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Electrolyte Disturbances. Pediatric Critical Care Medicine Emory University Children’s Healthcare of Atlanta. Objectives. Recognize common fluid and electrolyte disorders Clinical presentations Management. Basic Metabolic Panel. Na + Cl - BUN Ca ++ Glu Mg ++

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slide1
Electrolyte Disturbances

Pediatric Critical Care Medicine

Emory University

Children’s Healthcare of Atlanta

objectives
Objectives
  • Recognize common fluid and electrolyte disorders
  • Clinical presentations
  • Management
basic metabolic panel
Basic Metabolic Panel

Na + Cl-BUN Ca++

Glu Mg++

K+ CO3--Cr Phos--

basic metabolic panel1
Basic Metabolic Panel

Na + Cl-BUN Ca++

Glu Mg++

K+ CO3--Cr Phos--

sodium na
Sodium (Na+)
  • Bulk cation of extracellular fluid  change in SNa 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
sodium na1
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
sodium na2
Sodium (Na+)
  • Normal SNa: 135-145
  • Major component of serum osmolality
    • Sosm = (2 x Na+) + (BUN / 2.8) + (Glu / 18)
    • Normal: 285-295
  • Alterations in SNa reflect an abnormal water regulation
sodium na3
Sodium (Na+)
  • Hypernatremia: Causes
    • Excessive intake
      • Improperly mixed formula
      • Exogenous: bicarb, hypertonic saline, seawater
    • Water deficit:
      • Central & nephrogenic DI
      • Increased insensible loss
      • Inadequate intake
sodium na4
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
sodium na5
Sodium (Na+)
  • Hypernatremia Clinical presentation
    • Dehydration
    • “Doughy” feel to skin
    • Irritability, lethargy, weakness
    • Intracranial hemorrhage
    • Thrombosis: renal vein, dura sinus
sodium na6
Sodium (Na+)
  • Hypernatremia Treatment
    • Rate of correction for Na+ 1-2 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 12-24 hrs
      • Remaining next 24 hrs
sodium na7
Sodium (Na+)
  • Hyponatremia
    • Na+<135
    • Seizure threshold ~125
    • <120 life threatening
sodium na8
Sodium (Na+)
  • Hyponatremia: Etiology
    • Hypervolemic
      • CHF Cirrhosis
      • Nephrotic syndrome Hypoalbuminemia
      • Septic capillary leak
    • Hypovolemic
      • Renal losses Cerebral salt wasting
      • Extra-renal losses aldosterone effect
        • GI losses
        • Third spacing
sodium na9
Sodium (Na+)
  • Hyponatremia: Etiology
  • Euvolemic hyponatremia
      • SIADH
      • Glucocorticoid deficiency
      • Hypothyroidism
      • Water intoxication
        • Psychogenic polydipsia
        • Diluted formula
        • Beer potomania
  • Pseudo-hyponatremia
    • Hyperglycemia
    • SNa decreased by 1.6/100 glucose over 100

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sodium na10
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
sodium na11
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
sodium na12
Sodium (Na+)

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sodium na13
Sodium (Na+)

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sodium na14
Sodium (Na+)

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sodium na15
Sodium (Na+)

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sodium na16
Sodium (Na+)

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sodium na17
Sodium (Na+)

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sodium na18
Sodium (Na+)

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sodium na19
Sodium (Na+)

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sodium na20
Sodium (Na+)

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sodium na21
Sodium (Na+)

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sodium na22
Sodium (Na+)

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sodium na23
Sodium (Na+)

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sodium na24
Sodium (Na+)

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sodium na25
Sodium (Na+)

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sodium na26
Sodium (Na+)

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sodium na27
Sodium (Na+)

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basic metabolic panel2
Basic Metabolic Panel

