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Philippine Obstetrical and Gynecological Society (POGS), Foundation, Inc.
November 2009
Task Force on Clinical Practice Guideline In the Management of Third Trimester Bleeding
Philippine Obstetrical and Gynecological Society (POGS), Foundation, Inc.
CLINICAL PRACTICE GUIDELINES on THIRD TRIMESTER BLEEDING
November 2009
Task Force on Clinical Practice Guideline in the Management of Third Trimester Bleeding
FOREWORD
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”. Natin”. This is the Clinical Practice Guidelines on Third Tri mester 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/Reviewer Contributors/Reviewers, s, and a nd 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
INTRODUCTION
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
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
ADHOC COMMITTEE ON CLINICAL PRACTICE GUIDELINES ON THIRD TRIMESTER BLEEDING
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. Raymun do, MD Elisa O. Tiu, MD FELLOWS Rachelle U. delos Reyes, MD Ana Victoria V. Dy Echo, MD May Nueva-Hipol ito, 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, Tomacruz , MD Ryan Capitulo, MD Lyla Reyes, MD
TASK FORCE REVIEWERS AND PLENARY R EVIEWERS
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, 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. Dueñas, MD Joseline A. Ferrolino, MD Ma. Corazon N. Gamilla, MD Erlinda Erlinda G. Germar, MD Ma. Antonia E. Habana, MD Myrna R. Habaña, MD Bernardita B. Javier, MD Milagros T. Jocson, 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 Wilhelmina Pineda, MD
Regional Dire ctors Ellen A. Manzano, MD (Region 1) Melchor C. dela Cruz, MD (Region 2) Concepcion P. Aronza, MD (Region 3) Ernesto 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, 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. Pañares, 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 •
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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.
CPG ON THIRD TRIMESTER BLEEDING TOPICS / CONTENTS / AUTHOR/S A. Third Trimester Bleeding Antepartum Hemorrhage ………………………………………............. Blance C. De Guia, MD, MSc Abruptio Placenta ……………………………………………………… Ernesto S. Uichanco, MD Placenta Previa ………………………………………………………… Blanca C. De Guia, MD, MSc Placenta Accreta ………………………………………………………. Angela Teotico, MD B. Postpartum Hemorrhage Postpartum Hemorrhage ……………………………………………….. Rafael S. Tomacruz, MD Uterine Atony …………………………………………………………… Rafael S. Tomacruz, MD Retained Placenta ………………………………………………………. Ryan B. Capitulo, MD Uterine Rupture …… …………………………………………………… Ryan B. Capitulo, MD Genital Tract Trauma Tra uma …………………………………………………… 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 common causes include placenta previa, placenta accreta, and others, others, which include reproductive tract lesions. It occurs in 2 to t o 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, International, 4th edition. The Society of Obstetrics and Gynecologists Gynecologists of Canada
ABRUPTIO PLACENTA Ernesto S. Uichanco, MD
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 cer vix 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 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 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 2 associated decidual necrosis and venous hemorrhage . In some cases, it i t may be due to acute processes resulting result ing from one of the following: 1. Shearing forces resulting from trauma 2. Sudden uterine decompression resulting from membrane rupture wit h 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 cor relation 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. perfor med. In cases of acute revealed abruptio, the examiner may detect no abnormal 3 ultrasonographic findings. Nyberg and colleagues , 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 colleagues 3 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 2 pain. The above-mentioned clinical tests, correlated with good history and thorough physical examination will help make m ake 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, 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 Center 1: 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, reassuring, the patient may be managed conservatively. 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. 9 Sholl , in a retrospective cohort and case–control 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 i n prolonging gestation and did not increase the th e 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 11 co-workers 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 Oyelese which may be useful in the Philippine setting.
2
*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. 1983;64:467-73. 2. Oyelese Y, Ananth C. Placental abruption. Obstet Gynecol 2006;108:1005-16. 2006;108:1005-16.
3. Nyberg GA, Cyr DR, Mack LA, Wilson DA, Shuman WP. Sonographic Sonograp hic spectrum of placental abruption. Am abruption. Am J Roen tgenol 1987;148:161-4. 1987;148:161-4. 4. Glatz C, Purnell I. Clinical utility of sonography in the diagnosis and treatment of placental abruption. J Ultrasound Med 2002 200 2;21:837-40. 5. Yeo L, Ananth CV, Vintzileos AM. Placental abruption. In: Sciarra J, editor. Gynecology and Obstetrics. Obstetrics. Vol 2. Hagerstown (MD). Lippincott, Williams & Wilkins; 2003. 6. Kayani SI, Walkinshaw SA, Preston C. Pregnancy outcome in severe placental abruption. BJOG abruption. BJOG 2003; 2003; 10:679-83. 7. Brame RG, Harbert GM Jr, McGaughey HS Jr, et. al. Maternal risk in abruption. Obstet Gynecol 1968; 1968; 31:224. 8. Pritchard JA, Brekken AL. Clinical and laboratory studies on severe abruptio placenta. Am J Obstet Gynecol 1967; 1967; 97:681. 9. Sholl JS. Abruptio placentae: clinical management in nonacute cases. Am J Obstet Gynecol . 1987; 156:40-51. 10. Towers CV, Pircon RA, Heppard M. Is tocolysis safe in the management of third trimester bleeding? Am J Obstet G ynecol 1999;180:1572-8. 1999;180:1572-8. 11. Rasmussen S, Irgens LM, Daleker A. Outcome of pregnancies subsequent to placental abruption: a risk assessment. Acta assessment. Acta Obstet G ynecol 2000; 2000; 79:496-501. 12. 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. 13. 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. 14. Bernischke K, Kauffman P. Pathology of the hum en placenta. 4th ed. New York (NY): Springer; 2000. 15. Dhanraj D, Lambers D. The incidence of positive Kleihauer-Betke test in low risk pregnancies and maternal trauma p atients. Am atients. Am J Obstet Gyn ecol 2004;190:1461-3. 2004;190:1461-3.
PLACENTA PREVIA Blanca C. De Guia, MD, MSc
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 fet al 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 and a vicious 1 cycle of bleeding – contractions – placental separation – bleeding occurs.
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 twotwothirds 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 e xamination 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. 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 with false positive rate of up 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 placenta may appear to overlie overlie the internal os. If the cervical length further exceeds 3-5 3-5 cm length, imaging should be done done after the 3 patient emptied her bladder. During myometrial contractions, two situations that assume placenta previa may occur. First, the wall 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 should be suspected if the myometrium myometrium is 3 thicker than 1.5 cm. Repeat ultrasound after 30 minutes may exclude this conditions. (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, 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 persi stence 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 placenta previa at 35 7 weeks results in more CS. (Level III)
6. Is vaginal delivery possible with wi th 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 on last ultrasound prior to delivery. At 353536 weeks gestational age, a distance of >20 mm away from the os was associated with high likelihood of vaginal delivery delivery (range 63-100%). Between 20 mm and 0 mm mm from the 6,8,9 os, CS varies from 40-90/%. (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 11 5.6; 95% CI 1.8-17.0) were associated with massive bleeding (>2500 ml).
