FlUIDS AND ELECTROLITESFlUIDS AND ELECTROLITES

BYBY Dr. Sawsan S. Dr. Sawsan S.

ShurrabShurrab

Maintenance Fluid Therapy Total body water (TBW) as a percentage of body weight varies with age.

During the first year of life, TBW is about 60% of body weight and remains at this level until puberty.

TBW is divided between two main compartments: intracellular fluid (ICF) and extracellular fluid (ECF).

In the fetus and newborn, the ECF volume is larger than the ICF volume.

By 1 year of age, the ratio of the ICF volume to the ECF volume approaches adult levels.

The ECF volume is 20%of body weight, and the ICF volume is 40% of body weight .

The ECF is divided further into plasma water and interstitial fluid .

Plasma water is about 5% of body weight.

The volume of plasma water can be altered by pathologic conditions, including dehydration, heart failure, abnormal plasma osmolality, and hypo-albuminemia.

The interstitial fluid, normally 15% of body weight, can increase dramatically in diseases associated with edema, such as heart failure, protein-losing enteropathy, liver failure, and nephrotic syndrome

The composition of the solutes in the ICF and ECF is different.

Sodium and chloride are the dominant

cation and anion in the ECF.

Potassium is the most abundant cation in the ICF, and its concentration within the cells is approximately 30 times higher than in the ECF.

The difference in the distribution of cations-sodium and potassium-is due to the activity of the Na+,K+-ATPase pump, which uses cellular energy to actively extrude sodium from cells and move potassium into cells.

REGULATION OF INTRAVASCULAR REGULATION OF INTRAVASCULAR VOLUME AND OSMOLALITYVOLUME AND OSMOLALITY

Proper cell functioning requires close regulation of plasma osmolality, intravascular volume, and intracellular and extracellular electrolytes.

Maintenance of a normal osmolality depends on control of water balance.

The plasma osmolality is tightly regulated to maintain it between 285 and 295mOsm/kg.

Modification of water intake and excretion maintains a normal plasma osmolality.

Water intake and water produced by the body from oxidation balances water losses from the skin, lungs, urine, and gastrointestinal tract.

Urinary water losses are regulated by the secretion of antidiuretic hormone (ADH), which stimulats renal tubular reabsorption of water and decreases urinary water losses.

Thirst is also stimulated

When volume depletion:

Because sodium is the principal extracellular cation, and sodium is restricted to the ECF, adequate body sodium is necessary for maintenance of intravascular volume.

The renin-angiotensin system is an important regulator of renal sodium reabsorption and excretion.

The juxtaglomerular apparatus produces renin in response to decreased effective intravascular volume.

Renin cleaves angiotensinogen, producing angiotensin I.

Angiotensin-converting enzyme converts angiotensin I into angiotensin II.

The actions of angiotensin II include direct stimulation of the proximal tubule to increase sodium reabsorption and stimulation of the adrenal gland to increase aldosterone secretion.

Through its actions in the distal nephron, aldosterone increases sodium reabsorption.

When volume expansion : Synthesis of atrial natriuretic peptide is increased,and it is produced by the atria in response to atrial wall distention.

Along with increasing glomerular filtration rate, atrial natriuretic peptide inhibits sodium reabsorption, facilitating an increase in urinary sodium excretion.

FLUIDS THERAPYFLUIDS THERAPYMaintenance 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.

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 and water losses from the urine and stool, skin, and lungs.

The glucose in maintenance fluids provides approximately 20% of the normal caloric needs of the patient.

This percentage is enough to prevent the development of starvation ketoacidosis and diminishes the protein degradation that would occur if the patient received no calories.

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% to 1% of real weight each day.

Parenteral nutrition is especially important in a patient with underlying malnutrition.

Sodium and potassium are given in maintenance fluids to replace losses from urine and stool.

Maintenance requirements are 2 to 3 mEq/kg/day for sodium and 1 to 2 mEq/kg/day for potassium.

Body Weight (kg)Volume Per Day

0-10100ml\kg

11-201000 ml+50 ml\kg for each 1 kg more than 10 kg

More than 201500 +20 ml \kg more than 20 kg

Maintenance fluids usually contain D5 in quarter normal saline (NS) plus 20 mEq/L of potassium chloride.

Or D5 in half NS plus 20 mEq/L of potassium chloride.

NS is isotonic to plasma; quarter or half NS is not isotonic.

Children weighing less than about 20 do best with the solution containing quarter NS because of their high water needs per kilogram.

In contrast, larger children and adults may receive the solution with half NS .

Dehydration and Replacement Dehydration and Replacement TherapyTherapy

Evaporative skin water losses can be especially significant in neonates, especially premature infants who are under radiant warmers or who are receiving phototherapy .

