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

The pattern of arginine vasopressin (AVP) secretion in the immediate neonatal period is unclear. Plasma concentrations of AVP are reflected by its urinary excretion, thus providing a noninvasive method for studying the pattern of AVP release in the neonate. In these studies, we determined the pattern of urinary AVP excretion (microU/mg creatinine) during the first 2-4 days after birth in 78 neonates, 53 of whom had various prenatal and/or neonatal complications. In well term (n = 12) and preterm (n = 13) infants mean urinary AVP excretion decreased gradually during the first 24-36 h after birth. Although term and preterm infants with perinatal asphyxia had highest initial levels of urinary AVP (greater than 200 microU/mg creatinine) and a significant negative correlation with the 1-min Apgar score was obtained, their pattern of excretion was similar to respective controls. After delivery, elevated values for urinary AVP excretion were found among infants with neonatal courses complicated by intracranial hemorrhage, hypoxic encephalopathy, and pneumothorax. Urine osmolality did not correlate linearly with urinary AVP levels, but rather attained a maximum value of approximately 400 mosmol/kg at urinary AVP levels less than 200 microU/mg creatinine and then plateaued. It is concluded that the decrease in urinary AVP excretion observed soon after birth generally reflects diminution of the hypersecretion of AVP during parturition; neonates with evidence of intrapartum asphyxia initially have increased urinary AVP excretion; however, the pattern of excretion is similar to normal infants. During the neonatal period insults such as pneumothorax and intracranial hemorrhage may cause hypersecretion of this hormone.
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PMID:Urinary arginine vasopressin: pattern of excretion in the neonatal period. 394 21

This is a report on six psychiatric patients who indulged in excessive ingestion of water and subsequently developed tonic-clonic seizures in the course of the underlying mental disorders. On the basis of the DSM-III criteria, they were diagnosed as follows: schizophrenic disorder, 4; schizo-affective disorder, 1; borderline personality disorder, 1. The levels of serum electrolytes were estimated during five episodes of seizures in three patients. Hyponatremia was a consistent finding (serum sodium: mean = 120.6 mEq/liter). Plasma osmolality and plasma levels of arginine vasopressin (AVP) were determined during two episodes in two patients. The inappropriately high circulating levels of AVP relative to plasma hypoosmolality were documented. However, the response to the overnight fluid deprivation and acute water load during the period of no seizures in two patients revealed no evidence of the persistent SIADH, suggesting the temporal association of hyponatremic encephalopathy with inappropriate AVP secretion. It is not conclusive whether the transient SIADH is the cause or the consequence of hyponatremic encephalopathy, although a delusion or an auditory hallucination could play a critical role in drinking water excessively in three patients.
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PMID:The syndrome of self-induced water intoxication in psychiatric patients. 406 56

Hypoxic ischemic encephalopathy is a major cause of mortality in neonates. Studies in experimental subjects have shown differing responses of plasma arginine vasopressin to hypoxia. Plasma arginine vasopressin levels, serum osmolality, urine osmolality and fluid intakes were measured in thirteen asphyxiated and nineteen control newborn infants during the first seventy-two hours of life. In the asphyxiated infants plasma arginine vasopressin was found to be elevated as compared to control infants on days one (p less than 0.001) and two (p less than 0.007) but not on day three of life. Urine osmolality was also elevated in the study patients on days one (p less than 0.01) and two (p less than 0.001) but not on day three, in spite of equal intakes of fluid on day one in both groups and significantly diminished fluid intake on days two and three in the study patients. Serum osmolality was not different between the two groups on any day studied, and was felt to be on the basis of diminished intake in the study infants. The data presented in this study support the concept that arginine vasopressin release occurs following perinatal asphyxia in term newborn infants.
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PMID:Elevation of plasma concentrations of arginine vasopressin following perinatal asphyxia. 648 79

