(+)Robert G.

Buckley, MD, MPH, FACEP

Captain, Medical Corps, United States Navy
Staff Department of Emergency Medicine,
Naval Medical Center, San Diego, California

Correcting Electrolyte Emergencies:

Not Too Fast But Not Too Slow
Identifying and correcting electrolyte abnormalities are often
challenges in ED patients. Some electrolyte disorders can be
life-threatening and require immediate treatment, while rapid
correction or other disorders can lead to life-threatening
complications. Other electrolyte disorders are not real
abnormalities but result from fluid shifts and will correct
without electrolyte replacement. Using a cased-base
approach, the speaker will present challenging electrolyte
abnormalities and strategies for successful management.
• Discuss challenging electrolyte abnormalities that
commonly present to the ED.
• Review management strategies for electrolyte
abnormalities.
• Review pseudo electrolyte abnormalities and the
common correction factors.

MO-55
Monday, October 27, 2008
4:00 PM - 4:50 PM
McCormick Place - Lakeside Building

(+)No significant financial relationships to disclose

 Fixing Electrolyte Abnormalities in
the Emergency Department
Robert G. Buckley, MD
CAPT/ MC/ USN
Department of
Emergency Medicine
Naval Medical Center
San Diego

The views expressed in this presentation are those of the author and do not
reflect the official policy or position of the Department of the Navy, Department
of Defense, or the United States Government.

Why Electrolytes are Important?

• IMMEDIATE LIFE THREAT .
• You can Save or KILL the patient fixing it.
• USEFUL CLUE to the UNDERLYING
DIAGNOSIS.
“Hum. What’s up with that ?”
• Y
You ORDERED IT IT, you deal
d l with
ith itit…aka
k
the Basic Metabolic Panel.

1
 Sodium Homeostasis
• SODIUM is the Main contributor to
extracellular osmolality. (Tonicity)
– OsM= 2(N +) + Gluc/18
O M 2(Na Gl /18 + BUN/2
BUN/2.8
8
• WATER will move IN & OUT of cells
until things are ISO-OSMOTIC.

Hyponatremia and Brain Volume

Few hours.

2 kidneys or
1 smart doctor
doctor.

Few days.

Androgue, NEJM, 2000 by permission

2
 Hypertremia and Brain Volume

Hours

2 kidneys or
1 smart doctor.

Days

Androgue, NEJM, 2000 by permission AKA: Idiogenic Osmoles.

The Role of ADH

• ADH sucks back FREE WATER at the
collecting
ll i tubules
b l andd llowers NNa+, .
• Trigger for ADH release is an increase
in serum osmolality above 280.
• Hypovolemia (baroceptors) and other
things: SIADH
SIADH, Tegretol
Tegretol, etc
etc. can lead to
ADH release even when things are
isotonic.

3
 Fluid Shifts in Hyponatremia
= K+
= K+ +
== Na
Na+

Squares: Permeable and impermeable solutes Androgue, NEJM 2000 by permission

Is the Hyponatremia Hypotonic,

Isotonic or Hypertonic?
Is it “real” Hypo-Na+ ?
• Hypertonic Hyponatremia: HONKS – low Na+ is
due to osmotic effects of other solutes: glucose
actually dehydrate cells. Add 1.6 meq for each 100
mg/dL increase in Glucose.
• Isotonic Hyponatremia: (Pseudohyponatremias:
Hypertriglyceridemia or paraproteinemias.)
• Hypotonic Hyponatremia: Most common
scenario. Practically speaking: If they are not
HONK or pseudohypernatremia, they are
hypotonic… and they are “real” Hypo-Na+. (Pt will
have a low measured serum OsM.)

4
Volume Status Points to Dx and
Directs Tx
• Hypovolemic: (Pediatric
diarrhea, thiazide diuretics,
blood loss.)

• Euvolemic: (SIADH, drugs,

polydipsia)

• Hypervolemic: (CHF,
(CHF
Nephrotic syndrome,
Cirrhosis, relative
hypovolemia)

Urine Na+ and Urine Osm Helps

Confirm Dx
• Concentrated Urine, OsM >300 mOSM/kg
i nearly
in l allll cases, (SIADH
(SIADH, h
hypovolemia).
l i )
• Less concentrated urine <300 mOSM/kg,
psychogenic polydipsia, diuretics,
hypoadrenal, and renal failure.
– High Urine Na+ (>30 mEq/L) in SIADH and
Renal Failure.
– Low Urine Na+ (<15 mEq/L) in Dehydration
and Edematous states.

5
 Euvolemic Hyponatremia DDx

Androgue,
NEJM,
2000, by
Permission.

Hypovolemic Hyponatremia DDx

Androgue,
NEJM,
2000,
By permission.

6
 Hypervolemic (Edematous)
Hyponatremia DDx

Androgue,
Think: Third Spacing, ie: relative hypovolemia.
NEJM,
2000, by permission.

Treatment Goals
Hyponatremia
• Is the Patient Symptomatic? (Szs/ AMS.
N + usually
Na ll <120)
120)
• What is the VOLUME status?
• Symptomatic Euvolemic & Hypervolemic
Patients Need Hypertonic Saline.
• Symptomatic Hypovolemic Patients Need
volume expansion with Normal Saline.

7
 3% Hypertonic Saline
(Indications)
• Postoperative hyponatremia due to the administration of
yp
hypotonic intravenous fluids, p
particularly
y in yyoung
g
(premenopausal) women.
• Exercise-associated hyponatremia, as in marathon
runners.
• Hyponatremia associated with the use of ecstasy.
• Hyponatremia in patients with known intracerebral
pathology (eg, meningitis, stroke, or brain tumor).
• Self-induced water intoxication in primary polydipsia.

