British Journal of Radiology (2005) 78, 553-557
© 2005 British Institute of Radiology
doi: 10.1259/bjr/21010811
Benign external compression of the inferior vena cava associated with thrombus formation
R A England, MRCP, FRCR1,
I P Wells, FRCP, FRCR1 and
C M Gutteridge, MRCP, FRCR2
1 Department of Clinical Imaging, Derriford Hospital, Plymouth, Devon PL6 8DH and 2 Department of Radiology, Royal Cornwall Hospital, Truro, Cornwall TR1 3LJ, UK
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Abstract
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Malignant and benign causes of inferior vena cava (IVC) occlusion and compression are recognized. Cases of benign IVC compression with associated distal thrombus formation have not however been frequently described. We present two cases of benign external IVC compression associated with distal thrombus formation; one resulting from a giant, benign, hepatic cyst, and another due to pelviureteric junction obstruction, resulting in massive hydronephrosis.
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Introduction
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Occlusion of the inferior vena cava (IVC) is a well recognized complication of malignancy, be this indirectly through an increased tendency to thrombus formation, or directly due to tumour thrombus extension as in the case of renal cell carcinoma. Benign causes of IVC obstruction are less frequently encountered and may also be due to external compression or internal occlusion. Benign occlusions may be membranous, a condition of disputed aetiology more frequently encountered in the Far East that predisposes to hepatocellular carcinoma, or may be due to congenital segmental deficiency. There are however few reports of benign cases of external compression of the IVC. We have found reports in the literature of three cases of benign, external IVC obstruction secondary specifically to bladder distension, two of which were in neonates. An association between IVC compression by polycystic kidneys resulting in infrarenal IVC thrombus formation and pulmonary embolus has been described [1, 2]. A single case of IVC obstruction specifically due to an enlarged renal pelvis has been reported [3]. This case was due to bladder outflow obstruction secondary to benign prostatic hypertrophy, and was not complicated by thrombus formation. External IVC compression by other uncommon causes such as hydatid cyst [4], haematoma due to blunt liver trauma [5], and ruptured abdominal aortic aneurysm [6] have been described, again with no thrombotic complications. The two cases presented here are unusual in the combination of the causes of IVC obstruction, and associated distal thrombus formation.
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Case 1
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A 70-year-old woman, who had an asymptomatic benign hyperplastic colonic tumour was noted on a pre-operative CT study to have a large simple cyst arising from within the right lobe of her liver. She had a medical history of ischaemic heart disease, atrial fibrillation, transient ischaemic attacks, anaemia and mild, chronic renal impairment.
Prior to resection of her colonic tumour, and 12 days following coronary artery angioplasty and stent insertion for lesions in the left anterior descending and right coronary arteries, she presented with pain and swelling of the right leg. The arterial puncture had been via the right groin (size 6 French catheter) and there was no documented puncture of the femoral vein. Duplex ultrasound demonstrated echogenic material within the right common femoral vein with no evidence of femoral artery puncture complications such as haematoma or false aneurysm. She was subsequently commenced on warfarin. At this time she had been vomiting and was both clinically and biochemically dehydrated on a background of chronic renal impairment (urea 26, creatinine 209). 1 week later, with an International Normalized Ratio (INR) of 3.4, she passed a moderate amount of blood per rectum. Warfarin therapy was ceased and a repeat CT arranged to assess the upper limit of thrombus and re-assess the hepatic cyst. Both common iliac veins were occluded and the thrombus extended within the IVC to a level 3 cm below the renal veins. The cyst, which measured 17 cm in maximum diameter, significantly compressed the IVC (Figure 1a
).
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Figure 1. (a) CT of the abdomen showing a simple, but very large cyst within the right lobe of the liver. The inferior vena cava (IVC) is barely visible as it is compressed to near total occlusion. (b) Initial inferior vena cavogram showing both the extent of luminal narrowing of the IVC, and the cephalic extent of the thrombus within. (c) Following deployment of the Tulip filter, and subsequent cyst aspiration, the hepatic IVC lumen has now returned to normal appearances.
