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 normal

Water content of the blood HIGH

Water content of the blood LOW

Too much water drunk

Too much salt or sweating

Brain producesMore ADH

Urine output LOW

Brain produces Less ADH

Urine output HIGH

High volume of waterreabsorbed by kidney

Low volume of waterreabsorbed by kidney

(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 are 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, HCO3 20, BUN 4, Cr 88,

Glucose 75, Urine Na 5, Urine osm 520.

HyponatremiaSerum OSM

Low Normal High

HypotonicHyponatremia

ECFv *

LowNormal

High

HyperglycemiaMannitol

Marked hyperlipidemia(lipemia, TG >35mM)Hyperproteinemia(Multiple myeloma)

•CHF•Cirrhosis•Nephrosis

•Hypothyroidism•AI•SIADH•Reset Osmostat•Water Intoxication 1° Polydipsia TURP post-op

Renal loss (UNa > 20)•Diuretics

•Thiazide•K-sparing

•ACE-I, ARB•IV RTA, Hypoaldo• Cerebral salt wasting

Extra-renal loss (UNa <10)•Bleeding•Burns•GI (N/V, diarrhea)•Pancreatitis

*Note: all have ↑ADH•SIADH: inappropriate•Rest: appropriate

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/dL 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, HCO2 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 Na154, • Bp 125/76mmHg, • 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 mmHg, 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 mEq/kg (ie,

approximately 3500 mEq in a 70-kg person).• potassium homeostasis:– GI absorption is complete • daily intake of 1 mEq/kg/d (60-100 mEq)

– 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 mEq/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.• HCO3=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


• 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


• Step 2: Estimate the deficit– For every 100 mEq below normal, serum K+ usually

drops by 0.3 mEq/L• Highly variable from patient to patient, however!!• For every 10 mEq below normal, serum K+ usually

drops by 0.1 mEq


• 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 mEq/L• 60-80 mEq PO (or IV) QD, divided doses• Sometimes will require up to 160 mEq 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 mEq/L)• Can use combination of IV and PO• Avoid more than 60-80 mEq PO in a single dose• Avoid IV infusion rates faster than 20 mEq/hour—can cause

arrhythmia!!!


• Step 6: Monitor/reassess– Severe hypokalemia, DKA patients• Reassess labs Q4-6 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• 1st 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 0.3mEq/L, suspect pseudohyperkalemia

– In any case, have low threshold to repeat labs


• 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


• Step 3: Is this an emergency?– How high is the potassium level?

• If serum K+ > or = 6.0 mEq/L, then treat as emergency– Are there any EKG changes consistent with hyperkalemia-

induced cardiac instability?• If yes, then treat as emergency• Remember, the lack of EKG changes is NOT always entirely

reassuring


• 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, 10mL 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 10U regular insulin IV push, together with 1 ampule (50mL) D50 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


• 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

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