Refractory Hypoxemia as a Trigger for Systemic Thrombolysis in Intermediate-High-Risk Pulmonary Embolism: A Case...

Background and Clinical Significance: Intermediate-high-risk pulmonary embolism is characterized by right-ventricular dysfunction and positive cardiac biomarkers in the absence of hemodynamic instability. Current guidelines recommend anticoagulation with vigilant monitoring, and reserve systemic fibrinolysis for patients who deteriorate hemodynamically. However, some patients may experience physiologic decompensation manifested by refractory hypoxemia rather than hypotension, despite preserved systemic perfusion and normal lung parenchyma. In such cases, oxygenation failure reflects the severity of perfusion impairment and incipient right-ventricular-circulatory collapse. Whether this scenario justifies systemic fibrinolysis remains uncertain. Case Presentation: We present a 75-year-old man, five days after arthroscopic meniscus repair, presenting with acute dyspnea, tachycardia, and severe respiratory failure despite normal chest radiography. Laboratory findings revealed elevated troponin-I and brain natriuretic peptide, and echocardiography demonstrated marked right-ventricular dilation. Computed tomographic pulmonary angiography confirmed extensive bilateral central emboli with preserved lung parenchyma. Despite high-flow nasal oxygen at 100% fraction of inspired oxygen, respiratory failure worsened, necessitating intubation under lung-protective settings. With catheter-directed therapy unavailable and transfer unsafe, a multidisciplinary team administered staged systemic fibrinolysis with alteplase, pausing heparin during infusion. No bleeding or surgical complications occurred. Oxygenation and right-ventricular indices improved promptly. The patient was extubated on day 2, discharged from intensive care unit on day 7, and remained asymptomatic with normal echocardiography at 3 months. Conclusions: Refractory hypoxemia in intermediate-high-risk, normotensive pulmonary embolism, particularly when parenchymal disease and ventilator confounding are excluded, may represent an early form of circulatory decompensation warranting rescue reperfusion. In the absence of catheter-directed options and with acceptable bleeding risk, staged full-dose systemic fibrinolysis can be life-saving and physiologically justified. This case supports expanding the concept of "clinical deterioration" in intermediate-risk pulmonary embolism to include isolated, unexplained respiratory failure, highlighting the need for future trials to refine individualized reperfusion thresholds.