Posterior reversible encephalopathy syndrome due to COVID-19

Introduction Human coronaviruses (HCoVs) are part of coronaviruses cluster (CoVs); which can cause a range of respiratory diseases ranging in severity from simple common cold to more sever pneumonia (1). During late 2019, a group of patients started to have unexplained chest infections in Wuhan, China. After days, the new causative microorganism was identified as a new coronavirus type (nCoV) by multiple laboratories (2). Although it is mainly a respiratory disease, there have been numerous reports of new clinical findings that develop in coronavirus disease 2019 (COVID-19) patients, not only affecting the lungs but can also cause cardiac, and neurological manifestations. Patients with COVID-19 are reported to have strokes, seizures, abnormal mental status, and inflammatory brain changes. One of earliest case reports mentioned a COVID-19 Chinese patient with left sided hemiparesis which was due to a stroke with occlusion in a large blood vessel. Other reports also described massive intracranial hemorrhage without prior history of anticoagulation or hypertension (3). One study showed that cerebrovascular pathology was seen in 1.4% of patients, while headache was reported in 13.6% of patients with COVID-19 (4). Here we present a case of COVID-19 infection that showed typical neuroimaging of posterior reversible encephalopathy syndrome (PRES) with no reported history of any precipitating risk factors mentioned in the literature.

patient had recurrent seizures which progressed to status epileptics and again she was intubated and admitted to the intensive care unit.
After stabilizing her condition, the CT-scan of her brain showed features suggestive of PRES (Figure 2), and MRI was requested to confirm the diagnosis.
MRI of the brain showed vasogenic edema bilaterally involving occipital lobes, parietal lobes and posterior parts of frontal lobes confirming PRES (Figure 3).
Her vital signs at this point showed mild hypertension of 154/93, heart rate of 90/min, intubated on FiO2 35%, and her ABG showed PaO2 120 mm Hg. She was extubated one day later and started medical management by a neurologist and antiepileptic and antihypertensive management continued until discharge.
Routine blood tests were done daily while she was in ICU. Her WBC ranged from 8.2 * 10^9/L to 30*^9/L, C-reactive protein reached 270, her ferritin peaked at 3799 μg/L, the highest recorded LDH was 1554 IU/L, and D-Dimer ranged between 5 at time of admission and reached to > 35 mg/dL.
We followed the patient throughout her stay in the hospital and it is worth mentioning that the patient had no prior concerning chronic conditions including renal impairment or epilepsy.
She recovered after staying in our hospital for a total of 62 days. She was fully conscious, oriented, and vitally stable. She was discharged on Keppra, and augmentin. She was followed up by internal medicine and neurology.

Discussion
PRES is considered as a neurological syndrome with a spectrum of neurological and radiological characteristics usually due to different factors. The most common presenting signs are headaches, visual disturbances, disturbed consciousness, and occasionally focal neurological deficit (5).
With the fast spread of COVID-19 infection, different neurological symptoms are being reported in which many of them are still not pathologically linked to the infection with coronavirus and need more studies. PRES was reported in a patient with COVID-19 (6) and two more patients who experienced severe COVID-19 infection (7). All these patients reported to have high blood pressure around the time of PRES diagnosis.   This report described a young patient with no prior medical history that suffered from severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) associated with PRES. Our case gives further evidence of different neurological manifestation that can be associated with COVID-19.
PRES was diagnosed in this patient although she had only mild rise in her blood pressure, which may point to the assumption that patients with COVID-19 may develop PRES with lower blood pressure. Thus, a stricter blood pressure control should be considered when managing those patients.
The cause behind this might be due to cerebral endothelial dysfunction secondary to SARS-CoV-2 and needs further studies and observations to reach a better understanding of risk factors and causes behind such presentations.

Conclusion
The literature is still far away from gripping an edge regarding COVID-19 infection. Although PRES happens in patients with high blood pressure and other risk factors, in patients with COVID-19, it can be manifested with much lower blood pressure and that is something physicians should remember.

Ethical Issues
Patient consent was taken from the patient for publication of this report.