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a Department of Cardiothoracic Surgery, Royal Melbourne Hospital, Victoria, Australia
b Department of Perfusion, Royal Melbourne Hospital, Victoria, Australia
c Department of Anesthesia, Royal Melbourne Hospital, Victoria, Australia
Accepted for publication February 1, 2007.
* Address correspondence to Dr Atkinson, Department of Cardiothoracic Surgery, 2 North, Royal Melbourne Hospital, Grattan St, Parkville, Victoria, 3050, Australia (Email: victoria.atkinson{at}mh.org.au).
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Abstract |
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Introduction |
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At normothermia, CAs are seldom of clinical significance; however, activation of CAs during CPB can lead to massive hemagglutination, hemolysis, and microvascular thrombosis [1, 3]. This can manifest intraoperatively as intracoronary thrombosis, incomplete cardioplegic delivery, or high pressures in the CPB circuit [3]. Clinical sequelae can include cerebral or myocardial infarction, hepatic or renal failure, and hemolysis.
The importance of CAs depends on two factors: the plasma titre of CAs and the thermal amplitude at which hemagglutination occurs. Low levels of CAs can be found in the sera of healthy individuals (about 1:16) [1]; however, at higher titres, CA activation is more likely. In addition, thermal amplitude, or the temperature below which antibody activation occurs, should be quantified preoperatively, thus giving the surgeon a temperature range in which to work.
We describe a patient undergoing aortic valve replacement (AVR) for aortic stenosis who had high titre CAs with high thermal amplitude. A brief literature review of management strategies is undertaken.
A 76-year-old man presented with severe aortic stenosis, with a peak gradient of 98 mm Hg and a calculated valve area of 0.6 cm2. There was associated moderate aortic regurgitation. An angiogram revealed no coronary artery disease. Left ventricular (LV) systolic function was preserved, with severe LV hypertrophy.
The patient had asymptomatic CAs due to an underlying lymphoproliferative disorder. Preoperative testing demonstrated an elevated CA titre (1:1025) with an unusually high thermal amplitude of 32°C. Lactate dehydrogenase was elevated at 738 IU/L, but bilirubin levels and coagulation profile were normal.
Precautions were taken intraoperatively to avoid exposure to agents within the active temperature range for cold agglutination. Anesthetic agents and fluids were warmed, including priming fluid for CPB. The operating room temperature was elevated, and a lower body-warming blanket was applied. The patient was anticoagulated with heparin to an activated clotting time (ACT) of 603 seconds.
Warm CPB was initiated, and the esophageal core temperature was maintained above 35°C. A myocardial temperature probe was placed into the anterior wall of the LV for continuous monitoring. The aortic cross clamp was applied, and induction cardioplegia was given retrograde into the coronary sinus at a temperature of 35°C.
Because of the aortic regurgitation, a transverse aortotomy was performed and warm antegrade cardioplegia was delivered directly into the left and right coronary orifices. Throughout the remainder of the procedure, continuous warm retrograde cardioplegia was given, supplemented by direct antegrade aliquots every 15 minutes. Cardioplegia was ceased for 10 minutes during aortic cross-clamping when required to optimize the operative view. The myocardial temperature was maintained above 32°C throughout, and electromechanical silence was sustained. Pressures within the CPB and cardioplegic circuits remained within normal limits. The circuitry was visually monitored for evidence of agglutination of the RBCs.
A 21-mm Edwards Magna pericardial bioprosthesis (Edwards Lifesciences, Irvine, CA) was inserted into the supraannular position and the aortotomy was closed. Total cross-clamp time was 66 minutes, and the patient weaned successfully from CPB and did not require support with inotropes. Once separated from CPB, the circuit cooled to room temperature, and RBC agglutination could be seen within cardioplegic lines.
The patient’s postoperative course was without evidence of hemolysis or end-organ dysfunction. The patient was discharged on the seventh postoperative day.
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CAs are largely asymptomatic and can first present with the initiation of hypothermic CPB, manifesting as high line pressures and visible agglutination in the cardioplegia circuit [2, 4]. No protection is afforded by anticoagulation or hemodilution. In such cases, immediate management should entail raising the core temperature to normothermia in conjunction with warm retrograde myocardial washout. Any resulting hemolysis or end-organ damage should then be treated.
Patients with low titre, low thermal amplitude CAs can safely undergo CPB with little change in practice. Preoperative plasmapheresis requiring high-volume blood product transfusion can achieve an eightfold to tenfold reduction in CA titers, with the accompanying risks of large volume shifts as well as infection and altered hemostasis. It should therefore be reserved for those patients requiring deep hypothermic arrest [1, 3].
The controversy comes with primary management of patients with high titre and high thermal amplitude patients during routine hypothermic CPB. This involves maintaining tissues above the documented activation threshold of agglutination by warming the operating room and all fluids and anaesthetic gases. Strict core temperature monitoring should be undertaken, together with the simple addition of myocardial temperature monitoring to prevent activation of cold agglutinins.
Normothermic CPB with varying techniques of myocardial protection have been described in such cases [1–4], including intermittent cross-clamping or induced ventricular fibrillation. Alternatively, some authors have used cold crystalloid cardioplegia alone or the combination of warm crystalloid cardioplegic washout, followed by cold crystalloid cardioplegia, although this risks microvascular thrombosis from collateral coronary circulation [3].
We have demonstrated that warm blood cardioplegia is an appropriate and safe technique. It should be infused continuously, whenever technically possible, to maintain tissue perfusion and prevent microvascular clotting. A small risk of reduced cardiac function after CPB exists compared with colder cardioplegic solution delivery [5]. The high thermal threshold identified in this patient meant that we were forced to sacrifice some of the benefits of hypothermia in myocardial protection to offset the risk of CA activation and thrombosis. We attempted to use continuous cardioplegia to counter some of the effects of warm ischemia.
In conclusion, patients displaying high titre, high thermal amplitude CAs require individualized planning before cardiac operations, including consultation with a hematologist. Careful temperature monitoring must be undertaken intraoperatively to avoid CA activation causing catastrophic hemagglutination and hemolysis. We report a safe technique with a successful outcome using normothermic CPB and continuous warm blood cardioplegia.
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