Electrolyte Disturbances

Pediatric Critical Care Medicine

Emory University
Childrens 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 (2 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, -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
Pagets 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: Crohns, UC, Whipples disease, celiac sprue
Renal loss: Bartters 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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