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PubMed2006

Chronic hypernatremia increases the expression of vasopressin and voltage-gated Na channels in the rat choroid plexus.

The choroid plexus (CP) epithelium is one of the extrahypothalamic sources of arginine vasopressin (AVP). However, it is unclear whether the regulation of choroidal AVP synthesis in response to pathophysiological stimuli, such as hyperosmotic stress, is similar to that observed in the hypothalamus. In the present study, rats chronically implanted with cisterna magna cannulas, enabling the collection of cerebrospinal fluid (CSF) in freely moving animals, were subjected to salt loading. CSF osmolality increased from the baseline normonatremic levels ranging between 292 +/- 0.5 and 295 +/- 2 to 309 +/- 4 mosm/kg H(2)O at 2 days of hypernatremia. This elevated CSF osmolality was maintained at a relatively stable level until the end of a 10-day observation period. Changes in choroidal and hypothalamic AVP expression in response to hyperosmotic stress were assessed by semiquantitative reverse-transcriptase polymerase chain reaction. An increase in hypothalamic AVP expression was accompanied by augmented AVP synthesis in the CP. Compared to normonatremia, choroidal levels of AVP mRNA increased 5- and 10-fold at 2 and 5 days of salt loading, respectively. Salt loading also resulted in increased hypothalamic expression of the alpha-II, beta(1), and beta(2) subunits of voltage-gated Na(+) channels. Similarly, the choroidal mRNA levels for the alpha-II and beta(1) subunits increased approximately 2-fold after 5 days of salt loading; however, no changes in the beta(2) subunit expression were found in the CPs of hypernatremic rats. These experiments support the hypothesis that the regulation of choroidal AVP synthesis is similar to that observed in the hypothalamus. It is also suggested that the increased expression of voltage-gated Na(+) channels found in the hypothalamus and CP after salt loading may play a role in the adaptation of AVP-producing cells to chronic hypernatremia.

Animals↗
PubMed1993

Treatment of acute hypernatremia with hemodialysis.

The prognosis of severe hypernatremia in the adult is dismal, and new approaches are needed to improve this situation. Here we describe 3 cases of patients with severe hypernatremia (sodium levels of 178, 172, 182 mEq/l) associated with cardiopulmonary or hepatorenal complications that were treated successfully with acute hypotonic hemodialysis (dialysate sodium 110 mEq/l). We provide information of our investigational protocol since the past literature has dealt mostly with peritoneal dialysis. Our preliminary experience has yielded adequate results without significant side effects, but additional studies are needed to refine this technique that might be life-saving in selective situations.

Acute Disease↗
PubMed1996

Cerebral infarction in two cynomolgus macaques (Macaca fascicularis) with hypernatremia.

Hypernatremia resulting in neurologic symptoms ranging from lethargy to coma, and with underlying lesions of cerebral hemorrhage and thrombosis, has been reported in human beings. Herein we report two cases of cerebral infarction with venous thrombosis in cynomolgus monkeys. Both animals were severely hypernatremic because of water deprivation, with serum sodium levels of 185 and 193 meq/liter, respectively. At necropsy, there were bilateral multiple hemorrhagic and malacic areas visible on the surface of the cerebrum and extending into the parenchyma, primarily involving the occipital lobes. These lesions were interpreted microscopically as infarcts because, in addition to hemorrhage and necrosis, multiple thrombi were present in small and medium-sized veins of gray matter and meninges. The pathogenesis of hypernatremia-induced cerebral lesions is believed to involve cellular dehydration that caused shrinkage of the brain. Because the vasculature of the brain is tightly adherent to the skull, this shrinkage results in tearing of blood vessels, with consequent hemorrhage and thrombosis.

Animals↗
PubMed1999

Extrapontine myelinolysis with involvement of the hippocampus in three children with severe hypernatremia.

