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Fluids and Electrolytes

Maintenance Fluid Requirements (mL/kg/day)

Body Weight (kg)

Fluid Requirement per 24 hours

Up to 10 kg

100 mL/kg

11 to 20 kg

1000 mL + 50 mL for each kg over

10 kg

>20 Kg

1500 mL + 20 mL for each kg over

20 Kg

Maintenance Electrolyte Requirements (mEq/kg/day)










Stool losses








water losses


Estimation of Serum Osmolality

Serum osmolality (mosm/kg) =

serum Na x 2
+ serum K x 2
+ glucose (mg/dl

BUN (mg/dl)

Changes in serum osmolality effect ECF space since fluids

equilibrate osmolality across a semi-permeable membrane.
1. hypotonicity leads to contraction of ECF.
2. hypertonicity leads to expansion of ECF.

Maintenance fluids. The important thing for all of you to remember is that when you are
giving maintenance fluids to any child of any age, the first thing to ask yourself is, "Do I
expect the insensible water loss, urinary loss and stool loss to be normal?" If it is, then
you can give normal maintenance amounts. But if there is either a reason to give more
or less depending upon these, you need to make modifications. If a child is up to 10 kg
of weight, we give 100 ml/kg to the normal child with normal renal function. That is a liter
for a child that weighs 10 kg. From 11 to 20, we give 1000 ml plus 50 ml/kg for each kg
between 10 and 20. For the child over 20 kg, we give 1500 ml for the first 20 then 20
ml/kg for each kg over 20.
Maintenance electrolytes are not so much related to age but to weight and it is important
to remember that insensible water loss of electrolytes is relatively small. Only about 0.5
mEq/kg of both sodium and potassium are lost. Most of the electrolytes which are lost
through the urine and on average it is about 3.0 mEq/kg of sodium and 2.0 mEq/kg of
potassium. All of that should be given in maintenance fluids in the form of chloride.
Bicarbonate is not needed in maintenance fluids, but is needed in correcting a
metabolic acidosis.
There are of course three major types of dehydration. The ultimate character of the net
deficits will be determined by the quantity of fluid intake as well as the losses. Isotonic
dehydration is the type of dehydration that you will see most commonly. In this case,
salts and water are lost and replaced proportionately. This is primarily caused by
diarrheal dehydration, involving losses from the GI tract. It is important to remember that
the range that we would call isotonic dehydration is broader than normal serum sodium.
I've listed here what I would consider isotonic, being from 130-150 mEq/l. That means
that the fluid intake and the diarrheal output were proportional. The fluids which we
commonly recommend for oral rehydration therapy in isotonic dehydration are designed
to replace fluids as they are lost. In the United States rotavirus is the most common
cause of diarrhea; the concentration of sodium in diarrhea from rotavirus is about 15
mEq/l, actually similar in toxigenic E. coli diarrhea. Most diarrheas that we will see will
have that, and therefore, the common electrolyte solutions like Pedialyte or Infalyte
have concentrations of sodium of 45 or 50 mEq/l, with appropriate amounts of chloride,
potassium, and citrate as a substitute for bicarbonate.
Hypotonic dehydration. The balance between water and salts is disturbed either
because salt is lost in excess of water, or because very hypotonic fluids have been
given as replacement. This is where, in oral rehydration, we should be very careful
about the so-called clear liquids, because the so-called clear liquids given, 7-Up or
juices, are often very high in carbohydrate and very low in electrolyte. If we give fluids
that are clear liquids to the child who is having diarrhea, we may then produce
hypotonic dehydration. In addition to GI losses, we see hypotonic dehydration if we are
wasting sodium as result of adrenal cortical insufficiency, or as the result of renal
insufficiency, or if we are losing it from the skin in cystic fibrosis, or occasionally in an
infant who is given a very hypotonic solution.
Hypertonic dehydration is of course the opposite. The balance between water and salt
is also disrupted because water is lost in excess or because sodium is given too much
in replacement. You see that sometimes if diarrheal dehydration is treated with soup
broth, which may be very high sodium containing. We see it, of course, in GI losses with
improper replacement, but we also see it in solute diuresis from glucose or urea. In
diabetics we may see hypernatremia. In a child who has transient renal failure and
acute tubular necrosis, during the recovery phase from acute tubular necrosis, where
the urea is being rapidly washed out, water will be carried along with the solute of urea.
With diabetes water will be carried along with the solute of glucose, and one may
develop hypernatremia. Diabetes insipidus, of course, is the classical circumstance in
which the kidney is unable to concentrate urine. It is extremely dilute and hypernatremia
is an important complication. Occasionally formula is improperly mixed. Now, most
people will be able to buy the premixed formula and we don't see this problem, but of
course it is much less expensive to use the formula powder. If one doesnt add the
proper amount of fluid to it, the child can develop hypernatremia.
In assessing a child who has diarrheal dehydration or other forms of dehydration, the
most important criteria is loss of weight. Hopefully most of the patients who have been
in your practice you will have previous weight so you'll know what their weight has been.
But even if the patient has not been in, if you can get a previous weight it is your most
reliable measure of weight loss. The clinical signs of dehydration are not terribly
reliable. They give you a rough idea but they're not nearly as reliable as weight. If you
dont have a weight, then clinical signs of dehydration can be helpful. Mild dehydration
is about 5% dehydration in infancy, and about 3% dehydration in older children. If the
infant is less than 5% dehydrated, or a child is less than 3% dehydrated, you will not see

