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Blood Transf Ped Anaesth

Blood Transf Ped Anaesth

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Review article
Intraoperative pediatric blood transfusion therapy: a review of common issues. Part I: hematologic and physiologic differences from adults; metabolic andinfectious risks
SANDRA L. BARCELONA
MDMD
*‡, ALEXIS A. THOMPSON
MDMD
†§ AND CHARLES J. COTE´
MDMD
*†‡
Departmentsof 
*
 Anesthesiologyand
Pediatrics,TheFeinbergSchoolofMedicineatNorthwesternUniversity, Chicago, IL, USA and Departments of 
Pediatric Anesthesiology and
§
 Hematology-Oncology-Stem Cell Transplantation, Children’s Memorial Hospital, Chicago, IL, USA
Summary
Pediatric intraoperative transfusion therapy, particularly the approachto massive blood transfusion (blood loss
one blood volume) can bequite complex because of the unique relationship between thepatient’s blood volume and the volume of the individual bloodproduct transfused. This paper is divided into two parts: part 1presents an overview of the physiologic and hematologic differences between children and adults as well as an overview of the metabolicconsequences of blood transfusions, risks of disease transmission, and blood compatibility issues.
Keywords: 
transfusion therapy; massive blood transfusion; hypo-calcemia; hypomagnesemia; hyperkalemia; hypothermia; diseasetransmission
Hematologic and physiologic differencesfrom adults
The physiologic and hematologic differences between adults and children dictate different guide-lines regarding perioperative blood transfusions.The threshold to transfuse a child may be alteredsecondary to these physiologic considerations.Although many of the complications associated withpediatric blood transfusions are similar to thoseencountered in adults, some complications occurmore readily and with a greater frequency inchildren. Familiarity with the differences betweenadult and pediatric transfusion management isof utmost importance when planning transfusionstrategies.Children have higher oxygen consumption and ahigher cardiac output to blood volume ratio thanadults (1,2). The neonatal myocardium operates atnear maximum level of performance as a baseline.Therefore, the newborn’s heart may be unable tocompensate for a decreased oxygen carrying capa-city by increasing cardiac output. The neonatalmyocardium will also suffer a greater degree of decompensation when exposed to decreased oxygendelivery; intraoperative cardiac ischemia has been
Correspondence to:
Sandra L. Barcelona, MD, Department of Pediatric Anesthesiology, PO Box 19, Children’s Memorial Hos-pital, 2300 Children’s Plaza, Chicago, IL 60614, USA (email:s-barcelona@northwestern.edu).
Pediatric Anesthesia 2005
15
: 716726 doi:10.1111/j.1460-9592.2004.01548.x
716
Ó
2005 Blackwell Publishing Ltd
 
reported in neonates (3). Therefore the optimalhemoglobin values in the newborn are generallyhigher than those of older patients. The normal termneonate has hemoglobin values in the 14–20 g
Æ
dl
)
1
range depending in part upon how long it takes toclamp the umbilical cord. These elevated hemoglob-in levels gradually decrease over the first severalmonths of life because of decreased erythropoietinand reduced red blood cell half-life such that thephysiologic nadir for hemoglobin occurs at approxi-mately 2–3 months of age (Table 1). Term infantswith hemoglobin levels <9 g
Æ
dl
)
1
and preterminfants with hemoglobin values <7 g
Æ
dl
)
1
at the timeof this nadir should be investigated for the presenceof hemoglobinopathy or other pathology. If concernover adequate oxygen carrying capacity exists, anelective procedure may be postponed pending eval-uation and treatment. Raising the hemoglobin levelmay be accomplished by transfusion, exogenouserythropoietin administration, or simply postponingthe case until the child’s natural hematopoieticmechanisms have taken effect. Higher hemoglobinlevels will increase oxygen carrying capacity and inthe premature infant, may protect from postanes-thetic apnea of prematurity although transfusion forthis purpose alone is not generally indicated (4).Transfusions are usually withheld unless clinicallyimportant blood loss is likely to occur.Fetalhemoglobin(HbF)comprises70
%
offulltermand 97
%
of premature infants’ total hemoglobin at birth(5). Redblood cells(RBCs)containing HbFhavea shorter life span (90 days) than those containingprimarily adult hemoglobin (HbA) (120 days). HbF interacts poorly with 2–3-diphosphoglycerate (2–3DPG). Therefore the P
50
(the partial pressure of oxygen at which hemoglobin is 50
%
saturated)decreases from 26 mmHg with HbA to 19 mmHgwith HbF. This leftward displacement of the oxygen–hemoglobin dissociation curve results in decreasedoxygen delivery to tissue because of the high affinityof HbF for oxygen. HbF production diminishesduring the first few months of life until only a traceis present at 6 months of age (Fig. 1) (5). In clinicalterms, the younger the infant, the higher the fractionof HbF and thus the lower the oxygen carryingcapacity. Premature infants have higher percentagesof HbF than their full-term counterparts and de-creased erythropoietin production which inhibitsthem from responding to anemia appropriately (6).Anotherconcerninallneonates isthattheymayhaveadecreasedabilitytooxygenatebloodbecauseoflungdisease or congenital heart disease. It is for thesereasons that hemoglobin levels that are adequate forthe older patient may be suboptimal in the youngerinfantorneonate. ThethresholdfortransfusingRBCsto aneonateshould beata higher hemoglobin triggerthan an older child or healthy adult. In the operatingroomthedecision to initiate RBCtransfusion isbasedupon a constellation of factors such as the rapidity of the blood loss, the presence of impaired oxygenation(pulmonary or cardiac in origin), and the generalmedical condition of the patient.
Metabolic consequences and infectiousdisease risks of transfusion therapy
The anesthesiologist must be well versed in theinfectious disease risks and metabolic consequences
Table 1
Normal hemoglobin values for full-term and premature infants
 Full term(g
Æ
dl
)
1
of blood)Premature(g
Æ
dl
)
1
of blood)
Birth 19.3 Slightly less thanfull term0.5 months 16.6 15.41 month 13.9 11.6Age at hemoglobin nadir 9–12 weeks 6–10 weeksMean hemoglobin at nadir 11.2 9.44 months 12.2 11.76 months 12.5 12.4Modified with permission from Barcelona & Cote´(10).
Age (months)
2 0 2 4 6
   F  e   t  a   l   h  e  m  o  g   l  o   b   i  n   (  p  e  r  c  e  n   t  o   f   t  o   t  a   l   )
020406080100
Figure 1
Percent of fetal hemoglobin in infants. The shaded area representsthe range of fetal hemoglobin in infants from preterm to 6 monthsof age. [Modified from Brown (5) p. 258.]
INTRAOPERATIVE PEDIATRIC BLOOD TRANSFUSION THERAPY 717
Ó
2005 Blackwell Publishing Ltd,
Pediatric Anesthesia
,
15
, 716–726
 
