Location via proxy:   [ UP ]  
[Report a bug]   [Manage cookies]                

B41. Su-Et-Al PPH PDF

Download as pdf or txt
Download as pdf or txt
You are on page 1of 21

Postpartum

Hemorrhage
Cindy W. Su, MD

KEYWORDS
 Postpartum hemorrhage  Uterine atony  Uterotonic agents
 Uterine tamponade  Perineal lacerations
 Active management of third stage of labor

Postpartum hemorrhage (PPH) is an obstetric emergency that can follow either vaginal
or cesarean delivery. It is the single most significant cause of maternal mortality
worldwide. Annually an estimated 140,000 women die of PPH worldwide: one every
4 minutes.1–3 The World Health Organization (WHO) estimates that approximately
one-quarter of maternal deaths worldwide are caused by PPH.1 In addition to death,
serious morbidity may follow PPH because of the complications of adult respiratory
distress syndrome, coagulopathy, shock, loss of fertility, and pituitary necrosis
(Sheehan syndrome).

DEFINITION

There is no consensus on the single best definition of PPH. Traditionally PPH has been
defined as estimated blood loss of 500 mL or more after vaginal delivery, or 1000 mL
or more after a cesarean delivery. There are, however, two problems with this defini-
tion. First, studies have shown that objectively measured average blood loss after
vaginal and cesarean deliveries is about 500 mL and 1000 mL, respectively.4,5
Second, clinicians are more likely to underestimate than overestimate the volume of
blood loss.5 Using the traditional definitions would thus inaccurately categorize at
least one-half of deliveries as having PPH.
Another classic definition of PPH is a 10% decline in postpartum hemoglobin
concentration from antepartum levels. The problem with this definition is that determi-
nations of hemoglobin or hematocrit concentrations may not reflect the current hema-
tologic status, because this change depends on the timing of the test and amount of
fluid resuscitation given.6 More importantly, the diagnosis would be retrospective,
perhaps useful for research but not so in the clinical setting.
Some clinicians have suggested defining PPH as excessive bleeding that makes the
patient symptomatic (eg, lightheadedness, weakness, palpitations, diaphoresis, and
syncope) and/or results in signs of hypovolemia (eg, hypotension, tachycardia,

The author has nothing to disclose.


Department of Obstetrics & Gynecology, Contra Costa Regional Medical Center, 2500 Alhambra
Avenue, Martinez, CA 94553, USA
E-mail address: cindy.su@hsd.cccounty.us

Prim Care Clin Office Pract 39 (2012) 167–187


doi:10.1016/j.pop.2011.11.009 primarycare.theclinics.com
0095-4543/12/$ – see front matter Ó 2012 Elsevier Inc. All rights reserved.
168 Su

oliguria, and low oxygen saturation [<95%]). However, this method of diagnosis also
has its shortcomings. Maternal blood volume expands 40% to 50% during pregnancy
because of an increase in both plasma volume and red blood cell mass. This increased
blood volume, to some extent, protects the mother from the consequences of hemor-
rhage during and after delivery. Thus, after delivery a woman may lose up to 20% of
her blood volume before clinical signs become apparent.7 Consequently, waiting for
signs of excessive bleeding may delay initiating appropriate treatment.

INCIDENCE

Because of these varied definitions, the exact incidence of PPH is difficult to ascertain.
However, estimates suggest that PPH complicates 4% to 6% of all deliveries.7

ETIOLOGY AND RISK FACTORS

PPH generally is classified as primary or secondary, with primary (also known as early)
PPH occurring within 24 h after delivery, and secondary (also known as delayed) PPH
occurring between 24 h and 6 to 12 weeks postpartum. Box 1 lists the most common
causes of primary and secondary PPH. The “Four Ts” mnemonic (Tone, Tissue,
Trauma, and Thrombin) is another simple and effective way to remember and detect
the specific causes (Table 1).

Tone
The most common cause of PPH is uterine atony (ie, lack of effective contraction of the
uterus after delivery), which complicates 1 in 20 births and is responsible for at least
80% of cases of PPH.6 At term, blood flow through the placental site averages 600
mL/min. After placental delivery, the uterus contracts its myometrial fibers to occlude
the spiral arterioles. If inadequate uterine contraction occurs, rapid blood loss will
ensue. Risk factors for uterine atony include6,8:
 Uterine overdistention (multiple gestation, polyhydramnios, and fetal macrosomia)
 Prolonged oxytocin use
 Rapid or prolonged labor
 Multiparity
 Chorioamnionitis

Box 1
Etiology of PPH

Primary (early or within 24 h)


Uterine atony
Retained placenta, especially placenta accreta
Defects in coagulation
Uterine inversion
Secondary (delayed or between 24 h and 12 weeks)
Subinvolution of placental site
Retained products of conception
Infection
Inherited coagulation defects
Postpartum Hemorrhage 169

Table 1
“Four Ts” mnemonic device for causes of postpartum hemorrhage

Four Ts Cause
Tone Uterine atony
Trauma Lacerations, hematomas, inversion, rupture
Tissue Retained tissue, invasive placenta
Thrombin Coagulopathies

 Preeclampsia
 Placenta previa and accreta
 Uterine-relaxing agents (tocolytic therapy, halogenated anesthetics, and
nitroglycerin)
 History of uterine atony in previous pregnancy
 Uterine inversion
 Retained placenta or placental fragment
 Asian or Hispanic ethnicity.

Trauma
Trauma-related bleeding can be caused by genital tract lacerations, episiotomies, or
uterine rupture. Genital tract lacerations involve the maternal soft-tissue structures,
and can be associated with large hematomas and rapid blood loss if unrecognized.
The most common lower genital tract lacerations include perineal, vulvar, vaginal,
and cervical. Upper genital tract lacerations are typically associated with broad liga-
ment and retroperitoneal hematomas. Although it is difficult to ascertain their exact
incidence, genital tract lacerations are the second leading cause of PPH.8 Risk factors
include8,9:
 Operative vaginal delivery (forceps or vacuum)
 Fetal malpresentation
 Fetal macrosomia
 Episiotomy, especially mediolateral
 Precipitous delivery
 Prior cerclage placement
 Shoulder dystocia.

