CONSUMPTIVE COAGULOPATHY

Obstetrical syndromes commonly termed consumptive coagulopathy

or disseminated intravascular coagulation (DIC) were described
in the 1901 report by DeLee in which “temporary hemophilia”
developed with placental abruption or with a long-dead macerated
fetus. In ensuing decades, similar—but frequently less
intense—coagulopathic syndromes have been described for
almost all areas of medicine (Levi, 2010b; Montagnana, 2010).
■ Disseminated Intravascular
Coagulation in Pregnancy
Because of many definitions used and its variable severity, citing
an accurate incidence for consumptive coagulopathy is not
possible in pregnant women. For example, as will be discussed,
some degree of significant coagulopathy is found with most
cases of placental abruption and amnionic-fluid embolism.
Other instances in which frequently occurring but insignificant
degrees of coagulation activation can be found include sepsis,

TABLE 41-5. Selected Maternal Outcomes in Women with Accrete Syndromes

Identified Prenatally and Delivered in Tertiary-Care Units
Outcomea San Diegob n 62 Utahc n 60 Torontod n 33
Gestational age (wk) 33.9 1.1 34 (17–41) ∼32 (19–39)
Operating time (min) 194 1.6 NS 107 (68–334)
Transfusions ∼75% 70%
RBC (units) 4.7 2.2 ≥4 (30%) 3.5 (0–20)
FFP (units) 4.1 2.3 NS NS
Surgical outcomes
Bladder injury 14 (23%) 22 (37%) 10 (30%)
Ureteral injury 5 (8%) 4 (7%) 0
Postoperative
ICU admission 43 (72%) 18 (30%) 5 (15%)
LOS (days) 7.4 1.8 4 (3–13%) 5 (2–13)
Readmission NS 7 (12%) 1 (3%)
Reoperation NS 5 (8%) 0
aOutcomes shown as mean 1SD; as median (range); or as number (%).
bData from Warshak, 2010.
cData from Eller, 2011.
dData from Walker, 2013.

FFP fresh-frozen plasma; ICU intensive care unit; LOS length of stay; NS not
stated; RBC red blood cells.

thrombotic microangiopathies, acute kidney injury, and preeclampsia

and HELLP (hemolysis, elevated liver enzyme levels,
low platelet count) syndromes (Rattray, 2012; Su, 2012).

Although profound consumptive coagulopathy can be associated

with fatty liver disease of pregnancy, diminished hepatic
synthesis of procoagulants makes a significant contribution
(Nelson, 2013).
When consumptive coagulopathy is severe, the likelihood
of maternal and perinatal morbidity and mortality is increased.
Rattray and colleagues (2012) described 49 cases from Nova
Scotia during a 30-year period. Antecedent causes included
placental abruption, obstetrical hemorrhage, preeclampsia and
HELLP syndromes, acute fatty liver, sepsis, and amnionicfluid
embolism. Of these, 59 percent received blood transfusions,
18 percent underwent hysterectomy, 6 percent were
dialyzed, and there were three maternal deaths. The perinatal
mortality rate was 30 percent.
Pregnancy-Induced Coagulation Changes
Several changes in coagulation and fibrinolysis can be documented
during normal pregnancy. Some of these include
appreciable increases in the plasma concentrations of factors I
(fibrinogen), VII, VIII, IX, and X. A partial list of these normal
values can be found in the Appendix (p. 1288) and in Chapter
4 (p. 57). At the same time, plasminogen levels are increased
considerably, but levels of plasminogen activator inhibitor-1
and -2 (PAI-1 and PAI-2) also increase. Thus, plasmin activity
usually decreases until after delivery (Hale, 2012; Hui, 2012).

The mean platelet count decreases by 10 percent during pregnancy,

and there is increased platelet activation (Kenny, 2014).
The net results of these changes include increased levels
of fibrinopeptide A, -thromboglobulin, platelet factor
4, and fibrinogen-fibrin degradation products, which includes
d-dimers. Along with decreased concentrations of anticoagulant
protein S, hypercoagulability, and decreased fibrinolysis,
there is augmented—yet compensated—intravascular coagulation
that may function to maintain the uteroplacental interface.
■ Pathological Activation of Coagulation
Normal coagulation and fibrinolysis can be pathologically
activated via two pathways. The extrinsic pathway is active by
thromboplastin from tissue destruction, whereas the intrinsic
pathway is initiated by collagen and other tissue components
that become exposed with loss of endothelial integrity
(Fig. 41-30). Tissue factor III is an integral membrane protein.
It is released by endothelial cells to complex with factor
VII, which in turn activates tenase (factor IX) and prothrombinase
(factor X) complexes. Uncontrolled thrombin generation
converts fibrinogen to fibrin, which polymerizes to
deposit in small vessels of virtually every organ system. This
seldom causes organ failure, because these vessels are protected
by enhanced fibrinolysis stimulated by fibrin monomers
released by coagulation. These monomers combine with tissue
plasminogen activator and plasminogen to release plasmin,
which lyses fibrinogen and fibrin monomers and polymers.

The products form a series of fibrinogen-fibrin derivatives that

are measured by immunoassay. These are the fibrin degradation
products or fibrin-split products, which include d-dimers
(see Fig. 41-30). There may also be evidence for microangiopathic
hemolysis from mechanical trauma to the red cell
membrane by fibrin strands in small vessels. This is likely a
contributing cause of hemolysis in women with preeclampsia
and HELLP syndromes (Pritchard, 1976a).

The pathologically activated cycle of coagulation and fibrinolysis

becomes clinically important when coagulation factors
and platelets are sufficiently depleted to cause bleeding—hence,
consumptive coagulopathy.
Several obstetrical conditions are
accompanied by release of potent inciting factors for clinically
significant consumptive coagulation. The best known and most
common, and therefore most serious, results from thromboplastin
release with placental abruption. Also, unique to obstetrics
is the immediate and profound coagulation factor depletion
that can follow entry of amnionic fluid into the maternal circulation.
This causes activation of factor X by abundant mucin
in fetal squames. Other causes include activation by release of
endotoxins from gram-negative bacteria and exotoxins from
gram-positive bacteria.
■ Diagnosis
The International Society on Thrombosis and Haemostasis has
promulgated a DIC score to aid identification and prognosis prediction
(Taylor, 2001). This algorithm, shown in Table 41-6,
has not been applied in obstetrical conditions but can serve as a
rough guideline to identify a pregnant woman with consumptive
coagulopathy. Again, although not including obstetrical patients,
the Prowess Trial evaluated 840 subjects with severe sepsis. The
mortality rate increased from approximately 25 percent with a
DIC score of 3 to 70 percent with a score of 7 (Dhainaut, 2004).

