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PubMed2000

Hypernatremia in neonatal elk calves: 30 cases (1988-1998).

OBJECTIVE: To characterize hypernatremia in neonatal elk calves, including clinical signs, incidence, physical examination findings, and possible causes. DESIGN: Retrospective case series. ANIMALS: 26 neonatal elk calves were examined; 4 calves were evaluated twice, for a total of 30 examinations. PROCEDURE: Medical records were reviewed for signalment, history, physical examination findings, results of diagnostic tests, and response to treatment. Hypernatremia was defined as serum sodium concentration > 153 mEq/L. RESULTS: Hypernatremia was diagnosed in 14 calves and was significantly associated with diarrhea, high WBC count, high anion gap, and high serum concentrations of albumin, chloride, creatinine, and urea. Hypernatremia was not significantly associated with survival, but high serum albumin concentration and rectal temperature were significantly associated with survival of calves. Animals given antibiotics and electrolyte solutions orally prior to evaluation were significantly more likely to die than those untreated. Dehydration was a common reason for evaluation but was not significantly associated with survival. CONCLUSIONS AND CLINICAL RELEVANCE: Hypernatremia was significantly associated with diarrhea. Treatment of diarrheic elk calves is often the same as that used in bovine calves with diarrhea; however, bovine calves are commonly hypo- or normonatremic. Our experience suggests that treatment protocols used in bovine calves are unsatisfactory for elk calves. The rate at which serum sodium concentration is reduced should be < 1.7 mEq Na/L/h to avoid development of neurologic signs associated with iatrogenically induced cerebral edema.

Animals↗
PubMed1999

Hypernatremia and subdural hematoma in the pediatric age group: is there a causal relationship?

Several researchers in the 1950's proposed that hypernatremia causes water to leave brain cells, shrinking the brain, thus tearing the bridging veins and resulting in subdural hematomas. Although the old literature suggests mechanisms linking the two in a cause and effect relationship, there is controversy as to whether hypernatremia leads to subdural bleeding or whether the reverse is true. This issue is important for forensic pathologists who must distinguish natural disease from trauma. An etiologic link between hypernatremia and subdural hematomas was suggested recently, and was proposed originally before Kempe's 1962 paper "The Battered Child Syndrome" which widely disseminated the concepts of child physical abuse, and of subdural bleeding resulting from non-accidental injury. Our study is a multifaceted investigation of infants which includes: a literature review, retrospective chart reviews of both living and deceased hypernatremic infants, a retrospective review of infants hospitalized with subdural hematoma, and a prospective collection of head injured, hypernatremic children. We conclude that hypernatremia, if present in association with subdural hemorrhage, is most likely secondary to intracranial pathology, and that hypernatremia often develops in critically ill infants suffering from a variety of medical conditions.

Child Abuse↗
PubMed2000

[Hypernatremia in the aged: clinical characteristics].

OBJECTIVE: Hypernatremia in young adults is a rare condition, sometimes occurring after gastrointestinal diseases, osmotic diuresis or diabetes insipidus. The clinical characteristics and prognosis of hypernatremia in geriatric patients would be different. Each case must be examined separately. PATIENTS AND METHODS: We conducted a prospective uncontrolled study among patients over 70 with sodium levels equal to or greater than 150 mmol/l (at admission or during the hospitalization). RESULTS: Hypernatremia was found in 77 patients. Mean age was 84.1 +/- 6.7 years. The mean peak serum sodium level was 157.3 +/- 7.4 mmol (two-thirds ranged from 150 to 160). Hypernatremia onset was produced by a wide range of symptoms: 48% had a febrile illness, 470% were on diuretics, 15% had had a stroke, but only 9% were suffering from diarrhea or vomiting. Most of the patients had disabling chronic illnesses (62% loss of two or more ADL of Katz), severe dementia (84% level = 6 on the Reisberg global deterioration scale). In spite of fluid replacement and follow-up treatment, outcome was poor: 62% of the patients died within three months. CONCLUSION: Besides digestive and renal losses, hypernatremia in elderly patients is increased by fluid supply disorders consecutive to hypodipsia contracted at the same time as disability and dementia. Hypodipsia is a sign of poor prognosis. Prevention must be undertaken early, emphasizing the importance of identifying dehydration early among elderly people with chronic disabling illnesses.

Adult↗
PubMed2000

[Fatal hypernatremia due to accidental administration of table salt].

