Severe Hypernatremia Research Articles

Successful treatment of severe salt intoxication in a dog

AbstractObjective: To report successful treatment of severe salt intoxication and hypernatremia in a dog.Case summary: A 5‐year‐old intact female Doberman Pinscher was admitted to the intensive care unit with a history of seizures and coma. The owner had administered approximately 100 g of cooking salt to induce vomiting following ingestion of a nontoxic dose (10 g) of chocolate. Upon admission, the dog was comatose with intermittent seizures and vomiting. Diagnostic tests confirmed salt intoxication (Na: 200 mEq/L, Cl: 180 mEq/L) and metabolic acidosis (pH: 7.18; pCO2: 39 mmHg; HCO3: 14.3 mmol/L). Immediate treatment included intravenous fluid therapy, an anticonvulsant, antiemetic, diuretic, low molecular weight heparin, and supplemental oxygen. A fluid therapy protocol was initiated to decrease serum sodium concentration by approximately 2 mEq/L/hr. After 24 hours of intensive care, the patient regained consciousness and volume and acid‐base abnormalities improved. The patient developed a variety of abnormal clinical signs as a result of the severe hypernatremia. After 5 days of treatment, the serum sodium concentration returned to the established reference range. The patient recovered completely in 10 days.New information provided: Severe hypernatremia due to salt ingestion is a rare condition in dogs. All dogs in previous case reports of salt intoxication have died. This case report is the first to report survival of a dog with severe salt intoxication.

Impact of an early weighing policy on neonatal hypernatraemic dehydration and breast feeding

Aims:To ascertain the effect of a policy of early weighing on the detection and severity of neonatal hypernatraemic dehydration (NHD) and on breastfeeding rates in the short and medium term.Methods:A...

Deep vein thrombosis complicating severe hypernatremia, rhabdomyolysis, and acute renal failure in a patient with untreated seizure disorder

We report a 22-year-old male patient with untreated seizure disorder, presenting with increased frequency of seizures followed by encephalopathy. Laboratory evaluation showed severe hypernatremia (175 meq/l sodium), rhabdomyolysis, and acute renal failure (ARF). Excessive insensible water loss in hot and humid weather, associated with an inability to obtain adequate water replacement, led to a hyperosmolar state (plasma osmolality, 398 mOsm/kg). He was vigorously treated with hypotonic fluid supplement and, further, needed dialysis therapy (peritoneal dialysis followed by hemodialysis) for acute renal insufficiency. The patient survived without any neurological sequelae, but the clinical course was complicated by acute deep vein thrombosis. This case represents what we believe is a unique report in the literature of severe hypernatremia developing via the pathogenic mechanism outlined above and the complication of acute peripheral venous thrombosis, which has not been reported in adults. The purpose of this report is to emphasize hyperosmolarity as a newly described cause of rhabdomyolysis, ARF, and a hypercoagulable state.

CRANIAL MR VENOGRAPHY FINDINGS OF SEVERE HYPERNATREMIC DEHYDRATION IN ASSOCIATION WITH CEREBRAL VENOUS THROMBOSIS IN THE NEONATAL PERIOD

Severe neonatal hypernatremia is an important electrolyte disorder that has serious effects on the central nervous system, including brain edema, intracranial hemorrhage, hemorrhagic infarct, and thrombosis. Cerebral venous thrombosis is relatively rare in severe neonatal hypernatremic dehydration. The English literature contains only a few reports of the cranial radiological findings in severe neonatal hypernatremia. The authors report cranial MR venography findings of a newborn infant with severe hypernatremic dehydration. To the best of their knowledge, this is the first such report in the English literature.

