Disorders of water balance are common in neurosurgical patients and usually manifest as hypo- or hypernatremia. They are most commonly seen after subarachnoid hemorrhage, traumatic brain injury, with intracranial tumors, and after pituitary surgery.
We reviewed the experience of endocrine evaluation and management of disorders of salt and water balance in a large cohort of inpatients attending the national neurosciences referral centre in Dublin, Ireland, and compared this experience with findings from other studies.
The study group included unselected neurosurgical patients admitted to our centre and requiring endocrine evaluation.
We conducted investigations to determine the underlying mechanistic basis for disorders of salt and water balance in neurosurgical patients and treatment to restore normal metabolism.
Morbidity and mortality associated with deranged salt and water balance were measured.
The underlying pathophysiology of disordered water balance in neurosurgical patients is complex and varied and dictates the optimal therapeutic approach.
A systematic and well-informed approach is needed to properly diagnose and manage disorders of salt and water balance in neurosurgical patients.
"L'incidence de ce trouble est de 3–10 % chez les patients de ré animation polyvalente et est associé a ` un risque accru de dé cè s et de complications  . Cette incidence est de 10–50 % chez le patient cé ré brolé sé en raison de mé canismes propres a ` la lé sion cé ré brale, notamment une perte de la sensation de soif et un diabè te insipide central, mais aussi de l'utilisation de l'osmothé rapie pour traiter une hypertension intracrânienne (HTIC)  . L'objectif de ce travail est de rappeler les grands principes de ré gulation de l'eau et du sel dans l'organisme, d'analyser les causes et consé quences de l'hypernatré mie, pour ré pondre a ` la question de l'utilité ou du danger de l'hypernatré mie chez le patient cé ré brolé sé . "
[Show abstract][Hide abstract] ABSTRACT: Hypernatremia is defined by a serum sodium concentration of more than 145 mmol/L and reflects a disturbance of the regulation between water and sodium. The high incidence of hypernatremia in patients with severe brain injury is due various causes including poor thirst, diabetes insipidus, iatrogenic sodium administration, and primary hyperaldosteronism. Hypernatremia in the intensive care unit is independently associated with increased mortality and complications rates. Because of the rapid brain adaptation to extracellular hypertonicity, sustained hypernatremia exposes the patient to an exacerbation of brain edema during attempt to normalize natremia. Like serum glucose, serum sodium concentration must be tightly monitored in the intensive care unit.
Annales francaises d'anesthesie et de reanimation 06/2014; DOI:10.1016/j.annfar.2014.05.006 · 0.84 Impact Factor
"Therefore, mechanical or neuroinflammatory damage to these regions or the pituitary stalk can inhibit the body's osmotic balance, thus causing post-traumatic DI    . Reports suggest that disruption of blood flow to these hypothalamic osmoreceptor cells disrupts water homeostasis in the body . Irreversible damage can result in permanent DI . "
[Show abstract][Hide abstract] ABSTRACT: Each year, over one million people in the United States are affected by traumatic brain injury (TBI). Symptoms of both acute and chronic neuroinflammation follow TBI, coinciding with a robust immune response and activation of the brain's endogenous repair mechanisms. TBI can lead to endocrine failure as a result of damage to the thalamic region of the brain, evidenced by excessive thirst and polyuria often accompanying TBI. These symptoms indicate the presence of diabetes insipidus (DI), a disruption of water homeostasis due to antidiuretic hormone deficiency. This deficiency accompanies a mechanical or neuroinflammatory damage to the thalamic region during TBI, evidenced by increased expression of inflammatory microglial marker MHCII in this brain region. Excessive thirst and urinations, which are typical DI symptoms, in our chronic TBI rats also suggest a close connection between TBI and DI. We seek to bridge this gap between TBI and DI through investigation of the Cluster of Differentiation 36 (CD36) receptor. This receptor is associated with Low-Density Lipoprotein (LDL) deregulation, pro-inflammatory events, and innate immunity regulation. We posit that CD36 exacerbates TBI through immune activation and subsequent neuroinflammation. Indeed, scientific evidence already supports pathological interaction of CD36 in other neurological disorders including stroke and Alzheimer's disease. We propose that DI contributes to TBI pathology via CD36 neuroinflammation. Use of CD36 as a biomarker may provide insights into treatment and disease pathology of TBI and DI. This unexplored avenue of research holds potential for a better understanding and treatment of TBI and DI.
Medical Hypotheses 08/2013; 81(5). DOI:10.1016/j.mehy.2013.08.022 · 1.07 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Thyroid hormone is central to normal development and metabolism. Abnormalities in thyroid function in North America often arise from autoimmune diseases, but they rarely present as critical illness. Severe deficiency or excess of thyroid hormone both represent life-threatening disease, which must be treated expeditiously and thoroughly. Such deficiencies must be considered, because presentation may be nonspecific.
Critical care clinics 04/2013; 29(2):335-58. DOI:10.1016/j.ccc.2012.11.006 · 2.16 Impact Factor
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.