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 4.54.511 3395.2) and where there was lack of a clear zone (OR 480; 95% CI, 38.0-604.7). (Level II-2)
9. Is placenta previa associated with placenta accreta, increta or percreta? Placenta accreta, accreta, increta, percreta percreta may co-exist. co-exist. Women who have placenta 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 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 who were not given 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 14 setting. (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 re st with minimal ambulation to hospital and 26 women were were discharged home. Overall, there was no difference in any 15 major outcome. (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? 13
Suggestions for good practice recommendation include: • 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 experienced obstetrician obstetrician and anesthesiologist. anesthesiologist. This is especially to those women with higher risk of complications namely previous uterine scars, anterior placenta previa or associated placenta accreta. accreta. (Grade C)
14. What some related issues to provide total care to the patient? 17
To provide total care, the following are recommended: • 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 17 subjected to clinical audit. • Anticipation of hemorrhage with adequate workshop • Appropriate personnel involvement i nvolvement • 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 sonograp hic placental localization. Obstet Gynecol 2001; 17:496-501. 3. Morrinan Q et al. Placenta previa: imaging. eMedicine. Medscape Continually Updated Clinic References. References. Updated November 6, 2008. 4. Taipale P, et. al. Transvagin al ultrasonography ultrason ography at 18-23 weeks in predicting placenta previa at delivery. Ultrasound Ultrasound Obs tet Gynecol 1998;12:420-425. 1998;12:420-425. 5. Becker RH, et. al. The relevance of placental location at 20-23 gestational weeks for prediction of placenta prev ia at delivery : evaluation of 8650 ca ses. Ultrasound Obstet Gynecol 2001;17:100-2. 2001;17:100-2. 6. Oppenheimer Oppenheim er L, L, et. al. Diagnosis of low-lying placenta: Can migration in the third trimester predict outcome? Ultrasound Obstet Gynecol 2001;8:100-2. 2001;8:100-2. 7. Predanic M, et. al. A sonographic sonograp hic assessmen assessmen t of different patterns of placenta previa “migration” “migration ” on the third trimester of pregnancy. J Ultrasoun d Medicine Medicin e 2005;24:773-80. 8. Salkaut B, B, et. al. al. The classification classification of placenta previa based on placenta edge distance at transvaginal transvaginal sonography. Am J Obstet G ynecol 2002;187(6):594. 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 prev ia. Br J Obstet G ynecol 2009;110:860-4. 2009;110:860-4. 10. Oppenheimer L, et. et. al. Diagnosis and Management of placenta previa SOGC Clinical Practice Practice Guideline. JOGC Guideline. JOGC 2007. 2007. 11. Hasegava J, et. al. Predisposing factors for massive hemorrhage during cesarean section in in patient with placenta prev ia. Ultrasound Obstet Gynecol 2009;34:80-84. 2009;34:80-84. 12. Clark S, et. al. Placenta previa/accreta previa/accreta and previous previous cesarean section. section. Obstet Gynecol 198 198 5;66:89-92. 13. Besinger R, et. al. The effect of tocolytic use in the management of symptoma tic placenta previa. Am J Obstet Gynecol 1995;172:1170-8. 1995;172:1170-8. 14. Towers C, et. al. Is tocolysis safe in the management managem ent of third trimester bleeding? Am J Obstet Ob stet Gynecol Gyn ecol 1999;180:1572-8. 15. Wing D, et. al. Managemen t of the symptomatic placenta previa; a randomized , controlled trial of in patient versus outpatient outpatien t expectant m anagemen t. Am J Obstet G ynecol 1996;175:806-11. 1996;175:806-11. 16. Parekli N, et. al. Cesarean section for for placental placental previa. A retrospective retrospective study of anesthetic anesthetic management. B J Anaesth 2000;84:725-30. Anaesth 2000;84:725-30. 17. Clinical Clinical Practice Guidelines Guidelines on Placenta Previa: Diagnosis Diagnosis and Management. Guidelines and Audit Sub-Committee Sub-Committee of the Royal College of Obstetricians and Gyn ecologists, ecologists, 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 seri ous 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 current trend in the incidence of placenta placenta accreta? 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 1930’s, to 1/20,000 in 1960’s, to 1/7,000 in 1980’s. 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 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 f uture 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 t he mother. (Grade B) Summary of Evidence In a retrospective cohort study from 1966-2005 by Flood 7 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 incre ased from 27-57% (P<.00001). (P<.00001). (Level II-2) Other authors have reported placenta accreta to comprise 30-50% of their 8-10 peripartum hysterectomy and previous cesarean delivery was a common factor. 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 12 observed in a study done by Clark 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 clinician’s 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 14 analysis conducted by Gielchinsky 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 placent a 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 15 delivery on maternal outcome was evaluated by Wong 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 T he exact mechanism is i s unknown. It i s 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 Plac enta previa itself raises the t he 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 Wu 3, 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 Asherma’s 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 18,19 increasing the risk of abnormal placentation.
6. How do we screen and diagnose placenta accreta antenatally? antenatal ly?
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 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 dilat ed 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). 20 Using the above criteria, Frinberg 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 pr edictive 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 incr eased 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. cer vix. 2. A focal lacunar flow pattern 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 hypoechoic zone. 21 Chou, et. al. 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, te chnique, 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 Shih 25 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 sensiti vity 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 wel l as topographical information informati on that optimizes diagnosis and surgical management. This is particularly helpful in cases of posterior 26 placenta where ultrasonographic evaluation is difficult or to confirm bladder invasion. However, it is the combination of different imaging modalities that may prove most effective in diagnosing this condition.
7. How should should we manage placenta accreta? 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 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 27 infertility. 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. 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 Eller 29, 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 patient’s wishes regarding conservative management and future fertility. 28 Adequate blood product should be secured prior to delivery. Bauer , 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 r atio of PRBC to FFP in cases of massive hemorrhage.
Surgery in the presence presence of placenta accreta 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 t iming 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 Eller 29 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 32
Chou 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 Shrivastava 34 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 hemorr hage 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 (fr om 11, 84.6 % to 3, 15%; P<.001), blood transfusion tra nsfusion (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 examinati on 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 37 month. Tong 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. arteri es. (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 4,41 on Methotrexate therapy given weekly at 50 mg IM for 4-6 doses. (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 f or 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 43 hemorrhage, infection and or emergent surgery. 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 f ails 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. Sherer 47 reported a case of placenta previa percreta in a 35 year old multigravid successfully successfull y managed with 3 courses of methotrexate and 3 bilateral uterine artery artery embolization. Placenta completely 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. Luo 48 reported a case of placenta percreta managed conservatively with methotrexate and uterine embolization however, the patient had heavy bleeding on the 44 th 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)
References 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14.
Breen JL et. al. Placenta accreta, increta and percreta: A survey of 40 cases. Obstet Gynecol 1977;49:43-47. Miller DA. Clinical risk factors for placenta previa-placenta accreta. Am J Obstet Gynecol 1997;177:210-4. Serena Wu. Abnormal placentation: Twenty-year Twenty-year analysis. Am analysis. Am J Obstet Gyn ecol 2005;192:1458-61. 2005;192:1458-61. Panganiban R, Teotico A. Conservative Conservative management of placenta previa percreta: A case report. Phil report. Phil J Obstet Gynecol 2006;30(4):192. 2006;30(4):192. Teotico, AR. Review of POGS National statistics, 2002-2007. Lee YM, D’Alton ME. Cesarean delivery on maternal request: the impact on mother and newborn. Clin Perinatol 2008;35:505-518. 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. 2009;200-632. Kwee A. Emergency peripartum hysterectomy: A prospective study in the Netherlands. Eur J Obstet Gynecol 2006;124:187-92. 2006;124:187-92. Sakse A. Weber T, Peripartum hysterectomy in Denmark 1995-2004. Acta Obstet Gynecol Scand 2007;86:1472-5. Glaze S. Peripartum hysterectomy hysterectomy 1999 to 2006. Obtet Gynecol 2008;111:732-8. 2008;111:732-8. Todd R. Placenta accreta and cesarean scar pregnancy: Overlooked costs of the rising cesarean section rate. Clin Perinatol 2008;35:519-529. 2008;35:519-529. Clark, SL, Belfort MA. Maternal death in the 21 st century: causes, prevention, and relationship to cesarean delivery. Am delivery. Am J Obstet G ynecol 2008;199:36.e1-36.e5. ynecol 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. 2004;104:527-538.
15. Wong HS, Hutton J. The maternal outcome in placenta accreta: the significance of antenatal antenatal diagnosis and non-separation of placenta at delivery. N delivery. N Z Med J 2008;121(1277). 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. 2006;107:1226-1232. 17. Clark SL, et. al. Placenta previa/accreta and pr ior cesarean section. Obstet Gynecol 1985; 1985; 66:89-92. 18. Read JA. Placenta accreta: changing clinical aspects and outcome. Obstet Gynecol 1980;56:3. 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;99:976–80. 2002;99:976–80. 20. Frinberg HJ, et. al. Placenta accreta: prospective sonographic diagnosis in patients with placenta previa and prior cesarean section. J section. J Ultrasou nd Med 1992;11:333-343. 1992;11:333-343. 21. Chou MM, et. al. Prenatal diagnosis of placenta previa accreta by transabdominal color doppler ultrasound. Ultrasound Obstet Gynecol 2000;15:28-35. 2000;15:28-35. 22. Warshak CR, Eskander R. Accuracy of ultrasonography and magnetic resonance imaging in the diagnosis of placenta accreta. Obstet Gynecol 2006;108:573-81. 2006;108:573-81. 23. Chou MM, et. al. Prenatal diagnosis of placenta previa accreta with power amplitude ultrasonic angiography. Am angiography. Am J Obstet G ynecol 1997;177:1523-1525. 1997;177:1523-1525. 24. Comstock CH, Lee W, Vettraino IM, et. al. The early sonographic appearance of placenta accreta. J Ultrasound Med 2003;22:19-23. 2003;22:19-23. 25. Shih JC. Role of 3D Power doppler in the antenatal diagnosis of placenta accreta: comparison with grey scale and color doppler techniques. Ultrasound Obstet Gynecol 2009;33(2):193-203. Gynecol 2009;33(2):193-203. 26. Thorp JM, et. al. Antepartum diagnosis of placenta previa percreta by magnetic resonance imaging. Obstet Gynecol 1992;80:506-508. 1992;80:506-508. 27. Lee R. Placenta accreta and percreta: incidence, risks, diagnosis, counseling and preparations for delivery. Division delivery. Division o f Maternal-Fetal Materna l-Fetal Medicin e, University of Southern California 28. Bauer ST. Abnormal placentation. Seminars in Perinatology 2009;12.003 Perinatology 2009;12.003 29. Eller AG. Optimal management strategies for p lacenta accreta. BJOG accreta. BJOG Published Published online Feb 2009. 30. ACOG. Placenta accreta. ACOG Committee Opinion No. 2 66. American College of Obstetricians and Gynecologist, 2002. 31. RCOG. Placenta previa and placenta accreta: diagnosis and management. RCOG Guideline No. 27, Revised 2005. 32. Chou MM. Iliac artery embolization before hysterectomy for placenta accreta. J Vascular Interventiona l Radio 2003;14:1195-1199. 33. Shih JC. Temporary occlusion of the common iliac artery: new approach to bleeding control during a cesarean hysterectomy for placenta percreta. Am percreta. Am J Obstet Gy necol 2005;193:1756-8. 2005;193:1756-8. 34. Shrivastava V. Case control comparison of cesarean hysterectomy with and without prophylactic placement of intravascular intravascu lar balloon catheters for placenta accreta. Am J Obstet Gynecol Gyneco l 2007;197:402.e1-402-402.e5. 35. Kayem G, e.t al. Conservative versus extirpative management in cases of placenta accreta. Obstet 2004. Gynecol 2004. 36. Thia E. Lessons learnt from two women with morbidly adherent placentas and a review of literature. Ann Acad M ed Singapo re 2007:36;298-303. re 2007:36;298-303. 37. Tong SY. Conservative management of placenta accreta: review of three cases. Singapore Med J 2008;49(6): e156. 38. Crespo R, et. al. Conservative treatment of placenta increta with methotrexate. Int J Gynecol Gyneco l Obstet Obste t 2005:91,162-163. 39. Panolskaltsis Panolskaltsis TA. Placenta increta: evaluation of radiological radiological investigations and therapeutic options of conservative conservative management. Br management. Br J Obstet Gyn ecol 2000;107:802-806. 2000;107:802-806. 40. Antenatal diagnosis of placenta percreta with planne in situ retention and methotrexate therapy in a woman infected with HIV, P MID: 12100427(Pubmed) 41. Ermita, M. Teotico A. Complete placental dissolution after methotrexate therapy: A case report. Phil J Obstet Gynecol 2008. 2008. 42. Hundley AF, Parritz AL. Managing placenta accreta. OBG Management 2002;14(8). 2002;14(8). 43. Jaffe R, et. al. Failure of Methotrexate for term placenta percreta. Am J Obstet O bstet Gynecol Gyneco l 1994;171:558 1994;171:558559. 44. Panganiban R, Teotico A. Conservative vs extripative management of placenta accreta: A provincial hospital experience, 2009 (unpublished). 45. Mussalli GM. Placenta accreta and methotrexte methotrexte therapy: three case reports. J reports. J Perinat 2000;5: 2000;5: 331-334. 46. Clement D, et. al. Conservative management of placenta percreta: a safe alternative. Eur J Obstet 2004;114(1):108-109. Gynecol Reprod Biol 2004;114(1):108-109.
