Electrolyte Vignette

Fluid and
Electrolyte
Conference
Joel topf, MD
Nephrology Faculty
Providence Hospital

Friday, February 27, 2009

CC: weakness

Social Hx: bum

physical exam:
starving


presentation

CC: weakness 12
128 92 128
2.8 22
Social Hx: bum 0.6
EtOH 44
physical exam: starving


least sick patient you
admitted


problem list


problem list

weakness

hyponatremia

hypokalemia


Hypokalemia: differential diagnosis


Decreased intake
Alcoholism
Starvation


Decreased intake
Alcoholism
Starvation
Renal losses
Diuretics
Vomiting
RTA
Hyperaldo


Decreased intake
Alcoholism
Starvation
Renal losses
Diuretics
Vomiting
RTA
Hyperaldo
GI Losses
Diarrhea

Decreased intake
945 outpatients with eating
disorders Serum Potassium
anorexia, bulemia, or both
2%
ALL of the hypokalemic 3%
patients were abusing
cathartics or inducing
vomiting
NONE of the hypokalemia
was due to restricted
caloric intake alone
95%
The restricted calorie
subgroup was the most
nutritionally deprived of >3.5 3.0-3.5 <3.0
all the subgroups.
Greenfeld, D., Et Al. Am. J. Psychiatry 152, 60-63 (1995).


Serum K with dietary restriction
Intake does matter in
4.00
experimental settings
but clinical

Serum K (mEq/dL)
3.25
relevance is
questionable
2.50

A compilation of 7 1.75
separate metabolic
balance studies 1.00
reveals the 0 200 400 600 800
following graph K defecit (mEq)


Alcoholism

61 patients with weekly alcohol ingestion
greater than 600g/wk.

No cirrhosis of hepatitis, renal disease or,
acute medical condition.

Admitted for inpatient detoxiﬁcation for 4
weeks

De Marchi, S. et al. N Engl J Med 1993;329:1927-1934

admission 28-days

3.8 4.4
potassium

1.4 1.7
magnesium


Vomiting induced hypokalemia
is not due to GI losses



potassium content
of stomach ﬂuid
is 15 mEq/L



potassium content
of stomach ﬂuid
is 15 mEq/L

How much vomit
to get a 120 mEq
potassium deﬁcit?


Distal convoluted
tubule
Glomerulus

Vomiting induced Proximal tubule
hypokalemia is Collecting
tubule
due to renal
losses

Loop of Henle


Vomiting induced
hypokalemia is
due to renal
losses


is due to renal losses
Vomiting causes
metabolic alkalosis

Increased serum
bicarbonate is
dumped into the
urine

urine potassium can
rise to 80-120 mEq/L


Hypokalemia: Treatment

Potassium is 2.8

How much poassium will you give:

100 x (4–k)


Orders:


