Thrombolysis For Massive Pulmonary Embolism Research Articles

Cerebral infarction following thrombolysis for massive pulmonary embolism

A 29-year-old male developed a fatal stroke 6 h after successful thrombolysis for massive pulmonary embolism. Autopsy showed thrombus protruding through a patent foramen ovale (PFO). A strand of thrombus extended from the aortic arch into the left common carotid artery. The brain showed extensive infarction of the left fronto-parietal area. Thrombolysis caused initial disintegration of the embolism. It is likely that thrombolysis caused fragments of clot to later break lose and embolise into the cerebral circulation. We discuss the need for risk stratification in patients who present with massive pulmonary embolism and PFO.

Images in Resuscitation: Bruising after thrombolysis for massive pulmonary embolism (PE)

Images in Resuscitation: Bruising after thrombolysis for massive pulmonary embolism (PE)

Should thrombolysis be contraindicated in patients with cerebral arteriovenous malformations?

To report the successful and uncomplicated use of systemic thrombolysis for massive pulmonary embolism in a patient with a known cerebral arteriovenous malformation and to suggest that the presence of an unruptured arteriovenous malformation or aneurysm should not be considered an absolute contraindication to systemic thrombolysis. Case report. A 16-bed adult neurologic/medical intensive care unit in a university hospital. A patient developed a massive pulmonary embolism the morning after elective cerebral embolization of a large unruptured cerebral arteriovenous malformation. Radial artery catheterization, arterial blood gas measurements, mechanical ventilation, vasopressors, pulmonary perfusion scan, echocardiogram, head computed tomography, heparin therapy, and systemic recombinant tissue plasminogen activator therapy. The patient required emergent mechanical ventilation and vasopressor support for respiratory and hemodynamic failure. Echocardiogram showed acute right heart failure, and pulmonary perfusion scan demonstrated massive pulmonary embolism. Despite intravenous heparin therapy, the patient had worsening hypotension and acidosis and we therefore treated with recombinant tissue plasminogen activator. Within the next day the patient was weaned from vasopressor support and extubated. Neurologic examination remained normal, and follow-up head computed tomography revealed no evidence of intracranial hemorrhage. Known arteriovenous malformations or aneurysms are considered a contraindication to thrombolysis, although the true risk of thrombolysis-precipitated intracranial hemorrhage is unknown. We believe that this risk is low in the setting of a previously unruptured arteriovenous malformation or aneurysm. The decision to use systemic thrombolysis in a patient with a known vascular malformation should be individualized.

Mechanical and Enzymatic Thrombolysis for Massive Pulmonary Embolism

To assess the efficacy and safety of mechanical fragmentation combined with intrapulmonary thrombolysis in massive pulmonary thromboembolism (PTE) with hemodynamic impairment. Fifty-nine patients diagnosed with massive PTE with hemodynamic impact were treated. The initial clinical symptoms were shock in 23 patients (38.9%), syncope in eight (13.5%), and dyspnea at rest in 28 (47.4%). Mean O2 saturation was 67.8%. Mean pulmonary artery pressure (PAP) was 42.1 mm Hg. During fragmentation, thrombolysis was administered in the form of a urokinase bolus of 200,000-500,000 U in 57 patients and 20 mg of recombinant tissue plasminogen activator (rt-PA) in two patients. The mean urokinase dose used was 2,500,000 IU, whereas the total dose of rt-PA was 100 mg. Heparin sodium infusion was performed to reach activated partial thromboplastin time ratios of 2. The follow-up consisted of clinical assessment, pulmonary scintigraphy, and echocardiography. The patients received treatment with dicoumarin for 6 months after the procedure. Clinical improvement was seen in 56 patients (94%). Three patients died. The mean PAP after the treatment was 21.8 mm Hg. The mean posttreatment Miller index was 0.35. Technical success was achieved in all cases and clinical symptoms improved in all cases except those in which the patients died. Pulmonary scintigraphy showed improved perfusion in all cases. Echocardiography was performed after 3-6 months, showing a mean pressure of 22.8 mm Hg (corrected values). There were no signs of recurrent PTE or arterial hypertension in the follow-up. The data provided confirm the efficacy and safety of mechanical fragmentation and pharmacologic thrombolysis in the treatment of massive PTE with hemodynamic impairment, showing improvement of symptoms and a decrease in PAP.

