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Obstentrics_Williams. Tornblom-Paulander S, Tingaker BK, Werner A, et al: Novel topical formulation of lidocaine provides signiicant pain relieffor intrauterine device insertion: pharmacokinetic evaluation and randomized placebo-controlled trial. Ferril Steriln103(2):422, 2015 Trussell J: Contraceptive eicacy. In Hatcher A, Trussell J, Nelson AL, et al (eds): Contraceptive Technology, 20th ed. New York, Ardent Media, 2011a Trussell J: Contraceptive failure in the United States. Contraception 70:89, 2011b Tsilidis KK, Allen NE, Key TJ, et al: Oral contraceptive use and reproductive factors and risk of ovarian cancer in the European Prospective Investigation into Cancer and Nutrition. Br J Cancer 105(9): 1436,n2011 Turok OK, Eisenberg DL, Teal SB, et al: A prospective assessment of pelvic infection risk following same-day sexually transmitted infection testing and levonorgestrel intrauterine system placement. Am J Obstet Gynecol 215(5):599.el, 2016


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Obstentrics_Williams. Urdl W, Apter 0, Alperstein A, et al: Contraceptive eicacy, compliance and beyond: factors related to satisfaction with once-weekly transdermal compared with oral contraception. Eur J Obstet Gynecol Reprod Bioi 121n:202, 2005 van H ylckama Vlieg A, Helmerhorst FM, Vandenbroucke JP, et al: The venous thrombotic risk of oral contraceptives, efects of oestrogen dose and progestogen type: results of the MEGA case-control study. BMJ 339:b2921, 2009 Van Vliet A, Grimes DA, Helmerhorsr FM, et al: Biphasic versus mono phasic oral contraceptives for contraception. Cochrane Database Syst Rev 6:CD002032, 2006, Reairmed 2011a Van Vliet HA, Grimes DA, Lopez LM, et al: Triphasic versus monophasic oral contraceptives for contraception. Cochrane Database Syst Rev 11:CD003553,n2011b Van Vliet HA, Raps M, Lopez LM, et al: Quadriphasic versus monophasic oral contraceptives for contraception. Cochrane Database Syst Rev 1ln:CD009038,n2011c


Obstentrics_Williams

Obstentrics_Williams. Van Vliet HA, Raps M, Lopez LM, et al: Quadriphasic versus monophasic oral contraceptives for contraception. Cochrane Database Syst Rev 1ln:CD009038,n2011c Veres S, Miller L, Burington B: A comparison between the vaginal ring and oral contraceptives. Obstet Gynecol 104:555, 2004 Verhoeven CH, Dieben TO: he combined contraceptive vaginal ring, NuvaRing, and tampon co-usage. Contraception 69(3): 197, 2004a Verhoeven CH, van den Heuvel MW, Mulders TM, et al: The contraceptive vaginal ring, NuvaRing, and antimycotic co-medication. Contraception 69(2): 129, 2004b Vessey MP, Johnson B, Doll R, et al: Outcome of pregnancy in women using intrauterine devices. Lancet 1 :495, 1974 Vessey MP, Meisler L, Flavel R, et al: Outcome of pregnancy in women using diferent methods of contraception. Br J Obstet Gynaecol 86:548, 9 Vickery Z, Madden T, Zhao Q, et al: Weight change at 12 months in users of three progestin-only contraceptive methods. Contraception 88(4):503, 2013


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Obstentrics_Williams. Vinogradova Y, Coupland C, Hippisley-Cox J: Use of combined oral contraceptives and risk of venous thromboembolism: nested case-control studies using the QResearch and CPRD data-bases. BMJ 350:h2135, 2015 Wallach M, Grimes DA (eds): Modern Oral Contraception. Updates from he Contraception Report. Totowa, Emron, 2000 Walsh T, Grimes 0, Frezieres R, et al: Randomised controlled trial of prophylactic antibiotics before insertion of intrauterine devices. IUD Study Group. Lancet 351:1005, 1998 Watson: Ella prescribing information. 2010. Available at: http://www.access data. fda.govl drugsatfda_docs/labell20 1 01022474s0001bl.pdf. Accessed December 27,n2016 Wechselberger G, Wolfram 0, Piilzl P, et al: Nerve injury caused by removal of an implantable hormonal contraceptive. Am J Obstet Gynecol 195(1):323, 2006 Westhof C: IUDs and colonization or infection with Actinomyces. Contraception 75:S48, 2007a


Obstentrics_Williams

Obstentrics_Williams. Westhof C: IUDs and colonization or infection with Actinomyces. Contraception 75:S48, 2007a WesthofC, Heartwell S, Edwards S, et al: Initiation of oral contraceptive using a quick start compared with a conventional start: a randomized controlled trial. Obstet Gynecoln109:1270, 2007b Westhof C, Jain JK, Milson, et al: Changes in weight with depot medroxyprogesterone acetate subcutaneous injection 104 mg/0.65 mL. Contraception 75:261,n2007c Westhof C, Kerns J, Morroni C, et al: Quick start: novel oral contraceptive initiation method. Contraception 66: 141, 2002 WesthofC, Wieland 0, Tiezzi L: Depression in users of depo-medroxyprogesterone acetate. Contraception 51(6):351,n1995 Westhof CL, T orgal AH, Mayeda ER, et al: Pharmacokinetics of a combined oral contraceptive in obese and normal-weight women. Contraception 81(6):474,n2010


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Obstentrics_Williams. Westhof CL, T orgal AH, Mayeda ER, et al: Pharmacokinetics of a combined oral contraceptive in obese and normal-weight women. Contraception 81(6):474,n2010 Whitaker AK, Chen BA, Borgatta L: Society of Family Planning Guidelines: postplacental insertion of intrauterine devices. Contraception October 5, 20n17 [Epub ahead of print) Wilailak S, Vipupinyo C, Suraseranivong V, et al: Depot medroxyprogesterone acetate and epithelial ovarian cancer: a multicentre case-control study. BJOG 119(6):672,2012 World Health Organization: A multinational case-control study of ectopic pregnancy. Clin Reprod Ferriln3:131, 1985 World Health Organization: Acute myocardial infarction and combined oral contraceptives: results of an international multi-center case-control study. Lancet 349:1202, 1997


Obstentrics_Williams

Obstentrics_Williams. World Health Organization: Acute myocardial infarction and combined oral contraceptives: results of an international multi-center case-control study. Lancet 349:1202, 1997 World Health Organization: Cardiovascular disease and use of oral and injectable progestogen-only contraceptives and combined injectable contraceptives. Resulrs of an international, multicenter, case-control study. Contraception 57:315, 1998 World Healrh Organization: Depot-medroxyprogesterone acetate (DMPA) and risk of endometrial cancer. Int J Cancer 49: 186, 1991a World Health Organization: Depot-medroxyprogesterone acetate (DMPA) and risk of invasive squamous cell cervical cancer. Contraception 45(4): 299, 1992 World Health Organization: Depot-medroxyprogesterone acetate (DMPA) and risk of liver cancer. Int J Cancer 49(2):182, 1991b World Health Organization: Efects of hormonal contraceptives on breast milk composition and infant growth. Stud Fam Plann 19/361, 1988


Obstentrics_Williams

Obstentrics_Williams. World Health Organization: Efects of hormonal contraceptives on breast milk composition and infant growth. Stud Fam Plann 19/361, 1988 World Health Organization: Ischaemic stroke and combined oral contraceptives: results of an international, multi-center case-control study. Lancet 348:498, 1996 World Health Organization: Mechanism of action, safety and eicacy of intrauterine devices. Technical Reporr No. 753, Geneva, Switzerland, WHO, 1987 World Health Organization: vledical Eligibility for Contraceptive Use, 5th ed. Geneva, World Health Organization, 2015 Wu S, Godfrey EM, Wojdyla 0, et al: Copper T380A intrauterine device for emergency contraception: a prospective, multicentre, cohort clinical trial. BJOG 117(10):1205,2010 XU JX, Remedios E, Duthie A, et al: Intrauterine contraceptive device: cause of small bowel obstruction and ischaemia. ANZ J Surg May 26, 2015 [Epub ahead of print)


Obstentrics_Williams

Obstentrics_Williams. XU JX, Remedios E, Duthie A, et al: Intrauterine contraceptive device: cause of small bowel obstruction and ischaemia. ANZ J Surg May 26, 2015 [Epub ahead of print) XU JX, Rivera R, Dunson TR, et al: A comparative study of two techniques used in immediate postplacental insertion (IPPI) of the Copper T-380A IUD in Shanghai, People's Republic of China. Contraception 54(1):33, 1996 Yamazaki M, Dwyer K, Sobhan M, et al: Efect of obesity on the efectiveness of hormonal contraceptives: an individual participant data meta-analysis. Contraception 92(5):445, 2015 Yonkers A, Brown C, Pearlstein TB, et al: Eicacy of a new low-dose oral contraceptive with drospirenone in premenstrual dysphoric disorder. Obstet Gynecol 106:492, 2005 Zeino MY, Wietfeldt ED, Advani V, et al: Laparoscopic removal of a copper intrauterine device from the sigmoid colon. JSLS 15(4):568,n2011


