الفهرس 
HypernatremiaOnly 14 pages are availabe for public view
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Abstract
Sodium disturbances (dysnatremias) are considered a common problem in adult patients admitted to hospital and intensive care units (ICU). In fact, the majority of these abnormalities develop after the patient is admitted to the ICU because of their incapacitation, lack of access to free water, reliance on intravenous fluid and nutritional support, and the usually serious nature of their underlying disease which often leads to impaired renal water handling, so patients in the ICU are at high risk of developing sodium disturbances.
The osmoreceptor-ADH system, the thirst mechanism and angiotensin II and aldosterone system are the main systems responsible for regulation of sodium concentration and ECF osmolarity.
Hyponatremia is defined as a serum sodium concentration of less than 135 mEq/L. The precise incidence of hyponatremia varies depending on the conditions underlying it.
Hyponatremic disorders are divided into euvolemic, hypovolemic and hypervolemic. Several causes can lead to hyponatremia the most common are: use of diuretics, extrarenal loss such as vomiting and diarrhea, SIADH and hypothyroidism.
CNS is the most affected system from hyponatremia. Symptoms may be mild in from of headache, nausea, lethargy and confusion, or may be severe in the form of hemiparesis, seizures, hallucinations, tremors, coma and even cardiac arrest.
Management of hyponatremia includes reversible of CNS symptoms by using of hypertonic saline in a slow rate to avoid harmful complications. The second step in the management is treating the underlying cause.
Hypernatremia is a disorder of water metabolism and is usually defined as a plasma sodium concentration above 145 mEq/L.
Hypernatremia is particularly common in critically ill patients, but there are no prospective data available on the prevalence of hypernatremia in intensive care unit (ICU).
The origin of hypernatremia requires several factors to develop in ICU patients such as: the administration of hypertonic sodium bicarbonate solutions; renal water loss through a concentrating defect from renal disease or the use of diuretics or solute diuresis from glucose or urea in patients on high protein feeds or in a hypercatabolic state; gastrointestinal fluid losses through nasogastric suction and lactulose administration, and water losses through fever, drainages, and open wounds. Thus, most etiologies of hypernatremia involve states of impaired water access in conjunction with excessive free water losses.
Clinical effects of hypernatremia result from plasma hyperosmolarity, leading to intracellular dehydration and decrease in cell volume, particularly in brain cells, producing shrinking of brain size. This may predispose to vascular stretching and subsequent rupture of meningeal vessels with potential risk of cerebral or subarachnoid hemorrhage and neurological deficit such as convulsions and even cardiac arrest.
Treatment of hypernatremia involve identification of underlying cause of ongoing fluid loss and replacement of fluid lost by a certain rate to prevent brain cell edema and further neurological consequences