2. Total Body Water (TBW)
•High in early fetal life (~90% of body weight)
•Decreases to 75-80% at birth
•Declines to ~60% by end of first year, stable until puberty
•Adolescent females and overweight children have lower TBW
percentage
TBW Distribution
•Two-thirds intracellular fluid (ICF)
•One-third extracellular fluid (ECF)
•ECF: One-fourth intravascular (plasma water), rest extravascular
(interstitial)
3. HORMONES THAT REGULATE BODY FLUIDS AND
ELECTROLYTES
Hormones Site Effect
Anti-Diuretic
Hormone (ADH)
synthesized in the supraoptic and
paraventricular nuclei of the
hypothalamus.
• Increased water reabsorption in the kidney
Angiotensin II Vascular tissue of the lungs • Increased sodium resorption
• Increased aldosterone secretion
Aldosterone It is released from adrenal cortex. • Increased Na+ reabsorption
• stimulates K+ excretion
Atrial Natriuretic
Factor
Secreted by the cardiac atrium • Powerful vasodilator
• Inhibits Renin secretion
• Inhibits sodium resorption in the collecting
duct.
4. Sodium Physiology:
• Most abundant ion in the extracellular fluid.
• Normal serum sodium concentration: 135-145 mEq/L.
• Daily requirement: 2-3 mEq/kg of body weight.
• Majority of losses occur through urinary excretion.
5. Hyponatremia:
• This refers to plasma sodium < 135 mEq/L.
Causes of Hyponatremia:
• Hypovolemic hyponatremia (sodium loss in excess of free water):
- Renal loss: Diuretic use, osmotic diuresis, renal salt-wasting, adrenal insufficiency,
pseudohypoaldosteronism.
- Extrarenal loss: Diarrhea, vomiting, drains, fistula, sweat (cystic fibrosis), cerebral
salt wasting syndrome, third-spacing (effusions, ascites).
• Normovolemic hyponatremia (conditions predisposing to SIADH):
- Inflammatory central nervous system disease (meningitis, encephalitis), tumors.
- Pulmonary diseases (severe asthma, pneumonia).
- Drugs (cyclophosphamide, vincristine).
- Nausea, postoperative.
• Hypervolemic hyponatremia (excess free water retention):
- Congestive heart failure, cirrhosis, nephrotic syndrome, acute or chronic kidney
disease.
6. Management of hyponatremia:
• Treat hypotension with 20 mL/kg of normal saline or Ringer's lactate.
Symptomatic hyponatremia:
• - Infuse 3-5 mL/kg of 3% sodium chloride over 1 hour, monitoring
sodium levels hourly.
• - Aim to increase serum sodium by 5-6 mEq/L within the first hour of
management, with resolution of symptoms (awake, alert, responsive
to commands, no headache or nausea).
• - Continue 3% saline infusion until the patient is asymptomatic and
serum sodium approaches 130 mEq/L or rises by 10 mEq/L in 4-6
hours; monitor serum sodium levels every 2-4 hours.
7. Asymptomatic and chronic hyponatremia:
• Treat underlying etiology.
• Calculate sodium deficit (mEq/kg) using the formula: (130 - serum
sodium) x 0.6 x body weight (kg).
• Limit the rise in serum sodium to 0.5 mEq/hour or 10 mEq/L in the
first 24 hours, with an additional 8 mEq/L every subsequent 24 hours
until serum sodium reaches 130 mEq/L.
8. Specific interventions based on etiology:
• Hypovolemia: Administer normal saline; consider WHO ORS
rehydration solution if the patient can tolerate oral intake.
• SIADH: Implement fluid restriction; consider furosemide and oral salt
supplementation if necessary.
• Hypervolemia: Implement sodium and fluid restriction, along with
diuretics.
• Cerebral salt wasting: Consider fludrocortisone.
9. Hypernatremia:
• Serum sodium > 150 mEq/L.
Causes:
• Loss of body water, inadequate intake, ADH deficiency, excessive sodium
intake.
Signs:
• Lethargy, changes in mental status; can progress to coma and convulsions.
Treatment:
• Fluid resuscitation with normal saline; monitor serum sodium regularly.
• Avoid rapid correction to prevent brain edema; consider 3% NaCl for
seizures.
• Replace ongoing losses; identify and treat underlying cause; renal
replacement therapy may be necessary.
