Emmanouil D. Stamatis, MD

• Department of Orthopaedic Surgery
• 401 General Army Hospital
• Athens, Greece

It also contributes to fetal mineral homeostasis in bone heart attack yahoo answers buy hytrin 5mg low price, amnionic fluid blood pressure chart for 70+ year olds cheap hytrin 1mg online, and the fetal circulation (Simmonds pulse pressure 16 buy discount hytrin line, 2010) arrhythmia dysrhythmia purchase 5 mg hytrin with visa. It functions as an antiobesity hormone that decreases food intake through its hypothalamic receptor arteria femoral buy 2mg hytrin. In the placenta hypertension vision buy cheap hytrin 1mg on line, leptin is synthesized by both cytotrophoblasts and syncytiotrophoblast (Henson, 2002). Relative contributions of leptin from maternal adipose tissue versus placenta are currently not well defined, although recent evidence highlights a key regulatory role of placental leptin in placental amino acid transport and fetal growth (Rosario, 2016a). Fetal leptin levels correlate positively with birthweight and likely function in fetal development and growth. Studies suggest that reductions in leptin availability contribute to adverse fetal metabolic programing in intrauterine growth-restricted offspring (Nusken, 2016). It also is found in sympathetic neurons innervating the cardiovascular, respiratory, gastrointestinal, and genitourinary systems. Neuropeptide Y has been isolated from the placenta and localized in cytotrophoblasts (Petraglia, 1989). Inhibin and Activin these glycoprotein hormones are expressed in male and female reproductive tissues and belong to the transforming growth factor- family (Jones, 2006). Inhibin is a heterodimer made up of one -subunit and one of two distinct subunits, either A or B. For example, elevation in inhibin A levels in the second trimester is indicative of fetal Down syndrome. Further, low inhibin levels early in pregnancy may indicate pregnancy failure (Prakash, 2005; Wallace, 1996). Elevations in circulating inhibin and activin levels are reported in women with preeclampsia (Bersinger, 2003). Surgical removal of the corpus luteum or even bilateral oophorectomy during the 7th to 10th week does not decrease excretion rates of urinary pregnanediol, the principal urinary metabolite of progesterone. Before this time, however, corpus luteum removal will result in spontaneous abortion unless an exogenous progestin is given (Chap. After approximately 8 weeks, the placenta assumes progesterone secretion, resulting in a gradual increase in maternal serum levels throughout pregnancy. By term, these levels are 10 to 5000 times those found in nonpregnant women, depending on the stage of the ovarian cycle. First, cholesterol is converted to pregnenolone within the mitochondria, in a reaction catalyzed by cytochrome P450 cholesterol side-chain cleavage enzyme. Pregnenolone leaves the mitochondria and is converted to progesterone in the endoplasmic reticulum by 3-hydroxysteroid dehydrogenase. Although the placenta produces a prodigious amount of progesterone, the syncytiotrophoblast has a limited capacity for cholesterol biosynthesis. Radiolabeled acetate is incorporated into cholesterol by placental tissue at a slow rate. Because of this, the placenta must rely on an exogenous source, that is, maternal cholesterol, for progesterone formation. This mechanism differs from placental production of estrogens, which relies principally on fetal adrenal precursors. Although there is a relationship between fetal well-being and placental estrogen production, this is not the case for placental progesterone. The metabolic clearance rate of progesterone in pregnant women is similar to that found in men and nonpregnant women. During pregnancy, the plasma concentration of 5-dihydroprogesterone disproportionately rises due to synthesis in syncytiotrophoblast from both placenta-produced progesterone and fetus-derived precursor (Dombroski, 1997). Thus, the concentration ratio of this progesterone metabolite to progesterone is elevated in pregnancy. Progesterone also is converted to the potent mineralocorticoid deoxycorticosterone in pregnant women and in the fetus. The concentration of deoxycorticosterone is strikingly higher in both maternal and fetal compartments (see Table 5-1). The extraadrenal formation of deoxycorticosterone from circulating progesterone accounts for most of its production in pregnancy (Casey, 1982a,b). Production of both progesterone and estrogens in the maternal ovaries drops significantly by the 7th week of pregnancy. By the 7th week, more than half of estrogen entering maternal circulation is produced in the placenta (MacDonald, 1965a; Siiteri, 1963, 1966). Subsequently, the placenta produces a continually increasing magnitude of estrogen. Near term, normal human pregnancy is a hyperestrogenic state, and syncytiotrophoblast is producing estrogen in amounts equivalent to that produced in 1 day by the ovaries of no fewer than 1000 ovulatory women. Biosynthesis In human trophoblast, neither cholesterol nor, in turn, progesterone can serve as precursor for estrogen biosynthesis. Ryan (1959a) found that the placenta had an exceptionally high capacity to convert appropriate C19 steroids to estrone and estradiol. The fetal adrenal glands are quantitatively the most important source of placental estrogen precursors in human pregnancy. Thus, estrogen production during pregnancy reflects the unique interactions among fetal adrenal glands, fetal liver, placenta, and maternal adrenal glands. Directional Secretion More than 90 percent of estradiol and estriol formed in syncytiotrophoblast enters maternal plasma (Gurpide, 1966). And, 85 percent or more of placental progesterone enters maternal plasma, and little maternal progesterone crosses the placenta to the fetus (Gurpide, 1972). This directional movement of newly formed steroid into the maternal circulation stems from basic characteristics of hemochorioendothelial placentation. In this system, steroids secreted from syncytiotrophoblast can enter maternal blood directly. They must first traverse the cytotrophoblast layer and then enter the stroma of the villous core and then fetal capillaries. The net result of this hemochorial arrangement is that entry of steroids into the maternal circulation is substantially greater than that into fetal blood. More than 85 percent of the fetal gland is composed of a unique fetal zone, which has a great capacity for steroid biosynthesis. This is exemplified by the continued growth of the fetal glands throughout gestation and by rapid involution immediately after birth and placental delivery. Placental Estriol