SEARCH · PubMed Health

Results for “Hypernatremia”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 37 records · Page 2Linked to original sources

PubMed1998

Hypernatremia and hypertonic syndromes.

Hypernatremia is the most common cause of hypertonicity in small animal medicine. Despite this fact, severe hypernatremia is an uncommon clinical entity in dogs and cats. The causes of hypernatremia are excessive water loss and increased sodium intake. Clinical signs are most often related to CNS dysfunction. Severe hypernatremia should be considered a life-threatening situation and treated as such. Initial fluid therapy should be given with care according to the rate of onset of hypernatremia, as deterioration of the animal's condition is a common sequela. The determination of the cause of hypernatremia and the treatment can be both challenging and rewarding. The other notable hypertonic syndrome in small animal medicine is hyperosmolar nonketotic diabetes mellitus. Judicious management of this disease with fluid therapy and insulin is the standard therapy. An understanding of the pathophysiology is essential to their diagnosis and appropriate medical management.

Animals↗

PubMed1999

Adipsic hypernatremia in two patients with AIDS and cytomegalovirus encephalitis.

In patients with acquired immune deficiency syndrome (AIDS), hypoosmolality is frequently observed, whereas hypernatremia is distinctly rare. We report two patients with advanced AIDS and cytomegalovirus (CMV) encephalitis, who developed severe hypernatremia without any thirst sensation, that is, adipsic hypernatremia. Both developed severe hypernatremia of up to 164 and 162 mmol/L, with serum osmolalities of 358 and 344 mOsmol/kg while remaining alert and denying thirst. Serum antidiuretic hormone (ADH) levels were 0.9 and 1.5 pg/mL, inappropriately low for the concomitant serum osmolalities. Vital signs were stable. During hypernatremia, urine osmolalities were 327 and 340 mOsmol/kg, and urine Na+ levels were 56 and 119 mmol/L, respectively. Periventricular white matter lesions were seen on cerebral nuclear magnetic resonance imaging (NMRI) in case 1, but the pituitary appeared normal in both cases. Survival after onset of hypernatremia was 6 and 4 weeks, respectively. Autopsy in case 1 showed typical findings of CMV encephalitis but normal pituitary, confirming that infection with HIV or CMV most likely caused the dysfunction of the central osmostat.

AIDS-Related Opportunistic Infections↗

PubMed2000

Heparin-free hemodialysis in the treatment of hypernatremia in severely burned patients.

BACKGROUND: Hypernatremia in severely burned patients is associated with high morbidity and mortality rates. As the causes of hypernatremia in major burn patients are still not clear, hemodialysis is the method of choice for the treatment. While hemodialysis is effective for the control of hypernatremia, it can cause bleeding complications that may be fatal for burn patients with extensive wounds and potential gastro-intestinal mucosal damage. CLINICAL DATA: In the present study heparin-free hemodialysis in which the heparin is firmly absorbed to the haemofiltration membrane, hemophan, dispensed with systemic use of heparin. In two extensively burned patients with burn area of 100% TBSA and 98% TBSA respectively and hypernatremia with serum sodium concentration as high as 169 and 158 mmol/l respectively, heparin-free hemodialysis was performed five times and three times each. RESULTS: Hypernatremia was satisfactorily corrected with no interference to the coagulation system in the two patients as indicated by clinical observation and biochemical analysis. The patient with burn area of 98% TBSA survived and the patient with burn area of 100% TBSA died of wound coverage failure 6 weeks after injury because of non-availability of autograft. CONCLUSION: Heparin-free hemodialysis is an effective and safe method in the treatment of hypernatremia in extensively burned patients.

Adult↗

PubMed1999

[Holoprosencephaly with neurogenic hypernatremia].

BACKGROUND: Semi-lobar holoprosencephalies can be seldom complicated by neurogenic hypernatremia, which must be distinguished from other causes of hypernatremia. CASE REPORT: In two admitted children with semi-lobar holoprosencephaly, 7 months and 4 years old, biological data revealed chronic hypernatremia and hyperosmolarity without clinical signs of dehydration, which were finally attributed to a neurogenic hypernatremia. CONCLUSION: Neurogenic hypernatremia must be clearly differentiated from other causes of hypernatremia since it never causes specific complications.

