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syndrome. In type 2 diabetes, EC dysfunction begins before
the clinical onset of diabetes [66–68]. Patients with insulindecient diabetes (type 1) have multiple EC dysfunctions.
EC dysfunction resulting in dysregulation of vascular tone,
organ perfusion derangement, inhibition of inammation/
trans-endothelial transport of blood solutes, prevention of
coagulation, and initiation of angiogenesis [68–75]. High
fat diet has been shown to impair delivery of insulin to the
interstitial space causing a dysfunction in endothelial insulin
signaling [73]. Hyperglycemia causes mitochondrial fragmentation, and dysfunction leading to increased mitochondrial reactive oxygen species (ROS) production and vascular
tone dysregulation, which is secondary to rapid breakdown
of nitric oxide (NO) [73, 76, 77]. This has been suggested
as the etiology of EC dysfunction in patients with diabetes.
However, various studies have shown it is multifactorial and
not just hyperglycemia (Fig.22.13).
Perivascular adipose tissue (PVAT) found in the abdomen
and blood vessels, have been described to control insulin
sensitivity and endothelial function. They have shown to be
critically involved in the regulation of local vascular tone and
inammation [68, 79–81]. PVAT is reported to be impaired
in obesity and type 2 diabetes [70, 77, 82]. PVAT inammation has been associated with hypoperfusion of adipose
tissue, leading to concomitant hypoxia, which may alter adipocyte secretion, thus causing dysfunction in vascular tone.
Neoplasm
There are multiple tumors of endothelial origin; some are
benign while others malignant. Examples of benign tumors
are hemangioma and lymphangioma, while angiosarcoma is
a malignant tumor. Benign tumors are lined with a layer of
normal endothelial cells, lled with blood cells or lymph.
Malignant tumors do not have well-organized conduits and
are composed of more disorganized cells, that are constantly
proliferating with no distinct morphology. CD-31 and von
Willebrand’s factor are endothelial markers used to identify
malignant cells with poor atypia immunohistochemically
[83]. Hemangiomas are very common tumors which are
characterized by normal and abnormal blood vessels lled
with blood. They are common in infancy and early childhood and are usually localized even though they are quite
ubiquitous. Capillary hemangiomas spontaneously regress
and rarely undergo malignant transformation. Cavernous
hemangiomas are associated with abnormal blood vessel formation in deep tissues and are likely to cause pressure symptoms or rupture. Lymphangiomas are analogous to blood
vessel hemangiomas but devoid of erythrocytes. There are
two types, simple (capillary) and cavernous lymphangioma
(cystic hygroma). They are quite common in the head, neck,
and axilla of children. Angiosarcomas are malignant endothelial cell tumors common in adults. Angiosarcomas are
associated with carcinogen exposure: arsenics, thorotrast,
Fig. 22.13 Schematic
diagram showing the effect of
hyperglycemia on endothelial
function. (Modied from Van
den Oever etal. [
78])
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polyvinyl chloride, and tumors such as lymphangiosarcoma
and are poorly differentiated. In contrast to angiosarcomas,
hemangiomas are well differentiated.
Anesthetic Considerations
Acute Critical Illness andEndotheliopathy
Acute critically ill patients scheduled for operative intervention may have multisystem organ dysfunction that emanates
from endotheliopathy [84]. The endothelium and glycocalyx
are normally naturally anticoagulated by heparinoids, tissue factor pathway inhibitor, thrombomodulin system, and
tissue plasminogen activator (tPA). These factors interact
with other mediators to dissolve forming clots [84]. In acute
severe trauma, sepsis, post cardiac arrest and MI, endothelial
inammation, and dysfunction in the anticoagulation system
causes hypocoagulation [85]. In addition, there is shockinduced sympatho-adrenal hyperactivation which leads to
endotheliopathy. This endothelial injury induces a severe
imbalance between the quiescent and activated state, leading
to hypoperfusion and increased mortality (Fig.22.14). One
in four patients admitted to and from the emergency room
have some form of coagulopathy [85]. While many patients
have other causes such as drug reaction or side effect, the
coagulopathy that is associated with acute trauma, septic
shock, bacteremia, myocardial infarction, and post cardiac
arrest syndrome has a mortality rate that is three to four times
higher (mortality rate of 50%) than patients with these same
diagnosis without coagulopathy [86].