Central pontine myelinolysis is a disorder of unknown etiology linked to overly aggressive correction of hyponatremia. In addition to the typical location of demyelination with preservation of neurons and axon cylinders in the basis pontis, similar lesions have been described in extrapontine locations. Central pontine myelinolysis and extrapontine myelinolysis usually occur together, and are identified at autopsy rather than in life because symptoms of extrapontine myelinolysis are often masked in the critically ill patient. Central pontine myelinolysis is described in children, usually in the clinical setting of hyponatremic dehydration. Extrapontine myelinolysis has not been described in children previously. We report three children with severe hypernatremia and extrapontine myelinolysis involving various combinations of thalamus, basal ganglia, external and extreme capsules, and cerebellar vermis. All three had additional involvement of the hippocampus seen on T2-weighted magnetic resonance imaging. None of the three had detectable pontine lesions. Clinical features of the three cases were dehydration in a 28-month-old girl, respiratory syncytial virus bronchiolitis in a 14-month-old girl, and acute respiratory failure due to anaphylaxis after consumption of walnuts in a 3-year-old boy. Peak sodium values in each child were 195, 168, and 177 mmol/L, respectively; each received aggressive treatment for hypernatremia. We believe this to be the first report of extrapontine myelinolysis in children, the first report of extrapontine myelinolysis without central pontine myelinolysis in children, and the first report in children of hippocampal formation involvement. The pathogenesis of the central and extrapontine myelinolysis complex in children is more complicated than previously believed, and might differ significantly from that of adults.

Child, Preschool↗
PubMed1984

Lactulose-induced hypernatremia.

We describe severe hypernatremia in a patient with hepatic encephalopathy, who was treated with lactulose. Lactulose produces hypernatremia via its osmotic effect and its degradation to organic acids. We recommend that patients who receive large quantities of lactulose and who lack access to free water have their electrolytes monitored and the dose tapered as quickly as possible.

Aged↗
PubMed1976

Hypernatremia and chorea. A report of two cases.

The appearance of transient, generalized chorea in conjunction with brief, symmetrical myoclonic movements is described in two adult patients with hypernatremia secondary to dehydration. The association of hypernatremia and chorea is rare, even in massive salt poisoning, and has not been described previously in adults. Since both patients recovered, no pathologic material was obtained; but a speculative commentary on the possible underlying pathophysiology is included.

Chorea↗
PubMedDate not supplied

Adipsic hypernatremia syndrome in infancy.

We report on an infant with chronic hypernatremia due to a congenital defect in osmo-regulation of thirst and the secretion of arginine vasopressin (AVP). A 12 month-old female infant who presented with irritability and signs of dehydration was found to have hypertonic dehydration; plasma osmolality was 430 mOsm/kg B.W. Despite rehydration she remained hypernatremic (serum Na+ 152-158 mEq/l). Lack of signs of thirst led us to the diagnosis of chronic hypernatremia due to adipsia. Laboratory investigation showed: 1. plasma AVP levels were low for plasma osmolality; 2. urine osmolality was normal for plasma AVP, and 3, there was a significant correlation of plasma to urine osmolality (r = 0.72, p < 0.02); however, the slope was markedly reduced indicating partial destruction of the AVP osmoreceptors.

Arginine Vasopressin↗
PubMed2005

Breastfeeding-associated hypernatremia: are we missing the diagnosis?