Severe Hypernatraemia Due to Nephrogenic Diabetes Insipidus - a Life-Threatening Side Effect of Chronic Lithium Therapy

Renal toxicity of long-term lithium therapy is a common problem. Nephrogenic diabetes insipidus is the most frequently encountered complication, but often remains unrecognised because of the rather benign symptoms. We present a patient with long-term lithium therapy who developed life-threatening hypernatraemia due to insufficient oral fluid intake after elective spinal surgery. Careful daily substitution of up to 25 l of hypotonic fluids led to full recovery within 9 days. Nephrogenic diabetes insipidus should always be considered in lithium-treated patients undergoing elective surgery in order to avoid severe hypernatraemia.

Rhabdomyolysis caused by hypernatremia

Rhabdomyolysis is a clinical picture which is rarely seen in children. In this case report here it is presented a patient who has biochemical and clinical signs of rhabdomyolysis and admitted to our clinic with hypernatremia. The authors think that it is necessary to be alert for rhabdomyolysis in severe hypernatremia cases.

Electrolytes Disturbances and Seizures

Electrolytes Disturbances and Seizures

CRITICAL CARE ISSUES FOR THE NEPHROLOGIST: Electrolyte Disturbances in the Intensive Care Unit

AbstractThe development of many electrolyte disturbances in the ICU can be prevented by attention to the use of intravenous fluids and nutrition. Hyponatremia is a relative contraindication to the use of hypotonic intravenous fluids and hypernatremia calls for the administration of water. Formulae have been devised to guide the therapy of severe hyponatremia and hypernatremia. All formulae regard the patient as a closed system, and none takes into account ongoing fluid losses that are highly variable between patients. Thus, therapy of severe hyponatremia and hypernatremia must be closely monitored with serial electrolyte measurements. The significance of hypocalcemia in the critically ill is controversial. Hypokalemia, hypophosphatemia, and hypomagnesemia should be corrected.

Shock Revealing Salt Poisoning in a Neonate

We report a case of shock, revealing a severe hypernatremia caused by salt poisoning in a 17-day-old male neonate. We consider the physiopathology of salt overload in this context and the diagnostic strategy in neonate with hypernatremia. We used patient history, weight, plasma, and urine osmolality to establish the diagnostic strategy. Salt poisoning in neonates manifests as intracellular dehydration without extracellular fluid accumulation. This poisoning underscores the need for providing appropriate help to mothers at discharge from the maternity ward or neonatology unit.

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.

Clinical Presentation of Hypernatremia in Elderly Patients: A Case Control Study

To assess early clinical signs and their prognostic value in elderly patients with hypernatremia. Prospective, case control study of 150 patients with hypernatremia matched to 300 controls. Multicenter study including seven short- and long-term geriatric care facilities. Clinical assessment of hydration status at bedside, such as abnormal skin turgor or dry oral mucosa. 30-day mortality rate and clinical indicators (assessed at the peak of natremia) associated with mortality. Patients and controls were comparable in terms of drugs and underlying diseases, except for history of dementia, which was more frequent in patients than in controls. Patients were significantly more likely than controls to have low blood pressure, tachycardia, dry oral mucosa, abnormal skin turgor, and recent change of consciousness. Only three clinical findings were found in at least 60% of patients with hypernatremia: orthostatic blood pressure and abnormal subclavicular and forearm skin turgor. The latter two signs were significantly more frequent in patients with hypernatremia. Four other signs (tachycardia, abnormal subclavicular skin turgor, dry oral mucosa, and recent change of consciousness) had a specificity of greater than 79%. Using logistic regression, four signs were significantly and independently associated with hypernatremia: abnormal subclavicular and thigh skin turgor, dry oral mucosa, and recent change of consciousness. The mortality rate was 41.5% and was significantly higher in patients with hypernatremia. The status of consciousness when hypernatremia was diagnosed was the single prognostic indicator associated with mortality (odds ratio=2.3, 95% confidence interval=1.01-5.2). Most of the classical signs of dehydration are irregularly present in patients with hypernatremia. Caregivers should carefully screen any variations in consciousness, because they may reveal severe hypernatremia.

Hypernatremia in the neurologic intensive care unit: how high is too high?

