Correction Of Hypernatremia Research Articles

Cell volume regulation and transport mechanisms across the blood-brain barrier: implications for the management of hypernatraemic states.

Onset and correction of hypernatraemia constitute major hypertonic stresses for mammalian cells. Cells respond by activating specific osmoregulatory mechanisms allowing to preserve their volume and to adapt to their new environmental conditions. These processes have major implications in the management of hypernatraemia. In particular, cells chronically exposed to hypertonic conditions progressively accumulate organic osmolytes to maintain optimal intracellular electrolyte concentrations. During treatment of hypernatraemia, elevated intracellular organic osmotic content exposes cells to cellular oedema if sodium concentrations are rapidly corrected. In addition, circulating ions equilibrate slowly across the blood-brain barrier during acute changes in plasma osmolality. This can generate major brain water shifts and severe cerebral lesions related to brain shrinking or cerebral oedema. The basic mechanisms involved in brain ion and water transport are reviewed. A proper understanding of these processes is essential to develop appropriate treatment strategies in managing children with hypernatraemia.

The changing pattern of hypernatremia in hospitalized children.

Past studies have revealed that hypernatremia occurs primarily in infants with diarrheal dehydration. With improved infant feeding practices and the advent of pediatric critical care medicine, the pattern of hypernatremia in children has likely changed. The purpose of this study was to evaluate the current pattern of hypernatremia in hospitalized children. Medical records were reviewed for 68 patients admitted to a large urban children's hospital during a 3-year period, all with a serum sodium greater than 150 mEq/L. The etiologies, predisposing factors, and morbidity and mortality associated with hypernatremia were evaluated. The average patient age was 3.9 years (range, 1 day to 19. 7 years), and the peak serum sodium concentration was 159 mEq/L (range, 151-184 mEq/L). Hypernatremia was hospital acquired in 60% of children. The majority of children (71%) were admitted for reasons other than hypernatremia. In 76% of the patients, inadequate fluid intake was the main cause of hypernatremia. Gastroenteritis contributed to the hypernatremia in only 20% (14 out of 68) of children. Eleven of these were infants <1 year of age with hypernatremia on admission. Eighty-eight percent of patients (60 out of 68) suffered from neurologic impairment, critical illness, chronic disease, or prematurity before developing hypernatremia. The overall mortality was 16%. Patients in whom hypernatremia was not corrected had a significantly higher mortality than those in whom hypernatremia was corrected (4 out of 8 [50%] vs 7 out of 60 [12%]). Peak serum sodium was no different for survivors than nonsurvivors. No deaths were attributable to cerebral edema caused by correction of hypernatremia. Neurologic complications related to hypernatremia occurred in 15% of patients. Hypernatremia occurs in children of all ages, with the vast majority having significant underlying medical problems. Hypernatremia caused by gastroenteritis in infants has become much less common than previously reported. Hypernatremia is primarily a hospital-acquired disease, produced by the failure to administer sufficient free water to patients unable to care for themselves. Failure to correct hypernatremia may result in a high mortality rate.

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.

Hypernatremic myopathy

We describe a 21-year-old man presenting with proximal muscle weakness associated with hypernatremia. His manifestations other than muscle weakness included dry skin, loss of axillary and public hair, decreased libido and loss of thirst sensation. His serum sodium level was elevated to 169–171 mEq./1 but all other electrolytes were normal. In addition, serum CK was elevated and an EMG study showed myogenic changes. Endocrinological studies revealed hypothalamic hypopituitarism, while MRI revealed a surprasellar mass. A partial correction of hypernatremia led to an immediate recovery of the muscle weakness as well as a normalization of both the serum CK level and EMG findings, suggesting a direct association between the muscle weakness and hypernatremia. The phosphocreatine/inorganic phosphorus ( sol PCr P i ) ratios in the resting calf muscle, obtained using 31P magnetic resonance spectroscopy (MRS), were very low during the state of muscle weakness, while they returned to nearly normal values after clinical improvement, suggesting that the muscle weakness in hypernatremic state was caused by a depletion of the intramuscular energy stores, probably due to an overworking Na-K pump to correct the intracellular electrolyte imbalance.

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)

Fatal Hypernatremia From Exogenous Salt Intake: Report of a Case and Review of the Literature

Hypernatremia is a common electrolyte disturbance, most often caused by volume depletion. Hypernatremia due to sodium excess occurs less frequently, and fatal hypernatremia solely from ingestion of table salt is rare. We describe a 41-year-old man who had seizures and hypernatremia after ingestion of a supersaturated salt water solution intended for gargling. He had consumed approximately a third cup of table salt (approximately 70 to 90 g of salt or 1,200 to 1,500 meq of sodium). His initial serum sodium concentration was 209 meq/liter. Hypotonic fluid therapy was given to provide free water and to correct the hypernatremia gradually. Our patient, however, failed to recover from the initial insult and died 3 days later. Review of the literature revealed 10 adult and 20 pediatric cases of hypernatremia attributable to exogenous intake of salt. The type of therapy (fluid or peritoneal dialysis), the type of fluid used, and the rate of correction of hypernatremia did not influence survival. The age of the patient and the initial serum sodium concentration were the most important prognostic indicators. Both very young patients and those with lesser degrees of hypernatremia had a better rate of survival than did other patients. In addition, our review illustrates the surprisingly small amount of salt that can cause severe hypernatremia and the danger of using salt or saline as an emetic.

Correction of hypernatraemia with continuous arteriovenous haemodiafiltration

Continuous arteriovenous haemodiafiltration was used successfully to achieve controlled correction of hypernatraemia in the presence of renal failure, when peritoneal dialysis was contraindicated, in a 4 year old girl.

Hypernatremia

Hypernatremia is a potentially life-threatening electrolyte abnormality. This problem develops most often because of loss of water from the animal, but in rare cases hypernatremia results from gain of sodium chloride. Important conditions predisposing to hypernatremia include diarrhea, vomiting, heat stroke, fever, limited access to water, excessive diuretic use, renal diseases, and pituitary diabetes insipidus. This condition rarely develops if animals have adequate access to water. Clinical signs relate to central nervous system derangements and can progress to seizures and coma. Diagnosis is based on the serum sodium concentration; treatment should be instituted if it is greater than 170 mEq per L. Treatment is based on knowledge of the volume status of the patient and the probable cause for the hypernatremia. In general, 5 per cent dextrose in water or other hypotonic fluids are given slowly intravenously. The rate of administration should be adjusted so the water deficit is replaced over 48 to 72 h. Too rapid correction of hypernatremia can lead to cerebral edema and worsening of the animal. In cases of salt intoxication, diuretics must be given in addition to slow water replacement to avoid the development of pulmonary edema.

"Essential" Hypernatremia

Three patients had "essential" hypernatremia due to hypothalamic lesions and their clinical features were compared with those of previously described cases. Key findings were (1) chronic but fluctuating elevation of serum sodium level that was not corrected by fluid administration, (2) evidence of normal extracellular fluid volume, (3) intact antidiuretic hormone (ADH) synthesis and renal tubular response to ADH, (4) impaired osmotic regulation of ADH secretion, and (5) correction of hypernatremia with exogenous vasopressin. Clinical and experimental observations suggest that the anatomic lesion leading to sustained hyperosmolality in this disorder is injury to osmoreceptors with relative sparing of neural elements synthesizing ADH. Loss of sensitive osmotic control of ADH secretion and preservation of less sensitive volume modulation may explain both the wide fluctuations in serum sodium levels and the inability to correct hyperosmolality with fluid loading.