Development and Diagnosis of PRES. The patient was ambulatory with physical therapy and a walker on postoperative day 1. Her albumin levels were noted to be decreased postoperatively (28 mg/mL; normal, >35 mg/mL). She developed intermittent hypertensive episodes and experienced transient peripheral vision loss. After her ophthalmologic symptoms cleared, she was discharged and transferred to a rehabilitation facility on postoperative day 9. Eleven days later, the patient was emergently readmitted for a deep spine wound infection after an onset of wound swelling and fever. She underwent irrigation and débridement of the spine wound with an estimated blood loss of 400 mL. The patient continued to have fevers and was placed on ciprofloxacin and vancomycin, which was changed to levofloxacin on postoperative day 5. Elevated creatinine was noted, and the patient was diagnosed with acute renal failure. On postoperative day 7, oxacillin therapy was commenced. After her cultures grew methicillin-resistant Staphylococcus aureus, a peripherally inserted central catheter line was placed on postoperative day 9. As a result of nausea and constipation, the patient received feeding tubes on postoperative day 11. Additionally, she was diagnosed with a pleural effusion on postoperative day 14. Although her creatinine levels were decreasing, she continued to experience intermittent hypertensive episodes with a mean peak systolic blood pressure of 148 mm Hg. On postoperative day 15, she had a seizure and again developed visual loss. The patient was lethargic and followed only simple commands. She moved all extremities and withdrew symmetrically to noxious stimuli. Upon emergent imaging, head CT showed posterior subcortical white matter hypodensity within the occipital and parietal lobes bilaterally (Figure 7). MRI showed focal regions of symmetric hemispheric edema involving the parietal and occipital lobes in a predominantly subcortical white-matter distribution. Additionally, extensive involvement of the splenium and of the corpus callosum, left greater than right, was observed (Figure 8).
Treatment and Clinical Course. The patient was transferred to the intensive care unit for neuromonitoring. Her hypokalemia and hypertension were treated aggressively to normalize her potassium levels and blood pressure. Her oxacillin therapy was changed to daptomycin. On postoperative day 17, the patient was transferred to another institution for further medical management after achieving full recovery of her eyesight after electrolyte and blood pressure corrections.
Discussion
Posterior reversible encephalopathy syndrome is a rare but frequently devastating complication of spinal surgery, with an estimated incidence of 0.094% to 0.2%.7,8 Pediatric patients, as well as patients undergoing deformity correction surgery and posterior lumbar fusion, which necessitate prone positioning, have a significantly increased risk of POVL after spinal surgery.9 There are several causes of POVL after spinal surgery, each with a unique pathophysiology, clinical presentation, and prognosis.
The most common cause of POVL, accounting for 89% of all cases, is ischemic neuropathy.10 Ischemic neuropathy refers to a hypoperfusion or infarction of the anterior or posterior portion of the optic nerve and presents as painless bilateral vision loss or complete blindness on waking from the surgical procedure.11 Risk factors associated with anterior ischemic neuropathy are primarily diabetes mellitus, prone positioning, nocturnal hypotension, and blood loss.11 Posterior ischemic neuropathy has been most strongly correlated with anemia and hypotension.12 The exact etiology of this complication has not been established, although the prognosis is generally unfavorable, with most vision loss being permanent.10-12
Another potential cause of POVL after spinal surgery is retinal artery occlusion. It is most commonly observed in patients who were improperly positioned, resulting in compression of an orbit on the surface of the headrest or the operating table.13 Retinal artery occlusion characteristically presents as an irreversible unilateral complete loss of vision with a red spot on the macula and an afferent pupillary defect.14
Cortical blindness, another possible common cause of POVL, results from the hypoperfusion of the occipital cortex and has a slightly better prognosis. Cortical blindness generally results from an embolic event that can be visualized through neuroimaging and may be unilateral or bilateral, ranging from mild peripheral vision loss to complete blindness.15
Posterior reversible encephalopathy syndrome, the cause of POVL diagnosed in the 2 patients in this case report, is a neurologic syndrome that differs significantly in its clinical presentation and pathophysiology from the more well-known etiologies. The precise pathophysiologic mechanism of the syndrome is yet to be elucidated. One theory revolves around the failure of cerebral vascular autoregulation. It postulates that intracerebellar hypertension leads to the extravasation of proteins and fluid, resulting in the characteristic vasogenic edema.16,17 The other equally discussed theory postulates that cerebellar vasospasm and subsequent hypoperfusion leading to cellular hypoxemia and ischemia may be responsible.18-20 Posterior reversible encephalopathy syndrome has been reported with increasing frequency, particularly in connection with hypertension, acute renal failure associated with malignancy, cytotoxicity, and corticosteroids, as well as preeclampsia, eclampsia, and autoimmune disorders.1-3,21-23 Traditionally, patients display a combination of different symptoms, including vision changes ranging from slightly decreased perception to complete blindness. Unlike retinal artery occlusion and ischemic optic neuropathy, the onset of vision loss often does not happen immediately after surgery and may occur several hours to days after surgery. Visual disturbance may progressively worsen if the medical cause for the syndrome is not determined and corrected.2,3 In contrast to other known etiologies of POVL, PRES has a relatively favorable prognosis if managed appropriately. Reported case series determined a resolution of the characteristic parieto-occipital vasogenic edema in 83% to 88% of all patients in follow-up neuroimaging after aggressive control of seizures and arterial hypertension.2-3