Gynecologic Surgery

Chapter 71 Gynecologic Surgery

Howard W. Jones, III

PELVIC EMBRYOLOGY AND ANATOMY

REPRODUCTIVE PHYSIOLOGY

CLINICAL EVALUATION

ALTERNATIVES TO SURGICAL INTERVENTION

TECHNICAL ASPECTS OF SURGICAL OPTIONS

SURGERY DURING PREGNANCY

Gynecologic surgery involves the operative treatment of benign and malignant conditions of the female genital tract. Because of the hormonal responsiveness of these tissues and organs during the menstrual cycle and during the premenarchal, reproductive, and postmenopausal periods of life, the diagnosis, management, and even surgical approach may differ because of the hormonal milieu and the patient’s desire for future fertility. All these factors may be even further complicated in pregnant women in whom the surgical and anesthetic approach must consider the pregnant uterus and fetus. The surgeon who understands and is able to consider the physiology, endocrinology, and anatomy of the female pelvis is most prepared to select the most appropriate and successful operative procedure. In addition, by knowing the alternatives to surgery and risks and advantages of several possible management approaches, a treatment most likely to correct the problem and be consistent with the patient’s desires for fertility preservation, minimally invasive surgical approach, or even no surgery at all can be accomplished with the best opportunity for a good outcome.

The general surgeon may be called on to assist the gynecologic surgeon when endometriosis or ovarian cancer involves the sigmoid colon, when a diverticular abscess or carcinoma of the colon involves the ovary, in the pregnant women with acute appendicitis or cholecystitis, or in smaller communities in which there is no gynecologist at all.

Although a full discussion of gynecologic surgery is beyond the scope of a single chapter, I will attempt to address the basics of pelvic anatomy, reproductive physiology, clinical evaluation of common gynecologic symptoms, surgical technique for several common operations, and surgical approach to the pregnant patient.

Pelvic Embryology And Anatomy

Embryology

The female external genitalia are derived embryologically from the genital tubercle, which, in the absence of testosterone, fails to undergo fusion and devolves to the vulvar structures. The labial structures are of ectodermal origin. The urethra, vaginal introitus, and vulvar vestibule are derived from uroepithelial entoderm. The lower third of the vagina develops from the invagination of the urogenital sinus.

The internal genitalia are derived from the genital ridge. The ovaries develop from the incorporation of primordial germ cells into coelomic epithelium of the mesonephric (wolffian) duct and the tubes, uterus, cervix, and upper two thirds of the vagina develop from the paramesonephric (mullerian) duct. The embryologic ovaries migrate caudad to the true pelvis. Primordial ovarian follicles develop but remain dormant until stimulation in adolescence by gonadotropins. The paired mullerian ducts migrate caudad and medially to form the fallopian tubes and fuse in the midline to form the uterus, cervix, and upper vagina. The wolffian ducts regress. Failure or partial failure of these processes can result in distortions of anatomy and potential diagnostic dilemmas (Table 71-1).

Table 71-1 Selected Anatomic Abnormalities as a Result of Disrupted Embryogenesis

ORGAN	ABNORMALITY
Ovary	Duplication of ovary; secondary ovarian rests; paraovarian cysts (wolffian remnants)
Tube	Congenital absence; paratubal cyst (hydatid of Morgagni)
Uterus	Agenesis; complete or partial duplication of the uterine fundus
Cervix	Agenesis; complete or partial duplication of the cervix
Vagina	Agenesis; transverse or longitudinal septum; paravaginal (Gartner’s duct) cyst
Vulva	Fusion; hermaphroditism; cyst of the canal of Nuck (round ligament cyst)

Anatomy

External Genitalia

The external genitalia consist of the mons veneris, labia majora, labia minora, clitoris, vulvar vestibule, urethral meatus, and ostia of the accessory glandular structures (Fig. 71-1). These structures overlie the fascial and muscle layers of the perineum. The perineum is the most caudal region of the trunk; it includes the pelvic floor and those structures occupying the pelvic outlet. It is bounded superiorly by the funnel-shaped pelvic diaphragm and inferiorly by the skin covering the external genitalia, anus, and adjacent structures. Laterally, the perineum is bounded by the medial surface of the inferior pubic rami, obturator internus muscle below the origin of the levator ani muscle, coccygeus muscle, medial surface of the sacrotuberous ligaments, and overlapping margins of the gluteus maximus muscles (Fig. 71-2).

FIGURE 71-1 The external genitalia. A, Mons pubis; B, prepuce; C, clitoris; D, labia majora; E, labia minora; F, urethral meatus; G, Skene’s ducts; H, vagina; I, hymen; J, Bartholin’s glands; K, posterior fourchette; L, perineal body.