Burns can result in massive

losses of water and electrolytes

Fever leads to a predictable increase in insensible losses, causing a 10% 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

The gastrointestinal tract is potentially a source of considerable water and electrolyte losses.

The losses should be replaced after they occur,

using a solution with the same electrolyte

concentration as the gastrointestinal fluid.

An increase in urine volume like the polyuric phase of acute tubular necrosis, diabetes mellitus, and diabetes insipidus .

The patient must receive more than standard maintenance fluids when the urine output is excessive to prevent dehydration.

Third space losses manifest with edema and ascites and are due to a shift of fluid from the intravascular space into the intersitial space.

Replacement of third space fluid is

empirical but should be anticipated.

DEHYDRATION Dehydration, most often due to

gastroenteritis, 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.

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.

The opposite occurs with hyponatremic dehydration.

An infant with mild dehydration (3% to 5% of body weight dehydrated) has few clinical signs or symptoms.

An infant with moderate dehydration has intravascular space depletion which is evident by an increased heart rate and reduced urine output. The patient is 10% dehydrated and needs fairly prompt intervention.

An infant with severe dehydration is gravely ill. The decrease in blood pressure indicates shock.

The infant is approximately 15% dehydrated and should receive immediate and aggressive IV therapy.

Mild, moderate, and severe dehydration represent 3%, 6%, and 9% of body weight lost in older children and adults.

Laboratory Evaluation Serum BUN and creatinine concentrations are useful in assessing a child with dehydration.

Volume depletion without renal insufficiency may cause a disproportionate increase in the BUN, with little or no change in the creatinine concentration.

A significant elevation of the creatinine concentration suggests renal insufficiency.

Calculation of Deficits A child with dehydration has lost water; there is usually a concurrent loss of sodium and potassium.

The water 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 severe dehydration requires acute intervention to ensure that there is adequate tissue perfusion.

The child is given a fluid bolus, usually 20 mL/kg of the isotonic solution or ringer lactate, over about 20 minutes and it could be repeated .

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.

After shock therapy,the child receives normal maintenance fluids and the remaining fluid deficit.

For a patient with isotonic dehydration, D5 half NS with 20 mEq/L of potassium chloride is usually an appropriate fluid.

Potassium usually is not included in the IV fluids until the patient voids, unless significant hypokalemia is present.

Half of the total fluid is given over the first 8 hours; previous boluses are subtracted from this volume.

The remainder is given over the next 16 hours. Children with significant ongoing losses need to receive an appropriate replacement solution

Hyponatremic dehydration

It produces a more substantial intravascular volume depletion owing to the shift of water from the extracellular space into the intracellular space.

Some patients develop neurologic symptoms.

Most patients with hyponatremic dehydration do well with the same general approach .

Rapid correction of hyponatremia (>12 mEq/L/24 hr) should be avoided because of the risk of central pontine myelinolysis

Hypernatremic dehydration The movement of water from the intracellular space to the extracellular space during hypernatremic dehydration partially protects the intravascular volume.

Urine output may be preserved longer, and there may be less tachycardia.

Children with hypernatremic dehydration are often lethargic and irritable when touched.

Hypernatremia may cause fever, hypertonicity, and hyperreflexia.

More severe neurologic symptoms may develop if cerebral bleeding or thrombosis occurs.

Idiogenic osmoles are generated within the brain during the development of hypernatremia.

These idiogenic osmoles increase the osmolality within the cells of the brain, providing protection against brain cell shrinkage .

These idiogenic osmoles dissipate slowly during correction of hypernatremia.

With rapid lowering of the extracellular osmolality during correction of hypernatremia, water moves from the extra-cellular space into the cells of the brain, producing cerebral edema which produces seizures, brain herniation, and death.

To minimize the risk of cerebral edema, the serum sodium concentration should not decrease more than 12 mEq/L every 24 hours.

The deficits in severe hypernatremic dehydration may need to be corrected over 2 to 4 days

Monitoring of the serum sodium concentration and adjustment of the therapy is based on the result.

Nonetheless, the initial resuscitation-rehydration phase of therapy remains the same as for other types of dehydration.

Oral RehydrationOral Rehydration Mild to moderate dehydration due to

diarrhea can be treated effectively using oral rehydration solution (ORS) .

The ORS relies on the coupled

transport of sodium and glucose in the intestine.

Oral rehydration therapy has significantly reduced the morbidity and mortality from acute diarrhea.

ORS containsORS contains::Na : 90 mmo/lK : 20 mmol/lChloride: 80 mmol/lBicarb.: 30 mmol/lGlucose :111 mmol/l

50 mL/kg of the ORS should be given within 4 hours to patients with mild dehydration.

