AND
MANAGEMENT OF
ELECTROLYTE
ABNORMALITIES IN
CHILDREN
PG
OVERVIEW
Introduction
Various electrolyte
imbalances&Management
1.Hyponatremia
2.Hypernatremia
3.Hyperkalemia
4.Hypokalemia
5.Hypocalcemia
6.Hypercalcemia
7.Hypo&Hypermagnesemia
Introduction
6
PLASM INTRACELLULA
A
Cations Anions
R
Cations
Prot(14) Prot(40)
K(4)
Others(6) Na(13)
Ca(2.
HCO3(1
5)
Mg(1. Phos(2)
Mg(7) 0)Cl(3)
1)
Effective osmolality= 2 Na +
glucose
It determines
18 the tonicity of
plasma
REGULATION OF WATER AND SODIUM
BALANCE :
REGULATION OF INTRAVASCULAR VOLUME
Adequate body sodium is necessary for the
maintenance of intravascular volume
SODIUM REABSORPTION:
Normal kidney excretes <1% of sodium filtered
at glomerulus
Proximal tubule : 65% of Na is reabsorbed .
Water reabsorption parallels Na at this site
Loop of Henle: Na ,K- 2Cl co-transporter is
responsible for Na absorption
In thick ascending loop: ADH stimulates Na
retention but this site is impermeable to water
This is responsible for medullary hypertonicity
Distal tubule:
Thiazide sensitive Na-Cl co transporter is
responsible for Na,Cl absorption, which is
relatively impermeable to water
Collecting duct: Na absorbed via Na
channel regulated by aldosterone
water is reabsorbed through aquaporins
inserted under the influence of ADH
Renin angiotensin system is also
responsible for restoration of intravascular
volume and osmolarity
Angiotensin II increases Na reabsorption and
stimulates aldosterone secretion .It is also
vasoconstictor
Volume expansion
Synthasis of ANP
Increases GFR
Lethargy,confusion
Headache
Seizures
Coma
Hyporeflexia
Musclecramps,weakness
Cheynestokes respiration.
Acute severe hyponatremia leads to
brainstem herniation and apnoea
Hypernatremia
Intracranial haemarrage
(Na)145-157mEq/L:24 hr
(Na)158-170mEq/L:48 hr
(Na)171-183mEq/L:72 hr
Contd
Administer fluid at constant rate
over time for correction:
Typical fluid :D5 half normal saline
Typical rate :1.25-1.5 times
maintenance
follow serum sodium concentration
Adjust fluid on basis of clinical
status & serum sodium
concentration.
Acute hypernatremia(>180mEq/L)
should be rapidly corrected by
Peritonial dialysis
Loopdiuretics
Na free IV fluids
POTASSIUM
Major intracellular cation (150mEq/L)
Normal serum K levels :3.5-5mEq/L
Major extracellular part of K is in bone
REGULATION OF K BALANCE :
HYPERKALEMIA(>5.5 mEq/L)
CAUSES:
1. Spurious hemolysis ,tissue ischemia
2. Increased intake
3. Transcellular shift
Acidosis
Tissue damage ,tumour lysis syndrome, digitalis
intoxication, exercise, malignant hyperthermia,
insulin deficiency,rhabdomyolysis
4. Decreased excretion
Renal failure
Adrenal failure addisons disease, hypoaldosteronism
Renal tubular disease psuedohypoaldostereonism type I &
type II,urinary tract obstruction
Drugs - ACE inhibitors, K sparing diuretics,
NSAIDS ,heparin
CLINICAL FEATURES
Cardiac conduction system is usually affected
Drugs - diuretics,
aminoglycosides
amphotericin B,
2. Decreased intake
3. Transcellular shifts - alkalosis, insulin, agonist,
Drugs - theophylline
CLINICAL FEATURES
Skeletal muscle and heart are vulnerable to
hypokalemia
Muscle weakness, cramps, hypotonia, paralytic
ileus ,urinary retention, some may have
respiratory paralysis
ECG changes :
Flattened T waves, depressed ST segment
,appearance of U wave between T&P wave
Ventricular fibrillation & Torsades de pointes may
occur
Susceptible to digitalis induced arrythmias
TREATMENT
Severe hypokalemia (<2.5mEq/L):
IV infusion of KCl 0.5-0.75mEq/kg in first
one hour, if no response 1mEq/kg/hr
given under cardiac monitoring
The concentration of K in IV fluids
should not exceed 40mEq/L
If asymptomatic oral supplementation
with KCl syrup 10% is given
CALCIUM
Normal levels 8.8-10.8mg/dl
It is present in the body in three proportions
1.Ionized or unbound -50%
2. Protein bound -40%
3. Calcium complexed with phosphate,sulphate and citrate
-10%
80-90% of protein bound form is to albumin
With decrease of 1g/dl of albumin, decrease of 0.8mg/dl of
total serum calcium occurs without altering ionized calcium
Homeostasis is maintained by vit D,PTH,calcitonin by
acting on bone,kidney and intestine
HYPOCALCEMIA
Hypocalcemia is defined as
Causes:
1. PTH excess parathyroid adenoma,
hyperplasia, paraneoplastic
syndromes
3. Thyrotoxicosis, prolonged
immobilization , sarcoidosis, williams
syndrome
CLINICAL FEATURES
GI system nausea, vomiting, constipation,
abdominal cramps, paralytic ileus
Nervous system- irritability, confusion,
personality changes, hallucinations,
unsteady gait
Renal renal stones causing colic &
hematuria, nephrocalcinosis, polyuria,
polydypsia
Bone changes- fractures, deformities
TREATMENT
Calcium intake restriction and increased
calcium excretion
Forced saline diuresis with furosemide or
peritoneal dialysis can rapidly lower serum
calcium levels
Bisphosphonates like pamidronate and
etidronate have been used in the treatment
of hypercalcemia due to malignancy
immobilization and hyperparathyroidism
MAGNESIUM
Normal serum concentration 1.5-
2.3mg/dl
CAUSES :
Always due to excessive intake in the
form of laxatives, enemas, antacids
Severe hypomagnesemia
IV MgSO4 (50%) 25-50mg/kg given
slowly
Rate of infusion is slowed if
diaphoresis, flushing, warm sensation
develops.
Repeated every 6th hourly for 2-3 days
long term therapy - orally in divided
doses
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