electrolyte vignette

Fluid and Electrolyte Conference

Joel topf, MDNephrology FacultyProvidence Hospital

Friday, February 27, 2009

CC: weakness

Social Hx: bum

physical exam: starving


CC: weakness

Social Hx: bum

physical exam: starving

presentation

EtOH 44

1282.8 22

92 12

0.6128


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

DiarrheaFriday, February 27, 2009

Decreased intake945 outpatients with eating disorders

anorexia, bulemia, or both

ALL of the hypokalemic patients were abusing cathartics or inducing vomiting

NONE of the hypokalemia was due to restricted caloric intake alone

The restricted calorie subgroup was the most nutritionally deprived of all the subgroups.

95%

3%2%

Serum Potassium

>3.5 3.0-3.5 <3.0

Greenfeld, D., Et Al. Am. J. Psychiatry 152, 60-63 (1995).


Intake does matter in experimental settings but clinical relevance is questionable

A compilation of 7 separate metabolic balance studies reveals the following graph

1.00

1.75

2.50

3.25

4.00

0 200 400 600 800

Serum K with dietary restriction

Ser

um

K (

mE

q/d

L)

K defecit (mEq)


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

Alcoholism

De Marchi, S. et al. N Engl J Med 1993;329:1927-1934Friday, February 27, 2009

admission 28-days

potassium

magnesium

3.8 4.4

1.4 1.7


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?


Vomiting induced hypokalemia is due to renal losses

Glomerulus

Proximal tubule

Loop of Henle

Distal convoluted tubule

Collectingtubule



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


1282.8 22

92 12

0.6128

Initial Labs


1323.2 24

100 10

0.694128

2.8 2292 12

0.6128

Initial Labs Next morning


120 mEq and he’s still low

1323.2 24

100 10

0.694



repeat treatment

check magnesium

1323.2 24

100 10

0.694



repeat treatment

check magnesium

Ca

PhosMg

1323.2 24

100 10

0.694



repeat treatment

check magnesium

8.8

2.21.2

Ca

PhosMg

1323.2 24

100 10

0.694


Problem list

hypokalemia

hypomagnesemia

hypophosphatemia

hyponatremia


Na, 2Cl+ -

K+

K+

Ca, Na, Mg+ + +

+

++

+

++

+

Ca++


Na, 2Cl+ -

K+

K+

Ca, Na, Mg+ + +

+

++

+

++

+

ATP

ATP

ATP

Na, 2Cl+ -

K+

K+

Ca, Na, Mg+ + +

+

++

+

++

+

ATP

ATP

ATP


Na, 2Cl+ -

K+

K+

Ca, Na, Mg+ + +

+

++

+

++

+

ATP

ATP

ATP

Na, 2Cl+ -

K+

K+

Ca, Na, Mg+ + +

+

++

+

++

+

ATP

ATP

ATP

Na, 2Cl+ -

K+

K+

Ca, Na, Mg+ + +

+

++

+

++

+

ATP

ATP

ATP Mg

Mg

Mg


Na, 2Cl+ -

K+

K+

Ca, Na, Mg+ + +

+

++

+

++

+

ATP

ATP

ATP

Na, 2Cl+ -

K+

K+

Ca, Na, Mg+ + +

+

++

+

++

+

ATP

ATP

ATP

Na, 2Cl+ -

K+

K+

Ca, Na, Mg+ + +

+

++

+

++

+

ATP

ATP

ATP

Mg

Mg

Mg


Na, 2Cl+ -

K+

K+

Ca, Na, Mg+ + +

+

++

+

++

+

ATP

ATP

ATP

Na, 2Cl+ -

K+

K+

Ca, Na, Mg+ + +

+

++

+

++

+

ATP

ATP

ATP

Na, 2Cl+ -

K+

K+

Ca, Na, Mg+ + +

+

++

+

++

+

K+

K+

K+


Na, 2Cl+ -

K+

K+

Ca, Na, Mg+ + +

+

++

+

++

+

ATP

ATP

ATP

Na, 2Cl+ -

K+

Ca, Na, Mg+ + +

+

++

+

++

++


FIX THE MAGNESIUMSAVE THE POTASSIUM


magnesium


magnesium2 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


1282.8 22

92 12

0.6128

3.0

day one labs


8.8

2.21.21323.2 24

100 10

0.694

1282.8 22

92 12

0.6128

3.0

day two labs


day three labs

8.9

1.42.31333.9 24

98 10

0.694

8.8

2.21.21323.2 24

100 10

0.694

1282.8 22

92 12

0.6128

3.0


problem list

hyponatremia

hypophosphatemia

muscle weakness


problem list

hyponatremia

hypophosphatemia

muscle weakness

0

1

2

3

4

Day 1 Day 2 Day 3

Ph

os (

mg

/dL

)


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 dxIntracellular shift

CalcitoninCatecholamines

EpinephrineDopamineTerbutalineAlbuterol

InsulinCarbohydrate infusionsrefeeding

Respiratory alkalosisRapid cell proliferation

Treatment of anemiaCML in blast crisisAML

Decreased phosphorous absorption

Dietary insufficiencyMalabsorptionPhosphate binders

CalciumMagnesiumAluminumSevelamerLanthium

Vitamin D deficiencySteatorrhea

Vitamin D resistant ricketsGlucocorticoids


differential dxIncreased renal excretion

Volume expansion/natriuretic states

IV BicarbonateBicarbonaturiaGlucosuriaDiuretics

Acetazolamide is the most phosphaturic

High salt diet or saline infusionHyperaldosteronismSIADH

Paraneoplastic syndromePTHrpTumor induced osteomalacia

Renal transplantationAcute malaria (falciparum)X-linked hypophosphatemic rickets

Fanconi syndromeAlcoholismMultiple myelomaAmoniglycosidesHeavy metal toxicityChinese herbsCongenitalIfosfamideCisplatinCystinosisWilson’s DiseaseHereditary fructose intolerance

GlucocorticoidsHyperparathyroidismHypercalcemiaMetabolic acidosis


differential dx

8.9

1.42.3

8.8

2.21.2

3.0


differential dx

alcoholism

refeeding syndrome

malabsorption

respiratory alkalosis

Saline infusion8.9

1.42.3

8.8

2.21.2

3.0


differential dx

refeeding syndrome

8.9

1.42.3

8.8

2.21.2

3.0


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.

W i t h r e f e e d i n g , i n s u l i n m o v e s 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 labsDay Na K P Mg

1

2

3

4

5

128 2.8 3.0

132 3.2 2.2 1.2

133 3.9 1.4 2.3

131 3.8 1.8 2.2

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


We start with an increase in the plasma osmolality


ADH


We start with an increase in the plasma osmolalityThis is detected by the brain


ADH


We start with an increase in the plasma osmolalityThis is detected by the brainThe brain releases ADH


ADH


We start with an increase in the plasma osmolalityThis is detected by the brainThe brain releases ADHADH acts on the kidney


ADH


We start with an increase in the plasma osmolalityThis is detected by the brainThe brain releases ADHADH acts on the kidneyThe kidney reacts by retaining water and producing asmall amount of concentrated urine.


ADH

The retained watergoes here

not here


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


ADH


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


ADH

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 litersFriday, February 27, 2009

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)







500 mL







500 mL

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?




2,000 mL




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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