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

Treatment of hypercalcemia of malignancy (HCM) is briefly reviewed, available treatments are compared, and treatment guidelines are presented. The most effective strategy is treatment of the underlying malignancy. For patients who have a poor prognosis and no viable treatment options, the most humane course may be no treatment at all since encephalopathy will cloud their consciousness. Patients with mild hypercalcemia (corrected serum calcium concentration < 12 mg/dL) may respond to oral hydration, salt restriction, and ambulation, which encourage the normal bone remodeling process. Patients with moderate (corrected serum calcium concentration 12.0-13.5 mg/dL) to severe (> 13.5 mg/dL) hypercalcemia may require rehydration with 0.9% sodium chloride injection. Furosemide may be indicated to counteract fluid overload from rehydration measures or in patients at risk of developing congestive heart failure. For patients with renal failure not caused by dehydration, dialysis with a calcium-free or low-calcium solution is the treatment of choice. The calciuric effect of rehydration lasts only two to three days, and antiresorptive therapy is indicated for patients who require a longer duration of effect. Calcitonin is useful if a rapid decrease in serum calcium is necessary, but tachyphylaxis limits its use. Corticosteroids should be used only in patients with tumors that produce 1,25-dihydroxycholecalciferol. The use of plicamycin is limited because of adverse effects. Before the availability of zolendronic acid, pamidronate disodium was the treatment of choice, because of its longer duration of action than etidronate disodium and potential safety advantages. Zolendronic acid (discussed elsewhere in this supplement) is likely to supercede pamidronate disodium as the drug of choice for HCM, but the presence of symptoms, the rate of rise in serum calcium concentration, and the overall status of the patient are important considerations in selecting therapy.
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PMID:Conventional treatment of hypercalcemia of malignancy. 1175 6

Dysnatremias are among the most common electrolyte abnormalities encountered in hospitalized patients. In most cases, a dysnatremia results from improper fluid management. Dysnatremias can occasionally result in death or permanent neurological damage, a tragic complication that is usually preventable. In this manuscript, we discuss the epidemiology, pathogenesis and prevention and treatment of dysnatremias in children. We report on over 50 patients who have suffered death or neurological injury from hospital-acquired hyponatremia. The main factor contributing to hyponatremic encephalopathy in children is the routine use of hypotonic fluids in patients who have an impaired ability to excrete free-water, due to such causes as the postoperative state, volume depletion and pulmonary and central nervous system diseases. The appropriate use of 0.9% sodium chloride in parenteral fluids would likely prevent most cases of hospital-acquired hyponatremic encephalopathy. We report on 15 prospective studies in over 500 surgical patients that demonstrate that normal saline effectively prevents postoperative hyponatremia, and hypotonic fluids consistently result in a fall in serum sodium. Hyponatremic encephalopathy is a medical emergency that should be treated with hypertonic saline, and should never be managed with fluid restriction alone. Hospital-acquired hypernatremia occurs in patients who have restricted access to fluids in combination with ongoing free-water losses. Hypernatremia could largely be prevented by providing adequate free-water to patients who have ongoing free-water losses or when mild hypernatremia (Na>145 mE/l) develops. A group at high-risk for neurological damage from hypernatremia in the outpatient setting is that of the breastfed infant. Breastfed infants must be monitored closely for insufficient lactation and receive lactation support. Judicious use of infant formula supplementation may be called for until problems with lactation can be corrected.
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PMID:Preventing neurological complications from dysnatremias in children. 1677 23

Dysnatremias are a common clinical entity that are often associated with poor outcomes. This review takes a case study approach to understand how dysnatremias can result in devastating neurologic consequences. Concrete guidelines are provided for prevention, early recognition and treatment along with a discussion of how urinary electrolytes and osmolality can be used to guide therapy. Case studies in hyponatremic encephalopathy include the post-operative state, thiazide diuretics, extreme exercise and DDAVP use. Reasons to avoid using hypotonic parenteral fluids, risk factors for hyponatremic encephalopathy such as age, gender, and hypoxia, and the appropriate use of 3% sodium chloride are discussed. Case studies in hypernatremia include hypernatremia in the ICU setting and the emerging condition of breastfeeding-associated hypernatremia in infants.
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PMID:Dysnatremias: why are patients still dying? 1663 44

The most recent (1996) drinking guidelines of the American College of Sports Medicine (ACSM) propose that athletes should drink "as much as tolerable" during exercise. Since some individuals can tolerate rates of free water ingestion that exceed their rates of free water loss during exercise, this advice has caused some to overdrink leading to water retention, weight gain and, in a few, death from exercise-associated hyponatraemic encephalopathy. The new drinking guidelines of the International Olympic Committee (IOC), recently re-published in this Journal, continue to argue that athletes must drink enough to replace all their weight lost during exercise and to ingest sodium chloride since sodium is "the electrolyte most critical to performance and health". In this rebuttal to that Consensus Document, I argue that these new guidelines, like their predecessors, lack an adequate, scientifically proven evidence base. Nor have they been properly evaluated in appropriately controlled, randomized, prospective clinical trials. In particular, these new guidelines provide erroneous recommendations on five topics. If novel universal guidelines for fluid ingestion during exercise are to be promulgated by important international bodies including the IOC, they should first be properly evaluated in appropriately controlled, randomized, prospective clinical trials conducted under environmental and other conditions that match those found in "out-of-doors" exercise. This, and the potential influence of commercial interests on scientific independence and objectivity, are the two most important lessons to be learned from the premature adoption of those 1996 ACSM drinking guidelines that are not evidence-based. These concerns need to be addressed before the novel IOC guidelines are accepted uncritically. Otherwise the predictable consequences of the premature adoption of the 1996 ACSM guidelines will be repeated.
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PMID:Drinking guidelines for exercise: what evidence is there that athletes should drink "as much as tolerable", "to replace the weight lost during exercise" or "ad libitum"? 1745 46

