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ommended to repeat testing every 30–45minutes until the
hemorrhage is controlled [43]. However, during an acute
event, there can be signicant uctuations and variability
in measurements, and therefore laboratory tests should not
be used as the sole criteria to transfuse packed red blood
cells (PRBCs). Anesthesiologists often use these values in
conjunction with evidence of hypovolemia and oxygen debt
such as oliguria, refractory hypotension/tachycardia, and
arterial lactate to guide PRBC transfusions. Other clinical
endpoints of successful resuscitation include a maintained
mean arterial pressure ≥65mmHg, sustained mental status,
and acid-based status [53]. It would make sense that institutions that perform QBL would integrate these values into
transfusion algorithms. As it stands current transfusion practice is a delicate balance between under- and over-resuscitation, with negative consequences for both.
Cell Salvage
For a long time, the use of cell salvage during obstetric hemorrhage was considered controversial due to the possibility of
amniotic uid embolism (AFE) and maternal alloimmunization to fetal RBC antigens [43, 47, 48]. Newer data suggests
that the risk of AFE and maternal-fetal alloimmunization can
be decreased by use of leukocyte depletion lters (LDF) and
separation of suction for blood and amniotic uid prior to placental delivery [48]. Newer generation LDF are effective in
decreasing the number of amniotic uid proteins, bacterial
contamination, free hemoglobin, and potassium [48]. With
these new separate lters, large case series have demonstrated
a lower risk prole for salvaged blood, with no cases of AFE
reported, and are now supported in current guidelines.
However, obstetric hemorrhage is unpredictable, and a
major challenge is the inability to set up cell salvage for
every delivery [43]. As such, emphasis has been put on
identication of those at high risk for obstetric hemorrhage, including multiple gestation, placenta previa, and
invasive placentation [43]. The ACOG and ASA support
cell salvage in parturients in whom large blood loss is
expected (>20% of blood volume) [43, 48, 55]. Cell salvage may be especially useful in settings with limited
blood product availability or in specic obstetric populations including rare blood types and Jehovah’s Witnesses
[43, 47]. Any patient receiving salvaged blood should
undergo testing for fetal RBC exposure and administered
Rh immunoglobulin if clinically indicated [43].
Goal-Directed Therapy andViscoelastic Testing
An obstacle to avoiding coagulopathy in PPH lies in the limitations of traditional coagulation testing. Traditional coagula-
tion tests such as prothrombin time (PT), partial thromboplastin
time (PTT), and clauss brinogen assays do not give the full
picture of hemostasis during obstetric hemorrhage and only
provide guidance on initial clot formation [
recognized that these traditional coagulation tests are poor
predictors of bleeding [42]. During obstetric hemorrhage, PT
and PTT often remain within normal range even until blood
loss reaches 4000–5000ml [42]. Further, these tests may have
long turnaround times (60–90minutes); thus results are less
relevant in an acutely changing situation, and many clinicians
may decide to transfuse based on a protocol-based approach
or upon clinical judgment [42]. The issue with formulaic
transfusion is that not all obstetric hemorrhage is the same,
and patients may present with a variety of bleeding phenotypes. In many cases administering FFP may cause a dilutional coagulopathy, especially in the case of
hypobrinogenemia. Plasma transfusion must occur in large
volumes to be effective, which may lead to volume overload
or other transfusion reactions [
Viscoelastic testing via thromboelasography (TEG) or
thromboelastometry (ROTEM) overcome many of the shortfalls of traditional coagulation tests. TEG and ROTEM assess
and graphically display the viscoelastic properties from clot
formation to clot lysis, provide actionable information within
minutes, and allow for specic goal-directed therapy. An
important advantage of these assays is the quick turnaround
time, with an evaluation of clot kinetics generated in
5–10minutes [42]. Studies in the obstetric population have
shown both agreement and correlation between viscoelastic
testing parameters and traditional coagulation assays, with a
decreased time for data acquisition [60, 61]. This is especially true for measurements of brinogen, which has been
shown to be a prognostic indicator and therapeutic target in
obstetric hemorrhage. A FibTEM A5, which is the amplitude
of the FibTEM trace at 5minutes after the start of clot formation, measures the effect of brinogen by eliminating the
contribution of platelets to clot strength by way of the addition of cytochalasin D and has been shown to correlate with
plasma brinogen level [62]. A FibTEM A5 of 12mm correlates approximately with a plasma brinogen level of
2.2g/L [62]. In 2019, McNamara etal. presented 4years of
data on a ROTEM-guided algorithm for obstetric hemorrhage. The data compared the use of shock packs, which
included four units of PRBC, four units of FFP, and one dose
of platelets, and a ROTEM-guided algorithm with administration of brinogen concentrates. The data showed a signicant reduction in morbidity, specically transfusion-associated
circulatory overload (TACO) likely secondary to a decrease
in the transfusion of FFP, and a decrease in the number of
units and total volume of blood products transfused per
patient [62]. Comparator studies are ongoing, with early
results demonstrating that viscoelastic testing driven
algorithms can decrease the amount of products given
58, 59].
56, 57]. It is well-

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[49,63, 64], ICU admission [49, 63], hysterectomy [49], and
length of stay with decreased cost [49].
Pharmacologic Adjuncts inPostpartum
Hemorrhage
Maternal death from postpartum hemorrhage may occur
within hours of onset, especially in clinical settings without
robust blood banks or with the ability to collaborate with a
nearby blood bank [53]. Pharmacologic adjuncts including
antibrinolytics, brinogen concentrates, prothrombin complex concentrate (PCC), recombinant factor VIIa (rFVIIa),
and calcium may aid in both high and low blood bank
resource settings as adjuncts to massive transfusion
protocols.