Tissue
Retained products of conception, namely placental tissue and amniotic membranes,
can inhibit the uterus from adequate contraction and result in hemorrhage. Retained
placenta (ie, failure of the placenta to deliver within 30 minutes of birth) complicates
1 in 100 to 1 in 200 deliveries.10 Risk factors include midtrimester delivery, chorioam-
nionitis, and accessory placental lobes.
Invasive placenta is a cause of PPH that has significant morbidity and can also, at
times, be life threatening.10 One study reported that abnormally adherent placentation
caused 65% of cases of intractable PPH requiring emergency peripartum hysterec-
tomy at Brigham and Women’s Hospital.11 The incidence is estimated at 1 in 2500
deliveries, a tenfold rise in the last 50 years that is most likely due to the increase in
cesarean section rates.12 Classification is based on the depth of invasion and can
be easily remembered through alliteration: placenta accreta adheres to the myome-
trium, placenta increta invades the myometrium, and placenta percreta penetrates
170 Su

the myometrium to or beyond the serosa.13 The greatest risk factor is a placenta previa
in the setting of a prior cesarean section (increasing to 67% with 4 or more14). Other
risk factors include prior myomectomy, prior cesarean delivery, Asherman syndrome,
submucous leiomyomata, and maternal age of 35 years or greater.12
Thrombin
Coagulation disorders are a rare cause of PPH, and are usually identified before
delivery. These disorders include idiopathic thrombocytopenic purpura (ITP), throm-
botic thrombocytopenic purpura (TTP), von Willebrand disease, and hemophilia.
Disorders of coagulation should be suspected in patients with a family history of
such abnormalities and in patients with a history of menorrhagia.15 Women with von
Willebrand disease are prone to postabortal bleeding, but are unlikely to experience
PPH at term. On the other hand, women with factor XI deficiency or who are hemo-
philia carriers are at increased risk of both early and late PPH (16%–22% for early
and 11%–24% for late).16–19 However, PPH alone is not a strong indication for
screening for these defects, given that bleeding disorders are rarely the cause of PPH.
Patients can also develop hemolysis, elevated liver enzyme levels, low platelets
(HELLP), and disseminated intravascular coagulation (DIC). The overall incidence of
DIC in the obstetric population has not been reported; however, several risk factors
have been documented. These include massive antepartum hemorrhage or PPH,
sepsis, severe preeclampsia, amniotic fluid embolism, tissue necrosis (eg, retained
intrauterine fetal demise and trauma), placental abruption, and acute fatty liver of
pregnancy.20

PREVENTION OF PPH

Two preventive methods that have been suggested to reduce PPH from uterine atony
are active management of the third stage of labor and spontaneous delivery of the
placenta after cesarean delivery. Active management of the third stage of labor
involves three steps: (1) giving a prophylactic uterotonic (most commonly oxytocin),
(2) early cord clamping, and (3) controlled cord traction to deliver the placenta. A
Cochrane review showed that patients who were actively managed during the third
stage of labor had significant reductions in mean blood loss (weighted mean differ-
ence 79.33 mL, 95% confidence interval [CI] 94.29 to 64.37), PPH of more
than 500 mL (relative risk 0.38, 95% CI 0.32–0.46), and the length of third stage of
labor (weighted mean difference 9.77 minutes, 95% CI 10.00 to 9.53).21 Contro-
versy exists regarding whether prophylactic oxytocin should be given before or after
delivery of the placenta. A systematic review showed that the timing of administration
of the uterotonic agent made no significant impact on the incidence of PPH, the rate of
placental retention, or the length of the third stage or labor.22 The recommended dose
of oxytocin (Pitocin) is 10 to 40 units in 1 L of lactated Ringer’s intravenously at a rate of
125 to 250 mL/h or 10 units intramuscularly.7
Spontaneous delivery of the placenta during a cesarean section (ie, delivery of the
placenta with cord traction as opposed to manual removal) has also been associated
with reduced blood loss. In a Cochrane review, spontaneous delivery reduced blood
loss by 30% and postpartum endometritis by sevenfold when compared with manual
removal.23

MANAGEMENT OF PPH

Prompt recognition of excessive bleeding after delivery is crucial. A healthy woman


may lose 10% to 15% of her blood volume without a drop in blood pressure.7 By
Postpartum Hemorrhage 171

the time her blood pressure drops appreciably, the patient frequently has lost at least
30% of her blood volume. Thus, relying on vital signs to initiate treatment or to assess
the severity of the bleeding could be misleading and may cause an unnecessary delay
in initiating appropriate treatment.

PRIMARY INTERVENTIONS FOR PPH

Because the single most common cause of hemorrhage is uterine atony, the first inter-
ventions should be directed toward ensuring that the uterus is contracted. The bladder
should be emptied and a bimanual pelvic examination performed. If the uterus is soft
(atonic), massage is performed by placing one hand made into a fist in the anterior fornix
and pushing against the body of the uterus while the other hand compresses the fundus
from above through the abdominal wall (Fig. 1).24 The posterior aspect of the uterus is
massaged with the abdominal hand and the anterior aspect with the vaginal hand. The
fundus should be massaged vigorously for at least 15 seconds and continued until the
uterus remains firm and bleeding has abated. Massage should be maintained while
other interventions are being initiated. These measures may include ensuring adequate
intravenous access (preferably with two large-bore 18-gauge catheters), ordering
appropriate laboratory tests, and requesting uterotonic agents.
The first-line treatment for ongoing blood loss in the setting of decreased uterine
tone is the administration of additional uterotonics.7 The 3 categories of uterotonic
agents include oxytocin, ergot alkaloids, and prostaglandins (Table 2). There is no
evidence that one sequence is better than another.25 The important point is not the
sequence of drugs, but the prompt initiation of uterotonic therapy and prompt assess-
ment of effect. The choice of the agent also depends on its side-effect profile as well
as its contraindications. It should be possible to determine within 30 minutes whether

Fig. 1. Bimanual massage. Bimanual uterine compression massage is performed by placing


one hand in the vagina and pushing against the body of the uterus while the other hand
compresses the fundus from above through the abdominal wall. The posterior aspect of
the uterus is massaged with the abdominal hand and the anterior aspect with the vaginal
hand. (From Gabbe SG, Niebyl JR, Simpson JL. Obstetrics: normal and problem pregnancies.
4th edition. New York: Churchill Livingstone; 2002. p. 468; with permission.)
172
Su
Table 2
Uterotonic agents for management of postpartum hemorrhage

Agent Dose/Route Frequency Contraindications Side Effects


Oxytocin IV: 10–40 units in Continuous None Nausea, vomiting, water
(Pitocin) 1 L normal saline or intoxication
lactated Ringer’s solution
IM: 10 units
Methylergonovine IM: 0.2 mg Every 2–4 h Hypertension, preeclampsia Hypertension, hypotension,
(Methergine) nausea, vomiting
15-Methyl prostaglandin F2a IM: 0.25 mg Every 15–90 min, 8 doses Asthma Nausea, vomiting, diarrhea,
(Carboprost, Hemabate) maximum headache, flushing, fever
Prostaglandin E2 Suppository: vaginal or Every 2 h Hypotension Nausea, vomiting, diarrhea,
(Dinoprostone) rectal fever, chills, headache
20 mg
Misoprostol (Cytotec) 800–1000 mg rectally Single dose None Shivering, fever, diarrhea

Abbreviations: IM, intramuscular; IV, intravenous.


