Electrolyte Management

1. Electrolyte Management Christopher Powe, Ph.D., ACNP-BC President | Principle Global Training Institute

2. Objectives • Discuss Electrolyte Abnormalities • Discuss Signs and Symptoms of Electrolyte Abnormalities • Discuss Causes of Electrolyte Abnormalities • Discuss Treatment for Electrolyte Abnormalities

3. Potassium • Normal value 3.5-4.5 • Major intracellular cation • Na+-K+-adenosine triphophatase pump actively transport Na out of the cell and K into the cell at a 3:2 ratio. • 90% is absorbed in the GI tract • Major route of excretion is the kidneys • Secretion is regulated by aldosterone and hyperkalemia • Aldosterone is regulated by the renin, angiotensin II or hyperkalemia • pH changes are 0.1 to 0.7(check this)

4. Potassium Alterations • Hypokalemia • Hyperkalemia

5. Hypokalemia • Potassium level <3.5 • Symptoms seldom seen until K+ less than 3.0 • Common • Fatigue, Myalgia, Muscular weakness • Severe Hypokalemia • Hypoventilation, paralysis, Arrhythmias, • EKG changes; Flatten or inverted T waves, U wave, ST segment depression, prolonged QU interval, that may progress to wide QRS, increased PR interval, low voltage states.

6. Hypokalemia Causes • Decreased intake • Transcellular Shift; pH changes, B2 adrenergic agonists • Non-Renal loss; NGT, vomiting, laxative abuse, diarrhea • Renal loss; Diuretics, primary hyperaldosteronism (CA), hyper-reninemia (renal HTN)

7. Hypokalemia Treatment • Replace K+ deficit • Prevent life threatening complications • Minimize ongoing losses • Treat underlying cause • P.O.; Change of 1mEq/L plasma may equal 200-400mEq deficit in total. • IV; Infusion at 10mEq by PIV and max of 20mEq central line access.

8. Hyperkalemia • K+ level > 4.5 • Symptoms are peaked T waves, widen QRS, and cardiac toxicity. • Partial depolarization of the cell membrane results in weakness, flaccid paralysis, and hypoventilation • Will cause an inhibition of renal ammoniagenesis and reabsorption of NH4+ resulting in metabolic acidosis and further resulting of cellular shifts and pH alterations.

9. Hyperkalemia Causes • Increased intake • Psuedohyperkalemia from cellular shifts following venipuncture • Transcellular shifts; rhabdomyolysis, succinylcholine, hyperglycemia • Decreased renal excretion; impaired Na+ reabsorption (Addison’s, Heparin if pt. is DM, CRF, ACE use, Diuretic use or NSAID’s), Increased Cl- reabsorption (renal failure)

10. Hyperkalemia Treatment • Depends on EKG changes • Calcium Gluconate 10%; lasts 30-60 minutes. Can be repeated if no EKG changes seen in 5-10 minutes. • Insulin 10-20 units & Glucose 25-50 gms. K+ level will fall 1-1.5 mEq/l in 15-30 minutes • NaHCO3 X3. Mix in dextrose 5%; only in severe cases. Renal patient will not respond • B2-adrenergic agonist; onset in 30 minutes and lasts 2-4 hours • Loop diuretics • Cation exchange resins; Kayexalate; 1-2 hours onset and lasts 4-6 hours. Lowers K+ by 0.5-1.0mEq/l. Dose of 25-50gms • Hemodialysis or peritoneal dialysis, (less effective)

11. Calcium • Bone formation and neuromuscular function. • 99% in bone. • 50% ionized. • Metabolism is regulated by the parathyroid hormone and vitamin D metabolites

12. Hypercalcemia • Almost always a result of entry into ECF, by bone absorption or intestinal absorption. • Primary hyperparathyroidism; most common in ambulatory patients. (85% are from adenoma of a single gland) • Malignancy; most cases in hospital patients. Tumors cells stimulate osteoclastic and bone absorption • Other causes; sarcoidosis, Vit D toxicity, hyperthyroidism, lithium use, immobolization.

13. Hypercalcemia Symptoms • Normal 8.6-10.3 mg/dl • Most common when exceeds 12 • Rapid onset may produce a more rapid symptom development • Renal; Polyuria, nephrolithiasis, (renal failure if above 13) • GI; anorexia, N/V and constipation • Neuro; weakness, fatique, confusion, stupor, and coma • ECG; QT shortened

14. Hypercalcemia Treatment • Replace ECF by normal saline and restore normal GFR (300-500ml/hr until normal volume has been replaced) • Saline induced diuresis, (100-200ml/hr) Measure chemistry Q 6-12 hours. • Pamidronate for inhibition of bone reabsorption. • Calcitonin for inhibition of bone absorption.Will lower Ca++ in 1-2 hours by 1-2 mg/dl. (less potent but fewer side effects. • Plicamycin for inhibition of bone reabsorption. Second line agent d/t side effects (thrombocytopenia, renal failure, liver failure) • Glucocorticoids lower CA by inhibiting cytokine release and by direct cytolytic effects on some tumors. Decrease intestinal absorption and increase renal excretion. • Oral Phosphate; inhibits Ca absorption and promotes Ca deposition in bone and soft tissue. Use only if Phos level is 3.0mg/dl and normal renal function. No IV phos. Treatments may cause soft tissue calcification. • Parathyroidectomy. Indications for hyperparathyroidism and • symptomatic • Nephrolithiasis • Reduced bone mass • Serum Ca >12mg/dl • Age under 50 • Ifesable long-term f/u

