Electrolytes in Pediatrics

8/13/2019 Electrolytes in Pediatrics

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Fluid & ElectrolytesFluid & Electrolytes

inin

Pediatric PatientsPediatric Patients

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Body Fluids

TBW (60% wt)

= Intracellular fluid (ICF, 30-40% wt) +Extracellular fluid (ECF, 20-25% wt)


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6 8 . total bodywater

A. 4 Litre

Body Fluids

C. 6 Litre


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Total body water (TBW)

Term infant: 75% wt

Age 1 yr: 60% wt

Male adult: 60% wt

Body Fluids

Female adult: 50% wt


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Body Fluids


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6 8 . total bodywater

A. 4 Litre

Body Fluids

C. 6 Litre

C ( 8 0.75 )


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34 2.5 . blood volume

A. 150 mL

Body Fluids

B. 200 mL

C. 250 mL


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ECF (20-25% wt)

= Interstitial fluid (15% wt) + plasma (5% wt) Intravascular (blood) fluid

Body Fluids

Preterm NB: 10% wt


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34 2.5 . blood volume

A. 150 mL

Body Fluids

B. 200 mL

C. 250 mL

B ( 2500 0.1 )


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Intravascular fluid Interstitial fluid

ExamplesHeart failure

Body Fluids

Sepsis


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Electrolyte composition


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Osmolality

Osmolol gapWhen Osm

measured

- Osmcalculated

> 10 mOsm/kg

Unmeasured osmoles e.g., methanol, ethylene glycol,ethanol, mannitol


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7 diabetic ketoacidosis serum Na 130 mmol/L sugar 300 mg/dLserum sugar 100 mg/dL serumNa

A. 130.0 mmol/L

B. 133.2 mmol/L

C. 136.4 mmol/L


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Osmolality

HyperglycemiaShift of H

2

O

Dilution of Na

[Na] = [Na] + 1.6 [ lucose] 100 /100


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7 diabetic ketoacidosis serum Na 130 mmol/L sugar 300 mg/dLserum sugar 100 mg/dL serumNa

A. 130.0 mmol/L

B. 133.2 mmol/L

C. 136.4 mmol/L

B


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Osmolality

PseudohyponatremiaNa content / serum vol. while high serum lipids or

proteins


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Osmolality

Osm regulationH

2O balance

IntakeIntake + oxidation = skin + lungs + urineurine + GI loss

Osmorece tor


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Osmolality


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Osmolality


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Osmolality

ExamplesNephrotic syndrome (recent onset)

SIADH

Diabetes insi idus


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Osmolality

Minimum urine Osm30-50 mOsm/kg

CH receiving little salt && inadequate protein Risk for hypo Na

Maximum urine Osm1200 mOsm/kg

Less urine conc. ability in newborn Risk for hyper Na dehydration


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Intravascular volume

Body content of Na & Cl

Urine Na excretion

Undetectable urine Na

RegulatorsRenin-angiotensin system

Atrial natriuretic peptide


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Intravascular volume


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Sodium


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Sodium

IntakeBreast milk: ~ 7 mEq Na /LFormula: 7-13 mEq Na /L

Excretion

Increase in diarrhea, cystic fibrosis (sweat Na loss),some renal diseases

Decrease in hyperaldosteronism, Liddles syndrome(dysregulation of ENaC)


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Hypernatremia

Level > 145-150 mEq/L

Etiology

Excessive Na

, ,

hyperaldosteronism

Water deficit

: DI, insensible loss in NB, inadequate intakeWater & Na deficit

: GI, cutaneous, or renal losses


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Hypernatremia

ManifestationsIf dehydrated, less symptoms at initial

If Na largely or rapidly increase, CNS symptom

H er l cemia & mild h o Ca occasional

Brain hemorrhage

Central pontine myelinolysis (occasional)

Brain edema in chronic case (due to rapid Nacorrection)

HYPERNATRAEMIA


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HYPERNATRAEMIA

H2O

Losses

Na++H2O

Deficits

Na+

Addition

ExcessHypovolemia

TBW

Body Na+

UNaVariable

UNa>20 mEq/l

Euvolemia

TBW

Normal body Na+

Hypervolemia

TBW

Body Na+

UNa>20 mEq/l

UNa


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Hypernatremia

Treatment of hyper Na dehydrationRestore intravascular vol.

