Spinal epidural haematoma is increasingly picked up using magnetic resonance imaging, especially following trauma. The presentation can be varied especially if there is a trivial history of trauma. Spontaneous subarachnoid haemorrhage can occur in spinal haematoma as a rare and unusual presentation and can be easily misdiagnosed. The key to early diagnosis is a strong suspicion and careful repeated neurological examination. We present an illustrative case.
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Spinal epidural haematoma (SEH) can cause rapid neurological deficit and permanent damage. Similarly, subarachnoid haemorrhage, usually presenting with headache and neck stiffness is a neurosurgical emergency. The differential diagnosis of an SEH seems far fetched, but should be borne in mind in cases of nonaneurysmal subarachnoid bleed. The following case report reflects the ease with which this diagnosis can be missed.
A 36-year-old black South African woman presented with sudden onset headache, neck stiffness with discomfort, and associated severe acute onset thoracolumbar pain, following bending and lifting up of a relatively small weight. The headache was lancinating and brief, but neck stiffness was persistent. The thoracolumbar pain was described as burning, deep seated, and radiating to the epigastrium. The pain was partially relieved by bed rest. She developed progressive weakness in her legs 2 days following the episode of pain with associated leg stiffness and bladder and bowel dysfunction. There was no sensory loss.
Clinical examination revealed an alert young woman with opisthotonic posturing, marked nuchal rigidity, and positive Kernig’s sign. All cranial nerves were intact. She had truncal weakness with absent abdominal reflexes, 4−/5 power in her hip flexors and internal rotators bilaterally, with 4+/5 power in all other muscle groups in the lower limbs. Tone was normal but reflexes diminished. All sensory modalities were normal, aside from slightly reduced perianal sensation. The anal sphincter was slightly weak.
Spinal examination revealed marked tenderness of the T6 spinous process and positive percussion test. There was limitation of thoracic movement due to severe pain. Plain x rays of the thoracic spine revealed <5% anterior wedging of T6 vertebrae. There was no soft tissue swelling. Vessel cranial angiogram and cranial computed tomography (CT) scan was normal. CT myelogram demonstrated incomplete block at T6 and magnetic resonance imaging (MRI) showed a hyperintense extradural lesion anteriolateral to the T5, T6, and T7 vertebrae, with attenuation of epidural fat and anterior to posterior compression of the spinal cord on T1 weighted image (fig 1). The lesion did not enhance with gadolinium, and no soft tissue anomaly was noted.
Emergency surgery was planned and while waiting for surgery the power in the patient’s lower limbs and trunk deteriorated to 3/5. She became hypotonic but hypereflexic. Sensation, apart from the perianal area, remained intact. Emergency costotransversectomy of the T6 vertebrae with right pediculectomy was performed. A liquid extradural haematoma under pressure was evacuated. A thin membrane around haematoma was biopsied and tissue histology was that of inflammatory membrane.
Within 3 days postoperatively, the patient regained full power in her lower limbs and trunk, and full bladder and bowel control. She was discharged home after a week.
Spinal cord compression requires quick and early diagnosis. Prompt management is essential to prevent irreversible cord damage. In an emergency situation, headache, neck stiffness, and leg weakness suggest spontaneous subarachnoid bleed, possibly from the anterior communicating artery. There have been reports of patients with SEH presenting with features typical of subarachnoid bleed.1 On CT myelogram, lumbar puncture in this patient revealed a subarachnoid bleed. Four vessel cerebral angiogram was negative.
SEH had been considered rare. With the advent of MRI, the diagnosis has been made easier and they are commonly demonstrated in cervical spine injuries.2 SEH have been considered spontaneous in most instances.3 Secondary causes such as coagulapathies, vascular malformation, cavernous angiomas, cord trauma, cord tumours, hypertension, low molecular weight heparin, chronic renal failure in patients undergoing haemodialysis, and pregnancy are well documented.4–8 Severe epidural venous hypertension following Valsalva manoeuvre has been reported to cause SEH9; that patient had normal coagulation profile as a prerequisite investigation for a four vessel angiogram.
In the emergency setting, spinal pain in the absence of any structural lesion should alert the physician as to the possibility of SEH even in the absence of any precipitating event. Progressive paraparesis with sphincter dysfunction is a feature of cord compression syndrome. Careful evaluation of patients by neurological staff is critical. In the accident and emergency unit, regular and careful neurological examination of any patient with unusual clinical presentation of subarachnoid bleed or spinal epidural bleed is important.
There should be no question as to the surgical intervention in a case of SEH in which the patient shows unrelenting pain and progressive neurological deficit. Most SEH are reported to be posterolateral to the cord, with MRI features that are characteristic but depend on the age of the haematoma.2,10,11 In our case the SEH was anterolateral and the lesion was hyperintense on T1 with the fluid level on axial scans. Since the introduction of MRI scans, the mean incidence of cases reported in the literature has increased from 2.2% to 6%,11 and MRI has greatly influenced the surgical intervention rate.11
The result of surgery in this case was encouraging in spite of a 24 hour delay in hospital while trying to ascertain the diagnosis. The patient’s pain, sphincter dysfunction, and leg weakness completely resolved. Spontaneous recovery in a rapidly improving patient has been documented.12,13 It is considered that conservative management is safe in cases of SHE if spontaneous neurological recovery has started.14 Critical factors for recovery include the level of preoperative neurology and the interval of surgical intervension.7,15 Surgical outcome may depend on duration of symptoms and perioperative neurological state.
Competing interests: none declared