47. Sherer DM. Placenta previa percreta managed conservatively with methotrexate and multiple bilateral uterine artery embolization. embolization. Ultrasound Obstet Gynecol 2007;227-230. 2007;227-230. 48. Luo G. Failure of conservative management in placenta previa-accreta. J Perinat Per inat Med 2005;33(6):5648. 49. Butt K. Failure of methotexate and internal iliac balloon catheterization to manage placenta percreta.
POSTPARTUM HEMORRHAGE Rafael S. Tomacruz, MD
Background
Postpartum hemorrhage (PPH) is the leading cause of maternal mortality, accounting 1 for nearly one third of all maternal deaths worldwide. PPH causes up to 60% of all maternal deaths in developing countries. The majority of these deaths occur within 4 hours of delivery, 2 indicating they are a consequence of events in the third stage of labor. 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). 1). The World Health Organization (WHO) subsequently proposed a classification of PPH similar and based on Bonnar’s definition where clinicians are now guided in managing this life-threatening condition (Table (Table 2). 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 t o organs or death.
Table 1. Correlation of Blood Loss to Blood Pressure and Clinical Signs and Symptoms 3 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 Classificati on of PPH Hemorrhage Class
Estimated Blood Loss (mL)
Blood Volume Loss (%)
Clinical Sings & Symptoms
0 (normal loss)
< 500
<10
None
1
500-1000
15
Minimal
2
1200-1500
20-25
Oliguria, tachycardia, tachypnea, postural hypotension
3
1800-2100
30-35
Hypotension, tachycardia, cold clammy
4
>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 patient’s hemodynamic status is rapidly evaluated while the underlying etiology of the bleeding is investigated and ascertained. In BREATHING, patient’s 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 T’s: 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 Rafael S. Tomacruz, MD
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 ( 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 baby’s birth, bir th, delayed cord cor d 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 management of the third stage of labor better 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). 1.52-2.42). 1-3 (Level 1)
2. Should we routinely administer administer oxytocin soon after after the baby’s birth to reduce the incidence of PPH? Administration of oxytocin soon after the baby’s 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 baby’s 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 cord clamping reduce the incidence incidence of PPH better compared 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 6-9 0.12, 95 % CI 0.03-0.95). 0.03-0.95). (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 µg) be given to prevent PPH instead of oxytocin? Oxytocin is better than oral misoprostol mi soprostol 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% 95% CI 0.6211-13 1.04). (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), 3.03-3.56), diarrhea diarrhea (RR 2.52, 95% CI 1.603.98), and pyrexia with a temperature > 38°C (RR 6.62, 95% CI 5.45.8.05).11-13 (Level I)
6. Should sublingual sublingu al misoprostol (600 µg) be given to prevent PPH instead of 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 µg) 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 µg 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 > 38°C (RR 2.74, 95% CI 1.08-6.93). (Level II-1)
8. Should hemostatic agents be routinely given in the management of uterine 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 µg/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 procedures to be performed if active active management of third stage 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 t he initial conservative, surgical means of arresting ar resting 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 sta nding between the patient’s 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 15 atony. It is not necessary to t o re-open the uterine incision in this method. (Level II-3)
Figure 2. B-Lynch Compression Suture Procedure 15
(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 patient’s left side and threaded through the uterine cavity to emerge 3 cm above the upper incision margin approximately 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 uterin e 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 i ncision margin. 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 patient’s legs swabs the vagina again and confirms that the bleeding has been controlled.
References 1. 2.
3.
Prendiville WJ, Elbourne D, McDonald S. Cochrane Database Syst Rev 2003; 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 Librar y Commentary, Nov. 17, 2000). Cochrane Database Syst Rev 2001, Rev 2001, Issue 4.
4. 5. 6.
7. 8. 9.
10. 11. 12. 13. 14. 15.
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, Rev 2001, Issue 4. Liabsuetrakul 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, 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 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; Rev 2004; 4:CD003248. van Rheenen P, Brabbin BJ. Late umbilical cord-clamping as an intervention for reducing iron deficiency deficiency anemia in term infants in developing and industrialized industrialized countries: A systematic review. Ann review. Ann Trop Paediatr 2004; 2004; 24:3-16. Hofmeyr GJ, Abdel-Aleem H, Abdel-Aleem MA. Uterine massage for preventing postpartum haemorrhage. Cochrane Database Syst Rev 2008, Rev 2008, Issue 3. Art. No.: CD006431. Gulmezoglu AM, et. al. Prostaglandins for prevention o f postpartum haemorrhage. Cochrane Database Syst Rev 2006, Rev 2006, Issue 4. Villar J, Gulmezoglu AM, Hofmeyr GJ, Forna F. Systematic review of randomized control trials of misoprostol misoprostol to prevent pos tpartum hemorrhage. Obstet Gynecol 2002; 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 Anesth 2008;21: 281-287. B-Lynch C, Keith LG, Lalonde AB, Karoshi M. A Textbook of Postpartum Hemorrhage, Sapiens Publishing, 2006.
RETAINED PLACENTA Ryan B. Capitulo, MD
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 of retained placenta? Manual removal of the placenta is warranted if the other maneuvers have failed to deliver the placenta and significant bleeding bl eeding 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, 7 but a single, small, randomized trial supports the practice. (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, Rev, Issue 2. Oxford, UK: Update Software. 2006. Abouzahr C. Antepartum and postpartum haemorrhage. In: Murray CJ, Lopez AD, eds. H ealth Dimensions of Sex and Reproduction. Boston, Reproduction. Boston, Mas s: Harvard Harvar d University Pre ss; 1998:172-4. 1998: 172-4. Baskett TF. Complications of the th ird stage of labour. In: Essential Man agement of Obst etrical Emergencies. 3rd ed. Bristol, UK: Clinical Press; 1999:196-201. 1999: 196-201. Begley CM. A comparison of ''active'' and ''physiological'' ''physiological'' management of the third stage of labour. Midwifery 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 1 1 996;88(2):161-7. Bullough CH, Msuku RS, Karonde L. Early suckling and postpartum haemorrhage: controlled trial in deliveries by traditional birth attendants. Lancet attendants. Lancet 1 1 989;2(8662):522-5. Chongsomchai C, Lumbiganon P, Laopaiboon M. Prophylactic antibiotics antibiotics for manual removal of retained retained placenta in vaginal birth. Cochrane Database Syst Rev 2006;CD004904. 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; McGraw-Hill; 2001:320-5. 2001: 320-5.
