Fluid and Electrolyte Disturbances In Children

Tatty Ermin Setiati

Department of Pediatric Medical Faculty
Diponegoro University Dr. Kariadi Hospital - Semarang
Introduction
Deranged fluid and electrolyte homeostasis commonly afflicts children in the Pediatric
intensive care unit (PICU). The cause of this condition: Kidney disorder, primary derangement as
in hypernatremic dehydration, hyponatremic dehydration, non-renal problems as in
chemotherapy of solid tumor, as well as hyponatremia in inappropriate anti diuretic hormone
syndrome (SIADH).
There are factors that influencing water and electrolyte movement and caused
disturbances in the equilibrium of water and electrolyte between intravascular and interstitial
compartment.
Many clinical circumstances will combine several of these abnormalities. For example,
acute renal failure due to illness (sepsis or postsurgical) often involves water intoxication,
hyponatremia, hyperkalemia, hypocalcemia, or acidosis. Children with multiorgan failure (MOF)
present more complicated management challenges which may be additive in their effects
(hypocalcemia and hyperkalemia) or even offset each other (severe vomiting with loss of acid
and potassium in the face of severe renal failure, which generates acidosis and hyperkalemia). 1-3
A basis of pathophysiology is essential to applying the principals of practice and management.1-3
Water Anatomy and distribution
There are important contrasts in water anatomy in the infant and the adult. The
extracellular fluid (ECF) constuitutes a higher fraction of body weight in infants than in adults
and highlight the higher (three times) body water turnover in infants, compares with adults. 4,5
(table 1) Thus dehydration is more common and more serious in children with high mortality.
The net maintenance fluid requirement is approximately 1500/ml/m 2/24 hr in healthy, non-febrile
child 6

Table 1. Body water (as percentage of total body weight)

Water anatomy
Total Body Water
Extracellular fluid
Intravascular fluid
Intracellular fluid
Turnover rateExtracellular fluid

Infants ( % )
70-80
35-45
5
30

Adult ( % )
60
15
5
40

50 per 24 hr

15 per 24 hr

Serum Osmolality
Normal serum osmolality is approximately 272-300 mOsm/L. Sodium (Na) is the major
intravascular ion that influence serum osmolality. However if the serum glucose concentration or
blood urea nitrogen (BUN) is extremely high (such as in diabetic ketoacidosis), these can also
influence serum osmolality.7 Serum osmolality can be estimated using the following formula:
2 x sodium concentrate (mEq/L) =A + glucose concentrate (mg/dl) = B + BUN (mg/dl) = C
18

2.8

A + B + C = Total approximate serum osmolality (mOsm/L)

If the serum glucose concentration and BUN are not elevated, serum osmolality can be
quickly estimated by doubling the serum concentration and adding 20. This formula is not
accurate in the presence of hyperlipidemia
Factors Influencing Water Movement
Under normal condition, free water, electrolytes, and osmolality are equilibrated across
the vascular membrane between the intravascular and interstitial spaces. 7 Acute changes in the
osmolality of the cellular, vascular, or interstitial fluid compartment will result in an acute free
water shift until osmolality is equalized. The most compelling fluid shift will occur to restore
equal osmolality across the vascular membrane, between the intravascular and interstitial
spaces.7
Any condition that produces an acute change in serum osmolality will create an acute
osmotic gradient across the vascular membrane, and free water will shift from the compartment
of lower osmolality to the compartment of higher osmolality until osmolality is equalized.
If intravascular osmolality acutely decreases (e.g. the serum sodium concentration falls
acutely or hyperglycemia is rapidly corrected), free water will shift out of vascular space to the

interstitial space until osmolality in this two compartments is again equal. Fluid shift into the
interstitial space may result in cerebral edema. (Fig.1)
If intravascular osmolality acutely increases (e.g. the serum sodium concentration rises
acutely or the serum glucose concentration increases to very high levels), free water will shift
into intravascular space from the interstitial space. Significant fluid shift from the interstitial
space to the vascular space may produce intracranial hemorrhage. (Fig 1)
Any acute shift into or out of brain tissue may result in tearing of cerebral bridging vein,
producing intracranial hemorrhage or a neurologic condition known as acute pontine
myelinolysis. In addition fluid shift out of the vascular space may produce cerebral edema. The
brain tissue contains no lymphatic to carry edema fluid back inton circulation; thus cerebral
edema may produce increase intracranial pressure (ICP).