Hypernatremia is associated with increased mortality in hospitalized patients and in medical/surgical intensive care units. This relationship has not been studied in neurologic/neurosurgical intensive care units (NNICUs), where hypernatremia is often a component of treatment of cerebral edema. We performed a retrospective analysis of prospectively collected data in patients admitted to the NNICU over a 6.5-year period. Hypernatremia (serum sodium >150 mEq/L) was seen in 339 patients (7.9%) and was more common (24.3%) in patients who were treated with mannitol. Hypernatremic patients had a lower median admission Glasgow Coma Scale score (8 vs 14, P < .001), higher initial Acute Physiology and Chronic Health Evaluation II probability of death (34.9% vs 19.1%, P < .001), higher incidence of mechanical ventilation (80.5% vs 41.1.5%, P < .001), higher mortality (30.1% vs 10.2%, P < .001), and higher incidence of renal failure (10.3% vs 0.9%, P < .001). Mortality increased with increasing hypernatremia; however, only severe hypernatremia (serum sodium >160 mEq/L) was independently associated with increased mortality. Other factors independently associated with mortality were age, mechanical ventilation, initial Acute Physiology and Chronic Health Evaluation II probability of death or low admission Glasgow Coma Scale score, and a diagnosis of cerebrovascular disease. In conclusion, hypernatremia is common in the NNICU, more so in patients treated with mannitol. In this population, severe (but not mild or moderate) hypernatremia is independently associated with increased mortality.

Hypernatemia : Successful Treatment

Hypernatremia reflects a net water loss or a hypertonic sodium gain, with inevitable hyperosmolality. Severe symptoms are usually evident only with acute and large increases in plasma sodium concentrations to above 158-160 mmol/l. Importantly, the sensation of intense thirst that protects against severe hypernatremia in health may be absent or reduced in patients with altered mental status or with hypothalamic lesions affecting their sense of thirst and in infants and elderly people. Non-specific symptoms such as anorexia, muscle weakness, restlessness, nausea, and vomiting tend to occur early. More serious signs follow, with altered mental status, lethargy, irritability, stupor, and coma. Acute brain shrinkage can induce vascular rupture, with cerebral bleeding and subarachnoid hemorrhage. However, in the vast majority of cases, the onset of hypertonicity is low enough to allow the brain to adapt and thereby to minimize cerebral dehydration. Organic osmolytes accumulated during the adaptation to hypernatremia are slow to leave the cell during rehydration. Therefore, if the hypernatremia is corrected too rapidly, cerebral edema results as the relatively more hypertonic ICF accumulates water. To be safe, the rate of correction should not exceed 12 mEq/liter/day.

Hypernatremia and Hyperlipidemia in a Dog with Central Nervous System Lymphosarcoma

