To present a case of severe hypercapnia causing Posterior Reversible Encephalopathy Syndrome (PRES).

A 60-year-old African-American male with a history of chronic obstructive pulmonary disease (COPD) on home oxygen and chronic CO₂ retention was admitted for hypoxemic respiratory failure. Chest X-ray showed bilateral pleural effusions and CT angiography of the chest with contrast showed bilateral consolidations with effusions. Several days into his hospital course, he was found to be encephalopathic. Arterial blood gas revealed PaCO₂ > 102 and a pH of 7.22.  Non-contrast CT of the head showed areas of hypodensity in the posterior right parietal and occipital lobes. MRI brain showed T2 FLAIR hyperintensities in the right parietal and bilateral occipital lobes. CT angiography of the head and neck, EEG, and TTE did not show pertinent acute findings. 

Patient was empirically started on azithromycin, metronidazole, cefepime, and vancomycin for his severe pneumonia. His oxygen requirement was increased from 2 L to 5 L. He was initially refusing BiPAP, but subsequently was placed on nightly BiPAP due to the development of acute encephalopathy. Thoracentesis was performed for his pleural effusion.

The patient was diagnosed with PRES and treated with oxygen and nightly BiPAP. His PaCO₂ improved once he was placed on BiPAP. Mental status also returned to baseline shortly thereafter. Repeat MRI brain six days later showed improvement of the bilateral hyperintensities. The patient left against medical advice three weeks after admission and was lost to follow-up.

Severe hypercapnia is an uncommon and under-recognized risk factor associated with PRES. This case demonstrates how acute elevations in PaCO₂ led to the development of PRES in a COPD patient with chronic CO₂ retention. It also highlights the importance of how swift correction of elevations in PaCO₂ can rapidly improve the clinical and radiographic manifestations of PRES.