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Normal serum total serum CO2:

1st year of life 20-22 mM/l
Subsequently 24-27 mM/l


A. The ultimate character of the net deficits will be determined by
the quantity and quality of fluid intake as well as losses. There
are three possible relationships between H20 and salt

Isotonic Dehydration - The balance between H20 and

salt is the same as in normal plasma because H20 and
salt have been either lost or replaced proportionally.
Na+ = 130-150 mEq/1
a. Primarily caused by loss of fluids from the GI tract


Hypotonic Dehydration. the balance between H20 and

salt is disturbed because either salt has been lost in
excess of H20 or because fluids with little salt have been
given to replace the fluid losses.
Na+ < 130
a. Causes:

GI losses


Adrenal cortical insufficiency


Chronic renal failure


Cystic fibrosis


Hypotonic intake in an infant


Factitious hyponatremia (Na in plasma while

normal in plasma water),in hyperlipidemia,


Hypertonic Dehydration. The balance between H20

and salt has been disrupted, either because of H20 has
been lost in excess of salt or fluids with extra salt have
been given to replace the fluid losses.
Na+ >150

Causes of Hypertonic Dehydration

any signs of dehydration. Thus, you cannot use the absence of signs of dehydration to
indicate that a child is well hydrated. So if you have a child who you feel the need to
keep well hydrated, as for example when treating a respiratory infection, it is important
that either you note that there is a high urinary output that is light in color, you measure
the specific gravity of the urine to determine that it is indeed dilute and that you have a
well hydrated child.
Moderate dehydration is 10% dehydration in infancy or 6% dehydration in older
children. It is the classical dehydration which has the classical signs in isotonic and
hypotonic dehydration of decreased skin turgor, dry mucous membranes, and in the
child whose fontanelle is open, sometimes with a sunken fontanelle, softness of the
orbit. The classical signs of dehydration are seen at 10% dehydration or greater, and
that is moderate dehydration.
Severe dehydration is 15% in infancy, 9% in older children, and it is characteristically
associated with cardiovascular instability. The child who is 15% dehydrated will have
either a low normal blood pressure or periods of hypotension and tachycardia. Once
you see 15% dehydration, the chance is great that the child will go into shock, often into
profound shock. Greater than 20% dehydration in infancy is often incompatible with
sustained life.
If you have a child who does have severe dehydration and is in shock, then it is very
important to be able to correct that intravenously. Although oral rehydration is
recommended for most mild and moderate dehydration, if the child is in shock you
cannot treat it orally because, of course, the intestine is also in shock and if you gave
any fluids orally, they would simply remain in the intestine and will not be absorbed.
You'd also have an ileus. Obviously, the best thing to do if possible is to use a
peripheral vein. If it is not available, central venous access is not difficult to do for an
experienced person, either in the subclavian or jugular veins, occasionally in the
femoral, one should achieve central venous access. But if that is not available, and
sometimes the child is in profound shock and we just can't get into a vein, it is important
that either you know how to provide intraosseous access. It is a marvelous way of
getting emergency fluids into the central circulation when no vessels are available.
