PEDIATRICS II

1.2. Fluids & Electrolytes

Sheryl Wong, MD, DPPS | 11 August 2022

OUTLINE
I. The Basics
II. Clinical Application: Dehydration
III. Electrolytes
IV. Electrolyte Imbalance

LEGEND
Important Lecturer Book PPT Transer
★ 📣 📚 🖥 ✍

OBJECTIVES
At the end of this lecture, the future Bedan doctor must be able
to:
1. Understand fluid composition of the body and regulation of body
fluids
2. Understand different types and degrees of dehydration and
management plans Figure 2. Total Body Water + Fluid Compartments
3. Define causes and manifestation of electrolyte imbalance
4. Formulate plan for rehydration TOTAL BODY WATER COMPUTATION: 
T/N: Please do not be alarmed at the length of the trans! We have 4 FORMULAS:
pages of Appendices, and the photos are enlarged for your TBW = 0.61 x body weight (kg) + 0.251
convenience. 🍀 For PRACTICAL APPROACH: TBW = 0.6 x body weight
I. THE BASICS (kg)
A. TOTAL BODY WATER
→ Percentage of body weight that is made up water EXAMPLE:
→ Changes with age Using Practical Approach compute for TBW of a 70 kg man.
TBW = 0.6 x 70 kg
TBW = 42 LITERS
Lifted from USMLE 1: 
HIKIN: High K INtracellularly.
★ ★ ★ 60-40-20 rule (% of body weight for average person):
- 60% TBW
- 40% ICF
- 20% ECF
*If ever nalilito kayo kung sino mas malaki just remember 60-40-
20 TIE!
Plasma volume measured by radiolabeled albumin.
Extracellular volume measured by inulin.
Osmolality = 285-295 mOsm/kg H20.
Lifted from 2023.

★ Overweight (high fat)  TBW decreases 

★ Dehydration  TBW decreases 
Figure 1. Total body water, intracellular fluid, and extracellular fluid B. FLUID COMPARTMENTS OF THE TBW
as a percentage of body weight as a function of age.
→ 2 main compartments:
o Extracellular fluid (20-25%)
 Fetus: Very high
● Interstitial (15%)
 At birth (term): 75% of body weight ● Plasma (5%)
 Premature infants have higher TBW than term infants o Intracellular fluid (30-
 1 year old: 55-60% (same as adult) 40%)
 Women/ Obese: 55% → Fetus/ Newborn: ECF > ICF
 Greater body fat → Postnatal diuresis:
 Fat has very low water content Decrease ECF
→ Cellular growth: Increase
 Men: 60% ICF
 More muscle mass → 1 year old: ICF (40%) > ECF
 Muscle has high water content (20%)
→ Puberty: Male has higher
muscle mass, therefore ICF
is greater than women.
 Newborn/Fetuses mas mataas yung volume nung ECF. As the
childgrows older mas tumataaas na yung level ng ICF as
compared to your ICF. Kunwari dahil umihi na yung bata
pagkapnganak mag dedecrease na din yung ECF nya.

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TG: DE GUZMAN, GASPILLO, MARIANO, GALUT🍀
PEDIATRICS II LE#1
1.2. Fluids & Electrolytes
And then because of the cellular growth, kailangan ng
metabolism ng water intracellulary kailangan ng tumaas yung
volume ng water inside the cell.

A. EXTRACELLULAR FLUID
→ 20-25% of body weight
→ Extracellular fluid is composed of:
o Plasma water (5%)

Table 1. ECF components comparison and its accompanying condition. Lifted

from 2023
Plasma can be altered (either Inc or Figure 3. Electrolyte Composition of ECF Component
Dec) by: ⭐Na is the dominant cation in plasma.
Dehydration (decrease ang plasma water) K is the dominant cation in ICF.
Anemia
PLASMA
Polycythemia → Concentrations of the major cations and anions in the
WATER (5%)
Abnormal plasma osmolality  intracellular space and the plasma are expressed in
Heart failure (may fluid overload so tataas
mEq/L.
ang plasma water)
→ ECF
Low albumin
o Na+: dominant cation; determinant of extracellular
Interstitial fluid increases in the presence
osmolality
of:
o Cl-: dominant anion
Edema
→ ICF 
Heart Failure 
o K+ : most abundant cation
INTERSTITIAL Protein-losing enteropathy 
o Most anion in the ICF are proteins, organic anions,
FLUID (15%) Liver failure
phosphate
Nephrotic syndrome
→ Difference in anion: Cell membrane
Sepsis
Ascites
o  The reason why there is a difference in the
Pleural effusion anion content between the ICF versus ECF is
because of the presence of the cell membrane.
ECF/ICF COMPUTATION:
FORMULAS: → Difference in cation: Na-K ATPase pump
ECF (LITERS) = 0.239 x weight (kg) + 0.325 o The reason why there is a difference in the
ICF (LITERS) = TBW – ECF cation content between the ICF versus plasma is
Practical approach: TBW = 0.6 x body weight (kg ) because of the Na-K ATPase pump

Practice Question: D. WATER REGULATION

5-year-old male that weighs 20 kg. PLASMA OSMOLALITY
What is the formula for calculating total body fluids?
RECALL the formula for TBW! (see page 1) → 🖥 ICF and the ECF are in osmotic equilibrium because
How much water does the patient have in his body? the cell membrane is permeable to water.
0.6 x 20 kg = 12 liters o If osmolality in 1 compartment changes, then water
Lifted from 2023 movement leads to a rapid equalization of osmolality,
with a shift of water between the ICS and
o Interstitial fluid (15%) extracellular space (ECS)
o 📣 Water is the one that moves across the gradient,
B. INTRACELLULAR FLUID to equalize the osmolality.
→ 30-40% of body weight → Concentration of solute particles in plasma
→ Starts to rise in the first year of life as the ECF falls o 📣 Kung ano makuha mong plasma osmolality is
→ Bounded by membranes of the cells of the soft tissues already reflective of your ICF osmolality
→ ⭐ constant at 285-295 mOsm/kg 
C. ELECTROLYTE COMPOSITION → estimated using:
glucose BUN
o Osmolality=2 x ( Na ) + +
18 2.8
→ Modification of water intake and water excretion 
o Maintains balance between water intake and water
produced by body from oxidation of carbohydrates,
fat and proteins of exogenous and endogenous
source (WATER INTAKE) as well as losses from
kidneys, lungs, skin and GI tract (WATER
EXCRETION)
o Only water intake and urinary losses can be
regulated
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Practice Question: 
WATER INTAKE  What would be the complaint of a child if he/she is getting
→ Stimulated by sensation of thirst dehydrated? “Nauuhaw po”
→ Thirst  What ways can water be excreted from the body?
o conscious desire to drink water and is regulated *REVIEW CONCEPTS IN WATER EXCRETION
by the mid-hypothalamus (osmoreceptors)
→ Major stimuli II. CLINICAL APPLICATION: DEHYDRATION
o Increase plasma osmolality as little as 1-2% → Diminution in volume of the ECF
→ Different types are based on:
o Depletion of ECF volume by 10% (such as in
o degree of water loss
hemorrhage/massive bleeding, sodium
o serum sodium concentration
depletion, severe shock)
o 📣 [nonverbatim] children in the ward suffering → 📣 Diarrhea is the 2nd leading causes of child mortality in
the country.
from shock will ask for water; it would herald the
progression of deterioration, until multi-organ
A. TYPES OF DEHYDRATION
failure.
ISOTONIC (ISONATREMIC) DEHYDRATION
WATER EXCRETION → Loss of TBW and loss of Sodium are EQUAL
→ Serum Sodium: NORMAL (135-145 mEq/L)
Obligatory Water Losses → Serum osmolality: NORMAL (280-300 mOsm/L)
 minimum volume of fluid a person must lose every day to → Prefix “iso-“ – equal
maintain fluid balance
HYPOTONIC (HYPONATREMIC) DEHYDRATION
→ Loss of sodium ions proportionally GREATER THAN
I. Insensible Water Losses water loss
→ evaporative water loss from lungs and skin → Serum Sodium: LOW (<130 mEq/L)
→ Serum osmolality: LOW (<260 mOs/L)
o ex. Mechanically ventilated na child
→ Seen in patients who lost both water and salt by a
→ regulated by factors independent of body water pathologic process and has received partial replacement
→ influenced by: of water with either insufficient or no salt
o body and environmental temperatures ex. Fever o 📣 Analogy: uminom ka ng pure water na walang
or mainit yung lugar or malamig asin → napalitan yung water pero hindi yung asin
o rate of respiration → Body water shifts from ECF to ICF
o 📣 Sa ECF, konti asin & madami tubig kaya
o partial pressure of water vapor in the environment
ginawa ng tubig, pumasok sa ICF [✍since dun mas
→ ⭐ proportionate to body surface area madaming asin. Remember: where sodium goes, water
II. Urinary Water Excretion follows!]
→ amount of water necessary to excrete a solute load by the → Circulatory disturbance occurs at small degrees of
kidneys ex. ICU patients- monitor dapat input and dehydration and may easily become severe
o 📣Circulatory disturbances: vital signs
ouput
o 📣Changes in BP, HR kapag may hypotonic
→ OBLIGATORY
(hyponatremic) dehydration
→ IMPORTANT FUNCTIONS OF THE KIDNEYS to maintain
body homeostasis HYPERTONIC (HYPERNATREMIC) DEHYDRATION
→ Closely regulate the composition and volume of the ECF → Losses of water are GREATER THAN salt losses
→ Affected by: → Serum Sodium: HIGH (>150 mEq/L)
o Anti-diuretic Hormone Secretion Regulation: → Serum osmolality: HIGH (>300 mOsm/L)
● Regulated by effective osmotic pressure of the → Body water shifts from ICF to ECF
→ Less circulatory disturbance
ECF that is produced by solutes (Na, Cl) that
DO NOT readily penetrate cell membranes
Case: Losing It All
● monitored by vesicles in the supraoptic nuclei A 6 y/o patient comes in with a history of voluminous
(osmoreceptors) so anyone with brain tumor diarrhea which was described as like rice water and there
can affect the ADH secretion was barely any stool. The patient was given almost 2 liters
● Threshold for release: 280 mOsm/L of distilled water as a way of correcting the dehydration.
● Release if vasopressin (ADH) may be What is the expected serum sodium?
initiated or inhibited by changes in plasma
osmolality as little as 1-2% a. 138 mmol/L
b. 154 mmol/L
● After >8% dehydration and exponential
c. 122 mmol/L (Hypotonic hyponatremic
with more marked dehydration dehydration)
III. Stool Water Losses 📣 The child was rehydrated, but only with pure water. This
→ amount of water lost in the stools; small in amount but can would cause hypotonic hyponatremic dehydration <130
be significant in intestinal diseases mEq/L.