Postpartum Hemorrhage 173

pharmacologic treatment will reverse uterine atony.26 If it does not, prompt invasive
intervention is usually warranted.

Oxytocin
Oxytocin (Pitocin) is usually given as a first-line agent, and is often already administered
prophylactically as part of active management of the third stage of labor.7 The recom-
mended dose is 10 to 40 units in 1 L of normal saline or lactated Ringer’s intravenously
at a rate of 125 to 250 mL/h or 10 units intramuscularly (including directly into the myo-
metrium in the setting of a cesarean section).7 As much as 500 mL can be infused over
10 minutes without complications.13 Higher doses of oxytocin (up to 80 units in 1000
mL) can be infused intravenously for a short duration to manage uterine atony.27
Oxytocin generally is well tolerated and has few side effects, but rapid intravenous
push may, rarely, contribute to hypotension and lead to cardiovascular collapse.28
Carbetocin, a long-acting analogue of oxytocin, is available in many countries (but
not the United States) for preventing uterine atony and hemorrhage. It seems to be as
effective as oxytocin and shares a similar toxicity spectrum.29 The recommended
dose is 100 mg given by a single, slow intravenous injection.29

Ergot Alkaloids
When oxytocin fails to produce adequate uterine tone, a second-line therapy must be
initiated. Ergot alkaloids such as methylergonovine (Methergine) and ergometrine (not
available in the United States) cause smooth muscle contractions and thus rapidly
induce strong tetanic uterine contractions. These agents may be given orally or intra-
muscularly, but never intravenously. In cases of PPH, the recommended dose is 0.2
mg given intramuscularly (including directly into the myometrium) and repeated at 2-
to 4-hour intervals as needed.7 These medications may cause significantly rapid
increases in blood pressure and are, therefore, contraindicated in patients who have
hypertension and preeclampsia. Other side effects include nausea and vomiting.30

Prostaglandins
Prostaglandins enhance uterine contractility and vasoconstriction.31 Carboprost
(Hemabate) is a 15-methyl prostaglandin F2a analogue that is potent and has a long
duration of action. The recommended dose is 250 mg intramuscularly (including
directly into the myometrium) every 15 to 90 minutes, as needed, to a total cumulative
dose of 2 mg (8 doses).7 Carboprost has been proved to control hemorrhage in up to
87% of patients.32,33 In cases where it is not effective, chorioamnionitis or other risk
factors for hemorrhage often are present.31 Asthma is a strong contraindication to
its use because it has bronchoconstrictive properties. Other side effects include diar-
rhea, nausea, vomiting, headache, flushing, and pyrexia.31
Misoprostol (Cytotec), a synthetic prostaglandin E1 analogue, has also been shown to
increase uterine tone and decrease PPH.33,34 Extremely inexpensive, misoprostol is
especially useful for reducing blood loss in resource-poor settings where injectable ute-
rotonics and/or refrigeration are unavailable. It can be administered sublingually, orally,
vaginally, and rectally. Doses range from 200 to 1000 mg; the dose recommended by the
American College of Obstetricians and Gynecologists (ACOG) is 800 to 1000 mg admin-
istered rectally.2,7,34,35 There are no contraindications to misoprostol, although
common side effects include shivering, pyrexia, and diarrhea.36 Although misoprostol
is widely used in the treatment of PPH, it is not approved by the US Food and Drug
Administration (FDA) for this indication.
Dinoprostone is a prostaglandin E2 that is not as commonly used but has also been
shown to be effective in treating PPH.37 The recommended dose is a 20 mg
174 Su

suppository administered either vaginally or rectally and repeated every 2 hours as


necessary.7 It is not to be given in the setting of hypotension and has known side
effects of nausea, vomiting, diarrhea, fever, chills, and headache.7

SECONDARY INTERVENTIONS FOR PPH

If bleeding persists despite the initial interventions described earlier, other etiological
factors besides atony must be considered. Even if atony is present, there may also be
other contributing factors.

Genital Tract Lacerations


Even if inspection for lacerations has been already performed at delivery, a thorough
examination should be repeated, as it is possible that a bleeding site was missed. The
lower genital tract (cervix and vagina) should be examined carefully starting superiorly
at the cervix and progressing inferiorly to the vagina, perineum, and vulva. This
examination requires proper patient positioning, adequate operative assistance,
good lighting, appropriate instrumentation (eg, Simpson or Heaney retractors), and
adequate anesthesia. If necessary, performing the laceration repair in a well-
equipped operating room should be considered.
Sutures should be placed if direct pressure does not stop the bleeding. Episiotomy
increases blood loss as well as the risk of anal sphincter tears (third-degree lacera-
tions) and rectal mucosa tears (fourth-degree lacerations).6,38 Consequently, this
procedure should be avoided unless urgent delivery is necessary, and the perineum
is thought to be a limiting factor.39
Figs. 2–4 illustrate second-, third-, and fourth-degree lacerations of the perineum
and the techniques for their repair. For third- and fourth-degree lacerations, a prophy-
lactic dose of a second-generation cephalosporin (cefotetan or cefoxitin) or of clinda-
mycin, if the patient is allergic to penicillin at the time of repair, has been shown to
decrease perineal wound complications at 2 weeks postpartum.40
In repairing cervical lacerations it is important to secure the apex of the laceration,
which is often a major source of bleeding. However, this area is frequently the most

Fig. 2. (A–D) Second-degree laceration repair. A first-degree laceration involves the four-
chet, the perineal skin, and the vaginal mucous membrane. A second-decree laceration
also includes the muscles of the perineal body. The rectal sphincter remains intact. (From
Gabbe SG, Niebyl JR, Simpson JL. Obstetrics: normal and problem pregnancies. 4th edition.
New York: Churchill Livingstone; 2002. p. 472; with permission.)
Postpartum Hemorrhage 175

Fig. 3. (A–E) Third-degree laceration repair. A third-degree laceration not only extends
through the skin, mucous membrane, and perineal body, but includes the anal sphincter. In-
terrupted figure-of-eight sutures should be placed in the capsule of the sphincter muscle.
(From Gabbe SG, Niebyl JR, Simpson JL. Obstetrics: normal and problem pregnancies. 4th
edition. New York: Churchill Livingstone; 2002. p. 473; with permission.)

