This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a colleague Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Aliç, Y. Articles by Aslamaci, S. Search for Related Content PubMed PubMed Citation Articles by Aliç, Y. Articles by Aslamaci, S. Related Collections Cardiovascular Blood Complications Pediatrics

---

PEDIATRIC ANESTHESIOLOGY

ABO-Incompatible Blood Transfusion and Invasive Therapeutic Approaches During Pediatric Cardiopulmonary Bypass

Yasin Aliç, MD^*, Elif A. Akpek, MD^*, Asl Dönmez, MD^*, Süleyman Özkan, MD, Güray Yener Perfusionist, and Sait Alamaci, MD

From the Departments of *Anesthesiology, and Cardiovascular Surgery, Bakent University Faculty of Medicine, Ankara, Turkey.

Address correspondence and reprint requests to Elif A. Akpek, MD, Department of Anesthesiology, Bakent University Faculty of Medicine, 10.sok, No 45 Bahçelievler, 06490–Ankara, Turkey. Address e-mail to elifakpek{at}baskent-ank.edu.tr.

Abstract

Human error has been identified as a major source of ABO-incompatible blood transfusion which most often results from blood being given to the wrong patient. We present a case of inadvertent administration of ABO-incompatible blood to a 6-mo-old child who underwent congenital heart surgery and discuss the use of invasive therapeutic approaches. Invasive techniques included total circulatory arrest and large-volume exchange transfusion, along with conventional ultrafiltration and plasmapheresis, which could all be performed rapidly and effectively. The combination of standard pharmacologic therapies and alternative invasive techniques after a massive ABO-incompatible blood transfusion led to a favorable outcome in our patient.

The frequency of ABO-incompatible transfusions has been reported to range from 2.5 to 253 per 100,000 transfusion units, from which 10% of patients die.1 Human error has been identified as a major source of ABO-incompatible blood transfusion and usually involves mistakes in identification such as faulty labeling of samples taken for testing before transfusion or misidentifying the patient receiving the transfusion. Most transfusion errors result from blood being given to the wrong patient.2–6

We present a case of erroneous transfusion of ABO-incompatible blood that occurred in a child undergoing congenital heart surgery and discuss the use of invasive therapeutic approaches in this situation.

CASE DESCRIPTION

A 6-mo female patient weighing 7400 g (ASA IV) with a diagnosis of pulmonary stenosis and hypoplasia of the pulmonary arteries was scheduled for biventricular corrective surgery. The results of preoperative laboratory analyses were within normal limits, and her blood type was O Rh⁺. The patient was premedicated with 1 mg/kg of hydroxyzine and 0.5 mg/kg of midazolam 1 h before surgery. After initial noninvasive hemodynamic monitoring (electrocardiogram, arterial blood pressure, heart rate, peripheral oxygen saturation), the patient received 0.1 mg/kg of midazolam, 20 µg/kg of fentanyl, and 0.15 mg/kg of pancuronium IV. Central, arterial, and urinary catheters, along with nasopharyngeal and rectal temperature probes were inserted, and invasive monitoring was initiated. Anesthesia maintenance was provided with isoflurane 0.5%–0.7% in O₂/air and fentanyl infusion at a rate of 20 µg · kg^–1 · h^–1. Heparin (300 IU/kg) was administered, surgical cannulation was performed, and cardiopulmonary bypass (CPB) was initiated approximately 40 min after surgical incision.

A calculated CPB priming volume (800 mL) was composed of 200 mL of lactated Ringer’s solution, 1 U of fresh frozen plasma, and 1 U of whole blood to achieve a target hematocrit level of 28%–30%. Additionally, 10 mg/kg of methylprednisolone, 1 mg/kg of furosemide, heparin, potassium, and sodium bicarbonate were added to the priming solution as part of our standard protocol. A membrane oxygenator was used for CPB. Systemic hypothermia at a target core temperature of 26°C to 28°C and cold crystalloid cardioplegia solution were used with an -stat pH strategy.

