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Electrolyte Disturbances Pediatric Critical Care Medicine Emory University Children’s Healthcare of Atlanta.

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Presentation on theme: "Electrolyte Disturbances Pediatric Critical Care Medicine Emory University Children’s Healthcare of Atlanta."— Presentation transcript:

1 Electrolyte Disturbances Pediatric Critical Care Medicine Emory University Children’s Healthcare of Atlanta

2 Objectives Recognize common fluid and electrolyte disorders Clinical presentations Management 2

3 Basic Metabolic Panel Na + Cl - BUN Ca ++ GluMg ++ K + CO 3 -- Cr Phos -- 3

4 Basic Metabolic Panel Na + Cl - BUN Ca ++ GluMg ++ K + CO 3 -- Cr Phos -- 4

5 Sodium (Na + ) Bulk cation of extracellular fluid  change in S Na reflects change in total body Na + Principle active solute for the maintenance of intravascular & interstitial volume Absorption: throughout the GI system via active Na,K- ATPase system Excretion: urine, sweat & feces Kidneys are the principal regulator 5

6 Sodium (Na + ) Kidneys are the principal regulator –2/3 of filtered Na + is reabsorbed by the proximal convoluted tubule, increase with contraction of extracellular fluid –Countercurrent system at the Loop of Henle is responsible for Na + (descending) & water (ascending) balance – active transport with Cl - –Aldosterone stimulates further Na + re-absorption at the distal convoluted tubules & the collecting ducts –<1% of filtered Na + is normally excreted but can vary up to 10% if necessary 6

7 Sodium (Na + ) Normal S Na : Major component of serum osmolality –S osm = (2 x Na + ) + (BUN / 2.8) + (Glu / 18) –Normal: Alterations in S Na reflect an abnormal water regulation 7

8 Sodium (Na + ) Hypernatremia: Causes –Excessive intake »Improperly mixed formula »Exogenous: bicarb, hypertonic saline, seawater –Water deficit: »Central & nephrogenic DI »Increased insensible loss »Inadequate intake 8

9 Sodium (Na + ) Hypernatremia: Causes –Water and sodium deficit »GI losses »Cutaneous losses »Renal losses Osmotic diuresis: mannitol, diabetes mellitus Chronic kidney disease Polyuric ATN Post-obstructive diuresis 9

10 Sodium (Na + ) Hypernatremia Clinical presentation –Dehydration –“Doughy” feel to skin –Irritability, lethargy, weakness –Intracranial hemorrhage –Thrombosis: renal vein, dura sinus 10

11 Sodium (Na + ) Hypernatremia Treatment –Rate of correction for Na mEq/L/hr –Calculate water deficit »Water deficit = 0.6 x wt (kg) x [(current Na + /140) – 1] –Rate of correction for calculated water deficit »50% first hrs »Remaining next 24 hrs 11

12 Sodium (Na + ) Hyponatremia –Na + <135 –Seizure threshold ~125 –<120 life threatening 12

13 Sodium (Na + ) Hyponatremia: Etiology –Hypervolemic »CHFCirrhosis »Nephrotic syndromeHypoalbuminemia »Septic capillary leak –Hypovolemic »Renal lossesCerebral salt wasting »Extra-renal losses aldosterone effect GI losses Third spacing 13

14 Sodium (Na + ) Hyponatremia: Etiology Euvolemic hyponatremia »SIADH »Glucocorticoid deficiency »Hypothyroidism »Water intoxication Psychogenic polydipsia Diluted formula Beer potomania Pseudo-hyponatremia –Hyperglycemia –S Na decreased by 1.6/100 glucose over

15 Sodium (Na + ) Hyponatremia Clinical presentation –Cellular swelling due to water shifts into cells –Anorexia, nausea, emesis, malaise, lethargy, confusion, agitation, headache, seizures, coma –Chronic hyponatremia: better tolerated 15

16 Sodium (Na + ) Hyponatremia Treatment –Rapid correction  central pontine myelinolysis –Goal 12 mEq/L/day –Fluid restriction with SIADH –Hyponatremic seizures »Poorly responsive to anti-convulsants »Hypertonic saline »Need to bring Na to above seizure threshold 16

