Case report: Superior vena cava obstruction: Unusual CT findings due to venous collaterals

Case report: Superior vena cava obstruction: Unusual CT findings due to venous collaterals

Clinical Radiology (1997) 52, 559-560 Case Report: Superior Vena Cava Obstruction: Unusual CT Findings Due to Venous Collaterals J. A. HOLEMANS, D. C...

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Clinical Radiology (1997) 52, 559-560

Case Report: Superior Vena Cava Obstruction: Unusual CT Findings Due to Venous Collaterals J. A. HOLEMANS, D. C. HOWLETT and S. C. RANKIN

Department of Radiology, Guy's Hospital, London, UK We describe a case of superior vena cava (SVC) obstruction in which there was intense pericardial enhancement and focal enhancement within the medial segment of the left lobe of the liver on post-contrast CT due to the collateral circulation. Pericardial collaterals have not been previously reported, but focal liver enhancement [1] and similar areas of increased uptake of radiotracers are both well recognized in SVC obstruction [2,3].

CASE REPORT An 85-year-old woman presented with increasing shortness of breath on exertion and rest. Over the previous 3 weeks she had noted facial swelling, which was worse on lying down. She had a past history of chronic bronchitis, ischaemic heart disease, left ventricular failure and hypothyroidism. She had smoked all her adult life and still smoked five cigarettes a day. On examination she was dyspnoeic with a plethoric facies and distended veins over the chest and upper abdomen. There was a right-sided pleural effusion. Full blood count and electrolytes were normal. A chest radiograph showed a large right mediastinal mass. A probable diagnosis of SVC obstruction secondary to primary lung carcinoma was made. Spiral CT was performed with 50 ml intravenous contrast medium (370mgI/ml) infused at 2ml/s using an automatic pump with a 15s scanning delay after the injection started. This revealed an extensive anterior mediastinal mass surrounding the innominate veins and the SVC which was compressed, with right paratracheal, right hilar and sub-carinal adenopathy. There was filling of multiple collaterals in the anterior chest wall, around the right breast and the internal mammary chain (Fig. 1). Contrast medium also refluxed down the azygos system into the inferior vena cava. A very dense wedge-shaped area in the liver adjacent to the falciform ligament was noted (Fig. 2) and the pericardium was also hyperdense (Fig. 3). These areas of enhancement were due to contrast medium in unusual collaterals due to the SVC obstruction (calcification was excluded as the attenuation decreased on delayed images). Biopsy of the mass revealed a small cell lung carcinoma and the SVC was stented. However the patient died 1 month later.

lumbar and sacral veins to the azygos and the internal mammary pathways. Also rarely reported in SVC obstruction are minor rightto-left shunts [6,7]. These are thought to result from anastomoses between the systemic and pulmonary venous circulations at sites of tumour invasion into the chest wall or mediastinum, or in fibrosing mediastinitis. With collateral flow via the internal mammary and epigastric veins there may also be a systemic-portal communication through recanalization of the left umbilical vein. Thus, venous blood flows through the round ligament that joins the left branch of the portal vein within tire medial segment of left lobe of the liver (quadrate lobe). This accounts for the focal hepatic enhancement, in this case on contrast-enhanced CT. Analogous areas of increased

Fig. 1 - Post-contrast CT. The mediastinal mass is shown compressing the SVC. Contrast medium outlines multiple venous collaterals including the internal mammary and azygos pathways. Bilateral pleural effusions noted.

DISCUSSION Superior vena cava obstruction is caused by malignancy in 80% of cases [4]. Less frequent causes include tuberculosis, histoplasmosis, pyogenic and fibrosing mediastinitis, aneurysm and thrombophlebitis of the innominate veins or SVC [5,6]. In SVC obstruction four systemic venous collateral pathways are generally recognized [6]: (1) Internal mammary pathway, including the internal mammary, superior epigastric, inferior epigastric and superficial veins of the thorax. (2) Azygos pathway, including the azygos, hemiazygos, intercostal and lumbar veins. (3) Lateral thoracic pathway, including the lateral thoracic, thoracoepigastric, superficial circumflex, long saphenous and femoral veins to the inferior vena cava. (4) Vertebral pathway, including the innominate, vertebral, intercostal, Correspondence to: Dr J. A. Holemans, Department of Radiology, 2nd Floor, Guy's Tower, Guy's Hospital, London SEI 9RT, UK. © 1997 The Royal College of Radiologists, ClinicalRadiology 52, 559-560.

Fig. 2 - Post-contrast CT. Denronstrates the full extent of the wedge of fiver enhancement in the medial segment of the left lobe of the liver.

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the sole umbilical vein and drainage is preferentially via the left side of the liver and ductus venosus [8]. The pericardial veins are tributaries of the azygos system [9], and we consider the pericardial enhancement on postcontrast CT to be an unusual effect of the collateral circulation via this pathway.

