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Two multicenter trials evaluating the effectiveness of high-dose epinephrine in cardiac arrest failed to demonstrate an improvement in survival or neurologic outcome [64 quality 10mg tadalafil impotence therapy,65] cost of tadalafil erectile dysfunction specialist, and doses above 1 mg (excepting endotracheal administration) should not be used discount tadalafil 5 mg fast delivery impotence due to diabetic peripheral neuropathy. Risks in the use of epinephrine and other α-agonists include tissue necrosis from extravasation and inactivation from admixture with bicarbonate. Initial coronary vasoconstriction usually gives way to coronary vasodilatation, probably as a result of increased myocardial metabolic activity. During cardiac arrest, its usefulness, like that of epinephrine, is most likely due to peripheral vasoconstriction with an increase in perfusion pressure. In patients with spontaneous circulation who are in cardiogenic shock (when peripheral vasoconstriction is often already extreme), its effect is more difficult to predict. Indications for the use of norepinephrine during cardiac arrest are similar to those for epinephrine, although there does not appear to be any reason to prefer it to epinephrine. Norepinephrine appears to be most useful in the treatment of shock caused by inappropriate decline in peripheral vascular resistance, such as septic shock and neurogenic shock. Norepinephrine bitartrate, 4 to 8 mg (2 to 4 mg of the base), should be diluted in 500 mL D W or 5% dextrose in normal saline. Precautions to the use of norepinephrine include its inappropriate use in hypovolemic shock and in patients with already severe vasoconstriction. Intraarterial pressure monitoring is recommended when using norepinephrine because indirect blood pressure measurement is often incorrect in patients with severe vasoconstriction. In patients with myocardial ischemia or infarction, the myocardial oxygen requirements are increased by all catecholamines, but there is limited evidence to guide vasopressor selection in this population. Its cardiac activity includes potent inotropic and chronotropic effects, both of which will increase the myocardium’s oxygen demand. In addition to bronchodilatation, the arterial beds of the skeletal muscles, kidneys, and gut dilate, resulting in a marked drop in systemic vascular resistance. Cardiac output can be expected to increase markedly unless the increased myocardial oxygen demand results in substantial myocardial ischemia. Systolic blood pressure is usually maintained because of the rise in cardiac output, but the diastolic and mean pressures usually decrease. As a result, coronary perfusion pressure drops at the same time that the myocardial oxygen requirement is increased. This combination can be expected to have deleterious effects in patients with ischemic heart disease, especially during cardiac arrest. The main clinical usefulness of isoproterenol is in its ability to stimulate pacemakers within the heart. If the aortic diastolic pressure is already low, epinephrine is likely to be better tolerated as a stimulus to pacemakers. The infusion rate should be only rapid5 enough to effect an adequate perfusing heart rate (2 to 20 mcg per minute, or 0. Depending on the adequacy of cardiac reserve, a target heart rate as low as 50 to 55 beats per minute may be satisfactory. Precautions in the use of isoproterenol are largely due to the increase in myocardial oxygen requirement, with its potential for provoking ischemia; this effect, coupled with the possibility of dropping the coronary perfusion pressure, makes isoproterenol a dangerous selection in patients with myocardial ischemia. Isoproterenol is usually contraindicated if tachycardia is already present, especially if the arrhythmia may be secondary to digitalis toxicity. If significant hypotension develops with its use, it may be combined with another β-agonist with α-activity. However, switching to dopamine or epinephrine is usually preferable; better yet is the use of pacing for rate control. Dopamine This naturally occurring precursor of norepinephrine has α-, β-, and dopamine-receptor–stimulating activities. The dopamine-receptor activity theoretically dilates renal and mesenteric arterial beds at low doses (1 to 2 mcg per kg per minute), though the clinical relevance of this is unclear [67]. A 200-mg ampule is diluted to 250 or 500 mL in D W or 5%5 dextrose in normal saline for a concentration of 800 or 400 mg per mL. As with all catecholamine infusions, the lowest infusion rate that results in satisfactory perfusion should be the goal of therapy. Tachycardia or ventricular arrhythmias may require reduction in