurate histologic diagnosis prior to starting therapy, and the upfront use of endovascular stents in severely symptomatic patients to provide more rapid relief than can be achieved using RT. Kvale PA, Selecky PA, Prakash UB, American College of Chest Physicians. Palliative care in lung cancer: ACCP evidence- based clinical practice guidelines (2nd edition). Chest 2007; 132:368S.
  64. 64. TREATMENT OF SVCO
  65. 65. Treatment Of SVCO  Depending on the underlying condition, multiple treatment options are available for superior vena cava obstruction. The primary treatment options include  Medical Care  Radiation  Chemotherapy  Thrombolytic therapy  Anticoagulation  Stents and balloon angioplasty and  Surgery.
  66. 66. Medical Care  The goals of SVCS management are to relieve symptoms and to attempt cure of the primary malignant Conservative treatment -symptomatic improvement  including elevation of the head end of the bed and supplemental oxygen.  Emergency treatment (Corticosteroids and diuretics )  For Brain edema,  decreased cardiac output,  or upper airway edema Their efficacy is questionable.
  67. 67. Dexamethasone (Decadron, Dexasone) For symptomatic management in tumor- associated edema.  8-40 mg IV once initially, followed by 4-6 mg IV/PO q6-8h
  68. 68. Other Medications  Loop Diuretic agents  Salt Restriction.  Oxygen
  69. 69. Radiation therapy Indications.  The majority of cases of SVCS are caused by malignancy; thus, most patients receive radiation treatment at some point in their illness. Emergency radiation treatment  To life-threatening cerebral or laryngeal edema prior to a tissue diagnosis of malignancy.  To relieve obstructive symptoms  Inappropriate for the treatment of an underlying thrombosis or granulomatosis causing the obstruction
  70. 70. Radiation Dosage  Initiated at high dose daily for the first few days. followed by conventional low daily doses. total dose is dependent on tumor histology.  Lymphomas (3000 to 4000 cGy,)  Carcinomas require (4000 to 5000 cGy or more) Lower doses of radiation treatment  When systemic disease is present and short- term palliation is the goal.  Radiation to Heart and Spinal cord.  who are receiving chemotherapeutic agents such as doxorubicin, which can enhance radiation toxicity.
  71. 71. Response to RT 3 to 4 days- Resolution of facial edema and venous distension of the upper extremities . 1 to 3 weeks- Radiographic improvement . Not effective -Thrombosis is cause for SVCO  When RT successfully completed in pts of SVCS with malignancies, 10% to 20% survive more than 2 years.
  72. 72. Side effects of RT.  Persistent fever,  Bleeding or SVC perforation at the site of tumor invasion,  Nausea, Vomiting,  Anorexia,  Leukopenia,  Hemoptysis, Late Complications  Skin irritation;  Esophagitis;  Pulmonary or mediastinal fibrosis;
  73. 73. Chemotherapy  Chemotherapy may be used as a primary therapy or as an adjunct to radiotherapy  treatment of choice for SVCS caused by Mediastinal lymphoma is a combination of chemotherapy and radiotherapy.
  74. 74. Thrombolytic Therapy  Pericatheter thrombosis is seen in approximately 50% of Non- anticoagulated patients with long term Central vein Catheters  Acute Cases- excellent results with thrombolytic therapy.
  75. 75. Benefits of Thrombolytic therapy  Fast dissolution of emboli,  Quickened recovery,  Prevention of recurrent thrombus formation,  Rapid restoration of hemodynamic disturbances.
  76. 76. Urokinase Action:-  Converts plasminogen to plasmin, which degrades fibrin clots, fibrinogen, and other plasma proteins. Adult Dose: Loading dose: 4400 U/kg IV over 10 min and increase to 6000 U/kg/h Maintenance dose: 4400-6000 U/kg/h IV
  77. 77. Anticoagulation  Patients with SVCS are at increased risk for deep vein thrombosis and pulmonary embolism.  In patients for whom thrombosis is the cause of SVCS, anticoagulation therapy should be administered after successful thrombolytic treatment.  Once the symptoms subside after thrombolytic therapy, anticoagulation should be maintained as long as the central venous catheter is present.
  78. 78. Anticoagulants - Heparin Action:-  Inhibits thrombosis by inactivating activated factor X and inhibiting conversion of prothrombin to thrombin. Adult:-  5000 U IV bolus, then infusion to maintain aPTT 2-3 times the reference range Pediatric:-  Initial dose: 50 U/kg IV Maintenance infusion: 15-25 U/kg/h IV Increase dose by 2-4 U/kg/h IV q6-8h using aPTT
  79. 79. Anticoagulants -Warfarin (Coumarin) Action:-  Inhibits synthesis of vitamin K–dependent coagulation factors (factors II, VII, IX, X). Adult:-  Initial: 5-10 mg PO Maintenance: 2-10 mg PO qd to maintain INR of 2-3 Pediatric:-  0.05-0.34 mg/kg/d PO; adjust dose according to desired INR
  80. 80. Stents  Recent advances in interventional radiology have contributed expandable wire stents and balloon angioplasty.  can be placed across the stenotic portion.  stents have little thrombogenic potential  After thrombolytic therapy, stent placement has been noted to be a more successful approach.  After stent, patients experience instantaneous relief of symptoms.  The placement of stents is performed under local anesthesia.  palliation of the symptoms
  81. 81. Balloon Angioplasty  For localized lesions, balloon angioplasty with or without stenting has also been shown to significantly reduce the symptoms of SVCS
  82. 82. Endovascular Treatment SVC syndrome Lt superior intercostal drainage SVC occlusion Stent mounted on a balloon Status post SVC stent Balloon deployment Patent SVC
  83. 83. Surgical Treatment  Surgical bypass is an additional alternative to relieve SVCS.  is usually recommended to benign disease and to only a few patients with malignancy.  Patients selected for surgery should have the Category-IV venographic signs, i.e, total vena caval obstruction.  Surgery in cases of fibrosing mediastinitis can be extremely complicated, because of the extensive collateral circulation under high venous pressure.  Advantage is definitive removal of the obstruction and direct tissue diagnosis.  Long-term results after surgical bypass are lacking, because their life expectancy is short.
  84. 84. PROGNOSIS Benign disease-life expectancy unchanged Malignant obstruction of SVC  Untreated - 30 days average life expectancy  Treated - < 7 month average life expectancy - 20% 1-year survival for lung cancer -NSCLC-poor prognosis, palliative care+RT - 50% 2-year survival for lymphoma

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