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C. LABORATORY EXAMS FOR DEHYDRATION ⭐📣
CBC & PLATELET – HEMATOCRIT → Neonate: 0 – 28 days
→ Simple and readily available → Infant: 28 days – 1 year old
→ Changes in direct proportion to severity of ECF volume → Older child: >1 year old – 18 years old
changes → Take note of the skin (touch) and skin turgor.
o 📣 Hematocrit ang talagang target mo, dapat mataas o Clammy – malagkit pag hinawakan
Hct ng dehydrated patients due to → Buccal Mucosa/Lips
hemoconcentration means the patient is already o Under severe, it will be parched/cracked and you
dehydrated might need to use a tongue depressor
→ ✍🏽 Blood is made up of plasma (55%), red cells (44%), → Pulse rate not cardiac rate, so check the radial or brachial
and buffy coat (<1%). Plasma’s major component is water pulse and correlate per age group
(92% by weight). So, in dehydrated patients, there will be → Ex. 6 hours na walang ihi at all = anuria
a decrease in plasma causing red cells/ hematocrit to be → Ex. 6 hours but urine output is less than normal = oliguria
falsely elevated due to hemoconcentration → Values on the top will be used for the formula on fluid
deficit, depending on how dehydrated the child is and if
URINALYSIS they fall in the older child or infant range
→ ↑ Specific gravity in dehydration (>1.020) due to demands
on kidney to conserve water
o 📣 Urine color: dark yellow to orange
→ Glucose and ketones may be elevated in Diabetic
Ketoacidosis
→ 📣 Correlate the whole urinalysis as sp. gravity or even
color may appear normal but other results like hyaline cast
may help raise suspicions of dehydration

ELECTROLYTES
→ Na, K, Cl

BLOOD UREA NITROGEN (BUN)

→ Elevated due to prerenal azotemia but may not be SIGNS OF DEHYDRATION
correlated with the degree of dehydration
→ 📣 Used for computing plasma/serum osmolality

Clinical Application
→ What are the PE findings in a child with dehydration?
→ What are the signs of dehydration?

Write your answers here:

Figure 4. Signs of dehydration ⭐

→ Tachypnea due to metabolic acidosis
→ Tachycardia, hypOtension and peripheral vasoconstriction
in response to low blood pressure.
→ Oliguria
o 📣 [nv] Clinical application: Diapers are weighed
in the hospital to measure urine output by getting
the difference of a new diaper to the used diaper.
o Inform parents to hand the diaper over as soon
as the child urinates since urine evaporates and
could cause inaccurate measurement of urine
output
→ Sunken eyeballs
o Practice in determining if sunken or not since
there are some who naturally have sunken eyes.
(Ask the parents!)
o Hence, why it can’t be your only basis for
dehydration
→ Dry tongue, dry buccal mucosa, cracked tongue
Figure. Table 11.2 Clinical Observations in Dehydration ★

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Table 2. Values for % dehydration – To be used for fluid deficit repletion
computation (From 2023 Trans) (Retracted from Figure.)
Required
%
Severity Volume
Dehydration
(mL/kg)
Mild 3% 30 mL/kg
CHILD Moderate 6% 60 mL/kg
Severe 9% 90 mL/kg
Mild 5% 50 mL/kg
INFANT Moderate 10% 100 mL/kg
Severe 15% 150/mL/kg
Figure 5. ✍🏽 Halos same lang, read na lang yung green boxes. Steps for Phase 2:
→ Replace half of remaining deficit over the 1 st 8 hours
TREATMENT (includes any fluid given in the initial stabilization phase)
Table 1. Important to differentiate → Replace second half of deficit over the following 16 hours
VOLUME REPLACEMENT making sure to also include maintenance fluid volume
MAINTENANCE THERAPY replacement during this time
THERAPY
→
No dehydration
→
Provision of fluids and
electrolytes to replace
Dehydration usual or normal ongoing
Ex. Vomiting, diarrhea losses and metabolic
needs
→ 📣 We are trying to
prevent dehydration
→ 📣 But for diarrhea, you will be combining these two to
address both the dehydration and for the patient’s
physiological needs.

Figure 6. Table 11.3 Composition of Frequently Used Parenteral

VOLUME REPLACEMENT STRATEGY Rehydration Fluids (Larger photo, see appendix)
→ 📣 This strategy is for those who are dehydrated/ have → 0.9% (isotonic) is the highest concentration of sodium (US
diarrhea only)
o Kasama na din yung maintenance ng volume dito → Colloids – used in dengue, but expensive

Phase 1: Initial Stabilization Phase 3: Recovery and Ongoing losses

→ Rapid fluid resuscitation with isotonic fluid → Ongoing replacement of continuing abnormal losses
→ 20 ml/kg represents on 2% volume replacement o Usually given after fluid deficit has been corrected
and while normal maintenance needs are being
Steps/ Choices for Phase 1: provided
→ Initial emergency treatment for only if with shock o Continue maintenance fluid replacement
(=hypotension, check BP first!) o Seen in persistent diarrhea, vomiting, or drainage
o PNSS/PLRS at 20ml/kg to infuse over 30-60 from enteral tubes
minutes → Choice of fluids will depend on the source of losses
→ Initial treatment for mild to moderate dehydration but → Losses should be determined and replaced every 6-8
normal BP hours
o PNSS/PLRS at 20ml/kg to infuse over 1-2 hours → But needs to be individualized
o Refer to table below
✍🏽Remember! Faster infusion for shock! o Ex. Diarrhea
● 10-90 mEq/L Na+
Sample Computation ● 10-80 mEq/L K+
Given: 20 kg child in shock ● 10-110 mEq/L Cl-
20 kg x 20 ml/kg = 400 ml
Order: Start PNSS 400ml to run over 30 minutes (as bolus)

Phase 2: Deficit Repletion, Maintenance Volume, and

Ongoing Losses
→ Determine type and degree of dehydration
→ History, PE, serum electrolytes, and acid-base status
→ Replacement protocol
→ Go back to Figure_ Clinical observations in dehydration

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Figure 7. Table 11.6 Electrolyte Composition of Various Fluids

Figure 10. ORS- 75

→ Oral Rehydration Solutions (ORS) may be used as long as

Table 3. ORS contents in mmol/L:
the patient tolerates fluids orally
o Ex. Diarrhea. Nacompute na natin yung IV fluids sa Na+: 75mmol/L Citrate: 10 mmol/L = HCO3: 30 mmol/L
Cl-: 65 mmol/L Glucose: 75 mmol/L
ER, kung ano yung state nya ng dehydration.
K+ 20 mmol/L
o Pag dating sa ward nagsusuka pa, nagtatae. Pero
nakakainom, pwede mo palitan yung total volume ng
naisusuka, with ORS → Na+ and Glucose are equimolar. We can say na okay lang
bigyan ORS ang bata since may asukal naman. So, kung
hindi makakain ng ayos yung bata, basta mapainom, doon
na kukunin yung energy/ calorie sa ORS na binibigay
habang hindi pa nagiimprove yung appetite ng patient
Magpapak daw tayo ng ORS so ospital para malaman natin kung alin
yung mas magugustuhan nung bata 😊

Case Analysis for Maintenance Therapy

A patient comes in for poor appetite. She good urine output
but does not want to eat. You hooked her to an IV fluid line.
There is no fever, no vomiting, nor diarrhea.

Your consultant asked you to check the IV fluid’s orders.

Her weight is 18 kg and her previous weight at the clinic was
also 18 kg.
Figure 8. Types of ORS

What would be the correct order in the chart if you are going
to calculate the amount of IV fluids per 24 hours. Please
give your formula.

Feel free to solve this on your own! The answers + solution

will be in the appendix!