Obstentrics_Williams

Obstentrics_Williams. Zeino MY, Wietfeldt ED, Advani V, et al: Laparoscopic removal of a copper intrauterine device from the sigmoid colon. JSLS 15(4):568,n2011 Zieman M, Guillebaud J, Weisberg E, et al: Contraceptive eicacy and cycle control with the Orrho Evra/Evra transdermal system: the analysis of pooled data. Fertil Steril 77:S13, 2002 PUERPERAL TUBAL STERILIZATION.................702 NON PUERPERAL TUBAL STERILIZATION............ 704 COMPLICATIONS. . . . . . . ............. 704 TRANSCERVICAL STERILIZATION................... 705 VASECTOMY....................................706 In order, therore, to render a woman permanenty sterile by an operation upon the tubes, they must be excised by wedge-shaped incisions at the cornua of the uterus and the wounds closed by sutures. -J. Whitridge Williams (1903)


Obstentrics_Williams

Obstentrics_Williams. -J. Whitridge Williams (1903) Sterilization is a popular choice of contraception for millions of men and women. Among women using contraception, one third rely on either male or female sterilization (Daniels, 2015). This procedure is indicated in those requesting sterilization and who clearly understand its permanence and its diicult and often unsuccessful reversal. All persons considering sterilization should also be counseled regarding alternative contraceptive choices (American College of Obstetricians and Gynecologists, 2017a,c). Female sterilization is usually accomplished by occlusion, excision, or division of the fallopian tubes. Puerperal sterilization procedures follow cesarean or vaginal delivery and approximately 7 percent of all live births in the United States (Moniz, 2017). Nonpuerperal tubal sterilization is done at a time unrelated to recent pregnancy and is also termed interval sterilization.


Obstentrics_Williams

Obstentrics_Williams. For several days postpartum, the uterine fundus lies at the level of the umbilicus, and fallopian tubes are accessible directly beneath the abdominal wall. Moreover, abdominal laxity allows easy repositioning of the incision over each uterine cornu.


Obstentrics_Williams

Obstentrics_Williams. On our service, puerperal tubal ligation is performed by a surgical team dedicated to this role the morning after delivery. This timing minimizes hospital stay but lowers the likelihood that postpartum hemorrhage would complicate recovery following surgery. In addition, the status of the newborn can be better ascertained before surgery. In contrast, some prefer to perform sterilization immediately following delivery and use neuraxial analgesia already placed for labor. In this model, barriers to sterilization can be lessened by designating these postpartum surgeries as urgent, especially in high-volume labor and delivery units, which usually prioritize limited operating-room availability for intrapartum procedures (American College of Obstetricians and Gynecologists, 2016; Potter, 2013).


Obstentrics_Williams

Obstentrics_Williams. Various techniques are now used to disrupt tubal patency. In general, a midtubal segment of fallopian tube is excised, and the severed ends seal by fibrosis and peritoneal regrowth. Commonly used methods of puerperal sterilization include the Parkland, Pomeroy, and modiied Pomeroy techniques (American College of Obstetricians and Gynecologists, 2017a). Less often, Filshie clips are used (Madari, 2011). Irving and Uchida techniques or Kroener fimbriectomy are rarely used because of their increased required dissection or unfavorably high failure rates. Also, in the absence of uterine or other pelvic disease, hysterectomy solely for sterilization at the time of cesarean delivery, early in the puerperium, or even remote from pregnancy is diicult to justiy. It carries significantly increased surgical morbidity compared with tubal sterilization.


Obstentrics_Williams

Obstentrics_Williams. Evidence suggests that the fallopian tube may be the origin of pelvic serous carcinomas, especially those of the ovary. With this knowledge, the Society of Gynecologic Oncologists (2013) and American College of Obstetricians and Gynecologists (2017b) recommend consideration of salpingectomy to lower cancer risks. Speciically, for women at average risk of ovarian cancer, risk-reducing salpingectomy should be discussed and considered with patients at the time of abdominal or pelvic surgery, at hysterectomy, or in lieu of tubal ligation. Spinal analgesia is typically selected for cases scheduled for the first postpartum day. If done more proximate to delivery, the same epidural catheter used for labor analgesia can be used for sterilization analgesia. Notably, for those with preeclampsia, HELLP (hemolysis, �levated liver enzyme levels, low 2latelet count) syndrome, or gestational thrombocytopenia, platelet levels should be > 100,000 for spinal blockade (Chap. 25, p.


Obstentrics_Williams

Obstentrics_Williams. HELLP (hemolysis, �levated liver enzyme levels, low 2latelet count) syndrome, or gestational thrombocytopenia, platelet levels should be > 100,000 for spinal blockade (Chap. 25, p. 496). General anesthesia may be less desirable due to residual pregnancy-related airway vulnerabilities (Bucklin, 2003). The bladder is emptied before surgery to avoid its laceration. A full bladder can also push the fundus above the umbilicus.


Obstentrics_Williams

Obstentrics_Williams. A small infraumbilical incision is ideal for several reasons. As noted, the fundus in most cases lies near the umbilicus. Second, the umbilicus usually remains the thinnest portion of the anterior abdominal wall and requires less subcutaneous dissection to reach the linea alba fascia. hird, an infraumbilical incision ofers fascia with suicient integrity to provide a closure that has minimal risk for later incisional hernia. Last, incisions that follow the natural curve of the lower umbilical skin fold yield suitable cosmesis. A 2-to 4-cm transverse or vertical skin incision is usually suicient for normal-weight women. For obese women, a 4-to 6-cm incision may be needed for adequate abdominal access.


Obstentrics_Williams

Obstentrics_Williams. Beneath this incision, the subcutaneous tissue is bluntly separated to reach the linea alba fascia. For this, an Allis clamp can be opened and closed as downward pressure is exerted. Similarly, the blades of two army-navy retractors both pulling in downward yet opposite directions can part the subcutaneous layer. Clearing this fatty tissue away from the fascia isolates the fascia for incision and for later closure without intervening fat, which may impede wound healing.


Obstentrics_Williams

Obstentrics_Williams. he fascial incision may be transverse or vertical and follows the same orientation of the skin incision. For this, once the linea alba is reached, it is grasped with two Allis clamps-one placed on either side of the planned fascial incision. The purchase of tissue with each clamp should be substantial and creates a small roll of fascia to be incised. Often, the peritoneum is incorporated simultaneously and entered. If not, the peritoneum is grasped with two hemostats and sharply cut. Others may prefer to bluntly enter with a single index finger. Notably, if the initial fascial incision is too small, it can be extended with curved Mayo scissors.


Obstentrics_Williams

Obstentrics_Williams. Adequate exposure is critical, and army-navy or appendiceal retractors are suitable. For obese women, a slightly larger incision and narrow deeper retractors may be required. If bowel or omentum is obstructing, Trendelenburg position can help displace these cephalad. Digitally packing with a single, moist, fanned-out piece of surgical gauze can also be used, but a hemostat should always be attached to the distal end to avert


Obstentrics_Williams

Obstentrics_Williams. FIGURE 39-1 Parkland method. A.An avascular site in the meso salpinx adjacent to the fallopian tube is perforated with a small hemostat. The jaws are opened to separate the fallopian tube from the adjacent mesosalpinx for approximately 2.5 cm. B. The freed fallopian tube is ligated proximally and distally with O-chromic suture. The intervening segment of approximately 2 cm is excised, and the excision site is inspected for hemostasis. This method was designed to avoid the initial intimate proximity of the cut ends of the fallopian tube inherent with the Pomeroy procedure. (Reproduced with permission from Hoffman BL, Corton MM: Surgeries for benign gynecologic conditions. In Hoffman BL, Schorge JO, Bradshaw KD, et al: Williams Gynecology, 3rd ed. New York, McGraw-Hili Education, 201o6.) its retention. At times, tilting the entire table to the opposite side of the tube being exposed assists tube isolation.


