Padraig S. J. Malone, MCh, FRCSI, FRCS, FEAPU

• Consultant Paediatric Urologist,
• Southampton University Hospitals, NHS Trust,
• Southampton, United Kingdom

The finding of characteristic centers of caseation in the endometrial stroma with giant cell formation is pathognomonic of the disease erectile dysfunction effects buy 100mg extra super levitra otc. In about half of the patients with genital tuberculosis erectile dysfunction medication for high blood pressure buy extra super levitra from india, the uterus is involved disease that causes erectile dysfunction discount extra super levitra 100 mg amex, but erectile dysfunction washington dc purchase 100 mg extra super levitra free shipping, as a rule impotence type 1 diabetes generic 100 mg extra super levitra amex, this is secondary to a tuberculous infection of the tubes or pelvic peritoneum erectile dysfunction diabetes symptoms buy 100mg extra super levitra with mastercard. Fibroids are found in 30% of all women, and 40% to 50% of women older than 50 (one study has demonstrated a rate of more than 80% in African Americans older than 50). They are a benign connective tissue tumor found in or around the uterus, which may be disseminated in rare cases. From the point of view of the pathologist, the tumors under discussion should be classified as leiomyomata (from leios, meaning smooth). However, it is progressive until the menopause, when production of estrogen ceases. Obviously, in such instances removal of the tumor alone will not guarantee freedom from subsequent hemorrhages. Symptoms of pain and pressure are not common complaints, except in the presence of massive fibroids; dysmenorrhea, menorrhagia, or intermenstrual bleeding occurs in 30% to 40% of patients. Pelvic examination is generally sufficient to establish the diagnosis, although this may be augmented by ultrasonography, but is generally not required. In microscopic section, myomata are dense and cellular, showing strands and bundles of characteristic spindle cells devoid of mitotic activity. Those that arise near the cornua may impinge upon the patency of the intramural portion of the fallopian tube. Historically, the indications for surgery were undue bleeding, increasing pressure on bladder or bowel, a rapid increase in size or change in consistency of the tumor, or some degenerative change causing pain. With improved imaging and more effective medical therapies available, the need for surgical intervention has been more limited: symptoms unresponsive to therapy and acute pain. There has also been a limited role for myomectomy when a few large fibroids are present and there has been recurrent pregnancy loss. When a leiomyoma is diagnosed in the absence of any of the indications just listed, a policy of watchful waiting is justified. If none of these signs or symptoms is present in younger women with fibroids, the problem may be complicated by the question of infertility. Pedunculated submucous fibroids may undergo torsion of the pedicle, cutting off the blood supply and causing slough and necrosis. In such cases, the characteristic tough, rubbery consistency is lost, and the differential diagnosis from sarcomatous change may have to await removal and gross sectioning. Cystic degeneration is typified by amorphous, jellylike material in contrast to the friable, red, solid appearance of a sarcoma. The relation of fibroids to the successful culmination of pregnancy is affected by the situation in the individual case. Those arising from the cervix or the lower segment may be so large as to cause obstruction of the passage of the fetal head through the birth canal. Although small subserous or interstitial fibroids may not interfere in any way with gestation, during the course of pregnancy (probably owing to pressure), the vascular supply to an interstitial fibromyoma is sometimes sufficiently embarrassed so that hemorrhage into the stroma of the tumor results. This "red degeneration" of the tumor may lead to necrosis and become a serious complication of the pregnancy. After the menopause, such bleeding from a benign endometrial hyperplasia may be a telltale sign of a functioning ovarian tumor that might be overlooked unless it is recalled that fibroids almost never initiate bleeding in the postmenopausal period and certainly never cause endometrial proliferation. In those with abnormal bleeding and small fibroids at the climacteric, after the possibility of cancer has been investigated by endometrial biopsy or curettage, the diagnosis of anovulatory cycles may suggest hormonal therapy, with the hope that the complaint may be controlled until ovarian function ceases. Occasionally and unfortunately, a patient may be told that she has a tumor, and she may become so concerned with undue anxiety with regard to cancer that no choice is left in order to set her mind at rest but operative removal of the fibroids. At times, a large fibroid may outgrow its blood supply, with resultant cystic degeneration. The arterial supply of myomas is significantly less than that of a similarly sized area of normal myometrium. Histologically, with hyaline degeneration, cellular detail is lost as the smooth muscle cells are replaced by fibrous connective tissue. Cystic degeneration Incarceration Fibroids retracted with cervix permitting passage of child Incarcerated fibroid causing dystocia A large fibroid originating from a sharply retroverted fundus may become incarcerated in the hollow of the sacrum, pressing on the rectum, causing obstipation, although obstruction from this cause is probably rare. Cervical fibroids in the uterus at term may retract upward as cervical dilation proceeds, allowing for an uncomplicated delivery, or they may be forced downward, causing dystocia and making delivery impossible. Rarely, the high levels of both growth and ovarian hormones can stimulate existing fibroids to grow rapidly during mid- to late pregnancy, resulting in problems for the pregnancy. This rapid growth may be associated with pain, especially when the growth outstrips the available blood supply and degeneration or necrosis ensues. This form of degeneration occurs in approximately 5% to 10% of gravid women with myomas. Of all malignancies of the female genital tract, sarcomas represent less than 5% of uterine malignancies, or roughly 1 of 800 smooth muscle tumors, with a prevalence of 0. There appear to be no genetic pattern, and though sarcomas are reported more often in black women, there is no racial predisposition. Even in children, tumors have been observed that were larger than a pregnant uterus at term. It is easily recognized on cross sections, as it is soft and meaty and lacks the firm, characteristic whorled appearance of a myoma. Sarcomas may originate in any part of the uterus that contains mesodermal tissue, but whether the tumor is a mural or endometrial sarcoma, whether it derives from connective tissue of the endometrium, endocervix, or blood vessels or develops from muscle cells of the myometrium or myoma cells, and whether it may be classified as spindle cell or round cell or mixed cell sarcoma, its invasive and metastatic tendencies are seemingly the same. Size and extent of the tumor are more important, as far as the prognosis is concerned, than is its location or its histologic classifications. Because of technical difficulties, biopsy specimens examined by the frozen-section technique are seldom helpful. A primary sarcoma arising directly from the uterine body may easily be mistaken for a benign submucous fibroid. This tumor carries a grave prognosis and occurs almost exclusively in young children. Clusters of tumor masses arising from the cervix or the vagina may present themselves at the introitus, or they may be extruded by hemorrhage. In view of the rapid growth of the neoplasm, a very early and radical hysterectomy with extensive pelvic node dissection offers the only hope of survival. On the occurrence of vaginal bleeding in any young child, the possibility of this serious neoplasm must not be overlooked. These cancers are the most frequent malignancy of the female reproductive tract, representing the eighth leading site of cancer-related deaths among American women. Risk factors for the