fluid and electrolytes disasters jose-marie el-amm nephrology division wsu/dmc/huh august, 2006

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FLUID AND ELECTROLYTES DISASTERS JOSE-MARIE EL-AMM NEPHROLOGY DIVISION WSU/DMC/HUH AUGUST, 2006

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FLUID AND ELECTROLYTES DISASTERS

JOSE-MARIE EL-AMMNEPHROLOGY DIVISION

WSU/DMC/HUH AUGUST, 2006

COMPOSITION OF BODY FLUID COMPARTMENTS

COMPOSITION OF ECF AND ICF

ECFECF ICFICFNa 141 10K 4.1 120-150Cl 113 3HCO3 26 10

PHOSPHATE 2.0 140(ORGANIC)

TOTAL BODY WATER= 0.6 X TOTAL TOTAL BODY WATER= 0.6 X TOTAL BODY WEIGHTBODY WEIGHT

(0.5 IN THE ELDERLY OR OBESE, 0.7 IN (0.5 IN THE ELDERLY OR OBESE, 0.7 IN INFANTS AND VERY YOUNG CHILDREN)INFANTS AND VERY YOUNG CHILDREN)

2/3 ICF 1/3 ECF

¼ IVV

¾ ISV

(Principal Cells)

CLINICAL APPROACH TO CLINICAL APPROACH TO HYPONATREMIAHYPONATREMIA

IS HYPONATREMIA REALLY HYPOTONICITY? Translocational vs. isotonic

WHAT IS THE VOLUME STATUS? What are the physiological signals to the

kidney and the brain

WHAT IS THE URINE SODIUM AND OSMOLALITY? Is ADH present and is it physiologically

appropriate

CASE STUDY 1CASE STUDY 1 

A 30 year old woman is admitted for an increase in edema and worsening jaundice. She is a known alcoholic and has had several admissions for jaundice and ascites. She stopped taking her diuretic approximately 10 days ago.

Physical examination: blood pressure 128/80, heart rate 76 supine. No orthostatic change in BP noted. She has icteric sclera, ascites, sacral and pedal edema. Her liver span is 10 cm.

Labs: 125 89 5 bilirubin= 12mg/dL 80 albumin= 2.5 g/Dl 3.2 28 0.8

UNa = 1mEq/L

Uosm= 300mOsm/kg H2O

What is her Posm? What is her cell size?

CASE STUDY 1CASE STUDY 1What is her effective

arterial volume? mild volume depletion(4%)

historychange in body weightno orthostatic changes BP or pulse

moderate volume depletion(5% to 10%)

HR 15/min on standingsystolic BP 15mm Hg on standing

severe volume depletion(10%)supine hypotensionsupine tachycardia

CASE STUDY 1CASE STUDY 1

Is her total body water high, low or normal?

Is her total body sodium high, low or normal?

EDEMA=INCREASED TOTAL BODY SODIUM AND WATER BUT DOES NOT! NOT! NOT!NOT! NOT! NOT! TELL YOU THE PROPORTIONS (SODIUM CONCENTRATION)

ORTHOSTATIC HYPOTENSION= DECREASED TOTAL BODY SODIUM AND WATER BUT DOES NOT! NOT! NOT! NOT! NOT!NOT! TELL YOU THE PROPORTIONS (SODIUM CONCENTRATION)

BODY COMPARTMENT BODY COMPARTMENT VOLUMESVOLUMES

70 kg person 0.6 =42 liters total body water

25 liters intracellular (ICF)-3/5 TBW 28 liters intracellular (ICF)-2/3 TBW

17 liters extracellular (ECF)-2/5 TBW 14 liters extracellular (ECF)-13 TBW

3.5 liters intravascular (IVV)-1/5 ECF 3.5 liters intravascular (IVV)-1/4 ECF

13.5 liters interstitial (ISV)-4/5 ECF 10.5 liters interstitial (ISV)-3/4 ECF

PRINCIPAL SENSORS IN VOLUME REGULATION

EFFECTIVE CIRC VOL/

VENOUS RETURN /

/ CARDIAC OUTPUT

/ BP

BARORECEPTOR STIMULATION/

/ SYMPATHETIC TONE

VENOUS CONSTRICTION/RELAXATION

/ CARDIAC CONTRACTILITY

ARTERIAL CONSTRICTION or RELAXATION

/ RENIN SECRETION

/ TUBULAR Na+ REABSORPTION

/ A II

/ ALDO

CASE STUDY 1CASE STUDY 1

Can you tell if ADH is being secreted? How?

