This document discusses electrolyte abnormalities in children. It begins by reviewing body composition and water balance in the human body. It then covers the composition and regulation of sodium, potassium, and other electrolytes. Specific conditions that can cause electrolyte imbalances like hyponatremia, hypernatremia, hypokalemia, and hyperkalemia are defined and their causes and treatment approaches are outlined. The document emphasizes the importance of determining the underlying cause and correcting imbalances gradually to avoid complications.
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Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
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Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
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Adaptation Towards the Sense of Smell:
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Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
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Characteristics of Smell:
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Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
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2. Composition of body fluids
Total body water as a percentage of body weight
declines with age.
Early fetal life TBW= 90%
At birth TBW= 75-80%
By the end of 1st year to puberty TBW= 60%
4. Water balance
Input Output
Water intake:
Fluid 60%
Food 30%
Urine 60%
Stool 8%
Sweat 4%
Water of
oxidation 10
%
Insensible
loss 28%
(skin, lungs)
Water intake is
regulated by
osmoreceptors in
hypothalamus
Water loss is
regulated by ADH
from post.
pituitary
6. Osmolality
Osmolality is the solute concentration of a fluid expressed
as mOsm/kg.
Fluid/water moves from lower osmolality to higher
osmolality across biological membranes.
Normal Plasma osmolality = 285 to 295 mOsm/kg
Tightly regulated within 1-2% of normal.
Sosm = (2 x Na+) + (BUN / 2.8) + (Glu / 18)
8. Maintenance fluid & electrolyte
requirements
Holliday-Segar method
Maximum fluid/day = 2400ml/day
Body weight Per day Per hour
0-10 kg 100ml/kg 4ml/kg
10-20 kg 50 ml/kg beyond 10 kg
2ml/kg beyond
10 kg
>20 kg 20ml/kg beyond 20 kg
1ml/kg beyond
20 kg
10. Maintenance fluid & electrolyte
requirements
Fluid/electrolyte requirements calculated on Holliday-segar
method are generally hypotonic (N/4 or N/5)
Recent evidence shows use of hypotonic fluids esp. in sick
children can cause hyponatremia.
0.9% NS can be safely used in standard maintenence
volume.
(except in CHF, renal/hepatic failure, diabetes insipidus).
11. Maintenance fluid & electrolyte
requirements
No single i.v fluid is suitable in all situations, therapy to be
individualized.
Monitor with daily wt, input/output, serum electrolytes.
Maintenance fluids provide only about 20% of calories, therefore
child will lose wt due to catabolism.
12. Conditions that alter maintenance
fluid requirements
Increased fluid requirement
Fever (10-15% per 0C above
380C )
Radiant warmer/Phototherapy
Burns
Excessive sweating
High physical activity
Hyperventilation
Diarrhoea/vomiting
Polyuria
VLBW babies
13. Conditions that alter maintenance
fluid requirements
Decreased fluid requirement
Oliguria/Anuria
Humidified ventilator/incubator
Hupothyroidism
14. Sodium
Most abundant ion of the extracellular compartment
Normal serum sodium = 135 to 145 mEq/l.
Daialy sodium requirement is 2 to 3 mEq/kg body weight.
Requirement is nearly 2 to 3 fold higher in term & VLBW
preterm babies.
Adult requirements decreases to 1.5mEq/kg/day.
Extrarenal sodium losses can be significant via profuse
sweating ,burns, severe vomiting or diarrhoea.
15. Hyponatremia
Defined as serum Na < 135 meq/l.
Usually symptomatic when Na is < 125mEq/l or the decline is
acute(<24 hour).
Early features : headache, nausea, vomiting, lethargy and
confusion.
Advance manifestations: seizures, coma, decorticate posturing,
dilated pupil, anisocoria, papilledema, cardiac arrhythmias,
myocardial ischemias and central diabetes insipidus.
16. Hyponatremia
CAUSES of hyponatremia
Hypovolemic hyponatremia
Renal loss: diuretic use, osmotic diuresis, renal salt
wasting, adrenal insufficiency.
Extra-renal loss: diarrhoea, vomiting, sweat,cerebral salt
wasting syndrome, third spacing(effusion,ascites)
17. Hyponatremia
CAUSES of hyponatremia
Normovolemic hyponatremia
Conditions that predispose to SIADH - Inflammatory central
nervous system disease(meningitis, encephalitis), tumors,
pulmonary disease(severe asthma, pneumonia),drugs
(cyclophosphamide, vincristine).
18. Hyponatremia
CAUSES of hyponatremia
Hypervolemic hyponatremia
CHF, Cirrhosis, Nephrotic syndrome, Acute or chronic
renal failure
19. Hyponatremia-Treatment
Determine whether hyponatremia is acute(<24 hr) or chronic(>48hr),
symptomatic/asymptomatic.
Evaluate the volume status (hypervolemia, euvolemia, hypovolemia).
Sodium deficit (meq) = 0.6*Body wt(kg) * [desired Na – observed Na]
20. Hyponatremia-Treatment
Treat hypotension first (NS/RL/5%albumin), asymptomatic cases
prefer ORS.
Rate of correction = 0.6 to 1.0 mEq/l/hr till Na is 125 then at slower
rate over 48 to 72 hours.
For symptomatic cases give 3%NS @ 3-5 ml/kg over 1-2 hr. (increases
serum Na by 5-6mEq/l)
Stop further therapy with 3%NS when patient is symptom free or
acute rise in serum sodium is 10mEq/l in first 5 hour.
