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FLUID AND ELECTROLYTE DISTURBANCES OCT 2008

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FLUID AND ELECTROLYTE DISTURBANCES

OCT 2008

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Composition of Body Fluids. Total Body Water:

• Water is the most plentiful constituent of the human body. The other components of the body include protein, minerals, fat, & carbohydrate.

• Total body water (TBW) varies with age: - The fetus has very high TBW, which decreases to about 75% of

B Wt for a term infant (Higher for premature). - During the 1st yr, TBW ↓ to ~ 60% of B Wt & remains at this

level until puberty. - At puberty, the ↑ in fat content of girls > boys, (more muscle

mass). B/c fat has very low & muscle high water content, by the end of puberty TBW in boys remains at 60%, but in girls ↓ to ~ 50% of B Wt.

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Total body water and its major subdivisions as a function of age

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Fluid Compartments:• TBW is divided between two compartments:

intracellular fluid(ICF) & extracellular fluid (ECF). • In the fetus & newborn, the ECF vol > than ICF vol.

The postnatal diuresis causes an immediate ↓ in ECF vol followed by continued expansion of the ICF vol, (cellular growth).

• By 1 yr ratio of ICF to ECF approaches adult levels. The ECF vol is ~ 20–25% of B Wt & ICF vol is ~ 30–40% of B Wt.

• With puberty, boys have higher ICF vol than girls. There is no significant d/c in the ECF volume between postpubertal girls and boys.

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• The ECF is further divided into the plasma water and the interstitial fluid. The plasma water is ~ 5% of B Wt. The blood volume (hct of 40%), is ~ 8%, (higher in newborns & young infants).

• The vol. of plasma water can be altered by d/t pathologies: DHN, polycythemia, anemia, CHF, abnormal plasma osmolality,& hypoalbuminemia.

• The interstitial fluid, ~15% of B Wt, can increase in diseases associated with edema: CHF, liver failure, NS, & other causes of hypoalbuminemia. An increase in interstitial fluid occurs with ascites or pleural effusions.

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Compartments of TBW, expressed as % of B Wt:

Plasma 5%

Intracellular (30-40%)

Extracellular (20-25%)Interstitial 15%

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• A delicate equilibrium b/n IVF and IF exists. - The balance b/n hydrostatic & oncotic forces regulates the IV

volume critical for proper tissue perfusion. The IVF has a higher concentration of albumin than the IF, and this oncotic force draws water into the IV space (gradient b/c of limited permeability of albumin across capillaries).

- In contrast, the hydrostatic pressure of the IV space, due to the pumping action of the heart, drives fluid out. In the capillaries these favor movement into the interstitial space at the arterial end of the capillaries.

- The ↓ed hydrostatic forces & ↑ed oncotic forces, from

dilutional increase in albumin concentration, cause movement of fluid into the capillaries at the venous end of the capillaries.

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• Overall, there is a net movement of fluid out of the IV space, which is returned to the circulation via the lymphatics.

• An imbalance may cause expansion of interstitial volume at the expense of IV volume.

- In hypoalbuminemia, ↓ oncotic pressure of IVF contributes to the development of edema & inadequate blood flow to vital organs.

- In contrast, with heart failure, ↑ in venous hydrostatic pressure from expansion of the IV volume, which is caused by impaired pumping by the heart, & ↑ in venous pressure causes fluid to move from the IV to interstitial space.

- Expansion of IV volume & ↑ in IV pressure also cause the edema that occurs with AGN.

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Electrolyte Composition• Sodium & chloride are the dominant cation & anion,

respectively, in the ECF; both concentrations in the ICF are much lower.

• Potassium is the most abundant cation in the ICF, its concentration within the cells is ~ 30 times higher than in the ECF. Proteins, organic anions, and phosphate are the most plentiful anions in the ICF.

• The d/c b/n anions in ICF & ECF is largely due to IC molecules that do not cross the cell membrane; d/c in the cations—Na & K—is due to activity of the Na+/K+ -ATPase, which moves Na out & K into cells.

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• The chemical gradient b/n IC & EC K+ concentration creates the electrical gradient across the cell membrane.

- Specifically, the concentration-dependent movement of K+ out of the cell makes the IC space negative relative to the EC space.

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Osmolality• The ICF & ECF are in osmotic equilibrium b/c the cell

membrane is freely permeable to water. If the osmolality in one compartment changes, then water movement leads to a rapid equalization of osmolality. This can lead to significant shifts of water between the intracellular space and the extracellular space.