Hypernatremia is a common electrolyte abnormality, but it is rarely attributable to excess sodium. Hypernatremia due to exogenous salt intake, caused either by accidental ingestion or as a form of child abuse, is rare, difficult to manage and results in high mortality. Although hypernatremia is easily recognized by laboratory tests, its etiology is often difficult to determine. A surprisingly small amount of salt intake can result in a fatal outcome. We report two cases of severe salt intoxication in two girls, aged 20 and 7 months, who presented with severe hypernatremia. Both had seizures after accidental salt ingestion. In the first case, salt instead of sugar was inadvertently added to two yoghurts, leading to hypernatremia and convulsions. In the second case, a mistake in the preparation of salt-saturated water as an oral rehydration solution provoked seizures, coagulopathy and longitudinal venous sinus thrombosis. Both cases developed encephalic death. We discuss the clinical course and the difficulties in the treatment of these cases in the context of the available literature.

Accidents↗
PubMed2002

Hypernatremia in the elderly.

Hypernatremia is defined as a plasma sodium concentration greater than 145meq/liter. This is primarily due to water loss in adults although increased salt ingestion may be a cause for it. When plasma sodium concentration rises above 145meq/liter, thirst is stimulated, this results in ingestion of water. Hypothalamic osmoreceptors cause synthesis and release of an antidiuretic hormone. Normal renal response causes reabsorption that prevents further loss of water. These normal physiological responses help bring plasma sodium back to normal. Persistent hypernatremia, therefore, implies an inability to sense thirst or lack of access to water, since ingestion of water will prevent development of significant hypernatremia even in the absence of antidiuretic hormone release or lack of renal response to its effect. Elderly persons have decreased thirst, and therefore, ingest less amounts of water than their younger counterparts. Hospitalized elderly patients and frail nursing home residents are at an increased risk for the development of hypernatremia because they rely on others for their water needs. Therefore, adequate water must be prescribed and given to these individuals. In this article, we review the risk factors, pathophysiology, causes, prevention, and management of hypernatremia in the elderly.

Aged↗
PubMed2004

[Exploration of the pathogenesis and the management of hypernatremia in burn patients].

OBJECTIVE: To explore the pathogenesis and the management of hypernatremia in burn patients. METHODS: Twenty eight burn patients with hypernatremia were enrolled in the study and were divided into infection and non-infection groups. The pathogenesis, clinical features, biochemical indices in blood, the therapeutic results and the prognosis were compared between the two groups. RESULTS: In non-infection group, the hypernatremia was mainly induced by improper fluid resuscitation and occurred on the 3.1 postburn day (PBD), while that in the infected group, on 7.2 PBD. The patients in non-infected group exhibited much more excited and the blood levels of glucose and urea nitrogen (BUN) were obviously decreased when compared with those in the infected group (P < 0.01). The survival rate in non-infected and infected group were 94.12% and 9.09%, respectively. CONCLUSION: The mortality rate of the patients with hypernatremia could be lowered by means of taking optimal measures according to the different patterns of hypernatremia.

Adult↗
PubMed1995

Increased incidence of severe breastfeeding malnutrition and hypernatremia in a metropolitan area.

OBJECTIVE: To identify common characteristics among infants with breastfeeding malnutrition in a region with an increasing incidence of breastfeeding malnutrition. DESIGN: Retrospective case series. SETTING: A 361-bed regional tertiary care children's hospital in a 1.7 million population metropolitan area. PATIENTS CASE SERIES: five infants with severe breastfeeding malnutrition and hypernatremia admitted to a tertiary care children's hospital over a 5-month period. Retrospective case review: 166 infants admitted between 1990 and 1994 with the diagnosis of dehydration, hypernatremia, or malnutrition. MAIN OUTCOME MEASURES: Maternal characteristics, age at presentation, percent loss from birth weight, serum sodium, average age at birth hospital discharge, neurologic, or cardiovascular complications. RESULTS: Five infants were admitted to a children's hospital over a 5-month period with severe breastfeeding malnutrition and hypernatremia. The average weight loss at time of readmission was 23% (+/- 8%) from birth weight. The average presenting sodium was 186 +/- 19 mmol/L. Three suffered significant complications. From 1990 through 1994, there was a statistically significant (P < .05) annual increase in the number of infants admitted with breastfeeding malnutrition and hypernatremia. CONCLUSIONS: While breastfeeding malnutrition and hypernatremia is not a new problem, this cluster of infants represents an increase in frequency and severity of the problem and could be a consequence of several factors, including inadequate parent education about breastfeeding problems and inadequate strategies for infant follow-up.

Adult↗
PubMed1993

[Hypernatremia and kidney function].