Synthesis Estradiol is the primary placental estrogen product at term. In addition, significant levels of estriol and estetrol are found in the maternal circulation, and levels also rise, particularly late in gestation. These hydroxylated forms of estrogen derive from the placenta using substrates formed by the combined efforts of the fetal adrenal gland and fetal liver. For this, high levels of fetal hepatic 16hydroxylase act on adrenal-derived steroids. Near term, the fetus is the source of 90 percent of placental estriol and estetrol precursors in normal human pregnancy. Maternal estriol and estetrol are produced almost solely by fetal steroid precursors. Thus, in the past, levels of these steroids were used as an indicator of fetal well-being. However, the low sensitivity and specificity of such tests have caused them to be discarded. Fetal Adrenal Steroid Precursor the precursor for fetal adrenal steroidogenesis is cholesterol. All enzymes involved in cholesterol biosynthesis are elevated compared with those of the adult adrenal gland (Rainey, 2001). Thus, the de novo cholesterol synthesis rate by fetal adrenal tissue is extremely high. Even so, it is insufficient to account for the steroids produced by fetal adrenal glands. Most fetal plasma cholesterol arises by de novo synthesis in the fetal liver (Carr, 1984). Fetal Conditions Affecting Estrogen Production Several fetal disorders alter the availability of substrate for placental steroid synthesis and thus highlight the interdependence of fetal development and placental function. Similarly, after ligation of the umbilical cord with the fetus and placenta left in situ, placental estrogen production declines markedly (Cassmer, 1959). However, as previously discussed, placental progesterone production is maintained. In sum, an important source of precursors of placental estrogen-but not progesterone- biosynthesis is eliminated with fetal death. With absence of the adrenal cortex fetal zone, the placental formation of estrogen-especially estriol-is severely limited because of diminished availability of C19 steroid precursors. Indeed, urinary estrogen levels in women pregnant with an anencephalic fetus are only about 10 percent of those found in normal pregnancy (Frandsen, 1961). Fetal adrenal cortical hypoplasia occurs in perhaps 1 in 12,500 births (McCabe, 2001). Estrogen production in these pregnancies is limited, which suggests the absence of C19 precursors. Namely, sulfatase deficiency precludes the hydrolysis of C19 steroid sulfates, the first enzymatic step in the placental use of these circulating prehormones for estrogen biosynthesis. Its estimated frequency is 1 in 2000 to 5000 births and is associated with delayed labor onset. It also is associated with the development of ichthyosis in affected males later in life (Bradshaw, 1986). This can cause virilization of the mother and the female fetus (Belgorosky, 2009; Harada, 1992; Shozu, 1991). It was discovered that serum unconjugated estriol levels were low in women with Down syndrome fetuses (Benn, 2002). The likely reason for this is inadequate formation of C19 steroids in the adrenal glands of these trisomic fetuses. Fetal erythroblastosis in some cases of severe fetal D-antigen alloimmunization can lead to elevated maternal plasma estrogen levels. A suspected cause is the greater placental mass from hypertrophy, which can be seen with such fetal hemolytic anemia (Chap. Maternal Conditions Affecting Estrogen Production Glucocorticoid treatment can cause a striking reduction in placental estrogen formation. With Addison disease, pregnant women show lower estrogen levels, principally estrone and estradiol levels (Baulieu, 1956). The fetal adrenal contribution to estriol synthesis, particularly in later pregnancy, is quantitatively much more important. Maternal androgen-producing tumors can present the placenta with elevated androgen levels. Fortunately, placenta is extraordinary efficient in the aromatization of C19 steroids. For example, Edman and associates (1981) found that virtually all androstenedione entering the intervillous space is taken up by syncytiotrophoblast and converted to estradiol. Second, a female fetus is rarely virilized if there is a maternal androgensecreting tumor. The placenta efficiently converts aromatizable C19 steroids, including testosterone, to estrogens, thus precluding transplacental passage. Indeed, virilized female fetuses of women with an androgen-producing tumor may be cases in which a nonaromatizable C19 steroid androgen is produced by the tumor-for example, 5-dihydrotestosterone. Another explanation is that testosterone is produced very early in pregnancy in amounts that exceed the placental aromatase capacity at that time. Complete hydatidiform mole and gestational trophoblastic neoplasias lack a fetus and also a fetal adrenal source of C19 steroid precursors for trophoblast estrogen biosynthesis. Consequently, placental estrogen formation is limited to the use of C19 steroids from the maternal plasma, and therefore estradiol is principally produced (MacDonald, 1964, 1966). Mol Cell Endocrinol 107:189, 1995 Arnholdt H, Meisel F, Fandrey K, et al: Proliferation of villous trophoblast of the human placenta in normal and abnormal pregnancies. Virchows Arch B Cell Pathol Incl Mol Pathol 60:365, 1991 Baker T: A quantitative and cytological study of germ cells in human ovaries. Arch Gynecol 239:63, 1986 Belgorosky A, Guercio G, Pepe C, et al: Genetic and clinical spectrum of aromatase deficiency in infancy, childhood and adolescence. Biochem Biophys Res Commun 144:674, 1987 Bleker O, Kloostermans G, Mieras D, et al: Intervillous space during uterine contractions in human subjects: an ultrasonic study. J Endocrinol 165:217, 2000 Borell U, Fernstrom I, Westman A: An arteriographic study of the placental circulation. Obstet Gynecol Surv 41:401, 1986 Brosens I, Dixon H: the anatomy of the maternal side of the placenta. Hum Reprod 11(Suppl 2):62, 1996 Cassmer O: Hormone production of the isolated human placenta. Acta Endocrinol Suppl 32(Suppl 45):1, 1959 Cervar M, Blaschitz A, Dohr G, et al: Paracrine regulation of distinct trophoblast functions in vitro by placental macrophages. J Endocrinol 173:219, 2002 Coya R, Martul P, Algorta J, et al: Progesterone and human placental lactogen inhibit leptin secretion on cultured trophoblast cells from human placentas at term. Gynecol Endocrinol 21:27, 2005 Crawford J: A study of human placental growth with observations on the placenta in erythroblastosis foetalis. Mol Human Reprod 6(8):743, 2000 Diczfalusy E, Troen P: Endocrine functions of the human placenta.

