British Journal of Radiology 74 (2001),759-761 © 2001 The British Institute of Radiology
Retrograde venous invasion causing vertebral metastases in renal cell carcinoma
R S Oeppen, MRCP, FRCR
and
K Tung, FRCP, FRCR
Department of Clinical Radiology, Southampton University Hospital, Tremona Road, Southampton SO16 6YD, UK
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Abstract
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A case of renal cell carcinoma is presented with renal vein and inferior vena cava tumour/thrombus extension and vertebral metastases centred on the basivertebral veins at three contiguous levels in the low thoracic spine. MRI demonstrated tumour in the intervertebral veins, suggesting that the vertebral deposits were due to retrograde venous spread. To our knowledge, vertebral metastatic deposits due to retrograde venous spread in renal cell carcinoma have not been previously demonstrated directly on imaging. A review is given of the venous anatomy relevant to this mode of spread.
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Case report
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A 63-year-old man underwent a radical left nephrectomy for a left lower pole renal cell carcinoma. Contrast enhanced staging CT of the chest and abdomen demonstrated tumour/thrombus within the inferior vena cava (IVC) extending from the confluence of the common iliac veins to a level above the renal pedicles but below the intrahepatic portion of the IVC. No focal lung lesions were present. Post-operatively the patient suffered a right occipital lobe infarction but otherwise made a good recovery.
3 months later he presented with pain in the lower thoracic spine, chest and left loin. A chest radiograph showed two nodules in the right hemithorax that had the appearance of metastases on subsequent CT. MRI of the abdomen and thoracolumbar spine was also performed. There was no evidence of recurrence in the left renal bed. The IVC was poorly visualized but of normal calibre. The liver contained numerous lesions with high signal on T2 weighting, consistent with metastases. The right kidney had a normal appearance.
Images of the thoracolumbar spine demonstrated central linear nodular foci of abnormal high signal in the vertebral bodies of T10, T11 and T12, which did not suppress on the short tau inversion recovery (STIR) sequence (Figure 1
). These foci were based on the basivertebral veins, with abnormal soft tissue extending posteriorly into the epidural space and along the course of the intervertebral veins bilaterally at all three levels. The posterior aspect of each of these vertebral bodies was expanded and the cortex was disrupted. The spinal canal appeared narrowed and there was effacement of the cerebrospinal fluid anterior to the spinal cord (Figures 2a,b). The patient was referred for ß-interferon therapy and radiotherapy, with some relief in his symptoms.
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Figure 1. Sagittal STIR sequences showing central foci of abnormal high signal in the T10, T11 and T12 vertebral bodies.
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2 (a,b). Fat suppressed axial images showing abnormal high signal tissue expanding the posterior aspect of the vertebral body, effacing the cerebral spinal fluid and following the course of the basivertebral and intervertebral veins.
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Discussion
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Renal cell carcinoma (RCC) metastases occur in lung, bone, liver and brain as well as at less common sites such as thyroid, orbit, paranasal sinuses, vagina, gall bladder and soft tissues of the distal extremities [1]. The presumed route of metastasis for RCC to sites other than the liver or lung parenchyma involves the paravertebral venous plexus of Batson. Invasion of the IVC occurs in up to 55% of cases, more commonly with right-sided and large tumours [2]. The most likely explanation for the contiguous vertebral metastases found in this case is retrograde venous invasion via the vertebral venous plexus. The regional venous anatomy is reviewed to understand this mode of spread.
Venous drainage from the lower thoracic vertebrae is via the posterior intercostal veins into the azygos and hemiazygos systems. The hemiazygos vein lies to the left of the spine and is formed by the confluence of the left ascending lumbar vein with a medial root from the left renal vein. The hemiazygos vein crosses the midline at T8 to drain into the azygos vein, which is formed by the confluence of the right ascending lumbar vein with a medial root from the IVC (Figure 3).
Branches of the lumbar and posterior intercostal veins anastomose with the valveless venous plexus extending along the vertebral column from the skull to the coccyx. There is free communication between the veins of the neck, thorax, abdomen and pelvis and the vertebral venous plexus owing to the lack of competent valves. During any activity that increases intraabdominal pressure, for example coughing, retrograde flow occurs into the vertebral venous plexus. The vertebral venous plexus communicates with the intervertebral veins, which follow the course of the spinal nerve roots, and thus with the anterior longitudinal venous sinuses and basivertebral veins (Figure 4).
It can reasonably be postulated that with reduced flow through the left renal vein owing to the presence of tumour, increased retrograde venous flow can occur into the intervertebral and basivertebral veins resulting in tumour deposition within contiguous vertebral bodies.
A variety of imaging modalities are used in the detection and staging of RCC [3, 4]. Contrast enhanced spiral CT is most often used at present as it is relatively readily available and provides good anatomical coverage and spatial resolution. MRI has been advocated as a superior technique in assessing IVC involvement without the need for intravenous contrast medium and it provides improved soft tissue contrast and multiplanar imaging [5, 6]. In particular, the cranial extent of IVC involvement is best shown on sagittal and coronal images of the IVC. It may also be possible to distinguish between tumour and thrombus using gadolinium enhancement [3]. This case report gives further reason to favour MRI in preference to CT for staging abdominal disease in RCC. Furthermore, the thoracolumbar spine is proposed as an important review area in the presence of renal vein/IVC tumour/thrombus.
Received for publication November 22, 2000.
Revision received March 13, 2001.
Accepted for publication April 4, 2001.
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