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At least 163 records · Page 9Linked to original sources
PubMedDate not supplied

Lateral pontine and extrapontine myelinolysis associated with hypernatremia and hyperglycemia.

Efforts to understand and prevent pontine and extrapontine myelinolysis have focused on the correction of hyponatremia, but controversy persists. We report a woman who presented in hyperosmolar diabetic coma with hypernatremia (169 mEq/l) and hyperglycemia (954 mg/dl). Plasma sodium rapidly increased to 188 mEq/l before gradually returning to normal. She remained obtunded and died 21 days later. Autopsy showed widespread, symmetrical demyelination involving the subcortical white matter, corpus callosum, anterior commissure, extreme, external, and internal capsules, fornix, thalamus, cerebellum, and lateral pons. The central pons and lateral geniculate nuclei were uninvolved. This case illustrates that lateral pontine and extrapontine myelinolysis can be associated with hypernatremia and hyperosmolality. In both hypo- and hypernatremic states, the significant event may be an increase in serum sodium or serum osmolality of sufficient rapidity and magnitude.

Blood Glucose↗
PubMedDate not supplied

[Neurogenic hypernatremia with adipsia and cerebral malformations in a child with ectrodactyly-ectodermal dysplasia-cleft lip-palate syndrome].

An infant with E.E.C. Syndrome (a genetic condition characterized by: Ectrodactyly, Ectodermal dysplasia, Cleft Lip-Palate) and delayed psychomotor development was found to have chronic hypernatremia and absence of thirst. Computerized brain tomography revealed abnormal lateral ventricles, agenesis of corpus callosum, calcified cortex. His plasma Anti Diuretic Hormone (ADH) levels were inappropriately low relative to his high values of plasma osmolality, whereas ADH responsiveness to nonosmotic stimuli was normal. E.E.C. Syndrome in this baby is characterized by: ectrodactyly of the feet, syndactyly of the 3rd and 4th finger of the hands, bilateral cleft lip and cleft palate, bilateral microtia, lacrimal ductular stenosis. To our knowledge, this is the first report of a case of chronic hypernatremia in conjunction with normal ADH stores, congenital abnormalities of brain structures, and E.E.C. syndrome.

Abnormalities, Multiple↗
PubMed1986

Congestive heart failure with hypernatremia.

A patient presented with hypernatremia (plasma sodium level equals 171 mEq/L), marked congestive heart failure, and fluid retention. A high-salt intake and an inappropriate lack of thirst in this patient with poor cardiac function resulted in hypernatremia accompanied by edema. Hypertonic salt intake may have been due, in part, to zinc deficiency.

Heart Failure↗
PubMedDate not supplied

[Edemas with hypernatremia. Mechanism and treatment (author's transl)].

The discrepancy between the finding of hypernatremia--a manifestation of extra-cellular fluid depletion--and the presence of edema--a manifestation of increased ECF--is best explained by the patient's inability to mobilize edemas to compensate intra-vascular dehydratation. Treatment must start by the administration of hypotonic solutions, as hypernatremia is dangerous for the brain.

Aged↗
PubMed1983

["Essential hypernatremia" as a result of on increased osmoreceptor threshold in a boy with Pierre-Robin disease and corpus callosum agenesis].

Hypernatremia was found as a cause of recurrent fever episodes in a 18 month old boy with Mb, Pierre-Robin and agenesia of the corpus callosum. We found values of serum-sodium until 160 mVal/l. Examinations of the osmotic regulation showed a so called "essential hypernatremia" without polyuria and polydipsi. Therefore must be responsible a defect of the osmotic center and thirst center in the hypothalamic area. As therapy a diet of 1000 ml = 1000 kcal = 100 mg Sodium/d. was successful.

Agenesis of Corpus Callosum↗
PubMed1981

Extreme hypernatremia as a presenting sign of child abuse and psychosocial dwarfism.

