Transcript FLUIDS AND ELECTROLYTESD

FLUIDS AND
ELECTROLYTES
MAINTENANCE FLUIDS
• Maintenance intravenous (IV) fluids are used
in children who cannot be fed enterally.
• Along with maintenance fluids, children may
require concurrent replacement fluids if they
have excessive ongoing losses, such as may
occur with drainage from a nasogastric tube.
• In addition, if dehydration is present, the
patient also needs to receive deficit
replacement.
• Maintenance fluids are composed of a
solution of water, glucose, sodium, potassium,
and chloride.
• This solution replaces electrolyte losses from
the urine and stool, as well as water losses
from the urine, stool, skin, and lungs.
• Maintenance fluids do not provide adequate
calories, protein, fat, minerals, or vitamins.
• Because of inadequate calories, a child on
maintenance IV fluids loses 0.5 o/o to 1 o/o of
real weight each day.
• Daily water losses are measurable (urine and
stool) and not measurable (insensible losses
from the skin and lungs).
• Failure to replace these losses leads to a
thirsty, uncomfortable child and, ultimately, a
dehydrated child.
• Sodium and potassium are given in
maintenance fluids to replace losses from
urine and stool.
• After calculation of water needs and electrolvte
needs, children typicalIy received either 5%
dextrose( D5)'in 1/4 normal saline (NS) plus
20 mEqlL of potassium chloride(KCl) or D5 in
1/2 NS plus 20 mEqlL of KCl.
• Children weighing less than 10 kg do best with
the solution containing 1/4 NS (38.5 mEq/L)
because of their high water needs per kilogram.
• In contrast, larger children and adults may receive
the solution with 1/2 NS (77 mEq/L).
Replacment Therapy
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Components of maintenance therapy
Urin:60%
Insensible losses (skin and lungs):35%
Stool:5%
• Insensible losses, composed of evaporative
losses from the skin and lungs, represent
approximately one third of total maintenance
water.
• Sweating is not insensible and, in contrast to
evaporative losses, sweat contains water and
electrolytes.
• A variety of clinical situations modify normal maintenance
water balance.
• Evaporative skin water losses can be significant in neonates,
especially premature infants who are under radiant
warmers or undergoing phototherapy.
• Burns can result in massive losses of water and electrolytes.
• Fever leads to a predictable increase in insensible losses,
causing a I0%to 15% increase in maintenance water needs
for each 1'C increase in temperature greater than 38'C.
• Tachypnea or a tracheostomy increases evaporative losses
from the lungs.
Causes of
lncreased
Water Needs
Causes of
Decreased Water
Needs
Skin
Radiant
warmer
Phototherapy
Fever
Sweat
Burns
Mist tent
Incubator
(premature
infants)
Lungs
Humidified
Tachypnea
Tracheostomy ventilator
Source
Mist tent
Gastrointestinal Diarrhea
Emesis
Nasogastric
suction
Renal
Polyuria
Oliguria/anuria
Miscellaneous Surgical drain Hypothyroidism
Third space
losses
DEHYDRATION
• Dehydration, most often due to
gastroenteriris, is common in children.
• The first step in caring for a child with
dehydration is to assess the degree of
dehydration.
• The degree of dehydration dictates the
urgency of the situation and the volume of
fluid needed for rehydration.
• An infant with mild dehydration (3%to 5% of
body weight dehydrated) has few clinical signs
or symptoms.
• The infant may be thirsty; the alert parent
may notice a decline in urine output.
• The history describes decreased intake and
increased fluid losses.
• An infant with moderate dehydration has
demonstrable physical signs and symptoms.
• Intravascular space depletion is evident by an
increased heart rate and reduced urine
output.
• The patient is 10% dehydrated and needs
fairly prompt inrervention.
• An infant with severe dehydration is gravely ill.
• The decrease in blood pressure indicates that
vital organs may be receiving inadequate
perfusion (shock).
• The infant is at least 15% dehydrated and
should receive immediate and aggressive
intravenous (IV) therapy.
• Mild, moderate, and severe dehydration
represent 3%,6 %,a nd 9% of body weight lost
in older children and adults.
• This difference is because water is a higher
percentage of body weight in infants.
• Clinical assessment of dehydration is only an
estimate; the patient must be continually reevaluated during therapy.
• The degree of dehydration is underestimated
in hypernatremic dehydration because the
osmotically driven shift of water from the
intracellular space to the extracellular space
helps to preserve the intravascular volume.
Laboratory Evaluation
• Serum blood urea nitrogen (BUN)
• Crearinine
• Urine specific gravity is usually elevated
(>1.025)
• Urinalysis: may show hyaline and granular
casts, a few white blood cells and red blood
cells, and 30 to 100 mg/dL of proteinuria
• Hemoconcentration from dehydration causes
an increase in the hematocrit and hemoglobin
Calculation of Fluid Deficit
• A child with dehydration has lost water; there
is usually a concurrent loss of sodium and
potassium.