Hypertonic Saline: How Fast?

• Small increases in serum sodium
(5 mmol/L)
l/L) generally
ll stop
t seizures.
i
BMJ 1986 & Crit Care Med 1991

• Most cases of CPM occur when Na+

increases >12 mmol/L over 24 hours.
Isolated case reports only 9-10 mmol/L.
Ann Neuro 1990.

• TARGET: 1-2 mmol/L/hr x 2- 4 hours not

to exceed 8 mmol/L/day.

8
 Do the math, if you are bored:
(3% Saline for Symptomatic Hyponatremia)

Androgue,
NEJM,
2000, by
permission

Math for doctors:

(3% Saline for Symptomatic Hyponatremia)

What is patient’s serum Na+? (eg:110

mmol/L)
l/L)

Estimate TBW. (eg: 0.5 x 80kg = 40 L. Add

1L “fudge factor” = 41 L.

Use 3% Saline (513 mmol/L)

Androgue,
NEJM,
2000, by
permission

9
 More Math for Doctors
(3% Saline for Symptomatic Hyponatremia)
Calculate how many mmols/L your serum Na+
will increase if you dumped 1 liter of 3% into
your TBW.

513 mmol/L - 110 mmol/L = 403 mmols.

403mmol / 41L) = 9.8 mmol/L.
or:
1 liter of 3% saline will increase the serum Na
from 110 mmol/L to 120 mmol/L.
Androgue,
NEJM,
2000, by
permission

But Don’t Stop There

(Hyponatremia)
Remember: We Want to GO SLOW - raising the
serum Na by only about:

1 mmol/L/hour
So: 1 mmol/L/hour x 4 hours = 4 mmols/L increase
at the end of 4 hours will need:
4 mmols divided by 99.88 mmol/L = 00.4
4 L of 3%
saline or 0.1 L/hour : 100 cc/hour x 4 hours. ‘

Androgue,
NEJM,
2000 by
permission

10
 3% Hypertonic Saline Made
Ridiculously Simple
• Use only if there are neurological sxs.
• Infuse at rate of: 1-2 ml/kg/hr, or roughly
100 ml/ hour for 4 hours.
• Check sodium every hour for first 4 hour.
• Stop infusion when Neuro Sxs resolve.

Androgue,
NEJM,
2000, by
permission

Vasopressin Receptor Antagonists

(Indications for Chronic Rx)
• Euvolemic or hypervolemic SIADH.
• Heart failure.
failure (may also have a favorable effect
on hemodynamics.
• Cirrhosis. NB: V1a receptor blockade might
lower the blood pressure and promote variceal
bleeding.
• Vasopressin
p receptor
p antagonists
g should not be
used in hyponatremic patients who are volume
depleted in whom volume repletion with saline is
the primary therapy.
Schrier RW, et al and SALT Investigators., Tolvaptan, a selective oral vasopressin
V2-receptor antagonist, for hyponatremia., N Engl J Med. 2006 Nov 16;355(20):2099-112.

11

Hyponatremia Fake-out?
(HONK, multiple myeloma?)
Or Mild Hyponatremia?
Hyponatremia DX
One EM doc’s
approach.
Recheck Labs/ Osm. Punt to Hospitalist.
Send urine OsM and Na. (It might just go away.)

Volume Status
(Take a stab at it.

Hypervolemic Euvolemic Hypovolemic

(Pitting Edema, (You’re not sure.) (Thirsty just
Ascites, CHF?) Looking at them.)

CHF/ Cirrhosis SIADH (almost always) Ur OsM >300

Ur OsM >300 Ur OsM >300
Ur Na <15 Ur Na>30 Dehydration
Ur Na <15
Renal Failure Polydipsia
Ur Na > 30 Ur OsM <300 Over Diuresis
Ur Na <15 Ur Na >30

Hyponatremia Tx
One EM doc’s
approach.

Recheck Lab.
Send urine OsM and Na.

Volume Status
(Take a stab at it.)

Hypervolemic Euvolemic Hypovolemic

(Pitting Edema, (You’re not sure.) (You are thirsty just
Ascites, CHF?) Looking at them.)

Stable Treat underlying +/- Normal Saline. (3%?) Normal Saline

problem Free Water restrict Admit/Obs
Free Water restrict. SIADH, almost always.
Punt to Hospitalist.
Coma/ 3% Saline* 3% Saline*
Sz ? Normal Saline
* 100 ml/hr x 4 hours. (Prepare to be berated by IM/ICU/Nephro.)

12
 Hypernatremia
• Defined as Na+ > 145 mmol/L
• Always causes cellular dehydration.
• Rapid
R id overcorrection Na+ with
ti off N ith
hypotonic fluids can lead to cerebral
edema due to the accumulation of
idiogenic osmoles.

Hypernatremia
• Defined as Na+ > 145 mmol/L
• Always hypertonic.
• Al
Always causes cellular
ll l d
dehydration.
h d ti
• Rapid overcorrection of Na+ with
hypotonic fluids can lead to cerebral
edema due to the accumulation of
idiogenic osmoles.

13
 Hypernatremia

DDx

Androgue,
NEJM,
2000, by
permission

Fluid/ Volume Shifts in

Hypernatremia
= K+
= Na+

Adrogue, NEJM 2000, by permission.