Preoperative Consideration
The widespread presence of EC throughout the body means
that EC dysfunction may lead to generalized organ derangements and various associated conditions. Preoperatively, it
is necessary to perform a thorough evaluation. Prior medical conditions such as a cerebral vascular accident, cardio-
vascular changes, pulmonary disease, diabetes mellitus,
and medication history need to be reviewed. The planned
surgical procedure and acuity of the surgery needs to be
ascertained. The risks and benets should be discussed with
the patient, surgeon, and anesthesiologist. Appropriate preoperative workup, anesthetic planning, and postoperative
course must be carefully addressed. Patient presenting to the
operating room with severe trauma, sepsis, acute MI, and
post cardiac arrest syndrome has coagulopathy and adrenalcatecholamine hyperstimulation. While the approach has
been supportive and addressing matters as they evolve in
the past, recent reports suggest that beta blockers and ACE
inhibitors may help to optimize microcirculation through
reduction or reversal of endothelial injury. This is accomplished through their impact on inhibiting the catecholamine
surge associated with endotheliopathy [84].
Intraoperative Consideration
On arrival to the operating room, the standard monitors and
other monitoring modalities needed should be applied based on
the patient’s comorbidities. Invasive versus non-invasive blood
pressure management, echocardiogram, glucose, and temperature monitoring should all be considered on a case-by-case
basis. It is imperative in each case to preclude potential intraoperative sequelae following induction and the possible effect
of the anesthetic administered. Intraoperative bleeding can be
decreased through efforts to reduce glycocalyx and endothelial
injury [87]. In a recent randomized study in patients undergoing emergent thoracic aortic dissection surgery, and required
transfusion, patients who received Octaplast LG (solvent/
detergent-treated pooled plasma) when compared to standard
FFP, the former patients (Octaplas LG) had reduced glycocalyx and endothelial injury, reduced bleeding, less transfusion requirements, use of prohemostatics, and ventilator days
post operatively [88]. The concern raised is routine transfusion with glycocalyx, leading to barrier erosion which may
cause coagulation dysfunction, endothelium inammation,
and injury due to contaminants or substances in the blood [87,
Fig. 22.14 Shock-induced
endotheliopathy (SHINE).
Schematic illustration of the
changes in the vascular
compartment with increasing
disease severity and
increasing sympatho-adrenal
activation. (Modied from:
Johansson etal. [84])
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89]. Furthermore, in animal models with hemorrhagic shock,
it has been shown that plasma administration when compared
to crystalloid is associated with improved endothelial integrity
and restoration of the glycocalyx layer [89].
Postoperative Consideration
Patients with EC dysfunction may be at risk for bleeding,
hyper-hypoglycemia, and cardiovascular or cerebrovascular
event. Depending on the severity of the clinical presentation,
postoperative care of patients with endotheliopathy and diseases associated vascular endothelial dysfunction needs to be
carefully planned before the end of the intraoperative course.
Transition of care for patients with conditions involving EC
dysfunction should be closely monitored. Appropriate care
assessment, discussion, and planning may preclude potential
complications.
Prevention/Management
The Western diet is high in unsaturated fats, and the lifestyle
has become more sedentary compared to Mediterranean and
Oriental diet [14]. Hence, there is a signicant progression
of adverse cardiovascular risk factors in western population.
Pharmacological, physical activity, and lifestyle modication often may not treat or prevent EC dysfunction.