Figure 1. Distribution of Total Body Water

Postoperative Water Distribution and Balance
Body fluid composition and distribution is altered postoperatively, secondary to secretion
of antidiuretic hormone (ADH) and aldosteron. ADH and aldosteron are secreted in response to
stimuli such as catecholamine release, hypotension, and pain. As a result, there may be a
decrease in urine output and an increase in urine concentration with fluid retention and
hemodilution.

Postoperative fluid administration should be determined by the type of fluid lost and the
adjustments in sodium and water balance necessary:

Gastrointestinal fluids are replaced with 0.45% NaCl

Urine and insensible losses are replaced with 5% or 10% dextrose solution containing 0.2%
or 0.45% NaCl.
Dextrose and water solution are generally avoided during the postoperative period, since

the postoperative patient may be prone to stress and ADH or aldosteron secretion, as well as
sodium and water retention.
Urine output should be closely monitored. If fluid administration is adequate, urine
volume should exceed 1ml/kg/hr. Fluid administration may be limited in the presence of
respiratory, cardiac, or renal failure or if the child is at risk for the development of increase ICP
or SIADH. In these situation (when fluid intake is limited), a urine output of 0.5 to 1 ml/kg/hr
may be acceptable.
Urine osmolality is a better indicator of renal function than urine specific gravity. Normal
urine osmolality is approximately 300 mOsm/l. If renal function is good, the urine plasma
osmolality ratio should be 1.1: 1 or higher. Urine osmolality should always be higher than
plasma osmolality. If renal function is poor, urine and plasma osmolality are often equal.
Common Clinical Conditions
Dehydration
Etiology/Pathophysiology
Dehydration occurs when the total output of all fluids and electrolytes exceeds the total
fluid and electrolyte intake. This may result from inadequate fluid intake or excess fluid loss.
Dehydration produces a deficiency in both fluids and electrolyte.
Vomiting and diarrhea not only produce large fluid loss, but also produce a significant
loss of sodium, chloride, hydrogen, and bicarbonate ions.
Clinical Presentation
Dehydration is classified in two ways: by the severity of the fluid deficit and by the
serum osmolality. Initially the severity of the dehydration is estimated from the patients clinical
appearance. Then, when the serum sodium concentration is available from the laboratory, the
dehydration is classified by osmolality, and adjustment is made, if needed, in the estimation of
dehydration severity.

Initial Assessment of Clinical Severity

Clinical severity is determined initially by the effect of dehydration on clinical
appearance and cardiovascular function. (table 2) The serum sodium concentration is assumed to
be normal
Table 2. Effect of isotonic, hypotonic, and hypertonic dehydration on clinical appearance and
cardiovascular function
Clinical

Mild

Moderate

Severe

Parameters
Isotonic
Dehydration
Body Weight loss
Infant
Adult
Skin turgor
Fontanelle
Mucous membranes
Skin perfusion
Heart rate
Peripheral pulses
Blood pressure
Sensorium
Urine output
Azotemia

5% (50ml/kg)
3% (30ml/kg)
Slightly
Flat / depressed
Dry
Warm,normal color

10% (100ml/kg )
6% ( 60ml/kg)

Depressed
Very dry
Extremitas
cool,

15% (150ml/kg )
9% ( 90 ml/kg )

Severely depressed
Parched
Extremitas cold

Mild tachycardia
Normal
Normal
N / Irritable
Slightly

pale color
Mod. tachycardia
Diminished
Normal
Irritable/lethargic
Mild oliguria

Mottled, gray color

Extreme tachycardia
Absent
Reduced
Unresponsive
Marked oliguria or

Present

anuria
Severe

Absent

Modification of Assessment Based on Serum Sodium and Osmolality

Hypotonic

Those above signs These

dehydration

are associated with associated

(Serum sodium<130

hypotonic

mod.hypotonic

meq/l

(hyponatremic)

dehydration

dehydration

signs

are
with
and

and moderate vol.deficit:

mild vol deficit : 100ml/kg in infants

Hypertonic

These

signs

dehydration (Serum associated

sodium>150meq/l)

mod.

