Hypernatremia and Hypertonic Syndromes

Marks, Steven L.; Taboada, Joseph

doi:10.1016/s0195-5616(98)50054-x

Cited by 17 publications

(28 citation statements)

References 8 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The use of D5W is equivalent to administration of pure water. The following formulae represent guidelines to calculate fluid therapy requirements 9,15 . To determine the amount of water required to correct sodium to the desired level in hypernatremia due to water loss or hypotonic fluid loss, the following formula can be utilized: …”

Section: Discussionmentioning

confidence: 99%

Successful treatment of severe salt intoxication in a dog

Pouzot

Descone-Junot

Loup

et al. 2007

J Vet Emergen Crit Care

View full text Add to dashboard Cite

Objective: 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.

show abstract

Section: Discussionmentioning

confidence: 99%

Successful treatment of severe salt intoxication in a dog

Pouzot

Descone-Junot

Loup

et al. 2007

J Vet Emergen Crit Care

View full text Add to dashboard Cite

show abstract

“…Several mechanisms may result in hypernatremia, including free-water loss greater than sodium loss, excess sodium intake, inadequate water consumption, abnormal thirst reflex, osmoreceptor dysfunction, diabetes insipidus, hyperaldosteronism, and hyperadrenocorticism. 3,4 Clinically relevant hypernatremia rarely develops if access to water and an intact thirst mechanism are present. 5 Primary hypodipsia or adipsia (essential hypernatremia) develops from dysfunction of specialized neurons called osmostats within the hypothalamus.…”

mentioning

confidence: 99%

“…6 In contrast to that associated with diabetes insipidus, ADH may still be released from the hypothalamus in primary adipsia by nonosmotic stimuli (eg, volume depletion, nausea), but there is decreased or no response to osmotic stimuli. 3,7 Primary adipsia is characterized by a history of normal sodium intake, adipsia, absence of polyuria, appropriate urine concentration, marked hypernatremia, and serum hyperosmolality. 3 In this dog, marked hypernatremia and hyperosmolality with appropriate urine concentration and increased urine osmolality were consistent with hypothalamic osmoreceptor dysfunction and not diabetes insipidus.…”

mentioning

confidence: 99%

“…3,7 Primary adipsia is characterized by a history of normal sodium intake, adipsia, absence of polyuria, appropriate urine concentration, marked hypernatremia, and serum hyperosmolality. 3 In this dog, marked hypernatremia and hyperosmolality with appropriate urine concentration and increased urine osmolality were consistent with hypothalamic osmoreceptor dysfunction and not diabetes insipidus.…”

mentioning

confidence: 99%

“…Signs commonly develop secondary to neuronal dehydration, tissue shrinkage, and vascular disruption from plasma hyperosmolality. 3,8 Rarely in humans, signs of neurologic dysfunction have been attributed to extrapontine myelinolysis, associated with acute, severe hypernatremia. 9,10 Concurrent signs of hypothalamic dysfunction, such as behavior changes, altered appetite, abnormalities in temperature or heart rate regulation, and endocrine disorders, may be present depending on the underlying disorder.…”

mentioning

confidence: 99%

See 2 more Smart Citations

Hypernatremia and Hyperlipidemia in a Dog with Central Nervous System Lymphosarcoma

et al. 2006

View full text Add to dashboard Cite

A 6-year-old, spayed female Labrador Retriever was referred to the Ontario Veterinary College, Veterinary Teaching Hospital (OVC-VTH) because of generalized weakness and ataxia. Progressive lethargy, exercise intolerance, and decreased interaction with family members were reported over the preceding 3 weeks. Decreased appetite, hypodipsia, vomiting, and left hind limb lameness subsequently developed. Abnormalities in serum electrolyte concentrations 1 week prior to examination included marked hypernatremia (193 mEq/L; reference interval [RI] 144-160 mEq/L) and hyperchloridemia (147 mEq/L; RI 109-122 mEq/L). Serum total thyroxine, thyroid-stimulating hormone, free thyroxine, triiodothyronine autoantibody, and thyroxine autoantibody concentrations and results of an ACTH stimulation test were within reference intervals.On examination, the dog was laterally recumbent with dull mentation and decreased responsiveness to external stimuli. In response to strong external stimuli, the dog could be roused to briefly ambulate. Mucous membranes were injected and tacky; 5-7% dehydration was estimated, and severe hypotension (60/43 mm Hg) a was detected. Submandibular and popliteal lymph nodes were mildly enlarged. Neurologic examination revealed abnormal mental status with dullness and disorientation. An absent menace response was detected in the left eye, with normal pupillary light reflexes and eyelid closure. Generalized weakness and proprioceptive ataxia were observed in all limbs, and were more pronounced on the left side. The neurologic lesion was localized to the right thalamocortex (diencephalon and telencephalon).Profound hypernatremia (193 mEq/L; RI 140-154 mEq/L) and hyperchloridemia (161 mEq/L; RI 104-119 mEq/L) with normokalemia (4.4 mEq/L; RI 3.8-5.4 mEq/L) were identified by serum electrolyte analysis. The serum was grossly lipemic, and biochemical abnormalities included mild hyperphosphatemia (6.1 mg/ dL; RI 2.8-5.7 mg/dL), hypermagnesemia (2.9 mg/dL; RI 1.7-2.4 mg/dL), hyperproteinemia (8.9 g/dL; RI 5.5-7.4 g/dL), hyperglobulinemia (5.2 g/dL; RI 2.1-4.2 g/ dL), and mildly increased urea concentration (71 mg/dL; RI 21-54 mg/dL) and alkaline phosphatase activity (181U/L; RI 22-143 U/L) with marked hypercholesterolemia (820 mg/dL; RI 139-394 mg/dL) and hypertri-

show abstract

Management of Dehydration

Allen-Durrance

Campos

2018

Textbook of Small Animal Emergency Medicine

View full text Add to dashboard Cite

Hypernatremia and Hypertonic Syndromes

Cited by 17 publications

References 8 publications

Successful treatment of severe salt intoxication in a dog

Successful treatment of severe salt intoxication in a dog

Hypernatremia and Hyperlipidemia in a Dog with Central Nervous System Lymphosarcoma

Management of Dehydration

Contact Info

Product

Resources

About