Showing posts with label SVC Syndrome. Show all posts
Showing posts with label SVC Syndrome. Show all posts
Superior Venecaval Syndrome
By Dr Deepu
SVCS will be discussed under the sub headings given below, select specific subheading to read further.
Images
Definition
History
Pathophysiology
Presentation and Findings
Causes
Diagnostic Workup
Management
Images:
Normal Anatomy
SVC Obstruction
SVCS will be discussed under the sub headings given below, select specific subheading to read further.
Images
Definition
History
Pathophysiology
Presentation and Findings
Causes
Diagnostic Workup
Management
Images:
Normal Anatomy
Definition
Superior Venecaval Syndrome
By Dr Deepu
Images
Definition
History
Pathophysiology
Presentation and Findings
Causes
Diagnostic Workup
Management
Images
Definition
History
Pathophysiology
Presentation and Findings
Causes
Diagnostic Workup
Management
Management
In the management of superior vena cava syndrome (SVCS),
the goals are to relieve symptoms and to attempt cure of the primary malignant
process.
Only a small percentage of patients with rapid-onset
obstruction of the superior vena cava (SVC) are at risk for life-threatening
complications.
Patients with clinical SVCS often gain significant
symptomatic improvement from conservative treatment measures, including
elevation of the head of the bed and supplemental oxygen.
Emergency treatment is indicated when brain edema,
decreased cardiac output, or upper airway edema is present.
Corticosteroids and diuretics are often used to relieve
laryngeal or cerebral edema, although documentation of their efficacy is
questionable.
Radiotherapy has been advocated as a standard treatment
for most patients with SVCS. It is used as the initial treatment if a
histologic diagnosis cannot be established and the clinical status of the
patient is deteriorating; however, reviews suggest that SVC obstruction alone
rarely represents an absolute emergency that necessitates treatment without a
specific diagnosis.
The fractionation schedule for radiotherapy usually
includes two to four large initial fractions of 3-4 Gy, followed by daily
delivery of conventional fractions of 1.5-2 Gy, up to a total dose of 30-50 Gy.
The radiation dose depends on tumor size and radioresponsiveness. The radiation
portal should include a 2-cm margin around the tumor.
During irradiation, patients improve clinically before
objective signs of tumor shrinkage are evident on chest radiography. Radiation
therapy palliates SVC obstruction in 70% of patients with lung carcinoma and in
more than 95% of those with lymphoma.
In patients with SVCS secondary to non–small-cell
carcinoma of the lung, radiotherapy is the primary treatment. The likelihood of
patients benefiting from such therapy is high, but the overall prognosis of
these patients is poor.
When SVCS is due to thrombus around a central venous
catheter, patients may be treated with thrombolytics (eg, streptokinase,
urokinase, or recombinant tissue-type plasminogen activator) or anticoagulants
(eg, heparin or oral anticoagulants).
Removal of the catheter, if possible, is another option,
and it should be combined with anticoagulation to prevent embolization. These
agents are most effective when patients are treated within 5 days after the
onset of symptoms.
Dexamethasone
Important therapeutic agent in a number
of malignant diseases. Exerts biologic action predominately by binding to
glucocorticoid receptor. For symptomatic management in tumor-associated edema.
Thrombolytics
The potential benefits of thrombolytics
for the treatment of pulmonary embolism include fast dissolution of
physiologically compromising pulmonary emboli, quickened recovery, prevention
of recurrent thrombus formation, and rapid restoration of hemodynamic
disturbances. For deep vein thrombosis, lysis of the thrombus can prevent
pulmonary embolism and permanent pathologic changes, such as venous valvular
dysfunction and postphlebitic syndrome.eg Urokinase
Anticoagulants
In superior vena cava syndrome (SVCS),
these agents are used mainly to prevent pulmonary embolism from superior vena
cava (SVC) thrombus.
Eg: Heparin and Warfarin
Superior Venecaval Syndrome
By Dr Deepu
Images
Definition
History
Pathophysiology
Presentation and Findings
Causes
Diagnostic Workup
Management
Images
Definition
History
Pathophysiology
Presentation and Findings
Causes
Diagnostic Workup
Management
Diagnostic
workup
Patients presenting with
overt superior vena cava syndrome (SVCS) may be diagnosed by means of physical
examination alone. However, subtle presentations necessitate diagnostic
imaging.
Chest X Ray
Chest radiography may
reveal a widened mediastinum or a mass in the right side of the chest. Only 16%
of the patients studied by Parish et al in 1981 had normal findings on chest
radiography.
CT
Scan
Computed tomography (CT)
has the advantage of providing more accurate information on the location of the
obstruction and may guide attempts at biopsy by mediastinoscopy, bronchoscopy,
or percutaneous fine-needle aspiration. It also provides information on other
critical structures, such as the bronchi and the vocal cords.
A CT scan of the chest is
the initial test of choice to determine whether an obstruction is due to external
compression or due to thrombosis. The additional information is necessary
because the involvement of these structures requires prompt action for relief
of pressure.
Magnetic
resonance imaging (MRI)
Magnetic resonance imaging (MRI) has not yet been
sufficiently investigated in this setting, but it appears promising. It has
several potential advantages over CT, in that it provides images in several
planes of view, allows direct visualization of blood flow, and does not require
iodinated contrast material (an especially important characteristic when
stenting is anticipated).
MRI is an acceptable alternative for patients with renal failure or those with contrast allergies.
Potential disadvantages include increased scanning time with attendant problems
in patient compliance and increased cost.
venography
Invasive contrast venography is the most conclusive
diagnostic tool (see the image below). It precisely defines the etiology of
obstruction. It is especially important if surgical management is being
considered for the obstructed vena cava.
