Blood Transfusion

Blood transfusion is one alternative for those who become anemic, but it’s not without its hazards. Chief among these is getting the wrong blood. In the UK nearly two thirds of all serious hazards are caused by the patient getting the wrong blood. It has been known for about 100 years that there are four main blood groups: A, O, B and AB. In the UK at least A is the commonest, then O then B then AB. The reason that they are important is that we have naturally occurring antibodies against these groups. Group A patients have anti-B, Group O have anti-A and anti-B, Group B have anti-A but Group AB don’t have antibodies. If you are transfused blood from a group that you have antibodies against you will have a severe reaction comprising fever, shakes, back pain, dark urine and possibly kidney failure. People still get these reactions.

I have seen these reactions twice in my career. On the first occasion the patient was in hospital for a prostate operation. It was a simple matter of the technician, who did not normally work in the blood bank, but who was an immunologist helping out, cross matching blood at night. He performed the task excellently and issued the blood. About half an hour later he double checked his work and discovered that he had cross matched the blood against a different patient’s sample. Inadvertently, he had issued Group A blood for a Group O patients. He rushed to the ward and stopped the transfusion. Only 50 ccs had gone in, and although the patient had a shivering attack and raised his temperature, no further harm was done.

On the second occasion the patient had had his hip replaced and was unconscious when he got the blood. He was one of two patients returning from the operating theater, not to the orthopedic ward, which had closed for the summer while he was being operated on, but to the general surgery ward. Because of this he was unknown to the nurses on the ward and when the ward sister told the nurse to put up a unit of blood on Mr Bloggs who had just returned from theater, she didn’t check his name on the wristband, she didn’t check the name on the bed, she didn’t get a second nurse to double check, she just gave a unit of group A blood to Mr Doe who was group O. His reaction was more severe and he went into kidney failure, but happily made a complete recovery.

The astonishing thing was that it was the same patient on both occasions. My callous colleague exclaimed, “Never mind, we’ll get him next time!”

The important point from this story was that it was not a technical error that nearly killed him, but because somebody didn’t follow the published protocol. Most wrong transfusions are because of clerical errors. Commonly an error on the ward in giving the wrong blood to the patients, next taking the sample from the wrong patient; straight laboratory errors are a minority. Note: that even applies with autotransfusions, where a patient deposits a pint of his own blood for future use. The other point is that there might have been other occasions when a patient got the wrong blood, but by luck it happened to be the right group and nobody told me about it. If instead of cross matching the blood a unit was withdrawn randomly from the blood bank, it would turn out to be compatible 64% of the time. Even when incompatible blood is given, in more than half the cases there are no clinical symptoms resulting and the death rate is only about 1 in 50.

You might ask about the other blood groups: Rhesus negative and the like. The difference is that we don’t have naturally occurring antibodies against these; we have to be sensitized. Sensitization is caused either by a previous transfusion or a previous pregnancy. The Rhesus blood groups have 5 separate antigens: c, C, D, e and E. There is no d. We normally only test for D as anti-D is the commonest acquired antibody. Consequently, we give Rhesus D negative blood to Rhesus D negative patients and give anti-D injections to Rhesus D negative mothers who have Rhesus D positive babies, to prevent sensitization. But patients do get sensitized against c, C, e and E, and against a range of other less well known antigens such as Kell and Duffy. Cross matching is done to screen out incompatibilities here, but a sensitized patient may have no detectable antibody, only producing it after re-stimulation by a transfusion. The antibodies produced then slowly (or sometimes not so slowly) destroy the transfused red cells. This is called a delayed transfusion reaction. About 10% of severe adverse complications of transfusions are delayed transfusion reactions.

One of the most serious types of reaction is called transfusion related acute lung injury or TRALI. TRALI is caused by transfusing blood that contains anti-white cell antibodies in the plasma. The usual cause of these antibodies is sensitization during pregnancy. It is not practical to exclude women who have had children from being blood donors, though in the UK women who have had children cannot donate plasma. Neutrophils are activated in the capillaries of the lungs and the resulting inflammation hurts the lung’s ability to transfer oxygen. TRALI accounts for over 150 deaths a year in the US.

Anaphylaxis after blood transfusion is rare. It usually occurs in the 1 in 500 people with selective IgA deficiency. They make anti-IgA antibodies which react with the IgA in the transfused blood. Transfusion associated graft-versus-host disease (GVHD) results because the donor lymphocytes are engrafted and recognise the recipient-host as foreign and starts to reject it. Although GVHD is common in bone marrow transplants, it is not usually lethal as it is in transfusion-related GVHD since in the former case the bone marrow is of donor origin, whereas in the latter it belongs to the host and is susceptible to attack. You can’t live long without a bone marrow. It is very rare today because we irradiate blood to stop it happening. Blood should be irradiated in patients who have had auto- or allo- marrow transplants, patients with immunodeficiency syndromes, those with Hodgkin’s disease and those who have received one of the purine analogues: fludarabine, cladribine or pentostatin.

Infection is the next problem. Hepatitis B and C, HIV, HTLV-1, CMV, are well known risks, Chagas disease and Malaria in certain parts of the world, in times past, syphilis, in times present West Nile Virus, and possibly parvovirus, Lyme disease and variant CJD are all possible hazards of transfusion. Scrupulous care is taken to avoid these problems but there is still a slight risk of acquiring HIV in one in 2-5 million transfusions. That might not seem much, but people still play the lottery with a one in 14 million chance of winning.

The final risk I want to highlight is iron overload. I will write about this separately but patients who receive 50-100 units of blood will get iron overload, which can damage skin, joints, liver, pancreas and heart and will need a special treatment.