Venographic appearance of portosystemic collateral pathways

June 16, 2017 | Autor: Harold Mitty | Categoria: Humans, Portal hypertension, Varicose Veins, Clinical Sciences
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T he British Journal of Radiology, 70 (1997), 1302–1306 © 1997 The British Institute of Radiology

Pictorial review

Venographic appearance of portosystemic collateral pathways J AHN, MD, J M COOPER, MD, J E SILBERZWEIG, MD and H A MITTY, MD Mount Sinai Medical Center, Department of Radiology, Box # 1234, 1 Gustave L Levy Place, New York, NY 10029, USA Abstract. Many imaging modalities can be used to evaluate various portosystemic collateral pathways seen in patients with portal hypertension. A knowledge of various typical and atypical pathways is essential for a proper understanding of the disease process. Transjugular transhepatic portographic appearance of such pathways are discussed in detail.

Introduction Portal hypertension is characterized by hepatofugal flow via various portosystemic collateral pathways. Gastrointestinal haemorrhage, one of the main complications of portal hypertension, may require endoscopic sclerotherapy, transjugular intrahepatic portosystemic shunt (TIPS) or surgical intervention. The commonest source of bleeding is oesophagogastric varices and occasionally mesenteric varices. Other rare sources include peristomal and ileal conduit varices. Many less invasive imaging modalities, such as Doppler sonography, CT [1], and MRI are widely advocated to evaluate these collaterals. Angiographic examination performed during TIPS procedure can also effectively demonstrate these collateral pathways. Angiographic evaluation includes indirect visualization of the venous phase via splenic and/or superior mesenteric arteriography and direct visualization via percutaneous transjugular transhepatic portography. We present the venographic appearances of various collateral pathways demonstrated on transjugular transhepatic portograms. A knowledge of the various collateral pathways is important in the evaluation and follow-up of patients with portal hypertension.

Normal portal venous anatomy The main portal vein is formed by the confluence of the splenic vein and the superior mesenteric vein (SMV). The inferior mesenteric vein drains into the splenic vein in two-thirds of individuals and the SMV in the remaining third. Other major tributaries of the splenic vein include short gastric and gastroepiploic veins, and occasionally the left gastric (coronary) vein. The coronary vein usually Received 29 May 1997 and in revised form 5 August 1997, accepted 13 August 1997. 1302

drains into the confluence of the SMV and the splenic vein.

Coronary and short gastric venous collateral Coronary (left gastric) venous collaterals (Figure 1) are the most commonly seen portosystemic collateral pathways in portal hypertension with a reported incidence of 30–69% [2, 3]. They are the most important collaterals in cranially directed hepatofugal flow. Coronary and short gastric venous collaterals (Figure 2) are usually drained via coexisting oesophageal or paraoesophageal varices and occasionally via spontaneous gastrorenal or splenorenal shunts.

Oesophageal or paraoesophageal varices These varices (Figure 1) usually arise from coronary and/or short gastric veins and drain into azygous and hemiazygous veins. Oesophageal varices are the most common source of gastrointestinal haemorrhage. Negative angiographic findings on the indirect venous phase does not rule out oesophageal varices. Endoscopy is the most reliable diagnostic procedure for detecting oesophageal varices. The paraoesophageal varices, however, cannot be detected by endoscopy. The size of the varices depends on the degree of portal hypertension and the presence of other portosystemic collateral pathways.

Umbilical or paraumbilical varices The recanalized umbilical vein (Figures 3a and b) originates from the left intrahepatic portal vein, courses vertically in the falciform ligament and drains into the superficial epigastric veins on the anterior abdominal wall, resulting in the caput medusae. The course of the umbilical vein may T he British Journal of Radiology, December 1997

Pictorial review: Portosystemic collateral pathways

mimic that of the portal vein on anteroposterior projections and cause inadvertent catherization during TIPS procedures. The paraumbilical veins also originate from the left intrahepatic portal vein, run within the ligamentum teres and course through the falciform ligament.

Duodenal varices Duodenal varices (Figure 4) are relatively common collaterals but are rarely a source of bleeding due to their deep location in the duodenal wall. They usually drain into the inferior vena cava via retroperitoneal collaterals.

Gastric and perisplenic varices Gastric and perisplenic varices are formed via coronary and short gastric veins. These varices, however, are not easily differentiated by angiography. CT may demonstrate these collaterals better due to its axial imaging ability. Isolated gastric varices resulting from splenic venous occlusion (segmental portal hypertension), will obviously not decompress with TIPS and are usually treated by splenectomy.

to keep a TIPS patent and decrease the incidence of encephalopathy [6].

Peristomal varices Peristomal varices (Figures 8a–c) are a rare type of portosystemic collateral seen in patients with portal hypertension who have had prior abdominal surgery. Sites of portosystemic collateral communications occur in post-operative adhesions at the peristomal mucocutaneous junctions or at the peritoneal adhesions. While peristomal varices may bleed, oesophageal varices may coexist and be responsible for the majority of gastrointestinal haemorrhages in such cases. The occurrence rate of haemorrhage from the gastrooesophageal varices is not significantly different between the patients with oesophageal varices alone and peristomal varices with coexisting oesophageal varices. Peristomal varices thus do not act as a ‘‘safety valve’’ for oesophageal bleeding [7, 8].