Nonsteroidal antiinflammatory drugs may also be beneficial but are used only in short courses to avoid fetal effects (Chap essential hypertension buy hytrin 5mg cheap. Muscle relaxants that include cyclobenzaprine or baclofen may be added when needed arrhythmia ablation buy cheap hytrin 1 mg on line. Once acute pain is improved blood pressure 50 over 20 2 mg hytrin sale, stabilizing and strengthening exercises provided by physical therapy help improve spine and hip stability blood pressure journal pdf buy cheap hytrin line, which is essential for the increased load of pregnancy heart attack waitin39 to happen best hytrin 1 mg. For some kamaliya arrhythmia purchase 1mg hytrin otc, a support belt that stabilizes the sacroiliac joint may be helpful (Gutke, 2015). Varicosities and Hemorrhoids Venous leg varicosities have a congenital predisposition and accrue with advancing age. They can be aggravated by factors that raise lower extremity venous pressures, such as an enlarging uterus. Femoral venous pressures in the supine gravida rise from 8 mm Hg in early pregnancy to 24 mm Hg at term. Thus, leg varicosities typically worsen as pregnancy advances, especially with prolonged standing. Symptoms vary from cosmetic blemishes and mild discomfort at the end of the day to severe discomfort that requires prolonged rest with feet elevation. Treatment is generally limited to periodic rest with leg elevation, elastic stockings, or both. Surgical correction during pregnancy generally is not advised, although rarely the symptoms may be so severe that injection, ligation, or even stripping of the veins is necessary. Vulvar varicosities frequently coexist with leg varicosities, but they may appear without other venous pathology. Treatment is with specially fitted pantyhose that will also minimize lower extremity varicosities. With particularly bothersome vulvar varicosities, a foam rubber pad suspended across the vulva by a belt can be used to exert pressure on the dilated veins. Hemorrhoids are rectal vein varicosities and may first appear during pregnancy as pelvic venous pressures rise. Pain and swelling usually are relieved by topically applied anesthetics, warm soaks, and stool-softening agents. This may be relieved by incision and removal of the clot following injection of a local anesthetic. Sleeping and Fatigue Beginning early in pregnancy, many women experience fatigue and need greater amounts of sleep. This likely is due to the soporific effect of progesterone but may be compounded in the first trimester by nausea and vomiting. In the latter stages, general discomforts, urinary frequency, and dyspnea can be additive. Sleep duration may be related to obesity and gestational weight gain (Facco, 2016; Lockhart, 2015). Moreover, sleep efficiency appears to progressively diminish as pregnancy advances. Wilson and associates (2011) performed overnight polysomnography and observed that women in the third trimester had poorer sleep efficiency, more awakenings, and less of both stage 4 (deep) and rapid-eye movement sleep. Daytime naps and mild sedatives at bedtime such as diphenhydramine (Benadryl) can be helpful. Cord Blood Banking Since the first successful cord blood transplantation in 1988, more than 25,000 umbilical cord blood transplantations have been performed to treat hemopoietic cancers and various genetic conditions (Butler, 2011). Public banks promote allogeneic donation, for use by a related or unrelated recipient, similar to blood product donation (Armson, 2015). Private banks were initially developed to store stem cells for future autologous use and charged fees for initial processing and annual storage. The American College of Obstetricians and Gynecologists (2015d) has concluded that if a woman requests information on umbilical cord banking, information regarding advantages and disadvantages of public versus private banking should be explained. Some states have passed laws that require physicians to inform patients about cord blood banking options. Importantly, few transplants have been performed by using cord blood stored in the absence of a known indication in the recipient (Screnci, 2016). The likelihood that cord blood would be used for the child or family member of the donor couple is considered remote, and it is recommended that directed donation be considered when an immediate family member carries the diagnosis of a specific condition known to be treatable by hemopoietic transplantation (Chap. Birth 44(1):29, 2017 Ahmad F, Hogg-Johnson S, Stewart D, et al: Computer-assisted screening for intimate partner violence and control. Ann Intern Med 151(2):94, 2009 American Academy of Pediatrics, American College of Obstetricians and Gynecologists: Guidelines for perinatal care, 8th ed. Accessed October 23, 2017 American College of Obstetricians and Gynecologists: Gestational diabetes mellitus. J Nutr 137(2):447, 2007 Borrelli F, Capasso R, Aviello G, et al: Effectiveness and safety of ginger in the treatment of pregnancy-induced nausea and vomiting. Accessed September 18, 2016 Chamberlain G, Broughton-Pipkin F (eds): Clinical Physiology in Obstetrics, 3rd ed. Am J Obstet Gynecol 183:1484, 2000 Clausson B, Granath F, Ekbom A, et al: Effect of caffeine exposure during pregnancy on birth weight and gestational age. Am J Epidemiol 155:429, 2002 Clement S, Candy B, Sikorski J, et al: Does reducing the frequency of routine antenatal visits have long term effects Am J Obstet Gynecol 214:S384, 2016 Facco F, Reid K, Grobman W, et al: Short and long sleep duration are associated with extremes of gestational weight gain. Am J Public Health 106(2):359, 2016 Institute of Medicine: Dietary Reference Intakes: the Essential Guide to Nutrient Requirements. Washington, the National Academies Press, 2011 Institute of Medicine and National Research Council: Weight Gain During Pregnancy: Reexamining the Guidelines. Curr Opin Clin Nutr Metab Care 9:388, 2006 Lacroix R, Eason E, Melzack R: Nausea and vomiting during pregnancy: a prospective study of its frequency, intensity, and patterns of change. Plast Reconstr Surg 117:301, 2006 Margulies R, Miller L: Fruit size as a model for teaching first trimester uterine sizing in bimanual examination. Pediatrics 123(3):917, 2009 Montagnana M, Trenti T, Aloe R, et al: Human chorionic gonadotropin in pregnancy diagnostics. Br J Nutr 114(2):274, 2015 Ota E, Mori R, Middleton P, et al: Zinc supplementation for improving pregnancy and infant outcome. Am J Perinatol 29(10):787, 2012 Phupong V, Hanprasertpong T: Interventions for heartburn in pregnancy. Am J Prev Med 33(4):297, 2007 Poskus T, Buzinskiene D, Drasutiene G, et al: Haemorrhoids and anal fissures during pregnancy and after childbirth: a prospective cohort study. Semin Perinatol 40(1):35, 2016 Rumbold A, Ota E, Nagata C, et al: Vitamin C supplementation in pregnancy. New York, Academic Press, 1970 Screnci M, Murgi E, Valle V, et al: Sibling cord blood donor program for hematopoietic cell transplantation: the 20-year experience in the Rome Cord Blood Bank. Preventive Services Task Force: Behavioral and pharmacotherapy interventions for tobacco smoking cessation in adults, including pregnant women: U. Am J Respir Crit Care Med 193(5):486, 2016 Staruch M, Kucharcyzk A, Zawadzka K, et al: Sexual activity during pregnancy. Neuro Endocrinol Lett 37(1):53, 2016 Stein Z, Susser M, Saenger G, et al: Nutrition and mental performance. Department of Health and Human Services: Reducing tobacco use: a report of the Surgeon General. