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At least 127 records · Page 7Linked to original sources
PubMed2005

Fatal hypernatremia after using salt as an emetic--report of three autopsy cases.

Although a plethora of reports on life-threatening complications of salt emesis has been published since the early 1960s, salt is still used to induce emesis in cases of intoxication in the clinical as well as in the domestic setting. We report three cases of fatal hypernatremia after salt was used as an emetic. All fatalities were subjected to medico-legal autopsy at the Institute of Legal Medicine in Hamburg, Germany. In all cases, symptoms of cerebral damage such as seizures, fever and somnolence developed within hours after salt ingestion. All individuals were admitted to hospital before their deaths. Here, severe hypernatremia (up to 245 mmol/l) was detected, and all patients died under the clinical picture of cerebral edema despite intensive medical treatment. At autopsy, unspecific signs of a central regulatory failure were present. Histology revealed crenated red blood cells and few venous microthrombi in internal organs. Neuropathological investigations yielded no specific results but confirmed fatal cerebral edema and excluded other cerebral causes of death. Viewing the results of clinical and post-mortem investigations together, death could clearly be attributed to excessive salt intake in all cases.

Adult↗
PubMed1976

Recurrent hypernatremia; a proposed mechanism in a patient with absence of thirst and abnormal excretion of water.

A 7-year-old girl twice developed severe hypernatremia (serum sodium values up to 194 mEq/l) without obvious cause. The ability of her kidneys to conserve water was normal, and increasing her plasma osmolality stimulated an appropriate ADH response. Unable to excrete a water load, her kidneys continued to conserve water even with a serum sodium concentration of 133 mEq/l. She was never thirsty and did not ingest sufficient fluid by choice. Although there was no demonstrable anatomic lesion, we postulate a localized defect of her thirst center. This may have modified release of ADH and resulted in an inability to dilute the urine by interrupting a pathway that could exist from the thirst center to the supraoptic nuclei. A therapeutic regimen based on these studies has prevented further hypernatremia.

Child↗
PubMed1977

Rhabdomyolysis with severe hypernatremia.

Three children with severe hypernatremia presented with profound generalized weakness and biochemical evidence of rhabdomyolysis and myoglobinuria. These findings in combination have not been previously reported, to our knowledge, in children with severe hypernatremia. Unusual complications included respiratory failure in one child and cardiac arrhythmias in two children. All three children had acute renal insufficiency; one required peritoneal dialysis.

Acute Kidney Injury↗
PubMed2003

Severe hypernatremia after cesarean delivery secondary to transient diabetes insipidus of pregnancy.

BACKGROUND: Transient diabetes insipidus is an uncommon complication of pregnancy, usually manifesting with polydipsia and polyuria. This condition is considered to result from excess placental vasopressinase activity and is managed with deamino D arginine vasopressin. CASE: While on restricted oral intake after cesarean delivery, the patient gradually became disoriented and agitated in conjunction with markedly increased urine output disproportional to her intravenous crystalloid fluid intake. Marked hypernatremia of 178 mEq/dL was noted. Urine osmolality was low at 248 mOsm/L. The clinical presentation and electrolyte abnormalities were considered consistent with transient diabetes insipidus of pregnancy. The patient responded well to nasal-spray-administered deamino D arginine vasopressin and increased intravenous fluid intake, with resolution of symptoms and gradual normalization of serum sodium levels. CONCLUSION: Transient diabetes insipidus of pregnancy should be considered in the differential diagnosis of severe hypernatremia in obstetric patients with restricted oral intake after operative delivery.

Adult↗
PubMed1976

Hypernatremia--problems in management.