• The fluid deficit is the percentage of
dehydration multiplied by the patient's weight
(For a 10-kg child, 10% of 10 kg >1 L deficit).
Approach to Dehydration
• The child with dehydration requires acute intervenrion to ensure
that there is adequate tissue perfusion.
• This resuscitation phase requires rapid restoration of the circulating
intravascular volume which should be done with an isotonic
solution, such as normal saline (NS) or ringer's lactate.
• Blood is an appropriate fluid choice for a child with acute blood
loss.
• The child is given a fluid bolus, usually 20 mLlkg of the isotonic
solution, over about 20 minutes.
• A child with severe dehydration may require multiple fluid boluses
and may need to receive fluid at a faster rate.
• The initial resuscitation and rehydration is complete when che child
has an adequate intravascular volume.
• Typically the child has some general clinical
improvement, including a lower heart rate,
normalization of the blood pressure,improved
perfusion,and a more alert affect.
• With adequate intravascular volume,it is now
appropriate to plan the fluid therapy for the next 24
hours.
• In order to assure that the intravascular volume is
restored, the patient receives an additional 20 mL/kg
bolus of isotonic fluid over 2 hours.
• The child's total fluid needs are added together
(maintenance + deficit).
• The volume of isotonic fluids the patient has received
as acute resuscitation is subtracted from this total.
• The remaining fluid volume is then administered over
24 hours.
Fluid Management of Dehydration
• Restore intravascular voiume
Normal saline: 20 ml/kg over 20 minutes
Repeat as needed
• Rapid volume repletion: 2O mLlkg normal saline
(maximum : 1L) over 2 hours
• Calculate 24-hosr fluid needs: maintenance + deficit volume
• Subtract isotonic fluid already administered from 24-hour
fluid needs
• Administer remaining volume over 24 hours using D5 1/2 normal
saline + 2O mEq/LKCl
• Replace ongoing losses as they occur
Monitoring and Management of
Dehidration
• All calculations in fluid therapy are only
approximations.
• Thus, the patient needs to be monitored
during treatment with therapy modifications
based on the clinical situation.
Monitoring Therapy
• Vital signs
Pulse
Blood pressure
• Intake and outpur
Fluid balance
Urine output and specific graviuy
• Physical examination
Weight
Clinical signs of depletion or overload
• Electrolytes
Treatment of Hypernatremic
Dehydration
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Restore intravascular volume
Normal saline: 20 ml/kg over 20 minutes (repeat until intravascular volume restored)
Determine time for correction based on initial sodium concentration
[Na] 145-157 mEq/L:24 hr
[Na] 158-170 mEq/L: 48 hr
Na] 171-183 mEq/L: 72 hr
[Na] 18a-196 mEq/L: 84 hr
Administer fluid at a constant rate over the time for correction
Typical fluid: D5 1/2 normal saline (wirh 20 mEq/L pocassium chloride unless contraindicated)
Typical rate: 1.25-1.5 times maintenance
Follow serum sodium concentration
Adjust fluid based on clinical status and serum sodium concentration
Signs of volume depletion: administer normal saline (20 mLlkg)
Sodium decreases too rapidly
Increase sodium concentration of IV fluid or
Decrease rare of IV fluid
Sodium decreases too slowly
Decrease sodium concentration of IV fluid or
Increase rate of IV fluid
Replace excessive ongoing losses as they occur
Sadium Disorders
• HYPONATREMIA
• HYPERNATREMIA
• Pseudohyponatremia
• Hyperosmolality, resulting from mannitol
infusion or hyperglycemi
• For every 100 mg/dl-increment of the serum
glucose,the serum sodium decreases by 1.6
mEq/L.
• In hypovolemic hyponatremia, the child has lost
sodium from the body.
• Water balance may be positive or negative, but there
has been a higher net sodium loss than water loss;
this is due to oral or intravenous (IV) water intake,
with water retention bv the kidneys to compensate
for the intravascular volume depletion.
• If the sodium loss is due to a nonrenal disease the
urine sodium concentration is very low, as the
kidneys attempt to preserve the intravascular volume
by conserving sodium.
• In renal diseases the urine sodium is inappropriately
elevated.
• Patients with hyponatremia and no evidence of volume
overload or volume depletion have euvolemic
hyponatremia.
• These patients typically have an excess of total body
water and a slight decrease in total body sodium.
• Some of these patients have an increase in weight,
implying that they are volume overloaded.
• Nevertheless, they usually appear normal or have only
subtle signs of fluid overload.
• In syndrome of inappropriate ADH (SIADH), there is
secretion of ADH that is not inhibited by either low
serum osmolality or expanded intravascular volume.