Despite several decades of research interest and productivity, many aspects of hyponatremia and hypo-osmolar disorders remain incompletely understood. Among these aspects are questions relating to the morbidity and mortality actually attributable to hyponatremia, possible hormonal and gender-associated risk factors underlying susceptibility to neurologic complications from hyponatremic encephalopathy, the stimuli to arginine vasopressin secretion in some atypical subsets of patients with the syndrome of inappropriate antidiuretic hormone secretion and other hyponatremic disorders, the contributions of natriuresis and natriuretic peptides to hyponatremic states, the pathologic determinants of brain demyelination that sometimes follow rapid correction of hyponatremia, and appropriate treatment guidelines for patients with acute and chronic hyponatremia. The recent literature confirms that acceptable answers to these questions and others are still not available, and a better understanding of basic issues regarding the pathophysiology of hyponatremia is needed. Several recent advances stand out as being likely to enhance our future understanding of hyponatremia and hypo-osmolar states. First are studies of cellular mechanisms of volume regulation in kidney and brain tissue in response to changes in osmolality. Many, though clearly not all, clinical observations can be better understood by considering them in the conceptual framework provided by knowledge of cell and body fluid compartment volume regulation. Second is the elucidation of several important protein structures via complementary DNA cloning, including the arginine vasopressin V1 and V2 receptors, several organic osmolyte transporters, and the CHIP28 water channel. Future application of these new tools to carefully designed and executed physiologic studies will likely add considerable new knowledge to our understanding of hyponatremia. Third is the development and increasing application of nuclear magnetic resonance spectroscopy and imaging methods that will allow more detailed analyses of acute changes in brain metabolism during hyponatremia and following correction. Finally, the recent development of nonpeptide antagonists to arginine vasopressin V1 and V2 receptors should enable clinical studies to assess more accurately the contribution of arginine vasopressin-induced antidiuresis to hyponatremia and more importantly holds the promise of more effective therapies for hyponatremic patients.
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PMID:Hyponatremia: epidemiology, pathophysiology, and therapy. 785 27

A case of colonoscopy-induced hyponatraemic encephalopathy led us to study the risk of hyponatraemia after gastrointestinal endoscopy. We assessed 40 patients before and after colonoscopy. 20 gastroscopy patients served as controls. Our findings show a high incidence (7.5%) of hyponatraemia after colonoscopy, in association with raised serum concentrations of arginine vasopressin. Physicians should be aware of this complication, since it may contribute to psychological and neurological symptoms after colonoscopy.
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PMID:Hyponatraemia as a complication of colonoscopy. 1138 19

Exercise-associated hyponatremia (EAH) has emerged in recent years as a life-threatening complication of endurance sports that may lead to fatal cerebral and pulmonary edema. Defined as a serum sodium concentration <135 mEq/L (1 mEq/L = 1 mmol/L), symptomatic EAH is a dilutional hyponatremia with abnormal fluid retention mediated by decreased urine production, which is a variant of the syndrome of inappropriate antidiuretic hormone secretion. Strategies for prevention and treatment must take into account the pathophysiology underlying this dominant clinical paradigm. Beyond educating runners to drink moderately, monitoring changes in body weight during endurance sports may facilitate the early detection of positive fluid balance characteristic of symptomatic cases. Rapid diagnosis by point-of-care testing indicates the need for fluid restriction in mild cases and emergent treatment with hypertonic (3%) NaCl to reverse acute hypotonic encephalopathy. The efficacy of arginine vasopressin V(2) receptor antagonists warrants study as an alternative treatment to loop diuretics for volume overload in these patients. Nonosmotic stimulation of arginine vasopressin secretion may be mediated in part by enhanced release of muscle-derived interleukin-6 during glycogen depletion, linking exertional rhabdomyolysis to the pathogenesis of EAH.
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PMID:Exercise-associated hyponatremia: role of cytokines. 1684 89

Exercise-associated hyponatraemia (EAH) is an acute-onset imbalance in the tonicity of extracellular fluids during or after endurance exercise which results in a blood sodium concentration <135 mmol/L. Both excessive fluid intake and a concurrent decrease in urine formation contribute to this rapid-onset, predominantly dilutional, decrease in serum sodium, which can result in life-threatening pulmonary and cerebral oedema. Marathon runners with hypotonic encephalopathy related to EAH, including two cases with fatal cerebral oedema, demonstrated non-osmotic secretion of arginine vasopressin and fulfilled the essential diagnostic criteria for the syndrome of inappropriate antidiuretic hormone secretion (SIADH). The pathophysiology of SIADH as the proximate cause of EAH accounts for otherwise puzzling clinical observations such as cases occurring after only moderate fluid intake or presenting hours after races. This formulation provides a framework for enhancing prevention by monitoring weight changes during races to detect positive fluid balance before the onset of mental status changes. Most importantly, SIADH supports a strategy for use of oral and intravenous hypertonic solutions, including 3% sodium chloride, for the emergent treatment of moderate and life-threatening symptoms of hypotonic encephalopathy, respectively.
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PMID:Hypertonic (3%) sodium chloride for emergent treatment of exercise-associated hypotonic encephalopathy. 1746 35

