Severe Platelet Transfusion Refractoriness after Open Thoracoabdominal Aneurysm Repair
Claire M Motyl, S. Danielle Brokus, Jori E. May, Adam W. Beck
University of Alabama at Birmingham, Birmingham, AL
Background: Severe thrombocytopenia after open aortic repair poses significant risk in the immediate postoperative period. We present the case of a 76-year-old female with refractory thrombocytopenia following thoracoabdominal aortic aneurysm repair secondary to alloimmunization, with resolution by cross-matched platelet administration.
Methods: Case Report
Results: A 76-year-old female with history of HTN, CKD (Cr 2.4), CAD, EF 45-50%, and tobacco use presented to clinic with a 60mm Extent IV thoracoabdominal aneurysm. She was not a candidate for complex endovascular repair due to heavily diseased bilateral iliac arteries, heavily diseased bilateral renal arteries (compressed by her severely angulated aneurysmal aorta, contributing to renovascular hypertension), and chronic thoracic aortic thrombus.
She underwent open thoracoabdominal repair via a left 8th interspace retroperitoneal approach, with proximal clamp in the mid-descending thoracic aorta, celiac and SMA Carrell patch, bilateral renal endarterectomy with bilateral aortorenal bypasses, and distal anastomosis to the infrarenal aorta. She tolerated the procedure well. Postoperatively, she was placed on modified Spinal Cord Ischemia prevention protocol (no lumbar drain), with transfusion parameters of hemoglobin >9g/dl, platelets >100x109/L, and INR<1.5.
Her initial platelet count in the ICU was 89x109/L, which declined to a nadir of 55x109/L despite transfusion of 7 units of platelets over 28 hours (Figure). There was no evidence of postoperative bleeding. Heparin-induced-thrombocytopenia testing was negative. Her platelet count rose in response to units 8 and 9 on the evening of POD1, but failed to respond to unit 10. Post-transfusion platelet count after unit 10 showed no rise, consistent with immune-mediated refractoriness. Cross-match demonstrated compatibility with only 2/14 random donor platelet units, supporting the diagnosis of transfusion refractoriness due to alloimmunization. She then received 3 cross-matched units which consistently resulted in an increase in platelet count. Her transfusion parameters were subsequently relaxed, and her platelets recovered to normal levels prior to hospital discharge.
Discussion: Refractoriness to platelet transfusion is defined as a suboptimal response to transfusion on more than one occasion, with a post-transfusion platelet increment of <10x109/L. The majority of causes of refractoriness are non-immune. Immune-mediated refractoriness occurs due to anti-HLA antibodies directed against transfused platelets. History of pregnancy is the
most important risk factor for HLA alloimmunization; prior transfusions and stem cell transplant are also risk factors. Our patient had a history of pregnancy and prior transfusions. Patients with platelet alloimmunization may be transfused with HLA matched platelets (identical or similar HLA antigens to the patient), HLA antigen-exclusion platelets (lack the antigen implicated in platelet refractoriness), or crossmatch-compatible platelets (cross-matched with patient serum). Cross-matched platelets were used for our patient and effectively increased her platelet count on each occasion. The platelet count increase in response to units 8 and 9 is likely due to coincidental HLA matching in those units.
Conclusion: Alloimmunization is a rare but important cause of platelet refractoriness after open aortic repair, and should be considered when suboptimal response to platelet transfusions is observed.
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