Posterior Reversible Encephalopathy Syndrome Associated with Acute Pancreatitis.: [Essay Example], 1017 words GradesFixer

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Posterior Reversible Encephalopathy Syndrome Associated with Acute Pancreatitis.

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Posterior Reversible Encephalopathy Syndrome (PRES) is a cliniconeuroradiologic entity characterized by variable associations of neurological symptoms. The brain abnormalities are often symmetric and predominate in the posterior white matter. PRES can develop in association with many conditions including hypertensive encephalopathy, eclampsia, and use of cytotoxic and immunosuppressant drugs. Only few cases in the literature show an association between PRES and acute pancreatitis. We report a case of a 61yo woman presenting PRES after Endoscopic Retrograde CholangioPancreatography related pancreatitis.


Introduction: Posterior Reversible Encephalopathy Syndrome (PRES) is a clinic-neuroradiologic entity that was first described by Hinchey et al. in 1996

[1]. It is increasingly recognized and reported in case reports but the real incidence is not known

[2]. Patients of all ages appear susceptible and case series suggest that it’s more common in women

[3,4]. PRES is characterized by variable associations of seizure activity, consciousness impairment, headaches, visual abnormalities, and focal neurological signs

[5]. Typical findings in magnetic resonance imaging (MRI) are symmetrical white matter edema in the posterior hemispheres, particularly the parieto-occipital regions

[6-9]. Both clinical and radiological features are typically reversible once the cause is removed. PRES occurs most often in the setting of hypertensive crisis, eclampsia, cytotoxic or immunosuppressant therapy and renal disease

[10-13]. Regardless the underlying cause, the main abnormality is cerebral vasogenic edema

[14]. Only few cases in the literature show an association between PRES and acute pancreatitis

[15-23]. Case report: A 61 years old caucasian woman, come to our attention from the emergency ward, complaining of abdominal pain lasting for 5 days. She referred to has been submitted in the past to cholecystectomy and appendectomy, she denied history of hypertension. The remaining medical history was unremarkable. At blood samples, it was discovered an increase of total bilirubin (2.1mg/dl), Gamma-Glutamyl-Transpeptidase (1105U/l) and Alkaline-Phosphatase (615U/l); inflammatory indexes, amylase and lipase serum levels were in the normal range. An abdomen-US was performed: a mild dilatation of main bile duct without evidence of stones was found; a dilatation of intrahepatic biliary ducts was also present. Thus, the patient was admitted to the HPB unit of our hospital where she underwent ERCP (Endoscopic Retrograde CholangioPancreatography). This examination revealed an inflamed papilla, conditioning a sub-stenosis of 1cm. Oddi’s sphinterotomy and brushing of the inflammatory lesion was performed (the cytology was negative for malignant tumor cell). A 10Fr biliary plastic stent was placed. After 3 hours from the procedure, the patient developed a post-ERCP pancreatitis, with an elevation of serum amylase (3262U/l) and lipase (3963U/l); WBC was 12,6mg/dl. She also complained abdominal pain rebound, responsive to pain relief with NSAID. The morning after the procedure the patient was in good general condition with less abdominal pain. In the afternoon the patient experienced the sudden appearance of complete bilateral blindness. Vital parameters were normal except of mild hypertension (160/80). At the Neurological examination the response of pupil to light was intact and no other focal signs where revealed. A vascular and encephalic CT-scan was performed and showed no evidences of organic diseases. After oculist examination, it was excluded either a opthalmological disease. Also EEG was normal. Than the patient was examined with encephalic contrast enhanced MRI that showed in both parietal and occipital lobes the presence of symmetrical areas of increased signal in the T2 FLAIR sequence (Figure 1). The radiological picture was compatible with PRES. An abdomen TC-scan was performed and confirmed a mild inflammation of pancreatic head. The patient was treated conservatively with oral anti-hypertensive therapy and parenteral hydration. After 36 hours from the outset, her vision slightly return normal, but for 3 days she experienced visual hallucinations. Bilateral normal visus reached after 6 days. At the same time, serum amylase and lipase levels decrease to normal range and the patient was discharged. A MRI was performed two weeks later and documented the complete recovery of the brain signal intensity in the areas before affected (Fig. 2). Discussion: Posterior reversible Encephalopathy occurs in association with various medical condition that include hypertension, sepsis, shock, eclampsia, cytotoxic/immunosuppressive therapy, uremia, porphyria, connective tissue disease, alcohol, intoxication, hematological, renal or autoimmune disorders[10-13]. PRES evolves over a matter of hours, with the most common presenting symptoms being seizures, consciousness impairment, visual abnormalities and headache. The severity of clinical symptoms varies. Seizures and status epilepticus are common

[24]. Consciousness impairment may range in severity from confusion, somnolence, and lethargy to encephalopathy or coma[25]. The visual abnormalities can manifest as blurred vision, homonymous hemianopsia, cortical blindness, and visual hallucinations

[25]. Other symptoms less commonly seen include nausea, vomiting, and brainstem deficits[1]. Hypertension is often observed in PRES, but its level is not correlated to the severity of PRES. Neuroimaging is essential to the diagnosis of posterior reversible encephalopathy syndrome. Typical findings are bilateral and symmetric regions of white matter edema and predominating in the parietal and occipital lobes

[26]. The pathophysiology of PRES remains unclear, but it appears to be related to disordered cerebral autoregulation and endothelial dysfunction that lead to breakdown of blood brain barrier witch may than trigger vasogenic cerebral edema[14]. In our case, patient developed cortical blindness, with typical neurological findings of PRES in course of acute pancreatitis. She also developed a moderate hypertension. The symptoms and MRI alteration regressed with the normalization of amylase and lipase levels. Only a few cases of PRES in the setting of acute pancreatitis, with or without other possible triggers for PRES, have been reported[15-23] (Table 1). The few reported cases of pancreatitis associated with PRES concern both genders and variable age (18-61 years). Various causes of pancreatitis are reported in association with PRES (alcohol, traumatic pancratitis, nephrotic syndrome, porphyria, steroids and antiphospholipid syndrome). In acute pancreatitis, the serum levels of pro-inflammatory cytokines, lipase, and amylase are elevated which could play a major role in the development of extra-pancreatic complications

[27-28]. Experimental models in rats suggested that during acute pancreatitis the pro-inflammatory cytokines, such as IL-6 and TNF, contribute to vasogenic brain edema through an alteration of the blood brain barrier permeability.


Therefore it can be assumed that the pancreatitis itself can be a cause, although rare, of PRES. Obviously the data in the literature are few and further studies are needed to confirm these supposition.

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Posterior Reversible Encephalopathy Syndrome Associated with Acute Pancreatitis. (2018, July 05). GradesFixer. Retrieved February 27, 2021, from
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