Why is her ADH status the way it is? What turns ADH off? What turns it on?

CONTROL OF ADH

ALL

NONE

ADH

POSM

UOSM

280 300

50 1200

CASE STUDY 1CASE STUDY 1 

A 30 year old woman is admitted for an increase in edema and worsening jaundice. She is a known alcoholic and has had several admissions for jaundice and ascites. She stopped taking her diuretic approximately 10 days ago.

Physical examination: blood pressure 128/80, heart rate 76 supine. No orthostatic change in BP noted. She has icteric sclera, ascites, sacral and pedal edema. Her liver span is 10 cm.

Labs: 125 89 5 bilirubin= 12mg/dL 80 albumin= 2.5 g/dL 3.2 28 0.8

UNa = 1mEq/L

Uosm= 300mOsm/kg H2O

CASE STUDY 1CASE STUDY 1

Which IV fluids would you select?

CASE STUDY 1CASE STUDY 1

What diuretic(s) would you use?What would be the most likely or

severe complications using diuretics in her case?

(Principal Cells)

CASE STUDY 1CASE STUDY 1

CLARISSA’S TEAM HAVE BEEN WORKING ON HER FOR THE LAST WEEK. WITH ‘JUDICIOUS’ USE OF DIURETICS AND FLUID RESTRICTION, THEY HAVE DROPPED HER WEIGHT BY 12 LBS AND INCREASED HER SODIUM BY 5 MEQ/L. THE ON-CALL CHECK-OUT TO YOU IS “DON’T WORRY ABOUT HER.” AT 2 AM YOU ARE CALLED BY THE NURSE BECAUSE CLARISSA’S BP IS 80/60 AND HER HR IS 110/MIN.

WHAT DO YOU DO?

CASE STUDY 1CASE STUDY 1

1. DON’T WORRY ABOUT IT.

2. START AN IV OF NS AT 150CC/HR

3. BOLUS HER WITH NS IN 100CC INCREMENTS UNTIL HER BP INCREASES

4. GIVE 25 GRAMS OF ALBUMIN IVPB

5. START DOPAMINE

A patient with severe congestive heart failure and massive edema is admitted to the hospital complaining of progressive dyspnea.

Laboratory values

12594 40

4.1 25 2

CASE STUDY 2CASE STUDY 2

What is his Posm?

What is his cell size?

1-Spironolactone is administered but no diuresis occurs despite 2 days of treatment. Why?

2-A thiazide diuretic is then added to spironolactone with equally discouraging results. Why?

3-What single diuretic might result in successful diuresis? Why?

CASE STUDY 2CASE STUDY 2

(Principal Cells)

CASE STUDY 2CASE STUDY 2

A loop diuretic is given with better results but still not impressive diuresis

What diuretic might you add to the loop diuretic to increase the loop diuretic potency?

A 60 year old man was evaluated for persistent cough and a 25 pound weight loss over a 3 month period. He smoked a pack a day for 40 years. P.E.: BP sitting 110/70, no signs of dehydration and no evidence of edema.

A pleural effusion is present on the right. PPD was positive. Weight 65 kg.

CASE STUDY 3CASE STUDY 3

CASE STUDY 4CASE STUDY 4

115 88 4

105

3.7 24 0.6

Posm245 mOsm/kg H2O

Uosm340 mOsm/kg H2O

UNa39 mEq/L

In order to get rid of a water load, one needs to produce very dilute urine. What are the requirements for such urinary dilution?

1)Extrarenal requirements

adequate GFR

adequate solute delivery

2)Intrarenal requirements

intact vasa recta and loop function

absence of ADH

CAUSES OF SIADHCAUSES OF SIADH

Carcinomas (lung, pancreas, duodenum)

Pulmonary disease(pneumonia, Tb, abscess, etc.)