Evaluation and Management

Obstetrical causes of consumptive coagulopathy are almost
always due to an identifiable, underlying pathological process
that must be eliminated to halt ongoing defibrination. Thus,
prompt identification and removal of the source of the coagulopathy
is given priority. With surgical incisions or extensive
lacerations accompanied by severe hemorrhage, rapid replacement
of procoagulants is usually indicated. Vigorous restoration
and maintenance of the circulation to treat hypovolemia
cannot be overemphasized. With adequate perfusion, activated
coagulation factors, fibrin, and fibrin degradation products are
promptly removed by the reticuloendothelial system, along with
restoration of hepatic and endothelial synthesis of procoagulants.
Some treatments for intravascular coagulation have been
conceived by armchair theorists and are mentioned here only
to be condemned. For example, in years past, some recommended
heparin administration to block consumption of procoagulants.
Others recommended epsilon-aminocaproic acid
to inhibit fibrinolysis by blocking plasminogen conversion to
plasmin. The dangers of giving heparin to an actively bleeding
woman are obvious. Fibrinolysis inhibition is probably not
quite as dangerous, but any putative benefits remain unproven.
Identification of Defective Hemostasis. Bioassay is an
excellent method to detect or suspect clinically significant
coagulopathy. Excessive bleeding at sites of modest trauma
characterizes defective hemostasis. Examples include persistent
bleeding from venipuncture sites, nicks from shaving
the perineum or abdomen, trauma from bladder catheterization,
and spontaneous bleeding from the gums, nose, or
gastrointestinal tract. Purpuric areas at pressure sites such as
sphygmomanometer cuffs or tourniquets suggest significant
thrombocytopenia. As discussed, any surgical procedure provides
the ultimate bioassay and elicits generalized oozing from
the skin, subcutaneous and fascial tissues, the retroperitoneal
space, the episiotomy, or incisions and dissections for cesarean
delivery or hysterectomy.
Fibrinogen and Degradation Products. In late pregnancy,
plasma fibrinogen levels typically have increased to 300
to 600 mg/dL. Even with severe consumptive coagulopathy,
levels may sometimes be high enough to protect against clinically
significant hypofibrinogenemia. For example, defibrination
caused by a placental abruption might lower an initial
fibrinogen level of 600 mg/dL to 250 mg/dL. Although this
would indicate massive fibrinogen consumption, there are
still adequate levels to promote clinical coagulation—usually
about 150 mg/dL. If serious hypofibrinogenemia—less than
50 mg/dL—is present, the clot formed from whole blood in
a glass tube may initially be soft but not necessarily remarkably
reduced in volume. Then, over the next half hour or so,
as platelet-induced clot retraction develops, the clot becomes
quite small. When many of the erythrocytes are extruded, the
volume of liquid in the tube clearly exceeds that of clot.
Fibrinolysis cleaves fibrin and fibrinogen into various fibrin
degradation products that are detected by several sensitive test
systems. There are many fragment types, and monoclonal antibodies
in assay kits usually measure d-dimers specific for that
assay. These values are always abnormally high with clinically
significant consumptive coagulopathy. At least in obstetrical
disorders, quantification has not been correlated with outcomes,
although “moderate” to “strong” increases constitute part of the
diagnostic algorithm shown in Table 41-6.

Thrombocytopenia
Seriously low platelet concentrations are likely if petechiae are
abundant or if clotted blood fails to retract within an hour or
so. Confirmation is provided by a platelet count. If there is
associated severe preeclampsia syndrome, there may also be
qualitative platelet dysfunction (Chap. 40, p. 738).
Prothrombin and Partial Thromboplastin Times
Prolongation of these standard coagulation tests may result
from appreciable reductions in procoagulants essential for generating
thrombin, from very low fibrinogen concentrations, or
from appreciable amounts of circulating fibrinogen-fibrin degradation
products. Prolongation of the prothrombin time and
partial thromboplastin time need not be the consequence of
consumptive coagulopathy.
■ Placental Abruption
This is the most common cause of severe consumptive coagulopathy
in obstetrics and is discussed on page 793.
■ Preeclampsia Syndrome
Endothelial activation or injury is a hallmark of preeclampsia,
eclampsia, and HELLP syndrome. In general, the clinical severity
of preeclampsia is directly correlated with thrombocytopenia
and fibrinogen-fibrin degradation products (Levi, 2010b;
Kenny, 2014). That said, intravascular coagulation is seldom
clinically worrisome. Delivery reverses these changes, and treatment
until then is supportive. These syndromes are discussed in
detail in Chapter 40.
■ Fetal Death and Delayed Delivery
Consumptive coagulopathy associated with prolonged retention
of a dead fetus is unusual today because fetal death can
be easily confirmed and there are highly effective methods for
labor induction. Currently, the syndrome is only occasionally
encountered when there is one dead twin fetus and an ongoing
pregnancy. With singleton pregnancies, if the dead fetus
is undelivered, most women enter spontaneous labor within 2
weeks. Gross disruption of maternal coagulation rarely develops
before 4 weeks (Pritchard, 1959, 1973). After 1 month, however,
almost a fourth will develop consumptive coagulopathy.
The pathogenesis of coagulopathy appears to be mediated
by thromboplastin released by the dead fetus and the placenta
(Jimenez, 1968; Lerner, 1967). Typically, the fibrinogen concentration
falls during 6 weeks or more to levels that are normal
for nonpregnant adults, but in some cases, this declines
to 100 mg/dL. Simultaneously, fibrin degradation product
and d-dimer levels become elevated in serum, and moderate
thrombocytopenia develops (Pritchard, 1973). If enough time
elapses to seal the placental-decidual interface, these coagulation
defects may correct spontaneously before evacuation
(Pritchard, 1959).

Discordant Fetal Death in Multifetal Gestation

Obvious coagulation derangement occasionally develops in a
multifetal pregnancy in which there is at least one fetal death
and survival of another (Chescheir, 1988; Landy, 1989). This
situation is uncommon, and in one study of 22 such pregnancies,
none developed a coagulopathy (Petersen, 1999). Most
cases are seen in monochorionic twins with shared circulations,
which are described in Chapter 45 (p. 904). The course
in such a woman cared for at Parkland Hospital is shown in
Figure 41-31. In this case, the coagulopathy ceased spontaneously,
and the surviving healthy twin was delivered near term.
The placenta of the long-dead fetus was filled with fibrin.

