31One-Step Conservative Surgery forAbnormal Invasive Placenta (PlacentaAccreta–Increta–Percreta)J. M. Palacios-Jaraquemada

INTRODUCTION

Fifty years ago, placenta accreta was an obstetric rarity.Today, however, placenta accreta and its variationsrepresent one of the principal causes of maternal mor-bidity and mortality. That this is the case is oftenattributed to the increased number of cesarean deliver-ies, but close examination of the numbers involvedsuggests that other factors may also be in operation.

The potential for the compromise of neighboringorgans, as well as the development of neo-vascularization, implies specific technical difficultiesassociated with the treatment of placenta accreta, all ofwhich directly relate to morbidity and mortality sec-ondary to hemorrhage. Placenta accreta, characterizedby the abnormal adherence of the placenta to themyometrium, may present different degrees of inva-sion, which are categorized as placenta accreta, incretaand percreta. Since these terms are all based onhistological examination, their proper use should bepostoperative as well as retrospective. From a clinicalperspective, the different degrees of invasion are moreappropriately termed placenta accreta or abnormalinvasive placenta.

The most common location of placenta accreta isthe anterior lower uterine wall, especially when associ-ated with a prior cesarean scar1–3. This associationimplies difficulties from a technical surgical point ofview including adherence to bladder, development ofneovascularization, destruction of myometrial tissueand access to the pelvic subperitoneal spaces. Theuteroplacental tissues of placenta accreta are noticeablyfragile and tend to bleed excessively. Absence of surgi-cal planes for dissection makes it difficult or nearlyimpossible to apply the usual hemostatic procedures ifan accurate tissue dissection between invaded tissuescannot be made.

Understanding the behavior and development ofplacenta accreta is essential in order to plan an appro-priate surgical approach. Various vascular occlusivemechanisms have been used to reduce the tendencyfor bleeding4–6, but they have not always been effec-tive and, in some cases, have been deficient. Issues

such as these have led to the need for a detailed studyof each aspect related to the treatment of placentaaccreta. One of the most important is to understandhow both the pelvic anastomotic system and thecollateral uterine vascular anastomoses work (seeChapters 1 and 22).

Predicting the surgical difficulty, as well as under-standing the specific invaded areas, is essential in orderto know which vascular pedicles are involved in agiven case. A combination of vascular control, fascialdissection and identification of specific pelvic elements(ureter or specific vessels) makes it possible to preventinjuries and to avoid complications. Once a primarydiagnosis has been arrived at, the next priority is toknow how and where the placenta invades theadjacent tissues.

Designing a one-time surgery implies solving all theproblems caused by placenta accreta at one operation.This involves vascular disconnection of the invadedorgans (uterus, placenta and bladder), correct compart-ment exposure of the pelvic organs (necessary forthe hemostatic procedures), total resection of theinvaded myometrium and, finally, uterine and vesicalreconstruction7.

One-step conservative surgery for abnormalplacentation (OSCS) was first implemented in 1990and, 20 years later, has been applied in more than 450patients. This series includes the most diverse typesand degrees of placental invasion, operated upon elec-tively as well as in emergency circumstances. To date,106 consecutive postrepair pregnancies have beenreported; of these, only two cases of partial recurrencewere noted. This number represents the lowest relapserate reported for conservative treatments in abnormalinvasive placenta.

PLACENTAL INVASION

For years, the absence of Nitabuch’s layer was consid-ered the main phenomenon that led to abnormal pla-cental invasion. However, numerous cases have beenreported where absence of Nitabuch’s layer coexisted

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with normal placentation. This observation suggeststhat the absence of this membrane might be a second-ary process, rather than the primary cause of abnormaladherence8. In mammals, damage to the uterine colla-gen modifies decidualization; as such, it is logical topropose that a deformed collagen scar (repeated cesar-ean, postsurgical damage, radiation, etc.) may have asimilar effect in the human being.

Placental invasion represents a highly complexphenomenon associated with numerous biochemicalinteractions. A series of myometrial mediators pro-mote a physiological limit to trophoblastic invasion. Incases of extreme myometrial thinning (e.g. previouscesarean scar), the placenta might not find this physio-logical limitation and thus invade the myometriumexcessively9. The absence of adequate vascular supportwould induce the secretion of vascular growth factors,the purpose of which would be to ensure sufficientplacental flow to the fetus. This phenomenon wouldpromote the opening and hypertrophy of microscopicanastomotic collaterals between the uteroplacental tis-sue, the bladder and the vagina. The vascular growthfactors allow the newly formed vessels to grow rapidlyand with a high flow. These characteristics are ideal tomaintain an optimal placental blood supply; on theother hand, they also represent a surgical nightmare.

