Transfusion reactions in pregnancy: the tip of the iceberg?

Transfusion reactions may accompany or follow intravenous administration of blood components. Their severity varies from mild (fever and chills) to severe (acute kidney failure or complete vascular collapse and death), depending on the amount of blood transfused, the type of reaction and the person's general health. Severe reactions often manifest after small volumes of mismatched blood or blood product. We report a case of a pregnant patient who received a whole unit of ABO incompatible red blood cells and subsequently underwent a successful caesarean delivery under combined spinal epidural anaesthesia.

A multiparous woman at 38 weeks gestation, with a single live foetus, was diagnosed with iron deficiency anaemia (serum haemoglobin concentration 6 g/dl). She had been receiving haematinics and in view of an impending labour, it was decided by the obstetricians to transfuse packed red blood cells to increase her oxygen carrying capacity. She was started on a transfusion of A-positive packed cells after cross checking the blood with the patient's cross-match form. After 30 ml of transfusion, the patient complained of mild chills and rigors. The supplied blood was rechecked, the transfusion rate decreased and chlorpheniramine 50 mg and hydrocortisone 100 mg were given intravenously by the resident medical officer. By next morning, after the entire unit had been transfused, the patient was complaining of chest discomfort and breathlessness. On examination, she was conscious and oriented, haemodynamically stable and had no abnormality on examination of the chest. However her pulse was irregular, with frequent missed beats. Her bladder was catheterised and wine-coloured urine suggested haemoglobinuria. Intravenous fluids were infused, supplemental oxygen given and an electrocardiogram performed, showing Mobitz type 1 block. A second venous sample was sent to the blood bank to re-check for the possibility of a mismatched transfusion. It was then learnt that the patient's blood group was B-positive but that she had been issued A-positive blood due to a clerical error. Over the next six hours the urine cleared and a repeat electrocardiogram returned to normal. All other biochemical investigations including liver function tests and coagulation profile were normal. The foetus was monitored and remained well, but a caesarean section was planned for delivery. Since the patient was haemodynamically stable and the coagulation profile was normal, she had combined spinal epidural anaesthesia using 0.5% hyperbaric bupivacaine 2.2 ml. The surgery was uneventful and a live female baby was delivered with Apgar scores of 8 and 10 at five and 10 minutes respectively. The patient was discharged home after three days.

ABO incompatible transfusion of as little as 10 to 15 ml blood can be fatal due to massive haemolysis occurring as a consequence of complement activation. Even if the reaction is not severe, delayed haemolysis in the extravascular reticuloendothelial system can cause renal failure, acute coronary syndrome and coagulation failure. This patient complained of only minor chills and rigors initially, with renal and cardiac manifestations appearing much later when the whole unit of blood had been transfused. Although inhibition of the complement system is an absolute necessity for normal pregnancy, there is an increase in the concentrations of the anaphylatoxins C3a, C4a and C5a in the maternal circulation (1). However, pregnancy-associated plasma protein-A markedly inhibits the haemolytic activity of complement (2), probably explaining the attenuated transfusion reaction in this patient. Similarly, indoleamine-2,3-dioxygenase activity during pregnancy protects the developing foetus from maternal immune responses, by suppressing T cell local inflammatory responses to foetal alloantigens (3). Thus, by inference, the severity of transfusion reactions may be attenuated in pregnancy. Hence, even a minor transfusion reaction in a pregnant patient may be a harbinger of a major mismatch and should be vigorously investigated, rather than treated symptomatically.

References

(1.) Richani K, Soto E, Romero R, Espinoza J, Chaiworapongsa T, Nien JK et al. Normal pregnancy is characterized by systemic activation of the complement system. J Matern Fetal Neonatal Med 2005; 17:239-245.

(2.) Bischof P. Pregnancy-associated plasma protein-A: an inhibitor of the complement system. Placenta 1981; 2:29-34.

(3.) Mellor AL, Sivakumar J, Chandler P, Smith K, Molina H, Mao D, Munn DH. Prevention of T cell-driven complement activation and inflammation by tryptophan catabolism during pregnancy. Nat Immunol 200; 12:64-68.

N. KUMAR

A. BHALOTRA

D. BEHERA

G. MANCHANDA

R. ANAND

K. K. GIRDHAR

New Delhi, India