Transcript Blood Product Utilization in Pediatric Anesthesia

Blood Product Utilization in
Pediatric Anesthesia
Gamal Fouad S Zaki, MD
Professor of Anesthesiology
Ain Shams University
Outline
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Why blood component therapy?
Why transfuse RBCs?
Hematologic and physiologic differences
Decision making for transfusion in pediatric
surgical patients
• Adverse reactions: metabolic, infectious,
compatibility issues
• Platelets, FFP and cryoprecipitate
Why component therapy?
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RBCs
FFP
Platelets
Cryoprecipitate
Coagulation
factors
• Leukocytes
Why component therapy?
• Storage of whole blood results in:
– Shorter T1/2 of factors V and VIII (4-36 hrs in vivo,
7-14 days in vitro)
– Refrigeration results in Platelets losing discoid
shape, accelerated platelet storage defect, with
reduced in vivo survival after transfusion
• Separation of components aims at optimizing
the number of transfusible components from
a single donor to treat specific pathology
Roseff et al. Transfusion 2002
Why transfuse RBCs?
• The one and only reason should be
to restore or maintain oxygen
delivery to vital organs. Any other
reason has no medical or
physiological basis.
Ward et al. in Perioperative Transfusion
Medicine (2nd Ed.), 2006
Oxygen Delivery
SaO2
Hb Conc
Circ Volume
HR, SV, Contr
Vasomotion
Physiologic differences
• Higher oxygen consumption & COP to blood
volume ratio
• Transition from fetal to neonatal circulation leads to
high PVR with impaired oxygenation
Neonatal myocardium:
• Operates at near maximum performance (baseline)
may be unable to compensate for decreased
oxygen carrying capacity by increasing COP
• Decreased DO2: greater decompensation
Optimal hemoglobin values in the newborn are
generally higher than those of older patients
Hematologic differences
• Normal term neonate Hb range 14–20 g/dl which gradually
decrease over first months because of  erythropoietin, 
RBC T1/2 , physiologic nadir at approx 2–3 months
• Term infants with Hb <9 g/dl & preterm <7 g/dl should be
investigated for hemoglobinopathy or other pathology
(postpone elective surgery to evaluate, treat)
• Raising Hb: transfusion, exogenous erythropoietin, or simply
postpone until natural hematopoietic mechanisms take effect
• Higher Hb increases O2 carrying capacity & in prematures, may
protect from postanesthetic apnea of prematurity although
transfusion for this purpose alone is not generally indicated
• Avoid transfusion unless clinically important blood loss is likely
Median, 95% confidence
intervals
Hematologic differences
• Fetal Hb (HbF) comprises 70% of full term & 97%
of premis’ total Hb at birth
• RBCs containing HbF have shorter life span (90
days) than those containing HbA (120 days)
• HbF interacts poorly with (2–3 DPG), P50 (PaO2 at
which Hb is 50% saturated) decreases from 26
with HbA to 19 mmHg with HbF. This leftward
shift of the oxygen–Hb dissociation curve results
in decreased oxygen delivery to tissue because of
the high affinity of HbF for oxygen
Oxygen-Hb dissociation curve
HbF
19
26
P50
Fetal Hb in infants
• Younger infants have
higher fraction of
HbF and lower
oxygen carrying
capacity
• Premis have higher
% of HbF than fullterm & decreased
erythropoietin
production:
impaired response
to anemia
Physiologic/Hematologic variables and
decision to transfuse RBCs
• Neonates may have decreased ability to
oxygenate Hb: lung disease, CHD
• Hb levels adequate for older patients may be
suboptimal in younger infants or neonates
• Threshold for RBCs Trx in neonate is at higher
Hb trigger than older child or healthy adult
Decision to Transfuse RBCs
Ready to defend your decision?