Journal of Veterinary Internal MedicineVolume 20, Issue 4 p. 1029-1032 Open Access Hypernatremia and Hyperlipidemia in a Dog with Central Nervous System Lymphosarcoma Beth Hanselman, Corresponding Author Beth Hanselman Department of Clinical Studies, Ontario Veterinary College, University of Guelph, Guelph, Ontario, Canada Department of Clinical Studies, Ontario Veterinary College, University of Guelph, Guelph, Ontario N1G2W1 Canada; e-mail: [email protected]Search for more papers by this authorStephen Kruth, Stephen Kruth Department of Clinical Studies, Ontario Veterinary College, University of Guelph, Guelph, Ontario, CanadaSearch for more papers by this authorRoberto Poma, Roberto Poma Department of Clinical Studies, Ontario Veterinary College, University of Guelph, Guelph, Ontario, CanadaSearch for more papers by this authorStephanie Nykamp, Stephanie Nykamp Department of Clinical Studies, Ontario Veterinary College, University of Guelph, Guelph, Ontario, CanadaSearch for more papers by this author Beth Hanselman, Corresponding Author Beth Hanselman Department of Clinical Studies, Ontario Veterinary College, University of Guelph, Guelph, Ontario, Canada Department of Clinical Studies, Ontario Veterinary College, University of Guelph, Guelph, Ontario N1G2W1 Canada; e-mail: [email protected]Search for more papers by this authorStephen Kruth, Stephen Kruth Department of Clinical Studies, Ontario Veterinary College, University of Guelph, Guelph, Ontario, CanadaSearch for more papers by this authorRoberto Poma, Roberto Poma Department of Clinical Studies, Ontario Veterinary College, University of Guelph, Guelph, Ontario, CanadaSearch for more papers by this authorStephanie Nykamp, Stephanie Nykamp Department of Clinical Studies, Ontario Veterinary College, University of Guelph, Guelph, Ontario, CanadaSearch for more papers by this author First published: 28 June 2008 https://doi.org/10.1111/j.1939-1676.2006.tb01824.xCitations: 8AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL References 1 Kamel KS, Ethier JH, Richardson RMA, et al. Urine electrolytes and osmolality: When and how to use them Am J Nephrol 1990; 10: 89– 102. 2 Kent M., Lahunta AD, Tidwell AS. MR imaging findings in a dog with intravascular lymphoma in the brain. Vet Radiol Ultrasound 2001; 42: 504– 510. 3 Marks SL, Taboada J. Hypernatremia and hypertonic syndromes. Vet Clin North Am Small Anim Pract 1998; 28: 533– 543. 4 Crawford MA, Kittleson MD, Fink GD. Hypernatremia and adipsia in a dog. J Am Vet Med Assoc 1984; 184: 818– 821. 5 Mackay BM, Curtis N. Adipsia and hypernatraemia in a dog with focal hypothalamic granulomatous meningoencephalitis. Aust Vet J 1999; 77: 14– 17. 6 Sullivan SA, Harmon BG, Purinton PT, et al. Lobar holoprosencephaly in a Miniature Schnauzer with hypodipsic hypernatremia. J Am Vet Med Assoc 2003; 233: 1783– 1787. 7 DiBartola SP, Johnson SE, Johnson GC, et al. Hypodipsic hypernatremia in a dog with defective osmoregulation of anti-diuretic hormone. J Am Vet Med Assoc 1994; 204: 922– 925. 8 Bagley RS, Lahunta AD, Randolph JF, et al. Hypernatremia, adipsia and diabetes insipidus in a dog with hypothalamic dysplasia. J Am Anim Hosp Assoc 1993; 29: 267– 271. 9 Chang L., Harrington DW, Mlikotic A., et al. Unusual occurrence of extrapontine myelinolysis associated with acute severe hypernatraemia caused by central diabetes insipidus. Clin Endocrinol 2005; 63: 232– 237. 10 van der Mil AHM, Van Vugt JPP, Lammers GJ, et al. Hypernatremia from a hunger strike as a cause of osmotic myelinolysis. Neurology 2005; 64: 574– 575. 11 Sugimura Y., Murase T., Takefuji S. Protective effect of dexamethasone on osmotic-induced demyelination in rats. Exp Neurol 2005; 192: 178– 183. 12 Crook M., Robinson R., Swaminathan R. Hypertriglycer-idaemia in a child with hypernatraemia due to a hypothalamic tumour. Ann Clin Biochem 1995; 32: 226– 228. 13 Hayek A., Bryant PD, Woodside WF. Hypernatremia induces hyperlipemia and a fatty liver. Metabolism 1983; 32: 1– 3. 14 Kippenes H., Gavin PR, Bagley RS, et al. Magnetic resonance imaging features of tumors of the spine and spinal cord in dogs. Vet Radiol Ultrasound 1999; 40: 627– 633. 15 Troxel MT, Vite CH, Massicotte C., et al. Magnetic resonance imaging features of feline intracranial neoplasia: Retrospective analysis of 46 cats. J Vet Intern Med 2004; 18: 176– 189. 16 Dubuisson A., Kaschten B., Lenelle J., et al. Primary central nervous system lymphoma: Report of 32 cases and a review of the literature. Clin Neurol Neurosurg 2004; 107: 55– 63. 17 Morozumi M., Miyahara K., Sato M., et al. Computed tomography and magnetic resonance findings in two dogs and a cat with intracranial lesions. J Vet Med Sci 1997; 59: 807– 810. Citing Literature Volume20, Issue4July 2006Pages 1029-1032 ReferencesRelatedInformation

