|Year : 2000 | Volume
| Issue : 8 | Page : 330-334
Blood transfusion associated fatalities
MV Jadhav, N Kurade, N Sahasrabudhe, VM Bapat
Department of Pathology, B.J. Medical College, Pune 411 001, India
M V Jadhav
8, Mulay Classic, Near M.S.E.B. Colony, Bhosalenagar, Pune-411007
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Jadhav M V, Kurade N, Sahasrabudhe N, Bapat V M. Blood transfusion associated fatalities. Indian J Med Sci 2000;54:330-4
Apprehension to the blood transfusion reaction particularly when it is fatal still remains in the minds of medical world though 60 years have passed since the set up of first blood bank in Barcelona in 1936.  While clinical staff is over enthusiastic iu blaming the death on blood transfusion even when it is unrelated, blood bank staff is busy denying it even in genuine reaction. A casual glance at historical aspects of Transfusion Medicine will emphasise the fact that this attitude has influenced the transfusion practice unfavourably. On the other hand, the long history of unsuccessful transfusions due to severe reaction like hemolysis and death led to tremendous growth in the amount of knowledge about the human blood groups and made blood transfusion practicable.  This has prompted us to share our experience with others.
| ¤ Materials and Methods|| |
15 blood transfusion associated fatalities occurring in Sassoon General Hospitals Pune over a period of 6 years and 1 month from January 1995 were studied. 13 of these cases had received blood transfusion from regional blood bank of present institute. 2 additional cases were transfused outside the hospitals and were admitted to present institute for management of reaction. Records of one more fatal transfusion reaction occurring in the same period in another blood bank were also reviewed on their kind permission. The study was conducted by reviewing the clinical and blood bank records, by performing clinical autopsies in 10 cases and medicolegal autopsies in 2 cases and by carrying out pertinent laboraory investigations on samples collected at post mortem. The data was analysed to find out the role of transfusion in cause of death.
| ¤ Observation|| |
It can be seen from [Table 1] that post transfusion endotoxaemia was the most frequent mode of death and occurred in 7 cases. The clinical presentation of these cases was in the form of disseminated intravascular coagulation (DIC) in 2 cases and shock with autonomic disturbances in rest of the cases. The bacterial culture was not done in 2 cases, showed. Citrobacter, Klebsiella and E coli in 3 cases and no growth in 2 cases. Post transfusion septicaemia cost the life of 3 patients who presented with febrile reactions, one such reaction was hemolytic in nature, another was associated with gangrene of transfused arm and the remaining case had septicaemic shock. The organisms encountered in responsible blood units were Aeromonas in 2 cases and Citrobacter in 1 case. Post transfusion cardiac overload was responsible for death in 5 cases, all of which were severely anaemic and in failure. One in addition had primary pulmonary hypertension and the other had calcific aortic stenosis. Boh these conditions were diagnosed at post-mortem. The amount of blood transfused ranged from 30 ml to 120 ml and the rate of transfusion exceeded the prescribed rate in 2 cases (case no. 10, 11). In 2 cases coexistence of post transfusion cardiac overload and endotoxaemia was thought of.
In 3 cases the death was not related to transfusion (case no. 5, 12, 15). 6 patients were clinically stable before transfusion while rest were morbidly ill. 3 patients were transfused intraoperatively and were mildly anaemic. Rest of the patients were transfused in the wards, 2 for acute blood loss, 2 for carcinoma of esophagus, 4 for moderate degree of anaemia and 5 for severe anaemia.
| ¤ Discussion|| |
Every registered post-transfusion death may not be necessarily transfusion associated fatality. The practice of attributing death to transfusion even when it is not related to it can be dated back to 17th century.  In present study it has occurred in 3 instances. One such case died of hemorrhagic shock following multiple injuries. In one case, patient developed post transfusion urticaria, which was cleared quite well before death. The patient died of hypovolemic shock due to loose motions with which he was suffering even before a transfusion. In one case death was due to adverse reaction to halothane (anaesthetic drug). This patient developed repeated cardiac arrests and succumbed to it. The only known cause of transfusion associated cardiac arrest is citrate toxicity which occurs after massive transfusion, and present patient had received only few millilitres of blood. The present study emphasizes the importance of critical evaluation of pre transfusion clinical status and clinical diagnosis in investigating a post transfusion fatality. Equally important is the consideration of post transfusion course of the patient and information regarding the technique of transfusion. The need to review original clinical condition and its diagnosis in investigating a post transfusion fatality has been stressed by Myhrt.  The diagnosis of septicaemia was based on clinical and autopsy findings in 2 cases and on clinical grounds in 1 case. The cases were labelled as endotoxaemia mainly on clinical grounds and on failure to find out evidence of septicaemia at autopsy. It could not be always substantiated with bacterial culture.
