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Query: UMLS:C0085584 (encephalopathy)
 18,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hyponatremia in advanced cirrhosis and ascites or congestive heart failure (CHF) is the result of an inappropriate increase in vasopressin secretion, which acts through activation of specific V(2) receptors in the distal renal nephron to increase water reabsorption. This study investigates the efficacy and safety of 3 different doses of the V(2) receptor antagonist, VPA-985, in correcting hyponatremia over a 7-day inpatient study period. Forty-four hospitalized patients (33 patients with cirrhosis, 6 with CHF, and 5 with syndrome of inappropriate antidiuretic hormone (SIADH) were studied on a constant sodium intake, with VPA doses of 25, 125, and 250 mg twice daily or placebo. Serum sodium measurements were repeated after every daily dose, and the next dose withheld for excessive serum sodium rises. Fluid intake was adjusted according to previous 24-hour urinary outputs. Adverse events were based on clinical signs of dehydration or encephalopathy. VPA-985 produced a significant overall aquaretic response compared with placebo, with significant dose related increases in free water clearance (P <.05) and serum sodium (P <.05), without significant changes in orthostatic blood pressure or serum creatinine levels. Five patients (50%) on 250 mg twice daily had to have medication withheld on multiple occasions. End-of-study plasma vasopressin levels increased significantly in the 2 larger dose groups. In conclusion, VPA-985 appears effective and safe in appropriate doses in correcting abnormal renal water handling and hyponatremia in conditions associated with water retention. Higher doses of VPA-985 may produce significant dehydration and will require close monitoring with their use.
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PMID:A vasopressin receptor antagonist (VPA-985) improves serum sodium concentration in patients with hyponatremia: a multicenter, randomized, placebo-controlled trial. 1499 23

Many patients develop confusion, lethargy, and cognitive and behavioral abnormalities during or after cardiac decompensation. Congestive heart failure and the accompanying elevation in systemic venous pressure and decrease in cardiac output can lead to changes within the cranial cavity that cause an encephalopathy. At times, excess cerebrospinal fluid accumulates within the cranium causing an apathetic state identical to that seen in patients with other causes of hydrocephalus. Awareness of the syndrome of cardiac encephalopathy and optimal management of congestive heart failure and body fluids can reverse the neurologic dysfunction. In some patients with excess cerebrospinal fluid, lumbar puncture with removal of cerebrospinal fluid can reverse the apathetic state.
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PMID:Cardiac Encephalopathy. 1509 13

Hyponatremia is an important electrolyte abnormality with the potential for significant morbidity and mortality. Common causes include medications and the syndrome of inappropriate antidiuretic hormone (SIADH) secretion. Hyponatremia can be classified according to the volume status of the patient as hypovolemic, hypervolemic, or euvolemic. Hypervolemic hyponatremia may be caused by congestive heart failure, liver cirrhosis, and renal disease. Differentiating between euvolemia and hypovolemia can be clinically difficult, but a useful investigative aid is measurement of plasma osmolality. Hyponatremia with a high plasma osmolality is caused by hyperglycemia, while a normal plasma osmolality indicates pseudohyponatremia or the post-transurethral prostatic resection syndrome. The urinary sodium concentration helps in diagnosing patients with low plasma osmolality. High urinary sodium concentration in the presence of low plasma osmolality can be caused by renal disorders, endocrine deficiencies, reset osmostat syndrome, SIADH, and medications. Low urinary sodium concentration is caused by severe burns, gastrointestinal losses, and acute water overload. Management includes instituting immediate treatment in patients with acute severe hyponatremia because of the risk of cerebral edema and hyponatremic encephalopathy. In patients with chronic hyponatremia, fluid restriction is the mainstay of treatment, with demeclocycline therapy reserved for use in persistent cases. Rapid correction should be avoided to reduce the risk of central pontine myelinolysis. Loop diuretics are useful in managing edematous hyponatremic states and chronic SIADH. In all instances, identifying the cause of hyponatremia remains an integral part of the treatment plan.
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PMID:Management of hyponatremia. 1516 58