development of endometrial cancer include unopposed (without progestins) estrogen stimulation (such as in polycystic ovary syndrome, obesity, chronic anovulation, and estrogen replacement therapy without concomitant progestin). Selective estrogen receptor modulators with uterine activity (such as tamoxifen) may also place the patient at increased risk. In 1988, a surgical staging classification was introduced that relies on an operative evaluation with particular emphasis on myometrial invasion in stage I. The histologic type is also related to prognosis, with the best prognosis associated with typical More extensive carcinoma deeply involving muscle Extensive carcinoma invading full thickness of myometrium and escaping through tube to implant on ovary adenocarcinomas as well as better differentiated tumors with or without squamous elements and secretory carcinomas. Tumor grade and stage both affect the risk of lymph node spread in endometrial cancer. The frequency of nodal involvement becomes much greater with higher grade tumors and with greater depth of myometrial invasion: the risk of lymph node involvement appears to be negligible for endometrial carcinoma involving only the endometrium and for lower grade tumors with a depth of invasion involving only the inner one-third of the myometrium. In general, of course, the more anaplastic tumors may be expected to grow more rapidly and to metastasize earlier than do the more mature adenocarcinomas. Uterine papillary serous carcinomas are a highly virulent histologic subtype of endometrial carcinomas (5% to 10% of cases). These tumors histologically resemble papillary serous carcinoma elsewhere in the body. Clear-cell carcinomas of the endometrium are less common (<5%), and histologically they are similar to clear-cell adenocarcinomas of the ovary, cervix, and vagina. Survival rates of 39% to 55% have been reported, versus 65% or better for endometrial carcinoma. Successful therapy primarily depends on the surgical extirpation of the disease while it is confined to the uterus. Unfortunately, many of these patients are not good surgical risks owing to chronic or intercurrent afflictions common to the sixth and seventh decades of life. For patients with significant medical comorbidities, radiation therapy alone can be used, though at a cost in efficacy. For patients with stage I, grade 1 tumors, postoperative radiation (vaginal brachytherapy and/or external beam irradiation) may be considered if there is deep myometrial invasion to the outer one-third or if there is any invasion and the surgical staging was limited. Three therapeutic options have been employed: primary operation (radical hysterectomy and pelvic node dissection), primary radiation (intrauterine and vaginal implant and external irradiation) followed by an operation (extrafascial hysterectomy), and simple hysterectomy followed by external beam irradiation. Both hormonal and cytotoxic agents have activity in patients with advanced endometrial cancer. In addition, there continues to be a role for radiation therapy to gain local control or to treat pelvic disease. Following treatment, patients should be monitored by follow-up Pap smears from the vaginal cuff every 3 months for 2 years, then every 6 months for 3 years, and then yearly. Death results from distant metastases to vital organs more commonly in endometrial carcinoma than in cervical neoplasms. On hysterosalpingography, this tiny tubal antrum either is connected with the shadow of the uterine cavity by a threadlike communication or is separated from it by a narrow, empty zone. This constriction of the tubal shadow, usually designated as the tubal sphincter, is caused by an annular fold of the uterine mucosa at the junction of both organs. The muscular coat is thicker in the medial section than in the ampullary portion, where the longitudinal muscle bundles are more widely separated. The blood vessels are strikingly abundant, particularly in the infundibulum and the fimbriae, where they form with interspersed muscle bundles a kind of erectile tissue, which, if engorged, enables the tube to sweep over the surface of the ovary. The mucosa consists of a single layer of columnar cells, some of which are ciliated, whereas others are secretory. A third group of peg-shaped cells with dark nuclei is intercalated between the ciliated and secretory cells and represents apparently worn-out cells, which are gradually cast out into the lumen of the tube. The numerical relationship between ciliated and secretory cells changes during the menstrual cycle. The more cephalad portions of the paramesonephric ducts, which open directly into the peritoneal cavity, form the fallopian tubes. The paramesonephric ducts, and similarly the wolffian duct, grow more slowly than the fetal trunk as a whole. As a result, the location of the coelomic ostia of the ducts gradually slides caudally to the fourth lumbar segment. The muscular and connective tissues of the tubes are first apparent in the third month of fetal life and may be clearly demonstrated in the fifth month. Complete absence of both tubes is sometimes observed in combination with aplasia of the uterus. Nuclear morphology shown under high power in circle Perisalpingeal cysts than a result of developmental failure. The nuclei of these Walthard cells show a median groove or fold, which is a fundamental characteristic of these cells. Frequently found on the surface of otherwise normal fallopian tubes are tiny multiple serosal (perisalpingeal) cysts. They apparently originate from an invagination and occlusion of the serosal epithelium and do not have any practical significance. The supposition of some authors that these cysts are caused by chronic inflammation is not generally accepted. The nature of the temporarily inhibiting factor responsible for the defects in the lumen or the continuity of these organs is unknown, and all attempts to explain these lesions have failed hitherto. The accessory tubes arise either from the main tube or from the mesosalpinx and consist of a more or less well-developed wreath of fimbriae with a pedicle, which is usually thin and may be either hollow or solid. Production of tubal fluids within this blind segment can result in cystic dilation, mimicking a hydrosalpinx or ovarian cyst. There has even been a single case report in which laparotomy demonstrated that the proximal portion of one fallopian tube was absent and that the distal end was separated into three portions. The hypoplastic tube is thin and ischemic, its musculature weak, and its ampulla poorly developed. It may be that the peritoneal bridges between the tubal windings interfere with the tubal peristalsis in the same way as do adhesions and predispose to retention of the fertilized ovum in the tube and thereby to the occurrence of ectopic pregnancy. Conventional therapy consisted of surgical correction, where possible, but the availability and success of oocyte harvesting, in vitro fertilization, and embryo transfer have generally supplanted surgical therapy. Appendicitis is a frequent source of infection of the right or of both tubes; sigmoiditis or diverticulitis often migrates to the left tube. The ciliary current of the tube is a very weak protective apparatus, and the narrow communication between tube and uterus is an ineffective barrier. Besides, the narrow lumen proves to be a serious handicap when the tube is inflamed. On the other hand, the occurrence of tubal inflammatory disease is favored by the tendency of the uterus to react to abnormal stimuli, such as bacteria or chemicals, by spasm of the internal cervical os and severe contractions, which drive these noxious agents into the tubes. Lipid imaging solutions, which are occasionally used for hysterosalpingography, may cause serious damage to the tubes. In contrast, chlamydial infections tend to engender a much milder but longer-lived inflammatory response, accounting for their often indolent course and greater degree of long-term tubal damage. Streptococci and staphylococci also propagate in the mucosa but rapidly penetrate the deeper structures and invade the lymphatics and blood vessels of the uterine and tubal walls and adjacent connective tissue.