Child, Preschool↗

PubMed2003

[Severe hypernatremia: survival without neurologic sequelae].

Hypernatremia is an electrolyte disturbance most frequently caused by excess water loss and less frequently by increased sodium intake. The few reported cases of severe hypernatremia (> 190 mEq/l) had an adverse outcome with high mortality and/or severe neurologic sequelae. The first case was a 7-year-old girl with renal failure undergoing continuous venovenous hemodiafiltration therapy who presented hypernatremia (216 mEq/l) after incorrect preparation of dialysis fluid. The patient was treated with hemodiafiltration and hypernatremia was resolved in 48 hours. She had a convulsive crisis without subsequent neurologic impairment. The second patient, a 3-year-old girl with pseudohypoaldosteronism type I and encephalopathy, had hypernatremia (203 mEq/l) due to erroneous sodium administration, which was corrected in 36 hours with intravenous fluid therapy. Her neurologic status was unchanged by treatment. We conclude that children with extreme hypernatremia survive without neurologic sequelae if treatment achieves a progressive decrease of natremia.

Child↗

PubMed2002

The effect of hypernatremia on liver allografts in rats.

UNLABELLED: Hypernatremia in the donor organ is one of the most dangerous risk factors that may cause primary graft loss after orthotopic liver transplantation (OLT). However, the viability of donor grafts from acute hypernatremic donors, which is likely to occur during resuscitation of trauma patients with hypertonic saline solution, has not been studied precisely. In the present study, we sought to evaluate whether the hypernatremia, per se, induced by hypertonic saline solution, affects the outcome of liver transplantation in the normal rat. Thirty minutes after the induction of hypernatremia (>160 mEq/L), the livers of nine Wistar rats were removed under ether anesthesia. Six livers were immediately transplanted into normal Wistar rats, whereas the other three were preserved in 4 degrees C University of Wisconsin solution for 6 h before transplantation in the recipients. Liver function variables of the donor rats at graft procurement and of the recipients at Day 7 after OLT were compared with a control group. The water content of the graft at procurement and the survival of the recipients at 7 days after OLT were, likewise, compared with the untreated control group. Results showed that there were no significant differences in the liver function tests of the donors and recipients, as well as in the water content of the grafts, between groups. All the rats survived the observation period of 7 days. This study showed that acute hypernatremia induced by the infusion of 10% saline solution before graft procurement in a nonbrain-dead donor rat model did not lead to a deterioration of liver graft viability after OLT. IMPLICATIONS: Hypernatremia in cadaveric donors may be detrimental to the graft in clinical liver transplantation, but acute donor hypernatremia induced by an IV infusion of 10% saline solution before graft procurement in nonbrain-dead rats did not affect the survival of the recipient rats in an experimental liver transplantation model.

Animals↗

PubMed1996

Brain myelinolysis following hypernatremia in rats.

Brain myelinolysis could develop after excessive correction (delta SNa > 20-25 mEq/1/24 hour [h]) of chronic hyponatremia; however, this neurological event is not recognized as a complication of hypernatremia when arising from a normonatremic baseline. Previous animal studies were unable to reproduce these brain lesions in hypernatremia after acute increase of serum sodium to moderately hypernatremic levels. We hypothesize that to produce brain dehydration and myelinolysis from normonatremic baseline requires a more important osmotic gradient than when starting from hyponatremic state. Rapid and sustained hypernatremia (at least > 6 to 12 h) was induced in male rats by i.p. administration of NaCl 2 M (3 injections at 6 h intervals). The NaCl doses were determined to define two groups of hypernatremic rats (moderate and severe hypernatremia) for further analysis of the neurological outcome. In group 1 (moderate hypernatremia, n = 26) 8 rats died early (< 12 h) after the beginning of the NaCl administration without specific neurologic manifestations. All the surviving rats fared well and were asymptomatic at time of death (day 8). They were submitted for at least 6 to 12 h to a serum sodium gradient of 28 +/- 6 mEq/l. Brain analysis was normal in all of them without brain demyelinating lesions. In group 2 (n = 51), 24 rats also died rapidly (< 12 h). The surviving rats developed severe neurologic symptoms as typically encountered in hyponatremic rats with myelinolysis. The majority of them died before day 8. The hypernatremic gradient in this group was significantly higher than rats in group 1 that completely recovered (mean delta SNa: 39 +/- 8 mEq/l, p < 0.001). In the 7 surviving rats (mean delta SNa: 33 +/- 3 mEq/l) brain analysis demonstrated severe demyelinating lesions similar to the histologic changes observed in hyponatremia-related myelinolysis. We demonstrated for the first time that high and sustained levels of hypernatremia could induce brain myelinolysis and that the osmotic gradient necessary to produce brain lesions is higher for normonatremic than for hyponatremic rats.