Management
Management
Superior Venecaval Syndrome
By Dr Deepu
Images
Definition
History
Pathophysiology
Presentation and Findings
Causes
Diagnostic Workup
Management
Causes
Images
Definition
History
Pathophysiology
Presentation and Findings
Causes
Diagnostic Workup
Management
More than 80% of cases of
SVCS are caused by malignant mediastinal tumors.
Bronchogenic carcinomas account for 75-80% of
all these cases, with most of these being small-cell carcinomas.
Non-Hodgkin lymphoma (especially the
large-cell type) account for 10-15%. Causes of SVCS appear similar to the
relative incidence of primary lung and mediastinal tumors
. Rare malignant diagnoses
include Hodgkin disease, metastatic cancers, primary
leiomyosarcomas of the mediastinal vessels, and plasmocytomas.
Nonmalignant conditions
that can cause SVCS include the following:
·
Mediastinal
fibrosis
·
Vascular
diseases, such as aortic aneurysm, vasculitis, and arteriovenous
fistulas
·
Infections,
such as histoplasmosis, tuberculosis, syphilis, and
actinomycosis
·
Benign
mediastinal tumors such as teratoma, cystic hygroma, thymoma, and dermoid
cyst
·
Cardiac
causes, such as pericarditis and atrial myxoma
·
Thrombosis
related to the presence of central vein catheters
Super Venecaval Syndrome
By Dr Deepu
Images
Definition
History
Pathophysiology
Presentation and Findings
Causes
Diagnostic Workup
Management
Images
Definition
History
Pathophysiology
Presentation and Findings
Causes
Diagnostic Workup
Management
Presentation
Early in the clinical course of superior vena cava
syndrome (SVCS), partial obstruction of the superior vena cava (SVC) may be
asymptomatic, but more often, minor symptoms and signs are overlooked.
As the syndrome advances toward total SVC obstruction,
the classic symptoms and signs become more obvious.
Dyspnea is the
most common symptom, observed in 63% of patients with SVCS.
Facial swelling, head fullness, cough, arm swelling, chest pain, dysphagia, orthopnea,
distorted vision, hoarseness, stridor, headache,
nasal stuffiness, nausea, pleural effusions, and light-headedness can be seen.
Findings
The characteristic physical findings of
SVCS include venous distention of the neck and chest wall, facial edema, upper
extremity edema, mental changes, plethora, cyanosis, papilledema, stupor, and
even coma. Bending forward or lying down may aggravate the symptoms and signs.
Superior Venecaval Syndrome
By Dr Deepu
Definition
History
Pathophysiology
Presentation and Findings
Causes
Diagnostic Workup
Management
Pathophysiology:
History
Pathophysiology
Presentation and Findings
Causes
Diagnostic Workup
Management
Pathophysiology:
The SVC is the major drainage vessel for venous blood
from the head, neck, upper extremities, and upper thorax. It is a thin-walled,
low-pressure, vascular structure. This wall is easily compressed as it
traverses the right side of the mediastinum.
It is located in
the middle mediastinum and is surrounded by relatively rigid structures such as
the sternum, trachea, right bronchus, aorta, pulmonary artery, and the
perihilar and paratracheal lymph nodes. It extends from the junction of the
right and left innominate veins to the right atrium, a distance of 6-8 cm.
Obstruction of the SVC may be caused by neoplastic
invasion of the venous wall associated with intravascular thrombosis or, more
simply, by extrinsic pressure of a tumor mass against the relatively
thin-walled SVC. Complete SVC obstruction is the result of intravascular
thrombosis in combination with extrinsic pressure. Incomplete SVC obstruction
is more often secondary to extrinsic pressure without thrombosis. Other causes
include compression by intravascular arterial devices.
The incidence is on the rise, in line with the increased
use of endovascular devices.
An obstructed SVC initiates collateral venous return to
the heart from the upper half of the body through four principal pathways. The
first and most important pathway is the azygous venous system, which includes
the azygos vein, the hemiazygos vein, and the connecting intercostal veins. The
second pathway is the internal mammary venous system plus tributaries and
secondary communications to the superior and inferior epigastric veins. The
long thoracic venous system, with its connections to the femoral veins and
vertebral veins, provides the third and fourth collateral routes, respectively.
Despite these collateral pathways, venous pressure is
almost always elevated in the upper compartment if obstruction of the SVC is
present. Venous pressure as high as 200-500 cm H2 O has been recorded in patients with
severe SVCS.
Superior Venecaval Syndrome
By Dr Deepu
Images
Definition
History
Pathophysiology
Presentation and Findings
Causes
Diagnostic Workup
Management
Definition
Images
Definition
History
Pathophysiology
Presentation and Findings
Causes
Diagnostic Workup
Management
Definition
Superior vena cava syndrome (SVCS) is obstruction of
blood flow through the superior vena cava (SVC). It is a medical emergency and
most often manifests in patients with a malignant disease process within the
thorax. A patient with SVCS requires immediate diagnostic evaluation and
therapy.
History
William Hunter first described the syndrome in 1757 in a
patient with syphilitic aortic aneurysm.
In 1954,
Schechter reviewed 274 well-documented cases of SVCS reported in the
literature; 40% of them were due to syphilitic aneurysms or tuberculous mediastinitis.
Since the early reports, these infections have gradually
decreased as the primary cause of SVC obstruction. Lung cancer,
particularly adenocarcinoma, is now the underlying process in approximately 70%
of patients with SVCS. However, as many as 40% of cases are
attributable to nonmalignant causes.
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