The obstetrician often is faced with a need to maintain the uterine activity or to plan a coordinated augmentation of the expulsive forces in which the striated abdominal and intercostal muscles are involved statistics for erectile dysfunction order extra super levitra in india, including the diaphragm erectile dysfunction treatment new zealand discount extra super levitra 100 mg mastercard. The pain of labor is characterized as rhythmically increasing and fading pain that occurs synchronously with uterine contractions impotence from blood pressure medication buy discount extra super levitra 100 mg on-line, coming every 3 to 4 minutes and lasting 30 to 40 seconds but may occur more often impotence juicing order 100mg extra super levitra with visa. Continuing without synapse in a cephalic direction erectile dysfunction causes natural treatment cheap extra super levitra 100mg line, these nerves traverse the gray rami of the 11th and 12th thoracic and probably also the 1st lumbar nerve to enter the communicating system of these three dorsal root ganglia with the preganglionic afferent system in the lateral spinothalamic fasciculus of the spinal cord to the thalamic pain center and its cortical radiations erectile dysfunction 20s discount extra super levitra 100 mg without a prescription. The second component of labor pain is the backache associated with cervical dilation. These stimuli are transmitted through the parasympathetic system of the second, third, and fourth sacral nerves (blue dotted lines). Low saddle or spinal block, as well as the infrequently used caudal block, will relieve this pain. The third component of childbirth pain is that transmitted from the stimulus of stretching the lower birth canal and the perineum. Pressure upon the bladder and rectum through the pudendal nerve or its perineal and hemorrhoidal branches may also be involved. This pain can be relieved by pudendal and perineal nerve block, anesthetizing the nerves indicated in the picture by the broken lines. Epidural anesthesia is commonly used for childbirth in the United States because it provides good analgesia with a wide margin of safety. Use of epidural anesthesia may be associated with reduced contraction frequency or strength, or an impaired ability to push as effectively, so interventions such as oxytocin or operative delivery may become necessary. Successful saddle or spinal anesthesia produces a more or less complete analgesia from the perineum and sacral plexus ascending to the 10th thoracic segment. Prior to the onset of labor, physicochemical changes occur in the cervix and are collectively called "ripening. The first stage of labor is further subdivided into the latent and active phases, demarcated by cervical dilation of roughly 3 to 5 cm and an accelerated rate of cervical change. Descent is a necessity for the successful completion of passage through the vagina. External rotation occurs after delivery of the head as the head restitutes relative to the shoulders. The latter may be accomplished by either intermittent auscultation after contractions or by continuous electronic fetal monitoring devices. Amelioration of pain may be accomplished by systemic analgesics early in labor or by regional anesthetics as labor progresses. Following the delivery of the placenta, the uterus must contract to prevent maternal hemorrhage. To accomplish this, the use of uterine massage as well as uterotonic agents such as oxytocin, methylergonovine maleate, or prostaglandins may be routinely used. Assisted or expedited vaginal delivery may become necessary because of maternal fatigue, prolonged second stage of labor, or certain types of pulmonary, cardiac, or neurologic disease. When there is evidence of a nonreassuring fetal status or acute fetal distress, operative vaginal delivery may provide a safer or more expeditious way of protecting fetal health. For successful operative delivery, adequate maternal anesthesia or analgesia should be ensured in all but the most extreme circumstances. The position of the fetal head must be ascertained by palpation of the sagittal suture and fontanelles. Current obstetric practice has rendered the challenging and difficult forceps deliveries of past eras exceedingly rare. With either modality, it is critical that the device be carefully placed to avoid iatrogenic trauma to either mother or baby. Traction begins in a horizontal or slightly downward (axis of the maternal pelvic canal) manner. Traditionally a timely median or mediolateral episiotomy was believed to reduce the likelihood that such tears will be extensive, but the role of routine episiotomy has come under question. The simplest type is a first-degree perineal laceration that extends posteriorly toward the anus through the vaginal epithelium and perineal skin. Bleeding may be brisk, but self-limited, although no vital structures have been damaged. They often extend upward along the sides of the vagina, producing a triangular defect because of retraction of the superficial perineal muscles. At the lower margin of a second-degree tear, the capsule of the external anal sphincter bulges upward into the wound. In this instance, the skin, vaginal epithelium, and perineal body are torn, and the external anal sphincter is ruptured anteriorly with retraction of its severed ends. Although the perineum receives the main expulsive force and is therefore more often lacerated, the incidence of damage to the anterior wall increases proportionately. A tear that includes the rectal mucosa or extends up the anterior rectal wall to compromise the internal sphincter is referred to as a fourth-degree laceration. If the tear extends to the vaginal fornices, as it often may, the end result may be dyspareunia or urinary incontinence due to downward pull on the internal vesical sphincter. More acute symptoms are hemorrhage, hematoma, or infection followed by purulent leukorrhea. First-degree perineal laceration Second-degree perineal laceration plus tear of clitoris Third-degree perineal laceration and labial tear High cervicovaginal laceration the early and late clinical manifestations of all these injuries serve to emphasize the necessity of instituting prompt surgical treatment. Transfusions may be necessary to combat hemorrhage and shock if bleeding is significant. Sutures should be carefully and economically placed, which, in the difficult cases, usually requires the services of an assistant for adequate exposure. To provide additional support, plication of the levator muscles in the rectovaginal space has been advocated in the past. Before 1900, when most babies were delivered at home, these injuries were more frequent. Regardless of refinements in obstetric management and surgical technique, such accidents, both minor and major, continue to occur. The pressure thus exerted on the vaginal tube and its muscular supports has spread in several directions, but especially posteriorly toward the anus. The vagina is completely separated from the rectum above the level of the external sphincter ani, and the separation continues laterally without damaging the major divisions of the pubococcygei. An aberrant application of forceps may cause a deep tear in the pubococcygeus muscle close to its origin on the inner surface of the superior pubic ramus. The tear often extends downward to separate the right lateral and posterior vagina from its