NS 20 mL/kg over 20 min (repeat till vol. stored)Determine time for correction

Reduce Na < 12 mEq/L q 24 hr

Administer fluid at constant rate D5 NS 20 mEq/L KCl at rate 1.25-1.5 time maintenance

Follow serum Na

Adjust fluid based on status & serum Na

Replace ongoing losses as they occur


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2 4.7 nephrogenic DI 4.0 serum Na 170 mmol/L free water deficit

A. 320 mL

B. 360 mL

C. 400 mL

F W t D fi it


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Free Water Deficit

Current total Na = Previous total Na

C1V

1= C

2V

2

Naactual TBW = Nadesired (TBW + H2ODef)

H2O

Def= TBW [(Na

actual/ Na

desired) 1 ]

( if TBW = 0.6 wt, Nadesired= 145 mEq/L )

H2O

Def= 0.6 wt* [(Na

actual/ 145) 1] 1000 mL

= [ 600 wt / 145 ] [ Naactual

145 ] mL

4 wt [ Naactual

145 ] mL

* actual weight


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Hyponatremia

Level < 130-135 mEq/L

Etiology1 Pseudohyponatremia

3 Hypovolemia: Extrarenal or renal loss

4 Euvolemia: SIADH, glucocorticoid def,

hypothyroidism, H2O intoxication5 Hypervolemia: CHF, hypoalbuminemia,

renal failure, capillary leak

HYPONATRAEMIA (


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Total body water

Total body Na+ Total body water

Total body Na+

( q )

PSEUDO-

HYPONATRAEMIA

Normal Plasma osmolality High FACTITOUS

HYPONATRAEMIALow

TRUE HYPONATRAEMIA

ECF volumeDecreased Increased

Normal

Total body water

Normal total body Na+

Extrarenal

GI lossSkin lossThirdspaceloss

UNa

20 mmol/l

Non-oedematous states

SIADHExcessive water intake

Antidiuretic drugsReset osmostate

Glucocorticoid deficiency

Hypothyroidism

Oedematous states

Nephrotic syndromeHepatic failureCardiac failureCapillary leak

syndrome

Acute and chronic

renal failure

UNa>20 mmol/l

UNa20 mmol/l


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H i


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Hyponatremia

Treatment of dehydrationRestore intravascular vol.

NS 20 mL/kg over 20 min (repeat till vol. stored)Rapid vol. repletion 20 mL/kg NS or Ringer lactate (max 1 L) over 2 hr

Calculate 24-hr fluid needs (subtract isotonic fluid alreadyadministered)

Administer remaining vol.

D5 NS 20 mEq/L KCl over 24 hr

Follow serum Na


H t i


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If active symptoms, give 3% NaCl (0.5 mEq/ mL)toraiseserum Na125 mEq/L

Volume = Na space wt (125 [Na]actual

)

Hyponatremia

or = 4 - 6 mL/kg


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PotassiumPotassium


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The majority of body K is contained in muscle

The majority of extracellular K is in bone

< 1% of total body K is in plasma

K t i t llK t i t ll K t t f llK t t f ll


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NaNa

150150 mEq KmEq K++/L/L

K movement into cellsK movement into cells

by effect ofby effect of

InsulinInsulin

--Adrenergic agonistsAdrenergic agonists

pHpH

K movement out of cellsK movement out of cells

by effect ofby effect of

--Adrenergic agonistsAdrenergic agonists

pHpH

plasma osmolalityplasma osmolality

ATPATPATPATP

KK

K channelK channelK channelK channel

K

K

Hyper KHyper K stimulatesstimulates

adrenal release ofadrenal release of

catecholaminescatecholamines

insulin secretioninsulin secretion


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Effect of intracellular potassium

K gradient generate action potential & rate ofcellular repolarization

Low conc raises intra-pH while high conc lowersintra-pH.

Maintaining cell volume because of its importantcontribution to intracellular osmolality.


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Most K absorption occurs in small intestine,whereas colon exchanges body K for luminal

Na.

Renal failure aldosterone and lucocorticoids

colonic K secretion.