■ Amnionic-Fluid Embolism
This uniquely obstetrical syndrome was described in 1941 by
Steiner and Lushbaugh and became classically characterized by
the abrupt onset of hypotension, hypoxia, and severe consumptive
coagulopathy. Even so, amnionic-fluid embolism has great
individual variation in its clinical manifestation. For example,
only one of these three clinical hallmarks predominates in some
affected women.
Despite variations in the reported incidence of this uncommon
but extremely important complication, many reports
describe a similar frequency. A study that included 3 million
births in the United States cited an estimated frequency of
7.7 cases per 100,000 births (Abenhaim, 2008). The United
Kingdom Obstetric Surveillance System reported an incidence
of 2.0 per 100,000 births (Knight, 2010). And review of more
than 4 million births in Canada yielded an incidence of 2.5
per 100,000 births (Kramer, 2012). Another review of data
from five high-resource countries cites frequencies from 1.9 to
6.1 per 100,000 deliveries. The case-fatality rates in all of these
studies ranged from 11 to 43 percent. From another perspective,
amnionic-fluid embolism was the cause of 10 to 15 percent
of all pregnancy-related deaths in the United States and
Canada (Berg, 2003; 2010; Clark, 2008; Kramer, 2012).
Predisposing conditions are rapid labor, meconium-stained
amnionic fluid, and tears into uterine and other large pelvic veins.
Other risk factors commonly cited include older maternal age;
postterm pregnancy; labor induction or augmentation; eclampsia;
cesarean, forceps, or vacuum delivery; placental abruption or previa;
and hydramnios (Knight, 2010, 2012; Kramer, 2012). The
association of uterine hypertonus appears to be the effect rather
than the cause of amnionic-fluid embolism. This is likely because
uterine blood flow ceases when intrauterine pressures exceed 35
to 40 mm Hg. Thus, a hypertonic contraction would be the least
likely circumstance for amnionic fluid and other debris to enter
uterine veins (Clark, 1995). Because of this, there is also no association
between this disorder and hypertonus from oxytocin.
In obvious cases of amnionic-fluid embolism, the clinical picture
is unquestionably dramatic. The classic example is that of
a woman in the late stages of labor or immediately postpartum
who begins gasping for air and then rapidly suffers seizures or
cardiorespiratory arrest complicated by massive hemorrhage
from consumptive coagulopathy. It has become apparent that
there is a variation in the clinical manifestations of this condition.
For example, we and others have managed several women
in whom otherwise uncomplicated vaginal or cesarean delivery
was followed by severe acute consumptive coagulopathy
without overt cardiorespiratory difficulties. In those women,
consumptive coagulopathy appears to be the forme fruste of
amnionic-fluid embolism (Kramer, 2012; Porter, 1996).
Etiopathogenesis
Some amnionic fluid commonly enters the maternal circulation
at the time of normal delivery through a minor breach
in the physiological barrier between maternal and fetal compartments.
Thus, it is fortunate that infused amnionic fluid
is generally innocuous, even in large amounts (Adamsons,
1971; Stolte, 1967). At delivery, squames, other cellular elements
of fetal origin, and trophoblasts can be identified in
maternal peripheral blood (Clark, 1986; Lee, 1986). These
are presumed to enter venous channels from the placental
implantation site or from small lacerations that inevitably
develop in the lower uterine segment or cervix with delivery.
Although these events are usually innocuous, amnionic
fluid constituents in some women initiate a complex series of
pathophysiological sequelae shown in Table 41-7. The wide
range of clinical manifestations underscores the subjective
nature of diagnosis of many of these women.
Considering the wide spectrum of cardiovascular pathophysiological
aberrations and sometimes profound coagulopathy, one
can reasonably conclude that amnionic fluid and its constituents
have a multitude of actions. For example, tissue factor in
amnionic fluid presumably activates factor X to incite coagulation
(Ecker, 2012; Levi, 2013). Others that have been described
include endothelin-1 expressed by fetal squames, phosphatidylserine
expressed by amnion, and complement activators (Khong,
1998; Zhou, 2009). An anaphylactoid reaction with complement
activation has been postulated because serum levels of tryptase
and histamine are also elevated (Benson, 2001; Clark, 1995).

Pathophysiology
Animal studies in primates and goats have provided important
insights into central hemodynamic aberrations caused
by amnionic fluid infused intravenously (Adamsons, 1971;
Hankins, 1993). In general, evidence for fetal debris embolization
and toxicity increases with the volume infused and
the amount of meconium contamination (Hankins, 2002). If
a response is evoked, its initial phase consists of pulmonary
and systemic hypertension. A similar response was reported
in a woman in whom transesophageal echocardiography was
performed within minutes of collapse. Findings included a
massively dilated akinetic right ventricle and a small, vigorously
contracting, cavity-obliterated left ventricle (Stanten,
2003). Profound oxygen desaturation is often seen in the
initial phase, and this is the cause of neurological injury in
most survivors (Harvey, 1996). All of these observations are
consistent with failure to transfer blood from the right to
the left heart because of severe and unrelenting pulmonary
vasoconstriction. This initial phase is probably followed by
decreased systemic vascular resistance and diminished cardiac
output (Clark, 1988). Women who survive beyond these first
two phases invariably have a consumptive coagulopathy and
usually lung and brain injury.
Postmortem Findings. Histopathological findings may
be dramatic in fatal cases of amnionic-fluid embolism such
as the one shown in Figure 41-32. The detection of such
debris, however, may require special staining, and even
then, it may not be seen. In one study, fetal elements were
detected in 75 percent of autopsies and in 50 percent of
specimens prepared from concentrated buffy coat aspirates
taken antemortem from a pulmonary artery catheter (Clark,
1995). Several other studies, however, have demonstrated
that fetal squamous cells, trophoblasts, and other debris of
fetal origin may commonly be found in the central circulation
of women with conditions other than amnionic-fluid
embolism. Thus, the diagnosis is generally made by identifying
clinically characteristic signs and symptoms and excluding
other causes.
Management and Clinical Outcomes
Immediate resuscitative actions are necessary to interdict the
high mortality rate. As discussed, the initial period of systemic
and pulmonary hypertension that frequently heralds
amnionic-fluid embolism is transient. Tracheal intubation,
cardiopulmonary resuscitation, and other supportive measures
must be instituted without delay. Treatment is directed
at oxygenation and support of the failing myocardium, along
with circulatory support that includes rapid blood and component
replacement. That said, there are no data indicating
that any type of intervention improves maternal or fetal
prognosis. In undelivered women undergoing cardiopulmonary
resuscitation, consideration should be given to emergency
cesarean delivery to perhaps optimize these efforts and
improve newborn outcome. Decision making for perimortem
cesarean delivery is more complex in a woman who is
hemodynamically unstable but who has not suffered cardiac
arrest (Chap. 47, p. 956).

