The study involved 47 patients with hypernatremia who have clinical symptoms and the blood sodium level more than 150 mmol/l between January 1998 and June 2001. Results: hypernatremia is observed at the Intensive Care Unit with rate of 2.7%. It is more likely to occur in 1-year children. It can be required during hospitalization and developed in the patients who are using manitol, bicarbonate sodium and diuretics. The central nervous symptoms include seizures, increase in muscular tone, unconsciousness, coma, fever and dehydration. 31.9% of patients high and very high blood sodium level. The treatment has low effect on patients who have blood sodium level more than 170 mmol/l. The average time to normalize sodium level is 1.8 days with amount of solution during 4 to 6 hours to correct Na+ level is 19.8 ml/kg/h. During subsequent hours, amount of solution is different depending on body fluid disorder of patient.
Hypernatremia ; Sodium

Hypernatremia developing in nonhospitalized adults is predominantly a disease of the elderly and mentally handicapped patients, possibly revealing inadequate nursing care of these patients. It has long been claimed that the duration of hypernatremia and its rate of correction are correlated with improvement in patients' neurologic status. Since there are only a handful of cases with serum sodium levels greater than 200 mEq/L until recently, it is not clear at what rate plasma sodium concentration can be safely normalized in severe hypernatremic patients. We report a case of severe hypernatremia with survival. This patient underwent rapid correction of serum sodium concentration during the management of this metabolic derangement using isotonic solution.
Journal Article ; Female ; Human ; Hypernatremia/therapy* ; Hypernatremia/physiopathology ; Hypernatremia/blood ; Middle Age ; Sodium/blood* ; Treatment Outcome

PURPOSE: To evaluate the long-term safety of polyethylene glycol (PEG) 4000 in children with constipation, particularly the biochemical aspects of safety. METHODS: Medical records were evaluated, and 100 children, who had been taking PEG 4000 for more than 6 months, and who had been under clinical and biochemical monitoring, were enrolled. Ages; 6.11+/-3.12 years, Duration of therapy; 16.93+/-7.02 months, dose of PEG 4000; 0.72+/-0.21 g/kg/d. RESULTS: None of the children complained of clinical adverse effect. The first biochemical test was performed at 8.05 months after beginning of PEG 4000. Serum phosphate (SP) value was high in 10 children, and leucopenia was noted in one child. The second test was performed in 44 children at 7.57 months after the first test. The SP value was high in four children, including the three children whose initial SP value was high and one new child. Six out of 10 children with high initial SP value became normal and one was lost. Hypernatremia was noted in one child. The third test was done in 15 children at 7.5 months after the second test. The SP value of the new child from the second test was high, but became normal after finishing treatment. Two out of 3 children with high SP value at the second test became normal and one was lost. The fourth test was done in 2 children few months after the third test. All of the results were normal. There were no relation between duration of therapy and hyperphosphatemia, or between dose of PEG 4000 and hyperphosphatemia. CONCLUSIONS: PEG 4000 is safe for long-term therapy in children with constipation with respect to biochemical parameters.
Child ; Constipation ; Humans ; Hypernatremia ; Hyperphosphatemia ; Medical Records ; Polyethylene Glycols

Breast Feeding ; Female ; Humans ; Hypernatremia ; etiology ; therapy ; Infant, Newborn ; Male

Hypematremia is a rare but important medical condition and is associated with mortality rate of 40 to 70%. However, little has been known about its prognostic factors or treatment guidlines. To evaluate the prognostic factors and the outcome following treatment, we reviewed 22 available medical records among twenty five hypernatremic patients (0.2%) in 12841 admissions at medical ward from January to December 1995. We defined hypernatremia as serum sodium concentration more than or equal to 150 mEq/L. Of these patients, two had hypematrernia at admission and the remaining patients became hypernatremic during admission. Mean peak serum sodium concentration was 158 (150-178) mEq/L and mean total body water deficit was 11.4 (6.7-21.3)%. Factors correlated with the development of hypernatremia were diverse and multiple, and the most frequent factor was diminished access to water. Mortality rate was 59%, but mortality was not correlated with age, correction rate of hyper-natremia, primary route of fluid loss, and the severity of hypernatremia or total body water deficit. Mortality rate was higher in patients whose serum sodium concentrations were below 130 mEq/L at admission (P<0.05). In our study, development of hypernatremia from initial hyponatremic state was significantly associated with poor outcome, and age, rapidity of correction, route of fluid loss, and the severity of hypernatremia or total body water deficit were not.
Body Water ; Humans ; Hypernatremia* ; Medical Records ; Mortality ; Sodium ; Water

