Electrolyte Disturbances

Name: Electrolyte Disturbances
Uploaded: 2017-07-06T07:30:46+00:00
Duration: PTM34S14
Channel: Earl Barrell
Description: 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--
- Not common BMP, other places call it chem 7

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 Intracellular Na is constant and important in cellular activity Balance btw intake & excretion. Poorly understood mechanism. Some salt craving in some salt wasting diseases High sodium concentration in cow’s milk. Children take in less

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 -active transport with Chloride at the Loop of Henle

Sodium (Na+) Normal SNa: 135-145 Major component of serum osmolality
Sosm = (2 x Na+) + (BUN / 2.8) + (Glu / 18) Normal: Alterations in SNa reflect an abnormal water regulation

Sodium (Na+) Hypernatremia: Causes Excessive intake Water deficit:
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 IDDM: glucose causes increases ECF osmotic pressure draws water out of cells  artificially decrease Na 1.6 mEq/L / 100mg/dL of glucose above 100 Glucosuria  polyuria with free water loss

Sodium (Na+) Hypernatremia Clinical presentation Dehydration
“Doughy” feel to skin Irritability, lethargy, weakness Intracranial hemorrhage Thrombosis: renal vein, dura sinus Intracellular fluid loss causes doughy feel to skin ICH: tearing of bridging veins

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 hrs Remaining next 24 hrs Fluid should contain additional lytes; watch for glucose infusion Fluid rate: maintenance + correction + on going losses Fluid lytes: start with ½ NS and decrease to ¼ NS if necessary if Na does correct appropriately

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

Sodium (Na+) Hyponatremia: Etiology Hypervolemic Hypovolemic
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 - Beer potomania: excessive consumption of beer Low na, poor intake of other nutrition  profound hyponatremia - Glucocorticoids stimulate Na absorption in the GI tract

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 Central pontine myelinolysis – rapid correction of hyponatremia  water shifts from cell to extracellular space; sx; quadraparesis, dysphagia, dysarthria, diploplia, LOC associated with brain stem damage; no tx; poor prognosis; most die; survival 1/3; 1/3; 1/3 (recovered, disabled and severely disabled) - Sz threshold 125; HS: 5cc/kg  3-4 mEq/L

Sodium (Na+) Fill in the blanks Urine Output Serum Na Urine Na
Serum Osm Urine Osm DI SIADH CSW

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 - Major secretion again active Na re-absorption; also associated with H+ and NH3 excretion

Potassium (K+) Solvent drag Acidosis
Increase in Sosmo  water moves out of cells  K+ follows 0.6 SK / 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 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 Increase intake
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 Succinylcholine: inhibits repolarization (required to cellular re-uptake of K) Digitalis overdose: inhibits Na-K exchange by cell membrane

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 calcium: increases threshold potential  decrease cardiac cell excitability Bicarb: stimulate an exchange of cellular H+ for Na+, thus stim Na,K ATPase Insulin: shift K into cells via Na,K-ATPase; last a few hours Beta agonist: promote K shift into cells

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 Hypokalemic periodic paralysis: defects of muscular ion channels and transporters Colas consumption: diuretic effect of caffeine, diarrhea caused by fructose ingestion

Potassium (K+) Hypokalemia Causes Renal losses DKA
Diuretics: thiazide, loop diuretics Drugs: amphotericin B, Cisplastin Hypomagnesemia Alkalosis Hyperaldosteronism Licorice ingestion Gitelman & Bartter syndrome DKA: urine loss due to polyuria & volume contracion, also as cationic partner to the negatively charge ketone, Beta-hydrocybutyrate Mg require to process K Alkalosis: 1/ shift K into cells; 2/elevate bicarb cause increase in urine excretion of bicarb dragged k as partner cation Licorice has glycyrhizin: deficiency in 11-beta hydroxysteroid dehydrogenase  stimulate aldosterone receptors Hereditary syndrome; similar mechanism as diuretics

Potassium (K+) Hypokalemia Presentation ECG changes
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

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 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 Panel Na + Cl- BUN Ca++ Glu Mg++ K+ HCO3-- Cr 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

Bicarb (HCO3--) Metabolic acidosis Anion gap: Na – (Cl + bicarb)
Normal range: 12 +/- 2

Bicarb (HCO3--) Metabolic acidosis: causes for increase anion gap M U
Methanol, Uremia, DKA, Paraldehyde or Propylene Glycol (anti freeze or ativan solvent), Isoniazid, Lactic Acidosis, Ethylene Glycol, salycilates