Pharmacological
The ubiquitous nature of ECs allow ECs to be plastic and
amendable to therapeutic intervention [14]. Hence, ECs
are reliable conduits for therapeutic interventions of various pathologic conditions. Multiple medications for hypertension, hyperlipidemia, diabetes, thrombosis, and cancers
have been synthesized and prescribed to patients to prevent
or treat the associated clinical sequelae of endothelial dysfunction. These medications have not shown to be curative
for the various disorders associated with vascular endothelial
dysfunction. There is a signicant need for physical activity
and lifestyle modication adjuncts.
selectin) for endothelial damage. However, these markers
were absent in CHF patients who exercised regularly [91,
92]. It was also interesting to note that diet and exercise have
synergistic effects as opposed to modication from either
modality diet or exercise.
Lifestyle Modication
It has been established that various types of fats, saturated,
monounsaturated, and trans-fatty acids [94–96], have been
implicated in endothelial dysfunction. These specic fats
have been found in partial hydrogenation of vegetable oils
commonly found in margarine, pastry products, and frozen
foods. A Mediterranean diet low in saturated fats, high in
vegetables content, and olive oil (which contains oleic and
linoleic acids) reduces endothelial dysfunction, insulin resistance, and markers of vascular inammation [97–100]. In
addition, polyphenols found in fruits, cereals, olive, vegetables, legumes, chocolate, tea, coffees and wine [101, 102]
have antioxidant properties and are known to prevent endothelial dysfunction [103]. Melatonin and red wine also have
antioxidant properties.
Conclusion
ECs play an important role in the homeostasis of the body,
but dysfunction of EC is implicated in various inammatory
states and multiple organ system pathology. The goal of this
chapter is to highlight the various pathologies associated
with EC dysfunction and how it impacts anesthetic care. An
overview of the potential complications and conditions associated with EC dysfunction is useful for the anesthesiologist
and other anesthesia care providers to prevent or decrease
perioperative morbidity and mortality. Knowledge of vascular endothelial dysfunction and inammatory states can help
guide anesthetic assessment, plan, and management. The
different pathologic states associated with endothelial dysfunction have signicant socioeconomic and public health
impact. Adequate knowledge and modalities to address these
various pathologies will ultimately improve the global and
public health burden associated with diabetes and other cardiovascular diseases.
Physical Activity
A few studies have shown that moderate-intensity aerobic exercise improves endothelial function in animals and
humans with and without cardiovascular risk factors [90–
93]. Exercise training has been shown to ameliorate inam-
mation [14]. Patients with chronic heart failure (CHF) have
increased markers (tumor necrosis factor a, ICAM-1, and E
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Obstetrical Blood Management
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ColleenB.Yen, MonicaM.DiLorenzo, andDanielKatz
23
Overview andIntroduction
Transfusion in obstetrics presents unique challenges and
considerations. The most common indication for transfusion
in this population is post partum hemorrhage (PPH).
Obstetrical blood management goes hand in hand with
PPH. One cannot become procient in obstetrical blood
management without intimate knowledge of PPH.Likewise,
properly managing PPH should lead to a decreased need for
blood products, which is the best strategy when it can be
attained. Therefore, this chapter will begin with the critical
management steps for PPH that should lead to a decreased
need for transfusion and will end with specic transfusion
management strategies.
Epidemiology andDenition
Post partum hemorrhage affects approximately 2% of parturients [1, 2] and is one of the leading causes of maternal
deaths worldwide, accounting for over 27% of maternal
deaths [3].