Orders:
banana bag


Orders:
banana bag

D5LR at 80 an hour


Orders:
banana bag

D5LR at 80 an hour

KCL 40 mEq IVPB


Orders:
banana bag

D5LR at 80 an hour

KCL 40 mEq IVPB

KCL 80mEq orally split over
two doses q4 hours


Initial Labs
12
128 92 128
2.8 22
0.6


Initial Labs Next morning
12 10
128 92 128 132 100 94
2.8 22 3.2 24
0.6 0.6


120 mEq and he’s still low

10
132 100 94
3.2 24
0.6



10
132 100 94
3.2 24
0.6
repeat treatment

check magnesium



10
132 100 94
3.2 24
0.6
repeat treatment
Ca
check magnesium Mg Phos



10
132 100 94
3.2 24
0.6
repeat treatment
Ca
check magnesium Mg Phos

8.8
1.2 2.2


Problem list

hypokalemia

hypomagnesemia

hypophosphatemia

hyponatremia


Na, 2Cl -
+

+
K
++
Ca
+
+
+
+

+
K +
+
+
+ + +
Ca, Na, Mg


Na, 2Cl -
+

+
K

+
+
+
+

+
K +
+
+
+ + +
Ca, Na, Mg


Na, 2Cl -
+

+
K
ATP
+
ATP
+
+
+

+
K ATP
+
+
+
+ + +
Ca, Na, Mg


Na, 2Cl -
+

+
K
Mg
ATP
+
ATP Mg
+
+
+

+
Mg
K ATP
+
+
+
+ + +
Ca, Na, Mg


Na, 2Cl -
+

+
K
ATP
+
K +
ATP
+
+
+
+
K
+
ATP
K +
+
+
K +
+ + +
Ca, Na, Mg


Na, 2Cl -
+

+
K

+
ATP
+
+ ATP
+
+
+
+
+
+

+
K ATP
+
+
+
+
+
+
+ + +
Ca, Na, Mg
Ca, Na, Mg+
+ +


FIX THE MAGNESIUM
SAVE THE POTASSIUM

magnesium


magnesium
2 grams of Magnesium Sulfate IVPB over an
hour or so


magnesium
doesn’t really work

the next day it’s still low

Most of the IV magnesium is immediately
dumped in the urine

you need to drip it in over as long as
possible

i like 6g (48.6 mEq) over 24 hours


day one labs
12
128 92 128
2.8 22 3.0
0.6


day two labs
12
128 92 128
2.8 22 3.0
0.6

8.8 10
132 100 94
1.2 2.2 3.2 24
0.6


day three labs
12
128 92 128
2.8 22 3.0
0.6

8.8 10
132 100 94
1.2 2.2 3.2 24
0.6

10
8.9 133 98 94
3.9 24
2.3 1.4 0.6

problem list

hyponatremia

hypophosphatemia

muscle weakness


problem list

4

hyponatremia
3

Phos (mg/dL)
hypophosphatemia 2

muscle weakness 1

0
Day 1 Day 2 Day 3


weakness

hypokalemia corrected

magnesium a little high

not enough to cause muscle weakness


hypermagnesemia
the most tolerated electrolyte abnormality

Upper limit of magnesium 1.8

pre-eclampsia magnesium 6-8

Lethal magnesium 14


Weakness

Hypophosphatemia


differential dx

Decreased phosphorous absorption

Intracellular shift

Increased renal excretion


differential dx
Intracellular shift Decreased phosphorous
absorption
Calcitonin
Dietary insufﬁciency
Catecholamines
Malabsorption
Epinephrine
Phosphate binders
Dopamine
Calcium
Terbutaline
Magnesium
Albuterol
Aluminum
Insulin
Sevelamer
Carbohydrate
infusions Lanthium
refeeding Vitamin D deﬁciency
Respiratory alkalosis Steatorrhea
Rapid cell proliferation Vitamin D resistant
rickets
Treatment of anemia
Glucocorticoids
CML in blast crisis
AML


differential dx
Increased renal excretion Fanconi syndrome
Volume expansion/ Alcoholism
natriuretic states Multiple myeloma
IV Bicarbonate Amoniglycosides
Bicarbonaturia Heavy metal toxicity
Glucosuria Chinese herbs
Diuretics Congenital
Acetazolamide is the Ifosfamide
most phosphaturic Cisplatin
High salt diet or Cystinosis
saline infusion Wilson’s Disease
Hyperaldosteronism Hereditary fructose
SIADH intolerance
Paraneoplastic syndrome Glucocorticoids
PTHrp Hyperparathyroidism
Tumor induced Hypercalcemia
osteomalacia Metabolic acidosis
Renal transplantation
Acute malaria
(falciparum)
X-linked
hypophosphatemic rickets

differential dx

3.0

8.8
1.2 2.2

8.9
2.3 1.4


differential dx
alcoholism
3.0
refeeding syndrome
8.8
malabsorption
1.2 2.2
respiratory alkalosis
8.9
Saline infusion
2.3 1.4


differential dx

3.0
refeeding syndrome
8.8
1.2 2.2

8.9
2.3 1.4


Transcellular redistribution is movement of phosphorous into
cells. This is usually transient and, in the face of
normal total body phosphourous is harmless.
However, in the face of pre-existing phosphorous depletion,
this transcellular movement can provoke serious symptoms
including death. The most severe cases are

found with refeeding syndrome.

