Unveiling the Neurological Aftermath: PRES After Cardiac Arrest

Background: Posterior Reversible Encephalopathy Syndrome (PRES), also known as ‘Reversible Posterior Leukoencephalopathy Syndrome (RPLS)’, is a clinical radiographic syndrome originally described by Hinchey et al in 1996. PRES has been significantly underdiagnosed due to difficulty in confirmation. As such, there is currently no epidemiological data regarding its incidence, but it has been diagnosed in all age groups with a preponderance in females. A variety of medical conditions have been implicated as causes of PRES, including severe hypertension, immunosuppressive therapy, sepsis, renal diseases and autoimmune disorders. The mechanism of PRES is thought to be related to disordered cerebral autoregulation and endothelial dysfunction. It typically involves the subcortical white matter in the posterior cerebral hemispheres; however, other brain regions may be affected. Clinical manifestations include headache, altered consciousness, visual disturbances, and seizures. It is usually diagnosed with a non-contrast CT of the head or brain MRI. Typical findings are bilateral areas of vasogenic edema in the posterior cerebral hemispheres, particularly the parieto-occipital regions, but variations occur. PRES is reversible in most patients. On average, 40% of PRES patients require intensive care monitoring and treatment due to complications such as cerebral ischemia, intracerebral hemorrhage, and intracranial hypertension. With treatment, resolution of) imaging findings within days to weeks is expected. Case Presentation: A 69-year-old Hispanic male with a history of asthma and hypertension was brought to the Emergency Department by Emergency Medical Services after a cardiopulmonary arrest due to status asthmaticus. He was admitted to the Intensive Care Unit for post-cardiopulmonary arrest care. During his hospitalization, he had fluctuations in blood pressure, with his systolic blood pressure ranging between 161-185 mmHg. On hospital day 9, he developed generalized tonic-clonic seizures. The CT of the head without contrast was unremarkable. An MRI of the brain was obtained which demonstrated areas of increased intensity that involved the parieto-occipital subcortical regions, the frontal lobe, and the basal ganglion, as can be seen in PRES. Neurology was consulted. Nicardipine drip for appropriate control of his blood pressure and Levetiracetam for seizure control were recommended. He did not develop any subsequent seizures. On hospital day 13, a repeat MRI of the brain demonstrated almost complete resolution of the findings suggestive of PRES. We continued administration of levetiracetam and antihypertensive medications. Conclusion: PRES is a reversible condition presenting with acute neurologic symptoms ranging from headaches to seizures with radiographic evidence of vasogenic edema in various areas of the brain, most commonly the parieto-occipital region. While cardiopulmonary arrest itself is not a typical cause of PRES, severe hypoperfusion to the brain during the arrest could potentially lead to PRES, especially with dramatic changes in blood pressure and malfunctioning of the brain’s autoregulatory system. This case highlights the importance of considering PRES when a patient develops seizures or visual disturbances following a cardiopulmonary arrest, especially when there is a high probability of brain hypoperfusion and uncontrolled hypertension. This will ensure prompt diagnosis with imaging tests and proper management, leading to a favorable outcome with less long-term neurological damage.