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A Tulip filter (Cook, UK) was placed within the infrarenal IVC above the distal thrombus via a right-sided jugular approach. Venography at the time had confirmed 90% caval compression by the hepatic cyst (Figure 1b
). With the filter in a satisfactory position the cyst was drained percutaneously with the aspiration of 2 l of fluid, in the knowledge that the risk of embolising thrombus, owing to the rapid increase in venous flow rate, would not result in significant pulmonary embolus. Further venography immediately following the drainage procedure demonstrated a normal appearance in the upper IVC with free flow of blood to the right atrium (Figure 1c). The drainage procedure was complicated by a localized sub-hepatic haematoma resulting in a fall in haemoglobin. This was a self-limiting problem and did not require transfusion.
Repeat ultrasound 3 weeks later demonstrated some recollection of fluid within the cyst that now measured 10 cm in diameter. Flow within the hepatic portion of the IVC was of normal characteristics and no echogenic material was seen within. Following resection of the benign hyperplastic colonic polyp, the presumed source of her bleeding per rectum, she was recommenced on warfarin and there have been no further complications.
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Case 2
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A 45-year-old man presented as an emergency with sudden increasing shortness of breath associated with chest pain. He had a 5-week history of anorexia and weight loss, with a 2-week history of shortness of breath. He had a past medical history of hepatitis C infection secondary to intravenous drug abuse, and a right sided pelviureteric junction obstruction diagnosed 2 years previously. Dynamic renography with frusemide performed within 3 months of diagnosis had demonstrated an obstructed kidney that contributed 1% to divided renal function (PATLAK analysis). Renal biochemistry on admission was normal. He denied ever injecting into veins in either leg and claimed to have not injected for several years however this was later corrected to 6 weeks previously.
A contrast enhanced CT study performed urgently on admission revealed thrombus in the right atrium extending from the IVC (Figure 2a), and within both pulmonary arteries extending into the lower lobe vessels. The right atrium and IVC were distended. The right kidney was markedly hydronephrotic with only a thin rim of cortex, and the adjacent IVC was filled with thrombus. He was transferred to the regional cardiothoracic centre for surgical consideration. Transthoracic echo again demonstrated an enlarged right atrium containing thrombus extending from the IVC. He underwent open exploration of the right atrium and main pulmonary trunk. Systolic pulmonary arterial pressure measured 70 mmHg prior to removal of thrombus from the right atrium, main pulmonary trunk, left pulmonary artery, and vena cava.
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Figure 2. (a) CT pulmonary angiogram showing a filling defect due to thrombus within the right atrium (arrows) and enlarged right heart chambers. (b) Post operative inferior vena cavogram demonstrating the degree of inferior vena cava (IVC) luminal compression at the level of the renal veins.
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Post-operative duplex ultrasound demonstrated echogenic material within the left popliteal and superficial femoral veins to the mid thigh level. The intrahepatic and sub-hepatic portions of the IVC now appeared clear; the thrombus having presumably migrated. His post-operative recovery was complicated by a wound infection resulting in septicaemia necessitating a protracted course of antibiotics. Nephrectomy was therefore postponed and performed electively at a later date. Femoral venography performed 9 days post-operatively did not demonstrate any thrombus within the IVC, but did reveal a reduction in lumen calibre at the level of the renal veins by 70% (Figure 2b). The degree of distortion of the caval anatomy, along with the complication of sepsis, precluded the deployment of a filter and the patient remained on warfarin whilst awaiting nephrectomy. The hydronephrosis was drained percutaneously via nephrostomy 3 weeks after initial presentation with the aspiration of 850 ml of fluid. Repeat ultrasound performed 6 weeks later demonstrated no recurrence of hydronephrosis. When right nephrectomy was performed 5 months later the hydronephrosis had recollected. Factor V Leiden and prothrombin gene mutations were excluded.
