Arthur Louis Burnett, M.D.

• Director, Basic Science Laboratory in Neuro-Urology
• Professor of Urology

https://www.hopkinsmedicine.org/profiles/results/directory/profile/0004242/arthur-burnett

Vagina and Perineum During pregnancy acne free reviews buy 20gm eurax with visa, greater vascularity and hyperemia develop in the skin and muscles of the perineum and vulva skin care quiz eurax 20gm overnight delivery, and the underlying abundant connective tissue softens acne x ray best purchase eurax. This augmented vascularity prominently affects the vagina and cervix and results in the violet color characteristic of Chadwick sign skin care chanel cheap eurax 20gm without a prescription. Within the vagina acne 3 step clinique eurax 20gm with mastercard, the considerably elevated volume of cervical secretions during pregnancy forms a somewhat thick acne neck purchase 20gm eurax fast delivery, white discharge. This pH results from increased production of lactic acid by Lactobacillus acidophilus during metabolism of glycogen energy stores in the vaginal epithelium. Pregnancy is associated with an elevated risk of vulvovaginal candidiasis, particularly during the second and third trimesters. Higher infection rates may stem from immunological and hormonal changes and from greater vaginal glycogen stores (Aguin, 2015). The vaginal walls undergo striking changes in preparation for the distention that accompanies labor and delivery. These alterations include considerable epithelial thickening, connective tissue loosening, and smooth muscle cell hypertrophy. In particular, vaginal lengthening, posterior vaginal wall and hiatal relaxation, increased levator hiatal area, and greater first-trimester vaginal elastase activity are all associated with uncomplicated spontaneous vaginal delivery (Oliphant, 2014). The larger hiatal area persists in women who deliver vaginally compared with women delivering by prelabor or early-labor cesarean delivery. However, all women show greater hiatal distensibility after delivery, which is potentially a factor in later pelvic floor dysfunction (van Veelen, 2015). In women with apical vaginal prolapse, the cervix, and occasionally a portion of the uterine body, can protrude variably from the vulva during early pregnancy. With further growth, the uterus usually rises above the pelvis and can draw the cervix up with it. As a preventive measure, the uterus can be replaced early in pregnancy and held in position with a suitable pessary. Attenuation of anterior vaginal wall support can lead to prolapse of the bladder, that is, a cystocele. Urinary incontinence affects nearly 20 percent of women during the first trimester and nearly 40 percent during the third trimester. A large defect may fill with feces that occasionally can be evacuated only digitally. During labor, a cystocele or rectocele can block fetal descent unless they are emptied and pushed out of the way. If the mass interferes with delivery, the hernia sac and its abdominal contents are gently reduced to permit fetal descent. After the second month, the breasts grow in size, and delicate veins are visible just beneath the skin. After the first few months, a thick, yellowish fluid-colostrum -can often be expressed from the nipples by gentle massage. Scattered through each areola are several small elevations, the glands of Montgomery, which are hypertrophic sebaceous glands. If breasts gain extensive size, skin striae similar to those observed in the abdomen may develop. Rarely, breasts can become pathologically enlarged-referred to as gigantomastia-which may require postpartum surgical reduction. These factors and gestation breast changes are further discussed in Chapter 36 (p. They found at least one physiological cutaneous change in 89 percent of the women examined. Abdominal Wall Beginning after midpregnancy, reddish, slightly depressed streaks commonly develop in the abdominal skin and sometimes in the skin over the breasts and thighs. In multiparas, glistening, silvery lines that represent the cicatrices of previous striae frequently coexist. In one study of 800 primiparas, 70 percent developed striae gravidarum on their abdomen; 33 percent on their breasts; and 41 percent on their hips and thighs (Picard, 2015). The strongest associated risk factors included younger maternal age, family history, and prepregnancy weight and weight gain during pregnancy. The etiology of striae gravidarum is unknown, and there are no preventive steps or definitive treatments (Korgavkar, 2015). Occasionally, the muscles of the abdominal walls do not withstand the tension of the expanding pregnancy. As a result, rectus muscles separate in the midline, creating diastasis recti of varying extent. If severe, a considerable portion of the anterior uterine wall is covered by only a layer of skin, attenuated fascia, and peritoneum to form a ventral hernia. Hyperpigmentation this develops in up to 90 percent of women and is usually more accentuated in those with darker complexion (Ikino, 2015). Of specific sites, the pigmented skin line in the midline of the anterior abdominal wall-the linea alba-takes on dark brown-black pigmentation to form the linea nigra. Occasionally, irregular brownish patches of varying size appear on the face and neck, giving rise to chloasma or melasma gravidarum-the mask of pregnancy. After delivery, these pigmentary changes usually disappear or at least regress considerably. The etiology of these pigmentary changes is incompletely understood, however, hormonal and genetic factors play a role. For example, levels of melanocytestimulating hormone, a polypeptide similar to corticotropin, are elevated remarkably throughout pregnancy, and estrogen and progesterone also are reported to have melanocyte-stimulating effects. Vascular Changes Angiomas, called vascular spiders, are particularly common on the face, neck, upper chest, and arms. These are minute, red skin papules with radicles branching out from a central lesion. Both conditions lack clinical significance and disappear in most gravidas shortly after pregnancy. In addition to these discrete lesions, increased cutaneous blood flow in pregnancy serves to dissipate excess heat generated by the augmented metabolism. Hair Changes Throughout life, the human hair follicle undergoes a pattern of cyclic activity that includes periods of hair growth (anagen phase), apoptosis-driven involution (catagen phase), and a resting period (telogen phase). Based on a study of 116 healthy pregnant women, the anagen phase lengthens during pregnancy and the telogen rate increases postpartum (Gizlenti, 2014). Neither is exaggerated in most gravidas, but excessive hair loss in the puerperium is termed telogen effluvium. By the third trimester, maternal basal metabolic rate rises by 20 percent compared with that of the nonpregnant state (Berggren, 2015). This rate grows by an additional 10 percent in women with a twin gestation (Shinagawa, 2005). Viewed another way, the additional total pregnancy energy demand associated with normal pregnancy approximates 77,000 kcal (World Health Organization, 2004). This is stratified as 85, 285, and 475 kcal/d during the first, second, and third trimester, respectively (Table 4-1). Of note, Abeysekera and coworkers (2016) reported that women accrue fat mass during pregnancy despite the increased total energy expenditure and without significant change in energy intake. Additional Energy Demands During Normal Pregnancya Weight Gain Most of the normal weight gain in pregnancy is attributable to the uterus and its contents, the breasts, and expanded blood and extravascular extracellular fluid volumes. A smaller fraction results from metabolic alterations that promote accumulation of cellular water, fat, and protein, which are so-called maternal reserves. Weight Gain Based on Pregnancy-Related Components Water Metabolism In pregnancy, greater water retention is normal and mediated in part by a drop in plasma osmolality of 10 mOsm/kg. This decline develops in early pregnancy and is induced by a reset of osmotic thresholds for thirst and vasopressin secretion. Thus, the minimum amount of extra water that the average woman accrues during normal pregnancy approximates 6. Clearly demonstrable pitting edema of the ankles and legs is seen in most pregnant women, especially at the end of the day. This fluid accumulation, which may amount to a liter or so, results from greater venous pressure below the level of the uterus as a consequence of partial vena cava occlusion. Longitudinal studies of body composition show a progressive accumulation of total body water and fat mass during pregnancy. These two components as well as initial maternal weight and weight gained during pregnancy are highly associated with neonatal birthweight (Lederman, 1999; Mardones-Santander, 1998). Protein Metabolism the products of conception, the uterus, and maternal blood are relatively rich in protein rather than fat or carbohydrate. At term, the normally grown fetus and placenta together weigh about 4 kg and contain approximately 500 g of protein, or about half of the total pregnancy increase. The remaining 500 g is added to the uterus as contractile protein, to the breasts primarily in the glands, and to maternal blood as hemoglobin and plasma