50ml/kg in infants
are These signs are
with associated

Hypertonic severe

dehydration
(100ml/kg

hypertonic

and dehydration

mod.vol.deficit

severe

with
and
volume

in deficit (150ml/kg in

infants)

infants)

Modified from Hazinski MF: Nursing care of the critically ill child,2nd ed, St Louis Mosby 1992

Management of Dehydration (general guidelines)

The goals of treatment of dehydration include:

Restoration and maintenance of intravascular volume and systemic perfusion

Replacement of the volume and electrolyte deficit,as well as any ongoing losses

Provision of maintenance fluid requirements

Shock Resuscitation: If shock present, volume resuscitation is provided with normal

saline or lactate Ringers solution in boluses 20ml/kg until systemic perfusion is adequate. Bolus
administration of fluid must be discontinued once systemic perfusion has been restored. This is
especially for hypernatremic dehydration. Once systemic perfusion is adequate, the fluid volume
deficit is calculated and replaced over the appropriate time period (24-48 hours), while
maintenance fluid requirements are provided and ongoing fluid losses are replaced.
Supportive therapy: Assessment and support of cardiovascular, neurologic, and
respiratory status; evaluation and support of electrolyte and acid base balance; maintenance of
temperature; monitoring of weight;monitoring of serum glucose concentration and continous
source of glucose intake if hypoglycemia is detected.
Isotonic Dehydration
Isotonic dehydration: Serum sodium concentration is approximately 130-150 mEq/l. Loss
of fluid is proportional to the loss of sodium, thus the serum sodium concentration is normal, and
fluid loss from all body compartment is proportional.
Hypernatremic Dehydration
Definition: Hypernatremia is defined as a serum sodium level 150meq/l. In
hypernatremic dehydration there is a deficit of free water.
Clinical Signs of Hypernatremic Dehydration

When hypertonic dehydration is present, fluid loss has occurred predominantly from the
extravascular space.
If dehydration reaches the level of 8-10% of body weight loss, predictable symptoms
result. Shock is unusual because plasma water and circulation are relatively spared by the
pathophysiology of hypernatremic dehydration. Skin turgor has a characteristic doughy feel,
evident where the skin is loose over the abdomen or forehead.

8, 9

The patients presents with

irritability and high pitch cry, unusual somnolence alternating with irritability.10With progression
of the hypernatremia, the CNS disturbances become more evident, with increasing somnolence,
seizures, and coma. As the sodium rises above 160 meq/l, irritability and tremulousness occur. If
the sodium rises between 180-200 meq/l the progression to coma and death is likely.
In half of the children with serum sodium > 155meq/l, hyperglycemia occurs. This
problem correct spontaneously with resolution of the hypernatremia. The slow metabolism og the
glucose provides a continuous release of free water and is helpful. Hypocalcemia also occurs
commonly with hypernatremia and tends to resolve with treatment.
Goal of therapy
Major goals of therapy are restoration of adequate perfusion and prevention of a
precipitous fall in the serum sodium concentration. Bolus fluid therapy is administered if needed
to restore systemic perfusion.
Management
If dehydration is severe, plasma volume replacement takes priority regardless of serum
sodium. Normal saline/Lactate ringer (bolus infusion 20 ml/kg) are appropriate. Repeated as
needed.11
Estimated volume deficit replacement
Replacement is gradual over 48 hours, with 50% replaced within the initial 24 hours and the
remaining 50% replaced within the next 24 hours.
Estimate of water deficit
50 ml/kg if serumNa +