Animals↗

PubMed2002

Pathogenesis and treatment of hypernatremia.

Two aspects of hypernatremia are emphasized in this discussion: pathogenesis and treatment. Hypernatremia rarely develops with increased water loss alone; there must be a mechanism that interferes with water intake. In treating hypernatremia, the speed of correction is important because the volume regulation mechanisms restore the brain volume to normal when hypernatremia is chronic. Thus, too rapid correction of chronic hypernatremia results in brain edema. The calculation of fluid volume needed to correct hypernatremia can be obtained with use of various formulae described here for the fluid that contains dextrose in water or for hypotonic saline solution. Accurate prediction of the fluid volume requirement demands the knowledge of urine output and its electrolyte content, but when the information is not available, urine may be assumed to be isotonic in its electrolyte content.

Body Water↗

PubMed1991

Altered regulation of atrial natriuretic peptide in essential hypernatremia.

Hypothalamic osmoreceptor dysfunction resulting in hypodipsia and altered regulation of vasopressin secretion is well established as the pathogenetic mechanism in the syndrome of 'essential hypernatremia'. However, little is known about the secretory pattern of atrial natriuretic peptide (ANP) in this syndrome. Therefore, we assessed ANP regulation by determining ANP concentrations in a patient manifesting this syndrome of essential hypernatremia during several well-established experimental protocols. The serum ANP level was within normal limits despite severe euvolemic hypernatremia (serum Na+ 163 mEq/l) during one of the many admissions and remained unchanged following normalization of serum Na+. Furthermore, a decline in serum ANP instead of an appropriate rise was noted when hypernatremia (serum Na+ 152 mEq/l) was induced by either hypertonic (3%) saline infusion or following a high-Na+ (300 mEq/day) diet for several days (serum Na+ 161 mEq/l). Similarly, exogenous pitressin administration failed to cause a rise in ANP, although an appropriate fall in ANP concentration occurred following fluid deprivation. Therefore, it is apparent that ANP regulation may be significantly altered in essential hypernatremia. However, further studies are required to define whether it plays a role in the pathogenesis of hypernatremia in this syndrome.

Adult↗

PubMed2001

Hypodipsic hypernatremia with intact AVP response to non-osmotic stimuli induced by hypothalamic tumor: a case report.

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↗

PubMed1979

Hypodipsia-hypernatremia syndrome.

The pathogenesis of the rare hypernatremia, usually described in the literature as "neurogenic" or "essential" hypernatremia, consists of defective thirst mechanism either alone or in combination with impaired osmoregulation of ADH release. As etiology, disturbances of the neoplastic, vascular and degenerative type and malformations in the hypothalamic area are known. In patients with the hypodipsia-hypernatremia syndrome, dysfunction of the anterior pituitary lobe, obesity, abnormal regulation of body temperature, psychomotor retardation and episodic muscular weakness are frequently encountered as additional abnormalities. A 6-year-old patient is described with hypodipsia-hypernatremia syndrome manifest for 3 years. Besides hypernatremia, hypodipsia and the relative insensitivity of the osmoreceptors regulating ADH release, elevated body temperature, polyphagia and obesity, partial hypothalamic-hypophyseal dysfunction, lethargy and psychomotor retardation are the principal findings. An inflammatory lesion or one occupying an intracranial space was not demonstrable until now. Under forced water intake and hypocaloric diet the patient has progressed well with nearly complete normalization of the hypernatremia, body temperature and obesity.