10. Potassium Physiology:
• Potassium is the primary intracellular cation.
• Normal serum potassium concentration falls within the range of 3.5
to 5 mEq/L.
• Potassium-rich foods include meats, beans, fruits, and potatoes.
• Gastrointestinal absorption of potassium is complete, and its
homeostasis mainly relies on renal excretion.
• Renal excretion is predominantly regulated by aldosterone at the
collecting duct.
11. Hypokalemia:
• Definition: Serum potassium level below 3.5 mEq/L.
Pathogenetic Mechanisms:
• Increased losses, decreased intake, or transcellular shift.
• Common causes include vomiting, leading to volume depletion and
metabolic alkalosis.
• Secondary hyperaldosteronism enhances potassium secretion in cortical
collecting tubules.
Signs and Symptoms:
• Severe hypokalemia (<2.5 mEq/L) can cause muscle weakness and cardiac
arrhythmias.
• Chronic hypokalemia associated with interstitial renal disease and
increased risk of digitalis toxicity
12. Treatment Approach:
• Evaluate underlying causes, hypertension, and acidosis.
• Hypertension may indicate primary hyperaldosteronism or other
genetic hypertension syndromes.
• Relative hypotension and alkalosis could suggest tubular disorders
like Bartter or Gitelman syndrome.
• Treatment involves discontinuing diuretics, replenishing potassium
stores orally or intravenously, and disease-specific therapy for
conditions like Bartter and Gitelman syndrome
13. Calcium Physiology:
• 98% of body calcium in skeleton, 1-2% in extracellular fluid (ECF).
Functions:
• Blood coagulation, cellular communication, muscle contraction,
neural transmission.
Regulation:
• calcium-binding proteins, reabsorption in proximal/distal tubules.
Plasma calcium forms:
• Ionized, bound to plasma proteins, complexed to phosphate and
citrate
15. Management of Hypocalcemia
• Immediate treatment: IV calcium gluconate for tetany, laryngospasm,
seizures.
• Oral calcium supplementation follows IV therapy.
• Correction of hypomagnesemia before hypocalcemia.
• Correction of acidemia may precede correction of hypocalcemia.
16. Hypercalcemia:
• Definition: serum calcium >11 mg/dL.
• Causes: primary hyperparathyroidism, malignancies, granulomatous
diseases, vitamin D or A intoxication.
• Clinical features: Confusion, lethargy, weakness, constipation, renal
manifestations.
17. Management of Hypercalcemia
Treatment:
• Hydration, isotonic sodium chloride, loop diuretics, bisphosphonates,
IV calcitonin, calcimimetics.
• Surgical intervention for hyperparathyroidism resistant to medical
management.
18. Magnesium Physiology
• Third-most abundant intracellular cation, primarily in muscle and liver
cells.
• Functions: Energy transfer, nerve conduction, metabolism, cell
membrane function.
• Dietary sources: green leafy vegetables, cereals, nuts, meats.
• Absorption: Small intestine, Influenced by PTH, glucocorticoids,
intestinal substances.
19. Hypomagnesemia
Causes:
• Decreased intake or increased losses, commonly gastrointestinal or
renal.
Symptoms:
• Muscle weakness, tremors, seizures, paresthesias, tetany.
Clinical Manifestations:
• Cardiovascular manifestations: prolonged QT interval, arrhythmias.
Treatment:
• Oral therapy for mild cases; intravenous magnesium sulfate for
severe cases.
• Doses repeated every 6 hours, adjusted for renal insufficiency.
20. Treatment of Hypomagnesemia
Oral Therapy:
• Sufficient for mild symptoms.
• Severe cases or intolerance to oral administration require
intravenous magnesium sulfate.
Administration:
• Intravenous doses repeated every 6 hours.
• Adjustments made for renal insufficiency.
Long-term Replacement:
• Sustained-release oral preparations for asymptomatic or long-term
replacement patients.
22. Treatment of Hypermagnesemia
Management:
• Removal of magnesium source for mild cases.
• Intravenous calcium antagonizes magnesium effects.
• Dialysis is reserved for severe cases with renal impairment or serious
cardiovascular effects.
23. Acid Base Disorders
Introduction to Acid-Base Equilibrium
• Body regulates blood pH (7.35 to 7.45) tightly.
• Mechanisms: Respiratory and renal regulation.