FIGURE 71-2 The muscles and fascia of the perineum: A, Suspensory ligament of clitoris; B, clitoris; C, crus of clitoris; D, vestibular bulb; E, bulbocavernosus muscle; F, inferior fascia of urogenital diaphragm; G, deep transverse perineal muscle; H, Bartholin’s gland; I, perineal body; J, ischiocavernosus muscle; K, external anal sphincter; L, levator ani muscle; M, anococcygeal body; N, coccyx; O, gluteus maximus muscle; P, pudendal artery and vein; Q, superficial transverse perineal muscle.

The pelvic outlet can be divided into two triangles separated by a line drawn between the ischial tuberosities. The anterior or urogenital triangle has its apex anteriorly at the symphysis pubis and the posterior or anal triangle has its apex at the coccyx.

The urogenital triangle contains the urogenital diaphragm, a muscular shelf extending between the pubic rami and penetrated by the urethra and vagina, and the external genitalia, consisting of the mons pubis, labia majora and minora, clitoris, and vestibule. The mons pubis is a suprapubic fat pad covered by dense skin appendages. The labia majora extend posteriorly from the mons, forming the lateral borders of the vulva. They have a keratinized, stratified squamous epithelium with all the normal skin appendages and extend posteriorly to the lateral perineum. Within the confines of the labium are fat and the insertion of the round ligament. Medial to the labia majora are interlabial grooves and the labia minora, of similar cutaneous origin, but devoid of hair follicles. The labia minora are richly vascularized, with an erectile venous plexus. The bilateral roots of the clitoris fuse in the midline to form the glans at the lower edge of the pubic symphysis. The labia minora fuse over the clitoris to form the hood and, to a variable degree, below to create the clitoral frenulum.

Contiguous to the medial aspect of the labia minora, demarcated by Hart’s line, is the vulvar vestibule, extending to the hymeneal sulcus. The vestibular surface is a stratified, squamous mucous membrane that shares embryology and has similar characteristics to the distal urethra and urethral meatus. Bartholin’s glands, at 5 and 7 o’clock, the paraurethral Skene’s glands, and minor vestibular glands positioned around the lateral vestibule are all under the vestibular bulb, subjacent to the bulbocavernosus muscle. The ostia of these glands pass through the vestibular mucosa, directly adjacent to the hymeneal ring.

The muscles of the external genitalia consist of the deep and superficial transverse perineal muscles, paired ischiocavernosus muscles that cover the crura of the clitoris, and bulbocavernosus muscles lying on either side of the vagina, covering the vestibular bulbs.

The anal triangle contains the anal canal, with surrounding internal and external sphincters, ischiorectal fossa, filled with fatty tissue, median raphe, and overlying skin.

Blood supply to the perineum is predominantly from a posterior direction from the internal pudendal artery, which, after arising from the internal iliac artery, passes through Alcock’s canal, a fascial tunnel along the obturator internus muscle below the origin of the levator ani muscle. On emerging from Alcock’s canal, the internal pudendal artery sends branches to the urogenital triangle anteriorly and to the anal triangle posteriorly. Anteriorly, there is blood supply to the mons pubis from the inferior epigastric artery, a branch of the femoral artery. Laterally, the external pudendal artery arises from the femoral artery and supplies the lateral aspect of the vulva. Venous return from the perineum accompanies the arterial supply and therefore drains into the internal iliac and femoral veins. It is important for the surgeon dissecting the external genitalia to be cognizant of the variability of direction from which the blood supply of the operative field is derived.

The major nerve supply to the perineum comes from the internal pudendal nerve, which originates from the S2 to S4 anterior rami of the sacral plexus and travels through Alcock’s canal, along with the internal pudendal artery and vein. Anterior branches supply the urogenital diaphragm and external genitalia, whereas posterior branches, the inferior rectal nerve, supply the anus, anal canal, ischiorectal fossa, and adjacent skin. Branches of the posterior femoral cutaneous nerve from the sacral plexus innervate the lateral aspects of the ischiorectal fossa and adjacent structures. The mons pubis and anterior labia are supplied by the ilioinguinal and genitofemoral nerves from the lumbar plexus; they travel through the inguinal canal and exit through the superficial inguinal ring. All these paired nerves routinely cross the midline for partial innervation of the contralateral side. The visceral efferent nerves responsible for clitoral erection are derived from the pelvic splanchnic nerves and reach the external genitalia along with the urethra and vagina as they pass through the urogenital diaphragm.