Fortunately, not all placental invasions havecharacteristic newly formed vessels. This is because themechanism through which the placenta reaches theserosa is different. For placental advancement to occurthrough the myometrium there must be a prior tissuelesion. That is to say that placental advancement is aphysical fact secondary to rupture of the myometrium.If, on the other hand, this fact depended on an inva-sive characteristic of the placenta, we would be able tosee a similar percentage of invasions on all sides of theuterus, a phenomenon which has not been observed todate. All the evidence seems to indicate that if placen-tal implantation is adequately supplied with blood, theplacenta only advances through the myometrial defect.In contrast, if the placenta does not obtain an adequatevascular supply, the intense release of vascular growthfactors promotes the thickening of the vascularmicroanastomoses (newly formed vessels, also calledneovascularization).

SURGICAL ANATOMY

Morphological classification

Although three types of adherent placenta are foundthroughout the obstetrics literature (accreta, incretaand percreta), this classification is retrospective, histo-pathological in nature and of uncertain use in surgicalpractice. Moreover, efforts to find the correspondingdiagnostic images of this histological classification havebeen elusive. Finally, not even pathologists considerthe histological examination of placenta accreta as adiagnostic gold standard10,11. This apparent contradic-tion is supported by the fact that, in one specimen, alltypes and degrees of invasion may coexist. Therefore,

histological diagnosis only provides a report of the sitefrom which the sample was taken, and this area mayor may not be representative of the remainder ofthe invaded area. Unfortunately, however, histologicalclassification is relative to the degree of surgical diffi-culty; therefore, it is not always necessary to persistwith presurgical studies. For example, countless casesdescribe simple surgery for placenta percreta, andextremely difficult surgery with bleeding for localizedplacenta accreta. In contrast, classification accordingto invasion areas bears a close correlation with thepossibility of bleeding and surgical complexity; bothfeatures correspond to the origin of the blood supplyand to the difficulty in pelvic dissection. The classifica-tion based on invaded areas makes it possible to knowand plan how and on which vessels to perform vascularcontrol12,13.

From a surgical morphological point of view, threemain types of anterior placental adherences may bedistinguished14. In type 1 the anterior segment isnoticeably thinner and the placenta reaches the seroussurface, no newly formed placental–vesical or vesico-uterine vessels are identified, and there is a lax dividingplane between the posterior bladder wall and the ante-rior surface of the uterine segment (Figure 1). In type2 both the lower uterine segment and the posteriorwall of the bladder are noticeably thinner, there is nolax plane between both organs and a fibrous scar con-nects them, and no newly formed placental–vesical orvesicouterine vessels are observed (Figure 2). Type 3 ischaracterized by a thinner uterine segment, vesicalwall of variable thickness, presence of placental–vesicaland vesicouterine neovascular circulation and vesico-uterine plane with or without fibrous adherence(Figure 3).

This morphological, diagnostic and intrasurgicaldivision establishes the type of approach advisable foreach type. Type 1 usually constitutes the typical caselabelled diagnostic false positive. In this type, bothultrasound and placental magnetic resonance imaging(pMRI) show dehiscence with placental advancementwhich reaches the serosa; therefore, and from an

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Figure 1 Superior view of anterior placental invasion. Theplacenta reaches to the uterine serosa, but there is a lax dissectibletissue between posterior bladder wall and the placenta. BL, bladder

exclusively diagnostic point of view, these are casesof placenta percreta. However, once the newborn isdelivered, placental detachment can be performedwithout difficulty. There is no bleeding, and ondirect examination no remains of adherent placentaare observed. A more detailed examination – whichincludes dissection of the retrovesical plane – wouldshow a circular area of dehiscence hardly detectable ifit is not explored specifically.

Type 2 provides an apparent sensation of safetywhen the vesicouterine pouch is opened; the dissec-tion plane is narrow though manageable. While dis-section progresses, small and persistent hemorrhagicfoci occur which are difficult to control. The dissec-tion plane continues to be identifiable until thesurgeon unexpectedly sees the vesical mucosa or theFoley catheter. Access inside the bladder is almostimperceptible because dissection is performed on afibrosed plane that connects the posterior vesical wallwith the uterine scar. If, during dissection, the anteriorside of the placental invasion is injured, a severe high-pressure hemorrhage ensues, aggravated by the fetal

content. Attempts to achieve hemostasis or suture ofthe placental invaded area (extremely thinning) usuallyaggravate the blood loss due to uterine tissue rupture,making it essential to evacuate the uterus in order tocontrol the hemorrhage.