Then you must assess why the child lost the fluids and give fluids that are appropriate
for loss. If there has been blood loss, we should give blood. If there has been crystalloid
loss, we should give crystalloid and so forth. Whenever you are treating a child who is
in shock, the initial therapy should be with isotonic fluids. So even if you are dealing with
hypertonic dehydration, the initial therapy for shock should be with isotonic fluids, and
the ones to give are normal saline, Ringer's lactate, Plasmanate, or, in the case of
blood loss, blood.
How much fluid do you give? If the child is in shock, you are probably going to need no
less than 20 ml/kg of either saline, Ringer's lactate, or Plasmanate. Generally, what I
like to do is give 10 ml/kg of an isotonic solution as a bolus, as rapidly as I can and then
assess whether the shock has been reversed. If it has not been reversed, I will give the
second 10 ml/kg of isotonic solution. If the shock is severe, very often you will need to
give 40 ml/kg or sometimes more. Again, I like to do it in 10 ml/kg boluses, and
frequently I find it very worthwhile, if I have a child who is in shock and I am not sure
why, to give half the solution as crystalloid and half the solution as powder.
If you have gotten the child out of shock and you are going on with your replacement
fluids, you calculated the fluids you want to give to the child. If treating intravenously, I
generally will replace one-half of the deficit in isotonic or hypotonic dehydration in the
first 8-12 hours, a quarter of the deficit in the second 12 hours, and the final quarter of
the deficit in the third 12 hours. In other words, completely correcting the deficit within
36 hours. With oral rehydration in a child who is slightly less severe, I often will correct
one-half in the first 6-8 hours and then the remainder over the subsequent 24 hours.
If you have hypotonic dehydration and the hypotonicity is severe, by severe I mean
generally a serum sodium that is less than 120, often less than 115, and associated with
CNS symptoms, severe lethargy or seizures, then 3% saline can be used to raise the
serum sodium to a safe level. A safe level is the low 120s. It is rare for a child to seize
whose serum sodium is above 120. I didn't say never. You can have a child whose
serum sodium started out at 135 who has rapidly diluted down, for example in water
intoxication, into the high 120s and see a seizure. But in most children with diarrheal
dehydration and other causes of hypotonic dehydration, you will have a gradual
decrease in the sodium. You will not see seizures characteristically until it gets below
120. Therefore, if you have a child who is seizing, is severely hypernatremic, I
recommend that you calculate the amount of 3% saline that you give to only raise the
sodium into the low 120s, and then calculate using more standard solutions, bringing
the child the rest of the way back up to lower edge of normal. It is extremely important
that you not raise a sodium that is very low all the way to normal rapidly. In the adult,
there has been in a number of circumstances, descriptions of lysis of the pons, pontine
myelinolysis brought about by rapid correction of serum sodium from severely

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GI losses


Solute diuresis from glucose, urea


Diabetes insipidus


Improperly mixed formula

II. Approach to the Patient with Diarrheal Dehydration

A. Assessment of the Degree of Dehydration
1. Loss of body weight
2. Clinical estimate of severity

Severity of Isotonic Dehydration



Older Children


50 ml/kg (5%)

30 ml/kg (3%)


100 ml/kg (10%)

60 ml/kg (6%)


150 ml/kg (15%)

90 ml/kg (9%)