Most reports describe dismal outcomes with amnionicfluid

embolism. However, this is likely influenced by underdiagnosis
and reporting biases that favor the most severe cases,
which are recognized but also have the greatest mortality
rates. Several reports are illustrative. From a California database
of 1.1 million deliveries, there was a 60-percent mortality
rate with amnionic-fluid embolism (Gilbert, 1999). In a
report from the Suzhou region of China, 90 percent of mothers
died (Weiwen, 2000). This latter report emphasizes that
death can be amazingly rapid because 12 of the 34 women
who died did so within 30 minutes. The mortality rate was
less dismal in the largest study from a Canadian database. Of
120 women with an amnionic-fluid embolism, only a fourth
died. In many reports, survivors commonly have profound
neurological impairment. Clark (1995) observed that only
8 percent of women who lived despite cardiac arrest survived
neurologically intact.
As perhaps expected, perinatal outcomes are also poor and
are inversely related to the maternal cardiac arrest-to-delivery interval. Even so, neonatal survival rate is 70 percent,
but
unfortunately, up to half of survivors suffer residual neurological
impairment. In the Canadian study, 28 percent of
infants were considered to be asphyxiated at birth (Kramer,
2012).

■ Sepsis Syndrome
Various infections that are accompanied by endo- or exotoxin
release can result in sepsis syndrome in pregnant women.
Although a feature of this syndrome includes activation of
coagulation, seldom does sepsis alone cause massive procoagulant
consumption. Escherichia coli bacteremia is frequently
seen with antepartum pyelonephritis and puerperal infections,
however, accompanying consumptive coagulopathy is usually
not severe. Some notable exceptions are septicemia associated
with puerperal infection or septic abortion caused by exotoxins
released from infecting organisms such as group A Streptococcus
pyogenes, Staphylococcus aureus, or Clostridium perfringens or
sordellii. Treatment of sepsis syndrome and septic shock is discussed
in Chapter 47 (p. 946).
Purpura Fulminans
This severe—often lethal—form of consumptive coagulopathy
is caused by microthrombi in small blood vessels leading to
skin necrosis and sometimes vasculitis. Debridement of large
areas of skin over the extremities and buttocks frequently
requires treatment in a burn unit. Purpura fulminans usually
complicates sepsis in women with heterozygous protein C deficiency
and low protein C serum levels (Levi, 2010b). Recall
that homozygous protein C deficiency results in fatal neonatal
purpura fulminans (Chap. 52, p. 1031).
■ Abortion
Septic abortion—especially associated with the organisms
discussed above—can incite coagulation and worsen hemorrhage,
especially with midtrimester abortions. Indeed, sepsis
syndrome accompanied by intravascular coagulation accounts
for 25 percent of abortion-related deaths (Saraiya, 1999).
In the past, especially with illegal abortions, infections with
Clostridium perfringens were a frequent cause of intense intravascular
hemolysis at Parkland Hospital (Pritchard, 1971).
More recently, however, septic abortions from infection
with Clostridium sordellii have emerged as important causes
(Chap 18, p. 357).
Second-trimester induced abortions can stimulate intravascular
coagulation even in the absence of sepsis. Ben-Ami and
associates (2012) described a 1.6-percent incidence in 1249
late second-trimester pregnancies terminated by dilatation
and evacuation. Two thirds were done for fetal demise, which
may have been contributory to coagulopathy. Another source
of intense coagulation is from instillation of hypertonic solutions
to effect midtrimester abortions. These are not commonly
performed currently for pregnancy terminations (Chap. 18,
p. 369). The mechanism is thought to initiate coagulation by
thromboplastin release into maternal circulation from placenta,
fetus, and the decidua by the necrobiotic effect of the hypertonic
solutions (Burkman, 1977).

MANAGEMENT OF HEMORRHAGE
One of the most crucial elements of obstetrical hemorrhage
management is recognition of its severity. As discussed on
page 781, visual estimation of blood loss, especially when
excessive, is notoriously inaccurate, and true blood loss is
often two to three times the clinical estimates. Consider
also that in obstetrics, part and sometimes even all of the
lost blood may be concealed. Estimation is further complicated
in that peripartum hemorrhage—when most severe
cases are encountered—also includes the pregnancy-induced
increased blood volume. If pregnancy hypervolemia is not
a factor, then following blood loss of 1000 mL, the hematocrit
typically falls only 3 to 5 volume percent within an
hour. The hematocrit nadir depends on the speed of resuscitation
using infused intravenous crystalloids. Recall that with
abnormally increased acute blood loss, the real-time hematocrit
is at its maximum whenever measured in the delivery, operating,
or recovery room.
A prudent rule is that any time blood loss is considered more
than average by an experienced team member, then the hematocrit
is determined and plans are made for close observation
for physiological deterioration. Urine output is one of the most
important “vital signs” with which to monitor the woman with
obstetrical hemorrhage. Renal blood flow is especially sensitive
to changes in blood volume. Unless diuretic agents are given—
and these are seldom indicated with active bleeding—accurately
measured urine flow reflects renal perfusion, which in turn reflects
perfusion of other vital organs. Urine flow of at least 30 mL,
and preferably 60 mL, per hour or more should be maintained.
With potentially serious hemorrhage, an indwelling bladder
catheter is inserted to measure hourly urine flow.
■ Hypovolemic Shock
Shock from hemorrhage evolves through several stages. Early
in the course of massive bleeding, there are decreases in mean
arterial pressure, stroke volume, cardiac output, central venous
pressure, and pulmonary capillary wedge pressure. Increases
in arteriovenous oxygen content difference reflect a relative
increase in tissue oxygen extraction, although overall oxygen
consumption falls.
Blood flow to capillary beds in various organs is controlled
by arterioles. These are resistance vessels that are partially controlled
by the central nervous system. However, approximately
70 percent of total blood volume is contained in venules, which
are passive resistance vessels controlled by humoral factors.
Catecholamine release during hemorrhage causes a generalized
increase in venular tone that provides an autotransfusion
from this capacitance reservoir (Barber, 1999). This is accompanied
by compensatory increases in heart rate, systemic and
pulmonary vascular resistance, and myocardial contractility. In
addition, there is redistribution of cardiac output and blood
volume by selective, centrally mediated arteriolar constriction
or relaxation—autoregulation. Thus, although perfusion to the
kidneys, splanchnic beds, muscles, skin, and uterus is diminished,
relatively more blood flow is maintained to the heart,
brain, and adrenal glands.