14
 Hypernatremia
EM Management Goals
• Look for causes of Diabetes Insipidus.
p
• 0.9% Normal Saline boluses to initially
correct hemodynamic compromise.
• Use D5W, D50.2 or D50.45 and the formula
to slowly correct Na+. @ 0.5 mmol/L/hour.
• Forget the formula
formula. D5 ¼ NS @ 150 ml/hr.
ml/hr
• Central DI: DDAVP, (Desmopressin) 2-4
mcg IV/SC divided BID or 2-4
mcg/kg/dose intranasally. (Not in ED.)

Correcting Hypernatremia by the Formula.

(Actualize your inner internist.)

• NS only to correct shock. Androgue,

NEJM,
2000, by
Permission.

15
 Cases
ED Tx of Sodium Emergencies

Your 1st Case :

• 20 y/o Marine Corps recruit brought in by
G
Gunny for
f a Psych
P h Eval.
E l
• Started acting weird when we told him he
had to take the “piss test”.
• Awake. Refuses to answer doctor’s
questions.
questions
• Na+=112

16
 Psychogenic Polydipsia
• Euvolemic Hyponatremia.
• Ur Na = 10 meq/L.
• No Szs. No Coma. No 3% Saline.
• Fluid restrict. Monitor Is/Os and Weights.
• Don’t do anything. His kidneys will do it all.
• Recheck Na+ q2-4h.
• 3% Saline if Szs or worsening AMS.

Your 2nd Case is a Triple:

1. 18 month old infant
with 3 d h/o fever
and diarrhea
presents s/p
GTCSz.
Temp=100.8,
Somnolent but
easily arousable.
Na+=112

17
 Hypovolemic Hyponatremia
• Treated with 0.9% NS – 20ml/kg x 3.
• Maintenance D5NS 1.5 x maintenance.
• Rechecked lytes q2-4 hrs.
• Serum sodium level normal after 9 hours.
• D/Ced next morning.

Skinny Cowboy

• 68 y/o with Lung CA presents

unresponsive
i with
ith iintermittent
t itt t GTCS
GTCSzs.
• Afeb/ VS –nl Cachectic, AxOx4, Neuro
non-focal. Head CT- nl.
• Na+=112. Ur OsM = 600. Ur Na=34

18
 SIADH from Lung CA
• Treat SZs: Lorazepam. (Phenytoin?)
• IVFs: NS 1 liter over 1 hour.
• 3% NS: 100 ml/hr for 4 hours.
– (1 ml/kg raises Na+ about 1 meq/L/hr.)
– Check lytes q1-2 hrs.

Another Case: Parrot Man

• 76 y/o 68 kg
obtunded male
BIBA from SRO
hotel.
• Pulse
P l = 110
110,
BP=142/82. A x
Ox1, dry mucous
membranes.
• Na+ = 168
• Hospitalist: “Can
you write some
orders on this
guy?”

19
 Gradual Correction of
Hypernatremia
• 76 y/o 68 kg obtunded male with dry
mucous membranes
membranes, HR 110 BP 142/82
142/82.
+
Na = 168 meq/L
– Goal: Decrease Na+ by 10 mmol/L/24 hrs.
– Formula: (0-168)/(34+1) = - 4.8
– 10/4.8 = 2.1 L/24 hours + 1.5 L average
insensible loss = 3
3.6
6 L/24 hours =
D5W: 150 ml./hr. x 24 hrs.
– Swag: D5 ½ NS @ 250 ml x 4 hrs.

Another Case: Miller Time

• 32 y/o alcoholic localizes to painful stimuli
after
ft a GTCSz.
GTCS D Drank k 18 b
beers CT ((-))
• Na=112
• Tx? Fluids?

20
 Beer Potomania
Clinical Nephrology. 45(1):61-4, 1996 Jan.
• These patients usually have a history of binge beer
drinking, poor dietary intake, and then present with
severe hyponatremia
h t i andd various
i mental t l status
t t changes
h
or seizures.
• Typical laboratory findings … a very dilute urine.
• We propose that the pivotal pathophysiologic
mechanism in beer potomania syndrome is the minimal
intake of solute and the hypoosmolality of the beer
ingested. This will lead to the inability to excrete
sufficient amounts of free water to keep up with the
ingestion of large quantities of the hyposmolar beer.
• Treatment with isotonic sodium chloride results in the
rapid clearance of the accumulated excess free water.

Another Case: Miller Time

• 32 y/o alcoholic localizes to painful stimuli
after
ft a GTCSz.
GTCS D Drank k 18 b
beers CT ((-))
• Na=112
• 0.9% NS x 1L
• Banana bag

21
 Ultra Man: Tx?
• 40 something Navy O-6 c/o anorexia,
fatigue after competing in an “Ultra”
Ultra in
Upper Mojave.
– Anorexia, mild HA, muscle fasciculations.
– Turns to wife and says, “Darling, don’t be
surprised if I have a seizure”.
– P=118, BP=122/72, Afeb
– Na+=118

Permission by RDML Roberts

Hyponatremia among 488 Runners

in the Boston Marathon
NEJM April 2005
• 13% had hyponatremia (Na+ < 135
mmol/L); 0.6
0 6 percent had critical
hyponatremia (Na+ < 120 mmol/L).
• Univariate Risks: (1) substantial weight
gain, (2) consumption of more than 3 liters
of fluids during the race, (3) consumption
off fluids
fl id every mile,
il (4) a racing
i titime off
>4:00 hours, (5) female sex, and (6) low
body-mass index.