= 150 mEq/l

90 ml/kg if serum Na+

= 160 mEq/l

140 ml/kg if serum Na+

= 170 mEq/l

When perfusion is normal, infuse one-half normal saline until urin output is established.
Subsequent to this, hypovolemic patients require hypotonic fluid infusion (half normal saline),
adjusting the rate of infusion to allow a slow steady fall in serum sodiumconcentration
(10mmol/day or 10meq/day maximum) to prevent cerebral edema. Measure the sodium level
every 4 hours. Calculate the Free Water Deficit: Normal Body Water-Current Body Water
Normal Body Water = 0.6 x Body Weight (kg)
Current Body Water = 0.6 x Body Weight (kg) x Normal serum Na+ / Observed
Serum Na+
TBW deficit in hypernatremia = TBW ( 1 serum Na / 140 1)
TBW = body weight x 0.6
The approach to treatment of hypernatremic dehydration is in table 3
Table 3. Treatment of hypernatremic dehydration
Na > 175 mEq/l
Na+ 155-175 mEq/l
Shock +
1st hr
4th hrs
4 48 hrs

Dyalisis
5% Albumin 20 ml/kg
10-20 ml/kg RL
10 ml/kg RL or 0.5

NS

with

added

NaHCO3 (35mEq/l) per 4 hrs

Aim to decrease serum sodium 10 meq/ d

Indication of improvement
A positive response to rehydration will include improvement in systemic perfusion,
including an increased urine output and improved level of conciousness.
Hyponatremia ( Hypotonic ) Dehydration
When hypotonic dehydration is present, fluid loss has occurred predominantly from the
intravascular space; thus clinical signs will be significant even at a relatively small fluid volume
deficit. Remember that the severity of volume deficit estimated from initial clinical evaluation
should be reduced one level or degree (from severe to moderate or from moderate to mild) if the
serum sodium concentration is < 130 mEq/l
Goal of Therapy: Restoration of systemic perfusion and intravascular volume is the
priority.11 Bolus fluid therapy: Isotonic crystalloid (20ml/kg) bolus is repeated until systemic
perfusion is adequate. Estimated volume deficit replacement: Replacement is 50% within the

initial 8 hours, with the remaining 50% replaced within the next 16 hours. Replacement fluids
are provided in addition to calculated maintenance fluid requirements and replacement of any
ongoing losses. The replacement fluid of choice is usually 0.9% sodium chloride (contains 154
mEq/l Na +) or 0.45% sodium chloride (contain 77 mEq/l Na +). The sodium deficit is calculated
as follows:
Na+ deficit (in mEq) = (135 mEq/l patients serum Na +) x (0.55 x weight in kg).
The childs serum sodium concentration should rise no faster than 1-2 mEq/l/hr and the
total increment should not exceed 8 mEq/ 24 hr to prevent neurologic complications. Rapid fall
in serum sodium may cause seizures and cerebral edema, where as rapid rise in serum sodium
may cause intracranial hemorrhage or other complication.
If neurologic symptoms of hyponatremia develop (seizures, decrease level of
conciousness, cerebral edema, and increase ICP) or the serum sodium < 120 mEq/l, administer
3% saline (provide 0.513mEq Na +/ml) 3-5 ml/kg. This dose of 3% Saline will provide 1.5-2.5
mEq/kg of NaCl and should raise the serum sodium 3.5-4.5 mEq/l. Repeat administration of the
hypertonic saline should be given if neurologic symptoms persists or deficit is severe. Acute
therapy can be slowed when one of the following endpoints is achieved: 1. symptoms are
improved 2. a safe serum sodium level (120-125 mEq/l) is attained, or 3. the total increment
goal in serum sodium for that 24-hour period has been achieved.
The following is an example for calculating both the sodium deficit and the treatment dose:
1. Sodium deficit in a -10 kg child with a serum sodium of 115 would be:
10 kg x 0.6 x ( 20 mEq deficit ) = 120 mEq sodium (total deficit)
2. To raise serum Na+ by 5 mEq/l acutely requires: 5mEq x 0.6 x 10 = 30 mEq
3. Dose of 3% saline solution:
30 mEq Na at 0.513 mEq Na+/ml = 60 ml of 3% NaCl
Indication of improvement
If the child becomes more alert and systemic perfusion and urine output improve while
electrolyte balance are maintained or restored, therapy has been effective. In hyponatremia
caused by excess water and excess sodium, patients will present pulmonary edema, ascites, or
peripheral edema. Usually they suffer from one of three diseases: 1. Hypoproteinemia due to
nephritic syndrome or liver cirrhosis; 2. Congestive heart failure; 3. Acute and chronic renal
failure.

