FLUIDS AND ELECTROLYTES CHAPTER 32-36

1. Total Body Water (TBW) – Core Concept

●​ Fetus: Highest TBW (fluid-filled baby!)

●​ Term baby: ~75% of weight is water
●​ Premature baby: Even more water
●​ 1-year-old onward: ~60% (boys), ~50% (girls) due to:
○​ Fat = less water (more in females)
○​ Muscle = more water (more in males)

2. Water Compartments

●​ Intracellular Fluid (ICF): 30–40% body weight

●​ Extracellular Fluid (ECF): 20–25% body weight
○​ Plasma: 5%
○​ Interstitial fluid: 15%
●​ Newborns have more ECF; it reduces after birth and ICF increases with growth.

3. Solutes in Fluid Compartments

●​ ECF: Sodium & Chloride (Na+ Cl−)

●​ ICF: Potassium (K+), proteins, phosphate
●​ Na+/K+ pump keeps Na+ out, K+ in (like bouncers at a club – one in, one out)

4. Regulation of Volume & Osmolality

●​ Osmolality (concentration): Controlled by water balance

○​ Detected by osmoreceptors → ADH + thirst
●​ Volume: Controlled by sodium balance
○​ Detected by baroreceptors → RAAS system

5. Key Hormones

●​ ADH (vasopressin): Retains water (especially in dehydration)

●​ Aldosterone: Retains sodium (and water follows)
●​ Angiotensin II: Constricts vessels, stimulates aldosterone
●​ ANP: Excretes sodium (helps in volume overload)
6. Maintenance IV Fluids – When?

Use when oral feeding not possible:

●​ Add replacement fluids if ongoing loss (e.g., diarrhea, NG tube)

●​ Add deficit correction if dehydrated

7. What’s in Maintenance Fluids?

●​ Water + Glucose (Dextrose): Basic calories to prevent ketoacidosis

●​ Na+, K+, Cl−: Replace urine/stool losses
●​ Glucose = ~20% of daily calorie need (not enough for growth)

8. What Maintenance Fluids to Give?

●​ Common: D5NS + 20 mEq/L KCl

●​ Exceptions:
○​ Renal disease / hyperkalemia: Skip or reduce KCl
○​ Adjust based on labs, disease, urine output

9. Daily Maintenance Fluid Calculation (Weight-Based)

Use "4-2-1 Rule" (per hour):

●​ 0–10 kg: 4 mL/kg/hr

●​ 11–20 kg: 40 mL + 2 mL/kg/hr for weight above 10
●​ 20 kg: 60 mL + 1 mL/kg/hr for weight above 20​
Max rate: 100 mL/hr​
Max volume/day: 2400 mL​
​

10. Breakdown of Normal l Loss

●​ Urine: 60%
●​ Insensible (skin, lungs): 35%
●​ Stool: 5%
●​ Note: Sweat contains electrolytes, unlike insensible loss
Quick Mnemonics to Help

●​ "Fat floats, muscle drinks": Fat has less water; muscle more
●​ "SIP for compartments" – Sodium in plasma, Intracellular = Potassium
●​ "ADH = Add H2O", "Aldo = Add Salt"
●​ "4-2-1 Rule" – for hourly fluid rates

CHAPTER 33: Dehydration and Replacement Therapy (Simplified)

Replacement Therapy

The body normally loses water in three main ways:

1.​ Urine – the biggest contributor, making up about 60% of daily water loss.
2.​ Insensible losses – about 35%, which includes water lost through the skin (not
sweat) and lungs during breathing.
3.​ Stool – contributes about 5% of total daily water loss.

Important note: Sweat is not considered part of insensible loss because it contains water
and electrolytes, whereas insensible loss is mainly pure water.

Factors That Change Water Needs

Different clinical conditions can increase or decrease normal water requirements.

●​ Skin-related increases:​
Radiant warmers, phototherapy, fever, sweating, burns, or skin conditions like
exfoliative dermatitis (e.g., toxic epidermal necrolysis) can increase water loss.​

●​ Lung-related increases:​
Faster breathing (tachypnea) or children with tracheostomy lose more water through
the lungs. Using humidified ventilators can help reduce this.​

●​ Gastrointestinal losses:​
Vomiting, diarrhea, and nasogastric suctioning can cause major losses of both water
and electrolytes. These should be measured and replaced with specific fluids.​

●​ Renal (kidney) issues:​

○​ Low urine output (oliguria/anuria): Seen in kidney failure or SIADH

(inappropriate ADH secretion). Giving routine fluids can cause overload in
these cases.
 ○​ High urine output (polyuria): Conditions like diabetes mellitus, diabetes
insipidus, or polyuric phase of AKI increase urine loss. These patients need
extra fluid beyond maintenance.
●​ Miscellaneous losses:​
Include significant output from surgical drains, chest tubes, or fluid moving into the
"third space" (like ascites or edema due to sepsis or abdominal surgery). Even
though these patients may gain weight (from fluid retention), their blood volume may
actually be low and need replacement with isotonic fluids like normal saline or
Ringer lactate.​