Hospital-acquired hyponatremia can be lethal. There have been multiple reports of death or permanent neurological impairment in both children and adults. The main factor contributing to the development of hospital-acquired hyponatremia is routine use of hypotonic fluids in patients in whom the excretion of free water, which is retained in response to excess arginine vasopressin (AVP), might be impaired. The practice of administering hypotonic parental fluids was established over 50 years ago, before recognition of the fact that there are numerous potential stimuli for AVP production in most hospitalized patients. Virtually all neurological morbidity resulting from hospital-acquired hyponatremia has been associated with administration of hypotonic fluids. Multiple prospective studies have shown that 0.9% NaCl is effective prophylaxis against hyponatremia. There is not a single report in the literature of neurological complications resulting from the use of 0.9% NaCl in non-neurosurgical patients. Patients at greatest risk of developing hyponatremic encephalopathy following hypotonic fluid administration are children, premenopausal females, postoperative patients, and those with brain injury or infection, pulmonary disease or hypoxemia. When hyponatremic encephalopathy develops, immediate administration of 3% NaCl is essential. In this Review, we discuss the question of why administering hypotonic fluids is unphysiologic and potentially dangerous, the settings in which isotonic fluids should be administered to prevent hyponatremia, and the appropriate treatment of hyponatremic encephalopathy.
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PMID:Hospital-acquired hyponatremia--why are hypotonic parenteral fluids still being used? 1759 70

Exercise-associated hyponatremia (EAH) is a potentially fatal fluid imbalance largely resulting from sustained fluid intake beyond the capacity for fluid excretion during endurance exercise. Common symptoms include vomiting, confusion, altered mental status, and seizures; however, these symptoms can also be seen with hypernatremic encephalopathy, making measurement of plasma sodium concentration imperative when athletes present with these symptoms. Recent evidence supports the inappropriate secretion of the antidiuretic hormone, arginine vasopressin (AVP), as the primary pathophysiological mechanism underlying the development of dilutional EAH. It appears that AVP is stimulated normally during prolonged endurance running by non-osmotic factors such as an exercise-induced plasma volume decrease; therefore, any excess fluid intake will likely be retained, and sodium will likely be excreted. The capacity for a small concentrated bolus of a hypertonic saline solution to rapidly reverse cerebral edema and remove any decreased plasma volume stimulus to AVP secretion is the most efficacious treatment for acute EAH encephalopathy to date. The prompt administration of an intravenous (IV) bolus of hypertonic saline in the field or hospital setting can be lifesaving once EAH is documented. Conversely, oral sodium supplementation will not prevent the development of EAH encephalopathy if exuberant fluid intake combined with non-osmotic secretion of AVP occurs during prolonged physical activity. As a result, the seemingly paradoxical use of sodium supplementation as the most effective practical management therapy (IV bolus) and ineffective preventive strategy can be reconciled through a more complete understanding of the pathophysiological mechanisms underlying EAH.
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PMID:Practical management of exercise-associated hyponatremic encephalopathy: the sodium paradox of non-osmotic vasopressin secretion. 1861 87

Hyponatremia is the most common electrolyte abnormality encountered in children. In the past decade, new advances have been made in understanding the pathogenesis of hyponatremic encephalopathy and in its prevention and treatment. Recent data have determined that hyponatremia is a more serious condition than previously believed. It is a major comorbidity factor for a variety of illnesses, and subtle neurological findings are common. It has now become apparent that the majority of hospital-acquired hyponatremia in children is iatrogenic and due in large part to the administration of hypotonic fluids to patients with elevated arginine vasopressin levels. Recent prospective studies have demonstrated that administration of 0.9% sodium chloride in maintenance fluids can prevent the development of hyponatremia. Risk factors, such as hypoxia and central nervous system (CNS) involvement, have been identified for the development of hyponatremic encephalopathy, which can lead to neurologic injury at mildly hyponatremic values. It has also become apparent that both children and adult patients are dying from symptomatic hyponatremia due to inadequate therapy. We have proposed the use of intermittent intravenous bolus therapy with 3% sodium chloride, 2 cc/kg with a maximum of 100 cc, to rapidly reverse CNS symptoms and at the same time avoid the possibility of overcorrection of hyponatremia. In this review, we discuss how to recognize patients at risk for inadvertent overcorrection of hyponatremia and what measures should taken to prevent this, including the judicious use of 1-desamino-8d-arginine vasopressin (dDAVP).
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PMID:New aspects in the pathogenesis, prevention, and treatment of hyponatremic encephalopathy in children. 1989 66


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