Treatments for these conditions are fluid restriction. Intensity of treatment must be
individualized based on underlying disease, chronicity of problem and acuteness of symptoms.
Syndrome of Inappropriate Anti Diuretic Hormone ( SIADH )
SIADH develops when ADH secreted in the absence of a physiologic stimulus. In fact,
ADH secretion continues despite a fall in serum sodium and osmolality. As a result water
retention produces a progressive fall in serum sodium and osmolality, whereas the urine
sodiumconcentration is high.
Clinical presentation
Symptomatic hyponatremia may develop with a serum sodium < 130 mEq/l if the drop of
sodium has been acute. If serum sodium falls gradually (e.g. with the development of adrenal
insufficiency), symptoms may not develop despite a very low serum sodium concentration.
Clinical signs of hyponatremia : seizures, abdominal cramps, anorexia, nausea, and diarrhea.
Clinical signs of SIADH: serum hyponatremia, a low serum osmolality, high urine
excretion of sodium and high urine osmolality, normal renal function, normal adrenal function,
and decrease urine output. 12,13,14
SIADH should be suspected in patients at risk, particularly following head injury,
meningitis, and neurosurgery.
Management
The major treatment for hyponatremia is the treatment of the cause, and supportive care.
Elimination of excess intravascular water or increase sodium administration is required.
If neurologic symptoms develop:
1. Saline administration: Hypertonic saline 3% 3-5 ml/kg will provide approximately 1.5-2.5
mEq sodium/kg. To raise serum sodium concentration 5 mEq/l a total dose of approximately
6 ml/kg will be required.
2. Diuresis: Furosemide 1-2 mg/kg
3. Fluid restriction 30-70% of the calculated normal total intake
Potassium
Potassium disorders frequently cause major threats to survival. Derangement of
hydration, renal function, and endocrine function cause potassium abnormalities.
Burns, tissue necrosis, tumor lysis accompanying cancer chemotherapy, and side effects
of medication often contribute to disorders potassium balance

Although potassium is the principal intracellular cation, we measure derangement on the

basis of plasma or serum determination reflecting only 5% of total body potassium. The
distribution of potassium between the ICF and ECF is heavily dependent upon the action of the
Na-K ATPase. This latter enzyme import 2x K+ from the ECF and export Na+ from ICF. Acidbase status, insulin and catecholamines all excert effects upon the distribution of potassium
across the cell membrane.

15

Acidosis causes an efflux of potassium from the cell and alkalosis

the reverse. The greater effect occurs with mineral acids rather than lactic or keto acids where the
cell is more permeable to the accompanying anions and the effects on potassium levels lag
behind those of pH. Approximate relations between total body potassium, plasma potassium
concentration, and pH will determine the precise potassium needed in hypokalemic patients. 15
High or low potassium level in the blood signal abnormal state due to excess, loss, or
redistribution of potassium, and demand prompt correction.
Hypokalemia
Hypokalemia is present when serum potassium concentration < 3.5 mEq/l. It can result
from true potassium losses, dilution of existing intravascular potassium and chloride depletion
and a possible metabolic alkalosis.
Hypokalemia has cardiovascular, neuromuscular, and metabolic concequences including
dysrhytmia, ileus, muscle weakness, and effects on carbohydrate and protein metabolism
Management
Symptomatic and Moderate to Severe Hypokalemia
Moderate to severe hypokalemia, hypokalemia associated with arrhythmia, paralytic
ileus, is treated with intravenous potassium chloride.
Administer potassium chloride 0.5-1 mEq /kg iv over 2-3 hours. Dilute iv potassium and
administer slowly over several hours to avoid vascular irritation or burns. If administer
peripheral iv line, the ideal concentration is 3-4 mEq/dl, and if central venous administration
fluid restriction is necessary, concentration 1mEq / 10-20 ml
Mild Hypokalemia
Asymptomatic mild hypokalemia may be corrected with oral potassium supplementation.
Total daily potassium requirements average 20-40 mEq/ kg/day.
Hypokalemia Metabolic Alkalosis