proteins. Amino acid concentrations are higher in the fetal than in the maternal compartment and generally result from facilitated transport across the placenta (Cleal, 2011; Panitchob, 2015). This greater concentration is largely regulated by the placenta through an incompletely understood process. In particular, placental transport is variable for individuals and for different amino acids. For example, tyrosine is a conditionally essential amino acid in the preterm neonate but not in the fetus (Van den Akker, 2010, 2011). The placenta concentrates amino acids into the fetal circulation and is also involved in protein synthesis, oxidation, and transamination of some nonessential amino acids (Galan, 2009). Maternal protein intake does not appear to be a critical determinant for birthweight among well-nourished women (Chong, 2015). Still, recent data suggest that current recommendations for protein intake may be too low. These guidelines are extrapolated from nonpregnant adults and may underestimate actual needs. Stephens and colleagues (2015) prospectively analyzed maternal protein intake and metabolism. The daily requirements for dietary protein intake during pregnancy are discussed in Chapter 9 (p. Carbohydrate Metabolism Normal pregnancy is characterized by mild fasting hypoglycemia, postprandial hyperglycemia, and hyperinsulinemia. This elevated basal level of plasma insulin in normal pregnancy is associated with several unique responses to glucose ingestion. Specifically, after an oral glucose meal, gravidas demonstrate prolonged hyperglycemia and hyperinsulinemia and a greater suppression of glucagon (Phelps, 1981). This cannot be explained by an increased metabolism of insulin because its half-life during pregnancy is not changed appreciably (Lind, 1977). Instead, this response reflects a pregnancy-induced state of peripheral insulin resistance, which ensures a sustained postprandial supply of glucose to the fetus. Indeed, insulin sensitivity in late normal pregnancy is 30 to 70 percent lower than that of nonpregnant women (Lowe, 2014). In particular, pregnancy-related hormones such as progesterone, placentally derived growth hormone, prolactin, and cortisol; cytokines such as tumor necrosis factor; and hormones derived from central adiposity, particularly leptin and its interplay with prolactin, all have a role in the insulin resistance of pregnancy. Even so, insulin resistance is not the only factor to elevate postprandial glucose values. Hepatic gluconeogenesis is augmented during both diabetic and nondiabetic pregnancies, particularly in the third trimester (Angueira, 2015). Overnight, the pregnant woman changes from a postprandial state characterized by elevated and sustained glucose levels to a fasting state characterized by decreased plasma glucose and some amino acids. Plasma concentrations of free fatty acids, triglycerides, and cholesterol are also higher in the fasting state. This pregnancy-induced switch in fuels from glucose to lipids has been called accelerated starvation. Certainly, when fasting is prolonged in the pregnant woman, these alterations are exaggerated and ketonemia rapidly appears. Fat Metabolism the concentrations of lipids, lipoproteins, and apolipoproteins in plasma rise appreciably during pregnancy (Appendix, p. Increased insulin resistance and estrogen stimulation during pregnancy are responsible for the maternal hyperlipidemia. Augmented lipid synthesis and food intake contribute to maternal fat accumulation during the first two trimesters (Herrera, 2014). This is a consequence of enhanced lipolytic activity, and decreased lipoprotein lipase activity reduces circulating triglyceride uptake into adipose tissue. This transition to a catabolic state favors maternal use of lipids as an energy source and spares glucose and amino acids for the fetus. Maternal hyperlipidemia is one of the most consistent and striking changes of lipid metabolism during late pregnancy. After delivery, the concentrations of these lipids, lipoproteins, and apolipoproteins decline. Hyperlipidemia is theoretically a concern because it is associated with endothelial dysfunction. From studies, however, endothelium-dependent vasodilation responses actually improve across pregnancy (Saarelainen, 2006). These findings suggest that the increased cardiovascular disease risk in multiparas may be related to factors other than maternal hypercholesterolemia. Leptin this peptide hormone is primarily secreted by adipose tissue in nonpregnant humans. It plays a key role in body fat and energy expenditure regulation and in reproduction. For example, leptin is important for implantation, cell proliferation, and angiogenesis (Vazquez, 2015).

One example is fetal renal agenesis acne nodule discount eurax online amex, in which amnionic fluid is absent at the beginning of lung growth skin care shiseido order 20 gm eurax with visa, and major defects occur in all four developmental stages acne yahoo order 20 gm eurax visa. In another instance acne dermatologist order eurax 20gm otc, the fetus with membrane rupture and subsequent oligohydramnios before 20 weeks usually exhibits nearly normal bronchial branching and cartilage development but has immature alveoli skin care 7 belleville nj cheap eurax line. In contrast acne zits cysts and boils popped order eurax from india, membrane rupture after 24 weeks may have minimal long-term effect on pulmonary structure. In another example, various growth factors are expressed abnormally in the fetus with a diaphragmatic hernia (Candilira, 2015). Finally, vitamin D is thought to be important for several aspects of lung development (Hart, 2015; Lykkedegn, 2015). Pulmonary Surfactant After the first breath, the terminal sacs must remain expanded despite the pressure imparted by the tissue-to-air interface, and surfactant keeps them from collapsing. These cells are characterized by multivesicular bodies that produce the lamellar bodies in which surfactant is assembled. During late fetal life, at a time when the alveolus is characterized by a water-to-tissue interface, the intact lamellar bodies are secreted from the lung and swept into the amnionic fluid during respiratory-like movements that are termed fetal breathing. At birth, with the first breath, an air-to-tissue interface is established in the lung alveolus. Surfactant uncoils from the lamellar bodies and spreads to line the alveolus to prevent alveolar collapse during expiration. Nearly 80 percent of the glycerophospholipids are phosphatidylcholines (lecithins). The apoproteins are produced in the endoplasmic reticulum, and the glycerophospholipids are synthesized by cooperative interactions of several cellular organelles. Phospholipid is the primary surface tension-lowering component of surfactant, whereas the apoproteins aid the forming and reforming of a surface film. Since Liggins (1969) observed accelerated lung maturation in lamb fetuses given glucocorticosteroids prior to preterm delivery, many suggested that fetal cortisol stimulates lung maturation and surfactant synthesis. It is unlikely that corticosteroids are the only stimulus for augmented surfactant formation. However, when these are administered at certain critical times, they may improve preterm fetal lung maturation. As fetal lung therapy, antenatal betamethasone and dexamethasone use and neonatal replacement surfactant therapy are discussed in Chapter 34 (p. Breathing Fetal respiratory muscles develop early, and chest wall movements are detected sonographically as early as 11 weeks (Koos, 2014). From the beginning of the fourth month, the fetus engages in respiratory movement sufficiently intense to move amnionic fluid in and out of the respiratory tract. Some extrauterine events have effects on fetal breathing, for example, maternal exercise stimulates it (Sussman, 2016). Digestive System After its embryogenic formation from the yolk sac as the primordial gut, the digestive system forms the intestines and various appendages. The foregut gives rise to the pharynx, lower respiratory system, esophagus, stomach, proximal duodenum, liver, pancreas, and biliary tree. The midgut gives rise to the distal duodenum, jejunum, ileum, cecum, appendix, and the right colon. The hindgut develops into the left colon, rectum, and the superior portion of the anal canal. Numerous malformations develop in these structures from improper rotation, fixation, and partitioning. Swallowing begins at 10 to 12 weeks, coincident with the ability of the small intestine to undergo peristalsis and actively transport glucose (Koldovsky, 1965). As a correlate, neonates born preterm may have swallowing difficulties because of immature gut motility (Singendonk, 2014). Much of the water in swallowed fluid is absorbed, and unabsorbed matter is propelled to the lower colon. Gitlin (1974) demonstrated that late in pregnancy, approximately 800 mg of soluble protein is ingested daily by the fetus. The stimulus for swallowing is unclear, but the fetal neural analogue of thirst, gastric emptying, and change in the amnionic fluid composition are potential factors (Boyle, 1992). The fetal taste buds may play a role because saccharin injected into amnionic fluid increases swallowing, whereas injection of a noxious chemical inhibits it (Liley, 