Five minutes after CPB began, the perfusionist realized that the blood type used in the priming solution was incorrect; A Rh⁺ blood had been used instead of O Rh⁺. The reason for this ABO-incompatibility was because another pump had been prepared in the perfusion room at the same time for a same-aged patient who was to undergo congenital cardiac surgery in the next operating room. After realizing that the blood transfusion was ABO incompatible, additional methylprednisolone (10 mg/kg), mannitol (20%; 0.5 g/kg), pheniramine maleate (Avil®, lsan) (20 mg), and furosemide (20 mg) were given. IV fluids were administered to maintain central venous pressure high-normal and IV furosemide infusion (1–3 mg · kg^–1 · h^–1) was started to diurese the patient. Urine alkalinization was accomplished with intermittent administration of IV bicarbonate (1 mEq/kg).

Although the pharmacologic therapy was given and the patient was cooled, we decided to perform an "exchange transfusion" because we knew that a second pump with the appropriate blood type was ready and had not been used. To do this, total circulatory arrest was done while her body temperature was 26°C and approximately 350 mL of venous blood from the patient was collected to the pump. The pump lines were disconnected, and the arterial/venous connections of the appropriate blood-matched pump were connected within 3.5 min of total circulatory arrest; CPB was then reinitiated.

In addition to an exchange transfusion, conventional ultrafiltration of 800 mL was performed. When the CPB was terminated, plasmapheresis using AB Rh⁺ plasma (150 mL) was done for 1 h so that potential production of immune complexes could be eliminated. A xenograft pericardial patch was used to surgically correct the right ventricular outflow tract. The duration of cross-clamping was 75 min, and the total operation time was 3 h.

After transfer to the pediatric cardiovascular intensive care unit, early laboratory values showed normal coagulation profiles and haptoglobin levels. Although plasma and urine were clear macroscopically, high plasma hemoglobin levels and microscopic erythrocytes were present in the urine. Moreover, a direct Coombs’ test was positive after 6 h, and minor elevations of the LDH levels (648–1085 U/L) with a subsequent decreased level (945 U/L) suggested red cell lysis (Table 1). There were no differences between preoperative and postoperative liver and renal function test results, standard laboratory blood values, and electrolyte measurements performed at 6-h intervals. Additional postoperative laboratory data are presented in Table 2. The patient’s postoperative course was uneventful. She did not exist hemodynamic instability, disseminated intravascular coagulopathy or renal failure. The patient was tracheally extubated 2 days after surgery, transferred to the pediatric unit on day 5, and discharged on day 10.

DISCUSSION

This report presents a case of inadvertent administration of ABO-incompatible blood to a 6-mo-old child during CPB that ended favorably. The most frequent cause of an inadvertent ABO-incompatible blood transfusion is administering properly labeled blood to the wrong patient as occurred here. The risk of transfusing the wrong blood is much more common than is the risk of viral infection due to blood transfusion. Contributing factors include similar names leading to misidentification, sequential patient identifiers without full names, telephone orders, rush situations, and simultaneous handling of specimens from multiple patients. The reason for misidentification in our case was that the perfusionist responsible for the case did not carry the pump into the operating room. The back-up perfusionist took the wrong pump from the perfusion room that was also primed but was supposed to be taken to the other operating room. The major error here was that the responsible perfusionist in the operating room did not check the blood type once again prior to initiation of CPB, so he failed to ensure that the correct blood was being given to the correct patient. As a result, the properly labeled blood was used to prime the pump for the properly identified patient, but still the wrong blood was used for the patient.