REFERENCES

Fig. 3 - Post-contrast CT. Cutting through the inferior pericardium there is dense enhancement. The superior extent of the fiver enhancement is also visible.

uptake are well described in radiolabelled sulphur colloid and radioparticle scintigraphy when they are trapped in the narrow hepatic vascular channels [2,3]. Dynamic in vitro Tc-99m labelled red blood cell scintigraphy in SVC obstruction has shown accumulation within the liver due to collaterals 30 s after injection into the antecubital vein [2]. The right lobe of the liver does not enhance because the right umbilical vein and its vascular anastomoses with the fight side of the liver are obliterated at about the sixth week of embryonic life; the remaining left umbilical vein becomes

1 Maldjian PD, Obolovich AT, Kyunghee CC. Focal enhancement of the liver on CT: A sign of SVC obstruction. Journal of Computer Assisted Tomography 1995;19:316-318. 2 Trombley BA, Marcus CS, Koci T. Unexpected demonstration of superior vena caval obstruction in third trimester lung imaging. Clinical Nuclear Medicine 1988; 13:407-409. 3 Suneja SK, Teal JS. Discrepant sulfur colloid and radioparticle liver uptake in superior vena cava obstruction: case report. Journal of Nuclear Medicine 1989;30:113-116. 4 Roberts DJ Jr, Dotter CT, Steinberg I. Superior vena cava and innominate veins: Angiographic study. American Journal of Roentgenology 1952; 66:341. 5 Kistler AM, Silverman ED, Sharpe MB, Yudt WM, Camponovo EJ. Superior vena cava obstruction in fibrosing mediastinitis: demonstration of fight-to-left shunt and venous collaterals. Nuclear Medicine Communications 1991 ; l 2:1067 - 1074. 6 Wilson ES. Systemic to pulmonary venous communication in the superior vena caval syndrome. American Journal of Roentgenology 1976; 127:247. 7 Hutchins WW, Kirchner PT, MacMahon H. Perfusion lung scan in superior vena cava obstruction: demonstration of venous collaterals and systemic-pulmonary venous shunt. American Journal of Roentgenology 1982;138:433. 8 Patten BM. Human Embryology, 3rd ed. New York: McGraw-Hill, 1968. 9 Williams PL, Warwick R, eds. Gray's Anatomy, 37th ed. Edinburgh: Churchill Livingstone, 1989.

Clinical Radiology (1997) 52, 560-561

Case Report: The MRI Diagnosis of Bone Marrow Infarction in a Child With Leukaemia Y. AMANO, J. TAKAURA and T. KUMAZAKI

Department of Radiology, Nippon Medical School, Tokyo, Japan CASE REPORT A 14-year-old boy presented with a 1-month history of painful limbs and hip joints. Conventional radiographs of the lower extremities showed periosteal reaction. Bone marrow biopsy revealed acute lymphocytic leukaemia (ALL). Magnetic resonance (MR) imaging was performed using a 0.5 T unit. T1weighted images showed decreased signal intensity of bone marrow (Fig. la), while T2-weighted images showed high signal intensity, isointense with fat (Fig. lb). Tl-weighted images after gadopentetate dimeglumine (Gd-DTPA) injection showed intense enhancement in the marrow of the right femoral diaphysis, and medially in the marrow of the left femoral diaphysis and pefiosteal region. The lateral part of the left femoral marrow did not enhance (Fig. lc,d). A diagnosis of bone marrow infarction with acute bone pain was made. Histologic confirmation was not obtained owing to the risks of biopsy. No change in the non-enhancing region of the left femur was observed in three follow-up MR examinations performed at monthly intervals. After 4 months of chemotherapy, the right femoral diaphyseal marrow and the medial side of the left femoral diaphysis showed high signal intensity on Correspondence to: Y. Amano, Department of Radiology, Nippon Medical School, 1-1-5 Sendagi, Bunkyo-ku, Tokyo 113, Japan

both T1- and T2-weighted images, and no definite enhancement. Pre- and post-contrast enhancement MR appearances of the lateral side of left femoral diaphyseal marrow were similar to those on the first examination, except for rim enhancement (Fig. 2a-c). Bone marrow aspiration demonstrated remission of ALL.Correspondence to: Y. Amano, Department of Radiology, Nippon Medical School, 1-1-5 Sendagi, Bunkyo-ku, Tokyo 1 l 3, Japan.

DISCUSSION Bone marrow infarction has many causes, and presents with bone and joint pains [1]. There have been several reports describing MR appearances of bone marrow infarction associated with haematologic disorders in adults [1,2]. Although the MR findings in this case are similar to those of the previous reports [1,2], the presentation in a child is unusual. Both leukaemic marrow and infarcted marrow showed decreased signal intensity on Tl-weighted images and © 1997 The Royal College of Radiologists, ClinicalRadiology, 52, 560-561.