of blood transfusions. The common metabolic con-sequences of transfusion include: hypocalcemia,hyperkalemia, hypomagnesemia, hypothermia,changes in acid–base status, and shifts in theoxygen–hemoglobin dissociation curve. These meta- bolic disturbances may occur to a greater degree inchildren than with adults because of the largertransfusion to blood volume ratio. For example, aunit of whole blood may represent the entirecirculating blood volume of an infant whereas thatsame unit of blood transfused into an adult repre-sents only one-tenth of the circulating blood volume.
 Metabolic implications
 Hypocalcemia
Ionized calcium is essential for the successful initi-ation of the coagulation cascade (7). Citrate ispresent in stored blood as a chelating agent forcalcium to prevent clot formation. However, upontransfusion, the deleterious effect of citrate is
in vivo
ionized hypocalcemia. All blood products containsome citrate but the resulting degree of ionizedhypocalcemia depends upon the blood producttransfused, the rate of transfusion, and hepatic bloodflow/function (8–11). Hypocalcemia is most oftenseen during transfusion of fresh frozen plasma (FFP)and whole blood because these components containthe greatest concentration of citrate per unit volume.Patients with hepatic dysfunction and neonates areat high risk secondary to their decreased ability tometabolize citrate (9–11). As the neonate’s heart hasreduced sarcoplasmic reticulum, it is greatlydependent on ionized calcium (calcium flux) fornormal contraction and relaxation. Therefore theneonatal heart is particularly vulnerable to myo-cardial dysfunction in the presence of citrate-induced ionized hypocalcemia. This is further con-founded by the concomitant administration of potent inhalational anesthetic agents because all of the potent inhalation agents cause myocardialdepression secondary to blocking of calcium chan-nels (Figure 2) (9,12–14).Severe cardiac dysfunction may be prevented byslowing the rate of infusion of citrate containingproducts to <1 ml
Æ
kg
Æ
min
)
1
, prophylactically infu-sing calcium during the transfusion, and by redu-cing the concentration of inhaled potent anestheticagent. If a patient becomes hemodynamicallyunstable during rapid blood transfusion, and thecirculating blood volume has been maintained, thenionized hypocalcemia is the most likely cause of thehypotension. The treatment for ionized hypo-calcemia is administration of exogenous calcium.There is no difference in the rate of ionization or thechange in blood ionized calcium concentrations if equivalent doses of calcium chloride vs calciumgluconate are administered. Generally three timesmore calcium gluconate is required than calciumchloride, e.g. 2.5 mg
Æ
kg
)
1
calcium chlor-ide
¼
7.5 mg
Æ
kg
)
1
calcium gluconate (Figure 3)(15). Calcium should not be administered in the blood container or even in the same intravenous line because this will rapidly allow clot formation. Areasonable starting dose for calcium chloride is 5–10 mg
Æ
kg
)
1
or 15–30 mg
Æ
kg
)
1
for calcium gluconateto treat ionized hypocalcemia during rapid infusionsof FFP or whole blood (>1 ml
Æ
kg
)
1
Æ
min
)
1
). Alternat-ively, with blood loss that is moderate but continu-ing over an extended period of time, e.g. redo livertransplantation, a baseline infusion of calcium par-ticularly during the anhepative phase may be useful.Our practice in this situation is to begin calcium
Time (min) citrate infusion
024681012
   M   A   P  r  e   d  u  c   t   i  o  n   (  m  m   H  g   )
–50–40–30–20–100
   I  o  n   i  z  e   d  c  a   l  c   i  u  m   r  e   d  u  c   t   i  o  n   (  m  m  o   l  ·   l
  –   1
   )
–0.8–0.6–0.4–0.20.00.2
MAP deep halothane (1.5% expired)MAP light halothane (0.85 expired)Ionized calcium - deepIonized calcium - light
Figure 2
The effects of an infusion of citrate on ionized calcium and meanarterial pressure (MAP) in a dog model. Note that with the higherexpired concentration of halothane there is a greater fall in ionizedcalcium and MAP. This suggests that the calcium channel blocking properties of inhalation agents are potentiated by thereduced ionized calcium while at the same time the reduced MAPdecreases citrate metabolism by reducing hepatic blood flow.Although this study examined halothane, the interaction betweenionized hypocalcemia and any potent anesthetic agent would besimilar as all potent anesthetics depress cardiac function throughcalcium channel blocking activity. [Modified from data in Cote´(13)].
718 S.L. BARCELONA
ET AL.
Ó
2005 Blackwell Publishing Ltd,
Pediatric Anesthesia
,
15
, 716–726

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