Hypercapnia increases intracranial pressure by inducing cerebral vasodilation and elevated blood flow. In rare cases, this may cause radiographically visible cerebral edema. Altered consciousness in hypercapnic respiratory failure is typically attributed to CO₂ narcosis rather than edema. Standard management often involves intubation, ventilation, and osmotherapy.

A 60-year-old man with chronic obstructive pulmonary disease and chronic respiratory failure on home oxygen presented with 4 days of progressive dyspnea, productive cough, and confusion after discontinuing his inhaled fluticasone furoate/ umeclidinium/vilanterol regimen. On arrival, he was encephalopathic, exhibiting garbled speech and somnolence. Blood gas analysis revealed severe hypercapnia (pH 7.33, pCO₂ 100 mmHg; nadir pH 7.19, pCO₂ 133 mmHg). Head CT demonstrated diffuse cerebral edema (Figure 1, a–d). He was started on BiPAP (initially 18/8 cmH₂O, later adjusted to 20/7 cmH₂O with a backup rate of 25), along with systemic corticosteroids, antibiotics, and bronchodilators. Over 24-48 hours, his ventilation improved (pH 7.37, pCO₂ 81 mmHg), mental status returned to baseline and repeat CT imaging showed complete resolution of cerebral edema (Figure 1, e–h). By hospital day 3, he was weaned to his baseline supplemental oxygen and discharged with plans for home BiPAP therapy.

This case demonstrates hypercapnic global cerebral edema as a reversible entity responsive to NIV. Unlike prior reports requiring intubation and osmotherapy, both encephalopathy and imaging abnormalities resolved rapidly with BiPAP alone. Prompt recognition may avoid unnecessary escalation of care and supports further exploration of NIV in managing hypercapnia-associated cerebral edema. This case shows that prompt BiPAP correction of hypercapnia can reverse cerebral edema without invasive measures, helping avoid intubation.