P023: COLD AGGLUTININS DURING CARDIAC BYPASS... WHEN COOLING IS NOT THAT COOL
Juan Mora, MD, Saurin Shah, MD; University of Florida - Jacksonville
Introduction: Cold agglutinin disease (CAD) is a hemolytic process with an incidence of 1 per million people per year. This anemia is mainly mediated by an IgM monoclonal protein directed against the I/i antigens on the RBC surface that activates the complement cascade resulting in extravascular hemolysis. The severity varies greatly among patients according to antibody titer and thermal amplitude.
IgM molecules can be polyclonal (typically seen in the postinfectious setting) or monoclonal. This last one classically presents in older adults as a long-term disease that often resists treatment and may be associated with an underlying lymphoproliferative disorder 70% of the cases.
Only around 40% of patients presents with symptoms and the diagnosis is established with reticulocytosis, hyperbilirubinemia, elevated lactate dehydrogenase, positive Coombs testing for anti-C3 and negative anti-IgG. After test findings suggest CAD, the antibody titer and thermal activity should be determined. Nonpharmacological measures are the cornerstone of management of CAD mainly avoiding cold exposure.
Cardiac surgery requiring cardiopulmonary bypass (CPB) and hypothermia carries a significant risk of morbidity in this patient population because it might lead to intracoronary thrombosis, inadequate delivery of cardioplegia and high line pressures in the CPB circuit associated with myocardial or end organ infarction
Case Description: 71 yo Male with PMH of HTN, HLD and heavy smoker who presented with ST elevation myocardial infarction. Heart catheterization revealed total ostial right coronary occlusion and severe left anterior descending artery disease. He was then scheduled for Coronary Artery Bypass Grafting (CABG). After CPB was started and patient was cooled down to 34 oC the cardioplegia line was noted to have high resistance to flow and became partially occluded. Surgeon in the field noticed “clot like formation” despite ACT been more than 400 seconds at all times after first dose of heparin. Recheck of the chart showed a positive cold reacting agglutinin with wide thermal amplitude 4+ at 4 oC and 2+ at 37 oC. Immediately plenty of warm cardioplegia was provided, patient was warmed up and the procedure continued until completion. Aortic clamp time was 45 minutes and no major changes in cerebral oximetry were noticed. He was extubated 3 hours postoperatively and left sided body paralysis with aphasia were identified. Head CT scan showed multifocal white matter hypodensities with no evidence of intracranial hemorrhage. He recovered his baseline neurologic status within 24 -36 hours and follow-up CT scan showed no changes from first exam.
Conclusion: CAD is a rare condition that represents a challenge for the perioperative management of these patients facing surgical interventions that conventionally require hypothermia. Due to its low incidence and high variability there is poor consensus regarding the best method to address these cases. Hematology should be involved as a part of a multidisciplinary approach; agglutinin titers and most importantly thermal range should be always obtained. Specifically, in CPB procedures, normothermia with warm cardioplegia should be attempted. Otherwise a judicious control of temperature based on the thermal range should be always performed.