UTERINE RUPTURE Ryan B. Capitulo, MD
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. dif fer. The peer-reviewed literature was searched using the PubMed–Medline 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 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 3 Marivate, the mean parity for women who had pregnancy-related uterine rupture was 4. 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 3 unscarred uteri, and 32 (12%) of the 260 were associated with oxytocin use. 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 1 was used in 26 of 61 cases (43%) that involved unscarred uterine rupture. However, Plauche, et. al. attributed only 1 of 23 unscarred uterine ruptures (4%) to the use of 6 oxytocin. 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 10 1788) in those with normal uteri ( P = = .013). 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 11 (OR 2.10; 95% CI 1.45-3.05). 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 12 of uterine rupture after previous CS in 1324 women who underwent a subsequent TOL. 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 13 cesarean scars who underwent an unplanned TOL. 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 15 T, or J or J incision incision who either presented in advanced labor or refused repeat CS. 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 16 CS without a TOL was 0.16%. 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 18 spontaneously, the uterine rupture rate was 0.72%. 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 ( P = = .001).19 In a study by Ravasia, et. al. of 575 patients who underwent labor l abor induction, the uterine rupture rate r ate was 1.4% compared with 17 0.45% for women who labored spontaneously ( P ( P = = .004). 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 E 2 (PGE 2) 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 21 patients with 1 previous CS who received PGE2 alone for labor induction. 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 PGE 2 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 PGE 2. 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 PGE 2 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 15 underwent induction with PGE 2 alone. 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, PGE 2 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 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 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 26 an interdelivery interval of greater than 24 months ( P < .01). 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 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 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 f rom cesarean delivery, Miller, Mille r, 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 1.9529 4.79]. 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 30 uterine scar (absolute rupture risk 1.8 vs 0.9%; adjusted OR 2.3; 95% CI 1.37-3.85). 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 deliver y 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 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%) ( 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 af ter cesarean delivery. Rozenberg, et. al. prospectively examined 642 642 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 36 uterine rupture. 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 occurrences in other, benign obstetric circumstances. 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 38 uterine rupture, occurring in 78%. 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 26 epidural analgesia but not in women who received an epidural block. Thus, abdominal pain is an unreliable and uncommon sign of uterine uter ine rupture. Initial Initi al 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 38 supported. 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. fet us. 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 37 than 6.8. 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 40 required admission to the neonatal intensive care unit (NICU). 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 41 rupture had a cystotomy. 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 42 blood loss was 1500 ml and great enough to be symptomatic in 3 patients (60%). In a study by Shipp, et. al., 7 of 28 women (25%) who had uterine rupture during a TOL after 43 a previous CS received a blood transfusion. 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 1 rupture developed signs and symptoms of hypovolemic shock. 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 12 necessary in 10 women women who had a uterine rupture. 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 3 delivery; rates were wer e 4.5% and 10.4%, respectively. (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 foll owing 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 Hysterectomy should be considered the treatment 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 la bor 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, r upture, 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 during a subsequent trial of labor. Am labor. Am J Obstet G ynecol 20 20 00;183(5):1184-6. 19. Zelop CM, Shipp TD, Repke JT, et. al. Uterine rupture during induced or augmented labor in gravid women with one prior cesarean delivery. Am delivery. Am J Obstet Gyn ecol 1999;181(4):882-6. 1999;181(4):882-6. 20. Blanchette H, Blanchette Blanchette M, McCabe J, Vincent S. Is vaginal birth after cesarean safe? Experience at a community hospital. Am hospital. Am J Obste t Gynecol 2001;184(7):1478-84; 2001;184(7):1478-84; discussion 1484-7. 21. Taylor DR, Doughty AS, Kaufman H, et. al. Uterine rupture with the use of PGE2 vaginal inserts for labor induction in women with previous cesarean sections. J sections. J Reprod Med 2 2 002;47(7):549-54. 22. Flamm BL, Anton D, Goings JR, Newman J. Prostaglandin E2 for cervical ripening: a multicenter study of patients with pr ior cesarean delivery. Am delivery. Am J Perina tol 19 19 97;14(3):157-60. 23. Delaney T, Young DC. Spontaneous versus induced labor after a previous cesarean delivery. Obstet Gynecol 200 200 3;102(1):39-44. 24. Esposito MA, Menihan CA, Malee MP. Association Association of interpregnancy interpregnancy interval with uterine scar failure in labor: a case-control study. Am study. Am J Obstet G ynecol 2000;183(5):1180-3. 2000;183(5):1180-3. 25. Shipp TD, Zelop CM, Rep ke JT, et. al. Interdelivery interval and risk of sy mptomatic uterin e rupture. Obstet Gynecol 2001;97(2):175-7. Gynecol 2001;97(2):175-7. 26. Bujold E, Gauthier RJ. Neonatal morbidity associated with uterine rupture: what are the risk factors? Am factors? Am J Obstet G ynecol 2 2 002;186(2):311-4. 27. Durnwald C, Mercer B. Uterine rupture, perioperative and perinatal morbidity after single-layer and double-layer double-layer closure at cesarean d elivery. Am elivery. Am J Obstet G ynecol 2003;189(4):925-9. ynecol 2003;189(4):925-9. 28. Gyamfi C, Juhasz G, Gyamfi P, Blumenfeld Y, Stone JL. Single- versus double-layer uterine incision closure and u terine rupture. J rupture. J Matern Fe tal Neonata l Med 2006;19(10):639-43. 2006;19(10):639-43. 29. Miller DA, Diaz FG, Paul RH. Vaginal bir th after cesarean: a 10-year ex perience. perien ce. Obstet Gynecol 1994;84(2):255-8. 30. Macones GA, Cahill A, Pare E, et. al. Obstetric outcomes in women with two prior cesarean deliveries: is vaginal birth after cesarean delivery a viable option? Am J Obstet Gynecol 2005;192(4):1223-8; discussion 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 deliveries. Am J Obstet G ynecol 19 19 99;181(4):872-6. 32. ACOG. Vaginal birth after previous cesarean delivery. ACOG practice bulletin no. 54. Washington, DC: American College of Obstetricians and Gynecologists;2004. Gynecologists;2004. 33. Elkousy MA, Sammel M, Stevens E, et. al. The effect of birth weight on vaginal birth after cesarean delivery success rates. Am rates. Am J Obstet Gyn ecol 2003 2003 ;188(3):824-30. 34. Shipp TD, Zelop C, Repke JT, et. al. The association of maternal age and symptomatic uterine rupture during a trial of labor after prior cesarean delivery. Obstet Gynecol 200 200 2;99(4):585-8. 35. Rozenberg P, Goffinet F, Philippe HJ, Nisand I. Thickness of the lower uterine segment: its influence in the management of patients with previous cesarean sections. Eur sections. Eur J Obstet Gynecol Reprod Biol 1999;87(1):39-45. 36. Gotoh H, Masuzaki H, Yoshida A, et. al. Predicting Predicting incomplete uterine rupture with vaginal sonography during the late second trimester in women with prior cesarean. Obstet Gynecol 2000;95(4):596-600. 37. Leung AS, Leung EK, Paul RH. Uterine rupture after previous cesarean delivery: maternal and fetal consequences. Am consequences. Am J Obstet Gyn ecol 1993;169(4):945-50. 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 diagnosis? Am J Obstet Gyn ecol 198 198 9;161(3):666-9. 39. Phelan JP, Ko rst LM, Settles DK. Uterine activity act ivity pattern s in uterine ru pture: a case-control c ase-control study. Obstet Gynecol 19 19 98;92(3):394-7. 40. Menihan CA. Uterine rupture in women attempting a vaginal birth following prior cesarean birth. J Perinatol 1998;18(6 1998;18(6 Pt 1):440-3. 41. Kieser K E, Baskett TF. A 10-year population-based study of uterine rupture. Obstet Gynecol 200 200 2;100(4):749-53. 42. Cowan RK, Kinch RA, Ellis B, Anderso n R. Trial of labo r following ces arean delivery . Obstet Gynecol . Jun 1994;83(6):933-6. 43. Shipp TD, Zelop CM, Repke JT, et al. Intrapartum uterine rupture and dehiscence in patients with prior lower uterine segment vertical and transverse incisions. Obstet Gynecol 1999;94(5 1999;94(5 Pt 1):735-40. 44. Eden RD, Parker RT, Gall SA. Rupture of the pregnant uterus: a 53-year review. Obstet Gynecol 1986;68(5):671-4. 45. Gordon CA. Ruptured pregnancy in the closed rudimentary horn of a bicornuate uterus. Am J Obstet Gynecol 1935;29:279-82. 1935;29:279-82.
