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Described is a patient who presented with hypernatremia in the absence of dehydration. Further investigation revealed a tumor in the hypothalamic area, and evidence of anterior pituitary hypofunction. Water loading did not correct hypernatremia, and the results of the water-loading test suggested that hypernatremia had resulted from an elevated "osmotic set point" for the release of antidiuretic hormone, ie, "essential hypernatremia."
OBJECTIVE: The aim of this study was to determine what proportion of newborns admitted with idiopathic non-hemolytic hyperbilirubinemia exhibit severe weight loss and hypernatremia. METHODS: The prospective study involved 115 infants >48 h old who were admitted with jaundice between July 2002 and July 2003, and had unconjugated bilirubin levels >12 mg/dL. Premature babies (gestational age <37 weeks) and those with hemolytic jaundice and other pathologic causes of non-hemolytic jaundice were excluded. Postnatal age (days) at admission, bodyweight at admission, weight change since birth (percentage weight loss calculated at admission) and mode of feeding (breast-feeding, formula feeding, mixed feeding) were recorded. Severe weight loss was defined in babies who showed >10% weight loss or had not regained enough to reach birthweight by postnatal day 10. Serum Na levels and breast-milk Na levels were also measured. RESULTS: Twenty-eight (33%) of the 86 newborns with idiopathic hyperbilirubinemia in the study exhibited severe weight loss. Almost all the 86 babies were exclusively breast-fed, and 10 babies (12%) had severe weight loss combined with hypernatremia. The group with severe weight loss and hypernatremia had higher breast-milk Na levels than the other infants. CONCLUSION: The results indicate that a large proportion of babies with non-hemolytic jaundice have severe weight loss, and that breast-fed newborns with the combination of weight loss and hypernatremia may present with non-hemolytic jaundice.
We studied the fluid and electrolyte response of the brain and cerebrospinal fluid (CSF) in the lightly anesthetized newborn puppy exposed to acute (1-3 h) mild hyponatremia (12% decrease) and hypernatremia (7% increase). The changes in CSF osmolality, sodium, and chloride were equal to those in plasma. Blood acid-base values and CSF PCO2 remained normal, but in CSF there was a transient dilution acidosis in hyponatremia and contraction alkalosis in hypernatremia. In brain tissue, with hyponatremia, brain water increased in proportion to the osmotic stress (a change which was greater than that previously observed in adults) and the chloride space increased in the puppy (a change that was opposite to that observed in adults). There were no significant changes in dry tissue potassium, sodium, or chloride content. In hypernatremia, brain water decreased less than predicted by the osmotic change, the chloride space was unchanged, dry tissue potassium and chloride increased, and sodium was unchanged. In the newborn puppy, brain cell and extracellular volume regulation is not apparent with acute hyponatremia but is with hypernatremia.
We analyzed the disorder of water metabolism in a 32 year-old female with chronic hypernatremia. She had meningitis at 4 years, and ventriculo-peritoneal shunt operation at 13 years because of normal pressure hydrocephalus. At 14 years hypernatremia of 166 mmol/l was initially found and thereafter hypernatremia ranging from 150 to 166 mmol/l has been persisted for the last 18 years. Physical and laboratory findings did not show dehydration. Urine volume was 750-1700 ml per day and urinary osmolality (Uosm) 446-984 mmol/kg, suggesting no urinary concentrating defect. Plasma arginine vasopressin (AVP) levels ranged from 0.4 to 1.2 pmol/l despite hyperosmolality of 298 through 343 mmol/kg under ad libitum water drinking. There was no correlation between plasma osmolality (Posm) and plasma AVP levels, but Uosm had a positive correlation with Posm (r=0.545, P < 0.05). Hypertonic saline (500 NaCl) infusion after a water load increased Uosm from 377 to 679 mmol/kg, and plasma AVP from 0.2 to 1.3 pmol/l. There was a positive correlation between Posm and plasma AVP levels in the hypertonic saline test (r=0.612, P<0.05). In contrast, an acute water load (20 ml/kg BW) verified the presence of impaired water excretion, as the percent excretion of the water load was only 8.5% and the minimal Uosm was as high as 710 mmol/kg. Urinary excretion of aquaporin-2 remained low in concert with plasma AVP levels. No abnormality in pituitary-adrenocortical function was found. These results indicate that marked hypernatremia is derived from partial central diabetes insipidus and elevated threshold of thirst, and that enhanced renal water handling may contribute to maintenance of body water in the present subject.