Post partum hemorrhage was classically dened as estimated blood loss (EBL) >500mL for a vaginal delivery and
EBL >1000mL for a cesarean delivery and was divided into
primary PPH, occurring within 24hours of birth, and secondary PPH, occurring more than 24 hours and up to
12weeks post partum. However, these denitions are overly
simplistic, and current denitions vary by society and expert
C. B. Yen (*) · M. M. DiLorenzo
The Mount Sinai Hospital, Department of Anesthesiology,
Perioperative and Pain Medicine, New York, NY, USA
e-mail: colleen.yen@mountsinai.org;
Monica.dilorenzo@mountsinai.org
D. Katz
Icahn School of Medicine at Mount Sinai, Department of
Anesthesiology, New York, NY, USA
e-mail: Daniel.katz@mountsinai.org
opinion [4–10]. Further, since blood loss is difcult to estimate and is often underestimated, societies including ACOG
[4] have created programs such as the reVITALize program
to standardize denitions in obstetrics and have included
other metrics in addition to blood loss such as vital sign
changes as supplemental criteria regardless of the estimated
blood loss (EBL). Additionally, although some dene PPH
as EBL >1000 mL, which would decrease the number of
patients labeled with PPH, blood loss greater than 500mL
for a normal spontaneous vaginal delivery (NSVD) is still
considered to be abnormal [4] and should prompt an escalation of care.
Risk Factors forObstetric Hemorrhage
Several studies have identied risk factors for postpartum
hemorrhage and are presented in Table23.1.
While identifying patients at risk for PPH is an important
step in hemorrhage planning and management, probably the
most important take away is that there is a very high incidence
Table 23.1 Risk factors for postpartum hemorrhage [4, 11–14]
Risk factors involving a highly or
overly distended uterus Other risk factors
Macrosomia Prolonged labor
Twin or multiple gestation Augmented labor
Polyhydramnios Rapid labor
History of PPH
Episiotomy
Pre eclampsia
BMI >40
Operative delivery
Coagulopathy
Anticoagulant or antithrombotic
medication use
Thrombocytopenia
Morbidly adherent placenta
Asian or Hispanic ethnicity
Chorioamonitis
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C. S. Scher et al. (eds.), Essentials of Blood Product Management in Anesthesia Practice,
https://doi.org/10.1007/978-3-030-59295-0_23
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of PPH in patients with no known risk factors. Risk stratication tools have not proven to be specic. In fact, Bateman
etal. in a population study of almost 900,000 deliveries with
more than 25,000 episodes of PPH found that in patients
aged 20–40 years who had a normal spontaneous vaginal
delivery (NSVD) complicated by atony that required transfusion, only 38% of patients had one of the risk factors tested
[13]. The conclusion is that even though we can identify high
risk patients with scoring systems, every patient on the labor
oor is at risk for PPH. This highlights the importance of
labor and delivery units being prepared with plans and
resources to rapidly respond to unexpected hemorrhage
events. Specic management strategies will be discussed
later in this chapter.
Preventing PPH andBlood Transfusion
The most important step in obstetrical transfusion management is preventing obstetrical hemorrhage. It is important to
recognize that PPH is frequently preventable and represents
an area for improvement in obstetric care and outcomes.
Several major obstetric and anesthesiology societies recommend the use of uterotonic medications as rst-line prevention of PPH. An active type and screen should also be
obtained and conrmed at the rst sign of hemorrhage, if not
in all obstetric patients at the time of presentation in labor [4,
15], as discussed above, unanticipated hemorrhage in
patients with few or no risk factors is not uncommon.
When thinking about preventing PPH, it is important to
recall that the vast majority of PPH cases (60–80%) are due
to uterine atony, followed by retained placenta, defects in
coagulation, uterine inversion, and genital tract trauma [13,
14], which are summarized as the 4 Ts in Table23.2.
Active management of the third stage of labor (delivery of
the placenta) reduces the risk of PPH and is dened as
administration of a prophylactic uterotonic [16], early umbilical cord clamping, and controlled cord traction to facilitate
Table 23.2 Common causes of PPH [13, 14]
Tone Uterine atony
Tissue Placental retention/morbidly adherent placenta
Trauma Tears and lacerations
Thrombin Coagulopathy
placental delivery. Active management of the third stage of
labor is recommended for every delivery, and oxytocin or its
analogue carbetocin, which causes uterine contraction and
prostaglandin production, is considered to be the drug of
choice for rst-line treatment. Per a Cochrane meta-analysis,
oxytocin was found to probably reduce blood loss and the
need for additional uterotonics, though optimal dose and
timing have yet to be determined [6, 16–19]. When necessary, additional uterotonics such as misoprostol, methylergonovine, and carboprost have been shown to be effective when
used with or immediately following oxytocin [20–26]. It is
important to keep in mind that each uterotonic comes with
potential side effects and may be contraindicated in patients
with certain conditions, summarized in Table23.3.