Surgical injury to the pelvic nerve plexus can result in neuropathic pain and diminished sexual, voiding, and excretory function.

The lymphatic drainage of the perineum, including the urogenital and anogenital triangles, travels for the most part with the external pudendal vessels to the superficial inguinal nodes. The deep parts of the perineum, including the urethra, vagina, and anal canal, drain in part through the lymphatics that accompany the internal pudendal vessels and into the internal iliac lymph nodes.

The fascia and fascial spaces of the perineum are important regarding the spread of extravasated fluids and superficial and deep infections. Fascia covers each of the muscles bounding the perineum, including the deep surface of the levator ani, obturator internus, and coccygeus, as well as other perineal muscles, such as the urogenital diaphragm. The fascia of the levator ani muscles fuses with the obturator internus fascia and pubic rami, creating well-defined fascial spaces, the ischiorectal fosse. Beneath the skin of the external genitalia is a layer of fat; deep to this is Colles’ fascia, which is attached to the ischiopubic rami laterally and the posterior edge of the urogenital diaphragm. Anteriorly, Colles’ fascia of the vulva is continuous with Colles’ fascia of the anterior abdominal wall.

Infections or collections of extravasated urine deep to the urogenital diaphragm are usually confined to the ischiorectal fossa, including the anterior recess, which is superior to the urogenital diaphragm. Collections of fluid or infections superficial to the urogenital diaphragm may pass to the abdominal wall deep to Colles’ fascia. Because of various fascial fusions, infections spreading from the vulva to the anterior abdominal wall do not spread into the inguinal regions or the thigh.

Internal Genitalia

The internal genitalia consist of the ovaries, fallopian tubes, uterus, cervix, and vagina, with associated blood supply and lymphatic drainage (Figs. 71-3 to 71-5).

FIGURE 71-3 The internal genitalia. A, A, Symphysis pubis; B, bladder; C, corpus uteri; D, round ligament; E, fallopian tube; F, ovary; G, utero-ovarian ligament; H, broad ligament; I, ovarian artery and vein; J, ureter; K, uterosacral ligament; L, cul-de-sac; M, rectum; N, middle sacral artery and vein; O, vena cava; P, aorta. B, A, Labium majus; B, labium minus; C, symphysis pubis, D, urethra; E, bladder; F, vagina; G, anus; H, rectum; I, cervix uteri; J, corpus uteri; K, endometrial cavity; L, round ligament; M, fallopian tube; N, ovary; O, cul-de-sac; P, uterosacral ligament; Q, sacrum; R, ureter; S, ovarian artery and vein.

FIGURE 71-4 Blood supply of the pelvis. A, Aorta; B, inferior vena cava; C, ureter; D, ovarian vein; E, ovarian artery; F, renal vein; G, common iliac artery; H, psoas muscle; J, ovary; K, rectum; L, corpus uteri; M, bladder; N, internal iliac (hypogastric) artery, anterior branch; O, external iliac artery; P, obturator artery; Q, external iliac vein; R, uterine artery; S, uterine vein; T, vaginal artery; U, superior vesicle artery; V, inferior epigastric artery.

FIGURE 71-5 Lymphatics of the pelvis. A, Aortic; B, sacral; C, common iliac; D, hypogastric; E, obturator; F, deep inguinal; G, Cloquet’s node; H, parametrial; I, superficial inguinal.

Ovary

The oblong ovaries, glistening white in color, vary in size, which is dependent on age and status of the ovulatory cycle. In the prepubescent girl, the ovary will appear as a white sliver of tissue smaller than 1 cm in any dimension. The ovary of a woman during her reproductive years will vary in size and shape. The size of the nonovulating ovary will typically be in the range of 3 × 2 × 1 cm. When a follicular or corpus luteum cyst is present, the size may extend up to 5 to 6 cm. A follicular cyst is an asymmetrical, translucent, clear structure. A corpus luteum cyst will generally be characterized by areas of golden yellow and, occasionally, by hematoma. The ovaries are suspended from the lateral side wall of the pelvis below the pelvic brim by the infundibulopelvic ligament and attach to the superolateral aspect of the uterine fundus by the utero-ovarian ligament.

The primary blood supply to the ovary is the ovarian artery. It arises directly from the aorta and courses with the vein through the infundibulopelvic ligament into the medulla on the lateral aspect of the ovary. The right ovarian vein generally drains to the inferior vena cava and the left ovarian vein drains to the common iliac vein; however, variations commonly occur. There is a rich anastomotic arterial complex arising from the uterine artery that spreads across the broad ligament and mesosalpinx. The venous return accompanies that arterial supply. There is no somatic innervation to the ovary, but the autonomic fibers arise from the lumbar sympathetic and sacral parasympathetic plexuses. Lymphatic drainage parallels the iliac and aortic arteries.

