Hyperkalemia and other electrolytes disorders

Virtual Potassium for the Intern
(and other related electrolytes)

Intern Lecture Series
June 28th, 2011

Scott Pawlikowski, MD
Cardiology
Loyola University Medical Center / Hines VA

Goals of this Lecture
 SESSION OBJECTIVES
 Learn to effectively assess and manage
hyperkalemia
 Learn to address various electrolyte deficiencies
(low K+, low Mg2+, low phos, low Ca2+)
 Learn what serum electrolyte levels to follow in the
hospital, and how often to follow them
 Apply your knowledge to real cases!
 LEARNING METHODS
 Lecture/material review
 Interactive case scenarios
 Real cases and real intern approaches to electrolyte
disorders

What this lecture IS:
 A practical approach to handling
electrolyte disorders in MOST
hospitalized patients
 A guideline for supplementing
electrolytes based on experiential
and some evidence-based medical
recommendations
 Hopefully an informative and useful
tool

What this lecture IS NOT:
 A be-all, end-all list of all the causes
of hyperkalemia, hypokalemia, etc.
 A thorough review of all the large
center, prospective, randomized
controlled trials on electrolyte
replacement
 There really aren’t any!!!
 A complete reference that applies to
every patient you will treat

Some Electrolyte Reference Ranges
and Units (Hines VA)

 Potassium: 3.5 – 5.1 mEq/L
 Magnesium: 1.8 – 2.4 mg/dL
 Phosphorus: 2.5 – 4.5 mg/dL
 Calcium: 8.5 – 10.5 mg/dL

Hyperkalemia Overview
 Commonly encountered in

 Most feared consequence:
 PEA
 Asystole

 Urgent vs. Emergent therapy?
 Stepwise approach

Approach to Hyperkalemia: Step 1
 Is it real?
 Assess for/exclude pseudohyperkalemia
 Hemolysis—ask RN/phlebotomist/lab tech
 If suspected—order STAT repeat K+ level
 Potassium infusion—ask RN
 If suspected—order STAT repeat K+ level from
peripheral vein AWAY from infusion site
 Check CBC (WBC > 70K, 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

 If real, why did it happen?
 Acute or chronic renal failure
 Medications (K+ sparing diuretics, ACE
inhibitors, ARB’s, BB’s, digoxin, etc.)
 Endocrinopathies (hypoaldo, Addison’s)
 K+ supplements or salt substitutes
 K+ in IV infusions/TPN

 Is this an emergency?
 Did the K+ increase quickly?
 If yes, treat as emergency

 How high is the potassium level?
 If serum K+ ≥7.0 mEq/L, treat as emergency

 Any EKG changes of cardiac instability?
 If yes, treat as emergency

 Remember, the lack of EKG changes is NOT

always entirely reassuring

 EKG assessment
 Four stages of EKG changes
 Peaked T waves
 PR prolongation/loss of P wave (unstable)

 QRS widening (unstable)

 Sine waves (very unstable)

 The “fifth” and final stage if
hyperkalemia not addressed…
 PEA or asystole (i.e. cardiac arrest)

 Emergency therapy
 Part A: oppose toxic effects on cell membrane
 IV calcium infusion

 Chloride: 3x the elemental calcium of gluconate
 Gluconate: less toxic if IV extravasates
 Give 10mL ampule of 10% Calcium chloride
vs. gluconate over 2-5 minutes
 Too fast—pukey pukey!!!
 Can repeat in 3-5 minutes if no EKG effect
 Keep EKG machine attached to patient!!!
 EKG changes will diminish in 1-3 minutes

 Emergency therapy
 Part B: Shift K+ into cells
 Will buy you 1-4 hours before direct
elimination methods “kick-in”
 Insulin/dextrose therapy
 Regular insulin10 units IV push
 50% Dextrose (“D50”) 1 ampule IV push
 Adjuncts (usually not necessary)
 Albuterol nebulizer (continuous neb)
 Sodium bicarbonate 1 ampule IV push
 Only really helpful with coexistant acidosis

 Beware rebound hyperkalemia!!!

 Direct elimination of K+ from body
 Usually takes 4-6 hours to work
 Kayexalate (K+ binding resin/laxative combo)
 Give 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!

