Electrolyte Disturbances
Pediatric Critical Care Medicine
Emory University
Children’s Healthcare of Atlanta
Objectives
• Recognize common fluid and electrolyte disorders
• Clinical presentations
• Management
2
Basic Metabolic Panel
Na +
Cl-
BUN
Glu
K+
3
CO3--
Cr
Ca++
Mg++
Phos--
Basic Metabolic Panel
Na +
Cl-
BUN
Glu
K+
4
CO3--
Cr
Ca++
Mg++
Phos--
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,KATPase system
• Excretion: urine, sweat & feces
• Kidneys are the principal regulator
5
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
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•
•
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Osmotic diuresis: mannitol, diabetes mellitus
Chronic kidney disease
Polyuric ATN
Post-obstructive diuresis
Sodium (Na+)
• Hypernatremia
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–
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–
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Clinical presentation
Dehydration
“Doughy” feel to skin
Irritability, lethargy, weakness
Intracranial hemorrhage
Thrombosis: renal vein, dura sinus
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
» Nephrotic syndrome
» Septic capillary leak
Cirrhosis
Hypoalbuminemia
– Hypovolemic
» Renal losses
» Extra-renal losses
• GI losses
• Third spacing
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Cerebral salt wasting
aldosterone effect
Sodium (Na+)
• Hyponatremia:
Etiology
• Euvolemic hyponatremia
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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
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–
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
Output
DI
SIADH
CSW
Serum
Na
Urine
Na
Serum
Osm
Urine
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Sodium (Na+)
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Urine
Output
DI
SIADH
CSW
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Urine
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SIADH
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Urine
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SIADH
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Urine
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Urine
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SIADH
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Urine
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Urine
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DI
SIADH
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Urine
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SIADH
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SIADH
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Urine
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SIADH
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Urine
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SIADH
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Urine
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SIADH
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Urine
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Sodium (Na+)
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Urine
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DI
SIADH
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Urine
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Urine
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DI
SIADH
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Urine
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Urine
Output
DI
SIADH
CSW
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Urine
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Sodium (Na+)
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Urine
Output
DI
SIADH
CSW
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Urine
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Urine
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Sodium (Na+)
Fill in the blanks
Urine
Output
DI
SIADH
CSW
Serum
Na
Urine
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Osm
Urine
Osm
Basic Metabolic Panel
Na +
Cl-
BUN
Glu
K+
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CO3--
Cr
Ca++
Mg++
Phos--
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
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Renal failure
Adrenal insufficiency or CAH
Hypoaldosteronism
Urinary tract obstruction
Renal tubular disease
ACE inhibitors
Potassium sparing diuretics
Potassium (K+)
• Hyperkalemia
Causes
– Trans-cellular shifts
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Acidemia
Rhadomyolysis; Tumor lysis syndrome; Tissue necrosis
Succinylcholine
Malignant hyperthermia
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
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~6: peak T waves
~7: increased PR interval
~8-9: absent P wave with widening QRS complex
Ventricular fibrillation
Asystole
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
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DKA
Diuretics: thiazide, loop diuretics
Drugs: amphotericin B, Cisplastin
Hypomagnesemia
Alkalosis
Hyperaldosteronism
Licorice ingestion
Gitelman & Bartter syndrome
Potassium (K+)
• Hypokalemia
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–
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–
Presentation
Usually asymptomatic
Skeletal muscle: weakness & cramps; respiratory failure
Flaccid paralysis & hyporeflexia
Smooth muscle: constipation, urinary retention
ECG changes
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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 (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
Glu
K+
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HCO3--
Cr
Ca++
Mg++
Phos--
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
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M
U
D
P
I
L
E
S
Bicarb (HCO3--)
• Metabolic acidosis: causes for increase anion gap
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Methanol
Uremia
DKA
Paraldehyde or propylene glycol
Isoniazid
Lactic acidosis
Ethylene glycol
Salicylates
Bicarb (HCO3--)
• Metabolic acidosis: causes for normal anion gap
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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
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Chest pain, palpitation
Kussmaul respirations
Hyperkalemia
Neuro: lethargy, stupor, coma, seizures
Cardiac; arrhythmias, decreased response to Epinephrine,
hypotension
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
Glu
K+
61
CO3--
Cr
Ca++
Mg++
Phos--
Glucose
• Hypoglycemia
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–
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Causes
Complication of DM therapies
Hyperinsulinemia
Inborn errors of metabolism
Alcohol
Starvations
Infections, organ failure
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
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0.5-1 g/kg of dextrose
5-10 ml/kg of D10W
2-4 ml/kg of D25W
Max 1 amp (50 g)
Treatments
Basic Metabolic Panel
Na +
Cl-
BUN
Glu
K+
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CO3--
Cr
Ca++
Mg++
Phos--
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:
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–
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Coagulation
Cellular signals
Muscle contraction
Neuromuscular transmission
• Controlled by parathyroid hormone and vitamin D
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Calcium
• Hypercalcemia:
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Excess parathyroid hormone, lithium use
Excess vitamin D
Malignancy
Renal failure
High bone turn over
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Causes
Prolonged immobilization
Hyperthyroidism
Thiazide use, vitamin A toxicity
Paget’s disease
Multiple myeloma
Calcium
• Hypercalcemia:
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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
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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:
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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
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
Glu
K+
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CO3--
Cr
Ca++
Mg++
Phos--
Magnesium
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•
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Normal range: 1.5-2.3
60% stored in bone
1% in extracellular space
Necessary cofactor for many enzymes
Renal excretion is primary regulation
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
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4.0 mEq/L hyporeflexia
>5 prolonged AV conduction
>10 complete heart block
>13 cardiac arrest
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
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Loop and thiazide diuretics
Abx: aminoglycoside, ampho B, pentamidine, gent, tobra
PPI
Others: digitalis, adrenergic, cisplastin, ciclosporine
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
Glu
K+
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CO3--
Cr
Ca++
Mg++
Phos--
Phosphorus
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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
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
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–
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–
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Re-feeding syndrome
Respiratory alkalosis
Alcohol abuse
Malabsorption
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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