dosage or discontinuation of the drug. If significant hypotension occurs from the dilating activity of dopaminergic or β-active doses, small amounts of an α-active drug may be added. Dobutamine Dobutamine is a potent synthetic β-adrenergic agent that differs from isoproterenol in that tachycardia is less problematic. Dobutamine is indicated primarily for the short-term enhancement of ventricular contractility in the patient with heart failure. It may be used for stabilization of the patient after resuscitation or for the patient with heart failure refractory to other drugs. Although nitroprusside lowers peripheral resistance, dobutamine maintains perfusion by augmenting the cardiac output. A 250-mg vial is dissolved in 10 mL of sterile water and then to 250 or 500 mL D W for a5 concentration of 1. Dobutamine may cause tachycardia, ventricular arrhythmias, myocardial ischemia, and extension of infarction. In high doses, it is a powerful constrictor of smooth muscles and as such has been studied as an adjunctive therapy for cardiac arrest in an attempt to improve perfusion pressures and organ flows. Vasopressin may be especially useful in prolonged cardiac arrest as it remains effective as a vasopressor even in severe acidosis [68]. It may be used as a first-line agent in arrest in lieu of epinephrine or as the second- line agent if the first dose of epinephrine failed to cause a return in pulse. Antiarrhythmic Agents Antiarrhythmic agents have been thought to play an important role in stabilizing the rhythm in many resuscitation situations; however, the data in support of their value are scant. Amiodarone Amiodarone is a benzofuran derivative that is structurally similar to thyroxine and contains a considerable level of iodine. Gastrointestinal absorption is slow; therefore, when given orally, the onset of action is delayed while the drug slowly accumulates in adipose tissue. Amiodarone decreases myocardial contractility and also causes vasodilatation, which counterbalances the decrease in contractility. In a major study of out-of-hospital cardiac arrest due to ventricular arrhythmias refractory to shock, patients were initially treated with either amiodarone (246 patients) or placebo (258 patients). On the basis of this study, amiodarone has been given status as an option for use after defibrillation attempts and epinephrine therapy in refractory ventricular arrhythmias during cardiac arrest. It is also an option for ventricular rate control in rapid atrial arrhythmias in patients with impaired left ventricular function. Supplemental infusions of 150 mg may be given for recurrent or resistant arrhythmias to a total maximum dose of 2 g for 24 hours. Premature ventricular complexes are not unusual in apparently healthy people and most often are benign. If the patient has suffered an acute myocardial infarction and has had ventricular arrhythmias, the infusion is continued for hours to days and tapered slowly. The dosage should be reduced in patients with low cardiac output, congestive failure, hepatic failure, and age older than 70 years because of the decreased liver metabolism of the drug.

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The type of repair is determined by the location of the rupture and the presence or absence of aortic valve involvement purchase tadalafil 2.5mg popular erectile dysfunction drugs. Dacron grafts are generally placed to replace the diseased vessel segment order 5mg tadalafil with amex smoking and erectile dysfunction causes, with various strategies for aortic valve repair or replacement when necessary order tadalafil 20 mg line erectile dysfunction drugs non prescription. Recent work indicates that a less invasive form of repair, retrograde endovascular stent placement, may be useful for the repair of aneurysms of the descending aorta. Standard methods entail surgical replacement of diseased segments in a “staged” fashion; however, newer methods involving a hybrid approach of surgical replacement of the ascending aorta, with subsequent endovascular therapy of the distal segments, appear promising. It may be that a particular patient presents with complaints raising concern for a ruptured aortic aneurysm. In the event that no rupture is found and the patient is hemodynamically stable, it is possible that expansion of the aneurysm is responsible for the symptoms. In such a case, the focus of immediate clinical treatment should be to decrease aortic wall strain and systemic blood pressure through the use of β- blockers in the context of a critical care setting. This trend has been linked to the increased prevalence of atherosclerosis, which is thought to be the major etiology responsible for abdominal aneurysms. In general, the