Electrolyte imbalance Dr Mohammed Al-Ghonaim MBBS FRCP C

Electrolyte imbalance Dr. Mohammed Al-Ghonaim MBBS, FRCP(C)

Goals of this Tutorial • SESSION OBJECTIVES – Learn to effectively assess and manage various electrolyte abnormalities (NA, K) – Apply your knowledge to real cases! • LEARNING METHODS – Lecture/material review – Interactive case scenarios

Body’s fluid compartments

Sodium disorders: body’s fluid compartments • • • TBW = WEIGHT x. 5 (women) or. 6 (men) TBW x 1/3 = ECF TBW x 2/3 = ICF ECF x 2/3 = Interstitial compartment ECF x 1/4 = Intravascular compartment What regulate Sodium balance?

Water content of the blood HIGH Water content of the blood LOW Too much water drunk Too much salt or sweating Brain produces More ADH Brain produces Less ADH Water content of the blood normal High volume of water reabsorbed by kidney Low volume of water reabsorbed by kidney Urine output LOW Urine output HIGH (small volume of Concentrated urine) (large volume of dilute urine)

Sodium disorders • [Na] is a measure of Na relative to water. • It tells you NOTHING about the total body sodium. Abnormalities in the Na concentration tell us that there abnormalities in the amount of WATER in the ECF compartment.

Hyponateremia • Plasma [Na+ <135 • Approach: – Calculate serum Osmolality • Osmolality = Osmoles/kg of water • 2(Na+) + Glucose + BUN • Normal is 285 -295 – Determine volume status

Case Study: (1) 23 yr old male develops watery diarrhea. He comes to your ER lightheaded and orthostatic. On exam: - dry MM and tachycardia. - Neuro exam is normal and he is alert. - Labs: Na 129, K 3, HCO 3 20, BUN 4, Cr 88, Glucose 75, Urine Na 5, Urine osm 520.

Hyponatremia Serum OSM Low Hypotonic Hyponatremia Normal High Marked hyperlipidemia (lipemia, TG >35 m. M) Hyperproteinemia (Multiple myeloma) Hyperglycemia Mannitol *Note: all have ↑ADH • SIADH: inappropriate • Rest: appropriate ECFv * Low Renal loss (UNa > 20) Extra-renal loss (UNa <10) • Diuretics • Bleeding • Thiazide • Burns • K-sparing • GI (N/V, diarrhea) • ACE-I, ARB • Pancreatitis • IV RTA, Hypoaldo • Cerebral salt wasting Normal • Hypothyroidism • AI • SIADH • Reset Osmostat • Water Intoxication 1° Polydipsia TURP post-op High • CHF • Cirrhosis • Nephrosis

Hyponateremia • Hyponatremia with high osmolality: [Na] is low since water will flow into the ECF compartment as a result of hyperglycemia for example. – The calculated and measured osm will be elevated in that case. Na will decrease by approx 1. 6 meq/d. L for every 100 mg/dl increase in glucose above 100. – In the case of mannitol the measured osm will be high but the calculated osm will be low.

Case Study: (1) continue • Diagnosis: – First step: calculate osmolality • Low ( ) – Second step: Volume status • Low ECF volume • Treatment: – Acute vs Chronic – Any neurological symptoms

Case study-2 • 72 yr old woman with DM presents to ER with polyuria and polydipsia x 5 days. • Normal physical examination. • Labs: – Na 129, K 4. 2, Cl 89, HCO 2 3. 4, BUN 5, Cr 88, Glucose 780. • What is the osm? • Why is he hyponatremic? • What is the corrected Na? • What is the treatment

Case study-3 • A 50 yr old male with h/o hyperlipidemia has the following labs: • Na 125, M-Osm 270, TGs 1000, total protein 85.

Case study-4 • 72 yr old male who is a heavy smoker presents with cough and hemoptysis. • His physical exam is completely normal in terms of volume status. • CXR reveals a 6 cm left sided chest mass. • Labs: Na 125, K 4. 2, Cr 1. 1, M OSM 270, Urine Na is 45. He takes no meds. TSH and am cortisol are normal. • What is causing the hyponatremia

Case Study: (5) • A 72 -year-old woman presents with a 2 -day history of presyncope when rising from a chair. – Over the last week she has had a bout of viral gastroenteritis with diarrhea. – She is drinking 2– 3 L of water per day • Medications: – Hydrochlorothiazide, 25 mg/d, for HTN • On examination: – She had postural hypotension, JVP is low • Labs: – sodium 128 mmol/L, potassium 3. 1 mmol/L, creatinine 125 mmol/L and urea nitrogen 10 mmol/L.

