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CLINICAL PRESENTATION

AND
MANAGEMENT OF
ELECTROLYTE
ABNORMALITIES IN
CHILDREN

Dr. D.Naga Ramani

PG
OVERVIEW
Introduction
Various electrolyte
imbalances&Management
1.Hyponatremia
2.Hypernatremia
3.Hyperkalemia
4.Hypokalemia
5.Hypocalcemia
6.Hypercalcemia
7.Hypo&Hypermagnesemia
Introduction

Infants and young children are at


greater risk than adults for
disturbance in fluid and
electrolyte balance due to
difference in body position, higher
metabolic rate, and immaturity
for physiologic regulation systems
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TOTAL BODY WATER
Most plentiful constituent of human body.
Total body water as a percentage of body
weight varies with age
Key Items
ECF
Interstitial fluid: fluid surrounding
the cell, including lymph fluid.
Intravascular fluid: fluid contained
with the blood vessel (e.g, plasma).
Transcellular space: cerebral fluid,
pericardial, pleural, synovial,
sweat, digestive secretions

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PLASM INTRACELLULA
A
Cations Anions
R
Cations

Cl(104 K(140) Phos(10


Na ) 7)
(140)

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)

Concentrations expressed in mEq/L


OSMOLALITY
Plasma osmolality = 2 Na + glucose
+ BUN 2.
18 8
Normal:285 -295 mOsm/kg

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

Inhibits Sodium reabsorbtion


In collecting duct

Increase in sodium excretion


Loop of henle
SODIUM

Normal serum level : 135-


145mEq/L

Less than 3% of the total body Na is intracellular


(10mEq/L)

More than 40% of the total body Na is in bone


Remainder in interstitial and intravascular space

The patients effective plasma volume determines


the amount of Na in urine
HYPONATREMIA
Serum Na levels <135mEq/L

Both Total body water &total body


sodium determine the serum Na conc.

Ratio of water to Na increases

This can occur with low, normal or high


levels of body Na or water
1.Hypovolemic hyponatremia:
Sodium loss>Water loss
Extra renal
GI losses- diarrhea MC cause
skin losses
third space losses
Renal
Adrenal insufficiency
Thiazide diuretics
RTA
polycystic kidney disease
congenital adrenal hyperplasia
2. Hypervolemic hyponatremia:
Excess Total body water than
Sodium
Heart failure, nephrotic syndrome ,
cirrhosis of liver , protein loosing
enteropathies, renal failure
3. Euvolemic hyponatremia:
SIADH, water intoxication,
glucocorticoid deficiency
4. Pseudohyponatremia:
Excess of lipids
Patho Physiology:
Hyponatremia

Decreased osmolality of ECF

water moves from ECF to ICF

Cell swells (Brain)

Increased intracranial pressure

Impaires cerebral blood flow

Leads to neurological symptoms.


Neurological symptoms include :

Lethargy,confusion
Headache
Seizures
Coma
Hyporeflexia

Musclecramps,weakness

Cheynestokes respiration.
Acute severe hyponatremia leads to
brainstem herniation and apnoea

chronic hyponatremia brain adopts by


decreasing internal osmolality, that is, may be
asymptomatic even with Na levels < 110mEq/L

Depending upon the levels of serum Na, the


symptoms are as follows:
- 125 mEq/L nausea and malaise
- 120 mEq/L headache, lethargy
- 115 mEq/L seizure and coma
Treatment
Hypovolemic hyponatremia :
First correct dehydration by isotonic
solution intravenously
Symptomatic hyponatremia Na
deficit is quickly corrected by
infusion of 3% saline, 4-6 mL/kg over
10-15min, to raise the serum levels
by 5 mEq/L which causes relief of
symptoms
If no improvement additional 3-4
mL/kg is administered
Hypervolemic hyponatremia:
Water and Na restriction is the main stay of
therapy
Diuretics may be helpful
Nephrotic syndrome better response to
diuretics after albumin infusion
Renal failure - fluid restriction
- dialysis
Isovolemic hyponatremia:
Water restriction
For Acute symptomatic hyponatremia due
to iatrogenic water intoxication 3% saline
is needed to reverse cerebral edema
Cont
In chronic hyponatremia rapid correction is
not indicated. Na requirement measured as
:

Na deficit (mEq) = (desired Na


present Na)weight 0.6

It is corrected over 48 hrs @0.5 mEq/L/hr


Correction should not exceed 12mEq/L in
first 24 hrs
Rapid correction may lead to central
pontine myelenolysis
HYPERNATREMIA
Defined as serum [Na+] more than 145 mEq/L
Causes :
Excessive Na+ intake : improperly mixed formula
ingestion of seawater, i.v hypertonic salin e
Water deficit
a.Diabetes insipidus central & nephrogenic
b.Increase insensible losses
c.Inadequate intake ineffective breast feeding

Water and sodium deficient water deficit >Na deficit


a. GI losses Diarrhea, Emesis, Osmotic cathartics
b. Cutaneous losses-Burns
c. Renal losses
1.acute tubular necrosis-polyuric phase
2.post obstructive diuresis
3.Renal dysplasia
4. osmotic diuresis
Pathophysiology

Hypernatremia

ECF Osmolality increases

Water moves from ICF to ECF

Cell shrinkage occurs

Decreases brain volume

Tearing of intra cerebral veins & bridging blood vessels

Leads to haemorrhages, seizures


CLINICAL FEATURES
Most children are dehydrated
Better preservation of intravascular volume
because water moves from intracellular space to
extracellular space, so BP &Urine Output is
maintained
ICF depletion results in peculiar doughy feel of
skin when pinched and woody consistency of
tongue
Breast feeding infants with hypernatremic
dehydration show profound dehydration and
failure thrive
CNS SYMPTOMS