Child↗

PubMed1983

Hypernatremia and lactulose therapy.

Lactulose is used in the treatment of portal-systemic encephalopathy. Although it is usually safe, a case of hypernatremia has been reported. To evaluate further the association of lactulose therapy and hypernatremia, records of patients with hepatic failure treated with lactulose for encephalopathy were analyzed. In 20 of 75 courses of lactulose treatment, serum sodium level exceeded 145 mEq/L. Mortality was 41% in patients in whom hypernatremia developed as compared with 14% in those who remained normonatremic. In persons who died, hypernatremia persisted; in patients who eventually recovered, the serum sodium level returned to normal. The precise mechanism of hypernatremia in these cases is not clearly defined. As an osmotic cathartic, however, lactulose may cause fecal water loss in excess of sodium, resulting in contraction of extracellular fluid volume and, therefore, hypernatremia.

Creatinine↗

PubMed1995

Hypernatremia in the aging: causes, manifestations, and outcome.

The incidence, clinical manifestations, morbidity, and mortality of all adult hypernatremic patients hospitalized during a 6-month period were studied. The impact of age on this parameter was evaluated, and the velocity of correction that produced best clinical results was established. Records of all patients who were admitted or developed hypernatremia (Na+ > 150 mEq/L) were reviewed. Demographic characteristics of age, gender, associated diagnosis, length of stay, source of admission, treatment, and outcome were recorded. Of 3209 hospitalizations, 111 patients were hypernatremic (3.46%). Sixty-five were admitted with hypernatremia, and 45 developed hypernatremia while hospitalized. Fifteen had recurrent episodes of hypernatremia. Forty-nine had associated hypokalemia and six had hypercalcemia. The etiology was multifactorial and varied with age. Correction of the hypernatremia within 4 days produced significant improvement in mental status. The overall mortality was 48.6%, and age did not favorably influence mortality. Hypernatremia is a common disorder of elderly hospitalized patients, associated with high mortality and morbidity. Other electrolyte disorders that impair the kidney concentrating ability frequently are observed. The etiology is multiple, and febrile illness due to bacterial infections is the most common cause among the elderly. Prompt treatment of infections and increased water intake in this group of patients could prevent its development. Correction over a 72-hour period significantly improved recovery of mental functions.

Adult↗

PubMed1998

Hypernatremia.

Renal water conservation minimizes the progression of hypernatremia, but the ultimate defense against progressive hypernatremia is the stimulation of thirst by hypertonicity with a resultant increase in water ingestion. Defects in thirst may result from focal lesions involving the hypothalamic osmoreceptors, but more commonly are the result of lesions that impair higher cortical processes required for thirst perception and water ingestion. In response to hypernatremia, the brain undergoes adaptive responses to minimize osmotic shrinkage. Initially there is a rapid uptake of electrolytes, while a slower adaptive phase involves the accumulation of organic osmolytes. The rate at which these solutes can be extruded from the brain dictates the rate at which water replacement can be safely administered during treatment. The incidence of hypernatremia ranges from less than 1% to more than 3% in clinical series. While hypernatremia in nonhospitalized patients is predominantly a disease of the elderly, and is commonly a manifestation of infection or inadequate nursing care, hospital-acquired hypernatremia occurs in a patient population more closely resembling the general hospitalized population and results from inadequate water prescription to patients who are unable to self-regulate water intake. Mortality rates range from approximately 40% to more than than 60%.

Adaptation, Physiological↗

PubMed1997

Hyponatremia and hypernatremia.