Hypernatremia may be produced under several different circumstances but most frequently is the result of excessive water loss with diarrhea and the excessive solute load secondary to inappropriate preparation of formula. The clinical manifestations vary and depend primarily on the degree of dehydration and the rate at which the hyperosmolar state has been reached. The management of the patient will, of course, depend upon the mechanism of hypernatremia and degree of dehydration and/or hypovolemia that is present. It seems clear that the exact nature of the rehydrating solution is not of major importance. The volume is of great concern but most vital seems to be the rate of rehydration. If rehydration is accomplished too rapidly the child becomes edematous, develops increased intracranial pressure, stupor, and convulsions. If fluids are given slowly and at a well regulated rate, these complications can usually be avoided. The patient should be monitored regularly with electrolytes, careful determination of weights, and records of intake and output. The rate of rehydration should be monitored to assure that the planned schedule of 24 to 72 hours (depending on the severity of the problem) is followed. Approximately 10 to 15 per cent of children with serum sodium of 160 mEq per liter or greater will have permanent neurological deficits.

Brain Diseases↗
PubMed1991

Hypernatremia due to repeated doses of charcoal-sorbitol.

Hypernatremic dehydration due to unreplaced stool water losses often complicates the use of the osmotic cathartic lactulose in the treatment of hepatic encephalopathy. Sorbitol, another osmotic cathartic commonly used in the treatment of drug intoxications, has been reported in the pediatric literature to induce severe hypernatremia, but there is only a rare case report in an adult. We report a dramatic case of severe hypernatremia secondary to repetitive administration of activated charcoal-sorbitol suspension for the treatment of phenobarbital intoxication in an adult. Based on our experience with this case, several recommendations are provided regarding management of drug intoxications with charcoal-sorbitol suspension, including meticulous attention to fluid-electrolyte balance, type of replacement fluid, and dosing of the suspension.

Adult↗
PubMed1989

Survival after severe iatrogenic hypernatremia.

The case of a 24-year-old woman who survived without subsequent neurological damage after severe iatrogenic hypernatremia is presented. This previously healthy woman who had given birth with an uncomplicated delivery developed hypernatremia (serum sodium, 178 mmol/L) after erroneous infusion of hypertonic sodium solution.

Adult↗
PubMed1997

Profound natriuresis, extracellular fluid volume contraction, and hypernatremia with hypertonic losses following trauma.

A young male sustained very serious head and soft tissue injuries in a motor vehicle accident (MVA). Three interesting problems developed in the sodium (Na) and water area in the second week in hospital. First, on day 11 after the MVA, his urine output increased to 3 liters per day; the urine osmolality was 1000 mOsm/kg H2O and Na and Cl were the principal urine osmoles. There appeared to be a salt wasting syndrome because he had a very large natriuresis (close to 900 mmol/24 hr) at a time when his central venous pressure was low. To help identify the nephron site responsible for a natriuresis with a high urine osmolality, additional studies were carried out in normal volunteers who took a loop or a thiazide diuretic on different occasions while ADH was acting. The pattern of natriuresis in the patient was similar to that after the thiazide but not the loop diuretic. The second problem concerned his hypernatremia (153 mM) because his urine was hypertonic and his intravenous therapy was isotonic saline. To explain hypernatremia while receiving more electrolyte-free water, we speculated that there was a water shift into cells resulting from particles generated and retained in his intracellular fluid. Given the large shift of water required, a lesion in muscle was suspected, a form of rhabdomyolysis. The third problem concerned the rate of catabolism of lean body mass. The metabolic consequences of generating these intracellular particles and the large amount of urea that was excreted could reflect a large degree of protein catabolism.

Adult↗
PubMed2007

Enteral water for hypernatremia and intestinal morbidity in infants less than or equal to 1000 g birth weight.

OBJECTIVE: To evaluate the relationship between enteral water infusion for hypernatremia and significant intestinal morbidity in infants or=150 (high sodium control), >or=150 and treated with sterile water (study group). Significant intestinal morbidity was defined as probable or proven necrotizing enterocolitis or spontaneous intestinal perforation. Statistical analysis included Student's t test for continuous variables and chi(2) with Yeats correction for frequency variables. Multivariate logistic regression analysis was then performed to evaluate confounding variables among groups. RESULTS: The incidence of intestinal morbidity was significantly higher in the high sodium-water treated group compared to each of the other groups (13/33 (38%) for high sodium-water versus 16/100 (16%) for high sodium control and 18/188 (10%) for normal sodium control, P<0.01 chi(2)). Logistic regression analysis indicated that enteral water and hydrocortisone were risk factors for significant intestinal morbidity. CONCLUSIONS: Enteral sterile water for hypernatremia appears to be associated with significant intestinal morbidity in infants <or=1000 g. Hydrocortisone is also a risk factor.