Fig. 4. Fourth-degree laceration repair. This laceration extends through the rectal mucosa.
(A) The extent of the laceration is shown, with a segment of the rectum exposed. (B)
Approximation of the rectal submucosa. This is the most commonly recommended method
for repair. (C) Alternative method of approximating the rectal mucosa in which the knots are
actually buried inside the rectal lumen. (D) After closure of the rectal submucosa, an addi-
tional layer of running sutures may be placed. The rectal sphincter is then repaired. (From
Gabbe SG, Niebyl JR, Simpson JL. Obstetrics: normal and problem pregnancies. 4th edition.
New York: Churchill Livingstone; 2002. p. 473; with permission.)
176 Su

difficult to visualize, especially in the setting of an active bleed. A helpful technique to


use in these cases is to start to suture the laceration at its proximal end, using the suture
for traction to expose the more distal portion of the cervix until the apex is in view
(Fig. 5).13 Risk factors for cervical lacerations associated with excessive bleeding or
requiring repair include precipitous labor, operative vaginal delivery, and cerclage.41

Retained Products of Conception


The uterus should be explored and any retained placental fragments of fetal
membranes should be removed manually, if possible, or with ring forceps. Ultrasound
examination can be helpful for the diagnosis of retained tissue and to guide removal.7
Curettage with a 16-mm suction catheter or a large blunt curette (banjo curette) is per-
formed if manual removal is unsuccessful in controlling hemorrhage.26

Uterine Tamponade Techniques


Uterine tamponade is effective in many patients with atony or lower uterine segment
bleeding. Such approaches can be particularly useful as a temporizing measure, but if
a prompt response is not seen, preparations should be made for exploratory lapa-
rotomy and, if necessary, hysterectomy.

Fig. 5. Cervical laceration repair. The cervical laceration repair begins at the proximal part of
the laceration, using traction on the previous sutures to aid in exposing the distal portion of
the defect. (From Gabbe SG, Niebyl JR, Simpson JL. Obstetrics: normal and problem pregnan-
cies. 4th edition. New York: Churchill Livingstone; 2002. p. 474; with permission.)
Postpartum Hemorrhage 177

Either a balloon or a pack can be used for tamponade. Packing with gauze requires
careful layering of the material, such as Kerlix, back and forth from one cornu to the
other using a sponge stick and ending with extension of the gauze through the cervical
os.7 The gauze can be impregnated with 5000 units thrombin in 5 mL sterile saline to
enhance clotting. Often, broad-spectrum antibiotics (such as gentamicin, 1.5 mg/kg
every 8 hours and clindamycin 300 mg every 6 hours) are administered while the
pack is in place.26 If packing does not control hemorrhage, repacking is not advised.42
The same effect often can be derived more easily using a balloon device such as
a Foley catheter, Rusch catheter, condom catheter, Sengstaken-Blakemore tube or,
more recently, the Surgical Obstetric Silicone (SOS) Bakri tamponade balloon.43 The
advantages of such devices are that they allow some assessment of ongoing hemor-
rhage, are easy to place, and are effective.44 A success rate of 84% has been re-
ported.45 The SOS Bakri balloon was specifically designed for placement in the
uterus for control of PPH, and is one of two such devices approved by the US FDA
for this application. It consists of a silicone balloon connected to a 24F, 54-cm long sili-
cone catheter. The balloon provides a tamponade to the uterine surface while the cath-
eter allows drainage of blood from the uterine cavity. Fig. 6 shows its proper placement.
Regardless of the method used, hemoglobin and urine output should be closely
monitored. Such monitoring is especially important when a gauze pack is used
because a large amount of blood can collect behind the pack.26 The balloon or
pack should be removed by 12 to 24 hours.43,44

Arterial Embolization
A patient who has persistent bleeding despite all the aforementioned measures but is
hemodynamically stable may be a candidate for arterial embolization.7 The technique
involves pelvic angiography to visualize the bleeding vessels and placement of Gel-
foam (gelatin) pledgets, coils, or glue into the vessels for occlusion. Balloon occlusion
is also a technique used in such circumstances. A cumulative success rate of 95% has
been reported.46
Arterial embolization has several advantages over surgical intervention. First, it allows
for selective occlusion of bleeding vessels, which can be extremely valuable in patients
with aberrant pelvic vasculature (eg, uterine arteriovenous malformations).47–49
Second, the uterus and potential future fertility are preserved as long as the uterus
and ovaries are intact.50–55 Finally, the procedure has minimal morbidity, enables the
physician to avoid or delay surgical intervention, and can be performed in coagulopathic
patients, allowing more time for blood and clotting factor replacement.13 Serious
complications are unusual, and the procedure-related morbidity of 3% to 6% is much

Fig. 6. SOS Bakri balloon. (Ó Lisa Clark, courtesy of Cook Medical Inc.)
178 Su

less than with laparotomy.46,56 Postembolization fever is the most common complica-
tion; other less common complications include buttock ischemia, vascular perforation,
and infection.

Surgical Interventions
When uterine atony is unresponsive to conservative management, surgical intervention
through laparotomy is necessary. Possible interventions include (1) those that decrease
blood supply to the uterus (arterial ligation), (2) those aimed at causing uterine contrac-
tion or compression (B-Lynch), and (3) those that remove the uterus (hysterectomy).

Arterial ligation techniques


The goal of arterial ligation is to decrease uterine perfusion and subsequent bleeding.
Success rates have varied from 40% to 95% in the literature, depending on which
vessels are ligated.56 Described by O’Leary nearly 40 years ago, uterine artery ligation
is one of the easiest and most effective techniques, and is the recommended initial
step in surgical intervention for refractory PPH.57 To perform the procedure, a large
curved needle with an absorbable suture is passed anterior to posterior through the
uterine myometrium at the level of the lower uterine segment, approximately 1 to 2
cm medial to the broad ligament. The suture then is directed posterior to anterior
through a cleared avascular space in the broad ligament close to the lateral border
of the uterus. The suture is then tied to compress the vessels (Fig. 7). Unilateral artery
ligation will control hemorrhage in 10% to 15% of cases, whereas bilateral ligation will
control an additional 75%.58
If bleeding persists despite bilateral uterine artery ligations, the utero-ovarian vessels
can be ligated in a similar fashion. Alternatively, the ovarian artery can be ligated
directly between the medial margin of the ovary and the lateral aspect of the fundus
in the area of the utero-ovarian ligament (also known as infundibulopelvic vessels). A
stepwise combination of unilateral and then bilateral ligatures starting with the uterine
artery and working toward the ovarian vessels is the recommended strategy.58
Hypogastric (internal iliac) artery ligation can be technically challenging and time
consuming, and should really be performed only by an experienced surgeon who is
familiar with pelvic anatomy. If this procedure fails, it is important to proceed quickly
to more definitive therapy (ie, hysterectomy).59