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2000 U. Environmental Protection Agency: Fish: what pregnant women and parents need to know. Preventive Services Task Force: Recommendation statement: clinical guidelines: folic acid for the prevention of neural tube defects. Obstet Gynecol 104:65, 2004 Washington State Health Care Authority: Ultrasonography (ultrasound) in pregnancy: a health technology assessment. Whitridge Williams (1903) X-ray techniques were just on the horizon when the first edition of this textbook was published. The first application focused on the maternal pelvis without attention to the fetus. With improvements in resolution and image display, anomalies are increasingly detected in the first trimester, and Doppler is used to manage pregnancies complicated by growth impairment or anemia. The American College of Obstetricians and Gynecologists (2016) recommends that prenatal sonography be performed in all pregnancies and considers it an important part of obstetrical care in the United States. Technology and Safety the real-time image on the ultrasound screen is produced by sound waves that are reflected back from fluid and tissue interfaces of the fetus, amnionic fluid, and placenta. Sector array transducers contain groups of piezoelectric crystals working simultaneously in arrays. These crystals convert electrical energy into sound waves, which are emitted in synchronized pulses. Sound waves pass through tissue layers and are reflected back to the transducer when they encounter an interface between tissues of different densities. Dense tissue such as bone produces highvelocity reflected waves, which are displayed as bright echoes on the screen. Digital images generated at 50 to more than 100 frames per second undergo postprocessing that yields the appearance of real-time imaging. Ultrasound refers to sound waves traveling at a frequency above 20,000 hertz (cycles per second). Higher-frequency transducers yield better image resolution, whereas lower frequencies penetrate tissue more effectively. Transducers use widebandwidth technology to perform within a range of frequencies. Examinations are performed only by those trained to recognize fetal abnormalities and artifacts that may mimic pathology, using techniques to avoid ultrasound exposure beyond what is considered safe for the fetus (American College of Obstetricians and Gynecologists, 2016; American Institute of Ultrasound in Medicine, 2013b). No causal relationship has been demonstrated between diagnostic ultrasound and any recognized adverse effect in human pregnancy. The International Society of Ultrasound in Obstetrics and Gynecology (2016) further concludes that there is no scientifically proven association between ultrasound exposure in the first or second trimesters and autism spectrum disorder or its severity. All sonography machines are required to display two indices: the thermal index and the mechanical index. The thermal index is a measure of the relative probability that the examination may raise the temperature, potentially high enough to induce injury. That said, fetal damage resulting from commercially available ultrasound equipment in routine practice is extremely unlikely. The potential for temperature elevation is higher with longer examination time and is greater near bone than in soft tissue. The thermal index is higher with pulsed Doppler applications than with routine B-mode scanning (p. In the first trimester, if pulsed Doppler is clinically indicated, the thermal index should be 0. To document the embryonic or fetal heart rate, motion-mode (M-mode) imaging is used instead of pulsed Doppler imaging. The mechanical index is a measure of the likelihood of adverse effects related to rarefactional pressure, such as cavitation-which is relevant only in tissues that contain air. In mammalian tissues that do not contain gas bodies, no adverse effects have been reported over the range of diagnostically relevant exposures. The use of sonography for any nonmedical purpose, such as "keepsake fetal imaging," is considered contrary to responsible medical practice and is not condoned by the Food and Drug Administration (2014), the American Institute of Ultrasound in Medicine (2012, 2013b), or the American College of Obstetricians and Gynecologists (2016). Operator Safety the reported prevalence of work-related musculoskeletal discomfort or injury among sonographers approximates 70 percent (Janga, 2012; Roll, 2012). The main risk factors for injury during transabdominal ultrasound examinations are awkward posture, sustained static forces, and various pinch grips used while maneuvering the transducer (Centers for Disease Control and Prevention, 2006). Maternal habitus can be contributory because more force is often employed when imaging obese patients. As a result, your elbow is close to your body, shoulder abduction is less than 30 degrees, and your thumb is facing up. If seated, use a chair with back support, support your feet, and keep ankles in neutral position. Face the monitor squarely and position it so that it is viewed at a neutral angle, such as 15 degrees downward. Gestational Age Assessment the earlier that sonography is performed, the more accurate the gestational age assessment. Specific criteria for "re-dating" a pregnancy, that is, reassigning the gestational age and estimated date of delivery using initial sonogram findings, are shown in Table 10-1. The only exception to revising the gestational age based on early sonography is if the pregnancy resulted from assisted reproductive technology, in which case accuracy of gestational age assessment is presumed. Starting at 140/7 weeks, equipment software formulas calculate estimated gestational age and fetal weight from measurements of the biparietal diameter, head and abdominal circumference, and femur length. The estimates are most accurate when multiple parameters are used but may over- or underestimate fetal weight by up to 20 percent (American College of Obstetricians and Gynecologists, 2016). Various nomograms for other fetal structures, including the cerebellar diameter, ear length, ocular distances, thoracic circumference, and lengths of kidney, long bones, and feet, may be used to address specific questions regarding organ system abnormalities or syndromes (Appendix, p. A transverse (axial) image of the head is obtained at the level of the cavum septum pellucidum (arrows) and thalami (asterisks). The biparietal diameter is measured perpendicular to the sagittal midline, from the outer edge of the skull in the near field to the inner edge of the skull in the far field.

