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Acute cauda equina syndrome caused by thrombosis of the inferior vena cava
  1. JELLE DE KRUIJK,
  2. ARTHUR KORTEN,
  3. JELIS BOITEN
  1. Department of Neurology
  2. Department of Radiology, University Hospital Maastricht, The Netherlands
  1. Dr JR de Kruijk, Department of Neurology, University Hospital, Maastricht, P Debeylaan 25, NL 6229 HX, Maastricht, The Netherlands. Fax 0031 43 3877055; emailJDK{at}SNEU.AZM.NL
  1. JAN WILMINK
  1. Department of Neurology
  2. Department of Radiology, University Hospital Maastricht, The Netherlands
  1. Dr JR de Kruijk, Department of Neurology, University Hospital, Maastricht, P Debeylaan 25, NL 6229 HX, Maastricht, The Netherlands. Fax 0031 43 3877055; emailJDK{at}SNEU.AZM.NL

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Deep venous thrombosis of the lower limbs is the most common vascular disorder in hospital. Although the clinical features are not specific, the most important symptoms are oedema, local tenderness, and pain. Well known complications of deep venous thrombosis are pulmonary embolism and chronic venous insufficiency. Neurological complications are uncommon after deep venous thrombosis.

We report on a patient who presented with an acute cauda equina syndrome, which turned out to be caused by thrombosis of the inferior vena cava.

A 58 year old previously healthy white man presented at the emergency department of our hospital with acute severe low back pain irradiating to both legs. The pain in the legs was severe and was located from the lower half of the upper legs down to the feet. He also had noted decreased strength as well as sensory disturbances of both legs. Spontaneous micturition was not possible.

On physical examination, blood pressure was 110 over 75 mm Hg. Heart, lungs, and abdomen were normal. Peripheral arterial pulsations were present. Both legs were slightly swollen and coloured red to purple and livido reticularis was present. On catheterisation of the bladder, there was no urine retention. Neurological examination showed weakness of both legs with proximal strength Medical Research Council (MRC) grade 2–3 and distal MRC grade 1–2. There was bilateral sensory loss in the dermatomes L 1 to S 1. Tendon reflexes of the legs were absent. Plantar responses were both indifferent. The patient was diagnosed as having an acute cauda equina syndrome with possibly deep venous thrombosis of both legs, and an immediate MRI of the thoracic and lumbar spine was performed. This MRI disclosed a strongly dilated anterior epidural venous plexus with compression of the cauda equina and nerve roots in the foramina (fig 1 A–C). Signal intensity of the thoracic spinal cord was normal. Ultrasound examination of the lower abdomen and legs showed thrombosis of the inferior caval vein. Abdominal CT confirmed the presence of thrombosis of the inferior caval vein (just below the insertion of the renal veins) extending into the iliac veins. No other abnormalities that could have caused the inferior vena cava thrombosis were seen on CT. Routine laboratory investigations (including coagulability testing) were unremarkable, except for slight increase in erythrocyte sedimentation rate.

Figure 1

Lumbar spine MRI. Strongly dilated epidural and foraminal veins as black tubular structures due to signal loss, consistent with increased speed of flow. (A) Axial T1 weighted cut at L4–5; Anterior epidural plexus indicated by arrows. (B) Mid-sagittal proton density weighted cut showing compression of dural sac at L5 and S1 levels. (C) Lateral sagittal T1 weighted cut showing dilated foraminal veins.

The patient was diagnosed as having an acute cauda equina syndrome due to dilated anterior epidural veins secondary to thrombosis of the inferior vena cava. He was treated with intravenous heparin and acenocoumarol to prevent spread of thrombosis. In the next few days, the neurological disturbances gradually diminished. Despite exhaustive testing, no cause of the thrombosis was found.

We report on a patient with an acute cauda equina syndrome due to thrombosis of the inferior vena cava. An acute cauda equina syndrome is usually caused by a prolapsed intervertebral disc and less often by a tumour, trauma, or epidural bleeding.

Well known complications of deep venous thrombosis are pulmonary embolism and chronic venous insufficiency. To our knowledge, an acute cauda equina syndrome secondary to thrombosis of the inferior vena cava has not been reported previously.

The mechanism by which the neurological symptoms and signs were produced is probably twofold. Firstly, there is compression of cauda equina nerve roots in the spinal canal and foramen by the dilated anterior internal vertebral veins. Secondly, the symptoms and signs may be due to ischaemia of the cauda equina caused by stasis of the blood flow in the radicular veins. The mentioned anterior internal vertebral veins and radicular veins are part of the spinal venous plexus. This valveless plexus is connected by the intervertebral veins to the ascending lumbar veins which drain to the inferior caval vein (fig 2). The ascending lumbar veins, however, also communicate with the azygos system and the occipital and basilar sinuses. After occlusion of the inferior vena cava, this vertebrolumbar collateral pathway can function as an alternative route for venous blood from the lower limbs. Due to this bypass effect running parallel to the inferior caval vein, the anterior epidural veins are dilated by increased blood flow. In our case, the dilated veins have probably compressed the cauda equina and certainly compressed spinal roots in the intervertebral foramina, as can be seen on the MRI.

Figure 2

Diagram of lumbar vertebral veins.5 (1) Lateral anterior internal vertebral vein (AIVV); (2) medial AIVV; (3) posterior internal vertebral venous plexus; (4) basivertebral vein; (5) intervertebral vein (IVV); (6) ascending lumbar vein (ALV); (7) posterior external vertebral venous plexus; (8) anterior external vertebral venous plexus; (9) left lumbar vein; (10) inferior caval vein.

Vascular spinal neurological complications are also known in spinal arteriovenous malformations (AVMs) and spinal angiomas. More than half of the patients with AVMs have bladder dysfunction, paresis, and sensory change caused by the ischaemic effect of venous hypertension. In patients with spinal AVMs, an apoplectiform onset of clinical presentation, as presented in our patient, is described in 30%-50% due to thrombosis or haemorrhage.1 Neurological signs are also known as a related phenomena to spinal angiomas. Although ischaemia of the cord in these angiomas is mostly caused by stealing blood through a significant arteriovenous shunt, spinal compression by very large draining veins is also important in some patients.2 Besides cauda equina compression, dilated veins secondary to thrombosis of the inferior vena cava can also lead to destruction of pedicles of lumbar vertebral bodies and partial obstruction of the ureter.3 4 In conclusion, an acute cauda equina syndrome may be rarely caused by a dilated venous spinal plexus secondary to thrombosis of the inferior vena cava. The list of causes of the cauda equina syndromes5 should therefore also include inferior vena cava thrombosis.

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