CNS disorders (meningitis, encephalitis, SDH, SAH, CVA, trauma, etc)

CASE STUDY 4CASE STUDY 4A 40 year old man is brought to the ER by EMS after a witnessed seizure. His family states that he has been complaining of a severe headache and has had progressive mental deterioration over the last week or 10 days. They say he takes no medications and has no significant medical history.

Physical exam is completely negative except for meningeal signs. There is no focal neurological deficit, no papilledema. He weighs 60 kg.

Labs: 110 80Uosm=275mOsm/kg

UNa=50 mEq/L

3.5 22 CSF: 100WBC:

75%mononuclear

CASE STUDY 5CASE STUDY 5

Is ADH present? (hint: look at Uosm)Why is this man hyponatremic?

 

 

(present TBW) (present SNa) =present TBS

(normal TBW) (normal SNa) =normal TBS

(0.6)(60kg) x (110) = (???) x (140)

(36L)(110)/(140) = (???) = 28L

36 – 28 = 8 liters excess water8 liters excess water

SYMPTOMS OF SYMPTOMS OF HYPONATREMIAHYPONATREMIA

Mainly neurologic Symptoms of cerebral edema

Nausea and malaise followed by headache, lethargy, obtundation, seizures,

coma and death

The rate at which the hyponatremia develops determines the degree and severity of the symptoms Several protective responses which act to minimize cell

swelling Within four hours of hyponatremia developing the cells start

to lose solutes & as intracellular solute amount decreases, water moves back out of the cells, returning the cell volumes toward normal

CASE STUDY 5CASE STUDY 5How would you treat this man?

For rapid correction of symptomatic euvolemic hyponatremia, hypertonic (3%) saline is used

Hypertonic (3%) saline has about 0.5mEq/ml. (500mEq/L)

What are your goals and end points? Goal for rapid/initial SNa is to increase SNa to 120-

125mEq/L or until symptoms improve-whichever is lower

Overly rapid correction of hyponatremia can lead to an osmotic demylination state

Patients should have plasma serum sodium concentrations increased at less than 12 mEq/L/day (0.5mEq/L/hr)

The amount of sodium needed to raise the serum sodium can be estimated by the sodium deficit. Multiply the total body water (0.5xlean body weight in kg in women, 0.6x weight in men) by the plasma sodium deficit per liter.

36L x 15 mEq/L = 540 mEq Na 540 mEq Na needneed

At <0.5mEq/L/hour need to change over 30 hours

1000mL/30hours 30 mL/hour30 mL/hour

CASE STUDY 6CASE STUDY 6A 30 year old man comes in complaining

of polyuria and polydipsia for the previous two weeks. He has a history of sarcoidosis diagnosed 10 years ago for which he has been on Prednisone intermittently. Except for bilateral pulmonary crepitants and for uveitis, the physical exam is normal.

Labs:

152 120 30

4 25 1.0

U/A: neg glucose, acetone

Uosm=75 mOsm/kg H2O

What are the causes of polyuria?

1.Diabetes mellitus

2.Diabetes insipidus

3.Hypokalemia

4.Hypercalcemia

5.Psychogenic water drinking

HYPERNATREMIABY DEFINITION, HYPERNATREMIA IS A HYPERTONIC STATE. YOU STILL DON’T KNOW THE VOLUME STATUS WITHOUT EXAMINING THE PATIENT. IN A VOLUME VOLUME CONTRACTEDCONTRACTED STATE, WATER AND SODIUM ARE LOST-JUST MORE WATER THAN SODIUM. IN AN APPARENTLY EUVOLEMICEUVOLEMIC PATIENT, PURE WATER IS LOST. THERE ARE FEW SIGNS OF VOLUME DEPLETION AS MOST OF THE WATER LOSS IS INTRACELLULAR. VOLUME EXPANDEDVOLUME EXPANDED STATES ARE THOSE IN WHICH HYPERTONIC VOLUME EXPANSION TAKES PLACE.