supports and from the anterior rectal wall, with loss of almost an entire wing of the pelvic diaphragm. When forceps delivery was more commonly employed, rare cases of uterine rupture occurred during the process of placing the forceps blades or during forceps rotation. When forceps are used, and vaginal bleeding persists, the possibility of a lower uterine tear should be considered and evaluated by manual uterine exploration. In the United States, the rate of cesarean births rose fivefold for the 20-year period ending in the early 1990s and was 30% in 2006. The exact reasons for this are open to conjecture but concerns about liability, almost universal use of electronic fetal monitoring, increasing birth weight, and an increased number of repeat cesarean deliveries have all been postulated. Potential risks of cesarean delivery include a longer maternal hospital stay, an increased risk of respiratory problems for the baby due to iatrogenic prematurity, and greater complications in subsequent pregnancies, including increased risks of uterine rupture and placental implantation problems. The risks of placenta previa, placenta accreta, and the need for cesarean hysterectomy all increase with each succeeding cesarean delivery. Some have suggested that cesarean delivery decreases the risk of subsequent pelvic floor dysfunction and urinary incontinence but analysis of stress urinary incontinence rates at 2 and 5 years after delivery has shown no difference based on the mode of delivery. Patients with classic incisions and those who have had incisions of the upper uterus for other reasons. Although vaginal birth after cesarean delivery is appropriate for most women with a history of a low-transverse cesarean delivery, several factors increase the likelihood of a failed trial of labor, which in turn leads to increased maternal and perinatal morbidity. In these cases, the rupture occurs usually in the fundus, in contrast to the ruptures during labor that are usually in the lower segment. The blood may enter the peritoneal cavity if the rupture opens the peritoneal sheath covering the uterus, or the blood may dissect between the sheets of the broad ligament, thus giving rise to retroperitoneal hematoma. Abdominal tenderness, particularly at the level of the lower segment, is a salient feature. The fetus lies in the abdominal cavity with the presenting parts out of the pelvis. Symptoms of shock may follow the episode, but the blood pressure may not fall precipitously. When vaginal delivery has been attempted in patients with a previous Placenta accreta Rupture through scar of classic cesarean section Rupture of lower uterine segment into broad ligament section, rupture occurs in 1% to 5% of cases, but the percentage is higher in the patients who have had more cesarean deliveries. The only sign that may be present is a slight abdominal tenderness on palpation of the region over the site of rupture. In some cases, herniation of the amniotic sac or of some fetal parts may be seen at operation. Cesarean hysterectomy is the method of choice for catastrophic ruptures, except when the patient is young and desires more babies, in which case attempts at repair may be worthwhile. Uncommon and most often iatrogenic, this may be associated with catastrophic bleeding and cardiovascular collapse. This is more likely to occur with excessive force and a poorly contracted uterus or lower uterine segment. The diagnosis of inversion of the uterus must be based on a high degree of suspicion. More often, there is simply brisk bright red vaginal bleeding accompanied by bradycardia (due to vagal stimulation) and/or tachycardia, hypotension, and vascular collapse due to blood loss. Uterine inversion must be differentiated from simple uterine atony following placental delivery, retained placental fragments or undiagnosed genital tract lacerations, which can generally be accomplished by simple clinical examination. Uterine inversion is treated by rapid evaluation, fluid support, or resuscitation and calls for anesthesia assistance. As the uterus is returned to the abdominal cavity, the body of the uterus must be allowed to revert to its normal configuration. If the uterine fundus cannot be repositioned vaginally through these maneuvers, immediate laparotomy is necessary. If a constriction ring is present and impeding replacement, the use of local anesthetics to break the muscular spasm or incision (generally along the posterior aspect of the uterus) may be needed. Although unrecognized or untreated uterine inversion can end in hysterectomy, hemorrhagic shock, and cardiovascular collapse, if it is rapidly treated, the outcome is generally good. Dilation and increased tortuosity of the ureters have been produced in experimental animals by the administration of estrogens. Functional examinations and pyelography have demonstrated that during pregnancy the excretion time is delayed and that the flow through the ureters slows down parallel to the tortuosity and enlargement of the ureter and the renal pelvis. In rare instances, all the consequences of hydronephrosis, such as flattened calyces and atrophy of the renal parenchyma may become manifest. Ultrasonography can be used to document and assess the degree of ureteral and renal dilation present. Pyelitis or pyelonephritis and ureteritis are relatively frequent complications of pregnancy. The exact route of infection in pyelonephritis in pregnant women has not yet been established. Clean-catch urine examinations during prenatal care may reveal infections in an early stage, although for a definite diagnosis a fresh specimen obtained by catheterization is preferred. The characteristic symptoms include back pain in the lumbar region, fever (usually high), vomiting, frequent urination with the sensation of burning, and leukocytosis. The severity of cystitis varies from a mild form without ureteritis to extensive ulcerative cystitis and ureteritis. Cystitis and urethritis will generally prompt the classic symptoms of frequency, urgency, and dysuria. It involves reduced organ perfusion, vasospasm, and endothelial activation and is characterized by hypertension, proteinuria, and other symptoms. Chronic hypertension may be worsened by being superimposed on pregnancy-induced changes. Another uncommon presentation for preeclampsia is in the postpartum period, when it has been reported to occur up to 7 days after delivery. However, before the stage of pitting edema is reached, the interstitial space may accumulate large quantities of fluid. Edema may precede hypertension, but for the clinical diagnosis of preeclampsia, the increased blood pressure is essential. These patients also have characteristic renal glomerular lesions (capillary endotheliosis) and increased vascular reactivity. Preeclamptic patients may undergo convulsions with only moderate blood pressure elevation and only a slight degree of edema. In some patients with visual changes in preeclampsia, a diffuse increase in macular thickness has been documented. Examination of the eye grounds is of great help in the differential diagnosis between preeclampsia, eclampsia, and other hypertensive states coexisting with pregnancy. In preeclampsia, the first change in the retinal vessels consists of a spasm of the arterioles. In preeclampsia, this ratio may change to 1:2 or even 1:3, indicating extreme narrowing of the retinal arterioles.

