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ELECTROLYTE DISORDERS
Dr. Camelia Diaconu
November 22, 2016
Homeostasis
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State of equilibrium in body

Naturally maintained by adaptive responses

Body fluids and electrolytes are maintained


within narrow limits
Major Compartments for Fluids
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INTRACELLULAR EXTRACELLULAR FLUID (ECF)


FLUID (ICF) Outside cell

Inside cell Intravascular fluid - within

Most of body fluid blood vessels (5%)


here - 63% weight Interstitial fluid - between

cells & blood vessels (15%)


Transcellular fluid -
cerebrospinal, pericardial,
synovial
Electrolytes
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Substances whose molecules dissociate into ions


(charged particles) when placed into water
CATION - positively charged electrolyte
ANION - negatively charged electrolyte

# Cations must = # Anions for homeostasis to


exist in each fluid compartment
Commonly measured in mEq/L
Functions of electrolytes
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Promote neuromuscular irritability

Regulate acid - base balance

Regulate distribution of body fluids among


body fluid compartments
ELECTROLYTES IN BODY FLUID COMPARTMENTS

INTRACELLULAR EXTRACELLULAR

POTASSIUM SODIUM

MAGNESIUM CHLORIDE

PHOSPHORUS BICARBONATE

Ca2+ = almost equal in ICF and ECF


METHODS OF FLUID & ELECTROLYTE MOVEMENT

Diffusion
Osmosis

Active transport

Filtration
Regulation of fluids
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Hypothalamus

Pituitary gland

Kidneys
ADH (Antidiuretic Hormone)
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Water-retaining hormone

Hypothalamus senses low blood volume and


increased serum osmolality; triggers its release
from the pituitary gland

Prompts kidneys to retain H2O

Increases concentration of urine


ALDOSTERONE
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Produced by adrenal cortex

Released as part of RAA mechanism

Acts on renal distal convoluted tubule

Aldosterone = fluid retention and secretion of K+;


triggers the thirst center

Responsible for reabsorption of Na & water into


the vascular compartment
Renin released by
kidneys in response
Angiotensinogen Renin to decreased blood
volume

Angiotensin
Lungs
I

Angiotensin Adrenal
II gland

Aldosteron

12 Peripheral
vasoconstriction
TONICITY
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Isotonic a solution that has the same solute


concentration as that of ICF
(0.9% NSS, Ringers solution)
TONICITY
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Hypertonic a solution with a higher solute


concentration than that of ICF
(Dextrose 5% in NSS)
TONICITY
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Hypotonic a solution with lower solute


concentration than that of ICF
(0.45% NaCl solution)
ISOTONIC SOLUTIONS
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0.9% NaCl solution

Ringers Solution

Lactated Ringers solution


HYPOTONIC SOLUTIONS
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5% Dextrose & water

0.45% NaCl

0.33% NaCl
HYPERTONIC SOLUTIONS
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3% NaCl
5% NaCl

Whole blood

Albumin

Total parenteral nutrition

Tube feedings

Concentrated dextrose (>10%)


ELECTROLYTES
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Na+: most abundant electrolyte in the body


K+: essential for normal membrane excitability for nerve impulse
Cl-: regulates osmotic pressure and assists in regulating acid-base
balance

Ca2+: usually combined with phosphorus to form the mineral salts


of bones and teeth, promotes nerve impulse and muscle
contraction/relaxation

Mg2+: plays role in carbohydrate and protein metabolism, storage


and use of intracellular energy and neural transmission. Important
in the functioning of the heart, nerves, and muscles
Normal values for main electrolytes
- mEq/L -

Cl 95-105

Na 135 145

K 3.5-5

Ca 8.5-10.2

Mg 1.5-2

Phosphate 2.5-4.5
Fluid and electrolyte imbalances
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Common in most patients with illness


Directly caused by illness or disease (burns or
heart failure)
Result of therapeutic measures (IV fluid
replacement or diuretics)
MAJOR ELECTROLYTE IMBALANCES
(mEq/L)
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Na
imbalance K imbalance
<135 or <3.5 or >5
>145

Chloride Mg
imbalance imbalance
<95 or >105 <1.5 or >2
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Natrium
SODIUM
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Imbalances typically associated with parallel


changes in osmolality
Regulated by the kidneys
Influenced by the hormone aldosterone
Chloride ion frequently appears with the Na ion
Primary regulator of ECF volume
Chloride
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Maintains serum osm along with Na


Helps to maintain acid/base balance
Combines with other ions for homeostasis:
Na, K, Ca
Closely tied to Na
Decreased level is most commonly due to GI
losses
Sodium Functions
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Transmission and conduction of nerve impulses