infrarenal segment of the aorta is most heavily affected by atherosclerosis, and this is also the segment where most abdominal aneurysms are observed. The risk factor most closely associated with abdominal aneurysms is smoking, followed by age, hypertension, and hyperlipidemia. Damage to the vessel wall, caused by atherosclerotic plaque, has been shown to cause local inflammation. This inflammatory process is thought to cause degradation of extracellular matrix proteins, notably elastin and collagen. In addition, it is thought that the proinflammatory cytokine milieu leads to cell death within the vessel wall. The full effects of smoking on aneurysm formation and expansion are not known, but increased atherosclerosis and hypertension are thought to be contributors. Such aneurysms are referred to as thoracoabdominal, and their management mirrors the management of aneurysms in the abdominal cavity. Aneurysms of the descending thoracic or abdominal aorta may also be caused by acute bacterial infections. Syphilis may also be associated with abdominal aneurysms, but it is more commonly associated with the ascending aorta. Connective tissue disorders, such as Marfan and Ehlers–Danlos syndromes, do not typically affect the abdominal aorta; however, some systemic inflammatory disorders, notably Takayasu arteritis or Behcet disease, may be associated with abdominal aneurysms. Clinical Manifestations As is the case with thoracic aneurysms, most abdominal aneurysms are asymptomatic and tend to be discovered with testing performed for other reasons. Those patients who do have aneurysm-related complaints tend to report pain in the hypogastric area and/or pain in the lower back. This pain is caused by the expansion of the aneurysm and tends to last for hours or days at a time, and is usually dull and steady. The most common consequence of aortic expansion is compression of the ureter or kidney, leading to hydronephrosis. An episode of rupture tends to be announced by a sudden onset or increase in abdominal and/or back pain. These patients may present with an initial episode of pain associated with the first rupture, followed by temporary tamponade of the retroperitoneal space. Consequently, the absence of a pulsatile mass on physical examination should not be interpreted as an absence of aneurysm. Laboratory analysis may reveal evidence of elevation in D-dimer or an elevation in cardiac biomarkers, due to demand-related myocardial ischemia. Imaging Transcutaneous ultrasound is a noninvasive and readily available technique for the evaluation of the abdominal aorta. This method is frequently used to track the size of abdominal aneurysms, though it is not the imaging modality of choice for the acute aortic syndromes. Open repair, with replacement of the diseased segment with a Dacron graft, is the most established technique. Retrograde endovascular stent placement is a promising technique [113–115], but it is not yet in common use in the acute setting [116,117]. Timely, but elective, surgical or endovascular intervention on the basis of size criteria, as assessed with longitudinal imaging, is the most effective means to prevent progression to rupture. Kuperstein R, Cahan T, Yoeli-Ullman R, et al: Risk of aortic dissection in pregnant patients with the marfan syndrome. Moza A, Al-Hudaif A, Sheikh M: Isolated aortic dissection during coronary intervention: rare but challenging. Girdauskas E, Rouman M, Disha K, et al: Aortic dissection after previous aortic valve replacement for bicuspid aortic valve disease. Ohlmann P, Morel O, Radulescu B, et al: D-dimer in ruling out acute aortic dissection: sensitivity is not 100%. Suzuki T, Katoh H, Tsuchio Y, et al: Diagnostic implications of elevated levels of smooth-muscle myosin heavy-chain protein in acute aortic dissection. Shinohara T, Suzuki K, Okada M, et al: Soluble elastin fragments in serum are elevated in acute aortic dissection. Bossone E, Evangelista A, Isselbacher E, et al: Prognostic role of transesophageal echocardiography in acute type A aortic dissection. Piccardo A, Regesta T, Zannis K, et al: Outcomes after surgical treatment for type A acute aortic dissection in octogenarians: a multicenter study. Li Z, Lu Q, Feng R, et al: Outcomes of endovascular repair of ascending aortic dissection in patients unsuitable for direct surgical repair. Fattori R, Cao P, De Rango P, et al: Interdisciplinary expert consensus document on management of type B aortic dissection. Midulla M, Renaud A, Martinelli T, et al: Endovascular fenestration in aortic dissection with acute malperfusion syndrome: immediate and late follow-up. Girish A, Padala M, Kalra K, et al: the impact of intimal tear location and partial false lumen thrombosis