Na + Cl-BUN Ca++

Glu Mg++

K+ CO3--Cr Phos--

potassium k
Potassium (K+)
  • Normal range: 3.5-4.5
  • Largely contained intra-cellular  SK does not reflect total body K
  • Important roles: contractility of muscle cells, electrical responsiveness
  • Principal regulator: kidneys
potassium k1
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
potassium k2
Potassium (K+)
  • Solvent drag
    • Increase in Sosmo water moves out of cells  K+ follows
    • 0.6 SK / 10 of Sosmo
    • Evidence of solvent drag in diabetic ketoacidosis
  • Acidosis
    • Low pH  shifts K+ out of cells (into serum)
    • Hi pH  shifts K+into cells
    • 0.3-1.3 mEq/L K+ change / 0.1 unit change in pH in the opposite direction
potassium k3
Potassium (K+)
  • Hyperkalemia
    • >6.5 – life threatening
    • Potential lethal arrhythmias
potassium k4
Potassium (K+)
  • Hyperkalemia Causes
    • Spurious
      • Difficult blood draw  hemolysis  false reading
    • Increase intake
      • Iatrogenic: IV or oral
      • Blood transfusions
potassium k5
Potassium (K+)
  • Hyperkalemia Causes
    • Decrease excretion
      • Renal failure
      • Adrenal insufficiency or CAH
      • Hypoaldosteronism
      • Urinary tract obstruction
      • Renal tubular disease
      • ACE inhibitors
      • Potassium sparing diuretics
potassium k6
Potassium (K+)
  • Hyperkalemia Causes
    • Trans-cellular shifts
      • Acidemia
      • Rhadomyolysis; Tumor lysis syndrome; Tissue necrosis
      • Succinylcholine
      • Malignant hyperthermia
potassium k7
Potassium (K+)
  • Hyperkalemia Clinical presentation
    • Neuromuscular effects
      • Delayed repolarization, faster depolarization, slowing of conduction velocity
      • Paresthesias  weakness  flaccid paralysis
potassium k8
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
potassium k10
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 (β2 selective agonist) nebulizer
potassium k11
Potassium (K+)
  • Hyperkalemia Treatment
    • Increase elimination
      • Hemodialysis or hemofiltration
      • Kayexalate via feces
      • Furosemide via urine
potassium k12
Potassium (K+)
  • Hypokalemia
    • <2.5: life threatening
    • Common in severe gastroenteritis
potassium k13
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
potassium k14
Potassium (K+)
  • Hypokalemia Causes
    • Renal losses
      • DKA
      • Diuretics: thiazide, loop diuretics
      • Drugs: amphotericin B, Cisplastin
      • Hypomagnesemia
      • Alkalosis
      • Hyperaldosteronism
      • Licorice ingestion
      • Gitelman & Bartter syndrome
potassium k15
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
potassium k16
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

potassium k17
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 0.5-1 mEq/kg over 1 hr (rate of 10 mEq/hr)
    • K Acetate or K Phos as alternative
    • Add K sparing diuretics
    • Correct hypomagnesemia
basic metabolic panel3
Basic Metabolic Panel

Na + Cl-BUN Ca++

Glu Mg++

K+HCO3--Cr Phos--

bicarb hco 3
Bicarb (HCO3--)
  • Normal range: 25-35
  • 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
bicarb hco 31
Bicarb (HCO3--)
  • Metabolic acidosis
    • Anion gap: Na – (Cl + bicarb)
    • Normal range: 12 +/- 2
bicarb hco 32
Bicarb (HCO3--)
  • Metabolic acidosis: causes for increase anion gap
    • M
    • U
    • D
    • P
    • I
    • L
    • E
    • S
bicarb hco 33
Bicarb (HCO3--)
  • Metabolic acidosis:causes for increaseanion gap
    • Methanol
    • Uremia
    • DKA
    • Paraldehyde or propylene glycol
    • Isoniazid
    • Lactic acidosis
    • Ethyleneglycol
    • Salicylates
bicarb hco 34
Bicarb (HCO3--)
  • 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:
bicarb hco 35
Bicarb (HCO3--)
  • Metabolic acidosis Clinical presentation
    • Chest pain, palpitation
    • Kussmaul respirations
    • Hyperkalemia
    • Neuro: lethargy, stupor, coma, seizures
    • Cardiac; arrhythmias, decreased response to Epinephrine, hypotension
bicarb hco 36
Bicarb (HCO3--)
  • Metabolic acidosis Treatment
    • pH<7.1, risk of arrhythmias
    • IV bicarb
    • Dialysis
bicarb hco 37
Bicarb (HCO3--)
  • 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
basic metabolic panel4
Basic Metabolic Panel