Antibrinolytics
TXA is a potent antibrinolytic that binds to lysine residues in plasminogen and plasmin, preventing plasmin activation and clot breakdown. It is used widely in the
management of hemorrhage in the cardiac surgery and
trauma patient [43, 53] and is shown to signicantly reduce
perioperative blood loss and RBC transfusion without an
increase in thrombotic events [47]. The utility of TXA in
postpartum hemorrhage has been recognized since the
release of data from the World Maternal Antibrinolytic
Trial (WOMAN Trial) in 2017 [65]. Including over 20,000
parturients across almost 200 hospitals in 21 countries,
women randomized to receive 1g IV TXA after losing
500mL of blood had a decreased incidence of death from
bleeding (RR 0.64 [95%CI: 0.49–0.85 p = 0.045]) when
compared to placebo. If the TXA was administered within
3hours of delivery, maternal death was decreased by over
30%. Importantly, the WOMAN trial found no increase in
thromboembolic events or renal dysfunction in patients
who received TXA.The recommended treatment dose of
TXA is 1 g intravenously, with a second gram administered if bleeding continues after 30minutes, or if hemorrhage recurs within 24hours of delivery [48]. The WHO,
ACOG, and CMQCC now include TXA recommendations
in their obstetric hemorrhage guidelines [43]. Several
small RCTs and meta-analyses studying antibrinolytic
therapy in the postpartum period demonstrate that TXA
use is associated with a reduction in blood loss, decreased
need for additional uterotonic agents, and higher hemoglobin levels after 24hours [47]. Another unanswered questioned is whether one should wait for hemorrhage to start
as was the study design in the WOMAN trial or if it should
be given prophylactically for high-risk situations such as
placenta percreta.
Fibrinogen Concentrates
While brinogen has been identied as a biomarker for
severe PPH, the optimal brinogen concentration to prevent
coagulopathy is not known. However, the threshold of
200mg/dl has been shown to be predictive of progression to
further hemorrhage, has been used as a cut off value for
repletion, and is the currently recommended threshold for
repletion by the American Society of Anesthesiologists [51].
With regard to repletion strategy, it is important to note that
prophylactic treatment prior to the onset of hypobrinogenemia is an ineffective strategy [66, 67]. Therefore, to optimize transfusion management, rstly the measurement of
brinogen levels should occur rapidly, and, secondly,
brinogen- containing products must be readily available.
The rst issue can be overcome with rapid lab protocols or
viscoelastic testing if available. The second issue is that due
to high levels of brinogen present in term parturients, products such as FFP can dilute brinogen levels until the
extremes of blood loss.
Two therapeutic options are available for brinogen
replacement: cryoprecipitate and brinogen concentrate
[42]. The brinogen concentration in cryoprecipitate ranges
from 3 to 30g/L, leading to a potentially inconsistent effect,
and requires two to three freeze-thaw cycles prior to administration, which can potentially cause a delay in administration [42]. Also, cryoprecipitate is not virally inactivated and
is not available in all locations [68]. Fibrinogen concentrate
has been used as a rapid alternative for brinogen repletion
in obstetric hemorrhage [49, 63, 67]. Fibrinogen concentrates are a manufactured concentrated form of brinogen
produced from human plasma. It comes as a powder to be
reconstituted, does not require refrigeration, and therefore
may easily be stored near the patient in a controlled release
compartment system such as Pyxis [42]. Unlike cryoprecipitate, brinogen concentrates do not require cross-match
[45, 48] and have decreased risk of infectious complications
since viral activation and the removal of antigens and antibodies occurs during the manufacturing process [42, 48].
Appropriate brinogen concentrate therapy can prevent
unnecessary product transfusion and complications of transfusion such as volume overload and allergic reactions [45].
The cost of brinogen concentrate varies by location; however studies looking at the cost of utilizing brinogen concentrate instead of traditional MTP or shock packs have
found it to be either cost saving or cost neutral when taking
into account the complications from transfusion reactions
and the cost of wasted blood products [49, 63]. The costeffectiveness of brinogen concentrate and cryoprecipitate
in the management of severe obstetric hemorrhage should
be further explored [49]. A nal and important limitation of
brinogen concentrate is that unlike cryoprecipitate, brinogen concentrate contains no brin stabilizing factors or

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factor XIII, which in very large hemorrhages can cause
coagulopathy if not repleted.
Prothrombin Complex Concentrates
andRecombinant Activated Factor VIIa
The data for proper dosing and safety of PCCs in PPH is
limited [48]. They carry a major risk of thrombosis with their
usage, and clinical experience in the obstetric population are
limited to case reports in women who have extreme coagulation derangements or refractory hemorrhage [69–71]. The
advantages of PCCs lie in that they are standardized in their
composition and activity, unlike FFP in which factor composition and efcacy are highly variable. They are also stored at
room temperature and can have shelf-lives of over 36months,
which make them highly advantageous in areas with limited
blood bank resources. More data in the obstetric population
are needed before they can be considered for anything other
than severe life-threatening hemorrhage that is refractory to
all other therapies, as indicated in the ACOG hemorrhage
bundle [50].
In the setting of intractable obstetric hemorrhage, recombinant activated factor VIIa (rFVIIa) may be considered.
Like PCC, rFVIIa is associated with arterial and venous
thrombosis [47], continues to be recommended only as a last
ditch effort to stop life-threatening bleeding when all other
efforts have failed, and has no proven survival benet [48].
Although there is no optimal dose range for the parturient,
60–90 μg/kg IV is mentioned in guidelines [47]; however
lower doses including 40 μg/kg and 20 μg/kg have been
attempted and may carry less risk of thrombosis [72]. It
should be noted that women who receive rFVIIa during management of amniotic uid embolism may have worse outcomes compared to those who did not [73]. A novel topical
application of rFVIIa has been described in a ve patient
case series in patients with placenta previa [74]. Bleeding
was well-controlled in all cases; however, more data is
needed to determine both safety and efcacy of this
technique.
Calcium
Vigilance of maternal calcium levels is of paramount importance during obstetric hemorrhage. Calcium is needed for
adequate myocardial contractility as well as vascular tone.
Additionally, it is a co-factor in almost every step of coagulation and is necessary for hemostasis [75]. Calcium levels can
drop precipitously during obstetric hemorrhage due to hemodilution from non-calcium containing IV uids and from the
administration of citrated blood products that chelate calcium. Citrate from blood products can be cleared relatively
quickly by the liver; however, any hepatic impairment from
underlying or acute disease including hypotension or hypothermia can delay clearance and cause hypocalcemia. As
such, ionized calcium should be checked frequently and kept
in the normal physiologic range during any major obstetric
hemorrhage. In any case where calcium levels cannot be
monitored, pre-emptive repletion should be considered.
Lastly, both acidosis and hypothermia can have profound
negative impacts on hemostasis and coagulation. Coagulation
function diminishes once pH drops below 7.2, with prolongation of PT and PTT as well as diminished platelet function
[76, 77]. Interestingly, coagulation function remains impaired
upon pH neutralization with sodium bicarbonate administration which may have other deleterious effects on physiology
[78, 79]. It would seem based on this evidence that the best
way to ameliorate dysfunction by acidosis is to prevent its
onset through oxygen delivery optimization when possible.