22
Consensus Statement of the
1st International
Exercise-Associated
Hyponatremia Consensus
Development Conference,
Cape Town,
South Africa 2005
Prevention:
1) drink only according to
thirst (ie, ad libitum) or
2) use the USATF guidelines, or
analogous methods, to estimate hourly
sweat losses during
exercise and avoid consuming amounts
greater than this during
endurance exercise events

Treatment:

(1) 100 mL or a 1 mL/kg bolus

of 3% NaCl and repeat hourly at
a rate of 100 mL/hr,
or

2) infuse 3% NaCl at a rate of

1–2 mL/kg/hr.
(Clin J Sport Med 2005;15:208–213)

Ultra Man: Tx?

• 40 something Navy O-6 c/o anorexia, fatigue
after competing
p g in an “Ultra” in Upper
pp Mojave
j
– Anorexia, mild HA, muscle fasciculations.
– P=118, BP=122/72, Afeb
– Na+=118
• 3% Saline @ 100 ml/hr.
• Check lytes q1
q1-2
2 hrs.
• Stop 3% when feeling better.

Permission by RDML Roberts

23
 Sick Seal
• 23 y/o with 5 days fever, cough,
weakness,
k multilobar
ltil b PNA
PNA, BP = 91/61
91/61,
HR=132
• Na+ = 128
• K+ = 5.6

Clues to Adrenal Insufficiency

• Low Na+/ High K+ always a tip-off.
• NS resuscitation for 3-4 liters.
• EGDTx for Severe Sepsis.
• Spot Serum Cortisol.
• Hydrocortisone 100 mg.

24
 Electrolyte Emergencies II Potassium
Disorders

Case 1: Weak in the legs

• 35 y/o Asian male c/o sudden onset of leg
weakness
k x4hhours now affecting
ff ti one
arm.
– Can not stand. No meds. PMHx – “Thyroid
problem”. No other sxs.
– Exam: 3/5 motor in (B) lower extremities and
(L) upper extremity.
– Hyporeflexia throughout.
• Guillain-Barre, right?

25
 Case 2: Why K+ really matters:
Honk of a Horn. Obtunded. Thready pulse.
PGY2: “Charging 300.”

Potassium Homeostasis
• 50 meq/kg
• 2% Extra-cellular: 98% in cells.
• Na/K ATP-ase cranks K+ in and
Na+ out.
• Beta-2, insulin and aldosterone
cranks the Na/ K+ ATP-ase.

26
 Potassium Homeostasis

• 50 meq/kg
• 2% Extra-
cellular
• Na+/K+ ATP-
K+ in and
Na+ out.
• Beta-2,
Beta 2
insulin and
aldosterone
all stimulate
Na/K ATP-
ase.
Image by permission NEJM:
Gennari FJ, Hypokalemia., N Engl J Med. 1998 Aug 13;339(7):451-8

Na+/ K+ ATPase pump:

Diagram by Judy Christensen. Medical Graphics Division. NMC San Diego

27
 Hypokalemia

You see this every shift.

Hypokalemia - Causes
Shifts Losses
• Drugs: Beta-2 agonists, • Drugs: Diuretics.
Xanthines, Insulin. (Barium,
Magic Shave, Licorice.)
Steroids.
• Alkalosis • Diarrhea,
• Hyperadrenergic Diaphoresis.
states: - Thyroid,
Thyroid DTs DTs. • Type I & II RTA
RTA.
• HPP
• Aldosteronism.
• Pseudo. Leukemia.
• Low Mg++

28
 Hyperadrenergic States:Trauma

Beal AL. Scheltema KE. Beilman GJ. Deuser WE. Hypokalemia following trauma.
Shock. 18(2):107-10, 2002 Aug.

Initial Work-up
• Monitor, EKG.
• C
CorrecttVVolume
l L
Loss.
• Review all Meds.
• Add: Mg++, PO43-,
Ca++ . (ERP2)
• Consider: (TSH,
Urine Lytes, ABG)
• Replace K+

29
 Potassium Replacement in the
ED
• What solution: KCl, K-Phos, KHCO3
• What route?
- PO vs. IV?
- Central vs. Peripheral.
• How much? / How fast?
• Balance risk of hyperkalemia with need
to replace K+.

How much?
For K+ loss states:

0.3 mmol/L = 100mmol

Highly variable and depends on
acid base status and shifts.
acid-base shifts

Almost always down 100 mmol.

30
 KCl: How fast IV?
• Kruse Arch Int Med 1990.
• Retrospective 495 ICU infusions.
• 20 meg/ 1 hour.
• Average elevation: 0.25 meq/L.
• 10 (2%) rate of “mild” hyperkalemia.

Kruse JA. Carlson RW. Rapid correction of hypokalemia using concentrated

intravenous potassium chloride infusions. Archives of Internal Medicine. 150(3):613-7,
1990 Mar.

KCl: How fast IV?

• Kruse. J. Clin Pharm 1994
• Prospective. 26 ICU patients.
• 20 meq/hour.
• Mean elevation 0.5 mmol/L
(0.1 - 1.7 mmol)

Kruse JA. Clark VL. Carlson RW. Geheb MA. Concentrated potassium chloride infusions
in critically ill patients with hypokalemia. Journal of Clinical Pharmacology.
34(11):1077-82, 1994 Nov.

31
 KCl: How fast IV? Peds
• Frantz, Crit Care 2000
• 50 infant ICU infusions.
• 1 meq/kg/hour = 1.1 meg/L increase.
(range 0.4 - 4.3 meq/L increase.)
• 2/50 (4%) had hyperkalemia.