Hypernatremia is caused by a water deficit. Cases with hypernatremia and dehydration appear to cluster among children and the elderly with alterations in the level of consciousness thus with no independent access to water. In general, central nervous symptoms prevail. However, thorough examination reveals impaired renal function in many such cases. Animal experiments have shown that rapid increases of the sodium concentration in the renal artery will cause a reduction of renal blood flow (RBF), glomerular filtration rate (GFR) and inhibition of renin secretion, particularly during states of sodium chloride or volume depletion (i.e. with high plasma renin activity). In any other organ hypernatremia leads to vasodilation. The kidney, however, responds with vasoconstriction which can be reversed by the adenosine antagonist theophylline. This finding led to the hypothesis that adenosine mediates the renal response to hypernatremia. Adenosine is generated by the tubules at a higher rate when the kidney is forced to reabsorb large amounts of sodium. In this concept adenosine links metabolic processes of sodium reabsorption with the regulation of organ blood flow causing vasoconstriction via adenosine receptors on the vasa afferentia. This mechanism can explain impaired renal function during acute hypernatremia. It is concluded from experimental evidence that-apart from other therapeutic measures-the recovery of impaired renal function can be improved by administration of the adenosine antagonist theophylline.

Acute Kidney Injury↗
PubMed1972

Hypernatremia from intravascular saline infusion during therapeutic abortion.

In response to a question on how to avoid the rare, inadvertent intravascular or ip injection of hypertonic saline solution during therapeutic abortion, 3 consultants replied. According to Reid and Frigoletto, to avoid intravascular or ip infusion, place a small indwelling polyethylene catheter in the amniotic sac rather than a metal needle. This virtually precludes the possibility of inadvertent iv injection. When and if necessary, correct catheter placement may be confirmed by the use of fluoroscopy and amniography prior to the injection of hypertonic saline solution. The chemical imbalances associated with this accident are those encountered in severe hypernatremia with resultant brain edema and hemorrhagic softening. Bizarre paresthesia, pyrexia, altered consciousness, and, eventually, convulsions preceded the fatal cases. Peritoneal dialysis may be life saving in the event of ip injection. Naturiuretics, appropriate parenteral fluid administration, and possibly exchange transfusion might be indicated for intravascular accidents. In Goodlin's hospital there have been no cases of acute hypernatremia in the last 500 therapeutic abortions done with hypertonic saline solution. This is believed to be related to 2 changes in technique: 1) not losing the amniotic space by removing only as much amniotic fluid as can easily be obtained and 2) using a simple gravity infusion technique for the instillation of the hypertonic saline solution. During infusion it is essential that the patient be alert, for the first symptoms of intravascular injection are a slight pain, burning, or a feeling of warmth in the pelvis. If these minor symptoms are ignored and the procedure is continued, a sensation of flushing occurs throughout the body with tingling in the scalp and ringing in the ears followed finally by seizures, apnea, or coma or both. Late symptoms are those of hemolytic anemia and renal failure. From experience, serum sodium levels during these events are as high as 185 mEq/1. Along with occurrence of acute hypernatremia the contents of the amniotic cavity are sometimes extruded extraovularly through the fallopian tube into the peritoneal cavity when labor begins. Cases with serum sodium levels of 170 mEq/1 some 6-7 hours after saline instillation were observed, but by contrast these patients' only symptoms were extreme thirst and peritoneal discomfort (Lancet 1: 305, 1968). The treatment of hypernatremia is to force fluids either by mouth or iv. Since most commercial 5% dextrose in water solutions are actually 4.5% (regulations permit a 10% error), such hypotonic fluids are useful for treating hypernatremia.

Abortion, Induced↗
PubMed1999

Hypernatremia with edema.

Hypernatremia is usually associated with water depletion. Seven very ill patients developed hypernatremia in association with marked edema during therapy in the hospital. All patients had hypoalbuminemia and azotemia. At the time of hypernatremia, urine output averaged 1880 mL/24 h and urine sodium concentration averaged 59 mmol/L, suggesting that low levels of antidiuretic hormone and/or a diminished effect of this hormone on the nephron may contribute to the pathophysiological mechanism of the hypernatremia. Recognition of this salt- and water-overloaded state should guide therapy.

Aged↗
PubMed2001

Acute peritoneal dialysis as both cause and treatment of hypernatremia in an infant.