17 Sodium (Na + ) Fill in the blanks Urine Output Serum Na Urine Na Serum Osm Urine Osm DI SIADH CSW

18 Sodium (Na + ) Fill in the blanks Urine Output Serum Na Urine Na Serum Osm Urine Osm DI SIADH CSW

19 Sodium (Na + ) Fill in the blanks Urine Output Serum Na Urine Na Serum Osm Urine Osm DI SIADH CSW

20 Sodium (Na + ) Fill in the blanks Urine Output Serum Na Urine Na Serum Osm Urine Osm DI SIADH CSW

21 Sodium (Na + ) Fill in the blanks Urine Output Serum Na Urine Na Serum Osm Urine Osm DI SIADH CSW

22 Sodium (Na + ) Fill in the blanks Urine Output Serum Na Urine Na Serum Osm Urine Osm DI SIADH CSW

23 Sodium (Na + ) Fill in the blanks Urine Output Serum Na Urine Na Serum Osm Urine Osm DI SIADH CSW

24 Sodium (Na + ) Fill in the blanks Urine Output Serum Na Urine Na Serum Osm Urine Osm DI SIADH CSW

25 Sodium (Na + ) Fill in the blanks Urine Output Serum Na Urine Na Serum Osm Urine Osm DI SIADH CSW

26 Sodium (Na + ) Fill in the blanks Urine Output Serum Na Urine Na Serum Osm Urine Osm DI SIADH CSW

27 Sodium (Na + ) Fill in the blanks Urine Output Serum Na Urine Na Serum Osm Urine Osm DI SIADH CSW

28 Sodium (Na + ) Fill in the blanks Urine Output Serum Na Urine Na Serum Osm Urine Osm DI SIADH CSW

29 Sodium (Na + ) Fill in the blanks Urine Output Serum Na Urine Na Serum Osm Urine Osm DI SIADH CSW

30 Sodium (Na + ) Fill in the blanks Urine Output Serum Na Urine Na Serum Osm Urine Osm DI SIADH CSW

31 Sodium (Na + ) Fill in the blanks Urine Output Serum Na Urine Na Serum Osm Urine Osm DI SIADH CSW

32 Sodium (Na + ) Fill in the blanks Urine Output Serum Na Urine Na Serum Osm Urine Osm DI SIADH CSW

33 Basic Metabolic Panel Na + Cl - BUN Ca ++ GluMg ++ K + CO 3 -- Cr Phos -- 33

34 Potassium (K + ) Normal range: Largely contained intra-cellular  S K does not reflect total body K Important roles: contractility of muscle cells, electrical responsiveness Principal regulator: kidneys 34

35 Potassium (K + ) Daily requirement 1-2 mEq/kg Complete absorption in the upper GI tract Kidneys regulate balance –10-15% filtered is excreted Aldosterone: increase K + & decrease Na + excretion Mineralocorticoid & glucocorticoid  increase K + & decrease Na + excretion in stool 35

36 Potassium (K + ) Solvent drag –Increase in S osmo  water moves out of cells  K + follows – 0.6 S K / 10 of S osmo –Evidence of solvent drag in diabetic ketoacidosis Acidosis –Low pH  shifts K + out of cells (into serum) –Hi pH  shifts K + into cells – mEq/L K + change / 0.1 unit change in pH in the opposite direction 36

37 Potassium (K + ) Hyperkalemia –>6.5 – life threatening –Potential lethal arrhythmias 37

38 Potassium (K + ) Hyperkalemia Causes –Spurious »Difficult blood draw  hemolysis  false reading –Increase intake »Iatrogenic: IV or oral »Blood transfusions 38

39 Potassium (K + ) Hyperkalemia Causes –Decrease excretion »Renal failure »Adrenal insufficiency or CAH »Hypoaldosteronism »Urinary tract obstruction »Renal tubular disease »ACE inhibitors »Potassium sparing diuretics 39

40 Potassium (K + ) Hyperkalemia Causes –Trans-cellular shifts »Acidemia »Rhadomyolysis; Tumor lysis syndrome; Tissue necrosis »Succinylcholine »Malignant hyperthermia 40

41 Potassium (K + ) Hyperkalemia Clinical presentation –Neuromuscular effects »Delayed repolarization, faster depolarization, slowing of conduction velocity »Paresthesias  weakness  flaccid paralysis 41

42 Potassium (K + ) Hyperkalemia Clinical presentation –EKG changes »~6: peak T waves »~7: increased PR interval »~8-9: absent P wave with widening QRS complex »Ventricular fibrillation »Asystole 42

43 Potassium (K + ) 43

44 Potassium (K + ) Hyperkalemia Treatment –Lower K + temporarily »Calcium gluconate 100mg/kg IV »Bicarb: 1-2 mEq/kg IV »Insulin & glucose Insulin 0.05 u/kg IV + D10W 2ml/kg then Insulin 0.1 u/kg/hr + D10W 2-4 ml/kg/hr »Salbutamol ( β 2 selective agonist) nebulizer 44

45 Potassium (K + ) Hyperkalemia Treatment –Increase elimination »Hemodialysis or hemofiltration »Kayexalate via feces »Furosemide via urine 45

46 Potassium (K + ) Hypokalemia –<2.5: life threatening –Common in severe gastroenteritis 46

47 Potassium (K + ) Hypokalemia Causes –Distribution from ECF »Hypokalemic periodic paralysis »Insulin, Β -agonists, catecholamines, xanthine –Decrease intake –Extra-renal losses »Diarrhea »Laxative abuse »Perspiration –Excessive colas consumption 47