This is a derivative of the primitive erectile dysfunction doctor san diego buy generic extra super levitra on-line, embryonic how does an erectile dysfunction pump work order extra super levitra 100 mg without a prescription, arched anastomosis between the left gastric and the left hepatic erectile dysfunction treatment in egypt purchase discount extra super levitra on-line. In the adult erectile dysfunction signs cheap extra super levitra 100 mg fast delivery, the arc may persist in its entirety; the upper half may give rise to an accessory left gastric erectile dysfunction pills amazon buy discount extra super levitra 100mg line, the lower half to a so-called accessory left hepatic from the left gastric (25%) lipitor erectile dysfunction treatment cheap 100 mg extra super levitra. An aberrant right hepatic or the entire hepatic, arising from the superior mesenteric, may communicate with the splenic through a branch of the dorsal pancreatic or gastroduodenal or through the transverse pancreatic and caudal pancreatic. Right left hepatic Right gastric Gastroduodenal Effects of hepatic artery obstruction A. This pathway may be affected by a communication between the short gastrics from the splenic terminals and the recurrent cardioesophageal branches of the left inferior phrenic or by a communication between the latter and the cardioesophageal branches given off by the left gastric, its aberrant left hepatic branch, or an accessory left gastric from the left hepatic. From here, the lymph flows to the subpyloric nodes, which lie in front of the head of the pancreas. In the region where the thorax borders on the neck, the thoracic duct-before opening into the angle formed by the left subclavian and left jugular veins-receives, among other things, the left subclavian lymphatic trunk. In cases of gastric tumor, palpable metastases may develop in the left supraclavicular nodes (also known as Virchow or Troisier nodes). The lymph flows in the direction of the greater and lesser curvatures, where the first regional lymph nodes are situated. From these nodes the lymph flows to the right toward the subpyloric (Spyl) nodes, which are situated in front of the head of the pancreas, below the pylorus and the first part of the duodenum. For purposes of simplification, a distinction can be made among four different draining areas into which the gastric lymph flows, although, in fact, these areas cannot be so clearly separated. The lymph from the upper left anterior and posterior walls of the stomach (region I in the diagram) drains through the lower left gastric and paracardial nodes. From here, the lymphatics follow the left gastric artery and the coronary vein toward the vascular bed of the celiac artery. Floch 37 T his description of the innervation of the stomach and duodenum, although complex and detailed, is important to those who want to understand the common motility disorders of the stomach, such as gastroparesis and dyspepsia. Sympathetic and parasympathetic nerves that contain efferent and afferent fibers innervate the stomach and the duodenum. The sympathetic supply emerges in the anterior spinal nerve roots as preganglionic fibers, which are axons of Plexus on gastro-epiploic arteries Stomach turned up and to right Anterior hepatic plexus Right gastric plexus lateral cornual cells located at about the sixth to the ninth or tenth thoracic segments. These fibers are carried from the spinal nerves in rami communicantes, which pass to the adjacent parts of the sympathetic ganglionated trunks, then into the thoracic splanchnic nerves to the celiac plexus and ganglia. Some fibers form synapses in the sympathetic trunk ganglia, but most form synapses with cells in the celiac and superior mesenteric ganglia. The axons of these cells, the postganglionic fibers, are conveyed Greater posterior gastric nerve (branch of posterior vagal trunk distributing gastric branches) Gastric branch of posterior vagal trunk Hepatic branch of anterior vagal trunk via lesser omentum Branch from hepatic plexus to cardia via lesser omentum (sympathetic These arterial plexuses are composed mainly of sympathetic fibers but also contain some parasympathetic fibers, which reach the celiac plexus through the celiac branches of the vagal trunks. Afferent impulses are carried in fibers that pursue the reverse route of that just described. However, afferent impulses do not form synapses in the sympathetic trunks; their cytons (perikaryons) are located in the posterior spinal root ganglia and enter the cord through the posterior spinal nerve roots. The celiac plexus is the largest of the autonomic plexuses and surrounds the celiac arterial trunk and the root of the superior mesenteric artery. It consists of right and left halves, each containing one larger celiac ganglion, a smaller aorticorenal ganglion, and a superior mesenteric ganglion, which is often unpaired. These and other, even smaller ganglia are united by numerous nervous interconnections to form the celiac plexus. It receives sympathetic contributions through the greater (superior), lesser (middle), and least (inferior) thoracic splanchnic nerves and through filaments from the first lumbar ganglia of the sympathetic trunks. Its parasympathetic roots are derived from the celiac division of the posterior vagal trunk and from smaller celiac branches of the anterior vagal trunk. The celiac plexus sends direct filaments to some adjacent viscera, but most of its branches accompany the arteries from the upper part of the abdominal aorta. Numerous filaments from the celiac plexus unite to form open-meshed nerve plexuses around the celiac trunk and the left gastric, hepatic, and splenic arteries. Subsidiary plexuses from the hepatic arterial plexus are continued along the right gastric and gastroduodenal arteries and from the latter along the right gastroepiploic and anterior and posterior superior pancreaticoduodenal arteries. The splenic arterial plexus sends offshoots along the short gastric and left gastroepiploic arteries. The superior mesenteric plexus is the largest derivative of the celiac plexus and contains the superior mesenteric ganglion or ganglia. The main superior mesenteric plexus divides into secondary plexuses, which surround and accompany the inferior pancreaticoduodenal, jejunal, and other branches of the artery. The left gastric plexus consists of one to four nervelets connected by oblique filaments that accompany the artery and supply "twigs" to the cardiac end of the stomach, communicating with offshoots from the left phrenic plexus. Other filaments follow the artery along the lesser curvature between the layers of the lesser omentum to supply adjacent parts of the stomach. They communicate with the right gastric plexus and with gastric branches of the vagus. The hepatic plexus also contains sympathetic and parasympathetic efferent and afferent fibers and gives off subsidiary plexuses along all its branches. Following the right gastric artery, these branches supply the pyloric region, and the gastroduodenal plexus accompanies the artery between the first part of the duodenum and the head of the pancreas, supplying fibers to both structures and to the adjacent parts of the common bile duct. When the artery divides into its anterosuperior pancreaticoduodenal and right gastroepiploic branches, the nerves also subdivide and are distributed to the second part of the duodenum, terminations of the common bile and pancreatic ducts, head of the pancreas, and parts of the stomach. The part of the hepatic plexus lying in the free margin of the lesser omentum gives off one or more hepatogastric branches, which pass to the left between the layers of the lesser omentum, to the cardiac end and lesser curvature of the stomach; they unite with and reinforce the left gastric plexus. The splenic plexus gives off subsidiary nerve plexuses around its pancreatic, short gastric, and left gastroepiploic branches, which supply the structures indicated by their names. A filament from the right phrenic plexus sometimes turns to the left, posteroinferior to the vena caval hiatus in the diaphragm, and passes to the region of the cardiac orifice. A delicate branch from the left phrenic nerve (not illustrated) supplies the cardia. The