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.Ntw Dd/d Exchange blood transfusion remains the i~!!~t effective method to treat critical hyper~!lrubinaemia o! the newborn. However, procedure is not without dangers (Tan # # ! e L 1976). The mortality during the " ~~-e d u r e 9 varies from !3,7 per cent for sick l~eterm or kernicteric neonates to 0.2 ::i~rcent for term babies (Bogg and West[~laa! 1960 and Taylor 1962). The cause of ~ r b l d i t y and mortality during exchange ll~tmftnion is often a matter of speculation ~ ' ~ h and Mittal 196~J. Dur'~ng the past ,~aontl~ we encounterred 3 instances' of ~ t | a e arrest, apparently due to hypocal~ e m i a , out of12 exchange transfusions done,

rate are monitored by a physician throughout tile procedure. Prewarmed ACID (acid citrate dextrose) blood is used which in no case is more than 3 days old. A total of about lf,0 to 170 ml. of blood is exchanged per kilogram of body weight by the conventional discontinuous technique in 10 ml aliquots Calcium gluconate 100 rag (i ml of 10% solution) is administered routinely after each 100 ml" of blood exchanged, The rate of exchange transfusion is regulated so as to exchange 2.0-2.5ml of blood per kilogram per minute. Blood samples are taken before and after exchange for haemoglobin, serum bilirubin, electrolyres, calcium ahd proteins.

Methods Exchange transfusion is contemplated ' ~ , t h e basis of conventional indications ($iagh and Ghai 1976). Feeds are withheld for three hours before the procedure and stomach aspiration is done. The infants are strapped on a padded dummy splint. A radiant overhead heater is used to keep the baby warm. The umbilical vein is catheterised. The tip of the catheter is placed in the thoracic segment of the inferior vena cave, and before insertion it is marked with a thread for the appropriate distance to be inserted (Dunn 1956). i~emperature, respiratory rate, and cardiac ~lom the Neonatal Section, Department of PatediaAll-India Instithte of Medical Sciences, New l~ihi~ 016. il~ceivedon September 2, 1978.

Report of Case~

Case I.

Baby G was born to a 7th gravida Rh negative mother after 34 weeks of gestation by LSCS. Al! previous babies had suffered from Rh haemoiytic disease, and none was alive. During the current pregnancy indirect Coomb's titre.;avas 1:32. The baby had birth anoxia, w i t h l-minute and 5-minute Apgar scores of 3 and 5 respectively. She was jaundiced at birth. The liver and spleen were palpable by 3 cm and t c m respectively. Cord blood showed haemoglobin of 5.6 gm/dl, total bilirubin S.0 mg/dI with direct of 1.0 mg/dl and reticulocyte count of 9 per cent. The baby's blood group was B Rh positive. Direct Coomb's test was positive. Exchange transfusion through the umbilical vein was started at three and a half hours of age. At



the end of 100 ml of exchange when we "were preparing to give calcium gluconate, the baby developed sudden cardiac arrest in association with typical tetanic spasms of the limbs. Calcium gluconate 500 mg (5 ml of 10% solution) diluted witi~ 5 ml of 10% glucose was given immediately along with external cardiac massage and oxygen by mask. prompt recovery occurred. The baby needed a second exchange transfusion at the age of 25 hours. This time 1 ml of calcium gluconate was given intravenously after each 50 ml of exchange with no complications. Case 1L Baby S. was born to a 4 t h gravida g h negative mother after an unc o m p l i c a t e d gestation by spontaneous vaginal delivery. T h e previous two babies suffered from P,h haemolytic disease and died during the neonatal period. Apgar scores were 7 and 10 at l and 5 minutes, respectively. H e weighed 2.1 kg. T h e baby's blood .group was O Rh positive, and cord serum bilirubin was 3.5 mg/dl. Clinical jaundice was noticed at the age of 10 hours. The spleen and liver were not palpable: T h e first er_change transfusion was needed at the age of 23 hours Double volume exchange with O Rh negative. ACD blood was done through the umbilical vein catheterisation. Calcium gluconate 100 mg was given at the end of each 50 ml exchanged. No complications were encountered. At the age of 59 hours, a second exchange transfusion was necessitated, ~is indirect serum bilirubin levels approached 20 mg/dl. Calcium gluconate this time was being given at the end o f each 100 ml blood exchanged. At the end o f 300 ml exchange, when calcium was due, the baby developed sudden cardiac arrest. Hypocal-