Hypothermia, which can be associated with uid administration, insensible loss, and redistribution with induction of
anesthesia, can impair coagulation with a 10% drop in factor
activity level per 1°C drop in temperature [80]. Although
clinically signicant coagulopathy does not seem to appear
until core temperature drops below 33°C, efforts to warm
patients during resuscitation should begin early [81].
Maintaining core temperature through monitoring and warming efforts such as forced air warming and administering
warmed uids and blood products is well within the expertise of the anesthesiologist. Rapid infusion devices that
deliver large volumes of warm uid are often employed in
major surgical procedures and ought to be used in PPH when
indicated and should be readily available on the labor oor.
Conclusion
PPH management is a complex process requiring constant
vigilance and support from every discipline. The goals of the
anesthesiologist in these cases are to place invasive monitors
and lines, coordinate the administration of uterotonic agents,
direct transfusion practices including interpretation of POC
coagulation and lab tests, manage patient hemodynamics, as
well as optimize non-transfusion based therapies such that
the obstetrician can focus on surgical modalities to manage
the uterus and achieve hemostasis.
References
1. Callaghan WM, Kuklina EVBC.Trends in postpartum hemorrhage:
United States, 1994-2006. Am J Obs Gynecol. 2010;202(4):353,
e1-6.
2. Tuncalp O, Souza JP, GMI.New WHO recommendations on prevention and treatment of postpartum hemorrhage. Int J Gynaecol
Obstet. 2013;123(3):254–6.

240
https://t.me/medicina_free
C. B. Yen et al.
3. Say L, Chou D, Gemmill A, etal. Global causes of maternal death:
A WHO systemic analysis. Lancet Glob Heal. 2014;2(6):e323.
4. Committee on Practice Bulletins-Obstetrics. Practice bulletin no. 183: postpartum hemorrhage. Obstet Gynecol.
2017;130(4):e168–86.
5. Prevention and management of postpartum haemorrhage: green-top
guideline no. 52. BJOG 2017;124(5):e106–49.
6. Lyndon A, Lagrew D.CMQCC OB Hemorrhage Tootkit V 2.0.
7. Leduc D, Senikas V, Lalonde A, etal. Active management of the
third stage of labour: Prevention and treatment of postpartum hemorrhage. J Obs Gynaecol Canada [J D’obstétrique Gynécologie du
Canada]. 2009;31(10):980–93.
8. WHO recommendations for the prevention and treatment of postpartum haemorrhage. 2012.
9. Abdul-Kadir R, McLintock C, Ducloy A-S, etal. Evaluation and
management of postpartum hemorrhage: consensus from an international expert panel. Transfusion. 2014;54(7):1756–68.
10. Sentilhes L, Vayssière C, Deneux-Tharaux C, etal. Postpartum
hemorrhage: guidelines for clinical practice from the French
College of Gynaecologists and Obstetricians (CNGOF): In collaboration with the French Society of Anesthesiology and Intensive
Care (SFAR). Eur J Obs Gynecol Reprod Biol. 2016;198:12–21.
http://www.ncbi.nlm.nih.gov/pubmed/26773243
11. Mhyre JM, Shilkrut A, Kuklina EV, etal. Massive blood transfusion
during hospitalization for delivery in NewYork State, 1998–2007.
Obstet Gynecol. 2013;122(6):1288–94. https://doi.org/10.1097/
AOG.0000000000000021.
12. Sheiner E, Sarid L, Levy A, Seidman DS, Hallak M. Obstetric
risk factors and outcome of pregnancies complicated with
early postpartum hemorrhage: A population-based study. J
Matern Fetal Neonatal Med. 2005;18(3):149–54.
org/10.1080/14767050500170088.
13. Bateman BT, Berman MF, Riley LE, Leffert LR.The epidemiology
of postpartum hemorrhage in a large, nationwide sample of deliveries. Anesth Analg. 2010;110(5):1368–73. https://doi.org/10.1213/
ANE.0b013e3181d74898.
14. Ring L, Landau R.Postpartum hemorrhage: anesthesia management. Semin Perinatol. 2019;43(1):35–43.
15. SOAP Postpartum Hemorrhage Protocol. 2019.
16. Salati J, Leathersich S, Williams M, Cuthbert A, Tolosa J.
Prophylactic oxytocin for the third stage of labour to prevent postpartum haemorrhage. Cochrane Database Syst Rev. 2019 April;
29(4):CD001808. PMID: 31032882
17. Goffman D, Ananth CV, Fleischer A, D’Alton M, Lavery JA, et al.
The New York State Safe Motherhood Initiative: EarlyImpact of
Obstetric Haemorrhage Bundle Implementation. Am J. Perinatol.
2019 Nov; 36(13):1344–50. PMID:30609429
18. WHO Recommendations for the prevention and treatment of
postpartum hemorrhage. WHO Recomm Prev Treat Postpartum
Haemorrhage. 2012.
19. Westhoff G, Cotter AM, Tolosa JE. Prophylactic oxytocin for
the third stage of labour to prevent postpartum haemorrhage.
Cochrane Database Syst Rev. 2013;10:CD001808. https://doi.
org/10.1002/14651858.CD001808.pub2
20. Gallos ID, Williams HM, Price MJ, et al. Uterotonic agents for
preventing postpartum haemorrhage: a network meta-analysis.
Cochrane Database Syst Rev. 2018;4:CD011689. https://doi.
org/10.1002/14651858.CD011689.pub2.
21. Roth JV. Some unanswered questions about temperature management. Anesth Analg. 2009;109(5):1695–9. https://doi.org/10.1213/
ANE.0b013e3181b763ae.
22. Harber CR, Levy DM, Chidambaram S, Macpherson MB. Lifethreatening bronchospasm after intramuscular carboprost for
postpartum haemorrhage. BJOG. 2007;114(3):366–8. https://doi.
org/10.1111/j.1471-0528.2006.01227.x.
.
https://doi.
23. Butwick AJ, Carvalho B, Blumenfeld YJ, El-Sayed YY, Nelson LM,
Bateman BT.Second-line uterotonics and the risk of hemorrhagerelated morbidity. Am J Obstet Gynecol. 2015;212(5):642.e1-7.
https://doi.org/10.1016/j.ajog.2015.01.008.
24. Magee LA, Namouz-Haddard S, Cao V, Koren G, von Dadelazen
P. Labetolol for hypertension in pregnancy. Expert Opin Drug Saf.
2015;14(3):453–61. PMID:25692529.
