Spinal epidural haematomas (SEH) are infrequent events caused mainly either by trauma or iatrogenic following invasive spinal procedures (lumbar puncture, surgery, or peridural anaesthesia). The spontaneous spinal epidural haematoma (SSEH) is a rare entity requiring an emergency intervention in most cases. The incidence is estimated at about two to six cases per year.¹ The posterior internal vertebral venous plexus seems to play an important role in the development of the SSEH;² the role of vascular anomalies is overestimated. Coagulopathy may facilitate the development of haematoma but is not the cause of SSEH. The relation between hypertension and SSEH is not proven.²

The clinical diagnosis is difficult despite the somewhat characteristic presentation with rapid onset of symptoms, such as sudden pain and rapidly progressing neurological deficits.³ We describe the management of the case of a rather extended SSEH with unexpected outcome.

CASE REPORT

An 80 year old man was admitted to our hospital presenting an acute onset of sciatica with rapid progress to high grade paraparesis and a cauda equina syndrome within the next 30 minutes. He arrived at the hospital 3 hours after onset of the first symptoms. The previous history was non-specific with the exception of medication treated high blood pressure. He has never received anticoagulants. On admission the general status was without pathological findings except from a blood pressure of 230/130 mmHg. He presented a weakness of the iliopsoas muscles (3/4), quadriceps (3/5), tibialis anterior and extensor hallucis longus (3/5 right, 4/5 left), and gastrocnemius (4/5) with a sensory disturbance from L4 level. The anal sphincter tonus was weakened, with disturbed anal sensation and urinary bladder retention of 300 ml after catheterisation. Patellar and Achilles tendon reflexes were lost. Magnetic resonance imaging (MRI) revealed an epidural haematoma from the inferior margin L1 posteriorly down to L5 anteriorly in the spinal canal (fig 1). During the initial diagnostic procedure, approximately 4 hours after onset, the symptoms started to decline so that the already planned surgical intervention could be cancelled. After 6 hours the sensory disturbances had disappeared. Already 24 hours after admission the patient was almost free of symptoms, mobile, and continent. He was discharged after the next day. The further course was uneventful. We could follow up the patient within 5 months free of complaints. Besides bilateral absent Achilles tendon reflexes, he was without any neurological deficits. The MRI showed a complete resolution of the spinal haematoma (fig 2).

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Figure 1

 MRI scan on admission showing compression of the cauda equina by a spontaneous spinal epidural haematoma (left T1 weighted, right T2 weighted).

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Figure 2

 MRI follow up after 5 months showing complete resolution of the haematoma. Reproduced with patient’s permission.

DISCUSSION

A SEH causing severe neurological deficits is considered a medical emergency. MRI is the method of choice for establishing the diagnosis⁴ and facilitates the differential diagnosis between epidural haematoma, disc herniation, epidural tumour, or infection. Follow up MRI is needed to follow the evolution of a presumed SEH.

The posterior internal vertebral venous plexus seems to play an important role in the aetiology of the SSEH.² In our case, the main part of the haematoma at L4 level is located anteriorly. However, the only obvious medical problem in our case—that is, arterial hypertension—appears to be unrelated to the SSEH.²

Early surgical decompression was formerly believed to be the only treatment method,^1,5,6 with the timing of surgery determining the quality of the result.⁴ Other authors⁷ reported an improvement even after delayed surgery. Conservative treatment was reserved for cases with only minimal neurological deficits.

In the recent literature a number of cases with spontaneous recovery have been presented.^8,9,10 Conservative management of the SSEH may be appropriate if early and substantial neurological recovery is noticed, such as in our case.

There have been a number of reports^8,9,10 of spontaneous and complete recovery of SEHs. The incidence is possibly higher then previously thought, because more cases with less severe deficits have probably been misdiagnosed as transient low back pain. The broad availability of MRI facilities will discover increasing numbers of SEH; nevertheless, the neurological status will continue to dictate whether management is surgical or conservative.

Although SEH causing compression of neural structures is considered usually for emergency decompression, astonishingly there are some cases with a good clinical regression of restricted function even with severe initial neurological impairment, which can be handled non-surgically.