CPG-3rd Trimester Bleeding and Postpartum Hemorrage 2009

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Philippine Obstetrical and

Gynecological Society (POGS), Foundation, Inc.
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CLINICAL PRACTICE GUIDELINES

on
THIRD TRIMESTER BLEEDING

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November 2009
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Task Force on Clinical Practice Guideline

In the Management of Third Trimester Bleeding
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Philippine Obstetrical and

Gynecological Society (POGS),
Foundation, Inc.
CLINICAL PRACTICE GUIDELINES

on
November 2009

in the Management of Third Trimester Bleeding

In the Management of
Abnormal Labor and Delivery
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FOREWORD!
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LOURDES B. CAPITO, MD
President
Philippine Obstetrical and Gynecological Society (Foundation), Inc. (POGS), 2009
I have envisioned and have implemented to completion the publication of a series of

Clinical Practice Guidelines on the major procedures and topics of Obstetrics and
Gynecology. This is in consonance with the theme of my Presidency, Babae, Kalusugan
Mo, Katungkulan Natin. This is the Clinical Practice Guidelines on Third Trimester Bleeding
and is the First Edition of this Publication, 2009.
In the role of the POGS to provide its members with updates, current and standard
practice recommendations and guidelines, this publication will fulfill the objective of
continuing education and implementation of refinements in Obstetrics and Gynecology. In
keeping with the highest standards of care, the Level and Grades of Clinical
Practice/Recommendation have been adopted for every recommendation that is completed
and decided.
In the process of the formulation of the guideline/recommendation, the entire
membership of the POGS was consulted. I take special effort to thank the AdHoc Committee
on Clinical Practice Guidelines, headed by its Chair, Dr. Efren J. Domingo, for the unceasing
tireless effort to complete this publication. I also gratefully acknowledge the Chairs and
Training Officers
of the Residency-Accredited Hospitals, the Task
Force
Contributors/Reviewers, and the CME Committee.
It becomes easy, dignified and scientific to conduct the practice of Obstetrics and
Gynecology specifically on Third Trimester Bleeding. Now, the Clinical Practice Guidelines
on Third Trimester Bleeding will hope to update and make the practice current and
responsive to world-class standards and make the patients under our care deserving of the
trust and confidence that we, Obstetricians, impart with utmost care and compassion.
LOURDES BLANCO-CAPITO, MD
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INTRODUCTION!
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EFREN J. DOMINGO, MD, PhD
Chair, AdHoc Committee on the Clinical Practice Guidelines, 2009
The Clinical Practice Guidelines on Third Trimester Bleeding is the First Edition of
this Publication, 2009. The Philippine Obstetrical and Gynecological Society, (Foundation),
Inc. (POGS), through the AdHoc Committee on Clinical Practice Guidelines initiated and led
to completion the publication of this manual in plenary consultation with the Residency
Accredited Training Hospitals Chairs and Training Officers, The Regional Board of
Directors, The Board of Trustees, The Task Force Contributors/Reviewers for Third
Trimester Bleeding, and the Committee on Continuing Medical Education.
This publication represents the collective effort of the POGS in updating the clinical
practice of Obstetrics and Gynecology, specifically on Third Trimester Bleeding, and making
it responsive to the most current and acceptable standard in this procedure. A greater part of
the inputs incorporated in this edition are the contributions originating from the day-to-day
academic interactions from the faculty of the different Residency-Accredited Hospitals in
Obstetrics and Gynecology in the country.
This Clinical Practice Guideline on Third Trimester Bleeding is envisioned to become
the handy companion of the Obstetrician-Gynecologist in his/her day-to-day rendition of
quality care and decision making in managing the Obstetric patient. This is also envisioned
to provide the academic institutions in the country and in Southeast Asia updated information
on Third Trimester Bleeding treatment refinements being practiced in the Philippines.
Profound gratitude is extended to all the members of the POGS, the Chairs and
Training Officers of the Residency-Training Accredited Institutions, the Regional Directors,
The Task Force on the Management of Third Trimester Bleeding Contributors/Reviewers,
The CME Committee members, and the 2009 POGS Board of Trustees.
EFREN J. DOMINGO, MD, PhD

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BOARD OF TRUSTEES 2009

OFFICERS
Lourdes B. Capito, MD
President
Regta L. Pichay, MD
Vice President
Ma. Carmen H. Quevedo, MD
Secretary
Ditas Christina D. Decena, MD
Treasurer
Christia S. Padolina, MD
Public Relations Officer
BOARD OF TRUSTEES
Mayumi S. Bismarck, MD
Virgilio B. Castro, MD
Efren J. Domingo, MD, PhD
Gil S. Gonzales, MD
Diosdado V. Mariano, MD
Ma. Socorro M. Solis, MD
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ADHOC COMMITTEE ON CLINICAL PRACTICE GUIDELINES ON

Efren J. Domingo, MD, PhD
Chair
MEMBERS
Jennifer T. Co, MD
Jericho Thaddeus P. Luna, MD
Josephine M. Lumitao, MD
Lisa Teresa P. Jabson, MD
Noel E. Raymundo, MD
Elisa O. Tiu, MD
FELLOWS
Rachelle U. delos Reyes, MD
Ana Victoria V. Dy Echo, MD
May Nueva-Hipolito, MD
Michelle R. Ong, MD
Renee Vina G. Sicam, MD
TECHNICAL STAFF ASSISTANTS
Ms. Emiliana C. Enriquez
Ms. Jhasmin G. De Guzman
TASK FORCE ON THIRD TRIMESTER BLEEDING
Blanca C. De Guia, MD, MSc
Chair
MEMBERS
Ernesto S. Uichanco, MD
Angelito Teotico, MD
Rafael S. Tomacruz, MD
Ryan Capitulo, MD
Lyla Reyes, MD
TASK FORCE REVIEWERS AND PLENARY REVIEWERS
Rainerio S. Abad, MD
Imelda O. Andres, MD
Cecilia Joyce M. Bascarra, MD
Mayumi S. Bismark, MD
Ricardo R. Braganza, MD
Sylvia A. Carnero, MD
Virgilio B. Castro, MD
Lyra Ruth Clemente-Chua, MD
Maria Lourdes B. Coloma, MD
Godofreda V. Dalmacion, MD
Ditas Cristina D. Decena, MD
Santiago A. del Rosario, MD
Rey H. Delos Reyes, MD
Virginia R. de Jesus, MD
Arcangel N. Diamante, MD
Rommel Z. Dueas, MD
Joseline A. Ferrolino, MD
Ma. Corazon N. Gamilla, MD
Erlinda G. Germar, MD
Ma. Antonia E. Habana, MD
Myrna R. Habaa, MD
Bernardita B. Javier, MD
Milagros T. Jocson, MD
Lilia P. Luna, MD
Augusto M. Manalo, MD
Diosdado V. Mariano, MD
Jocelyn Z. Mariano, MD
Christia S. Padolina, MD
Mildred N. Pareja, MD
Wilhelmina Pineda, MD
Regional Directors
Ellen A. Manzano, MD (Region 1)
Melchor C. dela Cruz, MD (Region 2)
Concepcion P. Aronza, MD (Region 3)
Ernesto S. Naval, MD (Region 4)
Rowena M. Auxillos, MD (Region 4A)
Cecilia Valdes-Neptuno, MD (Region 5)
Patria P. Punsalan, MD
Ma. Carmen H. Quevedo, MD
Rebecca M. Ramos, MD
Cristina C. Raymundo, MD
Rosendo R. Roque, MD
Marilyn D. Ruaro, MD
Ma. Socorro M. Solis, MD
Sherri Ann L. Suplido, MD
Walfrido W. Sumpaico, MD
Carmencita B. Tongco, MD
Ma. Victoria Torres, MD
Milagros P. Torres, MD
Ma. Trinidad R. Vera, MD
Ma. Guadalupe N. Villanueva, MD
Evelyn R. Lacson, MD (Region 6)

Belinda N. Paares, MD (Region 7)
Realino G. Molina, MD (Region 8)
Suzette S. Montuno, MD (Region 9)
Jana Joy R. Tusalem, MD (Region 10)
Amelia A. Vega, MD (Region 11) !
DISCLAIMER, RELEASE AND WAIVER OF RESPONSIBILITY
This is the Clinical Practice Guidelines (CPG) on Third Trimester Bleeding, First Edition,
November 2009.
This is the publication of the Philippine Obstetrical and Gynecological Society,
(Foundation), Inc. (POGS).
This is the ownership of the POGS, its officers, and its entire membership.
The obstetrician-gynecologist, the general practitioner, the patient, the student, the allied
medical practitioner, or for that matter, any capacity of the person or individual who may
read, quote, cite, refer to, or acknowledge, any, or part, or the entirety of any topic,
subject matter, diagnostic condition or idea/s willfully release and waive all the liabilities
and responsibilities of the POGS, its officers and general membership, as well as the
AdHoc Commiittee on the Clinical Practice Guidelines and its Editorial Staff in any or all
clinical or other disputes, disagreements, conference audits/controversies, case
discussions/critiquing.
The reader is encouraged to deal with each clinical case as a distinct and unique clinical
condition which will never fit into an exact location if reference is made into any or all
part/s of this CPG.
The intention and objective of this CPG is to serve as a guide, to clarify, to make clear the
distinction. It is not the intention or objective of this CPG to serve as the exact and precise
answer, solution and treatment for clinical conditions and situations. It is always
encouraged to refer to the individual clinical case as the one and only answer to the case
in question, not this CPG.
It is hoped that with the CPG at hand, the clinician will find a handy guide that leads to
the a clue, to a valuable pathway that leads to the discovery of clinical tests leading to
clinical treatments and eventually recovery.
In behalf of the POGS, its Board of Trustees, the AdHoc Committee on The Clinical
Practice Guidelines, 2009, this CPG is meant to make each one of us a perfect image of
Christ, the Healer.
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CPG ON THIRD TRIMESTER BLEEDING

TOPICS / CONTENTS / AUTHOR/S!
A. Third Trimester Bleeding
Antepartum Hemorrhage .............
Blance C. De Guia, MD, MSc
Abruptio Placenta
Placenta Previa
Placenta Accreta .
Angela Teotico, MD
B. Postpartum Hemorrhage
Postpartum Hemorrhage ..
Uterine Atony
Retained Placenta .
Ryan B. Capitulo, MD
Uterine Rupture
Genital Tract Trauma
Lyla D. Reyes, MD
Uterine Inversion ..
Lyla D. Reyes, MD
C. Appendix
Level and Grade of Recommendation ..
Guidelines for Blood Transfusion .
ANTEPARTUM HEMORRHAGE
Definition and Incidence
Antepartum hemorrhage is defined as vaginal bleeding from 22 weeks of gestation up
to delivery. The most common causes include placenta previa, placenta accreta, and others,
which include reproductive tract lesions.
It occurs in 2 to 5% of pregnancies.
Physiology
The uterus receives 1% of cardiac output in the nonpregnant state but receives 20% of
the cardiac output in the third trimester of pregnancy.1
When massive bleeding occurs during the third trimester the loss of blood greatly
alters the hemodynamics of blood distribution resulting in a very unstable pregnant woman.
Reference
1. Alarm International, 4th edition. The Society of Obstetrics and Gynecologists of Canada
ABRUPTIO PLACENTA
Background
By definition, abruptio placenta is the premature separation of a normally implanted
placenta. When there is placenta previa, it is not conventionally considered abruptio in the
true sense. It is an important cause of vaginal bleeding in the second half of pregnancy,
complicating about 1% of births1.
It may be a revealed type of abruptio, in which case blood tracks down revealed
between the membranes and the decidua, and escapes through the cervix into the vagina. Less
commonly, it may be a concealed type of abruptio when blood accumulates behind the
placenta, with no obvious external bleeding.
Abruptio placenta may be total, involving the entire placenta, in which case it
typically leads to fetal death. Or it may be partial, with only a portion of the placenta
detached from the uterine wall.
In the past, expectant management has resulted in perinatal death rates as high as 50%
among infants alive at the time of admission. In an attempt to improve fetal outcome, some
authors have suggested immediate delivery, usually by cesarean section (CS), in all but the
mildest cases. More recently, in an effort to optimize fetal survival and to attain a more
acceptable CS rate, selective management of abruptio placenta has evolved.
The precise pathophysiology that leads to abruptio placenta is still not fully
understood in many cases. It may result from hemorrhage at the decidual-placental interface
and it seems that acute vasospasm of small vessels may be the event that immediately
precedes the placental separation. There may be thrombosis of the decidual vessels with
associated decidual necrosis and venous hemorrhage 2.
In some cases, it may be due to acute processes resulting from one of the following:
1. Shearing forces resulting from trauma
2. Sudden uterine decompression resulting from membrane rupture with hydramnios,
3. Cocaine usage leading to acute vasoconstriction with resultant placental separation.
In the majority of cases it is thought to involve chronic processes, abruptio placenta as
the consequence of a long-standing process that probably dates back to the first trimester.
Placental bed biopsies in women with abruptio demonstrate a lack of adequate trophoblastic
invasion 2 and in some, evidence of chronic pathologic lesions. Uteroplacental insufficiency
seems to play a role in the cause of abruptio, with bleeding in the first two trimesters of
pregnancy associated with an increased risk of subsequent placental separation. Thrombin,
found within the hemorrhage, is a potent uterotonic agent and uterine contractions are
frequently present.
Acute separation of the placenta deprives the fetus of oxygen and nourishment, with
the consequence that the fetus frequently dies if the abruptio is severe.
On the maternal side, the coagulation cascade is activated with consumption of
coagulation factors and consequent disseminated intravascular coagulopathy (DIC). This risk
is highest when there is such a large placental detachment as to cause fetal death.
Hemorrhage associated with DIC leads to further consumption of coagulation factors setting
off a vicious cycle.
The evolution and acceptance of the concept of a long-standing or Chronic abruptio
may have changed the old perception and management of this hemorrhagic complication.
Recommendations
1. When is abruptio placenta suspected?
The diagnosis of abruptio placenta is a clinical one and it is suspected in women who
present with vaginal bleeding or abdominal pain or both, a history of trauma, or
those who present in otherwise unexplained preterm labor. (Grade C)
Summary of Evidence
The classically described symptoms of abruptio placenta are vaginal bleeding and
abdominal pain but may occur with neither or just of one of these signs. It is diagnosed
clinically when 2 or more of the following criteria are present 1:
1. Significant unexplained vaginal bleeding after 20 weeks gestation.
2. Uterine irritability manifested as high frequency uterine contractions or uterine
hypertonus.
3. Uterine tenderness or back pain significant in the presence of sonographic evidence
of a posterior placenta.
4. Evidence of fetal distress on electronic fetal heart rate monitoring.
The severity of symptoms depends on the location of the abruptio, whether it is
revealed or concealed, and the degree of separation. Admittedly, the amount of bleeding
may be just a subjective estimate.
Typically, there is uterine hypertonus with associated high-frequency, lowamplitude uterine contractions occurring five or more times in ten minutes. Likewise, it
may manifest as baseline uterine tone that is excessive by palpation.
The uterus is frequently tender and may feel hard on palpation. The clinician,
though, must be careful to exclude local factors like costovertebral angle tenderness due
to pyelonephritis or musculoskeletal pain. Backache may be the only symptom, especially
when the placental location is posterior.
There may be acute fetal distress, and in cases where more than 50% of the
placenta has separated, fetal demise. There is a correlation between the extent of placental
separation and the risk of stillbirth, with stillbirth occurring in most cases in which there is
greater than 50% placental separation. Fetal distress may be manifest on heart rate
monitoring as repetitive late decelerations, severe variable decelerations with loss of
baseline variability, or sustained bradycardia. (Level III)
2. Which clinical tests are useful in the evaluation of pregnant women suspected of
having abruptio placenta?
The clinical tests most useful are the ultrasonographic examination of the uterus and
placenta and electronic fetal heart rate monitoring. (Grade A)
Summary of Evidence
Fetal heart rate patterns described in association with abruptio are recurrent late or
variable decelerations, reduced variability, bradycardia, or a sinusoidal fetal heart rate
pattern. (Level III)
The ultrasonographic appearance of abruptio depends to a large extent on the size

and location of the bleeding, as well as the duration between the abruption and the time
the ultrasonographic examination was performed.
In cases of acute revealed abruptio, the examiner may detect no abnormal
ultrasonographic findings. Nyberg and colleagues3, in a retrospective cohort study of
images in 57 cases of abruptio, found that the ultrasonographic appearance of abruptio in
the acute phase was hyperechoic to isoechoic when compared with the placenta. Later on,
as the hematomas resolved, they became hypoechoic within 1 week and sonolucent within
2 weeks. In some cases, only a thickened heterogenous placenta could be seen. Thus, it is
important to realize that abruptio may have a variety of ultrasonographic appearance.
(Level II-2)
Ultrasonography will fail to detect at least one half of cases of abruptio. However,
when the ultrasonogram seems to show an abruptio, the likelihood that there is indeed an
abruptio is extremely high. Importantly, a negative ultrasonogram does not rule out an
abruption.4 (Level II-2)
Yeo and colleagues5, in a prospective cohort study of 73 patients presenting with
vaginal bleeding in the second half of pregnancy, using 7 ultrasonographic parameters,
showed that the sensitivity of ultrasound for abruptio placenta was 80% whereas the
specificity was 92%. Positive and negative predictive values were 95% and 69%,
respectively. These are the Ultrasonographic Criteria for Diagnosis of Abruptio Placenta
used:
1. Preplacental collection under the chorionic plate (between the placenta and amniotic
fluid)
2. Jello-like movement of the chorionic plate with fetal activity
3. Retroplacental collection
4. Marginal hematoma
5. Subchorionic hematoma
6. Increased heterogenous placental thickness (more than 5 cm in a perpendicular plane)
7. Intra-amniotic hematoma (Level II-2)
Ultrasonography may also predict prognosis in abruptio. Nyberg and colleagues3
in a retrospective review of 69 cases of abruptio, found that fetal mortality correlated with
the ultrasonographically estimated percentage of abruptio and with the location, with the
worst prognosis occurring in retroplacental abruptios. An important role of
ultrasonography in evaluation of bleeding in the second half of pregnancy is placental
location; if there is a placenta previa, it makes it less likely that abruptio is the cause of
the bleeding. (Level II-2)
3. What other pregnancy conditions should be considered in patients suspected of
abruptio?
All other pregnancy conditions that can cause abdominal pain and bleeding should
also be considered. These include placenta previa, appendicitis, urinary tract
infections, preterm labor, fibroid degeneration, ovarian pathology, and muscular
pain.2 The above-mentioned clinical tests, correlated with good history and thorough
physical examination will help make a proper diagnosis. (Grade C)
4. What is the optimal method of initial management of a patient with abruptio

placenta?
Initial management of a patient with abruptio placenta consists of stabilizing the
pregnant patient, detecting any coagulation derangement, and instituting monitoring
methods to detect maternal as well as fetal compromise. (Grade C)
Summary of Evidence
The following measures are instituted as recommended by the University of
Cincinnati Medical Center1:
1.
2.
3.
4.
Nasal oxygen
Intravenous hydration using large bore catheter
Type and crossmatch for 4 units of packed red blood cells (RBC)
Evaluation of hematologic and clotting studies (complete blood count, prothrombin
time, partial thromboplastin time, fibrinogen, platelet count)
5. Monitoring of urinary output with indwelling bladder catheter
6. Continuous electronic fetal heart rate and uterine activity monitoring (Level III)
It is important to stabilize the patient and to correct any coagulation derangement
before and during delivery or surgery. It is prudent to involve an anesthesiologist in the
early care.
At present, opinion on the management of abruptio range from a conservative
approach, with resultant low CS rate and a high perinatal mortality, to a more aggressive
approach of immediate delivery by CS in all but the mildest cases. Some authors have
suggested that intensive fetal monitoring and a readiness to do a CS for the sake of the
fetus alone may result in improved fetal survival. (Level III)
5. When is immediate CS indicated in patients with abruptio placenta?
At term or near term with a live fetus, prompt delivery is indicated once there is
evidence of fetal compromise, severe uterine hypertonus, life-threatening vaginal
bleeding or DIC when vaginal delivery is not imminent. Cesarean delivery should be
performed promptly because total placental detachment could occur without
warning. (Grade B)
Summary of Evidence
In a case-control study examining the relationship between decision-delivery
interval and perinatal outcome in 33 patients with clinically overt abruption and fetal
bradycardia, Kayani and colleagues6 found that longer decision-delivery intervals were
associated with poorer perinatal outcomes. In severe abruptio placenta complicated by
fetal bradycardia, a decision to delivery interval of 20 minutes or less was associated with
substantially reduced neonatal morbidity and mortality. (Level II-2)
6. Is there room for expectant management in abruptio placenta?

With labor well established, expectant management in abruptio placenta is an option
when both maternal and fetal status are reassuring or when there is fetal demise as
long as the mother is stable. (Grade B)
Summary of Evidence
It is important to individualize management on a case-by-case basis. More
aggressive management, desirable in cases of severe abruptio, may not be appropriate in
milder cases. The proper choice depends on the presentation, the gestational age, and the
degree of maternal and fetal compromise
When both maternal and fetal status is reassuring, conservative management, with
the goal of vaginal delivery, is reasonable. Near term, labor, if established, should be
allowed to progress; otherwise induction of labor should be considered. Both mother and
fetus should be monitored closely during labor 2. (Level III)
In severe abruptio with fetal death, regardless of gestational age, expectant
management is acceptable as long as the mother is stable. When the fetus is dead or
previable, there is no evidence that establishing an arbitrary time limit for delivery is
necessary. Experiences at both the University of Virginia7 and Parkland8 Hospitals
indicate that maternal outcome depends on the diligence with which adequate fluid and
blood replacement therapy is pursued, rather than the interval to delivery. At the
University of Virginia Hospital, women with severe abruptio placenta who were
transfused for 18 hours or more before delivery experienced complications that were
neither more numerous nor greater in severity than the group in which delivery was
accomplished sooner. (Level II-2)
7. Is there room for a conservative approach when there is abruptio placenta in very
preterm pregnancies (20-34 weeks gestation)?
When there is only partial abruptio placenta and the maternal and fetal status are
reassuring, the patient may be managed conservatively. (Grade B)
Summary of Evidence
Preterm birth is the leading cause of perinatal death in women with abruptio, and
to optimize perinatal outcomes, it is desirable, if possible, to prolong gestation. Extremely
close fetal monitoring is necessary because there is a significant risk of fetal death.
Steroids should be administered to promote fetal lung maturation. Serial ultrasonography
is recommended to evaluate progression or regression of the abruptio.
Initial hospitalization for further evaluation and assessment of fetal well-being is
reasonable. Prolonged hospitalization and monitoring may be necessary. It may be
possible to discharge these patients to outpatient management if the fetal status is
reassuring once they have remained stable for several days. Patients should, however, be
delivered in a center with adequate neonatal facilities and the parents should be counseled
by a neonatologist regarding potential treatments and outcomes for the neonate.2 (Level
III)
8. Are tocolytic agents a safe option in the management of abruptio placenta in

pregnancies very far from term?
It seems reasonable to use tocolytics with caution in stable women who have partial
abruptio placenta but are remote from term. (Grade B)
Summary of Evidence
It has been generally taught that tocolytics, especially !-sympathomimetics such
as terbutaline, are contraindicated in the presence of vaginal bleeding, because side effects
such as tachycardia could mask the clinical signs of blood loss.
Sholl9, in a retrospective cohort and casecontrol study, evaluated the safety of
tocolytics (including intravenous magnesium sulfate and intravenous/oral !sympathomimetics) in the presence of bleeding in the second half of pregnancy, including
patients with suspected stable abruptio placenta. They concluded that tocolysis for the
preterm patients appeared to be beneficial in prolonging gestation and did not increase the
likelihood of cesarean delivery, hemorrhage, or fetal distress. (Level II-2)
Bond and colleagues10 expectantly managed 43 women with clinical evidence
of abruptio placenta before 35 weeks gestation, using tocolysis in cases where there were
contractions. There were no intrauterine deaths. They achieved a mean latency period to
delivery of 12.4 days. (Level II-2)
Towers and colleagues10 reviewed 236 cases of third trimester bleeding, which included
131 cases of abruptio placenta, with a mean gestational age of 28.9 weeks at the time of
first bleeding. In 95 (73%) of these women, tocolysis had been used. The mean time from
bleeding until delivery was 18.9 days. Fetal mortality was related to prematurity and no
adverse maternal or fetal effects of tocolysis occurred. (Level II-2)
9. Are patients with abruptio placenta at increased risk for adverse pregnancy
outcomes in future pregnancies?
There is a ten-fold increased risk of abruptio in a subsequent pregnancy and likewise
an increased risk of other adverse pregnancy outcomes, including preterm birth and
preeclampsia. Patients will also have an increased risk of impaired uteroplacental
perfusion. (Grade A)
Summary of Evidence
In a records review of births in Norway from 1967 through 1992, Rasmussen and
co-workers11 studied deliveries occurring immediately after an index case of abruptio
placenta and were able to identify 3074 non-abruptio births and 139 cases of recurrent
abruptions. They also found an increased risk of small for gestational age babies, preterm
birth, pregnancy induced hypertension (PIH), and perinatal death in immediate subsequent
deliveries.
Results were interpreted as epidemiological evidence for the hypothesis that PIH,
intrauterine growth restriction, preterm delivery and abruptio placenta all share an
etiological factor or represent clinical expressions of recurring placental dysfunction.
Histopathologic studies demonstrated lesions that indicate placental dysfunction12 (such
as acute atherosis in uteroplacental arteries and excess of decidual vascular lesions) and it
was suggested that these can recur in subsequent pregnancies.
Although no interventions have been demonstrated to reduce this risk, some

recommendations are possible. Hypertension should be controlled before and during the
subsequent pregnancy. Women who smoke tobacco or use cocaine should be counseled
on the adverse effects of exposure to these substances, and encouraged to quit before the
next pregnancy. In subsequent pregnancies, it will be reasonable to consider serial growth
scans every 4 weeks in the second half of pregnancy.
Where the mother has had two or more prior abruptions, amniocentesis for lung
maturity and delivery at about 37 weeks gestation should be seriously considered. (Level
II-2)
Summary
There are no randomized control trials (RCT) that have specifically examined
abruptio and the overwhelming majority of studies are observational (cohort, case-control, or
case series). Studies that have examined management strategies are typically limited by small
numbers. Levels of available evidence for the diagnosis and management of abruptio are
mainly II-1, II-2, and III.
Abruptio placenta remains an important cause of perinatal mortality and morbidity.
Perinatal mortality is determined by the severity of the abruptio and the gestational age at
which it occurs. Unfortunately neither accurate prediction nor prevention of abruptio is
possible at the present time. Despite advances in medical technology, the diagnosis of
abruptio is still a clinical one. When abruptio does occur, there are some strategies that may
help minimize the risk of morbidity and mortality associated with this condition.
These include early recognition and prompt delivery in cases in which the fetus is
mature and, in stable cases remote from term, conservative management to enable steroid
administration, allow transfer to a center with facilities for care of the preterm infant, and in
some cases, permit fetal maturation before delivery. Finally, close attention to maternal
condition, with replacement of blood and blood products as indicated, may improve outcomes
for the mother
With assurance of fetal well-being, and in the absence of other obstetric indications
for CS, studies suggest that more than 50% of patients diagnosed to with abruptio may
deliver vaginally with good neonatal outcome. Performing immediate CS on all patients with
diagnosis would result in an unnecessary high CS rate and may not improve neonatal
outcome.
The following are algorithms for management of abruption placenta from Oyelese2
which may be useful in the Philippine setting.
*Algorithm for the management of placental abruption in term or near term (A) and preterm births (B). In all
cases, complete blood count and coagulation indices should be checked; blood or blood volume should be
replaced; coagulopathy should be corrected; and intake, output, and renal function should be monitored.
References
1. Hurd W, Miodovnic M, Hertzberg V, Lavin J. Selective management of abruption placenta: a
prospective study. Obstet Gynecol 1983;64:467-73.
2. Oyelese Y, Ananth C. Placental abruption. Obstet Gynecol 2006;108:1005-16.
3.
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8.
9.
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14.
15.
Nyberg GA, Cyr DR, Mack LA, Wilson DA, Shuman WP. Sonographic spectrum of placental
abruption. Am J Roentgenol 1987;148:161-4.
Glatz C, Purnell I. Clinical utility of sonography in the diagnosis and treatment of placental abruption.
J Ultrasound Med 2002;21:837-40.
Yeo L, Ananth CV, Vintzileos AM. Placental abruption. In: Sciarra J, editor. Gynecology and
Obstetrics. Vol 2. Hagerstown (MD). Lippincott, Williams & Wilkins; 2003.
Kayani SI, Walkinshaw SA, Preston C. Pregnancy outcome in severe placental abruption. BJOG 2003;
10:679-83.
Brame RG, Harbert GM Jr, McGaughey HS Jr, et. al. Maternal risk in abruption. Obstet Gynecol 1968;
31:224.
Pritchard JA, Brekken AL. Clinical and laboratory studies on severe abruptio placenta. Am J Obstet
Gynecol 1967; 97:681.
Sholl JS. Abruptio placentae: clinical management in nonacute cases. Am J Obstet Gynecol. 1987;
156:40-51.
Towers CV, Pircon RA, Heppard M. Is tocolysis safe in the management of third trimester bleeding?
Am J Obstet Gynecol 1999;180:1572-8.
Rasmussen S, Irgens LM, Daleker A. Outcome of pregnancies subsequent to placental abruption: a
risk assessment. Acta Obstet Gynecol 2000; 79:496-501.
Redline RW. Placenta and adnexae in late pregnancy. In: Reed CB, Claireaux GB, Cockburn F, ed.
Diseases of the fetus and newborn. Pathology, imaging, genetics and management. London: Chapman
& Hall Medical, 1995: 328-34.
Ananth CV, Oyelese Y, Srinivas N, Yeo L, Vintzileos AM. Preterm premature rupture of membranes,
intrauterine infection, and oligohydramnios: risk factors for for placental abruption. Obstet Gynecol
2004;104:71-77.
Bernischke K, Kauffman P. Pathology of the humen placenta. 4th ed. New York (NY): Springer; 2000.
Dhanraj D, Lambers D. The incidence of positive Kleihauer-Betke test in low risk pregnancies and
maternal trauma patients. Am J Obstet Gynecol 2004;190:1461-3.
PLACENTA PREVIA
Background
Placenta previa is defined as a placenta implanted in the lower segment of the uterus,
presenting ahead of the leading pole of fetus. Maternal and fetal morbidity and mortality from
this are considerable.
It involves implantation of the placenta over the internal cervical os. Variants include:
1. complete implantation over the os (complete placenta previa)
2. a placental edge partially covering the os (partial placenta previa)
3. placenta approaching the border of the os (marginal placenta previa)
4. a low lying placenta implants within 2-3 cm from the os.
Pathophysiology
Placental implantation is initiated by the embryo (embryonic plate) implanting into
the lower uterus. A defective decidual vascularization occurs causing adherence over the
cervix, possibly secondary to inflammatory or atrophic change. When the lower segment
develops in the third trimester, bleeding occurs with disruption of placental attachment in this
area. Thrombin release from the bleeding sites promotes uterine contractions and a vicious
cycle of bleeding contractions placental separation bleeding occurs.1
Frequency
Placenta previa occurs in 0.3-0.5% of all pregnancies. The perinatal mortality
associated with it ranges from 2-3% and the maternal mortality (US) is 0.03%.1
The maternal morbidities include anterpartum bleeding, need for hysterectomy, blood
transfusion, septicemia and thrombophlebitis.
Risk Factors
These include advancing age, multiparity, infertility treatment, multiple gestation,
erythroblastosis, prior uterine surgery, recurrent abortions, nonwhite ethnicity, low
socioeconomic status, short interpregnancy interval, smoking, cocaine use and others (digital
exam, abruption, and trauma).
Diagnosis
Clinical History
The classic presentation of placenta previa is painless vaginal bleeding. Nearly twothirds of symptomatic patients present before 36 weeks, with half presenting before 30
weeks.
This hemorrhage stops spontaneously and recurs with labor.
Physical Examination
Any pregnant patient beyond the first trimester who presents with vaginal bleeding
requires a speculum examination followed by diagnostic ultrasound.
A digital examination is absolutely contraindicated until placenta previa is excluded.
Concurrent uterine contractions have to be monitored as 20% developed these with bleeding.
Laboratory Work-up
Complete blood count with platelets and blood typing are important.
Recommendations
1. What is the best way to diagnose placenta previa?
Transvaginal ultrasound (TVS) is safe in the presence of placenta previa, and is
more accurate than transabdominal ultrasound (TAS) in locating the placenta.
(Grade A)
Summary of Evidence
The only randomized control trial (RCT) to date comparing TVS and TAS
confirmed that TVS is more beneficial. TVS has also been shown to be safe in the
presence of placenta previa even in the presence of vaginal bleeding.
TAS is associated with false positive rate of up to 25%. Accuracy rates for TVS
are high (sensitivity 87.5%, specificity 98.8%, positive predictive value 93.3%, negative
predictive value 97.6%), establishing TVS as the gold standard for the diagnosis of
placenta previa.2 (Level I)
2. What are the conditions that can lead to false positive diagnosis of placenta previa
sonographically?
These are:
1) overdistended bladder
2) myometrial contractions (Grade C)
Summary of Evidence
Overdistention of the maternal urinary bladder places pressure on the anterior
aspect of the lower uterine segment, compressing it against the posterior wall and causing
the cervix to appear elongated. Thus a normal placenta may appear to overlie the internal
os. If the cervical length further exceeds 3-5 cm length, imaging should be done after the
patient emptied her bladder.3
During myometrial contractions, two situations that assume placenta previa may
occur. First, the wall of the uterus may thicken and imitate placental tissue. Second, the
lower uterine segment may shorten and bring the inferior edge of the placenta into contact
with the uterine cervical os. A contraction should be suspected if the myometrium is
thicker than 1.5 cm. Repeat ultrasound after 30 minutes may exclude this conditions.3
(Level III)
3. What is the value of Magnetic Resonance Imaging (MRI)?