 Lasix?
 Works best when volume overloaded

 Hemodialysis (always discuss with renal fellow)
 Last resort or in severe cases

 Housekeeping/Follow Up
 Try to reverse/prevent/treat the cause
 Treatment of acute kidney injury
 Medication adjustment
 Monitor and reassess closely
 Should check serum K+ 4-8 hours after Rx initiated
 Beware of rebound hyperkalemia, especially if
cellular shift Rx used!!
 ALWAYS discuss digitalis-toxicity associated
hyperkalemia with your senior resident!!!
 Calcium infusion can potentiate the toxicity!!!

Hypokalemia Overview
 Occurs in over 20% of hospitalized patients

 Dangers
 Arrhythmia

 Rhabdomyolysis

 Paralysis

 Usually does NOT require emergency
supplementation over minutes to hours

Approach to Hypokalemia: Step 1
 Redistribution or depletion?
 Redistribution causes (cellular shift)
 Insulin therapy (usually in DKA)
 Beta 2 agonists (e.g. albuterol)

 Metabolic alkalosis

 Replacing K+ in these settings may
cause overshoot and hyperkalemia

 Redistribution or depletion?
 Depletion causes (common)
 GI tract losses (diarrhea, vomiting)

 Loop/thiazide diuretic therapy

 Other medications (e.g. amphotericin B)

 Osmotic diuresis (DKA)

 Refeeding syndrome (NEVER underestimate!)

 Endocrinopathies (Conn’s syndrome, e.g.)

 Salt wasting nephropathies/RTA’s

 Magnesium deficiency (NEVER overlook!)

What is Refeeding Syndrome?
 Spectrum of electrolyte/volume disorders

 Occurs when previously malnourished patients are
fed carbohydrate loads (PO or IV!)

 Triggered by intense insulin secretion

 Low phos/K+/Mg2+ (sometimes low blood sugar)

 Severe cases with unexplained CHF-like picture

 First identified/described in liberated POW’s,
concentration camp survivors from WWII

 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!!

 Dr. Popli’s estimation scheme
 For every 10 mEq below normal, serum
K+ usually drops by 0.1 mEq

 Choose route to replace K+
 In nearly all situations, ORAL
replacement PREFERRED over IV
 Oral is quicker
 Oral has less side effects (IV burns!)

 Oral is less dangerous

 Choose IV therapy ONLY in patients
who are NPO (for whatever reason) or
who have severe depletion

 Choose K+ preparation
 Oral therapy
 Potassium Chloride is PREFERRED AGENT
 Especially useful in Cl-responsive metabolic
alkalosis
 Potassium Phosphate useful when
coexistant phosphorus deficiency
 Often useful in DKA patients
 Potassium bicarbonate, acetate,
gluconate, or citrate useful in metabolic
acidosis (“-ate” = bicarb former)

 Choose K+ preparation
 IV therapy
 Adjunct to maintenance fluids (10-20 mEq/L)
 “The surgical intern’s way”
 Try to avoid using it!!!
 you often forget it’s there

 hyperkalemia can then develop, especially in

patients that get ARF in the hospital
 IV rider/”piggyback” (+/- lidocaine)
 Generally 40-60 mEq
 KCl is PREFERRED AGENT again
 Can also use KPhos, Kbicarb, etc.

 Avoid dextrose solution (trigger insulin, shift K+)

 Choose dose/timing
 Mild/moderate hypokalemia
 3.0 to 3.5 mEq/L
 60-80 mEq PO (or IV) QDay divided doses

 Sometimes will require up to 160 mEq per

day (refeeders, lots of diarrhea, IV
diuretics)
 Avoid too much PO at once

 GI upset or just poor response
 Usually divide as BID or TID dosing

 Choose dose/timing
 Severe hypokalemia (< 3.0 mEq/L)
 Can use combination of IV and PO, again
with PO preferred if at all possible
 Avoid more than 60-80 mEq PO in a

single dose
 Avoid IV infusion rates >20 mEq/hour

 Can cause arrhythmia!!!
 Most RN protocols won’t allow >10 mEq/hour
rates on the floors (ICU’s too?)

 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 QDay or less as needed

 BE AGGRESSIVE in DKA patients and IV
diuresis patients
 “Moran’s Rule” for cardiac patients: keep
K+ > 4.0 or even 4.5 mEQ/L
 BE GENTLE in patients with acute or chronic
renal failure, and monitor very closely
 Cut dose in half
 Double dosing interval
 Do not replace at all

 NEVER forget to check for and treat
hypomagnesemia in refractory hypokalemia!!!

