Cold agglutinins are serum antibodies that are activated by decreased blood temperature to produce RBC agglutination or hemolysis. Hemolysis results from compliment activation.

Table 9.2. Management of patients at risk for sickle cell disease

Reduce risk of perioperative sickle cell crisis by preoperative partial exchange transfusion with Hb-A donor blood to dilute Hb-S RBCs

The ideal ratio of Hb-S to Hb-A has not been established. However, recommendations range from reducing the proportion of Hb-S containing RBCs from less than 5% to less than 33%

Avoid arterial or venous hypoxemia, acidosis, dehydration, hypothermia and hyperosmolarity

Treat hypotension with volume administration and avoid vasopressors if possible

If unrecognized, RBC agglutination during hypothermic bypass may lead to multiorgan ischemia from prolonged vascular occlusion.

Cold agglutinins may be caused by:

• Monoclonal antibodies associated with lymphoreticular neoplasms which are generally irreversible.

• Polyclonal variants associated with acute infectious disease (e.g., mycoplasma, infectious mononucleosis, cytomegalovirus) which may remit spontaneously in weeks.

Preoperatively screen the blood of all patients undergoing hypothermic car-diopulmonary bypass for cold agglutinins. A positive screen at 4°C requires further determination of the thermal amplitude and antibody titer. The thermal amplitude defines the temperature below which the antibodies become active. Activation of antibodies increases exponentially as temperature decreases below the thermal amplitude. The higher the titer of cold agglutinins the greater the clinical significance. Consult the hematology service preoperatively if cold agglutinins are identified in routine preoperative screening of patients' blood.

Evidence of agglutination during hypothermic bypass includes:

• agglutination within vessels in the surgical field

• agglutination in the blood cardioplegia reservoir as blood from the patient is mixed with cold cardioplegia solution

• hemolysis with hemoglobinuria

• agglutination of blood in a syringe during phlebotomy

If cold agglutination occurs, it may or may not be reversed by rewarming the patient to temperatures above the thermal amplitude.

Perioperative management involves prevention of complement activation and resultant problems of agglutination and hemolysis:

• If cold agglutinins have been caused by an acute infection, postpone elective hypothermic cardiac surgery for several weeks until antibody has cleared.

• Use warm cardioplegia for myocardial protection and maintain nor-mothermic or mildly hypothermic systemic temperatures to ensure that blood temperature remains above the thermal amplitude.

• If cold cardioplegia is used, wash out blood from the coronary circulation with warm cardioplegia at the onset of bypass and rewarm the heart with warm cardioplegia before myocardial reperfusion.

• Low systemic flows during bypass may reduce noncoronary collateral flow and subsequent cooling of this blood.

• Vent the left ventricle to avoid cooling and stagnation of blood.

• Use crystalloid cardioplegia to avoid agglutination of the cells in the solution when delivered at low temperature.

• Use a septal temperature probe to monitor myocardial temperature.

• Warm cold intravenous fluids, blood, and plasma administered during surgery.

• Consider plasmapheresis or total exchange transfusions in patients with high titer, high thermal amplitude cold agglutinins who must undergo hypothermic bypass.

Treatment of suspected cold agglutination during hypothermic bypass:

• Confirm satisfactory ACT (i.e., rule out inadequate anticoagulation).

• Verify with blood bank that cold agglutination is present rather than an unrecognized alloantibody.

• Use crystalloid cardioplegia to dilute the antibody in the coronary circulation.

• Rewarm patient to systemic temperatures greater than 28-30°C.

• Inspect extracorporeal circuit and oxygenator carefully for cell aggregates.

Selected Readings

1. Coursin DB. Perioperative management of diabetes and other endocrine abnormalities. In: Annual Refresher Course Lectures. Amer Soc Anes, 1997.

2. Oliver WC, DeCastro MA, Strickland RA. Uncommon diseases and cardiac anesthesia. In: Kaplan JA, ed. Cardiac anesthesia. 3,d edition. Philadelphia: WB Saunders, 1993.

3. Mangano CM, Diamondstone LS, Ramsay et al. Renal dysfunction after myocar-dial revascularization: risk factors, adverse outcomes, and hospital resource utilization. The multicenter study of perioperative ischemia research group. Ann Internal Med 1998; 128:194-203.

4. Hockmuth DR and Mills NL. Management of unusual problems encountered initiating and maintaining cardiopulmonary bypass. In: Gravlee GP, Davis RF, Utley JR, eds. Cardiopulmonary Bypass Principles and Practice. Baltimore: Williams & Wilkins, 1993.

5. Esseltine DW, Baxter MRN, Bevan JC. Sickle cell states and the anesthetist. CJA 1988; 35:385.

6. Heiner M, Teasdale SJ, David T et al. Aorto-coronary bypass in a patient with sickle cell trait. CJA 1979; 26:428-434.

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