The pre transfusion compromised clinical status of the patient had an important bearing on post transfusion clinical course. The patient with compromised cardio-respiratory status due to severe anaemia in failure along with primary pulmonary hypertension and calcific aortic stenosis readily developed post transfusion cardiac over load which was intractable and fatal. Severe and symptomatic anaemia is considered a fairly valid indication of transfusion. At the same time such patients are prone to fatal post transfusion cardiac overload.  One is faced with the dilemma as there is no other option but to transfuse the patient with blood to alleviate the symptoms. This increases the haemoglobin by merely 1 gm%, per unit of blood but may put the life of a patient at stake. Use of packed red cells would not have changed the destiny of 5 patients with fatal post transfusion cardiac overload in present study as none was transfused with more than 120 cc of blood. Here comes the role of meticulous dissection technique during surgical procedures which definitely reduce the blood loss and , transfusion requirements. Khurana et al  have stressed the need to improve the medical education in proper management of blood transfusion in clinical practice and strategies to avoid the need for blood transfusion. It was a relief to note that none of the fatalities in present study were attributable to clerical or technical error on part of blood bank or hospital staff.
Myhre  and Honig and Bove  in 1980 studied Food and Drug Administration records of 1975 to 1979 to find out the details of blood bank associated fatalities. There were 113 such fatalities in 37 million transfusions with the incidence of 0.00023%. 33 of such fatalities were due to hepatitis which is a late transfusion reaction and 3 cases were donor associated. 73 fatalities were the recipient associated immediate post transfusion fatalities, 47 of which were due to clerical error and 8 were due to laboratory errors. One case was contributed by wrong technique (over warming of blood). All these can be considered as preventable. The unpreventable and unpredictable fatalities consisted of anaphylaxis (4 cases), multiple antibodies (5 cases), delayed reactions (3 cases), respiratory distress (4 cases), DIC (2 cases), Graft verses host reaction (1 case) and Gram negative endotoxaemia (2 cases). Honig and Bove  have referred io aetiology of these fatalities. Antibody mediated hemolysis was the most frequent cause. Thermal hemolysis was observed once. Mehta et al' have reported 2 fatalities amongst 94 transfusion reactions and 32126 transfusions with the incidence of 0.006 amongst total transfusions and 2.14 amongst total reactions. Incidence of fatal transfusion reactions was high in present institute when compared with other institutes and in literature. However it should be viewed in the light of socio-economic status of the patients that we are catering for. Most of these patients were morbidly ill and had compromised clinical status when they were admitted, thus leaving us with very few treatment options. Nonetheless part of the high incidence still can be attributed to overuse of transfusion services and prompt recording which is possible due to location of blood bank within the hospital. Some of the cases were included form autopsy records though they were not registered in blood bank.
In conclusion, one can expect safe and fruitful transfusion only when administered to a properly selected patient and for absolutely indicated clinical condition.
| ¤ Summary|| |
16 post transfusion deaths were studied by reviewing clinical and blood bank records and by postmortem examination whenever possible. 13 of these cases belonged to regional blood bank, 2 were transfused in other hospitals and referred for management of transfusion reactions and one case belonged to other blood bank in the city. 3 deaths could not be attributed to transfusion reaction. Post transfusion endotoxaemia (7 cases) was the most frequent mode of transfusion associated fatality followed by cardiac overload (5 cases) and septicaemia (3 cases). In two cases endotoxaemia coexisted with cardiac overload. The pretransfusion compromised clinical course unfavourably thereby contributing significantly in death. The 3 clinically stable patients succumbed to post-transfusion endotoxaemia. The incidence of transfusion associated fatality in the present institute was 0.028% amongst total transfusions.
| ¤ References|| |
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