IgE- and IgG mediated severe anaphylactic platelet transfusion reaction in a known case of cerebral malaria
An 18-year-old male patient presented with the signs and symptoms of continuous, high-grade fever without chills and rigors since one week. He also had associated vomiting, altered sensorium, and was unconscious with delirium of one-day duration. On examination, the patient was unconscious, pulse: 82/minute, respiratory rate: 14/minute, blood pressure (BP): 110/60 mm of Hg. On auscultation, S1 and S2 were heard, and lungs were clear. There was no organomegaly, but tenderness in the right hypochondrium was present. Plantars were downgoing; he was started on antimalarial therapy. As per altered sensorium and deterioration, mechanical ventilation and intubation were done.\nBasic laboratory investigations were done. Hemoglobin was 12.9g/dL, total leukocyte count was normal with normal differential count, and there was severe thrombocytopenia. Erythrocyte sedimentation rate (ESR) was normal. Plasmodium falciparum ring forms: 1/1000 RBC were seen. Complete urine examination showed trace amount of albumin. Biochemical analysis showed elevated serum bilirubin (2.4mg/dL), alkaline phosphatase, and transaminases. Disseminated intravascular coagulation (DIC) profile showed prolonged prothrombin time (PT), activated partial thromboplastin time (APTT), fibrinogen -64mg/dL, and markedly reduced platelets. Lactate dehydrogenase was raised significantly.\nThe patient received blood components and platelets, and requested for fresh frozen plasma in view of DIC. Transfusion therapy received by the patient from day one of admission until death was reviewed [] and the description of the anaphylactic reaction [] was taken into consideration for investigating the adverse reaction. During the same period, plasma units of the same implicated platelet components were transfused to three different patients with bleeding, without any adverse transfusion reactions.\nInvestigation of transfusion reaction included clerical check of patient identification; labels of blood components, and grouping and typing, along with requisition forms revealed no misidentification. Visual inspection of the postreaction sample of the patient was negative for hemolysis. Pretransfusion testing done on day one of admission revealed ‘O’, Rh-positive blood group and negative antibody screening. On day five, the patient was transfused with ‘O’, Rh-positive platelets and no pretransfusion sample was available. Direct Coomb's test and IgG monospecific antibody were positive in the post-transfusion sample. In view of the positivity of the direct Coomb's test, antibody screening for any irregular or clinically significant red cell antibody was done to rule out immune-mediated hemolytic transfusion reaction. Indirect Coomb's test was negative. Antibody screening by commercial three red cell panel was also negative. Based on this workup, the possibility of immune-mediated hemolytic transfusion reaction was ruled out.\nBlood components as well as the sample of the patient were submitted for culture, and the result was negative for both. The activity of anti-IgA, IgG, and IgM was tested by gel column hemagglutination method.[] Gel column hemagglutination was positive for IgG antibodies and negative for IgA []. Serum imunoglobulins were measured by capture sandwich immunoassay using direct chemiluminescent technology and the results showed raised IgE antibody levels [].\nSigns and symptoms of transfusion reaction such as rashes all over the body, bronchospasm, endotracheal secretions, hypoxemia, tachycardia, and breathlessness developed immediately after the platelet transfusions. As the gel hemagglutination assay was positive for IgG and serum IgE levels were raised, we considered non-IgA-mediated or IgE- and IgG-mediated severe anaphylactic transfusion (alternate pathway) reaction.[]\nBased on some of the pulmonary signs and symptoms like breathlessness, hypoxia, and chest radiograph with lung infiltrates, transfusion-related acute lung injury (TRALI) might have been considered as the important differential diagnosis. However, the underlying critical illness of the patient with ventilator-associated pneumonia may explain the cause for acute lung injury. Subsequent transfusion of the plasma units of the implicated platelet components was uneventful.[]