Uterine suturing techniques


Two uterine suturing techniques that have been described for atony control include
placement of a B-Lynch compression suture and multiple square sutures.60,61 The

Fig. 7. Uterine artery ligation. (From Gabbe SG, Niebyl JR, Simpson JL. Obstetrics: normal and
problem pregnancies. 4th edition. New York: Churchill Livingstone; 2002. p. 470; with
permission.)
Postpartum Hemorrhage 179

B-Lynch compression suture technique involves anchoring a large absorbable suture


within the uterine myometrium, both anteriorly and posteriorly.62 It is then passed in
a continuous fashion around the external surface of the uterus and tied firmly so
that adequate uterine compression occurs (Fig. 8). Numerous case reports have
demonstrated the efficacy of B-Lynch compression sutures in resolving PPH due to
uterine atony.63,64 Furthermore, successful term pregnancies after the B-Lynch tech-
nique have been reported.65,66
A recent report demonstrated efficacy of multiple square sutures within the uterine
wall to control PPH caused by uterine atony, placenta previa, or placenta accreta.61
This technique involves the use of a large absorbable suture on a blunt straight needle.
The needle is passed from the anterior to the posterior aspects of the uterus and back
in the opposite directions, to form a square. The suture is tied firmly to provide
compression to the bleeding surfaces.
Hysterectomy
The final surgical intervention for refractory bleeding caused by uterine atony is hyster-
ectomy. Hysterectomy provides definitive therapy, and is required in the management
of PPH in approximately 1 in 1000 deliveries.67 The procedure should be reserved for
cases in which other measures have failed, and the ACOG recommends that if hyster-
ectomy is performed for uterine atony, there should be documentation of first attempt-
ing other therapies.7

SPECIAL SITUATIONS
Retained Placenta
When there is failure to spontaneously deliver the placenta within 30 minutes after
birth, it is considered a retained placenta. This can occur in 0.5% to 3% of deliveries.10

Fig. 8. (A–C) B-Lynch compression suture. (From Gabbe SG, Niebyl JR, Simpson JL. Obstetrics:
normal and problem pregnancies. 4th edition. New York: Churchill Livingstone; 2002. p. 471;
with permission.)
180 Su

The most popular approach in this situation is an attempt at manual extraction of the
placenta, which can be performed in the delivery room with proper pain control or,
preferably, in the operating room under anesthesia. Although it has become common
practice to administer prophylactic antibiotics to patients who require a manual
extraction of a retained placenta after vaginal delivery, no data exist to support its
effectiveness in preventing subsequent endometritis.68 If manual removal is unsuc-
cessful in controlling hemorrhage, a curettage with a 16-mm suction catheter or
a larger blunt curette (banjo curette) can be used to remove remaining placental frag-
ments or fetal membranes. Often, transabdominal ultrasound guidance is helpful in
determining that the evacuation of tissue is complete.
Two alternative approaches to manual removal of a retained placenta include
intraumbilical-vein injection of oxytocin and sublingual nitroglycerin. A large meta-
analysis study has shown that injection of oxytocin into the intraumbilical vein has no
clinically significant effect in preventing the need for manual extraction.69 Sublingual
nitroglycerin, however, may be effective, although it may cause hemodynamic changes
in blood pressure and thus warrants more clinical trials on its safety for this use.70

Uterine Inversion
Uterine inversion is a life-threatening obstetric emergency that occurs when the
uterine fundus collapses into the endometrial cavity. Its reported incidence ranges
from 1 in 2000 to 23,000 deliveries.71,72 The most common causes of a uterine inver-
sion are excessive umbilical cord traction with a fundally attached placenta, and fun-
dal pressure in the setting of a relaxed uterus (Crede maneuver).73 Once diagnosed,
a uterine inversion should elicit immediate intervention because of the high maternal
mortality that results from hemorrhage and shock. Uterotonic agents should be
discontinued promptly. A call for additional personnel, including anesthesiology,
obstetric, and operating room staff, should be placed. Adequate intravenous access
for maternal fluid resuscitation should be established. The obstetric provider should
then immediately attempt to manually replace the inverted uterus in its normal posi-
tion. This is best accomplished by placing a hand inside the vagina and pushing the
fundus cephalad along the long axis of the vagina. Prompt intervention is important
because the lower uterine segment and cervix contract over time, thus making manual
replacement progressively more difficult.
When immediate uterine replacement is unsuccessful, pharmacologic agents
should be given to relax the uterus. Manual replacement is then reattempted. The
most common uterine relaxants used are terbutaline (0.25 mg intravenously or subcu-
taneously) and magnesium sulfate (4–6 g intravenously over 15–25 minutes). Nitro-
glycerin has also been shown to be an effective uterine relaxant at doses of 50 to
500 mg intravenously.74 Furthermore, with its extremely short half-life, nitroglycerin
may be advantageous in cases of severe hemorrhage and hemodynamic instability.75
When manual replacement is unsuccessful despite the aforementioned measures,
the patient should be taken promptly to the operating room for surgical intervention.

Puerperal Hematomas
Because of the rich vascular supply of the pregnant uterus, vulva, and vagina, on
occasion a blood vessel laceration may lead to the formation of a pelvic hematoma
in the lower or upper genital tract. The most common locations for puerperal hema-
tomas are the vulva, vaginal/paravaginal area, and retroperitoneum; they often present
with pain within the first 24 hours of delivery.
Postpartum Hemorrhage 181

Vulvar hematoma
Most vulvar hematomas result from injury to the branches of the pudendal artery that
occur from episiotomies or spontaneous perineal lacerations. These vessels lie in the
superficial fascia of the anterior and/or posterior pelvic triangle. Blood loss is tampo-
naded by Colle’s fascia, the urogenital diaphragm, and the anal fascia (Fig. 9).
Because of these fascial boundaries, the mass will extend to the skin and a visible
hematoma will develop.
Vulvar hematomas usually present with rapid development of a severely painful,
tense, compressible mass covered by skin with purplish discoloration.76 The most
common initial approach to a vulvar hematoma is conservative management (anal-
gesia and application of cold packs). Most small (<5 cm), nonexpanding vulvar hema-
tomas will resolve spontaneously with supportive care.77 In cases of rapidly expanding
vulvar hematomas resulting in hemodynamic changes or dropping hematocrit,
surgical drainage is indicated.13 A wide linear incision through the skin is recommen-
ded. Once the clot is evacuated, the dead space should be closed in layers with
absorbable suture and a sterile pressure dressing applied. A transurethral Foley cath-
eter should be placed until significant tissue edema subsides.

