A case of acute spontaneous epidural haematoma in a chronic renal failure patient undergoing haemodialysis: successful outcome with surgical management

Keiko Takahashi, Fumihiko Koiwa, Hironori Tayama, Akiyo Satomi, Tadao Akizawa and Terukuni Ideura

Department of Internal Medicine, Division of Nephrology, Showa University Fujigaoka Hospital, Yokohama, Japan

Correspondence and offprint requests to: Keiko Takahashi, Department of Internal Medicine, Division of Nephrology, Showa University Fujigaoka Hospital,Yokohama, Japan.

Keywords: chronic renal failure; haemodialysis; MRI; spontaneous spinal epidural haematoma; surgical decompression

Introduction

The incidence of spinal epidural haematoma is rare. Neurological disorders resulting from compression of the spinal cord frequently are irreversible unless the patient is adequately treated rapidly after onset [1].

We report on a haemodialysis patient with spinal epidural haematoma with a successful outcome due to surgical management 12 h after onset.

Case

A 67-year-old female with end-stage renal disease (ESRD) undergoing haemodialysis was admitted to our hospital because of severe back pain and lumbago. She had suffered ESRD due to polycystic kidney disease and received regular haemodialysis treatment for 9 years. She had a history of hypertension for >10 years and angina pectoris for 3 years.

On May 19, 1997, 1 h after the start of her regular haemodialysis session in another dialysis clinic, she suffered from sudden, severe back pain and lumbago, and was transferred to our hospital. On admission, she was conscious, her heart rate was 116/min, blood pressure 222/120 mmHg, blood temperature 36.9°C, and bilateral flank and back tenderness was observed without sensory–motor neurological disturbances. Laboratory indices were: white blood cell count 14&thinsp;700/µl, haemoglobin 11.7 g/dl, platelet count 23.7x104/µ1, prothrombin time 74.6% (normal 70–130%), activated partial thromboplastin time 90.3% (normal 70–130%), FDP-E fraction 548 ng/dl, Ivy bleeding time 6.5 min (control 3–8 min), total protein 7.6 g/dl, albumin 4.6 g/dl, serum urea nitrogen 50.0 mg/dl, creatinine (Cr) 8.4 mg/dl, normal liver function except a high level of alkaline phosphatase (384 IU/l, normal 68–220 IU/l) and CRP <0.2 mg/dl. Chest, abdominal and thoraco-lumbar radiographs and electrocardiogram were unremarkable. Abdominal ultrasonography and computed tomography (CT) did not reveal intrarenal-cystic bleeding nor any other reasons for lumbago. Because an abnormality of the chest and abdominal visceral organs could be ruled out by the above findings, she was examined by magnetic resonance imaging (MRI) at 5 h after onset. MRI showed an extra-dural mass on the dorsal side of the spinal cord at the T8–L2 level and a marked compression of the spinal cord. The mass was isointense with the spinal cord on T1-weighted images, and of high intensity on T2-weighted images (Figure 1Go). The Myelo-CT revealed that only a trace contrast medium was observed in the spinal cord at L1 after the injection, but it did not flow one cephalad above the T9 level (Figure 2Go). The mass was identified as an epidural haematoma.



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Fig. 1. MRIs of the epidural haematoma at the T8–L2 vertebral body level. A sagittal T1-weighted image (left) demonstrates a dorsal extra-dural isointensity mass (arrows). A sagittal T2-weighted image (right) reveals a dorsal high intensity mass, and a marked compression of the spinal cord (arrows). Surgical findings showed this shadow to represent a large encapsulated epidural haematoma.

 


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Fig. 2. Axial Myelo-CT images of the epidural haematoma, at the level of T9 (left) and at the level of L1–2 (right). Only a small amount of contrast medium could be detected in the spinal cord at the L1 level after the injection (right: arrow). Contrast medium did not flow to the cephalad above the T9 level because of obstruction by the haematoma (left: arrow).

 
At 8 h after onset, bilateral muscle weakness developed, followed by complete sensory and motor loss within 2 h. She underwent emergency decompression laminectomy between T11 and L1 with excision of the extradural mass. Histopathological examination of the mass revealed a haematoma without any tumorous or vascular tissue.

Her post-operative recovery was satisfactory. Bilateral leg muscle strength was normalized at 2 days after the operation and, by the fourth day, other sensory–motor deficits had completely disappeared.

Discussion

Since the first case report of a spinal epidural haematoma described by Jackson in 1869, >350 case reports of spinal epidural haematoma have been reviewed in the international literature.

Underlying diseases and factors inducing spinal epidural haematoma include: vascular abnormality including congenital anomaly [2,3] and haemangioma [4], external factors such as trauma or catheterization for anaesthesia or lumbar punctures [5], haemorrhagic diseases [612], pregnancy [13] and drugs including cocaine [14]. However, a substantial number of epidural haematomas with unknown origin have also been reported. In this case, the above diseases or factors could be ruled out except for the use of anticoagulant for haemodialysis. Therefore, this case was diagnosed as a spontaneous spinal epidural haematoma.

The aetiological mechanism of spinal epidural haematoma still remains controversial. The spinal epidural venous plexus is postulated commonly to be the origin of the haematoma [15]. Usually, a high intracavitary pressure induced by, for example, pregnancy increases the plexus pressure, and it finally brings about rupture. In these situations, the small spinal artery was reported to be responsible for the bleeding. Abnormal coagulability, atherosclerosis or mechanical compression by a spinal tumour further facilitate vessel rupture.

The first clinical symptom of acute spinal epidural haematoma is the sudden onset of severe spinal pain, various degrees of sensory loss due to compression of the spinal cord by the localized bleeding and a rapidly progressive muscle weakness of the legs, followed by a complete or partial paraplegia within several hours to days after onset. In some cases, bladder and rectal disorders develop. The severe neurological symptoms such as total sensory and motor loss were observed at 10 h after onset in this case.

The diagnosis of spinal epidural haematoma, localization of bleeding and evaluation of the severity of spinal cord compression can be achieved easily and precisely with MRI [16]. In this case, the haematoma was detected to be isointense with the cord on the T1-weighted image, and high intense on the T2-weighted image at 6 h after onset. These results are consistent with previous reports describing these findings within 24 h after the onset of spinal epidural haematoma [17,18]. Since the introduction of MRI to diagnose spinal epidural haematoma in 1987, the prevalence of spinal epidural haematoma has increased from 2.2 to 6.4 patients per year [19]. MRI is a less complex procedure than myelo-CT and provides the same information.

In recent years, the number of spinal epidural haematoma cases which improved without surgical decompression has tended to increase. It was reported that 16 out of 22 cases with spontaneous spinal epidural haematoma resolved completely without surgical management [20]. Patients who underwent surgical decompression >40 h after the onset of symptoms had neurological symptoms after the surgery [20].

The post-operative outcome of 333 spontaneous spinal epidural haematomas with decompression correlated highly with the pre-operative neurological condition and the interval between onset and surgery [21]. Moreover, patients operated on within 12 h after onset had a better neurological outcome than patients operated on after 12 h, even though the pre-operative neurological conditions were comparable between the two groups [1]. Therefore, surgical decompression should be applied as soon as possible after the diagnosis.

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