B. Determine the Type of Dehydration

1. Pathophysiology of specific illness
2. Specific physical signs
3. Measurement of initial plasma sodium

hypernatremic levels. That has not been reported in children. It hasn't been reported but
it certainly is a risk and; therefore, I recommend that you bring it only to the low 120s
initially, and then calculate your fluid to bring the child to the edge of normal, just into the
If you have hypertonic dehydration, the basic goal is to bring the serum sodium down
slowly. If it comes down too rapidly the child may seize. The reason the child will seize
when you bring down the sodium too rapidly is that you are bringing the extracellular
osmology down faster than the intracellular osmology can accommodate it. So fluid
shifts from extracellular to intracellular and you get brain swelling and seizures.
Therefore, the secret of success in treating hypernatremic dehydration is to go slow. A
general rule of thumb is to calculate your fluids so that you reduce the serum sodium by
5 mEq/l each 12 hours. With hypernatremic dehydration, rather than taking 36 hours to
correct the sodium as I recommended in isotonic or hypotonic, I like to take 72 hours. A
more slow correction in order to minimize the chances that you will have seizure. In
addition to that, no matter how little sodium is needed in your calculation, you should
never use a lower concentration than a quarter normal saline. You should not use less
than 30 mEq/l in your fluid. If you do, you are more likely to get into problems with
rapidly falling sodium because as renal function is restored, the kidney will try to kick out
that sodium as rapidly as it can, and the sodium will drop faster than your calculations
How should you assess the child? The child that is severely ill should be assessed at
least every 12 hours. You should repeat the electrolytes and creatinine, BUN and a
measure of their degree of acidosis. If the child has prerenal failure and their BUN is
elevated to 30 or 40, it should fall very rapidly as you correct the dehydration. So one
should expect in 6-12 hours, the BUN, if elevated, should fall by 50%. If the BUN does
not fall, or if your initial BUN is greater than 50, that suggests that the degree of
dehydration, the inadequate perfusion, has led to some acute tubular necrosis in
addition to the prerenal acidemia, and you are dealing with intrarenal as well as prerenal
failure. But in the majority of circumstances, with your moderate elevation of urea, it will
fall very rapidly. That is a good sign that you are only dealing with prerenal failure.
If the potassium is also elevated, as it may be with acidosis despite total body
potassium loss, it should fall as acidosis regresses. You should reassess a child
frequently. One of the things to remember about oral rehydration in the mild to moderate
child is that, although you may not be giving electrolytes, you may be treating the child
at home, it is important that you assess that child on a regular basis. Do not feel that
because you are treating the child orally that the child is any less sick. Periodic
reassessment to make sure the child is gaining weight and recovering from the
dehydration is essential.

plasma (Na+) = 130 - 150 mEq/1


plasma (Na+) >150 mEq/1


plasma (Na+) <130 mEq/1

C. Fluid Resuscitation. If the patient is in shock, give 10-20

ml/kg of plasmanate, Ringers lactate or normal saline over
15-30 minutes. In severe shock, 40 ml/kg may be needed (20
ml/kg plasmanate + 20 ml/kg Ringers lactate or normal
D. Replacement of Losses. Once shock has been reversed, or
if the patient is not in shock, the time for replacement of salt
and H20 vary:

Isotonic dehydration
1st 12 hours

1/2 deficit

2nd 12 hours 1/4 deficit

3rd 12 hours

1/4 deficit

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Hypotonic dehydration
a. If the hypotonicity is severe (Na+ <115) and associated
with convulsions, 3% NaCl can be rapidly infused to
raise the Na+ to 120 mEq/1. 3% NaCl contains 513
mEq/1 or about 0.5 mEq/ml. Symptoms seldom occur at
a serum level of Na+ > 120 mEq/1.
b. Otherwise the rate of replacement is similar to isotonic


