Electrolyte Disturbances

Pediatric Critical Care Medicine

Emory University
Children’s Healthcare of Atlanta
 Objectives
• Recognize common fluid and electrolyte disorders
• Clinical presentations
• Management

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 Basic Metabolic Panel

Na + Cl- BUN Ca++

Glu Mg++
K+ CO3-- Cr Phos--

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 Basic Metabolic Panel

Na + Cl- BUN Ca++

Glu Mg++
K+ CO3-- Cr Phos--

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 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

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 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

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 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

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

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 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

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

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 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

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

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 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

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 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 (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

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 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

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 Sodium (Na+)
Fill in the blanks
Urine Serum Urine Serum Urine
Output Na Na Osm Osm

DI

SIADH

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

DI

SIADH

CSW
 Sodium (Na+)
Fill in the blanks

Urine Serum Urine Serum Urine

Output Na Na Osm Osm

DI

SIADH

CSW
 Sodium (Na+)
Fill in the blanks

Urine Serum Urine Serum Urine

Output Na Na Osm Osm

DI

SIADH

CSW
 Sodium (Na+)
Fill in the blanks

Urine Serum Urine Serum Urine

Output Na Na Osm Osm

DI

SIADH

CSW
 Sodium (Na+)
Fill in the blanks

Urine Serum Urine Serum Urine

Output Na Na Osm Osm

DI

SIADH

CSW
 Sodium (Na+)
Fill in the blanks

Urine Serum Urine Serum Urine

Output Na Na Osm Osm

DI

SIADH

CSW
 Sodium (Na+)
Fill in the blanks

Urine Serum Urine Serum Urine

Output Na Na Osm Osm

DI

SIADH

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

DI

SIADH

CSW
 Sodium (Na+)
Fill in the blanks

Urine Serum Urine Serum Urine

Output Na Na Osm Osm

DI

SIADH

CSW
 Sodium (Na+)
Fill in the blanks

Urine Serum Urine Serum Urine

Output Na Na Osm Osm

DI

SIADH

CSW
 Sodium (Na+)
Fill in the blanks

Urine Serum Urine Serum Urine

Output Na Na Osm Osm

DI

SIADH

CSW
 Sodium (Na+)
Fill in the blanks

Urine Serum Urine Serum Urine

Output Na Na Osm Osm

DI

SIADH

CSW
 Sodium (Na+)
Fill in the blanks

Urine Serum Urine Serum Urine

Output Na Na Osm Osm

DI

SIADH

CSW
 Sodium (Na+)
Fill in the blanks

Urine Serum Urine Serum Urine

Output Na Na Osm Osm

DI

SIADH

CSW
 Sodium (Na+)
Fill in the blanks

Urine Serum Urine Serum Urine

Output Na Na Osm Osm

DI

SIADH

CSW
 Basic Metabolic Panel

Na + Cl- BUN Ca++

Glu Mg++
K+ CO3-- Cr Phos--

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 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

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 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

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 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

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

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

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

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

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

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 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

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 Potassium (K+)

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 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

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

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

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 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

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

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 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

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 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

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 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

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 Basic Metabolic Panel

Na + Cl- BUN Ca++

Glu Mg++
K+ HCO3-- Cr Phos--

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 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

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 Bicarb (HCO3--)
• Metabolic acidosis
– Anion gap: Na – (Cl + bicarb)
– Normal range: 12 +/- 2

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 Bicarb (HCO3--)
• Metabolic acidosis: causes for increase anion gap
– M
– U
– D
– P
– I
– L
– E
– S

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 Bicarb (HCO3--)
• Metabolic acidosis: causes for increase anion gap
– Methanol
– Uremia
– DKA
– Paraldehyde or propylene glycol
– Isoniazid
– Lactic acidosis
– Ethylene glycol
– Salicylates

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 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:

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 Bicarb (HCO3--)
• Metabolic acidosis Clinical presentation
– Chest pain, palpitation
– Kussmaul respirations
– Hyperkalemia
– Neuro: lethargy, stupor, coma, seizures
– Cardiac; arrhythmias, decreased response to Epinephrine,
hypotension

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 Bicarb (HCO3--)
• Metabolic acidosis Treatment
– pH<7.1, risk of arrhythmias
– IV bicarb
– Dialysis

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 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

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 Basic Metabolic Panel

Na + Cl- BUN Ca++

Glu Mg++
K+ CO3-- Cr Phos--

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

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 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

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 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)

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 Basic Metabolic Panel

Na + Cl- BUN Ca++

Glu Mg++
K+ CO3-- Cr Phos--

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 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)]

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

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 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
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 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

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 Calcium
• Hypercalcemia Treatments
– Fluid & diuretics
» Forced diuresis
» Loop diuretic
– Oral supplement: biphosphate or calcitonine
– Glucocorticoids
– Dialysis

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 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

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 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

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

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 Basic Metabolic Panel

Na + Cl- BUN Ca++

Glu Mg++
K+ CO3-- Cr Phos--

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 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

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

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 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

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

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 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
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 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

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

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 Basic Metabolic Panel

Na + Cl- BUN Ca++

Glu Mg++
K+ CO3-- Cr Phos--

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 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

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

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 Phosphorus
• Hypophosphatemia Causes
– Re-feeding syndrome
– Respiratory alkalosis
– Alcohol abuse
– Malabsorption

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 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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