100 mL/kg should be given over 4 hours to patients with moderate dehydration.

An additional 10 mL/kg of ORS is given for each stool.

Breastfeeding and formula milk should be allowed after rehydration and not delayed more than 24 hours.

HYPONATREMIAHYPONATREMIAEtiology Pseudohyponatremia is a laboratory artifact that is present when the plasma contains high concentrations of protein or lipid. Hyperosmolality, resulting from mannitol infusion or hyperglycemia so water moves down its osmotic gradient from the intracellular space into the extracellular space, diluting the sodium concentration.

Hypovolemic Hyponatremia

There has been a higher net sodium

loss than water loss; this is due to

either renal or extrarenal.

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 salt-wasting diseases, the urine sodium is inappropriately elevated.

Euvolemic Hyponatremia o These patients typically have an

excess of total body water and a slight decrease in total body sodium.

o They usually appear normal or have subtle signs of fluid overload.

o In SIADH, there is secretion of ADH .

o SIADH is associated with pneumonia, mechanical ventilation, meningitis, and other CNS disorders (trauma).

o Infants also can develop euvolemic hyponatremia as a result of consumption of large amounts of water or inappropriately diluted formula in the absence of dehydration.

Hypervolemic Hyponatremia

There is an excess of total body water and sodium, although the increase in water is greater than the increase in sodium like

In renal failure and heart failure.

Clinical Manifestations Hyponatremia causes a fall in the osmolality of the extracellular space.

Water moves from the extracellular space to the intracellular space to maintain osmotic equilibrium.

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.

Treatment Rapid correction of hyponatremia can produce central pontine myelinolysis. Avoiding more than a 12 mEq/L increase in the serum sodium every 24 hours is prudent, especially if the hyponatremia developed gradually.

Treatment of hypovolemic hyponatremia requires administration of IV fluids with sodium to provide maintenance requirements and deficit correction and to replace ongoing losses.

For children with SIADH, water restriction is the cornerstone of the therapy.

Treatment of hypervolemic hyponatremia centers on restriction of water and sodium intake, but disease-specific measures, such as dialysis in renal failure, also may be necessary.

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.

A child often improves after receiving 4 to 6 mL/kg of 3% sodium chloride.

HYPERNATREMIAHYPERNATREMIA Etiology Sodium intoxication is frequently iatrogenic in a hospital setting resulting from correction of metabolic acidosis with sodium bicarbonate.

In hyperaldosteronism, there is renal retention of sodium and resultant hypertension; the hypernatremia is mild.

Hypernatremia resulting from water losses develops only if the patient cannot drink adequately because of neurologic impairment, emesis, or anorexia.

Hereditary nephrogenic diabetes insipidus which is x- linked causes massive urinary water losses and dilute urine.

Acquired nephrogenic diabetes insipidus may be secondary to interstitial nephritis, sickle cell disease, hypercalcemia, hypokalemia, or medications (lithium or amphotericin).

Children with diabetes insipidus have inappropriately dilute urine.

If the defect is due to central diabetes insipidus, the urine output decreases, and the urine osmolality increases in response to administration of an ADH analogue (central causes of ADH deficiency include tumor, infarction, or trauma).

There is no response to an ADH analogue in a child with nephrogenic diabetes insipidus

Clinical Manifestations

Most children with hypernatremia are dehydrated and have the typical signs and symptoms of dehydration .

Children with hypernatremic dehydration tend to have better preservation of intravascular volume .

Blood pressure and urine output are maintained.

Probably because of intracellular water loss, the pinched abdominal skin of a dehydrated, hypernatremic infant has a doughy feel.

As the extracellular osmolality increases, water moves out of brain cells, resulting in a decrease in brain volume which 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.

TreatmentIf the serum sodium concentration is lowered rapidly, brain swelling results and manifests as seizures .

The goal is to decrease the serum sodium by less than 12 mEq/L every 24 hours, a rate of 0.5 mEq/L/hr.

If a child develops seizures from brain edema secondary to rapid correction, administration of hypotonic fluid should be stopped, and an infusion of 3% saline can increase the serum sodium acutely, reversing the cerebral edema or coma.

In a child with hypernatremic dehydration, as in any child with dehydration, the first priority is restoration of intravascular volume with isotonic fluid.

A child with central diabetes insipidus should receive an ADH analogue to prevent further excessive water loss.

A child with nephrogenic diabetes insipidus requires a urine replacement solution to offset ongoing water losses.

Chronically, reduced sodium

intake, thiazide diuretics, and nonsteroidal anti-inflammatory drugs can decrease water losses in nephrogenic diabetes insipidus.