Decision should be based on evidence that
anemia with reduced oxygen delivery is
injurious and RBC transfusion will correct
DO2 and improve outcome
Optimum Hb / Hct
• Classical Teaching: >10g/dl do not transfuse,
<7g/dl always transfuse “10/30 rule” (not useful)
• Animal studies: Hct 30-40% for optimum DO2
(good O2 carrying capacity, low viscosity), Hct 1020% well tolerated in normal animals
• Normal human volunteers: Hb 5g/dl tolerated
with occasional signs of inadequate DO2:
memory impairement, ST-segment change
Optimum Hb / Hct
Surgical Patients:
• Jehova’s Witnesses (n=125) no mortality if Hb>8
• Death more likely in pts with low Hb in the
presence of coexisting cardiovascular disease
Critically
ill patients:
“restrictive
strategy
of red-cell transfusion is at least as effective as and possibly
superior to a liberal transfusion strategy in critically ill patients, with the possible
• Comparing liberal (10-12g) & restrictive (7-9g) Trx
exception of patients with AMI and unstable angina”
strategy showed reduced mortality with restrictive
strategy
• In pediatric pts restrictive strategy seems not
worse than liberal strategy
Decision to Transfuse RBCs
• No Universal Indications or Triggers for RBC trx
• Intraoperatively: decision is multifactorial:
– rapidity of blood loss
– Hb concentration
– Hemodynamic instability
– presence of impaired oxygenation (pulmonary or
cardiac in origin)
– Evidence of impaired O2 delivery
– general medical condition of the patient
Dose
• A transfusion of 10cc/kg will increase the
hemoglobin 2.5-3.0 g/dl
Metabolic consequences
Hypocalcemia:
• Ca++ essential for initiation of coagulation
• All blood products contain citrate
• Degree of hypocalcemia depends on:
– Type of blood product (FFP, whole blood)
– Rate of administration
– Hepatic blood flow and function
• Risk with neonates, liver disease (decreased
citrate metabolism)
Metabolic consequences
Hypocalcemia:
Equi-ionizable doses
• Neonatal myocardium has reduced sarcoplasmic
reticulum, is dependent on Ca++ to maintain function, and
thus vulnerable to citrate-induced ionized hypocalcemia
• Volatile anesthetics (given concomitantly) exert
myocardial depression via blocking Ca++ channels
• If hypotension with adequate volume:
– Slow transfusion of citrate-containing product <1ml/kg/min
– Decrease volatile inhaled agent concentration
– Calcium chloride (2.5mg/kg) or gluconate (7.5mg/kg) in
different IV line, or CaCl2 10-15mg/kg/hr for ongoing losses
Cote et al. Anesthesiology, 1987
Metabolic consequences
Hyperkalemia:
• K+ leaks from older RBC as cell membrane deteriorate
• Large volume Trx may result in fatal hyperkalemia in
children with small bld volume
• Highest K+ in whole blood, units near expiration date,
irradiated units
• Washed RBCs: reduced K+
• In neonates use “newer” units < 7 days old
• If dangerous arrhythmia: CaCl2 15mg/kg q 2min, then
definitive lowering of K+ by hyperventilation,
glucose/insulin, B-adrenergic stimulants, ..
