A 64-year-old male underwent living donor liver transplantation for recurrent hepatocellular carcinoma (HCC) within the Milan criteria. He was not known to have a history of diabetes or hypertension. His donor was related (his sister), 40 years old, no past medical history, BMI = 27, liver biopsy showed 10–12% steatosis; graft to recipient weight ratio (GRWR) was 0.8%. PET scan was normal 1 month before transplantation.
On day 11, following liver transplantation and during regular daily assessment, painless left upper limb weakness (grade 0) was observed. Shortly after, an attack of status epilepticus started and followed by loss of consciousness (GCS less than 8). The patient was readmitted to ICU, sedated, and needed mechanical ventilated for 3 days due to his current conscious level and the state of status epilepticus. Convulsions were controlled with anticonvulsant treatment and a continuous infusion of midazolam; after that, the patient progressively regained normal conscious level and was weaned from the mechanical ventilation. Following regaining consciousness, the patient developed bilateral blindness. The neurological assessment revealed bilateral complete loss of vision with left upper limb monoplegia, other neurological examination was normal. Ophthalmologic examination revealed bilateral complete loss of vision up to no light perception. Pupils were non-reactive and pinpoint. Eye movements, intraocular tensions, fundus examination, and anterior slit-lamp examination were normal.
The patient’s initial blood work-up included a complete blood count, chemistry panel including electrolytes, creatinine, liver function tests, and thyroid function tests and were all within normal ranges.
His medication included tacrolimus 2 mg twice a day since day 1 of transplantation. Tacrolimus blood level was 8.12 ng/ml (target therapeutic level in blood is 10–15 ng/mL) [7].
CT brain with contrast was normal. Magnetic resonance imaging (MRI) demonstrated bilateral, multifocal, cortical and subcortical areas of bright T2 and FLAIR signal intensity in the occipital and fronto-parietal regions. They show no diffusion restriction on DWI and ADC map. Those changes were consistent with atypical radiological features of posterior reversible encephalopathy syndrome (PRES) (Fig. 1). Also, atypical MRI findings that may be found with PRES could include diffusion restriction on DWI, post-gadolinium contrast enhancement on T1W images, and hemorrage [8].
He was not hypertensive and his workup excluded any infectious or metabolic causes.
Tacrolimus toxicity was considered the most probable suggested cause and accordingly was discontinued. Immunosuppressive regiment of was changed into mycophenolic acid 1000 mg three times a day and prednisone 40 mg daily. All manifestations including weakness and loss of vision progressively improved with complete normalization in a couple of weeks.
The patient had not had any further deterioration of his vision, attacks of convulsions, or weakness. His follow-up MRI 2 weeks later was completely normal.