The true incidence of erroneous blood transfusion may be much higher than that reported in the literature. During the 10-yr period from 1997 to 2006, during which more than 7000 U of blood were given to 4092 congenital cardiac patients, this is the first instance of ABO-incompatible transfusion during pediatric cardiovascular surgery at our institution. This rate is comparable to that from other centers.1,3

The standard, noninvasive methods of treating ABO-incompatible transfusion include maintaining urine output to overcome precipitates in the renal tubules that have been created secondary to intravascular hemolysis. Intravascular fluids, mannitol, and diuretics are given for this purpose. Alkalinization of the urine to prevent precipitates is controversial but still recommended. Besides these standard therapeutic approaches, several other factors could have led to the favorable outcome in our patient. First, the patient had a congenital heart disease and was scheduled to undergo open heart surgery. Thus, we had the advantage of preexisting arterial/venous pump lines which made hemodilution, hypothermia, and total circulatory arrest easier. Also, there was an appropriate blood-matched pump ready for rapid, effective, and high-volume exchange transfusion. Other invasive techniques including conventional ultrafiltration and plasmapheresis were rapidly available as well. A case of erroneous administration of blood similar to ours was reported in a 2.5-yr-old child who received a Glenn shunt while undergoing CPB.7 In that case, the blood was properly labeled but was used for the wrong patient to prime the CPB circuit. Use of heparin and reduced complement levels may have offset intravascular coagulopathy in that case. Neutropenia and decreased total hemolytic complement concentrations secondary to the CPB led to reduced hemolysis.

Because they have the highest concentrations of potent antibodies directed against A and B antigens, patients with blood group O are most at risk of dying of ABO incompatibility.2,3,8 However, the fact that ABO antibody levels are under-developed until infancy and reach peak levels between the ages of 5 and 10 yr might be another factor to have influenced the outcome in our patient.7,9,10 Foreman et al.11 reported a case series of 16 infants <14-mo-of-age who had ABO-incompatible heart transplantations using a standard perfusion strategy. A survival rate of 87% was suggested to be related to recipients’ immunologic immaturity.

Although not part of a standard protocol after an ABO-incompatible blood transfusion, plasmapheresis, conventional ultrafiltration, and exchange transfusion in our patient were rapidly and effectively performed. Plasmapheresis has long been used for ABO-incompatible bone marrow or solid organ transplants12–14 and exchange transfusion in newborns for hemolytic jaundice caused by ABO incompatibility.15,16 The mechanism in both treatments is to eliminate anti-A and anti-B antibodies and to reduce isohemagglutinins. Conventional ultrafiltration, although there is no evidence for its effectiveness in the treatment of ABO incompatibility, has been suggested to remove proinflammatory cytokines after CPB; thus it might have a supplementary role in other organ functions during the postoperative period. Although the exchange transfusion in our patient may not have been precise in terms of technique; it did modify the intravascular circulating volume in a short time during complete circulatory arrest and replacing the intravascular volume with properly matched blood. This resulted in high-volume, rapid and effective exchange transfusion. We found no reports in the literature of this method being used for a similar purpose.

Many systems have been described for minimizing risks of misidentification.17 Guidelines on documentation and procedures have been prepared by the Blood Transfusion Task Force.18 Thus, all hospitals must initiate standard procedures for accurately identifying patients and recognizing the signs of transfusion reactions. However, most centers still do not fully document transfusions or report transfusion complications.

We conclude that the combination of standard pharmacologic therapies and alternative invasive techniques after a massive ABO-incompatible blood transfusion led to a favorable outcome in our patient. However, the rapid and effective use of invasive techniques was possible in this case because of the type of operation the patient was undergoing and the technology at hand. Thus, consideration of these invasive techniques may not be the first-line approach for other situations. The most important steps in preventing transfusion-related adverse events are taking precautions and preparing standard institutional protocols against potential hazards.

Footnotes

Accepted for publication March 16, 2008.