Closely related to the latter include abnormalities of the course of the coronary arteries arteria meningea media buy hytrin with paypal, such as interarterial heart attack jack 1 life 2 live hytrin 5mg overnight delivery, or anterior to the right ventricular outflow tract in patients with tetralogy of Fallot hypertension updates 2014 buy 5mg hytrin overnight delivery. There may also be abnormalities of the coronary artery terminations hypertension at 60 discount hytrin amex, namely pulse pressure method order hytrin uk, fistulae or coronary artery sinusoids artaria string quartet generic hytrin 1 mg otc. Finally, congenital coronary arteries can also be seen as part of the findings of other congenital heart diseases. Coronary artery abnormalities associated with various types of congenital heart lesions are discussed in their respective chapters. Parasternal short-axis view of the anomalous left coronary artery arising from the posterior aspect of the pulmonary artery. The right coronary artery fills with contrast, which arises normally from the right sinus of Valsalva. Anomalous origins of the coronary arteries are a rare congenital malformation, occurring in 0. The history and laboratory findings are all consistent with an ischemic dilated cardiomyopathy. Less hemodynamically important congenital coronary artery lesions that may place patients at risk for sudden cardiac death include coronary artery origins from the opposite sinus of Valsalva. Symptoms do not typically arise in the neonatal period, though sudden death has been reported in infants [9]. Invariably, these have an intramural course if there is a separate ostium and an interarterial course. Myocardial ischemia from coronary ostial stenosis has also been described in neonates [10, 11]. This results in cardiac dysfunction with the associated signs and symptoms, and is a cause of early neonatal death. The right and left coronary arteries arise from their respective sinuses of Valsalva. Echocardiogram in the short axis of the aortic root in: (a) 2D; and (b) with color Doppler. The left coronary artery ostium is located in the posterior aspect of the left sinus of Valsalva. The acquired coronary artery abnormalities are unlikely to be encountered in neonates but should still be considered. Within each type of acquired abnormality, there are a number of causes including primary diseases which may be congenital. Examples of this are coronary thrombosis, disruption, narrowing after an intervention involving the coronary arteries, stenosis caused by a prior inflammatory illness. Although unlikely to be seen in the neonate, these are mentioned for completeness. Those associated with other congenital heart defects will most likely be diagnosed as part of the cardiac evaluation or caused by signs and symptoms of myocardial ischemia, including postsurgical complication of arterial switch for transposition of the great arteries involving transfer of the coronary arteries. Cardiac catheterization with selective injection of the left coronary artery shows single left coronary artery. As a result, systolic ventricular ejection occurs through both the semilunar valve and the tunnel. However, in diastole flow reverses and is directed from the aorta to the ventricle. Most tunnels are large and result in significant ventricular volume overload and infantile onset of congestive heart failure. Clinically, aorto-ventricular tunnel must be distinguished from other connections between the aortic root and adjacent structures, such as a ruptured sinus of Valsalva or aortopulmonary window. Physical findings and hemodynamic consequences are similar to the patient with an aorto-pulmonary window (prominent aortic diastolic run-off, a murmur, and signs of pulmonary hypertension). In contrast, rupture of a dilated sinus of Valsalva occurs below the sinotubular junction within the sinus itself. A ruptured sinus will usually have a tapering dimension (smaller exit than entrance) and may even have multiple exit orifices. As a result, there is no shunt at the ventricular level, rather the shunt volume travels directly from the aorta to the pulmonary circulation. The yellow arrow indicates the aortic orifice of the tunnel, which in this case was elliptical and somewhat restrictive. The red arrow indicates the ventricular orifice which in this patient was quite large. The asterisk is positioned in the immediate subaortic portion of the left ventricular outflow tract. Both the aortic and ventricular orifice of this tunnel were large and the amount of diastolic flow was torrential (b). The arrow in (a) indicates the aortic orifice from the tubular ascending aorta, just above the sinotubular junction. When additional abnormalities are present, they most often involve the semilunar valves and coronary arteries. The most common coronary malformation, occurring in about 5%, is anomalous origin of the right coronary artery from the body of the tunnel rather than from the aortic sinus. Presence of such an anomalous coronary origin will significantly impact the approach to repair. The asterisk indicates the area of the tubular ascending aorta that gives rise to the aortic orifice. Note the tapering of the aneurysm from the aortic end to its right atrial exit (*). Note that there are actually two defects (ruptures) in the distal sinus, creating a "Y-shaped" color jet. The exit was into the right atrium, so the shunt flow was continuous in this case. Diagnostic Methods 241 failure during the first year of life, although isolated adult presentations of smaller tunnels have been reported. The course and severity of heart failure is variable; ranging from prenatal hydrops, to the typical infantile onset of heart failure with a prominent systolic/diastolic murmur, to rapid neonatal hemodynamic collapse (combined regurgitation and obstructive physiology), to years of compensated function without symptoms [2]. Those with the most rapid decline and demise tend to be patients with large tunnels and severe aortic outflow obstruction. Early reports suggested greater than 50% mortality in those detected by fetal echocardiography. A more recent series has shown improved survival, but this likely represents an enhanced ability to detect less severe cases. The outlook remains very poor for the fetus with prenatal onset of heart failure resulting from an aorto-ventricular tunnel. In contrast to both an aorto-ventricular tunnel and a ruptured sinus of Valsalva aneurysm, this malformation has no "length. Echocardiography is the most common