• Hyponatremia in hospitalized patients is often
due to inappropriately produced ADH secondary
to stress in the presence of hypotonic fluids.
• SIADH is associated with pneumonia, mechanical
ventilation, meningitis, and other central nervous
system disorders (trauma).
• Ectopic (tumor) producrion of ADH is rare in
children.
• Infants also can develop euvolemic hvponatremia
as a result of excessive water consumption or
• inappropriately diluted formula.
• In hypervolemic hyponatremia, there is an excess of
total body water and sodium, although the increase in
water is greater than the increase in sodium.
• In renal failure, there is an inability to excrete sodium
or water; the urine sodium may be low or high,
depending on the cause of the renal insufficiency.
• In other causes of hypervolemic hyponatremia, there is
a decrease in the effective blood volume because of
either third space fluid loss or poor cardiac output.
Clinical Manifestation
• Brain cell swelling is responsible for most of the symptoms
of hyponatremia.
• Neurologic symptoms of hyponatremia include anorexia,
nausea, emesis, malaise, lethargy, confusion, agitation,
headache, seizures, coma and decreased reflexes.
• Patients may develop hypothermia and Cheyne-Stokes
respirations.
• Hyponatremia can cause muscle cramps and weakness.
• Symptoms are more severe when hyponatremia develops
rapidly; chronic hyponatremia can be asymptomatic
because of a compensatory decrease in brain cell
osmolality, which limits cerebral swelling.
Treatment
• Rapid correction of hyponatremia can produce
central pontine myelinolysis.
• Avoiding more than a I2-mEq/L increase in the
serum sodium every 24 hours is prudent,
especially if the hyponatremia developed
gradually.
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Treatment of hypovolemic hyponatremia
Treatment of children with SIADH
Treatment of acute water intoxication
Treatment of hypervolemic hyponatremia
• Emergency treatment of symptomatic
hyponatremia, such as seizures, uses IV
hypertonic saline to increase the serum sodium
concentration rapidly, which leads to a decrease
in brain edema.
• One milliliter per kilogram of 3% sodium chloride
increases the serum sodium by approximately 1
mEq/L.
A child often improves after receiving4 ro 5
mL/kg of 3% sodium chloride.
HYPERNATREMIA
Etiology
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Sodium intoxication
Hyperaldosteronism
Diabetes insipidus
Water losses
Diarrhea
Some renal diseases including obstructive
uropathy, renal dysplasia, and juvenile
nephronophrhisis, can cause losses of sodium
and water
Clinical Manifestations
• Probably because of intracellular water loss, the pinched
abdominal skin of a dehydrated, hypernatremic infant has a
doughy feeI.
• Patients are irritable, restless, weak, and lethargic.
• Some infants have a high-pitched cry and hyperpnea.
• Alert patients arc very thirsty, although nausea may be
present.
• Hypernatremia causes fever, although many patients have
• an underlying process that contributes to the fever.
• Hypernatremia is associated with hyperglycemia and mild
hypocalcemia; the mechanisms are unknown.
• Brain hemorrhage is the most devastating consequence
of hypernatremia.
• As the extracellular osmolaliry increases, water moves
out of brain cells, resulting in a decrease in brain
volume.
• This decrease in volume can result in tearing of
intracerebral veins and bridging blood vessels as the
brain moves away from the skull and the meninges.
• Patients may have subarachnoid, subdural, and
parenchymal hemorrhage.
• Seizures and coma are possible sequelae of the
hemorrhage.
Potassium Disorder
• HYPOKALEMIA
• HYPERKALEMIA
HYPOKALEMIA
Etiology
• Spurious
High white blood cell counr
• Transcellular shifts
Alkalemia
Insulin
Beta-Adrenergic agonists
Drugs/toxins (theophylline, barium, toluene)
Hypokalemic periodic paralysis
• Decreased intake
• Extrarenal losses
Diarrhea
Laxative abuse
Sweating
• Renal losses
With metabolic acidosis
Distal RTA
Proximal RTA
Ureterosigmoidostomy
Diabetic ketoacidosis
Without specific acid-base disturbance
Tubular roxins (amphorericin, cisplacin, aminoglycosides)
Intersririd nephritis
Diuretic phase of acuce rubular necrosis
Postobstrucdve diuresrs
Hypomagnesemia
High urine anions (e.g:penicillin or penicillin derivatives)
With merabolic alkalosis
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Low urine chloride
Emesis/nasogastric suction
Pyoric stenosis
Chloride-losing diarrhea
Cystic fibrosis
Low-chloride formula
Posthypercapnia
Previous loop or thiazide diuretic use
High urine chloride and normal blood pressure
Gitelman syndrome
Bartter syndrome
Loop and thiazide diurerics
High urine chloride and high blood pressure
Adrenal adenoma or hyperplasia
Glucocorricoid-remediable aldosreronism
Renovascular disease
Renin-secreting tumor
17 a-Hydroxylase deficiency
1 1B-Hydroxylase deficiency
Cushing syndrome
1 1 B-Hydroxysteroid dehydrogenase deficiency
Licorice ingescion
Liddle syndrome
clinical Manifestations
• The heart and skeletal muscle are especially vulnerable to
hypokalemia.
