Electrolyte Disturbances
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Electrolyte Disturbances. Pediatric Critical Care Medicine Emory University Children’s Healthcare of Atlanta. Objectives. Recognize common fluid and electrolyte disorders Clinical presentations Management. Basic Metabolic Panel. Na + Cl - BUN Ca ++ GluMg ++

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Electrolyte disturbances

Electrolyte Disturbances

Pediatric Critical Care Medicine

Emory University

Children’s Healthcare of Atlanta


Objectives

Objectives

  • Recognize common fluid and electrolyte disorders

  • Clinical presentations

  • Management


Basic metabolic panel

Basic Metabolic Panel

Na+Cl-BUN Ca++

GluMg++

K+CO3--CrPhos--


Basic metabolic panel1

Basic Metabolic Panel

Na+Cl-BUN Ca++

GluMg++

K+CO3--CrPhos--


Sodium na

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


Sodium na1

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


Sodium na2

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


Sodium na3

Sodium (Na+)

  • Hypernatremia: Causes

    • Excessive intake

      • Improperly mixed formula

      • Exogenous: bicarb, hypertonic saline, seawater

    • Water deficit:

      • Central & nephrogenic DI

      • Increased insensible loss

      • Inadequate intake


Sodium na4

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


Sodium na5

Sodium (Na+)

  • Hypernatremia Clinical presentation

    • Dehydration

    • “Doughy” feel to skin

    • Irritability, lethargy, weakness

    • Intracranial hemorrhage

    • Thrombosis: renal vein, dura sinus


Sodium na6

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


Sodium na7

Sodium (Na+)

  • Hyponatremia

    • Na+<135

    • Seizure threshold ~125

    • <120 life threatening


Sodium na8

Sodium (Na+)

  • Hyponatremia: Etiology

    • Hypervolemic

      • CHFCirrhosis

      • Nephrotic syndromeHypoalbuminemia

      • Septic capillary leak

    • Hypovolemic

      • Renal lossesCerebral salt wasting

      • Extra-renal losses aldosterone effect

        • GI losses

        • Third spacing


Sodium na9

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

  • -


    Sodium na10

    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


    Sodium na11

    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


    Sodium na12

    Sodium (Na+)

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    Sodium na13

    Sodium (Na+)

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    Sodium na14

    Sodium (Na+)

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    Sodium na15

    Sodium (Na+)

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    Sodium na16

    Sodium (Na+)

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    Sodium na17

    Sodium (Na+)

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    Sodium na18

    Sodium (Na+)

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    Sodium na19

    Sodium (Na+)

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    Sodium na20

    Sodium (Na+)

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    Sodium na21

    Sodium (Na+)

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    Sodium na22

    Sodium (Na+)

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    Sodium na23

    Sodium (Na+)

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    Sodium na24

    Sodium (Na+)

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    Sodium na25

    Sodium (Na+)

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    Sodium na26

    Sodium (Na+)

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    Sodium na27

    Sodium (Na+)

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    Basic metabolic panel2

    Basic Metabolic Panel

    Na+Cl-BUN Ca++

    GluMg++

    K+CO3--CrPhos--


    Potassium k

    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


    Potassium k1

    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


    Potassium k2

    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


    Potassium k3

    Potassium (K+)

    • Hyperkalemia

      • >6.5 – life threatening

      • Potential lethal arrhythmias


    Potassium k4

    Potassium (K+)

    • Hyperkalemia Causes

      • Spurious

        • Difficult blood draw  hemolysis  false reading

      • Increase intake

        • Iatrogenic: IV or oral

        • Blood transfusions


    Potassium k5

    Potassium (K+)

    • Hyperkalemia Causes

      • Decrease excretion

        • Renal failure

        • Adrenal insufficiency or CAH

        • Hypoaldosteronism

        • Urinary tract obstruction

        • Renal tubular disease

        • ACE inhibitors

        • Potassium sparing diuretics


    Potassium k6

    Potassium (K+)

    • Hyperkalemia Causes

      • Trans-cellular shifts

        • Acidemia

        • Rhadomyolysis; Tumor lysis syndrome; Tissue necrosis

        • Succinylcholine

        • Malignant hyperthermia


    Potassium k7

    Potassium (K+)

    • Hyperkalemia Clinical presentation

      • Neuromuscular effects

        • Delayed repolarization, faster depolarization, slowing of conduction velocity

        • Paresthesias  weakness  flaccid paralysis


    Potassium k8

    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


    Potassium k9

    Potassium (K+)


    Potassium k10

    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


    Potassium k11

    Potassium (K+)

    • Hyperkalemia Treatment

      • Increase elimination

        • Hemodialysis or hemofiltration

        • Kayexalate via feces

        • Furosemide via urine


    Potassium k12

    Potassium (K+)

    • Hypokalemia

      • <2.5: life threatening

      • Common in severe gastroenteritis


    Potassium k13

    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


    Potassium k14

    Potassium (K+)

