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J Thorac Cardiovasc Surg 1994;108:187-188
© 1994 Mosby, Inc.
LETTERS TO THE EDITOR |
Department of Cardiothoracic Surgerya
Department of Pediatric Cardiologyb
Stanford University School of Medicine
Stanford, CA 94305
To the Editor:
At 14 days of age, a male infant weighing 4 kg underwent mitral valve replacement for mixed congenital mitral valve disease. An inverted 19 mm St. Jude Medical aortic prosthesis (St. Jude Medical, Inc., St. Paul, Minn.) was placed in a supraannular position. The postoperative course was uncomplicated, and the patient was discharged to his home receiving warfarin (alternating doses of 0.5 and 1 mg daily). Prothrombin times were monitored on a regular basis but varied widely from 12 to 30 seconds (reference range of 10.9 to 12.2 seconds) on the discharge regimen. He was readmitted to the hospital at 2 months of age to optimize the anticoagulant control. While he was in the hospital acute congestive cardiac failure and pulmonary edema developed suddenly, necessitating intubation and mechanical ventilation. Transthoracic two-dimensional and Doppler echocardiography of the mitral prosthesis showed both leaflets to be immobile and surrounded by thrombus. A mean gradient of 17 mm Hg was measured across the prosthesis. At this time the prothrombin time was 21 seconds.
In view of the patient's young age and the likelihood of several operative procedures in the future, we decided to attempt thrombolysis with urokinase. A dosage protocol, as reported in adults,
1 was selected. A bolus of 4222 U/kg was given intravenously followed by a maintenance infusion of 4222 U/kg per hour for 24 hours. Fibrinogen levels were monitored and these remained within the reference range of 160 to 350 mg/dl. No bleeding complications resulted from the urokinase therapy, and the patient's clinical condition rapidly improved. A second echocardiogram 24 hours after urokinase therapy was begun showed normal movement of the posterior prosthetic leaflet, but the anterior leaflet remained immobile. By the following day both leaflets were moving normally and the transmitral gradient had fallen to 2.5 mm Hg. The patient was extubated 1 day after completing the course of urokinase. At this time an infusion of heparin was commenced and subsequently warfarin was recommenced. No underlying coagulation disturbance was identified in this infant and he remains well receiving warfarin therapy at follow-up.
Valve thrombosis remains a significant cause of prosthetic valve dysfunction. Infants and children of all ages with St. Jude Medical valves should receive warfarin to prevent this complication.
2 Anticoagulant control can be difficult in young infants. Our patient had widely fluctuating prothrombin times on the same dosage regimen, although at the time of his clinical deterioration the prothrombin time was high. Thrombus formation may have begun at a time when the prothrombin time was subtherapeutic.
Thrombolytic therapy for mechanical cardiac valve thrombosis using streptokinase, urokinase, or tissue-type plasminogen activator has been effective in 70% to 80% of adults with this problem.
1,3 Reports of prosthetic valvethrombolysis in the pediatric population are rare,
3-5 and this therapy has not previously been described in infants. Adopting a reported adult dosage protocol for urokinase, we were able to lyse a thrombus that had resulted in severe prosthetic mitral valve dysfunction. We, along with others,
4 found two-dimensional and Doppler echocardiography to be a valuable aid in the diagnosis and serial evaluation of the prosthetic valve.
We considered thrombolysis an acceptable option in this critically ill infant in whom we wished to avoid another high-risk operation, either thrombectomy or prosthetic valve replacement. Fortunately, a successful outcome was achieved and no bleeding complications occurred.
References
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