25. Sumikura H, Inada E. Uterotonics and tocolytics for anesthesiologists. Curr Opin Anaesthesiol. 2016;29(3)282–7. PMID 26974052.
26. Allen R, O’Brien BM.Uses of misoprostol in obstetrics and gynecology. Rev Obstet Gynecol. 2009;2(3):159–68.
nlm.nih.gov/pubmed/19826573
27. Novartis Pharmaceuticals Corporation. Methylergonovine
drug label.
label/2012/006035s078lbl.pdf
28. Carboprost tromethamine. National Center for Biotechnology
Information PubChem Database.
pound/Carboprost-tromethamine
29. Shahin Y, Pang CL. Endovascular interventional modalities for
haemorrhage control in abnormal placental implantation deliveries:
a systematic review and meta-analysis. Eur Radiol. 2018. https://
doi.org/10.1007/s00330-017-5222-0
30. Pan Y, Zhou X, Yang Z, Cui S, De W, Sun L. Retrospective
cohort study of prophylactic intraoperative uterine artery embolization for abnormally invasive placenta. Int J Gynaecol Obstet.
2017;137(1):45–50. https://doi.org/10.1002/ijgo.12090.
31. Aoki M, Tokue H, Miyazaki M, Shibuya K, Hirasawa S, Oshima
K. Primary postpartum hemorrhage: outcome of uterine artery
embolization. Br J Radiol. 2018:20180132. https://doi.org/10.1259/
bjr.20180132.
32. Kim J-E, So YH, Kim BJ, Kim SM, Choi YH, Sung CK.Postpartum
hemorrhage from non-uterine arteries: clinical importance of their
detection and the results of selective embolization. Acta Radiol.
2017: https://doi.org/10.1177/0284185117738547.
33. Baird E. Identication and management of obstetric hemorrhage.
Anesth Clin. 2017;35(1):15–34.
34. Kodkany B, Derman R. Pitfalls in assessing blood loss and decision to transfer. In: Lynch C, Keith L, Lalonde A, Karoshi M, editors. A Textbook of Postpartum Hemorrhage. Dumfries: Sapiens
Publishing; 2006. p.35–3.
35. Bills VL, Salmon AH, Harper SJ, et al. Impaired vascular permeability regulation caused by the VEGF
in pre-eclampsia. BJOG. 2011;118(10):1253–61. https://doi.
org/10.1111/j.1471-0528.2011.02925.x.
36. Dai D-M, Cao J, Yang H-M, etal. Hematocrit and plasma albumin levels difference may be a potential biomarker to discriminate
preeclampsia and eclampsia in patients with hypertensive disorders of pregnancy. Clin Chim Acta. 2017;464:218–22. https://doi.
org/10.1016/j.cca.2016.12.001
37. Hamada SR, Rosa A, Gauss T, et al. Development and validation of a pre-hospital “Red Flag” alert for activation of intrahospital haemorrhage control response in blunt trauma. Crit Care.
2018;22(1):113.
38. Javali RH, Ravindra P, Patil A, etal. A clinical study on the initial
assessment of arterial lactate and base decit as predictors of outcome in trauma patients. Indian J Crit Care Med. 2017;21(11):719–
25. https://doi.org/10.4103/ijccm.IJCCM_218_17.
39. Ryoo SM, Lee J, Lee Y-S, etal. Lactate level versus lactate clearance for predicting mortality in patients with septic shock dened
by sepsis-3. Crit Care Med. 2018;46(6):e489–95.
org/10.1097/CCM.0000000000003030
40. Shah A, Chisolm-Straker M, Alexander A, Rattu M, Dikdan S,
Manini AF. Prognostic use of lactate to predict inpatient mortality in acute gastrointestinal hemorrhage. Am J Emerg Med.
2014;32(7):752–5. https://doi.org/10.1016/j.ajem.2014.02.010.
https://www.accessdata.fda.gov/drugsatfda_docs/
https://doi.org/10.1186/s13054-018-2026-9.
.
. Accessed 22 Aug 2019.
pubchem.ncbi.nlm.nih.gov/com-
. Accessed 22 Aug 2019.
.
.
.
https://www.ncbi.
b splice variant
165
https://doi.

23 Obstetrical Blood Management
https://t.me/medicina_free
241
41. Collins PW, Bell SF, de Lloyd L, Collis RE.Management of postpartum haemorrhage: from research into practice, a narrative review
of the literature and the Cardiff experience. Int J Obstet Anesth.
2019;37:106–17.
42. Shah A, Collis RE. Managing obstetric haemorrhage: is it time for
a more personalised approach? Anaesthesia. 2019;74(8):961–4.
https://doi.org/10.1111/anae.14661. PMID:30950513.
43. O’Brien KL, Shainker SA, Lockhart EL.Transfusion management
of obstetric hemorrhage. Transfus Med Rev. 2018;32(4):249–55.
https://doi.org/10.1016/j.tmrv.2018.05.003.
44. Butwick AJ, Goodnough LT. Transfusion and coagulation management in major obstetric hemorrhage. Curr Opin
Anaesthesiol. 2015;28(3):275–84. https://doi.org/10.1097/
ACO.0000000000000180
45. Sahin AS, Ozkan S.Treatment of obstetric hemorrhage with brinogen concentrate. Med Sci Monit. 2019;25:1814–21.
org/10.12659/msm.914234
46. Collis RE, Collins PW.Haemostatic management of obstetric haemorrhage. Anaesthesia. 2015;70:78–86.
anae.12913
47. Baird EJ.Identication and management of obstetric hemorrhage.
Anesthesiol Clin. 2017;35(1):15–34.
anclin.2016.09.004.
48. Higgins N, Patel SK, Toledo P.Postpartum hemorrhage revisited: new
challenges and solutions. Curr Opin Anaesthesiol. 2019;32(3):278–
84. https://doi.org/10.1097/aco.0000000000000717.
49. Snegovskikh D, Souza D, Walton Z, etal. Point-of-care viscoelastic
testing improves the outcome of pregnancies complicated by severe
postpartum hemorrhage. J Clin Anesth. 2018;44:50–6. https://doi.
org/10.1016/j.jclinane.2017.10.003
50. American College of Obstetricians and Gynecologists. Maternal
safety bundle for obstetric hemorrhage. 2015;(November):1–29.
https://www.acog.org/-/media/Districts/District-II/Public/SMI/v2/
HEMSlideSetNov2015.pdf?dmc=1&ts=20190625T1556366928.