In type 3 the neovascular component must beligated and divided between double ligatures so as toaccess the vesicouterine space; the ligature maneuvermust always leave the main segment of the ligated ves-sel on the uterine side, because if the ligature is cut orreleased, the vessel which was cut off may easily beclamped with a hemostatic clamp. If this happens overthe vesical sector, it is convenient to perform a vascu-lar suture with polyglactin 000, which will includethe vesical muscular tunic, to provide the mechanicalsupport when suture is adjusted.

For the cases of fibrosis of the vesicouterine plane,it is advisable to open the anterior side of the para-metrium and to dissect medially the cervicovesicalspace. This plane is only rarely invaded; however,if this occurs, it may be dissected through stepwisevascular ligatures and vascular section. Once insidethis space, both fingers can be introduced laterally(Pelosi’s maneuver) through the vesicocervical plane.After this, dissection and ligature can be performedon all the newly formed vessels towards the cephalicsector15.

Induced neovascularization

Neovascularization is one of the main surgical prob-lems in abnormal invasive placenta. These vessels areusually of high caliber and flow, and even though theymay initially appear to have an anarchical pattern, theydo not. From an embryological point of view, the vas-cular growth to the pelvis is formed by magma ofinteranastomosed vessels. Once organ differentiationhas been established, many vessels develop whereasothers regress until they become invisible. However,when the appropriate conditions are present (vasculargrowth factors), these vessels can develop and establishanatomical connections not described in normalconditions.

In cases of anterior placenta accreta, newly formedvessels can be observed between the uterine, vesicaland vaginal arteries. Preoperative identification of theabnormal placental invasion enables planning ofthe approach and the technical tactics necessary toperform the specific vascular control of the pediclesinvolved.

Anatomy of newly formed vessels

It is usual to associate placenta accreta with newlyformed vessels that communicate with the placenta,uterus, bladder and neighboring tissues. Newlyformed vessels are generally of a large axial diameter,and they make adequate vascular exchange with theplacenta possible. Once abnormal placentation hasbeen established, the proliferation of angiogenic growthfactors enables the development of high-volume

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Figure 2 Superior view of anterior placental invasion. Noticethe dense fibrous bands between the posterior bladder wall and theplacenta. BL, bladder

Figure 3 Superior view of anterior placental invasion. Newlyformed vessels are present between posterior bladder wall and theabnormal placental invasion (black arrows) is evident. BL, bladder

newly formed vessels with fragile and less developedmedial muscular layers. Although these latter vesselsinitially appear to have an anarchic pattern, thisspecific arterial and venous vascular group has an orga-nized distribution14 at three anastomotic levels: (1)vesicouterine system (VUS), (2) placental–vesical sys-tem (PVS) and (3) colpouterine system (CUS). TheVUS habitually involves vessels that connect the uter-ine artery with the posterior-superior bladder wall andalso with the contralateral uterine artery. These aresuperficial vessels, and can be observed through thevesicouterine fold running transversally. The presenceof direct anastomoses of considerable size between theuterine arteries and the bladder must be consideredduring embolization, because this communication canbe a direct means to perform an undesired occlusion inthe vesical parenchyma (Figure 4).

The PVS is probably the best known, as it estab-lishes a connection between the placental vasculatureand the vesicular muscular layer, and is perpendicularto the vesicouterine plane. Anastomoses between thebladder and placenta (PVS) could be observed as thininterconnected net (Figure 5) as well as easily identifi-able thick cords (Figure 6). The PVS can send andreceive vessels from the entire surface of the posteriorbladder wall, and therefore make connections withbranches of the upper and lower vesical arteries,although it frequently does so with the upper vesicalpedicle.

Finally, the CUS is the anatomically most hidden(obscure) system, though probably it is the mostimportant physiologically. The CUS is located in thethickness of the anterior bladder wall and is parallel toits long axis; thus, it can only be identified throughdeep dissection of the retrovesical space. Nevertheless,on occasions CUS may not be visible at first sight,because its macroscopic visualization depends on thedegree of anastomotic vascular development, whichmay vary from imperceptible cords to the replacementof the vaginal muscular tunic for a noticeably devel-oped vascular plexus. The CUS connects the lower,middle and upper vaginal pedicles to the caudalbranches of the uterine artery, as well as theanastomotic intrauterine arcade, and is anatomicallylocated between its muscular fibers.

From a merely vascular point of view, thevesicouterine and placental–vesical anastomotic pedi-cles are likely to be controlled by endovascular occlu-sion of the uterine arteries (via transanastomotic flow).However, hemostasis of the colpouterine pediclecan be very difficult or nearly impossible, since itwould represent a high-flow anastomotic arcadebetween the vaginal and uterine pedicles. Endo-vascular access to CUS is improved by catheterizationof the internal pudendal artery, which is a branch ofthe posterior division of the iliac internal artery. Onthe other hand, CUS hemostasis can be performed in asimple, efficient and safe manner through square com-pression sutures, as described by Cho et al.16. Thismethod stops bleeding from specific areas regardless ofvessel origin.

