الفهرس 
About the Electrolytes under study
Sympathetic Nervous SystemOnly 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.