Excessive Hypernatremia and Hyperosmolality Associated with Germinoma in the Hypothalamic and Pituitary Region

Zazgórnik, J; Jellinger, K.; Waldhäusl, W.; Schmidt, Philip H

doi:10.1159/000114603

Cited by 15 publications

(5 citation statements)

References 5 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Namely,(1) if hypernatrmeia was caused by hypodipsia and consequent reduced fluid intake, it could not be reversed by forced high fluid intake (Avioli et al, 1962;Kastin et al, (1965;deRubertis et al, 1971;Alford et al, 1973;Zazgornik et al, 1974;Shaad et al, 1979;avRaskin et al, 1981);(2) the measured blood or plasma volume of some patients with this syndrome was more or less reduced (Kastin et al, 1965;Goldberg et al, 1967;deRubertis et al, 1971;Vajjajiva et al, 1979;Luciani et al, 1980); (3) the blood pressure was borderline low (Vajjajiva et al, 1969;Zazgornik et al, 1974;Brezis and Weiler-Ravall, 1980;Luciani et al, 1980;Rosansky and Nidus, 1981;avRaskin et al, 1981;(4) the plasma renin activity (PRA) was increased and dissociated from the plasma aldosterone concentration (PAC) (Alford et al, 1973;Nichelli et al, 1982;Inoue et al, 1985); (5) if AVP secretion is mainly regulated by a volume-dependent mechanism, a certain degree of hypovolemia must exist, for reduction of the blood volume by more than 10% is needed in order to experimentally elicit a sufficient increase in plasma AVP (Goetz et al, 1974;Kimura et al, 1976).…”

mentioning

confidence: 99%

Pathogenesis of Extracellular Fluid Abnormalities of Hypothalamic Hypodipsia-Hypernatremia Syndrome.

et al. 1988

View full text Add to dashboard Cite

A 26-year-old man with hypothalamic hypodipsia-hypernatremia syndrome is reported, who presented with adipsia, hypernatremia, and impaired osmolalitymediated arginine vassopressin (AVP) secretion. A chorionic gonadotropinsecreting tumor was detected in the anterior hypothalamus and treated with external irradiation.After the treatment, hypernatremia persisted and was not corrected by fluid loading, osmolality-mediated AVP secretion remained impaired. Despite the absence of signs of hydropenia, hypovolemia was suggested by low blood pressure and elevated plasma indices of the renin-angiotensin system, and supported by blood volume determination.The plasma aldosterone concentrations were inappropriately low for the renin-angiotensin status. The plasma atrial natriuretic polypeptide (ANP) level was normal in spite of hypovolemia and increased more than double after fluid loading.Hypernatremia, primarily caused by hypodipsia and impaired osmolality-mediated AVP secretion, secondarily sustained ANP secretion and suppressed aldosterone release, which conceivably contributed to the development and perpetuation of hypovolemia in this patient.

show abstract

mentioning

confidence: 99%

Pathogenesis of Extracellular Fluid Abnormalities of Hypothalamic Hypodipsia-Hypernatremia Syndrome.

et al. 1988

View full text Add to dashboard Cite

show abstract

“…When essential hypernatremia is associated with loss of osmoregulation of both thirst and ADH release but with preservation of baroreceptor mediated ADH release, it is usually due to destruction of the osmoreceptors, rather than a resetting of their threshold [37][38][39][40][41][42]. Hypothalamic damage or tumors and association with other endocrine or structural brain abnormalities are commonly found [37,[43][44][45][46][47][48][49][50][51][52]. Essential hypernatremia without an associated structural lesion of the hypothalamus is very rare.…”

Section: Essential Hypernatremiamentioning

confidence: 99%

Hypernatremia in children

Narchi

2016

J Pediatr Biochem

View full text Add to dashboard Cite

Hypernatremia results from a deficit of total body water in relation to the total body's sodium stores. This is caused by two main mechanisms: 1) net water depletion exceeding sodium losses or 2) increased sodium gain exceeding water gain. Net water depletion occurs when increased water loss exceeds sodium loss, either due to extrarenal losses (increased evaporative water losses, hypernatremic dehydration caused by diarrhea) or to renal losses (central and nephrogenic diabetes insipidus, intrinsic renal disease). Insufficient water intake occurs with neonatal hypernatremic dehydration secondary to lactation failure, essential hypernatremia or osmoreceptor dysfunction. Increased sodium gain can be caused by iatrogenic hypernatremia, administration of concentrated infant formula, deliberate abusive water restriction and deliberate or non-accidental salt poisoning. Hypernatremia results in a movement of water across cell membranes from the intracellular to the extracellular space, resulting in cellular dehydration, which, in cells of the central nervous system results in brain shrinkage leading to tearing of cerebral blood vessels and neurological complications. As a protective mechanism, idiogenic osmoles accumulate inside the brain cells to help them retain water intracellularly. However this may lead to cerebral edema during rapid rehydration as these idiogenic osmoles attract water inside the neurons. As the appropriate management of hypernatremia invariably depends on the underlying mechanism and cause, a methodical history taking and clinical examination, with the judicious use of laboratory tests will lead to a precise etiological diagnosis to enable appropriate and timely therapy.

show abstract

“…31 In surgeries for removal of craniopharyngiomas there might be diabetes insipidus if part of the pituitary gland is not preserved, which could produce severe and hard-to-control cases. 34 Clinical signs are also associated with the movement of water through the brain, which could cause intracranial hemorrhage due to the rupture of veins of the dura mater and venous sinus. Exogenous desmopressin (DDAVP) should be used and sodium correction should not exceed 10 mosm/l/24 hour.…”

Section: Hypernatremiamentioning

confidence: 99%

Suporte de terapia intensiva no paciente oncológico

Sapolnik¹

2003

J. Pediatr. (Rio J.)

View full text Add to dashboard Cite

Objective: To review the most important aspects of the clinical presentation and treatment of children with cancer in intensive care units. Medline (1970Medline ( to 2003; search terms: children, cancer, oncology, intensive care, complications. General and pediatric oncology textbooks. Sources of data: Summary of the findings:Practically all organs may be affected by cancer or by its treatment. The main complications include infections, hematological problems and electrolyte/ metabolic disturbances. Intensive care therapy is necessary to correct organic dysfunctions (cardiovascular, respiratory, renal, gastrointestinal, and neurologic). Nutritional and emotional support, as well as pain control are fundamental aspects for recovery in children. The intensivist should be alert to interrupt intensive care measures if required. Conclusions:Many studies show that the use of intensive care therapy in children with cancer is not futile, with a reduction in mortality and improvement in the quality of life of these children in the medium and long terms.

show abstract

Excessive Hypernatremia and Hyperosmolality Associated with Germinoma in the Hypothalamic and Pituitary Region

Cited by 15 publications

References 5 publications

Pathogenesis of Extracellular Fluid Abnormalities of Hypothalamic Hypodipsia-Hypernatremia Syndrome.

Pathogenesis of Extracellular Fluid Abnormalities of Hypothalamic Hypodipsia-Hypernatremia Syndrome.

Hypernatremia in children

Suporte de terapia intensiva no paciente oncológico

Contact Info

Product

Resources

About