Thrombolysis for massive pulmonary tumour embolism in a patient with cavoatrial renal carcinoma
Padova, Italy
* E-mail: micarron{at}libero.it
Editor—We would like to report a case in which the treatment with recombinant tissue plasminogen activator (rt-PA) appears as a key element of the successful management of a massive pulmonary tumour embolism in a patient with renal cell carcinoma (RCC) extending into the right heart. This catastrophic event has a high perioperative mortality1 and represents an important challenge for physicians. Few reports of successful surgical management have appeared,1 and no data are available to support the efficacy of thrombolytic treatment in this condition.
A 48-yr-old man, scheduled for surgery for cavoatrial renal carcinoma, presented with syncope followed by respiratory distress (pH, 7.12; PaO2, 7.3 kPa; PaCO2, 8.9 kPa; 8 litre min–1 of oxygen by face mask) and cardiogenic shock (arterial blood pressure, 60/40 mm Hg; heart rate, 140 beats min–1). Pulmonary embolism was suspected and the patient was transferred to the intensive care unit. Initial management consisted of pressure control ventilation (PEEP 8 cm H2O, peak airway pressure 28 cm H2O, FIo2 1), fluid loading and continuous infusion of dobutamine (10 µg kg–1 min–1) and norepinephrine (0.6 µg kg–1 min–1). Despite the therapy, impairment of gas exchange (pH, 7.29; PaO2, 10.4 kPa; PaCO2, 4.8 kPa) and haemodynamic instability (arterial blood pressure, 80/40 mm Hg; heart rate, 155 beats min–1) persisted. An ECG showed tachycardia, right bundle-branch block, and T-wave inversion in leads V1–4. The transthoracic echocardiography showed a dilated right heart, right ventricular hypokinesis (ejection fraction, 35%), and raised pulmonary artery systolic pressure (55 mm Hg) (Fig. 1). It showed the tumour thrombus in the right atrium prolapsing through the tricuspid valve into the right ventricle during diastole. Doppler ultrasonography of the lower limbs did not show evidence of deep venous thrombosis. The compromised condition of the patient did not permit emergency surgical treatment. After consultation with the cardiothoracic surgeon, thrombolytic treatment was adopted. An i.v. bolus of rt-PA 10 mg was administered, followed by an i.v. infusion of rt-PA 90 mg over 2 h. Haematuria was observed in the following 4 h with the decrease of red cells count from 4.56 to 3.75x109 litre–1 and of haemoglobin from 14 to 11.7 g dl–1. A clinical improvement was noted after 6 h of rt-PA administration. Vasopressor dosages were gradually reduced and stopped at 38 h after thrombolysis. Fifteen days later, an elective radical right nephrectomy and tumour embolectomy were successfully performed.
Approximately 1% of patients with RCC demonstrate tumour extension to the right atrium and, in exceptional cases, into the right ventricle.2 While microscopic or clinically insignificant tumour emboli have been reported in 26–31% of the patients, massive pulmonary tumour embolism from RCC occurs rarely and has a high mortality rate.2 3 When a large tumour embolus is partially or completely occluding the main pulmonary artery, surgical embolectomy is warranted.4 It has not previously been shown that thrombolysis could be an adequate treatment for an acute massive pulmonary embolism caused by small tumour emboli. Obstruction of pulmonary arteries is undoubtedly the most important cause of compromised physiology,4 but the release of vasoactive amines, such as serotonin, and pro-coagulant agents from platelets may lead to deleterious changes in pulmonary circulation and ventilation.4 5 Platelets initially adhere to the surface of tumour emboli. The activation of coagulation in situ at the level of pulmonary vessels induces adhesion, aggregation, and degranulation of circulating platelets.4 5 The rt-PA acts by converting plasminogen into plasmin. Plasmin, in turn, rapidly breaks down fibrin, which leads to clot lysis.6 Systemic plasminogen activation also interferes with blood coagulation.6 Therefore, rt-PA promotes a rapid recovery of pulmonary blood flow and improved right ventricular function.4 6 Thrombolytic treatment has the advantages of simplicity and rapid initiation, but the disadvantage of the risk of bleeding,4 6 but rt-PA has the advantage of its rapid in vivo clearance (half-life of approximately 5 min) and cryoprecipitate can be administered if adverse bleeding becomes problematic.7
In conclusion, thrombolysis with rt-PA may be a therapeutic option that can prevent a fatal evolution of massive pulmonary tumour embolism.
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References
1 Kubota H, Furuse A, Kotsuka Y, Yagyu K, Kawauchi M, Saito H. Successful management of massive pulmonary tumor embolism from renal cell carcinoma. Ann Thorac Surg (1996) 61:708–10.
2 Patel R, Schwartzbard A, Bosco J, Torre P, Taneja SS. Renal tumor with associated venous tumor thrombus prolapsing through tricuspid valve during diastole. Urology (2005) 66:195.[Medline]
3 Heaton BW, Sorenson CW, Middleton RG. Renal cell cancer tumor thrombi causing a massive pulmonary embolus in 34-year- old man. J Urol (1993) 150:1225–6.[Web of Science][Medline]
4 Tapson VF. Acute pulmonary embolism. N Engl J Med (2008) 358:1037–52.
5 Elliott CG. Pulmonary physiology during pulmonary embolism. Chest (1992) 101:163S–71S.[CrossRef][Medline]
6 Arcasoy SM, Kreit JW. Thrombolytic therapy of pulmonary embolism. Chest (1999) 115:1695–707.[CrossRef][Web of Science][Medline]
7 Jackson D, Botea A, Gubenko Y, Delphin E, Bennett H. Successful intraoperative use of recombinant tissue plasminogen activator during liver transplantation complicated by massive intracardiac/pulmonary thrombosis. Anesth Analg (2006) 102:724–8.
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