Acid-base problems. Correction of acid-based dysequilibrium is dependent on several

factors. In the first place, we have respiratory compensation for the metabolic changes.
Secondly, we have tissue buffering capacity. The buffers are hemoglobin, albumin, and
bicarbonate in our tissues. With acidosis, we try to renally excrete excess hydrogen ions
and we try to reabsorb bicarbonate.
First example is metabolic acidosis, which we see commonly with hypoxia or in
diarrheal dehydration, the main problem that we have in diarrheal dehydration is the
loss of bicarbonate and then the loss of fluid and water. The way that the lung attempts
to compensate is to breathe more rapidly, blow off CO2 and to superimpose a
respiratory alkalosis to compensate for the metabolic acidosis. That would not make the
correction completely but it will make a partial correction. Then renal bicarbonate
reabsorption will hopefully do the rest, but if the acidosis is severe, then we must
provide sodium bicarbonate in our intravenous or oral rehydration fluids in order to
correct the metabolic acidosis.

Hypertonic dehydration
a. Intracranial hemorrhage can occur during the
development of hypernatremia, and seizures during
b. The basic goal of therapy is to bring the serum into the
normal range slowly (over 72 hours). This can usually be
accomplished by lowering the Na+ by 5 mEq/1 every 12
hours. b.

The H20 deficit is replaced in 36 hours. c.

No fluids are used with < 30 mEq Na+/1.

III. Acid-Base Equilibrium

A. Acid-base equilibrium is dependent on respiratory
compensation, tissue buffering capacity (hemoglobin,
albumin, bicarbonate), renal excretion of hydrogen ion, and
renal reabsorption of bicarbonate.
B. The anion gap estimation is useful in assessing acid-base
Normal anion gap = Na+ + K+ - (HCO3 + Cl-) = 9-13 mEq/L.

If you have a metabolic alkalosis the problem is the opposite. Pyloric stenosis is an
example of that, where the child is vomiting hydrochloric acid. We lose hydrochloric
acid, our bicarbonate goes up and we develop a metabolic alkalosis. Our lungs try to
help us compensate by slowing down respiration, so the pCO 2 rises, so that we try then
to add a respiratory acidosis as compensation for the metabolic alkalosis. The kidney
then will produce renal bicarbonate excretion, particularly when the vomiting stops
because we are not feeding the child. Then the renal bicarbonate excretion increases
and the metabolic alkalosis is replaced.
An anion gap, whether it is present or absent, can be helpful particularly in a child who
has an acidosis, in determining whether we are dealing with the classical acidoses or
we are dealing with an organic acidosis. The anion gap is very easy to calculate. It is
simply the sodium, plus the potassium, minus the bicarbonate and the chloride. So the
cations minus the anions should give the normal anion gap which I've listed for you
which is characteristically between 9 and 13 mEq/l. Conditions that produce acidosis
that are associated with an increased anion gap may be endogenous or exogenous.
The classical endogenous one is diabetes where we retain ketones and produce a
combination of the metabolic acidosis for disordered metabolism, and an organic
acidosis with ketone retention and characteristically we will get an increased anion gap.
Exogenous acids, the common ones, are salicylate intoxication, ethanol intoxication,
and we do see it also in some drugs like paraldehyde.
The other area that you should remember that is important in terms of the acidosis and
the alkalosis is diuretics. We use diuretics quite a bit. There are many different
indications for diuretics, but it is important to remember the complications, particularly
the acid-based complications. Metabolic acidosis is the least frequent thing that we see
where the carbonic anhydrase inhibitors. Diamox is the classical example; it will
produce a metabolic acidosis with chronic use. Also, potassium retaining diuretics such
as spironolactone and amiloride will also produce a pronounced metabolic acidosis.
More important is the metabolic alkalosis which occurs with chronic use of either the
thiazide diuretics or the loop diuretics, furosemide being the classical loop diuretic. Each
of those diuretics will cause a marked potassium wasting by the kidney. They are
natriuretic and diuretic but they are also kaluretic. When acid is lost from the body and
our total body potassium gets low, then potassium is not available to exchange for
sodium at the distal tubule. Hydrogen ions are then preferentially secreted in exchange
for sodium, and that wasting of hydrogen ions leads to a metabolic alkalosis. Chronic
therapy with diuretics, if not accompanied by the provision of potassium chloride, will
lead to a metabolic alkalosis.