46. Tien DSP. Pregnancy in the rudimentary horn of the uterus. Review of the literature and report of one case. Chin Med J 1949;67:485-8. 1949;67:485-8. 47. Schauffler Schauffler GC. Double uterus with pregnancy. JAMA pregnancy. JAMA.. 1941;117:1516-20. 48. Erez O, Dukler D, Novack L, Rozen A, Zolotnik L, Bashiri A. Trial of labor and vaginal birth after cesarean section in patients with uterine Müllerian anomalies: a population-based study. Am J Obstet Gynecol 2007;196(6):537.e Gynecol 2007;196(6):537.e1-11. 1-11. 49. Golan D, Aharoni A, Gon en R, et al. Early spontan eous rupture rup ture of the post myomecto my gravid uterus. Int uterus. Int J Gynaeco l Obstet 1990 1990 ;31(2):167-70. 50. Brown AB, Chamberlain R, Te Linde RW. Myomectomy. Am Myomectomy. Am J Obstet Gyn ecol 195 195 6;71(4):759-63. 51. Garnet JD. Uterine rupture during pregnancy. An analysis of 133 patients. Obstet Gynecol 1964;23:898-905. 52. Dubuisson JB, Fauconnier A, Deffarges JV, e t al. Pregnancy outcome and d eliveries eliveries following laparoscopic myomectomy. Hum myomectomy. Hum Reprod 2000 Reprod 2000 ;15(4):869-73. 53. Seinera P, Farina C, Todros T. Laparoscopic myomectomy and subsequent pregnancy: results in 54 patients. Hum patients. Hum Reprod Rep rod 200 200 0;15(9):1993-6. 54. Nezhat CH, Nezhat F, Roemisch M, et al. Pregnanc y following laparoscop ic myomectomy: myomec tomy: preliminary resu lts. Hum lts. Hum Reprod Rep rod 1999;14(5):1219-21. 1999;14(5):1219-21. 55. Seracchioli R, Rossi S, Govoni F, et al. Fertility and obstetric outcome after laparoscopic myomectomy of large myomata: a randomized comparison with abdominal myomectomy. myomectomy. Hum Hum Reprod 2000 2000 ;15(12):2663-8. 56. Seracchioli R, Man uzzi L, Viane llo F, Gualerzi B, Sav elli L, Paradisi R. Obstetric an d delivery outcome of pregnancies achieved after laparoscopic myomectomy. Fertil myomectomy. Fertil Steril 2006;86(1):159-65. 2006;86(1):159-65. 57. Oktem O, Gokaslan H, Durmusoglu F. Spontaneous uterine rupture in pregnancy 8 years after laparoscopic myomectomy. J myomectomy. J Am Assoc G ynecol Laparosc Lap arosc 20 20 01;8(4):618-21. 58. Naef RW 3rd , Ray MA, Ch auhan SP, e t. al. Trial of labor after c esarean de livery with a lo wer-segment, vertical uterine incision: is it safe? Am safe? Am J Obs tet Gynecol 199 199 5;172(6):1666-73; discussion discussion 1673-4. 59. Adair CD, Sanche z-Ramos L, Whitak er D, et. al. Trial of labor in pat ients with a prev ious lower uterine vertical cesarean section. Am section. Am J Obste t Gynecol 1996;174(3):966-70. 1996;174(3):966-70. 60. Martin JN, Perry KG, Roberts WE, Meydrech EF. The case for trial of labor in the patient with a prior low-segment vertical cesarean incision. Am incision. Am J Obstet Gyn ecol 1997 1997 ;177(1):144-8. 61. Kayani SI, Alfirevic Z. Uterine rupture after induction of labour in women with previous caesarean section. BJOG section. BJOG 200 200 5;112(4):451-5. 62. Grobman WA, Gilbert S, Landon MB, Spong CY, Leveno KJ, Rouse DJ. Outcomes of induction of labor after one prior cesarean. Obstet Gynecol 2007;109(2 2007;109(2 Pt 1):262-9. 63. Miller DA, Goodwin TM, Gh erman RB, Paul RH. Intrapartum Intrapartum rupture of the unscarred uterus. Obstet Gynecol 1997;89(5 1997;89(5 Pt 1):671-3. 64. Johnson C, Oriol N. The role of epidural anesthesia in trial of labor. Reg labor. Reg Anesth 1990 ;15(6):304-8. 65. Asakura H, Myers SA. More than one previous cesarean delivery: a 5-year experience with 435 patients. Obstet Gynecol 199 199 5;85(6):924-9. 66. Bujold E, Bujold C, Hamilton EF, et. al. The impact of a single-layer or double-layer closure on uterine rupture. Am rupture. Am J Obstet G ynecol 2002;186(6):1326-30. 2002;186(6):1326-30. 67. Bujold E, Mehta SH, Bujold C, Gauthier RJ. Interdelivery interval and uterine rupture. Am rupture. Am J Obstet Gynecol 200 200 2;187(5):1199-202. 68. Yap OW, Kim ES, Laros RK Jr. Maternal and neonatal outcomes after uterine rupture in labor. Am J Obstet Gynecol 2001;184(7):1576-81. 2001;184(7):1576-81. 69. Flamm BL, Goings JR, Liu Y. Elective repeat cesarean delivery versus trial of labor: a prospective multicenter study. Obstet Gynecol 1994;83(6):927-32. 1994;83(6):927-32. 70. Achiron R, Tadmor O, Kamar R, et al. Prerupture ultrasound diagnosis of interstitial and rudimentary uterine horn pregnancy in the second trimester. A report of two cases. J cases. J Reprod Med 1992;37(1):89 1992;37(1):8992. 71. Gregory KD, Kor st LM, Cane P, et a l. Vaginal b irth after cesarean and uterine rup ture rates in California. Obstet Gynecol 199 199 9;94(6):985-9. 72. Lin C, Raynor BD. Risk of uterine rupture in labor induction of patients with prior cesarean section: an inner city hospital experience. Am experience. Am J Obstet Gyn ecol 200 200 4;190(5):1476-8. 73. Locatelli A, Regalia AL, Ghidini A, et al. Risks of induction of labour in women with a uterine scar from previous low transverse caesarean section. BJOG section. BJOG 2004;111 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 1,2 approximate incidence of 20 percent. 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 well being 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 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 2-5 tears according to the degree or depth of the laceration this includes: First Degree Second Degree Third Degree
Fourth Degree
involves the fourchette, perineal skin, and vaginal mucous membrane but not the underlying fascia and a nd muscle aside from the skin skin and and mucous 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, 6 this classification system has not been extensively validated yet. 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 3 since most of these would be less than 0.5 cm. 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 art ery 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. 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 15-16 and anal sphincter tears. 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 t rauma (RR 0.92, 95% CI 0.72-1.18), dyspareunia (RR 1.02, 95% CI 0.90-1.16), 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; 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 14 trauma during childbirth. (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 21,22 23 trauma and third-degree tears with vacuum extraction compared with forceps delivery. But the risk of perineal trauma between the 2 groups was not significantly 21 22 different (RR 0.50, 95% CI 0.10-2.64 ; RR 0.58, 95% CI 0.19-3.15 ; and RR 0.44, 95% CI 0.16-1.22 23). (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, deliver y, hence reducing the risk 24 of perineal trauma. 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 b etween the trials t rials was noted. The T he 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 26 trimester of pregnancy reduces the likelihood of perineal trauma and postpartum pain. 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 a ppropriate 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 1 entire circumference has been inspected. (Level III)
4. Once the lacerations lacerations are 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 r educed (RR 0.80, 95% CI 0.64-0.99). 28 Another RCT was conducted in Nigeria, involving 823 women who sustained a 29 second-degree tear or episiotomy. 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 6 th 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 wit h 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 28 study of Gordon, et. al., 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., 28 the risk of wound gaping was also noted to increase at 10 days after delivery. 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) 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. 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 32 cannot be closed securely, then a vaginal pack should be inserted. 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? laceratio ns? 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 34
A meta-analysis, 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) 0.64-1.08) or dyspareunia (RR ( RR 0.95, 95% CI 0.79-1.15) 0.79-1.15) between absorbable synthetic sutures and catgut chromic c hromic catgut. cat gut. But rates of dyspareunia were lower after 3 months from delivery with absorbable synthetic sutures than with
chromic catgut (RR 0.59, 95% CI 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 21–28 days after repair and it is not totally absorbed from the wound until 60–90 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 10–14 days and completely absorbed from the ti ssue 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 t o assess asses s the best suture material for repair of the external 38-40 anal sphincter were found. Only one RCT reported on the use of 3-0 PDS and 2-0 38 polyglactin (Vicryl). Out of the 103 women who followed up on the 6 th 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 27,30,38,40 associated with less irritation and discomfort. (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 t he 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 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 42 interrupted-suture group than in the continuous group (RR 1.41, 95% Cl 1.16-1.72). (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. In a large trial involving 1542 women with second-degree tears or episiotomy 37 in the UK continuous sutures significantly reduced the risk of developing pain among women with perineal tears at 10 days with continuous as compared with interrupted suture 37,43
(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). 0.77-1.43). 43 In a smaller RCT, 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). 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 c onclusions 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 24 primary repair of the external anal sphincter compared with the end-to-end method. (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 o’clock) 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 tr ials regarding repair r epair 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 39 to maternal morbidity, especially subsequent anal incontinence. A survey 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 would be appropriate for the postoperative 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 v agina 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 9,31,39 to achieve vaginal tamponade. 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 24–36 hours before removal. A urinary foley catheter and broad spectrum antibiotic cover should be given where packs are used.50 Balloon tamponade using Rüsch 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 arter ial embolization.52 (Level III) The success rates of these forms of management were evaluated in a systematic 52 review, 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 i ncrease the risk of anal incontinence incontinenc e and fistula 48 formation if the repaired anal sphincter breaks down. (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 54 sphincter repair. 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 6–12 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 6–12 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 58,59 postoperatively. 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 5 secondary sphincter repair. (Level III)
8. What is the prognosis after repair of the genital tract laceration? lacerati on? 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 10–12 days or even up to 3–18 months after giving birth. Women may also complain of dyspareunia up to t o three months postpartum. (Level III) Regarding breakdown of perineal laceration repair after vaginal delivery, a 61 retrospective, case-control study 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 ( 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 60–80% 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 20–67% 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 54–88% 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 19–36% of cases.45,74,75 (Level I)
9. When would it be comfortable comfortable for women to have sexual sexual intercourse after 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, reac tions, decreased libido, and decreased dec reased vaginal lubrication l ubrication correlated to 78 hormonal changes in the early puerperium. 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 79 deliveries.
