- Delayed Haemolytic Transfusion Reaction (DHTR) A DHTR usually manifests between 24 hours and 28 days after a transfusion and clinical or laboratory features of haemolysis are present. Signs and symptoms are similar to AHTR but are usually less severe. They may sometimes manifest as an inadequate rise of post-transfusion haemoglobin level or unexplained fall in haemoglobin after a transfusion. Blood group serology usually shows abnormal results. The incidence of DHTRs is one per 2500 transfusions, but rises to 11% in patients with sickle-cell disease (74). Patients at risk for delayed haemolytic or delayed serological transfusion reactions (DSTR) include those with a history of red blood cell antibodies (through pregnancy or transfusion exposure) in which the antibody titre subsequently decreases to levels undetectable by routine antibody detection testing. There is a DSTR when, after a transfusion, there is demonstration of clinically significant antibodies against red blood cells which were previously absent (as far as is known) and when there are no clinical or laboratory features of haemolysis (synonymous with alloimmunisation). With standard laboratory techniques, 25% of red blood cell alloantibodies become undetectable over a median follow-up of 10 months after initial development, thus putting patients at risk for delayed transfusion reactions. DHTR is usually due to an anamnestic immune response when the recipient is unknowingly transfused with a red blood cell unit that expresses the cognate antigen. Re-exposure to the foreign antigen causes a rise in red blood cell antibody titres 24 h to 28 days after transfusion, accompanied by either a fall in hemoglobin or failure of increment, rise in indirect bilirubin, or a positive direct antiglobulin (Coombs’) test. Hyperhemolytic transfusion reactions can occur in multiply transfused patients such as those with sickle cell disease of thalassemia, often due to pre-existing antibodies although the pathophysiologic basis is not completely understood.
-  Delayed serologic transfusion reaction (DSTR).  is an under-recognized reaction, affecting about 1–8% of patients who are transfused (68-70). It’s caused by an excessive quantity of transfused blood components or an excessive rate of transfusion (excessive being relative to each patient). The initial stages of TACO may be difficult to distinguish from haemolytic transfusion reaction, FNHTR, allergic reaction, or TRALI. Risk factors include being in the neonatal or elderly population, renal failure (especially if on dialysis), pre-existing fluid overload, cardiac dysfunction, administration of large volumes of blood products, and rapid administration rate. Prevention is based on assessment of patient risk and judicious transfusion practice.
Post Transfusion Purpura (PTP) Occurs roughly 1 in 100,000 transfusions, is a rare, self-limited thrombocytopenia occurring 5 to 10 days after transfusion in patients lacking a specific platelet antigen, usually HPA-1a, phenotypic frequency up to 2% depending on patient ethnic origin, (GPIIIa, CD61)(75), who have previously been alloimmunised by pregnancy, Indeed, approximately 85% of cases occur in women. However, other HPA antigens might be implicated. In elderly patients, platelet transfusions, multiple transfusions, and the presence of comorbidities are risk factors (76). Prevention of recurrence of PTP is uncertain but can include use of washed red blood cell units, or use of platelet and red blood cell units from HPA compatible donors. 
Transfusion Associated Graft Versus Host Disease (TA-GVHD) is an extremely rare adverse event caused by transfusion of cellular components containing viable donor lymphocytes that recognize their new host as foreign and engraft in the recipient. It is a clinical syndrome characterized by symptoms of fever, rash, liver dysfunction, diarrhea, pancytopenia and findings of characteristic histological appearances on biopsy occurring 1-6 weeks following transfusion with no other apparent cause. The diagnosis of TA-GVHD is further supported by the presence of chimerism. At risk are severely immunodeficient patients such as recipients of haemopoietic stem cell transplantation (past and current) or patients with congenital immunodeficiency affecting T cells or Hodgkin’s lymphoma; those in need of neonatal exchange transfusions; and patients taking high-dose chemotherapy or radiotherapy, purine- analogue drugs, or anti-thymocyte globulin for aplastic anaemia (77,78). Fetuses who need intrauterine transfusions are also at risk. Immunocompetent patients are at risk when receiving cellular components from blood relatives or if being transfused in a donor population with little HLA diversity. TA-GVHD can be prevented by irradiating cellular blood components with gamma-rays or x-rays, or by treating blood products with pathogen reduction technology to disrupt the residual lymphocytes’ ability to proliferate (78).
Cumulative iron overload Patients receiving regular RBC transfusions unavoidably and invariably develop iron overload and, thereby, are at risk for iron toxicity (79). Excess iron accumulation in tissues results in a number of adverse clinical outcomes, with an associated increase in morbidity and mortality that correlates with the degree of iron toxicity. The main sequelae of excess iron deposition depend on the organ that is damaged: liver fibrosis/cirrhosis and hepatocellular carcinoma, in the heart congestive cardiomyopathy, endocrine dysfunction: pancreas (diabetes mellitus), anterior pituitary (growth hormone deficiency with short stature), testes/ovaries (hypogonadism with delayed puberty and infertility), thyroid (hypothyroidism), parathyroids (hypoparathyroidism), and adrenals (adrenal insufficiency). Because symptoms may not appear until substantial organ damage has occurred, it is important for clinicians to maintain a high degree of awareness of iron overload. Screening and monitoring tests include indirect measurements of iron, such as laboratory and imaging studies.