Characteristics of Acid-base Disorders









 renal HCO3

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C. Acidosis Associated with an Increased Anion Gap


Increased endogenous anions: uremia (lactate, sulfate,

phosphate) ketones (diabetes)


Increased exogenous acids: salicylate, ethanol,


D. Acid-Base disorders induced by diuretics


Metabolic acidosis: carbonic anhydrase inhibitors

Potassium. Potassium may be high or low. We often use EKG, in addition to measuring
serum potassium, to determine the events of the hyperkalemia or hypokalemia. It is
important to remember there is not a one to one relationship between the serum level
and what the EKG will show. What the EKG reflects is the ratio between extracellular
and intracellular potassium. Therefore, in a diabetic, whose total body potassium may
be quite low, because a diabetic wastes potassium, a serum potassium of just 5 may be
associated with EKG signs of hyperkalemia. In contrast, a patient with chronic renal
failure, who chronically retains potassium, has potassium in all tissues, all of the time,
might have a serum potassium of 6 or 7 and show no electrocardiographic signs at all.
So it is a balance between intra and extracellular potassium which is reflected in the
electrocardiogram. But in the child with acute changes or chronic changes, if the
potassium is below 3, we will see low T-waves first and sometimes a prominent Uwave. If it is more severe, you may see dysrhythmias and ST depression.
Hyperkalemia. If the potassium is around 7, you will see peaked, intensive T-waves. If it
gets between 7 and 8, you see prolongation of the P-R interval. Very dangerous levels
are at a potassium of 8 or slightly more wirh ST depression, the absence of P waves,
and gradual widening of the QRS. As we approach fatal levels of hyperkalemia, the
QRS will widen more and more, eventually develop a sine wave and cardiac arrest and
Treatment of severe hyperkalemia. There are three elements to the treatment of
hyperkalemia. One is to reverse membrane effects. Calcium gluconate is the agent that
is recommended for treating for short-term therapy of severe hyperkalemia. The second
thing we can do is to transfer potassium into cells - to remove the hyperkalemia by
moving potassium out of the circulation and into cells. That can be done with sodium
bicarbonate and with glucose. The third thing is to remove potassium from the body,
which can be done with ion exchange resin, of which Kayexalate is an example, or by