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Figure 4 Superior view of lower uterus after reconstructivesurgery for abnormal invasive placenta. Black arrow shows a directanastomosis between transmedial interuterine anastomosis and thebladder

Figure 5 Superior viewing of anterior placental invasion. Blackarrows show a group of thin newly formed vessels between theposterior bladder wall and the placenta. BL, bladder

Figure 6 Superior view of anterior placental invasion. Blackarrows show evident and thick newly formed vessels between theplacenta and the bladder

Uterine anastomotic system

The uterus has two anastomotic systems: an upperone, supplied by the ovarian arteries; and a lowerone, supplied by the vaginal arteries (see Chapter 1)13.Of the two, the lower or vaginal pedicle is the onlyone that can maintain uterine vascular integrity whenboth uterine arteries have been occluded or ligated. Itis necessary to be aware, that simultaneous occlusionof the uterine arteries and the inferior vaginal artery(lower anastomotic pedicle) could produce uterinenecrosis by over devascularization. This lower anasto-motic system supplies collateral blood flow throughvessels of a higher caliber than the uterine artery, and ithas been shown that it is the major vascular supple-mentary system when the uterine arteries have beenoccluded.

The one-step surgery described below makes useof the occlusion of the uterine arteries, since mostanterior invasions are not supplied by collaterals of theuterine artery.

ONE-STEP CONSERVATIVE SURGERY

Stage 1: invasion area

Even though ultrasound represents an accuratemethod to diagnose placenta accreta, pMRI is themost useful technique to establish the exact area (topo-graphy) of the invasion. Certain aspects related to thespecific location of the invasion are essential whenresective surgery is performed, such as parametrialinvasion, and presence and location of newly formedvessels.

From a vascular point of view, the blood supply ofthe female generative tract can be divided into twoclearly defined areas. One involves the uterine bodyitself, labelled sector one (S1), and the other involvesthe lower uterine segment, cervix and vagina, labelledsector two (S2)13 (see also Chapter 1). S1 receives itsblood supply mainly from the respective bilateral uter-ine and ovarian arteries; S2, in contrast, is supplied bya series of subperitoneal vessels originating primarilyfrom internal pudendal arteries, secondarily fromcollaterals of the internal iliac artery and, to a lesserextent, by the uterine arteries. Precise knowledge ofthe location of the area of invasion makes it possible toplan efficient vascular control. For example, the occlu-sion of the uterine arteries or ligature of the anteriorbranch of the internal iliac artery in invasions in the S2area implies a high possibility of continued bleeding,because their branches arise from the posterior divisionof the internal iliac artery. This trunk connects theinternal iliac system with collaterals of the external iliacand the femoral arteries; therefore, this circumstanceleaves only two alternatives to control bleeding: aproximal vascular control at the level of the infrarenalaorta or a specific hemostatic control over tissue andprior to fascial dissection of the pelvis.

Both areas can be identified using images of amediosagittal pMRI slice12. If a perpendicular line isdrawn in the medial sector of the posterior side of the

bladder, two areas can be delineated, an upper onecorresponding to S1 invasions and a lower one, corre-sponding to S2 invasions. The sagittal plane also pro-vides information on the healthy myometrium abovethe cervix. In general, abnormal placental invasionnear the cesarean scar promotes an anterior bulge. Thisdetermines that healthy myometrium will move in acephalic and caudal direction. The myometrium supe-rior to the placental invasion is easily shown withultrasound, but this is not the case with the lowermyometrium. This detail is essential when planning aconservative procedure, since the absence of a healthymyometrium below the area of invasion – minimum2 cm – technically reduces the possibility of resectingthe invaded myometrium and of performing a safereconstruction.