A 21-month-old girl presented with seizures and a serum sodium concentration of 206 meq/l. She had many of the features of psychosocial dwarfism, including short stature, bizarre eating and drinking habits, absent growth hormone response to arginine and insulin infusion and a rapid weight gain during her hospitalization. During the initial rehydration, the patient's weight gain was only 2 percent of her body weight. This finding probably indicates that her hypernatremia was chronic, did not represent acute dehydration and may well have derived from willful denial of water, although a chronic salt load could not be ruled out. This report further emphasizes that extreme hypernatremia may be the presenting feature of child abuse.

Adult↗
PubMed1995

Ependymoma of the neurohypophysis and hypernatremia in a horse.

A 2-year-old Standardbred gelding was examined because of prolapse of the third eyelid; myoclonus of the muscles of the head, neck, and forelimbs; and persistent tail swishing. The horse had a high plasma sodium concentration but was not drinking water. The hypernatremia could not be corrected by means of IV administration of fluids, and the horse became worse and, 6 days later, died. At necropsy, a tumor was found to be compressing the neurohypophysis and the area in the brain in which the thirst centers are believed to be located. It is believed that hypernatremia in this horse was a result of altered thirst.

Animals↗
PubMed1994

Hypodipsic hypernatremia in a dog with defective osmoregulation of antidiuretic hormone.

Hypernatremia was detected in a dog that was evaluated because of seizures. During hospitalization, the dog was fully conscious and remained hypernatremic when drinking voluntarily and when water was added to the food. Urine volume increased and urine osmolality decreased during an infusion of hypertonic saline (2.5% NaCl) solution, despite development of progressive hyperosmolality. There was no correlation between plasma antidiuretic hormone concentration and osmolality during the infusion study. The dog released antidiuretic hormone normally after nonosmotic stimulation (ie, apomorphine administration). These findings allowed a diagnosis of hypodipsic hypernatremia caused by destruction of hypothalamic osmoreceptors. At necropsy, there was hydrocephalus, atrophy of the septum pellucidum, and neuraxonal dystrophy of the cuneate nuclei. The underlying neurologic disease responsible for the CNS lesions could not be determined, but hydrocephalus may have led to pressure atrophy in the region of the hypothalamus that contains osmoreceptors.

Animals↗
PubMed1993

Effects of hypertonic and isotonic fluid infusion on the flash evoked potential in rats: hemorrhage, resuscitation, and hypernatremia.

In resuscitation from hemorrhagic shock, very small volumes of hypertonic saline (HS) improve blood pressure while reducing intracranial pressure and edema formation. The effects of hypertonic resuscitation fluids and hypernatremia on electrophysiologic brain function have not been studied. The present study was done in two parts. First we examined the effects of hemorrhagic shock and resuscitation with either 7.5% HS or lactated Ringer's (LR) solution on the flash evoked potential (FEP). Rats were bled to a mean arterial pressure (MAP) of 35 mm Hg for 1 hour, then resuscitated with HS (n = 10) or LR (n = 10) to a MAP of 80 mm Hg for another hour. Resuscitation required 3.8 +/- 0.5 mL/kg HS and 42.9 +/- 7.5 mL/kg LR (p < 0.05). During hemorrhage, FEP latencies increased and amplitudes decreased. During resuscitation, these variables returned toward baseline values. There were no significant differences between groups, although HS tended to restore the FEP better than LR. We next examined the effects on the FEP of hypernatremia and hyperosmolarity produced by two different hyperosmotic fluids. Over a 1-hour period, 16 mL/kg HS (n = 8), 16 mL/kg IsoSal (4.5% saline, 5.9% glucose, 6.4% mixed amino acids; n = 8), or 40 mL/kg LR (n = 8) was infused into normovolemic rats. Plasma sodium levels increased in both hyperosmotic groups (baseline = 145.2 +/- 0.7 mEq/L; after infusion, HS = 202.4 +/- 9.8 mEq/L, IsoSal = 163.3 +/- 4.2 mEq/L; p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Effects of plasma hypernatremia on nucleus tractus solitarius neurons.