Hyponatremia and hypernatremia are common electrolyte disorders resulting from disorders in water homeostasis. Hyponatremia usually results from defects in free water excretion, although increased intake may also contribute. The treatment of hyponatremia has been controversial because of the high associated morbidity and mortality and the observation that rapid correction of hyponatremia is associated with the development of central pontine myelinolysis. Mild hyponatremia should be treated with water restriction alone, whereas severe acute or symptomatic hyponatremia should initially be corrected rapidly until symptoms resolve followed by more gradual correction. In all cases, treatment should be individualized on the basis of severity, cause, and duration of the hyponatremia. Hypernatremia results from impaired water ingestion, although increased water losses are often contributory. Hospital-acquired hypernatremia is usually iatrogenic because of inadequate water prescription and is therefore preventable. Hypernatremia is also associated with high morbidity and mortality, both as a result of the underlying disease and inadequate treatment. The primary treatment of hypernatremia is water replacement-repleting water deficits and replacing ongoing losses. Additional treatment should be directed at eliminating excess water losses.

Body Water↗

PubMed1989

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.

Animals↗

PubMed1986

Hypernatremia inhibits NaHCO3 reabsorption and associated NaCl reabsorption in dogs.

To examine the effect of selective rise of plasma NaCl concentration (hypernatremia) on NaHCO3 reabsorption and associated NaCl reabsorption remaining during continuous ethacrynic acid infusion, hypertonic NaCl solution was infused in three groups of anesthetized volume-expanded dogs. In six dogs examined at constant hematocrit and plasma pH, bicarbonate and water reabsorptions were inversely related to PNa and reduced by 37% and 39% respectively by raising PNa from 140 to 200 mM. Chloride reabsorption remained essentially constant until PNa exceeded 170 to 180 mM. At PNa 200 mM, sodium reabsorption was reduced by 22 +/- 6%. In six other dogs, mechanical variations of GFR showed that the inhibitory effects of hypernatremia (PNa 199 +/- 3 mM) were less pronounced at low GFR. After subsequent administration of acetazolamide (30 mg/kg body wt), only 20% of control bicarbonate reabsorption remained and glomerulo-tubular balance was completely abolished. Both hypernatremia and acetazolamide inhibited NaHCO3 and NaCl reabsorption in a molar ratio of about 1:2, as in normonatremic dogs. Finally, experiments in six dogs showed that the inhibitory effects of hypernatremia (PNa 213 +/- 4 mM) were not altered by varying PCO2 and plasma pH. We conclude that hypernatremia inhibits paracellular water and NaCl reabsorption in the proximal tubules by reducing the osmotic force caused by transcellular NaHCO3 reabsorption. A rise in PNa does not stimulate transcellular NaCl reabsorption during distal inhibition by ethacrynic acid.

Acetazolamide↗

PubMed2006

Hypernatremia associated with intracranial B-cell lymphoma in a cat.

An 8-year-old, spayed female, domestic shorthair cat with a history of hyperthyroidism, anorexia, dehydration, cervical ventroflexion, and behavioral changes was referred to the Iowa State University College of Veterinary Medicine. The cat was obtunded, with severe dehydration (15%) and hypothermia (86 degrees F), and severe muscle atrophy and fasciculations. Serum biochemical abnormalities included severe hypernatremia (195 mmol/L, reference interval 155-165 mmol/L), hyperchloridemia (161 mmol/L, reference interval 123-131 mmol/L), and hypokalemia (3.6 mmol/L, reference interval 4.0-5.7 mmol/L). Calculated osmolality was 418 mOsm/kg (reference interval 280-305 mOsm/kg), attributable to the hypernatremia. The cat was kept warm and given fluid and glucocorticoid therapy and supportive measures but remained unresponsive. Hypernatremia and hyperosmolality improved through day 3, when the cat died suddenly. At necropsy, a 1.25-cm mass was found in the area of the thalamus and interthalamic adhesion that extended to the ventral aspect of the cerebrum. The histologic and immunohistochemical diagnosis was B-cell lymphoma. Hypernatremia and hyperosmolality in this cat were attributed to primary adipsia and hypothalamic dysfunction secondary to effacement of central nervous system tissue by neoplastic lymphocytes. To the authors' knowledge, this is the first reported case of central nervous system lymphoma, confirmed by use of immunohistochemical analysis as a B-cell phenotype, associated with hypernatremia. It also is the first reported case of lymphoma in animals limited to the thalamus, hypothalamus, and cerebrum, with no involvement of the spinal cord.

Animals↗