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Discussion
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Compression of the lumen of a vein results in decreased flow caudally which, with time, may predispose to thrombus formation. In both cases presented, the external IVC obstruction was of a chronic nature, inferred from the size of the giant hepatic cyst in case 1, and the longstanding hydronephosis in the second case. It is reasonable to postulate that the marked narrowing of the IVC with resultant flow disturbance was one factor which predisposed to the thrombosis, and in one case embolism, seen in our cases. Other factors however may well have contributed. The patient in case 1 had been vomiting for 2 days and was dehydrated, which is widely accepted as a risk factor for thrombus formation. Deep vein thrombosis (DVT) following cardiac catheterization is an uncommon but recognized complication [7] although more frequently associated with venous cannulation and multiple attempts. There was no documented venous cannulation and no ultrasound evidence of arterial puncture complication in this case.
Injection into the groin veins is the most likely compounding risk factor in an intravenous drug abuser [8, 9]. This however was denied by our patient. Hepatitis C is associated with the increased incidence of anticardiolipin antibodies, however studies have failed to show any significant increase in thrombotic tendency or anticardiolipin syndrome [10, 11]. There is a recognized association between advanced hepatic fibrosis secondary to Hepatitis C and an increased incidence of thrombotic risk factors [12, 13], although it is not yet clear whether this risk extends to the larger veins. Our patient did not have hepatic fibrosis, however we cannot fully exclude all associated thrombotic risk factors.
There are certain signs that should alert to the possibility of IVC flow interruption such as bilateral limb swelling in the absence of cardiac impairment, and collateral formation in the absence of chronic liver disease. In the case presenting with massive pulmonary embolus, imaging by both contrast enhanced CT and echocardiography had demonstrated thrombus extending from the IVC to the right atrium prior to surgery. At surgery later that day, the thrombus had migrated proximally from the IVC, underlining the serious and unstable nature of this condition.
Various means of imaging were employed in the diagnosis and management of these cases. Ultrasound, CT and lower limb venography all have roles to play, and vary slightly in the information that they can offer. Traditionally venography has been considered the gold standard in venous assessment, however it can have limitations, particularly in the assessment of the proximal veins, and ultrasound and CT are now often thought to be advantageous [14, 15]. Femoral venography will provide accurate information about the IVC lumen calibre, the caudal extent of narrowing or occlusion, and will demonstrate any functioning collateral vessels. Intervening bowel gas is not usually a concern when using digital subtraction, unlike with ultrasound when it may seriously compromise the image quality. It may not be possible however to define accurately the cephalad extent of complete obstruction by femoral venography alone. Both ultrasound and CT have been shown to demonstrate accurately the cephalad extent of the thrombus, although parasagittal imaging in ultrasound achieves this more definitively [15]. Both ultrasound and CT also allow further assessment of the cause of IVC flow interruption, be this detection of primary malignancy or the cause of external compression as in our cases.
Benign intra-abdominal causes of external IVC compression as a predisposition to DVT have not been widely described in the literature. Given the incidence of gross hydronephrosis and large hepatic cysts, it is surprising that associated thromboembolism has not been described more frequently. Often a pelvic ultrasound examination is requested in a hunt for malignancy, yet the abdominal viscera and IVC are usually not routinely examined in such cases. It may be postulated therefore, that some similar cases remain undetected. Ultrasound is a reliable way of assessing the upper extent of the thrombus, which is often not demonstrated on venography alone, and allows assessment of other viscera. It remains the safest and most accessible means of follow-up. When transluminal, interventional therapy is considered, such as filter insertion or venoplasty, venography remains essential.
Received for publication January 15, 2004.
Revision received July 22, 2004.
Accepted for publication January 26, 2005.