Occasionally, in cases where severe hemorrhage is anticipated and would be challenging to control, such as in placenta percreta, surgical strategies to prevent bleeding may be
employed. Arterial balloon catheters may be placed in a preemptive manner and are most commonly placed in the uterine arteries; however more proximal balloons in the iliac
arteries and the aorta have also been used [29]. Uterine artery
embolization has been used in such a manner for both prophylactic control of bleeding [30] or as a rescue measure as
part of a uterine conservation strategy [31]. A signicant
number of patients, however, will continue to bleed in spite
of uterine artery embolization given the redundancy of blood
ow to the uterus [32], and in these cases emergent uterine
artery embolization or hysterectomy may be required.
Recognition andQuantication ofPPH
One of the largest challenges in obstetrical blood management is estimating how much blood has been lost and determining how much blood to replace. Physiologic perturbations
are often late signs of hypovolemia in young, healthy parturient [33]. Peripheral and splanchnic vasoconstriction facilitates the relocation of blood from venous capacitance vessels
to the central circulation, allowing blood pressure and heart
rate to remain near normal until blood loss exceeds 1500mL
in most parturient [33].
Other indicators of blood loss, such as hematocrit and lactate levels, also present challenging limitations. Changes in
hematocrit and hemoglobin often take hours to manifest, and
Table 23.3 Second-line uterotonics [26–28]
Uterotonic Mechanism of action Common side effects Possible contraindications
Misoprostol Prostaglandin E1 causes uterine contraction Nausea, vomiting, maternal
Methylergonovine Semi-synthetic ergot alkaloid increases tone, rate,
and amplitude of rhythmic contractions
Carboprost Analogue of prostaglandin F2 alpha causes
smooth muscle contractions
pyrexia
Hypertension Hypertension, coronary artery
Bronchospasm, hypertension,
nausea, vomiting, diarrhea
Concern for aspiration or
increased oxygen demand
disease, preeclampsia
Asthma, hypertension, concern
for aspiration
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a nadir may not be reached until post partum day 2 or 3 [34]
and are further confounded by crystalloid administration as
well as clinical states such as pre eclampsia where vascular
permeability is altered [35, 36]. Arterial lactate levels have
been successfully used as a surrogate marker for tissue perfusion in trauma [37, 38], sepsis [39], and gastrointestinal bleeding [40], and the lactate level trend and absolute value have
been used in obstetrics to assess oxygen delivery and the need
for transfusion or to assess for the efcacy of interventions
aimed at facilitating tissue perfusion, though data supporting
their use in PPH is limited. However, the utility of both hematocrit and lactate testing may be limited by the availability of
point-of-care testing and laboratory turn around times. In fact,
they may result so late as to provide no clinical value to a provider managing an acute or rapid hemorrhage.
Patient Blood Management andPPH
Current guidelines for transfusion are based on evidence specic to the non-pregnant adult major trauma and military
medicine patient and recommend the use of formulaic transfusion of packed red blood cells (PRBC), fresh frozen plasma
(FFP), and cryoprecipitate in xed ratios [41, 42]. However,
the baseline coagulation prole of a pregnant patient and a
non-pregnant patient is very different, and there is no data to
extrapolate the formulaic transfusion used in trauma and
military medicine to obstetric hemorrhage [41–43]. This is
especially true in regard to components such as brinogen
(discussed below) in which transfusion of plasma-based
products can incite a dilutional coagulopathy.