48 Potassium (K + ) Hypokalemia Causes –Renal losses »DKA »Diuretics: thiazide, loop diuretics »Drugs: amphotericin B, Cisplastin »Hypomagnesemia »Alkalosis »Hyperaldosteronism »Licorice ingestion »Gitelman & Bartter syndrome 48

49 Potassium (K + ) Hypokalemia Presentation –Usually asymptomatic –Skeletal muscle: weakness & cramps; respiratory failure –Flaccid paralysis & hyporeflexia –Smooth muscle: constipation, urinary retention ECG changes »Flattened or inverted T-wave »U wave: prolonged repolarization of the Purkinje fibers »Depressed ST segment and widen PR interval »Ventricular fibrillation can happen 49

50 Potassium (K + ) Hypokalemia - Flattened or inverted T-wave - U wave: prolonged repolarization of the Purkinje fibers - Depressed ST segment and widen PR interval - Ventricular fibrillation can happen 50

51 Potassium (K + ) Hypokalemia Treatment –Address the causes & underlying condition –Dietary supplements : leafy green vegetables, tomatoes, citrus fruits, oranges or bananas –Oral K replacement preferred –IV: KCl mEq/kg over 1 hr (rate of 10 mEq/hr) –K Acetate or K Phos as alternative –Add K sparing diuretics –Correct hypomagnesemia 51

52 Basic Metabolic Panel Na + Cl - BUN Ca ++ GluMg ++ K + HCO 3 -- Cr Phos -- 52

53 Bicarb (HCO 3 -- ) Normal range: Important buffer system in acid-base homeostasis Increased in metabolic alkalosis or compensated respiratory acidosis Decreased in metabolic acidosis or compensated respiratory alkalosis 0.15 pH change/10 change in bicarb in uncompensated conditions 53

54 Bicarb (HCO 3 -- ) Metabolic acidosis –Anion gap: Na – (Cl + bicarb) –Normal range: 12 +/- 2 54

55 Bicarb (HCO 3 -- ) Metabolic acidosis: causes for increase anion gap –M –U –D –P –I –L –E –S 55

56 Bicarb (HCO 3 -- ) Metabolic acidosis: causes for increase anion gap –Methanol –Uremia –DKA –Paraldehyde or propylene glycol –Isoniazid –Lactic acidosis –Ethylene glycol –Salicylates 56

57 Bicarb (HCO 3 -- ) Metabolic acidosis: causes for normal anion gap –Diarrhea –Pancreatic fistula –Renal tubular acidosis or renal failure –Intoxication: ammonium chloride, Acetazolamide, bile acid sequestrants, isopropyl alcohol –Glue sniffing –Toluene: 57

58 Bicarb (HCO 3 -- ) Metabolic acidosis Clinical presentation –Chest pain, palpitation –Kussmaul respirations –Hyperkalemia –Neuro: lethargy, stupor, coma, seizures –Cardiac; arrhythmias, decreased response to Epinephrine, hypotension 58

59 Bicarb (HCO 3 -- ) Metabolic acidosis Treatment –pH<7.1, risk of arrhythmias –IV bicarb –Dialysis 59

60 Bicarb (HCO 3 -- ) Metabolic alkalosis Causes –Chloride responsive »Compensated respiratory acidosis »Diuretics  contraction alkalosis »Vomiting –Chloride resistant »Retention of bicarb, shift hydrogen ion into IC space »Alkalotic agents »Hyperaldosteronism 60

61 Basic Metabolic Panel Na + Cl - BUN Ca ++ GluMg ++ K + CO 3 -- Cr Phos -- 61

62 Glucose Hypoglycemia Causes –Complication of DM therapies –Hyperinsulinemia –Inborn errors of metabolism –Alcohol –Starvations –Infections, organ failure 62

63 Glucose Hypoglycemia Clinical presentation –Adrenergic »Shakiness, anxiety, nervousness, palpitations, tachycardia »Sweating, pallor, coldness, clamminess –Glucagon »Hunger, borborygmus, nausea, vomiting, abd. Discomfort »Headache –Neuroglycopenic »AMS, fatigue, weakness, lethargy, confusion, amnesia. »Ataxia, incoordination, slurred speech 63

64 Glucose Hypoglycemia Treatments »0.5-1 g/kg of dextrose »5-10 ml/kg of D10W »2-4 ml/kg of D25W »Max 1 amp (50 g) 64

65 Basic Metabolic Panel Na + Cl - BUN Ca ++ GluMg ++ K + CO 3 -- Cr Phos -- 65

66 Calcium Normal range: with half bound to albumin Ionized (free or active)calcium: – relevant for cell function Majority is stored in bone Hypoalbuminemia  falsely decreased calcium –Ca c = Ca m + [0.8 x (Alb n – Alb m )] 66