KCl: How fast IV? Bottom Line

• Mild cases. (K+ >2.5) No Sxs. Tol PO.
20 - 40 meg PO

• Moderate cases. (K+ = 2.0-2.5) or not tol PO:

KCL using 10 meq/hr. riders.

• Severe cases. (K+ <2.0 or Sxs) or card/neuro

sxs: 20 meq/hr. (max 40 meq/hr central.). Use
2 peripheral IV s.

32
 Weak in the legs
• 35 y/o Asian male c/o sudden onset of leg
weakness
k x4hhours now affecting
ff ti one
arm.
– Can not stand. No meds. PMHx – “Thyroid
problem”. No other sxs.
– Exam: 3/5 motor in (B) lower extremities and
(L) upper extremity.
– Hyporeflexia throughout.
• Guillain-Barre, right?

Hypokalemic Periodic Paralysis

(HPP)
• Insidious onset of diffuse prox>distal
weakness and hyporeflexia
hyporeflexia.
• Etiol: Sudden transcellular shifts.
• Familial HPP. Autosomal dominant.
Gene defect leads to “channelopathy”.
Most common cause in Western
C
Countries.
ti
• Thyrotoxic HPP most common cause in
Asians (males) up to 8% incidence.
• Response rapidly to PO/IV KCl + Beta-
blockers.

33
 Foods with High Potassium Content

Gennari, F. J. N Engl J Med 1998;339:451-458

Hypokalemia - Summary
• Beta-2 agonists & aldosterone pump K+
i t cells
into ll via
i N
Na/K
/K ATP
ATP-ase.
• Drugs (Diuretics) & Diarrhea most
common cause.
• Consider unusual causes: Periodic
paralysis RTA
paralysis, RTA, Hyperaldosteronism
Hyperaldosteronism,
Hyperthyroid.
• Replace carefully: Max 20 meq/hour. Re-
check levels in 1-2 hours in ED.

34
 Hyperkalemia

Beep of a Horn
• 52 y/o obtunded with
thready pulse
pulse.
• BP = 70/P
• Intubated. 100%.
• Monitor/ EKG as
shown:
• PGY
PGY-2:2: “Charging
Charging to
300 Joules…”
• Med-alert: Renal
Failure.

35
Hyperkalemia: Common Causes
• Spurious: Hemolysis
• Iatrogenic: KCL Riders, Succ Chol.,
transfusions.
• Renal Failure
• Acidosis: (variable)
• Myonecrosis & Hemolysis
• Addisons / hypoadrenal states. (mild)
• Drugs: Digoxin and Beta-blockers.

Hyperkalemia: Management
• Immediate monitoring and EKG.
• Repeat level if EKG normal.
• What if EKG is not normal?

36
 Common EKG Findings

Peaked T-waves

Common EKG Findings

Widened QRS

37
 Treatment Goals for
Hyperkalemia
• Immediately Protect the Heart. Calcium.

• Temporarily Shift the K+ into muscle cells.

Insulin/ D50W. Beta agonists. Bicarb.

• Get rid of K+ . Kaexolate and Dialysis.

Calcium
• Antagonizes the membrane effects of K+.
• Immediate onset lasting 30 - 60 minutes.
• Calcium gluconate 10% (90 mg elemental
calcium per 10-mL amp) less venous
irritation than CaCl 10% (272 mg of
elemental calcium per 10-mL amp)
amp).
• Relatively contraindicated
in Digoxin toxicity.

38
 Digoxin and Hyperkalemia
• Digitalis poisons the
Na+/ K+ -ATPase
ATPase.
• Increased intracellular
Na+ leads to
increased exchange
with Calcium
triggering massive
Ca++ release from the
sarcoplasmic
reticulum.
• Calcium theoretically
could worsen Dig
Image of foxgloves from: http://www.squidoo.com/rosesdigitalis toxicity.

Beta-2 Agonists
• Stimulates a separate segment of the Na/
K+ ATP-ase
ATP i d
independent d t off
insulin/glucose.
• Albuterol neb 10-20 mg + insulin/gluc
showed decrease of 1.2 compared to
insulin/ gluc alone of 0.6. Allon et al, Kidney Int 1990
• Rebound post-dialysis due as K+ shift out
of cells. Allon Am J Kid Dis 1995.
• Albuterol buys you time in severe cases.

39
 Insulin & Glucose
• Insulin activates Na/ K+ ATP-ase driving
K+ into
i t cells.
ll
• Onset 15 minutes lasting 2 hours.
• Lowers K+ by 0.5 to 1.0 meq/L.
• Regular Insulin 10 U with 50 ml of D50W if
any EKG changes or K+ > 6 6.0-6.5.
065
• Recheck D-stick q 1 hour with lytes.

NaHCO3
• Best study (n=14) showed average dose
off 100 meq over 4 4-6 6h hours d d K+
decreased
by 1.6 meq/L. Fraley, Kid Int 1977.
• Recent evidence does not support use in
non-acidotic patient. Kim, Nephon 1996
• One ampule (50 meq) in presence of
metabolic acidosis - concurrent with other
Tx.

40
 Polystyrene Sulfate (Kayexelate)
• Na+ bound anionic resin exchanges with
gutt cations
ti lik K+.
like
• PO: 30 gms = 120ml
• PR: 100 gms.
• Lowers K+ by 1 meq
over 24 hours.
• Na+ overload.

Dialysis
• Hemodialysis
removes 40 meq per
hour.
• Peritoneal dialysis
removes 5 meq per
hour.