First, we will discuss the change in coagulation status in
the term parturient and subsequently the impact of the coagulopathy of PPH on this coagulation status, with emphasis
on brinogen level as a therapeutic target. Next, we will discuss steps in anticipation for PPH including blood product
availability and triggers for transfusion of PRBC specically.
Further, we will discuss massive transfusion protocols in
obstetric anesthesia, transfusion of incompatible blood in a
patient with multiple antibodies, and cell salvage.
Importantly, we will stress the ability of viscoelastic testing
to overcome many of the shortfalls of traditional coagulation
testing in the management of PPH.Finally, we will discuss
pharmacologic adjuncts including antibrinolytics, brinogen concentrates, prothrombin complex concentrates,
recombinant activated factor VIIa, and calcium in obstetrical
blood management.
Change inCoagulation Factors inthePregnant
Patient
Pregnancy is a hypercoagulable state [43, 44]. In the pregnant patient, there is an increase in procoagulant activity
(characterized by increases in factors V, VII, VIII, IX, X, XII,
von Willebrand factor, and brinogen) and a decrease in
endogenous anticoagulant activity (characterized by
increases in heparin cofactor I1 antitrypsin, protein S activity, and activated protein C resistance) [
count may decrease during pregnancy (gestational thrombocytopenia) but rarely occurs to a level that contributes to risk
of bleeding [45].
The change in brinogen in a term pregnancy is important
and signicant; brinogen level in a pregnant patient at term
ranges from 350 to 650mg/dL, which is nearly double in the
brinogen level in a non-pregnant patient [43]. The change
in brinogen may not be reected in a facility’s reference
range, which may cause the under-recognition of hypobrinogenemia. Other laboratory markers of coagulation such as
the prothrombin time (PT) and partial thromboplastin time
(PTT) do not usually become abnormal during obstetric
hemorrhage until large volumes of blood have already been
lost [
43].
43, 44]. Platelet
Coagulopathy inPostpartum Hemorrhage
Coagulopathy associated with PPH is likely a complex interaction between dilution, local consumption, disseminated
consumption, and increased brinolysis [46, 47]. Although
an increase in procoagulant activity is seen in the pregnant
patient, these protective mechanisms may be quickly overcome in the setting of massive blood loss [47]. The rapid
consumption of clotting factors and platelets in massive
hemorrhage can quickly exceed the normal surplus of coagulation factors [47]. Furthermore, critical levels of prothrombin, factor V, factor VII, and platelets are reached after a loss
of greater than 200% of calculated blood volume, whereas
life-threatening levels of brinogen are reached after a loss
of only 140% [47].
Fibrinogen
Although factor repletion is an important component of
preventing coagulopathy, brinogen deserves special consideration as a biomarker in the diagnosis of hemorrhage
and as a potential therapeutic target for the management of
hemorrhage. Fibrinogen is one of the main building blocks
in coagulation, and a low brinogen level has been identied as an early predictor of severe PPH [44, 48]. Charbit
et al. assessed coagulation proles of 128 patients with
atonic PPH (after administration of a second-line uterotonic) for 24hours after onset of bleeding. Maternal brinogen level was independently associated with severe PPH;
for every 1g/L decrease in brinogen, there was a 2.6-fold
increased odds of severe PPH.A baseline brinogen level
≤2g/L taken at the time of bleeding onset had a positive
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predictive value of 100% [42, 44, 49]. These results demonstrate that a low brinogen level during the early phase
of postpartum bleeding can predict the later development of
severe PPH [44].
