Electrolyte Disturbances

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++ Glu Mg++ K+ CO3--Cr 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,K-ATPase system • Excretion: urine, sweat & feces • Kidneys are the principal regulator

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 (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 (Na+) • Hypernatremia: Causes • Excessive intake • Improperly mixed formula • Exogenous: bicarb, hypertonic saline, seawater • Water deficit: • Central & nephrogenic DI • Increased insensible loss • Inadequate intake

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 (Na+) • Hypernatremia 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

Sodium (Na+) • Hyponatremia • Na+<135 • Seizure threshold ~125 • <120 life threatening

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

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 (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 (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 (Na+) Fill in the blanks

Basic Metabolic Panel Na + Cl-BUN Ca++ Glu Mg++ K+ CO3--Cr 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

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 (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 (K+) • Hyperkalemia • >6.5 – life threatening • Potential lethal arrhythmias

Potassium (K+) • Hyperkalemia Causes • Spurious • Difficult blood draw  hemolysis  false reading • Increase intake • Iatrogenic: IV or oral • Blood transfusions

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 (K+) • Hyperkalemia Causes • Trans-cellular shifts • 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

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 (K+)

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 (K+) • Hyperkalemia Treatment • Increase elimination • Hemodialysis or hemofiltration • Kayexalate via feces • Furosemide via urine

Potassium (K+) • Hypokalemia • <2.5: life threatening • Common in severe gastroenteritis

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 (K+) • Hypokalemia Causes • Renal losses • DKA • Diuretics: thiazide, loop diuretics • Drugs: amphotericin B, Cisplastin • Hypomagnesemia • Alkalosis • Hyperaldosteronism • Licorice ingestion • Gitelman & Bartter syndrome

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 (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

Electrolyte Disturbances