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Query: UMLS:C0028961 (oliguria)
 1,847 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ovarian hyperstimulation syndrome (OHS) is an iatrogenic syndrome in which induction of ovulation results in a wide spectrum of clinical symptoms and signs and laboratory manifestations. Based on the severity of the symptoms and signs, three degrees of hyperstimulation have been described: mild, moderate and severe. The most severe manifestation, presented in this paper with reference to the case of a 27-year-old woman, takes the form of massive ovarian enlargement with multiple cysts, hemoconcentration and third-space accumulation of fluid in the form of ascites, pleural and pericardial effusion. The full-blown clinical syndrome may be complicated by renal failure and oliguria, hypovolemic shock, thromboembolic episodes, adult respiratory distress syndrome (ARDS) and even death. The pathophysiologic mechanisms responsible for the development of OHS are still not known. The incidence of this iatrogenic syndrome can be reduced by monitoring plasma estradiol and by ultrasonographic evaluation of growing follicles. The anesthesiological aspects of OHS are discussed. A strategy for treatment, based on repeated ultrasonographic examination, clinical and biochemical evaluation, plasma volume replacement, abdominal paracentesis and aspiration puncture of the pleural effusion, is suggested.
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PMID:[The ovarian hyperstimulation syndrome. Anesthesiologic aspects based on a severe case]. 237 89

Ovarian hyperstimulation syndrome (OHS) is the most serious complication of ovulation induction, particularly in in vitro fertilization. It is a potentially life-threatening situation. Its pathophysiology is poorly understood. This syndrome is explained by a sudden increase in capillary permeability which results in a rapid fluid shift from the intravascular space into a third space leading to haemodynamic changes. In its most severe forms. OHS is characterized by multicystic ovarian enlargement, hemoconcentration, hypovolemia, oliguria, third space accumulation of fluid in the form of ascites and pleural effusion, renal failure, thrombotic disorders. Mild and the most of moderate forms of OHS usually do not require any active form of therapy. Severe OHS requires hospitalization, correction of fluid and electrolyte imbalance, prevention of thromboembolism, aspiration of the ascites and pleural effusion causing respiratory discomfort and dyspnea. Surgical interventions are exceptionally indicated and reserved for ovarian or rupture of ovarian cyst. Although severe OHS may not be completely avoided, early recognition of high-risk factors, judicious monitoring of ovulation induction (plasma estradiol levels and ultrasonography), and, perhaps in future, substitution of hCG for triggering ovulation should reduce the incidence of this iatrogenic syndrome.
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PMID:[Ovarian hyperstimulation syndrome in medically assisted reproduction]. 781 78

Ovarian hyperstimulation syndrome may be a serious complication of ovulation induction usually manifested by ovarian enlargement and ascites. In its severe form, haemoconcentration, oliguria and hydrothorax may ensue. As evident from this case report, the usual sequence of events does not necessarily occur in all cases. Unilateral hydrothorax may be the only extra-ovarian manifestation of ovarian hyperstimulation syndrome.
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PMID:Ovarian hyperstimulation syndrome manifests as acute unilateral hydrothorax. 858 61

Ovarian hyperstimulation syndrome (OHSS) is a serious complication affecting ovulation induction. Its most severe manifestation takes the form of massive ovarian enlargement and multiple cysts, haemoconcentration and third-space accumulation of fluid. The full-blown clinical syndrome may be complicated by renal failure and oliguria, hypovolaemic shock, thromboembolic episodes, adult respiratory distress syndrome (ARDS), and death. Although the pathophysiology of this syndrome has not been completely elucidated, it seems likely that the increased capillary permeability triggered by the release of vasoactive substance secreted by the ovaries under human chorionic gonadotrophin (HCG) stimulation plays a key role in this syndrome. Several factors such as histamine, serotonin, prostaglandins, prolactin, and a variety of other substances have been implicated in this process in the past. At present, factors belonging to the renin-angiotensin system, cytokines including the interleukins, tumour necrosis factor alpha, endothelin-1 and vascular endothelial growth factor (VEGF) are thought to be involved in triggering increased vascular permeability after ovulation induction treatment. This manuscript summarizes the current knowledge of the pathophysiology of ovarian hyperstimulation syndrome with emphasis on the correlation of the various factors with the clinical phenomena of this iatrogenic syndrome.
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PMID:The pathophysiology of ovarian hyperstimulation syndrome--views and ideas. 957 53

Ovarian hyperstimulation syndrome (OHSS) is a potentially fatal condition associated with the use of ovulation-inducing drugs. We describe a 28-year-old woman who presented with ascites, oliguria and vomiting. Over 2 weeks, the combination of intractable vomiting, intravenous rehydration, paracentesis, hypercatabolism and proteinuria led to severe hypoalbuminaemia with gross oedema and progressively worsening liver function. The patient's albumin dropped to 9 g/l with liver function abnormalities peaking at: alanine aminotransferase, 462 IU/l; alkaline phosphatase, 706 IU/l; bilirubin, 26 micromol/l; and prothrombin time, 19 s. The judicious use of paracentesis and commencement of total parenteral nutrition coincided with a rapid clinical improvement. One month after discharge, the patient was asymptomatic with normal liver function. This case demonstrates the severity of malnutrition and liver dysfunction that can occur with severe OHSS. Increasing use of in-vitro fertilization techniques makes it mandatory for clinicians to be aware of the clinical features, complications and treatment of this condition, and we would suggest that patients with severe OHSS should be jointly managed by physicians and obstetricians.
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PMID:A severe case of ovarian hyperstimulation syndrome with liver dysfunction and malnutrition. 1216 89