Approach to Altered Urine Output

●​ Oliguria/Anuria:​
Give only "insensible" fluids (about one-third of normal maintenance). Monitor
closely, because this is only an estimate. Watch weight, hydration status, and signs
of overload.​

●​ Polyuria:​
Give insensible fluids plus replace urine loss milliliter for milliliter using a solution
that matches the lost urine electrolytes (usually based on lab analysis).​

Special GI Losses: How to Replace

●​ Diarrhea:​
Replace each mL of stool with an equal amount of fluid. A good choice is 5%
dextrose in quarter-normal saline with added bicarbonate and potassium
chloride, because stool contains sodium, potassium, and bicarbonate.​

●​ Gastric fluid loss (vomiting or suction):​

Replace with normal saline plus potassium chloride, because gastric fluid is rich
in sodium and chloride.​

Third Space Losses and Drains

●​ Fluids lost into third space (like ascitic fluid or tissue edema) or through
chest/surgical drains cannot be precisely measured, but they must be considered in
replacement plans.
●​ Use isotonic fluids like normal saline or Ringer lactate. Adjust based on clinical
monitoring: look at heart rate, blood pressure, and urine output for clues to
intravascular volume status.
Here's a simplified and easy-to-study version of the content from those tables — with all
information converted to text as you asked, no grids:

Adjustments in Maintenance Water Needs

In different clinical situations, the water needs of a child may increase or decrease based on
the source of fluid loss:

1. Skin-related causes:

●​ Increased water loss happens in babies placed under radiant warmers, receiving
phototherapy, or having a fever, sweating a lot, burns, or severe skin conditions (like
epidermolysis bullosa or toxic epidermal necrolysis).
●​ Decreased water loss from skin may happen in incubator settings for premature
infants where the environment is humidified.

2. Lung-related causes:

●​ Increased water loss occurs if the child is breathing very fast (tachypnea) or has a
tracheostomy — both lead to more water being lost through breathing.
●​ Decreased water loss happens when the child is on a humidified ventilator, which
reduces evaporation from the airways.

3. Gastrointestinal (GI) causes:

●​ Conditions like diarrhea, vomiting (emesis), and nasogastric (NG) suctioning increase
GI fluid losses and therefore increase the need for fluid replacement.

4. Renal (kidney-related) causes:

●​ When the child has polyuria (passing too much urine), more fluid is needed.
●​ In contrast, with oliguria or anuria (very little or no urine output), the body conserves
water, and fluid needs are reduced.

5. Miscellaneous causes:

●​ Increased needs include situations like having surgical drains or fluid being lost into
the “third space” (like in ascites or severe infections).
●​ Decreased needs can occur in conditions like hypothyroidism where metabolism
slows down.

Fluid Therapy Adjustments for GI Losses

When a child is losing fluid through diarrhea or vomiting, we replace what is lost with
fluids that mimic what the body lost. The type of replacement depends on where the fluid
is coming from:
For Diarrhea (Stool Loss):

●​ The lost stool typically contains sodium, potassium, and bicarbonate.

●​ Use a solution like 5% dextrose in ¼ normal saline, with added 20 mEq/L of
sodium bicarbonate and 20 mEq/L of potassium chloride.
●​ Replace the exact amount lost — that means give back the same volume of fluid
the child loses in stool, every 1 to 6 hours depending on clinical status.

For Gastric Losses (Vomiting or NG suction):

●​ Gastric fluid contains mostly sodium, potassium, and chloride.

●​ Use normal saline (0.9% NaCl) with 10 mEq/L of potassium chloride.
●​ Again, replace mL for mL — whatever is lost in gastric output (vomit or NG
aspirate), give back the same volume in fluid every 1 to 6 hours.

Dehydration in Children

Most commonly caused by gastroenteritis.

First step: Assess the degree of dehydration, as this determines urgency and volume of
fluid needed.

●​ Mild dehydration:​
Subtle or no signs. Usually only a history of poor intake or increased loss.​

●​ Moderate dehydration:​
Visible clinical signs like dry mouth, sunken eyes, reduced skin turgor. Needs prompt
correction.​

●​ Severe dehydration:​
Life-threatening. Blood pressure may be low or unrecordable, urine output very low
or absent, child lethargic or unconscious. Immediate resuscitation required.​

Got it — from now on, when you say "make it simple", I will:

Simplify the text for easier study, understanding, recall, and repetition — without
losing important clinical meaning.