Correction of the hypokalemia can be provided with oral potassium supplements that
provide approximately 2-4 mEq/kg/day of potassium. If hypokalemia is associated with
hypochloremia, administration of ammonium chloride may be indicated. Half of the corrective
dose can be calculated as follows:
mEq ammonium chloride for 50% correction = 0.25 l/kg x weight in kg x (HCO3 - - 24)
Hypokalemia Respiratory Alkalosis
Correction of alkalosis is the treatment of choice. If the alkalosis will be maintained (in
the treatment of pulmonary hypertension), potassium administration will correct the hypokalemia
but must be tapered when the respiratory alkalosis will be discontinued.
Hyperkalemia
Hyperkalemia can result from excessive potassium administration, inadequate potassium
excretion by the kidney, or a shift of potassium from the cellular to the vascular space with a fall
in serum pH. Hyperkalemia may also result from potassium release from injured cells, which
may occur in association with severe dehydration, trauma or burns, shock, sepsis, transfusion, or
acute tumor lysis syndrome.
Potassium excess is present when the serum potassium value is > 5.5 mEq/l. When
potassium concentration increases, the membrane potential in excitable tissue is affected.
Acidosis can be associated with an acute increase in the serum potassium concentration because
it produces an intravascular shift of potassium as hydrogen ions move from the vascular space
into cells in exchange for potassium.
Clinical Presentation
Severe Hyperkalemia
Serum potassium concentration is > 7 to 8 mEq/l, symptoms of hyperkalemia,
particularly cardiac arrhytmias, should be anticipated and treatment should be initiated. ECG
changes are most common, including a prolonged PR interval, absence of a P wave, ventricular
arrhythmias or fibrillation, and cardiac arrest.
Mild to Moderate Hyperkalemia
Skeletal and muscle weakness, flaccid muscles, decreased reflexes. ECG changes include
peaked T waves, a widening QRS complex, ST segment depression, and dcreasing amplitude of
the R wave.

Management of Hyperkalemia
Severe, Symptomatic Hyperkalemia
Potassium concentration > 7 to 8 mEq/l or is associated with ECG changes, intravascular
potassium must be emergently reduced by one or more of the following methods:

Stabilize myocardial membranes: Calcium gluconate 60-100 mg/kg iv or calcium chloride

20-25 mg/kg iv slow (no more than 100 mg/minute)

Shift potassium into cells: Create serum alkalosis with sodium bicarbonate 1 mEq/kg iv bolus
and glucose plus insulin (Regular Insulin 0.1 U/kg iv plus 25% glucose (1-2 ml/kg)

Prevent ongoing gastrointestinal absorption of potassium: Sodium polystyrene sulfonate

(Kayexalate)

Remove potassium: Provide exchange transfusion or dyalisis

Mild, Asymptomatic Hyperkalemia

Elimination of potassium intake, treatment of the underlying cause (acidosis,
dehydration), and dilution (administration of potassium-free fluids to expand the extracellular
fluid space and reduce the serum potassium concentration).
Calcium
The key component of plasma calcium with respect to its effectiveness in neuroexcitation
and muscle contraction is ionized calcium. This component represents 45-50% of the plasma
ion, which distributed among an equal amount of calcium that is protein-bound to albumin and a
small component complexed with anions such as lactate phosphate, and bicarbonate.
Ionized hypocalcemia has been reported particularly among sick newborn infants and in
severely ill pediatric ICU patients.16
Hypocalcemia
The clinical manifestation of low calcium include seizures, tetany, depressed cardiac
function, and rarely laryngospasm. 17
The rhytm disturbance brought about by hypocalcemia for QT interval corrects for heart
rate and is especially important The standard formula for QT interval corrects for heart rate and
specially important in the infants with a normal heart rate double that of an adult
Treatment
In a prospective randomized double blind comparison of calcium chloride and calcium
gluconate therapies for hypocalcemia in critically ill children, data presented that calcium