MAINTENANCE THERAPY
→ Goals of maintenance fluids:
Figure 9. Table 11.4 Composition of ORS (See appendix for larger photo) o Prevent dehydration
→ We can use this to explain why coke or gatorade are not o Prevent electrolyte disorders
recommended for oral rehydration o Prevent ketoacidosis
o Hindi enough yung kayang ibigay nitong mga not o Prevent protein degradation
recommended fluids for a child with dehydration → Maintenance fluid needs
o Depends on the metabolic rate of the child
o Allow 100ml/ 100 calories expended
→ Estimation of caloric expenditure (using Holliday-Segar
Method)

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→ Solve for Maintenance Fluid Rate/ Maintenance fluid
requirements using Holliday-Seagar Method
o First 10: 100ml/kg/day x 10kg = 1000ml/day
o Remaining 5kg: 50ml/kg/day x 5 kg = 1250ml/day
o 1250ml/day divided by 24 hours = 52ml/hr
→ Solve for Fluid Deficit (since patient is moderately
dehydrated [10% or 100ml/kg])
o 100ml/kg x 15 kg = 1500 ml
o Just use the ml/kg since same lang naman and
much easier!
o If you want to know the long version, see
appendix.
→ Solve for Fluid Replacement Rate Over 24 hours
o HALF of the fluid deficit must be given for the 1 st
8 hours + maintenance fluid rate
● 1500ml / 2 = 750ml
● 750ml / 8 hrs = 94 ml/hr
Figure 11. Holliday-Segar Method ● 94ml/hr + 52ml/hr = 146ml/hr
⭐ For uniformity’s sake: use ml/kg/day o OTHER HALF must be given for the next 16
→ Remember: allowances should be made for factors that hours + maintenance fluid rate
increases insensible water losses ● 750ml / 16 hrs = 47 ml/hr
→ Extra fluids required: ● 47ml/hr + 52 ml/hr = 99 ml/hr
o Fever (Add 12% every 1°C above 37.5°C) → Note: If the patient received an initial 20ml/kg bolus (20ml
● [Using the example above] 1600 ml/d x 12% = x 15kg = 300ml), subtract it from the fluid deficit.
192 o 1500ml – 300ml = 1200 ml
● 1600 mL/d + 192  to account for the fever o 1200 ml / 2 = 600 ml
o Sustained hyperventilation or excessive muscular o 600ml / 8hrs = 75ml/hr
activity (↑25-50%) o 75 ml/hr + 52 ml/hr = 127ml/hr in the first 8hr
o Hypermetabolic states (severe thermal injury, o 600 ml / 16 hr = 38ml/hr
salicylate intoxication, thyrotoxicosis) (↑25-75%) o 38 ml/hr + 52ml/hr = 90ml/hr over the next 16 hrs
o Abnormal water and electrolyte losses (diarrhea and
vomiting) Sample Case
o Sweating (↑10-25%) Weight: 39.5kg
→ Less fluids required: Assumption: Isonatremic dehydration
o Hypothermia (subtract 12% for every 1°C below Moderate dehydration on older child
37.5°C) Phase 1: PLRS/PNSS 20ml/kg x 39.5kg (weight of
o Very high humidity Initial patient)
o Oliguria or anuria Stabilization
o Sedated or paralyzed patients (↓40% due to ↓energy Order: Give PLRS 790ml over 1 hour*
expenditure)
o Edematous and antidiuretic states (Cardiac failure) *1 hour since moderate palang naman
yung dehydration
Phase 2: Maintenance therapy: 1890 ml = 79ml/
Deficit, hour
Maintenance, ✍🏽Remember: 100-50-20!!!!
and Ongoing
Losses Deficit:
2370ml – 790ml** = 1580ml
1580 ml/ 2*** = 790ml

*2370ml
 60ml/hr (6% dehydration)
60 ml x 39.5kg = 2370 ml
**790ml from bolus given
***2 since hahatiin yung pagbigay to 1st
8hrs, tapos next 16hrs

First 8 hrs: 790ml / 8hrs = 98.75ml +

maintenance of 97ml/hr = 178ml/hr
Figure 12. Sample Calculation: Isonatremic Dehydration
Step by step: Next 16 hrs: 790ml / 16hrs = 49.375ml/hr +
→ Given: 15kg child with 10% dehydration (Moderate) and 79 ml/hr = 128ml/hr
normal serum Na+
Order: Start IV fluids D5LRS 1L to run at

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178ml/hr (180ml/hr) for the first 8 hrs ● An increase also prevents the use of the
followed by 128ml/hr (130ml/hr) over 16 formula for serum osmolality (2 x [Na])
hrs. For reassessment of pediatric resident ● Increase in CHONs and lipids decreases
after 6 hours* water content because of displacement by
the lipids
First 8 hrs: 178 x 8hrs = 1424ml
Next 16 hrs: 128 x 16 hrs = 2-48 ml ● Electrolytes appear to be decreased even
though its concentration per liter of serum water
1424ml + 2048ml = 3472ml + 790ml = is normal
4262ml/24 hrs
BODY CONTENT AND PHYSIOLOGIC FUNCTION 📚
*Dapat icheck pa din kasi you might need → Predominant cation of ECF
to adjust maybe nag progress or is o Extracellular component: 140 mEq/L
responding to the IV fluid resuscitation o Intracellular component: 10 mEq/L
→ Principal determinant of extracellular osmolality
Phase 3: Order: Replace ongoing losses volume per o Necessary for maintenance of intravascular volume
Recovery volume with PLRS ___ml over 3 hrs
and Ongoing
ABSORPTION
Losses *ORS75 if no vomiting
→ Occurs throughout the gastrointestinal tract (maximally in
75 x weight of the px  consume within 4
the jejunum)
hours
→ Via Na-K-ATPase system for sodium balance
Either through teaspoon or through the
o 📚 Presence of glucose enhances Na absorption
barrel of a needle – less syringe
administered to the side of the inside of the owing to the presence of a co-transport system
cheek. o Augmented by aldosterone

MONITORING THERAPY EXCRETION

→ While admitted in the hospital: → Through urine, sweat, feces
o Vital signs (Pulse, BP) → Kidney: principal organ for regulation of sodium
o Intake and output (fluid balance, urine output) output
→ Sweat, sodium conc.: 5-40 mEq/L
o Physical examination (weight, clinical signs of
→ Feces, sodium conc.: LOW
depletion or overload)
→ 📚 Sweat Na+ concentration is increased in children with
o Electrolyte levels
cystic fibrosis, aldosterone deficiency, or pseudo
→ See appendix: WHO IMCI Booklet and Chart for Diarrhea hypoaldosteronism.
→ Factors regulation Sodium Excretion:
Urine output computation o Renin-Angiotensin-Aldosterone System (RAAS)
Given: In an 8hr shift, what is the urine output of this o Atrial Natriuretic Peptide (ANP)
patient? ● Potent natriuretic and diuretic peptide hormone
Weight: 15 kg
produced and stored in atrial myocytes
Moderately dehydrated
● Target organ: kidneys
Urine for 8hrs: 400ml
● Increases Na H2O excretion
● Released as a response to ECF volume
Formula: UO = cc/kg/hr
expansion and resulting stretch of the atrial
Nv: 0.5-1 cc/kg/hr
walls
● Antagonizes the sodium-retaining function of
= 400ml / 15kg / 8 hrs
the renin-angiotensin system
= 3.3 / good urine output
● Regulates acute or short-term changes in ECF
volume
⭐Doc wants us to remember:
When giving boluses for resuscitation, you are not supposed to
give fluids that contain dextrose (GLU), as giving this in a
faster rate can be detrimental for the patient’s kidney.

II. ELECTROLYTES
SODIUM
→ Most important cation contributing to extracellular
osmolality
→ With accompanying anions: chloride & bicarbonate
→ > 90% of plasma osmolality
→ Rough estimate of serum osmolality: 2 x [serum Na]
→ IMPORTANT EXEMPTIONS:
o Serum Solids

Figure 13. RAAS (bigger at appendix)

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⭐The aldosterone effect = increase Na reabsorption and K REGULATION
secretion → Intake and output parallel to those of sodium, but can
POTASSIUM occur independently
→ Daily turnover and renal conservation is excellent through
BODY CONTENT & DISTRIBUTION
an efficient renal regulation
→ Principal intracellular cation
→ Intracellular concentration: 150 mEq/L Sample Questions
→ Extracellular concentration: 4 mEq/L Which of the following is lost the most if you are vomiting
→ Maintained by action of Na-K-ATPase exchange immediately after ingestion?
o Maintains the resting membrane potential difference a. Sodium
across the cell membrane b. Potassium
→ Critical for excitability of nerve and muscle cells for c. Calcium
the contractility of cardiac, skeletal, and smooth Which of the following is lost the most if you are having
muscles diarrhea?
o Manifestation of hyperkalemia: ⭐ arrythmia a. Sodium
o Manifestation of hypOkalemia: ⭐muscle weakness b. Potassium
→ Important for the maintenance of cell volume c. Calcium
Answer: A, B

