- The Harriet Lane Handbook 21th edition

A. Maintenance requirements
B. Deficit repletion
C. Ongoing losses
▪ Constitute the amount of water and
electrolytes lost during basal
metabolism
▪ Metabolism → heat + solute
▪ 100 calories metabolized in 24
hours = 55-60 ml of fluid is
required to provide for insensible
losses, basal stool, sweat losses
▪ 50 ml of fluid is required for the
kidneys to excrete an ultrafiltrate
of plasma 300 mOsm/L, without to
concreate the urine
1. Basal calorie method
2. Holliday-Segar method
3. BSA method
▪ Estimated energy
requirements ( age &
activity level)
▪ Each 100 calories
metabolized in 24
hours, need:
✓100-200ml H2O
✓2-4 mEq Na+
✓2-3 mEq K+
* Not suitable for neonates < 14 days old
▪ Insensible water losses (skin & respiratory tract) → electrolyte free
▪ Urine → Primary source of electrolyte loss
▪ Addition 5-10 % dextrose → prevent: ketosis
▪ D5 ¼ NS + 20 mEq/L KCL
▪ Outside of the neonatal period ¼ NS is generally not used as a
maintenance fluid
▪ 3 mEq of Na+ per 100 ml of water → sufficient to maintain basic sodium
needs
▪ Hypotonic fluid to hospitalized children → hyponatremia
▪ ↑ secretion of ADH → retention of free water – in the same time: prior or ongoing
losses of water & electrolytes → unsuitable candidates for mere “maintenance”
fluid replacement
A. Water Deficit Volume

*if weight loss is not known, clinical observation may be used.

Each 1% dehydration = 10 mL/kg fluid deficit
1. Phase I: Initial stabilization
A. Rapid fluid resuscitation with isotonic fluid (NS/RL) for patient
with need for rapid volume expansion
Isotonic fluid expands the intravascular volume without causing
significant fluid shifts
Excessive administration of isotonic fluid → dangerous in patients
with hyperosmolarity (ex: DKA with hyperglycemia)
B. Symptomatic hyponatremic dehydration (CNS symptoms) →
hypertonic saline (HTS) over 3-4 hours to correct the
hyponatremia by ~5mEq/L. If severe CNS symptoms persist, HTS
may be repeated
1. Phase I: Initial stabilization
C. Severe hypernatremic dehydration (>175 mEq/L) → initial
resuscitation with NS → ↓ serum Na+ too rapidly →
cerebral edema. Because NS (154 mEq/L) is significantly
lower than the child’s serum Na+ . Use NS + HTS → to avoid
giving a fluid whose concentration is >15mEq/L below of
the serum Na+
D. Bolus of 20 mL/kg = 2% body weight replacement
2. Phase II: Deficit repletion, maintenance, ongoing losses. After initial
stabilization, the remaining deficit is replaced over the next 24-48
hours.
A. Isonatremic dehydration
▪ Proportional loss of sodium + water (serum Na+ 130-149 mEq/L)
▪ Replace half of the remaining deficit after stabilization over the 1st 8 hours,
2nd half over the following 16 hours
B. Hyponatremic dehydration (serum Na+ <130 mEq/L)
▪ Correct the sodium deficit by ~10 mEq/24 hours until isonatremia
▪ Rapid correction → central pontine myelinolysis (symptomatic)
▪ In asymptomatic → the rate of rise should not exceed 0.5-1 mEq/L/hour or
10-12 mEq/L in 24 hours
2. Phase II:
C. Hypernatremic dehydration (serum Na+ > 150 mEq/L)
▪ Lowering the serum Na+ no > 10 mEq/L/24 hours → minimize the risk of
cerebral edema
▪ Obtain frequent lab draws every 2-4 hours wen correcting solute/free
water deficits
▪ Expected change in Na+ per 1 L of parenteral fluid
▪ Indication:
Mild-moderate dehydration without sign of shock, coma, acute abdomen, gastric distention,
intractable vomiting, sodium derangements, excess stool losses
▪ Method:
5-10 mL ORS every 5-10 minutes, gradually increasing the volume as tolerated
▪ Deficit replacement:
1) Mild dehydration = 50 mL/kg pre-illness weight over 4 hours
2) Moderate dehydration = 100 mL/kg pre-illness weight over 4 hours