parasympathetic supply for the stomach and duodenum arises in the dorsal vagal nucleus in the floor of the fourth ventricle. The afferent fibers also end in the dorsal vagal nucleus, which is a mixture of visceral efferent and afferent cells. The fibers are conveyed to and from the abdomen through the vagus nerves, esophageal plexus, and vagal trunks. The anterior vagal trunk gives off gastric branches that run downward along the lesser curvature, supplying the anterior surface of the stomach almost as far as the pylorus. The pyloric branches (not illustrated) arise from the anterior vagal trunk or from the greater anterior gastric nerve and run to the right between the layers of the lesser omentum, before turning downward through or close to the hepatic plexus to reach the pyloric antrum, pylorus, and proximal part of the duodenum. Small celiac branches run alongside the left gastric artery to the celiac plexus, often uniting with corresponding branches of the posterior vagal trunk. The posterior vagal trunk gives off gastric branches that radiate to the posterior surface of the stomach, supplying it from the fundus to the pyloric antrum. One branch, the greater posterior gastric nerve, is usually larger than the others. As on the anterior aspect, these branches communicate with adjacent gastric nerves, although no true posterior gastric plexus exists. The celiac branch is large and reaches the celiac plexus alongside the left gastric artery. Vagal fibers from this celiac branch are distributed to the pylorus, duodenum, pancreas, and so on, through the vascular plexuses derived from the celiac plexus. Hormonal stimulation of the secretion occurs by humoral and paraendocrine methods through receptors and intracellular signal transduction. The intestinal phase begins when chyme enters the duodenum and humoral effects occur. By the time a significant amount of the gastric content has been delivered to the intestine, regulatory mechanisms are already in operation to terminate the digestive period of gastric secretion. When the stomach is filled and absorption begins, satiety sets in, eating ceases, and psychic stimuli are withdrawn. The production of secretoinhibitory hormones from the antrum results in the withdrawal of humoral and mechanical stimuli of the gastric phase. Other polypeptides, such as tropin-releasing hormone, peptide-y, and peptide-yy, have action, but their roles are unclear. The mucous layer, consisting of a glycoprotein, coats the stomach and measures approximately 0. Transport occurs across this mucous barrier of hydrogen ions (H+), which is constantly being digested by pepsin and then replaced as it acts as an interface between the passage of H+ and the neutralization by bicarbonate. The role of prostaglandins has some importance in gastric physiology, but their exact effect is not clear. The exocrine secretions are water, electrolytes (hydrogen, potassium, sodium, chlorate, bicarbonate), pepsinogen, lipase, intrinsic factor, and mucins. Gastric secretion varies greatly during the day, from resting periods to active periods while eating. Actual secretion is integrated and includes many stimulatory and inhibitory factors. Observations on gastric secretion clearly identify an interdigestive period and a digestive period. The interdigestive phase includes the basic secretion and is influenced heavily by emotional factors. Although most experiments have been on animals, human experiments have shown that anger, resentment, hostility, and fear can influence the volume and content of secretion. The digestive period can be divided into three phases: cephalic, gastric, and intestinal. The cephalic phase includes the secretory response to all stimuli acting in the region of the brain. These may be unconditional (unlearned) reflexes, such as the secretion to sham feeding in a decorticate animal or the conditioned (learned) reflexes exemplified by the secretory effect of the thought, odor, sight, or taste of food. Conditioned or psychic secretion (Pavlov) is the principal component of the cephalic phase; the copious flow of gastric juice that occurs when appetizing food is masticated amounts to almost half the volume output of the gastric glands. Its presence contributes to the effective initiation and the subsequent efficiency of gastric digestion. The cephalic phase is mediated primarily through the vagus nerve and hormonal stimuli as gastrin release from the antrum. Floch 39 general rule that liquids are weak stimulants of gastric secretion are (1) the broth of meat or fish, because of their high secretagogue content, and (2) coffee, which derives its secretory potency from its content of caffeine and of the secretagogues formed in the roasting process. A meal eaten at a time of intense hunger tends to be evacuated more rapidly than normal, apparently in consequence of the heightened gastric tonus. Because hunger results from the depletion of body nutrient stores (see Section X), it is understandable on teleologic grounds that in the hunger state, the body should have some mechanism for hastening the delivery of ingested nutrients into the intestine. Mild exercise, particularly just after eating, shortens the emptying time of the meal. With strenuous exercise, gastric contractions are temporarily inhibited, then augmented, so that final emptying is not significantly delayed. In some persons, gastric emptying is facilitated when the position of the body is such that the pylorus and the duodenum are in a dependent position, that is, with the person lying on the right side. In the supine position, particularly in infants and adults with cascade stomach, the gastric content pools in the dependent fundic portion, and emptying is delayed. The impairing effect of emotional states on gastric motility and secretion has been well documented by clinical and experimental observations. Evidence indicates that the influence of emotions on gastric activity may be augmentative or inhibitory, depending on whether the emotional experience is of an aggressive (hostility, resentment) or a depressive (sorrow, fear) type, respectively. One point of view holds that it is not the manifest or conscious emotion that determines whether the stomach is stimulated or inhibited, but rather the unconscious or symbolic content of the emotional state, and further, that certain emotions may be accompanied by dissociation in the response among the various components of the gastric secretions. S tomach activity is modified by the factors that stimulate and inhibit gastric secretion. Emptying of the stomach is affected by many factors; the types of food eaten and the environment in which they are eaten play major roles through direct nerve and hormonal influences. Factors that modify motor and secretory activities of the stomach, usually simultaneously and in the same direction, include the following: 1. The hypertonic, or "steerhorn," stomach is hypermotile and empties relatively rapidly compared with the hypotonic, or "fishhook," type. A meal sufficiently high in fat to yield an intragastric fat content in excess of approximately 10% empties more slowly and stimulates considerably less acid secretion than does a meal consisting predominantly of protein. The inhibitory effect of fat on gastric secretion is not local but is a primarily a result of enterogastric neural reflexes and hormones, primarily cholecystokinin, after fat has entered the upper intestine. A meal consisting exclusively or mainly of starch tends to empty more rapidly, although stimulating less secretion, than does a protein meal. Thus, other factors being equal, a person may expect to be hungry sooner after a breakfast of fruit juice, cereal, toast, and tea than after bacon, eggs, and milk. The amount of total secretion and of acid content is highest with the ingestion of proteins. However, the relationship of quantity and rate of secretion to its acid or pepsin concentration varies greatly among individuals and in a single person under different conditions. Liquids, whether ingested separately or with solid food, leave the stomach more rapidly than do semisolids or solids. This does not apply to liquids such as milk, from which solid material is precipitated on contact with gastric juice.

