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Perfusion Policies 101: Cold Agglutinins



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FA 2016

Editor’s Note:


Welcome to PERFUSION POLICIES 101.  This will be a continuing series provided to assist your programs with that one puzzle piece we all run into now and then- that one time that an unexpected patient condition may give you pause…

The intention here is to disseminate some basic recipes that have probably been implemented at countless institutions, for God knows how long.  The usual disclaimers obviously apply:

Due Diligence is the Responsibility of the Reader!

Use the information as you feel fit, recognizing that this is information gleaned from multiple sources, it is recruited from the public domain of the internet, with no implied assurance of accuracy- but is cogent, and based on logical and reasonable clinical rationale.

Frank Aprile ?

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Cold agglutinins, also called autoimmune hemolytic anemia, is a condition where imminoglobulins IgM, autoantibodies in plasma, react with antigens, mainly the Anti-I, on a patient’s red blood cell or with exogenous red blood cells and cause agglutination or hemolysis.  This condition results in a variety of symptoms, including intravascular hemolysis, hemoglobinuria, cold-induced vasoocclusive symptoms, hemolytic anemia, microvascular occlusion in renal, peripheral, and cardiac vasculature, myocardial infaction Z(MI), and cyanosis.

Testing for cold agglutinins is performed using the direct or indirect Coomb’s test, and it is usually done at room temperature or 18-20*C with observation for the presence of clot in saline suspended red blood cells (RBCs).  Test results include:

-Thermal amplitude: the temperature range over which the antibodies eact.  May be a narrow or broad spectrum or be close to 3*C.

-Titer: the percentage level of the blood’s reactive antibody.

-Critical temperature: the temperature abovewhich agglutination activity ceases.

-Indirect Coomb’s” establishes the presence of antibodies in the serum that react with autologous or exogenous blood.

-Direct Coomb’s: demonstrates complement component attached by the antibody to the patient’s washed RBC membrane.


Cold aggluninins are found in all subjects, and normally only react at temperatures of 0-4*C.  There is an exponent tial increase in antibody activity (titer) upon cooling below the threshold of thermal amplitude, and rapid reversal of antibody activation and RBC aggluntination with rewarming above the thermal amplitude threshold.  Aggluitination is not affected by hemodilution or heparinazation.


CPB Management

-Preoperative plasma pheresis to remove 90% of the antibodies.  Replacement of volume with fresh frozen plasma.

-Maintenance of patient’s temperature above the critical temperature at all times.  Use mild or moderate hypothermic bypass, warm operating room environment, hjypothermia blanket on warm , and radiant lights.

-Normothermic b ypass with continous normothermic coronary perfusion.

-Use of warm blood cardioplegia or warm crystalloid cardioplegia.

-Coronary washout with warm crystalloid cardioplegia, followed by administration of cold crystalloid cardioplegia.

-Warming of all solutions, medications, and blood products before administration to the patient.


Cold Agglutinins

If cold agglutinins are encountered during hypothermic bypass:

-Systemic rewarming to 32-37*C.  This is the only immediate counteraction to reverse RBC agglutination.

-Re-check activatal clothing time frist to rule out insufficient heparinization.

-Administer only warm cardioplegia (either crystalloid or blood).  If the surgeon wishes to give crystalloid cardioplegia, you will neeed to change out the MP-4 for a clear set.

-Use of a posterior pericardial insulating pad to insulate the heart from the underlying warm tissues.

-Snared bicaval cannulation to prevent warm systemic clood from entering the heart.  Left heart venting to evacuate any warm bronchial or mediastinal return.

-Check a blood sample in a red top tube by placing in ice and observing for agglutination, then rewarming by hand and observing for disappearance of agglutination.

-Send complete lab screening for cold agglutinins with dermination of critical temperature and titer (this lab result may take several hours).  Send a sample for plasma-free hemoglobin.

-Administer microcirculatory enhancers (NTG, SNP) to alleviate central nervous system andkidney ischemia and dysfunction secondary to increased blood viscosity.

-Administer steroids to alter macrophage-complement receptor function (macrophages are unable to recognize RBCs in the presence of steroids).

-Washed RBSs should be used to avoid using fresh serum complement.

Cold blood or crystalloid cardioplegia administration may cause intracoronary hemaagglutination with poor distribution may cause intracoronary hemaagglutination with poor distribution of solution, coronary thrombosis, subendocardial ischemia, and MI.

Administration of normothermic asanguinous cardioplegia to washout coronary circulation until sinus return is clear before infusion of cold cardioplegia is advisable.  Before removal of the XCL, reperfusion of the heart with normothermic cardioplegia to prewar the myocardium and prevent cooling of intracoronary blood by cold muscle tissues.

NOTE:  Landymore states, “Although the red cell population is temporarily removed by the first injection of normothermic crystalloid cardioplegia, and is subsequently followed by cold crystalloid injections, blood soon returns to the arrested heart through non-coronary collaterals.”

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