Slide 1
SUPERIOR VENA CAVA SYNDROMEDr. PRAPULLA CHANDRA
OBJECTIVES
DEFINITIONHISTORYANATOMYPATHOGENESIS ETIOLOGYCLINICAL
FEATURESDIAGNOSISTREATMENTPROGNOSIS
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
HISTORYFirst 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
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.
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.
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 SVCs length ranges from 6 to 8 cm.
Its diameter is usually 20-22 mm.
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.
Novalvedivides the superior vena cava from the right atrium. As
a result, the right atrial and right ventricular contractions are
conducted up into theinternal jugular veinand, through
thesternocleidomastoid muscle, can be seen as thejugular venous
pressure.
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.
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.
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.
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.
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.
Posterior intercostal veinsThere 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.
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.
There are four possible collateral systems which were first
described in 1949 by McIntire and Sykes.
They are represented by Azygos venous system, Internal thoracic
venous system, Vertebral venous system and External thoracic venous
system.
Azygos venous system is the only direct path into the SVC.
Internal thoracic vein is the collector between SVC and inferior
vena cava (IVC) via epigastric and iliac veins.
Vertebral veins with intercostals, lumbar and sacral veins,
represent the posterior network between SVC and IVC.
External thoracic vein system is the most superficial and it is
represented by axillary, lateral thoracic and superficial
epigastric veins.
ETIOLOGY
MalignantLung cancerLymphomasThymomaMediastinal germ cell
tumorsMediastinal metastases
MesotheliomaLeiomyosarcoma and angiosarcomaNeoplastic
thrombiAnaplastic thyroid cancer
Benign
Fibrosing mediastinitis (idiopathic or radiation-induced)
Infectious diseases Tuberculosis, Histoplasmosis,
Echinococcosis, Syphilis, Aspergillosis, Blastomycosis, Filariasis,
Nocardiosis.
Thrombosis (non-neoplastic)
Lymphadenopathies sarcoidosis, Behets syndrome, Castlemans
disease
Aortic aneurysm
Substernal goiter
Pericardial, thymic, bronchogenic cysts
IatrogenicPacemaker and defibrillator placementCentral venous
catheters
PATHOPHYSIOLOGYPathogenetic basis of SVCS is obstruction to the
blood flow.
It can be intrinsic or extrinsic obstruction.
Intrinsicuncommon, 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.
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.
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
The clinical seriousness is related to several factors:Level of
obstruction and rapidity of development, determining the
effectiveness of collateral circulation
Impairment of lymphatic drainage (pulmonary interstitial edema
or pleural effusion)
Involvement of other mediastinal structures (compression or
invasion of heart, pulmonary artery and central airways, phrenic
nerve paralysis)
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:Obstruction of the upper SVC, proximal to (above the
level of) azygos entry point.Obstruction with azygos
involvement.Obstruction of the lower SVC, distal to (below the
level of) azygos entry point.
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.
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.
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.
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.
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.
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.
Classification of SVCS
There are three main classification proposals which follow
different methods of categorization.
Doty and Standfords classification (anatomical) Type I: stenosis
of up to 90% of the supra-azygos SVC Type II: stenosis of more than
90% of the supra-azygos SVC Type III: complete occlusion of SVC
with azygos reverse blood flow Type IV: complete occlusion of SVC
with the involvement of the major tributaries and azygos vein
Yus classification (clinical)
Grade 0: asymptomatic (imaging evidence of SVC obstruction)
Grade 1: mild (plethora, cyanosis, head and neck edema)
Grade 2: moderate (grade 1 evidence + functional impairment)
Grade 3: severe (mild/moderate cerebral or laryngeal edema,
limited cardiac reserve)
Grade 4: life-threatening (significant cerebral or laryngeal
edema, cardiac failure)
Grade 5: fatal
Bigsbys classification (operative risk)Low riskHigh 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.
Clinical Presentation
Diagnosis is made by history, physical examination, and lab
studies findings will depend onThe degree of occlusionThe rapidity
of developmentPresence or absence of collateral circulation
PRESENTING SYMPTOMS OF SVCO These symptoms may be worsened by
positional changes such as bending forward, stooping, or lying
down.
Common symptomsLess commonFacial 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 effusionsLethargy(1%) Stridor
(1%)Dizziness,Epistaxis Hemoptysis Confusion
Symptoms increase bending forward,lying down.43
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
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).
DIFFERENTIAL DIAGNOSISHeart failure and pericardial
tamponadeNephrotic syndrome
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.