This report describes a 4-month-old infant with multisystem organ failure who developed severe hypernatremia (sodium 168 mEq/l) due to rapid free water removal associated with acute peritoneal dialysis instituted for fluid overload. The current report describes the pathophysiology of the hypernatremia, and its correction by low-sodium hypertonic peritoneal dialysis without compromising ultrafiltration or supplementing with free water. Although peritoneal dialysis can cause hypernatremia, a modified solute concentration in the dialysate can treat the hypernatremia successfully.

Female↗
PubMed1986

Selective osmoreceptor dysfunction presenting as intermittent hypernatremia following surgery for a pituitary chromophobe adenoma.

Intermittent hypernatremia following hypothalamic surgery or trauma is usually attributed to the triphasic dysfunction of vasopressin release (diabetes insipidus, inappropriate vasopressin release, and diabetes insipidus). A 39-year-old patient had hypodipsia and intermittent hypernatremia following hypothalamic surgery for a chromophobe adenoma. Mean arterial pressure fell by 25 percent during orthostasis testing and was associated with an increase in vasopressin levels from 1.3 microU/ml to 12 microU/ml. Plasma renin activity and aldosterone increased from 1.1 to 16 ng/ml per hour and from 6.7 to 39 ng/dl, respectively, and remained elevated for three and a half hours after tilt testing. Hypertonic saline infusion, on the other hand, increased serum osmolality from 290 to 304 mOsm/kg but did not result in a significant rise in vasopressin levels (all were less than 1 microU/ml). These results are consistent with a selective dysfunction of the osmoreceptor pathways of vasopressin release and intact volume receptor-mediated pathways. Patients with intermittent hypernatremia following hypothalamic surgery or trauma should be questioned specifically regarding thirst. If it is impaired or absent, these patients should be watched carefully, not only for the development of triphasic dysfunction of vasopressin release, but also for a selective osmoreceptor dysfunction associated with thirst deficits as found in patients with "essential hypernatremia."

Adult↗
PubMed1995

Cerebral cell volume regulation during hypernatremia in developing rats.

Cell volume regulation is a vital biological function in all species. Maintenance of cerebral cell size in the face of osmotic stress is especially important because the brain is contained in the non-complaint skull. The developmental aspects of this adaptive process are not known. Therefore, we evaluated cerebral cell volume regulation during hypernatremia in pre-weaning and adult rats. Hypernatremia was induced by injections of 1 M NaCl for 48 h. Brain water, electrolyte, and organic osmolyte contents were measured in hypernatremia and sham injected littermate control rats at the following ages: 12, 18 and 20 days and adults. In normonatremic rats, there was a steady decline in brain water content during development that was paralleled by a gradual fall in the cerebral levels of Na+, K+, and all organic osmolytes. The change in brain water content correlated most closely with the decrease in cerebral taurine content. In the face of equivalent elevations in serum Na+ concentration, there was comparable brain cell shrinkage and similar increases in total cerebral electrolyte and organic osmolyte content in rats at all 4 ages studied. Taurine was the predominant organic osmolyte prior to weaning, constituting 16-49% of the increment in nonperturbing solute content in hypernatremic animals between 12-20 days of age; in contrast, taurine contributed only 10% to the cerebral organic osmolyte pool in adult rats. We conclude that the capacity of brain cells to accumulate inorganic electrolytes and organic osmolytes during adaptation to hypernatremia is adequately expressed in developing rats, aged 12 days or older. Moreover, we speculate that the immature animal behaves as if it has an elevated 'set point' to protect the higher brain water content that is present earlier in development.

Age Factors↗
PubMed2003

Age and gender as risk factors for hyponatremia and hypernatremia.

BACKGROUND: This study assesses gender and age as independent risk factors for hypo- and hypernatremia and describes the prevalence of hypo- and hypernatremia in different population groups. METHODS: Details of all serum Na results with accompanying patient demographics for 2 years were downloaded from the laboratory database into Microsoft Access for multiple logistic regression analysis using SPSS. Female gender and age <30 years were the reference groups. RESULTS: Data from 303577 samples on 120137 patients were available for analysis. Prevalence at initial presentation to a health care provider of Na<136, <116, >145, and >165 mmol/l were for acute hospital care patients: 28.2%, 0.49%, 1.43%, and 0.06%; ambulatory hospital care: 21%, 0.17%, 0.53%, and 0.01%; community care: 7.2%, 0.03%, 0.72%, and <0.01%. Age odds ratios rose with increasing age to 1.89 and 8.70 (Na<136 and <116 mmol/l) and 7.09 and 24.39 (Na>145 and >165 mmol/l, respectively) for age >81 years. Male gender was a mild risk factor for Na<136 mmol/l and was otherwise unimportant. CONCLUSIONS: Hyponatremia is a common but generally mild condition while hypernatremia is uncommon. Increasing age is a strong independent risk factor for both hypo- and hypernatremia. Gender is not an important risk factor for disturbances of serum Na concentration.

