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Transcript of Electrolyte Disturbances Pediatric Critical Care Medicine Emory University Children’s Healthcare...
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Electrolyte Disturbances
Pediatric Critical Care MedicineEmory University
Children’s Healthcare of Atlanta
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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 Outpu
t
SerumNa
UrineNa
Serum Osm
UrineOsm
DI
SIADH
CSW
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Sodium (Na+)
Fill in the blanks
Urine Outpu
t
SerumNa
UrineNa
Serum Osm
UrineOsm
DI
SIADH
CSW
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Sodium (Na+)
Fill in the blanks
Urine Outpu
t
SerumNa
UrineNa
Serum Osm
UrineOsm
DI
SIADH
CSW
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Sodium (Na+)
Fill in the blanks
Urine Outpu
t
SerumNa
UrineNa
Serum Osm
UrineOsm
DI
SIADH
CSW
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Sodium (Na+)
Fill in the blanks
Urine Outpu
t
SerumNa
UrineNa
Serum Osm
UrineOsm
DI
SIADH
CSW
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Sodium (Na+)
Fill in the blanks
Urine Outpu
t
SerumNa
UrineNa
Serum Osm
UrineOsm
DI
SIADH
CSW
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Sodium (Na+)
Fill in the blanks
Urine Outpu
t
SerumNa
UrineNa
Serum Osm
UrineOsm
DI
SIADH
CSW
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Sodium (Na+)
Fill in the blanks
Urine Outpu
t
SerumNa
UrineNa
Serum Osm
UrineOsm
DI
SIADH
CSW
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Sodium (Na+)
Fill in the blanks
Urine Outpu
t
SerumNa
UrineNa
Serum Osm
UrineOsm
DI
SIADH
CSW
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Sodium (Na+)
Fill in the blanks
Urine Outpu
t
SerumNa
UrineNa
Serum Osm
UrineOsm
DI
SIADH
CSW
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Sodium (Na+)
Fill in the blanks
Urine Outpu
t
SerumNa
UrineNa
Serum Osm
UrineOsm
DI
SIADH
CSW
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Sodium (Na+)
Fill in the blanks
Urine Outpu
t
SerumNa
UrineNa
Serum Osm
UrineOsm
DI
SIADH
CSW
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Sodium (Na+)
Fill in the blanks
Urine Outpu
t
SerumNa
UrineNa
Serum Osm
UrineOsm
DI
SIADH
CSW
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Sodium (Na+)
Fill in the blanks
Urine Outpu
t
SerumNa
UrineNa
Serum Osm
UrineOsm
DI
SIADH
CSW
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Sodium (Na+)
Fill in the blanks
Urine Outpu
t
SerumNa
UrineNa
Serum Osm
UrineOsm
DI
SIADH
CSW
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Sodium (Na+)
Fill in the blanks
Urine Outpu
t
SerumNa
UrineNa
Serum Osm
UrineOsm
DI
SIADH
CSW
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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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