Experiments were done in chloralose-anesthetized, paralyzed, and artificially ventilated rats to investigate the effect of plasma hypernatremia and baroreceptor activation on the excitability of nucleus tractus solitarius (NTS) neurons. Extracellular, single unit recordings were made from 67 histologically verified neurons in the region of NTS. The firing frequency of 29 (43%) NTS neurons was increased by the intracarotid infusion of hypertonic saline (0.5 M). The acute activation of baroreceptors after the intravenous infusion of phenylephrine resulted in the excitation of seven (31.8%) or the inhibition of five (22.7%) of the units responsive to plasma hypernatremia. Thirteen of the hypertonic saline-responsive neurons were recorded in animals in which the organum vasculosum lamina terminalis and subfornical organ were lesioned and/or the left vagus nerve was cut. These data suggest that within NTS there exists a pool of neurons that alter their discharge rate in response to changes in plasma sodium levels and that these neurons may also function in cardiovascular regulation.

Animals↗
PubMed1991

Adipsic hypernatremia in two sisters.

We describe two sisters with chronic hypernatremia, lack of thirst, and inappropriate osmoregulated vasopressin secretion. Only one sister, who presented with microcephaly and developmental delay, showed signs of dysplasia of the midline structures (ie, septum pellucidum and corpus callosum) and a large intracranial cyst. Neither sister showed any signs of thirst, even when osmolality exceeded 337 mmol/kg. In both patients, the vasopressin secretion did not respond to either osmotic or nonosmotic stimuli or was suppressed by a water load. Plasma osmolality values returned to normal after treatment with forced hydration and a vasopressin analogue, desamino-D-arginine vasopressin. These findings indicate a severe defect in the hypothalamic osmoreceptors that control thirst and vasopressin secretion. To our knowledge, this is the first report of such a disorder in two sisters.

Aldosterone↗
PubMed1977

Ectopic ACTH, prostatic oat cell carcinoma, and marked hypernatremia.

Locally recurrent, poorly differentiated carcinoma of the prostate was associated with hypokalemic alkalosis, marked hypernatremia, diabetes mellitus of recent onset, and hyperosmolar syndrome. These findings, with mild hypertension, in the absence of clinical features of Cushing's syndrome, suggested an ectopic ACTH syndrome. Plasma ACTH and cortisol levels were markedly elevated, and failed to suppress in response to either low or high-dose dexamethazone administration. The patient's condition deteriorated rapidly. Autopsy findings included carcinoma extensively infiltrating the prostate with extension to the urinary bladder, and metastases confined to the pelvic nodes and soft tissues. The adrenal glands weighed 23 g and showed diffuse hyperplasia. Extract of the prostatic tumor was analyzed for ACTH and showed approximately 40 times normal plasma levels (or about 4,010 pg/g of tissue); ultrastructural features showed secretory granules consistent with ACTH content of the tumor cells. Such cells were positive when stained for ACTH by peroxidase-tagged immunochemical methods. The case fulfills all established criteria for relating excess corticosteroid production and nonpituitary tumors.

Adrenocorticotropic Hormone↗
PubMed1975

Hypernatremia following gastrointestinal bleeding in cirrhosis with ascites.

3 patients with hepatic cirrhosis and ascites underwent increased diuresis on six occasions, closely related to episodes of gastrointestinal bleeding. In each instance the increased urine volume was preceded by a sharp increase in blood urea nitrogen, presumably due to absorption of nitrogenous compounds from the gastrointestinal tract, suggesting a mechanism of osmotic diuresis. In each case there was a signigicant increase in serum sodium and osmolality, related to the greater-water-than-sodium diuresis induced by urea, which was promptly reversed by the administration of water or isotonic solution. Clinically this syndrome may be defined as the association of hypernatremia and hyperosmolality due to osmotic diuresis from urea appearing in a cirrhotic patient with ascites and gastrointestinal bleeding.

Adult↗
PubMed1991

Excessive hypernatremia in a patient with renal amyloid disease.