ABSORPTION CALCIUM
→ Upper gastrointestinal tract → 99% is found in bones
o Most occurs in the small intestine o Infants have less densely mineralized bone
→ Exchanged for sodium in lumen of lower bowel o 📣 That is why calcium is only 400mEq/kg of body
weight in infants vs. 950mEq/kg body weight in adult
REGULATION → Serum calcium concentration is fairly constant at 10mg/dl
→ Recommended daily intake: 1-2 mEq/kg body weight o 40% is protein-bound
(from most animal and vegetable tissues) ● 80-90% is bound to albumin
o 📣 Important in children with renal issues ● 10-20% is bound to globulin
→ Aldosterone ● 1g of albumin binds 0.80mg of calcium
o Regulates renal and extra-renal mechanisms while 1g of globulin binds only 0.16mg of
o Secreted in response to ↓blood volume via calcium
Angiotensin 2 and ↑plasma K+ which causes ↑Na+ ● ✍ If you have changes in albumin levels, your
reabsorption, ↑K+ secretion, ↑H+ secretion serum calcium also changes
o Primary extra-renal site: Gastrointestinal tract ● ✍ Decrease in albumin - increase in serum
→ Acid-base Balance calcium kasi walang kakapit kay calcium
o Systemic acidosis → movement of K+ out of the cell → 60% is ultra-filtrable
= hyperkalemia o 14%: complexed with anions (phosphate, citrate)
o Systemic alkalosis → movement of K+ into the cells o 46%: free ionic calcium (4.8mg/dL)
o For every 0.1 unit change in blood pH, plasma K+
conc. Inversely changes by 0.3-1.3 mEq/L IONIZED CALCIUM
→ Fetal Excretion → Exist in equilibrium with protein- bound form.
o Accounts only for a small amount → Affected by changes in hydrogen ion activity by change of
o Exchange of plasma K+ for sodium in caloric 0.1 units in pH alters the concentration of ionized calcium
contents leads to sodium conservation by 10% inversely
o Human colon responds to mineralocorticoids and → Major role in:
o Bone formation
glucocorticoids by decreasing sodium and increasing
potassium content of stool o Cell division and growth
o Coagulation
o Hormone-response coupling
o Electrical stimulus-response coupling in muscle
contraction and neurotransmitter release

REGULATION
CHLORIDE INTESTINAL ABSORPTION
→ Major anion of ECF
→ Plasma – 13.6% → Absorbed in SMALL INTESTINE ⭐ (duodenum and early
→ Interstitial lymph – 37.3% jejunum)
→ Dense connective tissue and cartilage – 17% → Via active, carrier-mediated transport mechanism
→ Bone – 15.2% → Stimulated by 1,25-dihydroxyvitamin D3
→ Transcellular fluid – 4.5% → Increased by low Ca intake in the growing child,
→ Intracellular Fluid – 12.4% pregnancy and during depletion of calcium stores
o ✍ Absorbed in the jejunum → Mechanism unknown but administering vitamin D and
parathyroid hormone will increase calcium absorption

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RENAL EXCRETION → Absolute or relative water deficit which can occur in the
→ Matches the amount of intestinal absorption face of normal, increased or even decreased total body
→ Plasma free calcium is filtered at glomerulus sodium
→ 99% is reabsorbed by tubules → Leads to a shift of water from ICF to ECF compartment →
o Proximal tubule (50-55%) cellular dehydration
o Loop of Henle (20-30%) → Extracellular fluid volume and plasma volume are
o DCT (10- 15%) relatively preserved: typical signs of dehydration are less
o Collecting duct ((2-8%) pronounced
→ ⭐ Hypertonicity stimulates secretion of antidiuretic
→ Stimulated specifically by 1,25 dihydroxyvitamin D3
hormone (ADH) and thirst
o ⭐ FIRST LINE OF DEFENSE: ADH
HORMONAL REGULATION ● Increases water reabsorption in kidney —>
→ Parathyroid Hormone (PTH) increases urine concentration and decreases
o Stimulates calcium reabsorption in the thick urine volume
ascending limb of the loop of Henle and distal tubule o ⭐ BEST LINE OF DEFENSE: THIRST
→ Thyrocalcitonin ● Water drinking as long as there is free access
o Produced in the parafollicular cells of the thyroid ● Not true for infants
gland in response to hypercalcemia
CAUSES
o Lowers plasma calcium by inhibiting bone resorption
→ Pure sodium excess – increased total body sodium
and increasing urinary calcium excretion
→ ★ Water deficit – normal total body sodium
→ ★ Water deficit in excess of sodium deficit – low total
HYDROGEN ION
body sodium
→ Acid is a proton (i.e hydrogen ion) donor
o E.g. hydrochloric, sulfuric, phosphoric, and carbonic ETIOLOGIES
acids Low Urine Osmolality
o Strong acid – highly dissociated; produces high → Diabetes insipidus (central and nephrogenic)
concentration of hydrogen ion → Post obstructive diuresis
o Weak acid – poorly dissociated → CKD
→ Base is a hydrogen ion acceptor → Diuretic use
o E.g. hydroxyl ion, ammonia, and anions of weak → Polyuric phase of ATN
acids Elevated Urine Osmolality
→ Buffer – substance that reduces the change in free →  Urine Na (<20 mEq/L)
hydrogen ion concentration of a solution based on the o GI losses
addition of an acid or base
o Skin losses
o It increases the amount of acid or alkali that must be
o Respiratory
added to cause a change in pH

Fact Check on your Bones NORMAL ACID-BASE REGULATION:

BUFFER SYSTEMS:
A 12 yr. old female comes to you with a history of recurrent
fractures. She has been cleared of any Congenital Principal buffer in the ECF Bicarbonate-Carbonic Acid
Abnormalities leading to these fractures. On further history, System
she had a perforated duodenal ulcer when she was 10 Principal buffer in the ICF Various Proteins and
years old and they had to resect majority of her duodenum. Organic Phosphates
a.) Is the history of the duodenal resection an Principal buffer in the urine Phosphate in the
important question to ask? monohydrogen and
b.) Why? dihydrogen forms
o Increased insensible losses
o Adipsia
→  Urine Na (>20 mEq/L)
o Exogenous Na+ (meds, infant formula)
o Mineralocorticoid excess (e.g., hyperaldosteronism)
IV. ELECTROLYTE IMBALANCES
A. HYPERNATREMIA SIGNS AND SYMPTOMS
→ Serum sodium greater than 145mEq/L Neurologic
→ Deficiency of water relative to total body sodium → Hypernatremia or hyponatremia, or when you have a
content problem with your sodium, it’s usually of a neurologic
→ Usually, a disorder of water balance manifestation because your brain is the most sensitive
→ Hypertonic hypernatremic dehydration part to loss of sodium.
o Results when losses of water are greater than salt → Restlessness
losses → Irritability
o Serum sodium is HIGH: >150 mEq/L → Lethargy
o Serum osmolality is HIGH: >300 mOsm/L → Muscular twitching
→ Increased concentration of solutes throughout all body → Hyperreflexia
fluids → Spasticity

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→ Coma
→ Seizures
→ Death
→ ⭐ Brain hemorrhages – Most devastating consequence
of untreated hypernatremia
Others
→ Decreased skin turgor (doughy)
o 📣 Particularly for hypernatremia, the character of the
skin is doughy
→ High-pitched cry/ wail
→ Fever
→ Hypocalcemia
→ Hyperglycemia
→ Avid thirst
Figure 14. Rapid correction of hypernatremia will lead to cerebral edema
because water moves from serum to brain cell
LABORATORY EXAMINATIONS
Blood: QUESTIONS
What is the level of serum sodium >145
→ Na, K, Cl, HCO3
to say it is high
→ BUN, Creatinine  for serum osmolality
→ Liver Function Test (glucose) Is the skin turgor decreased or decreased
→ Complete serum osmolality = 2[Na] + serum increased in hypernatremia
glucose(mg/dl) /18 + BUN (mg/dl)/2.8 What is the complication of rapidly Cerebral edema
correcting hypernatremia
Urine
What is an early symptom in a Thirst
→ Urinalysis patient with hypernatremia
→ Urine Na
→ Urine Creatinine or Urine Osmolality B. HYPONATREMIA
o 📣 Most important test is serum electrolytes so you → SERUM SODIUM concentration less than 135 mEq/L
would know if patient is hypernatremic or not → Reflects hypoosmolality
→ Kidney protects the body against hyponatremia by
TREATMENT excreting a dilute urine.
→ Proper management of hypernatremia involves identifying o Dependent on:
the underlying condition and correcting the hypertonicity. ● Glomerular filtration rate
→ The goal of therapy is to correct both the serum sodium ● Reabsorption of Na in proximal tubules
and the intravascular volume. ● Delivery of sodium to the distal tubules and
→ In patients with severe dehydration or shock, the initial collecting ducts
step is fluid resuscitation with isotonic fluids (PNSS ● Levels of antidiuretic hormone
20ml/kg) before free water deficit correction
Free water deficit CAUSES
→ Formula (✍🏽will not be part of the exam) Deficit of total body water & larger deficit of total body
o TBW= 0.6 x body wt in kg x [(actual Na/desired Na)- sodium (ECF volume depletion)
1] → Renal losses: diuretic excess especially thiazides, renal
o Used D5 0.45% NaCl tubular acidosis, salt-losing nephritis, osmotic diuresis,
o Example: actual 158/ desired 148 metabolic alkalosis
o 0.6 x 40kg x [(158/148)-1] → Adrenal (mineralocorticoids) insufficiency (aldosterone)
o FWD plus maintenance volume using Holiday Segar → GI losses: Vomiting, diarrhea, fistulas, enteric tubes
Method= total volume per day or 24 hours → Third spacing: burns, pancreatitis, traumatized muscles,
→ Correction of water deficit and maintenance should be ascites, peritonitis, effusions
done over 48 hours, lowering the sodium by <10 → Excessive sweating
mmol/day Excess total body water with normal total body sodium
→ ⭐ Correcting too rapidly will result in cerebral edema → SIADH secretion
and seizure o 📣 Too much ADH  anuria  excess TBW, while
→ Close, serial monitoring of serum sodium every 2 to 4 total body sodium is normal
hours is essential during the acute phase of correction → Glucocorticoid deficiency
→ Water intoxication (intravenous therapy, psychogenic
water drinking)
→ Hypothyroidism
Excess total body sodium and larger excess of total body
water (ECF volume excess, Edema)
→ Renal: Nephrotic syndrome, acute and chronic renal
failure
→ Cardiac: Congestive Heart Failure
→ GI: Cirrhosis