In most situations, MRI is no more sensitive than ultrasonography on diagnosing
placenta accreta, which is usually associated with placenta previa. For women at
high risk for placenta accreta, a 2 step-protocol that uses ultrasonography first and
then MRI for cases with inconclusive ultrasonographic features may optimize
diagnostic accuracy. (Grade C)
Summary of Evidence
MRI may be used for planning the delivery as it helps identify placenta accreta,
increta or percreta. MRI may be superior for the posterior placenta accreta or the more
invasive increta and percreta as these abnormally adherent placentas are closely associated
with placenta previa.3 (Level III)
4. How should sonographic findings for placental location be interpreted reported?
Sonographers at TVS are encouraged to report the actual distance from the placenta
edge to the internal os, using standard terminology starting at 18 weeks of gestation.
! A placental edge exactly reaching the internal os is described as 0 mm.
! Placental edge may extend from 0 mm and 20 mm away from the os.
! Placenta edge may extend from 0 mm to 20 mm beyond the os and maybe
reported as mm overlap. (Grade A)
Summary of Evidence
There are several studies that have examined various distance of overlap (mm) at
18-23 weeks gestation and the persistence of placenta previa.
The likelihood of persistent placenta previa was effectively zero at term when the
placental edge reached but did not overlap the os (0 mm) at second trimester scan.4
It increased significantly beyond 15 mm overlap such that a distance of >25 mm
overlap had a likelihood of placenta previa at delivery of 40% and 100%.5 (Level II-2)
5. How should one proceed after placental localization at the second trimester?
When the placental edge lies between 20 mm away from the internal os and 20 mm
overlap at second trimester, ultrasound should be repeated at regular interval
depending on the gestational age, distance from the internal os, and clinical features
such as bleeding, because continued change in placental location is likely.
Overlap of 20 mm or more at anytime in the third trimester is highly predictive of
the need for cesarean section (CS). (Grade C)
Summary of Evidence
The process of placenta migration or relative upward shift of the placenta due to
differential growth of lower segment is continuous into the late third trimester.
In a study of 26 patients scanned at an average of 29 weeks, with the placenta
lying between 20 mm away from the os and 20 mm overlap, 3(1.5%) required CS at
delivery.6
At 35 weeks, when the placenta lie between 20 mm away from the os and 20 mm
overlap, CS ranged from 40-90%. This shows that persistence of placenta previa at 35
weeks results in more CS.7 (Level III)
6. Is vaginal delivery possible with placenta previa?
The os-placental edge distance on TVS after 35 weeks is valuable in planning route
of delivery.
When the placental edge lies > 20 mm away from the internal os, women may go into
labor with a high expectation of success.
A distance of 20 to 0 mm from the os is associated with a high CS rate, although
vaginal delivery is still possible depending on the clinical circumstances. (Grade A)
Summary of Evidence
Five studies have examined the likelihood of vaginal delivery for placenta previa
on the basis of distance to the placenta edge on last ultrasound prior to delivery. At 3536 weeks gestational age, a distance of >20 mm away from the os was associated with
high likelihood of vaginal delivery (range 63-100%). Between 20 mm and 0 mm from the
os, CS varies from 40-90/%.6,8,9 (Level II-2)
7. When is CS indicated?
In general, any degree of overlap (> 0 mm) after 35 weeks is an indication for CS as
a route of delivery. (Grade B)
Summary of Evidence
When the placenta overlaps the os by any amount on the last scan prior to
delivery, CS is required in all cases.10 (Level II-2)
8. What are the risk factors for massive hemorrhage during CS in patients with
placenta previa?
Advanced maternal age, previous CS, and presence of sponge-like sonographic
findings in the cervix are risk factors for massive bleeding during CS in cases of
placenta previa regardless of whether adherence is present.
In addition, ultrasound findings of a placenta located on the scar of a previous CS
and lack of clear zone are risk factors for placental adherence.
When these findings are identified pre-operatively, management should be tailored
to account for the risk of massive intraoperative bleeding and a multidisciplinary
team alerted and prepared for intensive treatment. (Grade A)
Summary of Evidence
In a study of 127 singleton pregnancies who had CS for placenta previa, logistic
regression analysis revealed that advanced maternal age (OR 5.4; 95% CI 1.8-16.4),
previous CS (OR 20.4; 95% CI 4.0-105.2), and sponge-like findings in the cervix (OR
5.6; 95% CI 1.8-17.0) were associated with massive bleeding (>2500 ml).11
Placental adherence occurred in 5 cases and was more frequent in cases where the
placenta was located at the rate of the scar of a previous CS (OR 123.1; 95% CI 4.53395.2) and where there was lack of a clear zone (OR 480; 95% CI, 38.0-604.7).11 (Level
II-2)
9. Is placenta previa associated with placenta accreta, increta or percreta?
Placenta accreta, increta, percreta may co-exist. Women who have placenta previa
with or without a CS scar should be considered at high risk of having a morbidly
adherent placenta.
Attention then should be focused in confirming this diagnosis using ultrasound and
when present, senior anesthetic and obstetric input are noted in planning the
delivery. (Grade A)
Summary of Evidence
The association between placenta previa and placenta accreta is strong, with RR of
2.065 compared to a normally-located placenta. This is also associated with scarring of
the lower segment of the uterus, and the risk of placenta previa rises relative to the
number of previous uterine incisions.12 (Level II-2)
10. Is tocolysis indicated in the treatment of uterine contractions in the presence of
bleeding due to placenta previa?
Tocolysis for treatment of uterine contractions in the presence of bleeding due to
placenta previa may be useful. (Grade B)
Summary of Evidence
The etiology of bleeding in placenta previa is thought to be due to the dynamics of
the development of the lower uterine segment, but may also be triggered by uterine
contractions. Besinger, et. al. conducted a prospective study on 112 women with acute
vaginal bleeding and known placenta previa and gave tocolysis to 72 who had significant
uterine activity (88%).13 This group of patients had a prolongation from admission to
delivery interval (39.2 vs 26.9 days, p<0.02) and an increase in birthweight (2520 vs 2124
g, p<0.03) compared to 40 women who were not given tocolysis. The largest series of
cases where tocolysis has been used for bleeding in the third trimester including 76 of 105
women with placenta previa is reported in a retrospective review by Towers, et. al. and
has suggested no increased morbidity or mortality associated with such use in a tertiary
setting.14 (Level II-2)
11. Is out patient management of placenta previa possible?
Outpatient management of placenta previa maybe appropriate for stable women
with support, close proximity to a hospital, and readily available transportation and
communication. (Grade C)
Summary of Evidence
Twenty-seven women were randomized to bed rest with minimal ambulation to
hospital and 26 women were discharged home. Overall, there was no difference in any
major outcome.15 (Level II-2)
12. Is it better to give regional anesthesia?
Regional anesthesia maybe employed for CS in the presence of placenta previa.
(Grade C)
Summary of Evidence
Two retrospective studies concluded that regional anesthesia is safe and one small
randomized trial suggests epidural anesthesia is superior to general anesthesia with
regards to maternal hemodynamics.16 (Level II-2)
13. What are some good practice recommendations in the management of placenta
previa?
Suggestions for good practice recommendation include:13
Prior to delivery, all women with placenta previa and their partners should have
had antenatal discussions regarding delivery and possible blood transfusion.
Blood should be available in the peripartum period.
In any case where a woman with placenta previa is being delivered, the
consultant can call or a senior resident should be involved.
Any woman going to the operating room with known placenta previs should be
attended by an experienced obstetrician and anesthesiologist. This is especially
to those women with higher risk of complications namely previous uterine scars,
anterior placenta previa or associated placenta accreta. (Grade C)
14. What some related issues to provide total care to the patient?
To provide total care, the following are recommended:17
Screening for infection
Use of antenatal corticosteroids in preterm labor
Thromboprophylaxis for any woman at increased risk of thromboembolism
(Grade C)
15. What are some auditable standards in the management of placenta previa?
All women with massive hemorrhage with or without placenta previa should be
subjected to clinical audit.17
Anticipation of hemorrhage with adequate workshop
Appropriate personnel involvement
Quick and effective resuscitation including blood and blood components
Appropriate monitoring instituted
Discharge hemoglobin
Careful documentation (Grade C)
References
1. Suyu J, et. al. Placenta previa. eMedicine. Medscape Continually Updated Clinic References.
Updated August 12, 2008.
2. Leerentveld RA et al. Accuracy and safety of transvaginal sonographic placental localization. Obstet
Gynecol 2001; 17:496-501.
3. Morrinan Q et al. Placenta previa: imaging. eMedicine. Medscape Continually Updated Clinic
References. Updated November 6, 2008.
4. Taipale P, et. al. Transvaginal ultrasonography at 18-23 weeks in predicting placenta previa at delivery.
Ultrasound Obstet Gynecol 1998;12:420-425.
5. Becker RH, et. al. The relevance of placental location at 20-23 gestational weeks for prediction of
placenta previa at delivery: evaluation of 8650 cases. Ultrasound Obstet Gynecol 2001;17:100-2.
6. Oppenheimer L, et. al. Diagnosis of low-lying placenta: Can migration in the third trimester predict
outcome? Ultrasound Obstet Gynecol 2001;8:100-2.
7. Predanic M, et. al. A sonographic assessment of different patterns of placenta previa migration on the
third trimester of pregnancy. J Ultrasound Medicine 2005;24:773-80.
8. Salkaut B, et. al. The classification of placenta previa based on placenta edge distance at transvaginal
sonography. Am J Obstet Gynecol 2002;187(6):594.
9. Bhide A, et. al. Placental edge to internal os distance in the late third trimester and mode of delivery in
placenta previa. Br J Obstet Gynecol 2009;110:860-4.
10. Oppenheimer L, et. al. Diagnosis and Management of placenta previa SOGC Clinical Practice
Guideline. JOGC 2007.
11. Hasegava J, et. al. Predisposing factors for massive hemorrhage during cesarean section in patient with
placenta previa. Ultrasound Obstet Gynecol 2009;34:80-84.
12. Clark S, et. al. Placenta previa/accreta and previous cesarean section. Obstet Gynecol 1985;66:89-92.
13. Besinger R, et. al. The effect of tocolytic use in the management of symptomatic placenta previa. Am J
Obstet Gynecol 1995;172:1170-8.
14. Towers C, et. al. Is tocolysis safe in the management of third trimester bleeding? Am J Obstet Gynecol
1999;180:1572-8.
15. Wing D, et. al. Management of the symptomatic placenta previa; a randomized, controlled trial of in
patient versus outpatient expectant management. Am J Obstet Gynecol 1996;175:806-11.
16. Parekli N, et. al. Cesarean section for placental previa. A retrospective study of anesthetic
management. B J Anaesth 2000;84:725-30.
17. Clinical Practice Guidelines on Placenta Previa: Diagnosis and Management. Guidelines and Audit
Sub-Committee of the Royal College of Obstetricians and Gynecologists, 2006.
PLACENTA ACCRETA
Angelita R. Teotico, MD, FPOGS
Background
Placenta accreta refers to abnormal adherence of the placenta to the uterus with
subsequent failure to separate after delivery of the fetus. It results when the placenta adheres
to the uterine wall because of abnormal development of the decidua basalis and imperfect
development of the fibrinoid layer allowing the trophoblasts, which have tissue-invasive
characteristics similar to malignant neoplastic cells, to break the barrier and invade the
myometrium, serosa and infiltrate even the neighboring organs such as urinary bladder and
the bowels.
Placenta accreta is a potentially catastrophic obstetric complication. Its most
significant feature is a tremendous uteroplacental neovascularization which causes lifethreatening hemorrhage. Careful assessment of pregnancies at risk is warranted because
maternal morbidity and mortality from this condition are considerable. Prenatal diagnosis is
important to establish an appropriate management plan to help reduce serious complications.
It has emerged as one of the common indications for emergency peripartum
hysterectomy and therefore, all obstetric care providers must be ready to handle this obstetric
emergency.
There are 3 types depending on the depth of invasion:
Placenta Accreta Vera (75%) - chorionic villi penetrate the decidua but not the
myometrium
Placenta Increta (15%) - chorionic villi penetrate and invade deeper into the myometrium
but not the serosa
Placenta Percreta (5%) - chorionic villi penetrate through myometrium, may perforate the
serosa and extend to adjacent structures like the bladder or the bowels
There are 3 types depending on the number of cotyledons involved:
Total placenta accreta, adherence involve all of the cotyledons
Partial placenta accreta, adherence involve few to several cotyledons
Focal placenta accreta, adherence involve a single cotyledon
Recommendations
1. What is the current trend in the incidence of placenta accreta?
The incidence of placenta accreta has increased 10-fold in the past 50 years and this is
attributed to the rapidly rising numbers of primary and repeat cesarean births. Placenta
accreta is an obstetric complication directly related to uterine surgery. This information
must be included in the informed consent particularly those cesarean delivery on maternal
request (CDMR). (Grade B)
Summary of Evidence
Reports in the literature have shown an increasing trend over the years from
1/30,000 in 1930s, to 1/20,000 in 1960s, to 1/7,000 in 1980s.1 Miller and colleagues
reported an incidence of histologically confirmed placenta accreta of 1 in 2510 for a 10year period ending in 1994.2 (Level III)
In a case-control study made by Wu, which is a twenty-year analysis of abnormal
placentation from 1882-2002 involving 64,359 deliveries, the overall incidence of
placenta accreta was reported at 1 in 533. In this study, the rate of placenta accreta
increased in conjunction with cesarean deliveries.3 (Level II-2)
In a review of our local statistics, the incidence of placenta accreta has increased
from 1/6000 in 2002 to 1/3500 in 2005 to 1/2000 in 2007. This is concurrent with an
increasing cesarean section (CS) rate of 16%, 26% and 30% in the respective years.4,5
The association of placenta accreta with cesarean delivery must be made known
to patients seeking CDMR as this condition poses a risk to future pregnancy.6 (Level III)
2. How does placenta accreta affect the mother?
Placenta accreta has emerged as a significant indication for peripartum hysterectomy
alongside the rising cesarean delivery rate. This condition can lead to massive obstetric
hemorrhage, disseminated intravascular coagulopathy (DIC), visceral injury, acute
respiratory distress syndrome (ARDS), renal failure, infection and death. Whenever this
condition is suspected, a management plan should be carefully formulated to maximize
outcome for both the fetus and the mother. (Grade B)
Summary of Evidence
In a retrospective cohort study from 1966-2005 by Flood7 comparing decades
1966-1975 with 1996-2005, it was reported that the indications for peripartum
hysterectomy have changed significantly with uterine rupture decreasing from 40.5-9.3%
(P<.0001) and placenta accreta increasing significantly from 5.4-46.5% (P<.00001).
During the 2 decades, the overall cesarean delivery rate has increased from 6-19% and the
percentage of peripartum hysterectomy that occurs in the setting of a previous cesarean
delivery has also increased from 27-57% (P<.00001). (Level II-2)
Other authors have reported placenta accreta to comprise 30-50% of their
peripartum hysterectomy and previous cesarean delivery was a common factor.8-10
Significant hemorrhage and severe maternal morbidity at the time of delivery are
common in cases of placenta accreta. The bleeding may become massive in cases of
placenta percreta. Todd11 reported 33 cases of placenta accreta/percreta managed in his
center between 2001-2006 all managed by hysteterctomy. Blood loss during surgery
ranged between 2500-5000 ml, necessitating transfusion of 3-29 units of packed RBC.
Admission to intensive care unit (ICU) was required for 51.6% of cases and 29% had
intraoperative while 40% had postpartum complications. (Level III)
The feared increase in maternal deaths because of placenta accreta was not
observed in a study done by Clark12 in his review of maternal deaths between 2000-2006.
In a series of 1.5 million deliveries, the author saw only 1 death from placenta accreta.
This could be attributed to the improved diagnostic and management technologies in his
center. (Level III)
In a review of our local statistic covering the period between 2002-2007, there
were 41 maternal deaths due to placenta accreta out of 1.48 million deliveries, although
there was a noticeable decrease from 8 cases (5.41% of direct maternal death) in 2002 to
only 2 cases (0.56% of direct maternal death) in 2007.13 This could be attributed to
increased clinicians awareness, improved diagnosis and management.
3. How does placenta accreta affect the fetus?
Pregnancies complicated by placenta accreta are at increased risk for adverse perinatal
outcome resulting from preterm deliveries and restricted fetal growth. Therefore,
whenever placenta accreta is being considered, close antenatal fetal surveillance must be
conducted. Giving corticosteroids to enhance pulmonary maturity should be considered in
anticipation of an iatrogenic preterm delivery. (Grade B)
Summary of Evidence
Because placenta accreta is characterized by an abnormal placental implantation,
it may be assumed that fetal development would also be affected. In a case-control
analysis conducted by Gielchinsky14 involving 34,450 deliveries in which 310 cases of
placenta accreta were diagnosed, they found a significant increase in preterm deliveries
(10.7% vs 1%, P<.001, OR 12.1) and small for gestational age babies (27.3% vs 14%,
P,.001, OR 5.05). (Level II-2)
4. Why should we screen for placenta accreta antenatally?
Antenatal diagnosis of placenta accreta may result to better maternal outcome as there will
be enough time to establish an appropriate management plan and prepare for surgery.
(Grade B)
Summary of Evidence
Antenatal diagnosis is the key to a successful management outcome in placenta
accreta. This allows enough time to make a multi-disciplinary management plan that is
most appropriate for the patient.
The effect of antenatal diagnosis and subsequent placental non-separation at
delivery on maternal outcome was evaluated by Wong15 in 16 confirmed cases of placenta
accreta (15 histologically and 1 visually). Antenatal diagnosis and placental nonseparation
resulted to lower mean blood loss (1.4 L vs 3.6 L, p=0.003) and lesser amount of blood
transfused (1.2 vs 5.1, p=0.005). When an antenatal diagnosis was not made, attempted
placental separation led to emergency hysterectomy. (Level III)
5. Who should be screened for placenta accreta?
All women with placenta previa and a previous uterine surgery should be screened for
placenta accreta. The major risk factor is a combination of placenta previa and a previous
CS and the risk for previa-percreta increases proportionately with the number of CS.
Whenever placenta previa and a previous uterine surgery co-exit diagnosis of placenta
accreta must be established antenatally. When antenatal diagnosis is not conclusive or not
possible, these women should still be managed as if they have placenta accreta. (Grade B)
Placenta previa with or without uterine surgery and advance maternal age are independent
risk factors for placenta accreta. Other risk factors include prior myomectomy or
reconstructive surgery, Asherman's syndrome, submucous leiomyomata and multiparity
(gravida 6 or more). All women with these risk factors must also be screened for placenta
accreta. (Grade B)
Summary of Evidence
CS is a well-established risk factor for abnormal placentation, both for placenta
previa and placenta accreta. The exact mechanism is unknown. It is hypothesized that the
early embryo implants preferentially into areas of uterine scarring and deficient decidua
because of relative deficiency of blood flow and oxygen tension in this area with the
trophoblasts invading deeply into the myometrium resulting to placenta accreta. In a large
propective observational study, the centers of Maternal and Fetal Medicine Units
(MFMU) Network evaluated the risk of placenta accreta with increasing number of CS.
In 143 cases of abnormal placentation among 30,132 cesarean deliveries, the investigators
found that the risk of abnormal placentation increased dramatically with each cesarean
delivery particularly after the third CS. The risk of abnormal placentation increased even
more dramatically with each previous cesarean section in the presence of placenta previa.
(Table 1). 16 (Level II-2)
Table 1. Risk of abnormal placentation by number of previous cesarean deliveries16
No of Prior
cesarean
deliveries
0
1
2
3
4
5 or more
Abnormal
Placentation %
(n=143)
0.2
0.3
0.6
2.3
2.3
6.7
Previa-Accreta %
(n=91)
3.3
11
40
61
67
A deficiency of decidualization may contribute to the development of abnormal

placentation. Placenta previa itself raises the risk for placenta accreta due to implantation
over a high vascular, poorly contractile lower uterine segment and an existing scar in the
same area compounds the risk. Clark and colleagues17, in a single center study showed the
effect of previous cesarean deliveries on the incidence of placenta previa and accreta.
(Table 2)
Table 2. Risk of placenta accreta relative to uterine scarring and presence of placenta
previa17
No of Prior cesarean
deliveries
0
1
2
3
4
Incidence of placenta previa

(%)
0.26
0.65
1.8
3.0
10
Incidence of concurrent
placenta accreta (%)
5
24
47
40
67
In a twenty-year analysis of abnormal placentation, a retrospective case control

study by Wu3, significant risk factors for placenta accreta indentified included advanced
maternal age > 35y (OR 1.13, 95% CI 1.089-1.194, P<.0001), 2 or more cesarean
deliveries (OR 8.6, 95% CI 3.536-21.078, P<.0001) and presence of placenta previa (OR
51.4, 95% CI 10.65-248.39,P<.0001). (Level III) Other risk factors for placenta acreta
include Ashermas syndrome, submucous myomas, uterine surgeries and multiparity. All
of these factors distort the uterine cavity and endometrial environment. Multiparity nd
advance maternal age in some way alters the nature of the endometrium, thereby
increasing the risk of abnormal placentation.18,19
6. How do we screen and diagnose placenta accreta antenatally?
The main screening modality used to make an antenatal diagnosis of placenta accreta is
gray-scale ultrasound imaging combined with clinical risk factors. (Grade B)
Diagnosis can be established by gray-scale ultrasound combined with Color and Power
Doppler ultrasound to increase accuracy of diagnosis. Magnetic resonance imaging (MRI)
must also be considered when results of gray scale and Color Doppler are equivocal and
non-conclusive or when the placenta is posteriorly implanted. (Grade B)
Summary of Evidence
Antenatal diagnosis of placenta accreta should begin with a high index of
suspicion in women having risk factors. All women with placenta previa and previous
CS (being the 2 most frequent predisposing factors) must have an ultasound exam to
screen for placenta accreta.
Diagnosis of placenta accreta can be established using gray scale ultrasound
combined with color and power Doppler.
Gray-scale sonographic signs of placenta accreta are:20
1. Loss of normally visible retroplacental hypoechoic zone, which corresponds to
the decidua basalis, myometrium and dilated venous channels
2. Progressive thinning of the retroplacental hypoechoic zone to < 2 mm on serial
exams
3. Presence of multiple placental lakes that represent dilated vessels extending
from the placenta through the myometrium giving the placenta the so-called
Swiss cheese appearance
4. Thinning or focal disruption of the uterine serosa-bladder wall complex

(placenta percreta)
5. Focal mass-like elevation of tissue with the same echogenicity as the placenta
beyond the uterine serosa (placenta percreta).
Using the above criteria, Frinberg20 reported a sensitivity of 93% and a specificity
of 79% for the use of ultrasound in diagnosis placenta accreta in high risk patients. Many
studies have found at 15-20 weeks of gestation, that the presence of lacunae in the
placenta is the most predictive sonographic sign of placenta accreta, with a sensitivity of
79% and a positive predictive value of 92%. After 20 weeks of gestation, the sensitivity of
these findings increases with values of 93% and 80% for lacunae and obliteration of the
retroplacental clear space, respectively.
Abnormal placental invasion induces angiogenesis resulting to uteroplacental
hypervascularity. Color Doppler ultrasound has been utilized as an aid in diagnosing
placenta accreta because it highlights abnormal areas of increased turbulent flow that may
extend from the placenta into the surrounding uterine wall and cervix.
Color Doppler signs suggestive of placenta accreta are:21
1. Dilated vascular channels with diffuse lacunar flow pattern scattered
throughout the whole placenta and the surrounding myometrium and cervix.
2. A focal lacunar flow pattern showing irregular sonoluscent vascular lakes with
turbulent lacunar flow distributed regionally or focally within the
intraparenchymal placental area.
3. Interface hypervacularity with abnormal vessels linking the placenta t the
bladder.
4. Markedly dilated peripheral subplacental vascular channels and pulsatile
venous-type flow over the cervix
5. Poor vascularity at sites of loss of hypoechoic zone.
Chou, et. al.21 prospectively followed 80 women with placenta previa using
transabdominal B-mode and colour Doppler ultrasonography with 17 cases of accreta
identified at delivery. Sixteen cases were suspected by color Doppler, 14 of which were
correctly diagnosed and 2 were false positives, while 3 cases were not diagnosed giving a
sensitivity of 82.4%, specificity of 96.8%, positive predictive value of 87.5% and negative
predictive value of 95.3%. (Level II-2)
A two-stage imaging protocol to evaluate women at high risk for placenta accreta
has been proposed, consisting of an initial ultrasonography followed by magnetic
resonance imaging (MRI) when ultrasound features are inconclusive to optimize
diagnostic accuracy. In a historical cohort study conducted by Warshak, et. al.22 on 453
women with placenta previa, previous cesarean delivery and low lying anterior placenta,
ultrasonography accurately predicted placenta! accreta in 30 of 39 women and correctly
ruled out placenta accreta in 398 of 414 without placenta accreta (sensitivity 77%,
specificity 96%). Of the 42 women who underwent MRI, 23 of 26 cases were correctly
identified and 14 of 14 were ruled out (sensitivity 88%, specificity 100%). (Level III)
Power ultrasonic angiography (power Doppler) has also been used to better
delineate the abnormal placental vascular architectural pattern in placenta accreta. This
modality is less dependent of blood flow direction and can pick up signals even from
small vessels giving better information on the degree of vascularity.23 Although this is a
promising technique, prospective studies comparing its effectiveness over gray scale and
color Doppler have yet to be published.
Power and color Doppler are often used for the diagnosis of placenta accreta,
demonstrating turbulent flow through placental lacunae. However, in the majority of cases
this imaging modality does not significantly improve the diagnosis over that achieved by
grayscale sonography alone. Thus, in majority of clinical situations, Doppler should not
be the primary!technique used to diagnose placenta accreta.24 Three-D Power Doppler was
reported by Shih25 as a useful complimentary tool to antenatal diagnosis or exclusion of
placenta accreta. In his report, the finding of numerous cohesive vessels visualized
using 3D power Doppler in basal view was the best single criterion for the diagnosis of
placenta accreta with a sensitivity of 97% and specificity of 92%.
MRI is also useful as an adjunct in the diagnosis of placenta accreta. Diagnosis
with high level of confidence can be achieved with this modality since high signals from
the placenta makes it easier to be distinguished from the myometrium. A placental MRI
provides a morphological description, as well as topographical information that optimizes
diagnosis and surgical management. This is particularly helpful in cases of posterior
placenta where ultrasonographic evaluation is difficult or to confirm bladder invasion.26
However, it is the combination of different imaging modalities that may prove most
effective in diagnosing this condition.
7. How should we manage placenta accreta?
The management approach often recommended in cases of placenta accreta is extirpative
surgery but conservative management approach can be done in selected case. (Grade B)
Antenatal Management
Counsel all patients with placenta accreta about delivery risks and complications and
future infertility if hysterectomy performed. (Grade C)
Consider early delivery (32-36 weeks) before labor and after pretreatment with
betamethasone for fetal lung maturity. (Grade C)
Prepare team-approach for delivery including a plan for emergent surgery prior to
scheduled delivery. Planning should include primary obstetric surgeon, blood bank,
perinatologist, anesthesiologist, gynecologic oncologist, urosurgeon, labor and delivery
nursing, operating room, personnel, nursery and pediatric teams. (Grade C)
Ensure availability of adequate blood products (at least 4-6 units of packed red blood cells
(RBC), fresh frozen plasma (FFP) and platelet concentrate) at the time of delivery. (Grade
C)
Summary of Evidence
Providers caring for patients with prenatally suspected placenta accreta should
extensively counsel patients about potential risks and complications well in advance of
their estimated due date. Patients with accreta are at increased risk for hemorrhage, blood
transfusion, bladder/ureteral damage, infection, need for intubation, prolonged
hospitalization, ICU admission, need for reoperation, thromboembolic events and death.
Discussions should involve relative likelihood for hysterectomy and subsequent
infertility.27
A scheduled delivery is ideal, as it is associated with less intraoperative blood loss
than emergent delivery. In patients with strong suspicion for placenta accreta it is strongly
advised to perform the delivery prior to hemorrhage or labor. Considerations should be

given to performing the cesarean birth electively and prematurely either after
corticosteroids for fetal lung maturation or after documentation of fetal lung maturity. The
optimal timing of delivery is unclear, some tertiary referral centers recommended 35-36
weeks and others 32-34 weeks. The timing of delivery should be individualized. Bauer
and colleagues28 advocates early delivery typically at 34 weeks gestation after a course of
corticosteroid in cases of placenta percreta or in cases complicated by recurrent antenatal
bleeding. Patients at high risk for emergent delivery are patients with recurrent vaginal
bleeding. In a study by Eller29, it was reported that women who underwent scheduled cshysterectomy had lower occurrence of ICU admission, ureteric admission, intraabdominal
infection, hospital re-admission and vesico-vaginal fistula, that women who underwent
emergency CS-hysterectomy. (Level III)
A team approach and preoperative preparation is essential in anticipation of
extensive surgery which may be difficult. Pre-operative planning must discuss location of
delivery, choice of anesthesia, type of abdominal incision and management of the
placenta. Incisions made through the placenta and attempts to deliver it will often incite
significant hemorrhage. Discussion by the operating team should also incorporate
patients wishes regarding conservative management and future fertility.
Adequate blood product should be secured prior to delivery. Bauer28, in his center,
prepares 20 units of packed RBC, 20 units of FFP, 6 packs of platelets and 10 units
cryoprecipitate. The use 1:1 ratio of PRBC to FFP in cases of massive hemorrhage.
!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!
Surgery in the presence of placenta accreta

