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Table of Contents
CASE REPORT
Year : 2021  |  Volume : 9  |  Issue : 3  |  Page : 186-189

Transfusion of Incompatible Blood


1 Department of Medicine, Katurba Medical College, Manipal University, Mangalore, Karnataka, India
2 Department of Emergency Medicine, KMC Hospital, Mangalore, Karnataka, India
3 Department of Pathology, KMC, Mangalore, Karnataka, India

Date of Submission15-Mar-2020
Date of Decision14-Jun-2020
Date of Acceptance27-Jun-2020
Date of Web Publication16-Jul-2021

Correspondence Address:
Dr. P Sandesh
Usha Kiran Appartments, Behind Falnir Palace, Mother Theresa Road, Mangalore - 575 001, Karnataka
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/AJIM.AJIM_18_20

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  Abstract 


Transfusion of incompatible blood is mostly accidental rather than therapeutic. However, at times, we are faced with challenges wherein we need to transfuse incompatible blood. Once such situation arise in autoimmune hemolytic anemia (AIHA) if it leads to severe anemia. Here, we report a case of AIHA with hypoxia and hemodynamic instability requiring urgent transfusion and later diagnosed to have systemic lupus erythematosus. In AIHA, typing and crossmatching are very difficult. Therefore, one should use the least incompatible blood if transfusion is indicated for the risk of hemolysis.

Keywords: Autoimmune hemolytic anemia, Red Blood Cell (RBC), systemic lupus erythematosus


How to cite this article:
Sandesh P, Shenoy D, Deepa Adiga S A. Transfusion of Incompatible Blood. APIK J Int Med 2021;9:186-9

How to cite this URL:
Sandesh P, Shenoy D, Deepa Adiga S A. Transfusion of Incompatible Blood. APIK J Int Med [serial online] 2021 [cited 2021 Jul 29];9:186-9. Available from: https://www.ajim.in/text.asp?2021/9/3/186/321655




  Introduction Top


Autoimmune hemolytic anemia (AIHA) is characterized by the production of autoantibodies against red cell antigen. The basic cause of autoantibody production in AIHA is the result of nonrecognition of self-antigens which is attributed to the failure of T-cell regulation of B-cell and least likely due to alteration in red blood cell (RBC) antigen.[1]

AIHA can be the first manifestation of systemic lupus erythematosus (SLE) or other underlying systemic disorders. It can appear several years before the diagnosis of SLE is made. AIHA is quite rare in SLE but found more commonly in the childhood form of disease than in the adults. It is relatively uncommon cause for anemia though in some cases hemolytic anemia can be the only presentation in SLE.[2]

The rate of hemolysis and the severity of anemia may vary from mild to severe and life-threatening. The diagnosis is made in the laboratory by the findings of anemia, reticulocytosis, a positive Coomb's test, and specific serological tests.[3] The prognosis is generally good, but renal failure and death sometimes occur, especially in cases mediated by drugs.[4],[5],[6]

Patients with AIHA may frequently develop anemic hypoxia that cannot be relieved by oxygen administration until therapeutic measures become effective.[7],[8] Apart from RBC transfusion, no drug is yet available which can immediately stop and/or compensate hemolysis in such patients. Transfusion is only indicated in life-threatening situations and if indicated the total volume should be transfused at a very slow rate after challenging with least incompatible blood under the cover of immunosuppression with corticosteroids.[9],[10]


  Case Report Top


An 18-year-old female with no comorbidities, apparently in normal health, presented with complaints of generalized weakness, and fever for 2 days. There was no history of vomiting, loose stools, pain abdomen, constipation, breathlessness, cough, rashes or joint pain, burning micturition passage of high-colored urine, or previous hospital admissions. No history of previous blood transfusions or antibiotic drug intake. She had regular monthly periods. On examination, the patient had severe pallor, mild jaundice, and tachycardia. Systemic examination revealed splenomegaly.

Laboratory findings

Complete blood count – hemoglobin– 3.9 gm/dl (13 gm/dl–17 gm/dl), packed cell volume– 20.4 (36–46), Tc – 16,000 cells/cu.mm (4000–11,000 cells/cu.mm), platelet count – 206,000 cells/cu.mm (150,000–400,000), erythrocyte sedimentation rate – 87 mm/h (0–15 mm/h), mean corpuscular volume – 143fl (80–96fl) mean cell hemoglobin – 51.5 pg/cell (27–33 pg/cell) mean corpuscular hemoglobin concentration – 44.6 gm/l (33.4–35.5 gm/dl) red cell distribution width – 22.7% (11.5%–14.5%) peripheral smear showed spherocytic hemolytic anemia, reticulocyte count – 60% (0.5%–1.5%), and reticulocyte production index-7.8 (1.5–2.5). Lactate dehydrogenase – 625U/l (0–250U/l). RFT-UREA-18 mg/dl (15–45 mg/dl), CREATININE-0.7 mg/dl (0.7–1.2 mg/dl), LFT-Total Bilirubin-3.79 mg/dl (0.30–1.20), indirect bilirubin- 3.34 mg/dl (0.1–1.0 mg/dl), total protein-7.0 g/dl (6.0–8.30), albumin – 5.30 gm/dl (3.20–5.50 g/dl), globulin-1.70 gm/dl (1.80–3.40 gm/dl), aspartate aminotransferase-49U/l5.0–40.00U/l, ALT-9U/l (5.00-40.00U/l), alkaline phosphatase-55U/l40.00–129.0U/l), URIC ACID– 6.8. Urine routine within the normal limits [Table 1].
Table 1: Antibody results of ANA