Stage 2: surgical scheduling

The literature on the ideal moment to performelective surgery in placenta accreta is contradictory.Despite this, tacit consensus exists to operate betweenweeks 35 and 38. This time interval is governed by thepossibility of additional fetal lung maturation. There isa statistical increase in complications after week 35related to placenta percreta; however, it is not alwaysclear whether the authors used the same criteria todefine invasion (clinical or histological). The mostcommon complication in placenta accreta is bleeding,which is related to the disruption of the invaded area(uterine distension) attached to the placenta. In casesof anterior invasions, from week 35 the upper edge ofthe invasion extends beyond the upper wall of bladder.This phenomenon causes a lack of anterior parietalsupport, producing (spontaneously or through uterinedynamics) an additional disruption in the myometriumwith higher risk of bleeding. Also, the dynamictraction on the invaded myometrium could producevariable activation of the coagulation system and,therefore, activate fibrinolysis. This phenomenon maygo completely unnoticed and cause marked hypo-fibrinogenemia during the cesarean surgery. If thisalteration is not detected through the quantification offibrinogen and its degradation products after removingthe placenta or performing the hysterectomy, a capil-lary and continuous hemorrhage occurs. This type ofbleeding is very hard to treat, by either compressionsutures or endovascular treatment. For this reason,if plasma fibrinogen reaches levels near 200 or250 mg/dl before surgery, 1 U of cryoprecipitate per10 kg body weight must be provided, thawed andinfused before the surgery begins. This precautionis vital, because both hysterectomy and placentalremoval generally cause a decrease in fibrinogen levelsto between 100 and 200 mg/dl. If fibrinolysis alreadyhas begun, a further postpartum physiological reduc-tion would bring the fibrinogen level below its mini-mum hemostatic level to maintain a stable clot in theplacental bed17. Because lyophilized fibrinogen is notavailable in all centers, it is necessary to take into con-sideration that the time required to use cryoprecipitate

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(request, defrost, transport and administer) is notusually less than 45 minutes to 1 hour. Under suchcircumstances, it would require an excessively anddangerously long time to correct the defibrinationassociated hemorrhage in conjunction with othertechnical problems during surgery (see Chapter 4).

The presence of a moderate, profuse or recurrenthemorrhage, as well as active labor, is an indication fortermination of pregnancy. Nevertheless, and in spiteof the urgency, the best clinical, hematologic andhemostatic control must be provided before surgerycommences, as well as the most experienced surgicalteam.

Emergency

Whether in the presence of an ultrasound diagnosis ordiagnostic suspicion due to clinical record and history, itis advisable to start the surgery with four or more unitsof red cells and plasma available ‘in the surgical room’.Promises of immediate supply ‘when called’ are notacceptable, since the time to request, prepare and trans-port these agents may be excessive in the presence ofbleeding of more than 500 ml per minute which is thenorm in this type of abnormal placental invasion.

Basic hemostatic evaluation is recommended, aswell as investigation of fibrinogen levels. However,factor-1 quantification is not always available, and inmany centers it is only available after significant delays.In order to avoid this inconvenience, a 5 ml bloodsample must be obtained prior to the start of surgeryand placed in a dry test tube. The tube can be placed ina liquid bath at 37°C or under an assistant’s armpit.The sample is examined after 15–20 min; if it pro-duces a clot which remains firm when the tube isshaken, the fibrinogen level is correct. If the clotbreaks up when moved, the fibrinogen level is near100–150 mg%, and it is necessary to request cryo-precipitate immediately. On the other hand, if theblood does not coagulate, its level is below 50 mg%, afact that indicates a severe fibrinolytic process. In suchcases, it is advisable to administer lyophilized fibrino-gen or cryoprecipitates and also to request immedi-ately the supply of an equivalent dose to administerduring surgery19.

Although better fluid and blood replacement isunder current discussion, we prefer to use two wellplaced large-bore venous accesses to administer crys-talloids or Ringer’s lactate solution on a 3:1 ratio withrespect to estimated blood loss. Volumetric replace-ment maintains peripheral oxygenation, protects themicrocirculation and avoids multisystemic damage.Administration of fluids and blood replacement mustbe accomplished early, according to the basic clinicalsigns and before the development of arterial hypo-tension, because the compensating mechanisms of thepregnant woman could maintain acceptable levelswith blood losses of up to 30–40% of total volume.Since the contents of the circulatory system representapproximately 7% of body weight, the risk of shock ishigher in women with a small body mass and in those

with previous anemia or bleeding. Common mistakesassociated with management of bleeding from placentaaccreta include deficiency in recognizing bleedingseverity, insufficient fluid administration duringresuscitation and delay in stopping the bleeding19.

Besides the clinical signs of shock, it is absolutelynecessary to check the patient’s acid–base status usingan arterial sample in order to assess the efficacy ofresuscitation.

Presurgical measures

Standard blood tests are recommended, including acomplete coagulation profile. In normal conditions,this type of surgery is performed under epidural orspinal anesthesia; however, the presence of clinical orsubclinical coagulation disorders contraindicates eithertechnique.

Two large-caliber venous accesses are recom-mended, and the blood bank and laboratory servicemust be warned of the singular characteristic of thissurgery. Because abnormal placentation is a possiblecause of exsanguinating hemorrhage, before startingsurgery four cross-matched units of packed red bloodcells (pRBC) and four bags of fresh frozen plasma(FFP) should be on hand in the surgical room. Anadditional amount of pRBC, FFP, cryoprecipitate andplatelets should be on reserve and ready for immediateuse20. During surgery, communication between theanesthesiologists and the surgeon must be directedto assessing the estimated volume, the speed of bloodloss and avoiding any predictable hemodynamic orhemostatic deterioration.

