Asian Journal of Transfusion Science
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Year : 2017  |  Volume : 11  |  Issue : 1  |  Page : 75-76
A case of anemia: How important is peripheral blood film before transfusing?


Department of Paediatrics, GMCH, Chandigarh, India

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Date of Web Publication22-Feb-2017
 

How to cite this article:
Kumar P, Jindal G, Guglani V. A case of anemia: How important is peripheral blood film before transfusing?. Asian J Transfus Sci 2017;11:75-6

How to cite this URL:
Kumar P, Jindal G, Guglani V. A case of anemia: How important is peripheral blood film before transfusing?. Asian J Transfus Sci [serial online] 2017 [cited 2017 Mar 25];11:75-6. Available from: http://www.ajts.org/text.asp?2017/11/1/75/200780


Sir,

Immediate management of a case of severe anemia presenting in CCF in the emergency room is reasonably simple with transfusion of blood or blood products. However, what is more difficult is to find out the cause of anemia and if one is scared to see such a child in emergency room, who definitely looks sick, and starts the definitive treatment, i.e. transfusion of blood/blood products, without investigating for the cause or at least preserving some pretransfusion samples for further work up, then it becomes difficult to establish the definitive diagnosis of the cause of anemia. We encountered such a case which had a reasonably simple and a common cause of anemia but had to undergo a variety of investigations just because of the fact that we did not have a pretransfusion peripheral smear examination report.

A 4½-month-old male child presented to the emergency room at 2 A.M. with complaints of fever, cough, rapid breathing, poor feeding, interrupted feeding, and excessive sweating over the forehead. On examination, the child had severe pallor, petechial and purpuric spots all over body and was in CCF and also had splenomegaly. Initial hemogram (done manually, not with cell counter) revealed severe anemia and thrombocytopenia (Hb - 2.0, platelet count - 27,000, total leukocyte count [TLC] - 10,500, and differential leukocyte count [DLC] - N56 L40 M2 E2). Hence, possibilities kept were of sepsis or some hematological malignancy and associated severe anemia leading to congestive cardiac failure, and the child was transfused with packed red blood cell (PRBC) and platelets, following which the child improved clinically. However, a mistake done while managing this patient while wee hours was that, before transfusing, a peripheral smear was not done and neither the pretransfusion samples were preserved. The sepsis workup came out to be negative, and peripheral blood smear in post-BT samples was not suggestive of malignancy and RBC indices were normal. However, the child continued to have thrombocytopenia and even anemia did not improve significantly and required one more PRBC transfusion. Bone marrow was done which was suggestive of megaloblastic anemia. Serum Vitamin B12 levels of the infant and mother were sent which came out be very low (86 pg/ml for infant and 111 pg/ml for mother, normal range being 220–1500 pg/ml). Hence, the child was started on Vitamin B12 supplementation daily, to which he responded with an increase in reticulocyte count and hemogram normalized on day 7 of supplementation, with platelet count returning to normal (Hb-10.7, platelet count-150,000, TLC-19100, and DLC-N66 L28 M2 E2). Hence, we made a final diagnosis of Vitamin B12 deficiency with megaloblastic anemia because of deficient maternal stores and the child being exclusively breast-fed. If we had a peripheral blood film before PRBC transfusion in this child, which definitely would have been suggestive of megaloblastic anemia, we could have very well managed this child without going in for an invasive investigation like bone marrow. Hence, the emphasis here is made of preserving blood sample for a peripheral smear examination if we cannot do it before transfusing a sick child with severe anemia.

Clinical features peculiar to MA include hyperpigmentation of knuckles and terminal phalanges (observed in Asian communities), enlargement of liver and spleen (seen in up to 30%–40% cases). Petechial and other hemorrhagic manifestations have been reported in up to 25% cases.[1] The presence of bleeding with severe anemia makes them clinically indistinguishable from aplastic anemia. Cases with megaloblastic anemia may mimic acute leukemia due to the presence of hepatosplenomegaly.[2],[3],[4]

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
   References Top

1.
Chandra J. Megaloblastic anemia: Back in focus. Indian J Pediatr 2010;77:795-9.  Back to cited text no. 1
    
2.
Bhende YM. Some experiences with nutritional megaloblastic anemia. J Postgrad Med 1965;11:145-55.  Back to cited text no. 2
    
3.
Gomber S, Kela K, Dhingra N. Clinico-hematological profile of megaloblastic anemia. Indian Pediatr 1998;35:55-8.  Back to cited text no. 3
    
4.
Marwaha RK, Singh S, Garewal G, Marwaha N, Walia BN, Kumar L. Bleeding manifestations in megaloblastic anemia. Indian J Pediatr 1989;56:243-7.  Back to cited text no. 4
    

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Correspondence Address:
Pankaj Kumar
Department of Paediatrics, GMCH, Sector 32, Chandigarh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0973-6247.200780

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2006 - Asian Journal of Transfusion Science | Published by Wolters Kluwer - Medknow
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