in acute type B aortic dissection. Kudo T, Mikamo A, Kurazumi H, et al: Predictors of late aortic events after stanford type B acute aortic dissection. Delsart P, Maldonado-Kauffmann P, Bic M, et al: Post aortic dissection: gap between activity recommendation and real life patients aerobic capacities. Kitai T, Kaji S, Yamamuro A, et al: Clinical outcomes of medical therapy and timely operation in initially diagnosed type A aortic intramural hematoma: a 20-year experience. Iida Y, Kawaguchi S, Koizumi N, et al: Thoracic endovascular aortic repair with aortic arch vessel revascularization. Garzon G, Fernandez-Velilla M, Marti M, et al: Endovascular stent- graft treatment of thoracic aortic disease. Larzon T, Lindgren R, Norgren L: Endovascular treatment of ruptured abdominal aortic aneurysms: a shift of the paradigm? Potential explanations for the higher prevalence of heart failure in the elderly include the high rate of hypertension; ventricular remodeling from prior myocardial infarction; age-related loss of functional myocytes; and increased extracellular matrix that contributes to alterations in left ventricular compliance. Several of these features combine to create a ventricular phenotype of “heart failure with preserved ejection fraction. The differentiation of new-onset decompensated heart failure from subacute or acute worsening of chronic heart failure is important, because their pathophysiologies differ.

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Cytochrome a3 is a key enzyme in the cytochrome oxidase system that is important for carrying out and sustaining aerobic metabolism within cells buy on line tadalafil erectile dysfunction the facts. Hyperpnea buy tadalafil line erectile dysfunction suction pump, dyspnea tadalafil 20 mg overnight delivery erectile dysfunction doctor orlando, tachycardia, agitation, anxiety, dizziness, headache, confusion, nausea, muscle weakness, and trembling are common. Hypotension, flushing, seizures, and Parkinson-like symptoms may occur among cases of severe intoxication. Coma, apnea, and cardiac dysrhythmias are poor prognostic signs unless prompt treatment is given [49,50]. It should be suspected in every individual with any of the above signs or symptoms for which there is no other obvious cause and a pertinent history such as smoke inhalation victims, victims of industrial accidents in which cyanide could have been released, and victims of terrorist attacks. Blood and urine cyanide concentrations can be obtained, but because these tests are not routinely performed in most laboratories, results take days to return and, therefore, are only be used to confirm the diagnosis. Treatment for this potentially life-threatening poisoning must be initiated immediately based on diagnostic suspicion alone. Arterial and venous blood gases can provide potentially useful information, with a high index of suspicion when the arteriovenous O difference is far less than normal. Because of poor2 cellular extraction and utilization of oxygen, the arterial oxygen tension is usually above 90 mm Hg, whereas venous oxygen tension may be significantly elevated above the normal range of 35 to 45 mm Hg. Similarly, arterial oxygen saturation is typically in the normal range of 95% to 100%, whereas the oxygen saturation of mixed venous blood may be in the vicinity of 85% or greater, significantly higher than the normal range of 60% to 80%. Hydroxocobalamin has no adverse effect on the oxygen-carrying capacity of the red blood cells and no negative impact on the patient’s blood pressure—significant benefits when treating victims of smoke inhalation. The mechanism of action is surprisingly simple: hydroxocobalamin binds to cyanide forming vitamin B12 (cyanocobalamin), a nontoxic compound excreted in the urine. Victims presenting with seizures, hypotension, or a coma in a setting consistent with cyanide toxicity should be considered candidates for empiric administration of hydroxocobalamin 5 g intravenously over 15 minutes through two intravenous or intraosseous lines. The most common adverse reactions (>5%) include transient chromaturia, erythema, rash (predominantly acneiform), hypertension, nausea, headache, decreased lymphocyte percentage, and injection site reactions. Less common allergic reactions include anaphylaxis, chest tightness, angioneurotic edema, and dyspnea. Because of its deep red color, hydroxocobalamin may cause hemodialysis machines to shut down because of an erroneous detection of a “blood leak. Sodium nitrite generates methemoglobin by changing the normal ferrous state of iron in the heme +2 +3 molecule of hemoglobin (Fe ) to the ferric state (Fe ). The adult dose of sodium nitrite is 300 mg in 10 mL of diluent (30 mg per mL) administered intravenously over 2 to 4 minutes, and the pediatric dose is 0. Following the administration of sodium nitrite, sodium thiosulfate should be administered intravenously. The inhalation of amyl nitrite from ampules can be used as a temporizing measure until venous access for the administration of sodium nitrite and sodium thiosulfate is obtained. The inhalation of amyl nitrite should never be considered a substitute for the administration of intravenous sodium nitrite and sodium thiosulfate. These effects are more pronounced in children, the elderly, and in patients with cardiopulmonary diseases. Dose regimen is difficult to control and could even result in exposure of the health care provider to amyl nitrite’s adverse effects. For these reasons, administration of amyl nitrite may be unwarranted, especially because hydroxocobalamin is now available [59]. The administration of sodium bicarbonate should be considered for the treatment of severe lactic acidosis in patients who are unconscious or hemodynamically unstable. Arterial blood gas analysis should be used to guide the need for repeat doses of sodium bicarbonate to ensure that metabolic alkalosis does not develop. Hydrogen Sulfide Pathophysiology Hydrogen sulfide (H S) is a colorless, highly flammable gas that has the2 characteristic odor of “rotten eggs. It’s noxious, “rotten eggs” odor is detectable by smell at low concentrations but may not be detectable at high concentrations or after prolonged exposure because of olfactory fatigue. As such, it can produce a variety of clinical effects, including central nervous system dysfunction [63], cardiac dysrhythmias, and pulmonary edema as a result of acute lung injury. After absorption through the lungs,2 H S easily dissolves in the blood and is rapidly distributed to tissues2 throughout the body. The respiratory system and organs with high oxygen demand, such as the brain and heart, are particularly vulnerable. The severity of clinical signs and symptoms associated with H S2 toxicity depends on the exposure dose. Local irritant effects dominate at low exposure doses, whereas pulmonary edema and life-threatening chemical asphyxiation dominate at higher exposure doses. Clinically detectable eye, mucous membrane, and respiratory tract irritation begin to occur at low exposure doses in the vicinity of 50 parts per million (ppm). Low-dose exposures in the range of 50 to 200 ppm are typically characterized by burning of the eyes, increased lacrimation, sore throat, nausea, cough, and occasional wheezing. Because olfactory function is lost at around 100 to 200 ppm, if exposed individuals can still smell the “rotten eggs” odor of H S, the2 concentration is usually not high enough to cause severe asphyxiation or irritant injury. At exposure concentrations of 200 to 250 ppm, H S2 produces intense irritation of mucous membranes, corneal ulceration, blepharospasm, and dyspnea. Pulmonary edema may occur at these concentrations as a result of irritant-induced acute lung injury [64]. At concentrations greater than 500 ppm, chemical asphyxiation of the brain may produce headache, seizures, delirium, confusion, and lethargy. The central nervous system effects of H S toxicity may be exacerbated by2 hypoxemia secondary to severe pulmonary edema. In survivors, long- term neurologic sequelae, such as ataxia, intention tremor, sensorineural hearing loss, muscle spasticity, and memory impairment, have been reported [61]. Myocardial ischemia, arrhythmias, and dilated cardiomyopathy have all been reported after significant exposures [65,66]. As doses increase, loss of consciousness, cessation of brainstem function, and cardiopulmonary arrest will occur. Diagnosis and Management A high index of suspicion is the key to making the diagnosis of H S2 intoxication. Although blood levels of thiosulfate are helpful in confirming the diagnosis of H S poisoning [2 67], these tests are not readily available in most clinical laboratories. When available, atmospheric measures of H S concentration can be used to increase diagnostic2 suspicion and in classifying the expected the severity of exposure and intoxication. In the absence of specific exposure information, signs of ocular irritation, inflammation of mucosal membranes, and the smell of “rotten eggs” on the clothing or breath of a patient should suggest the diagnosis of H S intoxication. As a result, blood gas analyses typically show a PaO in the normal range and an2 elevated mixed venous oxygen tension (PvO ), typically in the range of 352 to 45 mm Hg. In addition, both methemoglobin and sulfhemoglobin are produced during the treatment of H S poisoning with sodium nitrite2 and amyl nitrite, as discussed later.