Stage 3: laparotomy and initial evaluation

Pfannenstiel incision may provide sufficient access ifthe location of the invasive adherence is known andthe surgeon is experienced. However, when vascularcontrol either is or may be required at the aortic level,the essential incision must be median infraumbilicalwith cephalic extension. Regardless of incision type,the primary objective at this stage will consist ofwidely exposing the retrovesical space. When this areais apparently adherent to and fused with the placenta,it is not as technically difficult as might be thought(Figure 7). In order to identify the correct place fordissection, the bladder must be elevated with two Allisclamps, a maneuver which will noticeably simplifydissection, repair, ligature and section of the newlyformed vessels between bladder-invaded uterus andthe placenta. Dissection should start immediatelyinside the round ligament, from which a small button-hole can be made, which will include the peritoneumand newly formed vessels, which always must beligated between double ligatures. The poor muscularlayer of the newly formed vessels often allows them togo unnoticed during the pulling maneuvers, since theycollapse as veins. If they are inadvertently cut, this canbe a cause of postsurgery rebleeding and secondarymorbidity.

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This stage is slow and requires care, and dissectionof the new vessels must be made meticulously, sincethey are fragile and have high blood flow. On occa-sions, there is not much tissue between the two liga-tures; in this case, an incision on the vesical side ispreferred. If the ligature moves or if bleeding occurs, astitch can be made, which includes the vesical muscu-lar layer with polyglactin 000. On occasions, dissec-tion may be hindered by tissue fibrosis, which makesit difficult to identify a well-defined anatomical plane.In these circumstances, dissecting the vesical surgicalplane makes it possible to make a bridge, pass a fingerand then exert upward traction. This maneuver,described as a retrovesical bypass, is of great use andallows access to the posterior-lower sector of bladder.

Retrovesical dissection is finished when all newlyformed vessels between bladder, uterus and placentaare ligated, and the upper portion of the vagina isaccessible. At this moment, hysterectomy must beconsidered if repair is not considered possible, as mightoccur when there is segmental tissue destruction ofgreater than 50% of the organ’s axial circumference,or when tissue loss in the distal uterine segment leavesless than 2 cm of healthy segment above the uterinecervix.

Stage 4: hysterotomy

Once the anterior side of the uterus has been exposedand the newly formed vesico–uterine–placental vesselshave been interrupted, control of the colpouterinepedicle remains when the placenta has been removed.This is the reason why there is no risk of hemorrhageduring hysterotomy. Several authors are very carefulnot to make an incision in the placenta duringhysterotomy, and many use intraoperative ultrasoundto this aim. Hysterotomy can be performed in theupper sector of the invasive area in a completely safemanner. Even though there is placenta in this area, itsinsertion is normal and the newly formed vessels havebeen ligated; therefore, bleeding is not a problem. Atthis stage, it is advisable to apply the hysterotomymethod described for placenta previa21. Whenhysterotomy is performed, only the muscular layer iscut (Figure 8). Next, the hand is introduced betweenthe myometrium and the placenta until the sac isreached. After that, the baby is gently extracted andthe uterus exteriorized for better handling.

Stage 5: resection and hemostasis

Once the uterus has been exteriorized, the dissectionof the posterior side of the bladder can be completed ifnecessary. This maneuver allows clean access to theupper side of the vagina and uterine cervix, and isessential to obtain hemostasis of the colpouterine ves-sels. The inferior edge of the invasion can be trimmedwith scissors, in order manually to remove the placentawith the invaded myometrium in one piece. Next, thecavity is cleaned with a gauze pad or a Pinard curette(Figure 9). After fetal delivery and placental

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Figure 7 Superior view of anterior placental invasion. Afterligature of newly formed vessels the posterior bladder wall is easilydissected. BL, bladder

Figure 8 Cutting of the myometrium above the abnormalinvasive placenta. Notice that the hysterotomy is performed overthe placenta, but not over the newly formed vessels, which wereligated in a previous step

Figure 9 The entire placenta and invaded myometrium areremoved in one surgical piece. In this way, uterine reconstruction isperformed using healthy tissues

extraction, uterotonic drugs are administered, such asoxytocin (SyntocinonTM, Novartis, Brazil) 20 IU i.v.after fetal extraction, plus 20 IU i.v. within the first24 h, or carbetocin (DuratocinTM, Ferring, Argentina)100 mg i.v. in a single dose.

