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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
    hospitalized patients

   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
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 (hypoaldo, Addison’s)
       K+ supplements or salt substitutes
       K+ in IV infusions/TPN
Approach to Hyperkalemia: Step 3
   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
Approach to Hyperkalemia: Step 3
   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)
Approach to Hyperkalemia: Step 4
   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
Approach to Hyperkalemia: Step 4
   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!!!
Approach to Hyperkalemia: Step 5
   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
Approach to Hyperkalemia: Step 6
   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
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)

          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
Approach to Hypokalemia: 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!!

       Dr. Popli’s estimation scheme
            For every 10 mEq below normal, serum
             K+ usually drops by 0.1 mEq
Approach to Hypokalemia: Step 3
   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
Approach to Hypokalemia: Step 4
   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)
Approach to Hypokalemia: Step 4
   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+)
Approach to Hypokalemia: Step 5
   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
Approach to Hypokalemia: Step 5
   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?)
Approach to Hypokalemia: 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 QDay or less as needed
Approach to Hypokalemia: Step 7
   Housekeeping/Follow Up
       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)
Approach to Hypomagnesemia
   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
Approach to Hypomagnesemia
   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
Approach to Hypomagnesemia
   Housekeeping/Follow Up
       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
    hospitalized patients
   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
Hypocalcemia Overview
   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
Hypocalcemia Overview
   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
Recap of Major Learning Points
   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
Recap of Major Learning Points
   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
Recap of Major Learning Points
   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)
   Here’s what the intern did…
       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?

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

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?

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

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)
   Here’s what the intern did…
       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?

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

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).

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

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?

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

140    4.7   99     29    11    1.1     89     9.6    1.3    3.4
Case #3 (continued)
   Here’s what the intern did…
       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?

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


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)
   Here’s what the intern did…
       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

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

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):




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

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):

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

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.


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


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:


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

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):

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

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:

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

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:

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

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
  electrolyte imbalance in congestive heart failure. Card Clin
  1994; 12: 37-50.

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-
  Based Core Curriculum. Dubuque, Kendall/Hunt, 2001, pp
  53-84.

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Hyperkalemia and other electrolytes disorders