Here’s your current extract simplified accordingly:

Severe Dehydration: What to Do

If a child has severe dehydration, it's a medical emergency. Low blood pressure means
vital organs (like the brain, kidneys, heart) are not getting enough blood — this is shock.

●​ Such patients need immediate IV fluids, given fast and aggressively.

●​ Ongoing monitoring is critical — check frequently to adjust fluids.
●​ In hypernatremic dehydration, the signs can underestimate the actual water loss
because water moves from inside cells to the blood to keep blood pressure up.

Lab Tests in Dehydration

●​ BUN and creatinine are key tests:​

○​ In simple dehydration (without kidney injury), BUN goes up, but creatinine
stays normal.
○​ Why? The kidneys are trying to save water and sodium, so they reabsorb
more urea (BUN).
○​ If the child eats very little protein, BUN may not rise much.
○​ If the child has a GI bleed or is on steroids, BUN can be very high.
○​ If creatinine is also high, think of kidney damage.
 ●​ Urine specific gravity (USG):​

○​ USG is usually high (≥1.025) in dehydration.

○​ It goes back to normal after fluids.
●​ Urinalysis may show:​

○​ Some protein, white and red blood cells, and casts.

○​ These findings go away after proper fluid therapy and usually don’t mean
permanent kidney damage.
●​ Hemoglobin and hematocrit increase due to blood concentration from fluid loss.​

How to Calculate Fluid Deficit

To find out how much fluid the child has lost:

●​ Use this formula:​

Fluid Deficit = % dehydration × weight (kg)

Example: A 10 kg child who’s 10% dehydrated has lost:​

10% of 10 kg = 1 L (1000 mL) of fluid.

Treatment Approach

Dehydrated children need quick treatment to restore blood flow to organs.

●​ Start with isotonic fluids like:​

○​ Normal Saline (NS)

○​ Ringer Lactate
●​ Blood transfusion is used only if there’s blood loss, not in usual dehydration.​

●​ Start with a bolus of 20 mL/kg over 20 minutes.​

●​ If dehydration is severe, more boluses may be needed, possibly faster.​

●​ Once the child:​

○​ Becomes more alert

○​ Heart rate slows
○​ Blood pressure normalizes
○​ Hands and feet warm up
●​ — initial fluid resuscitation is considered complete.​
fluid management and types of dehydration for easy study:

1. First Step: Restore Blood Flow (Intravascular Volume)

●​ Give NS (Normal Saline):​

20 mL/kg over 20 minutes​
→ Repeat if still signs of poor perfusion (e.g., weak pulse, low BP, cold hands/feet).​

●​ Next:​
Another 20 mL/kg over 2 hours to stabilize.​

2. Calculate Total Fluids Needed (for 24 hrs)

●​ Formula:​
Maintenance + Deficit – Bolus already given​

●​ Give remaining fluids over 24 hours using:​

D5 NS + 20 mEq/L KCl (only after child urinates)​

●​ Also: Replace ongoing losses (vomit/diarrhea) as they happen.​

3. Monitor Closely (Table 33.7)

Check:

●​ Vitals: HR, BP
●​ Urine output & Specific gravity
●​ Intake-output & Weight
●​ Electrolytes
●​ Physical signs of dehydration or overload

4. Types of Dehydration (Key Differences)

A. Hyponatremic Dehydration (Low Sodium):

●​ Due to: drinking water or diluted milk when dehydrated

●​ Risk: Brain swelling if Na is corrected too fast
 ●​ Rule: Do not increase sodium >10–12 mEq/L in 24 hrs

B. Hypernatremic Dehydration (High Sodium):

●​ Due to: lack of access to water, vomiting, neuro issues

●​ Looks: Child may not look very dry (water shifts from cells to blood)
●​ Danger: Seizures, brain bleeding, cerebral edema
●​ Rule: Decrease Na <12 mEq/L per 24 hrs, go slow
●​ Monitor Na every 4–6 hrs

5. Oral Rehydration (For Mild–Moderate Dehydration)

●​ ORS (Oral Rehydration Solution) is best when:​

○​ Child is alert, not vomiting much, and not in shock

●​ How much to give:​

○​ Mild dehydration: 50 mL/kg over 4 hrs

○​ Moderate: 100 mL/kg over 4 hrs
●​ Vomiting? Use ondansetron to help ORS stay down​

6. Key Signs That Fluid Therapy is Working:

●​ Child becomes alert, HR drops, BP normalizes, perfusion improves (warm hands,

capillary refill <2s)
Oral Rehydration Plan – Moderate Dehydration

Phase 1: Rehydration (First 4 hours)

●​ Give 100 mL/kg of ORS over 4 hours

●​ Example: If child weighs 10 kg → give 1000 mL over 4 hrs (~250 mL/hr)

Add Extra for Each Loose Stool or Vomit

●​ Give 10 mL/kg of ORS per stool or vomit​

(e.g., 10 kg child → 100 mL extra each time)

Phase 2: Maintenance After Rehydration

●​ Give 100 mL/kg/day of ORS until diarrhea stops

 ●​ Continue breastfeeding or formula as usual — don’t delay feeds >24 hours

General Rules

●​ If child becomes hydrated early (looks well, no signs of dehydration) → reduce ORS
●​ Watch for puffy eyes (periorbital edema) → sign of excess fluid
●​ If exact stool volume can't be measured, give 10–15 mL/kg/hour of ORS

Parenteral Nutrition (PN) – Quick Overview

When is PN Needed?

