What is the role of compression in the pathogenesis of inferior vena caval thrombosis (IVCT)?

Updated: Jun 12, 2018
  • Author: Luis G Fernandez, MD, FACS, FASAS, FCCP, FCCM, FICS, KHS, KCOEG; Chief Editor: John Geibel, MD, DSc, MSc, AGAF  more...
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Extrinsic compression may also result from nontumoral sources and increase the likelihood of IVCT. The distortion of the normal caval anatomy generates both venous stasis and turbulent flow. This situation facilitates the formation of a thrombus. An activity as innocuous as bicycle riding has reportedly caused IVCT. [9] The spectrum of medical diagnoses that can cause compression of the IVC is determined by those structures anatomically adjacent to the IVC.

Abdominal aortic aneurysms (AAAs) can compress the IVC and cause thrombosis. Although this clinical situation is uncommon, the implications for surgical repair of the aneurysm are significant. The surgeon must be prepared for enlarged venous collaterals and the possibility of unusual tissue-plane configurations. One reported case described incorporation of the IVC into the aneurysm [10] ; the wall of the IVC was actually part of the wall of the aneurysm. Knowing that AAA is a risk factor for IVCT should heighten clinical suspicion in appropriate cases.

Hepatic abscesses, either from amebae or echinococci, can also generate thrombosis of the IVC from compression. Because of the propensity of these processes to evolve over time, patients may present without symptoms suggestive of IVC occlusion. They may only demonstrate evidence of the primary process or of collateral venous hypertrophy. The initial presenting symptom may even be pulmonary embolization.

Other retroperitoneal organ systems that have been shown to cause IVCT include the pancreas and the kidneys. Polycystic disease of the right kidney has reportedly been clinically associated with thrombosis of the IVC. [11] Pancreatic pseudocysts have been observed to cause thrombosis of the IVC. [12] Acute pancreatitis has also been found to generate thrombosis of the IVC. [13, 14]

The pathophysiology of the evolution of the thrombosis may reflect either the local impact of inflammation of the pancreatic head or the impact of a hypercoagulable state on the IVC. Although IVCT in the setting of pancreatitis is uncommon, this clinical entity may account for an unexplained deterioration in the status of a patient with acute pancreatitis.


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