When the blood volume deficit exceeds approximately 25

percent, compensatory mechanisms usually are inadequate
to maintain cardiac output and blood pressure. Importantly,
additional small losses of blood will now cause rapid clinical
deterioration. Following an initial increased total oxygen
extraction by maternal tissue, maldistribution of blood
flow results in local tissue hypoxia and metabolic acidosis.
This creates a vicious cycle of vasoconstriction, organ ischemia,
and cellular death. Another important clinical effect
of hemorrhage is activation of lymphocytes and monocytes,
which in turn cause endothelial cell activation and platelet
aggregation. These cause release of vasoactive mediators with
small vessel occlusion and further impairment of microcirculatory
perfusion. Other common obstetrical syndromes—preeclampsia
and sepsis—also lead to loss of capillary endothelial
integrity, additional loss of intravascular volume into the
extracellular space, and platelet aggregation (Chaps. 40, p. 734
and 47, p. 947).
The pathophysiological events just described lead to the
important but often overlooked extracellular fluid and electrolyte
shifts involved in both the genesis and successful treatment
of hypovolemic shock. These include changes in the cellular
transport of various ions such as sodium and water into skeletal
muscle and potassium loss. Replacement of extracellular
fluid and intravascular volume are both necessary. Survival is
enhanced in acute hemorrhagic shock if blood plus crystalloid solution
is given compared with blood transfusions alone.

■ Immediate Management and

Resuscitation
Whenever there is suggestion of excessive blood loss in a pregnant
woman, steps are simultaneously taken to identify the
source of bleeding and to begin resuscitation. If she is undelivered,
restoration of blood volume is beneficial to mother and
fetus, and it also prepares for emergent delivery. If she is postpartum,
it is essential to immediately identify uterine atony,
retained placental fragments, or genital tract lacerations. At
least one and preferably more large-bore intravenous infusion
systems are established promptly with rapid administration of
crystalloid solutions, while blood is made available. An operating
room, surgical team, and anesthesia providers are assembled
immediately. Specific management of hemorrhage is further
dependent on its etiology. For example, antepartum bleeding
from placenta previa is approached somewhat differently than
that from postpartum atony.
Fluid Resuscitation
It cannot be overemphasized that treatment of serious hemorrhage
demands prompt and adequate refilling of the intravascular
compartment with crystalloid solutions. These rapidly
equilibrate into the extravascular space, and only 20 percent of
crystalloid remains intravascularly in critically ill patients after
1 hour (Zuckerbraun, 2010). Because of this, initial fluid is
infused in a volume three times the estimated blood loss.
Resuscitation of hypovolemic shock with colloid versus
crystalloid solutions is debated. In a Cochrane review of
resuscitation of nonpregnant critically ill patients, Perel and Roberts (2007) found equivalent benefits but concluded
that
colloid solutions were more expensive. Similar results were
found in the Saline versus Albumin Fluid Evaluation (SAFE)
randomized trial of almost 7000 nonpregnant patients (Finfer,
2004). We concur with Zuckerbraun and colleagues (2010)
that acute volume resuscitation is preferably done with crystalloid
and blood.
Blood Replacement
There is considerable debate regarding the hematocrit level or
hemoglobin concentration that mandates blood transfusion.
Cardiac output does not substantively decrease until the hemoglobin
concentration falls to approximately 7 g/dL or hematocrit
of 20 volume percent. At this level the Society of Thoracic
Surgeons (2011) recommends consideration for red-cell transfusions.
Also, Military Combat Trauma Units in Iraq used a
target hematocrit of 21 volume percent (Barbieri, 2007). In
general, with ongoing obstetrical hemorrhage, we recommend
rapid blood infusion when the hematocrit is 25 volume percent.
This decision is dependent on whether the fetus has been
delivered, surgery is imminent or ongoing operative blood loss
is expected, or acute hypoxia, vascular collapse, or other factors
are present.
Scant clinical data elucidate these issues. In a study from the
Canadian Critical Care Trials Group, nonpregnant patients
were randomly assigned to restrictive red cell transfusions to
maintain hemoglobin concentration 7 g/dL or to liberal transfusions
to maintain the hemoglobin level at 10 to 12 g/dL. The
30-day mortality rate was similar—19 versus 23 percent in the
restrictive versus liberal groups, respectively (Hebert, 1999).
In a subanalysis of patients who were less ill, the 30-day mortality
rate was significantly lower in the restrictive group—9
versus 26 percent. In a study of women who had suffered postpartum
hemorrhage and who were now isovolemic and not
actively bleeding, there were no benefits of red cell transfusions
when the hematocrit was between 18 and 25 volume percent
(Morrison, 1991). The number of units transfused in a given
woman to reach a target hematocrit depends on her body mass and
on expectations of additional blood loss.
Blood Component Products. Contents and effects of transfusion
of various blood components are shown in Table 41-8.
Compatible whole blood is ideal for treatment of hypovolemia
from catastrophic hemorrhage. It has a shelf life of 40 days, and
70 percent of the transfused red cells function for at least 24
hours following transfusion. One unit raises the hematocrit by
3 to 4 volume percent. Whole blood replaces many coagulation
factors—which is important in obstetrics—especially fibrinogen—
and its plasma treats hypovolemia. A collateral derivative
is that women with severe hemorrhage are resuscitated with
fewer blood donor exposures than with packed red cells and
components (Shaz, 2009).
There are reports that support the preferable use of whole
blood for massive hemorrhage, including our experiences at
Parkland Hospital (Alexander, 2009; Hernandez, 2012). Of
more than 66,000 deliveries, women with obstetrical hemorrhage
treated with whole blood had significantly decreased
incidences of renal failure, acute respiratory distress syndrome,

pulmonary edema, hypofibrinogenemia, ICU admissions, and

maternal death compared with those given packed red cells
and component therapy. Freshly donated whole blood has also
been used successfully for life-threatening massive hemorrhage
at combat support hospitals in Iraq (Spinella, 2008).
It is problematic that in most institutions today, whole
blood is rarely available. Thus, most women with obstetrical
hemorrhage and ongoing massive blood loss are given packed
red cells and crystalloid in 2:1 or 3:1 proportions. In these
instances, there are no data to support a 1:1 red cell:plasma
transfusion ratio. Many institutions use massive transfusion
protocols designed to anticipate all facets of obstetrical hemorrhage
defined as massive. These “recipes” commonly contain a
combination of red cells, plasma, cryoprecipitate, and platelets
(Pacheco, 2011; Shields, 2011). If time permits, we usually
prefer to await results of emergently performed hematological
laboratory assessments to treat deficiencies of fibrinogen or
platelets. If time does not permit this, however, the massive
transfusion protocol is activated.
Dilutional Coagulopathy. A major drawback of treatment
for massive hemorrhage with crystalloid solutions and packed
red blood cells is depletion of platelets and clotting factors. As
discussed on page 808, this can lead to a dilutional coagulopathy
clinically indistinguishable from disseminated intravascular
coagulation (Hossain, 2013). In some cases, impaired hemostasis
further contributes to blood loss.
Thrombocytopenia is the most frequent coagulation defect
found with blood loss and multiple transfusions (Counts,
1979). In addition, packed red cells have very small amounts
of soluble clotting factors, and stored whole blood is deficient
in platelets and in factors V, VIII, and XI. Massive replacement
with red cells only and without factor replacement can also
cause hypofibrinogenemia and prolongation of the prothrombin
and partial thromboplastin times. Because many causes of
obstetrical hemorrhage also cause consumptive coagulopathy,
the distinction between dilutional and consumptive coagulopathy
can be confusing. Fortunately, treatment for both is similar.