51. Practice guidelines for perioperative blood management.
Anesthesiology. 2015;122(2):241–75. https://doi.org/10.1097/
aln.0000000000000463.
52. Einerson BD, Stehlikova Z, Nelson RE, Bellows BK,
Kawamoto K, Clark EAS. Transfusion preparedness strategies for obstetric hemorrhage: a cost-effectiveness analysis.
Obstet Gynecol. 2017;130(6):1347–55. https://doi.org/10.1097/
AOG.0000000000002359.
53. Kogutt BK, Vaught AJ. Postpartum hemorrhage: blood product management and massive transfusion. Semin Perinatol.
2019;43(1):44–50.
54. Lyndon A, Lagrew D, Main E, Cape V. A California toolkit to
transform maternity care improving ealth care response to obstetric
hemorrhage version 2. 0 a California quality improvement toolkit
THE OBSTETRIC HEMORRHAGE TASK FORCE improving
health care response to obstetric hemorrhage Versi. 2015.
55. Wong CA, Toledo P. To salvage (routinely) or not to salvage:
that is the question. Anaesthesia. 2019;74(8):957–60. https://doi.
org/10.1111/anae.14667. PMIAD:30963553.
56. De Lloyd L, Bovington R, Kaye A, etal. Standard haemostatic
tests following major obstetric haemorrhage. Int J Obstet Anesth.
2011;20(2):135–41. https://doi.org/10.1016/j.ijoa.2010.12.002.
57. Larsen JB, Hvas AM.Predictive value of whole blood and plasma
coagulation tests for intra- and postoperative bleeding risk: a systematic review. Semin Thromb Hemost. 2017;43(7):772–805.
https://doi.org/10.1055/s-0037-1602665.
58. Solomon C, Collis RE, Collins PW.Haemostatic monitoring during
postpartum haemorrhage and implications for management. Br J
Anaesth. 2012;109(6):851–63. https://doi.org/10.1093/bja/aes361.
59. Hendrickson JE, Roubinian NH, Chowdhury D, Brambilla
D, Murphy EL, Wu Y, Ness PM, Gehrle EA, Snyder EL,
https://doi.org/10.1016/j.ijoa.2018.08.008.
.
https://doi.
.
https://doi.org/10.1111/
.
https://doi.org/10.1016/j.
.
https://doi.org/10.1053/j.semperi.2018.11.008.
Hauser RG, Gottschall JL, Kleinman S, Kakaiya R, Strauss
R. Incidence of transfusion reactions: a multi-center study utilizing systematic active surveillance and expert adjudication.
Transfusion. 2016;56(10):2587–96.
CCM.0b013e31823da96d.Hydrogen
60. Katz D, Hamburger J, Batt D, Zahn J, Beilin Y.Point-of-care brinogen testing in pregnancy. Anesth Analg. 2018;XXX(Xxx):1–3.
https://doi.org/10.1213/ane.0000000000003301.
61. Girard T, Mörtl M, Schlembach D. New approaches to obstetric
hemorrhage: the postpartum hemorrhage consensus algorithm. Curr
Opin Anaesthesiol. 2014;27(3):267–74. https://doi.org/10.1097/
ACO.0000000000000081
62. McNamara H, Kenyon C, Smith R, Mallaiah S, Barclay P. Four
years’ experience of a ROTEM ® -guided algorithm for
coagulopathy in obstetric haemorrhage. Anaesthesia.2019;74(8):
https://doi.org/10.1111/anae.14628. PMID:30950521.
984–91.
63. Mallaiah S, Barclay P, Harrod I, Chevannes C, Bhalla A.Introduction
of an algorithm for ROTEM-guided brinogen concentrate
administration in major obstetric haemorrhage. Anaesthesia.
2015;70(2):166–75.
64. Mallaiah S, Chevannes C, McNamara H. Use of ROTEM® in
major obstetric haemorrhage. Anaesthesia. 2015;70(6):759–60.
https://doi.org/10.1111/anae.13103.
65. Shakur H, Roberts I, Fawole B, etal. Effect of early tranexamic
acid administration on mortality, hysterectomy, and other morbidities in women with post-partum haemorrhage (WOMAN):
an international, randomised, double-blind, placebo-controlled
trial. Lancet. 2017;389(10084):2105–16. https://doi.org/10.1016/
S0140-6736(17)30638-4.
66. Wikkelsø AJ, Edwards HM, Afshari A, etal. Pre-emptive treatment
with brinogen concentrate for postpartum haemorrhage: randomized controlled trial. Br J Anaesth. 2015;114(4):623–33. https://doi.
org/10.1093/bja/aeu444.
67. Collins PW, Cannings-John R, Bruynseels D, et al.
Viscoelastometric-guided early brinogen concentrate replacement
during postpartum haemorrhage: OBS2, a double-blind randomized controlled trial. Br J Anaesth. 2017;119(3):411–21.
org/10.1093/bja/aex181.
68. McDonnell NJ, Browning R. How to replace brinogen in
postpartum haemorrhage situations? (Hint: Don’t use FFP!).
Int J Obstet Anesth. 2018;33:4–7. https://doi.org/10.1016/j.
ijoa.2017.08.008.
69. Nakauchi-Tanaka T, Sohda S, Someya K, Kono K, Hamada H,
Yoshikawa H.Acquired haemophilia due to factor VIII inhibitors
in ovarian hyperstimulation syndrome: case report. Hum Reprod.
2003;18(3):506–8. https://doi.org/10.1093/humrep/deg112.
70. Matsuoka A, Sasaki H, Sugimori C, Hirabuki S, Hoshiba T, Fujiwara
H. Acquired hemophilia A manifesting as plasma transfusionuncontrolled severe bleeding 2 weeks after chorioamnionitis- induced
abortion. J Obstet Gynaecol Res. 2017;43(4):763–7. https://doi.
org/10.1111/jog.13270.
71. Glynn JC. Prothrombin complex for massive obstetric haemorrhage. Anaesthesia. 2007;62:202–3.
72. Shaylor R, Weiniger CF, Austin N, et al. National and international guidelines for patient blood management in obstetrics: a
qualitative review. Anesth Analg. 2017;124(1):216–32. https://doi.
org/10.1213/ANE.0000000000001473.
73. Leighton Barbara L, Wall Michael H, Lockhart Ellen M,
Phillips Louise E, Zatta AJ. Use of recombinant factor VIIa
in patients with warfarin-associated intracranial hemorrhage.