1972). Fetal swallowing appears to have little effect on amnionic fluid volume early in pregnancy because the volume swallowed is small compared with the total. However, term fetuses swallow between 200 and 760 mL per day-an amount comparable to that of the term neonate (Pritchard, 1966). Thus at term, amnionic fluid volume regulation can be substantially altered by fetal swallowing. Hydrochloric acid and some digestive enzymes are present in the stomach and small intestine in minimal amounts in the early fetus. The preterm neonate, depending on its gestational age, may have transient deficiencies of these enzymes (Lebenthal, 1983). Movement of amnionic fluid through the gastrointestinal system may enhance growth and development of the alimentary canal. For example, anencephalic fetuses, in which swallowing is limited, often have normal amnionic fluid volume and normal-appearing gastrointestinal tract. Meconium Fetal bowel contents consist of various products of secretion, such as glycerophospholipids from the lung, desquamated fetal cells, lanugo, scalp hair, and vernix. Meconium can pass from normal bowel peristalsis in the mature fetus or from vagal stimulation. Meconium is toxic to the respiratory system, and its inhalation can result in meconium aspiration syndrome (Chap. Liver the hepatic diverticulum is an outgrowth of the endodermal lining of the foregut. Epithelial liver cords and primordial cells differentiate into hepatic parenchyma. Still, the fetal liver has a gestational-age-related diminished capacity for converting free unconjugated bilirubin to conjugated bilirubin (Morioka, 2015). Because of hepatic immaturity, the preterm newborn is at particular risk for hyperbilirubinemia (Chap. And because the life span of normal fetal macrocytic erythrocytes is shorter than that of the adult, relatively more unconjugated bilirubin is produced. As just noted, the fetal liver conjugates only a small fraction, and this is excreted into the intestine and ultimately oxidized to biliverdin. Most of the unconjugated bilirubin is excreted into the amnionic fluid after 12 weeks and transferred across the placenta (Bashore, 1969). Thus, a woman with severe hemolysis from any cause has excess unconjugated bilirubin that readily passes to the fetus and then into the amnionic fluid. Conversely, conjugated bilirubin is not exchanged to any significant degree between mother and fetus. Hepatic glycogen is present in low concentration during the second trimester, but near term, levels rise rapidly and markedly to reach concentrations that are two- to threefold higher than those in the adult liver. Pancreas this organ arises from dorsal and ventral pancreatic buds from the endoderm of the foregut. Insulin-containing granules can be identified by 9 to 10 weeks, and insulin is detectable in fetal plasma at 12 weeks (Adam, 1969). Although hypoglycemia does not cause an increase in fetal glucagon levels, similar stimuli do so by 12 hours after birth (Chez, 1975). At the same time, however, fetal pancreatic cells do respond to Ldopa infusions (Epstein, 1977). Therefore, unresponsiveness to hypoglycemia is likely the consequence of failed glucagon release rather than inadequate production. This is consistent with developmental expression of pancreatic genes in the fetus (Mally, 1994). Trypsin, chymotrypsin, phospholipase A, and lipase are found in the 14-week fetus, and their concentrations increase with gestational age (Werlin, 1992). Physiologically important secretion occurs only after stimulation by a secretagogue such as acetylcholine, which is released locally after vagal stimulation (Werlin, 1992). Cholecystokinin normally is released only after protein ingestion and thus ordinarily would not be found in the fetus. Urinary System Renal development involves interaction between pluripotential stem cells, undifferentiated mesenchymal cells, and epithelial components (Fanos, 2015). Two primitive urinary systems-the pronephros and the mesonephros-precede development of the metanephros, which forms the final kidney (Chap. The pronephros involutes by 2 weeks, and the mesonephros produces urine at 5 weeks and degenerates by 11 to 12 weeks. Failure of these two structures either to form or to regress may result in anomalous urinary system development. Between 9 and 12 weeks, the ureteric bud and the nephrogenic blastema interact to produce the metanephros. By week 14, the loop of Henle is functional and reabsorption occurs (Smith, 1992). Although the fetal kidneys produce urine, their ability to concentrate and modify the pH is limited even in the mature fetus. Fetal urine is hypotonic with respect to fetal plasma and has low electrolyte concentrations. Renal vascular resistance is high, and the filtration fraction is low compared with adult values (Smith, 1992). Fetal renal blood flow and thus urine production are controlled or influenced by the renin-angiotensin system, the sympathetic nervous system, prostaglandins, kallikrein, and atrial natriuretic peptide. In later gestation, the rate remains constant when corrected for fetal weight (Smith, 1992). Hemorrhage or hypoxia generally results in a decrease in renal blood flow, glomerular filtration rate, and urine output. By 18 weeks, they are producing 7 to 14 mL/day, and at term, this increases to 650 mL/day (Wladimiroff, 1974). Maternally administered furosemide increases fetal urine formation, whereas uteroplacental insufficiency, fetal growth restriction, and other fetal disorders can lower it. Kidneys are not essential for survival in utero but influence control of amnionic fluid composition and volume. Thus, abnormalities that cause chronic fetal anuria are usually accompanied by oligohydramnios and pulmonary hypoplasia. Pathological correlates and prenatal therapy of urinary tract obstruction are discussed in Chapter 16 (p. Endocrine Gland Development Pituitary Gland the fetal endocrine system is functional for some time before the central nervous system reaches maturity (Mulchahey, 1987). The anterior pituitary gland develops from oral ectoderm # 8212;Rathke pouch, whereas the posterior pituitary gland derives from neuroectoderm. As with other organ systems, embryonic development involves a complex and highly spatiotemporally regulated network of signaling molecules and transcription factors (Bancalari, 2012; de Moraes, 2012). The adenohypophysis, or anterior pituitary, differentiates into five cell types that secrete six protein hormones. By the end of the 17th week, the fetal pituitary gland synthesizes and stores all pituitary hormones. Moreover, the fetal pituitary is responsive to tropic hormones and is capable of secreting these early in gestation (Grumbach, 1974). The cells of this structure begin to disappear before term and are absent from the adult pituitary. The posterior pituitary gland or neurohypophysis is well developed by 10 to 12 weeks, and oxytocin and arginine vasopressin are demonstrable. Both hormones probably function in the fetus to conserve water by actions directed largely at the lung and placenta rather than kidney. Vasopressin levels in umbilical cord plasma are increased strikingly compared with maternal levels (Chard, 1971). The thyroid migrates to its final position and the obliterated thyroglossal duct connects to the foramen cecum of the tongue. The placenta actively concentrates iodide on the fetal side, and by 12 weeks and throughout pregnancy, the fetal thyroid concentrates iodide more avidly than does the maternal thyroid. Thus, maternal administration of either radioiodide or appreciable amounts of ordinary iodide is hazardous after this time (Chap. Normal fetal levels of free thyroxine (T4), free triiodothyronine (T3), and thyroxin-binding globulin increase steadily throughout gestation (Ballabio, 1989). This suggests that the fetal pituitary may not become sensitive to feedback until late pregnancy (ThorpeBeeston, 1991). Fetal thyroid hormone plays a role in the normal development of virtually all fetal tissues, especially the brain (Forhead, 2014; Rovet, 2014). Its influence is illustrated by congenital hyperthyroidism, which develops when maternal thyroidstimulating antibody crosses the placenta to stimulate the fetal gland to secrete thyroxine (Donnelley, 2015). They also display tachycardia, hepatosplenomegaly, hematological abnormalities, craniosynostosis, and growth restriction. As children, they have perceptual motor difficulties, hyperactivity, and reduced growth (Wenstrom, 1990). The placenta prevents substantial passage of maternal thyroid hormones to the fetus by rapidly deiodinating maternal T4 and T3 to form reverse T3, a relatively inactive thyroid hormone (Vulsma, 1989). Several antithyroid antibodies cross the placenta when present in high concentrations (Pelag, 2002). It was previously believed that normal fetal growth and development, which occurred despite fetal hypothyroidism, provided evidence that T4 was not essential for fetal growth. It is now known, however, that growth proceeds normally because small quantities of maternal T4 prevent antenatal cretinism in fetuses with thyroid agenesis (Forhead, 2014; Vulsma, 1989). The fetus with congenital hypothyroidism typically does not develop stigmata of cretinism until after birth (Abduljabbar, 2012).