Adipsic hypernatremia cause chronic hyperosmolality and hypernatremia through a combination of impaired thirst and osmotically stimulated antidiuretic hormone secretion. This syndrome can be grouped together as disorders of osmoreceptor dysfunction due to the various degrees of osmoreceptor destruction related with different types of intracranial lesions around the anterior hypothalamus, consistent with the location of primary osmoreceptor cells. Adipsic hypernatremia, associated with developmental disorder of corpus callosum, is very rare. Most cases are diagnosed at infancy and early childhood; the replacement of desmopressin is necessary. Herein, we report adipsic hypernatremia associated with anomalous corpus callosum in adult with mental retardation; they were treated with only free water without desmopressin.
Adult ; Corpus Callosum ; Deamino Arginine Vasopressin ; Humans ; Hypernatremia ; Hypothalamus, Anterior ; Intellectual Disability ; Thirst ; Water

Adipsic hypernatremia is a rare disorder of hypothalamic osmoreceptor dysfunction for thirst. It is frequently associated with a deficiency in antidiuretic hormone (ADH) release. We report the first case in Korea of adipsic hypernatremia combined with subnormal ADH response to osmotic stimuli without any demonstrable structural lesion. A 69-year-old woman was admitted to the hospital with general weakness. In a hypernatremic hyperosmolar state, she denied thirst and did not drink spontaneously. Her plasma ADH level was markedly subnormal but she had no large volume of dilute urine. Investigation of osmoregulation by infusion of hypertonic saline revealed adipsia and an absolute deficiency in antidiuretic hormone release, despite a serum osmolarity in excess of 321 mOsmol/kg. There was no structural lesion of the hypothalamus and no abnormal finding in hypothalamic-pituitary function. After diagnosis, she was treated successfully with intentional water intake alone.
Aged ; Female ; Humans ; Hypernatremia ; Hypothalamus ; Korea ; Osmolar Concentration ; Plasma ; Thirst ; Water-Electrolyte Balance

Sodium is the major cation of the extracellular fluid and the primary determinant of extracellular osmolality. Therefore, hypernatremia causes water movement out of cells, while hyponatremia causes water movement into cells, resulting in cellular shrinkage and cellular swelling, respectively. Serious central nervous system symptoms may complicate both conditions. Since hypernatremia and hyponatremia are accompanied by abnormalities in water balance, it is essential to understand the mechanisms regulating extracellular osmolality and volume as well as the pathophysiology of hypernatremia and hyponatremia, in order to manage both conditions with swiftness and safety.
Central Nervous System ; Extracellular Fluid ; Hypernatremia* ; Hyponatremia* ; Osmolar Concentration ; Sodium ; Water Movements

Anatomical lesions of hypothalamic area associated with hypodipsic hypernatremia have been reported only rarely. We report here a case of hypodipsic hypernatremia induced by a hypothalamic lesion. A 25-yr-old man, who had been treated with radiation for hypothalamic tumor 5-yr before, was admitted for evaluation of hypernatremia and hypokalemia. He never felt thirst despite the elevated plasma osmolality and usually refused to drink intentionally. Plasma arginine vasopressin (AVP) level was normal despite the severe hypernatremic hyperosmolar state and urine was not properly concentrated, while AVP secretion was rapidly induced by water deprivation and urine osmolality also progressively increased to the near maximum concentration range. All of these findings were consistent with an isolated defect in osmoregulation of thirst, which was considered as the cause of chronic hypernatremia in the patient without an absolute deficiency in AVP secretion. Hypokalemia could be induced by activation of the renin-angiotensin-aldosterone system as a result of volume depletion. However, inappropriately low values of plasma aldosterone levels despite high plasma renin activity could not induce symptomatic hypokalemia and metabolic alkalosis. The relatively low serum aldosterone levels compared with high plasma renin activity might result from hypernatremia. Hypernatremia and hypokalemia were gradually corrected by intentional water intake only.
Adult ; Argipressin/*secretion ; Case Report ; Human ; Hypernatremia/*etiology ; Hypothalamic Neoplasms/*metabolism ; Male ; Osmolar Concentration ; *Thirst

Diabetes insipidus caused by impaired production or reduced responses to vasopressin, can occasionally be seen postoperatively in neurosurgical patients, but rarely occurs during anesthesia and surgery. An 8-year old female patient with suprasellar germinoma was scheduled for tumor resection. Anesthesia was induced smoothly and maintained mainly with sevoflurane. Several hours after anesthesia and surgery, urine output was increased with increased serum sodium concentration, indicating the occurrence of diabetes insipidus. To prevent sodium increase and replace fluid loss, 2.5% dextrose half saline was used. Though sodium concentration did not increase further, the concomitant increase of glucose complicated anesthetic management. After the completion of anesthesia and surgery, serum sodium increased further but then gradually returned to normal with conservative management. The patient was discharged without any complications.
Anesthesia ; Brain ; Child ; Diabetes Insipidus ; Female ; Germinoma ; Glucose ; Humans ; Hypernatremia ; Methyl Ethers ; Sodium ; Vasopressins