21. Hyponatremia-Treatment
Rise in serum Na can be estimated by Adrogue Madias formula-
Δ 𝑁𝑎 =
𝐼𝑛𝑓𝑢𝑠𝑎𝑡𝑒 𝑁𝑎 + 𝐼𝑛𝑓𝑢𝑠𝑎𝑡𝑒 𝐾 −𝑆𝑒𝑟𝑢𝑚 𝑁𝑎
[𝑇𝐵𝑊+1]
Δ[Na]= expected change in serum sodium/L of fluid given
TBW= total body water is 0.6*Body wt (kg)
22. Hyponatremia-Treatment
Fluid restriction alone is needed for SIADH.
Sodium and water restriction for hypervolemic hyponatremia.
V2-receptor antagonists or vaptans may be used in SIADH &
hypervolemic hyponatremia.
Diuretics for refractory cases.
23. Hypernatremia
Defined as serum Na >150mEq/l
Clinical features
Lethargy or mental status change which can proceed to coma and
convulsions.
Acute severe hypernatremia leads to osmotic shift of water from
neurons causing shrinkage of brain and tearing of meningeal vessels -
intracranial hemorrhage.
24. Hypernatremia
Causes of Hypernatremia
Net water loss
Insensible losses
Diabetes insipidus
Inadequate breastfeeding
Hypotonic fluid loss
Renal: osmotic diuretics, post obstructive, polyuric phase of acute tubular
necrosis
GI: vomiting,nasogastric drainage, diarrhea, laxative.
26. Hypernatremia- Treatment
Treat hypotension first (NS/RL/5% Albumin bolus)
Correct deficit over 48 to 72 hours. Recommended rate of drop is
0.5mEq/l/hr (10-12mEq/l/day)
Hypotonic infusates are used as N/4 or N/5 saline, avoid sodium free
fluids. ( Calculate expected fall in Na by Adrogue Madias formula ).
27. Hypernatremia- Treatment
Seizures during correction of hypernatremia are treated using
3%NS as 5-6ml/kg infusion over 1-2 hr.
For significant hypernatremia ( >180-200mEq/l ) with concurrent
renal failure and or volume overload, renal replacement therapy
(peritoneal or hemodialysis, hemofiltration) is indicated.
29. Potassium
Normal serum concentration=3.5-5.0mEq/l and intracellular 150mEq/l .
Source of potassium include meats, beans, fruits and potatoes.
Majority in muscles and majority of extracellular K in bones.
More significant in males around puberty.
Serum K concentration increases by approximately 0.6mEq/l with each
10 mOsm rise in plasma osmolality
30. Physiologic function of Potassium
Electrical responsiveness of nerve and muscle cells.
Contractility of cardiac, skeletal and smooth muscle cells.
Maintains cell volume.
31. Potassium Excretion
Normally 10% of K is excreted.
Excretion is increased by aldosterone, loop diuretics, osmotic diuresis,
glucocorticoids, ADH and delivery of negatively charged ions to the
collecting duct(e.g. bicarb).
Insulin, ß agonists and alkalosis enhance potassium entry into cells.
32. Hypokalemia
Serum K<3.5mEq/l.
Clinical features
Severe hypokalemia (<2.5mEq/l) cause muscle weakness (neck
flop, abdominal distension, ileus) and arrhythmia.
Hypokalemia increases the risk of digoxin toxicity by promoting
its binding to myocyte, potentiating its action and decreasing its
clearance.
39. Hypokalemia-Treatment
Determine the underlying cause, whether associated with
hypertension and acidosis or alkalosis.
Hypertension may be due to primary hyperaldosteronism, renal
artery stenosis, CAH, glucocorticoid, liddle syndrome.
Relative hypotension and alkalosis suggest diuretic use or
tubular disorder (Bartter/Gittelman syndrome).
40. Hypokalemia-Treatment
Decrease ongoing losses (stop loop diuretics, replace GI losses). Use K
sparing diuretics, restore i.v volume, correct hypomagnesemia.
Disease specific therapy , e.g Indomethacin/ACE inhibitors for
Bartter/Gittelman syndrome.
Correct deficit over 24 hours.
Replace the deficit : oral route safer. Dose 2-4mEq/kg/day (max-120-
240mEq/day) in 3 or 4 divided doses.
41. Hypokalemia-Treatment
IV correction is used under strict ECG monitoring.
For rapid correction in severe hypokalemia (<2.5 or
arrhythmias) 0.5 to 1.0mEq/kg (max-40 mEq ) is given over 1
hour.
Infusate K should not exceed 40-60 meq/L.
42. Hyperkalemia
Serum K>5.5mEq/l.
Factitious or pseudo hyperkalemia: squeezing of extremities during
phlebotomy, sample from limb being infused with K containing fluid or
hemolysed sample.
Clinical features: nausea vomiting paresthesias, muscle weakness(skeletal,
respiratory), fatigue, ileus, arrhythmia.
47. Hyperkalemia- Treatment
It’s a medical emergency.
Discontinue K+ containing fluids.
ECG monitoring.
If K > 7 or symptomatic with ECG changes- Administer Calcium
gluconate to stabilise myocardium (0.5ml/kg of 10%
Ca.gluconate over 5-10 min).
48. Hyperkalemia- Treatment
Enhance Cellular uptake of potassium-
Regular Insulin with glucose i.v (0.3 IU/g glucose over 2 hr).
NaHCO3 i.v 1-2 meq/kg over 20-30 min.
ß- agonist (salbutamol/terbutaline nebulized or i.v)
49. Hyperkalemia- Treatment
Ensure K elimination
K binding resin (kayexalate oral/per rectal 1g/kg)
Loop or thiazide diuretic ( if renal functions maintained )
Hemodialysis
Correct hypoaldosteronism if present : steroids.