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Ann Thorac Surg 2002;74:910-912
© 2002 The Society of Thoracic Surgeons
a Department of Anesthesiology and Intensive Care Medicine, University Hospital Charité, Campus Mitte, Berlin, Germany
b Department of Cardiovascular Surgery, University Hospital Charité, Campus Mitte, Berlin, Germany
c Institute of Laboratory Medicine and Pathological Biochemistry, University Hospital Charité, Campus Mitte, Berlin, Germany
Accepted for publication April 1, 2002.
* Address reprint requests to Dr von Heymann, Department of Anesthesiology and Intensive Care Medicine, University Hospital Charité Campus Mitte, Schumannstr 20-21, D-10117 Berlin, Germany
e-mail: christian.von.heymann{at}rz.hu-berlin.de
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Abstract |
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Introduction |
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Recombinant factor VIIa (rFVIIa) has been developed for the treatment of hemophiliac patients with inhibitors and has proven its clinical effectiveness in patients with thrombocytopenia and congenital platelet defects [3].
Recombinant FVIIa has also been shown to be an effective treatment for severe, uncontrolled bleeding in patients undergoing heart valve replacement [4]. The mechanism of action is not fully understood.This is the first report of an OI patient with severe postoperative bleeding after aortic valve replacement that was successfully treated with rFVIIa.
A 26-year-old man with osteogenesis imperfecta, hyperlipemia, and arterial hypertension was seen for follow-up. Aortic regurgitation had been diagnosed 3 years earlier. The patient’s condition was clinically stable on a regimen of diuretic, angiotensin-converting enzyme inhibitor, and statin therapy. The preoperative cardiac catheterization findings showed severe aortic valve regurgitation with dilation of the left ventricle and a normal ejection fraction of 50%. There were no pathologic findings in the coronary arteries. Because the dilation of the left ventricle had increased over the 3-year follow-up period, the patient was scheduled for aortic valve replacement. The preoperative laboratory findings including the coagulation studies were within normal range. Aspirin and other platelet-inhibiting drugs were not administered before surgery.
A 23-mm aortic valve (On-X) was implanted under normothermic cardiopulmonary bypass. Because of the friability of the aortic tissue 3.0 mL of fibrin sealant (Tissucol Duo S Immuno) was used to stop bleeding from the aortic root. Transfusion of packed red blood cells (RPBC) or fresh frozen plasma (FFP) was not required during surgery. After admission to the intensive care unit an average blood loss of more than 150 mL per hour from the mediastinal chest drain for the first 6 hours required the transfusion of 3 U RPBC, 4 U FFP, and 2 U platelets (Fig 1). A continuous infusion of aprotinin at 100,000 IU/h was started immediately after admission and did not reduce the amount of bleeding. The systolic blood pressure was kept between 80 and 100 mm Hg with a continuous infusion of nitroglycerine. The coagulation determinants did not show major abnormalities at this time (see Fig 1). After the blood loss from the mediastinal chest drain exceeded 1,000 mL without any reduction in bleeding rFVIIa was applied at a dose of 40 µg/kg because revision was not considered appropriate owing to the high surgical risk. Bleeding was stopped immediately. No further blood products were needed. The patient was extubated on the morning of the first postoperative day. Myocardial enzymes were raised on the second postoperative day. Creatine kinase (CK) was 5,368 U/L with an MB-fraction of 131.4 U/L and the troponine level was at 67.1 U/L. The ST segments in the lateral leads of the ECG were elevated. The coronary catheterization, which was performed immediately on the same day, showed good aortic prosthesis function. No alterations in the coronary arteries could be identified. The patient was discharged from the intensive care unit on the second day after surgery in stable clinical condition.
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Comment |
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As a possible explanation for the mechanism of rFVIIa action we hypothesize that the formation of a tissue factor-FVIIa complex locally at the site of vessel injury initiated a local plug formation. Vessel injury exposes tissue factor to the blood stream where it complexes with rFVIIa, resulting in a local thrombin formation. Thrombin itself activates platelets and factors V and VIII, resulting in a further generation of thrombin [5]. Conversely, a tissue-factor independent effect on hemostasis has been described with high doses of rFVIIa [5]. High levels of rFVIIa can activate enough FX and FIX on platelets resulting in the further generation of thrombin, which in turn activates other platelets. That leads to a massive generation of thrombin ("thrombin burst") that promotes the formation of a stable clot at the site of bleeding [5].
Although we do not know the exact mechanism of action in our patient we have to assume some systemic activation due to the decrease in prothrombin time (international normalized ratio) and the increase of factor VIIc activity after the administration of low-dose rFVIIa. FVIIc activity has been proposed as a reliable monitoring marker for high-dose rFVIIa treatment [6].
In the patient in this case report, signs of myocardial ischemia developed postoperatively. To rule out any thromboembolic complication in the coronary system after the application of rFVIIa, a coronary catheterization was performed on the first postoperative day. All findings were normal.
This is a report of successful treatment with rFVIIa of postoperative bleeding in a patient with osteogenesis imperfecta and aortic valve replacement. Considering the high rate of bleeding complications after cardiac surgery and the high risk associated with surgical reexploration in these patients, rFVIIa treatment may represent a novel and effective therapeutic option.
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