• Electrocardiographic (ECG) changes include a flattened T
wave, a depressed ST segment, and the appearance of a U
wave.
• The clinical consequences in skeletal muscle include muscle
weakness and cramps.
• Paralysis is a possible complication (generally only at
potassium levels <2.5 mEq/L).
• Paralysis usually starts with the legs, followed by the arms.
• Respiratory paralysis may require mechanical ventilation.
• Some patients develop rhabdomyolysis; the risk
increases with exercise.
• Hypokalemia slows gastrointestinal motility; potassium
levels less rhan 2.5 rmEqlL may cause an ileus.
• Hypokalemia impairs bladder function, potentially
Ieading to urinary retention.
• Hypokalemia causes polyuria by producing secondary
nephrogenic diabetes insipidus.
• Chronic hypokalemia may cause kidney damage,
including interstitial nephritis and renal cysts.
• In children, chronic hypokalemia, as in Bartter
syndrome, leads to poor linear growth.
Diagnosis
• It is important to review the child's diet, history of gastrointestinal
losses, and medications.
• Emesis and diuretic use can be surreptitious.
• The presence of hypertension suggests excess mineralocorticoids.
• Concomitant electrolyte abnormalities are useful clues.
• The combination of hvpokalemia and metabolic acidosis is
characteristic of diarrhea, distal renal tubular acidosis, and proximal
renal tubular acidosis.
• A concurrent metabolic alkalosis is characteristic of gastric losses,
aldosterone excess, diuretics, and Bartter syndrome or Gitelman
syndrome.
• Alkalosis also causes a transcellular shift of potassium and increased
urinary losses of potassium.
HYPERKALEMIA
Causes of Hyperkalemia
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Spurious laboratory value
Hemolysis
Tissue ischemia during blood drawing
Thrombocytosis
Leukocytosis
Increased incake
IV or PO
Blood transfusions
Transcellular shifts
Acidemia
Rhabdomyolysis
Tumor lysis syndrome
Tissue necrosrs
Hemolysis/hematomas/gastrointestinabl leeding
Succinylcholine
Digitalis intoxication
Fluoride intoxication
B-Adrenergic blockers
Exercrse
Hyperosmolaiiry
Insulin deficiency
Malignanc hyperchermra
Hyperkalemic periodic ParalYsis
Decreased excretion
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Renal failure
Primary adrenal disease
Acquired Addison disease
2 l-Hydroxylase deficiency
3 Beta-Hydroxysteroid-dehydrogenase deficiency
Lipoid congenital adrenal hyperplasia
Adrenal hypoplasia congenira
Aldoscerone synthase deficiencY
Adrenoleukodystrophy
Hyporeninemic hypoaldosteronism
Urinary tract obscruction
Sickle cell disease
Kidney transplant
Lupus nephritis
Decreased excretion
• Renal tubular disease
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Pseudohypoaldosteronismr type 1
Pseudohypoaldosteronismr type 2
Urinary tract obstruction
Sickle cell disease
Kidney transplant
• Medications
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ACE inhibitors
Angiotensin II blockers
Potassium-sparing diuretics
Cyclosporine
NSAIDS
Trimethoprim
Clinical manifestations
• The most important effects of hyperkalemia are
due to the role of potassium in membrane
polarization.
• The cardiac conduction system is usually the
dominant concern.
• ECG changes begin with peaking of the T waves.
• As the potassium level increases, an increase P-R
interval, flattening of the P wave, and widening of
the QRS complex occur,this eventually can
progress to ventricular fibrillation.
Treatment
• The first action in a child with a concerning
elevation of plasma potassium is to stop all
sources of additional potassium (oral and IV).
• If the potassium level is greater than 6 to 6.5
mEq/L, an ECG should be obtained to help assess
the urgency of the situation.
• Therapy of hyperkalemia has two basic goals:
• 1. Prevent life-threatening arrhythmias.
• 2. Remove potassium from the body
Treatment of hyperkalemia
• Rapidly decrease the risk of life-threatening arrhythmias
Shift pocassium inrracellularly
Sodium bicarbonare administration (IV)
Insulin and glucose (IV)
B-Agonist (albuterol via nebulizer)
Cardiac membrane stabilization
IV calcium
• Remove potassium from the body
Loop diurecic (IV or PO)
Sodium polystyrene (PO or rectal)
Dialysis