Electrolytes abnormalities

Electrolyte Abnormalities in

Children

Presenter- Dr Aftab Ahmad SiddiquiModerators- Dr. Z Z Rab, Dr. Uzma Firdaus, Dr. Ayesha Ahmad, Dr Shaad Abqari

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%

Body Composition

40% Intracellu-lar fluid

40%Intracellular

15% Interstitial

5% Intravascular

Body Composition

Intracellular fluid Non Water Interstitial fluid Intravascular volume

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

Electrolyte composition of extracellular and intracellular fluid compartments

Sodiu

m

Potass

ium

Calcium

Magne

sium

Chlorid

e

Bicarb

.

Protein

s

Others

Phosp

hate

0

20

40

60

80

100

120

140

160140

4 2.5 1.1

104

2414

6 2

Plasma

mm

ol/l

Potass

ium

Sodiu

m

Magne

sium

Phosp

hate

Protein

s

Bicarb

.

Chlorid

e0

20

40

60

80

100

120

140

160140

13 7

107

40

103

Intracellular

mm

ol/l

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)

Regulation of sodium and water balance

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


Daily sodium requirement = 3meq/kg (children)

Daily potassium requirement = 2meq/kg

Daily chloride requirement = 2meq/kg


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).


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.

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

Conditions that alter maintenance fluid requirements

Decreased fluid requirement

Oliguria/Anuria Humidified ventilator/incubator Hupothyroidism

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.

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.

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)

Hyponatremia


Normovolemic hyponatremia

Conditions that predispose to SIADH - Inflammatory central nervous system disease(meningitis, encephalitis), tumors, pulmonary disease(severe asthma, pneumonia),drugs (cyclophosphamide, vincristine).

Hyponatremia


Hypervolemic hyponatremia

CHF, Cirrhosis, Nephrotic syndrome, Acute or chronic renal failure

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]


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.


Rise in serum Na can be estimated by Adrogue Madias formula-

Δ

Δ[Na]= expected change in serum sodium/L of fluid givenTBW= total body water is 0.6*Body wt (kg)


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.

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.

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.

Hypernatremia

Causes of Hypernatremia

Hypertonic Sodium gain Excess sodium intake Sodium bicarbonate, saline infusion Hypertonic feeds, boiled skimmed milk Ingestion of sodium chloride Hypertonic dialysis Endocrine: Primary hyperaldosteronism, Cushing syndrome

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 ).

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.

Differentiation b/w few important conditions

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

Physiologic function of Potassium

Electrical responsiveness of nerve and muscle cells.

Contractility of cardiac, skeletal and smooth muscle cells.

Maintains cell volume.

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.

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.

Hypokalemia

ECG changes-

Hypokalemia

The trans-tubular potassium gradient (TTKG) is used to interpret urinary potassium concentration.

TTKG

TTKG<4 suggest that kidney is not wasting excessive potassium, TTKG ≥4 signify renal loss.

Causes of Hypokalemia

Incresed Lossed Renal Extrarenal

Decreased intake or stores

Intracellular shift


Increased losses

Renal – RTA(proximal or distal) Drugs (diuretics, amphotericin B, aminoglycosides,

corticosteroids), Cystic fibrosis Mineralocorticoid excess (cushing syndrome, CAH, high

renin(renin secreting tumors, renal artery stenosis) Gittelman, Bartter and Liddle syndrome


Increased losses

Extrarenal – Diarrhea/vomiting/nasogastric suction Sweating Potassium binding resins(sodium polystyrene

sulfonate).


Decreased intake or stores

Potassium poor parenteral nutrition Malnutrition, anorexia nervosa

Intracellular shift

alkalosis, high insulin state, drugs (ß agonist, theophylline, barium, hydroxycholoroquine), refeeding syndrome, hypokalemic periodic paralysis, malignant hyperthermia.

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).


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.


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.

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.

Hyperkalemia ECG changes-

Causes of Hyperkalemia

Decreased losses

Increased intake

Extracellular shift

Cellular breakdown


Decreased losses:

Renal failure Renal tubular disorder- pseudohypoaldosteronism,

urinary tract obstruction. Drugs- ACE inhibitors, ARB, K sparing diuretics, NSAIDS,

heparin. Mineralocorticoid deficiency - Addision disease and

21-hydroxylase deficiency.


Increased intake IV/Oral intake, PRBC transfusion.

Extracellular shift Acidosis, low insulin state, drugs (ß blocker, digitalis,

succinylcholine, fluoride), hyperkalemic periodic paralysis, malignant hyperthermia.

Cellular breakdown tumor lysis syndrome, crush injury, massive hemolysis.

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).


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)


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.

Thank you

Health & Medicine

Electrolytes abnormalities