Responsible for osm of vascular fluids
Regulation of body fluid levels
Na shifts into cells and K shifts out of the
cells (Na/K pump)
Assists with regulation of acid-base balance by
combining with Cl or HCO3
Hyponatremia epidemiologic
data

The most common electrolytic disorder in


hospitalized pts:

30% of pts hospitalized in ICU


87% of pts admitted for heart failure

Sometimes it is a medical emergency, that


requires prompt intervention to prevent
cerebral edema !
Upadhyay A et al. Am J Med 2006
London Marathon, April 2007
A 22 yo man died after
completing his first London
Marathon because he drank too
much water. David Rogers
collapsed at the end of the race
and died yesterday in Charing
Cross Hospital.

Today it emerged the fitness


instructor died from
hyponatremia, or water
intoxication.
www.dailymail.co.uk

Na 122 mmol/L
Hyponatremia is associated with
unfavorable evolution

High risk of mortality


Prolonged hospitalization
High costs

Patients with chronic asymptomatic


hypoNa are hospitalized for diverse
trauma
HypoNa increases the risk of fractures

Gheorghiade M et al. Arch Intern Med 2007


Wald R et al. Arch Intern Med 2010.
Osmolality

Osmolality is the number of osmotic


active particles per unit of solvent

Plasmatic osm is determined by the plasm. Na


Plasmatic osm is maintained within normal range
(275-290 mOsm/Kg H2O) by the variation of
sodium intake and output, as a result of
vasopressin changes and thirst

Plasmatic osmolality
2 x seric Na + seric glucose /18 + BUN/2.8
Hyponatremia (Na<135 mEq/L)
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Excessive Na loss or H2O gain


CAUSES
Prolonged diuretic therapy

Excessive diaphoresis

Insufficient Na intake

GI losses suctioning, laxatives, vomiting

Administration of hypotonic fluids

Compulsive water drinking

Alcoholism
Hyponatremia is an
alteration of water balance

Water input
> Renal water
excretion
Hyponatremia
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Causes an osmotic fluid shift from


plasma into brain cells
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Types of hyponatremia

Hypovolemic
Euvolemic
Hypervolemic
Redistribution
Pseudohyponatremia
Hypovolemic hyponatremia
Volume replacement with hypotonic
fluids, vomiting, diarrhea, 3rd space
sequestration, renal losses

Na deficit > Water deficit


Euvolemic Hyponatremia

Normal quantity of Na but free water excess


SIADH: most common cause
Physical and emotional stress or pain

Myxedema, Addison disease

Drugs

Preparation for colonoscopy or colorectal surgery

35% of hypoNas of hospitalized pts


Euvolemic Hyponatremia - SIADH

HypoNa with:

Urinary osm (>100 mmol/L)


Urinary excretion of Na (>20 mmol/L)

Hypouricemia

Normal renal and endocrine function

Without diuretic treatment, dehydration or edema

SIADH is an exclusion diagnosis !


Hypervolemic Hyponatremia
Total Na increased, as well as TBW

Water excess
> Na excess

May be renal or nonrenal


Acute or chronic renal insufficiency
Cirrhosis, CHF, nephrotic syndrome

20% of hospitalized hyponatremic pts


Hypertonic Hyponatremia
(Posm > 295)
Hyperglycemia
Manitol excess
Glycerol use
Pseudohyponatremia
(Posm 275-295)

Hyperproteinemia Hyperlipidemia
Lab evaluation of hypoNa

Seric Osm
Urine Osm
Glycemia: seric Na with 1.6-2.4 mmol/L for each
100 mg/dL increase of glycemia > 100 mg/dL

Tests for thyroid and adrenal function : TSH,


FT4, ACTH

Uric acid and BUN


Hyponatremia ED treatment
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Correct volume and perfusion deficits with


NS

In euvolemic or hypervolemic pts, restrict fluids to


500-1500 ml water daily

In severe hypoNa (<120) developed rapidly, with


CNS changes, give hypertonic saline, 3% NS (513
mEq/L) at 25-100 mL/h;
The Na correction should not exceed 12 mEq/L/day
Hyponatremia - treatment
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Rapid correction

central pontine myelinolysis

Fluid restriction with SIADH


Hyponatremic seizures
Poorly responsive to anticonvulsants
Hypertonic
Na saline
deficit=weight (Kg) x 0.6 x (desired Na+
measured Na+)
Hypernatremia (Na>145 mEq/L)
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Occurs with excess loss of H2O or excessive retention


of Na

Can lead to death if not treated


Hypernatremia - causes
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Loss of water Gain of Na