Hypomagnesemia Overview
 Most of total body magnesium is intracellular
 Serum levels may NOT reflect intracellular status
 Low intracellular Mg2+ can occur in the setting of
low, normal, and high serum magnesium levels
 Highest risk patients for hypomagnesemia
 Alcoholics
 Diabetics
 Critically ill patients
 Refeeding syndrome patients
 Rare symptoms (most patients asymptomatic)
 Neurologic
 Muscular
 Cardiac

Causes of Hypomagnesemia
 Poor PO intake and malabsorptive syndromes
 Alcohol ingestion (renal losses)
 Thiazide/loop diuretic administration
 Amphotericin administration
 Acute/chronic diarrhea
 DKA
 Refeeding syndrome
 Inadequate TPN dosing

 Diabetes mellitus? (at least an association)

Approach to Hypomagnesemia
 Unlike potassium replacement,
magnesium replacement usually
involves IV replacement
 All PO magnesium salts are all poorly
absorbed
 High doses of PO magnesium usually
leads to diarrhea
 Conversion rule: 8 mEq of
magnesium sulfate equals 1 gram of
magnesium sulfate (Hines CPRS)

 Rx in hospitalized patients
 1.6-2.0 mg/dL
 Give 2-4 gram IVPB (16-32 mEq)
 Usually infused at 1 gram/hour
 1.0-1.6 mg/dL
 Give 4-8 gram IVPB (32-64 mEq), usually
in divided doses BID to TID
 <1.0 mg/dL
 Can give up to 8-12 gram IVPB (64-96
mEq) in a single day, would divide into
three-four doses

 Treating chronic low Mg2+ patients
 Give oral magnesium salt daily
 Sulfate, oxide, hydroxide, citrate, lactate,
chloride, and gluconate available
 Gluconate less likely to cause diarrhea

 Periodic IM/IV dosing if/when needed

 My approach: Magnesium Oxide 420mg
PO QDay to TID, based on level and
tolerability

 BE AGGRESSIVE in DKA patients and IV
diuresis patients
 “Moran’s Rule” for cardiac patients: keep
Mg2+ > 2.0 or even 2.5 mEQ/L

 BE GENTLE in patients with acute or chronic
renal failure, and monitor very closely
 Cut dose in half
 Double dosing interval
 Do not replace at all

Hypophosphatemia Overview
 Phosphorus is a critically important
element in every cell
 Remember what the “P” stands for in
ATP?
 Low phos commonly encountered in
 Feared complication of severe
deficiency is rhabdomyolysis

Causes of Hypophosphatemia
 Refeeding syndrome
 DKA
 Vitamin D deficiency
 Malabsorptive syndromes
 Alcoholism
 Inadequate TPN dosing

Approach to Hypophosphatemia
 Rx in hospitalized patients
 Mild to moderate hypophosphatemia
 1.5 -2.4 mg/dL
 Give phosphorus in the form of K+ or Na+
salts PO BID to TID as needed
 Usually given as 1-2 packets of “neutraphos” BID
to TID
 Severe deficiency
 <1.5 mg/dL
 Give IVPB in the form of sodium or
potassium phosphate
 Usually given as 20-40 mEq/mmol rider infused
over 2-4 hours
 Reasess labs QDay to TID as needed

Hypocalcemia Overview
 Hypocalcemia in hospitalized
patients is usually spurious and/or
DOES NOT need to be treated
 Aggressive management of
hypocalcemia is usually ONLY
indicated in “symptomatic” patients
 Active or latent tetany
 Cardiac dysrhythmia/prolonged QT

 Spurious hypocalcemia: low albumin
 Corrected Ca2+ = measured Ca2+ + [(normal
albumin - measured serum albumin) x 0.8]
 Works well unless albumin < 2 mg/dL

 Hypocalcemia due to hyperphosphatemia
from CKD/ESRD
 Aggressive calcium replacement is DANGEROUS
—serum/tissue precipitation!!!
 Treat high phos and calcium level will improve
 Renal consults/senior resident can help with
phosphate binder dosing/orders

