Posterior Reversible Encephalopathy Syndrome after Heart Transplantation: Diagnosis and Immunosuppressive Therapy

Abstract

Posterior reversible encephalopathy syndrome (PRES) is an infrequent neurologic sequela occurring in response to tacrolimus therapy. One of our recent cases is a prime example of the difficulties faced by physicians when they attempt to balance immunosuppression and drug toxicities. We highlight the most relevant features of our case, in an attempt to bring greater understanding of the pathophysiology of PRES. Further, we discuss the methods typically used to diagnose PRES, and we attempt to consolidate previous knowledge within the scope of PRES in a patient who was receiving immunosuppression after orthotopic heart transplantation. Case ReportA 37-year-old woman with a medical history of type 2 diabetes mellitus and hypothyroidism presented with generalized tonic-clonic seizures 16 days after orthotopic heart transplantation. Her home medications included 6 mg of tacrolimus, 1,500 mg of mycophenolate mofetil, and 20 mg of prednisone, each taken orally twice daily; trimethoprim/sulfamethoxazole; and valganciclovir. She had had 3 seizures that involved tongue-biting and stool incontinence. Initially, she was treated with diazepam, intravenous phenytoin, and intravenous ceftriaxone for suspected meningitis, a frequent sequela in an immunocompromised patient. On admission, the patient was somnolent but rousable and reported a throbbing temporal headache. Her blood pressure was 130/77 mmHg, and her pulse was 110 beats/min. No focal deficits were present upon neurologic examination. Laboratory data included a white blood cell count of 16.4 ×10 9 cells/L, a potassium level of 5.4 mmol/L, a magnesium level of 1.77 mmol/L, a blood urea nitrogen level of 47 mg/dL, and a creatinine level of 1.25 mg/dL with an anion gap of 23 mmol/L. Her tacrolimus levels at the time of admission were 8.4 ng/mL. Her previous tacrolimus levels had been 9.7 to 13.9 µg/mL, which, in a normotensive patient without a tremor, made toxicity less likely. Her examination included a lumbar puncture that was negative for any infectious process, an electroencephalogram that showed no evidence of seizure activity, and a computed tomogram of the head that showed no intracranial bleeding. A brain magnetic resonance image (MRI) was ordered, and the findings suggested PRES (Fig. 1A).On the basis of these findings, we discontinued tacrolimus and replaced it with 2 mg/d of oral sirolimus. A repeat MRI showed resolution of the patient's high signal intensities (Fig. 1B). The mycophenolate mofetil was continued at 1,500 mg and the prednisone was slightly reduced to 15 mg, twice a day. The patient was discharged

A Case of Antibiotic-Induced Posterior Reversible Encephalopathy Syndrome

“…3 Early detection and prompt correction of the underlying causative factor decrease the risk of damage to the cerebral vascular system. 6 As for this presented case, the patient was never hypertensive and upon presentation actually required vasopressor support. With respect to sepsis and inflammatory status, the patient was never febrile and had an initial leukocytosis which was considered reactive secondary to the patient seizing.…”

“…4,11 The current literature suggests that MRI is superior to CT in the identification of PRES. 6 Typical PRES lesions are seen as hyper-to isointense on FLAIR/T2-weighted images seen on MRI. 4 Wernicke's encephalopathy and PRES have overlapping MRI findings and symptoms, making the diagnosis difficult in some cases where a patient may have an extensive alcohol use history.…”

“…7 Differentiating between MIE and PRES can be difficult when the patient presents with signs and symptoms consistent with both disorders. [3][4][5][6][7] Imaging was a major factor in determining PRES versus MIE in this patient, as symptomatically they present very similar symptoms. The patient had hyperintensity in the parietal occipital regions on MRI, which is indicative of PRES, whereas MIE is associated with lesions in a variety of areas, for example, the cerebellar dentate nucleus.…”

“…Metronidazole-induced encephalopathy (MIE) is a disorder associated with metronidazole use and presents with altered mental status, aphasia, dysarthria, and, in some instances, seizures. [6][7][8] Prolonged exposure to metronidazole has been identified as the most likely cause and is associated with unique neuroimaging such as symmetric bilateral fluidattenuated inversion recovery (FLAIR) seen on MRI at the dentate nuclei, dorsal medulla, pons, or midbrain regions.…”

Malaria and encephalopathy in a heart transplant recipient: A case report in the context of multiorgan donation

“…Therefore, it is important to identify the most common signs and symptoms to guide clinicians on conducting adequate blood tests for determining the presence of malarial parasites. It is important to recognize that both plasmodial infection (inducing blood-brain barrier dysfunction and endothelial leakage) 18 and the use of calcineurin inhibitors (that favors autoregulatory vasoconstriction and vasogenic edema) 19 can produce neurological symptoms compatible with PRES.…”