Vaginal hematoma
Vaginal hematomas result from injury to branches of the uterine artery that most often
result from forceps deliveries, but may also occur with spontaneous vaginal deliveries.
These hematomas accumulate above the pelvic diaphragm (Fig. 10). It is unusual for
large amounts of blood to collect in this region, and protrusion of the hematoma into
the vaginal-rectal area is common.13 Consequently, vaginal hematomas often present
with rectal pressure, and on physical examination a large mass protruding into the
vagina is obvious.78
Conservative treatment is also recommended as the initial step for small (<5 cm),
nonexpanding vaginal hematomas.77 When surgical drainage is indicated, it should
generally be performed under good anesthesia and lighting in an operating room.
Unlike vulvar hematomas, the incision of a vaginal hematoma does not require closing;
rather, a vaginal pack should be placed to tamponade the raw edges.13 If bleeding
persists, selective arterial embolization may be considered.

Fig. 9. Vulvar hematoma fascial boundaries. (From Gabbe SG, Niebyl JR, Simpson JL. Obstet-
rics: normal and problem pregnancies. 4th edition. New York: Churchill Livingstone; 2002.
p. 474; with permission.)
182 Su

Fig. 10. Vaginal hematoma. (From Gabbe SG, Niebyl JR, Simpson JL. Obstetrics: normal and
problem pregnancies. 4th edition. New York: Churchill Livingstone; 2002.)

Retroperitoneal hematoma
Although the least common puerperal hematoma, retroperitoneal hematomas are the
most serious and life threatening. They are usually caused by injury to the branches of
the hypogastric (ie, internal iliac) artery (Fig. 11). The most common childbirth-related
causes are (1) laceration of a uterine artery during a cesarean delivery or uterine
rupture and (2) extension of a paravaginal hematoma. Patients with retroperitoneal
hematomas generally do not present with pain and are often asymptomatic initially.
Rather, because of the significant amount of blood that can accumulate in the

Fig. 11. Retroperitoneal hematoma. (From Gabbe SG, Niebyl JR, Simpson JL. Obstetrics:
normal and problem pregnancies. 4th edition. New York: Churchill Livingstone; 2002.
p. 476; with permission.)
Postpartum Hemorrhage 183

retroperitoneal space, these patients often present with symptoms of hemodynamic


instability from hemorrhage or shock. Treatment of a retroperitoneal hematoma
requires either prompt surgical (incision and evacuation of hematoma) or angiographic
(arterial ligation) intervention.

SIMULATION-BASED TRAINING FOR PPH

A small but growing body of literature has shown that designing a PPH protocol that
involves training in a simulation-based setting with a multidisciplinary team may help
optimize outcomes after PPH.79–83 One study noted improvement in perinatal
outcomes in terms of 5-minute Apgar scores and hypoxic-ischemic encephalop-
athy.84 Several other studies showed an improvement of knowledge, practical skills,
communication, and team performance in acute obstetric situations.79 Running
mock drills can also help identify the obstacles encountered and errors made in
obstetric emergency settings that lead to delayed appropriate care.85 The California
Maternal Quality Care Collaborative has developed an excellent “Obstetric (OB)
Hemorrhage Toolkit” as a resource for health care providers interested in initiating
a standardized PPH protocol on their hospital’s Labor & Delivery floor.86

SUMMARY

PPH is an obstetric emergency that all providers should be prepared for, because it is
one of the most common complications after either vaginal or cesarean delivery. In
managing PPH, one should remember the Four Ts mnemonic (Tone, Tissue, Trauma,
Thrombin)83 to aid in evaluating the possible etiology. Medical management should
always be initiated before progressing to more aggressive interventions such as
a laparotomy. If available, placement of a uterine tamponade balloon may prevent
the necessity for surgical intervention. Also, if the patient is hemodynamically stable,
arterial embolization is an option to consider. Active management of the third stage of
labor can also prevent PPH and may, thus, be encouraged as the standard of practice.
There is also a growing body of literature showing that the creation of a standardized
PPH protocol that involves simulation-based training with a multidisciplinary team may
help decrease maternal morbidity and improve perinatal outcomes.

REFERENCES

1. Kahn KS, Wojdyla D, Say L, et al. WHO analysis of causes of maternal death:
a systematic review. Lancet 2006;367:1066–74.
2. Mous HA, Alfirevic Z. Treatment for primary postpartum haemorrhage. Cochrane
Database Syst Rev 2003;1:CD003249.
3. Lu MC, Fridman M, Korst LM, et al. Variations in the incidence of postpartum
hemorrhage across hospitals in California. Matern Child Health J 2005;9:297–306.
4. Andolina K, Daly S, Roberts N, et al. Objective measurement of blood loss at
delivery: is it more than a guess? Am J Obstet Gynecol 1999;180:S69.
5. Stafford I, Dildy GA, Clark SL, et al. Visually estimated and calculated blood loss
in vaginal and cesarean delivery. Am J Obstet Gynecol 2008;199:519.e1–7.
6. Combs CA, Murphy EL, Laros RK Jr. Factors associated with postpartum hemor-
rhage with vaginal birth. Obstet Gynecol 1991;77:69–76.
7. American College of Obstetricians, Gynecologists. American College of Obstet-
rics and Gynecology practice bulletin: clinical management guidelines for
obstetrician-gynecologists number 76, October 2006: postpartum hemorrhage.
Obstet Gynecol 2006;108:1039–47.
184 Su

