Fulminant Pulmonary Edema Triggered by Phenylephrine-Induced Hypertension for Early Neurological Deterioration in Ischemic Stroke

Dear Editor,Phenylephrine-induced hypertension (PIH) is used to treat early neurological deterioration in acute ischemic stroke (AIS).1,2 However, phenylephrine may cause serious cardiovascular complications.We report a case of fulminant pulmonary edema following PIH therapy.A 63-year-old female with hypertension and diabetes mellitus was admitted for pneumonia with consolidation in the left lower lobe on chest radiography.She developed acute right hemiparesis during hospitalization.A neurological examination revealed right hemiparesis with a score on the National Institutes of Health Stroke Scale (NIHSS) of 7. Brain MRI revealed an acute infarction in the left middle cerebral artery territory with focal stenosis of the M1 segment (Fig. 1A).Transthoracic echocardiography (TTE) revealed low-normal left ventricular (LV) systolic function (ejection fraction [EF] of 54%) and mild pulmonary hypertension, with an estimated right ventricular systolic pressure (RVSP) of 48.6 mm Hg based on the peak tricuspid regurgitation velocity.The mean E/e' ratio was 21.2, suggesting elevation of the LV filling pressure.The inferior vena cava was not dilated, and there were no clinical signs of volume overload.The patient exhibited neurological deterioration at 4 days after stroke onset, with her NI-HSS score increasing to 9. Before PIH initiation, the patient received only maintenance intravenous fluids without volume expanders or other vasoactive agents.Over the preceding 3 days her intravenous fluid intakes were 1,270 mL, 880 mL, and 930 mL.Her total intake over the same period (including oral fluids) was 5,740 mL, and her total output was 5,710 mL, giving a net balance of +30 mL.Her pneumonia was clinically improving, with resolution of fever and decreasing inflammatory markers; parapneumonic effusion that had been managed with pigtail catheters placed 3 days previously showed interval radiographic improvement.PIH was initiated at 0.15 μg/kg/min targeting a 20%-30% increase in the mean arterial pressure (MAP) from the baseline of 87 mm Hg (blood pressure was 124/69 mm Hg).Titrating the infusion resulted in MAP reaching 106 mm Hg at the maximum dose of 1.35 μg/kg/ min (Fig. 1B).Nine hours after PIH initiation, the patient developed acute respiratory distress and desaturation.An arterial blood gas analysis showed hypoxemia (pH 7.32, PaCO2=39.3mm Hg, PaO2=60.7 mm Hg).High-flow nasal cannula (HFNC) oxygen therapy was initiated at an FiO2 of 40% and a flow rate of 40 L/min.Chest radiography revealed diffuse bilateral pulmonary edema (Fig. 1C), and PIH therapy was immediately discontinued.HFNC support was escalated by incrementing FiO2 to 60%, 80%, and 100% (all at 60 L/min), but hypoxemia worsened despite maximal oxygen support.