The colpouterine hemostasis component of theoperation is performed with a pair of square stitchesfollowing the technique described by Cho et al.16.With the aim of preventing hematometra, a Hegar’sbougy dilator #10 is placed in the uterine cervix,which will move towards one of the sides (Figure 10).In this manner the application of a square stitch is eas-ier, and the potential for accidental closure of theinternal cervical os is minimized. The advantage ofusing Cho’s suture relies on the fact that the surgeonworks on a surface instead of a specific pedicle. Inaddition, this procedure prevents inadvertent ureteralinjury, since it is applied on uterine tissue. When thehemostatic suture has been placed, any additionalbleeding can be checked. Due to the fragility of thenewly formed vessels, it is preferable to apply U-stitches in order to minimize the suture cutting effect.

Stage 6: repair

Once hemostasis has been achieved, it is necessaryto check that the fibrinogen level is higher than200 mg%. The repair is performed in two stages. Inthe first, U-stitches are made with polyglactin suture1 cm from the myometrial border. The aim with thesestitches is to coapt the borders and reduces tension onthe primary suture. In the first years of performing thissurgery, a reabsorbable net was applied with excellentresults; however, the net was not always available.For this reason, another anti-tension mechanism wasdesigned (Vicryl™ mesh (polyglactin 910) Ethicon,USA), which yielded identical results. The secondstage is to use a continuous suture with polyglactin1, which closes the borders and provides securehemostasis. On occasion, small muscular defects areobserved in some areas of the posterior wall of bladder.Such defects as well as any residual focal bleeding aresutured with polyglactin 000 (Figure 11).

When the repair has been completed, the incisionand dissection surfaces are inspected one more time,and a sheet of regenerated cellulose is placed as ananti-adhesion barrier between the bladder and theuterine repair.

Stage 7: postoperative care

Special attention must be paid to pain after one-stepsurgeries, as this type of surgery involves far moretissue disruption than is the case with a cesarean deliv-ery. A useful plan includes morphine administrationtogether with other painkillers starting in theimmediate postsurgery period, modified dependingon demand, and reduced on the second or third post-operative day.

One additional but important aspect of postopera-tive care is deep venous thrombosis prophylaxis.

Pregnancy, pelvic surgery and bed rest should beregarded as risk factors22. From an ideal point of view,it is advisable to use intermittent pneumatic compres-sors23. Low-molecular weight heparin can be adminis-tered when the platelet count is over 100,000/mm3,and until there is effective ambulation.

FOLLOW-UP

Control uterine studies were performed between5 and 10 months after repair. The first 100 patientswho underwent one-step conservative surgeries subse-quently had hysteroscopy to explore the cavity andscar characteristics. The study showed only two casesof uterine synechiae, which were related to the use ofchromic catgut. This follow-up procedure was laterreplaced by uterine T2-weighted MRI performedbetween 5 and 6 days before patient menses. UterineMRI makes it possible to observe the repaired areaclearly. Prior to the study, moderate urinary retentionis requested, which renders a whitish color on T2.This contrast, added to the whitish color of the

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Figure 10 Superior viewing of lower uterus, a Hegar bougy(black arrow) is placed in cervical canal to avoid unwanted lochiaocclusion during placement of Cho’s hemostatic sutures

Figure 11 Superior viewing of lower uterus, on the left, themuscular bladder defects is sutured with 000 polyglactin. Repaireduterus (black arrow)

premenstrual endometrium, makes it possible todefine precisely the repaired myometrium.

SUBSEQUENT PREGNANCIES

To date, 106 subsequent pregnancies have beenreported following this type of surgery, two cases ofanterior placenta previa coincided with both cases ofpartial recurrence.

GENERAL OVERVIEW

Placenta accreta is a leading cause of emergency post-partum hysterectomy. Although hysterectomy canbe a life-saving operation, it is associated with highmaternal mortality and subsequent morbidities24. Onother hand, conservative treatment leaving the pla-centa in situ has fewer complications of hemorrhagebut more of an infectious nature including septicshock, sepsis, infection, endometritis, wound infec-tion, peritonitis, pyelonephritis, vesicouterine fistulaand uterine necrosis25 among other medicalcomplications.

One-step conservative surgery eliminates uterinedamage and the entire placenta in the same surgicalact. Its technical complexity can be learned withsupervised instruction, as was the case with laparos-copy some years ago. Collaboration between countriescould help to introduce this procedure as standardtreatment for abnormal invasive placenta in the yearsto come.