Obstentrics_Williams

Obstentrics_Williams. he fallopian tube is identiied and grasped at its midportion with a Babcock clamp, and the distal fimbria conirmed. his prevents confusing the round ligament with the midportion of the tube. A common reason for sterilization failure is ligation of the wrong structure, typically the round ligament. Therefore, identiication and isolation of the distal tube prior to ligation is necessary. Whenever the tube is inadvertently dropped, it is mandatory to repeat this identification process. Surgical steps for ligation are outlined in Figures 39-1 and 39-2. FIGURE 39-2 Pomeroy method. During ligation of a tubal loop, plain catgut is used to ensure prompt absorption of the ligature and subsequent separation of the severed tubal ends. (Reproduced with permission from Hoffman BL, Corton MM: Surgeries for benign gynecologic conditions. In Hoffman BL, Schorge JO, Bradshaw KD, et al: Williams Gynecology, 3rd ed. New York, McGraw-Hili Education, 201o6.)


Obstentrics_Williams

Obstentrics_Williams. Steps of salpingectomy are shown in Figure 39-3. he umbilical incision generally will need to be larger to allow an adequate view of the tube and mesosalpinx and to place clamps. With total salpingectomy, the entire mesosalpinx must be divided to free the fallopian tube. In two small cohorts undergoing salpingectomy ater vaginal birth, surgical times were longer than for tubal occlusion, and in one report, blood loss was increased (Danis, 2016; Powell, 2017). With salpingectomy and cesarean delivery, total blood loss rates were not statistically higher (Powell, 2017; Shinar, 2017). After surgery, diet is given as tolerated. Ileus is infrequent and should prompt concern for bowel injury, albeit rare. Most women have an uncomplicated course and are discharged on the first postoperative day.


Obstentrics_Williams

Obstentrics_Williams. These techniques and other modiications basically consist of (1) ligation and resection at laparotomy as described earlier for puerperal sterilization; (2) application of permanent rings, clips, or inserts to the fallopian tubes by laparoscopy or hysteroscopy; or (3) electrocoagulation of a tubal segment, usually through a laparoscope. A detailed description and illustration of these can be found in Wiliams Gynecoloy, 3rd edition (hompson, 2016).


Obstentrics_Williams

Obstentrics_Williams. In the United States, a laparoscopic approach to interval tubal sterilization is the most common. The procedure is frequently performed in an ambulatory surgical setting under general anesthesia. In almost all cases, the woman can be discharged within several hours. Minilaparotomy using a 3-cm suprapubic incision is also popular, especially in resource-poor countries. Major morbidity is rare with either minilaparotomy or laparoscopy. lthough not often used, the peritoneal cavity can be entered through the posterior vaginal fornix via colpotomy to perform tubal interruption. Pregnancy following sterilization is infrequent. The Collaborative Review of Sterilization (CREST) study followed 10,863 women who had undergone tubal sterilization from 1978 through 1986 (Peterson, 1996). he cumulative failure rate for the various tubal procedures was 18.5 per 1000 or approximately


Obstentrics_Williams

Obstentrics_Williams. FIGURE 39-3 A. With salpingectomy, the mesosalpinx is sequentially clamped, cut, and ligated. B. At the cornu, clamps are placed across the fallopian tube and its adjacent mesosalpinx prior to tubal transection. (Reproduced with permission from Stuart GS: Puerperal sterilization. In Yeomans ER, Hoffman BL, Gilstrap, III, et al (eds): Cunningham and Gilstrap's Operative Obstetrics, 3rd ed. New York, McGraw-Hili, 201o7.) 0.5 percent. The study found puerperal sterilization to be highly efective. The 5-year failure rate was 5 per 1000, and for 12 years, it was 7 per 1000. Puerperal sterilization fails for two major reasons. First, sur gical errors occur and include transection of the round ligament or only partial transection of the tube. For this reason, both tubal segments are submitted for pathological confirmation. Second, a fistulous tract or spontaneous reanastomosis may form between the severed tubal stumps.


Obstentrics_Williams

Obstentrics_Williams. Second, a fistulous tract or spontaneous reanastomosis may form between the severed tubal stumps. Approximately 30 percent of pregnancies that follow a failed tubal sterilization procedure are ectopic. his rate is 20 percent for those following a postpartum procedure (Peterson, 1996, 1997). hus, any symptoms of pregnancy in a woman after tubal sterilization must be investigated, and an ectopic preg nancy excluded. Overall, risks for ovarian cancer decline and for breast cancer are unafected following sterilization (Gaudet, 2013; Pearce, 2015). Women who have undergone tubal sterilization are highly unlikely to subsequently have salpingitis (Levgur, 2000). For menorrhagia and intermenstrual bleeding following tubal sterilization, most studies of the risk have found no association (DeStefano, 1985; Peterson, 2000; Shy, 1992).


Obstentrics_Williams

Obstentrics_Williams. Less objective but important psychological sequelae of sterilization have also been evaluated. In the CREST study, Costello (2002) found that tubal ligation did not change sexual interest or pleasure in 80 percent of women. In most of the 20 percent of women who did report a change, positive efects were 10 to 15 times more likely. Invariably, a number of women express regrets regarding sterilization, and this is especially true if it is performed at a younger age (Curtis, 2006; Kelek:i, 2005). In the CREST study, Jamieson (2002) reported that 7 percent of women who had undergone tubal ligation had regrets by 5 years. his is not limited to their own sterilization, because 6.1 percent of women whose husbands had undergone vasectomy had similar regrets.


Obstentrics_Williams

Obstentrics_Williams. No woman should undergo tubal sterilization believing that subsequent fertility is guaranteed either by surgery or by assisted reproductive techniques. Both approaches are technically dificult, expensive, and not always successful. In general, pregnancy rates after tubal reversal favor women with age younger than 35 years, with 7 cm of remaining tube, with a short time from antecedent sterilization, and with isthmic-isthmic repairs. With reanastomosis via laparotomy, rates of live births range from 44 to 82 percent (Deieux, 2011; Malacova, 2015). The rate of ectopic pregnancy is 2 to 10 percent after reanastomosis (American Society for Reproductive Medicine, 2015). With reanastomosis to reverse Essure sterilization, only 27 percent of women had subsequent live births (Monteith, 2014).


Obstentrics_Williams

Obstentrics_Williams. Devices can be inserted via hysteroscopy to occlude the proximal fallopian tubes. he Essure micro insert has a ine stainless-steel inner coil enclosed in polyester fibers and an expandable outer coil of Nitinol-a nickel and titanium alloy (Fig. 39-4). he outer coil expands after placement, allowing the inner fibers to expand. These synthetic fibers incite a chronic inflammatory response to prompt local tissue ingrowth that leads to complete tubal lumen occlusion. For hysteroscopic placement, sedation, paracervical block, or both may be used, and in-oice insertion is often elected. Devices cannot be placed in all women, and some do not tolerate the procedure while awake (DuY, 2005). Bilateral placement is achieved in 81 to 98 percent of cases on a first attempt (la Chapelle, 2015).


Obstentrics_Williams

Obstentrics_Williams. FIGURE 39-4 Essure microinsert placement hysteroscopically and ingrowth of tissue. (Reproduced with permission from Thompson M, Kho K: Minimally invasive surgery. In Hoffman BL, Schorge JO, Bradshaw KD, et al (eds): Williams Gynecology, 3rd ed. New York, McGraw-Hill,o201o6.) Since the introduction of Essure, cited adverse events include abnormal bleeding, perforation of the uterus or fallopian tubes from device migration, and allergy or hypersensitivity reactions, especially to the nickel component (Al-Sai, 2013; IIao, 2015). Some events resulted in device removal that requires abdominal surgery (Casey, 2016; Lazorwitz, 2017). To provide more information of the risks and beneits, the Food and Drug Administration (2016) has drafted a black box warning and patient-decision checklist to aid counseling.


Obstentrics_Williams

Obstentrics_Williams. Because complete tubal blockage is not 100 percent, it must be conirmed by hysterosalpingography (HSG) 3 months following surgery (Bayer Healthcare, 2002). With such confirmation, eicacy rates for these devices reach 98 to 99 percent (Chudnof, 2015; Munro, 2014). In real-world settings, pregnancies following transcervical sterilization are most frequently attributed to conception before insertion or HSG and to noncompliance with HSG or its misinterpretation. Although data are limited to small case series, pregnancies conceived with Essure in place do not appear to be at increased risk from the device (Arora, 2014; Veersema, 2014). Another insert, Adiana, also stimulates tissue ingrowth for tubal occlusion using a cylindrical, nonabsorbent silicone elastomer matrix. However, for inancial reasons, production of this device has now been discontinued by the manufacturer


Obstentrics_Williams

Obstentrics_Williams. Vasectomy is safer than tubal sterilization because it is less invasive and is performed with local analgesia (American College of Obstetricians and Gynecologists, 2017a). In a review to compare the two, Hendrix and associates (1999) found that, compared with vasectomy, female tubal sterilization rate, a 10-to 37 -fold failure rate, and costs three times as much. Incision on left side of One disadvantage is that sterilizascrotum, and in tunica tion following vasectomy is not immediate. Complete release of sperm stored V2" of duct removed Incision on in the reproductive tract beyond the right side Ends are sealed interrupted vas deferens takes approximately 3 months or 20 ejaculations.Epididymis The American Urological Association recommends a postprocedural semen analysis at 8 to 16 weeks to document sterility (Sharlip, 2012). During the period before azoospermia is documented, another form of contraception should be used.