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

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

Gastroenteritis is one of the most common medical conditions seen by pediatricians. The standard approach to intravenous fluid therapy for these children has been to administer a 0.9% sodium chloride (NaCl) bolus followed by a hypotonic solution ranging from 0.2-0.45% NaCl to replace the remaining deficit plus maintenance. We have questioned the safety of this approach as there have been reports of death or permanent neurologic impairment from hyponatremic encephalopathy. Hanna and Saberi (Pediatr Nephrol. doi: 10.1007/s00467-009-1428-y ) found the incidence of hospital-acquired hyponatremia (sodium < 135 mEq/L) to be 18.5% for patients presenting with isonatremic dehydration from gastroenteritis. This confirms that the current approach of using hypotonic fluids results in a high incidence of hyponatremia. Hypotonic fluids are not appropriate for rehydration in patients with gastroenteritis as it is a state of arginine vasopressin (AVP) excess due to both hemodynamic stimuli from volume depletion and non-hemodynamic stimuli such as nausea and vomiting. Free water will be retained until the volume deficit is corrected and the hemodynamic stimulus for AVP production abates. A safer and more effective approach is the administration of 0.9% NaCl in a continuous infusion following bolus therapy. 0.9% NaCl not only serves as prophylaxis against hyponatremia, but it is superior to hypotonic fluids as an extracellular volume expander and corrects the volume deficit more rapidly.
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PMID:Improving intravenous fluid therapy in children with gastroenteritis. 2010 2

The present study included 161 patients with vibration disease associated with dyscirculatory encephalopathy. It was designed to estimate the degree of cognitive dysfunction and the efficacy of its treatment by physiobalneotherapeutic techniiques including low-frequency pulsed currents in combination with general artificial sodium chloride and iodine bromide baths. In addition, the influence of combined therapy on the clinical course of the disease, results of neuropsychological tests, and cerebral hemodynamics was evaluated.
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PMID:[Combined physiobalneotherapy of vibration disease associated with dyscirculatory encephalopathy in the miners]. 2321 Mar 56

Disorders in serum sodium, hyponatremia and hypernatremia, are frequently encountered in both inpatient and outpatient settings. Many sodium disorders are iatrogenic, caused by inappropriate intravenous fluid management. The methods of prevention and treatment of serum disorders differ based on the underlying disease states. Nine cases are presented to illustrate different aspects of fluid management, with an emphasis on the prevention and treatment of disorders in serum sodium. Key concepts that are discussed are (1) when to use an isotonic fluid versus a hypotonic fluid, (2) when to restrict or liberalize maintenance intravenous fluids, (3) how to use 3% sodium chloride for the treatment of hyponatremic encephalopathy, (4) when to use desmospressin to prevent the overcorrection of chronic hyponatremia, and (5) strategies to treat different causes of hypernatremic dehydration in children.
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PMID:Case studies in fluid and electrolyte therapy. 2382 3

Gitelman syndrome is an autosomal recessive renal tubular disorder characterized by hypokalemic metabolic alkalosis, hypomagnesemia and hypocalciuria. The syndrome is caused by a defective thiazide-sensitive sodium chloride co-transporter in the distal convoluted tubules of the kidneys. Gitelman syndrome could be confused with Bartter syndrome; the main differentiating feature is the presence of low urinary calcium excretion in the former. Descriptions of neuroradiological imaging findings associated with Gitelman syndrome are very scarce in the literature and include basal ganglia calcification, idiopathic intracranial hypertension and sclerochoroidal calcification. Cauda equina syndrome-like presentation has been reported, but without any corresponding imaging findings on lumbar spine MRI. We report a 13-year-old male with Gitelman syndrome who presented with altered mental status following a fall and scalp laceration and unremarkable brain CT, followed during hospitalization by somnolence and seizures. Metabolically the patient demonstrated hypokalemia and hypomagnesemia. MRI demonstrated features of encephalopathy including predominantly right-sided cerebral hemispheric signal abnormality and cytotoxic edema, with bilateral symmetric involvement of the thalami, midbrain tegmentum and tectum and cerebellar dentate nuclei. MRI after five months obtained during a later episode of encephalopathy showed resolution of the signal abnormalities with setting in of brain atrophy and also areas of newly developed cytotoxic edema in the left thalamus, bilateral dorsal midbrain and right greater than left dentate nuclei. The described abnormalities, either recurrent or in isolation, have not previously been published in patients with Gitelman syndrome. We believe that the findings are due to alteration of respiratory chain function secondary to the metabolic derangement and hence have a similar imaging appearance as encephalopathy related to mitochondrial cytopathy or metabolic encephalopathy.
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PMID:Novel brain MRI abnormalities in Gitelman syndrome. 2644 1


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