▪ Maintenance:
a. Infant → resume formula/breast milk PO
b. Children → continue regular bland diet

▪ Ongoing losses:
✓ Additional 10 mL/kgBW of ORS for each additional diarrheal stool
✓ Additional 2 mL/kgBW of ORS for each additional episode of emesis
✓ If the losses can be measured → replaced 1:1 based on bodily fluid electrolyte composition
• Isonatremic
• Hyponatremic
• Hypernatremic
▪ Factitious Etiologies:
1. Hyperglycemia
✓ ↓ Na+ 1.6 mEq/L for each
100-mg/dL rise in glucose

2. Hyperlipidemia
✓ ↓ Na+ by 0.002 x lipid
(mg/dL)

3. Hyperproteinemia
✓ ↓ Na+ by 0.25 x [protein
(g/dL) ─ 8]

▪ Clinical manifestations:
nausea, headache,
letargy, seizure, coma
B. Solute Deficit: Isonatremic Dehydration
✓Estimated: Sodium repletion requirement of 8-10 mEq/100 mL

fluid deficit (in addition to 3 mEq/100 mL of maintenance fluid)

✓Unless hypokalemia is present → maintenance K + requirements

20 mEq/L of fluid (not in renal failure)

B. Solute Deficit: Hyponatremic Dehydration

▪ 0.6 → % of body water for a child/infant

▪ 0.6 x weight = TBW
▪ Extracellular fluid compartement:
✓≈ 20% of the body’s weight (40% in the newborn)
✓3 : 1 = interstitial : intravascular
B. Solute Deficit: Hyponatremic Dehydration
▪ Percentage deficit from each compartements based on the
total duration of illness
a) Illness < 3 days: 80% (0.8) ECF deficit, 20% (0.2) ICF deficit
b) Illness ≥ 3 days: 60% (0.6) deficit, 40% (0.4) ICF deficit
B. Solute Deficit: Hyponatremic Dehydration
▪ Na+ Deficit
B. Solute Deficit: Hyponatremic Dehydration
▪ K + Deficit
C. Water & Solute Deficit: Hypernatremic Dehydration
▪ In case: unavailable/restricted free water, excessive loss of
solute-free water
▪ Requires 4 mL/kg to ↓ serum Na+ by 1 mEq/L, and 3 mL/kg if
serum Na+ > 170

▪ *SFD: amount of additional fluid volume loss beyond free water loss in hypernatremic
dehydration
• Hypokalemia
• Hyperkalemia
▪ Clinical manifestations:
✓ Skeletal muscle weakness
✓ Paralysis
✓ Ileus
✓ Cardiac arrhythmias
✓ ECG change: delayed
depolarization, flat/absent
T waves, U waves
▪ Diagnostic studies
1. Blood: electrolytes,
BUN/Cr, CK, glucose,
renin, ABG
2. Urine: urinalysis, K+,
Na+ , Cl-, osmolality, 17-
ketosteroids
3. ECG
▪ Management:
1. Acute:
• Calculate deficit
• Replace with Potassium acetate or Potassium chloride
• Enteral replacement is safer when feasible with less risk for iatrogenic
hyperkalemia
• Closely follow serum K+

2. Chronic
• Determine daily requirement
• Replace with Potassium chloride or Potassium gluconate
▪ Clinical manifestations:
✓ Skeletal muscle weakness
✓ Paresthesias
✓ ECG changes: peaked T
waves, loss of P waves with
widening of QRS,
✓ Bradycardia, AV block,
ventricular arrhythmias,
torsades de pointes, cardiac
arrest
▪ Management: stop all IV
infusions containing
potassium!
• Hypocalcemia
• Hypercalcemia
 Etiologies

▪ Clinical manifestations:
✓ Tetany ✓ Laryngospasm
✓ Neuromuscular ✓ Cardiac
irritability with arrhythmias
weakness ✓ ECG changes:
✓ Paresthesias prolonged QT
✓ Fatigue interval
✓ Cramping ✓ Trousseau’s
✓ Altered mental sign
status ✓ Chovstek’s sign
✓ Seizures