Obstentrics_Williams

Obstentrics_Williams. FIGURE 39-5 Anatomy of male reproductive system showing procedure for vasectomy. The failure rate for vasectomy dur (Hologic, 2012). hat said, patients with these inserts may be encountered and can consider their device efective. lthough not currently available in the United States, quinacrine pellets cause sclerosis at the tubal ostia. Placement at the uterine fundus with an IUD-type inserter method allows pellet migration into the tubal ostia. Of drawbacks, prior cancer associations have been disproved (Sokal, 201 Oa,b). Eicacy appears enhanced by technique modification. In one early cohort of 1335 treated women, pregnancy rates at 10 years were 12 percent (Sokal, 2008). Following insertion technique improvement, a 2-year failure rate of 1.2 percent was calculated by Lippes (2015).


Obstentrics_Williams

Obstentrics_Williams. Currently, up to a half million men in the United States undergo vasectomy each year (Barone, 2006; Eisenberg, 2010). And 5 percent of women rely on this method for contraception (Daniels, 2015). For sterilization, the vas deferens lumen is disrupted to block the passage of sperm from the testes. Most commonly, a no-scapel vasectomy (NS) accomplishes this with one specialized instrument that grasps the vas deferens and surrounding skin together. A second dissector tool punctures the skin and then isolates the vas (Rogers, 2013). As clariied by the American Urological Association, minimaly invasive vasectomy includes any vas isolation procedure, including the no-scalpel technique, which uses a skin incision measuringr:;1 cm and requires minimal vas dissection (Fig. 39-5) (Sharlip, 2012). Compared with conventional vasectomy that employs incisions > 1 cm and greater dissection, the no-scalpel technique is associated with fewer minor surgical complications, but each is equally efective


Obstentrics_Williams

Obstentrics_Williams. Compared with conventional vasectomy that employs incisions > 1 cm and greater dissection, the no-scalpel technique is associated with fewer minor surgical complications, but each is equally efective (Cook, 2014).


Obstentrics_Williams

Obstentrics_Williams. ing the first year is 9.4 per 1000 procedures and 11.4 per 1000 at 2,r3, and 5 years Qamieson, 2004). Failures result from unprotected intercourse too soon after ligation, incomplete occlusion of the vas deferens, or recanalization (Awsare, 2005; Deneux-haraux, 2004). Other than regrets, long-term consequences are rare. One is troublesome chronic scrotal pain, which develops in up to 15 percent of men (Leslie, 2007; vlanikandan, 2004). Previous concerns for atherogenesis, immune-complex mediated disease, testicular cancer, and prostate cancer have been allayed by a number of investigators (Bernal-Delgado, 1998; Giovannucci, 1992; Goldacre, 1983; M0ller, 1994).


Obstentrics_Williams

Obstentrics_Williams. Reanastomosis of the vas deferens can be completed most efectively using microsurgical techniques. In general, conception rates following reversal are adversely afected by longer duration from vasectomy, poor sperm quality found at reversal, and type of reversal procedure required (American Society for Reproductive Medicine, 2008). Al-Safi ZA, Shavell VI, Hobson DT, et al: Analysis of adverse events with Essure hysteroscopic sterilization reported to the Manufacturer and User Facility Device Experience database. J Minim Invasive Gynecol 20(6):825, 2013 American College of Obstetricians and Gynecologists: Access to postpartum sterilization. Committee Opinion No. 530, July 2012, Reairmed 2016 American College of Obstetricians and Gynecologists: Benefits and risks of sterilization. Practice Bulletin No. 133, February 2013, Reairmed 2017a


Obstentrics_Williams

Obstentrics_Williams. American College of Obstetricians and Gynecologists: Salpingectomy for ovarian cancer prevention. Committee Opinion No. 620, January 2015b, Reairmed 2017b American College of Obstetricians and Gynecologists: Sterilization of women: ethical issues and considerations. Committee Opinion No. 695, Apri 20l7c American Society for Reproductive Medicine: Vasectomy reversal. Fertil Steril 90:S78, 2008 American Society for Reproductive Medicine: Role of tubal surgety in the era of assisted reproductive technology: a committee opinion. Fertil Steril 103(6):e37,n2015 Arora P, Arora RS, Cahill 0: Essure for management of hydrosalpinx prior to in vitro fertilisation-a systematic review and pooled analysis. B]OG 121(5):527,n2014 Awsare N, Krishnan ], Boustead GB, et al: Complications of vasectomy. Ann R Coli Surg Engl :406, 2005 Barone A, Hutchison PL, Johnson CH, et al: Vasectomy in the Unites States, 2002. ] U rol 176:232, 2006


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Obstentrics_Williams. Bayer Healthcare: Essure: instruction for use. 2002. Available at: http://www. hcp.essure-us.com/ assets/ pdf/Link%20 Essure%20 IFU. pdf. Accessed April 28, 2016 Benal-Delgado E, Latour-Perez ], Pradas-Arnal F, et al: The association between vasectomy and prostate cancer: a systematic review of the literature. Fertil Steril 0:201, 1998 Bucklin BA: Postpartum tubal ligation: timing and other anesthetic consideradons. Clin Obstet Gynecol 46(3):657, 2003 Casey], Aguirre F, Yunker A: Outcomes of laparoscopic removal of the Essure sterilization device for pelvic pain: a case series. Contraception 94(2): 190, 2016 Chudnof SG, Nichols JE ]r, Levie M: Hysteroscopic Essure inserts for permanent contraception: extended follow-up results of a phase III multicenter international study. J Minim Invasive Gynecol 22(6):95n1, 2015 Cook A, Pun A, Gallo MF, et al: Scalpel versus no-scalpel incision for vasectomy. Cochrane Database SYSt Rev 3:CD004112, 2014


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Obstentrics_Williams. Cook A, Pun A, Gallo MF, et al: Scalpel versus no-scalpel incision for vasectomy. Cochrane Database SYSt Rev 3:CD004112, 2014 Costello C, Hillis S, Marchbanks P, et al: he efect of interval tubal sterilizadon on sexual interest and pleasure. Obstet Gynecol 100:3, 2002 Curtis M, Mohllajee AP, Peterson HB: Regret following female sterilization at a young age: a systematic review. Contraception 3:205, 2006 Daniels K, Daugherty ], Jones ], et al: Current contraceptive use and variation by selected characteristics among women aged 15-44: United States, 2011-2013. Nat! Health Stat Report 86:1,n2015 Danis RB, Della Badia CR, Richard SD: Postpartum permanent sterilization: could bilateral salpingectomy replace bilateral tubal ligation? J Minim Invasive GynecoIn23(6):928, 2016 Deieux X, Morin Surroca M, Faivre E, et al: Tubal anastomosis after tubal sterilization: a review. Arch Gynecol Obstet 83(5):1n149,n201n1


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Obstentrics_Williams. Deieux X, Morin Surroca M, Faivre E, et al: Tubal anastomosis after tubal sterilization: a review. Arch Gynecol Obstet 83(5):1n149,n201n1 Deneux-Tharaux C, Kahn E, Nazerali H, et al: Pregnancy rates after vasectomy: a survey of U.S. urologists. Contraception 69:401, 2004 DeStefano F, Perlman ]A, Peterson HB, et al: Long term risk of menstrual disturbances after tubal sterilization. Am J Obstet GynecoIn152:835, 1985 DuY S, Marsh F, Rogerson L, et al: Female sterilization: a cohort controlled comparative study of Essure versus laparoscopic sterilization. BJOG 112: 1522, 2005 Eisenberg ML, Lipshultz LI: Estimating the number of vasectomies performed annually in the United States: data from the National Survey of Family Growth. J Urol 184(5):2068,n2010


