The effect of end-tidal carbon dioxide on optic nerve diameter in COPD patients: A cross-sectional study.

Chronic obstructive pulmonary disease (COPD) is a heterogeneous condition that causes persistent and often progressive airway obstruction with symptoms such as dyspnea, cough, expectoration, and/or exacerbations due to abnormalities in the airways and/or alveol. It is known that hypercarbia causes headaches by increasing intracranial pressure (ICP). Ultrasonographic measurement of optic nerve sheath diameter (ONSD) noninvasively has been shown to be as successful as invasive measurements in demonstrating increased intracranial pressure. The aim of this study was to determine the effect of the decrease in end-tidal carbon dioxide pressure on the optic nerve diameter and thus get an idea about ICP and its correlation with symptoms such as headache in hypercarbic patients with severe exacerbations of COPD. Patients with COPD ICD codes who needed noninvasive mechanical ventilation (NIMV) were included in the study. Patients who were incompatible with NIMV or who were switched to invasive mechanical ventilation due to treatment failure were excluded from the study. The decrease in end-tidal carbon dioxide, the change in ONSD, in the state of consciousness, and in symptoms such as headache was evaluated. There was no statistically significant difference in optic nerve diameter between those with and without headache at baseline. This difference was not significant: 6.45 (6-6.7) mm in those with ONSD headache and 6.4 (6-6.7) mm in those without. As a result, although the ONSD was wider than expected in patients with hypercarbic COPD, no relationship was found with headache.