If risk factors and prenatal imaging together strongly suggest this diagnosis, cesarean
hysterectomy is generally planned, especially for patients who do not wish continued
fertility. Profuse hemorrhage can occur when attempting to separate the placenta, thus if
the clinician is confident in the diagnosis, it is prudent to proceed with hysterectomy with
the placenta attached. (Grade B)
Uterine incision must be done away from the placenta. For placenta previa acrreta,
incision must be a fundal classical incision, cutting thru the placenta must be avoided.
Ancillary procedures to lessen intraoperative hemorrhage may be employed when feasible
and available like bilateral hypograstric artery ligation, internal iliac artery embolization,
common iliac artery balloon occlusion. (Grade B)
Summary of Evidence
The American College of Obstetrician and Gynecologists has issued the following
committee opinion on surgical management of placenta accreta.30
If the diagnosis of placenta accreta before delivery is suspected:
1. The patient must be counseled about the likelihood of hysterectomy and blood
transfusion.
2. Blood products and clotting factors should be available
3. The appropriate location and timing for delivery should be considered to allow
access to adequate surgical personnel and equipment
4. A preoperative anesthesia assessment should be obtained.
5. If the diagnosis is made after a vaginal delivery when the placenta fails to
separate or when profuse bleeding is encountered selective pelvic vessel
embolization (if this is available) may be an alternative to hysterectomy.
The Royal College of Obstetrcians and Gynecologist (RCOG)31 issued the
following guidelines:
1. When placenta accreta is thought to be likely, consultant anesthetic and
obstetric input are vital in planning and conducting the delivery. Crossed
marched blood should be available and collegues from other subspecialties
may be alerted to be on standyby to attend as needed.
2. In case of placenta accreta, increta and percreta, the risk of hemorrhage,
transfusion and hysterectomy should be discussed with the patient as part of
the consent procedure.
3. All CS performed in women with placenta previa who had a previous
caesarean section should be conducted by a consultant-obstetrician because of
the high risk of major morbidity.
A retrospective cohort study done by Eller29 involving 2 tertiary centers from
1996-2008 wherein 76 cases of placenta accreta were identified, showed that scheduled
cesarean hysterectomy without attempting placental removal was associated with reduced
rate of early morbidity compared with cases in which placental removal was attempted
(67 vs 36%, P=0.038). Women with pre-operative bilateral ureteric stents had a lower
incidence of morbidity compared with women without stents (18 vs 55%, P=.018). (Level
II-2)
Ancillary procedures
Chou32 also reported the use of internal iliac artery embolization before
hysterectomy for placenta accreta in 6 cases and found a mean blood loss of 300-3000 ml
but concluded that there is a need for further investigation of its effectiveness. (Level III)
Another approach to minimize blood loss during hysterectomy and facilitate
surgery is the use of balloon catheters for occlusion and/or embolization of the pelvic
vasculature. To date however, the literature regarding this modality is limited. The
successful use of pre-operative occlusive balloon catheters for cesarean hysterectomy has
been described in few case reports.33 However, in a case control study by Shrivastava34
involving 69 cases of placenta accreta wherein 19 cases had balloon catheters plus
hysterectomy while 50 cases had hysterectomy alone, difference in outcome between the
2 groups in terms of blood loss (P=.79), transfused blood (P=.6) operative time (P=.85)
and postoperative hospital days (P=.85) were not significant. In this study, prophylactic
intravascular balloon catheters did not benefit women with placenta accreta undergoing
hysterectomy. (Level II-2)
Conservative management of placenta accreta
Conservative management of placenta previa accreta can be successful in selected cases.
It should be considered when fertility is desired, the condition for extensive surgery is not
optimum or in severe invasion like placenta percreta. However, this must be considered
only when the woman is hemodynamically stable. Conservative approach may involve
leaving the placenta in situ or giving Methotrexate therapy. No standard dose for
methotrexate has been recommended and certain guidelines must be followed when this
modality is chosen. Management modalities should be individualized and patients should

be carefully selected. (Grade B)
Ancillary procedures like uterine artery embolization can be done in conjunction with
conservative approach, whether leaving the placenta in situ or with methotrexate therapy.
(Grade B)
For focal accreta, a wedge resection of the area can be performed followed by repair of
the myometrium. (Grade B)
Summary of Evidence
Conservative management of placenta accreta involves different management
strategies which include the following: leaving the placenta in situ, uterine artery
embolization, internal iliac artery ligation as initial surgery, and methotrexate therapy to
dissolve the placenta. Conservative management approach preserves fertility and in
selected cases of severe invasion like placenta percreta, this approach may even reduce
maternal morbidity from massive hemorrhage and blood transfusion.
Leaving the placenta in situ
Kayem, et. al.35 compared the impact of conservative and extirpative strategies
for placenta accreta on maternal morbidity and mortality in a retrospective review of 33
cases and found a reduction in the hysterectomy rate (from 11, 84.6 % to 3, 15%; P<.001),
blood transfusion (3.2 L versus 1.5 L (P<.01) and DIC (5, 38.5% versus 1, 5%, P=.02).
(Level III)
Conservative management of leaving the placenta in situ involves the following steps:35
1. The precise position of the placenta determined by ultrasound.
2. CS planned, with the abdominal incision at the infraumbilical midline, enlarged
above the umbilicus.
3. A vertical uterine incision carried out at a distance from the placental edge.
4. After delivery of the infant, delivery of the placenta attempted prudently, with the
injection of 5 IU oxytocin and moderate cord traction.
5. If the placenta failed to separate, this is considered placenta accreta and left in
situ.
6. The cord cut at the placental insertion and left in the uterine cavity and the uterine
incision closed.
7. Prophylactic antibiotic therapy (amoxicillin and clavulanic acid) administered
systemically for 10 days.
8. Postoperative follow up including weekly evaluation for 6 months with
ultrasonography, clinical examination and blood counts.
There are several case reports on leaving the placenta in situ without giving
methotrexate. Thia36 reported a case of placenta previa-percreta with bladder invasion.
Surgery was done at 36 weeks, leaving the placenta in situ followed by embolization.
Postpatum course was uneventful, HCG dropped to < 2 U/L at 13 weeks postpartum. The
placenta passed out partially and rest involuted. Uterus returned to normal on the 5th
month. Tong37 reported 3 cases of placenta accreta managed conservatively in different
strategies: (1) placenta left in situ followed by uterine artery embolization, (2) placenta
left in situ followed by methotrexate therapy, (3) focal area of accreta managed by
underrunning sutures. One patient had sepsis managed with antibiotics. In all cases,
balloon occlusion catheters were inserted in the bilateral internal iliac arteries. (Level III)
Medical management with methotrexate
Conservative approach can also be done by medical management using
methotrexate, a folic acid antagonist that inhibits DNA synthesis and cell reproduction,
primarily in actively proliferating cells. It is possible that methotrexate hastens placental
dissolution. Several case reports have documented decreased placental size and
vascularity to complete dissolution.38-40 Local literature also reports successful outcome
on Methotrexate therapy given weekly at 50 mg IM for 4-6 doses.4,41 (Level III)
Guidelines for Medical management include the following:42
1. The cord and membranes should be ligated as high as possible.
2. Broad spectrum antibiotics, for prophylaxis, and oxytocin should be administered
during the initial 72 hours.
3. Ultrasound should be performed daily to monitor involution and placental
vascularity, which should decrease over time.
4. If HCG plateau, placental vascularity persists, or placental involution stalls after
the initial 72-hour period, methotrexate (MTX) should be administered (1mg/kg)
on alternate days for a total of 4-6 doses.
5. Medical management should be stopped if liver function tests are 2 or more times
the normal value or there is evidence of thrombocytopenia (platelet leves below
100,000), neutropenia (WBC< 2,000), or renal dysfunction (creatinine levels >
1.5mg/dL).
6. If patient becomes clinically unstable or placenta tissue fails to resolve following
MTX therapy, hysterectomy should be considered.
Opponents of medical management suggest it increased the risk of sudden
hemorrhage, infection and or emergent surgery.43 Patients may develop vaginal bleeding
several weeks after delivery. In a local data, bleeding in some cases was observed on the
5th-6th week postdelivery.44 An elective hysterectomy can be considered earlier (between
2-4 weeks postpartum) to avoid further complications. But even in cases when the
placental mass fails to resolve or vaginal bleeding occurs, an interval of even a few days
after the delivery may simplify hysterectomy due to uterine involution and concurrent
decrease in vascularity. Mussali, et. al.45 reported 3 cases of placenta accreta managed
with methotrexate which resulted to preservation of the uterus in 2 patients. Delayed
hemorrhage on day 46 which necessitated hysterectomy was encountered in 1 case but
there was no catastrophic hemorrhage encountered as reported in immediate surgical
management. (Level III) Side effects of methotrexate include nausea, vomiting,
indigestion, stomatitis, sore throat, fatigue, dizziness, lightheadedness, temporary hair
loss, anemia, leucopenia, inflammation of the lungs. These are observed with very high
doses or prolonged use. In a local series46, no adverse effects have been observed.
Ancillary Procedures
Uterine artery embolization is an option to employ in conjunction with leaving
the placenta in situ or with methotrexate therapy, although in our setting this may still be
limited, but whenever possible, this modality may be used. Sherer47 reported a case of
placenta previa percreta in a 35 year old multigravid successfully managed with 3 courses
of methotrexate and 3 bilateral uterine artery embolization. Placenta completely dissolved
after 9 months. (Level III)
Focal accreta
If the area of accreta is focal and majority of the placenta has been removed, then
a wedge resection of the area can be performed. The myometrium is subsequently
oversewn in two layers.37
Failure of conservative management
Failure of methetrexate has also been reported in the literature. Luo48 reported
a case of placenta percreta managed conservatively with methotrexate and uterine
embolization however, the patient had heavy bleeding on the 44th postoperative day
necessitating a hysterectomy in an unstable hemodynamic condition. Butt49 reported a
case of placenta percreta in a 30 weeks gestation previously delivered by classical CS
managed by leaving the placenta in situ followed by methotrexate therapy. Postpartum
bleeding occurred 1 week later which was managed by internal iliac balloon
catheterization and manual transcervical removal of the placenta which resulted to
hysterectomy and required massive blood transfusion. (Level III)
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Panganiban R, Teotico A. Conservative management of placenta previa percreta: A case report. Phil J
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Teotico, AR. Review of POGS National statistics, 2002-2007.
Lee YM, DAlton ME. Cesarean delivery on maternal request: the impact on mother and newborn. Clin
Perinatol 2008;35:505-518.
Flood KM, Soha S, et al. Changing trends in peripartum hysterectomy over the last 4 decades. Am J
Obstet Gynecol 2009;200-632.
Kwee A. Emergency peripartum hysterectomy: A prospective study in the Netherlands. Eur J Obstet
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Sakse A. Weber T, Peripartum hysterectomy in Denmark 1995-2004. Acta Obstet Gynecol Scand
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Glaze S. Peripartum hysterectomy 1999 to 2006. Obtet Gynecol 2008;111:732-8.
Todd R. Placenta accreta and cesarean scar pregnancy: Overlooked costs of the rising cesarean section
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Clark, SL, Belfort MA. Maternal death in the 21st century: causes, prevention, and relationship to
cesarean delivery. Am J Obstet Gynecol 2008;199:36.e1-36.e5.
Review of Maternal Mortality, POGS statistics, 2002-2007.
Gielchinsky Y, et. al. Perinatal outcome of pregnancies complicated by placenta accreta. Obstet
Gynecol 2004;104:527-538.
15. Wong HS, Hutton J. The maternal outcome in placenta accreta: the significance of antenatal diagnosis
and non-separation of placenta at delivery. N Z Med J 2008;121(1277).
16. Silver RM, Landon MB, et al. Maternal morbidity associated with multiple repeat cesarean deliveries.
NICHD-MFMU Network Obstet Gynecol 2006;107:1226-1232.
17. Clark SL, et. al. Placenta previa/accreta and prior cesarean section. Obstet Gynecol 1985; 66:89-92.
18. Read JA. Placenta accreta: changing clinical aspects and outcome. Obstet Gynecol 1980;56:3.
19. Gilliam M, et. al. The likelihood of placenta previa with greater number of cesarean deliveries and
higher parity. Obstet Gynecol 2002;99:97680.
20. Frinberg HJ, et. al. Placenta accreta: prospective sonographic diagnosis in patients with placenta previa
and prior cesarean section. J Ultrasound Med 1992;11:333-343.
21. Chou MM, et. al. Prenatal diagnosis of placenta previa accreta by transabdominal color doppler
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22. Warshak CR, Eskander R. Accuracy of ultrasonography and magnetic resonance imaging in the
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23. Chou MM, et. al. Prenatal diagnosis of placenta previa accreta with power amplitude ultrasonic
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49. Butt K. Failure of methotexate and internal iliac balloon catheterization to manage placenta percreta.
POSTPARTUM HEMORRHAGE
Background
Postpartum hemorrhage (PPH) is the leading cause of maternal mortality, accounting
for nearly one third of all maternal deaths worldwide.1 PPH causes up to 60% of all maternal
deaths in developing countries. The majority of these deaths occur within 4 hours of delivery,
indicating they are a consequence of events in the third stage of labor.2
Traditionally, PPH has been defined as blood loss in excess of 500 ml in vaginal
deliveries, 1000 ml in cesarean deliveries, 1.4 L in an elective cesarean hysterectomy, and 3.0
L in an emergency cesarean hysterectomy. It has also been defined as a decrease in
postpartum hematocrit levels >10% of prenatal values. However, due to difficulty in
accurately estimating and the non-reproducibility of measuring blood loss in these situations,
these definitions of PPH have not gained wide acceptance. For clinical purposes, any blood
loss that results in signs and symptoms of hemodynamic instability should be considered as
PPH. Bonnar, et. al.3 in 2000 correlated the amount of blood loss (with its subsequent
percentage of total blood lost in the body) to blood pressure and clinical signs and symptoms
(Table 1). The World Health Organization (WHO) subsequently proposed a classification of
PPH similar and based on Bonnars definition where clinicians are now guided in managing
this life-threatening condition (Table 2). As blood loss after delivery exceeds 500 ml, an
ALERT signal is raised and clinicians should anticipate the possible consequences of
continued bleeding. Although the total blood volume loss is more than 10%, signs and
symptoms are minimal and blood pressure is generally maintained. Once blood loss exceeds
1000 ml (total blood volume loss > 15%) and now with signs and symptoms of hemodynamic
instability (tachycardia, hypotension, oliguria), an ACTION signal is raised and clinicians
should begin aggressive resuscitative measures to prevent its progression to hypovolemic
shock and prevent irreversible damage to organs or death.
Table 1. Correlation of Blood Loss to Blood Pressure and Clinical Signs and Symptoms3
Blood Loss
%
mL
Systolic Blood
Pressure,
(mmHg)
Signs & Symptoms
10-15
500-1000
Normal
Palpitations, dizziness, tachycardia
15-25
1000-1500
Slightly low
Weakness, sweating, tachycardia
25-35
1500-2000
70-80
Restlessness, pallor, oliguria
35-45
2000-3000
50-70
Collapse, air hunger, anuria
Table 2. WHO Classification of PPH

Hemorrhage
Class
Estimated
Blood Loss
(mL)
Blood Volume
Loss (%)
Clinical Sings & Symptoms
0
(normal loss)
< 500
<10
None
500-1000
15
Minimal
1200-1500
20-25
Oliguria, tachycardia, tachypnea, postural

hypotension
1800-2100
30-35
Hypotension, tachycardia, cold clammy
>2400
>40
Profound shock
The general management of PPH involves anticipation, prompt recognition and

appropriate treatment. Anticipation of PPH begins in the antenatal period, when clinicians
recognize and identify risk factors or situations that may increase the risk or predispose the
gravid to PPH. Some of these risk factors are parity, presence of situations that would tend to
overdistend the uterus (macrosomia, multiple gestation), number and type of cesarean
sections (CS), and even prenatal ultrasound findings suggestive of placental abnormalities.
During labor, prolonged use of oxytocics for induction or augmentation may likewise
predispose a woman to PPH secondary to uterine atony.
Once PPH is recognized, the three basic steps of management include: A
Assessment, B Breathing, and C Circulation. In ASSESSMENT, the patients
hemodynamic status is rapidly evaluated while the underlying etiology of the bleeding is
investigated and ascertained. In BREATHING, patients airway has to ensured and
maintained and oxygen supplementation is administered, in order to increase the oxygencarrying capacity of blood. In CIRCULATION, intravenous access is maximized by inserting
multiple large-bore intravenous lines with maintenance of adequate circulating blood volume
by infusing appropriate amounts of crystalloids and transfusing the adequate proportions of
blood components. Management of PPH requires a simultaneous and coordinated
multidisciplinary approach involving the obstetrician(s), anesthesiologists, critical care
nurses, and other surgical disciplines suitable to a particular situation.
It would be helpful to remember the various etiologies of PPH based on the four Ts:
TONE, TISSUE, TRAUMA, and THROMBIN. In TONE, uterine atony is the primary
etiology. In TISSUE, retained placenta or its secundines are the considerations. In TRAUMA,
lower genital tract lacerations, pelvic/perineal hematomas, and uterine inversion should be
primary considerations. And in THROMBIN, a pre-existing or acquired coagulopathy
(disseminated intravasculat coagulopathy (DIC)) should be primary causes. The specific
pathophysiology and clinical risk factors for each cause are listed in Table 3.
Table 3. Etiology, Pathophysiology and Risk factors of Postpartum Hemorrhage
References
1. Derman 2006
2. Ramanthan, 2006.
3. Bonnar J. Baillieres Best Pract Res Clin Obstet Gynaecol 2000;14:1.
UTERINE ATONY
Background
Uterine atony is the leading cause of postpartum hemorrhage (PPH), observed alone
in 40%-50% of all cases of PPH. It is defined as failure of the uterus to contract and retract
following childbirth. Uterine atony is a condition which, in spite of the presence of effective
medical interventions, still claims thousands of maternal lives. It is generally associated with
an overdistended uterus (secondary to multiple gestation, macrosomia, or polyhydramnios),
uterine muscle fatigue (secondary to labor induction/augmentation, Couvelaire uterus),
uterine distortion (like the presence of myoma), chorioamnionitis from prolonged rupture of
membranes) and the administration of uterine-relaxing drugs (such as beta-mimetics, and
anesthetic drugs).
Management of uterine atony starts with its prevention and later follows a stepwise
algorithm (if these preventive measures fail) designed to guide the clinician in maximizing all
the possible options prior to the performance of hysterectomy (Figure 1). Prevention of
uterine atony begins with Active Management of the Third Stage of Labor (AMTSL). At
present, this includes: Administration of uterotonic soon after the babys birth, delayed cord
clamping, and controlled cord traction followed by uterine massage. This standard
management may be supplemented with the therapeutic administration of additional
uterotonic drugs (methylergometrine, prostaglandins) and hemostatics (tranexamic acid,
recombinant activated factor VII).
If bleeding persists despite AMTSL and other standard measures, we should attempt
to perform conservative procedures to prevent continued hemorrhage and the performance of
a hysterectomy. Conservative measures include non-surgical and surgical procedures. It is but
proper to state that one may not go through all these measures one-by-one in the
management of persistent hemorrhage from uterine atony. Each procedure has its pros and
cons and many of these measures require skill, experience and technology to perform. Thus,
one should not hesitate to skip procedures he/she is not experienced or skilled to perform
these. Bypassing the conservative approaches and doing an outright hysterectomy is an
acceptable option in various situations: when the woman has completed her family and
reproductive function is no longer an issue, when the woman is hemodynamically unstable
and the most prudent and rapid way to alleviate the condition is to perform a hysterectomy, or
when the obstetrician is not adept or experienced in performing the more complex
conservative measures.
Figure 1. Management Algorithm for Uterine Atony
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Recommendations
1. Is active management of the third stage of labor better in reducing PPH compared
with expectant management?
Active management of the third stage of labor is associated with reduced maternal
blood loss, postpartum anemia, need for blood transfusion and additional oxytocics.
(Grade A)
Summary of Evidence
Active management of the third stage of labor is associated with reduced PPH
greater than 500 ml (OR 0.37, 95% CI 0.33-0.41), reduced PPH greater than 1000 ml (OR
0.36, 95% CI 0.25-0.52), reduced postpartum anemia (OR 0.40, 95% CI 0.30-0.54),
reduced need for blood transfusion (OR 0.36, 95% CI 0.24-0.54), and reduced need for
additional oxytocics (OR 0.22, 95% CI 0.19-0.26). However, it is also associated with
increased incidence of nausea (OR 1.95, 95% CI 1.52-2.42).1-3 (Level 1)
2. Should we routinely administer oxytocin soon after the babys birth to reduce the
incidence of PPH?
Administration of oxytocin soon after the babys birth is associated with reduced
maternal blood loss and decreased trend for therapeutic oxytocin. (Grade A)
Summary of Evidence
Routine administration of oxytocin after the babys birth reduced PPH greater
than 500 ml (RR 0.5, 95% CI 0.43-0.59), reduced PPH greater than 1000 ml (RR 0.61,
95% CI 0.44-0.87), and reduced need for additional oxytocics (RR 0.5, 95% CI 0.390.64).4,5 (Level I)
3. Does delayed cord clamping reduce the incidence of PPH better compared with early
cord clamping?
Delayed cord clamping does not reduce the incidence of PPH compared with early
cord clamping. (Grade B)
Delayed cord clamping is more beneficial to the baby in terms of improvement of
iron status and increase in hemoglobin. (Grade B)
Summary of Evidence
There is no significant difference between delayed and early cord clamping in
terms of postpartum hemorrhage.6-9 (Level II-2)
Delayed cord clamping is more beneficial to the baby in terms of significant
increases in hemoglobin, improvement in iron status and, among preterm infants, less
intraventricular hemorrhage (RR 0.28, 95% CI 0.09-0.9) and less late onset sepsis (RR
0.12, 95 % CI 0.03-0.95).6-9 (Level II-2)
4. Should uterine massage be routinely performed after delivery of the placenta?