A transverse fracture follows a linear path from the foramen magnum to the foramen spinosum across the foramen lacerum skin care essentials purchase eurax with american express, also traversing and affecting on its way the jugular foramen skin care usa order eurax with visa, hypoglossal foramen skin care kiehls buy eurax 20 gm lowest price, and internal auditory meatus acne 60 year old woman 20 gm eurax with mastercard. A longitudinal fracture is roughly perpendicular to this skin care vancouver purchase 20 gm eurax visa, that is acne rash order eurax 20gm otc, it extends across the squamous part of the temporal bone to the foramen spinosum, passing on its way the posterior superior part of the external auditory canal, upper portion of the middle ear, and the carotid canal. The relative incidences of longitudinal and transverse fractures mentioned above, though the most often cited, are not constant and vary rather widely across the published literature on this topic. This is a more practical classification, and features of both transverse and longitudinal fractures are seen. Temporal bone fractures in children may have a similar presentation as in adults but with less morbidity as the pneumatization of the mastoid air cells lends a good amount of elasticity and shockabsorbing capacity to the temporal bone and the involved structures. Ear canal lacerations if circumferential need to be gently packed with a steroid antibiotic ointment to minimize chances of stenosis, whereas isolated areas of injury may be left to heal on their own without packing, taking care only to maintain aseptic conditions, or prophylactic antibiotics orally if required. Presence of a hemotympanum does not always mean active intervention, aspiration, or drainage, but a strict vigil must be maintained to promptly detect and treat ossicular chain damage or fibrosis. Blast trauma is due to the transmission of a very strong pressure wave across all the components of the ear-external, middle, and inner. It may be due to an excessively loud noise or an explosive force as is seen in bomb blasts, gunshot, and other ballistic wounds. While loud noise spares the external ear and tends to damage the more delicate middle and inner ear structures, explosions could damage all the three components as they also carry physical particles such as shrapnel and gunpowder and also chemicals or toxins. External ear lacerations, perichondritis, eardrum perforations, ossicular damage, and inner ear barotrauma can also occur. In addition, the spiral lamina of the cochlea may be disrupted leading to various degrees of hearing loss which is usually permanent. They may be pierced into the tissue or attached with a press-style clamp or have a combination of both. Piercing methods may not always be aseptic in nature, and infections are very common and in some cases may lead to serious problems such as perichondritis. Ear manipulation with buds and other solid objects such as hairpins and safety pins is very common and can cause direct trauma to the skin of the ear canal and may even perforate the tympanic membrane if forcibly introduced deeper into the ear, such as when another person pushes or brushes against the user. Medication abuse or routine use of potentially ototoxic eardrops may be considered a form of trauma-both self-induced and iatrogenic. Medication abuse with antibiotic eardrops may lead to fungal infections of the ear canal, while ototoxic medications may cause hearing impairment. External ear trauma has been classified by Weerda [1] into the following four types: 1. Minor abrasion-this type, as the definition suggests, involves minimal intervention in the form of an antibiotic cream for superficial abrasion and primary suturing of the wound with topical or oral antibiotic cover. Minor avulsion-where only a part of the pinna has been avulsed but has a pedicle about 5 mm in size with a feeding vessel, primary suturing may be done with fine nonabsorbable monofilament material, taking care to approximate the edges carefully. Major avulsion-if the pinna is avulsed and a large piece up to several millimeters in size is lost or devitalized, the missing part may be sacrificed and primary suturing is still possible. In some areas of the pinna, some distortion of normal anatomy may be acceptable, as over the lobule or rim. The pinna may look 64 4 Trauma to Ear slightly smaller in size as compared to the unaffected side but structurally similar and hence cosmetically all right. Primary repair and direct reattachment of an avulsed auricle as a composite graft can be done if the size of the amputated part is smaller than 15 mm in diameter [2]. Another method of primary repair is by repositioning the cartilage and covering it with local skin flaps such as a platysma or temporoparietal fascia flap [4]. Complete avulsion-when there is complete loss of the pinna, or a wound size larger than one and a half centimeter, bringing the skin edges together may not be possible. A soft tissue flap harvested from the same site, or a free flap from another region, may then be necessary. For example, blunt soft tissue impact may cause enough shearing forces to tear the auricle apart including both the skin and the underlying cartilage. This could be seen in direct impact as in assault or contact sport, motor vehicle accidents with exposure of the side of head, blast trauma with shattering of soft tissue, and penetrating injury with gunshot or sharp weapons. Loss of cartilage from the pinna results in severe scarring and distortion of anatomy. In certain cases, the cartilage may be present but unhealthy and devitalized and hence must be sacrificed. A cartilage graft from the nasal septum or rib (costal cartilage) may be required. These sites offer the ideal thickness of cartilage which may be molded into the desired shape. For larger defects or in those patients where the general condition of the patient is poor or the remaining soft tissue in the area is not viable, primary repair is not possible. The wound may be left to heal with secondary intention, and a tertiary repair could be undertaken at a later stage. A prosthetic appliance may also be used where it is impossible to restore a normal or esthetically acceptable appearance. Perichondritis of pinna may result from frostbite, thermal or chemical injury, and radiation injury following accidental exposure or radiotherapy. It occurs due to inflammation of the cartilage if exposed or even due to contamination of the overlying skin resulting in infection. The affected area becomes discolored and devitalized and is extremely tender and painful. It may lead to a spreading cellulitis of the surrounding skin and soft tissue, with the potential for hematogenous spread of infection and sepsis in severe cases. It is thus to be detected and treated early with antibiotics, given systemically if necessary. Failure to arrest the process may lead to loss of tissue with cosmetic deformity or systemic complications threatening life. It may also be caused by shearing forces on the auricle as in the case of motor vehicle accidents, in which case it may be associated with abrasions over the skin and bleeding/oozing. A seroma or pseudocyst of pinna is a collection of clear or serous fluid under the skin and perichondrium of the auricular cartilage. It is believed to be idiopathic in nature, but minor trauma such as an insect bite or scratch cannot be ruled out, and many a time a telltale sign of such trauma may be present if looked for closely. Auricle hematomas, apart from getting infected and causing an abscess, are potentially disfiguring because the underlying cartilage undergoes aseptic necrosis and gets absorbed, thus permanently altering the appearance of the auricle. Fibrosis occurs in the spots where cartilage loss has occurred, adding to the deformity. Recurrent hematomas lead to a deformity of the auricle known as "cauliflower