●​ When the gut can’t be used or isn't enough (e.g., ileus, bowel surgery, severe
diarrhea).
●​ Preferred only when enteral feeding fails—because gut feeding is:
○​ More natural (physiologic)
○​ Cheaper
○​ Safer with fewer complications

Common Indications

Acute:

●​ Prematurity
●​ Trauma, burns
●​ Post-bowel surgery
●​ ICU cases (e.g., multiorgan failure)
●​ Bone marrow transplant, malignancy

Chronic:

●​ Short bowel syndrome (e.g., post-NEC)

●​ Intractable diarrhea
●​ Chronic gut motility issues
●​ IBD, Immunodeficiency

Types of Access for PN

●​ Peripheral IV line:​
 ○​ Easier, but veins inflame with high concentration
○​ Limited to dextrose ≤12%
○​ Lipids can still be given
●​ Central Venous Line (CVL):​

○​ Needed for long-term PN

○​ Can deliver concentrated solutions (dextrose up to 25–30%)
○​ Preferred in cancer, transplant, or prolonged illness
○​ Safer option: PICC (Peripherally Inserted Central Catheter)

What’s in PN?

●​ Calories: From dextrose (sugar) and lipids (fat)

●​ Proteins: As amino acids
●​ Vitamins, minerals, electrolytes, trace elements
●​ Iron (if needed)

Typical Daily Protein Goals:

●​ Preterm infant: 2.5–3.5 g/kg/day

●​ Full-term infant: 1.5–3 g/kg/day
●​ Older child: 0.8–2 g/kg/day

Lipids:

●​ Start slow: 0.5–1 g/kg/day, build up to 2.5–3.5 g/kg/day

●​ Should give 30–40% of total calories
●​ Monitor: serum triglycerides to avoid overload

Complications to Watch For

Line-Related:

●​ Insertion risks: Pneumothorax, bleeding

●​ Long-term: Clots (thrombosis), line infections
○​ Common bugs: Coagulase-negative staph, S. aureus, GNB, fungi

Metabolic/Nutritional:

●​ Hyperglycemia
●​ Electrolyte imbalance
●​ Excess protein: May cause azotemia or hyperammonemia
●​ Micronutrient deficiencies

Liver Problems (Long-term PN):

 ●​ Cholestatic liver disease: Jaundice → Cirrhosis → Liver failure
●​ Risk reduced by:
○​ Lower toxic amino acids
○​ Using fish-oil-based lipids
○​ Early minimal gut feeds (trophic feeding)

Quick Tip:​
Even if full feeding isn’t possible, start small gut feeds early—they help prevent liver
issues and promote gut health.

CHAPTER 35: Sodium Disorders

The kidneys control sodium balance by deciding how much sodium to throw out in urine.​
But, water balance, not sodium itself, usually controls the blood sodium concentration.

●​ If sodium levels go up, blood becomes more concentrated.​

○​ This makes you thirsty and causes release of ADH (antidiuretic hormone).
○​ ADH makes kidneys hold on to water, diluting the sodium and bringing the
level back to normal.
●​ If sodium levels fall (hyponatremia), the blood becomes dilute.​

○​ Less ADH is released.

○​ Kidneys pee out more water, making sodium concentration rise back to
normal.

Important: If your body is low on fluid (volume depletion), it prioritizes saving water —
even if blood sodium is low.​
Saving water is more important than fixing sodium level!

The amount of sodium in the urine depends mainly on your blood volume, not directly on
your blood sodium number.

HYPONATREMIA (Low Sodium)

Causes:
 ●​ Pseudohyponatremia: A false low reading when there’s too much fat or protein in
the blood.​
(Modern machines mostly avoid this mistake.)​

●​ True hyponatremia: Really low sodium, and low measured osmolality.​

○​ High blood sugar (hyperglycemia) can also lower sodium readings (not true
hyponatremia).​
For every 100 mg/dL increase in blood sugar, sodium drops by 1.6 mEq/L.​
These patients don’t need sodium correction — just fix the sugar!
○​

Types (based on body fluid status):

1.​ Hypovolemic hyponatremia (low sodium + low fluid volume):​

○​ More sodium lost than water.