▪ Diagnostic:
1) Blood: total & ionized Ca2+, phosphate, alkaline phosphatase, Mg2+, total protein, BUN, Cr, 25-
hydroxy vitamin D, PTH
2) Urine: Ca2+, phosphate, Cr
3) Chest X-ray (thymus), ankle, wrist films (rickets), ECG (QT interval)
▪ Management:
1) Acute
Consider IV replacement → Calcium gluconate, calcium gluceptate, calcium
chloride (cardiac arrest dose)
2) Chronic
Oral supplements: calcium carbonate, calcium gluconate, calcium glubionate,
calcium lactate
▪ Special considerations:
o Hypomagnesemia → symptoms of hypocalcemia refractory to Ca2+ supplementation
o Significant hyperphosphatemia should be corrected before the correction of
hypocalcemia if total [Ca2+]x[PO43− ] ≥ 55 → induced renal calculi or soft tissue
calcification
Etiologies
▪ Clinical manifestations:
✓ Weakness ✓ Nausea, vomiting
✓ Irritability ✓ Polyuria
✓ Lethargy ✓ Polydipsia
✓ Seizures ✓ Renal calculi
✓ Coma ✓ Pancreatitis ECG
✓ Abdominal changes (shortened
cramping QT interval)
✓ Anorexia

▪ Diagnostic studies
1) Blood: total & ionized Ca2+, phosphate, alkaline
phosphatase, albumin, total protein, BUN, Cr, 25-hydroxy
vitamin D, PTH
2) Urine: Ca2+, phosphate, Cr
3) Other: ECG (calculate interval QT), kidney, ureter, bladder
radiograph, renal ultrasound (assess renal calculi)
▪ Management:
1) Treat the underlying disease
2) Hydration: ↑ UO & Ca2+ excretion
3) Diuresis → furosemide
4) Consider HD for severe/refractory cases
5) Consider steroids in malignancy, granulomatous disease, vitamin D
toxicity → ↓ vitamin D & Ca2+ absorption
6) Severe/persisten ↑ Ca2+ → consider calcitonin/biphosphonate
• Hypomagnesemia
• Hypermagnesemia
 ▪ Clinical manifestations:
Etiologies ✓ Anorexia spasm
✓ Weakness ✓ Clonus
✓ Nausea ✓ Tetany
✓ Malaise ✓ ECG changes
✓ Depression (atrial &
✓ Nonspecific ventricular
psychiatric ectopy, torsades
symptoms de pointes)
✓ Hyperreflexia
✓ Carpopedal

▪ Diagnostic studies
1) Blood: Mg2+, total & ionized Ca2+
2) Consider evaluation for renal/GIT
lossess/endocrine etiologies
▪ Management:
1) Acute
Magnesium sulfate
2) Chronic
Magnesium oxide/magnesium sulfate
 Etiologies

▪ Clinical manifestations:
✓ Depressed deep ✓ Respiratory
tendon reflexes failure (extreme
✓ Letarghy case)
✓ Confusion

▪ Diagnostic studies
1) Blood: Mg2+, total & ionized Ca2+, BUN, Cr

▪ Management:
1. Stop supplemental Mg2+
2. Diuresis
3. Ca2+ supplements: calcium chloride, calcium gluconate
4. Dialysis (if life threatening)
• Hypophosphatemia
• Hyperphosphatemia
Etiologies ▪ Clinical manifestations: symptomatic only at
very low levels (<1 mg/dL)
✓ Irritability ✓ Myocardial
✓ Paresthesias depression
✓ Confusion ✓ Apnea in VLBW
✓ Seizures ✓ Coma

▪ Diagnostic studies
1) Blood: Phosphate, total & ionized Ca2+, BUN,
Cr, Na+, K+, PTH, vitamin D
2) Urine: Ca2+, phosphate, Cr, pH

▪ Management:
1. Insidious onset of symptoms → PO potassium
phosphate/sodium phosphate
2. Acute onset of symptoms → IV potassium
phosphate/sodium phosphate
 Etiologies

▪ Clinical manifestations: = hypophosphatemia

▪ Diagnostic studies
1) Blood: Phosphate, total & ionized Ca2+, BUN,
Cr, Na+, K+, PTH, vitamin D, CBC, ABG
2) Urine: Ca2+, phosphate, Cr, urinalysis

▪ Management:
1. Restrict dietary phosphate
2. Phosphate binders: calcium carbonate,
aluminium hydroxide
3. For cell lysis (with normal renal function) →
NS bolus & IV mannitol
4. Dialysis if poor renal function