ear," commonly seen in boxers. Professional sportspersons, however, are not much affected by this deformity and flaunt it as a symbol of a scintillating career in the sport. Treatment of hematoma of auricle is similar to that of a seroma, but an open approach is recommended especially for a hematoma. Aspiration of contents followed by instillation of steroid is practiced widely but is more appropriate for seromas than traumatic hematomas. The window technique and de-roofing of hematoma (or pseudocyst) is a more reliable technique whereby the contents can be removed properly, the cartilage inspected for areas of necrosis or devitalization and recurrence rates reduced along with a better cosmetic result [8]. Keloids are a type of hypertrophic scar where florid, uncontrolled, and lateral growth of scar occurs, leading to considerable cosmetic deformity. The word "keloid" is derived from "kelos" meaning "crab," suggesting a creeping pattern of spread, usually beyond the margins of the original wound in all directions including laterally, and therefore often visible externally. Since a keloid is a sequel to wound healing, it is best to leave it undisturbed, but treatment may be required for cosmetic and esthetic reasons. Foreign bodies in the ear usually get impacted at the region of the isthmus of the external auditory canal, which is the narrowest part. The hairs in the outer cartilaginous part may help trap a foreign body and prevent its further progress down the canal, but some may still be found even up to the deep meatus, especially if they are animate or small, smooth, and rounded and easily able to slip inside. Inept handling of foreign bodies in the ear by inexperienced persons may cause more harm than good. Insects and vegetable matter are removed more efficiently with a pair of forceps or a blunt hook. Examination and removal of a foreign body in the ear are greatly facilitated by the use of an operating microscope. The removal of the foreign body is usually carried out in the office or outpatient department without the use of anesthesia. The doctor meanwhile retracts the pinna with one hand (usually the left) and removes the foreign body holding the instrument in the other hand. If the microscope is used, the child may be "mummified" by swaddling it in a thick sheet to prevent movements of the arms and legs and keeping the child still. If the child is extremely uncooperative, it is better to remove the foreign body using a short general anesthetic agent such as ketamine or even holding down a mask if the procedure is anticipated to be easy. Impaction of the foreign body in the isthmus or deep meatus may necessitate a postaural approach under general anesthesia, especially in children. Struggling to remove the foreign body in such cases may cause it to rupture the tympanic membrane and enter the middle ear, causing predictable complications. Foreign bodies such as maggots may be removed manually after instillation of turpentine, chloroform, or liquid paraffin. Once suffocated and dead, syringing may be done to remove them en masse and debride the wound if necessary. A variety of foreign bodies may be encountered in the head and neck region- from plastic beads and metal batteries to glue and adhesive items being introduced into the ear by unsuspecting persons. In our experience, we have come across cyanoacrylate glue (Fevistick) that was squeezed into the ear of a young girl by her illiterate father in order to relieve an earache. It ended up forming a tight mold in the ear canal and caking the facial hair outside. After managing the patient with painkillers and allowing for the glue mold to separate on its own without any sign of success, it was finally removed under general anesthesia. Blunt injury occurs when the soft tissues of the lateral surface of the skull are subjected to contusion, laceration, or blast impact. This is seen in slaps or blows to the face, falls on the side of the head, and loud explosions. Penetrating trauma is seen with foreign bodies entering the ear in self-inflicted wounds by ear manipulation using fingers, ear buds, safety pins, hair clips, sticks, nails, etc. The perforation most commonly occurs in the anteroinferior quadrant slightly below the umbo, as this is directly in line with the forces of injury and also has the widest area of exposure where the tensile strength of the eardrum is just balanced by its fragile structure, as might be seen in any stretched membrane along its center point. Pain and bleeding usually occur at the onset but are not marked, while the hearing loss could be conductive or mixed depending on the impact and transmission of a pressure wave into the inner ear through the conducting apparatus. The history taking should be directed toward causation and nature of trauma and the need for establishing a medicolegal case if required. The edges of the perforation may be gently everted to prevent migration of squamous epithelium into the middle ear. The defect is patched with a piece of moistened Gelfoam or cigarette paper to act as a scaffold and promote rapid healing. Even if no active intervention is done, medium to large traumatic perforations have the potential for complete and spontaneous repair in the absence of infection or contamination. Follow-up is important for the first 3 months to ensure that no complications have occurred and normalcy has been restored. This results in a conductive type of hearing loss, which may be missed when other injuries of the ear are present. Treatment is simple and consists of exploration of the middle ear, reduction and alignment of the joint, or bridging the gap in the ossicular chain using a piece of cartilage harvested from the tragus or concha. If a lot of time has elapsed after the injury, fibrosis or ankylosis of the joint occurs and is difficult to treat. Hence a suspicion of this type of injury must always accompany trauma to the ear and be promptly treated. Established fibrosis or fixation of the joint is addressed with the use of a hearing aid. Barotrauma can be graded from 1 to 5 on the basis of signs and symptoms, 1 being mildest and causing only discomfort without any changes in the eardrum and 70 4 Trauma to Ear 5 the most severe, with perforation of the eardrum. The intermediate grades are characterized by tympanic membrane congestion, presence of fluid in the middle ear cavity, and bleeding from the capillaries in the tympanic membrane and middle ear. Tympanic membrane congestion and capillary rupture may also occur in cases of severe hypoxia as may be seen in cases of hanging or strangulation, due to compression of the carotid artery in the neck [9]. Usually as a result of such hypoxia, the victim has already been rendered unconscious. Hemotympanum is characterized by a "blue drum" due to the presence of dark blood (mainly venous) behind an intact tympanic membrane. Other causes for a blue drum are glomus tympanicum or glomus jugulare, otitis media with effusion, and cholesterol granuloma. Middle ear barotrauma generally does not require any active treatment except for the primary or precipitating condition. Active swallowing aided by chewing gum, steam inhalation, and gentle autoinflation usually suffices. Steroids may be added in individual cases where the fluid takes too long to be resorbed or the patient wishes to have a more rapid recovery. This occurs due to the impact of pressure disequilibrium or transmission of a pressure wave from blast trauma. The risk of perilymph fistula is greater in case of congenital weakness or anomalies of the stapes footplate or vestibular apparatus or following stapedotomy/stapedectomy. Labyrinthine concussion is a broad and nonspecific term given to inner injury due to barotraumas, resulting in a disturbance of inner ear fluids and electric potentials. Symptoms due to the above two are hearing and balance impairments, and diagnosis is more often than not delayed.