67 Calcium Roles: –Coagulation –Cellular signals –Muscle contraction –Neuromuscular transmission Controlled by parathyroid hormone and vitamin D 67

68 Calcium Hypercalcemia: Causes –Excess parathyroid hormone, lithium use –Excess vitamin D –Malignancy –Renal failure –High bone turn over »Prolonged immobilization »Hyperthyroidism »Thiazide use, vitamin A toxicity »Paget’s disease »Multiple myeloma 68

69 Calcium Hypercalcemia:Clinical presentation –Groans: constipation –Moans: psychic moans (fatigue, lethargy, depression) –Bones: bone pain –Stones: kidney stones –Psychiatric overtones: depression & confusion –Fatigue, anorexia, nausea, vomiting, pancreatitis –ECG: short QT interval, widened T wave 69

70 Calcium HypercalcemiaTreatments –Fluid & diuretics »Forced diuresis »Loop diuretic –Oral supplement: biphosphate or calcitonine –Glucocorticoids –Dialysis 70

71 Calcium HypocalcemiaCauses –Eating disorder –Hungry bone syndrome –Ingestion: mercury, excessive Mg –Chelation therapy EDTA –Absent of PTH –Ineffective PTH: CRF, absent or ineffective vitamin D, pseudohypoparathyroidism –Deficient in PTH: acute hyperphos: TLS, ARF, Rhabdo –Blood transfusions 71

72 Calcium Hypocalcemia: Clinical presentation –Neuromuscular irritability –Paresthesias: oral, perioral and acral, tingling or pin & needles –Tetany (Chvostek & Trousseau signs) –Hyperreflexia –Laryngospasm –Jittery, poor feedings or vomiting in newborns –ECG changes: prolonged QT intervals 72

73 Calcium Hypocalcemia: Treatments –Supplements »IV: gluconate or chloride with EKG change »Oral calcium with vitamin D 73

74 Basic Metabolic Panel Na + Cl - BUN Ca ++ GluMg ++ K + CO 3 -- Cr Phos -- 74

75 Magnesium Normal range: % stored in bone 1% in extracellular space Necessary cofactor for many enzymes Renal excretion is primary regulation 75

76 Magnesium Hypermagnesemia: Causes –Hemolysis –Renal insuficiency –DKA, adrenal insufficiency, hyperparathyroidism, lithium intoxication 76

77 Magnesium Hypermagnesemia: Clinical presentation –Weakness, nausea, vomiting –Hypotension, hypocalcemia –Arrhythmia and asystole »4.0 mEq/L hyporeflexia »>5 prolonged AV conduction »>10 complete heart block »>13 cardiac arrest 77

78 Magnesium Hypermagnesemia: Treatments –Calcium infusion –Diuretics –Dialysis 78

79 Magnesium HypomagnesemiaCauses –Alcoholism: malnutrition + diarrhea; Thiamine deficiency –GI causes: Crohn’s, UC, Whipple’s disease, celiac sprue –Renal loss: Bartter’s syndrome, postobstructive diuresis, ATN, kidney transplant –DKA –Drugs »Loop and thiazide diuretics »Abx: aminoglycoside, ampho B, pentamidine, gent, tobra »PPI »Others: digitalis, adrenergic, cisplastin, ciclosporine 79

80 Magnesium Hypomagnesemia: Clinical presentation –Weakness, muscle cramps –Cardiac arrhythmias »Prolonged PR, QRS & QT »Torsade de pointes »Complete heart block & cardiac arrest with level >15 –CNS: irritability, tremor, athetosis, jerking, nystagmus –Hallucination, depression, epileptic fits, HTN, tachycardia, tetany 80

81 Magnesium Hypomagnesemia: Treatments –Oral or IV supplement –Correct on going loss 81

82 Basic Metabolic Panel Na + Cl - BUN Ca ++ GluMg ++ K + CO 3 -- Cr Phos -- 82

83 Phosphorus Normal range: Most store in bone or intracellular space <1% in plasma Intracellular major anion, most in ATP Concentration varies with age, higher during early childhood Necessary for cellular energy metabolism 83

84 Phosphorus Hyperphosphatemia –Causes »Hypoparathyroidism »Chronic renal failure »Osteomalacia –Presentations »Ectopic calcification »Renal osteodystrophy –Treatments »Dietary restriction »Phosphate binder 84

85 Phosphorus HypophosphatemiaCauses –Re-feeding syndrome –Respiratory alkalosis –Alcohol abuse –Malabsorption 85

86 Phosphorus Hypophosphatemia –Clinical presentation »Muscle dysfunction and weakness: diploplia, low CO, dysphagia, respiratory depression »AMS »WBC dysfunction »Instability of cell membrane  rhabdomyolysis –Treatments »supplementation 86


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