Abstract

Posterior reversible encephalopathy syndrome (PRES) is a disorder characterized by grey and white matter abnormalities in the temporal, parietal, and occipital lobes of the brain. Clinical findings involve headache, mental status changes, focal neurological deficits, as well as visual disturbance which are also associate with characteristic imaging features of subcortical white matter lesions on computed tomography (CT) and magnetic resonance imaging (MRI). it may lead to significant morbidity and mortality if it is not diagnosed instantly. The study sheds light on importance of magnetic resonance imaging in prompt recognition of this syndrome, withholding tacrolimus may be consider to be diagnostic tool, if symptoms persists or other complications require this approach. We aimed to present our 44 years old secondary membranous nephropathy with nephrotic syndrome secondary to lupus nephritis with ANA profile S1RNP positive, right lower limb DVT provoked due to nephrotic syndrome, complicated pyelonephritis S/P D-J stent removal patient in whom we observed press following tacrolimus treatment in the light of clinical and MRI findings.

Keywords

Introduction

MRI : vasogenic edema in the Parieto-occipital lobe and cerebellum in axial FLAIR.
TREATMENT GIVEN DURING HOSPITALIASATION

DISCGARGE MEDICATIONS

DISCUSSION

PRESS is clinicoradiological diagnosis that is based on combination of typical clinical features and risk factors, and supported by magnetic resonance imaging findings.² PRES , as the name suggests, is a constellation of symptoms associated with vasogenic edema, most commonly, the posterior cerebral vasculature, of the posterior cerebral vasculature, often affecting the parietal occipital region. Other vascular territories can also be affecting in PRES, such as the posterior portion of frontal lobe and temporal lobe.¹⁰ Numerous investigations have noted varying frequency of signs and symptom in PRES by Fisher M et al i.e Encephalopathy 28-92% Disorder of consciousness 67-90?ute arterial hypertension or blood pressure fluctuations 61-80% Epileptic seizures 70-74% Visual disturbance 20-67% Headache 26-53% Focal neurological signs 5-15%.⁵ Our patient developed sudden onset of convulsions 4 episodes, and weakness of right upper and lower limb (symptoms consistent with PRES). Tab. tacrolimus can cause hypertension,  as the risk factor mentioned in literature, our patient also had high blood pressure while on oral Tab. Tacrolimus therapy which promptly responded to discontinuations of accused  medication. Although the precise pathogenesis of PRES remains unclear, Hypertension & endothelial damage appear to be constant feature. Hypertension is the most common precipitating factor with endothelial dysfunction, the pathogenesis of PRES can be explained by multiple process such as (i) Failure of auto regulation causing vasogenic edema (ii) Disruption or damage of Blood Brain Barrier (BBB) (iii) cerebral vasoconstriction.  Upon disruption of autoregulation, which mains as steady blood supply to the brain despite variations in systemic pressure, elevated perfusion pressure leads to disruption resulting in hyper perfusion and extravasation of protein and fluid into interstitial space, which inter cause vasogenic edema.⁴

Diagnosis fugate et al. suggested the following criteria for the diagnosis of PRES 1. Acute onset of Neurological symptoms 2. Neuroimaging abnormalities of vasogenic edema (focal / confluent) 3. Reversibility of clinical and/or radiological findings. The most sensitive routine magnetic resonance imaging (MRI) sequence for identifying subcortical and cortical lesions in PRES is fluorescence-assisted inversion recovery, or FLAIR. Vasogenic edema-induced bilateral and symmetrical regions of hyperintensity in the posterior parietal and occipital lobes have been the traditional descriptions of PRES on T2-weighted MRI and FLAIR. In our patient, MRI finding that symmetric bilateral white matter lesions with cortical involvement in parietooccipital lobe and cerebellum. In our case unlike those described in literatures. ⁵   Treatment early diagnosis and therapy beginning are crucial components of PRES management. An intensive care unit (ICU) may be necessary for many patients in order to aggressively manage symptoms such seizures, encephalopathy, and status epilepticus.⁴ Tacrolimus dose adjustment involves immediate reduction or discontinuation of tacrolimus to resolve symptoms and prevent permanent neurological damage. The acute management of PRES is supportive and includes removing or reversing any suspected cause. supportive measures such as controlling blood pressure, manging seizure or other cause and correcting electrolyte imbalances. Blood pressure control is still the cornerstone of management. In order to prevent fluctuations, continuous IV infusion is typically necessary. However, the selection of antihypertensive medications is based on standard guidelines for the treatment of hypertensive emergencies or crises in the general public. The objective is to lower blood pressure to 160/100 mmHg in the first six hours and to lower MAP by 20 –25% in the first two hours. Nevertheless, despite a known link between hypertension and other conditions.⁵ The management of PRES primarily adopts a symptomatic approach , with a key emphasis on regulating blood pressure. Additionally, when feasible, discontinuation of the causative drug is recommended. In cases where immediate cessation is impractical, considering dose reduction becomes a viable alternative. For individuals presenting with seizures , the administration of anti-seizures medications (ASMs) may be necessary. A standard practice involves tapering ASMs as symptoms alleviates and MRI findings show resolutions, a trend observed in majority of patients.⁹  PRES is generally reversible with timely intervention, but delays in recognizing symptoms or adjustment in tacrolimus levels can lead to lasting neurological deficits. prevention strategies include regular monitoring of the blood levels for patients taking Tab tacrolimus, particular in patient with renal or hepatic impairment. propose routine neurological assessment for patient with risk factors to help detect PRES symptoms early. an individualized treatment plan, tailored to each patient need and risk profile is critical for achieving a balance between effective immunosuppression and neurological safety. This careful, proactive management strategy is essential for maximizing the risk of adverse neurological outcomes.⁶

CONCLUSION

Tacrolimus associated PRES is a rare and serious complication. This syndrome should be promptly recognised as it recognised potentially reversible and generally response to withholding or decreasing the dose of tacrolimus in addition to controlling hypertension and seizures¹. PRES generally has good prognosis; prompt recognition and management are important in preventing significant disease morbidity and mortality.⁷

REFERENCES

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