Critical Care |

Anesthesia-Induced Posterior Reversible Encephalopathy Syndrome (PRES) in a Postoperative Patient FREE TO VIEW

Eric Boccio, BS; Fiore Mastroianni, BS; Todd Slesinger, MD
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North Shore University Hospital, Manhasset, NY

Chest. 2014;146(4_MeetingAbstracts):289A. doi:10.1378/chest.1991815
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SESSION TITLE: Critical Care Student/Resident Case Report Posters I

SESSION TYPE: Medical Student/Resident Case Report

PRESENTED ON: Tuesday, October 28, 2014 at 01:30 PM - 02:30 PM

INTRODUCTION: Posterior Reversible Encephalopathy Syndrome (PRES) is a neurotoxic state defined by variable clinical signs and symptoms, unique radiological features, and general reversibility of the condition. Presentation may include headache, nausea, vomiting, altered mental status, seizures, and visual loss or disturbances. Neuroimaging shows characteristic transient changes, and diagnosis is typically made using MRI. Treatment of PRES should focus on the underlying cause which may include hypertension, severe infection, shock, eclampsia, immunosuppressive therapies, renal insufficiency, lupus, and therapeutic agents.

CASE PRESENTATION: A 68-year-old female with known history of diverticulosis presented to the emergency department (ED) complaining of 3 days of worsening LLQ pain. Review of systems was notable for fever, chills, diarrhea, and vomiting. On physical exam, the abdomen was distended and diffusely tender with guarding. CT showed perforated sigmoid diverticulitis with local extraluminal air. The patient was brought for surgical resection of the perforated bowel. A successful Hartmann’s procedure was performed under general anesthesia with minimal blood loss. Following a postoperative course complicated by ARDS and septic shock, the patient failed to regain normal mental status becoming uncooperative and combative. On POD7, head CT showed bilateral parietal-occipital white matter lucencies. Follow up MRI showed bilateral and symmetric T2 hyperintensities confined to posterior cerebral and cerebellar white matter. The symmetrical nature and location of the abnormality made it highly suspicious for PRES. The patient continued to receive supportive measures and was discharged on POD21 with minimal deficit.

DISCUSSION: The cause of acute PRES is not completely understood, and proposed mechanisms attribute the condition to vasogenic edema resulting from a disruption of the blood-brain barrier and autoregulatory function. If untreated, vasogenic edema will progress to cytotoxic edema, ischemia, and infarction of brain tissues. On T2 MRI, PRES appears as bilateral hyperintensities predominantly in the white matter of the posterior cerebral hemispheres. On T1 MRI, hypointensities/isointensities appear in the same localized regions.1 CT studies are inconsistent, making MRI the favored modality.

CONCLUSIONS: This case highlights the need to recognize the non-specific neurological symptoms associated with PRES especially when monitoring critically ill and intubated postoperative patients. Reversible with appropriate treatment, early recognition and diagnosis is crucial to prevent the complicating factors of prolonged PRES, specifically cytotoxic edema. Increased awareness will allow for rapid ordering of appropriate neuroimaging, and confirmation of characteristic radiological findings will prevent misdiagnosis.

Reference #1: Lamy C, et al. Neuroimaging in posterior reversible encephalopathy syndrome. J Neuroimaging. 2004 Apr;14(2):89-96.

DISCLOSURE: The following authors have nothing to disclose: Eric Boccio, Fiore Mastroianni, Todd Slesinger

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