REFERENCES

1. Tsubaki K, Nagao A. Examination for prevent of blood transfusion errors [Japanese]. Rinsho Byori 2003;51:146–9[Medline]
2. Contreras M, de Silva M. Preventing incompatible transfusions. BMJ 1994;308:1180–1[Free Full Text]
3. Linden JV, Paul B, Dressler KP. A report of 104 transfusion errors in New York State. Transfusion 1992;32:601–6[Web of Science][Medline]
4. Wallace J. Blood Transfusion For Clinicians. Edinburgh: Churchill Livingstone, 1977
5. Baele PL, De Bruyere M, Deneys V, Dupont E, Flament J, Lambermont M, Latinne D, Steensens L, van Camp B, Waterloos H. Bedside transfusion errors. A prospective survey by the Belgium SAnGUIS Group. Vox Sang 1994;66:117–21[Web of Science][Medline]
6. Schmidt PJ. The mortality from incompatible transfusion in immunobiology of the erythrocyte. In: Sandler SG, Nussbacher J, Schanfield MS, Alan R, eds. Immunobiology of the Erythrocyte. New York: Liss, 1980: 251–61
7. Ti LK, Ang SB, Chen FG. Survival after large ABO-incompatible blood transfusion. Can J Anaesth 1998;45:916[Web of Science][Medline]
8. Sazama K. Reports of 355 transfusion-associated deaths: 1976 through 1985. Transfusion 1990;30:583–90[Web of Science][Medline]
9. Mollison PL, Englelfriet GP, Contreras M. Hemolytic Transfusion Reactions. In: Blood Transfusion in Clinical Med. 5th ed. Oxford: Blackwell Scientific Publication, 1993
10. West LJ, Polloock-Barziv SM, Dipchand AI, Lee KJ, Cardella CJ, Benson LN, Rebeyka IM, Coles JG. ABO-incompatible heart transplantation in infants. N Engl J Med 2001;344:793–800[Abstract/Free Full Text]
11. Foreman C, Gruenwald C, West L. ABO-incompatible heart transplantation: a perfusion strategy. Perfusion 2004;19:69–72[Abstract/Free Full Text]
12. Squifflet JP, De Meyer M, Malaise J, Latinne D, Pirson Y, Alexandre GP. Lessons learned from ABO-incompatible living donor kidney transplantation: 20 years later. Exp Clin Transplant 2004;2:208–13[Medline]
13. Farges O, Kalil AN, Samuel D, Saliba F, Arulnaden JL, Debat P, Bismuth A, Castaing D, Bismuth H. The use of ABO-incompatible grafts in liver transplantation: a life-saving procedure in highly selected patients. Transplantation 1995;59:1124–33[Web of Science][Medline]
14. Botha P, Hasan A, Haynes S, Cassidy J, Roe J, Wallis J, Smith J. Exchange transfusion during extra corporeal membrane oxygenation used as a bridge to ABO-mismatch cardiac transplantation. Ann Thorac Surg 2006;81:1105–7[Abstract/Free Full Text]
15. Thayyil S, Milligan DW. Single versus double volume exchange transfusion in jaundiced newborn infants. Cochrane Database Syst Rev 2006;4:CD004592[Medline]
16. Ebbesen F. Effect of exchange transfusion on serum reserve albumin for binding of bilirubin and index of serum bilirubin toxicity. Acta Paediatr Scand 1981;70:643–8[Web of Science][Medline]
17. Shulman IA, Lohr K, Derdiarian AK, Picukaric JM. Monitoring transfusionist practices: a strategy for improving transfusion safety. Transfusion 1994;34:11–15[Web of Science][Medline]
18. [No authors listed.] Guidelines on hospital blood bank documentation and procedures. British Committee for Standards in Haematology, Blood Transfusion Task Force. Clin Lab Haematol 1990;12:209–20[Medline]

This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a colleague Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Aliç, Y. Articles by Aslamaci, S. Search for Related Content PubMed PubMed Citation Articles by Aliç, Y. Articles by Aslamaci, S. Related Collections Cardiovascular Blood Complications Pediatrics