Clinical practice guideline on diagnosis ... - edc.mui.ac.ir practice guideline on... · congestive heart failure, GI loss, yg pypychogenic polydipsya H enal from renal causes Physiology

Clinical practice oand treatment of hyponatraemiahyponatraemiaDR MOJGAN MORTAZAVIASSOCIATE PROFESSOR OF NEPHROLOGYASSOCIATE PROFESSOR OF NEPHROLOGYISFAHAN UNIVERSITY OF MEDICAL SCIEN

on diagnosis

YYCES

PhysiologyPhysiologyDefinition of hyponatDifferent type of hypClinical featuresClinical featuresHyponatremia/DiagnTreatment

tremiaponatremia

nosis

SODSODDIUMDIUM

Hyponatremiayp Physiology

Serum sregulati

tistimusecrefeedb

the realdoswww.daviddarling.info aldos

renal sodiu

odium concentration on:l ti f thi tlation of thirst

etion of ADHback mechanisms of enin-angiotensin-sterone systemsterone system handling of filtered m

Sodium

www.merricks.com/tech_eelectrolyte_new.htm

Osmoregulation and Osmoregulation and eleaseUnder normal circumsta

regulation of the releaseregulation of the releasefrom the posterior pituitadepends on the effectivdepends on the effectivserum.

vasopressin vasopressin

ances, osmotic e of vasopressin e of vasopressin ary primarily ve osmolality of the ve osmolality of the

Hyponaatremia


tremiaponatremia

nosis

ntroductionntroduction

Hyponatraemia, defined as a sconcentration

<135 mmol/l, is the most commonand electrolyte balance encount It occurs in up to 30% of hospita

leadt id t f li i l to a wide spectrum of clinical symsevere or even life threatening

erum sodium

n disorder of body fluidtered in clinical practice.alised patients and can

t f btl tmptoms, from subtle to

ntroductionntroduction

Hyponatraemia is primarily a dibalance, with a relative excess ofto total body sodium and potassiu It is usually associated with a dy

hormone that governswater balance, vasopressin (also h )hormone).

isorder of waterf body water comparedy pum content.disturbance in the

called antidiuretic

yponatremiayponatremia

Low plasma osmolality cau

into the cells and then cellul

particularly in brain cells

uses water movement

lar overhydration


Mortality/Morbidity

Acute hyponatremia (devare subject to more severare subject to more severedemasodium level is less than

is over 50%Chronic hyponatremia (d

48 h) experience milder d48 h) experience milder dedema Brainstem herniation ha

ti t ith h i hpatients with chronic h

veloping over 48 h or less) re degrees of cerebral re degrees of cerebral

n 105 mEq/L, the mortality

eveloping over more than egrees of cerebral egrees of cerebral

as not been observed in h t ihyponatremia


tremiaponatremia

nosis


Types Hypovolemic hyponatremia Euvolemic hyponatremia Hypervolemic hyponatremia Redistributive hyponatremia Redistributive hyponatremia Pseudohyponatremia

Which one of these serums smolality?

A- Half salineB-RingerC-dextrose / salineC-dextrose / salineD-serum1/3,2/3

has lower

Which one of these serums smolality?

A- Half salineB-RingerC-dextrose / salineC-dextrose / salineD-serum1/3,2/3

has lower

uvolemic hyponatreuvolemic hyponatre

SIADH Pulmonary Disease

Small cell, pneumonia, TB, sarc Cerebral Diseases

CVA T l t iti iCVA, Temporal arteritis, mening Medications

SSRI Antipsychotics Opiates D SSRI, Antipsychotics, Opiates, D

emiaemia

coidosis

iti h litigitis, encephalitis

Depakote TegratolDepakote, Tegratol

Diagnostic criteria for the sgantidiuresis

syndrome of inappropriatey pp p

edistributive hyponaedistributive hyponaWater shifts from the

t ll l extracellular comparesultant dilution of total body sodium atotal body sodium aThis condition oc

hyperglycemiahyperglycemiaAdministration of

atremiaatremiae intracellular to the

t t ith artment, with a sodium. The TBW and are unchanged are unchanged. curs with

f mannitol

stimates of the serum sodium orrected fore presence of hyperglycaem This translates into adding 2.4 mmeasured serum sodium concent5.5 mmol/l (100 mg/dl) incrementconcentration above a standard concentrationof 5.5 mmol/l (100 mg/dl).

concentration

miammol/l to thetration for everyytal rise in serum glucose serum glucose g

he sodium of a patient is 125mucose is 500mg/dl. what is the

odium in this patient?

A-135B 145B-145C-130D-140

mg/dl and the blood e exact number of the

he sodium of a patient is 125mucose is 500mg/dl.what is the

odium in this patient?