A few studies have assessed the relationship between massive

transfusion and resultant coagulopathy in civilian trauma units
and military combat hospitals (Bochicchio, 2008; Borgman, 2007;
Gonzalez, 2007; Johansson, 2007). Patients undergoing massive
transfusion—defined as 10 or more units of blood—had much
higher survival rates as the ratio of plasma to red cell units was near
1.4, that is, one unit of plasma given for each 1.4 units of packed
red cells. By way of contrast, the highest mortality group had a 1:8
ratio. Most of these studies found that component replacement is rarely
necessary with acute replacement of 5 to 10 units of packed red cells.
From the foregoing, when red cell replacement exceeds five
units or so, a reasonable practice is to evaluate the platelet count,
clotting studies, and plasma fibrinogen concentration. In the
woman with obstetrical hemorrhage, the platelet count should
be maintained above 50,000/L by the infusion of platelet concentrates.
A fibrinogen level 100 mg/dL or a sufficiently prolonged
prothrombin or partial thromboplastin time in a woman
with surgical bleeding is an indication for replacement. Freshfrozen
plasma is administered in doses of 10 to 15 mL/kg, or
alternatively, cryoprecipitate is infused (see Table 41-8).
Type and Screen versus Crossmatch. A blood type and
antibody screen should be performed for any woman at significant
risk for hemorrhage. Screening involves mixing maternal
serum with standard reagent red cells that carry antigens
to which most of the common clinically significant antibodies
react. Crossmatching involves the use of actual donor erythrocytes
rather than the standardized red cells. Clinical results
show that the type-and-screen procedure is amazingly efficient.
Indeed, only 0.03 to 0.07 percent of patients identified to
have no antibodies are subsequently found to have antibodies
by crossmatch (Boral, 1979). Importantly, administration of
screened blood rarely results in adverse clinical sequelae.
Packed Red Blood Cells. One unit of packed erythrocytes
is derived from one unit of whole blood to have a hematocrit
of 55 to 80 volume percent, depending on the length of gentle
centrifugation. Thus one unit contains the same volume of erythrocytes as one whole blood unit. It will increase the
hematocrit by 3 to 4 volume percent depending on patient size.
Packed red blood cell and crystalloid infusion are the mainstays of
transfusion therapy for most cases of obstetrical hemorrhage.
Platelets. With operative delivery or with lacerations, platelet
transfusions are considered with ongoing obstetrical hemorrhage
when the platelet count falls below 50,000/L (Kenny, 2014).
In the nonsurgical patient, bleeding is rarely encountered if the
platelet count is 10,000/L or higher (Murphy, 2010). The
preferable source of platelets is a bag obtained by single-donor
apheresis. This is the equivalent of six units from six individual
donors. Depending on maternal size, each single-donor apheresis
bag raises the platelet count by approximately 20,000/L
(Schlicter, 2010). If these bags are not available, then individualdonor
platelet units are used. One unit contains about 5.5 
1010 platelets, and six to eight such units are generally transfused.
Importantly, the donor plasma in platelet units must be
compatible with recipient erythrocytes. Further, because some
red blood cells are invariably transfused along with the platelets,
only units from D-negative donors should be given to
D-negative recipients. If necessary, however, adverse sequelae
are unlikely. For example, transfusion of ABO-nonidentical
platelets in nonpregnant patients undergoing cardiovascular
surgery had no clinical effects (Lin, 2002).
Fresh-Frozen Plasma. This component is prepared by
separating plasma from whole blood and then freezing it.
Approximately 30 minutes are required for frozen plasma to
thaw. It is a source of all stable and labile clotting factors,
including fibrinogen. Thus, it is often used for treatment of
women with consumptive or dilutional coagulopathy. Plasma
is not appropriate for use as a volume expander in the absence of
specific clotting factor deficiencies. It should be considered in a
bleeding woman with a fibrinogen level 100 mg/dL or with
an abnormal prothrombin or partial thromboplastin time.
An alternative to frozen plasma is liquid plasma (LQP).
This never-frozen plasma is stored at 1 to 6ºC for up to 26
days, and in vitro, it appears to be superior to thawed plasma
(Matijevic, 2013).
Cryoprecipitate and Fibrinogen Concentrate. Each unit
of cryoprecipitate is prepared from one unit of fresh-frozen
plasma. Each 10- to 15-mL unit contains at least 200 mg of
fibrinogen, factor VIII:C, factor VIII:von Willebrand factor,
factor XIII, and fibronectin (American Association of Blood
Banks, 2002). It is usually given as a “pool” or “bag” using an
aliquot of fibrinogen concentrate taken from 8 to 120 donors.
Cryoprecipitate is an ideal source of fibrinogen when levels are
dangerously low and there is oozing from surgical incisions.
Another alternative is virus-inactivated fibrinogen concentrate.
Each gram of this raises the plasma fibrinogen level approximately
40 mg/dL (Ahmed, 2012; Kikuchi, 2013). Either is
used to replace fibrinogen. However, there are no advantages
to these compared with fresh-frozen plasma for general clotting
factor replacement. Exceptions are general factor deficiency
replacement for women in whom volume overload may be a
problem—an unusual situation in obstetrics—and for those
with a specific factor deficiency.

