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Body fluid compartments

Total body fluid = 60% body weight

Two-thirds is in the intracellular K+ rich

(120 mmol/L)

One-third is in the extracellular space

Na+ rich (140 mmol/L)

One-quarter of extracellular fluid is in

the intravascular space

In a 70-kg man Total body fluid = 42 L

Intracellular fluid = 28 L

Extracellular fluid = 14 L

Intravascular fluid = 3.5 L

There is movement of water

between these compartments

Plasma sodium concentration is

an index of total body fluid

osmolality

Body fluid compartments and osmolality(Robert U, NEPHROLOGY Medical Progress December 2003)


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Plasma sondium (Na+) concentration :

the ratio between sodium and water in the plasma

Normal : 135 145 mmol/L

Hyponatremia : < 135 mmol/L

Is, Na+ loss or water gain

HYPONATREMIA


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Types and Causes of Hyponatremia

Pseudohyponatremia

A rare measurement artefact caused by reduced plasma water, as a

result of excess lipids (triglycerides) or abnormal proteins (e.g. IgM)

Hyperosmolar (iso-osmolar and other) hyponatremia

Hyperglycaemia (and other impairment solutes, but not urea)

Surgical (e.g. transurethral prostatectomy) irrigation fluids (mannitol,

sorbitol, glycine)

Subarachnoid haemorrhage

True (hypo-osmolar) hyponatremia

q ECF (q TBNa+) reduced effective arterial volume (Na+ loss)

o ECF (o TBNa+) reduced effective arterial volume (oedema)

q ECF ( TBNa+) normal effective arterial volume (no oedema),

SIADH, drugs, stress, q cortisol, q thyroxine)


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The formula of osmolality

Posm = 2[Na+] + [glucose]/18 + [BUN]/2.8


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Hiponatremia

Translocational

hyperglycemia

irrigation fluids

(mannitol, sorbitol)

surgical

(transurethral prostatectomy)

Normal or high osmotic Low osmotic

(true hyponatremia)

Psudohyponatremia

protein

lipid

Urinary osmolality *)

> 100 mosm/kgUrinary osmolality


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A Clinical Approach to Hyponatremia

Hypo-osmotic hyponatremia

Urinary sodium

concentration

Urinary

osmolality

Treatment Normal saline Water restriction Treat + restrict water

Hypovolaemia Euvolaemia Hypervolaemia

Renal loss

Diuretic

Na+ loss

Extra Renal loss

Gastrointestinal

tract Skin

Heart failure

Liver failure

Nephrotic syndrome

Syndrome of

inappropriate

antidiuretic

PsychogenicHypothyroid

Drugs

(Robert U, NEPHROLOGY Medical Progress December 2003)


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SALT LOSING NEPHRITIS

Nephritis with an excessive urinary loss of Na

hypovolemic hyponatremia

urinary Na+ >20 mmil/L

mostly without hypertension

medullary cystic disease

chronic interstitial nephritis

polycystic kidney disease analgetic nephropathy

partial urinary tract obstruction

chronic glomerulonephritis (rarely)


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Diagnosis criteria for SIADH

(Syndrome of inappropriate ADH secretion

Essential

ECF effective osmolality below 270 mosmol/kg water

Inappropriate urinary concentration (> 100 mosmol/kg)

Clinical euvolemia

Increased urinary [Na+

] while on a normal salt and water intake Absence of adrenal, thyroid, pituitary or renal insufficiency or

diuretic use

Supplemental

Abnormal water load test (inability to excrete at least 90% of 20

mL/kg water load in 4 h and/or failure to dilute urinary osmolality tobelow 100 mosmol/kg)

Plasma ADH level inappropriately raised relative to plasma

osmolality

No significant correction of plasma [Na+] with volume expansion but

improvement after fluid restriction THE LANCET, Vol 352, July 18, 1998)


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CLINICAL MANIFESTATION:

Symtoms of hyponatremia due to the

consequences of plasma hypoosmolality

HypoosmolalityMove of water from extra

to intracellular

intracellular

edema

Particularly in CNS

Symptoms:

- Lethargy

- confusion

- nausea-vometing

- muscle cramps

- seizures- coma

Note:

Permanent neurologic damage may be occur in premenopausal women

- the cause is not well understood

- so: hyponatremic women must be watched carefully

Lauriat, SM. J. Am Soc Nephrol. 8 : 1997


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postoperative menstrual women

elderly women in thiazide diuretics

children

psychiatric polydipsic patients

hypoxemic patients

PATIENTS AT RISK FOR PERMANENTNEUROLOGIC COMPLICATION


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Important questions must be answered :

1. Is the patients symptomatic ? Symptomatic patients have to

treat aggressively but promptly

2. is the hyponatremia

- acute (before 48 hrs) ?

- chronic (after 48 hrs) ?