There are three important relationships to be considered when carrying out surgical dissection. The infundibulopelvic ligament, with the ovarian blood supply, crosses over the ureter as it descends into the pelvis. As the surgeon divides and ligates the ovarian vessels, it is critical that this relationship be identified to avoid transecting, ligating, or kinking the ureter. The risk for ureteral injury is greater with a more proximal dissection of the ligament. Also, in its natural position, the suspended ovary drops along the pelvic sidewall along the course of the midureter. If there are adhesions between the ovary and peritoneum of the pelvic sidewall, careful dissection is necessary to avoid tenting the peritoneum with the attached ureter and causing injury. The third surgical relationship is the complex of external iliac vessels and femoral nerve, which course along the iliopsoas muscle, directly below the course of the ovarian vessels; with anterior adhesions of an ovary, these structures may be subjacent to the malpositioned ovary.

Fallopian Tubes

The fallopian tubes are cylindrical structures approximately 8 cm in length. They originate at the uterine cavity in the uterine cornua, with an intramural segment of 1 to 2 cm and a narrow isthmic segment of 4 to 5 cm, flaring over 2 to 3 cm to the funnel of the infundibular segment and terminating in the fimbriated end of the tube. The fimbria are fine, delicate mucosal projections that are positioned to allow for capture of the extruded oocyte to promote the potential for fertilization. The blood supply to the tube is derived primarily from branches of the uterine artery, with a delicate cascade of vessels in the mesosalpinx. There is a secondary supply from the anastomosis with the ovarian vessels.

The surgeon must be aware of the fragility of the fallopian tube and handle this structure delicately, especially in women wishing to preserve their fertility. The mucosa lining the tubal lumen, especially at the fimbriated end, is highly specialized to facilitate transport of the oocyte and fertilized zygote. Traumatic manipulation of the tube can induce tubal infertility or predispose to later tubal pregnancy through damage to the mucosa or distortion of the tubal position by adhesions, thereby interfering with the access or transport mechanisms.

Uterus and Cervix

The uterus, with the cervix, is a midline, pear-shaped organ suspended in the midplane of the pelvis by the cardinal and uterosacral ligaments. The cardinal ligaments are dense fibrous condensations arising from the fascial covering of the levator ani muscles of the pelvic floor and inserting into the lateral portions of the uterocervical junction. The uterosacral ligaments arise posterolaterally from the uterocervical junction and course obliquely in a posterolateral direction to insert into the parietal fascia of the pelvic floor at the sacroiliac joint. The round ligaments of the uterus arise from the anterolateral superior aspect of the uterine fundus, course anterolaterally to the internal inguinal ring, and insert into the labia majora. The round ligaments are highly stretchable and serve no function in pelvic organ support. The broad ligaments are composed of a visceral peritoneal surface containing loose adventitious tissue. These ligaments also provide no pelvic organ support, but do allow access to an avascular plane of the pelvis through which the retroperitoneal vasculature and ureter can be exposed.

The size of the uterus is influenced by age, hormonal status, prior pregnancy, and common benign neoplasms. The normal uterus during the reproductive years is approximately 8 × 6 × 4 cm and weighs approximately 100 g. The prepubertal or postmenopausal uterus is substantially smaller. The mass of the uterus is almost exclusively made up of myometrium, a complex of interlacing bundles of smooth muscle. The uterine cavity is 4 to 6 cm from the internal cervical os to the uterine fundus, shaped as an inverted triangle, 2 to 3 mm wide at the cervix, and 3 to 4 cm across the fundus, extending from cornua to cornua. It is only a few millimeters deep between the anterior and posterior walls, with no defined lateral walls in the nonpregnant state. The most common reason for variation in size is current pregnancy followed by uterine fibroids.

If, during a surgical procedure, the surgeon encounters an enlarged uterus, undiagnosed pregnancy must be considered. The morphologic differences between a uterus enlarged by a pregnancy and one enlarged by fibroid include symmetrical enlargement in pregnancy with generally asymmetrical enlargement with fibroids. If symmetrical, consider the origin of the round ligaments. With pregnancy, the round ligaments stretch as the uterus grows and continue to originate from the normal site; even with an apparently symmetrical fibroid uterus, the origin of the round ligaments is frequently displaced from the top of the uterine fundus or asymmetrical course through the pelvis. Finally, the pregnant uterus is usually dusky and soft, whereas fibroids are generally firm and nodular masses can be palpated in the myometrial wall.