Mesenteric varices Mesenteric varices (Figures 5a–c and 6) include collaterals originating from the superior mesenteric and inferior mesenteric veins. The reported incidence of gastrointestinal haemorrhage from intestinal varices is 5–6.6% [4]. These varices communicate with systemic veins via the retroperitoneal and mesenteric venous plexus. Extensive collaterals may develop between branches of the inferior mesenteric vein such as anorectal veins and haemorrhoidal veins which drain into the inferior vena cava via internal iliac veins or gonadal veins. Bleeding mesenteric varices can also be treated successfully with TIPS [5]. Mesenteric varices due to focal venous obstruction (segmental portal hypertension), however, cannot be treated with TIPS.

Spontaneous gastrorenal and splenorenal shunts Gastrorenal and splenorenal portosystemic (Figures 7a and b) shunts are occasionally seen in patients with portal hypertension. These shunts divert blood to the inferior vena cava via an enlarged left renal vein. They can decompress the high pressure portal flow and produce a low portosystemic pressure gradient. Following TIPS procedure, these spontaneous shunts can decrease the effective flow and cause early closure of the newly created portosystemic shunt. Intentional embolization of these spontaneous shunts may be needed T he British Journal of Radiology, December 1997

Figure 1. Subtracted transjugular transhepatic portogram demonstrates a coronary vein ( large arrow), feeding prominent gastric varices (small arrow) which drains via oesophageal varices (arrowhead). There is a partially inflated Blakemore tube. 1303

J Ahn, J M Cooper, J E Silberzweig and H A Mitty

Figure 2. Transjugular transhepatic portogram demonstrates a prominent short gastric vein (arrow), feeding gastric varices (arrowhead). A curved arrow indicates a patent splenic vein.

Figure 4. Transjugular transhepatic splenoportogram demonstrates duodenal varices (arrow). Also shown are coexisting short gastric varices (arrowhead).

(a)

(b)

Figure 3. Subtracted transjugular transhepatic splenoportogram demonstrates prominent recanalized umbilical vein (arrow in (a)) arising from the intrahepatic left portal vein, continuing as a superficial epigastric vein on the anterior abdominal wall (arrowheads), and draining via bilateral iliac veins (arrows in ( b)). Also seen is retrograde filling of the inferior mesenteric vein (curved arrows). 1304

T he British Journal of Radiology, December 1997

Pictorial review: Portosystemic collateral pathways

(a)

(b)

Figure 5. Subtracted (a) and nonsubtracted (b) transjugular transhepatic splenoportograms demonstrate prominent mesenteric varices (open arrows in (a) and (b)) filling retrogradely from the anorectal branch of the inferior mesenteric vein (arrowheads in (a) and ( b)) and ileocolic branch of the superior mesenteric vein (arrows in (a) and (b)). These mesenteric varices are drained via right gonadal vein (curved arrows) which joins the inferior vena cava (arrowheads in (c)), best seen on delayed phase.

(c)

Figure 6. Subtracted transjugular transhepatic portogram demonstrates prominent inferior mesenteric vein (arrow), forming mesenteric varices (arrowhead) which drain via retroperitoneal collaterals and into inferior vena cava (curved arrow).

(a)

(b)

Figure 7. Subtracted transjugular transhepatic splenoportogram demonstrates prominent perisplenic varices (arrows in (a) and (b)) draining via oesophageal varices (arrowhead in (a)) and a spontaneous splenorenal shunt (arrowheads in (b)) which drain into the inferior vena cava (large arrow in ( b)) via the left renal vein (curved arrow in ( b)).

T he British Journal of Radiology, December 1997

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J Ahn, J M Cooper, J E Silberzweig and H A Mitty

(a)

(b)

Figure 8. Subtracted transjugular portogram demonstrates prominent retrograde filling of the superior mesenteric vein (arrow in (a)) in a patient with diverticular disease treated with an ileostomy. Unsubtracted (b) and subtracted (c) images of selective injection into the superior mesenteric vein demonstrates prominent peristomal varices (arrows in ( b) and (c)), draining via the right iliac vein (arrowhead in (c) and eventually into the inferior vena cava (curved arrow in (c)).

(c)

References 1. Cho KC, Patel YD, Wachsberg RH, Seeff J. Varices in portal hypertension: Evaluation with CT. Radiographics 1995;15:609–22. 2. Doehner GA, Ruzicka FF Jr, Rousselot LM, Hoffman G. The portal venous system: on its pathological anatomy. Radiology 1956;66:206–17. 3. Rousselot LM, Moreno AH, Panke WF. The clinical and physiopathologic significance of self established (nonsurgical) portosystemic shunts. Ann Surg 1959;150:384–410. 4. Nunez D, Russell E, Yrizarry J, et al. Portosystemic communications studied by transhepatic portography. Radiology 1978;127:75–9.

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5. Katz JA, Rubin RA, Cope C, Holland G, Brass CA. Recurrent bleeding from anorectal varices: Successful treatment with a transjugular intrahepatic portosystemic shunt. Am J Gastroenterol 1993;88:1104–7. 6. Shioyama Y, Matsueda K, Horihata K, et al. PostTIPS hepatic encephalopathy treated by occlusion balloon-assisted retrograde embolization of a coexisting spontaneous splenorenal shunt. Cardiovasc Intervent Radiol 1996;19:53–5. 7. Wiesner RH, LaRusso NF, Dozois RR, Beaver SJ. Peristomal varices after proctocolectomy in patients with primary sclerosing cholangitis. Gastroenterology 1986;90:316–22. 8. Fucini C, Wolff BG, Dozois RR. Bleeding from peristomal varices: Perspectives on prevention and treatment. Dis Colon Rectum 1991;34:1073–8.

T he British Journal of Radiology, December 1997

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