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This appearance is typical of normal in athletes under the age of 30 years and is particularly puberty and is seen when there are several cysts (about common in women involved in the endurance events Polycystic Ovary Syndrome and Secondary Amenorrhoea 651 (such as long‐distance running) buy tadalafil in united states online impotence at 16. Up to 50% of competi­ age when the attainment of peak bone mass is impor­ tive runners training 80 miles per week may be amenor­ tant for long‐term skeletal strength cheap 5 mg tadalafil otc impotent rage violet. Physiological changes are consistent with those associated with starvation and chronic illness cheap tadalafil 10mg with visa impotence grounds for annulment philippines. Iatrogenic causes of amenorrhoea Ballet dancers provide an interesting subgroup of There are many iatrogenic causes of amenorrhoea, which sportswomen, because their training begins at an early may be either temporary or permanent. They have been found to have a significant delay in malignant conditions that require either radiation to the menarche (starting at the age of 15. Menstrual irregularities are common, and patient, the cumulative dose and the patient’s previous up to 44% have secondary amenorrhoea. However, iatrogenic causes disposition to scoliosis, as oestrogen is required for epi­ of ovarian quiescence have the same consequences of physeal closure. However, the these dancers does not compensate for these osteoporo­ demineralization is reversible with the cessation of ther­ tic changes. Oestrogen is also important in the forma­ apy, especially for the treatment of benign conditions in tion of collagen, and soft‐tissue injuries are also common young women who are in the process of achieving their in dancers. The concurrent use of an androgenic to reduce the incidence of postmenopausal osteoporosis, progestogen or oestrogen ‘add‐back’ therapy may pro­ young athletes may be placing themselves at risk at an tect against bone loss. Mortality of women with polycystic ovary polycystic ovary syndrome, oligo amenorrhoea and syndrome at long‐term follow‐up. J to impaired glucose tolerance or non‐insulin dependent Obstet Gynaecol Br Empire 1950;57:892–896. The management Legal/Guidelines/Management‐of‐premature‐ovarian‐ of anovulatory infertility in women with polycystic insufficiency. Simmond’s disease due to post‐partum reproductive health: British Fertility Society, Policy necrosis of the anterior pituitary. In addition to the tom description as it is simple and easily translatable into direct effect on the woman and her family, there are sig­ other languages. The recent national Cullen, a professor at the University of Edinburgh in the audit in England and Wales [3] reported that at 1‐year late 1700s. The term is confusing, being used as a symp­ post referral, only one‐third of women (including those tom, sign and diagnosis. As many as one in origin which was not due to pelvic pathology or sys­ five women discontinue use of progestin therapies (sys­ temic disease. It is also important in clinical practice to distinguish between regular and abnormal bleeding, such as inter­ Aetiology menstrual and post‐coital bleeding. Adenomyosis, Leiomyoma [fibroids], Malignancy) are ● ‘Bleeding of endometrial origin’ replaces ‘dysfunctional assessed visually (imaging and histopathology) and the uterine bleeding’. About abnormalities are present, many women may in fact be 50% of fibroids cause no symptoms. Theories include an increased endo­ Polyps metrial surface area and the presence of fragile and dilated Polyps are common (incidence increasing with age), fre­ vasculature around the fibroid [6]. Knowledge regarding quently asymptomatic and their exact cause remains the complex cellular and molecular changes found in unknown. It is important to be aware that both polyps association with fibroids is increasing. Data are emerging and fibroids may frequently coexist, and that polyps may on the impact of uterine fibroid presence on angi­ be mistaken for submucous fibroids on ultrasound. The most relevant premalignant and often coexists with endometriosis and fibroids. Sarcomas of myometrial origin, and ultrasonography but it is harder to establish