8. Stones RW, Paterson CM, Saunders NJ. Risk factors for major obstetric haemor-
rhage. Eur J Obstet Gynecol Reprod Biol 1993;48:15–8.
9. Christianson LM, Bovbjerg VE, McDavitt EC, et al. Risk factors for perineal injury
during delivery. Am J Obstet Gynecol 2003;189:255–60.
10. Weeks AD, Mirembe FM. The retained placenta—new insights into an old
problem. Eur J Obstet Gynecol Reprod Biol 2002;102:109–10.
11. Zelop CM, Harlow BL, Frigoletto FD Jr, et al. Emergency peripartum hysterec-
tomy. Am J Obstet Gynecol 1993;168:1443–8.
12. Wu S, Kocherginsky M, Hibbard JU. Abnormal placentation: twenty-year anal-
ysis. Am J Obstet Gynecol 2005;192:1458–61.
13. Gabbe SG, Niebyl JR, Simpson JL. Obstetrics: normal and problem pregnancies.
4th edition. New York: Churchill Livingstone; 2002.
14. Sl Clark, Koonings PP, Phelan JP. Placenta previa/accreta and prior cesarean
section. Obstet Gynecol 1985;66:89–92.
15. Silver RM, Major H. Maternal coagulation disorders and postpartum hemorrhage.
Clin Obstet Gynecol 2010;53:252–64.
16. Nichols WL, Hultin MB, James AH, et al. von Willebrand disease (VWD):
evidence-based diagnosis and management guidelines, the National Heart,
Lung, and Blood Institute (NHLBI) Expert Panel report (USA). Haemophilia
2008;14:171–232.
17. Kadir RA, Lee CA, Sabin CA, et al. Pregnancy in women with von Willebrand’s
disease or factor XI deficiency. Br J Obstet Gynaecol 1998;105:314–21.
18. Kadir RA, Economides DL, Braithwaite J, et al. The obstetric experience of
carriers of haemophilia. Br J Obstet Gynaecol 1997;104:803–10.
19. Myers B, Pavord S, Kean L, et al. Pregnancy outcome in Factor XI deficiency:
incidence of miscarriage, antenatal and postnatal haemorrhage in 33 women
with Factor XI deficiency. BJOG 2007;114:643–6.
20. Richey ME, Gilstrap LC 3rd, Ramin SM. Management of disseminated intravas-
cular coagulopathy. Clin Obstet Gynecol 1995;38:514–20.
21. Begley CM, Gyte GM, Murphy DJ, et al. Active versus expectant management for
women in third stage of labour. Cochrane Database Syst Rev 2010;7:CD007412.
22. Soltani H, Hutchon DR, Poulose TA. Timing of prophylactic uterotonics for the
third stage of labour after vaginal birth. Cochrane Database Syst Rev 2010;8:
CD006173.
23. Anorlu RI, Maholwana B, Hofmeyr GJ. Methods of delivering the placenta at
caesarean section. Cochrane Database Syst Rev 2008;3:CD004737.
24. Anderson J, Etches D, Smith D. Postpartum hemorrhage. In: Baxley E, editor.
Advanced life support in obstetrics course syllabus. 4th edition. Leawood (KS):
American Academy of Family Physicians; 2001.
25. Rajan PV, Wing DA. Postpartum hemorrhage: evidence-based medical interven-
tions for prevention and treatment. Clin Obstet Gynecol 2010;53:165–81.
26. Jacobs AJ. Management of postpartum hemorrhage at vaginal delivery. Avail-
able at: www.uptodate.com. Accessed October 3, 2011.
27. Munn MB, Owen J, Vincent R, et al. Comparison of two oxytocin regimens to
prevent uterine atony at cesarean delivery: a randomized controlled trial. Obstet
Gynecol 2001;98:386–90.
28. Archer TL, Knape K, Liles D, et al. The hemodynamics of oxytocin and other vaso-
active agents during neuraxial anesthesia for cesarean delivery: findings in six
cases. Int J Obstet Anesth 2008;17:247–54.
29. Su LL, Chong YS, Sameul M. Oxytocin agonists for preventing postpartum hae-
morrhage. Cochrane Database Syst Rev 2007;3:CD005457.
Postpartum Hemorrhage 185

30. Mosby’s drug consult 2005. St Louis (MO): Mosby; 2005.


31. Lamont RF, Morgan DJ, Logue M, et al. A prospective randomised trial to
compare the efficacy and safety of hemabate and syntometrine for the prevention
of primary postpartum haemorrhage. Prostaglandins Other Lipid Mediat 2001;66:
203–10.
32. Oleen MA, Mariano JP. Controlling refractory atonic postpartum hemorrhage with
Hemabate sterile solution. Am J Obstet Gynecol 1990;162:205–8.
33. Gulmezoglu AM, Forna F, Villar J. Prostaglandins for preventing postpartum hae-
morrhage. Cochrane Database Syst Rev 2007;3:CD000494.
34. Hofmeyr GJ, Walraven G, Gulmezoglu AM, et al. Misoprostol to treat postpartum
haemorrhage: a systematic review. BJOG 2005;112:547–53.
35. Chong YS, Chua S, Shen L, et al. Does the route of administration of misoprostol
make a difference? The uterotonic effect and side effects of misoprostol given by
different routes after vaginal delivery. Eur J Obstet Gynecol Reprod Biol 2004;
113:191–8.
36. Lumbiganon P, Villar J, Piaggio G, et al. Side effects of oral misoprostol during the
first 24 hours after administration in the third stage of labour. BJOG 2002;109:
1222–6.
37. Dildy GA 3rd. Postpartum hemorrhage: new management options. Clin Obstet
Gynecol 2002;45:330–44.
38. Carroli G, Belizan J. Episiotomy for vaginal birth. Cochrane Database Syst Rev
1999;3:CD000081.
39. Malhotra M, Sharma JB, Batra S, et al. Maternal and perinatal outcome in varying
degrees of anemia. Int J Gynaecol Obstet 2002;79:93–100.
40. Duggal N, Mercado C, Daniels K, et al. Antibiotic prophylaxis for prevention of
perineal wound complications: a randomized controlled trial. Obstet Gynecol
2008;111:1268–73.
41. Melamed N, Ben-Haroush A, Chen R, et al. Intrapartum cervical lacerations: char-
acteristics, risk factors, and effects on subsequent pregnancies. Am J Obstet
Gynecol 2009;200:388, e1–4.
42. Maier RC. Control of postpartum hemorrhage with uterine packing. Am J Obstet
Gynecol 1993;169:317–21.
43. Bakri YN, Amri A, Abdul Jabbar F. Tamponade-balloon for obstetrical bleeding.
Int J Gynaecol Obstet 2001;74:139–42.
44. Georgiou C. Balloon tamponade in the management of postpartum haemor-
rhage: a review. BJOG 2009;116:748–57.
45. Doumouchtsis SK, Papageorghiou AT, Arulkumaran S. Systematic review of
conservative management of postpartum hemorrhage: what to do when medical
treatment fails. Obstet Gynecol Surv 2007;62:540–7.
46. Ganguli S, Stecker MS, Pyne D, et al. Uterine artery embolization in the treatment
of postpartum uterine hemorrhage. J Vasc Interv Radiol 2001;22:169–76.
47. Barber JT Jr, Tressler TB, Willis GS, et al. Arteriovenous malformation identifica-
tion after conservative management of placenta percreta with uterine artery
embolization and adjunctive therapy. Am J Obstet Gynecol 2011;204(5):e4–8.
48. Sidhu HK, Prasad G, Jain V, et al. Pelvic artery embolization in the management
of obstetric hemorrhage. Acta Obstet Gynecol Scand 2010;89:1096–9.
49. Ghai S, Rajan DK, Asch MR, et al. Efficacy of embolization in traumatic uterine
vascular malformations. J Vasc Interv Radiol 2003;14:1401–8.
50. Ornan D, White R, Pollak J, et al. Pelvic embolization for intractable postpartum
hemorrhage: long-term follow-up and implications for fertility. Obstet Gynecol
2003;102:904–10.
186 Su