Uterine massage is associated with reduced mean blood loss at 30 and 60 minutes
and a reduced need for additional oxytocics. (Grade A)
Summary of Evidence
The women who underwent uterine massage after delivery of the placenta had a
lower mean blood loss at 30 minutes (Mean difference -41.60 m, 95% CI -75.16 to -8.04),
lower mean blood loss at 60 minutes (Mean difference -77.40 ml 95% CI -118.71 to 36.09), and reduced need for additional uterotonics (RR 0.20, 95% CI 0.08-0.50).10 (Level
I)
5. Should oral misoprostol (600 g) be given to prevent PPH instead of oxytocin?
Oxytocin is better than oral misoprostol in preventing PPH. (Grade A)
Oral misoprostol is associated with more adverse effects compared with oxytocin.
(Grade A)
Summary of Evidence
Compared to oxytocin, oral intake of misoprostol is associated with increased
blood loss greater than 1000 ml (RR 1.34, 95% CI 1.16-1.55), increased use of additional
uterotonics (RR 1.41, 95% CI 1.31-1.50). There was no significant differences between
misoprostol and oxytocin in the need for blood transfusion (RR 0.8, 95% CI 0.621.04).11-13 (Level I)
Compared to oxytocin, oral intake of misoprostol is associated with more adverse
effects, such as shivering (RR 3.29, 95% CI 3.03-3.56), diarrhea (RR 2.52, 95% CI 1.603.98), and pyrexia with a temperature > 38C (RR 6.62, 95% CI 5.45.8.05).11-13 (Level I)
6. Should sublingual misoprostol (600 g) be given to prevent PPH instead of oxytocin?
Oxytocin is the preferred uterotonic compared with sublingual misoprostol in
preventing PPH. (Grade A)
Summary of Evidence
One systematic review (covering 2 clinical trials) with less than 200 women
revealed that there was no difference in blood loss over 1 liter or in any other outcome
related to PPH. Further research is needed to define the role of sublingual misoprostol
administration for the prevention of PPH.11-13 (Level II-1)
7. Should rectal misoprostol (600 g) be administered to prevent PPH instead of
oxytocin?
Oxytocin is the preferred uterotonic compared with rectal misoprostol in preventing
PPH. (Grade A)
Rectal misoprostol is associated with more adverse effects compared with oxytocin.
(Grade A)
Summary of Evidence
There was only 1 study in the systematic review that compared misoprostol 600 g
administered rectally with oxytocin 10 IU IM in 803 women. There were no differences in
the blood loss of >1 L and the use of blood transfusion.11-13 (Level II-1)
Compared to oxytocin, oral intake of misoprostol is associated with more adverse
effects, such as shivering (RR 3.02, 95% CI 1.74-5.23) and pyrexia with a temperature >
38C (RR 2.74, 95% CI 1.08-6.93). (Level II-1)
8. Should hemostatic agents be routinely given in the management of uterine atony?
Hemostatics are adjunctive forms of management for uterine atony. (Grade C)
Summary of Evidence
An antifibrinolytic agent, tranexamic acid, may be useful in emergencies. A dose
of 1 gm is given intravenously and can be repeated every 4-6 hours. Recombinant
Activated Factor VII, on the other hand, is used for the prevention and treatment of
hemorrhage in patients with hematologic disorders. Although not generally used in
obstetrics, there are numerous reports of its successful use in cases of intractable
hemorrhage from uterine atony. It is given in a dose of 60-120 g/kg BW. Both
tranexamic acid and recombinant activated factor VII can be used in conjunction with or
after primary measures.14 (Level III)
9. What is/are the procedures to be performed if active management of third stage of
labor and other standard measures to prevent uterine atony fail to control the
bleeding?
Conservative, non-surgical measures in the management of uterine atony may be
performed if bleeding persists after standard treatments. (Grade C)
Summary of Evidence
If bleeding persists despite AMTSL and other standard forms of treatment and the
patient is desirous of maintaining her reproductive potential, conservative measures may
be utilized. Among the non-surgical aspects of this form of treatment are bimanual uterine
compression and the internal uterine tamponade procedures. There are numerous case
reports and descriptive analyses of various devices used in internal uterine tamponade.
These include the Sengstaken-Blakemore tube (more popularly used for bleeding
esophageal ulcers), Rusch hydrostatic urological balloon, SOS Bakri balloon, foley
catheter with large volume capacity, hydrostatic condom catheter, and rubber glove
catheter. There have been no case-control, cohort or randomized trials comparing any of
these devices with other established forms to control PPH from uterine atony.15 (Level II3)
10. What is/are the procedures to be performed if active management of third stage of
labor, other standard measures, and non-surgical procedures to prevent uterine
atony fail to control the bleeding?
Brace compression suture procedures may be performed for uterine atony if
bleeding persists after standard and non-surgical measures. (Grade C)
Summary of Evidence
If bleeding persists despite AMTSL, other standard forms of treatment, and
other non-surgical interventions, and the patient is still desirous of maintaining her
reproductive potential, surgical measures may be utilized. These are the Brace
Compression Suture Procedures (more popularly known as the B-Lynch procedure), vasoocclusive measures (uterine and/or internal iliac artery ligation) and the angiographic
arterial embolization.
Because of its relative ease in performance, the brace compression suture should
be the initial conservative, surgical means of arresting PPH from uterine atony. It should
be attempted prior to the vaso-occlusive procedures. Its objectives are to prevent or
minimize uterine bleeding, maintain a tonically-contracted uterus, and promote normal
uterine involution.
Prior to performing this procedure, a test for potential efficacy has to be done. The
patient is placed in a semi-lithotomy position (frog-leg position) with an assistant standing
between the patients legs. The uterus is exteriorized by the surgeon/obstetrician and
bimanual compression is performed. The assistant intermittently swabs the vagina to
determine the presence of bleeding. If the bleeding stops on applying such as
compression, there is a good probability that the B-Lynch suture will work. If bleeding
persists, B-Lynch procedure may not be efficacious since a possible coagulation disorder
exists.
The steps in performance of the B-Lynch compression suture are detailed in
Figure 2.
There have been over 1,827 cases reported on the use of this procedure in the
management of PPH secondary to uterine atony with only 31 reported failures. These
failures are usually secondary to wrong surgical technique leading to uterine necrosis, no
pre-operative testing done, brace sutures not correctly applied, and uncontrolled DIC.
Modifications of the B-Lynch compression suture are the Hayman compression
suture and the Cho Multiple Squares Suture. The former is used when atony ensues after a
vaginal delivery and opening the uterus (akin to performing a low transverse CS) to guide
the sutures is not performed. The latter, on the other hand, is the alternative to the BLynch when the uterine incision has already been sutured prior to determining uterine
atony. It is not necessary to re-open the uterine incision in this method.15 (Level II-3)
Figure 2. B-Lynch Compression Suture Procedure15
(1) First stitch relative to the low transverse cesarean section: With the bladder displaced
inferiorly, the first stitch is placed 3 cm below the CS incision on the patients left side and
threaded through the uterine cavity to emerge 3 cm above the upper incision margin
approximately 4 cm from the lateral border of the uterus.
(2) The fundus: The suture is now carried over the top of the uterus and to the posterior side.
Once situated over the fundus, the suture should be more or less vertical and lie about 4 cm
from the cornu.
(3) The posterior wall: The location on the posterior uterus where the suture is placed through
the uterine wall is on the horizontal plane at the level of the uterine incision at the insertion of
the uterosacral ligament.
(4) Role of the assistant: As the operation proceeds, the assistant continues to compress the
uterus as the suture is fed through the posterior wall into the cavity. This will enable
progressive tension to be maintained as the suture begins to surround the uterus. Assistant
compression will also help to pull the suture material through to achieve maximum
compression, without breaking it, at the end of the procedure. Furthermore, it will prevent
suture slipping and uterine trauma. The suture now lies horizontally on the cavity side of the
posterior uterine wall.
(5) The fundus: As the needle pierces the uterine cavity side of the posterior wall, it is placed
over the posterior wall, bringing the suture over the top of the fundus and onto the anterior
right side of the uterus. The needle re-enters the cavity exactly in the same way as it did on
the left side, that is 3 cm above the upper incision and 4 cm from the lateral side of the uterus
through the upper incision margin, into the uterine cavity and then out again through 3 cm
below the lower incision margin.
(6) Later role of the assistant: The assistant maintains the compression as the suture material is
milked through from its different portals to ensure uniform tension and no slipping. The two
ends of the suture are put under tension after the lower segment incision has been closed by
either a one- or two-layer method.
(7) Relation to the hysterometry incision: The tension on the two ends of the suture material
can be maintained while the lower segment incision is closed, or the knot can be tied first,
followed by closure of the lower segment.
(8) Post-application and hysterotomy closure: It is probable that the maximum effect of suture
tension lasts for only about 24-48 hours. Because the uterus undergoes its primary
involutionary process in the first week after vaginal or cesarean delivery, the suture may have
lost some tensile strength, but hemostasis would have been achieved by that time. There is no
need for delay in closing the abdomen after the application of the suture. The assistant
standing between the patients legs swabs the vagina again and confirms that the bleeding has
been controlled.
References
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3.
Prendiville WJ, Elbourne D, McDonald S. Cochrane Database Syst Rev 2003; Issue 2.
Rogers J, Wood J, McCandlish R, Ayers S, Truesdale A, Elbourne D. Active versus expectant
management of third stage of labour: the Hinchingbrooke randomized controlled trial. Lancet 1998;
351:693-699.
Caroli G. Active versus expectant management in the third stage of labour (WHO Reproductive Health
Library Commentary, Nov. 17, 2000). Cochrane Database Syst Rev 2001, Issue 4.
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Elbourne DR, Prendiville WJ, Carroli G, Wood J, McDonald S. Prophylactic use of oxytocin in the
third stage of labor. Cochrane Database Syst Rev 2001, Issue 4.
Liabsuetrakul T, Choobul T, Peeyananjarassri K, Q Monir Islam. Prophylactic use of ergot alkaloids in
the third stage of labour. Cochrane Database Syst Rev 2009, Issue 3.
Ceriani Cernadas JM, Carroli G, Pellegrini L, et. al. The effect of timing of cord clamping on neonatal
venous hematocrit values and clinical outcome at term: A randomized controlled trial. Pediatr 2006;
117:e779-e786.
Chaparro CM, Neufeld LM, Tena Alvarez G, et. al. Effect of timing of umbilical cord clamping on iron
status in Mexican infants: A randomized controlled trial. Lancet 2006; 367:1997-2004.
Rabe H, Reynolds G, Diaz-Rossello J. Early versus delayed umbilical cord clamping in preterm
infants. Cochrane Database Syst Rev 2004; 4:CD003248.
van Rheenen P, Brabbin BJ. Late umbilical cord-clamping as an intervention for reducing iron
deficiency anemia in term infants in developing and industrialized countries: A systematic review. Ann
Trop Paediatr 2004; 24:3-16.
Hofmeyr GJ, Abdel-Aleem H, Abdel-Aleem MA. Uterine massage for preventing postpartum
haemorrhage. Cochrane Database Syst Rev 2008, Issue 3. Art. No.: CD006431.
Gulmezoglu AM, et. al. Prostaglandins for prevention of postpartum haemorrhage. Cochrane Database
Syst Rev 2006, Issue 4.
Villar J, Gulmezoglu AM, Hofmeyr GJ, Forna F. Systematic review of randomized control trials of
misoprostol to prevent postpartum hemorrhage. Obstet Gynecol 2002; 100 (6): 1301-12.
Mousa HA, Alfirevic Z. Treatment for primary postpartum haemorrhage. Cochrane Database Syst Rev
2009, Issue 3.
Wise A and Clark V. Strategies to Manage major obstetric hemorrhage. Curr Opin Anesth 2008;21:
281-287.
B-Lynch C, Keith LG, Lalonde AB, Karoshi M. A Textbook of Postpartum Hemorrhage, Sapiens
Publishing, 2006.
RETAINED PLACENTA
Background
Retained placenta is defined in various ways. The most common definition is
retention of the placenta in-utero for more than 30 minutes. This is an arbitrary definition,
and management is greatly influenced by the clinical assessment of whether significant
bleeding is occurring. This bleeding may be visible or may manifest only by the increasing
size of the uterus. In the absence of any evidence of placental detachment, consider the
diagnosis of complete placenta accreta or a variant. This condition may be present with
bleeding if only a portion of the placenta is abnormally implanted.
Recommendations
1. What is the role of umbilical vein injection in the management of retained placenta?
Umbilical vein injection may reduce the need for manual removal of a retained
placenta. (Grade B)
Summary of Evidence
A number of trials have evaluated the role of injection into the umbilical cord in
the management of retained placenta in women not experiencing significant bleeding.1
The definitions of retained placenta range from 15-60 minutes without placental delivery
but are most commonly 20-30 minutes. Injections into the cord vein have used isotonic
sodium chloride solution (normal saline), oxytocin and saline, prostaglandin and saline,
and dextran 70.
The studies comparing injection of oxytocin (commonly, 10 IU) and saline
(commonly, 20 ml) with expectant management (OR, 0.7; 95% CI 0.48-1.02) or saline
injection alone (OR, 0.59; 95% CI 0.43-0.82 and NNT, 8; 95% CI 5-20) suggest that this
practice indeed reduces the need for manual removal of the placenta. This intervention
seems reasonable in stable women with minimal bleeding while preparations for a manual
removal are being made. (Level II-2)
2. What is the definitive management of retained placenta?
Manual removal of the placenta is warranted if the other maneuvers have failed to
deliver the placenta and significant bleeding occurs. This followed by administration
of antibiotics. (Grade B)
Summary of Evidence
The retained or partially detached placenta interferes with uterine contraction and
retraction and leads to bleeding. Perform manual removal with a level of analgesia that
matches the clinical urgency of the situation. The cessation of an oxytocin infusion or the
administration of uterine relaxants to promote uterine exploration and manual removal is
of questionable value and may lead to increased bleeding. Ultrasound may be useful in
select cases.
When possible, an elbow-length glove is worn and attention is paid to asepsis.
The perineum and vagina must be prepared. The vaginal hand may be immersed in
povidone-iodine solution to facilitate easier entry. The hand is passed into the vagina
through the cervix and into the lower segment following the umbilical cord. Care is taken
to minimize the profile of the hand as it enters, keeping the thumb and fingers together in
the shape of a cone to avoid damage.
Control of the uterine fundus with the nonvaginal hand is essential. If the placenta
is encountered in the lower segment, it is removed. If the placenta is not encountered, the
placental edge is sought. Once found, the fingers gently develop the space between the
placenta and uterus and shear off the placenta. The placenta is pushed to the palmar aspect
of the hand and wrist; when it is entirely separated, the hand is withdrawn. Ensure that an
oxytocin infusion is running rapidly as the hand is withdrawn in order to encourage strong
uterine contraction, and then perform uterine massage. Care must be taken to tease out the
membranes. Once uterine contraction is established, examine the placenta and membranes
to determine whether further exploration or curettage is necessary. The administration of
antibiotics following manual removal is sometimes advocated. Evidence is very limited,
but a single, small, randomized trial supports the practice.7 (Level II-3)
References
1.
2.
3.
4.
5.
6.
7.
8.
Carroli G, Bergel E. Umbilical vein injection for management of retained placenta (Cochrane Review).
Cochrane Database Syst Rev, Issue 2. Oxford, UK: Update Software. 2006.
Abouzahr C. Antepartum and postpartum haemorrhage. In: Murray CJ, Lopez AD, eds. Health
Dimensions of Sex and Reproduction. Boston, Mass: Harvard University Press; 1998:172-4.
Baskett TF. Complications of the third stage of labour. In: Essential Management of Obstetrical
Emergencies. 3rd ed. Bristol, UK: Clinical Press; 1999:196-201.
Begley CM. A comparison of ''active'' and ''physiological'' management of the third stage of
labour. Midwifery 1990;6(1):3-17.
Berg CJ, Atrash HK, Koonin LM, Tucker M. Pregnancy-related mortality in the United States, 19871990. Obstet Gynecol 1996;88(2):161-7.
Bullough CH, Msuku RS, Karonde L. Early suckling and postpartum haemorrhage: controlled trial in
deliveries by traditional birth attendants. Lancet 1989;2(8662):522-5.
Chongsomchai C, Lumbiganon P, Laopaiboon M. Prophylactic antibiotics for manual removal of
retained placenta in vaginal birth. Cochrane Database Syst Rev 2006;CD004904.
Cunningham FG, Gant NF, Leveno KJ, et al. Conduct of normal labor and delivery. In: Williams
Obstetrics. 21st ed. New York, NY: McGraw-Hill; 2001:320-5.
UTERINE RUPTURE
Background
Uterine rupture in pregnancy is a rare and often catastrophic complication with a high
incidence of fetal and maternal morbidity. Several factors are known to increase the risk of
uterine rupture, but even in high-risk subgroups, the overall incidence of uterine rupture is
low. From 1976-2005, 19 peer-reviewed publications that described the incidence of uterine
rupture reported 1654 cases of uterine rupture among 2,504,456 pregnant women, yielding an
overall rupture rate of 1 in 1514 pregnancies (0.07%). The initial signs and symptoms of
uterine rupture are typically nonspecific, a condition that makes diagnosis difficult, which
sometimes delays definitive therapy. From the time of diagnosis to delivery, only 10-37
minutes are available before clinically significant fetal morbidity becomes inevitable. Fetal
morbidity invariably occurs because of catastrophic hemorrhage, fetal anoxia, or both. The
inconsistent premonitory signs and the short time for instituting therapeutic action make
uterine rupture a fearful event.
Uterine rupture during pregnancy is a rare occurrence that frequently results in lifethreatening maternal and fetal compromise, whereas uterine scar dehiscence is a more
common event that seldom results in major maternal or fetal complications. By definition,
uterine scar dehiscence constitutes separation of a preexisting scar that does not disrupt the
overlying visceral peritoneum (uterine serosa) and that does not significantly bleed from its
edges. In addition, the fetus, placenta, and umbilical cord must be contained within the
uterine cavity, without a need for cesarean section (CS) because of fetal distress. By contrast,
uterine rupture is defined as a full-thickness separation of the uterine wall and the overlying
serosa. Uterine rupture is associated with clinically significant uterine bleeding; fetal distress;
expulsion or protrusion of the fetus, placenta, or both into the abdominal cavity; and the need
for prompt CS, uterine repair, or hysterectomy. Although a scar from CS is a well-known risk
factor for uterine rupture, most events that involve disruption of the uterine scar result in
uterine-scar dehiscence rather than frank uterine rupture. These 2 entities must be clearly
distinguished because their options for clinical management and outcomes analyses differ.
The peer-reviewed literature was searched using the PubMedMedline and Cochrane
databases for articles published in the English language. The search terms were uterine
rupture, pregnancy and prior CS, vaginal birth after cesarean (VBAC), trial of labor (TOL),
uterine scar dehiscence, and pregnancy and myomectomy. Standard reference tracing was
also used. Articles published in 1976-2009 that described the incidence of uterine rupture and
that included sufficient information regarding the authors' definitions of uterine rupture and
of uterine-scar dehiscence were incorporated for review. All studies were observational or
reviews. A total of 73 published articles were included for data extraction and analysis.
Recommendations
1. What are the risk factors that predispose to rupture of the unscarred uterus?
The normal, unscarred uterus is least susceptible to rupture. Grand multiparity,
neglected labor, malpresentation, breech extraction, uterine instrumentation and
congenital uterine anomalies are all predisposing factors for uterine rupture. The
increased risk of uterine rupture attributable to the use of oxytocin in gravidas with
unscarred uteri is uncertain. (Grade B)
Summary of Evidence
Many authors have considered multiparity a risk factor for uterine rupture. Golan,
et. al. noted that, in 19 (31%) of 61 cases, uterine rupture occurred in women with a parity
of more than 5.1 Schrinsky and Benson found that 7 of 22 women (32%) who had
unscarred uterine rupture had a parity of greater than 4.2 In a study by Mokgokong and
Marivate, the mean parity for women who had pregnancy-related uterine rupture was 4.3
Despite the apparent increase in the risk of uterine rupture associated with high parity,
Gardeil, et. al. found only 2 (0.005%) women with uterine rupture among 39,529
multigravidas who had no previous uterine scar.4
Schrinsky and Benson reported 22 cases of uterine rupture in gravidas with
unscarred uteri.2 Nineteen (86%) ruptures occurred during labor, and 3 (14%) occurred
before labor. This percentage was markedly different from that of gravidas with a
previous uterine scar, for whom the timing of uterine rupture between labor and the
antepartum period was nearly evenly distributed.
Although distinguishing oxytocin use for labor induction versus labor
augmentation is useful, many researchers who investigate the use of oxytocin and the risk
of uterine rupture in unscarred uteri do not make this distinction. In 1976, Mokgokong
and Marivate reported 260 uterine ruptures among 182,807 deliveries that involved
unscarred uteri, and 32 (12%) of the 260 were associated with oxytocin use.3 Rahman, et.
al. similarly found that oxytocin was administered in 9 of 65 cases (14%) that involved
unscarred uterine rupture.5 Golan, et. al. noted that, among 126,713 deliveries, oxytocin
was used in 26 of 61 cases (43%) that involved unscarred uterine rupture.1 However,
Plauche, et. al. attributed only 1 of 23 unscarred uterine ruptures (4%) to the use of
oxytocin.6 Therefore, the increased risk of uterine rupture attributable to the use of
oxytocin in gravidas with unscarred uteri is uncertain.
In a review article by Nahum, congenital uterine anomalies affected
approximately 1 in 200 women.7-9 The walls of the abnormal uteri in such cases tend to
become abnormally thin as pregnancies advance, and they can be inconsistent over
different aspects of the myometrium. Ravasia, et. al. reported an 8% incidence of uterine
rupture (2 of 25) in those with congenitally malformed uteri compared with 0.61% (11 of
1788) in those with normal uteri (P = .013).10 Both cases of uterine rupture involved labor
induction with prostaglandin E2. Pregnancies implanted in the rudimentary horn of the
uterus pose special risk for uterine rupture up to 81% (387 of 475) in those women
attempting induction of labor. Importantly, 80% of ruptures occurred before the third
trimester, with 67% occurring during the second trimester. Although the uterine rupture
rate in anomalous, unscarred uteri during pregnancy appears to be increased relative to
that for normal uteri; the precise risk for different uterine malformations remains
uncertain. (Level II-2)
2. What are the risk factors that predispose to rupture of the scarred uterus?
For women with a single previous CS scar (whether vertical or transverse) at the
lower uterine segment, the risk for uterine rupture during spontaneous labor is
increased compared to those with unscarred uteri. The risk for rupture increases
with oxytocin induction or augmentation, cervical ripening with prostaglandins,
shorter inter-delivery interval, one-layer closure of uterine incision, lower uterine

wall thickness of less than 2-3.5 millimeters, fetal macrosomia and increasing
maternal age. The risk for uterine rupture is highest with multiple CS scars,
previous classical CS and previous myomectomies. (Grade B)
Summary of Evidence
The effect of previous CS on the risk of uterine rupture has been studied
extensively. In a meta-analysis, Mozurkewich and Hutton used pooled data from 11
studies and showed that the uterine rupture rate for women undergoing TOL after
previous CS was 0.39% compared with 0.16% for patients undergoing elective repeat CS
(OR 2.10; 95% CI 1.45-3.05).11 Restricting the meta-analysis to 5 prospective cohort trials
generated similar results (OR, 2.06; 95% CI, 1.40-3.04). Hibbard, et. al. examined the risk
of uterine rupture after previous CS in 1324 women who underwent a subsequent TOL.12
They reported a significant difference in the risk of uterine rupture between women who
achieved successful vaginal birth compared with women in whom attempted vaginal
delivery failed (0.22% vs 1.9%; OR, 8.9; 95% CI 1.9-42). The effect of previous CS on
the rate of subsequent pregnancy-related uterine rupture can be further examined
according to additional subcategories.
Classical CS is infrequently performed in the modern era and currently account
for 0.5% of all births in the United States. In a meta-analysis, Rosen, et. al. reported an
11.5% absolute risk of uterine rupture (3 of 26 cases) in women with classic vertical
cesarean scars who underwent an unplanned TOL.13 Chauhan, et. al. reported that the
uterine rupture rate for 157 women with classic uterine cesarean scars was 0.64% (95% CI
0.1-3.5%).14 All patients underwent repeat CS, but a high rate of preterm labor resulted in
49% of the patients being in labor at the time of their CS. Landon, et. al. reported a 1.9%
absolute uterine rupture rate (2 of 105 cases) in women with a previous classic, inverted
T, or J incision who either presented in advanced labor or refused repeat CS.15 However,
Chauhan, et. al. observed a 9% rate of asymptomatic uterine scar dehiscence (95% CI 515%).14
A meta-analysis of pooled data from 5 studies demonstrated a 1.1% absolute risk
(12 of 1112 cases) of symptomatic uterine rupture in women undergoing a TOL with a
low vertical cesarean scar. Compared with women with low transverse cesarean scars,
these data suggest no significantly increased risk of uterine rupture or adverse maternal
and perinatal outcomes.
The risk of uterine rupture after a low transverse CS varies depending on whether
patients undergo a TOL or an elective repeat CS and on whether labor is induced or
spontaneous, as well as other factors. The vast majority of CS in the United States are of
the low transverse type. For women who have had 1 previous CS, examining the various
risks of uterine rupture is instructive. These absolute risks for uterine rupture are
discussed below.
In a study of 20,095 women by Lydon-Rochelle, et. al., the spontaneous uterine
rupture rate among 6980 women with a single CS scar who underwent scheduled repeat
CS without a TOL was 0.16%.16 This finding indicates that uteri with cesarean scars have
an intrinsic propensity for rupture that exceeds that of the unscarred organ during
pregnancy, which is 0.013% (OR increased by approximately 12-fold). Therefore, all
other uterine rupture rates must be referenced to this expected baseline rate.
Lydon-Rochelle, et. al. showed that the uterine rupture rate among 10,789 women
with a single previous CS who labored spontaneously during a subsequent singleton
pregnancy was 0.52%.16 This rate of uterine rupture implies an increased relative risk
(RR) of 3.3 (95% CI 1.8-6.0) for women who labor spontaneously compared with women
who undergo elective repeat CS. In a study by Ravasia, et. al. of 1544 patients with a
previous CS who later labored spontaneously, the uterine rupture rate was 0.45%.17
Zelop, et. al. found that among 2214 women with 1 previous CS who labored
spontaneously, the uterine rupture rate was 0.72%.18 The authors of this article
performed a meta-analysis of 29,263 pregnancies from 9 studies from 1987-2004 and
showed that the overall risk of uterine rupture was 0.44% for women who labor
spontaneously after a previous CS.
Zelop, et. al. found that the rate of uterine rupture in 560 women who underwent
labor induction after a single previous CS was 2.3% compared with 0.72% for 2214
women who had labored spontaneously (P = .001).19 In a study by Ravasia, et. al. of 575
patients who underwent labor induction, the uterine rupture rate was 1.4% compared with
0.45% for women who labored spontaneously (P = .004).17 Blanchette, et. al. found that
the uterine rupture rate after previous CS when labor was induced was 4.0% compared
with 0.34% for women who labored spontaneously.20 This last finding suggests a 12-fold
increased risk of uterine rupture for women who undergo labor induction after previous
CS.
Lydon-Rochelle, et. al. reported a 15.6-fold increased risk for uterine rupture
(95% CI 8.1-30) when prostaglandins E2 (PGE2) were used in gravidas who underwent a
TOL after previous CS.16 In 366 women with scars from a previous CS who underwent
labor induction with prostaglandins, the uterine rupture rate was 2.45% compared with
0.77% without prostaglandin use. Taylor, et. al. identified 3 uterine ruptures among 58
patients with 1 previous CS who received PGE2 alone for labor induction.21 The uterine
rupture rate was 5.2% compared with 8 (1.1%) ruptures among 732 patients not treated
with PGE2. Ravasia, et. al. found that 3 ruptures occurred among 172 patients who
underwent labor induction with PGE2 alone (1.7%), which was significantly higher than
0.45%, or 7 of 1544 women who labored spontaneously.17 In contrast, Flamm, et. al.
found a uterine rupture rate of 6 (1.3%) of 453 patients with a previous CS who were
treated with PGE2 in combination with oxytocin.22 This result was not significantly
different from the rate of 33 (0.7%) of 4569 women who were not treated with PGE2. In a
small study, Delaney and Young also did not find a significant difference in uterine
rupture rates between patients with scars from a previous CS who underwent labor
induction with PGE2 and patients with previous CS who labored spontaneously (1.1 vs
0.3%; P = .15).23 Landon, et. al. reported no uterine ruptures among 227 patients who
underwent induction with PGE2 alone.15 Although the study was underpowered to detect
small differences, the particular type of prostaglandin administered did not appear to
significantly affect the uterine rupture rate. (Fifty-two patients received misoprostol; 111,
dinoprostone; 60, PGE2 gel; and 4, combined prostaglandins).
In a study by Blanchette, et. al., the rate of uterine rupture for 288 women who
underwent oxytocin augmentation of labor after a previous CS was 1.4% compared with
0.34% for 292 women who underwent a trial of spontaneous labor.20 This finding suggests
a 4-fold increased risk of uterine rupture in women who undergo labor augmentation with
oxytocin compared with spontaneous labor after previous CS.
Several studies have shown a protective association of previous vaginal birth on
uterine rupture risk in subsequent attempts at vaginal birth after previous CS. Zelop, et. al.
compared 1021 women who underwent a TOL after a single CS with 1 previous vaginal
delivery with 2762 women who underwent a TOL with no previous vaginal delivery.18
The uterine rupture rate was 0.2% versus 1.1% (P = .01).
In a study by Esposito, et. al., an interpregnancy interval between CS and a
subsequent pregnancy of <6 months was nearly 4 times as common among patients who
had uterine rupture than in control subjects (17.4 vs 4.7%; OR 3.92; 95% CI 1.09-14.3).24
Among 23 patients who had uterine rupture after a previous CS, the mean interpregnancy
interval was 20.4 4 15.4 months compared with 36.5 4 30.4 months for control subjects
(P = .01). Shipp, et. al. similarly found that the risk of symptomatic uterine rupture was
increased 3-fold in women with interdelivery intervals of less than 18 months when they
underwent a TOL after 1 previous CS (OR 3.0; 95% CI 1.2-7.2).25 In support of this
observation, Bujold and Gauthier reported 1527 women who underwent a TOL after a
single previous low transverse CS, finding that 2.8% of patients who had an interdelivery
interval of less than 24 months had a uterine rupture compared with 0.9% for those with
an interdelivery interval of greater than 24 months (P < .01).26 The OR for a uterine
rupture during a subsequent TOL (after adjustment for confounding variables) was 2.65
for women who had an interdelivery interval of less than 24 months compared with
women who had an interdelivery interval longer than this (95% CI, 1.08-5.46). The
authors speculated that a prolonged interpregnancy interval may allow time for the
previous CS scar to reach its maximal tensile strength before the scar undergoes the
mechanical stress and strain with a subsequent intrauterine pregnancy.
In a Canadian study of 1,980 women who underwent a TOL after a single
previous low transverse CS, Bujold and Gauthier found a 4 to 5-fold increased risk of
uterine rupture for women who had a previous single-layer uterine closure compared with
a 2-layer closure.26 Uterine rupture occurred in 15 (3.1%) of 489 cases of single-layer
closure versus 8 (0.5%) of 1,491 cases of double-layer closure (P < .001). Using stepwise
multivariate logistic regression, the authors concluded that the OR for uterine rupture in
women who had undergone single previous 1-layer cesarean hysterotomy closure was
3.95 (95% CI, 1.35-11.49) compared with those who had a 2-layer closure. Durnwald and
Mercer found that 182 patients with single-layer closure did not have an increased rate of
uterine rupture, but the rate of uterine windows at subsequent delivery was increased (3.5
vs 0.7%; P = .046).27 Gyamfi, et. al. reported an 8.6% (3 of 35) rate of uterine rupture in
patients with a single-layer closure compared with 1.3% (12 of 913) in those with doublelayer closure (P = 0.015).28 Although the single-layer group had a shorter interdelivery
interval, the uterine rupture rate remained significantly elevated even when the time
interval was controlled for using logistic regression (OR 7.20, 95% CI, 1.81-28.62, P =
0.005).
For women with a history of 2 or more CS, 9 studies published in 1993-2005
showed that the risk of uterine rupture in a subsequent pregnancy is 0.9-6.0% (1 per 17112 pregnancies). This risk is increased 2- to 16-fold for women with only a single
previous CS. In a study of 17,322 women with scars from cesarean delivery, Miller, et. al.
found that, when women underwent a TOL, uterine rupture was 3 times more common
with 2 or more scars (1.7%) than with 1 scar (0.6%) [OR 3.06; P < .001; 95% CI 1.954.79].29 In the largest analysis to date, Macones, et. al. reviewed data from 17 tertiary and
community hospitals and found that, in 1082 women with 2 uterine scars who underwent
a TOL, the risk of uterine rupture was increased 2-fold compared with women with only 1
uterine scar (absolute rupture risk 1.8 vs 0.9%; adjusted OR 2.3; 95% CI 1.37-3.85).30 In
the only study to control for potential confounding variables, Caughey, et. al. concluded
that, in women who had 2 previous CS who then attempted vaginal birth, the risk of
uterine rupture was almost 5 times the risk of those with only 1 previous CS (3.7 vs 0.8%;
P = .001).31 They also found that women with a previous vaginal delivery were about one
fourth as likely to have a uterine rupture as patients without a previous vaginal delivery
(OR, 0.26; 95% CI, 0.08-0.88). A 2004 American College of Obstetrics and Gynecology
(ACOG) Guideline suggests that, in women with 2 previous cesarean deliveries, only
those with a previous vaginal delivery should be considered candidates for a TOL. 32
Elkousy, et. al. found that, in 9960 women who underwent a TOL after 1 previous
CS, the risk of uterine rupture was significantly greater for fetuses that weighed more than
4000 g (2.8%) than in those weighing less than 4000 g (1.2%; RR 2.3, P < .001).33 For
women with 1 previous CS and no previous vaginal deliveries, the uterine rupture rate
was 3.6% for women with fetal weights of more than 4000 g compared with women with
fetal weights of less than 4000 g (RR 2.3, P < .001).
Shipp, et. al. showed that increasing maternal age has a detrimental effect on the
rate of uterine rupture.34 In a multiple logistic regression analysis that was designed to
control for confounding factors, the overall rate of uterine rupture rate in 3015 women
with 1 previous CS was 1.1%. The rate of uterine rupture in women older than 30 years
(1.4%) versus younger women (0.5%) differed significantly (OR, 3.2; 95% CI, 1.2-8.4).
Several reports have suggested that transabdominal (TAB), transperineal,
transvaginal, or sonohysterographic ultrasonography may be useful for detecting uterinescar defects after cesarean delivery. Rozenberg, et. al. prospectively examined 642 women
and found that the risk of uterine rupture after previous CS was directly related to the
thickness of the lower uterine segment, as measured during TAB ultrasonography at 3638 weeks of gestation.35 The risk of uterine rupture increased significantly when the
uterine wall was thinner than 3.5 mm. Using a 3.5 mm cutoff, the authors had a sensitivity
of 88%, specificity of 73.2%, positive predictive value of 11.8%, and a negative
predictive value of 99.3% in predicting subsequent uterine rupture. In a study of 722
women, Gotoh, et. al. reported that a uterine wall thinner than 2 mm, as determined with
ultrasonography performed within 1 week of delivery, significantly increased the risk of
uterine rupture.36 Positive and negative predictive values were 73.9% and 100%,
respectively.
3. What are the signs and symptoms of uterine rupture during pregnancy?
The classic signs and symptoms of uterine rupture are as follows: fetal distress (as
evidenced most often by pattern of abnormalities in fetal heart rate), diminished
baseline uterine pressure, loss of uterine contractility or hyperstimulation, abnormal
labor or failure to progress, abdominal pain, recession of the presenting fetal part,
hemorrhage, and shock. However, modern studies show that some of these signs and
symptoms are rare and that many may not be reliably distinguished from their
occurrences in other, benign obstetric circumstances. (Grade B)
Summary of Evidence
The signs and symptoms of uterine rupture largely depend on the timing, site, and
extent of the uterine defect. Uterine rupture at the site of a previous uterine scar is
typically less violent and less dramatic than a spontaneous or traumatic rupture because
the scar is relatively avascular.
Prolonged, late, or recurrent variable decelerations or fetal bradycardias are often
the first and only signs of uterine rupture. Bujold and Gauthier showed that abnormal
patterns in fetal heart rate were the first manifestations of uterine rupture in 87% of
patients.26 In a study by Leung, et. al., prolonged decelerations in fetal heart rate occurred
in 79% of cases and was the most common finding associated with uterine rupture.37
Rodriguez, et. al. found that fetal distress was the most common finding associated with
uterine rupture, occurring in 78%.38 Overall, in 4 studies from 1983-2000, prolonged
decelerations of fetal heart rate or bradycardias occurred in 114 (80%) of 143 cases of
uterine rupture. In cases that involved the extrusion of the placenta and fetus into the
abdominal cavity, prolonged decelerations in fetal heart rate occurred invariably.
Sudden or atypical maternal abdominal pain occurs more rarely than do
decelerations or bradycardia. In 9 studies from 1980-2002, abdominal pain occurred in
13-60% of cases of uterine rupture. In a review of 10,967 patients undergoing a TOL,
only 22% of complete uterine ruptures presented with abdominal pain and 76% presented
with signs of fetal distress diagnosed by continuous electronic fetal monitoring.
Moreover, in a study by Bujold and Gauthier, abdominal pain was the first sign of rupture
in only 5% of patients and occurred in women who developed uterine rupture without
epidural analgesia but not in women who received an epidural block.26 Thus, abdominal
pain is an unreliable and uncommon sign of uterine rupture. Initial concerns that epidural
anesthesia might mask the pain caused by uterine rupture have not been verified and there
have been no reports of epidural anesthesia delaying the diagnosis of uterine rupture. A
Guideline from the ACOG from 2004 suggests there is no absolute contraindication to
epidural anesthesia for a TOL because epidurals rarely mask the signs and symptoms of
uterine rupture. 32
Phelan, et. al. found that abnormal patterns of uterine activity, such as tetany and
hyperstimulation, are often not associated with uterine rupture.39 In their study, in which
monitoring of uterine activity was limited to external tocodynamometry, tetany was
defined as a contraction lasting longer than 90 seconds, and hyperstimulation was defined
as more than 5 contractions in 10 minutes. Rodriguez, et. al. found that the usefulness of
intrauterine pressure catheters (IUPCs) for diagnosing uterine rupture was not
supported.38 In 76 cases of uterine rupture, the classic description of decreased uterine
tone and diminished uterine activity was not observed in any patients, 39 of whom had
IUPCs in place. In addition, rates of fetal and maternal morbidity and mortality associated
with uterine rupture did not differ with the use of an IUPC compared with external
tocodynamometry.
In 8 reports published in 1980-2002 in which investigators examined the
frequency of vaginal bleeding in cases of uterine rupture, vaginal bleeding occurred in 1167% of cases. In 3 studies, maternal shock from hypovolemia was associated with uterine
rupture in 29-46% of cases. (Level II-2)
4. What are the fetal and neonatal consequences of uterine rupture?
The consequences of uterine rupture to the fetus or neonate include hypoxia or
anoxia, acidosis, depressed APGAR scores, admission to the neonatal intensive care
unit and perinatal death. (Grade B)
Summary of Evidence
The consequences of uterine rupture during pregnancy depend on the time that
elapses from the rupture until the institution of definitive therapy. In this regard,
appropriate therapy for the fetus and the mother are fundamentally different. Definitive
therapy for the fetus is delivery and must generally be accomplished with alacrity to avoid
major fetal morbidity and mortality. In the converse, therapy for the mother can generally
be supportive and resuscitative until surgical intervention can arrest the often lifethreatening uterine hemorrhage. Several studies have shown that delivery of the fetus 1037 minutes after uterine rupture is necessary to prevent serious fetal morbidity and
mortality. If proper supportive measures (including fluid resuscitation and blood
transfusion), are available to treat the mother, the time for definitive surgical intervention
before the onset of major maternal morbidity and mortality may often be substantially
longer than that for the fetus.
Leung, et. al. found that 5 of 99 neonates (5%) born to women who had uterine
ruptures developed neonatal asphyxia (defined as umbilical-artery pH <7 with seizures
and multiorgan dysfunction).37 No neonate had clinically significant perinatal morbidity
when delivery was accomplished within 17 minutes of an isolated and prolonged
deceleration of fetal heart rate. If severe late decelerations preceded prolonged
deceleration, perinatal asphyxia was observed as soon as 10 minutes from the onset of the
prolonged deceleration to delivery. In a study by Menihan, 6 of 11 fetuses born after
uterine rupture had bradycardias occur between 18-37 minutes prior to delivery.40
Although the rate of fetal acidosis was high (91%), no permanent neurologic injuries or
neonatal deaths occurred. In 23 cases of uterine rupture, Bujold and Gauthier found that,
even with rapid (<18-min) intervention between prolonged deceleration in fetal heart rate
and delivery, 2 neonates developed hypoxic-ischemic encephalopathies with impaired
motor development.26 They concluded that, though rapid intervention did not always
prevent severe metabolic acidosis and serious neonatal disease, it probably did limit the
occurrence of neonatal death.
In 99 cases of uterine rupture, Leung, et. al. found that 43 newborns (43%) had an
umbilical-artery pH level of less than 7, and 25 of these newborns had a pH level of less
than 6.8.37 In association with these pH levels, 39 newborns (39%) had 5-minute Apgar
scores of less than 7, 12 of whom had 5-minute Apgar scores of less than 3. Menihan
found that 10 of 11 fetuses (91%) who were born after uterine rupture had an umbilicalartery cord pH level of less than 7.0, and 5 (45%) had 5-minute Apgar scores of less than
7.40 The most important factor for the development of fetal acidosis was complete
extrusion of the fetus and placenta into the maternal abdomen.
Menihan found that 8 of 11 newborns (73%) delivered after uterine rupture
required admission to the neonatal intensive care unit (NICU).40 Kieser and Baskett found
an NICU admission rate for newborns after uterine rupture of 8 of 18 (45%).41 Landon, et.
al. found a similar NICU admission rate of 46 of 144 newborns (32%) after uterine
rupture. 15
In studies reported before 1978, the fetal mortality rate associated with uterine
rupture was high. In a review of 33 studies by Schrinsky and Benson, 960 cases of uterine
rupture resulted in 620 infant deaths, yielding a perinatal mortality rate of 65%.2
Blanchette, et. al. reported that 2 neonates (17%) died among 12 women who had uterine
rupture and that 1 of these neonates died after a decision-to-delivery time of only 26
minutes after the acute onset of fetal bradycardia, lower abdominal pain, and vaginal
bleeding, which signaled the acute uterine rupture.20 Leung, et. al. reported that 6 perinatal
deaths (6%) occurred among 99 patients who had uterine rupture.37 In a study by LydonRochelle, et. al., the perinatal death rate among fetuses in 91 cases of uterine rupture was
5.5% compared with 0.5% in control subjects.16 Landon, et. al. reported a perinatal death
rate from uterine rupture of 2% (2 of 124) among 19 academic centers in the United
States.15 These studies indicate that the incidence of perinatal death associated with
uterine rupture is decreasing in the modern era. (Level II-2)
5. What are the maternal consequences of uterine rupture?