A-135B 145B-145C-130D-140

mg/dl and the blood e exact number of the

PseudohyponatremPseudohyponatrem The aqueous phase is diluted

lipids The TBW and total bodlipids. The TBW and total bodyhypertriglyceridemia lti l lmultiple myeloma

miamiaby excessive proteins or sodi m are nchanged y sodium are unchanged.

seudohyponatraemseudohyponatraem Pseudohyponatraemia is a labowhen abnormally high concentrablood interfere with the accurate SodiumSodium

miamiaoratory artefact that occurs

ations of lipids or proteins in the measurement of

eset osmostateset osmostat

In reset osmostat, there is a chawell as in the slope of the osmorep The response to changes in osm We see this phenomenon, for epwhere the serum sodium concentdecrease 4–5 mmol/l./

ange in the set point asgulation curveg

molality remains intact.xample, in pregnancyp p g ytration may mildly


tremiaponatremia

nosis

Clinical Clinical features features

Clinical featuresClinical features

Symptoms can vary from mild, and

life-threatening Severe symptoms of hyponatraare caused by brain oedema andintracranial pressure. Brain cells start to swell whenwater moves from the extracellula

non-specific to severe

aemiad increased

ar to the intracellular

efinition of hyponatraemiaiochemical severity

We define ‘mild’ hyponatraemia as a bfinding of a serum sodium concentration b130 and 135 mmol/l as measured by ion-sp130 and 135 mmol/l as measured by ion spelectrode. We define ‘moderate’ hyponatraemiafi di f di t tifinding of a serum sodium concentrationbetween 125 and 129 mmol/l as measuredelectrode. We define ‘profound’ hyponatraemiafinding of a serum sodium concentration<125 mmol/l as measured by ion-specific e/ y p

a based on

biochemicalbetweenpecificpecific

a as a biochemical

d by ionspecific

as a biochemical

electrode

efinition of hyponatraemia ba development

We define ‘acute’ hyponatraemthat is documented to exist <48 h. We define ‘chronic’ hyponatraethat is documented to exist for at If hyponatraemia cannot be clbeing chronic, unless there is clinig ,evidence of the contrary

sed on time

mia as hyponatraemia.emia as hyponatraemia least 48 h.lassified, we consider itical or anamnestic

ymptoms of hyponaymptoms of hypona

The changes induced by a(developing over 1-3 days)( p g y )permanent neurological dprimarily duo to cerebral o

Nausea and malaise as theacutely below 125 meq/l

Headache, lethargy, and oappear in Na+ between 11

atremiaatremia

acute hyponatremia ) may result in ) yamage and are verhydratione plasma Na+ falls

obtundation may 15-120

ymptoms of hyponaymptoms of hypona

The more sever changes oare not seen until the plasmp110-115 meq/l

Women particularly premep y p,appear to be at much gredeveloping sever neurologi ibl l i dirreversible neurologic dammay be related to differenmetabolism and sex hormometabolism and sex hormo

atremia…..atremia…..

f seizures and coma ma Na+ is less than

enopausal women peater risk of gic symptoms and of

th th t mage than men that ces in cerebral

ones ones.


tremiaponatremia

nosis

Hyponatremia/D Diagnosis

CT head, EKG, CXR if symptom Repeat Na level Correct for hyperglycemia Laboratory tests provide impo Laboratory tests provide impo

differential diagnosis of hypon Plasma osmolality Urine osmolality Urine sodium concentratio Uric acid level Uric acid level FeNa

Diagnosis

matic

ortant initial information in the ortant initial information in the natremia

on

Hyponatremia/D

Laboratory tests Cont. Pl l lit Plasma osmolality

normally ranges fromIf >290 l/k If >290 mosmol/kg :

Hyperglycemia omannitolmannitol

If 275 – 290 mosmol/hyperlipidemia ohyperlipidemia o

If <275 mosmol/kg :Eval volume statuEval volume statu

Diagnosis

m 275 to 290 mosmol/kg or administration of

/kg :or hyperproteinemiaor hyperproteinemia

usus

yponatremia/Diagnyponatremia/Diagn

Laboratory tests Cont. Plasma osmolality < 275 mosmol/k

Increased volume:CHF, cirrhosis, nephrotic sy

E l i Euvolemic SIADH, hypothyroidism, psy

postoperative statesDecreased volume

GI loss, skin, 3rd spacing, di

nosisnosis

kg

yndrome

ychogenic polydipsia,

uretics

yponatremia/Diagnyponatremia/Diagn Laboratory tests Cont.

Urine osmolality Normal value is > 100 mos N l t hi h Normal to high:

Hyperlipidemia, hyper < 100 mosmol/kgg

hypoosmolar hyponat Excessive sweatin Burns Vomiting Diarrhea Diarrhea Urinary loss

nosisnosis

mol/kg

rproteinemia, hyperglycemia, SIADH

tremiag

Hyponatremia/D Laboratory tests Cont.