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With the above clinical and laboratory findings, hemolytic anemia probably due to hereditary spherocytosis or AIHA is considered. Accordingly, an osmotic fragility test and coombs test were done, and osmotic fragility test was normal.

Direct agglutination test (DAT, Coombs test) turned out to be positive (washed red cell with low ionic salt solution suspension was used for grouping and DAT,) and hence, AIHA was considered. The grouping and crossmatching were done and confirmed both by the matrix gel card and repeated again by tube method.

Washed red cell with low ionic salt solution suspension was used for grouping and DAT. Agglutination was noted with A, B, and Rh antisera, DAT as well as autoagglutination in neutral gel column. Serum grouping showed that the blood group was “0”. Further presence of irregular antibodies was detected by the reaction of patient's serum with commercially prepared pooled O cells.

As a part of evaluation of cause of AIHA imaging (contrast-enhanced computed tomography CHEST, ABDOMEN and NECK), blood markers for lymphoma and SLE were done. ANA (done by immunofluorescence method) was positive for and autoantibodies against histones, AMA-M2, Sm, SS-A, RO-52, SS-B, PM-SCL100, ribosomal protein, and proliferating cell nuclear antigen (done through immunoblot technique) suggestive of SLE as per Systemic Lupus International Collaborating Clinics (SLICC) criteria. SLICC includes clinical criteria-acute cutaneous lupus, chronic cutaneous lupus, oral or nasal ulcer, nonscarring alopecia, arthritis, serositis, renal, neurologic, hemolytic anemia, leukopenia, and thrombocytopenia (<100,000/mm).

Immunological criteria ANA, Anti-DNA, Anti-Sm, antiphosholipid, low complement and direct coombs.

Requirements are more than or equal to 4 criteria (at least one 1 clinical and 1 laboratory criteria).

This patient had ANA, Anti-Sm, and hemolytic anemia positivity. In clinical situation, when SLE is of very high probability, the patient usually fulfils the criteria over a period of time when new manifestation of disease develops.

As the patient was in hypoxia and hemodynamically unstable due to severe anemia blood transfusion was planned. However, recipient's blood was incompatible for all available blood groups due to the high level of antibodies. Hence, among the available blood groups, least incompatible blood (O negative) was transfused patient is given high-dose corticosteroids at least 1 h before transfusion is initiated. In this patient, 1 g IV methylprednisolone was given as infusion. Moreover, then the transfusion was started very slowly for about 15 min to look for any untoward reaction. As the volume of blood in the bag is too huge for this slow transfusion rate, it is ideal to divide this volume of blood in 2 or 3 bags so that the rate of transfusion does not allow the blood to be in the room temperature for more than 4–5 h. Patient's baseline vitals were normal before the initiation of transfusion. As there were no adverse reactions, the rest of the blood was transfused slowly over 4 h. Patient's hemoglobin improved to 8 gm/dl after two units of packet RBC (PRBC) transfusion. In mild-to-moderate anemia, only steroids are preferred. In patients with severe decompensated anemia, transfusion of least incompatible blood under cover of steroids to be followed. Requirement of further transfusion depends upon the hemoglobin rise. The patient was started on oral steroids after 5 days of pulse therapy (Tablet prednisolone– 40 mg od), hydroxychloroquine 400 mg od, and tablet azathioprine 50 mg od.


  Discussion Top


Transfusion of incompatible blood is rarely therapeutic, more often accidental. At times, we face the challenge of incompatible blood transfusion in rare cases such as AIHA due to the high level of antibodies. Hence, blood transfusion is avoided as far as possible except in severe cases. Here is a case of AIHA in a 18-year-old girl with severe anemia with hypoxia and hemodynamic instability requiring urgent transfusion and later diagnosed to have SLE. In AIHA typing and cross-matching is very difficult. Therefore, one should use the least compatible blood if transfusion is indicated for the risk of hemolysis. While transfusing incompatible blood, certain precautions have to be taken. Initially, patient's guardians have to be appraised of possible risk involved, and proper written consent is obtained.