During early pregnancy acne 7 weeks pregnant cheap eurax 20gm on-line, there is a space between the decidua capsularis and parietalis because the gestational sac does not fill the entire uterine cavity acne studios order cheap eurax. The gestation sac is the extraembryonic coelom and also called the chorionic cavity acne treatments that work order eurax canada. The resulting apposition of the decidua capsularis and parietalis creates the decidua vera skin care myths purchase cheap eurax line, and the uterine cavity is functionally obliterated skin care basics eurax 20 gm on-line. In early pregnancy acne vulgaris icd 10 discount eurax 20 gm with amex, the decidua begins to thicken, eventually attaining a depth of 5 to 10 mm. With magnification, furrows and numerous small openings, representing the mouths of uterine glands, can be detected. Later in pregnancy, the decidua becomes thinner, presumably because of pressure exerted by the expanding uterine contents. There is a surface or compact zone-zona compacta; a middle portion or spongy zone-zona spongiosa-with remnants of glands and numerous small blood vessels; and a basal zone-zona basalis. In human pregnancy, the decidual reaction is completed only with blastocyst implantation. Predecidual changes, however, commence first during the midluteal phase in endometrial stromal cells adjacent to the spiral arteries and arterioles. Thereafter, they spread in waves throughout the uterine endometrium and then from the implantation site. The nuclei become vesicular, and the cytoplasm becomes clear, slightly basophilic, and surrounded by a translucent membrane. These arteries retain a smooth-muscle wall and endothelium and thereby remain responsive to vasoactive agents. In contrast, the spiral arterial system that supplies the decidua basalis and ultimately the placental intervillous space is altered remarkably. These spiral arterioles and arteries are invaded by trophoblasts, and during this process, the vessel walls in the basalis are destroyed. Importantly, as a result, these vascular conduits of maternal blood-which become the uteroplacental vessels-are unresponsive to vasoactive agents. Conversely, the fetal chorionic vessels, which transport blood between the placenta and the fetus, contain smooth muscle and thus do respond to vasoactive agents. Decidual Histology Early in pregnancy, the zona spongiosa of the decidua consists of large distended glands, often exhibiting marked hyperplasia and separated by minimal stroma. At first, the glands are lined by typical cylindrical uterine epithelium with abundant secretory activity that contributes to blastocyst nourishment. The spongy zone of the decidua basalis consists mainly of arteries and widely dilated veins, and by term, glands have virtually disappeared. Also, the decidua basalis is invaded by many interstitial trophoblasts and trophoblastic giant cells. Although most abundant in the decidua, the giant cells commonly penetrate the upper myometrium. If the decidua is defective, as in placenta accreta, the Nitabuch layer is usually absent (Chap. There is also a more superficial, but inconsistent, deposition of fibrin-Rohr stria-at the bottom of the intervillous space and surrounding the anchoring villi. Decidual necrosis is a normal phenomenon in the first and probably second trimesters (McCombs, 1964). Thus, necrotic decidua obtained through curettage after spontaneous abortion in the first trimester should not necessarily be interpreted as either a cause or an effect of the pregnancy loss. Both decidua types contain numerous cell groups whose composition varies with gestational stage (Loke, 1995). The primary cellular components are the true decidual cells, which differentiated from the endometrial stromal cells, and numerous maternal bone marrow-derived cells. These include regulatory T cells, decidual macrophages, and decidual natural killer cells. Collectively, these cells not only provide immunotolerance but also play an important role in trophoblast invasion and vasculogenesis (PrabhuDas, 2015). Decidual Prolactin In addition to placental development, the decidua potentially provides other functions. The decidua is the source of prolactin, which is present in enormous amounts in amnionic fluid (Golander, 1978; Riddick, 1979). Decidual prolactin is a product of the same gene that encodes for anterior pituitary prolactin, but the exact physiological role of decidual prolactin is unknown. This compares with fetal serum levels of 350 ng/mL and maternal serum levels of 150 to 200 ng/mL. As a result, decidual prolactin is a classic example of paracrine function between maternal and fetal tissues. These are accomplished through the anatomical relationship of the placenta and its uterine interface. In overview, maternal blood spurts from uteroplacental vessels into the placental intervillous space and bathes the outer syncytiotrophoblast. This allows exchange of gases, nutrients, and other substances with fetal capillary blood within the core of each villus. Thus, fetal and maternal blood does not normally mix in this hemochorial placenta. A paracrine system also links mother and fetus through the anatomical and biochemical juxtaposition of the maternal decidua parietalis and the extraembryonic chorion laeve, which is fetal. This is an extraordinarily important arrangement for communication between fetus and mother and for maternal immunological acceptance of the conceptus (GuzelogluKayisli, 2009). Although technically this mass of cells is released into the peritoneal cavity, the oocyte is quickly engulfed by the fallopian tube infundibulum. Further transport through the tube is accomplished by directional movement of cilia and tubal peristalsis. Fertilization, which normally occurs in the oviduct, must take place within a few hours, and no more than a day after ovulation. Because of this narrow window, spermatozoa must be present in the fallopian tube at the time of oocyte arrival. Almost all pregnancies result when intercourse occurs during the 2 days preceding or on the day of ovulation. Molecular mechanisms allow spermatozoa to pass between follicular cells; through the zona pellucida, which is a thick glycoprotein layer surrounding the oocyte cell membrane; and into the oocyte cytoplasm. Fusion of the two nuclei and intermingling of maternal and paternal chromosomes creates the zygote. Early human development is described by days or weeks postfertilization, that is, postconceptional. After fertilization, the zygote-a diploid cell with 46 chromosomes-undergoes cleavage, and zygote cells produced by this division are called blastomeres. In the two-cell zygote, the blastomeres and polar body continue to be surrounded by the zona pellucida. The zygote undergoes slow cleavage for 3 days while still remaining in the fallopian tube. As the blastomeres continue to divide, a solid mulberry-like ball of cells-the morula-is produced. Gradual accumulation of fluid between the morula cells leads to formation of the early blastocyst. The morula period begins at the 12- to 16-cell stage and ends when the blastocyst forms, which occurs when there are 50 to 60 blastomeres present. The polar bodies, shown in the 2-cell stage, are small nonfunctional cells that soon degenerate. Blastocyst As early as 4 to 5 days after fertilization, the 58-cell blastula differentiates into five embryo-producing cells-the inner cell mass. The remaining 53 outer cells, called the trophectoderm, are destined to form trophoblasts (Hertig, 1962). Interestingly, the 107-cell blastocyst is found to be no larger than the earlier cleavage stages, despite the accumulated fluid within the blastocyst cavity. At this stage, the eight formative, embryo-producing cells are surrounded by 99 trophoblastic cells. Release from the zona pellucida allows blastocyst-produced cytokines and hormones to directly influence endometrial receptivity (Lindhard, 2002). Implantation Six or 7 days after fertilization, the blastocyst implants into the uterine wall. This process can be divided into three phases: (1) apposition-initial contact of the blastocyst to the uterine wall; (2) adhesion-increased physical contact between the blastocyst and decidua; and (3) invasion-penetration and invasion of syncytiotrophoblast and cytotrophoblasts into the decidua, inner third of the myometrium, and uterine vasculature. Successful implantation requires a receptive endometrium appropriately primed with estrogen and progesterone by the corpus luteum. Adherence is mediated by cell-surface receptors at the implantation site that interact with blastocyst receptors (Carson, 2002; Lessey, 2002; Lindhard, 2002). If the blastocyst approaches the endometrium after cycle day 24, the potential for adhesion is diminished because antiadhesive glycoprotein synthesis prevents receptor interactions (Navot, 1991). At the time of its interaction with the endometrium, the blastocyst is composed of 100 to 250 cells. Attachment