and useful imaging modality for the infant with aorto-ventricular tunnel. The diastolic signal (above the baseline) represents the "regurgitant" flow traveling from the aorta, through the tunnel, and into the left ventricle. In addition to normal systolic forward flow (above the baseline), there is also prominent, holodiastolic reversal of flow (arrows). This image reveals that the right coronary artery (*) originates from the distal aspect of the tunnel. The unbranched segment is short with a large anterior branch and a small right/posterior branch noted immediately beyond the asterisk. These alternative imaging strategies can be very helpful in defining the origin of the right coronary artery, especially in the older patient. Invasive studies (cardiac catheterization with angiocardiography) are rarely necessary, unless it is not possible to define coronary arterial anatomy by any other means. The images oriented similar to parasternal long-axis transthoracic echocardiographic images. There was a normal pulmonary valve and no ventricular septal defect, eliminating truncus arteriosus as a possible diagnosis. Despite the combination of these two abnormalities, the fetus did not develop hydrops. Tunnels that open into the right ventricle are more optimally visualized in the short-axis view, because the body of the tunnel lies more parallel to the transverse axis of the heart. Coexisting aortic valve and coronary arterial abnormalities can also be detected in these views. Apical, subcostal, and suprasternal images can provide additional confirmation of the hemodynamic significance of the tunnel. Management Medical therapy provides only temporary palliation for heart failure symptoms. Surgery to eliminate a tunnel with significant blood flow should be undertaken without delay, even in asymptomatic patients. Such early intervention is warranted as the risk of surgery is low and likelihood of long-term ventricular dysfunction is increased if repair occurs after 6 months of age. Repair consists of closing the tunnel in a way that supports the aortic valve, and does not impair ventricular outflow or coronary blood flow. Closure of the ventricular orifice, in addition, supports the right coronary leaflet and theoretically reduces the incidence and severity of late regurgitation. When a coronary artery arises directly from the tunnel, more complex repairs are required. Most often, the anomalous coronary artery is surgically "transferred" and reattached to the ascending aorta (similar to the technique used in the arterial switch operation). Catheter-based interventions (device closure) are not usually appropriate because of the small size of most of these patients, and the fact that such devices do not give the extra support to the aortic valve that is gained with surgical closure. Associated abnormalities should be treated as clinically indicated, either separately or at the time of repair. Aortic valve regurgitation can progress, with up to half of patients reported to need aortic valve replacement later in life. It is not clear whether aortic enlargement after repair carries an increased risk of dissection in adulthood. Patients present with signs and symptoms similar to those for severe aortic valve regurgitation. Echocardiography will detect an anterior extracardiac channel connecting the tubular ascending aorta to the left ventricular outflow tract in most of these patients. Treatment involves early surgical closure and results in excellent short and intermediate term outcomes. Progressive aortic valve regurgitation is the most common late problem, highlighting the potential benefit to patch closing both the aortic and ventricular orifices of the tunnel in an effort to provide added support to the aortic valve leaflets. The morphology, origin, and exit points are variable, allowing potential connections between any coronary artery branch and any cardiac chamber, venous channel, or pulmonary artery [1]. The typical murmur is continuous, peaking in diastole when the pressure gradient is maximal. The clinical features are the same as any other cause of left-to-right shunt causing heart failure. The abnormal coronary connections that course from the ventricles in the setting of pulmonary atresia with intact ventricular septum or hypoplastic left heart syndrome should be discussed in the context of their primary disease entity and will not be discussed further here [2]. This accounts for the wide distribution of the anomalies throughout the coronary tree [3]. The incidence is unknown; however, it is likely to be between 1 in 100 000 and 1 in 10 000. Approximately 60% arise from the right coronary artery; 20% from the left descending coronary artery; and 20% from the left main stem or circumflex artery. The key echocardiographic features include a larger than normal coronary artery brought about by increased flow into the low pressure exit chamber. This position was achieved by first forming a guide wire loop through the fistula from the native coronary artery. Occlusion here was achieved using coils which were deployed directly from a catheter placed through the length of the coronary artery. The course of the fistula can sometimes be traced from the origin to the exit by color Doppler, allowing appreciation of the degree of tortuosity and relationship to standard coronary branches. Pulsed and continuous wave Doppler interrogation should show a continuous trace with more prominent diastolic than systolic flow. The diastolic predominance is because the aortic root (the origin of the coronary fistula flow) usually has the highest diastolic pressure in the circulation, resulting in a pressure gradient to the exit chamber. The exact nature of the flow pattern will depend on the exit chamber involved and its pressure profile. Following echocardiographic diagnosis, a decision needs to be made about further diagnostic imaging. In some cases, it may be appropriate to proceed straight to cardiac catheterization with a view to occlusion of the defect at the same procedure. Management Strategies the management strategy depends on symptoms or evidence of deleterious effects on the heart and circulatory function. Evidence of chamber dilation or an increase in pulmonary artery pressure should be sought. In these cases, standard medical management to control heart failure should be instituted alongside contemplation of definitive treatment [10]. Interventional Catheterization Currently, interventional catheterization is the mainstay of definitive management.