Anesthesiology. 2011;115(6):1201–8. http://ovidsp.ovid.com/
ovidweb.cgi?T=JS&PAGE=reference&D=emed7&NEWS=N
&AN=2005358465.
74. Schjoldager BTBG, Mikkelsen E, Lykke MR, etal. Topical application of recombinant activated factor VII during cesarean delivery
.
https://doi.org/10.1111/anae.12859.
https://doi.org/10.1097/
.
treatment of
https://doi.

242
https://t.me/medicina_free
C. B. Yen et al.
for placenta previa. Am J Obstet Gynecol. 2017;216(6):608.e1–5.
https://doi.org/10.1016/j.ajog.2017.02.024.
75. Palta S, Saroa R, Palta A. Overview of the coagulation system. Indian J Anaesth. 2014;58(5):515–23.
org/10.4103/0019-5049.144643
76. Ganter MT, Pittet JF. New insights into acute coagulopathy in
trauma patients. Best Pract Res Clin Anaesthesiol. 2010;24(1):15–
25. https://doi.org/10.1016/j.bpa.2009.09.010.
77. Meng ZH, Wolberg AS, Monroe DM, Hoffman M.The effect of
temperature and pH on the activity of factor VIIa: implications for
the efcacy of high-dose factor VIIa in hypothermic and acidotic
patients. J Trauma. 2003;55(5):886–91.
TA.0000066184.20808.A5
.
https://doi.org/10.1097/01.
.
https://doi.
78. Graf H, Leach W, Arieff AI.Evidence for a detrimental effect of
bicarbonate therapy on hypoxic lactic acidosis. Science (80- ).
1984;227(4688):754–5.
79. Martini WZ, Dubick MA, Pusateri AE, Park MS, Ryan KL, Holcomb
JB.Does bicarbonate correct coagulation function impaired by acidosis in swine? J Trauma– Inj Infect Crit Care. 2006;61(1):99–106.
https://doi.org/10.1097/01.ta.0000215574.99093.22.
80. Elmer J, Wilcox SR, Raja AS. Massive transfusion in traumatic
shock. J Emerg Med. 2013;44(4):829–38.
jemermed.2012.11.025
81. De Robertis E, Kozek-Langenecker SA, Tufano R, Romano GM,
Piazza O, Zito Marinosci G. Coagulopathy induced by acidosis, hypothermia and hypocalcaemia in severe bleeding. Minerva
Anestesiol. 2015;81(1):65–75.
.
https://doi.org/10.1016/j.

Pediatric Blood Management
https://t.me/medicina_free
MichelleM.Sheth, MeeraGangadharan, DestinyF.Chau,
NormaJ.Klein, andReniraRugnath
24
Introduction
Pediatric patient blood management (PBM) is an
interdisciplinary, evidence-based approach to improving
patient outcomes through anemia prevention and treatment,
optimization of hemostasis, and minimization of perioperative
blood loss. These practices are well established in the adult
literature and are supported by various health organizations
including the World Health Organization, the American
Society of Anesthesiology, the Australian National Blood
Authority, and the European Society of Anesthesiology.
However, while these practices have been well established
for the adult patient population, pediatric PBM lags behind
[1–5].
In general, the anesthesiology literature reafrms that
children are not little adults and that unique differences must
be recognized for successful outcomes. Adult PBM strategies may not be directly extrapolated to pediatric patients, so
guidelines addressing patient physiology and disease processes are necessary. Pediatric patients must always be
treated with attention to unique features of each growth
phase. For instance, neonates and children have higher
M. M. Sheth (*)
UMMC, Department of Anesthesiology, Jackson, MS, USA
e-mail: Msheth2@umc.edu
M. Gangadharan
Department of Anesthesiology, UAMS, Little Rock, AR, USA
D. F. Chau
Department of Anesthesiology and Pain Medicine, Arkansas
Children’s Hospital, University of Arkansas for Medical Sciences,
Little Rock, AR, USA
N. J. Klein
University of California Medical Center Davis (UCDMC),
University of California, Davis, Department of Anesthesiology &
Pain Medicine, Sacramento, CA, USA
R. Rugnath
University of Mississippi Medical Center, School of Medicine,
Jackson, MS, USA
average hemoglobin concentrations and oxygen requirements than adults [6]. Additionally, transfusion practices
may differ signicantly between children’s hospitals [7]. In
response, recent steps have been taken to standardize methodology. Comprehensive standards were released in 2010 by
the Society of Advancement of Blood Management (a
Pediatric section was added in 2016), who dene PBM as,
“the timely application of evidence-based medical and surgical concepts designed to maintain hemoglobin concentration, optimize hemostasis, and minimize blood loss as to
improve patient outcome” [1]. Blood transfusions are not
without risk, so the decision to transfuse must involve a consideration of the risks and benets [8]. Thus, this chapter will
describe pediatric physiology from the premature neonate
through adolescence, the preoperative evaluation, blood conservation strategies, surgical discipline-specic considerations, and evidence-based transfusion guidelines.
History ofPediatric Blood Transfusion
Among the early documented experiments with blood transfusions is the transfusion to a 15-year-old with fever who
became weak and pale after leeching proved unsuccessful.
He was transfused with blood from a lamb donor. He survived, but the donor succumbed. This sacricial act was
repeated a few more times with only one recipient surviving
the procedure. These transfusions were provided by JeanBaptiste Denys, the personal physician to King Louis XIV in
the seventeenth century. Subsequently, Jean-Baptiste was
charged with murder, and the procedure was banned [9].
Centuries passed before blood transfusions were conducted
in the pediatric patient population. The rst neonatal blood
transfusion occurred on March 4, 1908, at a New York
children’s hospital. The newborn was delivered with forceps; however, within 12 hours, the neonate developed a
tongue hematoma and facial swelling. She became febrile,
© Springer Nature Switzerland AG 2021
C. S. Scher et al. (eds.), Essentials of Blood Product Management in Anesthesia Practice,
https://doi.org/10.1007/978-3-030-59295-0_24
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restless, and pale, and it became evident a transfusion was
required. Her father was the donor for the transfusion, and
both the neonate and the father survived. With that, the foundation for the practice of pediatric blood transfusion was
established [10].
Anatomical andPhysiological Characteristics
ofBlood inPremature Neonates, Infants,
andChildren
Many anatomic, physiologic, and hematologic differences
between children and adults, even between different age
groups, have been identied. The following sections will discuss current standards in pediatric PBM and transfusion
guidelines in light of these differences.
