الفهرس 
: causes & pathophysiology of electrolyteOnly 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.
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.
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.
Hypomagnesemia is reported in as many as 65% of patients in ICU’s. Because magnesium depletion may not be accompanied by hypomagnesemia, the incidence of magnesium depletion is probably higher. In fact, magnesium depletion has been described as “the most underdiagnosed electrolyte abnormality incurrent medical practice”.
The neurologic manifestations of magnesium deficiency include altered mentation, generalized seizures, tremors, and hyperreflexia. All are uncommon. The serum Mg level is an insensitive marker of magnesium depletion. When magnesium depletion is due to nonrenal factors (e.g., diarrhea), the urinary magnesium excretion is a more sensitive test for magnesium depletion.
The serum Mg can be normal in patients who are magnesium depleted. Magnesium depletion should be suspected in any patient with diuretic-induced hypokalemia, and especially when hypokalemia is refractory to potassium replacement.
Magnesium replacement will correct the serum Mg before total body stores of magnesium are replenished. The best indicator of magnesium repletion is the urinary retention test.
Hypercalcemia is an abnormality of the balance between different body compartments and can result from increased bone resorption, decreased renal excretion, increased GI absorption, or any combination of these mechanisms.
The signs and symptoms of hypercalcemiacan be divided into mental, neurologic, musculoskeletal, GI, urologic, and cardiovascular.
The mental manifestations of hypercalcemia include stupor, obtundation, apathy, lethargy, confusion, disorientation, and Coma. In general, for a given level of hypercalcemia, older patients exhibit more of the mental signs than younger patients.
The neurologic and musculoskeletal effects of hypercalcemia are reduced muscle tone and strength, myalgias, and decreased deep tendon re exes. The GI and urologic signs are vomiting, constipation, polyuria, and polydipsia. The major cardiovascular effect of hypercalcemia, which the intensive care physician must address, is shortening of the QT interval. In the presence of ventricular ectopic beats, the calcium-induced shortening of the QT interval increases the potential for fatal arrhythmias or asystole.
The aim of treatment of hypercalcemia is to minimize its effects on central nervous system (CNS), renal, and cardiovascular function. Appropriate treatment of hypercalcemia depends, in part, on the cause. General concepts in themanagement involve attempts to increase renal calcium clearance, decrease boneresorption, and decrease intestinal calcium absorption.
To this end, it is critical that the pathophysiology of the disease process be understood.