Urine Sodium >20 mEq/L

SIADH, diuretics <20 mEq/L

cirrhosis, nephrosis, skin, 3rd spacing, psy, p g, p y

Uric Acid Level < 4 mg/dl consider SIAD

FeNaHelp to determine pre-r

Diagnosis

congestive heart failure, GI loss, ychogenic polydipsya y g p y p y

DH

enal from renal causes


tremiaponatremia

nosis

Treatment of Treatment of hyponatremiahyponatremia

reatmentreatment

There are two basic There are two basic involved in the treathyponatremia: hyponatremia: 1-rasing the plasmarate rate 2-treating the under

principles principles tment of

a Na+ at a safe rlying cause

reatmentreatment

Goal:

raise Na by <10-12 meq/L in the 1st 24

raise Na by <18 meq/L in the 1st 48 hou

hours

urs

Available therapies foAvailable therapies foyponatraemia The treatment of hyponatraemia is de1-the symptoms present,2- the duration of hyponatraemia, 3-and the diagnostic category (namely or euvolaemic hyponatraemia)or euvolaemic hyponatraemia)

or or

ependent on several factors

hypovolaemic, hypervolaemic

hyponatraemic patients withcluding obtundation, coma, sspiratory arrest (Acute)

the treatment of choice is 3% hmmol/l) to decrease brain oed/ )herniation and cardiorespirator

a practical approach is a 100 mhl id t b t d ithi chloride to be repeated within

improvement occurs. This approsodium concentration by 2–4 myattenuate the brain oedema.

Concomitant furosemide use codi t ti sodium concentration even mo

severe symptoms seizures, and

ypertonic saline (513 ema and avoid brainstem ry arrest. ml bolus of 3% sodium 30 i if li i l 30 min if no clinical oach will increase serum

mmol/l and thereby / y

ould increase serum ore.

moderate neurologicmoderate neurologicconfusion, disorientation, nausea acute or chroniccute or chronic Treatment with hypertonic Thi h h h This approach, however, sh

caution so as to avoid too hyponatraemiahyponatraemia.

In patients with either sevesymptoms fluid restriction ssymptoms, fluid restriction sand the patient followed ca

cal symptomscal symptomsnd alerted mental status)

saline h ld b d ith hould be used with rapid a correction of

re or moderate should be instituted should be instituted arefully in hospital

Minimal symptoms ( incMinimal symptoms ( incncentrate, irritability, altered mood and d

fluid restriction The degree of fluid restriction depend For example, if a patient’s daily urine

oral fluid intake should be restricted to

Such fluid restriction will generally incsodium concentration by 1–2 mmol p

clude headache inability to clude headache, inability to depression.)more are chronic

ds on the patient’s urine output output is 1,200 ml, their daily o 750 ml

crease the patient’s serum per day.

Minimal symptomsMinimal symptoms

The higher the urinary-to-plasma osmg y pfluid restriction becomes, and long-teoutside the hospital, is poor

In elderly females with chronic hypon In elderly females with chronic hyponnormal saline infusion was reported tobetter outcomes than was fluid restric

molality ratio, the less effective y ,erm compliance, particularly

natraemic encephalopathy natraemic encephalopathy, o be associated with much ction alone.

DemeclocyclineDemeclocycline

Administration of demeclocycline caresistant diabetes insipidus and enabl

H i t d l ti However, owing to drug accumulatiodemeclocycline is contraindicated infailure or cirrhosis

n result in a vasopressin-le more liberal fluid intake

d t i ff t on and toxic effects, n patients with either heart

Oral ureaOral urea

(15–30 g per day in divided doses) hahyponatraemia;

thi t k b i l t this agent works by causing a solute solute-free water excretion).

The main criticism associated with ure Because of its poor palatability, oral u

orange juice. In the intensive care unit setting urea In the intensive care unit setting, urea

given via gastric tube

as been used to treat

di i (th t i i d diuresis (that is, increased

ea is its bitter taste.urea should be given with

a (0 5 1 g/kg per day) can be a (0.5–1 g/kg per day) can be

OOP diureticOOP diuretic

loop diuretic adminiswith increased sodiumwith increased sodiumalso enhance solute-

tiexcretion.

stered together m intake can m intake can -free water

asopressin-receptorasopressin receptorhypervolaemic hyponatraemia / eyponatraemia )yponatraemia )

Conivaptan was the first FDA-approveT l t Tolvaptan

In hyponatraemic patients starting theshould not be restricted and the patieconcentration should be monitored eexcessive increase in serum sodium c