The uterine cavity is lined by the endometrium, a complex epithelial-stromal-vascular secretory tissue. The arterial supply to the endometrium is derived from branches of the uterine artery that perforate the myometrium to the inactive basalis layer. There, they form the arcuate vessels, which produce radial branches extending through the functional layer toward the compacted surface layer. There will be further description of the menstrual cycle here but, during the postovulatory phase, these vessels differentiate into spiral arteries, uniquely suited to allow menstruation and subsequent hemostasis.

The uterine cervix is histologically dynamic, with changes in cervical mucus production during the ovarian cycle. In the follicular phase, under estrogen stimulation, copious clear mucus is produced that facilitates the transport of sperm through the cervical canal to ascend through the uterine cavity to the fallopian tubes. During progesterone-dominant states, either luteal phase, or with exogenous hormones, the mucus becomes viscous and plugs the cervix. The secretory epithelium of the endocervical canal has a dynamic metaplastic interaction with the stratified squamous epithelium of the portio vaginalis of the ectocervix under hormonal stimulation. Because the cervical canal is continuous with the vagina, surgical procedures involving the uterus and tubes are considered to be clean-contaminated cases.

The major sources of blood supply for the uterus and cervix are the uterine arteries, which are branches of the anterior division of the internal iliac (hypogastric) arteries. Although the origin of the uterine artery is usually a single identifiable vessel, it divides into multiple ascending and descending branches as it courses medially to the lateral margins of the cervicouterine junction. The distance from the uterus at which this division occurs is highly variable. Venous return from the uterus flows into the companion internal iliac vein. Lymphatics from the cervix and upper vagina drain primarily through the internal iliac nodes but, from the uterine fundus, drainage occurs primarily along a presacral path directly to the para-aortic nodes.

The primary surgical consideration for managing the uterine vessels is the close proximity of the ureter, which courses approximately 1 cm below the artery and 1 cm lateral to the cervix. If the surgeon loses control of one of the branches of the vessel, it is important to use techniques that avoid clamping or kinking the ureter. Often, the most prudent way to secure the uterine artery is to expose its origin and place hemostatic clips on the vessel.

Innervation of the uterus and cervix is derived from the autonomic plexus. Autonomic pain fibers are activated with dysmenorrhea, in labor, and with instrumentation of the cervix and uterus.

In the retroperitoneal space lateral to the uterus is the obturator nerve, which arises from the lumbosacral plexus and passes through the pelvic floor by way of the obturator canal to innervate the medial thigh. With relatively normal pelvic anatomy, it is unlikely to be subjected to injury; however, under circumstances in which the surgeon must dissect the retroperitoneal or paravaginal spaces, this relatively subtle structure can be injured, with significant neuropathic residual.

Vagina

The vagina originates at the cervix and terminates at the hymeneal ring. The anatomic axis of the upper vagina is posterior to anterior in a caudad direction. The anterior and posterior walls of the upper two thirds of the vagina are normally opposed to each other to create a transverse potential space, distensible through pliability of the lateral sulci. The lower third of the vagina has a relatively vertically oriented caudad lumen. The mucosa of the vagina is nonkeratinized, stratified, squamous epithelium that responds to estrogen stimulation.

The blood supply to the vagina is provided by descending branches of the uterine artery and vein and ascending branches of the internal pudendal artery and its companion vein. These vessels course along the lateral walls of the vagina. Innervation is derived from the autonomic plexus and pudendal nerve, which track with the vessels.

Traumatic lacerations of the vagina are usually located along the lateral sidewalls, and the degree to which there is major injury to the vessels can be associated not only with significant evident hemorrhage, but also with concealed hemorrhage. Spaces in which a hematoma can be concealed are the retroperitoneum of the broad ligaments, paravesical and pararectal spaces, and ischiorectal fossa. Because of the proximity of the pudendal nerve, attempts to ligate the vessels require maintaining orientation to the location of Alcock’s canal to avoid creating neuropathic injury. In the absence of an accumulating hematoma, the best approach to management is often a bulk vaginal pack to achieve tamponade. To accomplish this requires significant sedation or anesthesia and an indwelling urinary catheter.

The uterus, cervix, and vagina, with their fascial investments, comprise the middle compartment of the pelvis. The structures of the anterior compartment, the bladder and urethra, and of the posterior compartment, the rectum, are each invested with a fascial layer. Avascular planes of loose areolar tissue separate the posterior fascia of the bladder and anterior fascia of the vagina and the anterior fascia of the rectum and posterior fascia of the vagina. Anteriorly, the bladder is attached to the lower uterine segment by the continuous visceral peritoneum. This vesicouterine fold can be incised transversely with minimal difficulty to expose the plane and allow dissection of the bladder from the cervix and vagina. Posteriorly, the proximity of the rectum to the posterior vagina is significant only below the peritoneum of the cul-de-sac of Douglas, unless the cul-de-sac anatomy is distorted by dense adhesions.