Enteral Nutrition↗
PubMed1986

[Severe hypernatremia within the scope of catatonic schizophrenia].

We report the case of a 57-year-old chronic schizophrenic patient who developed an acute catatonic stupor after postoperative withdrawal of neuroleptics with excessive and firstly therapy-resistant hypernatremia. Only after re-treatment with neuroleptics the hypernatremia could be compensated. A relationship between the catatonic schizophrenia and the electrolyte-disturbances can be supposed; probably in both diencephalic structures are involved. Therefore the syndrome of "acute life threatening catatonia" should be included into the differential diagnosis of uncertain metabolic disorders.

Antipsychotic Agents↗
PubMed2002

Severe hypernatremia after hypertonic saline irrigation of hydatid cysts.

IMPLICATIONS: Patients with iatrogenic hypernatremia and serum sodium levels >170 mmol/L either die or sustain severe central nervous system damage. We report the first case of an adult patient who survived an extreme iatrogenic acute hypernatremia (200 mmol/L) resulting from a hypertonic saline irrigation of multiple intraabdominal hydatid cysts. It is a unique report of an intraoperatively developed serum sodium increase without subsequent neurological damage.

Adult↗
PubMed1992

Disorders of sodium metabolism: hypernatremia and hyponatremia.

OBJECTIVE: Discussion of abnormal plasma sodium concentrations with an emphasis on the pathogenesis, diagnosis, and treatment. DATA SOURCES: Relevant literature in the English language and the authors' clinical experience. STUDY SELECTION: No special study has been carried out for the present discussion. DATA EXTRACTION: The information from the literature and the data from the authors' clinical experience have been used to illustrate important points in the discussion. DATA SYNTHESIS: A most important aspect in the approach to hypernatremia is determination of the mechanism responsible for impaired water intake. Various mechanisms of abnormal water loss can be determined from measurement of urine osmolality. Hypernatremia is treated by water replacement and measures to reduce abnormal water loss. In most instances, hyponatremia is caused by inappropriate concentration of urine because of either appropriate or inappropriate antidiuretic hormone secretion. The determination of appropriateness of antidiuretic hormone secretion requires the assessment of effective arterial volume. Treatment depends on the pathogenetic mechanism. CONCLUSIONS: Abnormal plasma sodium concentration results from abnormal water intake or water output. Treatment is guided by determining the pathogenetic mechanism.

Diagnosis, Differential↗
PubMed1981

Hypernatremia during lithium and ticarcillin therapy.

A patient being treated for leukemia received lithium carbonate and ticarcillin for sepsis, and polyuria and severe hypernatremia developed. Although useful in neutropenic patients, the simultaneous use of these drugs may result in life-threatening hypernatremia.

Aged↗
PubMed1983

Hypernatremia with choroid plexus hematomas and elevated CSF protein level.

A 3-month-old infant had hypernatremia, neurologic dysfunction, and an unusually high level of cerebrospinal fluid protein. The autopsy findings included cerebral edema, intravascular coagulation, and bilateral choroid plexus hematomas. Extensive destruction of the choroid plexus, in combination with diffuse intravascular coagulation may explain the much greater elevation of CSF protein than previously described with hypernatremia.

Cerebral Hemorrhage↗
PubMed1987

Recumbent cranial diabetes insipidus. Studies in a patient with adipsia, hypernatremia, poikilothermia and polyphagia.