The consequences of uterine rupture to the mother include bladder injury, severe
blood loss or transfusion, hypovolemic shock, need for hysterectomy and death.
(Grade B)
Summary of Evidence
Lydon-Rochelle, et. al. reported significant maternal bladder injuries in 7 of 91
women (8%) whose uteri ruptured compared with 240 of 20,004 control subjects (1.2%)
in whom rupture did not occur (P = .001).16 Shipp, et. al. found that bladder injuries
occurred in 5 of 28 women (18%) who had a uterine rupture after previous low transverse
CS.42 In a study by Kieser and Baskett, 3 of 18 patients (17%) who developed uterine
rupture had a cystotomy.41 Leung, et. al. found that 12 of 99 patients (12%) who
developed uterine rupture had incidental cystotomies at the time of surgery, and 7 more
(7%) had either a ruptured bladder or an accidental cystotomy; the combined total
urologic injury rate was 19%. 37
Cowan, et. al. found that, among 5 patients who developed uterine rupture, mean
blood loss was 1500 ml and great enough to be symptomatic in 3 patients (60%).42 In a
study by Shipp, et. al., 7 of 28 women (25%) who had uterine rupture during a TOL after
a previous CS received a blood transfusion.43 Kieser and Baskett found that 8 of 18
patients (44%) who had a complete uterine rupture required blood transfusion.41 Leung, et.
al. found that 29 of 99 (29%) patients who had uterine rupture required a blood
transfusion. 37
In a study of 93 uterine ruptures by Golan, et. al., 29% of women who had uterine
rupture developed signs and symptoms of hypovolemic shock.1 Rahman, et. al. reported
that, of 96 women who had uterine rupture, 33 (34%) developed hypovolemic shock.5
These modern rates of maternal shock after uterine rupture appear to be reduced compared
with the early rates reported in a 53-year review of the literature by Eden, et. al.44; their
observed incidence was 11 of 24 cases (46%).
In a study from South Africa, 261 of 335 women (78%) who had uterine rupture
were treated with hysterectomy. Flamm, et. al. found that 3 of 39 patients (8%) who
developed uterine rupture required hysterectomy.22 Kieser and Baskett found that 1 of 18
patients (6%) who developed complete uterine rupture required hysterectomy.41
Blanchette, et. al. reported that hysterectomy was necessary in 2 of 12 women (17%) who
developed uterine rupture.20 Hibbard, et. al. found that 6 hysterectomies (60%) were
necessary in 10 women who had a uterine rupture.12 Leung, et. al. reported that 19 of 99
patients (19%) with sustained uterine rupture required hysterectomy.37 Thirteen
hysterectomies (68%) were performed because the uterus was not deemed repairable, 4
(21%) were performed for irremediable uterine atony, and 1 (5%) was performed because
of placenta accreta.
Maternal death as a consequence of uterine rupture occurs at a rate of 0-1% in
modern developed nations, but the mortality rates in developing countries are 5-10%. The
availability of modern medical facilities in developed nations is likely to account for this
difference in maternal outcomes. In a South African study (1976), 22 of 260 women who
had pregnancy-related rupture of an unscarred uterus died (mortality rate 8.5%). These
deaths could be further subdivided into mortality for women with longitudinal uterine
tears (15 of 183 patients [8.2%]), transverse tears (2 of 49 patients [4%]), posterior-wall
tears (2 of 16 patients [13%]), and multiple uterine tears (3 of 12 patients [25%]). Golan,
et. al. reported no deaths among 32 mothers who developed rupture of a scarred uterus
compared with 9 deaths among 61 women with an intact uterus (15%).1 In a study from
Los Angeles, Leung, et. al. reported 99 patients with uterine ruptures; 1 woman (1%)
died.37 Mokgokong and Marivate noted that the maternal mortality rate associated with
uterine rupture largely depends on whether the diagnosis is established before or after
delivery; rates were 4.5% and 10.4%, respectively.3 (Level II-2)
6. What are the management options for uterine rupture?
Conservative surgical management involving uterine repair should be reserved for
women who have the following findings:
Low transverse uterine rupture
No extension of the tear to the broad ligament, cervix, or paracolpos
Easily controllable uterine hemorrhage
Hemodynamic stability
Desire for future childbearing
No clinical or laboratory evidence of an evolving coagulopathy
Hysterectomy should be considered the treatment of choice when intractable uterine
bleeding occurs or when the uterine rupture sites are multiple, longitudinal, or low
lying.
Rupture of a previous CS scar often can be managed by revision of the edges of the
prior incision followed by primary closure. (Grade C)
Summary of Evidence
The most critical aspects of treatment in the case of uterine rupture are
establishing a timely diagnosis and minimizing the time from the onset of signs and
symptoms until the start of definitive surgical therapy. Once a diagnosis of uterine rupture
is established, the immediate stabilization of the mother and the delivery of the fetus are
imperative. After the fetus is delivered, the type of surgical treatment for the mother
should depend on the following factors:
Type of uterine rupture

Extent of uterine rupture
Degree of hemorrhage
General condition of the mother
Mother's desire for future childbearing
No clinical or laboratory evidence of an evolving coagulopathy
As a rule, the time available for successful intervention after frank uterine rupture and
before the onset of major fetal morbidity is only 10-37 minutes. Therefore, once the
diagnosis of uterine rupture is considered, all available resources must quickly and
effectively be mobilized to successfully institute timely surgical treatment that results in
favorable outcomes for both the newborn and mother. Because of the short time available
for successful intervention, the following 2 premises should always be kept firmly in
mind: (1) Maintain a suitably high level of suspicion regarding a potential diagnosis of
uterine rupture, especially in high-risk patients. (2) When in doubt, act quickly and
definitively. (Level III)
7. What are the preventive strategies for uterine rupture?

The most direct prevention strategy for minimizing the risk of pregnancy-related
uterine rupture is to minimize the number of patients who are at highest risk. (Grade
B)
Summary of Evidence
The absolute risk of uterine rupture in pregnancy is low, but it is highly variable
depending on the patient subgroup. Women with normal, intact uteri are at the lowest risk
for uterine rupture (1 in 7440 pregnancies [0.013%]).
The most direct prevention strategy for minimizing the risk of pregnancy-related
uterine rupture is to minimize the number of patients who are at highest risk. The salient
variable that must be defined in this regard is the threshold for what is considered a
tolerable risk. Although this choice is ultimately arbitrary, it should reflect the prevailing
risk tolerance of patients, physicians, and of society as a whole. If this threshold is chosen
as 1 in 200 women (0.5%), the categories of patients that exceed this critical value are
those with the following:
Several previous CS
Previous classic midline CS
Previous low vertical CS
Previous low transverse CS with a single-layer hysterotomy closure
Previous CS with an interdelivery interval of less than 2 years
Previous low transverse CS with a congenitally abnormal uterus
Previous CS without a previous history of a successful vaginal birth
Previous CS with either labor induction or augmentation
Previous CS in a woman carrying a macrosomic fetus who weighs more than
4000 g
Previous uterine myomectomy accomplished by means of laparoscopy or
laparotomy
If a gravida falls into any 1 of these categories, her risk for uterine rupture is
increased to more than 1 in 200, and a clinical management plan should be specifically
designed with this increased risk in mind. (Level II-2)
Conclusion
Uterine rupture is a rare but often catastrophic obstetric complication with an overall
incidence of approximately 1 in 1514 pregnancies (0.07%). In modern industrialized
countries, the uterine rupture rate during pregnancy for a woman with a normal, unscarred
uterus is 1 in 7440 pregnancies (0.013%).
The vast majority of uterine ruptures occur in women who have uterine scars, most of
which are the result of previous cesarean deliveries. A single cesarean scar increases the
overall rupture rate to 0.51%, with the rate for women with 2 or more cesarean scars
increasing to 2%. Other subgroups of women who are at increased risk for uterine rupture are
those who have a previous single-layer hysterotomy closure, a short interpregnancy interval
after a previous cesarean delivery, a congenital uterine anomaly, a macrosomic fetus, a
history of prostaglandin use, and a failed trial of a vaginal delivery.
Surgical intervention after uterine rupture in less than 10-37 minutes is essential to
minimize the risk of permanent perinatal injury to the fetus. However, delivery within this
time cannot always prevent severe hypoxia and metabolic acidosis in the fetus or serious
neonatal consequences.
The most consistent early indicator of uterine rupture is the onset of a prolonged,
persistent, and profound fetal bradycardia. Other signs and symptoms of uterine rupture, such
as abdominal pain, abnormal progress in labor, and vaginal bleeding, are less consistent and
less valuable than bradycardia in establishing the appropriate diagnosis.
The general guideline that labor-and-delivery suites should be able to start cesarean
delivery within 20-30 minutes of a diagnosis of fetal distress is of minimal utility with respect
to uterine rupture. In the case of fetal or placental extrusion through the uterine wall,
irreversible fetal damage can be expected before that time; therefore, such a recommendation
is of limited value in preventing major fetal and neonatal complications. However, action
within this time may aid in preventing maternal exsanguination and maternal death, as long
as proper supportive and resuscitation methods are available before definitive surgical
intervention can be successfully initiated.
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18. Zelop CM, Shipp TD, Repke JT, et. al. Effect of previous vaginal delivery on the risk of uterine rupture
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factors? Am J Obstet Gynecol 2002;186(2):311-4.
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closure and uterine rupture. J Matern Fetal Neonatal Med 2006;19(10):639-43.
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30. Macones GA, Cahill A, Pare E, et. al. Obstetric outcomes in women with two prior cesarean deliveries:
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discussion 1228-9.
31. Caughey AB, Shipp TD, Repke JT, et. al. Rate of uterine rupture during a trial of labor in women with
one or two prior cesarean deliveries. Am J Obstet Gynecol 1999;181(4):872-6.
32. ACOG. Vaginal birth after previous cesarean delivery. ACOG practice bulletin no. 54. Washington,
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36. Gotoh H, Masuzaki H, Yoshida A, et. al. Predicting incomplete uterine rupture with vaginal
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37. Leung AS, Leung EK, Paul RH. Uterine rupture after previous cesarean delivery: maternal and fetal
consequences. Am J Obstet Gynecol 1993;169(4):945-50.
38. Rodriguez MH, Masaki DI, Phelan JP, Diaz FG. Uterine rupture: are intrauterine pressure catheters
useful in the diagnosis? Am J Obstet Gynecol 1989;161(3):666-9.
39. Phelan JP, Korst LM, Settles DK. Uterine activity patterns in uterine rupture: a case-control
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40. Menihan CA. Uterine rupture in women attempting a vaginal birth following prior cesarean birth. J
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41. Kieser KE, Baskett TF. A 10-year population-based study of uterine rupture. Obstet
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48. Erez O, Dukler D, Novack L, Rozen A, Zolotnik L, Bashiri A. Trial of labor and vaginal birth after
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49. Golan D, Aharoni A, Gonen R, et al. Early spontaneous rupture of the post myomectomy gravid
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51. Garnet JD. Uterine rupture during pregnancy. An analysis of 133 patients. Obstet Gynecol
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55. Seracchioli R, Rossi S, Govoni F, et al. Fertility and obstetric outcome after laparoscopic myomectomy
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58. Naef RW 3rd, Ray MA, Chauhan SP, et. al. Trial of labor after cesarean delivery with a lower-segment,
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59. Adair CD, Sanchez-Ramos L, Whitaker D, et. al. Trial of labor in patients with a previous lower
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60. Martin JN, Perry KG, Roberts WE, Meydrech EF. The case for trial of labor in the patient with a prior
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Gynecol 1997;89(5 Pt 1):671-3.
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66. Bujold E, Bujold C, Hamilton EF, et. al. The impact of a single-layer or double-layer closure on uterine
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from previous low transverse caesarean section. BJOG 2004;111(12):1394-9.
GENITAL TRACT TRAUMA

Lylah D. Reyes, MD
Background
Genital trauma is the second most common cause of postpartum bleeding with an
approximate incidence of 20 percent.1,2 It involves lacerations to the perineum, vagina, or
cervix; large episiotomy including extensions; ruptured uterus; and uterine inversion.2-5
Bleeding from genital injury is a major cause of morbidity and mortality in several
disorders involving the female reproductive tract.6 Such morbidity associated with childbirth
may have immediate and long-term effects on the physical, psychological, and social wellbeing of the woman after delivery.4,5 Hence, appropriate management of genital tract trauma
is an essential concern of obstetricians and gynecologists.
A. GENITAL TRACT LACERATIONS
Background
Lacerations can occur within the genital tract during childbirth (OR 2.4; 95% CI 2.02.8). This often occurs at the vaginal vault as the fetal head passes through. Lacerations can
involve the perineum, vagina, and the cervix.1-3
Perineal trauma may occur spontaneously or arise from episiotomy during vaginal
delivery. There are several classifications of spontaneous perineal trauma. It can be classified
according to location or depth of the perineal tissue involved. The classification based on
location include anterior and posterior perineal trauma.4,5 Anterior perineal trauma is
described as an injury involving the labia, anterior vagina, urethra or clitoris. Posterior
perineal trauma involves injury to the posterior vaginal wall, perineal muscles or anal
sphincters and may extend through the rectum. Regarding the classification of spontaneous
tears according to the degree or depth of the laceration this includes: 2-5
First Degree
Second Degree
Third Degree
Fourth Degree
involves the fourchette, perineal skin, and vaginal mucous membrane but
not the underlying fascia and muscle
aside from the skin and mucous membrane, the fascia and muscles of the
perineal body are involved
lacerations extend through skin, mucous membrane, perineal body, and
anal sphincter
3a: less than 50% of external anal sphincter thickness torn
3b: more than 50% of external anal sphincter thickness torn
3c: internal anal sphincter torn
there is extension of laceration through the rectal mucosal to expose lumen
of the rectum
The current classification based on depth was adopted from the guidelines published
by Royal College of Obstetricians and Gynaecologists (RCOG).5 The guidelines as shown
above further classified the third degree laceration according to the extent of anal sphincter
injury. This additional classification was included to allow the differentiation between future
incontinence related to internal anal sphincter injury rather than external anal sphincter alone.
According to the meta-analysis cited by RCOG conducted by Gupta, et. al., the incidence of
anal incontinence is increased in women who had both internal and external anal sphincter
damage compared with those who had external anal sphincter damage alone. However, in
acute obstetric trauma, identification of the internal anal sphincter may not be feasible but
recognizing the degree of external anal sphincter damage is possible in all cases. However,
this classification system has not been extensively validated yet.6 In a survey conducted
among doctors repairing third and fourth degree lacerations revealed that the physicians
concur with the classification of OASI (Obstetric Anal Sphincter Injuries), and that further
definitive research is strongly recommended.7
Intrapartum cervical lacerations have an overall incidence of 25-90% and most cases
are asymptomatic. On the other hand, the clinically significant cervical lacerations complicate
0.2 to 4.8% of all vaginal deliveries.8 Minor cervical lacerations are most often undetected
since most of these would be less than 0.5 cm.3 On the other hand, cervical tears may extend
to the upper third of the vagina. In certain instances the cervix may be avulsed, partially or
completely. Although rare, lacerations of the cervix may also extend to the lower uterine
segment, peritoneum, and even involve the uterine artery including its major branches.3,8
It has been reported that women who had episiotomies or spontaneous perineal
lacerations have greater perineal pain or discomfort, decreased sexual satisfaction postnatally,
and delayed return of sexual activity than those who had an intact perineum after delivery.2,4
This may disrupt breastfeeding, family life and sexual relations. Such may occur depending
on the severity of perineal trauma and on the effectiveness of treatment. The type of suturing
material, the technique of repair and the skill of the operator are considered as the three main
factors that influence the outcome of perineal repair.4, 7
Recommendations
1. What factors will increase the suspicion for genital tract laceration?
Genital tract laceration should be suspected if bleeding will persists despite a wellcontracted uterus. (Grade C)
Summary of Evidence
Most of the risk factors identified cannot be promptly used to prevent or predict
the occurrence genital tract lacerations. However, the presence of bleeding despite a wellcontracted uterus along with any of the risk factors mentioned below will increase the
possible occurrence of such injury.1,3,5,9-11
It is essential for clinicians to be aware of the factors that increase the risk for the
development of genital tract laceration. The factors9,12-14 associated with such injury
include induction of labor with oxytocin (OR 11.9; 95% CI 4.7-30.4), operative vaginal
delivery (adjusted OR 10.8; 95% CI 5.2-22.3), nulliparity (adjusted OR, 10.0; 95% CI
3.0-33.3), mediolateral episiotomy with forceps delivery (OR 5.62, 95% CI 2.16-14.62),
midline episiotomy (adjusted OR 2.5; 95% CI 1.0-6.0), and birth weight over 4 kg
(adjusted OR 1.68, 95% CI 1.18-2.41). The other factors include second stage longer than
1 hour (4%), shoulder dystocia (4%), persistent occipitoposterior position (3%), epidural
analgesia (2%), and precipitous delivery.
Perineal lacerations may occur in women with no apparent risk factors3,9 but the
presence of any of these risk factors increase the possible occurrence of such injury.
(Level III)
2. How can the occurrence of genital tract lacerations be prevented?