○​ Common causes: Diarrhea, kidney problems.
○​ Urine sodium:
■​ Low if losses are outside kidneys (like diarrhea).
■​ High if kidney disease is causing the problem.
2.​ Euvolemic hyponatremia (normal fluid volume, low sodium):​

○​ Body water slightly increased, sodium slightly decreased.​

 ○​ Example: SIADH (Syndrome of Inappropriate ADH Secretion).​

■​ ADH is secreted even when it’s not needed.

■​ Causes: stress, pneumonia, meningitis, brain injury.
○​ SIADH vs Cerebral Salt Wasting:​

■​ SIADH = normal or slightly overloaded volume.

■​ Cerebral Salt Wasting = true volume loss.
○​ In infants: can happen with excess water intake or over-diluted formula.​

3.​ Hypervolemic hyponatremia (high sodium and water, but more water than
sodium):​

○​ Seen in renal failure, heart failure, liver disease.

○​ Kidneys keep both sodium and water, but because more water is kept,
sodium looks low.

Symptoms:
●​ Water moves into brain cells → Brain swelling.
●​ Symptoms:
○​ Mild: nausea, tiredness, headache.
○​ Severe: confusion, seizures, coma.
●​ Faster sodium drops → worse symptoms.
●​ In long-standing hyponatremia, brain adapts and symptoms may be milder.

Treatment:
●​ Correct slowly — if you fix sodium too fast, it can cause central pontine
myelinolysis (brain damage).
●​ Rule of thumb: Raise sodium by no more than 10 mEq/L in 24 hours.

Depending on the cause:

●​ Hypovolemic hyponatremia: Give IV fluids with sodium.

●​ SIADH: Restrict water intake; special drugs (vaptans) can be used.
●​ Hormone issues: Replace missing hormones (thyroid, cortisol).
●​ Water intoxication: Limit water; let the body balance itself.

If emergency (seizures):

●​ Give hypertonic saline (3% NaCl).

●​ 1 mL/kg of 3% saline raises sodium by 1 mEq/L.
 ●​ Usually 4–6 mL/kg given for quick improvement.

HYPERNATREMIA (High Sodium)

Causes:
1.​ Too much sodium intake:​

○​ Example: hospital error with sodium bicarbonate.

2.​ Too little water:​

○​ Common cause!
○​ Happens when people can’t drink water — infants, neurologic issues,
vomiting, poor breastfeeding.
○​ Premature babies lose more water through skin (especially under
warmers/phototherapy).
3.​ Excess water loss through kidneys:​

○​ Diabetes insipidus (kidney can’t respond to ADH or brain doesn’t make

ADH):​

■​ Central DI (brain problem): improves with ADH analog.

■​ Nephrogenic DI (kidney problem): no improvement with ADH.
○​ Nephrogenic DI can be inherited (common in boys) or acquired (e.g., sickle
cell disease, lithium use).​

4.​ Diarrhea:​

○​ If a child can't drink enough to replace stool losses, can develop

hypernatremia.
5.​ Renal causes:​

○​ Some kidney diseases cause water loss with sodium loss — if the child can’t
drink enough, hypernatremia can happen.

Diagnosis clues:
●​ Extrarenal losses (diarrhea, sweat):​

○​ Kidneys save water → concentrated urine, low urine sodium (<10 mEq/L).
 ●​ Renal losses (kidney disease, DI):​

○​ Diluted urine even when body needs to save water.

Got it! Here's the information on Hypernatremia in a simplified notes format:

Hypernatremia

Definition: High sodium levels in the blood.

Etiology (Causes)

1.​ Sodium Intoxication​

○​ Often occurs in hospitals due to sodium bicarbonate used to treat metabolic

acidosis.
○​ Hyperaldosteronism: Sodium retention by kidneys, causing mild
hypernatremia and high blood pressure.
2.​ Water Loss​

○​ No access to water or can't drink properly: Caused by neurological issues,

vomiting, or anorexia (loss of appetite).
○​ Infants at risk: They can't control their water intake.
■​ Improper breastfeeding in first-time mothers can lead to severe
dehydration and hypernatremia.
■​ Premature infants have higher water loss (due to radiant warmers,
phototherapy).
3.​ Diabetes Insipidus​

○​ Nephrogenic Diabetes Insipidus:

■​ Genetic (X-linked), mainly affects males. Causes massive water loss
in urine.
■​ May result in failure to thrive and severe hypernatremic
dehydration.
○​ Acquired Nephrogenic Diabetes Insipidus:
■​ Caused by kidney disease, medications (like lithium), high calcium, or
low potassium.
○​ Central Diabetes Insipidus:
■​ ADH (antidiuretic hormone) deficiency due to tumor, trauma, or
infarction.
■​ Responds to ADH analog (synthetic ADH), unlike nephrogenic.
4.​ Diarrhea​
 ○​ Causes sodium and water loss.
○​ Most children with gastroenteritis (stomach infection) don't develop
hypernatremia because they drink enough fluids.
○​ Risk factors: Inadequate intake due to vomiting, lack of water access, or
anorexia.
5.​ Renal Causes​

○​ Conditions like obstructive uropathy, renal dysplasia, and juvenile

nephronophthisis can cause water and sodium loss, leading to
hypernatremia.

