Introduction:
Several theories exist regarding the pathogenesis of posterior reversible encephalopathy syndrome (PRES). One theory suggests that PRES occurs when systemic blood pressure exceeds the upper limit of cerebral autoregulation. Endothelial dysfunction has been proposed as an alternative pathogenesis to account for PRES outside the setting of acute hypertension. This mechanism has been implicated in other conditions associated with PRES including autoimmune diseases, cytotoxic medications, sepsis, and eclampsia. The purpose of this study was to determine if COPD, a disease known to cause endothelial dysfunction, has a causative association with the development of PRES.
Methods:
A single center retrospective, age-matched, case-control study was performed from January 2013 to June 2019 comparing patients discharged with a primary diagnosis of PRES to a control group with acute ischemic stroke. Demographics, medical comorbidities, initial blood pressure, and clinical outcomes were compared between the two groups. For categorical variables, p-values were calculated using χ2 and Fisher’s exact tests. For continuous variables, p-values were calculated using two-sample t-tests. The effect of COPD and acute hypoxic respiratory failure on PRES status was investigated using multivariate logistic regression.
Results:
A total of 94 PRES subjects and 109 control subjects were included for analysis. Mean age did not differ between the two groups; however, the PRES group was more likely to be female (78.7% vs. 49.5%, p<0.001). COPD was present in 26.6% (n=25) of cases and 11% (n= 12) of controls (odds ratio 4.12, p=0.003). Occurrence of hypertension did not differ significantly between the two groups (78.0% vs 86.2%). Among patients with PRES in the setting of COPD (n=25), 60% (n=16) did not meet criteria for hypertensive emergency. Controlling for hypertensive emergency status in a multivariate logistic regression analysis, patients with COPD were 3.21 times more likely to develop PRES (p= 0.004).
Conclusions:
To our knowledge, very few reports of PRES in the setting of COPD have been described in the literature and no association of PRES and COPD has been defined to date. Our data support the role of COPD as a risk factor in the development of PRES.