    • Hypokalemia Causes

      • Renal losses

        • DKA

        • Diuretics: thiazide, loop diuretics

        • Drugs: amphotericin B, Cisplastin

        • Hypomagnesemia

        • Alkalosis

        • Hyperaldosteronism

        • Licorice ingestion

        • Gitelman & Bartter syndrome


    Potassium k15

    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


    Potassium k16

    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


    Potassium k17

    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


    Basic metabolic panel3

    Basic Metabolic Panel

    Na+Cl-BUN Ca++

    GluMg++

    K+HCO3--CrPhos--


    Bicarb hco 3

    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


    Bicarb hco 31

    Bicarb (HCO3--)

    • Metabolic acidosis

      • Anion gap: Na – (Cl + bicarb)

      • Normal range: 12 +/- 2


    Bicarb hco 32

    Bicarb (HCO3--)

    • Metabolic acidosis: causes for increase anion gap

      • M

      • U

      • D

      • P

      • I

      • L

      • E

      • S


    Bicarb hco 33

    Bicarb (HCO3--)

    • Metabolic acidosis:causes for increaseanion gap

      • Methanol

      • Uremia

      • DKA

      • Paraldehyde or propylene glycol

      • Isoniazid

      • Lactic acidosis

      • Ethyleneglycol

      • Salicylates


    Bicarb hco 34

    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:


    Bicarb hco 35

    Bicarb (HCO3--)

    • Metabolic acidosis Clinical presentation

      • Chest pain, palpitation

      • Kussmaul respirations

      • Hyperkalemia

      • Neuro: lethargy, stupor, coma, seizures

      • Cardiac; arrhythmias, decreased response to Epinephrine, hypotension


    Bicarb hco 36

    Bicarb (HCO3--)

    • Metabolic acidosis Treatment

      • pH<7.1, risk of arrhythmias

      • IV bicarb

      • Dialysis


    Bicarb hco 37

    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


    Basic metabolic panel4

    Basic Metabolic Panel

    Na+Cl-BUN Ca++

    GluMg++

    K+CO3--CrPhos--


    Glucose

    Glucose

    • Hypoglycemia Causes

      • Complication of DM therapies

      • Hyperinsulinemia

      • Inborn errors of metabolism

      • Alcohol

      • Starvations

      • Infections, organ failure


    Glucose1

    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


    Glucose2

    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)


    Basic metabolic panel5

    Basic Metabolic Panel

    Na+Cl-BUNCa++

    GluMg++

    K+CO3--CrPhos--


    Calcium

    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)]


    Calcium1

    Calcium

    • Roles:

      • Coagulation

      • Cellular signals

      • Muscle contraction

      • Neuromuscular transmission

    • Controlled by parathyroid hormone and vitamin D


    Calcium2

    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


    Calcium3

    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


    Calcium4

    Calcium

    • HypercalcemiaTreatments

      • Fluid & diuretics

        • Forced diuresis

        • Loop diuretic

      • Oral supplement: biphosphate or calcitonine

      • Glucocorticoids

      • Dialysis


    Calcium5

    Calcium

    • HypocalcemiaCauses

      • 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


    Calcium6

    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


    Calcium7

    Calcium

    • Hypocalcemia: Treatments

      • Supplements

        • IV: gluconate or chloride with EKG change

        • Oral calcium with vitamin D


    Basic metabolic panel6

    Basic Metabolic Panel

    Na+Cl-BUN Ca++

    GluMg++

    K+CO3--CrPhos--


    Magnesium

    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


    Magnesium1

    Magnesium

    • Hypermagnesemia: Causes

      • Hemolysis

      • Renal insuficiency

      • DKA, adrenal insufficiency, hyperparathyroidism, lithium intoxication


    Magnesium2

    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


    Magnesium3

    Magnesium

    • Hypermagnesemia: Treatments

      • Calcium infusion

      • Diuretics

      • Dialysis


    Magnesium4

    Magnesium

    • HypomagnesemiaCauses

      • 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


    Magnesium5

    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


    Magnesium6

    Magnesium

    • Hypomagnesemia: Treatments

      • Oral or IV supplement

      • Correct on going loss


    Basic metabolic panel7

    Basic Metabolic Panel

    Na+Cl-BUN Ca++

    GluMg++

    K+CO3--CrPhos--


    Phosphorus

    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


    Phosphorus1

    Phosphorus

    • Hyperphosphatemia

      • Causes

        • Hypoparathyroidism

        • Chronic renal failure

        • Osteomalacia

      • Presentations

        • Ectopic calcification

        • Renal osteodystrophy

      • Treatments

        • Dietary restriction

        • Phosphate binder


    Phosphorus2

    Phosphorus

    • HypophosphatemiaCauses

      • Re-feeding syndrome

      • Respiratory alkalosis

      • Alcohol abuse

      • Malabsorption


    Phosphorus3

    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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