A 26-year-old man with hypothalamic hypodipsia-hypernatremia syndrome is reported, who presented with adipsia, hypernatremia, and impaired osmolality-mediated arginine vassopressin (AVP) secretion. A chorionic gonadotropin-secreting tumor was detected in the anterior hypothalamus and treated with external irradiation. After the treatment, hypernatremia persisted and was not corrected by fluid loading, osmolality-mediated AVP secretion remained impaired. Despite the absence of signs of hydropenia, hypovolemia was suggested by low blood pressure and elevated plasma indices of the renin-angiotensin system, and supported by blood volume determination. The plasma aldosterone concentrations were inappropriately low for the renin-angiotensin status. The plasma atrial natriuretic polypeptide (ANP) level was normal in spite of hypovolemia and increased more than double after fluid loading. Hypernatremia, primarily caused by hypodipsia and impaired osmolality-mediated AVP secretion, secondarily sustained ANP secretion and suppressed aldosterone release, which conceivably contributed to the development and perpetuation of hypovolemia in this patient.
The causes, therapy for, and consequences of hypernatremia in elderly patients are not well understood. We found that in 15,187 consecutive hospital admissions, 162 (1.1%) patients who were at least 60 years of age had serum sodium levels that measured greater than 148 meq/L. Of that 162, 57% had become hypernatremic in the hospital; the remaining 43% were hypernatremic at hospitalization. The mean peak serum sodium level was 154 meq/L (range, 149 to 182), and mean water deficit, 9% of total body water (range, 6% to 30%). The most frequent primary causes were complications of surgery (21%), febrile illness (20%), infirmity (11%), and diabetes mellitus (11%), with more than 40 causal factors identified. Depression of sensorium correlated with severity of hypernatremia (p less than 0.001). The mortality rate (42%) was seven times that of age-matched hospitalized patients, but was not predicted by severity of hypernatremia. Mortality increased with increasing rates of fluid replacement (p less than 0.008). Hypernatremia in elderly patients is usually iatrogenic and often a marker for severe associated systemic illness.
We here report a 17-year-old high school boy having suprasellar germinoma who presented marked hypernatremia probably due to damages of both the osmoregulation and thirst centers. He was in good health until July, 1996, when he noticed slight general malaise and complained of dryness of the mouth, but without polyuria. He was found to have hypernatremia of mild degree (serum Na 151 mEq/l), but dropped out from the follow-up. In April, 1997, he was admitted to our hospital with complaints of general malaise and weakness of the upper and lower extremities. Serum Na was high at 202 mEq/l with a plasma osmolality of 390 mOsm/kg H2O. He completely lacked a sense of thirst and polydipsia/polyuria. Computed tomography and magnetic resonance imaging indicated a suprasellar tumor, possibly a germinoma. Hypernatremia was first treated with intravenous infusion of a half-normal saline solution, followed by immediate polyuria of 3 to 6 l/day. Subsequently, nasal administration of desamino-D-arginine vasopressin (DDAVP) induced stabilization of serum Na to a range between 140 and 160 mEq/l. The tumor disappeared following steroid pulse therapy and irradiation of 50 Gy to the brain. At the time of discharge, he and his family were instructed to record the urine volume, amount of water intake, body weight and amount of DDAVP used. The patient was instructed to drink water corresponding to the urine volume while maintaining the dose of DDAVP. One year after treatment, the water balance reverted to a positive direction, leading to a normal range of serum Na probably because of partial recovery of the osmoreceptors and/or trained drinking habit. This case illustrates the so-called adipsic hypernatremia which is attributed to partial osmoreceptor destruction by a suprasellar germinoma.
This is a case report involving a 9 year old girl with a teratoma that infaced mainly the bilateral hypothalamus. The girl was observed for 14 months after partial surgical removal. During that time she showed aphagia, adipsia, hypopituitarism, and visual and psychiatric disturbances. Severe hypernatremia also was present, even though large amounts of 5% glucose solution without salt were given I.V. Food and water were given by nasal gastric gavage and later gavage via gastric fistula, but the hypernatremia remained unchanged. When pitressin or spironolacton (anti-aldosterone) were administered, remarkable effect on the hypernatremia couldn't be found. Upon autopsy it was discovered that the bilateral hypothalamus, left subthalamus and ventral part of the thalamus were invaded by teratoma. Comparing many similar clinical reports and manifestations of hypothalamic lesions in experimental animals, it is reasonable to assume that the mechanisms of hypernatremia were caused by the disturbances of ADH secretion, thirst centre and osmoreceptor in the hypothalamus.