• Intracellular and extracellular buffers maintain balance.
24. Metabolic Acidosis:
• Metabolic acidosis refers to reduction in serum pH due to
decreased plasma bicarbonate or increased hydrogen ion
concentration.
• Primary indication: arterial pH < 7.35 with diminished
bicarbonate and normal or low PaCO2.
• Compensation: initial increase in alveolar ventilation mediated
by medullary chemoreceptors.
25. Clinical Manifestations:
• Compensatory tachypnea and hyperpnea.
• Potential progression to respiratory distress, indicated by
Kussmaul breathing.
• Pulmonary effects: vasoconstriction, increased pulmonary
artery pressure, resistance.
26. Physiological Effects:
• Tachycardia in mild cases but cerebral vasodilation can elevate
intracranial pressure.
• Shift in oxygen-hemoglobin dissociation curve: decreased
oxygen affinity of hemoglobin.
• Severe complications: arrhythmias, myocardial depression,
respiratory muscle fatigue, seizures, shock, multiorgan failure.
27. Treatment and Management:
• Identify underlying cause; correction often resolves acidosis.
• Alkali therapy is limited in acute cases but indicated in salicylate
poisoning and inborn errors of metabolism.
• Dosage of bicarbonate is based on body weight and base
deficit. Monitor for complications like volume expansion and
electrolyte imbalances.
• Gradual correction if acidosis is advised, especially in cardiac
failure.
• Caution is needed in newborns to prevent complications like
intracranial hemorrhage from hypertonic solutions.
28. Metabolic Alkalosis:
• pH > 7.45 indicates metabolic alkalosis with elevated plasma
bicarbonate (HCO3).
• Two types: chloride-responsive and chloride-resistant, based on
urine chloride levels.
• Causes include loss of fluid with excess chloride seen in
vomiting or diuretic use.
29. Pathophysiology of Metabolic Alkalosis
• Compensation: body buffers excess bicarbonate and induces
hypoventilation.
• Intracellular buffering involves sodium-hydrogen and potassium-
hydrogen ion exchange.
• Hypoventilation raises PCO2 levels, counteracting alkalosis.
30. Clinical Manifestations:
• Symptoms reflect underlying cause: increased neuromuscular
excitability could present as tetany, seizures.
• Generalized weakness, especially with hypokalemia.
• Severe cases may present with signs of volume depletion and
dehydration.
31. Management Strategies
•Discontinue diuretic therapy in severe cases.
•Chloride-responsive: respond well to volume resuscitation and
chloride supplementation.
•Chloride-resistant: may require cautious use of HCl or ammonium
chloride.
•Acetazolamide may help in chloride-resistant cases with adequate
renal function.
•Correction in renal failure may require hemodialysis or continuous
renal replacement therapy.
32. Respiratory Acidosis:
• Definition: Respiratory acidosis results from decreased alveolar
ventilation or increased carbon dioxide production.
• Key Parameters: Elevated PaCO2 (>45 mm Hg) and blood pH
< 7.35 characterize this condition.
33. Physiological Response:
• Kidney Response: Increased bicarbonate (HCO3-) reabsorption
initiates within 6-12 hours and peaks in 3-5 days.
• Compensation Mechanism: Enhanced excretion of hydrogen
ions, primarily as ammonium, leading to a rise in plasma
bicarbonate levels.
34. Clinical Manifestations:
• Respiratory Signs: Air hunger, retractions, and use of accessory
muscles are common.
• Neurological Symptoms: Range from anxiety to coma as
PaCO2 levels rise.
• Cardiovascular Signs: Tachycardia, bounding arterial pulses,
and hypotension may occur in severe cases.
35. Treatment Approach
•Aim: Correct or compensate for the underlying cause.
•Intervention: Assisted ventilation often necessary to support
respiratory function.
36. Respiratory Alkalosis
• Respiratory alkalosis results from hyperventilation, leading to a
primary decrease in PaCO2.
• Renal Compensation: Begins within hours, reaching maximal
response over several days.
37. Treatment Approach
• Addressing Underlying Cause: Focuses on treating the
condition triggering hyperventilation.
• Symptomatic Relief: Addressing neurological symptoms and
providing supportive care as needed.
38. Contributing Factors:
1.Hypoxia and Hypoxemia: At high altitudes, low fraction of
inspired oxygen, anemia, hypotension, or lung disease.