Diagnosis

●​ Urine Analysis: To differentiate between renal and non-renal causes of

hypernatremia.
○​ Non-renal causes (e.g., dehydration): Kidneys conserve sodium, produce
concentrated urine (urine sodium <10 mEq/L).
○​ Renal causes: Kidneys lose sodium, produce dilute urine (urine sodium
elevated).

Clinical Manifestations of Hypernatremia:

●​ Dehydration: Most children with hypernatremia are dehydrated and show typical
dehydration signs (refer to Chapter 33).
 ●​ Better Preservation of Intravascular Volume: Due to water shifting from
intracellular to extracellular space, children with hypernatremic dehydration often
have better intravascular volume.
●​ Doughy Skin: In hypernatremic infants, skin feels doughy due to intracellular water
loss.
●​ Central Nervous System (CNS) Symptoms: Even without dehydration,
hypernatremia affects the CNS, with symptoms linked to the sodium level and speed
of increase. These include:
○​ Irritability
○​ Restlessness
○​ Weakness
○​ Lethargy
○​ High-pitched cry and hyperpnea in infants
○​ Fever
○​ Excessive thirst
○​ Nausea
●​ Brain Hemorrhage: This is the most serious complication. High extracellular
osmolality causes water to leave brain cells, reducing brain volume and leading to
tearing of blood vessels (subarachnoid, subdural, and parenchymal hemorrhage).
○​ Seizures and coma can occur due to brain hemorrhage.

Treatment of Hypernatremia:

1.​ Slow Correction:​

○​ The brain generates idiogenic osmoles to prevent water loss. Rapid reduction
of sodium can cause water to move into brain cells, causing swelling,
seizures, or coma.
○​ Goal: Decrease serum sodium by less than 12 mEq/L per 24 hours.
2.​ Restoring Intravascular Volume:​

○​ Isotonic fluid is used to restore volume initially, especially in hypernatremic

dehydration due to gastroenteritis.
○​ For diabetes insipidus-related hypernatremia, hypotonic fluids are used.
3.​ Monitoring:​

○​ Frequent monitoring of serum sodium is critical for adjusting fluid therapy and
ensuring gradual correction.
4.​ Specific Causes:​

○​ Central Diabetes Insipidus: Administer ADH analog to reduce excessive

water loss.
○​ Nephrogenic Diabetes Insipidus: Use urine replacement solutions to
counteract water losses. Long-term, reduce sodium intake, use thiazides, and
NSAIDs to manage nephrogenic DI.
 5.​ Acute Hypernatremia:​

○​ For acute hypernatremia (e.g., due to sodium intoxication), rapid correction is

possible, as idiogenic osmoles haven’t formed.
○​ Loop diuretics or dialysis may be necessary if rapid correction is needed
without causing volume overload.
○​ Severe hypernatremia from sodium intoxication may require controlled water
administration.

CHAPTER 36: Potassium Disorders

Introduction to Potassium Balance

The kidneys primarily regulate potassium balance by adjusting its excretion based on intake,
influenced by factors like aldosterone, acid-base status, serum potassium levels, and kidney
function. Intracellular potassium is significantly higher (about 30 times) than in the
extracellular space. Alterations in potassium distribution can lead to either hypokalemia or
hyperkalemia, and the plasma potassium concentration does not always reflect the total
body potassium content.

Hypokalemia

Etiology of Hypokalemia

Hypokalemia is common in children, often due to gastroenteritis, with loss of potassium

through diarrhea. It can also result from spurious hypokalemia (such as in leukemia, where
the plasma sample is left at room temperature, causing white blood cells to absorb
potassium). Four main mechanisms cause hypokalemia:

1.​ Low intake

2.​ Nonrenal losses (e.g., diarrhea, laxative abuse)
3.​ Renal losses (e.g., diuretics, renal tubular acidosis)
4.​ Transcellular shifts (e.g., insulin therapy in diabetic ketoacidosis)

For example:

●​ Insulin therapy in diabetic ketoacidosis shifts potassium from the extracellular to the
intracellular space.
●​ β-adrenergic agonists (like albuterol) used for asthma treatment can cause
potassium to shift into cells, leading to hypokalemia.

