Where There Is Blood, There Is a Way: Unusual Collateral Vessels in Superior and Inferior Vena Cava Obstruction

Kapur, Sangita; Paik, Eugene; Rezaei, Ario; Vũ, Đoàn

doi:10.1148/rg.301095724

Cited by 126 publications

(117 citation statements)

References 23 publications

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“…In exceptional cases spleno-gonado-renal collateral vessels can drain from the splenic vein to the left renal vein via a gonadal vein. 44 Figure 4 …”

Section: The Afferents To Gastric Varicesmentioning

confidence: 99%

Collateral Pathways in Portal Hypertension

Sharma

Rameshbabu²

2012

Journal of Clinical and Experimental Hepatology

127

104

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Presence of portosystemic collateral veins (PSCV) is common in portal hypertension due to cirrhosis. Physiologically, normal portosystemic anastomoses exist which exhibit hepatofugal flow. With the development of portal hypertension, transmission of backpressure leads to increased flow in these patent normal portosystemic anastomoses. In extrahepatic portal vein obstruction collateral circulation develops in a hepatopetal direction and portoportal pathways are frequently found. The objective of this review is to illustrate the various PSCV and portoportal collateral vein pathways pertinent to portal hypertension in liver cirrhosis and EHPVO. ( J CLIN EXP HEPATOL 2012;2:338-352) A lmost any vein in the abdomen may serve as a potential collateral channel to the systemic circulation. Presence of abnormal collateral vessels appears to be one of the most sensitive (70-83%) and specific sonographic signs for the diagnosis of portal hypertension. 1 When blood flow through a vessel or a vascular bed is obstructed due to occlusion, as in EHPVO, or distortion, as in liver cirrhosis, collateral pathways open up as blood bypasses the occlusion or obstruction, always flowing down a pressure gradient from a high pressure to a low-pressure vessel or bed. The formation of portosystemic pathways occurs due to reopening of collapsed embryonic channels or reversal of the flow within existing adult veins. 2,3 The number of collateral channels depends on the severity of portal hypertension i.e. the differential gradient driving the flow between the portal and the systemic circulations and the duration of portal hypertension. The more severe and more prolonged the portal hypertension, the higher are the number of portosystemic pathways. However, this traditional hypothesis has been challenged and it has been suggested that the formation of portosystemic collateral circulation may be due in part to angiogenesis driven by vascular endothelial growth factor. 4,5 Almost 50 years have passed since the first detailed description of portosystemic collateral veins (PSCV) in portal hypertension appeared. 6 Precise mapping of PSCV is essential to therapeutic decisions and multidetector computerized tomography (MDCT) is sometimes used for cartography of PSCV. 7 EUS is increasingly being used for evaluation of PSCV and additionally provides an option for performing therapeutic interventions. 8 In addition to PSCV, PPCV pathways are frequently found in extrahepatic portal vein obstruction (EHPVO). The objective of this review is to illustrate the various PSCV and PPCV pathways pertinent to portal hypertension in liver cirrhosis and EHPVO. NORMAL PORTOSYSTEMIC ANASTOMOSESThe left gastric vein (LGV) anastomoses with the esophageal veins, which in turn drain into the azygos vein (AV). The superior rectal vein (SRV) anastomoses with the middle and inferior rectal veins (IRV), which are, respectively, tributaries of the internal iliac and the pudendal veins. The paraumbilical vein (PUV) anastomoses with subcutaneous veins in the anterior abdominal...

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“…In exceptional cases spleno-gonado-renal collateral vessels can drain from the splenic vein to the left renal vein via a gonadal vein. 44 Figure 4 …”

Section: The Afferents To Gastric Varicesmentioning

confidence: 99%

Collateral Pathways in Portal Hypertension

Sharma

Rameshbabu²

2012

Journal of Clinical and Experimental Hepatology

127

104

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“…7 IVC occlusion may also be secondary to coagulopathy, congestive heart failure, vasculitis, trauma, and extrinsic compression, among other conditions. 8 It is unclear which of these factors may have contributed to this patient's IVC thrombosis.…”

Section: Discussionmentioning

confidence: 96%

Complete infrahepatic inferior vena cava occlusion presenting as congenital absence

Baxi

Shah

Clair

2011

Journal of Vascular Surgery

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Inferior vena cava (IVC) occlusion may have widely varying clinical presentations that overlap with congenital IVC anomalies. Nevertheless, appropriate diagnosis, including differentiation from congenital absence, is mandatory. Endovascular therapy of chronic occlusions appears to yield results comparable to those of open repair. We report a case of infrahepatic IVC occlusion misdiagnosed as congenital absence of the IVC. The IVC occlusion was successfully recanalized and treated with angioplasty and stent placement.