2.Pulmonary Disorders: Including pulmonary edema, embolism,
airway obstruction, pneumonia, and interstitial lung disease.
3.Mechanical Ventilation: Excessive ventilatory rate or tidal
volume during mechanical ventilation.
4.Extrapulmonary Disorders: Such as stress, neurologic
diseases (stroke, infection, trauma, tumor), and medications like
catecholamines, progesterone, methylxanthines, salicylates,
doxapram, and nicotine.
5.Other Factors: Hyperthermia, hepatic encephalopathy, sepsis,
and recovery from metabolic acidosis.
39. Clinical Manifestations
• Altered Calcium Levels: Increased binding of calcium to albumin
due to alkalosis, leading to symptoms like tingling, paresthesias,
and seizures.
• Sensations: Dizziness, palpitations, tetany, reflecting the
underlying disorder.
40. Maintenance Fluid Therapy
Maintenance fluids are used in children who cannot be fed
enterally.
Goals of maintenance therapy are;
• Prevent Dehydration
• Prevent electrolyte disorders
• Prevent Ketoacidosis
• Prevent Protein degradation
41. Maintenance Fluid Therapy :
• Maintenance fluids are composed of a solution of water, glucose,
sodium and potassium.
• This solution has the advantage of simplicity, long shelf life, low cost
and compatibility with peripheral IV administration.
• The glucose provides approximately 20% of the caloric needs of the
patient, prevents the development of starvation ketoacidosis and
diminishes the protein degradation that would occur if the patient
received no calories.
• Maintenance therapy however does not provide adequate calories,
proteins, fat, minerals and vitamins
42. Body weight method for calculating daily maintenance fluid volume.
• The maximum total fluid per day is normally 2400mL.
BODY WEIGHT FLUID PER DAY
0-10 Kg 100mL/Kg
11-20Kg 1000mL+ 50mL/Kg for each Kg > 10 Kg
>20 kg 1500 mL + 20 mL /Kg for each Kg > 20 kg
43. Composition of intravenous solutions
• These solutions are available with 5% dextrose, 10% dextrose or
without dextrose. Except for Ringer lactate, they are also available
with added potassium.
• A balanced IV fluid contains a base (lactate or acetate), a more
physiologic chloride concentration than Normal saline, and additional
physiologic concentrations of electrolytes like potassium calcium and
magnesium
• Intravenous solutions include Normal saline, Half normal saline, 0.2%
normal saline and Ringer lactate
44. Considerations in Fluid Selection:
• Avoidance of fluids with osmolality lower than plasma osmolality
to prevent hemolysis.
• Hypotonic fluids reserved for replacing electrolyte-free water
loss.
• Debate on volume: Conventional weight-based calculations
may overestimate needs, posing hyponatremia risk.
Recommendation to limit to 40-60%, especially in critically ill
children.
45. Monitoring and Assessment:
• Regular monitoring of children receiving IV maintenance fluids.
• Parameters include daily weight, fluid balance, and clinical and
biochemical assessments.
• Maintenance IV fluids provide only 20% of daily calories and do
not meet nutrient requirements.
46. Management of Fluid Deficit:
1. Assessment of Volume Depletion:
• Evaluate physical signs such as the degree of dehydration, signs of
tachycardia or tachypnea.
• Severity may be masked by hypernatremia or hypertonicity.
• Replace all lost fluids daily to maintain a euvolemic state.
2. Steps for Providing Fluids and Electrolytes:
• Rapidly infuse isotonic fluids for shock, compensated shock, or severe
dehydration.
• Administer 1 to 3 fluid boluses of isotonic saline or Ringer's lactate.
• Rate: 20 mL/kg of body weight.
47. 3. Replace Fluids for Volume Deficit:
• Calculate or observe volume deficit.
• Replacement: 10 mL for each percentage of weight loss.
• Example: 75 mL/kg of body weight for moderate dehydration (7.5% weight loss
on average).
4. Provide Fluids and Electrolytes for Maintenance:
• Replace fluids lost during normal daily metabolism.
• Ensure adequate replacement for ongoing losses from bodily fluids.
5. Considerations for Fluid Choice:
• Growing concern about hyperchloremic metabolic acidosis with normal saline.
• Balanced fluids like Ringer's lactate may be preferable, especially in cases
involving acidosis.