Metabolic consequences
Hypomagnesemia:
• Mg++: for RMP, cardiovascular &
electrophysiologic stabilization
• Ionized hypomagnesemia results from massive
transfusion because of citrate chelation of Mg++
• Anhepatic phase of liver Tx
• Arrhythmia refractory to CaCl2: give IV MgSO4
25-50mg/kg then infuse 25mg/kg/24hrs
Metabolic consequences
Acid / Base disturbance
• RBCs continue metabolism inside bag: PCO2 reaches
180-210mmHg, O2 consumed, lactate accumulates
• Rapid whole blood trx causes transient metabolic &
respiratory acidosis, CO2 excreted in lungs, lactate
rapidly buffered (no need for ttt)
• Metabolic acidosis during massive trx reflects
inadequate perfusion, severe hypovolemia prior to
Trx, sepsis, or hypoxemia
• Citrate metabolism: causes delayed metabolic
alkalosis (better limit empirical use of NaHCO3)
Metabolic consequences
Hypothermia
• Maintaining normothermia in children is
challenging even without Trx: large BSA/Wt, GAinduced heat redistribution from core to periphery,
respiratory & surgical evaporative losses, cold OR
• Consequences: apnea, hypoglycemia, delayed
drug metabolism and prolonged effects, left shift
of oxyHb dissociation curve, increased oxygen
consumption, coagulopathy, increased mortality
• Type of warming device depends on rate of Trx
Infectious disease transmission risk
• Risk less than metabolic & immunologic risks
• Will further improve with wide adoption of
nucleic acid amplification technique (PCR)
• Viral risk includes Cytomegalovirus, hepatitis C,
hepatitis B, HIV, and human T-lymphotropic virus
• Others: West Nile Virus, SARS, Malaria, Chagas
disease
• In countries where testing is incomplete, anemia
may be a better risk
Evolution of viral risks of transfusion over time in the USA
Infectious disease transmission risk
• Evidence exists that RBC transfusion is associated
with impairment of immune mechanisms, possibly
increasing risk of bacterial infection
• Multiple observational studies link RBC transfusions
with infection, immunosuppression, and mortality
• Transfusion induce immunomodulation
• Patients in a medical–surgical ICU had a 10%
increased risk of nosocomial infection/unit of RBCs
Taylor et al. Red blood cell transfusions and nosocomial infections
in critically ill patients. Crit Care Med 2006; 34:2302–8.
Incompatibility & immunologic
considerations
• ABO incompatibility: acute hemolytic reaction,
Clerical error is the most common cause: fever,
tachycardia, hypotension, abn bleeding: stop Trx,
maintain ABP, UOP
• Transfusion-related graft vs host disease occurs in
immuno-compromised pts when lymphocytes
contained in a transfused blood component
proliferate and cause host tissue destruction: TAGVHD prevented by Gamma irradiation of blood
products (RBCs, platelets, granulocytes)
Transfusion-Related Acute Lung Injury
TRALI: abrupt onset of respiratory failure within
hours of the transfusion of a blood product. Usually
caused by anti-leukocyte antibodies, resolves rapidly,
low mortality. Most likely with plasma rich products:
FFP, apheresis Platelets
Clinically: a nonspecific constellation of dyspnea,
hypotension, noncardiogenic pulmonary edema,
fever,may overlap with ARDS: dyspnea, bilateral
infiltrates, hypoxemia, & noncardiogenic edema
Leading cause of transfusion-related mortality
Prevention: Plateletpheresis from male donors and
never pregnant females
Platelets
• Either from platelet rich plasma or apheresis
• Stored in a special permeable plastic at room
temperature, high risk of bacterial contamination
• Apheresis platelets: less donor exposure, decreased
risk of disease transmission & allo-immunization,
less exposure of platelets to centrifuge
• Risks: TRALI, febrile reactions, circulatory overload.
Observational data from CABG: association with
increased risk of stroke, inotrope use, pulmonary
dysfunction, death.Spiess. Transfusion.2004
Platelets
• ABO compatible
• Indications and dosage: not clear
• Prophylactic: keep platelets above certain count,
versus Therapeutic: transfuse only for active
bleeding or before procedure
• Dosage:
– 1 Unit / 10kg Body Wt which is expected to raise the
platelet count by 50,000 platelets/microliter
– Higher doses can be considered in septic patients, or
patients with DIC, or splenomegaly
• Benefit / Risk consideration
FFP
• Indications: prolonged PT, PTT, low fibrinogen
• Dosage: 10cc’s/kg of ABO compatible product
• Cryoprecipitate is made from FFP, contains higher
concentrations of fibrinogen, von Willebrand
factor, and factor VIII
• Risks: infection, allergic reactions, hemolysis, and
volume overload. Risk of TRALI 1:60000/FFP unit.
• Strong association of TRALI and female gender of
donor. Hypothesis: pregnancy induces human
leukocyte antibodies among female donors. Led to
preferential use of male-derived plasma for FFP
Summary
• Utilize blood products only when strongly indicated
• In addition to hemoglobin concentration Consider
comorbidity & rate of blood loss when giving RBCs
• Blood Products are scarce resources
• Remain conscious of complications: incompatibility,
bacterial and viral transmission, TRALI
• Each hospital should setup its own protocols