Ovarian hyperstimulation syndrome is a complication of the ovulation stimulation, most commonly by gonadotrophins. It frequently occurs in patients included in in vitro fertilization program. The exact mechanism of development of this syndrome has not been elucidated yet. The basic pathogenic mechanism of development of this syndrome is vasodilation of the ovarian blood vessels. Dilated ovarian blood vessels become permeable. Permeability of dilated ovarian blood vessels is more increased by released ovarian mediators. Due to increased permeability of the blood vessels, there is leakage of the intravascular fluid into the extravascular areas resulting in hypovolemia, edema and ascites. Hypovolemia leads to renal perfusion decrease. Increased salt and water reabsorption occurs in the renal tubules so oliguria develops. Decreased arterial blood volume results in stimulation of the renin-angiotensin-aldosterone system, the sympathetic nervous system as well as the antidiuretic hormone. The activation of the sympathetic nervous system via beta adrenergic receptors stimulates renin release and aldosterone secretion. Renin stimulates release of angiotensin I which transforms into angiotensin II. Angiotensin II increases the pressure and stimulates aldosterone secretion. In patients with this syndrome, there is an elevated plasma endothelin and natriuretic peptide level. Endothelin is an important vasoconstrictor. It increases secretion of renin, aldosterone, catecholamines, antidiuretic hormone, and atrial natriuretic peptide, and enhances the vasoconstrictive effect of norepinephrine and angiotensin II. The platelet number increase together with the elevated factor of blood coagulation and hyperviscosity in a severe form of this syndrome may result in development of intravascular thrombosis. The treatment consists of maintenance of circulatory function, i.e. the increase of effective arterial blood volume by applying the plasma volume expanders.
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PMID:[The significance of the ovarian arteriolar vasodilatation in pathogenesis of the ovarian hyperstimulation syndrome]. 1700 17

Ovarian hyperstimulation syndrome (OHSS) is an iatrogenic complication, the basis for which is a hyperergic uncontrolled ovarian response to gonadotropins in the ovulation stimulation cycles and assisted procreation programs. The clinical picture of OHSS is characterized by a broad spectrum of clinical and laboratory manifestations: increased vascular permeability resulting in the excess release of liquid into the third space and its storage with the development of hypovolemia, hemoconcentration, oliguria, hypoproteinemia, electrolyte imbalance, polyserositis; in severe cases, acute renal failure, thromboembolic events, and adult respiratory distress syndrome develop. The goal of treatment is to prevent the development of multiply organ dysfunctions. Its leading methods are infusion therapy with colloid-crystalloid solutions and anticoagulant therapy. Whether diuretics and other drugs are administered is under consideration. Indications for laparocentesis and peritoneal transudate evacuation are discussed. Complications requiring surgery are identified.
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PMID:[Ovarian overstimulation syndrome: problem of intensive care]. 1832 63

Ovarian hyperstimulation syndrome (OHSS) is an iatrogenic complication of controlled ovarian hyperstimulation (COH) protocols performed in women undergoing assisted reproductive technologies. Overstimulation of the ovaries results in the overproduction of vasoactive cytokines and mediators by the ovaries, thereby causing a generalized capillary leak and acute shift of protein-rich fluid from the intravascular compartment into the third space. This may lead to the development of ascites, pleural effusions, pericardial effusion, anasarca, intravascular volume depletion, hemoconcentration, oliguria, hypoalbuminemia and hypoproteinemia, electrolyte imbalances, acute renal failure, abdominal compartment syndrome, thromboembolic events, and adult respiratory distress syndrome. The only effective treatment available is prevention of the syndrome from developing by individualizing the stimulation protocol, especially in high-risk patients. Once the syndrome develops, the management is mainly supportive. Oliguria and some degree of acute renal failure commonly develop in patients with moderate to severe OHSS and are usually due to prerenal causes. Acute renal failure (ARF) secondary to obstructive uropathy is rare. Here we report a case of severe, life-threatening OHSS resulting in ARF secondary to obstructive uropathy.
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PMID:Ovarian hyperstimulation syndrome as an etiology of obstructive uropathy. 2387 50

Ovarian hyperstimulation syndrome (OHSS) is a severe iatrogenic complication of ovulation induction, which has a very serious impact on the patient's health, as it is often associated with a high morbidity and mortality risk. Indeed, patients classified as having severe OHSS presented with liquid imbalance signs (such as rapid weight gain, tense ascites, respiratory difficulty and progressive oliguria), which are related to the fluid shift from the intravascular space to third space compartments subsequent to an increased capillary permeability. In this way, cardiovascular system findings include decreased intravascular volume, decreased blood pressure, decreased central venous perfusion, and compensatory increased heart rate and cardiac output with arterial vasodilation might be found concomitantly. Notwithstanding that venous thromboembolic phenomena are a possible complication in advanced phases of OHSS, arterial ischemia involving the cerebral circulation is a rare but recently reported problem. The pathogenesis of thromboembolism in OHSS is not fully understood, even though hemoconcentration and blood hyperviscosity seem to play a role in developing thrombotic changes into both venous and arterial system. Interestingly, the presence of cardiac abnormalities in combination with inherited or acquired hypercoagulable state seems to increase the risk of cerebral infarct in these subjects, as recently shown by our group. This review is aimed at investigating the pathomechanism and the management of neurovascular complications related to OHSS, including new treatment options.
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PMID:Neurovascular complications of ovarian hyperstimulation syndrome (OHSS): from pathophysiology to recent treatment options. 2490 9