Restricting the use of episiotomy can reduce the incidence of severe perineal trauma.
(Grade A)
Summary of Evidence
The purpose of performing an episiotomy is to prevent perineal lacerations.
Although, the routine use of such procedure was found to increase the risk for blood loss
and anal sphincter tears.15-16 A Cochrane review which included 8 randomized trials,
involving 5541 women, compared the effects of restrictive and routine episiotomy.15 The
proportion of women who had episiotomies was 75.15% (2035/2708), while the
proportion of those with restrictive episiotomy was 28.40% (776/2733). The review
demonstrated that liberal use of episiotomy does not reduce the incidence of anal
sphincter lacerations and is associated with increased perineal trauma. The result of the
review showed that restricting the use of episiotomy to specific fetal and maternal
indications, compared with routine use during vaginal birth, was associated with lower
rates of posterior perineal trauma (RR 0.67, 95% CI 0.49-0.91), less suturing (RR 0.71,
95% CI 0.61-0.81), and fewer healing complications (RR 0.69, 95% CI 0.56-0.85). But
restrictive episiotomy was noted to be associated with more anterior perineal trauma (RR
1.84, 95% CI 1.61-2.10). For the other outcome measures such as severe vaginal or
perineal trauma (RR 0.92, 95% CI 0.72-1.18), dyspareunia (RR 1.02, 95% CI 0.90-1.16),
and urinary incontinence (RR 0.98, 95% CI 0.79-1.20), no significant difference between
the 2 groups was noted. (Level I)
The American College of Obstetricians and Gynecologists (ACOG)3 recommends
restrictive use of episiotomy rather than routine. This is based on level B evidence that
median episiotomy is associated with higher rates of injury to the anal sphincter and
rectum as compared to mediolateral episiotomy. Thus, routine episiotomy does not
prevent pelvic floor damage that may lead to incontinence.
Minimizing the use of operative vaginal delivery can decrease the incidence of severe
perineal trauma. Vacuum extraction is more effective in reducing the severity of
perineal trauma compared with forceps. (Grade B)
Summary of Evidence
Vaginal sidewall laceration is also most commonly associated with operative
vaginal delivery, but it may occur spontaneously. Lacerations often occur in the region
overlying the ischial spines. Cervical laceration is most commonly associated with forceps
delivery, and the cervix should be inspected following such deliveries. To further avoid
trauma to the cervix, assisted vaginal delivery (forceps or vacuum) should never be
attempted without the cervix being fully dilated. The frequency of sidewall and cervical
lacerations has probably decreased in recent years since there has been a reduction in the
use of midpelvic forceps and, especially, midpelvic rotational procedures.18,19 (Level III)
In multivariate regression models, high birth weight (OR 1.68, 95% CI 1.18-2.41;
P=0.004), and forceps delivery combined with mediolateral episiotomies (OR 5.62, 95%
CI 2.16-14.62; P<0.001) were proven as independent risk factors for severe perineal
trauma during childbirth.14 (Level II-1)
In a meta-analysis in published in 200120 there were 10 randomized control trials
(RCTs), involving 2885 women, which reviewed the occurrence of perineal trauma with
forceps delivery and vacuum forceps extraction. The review was able to demonstrate that
perineal injury and pain at 24 hours was significantly reduced with vacuum forceps
extraction as compared to forceps delivery (RR 0.46, 95% CI 0.38-0.56). The number
needed to treat (NNT) is 10, which means that to prevent 1 woman having perineal injury
10 women should undergo vacuum forceps extraction rather than forceps delivery.
However, none of the trials attempted to blind the allocated intervention during the
postnatal assessments. (Level I)
The subsequent RCTs conducted found that fewer women had severe perineal
trauma21,22 and third-degree tears23 with vacuum extraction compared with forceps
delivery. But the risk of perineal trauma between the 2 groups was not significantly
different (RR 0.50, 95% CI 0.10-2.6421; RR 0.58, 95% CI 0.19-3.1522; and RR 0.44, 95%
CI 0.16-1.2223). (Level II-1)
In an observational study, vacuum extraction was found to be more effective in
decreasing the proportion of women with severe perineal injury, severe perineal pain at 24
hours, and altered fecal continence at 3 months. However, due to the low quality of
evidence no definite conclusion can be drawn.24 (Level III)
Continuous support may be more effective in reducing perineal trauma. (Grade A)
Summary of Evidence
Continuous support during labor may be more effective in decreasing the
proportion of women who would need assisted vaginal delivery, hence reducing the risk
of perineal trauma.24 We don't know whether continuous support during labor may be
more effective in reducing perineal trauma or in reducing rates of episiotomy.
One systematic review conducted in 2005, which included 15 RCTs, involving
12,791 women, compared continuous one-to-one intrapartum support from a professional
nurse, midwife, or layperson versus usual care.25 The RCTs were of reasonable quality.
Although the experimental intervention was always described as one-to-one support, but
the experience, relationship to the laboring woman, timing, and duration of support varied
between trials. Despite of this no heterogeneity between the trials was noted. The review
found that continuous support significantly reduced assisted vaginal birth compared with
usual care (RR 0.89, 95% CI 0.83-0.96). However, there was no significant difference in
the overall rate of episiotomy or perineal trauma with continuous support (RR 0.97, 95%
CI 0.90-1.05); and perineal trauma (episiotomy or laceration requiring suturing) with
usual care (RR 0.99, 95% CI 0.95-1.03). Although, there is some evidence of benefit for
continuous support during labor compared with usual care, particularly in reducing the
rate of assisted vaginal birth. However, no reduction was noted with the overall rates of
perineal trauma. (Level I)
Antenatal perineal massage reduces perineal trauma. (Grade A)
Summary of Evidence
A Cochrane Review documented that antenatal perineal massage during the last
trimester of pregnancy reduces the likelihood of perineal trauma and postpartum pain.26
Four good quality trials were included in the review, which involved 2497 women,
comparing digital antenatal perineal massage with control. Perineal massage done at least
once or twice a week from 35 weeks of pregnancy performed by the woman or her
husband was associated with an overall reduction in the incidence of trauma requiring
suturing (RR 0.91, 95% CI 0.86-0.96). The NNT is 15. Women practicing perineal
massage were found to be less likely to have an episiotomy (RR 0.84, 95% CI 0.74-0.95),
with NNT of 21. These findings were significant for women without previous vaginal
birth only. For women who previously had vaginal delivery, a statistically significant
reduction in the incidence of pain at three months postpartum (RR 0.45, 95% CI 0.240.87) was reported, with NNT of 13. Regarding the incidence of first- or second-degree
perineal tears or third/fourth-degree perineal trauma, no statistically significant
differences were reported between perineal massage and no massage. Similarly, no
significant differences were observed in the incidence of instrumental deliveries, sexual
satisfaction, or incontinence of urine, feces or flatus for any of the women who practiced
perineal massage compared with those who did not massage. (Level I)
Antenatal perineal massage reduces the occurrence of perineal trauma, particularly
episiotomies, and the reporting of ongoing perineal pain. It is generally found to be well
accepted by women.24 Thus, women should be made aware of the possible benefit of
perineal massage and provided with information on the process of massage. For further
details regarding perineal massage please refer to Appendix.
3. What measures can be done to properly identify genital tract lacerations?
All women undergoing vaginal delivery suspected to have genital tract lacerations
should be assessed thoroughly by exploration of the lower genital tract to properly
evaluate the extent of the injury. Most especially when uterine atony and retained
placenta has been ruled out. (Grade C)
Summary of Evidence
In assessing genital tract lacerations, careful visual inspection of the lower genital
tract should be done. 1,9,12,17,27 The patient should be in a dorsal or lithotomy position
assessed with appropriate assistance and good lighting to adequately visualize the
presence and extent of the lacerations. During the process, adequate anesthesia is often
essential to allow ease of exploration. In some instances, it may be necessary to move the
patient to the operating room, as surgical assistance may be needed to obtain appropriate
exposure.
Inspection of the cervix should be aided with the use of ring or sponge forceps and
appropriate retractors to ensure adequate visualization. The anterior lip is grasped, and the
cervix is inspected by using a second ring forceps placed at the 2-o'clock position,
followed by progressively "leap-frogging" the forceps ahead of one another until the
entire circumference has been inspected.1 (Level III)
4. Once the lacerations are identified, how should it be managed?
Nonsuturing of first- and second-degree tears may be associated with reduced
wound gaping up to 48 hours to 14 days after birth. However, leaving perineal skin
unsutured reduces dyspareunia and pain up to 3 months. (Grade B)
Summary of Evidence
In women with first- and second-degree tears or episiotomies, nonsuturing of the
perineal skin but apposing it with the sutured vagina and perineal muscles may be more
effective than suturing all three layers in decreasing the incidence of dyspareunia at 3
months but not at reducing pain. However, this method may be less effective in
decreasing the incidence of gaping wound at 48 hours and at 10 days, but not at 14 days
postpartum. There were two RCTs that compared non-suturing of but apposed skin of
perineal tears versus repair or suturing all three layers.28,29 However, these RCTs were
found to be of low-quality evidence.
In one RCT conducted in a large center in UK, involving 1780 primiparous and
multiparous women with first- and second-degree tears or episiotomies after spontaneous
or assisted vaginal delivery, nonsuturing of the skin was compared with the skin sutured.
In this RCT, no significant difference was noted in the proportion of women reporting
perineal pain at 10 days after birth (RR 0.91, 95% CI 0.77-1.06). With regards to
dyspareunia at 3 months postpartum, the unsutured skin compared with sutured skin
group was significantly reduced (RR 0.80, 95% CI 0.64-0.99).28
Another RCT was conducted in Nigeria, involving 823 women who sustained a
second-degree tear or episiotomy.29 The trial showed that leaving the perineal skin
unsutured significantly decreased the proportion of women with perineal pain at 48 hours,
14 days, 6 weeks, and 3 months after delivery. Forty-eight hours after delivery the risk of
developing perineal pain with the skin unsutured was significantly reduced as compared
when the skin is sutured (RR 0.87, 95% CI 0.78-0.97). At 14 days postpartum, the risk of
perineal pain further decreased significantly in women with unsutured skin had as
compared to those with the skin sutured (RR 0.77, 95% CI 0.61-0.98). On the 6th week
postpartum, the risk of perineal pain was reduced by 36% for the unsutured skin group
compared with the skin sutured (RR 0.64, 95% CI 0.44-0.93). By 3 months postpartum,
there is 81% reduction in the risk of perineal pain among women with unsutured skin
compared with the skin sutured (RR 0.19, 95% CI 0.06-0.54). When dyspareunia as an
outcome was assessed, there was also a significant reduction noted after 3 months
postpartum with unsutured skin of perineal tears as compared to those sutured (RR 0.52,
95% CI 0.33-0.81).
However, the two RCTs found that leaving the perineal skin unsutured increased
the rates of wound gaping 48 hours postpartum compared with suturing the skin. In the
study of Gordon, et. al.,28 the reported RR is 5.10 (95% CI 3.68-7.0) and a RR of 4.96
(95% CI 3.17 to 7.76) was accounted from Obovo, et. al.29 In the study of Gordon, et. al.,
the risk of wound gaping was also noted to increase at 10 days after delivery.28 However,
with Obovo, et. al.29 no significant difference in wound gaping was reported at 14 days
postpartum (RR 1.25, 95% CI 0.94-1.67) unlike with the study of Gordon, et. al.28 (RR
1.56, 95% CI 1.30-1.88). Regarding wound breakdown at 14 days postpartum, no
significant differences were noted between the unsutured and sutured skin groups (RR
1.27, 95% CI 0.56-2.85). (Level II-1)
Any cervical tear, which is actively bleeding and/or 2 centimeters in length or longer
should be sutured. (Grade C)
Summary of Evidence
Cervical lacerations up to 2 cm in length occur frequently and can be expected
during childbirth. They usually heal rapidly and are of little consequence. If the
lacerations are actively bleeding or if alterations in the anatomical relationship of the
cervix occur, such lacerations should be repaired.3,27,30 (Level III)
In repairing genital tract lacerations an anchoring suture is placed 1 cm above the
apex of the vaginal tear and or episiotomy incision, and just above the angle for
cervical lacerations. (Grade C)
Summary of Evidence
Applying the suture above the apex of the laceration ensures hemostasis of any
bleeding vessels that may have retracted above it.3,31 (Level III)
Obliteration of dead spaces and prevention of overtightened sutures should be
ensured when repairing genital tract lacerations. (Grade C)
Summary of Evidence
Presence of dead spaces cannot assure hemostasis. This predisposes the woman to
hematoma formation, pain, infection, and wound breakdown as well. If dead spaces
cannot be closed securely, then a vaginal pack should be inserted.32 Avoid over-tightened
sutures since this can cause unnecessary pain when reactionary edema and swelling occur,
and also may cause tissue ischemia which delays healing.31,33 (Level III)
4. What suture material should be used in the repair of genital tract lacerations?
The use of absorbable synthetic material (polyglycolic acid and polyglactin 910) for
repair of perineal trauma is preferred. Such material is associated with less perineal
pain, analgesic use, dehiscence and resuturing, although there is increased suture
removal, when compared with catgut. (Grade A)
Summary of Evidence
A meta-analysis,34 which included eight trials, involving 3681 women, reviewed
the evidence on absorbable synthetic versus catgut suture material for perineal repair.
There were 5 RCTs, which examined the use of analgesics as the outcome, while the other
3 trials assessed the outcome perineal pain. Three out of the 8 RCTs assessed the presence
of dyspareunia. With all the RCTs, blinding of the outcome assessment was not possible
due to the noticeable difference between the sutures. The findings were consistent among
the RCTs. Compared with catgut, the polyglycolic acid and polyglactin groups were
significantly associated with less pain (RR 0.78, 95% CI 0.67-0.90) and analgesic use (RR
0.74, 95% CI 0.65-0.85) in first 10 days postpartum. The NNT is 18, which means that
using polyglycolic acid or polyglactin suture in 18 women with perineal tears will reduce
1 event of perineal pain. By 3 months postpartum, there was no significant difference in
perineal pain (RR 0.86, 95% CI 0.64-1.08) or dyspareunia (RR 0.95, 95% CI 0.79-1.15)
between absorbable synthetic sutures and catgut chromic catgut. But rates of dyspareunia
were lower after 3 months from delivery with absorbable synthetic sutures than with
chromic catgut (RR 0.59, 95% CI 0.39-0.91) with NNT of 20. Therefore, you need to use
absorbable synthetic sutures in repairing perineal tears of 20 women to prevent one event
of dyspareunia.
However, in the same systematic review suture removal was significantly more
common in the absorbable synthetic group as compared to the catgut group up to 3
months after postpartum (RR 1.78, 95% CI 1.44-2.20). The number needed to harm
(NNH) is 13, wherein among 13 women with perineal tears repaired with absorbable
synthetic sutures there will be 1 event of dehiscence. This was based on the findings of 2
RCTs, involving 2129 women.
There were 3 RCTs which compared rapidly absorbed suture polyglactin 910
suture and standard polyglactin suture for surgical repair. There was no systematic review
found. One RCT did not report their data in a standard format, hence, it was not included
for appraisal.35 With the other 2 RCTs,36,37 rapidly absorbed sutures significantly reduced
pain on ambulation within 2 weeks postpartum compared with standard absorbable
sutures. This accounted for the RR of 0.69 (95% CI 0.51-0.92) in the trial of Gemynthe,
et. al., and RR of 0.83 (95% CI 0.73-0.94) with the study of Kettle, et. al. No significant
difference between suture groups was found in terms of the risk of developing perineal
pain, pain on sitting, or dyspareunia. Outcome assessors were blinded as to the type of
suture material used since the manufacturers produced identical suture materials. Only the
trial of Kettle, et. al. reported on the adverse effect of the suture material, which is suture
removal. In this trial rapidly absorbed sutures were significantly removed less frequently
during the 3 months postpartum than standard absorbable sutures (RR 0.23, 95% CI 0.140.35). (Level I)
The standard polyglactin 910 takes time to be absorbed. About 60% of the suture
remains up to 2128 days after repair and it is not totally absorbed from the wound until
6090 days. But current evidence reported a more rapidly absorbed synthetic suture
material when compared to standard polygalctin 910 material is associated with less
perineal pain with ambulation or need for suture removal up to 6 months after repair.
According to the product information sheet of the suture material, the tensile strength is
reduced at 1014 days and completely absorbed from the tissue by 42 days.36
In repairing the external anal sphincter muscle use of either monofilament sutures
such as polydiaxanone or braided sutures such as polyglactin can be used with
equivalent outcome. (Grade A)
Summary of Evidence
No systematic reviews to assess the best suture material for repair of the external
anal sphincter were found.38-40 Only one RCT reported on the use of 3-0 PDS and 2-0
polyglactin (Vicryl).38 Out of the 103 women who followed up on the 6th week after repair
of perineal tears after childbirth, no difference in suture-related morbidity between the 2
suture material groups was found. Seventy percent of these women were asymptomatic.
Up to 12 months of follow-up no significant difference in morbidity from anal
incontinence, perineal pain or suture migration.
Use of fine suture size such as 3-0 PDS and 2-0 polyglactin (Vicryl) may cause
less irritation and discomfort.39 Use of these sutures is preferable since these are delayed
absorbable monofilament suture with a longer half-life and is less likely to precipitate
infection than braided sutures. (Level I)
With the repair of the internal anal sphincter muscle, fine suture size such as 3-0
PDS and 2-0 Vicryl may produce less irritation and discomfort. (Grade C)
The use of and 2-0 Vicryl or 3-0 PDS absorbable sutures with tapered needle is
suitable to repair cervical lacerations. (Grade C)
Summary of Evidence
Similarly, there are no systematic reviews or randomized studies conducted to
evaluate the type of suture materials use for the repair of internal anal sphincter and
cervical lacerations. The use of fine suture size such as 3-0 PDS and 2-0 Vicryl may be
associated with less irritation and discomfort.27,30,38,40 (Level III)
5. What techniques should be used to accomplish the repair of genital tract
lacerations?
Continuous subcuticular suture for repair of perineal skin is more effective in
reducing the proportion of women with short-term pain as compared to interrupted
sutures. (Grade A)
Summary of Evidence
A Cochrane systematic review41 of four RCTs, involving 1864 primiparous and
multiparous women, found that a continuous subcuticular technique of perineal skin
closure, when compared with interrupted transcutaneous stitches, was associated with less
short-term pain. Three of the trials presented data on pain up to day 10 in a suitable format
for inclusion in the analysis and only one study actually demonstrated any statistical
significance between the two intervention groups. Continuous sutures significantly
reduced the risk for perineal pain up to 10 days compared with interrupted sutures (RR
0.75, 95% CI 0.63-0.89) with NNT of 14. This means to prevent one event of perineal
pain the perineal tears of 14 women should be repaired by continuous subcuticular suture.
However, there was no significant difference in the risk of women with pain at 3 months
between the subcuticular and interrupted suture groups (RR 1.10, 95% CI 0.77-1.57).
But in 1 RCT identified by the systematic review of Kettle, et. al. suture removal
was significantly more common up to 3 months from perineal skin repair in the
interrupted-suture group than in the continuous group (RR 1.41, 95% Cl 1.16-1.72).42
(Level I)
A loose, continuous non-locking suturing technique used to appose the vaginal
(anterior and posterior perineum) tissue, perineal muscle and skin is associated with
less short-term pain compared with the traditional interrupted method. (Grade A)
Summary of Evidence
Two RCTs compared loose continuous suture for all layers versus interrupted
sutures.37,43 In a large trial involving 1542 women with second-degree tears or episiotomy
in the UK37 continuous sutures significantly reduced the risk of developing pain among
women with perineal tears at 10 days with continuous as compared with interrupted suture
(OR 0.47, 95% CI 0.38-0.58). However, no significant difference in the risk of perineal
pain was noted among these women at 3 months postpartum with continuous and
interrupted sutures (OR 0.70, 95% CI 0.54-1.47) even up to 12 months (OR 0.64, 95% CI
0.35-1.16). The odds of developing dyspareunia is not significantly different after 3
months with continuous and with interrupted suture groups (OR 0.98, 95% CI 0.72-1.33)
as well as at 12 months (OR 1.05, 95% CI 0.77-1.43).
In a smaller RCT,43 212 primiparous women in Italy with a second-degree tear or
episiotomy were assessed to compare the effects of continuous and interrupted sutures on
perineal pain and dyspareunia. The suture material used was fast-absorbing polyglactin
910 suture material for perineal repair in both comparison groups. The trial reported that
continuous sutures significantly reduced the risk of women having perineal pain at 10
days compared with interrupted sutures (OR 0.32, 95% CI 0.19-0.57). However, no
significant difference between groups in the risk of developing dyspareunia at 3 months
(OR 0.87, 95% CI 0.42-1.82).
The trial of Kettle, et. al. accounted for significant suture removal 3 months
postpartum in the interrupted suture group than in the continuous group (RR 4.01, 95% CI
2.59-6.19).24 No information regarding adverse effects was reported by Morano, et. al.43
(Level I)
The use of a two-layer procedure of perineal repair, where the skin is apposed but
not sutured, is associated with an increase in wound gaping up to 10 days following
birth but less dyspareunia at 3 months postpartum than a three-layer technique
involving skin closure. (Grade A)
Summary of Evidence
Two large RCTs compared leaving the perineal skin unsutured but apposed (the
vagina and perineal muscle were sutured) to the traditional repair whereby all three layers
(vagina, perineal muscles and skin) were each sutured. One of the RCTs carried out in a
single centre in the UK involving 1780 women found no difference in short- or long-term
pain between the two groups.28 However, the other RCT carried out in Nigeria among 823
women found that leaving the skin unsutured was associated with a reduction in perineal
pain up to 3 months postpartum.29 Both trials reported lower rates of dyspareunia at 3
months postpartum in the groups that had the perineal skin left unsutured. Both studies
found that leaving the perineal skin unsutured was associated with a significant increase
in wound gaping up to 10 days following birth. (Level I)
For repair of the external anal sphincter, either an overlapping or end-to-end
(approximation) method can be used, with equivalent outcome. Where the internal
anal sphincter can be identified, it is advisable to repair separately with interrupted
sutures. (Grade A)
Summary of Evidence
A systematic review44 on the method of repair for third-degree tears examined
three trials involving 279 women. This review showed that there was no significant
difference in perineal pain (RR 0.08, 95% CI 0.00-1.45), dyspareunia (RR 0.62, 95% CI
0.11-3.39), flatus incontinence (RR 0.93, 95% CI 0.26-3.31) and fecal incontinence (RR
0.07, 95% CI 0.00-1.21) between the two repair techniques at 12 months. But a
significantly lower incidence in fecal urgency (RR 0.12, 95% CI 0.02-0.86, one trial, 52
women) and lower anal incontinence score (weighted mean difference 1.70, 95% CI
3.03 to 0.37) in the overlap group was noted. Overlap technique was also associated with
a significant lower risk of deterioration of anal incontinence symptoms over 12 months
(RR 0.26, 95% CI 0.09-0.79, one trial, 41 women). There was no significant difference in
quality of life. The reviewers concluded that the limited data available show that
compared with immediate primary end-to-end repair of obstetric anal sphincter injuries,
early primary overlap repair appears to be associated with lower risks for fecal urgency
and anal incontinence symptoms. As the experience of the surgeon is not addressed in the
three studies reviewed, it would be inappropriate to recommend one type of repair over
another. However, most of these conclusions were based on one study.
One of the RCTs included in the review assessed the presence of residual defects
of the external anal sphincter with ultrasound, and found no significant difference
between groups.45 Sixty six percent of women had a residual full-thickness defect in the
external anal sphincter ultrasound after 3 months from primary repair with overlap 40/57
[70%] and end-to-end (RR 0.88, 95% CI 0.67 to 1.15).
There is weak evidence of benefit associated with the overlap technique for
primary repair of the external anal sphincter compared with the end-to-end method.24
(Level I)
The external anal sphincter appears as a band of skeletal muscle with a fibrous
capsule. Traditionally, an end-to-end technique is used to bring the ends of the sphincter
together at each quadrant (12, 3, 6 and 9 oclock) using interrupted sutures placed through
the capsule and muscle. Allis clamps are placed on each end of the external anal sphincter.
The use 2-0 PDS, a delayed absorbable monofilament suture, will allow the sphincter
ends to have adequate time to scar together. Recent evidence suggests that end-to-end
repairs have poorer anatomic and functional outcomes than was previously believed.46,47
(Level II-2)
The cervical laceration is repaired with interrupted or running sutures. (Grade C)
Summary of Evidence
No randomized controlled trials regarding repair of cervical laceration was found.
But according to case reports either running or interrupted absorbable sutures are suitable
to repair such lacerations. Although, overzealous suturing aimed to restore anatomical
appearance of the cervix may lead to stenosis as the uterus returns to its non-pregnant
state.3,27,30 (Level III)
6. Who should repair obstetric anal sphincter injury?
An experienced health provider should repair difficult trauma under regional or
general done in the operating room. (Grade C)
The practitioner must be able to demonstrate clinical competence in suturing an
episiotomy and/or genital laceration before undertaking the procedure without
supervision. (Grade C)
Summary of Evidence
Repair done in the operating room will allow ease in performing the procedure
under aseptic conditions with appropriate instruments, adequate light and an assistant.48 In
this set up the patient can be adequately given regional or general anesthesia. This will
permit access to deeper tears, and promote relaxation of the perineal muscles and anal
sphincter. Thus, there will be ease in retrieving the retracted severed ends of the anal
sphincter, and help affix the ends of together without any tension.
Repair of the anal sphincter by an inexperienced health provider may contribute
to maternal morbidity, especially subsequent anal incontinence. A survey39 conducted
among consultant and training obstetricians in two regions in the UK stressed on the
deficiency and dissatisfaction of these practitioners with their training in the management
of third-degree tears.
Limited research has been carried out to assess the techniques of teaching and
evaluating surgical skills in obstetrics. However, training may be improved by
implementation of structured surgical skills courses with the use of models, perineal
repair simulators, case scenarios and audiovisual material.5 A report on the effect of
hands-on training workshops on repair of third- and fourth-degree perineal tears showed
that such increased awareness on perineal anatomy and recognition of anal sphincter
injury.49 (Level III)
In our setting, the four-year residency-training program in Obstetrics and
Gynecology among Philippine Obstetrical and Gynecological Society, Inc. (POGS)
accredited institutions ensures to provide teaching methods and the means to evaluate the
skill regarding the different approaches for perineal repair. An accredited staff member
assesses the competency of such training. Training among midwives of local health
centers is also being improved through the implementation of surgical skills workshops
with the use of models and audiovisual material. Nevertheless, practitioners appropriately
trained on perineal repair are more likely to provide consistent, and high standard of
surgical skill. Thereby, contributing in the effort to lower the maternal morbidity and
litigation associated with this procedure.
7. What measures would be appropriate for the postoperative care and follow-up of
women with puerperal genital tract lacerations?
Perform a vaginal and rectal examination postoperatively to check for bleeding,
hematoma, and ensure that suture material has not been accidentally inserted
through the rectal mucosa. (Grade C)
If there is any significant dead space or if the vagina is too friable to accept suturing,
then pressure or packing is indicated for at least 24 hours. (Grade C)
Summary of Evidence
The literature contains little information on patient care after the repair of perineal
lacerations. No data in the literature from controlled studies regarding the best mode of
subsequent delivery following repair of genital tract lacerations.
The laceration must be observed for bleeding after the torn edges of the
lacerations are approximated. Vaginal packing using gauze is the most common method
to achieve vaginal tamponade.9,31,39 Pressure or packing over the repair may achieve
hemostasis or allow for better placement of further hemostatic stitches. Generally, packs
are left in place for 2436 hours before removal. A urinary foley catheter and broad
spectrum antibiotic cover should be given where packs are used.50 Balloon tamponade
using Rsch catheters or Blakemore-Sengstaken tubes, as described for treatment of
uterine bleeding, can also be used.51 Cervical and vaginal vault lacerations that continue to
ooze despite treatment as detailed above or those that are associated with hematomas may
be amenable to selective arterial embolization.52 (Level III)
The success rates of these forms of management were evaluated in a systematic
review,52 which included all cases causing postpartum hemorrhage. The cumulative
success rates reported was 90.7% (95% CI 85.7-94.0%) for arterial embolization, 84.0%
(95% CI 77.5-88.8%) for balloon tamponade, and 84.6% (95% CI 81.2-87.5%) for iliac
artery ligation or uterine devascularization (P = 0.06). Currently, no evidence suggests
that any one the method is better than the other for the management of severe postpartum
hemorrhage. No randomized controlled trials on the various treatment options were found.
(Level II-3)
The use of broad-spectrum antibiotics is recommended following obstetric anal
sphincter repair to reduce the incidence of postoperative infections and wound
dehiscence. (Grade C)
Summary of Evidence
A systematic review regarding antibiotic prophylaxis for fourth-degree perineal
tear designed to compare prophylactic antibiotics with placebo or no antibiotics was not
able to find any randomized controlled trials.53 Hence, there is limited data to support a
policy for routine prophylactic antibiotics in fourth-degree perineal tear during vaginal
birth. To carry out this policy a well-designed randomized controlled trial is needed.
However, intra-operative and postoperative broad-spectrum antibiotics are advised
because the occurrence of infection will increase the risk of anal incontinence and fistula
formation if the repaired anal sphincter breaks down.48 (Level III)
The use of postoperative laxatives is recommended to reduce the incidence of
postoperative wound dehiscence. (Grade C)
Summary of Evidence
Laxatives are recommended during the postoperative period to minimize the
potential for repair breakdown from straining during defecation.48 Use of lactulose, and
bulk laxatives are recommended for about 10 days after the repair. An RCT compared
laxatives and constipating agents given postoperatively after primary obstetric anal
sphincter repair.54 In this trial, women in the laxative arm had significantly earlier and less
painful bowel movement. There was no significant difference in the symptomatic or
functional outcome of repair between the two groups. However, no systematic reviews
were reported to assess the use of postoperative laxatives and stool softeners as part of the
postoperative care for patients who had episiotomies or perineal injury. (Level III)
All women who incurred such injury should be informed regarding the extent of
trauma and discuss pain relief, diet, hygiene and the importance of pelvic-floor
exercises. (Grade C)
Summary of Evidence
According to the RCOG guidelines women should be offered physiotherapy and
pelvic-floor exercises for 612 weeks after obstetric anal sphincter repair. However, this
recommendation was regarded as best practice based on the clinical experience of the
guideline development group. For proper wound care and healing women should also be
advised on the importance of appropriate diet and perineal hygiene.40,55-57 (Level III)
All women who have had obstetric anal sphincter repair should be reassessed 612
weeks postpartum by an obstetrician and gynecologist. If incontinence develops
referral to a colorectal surgeon should be considered. (Grade C)
Summary of Evidence
No systematic reviews or RCTs were found to recommend the best method for
follow-up of repaired puerperal genital tract lacerations. It is useful to discuss the injury
sustained during childbirth and evaluate for symptoms of its complication
postoperatively.58,59
When such symptoms develop the woman should be advised to follow up. If a
woman is having incontinence or pain at follow-up, referral to a specialist gynecologist or
colorectal surgeon for endoanal ultrasonography and anorectal manometry should be
considered. Some women may require referral to a colorectal surgeon for consideration of
secondary sphincter repair.5 (Level III)
8. What is the prognosis after repair of the genital tract laceration?
Women should be informed regarding the complications that may arise after repair
of the genital tract laceration. (Grade C)
Summary of Evidence
The complications of repaired genital tract lacerations postoperatively include
perineal pain and discomfort, dyspareunia, fecal and urinary incontinence, and breakdown
of the repaired perineal laceration.58-60 Perineal pain and discomfort as a complication of
the injury may last for 1012 days or even up to 318 months after giving birth. Women
may also complain of dyspareunia up to three months postpartum. (Level III)
Regarding breakdown of perineal laceration repair after vaginal delivery, a
retrospective, case-control study61 reviewed and identified the associated risk factors. The
significant risk factors identified were mainly mediolateral episiotomy (OR 6.9, 95% CI
2.6-18.7), operative vaginal delivery (OR 3.6, 95% CI 1.8-7.3), third- and fourth-degree
lacerations (OR 3.1, 95% CI 1.5-6.4), and meconium-stained amniotic fluid (OR 3.0; 95%
CI 1.1-7.9). Longer second stage of labor (142 vs 87 minutes; P = .001) was found to have
the least association. Previous vaginal delivery was found to be protective (OR 0.38; 95%
CI 0.18-0.84). But the most significant factor reported was mediolateral episiotomy in
concurrence with operative vaginal delivery (OR 6.36; 95% CI 2.18-18.57). (Level II-2)
Women should be advised that the prognosis following external anal sphincter
repair is good, with 6080% asymptomatic at 12 months. Women who remained
symptomatic mostly reported the occurrence of incontinence of flatus or fecal
urgency. (Grade A)
Summary of Evidence
The outcome of repaired genital tract lacerations based on reported symptoms and
consequences of anal sphincter investigations were accounted by 7 prospective casecontrol47,62-67 and 7 retrospective studies.46,68-73 Most of these studies only described the
technique of suturing the external anal sphincter either by interrupted or figure-of-eight
sutures. Only a few studies reported on the method of suturing the internal anal sphincter.
(Level II-2)
Majority of these studies reported symptoms of anal incontinence was in 2067%
of women who had third-degree laceration repair. The types of incontinence accounted
were passage of flatus in 59%, leakage of fluid or solid stool in 11%, and fecal urgency
occurred in 26% of these women. One study even reported that symptoms of anal
incontinence markedly increased in 17 to 42% of cases after four years. However, there
was no standard questionnaire utilized by these studies to assess for symptoms on anal
incontinence. Hence, it is difficult to compare their study outcomes. (Level II-3)
But recently, RCTs comparing the techniques of external anal sphincter repair,
reported that there is a decreasing incidence of anal incontinence symptoms with both
overlap and end-to-end suturing.38,45,48,68 Sixty to eighty percent of women who have
undergone such repair were noted to be asymptomatic after 12 months.38,75,76 But there
were 3 studies, which confirmed the presence of persistent defects in 5488% women
who had third-degree laceration repair followed up by endoanal ultrasound.46,68,77 On the
contrary, more recent randomized controlled trials reported fewer residual defects, which
accounted to 1936% of cases.45,74,75 (Level I)
9. When would it be comfortable for women to have sexual intercourse after repair of
the genital tract laceration?
Women resume sexual intercourse at 3 to 6 months after repair of laceration.
(Grade C)
Summary of Evidence
Dyspareunia or sexual problems after childbirth is reported as 17 to 83% at 8 to12
weeks postpartum declining to 8-64% at six months postpartum.6 It is not just due to pain
from the scar which resulted from perineal repair but to several factors as well such as
psychological reactions, decreased libido, and decreased vaginal lubrication correlated to
hormonal changes in the early puerperium.78 Postpartum dyspareunia has previously been
associated with the extent of trauma. Such that in a German observational study,
involving 655 primipara, intact perineum after vaginal delivery (3.5%) or CS (3.4%) was
noted to be associated with the least dyspareunia at six months postpartum as compared
with 11% among women who had episiotomies and 14% after operative vaginal
deliveries.79
The first sexual intercourse after childbirth may be difficult for women due to
dyspareunia, especially if there were injuries incurred in the genital area. Hence, they may
opt to delay resumption of their first sexual intercourse. The data from British randomized
trials on suture techniques and suture materials, including 178028 and 154278 participants,
showed that 76 to 83% had resumed intercourse at three months and 86 to 99% at six
months postpartum.
A population-based cohort conducted in Sweden80 investigated on the effect of
lacerations in the vagina, perineum, anal sphincter, or rectum on sexual intercourse during
the first year postpartum. In this cohort 2490 women were asked to fill up a questionnaire
to gather information about their first sexual intercourse 1 year after birth. The results
showed that risk of not having sexual intercourse within 3 months after childbirth were
1.5 (95% CI 1.2-1.8) for tears in the vagina, 1.4 (95% CI 1.1-1.6) for tears in the
perineum, and 2.1 (95% CI 1.4-3.1) for tears in the anal sphincter and rectum. On the
other hand the risk of abstaining from intercourse after 6 months were 1.6 (95% CI 1.22.3) for vaginal tears, 1.5 (95% CI 1.1-2.1) for perineal lacerations, and 2.2 (95% CI 1.14.6) due to anal sphincter and rectal lacerations. No statistically significant differences
were found at 1-year follow-up. There were no associations found between episiotomy
and delay in resuming intercourse after adjusting the relative risks. Therefore, lacerations
in the genital tract significantly delay the womans capacity to have resume sexual
intercourse by 3 to 6 months from childbirth.
In the Ipswich Childbirth study, the occurrence of dyspareunia one year
postpartum was associated with the suture material used during repair.28,81 They
documented that 8% of women sutured with polyglactin 910, compared with 14% sutured
with chromic catgut, experienced dyspareunia. (Level II-2)
References
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2. Anderson J, Etches D. Prevention and management of postpartum hemorrhage. Am Fam Physician
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3. Cunningham FG, Gant NF, Leveno KJ, Gilstrap LC 3rd, Hauth JC, Wenstrom KD, Bloom SL.
Obstetrical hemorrhage. Williams Obstetrics 2005;22nd ed(28):809-854.
4. Leeman L, Rogers R, Greulich B, Albers L. Do unsutured second-degree perineal lacerations affect
postpartum functional outcomes? J Am Board Fam Med 2007;20:451-457.
5. Guideline and Audit Committee of the Royal College of Obstetricians and Gynaecologists. Methods and
materials used in perineal repair. Guideline No. 23, June 2004.
6. Kinberg SF. Introduction. Perineal lacerations after childbirth. Section 2008; Section 5:12-27.
7. Fernando RJ, Sultan AH, Radley S, Jones PW, Johanson RB. Management of obstetric anal sphincter
injury: a systematic review & national practice survey. BMC Health Serv Res 2002;2(1):9.
8. Melamed N, Ben-Haroush A, Chen R, et al. Intrapartum cervical lacerations: characteristics, risk
factors, and effects on subsequent pregnancies. Am J Obstet Gynecol 2009; 200: 388.e1-388.e4.
9. Ramanathan G, Arulkumaran S. Postpartum hemorrhage. J Soc Obstet Gynecol Can 2000; 22(4): 27181.
10. Williams A, Tincello DG, White S, Adams EJ, Alfirevic Z, Richmond DH. Risk scoring system for
prediction of obstetric anal sphincter injury. BJOG 2005;112:10669.
11. Bhau U, Koul I. Recent advances in the management of postpartum hemorrhage. JK Science 2008;
10(4).
12. Schuurmans N, Mackinnon C, et al. Prevention and management of postpartum hemorrhage. J Soc
Obstet Gynaecol Can 2000;22(4):271-81.
13. Christianson LM, Bovbjerg VE, McDavitt EC, Hullfish KL. Risk factors for perineal injury during
delivery. Am J Obstet Gynecol 2003;189(1):255-60.
14. Hudelist G, Gelle'n J, Singer C, Ruecklinger E, Czerwenka K, Kandolf O, Keckstein J. Factors
predicting severe perineal trauma during childbirth: role of forceps delivery routinely combined with
mediolateral episiotomy. Am J Obstet Gynecol 2005;192(3): 875-81.