the such as leiomyosarcoma, are rare but not infrequently diagnosis of adenomyosis if fibroids are also present. Age is a cally associated with continuous oestrogen or progestin risk factor for the development of leiomyosarcoma, therapies (intrauterine, systemic or oral delivery). Data exist to be inherited or acquired and severity of disorder varies support an association between chronic endometrial (but the majority are mild to moderate). The overall clin­ infection and abnormal uterine bleeding, both intermen­ ical impact is unknown. Acquired condi­ by the fact that 85% of cases of chlamydial infection are tions include severe thrombocytopenia, thrombocy­ asymptomatic. When they occur in the uterus they have been associated with episodes Ovulatory dysfunction of acute excessive bleeding. This most com­ of the uterus pose difficult management decisions and monly occurs at the extremes of reproductive age may present with heavy uterine bleeding following early (adolescence and perimenopause). Women in this group due to sub‐involution of the placental bed), the uterine often report menstrual cycles that extend beyond 38 lesion resolves once the human chorionic gonadotrophin days or vary by more than 21 days. An accurate history may also indicate the cause of the Investigation Indication bleeding. A coagulation disor­ der is likely if there is: Colposcopic Suspicion of cervical pathology examination 1) a history of excessive bleeding since menarche, post­ Histological Symptomatic women ≥45 years old, partum haemorrhage, surgery‐related bleeding, or assessment of the younger women when medical bleeding associated with dental work; or endometrium treatment has failed, younger women 2) a history of two or more of (i) bruising greater than with risk factors (e. Examination A general evaluation of the patient should be performed aged 45 years and above who have persistent intermen­ to exclude signs of anaemia, evidence of systemic coagu­ strual bleeding or treatment failure. This imaging modality will assist in further identi­ women in whom medical treatment has failed, further fication and localization of fibroids and also features of investigation is warranted (Table 48. For some women the demonstration that their ● Perform structured history to determine coagulation blood loss is in fact ‘normal’ may be sufficient to reassure disorder. These options include non‐hormonal, hormo­ intervention, and should be considered in women nal and surgical approaches [11]. As its action is local, progestogen‐related Antifibrinolytics, such as tranexamic acid, reduce blood side effects are much less than with oral agents. However, loss by up to 50% by inhibiting endometrial fibrinoly­ women should be fully counselled that they are likely to sis [12]. Side effects are rare but include gastrointesti­ experience unscheduled spotting/bleeding during the nal symptoms. Cyclical quently used agent and reduces blood loss by approxi­ administration of progestogens for less than 21 days each mately 25% [13]. Shorter courses of oral progestogens (14 days) are appropriate for women with definite anovulatory cycles Hormonal treatments (e. Furthermore, as amenorrhoea has become more a proportion of women will experience unscheduled acceptable (and indeed for some women even desirable), bleeding. A clinically and Endometrial ablation is the targeted destruction of the statistically significant reduction in fibroid volume was endometrium and some of the underlying myometrium. Further research is needed into or under local anaesthetic in the outpatient setting. Prophylactic antibiotic therapy is often ● Antifibrinolytics and prostaglandin synthetase inhibi- used to reduce the risk of endometritis. Typically, become amenorrhoeic, 40–60% will have markedly surgical management is only considered in women who reduced menstrual loss and 20% will have no difference have completed their family, with the exception of pol­ in their bleeding. Nonetheless, it is clear from longer‐ ypectomy and myomectomy where fertility may be term trials that while most women are initially satisfied, retained. Dilatation and curettage should not be used as many subsequently choose or require repeat endome­ a therapeutic treatment in any clinical situation.