Hypernateremia • Plasma [Na] >145 • Caused primarily by Na+ gain, or water deficit • Etiology: – Impaired thirst – Water loss • Renal • Extra renal – Na+ gain – Trans cellular shift

Hypernateremia

Case study: (1) • • • 76 yrs old male HTN, DM II, dementia Admitted to ICU with septic shock, intubated Called to see due to Na 154, Bp 125/76 mm. Hg, Urine out put 1. 3 L/day

Case study: (2) • • • 25 yrs old male presented with polyuria Found to have Na 156 Bp 110/67 mm. Hg, low JVP Urine out put=6 L/day Urine osmolality 100 Calculate the osmolar excretion rate – 6 x 100 = 600 Mosmole • Replace the fluid deficit • Dx Diabetes insipidis (central Vs nephrogenic)

Potassium disorders • Potassium is one of the body's major ions. – 98% of the body's potassium is intracellular – Total body potassium stores 50 m. Eq/kg (ie, approximately 3500 m. Eq in a 70 -kg person). • potassium homeostasis: – GI absorption is complete • daily intake of 1 m. Eq/kg/d (60 -100 m. Eq) – 90% of this excess is excreted through the kidneys – 10% is excreted through the gut • Normal K level: 3. 5 – 5. 0

Hypokalemia • K < 3. 5 m. Eq/L • Clinical manifestations: – Fatigue – Cramps – Constipation – Weakness / Paralysis – Parasthesias – Arrhythmias

EKG Changes in Hypokalemia – Flattened T waves – ST depressions – Prominent U waves – Prolonged QT – Prolonged PR interval

Pathophysiology of hypokalemia • Deficient intake (Poor potassium intake) • Due to a shift from extracellular to intracellular • Increased excretion – Renal – Extra renal

Case study: (1) • 35 yrs old male • HTN on treatment • Found to have hypokalemia (K=2. 9) referred for evaluation. • HCO 3=29 • Urine K (spot)= 30

How to asses kidney response? • Urinary excertion of K – U k < 15 mmol/l in hypokalemia – U k > 200 mmol/l in hyperkalemia • TTKG < 2 in hypokalemia • >8 in hyperkalemia

Approach to Hypokalemia • Step 1: Redistribution or depletion? – Redistribution causes • Insulin therapy (usually in DKA) • Beta 2 agonists (e. g. albuterol) • Metabolic alkalosis – Replacement of potassium in these settings may lead to overshoot and hyperkalemia

Approach to Hypokalemia • Step 1: Redistribution or depletion? – Depletion causes (common) • • GI tract losses (diarrhea, vomiting) Loop/thiazide diuretic therapy Other medications (e. g. amphotericin B) Osmotic diuresis (DKA) Endocrinopathies (mineralocorticoid excess) Salt wasting nephropathies/RTA’s Magnesium deficiency

Approach to Hypokalemia • Step 2: Estimate the deficit – For every 100 m. Eq below normal, serum K+ usually drops by 0. 3 m. Eq/L • Highly variable from patient to patient, however!! • For every 10 m. Eq below normal, serum K+ usually drops by 0. 1 m. Eq

Approach to Hypokalemia • Step 3: Choose route to replace K+ – In nearly all situations, ORAL replacement is PREFERRED over IV replacement • Oral is quicker • Oral is less dangerous • Increase dietary intake – Potatoes / Bananas – Choose IV therapy ONLY in patients who are NPO (for whatever reason) or who have severe depletion

Approach to Hypokalemia • Step 5: Choose dose/timing – Mild/moderate hypokalemia • 3. 0 to 3. 5 m. Eq/L • 60 -80 m. Eq PO (or IV) QD, divided doses • Sometimes will require up to 160 m. Eq QD (severe diarrhea, IV diuretics) • Avoid too much PO at once – GI upset or just poor response • Usually divide as BID or TID dosing – Severe hypokalemia (< 3. 0 m. Eq/L) • Can use combination of IV and PO • Avoid more than 60 -80 m. Eq PO in a single dose • Avoid IV infusion rates faster than 20 m. Eq/hour—can cause arrhythmia!!!