Adult↗
PubMed1990

Hypernatremia.

Hypernatremia results when the water content of body fluids is deficient compared with sodium content. Hypernatremia can be the result of pure sodium excess but is usually associated with dehydration, secondary to excess losses of water or hypotonic fluids. Hypernatremic dehydration is less common than hyponatremic or isonatremic dehydration, but is associated with the highest morbidity and mortality rate, primarily related to CNS dysfunction. Except when hypernatremia has developed rapidly, the serum sodium concentration should be corrected slowly with frequent monitoring of serum electrolytes. Even then CNS damage can result, either as a consequence of the hypernatremia itself or of rapid lowering of the serum sodium concentration.

Child↗
PubMed1993

Reversible vasopressin deficiency in severe hypernatremia.

Studies to assess the relationship between plasma arginine vasopressin concentration (Pavp) and plasma osmolality (Posm) were performed on an elderly patient with dementia who developed severe hypernatremia due to inadequate water intake following a debilitating hip fracture. Serum sodium concentrations were 174 and 196 mEq/L on two consecutive hospital admissions. During the second of these admissions, sequential measurements of Pavp and Posm were obtained as hypernatremia was gradually corrected. Pavp during this period was correlated with Posm (r = 0.887, P < 0.01), but was low despite the presence of hyperosmolality and volume depletion. Pavp decreased from 0.56 microU/mL to 0.18 microU/mL as Posm decreased from 396 to 338 mOsm/kg H2O. The regression line of this relationship intercepted the abscissa at 320 mOsm/kg H2O. Hypertonic sodium chloride infusion to reassess this relationship 2 days following the correction of hypernatremia increased Pavp only to 0.67 microU/mL while increasing Posm from 297 to 316 mOsm/kg H2O. Nevertheless, Pavp and Posm were significantly correlated (r = 0.937, P < 0.001). The slope of the regression line was 0.031, and Posm at the abscissal intercept was 292 mOsm/kg H2O. A similar increase in Posm from 290 to 310 mOsm/kg H2O during hypertonic sodium chloride infusion 11 days following the correction of hypernatremia increased Pavp to 1.95 microU/mL (r = 0.786, P < 0.05). The magnitude of the increase in Pavp at this time was equivalent to that previously observed in studies of normal subjects. The slope (0.048) and abscissal intercept (280 mOsm/kg H2O) of linear regression were also consistent with observations in studies of normal subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1999

Transient thalamic changes on MRI in a child with hypernatremia.

Severe hypernatremia has been associated with a wide variety of central nervous system lesions. Neurologic sequelae are the usual outcome in those cases in which a lesion has been documented neuroradiologically. The authors report a 7-month-old male with severe hypernatremia who developed obtundation after correction of the electrolyte imbalance. Magnetic resonance imaging revealed bilateral thalamic signal changes that resolved on follow-up study, in accordance with complete clinical recovery. To the authors' knowledge, bilateral thalamic signal changes are previously unreported findings associated with hypernatremia. Pertinent literature and the clinical course of the authors' patient are the basis for questioning currently recommended guidelines for the rate of correction of hypernatremia.

Brain Edema↗
PubMedDate not supplied

[Functional disorder of the hypothalamic osmoreceptor as the cause of excessive hypernatremia in a girl with absence epilepsy].

BACKGROUND: Chronic hypernatremia is a rare disorder in childhood and normally results from impairment of the water homeostasis. In some cases, chronic hypernatremia is caused by decreased intake of water based on impaired thirst perception. CASE REPORT: We report a girl with microcephaly, partial agenesis of the corpus callosum, mild midface hypoplasia and absence seizures, who presented with severe hypernatremia (serum sodium concentration 189 mmol/l). Though serum osmolality was increased up to 382 mOsm/kg, the girl showed no signs of thirst. After normalization by intravenous fluid therapy, serum osmolality and serum sodium concentration remained in the normal range with an oral water intake of at least 1500 ml/d. Polyuria was never present, the ability to concentrate urine was preserved. CONCLUSIONS: In summary, we speculate that the chronic hypernatremia in our patient is caused by a selective hypothalamic osmoreceptor dysfunction associated with mild dysplasia of the midline structures. Only very few similar cases have been documented in the literature.

Agenesis of Corpus Callosum↗