OBJECTIVES: To assess the incidence and complications of breastfeeding-associated hypernatremic dehydration among hospitalized neonates. STUDY DESIGN: A retrospective study was conducted at Children's Hospital of Pittsburgh over a 5-year period, to identify otherwise healthy term and near-term (> or =35 weeks of gestation) breastfed neonates (<29 days of age) who were admitted with serum sodium concentrations of > or =150 mEq/L and no explanation for hypernatremia other than inadequate milk intake. RESULTS: The incidence of breastfeeding-associated hypernatremic dehydration among 3718 consecutive term and near-term hospitalized neonates was 1.9%, occurring for 70 infants. These infants were born primarily to primiparous women (87%) who were discharged within 48 hours after birth (90%). The most common presenting symptom was jaundice (81%). Sixty-three percent of infants underwent sepsis evaluations with lumbar puncture. No infants had bacteremia or meningitis. Infants had hypernatremia of moderate severity (median: 153 mEq/L; range: 150-177 mEq/L), with a mean weight loss of 13.7%. Nonmetabolic complications occurred for 17% of infants, with the most common being apnea and/or bradycardia. There were no deaths. CONCLUSION: Hypernatremic dehydration requiring hospitalization is common among breastfed neonates. Increased efforts are required to establish successful breastfeeding.

Apnea↗
PubMed2003

Lobar holoprosencephaly in a Miniature Schnauzer with hypodipsic hypernatremia.

A 9-month-old male Miniature Schnauzer was examined because of a lifelong history of behavioral abnormalities, including hypodipsia. Diagnostic evaluation revealed marked hypernatremia and a single forebrain ventricle. The behavioral abnormalities did not resolve with correction of the hypernatremia, and the dog was euthanatized. At necropsy, midline forebrain structures were absent or reduced in size, and normally paired forebrain structures were incompletely separated. Findings were diagnostic for holoprosencephaly, a potentially genetic disorder and the likely cause of the hypodipsia. Similar evaluation of affected Miniature Schnauzer dogs may reveal whether holoprosencephaly routinely underlies the thirst deficiency that may be seen in dogs of this breed.

Animals↗
PubMedDate not supplied

Fatal hypernatremia in a dog from salt ingestion.

An eight-year-old, neutered male Airedale terrier was presented for the evaluation of a 45-minute episode of continuous seizure activity after ingesting a salt-flour mixture used as clay for the sculpting of small figurines. Levels of serum sodium (211 mEq/L; reference range, 145 to 158 mEq/L) and chloride (180 mEq/L; reference range, 105 to 122 mEq/L) were elevated. The dog died despite aggressive therapy directed at the hypernatremia. Tissue levels of sodium and chloride were elevated. Brain sodium level (108 mEq/L; reference range, has less than 80 mEq/L) was diagnostic for salt toxicosis. All necropsy findings, except severe hepatocellular necrosis, were consistent with reports of salt poisoning in humans and other species. Hypernatremia from ingestion of salt has not been described previously in the dog.

Administration, Oral↗
PubMed1999

Treatment of hypernatremia in an acidotic neonatal calf.

A 7-day-old Jersey calf was evaluated because of diarrhea and pneumonia. The calf was hypernatremic, hypoproteinemic, and acidemic, and was treated initially with i.v. administration of fluids with sodium concentration (175 mEq/L) similar to the calf's serum sodium concentration. Sodium concentration of the administered fluids was gradually decreased over the following days, but the calf's serum sodium concentration decreased too rapidly, and the calf developed neurologic signs attributed to cerebral edema. Treatment with mannitol and i.v. administration of fluids with a higher concentration of sodium resulted in abatement of clinical signs. In calves, hypernatremia may develop over several days. Prescribing traditional isotonic or hypotonic fluids in such cases will be harmful, because during chronic hypernatremia, the brain's adaptive mechanisms involve accumulation of organic osmoles that may take several days to equilibrate across cell membranes, and cerebral edema may result. Administration of fluids containing sodium concentration approximately equal to the patient's measured serum sodium concentration is required to decrease serum sodium concentration more slowly than is possible with traditional isotonic fluids.

Acidosis↗
PubMed2000

Unusual combination: polydipsia with hypernatremia in a schizophrenic patient.

OBJECTIVE: The authors describe a patient with an unusual combination of polydipsia and isolated hypernatremia without any other changes of electrolytes. The patient had two attacks of hypernatremia which were successfully treated with clozapine. Some speculations about possible mechanisms of this unusual combination are discussed.