51. Wang H, Garmel S. Successful term pregnancy after bilateral uterine artery
embolization for postpartum hemorrhage. Obstet Gynecol 2003;102:603–4.
52. Chauleur C, Fanget C, Tourne G, et al. Serious primary post-partum hemorrhage,
arterial embolization and future fertility: a retrospective study of 46 cases. Hum
Reprod 2008;23:1553–9.
53. Fiori O, Deux JF, Kambale JC, et al. Impact of pelvic arterial embolization for
intractable postpartum hemorrhage on fertility. Am J Obstet Gynecol 2009;200.
384.e1–4.
54. Sentilhes L, Gromez A, Calvier E, et al. Fertility and pregnancy following pelvic
arterial embolisation for postpartum haemorrhage. BJOG 2010;117:84–93.
55. Kirby JM, Kachura JR, Rajan DK. Arterial embolization for primary postpartum
hemorrhage. J Vasc Interv Radiol 2009;20:1036–45.
56. Mousa HA, Walkinshaw S. Major postpartum haemorrhage. Curr Opin Obstet Gy-
necol 2001;13:595–603.
57. O’Learly JL, O’Leary JA. Uterine artery ligation in the control of intractable post-
partum hemorrhage. Obstet Gynecol 1974;43:849–53.
58. Adrabbo F, Salah J. Stepwise uterine devascularization: a novel technique for
management of uncontrolled postpartum hemorrhage with preservation of the
uterus. Am J Obstet Gynecol 1984;171:694–700.
59. Evans S, McShane P. The efficacy of internal iliac artery ligation in obstetric
hemorrhage. Surg Gynecol Obstet 1985;160:250–3.
60. B-Lynch C, Coker A, Lawal AH, et al. The B-Lynch surgical technique for the
control of massive postpartum haemorrhage: an alternative to hysterectomy?
Five cases reported. Br J Obstet Gynaecol 1997;104:372–5.
61. Cho JH, Jun HS, Lee CN. Hemostatic suturing technique for uterine bleeding
during cesarean delivery. Obstet Gynecol 2000;96:129–31.
62. Price N, B-Lynch C. Technical description of the B-Lynch brace suture for treat-
ment of massive postpartum hemorrhage and review of published cases. Int J
Fertil Womens Med 2005;50:148–63.
63. Kayem G, Kurinczuk JJ, Alfirevic Z, et al. Uterine compression sutures for the
management of severe postpartum hemorrhage. Obstet Gynecol 2011;117:14–20.
64. Baskett TF. Uterine compression sutures for postpartum hemorrhage: efficacy,
morbidity, and subsequent pregnancy. Obstet Gynecol 2007;110:68–71.
65. Sentilhes L, Gromez A, Trichot C, et al. Fertility after B-Lynch suture and stepwise
uterine devascularization. Fertil Steril 2009;91. 934.e5–9.
66. Tsitlakidis C, Alalade A, Danso D, et al. Ten year follow-up of the effect of the B-
Lynch uterine compression suture for massive postpartum hemorrhage. Int J Fer-
til Womens Med 2006;51:262–5.
67. Habek D, Becarevic R. Emergency peripartum hysterectomy in a tertiary
obstetric center: 8-year evaluation. Fetal Diagn Ther 2007;22:139–42.
68. Chongsomchai C, Lumbiganon P, Laopaiboon M. Prophylactic antibiotic for
manual removal of retained placenta in vaginal birth. Cochrane Database Syst
Rev 2006;2:CD004904.
69. Nardin JM, Weeks A, Carroli G. Umbilical vein injection for management of re-
tained placenta. Cochrane Database Syst Rev 2011;5:CD001337.
70. Abdel-Aleem H, Abdel-Aleem MA, Shaaban OM. Tocolysis for management of re-
tained placenta. Cochrane Database Syst Rev 2011;1:CD007708.
71. Baskett TF. Acute uterine inversion: a review of 40 cases. J Obstet Gynaecol Can
2002;24(12):953–6.
72. Shah-Hosseini R, Evrard JR. Puerperal uterine inversion. Obstet Gynecol 1989;
73(4):567–70.
Postpartum Hemorrhage 187

73. Lipitz S, Frenkel Y. Puerperal inversion of the uterus. Eur J Obstet Gynecol Re-
prod Biol 1988;27:271–4.
74. Smith GN, Brien JF. Use of nitroglycerin for uterine relaxation. Obstet Gynecol
Surv 1998;53(9):559–65.
75. Dayane SS, Schwalbe SS. The use of small-dose intravenous nitroglycerin in
a case of uterine inversion. Anesth Analg 1996;82(5):1091–3.
76. Zahn CM, Yeomans ER. Postpartum hemorrhage: placenta accreta, uterine inver-
sion, and puerperal hematomas. Clin Obstet Gynecol 1990;33(3):422–31.
77. Zahn CM, Hankins GD, Yeomans ER. Vulvovaginal hematomas complicating
delivery. Rationale for drainage of the hematoma cavity. J Reprod Med 1996;
41(8):569–74.
78. Guerriero S, Ajossa S, Bargellini R, et al. Puerperal vulvovaginal hematoma: sono-
graphic findings with MRI correlation. J Clin Ultrasound 2004;32(8):415–8.
79. Merien AE, van de Ven J, Mol BW, et al. Multidisciplinary team training in a simu-
lation setting for acute obstetric emergencies: a systematic review. Obstet Gyne-
col 2010;115(5):1021–31.
80. Skupski DW, Lowenwirt IP, Weinbaum FI, et al. Improving hospital systems for the
care of women with major obstetric hemorrhage. Obstet Gynecol 2006;107(5):
977–83.
81. Fuchs KM, Miller RS, Berkowitz RL. Optimizing outcomes through protocols,
multidisciplinary drills, and simulation. Semin Perinatol 2009;33(2):104–8.
82. Clark EA, Fisher J, Arafeh J, et al. Team training/simulation. Clin Obstet Gynecol
2010;53(1):265–77.
83. Advanced Life Support in Obstetrics (ALSO) Curriculum, American Academy of
Family Physicians proprietary materials.
84. Draycott T, Sibanda T, Owen L, et al. Does training in obstetric emergencies
improve neonatal outcome? BJOG 2006;113:177–82.
85. Maslovitz S, Barkai G, Lessing JB, et al. Recurrent obstetric management
mistakes identified by simulation. Obstet Gynecol 2007;109:1295–300.
86. California maternal quality care collaborative (CMQCC): OB Hemorrhage Toolkit.
Available at: http://www.cmqcc.org/ob_hemorrhage. Accessed October 25,
2010.

You might also like