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→ All above present with ascites Figure 15. Rapid correction of hyponatremia will lead to central pontine
myelinosis/ osmotic demyelination
→ ★ Infants are more prone to hyponatremia from excess
water ingestion because they have lower GFR.
→ ★ Diarrhea as a result of gastroenteritis is the most ]
common cause of hypovolemic hyponatremia in children.
QUESTIONS
Pseudohyponatremia In SIADH: Hyponatremia or Hyponatremia
→ is a laboratory artifact present when the plasma contains hypernatremia?
very high concentrations of: Complication of rapidly correction Central pontine
o Protein (multiple myeloma, IVIG infusion) hyponatremia myelinosis
o Lipid (hypertriglyceridemia, hypercholesterolemia) Serum sodium level to say it is <135 mEq/L
hyponatremia?
SIGNS AND SYMPTOMS What is pseudohyponatremia? Protein and lipid
→ Neurologic: due to cerebral overhydration
o Anorexia HYPERKALEMIA
o Nausea → Serum potassium greater than 5.0 mEq/L
o Vomiting → Potassium most importantly affects membrane potential
o Agitation and the cardiac conduction system.
o Headache
o Muscle cramps CAUSES
o Clouded or decreased sensorium ALTERED RENAL EXCRETION
o Pathologic reflexes → Acute Renal Failure
o Cheyne-Stokes Respiration → Chronic Hydronephrosis
o Hypothermia → Potassium-sparing diuretics
o Seizures IMPAIRED EXTRARENAL REGULATION:
o Muscle weakness → Diabetes mellitus
📣 If the child comes in with seizure or decreased in → Adrenalin sufficiency
sensorium, one of your differentials would be electrolyte → Drugs: beta blockers, ACE inhibitors
imbalance. Either hyponatremia or hypernatremia. SHIFT FROM INTRACELLULAR TO EXTRACELLULAR
FLUID:
LABORATORY EXAMINATIONS → Acidosis
→ Serum electrolytes: Na, K, Cl, HCO3 INCREASED INTAKE:
→ Serum and urine osmolalities
→ Intravenous solutions
→ Urinalysis (specific gravity)
→ Potassium-containing salts
→ Urine Sodium
→ Liver function test for cirrhosis, BUN, creatinine, serum SPURIOUS HYPERKALEMIA:
albumin, glucose → Hemolyzed blood 📣 False positive elevation of potassium

TREATMENT SIGNS AND SYMPTOMS

Asymptomatic → Paresthesia, weakness, flaccid paralysis
→ ⭐ Peaked T waves, widened QRS complexes, prolonged
→ Na deficit= 0.6 x body wt in kg x (desired Na-actual Na)
PR interval, ventricular arrhythmias, cardiac arrest
PLUS
(admit to ICU)
→ Na maintenance = wt (kg) x 2-3 mEqs
→ Stimulate the release of:
Symptomatic (seizure, altered mental status) o Aldosterone (increases urine K excretion)
→ 3% NaCl at 4-5 ml/kg over 30 minutes = Fast correction o Insulin & epinephrine (increases cellular K uptake)
→ Achieve safe level of 125 mmol/L then correct for 24-48 o Glucagon (prevents hypoglycemia produced by
hours increased insulin)
→ ⭐ Recommended target route of correction: 8-
10mmol/L/day

Figure 16. The typical ECG progression with increasing serum K+ values:
Peaked T waves; prolonged PR and widening of QRS; loss of P waves; ST
segment of depression with further widening of QRS; bradycardia,

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atrioventricular (AV block), ventricular arrythmias, torsades de pointes;
cardiac arrest

TO TRANSFER K+ INTO CELLS:

→ Sodium Bicarbonate
o dose: 1-2 mEq/kg
o rate of admin.: 10-30 minutes IV
o onset/ duration of action: 30-60 min./1-4 hours
o caution in use if without acidosis
→ Glucose (INSULIN)
o DOSE: 0.5 – 1.0 g/kg. (0.1 unit per kg. IV or SC)
o rate of admin.: 15-30 mins. IV with insulin
o onset/duration: 30-60 mins. / hours
o monitor blood glucose
TO ΕNHANCE RENAL EXCRETION OF K+:
→ Sodium polystyrene sulfonate (Kayexalate)
o Targets the kidney
o Dose: 1g/kg
o Rate of admin: Orally or per rectum diluted with 2-4ml
of sorbitol or 10% dextrose per gram of resin every 4-6
Figure 17.
hours
o Onset/Duration: 60 mins/hours
LABORATORY EXAMINATIONS
→ Sodium Chloride
→ Blood o Dose: 0.9%NaCl:10-20ml/kg
→ Na, K, Cl, HCO3, BUN, Creatinine, glucose
o Rate of admin: 45-60 mis
→ Arterial blood gas
o Onset/duration: 30-60 mins/hours
→ Urine
→ Urinalysis, Na, K, Cl Table 7. Mnemonic for management of hyperkalemia
→ pH, Osmolality
MNEMONIC- CBIGKDrop Treatment
→ ECG ⭐15-lead ECG in children
Check the EKG -> If EKG changes, calcium gluconate IV
TREATMENT Bicarbonate/ Beta Agonist
Table __. Treatment for Hyperkalemia
Insulin
Plasma K Level Maneuver
< 6.5 meq/L 1. Decrease K+ intake Glucose- Dextrose
(no ECG changes or only 2. Discontinue drug that Kayexalate
peaked T waves) decreases K+ excretion D- Hemodialysis for refractory Hyperkalemia
(K+ sparing diuretics)
3. Correct acidosis (except in QUESTION:
acute oliguric renal failure In which electrolyte abnormality in the Hyperkalemia
where you need more advanced stage would you expect to see a
aggressive tx) widening of the QRS and decreased P
>7.0 meq/L 1. Therapies to move K into wave amplitude?
(more advanced ECG cells acutely (Eg. Calcium
changes) gluconate, sodium HYPOKALEMIA
bicarbonate, glucose (insulin) → Serum potassium less than 3.5mEq/L
PATHOPHYSIOLOGY:
⭐ REVERSE MEMBRANE EFFECTS
→ K+ shift into cells in exchange for H+ ions
→ Increase threshold potential and allow excitable cells to
o 0.1 unit shift in pH = converse change of 0.6 mEq/L of
repolarize and fire a signal again
K+
o 10% calcium gluconate = cardioprotective (protects
→ Extrarenal/Renal Losses:
the heart from arrhythmia brought about by
o Clinical use of diuretics – increases flow rate and
hyperkalemia)
delivery of sodium to the distal nephron and promote
📣 In practice, calcium gluconate is given by GP or
K+ excretion
pediatrician through slow IV push (within 30 mins)
along with the use cardiac monitor. You should also
have a baseline cardiac rate prior to the administration CAUSES
of the medication. Without K+ deficit
o Dose: 0.5-1.0ml/kg (Shift from extracellular to intracellular fluid)
o Rate of admin: 2-10 mins IV → 📣 Normal ang potassium level sa body but ang
o Onset/duration of action: immediate/30-60 mins nangyayari dito, napapasok siya sa loob ng cell (yung
o NEED FOR ECG MONITORING potassium)
o Discontinue if pulse rate <100/min → Insulin
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o 📣 Sa mga DKA patient na kailangan ng insulin in the TREATMENT
management, as you monitor the patient dahil MILD HYPOKALEMIA
nagbigay ka ng insulin magkakaroon ng hypokalemia.
→ in asymptomatic persons may not require specific therapy;
Kasi ang effect ng insulin would be shift the potassium
if on digitalis glycosides, will need supplemental potassium
into the intracellular fluid. After giving insulin, you have
→ Most are NOT life threatening, so may correct via oral
to give potassium supplement to prevent hypokalemia.
route, slowly (over days), and started once with urine
→ Beta-2 catecholamines
output
→ Alkalosis
o Oral route is preferred as it rarely causes
→ Familial hypokalemic periodic paralysis
HYPERKALEMIA if the patient has a normal renal
With K+ deficits function
→ Poor dietary intake o 📣 May potassium tablets na pwede painom sa bata
o Anorexia nervosa para ma-correct yung hypokalemia
o Alcoholism → 📣 Kapag yung patient is oliguric, you cannot use IV fluids
→ Gastrointestinal losses with potassium because the potassium will cause acute
o Protracted vomiting (e.g. pyloric stenosis or gastric tubular necrosis. So the only time you can give potassium
suctioning) is when you’ve established good urine output.
o Laxative abuse IF DEFICIT IS SEVERE
o Obstructed or long ileal loop → And is causing cardiac arrhythmias, rhabdomyolysis,
→ Renal losses extreme muscular weakness (quadriplegia, respiratory
o Tubular diseases (e.g. cytinosis) distress), INTRAVENOUS THERAPY IS NEEDED
o Diuretic abuse
INTRAVENOUS
o Renal tubular acidosis (RTA)
→ 📣 In the future pag nagging doctor na kayo, mag-iinsert
o Diabetic ketoacidosis (DKA)
kayo ng IV line sa patient. Once na na-insert mo na,
o Excess mineralocorticoid effect
kailangan mo i-flush yung cannula with plain NSS para
● Primary/Secondary hyperaldosteronism hindi mag-clot yung blood at para malaman mo ok yung
● Bartter’s Syndrome blood flow you’re inside the vein. Rule of thumb: ikaw
● Cushing Syndrome dapat mag-aspirate ng pang-push mo na fluid. Dapat
o Non-reabsorbable anions (penicillin, bicarbonate) malaman mo kung ano ang content nung pang-push mo.
o Leukemias → Peripheral vein: < 40 mEq/L concentration
→ Central vein: maximum of 80 mEq/L; monitor ECG
SIGNS AND SYMPTOMS continuously
Neuromuscular: → Quantitative rate of replacement: 0.2 – 0.3 mEq/kg/hr
→ Ileus 📣 hindi gagalaw yung bituka, kaya common yung o IF WITH LIFE THREATENING SYMPTOMS: up to 1
ileus sa suka ng suka na bata mEq/kg/hr; but needs ECG monitoring and placed in
→ Muscle weakness the IC
→ Areflexia → Use KCl in alkalosis and KHCO3 if with acidosis
→ Tetany → Admit the patient if symptomatic or asymptomatic but
→ Autonomic insufficiency (orthostatic hypotension) potassium is < 3.0 mEq/L
Cardiac: → START ONLY if patient has voided urine or with LIFE-
THREATENING hypokalemia – BUT USE WITH
→ Arrhythmias CAUTION
→ ⭐ ECG changes: flattened T waves 📣 compared to → Correct all possible causes
hyperkalemia na peak T waves, U waves, ST segment → Frequent measurement of potassium during correction
changes, arrhythmias
→ The dose of IV potassium is 0.5- 1.0 mEq/L, usually given
Renal: over 1 hour. The adult maximum dose is 40 mEq/L.
→ Polydipsia, polyuria
→ Edema, sodium retention