Na + Cl-BUN Ca++

Glu Mg++

K+ CO3--Cr Phos--

glucose
Glucose
  • Hypoglycemia Causes
    • Complication of DM therapies
    • Hyperinsulinemia
    • Inborn errors of metabolism
    • Alcohol
    • Starvations
    • Infections, organ failure
glucose1
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
glucose2
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)
basic metabolic panel5
Basic Metabolic Panel

Na + Cl-BUNCa++

Glu Mg++

K+ CO3--Cr Phos--

calcium
Calcium
  • Normal range: 8.8-10.1 with half bound to albumin
  • Ionized (free or active)calcium: 4.4-5.4 – relevant for cell function
  • Majority is stored in bone
  • Hypoalbuminemia  falsely decreased calcium
    • Cac = Cam + [0.8 x (Albn – Alb m)]
calcium1
Calcium
  • Roles:
    • Coagulation
    • Cellular signals
    • Muscle contraction
    • Neuromuscular transmission
  • Controlled by parathyroid hormone and vitamin D
calcium2
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
calcium3
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
calcium4
Calcium
  • Hypercalcemia Treatments
    • Fluid & diuretics
      • Forced diuresis
      • Loop diuretic
    • Oral supplement: biphosphate or calcitonine
    • Glucocorticoids
    • Dialysis
calcium5
Calcium
  • Hypocalcemia Causes
    • 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
calcium6
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
calcium7
Calcium
  • Hypocalcemia: Treatments
    • Supplements
      • IV: gluconate or chloride with EKG change
      • Oral calcium with vitamin D
basic metabolic panel6
Basic Metabolic Panel

Na + Cl-BUN Ca++

Glu Mg++

K+ CO3--Cr Phos--

magnesium
Magnesium
  • Normal range: 1.5-2.3
  • 60% stored in bone
  • 1% in extracellular space
  • Necessary cofactor for many enzymes
  • Renal excretion is primary regulation
magnesium1
Magnesium
  • Hypermagnesemia: Causes
    • Hemolysis
    • Renal insuficiency
    • DKA, adrenal insufficiency, hyperparathyroidism, lithium intoxication
magnesium2
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
magnesium3
Magnesium
  • Hypermagnesemia: Treatments
    • Calcium infusion
    • Diuretics
    • Dialysis
magnesium4
Magnesium
  • Hypomagnesemia Causes
    • 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
magnesium5
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
magnesium6
Magnesium
  • Hypomagnesemia: Treatments
    • Oral or IV supplement
    • Correct on going loss
basic metabolic panel7
Basic Metabolic Panel

Na + Cl-BUN Ca++

Glu Mg++

K+ CO3--CrPhos--

phosphorus
Phosphorus
  • Normal range: 2.3 - 4.8
  • 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
phosphorus1
Phosphorus
  • Hyperphosphatemia
    • Causes
      • Hypoparathyroidism
      • Chronic renal failure
      • Osteomalacia
    • Presentations
      • Ectopic calcification
      • Renal osteodystrophy
    • Treatments
      • Dietary restriction
      • Phosphate binder
phosphorus2
Phosphorus
  • Hypophosphatemia Causes
    • Re-feeding syndrome
    • Respiratory alkalosis
    • Alcohol abuse
    • Malabsorption
phosphorus3
Phosphorus
  • Hypophosphatemia
    • Clinical presentation
      • Muscle dysfunction and weakness: diploplia, low CO, dysphagia, respiratory depression
      • AMS
      • WBC dysfunction
      • Instability of cell membrane  rhabdomyolysis
    • Treatments
      • supplementation
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