A male, aged 16, with chronic hypernatremia, adipsia, polyphagia, and poikilothermia was studied regarding regulation and secretion of arginine vasopressin. During recumbency at night, low plasma arginine vasopressin levels and increased volumes of dilute urine were found; whereas plasma arginine vasopressin levels and urine osmolalities rose and urine volumes decreased during ambulation in the daytime. Neither a 25% reduction of mean arterial pressure nor hypertonic saline infusion increased plasma arginine vasopressin or urine osmolalities. Treatment with 1-desamino-D-arginine-vasopressin at 6 p.m. and a scheduled fluid intake according to actual body weight eradicated hypernatremia and hyperosmolality. These data demonstrate a complete loss of arginine vasopressin secretion to osmotic stimulation, a partial defect of arginine vasopressin secretion to non-osmotic stimulation, an abolished response to stimulation of high-pressure-baroreceptors, but an intact responsiveness to stimulation of low-pressure-baroreceptors.

Adolescent↗
PubMed2004

Effects of forebrain circumventricular organ ablation on drinking or salt appetite after sodium depletion or hypernatremia.

In many previous studies, one or the other forebrain circumventricular organ, the subfornical organ (SFO) or organum vasculosum laminae terminalis (OVLT), was lesioned to test whether it was critical for the behavioral or physiological responses to sodium depletion and hypernatremia. These studies conflict in their conclusions. The present study was designed to create discrete lesions of both the SFO and OVLT in the same animals and to compare these with rats having a lesion of only the SFO or OVLT. Both the OVLT-lesioned group and the combined SFO + OVLT-lesioned group drank significantly more water and saline on a daily basis than Controls or SFO-lesioned rats. In both sodium depletion and hypertonic saline testing, rats with SFO lesions displayed transient deficits in salt appetite or thirst responses, whereas the rats with single OVLT lesions did not. In the sodium depletion test, but not in the hypernatremia test, rats with lesions of both the SFO and OVLT exhibited the largest deficit. The data support the hypothesis that a combined lesion eliminates redundancy and is more effective than a single lesion in sodium depletion tests. The interpretation of the OVLT lesion-only data may have been complicated by a tendency to drink more fluid on a daily basis, because some of those animals drank copious water in addition to saline even very early during the salt appetite test.

Analysis of Variance↗
PubMed1988

Effects of plasma angiotensin II and hypernatremia on subfornical organ neurons.

Experiments were done in urethan-anesthetized rats to investigate the effect of plasma angiotensin II (ANG II) and hypernatremia on the excitability of subfornical organ (SFO) neurons projecting directly to paraventricular nucleus of the hypothalamus (PVH), supraoptic nucleus (SON), and nucleus medianus (NM). Extracellular recordings were made from 106 antidromically identified neurons in the SFO. The firing frequency of 53 (50%) was increased by the intracarotid infusion of ANG II and/or 0.5 M hypertonic NaCl. The intracarotid infusion of isotonic saline or the intravenous infusion of phenylephrine did not alter the discharge rate of these SFO neurons. Of 38 PVH projecting neurons, 21 (55%) responded to ANG II and/or hypertonic NaCl: 9 to ANG II only, 8 to hypertonic NaCl only, and 4 to both. Similarly, of 42 SON projecting neurons, 30 (71%) responded to ANG II and/or hypertonic NaCl: 10 to ANG II only, 15 to hypertonic NaCl only, and 5 to both. Finally, of 26 NM projecting neurons, one increased its firing frequency to ANG II and one other to 0.5 M NaCl. An additional eight SFO neurons were found to send collateral axons to both the PVH and SON (n = 6) and PVH and NM (n = 2): four responded in various combinations to intracarotid infusion of ANG II and 0.5 M NaCl. These data suggest that blood-borne ANG II and plasma hypernatremia can influence arterial pressure and the release of vasopressin from the neurohypophysis by altering the discharge rate of SFO neurons projecting to forebrain structures that contain magnocellular neurosecretory vasopressin neurons and neurons that are components of sympathoexcitatory pathways.

Angiotensin II↗