Hereditary hemorrhagic telangiectasia (HHT), also known as Rendu-Osler-Weber disease, is an autosomal-dominant vascular disease characterized by mucocutaneous or visceral angiodysplastic lesions (telangiectases and arteriovenous malformations) that may be widely distributed throughout the cardiovascular system. The recognition of mucocutaneous telangiectases, the occurrence of spontaneous and recurrent episodes of epistaxis, the presence of visceral involvement, and a family history of this disease are the clinical criteria that allow diagnosis. In comparison with skin, lungs, gastrointestinal tract, and brain involvement, hepatic involvement defined by clinical criteria alone has long been considered uncommon. Our experience with a large group of HHT patients, even those asymptomatic for liver involvement, demonstrates that it is more frequent than reported and is characterized by the presence of intrahepatic shunts, disseminated intraparenchymal telangiectases, and other vascular lesions. Congestive cardiac failure, portal hypertension, portosystemic encephalopathy, cholangitis, and atypical cirrhosis have been reported as possible serious complications related to this condition. Thus, a correct diagnosis is important, and diagnostic imaging has a fundamental role in detecting alterations involving the liver. The possibilities to perform a multiphasic study and to provide high-quality multiplanar and angiographic reconstructions, gives multidetector row helical computed tomography the ability to detect and characterize the complex anatomopathologic alterations typical of this disease.
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PMID:Hepatic involvement in hereditary hemorrhagic telangiectasia: CT findings. 1529 Sep 48

Little is known about differences in practice patterns or outcomes in the management of patients who have atrial fibrillation in Canada compared with those in the United States (US). We evaluated the effect that the country of enrollment may have on the management patterns and clinical outcomes in patients who participated in the AFFIRM study. Three thousand four hundred patients came from the US and 660 from Canada. In the US, patients were more likely to have a history of coronary artery disease (39% vs 35%, p = 0.03), hypertension (72% vs 67%, p = 0.01), or congestive heart failure (24% vs 18%, p = 0.0002). More US participants were <65 years of age (25% vs 19%, p = 0.003). Although at randomization the use of warfarin was comparable, during follow-up Canadians were more likely to be treated with warfarin and to be therapeutically anticoagulated. Mortality rate at 5 years was higher in US patients (24% vs 16%, p = 0.001), and the composite end point (death, disabling stroke, major bleeding, cardiac arrest, or anoxic encephalopathy) was also higher in US patients (30% vs 22%, p = 0.0005). Even after adjusting for known differences in baseline characteristics, the risk of death was lower in Canada (hazard ratio 0.70, p = 0.02). In conclusion, in the AFFIRM study, US subjects were more likely to have preexisting cardiovascular diseases despite being younger (<65 years old) than those in Canada. Effective warfarin therapy was more commonly employed in Canada. After correcting for the known differences in baseline characteristics, Canadian patients who had atrial fibrillation had a lower mortality risk.
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PMID:Comparison of management patterns and clinical outcomes in patients with atrial fibrillation in Canada and the United States (from the analysis of the Atrial Fibrillation Follow-up Investigation of Rhythm Management [AFFIRM] database). 1616 68

Mitochondrial diseases represent a heterogeneous group of disorders associated with a wide array of clinical manifestations. The presentation of patients with mitochondrial pathology largely depends upon the dysfunction of organ systems with large metabolic/energy requirements, including cardiac, neurologic, and musculoskeletal. In particular, mitochondrial myocardial disease can be progressive resulting in congestive heart failure and end-stage heart disease. This article reviews the role of heart transplantation for a particular variant of mitochondrial disorder, mitochondrial encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) syndrome, and discusses perioperative management issues related to transplantation for mitochondrial cardiomyopathies.
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PMID:Heart transplantation for progressive cardiomyopathy as a manifestation of MELAS syndrome. 1636 83

Many patients with congestive heart failure develop neurologic dysfunction. This may take the form of a cardiac encephalopathy that shares clinical features with other metabolic encephalopathies. The causes are multiple. There is a particular, previously unreported, syndrome that occasionally develops in some patients with congestive heart failure that resembles the findings in patients with normal pressure hydrocephalus. This syndrome is characterized by apathy and abulia with preserved alertness; it is caused by fluid retention within the cranial cavity. The syndrome may also develop in patients with other conditions that cause anasarca, e.g., severe liver or kidney disease or hypoalbuminemia. Because patients with these conditions are often quite ill, it has been difficult to verify the pathophysiologic aspects of the syndrome so that its mechanism must remain a hypothesis that awaits more definitive study in a series of patients. I have not seen this syndrome discussed in any cardiology or neurology texts or reports, and it seems to be completely unknown to cardiologists and neurologists. I have recognized about one patient per year with this syndrome.
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PMID:Cardiac encephalopathy and congestive heart failure: a hypothesis about the relationship. 1640 54