41
 Hyperkalemia: Summary
• Always get EKG, monitor & re-check level.
• Institute Tx based on EKG
EKG, Sxs and level
level.
• C BIG K:
– Calcium
– B2-Agonist (Bicarb)
– Insulin/Glucose
– Kayexelate
y
• Na Bicarbonate only if acidotic.
• Consult Nephrology in all CRF patients.
• Stop ACE/ARBs/Spironolactone if K+>5.5.

Calcium, Phosphate and

Magnesium
Hang in there.

42
 Calcium and Phosphorus
Homeostasis
• 99% in bone as Ca –Phos/Carb “apatite”
Thi k off your skeleton
Think k l t as a hhuge calcium
l i
infusion machine.
• Normal Ca++ 9.0-10.5 mg/dL
• Serum Ca++: Half albumin bound – half
free “ionized”.
• Normal ionized level Cai++= 1.0 –1.15
mmol/L, under tight control - maintained at
“expense” of bone.

Calcium Level Modulation

• PTH causes a rapid increase in calcium
resorption from bone and reabsorption in the
distal renal tubules.
• PTH also stimulates renal production of 1,25 –
dihydroxy-vitamin D which leads to increased
absorption of calcium in the gut.
• Rising calcium levels lead to a decrease in PTH
release
l with
ith subsequent
b t calcium
l i b
bone
deposition, renal excretion and diminished GI
uptake.

43
 Hyperparathyroidism
• Most common cause in
minimallyy symptomatic
y p
outpatients.
• 85% due to solitary
adenoma.
• Incidence: 4 per 100,000
per year.
• Peak incidence in 50s
andd 60
60s.
• Uncommon: Bones,
stones, abdominal
groans.

Hypercalcemia in Cancer
• Cancer is most common cause in SICK pts.
• Tumors
T secreting
ti PTH-related
PTH l t d proteint i ((e.g.
squamous cell carcinomas) or calcitrol (e.g. B-
cell lymphomas).
• Local osteolytic hypercalcemia occurs when
tumor within the bone itself (e.g. multiple
myeloma) causes cytokin release and increased
osteoclastic calcium resorption from bone

44
 Hypercalcemia
DDx
• Incidental finding on ERP2 – not a laboma.
• Hyperparathyroidism:
H th idi 90% off ambulatory
b l t
cases. Most due to single adenoma.
• Cancers(1) : Boney mets - PTBLK.
• Cancers(2): Humoral hypercalcemia due
to PTH-related protein.
• Lithium. Excess Antacids. Sarcoid.
Supplements (Vitamin D)

Clinical Presentation of
Hypercalcemia
• Mild hypercalcemia (up to 12 mg/dL) vague
changes in cognitive function
function, depression
depression, and
fatigue.
• Higher levels are more frequently associated
with GI symptoms, (nausea, anorexia,
constipation, and abdominal pain), muscle
weakness and more profound changes in mental
status.
• The EKG may reveal QTC shortening and PR or
QRS widening.

45
 Hypercalcemia
Initial ED Treatment
• Always check ionized Ca++ or adjust for
elevated
l t d protein.
t i
• 0.9% NS: 2 Liters over 1-2 hours.
• Lasix 40 mg IVP only AFTER VOLUME
restored and good urine output.

Hypercalcemia
Further therapy
• Biphosphonates directly inhibit osteoclastic
activity.
activity
Pamidronate 60mg IV in 1 L D5W or
Zolendronic acid 4mg IV
Plicamycin (25 mg/kg over four hours)
• Steroids: Inhibit cytokine release. (Cancer/
Sarcoid)
• Calcitonin (4 IU/kg sq) has a more rapid onset
but is associated with GI upset and flushing.

46
 Critical Actions in
Hypercalcemia
• Measure a calcium level in all patients with
known or suspected malignancy who present
with fatigue, weakness, or change in mental
status.
• Rule out pseudohypercalcemia in the presence
of elevated protein by checking an ionized
calcium level.
• Treat
T t allll cases off hypercalcemia
h l i with
ith profound
f d
muscle weakness, altered mental status, cardiac
dysrhythmias, or a serum calcium level of 14
mg/dL or greater.

Critical Actions (cont)

ƒ Restore intravascular volume with one to two
liters of normal saline followed by a loop
loop-diuretic
diuretic
is the cornerstone of initial therapy.
ƒ Initiate therapy to decrease osteoclastic activity
using a biphosphonate, plicamycin or calcitonin.
ƒ Minimally symptomatic or assymptomatic
patients with mild
mild-to-moderate
to moderate hypercalcemia
and no known malignancy should have a PTH
level ordered and close outpatient follow-up.

47
 Hypocalcemia
Presentation
• Neuro-excitability:
• T t
Tetany, SZs
SZ
• Trousseau’s sign.
• Chvostek’s sign.
• Cardiac conduction.

Photo courtesy of LCDR David Durkovich, MC, USN

Hypocalcemia
Presentation
• Neuro-excitability:
• T t
Tetany, SZs
SZ
• Trousseau’s sign.
• Chvostek’s sign.
• Cardiac conduction:

Photo courtesy of LCDR David Durkovich, MC, USN

48
 Hypocalcemia
Cardiac Manifestations

Hypocalcemia
DDx/ Etiology
• Hypoalbuminemia fake out : Add 0.8 mg/dL per
1 g/dL below 4 g/dL of Albumen
Albumen.
• Hyperventilation syndrome: H+ knocks Ca++ off
of albumin.
• Hypomagnesemia.
• Renal failure (high phosphate)
• Hypoparathyroidism.
– High Phosphate.
– Look for scar on neck.
• Rhabdomyolysis due to increase phosphate
• Pancreatitis – unknown mechanism,
(saponification?).