15. Carroli G, Belizan J. Episiotomy for vaginal birth. Cochrane Database Syst Rev 2003;(1):CD000081.
16. Combs CA, Murphy EL, Laros RK, Jr. Factors associated with postpartum hemorrhage with vaginal
birth. Obstet Gynecol 1991;77(1):69-76.
17. ACOG Committee on Practice Bulletin. Postpartum hemorrhage. ACOG Practice Bulletin Clinical
Management Guidelines for Obstetrician-Gynecologist No. 71. Obstet Gynecol 2006; 107:957-62.
18. Sheiner E, Sarid L, Levy A, et al. Obstetric risk factors and outcome of pregnancies complicated with
early postpartum hemorrhage: a population-based study. J Matern Fetal
Neonatal Med
2005;18(3):149-54.
19. Stones RW, Paterson CM, Saunders NJ. Risk factors for major obstetric haemorrhage. Obstet Gynecol
1997;90:924-7.
20. Johanson RB, Menon BKV. Vacuum extraction versus forceps for assisted vaginal delivery (Cochrane
Review). Cochrane Pregnancy and Childbirth Group Trials Register 2001;108: 3440.
21. Pliego Perez AR, Moncada Navarro O, Neri Ruz ES, et. al. Comparative assessment of efficacy and
safety of assisted vaginal delivery with forceps and with vacuum extractor. Ginecol Obstet Mex
2000;68:453459.
22. Weerasekera DS, Premaratne S. A randomised prospective trial of the obstetric forceps versus vacuum
extraction using defined criteria. J Obstet Gynaecol 2002;22:344345.
23. Fitzpatrick M, Behan M, O'Connell PR, et al. Randomised clinical trial to assess anal sphincter function
following forceps. Br J Obstet Gynaecol 2003;110:424429.
24. Kettle C, Tohill S. Perineal Care. BMJ Clinical Evidence 2008;09:1401.
25. Hodnett ED, Gates S, Hofmeyr GJ, et al. Continuous support for women during childbirth. Cochrane
Database Syst Rev 2006, Issue 1.
26. Beckmann MM, Garrett AJ. Antenatal perineal massage for reducing perineal trauma. Cochrane
Database Syst Rev 2006, Issue 1. Art. No.: CD005123.
27. Riggs W, Blanco J. The Puerperium. Management of Labor and Delivery 1997; Chapter 10: 223-257
28. Gordon B, Mackrodt C, Fern E, et. al. The Ipswich Childbirth study: A randomised evaluation of two
stage after birth perineal repair leaving the skin unsutured. Br J Obstet Gynaecol 1998;105:435440.
29. Oboro VO, Tabowei TO, Loto OM, et. al. A multicentre evaluation of the two-layer repair of after birth
perineal trauma. J Obstet Gynaecol 2003;1:58.
30. DeCherney AH, Pernoll ML. Postpartum hemorrhage. Current Obstetric & Gynecologic Diagnosis &
Treatment: 9th Ed Aug 2002;Chapter 12:499-530.
31. Kettle C. The Pelvic Floor. In: Henderson C, Macdonald S, editors. Mayes' Midwifery A textbook for
Midwives. 13th Edition ed. London: Bailliere Tindall; 2004: 476-91.
32. White C. Perineal repair workshop. Perth: Australian College of Midwives (WA Branch)
33. Gould D. Perineal tears and episiotomy. Nursing Standard. 2007; 21(52): 41-6.
34. Kettle C, Johanson R. Absorbable synthetic versus catgut suture material for perineal repair. Cochrane
Database Systematic Revs1999, Issue 4. Art. No.: CD000006.
35. McElhinney BR, Glenn DRJ, Dornan G, Harper MA. Episiotomy repair: vicryl versus vicryl rapide.
Ulster Med J 2000;69:279.
36. Gemynthe A, Langhoff-Roos J, Knudsen SS. New VICRYL formulation: an improved method of
perineal repair? Br J Midwifery 1996;4:2304.
37. Kettle C, Hills RK, Jones P, Darby L, Gray R, Johanson R. Continuous versus interrupted perineal
repair with standard or rapidly absorbed sutures after spontaneous vaginal birth: a randomised
controlled trial. Lancet 2002;359:221723.
38. Williams A, Adams EJ, Tincello DG, Alfirevic Z, Walkinshaw SA, Richmond DH. How to repair an
anal sphincter injury after vaginal delivery: results of a randomised controlled trial. BJOG
2006;113:2017.
39. Fernando RJ, Sultan AH, Radley S, Jones PW, Johanson RB. Management of obstetric anal sphincter
injury - A systematic review and national practice survey. BMC Health Serv Res 2002;2:9.
40. Guideline and Audit Committee of the Royal College of Obstetricians and Gynaecologists. The
management of third- and fourth-degree perineal tears. Green-top Guideline No. 29, March 2007.
41. Kettle C, Johanson RB. Continuous versus interrupted sutures for perineal repair. Cochrane Database
Syst Rev 2003;CD000947.
42. Mahomed K, Grant A, Ashurst A, James D. The Southmead Perineal Suture Study. A randomised
comparison of suture materials and suturing techniques for repair of perineal trauma. Br J Obstet
Gynaecol 1989;96:127280.
43. Morano S, Mistrangelo E, Pastorino D, et. al. A randomized comparison of suturing techniques for
episiotomy and laceration repair after spontaneous vaginal birth. J Minim Invasive Gynecol
2006;13:457462.
44. Fernando R, Sultan AH, Kettle C, Thakar R, Radley S. Methods of repair for obstetric anal sphincter
injury. Cochrane Database Syst Rev 2006;(3):CD002866.
45. Fitzpatrick M, Fynes M, Behan M, et al. A randomized clinical trial comparing primary overlap with
approximation repair of third-degree obstetric tears. Am J Obstet Gynecol 2000; 183:12201224.
46. Sultan AH, Kamm MA, Hudson CN, Bartram CI. Third degree obstetric anal sphincter tears: risk
factors and outcome of primary repair. BMJ 1994;308:877-91.
47. Kammerer-Doak DN, Wesol AB, Rogers RG, Dominguez CE, Dorin MH. A prospective cohort study
of women after primary repair of obstetric anal sphincter laceration. Am J Obstet Gynecol
1999;181:1317-2.
48. Sultan AH, Monga AK, Kumar D, Stanton SL. Primary repair of obstetric anal sphincter rupture using
the overlap technique. BJOG1999;106:31823.
49. Thakar R, Sultan AH, Fernando R, Monga A, Stanton S. Can workshops on obstetric anal sphincter
rupture change practice? Int Urogynecol J 2001;12:S5.
50. Johanson R, Kumar M, Obhrai M, et. al. Management of massive postpartum haemorrhage: use of a
hydrostatic balloon catheter to avoid laparotomy. Br J Obstet Gynaecol 2001;108: 420-2.
51. Katesmark M, Brown R, Raju K. Successful use of a Sengstaken-Blakemore tube to control massive
postpartum haemorrhage. Br J Obstet Gynaecol 1994;101:259-60.
52. Doumouchtsis SK, Papageorghiou AT, Arulkumaran S. Systematic Review of Conservative
Management of Postpartum Hemorrhage: What to Do When Medical Treatment Fails.
Obstet
Gynecol Survey 2007;62(8):540-547.
53. Buppasiri P, Lumbiganon P, Thinkhamrop J, Thinkhamrop B. Antibiotic prophylaxis for fourth-degree
perineal tear during vaginal birth. Cochrane Database Syst Rev 2005, Issue 4. Art. No.: CD005125.
54. Mahony R, Behan M, OHerlihy C, OConnell PR. Randomised clinical trial of bowel confinement vs.
laxative use after primary repair of a third degree obstetric anal sphincter tear. Dis Colon Rectum
2004;47:12-17.
55. Sleep J, Grant A. Pelvic floor exercises in postnatal care. Br J Midwifery 1987;15864.
56. Sultan AH, Kamm MA, Hudson CN. Anal sphincter disruption during vaginal delivery. N Engl J Med
1993;329:1905-11.
57. National Institute for Clinical Excellence. Intrapartum care. Care of healthy women and their babies
during childbirth. London; 2007.
58. Sleep J, Grant A, Garcia, et. al. West Berkshire perineal management trial. BMJ 1984;289: 587-690.
59. Glazener CMA, Abdalla M, Stroud P. Postnatal maternal morbidity: extent, causes, prevention and
treatment. Br J Obstet Gynaecol 1995;102:286-7.
60. Leeman L, Rogers R, Greulich B, Albers L. Do unsutured second-degree perineal lacerations affect
postpartum functional outcomes? J Am Board Fam Med 2007;20:451-457.
61. Williams MK, Chames MC. Risk factors for the breakdown of perineal laceration repair after vaginal
delivery. Am J Obstet Gynecol 2006;195:7559.
62. Haadem K, Dahlstrom JA, Lingman G. Anal sphincter function after delivery: a prospective study in
women with sphincter rupture and controls. Eur J Obstet Gynaecol Reprod Biol 1990;35:7-13.
63. Haadem K, Dahlstrom JA, Ling L, Ohrlander S. Anal sphincter function after delivery rupture. Obstet
Gynecol 1987;70:53-6.
64. Walsh CJ, Mooney EF, Upton GJ, Motson RW. Incidence of thirddegree perineal tears in labour and
outcome after primary repair. Br J Surg 1996;83:218-21.
65. Fornell EK, Berg G, Hallbook O, Matthiesen LS, Sjodahl R. Clinical consequences of anal sphincter
rupture during vaginal delivery. J Am Coll Surg 1996;183:5538.
66. Nazir M, Stein R, Carlsen E, Jacobsen AF, Nesheim BI. Early evaluation of bowel symptoms after
primary repair of obstetric perineal rupture is misleading: an observational cohort study. Dis Colon
Rectum 2003;46:24550.
67. Crawford LA, Quint EH, Pearl ML, DeLancey JO. Incontinence following rupture of anal sphincter
during delivery. Obstet Gynecol 1993;82:52731.
68. Poen AC, Felt-Bersma RJF, Strijers RL, Dekker GA, Cuesta MA, Meuwissen SG. Third degree
obstetric perineal tear: long-term clinical and functional results after primary repair. Br J Surg
1998;85:14338.
69. Gjessing H, Backe B, Sahlin Y. Third degree obstetric tears: outcome after primary repair. Acta Obstet
Gynecol Scand 1998;77:73640.
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Obstet Gynaecol 1998;38:414-7.
71. de Leeuw JW, Sruijk PC, Vierhout ME, Wallenburg HC. Risk factors for third degree perineal ruptures
during delivery. BJOG 2001;108:383-7.
72. Tetzschner T, Sorensen M, Lose G, Christiensen J. Anal and urinary incontinence in women with
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73. Goffeng AR, Andersch B, Andersson M, Berndtsson I, Hulten L, Oresland T. Objective methods
cannot predict anal incontinence after primary repair of extensive anal tears. Acta Obstet Gynecol
Scand 1998;77:439-43.
74. Garcia V, Rogers RG, Kim SS, Hall RJ, Kammerer-Doak DN. Primary repair of obstetric anal
sphincter laceration: A randomized trial of two surgical techniques. Am J Obstet Gynecol
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75. Fernando RJ, Sultan AH, Kettle C, Radley S, Jones P, OBrien S. Repair techniques for obstetric anal
sphincter injuries: a randomized controlled trial. Obstet Gynecol 2006;107: 1261-8.
76. Malouf AJ, Norton CS, Engel AF, Nicholls RJ, Kamm MA. Long-term results of overlapping anterior
anal sphincter repair for obstetric trauma. Lancet 2000;355:260-5.
77. Gjessing H, Backe B, Sahlin Y. Third degree obstetric tears: outcome after primary repair. Acta Obstet
78. Kettle C, Ismail K, O "Mahony F. Dyspareunia following childbirth. The Obstetrician & Gynaecologist
2005;7:245-249.
79. Buhling KJ, Schmidt S, Robinson JN, Klapp C, Siebert G, Dudenhausen JW. Rate of dyspareunia after
delivery in primiparae according to mode of delivery. Eur J Obstet Gynecol Reprod Biol
2006;124(1):42-46.
80. Radestad I, Olsson A, Nissen E, Rubertsson C. Tears in the vagina, perineum, sphincter ani, and
rectum and first sexual intercourse after childbirth: A nationwide follow-up. Birth 2008; 35(2):98-106.
81. Mackrodt C, Gordon B, Fern E, Ayers S, Truesdale A, Grant A. The Ipswich Childbirth Study: 2. A
randomised comparison of polyglactin 910 with chromic catgut for postpartum perineal repair. Br J
Obstet Gynaecol 1998;105(4):441-445.
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B. GENITAL TRACT HEMATOMAS

Background
The pregnant uterus, vagina, and vulva have rich vascular supplies that are at risk of
trauma during the birth process, and trauma may result in formation of a hematoma.
Puerperal genital hematomas are relatively uncommon but can be a cause of serious
morbidity and even maternal death.1 Hematomas occur in 1:300 to 1:1500 deliveries and,
rarely, are a potentially life-threatening complication of childbirth.4 In a case series the
estimated incidences are 1 in 500 to 1 in 12,500 deliveries, with surgical intervention required
in approximately 1 in 1 000 deliveries.1,2 However, there may be difficulty in diagnosing such
condition, as symptoms can be non-specific and bleeding is often concealed.
Genital tract hematomas are classified according to their anatomical location.3,4 The
most common locations for puerperal hematomas are the vulva, vaginal/paravaginal area, and
retroperitoneum/subperitoneal.1
The vulval hematomas tend to be limited to the vulval tissues superficial to the
anterior urogenital diaphragm, while a vulvovaginal hematoma may extend to the paravaginal
area.1-3 These types of hematoma arise from injury to the branches of the pudendal artery
including the inferior rectal, transverse perineal, or posterior labial branches, as a result of
episiotomy or perineal lacerations. Bleeding is then directed toward the skin and the loose
subcutaneous tissues exert little resistance to hematoma formation. The hematoma can extend
from the posterior margin of the anterior triangle, at the level of the transverse perineal
muscle, anteriorly over the mons to the fusion of the fascia at the inguinal ligament.
On the other hand, paravaginal hematomas1,3 occur from damage to the descending
branch of the uterine artery. It is confined to the space bounded inferiorly by the pelvic
diaphragm and superiorly by the cardinal ligament. This type of hematoma may not be
obvious externally but can be palpated through vaginal examination. Blood vessels in the
vagina are surrounded by soft tissue and are not found in the superficial fascia, thus, injury to
these vessels can result to the collection of blood in the paravaginal space or ischiorectal
fossa. Extension and dissection of the bleeding into the retroperitoneum may occur and form
a palpable tumor above Poupart's ligament. Dissection of blood may also extend cephalad
and reach the lower margin of the pelvic diaphragm. Most vaginal or paravaginal hematomas
often blocks the vaginal canal. They are commonly associated with operative vaginal
deliveries but may also occur spontaneously.1
The supravaginal or subperitoneal hematomas are the result of damage to the uterine
artery branches in the broad ligament. The hematoma can dissect retroperitoneally or develop
within the broad ligament.1
Recommendations
1. Can the occurrence of genital tract hematoma be predicted and prevented?
The practitioner should be aware of the risk factors for genital tract hematoma but
also acknowledge that these risk factors will not frequently permit its prediction or
prevention. (Grade C)
Good surgical technique, with attention to hemostasis in the repair of lacerations,
should limit the occurrence of puerperal hematoma. (Grade C)
Summary of Evidence
The risk factors for genital tract hematoma include nulliparity, prolonged second
stage of labor, instrumental delivery, having a baby greater than 4000 grams, genital tract
varicosities, maternal age more than 29 years, preeclampsia, multifetal pregnancy, and
clotting disorders.3,5 In several case series, 87% of puerperal hematomas were reported to
occur from bleeding lacerations related to operative deliveries, sutured perineal tears, or
episiotomies.3,4,6 Hence, a good surgical technique with appropriate hemostasis may
reduce the incidence of puerperal hematomas. Even without lacerations or incisions of the
surrounding tissue, hematomas can still occur as long as there is injury to a blood
vessel.3,5,6 Hematomas are not unavoidable. However, no published information on the
risk of recurrence of puerperal hematomas was found in subsequent deliveries.
These risk factors may help the practitioner to be attentive to the occurrence
puerperal hematomas. But it should be recognized that these factors will not completely
prevent or predict hematoma formation.3,5 As this type of injury may occur in both
spontaneous and operative vaginal delivery even without lacerations. (Level III)
2. What signs and symptoms will facilitate the recognition of genital tract hematoma?
Excessive perineal pain is a hallmark symptom of puerperal hematomas. But a
change in vital signs disproportionate to the amount of blood loss should also prompt
a gentle pelvic examination. It may present with non-specific signs and symptoms as
well. (Grade C)
A high index of suspicion is required to diagnose and manage these hematomas
promptly before signs of cardiovascular collapse develop. (Grade C)
Summary of Evidence
Clinical awareness is the most important factor to arrive at a correct diagnosis.
Recognition of the hematoma will depend on the extent of the bleeding, its associated
consequences and the level of awareness of the practitioner.1,4,8 Thus, a woman with a
large hematoma may present with cardiovascular collapse within a few hours of delivery,
while a woman with a small hematoma in an episiotomy may present with persisting pain
over a few days.1,4,6 Puerperal hematomas aside from pain usually present with pressure
symptoms, swelling as well as urinary retention due to inability to void or, rarely,
unexplained pyrexia.1
The typical symptoms of hematomas will depend on its location. Vulvar and
vulvovaginal hematomas1,9 usually presents with pain and swelling in the perineum.
These hematomas are easy to detect if the woman is examined thoroughly and gently but
can be confused with abscesses. Failure to examine the patient can lead to incorrectly
attributing the pain to pain from the episiotomy site, a tear or hemorrhoids.
Paravaginal hematomas1 typically present with rectal pain, vague lower abdominal
pain, and signs of hypovolemia. These non-specific symptoms can be ascribed to other
causes, and may delay diagnosis. The degree of shock is often not proportional to revealed
blood loss.
In case of supravaginal hematomas,1 signs of hypovolemia frequently present first
but abdominal pain may also be noted. For broad ligament hematomas, approximately
50% of cases present early with symptoms of lower abdominal pain, hemorrhage and
shock.1,6 On abdominal examination the uterus is deviated upward and laterally, to the
opposite side from the broad ligament hematoma. Usually, there are no vaginal
symptoms. It may be mistaken as a pelvic mass such as abscess, or other sources of intraabdominal bleeding. It can be clinically occult despite significant blood loss; hence, a
high index of suspicion is required to recognize these hematomas. (Level III)
3. What diagnostic modalities can aid in the investigation of genital tract hematoma?
Imaging may be helpful to confirm the diagnosis when there is a high clinical
suspicion for hematoma but the patient remains hemodynamically stable. (Grade B)
Summary of Evidence
The clinical presentation of the patient is the key to diagnose genital tract
hematoma. However, in cases when the patient is hemodynamically stable and if the
hematomas are located supravaginally or subperitoneally, imaging modalities may serve
to be useful.1
According to descriptive studies,10,11 ultrasound, computed tomography (CT), and
magnetic resonance imaging (MRI) scans are mainly useful for diagnosing hematomas
above the pelvic diaphragm. These modalities are also useful to assess any extension into
the pelvis, particularly as bimanual examination may not detect them until they become
quite large and palpable. Aside from location, information regarding the size, extent and
progress or resolution of these hematomas may be provided by these modalities as
well.1,7,10,11 The added advantage of MRI is that it can help differentiate between other
causes of a pelvic mass, such as an abscess or endometrioma. (Level III)
A complete blood count and coagulation screen are mandatory to aid in estimating
blood loss and to monitor coagulation status. (Grade C)
Summary of Evidence
Blood tests are necessary to determine baseline values and should be repeated as
necessary. Blood should be drawn for crossmatching, based on the clinical picture of the
patient. Transfusion is usually necessary with paravaginal and subperitoneal than with
vulvar hematomas. With monitoring of the coagulation status, this will guide the
practitioner in giving the appropriate management.1,12 (Level III)
4. How will genital tract hematoma be managed?
Initial treatment of puerperal hematomas includes early recognition followed by
prompt attention to resuscitation and simultaneous search for the cause of the
bleeding. (Grade C)
Management aims to prevent further blood loss, minimize tissue damage, ease pain
and reduce the risk of infection. (Grade C)
Summary of Evidence
There are limited literatures on the management of paragenital hematomas and no
randomized studies on the efficacy of various treatments have been published.9
The clinical presentation of pelvic hematomas can be useful in defining the
location of the bleeding vessel.4 Once identified, these vessels should be ligated, and
sutured to stop the bleeding. If with lower genital tract hematomas, these are usually
managed by incision and drainage, although expectant management is acceptable if the
lesion is not enlarging.13
Resuscitative measures should be considered the first line of treatment followed
by close observation.4,9,13 The extent of the blood loss is often underestimated and a high
index of suspicion is required. Aggressive fluid replacement and assessment of
coagulation status is essential if there is heavy bleeding or signs of hypovolemia. Blood
should be available for transfusion. Vaginal packing or balloon/blood pressure cuff
tamponade and antibiotics are commenced as other appropriate measures. A foley catheter
is inserted to avoid possible urinary retention that can occur due to pain, tissue distortion
from edema, or pressure of a vaginal pack. It is also advocated to monitor fluid balance.
(Level III)
Large (> 3 cm) hematomas are best managed with surgical evacuation, primary
closure and compression for 1224 hours, while small, non-expanding hematomas (<
3 cm in diameter) can be managed conservatively. (Grade C)
Summary of Evidence
Small hematomas, less than 5 cm, can be managed with close observation.14
However, according to the South Australian Perinatal Practice Guidelines, conservative
management is confined to non-expanding hematomas less than 3 cm.15 The latter
recommendation was preferred by the stakeholders who attended the presentation of this
practice guideline. Conservative treatment entails the use of ice packs, pressure dressing
and analgesia.16-17
Patients with persistent signs of volume loss despite fluid replacement, as well as
those with large (> 3 cm) or enlarging hematomas, are best managed with surgical
evacuation of the clot.14 The involved area should be irrigated and the bleeding vessels
ligated. In patients with diffuse oozing, a layered closure will help to secure hemostasis
and eliminate dead space. The primary closure is done with deep mattress sutures and the
overlying skin re-approximated without tension. Care must be taken to avoid damage to
contiguous structures such as the ureters, bowel and bladder during repair procedures.
Adequate anesthesia is mandatory. The surgical procedure should be conducted in the
operating room.
Small, stable subperitoneal hematomas, broad ligament and retroperitoneal
hematomas can be also managed conservatively particularly if the patient is stable and the
lesions are not expanding.18 If it is not possible to maintain a stable hemodynamic state, or
if these hematomas are enlarging and expanding, surgical management is indicated. The
surgical management for these hematomas requires an abdominal approach with
identification and ligation of bleeding vessels.1 (Level III)
Vaginal packing/pressure or insertion of drains for 24 to 36 hours may be useful