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. 80 A population-based cohort conducted in Sweden 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 woman’s capacity to have resume sexual intercourse by 3 to 6 months from childbirth. chil dbirth. 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 1. Clark SL. Managing Managing postpartum postpartum hemorrhage: hemorrhage: establish establish a cause. cause. J Fam Prac t 2002;14(11). 2002;14(11). 2. Anderson J, Etches D. Prevention and management management of postpartum postpartum hemorrhage. Am Fam Physician 2007;75:875-82 3. Cunningham FG, Gant NF, Leveno KJ, Gilstrap Gilstrap LC 3rd, Hauth Hauth JC, Wenstrom KD, Bloom SL. nd Obstetrical Obstetrical hemorrhage. Williams Obstetrics 2005;22 Obstetrics 2005;22 ed(28):809-854. 4. Leeman L, Rogers Rogers R, Greulich B, Albers L. Do unsutured unsuture d second-degree perineal lacerations affect postpartum fu nctional ou tcomes? J tcomes? J Am Board Fam Med 2007;20:451-457. 2007;20:451-457. 5. Guideline and and Audit Committee of the Royal College College of Obstetricians Obstetricians and Gynaecologists. Gynaecologists. Methods Methods and materials used in perineal repair. Guideline No. 23, June 2004. 6. Kinberg SF. Introduction. Perineal lacerations lacerations after after childbirth. Section Section 2008; Section Section 5:12-27. 5:12-27. 7. Fernando RJ, RJ, Sultan AH, Radley Radley S, Jones PW, Johanson RB. RB. Management of obstetric obstetric anal sphincter sphincter injury: a systematic review & national practice survey. BMC survey. BMC Health Heal th Serv Res 2002;2(1):9. 8. Melamed N, Ben-Harou Ben-Haroush sh A, Chen R, et al. Intrapartum cervical lacerations: character istics, risk factors, and effects on subsequent pregnancies. Am pregnancies. Am J Obstet Gynecol 2009; 2009; 20 0: 388.e1-388.e4. 9. Ramanathan G, Arulkumaran Arulkumaran S. Postpartum hemorrhage. J hemorrhage. J Soc Obstet Gynecol Gyneco l Can 2000; Can 2000; 22(4): 27181. 10. Williams A, Tincello DG, White S, Adams EJ, Alfirevic Z, Richmond DH. Risk scoring system for prediction of ob stetric anal ana l sphincter inju ry. BJOG ry. BJOG 2005;112:1066–9. 2005;112:1066–9. 11. Bhau U, Koul I. Recent advances in the management of postpartum hemorrhage. JK Science Science 2008; 10(4). 12. Schuurmans N, Mackinnon C, et al. Prevention and management of postpartum hemorrhage. J Soc Obstet Gynaecol Can 2 Can 2 000;22(4):271-81. 13. Christianson LM, Bovbjerg VE, McDavitt EC, Hullfish KL. Risk factors for perineal injury during delivery. Am delivery. Am J Obstet Gyn ecol 2003 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: childbirth : role of forceps delivery routinely combined with
mediolateral mediolateral episiotomy. Am episiotomy. Am J Obstet G ynecol 2005;192(3): 2005;192(3): 875-81. 15. Carroli G, Belizan 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. Gynecol 1991;77(1):69-76. 17. ACOG Committee on Practice Bulletin. Postpartum hemorrhage. ACOG Practice Bulletin Clinical Management Guidelines for Obstetrician-Gynecol Obstetrician-Gynecologist ogist No. 71. Obstet Gynecol 2006; 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 Childbirth Group Trials Register 2001;108: 34–40. 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;68:453–459. 22. Weerasekera DS, Premaratne Premaratne S. A randomised prospective trial of the obstetric forceps versus vacuum extraction using defined criteria. J criteria. J Obstet Gyna ecol 2002;22:344–345. 2002;22:344–345. 23. Fitzpatrick M, Behan M, O'Connell PR, et al. Randomised clinical trial to assess anal sphincter function following following forceps. Br forceps. Br J Obste t Gynaecol Gynaeco l 2003;110:424–429. 2003;110:424–429. 24. Kettle C, Tohill S. Perineal Perinea l Care. BMJ Care. BMJ Clinica l Evidence 2008;09:1401. Evidence 2008;09:1401. 25. Hodnett ED, Gates S, Hofmeyr GJ, et al. Continuous support for women during childbirth. Cochrane Database Sy st Rev 2006, Issue 1. 26. Beckmann MM, Garrett AJ. Antenatal perineal massage for reducing perineal trauma. Cochrane Database Sy st Rev 2006, 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 evalua tion of two stage after birth perineal repair leaving the skin unsutured. Br unsutured. Br J Obstet Gyn aecol 1998;105:435–440. 1998;105:435–440. 29. Oboro VO, Tabowei TO, Loto OM, et. al. A multicentre evaluation of the two-layer repair of after birth perineal trau ma. J ma. J Obstet Gyna ecol 2003;1:5–8. 2003;1:5–8. 30. DeCherney AH, Pernoll ML. ML. Postpartum hemorrhage. hemorrhage. Current Obstetric & Gynecologic Diagnosis Diagnosis & Treatment: 9th Ed Aug 2002;Chapter 12:499-530. 31. Kettle C. The The Pelvic Floor. In: Henderson Henderso n C, Macdonald S, editors. Mayes' Midwifery A textbook for Midwives. 13th Edition ed. London: Bailliere Tindall; 2004: 476-91. 32. White C. Perineal repair repair workshop. Perth: Perth: Australian Australian College of Midwives (WA Branch) 33. Gould D. Perineal tears tears and episiotomy. Nursing Nursing Standard. 2007; 21(52): 41-6. 41-6. 34. Kettle C, Johanson R. Absorbable synthetic versus catgut suture material for perineal repair. Cochrane Database Sy stematic Revs1999, Revs 1999, Issue 4. Art. No.: CD000006. 35. McElhinney BR, Glenn DRJ, Dornan G, G, Harper MA. Episiotomy Episiotomy repair: repair: vicryl versus vicryl rapide. Ulster Med J 2000;69:27–9. 2000;69:27–9. 36. Gemynthe A, Langhoff-Roos J, Knudsen SS. New VICRYL formulation: an improved method of perineal repa ir? Br ir? Br J Midwifer y 1996;4:230–4. 37. Kettle C, Hills RK, Jones Jones P, Darby L, Gray R, Johanson R. Continuous versus interrupted interrupted perineal repair with standard or rapidly absorbed absorbed sutures after spontaneous vaginal birth: a randomised controlled trial. Lancet trial. Lancet 2002;359:2217–23. 2002;359:2217–23. 38. Williams A, Adams EJ, Tincello DG, Alfirevic Z, Walkinshaw SA, Richmon d DH. How to repair an anal sphincter injury after vaginal delivery: results of a randomised controlled trial. BJOG 2006;113:201–7. 39. Fernando RJ, Sultan Sultan AH, Radley S, Jones PW, Johanson RB. Management of obstetric obstetric anal sphincter sphincter injury - A systematic review and n ational practice survey. BMC survey. BMC Health S erv Res 2002;2:9. 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 Guideline No. 29, March 2007 . 41. Kettle C, Johanson RB. Continuou s versus interrupted sutur es for perineal repair. Cochrane Database Syst Rev 2003;CD000947. Rev 2003;CD000947. 42. Mahomed K, Grant A, Ashurst A, James D. The Southmead Perineal Suture Suture Study. A randomised comparison of suture suture materials and suturing suturing techniques for repair of perineal trauma. Br J Obstet Gynaecol 1989;96:1272–80. 1989;96:1272–80. 43. Morano S, Mistrangelo E, Pastorino Pastorino D, et. al. A randomized comparison of suturing techniques for episiotomy and laceration repair after spontaneous vaginal birth. J Minim Invasive Invasiv e Gynecol Gyneco l 2006;13:457–462.
