Case Presentation: Posterior reversible encephalopathy syndrome (PRES) is a neurological disorder characterized by symptoms of encephalopathy and radiographic findings suggestive of vasogenic edema. Although PRES is most often triggered by hypertensive emergencies, sepsis and immunosuppressive medications have also been implicated in its pathogenesis. We present a case of PRES due to lithium toxicity.A 47-year-old female with bipolar disorder presented with dizziness and was found to have acute kidney injury (creatinine 4.58) with toxic lithium levels (3.7 mmol/L) after an intentional lithium overdose. The patient initially improved with aggressive hydration, with down-trending lithium levels. However, on day 2 of admission the patient developed rapidly worsening encephalopathy, with progression to a nonverbal state with catatonia. An MRI of her brain was performed, which showed increased T2/flair signal involving the bilateral occipital lobes and parietal lobes without infarction, highly concerning for posterior reversible encephalopathy syndrome. Her blood pressure consistently remained in normal range, with her systolic below 150 mmHg throughout the hospitalization. Hemodialysis was deferred given her improving kidney function and low lithium levels. She was closely monitored in the neurocritical care unit with continuous EEG not showing epileptic events. She also underwent an infectious work-up, including a lumbar puncture, all of which were negative. She was aggressively fluid resuscitated in the critical care unit, with eventual improvement around in encephalopathy and catatonia around day 6. She was discharged with a close psychiatry follow-up.
Discussion: The pathogenesis of PRES is uncertain; however, hyperperfusion due to hypertension and endothelial damage due to toxins are the prevailing theories. Our patient was never hypertensive, and negative for infection, and other causes for encephalopathy (such as seizures) were ruled out. We suspect that lithium toxicity primarily induced her PRES. There have been rare case reports of PRES triggered by lithium toxicity. In each of these cases, the patients developed PRES shortly after withdrawal of lithium due to toxic amounts. Their creatinine and lithium levels were normalizing when the symptoms of PRES began; however, most of the patients did also develop elevated blood pressures. Our patient’s MRI findings were significant for PRES, but her blood pressure remained normal throughout hospitalization. Although neurological manifestations of lithium toxicity are well-documented, there is no management guideline for lithium toxicity-induced PRES. There is some data to suggest that lithium may induce PRES through VEGF-mediated endothelial dysfunction, or through ADH-mediated cerebral edema however more data needs to be collected on the subject.
Conclusions: Although PRES is commonly associated with hypertension, there can be other causes for it. There are currently no guidelines in managing lithium toxicity leading to PRES given its rarity; however our management primarily involved avoiding nephrotoxicity and aggressive fluid resuscitation with supportive care.