Approach to Hypokalemia • Step 6: Monitor/reassess – Severe hypokalemia, DKA patients • Reassess labs Q 4 -6 hours – Moderate hypokalemia, IV diuresis patients • Reassess labs BID to TID as needed – Mild hypokalemia • Reassess labs QD or less as needed

Summary: Hypokalemia – PO almost always preferred over IV – KCl is preferred preparation – Don’t give too much too quickly – Be gentle in renal failure patients – Don’t forget to check magnesium levels in refractory patients

Hyperkalemia • Symptoms – Usually asymptomatic – Muscle weakness / paralysis – EKG abnormalities • • • Peaked T waves ST depression 1 st degree AVB QRS widening “Sine wave sign”

Hyperkalemia • Elevated potassium level should be evaluated as to the following: • Step 1: Is it real? • Step 2: If real, why did it happen? • Step 3: Is this an emergency? • Step 4: Emergency Rx

Pathophysiology of Hyperkalemia • Increase dietary intake • shift of K from ICF to ECF such as: – acidosis – beta blocker – insulin deficiency – periodic paralysis • Decrease renal excretion :

EKG changes in Hyperkalemia

Approach to Hyperkalemia • Step 1: Is it real? – Assess for/exclude pseudohyperkalemia • Hemolysis—ask the nurse/phlebotomist/lab tech – If suspected—order STAT repeat K+ level • Potassium infusion—ask the nurse – If suspected—order STAT repeat K+ level from peripheral vein AWAY from infusion site • Check CBC (WBC > 70, 000, PLT > 1, 000) – K+ moves out of WBC’s, PLT’s after clotting – If suspected—order STAT serum/plasma K+ levels » if serum K+ > plasma K+ by more than 0. 3 m. Eq/L, suspect pseudohyperkalemia – In any case, have low threshold to repeat labs

Approach to Hyperkalemia • Step 2: If real, why did it happen? – Acute or chronic renal failure – Medications (K+ sparing diuretics, ACE inhibitors, ARB’s, BB’s, digoxin, etc. ) – Endocrinopathies – K+ supplements or salt substitutes – K+ in IV infusions/TPN

Approach to Hyperkalemia • Step 3: Is this an emergency? – How high is the potassium level? • If serum K+ > or = 6. 0 m. Eq/L, then treat as emergency – Are there any EKG changes consistent with hyperkalemiainduced cardiac instability? • If yes, then treat as emergency • Remember, the lack of EKG changes is NOT always entirely reassuring

Approach to Hyperkalemia • Step 3 (con’t): EKG assessment – Four stages of EKG changes • • Peaked T waves PR prolongation QRS widening Sine waves • PEA or asystole

Approach to Hyperkalemia • Step 4: Emergency Rx – Part A: oppose toxic effects on cell membrane • IV calcium infusion (gluconate preferred over chloride) – Less toxic effects if IV extravasation • Give 1 -2, 10 m. L ampules of 10% Calcium gluconate over 2 -5 minutes • Keep EKG machine attached to patient!!! – EKG changes will diminish in 1 -3 minutes – Action: Stabilization of cardiac cells. Does not lower potassium. Used for hyperkalemia with EKG changes. – If EKG changes do not immediately resolve, dose can be repeated in 5 minutes.

Approach to Hyperkalemia • Step 4 (con’t): Emergency Rx – Part B: Shift K+ into cells • Will buy you 1 -4 hours before direct elimination methods “kick-in” • Insulin/dextrose therapy – – Give 10 U regular insulin IV push, together with 1 ampule (50 m. L) D 50 IV push Follow this with a D 5 containing IV maintenance fluid for several hours. Effect within 15 minutes. Peak effect 60 min. Duration 3 -4 hours. • Adjuncts – Beta agonist: – Albuterol nebulizer » Peak effect in 90 minutes – Sodium bicarbonate 1 ampule IV push – Onset: 30 minutes – Duration: 60 -120 minutes

Approach to Hyperkalemia • Step 5: Emergency or non-emergency therapy (usually takes 4 -6 hours to work) – Direct elimination of K+ from body – Sodium polystyrene sufonate (K+ binding resin) plus sorbitol • Give Kayexalate 30 -60 gm – PO if patient can tolerate – PR (retention enema) if upper GI problems – Patient needs to have a colon for this to work! – Hemodialysis as last resort or in severe cases

Summary: Hyperkalemia – Make sure it’s real – Determine emergent or not • Degree of hyperkalemia, EKG – Treat emergent cases with calcium gluconate, insulin, dextrose, and kayexalate +/- dialysis – Monitor closely for response to treatment—watch for rebound – Fix the cause if possible