chloride produces a greater rise in ionized calcium than did calcium gluconate. But other
investigators studying the same question have not found any difference between calcium salts
tested for biovialability.18 Usually 10 mg/kg of elemental CaCl is given in a drip over several
minutes to treat acute hypocalcemia which may be followed by continuous infusions of calcium
as needed.Treat the underlying disease is very important.
Hypercalcemia
In the young infantsan familial hypercalcemia can present with a toxic level of calcium,
warranting acute intervention. In older patient, hyperparathyroidism and malignancy are the
conditions with toxic levels of calcium need intensive care management.
Infants with severe hypercalcemia presen neuromuscular symptoms, including lethargy
and difficulty feeding as well as hypotonia. Older children may manifest a variey of symptoms,
including CNS disturbance up to and including coma, nausea, and vomiting.
Hypercalcemia constitutes a medical emergency when blood level exceed 15 mg/dl. With
elevated phosphorus complicating hypercalcemia, the risk of metastatic calcification of soft
tissue,nephrocalcinosis, and metastatic calcification of the cornea or in the vascular tree may
occur.
Magnesium
Hypomagnesemia
Newborn infants and the patient with renal failure are two groups prone to
hypomagnesemia.19 Symptoms of hypomagnesemia including similar to hypocalcemia: tetany,
muscular weakness, and cardiac rhytm disturbance. Because hypomagnesemia impairs PTH
function, hypocalcemia is often accompaniment.
Treatment of hypomagnesemia:50% MgSO4 5-10 mg/kg/ 12-24 hr. Oral repletion can be
carried out by giving 10-30 mg/kg/24 hr of magnesium as chloride or citrate .
Hypermagnesmia
Excert clinical effects when the concentration exceed 5 mg/dl. Weakness, neuromuscular
abnormalities, including loss of deep tendon reflex, and paralysis become evident when
magnesium rise above 7.5 mg/dl. Abnormal cardiac rhythms become more pronounced,
displaying an array of conduction defects on ECG.

There is no specific treatment for hypermagbesemia, but 10 mg/kg elemental calcium as a

slow intravenous infusion to minimize the effects of hypermagnesemia on the heart. Dyalisis
may be needed if neurologic or cardiac arrhythmia are severe.19
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2. Maxwell MH, Kleeman CR, Narins RC. Clinical Disorders of Fluid and Electrolyte
Metabolism 4th ed. New York. McGraw-Hill, 1987
3. Ichikawa I. Pediatric Textbook of Fluid and Electrolyte. Baltimore. Williams & Wilkins,
1990
4. Friis- Hansen B. Changes in body water compartments during growth. Acta Paediatr
Scand 1957; 110: 1-68
5. Friis-Hansen B. Body water compartments in children: Changes during growth and
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6. Link DA. Accurate assessment in therapy of pediatric dehydration. In Link DA ed.
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Care 2nd ed St.Louis Mosby 1999; pp 454-57
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Conventional and novel aspects. J Am Soc Nephrol 2001; 12( Suppl 17) : S10-14
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11-23
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RG eds. Clinical Disorders of Fluid and Electrolyte Metabolism 4 th ed New York .
McGraw-Hill. 1987
18. Bronner CW et al.A Prospective, randomized, double blind comparison of calcium
chloride and calcium gluconate therapies for hypocalcemia in critically ill children. J
Pediatr 1990; 117: 986
19. Link D. Fluid, Electrolyte, Acid- Base Disturbances, and Diuretics. In: Critical Care of
Infants and Children. Todres ID, Fugate JH eds. 1st ed Little, Brown and Company 1996
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