Fetal Blood Development
To understand physiological characteristics of blood, one
must rst review fetal blood development. A fetus attains
viability between the 23rd and 26th weeks of gestation. The
hematologic system of these fragile patients differs considerably from that of an older child. In utero, erythrocyte production begins in the yolk sac (at 3–6weeks of gestation), then
it migrates to the liver (6–22weeks of gestation) and nally
to the bone marrow. Erythrocyte production and maturation
in the fetus is controlled by growth factors produced by the
fetus, rather than maternally transferred factors.
Erythropoietin is produced by the liver in utero. After birth,
the kidneys become the site of erythropoietin synthesis [11].
The quantity of iron in the fetus increases throughout gestation. Preterm infants have less iron than full-term infant [12].
In extremely premature infants, the hematologic system is
frequently supported with blood component transfusions and
nutritional support.
may be more indicative of signicant blood loss than hypotension and tachycardia. In the case of premature infants and
neonates, signicant anemia may be reected in nonspecic
signs such as poor feeding, slow weight gain, apnea, bradycardia, and decreased activity. Furthermore, the neonatal
heart contains proportionally less contractile tissue and has a
limited ability to increase cardiac output in the face of a
hemorrhage-
induced reduction in oxygen carrying capacity
[14, 15].
Normal Red Blood Cell Parameters inPreterm
andTerm Neonates
The normal red blood cell parameters listed in Table 24.1
were obtained by analyzing a very large database (17,634
tests performed on 12,016 neonates in western USA) who
had blood tests during their routine care [11]. Only tests
from neonates who were expected to have normal values
were included. Mean corpuscular volume (MCV) and mean
corpuscular hemoglobin (MCH) decreased in a linear fashion with increasing gestational age. Mean corpuscular
hemoglobin concentration (MCHC) does not change based
on gestational age. The hemoglobin and hematocrit increase
from 22 weeks to 40 weeks gestation. The hemoglobin
increases by 0.21 g/dl and the hematocrit by 0.64% for
every week increase in gestational age. In neonates
35 weeks to 42 weeks of gestation, the hematocrit levels
increase by 3.6 +/− 0.5% in the rst 4 hours after birth,
secondary to uid shifting out of the intravascular space.
Hematocrit levels remained unchanged in the same time
period for neonates 29 to 34 weeks of gestation but are
reduced by 6 +/− 0.3% in neonates less than 29 weeks of
gestation [16].
Neonatal Hemoglobin Levels andOxygen
Dissociation
Blood Volume
Estimation of a child’s blood volume and blood loss may be
difcult, as children have an increased blood volume: body
mass ratio compared to adults. The increased blood volume
varies with age, such that the blood volume of a child may be
as high as 90, 80, and 70 mL/kg at birth, 1 month, and 5
years, respectively. During active bleeding, the hemoglobin
and hematocrit values may not accurately predict blood cell
mass. Therefore, a child may maintain a normal blood pressure value in spite of a 15–20% blood volume loss [13].
Mottling, altered consciousness, and delayed capillary rell
>3 seconds are likely to precede evident hypotension, but a
narrowed pulse pressure and loss of arterial pulse contour
At birth, a term neonate’s hemoglobin is ~70% hemoglobin
F (HgbF) and~30 hemoglobin A (HgbA) [15]. The p50 of
HgbF is 18mmHg, but the p50 in HgbA is 25mmHg. Thus,
HgbF is associated with a leftward shift in the oxyhemoglobin dissociation curve, or an increased oxygen
afnity. This increased oxygen afnity results from HgbF’s
decreased afnity for 2,3 diphosphoglycerate (2,3-DPG),
Table 24.1 Normal red cell parameters in preterm and term neonates
Parameter <25weeks 40weeks
MCV
MCH
MCHC
Table information from: Christensen etal. [72]
119 +/− 7 106 +/− 4
40 +/− 2pg 36 +/− 2pg
34 +/− 1g/dl 34 +/− 1g/d

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245
the stabilizer of the deoxyhemoglobin state. Although this
is associated with an increased ability of the fetus to extract
oxygen from the maternal placental circulation, it is a theoretical disadvantage in the extrauterine environment under
conditions of hypoxic stress. During the rst several months
of life, an infant’s hemoglobin levels fall from 14 to 20g/
dL to a mean~11g/dL in term infants and as low as ~7g/
dL in preterm infants. This “physiologic anemia” is the
result of decreased erythropoietin production and the
shorter life span of HgbF (e.g., 90 vs. 120days for HgbA)
[14]. This transient but functional anemia tends to occur
earlier and to a more notable degree in preterm infants. In
preterm infants, the switch from fetal hemoglobin production to predominantly HgbA production occurs at the postconceptional age of 37 weeks. It is unaffected by the
duration of time that the infant spends in the extrauterine
environment [17]. Also, neonatal erythropoietin is produced in monocytes, the adrenal cortex, and the kidney, but
postnatally, it is produced in the peritubular renal cells. A
confounding issue for sick neonates is that they often
undergo repeated blood testing, amounting to 0.8–3.1mL/
kg/day blood loss [18]. For example, a 0.5mL blood sample in a 1kg neonate, if extrapolated to a 70kg patient, is a
35mL blood sample, something rarely removed at one time
in an adult patient [19].
Coagulation System Development
The coagulation system undergoes developmental changes
as the fetus grows in utero and changes continue after birth.
Coagulation factors do not cross the placenta; instead, they
are synthesized by the fetus and can be detected as early as
10 weeks of gestation. Challenges to studying developmental hemostasis in the newborn include small sample
sizes in studies, the need for small volumes of blood for
assays, and the different physiological states of test subjects especially the premature neonatal population.