Reduced water intake Increased intake
Unconsciousness
Inability to drink water Increase salt use
Lack of access to water Sodium bicarbonate
Water loss in excess of Na adm
Vomiting, diarrhea

Sweating, fever
Mineralocorticoid or
glucocorticoid

Diabetes insipidus
Drugs: lithium, phenytoin excess
Dialysis
Primary

Thyrotoxicosis

Severe burns
aldosteronism
Cushing syndrome
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Hypernatremia S/S
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Thirst, dehydration
Dry mucus membranes
Flushed skin
Tachycardia
Irritability, lethargy, weakness
Seizures, coma
Hyperactive deep tendon reflexes
Dry, swollen tongue
Hypernatremia treatment in ED
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Correct volume Each liter of If no urine


deficits with water deficit output after
NS or lactated causes the Na rehydration,
Ringer sol; to increase 3-5 rapidly switch
avoid lowering mEq/L to NS; give
Na+ more than furosemide 20-
10 mEq/L/day 40 mg IV
Hypernatremia treatment
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Rate of correction for Na+ 1-2 mEq/L/hr

Calculate water deficit


= 0.6 x weight (Kg) x [(current Na+/140) 1]

Rate of correction for calculated water deficit


50% in the first 12-24 hrs
Remaining next 24 hrs
Hypernatremia - treatment
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Low Na diet
May use salt substitutes if K+ OK

Encourage H2O consumption

Monitor fluid intake in patients with heart or renal disease

Observe changes in BP and HR if hypovolemic

Monitor serum Na levels

Assess respiratory for crackles

Weigh daily
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Potassium
Potassium Imbalances
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K is the most abundant cation in the body cells

97% is found in the intracellular fluid


Also plentiful in the GI tract

Normal extracellular K+ is 3.5-5 mEq/L


A serum K+ level < 2.5 or > 7.0 can cause cardiac
arrest

80-90% is excreted through the kidneys


Daily intake of K is necessary because it is
poorly conserved by the body
Hypokalemia (K+<3.5 mEq/L)-causes
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Increased loss:
Shift into the cell:
- Hyperaldosteronism
- Alkalosis and sodium - Diuretics
bicarbonate
- Beta-agonists - Renal tubular acidosis
- Adm. of insulin and glucose - Renal artery stenosis
- GI loss: vomiting, diarrhea

HypoK
Miscellanous:
- Hypercalcemia
- Mg deficiency Reduced intake
- Acute leukemia
- Drugs and toxins (penicilin,
theophylline)
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19/10/2009
HypoK ECG changes
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HypoK ED treatment
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IV or PO replacement
Give K+ IV diluted in a large vein
* Never push K+ as a bolus *
Monitor site for infiltration

In stable pts oral replacement is preferred: 20-40 mEq


K+

In unstable pts: iv KCl 10-20 mEq/h, no more than 40


mEq KCl to each liter of iv fluid, infusion rate should not
exceed 40 mEq/h
A 20 mEq/dose K+ will raise the K+ by 0.25 mEq/L
Monitor EKG for dysrhythmias
Hyperkalemia (K+>5.5 mEq/L)
Etiology
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Increased dietary intake


Excessive adm. of K+
Excessive use of salt substitutes
Burns, trauma
Renal failure
Potassium sparing diuretics
Addison disease
Digitalis intoxication
Hyperkalemia S/S
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Hyperkalemia
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ECG changes: K>8 ventricular fib, blocks


decreased pH, metabolic acidosis
Hyperkalemia tests for
management
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Arterial
ECG blood gases
(check for
acidosis)

Digoxin
Electrolytes level in
appropriate
pts
Hyperkalemia ED treatment
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Give IV calcium chloride (10%) 5-10


If K>7.0 mEq/L
mL or IV calcium gluconate (10%) 10-
or ECG changes 20 mL

If digoxin
Avoid calcium, give digoxin immune
toxicity with Fab therapy
hyperK

Consider giving 50-100 mEq sodium


In acidotic pts bicarbonate slow IV

Give 50 mL (25 g) of D50W


with 10-20 U regular insulin IV
push (5-10 U in dialysis pts)
Hyperkalemia ED treatment
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Diuresis is
maintained Kayexalate (po
with or rectal) 1 g
furosemide binds 1 mEq K
20-40 mg IV

In pts with Albuterol 5-10


acute renal mg by
failure, consult nebulization
a nephrologist may also be
for dialysis used
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Calcium
Calcium
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Regulated by the parathyroid gland

Parathyroid hormone
Helps
with Ca retention and phosphate
excretion through the kidneys