A 24-year-old Italian male presented with a nephrotic syndrome in September 1984. In February 1985 renal biopsy showed amyloid disease with tubular atrophy and interstitial fibrosis. Edema was treated with furosemide, and cholchicine was started. Because he feared side effects of drug therapy, the patient stopped all medication by July 1985. Instead, he decided to restrict severely fluids in order to fight edema. In early November 1985 his family noted he was becoming increasingly lethargic. Two weeks later, on his admission to the hospital, he had a serum sodium concentration of 193 mmol/l and serum osmolality of 397 mosm/kg. Apart from mild mental status changes neurological examination was normal. The fluid deficit was slowly corrected. He was discharged three weeks later with normal serum electrolytes. This case demonstrates that (1) severe hypernatremia can present with mild neurological symptoms and (2) it can be survived provided that it develops slowly and is corrected cautiously.

Adult↗
PubMed1986

Arginine-vasopressin in essential hypernatremia.

Dynamics of AVP secretion in a 14-year-old girl with essential hypernatremia, psychomotor retardation and optic nerve coloboma, are reported. Basal levels of AVP were similar to those of a control population, but disproportionately low in relation with natremies. Hypertonic saline and hydric restriction did not alter the AVP basal values, which were, instead, stimulated with orthostatism. AVP decreased during a water surcharge, but delayed elimination of water was observed. The existence of a moderate volume deficit, not corrigible with a chronic surcharge of water, together with the reversed diurnal pattern of water excretion and the AVP data, suggest--as a physiopathological basis of the syndrome--a severe anomaly of the osmoreceptors, with alteration of thirst and of the osmodependent AVP responses, so that the AVP secretion was regulated exclusively through volumetric mechanisms.

Adolescent↗
PubMed1996

Effect of lesions of forebrain circumventricular organs on c-fos expression in the central nervous system to plasma hypernatremia.

Experiments were carried out on conscious adult male Wistar rats to investigate the effect of selective ablation of the subfornical organ (SFO), and/or the anteroventral third ventricular (AV3V) region on the induction of Fos in central structures in response to plasma hypernatremia. Fos induction, detected immunohistochemically, was used as a marker for neuronal activation. Intravenous infusions of hypertonic saline resulted in dense Fos-like immunoreactivity in several forebrain (paraventricular nucleus of the hypothalamus (PVH), supraoptic nucleus (SON), median preoptic nucleus (MnPO), medial preoptic nucleus, organum vasculosum of the laminae terminalis and (SFO) and brainstem (nucleus of the solitary tract, ventrolateral medulla, and parabrachial nucleus) structures. Intravenous infusions of the hypertonic saline solution into animals with lesions of either the SFO, the AV3V or both resulted in a decreased number of Fos-like immunoreactive neurons in the MnPO, PVH and SON. In addition, the number of Fos-labeled neurons in the SON after lesions of both the SFO and the AV3V was significantly greater than that observed in isotonic saline infused controls. Finally, lesions of the forebrain circumventricular structures did not alter the Fos labeling in brainstem structures as a result of the infusion of the hypertonic solution. These data suggest that changes in plasma osmolality and/or concentration of sodium alter the activity of SON and brainstem neurons in the absence of afferent inputs from the SFO and AV3V.

Animals↗
PubMedDate not supplied

Changes of auditory brainstem responses in electrolyte-induced myelinolysis in rats. Role of hyponatremia and hypernatremia.

Electrolyte-induced myelinolysis was produced in rats to evaluate electrophysiological derangement in the brainstem. Auditory brainstem responses (ABRs) were used to assess the brainstem function. Rats treated with hypertonic saline for 2 days had normal interpeak latencies in ABRs. Rats treated with vasopressin-induced hyponatremia alone and those with hypertonic saline after 3 days of hyponatremia had significantly prolonged interpeak latencies between waves II-III and III-IV in ABRs. These prolongations indicate electrophysiological derangement of the upper pons and mesencephalon in hyponatremic rats as well as in rats with hyponatremia followed by hypernatremic myelinolysis. In view of these data, hyponatremia may be a prerequisite for electrolyte-induced myelinolysis and electrolyte derangements such as hyponatremia, and rapidly correcting hypernatremia may be the cause of electrolyte-induced myelinolysis in rats.

Animals↗