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					Virtual Potassium for the Intern
       (and other related electrolytes)



Intern Survival Lecture Series
July 2009

Scott Pawlikowski, M.D.
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
            Based on 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 for future interns
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 (HVA)

   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
   Hyperkalemia is a commonly
    encountered electrolyte disorder in
    hospitalized patients
   The most feared consequence is life
    threatening arrhythmia (PEA,
    asystole)
   Urgent vs. emergent therapy is best
    decided upon using a 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
       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, then treat as emergency

       How high is the potassium level?
          If serum K+ > or = 7.0 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
Approach to Hyperkalemia
   Step 3 (con’t): EKG assessment
       Four stages of EKG changes
         Peaked T waves
         PR prolongation
                Eventually, loss of P waves (unstable)
         QRS widening (unstable)
         Sine waves (very unstable!)

       The ―fifth‖ and final stage if
        hyperkalemia is not addressed…
           PEA or asystole (yikes!!!)
Approach to Hyperkalemia
   Step 4: Emergency Rx
       Part A: oppose toxic effects on cell membrane
          IV calcium infusion
                 Chloride has 3x the concentration of elemental
                  calcium compared to Gluconate
                 Gluconate has less toxic effects if IV extravasation
            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 (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 units regular insulin IV push, together
                  with 1 ampule (50mL) D50 IV push
            Adjuncts (usually not necessary)
                 Albuterol nebulizer (continuous neb)
                 Sodium bicarbonate 1 ampule IV push
                     Only really helpful with coexistant acidosis

                 Lasix: yes or no? USE WITH CAUTION
            Beware rebound hyperkalemia!!!
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
        (always discuss with renal fellow)
Approach to Hyperkalemia
   Step 6: Housekeeping/follow up
       Try to reverse/prevent/treat the cause
          Rx acute renal failure

            Medication adjustment
       Be sure to monitor closely, reassess/follow serum
        K+ closely
            Generally 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 in these patients can potentiate
             the toxicity!!!
Hypokalemia Overview

   Hypokalemia occurs in more than
    20% of hospitalized patients
   Can be dangerous due to
    arrhythmia, rhabdomyolysis, and
    paralysis
   Usually does not require emergency
    supplementation over minutes to
    hours
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)

          Refeeding syndrome (NEVER underestimate!)

          Endocrinopathies (mineralocorticoid excess)

          Salt wasting nephropathies/RTA’s

          Magnesium deficiency (NEVER overlook!)
But I Digress…
   What the heck is refeeding syndrome?
       Spectrum of electrolyte/volume disorders
       Occurs when previously malnourished patients are
        fed with carbohydrate loads (PO or IV!)
       Triggered by intense insulin secretion
       Results in hypophosphatemia, hypokalemia,
        hypomagnesemia, and sometimes hypoglycemia
       Can also result in unexplained expansion of ECF
        volume, leading to CHF-like picture (usually only in
        severe cases)
   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 is PREFERRED over IV
        replacement
          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
Approach to Hypokalemia
   Step 4 (con’t): Choose K+ prep
       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 (con’t): 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 faster than 20
          mEq/hour—can cause arrhythmia!!!
               Most RN protocols won’t allow more than 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
          May want to keep K+ over 4.0 or even 4.5
           mEQ/L in cardiac patients, especially in
           those with arrhythmias (―Moran’s Rule‖)
       BE GENTLE in patients with acute or chronic
        renal failure
          May wish to cut doses in half, double
           intervals, or not replace at all
          May need to monitor very closely
       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
       Intracellular magnesium depletion has been shown
        to occur in the setting of decreased, normal, and
        elevated serum magnesium levels
   Highest risk patients for hypomagnesemia are
    alcoholics, critically ill patients, and refeeding
    syndrome patients
   Most patients are asymptomatic
   Rare symptoms: usually neurologic, muscular,
    cardiac in nature
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
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 (HVA 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
   Rx in chronically hypomagnesemic
    patients
       Give oral magnesium salt daily
          Available as sulfate, oxide, hydroxide,
           citrate, lactate, chloride, and gluconate
           salts
          Gluconate preps theoretically less likely to
           cause diarrhea
       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, IV diuresis
        patients, and alcoholics
          May want to keep magnesium over 2.0 or
           even 2.5 mg/dL in cardiac patients, especially
           in those with arrhythmias
               ―Moran’s Rule‖
       BE GENTLE in patients with acute or chronic
        renal failure
          May wish to cut doses in half, double
           intervals, or not replace at all
          May need to monitor very closely
Hypophosphatemia Overview

   Phosphorus is a critically important
    element in every cell
       Remember what the ―P‖ stands for in
        ATP?
   Hypophosphatemia 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 or
    DOESN’T 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: hypoalbuminemic
    states (remember correction rule!)
       Corr. calcium = measured calcium + [(normal
        albumin-measured serum albumin) x 0.8]
   Hypocalcemia due to hyperphosphatemia
    from CRF/ESRD
       Aggressive calcium replacement is
        DANGEROUS—serum/tissue precipitation!!!
       General rule is to Rx the hyperphosphatemia,
        and the serum 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
    site into subcutaneous tissues
       May threaten limb or necessitate skin
        grafting!!!
   If replacement is needed, can give TUMS
    PO or discuss with senior
    resident/endocrinology on IV dosing
    protocol
   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
       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 CRF/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 Q other 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, ARF/CRF/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 HVA
          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 CRI 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 CRI
            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 CRI 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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