Successful thrombolysis for massive pulmonary embolism after pulmonary resection

We report the successful use of thrombolysis for acute massive pulmonary embolism 2 days after right lower lobectomy for bronchial adenocarcinoma. Pulmonary angiography revealed extensive clot unsuitable for surgical embolectomy. A bolus infusion of recombinant tissue plasminogen activator produced an immediate improvement in the patient’s hemodynamic state. There was substantial blood loss requiring the transfusion of 21 units of blood over the postoperative period. The patient made a successful recovery and remained well at 1 year.

Mechanical Fragmentation and Pharmacologic Thrombolysis in Massive Pulmonary Embolism

To evaluate the usefulness of mechanical fragmentation associated with intrapulmonary thrombolysis in acute massive pulmonary embolism (PE). Sixteen cases of massive PE treated with mechanical fragmentation associated with pharmacologic thrombolysis were retrospectively studied. Severity of PE was assessed with the angiographic index according to the Urokinase Pulmonary Embolism Trial (maximum value of 18; score according to whether obstruction was central or peripheral, complete or partial). Mechanical fragmentation of the emboli was performed with angiographic catheters and angioplasty balloons. Urokinase was infused directly into the thrombus during the course of 8-24 hours. The effect of therapy was measured with direct pulmonary artery pressure (PAP) and blood O2 values. Pre- and postinfusion angiographic index mean values (+/- standard deviation) were 13.7 +/- 1.4 and 6.1 +/- 2.2 (P < .0001). Mean pre- and postinfusion PAPs were 48.2 +/- 13.4 and 18.5 +/- 7.2 mm Hg (P < .0001). PaO2 increased from 60.1 +/- 12.1 to 88.7 +/- 23.4 mm Hg (P = .01). Fourteen patients (87.5%) completely recovered. One patient died during treatment despite improvement in PAP and PaO2 parameters. There were no major hemorrhagic complications. The data support the efficacy of mechanical fragmentation associated with pharmacologic thrombolysis in the treatment of acute massive PE, resulting in improved hemodynamics and-blood oxygenation and in decreased PAP, with low morbidity.

Effects of the dosing regimen of tissue-type plasminogen activator on blood coagulation system in experimental pulmonary embolism.

Background: As a physiologic plasminogen activator, tissue-type plasminogen activator (t-PA) could induce effective thrombolysis in massive pulmonary embolism, without the risk of systemic hemorrhage. However, therapeutic doses of t-PA has been associated with systemic lytic state, and fibrin selectivity may be influenced by the dosing regimen of t-PA. To investigate the effects of duration of t-PA infusion on blood coagulation system, we performed this study. Method: In a canine model of pulmonary embolism, which was induced by injection of autologous blood clots, we administered equal doses of t-PA (1 mg/kg) over 15 minutes in group, over 180 minutes in group, and only saline in control group. Then serial blood samplings were made to check complete blood count, prothrombin time, activated partial thromboplastin time, thrombin time, fibrin, plasminogen, -antiplasmin, coagulation factor V and VIII, and fibrin(ogen) degradation products. Results: 1) In all 3 groups, complete blood count showed same changes. Hemoglobin, hematocrit and platelet count decreased, but WBC count increased. 2) Prothrombin time, activated partial thromboplastin time, and thrombin time were prolonged during 15-60 minutes after t-PA administration in group, and from 30 minutes through 180 minutes after administration in gorup. 3) Fibrin, -antiplasmin, and cogulation factor V and VIII decreased in both and group, but returned to basal levels earlier in group. 4) Fibrin(ogen) degradation products increased after pulmonary embolism in all groups, and further increased in both and groups after t-PA infusion. But more pronounced increment was noted in gorup. Conclusion: In pulmonary embolism, the shorter (15 minutes) infusion of t-PA would have less risk of systemic hemorrhage than the longer (180 minutes) infusion when the doses is equal. And, this suggests that manipulating the duration of t-PA infusion can reduce the risk of major bleeding.