• The osmolality of the ECF equals the ICF osmolality. The plasma osmolality is normally 285–295mOsm/kg. It can also be calculated based on the following formula:

Osm= 2x[Na] + [Glucose]/18 + [BUN]/2.8 - Glucose & BUN are measured in mg/dL. Division by 18 & 2.8

converts units into mmol/L. Multiplication of sodium by 2 accounts for its accompanying anions, principally chloride and bicarbonate.

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• The effective osmolality can be calculated as: Effective Osm= 2x[Na] + [Glucose]/18• The effective osmolality (tonicity) determines the

osmotic force mediating the shift of water b/n the ECF & ICF.

• Hyperglycemia ↑ the plasma osmolality & thus there is a shift of water from the IC space to the EC space. This is clinically important in DKA: shift of water causes dilution of the sodium in the EC space, causing hyponatremia despite an elevated plasma osmolality. The magnitude of this effect can be calculated as follows:

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Corrected sodium concentration

- [Na]corrected= [Na]measured + 1.6x ([Glucose]-100mg/dl)/100

where [Na]corrected = corrected Na concentration

(the Na conc IF the glucose concentration were normal & its accompanying water moved back into the cells).

• The [Na]corrected is the more reliable indicator of the true ratio of total body sodium to TBW, the normal determinant of the Na conc.

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Regulation of Osmolality

• The plasma osmolality is tightly regulated to b/n 285 and 295 mOsm/kg.

- Modification of water intake and excretion maintains a normal plasma osmolality. In the steady state, intake & that produced by the body from oxidation balances water losses from the skin, lungs, urine, and gastrointestinal tract.

- Only intake & urinary losses can be regulated.• Osmoreceptors in the hypothalamus sense the

plasma osmolality.

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Regulation of Volume

• An appropriate IV volume is critical for survival. B/c Na is the principal EC cation & is restricted to the ECF, adequate Na is necessary for maintenance of IV volume.

• The principal EC anion, Cl, is also necessary, but for simplicity, sodium balance is considered the main regulator of volume status b/c body content of Na & Cl change proportionally given the need for equal numbers of cations & anions.

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• The kidney regulates sodium balance by altering the percentage of filtered sodium that is reabsorbed along the nephron. In the absence of disease, extrarenal losses and urinary output match intake,

• The most important determinant of renal Na excretion is the effective IV volume.

• Volume overload occurs when Na intake exceeds output, e.g. in RF with impaired ability to excrete sodium.

• Renal retention occurs during volume depletion, but this appropriate response causes the severe excess in total body Na present in CHF, liver failure, NS, & other causes of hypoalbuminemia.

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Maintenance and Replacement Therapy

• Maintenance intravenous fluids are used in a child who cannot be fed enterally.

• Patients lose water, Na, & K in their urine and stool; water is also lost from the skin and lungs. Maintenance fluids replace these losses & thus avoid development of dehydration & deficiencies of Na/ K.

• Maintenance fluids do not provide adequate calories, protein, fat, minerals, or vitamins not problematic for patients on IV fluids for few days.

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Maintenance water

• a crucial component of maintenance fluid b/c of obligatory losses which are both measurable (urine and stool) and not measurable (insensible losses from the skin and lungs). Failure to replace these losses leads to thirst & dehydration.

TABLE -- Calculating Maintenance Fluid Volume Body Weight Fluid per Day - 0–10 kg 100 mL/kg - 11–20 kg 1,000 mL + 50 mL/kg for

each kg > 10 kg - > 20 kg 1,500 mL + 20 mL/kg for each kg > 20 kg

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Maintenance electrolytes:• Na, K, & Cl are given in maintenance fluids to replace

losses from urine & stool.• Adequate chloride is provided if at least half of the Na

& K are given as Cl salts. - Sodium: 2–3 mEq/kg/24 hr - Potassium: 1–2 mEq/kg/24 hr

Glucose:• Maintenance fluids contain 5% DW, provide 17 cal/100

ml, ~ 20% of daily caloric needs. This is enough to prevent ketone production & helps minimize protein degradation.

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• Half NS & 1/4 NS are the choices for maintenance in children. These solutions are available with 5% dextrose.

• Infusing IV soln with lower osm can cause water to move into RBCs hemolysis.

• Fever ↑s evaporative losses from the skin, leading to 10–15% ↑ in maintenance water needs for each 1°C increase in Tº >38°C.