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“…These include infraphrenic and hepatic parenchymal collaterals and systemic to pulmonary venous shunting [5][6][7]. Infraphrenic and hepatic parenchymal collaterals are said to be more likely if there is obstruction of the azygoatrial portion of the SVC [8].…”

Section: Discussionmentioning

confidence: 99%

Vanishing bone metastases — a pitfall in the interpretation of contrast enhanced CT in patients with superior vena cava obstruction

Thomas

Oliver²,

Sudarshan³

2011

BJR

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ABSTRACT. We describe a previously unreported case of vertebral marrow enhancement owing to collateral circulation in a patient with superior vena cava obstruction. Failure to recognise this phenomenon led to the misdiagnosis of sclerotic bone metastases. We describe a patient with superior vena cava (SVC) obstruction who had retrograde filling of the thoracic and vertebral venous collateral systems, which caused enhancement of the thoracic vertebrae and was mistaken for metastatic infiltration.Several other venous collateral imaging patterns have been reported in patients with SVC obstruction, but we are not aware of any previous description of the above phenomenon, which we believe to be of general interest to radiologists. Case reportA 60-year-old male smoker presented with weight loss and clinical features suggestive of SVC obstruction. A chest radiograph showed a superior mediastinal mass and a contrast enhanced CT (CECT) of the chest and abdomen was performed using the following parameters: 64 slice Lightspeed VCT (GE Medical Systems, Milwaukee, WI), 0.625 mm source image thickness, 100 ml iodinated contrast (Ultravist 300, Schering, Berlin, Germany), via iv cannula in left antecubital fossa injected by pump at 3 ml s 21 with a 26 s delay. CT confirmed a large anterior mediastinal mass. This occluded the left brachiocephalic vein and the SVC, proximal to the azygocaval junction. Contrast filled an extensive collateral circulation involving the mediastinum, left chest wall and vertebral venous plexus, passing into the distal SVC via the azygos vein.High attenuation was observed within the vertebral bodies and left posterior elements of several upper thoracic vertebrae. This was ascribed to metastatic disease (Figure 1a,b).Following biopsy diagnosis of squamous cell carcinoma, a CT positron emission tomography (PET) staging study was performed. The non-contrast enhanced CT study showed that the upper thoracic vertebrae were normal (Figure 2). On re-examination of the initial CECT, it was noted that much of the vertebral abnormality was centred around the opacified basivertebral and the anterior vertebral body veins and it was realised that retrograde opacification of the capillary spaces within the vertebrae had been mistaken for sclerotic metastatic disease (Figure 3). DiscussionSVC obstruction is due to malignancy in 80% of cases, but is also a recognised complication of iatrogenic or noniatrogenic trauma and fibrosing mediastinitis owing to granulomatous infection, autoimmune disease or drugs [1].When SVC obstruction develops, blood is diverted via venous collaterals. Four classic collateral pathways involving the azygos and hemiazygos, internal mammary and lateral thoracic, superficial thoraco-abdominal and vertebral venous plexuses have been described and proven by venography [2][3][4]. In practice, several collateral pathways may be involved together and the specific pattern in a given patient will depend on the cause, exact location and duration of venous obstruction, along with individual variations ...

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Where There Is Blood, There Is a Way: Unusual Collateral Vessels in Superior and Inferior Vena Cava Obstruction

Cited by 126 publications

References 23 publications

Collateral Pathways in Portal Hypertension

Collateral Pathways in Portal Hypertension

Complete infrahepatic inferior vena cava occlusion presenting as congenital absence

Vanishing bone metastases — a pitfall in the interpretation of contrast enhanced CT in patients with superior vena cava obstruction

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