Water or milk should not be given vasodilator drugs erectile dysfunction extra super levitra 100 mg amex, vomiting should be prevented impotence clinics purchase 100mg extra super levitra visa, and no nasogastric tube should be placed erectile dysfunction age onset trusted 100mg extra super levitra. In the patient with minor burns erectile dysfunction test yourself order extra super levitra from india, high-dose corticosteroids may improve the prognosis and prevent the formation of esophageal strictures erectile dysfunction 9 code order 100mg extra super levitra fast delivery. Corticosteroids have not shown benefit in the treatment of caustic injuries or in the prevention of esophageal strictures erectile dysfunction pills in pakistan cheap 100mg extra super levitra, but rather increase the risk for other complications. Patients who survive beyond several weeks should undergo esophagoscopy to reassess for esophageal strictures. Strictures, a severe complication of caustic ingestion, develop in 5% to 47% of patients and are accompanied by severe esophagitis. Initially, chronic strictures may necessitate serial dilatation so that patency can be established. Some patients require repeat dilatation to maintain adequate Esophageal Rupture and Perforation Neil R. T raumatic perforation represents 75% of esophageal injuries, with spontaneous rupture of the esophagus less common; however, both are surgical emergencies. Mechanisms of perforation include iatrogenic injuries, trauma, malignancy, inflammation, and infection. Iatrogenic injuries can occur from endoscopy with dilatation, ultrasound, ablation, resection, and endoscopic antireflux procedures. Esophageal perforation usually occurs at narrow areas of the anatomy and at points weakened by benign or malignant disease. Perforation of the cervical esophagus through endoscopy is likely in areas of blind pouches, such as a Zenker diverticulum or the pyriform sinus. It is common in elderly persons who have kyphosis and are unable to open their mouths completely because of muscle contracture. The endoscopist typically is immediately aware of the perforation because bleeding occurs and the anatomy is difficult to discern. Overall, the distal third of the esophagus is the most common site of perforation because it is also the most frequent location for tumors and inflammation. Patients with evidence of a malignancy at the time of esophagogastroduodenoscopy may have as high as a 10% incidence of perforation. Boerhaave syndrome, or spontaneous rupture of the esophagus, occurs from barotrauma with violent coughing, vomiting, or weightlifting or from the Heimlich maneuver. A sudden pressure transfer of 150 to 200 mm Hg across the gastroesophageal junction causes damage. Spontaneous rupture occurs in the distal or lower third of the esophagus on the posterolateral wall and results in a 2- to 3-mm linear tear, frequently on the left side of the chest and in alcoholic patients. Tearing may occur during misidentification of the retroesophageal space during laparoscopy or with improper passage of a bougie. With only a sparse connective tissue barrier and no adventitia, the esophagus has limited defenses. The mortality rate from perforation is high because the anatomy of the esophagus enables direct communication with the mediastinum, allowing the entry of bacteria and digestive enzymes and leading to sepsis, mediastinitis, empyema, and multiorgan failure. Meglumine diatrizoate (Gastrografin) esophagraphy is performed next because the material used is better tolerated if leaked into the mediastinum. If no leak is found, a barium study is performed because it has 90% sensitivity for finding a small leak. Patients at risk for aspiration should have a barium swallow, given that Gastrografin may cause pulmonary edema. Computed tomography can confirm the diagnosis by revealing extraluminal air, periesophageal fluid, esophageal thickening, or extraluminal contrast. Esophagoscopy may demonstrate small bruises or tears and has not been shown to worsen the clinical situation. Treatment depends on the location of the injury and presence of any underlying disease. Cervical esophageal injuries may be treated conservatively, but midthoracic and distal injuries are usually treated surgically. Most patients seek treatment in the first 24 hours and may undergo primary surgical closure, with or without cervical esophagotomy. Patients with associated malignancy, long-segment Barrett esophagus, or chronic strictures will require esophagectomy. Other patients, with severe reflux, dysphagia, aspiration, or severely dilated esophagus from achalasia, may be considered for esophagectomy. Surgery is not performed if patients seek treatment late, have minimal symptoms, do not have sepsis, or are in a poor medical condition. Patients who have intramural perforation after balloon dilatation may also be treated conservatively. Best results are achieved in patients who have normal white blood cell counts, free communication of the injury with the esophagus, no fever, and no sepsis. They may be treated with antibiotics and total parental nutrition, and no food may be allowed by mouth for 1 to 2 weeks. Another option is endoscopic clipping of a mucosal defect, which can be performed with a doublelumen endoscope. Percutaneous drainage or closure may be performed to treat cervical rupture, if diagnosed early. If severe soilage occurs, patients should undergo esophagectomy with delayed reconstruction, because they will do better than with drainage alone. For patients with lifethreatening illness, excision of the esophagus is performed. Covered metallic stents may be used to seal perforations in patients with distal esophageal perforation. Large-diameter stents are placed, thoracostomy tubes drain pleural cavities, and antibiotics are administered. Complete sealing occurs in 80% of patients; no further therapy is necessary except for eventual removal of the stent. Treatment is shifting toward the possibility of primary esophageal repair of nonmalignant esophageal perforations that present at any time. Often, however, patients with esophageal injury have an acute attack or "ripping" chest, back, and epigastric pain. Patients with cervical injuries frequently have dysphagia and odynophagia, which increases with neck flexion. Thoracic perforations cause not only substernal chest pain but also epigastric pain. Substernal pain, cervical crepitus, and vomiting affect 60% of patients with spontaneous rupture from barotrauma. Fever, dyspnea, cyanosis, sepsis, shock, and