VOL. 46, N o . ~ cacmlc tetany did not manifest itself, i ~ 9 was resuscitated with intravenous calciu]U gluconate and external cardiac massage.: C~se 3. Baby H, a full term male, was b o ~ to a second gravida O Rh positive m o t h ~ by spontaneous vagina] de]ivery after axE2 uneventful gestation. Apgar score at 1 a ~ 5 minutes were 9 and t0 respectively. B i i J weight was 2.95 kg. Jaundice was notice'~m at the age of 36 hours and increased p r o g r e ~ sively. At the age of 90 hours the b a b y l was found to be deeply jaundiced. H i l haemoglobin was I0.4 gm/di and peripherY! smear showed crenated RBCs. No micr0m spherocytes were seen. Blood group o f baby was A Rh positive. Direct Coomb~]m test was negative and G-6-PD assay warn normal. Total serum bilirubin Wa-~ 25.0 mg/dl with an indirect bilirubin levens of 23.7 mg/dl. Exchange transfusion w a ~ done at the age of 94 hours with 470 ml o ~ A Rh positive ACD blood. Calciuxifll gluconate 100 mg was given after evervi 50 ml of blood exchanged. The procedurei was uncomplicated. The second exchangel transfusion was indicated at the age _of~ 118 hours when serum bilirubin rose to.~ 21.5 mg/di. After 80 ml blood was ex- I changed the baby developed sudden cardiac arrest. The baby was successfully resus-, citated by intravenous administration of" 500 mg of calcium gluconate and external cardiac massage. "l-hree additional exchange ~ transfusions were needed in this baby. Each time ACD blood was used for double~ volume exchange and 100 mg calcium~ gluconate ~as given after eveiy 50 ml o~ exchange. No complications were en-~ countered during any of the snbsequent exchange transfusions


Cardiac arrest is known to occur during ,atcliange transfusion (Tan et el. 1976, T~yl0r 1962). The various aetiological ~ctors include malpositioning of the ~dieter, hyperkalaemia, hvpocalcaemia itidrapidity of exchange transfusion result~n~iii|a:iacute haemodynamie alterations. ~ b c e u r r e n e r of cardiac arrest in all the ~ e babies and clinical tetany in one of them, wlaen calcium gluconate was due, ~ m p t s the diagnosis of hypocalcaemia ~diae arrest. A prompt response to Intravenous infusion of 500 mg of calcium il'~Ileonate i .... "In all these eases confirms the W!d610gi~a]! role of hypocalcaemia in the r cardiac arrest.:: Whenl calcium ~itdo~aiewas: given after each 50 ml Of iil~/tnge transfusion, none of the babies developed cardiac arrest or tetany. ACD stored blood is widely used for ~xehange transfusion although it is well known that citrate chelates serum calcium i(Furquhar and Smith" 1958). The chelation ofealcium is thought to be counteracted by the administration of calcium gluconate at !egular intervals during the exchange transfusion (Allen and Diamond 1958). I t h a s been shown experimentally that during exchange transfusion significant :reduction in ionised calcium occurs (Radde a oJ. 1972, Gershanik #tel. 1973) although total calcium levels are unaffected. In a total of 26 exchange transfusions monitored by Radde et el. (1972), serum ionised calcium levels came down to 1.2 mEq/t in 8 infants despite administration of the Ilandard,dose of calcium gluconate (100 mg ,ig'r:100 ml of exchange), Clinically manifest hypocalcaemic tetany occurred in 4 babies. Other workers have also shown that administration of 100 ml calcium gluco-