Recombinant Activated Factor VII (rFVIIa). This synthetic

vitamin K-dependent protein is available as NovoSeven.
It binds to exposed tissue factor at the site of injury to generate
thrombin that activates platelets and the coagulation
cascade. Since its introduction, rFVIIa has been used to help
control hemorrhage from surgery, trauma, and many other
causes (Mannucci, 2007). More than three fourths of Level I
trauma centers include it in their massive transfusion protocols
(Pacheco, 2011). It is included in the massive transfusion protocol
at Parkland Hospital.
One major concern with rFVIIa use is arterial—and to a
lesser degree venous—thrombosis. In a review of 35 randomized
trials with nearly 4500 subjects, arterial thromboembolism
developed in 55 percent (Levi, 2010a). A second concern is that
it was found to be only marginally effective in most of these
studies (Pacheco, 2011). In obstetrics, recombinant FVIIa has
also been used to control severe hemorrhage in women with
and without hemophilia (Alfirevic, 2007; Franchini, 2007).
It has been used with uterine atony, lacerations, and placental
abruption or previa. In approximately a third of cases, hysterectomy
was required. Importantly, rFVIIa will not be effective if
the plasma fibrinogen level is 50 mg/dL or the platelet count
is 30,000/L.
Topical Hemostatic Agents. Several agents can be used to
control persistent oozing. These were recently reviewed by dos
Santos and Menzin (2012). In general, these are rarely used in
obstetrical hemorrhage.
Autologous Transfusion. Patient phlebotomy and autologous
blood storage for transfusion has been disappointing.
Exceptions are women with a rare blood type or with unusual
antibodies. In one report, three fourths of women who began
such a program in the third trimester donated only one unit
(McVay, 1989). This is further complicated in that the need for
transfusion cannot be predicted (Reyal, 2004). For these and
other reasons, most have concluded that autologous transfusions
are not cost effective (Etchason, 1995; Pacheco, 2011, 2013).
Cell Salvage. To accomplish autotransfusion, blood lost intraoperatively
into the surgical field is aspirated and filtered. The
red cells are then collected into containers with concentrations
similar to packed red cells and are infused as such. Intraoperative
blood salvage with reinfusion is considered to be safe in obstetrical
patients (Pacheco, 2011; Rainaldi, 1998). That said, Allam
and associates (2008) reported the lack of prospective trials but
also found no reports of serious complications.
Complications with Transfusions. During the past several
decades, substantial advances have been achieved in blood
transfusion safety. Although many risks are avoided or mitigated,
the most serious known risks that remain include errors
leading to ABO-incompatible blood transfusion, transfusionrelated
acute lung injury (TRALI), and bacterial and viral transmission
(Lerner, 2010).
The transfusion of an incompatible blood component
may result in acute hemolysis. If severe, this can cause disseminated
intravascular coagulation, acute kidney injury, and
death. Preventable errors responsible for most of such reactions frequently include mislabeling of a specimen or
transfusing an
incorrect patient. Although the rate of such errors in the United
States has been estimated to be 1 in 14,000 units, these are
likely underreported (Lerner, 2010; Linden, 2001). A transfusion
reaction is characterized by fever, hypotension, tachycardia,
dyspnea, chest or back pain, flushing, severe anxiety, and hemoglobinuria.
Immediate supportive measures include stopping the
transfusion, treating hypotension and hyperkalemia, provoking
diuresis, and alkalinizing the urine. Assays for urine and plasma
hemoglobin concentration and an antibody screen help confirm
the diagnosis.
The syndrome of transfusion-related acute lung injury
(TRALI) can be a life-threatening complication. It is characterized
by severe dyspnea, hypoxia, and noncardiogenic pulmonary
edema that develop within 6 hours of transfusion
(Triulzi, 2009). TRALI is estimated to complicate at least 1
in 5000 transfusions. Although the pathogenesis is incompletely
understood, injury to the pulmonary capillaries may
arise from anti-human leukocyte antigen (HLA) antibodies in
donor plasma (Lerner, 2010; Schubert, 2013). These antibodies
bind to leukocytes that aggregate in pulmonary capillaries
and release inflammatory mediators. A delayed form of TRALI
syndrome has been reported to have an onset 6 to 72 hours
following transfusion (Marik, 2008). Management is with
supportive therapy that may include mechanical ventilation
(Chap. 47, p. 944).
Bacterial infection from transfusion of a contaminated blood
component is unusual because bacterial growth is discouraged
by refrigeration. The most often implicated contaminant of red
cells include Yersinia, Pseudomonas, Serratia, Acinetobacter, and
Escherichia species. The more important risk is from bacterial contamination
of platelets, which are stored at room temperature.
Current estimates are that 1 in 1000 to 2000 platelet units are contaminated.
Death from transfusion-related sepsis is 1 per 17,000
for single-door platelets and 1 per 61,000 for
apheresis-donor packs (Lerner, 2010).
Risks from many transfusion-related viral
infections have been curtailed. Fortunately,
the most feared infection—HIV—is the least
common. With current screening methods
using nucleic acid amplification, the risk of
HIV or hepatitis C virus infection in screened
blood is estimated to be 1 case per 1 to 2 million
units transfused (Stramer, 2004). The risk
for HIV-2 infection is less.
Other viral infections include hepatitis B
transmission, which is estimated to be 1
per 100,000 transfused units (Jackson, 2003).
Choosing donors who have been vaccinated
will lower this incidence. Because of its high
prevalence, cytomegalovirus-infected leukocytes
are necessarily often transfused. Thus,
precautions are taken for immunosuppressed
recipients, keeping in mind that this includes
the fetus (Chap. 15, p. 310). Finally, there are
slight risks for transmitting West Nile virus,
human T-lymphotropic virus Type I, and parvovirus
B19 (American Association of Blood
Banks, 2013).

Red Cell Substitutes. Use of these artificial carriers of oxygen

has been abandoned (Ness, 2007; Spiess, 2009). Three that
have been studied include perfluorocarbons, liposome-encapsulated
hemoglobin, and hemoglobin-based oxygen carriers.
■ Adjunctive Surgical Procedures
to Treat Hemorrhage
Uterine Artery Ligation
Several surgical procedures may be helpful to arrest of obstetrical
hemorrhage. Of these, the technique for unilateral or bilateral
uterine artery ligation is used primarily for lacerations at
the lateral part of a hysterotomy incision (Fig. 41-33). In our
experiences, this procedure is less helpful for hemorrhage from
uterine atony.
Uterine Compression Sutures. Almost 20 years ago a surgical
technique to arrest hemorrhage for severe postpartum atony
was introduced by B-Lynch and coworkers (1997). The procedure
involves placement of a No. 2-chromic suture to compress
the anterior and posterior uterine walls together. Because they
give the appearance of suspenders, they are also called braces
(Fig. 41-34). Several modifications of the B-Lynch technique
have been described (Cho, 2000; Hayman, 2002; Matsubara,
2013b; Nelson, 2007). Indications vary for its application, and
this will affect the success rate. For example, B-Lynch (2005)
cited 948 cases with only seven failures. Conversely, Kayem and
associates (2011) described 211 women in whom compression
sutures were employed. The overall failure rate of 25 percent
did not differ between B-Lynch sutures and their modifications.
Our experiences at Parkland Hospital are not nearly so
successful. The technique has been effective in perhaps half of
cases in which it is used.