eventually multiorgan failure may develop with increasing contamination of the mediastinum and chest. An hour after the incident, the chest radiograph may show air under the diaphragm or subcutaneous or mediastinal emphysema in 40% of patients. Survival rates are 92% for patients with thoracic perforations closed primarily within 1 day of injury and 30% to 35% for patients with thoracic perforations discovered after 24 hours. In the past, results included 10% to 25% mortality if the perforations were treated within the first 24 hours and 40% to 60% mortality if treated after 48 hours. The mortality rate is highest, 67%, in patients with spontaneous rupture of the esophagus. Zubarik R, Eisen G, Mastropietro C, et al: Prospective analysis of complications 30 days after outpatient upper endoscopy, Am J Gastroenterol 94:15391545, 1999. Floch 20 ties, because surgical treatment may need to be modified if these have developed. A typical finding is a "honeycomb" formation produced by a thin layer of barium surrounding the venous protrusion that does not constrict the lumen. Endoscopic color Doppler ultrasonography is a useful modality for obtaining color flow images of esophageal varices and their hemodynamics. Capsule endoscopy is now being studied as a possible screening tool for esophageal varices; it has a sensitivity and specificity of 84% and 88%, respectively. It also has the benefit of detecting extraluminal pathology that cannot be seen by endoscopy. V aricosities occur secondary to portal hypertension and are defined as a dilatation of various alternative pathways when cirrhosis obstructs the portal return of blood. Varicosities occur most often in the distal third but may occur throughout the esophagus. Varices of the esophagus are a less common cause of upper gastrointestinal hemorrhage, but the consequences of bleeding are an ever-impending threat to life. The most common cause for portal hypertension, affecting 94% of patients, is cirrhosis. The most common causes of cirrhosis are alcoholism (57%), hepatitis C virus (30%), and hepatitis B virus (10%). Mortality rates from the initial episode of variceal hemorrhage range from 17% to 57%. Hospitalizations for acute bleeding from esophageal varices have been declining in recent years, believed to be a result of more active primary and secondary prophylaxis. Bleeding occurs when the tension in the venous wall leads to rupture, and shock may occur. Occasionally, the bleeding may stop spontaneously, but more often the bleeding will recur. Thrombocytopenia and impaired hepatic synthesis of coagulation factors both interfere with hemostasis. Treatment includes pharmacologic, endoscopic, and radiologic shunting and surgery. Once large varices are identified, patients should begin -blocker therapy, such as propranolol, which reduces portal pressure and variceal blood flow and decreases risk of bleeding by 50%. Hepatic venous pressure measurements are used to monitor the success of this combination pharmacologic therapy, shown to be superior to sclerotherapy and possibly superior to band ligation. A recent meta-analysis showed that a combination of endoscopic and pharmacologic therapy reduces overall and variceal rebleeding in cirrhosis more than either therapy alone. If -blockers are not tolerated or are contraindicated, or if patients are at high risk for bleeding, endoscopic band ligation is preferred over sclerotherapy because of fewer complications and lower cost. Surveillance of varices, with potential rebanding, should be repeated every 6 months. Bleeding requires simultaneous control, resuscitation, and prevention/treatment of complications. Medical treatment of bleeding with vasopressin, terlipressin, somatostatin, or octreotide is started. These medications stop the bleeding in 65% to 75% of patients, but 50% will bleed again within a week. Vasopressin is a posterior pituitary hormone that constricts splanchnic arterioles and reduces portal flow and pressure. Definitive therapy is first performed with sclerotherapy or band ligation, which is successful in 90% of patients. Patients with acute variceal bleeding have hemodynamic instability (61%), tachycardia (22%), hypotension (29%), and orthostatic hypotension (10%). Screening should be performed for patients with low platelet counts, splenomegaly, or advanced cirrhosis. Endoscopy should also be performed for any patient who has hemorrhage of unexplained cause. In 25% of patients with varices that bleed, the cause is something other than varices. Esophageal varices are believed to be the cause of bleeding if no other source of bleeding is found. Other causes include gastric or duodenal ulcers, gastritis, Mallory-Weiss tear, and gastric varices. At endoscopy, the varices are blue, round, and surrounded by congested mucosa as they protrude into the lumen of the distal esophagus. They are soft and compressible, and an esophagoscope can be passed easily beyond them. Erosion of the superficial mucosa, with an adherent blood clot, signifies the site of a recent hemorrhage. However, recurrence is common before complete obliteration, and esophageal strictures typically develop. Endoscopic band ligation results in fewer strictures and ulcers than sclerotherapy and faster eradication. When bleeding is under control, endoscopic ligation and sclerotherapy are repeated every 1 to 2 weeks until the varices are eradicated. This technique has the fewest complications and the lowest incidence of recurrence. Surveillance is performed at 3- to 6-month intervals to detect and treat any recurrence. Patients who have two or more rebleeding episodes should be considered for surgery or transplantation. Balloon tamponade is used as a bridge to definitive therapy in 6% of patients when hemostasis is not achieved. Bleeding stops in 80% to 90% of patients, but unfortunately, 60% of them have recurrences. A new method involves the use of a self-expanding stent to stop acute bleeding from esophageal varices; initial studies reveal no method-related mortality or complications. Patients must be followed closely because the shunt may occlude in up to 50% of cases within 18 months. Shunt procedures are not the modality of choice because they result in a high rate of complications compared with medical therapy. Emergency bleeding may be controlled with a central portacaval shunt or with combined esophageal transaction, gastric devascularization, and splenectomy in patients hopeful for liver transplantation.

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