(diamox), potassium retaining diuretics (spironolactone,


Metabolic alkalosis: loop diuretics (furosemide), thiazide

diuretics, mercurials

IV. Disorders of Potassium Balance

Electrocardiographic Changes Associated with Hypokalemia

and Hyperkalemia
Serum Potassium

EKG Changes


Ventricular or atrial arrhythmias

Low T wave, prominent U
wave, S-T segment depression


Peaked T waves


Prolonged P-R interval


ST depression, absent P wave,

widened QRS


Continued widening of QRS,

sine wave pattern; arrhythmias

A. Hypokalemia

Causes of Hypokalemia

If we have a child who has hyperkalemia, we don't need to use all of those agents for
every child. It is important that we think about the specific usage which may be most
appropriate. If the potassium is in the range of 5.5 to 7 in a previously normal child and
we see peaked, intensive T-waves, that is, of course, hyperkalemia that requires
treatment, but it is not life-threatening hyperkalemia. My recommendation here is that
you treat it with sodium bicarbonate. Dosage recommendation is between 1 and 3
mEq/kg. I generally will give the one right in between, I would use 2 mEq/kg, and that
can be used whether the child is acidotic or not. Two mEq/kg of sodium bicarbonate,
infused over about a 15 minute period would be effective in driving potassium into cells.
It will begin to work in about 10 minutes. It will drive potassium into cells and potassium
will stay in cells for about two hours, and then the potassium will begin to leech back out
of cells, and probably by four hours it will be back out of the cells. So bicarbonate will
drive into the cells. If you have an acidosis you have corrected, it will drive into cells to
stay. Without an acidosis, it will drive it in still transiently. So after you have given
sodium bicarbonate I recommend that you give Kayexalate, 1 gm/kg given by high
rectal enema. The Kayexalate takes about an hour to begin to work. It peaks at about
two hours. By the time the sodium bicarbonate is stopping working, the Kayexalate is
then peaking and removing potassium from the body. If you give 1 gm/kg of Kayexalate,
you will generally, on average, lower the serum potassium by 1 mEq/l. So that that
therapy in this child would do quite well. You can repeat that in 6-12 hours and bring the
potassium down.
If you have major EKG changes, widening QRS certainly is a very important major one,
then I like to give calcium gluconate first. Calcium gluconate will act immediately, but the
effect will be gone in about 15 minutes. 10% calcium gluconate is recommended, 0.5
ml/kg and it should be given fairly rapidly over two to four minutes. It is very important
that when you give intravenous calcium rapidly that you monitor the heart and that if
there is any sign of bradycardia that you stop the infusion immediately. There is an
immediate toxic effect of calcium. But given safely, what will happen is the EKG will
normalize or improve even though the potassium will not change. The calcium does is
stabilize the membrane transiently. You follow that right away with sodium bicarbonate 2
mEq/kg in order to drive potassium into cells. You give the calcium gluconate to
stabilize the membrane, and you can then give the sodium bicarbonate to drive into the
cells, in the meantime call in a critical care or in nephrology specialist to institute dialysis
in order to remove potassium from the body.
Kayexalate can then be given with severe hyperkalemia. Since use of Kayexalate only
reduces the potassium by 1 mEq/l it usually is not sufficient and you need to give the
child dialysis. Now glucose can be given at a 0.5 gm/kg ,and that can be given at the
same time. That will also drive potassium into cells. Notice I didn't put up there glucose
and insulin. In the adults, you will see the use of glucose and insulin, but particularly in
dealing with infants, they have generally plenty of insulin around. If you infuse glucose
alone, that will be sufficient. If the child begins to show moderate hyperglycemia, then of

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a. Decreased intake

course insulin and glucose can be used. One unit of insulin per 10 gm of glucose is

b. Increased renal losses

(1) Diuretics
(2) Acid-base disturbances - acidosis may mask total K
(3) Adrenocortical hypersecretion
c. Extrarenal losses
(1) Gastrointestinal losses
(2) Profuse sweating

Clinical Manifestations of Hypokalemia

a. Neuromuscular Complications. Ileus, muscle weakness,
areflexic paralysis
b. Cardiac Manifestations. Arrhythmias, ST depression
c. Renal Manifestations. Polyuria, nephrogenic diabetes


Treatment of Hypokalemia
a. Oral replacement is preferred over IV
b. It is rarely necessary to give more that potassium at
more than 40 mEq/L of IV solution

B. Hyperkalemia

Causes of Hyperkalemia
a. Increased Intake or Production of Potassium
(1) Increased intake, PO or IV
(2) Cell breakdown
b. Decreased Excretion
(1) Renal failure
(2) Adrenal insufficiency
(3) Potassium-sparing diuretics
c. Internal Redistribution
(1) Acid-base abnormalities
(2) Extreme exercise
(3) Drug induced
(4) Hyperkalemia periodic paralysis


Clinical Manifestations of Hyperkalemia

a. Cardiac arrhythmias
b. Neuromuscular Manifestations. Paresthesias, muscle
weakness, or paralysis


Treatment of Hyperkalemia
a. Reversal of membrane effects: Calcium gluconate
b. Transfer of potassium into cells: Sodium bicarbonate
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and glucose
c. Removal of potassium from the body: Kayexalate,
d. Approach to therapy based on EKG and serum K+
(1) Potassium of 5.5 - 7.0 with peaked T-waves on
EKG (potassium >7.0).
(a) NaHCO3 1-3 mEq/kg over 15-30 minutes
(b) Kayexalate enema 1 gm/kg
(2) Major EKG changes
(a) Calcium gluconate, 10% 0.5 ml/kg over 2-4
minutes, may be repeated
(b) Sodium bicarbonate, 1-3mEq/kg over 15-30