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Obstentrics_Williams. Eisenberg ML, Lipshultz LI: Estimating the number of vasectomies performed annually in the United States: data from the National Survey of Family Growth. J Urol 184(5):2068,n2010 Food and Drug Administration: Labeling for permanent hysteroscopicallyplaced tubal implants itended for sterilization. 2016. Available at: http:// ww.fda.gov/downloads/MedicaIDevices/DeviceRegulationandGuidance/ GuidanceDocuments/UCM488020.pdf. Accessed April 28, 2016 Gaudet MM, Patel AV, Sun J, et al: Tubal sterilization and breast cancer incidence: results from the cancer prevention study II nuuition cohort and meta-analysis. Am J Epidemiol 7(6):492,n2013 Giovannucci E, Tosteson TD, Speizer FE, et al: A long-term study of mortality in men who have undergone vasectomy. N Engl ] Med 326: 1392, 1992 Goldacre ]M, Holford TR, Vessey MP: Cardiovascular disease and vasectomy. N Engl ] Med 308:805, 1983 Hendrix NW, Chauhan SP, Morrison JC Sterilization and its consequences. Obstet Gynecol Surv 66, 1999


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Obstentrics_Williams. N Engl ] Med 308:805, 1983 Hendrix NW, Chauhan SP, Morrison JC Sterilization and its consequences. Obstet Gynecol Surv 66, 1999 Hofman BL, Corton MM: Surgeries for benign gynecologic conditions. In Hofman BL, Schorge JO, Bradshaw KD, et al: Williams Gynecology, 3rd ed. New York, McGraw-Hill Education, 2016 Hologic: Hologic announces second quarter iscal 2012 operating results. 2012. Available online at: ile:/ / /C/Users/bhofm/Downloads/Hologic-AnnouncesSecond-Quarter-Fiscal-20 12-0perating-Results. pdf. Accessed May 19, 2016 Jamieson DJ, Costello C, Trussell ], et al: The risk of pregnancy after vasectomy. Obstet Gynecol 103:848, 2004 Jamieson DJ, Kaufman SC, Costello C, et al: A comparison of women's regret after vasectomy versus tubal sterilization. Obstet Gynecol 99: I073, 2002


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Obstentrics_Williams. Jamieson DJ, Kaufman SC, Costello C, et al: A comparison of women's regret after vasectomy versus tubal sterilization. Obstet Gynecol 99: I073, 2002 Kelek:i S, Erdemoglu E, Kuduk S, et al: Risk factors for tubal ligation: regret and psychological efects. Impact of Beck Depression Inventoty. Contraception ,2005 la Chapel Ie CF, Veersema S, Brolmann HA, et al: Efectiveness and feasibility of hysteroscopic sterilization techniques: a systematic review and metaanalysis. Ferril Steriln103(6):1516, 2015 Lazorwitz A, Tocce K: A case series of removal of nickel-titanium sterilization microinserts from the uterine cornua using laparoscopic electrocautety for salpingectomy. Contraception 96(2):96, 2017 Leslie TA, Illing RO, Cranston DW, et al: he incidence of chronic scrotal pain after vasectomy: a prospective audit. BJU Int 100:n1330,n2007 Levgur M, Duvivier R: Pelvic inAammatory disease after tubal sterilization: a review. Obstet Gynecol Surv 55:41, 2000


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Obstentrics_Williams. Levgur M, Duvivier R: Pelvic inAammatory disease after tubal sterilization: a review. Obstet Gynecol Surv 55:41, 2000 Lippes J: Quinacrine sterilization (QS): time for reconsideration. Contraception 92(2):91, 2015 Madari S, Varma R, Gupta J: A comparison of the modified Pomeroy tubal ligation and Filshie clips for immediate postpartum sterilisation: a systematic review. Eur] Contracept Reprod Health Care 16(5):341,n2011 Malacova E, Kemp-Casey A, Bremner A, et al: Live delivety outcome after tubal sterilization reversal: a population-based study. Ferril Steril 104(4):92, 2015 Manikandan R, Srirangam SJ, Pearson E, et al: Early and late morbidity after vasectomy: a comparison of chronic scrotal pain at 1 and 10 years. BJU Int 93:571,n2004 Mao], pfeifer S, Schlegel P, et al: Safety and eicacy of hysteroscopic sterilization compared with laparoscopic sterilization: an observational cohort study. BM] 351:h5162, 2015


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Obstentrics_Williams. Mao], pfeifer S, Schlegel P, et al: Safety and eicacy of hysteroscopic sterilization compared with laparoscopic sterilization: an observational cohort study. BM] 351:h5162, 2015 M01ler H, Knudsen LB, Lynge E: Risk of testicular cancer after vasectomy: cohort study of over 73,000 men. BM] 309:295, 1994 Moniz MH, Chang T, Heisler M, et al: Inpatient postpartum long-acting reversible conuaception and sterilization in the United States, 2008-2013. Obstet Gynecol 129(6): 1078,n20] Monteith CW, Berger GS, Zerden ML: Pregnancy success after hysteroscopic sterilization reversal. Obstet Gynecol 124(6):1183,n2014 Munro MG, Nichols ]E, Levy B, et al: Hysteroscopic sterilization: lO-year retrospective analysis of worldwide pregnancy reportS. ] Minim Invasive Gynecol 21(2):245, 2014 Pearce CL, Stram DO, Ness RB, et al: Population distribution of lifetime risk of ovarian cancer in the United States. Cancer Epidemiol Biomarkers Prev 24(4):671,n2015


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Obstentrics_Williams. Pearce CL, Stram DO, Ness RB, et al: Population distribution of lifetime risk of ovarian cancer in the United States. Cancer Epidemiol Biomarkers Prev 24(4):671,n2015 Peterson HB, ]eng G, Folger SG, et al: he risk of menstrual abnormalities after tubal sterilization. N Engl ] Med 343: 1681, 2000 Peterson HB, Xia Z, Hughes ]M, et al: The risk of ectopic pregnancy after tubal sterilization. U.S. Collaborative Review of Sterilization Working Group. N Engl J Med 336(11):762, 1997 Peterson HB, Xia Z, Hughes ]M, et al: The risk of pregnancy after tubal sterilization: findings from the U.S. Collaborative Review of Sterilization. m ] Obstet Gynecol 1 4: 1161, 1996 Potter JE, Stevenson A], White K, et al: Hospital variation in postpartum tubal sterilization rates in California and Texas. Obstet Gynecol 121 (1): 152,n2013


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Obstentrics_Williams. Potter JE, Stevenson A], White K, et al: Hospital variation in postpartum tubal sterilization rates in California and Texas. Obstet Gynecol 121 (1): 152,n2013 Powell CB, Alabaster A, Simmons S, et al: Salpingectomy for sterilization: change in practice in a large integrated health care system, 2011-2016. Obstet Gynecol 130(5):961,n2017 Rogers MD, Kolettis PN: Vasectomy. Urol Clin North Am 40(4):559, 2013 Sharlip 10, Belker AM, Honig S, et al: Vasectomy: AUA guideline. Outcomes of microsurgical vasovasostomy for vasectomy reversal: a meta-analysis and systematic review.n] Urol 188(6 Suppi):2482, 2012 Shinar S, Blecher Y, Alpern S, et al: Total bilateral salpingectomy versus partial bilateral salpingectomy for permanent sterilization during cesarean delivety. Arch Gynecol Obstet295(5):1185, 2017 Shy KK, Stergachis A, Grothaus LG, et al: Tubal sterilization and risk of subsequent hospital admission for menstrual disorders. Am ] Obstet Gynecol 166:n1698,n1992


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Obstentrics_Williams. Shy KK, Stergachis A, Grothaus LG, et al: Tubal sterilization and risk of subsequent hospital admission for menstrual disorders. Am ] Obstet Gynecol 166:n1698,n1992 Society of Gynecologic Oncologists: SGO Clinical Practice Statement: Salpingectomy for ovarian cancer prevention. Available at: https://www.sgo.org/ cl inical-practice/ gu idel i nes/ sgo-cl inical-p ractice-statemen t -sal pi ngecto m yfor-ovarian-cancer-prevention.l Accessed December 13,n2013 Sokal DC, Hieu do T, Loan NO, et al: Contraceptive efectiveness of two insertions of quinacrine: results from 10-year follow-up in Vietnam. Con 8:61, 2008 Sokal DC, Trujillo V, Guzman SC, et al: Cancer risk after sterilization with transcervical quinacrine: updated indings from a Chilean cohort. Contraception 81(1): 5,n2010a Sokal DC, Vach TH, Nanda K, Quinacrine sterilization and gynecologic cancers: a case-control study in northen Vietnam. Epidemiology 21 (2): 164, 201 Ob