LABORATORY
Blood:
→ Na, K, Cl, HCO3, BUN, Creatinine, Glucose
→ Arterial blood gas

Urine:
→ Urinalysis, Na, K, Cl
→ pH, Osmolality
ECG

Others
→ Plain abdominal x-ray (to check for ileus), Upper
gastrointestinal series

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Which is it? SIGNS AND SYMPTOMS

Neurologic
A 15-year-old Male comes to the Emergency Room with a → headache, irritability, lethargy, fatigue, weakness, seizure,
chief complaint of lethargy and irritability. He has been coma, hyporeflexia, behavioral changes
vomiting for several days already and could not eat → 📣 Seizure hindi lang sa hypo- or hypernatremia, pwede
properly. Which of the following laboratory result will you rin sa hypercalcemia
expect? Gastrointestinal
→ anorexia, nausea, vomiting, constipation 📣 hypercalcemia
a. Serum Sodium = 125 mmol/L
= constipation, dehydration
b. Serum Potassium = 3.8 mmol/L
c. Serum Calcium = 9.2 mg/dl Cardiovascular
→ bradycardia, hypertension, short QTc interval in the ECG
Answer: B. → Using Bazett’s formula: QTc = QTa / square root of R-R’
interval
📣 The child is vomiting and not eating properly. What is Renal
the possible electrolyte disturbance here? Mataas yung → polydipsia, polyuria, hypokalemia, aminoaciduria,
potassium content ng vomitus so pwede siyang nephrocalcinosis, nephrolithiasis
magkaroon ng hypokalemia. Dermatologic
→ pruritus, band keratopathy, ectopic calcification
HYPERCALCEMIA
→ TOTAL SERUM CALCIUM GREATER THAN 11 mg/dl LABORATORY
→ Normal range must be established for each laboratory Blood
→ 3 types: → Calcium
o Protein-bound: 39.5% → Phosphorus
o Complexed: 13.6% → Alkaline phosphatase
o Ionized: 46.9% → Total protein
→ Albumin
PATHOPHYSIOLOGY → BUN
→ Increased intestinal absorption of calcium (secondary to → Creatinine
Vitamin D) → Parathyroid hormone
→ Increased mobilization of calcium from bone with or → Vitamin D
without increased absorption from the intestinal tract Urine
(secondary to Parathormone) → Calcium
→ Phosphorus
CAUSES → Creatinine
Primary hyperparathyroidism: Others
→ Adenoma & carcinoma → ECG
→ Hyperplasia → Skull and abdominal x-rays
→ Multiple endocrine adenomatosis → Skeletal survey
Secondary hyperparathyroidism → Work-up for any hidden malignancy
→ Malabsorption of Vitamin D; vitamin D deficiency
→ Chronic renal failure TREATMENT
→ Following kidney failure ⭐ Symptomatic
Neoplastic diseases → initial emergency management is infusion of saline at a
→ Malignant tumor with metastases to bone rate twice the maintenance followed by infusion of
→ Tumors secreting humoral non-parathyroid-like substance furosemide 📣 which is a diuretic at 1-2 mg/kg every 6-8
→ Tumors secreting parathyroid hormone-like substances hours
→ Multiple myeloma and lymphoproliferative disorders o Should have a normal functioning kidney
Other Causes → If no pre-existing cardiac disease, subsequent amount of
saline may be given at 2-3 times the daily requirements
→ Hypervitaminosis D
until serum Calcium returns to normal; may also be guided
→ Hypervitaminosis A
by state of hydration
→ Sarcoidosis & Tuberculosis
→ Hyperthyroidism Hypercalcemic crisis
→ Adrenocortical insufficiency → admit to ICU and manage depending on etiology, serum
→ Infantile hypercalcemia Calcium, and severity of signs & symptoms
→ Immobilization Vitamin D intoxication
→ Milk-alkali syndrome → infuse PO4 or SO4 salts followed by oral prednisone (1-2
→ Use of calcium-ion exchange resins mg/kg/day)
→ Hypercalcemia associated with acute renal failure Malignancy
→ Thiazide induced hypercalcemia
→ mithramycin 25 ug / kg IV may be given

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Acute oliguric renal failure
→ peritoneal dialysis or hemodialysis

HYPOCALCEMIA
→ Total serum calcium less than 9.0 mg/dl beyond the
neonatal period
→ DOES NOT result from a decreased amount in the body,
rather as a result of an inability to mobilize from bone into
the extracellular and intravascular compartments
o Failure of secretion of adequate amounts of
parathormone (PTH) or an inadequate responsiveness
of end organs to PTH, despite adequate secretion
→ PTH increases calcium resorption from bone & increase
renal excretion of phosphorus (reciprocal relationship)
→ Active form of vitamin D (1,25-dihydroxyvitamin D3)
promotes calcium and phosphorus absorption from the
gut, enhance PTH-dependent mobilization of calcium from Figure . Chvostek’s Sign. Manifestation of heightened neuromuscular
mineralized bone excitability. Tapping of the facial nerve in front of the ear causes ipsilateral
contraction of the facial muscles.

CAUSES
True Hypoparathyroidism
→ Familial with or without multiple endocrine abnormalities
→ Di George Syndrome
→ Postsurgical
→ Idiopathic
o Magnesium deficiency
End-organ resistance to PTH
→ Pseudohypoparathryoidism
→ Insensitivity to cyclic AMP
Abnormalities of vitamin D metabolite
→ Primary D deficiency (dietary, sunlight) Figure . Trosseau’s Sign. It represents increased neuromuscular
→ Secondary D deficiency excitability which may be related to the gating function of calcium ions for
ion channels at a cellular level (particularly in neurons). It manifests as a
o malabsorption, anticonvulsant therapy, chronic renal
spasm of the hand characterized by adduction of the thumb, flexion of the
failure metacarpophalangeal joints, an extension of the interphalangeal joints, and
→ Primary D resistance (familial hypophosphatemic rickets) flexion of the wrist when a sphygmomanometer is inflated above systolic
→ Secondary D resistance blood pressure for three minutes.
o Fanconi syndrome, renal tubular acidosis
→ Primary D dependence LABORATORY
o Type 1 (deficient 1-alpha-hydroxylase) Blood
o Type 2 (end-organ resistance to 1,25 dihydroxyvitamin → Calcium
D3 → Phosphorus
Others → Alkaline phosphatase
→ Hypoproteinemia → Mg
→ Hypernatremic dehydration → Total protein
→ Postacidotic tetany → Albumin (low levels affect the protein bound portion but
→ Diuretic abuse (ethacrynic acid, furosemide) not the free ionized calcium)
→ Phosphate loading → PTH
→ pH
SIGNS AND SYMPTOMS → BUN
→ Tetany (i.e., Chvostek and Trosseau signs) → Creatinine (over-vigorous correction of acidosis drives
→ Frank seizures (short, generalized, tonic - clonic) calcium into the bones)
→ Laryngospasm Urine
→ Non-specific: vomiting, muscle weakness, irritability, → Ca
lethargy, bone pain, generalized feeling of debilitation → Phosphorus
→ In the neonate: poor feeding, apnea, abdominal distention → Creatinine
Early signs: Others
→ Spontaneous tonic contractions of muscles of the upper → ECG
and lower extremities → Skull and abdominal x-rays
→ Carpopedal spasm (hand is held with fingers extended & → Skeletal survey
wrist flexed)
ECG changes
→ prolonged QT interval, normal T waves