Now, let me mention briefly the syndrome of inappropriate ADH, and it is characterized
by hyponatremia and hypoosmolality with continuing sodium loss in the urine. If you
have either a central nervous system or pulmonary cause of SIADH, it will lead to over
absorption of water by the distal tubule collecting duct. You will get volume expansion
and get hyponatremia and hypoosmolality. Because you have volume expansion, that is
a signal to the proximal tubule of the kidney to put out sodium, and you will waste
sodium. So despite the hyponatremia, you will have continued loss of sodium in the
urine and an inappropriately high urine osmolality because of the water reabsorption
and the sodium wasting. In order to make the diagnosis, you can't have an appropriate
reason to have ADH secreted. In other words, if you increase the blood volume, you
have normal renal function, because if you have chronic renal failure you are going to
waste sodium because the damaged tubule will waste sodium, and you need to have
normal adrenal function because if you have adrenal insufficiency, you will waste
The therapy in SIADH is to restrict fluids. The goal is to create a negative water
balance. Fluid restriction of 65-75% of maintenance requirements. The use of
hypertonic saline can be given if you have severe hyponatremia, but as I mentioned to
you in hyponatremic dehydration, I would only use it if the hyponatremia is severe and
then only to raise the sodium into the 120s. Otherwise, you should treat SIADH with fluid
restriction. What has been in the literature sometimes that I feel should not be used,
diuretics, ethanol and lithium have been suggested from time to time, and they are not

(c) Dialysis
(d) Glucose 0.5 gm/kg can be given over 30-60
minutes when there are EKG changes.
V. Syndrome of Inappropriate Antidiuretic Hormone (SIADH)
A. Clinical Manifestations of SIADH
1. Hyponatremia and serum hypoosmolality
2. Continuing sodium loss in the urine, despite hyponatremia
3. Inappropriately high urine osmolality
4. Absence of decreased blood volume
5. Normal renal function
6. Normal adrenal function
B. Treatment of SIADH
1. The goal of therapy is to create a negative water balance.
2. Fluid restriction to 65-75% of maintenance requirements.
3. Hypertonic saline only if symptomatic from hyponatremia.
VI. Diabetes Insipidus
A. Caused by lack of ADH secretion (pituitary diabetes
insipidus) or lack of response to ADH (nephrogenic diabetes
B. Causes of Pituitary Diabetes Insipidus
1. Congenital, hereditary defect
a. Autosomal dominant
b. Sex-linked recessive
2. Acquired
a. Idiopathic
b. Tumor. Craniopharyngioma, pinealoma, optic glioma,
D:\FILES\Review Courses\Prep 1\Metabolic Disorders.WPD

melanoma, metastatic
3. Other Causes. Neurosurgical complication, xanthoma
(Hand-Schuller-Christian disease), degenerative disease
(Laurence-Moon-Biedl syndrome), basal skill fracture
C. Causes of Lack of Response to ADH
1. Nephrogenic diabetes insipidus
2. Congenital x-linked
3. Acquired. Hypercalcemia, hypokalemia, obstructive
uropathy, medullary cystic disease, sickle cell disease,
D. Diagnosis of Diabetes Insipidus
1. High urine flow, negative water balance, urine osmolality
and specific gravity less that of plasma.
2. Mild degree of hypernatremia and hyperosmolality with or
without dehydration or azotemia
3. Thirst


Lewy, John E.: Nephrology, Fluids and Electrolytes. Nelson

Essentials of Pediatrics, Behrman and Kleigman editors, pp 573610,1994.
Stapleton FB, Roy SIII, Noe HN, Jenkins G: Hypercalciuria in
children with hematuria. New England Journal of Medicine, 310:
1345-1350, 1984.
Becker, N., and Avner, E.: Congenital Nephropathies and
Uropathies. Pediatric Clinics of North America, 42: 1319-1342, 1995.
Siegler, R. L.: The Hemolytic Uremic Syndrome, Pediatric Clinics of
North America, 42: 1505-1530, 1995.

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