Bicarb (HCO3--) Metabolic acidosis: causes for increase anion gap
Methanol Uremia DKA Paraldehyde or propylene glycol Isoniazid Lactic acidosis Ethylene glycol Salicylates Methanol, Uremia, DKA, Paraldehyde or Propylene Glycol (anti freeze), Isoniazid or iron, Lactic Acidosis, Ethylene Glycol, salicylates - Propylene glycol – Lorazepam solvent

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: - Toluene: paint thinner

Bicarb (HCO3--) Metabolic acidosis Clinical presentation
Chest pain, palpitation Kussmaul respirations Hyperkalemia Neuro: lethargy, stupor, coma, seizures Cardiac; arrhythmias, decreased response to Epinephrine, hypotension - Exacerbation of pulmonary hypertension

Bicarb (HCO3--) Metabolic acidosis Treatment
pH<7.1, risk of arrhythmias IV bicarb Dialysis - Exacerbation of pulmonary hypertension

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 Vomiting: loss of hydrochloric acid Contraction alkalosis: loss of water in the EC space which is poor in bicarb Hyperaldosteronism: increase excretion of H+ via Na,H exchange protein  alkalosis

Glucose Hypoglycemia Causes Complication of DM therapies
Hyperinsulinemia Inborn errors of metabolism Alcohol Starvations Infections, organ failure

Glucose Hypoglycemia Clinical presentation Adrenergic Neuroglycopenic
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 - borborygmus; stomach rumbling, growling, gurgling, grumbling or wambling

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) Lower in neonates Limitation of D25 is IV access. D10 is readily available

Calcium Normal range: 8.8-10.1 with half bound to albumin
Ionized (free or active)calcium: – relevant for cell function Majority is stored in bone Hypoalbuminemia  falsely decreased calcium Cac = Cam + [0.8 x (Albn – Alb m)] 99% stores in bone

Calcium Roles: Controlled by parathyroid hormone and vitamin D
Coagulation Cellular signals Muscle contraction Neuromuscular transmission Controlled by parathyroid hormone and vitamin D

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 - malignancy: breast, squamous cell carcinoma

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

Calcium Hypercalcemia Treatments Fluid & diuretics
Forced diuresis Loop diuretic Oral supplement: biphosphate or calcitonine Glucocorticoids Dialysis Biphosphate: high affinity for bone, taking up by osteoclasts and inhibit osteroclast bone resorption Calcitonin: blocks bone resorption and also increases urinary calcium excretion by decrease absorption Glucocorticoids: increase urinary excretion and decrease intestinal absorption

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 Hungry bone syndrome: severe and prolonged hypocalcemia despite high to normal PTH level Absent of vitamin D: decrease intake or sun exposure, defective metab in AED, Rickets Ineffective vitamin D: malaborsorption, Rickets, type II - acrodynia

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 Trousseau; eliciting carpal spasm by inflating the blood pressure cuff above systole for three min Chvostek’s sign: tapping of the inferior portion of the zygoma will produce facial spasm

Calcium Hypocalcemia: Treatments Supplements
IV: gluconate or chloride with EKG change Oral calcium with vitamin D

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

Magnesium Hypermagnesemia: Causes Hemolysis Renal insuficiency
DKA, adrenal insufficiency, hyperparathyroidism, lithium intoxication

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 - Mg acts as physiology calcium blocker causing arrhythmias

Magnesium Hypermagnesemia: Treatments Calcium infusion Diuretics
Dialysis - Calcium to counteract the activity on the neuromuscular and cardiac function

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 Increase renal excretion: via alcohol stim or DKA, hypophos, hyperaldosterron

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 Athetosis: involuntary convoluted involuntary movement of the fingers, arms, legs and necks.

Magnesium Hypomagnesemia: Treatments Oral or IV supplement
Correct on going loss

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

Phosphorus Hyperphosphatemia Causes Presentations Treatments
Hypoparathyroidism Chronic renal failure Osteomalacia Presentations Ectopic calcification Renal osteodystrophy Treatments Dietary restriction Phosphate binder - PTH inhibits renal absorption of Phos

Phosphorus Hypophosphatemia Causes Re-feeding syndrome
Respiratory alkalosis Alcohol abuse Malabsorption Refeeding syndrome: demand phos in cells due to the action of phosphofructokinase, attach phos to glucose for metabolism Alkalosis move phos into cells Alcohol: impairs phos absorption, poor nutrition, DT cause respiratory alkalosis Malabsorption: GI damage, lack of vit D, use of phosphate binders (sucrafate), aluminum containing antacids

Phosphorus Hypophosphatemia Clinical presentation Treatments
Muscle dysfunction and weakness: diploplia, low CO, dysphagia, respiratory depression AMS WBC dysfunction Instability of cell membrane  rhabdomyolysis Treatments supplementation -

Electrolyte Disturbances

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