Operative techniques for gynecologic procedures are optimized by careful identification of these planes to separate and protect the adjacent organs from operative injury. The surgeon can create an incidental cystotomy, which may or may not be recognized, or devitalize the bladder wall with a crush or stitch, with delayed development of a vesicovaginal fistula.

In the lower pelvis, the ureter courses anteromedially after it passes under the uterine vessels and progresses toward the trigone of the bladder through a fascial tunnel on the anterior vaginal wall. The fixation of the ureter by the tunnel precludes effective displacement from the operative site by retracting. Although the location of the fascial tunnel is generally 1 to 2 cm safely below the usual site for vaginotomy during hysterectomy, in patients with a large cervix, distorting uterine myoma, prior cesarean birth, or bleeding from the bladder base or vaginal wall, the ureter can be transected, crushed, or kinked with a stitch.

The rectovaginal septum is surgically relevant during the repair of an episiotomy or obstetric laceration, repair of rectovaginal fistula, or pelvic support procedures. Identification of the fascial layers investing the subjacent structures and using the tissue strength is critical to an optimal repair.

Reproductive Physiology

The development of a differential diagnosis of gynecologic complaints is facilitated by an understanding of the reproductive cycle and eliciting a careful menstrual history. Many conditions are a direct consequence of aberrations in the hypothalamic-pituitary-ovarian cycle and the effects of the hormonal milieu on the endometrium. Others tend to be mere variations in the presentation of different phases of the cycle. A detailed description of the cycle is beyond our scope here, but the surgeon needs to have a basic understanding of the relationships in this complex process to elicit an adequate history, interpret the findings on physical examination, use ancillary tests appropriately, and formulate the differential diagnosis (Fig. 71-6).

FIGURE 71-6 Hormonal changes during the menstrual cycle. Menses, days 0 to 5; ovulation, day 14.

Ovarian Cycle

Under the stimulus of hypothalamic secretion of gonadotropin-releasing hormone (GnRH) to the pituitary gland, follicle-stimulating hormone (FSH) is released into the systemic circulation. During this secretory phase of the ovarian cycle, the primordial follicles of the ovary are targeted and stimulated toward growth and maturity. Multiple follicles are recruited each cycle, but generally only one follicle becomes dominant, destined to reach maturity and extrusion at ovulation. The effects of the maturation process include not only the completion of meiotic germ cell development but also the stimulation of the granulosa cells that surround the follicle to secrete estradiol, other estrogenic compounds, and inhibin. As the estradiol level increases in the circulation, it has a positive regulatory effect on GnRH, which in turn stimulates the pituitary gland to release a surge of luteinizing hormone (LH). The LH surge stimulates the release of the oocyte from the follicle. After release, the follicle site converts to the corpus luteum; the dominant hormone secreted during this luteal phase is progesterone. This sequence of hormonal events prepares the cervix, uterus, and tubes for sperm transport into the upper genital tract, fertilization, implantation, and support of the early gestation. In the absence of conception, the corpus luteum undergoes atresia and the next ovarian cycle begins.

Endometrial Cycle

The hormonal sequence of the ovarian cycle controls the physiologic changes in the endometrium. By convention, each endometrial cycle begins on day 1, defined as the onset of menses. In an idealized cycle, the LH surge and ovulation occur on day 14. Atresia of the corpus luteum occurs on day 28 and menses begin the next day, day 1 of the new cycle.

During the follicular phase of the ovarian cycle, estrogen exerts a stimulatory effect on the endometrium, producing the proliferative phase of the endometrial cycle. The endometrial tissues that are affected include the surface and glandular epithelium, stromal matrix, and vascular bed. The stromal layer thickens, the glandular elements elongate, and the terminal arterioles of the endometrial circulation extend from the basalis toward the endometrial surface. The mucous secretions of the glands of the endometrium, and the endocervix, become profuse and watery, facilitating the ascent of spermatozoa for potential fertilization.

During the luteal phase of the ovarian cycle, corresponding to the secretory phase of the endometrial cycle, progesterone domination converts the endometrium toward receptivity for implantation of the fertilized oocyte. Several endometrial changes occur under progesterone stimulation. The growth of the endometrial stroma is terminated, the surface layer of the endometrium becomes compacted, the glandular secretions become more viscous, and the terminal arterioles become coiled, creating the spiral arterioles. Cervical mucus similarly becomes more viscous and tenacious, creating a relative barrier between the vagina and uterine cavity.