References

1. Clark SL, Koonings PP, Phelan JP. Placenta previa/accretaand prior cesarean section. Obstet Gynecol 1985;66:89–92

2. Miller DA, Chollet JA, Goodwin TM. Clinical risk factors forplacenta previa/placenta accreta. Am J Obstet Gynecol 1997;177:210–4

3. Usta IM, Hobeika EM, Musa AA, Gabriel GE, Nassar AH.Placenta previa-accreta: risk factors and complications. Am JObstet Gynecol 2005;193:1045–9

4. Shih JC, Liu KL, Shyu MK. Temporary balloon occlusion ofthe common iliac artery: new approach to bleeding controlduring cesarean hysterectomy for placenta percreta. Am JObstet Gynecol 2005;193:1756–8

5. Andoh S, Mitani S, Nonaka A, et al. Use of temporary aorticballoon occlusion of the abdominal aorta was useful duringcesarean hysterectomy for placenta accreta. Masui 2011;60:217–9

6. Dubois J, Garel L, Grignon A, Lemay M, Leduc L. Placentapercreta: balloon occlusion and embolization of the internaliliac arteries to reduce intraoperative blood losses. Am JObstet Gynecol 1997;176:723–6

7. Palacios-Jaraquemada JM, Pesaresi M, Nassif JC, Hermosid S.Anterior placenta percreta: surgical approach, hemostasis anduterine repair. Acta Obstet Gynecol Scand 2004;83:738–44

8. Pijnenborg R, Vercruysse L. Shifting concepts of the fetal-maternal interface: A historical perspective. Placenta 2008;29(Suppl A):S20–5

9. Tantbirojn P, Crum CP, Parast MM. Pathophysiology of pla-centa creta: the role of decidua and extravillous trophoblast.Placenta 2008;29:639–45

10. Khong TY, Werger AC. Myometrial fibers in the placentalbasal plate can confirm but do not necessarily indicate clinicalplacenta accreta. Am J Clin Pathol 2001;116:703–8

11. Jacques SM, Qureshi F, Trent VS, Ramirez NC. Placentaaccreta: mild cases diagnosed by placental examination. Int JGynecol Pathol 1996;15:28–33

12. Palacios-Jaraquemada JM, Bruno CH. Magnetic resonanceimaging in 300 cases of placenta accreta: surgical correlationof new findings. Acta Obstet Gynecol Scand 2005;84:716–24

13. Palacios-Jaraquemada JM, García Mónaco R, Barbosa NE,Ferle L, Iriarte H, Conesa HA. Lower uterine blood supply:extrauterine anastomotic system and its application in surgicaldevascularization techniques. Acta Obstet Gynecol Scand2007;86:228–34

14. Palacios-Jaraquemada JM. Abnormal Invasive Placenta, 1stedn. Berlin: DeGruyter, 2012

15. Pelosi MA 3rd, Pelosi MA. Modified cesarean hysterectomyfor placenta previa percreta with bladder invasion: retrovesicallower uterine segment bypass. Obstet Gynecol 1999;93:830–3

16. Cho JH, Jun HS, Lee CN. Hemostatic suturing technique foruterine bleeding during cesarean delivery. Obstet Gynecol2000;96:129–31

17. Palacios-Jaraquemada JM, Bruno CH, Clavelli WA. Morbidadherent placenta: prediction, diagnosis and management.Fetal Matern Med Rev 2007;18:357–81

18. de Lloyd L, Bovington R, Kaye A, et al. Standard haemostatictests following major obstetric haemorrhage.Int J ObstetAnesth 2011;20:135–41

19. Lombaard H, Pattinson RC. Common errors and remediesin managing postpartum haemorrhage. Best Pract Res ClinObstet Gynaecol 2009;23:317–26

20. Snegovskikh D, Clebone A, Norwitz E. Anesthetic manage-ment of patients with placenta accreta and resuscitationstrategies for associated massive hemorrhage. Curr OpinAnaesthesiol 2011;24:274–81

21. Ward CR. Avoiding an incision through the anterior previaat cesarean delivery. Obstet Gynecol 2003;102:552–4

22. Davis SM, Branch DW. Thromboprophylaxis in pregnancy:who and how? Obstet Gynecol Clin North Am 2010;37:333–43

23. Casele H, Grobman WA. Cost-effectiveness of thrombo-prophylaxis with intermittent pneumatic compression atcesarean delivery. Obstet Gynecol 2006;108:535–40

24. Varras M, Krivis Ch, Plis Ch, Tsoukalos G. Emergencyobstetric hysterectomy at two tertiary centers: a clinicalanalysis of 11 years experience. Clin Exp Obstet Gynecol2010;37:117–9

25. Sentilhes L, Kayem G, Ambroselli C, et al. Fertility andpregnancy outcomes following conservative treatment forplacenta accreta. Hum Reprod 2010;25:2803–10

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One-Step Conservative Surgery for Abnormal Invasive Placenta (Placenta Accreta–Increta–Percreta)