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Ann Thorac Surg 1999;67:1778-1780
© 1999 The Society of Thoracic Surgeons
a Department of Cardiothoracic Anesthesia and Intensive Care, Vienna General Hospital, Vienna, Austria
b Department of Cardiothoracic Surgery, Vienna General Hospital, Vienna, Austria
Accepted for publication November 4, 1998.
Address reprint requests to Dr Gruber, Department of Cardiothoracic and Vascular Anesthesia & Intensive Care Unit, Vienna General Hospital, Waehringer Gurtel 18-20, A-1090 Vienna, Austria;
e-mail: eva.gruber{at}univie.oc.at
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Abstract |
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Introduction |
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A 23-year-old man was admitted with increasing dyspnea and peripheral edema. Echocardiography demonstrated acute aortic valve insufficiency and severe reduction in left ventricular function, but no regional hypokinetic areas. ECG at admission showed accelerated heart rate, sinus rhythm, and ST depression in the precordial leads. Creatine kinase levels were in the upper normal range. Surgery for valve replacement was scheduled for the same day. Preoperatively the patient developed ventricular fibrillation, which was immediately treated with defibrillation; however, inotropic support (epinephrine 2 µg/kg/min), intubation, and sedation became necessary.
Surgery was then performed and, despite uneventful aortic valve replacement (23 mm Medtronic Freestyle stentless bioprothesis, subcoronary implantation technique), biventricular heart failure occurred when weaning from cardiopulmonary bypass was attempted. Valve function was checked immediately and opening confirmed. The patient did not respond to drug support with inotropic agents (epinephrine 1 µg/kg/min) and vasodilators (diltiazem 1.2 µg/kg/min). Consequently, a left ventricular assist device was implanted (Bio-Medicus, Minneapolis, MN). In addition, because of right ventricular failure a right ventricular assist device also became necessary. All cannulae, tubing, and connectors were heparin-coated (Carmeda Bioactive Surface, Medtronic, Inc, Anaheim, CA). As soon as postoperative bleeding was controlled, anticoagulation was started with continuous infusion of heparin to maintain activated clotting time (ACT) between 150 and 160 seconds. Laboratory data and dosing of heparin are shown in Table 1. With flow rate of the ventricular assist devices (VADs) set at 4.5 L/min (range 3.9 to 6.0 L/min) and pharmacological therapy (norepinephrine 0.51 µg/kg/min), the patient’s hemodynamic values were stabilized during the immediate postoperative period. ECG did not show any sign of myocardial infarction. To evaluate recovery of ventricular function, transesophageal echocardiography (TEE) was performed on the second postoperative day. This revealed complete obstruction of the left ventricular outflow tract by a clot (Fig 1). No blood flow through the implanted valve in either direction was found by color Doppler assessment. A cerebral CT scan was performed to evaluate possible cerebral thromboembolic events. The scan revealed extensive occipital subarachnoid bleeding (SAB) and cerebral edema. This was treated with mild hypothermia, sedation, maintenance of mean cerebral perfusion pressure > 50 mmHg and minimal handling of the patient during the following 48 hours. Follow up CT scan showed reduced edema and bleeding. The ventricular clot was removed surgically and left atrial cannulation was changed to cannulation of the left ventricular apex to prevent stasis. Inspection of the stentless valve did not reveal any functional or morphological abnormality. Despite maintaining ACT at 160 to 180 seconds, recurrent thrombosis was detected 24 hours later. No immediate surgical intervention was undertaken, because of development of hemodynamic instability, intestinal malfunction, and renal failure. Hemofiltration was commenced. Recovery of ventricular function began on the 8th postoperative day. On the 12th postoperative day surgical removal of the clot in the left ventricular outflow tract was again performed. Thereafter the patient could be weaned from both assist devices. During weaning, pharmacological treatment with epinephrine and milrinone was necessary and the chest remained open. The patient stabilized hemodynamically during the following 4 days (mean cardiac output 5.3 L/min) and the chest was closed. After 32 days the renal function recovered and hemofiltration was terminated. Finally, on postoperative day 52, the patient was successfully extubated. Neurologic, cardiac, renal, and intestinal function were fully recovered after 57 days of ICU stay, and the patient was discharged. On his follow-up visit 6 months later the patient was doing well.
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In our institution an ACT of 180 to 200 seconds is usually maintained for management of patients with VADs. This, up until now, seemed an acceptable regimen to prevent clotting and bleeding problems. In this case it had to be adapted because of bleeding problems immediately after surgery. Thrombus formation in the left ventricle and SAB occurred simultaneously in our patient, although no inherited coagulation disorder was known and he had never before suffered from any coagulation related problem. This led to a therapeutic dilemma since anticoagulation is essential during the use of cardiac assist devices but increases the risk of further cerebral bleeding. No recommendations are available on how to proceed in such circumstances. Usually a ventricular clot is removed immediately after detection to minimize the risk of thromboembolism. However, immediate surgery was contraindicated, as hemodynamic instability induced by such surgery would be unacceptable in a patient with severe cerebral edema and SAB. Furthermore complete anticoagulation, as necessary during open-heart surgery, could lead to further, potentially lethal, cerebral bleeding. It may be that the SAB was caused by septic emboli in the preoperative period and was aggravated by the systemic anticoagulation during the aortic valve operation. The treatment of cerebral edema and SAB was given priority over the removal of the ventricular clot in the presented case. The ventricular clot was removed after a follow up CT scan showed significant reduction of cerebral edema.
The induction of inflammatory reactions is known to occur after cardiac surgery [7]. The production of platelets and acute phase proteins like C-reactive protein and fibrinogen is mediated by cytokines like interleukin 6 [8]. During this period the coagulation cascade is influenced by activation of both procoagulatory and anticoagulatory proteins leading to thrombin generation and possibly thrombus formation. Unfractionated heparin, which together with antithrombin III counteracts thrombin formation, may per se lead to thrombotic events by provoking an immunoglobulin G antibody and Heparin-induced thrombocytopenia (HIT) [9]. In our patient, HIT was ruled out by repeated negative measurements of antibodies reactive with heparin:platelet factor 4 complexes.
In addition to prothrombin time, partial thrombin time, fibrinogen, and platelet count, ACT is measured routinely in our institution to manage patients on VADs. Platelet function tests like ADP, Collagen, and Ristocetin mediated platelet aggregation are not available for urgent correction of coagulation disturbances. Thromboelastography, which evaluates coagulation factors, platelets, and fibrinolytic activity, could provide a supplementary tool for evaluating a critical patient and, in the future, will be used in our institution.
Temporary renal insufficiency and dysfunction of the intestinal organs during use of biventricular assist devices is frequently observed [3]. Nevertheless, renal and intestinal function recovered completely with standard treatment and the patient was discharged with normal organ function.
We conclude that in this patient simultaneous ventricular clotting and SAB during treatment with cardiac assist devices could not be prevented. Nevertheless, timely diagnosis and careful treatment of these complications enabled full recovery.
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This article has been cited by other articles:
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  S. Chumnanvej, M. J. Wood, T. E. MacGillivray, and M. F. V. Melo Perioperative Echocardiographic Examination for Ventricular Assist Device Implantation Anesth. Analg., September 1, 2007; 105(3): 583 - 601. [Abstract] [Full Text] [PDF]
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 D. Fries, P. Innerhofer, W. Streif, W. Schobersberger, J. Margreiter, H. Antretter, and C. Hormann Coagulation monitoring and management of anticoagulation during cardiac assist device support Ann. Thorac. Surg., November 1, 2003; 76(5): 1593 - 1597. [Abstract] [Full Text] [PDF]
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