49
 Hypocalcemia
Treatment
• Measure Cai++. Check + replace Mg++.
• Benzodiazepine/ Paper bag in hyperventilation
hyperventilation.
• Calcium gluconate 10% soln. (10 ml.)
2 x 10cc AMPS over 10 minutes
6 x 10cc AMPS/L over 6 hours
• Calcium gluconate (90 mg elemental calcium
per 10-mL ampule) less venous irritation than
calcium chloride (272 mg of elemental calcium
per 10-mL ampule).
• Never, ever, thru line with Bicarbonate. Lime.
• Goal: Ca++ = 8.0-8.5, (low nl).

Phosphorus
• Key for ATP production and cell membranes
• C x Phos
Ca Ph > 70 = ectopict i calcification
l ifi ti
• 85% bone, 14% other ICF, 1% ECF
• NL Phosphorus level: 3.0 – 4.5 mg/dL
• 90% renally excreted
• PTH increases renal loss
• Like potassium, H+ drives Phosphate out.
Insulin drives it in.

50
 Hyperphosphatemia
• Key for ATP production and cell membranes
• Ca x Phos > 70 = ectopic calcification
• Causes/DDx:
– Chronic renal failure – far & away most common.
– Hypoparathyroidism
– Rhabdomyolysis
– Tumor lysis
y syndrome
y
– Acidosis (DKA)
– Excess phosphate intake.
• Treatment: Saline. Dialysis in CRF > 14 meq/L.

Hypophosphatemia
• Common: 3% of all hospitalized patients
– Up to 50% in VA series.
series EtOH
• Rarely needs emergent IV treatment unless
Phoshate < 1.0 mg/dL and symptomatic.
• Neutra-Phos or K-Phos (0.25 mMol/kg/6 hours).
Must be monitored for hypotension and tetany
due to hypocalcemia
hypocalcemia.
• Oral replacement Neutra-Phos 250mg TID

51
 Etiology of Hypophosphatemia
• Renal loss • Transcellular shifts
Renal tubular dysfunction
y
Diuretic therapy R
Respiratory
i t alkalosis
lk l i
Hyperosmotic states (DKA, (COPD, sepsis, ASA
HONK Hyperglycemia)
Hyperparathyroidism
poisoning)
Hyperadrenergic states
• Decreased intake (Etoh withdrawal)
Malnutrition
Phosphate binding antacids
H
Hyperglycemia
l i
Chronic diarrhea Insulin therapy
Inflammatory bowel disease
Vitamin D deficiency

Magnesium Ion
A Magic Little Ion
• Cofactor in a
multitude of
enzymatic reactions:
-Na+/K+ ATPase
-Ca++ ion channels
• Cardiac/ Neuro
function
• <1% in ECF (Nl=1.3-
2.2 mEq/L)

Image by permission NEJM:

Gennari FJ, Hypokalemia., N Engl J Med. 1998 Aug 13;339(7):451-8

52
 Magnesium
<1% in ECF (Nl=1.3-2.2 mEq/L)
• Cofactor in a multitude of enzymatic reactions:
Na+/K+ ATPase,
-Na ATPase Ca++ ion channels
channels.
• Low magnesium : Often have NORMAL levels.
Malnutrition, Renal loss, eg: diuretics. Drugs.
• Assx. If Sxs, similar to hypocalcemia:
prolonged QTc, Torsade de Points,
fasciculations, AMS.
• Tx: MgSO4 2-4gms over 5 – 60 mins.
• Hypermagnesemia: CRF w/ Mg Antacids, or
L+D. Tx: Calcium Gluconate 10% x 2 amps.

Minor Electrolytes
Indications for ERP2
• 260 (18%) abnls
• Only
O l 5 (0(0.3%)
3%) needed
d d
ED Tx
• Only 75 (5%) needed
hospital Tx
• All needing Tx were
di b ti alcoholic
diabetic, l h li or
renal failure patients.

53
 Electrolytes I: Recap
• Low Na+: Don’t hurt the brain. (CPM)
– Volume status, Ur OsM and Ur Na are key.
– 3% Saline – only if coma, seizing or post 26.2
miles .
• High Na+: Don’t hurt the brain. (Edema)
– NS bolus then D51/2 NS @ 150 ml/hr.
– Let internist correct over 24-48 hours.

Electrolytes II Recap
• Low K+: Arrhythmias and HPP only drama.
– KCL 20 meq/hr is safe. 40 meq/hr central.
• High K+: Save the heart.
– C/BIG/K can save the day.
– NaBicarb only if acidotic and not in CHF.
– Dialysis if high K+ and no urine output
output.

54
 Electrolytes III: Recap
• High Ca++: PTH and Cancer.
– NS,
NS NS,
NS NS then Lasix
Lasix, Biphosphates
Biphosphates, Steroids
Steroids.
• Low Ca++: Avoid hypoalbumen fake out.
– CRF, low PTH, Rhabdo, Pancreatitis
– 20 ml 10% CaGluconate
• High Phos: See low Ca++
• Low Phos: Ignore unless <1.0 mg/dL + Sxs
• High Mg++: L&D. Tx: CaGluconate.
• Low Mg++: EtOH. 2 gms MgSO4.

