Sir,A 25-years-old female, a known case of sickle cell anemia (SCA) with avascular necrosis of left hip joint was posted for total hip replacement. She was diagnosed as SCA since childhood and gave a history of receiving blood transfusions since 9 years of age. She had undergone splenectomy 15 years back under general anaesthesia.On examination she was afebrile, no pallor, cyanosis and clubbing but sclera showed icteric tinge. Pulse rate was 78/min, blood pressure (BP) 110/80 mmHg, and respiratory rate 14/min. Respiratory and cardiovascular system were within normal limits. Airway assessment revealed no abnormality with adequate mouth opening and Mallampatti airway grade 1.Investigations revealed haemoglobin of 9.7 g%, haematocrit of 30%. Electrocardiogram, chest X-ray and laboratory investigations were within normal limits except for raised serum bilirubin (total 2.6 mg% and direct 0.9 mg%); the other serum glutamic oxaloacetic transaminase 108 IU/L, serum glutamic pyruvic transaminase 116 IU/L, serum alkaline phosphatase 127IU/L, A: G 4.0:3.9, INR 1. The surgery was planned under combined spinal-epidural anaesthesia. A double-lumen central venous catheter was passed under local anaesthesia through a right internal jugular vein with the patient in supine position. Central venous pressure measured was 6 cm H2O.An epidural catheter was passed under aseptic pre-cautions at the L2-L3 space with the loss of resistance to air technique. A test dose of 3cc of 2% lignocaine with adrenaline was given to rule out intravascular or intrathecal placement. This was followed by spinal anaesthesia in L3-L4 intervertebral space with injection of 2.6cc 0.5% (H) bupivacaine and 30 mcg of clonidine via 25 gauges spinal needle.Oxygen was given to the patient via facemask with 5 L/min flow. 10 mg/kg tranexamic acid was given as infusion before incision. An epidural top up of 5cc 0.25% bupivacaine was given after 2 h after assessing the sensory level of anaesthesia.Intraoperatively, 1 L of warm crystalloids, 500 ml of 6% hydroxyl ethyl starch, 500 ml of whole blood were given. Duration of surgery was 3 h, intraoperative urine output was 300 cc and total blood loss was around 1 L. At the end of surgery, the patient was stable, with O2 saturation of 100% on room air, central venous pressure of 5 cm H2O, BP of 98/64 mmHg and heart rate of 80/min.The intraoperative period was uneventful. The perioperative arterial blood gases were normal. Post-operatively oxygen was continued and saturation was maintained around 100%. For analgesia, the patient received 150 µg of buprenorphine diluted with 6 cc sterile saline via epidural catheter 8 hourly for next 48 h with a pulse, BP, and Spo2 monitoring.The possible predictors of post-operative SCD complications according to a study by Curro et al. are: (1) Type of surgical procedure (2) increased age (3) frequency of recent complications (4) recurrent hospitalization (5) temporal clustering of acute chest syndrome (6) abnormal lung fields on radiograph (7) pregnancy (8) pre-existing infection (9) haplotype-African haplotypes have more severe disease than the Asian haplotype.[1] History and examination should, therefore, establish the frequency, pattern and severity of recent SCD events and the presence and degree of various organ damages. Pre-operative screening includes haematocrit - baseline 15–30%, Plasma urea/creatinine - baseline lower than general population, if no proteinuria, urine dipstick test -haematuria, proteinuria, screening for occult infection, pulse oximetry - haemoglobin oxygen saturation atleast 90%. Investigations include screen - for antibodies, extended cross-match for E, C, K groups, pulmonary function tests, arterial blood gas analysis, electrocardiogram, chest radiograph, liver function tests, stool examination (mucosal ischaemia) and neurological imaging. In patients with SCA, red blood cells are transfused to bring the haemoglobin level to 10 g/dl prior to a surgical procedure involving general anaesthesia.[2] If the haemoglobin level is higher than 8.5 g/dl without transfusion in patients who undergo high-risk surgery, consultation with a sickle cell expert for guidance as to the appropriate transfusion method is advised.[2] Hydroxyurea has shown to reduce the incidence of painful vaso-occlusive crisis.[3] Purified poloxamer 188, fructose 1-6 diphosphates, and inhaled nitric oxide are being studied clinically and have promising applications to perioperative care.[3] Alternative to opiates, in the form of non-steroidal anti-inflammatory drugs like ketorolac and agonist-antagonists like nalbuphine, avoid the adverse effects that may exacerbate the frequency of sickling crisis and effective in the treatment of vaso-occlusive pain.[3] The general pre/perioperative management includes erythrocyte transfusion,[4] improvement of oxygen delivery, thermoregulation, hydration and acid-base regulation. Avoid hypothermia, hypoxaemia, hypovolaemia, acidosis and hypotension. The use of regional anaesthesia appears to be a useful means of pain control with effective blocking of nociceptive pathways and also prevent a vaso-occlusive crisis.[5] Use of tourniquet is safe to use provided optimum acid-base status and oxygenation are maintained throughout.[6] Adequate analgesia, incentive spirometry, early mobilisation and oxygen supplementation as needed to prevent hypoxaemia is the mainstay of post-operative management. With the advent of the new therapies, the perioperative course of sickle cell diseasepatient should become less complicated and hospital stays shortened.