Acute hyponatremic, carries a

greater risk of permanent

neurologic sequelae if the

correction is not expeditiously

3. Whats the Na+ level ? Severe hypoNa+ is Na level


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SEVERE

HYPONATREMIA

(Na+


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HypoN+ present for


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HypoNa+ present for >48 hrs or the duration is unknown

increase the serum Na+ by 10% with hypertonic saline

infusion at rate 1,5 -2 ml/kg/hr (or in 4-6 hrs)

after the initial correction, do not exceed a correction

rate of 1-1,5 ml/kg/hr

coadministration of loop diuretic

until the symptoms resolved or Na+ level 130 mmol/L

do not increase the serum Na+ by more than 15 mmol/L

24 hrs serum Na+ should be carefully monitored (every 4-6 hrs)

SEVERE CHRONIC SYMPTOMATIC HYPONa+


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TreatmentTreatment MechanismMechanism

Fluid restrictionFluid restriction Decreases free waterDecreases free water

Pharmacological inhibition of ADHPharmacological inhibition of ADH

LithiumLithium Inhibits renal response to ADHInhibits renal response to ADH

DemeclocyclineDemeclocycline Inhibits renal response to ADHInhibits renal response to ADH

VV22 receptor antagonistreceptor antagonist Antagonises vasopressinAntagonises vasopressin

Increased solute intakeIncreased solute intake

FurosemideFurosemide Increases free water clearanceIncreases free water clearance

UreaUrea Osmotic diuresisOsmotic diuresis

THE LANCET, Vol 352, July 18, 1998)

CHRONIC ASYMPTOMATIC HYPONa+

No immediate therapy is required and underlying diseasecan be sought

No urgency to coorect the serum Na+


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HYPOKALEMIA

Serum K level < 3.5 mmol/L (normal: 3.5 5.5 mmol/L)

True hypokalemia : decreased of serum K level

False (spurious) hypokalemia :

false in laboratory result

in extreme leucocytosis (in vitro), wbc uptake kalium

in the test tube


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DIAGNOSTIC APPROACH OF HYPOKALEMIA

Hypokalemia

Kalium depletionTranscelular shift

insulin therapy

beta2 agonists

alkalosis

Urine K 20 meq/L renal losses

Viarable PH

post obstructive

ATN recovery

aminoglycoside

Metabolic acidosis

RTA

Diabetic ketoacidosis


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CLINICAL MANIFESTATIONS

Cardiac

ventricular irritability

abnormal ECG

predisposition of digitalis intoxication

coronary artery spasm Neuromuscular

muscle spasm, tetany, paralysis

gastrointestinal (constipation, ileus)

Renal polyuria

increased amoniogenesis

Endocrene

carbohydrate intolerance


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MANAGEMENT

Emergency or not emergenny ? clinical manifestation

ECG

degree of hypo K

Estimated degree of decreases in total body kalium decreased in average of 0,3 mmol/L for each 100 mmol of

kalium depletion

Serum K level Deficit

Mild 3.00 3.4 meq/L 150 200 meq/L

Moderate 2.00 3.0 meq/L 200 400 meq/L

Severe < 2 meq/L 500 1000 meq/L


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Treat the underlying causes

In mild hypo K : oral K preparation 600 -1200 meq/day

- small risk of hyper K

MANAGEMENT


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Mild and severe hypo K : intravenous administration

do not give direct i.v injection : CRIME

intravenous drips peripheral or central venous line

10 20 meq/hr : into peripheral vein

> 40 meq/hr : into central vein

with ECG monitor

Monitoring K level carefully (every 4-6 hrs)


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TAKE- HOME MESSAGE :

In diagnostic and treatment of water and electrolyte

dysbalance :

knowledge of basic renal physiology is useful for

understanding.

a promptly management and monitoring is needed


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A Clinical Approach to Hyponatremia

Pseudohyponatremia

High protein

High Lipid

Hypo-osmotic

hyponatremia

Assess extracellular fluid

(volume) status

Jugular venous pressure

Postural blood pressure

Presence of edema

Hyperosmotic

hyponatremia

HyperglycaemiaMannitol


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Acute Hyponatremia

Iatrogenic often post-op

Large volumes hypotonic fluids

Pain, hypotension, nausea,

drugs - may increase ADH


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Acute Symptomatic Hyponatremia

Risk of cerebral oedema greater than the risk

treatment complications

Treat with furesemide and hypertonic saline (3%) untilconvulsions subside usually means increasing [Na]

by 10%

3% NaCl @ 1-2 ml/kg/hr (for ~ 4 hrs) or 1.0-1.5

mEq/1/hr

Do not exceed correction of 1.5 meq/1/hr

Do not increase [Na] more than 12-15 meq/l/day


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Chronic Hyponatremia

Often asymptomatic

No hurry

Water restriction

Treat th eunderlying cause if possible eg. Heart

failure, SIADH, thiazides

Increase In [Na] may be associated with subtle

improvements eg less falls

Tolvaptan trials-improved Mental Component of

SF-36 despite normal baseline


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Severe hyponatremia

(


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1. Because cerebral water is increased only byapproximately 10% in severe chronic

hyponatremia, promptly increase the serum

sodium level by 10%, or by approximately

10 mmol/L

2. After the initial correction, do not exceed a

correction rate of 1 to 1.5 mmol/L hr

3. Do not increase the serum sodium by more

than 12 mmol/L in 24 hours


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Hyponatremia and Hypernatremia

Sodium concentration is simply the ratio od

sodium to water; thus, hyponatremia (plasma

sodium (PNa] < 130 mmol/L) is Na+ loss or water

gain

In clinical practice, hyponatremia usually results

from gain of water or failure to excrete it, and cells

may or may not be swollen


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(Robert U, NEPHROLOGY Medical Progress December 2003)

K+ Secretion Along the Collecting Duct

AldosteroneAldosterone Distal NDistal N++

deliverydelivery

KK++

secretionsecretion

ooECFECF qq oo mm

qqECFECF oo qq mm

Conns syndrome (Conns syndrome (ooECF)ECF) oo oo oo

Diuretics (Diuretics (qqECF)ECF) oo oo oo

Addisons disease (Addisons disease (qqECF)ECF) qq qq qq

Acute glomerulonephritis (Acute glomerulonephritis (ooECF)ECF) qq qq qq

Hyperkalemia vs. normokalemia occurs in oliguric vs. non-oliguric acute renal failure

ECF = extracellular fluid

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