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Obstentrics_Williams. Sokal DC, Vach TH, Nanda K, Quinacrine sterilization and gynecologic cancers: a case-control study in northen Vietnam. Epidemiology 21 (2): 164, 201 Ob Stuart GS: Puerperal sterilization. In Yeomans ER, Hofman BL, Gilstrap, III, et al (eds): Cunningham and Gilstrap's Operative Obstetrics, 3rd ed. New York, McGraw-Hill, 201 Thompson M, Kho K: Minimally invasive surgery. In Hofman BL, Schorge JO, Bradshaw KD, et al (eds): Williams Gynecology, 3rd ed. New York, McGraw-Hill, 2016 Veersema S, Mijatovic V, Dreyer K, et al: Outcomes of pregnancies in women with hysteroscopically placed micro-inserts in situ. ] Minim Invasive Gynecol 21(3):492, 2014 TERMINOLOGY AND DIAGNOSIS .................. 710 INCIDENCE AND RISK FACTORS ................... 713 ETIOPATHOGENESIS ............................ 713 PATHOPHYSIOLOGY ............................ 717 PREDICTION.. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 725


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Obstentrics_Williams. ETIOPATHOGENESIS ............................ 713 PATHOPHYSIOLOGY ............................ 717 PREDICTION.. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 725 PREVENTION . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 726 PREECLAMPSIA . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 728 ECLAMPSIA. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 734 MANAGEMENT CONSIDERATIONS ................. 738 LONG-TERM CONSEQUENCES .................... 744 An eclamptic convulsion sometimes occurs without warning, "like a bolt from a clear sky': in women who are apparenty in peect health. In the majoriy of cases, however, the outbreak is preceded or a longer or shorter period by premonitoy symptoms indicative of toxemia of pregnancy, among the more common being oedema, headache, epigastric pain, and possiby disturbances of vision. -J. Whitridge Williams (1903)


Obstentrics_Williams

Obstentrics_Williams. At the time of this textbook's irst edition, it was accepted that "toxemia" preceded most cases of eclampsia. he central role of hypertension had not yet been discovered, and after many years, it became apparent that preeclampsia was a syndrome of which hypertension was only one important facet. Still, the mechanisms by which pregnancy incites or aggravates hypertension remain unsolved. Indeed, hypertensive disorders remain among the most signiicant and intriguing unsolved problems in obstetrics. hese disorders complicate 5 to 10 percent of all pregnancies, and together they are one of the deadly triad-along with hemorrhage and infection-that contributes greatly to maternal morbidity and mortality rates. Of hypertensive disorders, the preeclampsia syndrome, either alone or superimposed on chronic hypertension, is the most dangerous. As subsequently discussed, new-onset hypertension during pregnancy-termed gestational hypertension-is followed by signs and symptoms of preeclampsia


Obstentrics_Williams

Obstentrics_Williams. on chronic hypertension, is the most dangerous. As subsequently discussed, new-onset hypertension during pregnancy-termed gestational hypertension-is followed by signs and symptoms of preeclampsia almost half the time, and preeclampsia is identiied in 4 to 5 percent of all pregnancies (Martin, 2012).


Obstentrics_Williams

Obstentrics_Williams. he World Health Organization (WHO) systematically reviews maternal mortality worldwide, and in developed countries, 16 percent of maternal deaths were attributed to hypertensive disorders (han, 2006). In the United States from 201r1 to 2013, 7.4 percent of2009 pregnancy-related maternal deaths were caused by preeclampsia or eclampsia (Creanga, 2017). A similar rate was 10 percent in France from 2003 through 2007 (Saucedo, 2013). Importantly, more than half of these hypertension-related deaths were deemed preventable (Berg, 2005). To update and codiy the terminology and classiication of hypertensive disorders of pregnancy, a Task Force of the American College of Obstetricians and Gynecologists (2013) has provided evidence-based recommendations for clinical practice. The previous basic classiication was retained and describes four types of hypertensive disease: 1. 2. Chronic hypertension of any etiology 3.


Obstentrics_Williams

Obstentrics_Williams. 2. Chronic hypertension of any etiology 3. 4. Gestational hypertension-definitive evidence for the preeclampsia syndrome does not develop and hypertension resolves by 12 weeks postpartum. Importantly, this classification diferentiates the preeclampsia syndrome from other hypertensive disorders because it is potentially more ominous. • Diagnosis of Hypertensive Disorders


Obstentrics_Williams

Obstentrics_Williams. Importantly, this classification diferentiates the preeclampsia syndrome from other hypertensive disorders because it is potentially more ominous. • Diagnosis of Hypertensive Disorders Hypertension is diagnosed empirically when appropriately taken blood pressure exceeds 140 mm Hg systolic or 90 mm Hg diastolic. Korotkofphase V is used to define diastolic pressure. Previously, incremental increases of 30 mm Hg systolic or 15 mm Hg diastolic above blood pressure values taken at midpregnancy had also been used as diagnostic criteria, even when absolute values were < 140/90 mm Hg. These incremental changes are no longer used to define hypertension, but it is recommended that such women be observed more closely because eclamptic seizures develop in some whose blood pressures have stayed below 140/90 mm Hg (Alexander, 2006). Also, a sudden rise in mean arterial pressure but still in a normal range-"delta hypertension"-may signiy preeclampsia (Macdonald-Wallis, 2012; Zeeman, 2007).


Obstentrics_Williams

Obstentrics_Williams. he systolic and diastolic blood pressure levels of 140/90 mm Hg have been arbitrarily used since the 1950s to define "hypertension" in nonpregnant individuals. However, these levels were selected by insurance companies to characterize a group of middle-aged men. It seems more realistic to deine normalrange blood pressures that fall between an upper and lower limit for a particular population-such as young, healthy, pregnant women. A schematic example using arbitrary mean arterial blood pressure readings is shown in Figure 40-1. Data curves for both women show blood pressure measurements near the ...Patient A ...Patient B )..:J, C,


Obstentrics_Williams

Obstentrics_Williams. C, FIGURE 40-1 Schematic shows normal reference ranges for mean arterial blood pressure changes across pregnancy. Patient A (blue) has mean blood pressures near the 20th percentile throughout pregnancy. Patient B (red) has a similar pattern with mean pressures at the 25th percentile until approximately 36 weeks when her blood pressure begins to rise. By term, it is substantively higher and in the 75th percentile, but she is still considered "normotensive." 25th percentile until 32 weeks. These begin to rise in patient B, who by term has substantively higher blood pressures. However, her pressures are still < 140/90 mm Hg, and thus she is considered to be "normotensive." We use the term delta hypertension to describe this rather acute rise in blood pressure. Some of these women will go on to have obvious preeclampsia, and some even develop eclamptic seizures or HELLP (hemolysis, devatedliver enzyme levels, low 2latelet count) syndrome while still normotensive.


Obstentrics_Williams

Obstentrics_Williams. his diagnosis is made in women whose blood pressures reach 140/90 mm Hg or greater for the irst time after midpregnancy, but in whom proteinuria is not identiie. Almost half of these women subsequently develop preeclampsia syndrome. Even so, when blood pressure increases appreciably, it is dangerous to both mother and fetus to ignore this rise only because proteinuria has not yet developed. As Chesley (1985) emphasized, 10 percent of eclamptic seizures develop before overt proteinuria can be detected. Finally, gestational hypertension is reclassiied by some as transient hypertension if evidence for preeclampsia does not develop and the blood pressure returns to normal by 12 weeks postpartum.


Obstentrics_Williams

Obstentrics_Williams. Preeclampsia is best described as a pregnancy-speciic syndrome that can aect virtualy evey organ system. In addition, it heralds a higher incidence of cardiovascular disease later in life (p. 744). Although preeclampsia is much more than simply gestational hypertension with proteinuria, appearance ofproteinuria remains an important diagnostic criterion. Thus, proteinuria is an objective marker and relects the system-wide endothelial leak that characterizes the preeclampsia syndrome. In some women with the preeclampsia syndrome, neither overt proteinuria nor fetal-growth restriction are features (Sibai, 2009). Because of this, the Task Force (2013) suggests other diagnostic criteria, which are shown in Table Evidence of multiorgan involvement may include thrombocytopenia, renal dysfunction, hepatocellular necrosis, central nervous system perturbations, or pulmonary edema. • Indicators of Preeclampsia Severity


Obstentrics_Williams

Obstentrics_Williams. • Indicators of Preeclampsia Severity The markers listed in Table 40-1 are also used to classiy preeclampsia syndrome severity. lthough many use a dichotomous "mild" and "severe" classiication, the Task Force (2013) discourages the use of "mild preeclampsia." It is problematic that there are criteria for the diagnosis of "severe" preeclampsia, but the default classiication is either implied or speciically termed as "mild," "less severe," or "nonsevere" (Alexander, 2003; Lindheimer, 2008b). here are no generally agreed-on criteria for "moderate" preeclampsia-an elusive third category. We use the criteria listed in Table 40-2, which are categorized as "severe" versus "nonsevere." Some symptoms are considered ominous. Headaches or visual disturbances such as scotomata can precede eclampsia, which is a convulsion not attributable to another cause. The TABLE 40-1. Classification and Diagnosis of Pregnancy-Associated Hypertension