Glycerol kinase deficiency presenting with hypodipsia, osmotic diuresis and severe hypernatraemia

A Chinese boy with glycerol kinase deficiency is reported. His presentation with severe hypernatraemia secondary to hypodipsia and glycerol-induced osmotic diuresis is unusual and not previously described in the literature.

Weight loss and hypernatremia in breast‐fed babies: Frequency in neonates with non‐hemolytic jaundice

The aim of this study was to determine what proportion of newborns admitted with idiopathic non-hemolytic hyperbilirubinemia exhibit severe weight loss and hypernatremia. 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. 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. 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.

Index of Suspicion in the Nursery

Index of Suspicion in the Nursery

Perioperative anesthetic management for cesarean section of a parturient with gestational diabetes insipidus

Gestational diabetes insipidus (GDI) is a rare endocrinopathy complicating about 4:100,000 deliveries. We present the case of a preterm parturient with GDI and severe hypernatremia (serum sodium concentration = 174 mmol.L(-1)) presenting for an urgent Cesarean section. Fluid resuscitation and desmopressin supplementation partially corrected the patient's homeostasis, allowing us to carefully titrate epidural anesthesia for an urgent Cesarean section. After delivery, the patient was transferred to the intensive care unit. The serum sodium concentration of the mother and the neonate was normalized over 48 hr and three days respectively. The careful perioperative management of GDI led to a favourable outcome of the mother and fetus.

Unusual occurrence of extrapontine myelinolysis associated with acute severe hypernatraemia caused by central diabetes insipidus

Unusual occurrence of extrapontine myelinolysis associated with acute severe hypernatraemia caused by central diabetes insipidus

Treating Hypernatremic Dehydration

1. Andrew L. Schwaderer, MD 1. Fellow, Pediatric Nephrology 1. George J. Schwartz, MD 1. Professor of Pediatrics Chief, Division of Pediatric Nephrology University of Rochester School of Medicine & Dentistry Rochester, New York In the November 2004 “Index of Suspicion,” Case 1 featured a patient who had hypernatremic dehydration. Dr Scott Hamilton raised the issue of which intravenous solution should be used to treat this condition, given the dangers inherent in lowering the serum sodium level too quickly. Drs Schwaderer and Schwartz have written this commentary to guide clinicians through the complexities of this therapeutic challenge. During most of January, an earlier version of this commentary was printed in the online edition of Pediatrics in Review. This amended version, which was substituted online in late January for the previous commentary, is the text that readers should consult because some corrections were made by the authors. — LFN Hypernatremia, a frequently encountered electrolyte disorder, is defined as a serum sodium level greater than 145 mEq/L (145 mmol/L) and represents a deficit of water in relation to total body sodium. Hypernatremic dehydration may be caused by pure water loss (diabetes insipidus), hypotonic fluid loss (vomiting or diarrhea), or hypertonic sodium gain (hypertonic feeding preparations such as improperly prepared infant formula). (1) Severe hypovolemic hypernatremic dehydration induces brain shrinkage, which can tear the cerebral blood vessels, leading to cerebral hemorrhage, seizures, paralysis, and encephalopathy. (2)(3) Infants who have severe hypernatremia (serum sodium, >160 mEq/L [160 mmol/L]) often present with muscle weakness, a high-pitched cry, insomnia, or lethargy. (1) Younger children tend to have both a higher morbidity and mortality with severe hypernatremia. (2) Breastfeeding hypernatremic dehydration results when a mother-infant feeding interaction is inadequate. In this case, human milk production is limited, and the physiologic decline in human milk sodium concentration does not occur. (4) Forty cases of hypernatremia due to human milk failure have been described in the medical literature. …