 IV Calcium infusion can cause skin and
muscle necrosis if it extravasates from IV
 May threaten limb or necessitate skin
grafting!!!
 If replacement is needed, can usually give
TUMS PO
 Severe depletion: discuss IV dosing with
senior resident or endo consults
 Maintenance calcium replacement in TPN
usually handled by nutrition support team

Recap of Major Learning Points
 Hyperkalemia
 Make sure it’s real
 Determine emergent or not
 Rate of rise, degree of hyperkalemia, EKG
 Treat emergent cases with calcium
gluconate, insulin, dextrose, and
kayexalate +/- dialysis/lasix
 Monitor closely for response to
treatment—watch for rebound
 Fix the cause if possible

 Hypokalemia
 PO almost always preferred over IV
 KCl is preferred preparation
 Don’t give too much too quickly
 Be aggressive in DKA and IV diuresis
patients
 Be gentle in renal failure patients
 Don’t forget to check magnesium levels
in refractory patients

 Hypomagnesemia
 IV almost always preferred over PO
 Give IVPB in 2 gram increments
 Be aggressive in DKA patients, IV
diuresis patients, and alcoholics
 Be gentle in renal failure patients
 PO does not work well and in high
doses causes diarrhea

 Hypophosphatemia
 Can be treated with neutraphos packets PO
BID/TID in mild cases
 Can be treated with sodium or potassium
phosphate IVPB’s in severe cases
 Hypocalcemia
 Usually spurious or does not require Rx
 Avoid calcium replacement in CKD/ESRD
patients with hyperphosphatemia
 Avoid IV calcium whenever possible
 Call for help if hypocalcemia really needs IV Rx

Getting Labs on Patients
 BMP
 QDay or Qother day on most hospitalized patients,
especially if they have PO intake issues or are on
maintenance fluids
 BMP with Mg levels
 QDay-BID on cardiology patients, alcoholics, and
patients on amphotericin B
 BMP with Mg/Phos levels
 QDay-TID on tube feeding patients, DKA patients,
or patients with suspected refeeding syndrome
 BMP with Ca/Mg/Phos levels
 QDay-4x/Day on TPN patients, AKI/CKD/ESRD
patients, oncology patients (chemo/TLS),
pancreatitis patients, critically ill patients

Ok, You Think You Got It???
 Let’s try it out on some cases
 3 Real cases from real patients at Hines

 Figure out what you would do...

 …then I’ll show you what the intern
actually DID and what actually
happened!

Case #1
 A 56 y/o male presents due to increased swelling
in his face, legs, and abdomen, as well as
increasing SOB and DOE. He is volume
overloaded on exam. His labs are listed below.
His serum albumin is 2.5 g/dL. Would you
replace or treat anything?

Na+ K+ Cl- CO2 BUN Creat Gluc Ca2+ Mg2+ Phos

133 5.5 101 18 51 9.5 83 8.2 2.1 6.0

Case #1 (continued)
 Patient’s EKG

Case #1 (continued)
 Here’s what the intern did…
 Gave 30gm Kayexalate PO
 Appropriate
 Gave lasix for volume overload, attempt at diuresis
and potassium lowering
 Appropriate
 No insulin/dextrose/calcium gluconate
 Probably appropriate
 Gave phosphate binders for high phosphorus and
DID NOT Rx low calcium (corrected calcium 9.4 mg/
dL--normal)
 Very appropriate
 Discussed possible hemodialysis with senior
 Appropriate

Case #1 (continued)
 Rechecked K+ 12 hours later, still 5.5
mEq/L
 Could have rechecked a little sooner

 Therfore gave another 30gm of

Kayexalate PO
 Appropriate
 Rechecked K+ 8 hours later, down to
5.1 mEq/L

Teaching Points
 Know the systematic approach to
assessing and treating
hyperkalemia
 Avoid unnecessary correction of low
serum calcium values, especially
when they are spuriously low

Case #2
 A 31 y/o male with a h/o severe HTN and
resultant CKD and diastolic dysfunction/CHF
presents with hypertensive urgency and CHF
exacerbation. He is started on IV lasix and BP
meds in the ED. His admission labs are below
(taken prior to any medication administration).
Would you replace or treat anything?