Obstentrics_Williams

Obstentrics_Williams. TABLE 40-1. Classification and Diagnosis of Pregnancy-Associated Hypertension Gestational hypertension Preeclampsia: Hypertension plus • 2300 mg/24 h, or Urine protein: creatinine ratio 20.3, or Platelet count < 1 OO,OOO/.LL 1.1 mg/dL or doubling of baselineb Headache, visual disturbances, convulsions aRecommended only if sole available test. bNo prior renal disease. CAST (aspartate transaminase) or ALT (alanine transaminase). BP = blood pressure. Modified with permission from American College ofObstetricians and Gynecologists; Task Force on Hypertension in Pregnancy: Hypertension in pregnancy. Report ofthe American College ofObstetricians and Gynecologists'Task Force on


Obstentrics_Williams

Obstentrics_Williams. Hypertension in Pregnancy, Obstet Gynecol. 201n3 Nov;122(S):n seizures are generalized and may appear before, during, or after labor. The proportion that develops seizures later, after 48 hours postpartum, approximates 10 percent (Sibai, 2005; Zwart, 2008). Another symptom, epigastric or right upper quadrantpain, frequently accompanies hepatocellular necrosis, ischemia, and edema that ostensibly stretches Glisson capsule. This characteristic pain is frequently accompanied by elevated serum TABLE40-2. Indicators of Severity of Gestational (< 1 OO,OOO/LL) None to positive None to positive aCompare with criteria in Table 40-1. blncludes "mild" and "moderate" hypertension not specifically defined. cMost disregard degrees of proteinuria to classify nonsevere or severe. BP = blood pressure.


Obstentrics_Williams

Obstentrics_Williams. blncludes "mild" and "moderate" hypertension not specifically defined. cMost disregard degrees of proteinuria to classify nonsevere or severe. BP = blood pressure. hepatic transaminase levels. Finally, thrombocytopenia also signifies worsening preeclampsia. It represents platelet activation and aggregation as well as microangiopathic hemolysis. Other factors indicative ofsevere preeclampsia include renal or cardiac involvement, obvious fetal-growth restriction, and early-onset disease. he more profound these signs and symptoms, the less likely it is that they can be temporized, and the more likely that delivery will be required. A caveat is that dierentiation between nonsevere and severe gestational hypertension or preeclampsia can be misleading because what might be apparenty mild disease may progress rapidy to severe disease.


Obstentrics_Williams

Obstentrics_Williams. Regardless of its cause, any chronic hypertensive disorder predisposes a woman to develop superimposed preeclampsia syndrome. Chronic underlying hypertension is diagnosed in women with documented blood pressures > 140/90 mm Hg before pregnancy or before 20 weeks' gestation, or both. Hypertensive disorders can create diicult problems with diagnosis and management in women who are not irst seen until after midpregnancy. This is because blood pressure normally drops during the second and early third trimesters in both normotensive and chronically hypertensive women (see Fig. 40-1). Thus, a woman with previously undiagnosed chronic vascular disease who is seen before 20 weeks frequently has blood pressures within normal range. During the third trimester, however, as blood pressures return to their originally hypertensive levels, it may be diicult to determine whether hypertension is chronic or induced by pregnancy. Even a careful search for evidence of preexisting end-organ damage may be


Obstentrics_Williams

Obstentrics_Williams. their originally hypertensive levels, it may be diicult to determine whether hypertension is chronic or induced by pregnancy. Even a careful search for evidence of preexisting end-organ damage may be futile, as many ofthese women have mild disease and no evidence ofventricular hypertrophy, retinal vascular changes, or renal dysfunction.


Obstentrics_Williams

Obstentrics_Williams. In some with chronic hypertension, blood pressure rises to obviously abnormal levels, typically after 24 weeks' gestation. If new-onset or worsening baseline hypertension is accompanied by new-onset proteinuria or other indings listed in Table 40-1, then superimposed preeclampsia is diagnosed. Compared with "pure" preeclampsia, superimposed preeclampsia commonly develops earlier in pregnancy. It also tends to be more severe and more often is accompanied by fetal-growth restriction. he same criteria shown in Table 40-2 are also used to further characterize severity of superimposed preeclampsia.


Obstentrics_Williams

Obstentrics_Williams. Young and nulliparous women are particularly vulnerable to developing preeclampsia, whereas older women are at greater risk for chronic hypertension with superimposed preeclampsia. he incidence is markedly inluenced by race and ethnicity-and thus by genetic predisposition. In one study by the Maternal-Fetal Medicine Units (MFMU) Network, the incidence of preeclampsia was 5 percent in white, 9 percent in Hispanic, and 11 percent in African-American women (Myatt, 2012a,b). In addition, black women have greater morbidity (Shahul, 2015). In several worldwide studies reviewed by Staf and coworkers (2015), the incidence of preeclampsia in nulliparous populations ranged from 3 to 10 percent. he incidence of preeclampsia in multiparas also varies and ranges from 1.4 to 4 percent (Fisher, 2015).


Obstentrics_Williams

Obstentrics_Williams. Bartsch and associates (2016) extracted data from more than 25 million pregnancies and calculated relative risks for several clinical factors shown in Table 40-3. Others include the metabolic syndrome and hyperhomocysteinemia (Karumanchi, 2016a; Masoudian, 2016; Scholten, 2013). Pregnancies with a male fetus are also at slightly higher risk a askolka, TABLE 40-3. Selected Clinical Risk Factors for Preeclampsia APA = antiphospholipid antibody; ART = assisted reproductive technology; BMI = body mass index; CHTN = chronic hypertension; CKD = chronic kidney disease; SLE = systemic lupus erythematosus. Data from Ba rtsch, 201 6. 2017). Although smoking during pregnancy causes various adverse pregnancy outcomes, ironically, it carries a reduced risk for hypertension during pregnancy (Bainbridge, 2005; Kraus, 2014). Other factors are human immunodeficiency virus (HIV) seropositivity and sleep-disordered breathing (Facco, 2017; Sansone, 2016).


Obstentrics_Williams

Obstentrics_Williams. For eclampsia, the incidence has declined in areas where health care is more readily available. In the United States in 1998, it afected 1 in 3250 births (Ventura, 2000). Except for Iceland, which has an extremely low rate, in countries with adequate resources the incidence averages 1 in 2000 to 3000 deliveries (Andersgaard, 2006; Jaatinen, 2016; O'Connor, 2013; Royal College of Obstetricians and Gynaecologists, 2006; Zwart, 2008). Any satisfactory theory concerning the origins of preeclampsia must account for the observation that gestational hypertensive disorders are more likely to develop in women with the following characteristics: Are exposed to chorionic villi for the irst time Are exposed to a superabundance of chorionic villi, as with twins or hydatidiform mole Have preexisting conditions associated with endothelial cell activation or inflammation, such as diabetes, obesity, cardiovascular or renal disease, immunological disorders, or hereditary inluences


Obstentrics_Williams

Obstentrics_Williams. Have preexisting conditions associated with endothelial cell activation or inflammation, such as diabetes, obesity, cardiovascular or renal disease, immunological disorders, or hereditary inluences Are genetically predisposed to hypertension developing during pregnancy. A fetus is not a requisite for preeclampsia to develop. And, although chorionic villi are essential, they need not be intrauterine. For example, preeclampsia can develop with an abdominal pregnancy (Worley, 2008). Regardless of precipitating etioloy, the cascade of events leading to the preeclampsia syndrome is characterized by abnormalities that result in systemic vascular endothelial damage with resultant vasospasm, transudation ofplasma, and ischemic and thrombotic sequelae.


Obstentrics_Williams

Obstentrics_Williams. • Phenotypic Expression of he preeclampsia syndrome varies widely in its clinical phenotypic expression. But, at least two major subtypes are diferentiated by whether or not remodeling of uterine spiral arterioles by endovascular trophoblasts is defective. his concept has given rise to the "two-stage disorder" theory of preeclampsia pathogenesis. According to Redman and coworkers (20 15a), stage 1 is caused by faulty endovascular trophoblastic remodeling that downstream causes the stage 2 clinical syndrome. Importantly, stage 2 can be modified by preexisting maternal conditions that are also manifest by endothelial cell activation or inlammation and are listed in the third prior bullet. Such staging is artiicial, and it seems logical that preeclampsia syndrome presents clinically as a spectrum of worsening disease. Moreover, evidence is accruing that many "isoforms" exist as discussed subsequently. Examples include diferences in


Obstentrics_Williams

Obstentrics_Williams. FIGURE 40-2 Schematic representation of normal placental implantation shows proliferation of extravillous trophoblasts from an anchoring villus. These trophoblasts invade the decidua and extend into the walls of the spiral arteriole to replace the endothelium and muscular wall to create a dilated low-resistance vessel. With preeclampsia, defective implantation is characterized by incomplete invasion of the spiral arteriolar wall by extravillous trophoblasts. This results in a small-caliber vessel with high resistance to flow. maternal and fetal characteristics, placental indings, and earlyversus late-onset disease (Phillips, 2010; Valensise, 2008; van der Merwe, 2010). n imposing number of mechanisms have been proposed to explain the cause of preeclampsia. Those currently considered important include: 1. Placental implantation with abnormal trophoblastic invasion of uterine vessels 2. Immunological maladaptive tolerance between maternal, paternal (placental), and fetal tissues 3.


