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Results for “Hypernatremia”

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At least 109 records · Page 6Linked to original sources
PubMed2006

[Continuous veno-venous hemofiltration treatment for acute hypernatremia].

OBJECTIVE: To investigate the effect of continuous veno-venous hemofiltration (CVVHF) for acute hypernatremia. METHODS: Seven patients with hypernatremia were studied and treated with CVVHF. The serum sodium concentration and its remedy speed, creatinine, osmolarity, and blood pressure, etc were observed before and after CVVHF. RESULTS: The patients were treated with CVVHF averagely for 40 hours. The serum sodium concentration, creatinine, osmolarity after the treatment decreased significantly and the APACHE II scores significantly improved. Among the 5 coma patients, 2 patients's consciousness was improved. CONCLUSION: CVVHF is effective and can be a new method for treating acute hypernatremia.

Acute Disease↗
PubMed1977

[Essential hypernatremia with hypovolemia caused by hypodipsia and partial diabetes insipidus].

The authors report the case of 13 year old girl presenting with chronic hypernatremia. This case should be considered as either neurogenic or essential hypernatremia. Partial diabetes insipidus and hypodipsia hypernatremia. Partial diabetes insipidus and hypodipsia are the cause of chronic hypovolemia and a new homeostasis with an exceptionally high level of sodium (isoosmotic point 154 mEq/l). No cause was found and in particular, the search for a cerebral disease was until now proved negative.

Adolescent↗
PubMedDate not supplied

[Neurogenic hypernatremia syndrome in children].

Chronic "neurogenic" hypernatremia is the consequence of defective thirst mechanism either alone or in combination with impaired osmoregulation of ADH release. Both the specific receptors and the structures involved in hormonal secretion are localised in the hypothalamic area. "Neurogenic" hypernatremia can be secondary to a hypothalamic lesion of different type (neoplastic, vascular, malformative) or rarely it can be idiopathic. We present three cases: two females 4 and 5 months old, affected by cerebral malformations involving midline structures of the brain (III ventricule, corpus callosum etc.) and a male 4 years old with a idiopathic form. We discuss the relationship between the origin of the cerebral malformations and the ontogeny of the structures involved in the control of the osmolarity. Moreover we have observed that the hypernatremia in associated with hyperlipemia: the pathogenetic hypothesis explaining this abnormality are discussed.

Brain↗
PubMed1988

[Renal protection in acute neurosurgical diseases--effect of a low dose dopamine with reference to acute renal failure and hypernatremia in patients with dehydration].

The authors reviewed the effect of low dose dopamine administration (1-5 micrograms/kg/min) in neurosurgical patients with acute renal failure (5 cases) or hypernatremia (7 cases) in whom cerebral dehydration therapy for intracranial hypertension was thought to be causative of these disorders. Cases with hypernatremia (serum sodium over 155 mEq/l) were considered in the stage of impending acute renal failure as in the majority of cases serum creatinine levels were mildly elevated while urinary sodium was markedly diminished. Associated with systemic hypovolemia, in cases with acute renal failure (with serum creatinine over 3.5 mg/dl and urinary output of less than 20 ml/hr for more than 4 hour duration) the urinary sodium levels were less than 20 mEq/l. In all the cases treated by low dose dopamine, urinary output and sodium increased within 6 hours and in the following 24 hours stabilized urinary output with its elevated sodium (some 100 mEq/l) was obtained. As the result, elevated urea-nitrogen or serum sodium was rather easily washed out and the patients were kept adequately hydrated afterwards. Any complications such as aggravation of cerebral edema or convulsive disorder were not associated with this regime. The authors, therefore, would emphasize that low dose dopamine administration resulting in sodium diuresis and increase in renal blood flow is a practical way of method in treating patients with hypernatremia or acute renal failure caused by hyperosmolar agent infusion in their acute stage.

Acute Kidney Injury↗
PubMed1987

Hypodipsic hypernatremia and associated myopathy in a hydrocephalic cat with transient hypopituitarism.

Hypodipsic hypernatremia developed in association with hypopituitarism and hydrocephalus in a 7-month-old cat. Initial clinical signs (generalized weakness, cervical ventroflexion) were related to a hypernatremia-induced polymyopathy. Forced water intake and dietary sodium restriction corrected the hypernatremia and signs of muscle dysfunction. After restoration of eunatremia, secretion of pituitary hormones normalized. It was speculated that hypothalamic dysfunction, possibly related to hydrocephalus, induced both hypodipsia and transient hypopituitarism.

Animals↗
PubMed1986

Severe hypernatremia in a patient with psychiatric illness.

A 17-year-old schizophrenic developed severe hypernatremia during a period of psychosis. The thirst-deficient abnormality that caused this hypernatremia resolved when his psychosis improved. The primary disorders causing a thirst deficiency leading to hypernatremia fall into three categories: lesions of the central nervous system, mineralocorticoid excess, and drug side effects. None of these disorders was found in our patient. We conclude that psychosis can severely impair the thirst mechanism directly.

Adolescent↗
PubMed1983

Hypernatremia in the very low birthweight infant.