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Urine K excretion byUrine K excretion by aldosteronealdosterone glucocorticoidsglucocorticoids

ADHADH

high urinary flow ratehigh urinary flow rate

high sodium delivery tohigh sodium delivery to

the distal nephronthe distal nephron

Urine K excretion by

insulin

catecholamines

urinary ammonia


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+

+


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HyperkalemiaHyperkalemia

S O S O O

DECREASED EXCRETION

Renal failure or renal diseaseRenal failure or renal diseaseEtiologiesEtiologies


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SPURIOUS LABORATORY VALUE

HemolysisHemolysis Tissue ischemia during blood drawingTissue ischemia during blood drawing Thrombocytosis or leukocytosisThrombocytosis or leukocytosisINCREASED INTAKE

Intravenous or oralIntravenous or oral

Blood transfusionsBlood transfusionsTRANSCELLULAR SHIFTS

AcidemiaAcidemia HyperosmolalityHyperosmolality

Renal failure or renal diseaseRenal failure or renal diseaseeg,. renal tubular disease, urinary tracteg,. renal tubular disease, urinary tract

obstruction, sickle cell disease, kidneyobstruction, sickle cell disease, kidneytransplant, lupus nephritistransplant, lupus nephritis

Mineralocorticoid disordersMineralocorticoid disorders-- Acquired Addison diseaseAcquired Addison disease

-- 2121--OH defOH def

-- 33--OH dehydrogenase defOH dehydrogenase def

-- Lipoid cong adrenal hyperplasiaLipoid cong adrenal hyperplasia

Insulin deficiencyInsulin deficiency

Cellular damage (eg,.Cellular damage (eg,.Rhabdomyolysis, tumor lysisRhabdomyolysis, tumor lysissyndrome, tissue necrosis,syndrome, tissue necrosis,hemolysis/hematomas/GI bleeding)hemolysis/hematomas/GI bleeding)

Medications (succinylcholine, digitalisMedications (succinylcholine, digitalis

intoxication, fluoride intoxication, Betaintoxication, fluoride intoxication, Beta--adrenergic blockers)adrenergic blockers)

ExerciseExercise Malignant hyperthermiaMalignant hyperthermia Hyperkalemic periodic paralysisHyperkalemic periodic paralysis

-- Adrenal hypoplasia congenitaAdrenal hypoplasia congenita

-- Aldosterone synthase defAldosterone synthase def

-- AdrenoleukodystrophyAdrenoleukodystrophy

-- Hyporeninemic hypoaldosteronismHyporeninemic hypoaldosteronism

-- Pseudohypoaldosteronism type I & IIPseudohypoaldosteronism type I & II

Medications (eg,. ACEIs, ARBs, KMedications (eg,. ACEIs, ARBs, K--sparing diuretics, cyclosporin, NSAIDs,sparing diuretics, cyclosporin, NSAIDs,

trimethoprim)trimethoprim)


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Serum K is 0.4 mEq/L higher than plasma K For platelet 100,000/L, serum K 0.15 mEq/L

WBCs > 200,000/L can cause dramatic serum K If significant WBCs or platelets, sample should be from

plasma that is evaluated promptly.


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Excessive K intake, by itself, not usually causehyper K.

T l t l t h K


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To evaluate renal response to hyper K

Transtubular potassium gradient (TTKG)

TTKG < 8 during hyper K

= Defect in renal K excretion due to either lack of

aldosterone or inability to respond to aldosterone


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In adrenal disorders causing decreased production of

aldosterone

Hyper K, metabolic acidosis and salt wasting with hypo Na


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A deficiency in renin, a result of kidney damage, canlead to decreased aldosterone production.

Impaired renal function in some patients partiallyaccounts for hyper K

Pseudohypoaldosteronism type 1


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In autosomal recessive variant,

- defect in renal Na channel

- severe symptoms, beginning in infancy

In autosomal dominant form,

- defect in aldosterone receptor

- milder, often remitting in adulthood



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Gordon syndrome

Autosomal dominant

Activating mutations in either WNK1 or WNK4 Hypertension due to salt retention and impaired

excretion of K and H+

Cardiac Manifestations


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Cardiac Manifestations

ECG changes begin with peaking T waves followed,as K level increases, by

PR interval,flattening P wave,

widening QRS complex and

eventually ventricular fibrillation

If K level > 6.06.5 mEq/L, ECG should be obtained.