Promotes Ca absorption in the intestines

Helps mobilize Ca from the bone

Normal Ca = 8.5-10 mEq/L


Calcium
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Calcium helps K and


Na move into and out
cells in the Na-K pump
mechanism
Hypocalcemia (Ca2+<8.5 mEq/L)
- Etiology -
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Surgically induced hypoparathyroidism

Renal failure

Vit. D defficiency

Inadequate exposure to ultraviolet light

Acute pancreatitis

Hyperphosphatemia
Hypocalcemia S/S
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Muscle cramps
Hyperactive deep tendon reflexes
Paresthesia of fingers, toes and
face
PositiveTrousseaus/Chvosteks
sign
Tetany
Laryngeal spasms
Confusion, memory loss
Cardiac dysrhythmias
Hypocalcemia - seizures,
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mental changes
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Hypocalcemia ED treatment
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If asymptomatic: use tb In symptomatic pts or


of Ca gluconate 1-4 those with severe hypoCa:
g/day PO divided every Ca gluconate or Ca chloride,
6 hrs vit. D (calcitriol 10 mL 10% solution IV
0.2g,2 times/day) slowly over 10 min

Replace Mg in conjunction with Ca2+


Hypercalcemia (>10.5 mEq/L)
- etiology -
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Etiology: PAM P. SCHMIDT


Parathyroid hormone
Addison disease
Multiple myeloma
Paget disease
Sarcoidosis
Cancer
Hyperthyroidism
Milk-alkali syndrome
Immobilization
Excess vit. D
Thiazides
Hypercalcemia S/S
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Stones: renal calculi


Bones: osteolysis
Psychic moans: lethargy, weakness, fatigue,
confusion
Abdominal groans: abdominal pain, constipation,
polyuria, polydipsia
ECG changes
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Short QT
Hypercalcemia ED treatment
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Initiate treatment in pts with severe


symptoms or significant dehydration
Restore fluid deficits, enhance calcium
elimination, decrease osteoclastic activity
Loop diuretics: only in isolated cases,
furosemide 10-40 mg IV after correction of
fluid deficits
Drugs that inhibit osteoclastic activity:
biphosphonates, calcitonin, glucocorticoids
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Magnesium
HypoMg (<1,5 mEq/L) - Causes
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Excessive dietary intake of Ca++ or vit. D


Gastrointestinal losses
Pancreatitis, alcoholism
Excessive diuretic therapy
Malabsorption syndromes
Hypercalcemia, hypoaldosteronism
High dose steroid use
Cancer chemotherapy
HypoMg S/S
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CNS symptoms: depression, vertigo, ataxia,


seizures, tetany
Cardiac symptoms: arrhythmias, prolonged
PR, QRS and QT
Anemia, hypotension, hypothermia, dysphagia
HypoMg ECG changes
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HypoMg ED treatment
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Cardiac monitoring
Seizure precautions
Treat with oral, IM, IV or Mg salts
Monitor urine output

In pts with severe symptoms and normal renal


function:

adm. 2 g magnesium sulfate IV over an


hour, followed by 6 g over the first 24 hrs
HyperMg (serum Mg>3 mEq/L)
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Causes

Renal failure
Excessive use of Mg containing antacids
Untreated diabetic ketoacidosis
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HyperMg ECG changes
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HyperMg ED treatment
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In many pts, stopping Mg intake is sufficient


In severely symptomatic pts, give 5 mL (10%
solution) of calcium chloride IV to antagonize
the effects of Mg
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Phosphorus
PHOSPHORUS
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Essential to the function of muscle and red


blood cells, maintenance of acid-base balance

Provides structural support to bones and teeth

N = 2.7-4.5 mg/dL
Hypophosphatemia (<2.7 mg/dL)
- Causes -
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insufficientintake
malnutrition, starvation

hyperparathyroidism
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A decrease in the serum phosphorus level is


accompanied by an increase in the serum Ca level
Hypophosphatemia S/S
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Decreased contractility and cardiac output


Decreased bone density
Irritability
Confusion
Seizures
Hypophosphatemia - treatment
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Monitor cardiovascular, respiratory,


neuromuscular, cerebral, renal and GI status

Adm. phosphorus orally along with vit. D


supplement

Prepare to administer phosphorus IV

Monitor for signs of fracture


Hyperphosphatemia (>4.5 mg/dL)
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Increase in serum phosphorus is accompanied


by a decrease in serum calcium

Causes: decreased renal excretion, increased


intake of phosphorus, hypoparathyroidism

S/S same as hypocalcemia


Hyperphosphatemia - treatment
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Entails management of hypocalcemia

Avoid phosphate containing medications


Last Slide

Its Over

THANK YOU !
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19/10/2009

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