electrolyte disturbances pediatric critical care medicine emory university children’s healthcare...

Electrolyte Disturbances

Pediatric Critical Care MedicineEmory 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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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


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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– Decrease excretion» Renal failure» Adrenal insufficiency or CAH» Hypoaldosteronism» Urinary tract obstruction» Renal tubular disease» ACE inhibitors» Potassium sparing diuretics

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– 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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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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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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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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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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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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electrolyte disturbances pediatric critical care medicine emory university children’s healthcare...

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