Agent Dose Onset Comments/side effects

Medication for Hyperkalemia


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Agent Dose Onset

(Duration)

Comments/side effects

NaHCO3

(1 mEq/mL)

1 mEq/kg IV over 10-30 min 15-30 min

(1-4 hr)

Assure adequate ventilation; do

not give simultaneously with

Ca

Ca gluconate

(10%)

0.5-1 mL/kg IV over 5-15 min Immediate

(30-60 min)

Monitor ECG for bradycardia; stop

infusion if pulse


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Normal ECG

(~K+= 6-7 mEq/L)

- Elimination K+ from all intake- Polystyrene resin (kalimate,

kayexalate)

Abnormal ECG

(~K+>7 mEq/L)

- 10% Ca gluconate 1 mL/kg IVin 5 min

- NaHCO3 1-2 mL/kg IV in 10 min

K+ > 6 mEq/L

po q 6 hr or enema over4-6 hr

- Regular insulin 0.1 U/kg IV withD25W 2 mL/kg in 30 min

- Dialysis if above unsuccessful


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HypokalemiaHypokalemia

EtiologiesEtiologiesSPURIOUS High white blood cell countTRANSCELLULAR SHIFTS

RENAL LOSSES ( t)


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TRANSCELLULAR SHIFTS

Alkalemia

Insulin, -adrenergic agonists, drugs/toxins(theophylline, barium, toluene) Hypokalemic periodic paralysisDECREASED INTAKE

EXTRARENAL LOSSES

Diarrhea

Laxative abuse SweatingRENAL LOSSES

With metabolic acidosis

Distal renal tubular acidosis (RTA)

RENAL LOSSES (cont)

With metabolic alkalosis- Low urine chloride

Emesis nasogastric suction Chloride losing diarrhea Cystic fibrosis

Low chloride formula Posthypercapnia Previous loop or thiazide diuretic use- High urine chloride and normal blood

Proximal RTA Ureterosigmoidostomy Diabetic ketoacidosisWithout specific acid-base disturbance

Tubular toxins: amphotericin, cisplatin,aminoglycosides

Interstitial nephritis Diuretic phase of acute tubular necrosis

Postobstructive diuresis Hypomagnesemia High urine anions (e.g., penicillin or penicillin

derivatives)

Gitelman syndrome Bartter syndrome Loop and thiazide diuretics- High urine chloride and high blood pressure

Adrenal adenoma or hyperplasia Glucocorticoid-remedial aldosteronism

Renovascular disease Renin-secreting tumor 17-hydroxylase def 11-hydroxylase def


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Hypokalemia is common in children, with mostcases related to gastroenteritis.

Clinical manifestration


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Muscle weakness, cramps or paralysis with the legs,followed by the arms (when K < 2.5 mEq/L)

Urinary retention, constipation orileus

(when K < 2.5 mEq/L) Primary polydipsia, impaired urinary concentrating ability,

interstitial nephritis and renal cysts Hypo K may worsen hepatic encephalopathy because

hypo K stimulates renal ammonia production

To evaluate renal response to hypo K


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p yp

Transtubular potassium gradient (TTKG)

TTKG > 4 in the presence of hypo K

= Excessive urinary losses of potassium

Management


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g

Type of therapy depends on K level, clinical symptoms,renal function, presence of K transcellular shifts, ongoing

losses, and the patient's ability to tolerate oral K. Oral K is safer, albeit not as rapid in urgent situations. Choice for supplementationdepends on concurrent

electrolyte abnormalities


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Fluid TherapyFluid Therapy

Maintenance Therapy

Body Surface Area Method 1500 mL/BSA (m2)/day


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Body Surface Area Method 1500 mL/BSA (m )/day

100/50/20 Method

Weight

0-10 kg

11-20 kg

> 20 kg

Fluid

100 mL/kg/day

100 mL + 50 mL/kg/day for every kg > 10 kg

1500 mL + 20 mL/kg/day for every lg > 20 kg

Weight

0-10 kg

11-20 kg

> 20 kg

Fluid

4 mL/kg/h

40 mL + 2 mL/kg/h for every kg > 10 kg

60 mL + 1 mL/kg/h for every kg > 20 kg

Insensible + Measured Losses Method

400-600 mL/BSA (m2)/day + urine output (mL/mL) + L

other measured losses (mL/mL)

