Electrolytes abnormalities
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Transcript of 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
Maintenance fluid & electrolyte requirements
Daily sodium requirement = 3meq/kg (children)
Daily potassium requirement = 2meq/kg
Daily chloride requirement = 2meq/kg
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).
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.
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
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).
Hyponatremia
CAUSES of 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]
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.
Hyponatremia-Treatment
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)
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.
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
Causes of Hypokalemia
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
Causes of Hypokalemia
Increased losses
Extrarenal – Diarrhea/vomiting/nasogastric suction Sweating Potassium binding resins(sodium polystyrene
sulfonate).
Causes of Hypokalemia
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).
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.
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.
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
Causes of Hyperkalemia
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.
Causes of Hyperkalemia
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).
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)
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.
Thank you