Part of TopicBrowse Topic in full-screen mode
Transient paraplegia following Epidural blood patch
C. Wijeratne, A. Avila
Sunnybrook Health Sciences Centre, University of Toronto
Spontaneous Intracranial Hypotension is a neurological condition caused by spontaneous spinal cerebrospinal fluid (CSF) leaks characterised by orthostatic headache and a variety of atypical neurological symptoms.
Imaging techniques including magnetic resonance (MRI) are fundamental in locating the precise anatomical site of the CSF leak. Management strategies include epidural infusion of crystalloids, colloids, fibrin glue or hematic blood patch (EBP), before a surgical repair is warranted.
We report a case in which a patient treated with EBP developed transient paraplegia for 90 minutes following the procedure.
Material and Methods
Patient informed consent was obtained for submission of a case report.
Results / Case Report
37-year-old male with clinical and radiological findings diagnostic of spontaneous intracranial hypotension presented for a planned epidural blood patch at T11-12 to be followed by an infusion via epidural catheter with colloid. He had a past history of two epidural blood patches with partial and temporary benefit. MRI showed a possible CSF leak at T11and also noted epidural lipomatosis along the length of the thoracic and lumbar spine with extradural compression most prominent from T4-T7 levels with mild flattening of the cord with no change in cord signal. L5-S1 disc protrusion was also noted without any compression. Other past medical history included treated obstructive sleep apnoea, obesity and hypertension.
Epidural blood patch was performed with autologous blood from forearm in sterile condition under fluoroscopy guidance.
The patient complained of crescendo back pain up to 7/10 on visual analogue scale (VAS) after only 14ml injection via epidural catheter. Epidural catheter was removed due to the discomfort. 25 minutes following procedure, patient became paraplegic at the level of T8 dermatome with sensorial and motor deficit and deep tendon hyperreflexia. Vital signs were stable including a blood pressure of 170/90mmHg. Patient was transferred for urgent MRI and Neurosurgical assessment. 90 minutes post event, the patient returned to his baseline neurological status except for back pain VAS 4/10. MRI at this time demonstrated evidence of recent epidural blood patch, but no other changes from his baseline MRI. Cord signal was normal.
This case illustrates a transient paraplegia following EBP in a patient with pre-existing epidural lipomatosis. Spinal Epidural lipomatosis is a rare cause of spinal cord compression and neurological deficits. We postulate that compression by the EBP may have unbalanced the cord transmural perfusion pressure. The increase in venous pressure may have been exacerbated by the pre-existing epidural lipomatosis. Resolution was likely due to redistribution of blood in the epidural space.
This rare case highlights the importance of evaluating the epidural space anatomical target and anatomical variances including spinal stenosis, disc protrusion, spondylolisthesis and in this case spinal epidural lipomatosis. Infusion or injection of foreign material in the neuraxial space could alter the fine perfusion balance of the spinal cord structures. Injection in aliquots and assessment of pain/pressure during the procedure may not be sufficient to prevent the catastrophic misadventure of spinal cord ischemia as seen with epidural hematoma.