Drinking↗
PubMedDate not supplied

Hypodipsia-hypernatremia syndrome associated with holoprosencephaly in a child: a case report.

We report a child with diabetes insipidus and hypodipsia associated with holoprosencephaly. A two-year-old girl with the history of several admittances to hospital during and after the newborn period with hypernatremic dehydration, acute renal failure and convulsions is presented. The patient had hypodipsia, hypernatremia, microcephaly, failure to thrive, and unilateral cleft lip and palate. Magnetic resonance imaging revealed lobar type holoprosencephaly. Increased plasma osmolality and decreased urinary osmolality were detected. Her urine ADH level was 10 ng/day. Plasma osmolality levels returned to normal after hydration and administration of a vasopressin analogue. These findings suggest that in children with hypernatremia-hypodipsia syndrome, the possibility of cerebral malformations should always be kept in mind.

Child, Preschool↗
PubMed2002

[Hypernatremia in newborns].

Two cases of severe hypernatremia in healthy newborns are described. They were term infants with normal birthweight and breastfed at the discharge from the maternity ward. The infants had not been weighed from the time of birth until the day of admission to hospital at an age of seven and nine days. At the admission, the weight loss was 18% and 22% and the sodium concentrations were 160 and 164 mmol/l. After rehydration mainly orally they were discharged bottle-fed after five and eight days, respectively. None of the mothers were able to breast-feed their infants at the time of admission. To prevent breast-feeding malnutrition and hypernatremia it is recommended that all newborns are seen and weighed by a professional during the second half of their first week of life.

Breast Feeding↗
PubMed2003

[Iatrogenic hypernatremia during hydatid cyst operation].

Hypernatremia due to salt gain is generally iatrogenic. This case report presents a 55 year-old woman who was operated because of hepatic hydatid cyst. At the end of the operation, following extubation the patient was unconscious and serum sodium concentration was found to be 185 mEq/ L. The patient was entubated again and transferred to the intensive care unit. When the patient awaked and became conscious at 36th hour in intensive care unit, she was extubated and transferred to ward with serum sodium concentration of 142 mEq/L. The serum sodium concentration should be monitored carefully in hydatid cyst operation, during which hypertonic saline is used for scelosidal effects as general anesthesia can mask neurologic signs due to hypernatremia.

Adult↗
PubMed2006

Hyponatremia, hypernatremia: a physiological approach.

Natremia belongs to the toolbox of the practicing intensivist. It is an indicator of the hydration status, which is an item that must be continuously monitored in critically ill patients. Hyponatremia is not rare (1% to 2% of hospitalised patients), and hypernatremia is about 10 times less frequent while hypernatremia always indicates hypertonicity, hyponatremia is not equivalent to hypotonicity. Diagnosis depends on the history, clinical examination and basic biochemical data. It should be kept in mind that obtaining urine samples is as important as plasma samples in this respect. The first step consists in confirming that hyponatremia is hypotonic. The second step is to assess the renal response to hypotonicity. Hypotonic hyponatremia will be considered in association with hypovolemia, euvolemia or hypervolemia. The constitution of a hyperosmolar state requires an inadequate water intake The main goal of the treatment is not to normalize numbers (they must always be checked first), but to treat symptoms. Tolerance must always be appreciated. The mathematical formulas proposed are of interest for a better understanding, but should not be followed strictly.

Humans↗
PubMed1989

Disorders of water metabolism: hyponatremia and hypernatremia.

Patients with disorders of sodium and water metabolism are seen frequently in Emergency Departments, but in most cases these disorders do not require treatment. Severe hypo- and hypernatremia are relatively uncommon but can result in severe neurologic sequelae or death. Appropriate therapy, based on an understanding of the physiology involved, can reduce the morbidity and mortality associated with these disorders. A systematic approach to the assessment and management of patients with hypo- and hypernatremia is presented.

Humans↗