Treatment of pulmonary embolism with low-dose prolonged infusion of tissue-type plasminogen activator in an 85-year-old woman
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CitationBiteker, M., Ekşi Duran, N., Gündüz, S. ve Özkan, M. (2009). Treatment of pulmonary embolism with low-dose prolonged infusion of tissue-type plasminogen activator in an 85-year-old woman. Journal of the American Geriatrics Society. 57(4), s. 745-746.
An 85‐year‐old woman was admitted to Kosuyolu Heart and Research Hospital for sudden dyspnea and chest pain. She had no chronic disease. On physical examination, she had a pale, cyanotic hue on the face, regular pulse of 108 beats per minute, and blood pressure of 70/40 mmHg. She had marked respiratory difficulty, with a respiratory rate of 27 breaths per minute. Her jugular veins were mildly distended, and lung fields were clear. She had normal heart sounds except for a mild systolic murmur on the left lower sternal border. Her electrocardiogram showed sinus tachycardia with S1 Q3 T3 pattern. A chest film showed a minimally enlarged cardiac silhouette without congestion or infiltrate. The patient was admitted to the coronary intensive care unit, where an arterial blood gas measurement obtained on room air showed a pH of 7.40, a partial pressure of carbon dioxide of 33 mmHg, and a partial pressure of oxygen of 60 mmHg. She was started on supplemental oxygen through a venturi mask. Oxygen saturation was 88% on room air. Her plasma d‐dimer level was 2,450 (normal <500 ng/mL). Transthoracic echocardiography (TTE) (Supporting Information, Video S1)* showed a worm‐like, mobile mass in the right atrium moving during diastole into the right ventricle. The right ventricle was enlarged, and paradoxical septal motion was present, indicating right ventricular pressure overload. Doppler examination showed moderate tricuspid regurgitation and pulmonary artery hypertension (pulmonary artery systolic pressure 65 mmHg). The diagnosis was right heart thrombosis with massive PE. She was deemed too high a surgical risk because of her age and general condition. After discussion of the treatment options (cardiac surgery, thrombolysis, intravenous heparin) with the patient and her family, the decision was made to initiate thrombolytic therapy. Considering not only her age, but also the possibility of decreasing thromboembolism, it was decided to administer a prolonged low‐dose tissue‐type plasminogen activator (t‐PA) without heparin. After 20 mg t‐PA was given in 90 minutes, without bolus, thrombus dimension was decreased nearly 50%. Then the second dose t‐PA was given using the same protocol (20 mg in 90 minutes). At the end of the second infusion, right heart thrombus was completely resolved on TTE, with a progressive clinical and hemodynamic improvement. Pulmonary artery systolic pressure decreased to 30 mmHg. The thrombolytic therapy was stopped after 40 mg t‐PA was given over 3 hours and started an unfractionated heparin infusion intravenously. At the end of the thrombolytic therapy, the patient's clinical status was normal; blood pressure was 130/80 mmHg, heart rate was 80 beats per minute, and there were no signs of dyspnea (17 breaths per minute). A Doppler ultrasound revealed bilateral femoral vein thrombosis, and high‐resolution computed tomography of the thorax, performed at the same day, did not reveal a significant lesion. The unfractionated heparin infusion was continued for 3 days, followed by warfarin therapy.
SourceJournal of the American Geriatrics Society
- Makale Koleksiyonu 
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