Background. Iron deficiency anaemia is the most common deficiency disorder in the world, affecting more than one billion people, with pregnant women at particular risk.

No abstract

Background: Improving preoperative anaemia is associated with a better surgical outcome. There is lack of data regarding treatment of preoperative anaemia with intravenous versus oral iron.Objective: Assessment of efficacy of oral iron sulphate versus a single intravenous iron polymaltose and subsequent effect on perceived quality of life in both treatment groups. Patients and methods:We conducted a prospective randomised controlled trial with iron therapy for the treatment of Iron Deficiency Anaemia (IDA) patients who were undergoing elective joint arthroplasty. At a single institution, we recruited 44 patients who were randomized to a single intravenous iron polymaltose infusion (16/22) versus oral daily iron sulphate (17/22). Median age was 68 years (range, 45-91) with a male to female ratio of 14:19.

A 58-year-old Caucasian female was known to have had autoimmune thrombocytopenia purpura (ITP) since childhood and had undergone splenectomy when she was 16 years old. She presented with a platelet count of 15 x 10 9 /l with bleeding manifestations and high dose intravenous immunoglobulin (IVIG) was therefore administered. The IVIG administered was Intragam-P (CSL Ltd., Parkville, Victoria, Australia). Her platelet count showed good improvement and had normalized by 48 h. However 48 h after a second dose of IVIG, the patient complained of reddish urine and her haemoglobin concentration (Hb) was found to have dropped from 122 g/l to 100 g/l, falling to 80 g/l after a further three days. Severe haemolysis was evidenced by polychromasia, spherocytes and nucleated red cells in her blood film (top). High lactate dehydrogenase (LDH), high bilirubin and low haptoglobin levels were also noted. A direct antiglobulin test (DAT) was strongly positive (4 + ), anti-IgG was strongly positive (4 + ) and anti-C3d was negative. Anti-A antibody was eluted from the red cells. The plasma was dark red in colour due to intravascular haemolysis (bottom left). Urine was also red in colour due to haemoglobinuria (bottom right), with no red cells on urine microscopy. There was no renal impairment. The patient's blood group was A RhD-positive. Tests for antinuclear antibody (ANA), anti-double stranded DNA and anti-extractable nuclear antigen were negative.The patient was managed conservatively and did not require transfusion. Urine colour became normal after four days. Hb and haemolytic markers started to show improvement after five days and had normalized within four weeks. The DAT became weak (1 + ) by four weeks and was negative by eight weeks. After the haemolysis had settled completely and the DAT had become negative, a small aliquot from the same batch of IVIG was cross-matched (using gel card technique) against the patient's red cells with A, B and O cells as controls. Strong agglutination was seen with the patient's and control A red cells up to 1:256 dilution confirming that anti-A antibody in IVIG was the cause of the haemolysis. IVIGinduced haemolysis is usually mild and self-limiting and can easily be un-noticed. Massive intravascular haemolysis due to anti-A antibody is a rare complication of high dose IVIG.