View clinical trials related to Hypernatremia.
Filter by:The purpose of this study is to estimate the effect of an early induced hypernatremia protocol (150-155 milliequivalent/L) versus normonatremia plus mannitol (135 - 145 milliequivalent/L) in terms of neurologic outcome in patients with severe traumatic brain injury managed at critical care unit.
Patients who are on mechanical ventilation in an intensive care unit often require diursis as part of their pre-extubation regimen. The drug of choice for diuresis has traditionally been furosemide. However, this drug cause hypernatremia (a rise in serum sodium) in a significant proportion of patients. Hypernatremia is traditionally treated by providing free water supplementation to the patient. This strategy creates a vicious and unproductive cycle of giving free water, and then diuresing it off. We propose a strategy for breaking this cycle by using a second diuretic-- metolazone-- which has a tendency to rid the body of more sodium, thereby minimizing hypernatremia.
Cerebral edema is seen heterogenous group of neurological disease states that mainly fall under the categories of metabolic, infectious, neoplasia, cerebrovascular, and traumatic brain injury disease states. Regardless of the driving force, cerebral edema is defined as the accumulation of fluid in the brain's intracellular and extracellular spaces. This occurs secondary to alterations in the complex interplay between four distinct fluid compartments within the cranium. In any human cranium; fluid is contained in the blood, the cerebrospinal fluid, interstitial fluid of the brain parenchyma, and the intracellular fluid of the neurons and glia. Fluid movement occurs normally between these compartments and depends on specific concentrations of solutes (such as sodium) and water. In brain-injured states, the normal regulation of this process is disturbed and cerebral edema can develop. Cerebral edema leads to increased intracranial pressure and mortality secondary to brain tissue compression, given the confines of the fixed-volume cranium. Additionally, secondary neuronal dysfunction or death can occur at the cellular level secondary to the disruption of ion gradients that control metabolism and function. While studies utilizing bolus dosing of hyperosmolar therapy to target signs or symptoms of increased intracranial pressure secondary to cerebral edema are numerous, there is a paucity of studies relating to continuous infusion of hyperosmolar therapy for targeted sustained hypernatremia for the prevention and treatment of cerebral edema. The investigators hypothesize that induced, sustained hypernatremia following traumatic brain injury will decrease the rate of cerebral edema formation and improve patient outcomes.
Hypo- and hypernatremia are the most frequent electrolyte disorders found in hospitalized patients. The increasing use of diuretics and other medications influencing the water and sodium homeostasis potentially lead to a rise in the prevalence of the electrolyte disorders. Only little data is available on the frequency and the mechanisms leading to hypo-/hypernatremia. Thus, the investigators aim to A.) determine the frequency of hypo- and hypernatremia in the emergency department of a large tertiary university hospital and B.) explore the mechanisms leading to the development of dysnatremias by detailed clinical and laboratory examinations.