Superior vena cava syndrome pathophysiology: Difference between revisions
No edit summary |
No edit summary |
||
| Line 33: | Line 33: | ||
On microscopic pathology, there are no characteristic findings of superior vena syndrome. | On microscopic pathology, there are no characteristic findings of superior vena syndrome. | ||
==References== | ==References== | ||
Revision as of 22:22, 11 January 2016
|
Superior Vena Cava Syndrome Microchapters |
|
Differentiating Superior Vena Cava Syndrome from Other Diseases |
|---|
|
Diagnosis |
|
Treatment |
|
Case Studies |
|
Superior vena cava syndrome pathophysiology On the Web |
|
American Roentgen Ray Society Images of Superior vena cava syndrome pathophysiology |
|
Directions to Hospitals Treating Superior vena cava syndrome |
|
Risk calculators and risk factors for Superior vena cava syndrome pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Maria Fernanda Villarreal, M.D. [2]
Overview
Superior vena cava (SVC) syndrome arises from the obstruction of venous blood drainage of the superior vena cava, which is normally is involved in the major blood flow return from head, neck, upper extremities, and upper thorax to the heart. Superior vena cava syndrome is a complication from a partial or complete obstruction due to malignant causes (60%) or benign causes (20%). This syndrome may be caused by the invasion of the venous wall associated with intravascular thrombosis, enlarged nodes, enlarged ascending aorta, or more simply, by extrinsic pressure of a tumor mass against the thin-walled superior vena cava (SVC) which leads to the development of SVC syndrome. SVC syndrome is associated with a number of conditions that include malignant tumors, tuberculosis, histoplasmosis, and syphilis.[1]
Pathogenesis
The superior vena cava (SVC) is the major blood vessel for drainage in the upper body (head, neck, upper extremities, and upper thorax). Extrinsic compression of the superior vena cava by a mediastinal tumor is possible because it has a low intravascular pressure. In addition, the superior vena cava is also surrounded by rigid structures, so it is relatively easy to compress. Moreover, the SVC is thin-walled, and the blood flowing therein is under low pressure. Therefore, when the nodes or ascending aorta enlarge, the SVC is compressed, blood flow slows, and complete occlusion may occur.
Knowledge of the anatomy of the SVC and its relationship to the surrounding lymph nodes is essential to understanding the development of the syndrome. The SVC is formed by the junction of the left and right brachiocephalic veins in the mid third of the mediastinum. The SVC extends caudally for 6 to 8 cm, coursing anterior to the right mainstem bronchus and terminating in the superior right atrium, and extends anteriorly to the right mainstem bronchus. The SVC is joined posteriorly by the azygos vein as it loops over the right mainstem bronchus and lies posterior to and to the right of the ascending aorta. The mediastinal parietal pleura is lateral to the SVC, creating a confined space, and the SVC is adjacent to the right paratracheal, azygous, right hilar, and subcarinal lymph node groups.
Associated Conditions
- Malignancy[2]
- Lymph node metastasis
- Non–small cell lung cancer
- Small cell lung cancer
- Lymphoma
- Metastatic lesions (most commonly from breast and testicular cancers)
- Infections
- Iatrogenic intravascular devices
- Thyroid goiter
- Thrombosis of SVC
- Pericardial constriction
- Idiopathic sclerosing mediastinitis
- Aortic aneurysm
Gross Pathology
On gross pathology, there are no characteristic findings of superior vena syndrome.
Microscopic Pathology
On microscopic pathology, there are no characteristic findings of superior vena syndrome.
References
- ↑ Menon A, Gupta A (2015). "Superior vena cava syndrome". Indian J. Med. Res. 142 (3): 350. doi:10.4103/0971-5916.166606. PMC 4669875. PMID 26458355.
- ↑ National Cancer Institute. http://www.cancer.gov/about-cancer/treatment/side-effects/cardiopulmonary-hp-pdq#link/_102_toc Accessed on January,11 2016