An 85-year-old male patient with no morbid history, except for old prostatic resection.
The patient presented left ankle trauma 3 weeks prior to admission, due to the fact that he remained at rest for seven days.
Progressively, he noticed increased volume of the left lower limb.
On the day of admission, the patient developed moderate back pain associated with lipothymia and dyspnea.
The patient was admitted to the emergency department with hypotension (70/40 mmHg), poor peripheral perfusion, heart rate of 60 per minute, regular rhythm, engorged jugular vein, with no palpable right ventricular edema.
Laboratory tests showed PaO2 96.4 mmHg, PaCO2 33 mmHg, pH 7.39, HCO3 20.1 (mmol/l), lactate 2.6 (mmol/l) and difference alveolar oxygen 29 mmHg.
The electrocardiogram showed complete right bundle branch block.
The diagnoses at admission were cardiogenic shock due to myocardial infarction of the RV versus obstructive shock due to massive embolism.
The surface echocardiogram showed marked RV dilatation, tricuspid reflux and estimated pulmonary artery pressure of 65 mmHg, with no communication ̄.
The left ventricle appeared normal, with preserved systolic function.
A computed axial tomography angiography (CAT) of the pulmonary arteries showed bilateral pulmonary artery involvement, with dilatation of the right ventricle and reflux of contrast to the inferior vena cava.
CT venography showed left deep iliac and femoropopliteal vein thrombosis.
The patient was taken directly from a scanner to the angiography room and was admitted to shock refractory to vasoactive drugs, with oxygen saturation of 70%.
Digital subtraction angiography confirmed the diagnosis of bilateral massive embolism.
Mechanical fragmentation of thrombi was performed with balloon angioplasty and angiographic guide, obtaining rapid improvement in oxygen saturation and hemodynamic parameters.
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In addition, local thrombolysis was performed with tissue endogenous activator (t-PA) (20 mg), followed by infusion of urokinase 60,000 U/h for 12 h.
The mean pulmonary artery pressure, measured directly, decreased from 47 to 30 mmHg after thrombolysis.
The patient developed mild gingivorragia and epistaxis after thrombolysis, which resolved spontaneously.
In the final control, there was a significant improvement in pulmonary perfusion.
Given the extensive deep venous thrombosis in the left lower limb, a vena cava filter was placed percutaneously, without complications.
The patient started intravenous heparin and on the second day began oral anticoagulant therapy (OAT) with acenocoumarol.
The patient was discharged on the fifth day of hospitalization, in good general condition, applying TACO for six months.
In the clinical follow-up performed at 6 months, the patient was in good condition, functional capacity I, with no complications derived from the TACO.