The incidence and cause of hypernatremia in twenty-five very low birthweight infants were determined by a retrospective analysis of their clinical course during the first 72 hours of life. Ten (40%) developed a serum sodium greater than or equal to 150 mEq/l. This was associated with a greater weight loss than found in normal infants (5.3 +/- 2.6%/day vs 1.7 +/- 2.3%/day, p less than .05) and with more time spent under radiant energy, but not with the amount of water, or sodium received. The severity of hypernatremia correlated with birthweight (r = -.47, p less than .05) and with postnatal weight loss but not with sodium intake. The excess weight loss in the hypernatremic group, when added to their average measured fluid intake suggests an estimated optimal fluid requirement of 150 ml/kg/day in the environment described. The hypothesized mechanism for hypernatremia is dehydration, possibly through insensible water loss.

Birth Weight↗
PubMed1984

Hypernatremia and adipsia in a dog.

Primary adipsia and defective osmoreceptor function were diagnosed in a 7-month-old female Miniature Schnauzer. Also, the dog was noted to be dehydrated and to have chronic hypernatremia. On multiple occasions the dog's urine osmolality: plasma osmolality was greater than 4. The dog had inappropriate responses to isoosmotic and hypertonic NaCl infusions. Chlorpropamide administration initiated water intake but the volume was insufficient to avoid hypernatremia. The chronic hypernatremia and dehydration were treated successfully by mixing the calculated maintenance fluid volume in canned food. At 25 months of age, the dog died several days after becoming dehydrated and severely hypernatremic. Astrogliosis and neuronal degeneration were noted in both the thalamic and hypothalamic regions, but were believed to be nonspecific degenerative lesions compatible with seizures and severe dehydration.

Animals↗
PubMed1977

Hyponatremia and hypernatremia.

The concentration of serum sodium is determined by the external balance of water. Hyponatremia occurs when total body water is in excess of sodium, and hypernatremia develops when body water is relatively decreased in relation to sodium. Both disorders may be present in patients with various disease states in which total body sodium is either decreased, normal or increased. The symptomatology in both disorders is related to the disturbance in central nervous system due to brain edema in patients with hyponatremia and brain dehydration, and cerebrovascular hemorrhages in patients with hypernatremia. The treatment of hypo and hypernatremia is achieved by correcting the abnormalities in body water content.

Adult↗
PubMed1988

[Severe hypernatremia in acquired disorder of thirst and vasopressin regulation].

Three patients with severe adipsic hypernatremia (greater than 171 mmol/l) are presented. In two of them, hypernatremia occurred after the operation of a ruptured aneurysm of the A. communicans anterior, in one patient the cause of the disease remained obscure. Despite high plasma osmolality, all patients had low or undetectable plasma vasopressin levels, even throughout hypertonic saline infusion. Urine concentrating ability was partially maintained, suggesting activation of alternative extra- and intrarenal concentrating mechanisms or increased renal sensitivity to low vasopressin concentration. Nonosmolar stimulation (insulin-induced hypoglycemia) did increase vasopressin concentration only subnormally in the two patients tested. This finding might be due to an extended and complex dysfunction of the anterior hypothalamus rather than to a circumscribed defect of the osmoreceptor/thirst center or the supraoptic nuclei.

Adult↗
PubMed2006

Dehydration and hypernatremia in breast-fed term healthy neonates.

OBJECTIVE: The aim of the study was to determine the incidence of significant weight loss, dehydration, hypernatremia and hyperbilirubinemia in exclusively breast-fed term healthy neonates and compare the incidence of these problems in the warm and cool months. METHODS: During the study period 496 neonates were recruited. RESULTS: 157 neonates (31.6%) had significant weight loss (> 10 % cumulative weight loss or per day weight loss > 5%). Clinical dehydration was present in 2.2% of neonates. Of these 157 neonates, 31.8% had hypernatremia and 28 % had hyperbilirubinemia. CONCLUSION: The incidence of the above mentioned problems were higher in the warm months but the difference was not statistically significant.

Breast Feeding↗
PubMed2006

Rhabdomyolysis caused by hypernatremia.

Rhabdomyolysis is a clinical picture which is rarely seen in children. In this case report here it is presented a patient who has biochemical and clinical signs of rhabdomyolysis and admitted to our clinic with hypernatremia. The authors think that it is necessary to be alert for rhabdomyolysis in severe hypernatremia cases.

Acute Disease↗
PubMed2001

[Hypernatremia as a rare complication in change from lithium to valproate].

This paper is about a female patient who suffered from bipolar disorders for several decades. Due to a change in medication from lithium to valproic acid by infusion, the patient fell into a coma. Hypernatremia, which had developed unnoticed, was later discovered as the reason. This hypernatremia was due to renal diabetes insipidus stemming from the decades of lithium therapy, with accompanying polydipsia and polyuria, and also to the failure to give enough fluid to the somnolent patient.

Antimanic Agents↗
PubMed1987

Polyuria and refractory hypernatremia after cardiopulmonary arrest.