following drainage and repair of a paravaginal hematoma. (Grade C)
Summary of Evidence
There is no evidence to support the best or optimal management for vaginal
hematomas, which include primary repair with or without drains, primary repair with
packing, and packing alone have all been advocated.1 Vaginal packing for 24-36 hours
aims to tamponade bleeding vessels. Some authors believe that drains defeat the object of
packing. Insertion of drains can be useful to highlight ongoing or recurrent bleeding.
A case series19 described the successful use of the blood pressure cuff in two
patients to control intractable vaginal bleeding following evacuation of vaginal hematoma
that developed after spontaneous vaginal delivery. A blood pressure cuff was inserted into
a sterile glove, which in turn was inserted into the vagina and the pressure then gradually
increased to 120 mmHg, 10 mmHg above the systolic pressure, to stop the bleeding. Eight
hours later, the pressure of the cuff was reduced by 10 mmHg and then taken out after 32
hours. Both patients had an uneventful recovery. (Level III)
If first line management fails, additional surgical intervention is indicated such as
ligation of the internal iliac artery, hysterectomy, or even selective arterial
embolization, may be necessary. Embolization of the bleeding vessel may be a
therapeutic option in centers where interventional radiologists are available and the
bleeding is not life threatening. (Grade C)
Summary of Evidence
Where there is continuing expansion of a supralevator hematoma without
extension into the cervix or uterus, selective arterial embolization is seen as the treatment
of choice over internal iliac artery ligation, which in itself has an uncertain chance of
success.20,21 Selective arterial embolization may be useful in situations in which
preservation of fertility is desired, when surgical options for managing hematomas have
been exhausted. However, no RCTs regarding its effectiveness have been conducted.
The technique of selective arterial embolization investigates these vessels by
preliminary transfemoral arteriography, followed by embolization using Gelfoam (gelatin)
pledglets. A case report20 on 35 patients with unanticipated postpartum hemorrhage
underwent this procedure conducted by Pelage, et. al. In the series, bleeding was
controlled in all but one, who required hysterectomy 5 days later for re-bleeding. All
women who had successful embolization resumed menstruation. Across published case
reports and series, the aggregate success rate in controlling bleeding from hematomas is
over 90%.22-24
The procedure, however, is not without risk and deaths have been reported due to
sepsis and multiple organ failure.25 Complications are uncommon (< 9%), which include
local hematoma formation at the insertion site; low-grade fever; pelvic infection; ischemic
phenomena, such as uterine necrosis in rare instances; temporary foot drop; vessel
perforation; and contrast-related adverse effects. Use of temporary embolic agents reduces
the risk of ischemic problems.
The major drawbacks of the procedure are the requirement for 24-hour
availability of radiological expertise and the time required to complete the procedure.
Patients must be stable to be candidates for this procedure.20,26 (Level III)
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Cunningham FG, Gant NF, Leveno KJ, Gilstrap LC 3rd, Hauth JC, Wenstrom KD, Bloom SL.
Obstetrical hemorrhage. Williams obstetrics 22nd ed 2005; Chapter 28: 809-854.
Anderson J, Etches D. Prevention and management of postpartum hemorrhage. Am Fam Physician
2007;75:875-82.
Ridgway LE. Puerperal emergency. Vaginal and vulvar hematomas. Obstet Gynecol Clin North Am
1995;22:275-82.
Nagayama M, Watanabe Y, Okumura A, Amoh Y, Nakashita S, Dodo Y. Fast MR imaging in
obstetrics. Radiographics 2002;22:563-82.
Rooholamini SA, Au AH, Hansen GC, Kioumehr F, Dadsetan MR, Chow PP, et. al. Imaging of
pregnancy-related complications. Radiographics 1993;13:753-70.
Mackinnon C, et. al. Prevention and management of postpartum hemorrhage. J Soc Obstet Gynecol
Can 2000;22(4):271-81.
Propst AM, Thorp JM Jr. Traumatic vulvar hematomas: conservative versus surgical management.
South Med J 1998;91(2):144-6.
Schuurmans N, Mackinnon C, et al. Prevention and management of postpartum hemorrhage. J Soc
Obstet Gynecol Can 2000;22(4):271-81.
South Australian Perinatal Practice Guidelines. Uterine inversion. Chapter 11; March 2008.
Zahn C, Yeomans E. Postpartum haemorrhage: placenta accrete, uterine inversion and puerperal
haematomas. Clin Obstet Gynaecol 1990;33:422.
Kean LH, Baker, Edelstone DI, editors. Other problems of the third stage. Best Practice in Labor Ward
Management, Edinburgh: Harcourt; 2000.
Lingam K, Hood V, Carty MJ. Angiographic embolisation in the management of pelvic haemorrhage.
BJOG 2000;107(9):1176-8.
Pinborg A, Bodker B, Hogdall C. Postpartum haematoma and vaginal packing with a blood pressure
cuff. Acta Obstet Gynecol Scand 2000;79:8879.
Pelage J, Le Dref O, Jacob D, et. al. Selective arterial embolisation of the uterine arteries in the
management of intractable postpartum haemorrhage. Acta Obstet Gynecol Scand 1999;78: 698-703.
Evans S, McShaneP. The efficacy of internal iliac artery ligation in obstetric haemorrhage. Surg
Gynecol Obstet 1985;160:250-327.
Johanson R. Continuous vs. interrupted sutures for perineal repair. In Keirse M, Renfrew M, Neilson J,
Crowther C, eds. Pregnancy and Childbirth Module. The Cochrane Pregnancy and Childbirth Database.
London: BMJ Publishing Group, 1994.
Bobrowski R, Jones T. A thrombogenic uterine pack for postpartum hemorrhage. Obstet Gynecol
1995;85:836-7.
Wax J, Channell J, Vandersloot J. Packing of the lower uterine segment: new approach to an old
technique? Int J Gynaecol Obstet 1993;43:1978.
Ledee N, Ville Y, Musset D, et. al. Management inintractable obstetric haemorrhage: an audit study on
61cases. Eur J Obstet Gynecol Reprod Biol 2001;94:18996.
Vedantham S, Goodwin SC, McLucas B, Mohr G. Uterine artery embolization: an underused method
of controlling pelvic hemorrhage. Am J Obstet Gynecol 1997;176(4):938-48.
UTERINE INVERSION
Lyla D. Reyes, MD
Background
Puerperal uterine inversion is due to displacement of the fundus of the uterus, usually
occurring during the third stage of labor. It is a complication of childbirth that occurs between
1 in 2148 and 1 in 6407 births.1 Other authors reported this as a rare condition, occurring in
0.05% of deliveries.2
Uterine inversion is classified not only by the degree of inversion but by the time of
onset as well.1,3,4 The first classification is according to the occurrence of uterine inversion
after delivery. Acute inversions occur immediately or within 24 hours after delivery. This is
the most common type of uterine inversion with a prevalence of 83.4%. The subacute
inversion occurs after the first 24 hours and within four weeks after delivery. This accounts
for 2.62% of all types of inversion. Finally the chronic inversion occurring after more than
four weeks after the delivery has been reported to take place in13.9 % of such cases.
The second classification of uterine inversion is based on the anatomical severity of the
inversion. This is most widely used classification.4,5 It includes four stages. In the first stage
the uterine base is in the uterine cavity and do not cross the cervix of the uterus. With the
second stage the uterine base crossed the cervix and passed through the vagina. The third
stage involves the visualization of the uterine base at the vulva. Lastly, in the fourth stage the
vaginal walls participate with the inversion.
However, others report the classification as partial or complete inversion.2,5 The
uterine fundus that has inverted and lies within the endometrial cavity without extending
beyond the external os is called an incomplete or partial inversion. In complete inversion the
fundus is inverted and extends beyond the external os. A prolapsed inversion is one in which
the inverted uterine fundus extends beyond the vaginal introitus. A total inversion, usually
nonpuerperal and tumor related, results in inversion of the uterus and vaginal wall as well.
Studies have yet to clearly demonstrate the mechanism for uterine inversion.3
However, clinical vigilance for inversion, secondary to these potential causes, is generally
practiced. Inversion prevents the myometrium from contracting and retracting, and it is
associated with life-threatening blood losses as well as profound hypotension from vagal
activation.6
Therefore, uterine inversion during the third stage of labor although unusual, is
potentially life threatening. But when managed promptly and aggressively, uterine inversion
can result in minimal maternal morbidity and mortality.
Recommendations
1. What factors will predispose to the occurrence of uterine inversion?
The causes of inversion remain undefined, but overly aggressive management of the
third stage of labor is commonly ascribed cause. (Grade C)
Summary of Evidence
Inversion of the uterus is principally a complication of the third stage of labor,
and the most common cause is traction applied to the umbilical cord while the uterus is
relaxed. In case of adherent or accretic placenta, the thin and relaxed myometrium is
predisposed to inversion when traction is applied.7 Inversion may occur more likely if the
placenta is situated at the fundal aspect of the uterus, where a direct traction may be
applied on the central portion of the non-contracted muscle.5,8
Aside from excessive umbilical cord traction the other extrinsic factor associated
uterine inversion is antepartum use of magnesium sulfate or oxytocin. Intrinsic risk
factors were also accounted in several case reports such as primiparity; uterine hypotonia
secondary to twin pregnancy and betamimetics; placenta accreta, particularly involving
the uterine fundus; fundal myoma; short umbilical cord; rapid emptying of the uterus after
prolonged distention; and congenital weakness or anomalies of the uterus.3,9 However, the
role of fundal pressure with undue cord traction is uncertain. The underlying causes are
not completely understood.1,2 (Level III)
2. How is uterine inversion diagnosed?
Clinical signs and symptoms such as hemorrhage, shock and severe pelvic pain
mainly support the diagnosis of the uterine inversion. Bimanual examination will
confirm the diagnosis and also reveal the degree of inversion. (Grade C)
Summary of Evidence
The classical presentation of uterine inversion is an obviously displaced uterus
while delivering the placenta, usually in association with post-partum hemorrhage and
clinical shock.1,3,5,10 The shock is often out of proportion to the degree of blood loss,
although if the placenta remains attached following inversion shock is less likely to occur.
Uterine inversion is also often associated with acute lower abdominal pain. Hence, the
profound shock may not only be hemorrhagic in origin but neurogenic as well.
According to case reports,2,4,6,11 when there is complete inversion, the diagnosis is
not difficult and easily made by palpating the inverted fundus at the cervical os or vaginal
introitus. The completely inverted uterus usually appears as a bluish-gray mass protruding
from the vagina. In incomplete inversion, palpating the fundal wall in the lower uterine
segment and cervix might be required for diagnosis. Profuse bleeding, absence of uterine
fundus, or an obvious defect of the fundus on abdominal examination, as well as evidence
of shock with severe hypotension, will further provide the clinician diagnostic clues for
uterine inversion. (Level III)
Imaging can help when the diagnosis is uncertain after examination, and the patient
is sufficiently stable clinically to undergo such evaluation. (Grade C)
Summary of Evidence
Although clinical symptoms will provide the diagnosis in most cases, radiographic
methods to diagnose inversion have also been reported. In one literature, uterine inversion
was discovered incidentally in an acute incident by ultrasound findings.12 The inverted
uterus in transverse images was described as a hyperechoic mass in the vagina with a
central hypoechoic H-shaped cavity. Longitudinal images showed a U-shaped depressed
longitudinal groove from the uterine fundus to the center of the inverted part. Magnetic
resonance imaging (MRI) for uterine inversion has also been reported. The appearance of
the uterus is similar to that found in sonographic imaging; however, MRI findings are
more prominent.13 Thus imaging can help when the diagnosis is uncertain after
examination, and the patient is sufficiently stable clinically to undergo such evaluation.
(Level III)
3. What are the management options for uterine inversion?
Successful management requires early recognition of the inversion and prompt
replacement of the uterus, with or without a general anesthetic and/or tocolytics.
Provide adequate analgesia before attempting to reposition the uterus. (Grade C)
Summary of Evidence
Management of uterine inversion has two important components: the immediate
treatment of the hemorrhagic shock and replacement of the uterus.1,14 If puerperal
inversion of the uterus is recognized immediately, the uterine corpus can usually be
pushed back through the cervical ring, by pressure directed toward the umbilicus, either
manually by Johnson maneuver1 or by hydrostatic pressure.15 (Level III)
Hydrostatic pressure, cited commonly in the British literature, is another method
used to reposition the uterus when inversion has occurred. In this method, first described
by O'Sullivan in the British Medical Journal in 1945, a bag of warmed fluid is hung on a
pole used for intravenous fluids above the level of the patient and allowed to flow, via
tubing, into the vagina. The pressure of the water, held in place by the clinician's hands,
results in correction of the inversion. It has been reported that successful correction in five
cases of inversion within a 7-year period using this method.16 More recently, a new
technique of hydrostatic pressure was described.15 Citing difficulty in maintaining an
adequate water seal to generate the pressure required, the authors suggest attaching the
intravenous tubing to a silicone cup used in vacuum extraction. By placing the cup within
the vagina, an excellent seal is created, and adequate hydrostatic pressure for inversion
correction is thus produced. Although success with this technique is cited in the literature,
there has been no discussion of the theoretical risk of air or amniotic fluid embolus. For
details regarding the hydrostatic pressure procedure please refer to Appendix D, and
Johnson maneuver at Appendix E. (Level II-3)
Occasionally, administration of a smooth muscle relaxant such as beta-adrenergic
agonist (terbutaline), nitroglycerin, or magnesium sulfate; may facilitate replacement of
the uterus. As uterine inversion is uncommon, it is difficult to compare these different
therapies. According to Abouleish, et. al., terbutaline 0.25 mg, and general anesthesia are
used as a last resort.17 They recommended terbutaline as a drug of rapid onset and short
duration. It was used successfully in five out of eight patients. In the study of Brar, et. al.,
terbutaline 0.25 mg was used successfully in 16 out of 18 patients, but they recommended
that it should not be used in patients with significant hypotension and shock.7 In these
patients, magnesium was used successfully in seven of eight patients. Catanzarite, et. al.19
and Wendel, et. al.24 recommend an intravenous dose of 4 grams magnesium sulfate.
However, in the study of Dayan, et. al., the benefits for the use of low-dose nitroglycerin
include quicker onset of uterine relaxation; quick dissipation of the effect, obviating the
need for reversal; and less effect on hemodynamics than magnesium sulfate.20 (Level II-3)
Immediately, provide intravenous access and resuscitation. (Grade C)

Summary of Evidence
Resuscitation should start immediately while attempts are made to replace the
uterus manually. If immediate replacement is not possible, aggressive support of
circulation by blood transfusion and intravenous fluid during rapid transport to the nearest
facility with operative obstetrics capability is urgently indicated.1,3,18,22,23 (Level III)
The placenta if still attached, should be left in place until after reduction. (Grade C)
Summary of Evidence
Controversy exists about whether the placenta should be removed before
repositioning the uterus. It is commonly suggested that removal of the placenta before
correction will result in increased blood loss and worsening of hemodynamics. Hence,
most authors advise replacement before removing the placenta.5,9,10,16,25-28 (Level III)
If the above method is unsuccessful, resuscitate and anaesthetise the woman, either
repeat the procedure or consider laparotomy to correct the defect or transvaginal
cervical incision and repair. (Grade C)
Summary of Evidence
When reduction under tocolysis fails, general anesthesia with halothane may be
induced to provide uterine relaxation and reduction attempted again. If unsuccessful,
further attempts should wait until the patient is hemodynamically stable. If further
attempts fail, laparotomy will frequently be indicated.5,18
At laparotomy, although several procedures have been described, the two most
commonly cited are the Huntington and Haultaim procedures.11 The Huntington
procedure requires a laparotomy which involves grasping the round ligaments and
sequentially locate the cup or depression of the uterus formed by the inversion. Clamps
are placed in the cup of the inversion below the cervical ring, and gentle upward traction
is applied. Repeated clamping and traction continues until the inversion is corrected. A
variant of this has been described using suction applied to the inverted fundus via a
vacuum instrument. If the Huntington method fails Haultain procedure is done. With this
procedure an incision is made in the posterior portion of the cervical ring, again through
the abdomen, to increase the size of the ring and allow repositioning of the uterus. For
further details and figures regarding these procedures please refer to Appendices F and G.
(Level III)
Uterotonic drugs should only be given immediately after repositioning of the uterus.
(Grade C)
Summary of Evidence
Uterotonics are not administered until the uterus has been repositioned.
Thereafter, oxytocic intravenous infusion should be given to maintain uterine contraction

and to prevent reinversion. If the uterus does not contract ergometrine or prostaglandins
may be given.5,18,29 (Level III)
Hysterectomy is regarded as the last resort of management after repositioning the
uterus and medical treatment failed. (Grade C)
Summary of Evidence
Hysterectomy is indicated for a gangrenous or hemorrhagic uterus despite the
reduction and medical treatment.3,5,18 (Level III)
Antibiotic prophylaxis is advisable. (Grade C)
Summary of Evidence
No RCTs have been published with regards to the benefit of antibiotic
prophylaxis for uterine inversion. Antibiotic prophylaxis should be instituted in order to
prevent any upward spread of infection. The use of antibiotics is left to the discretion of
the provider because data from the literature do not mandate its use.3,5
The recommendation of World Health Organization (WHO) is to give a single
dose of prophylactic antibiotics, ampicillin 2 g IV or cefazolin 1 g IV plus metronidazole
500 mg IV, after repositioning the inverted uterus. If the woman shows signs of infection
or has fever, give a combination of antibiotics, ampicillin 2 g IV every 6 hours,
gentamicin 5 mg/kg body weight IV every 24 hours, and metronidazole 500 mg IV every
8 hours. Continue the IV antibiotics until she is afebrile for 48 hours.29 (Level III)
4. Can uterine inversion be prevented?
The application of active management of the third stage of labor including controlled
cord traction decreases the incidence of acute uterine inversion following vaginal
delivery. (Grade C)
Summary of Evidence
As a measure to prevent postpartum hemorrhage, active management has been
widely adopted. Active management generally involves all three of the following
interventions: administration of routine prophylactic uterotonic agent, early cord clamping
and controlled cord traction. It has been noted that faulty management of the third stage of
labor may increase the risk of inversion of the uterus. The use of active management of
the third stage of labor decreases the incidence of acute uterine inversion by fourfold.
However, no randomized controlled trial has examined the third component of active
management, which is controlled cord traction, particularly in cases of preventing uterine
inversion.10,30 (Level III)
References
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
19.
20.
21.
22.
23.
24.
25.
26.
27.
28.
29.
30.
Beringer RM and Patteril M. Puerperal uterine inversion and shock. Br J Anaesth 2004;92(3),439-441.
Anderson J, Etches D. Prevention and management of postpartum hemorrhage. Am Fam Physician
2007;75:875-82.
Bouchikhi C, Saadi H, Fakhir B, Chaara H, Bouguern H, Banani A and Melhouf MA. Uterine
Inversion: A case report. Libyan J Med, AOP:071218;58-59.
Shah-Hosseini R, Evrard JR. Puerperal uterine inversion. Obstet Gynecol 1989;73:567-70.
Evans DG and B-Lynch C. Obstetric Trauma. Postpartum Hemorrhage. Chapter 9:70-79.
South Australian Perinatal Practice Guidelines. Uterine inversion. Chapter 11; March 2008.
Brar HS, Greenspoon JS, Platt LD, Paul RH: Acute puerperal uterine inversion. New approaches to
management. J Reprod Med 1989;34:173-177.
O'Leary JA: Uterine artery ligation for control of postpartum hemorrhage. Obstet Gynecol
1974;43:849-853.
Gumming D, Taylor P. Puerperal uterine inversion: report of nine cases. CMA Journal 1978;118:12681270.
Baskett TF. Acute uterine inversion: a review of 40 cases. J Obstet Gynaecol Can 2002;24(12):953-6.
Varner M. Postpartum hemorrhage. Crit Care Clin 1991;7:883-97.
Hsieh TT, Lee JD. Sonographic findings in acute puerperal uterine inversion. J Clin Ultrasound
1991;19:306-9.
Lewin JS, Bryan PJ. MR imaging of uterine inversion. J Comput Assist Tomogr 1989;13:357-9.
Hostetler DR, Bosworth MF: Uterine inversion: A life-threatening obstetric emergency. J Am Board
Fam Pract 2000;13:120-123.
Ogueh O, Ayida G. Acute uterine inversion: A new technique of hydrostatic replacement. BJOG
1997;104:951-952.
Momani AW, Hassan A. Treatment of puerperal uterine inversion by the hydrostatic method: reports of
five cases. Eur J Obstet Gynecol Reprod Biol 1989;32:281-5.
Abouliesh E, Ali V, Joumaa B, Lopez M, Gupta D. Anaesthetic management of acute puerperal uterine
inversion. Br J Anaesth 1995;75:486-7.
Cunningham FG, Gant NF, Leveno KJ, Gilstrap LC 3rd, Hauth JC, Wenstrom KD, Bloom SL.
Obstetrical hemorrhage. Williams obstetrics 22nd ed 2005; 28: 809-854.
Catanzarite VA, Moffitt KD, Baker ML, Awadalla SG, Argubright KF, Perkins RP. New approaches to
the management of acute puerperal uterine inversion. Obstet Gynecol 1986;68:710.
Dayan SS, Schwalbe SS. The use of small-dose intravenous nitroglycerin in a case of uterine inversion.
Anesth Analg 1996;82:1091-3.
Harnett MJ, Segal S: Presence of placental tissue is necessary for TNG to provide uterine relaxation.
Anesth Analg 2000;91:1043-1044.
Tews G, Ebner T, Yaman C, et al: Acute puerperal inversion of the uterus - treatment by a new
abdominal uterus preserving approach. Acta Obstet Gynecol Scand 2001;80:1039-1040.
Watson P, Besch N, Bowes WA, Jr. Management of acute and subacute puerperal inversion of the
uterus. Obstet Gynecol 1980;55(1):12-16.
Wendel PJ, Cox SM. Emergency obstetric management of uterine inversion. Obstet Gynaecol Clin
North Am 1995;22:26174.
Mirza FG, Gaddipati S. Obstetric emergencies. Semin Perinatol 2009;33:97-103.
Kitchin JD, Thiagarajah S, May HV, Thornton WN. Puerperal inversion of the uterus. Am J Obstet
Gynecol 1975;123:51-58.
Kochenour NK. Intrapartum obstetric emergencies. Crit Care Clin 1991;7(4):851-64.
You WB, Zahn CM: Postpartum hemorrhage: Abnormally adherent placenta, uterine inversion, and
puerperal hematomas. Clin Obstet Gynecol 2006;49:184-197.
World Health Organization. Managing Complications in Pregnancy and Childbirth A Guide for
Midwives and Doctors, Department of Reproductive Health and Research, World Health Organization.
2000.
Pea-Mart GE, Comunin-Carrasco G. Fundal pressure versus controlled cord traction as part of the
active management of the third stage of labour. Cochrane Database Syst Rev 2007, Issue 4. Art. No.:
CD005462.
APPENDIX
LEVELS OF EVIDENCE AND GRADES OF RECOMMENDATION

LEVEL
I
II-1
II-2
II-3
III
DEFINITION
Evidence obtained from at least one properly randomized controlled trial
Evidence obtained from well-designed controlled trials without
randomization
Evidence obtained from well-designed cohort or case-control analytic
studies, preferably from more than one center or research group
Evidence obtained from multiple time series with or without the
intervention.
Opinions of respected authorities, based on clinical experience; descriptive
studies and case reports or reports of expert committees.
GRADE
A
B
C
D
E
GPP
!
!
!
DEFINITION
There is good evidence to support the recommendation of the practice in
third trimester bleeding.
There is fair evidence to support the recommendation of the practice in
third trimester bleeding.
There is insufficient evidence to recommend for or against the inclusion of
the practice in abnormal uterine bleeding.
There is fair evidence to support the recommendation that the practice be
excluded in third trimester bleeding.
There is good evidence to support the recommendation that the practice be
excluded in third trimester bleeding.
A good practice point (GPP) is a recommendation for best practice based
on the experience of the Task Force3!
ANTENATAL PERINEAL MASSAGE

Perineal massage is usually done 3 to 4 times a week for 5 to 10 min starting 6 weeks
before their estimated due date.1 The pregnant woman is advised to acquire a comfortable
position for the massage: semi-sitting, squatting against a wall, or standing with one foot
raised and resting on tub, toilet or chair. Some women prefer to have the massage performed
on them while lying in bed. Advise the pregnant woman to try different positions and find
what position will make her comfortable.
Perineal massage entails the use of one or two fingers inserted 3 to 4 cm deep into the
vagina. These fingers apply and maintain pressure, first downwards and then to each side of
the vaginal entrance. To allow the fingers to move smoothly, the use of any of these
lubricants - vitamin E, wheat germ oil, mineral oil, virgin olive oil, almond oil, and
lubricating gel (such as KY). Avoid using baby oil, petroleum jelly, hand lotion, or perfumed
oils as these are less well absorbed by the body and are believed to be associated with allergic
reactions as compared to vegetable or water-based products.2
After lubricating the fingers, massage is initially applied diagonally on either side of the
top of the vestibule, just below the urethra. The muscles of the vagina should be allowed to
relax, and this helps prepare the pregnant woman to the sensations of childbirth. This should
be followed by insertion of the index finger of both hands into the vagina approximately 3 to
4 cm deep while the thumb presses on the perineum. A steady gentle pressure is maintained
as the fingers press downward on the area between the vagina and the rectum and upward
along the sides of the vagina in a "U" sling-type motion. This pressure will stretch the vaginal
tissue, the muscles surrounding the vagina, and the outer rim of the perineum. Then, massage
the fourchette edge of the perineum and outer layer of the perineum, towards the anus. Once
at the anus, the massage pattern is complete.
Explain to the woman that she will feel some pressure and uncomfortable stretching or
burning sensation. As the purpose of perineal massage is to help the woman get used to the
burning sensation that occurs when the fetal head presses against the perineum. The vaginal
and perineal sensations will be of tightness at first, but as the weeks would progress, daily
massage will relax and stretch the tissue.
References
1.
2.
Bodner-Adler B, Bodner K, Mayerhofer K. Perineal massage during pregnancy in primiparous

women. Int J Gynecol Obstet 2002; 78: 5153.
Bruce E. "Everything You Need to Know to Prevent Perineal Tearing." Midwifery Today Issue 65; 5:
25
METHOD OF HYDROSTATIC REDUCTION (O'Sullivan's hydrostatic maneuver)

The hydrostatic method does not always require anesthesia and may be done in the
labor and delivery room. However, it is preferable to perform the procedure in the operating
room. The woman should be placed in the lithotomy position. Two bottles of 1 liter of warm
(40C) irrigation fluid (e.g. sodium chloride 0.9 %) are attached to a wide bore giving set or
cystoscopy irrigation set. The intravenous bottle should be placed on an IV stand and kept
about 2 m above the ground level. The labia should be held tightly around the forearm, using
the other hand, to prevent the water from leaking out. An assistant may be required. The
nozzles of the two long rubber tubes should be directed to the posterior fornix of the vagina.
Run the warmed fluid by gravity or by pressure on the bag. The fluid must be allowed to flow
quickly and prevented from escaping. Up to 4 liters of fluid may be required. As the vaginal
walls distend, the fundus of the uterus will begin to rise. In most cases this will reduce the
inversion, with rapid resolution of the shock. The placenta can then be removed under
anesthesia.
After correction of the inversion, the fluid in the vagina should be allowed to flow out
slowly. The uterus must be checked for complete replacement. Thereafter contraction of the
uterus must be maintained by appropriate oxytocic treatment. An intravenous infusion
containing 1 liter 5% dextrose with 20 units of oxytocin should also be provided.
Ergometrine 0.5 mg should be administered intravenously as well.
Reduction of the inverted uterus may be achieved in about 5 to 10 min after
commencement of the hydrostatic technique. If this method is unsuccessful, resuscitate and
anesthesize the woman, either repeat the procedure or consider laparotomy to correct the
defect or transvaginal cervical incision and repair.
References
1. Momani AW, Hassan A. Treatment of puerperal uterine inversion by the hydrostatic method; reports of
five cases. Eur J Obstet Gynecol Reprod Biol 1989;32:281-285.
2. South Australian Perinatal Practice Guidelines. Maternity Care in South Australia. Chapter 11; May
2009.
JOHNSON MANEUVER
The placenta is left in place. The operators hand grasps the inverted uterus with the
placenta (see figure A). The fundus is allowed to rest on the palmar surface of the operators
hand with the fingertips exerting equal pressure around the collar of the uterus within the
cervical opening. The fundus is then replaced with upward pressure (see figure B). After
repositioning the uterus, the placenta is manually removed followed by uterine exploration.
The operators hand is kept inside the uterus until it begins to contract around the hand (see
figure C). A tight uterovaginal pack may be inserted before the hand is removed from the
uterine cavity (see figure D). The pack can be removed after 24 hours.
Figures A to D
Reference
World Health Organization. Managing Complications in Pregnancy and Childbirth A Guide for Midwives
and Doctors, Department of Reproductive Health and Research, World Health Organization. 2000.
HUNTINGTON MANEUVER
This maneuver is done during laparotomy. The surgeon grasps the surface of the
uterus in the crater created by the inversion with an allis clamp or a babcock (see figure A).
The clamps are used to simultaneously pull the uterus upward out of the cervical ring until it
is restored back into the peritoneal cavity. As the clamps steadily hold the uterus, the surgeon
now inserts another allis clamp into the crater and the uterus is further pulled upward (see
figure B). Through successive bites of the clamp on the surface of the uterus with upward
traction applied, the uterus is gradually restored to its normal position in the abdominal cavity
(See figure C).
Figures A to C
Reference
Gilstrap III LC, Cunningham FG, Vandorsten JP. Diagnosis and management of uterine inversion.
Operative obstetrics 2nd edition 2002; 15: 241-248.
HULTAIN MANEUVER
The maneuver is done through an abdominal-vaginal approach. As such procedure
requires a malleable retractor to be inserted vaginally. The retractor is inserted at the posterior
aspect of the vagina, with its tip placed between the posterior lip of the cervix and the
inverted uterine wall at the point at which the muscle will be incised abdominally (see figure
A). The rectosigmoid is held aside while an incision is made entirely through the uterine wall
at the point of constriction (see figure B). The length of the incision should be sufficient to
permit the passage of the uterine fundus. The purpose of the previously placed malleable
retractor is to ensure that only the uterus will be incised and prevent possible injury to the
vagina. The fundus is restored by combined traction on the uterine wall from above by the
surgeon and pressure from the vagina by an assistant (see figure C). When the uterus is
completely restored the incision is closed with interrupted sutures.
Figures A to C
References
1. Gilstrap III LC, Cunningham FG, Vandorsten JP. Diagnosis and management of uterine inversion.
Operative obstetrics 2nd edition 2002; 15: 241-248.
2. World Health Organization. Managing Complications in Pregnancy and Childbirth A Guide for
Midwives and Doctors, Department of Reproductive Health and Research, World Health Organization.
2000.

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Philippine Obstetrical and

CLINICAL PRACTICE GUIDELINES

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Task Force on Clinical Practice Guideline

Philippine Obstetrical and

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BOARD OF TRUSTEES 2009

ADHOC COMMITTEE ON CLINICAL PRACTICE GUIDELINES ON

Evelyn R. Lacson, MD (Region 6)

DISCLAIMER, RELEASE AND WAIVER OF RESPONSIBILITY

CPG ON THIRD TRIMESTER BLEEDING

The ultrasonographic appearance of abruptio depends to a large extent on the size

4. What is the optimal method of initial management of a patient with abruptio

6. Is there room for expectant management in abruptio placenta?

8. Are tocolytic agents a safe option in the management of abruptio placenta in

Although no interventions have been demonstrated to reduce this risk, some

3. What is the value of Magnetic Resonance Imaging (MRI)?

Careful documentation (Grade C)

A deficiency of decidualization may contribute to the development of abnormal

Incidence of placenta previa

In a twenty-year analysis of abnormal placentation, a retrospective case control

4. Thinning or focal disruption of the uterine serosa-bladder wall complex

advised to perform the delivery prior to hemorrhage or labor. Considerations should be

Surgery in the presence of placenta accreta

modality is chosen. Management modalities should be individualized and patients should

Signs & Symptoms

Palpitations, dizziness, tachycardia

Weakness, sweating, tachycardia

Restlessness, pallor, oliguria

Collapse, air hunger, anuria

Table 2. WHO Classification of PPH

Clinical Sings & Symptoms

Oliguria, tachycardia, tachypnea, postural

Hypotension, tachycardia, cold clammy

The general management of PPH involves anticipation, prompt recognition and

Table 3. Etiology, Pathophysiology and Risk factors of Postpartum Hemorrhage

Figure 1. Management Algorithm for Uterine Atony

4. Should uterine massage be routinely performed after delivery of the placenta?

Figure 2. B-Lynch Compression Suture Procedure15

shorter inter-delivery interval, one-layer closure of uterine incision, lower uterine

5. What are the maternal consequences of uterine rupture?

Type of uterine rupture

7. What are the preventive strategies for uterine rupture?

GENITAL TRACT TRAUMA

2. How can the occurrence of genital tract lacerations be prevented?

mediolateral episiotomy. Am J Obstet Gynecol 2005;192(3): 875-81.

obstetric anal sphincter rupture. BJOG 1996;103:1034-40.

B. GENITAL TRACT HEMATOMAS

Vaginal packing/pressure or insertion of drains for 24 to 36 hours may be useful

Mawhinney S, Holman R. Puerperal genital haematoma: a commonly missed diagnosis. The

Immediately, provide intravenous access and resuscitation. (Grade C)

Thereafter, oxytocic intravenous infusion should be given to maintain uterine contraction

LEVELS OF EVIDENCE AND GRADES OF RECOMMENDATION

ANTENATAL PERINEAL MASSAGE

Bodner-Adler B, Bodner K, Mayerhofer K. Perineal massage during pregnancy in primiparous

METHOD OF HYDROSTATIC REDUCTION (O'Sullivan's hydrostatic maneuver)

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