Sodium References
• Adrogué HJ, Madias NE., Hypernatremia., N Engl J Med. 2000 May 18;342(20):1493.
• Adrogué HJ, Madias NE., Hyponatremia., N Engl J Med. 2000 May 25;342(21):1581.
• Almond CS,, Shin AY,, Fortescue EB,, Mannix RC,, Wypij
yp j D,, Binstadt BA,, Duncan CN,,
Olson DP, Salerno AE, Newburger JW, Greenes DS., Hyponatremia among runners
in the Boston Marathon, N Engl J Med. 2005 Apr 14;352(15):1550-6.
• Budisavljevic, MN, Stewart, L, Sahn, SA, Ploth, DW. Hyponatremia associated with
3,4-methylenedioxymethylamphetamine ("Ecstasy") abuse. Am J Med Sci 2003;
326:89.
• Ellison DH, Berl T., Clinical practice. The syndrome of inappropriate antidiuresis., N
Engl J Med. 2007 May 17;356(20):2064-72
• Hartung, TK, Schofield, E, Short, AI, et al. Hyponatraemic states following 3,4-
methylenedioxymethamphetamine (MDMA,'ecstasy') ingestion. QJM 2002; 95:431.
• Schrier RW, Gross P, Gheorghiade M, Berl T, Verbalis JG, Czerwiec FS, Orlandi C;
SALT Investigators
Investigators., Tolvaptan,
Tolvaptan a selective oral vasopressin V2-receptor antagonist,
antagonist
for hyponatremia., N Engl J Med. 2006 Nov 16;355(20):2099-112.
• Upadhyay A, Jaber BL, Madias NE., Incidence and prevalence of hyponatremia., Am
J Med. 2006 Jul;119(7 Suppl 1):S30-5.

55
 Potassium References
• Acker CG, Johnson JP, Palevsky PM, Greenberg A., Hyperkalemia in hospitalized patients:
causes, adequacy of treatment, and results of an attempt to improve physician compliance with
published therapy guidelines., Arch Intern Med. 1998 Apr 27;158(8):917-24.
• Beal AL.
AL Scheltema KE KE. Beilman GJ
GJ. Deuser WE
WE. Hypokalemia following trauma
trauma. Shock.
Shock
18(2):107-10, 2002 Aug.
• Carvalhana V, Burry L, Lapinsky SE., Management of severe hyperkalemia without hemodialysis:
case report and literature review., J Crit Care. 2006 Dec;21(4):316-21.
• Charytan D, Goldfarb DS., Indications for hospitalization of patients with hyperkalemia., Arch
Intern Med. 2000 Jun 12;160(11):1605-11.
• Freeman K, Feldman JA, Mitchell P, Donovan J, Dyer KS, Eliseo L, White LF,
• Temin ES. Effects of presentation and electrocardiogram on time to treatment of hyperkalemia.,
Acad Emerg Med. 2008 Mar;15(3):239-49.
• Gennari FJ., Hypokalemia., N Engl J Med. 1998 Aug 13;339(7):451-8.
• Kruse JA. Carlson RW. Rapid correction of hypokalemia using concentrated intravenous
potassium chloride infusions. Archives of Internal Medicine. 150(3):613-7, 1990 Mar.
• K
Kruse JA.
JA Clark
Cl k VL
VL. CCarlson
l RW.
RW Geheb
G h b MA.
MA Concentrated
C t t d potassium
t i chloride
hl id iinfusions
f i iin
critically ill patients with hypokalemia. Journal of Clinical Pharmacology. 34(11):1077-82, 1994
Nov.
• Mattu A, Brady WJ, Robinson DA., Electrocardiographic manifestations of hyperkalemia., Am J
Emerg Med. 2000 Oct;18(6):721-9.
• Tassone H, Moulin A, Henderson SO. The pitfalls of potassium replacement in thyrotoxic periodic
paralysis: a case report and review of the literature. J Emerg Med. 2004 Feb;26(2):157-61.

Calcium, Phosphate & Magnesium

References
• Bilezikian JP. Management of acute hypercalcemia. N Engl J Med 1992;326:1196–1203.
• Deftos L. Hypercalcemia in malignant and inflammatory diseases. Endocrinol Metab Clin North
Am 2002;31:141–158.
• Fouad A, A Hutchinson AJ
AJ. Hyperphosphataemia in renal failure: causes,
causes consequences and
current management. Drugs 2003;63:577–596.
• Gibbs MA, Wolfson AB, Tayal VS. Electrolyte disorders. In: Rosen P, Barkin RM, eds. Emergency
medicine: concepts and clinical practice, 5th ed. St. Louis: Mosby-Year Book, 2002:1724–1745.
• Noronha JL, Matuschak GM. Magnesium in critical illness: metabolism, assessment, and
treatment. Intensive Care Med 2002;28:667–679.
• Pollak, MR, Yu, ASL. Clinical Disturbances of Calcium, Magnesium, and Phosphate Metabolism.
In: Brenner, BM, ed. Brenner and Rector’s, The Kidney, 7th Ed, St. Louis, MO, W.B. Saunders
Company, 2004: 1041-1064.
• Reber PM, Heath H. Hypocalcemic emergencies. Med Clin North Am 1995;29:93–106.
• Rosen GH, Boullata JI, O’Rangers EA, et al. Intravenous phosphate repletion regimen for critically
ill patients with moderate hypophosphatemia. Crit Care Med 1995;23:1204–1210.
• Shib JG,
Shiber JG Mattu
M tt A.
A Serum
S phosphate
h h t abnormalities
b liti in
i the
th emergency department.
d t t J Emerg
E M
Medd
2002;23:395–400.
• Subramanian R, Khardori R. Severe hypophosphatemia: Pathophysiologic implications, clinical
presentations and treatment. Medicine 2000;79:1–8.
• Zaloga, G. Ionized hypocalcemia during sepsis. Crit Care Med 2000;28:266–268.

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