Obstentrics_Williams

Obstentrics_Williams. Placental implantation with abnormal trophoblastic invasion of uterine vessels 2. Immunological maladaptive tolerance between maternal, paternal (placental), and fetal tissues 3. Maternal maladaptation to cardiovascular or inlammatory changes of normal pregnancy 4. Genetic factors including inherited predisposing genes and epigenetic inluences. Discussed in Chapter 5 (p. 88), normal implantation is characterized by extensive remodeling of the spiral arterioles within the decidua basalis (Fig. 40-2). Endovascular trophoblasts replace the vascular endothelial and muscular linings to enlarge the vessel diameter (Zhou, 1997). The veins are invaded only superficially.


Obstentrics_Williams

Obstentrics_Williams. In some cases of preeclampsia, however, trophoblastic invasion may be incomplete. With this, decidual vessels, but not myometrial vessels, become lined with endovascular trophoblasts. The deeper myometrial arterioles thus do not lose their endothelial lining and musculoelastic tissue, and their mean external diameter is only half that of corresponding vessels in normal placentas (Fisher, 2015). In general, the magnitude of defective trophoblastic invasion correlates with the severity of the hypertensive disorder (Madazli, 2000). And importantly, it is more prevalent in women with early-onset preeclampsia (Khodzhaeva, 2016). cMahon and associates (2014) found that lower levels of soluble antiangiogenic growth factors may be involved in this faulty endovascular remodeling.


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Obstentrics_Williams. From placental electron microscopy studies, early preeclamptic changes include endothelial damage, insudation of plasma constituents into vessel walls, proliferation of myointimal cells, and medial necrosis (De Wolf, 1980). Hertig (1945) referred to lipid accumulation in myointimal cells and macro phages as atherosis. These indings are more common in placentas from women diagnosed with preeclampsia before 34 weeks (Nelson, 2014b). Acute placental vascular atherosis may also identiy a group of women at greater risk for later atherosclerosis and cardiovascular disease (Staf, 2015). In pregnancy, the abnormally narrow lumen of spiral arterioles likely impairs placental blood flow. Diminished perfusion and a hypoxic environment eventually lead to release of placental debris or microparticles.


Obstentrics_Williams

Obstentrics_Williams. At this point, these changes incite a systemic inlammatory response, which is stage 2 of the preeclampsia syndrome (Lee, 2012; Redman, 2012). Defective placentation is posited to further cause the susceptible woman to develop gestational hypertension, the preeclampsia syndrome, preterm delivery, a growth-restricted fetus, and/or placental abruption (Brosens, 2011; Labarrere, 2017; Nelson, 2014b). IVlaternal immune tolerance to paternally derived placental and fetal antigens is discussed in Chapter 5 (p. 95). Loss of this tolerance is another cited theory for preeclampsia (Erlebacher, 2013). Certainly, the histological changes at the maternalplacental interface are suggestive of acute graft rejection.


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Obstentrics_Williams. Inferential data also suggest that preeclampsia is an immunemediated disorder. For example, the risk of preeclampsia is appreciably enhanced in circumstances in which formation of blocking antibodies to placental antigenic sites might be impaired. In this scenario, the irst pregnancy would carry a higher risk. Tolerance dysregulation might also explain an ele vated risk when the paternal antigenic load is increased, that is, with two sets of paternal chromosomes-a "double dose." Namely, women with molar pregnancies have a high incidence of early-onset preeclampsia. Women with a trisomy 13 fetus also have a 30-to 40-percent incidence of preeclampsia. hese women have elevated serum levels of antiangiogenic factors. he gene for one of these factors, soluble ins-like tyrosine kinase 1, is on chromosome 13 (Bdolah, 2006). Conversely, women previ ously exposed to paternal antigens, such as a prior pregnancy with the same partner, are "immunized" against preeclampsia.


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Obstentrics_Williams. his phenomenon is not as apparent in women with a prior abortion (Strickland, 1986). Multiparas impregnated by a new consort have a greater risk of preeclampsia (Mostello, 2002).


Obstentrics_Williams

Obstentrics_Williams. Redman and colleagues (2015a) reviewed the possible role of immune maladaptation in preeclampsia pathophysiology. In women destined to be preeclamptic, extravillous trophoblasts early in pregnancy express reduced amounts of immunosuppressive nonclassic human leukocyte antigen G (HLA G). Black women more commonly have the 1597 �C gene allele that further predisposes to preeclampsia (Loisel, 2013). hese changes may contribute to the defective placental vascularization in stage 1 of the preeclampsia syndrome. As discussed in Chapter 4 (p. 59), T-helper (h) lymphocytes during normal pregnancy are produced so that type 2 activity is increased in relation to type 1-so-called ype 2 bias (Redman, 2012, 2015a). h2 cells promote humoral immunity, whereas Th1 cells stimulate inlammatory cytoine secretion. Beginning in the early second trimester in women who develop preeclampsia, Th1 action is increased.


Obstentrics_Williams

Obstentrics_Williams. Inflammatory changes are believed to be a continuation of stage 1 alterations. In response to ischemia or other inciting causes, placental factors are released and begin a cascade of events (Davidge, 2015). Thus, antiangiogenic and metabolic factors and other inflammatory leukocyte mediators are thought to provoke systemic endothelial cell injury, which is used synonymously here with endothelial cel activation or dyfunction.


Obstentrics_Williams

Obstentrics_Williams. Endothelial cell dysfunction may result from an extreme activated state of leukocytes in the maternal circulation (Faas, 2000; Gervasi, 2001). Briefly, cytokines such as tumor necrosis factor-a (TNF-a) and the interleukins may contribute to the systemic oxidative stress associated with preeclampsia. This is characterized by reactive oxygen species and free radicals that lead to formation of self-propagating lipid peroxides (Manten, 2005). hese peroxides in turn generate highly toxic radicals that injure systemic vascular endothelial cells, modiy nitric oxide production by these cells, and interfere with prostaglandin balance. Other consequences of oxidative stress include production of the lipid-laden macrophage foam cells seen in placental atherosis, activation of systemic microvascular coagulation manifested by thrombocytopenia, and greater systemic capillary permeability relected by edema and proteinuria.


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Obstentrics_Williams. Preeclampsia appears to be a multifactorial, polygenic disorder. In one study of almost 1.2 million Swedish births, a genetic Data from Buurma, 2013; Staines-Urias, 2012; Triche, 2014; Ward, 2014; Ye, 2016. association for gestational hypertension and for preeclampsia was found (Nilsson, 2004). Ward and Taylor (2015) cite an incident risk for preeclampsia of 20 to 40 percent for daughters of preeclamptic mothers; 11 to 37 percent for sisters of preeclamptic women; and 22 to 47 percent for twins. Ethnoracial factors are important, as evidenced by the high incidence of preeclampsia in African-American women. It may be that Latina women have a lower incidence because of interactions of American Indian and white race genes (Shahabi, 2013).


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Obstentrics_Williams. he hereditary predisposition for preeclampsia likely stems from interactions of literally hundreds of inherited genesboth maternal and paternal-that control myriad enzymatic and metabolic functions throughout every organ system (Triche, 2014). Plasma-derived factors may induce some of these genes in preeclampsia (Mackenzie, 2012). Thus, the clinical manifestation in any given woman with the preeclampsia syndrome will occupy a spectrum. In this regard, phenotypic expression will difer among similar genotypes depending on interactions with environmental components (Yang, 2013).


Obstentrics_Williams

Obstentrics_Williams. Hundreds of genes have been studied for their possible association with preeclampsia (Buurma, 2013; Sakowicz, 2016; Ward, 2015). Several that may have a significant association with the syndrome are listed in Table 40-4. However, because of the complex phenotypic expression of preeclampsia, it is doubtful that anyrone candidate gene will be found responsible. Indeed, Majander and associates (2013) have linked preeclampsia predisposition to evenetal genes on chromosome 18.