Hereditary Haemorrhagic Telangiectasia (HHT), also known as Rendu-Osler-Weber disease, is an autosomal-dominant vascular disease characterised by mucocutaneous or visceral angiodysplastic lesions (telangiectases and arteriovenous malformations), which may be widely distributed throughout the cardiovascular system. Its diagnosis is based on clinical criteria. Liver, lungs and brain, in order of prevalence, are the most frequently involved visceral districts of the body other than skin and nasal mucosa. Liver involvement is frequent and characterised by the presence of intrahepatic shunts, disseminated intraparenchymal telangiectases and other vascular lesions. Although it is usually asymptomatic, congestive cardiac failure, portal hypertension, portosystemic encephalopathy, cholangitis or atypical cirrhosis are possible complications. Pulmonary arteriovenous malformations involve more than one third of HHT patients and can consist of diffuse telangiectases or high-flow low-pressure shunts between pulmonary arteries and veins. Pulmonary involvement can cause serious complications: hypoxaemia, pulmonary or pleural hemorrhage, paradoxical embolism into cerebral circulation. Various types of cerebrovascular malformations can affect HHT patients and the most common are arteriovenous malformations, consisting of one or more feeding arteries connected to one or more draining veins. Diagnostic imaging has a fundamental role in detecting the alterations involving these various districts in the body. The possibility to perform fast and complete studies and to provide high quality multiplanar and angiographic reconstructions, gives multi-detector row helical computed tomography and magnetic resonance the ability to detect and characterise the complex anatomo-pathological alterations typical of HHT. Ultrasonography seems to be the best screening modality for hepatic and pulmonary involvement.
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PMID:Hereditary haemorrhagic teleangiectasia: diagnostic imaging of visceral involvement. 1661 Nov 5

We present the case of a post-menopausal female who, following a prolonged period of vomiting and diarrhoea, presented acutely with Wernicke's; encephalopathy, chest pain, ST-segment elevation and congestive cardiac failure associated with hypotension. Coronary angiography demonstrated no abnormality. Haemodynamics improved significantly in the short-term following intravenous thiamine replacement, with complete resolution of all ST-segment abnormalities and normalization of left ventricular function at six-week follow-up. Shoshin beriberi in the context of metabolic alkalosis, secondary to severe electrolyte depletion, is exceptional and is a differential diagnosis to be considered in all malnourished patients presenting with symptoms and signs suggestive of an acute coronary syndrome, especially those with a history of alcohol-dependence.
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PMID:A case of ST-elevation and nystagmus--when coronary thrombosis is not to blame. 1962 76

The aim of this study was to define the current demographic, clinical and prognostic characteristics of acute post-streptococcal glomerulonephritis (APSGN) in French Polynesia and to compare these features with those of other populations. Fifty children, all of whom were <15 years old and had been admitted to the Territorial Hospital of Papeete for APSGN between January 2005 and December 2007, were retrospectively enrolled in the study. Diagnostic criteria were microscopic or macroscopic haematuria, decreased C3 fraction of the complement and evidence of recent streptococcal infection. The annual incidence was 18 cases per 100,000 children <15 years of age in 2007. Most of the children (98%) enrolled in the study were of Polynesian ethnic origin, 27 were male (54%), and the average age at presentation was 6.7 years. Signs of previous respiratory infections were clearly evident in 40% of the children. Most of the patients presented during the rainy season, correlating with the relatively high incidence of skin infections at this time. The majority of patients had proteinuria (98%), with 25% having proteinuria in the nephrotic range (proteinuria/urinary creatinine >3 g/g). The presentation was severe in 22% of the children (congestive cardiac failure, severe hypertension and/or encephalopathy), and renal failure was an initial presenting symptom in 43.7%. The C3 fraction was lower in severe presentations, but the type of haematuria, level of proteinuria and inflammatory syndrome were not correlated with immediate severe forms or with initial renal failure. Haematuria resolved in a mean of 7.7 months and proteinuria in a mean of 3.9 months. None of the children had hypocomplementemia for more than 8 weeks. Acute post-streptococcal glomerulonephritis is endemic among French Polynesians, and they can be considered to be a high-risk population. Despite a high incidence of skin infections, however, the predominance of respiratory infections potentially indicates that French Polynesia is on the way to become a low-incidence area. Systematic detection and treatment of group A Streptococcus should be intensified.
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PMID:Acute post-streptococcal glomerulonephritis in children of French Polynesia: a 3-year retrospective study. 1987 55


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