We studied 18 consecutive in-hospital patients with hypernatremia, as well as developed an animal model to simulate hypernatremic dehydration to determine the occurrence of rhabdomyolysis associated with hypernatremia. Mean serum creatine kinase (CPK) levels for the patient group at peak rhabdomyolysis were 3279 +/- 887 IU/L. There was a significant linear correlation between serum sodium and corrected sodium versus CPK (R = 0.585 and 0.713, respectively). In the animal study, mean serum sodium and CPK values were significantly different (p less than 0.0010 and p less than 0.010, respectively). Pre- and post-hypernatremia values of all other electrolytes measured were unchanged. We conclude that hypernatremia has a direct cause and effect relationship with rhabdomyolysis.
A case of a patient with the syndrome of chronic hypernatremia and hypodispia due to hypothalamic tumor was studied to evaluate the change of ADH response to plasma osmolality during the clinical course. A 23-year-old man was admitted for investigation of anorexia, hypodipsia and gait disturbance. Examination showed memory disturbance and generalized muscle weakness. Investigation showed marked hypernatremia (177 mEq/l) and hypopituitarism. Water loading test showed that ADH was not stimulated by hyperosmolality but continued to be secreted at a more or less constant level approximating normal basal state. CT scan revealed hypothalamic tumor. The tumor was suspected to be germinoma due to its radiosensitivity and high serum hCG level. After irradiation, the tumor lesion disappeared. ADH secretion came to be responsive to changes in osmolality but the response of the system was markedly reduced compared with the normal response, and hypodipsia and hypernatremia still remained. We conclude that the adipsia and complete destruction of the osmoreceptor in the patient caused marked hypernatremia and the destruction of ADH osmostat improved partially after irradiation. We believe it very useful for analyzing the disturbance of osmoregulatory system to evaluate the relationship of plasma ADH to plasma osmolality.
A short burst of intensive exercise (100-m swim lasting one minute and resulting in a 12-fold rise in the level of blood lactate) resulted in frank hypernatremia (serum sodium level, greater than 150 mEq/L) in 30% to 40% of well-trained athletes. In contrast, less intensive exercise (800-m swim lasting ten minutes and resulting in a sevenfold rise in the level of blood lactate) failed to cause a rise in serum sodium level despite comparable elevations in hematocrit reading and serum protein levels. Hypernatremia induced by intensive exercise cannot be explained by losses in body fluid or solute ingestion, but is probably a consequence of a shift of hypotonic fluid from the extracellular to the intracellular compartment. Thus, the mechanism of exercise-induced hypernatremia may be unique, as compared with other clinically recognized forms of hypernatremia.
The presence of hypernatremia in patients with hepatic failure has not received major attention. We examined the records of 25 patients admitted to the hospital with decompensated liver disease (usually Laënnec's cirrhosis) and found hypernatremia in 15. Probable causes include increased insensible water losses, impairment of water intake due to encephalopathy, and the use of osmotic cathartics with hypotonic enteric losses. Patients in this series showing hypernatremia had a mortality of 87%. Mortality in those without hypernatremia was 60%. The presence of increased serum sodium concentrations in patients with decompensated liver disease is an ominous but correctable abnormality reflecting a disturbance in water balance.
A 69-year-old woman was admitted because of severe dehydration due to anorexia. Consciousness disturbance was found to be due to severe abnormalities of serum electrolyte balance, but recovered quickly by correcting the hyperosmolality. While the initial serum sodium value of 186 mEq/L was corrected to 139 mEq/L in 5 days, locked-in syndrome, bilateral hand tremor and tetraparesis appeared. Brain magnetic resonance imaging (MRI) revealed symmetrically high signal intensity areas on T2-weighted images and low signal intensity areas on T1-weighted images in central part of pons and bilateral middle cerebellar peduncles. One and a half month later, these neurologic symptoms were improved and the MRI abnormalities also disappeared. Auditory brain stem responses which showed prolongations of III to V wave peak to peak latency at the onset returned to normal. It is noted in this case that central pontine myelinolysis (CPM) and extrapontine myelipolysis (EPM) appeared during the period of rapid correction of hypernatremia. Although it is known CPM and EPM are caused by hypernatremia or the rapid correction of hyponatremia, there has been reported only one case of CPM and EPM after rapid correction of hypernatremia. According to the hypothesis of Norenberg, rapid rise in serum sodium may cause CPM and EPM, but if CPM and EPM are caused by the rapid correction of hypernatremia in this case, CPM and EPM may be caused by another pathogenesis of the disorder.