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TREATMENT What is an ECG finding in hypocalcemia:

IF SYMPTOMATIC:
→ Calcium gluconate 10% (9.2 mg elemental Ca/ml) _____ that can lead to Torsades de pointes that can be
o Dose: 0.5 – 1.0 ml/kg IV bolus over 3-5 mins. under fatal?
cardiac monitoring. STOP if HR <60/min.
o 📣 Kasi it will leak outside the vein causing severe
tissue necrosis and calcification kapag binigay mo ng
mabilis
Answer: QTc prolongation: This can lead to Torsades de pointes
o 📣 Dalawa ang magiging complication: either
that can be fatal.
magkaka-tissue necrosis at extravasation or
bradycardia
o Maintenance should follow once symptoms are
REMINDERS
relieved
→ Check plasma Ca levels 12-24 hours after treatment; or
o Dose: 100 mg. elemental calcium/kg/day added to IV
earlier if necessary, and again after 2-3 days after
solution stopping
→ Oral Calcium supplement 📣 Kapag di naman severe o It is necessary to demonstrate a normal level can be
ang hypocal
maintained after treatment is stopped
o Calcium Lactate (13% Calcium by weight)
→ Use of calcium gluconate is reserved for emergency
o Calcium Gluconate (9% Calcium by weight) treatment:
o Calcium Chloride (21% Calcium by weight) o Rarely indicated urgently and danger of cardiac arrest
o Oral calcium Sandoz contains Ca glubionate 1.437 g. o Leakage outside of a vein causes severe tissue
and Ca lactobionate 0.295 g. equivalent to 110 mg. necrosis and calcification
ionizable Ca PER 5 ml. o Effect extremely brief; unnecessary in most cases of
● Dose: up to 3 y.o.: 10-25 ml. per day transient hypocalcemia and ineffective in persistent
● 4 – 12 y.o.: 30-45 ml. per day cases
● In severe deficiency states as high as 75 ml. /day → Precipitates with bicarbonate containing solutions
→ Magnesium deficiency is suspected or confirmed, give
magnesium METABOLIC ACIDOSIS
o 📣 You have to measure magnesium level kasi you → Systemic disorder characterized by primary decrease in
also expect magnesium deficiency in hypocalcemia plasma bicarbonate concentration which causes a fall in
o Dose: 0.5 mEq/kg or 0.125 ml/kg of 50% MgSO4 I.M. pH
o (1 g. of 50% MgSO4 contains 99 mg Magnesium or → Lower limit of normal plasma HCO3 for infants and
about 8 mEq) children is 20 mEq/L

PATHOPHYSIOLOGY
IF ASYMPTOMATIC: → Loss of HCO3 through the gastrointestinal tract or kidney
→ Oral calcium supplements should be given and admitted → Addition of acids to the body → hydrogen ion load that
for workups consume bicarbonate, depleting buffer system
→ IN ALL CASES, milk should be changed to low- → Decreased hydrogen ion excretion resulting in depletion of
phosphate milk (human or modified cow’s milk) HCO3 stores

Figure _. Cheatsheet

CAUSES
Loss of Bicarbonate:
→ Gastrointestinal losses:
o Diarrhea
● Most common etiology
Figure . Notes from Doc. ● Most common cause of metabolic acidosis in
children

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●
It causes volume depletion as a result of losses of
sodium and water, potentially exacerbating the
acidosis by causing shock and a lactic acidosis.
o Small bowel tube or fistula drainage
o Pancreatic tube or fistula drainage
o Biliary tube
o Ureterosigmoidostomy
→ Renal losses
o Proximal renal tubular acidosis (RTA)
o Use of carbonic anhydrase inhibitors
o Chronic renal failure
o Adrenal insufficiency
→ Increased H+ load
o Endogenous production
● Lactic acidosis Figure . Arterial Blood Gas. 📣 Example of ABG result, pH of 7.332, PCo2
of 50.1 and PO2 of 189, PO2. HC03 is 26.5 and O2 SAT of 99 %. Sa PH, di
● Tissue hypoxia talaga natin minemeasure yung serum bicarbonate, sa US minemeasure
● Inborn errors of metabolism nila. Kinukuha lang natin yung bicarbonate level sa pag-compute ng anion
o Exogenous production gap ditto sa arterial blood gas. Yung formula, dito natin kukunin yung
● NH4Cl, HCl bicarb, yung chloride sa serum sample, yung sodium sa serum result, pero
● Toxins (Salicylates, Methanol, Ibuprofen, Ethylene yung bicarb sa ABG. Base excess (BE), important. Ilan nalang natitirang
base, which is bicarbonate divide sa base, pag nag-negative nay an kulang
glycol, Paraldehyde, etc.) na kulang na.
→ Decreased H+ load
o Renal failure (acute & chronic)
o Distal RTA
o Carbonic anhydrase inhibitors

ANION GAP
→ SUM OF THE TOTAL CATIONS IS EQUAL TO THE SUM
OF TOTAL ANIONS
→ = serum [Na] mEq/L – ([Cl] + [HCO3] mEq/L)
→ Normal anion gap: 8-12

Figure . Arterial Blood Gas. 📣 Kung parehong down/low ang arrow,

metabolic siya kaya nga metabolic equal. Respiratory opposite. Sa
respiratory, PCO2. Sa metabolic, bicarbonate.

Figure . Anion Gap. 📣 You have to check the arterial pH, if it’s less than 7.35
acidotic. Metabolic acidosis, the bicarbonate is low. Less than 20 mEq/L,
that’s metabolic acidosis. And you have to check the anion gap (check
formula). Normal anion gap is 8-12. NAGMA (normal anion gap metabolic
acidosis), so ito yung cause mnemonic is HARDASS. If high ang anion gap
ng metabolic acidosis, more than 12, so HAGMA naman, MUDPILES.

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Decreased Anion Gap
→ Does not help in the diagnosis of acid-base disorder
→ Suggest the presence of hypoalbuminemia increased
concentration of K, Ca, Mg or laboratory error

SIGNS AND SYMPTOMS

Respiratory
→ Deep, rapid respiration (Kussmaul’s); prominent when
arterial pH falls below 7.2
Cardiovascular
→ Secondary to depressed myocardial contractility and
decreased peripheral vascular resistance
→ Hypotension
o With acidemia, there may be a decrease in the
cardiovascular response to catecholamines,
potentially exacerbating hypotension in children with
volume depletion or shock.
→ Pulmonary edema
→ Tissue hypoxia
→ Ventricular fibrillation
→ Splanchnic vasoconstriction
Figure . Nomogram. Interpretation of Arterial Blood Gas. 📣 The easiest way, if
you’re confused, to analyze ABG. Example: arterial blood pH 7.2, HCO3 8, Central Nervous System
saan siya nakasama dito sa shaded area? Metabolic acidosis. → Disturbance of consciousness (coma in severe acidosis)
Seizures
Hematologic
→ Leukocytosis
Others:
→ anorexia, nausea, vomiting

LABORATORY
Blood
→ Na, K, Cl, HCO3
→ ABG
→ BUN, Creatinine
→ Glucose
Figure . Calculation of expected compensatory response. 📣 No need to → Lactate, pyruvate
memorize, I’m just showing you for you to know if there’s an adequate → Toxic screen
compensation.
Urine
Normal Anion Gap (NAGMA) → pH, glucose, protein
→ Normal anion gap is 4-11
→ AG = Na – (Cl + HCO3) TREATMENT
→ A 1 g/dL decrease in albumin concentration decreases the → Directed towards the underlying cause
anion gap by approximately 2.5 mEq/L → Treatment should be done if acidosis is severe and
→ Hyperchloremic metabolic acidosis is an alternative term causes serious acute or chronic organ system dysfunction
for a normal-anion gap metabolic acidosis → Correct extracellular volume, K+ or Cl- deficiency
→ Suggests loss of HCO3 via the kidneys or gastrointestinal → When blood pH is less than 7.20 (serum HCO3 less than
tract or rapid dilution of the ECF 15 mEq/L) patient is at risk for complications of acidosis
o Rise in chloride concentration equal to the lowering per se
of HCO3 concentration, thus keeping the anion gap → ⭐ HCO3 treatment dose can be estimated as:
unchanged o Mild to moderate acidosis (pH 7.20 – 7.37)
● HCO3 deficit (mEq) = desired serum [HCO3] –
Increased Anion Gap (HAGMA)
actual serum
→ Suggests addition of strong acids (endogenous or ● [HCO3] x 0.20 of total body weight (kg.)
exogenous) o Severe acidosis (pH <7.20)
→ HCO3 is consumed by the additional acid
● HCO3 deficit (mEq) = desired serum [HCO3] –
→ Examples of organic anions that may elevate the anion
actual serum [HCO3] x 0.50 of total body
gap: ketoacids in DKA, lactate in lactic acidosis, and
weight (kg.)
formic acid in methanol poisoning
→ Full correction SHOULD NEVER be attempted
→ May be due to a decrease in serum Ca, Mg, or K, a falsely
→ Reasonable goal is to increase serum HCO3 in
elevated serum Na, or an increase in serum total protein
increments of 5-10 mEq/L until a level of 15-18 mEq/L is
concentration
achieved 📣 Ang normal value ng bicarbonate is 22-28,
ayaw mo masyadong taasan