15. Hypocalcemia Symptoms • Chronic may be asymptomatic • Alkalosis augments Ca binding to albumin and increases severity. • Trouseau’s = carpal spasm with BP cuff inflated above systolic for 3 minutes • Chvostek’s = twitching of facial muscle with tapping facial nerve anterior to ear • Latent tetany • Lethargy and confusion • Rare laryngospasm • Seizures • Heart failure • ECG with prolonged QT interval • Chronic will have cataracts and calcification in the basal ganglia

16. Hypocalcemia Treatment • Acute emergency for symptomatic patient with Calcium Gluconate 2 gms over 10 mins. • Ca gluc. 6gms in D5W over 4-6 hours (treat Mg if low) • Monitor for digoxin toxicity • Ca suppliments and Vit D for absorption 1-2 gms elemental Ca p.o., TID. Vit D 400-1000IU/day. • Lower phosphate before treatment if hyperphosphatemia <6.5mg/dl • Calcitrol 0.25-0.5mcg p.o. each day

17. Phosphorus • Hyperphosphatemia • Hypophosphatemia • Critical for bone formation (85%) and cellular metabolism (14%) and 1% in ECF • Major regulatory factors; PTH that lowers phos by renal excreation, Insulin which lowers phos by shifting into cells, 1,25(OH)2D3 which enhances intestinal absorption.

18. Hyperphosphatemia • Causes • Most often resulting from renal failure • Hypoparathyroidism • Rhabdomyolysis • Tumor lysis syndrome • Metabolic and respiratory acidosis • Excessive Phosphate administration

19. Hyperphosphatemia • Signs and Symptoms • Same as hypocalcemia • Trouseau’s = carpal spasm with BP cuff inflated above systolic for 3 minutes • Chvostek’s = twitching of facial muscle with tapping facial nerve anterior to ear • Latent tetany • Lethargy and confusion • Rare laryngospasm • Seizures • Heart failure • ECG with prolonged QT interval • Chronic will have cataracts and calcification in the basal ganglia

20. Hyperphosphatemia • Management • Restrict dietary intake of phosphate • Calcium Carbonate 0.5-1.0gm elemental • Calcium p.o. intake with meals, alter dose every 2-4 weeks to max dose of 3gms TID • Goal is phosphate of 4.5-6.0 mg/dl • Keep serum Ca at 11 or greater by dose adjustment • Sevelamer; Binds phos through ion exchange. (may worsen metabolic acidosis) • N/S diuresis • Dialysis

21. Hypophosphatemia • Causes • Impaired intestinal absorption, excessive renal excretion, or redistribution into cells

22. Hypophosphatemia • Severe <1.0mg/dl • Alcohol abuse and withdrawal • Respiratory alkalosis • Malabsorption • Oral phosphate binders • Refeading after malnutrition • Hyperalimentation • Severe burns • DKA therapy. (IV phosphate should not be used in DKA)

23. Hypophosphatemia • Moderate hypophosphatemia (1-2.5mg/dl) • Common in hospitalized patients • Glucose infusions • Vitamin D deficiency • Renal phosphate loss d/t hyperparathyriodism • ATN diuresis • Renal transplant • Fanconi’s syndrome

24. Hypophosphatemia • Treatment • Oral • Nuetro-Phos • Neutro-Phos K • Fleet Phospho-Soda • IV • Potassium Phosphate • Sodium Phosphate • 0.08-0.16 mmol/kg for levels 2.5-5.0mg/dl

25. Magnesium Abnormalities (Causes) • Hypomagnesemia • Malnutrition • Malabsorption • Prolonged diarrhea • NGT suctioning • Increased renal excretion due to hypercalcemia, diuresis, aminoglycosides, amp.B • Hypermagnesemia • Occurs in renal failure • Antacids, laxatives • Treatment of pre-eclampsia with IV Mg

26. Magnesium Abnormalities Signs and Symptoms • Hypomagnesemia • Hypokalemia, hypocalcemia s/s, • Neuro • Lethargy, confusion, tremors, fasciculations, ataxia, nystagmus, tetany, siezures • Cardiac • Prolonged PR’, QT, atrial and ventricular arrhythmias • Hypermagnesemia • Seen only with levels >4 • Neuro • Areflexia, lethargy, weakness, paralysis, respiratory failure • Cardiac • Hypotensive, bradycardia, prolonged PR’ QT” QRS, asystole and heart block

27. Magnesium Treatment • Hypomagnesemia • Mild-or chronic with oral tab therapy • Mag-Ox 400 • Uro-Mag 140mg • Severe symptomatic • 1-2 gms IV over 15 minutes • Hypermagnesemia • Treat with 10% calcium glucanate in severe symptomatic cases • Withdraw intake of magnesium

28. Sodium • Hyponatremia <135mmol/l without hypoglycemia • S/S Extensive • Hypernatremia > 145mmol/l • Signs and symptoms • Altered L.O.C., weakness, seizures in severe cases • D/T water loss • Diuresis evaporation, GI, fever, exercise, burns and MV patients, diarrhea, • Na gain

29. Treatment for Hypernatremia • Correct slowly over 48-72 hours • No more than 12 mmol/l in 24 hours • DI with DDAVP 10mcg intranasal

30. Hyponatremia