There are complications with compression sutures, and

some are unique (Matsubara, 2013b). Their precise frequency
is unknown, but it is likely low. The most common involve
variations of uterine ischemic necrosis with peritonitis (Gottlieb,
2008; Joshi, 2004; Ochoa, 2002; Treloar, 2006). Total uterine
necrosis was described by Friederich and associates (2007) in
a woman in whom B-Lynch sutures were placed along with
bilateral ligation of uterine, uteroovarian, and round ligament
arteries. In most cases, subsequent pregnancies are uneventful
if compression sutures are placed. A few women, however, with
B-Lynch or Cho sutures have been reported to have defects in the uterine wall (Akoury, 2008; An, 2013). Another
long-term
complication is uterine cavity synechiae, which may develop in
20 to 50 percent of these women by 3 months (Alouini, 2011;
Ibrahim, 2013; Poujade, 2011).
Internal Iliac Artery Ligation
Ligation of one or both internal iliac arteries has been used
for many years to reduce hemorrhage from pelvic vessels
(Allahbadia, 1993; Joshi, 2007). Drawbacks are that the procedure
may be technically difficult and is only successful half of
the time (American College of Obstetricians and Gynecologists, 2012b). It is not particularly helpful to abate
hemorrhage with
postpartum atony (Clark, 1985; Joshi, 2007).
Adequate exposure is obtained by opening the peritoneum over
the common iliac artery and dissecting down to the bifurcation of
the external and internal iliac arteries (Fig. 41-35). Branches distal
to the external iliac arteries are palpated to verify pulsations at or
below the inguinal area. Ligation of the internal iliac artery 5 cm
distal to the common iliac bifurcation will usually avoid the posterior
division branches (Bleich, 2007). The areolar sheath of the
artery is incised longitudinally, and a right-angle clamp is carefully
passed just beneath the artery from lateral to medial. Care must be
taken not to perforate contiguous large veins, especially the internal
iliac vein. Suture—usually nonabsorbable—is passed under
the artery with a clamp, and the vessel is then securely ligated.
Following ligation, pulsations in and distal to the external
iliac artery are again confirmed. If not, pulsations must be identified
after arterial hypotension has been successfully treated to
ensure that the artery has not been compromised. The most
important mechanism of action with internal iliac artery ligation
is an 85-percent reduction in pulse pressure in those arteries
distal to the ligation (Burchell, 1968). This converts an
arterial pressure system into one with pressures approaching
those in the venous circulation. This creates vessels more amenable
to hemostasis via pressure and clot formation.
Even bilateral internal iliac artery ligation does not appear to
interfere with subsequent reproduction. Nizard and colleagues
(2003) reported follow-up in 17 women who had bilateral
artery ligation. From a total of 21 pregnancies, 13 were normal,
three ended with miscarriage, three were terminated, and there
were two ectopic pregnancies.

Angiographic Embolization
This tool is now used for many causes of intractable hemorrhage
when surgical access is difficult. In more than 500 women reported,
embolization was 90-percent effective (Bodner, 2006; Lee, 2012;
Poujade, 2012; Sentilhes, 2009). Rouse (2013) recently reviewed
the subject and concluded that embolization can be used to arrest
refractory postpartum hemorrhage. However, the author cautioned
that the procedure is less effective with placenta percreta or with
concurrent coagulopathy. Other reports have been less enthusiastic,
and the American College of Obstetricians and Gynecologists
(2012b) describes its efficacy as “unclear.” Fertility is not impaired,
and many subsequent successful pregnancies have been reported
(Chauleur, 2008; Fiori, 2009; Kolomeyevskaya, 2009). There
are limited data describing its antepartum use. Embolization in a
20-week pregnant woman was reported for a large lower uterine
segment arteriovenous malformation (Rebarber, 2009). It has also
been used for renal hemorrhage (Wortman, 2013b).
Complications of embolization are relatively uncommon,
but they can be severe. Uterine ischemic necrosis has been
described (Coulange, 2009; Katakam, 2009; Sentilhes, 2009).
Uterine infection has been reported (Nakash, 2012). Finally,
Al-Thunyan and coworkers (2012) described a woman with
massive buttock necrosis and paraplegia following bilateral
internal iliac artery embolization.
Preoperative Pelvic Arterial Catheter Placement
There are a few instances in which massive blood loss and difficult
surgical dissection is anticipated. For these, investigators
have described use of balloon-tipped catheters inserted into
the iliac or uterine arteries preoperatively. Catheters can then be inflated or embolization performed to mitigate
heavy blood
loss if it develops (Desai, 2012; Matsubara, 2013a). These techniques
are used more commonly in cases of accrete syndromes
(p. 804), and they have also been described for abdominal pregnancy
(Chap. 19, p. 388). The reported success rates have been
variable, and these techniques are not universally recommended
(Angstmann, 2012; Pacheco, 2011, 2013; Zacharias, 2003).
Again the American College of Obstetricians and Gynecologists
(2012b) considers the use and efficacy of these techniques to
be “unclear.” Adverse effects are uncommon, but postoperative
iliac and popliteal artery thrombosis and stenosis have been
reported (Greenberg, 2007; Hoffman, 2010; Sewell, 2006).

Pelvic Umbrella Pack

The umbrella or parachute pack was described by Logothetopulos
(1926) to arrest intractable pelvic hemorrhage following hysterectomy.
Although seldom used today, it can be lifesaving if all
other measures have failed. The pack is constructed of a sterile
x-ray cassette bag that is filled with gauze rolls knotted together
to provide enough volume to fill the pelvis (Fig. 41-36). The
pack is introduced transabdominally with the stalk exiting the
vagina. Mild traction is applied by tying the stalk to a 1-liter fluid bag, which is hung over the foot of the bed. An
indwelling
urinary catheter is placed to prevent urinary obstruction and
to monitor urinary output. Percutaneous pelvic drains can be
placed to monitor ongoing bleeding within the peritoneal cavity.
Broad-spectrum antimicrobials are given, and the umbrella
pack is removed vaginally after 24 hours.
Dildy and colleagues (2006) described use of the pelvic pack
to arrest hemorrhage following hysterectomy in 11 women.
These women were given seven to 77 units of red cells, and the
pack successfully stopped bleeding in all but two women. Over
the years, we have had mixed results with this technique, but
we can recommend it as a “last-ditch” attempt when exsanguination
is inevitable, especially in “low-resource” areas.