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. 2006;(3):CD002866. 45. Fitzpatrick M, Fynes M, Behan M, et al. A randomized clinical trial comparing primary overl ap with approximation approximation r epair of third-degree third-degree obstetric tears. Am tears. Am J Obstet G ynecol 2000; 2000; 183:1220–1224. 46. Sultan AH, Kamm MA, Hudson CN, Bartram CI. Third degree obstetric anal sphincter tears: risk factors and outcome of primary repair. BMJ repair. BMJ 1994;308:877-91. 47. Kammerer-Doak Kammerer-Doak DN, Wesol AB, Rogers RG, Dominguez CE, Dorin 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 Primary repair of obstetric anal sphincter rupture rupture using the overlap technique. BJOG technique. BJOG1999;106:318–23. 1999;106:318–23. 49. Thakar R, Sultan AH, Fernando R, Monga A, Stanton Stanton S. Can workshops on obstetric anal sphincter rupture change practice? Int practice? Int Urogyn ecol J 2001;12:S5. 2001;12:S5. 50. Johanson R, Kumar M, Obhrai M, et. al. Management of massive postpartum haemorrh age: use of a hydrostatic hydrostatic balloon catheter to avo id laparotomy. Br laparotomy. Br J Obstet Gyn aecol 2001;108: 420-2. 51. Katesmark M, Brown R, Raju K. Successful use of a Sengstaken-Blakemore tube to control massive postpartum h aemorrhage. aemorrhag e. Br Br J Obstet Gyn aecol 1994;101:259-60. 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. Survey 2007;62(8):540-547. 53. Buppasiri P, Lumbiganon Lumbiganon P, Thinkhamrop J, Thinkhamrop B. Antibiotic prophylaxis for fourth-degree fourth-degree perineal tear du ring vagin al birth. Cochrane Database Syst Rev 2005, Rev 2005, Issue 4. Art. No.: CD005125. 54. Mahony R, Behan M, O’Herlihy C, O’Connell O’Conn ell PR. Randomised clinica l trial of bowel confinement vs. laxative use after primary repair of a third degree obstetric obstetri c 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;158–64. 56. Sultan AH, Kamm MA, Hudson CN. Anal sphincter sphincter disruption during vaginal delivery. delivery. N N Engl J Med M ed 1993;329:1905-11. 57. National Institute Institute for Clinical Clinical Excellence. Excellence. Intrapartum care. care. Care of healthy women and their their babies during childbirth. London; 2007. 58. Sleep J, Grant A, Garcia, et. al. West Berkshire perineal managem ent trial. BMJ trial. BMJ 1984;289: 1984;289: 587-690. 59. Glazener CMA, Abdalla M, Stroud P. Postnatal maternal morbidity: morbidity: extent, causes, prevention and treatment. Br treatment. Br J Obstet Gyn aecol 1995;102:286-7. 1995;102:286-7. 60. Leeman L, Rogers R, Greulich B, Albers L. Do unsutured second-degre e perineal lacerations affect postpartum fu nctional ou tcomes? J tcomes? J Am Board Fam Med 2007;20:451-457. 2007;20:451-457. 61. Williams MK, Chames MC. Risk Risk factors for the breakdown of perineal perineal laceration repair after after vaginal delivery. Am delivery. Am J Obstet G ynecol 2006;195:755–9. 2006;195:755–9. 62. Haadem K, Dahlstrom Dahlstrom JA, Lingman Lingman G. Anal sphincter sphincter function after after delivery: a prospective study in women with sphincter rupture and controls. Eur controls. Eur J Obst et Gynaecol Gyna ecol Reprod B iol 1990;35:7-13. 1990;35:7-13. 63. Haadem K, Dahlstrom JA, Ling Ling L, Ohrlander S. Anal sphincter function after delivery rupture. Obstet Gynecol 1987;70:53-6. 1987;70:53-6. 64. Walsh CJ, Mooney EF, Upton GJ, Motson RW. Incidence of third–degree third–degree perineal tears in labour and outcome after primary repair. Br repair. Br J Surg 1996;83:218-21. 1996;83:218-21. 65. Fornell EK, Berg G, Hallbook O, Matthiesen Matthiesen LS, Sjodahl R. Clinical consequences of anal sphincter sphincter rupture during vaginal delivery. J delivery. J Am Coll Surg 1996;183:553–8. Surg 1996;183:553–8. 66. Nazir M, Stein R, Carlsen Carlsen E, Jacobsen AF, Nesheim BI. Early evaluation of bowe l symptoms after primary repair of obstetric perineal rupture is misleading: misleading : an observation al cohort study. Dis Colon Rectum 2003;46:245–50. Rectum 2003;46:245–50. 67. Crawford LA, Quint EH, Pearl ML, DeLancey JO. Incontinence Inconti nence following rupture of anal sphincter during delivery. Obstet Gynecol 1993;82:527–31. 1993;82:527–31. 68. Poen AC, Felt-Bersma Felt-Bersma RJF, RJF, Strijers Strijers RL, Dekker GA, Cuesta MA, Meuwissen Meuwissen SG. Third degree obstetric perineal tear: long-term clinical and functional results after primary repair. Br J Surg 1998;85:1433–8. 69. Gjessing H, Backe B, Sahlin Y. Third degree obstetric tears: outcome after primary repair. Acta repair. Acta Obstet Ob stet Gynecol Scand 1998;77:736–40. 1998;77:736–40. 70. Wood J, Amos L, Rieger N. Third degree anal sphincter tears: risk factors and outcome. Aust NZ J Obstet Gynaecol 1998;38:414-7. 71. de Leeuw JW, Sruijk PC, Vierhout Vierhou t ME, Wallenburg Wallenbu rg HC. Risk Risk factors for third third degree perineal ruptures during delivery. BJOG delivery. BJOG 2001;108:383-7. 2001;108:383-7. 72. Tetzschner T, Sorensen M, Lose G, Christiensen J. Anal and urinary incontinence in women with
obstetric obstetric anal sphincter rupture. BJOG rupture. BJOG 1996;103:1034-40. 1996;103:1034-40. 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 2005;192:1697-701. 75. Fernando RJ, Sultan AH, Kettle C, Radley S, Jones P, O’Brien S. Repair techniques for obstetric anal sphincter injuries: a randomized controlled trial. Obstet Gynecol 2006;107: 2006;107: 1261-8. 76. Malouf AJ, Norton CS, Engel AF, Nicholls Nicholls RJ, Kamm MA. Long-term results results of overlapping anterior anal sphincter repair for obstetric trauma. Lancet trauma. Lancet 2000;355:260-5. 2000;355:260-5. 77. Gjessing H, Backe B, Sahlin Y. Third degree obstetric tears: outcome after primary repair. Acta repair. Acta Obstet Ob stet Gynecol Scand 1998;77:736–40. 1998;77:736–40. 78. Kettle C, Ismail K, O "Mahony Mahony F. Dyspareunia following childbirth. The Obstetrician & Gynaecologist 2005;7:245-249. 79. Buhling KJ, Schmidt 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 Gyneco l Reprod Biol 2006;124(1):42-46. 80. Radestad I, Olsson A, Nissen E, Rubertsson Rubertsson C. Tears in the vagina, perineum, sphincter ani, and rectum and first sexual intercourse intercourse after childbirth: childbirth: A na tionwide follow-up. follow-up. Birth Birth 2008; 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 repair. Br J Obstet Gynaecol 1998;105(4):441-445. 1998;105(4):441-445.
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 a lso 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 1 within the broad ligament.
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. 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 f actors will not completely 3,5 prevent or predict hematoma formation. As this type of injury may occur in both spontaneous and operative vaginal delivery even without lacerations. (Level III)
2. What signs and symptoms symptoms will facilitate the recognition of genital genital tract hematoma? 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 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 1,4,6 over a few days. Puerperal hematomas aside from pain usually present with pressure symptoms, swelling as well as urinary retention due to inability to void or, rarely, 1 unexplained pyrexia. 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 intraintraabdominal 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 diagnostic modalities can aid in the the investigation of of genital tract hematom hematoma? a? 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 1,12 practitioner in giving the appropriate management. (Level III)
4. How will genital genital tract hematoma be managed? 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 12–24 hours, while small, non-expanding 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 14 evacuation of the clot. 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 18 lesions are not expanding. 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 or recurrent bleeding. 19 A case series 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. ef fects. 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)
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.