Blood Product Availability
One of the earliest steps in patient blood management is to
have blood products available when needed. Practices in
routine laboratory testing of the obstetric patient vary by
institution and can vary from no routine testing to a universal type and screen. Although hemorrhage bundles encourage use of preemptive type and screen for moderate-risk
patients and type and cross-match for high-risk patients,
less guidance is given as to what should be done in the lowrisk population who still contribute to a signicant portion
of patients with PPH [50]. The ASA Task Force on Obstetric
Anesthesia practice guidelines state that the literature is
insufcient to determine whether type and screen leads to
fewer maternal anesthetic complications and whether type
and cross-match is necessary for healthy and uncomplicated parturients [51]. From a cost analysis perspective,
universal type and screen for all patients is not cost-effective and only marginally reduces the need to transfuse
uncrossed blood [52]. Each institution must determine their
own approach based on local guidelines, patient mix, and
cost-effectiveness while maximizing the degree of clinical
impact [44].
Massive Transfusion Protocol
When the maternal rate of bleeding is rapid, several units of
blood products will not sufce to ensure avoidance of maternal morbidity and mortality. In the event of massive hemorrhage, large volumes of blood products are needed
expeditiously, and massive transfusion protocols (MTPs)
were developed for this purpose. The criteria to meet massive transfusion is discussed elsewhere.
As discussed, there is no consensus on the optimal RBCto- plasma ratio in the management of obstetric hemorrhage.
Popular ratios for transfusion include PRBC/FFP/platelet
ratio of 6:4:1 or 4:4:1. While some societies such as ACOG
recommend xed product ratios for obstetric hemorrhage
MTPs, others such as the Royal College of Obstetricians and
Gynecologists (RCOG) recommend set volumes of plasma
following RBC transfusion [43]. The CMQCC recommends
that transfusion be based on vital signs and should not be
delayed while awaiting laboratory results [43]. In the obstetric patient, many transfusion protocols include cryoprecipitate, in anticipation of a rapid decrease in brinogen during
severe hemorrhage.
Implementation of a massive transfusion protocol has
been shown to improve the timeline of blood transfusion and
to be cost-effective due to a lower overall usage of blood
products [
improves the line of communication for ordering and transporting blood products from the blood bank to the labor and
delivery unit but also ensures that blood products continue to
be available until surgical and hemostatic control of hemorrhage has occurred [44].
units across the United States reported that 95% of labor and
delivery units had an MTP protocol [44, 53]. However, most
centers lacked a standardized initiation cut off which caused
variability in use. Most institutions with an initiation standard
used a cut-off of 1500mL with uncontrolled bleeding [53].
44]. Additionally, utilization of the MTP not only
A survey of 60 directors of academic obstetric anesthesia
Multiple Antibodies andTransfusion
ofIncompatible Blood
Specic patient populations including patients with sickle
cell disease, thalassemia, and hemophilia have higher rates
of blood antibodies [53]. These patients are still at risk for
obstetric hemorrhage and may require transfusion. Usually,
every effort is made to avoid the transfusion of incompatible
blood, through efforts including prophylactic preparation of
cross-matched blood products 48hours prior to induction of
labor, use of cell salvage, and early intervention for obstetric
hemorrhage such as uterine artery embolization and hysterectomy to obtain surgical control [53]. If the transfusion of
incompatible units becomes necessary, the clinician should
transfuse in ascending order of clinical hemolytic severity of
the antibody of concern. The blood bank, hematology, and
maternal fetal medicine should be involved if transfusion of
known incompatible blood is to take place [53].
Transfusion Triggers forPRBC Transfusion
inNon-MTP Circumstances
There is no optimal Hob/Hot goal that must be met during
obstetric hemorrhage; however the common threshold of a
Hob of 7g/ld. or a Hot of 21% is commonly cited [50, 54].
Although a Hot of 18–25% may be tolerated in an otherwise
healthy parturient, most experts agree that PRBC transfusion is warranted with a Hot of less than 25% in the setting of active bleeding [47]. A higher Hot during ongoing
hemorrhage both maintains tissue and organ perfusion and
improves overall coagulation status [47]. Clinical markers
including serum pH, lactate, base decit, and bicarbonate
have been extensively studied as markers of resuscitation
success in shock [53]. As a patient’s volume status may
change rapidly during hemorrhage resuscitation, it is rec-
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