CENTRAL DIABETES INSIPIDUS:

Idiopathic

Trauma

Hypoxic encephalopathy

Posthypophysectomy

Neoplastic 1:craniopharyngioma, pinealoma, cyst

metastatic: breast, lung

Misc: sarcoidosis, aneurysm, Histiocytosis X, encephalitis, meningitis

NEPHROGENIC DIABETES INSIPIDUS:

Hereditary: usually X-linked, very rare AR form

Drugs: lithium, cidofovir, foscarnet

Electrolyte disorders: hypokalemia, hypercalcemia

Misc: sickle cell anemia or trait, renal amyloidosis, Sjögren’s syndrome, transient DI in pregnancy

DIABETES INSIPIDUS THERAPYDDAVP

a 2 amino acid substitute of ADH with potent antidiuretic effect but little to no pressor effects

Mild volume depletion(1-2 kg), a low salt diet and a thiazide diuretic increases proximal sodium and water resorption and

decreases water delivery to the ADH sensitive collecting tubule

Don’t use loop diuretics induce a relative resistance to ADH by decreasing the

maximal interstitial concentrationNSAIDs

potentiate ADH and are additive to the thiazide effect(renal prostaglandins oppose ADH effects)

A 78 year old woman was admitted with right hemiparesis. She had a 9 year history of hypertension.

PE: Her BP was 190/95 mm Hg. Pulse 80 beats per min.

CASE STUDY 7CASE STUDY 7

CASE STUDY 7CASE STUDY 7

LABS: Hct 40%. Urine: SpGr 1.025, negative for protein and glucose. Sediment: Occasional WBC and RBC. BUN 17, Creat. 1.0 mg/dl. Glucose 140 mg/dL, Na 140 mEq/L, K 3.7 mEq/L, CO2 24 mEq/L and Cl 103 mEq/L.

After admission she was managed with tube feedings and eventually transferred to a nursing home.

Three weeks later she was readmitted because of vomiting and tachypnea.

PE: Wt. 67 kg., BP 115/80. P=120, Temp. = 101.6 F. She was unresponsive and had poor skin turgor.

LABS Urine: SpGr 1.022, protein 1+, glucose neg. Sediment: Few hyaline casts. BUN 120 mg/dl, creatinine 3 mg/dl, glucose 150 mg/dL, Na 160 mEq/L, K 5.9 mEq/L, Cl 125 mEq/L, CO2 18 mEq/L. Hct 48%.

Is total body sodium increased, normal or decreased?

It total body water increased, normal or decreased?

How did this occur?

CASE STUDY 7CASE STUDY 7

Is total body water increased, normal or decreased?

poor skin turgor

Water Sodium

Normal Our patient

Is total body sodium increased, normal or decreased?BP 115/80 P=120

How did this occur?

Loss of sodium and water-more water than sodium

Water losses: insensible (temp 101F), urine

(conc.), GI

Sodium losses: poor intake and vomiting

THE TRAGEDY OF THE VERY YOUNG & VERY OLDMobile people lose salt and water

(N/V) but as IVV , ADH and they become thirsty/seek out fluids. fluid intake with ADH present can

lead to hyponatremiaNon-mobile people (playpens,

restraints, strokes) cannot respond to thirst if they lose more water than sodium,

they become hypernatremic

CASE STUDY 7CASE STUDY 7

What is the first priority in her therapy? IVV resuscitation

What IV would you first order? 0.9% NaCl

How much would you give? Until she is better

CASE STUDY 7CASE STUDY 7

Once she has a stable blood pressure, her total body sodium (TBS) has been returned to normal

How much water would be needed to lower her serum sodium to 140 mEq/L?

PE: Wt. 67 kg.

LABS: BUN 120 mg/dl, creatinine 3mg/dl, glucose 150 mg/dL, Na 160 mEq/L, K 5.9 mEq/L, Cl 125 mEq/L, CO2 18 mEq/L. 67kg x .5=33.5L=TBW

160 x 33.5=140 x desired TBW

desired TBW=38 liters

She needs 4.5 liters of water to drop her serum Na to 140 mEq/L

Rates of correction should be carefully controlled as cerebral edema can occur with over-rapid corrections. Correcting at less than 0.5mEq/L/hr (12 mEq/day) is safe.

TREATMENT OF HYPERNATREMIA

Eg: 5 liters of water need to be given to replace the water deficit.

Serum sodium 165 140mEq/L 25mEq/L

This will take 50 hours to drop it less than or equal to 0.5 mEq/hour

5000mL/50hours = 100 mL/hour of D5W or

200 mL/hour of D21/2NS