Mawhinney S, Holman R. R. Puerperal genital genital haematoma: a commonly commonly missed diagnosis. The Obstetrician Obstetrician & Gynaecologist 2007;9:195–200. 2007;9:195–200. Morgans D, Chan Chan N, Clark Clark CA. Vulval Vulval perineal haematomas in the immediate postpartum period and their management. Aust management. Aust N Z J Obst et Gynaecol 1999;39:223–7. Gynaecol 1999;39:223–7. Resnik R. Vaginal and vulval hematoma. Contemporary OB/GYN 1996;41:19–23. 1996;41:19–23. Mirza FG, Gaddipati S. Obstetric emergencies. Semin Perinatol 2009; 2009; 33:97-103. Saleem Z, Rydhstrom H. Vaginal hematoma during parturition: parturitio n: a population-based study. Acta Obstet Gynecol Scand 2004;83:560–2. 2004;83:560–2. Sheikh GN. Perinatal Perinatal genital genital hematomas. Obstet Gynecol Gynecol 1971; 38: 571–5. 571–5. Cunningham FG, Gant NF, Leveno Leveno KJ, Gilstrap Gilstrap LC 3rd, Hauth JC, Wenstrom KD, Bloom Bloom SL. nd Obstetrical Obstetrical h emorrhage. Williams obstetrics 22 ed 2005; Chapter 28: 809-854. Anderson J, Etches D. D. Prevention and management of postpartum hemorrhage. Am hemorrhage. Am Fam Physician 2007;75:875-82. Ridgway LE. Puerperal emergency. emergency. Vaginal Vaginal and vulvar hematomas. 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. Radiograp obstetrics. Radiograp hics 2002;22:563-82. hics 2002;22:563-82. Rooholamini SA, Au AH, Hansen GC, Kioumehr F, Dadsetan MR, Chow PP, et. al. Imaging of pregnancy- related comp lications. Radiograp lications. Radiograp hics 1993;13:753-70. hics 1993;13:753-70. Mackinnon C, et. al. Prevention and management of postpartum hemorrhage. J Soc Obstet Gyneco l Can 2000;22(4):271-81. Propst AM, Thorp JM Jr. Traumatic vulvar hematomas: conservative versus surgical management. South Med J 1 1 998;91(2):144-6. Schuurmans N, Mackinnon C, et al. Prevention and management of postpartum hemorrhage. hemorrhage. J Soc Obstet Gynecol Can 200 Can 200 0;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. 1990;33:422. Kean LH, Baker, Edelstone Edelstone DI, editors. Other problems problems of the third stage. Best Practice in in Labor Ward Management, Edinburgh: Harcourt; 2000. Lingam K, Hood V, Carty MJ. Angiographic Angiographic embolisation in the management of pelvic haemorrhage. haemorrhage. BJOG 20 BJOG 20 00;107(9):1176-8. Pinborg A, Bodker B, Hogdall Hogdall C. Postpartum haematoma haematoma and vaginal packing with a blood pressure cuff. Acta cuff. Acta Obstet G ynecol yneco l Scand 2000;79:887–9. 2000;79:887–9. Pelage J, Le Dref O, Jacob D, et. al. Selective arterial embolisation of the uterine arteries in the management of intractable intractable po stpartum haemorrhage. Acta haemorrhage. Acta Obstet Ob stet Gyneco l Scand 1999;78: 1999;78: 698-703. Evans S, McShaneP. The efficacy of internal iliac artery ligation in obstetric haemorrhage. Surg Gynecol Obstet 1985;160:250-327. 1985;160:250-327. Johanson R. Continuous vs. interrupted interrupted sutures for perineal perineal repair. In Keirse M, Renfrew M, Neilson 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 technique? Int J Gyna ecol Obstet 1993;43:197–8. 1993;43:197–8. Ledee N, Ville Y, Musset D, et. al. al. Management inintractable obstetric obstetric haemorrhage: an audit study on 61cases. Eur 61cases. Eur J Obstet G ynecol Reprod Rep rod Biol 2001;94:189–96. 2001;94:189–96. Vedantham S, Goodwin SC, McLucas B, Mohr G. Uterine Uterine artery embolization: an underused underused method of controlling pelvic hemorrhage. Am hemorrhage. Am J Obstet G ynecol 1997;176(4):938-48. 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 2 0.05% of deliveries. 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. 2,5 However, others report the classification as partial or complete inversion. 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? 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 porti on 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 3,9 prolonged distention; and congenital weakness or anomalies of the uter us. However, the role of fundal pressure with undue cord traction is uncertain. The underlying causes are 1,2 not completely understood. (Level III)
2 . How is uterine inversion diagnosed? di agnosed? 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 1 15 manually by Johnson maneuver or by hydrostatic pressure. (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 f luid 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 16 cases of inversion within a 7-year period using this method. 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 7 that it should not be used in patients with significant hypotension and shock. In these patients, magnesium was used successfully successfull y in seven of eight patients. pat ients. Catanzarite, et. al.19 24 and Wendel, et. al. 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 unti l 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 i s 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 3,5,18 reduction and medical treatment. (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 29 8 hours. Continue the IV antibiotics until she is afebrile for 48 hours. (Level III)
4. Can uterine uterine inversion be prevented? 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 Puerperal uterine inversion and shock. Br shock. Br J Anaesth 200 4;92(3),439-441. Anderson J, Etches D. Prevention Prevention and management of postpartum postpartum hemorrhage. Am hemorrhage. Am Fam Physician 2007;75:875-82. Bouchikhi C, Saadi H, Fakhir Fakhir B, Chaara H, Bouguern Bouguern H, Banani A and and Melhouf MA. Uterine Inversion: A case report. Libyan report. Libyan J Med , AOP:071218;58-59. Shah-Hosseini Shah-Hosseini R, Evrard JR. Puerperal uterine inversion. Obstet Gynecol 1989;73:567-70. 1989;73:567-70. Evans DG and B-Lynch B-Lynch C. Obstetric Trauma. Postpartum Hemorrhage. Chapter Chapter 9:70-79. 9:70-79. South Australian Australian Perinatal Practice Guidelines. Uterine Guidelines. Uterine inversion. Chapter 11; March 2008. Brar HS, Greenspoon Greenspo on JS, Platt LD, Paul RH: Acute puerperal uterine inversion. New approaches to management. J Reprod Med 1989;34:173-177. 1989;34:173-177. O'Leary JA: Uterine artery ligation for control of postpartum hemorrhage. hemorrhag e. Obstet Gynecol 1974;43:849-853. Gumming D, Taylor P. Puerperal Puerperal uterine uterine inversion: inversion: report report of nine cases. cases. CMA Journal 1978;118:1268 1978;118:12681270. Baskett TF. TF. Acute uterine inversion: inversion: a review of 40 cases. J cases. J Obstet Gyna ecol Can 2002 Can 2002 ;24(12):953-6. Varner M. Postpartum hemorrhage. Crit Care Clin 1991;7:883-97. 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 Bryan PJ. MR imaging imaging of uterine inversion. inversion. J J Comput Compu t Assist Tomog r 198 198 9;13:357-9. Hostetler DR, Bosworth MF: Uterine inversion: A life-threatening obstetric emergency. J Am Board 2000;13:120-123. 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 Treatment of puerperal uterine inversion by the hydrostatic hydrostatic method: reports of five cases. Eur cases. Eur J Obste t Gynecol Repro d Biol 1989;32:281-5. 1989;32:281-5. Abouliesh Abouliesh E, Ali V, Joumaa B, Lopez M, Gupta D. Anaesthetic management of acute puerperal puerperal uterine uterine inversion. Br inversion. Br J Anaesth 1995;75:486-7. Cunningham FG, Gant NF, Leveno KJ, Gilstrap LC 3rd, Hauth JC, Wenstrom KD, Bloom SL. Obstetrical Obstetrical h emorrhage. Williams obstetrics 22 nd ed 2005; 28: 809-854. Catanzarite VA, Moffitt KD, Baker ML, Awadalla SG, Argubright Argubrigh t KF, Perkins RP. New approaches to the management of acute puerperal uterine inversion. Obstet Gynecol 1986;68:7–10. 1986;68:7–10. Dayan SS, Schwalbe SS. The use of small-dose intravenous nitroglycerin in a case of uterine inversion. Anesth Analg 1996;82:1091-3. 1996;82:1091-3. Harnett MJ, Segal S: Presence of placental placental tissue is is necessary for TNG TNG to provide uterine uterine relaxation. 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 approach. Acta Obste t Gynecol Sca nd 2001;80:1039-1040. Watson P, Besch N, Bowes WA, Jr. Management of acute and subacute puerperal puerperal inversion of the uterus. Obstet Gynecol 19 19 80;55(1):12-16. Wendel PJ, Cox SM. Emergency obstetric management of uterine inversion. Obstet Gynaecol Clin North Am 1995;22:261–74. Am 1995;22:261–74. Mirza FG, Gaddipati S. Obstetric Obstetric emergencies. emergencies. Semin Perinatol 2009;33:97-103. 2009;33:97-103. Kitchin JD, Thiagarajah Thiagarajah S, May HV, Thornton WN. Puerperal inversion of the uterus. Am J Obstet Gynecol 1975;123:51-58. 1975;123:51-58. Kochenour NK. Intrapartum Intrapartum obstetric obstetric emergencies. Crit Care Clin 1991;7(4):851-64. You WB, Zahn CM: Postpartum hemorrhage: Abnormally adherent placenta, uterine uterine inversion, and puerperal hem atomas. Clin Obstet Gynecol 2006;49:184-197. 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 H ealth Organization. Organization. 2000. Peña-Martí GE, Comunián-Carras Comunián-Carrasco co G. Fundal pressure versus controlled cord traction 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
GRADE A B C D E GPP
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.
DEFINITION There is good evidence to support the recommendation of the practice in 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 1 before their estimated due date. 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 t he purpose of perineal massage is to help the woman get g et 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 Bodner-Adler B, Bodner K, Mayerhofer K. Perineal Perineal massage massage during during pregnancy pregnancy in primiparous women. Int women. Int J Gynecol Gyn ecol Obstet Obste t 2002; 2002; 78: 51–53. Bruce E. "Everyth ing You Need to Know to to Prevent Perineal Tearing." Midwifery Today Issue 65; 5: 25
METHOD OF HYDROSTATIC 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 (40°C) 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 puerpera l uterine inversion by the the hydrostatic method; reports of five cases. Eur cases. Eur J Obste t Gynecol Repro d Biol 1989;32:281-285. 1989;32:281-285. 2. South Australian Perinatal Practice Guidelines. Guidelin es. Maternity Care in in South Australia. Chapter 11; May 2009.
JOHNSON MANEUVER
The placenta is left in place. The operator’s hand grasps the inverted uterus with the placenta (see ( see figure fi gure A). The fundus is allowed all owed to rest on the palmar surface of the operator’s 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 operator’s 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 ( 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 Vando rsten JP. Diagnosis and management of uterine inversion. Operative obstetrics 2nd edition 2002; 15: 241-248. 2. World Health Organization. Organization. Managing Complications Complications in Pregnancy Pregnancy and Childbirth A Guide for Midwives and Doctors, Department of Reproductive Reproductive Health and Research, World Health Organization. Organization. 2000.