Laboratory studies:Exercise testLower chest torniquet test
RadiologicChest x rayUltrasonography CTMRIContrast
venographyRadionucleide venography
HistologicSputum/pleural fluid cytologyBone marrow biopsyLymph
node biopsy
ProceduresBronchoscopyThoracotomyThoracocentesis
Laboratory Studies
Localizing ObstructionPressure readings are taken from the
ante-cubital vein with a 3-way stopcock spinal mannometer using 2.5
% citrate solutionExercise 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
constantIn SVCO pressure will rise 10 cm. or more and then
gradually recedes to normal.
Lower chest tourniquet testin which a tourniquet constricts the
superficial thoracic collaterals and raises the venous pressure if
obstruction is below the azygos.Other TestCirculatory time is
prolonged in SVCOInfra red photography demonstrates superficial
collateralsPhlebography
RADIOLOGICAL STUDIESa) 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.
Chest radiography..X-Ray findings suggestive of underlying
malignancy, Mediastinal widening Pleural effusion(s) Right hilar
mass Cardiomegaly Calcified paratracheal lymph nodes- Granulomatous
diseaseAnterior mediastinal massNormal(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.
Aortic NippleSeen 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.
Aortic Nipple
Aortic NippleConditions that can cause an aortic nipple area)
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
Aortic Nipplec) 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
Impending Superior Vena Cava SyndromeDetection of aortic nipple
on chest roentgenogram predates the clinical syndrome by 7 to10
weeksDevelopment 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
ULTRASONOGRAPHYSVC cannot be imaged because of poor acoustic
windowPatency can be indirectly determined with normal wave forms
in brachiocephalic and subclavian veins. Exclusion of thrombus in
upper extremity, subclavian, brachiocephalic and axillary
veins.
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.
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
Surgery
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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.
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 vesselsthe degree of
venous distension of the neck and arms
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 andRepeat venography can be
used to evaluate treatment efficacy.
Venographic classification Type I: stenosis of up to 90% of the
supra-azygos SVC Type II: stenosis of more than 90% of the
supra-azygos SVC Type III: complete occlusion of SVC with azygos
reverse blood flow Type IV: complete occlusion of SVC with the
involvement of the major tributaries and azygos vein
Extrinsic compression of svc
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.
Diagnostic surgery.
When all other diagnostic procedures fail to provide information
about the cause of SVCS, Exploratory thoracotomy be the last
alternative.
Advantagessurgery 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.
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.
TREATMENT OF SVCO
Treatment Of SVCODepending on the underlying condition, multiple
treatment options are available for superior vena cava obstruction.
The primary treatment options include Medical
CareRadiationChemotherapyThrombolytic therapyAnticoagulationStents
and balloon angioplasty andSurgery.
Medical Care
The goals of SVCS management are to relieve symptoms and to
attempt cure of the primary malignantConservative 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.
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
Other MedicationsLoop Diuretic agents Salt
Restriction.Oxygen
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
Radiation DosageInitiated 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.
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 SVCOWhen RT successfully
completed in pts of SVCS with malignancies, 10% to 20% survive more
than 2 years.
Side effects of RT.
Persistent fever,Bleeding or SVC perforation at the site of
tumor invasion, Nausea, Vomiting, Anorexia,
Leukopenia,Hemoptysis,Late ComplicationsSkin
irritation;Esophagitis;Pulmonary or mediastinal fibrosis;
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.
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.
Benefits of Thrombolytic therapyFast dissolution of emboli,
Quickened recovery, Prevention of recurrent thrombus formation,
Rapid restoration of hemodynamic disturbances.
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/hMaintenance dose: 4400-6000 U/kg/h IV
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.
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
rangePediatric:-Initial dose: 50 U/kg IVMaintenance infusion: 15-25
U/kg/h IVIncrease dose by 2-4 U/kg/h IV q6-8h using aPTT
Anticoagulants -Warfarin (Coumarin) Action:-Inhibits synthesis
of vitamin Kdependent coagulation factors (factors II, VII, IX,
X).Adult:-Initial: 5-10 mg POMaintenance: 2-10 mg PO qd to maintain
INR of 2-3Pediatric:-0.05-0.34 mg/kg/d PO; adjust dose according to
desired INR
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
potentialAfter 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
Balloon Angioplasty
For localized lesions, balloon angioplasty with or without
stenting has also been shown to significantly reduce the symptoms
of SVCS
Endovascular Treatment
SVC syndrome
Lt superior intercostal drainage
SVC occlusion
Stent mounted on a balloon Status post SVC stent
Balloon
deployment Patent SVC
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.
PROGNOSIS Benign disease-life expectancy unchangedMalignant
obstruction of SVCUntreated - 30 days average life
expectancyTreated - < 7 month average life expectancy - 20%
1-year survival for lung cancer -NSCLC-poor prognosis, palliative
care+RT - 50% 2-year survival for lymphoma