of the blastocyst trophectoderm to the decidual surface by apposition and adherence appears to be closely regulated by paracrine interactions between these two tissues. Endometrial integrins are hormonally regulated, and a specific set of integrins is expressed at implantation (Lessey, 1995). Recognition-site blockade of integrins needed for binding will prevent blastocyst attachment (Kaneko, 2013). Trophoblast Development Human placental formation begins with the trophectoderm, which gives rise to a trophoblast cell layer encircling the blastocyst. Trophoblasts exhibit the most variable structure, function, and developmental pattern of all placental components. Their invasiveness promotes implantation, their nutritional role for the conceptus is reflected in their name, and their endocrine organ function is essential to maternal physiological adaptations and to pregnancy maintenance. By the eighth day postfertilization, after initial implantation, trophoblasts have differentiated into an outer multinucleated syncytium-primitive syncytiotrophoblast, and an inner layer of primitive mononuclear cells -cytotrophoblasts. As cytotrophoblasts proliferate, their cell walls disappear, and the cells fuse to add to the expanding outer layer of syncytiotrophoblast. These are lacking in the syncytiotrophoblast, which provides transport functions of the placenta. It is so named because instead of individual cells, it has an amorphous cytoplasm without cell borders, nuclei that are multiple and diverse in size and shape, and a continuous syncytial lining. After implantation is complete, trophoblasts further differentiate along two main pathways, giving rise to villous and extravillous trophoblasts. Villous trophoblasts generate chorionic villi, which primarily transport oxygen, nutrients, and other compounds between the fetus and mother. Extravillous trophoblasts migrate into the decidua and myometrium and also penetrate maternal vasculature, thus coming into contact with various maternal cell types (Pijnenborg, 1994). Extravillous trophoblasts are further classified as interstitial trophoblasts and endovascular trophoblasts. The interstitial trophoblasts invade the decidua and eventually penetrate the myometrium to form placental-bed giant cells. The endovascular trophoblasts penetrate the spiral artery lumens (Pijnenborg, 1983). Endovascular trophoblasts invade and transform spiral arteries during pregnancy to create low-resistance blood flow that is characteristic of the placenta. Early Invasion After gentle erosion between epithelial cells of the surface endometrium, invading trophoblasts burrow deeper. At 9 days of development, the blastocyst wall facing the uterine lumen is a single layer of flattened cells. The blastocyst wall opposite the uterine lumen is thicker and comprises two zones-the trophoblasts and the embryo-forming inner cell mass. Some small cells appear between the embryonic disc and the trophoblasts and enclose a space that will become the amnionic cavity. This stage is characterized by the intercommunication of the lacunae filled with maternal blood. Note in (B) that large cavities have appeared in the extraembryonic mesoderm, forming the beginning of the extraembryonic coelom. Also note that extraembryonic endodermal cells have begun to form on the inside of the primitive yolk sac. Spaces form and then fuse within the extraembryonic mesoderm to form the chorionic cavity (extraembryonic coelom). This stalk joins the embryo to the nutrient chorion and later develops into the umbilical cord. The body stalk can be recognized at an early stage at the caudal end of the embryonic disc. As the embryo enlarges, more maternal decidua basalis is invaded by syncytiotrophoblast. Beginning approximately 12 days after conception, the syncytiotrophoblast is permeated by a system of intercommunicating channels called trophoblastic lacunae.

A soft diastolic murmur was noted transiently in 20 percent acne definition order eurax with mastercard, and continuous murmurs arising from the breast vasculature in 10 percent acne 5 months after baby order eurax 20gm without a prescription. Structurally skin care jobs purchase 20 gm eurax free shipping, the expanding plasma volume seen during normal pregnancy is reflected by enlarging cardiac end-systolic and end-diastolic dimensions acne 8 month old purchase eurax overnight delivery. This is because the dimensional changes are accompanied by substantive ventricular remodeling acne inversa images best 20 gm eurax, which is characterized by left-ventricular mass expansion of 30 to 35 percent near term acne 19 year old male generic eurax 20gm amex. In the nonpregnant state, the heart is capable of remodeling in response to stimuli such as hypertension and exercise. Such cardiac plasticity likely is a continuum that encompasses physiological growth-such as that in exercise, and pathological hypertrophy-such as with hypertension (Hill, 2008). This remodeling is concentric and proportional to maternal size for both normal and overweight women and resolved within 3 months of delivery. For the given filling pressures, cardiac output is appropriate and thus cardiac function during pregnancy is eudynamic. The associated increase in oxygen consumption is primarily accomplished via increased coronary blood flow rather than increased extraction (Liu, 2014). In a supine woman, a large uterus rather consistently compresses veins and diminishes venous return from the lower body. Consistent with this, Simpson and James (2005) found that fetal oxygen saturation is approximately 10 percent higher if a laboring woman lies in a lateral recumbent position compared with supine. Upon standing, cardiac output falls to the same degree as in the nonpregnant woman (Easterling, 1988). In multifetal pregnancies, compared with singletons, maternal cardiac output is augmented further by almost another 20 percent. Ghi and coworkers (2015) used transthoracic echocardiography to show that first-trimester cardiac output with twins (mean 5. Left atrial and left ventricular end-diastolic diameters are also longer with twins due to augmented preload (Kametas, 2003). The greater heart rate and inotropic contractility imply that cardiovascular reserve is reduced in multifetal gestations. During the second stage, with vigorous expulsive efforts, it is appreciably greater. The pregnancyinduced increase is lost after delivery, at times dependent on blood loss. Hemodynamic Function in Late Pregnancy Clark and associates (1989) conducted invasive studies to measure hemodynamic function late in pregnancy (Table 4-4). Late pregnancy was associated with the expected increases in heart rate, stroke volume, and cardiac output. Systemic vascular and pulmonary vascular resistance both dropped significantly, as did colloid osmotic pressure. Pulmonary capillary wedge pressure and central venous pressure did not change appreciably. Thus, although cardiac output rises, left ventricular function as measured by stroke work index remains similar to the nonpregnant normal range. Central Hemodynamic Changes in 10 Normal Nulliparous Women Near Term and Postpartum Circulation and Blood Pressure Changes in posture affect arterial blood pressure. Brachial artery pressure when sitting is lower than that when in the lateral recumbent supine position (Bamber, 2003). Additionally, systolic blood pressure is lower in the lateral positions compared with either the flexed sitting or supine positions (Armstrong, 2011). Compared with healthy nonpregnant controls, significant declines in mean arterial pressure and arterial stiffness, measured using pulse wave velocity, were observed between the prepregnant and the postpartum time periods. These findings suggest that pregnancy confers a favorable effect on maternal cardiovascular remodeling and may possibly help explain why the risk of preeclampsia is reduced in subsequent pregnancies. In the supine position, however, femoral venous pressure rises steadily, from approximately 8 mm Hg early in pregnancy to 24 mm Hg at term. Venous blood flow in the legs is retarded during pregnancy except when the lateral recumbent position is assumed (Wright, 1950). This tendency toward blood stagnation in the lower extremities during later pregnancy is attributable to occlusion of the pelvic veins and inferior vena cava by the enlarged uterus. The elevated venous pressure returns to normal when the pregnant woman lies on her side and immediately after delivery (McLennan, 1943). These alterations contribute to the dependent edema frequently experienced and to the development of varicose veins in the legs and vulva, as well as hemorrhoids. Supine Hypotension In approximately 10 percent of women, supine compression of the great vessels by the uterus causes significant arterial hypotension, sometimes referred to as the supine hypotensive syndrome (Kinsella, 1994). Also when supine, uterine arterial pressure-and thus uterine blood flow-is