  • 1. 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
  • 2. 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
  • 3. 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
  • 4. 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
  • 5. 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
  • 6. Hyperkalemia Overview  Commonly encountered in hospitalized patients  Most feared consequence:  PEA  Asystole  Urgent vs. Emergent therapy?  Stepwise approach
  • 7. 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
  • 8. 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 (hypoaldo, Addison’s)  K+ supplements or salt substitutes  K+ in IV infusions/TPN
  • 9. Approach to Hyperkalemia: Step 3  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
  • 10. Approach to Hyperkalemia: Step 3  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)
  • 11. Approach to Hyperkalemia: Step 4  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
  • 12. Approach to Hyperkalemia: Step 4  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!!!
  • 13. Approach to Hyperkalemia: Step 5  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
  • 14. Approach to Hyperkalemia: Step 6  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!!!
  • 15. Hypokalemia Overview  Occurs in over 20% of hospitalized patients  Dangers  Arrhythmia  Rhabdomyolysis  Paralysis  Usually does NOT require emergency supplementation over minutes to hours
  • 16. 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
  • 17. 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)  Refeeding syndrome (NEVER underestimate!)  Endocrinopathies (Conn’s syndrome, e.g.)  Salt wasting nephropathies/RTA’s  Magnesium deficiency (NEVER overlook!)
  • 18. 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
  • 19. Approach to Hypokalemia: 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!!  Dr. Popli’s estimation scheme  For every 10 mEq below normal, serum K+ usually drops by 0.1 mEq
  • 20. Approach to Hypokalemia: Step 3  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
  • 21. Approach to Hypokalemia: Step 4  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)
  • 22. Approach to Hypokalemia: Step 4  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+)
  • 23. Approach to Hypokalemia: Step 5  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
  • 24. Approach to Hypokalemia: Step 5  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?)
  • 25. Approach to Hypokalemia: 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 QDay or less as needed
  • 26. Approach to Hypokalemia: Step 7  Housekeeping/Follow Up  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!!!
  • 27. 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
  • 28. 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)
  • 29. 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)
  • 30. Approach to Hypomagnesemia  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
  • 31. Approach to Hypomagnesemia  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
  • 32. Approach to Hypomagnesemia  Housekeeping/Follow Up  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
  • 33. Hypophosphatemia Overview  Phosphorus is a critically important element in every cell  Remember what the “P” stands for in ATP?  Low phos commonly encountered in hospitalized patients  Feared complication of severe deficiency is rhabdomyolysis
  • 34. Causes of Hypophosphatemia  Refeeding syndrome  DKA  Vitamin D deficiency  Malabsorptive syndromes  Alcoholism  Inadequate TPN dosing
  • 35. 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
  • 36. 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
  • 37. Hypocalcemia Overview  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
  • 38. Hypocalcemia Overview  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
  • 39. 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
  • 40. Recap of Major Learning Points  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
  • 41. Recap of Major Learning Points  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
  • 42. Recap of Major Learning Points  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
  • 43. 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
  • 44. 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!
  • 45. 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
  • 46. Case #1 (continued)  Patient’s EKG
  • 47. 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
  • 48. Case #1 (continued)  Here’s what the intern did…  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
  • 49. 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
  • 50. 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? Na+ K+ Cl- CO2 BUN Creat Gluc Ca2+ Mg2+ Phos 137 3.5 100 26 25 2.8 125 9.1 1.9 3.5
  • 51. 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
  • 52. 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? Na+ K+ Cl- CO2 BUN Creat Gluc Ca2+ Mg2+ Phos 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
  • 53. Case #2 (continued)  Patient’s EKG
  • 54. Case #2 (continued)  Here’s what the intern did…  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…
  • 55. 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? Na+ K+ Cl- CO2 BUN Creat Gluc Ca2+ Mg2+ Phos 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
  • 56. 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
  • 57. 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). Na+ K+ Cl- CO2 BUN Creat Gluc Ca2+ Mg2+ Phos 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
  • 58. 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
  • 59. 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? Na+ K+ Cl- CO2 BUN Creat Gluc Ca2+ Mg2+ Phos 140 4.7 99 29 11 1.1 89 9.6 1.3 3.4
  • 60. Case #3 (continued)  Here’s what the intern did…  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
  • 61. 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? Na+ K+ Cl- CO2 BUN Creat Gluc Ca2+ Mg2+ Phos 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
  • 62. Case #3 (continued)  Here’s what the intern did…  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!!!
  • 63. 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 Na+ K+ Cl- CO2 BUN Creat Gluc Ca2+ Mg2+ Phos 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!
  • 64. Case #3 (continued)  Nothing gets replaced/addressed. New labs 12 hours later below (at bottom): Na+ K+ Cl- CO2 BUN Creat Gluc Ca2+ Mg2+ Phos 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
  • 65. Case #3 (continued)  6gm magnesium sulfate IVPB given  Labs redrawn 8 hours later, listed below (at bottom): Na+ K+ Cl- CO2 BUN Creat Gluc Ca2+ Mg2+ Phos 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
  • 66. 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. Na+ K+ Cl- CO2 BUN Creat Gluc Ca2+ Mg2+ Phos 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
  • 67. Case #3 (continued)  Nothing gets addressed/replaced by intern (Ouch, that hurts!)  New labs 24 hours later, listed at bottom: Na+ K+ Cl- CO2 BUN Creat Gluc Ca2+ Mg2+ Phos 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
  • 68. 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): Na+ K+ Cl- CO2 BUN Creat Gluc Ca2+ Mg2+ Phos 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!
  • 69. Case #3 (continued)  Gets 4gm magnesium sulfate IVPB  Gets new labs in 12 hours, listed below at bottom: Na+ K+ Cl- CO2 BUN Creat Gluc Ca2+ Mg2+ Phos 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
  • 70. Case #3 (continued)  Nothing supplemented (oh boy, here we go again…)  New labs 12 hours later, at bottom: Na+ K+ Cl- CO2 BUN Creat Gluc Ca2+ Mg2+ Phos 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
  • 71. 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!!!
  • 72. References Cody RJ, Pickworth KK: Approaches to diuretic therapy and electrolyte imbalance in congestive heart failure. Card Clin 1994; 12: 37-50. 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- Based Core Curriculum. Dubuque, Kendall/Hunt, 2001, pp 53-84. Up to Date On-line