Diagnosis of bleeding disorders in newborns requires an
understanding of normal values of coagulation factor levels
in these patients. Table 24.2 shows how various levels of
coagulation proteins in newborn infants differ from adult
values. Although newborns have lower levels of coagulation factors than adults, their hemostatic system appears to
function without spontaneous hemorrhage. Extremely low
birth weight infants, at a corrected age of 6months, achieve
the same levels of factor II, V, VII, and X as healthy fullterm infants of the same age. Antithrombin III, protein C,
and protein S showed the same pattern of development as
that of term infants [20]. These ndings have clinical implications. Newborns are fairly resistant to heparin probably
because of low levels of AT III.Since APTT is prolonged
in infants, one should monitor factor Xa activity to titrate
Table 24.2 Various tests of coagulation and levels of coagulation pro-
teins in premature vs term newborns
Various tests of coagulation and levels of coagulation proteins in
newborn infants
Test 30–36weeks Term
Fibrinogen = =
II
VII = = by day 5
IX
X
XI
XII
Prekallikrein
HMWK
V = by day 5 of
VIII
VwF
XIII = by day 5 of
Plasminogen
Antithrombin III
Heparin cofactor II
Protein S
Protein C
α
Macroglobulin ↑ ↑
2
C1 INH
Antiplasmin ↓
α
2
Antitrypsin
α
1
Table information from: Andrew M 1987 [
[74]
HMWK high molecular weight kininogen, VwF von Willebrand factor,
C1 INH C1 esterase inhibitor
↓ ↓
↓ ↓
↓ ↓
↓ ↓
↓ ↓
↓ ↓
↓
life
↑ ↑
↑ ↑
life
↓ ↓
↓ ↓, = by
↓ ↓
↓ ↓
↓ ↓
↓ ↓
= =
73], and Andrew M 1988
= by 1 month
= by day 5 of
life
= by day 5 of
life
3months
= by day 5
unfractionated heparin in this age group [21]. Homozygous
deciency of factor II, X, and XI can be difcult to diagnose because the lower limits of normal coincide with the
levels found in these decient states. Homozygous factor
V, VII, IX, XIII and brinogen deciency can be diagnosed
at birth, because the levels in the disease state are much
lower than the lower limit of normal in this age group.
Moderate and severe forms of factor VIII deciency (hemophilia A) can also be diagnosed in the newborn period. Von
Willebrand factor levels are high in the neonate, and there
is a greater percentage of the efcacious high molecular
weight multimers. Hence only severe forms of von
Willebrand’s disease are likely to be diagnosed in the newborn period. Neonatal brinogen is different from the adult
form. Thromboelastography (TEG) studies indicate that a
dysfunctional state of brinogen exists in infancy [22].
Neonatal plasminogen function is also less effective than
its adult counterpart. However, tissue plasminogen activator inhibitor levels are high. This indicates that brinolytic
activity is attenuated in the neonate compared to the
adult[23].

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Table 24.3 Diseases that require special consideration
Disease
process Abnormality Recommendation
Sickle cell
disease
Anemia of
prematurity
Liver failure Coagulation
Cirrhosis Thrombocytopenia, low
Renal failure Anemia of chronic
Congenital
heart disease
(cyanotic)
Noncyanotic
heart disease
Pediatric
oncology
Low hematocrit, iron
overload
Low hematocrit, low
iron stores
abnormalities. Anemia
of chronic disease
serum albumin, clotting
factors II, VII, IX, X
abnormalities
disease
Decreased oxygen
delivery
Intracardiac shunting,
cardiac failure
Pancytopenia,
thrombocytopenia,
aplastic anemia
Threshold of Hb 10g/dL
prior to surgery requiring
general anesthesia if at
risk of critical illness [25]
Limit preoperative blood
draws; add iron
supplementation [
Coagulation lab tests
prior to surgery to assess
baseline [26]
Platelet and FFP
+/− cryoprecipitate
administration
preoperatively if indicated
by test results or clinical
coagulopathy [
Erythropoiesisstimulating agents [4]
Threshold of Hb 9g/dL if
adequate oxygenation and
normal end organ
perfusion [
Threshold of Hb 7g/dL if
19, 27]; 8g/dL if
stable [
clinical signs of
symptomatic anemia [27]
Preoperative labs and
appropriate transfusion
[28]
19]
26]
25, 27]
Preoperative Assessment
Preoperative assessment to stratify hemorrhage risk is important. Neonates and infants are less tolerant of blood loss compared to older children and adults, and signicant blood loss
may go unrecognized. Poor hematopoiesis with reduced
erythropoietin levels and production, repeat blood draws,
and poor iron availability contribute to the high rate of anemia seen in critically ill children [24]. Specic disease processes that require special preoperative consideration are
detailed in Table24.3. The impact of each of these conditions
on the requirement for an allogeneic blood transfusion may
vary depending on the patient’s age and disease severity.
Estimating Allowable Blood Loss
Prior to all surgeries, it is important to assess the child’s tolerance for and likelihood of requiring a blood transfusion. A
restrictive red blood cell (PRBC) transfusion threshold in the
adult patient population is associated with unchanged, if not
improved, morbidity and mortality [29]. Application of similar
thresholds in the pediatric patient population, along with nutrition and anemia support, is thought to produce similar outcomes [30–34].
Table 24.4 Calculation technique for estimated blood volume (EBV)
Estimated blood volume calculation
Age Estimated blood volume (EBV)
Preemies 90–100mL/kg
Term neonate to 3months 80–90mL/kg
>3months of age to 3years 70–80mL/kg
>3years of age 70mL/kg
Estimating the maximum allowable blood loss requires
calculation of the child’s estimated blood volume (EBV),
which is a product of both age and weight. This is described
in Table24.4 and Eq.24.1.
Equation 24.1 The maximum allowable blood loss
(MABL) is a function of the EBV, the patient’s initial hematocrit (H0), and the minimal or target hematocrit (H1)
MABL
EBV
H
0
(24.1)
Perioperative Conservation Strategies
inPediatric Patients
PBM Standards andGoals
Due to these anatomical, physiological, and hematological variances, special considerations and strategies should
be employed during the use of PBM tactics. Recent data
highlighting the serious hazards of allogeneic blood transfusions have contributed to the development of perioperative patient blood management (PBM) and conservation
strategies. Patient blood management is most useful for
procedures with expected severe blood loss, as it focuses
on blood conservation and preventative measures and has
been shown to reduce blood product transfusions, mortality, and costs [35, 36]. However, dening PBM standards
for infants and children is much more challenging than for
adults, as transfusion practices vary considerably by
patient categories, conditions, and settings. Therefore, in
order to develop and implement an institutional pediatric
PBM program as supported as its adult-centered counterpart, multidisciplinary health professionals and administrative support system involvement is critical, with proper
education for the involved team members an essential factor for its success. The team should include the
Anesthesiology, Surgery, Pharmacy, Transfusion Services,
ICU, and administrative support. PBM goals involve optimizing and maintaining hemoglobin levels, optimizing
hemostasis, minimizing blood loss, and improving patient
outcomes.
Updated clinical and administrative standards for pediatric PBM were recently published by The Society for
Advancement of Blood Management [1]. It is urged that a
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