significantly lower than that in the brachial artery. Renin is produced by both the maternal kidney and the placenta, and greater amounts of renin substrate (angiotensinogen) are produced by both maternal and fetal liver. Elevated angiotensinogen levels result, in part, from augmented estrogen production during normal pregnancy and are important in first-trimester blood pressure maintenance (Lumbers, 2014). Conversely, those who ultimately became hypertensive developed, but then lost, this refractoriness. Large amounts of intramuscular progesterone given during late labor delay this diminishing refractoriness. These peptides regulate blood volume by provoking natriuresis, diuresis, and vascular smooth-muscle relaxation. Prostaglandins Elevated prostaglandin production during pregnancy is thought to have a central role in control of vascular tone, blood pressure, and sodium balance. Renal medullary prostaglandin E2 synthesis is markedly elevated during late pregnancy and is presumed to be natriuretic. It helps maintain vasodilation during pregnancy, and its deficiency is associated with pathological vasoconstriction (Shah, 2015). Endothelin-1 is a potent vasoconstrictor produced in endothelial and vascular smooth muscle cells and regulates local vasomotor tone (George, 2011; Lankhorst, 2016). Nitric Oxide this potent vasodilator is released by endothelial cells and may modify vascular resistance during pregnancy. Moreover, nitric oxide is an important mediator of placental vascular tone and development (Krause, 2011; Kulandavelu, 2013). Abnormal nitric oxide synthesis has been linked to preeclampsia development (Laskowska, 2015; Vignini, 2016). The subcostal angle widens appreciably as the transverse diameter of the thoracic cage lengthens approximately 2 cm. The thoracic circumference increases about 6 cm, but not sufficiently to prevent reduced residual lung volumes created by the elevated diaphragm. Even so, diaphragmatic excursion is greater in pregnant than in nonpregnant women. The subcostal angle increases, as does the anteroposterior and transverse diameters of the chest wall and chest wall circumference. These changes compensate for the 4-cm elevation of the diaphragm so that total lung capacity is not significantly reduced. This capacity is composed of expiratory reserve volume-which drops 15 to 20 percent or 200 to 300 mL-and residual volume-which decreases 20 to 25 percent or 200 to 400 mL. Kolarzyk and coworkers (2005) reported significantly greater mean tidal volumes-0. These include enhanced respiratory drive primarily due to the stimulatory action of progesterone, low expiratory reserve volume, and compensated respiratory alkalosis (Heenan, 2003). Decreased plasma osmolality also results in less respiratory depression (Moen, 2014). This provides an additional mechanism for the increased minute ventilation seen in pregnancy, and one that is not dependent on progesterone. Regarding pulmonary function, peak expiratory flow rates rise progressively as gestation advances (Grindheim, 2012). Airway conductance is increased and total pulmonary resistance reduced, possibly as a result of progesterone. The maximum breathing capacity and forced or timed vital capacity are not altered appreciably. It is unclear whether the critical closing volume-the lung volume at which airways in the dependent parts of the lung begin to close during expiration-is higher in pregnancy (Hegewald, 2011). Pulmonary function with a singleton pregnancy does not significantly differ from that with twins (McAuliffe, 2002; Siddiqui, 2014). Importantly, the greater oxygen requirements and perhaps the increased critical closing volume imposed by pregnancy make respiratory diseases more serious. Although the minimal cross-sectional area decreased between the first and third trimesters, subjective reports of nasal congestion or total nasal resistance did not significantly differ among trimesters or compared with nonpregnant controls. Oxygen Delivery the amount of oxygen delivered into the lungs by the increased tidal volume clearly exceeds oxygen requirements imposed by pregnancy. Moreover, the total hemoglobin mass and, in turn, total oxygen-carrying capacity rise appreciably during normal pregnancy, as does cardiac output. Oxygen consumption grows approximately 20 percent during pregnancy, and it is approximately 10 percent higher in multifetal gestations (Ajjimaporn, 2014). This may be interpreted as dyspnea, which may suggest pulmonary or cardiac abnormalities when none exist. To compensate for the resulting respiratory alkalosis, plasma bicarbonate levels normally drop from 26 to 22 mmol/L. Although blood pH is increased only minimally, it does shift the oxygen dissociation curve to the left. This shift increases the affinity of maternal hemoglobin for oxygen-the Bohr effect- thereby lowering the oxygen-releasing capacity of maternal blood. This is offset because the slight pH rise also stimulates an increase in 2,3-diphosphoglycerate in maternal erythrocytes. First, hypervolemia-induced hemodilution lowers the protein concentration and oncotic pressure of plasma entering the glomerular microcirculation. Second, renal plasma flow increases by approximately 80 percent before the end of the first trimester (Conrad, 2014b; Odutayo, 2012). A reversal of the gestational hypervolemia and hemodilution, still evident on the first postpartum day, eventuates by the second week postpartum (Odutayo, 2012). Relaxin boosts renal nitric oxide production, which leads to renal vasodilation and lowered renal afferent and efferent arteriolar resistance. Relaxin may also increase vascular gelatinase activity during pregnancy, which leads to renal vasodilation, glomerular hyperfiltration, and reduced myogenic reactivity of small renal arteries (Odutayo, 2012). As with blood pressure, maternal posture may considerably influence several aspects of renal function. Late in pregnancy, the sodium excretion rate in the supine position averages less than half that in the lateral recumbent position. One unusual feature of the pregnancy-induced changes in renal excretion is the remarkably increased amounts of some nutrients lost in the urine. Amino acids and water-soluble vitamins are excreted in much greater amounts (Shibata, 2013). Renal Function Tests Of renal function tests, serum creatinine levels decline during normal pregnancy from a mean of 0. Creatinine clearance in pregnancy averages 30 percent higher than the 100 to 115 mL/min in nonpregnant women. This is a useful test to estimate renal function, provided that complete urine collection is made during an accurately timed period. During the day, pregnant women tend to accumulate water as dependent edema, and at night, while recumbent, they mobilize this fluid with diuresis. This reversal of the usual nonpregnant diurnal pattern of urinary flow causes nocturia, and urine is more dilute than in nonpregnant women. Failure of a pregnant woman to excrete concentrated urine after withholding fluids for approximately 18 hours does not necessarily signify renal damage. In fact, the kidneys in these circumstances function perfectly normally by excreting mobilized extracellular fluid of relatively low osmolality. Chesley (1963) calculated that about a sixth of pregnant women will spill glucose in the urine. That said, although common during pregnancy, when glucosuria is identified, a search for diabetes mellitus is pursued. Hematuria is common after difficult labor and delivery because of trauma to the bladder and urethra. Proteinuria is typically defined in nonpregnant subjects as a protein excretion rate of more than 150 mg/d. Because of the aforementioned hyperfiltration and possible reduction of tubular reabsorption, proteinuria during pregnancy is usually considered significant once a protein excretion threshold of at least 300 mg/d is reached (Odutayo, 2012). Higby and coworkers (1994) measured protein excretion in 270 normal women throughout pregnancy. Mean 24-hour excretion for all three trimesters was 115 mg, and the upper 95-percent confidence limit was 260 mg/d without significant differences by trimester. The three most commonly employed approaches for assessing proteinuria are the qualitative classic dipstick, the quantitative 24-hour collection, and the albumin/creatinine or protein/creatinine ratio of a single voided urine specimen. The pitfalls of each approach have been reviewed by Conrad (2014b) and Bramham (2016) and their colleagues. The principal problem with dipstick assessment is that it fails to account for renal concentration or dilution of urine. For example, with polyuria and extremely dilute urine, a negative or trace dipstick could actually be associated with excessive protein excretion. The 24-hour urine collection is affected by urinary tract dilatation, which is discussed in the next section.

Buy eurax 20gm without prescription. The Ordinary Skincare Retinoid 2% VS Retinol 1% - What isn't being said!.