Hyponatraemia in acute brain disease

Kroll, Maja; Juhler, Marianne; Lindholm, Jörgen

doi:10.1111/j.1365-2796.1992.tb00588.x

Cited by 43 publications

(16 citation statements)

References 63 publications

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“…Natriuretic peptides and intrinsic renal mechanisms counter-regulate weight gain associated with prolonged AVP-receptor activation [38], and an abrupt increase in urine sodium excretion coincident with antidiuresis represents a precarious clinical state in patients with MSD. Hyponatremia and critical brain edema can evolve rapidly in this setting [40].…”

Section: Pathophysiologymentioning

confidence: 99%

Branched-chain ketoacyl dehydrogenase deficiency: Maple syrup disease

Strauss

Morton²

2003

Curr Treat Options Neurol

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Classic maple syrup disease can be managed to allow a benign neonatal course, normal growth, and low hospitalization rates. The majority of affected infants that are prospectively managed have good neurodevelopmental outcome; however, acute metabolic intoxication and neurologic deterioration can develop rapidly at any age. Each episode is associated with a risk for cerebral edema, cerebrovascular compromise, and brain herniation. High plasma leucine and, possibly, alpha-ketoisocaproate are the principal neurotoxins in maple syrup disease. Plasma levels rise rapidly in association with net protein catabolism provoked by common infections and injuries. Transient periods of maple syrup disease encephalopathy appear fully reversible, leaving no clinically detectable neurologic sequelae. In contrast, prolonged amino acid imbalance, particularly if occurring during the critical period of brain development, leads to neuronal hypoplasia, a paucity of synapses, and undermyelination. Stagnated maturation and inadequate nutritional maintenance of brain structure have lifelong neurologic and behavioral consequences. Core elements of effective long-term therapy include screening and identification of asymptomatic newborns, frequent plasma amino acid monitoring, careful attention to branched-chain amino acid nurtriture, prevention of cerebral essential amino acid deficiencies, adequate provision of essential omega-3 class fatty acids and micronutrients deficient in commercial formulas, methods for home monitoring of metabolic control, and a commitment to lifelong therapy. Recognizing the risk for acute leucine intoxication depends on anticipating effects of common childhood infection and physiologic stresses on whole body protein turnover. Successful management of metabolic decompensation is based on the use of home sick-day regimens, rapid availability of branched-chain amino acid-free hyperalimentation solutions for hospitalized children, prevention of hyponatremia in patients with leucinosis, and frequent adjustments of intravenous therapies guided by plasma amino acid levels and indices of metabolic and clinical response.

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Section: Pathophysiologymentioning

confidence: 99%

Branched-chain ketoacyl dehydrogenase deficiency: Maple syrup disease

Strauss

Morton²

2003

Curr Treat Options Neurol

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“…63 Many studies support the concept that delayed hyponatremia following transsphenoidal surgery is based on an adrenocortical insufficiency. 22,39 Secondary adrenal insufficiency may indeed be the causative factor behind the SIADH-like syndrome because cortisol has been shown to be an inhibitor of vasopressin secretion.…”

mentioning

confidence: 99%

Hyponatremia in the neurosurgical patient: diagnosis and management

Cole¹,

Gottfried²,

Liu³

et al. 2004

FOC

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Hyponatremia is frequently encountered in patients who have undergone neurosurgery for intracranial processes. Making an accurate diagnosis between the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) and cerebral salt wasting (CSW) in patients in whom hyponatremia develops is important because treatment differs greatly between the conditions. The SIADH is a volume-expanded condition, whereas CSW is a volume-contracted state that involves renal loss of sodium. Treatment for patients with SIADH is fluid restriction and treatment for patients with CSW is generally salt and water replacement. In this review, the authors discuss the differential diagnosis of hyponatremia, distinguish SIADH from CSW, and highlight the diagnosis and management of hyponatremia, which is commonly encountered in patients who have undergone neurosurgery, specifically those with traumatic brain injury, aneurysmal subarachnoid hemorrhage, recent transsphenoidal surgery for pituitary tumors, and postoperative cranial vault reconstruction for craniosynostosis.

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“…Although tuberculosis is considered a cause of the syndrome of inappropriate antidiuretic hormone secretion (SIADH), circulating vasopressin has been documented in only a few cases. 15,16,17,18 SIADH is a volume-expanded state because of antidiuretic hormone-mediated renal water retention. CSW is characterized by a contracted effective arterial blood volume resulting from renal salt wasting.…”

Section: Resultmentioning

confidence: 99%