Maintenance Therapy


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High water needs of smaller, less mature patients

Upper limit of 2.4 L/ 24 hr in adult-sized patients Maximum fluid rate 100 mL/hr

Maintenance Therapy


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Composition of Intravenous Solutions

Fluid [Na+ ] [Cl- ] [K+ ] [Ca2+ ] [Lactate- ]

Normal saline (0.9% NaCl) 154 154

Normal saline (0.45% NaCl) 77 77

Normal saline (0.225% NaCl) 38.5 38.5

Ringer lactate 130 109 4 3 28

Maintenance Therapy


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In all children,

carefully monitor wt, urine output, and elytes.

Maintenance Therapy


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Sources of Water lossUrine 60%

Insensible loss (ISL) ~35% (skin & lungs)Stool 5%

ISL, 40% in infants; 25% in adolescents

Maintenance Therapy


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Fever - Increase maintenance fluids by 10-15%

for each degree > 38 oC

Tachypnea

(nonhumidified environment)

- Increase maintenance fluids by 5-10%

Replacement Therapy


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AVERAGE COMPOSITION OF DIARRHEA

- Sodium: 55 mEq/L

- Potassium: 25 mEq/L

- Bicarbonate: 15 mEq/L

APPROACH TO REPLACEMENT OF ONGOING LOSSES

- Solution: D5 0.2 NS + 20 mEq/L NaHCO3

+ 20 mEq/L KCl

- Replace stool mL/mL q 16 hr

Replacement Therapy


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AVERAGE COMPOSITION OF GASTRIC FLUID

- Sodium: 60 mEq/L

- Potassium: 10 mEq/L

- Chloride: 90 mEq/L

APPROACH TO REPLACEMENT OF ONGOING LOSSES

- Solution: NS + 10 mEq/L KCl

- Replace output mL/mL q 16 hr

Deficit Therapy


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1. Mild dehydration

6% in older child or adult

Body weight lossa

15% (9%)


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( ) ( ) ( )

Symptoms interstitial fluid

- Colour

- Mucous membranes- Eyes

- Skin tur or

Thirst

Pale

Dry

Restless

Grey

ParchedDeep set

Tentin

Lethargic/obtunded

Mottled

Crackedsunken

Loss

- Fontanelle

intra-vascular vol

- Pulse

- CRTb

- BP

- Urine output

Flat Soft

rate, weak

~ 2 sec

Normal/low

Oliguria

Sunken

rate, feeble

> 3 sec

Low/unrecordable

Anuria

a, Percentage outwith parentheses indicate estimates for infancy and those within are estimates beyond infancy.

b, capillary refill time

Dehydration Therapy


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Treatment of dehydrationRestore intravascular vol.

NS 20 mL/kg over 20 min (repeat till vol. stored)

Rapid vol. repletion 20 mL/kg NS or Ringer lactate (max 1 L) over 2 hr

Calculate 24-hr fluid needs (subtract isotonic fluid alreadyadministered)

Administer remaining vol.

D5 NS

20 mEq/L KCl over 24 hrFollow serum Na


Dehydration Therapy


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Monitoring TherapyVITAL SIGNS Pulse

Blood pressureINTAKE AND OUTPUT

Urine output and specific gravityPHYSICAL EXAMINATION Weight

Clinical signs of depletion or overload

ELECTROLYTES

Dehydration Therapy


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Acute diarrheaIntravenous therapy may be required in

severe dehydration

uncontrollable vomiting

, ,

gastric or intestinal distention

Dehydration Therapy


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Acute diarrheaDeficit

Mild dehydration: ORS 50 mL/kg within 4 hr

Moderate dehydration: ORS 100 mL/kg over 4 hr

Maintenance (after rehydration) Mild diarrhea: ORS 100 mL/kg/24 hr until the diarrhea

stops.

severe diarrhea: ORS 1015 mL/kg/hr under closesupervision

Dehydration Therapy


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A risk of hypernatremia with the WHO ORS

if maintenance solution is usedwithout supplemental water or formula


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Electrolytes in Pediatrics