137 3.5 100 26 25 2.8 125 9.1 1.9 3.5

Case #2 (continued)
 Here’s what the intern(s) did…
 No initial Rx for low normal K+ or Mg2+
in the setting of CKD
 Probably appropriate, though could have
given a little K+ PO (20 mEq) or Mg2+ IV
(2 grams), given plans for IV lasix
 Repeated BMP and Mg2+ level in 12
hours
 Appropriate

Case #2 (continued)
 The patient is responding to IV diuretics
in terms of volume status and BP. His
repeat labs are below (bottom row).
What would you do now?


137 3.5 100 26 25 2.8 125 9.1 1.9 3.5

139 5.4 106 29 23 2.4 102 1.9

Case #2 (continued)
 Patient’s EKG

Case #2 (continued)
 Did NOT bother to notice that hemolysis was
noted on the lab report
 Ooops!

 Did NOT repeat BMP values before deciding
treatment
 Ooops!

 Gave 15gm Kayexalate PO
 Big Ooops!

 Repeated BMP and Mg2+ level in 8 hours
 Appropriate, though intervention is suspect…

Case #2 (continued)
 The patient experienced 3-4 loose, watery
BM’s and is now very frustrated. He is
still receiving high dose IV diuretics. His
repeat labs are listed below (bottom row).
What would you do now?


137 3.5 100 26 25 2.8 125 9.1 1.9 3.5

139 5.4 106 29 23 2.4 102 1.9

142 3.3 105 29 25 2.7 115 2.0

Case #2 (continued)
 Here’s what the intern(s) did…
 Gave 20mEq KCl PO and 20mEq KCl
IVPB
 Most likely needed only PO potassium
therapy, low dose probably appropriate,
given CRI
 Repeated BMP and Mg2+ level in 12
hours
 Probably appropriate

Case #2 (continued)
 The patient complains bitterly about the IV
potassium infusion burning his arm. He’s still
mad about the diarrhea from last night. He
threatens to leave AMA and requires three
separate MD conferences to keep him in the
hospital! Repeat labs listed below (bottom row).


137 3.5 100 26 25 2.8 125 9.1 1.9 3.5
139 5.4 106 29 23 2.4 102 1.9
142 3.3 105 29 25 2.7 115 2.0
139 3.6 102 29 24 2.6 96 2.1

Teaching Points
 Consider “staying ahead” of potassium
and magnesium depletion in IV diuresis
patients with replacement for low-normal
values
 Suspect pseudohyperkalemia when things
“just don’t add up”
 Be gentle in CKD patients
 PO potassium is PREFERRED over IV
potassium in most situations

Case #3
 A 56 y/o male with a h/o chronic alcoholism and
chronic dysphagia from prior CVA presents due to
heavy drinking with nausea and vomiting at home.
Patient is a poor historian and is VERY CACHECTIC on
exam. He is placed on dextrose-containing IV fluids
and made NPO. His labs are listed below. His serum
albumin is 3.2 g/dL. Would you replace or treat
anything?


140 4.7 99 29 11 1.1 89 9.6 1.3 3.4

Case #3 (continued)
 Gave thiamine and folate in addition to IVF as
adjunctive therapy for chronic ETOHism
 Appropriate

 Did NOT supplement with any magnesium
preparations
 Ooops!

 Repeated BMP, Mg2+ level, Phos level in 8
hours
 Appropriate

Case #3 (continued)
 Patient continues to have dysphagia and
nausea/vomiting problems. His repeat labs are
listed below (bottom row)—these were drawn 36
hours after admission (patient kept refusing labs).
Service is planning on Dobhoff until full
ENT/speech pathology workup complete. What
would you do now?


140 4.7 99 29 11 1.1 89 9.6 1.3 3.4

136 3.9 100 23 5 0.9 46 1.3 2.4

Case #3 (continued)
 Gave 4gm magnesium sulfate IVPB
 Appropriate
 DID NOT further address the hypoglycemia
 Ooops!
 DID NOT supplement with any potassium or
phosphorus
 Ooops!
 Repeated labs in 24 hours
 Probably should have repeated in 8-12 hours
 DID NOT ANTICIPATE this patient’s potential for
continued electrolyte problems, given his alcoholism
and high risk for refeeding syndrome
 Can happen even with IV dextrose infusion!!!