In the absence of fertilization, and with the withdrawal of progesterone because of atresia of the corpus luteum, there is a complex sequence of arteriolar spasm, leading to ischemic necrosis of the endometrial surface and endometrial shedding, or menses. Normal menses, in the absence of structural pathology, is an orderly process because these arteriolar changes occur in the entire mucosa simultaneously and universally, with vasospasm and coagulation occluding the terminal vessels. Bleeding associated with normal menses is notable for the absence of clotting because of fibrinolysis within the uterine cavity before flow. With fertilization and implantation, menses are absent (amenorrhea). Alternatively, a disordered ovarian cycle leads to a disordered endometrial cycle and abnormal uterine bleeding patterns.

Early Pregnancy

A brief description of the events leading to pregnancy is useful for understanding the possible complications of early pregnancy. Coitus during the 48 hours before ovulation or during the periovulatory period establishes the conditions for fertilization. As noted, sperm transport is facilitated by the estrogenic environment; the spermatozoa ascend through the cervix and uterine cavity to the fallopian tube. When a mature oocyte and spermatozoa come into contact in the distal fallopian tube, fertilization can occur, usually 3 to 5 days after ovulation. During tubal transport, the zygote undergoes multiple divisions to reach the stage of the morula by the time it reaches the cavity. Implantation generally occurs approximately 5 to 7 days after fertilization.

There are two significant clinical implications to delay in the fertilization-transport sequence. If the zygote has not matured adequately before reaching the endometrial cavity, implantation will not occur and a preclinical unrecognized pregnancy will be lost. If there is delay in the fertilization-transport sequence, either because of the randomness of coital timing or because of altered tubal structure or function, the zygote can reach the stage at which it is programmed to adhere to genital mucosa while still in the fallopian tube, resulting in an ectopic pregnancy.

Amenorrhea and Abnormal Menses

A disrupted sequence of the hypothalamic-pituitary-ovarian interaction has a profound effect on the endometrium and menses. There are two broad classes of amenorrheic disorders, hypogonadotropic and anovulatory. Although the details of the pathology and evaluation are beyond our scope of this text, hypogonadotropic conditions result from central disruption of the hypothalamic-pituitary axis. Common causes for this condition include stress, hyperprolactinemia, and low body mass (e.g., those with anorexia nervosa, athletes [distance runners, gymnasts, ballerinas]). Because of the hypogonadotropic state, follicles are not stimulated, estrogen is not secreted, and endometrial proliferation does not occur. The result is an atrophic endometrium.

An atrophic endometrium can be identified with ultrasound, measuring the endometrial bilayer. Although local equipment and operator experience will vary, an endometrial bilayer less than 5 mm in a young amenorrheic woman is highly supportive of the diagnosis. This must be followed by a thorough investigation of the entire axis.

Anovulation results from a disrupted sequence of the axis from failure of the feedback loop to trigger the LH surge. The patient may have normal or elevated FSH levels, but FSH continues to stimulate the continuous production of estrogen from the granulosa cells. The chronic unopposed estrogen promotes continuous proliferation of the endometrium, without the maturing sequence induced by progesterone. The proliferation of the endometrium results in excessive thickness. This becomes clinically manifest by prolonged amenorrhea, often followed by prolonged and profuse uterine bleeding (hypermenorrhea, menorrhagia). The most common cause for this presentation is polycystic ovarian disease, but physiologic or social stress can produce a similar clinical scenario.

Ultrasound measurement of the endometrial bilayer can exceed 20 mm. Patients with chronic anovulation with chronic unopposed estrogen are at risk for endometrial hyperplasia and even endometrial cancer. The evaluation of the patient must address the cause for the chronic anovulation and the endometrial consequences. Histologic diagnosis requires an endometrial biopsy or curettage.

After prolonged amenorrhea with excessive proliferation of the endometrial lining, hypermenorrhea and menorrhagia may occur as a result of four parallel mechanisms. The growth of tissue from the basalis to the surface extends beyond the terminal branches of the arterioles, resulting in surface ischemia and necrosis. The volume of endometrial tissue is obviously increased. The normal hemostatic mechanisms of the spiral arterioles in the menstrual cycle are absent. Finally, the shedding of the endometrial surface is not a universal event, but is random and leads to multiple foci of bleeding that are dyssynchronous and occur over a prolonged time. Frequently, the rate of bleeding exceeds the capacity of the normal intracavitary fibrinolytic processes, and blood clots are common in the flow.