Hypernatremia, a common finding among the elderly, is believed to be due to water deficit. In the present study, in 12 consecutive hospitalized elderly patients (mean age 82.2 years) with moderate to severe hypernatremia (mean serum sodium 166.9 mEq/l), inappropriately low plasma levels of vasopressin were found in relation to serum osmolality (mean 1.8 pg/ml and 343 mosmol/l, respectively). All patients but 1 were hospitalized with acute febrile disease and all but 2 had underlying neurological disease. Hypernatremia persisted for at least 3 days despite the patients' rehydration. It seems, therefore, that temporary hypernatremia in elderly patients with acute febrile disease, especially in the presence of underlying neurological disorder, reflects an inadequate vasopressin response to the hyperosmolar state.
Central diabetes insipidus (DI) is a rare but recognized complication of myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML) that is caused by leukemic infiltration to the hypothalamo-neurohypophyseal system. In rare patients in whom a wide region of the hypothalamus is involved, central DI results in hypodipsic hypernatremia and dehydration. Typical DI symptoms such as polydipsia, polyuria, and marked thirst are concealed in these cases, because the hypothalamic "thirst center" cannot send thirst stimuli to the cerebral cortex. Herein we describe a patient with MDS developing into AML, who presented with hypodipsic hypernatremia and dehydration. A diagnosis of central DI was made on the ground of a low level of serum anti-diuretic hormone (ADH) despite high serum osmolality. A magnetic resonance imaging study revealed attenuation of a physiological "bright spot" of the neurohypophysis. An induction course chemotherapy including regular-dose cytarabine and daunorubicin produced a rapid improvement of hypernatremia. The bone marrow aspirate after two courses of chemotherapy showed complete remission. At that point, ADH release and the "bright spot" were recovered. In order to correctly diagnose central DI in association with hematological malignancies, we should not overlook this atypical type of DI.
1. Graded hypovolemia was induced by hemorrhagic blood loss and graded hypernatremia by salt load in the toad, Bufo marinus, and the bullfrog, Rana catesbeiana. Maximal blood flow rates in the systemic arches and arterial and venous pressures were measured during activity after each stress. 2. Maximal blood flow rates in the B. marinus did not decline until blood loss exceeded 5% of initial body mass. In R. catesbeiana, losses of 2% initial body mass caused a decline (Fig. 1). 3. Maximal heart rates did not change with hemorrhage (Fig. 2). The decline in blood flow rates with hemorrhage was due to declining pulse volumes in both species (Fig. 3). 4. Arteriovenous pressure difference declined with hemorrhage in both species (Fig. 4). Peripheral resistance increased with hemorrhage in parallel with compromised blood flow rates (Fig. 5). 5. Plasma sodium concentration slightly increased with hemorrhage, while plasma protein concentration and hematocrit declined. Lymphatic compensation for hemorrhagic loss is indicated in both species (Fig. 6). 6. Induced hypernatremia compromised blood flow rates in both species at plasma sodium concentrations above 175 mM. The decline in flow rates was principally a result of a decrease in pulse volume, though maximal heart rates also declined (Figs. 2, 3, 7). 7. Induced hypernatremia had no effect on the arteriovenous pressure difference in B. marinus but caused it to decline in R. catesbeiana. Peripheral resistance increased in only B. marinus but not R. catesbeiana (Figs. 4, 5). Hematocrit did not change with salt load, indicative of a constant vascular volume.
Rats drinking taurine and hypertonic saline (T + S) develop severe hypernatremia, but rats drinking either T or S alone do not. One hypothesis for this disruption of homeostasis is that the T + S combination interferes with the actions of antidiuretic hormone (ADH). Rats drinking T + S developed severe hypernatremia (170 mmol/L) by day 8 when infused with distilled water by osmotic minipumps, but maintained plasma sodium below 150 mmol/L when infused with ADH. Cumulative water balance in T + S drinkers receiving ADH was consistently higher than in those not receiving ADH. However the ratio of cumulative sodium balance to cumulative water balance suggests little uniform advantage to rats receiving ADH nor does comparison of urine osmolality in the two groups. Precisely how ADH administration reduces hypernatremia in T + S drinking rats remains unclear, but the hypothesis that T + S interferes with the action of ADH in its regulation of extracellular fluid volume and osmolality remains viable.
Adipsic hypernatremia, a rare disorder, usually secondary to a hypothalamic lesion, is caused by the combination of partial central diabetes insipidus with hypo- or adipsia. We studied a patient who presented with a global hypothalamic dysfunction including adipsic hypernatremia. An extensive work-up disclosed the presence of pseudotumor cerebri and an empty sella turcica. Although endocrine abnormalities including true diabetes insipidus have been reported in conjunction with pseudotumor cerebri or an empty sella, no patient described presented such a global hypothalamic dysfunction or adipsic hypernatremia. The increased intracranial pressure is postulated to be the responsible mechanism for both the empty sella and the hypothalamic dysfunction.