A 61–year–old male with worsening back pain and right leg weakness secondary to lumbar spinal stenosis underwent an elective L2–S1 laminectomy with L4–L5 fusion. His past medical history included essential hypertension with medication noncompliance and laparoscopic cholecystectomy. Preoperatively, his blood pressure ranged between 106–142 systolic and 69–76 diastolic. On postoperative day 1, he complained of severe back pain and headache. His systolic blood pressure increased to 160–220. Physical examination demonstrated encephalopathy with decreased visual acuity and absent blink reflex to visual threat testing. The remainder of his examination was unchanged. Head CT scan was unremarkable. An MRI of the brain demonstrated patchy hyperenhancement in the bilateral parieto–occipital cortices consistent with posterior reversible encephalopathy syndrome (PRES). Intravenous nicardipine was started leading to blood pressure normalization; however, his headache and back pain remained unchanged. A lumbar JP drain showed continued output of serous fluid. Beta–2 transferrin analysis of the fluid was positive suggesting a CSF leak. A lumbar spine MRI showed a fluid collection in the lumbar vertebrae. The patient then underwent a revision L3–L4 decompressive laminectomy which demonstrated spinal nerve root herniation through a complex dural tear at the L3–L4 interspace. The nerve roots were reduced, and the dural defect was repaired. Following the procedure, the patient was weaned off intravenous nicardipine and continued on Metoprolol tartrate twice daily. A workup for secondary causes of hypertension was unremarkable.
PRES is characterized by headache, confusion, visual loss, and seizures and is associated with white matter vasogenic edema predominantly affecting the posterior occipital and parietal lobes of the brain. It is believed to be related to disordered cerebral autoregulation and endothelial dysfunction. PRES is associated with a number of medical conditions including poorly controlled hypertension, eclampsia, vasculitides, toxic/metabolic etiologies, immunosuppressive therapy, and traumatic spinal cord injury. Recent case studies describe the onset of PRES in the setting of inadvertent dural tears created during spinal anesthesia and lumbar puncture. Our patient developed PRES after lumbar laminectomy and unintentional spinal cord injury with spinal nerve herniation through a dural defect. With prompt surgical treatment, this patient was able to make a complete recovery.
The development of PRES following spinal surgery may signal a dural defect with CSF leakage and resultant spinal nerve injury. Prompt recognition and treatment of this disorder can prevent devastating consequences.