The patient was transfused with two units of least incompatible blood (O negative) under the cover of steroids (1 g IV methylprednisolone). Within 24 h hemoglobin improved to 8 gm/dl after two units of packed RBC transfusion. She was continued with steroids for the next 2 weeks with tapering dose along with hydroxychloroquine and azathioprine was introduced later. The patient on discharge had hemoglobin of 10 gm/dl and was hemodynamically stable.

Steroids are often the mainstay of therapy in AIHA. Steroids decrease the production of autoantibodies by B-cells. Prednisolone is started at 1 mg/kg/day and depending on the clinical response tapered slowly. In case of steroid failure or intolerable side effects, steroid sparing therapies such as cyclophosphamide (100 mg/d) or azathioprine (100–150 mg/d) can be administered as monotherapy or in the combination with steroids.[11],[12],[13],[14],[15] In case of severe anemia, the patient needs transfusion under cover of immunosuppression after the consent from the guardian. Transfusion is started very slowly sometime 1 ml of blood over a period of 15–30 min. If there are no untoward reactions may hasten the transfusion rate. The whole unit of PRBC has to be divided into 2–3 parts and transfused to avoid long hours of thawing in the room temperature.

Seventy-five percent–96% of patients with AIHA respond to steroids. Steroids can be tapered once there is rise in hematocrit and fall in reticulocyte count. Azathioprine, cyclophosphamide, or splenectomy are the next resorts if there is no response. Intravenous immunoglobulin, danazol, mycophenolate, and rituximab are the other options for refractory AIHA.[16] The recurrence of autoimmune hemolysis during the course of SLE is rare with an estimated recurrence of 3%–5%.[17]

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Velo-García A, Castro SG, Isenberg DA. The diagnosis and management of the haematologic manifestations of lupus. J Autoimmune 2016;74:139-60.  Back to cited text no. 1
    
2.
Gormezano NW, Kern D, Pereira OL, Esteves GC, Sallum AM, Aikawa NE, et al. Autoimmune hemolytic anemia in systemic lupus erythematosus at diagnosis: Differences between pediatric and adult patients. Lupus 2017;26:426-30.  Back to cited text no. 2
    
3.
Packman CH. Hemolytic anemia resulting from immune injury. In: Kaushansky K, Lichtman MA, Prchal JT, Levi MM, Press OW, Burns LJ, Caligiuri MA, editors. Williams Hematology. 9th ed., Ch. 54. New York: McGraw-Hill; 2016.  Back to cited text no. 3
    
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Dacie JV. The Haemolytic Anaemias. The Autoimmune Haemolytic Anaemias, 3rd ed., Vol. 3. New York: Churchill Livingstone; 1992.  Back to cited text no. 4
    
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Garratty G. Drug-induced immune hemolytic anemia. Hematology Am Soc Hematol Educ Program 2009:73-9.  Back to cited text no. 6
    
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Dacie J. The Haemolytic Anaemias. London: Churchill Livingstone; 1992.  Back to cited text no. 8
    
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Petz L, Garratty G. Immune Hemolytic Anemias. New York: Chrurchill Livingstone; 2004.  Back to cited text no. 9
    
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Petz LD. A physician's guide to transfusion in autoimmune haemolytic anaemia. Br J Haematol 2004;124:712-6.  Back to cited text no. 10
    
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Eaton WW, Rose NR, Kalaydjian A, Pedersen MG, Mortensen PB. Epidemiology of autoimmune diseases in Denmark. J Autoimmun 2007;29:1-9.  Back to cited text no. 11
    
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Jeffries M, Hamadeh F, Aberle T, Glenn S, Kamen DL, Kelly JA, et al. Haemolytic anaemia in a multi-ethnic cohort of lupus patients: A clinical and serological perspective. Lupus 2008;17:739-43.  Back to cited text no. 12
    
13.
Packman CH. Hemolytic anemia due to warm autoantibodies. Blood Rev 2008;22:17-31.  Back to cited text no. 13
    
14.
Evans RS, Bingham M, Boehni P. Autoimmune hemolytic disease. Antibody dissociation and activity. Arch Intern Med 1961;108:338-52.  Back to cited text no. 14
    
15.
Zupańska B, Sylwestrowicz T, Pawelski S. The results of prolonged treatment of autoimmune haemolytic anaemia. Haematologia (Budap) 1981;14:425-33.  Back to cited text no. 15
    
16.
Schur PH, Berliner N. Hematological manifestations of systemic lupus erythematosus in adults. USA: Up To Date 2012.  Back to cited text no. 16
    
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Engelfriet CP, Overbeeke MA, von dem Borne AE. Autoimmune hemolytic anemia. Semin Haematol 1992;29:3-12.  Back to cited text no. 17
    



 
 
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