Neuron shrinkage-irritable, restless, lethargic

Infants high pitched cry

Intracranial haemarrage

Seizures and coma

Thrombotic complications stroke , renal


veinthrombosis
Cenral pontine myelinolysis
Treatment
In hypernatremic dehydration, if the patient is
conscious ,standard WHO ORS solution is given and
dehydration corrected
Incase of severe dehydration intravascular volume
is restored by isotonic fluid ( NS)
Water deficit = Body weight 0.6[1-145/(current
Na)]
That is equivalent to 3-4 ml/kg for each 1 mEq that
the current Na exceeds 145 mEq
This fluid deficit +maintenance requirement of 2
days given over 48 hrs
Decrease in Na levels should be < 12 mEq/L for
every 24 hrs
Rapid correction leads to cerebral edema
Restoration of intravascular volume
Normal saline:20ml/kg Over 20 min

Determine time for correction on basis


of initial sodium concentration:

(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

serum K levels ECGchanges


>6mEq/L - peaking of T waves
>7.5mEq/L - increased P-R interval,
widening of QRS complex, heart blocks
>9mEq/L - flattening of T waves

Finally ventricular fibrillation , asystole may occur


Some patients may show weakness, parasthesias, tingling
But cardiac toxicity usually preceeds these symptoms
ANAGEMENT
Depends upon serum K levels and ECG changes
I. Mild (5.5-6mEq/L)
Stop all sources of additional K and offending
drugs

II. Moderate (6.6-8mEq/L) or peaked T waves


- Glucose insulin infusion 0.5g/kg of glucose with
0.3 regular insulin per gram of glucose over 2 hrs

- Sodium bicarbonate infusion 2mEq/kg over


5-10
III. Severe > 8 mEq/L
1. 10 % calcium gluconate 0.5mL/kg IV over
3-5
Acts immediately and reverses cardiac
effects
2. NaHCO3 infusion
3. Insulin glucose infusion
4. IV /nebulized salbutamal produces rapid
intracellular movement of K
5. Refractory Dialysis

For long term treatment of hyperkalemia-


sodium polystyrene sulphonate (kayexalate)
an K ion binding ion exchange resin
HYPOKALEMIA
K levels < 3.5 mEq/L
CAUSES:
1. Increased losses
Extrarenal losses - diarrhoea, laxative
abuse , exercise
Renal losses - RTA type I & type II,
DKA, Barters syndrome ,
Gitelmansyndrome

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

< 8.5mg/dl in children


< 8 mg/dl in neonates
<7mg/dl in preterm
neonates
USES
VitD deficiency malnutrition
,malabsorption,prolonged phenytoin
therapy
Increased losses idiopathic
hypercalciuria ,RTA,furosemide
therapy
Metabolic
hypoparathyroidism,hypomagnesemia
Metabolic alkalosis,
hypoproteinemia,sepsis
CLINICAL FEATURES
CNS-tremors , jitteriness, seizures, latent
tetany, apnoea
Neuromuscular numbness, tingling of lips,
hands and toes, carpopedal spasms,
muscle cramps, laryngeal stridor
CVS- hypotension, poor myocardial
contraction, bradycardia,prolonged QT
interval
Prolonged hypocalcemia manifests as
rickets and osteomalacia
TREATMENT
Severe symptomatic
hypocalcemia(seizures,laryngospasm):
Immediately treated with 2ml/kg of 10% Calcium
gluconate slowly IV
then oral Calcium supplements are provided at 40-
80mg/kg/day after stabilization
If hypocalcemia is severe or persistant then
hypomagnesemia is suspected and treated with
0.5ml of 50% MgSO4 IM twice daily followed by 25-
50mg/kg daily orally
Then vit D deficiency is treated
HYPERCALCEMIA (>11mg/dl)

Causes:
1. PTH excess parathyroid adenoma,
hyperplasia, paraneoplastic
syndromes

2. Vit D excess, hypervitaminosis A

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

It is a cofactor many enzymes,


important for membrane stabilization
and nerve conduction

15% of the filtered Mg is reabsorbed


at proximal tubule, 70% at thick
ascending limb 5-10% at distal
HYPER MAGNESEMIA

CAUSES :
Always due to excessive intake in the
form of laxatives, enemas, antacids

Also seen in neonates born to mother


who are receiving IV MgSO4 for
eclampsia and preeclampsia
Clinical features
Symptoms appear when serum Mg levels >4
Hypotonia, hyporeflexia, weakness,
Paralysis at high concentrations
Direct CNS depression lethargy,sleepiness
infants - poor suck
Hypotension
ECG changes- prolonged PR,QRS,QT interval
>15mg/dl- complete heart block and arrest
Treatment
Patients with normal renal function
rapidly clear excessive Mg
IV hydration, loop diuretics
accelerates this process
If renal insufficiency dialysis
In acute emergencies -IV Calcium
gluconate 100mg/kg is transiently
effective
HYPOMAGNESIMIA
Causes:
GI disorders
diarrhoea,vomitings,celiac
disease,small bowl resection
Renal disorder Acute Tubular
Necrosis ,glomerulonephritis
,interstitial nephritis
Poor intake, insulin administration
CLINICAL FEATURES

Appears at levels < 0.7 mg/dl


It causes secondary hypocalcemia by
impairing PTH release and blunting of
tissue response to PTH
Manifestations are due to hypocalcemia-
tetany, positive chvostek and trousseau
signs, seizures
ECG changes- T wave
flattening,lengthening of ST segment
TREATMENT

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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