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Replacement therapy:• AVERAGE COMPOSITION OF DIARRHEA

- Na: 55mEq/L, K: 25mEq/L,HCO3 : 15mEq/L• REPLACEMENT OF ONGOING LOSSES

- Soln: D5 1/4 NS + 15mEq/L HCO3 + 25mEq/LKCl, - Replace stool ml for ml every 1–6hr.• OLIGURIA/ANURIA

- Put on insensible fluids (1/3 maintenance)• Replace urine output ml for ml with 1/2 NS.

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Deficit Replacement:• With DHN water is lost with concurrent loss of Na & K

isotonic DHN (normal serum Na values).• Water deficit is the % DHN X B Wt. Na & K deficits are derived

from the water deficit.• Dehydration needs acute intervention so that there is

adequate tissue perfusion. - isotonic soln: NS or RL usu satisfactory, - Blood, 5% albumin, & plasma are occasionally used for fluid

boluses.• Blood transfusion: with significant anemia/ blood loss. Plasma

is useful for children with a coagulopathy. The child with hypoalbuminemia may benefit from 5% albumin.

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Fluid & Electrolyte Rx: Specific Disorders 1. Pyloric Stenosis: - infants will have SSx of DHN, and hypokalemic metabolic

alkalosis.• Severe depletion of IC K ↑ exchange of H+ for Na (distal

nephrons of the kidney). *paradoxical presence of an acid urine with systemic alkalosis should be taken as signifying a marked K deficit & a need to increase amount of K used for repletion.

• only volume repletion, via administration of NaCl & KCl, corrects the metabolic alkalosis. Saline with added KCl is fluid of choice.

• Serum e’ normalize within 6–12 hr, but delay surgery for at least 24–48 hr for optimal readjustment of body functions.

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2. Adrenal Insufficiency:• Hypoglycemia prominent, + ketosis as the body attempts to

utilize FA as an alternative energy source. • Cortisol def ↓ CO & vascular tone; catecholamines such as EP

have ↓ inotropic & pressor effects in the absence of cortisol. • Aldosterone def results in hypovolemia due to decreased

resorption of Na in the distal nephron.• Hypotension & ↓CO lead to ↓GFR & thus decrease the

ability of the kidney to excrete free water. • Vasopressin (AVP) is secreted in response to hypotension,

decrease plasma osm & hyponatremia.• Aldosterone deficiency causes hyperkalemia by decreasing

potassium excretion.

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• IV 5% Glu in NS: to correct hypoglycemia, hypovolemia, & hyponatremia. If hyperkalemia is severe, it may require treatment.

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3. DKA

• Metabolic abnormalities resulting from a severe def/ ineffectiveness of insulin. The latter during stress as counter-regulatory hormones block insulin action.

• In 20–40% of children with new-onset diabetes, • the range of Sx depends on the depth of KA. - ketonuria, ↑ed ion gap, ↓serum HCO3/total CO2 &

↓pH, ↑ effective serum osm hypertonic DHN.• Severe insulinopenia/ lack of effective insulin action

results in a physiologic cascade of events in three general pathways:

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1. ↑ glu + ↓ glu utilization ↑ serum glu osmotic diuresis, loss of fluid & e’, DHN, & activation of RAA with K loss.

If glu ↑ & DHN are severe & persist for hours, risk of cerebral edema.

2. Increased catabolic processes cellular losses of Na, K, & PO4.

3. Increased FFA from fat stores, substrate for hepatic KA production. When ketoacids ↑, buffer systems are depleted & metabolic acidosis ensues.

• Reversal of DKA is associated with inherent risks that include hypoglycemia, hypokalemia, and cerebral edema.

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• Time Therapy - 1st hour 10–20mL/kg IV bolus NS/ LR Insulin 0.05 to 0.10u/kg/hr * may be repeated. NPO. Monitor I/O, flow sheet. Have mannitol - 2nd hr till DKA resolution 0.45 % NaCl, continue insulin drip 20mEq/L KPhos, 5% glu if BG <250mg IV rate= 85ml/kg+ maintenance-bolus/ 23 hr If K <3mEq/L, 0.5 to 1.0mEq/kg as PO K solution OR increase IV K to 80mEq/L

• Note that initial IV bolus is considered part of the total fluid allowed in the first 24 hr and is subtracted before calculating the IV rate.

• Sample calculation for a 30-kg child:• 1st hour = 300mL IV bolus NS/ RL.• Depending on the degree of DHN, the fluid deficit can be corrected with

larger volume & over 30-36 hr.