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References
|
|---|
- O'Sullivan DA, Torres VE, Heit JA, Liggett S, King BF. Compression of the inferior vena cava by right renal cysts: an unusual cause of IVC and/or iliofemoral thrombosis with pulmonary embolism in autosomal dominant polycystic kidney disease. Clin Nephrol 1998;49:332–4.[Medline]
- Leimenstoll G, Loose G, Harder T, Herrmann G, Papadopoulos I, Burck HC, et al. Inferior vena cava compression syndrome in cystic kidney. Duplex ultrasonic diagnosis. Dtsch Med Wochenschr 1991;116:1583–7.[Medline]
- Davis GC, Aronson NE, Moul JW. Inferior vena cava compression due to massive hydronephrosis from bladder outlet obstruction. Tech Urol 2000;6:226–7.[Medline]
- Rajagopal KV, Bishwas R. Hydatid cyst of the liver presenting as an inferior cava obstruction. J Clin Ultrasound 2002;30:114–6.[CrossRef][Medline]
- Markert DJ, Shanmuganathan K, Mirvis SE, Nakajima Y, Hayakawa M. Budd-Chiari syndrome resulting from intrahepatic IVC compression secondary to blunt hepatic trauma. Clin Radiol 1997;52:384–7.[CrossRef][Medline]
- Ohno A, Nishimura T, Uehara T, Shimonagata T, Kumita S, Ogawa Y, et al. Interesting finding of RI venogram in a case with obstruction of inferior vena cava due to compression by the ruptured abdominal aortic aneurysm. Kaku Igaku 1993;30:557–61.[Medline]
- Zahn R, Fromm E, Thoma S, Lotter R, Zander M, Wagner S, et al. Local venous thrombosis after cardiac catheterisation. Angiology 1997;48:1–7.
- Roszler MH, McCarroll KA, Donovan KR, Rashid T, Kling GA. The groin hit: complications of intravenous drug abuse. Radiographics 1989;9:487–508.[Abstract]
- McColl MD, Tait RC, Greer IA, Walker ID. Injecting drug use is a risk factor for deep vein thrombosis in women in Glasgow. Br J Haematol 2001;112:641–3.[CrossRef][Medline]
- Harada M, Fujisawa Y, Sakisaka S, Kawaguchi T, Taniguchi E, Sakamoto M, et al. High prevalence of anticardiolipin antibodies in hepatitis C virus infection: lack of effects on thrombocytopenia and thrombotic complications. J Gastroenterol 2000;35:272–7.[CrossRef][Medline]
- Ordi-Ros J, Villarreal J, Monegal F, Sauleda S, Esteban T, Vilardell M. Anticardiolipin antibodies in patients with chronic hepatitis C virus infection: characterisation in relation to antiphospholipid syndrome. Clin Diagn Lab Immunol 2000;7:241–4.[Abstract/Free Full Text]
- Poujol-Robert A, Rosmorduc O, Serfaty L, Coulet F, Poupon R, Robert A. Genetic and acquired thrombotic factors in chronic hepatitis C. Am J Gastroenterol 2004;99:527–31.[CrossRef][Medline]
- Papatheodoridis GV, Papakonstantinou E, Andrioti E, Cholongitas E, Petraki K, Kontopoulou I, et al. Thrombotic risk factors and extent of liver fibrosis in chronic viral hepatitis. Gut 2003;52:404–9.[Abstract/Free Full Text]
- Park JH, Lee JB, Han MC, et al. Sonographic evaluation of inferior vena caval obstruction: correlative study with vena cavography. AJR Am J Roentgenol 1985;145:757–62.[Abstract/Free Full Text]
- Didier D, Racle A, Etievent JP, Weill F. Tumour thrombus in the inferior vena cava secondary to malignant abdominal neoplasms: US and CT evaluation. Radiology 1987;162:83–89.[Abstract/Free Full Text]
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Abstract
Introduction