Of surgical relevance arrhythmia dysrhythmia buy hytrin visa, the inferior epigastric vessels initially course lateral to blood pressure prescriptions order hytrin paypal, then posterior to the rectus abdominis muscles arrhythmia band cheap hytrin 2mg fast delivery, which they supply blood pressure normal numbers discount 5 mg hytrin with visa. Above the arcuate line blood pressure chart for 19 year old buy generic hytrin pills, these vessels course ventral to the posterior rectus sheath and lie between this sheath and the posterior surface of the rectus muscles pulmonary hypertension 60 mmhg order hytrin with american express. Near the umbilicus, the inferior epigastric vessels anastomose with the superior epigastric artery and vein, which are branches of the internal thoracic vessels. Clinically, when a Maylard incision is used for cesarean delivery, the inferior epigastric vessels may be lacerated lateral to the rectus belly during muscle transection. These vessels rarely may rupture following abdominal trauma and create a rectus sheath hematoma (Tolcher, 2010; Wai, 2015). On each side of the lower anterior abdominal wall, Hesselbach triangle is the region bounded laterally by the inferior epigastric vessels, inferiorly by the inguinal ligament, and medially by the lateral border of the rectus abdominis muscle. Hernias that protrude through the abdominal wall in Hesselbach triangle are termed direct inguinal hernias. In contrast, indirect inguinal hernias do so through the deep inguinal ring, which lies lateral to this triangle, and then may exit out the superficial inguinal ring. Of these, the intercostal and subcostal nerves are anterior rami of the thoracic spinal nerves and run along the lateral and then anterior abdominal wall between the transversus abdominis and internal oblique muscles. This space, termed the transversus abdominis plane, can be used for postcesarean analgesia blockade (Chap. Others report rectus sheath or ilioinguinal-iliohypogastric nerve blocks to decrease postoperative pain (Mei, 2011; Wolfson, 2012). In this figure, an intercostal nerve extends ventrally between the transversus abdominis and internal oblique muscles. During this path, the nerve gives rise to lateral and anterior cutaneous branches, which innervate the anterior abdominal wall. Thus, these nerve branches may be severed during a Pfannenstiel incision creation during the step in which the overlying anterior rectus sheath is separated from the rectus abdominis muscle. In contrast, the iliohypogastric and ilioinguinal nerves originate from the anterior ramus of the first lumbar spinal nerve. They emerge lateral to the psoas muscle and travel retroperitoneally across the quadratus lumborum inferomedially toward the iliac crest. Near this crest, both nerves pierce the transversus abdominis muscle and course ventromedially. At a site 2 to 3 cm medial to the anterior superior iliac spine, the nerves then pierce the internal oblique muscle and course superficial to it toward the midline (Whiteside, 2003). The iliohypogastric nerve perforates the external oblique aponeurosis near the lateral rectus border to provide sensation to the skin over the suprapubic area. The ilioinguinal nerve in its course medially travels through the inguinal canal and exits through the superficial inguinal ring, which forms by splitting of external abdominal oblique aponeurosis fibers. This nerve supplies the skin of the mons pubis, upper labia majora, and medial upper thigh. The ilioinguinal and iliohypogastric nerves can be severed during a low transverse incision or entrapped during closure, especially if incisions extend beyond the lateral borders of the rectus abdominis muscle (Rahn, 2010). These nerves carry sensory information only, and injury leads to loss of sensation within the areas supplied. Regional analgesia for cesarean delivery or for puerperal sterilization ideally extends to T4. This includes the mons pubis, labia majora and minora, clitoris, hymen, vestibule, urethral opening, greater vestibular or Bartholin glands, minor vestibular glands, and paraurethral glands. After puberty, the mons pubis skin is covered by curly hair that forms the triangular escutcheon, whose base aligns with the upper margin of the symphysis pubis. In men and some hirsute women, the escutcheon extends farther onto the anterior abdominal wall toward the umbilicus. They are continuous directly with the mons pubis superiorly, and the round ligaments terminate at their upper borders. Hair covers the labia majora, and apocrine, eccrine, and sebaceous glands are abundant. Beneath the skin, a dense connective tissue layer is nearly void of muscular elements but is rich in elastic fibers and fat. This fat mass provides bulk to the labia majora and is supplied with a rich venous plexus. During pregnancy, this vasculature may develop varicosities, especially in multiparas, from increased venous pressure created by the enlarging uterus. They appear as engorged tortuous veins or as small grapelike clusters, but they are typically asymptomatic and require no treatment. From each side, the lower lamellae fuse to form the frenulum of the clitoris, and the upper lamellae merge to form the prepuce. Inferiorly, the labia minora extend to approach the midline as low ridges of tissue that join to form the fourchette. The labia minora dimensions vary greatly among individuals, with lengths from 2 to 10 cm and widths from 1 to 5 cm (Lloyd, 2005). Structurally, the labia minora are composed of connective tissue with numerous vessels, elastin fibers, and very few smooth muscle fibers. They are supplied with many nerve endings and are extremely sensitive (Ginger, 2011a; Schober, 2015). Thinly keratinized stratified squamous epithelium covers the outer surface of each labium. On their inner surface, the lateral portion is covered by this same epithelium up to a demarcating line, termed Hart line. Medial to this line, each labium is covered by squamous epithelium that is nonkeratinized. It is located beneath the prepuce, above the frenulum and urethra, and projects downward and inward toward the vaginal opening. The clitoris rarely exceeds 2 cm in length and is composed of a glans, a corpus or body, and two crura (Verkauf, 1992). Extending from the clitoral body, each corpus cavernosum diverges laterally to form a long, narrow crus. Each crus lies along the inferior surface of its respective ischiopubic ramus and deep to the ischiocavernosus muscle. Specifically, the deep artery of the clitoris supplies the clitoral body, whereas the dorsal artery of the clitoris supplies the glans and prepuce. Vestibule In adult women, the vestibule is an almond-shaped area that is enclosed by Hart line laterally, the external surface of the hymen medially, the clitoral frenulum anteriorly, and the fourchette posteriorly. The