Case #3 (continued)
 Patient is getting more lethargic, starts to have
fevers, service suspects aspiration pneumonia,
eventually goes to MICU. He gets nutritional
support off/on with Dobhoff, but keeps pulling it
out. Here’s the next several days’ labs, with
notes on replacement in-between


140 4.7 99 29 11 1.1 89 9.6 1.3 3.4

136 3.9 100 23 5 0.9 46 1.3 2.4

137 3.8 100 24 6 0.8 65 Oops! Oops!

Case #3 (continued)
 Nothing gets replaced/addressed. New
labs 12 hours later below (at bottom):


140 4.7 99 29 11 1.1 89 9.6 1.3 3.4
136 3.9 100 23 5 0.9 46 1.3 2.4
137 3.8 100 24 6 0.8 65 Oops! Oops!

134 3.9 100 25 65 1.3 4.1

Case #3 (continued)
 6gm magnesium sulfate IVPB given
 Labs redrawn 8 hours later, listed below
(at bottom):


140 4.7 99 29 11 1.1 89 9.6 1.3 3.4
136 3.9 100 23 5 0.9 46 1.3 2.4
137 3.8 100 24 6 0.8 65 Oops! Oops!

134 3.9 100 25 65 1.3 4.1
137 3.8 103 24 9 1.0 80 2.4 3.6

Case #3 (continued)
 Finally making some progress!!! At this point
tube feeds get started with some regularity. New
labs drawn 24 hours later, listed below at bottom
(line above is yesterday’s “perfect” labs). Serum
albumin around this time is 2.1 g/dL.


137 3.8 103 24 9 1.0 80 2.4 3.6

138 3.4 106 26 8 0.9 129 7.9 1.3 2.7

Case #3 (continued)
 Nothing gets addressed/replaced by
intern (Ouch, that hurts!)
 New labs 24 hours later, listed at bottom:


137 3.8 103 24 9 1.0 80 2.4 3.6

138 3.4 106 26 8 0.9 129 7.9 1.3 2.7

141 2.9 105 28 4 0.8 124 7.7 0.9 2.9

Case #3 (continued)
 Finally, something starting to happen!!!
 Gets 20mEq KCL IVPB x 2 doses 4 hours apart
 Probably not enough, if you ask me…
 Gets 4gm magnesium sulfate IVPB
 Gets new labs in 12 hours this time (below, at
bottom):


137 3.8 103 24 9 1.0 80 2.4 3.6
138 3.4 106 26 8 0.9 129 7.9 1.3 2.7
141 2.9 105 28 4 0.8 124 7.7 0.9 2.9
138 3.6 106 27 3 0.8 89 1.6 Oops!

Case #3 (continued)
 Gets 4gm magnesium sulfate IVPB
 Gets new labs in 12 hours, listed below at
bottom:


137 3.8 103 24 9 1.0 80 2.4 3.6
138 3.4 106 26 8 0.9 129 7.9 1.3 2.7
141 2.9 105 28 4 0.8 124 7.7 0.9 2.9
138 3.6 106 27 3 0.8 89 1.6 Oops!

141 3.3 104 27 2 0.7 107 1.8 2.2

Case #3 (continued)
 Nothing supplemented (oh boy, here we
go again…)
 New labs 12 hours later, at bottom:


137 3.8 103 24 9 1.0 80 2.4 3.6
138 3.4 106 26 8 0.9 129 7.9 1.3 2.7
141 2.9 105 28 4 0.8 124 7.7 0.9 2.9
138 3.6 106 27 3 0.8 89 1.6 Oops!

141 3.3 104 27 2 0.7 107 1.8 2.2
140 3.1 105 28 2 0.9 100 1.2 2.3

Some Take Home Points
 Try to avoid “chasing your tail” on
patients at high risk for continued
electrolyte deficiencies
 Be aggressive in these patients, do not be
afraid to replace lytes when at low-normal
end of reference range
 Never underestimate the importance of
maintainting electrolyte homeostasis, for
the patient’s benefit and for YOUR benefit
 Your seniors and attendings will LOVE you!!!

References
Cody RJ, Pickworth KK: Approaches to diuretic therapy and
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Kim G, Han J: Therapeutic approach to hypokalemia.
Nephron 2002; 92(suppl 1): 28-32.

Kim H, Han S: Therapeutic approach to Hyperkalemia.
Nephron 2002; 92(suppl 1); 33-40.

Whitmire SF: Fluid and electrolytes; in Gottschlich MM (ed):
The Science and Practice of Nutrition Support; A Case-
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