Causes of Hypokalemia (Table 36.1)

 ●​ Spurious: High white blood cell count.
●​ Transcellular shifts: Alkalemia, insulin, β-adrenergic agonists, etc.
●​ Decreased intake: Uncommon unless associated with anorexia.
●​ Extrarenal losses: Diarrhea, laxative abuse, sweating.
●​ Renal losses:
○​ With metabolic acidosis: Renal tubular acidosis (RTA), diabetic
ketoacidosis.
○​ Without specific acid-base disturbance: Tubular toxins, diuretic use.
○​ With metabolic alkalosis: Vomiting, nasogastric suction, cystic fibrosis, etc.
●​ Adrenal disorders: Hyperaldosteronism, Liddle syndrome, etc.

Clinical Manifestations of Hypokalemia

●​ Heart:​

○​ ECG changes: Flattened T waves, depressed ST segments, U waves.

○​ Severe hypokalemia can lead to ventricular fibrillation or torsades de
pointes.
●​ Skeletal muscle:​

○​ Muscle weakness, cramps, and paralysis (especially when potassium is <2.5

mEq/L).
○​ Respiratory paralysis can occur and may require mechanical ventilation.
●​ Other effects:​

○​ Rhabdomyolysis after exercise.

○​ Gastrointestinal: Hypokalemia can slow motility, causing ileus (especially at
potassium levels <2.5 mEq/L).
○​ Bladder function: Urinary retention may occur.
○​ Polyuria and secondary nephrogenic diabetes insipidus.
○​ Chronic hypokalemia can cause kidney damage, interstitial nephritis, and
renal cysts.

Diagnosis of Hypokalemia

●​ Review the child’s diet, gastrointestinal losses, and medications.

●​ Hypertension may indicate excess mineralocorticoids.
●​ Electrolyte abnormalities (hypokalemia with metabolic acidosis suggests diarrhea or
RTA; with metabolic alkalosis, suggests gastric losses, diuretics, etc.).

Treatment of Hypokalemia

Treatment depends on:

 ●​ Potassium level, clinical symptoms, renal function, and ongoing losses.​

●​ Severe, symptomatic hypokalemia requires aggressive treatment, while mild

hypokalemia can be treated more cautiously.​

●​ The plasma potassium level may not reflect total body potassium due to shifts in
potassium between compartments (e.g., in diabetic ketoacidosis, where plasma
potassium may be normal but total body potassium is reduced).​

Bartter and Gitelman Syndromes

Bartter Syndrome and Gitelman Syndrome are inherited disorders that lead to
hypokalemia and metabolic alkalosis, among other signs.

●​ Bartter Syndrome: Characterized by nephrocalcinosis, polyhydramnios, and

sometimes hypercalciuria.
●​ Gitelman Syndrome: Features include hypomagnesemia, hypocalciuria, and
metabolic alkalosis.

Both conditions cause renally induced hypokalemia and are important in differential
diagnosis.
HYPOKALEMIA (Low Potassium)
Why it happens:

●​ Either potassium is lost (via urine, gut, etc.)

●​ Or it shifts from blood into cells (common during treatment of other problems like
acidosis or insulin therapy)

Treatment:

●​ Oral potassium is safer if not urgent.

●​ IV potassium is used in urgent cases:
○​ Dose: 0.5–1 mEq/kg over 1 hour
○​ Max adult dose: 40 mEq
○​ Always monitor ECG and vitals
●​ If potassium loss is through urine (like due to diuretics), potassium-sparing
diuretics can help.
●​ In volume-depleted patients, correcting fluid status also reduces potassium loss.

HYPERKALEMIA (High Potassium)

Why it happens:

Three main categories:

1.​ Spurious (lab error)

○​ Due to hemolysis during blood draw, tight tourniquet, or excessive muscle use
(fist clenching)
2.​ Potassium moving out of cells (shift to extracellular space)
○​ Happens in:
■​ Acidosis
■​ Cell destruction (rhabdomyolysis, tumor lysis, trauma)
■​ Lack of insulin
■​ Meds (like succinylcholine, β-blockers)
■​ Exercise, hyperosmolality, etc.
3.​ Reduced excretion (kidney/adrenal issues)
○​ Seen in:
■​ Renal failure
■​ Addison’s disease or CAH (e.g., 21-hydroxylase deficiency)
■​ Pseudohypoaldosteronism
 ■​ Drugs like ACE inhibitors, ARBs, NSAIDs, potassium-sparing
diuretics

Symptoms:

●​ Cardiac effects come first:

○​ ECG changes: Peaked T waves → wide QRS → arrhythmia → cardiac arrest
●​ Others: Muscle weakness, tingling, paresthesias (but these usually follow heart
issues)

Diagnosis:

●​ Rule out lab error (repeat sample, use plasma if high WBC/platelet)
●​ Look at history: potassium intake, kidney function, drugs
●​ Test for acid-base imbalance
●​ Watch for signs of cell lysis (↑LDH, uric acid, phosphate)