Clinical Evaluation

Acute life-threatening conditions frequently involve pregnancy, such as a ruptured ectopic pregnancy and heavy vaginal bleeding associated with miscarriage. Therefore, in the acute setting, the possibility of pregnancy must be considered and history focused on this area. It is immediately apparent that many questions in a gynecologic or obstetric history are personal and sensitive, so it may be helpful to conduct the interview or at least part of it in private, without the presence of family members and after attempting to gain the patient’s trust and understanding.

Patients will typically present with aberrant bleeding patterns, pelvic-abdominal pain or ill-defined discomfort, or a combination of these symptoms. With a focused history, the differential diagnosis can be constructed with further refinement from physical findings and ancillary tests. The key elements to be elicited are age, pregnancy history, recent and past menstrual history, sexual history, contraception, prior gynecologic disease and procedures, and evolution of the current complaints.

Diagnostic Considerations

Although there are always atypical crossover presentations for any of the possible diagnoses, the most common considerations for the differential diagnosis of symptom complexes are as presented here.

Bleeding Without Pain

• Anovulatory cycle

• Threatened or spontaneous abortion (miscarriage of intrauterine pregnancy)

• Vaginal laceration

• Vaginal or cervical neoplasm

Midline Pelvic Pain Without Bleeding

• Endometritis or pelvic inflammatory disease (PID)

• Endometriosis

• Pelvic neoplasm

• Urinary tract infection

• Constipation

Generalized Abdominal Pain Without Bleeding

• Ruptured extrauterine pregnancy

• Ruptured ovarian cyst

• PID with pelvic peritonitis

• Endometriosis

Obstipation

• Cul-de-sac hematoma

• Cul-de-sac adnexal mass

• Posterior uterine fibroid

• Pelvic abscess

• Endometriosis

Flank Pain

• Pyelonephritis

• Ureteral obstruction

• Ovarian remnant syndrome, with or without ureteral obstruction

Other Acute Clinical Presentations

Acute Vulvovaginitis

Acute vulvovaginitis is a common presenting emergency complaint. Presenting symptoms are intense pruritus or cutaneous pain with discharge. The most frequent pathogens are mycotic or herpetic infections. Mycotic infections are generally characterized by a thick, white, cottage cheese–like discharge. Primary herpetic infections often present with profuse watery discharge, inguinal adenopathy, and signs of a viremia. In contrast, other common vaginal infections, such as bacterial vaginosis and trichomoniasis, may cause irritative symptoms and malodorous discharge, but rarely cause pain.

Common acute vulvar complaints include infection of skin appendages—folliculitis, furunculosis, and cellulitis. The ostium of the Bartholin’s gland may become occluded, with or without infection. Sterile cysts are only minimally uncomfortable, but a Bartholin’s cyst abscess is exquisitely painful.

Necrotizing Fasciitis

Necrotizing fasciitis is a life-threatening infection that can occur in the vulva. It can begin as a cellulitis, from infected skin appendages, or following biopsy or episiotomy. Once established, it can quickly extend through the fascial planes. Women at risk are patients with obesity, diabetes, and steroid or other immunosuppressive drug use. Treatment is immediate surgical débridement. Patients may require several débridements to determine the extent of the fascial involvement. Skin grafts are often needed to repair large defects. It is important that women with risk factors for necrotizing fasciitis who present with a vulvar cellulitis be admitted for treatment with IV antibiotics and possible surgery.

Pelvic Masses

Masses identified in the pelvis can be functional, congenital, neoplastic, hemorrhagic, or inflammatory and can arise from the ovary or the uterus. Also, the anatomy of the cul-de-sac of Douglas in its dependent position in the pelvis facilitates restriction of pelvic infection as collections or abscesses to that location.

Common ovarian masses include functional cysts, hemorrhagic cysts, paraovarian or paratubal wolffian remnants, endometrioma, and benign or malignant tumors (e.g., epithelial, germ cell, stromal). The most common neoplastic mass in young women is the benign cystic teratoma. Because of the sebaceous content of these lesions, they frequently float to the anterior cul-de-sac between the uterus and bladder. Diagnostic considerations for differentiating among ovarian masses of various causes are discussed in detail in the later section on ovarian cancer.

Common uterine masses include leiomyoma, adenomyoma, and bicornuate uterus. Common inflammatory masses are tubo-ovarian abscesses (TOAs), pelvic collection, and appendiceal or diverticular abscesses.

Inflammatory masses in the anterior cul-de-sac most commonly originate from sigmoid diverticular disease.

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Aug 1, 2016 | Posted by admin in CARDIAC SURGERY | Comments Off

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