Contributed by Nicole Nicosia Esposito, MD, Don Kelley, MD, Beth Jochum and Mark H Yazer, MD, FRCPC
Published on line in December 2005
A 79-year-old man with stage IV mantle cell lymphoma, previously untransfused, presented to a peripheral hospital with symptomatic anemia (Hgb=7 g/dL, Hct=23%). A type and screen revealed that he was group AB with no unexpected antibodies (Table 1).
Two units of group A blood were issued by computer crossmatch. Both units were transfused without incident. Six days later, he returned to hospital with a hemoglobin of 6.8 g/dL (Hct=22%). Routine type and screen at that time was unchanged from the previous specimen. On Day 7, he was transfused with one computer crossmatch compatible unit of group A RBCs followed by 30 cc of another group A unit when he noted painless bright red urine and complained of chills, lower abdominal pain, and required intubation. Chest x-ray performed at the time was unremarkable. He was transferred to the MICU where he was dialyzed for anuria. The patient's blood film was unremarkable.
1. What is the differential diagnosis of the patients' symptoms? [ Answer ]
2. From a blood bank perspective, what should the nursing staff do at the bedside when a transfusion reaction is suspected? [ Answer ]
3. What actions does the blood bank take when notified about a transfusion reaction? [ Answer ]
Later that evening, the patient's hemoglobin continued to decline from 6.6 g/dL to a nadir of 5.7 g/dL at midnight. A total of two more units of computer crossmatch compatible group A RBCs were transfused shortly after midnight and in the early morning of Day 8, respectively. His hemoglobin was 6.3 g/dL after the first unit and 6.2 g/dL after the second unit. Subsequently, RBC transfusions were withheld, and his hemoglobin decreased to 5.8 g/dl on the morning of Day 9. That evening, an anti-A1 was identified on reverse typing in a new blood sample, and the DAT was positive with IgG (Table 2):
An eluate was then performed and tested against selected cells using polyethylene glycol (Table 3):
He then received one unit of O RBCs on Day 10, with a resultant increase in hemoglobin to 6.2 g/dL four hours after transfusion. An additional unit of O RBCs was administered, with a further rise in hemoglobin to 8 g/dL. The patient continued to respond well to O RBCs and was discharged from the MICU.
ADDITIONAL LABORATORY INVESTIGATIONS:
Routine pretransfusion serological testing did not reveal the anti-A1 antibody (Table 1); however, when the serum:cell ratio of the pre-transfusion specimen was increased, a weak and 1+ reaction was seen at the immediate spin phase and after a 15 minute incubation at room temperature, respectively (Table 4):
Additionally, a screen using the patient's post-transfusion serum from Day 11 against A1 and A2 cells revealed agglutination at the immediate spin and IgG antiglobulin phase only (Table 5):
4. How can a group AB individual produce an anti-A1 antibody? [ Answer ]
5. What is the typical clinical significance of an anti-A1? [ Answer ]