Weinsier and Krumdieck, 1981, Am J Clin Nutr, 34, 393-9


Starvation decreases total body phosphorous.
However, serum phos remains normal due
to movement of phosphorous out of cells.
With refeeding, insulin moves
phosphorous into cells, in order to
phosphorylate carbs as part of glycolysis.

This unmasks the previous
phosphorous depletion.

this is worse with fructose

conversion of fructose to fructose-P
is unregulated

causes rapid consumption of Phos and
ATP

the loss of ATP is thought to be the
cause of fructose toxicity


give phos

stop carbs


Stop the D5LR

Started 8 ounces of
milk four times a
day

Used a packet of
KPhos


IV sodium phosphorous

8mmol q6 hours

target 32 mmol in a day

careful in renal failure


day four and ﬁve labs
Day Na K P Mg

1 128 2.8 3.0

2 132 3.2 2.2 1.2

3 133 3.9 1.4 2.3

4 131 3.8 1.8 2.2

5 130 4.2 2.8 1.8


problem list

hyponatremia


Speciﬁc gravity on admission:

1.005

What’s the speciﬁc gravity in:
hypervolemic hyponatremia: heart
failure? Cirrhosis? Nephrotic
syndrome?

Euvolemic hyponatremia: SIADH?

Hypovolemic hyponatremia:
diuretics? GI losses?

What regulates speciﬁc gravity?



ADH



ADH

We start with an increase in the plasma osmolality



ADH

This is detected increase in
We start with an by the brainthe plasma osmolality



ADH

The is detected increase
Thisbrain releases the in
We start with an by ADHbrainthe plasma osmolality



ADH

ADH acts releases the
The is detected kidney
Thisbrain on an increase in
We start withthe by ADHbrainthe plasma osmolality



ADH

The retained water
goes here

not here

The kidney reacts by retaining water and producing a
small amount of kidney
The is detected concentrated
Thisbrain on an increase in urine.
ADH acts releases the
We start withthe by ADHbrainthe plasma osmolality



ADH

What do all of the etiologies of
hyponatremia have in common?



ADH

What do all of the etiologies of
hyponatremia have in common?

ADH


Hyponatrmia Occurs When Water
Intake Exceeds Excretion

ADH Decreases Urine Volume

Our patient has a low speciﬁc gravity.



ADH independent hyponatremia




psychogenic polydipsia





tea and toast or beer drinkers
potomania



18 liters

The kidney is able to
concentrate urine to 1200
mOsm/L

The kidney is able to dilute
urine to 50 mOsm/L

If a patient has a daily
solute load of 600 mOsms.
What is:

The minimal amount of
urine he can produce
(maximum ADH)

The maximum amount of
urine he can make
(minimal ADH)


mOsm/L

urine to 50 mOsm/L

What is:

(maximum ADH) 500 mL

urine he can make
(minimal ADH)


mOsm/L

urine to 50 mOsm/L

What is:

(maximum ADH) 500 mL

urine he can make
(minimal ADH) 12,000 mL

600 mOsms is the typical daily solute
load

so a patient requires a minimum of
500 mL of urine to remove the daily
solute load

A patient making less than that is
unable to clear the daily solute load

what is the deﬁnition of oliguria


What if the daily solute load is 100
mOsms?

What is the most urine they can make?


mOsms?


2,000 mL


mOsms?


2,000 mL
What happens if they are getting IV
ﬂuids at 100 mL/hour?


An alcoholic gets much of
his daily calories from
alcohol.

Alcohol is metabolized to
CO2 and water

no solute for the kidney
to excrete

Low daily solute load


A tea and toast diet refers to
a carbohydrate rich diet free
of proteins

Both beer drinker’s and Tea and Toast
respond to increased protein intake

Usually get a brisk response to
crystalloids


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