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→ Then, maintenance therapy can be continued at roughly 2 → PCO2 increases by 7 mm Hg for each 10 mEq/L increase
mEq/kg/day unless the underlying acidosis has been in the serum [HCO3−].
successfully corrected
PATHOPHYSIOLOGY
→ Loss of hydrogen ion
→ Gain of bicarbonate
→ Loss of extracellular fluid with more chloride than HCO3
→ Factors that prevent the kidneys from excreting HCO3
must also be present

CAUSES
LOSS OF HYDROGEN ION
→ Gastrointestinal
o Vomiting
o Nasogastric suction
o Congenital chloride-wasting diarrhea
o Antacid therapy (cation exchange resin)
→ Renal
Figure. 📣 For example, 8.4 NaHCO3. Half correction lang daw tayo, we o Diuretics: Thiazides, Furosemide, Ethacrynic acid
don’t give full correction. 0.3 times weight times base excess. 0.3 is a
constant, 16kg yung patient, times -19.3 kasi yun nalang natitirang base. o Excess mineralocorticoid: (aldosterone increases
That’s 106 mL na kukunin mong NaHCO3, pero dilute mo pa sa equal secretion of H+ in kidney alpha intercalated cells)
amount of D10 water to infuse over 7 hours kasi dapat 1mEq/kg/hr. 106 o Endogenous: Hyperaldosteronism, Cushing’s
divided by 16, kasi 1mEq is equal to 1mL. 6.6 hours, ginawa nalang 7 hrs disease, Adrenogenital syndrome
ang infusion time.
o Exogenous: Steroid therapy, licorice, Bartter’s
→ Based on the assumption that HCO3 space of one-third of syndrome, Cl-deficient infant formula
the body weight: o Post-chronic hypercapnia
o NaHCO3 required (mEq/L) = weight (kg.) x base o Occurs after the correction of a chronic respiratory
excess x 1/3 acidosis. This is typically seen in patients with
→ Usual physiologic compensatory mechanisms may be in chronic lung disease who are started on mechanical
the process, so the full dose may not be needed ventilation
o 1⁄2 dose may be given over 30 mins. as an isotonic → H+ movement into cells
solution of NaHCO3 and then the blood gas repeated o Hypokalemia
and adjust accordingly o Refeeding with carbohydrate after a prolonged fast
o If the pH is 7.3 or higher, NaHCO3 infusion may be GAIN OF HCO3
discontinued; but if still low, may continue the → Exogenous alkali: HCO3, citrate, acetate, lactate
infusion
Contraction of extracellular volume
→ If blood gases are still not available, empiric therapy may
be given at 1-2 mEq NaHCO3 per kg. body weight → Sweat losses in cystic fibrosis (infants)
→ In acidosis, potassium shifts out of cells in response to → Loop or thiazide-type diuretics
increased H+ ion concentration, but with correction of → Gastric losses in patients with achlorhydria
acidosis, ECF potassium will shift back
→ If serum K is normal or frankly low prior to start, potassium SIGNS AND SYMPTOMS
supplement / correction must be done to prevent life- ASYMPTOMATIC
threatening arrhythmia or respiratory paralysis → If symptomatic, complaints directly related to alkalemia are
→ In chronic metabolic acidosis, NaHCO3 may be given by uncommon
mouth. One-gram tablets contain about 12 mmoles of → Usually related to volume depletion (weakness, muscle
NaHCO3 cramps, postural dizziness) or to hypokalemia (polyuria,
polydipsia, muscle weakness)
ABG → Arrythmias are a potential complication of a metabolic
alkalosis, and the risk for arrythmia increases if there is
pH 7.32 concomitant hypokalemia.
PCO2 30
HCO3 16 LABORATORY
→ Arterial blood gas
→ Urinary chloride concentration on spot urine MOST
Answer: Metabolic acidosis useful diagnostic test
o The urine [Cl-] is superior to the urine [Na+] in
METABOLIC ALKALOSIS assessment of volume status in patients with
→ Systemic disorder caused by a process that leads to an metabolic alkalosis because the normal response to
increased pH (above 7.45) due to primary increase in a metabolic alkalosis is to excrete bicarbonate.
o The urine [Cl-] is usually a good indicator of volume
HCO3 concentration
status, and it differentiates Cl- resistant and Cl-
responsive causes of a metabolic alkalosis

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→ If urinary Cl- is <10 mEq/L (saline-responsive metabolic o Vomiting
alkalosis) avid renal reabsorption of Cl- has occurred, o Nasogastric suction
suspect the following:
o Congenital Cl- wasting diarrhea → Directed at releasing the constraints on renal HCO3
o Cl- deficient formula intake excretion
o Post-hypercapnea → Volume of fluids with NaCl plus K must be provided to
o Infants with cystic fibrosis excrete HCO3 and retain NaCl and K
→ If urinary Cl- is > 20 mEq/L (saline-resistant metabolic → NaCl – responsive varieties may be corrected by giving
alkalosis), suspect the following: NaCl alone
o Recent ingestion of diuretics → But KCl should be provided to replenish K stores
o Excess mineralocorticoid production or → Excess mineralocorticoid varieties of metabolic alkalosis
require:
administration
o Removal or ablation of secretory tumors
o Bartter’s syndrome (renal problem)
o Blockage of the renal tubular effects of the
o Profound hypokalemia (serum K+ < 2.0 mEq/L)
mineralocorticoids with spironolactone
→ Patients with severe K depletion and NaCl resistant
TREATMENT
alkalosis require provision of very large amounts of KCl
→ TREAT the underlying disease process before NaCl can be effective in correcting alkalosis
→ Promote renal HCO3 excretion

APPENDIX
Pediatric Reference Values can be found in Chapter 28 of Harriet Lane (if we include it here super haba na :<)
Quiz at the very end~

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Case Analysis for Maintenance Therapy: ANSWER

A patient comes in for poor appetite. She good urine output but Given: 18kg
does not want to eat. You hooked her to an IV fluid line. There is Formula: Holliday-Segar Method
no fever, no vomiting, nor diarrhea.
First 10 kg x 100ml/kg/day = 1000ml/day
Your consultant asked you to check the IV fluid’s orders. Her Second 8 kg x 50ml/kg/day = 400ml/day
weight is 18 kg and her previous weight at the clinic was also 18
kg. 1000 ml/day + 400 ml/day = 1400ml/day
1400ml/day / 24 = 58.33ml/hr
What would be the correct order in the chart if you are going to
calculate the amount of IV fluids per 24 hours. Please give your
formula.

Scan QR to download IMCI’s Booklet &

Chart (ʘᴥʘ)

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→ I think it’s derived from %dehydration’s formula (but I’m not so sure. Here’s %dehydration’s formula from Hariett Lane)

→ Then simplified to:

Fluid deficit ( ml )=% dehydration x preillness weight ( kg ) x 10
→ Note: when using this formula, you don’t have to use the percentage sign. Also, 10 is a constant and not in mL!

ml=10 ( % dehydration ) x 15 kg x 10
ml=1500

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Answers: Mix and Match c, e, f, a, b, g, d

1. ATPase system
2. Jejunum
3. 1-2 meq/kg
4. Thirst
5. ADH
6. Various proteins and organic phosphates
7. Hyperproteinuria and hyperlipidemia
8. Potassium; Sodium
9. Bicarbonate and chloride
10.Pure sodium excess – increased total body sodium; Water deficit – normal total body sodium; Water deficit in
excess of sodium deficit – low total body sodium

PRACTICE TEST: MIX AND MATCH

1. Hyponatremia a. Muscle weakness & Ileus
2. Hyperkalemia b. Hypervitaminosis D &
3. Metabolic Acidosis Hyperparathyroidism
4. Hypokalemia c. Syndrome of Inappropriate
5. Hypercalcemia Anti-diuretic Hormone
6. Hypernatremia d. QTc Interval = 0.50
7. Hypocalcemia e. Peaked T waves with
Ventricular Arrhythmia
f. Kussmaul’s Respiration
g. Serum Osmolality = 350
mOsm/L
Identify:

1. Mechanism by which Na and K are controlled? ______

2. Where is Sodium absorbed? ______
3. Recommended daily intake of potassium? _____
4. Best line of defense of hypernatremia? ______
5. First line of defense of hypernatremia? ______
6. Principal buffer in the ICF? ______
7. Causes of Pseudohyponatremia? _____
8. What is the major intracellular and extracellular cation?
____
9. Anions that accompany the sodium? ____
10. What are the causes of hypernatremia? ____

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