vestibule is usually perforated by six openings: the urethra, the vagina, two Bartholin gland ducts, and two ducts of the largest paraurethral glands-the Skene glands. The posterior portion of the vestibule between the fourchette and the vaginal opening is called the fossa navicularis. On their respective side, each lies inferior to the vestibular bulb and deep to the inferior end of the bulbospongiosus muscle (former bulbocavernosus muscle). Following trauma or infection, either duct may swell and obstruct to form a cyst or, if infected, an abscess. In contrast, the minor vestibular glands are shallow glands lined by simple mucin-secreting epithelium and open along Hart line. The paraurethral glands are a collective arborization of glands whose numerous small ducts open predominantly along the entire inferior aspect of the urethra. The two largest are called Skene glands, and their ducts typically lie distally and near the urethral meatus. Clinically, inflammation and duct obstruction of any of the paraurethral glands can lead to urethral diverticulum formation. Vagina and Hymen In adult women, the hymen is a membrane of varying thickness that surrounds the vaginal opening more or less completely. It is composed mainly of elastic and collagenous connective tissue, and both outer and inner surfaces are covered by nonkeratinized stratified squamous epithelium. The aperture of the intact hymen ranges in diameter from pinpoint to one that admits one or even two fingertips. However, identical tears may form by other penetration, for example, by tampons used during menstruation. For example, over time, the hymen transforms into several nodules of various sizes, termed hymeneal or myrtiform caruncles. Proximal to the hymen, the vagina is a musculomembranous tube that extends to the uterus and is interposed lengthwise between the bladder and the rectum. Anteriorly, the vagina is separated from the bladder and urethra by connective tissue-the vesicovaginal septum. Posteriorly, between the lower portion of the vagina and the rectum, similar tissues together form the rectovaginal septum. The upper fourth of the vagina is separated from the rectum by the rectouterine pouch, also called the cul-de-sac or pouch of Douglas. Vaginal length varies considerably, but commonly, the anterior wall measures 6 to 8 cm, whereas the posterior vaginal wall is 7 to 10 cm. The upper end of the vaginal vault is subdivided by the cervix into anterior, posterior, and two lateral fornices. Clinically, the internal pelvic organs usually can be palpated through the thin walls of these fornices. The vaginal lining is composed of nonkeratinized stratified squamous epithelium and underlying lamina propria. In premenopausal women, this lining is thrown into numerous thin transverse ridges, known as rugae, which line the anterior and posterior vaginal walls along their length. Beneath this muscularis lies an adventitial layer consisting of collagen and elastin (Weber, 1997). Instead, it is lubricated by a transudate that originates from the vaginal subepithelial capillary plexus and crosses the permeable epithelium (Kim, 2011). Due to increased vascularity during pregnancy, vaginal secretions are notably increased. At times, this may be confused with amnionic fluid leakage, and clinical differentiation of these two is described in Chapter 22 (p. After birth-related epithelial trauma and healing, fragments of stratified epithelium occasionally are embedded beneath the vaginal surface. Similar to its native tissue, this buried epithelium continues to shed degenerated cells and keratin. As a result, epidermal inclusion cysts, which are filled with keratin debris, may form. The proximal portion is supplied by the cervical branch of the uterine artery and by the vaginal artery. The latter may variably arise from the uterine or inferior vesical artery or directly from the internal iliac artery. The middle rectal artery contributes supply to the posterior vaginal wall, whereas the distal walls receive contributions from the internal pudendal artery. At each level, vessels supplying each side of the vagina course medially across the anterior or posterior vaginal wall and form midline anastomoses. An extensive venous plexus also surrounds the vagina and follows the course of the arteries. Lymphatics from the lower third, along with those of the vulva, drain primarily into the inguinal lymph nodes. Those from the middle third drain into the internal iliac nodes, and those from the upper third drain into the external, internal, and common iliac nodes. Perineum this diamond-shaped area between the thighs has boundaries that mirror those of the bony pelvic outlet: the pubic symphysis anteriorly, ischiopubic rami and ischial tuberosities anterolaterally, sacrotuberous ligaments posterolaterally, and coccyx posteriorly. An arbitrary line joining the ischial tuberosities divides the perineum into an anterior triangle, also called the urogenital triangle, and a posterior triangle, termed the anal triangle. The perineal body is a fibromuscular pyramidal mass found in the midline at the junction between these anterior and posterior triangles. Also called the central tendon of the perineum, the perineal body sonographically measures 8 mm tall and 14 mm wide and thick (Santoro, 2016). It serves as the junction for several structures and provides significant perineal support (Shafik, 2007). Superficially, the bulbospongiosus, superficial transverse perineal, and external anal sphincter muscles converge on the perineal body. More deeply, the perineal membrane, portions of the pubococcygeus muscle, and internal anal sphincter contribute (Larson, 2010). The perineal body is incised by an episiotomy incision and is torn with second-, third-, and fourth-degree lacerations. Structures on the left side of the image can be seen after removal of Colles fascia. Those on the right side are noted after removal of the superficial muscles of the anterior triangle. This membranous partition is a dense fibrous sheet that was previously known as the inferior fascia of the urogenital diaphragm. The perineal membrane attaches laterally to the ischiopubic rami, medially to the distal third of the urethra and vagina, posteriorly to the perineal body, and anteriorly to the arcuate ligament of the pubis. The superficial space of the anterior triangle is bounded deeply by the perineal membrane and superficially by Colles fascia. As noted earlier, Colles fascia is the continuation of Scarpa fascia onto the perineum. On the perineum, Colles fascia securely attaches laterally to the pubic rami and fascia lata of the thigh, inferiorly to the superficial transverse perineal muscle and inferior border of the perineal membrane, and medially to the urethra, clitoris, and vagina.

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