Electrolytes abnormalities

Dr Aftab Ahmad Siddiqui JNMC AMU Aligarh

1. Electrolyte Abnormalities in Children Presenter- Dr Aftab Ahmad Siddiqui Moderators- Dr. Z Z Rab , Dr. Uzma Firdaus , Dr. Ayesha Ahmad, Dr Shaad Abqari

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 1 st year to puberty TBW= 60%

3. Body Composition

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

5. Electrolyte composition of extracellular and intracellular fluid compartments

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. S osm = (2 x Na + ) + (BUN / 2.8) + ( Glu / 18)

7. Regulation of sodium and water balance

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

9. Maintenance fluid & electrolyte requirements Daily sodium requirement = 3meq/kg (children ) Daily potassium requirement = 2meq/kg Daily chloride requirement = 2meq/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 C above 38 C ) 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. H yponatremia CAUSES of hyponatremia Hypervolemic hyponatremia CHF, Cirrhosis, Nephrotic syndrome, Acute or chronic renal failure

19. Hyponatremia -Treatment D etermine whether hyponatremia is acute(<24 hr ) or chronic(>48hr), symptomatic/asymptomatic. E valuate 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 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 L ethargy 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.

25. 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

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.

28. Differentiation b/w few important conditions

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. C ontractility 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.

33. Hypokalemia ECG changes-

34. 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.  

35. Causes of Hypokalemia Incresed Lossed Renal Extrarenal Decreased intake or stores Intracellular shift

36. Causes of Hypokalemia Increased losses Renal – RTA(proximal or distal) Drugs (diuretics, amphotericin B, aminoglycosides, corticosteroids), C ystic fibrosis M ineralocorticoid excess ( cushing syndrome, CAH, high renin(renin secreting tumors, renal artery stenosis) Gittelman , Bartter and Liddle syndrome

37. Causes of Hypokalemia Increased losses Extrarenal – Diarrhea/vomiting/nasogastric suction Sweating Potassium binding resins(sodium polystyrene sulfonate).

38. 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.

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.

43. Hyperkalemia ECG changes-

44. Causes of Hyperkalemia Decreased losses Increased intake Extracellular shift Cellular breakdown

45. Causes of Hyperkalemia Decreased losses: Renal failure Renal tubular disorder- pseudohypoaldosteronism , urinary tract obs t ruction. Drugs- ACE inhibitors, ARB, K sparing diuretics, NSAIDS, heparin. Mineralocorticoid deficiency - A ddision disease and 21-hydroxylase deficiency.

46. 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.

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 ). NaHCO 3 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 .

50. Thank you