nate after each 100 ml of blood exchanged may not effectively prevent a fall in ionised calcium (Radde et el. 1972, Gershanik et el. 1973, Maisels et el. 1974). Following that schedtde a transient rise in serum calcium does occur but by the time the next dose of calcium is due, serious hypocalcaemia may manifest itself. On the basis of these data it is, therefore, recommended that calcium should ha administered after each 50 ml of blood exchanged in Order to prevent hypocalcaemia. Smooth and uncomplicated subsequent exchange transfusions in case I a~ad I I I further support this recommendation. . . . . Objections have also been raised regard. ling the safety: of routlne ~admfnistration of calcium gluconate during exchange trans ~ fusion with ACD blood (Radde et al. 1972). It has been suggested that rise in serum total calcium following its intravenous administration may cause imbalance of delicate renal homeostatic mechanisms of the newborn. However, this fear is unfounded because the amount of calcium administered is insufficient to result in neonatalhypercalcaemia and a marginal rise in serum calcium is not likely to lead to any serious side effects (Freidman tt ai 1972). Summary Three instances of cardiac arrest due to hypocalcaemia during exchange blood transfusion with ACD-blood are described. One of the babies showed clinical manifestations of tetany. All infants were successfully resuscitated by intravenous administration of calcium gluconate. It is recommended that during exchange blood transfusion with ACD-blood, calcium should be administered after each 50 m| of blood exchanged.



Allen, F'H., Diamond, L.K. (1058). In erythro. blastosis foetalis including exchange trarlsiusion technic. Little Brown and Co., Boston. Bogg, T.R, Jr., Westphal, M.C., Jr. (1960). Mortality of exchange trausfusion. Pedialrics 26, 747.

Dunn, P,M. (1966). Localisation of the umbilical catheter by postmortem measurements. Arch. Dis. Chlldh. 41, 69. Freidman, Z., Hanley, W,.B., Radde, 1.C. (1972). Ionised calcium in exchange transfusion with THAM buffered ACD blood. Canad. Med. dJsoc. J. 107, 742. Furquhar, J.W., Smith, H. (1958). Clinical ~nd biochemical changes during exchange transfusion. Arch. Dis. Childh. 38, 142.

VOL. 46, N o ~ Gcr|hanik, J.J., Levkoff. A.H., Duncan, R. ( | 9 ~ Serum ionised calcium values in relation to e a : r transfusion..7. Pediatr. 82, 847. Mabel*, M J., Li. T.K., Peichocki, J.T., W ~ man, M.W. (1974). Effect of exchange transfgs~ on serum ionised calcium. P#diar 53, 683. Radde, I.C. Parkinsc!n, D.C. Hoffken, BI A p ~ K.E, Hanky, W,B. (1975). Calcium ion actlv|~y~ll Jick neonates. Effect o f bicarbonate administra~ and exchange transfusion. Pediatr Res. 6, 43. Singh, M. and Mittal, $.K. (1969). Exchacl transfusion in the newborn. A four year experien~ india n .7. P, diatr. 86, 161. Singh, M., Ghai. O.P. (1978). In Care of A~[ Newborn. Sagar Publication, New Delhi, p. 296. Tan, K.L, Phua, K.B., Arts. P.L. (1976). M o / ~ lity ef exchange transfusions. Mrd. J . At,st. 1, 473~

Cardiac arrest during exchange transfusions.

/~i~3Pdialr, 4e t 131,10"1~ CARDIAC ARRF.,ST DURINC, EXCHANGE TRANSFUSIONS* MEtlARBAN SINOH AND SUN|T Slblr .Ntw Dd/d Exchange blood transfusion rem...
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