TREATMENT OF HYPERKALEMIA
2 Main Goals:

1.​ Prevent deadly heart rhythms (arrhythmias):​

○​ Stabilize heart:
■​ IV calcium gluconate
○​ Shift K+ into cells:
■​ Insulin + glucose (pushes K+ into cells)
■​ Sodium bicarb (especially if acidosis is present)
■​ Albuterol (β-agonist via nebulizer)
2.​ Remove potassium from body:​

○​ Loop diuretics
○​ Sodium polystyrene sulfonate (Kayexalate) – oral or rectal
○​ Dialysis – if kidney failure or severe/refractory hyperkalemia

Special Scenarios:

●​ Aldosterone deficiency (like CAH or Addison) → treat with fludrocortisone

●​ Chronic cases → dietary changes, adjust medications

Key ECG Tip:Always check ECG if K+ > 6.5 mEq/L, even if patient is stable.
QUICK REVISION PEARLS

CHAPTER 32: Maintenance Fluid Therapy

●​ Water balance is regulated by ADH and thirst; osmolality triggers these systems.
●​ In volume depletion, ADH increases even if osmolality is normal — volume >
osmolality in priority.
●​ Sodium balance depends on effective circulating volume, not serum sodium
levels.
●​ Maintenance IV fluids are needed when oral intake is not possible; they replace:
○​ Insensible losses (skin, lungs)
○​ Urinary/stool losses
●​ Glucose (D5) in fluids provides ~20% of daily caloric needs, preventing
ketoacidosis and muscle breakdown.
●​ Typical maintenance solution: D5 NS + 20 mEq/L KCl

CHAPTER 33: Dehydration & Replacement Therapy

●​ 35% of water loss is via insensible routes — skin and respiration.

 ●​ An anuric child (not eating or peeing) needs only insensible fluids to maintain
volume.
●​ Children with diarrhea, vomiting, polyuria need fluid replacement to prevent
hypovolemia.
●​ Emergency fluid bolus: 20 mL/kg of NS or RL over 20 minutes for significant
dehydration.
●​ BUN > creatinine suggests pre-renal dehydration.
●​ Hyponatremic dehydration: Giving plain water/diluted milk during gastro → low
Na.
●​ Hypernatremic dehydration: Seen in poor intake, DI, or excessive water loss.
●​ Mild/moderate dehydration: Treat with ORS unless contraindicated.

CHAPTER 34: Parenteral Nutrition (PN)

●​ Use PN when enteral feeds are inadequate.

●​ Short bowel syndrome is a classic indication.
●​ PN provides calories mainly via dextrose & fats; proteins are for tissue repair.
●​ Complications:
○​ Thrombosis, line infections
○​ Cholestatic liver disease (especially long-term PN)
●​ Trophic feeds (minimal gut feeds) reduce PN-related liver issues — “gut keeps the
liver healthy.”

CHAPTER 35: Sodium Disorders

●​ Most sodium disorders are actually water balance issues.

●​ Hyponatremia: Water enters brain cells → cerebral edema, risk of seizures.
●​ Hypernatremia: Water leaves brain cells → brain shrinkage, risk of bleed.
●​ Rapid shifts are dangerous:
○​ Correct hyponatremia <10 mEq/L/day
○​ Correct hypernatremia <12 mEq/L/day
●​ Volume status is the first clue: Hypovolemic, euvolemic, hypervolemic?
●​ Common causes:
○​ Hyponatremia: GE (hypovolemic), SIADH (euvolemic), CHF/cirrhosis
(hypervolemic)
○​ Hypernatremia: GE or diabetes insipidus
●​ Hypertonic saline (3%) is used only in severe symptomatic hyponatremia (e.g.,
seizures).
●​ Water intoxication often self-corrects when excess water intake stops.

CHAPTER 36: Potassium Disorders

●​ Kidneys are the main regulators of potassium.
●​ Hypokalemia causes:
1.​ Renal losses (diuretics), GI losses (diarrhea)
2.​ Poor intake, or intracellular shifts (e.g., insulin, salbutamol)
●​ Symptoms: Muscle cramps, weakness, even paralysis
●​ Clues from ABG:
1.​ With acidosis: think diarrhea, RTA
2.​ With alkalosis: think vomiting, NG suction, diuretics, Bartter/Gitelman
●​ Hyperkalemia:
1.​ Causes: ↓ Excretion (renal failure), ↓ aldosterone (CAH), or IC→EC shift
2.​ Symptoms: Paresthesia, muscle weakness, arrhythmias
3.​ ECG: Tall, peaked T waves
●​ Management of hyperkalemia:
1.​ Stabilize heart – IV calcium gluconate
2.​ Shift K+ into cells – Insulin + glucose, salbutamol
3.​ Remove K+ – Loop diuretics, dialysis, resins