A patient exhibited brain damage, polyuria, and refractory hypernatremia after myocardial infarction and cardiopulmonary arrest. Serum vasopressin levels were relatively fixed and inappropriately low for the elevated serum osmolality. Hypernatremia persisted despite administration of vasopressin; after vasopressin was discontinued, serum sodium value was corrected with small doses of furosemide and replacement of free water. In her case, impairment of osmotic homeostasis could not be attributed to either simple resetting or complete destruction of osmoreceptors; metabolic normalization required an unusual therapeutic approach.

Diabetes Insipidus↗
PubMed1996

Arcuate nucleus inputs onto subfornical organ neurons that respond to plasma hypernatremia and angiotensin II.

Experiments were done in urethane anesthetized rats to investigate the effect of electrical and glutamate stimulation of arcuate nucleus (Arc) on the discharge rate of subfornical organ (SFO) neurons that responded to either plasma hypernatremia or angiotensin II (ANG II). Extracellular recordings were made from 253 histologically verified single neurons in SFO. Of these, 40.3% (102/253) responded with excitation and 10% (25/253) with inhibition to Arc stimulation. Thirty-five (34.3%) of the units excited by Arc were also excited by intracarotid infusion of hypertonic (0.5 M) NaCl. In addition, 37 (36.3%) of the units excited by Arc were also excited by intracarotid infusion of ANG II. Furthermore, 10 (40.0%) of the units inhibited by Arc were found to be excited by ANG II. None of the units inhibited by Arc stimulation were responsive to plasma hypernatremia. These data indicate that inputs from Arc neurons converge onto SFO neurons that alter their discharge rate during changes in plasma concentration of Na+ or ANG II. These results suggest that Arc may be involved in body fluid balance and circulatory regulation by modulating the activity of SFO neurons that function in the detection of blood-borne signals from the depletion of intra- and extra-cellular fluid volumes.

Angiotensin II↗
PubMed1992

Changes in Na concentration in cerebrospinal fluid during acute hypernatremia and their effect on drinking in juvenile rats.

To clarify if there are age-related differences in osmoreception, we measured changes in Na concentration in cerebrospinal fluid ([Na]csf) during and after acute hypernatremia in juvenile (JR) and adult rats (AR). The Na concentrations in plasma ([Na]pl) and [Na]csf were measured during intravenous infusion of 1 M NaCl solution (INF, 0.2 ml/100 g body wt. for 10 min) and for 20 min thereafter in anesthetized rats. To measure [Na]pl, a flow-through Na-sensitive electrode was placed in an extracorporeal shunt from a carotid artery to a jugular vein, and to measure [Na]csf, a Na-sensitive electrode was placed in the right lateral ventricle. There was a linear relationship between delta[Na]pl and delta[Na]csf during INF. The slope of delta[Na]pl vs. delta[Na]csf was 0.42 +/- 0.03 (n = 7) in JR, which was significantly higher (p less than 0.01) than in AR (0.23 +/- 0.04, n = 6). We also measured water intake during and after INF of the same amount of 1 M NaCl solution in conscious JR (n = 6) and AR (n = 6). The JR drank 1.93 +/- 0.22 ml/100 g body wt. of water within 30 min of the start of INF, which was significantly more (p less than 0.05) than AR drank (1.20 +/- 0.13 ml/100 g body wt.). These results indicate that the movement of Na or water, or both, between the blood and cerebrospinal fluid in acute hypernatremia is greater in JR, and that the osmoreceptors in JR are more sensitive than those in AR.

Animals↗
PubMed1980

Severe hypernatremia complicating urinary tract obstruction.

Severe hypernatremia and hyperosmolar dehydration developed in a patient with partial urinary tract obstruction. The urine was initially hypotonic, and there was no response to exogenous vasopressin. These abnormalities resolved with relief of the urinary tract obstruction and replacement of the water deficit. This case documents lower urinary tract obstruction as a cause of nephrogenic diabetes insipidus and severe hypernatremia and illustrates its reversible nature.

Dehydration↗
PubMed2006

[Controlled hypernatremia].

Hypernatremia exerts its main effect on the brain through the osmotic gradient it creates on either side of the blood brain barrier, which is impermeable to sodium. This generates a transfer of water from the intracellular to the vascular sector leading to temporary cell shrinkage. Osmoregulation permits cerebral cells to accumulate osmoactive molecules in order to restore their initial volume. It has been demonstrated in animals with brain injury that intracellular dehydration occurs essentially in the nonlesioned hemisphere. In most experimental studies, the reduction in cerebral volume obtained by hypertonic saline (HS) perfusion is accompanied by an intracranial pressure decrease, even under hemorrhagic shock conditions. Initially, clinical studies successfully used HS, as an alternative to mannitol, in the treatment of acute and refractory intracranial hypertension. Then continuous infusion of HS, with the objective of inducing hypernatremia, had produced encouraging effects on intracranial pressure control. However, these results were limited to non-randomized studies, without control groups and mainly in pediatric patients. Nevertheless, the use of HS on intracranial hypertension, refractory to conventional treatments, could be reasonable under strict monitoring of natremia as well as its adverse effects.

Animals↗