The use of tolvaptan is FDA approved p ppconcentrations of less than 125 mmolrelated symptoms

r blockerr blockereuvolaemic

ed AVP-receptor blocker

ese V2-receptor blockers, fluid ent’s serum sodium every 6–8 h so as to avoid an oncentration

d for patients with serum sodium p/l or patients with clinically

n which diseases the waterestricted for treatment of hy

A-SIADHB-Primary polydipsiaC-Renal failureD-All of them

r should be yponatremia?

n which diseases the waterestricted for treatment of hy

A-SIADHB-Primary polydipsiaC-Renal failureD-All of them

r should be yponatremia?

reatment with Naclreatment with Nacl

True volume depletioDi tiDiuretics

Adrenal insufficiency y

on

yy

reatment with H2O rereatment with H2O re

SIADHEd t t tEdematous state

Renal failure

Primary polydipsia

estrictionestriction

osmotic demyelinatosmotic demyelinat

Symptoms: flaccid paralysis, dy Evolve over days – weeks May extend dorsally Sensory

tion tion

ysarthria, dysphagia

y Tracts

he risk factors for develoemyelination

1-More than a 12 meq/l elevation

2-Over correction of the Na+ to afirst 2 days

3-Hypoxic or anoxic episodes prio4-Osmotic demyelination has beemostly in patients who have an inlower than 115–120 mmol/llower than 115–120 mmol/l

oping osmotic p g

n in Na+ in the first day

bove 140 meq/l within the

or to therapy en reported to occur itial serum sodium level

isk factors for developinp

concomitant liver dishypokalaemia malnhypokalaemia, malnchange in serum sodth 25 l/l i ththan 25 mmol/l in thetreatment

ng demyelination g y

seases, hypoxia, utrition and a utrition and a

dium of more i iti l 48 h f e initial 48 h of

sk factors for developing dgatients on dialysis

Patients with a chronic serum sodium mmol/l,

li di liver disease, malnutrition, alcoholism and hypokalaemia are at alcoholism and hypokalaemia are at

osmotic demyelination. In these settings, serum sodium correc

mmol in 24 hmmol in 24 h

demyelination in

concentration of less than 105

t increased risk of developing t increased risk of developing

ction should not exceed 8

Which serum and how m

Symptomatic or Acute Treatment Cont. - Here comes th

estimate SNa change on the estimate SNa change on the infusate

ΔSNa = {[Na + K]inf − SNa} ÷ (T ΔSN i h i SN ΔSNa is a change in SNa [Na + K]inf is infusate Na a

solution OH MY GOD, what did he just say

much is better?

e Math!!! basis of the amount of Na in the basis of the amount of Na in the

TBW + 1)

and K concentration in 1 liter of

y!!!!!!!!!!!!!!!!!!

Hyponatremia/t IV Fluids

One liter of Lactated Ringer's S 130 mEq of sodium ion = 13 109 mEq of chloride ion = 1 28 mEq of lactate = 28 mm 28 mEq of lactate = 28 mm 4 mEq of potassium ion = 4 3 mEq of calcium ion = 1.5

One liter of Normal Saline con 154 mEq/L of Na+ and Cl−

O lit f 3% li t i One liter of 3% saline contains 514 mEq/L of Na+ and Cl−

treatment

Solution contains:30 mmol/L109 mmol/L

mol/Lmol/L4 mmol/L 5 mmol/L ntains:

s:

Example:A 60 kg women witA 60 kg women wit

110 meq/LFormula:Formula:

ΔSNa = {[Na + K]iWhat is the TBW?What is the TBW?How high will 1 liter

the plasma sodiumthe plasma sodiumA-30/ 1.4 meq/L B- 35/1 8B 35/1.8C- 35/1.4D- 30/1 8D- 30/1.8

h a plasma sodium of h a plasma sodium of

inf − SNa} ÷ (TBW + 1)

of normal saline raise ??

Answer: AAnswer: A

TBW is 30 LSerum sodium will increaSerum sodium will increa

1.4 meq/L for a total SNaase by approximately ase by approximately a of 111.4 meq/L

Example: a 90 kg man with a pla a 90 kg man with a pla Formula:

ΔSNa = {[Na + K] ΔSNa = {[Na + K]inf − What is the TBW? How high will 1 liter of 3 How high will 1 liter of 3

sodium? A-54/1.3 meq/L A 54/1.3 meq/L B-65/7.3 C- 54 / 7.3 C 54 / 7.3 D -65/1.3

sma sodium of 110 meq/Lsma sodium of 110 meq/L

SNa} ÷ (TBW + 1) SNa} ÷ (TBW + 1)

3% saline raise the plasma 3% saline raise the plasma

Answer: CAnswer: C

TBW is 54 L Serum sodium will increase b

meq/L for a total SNa of 117.by approximately 7.3 y pp y3 meq/L

Example: 63 y/o female at 75 Kg with N/V

SNa is 108 mEq/L

She has had one seizure in the a

Plasma osmolality is Urine osmolality is 47 Uric acid is 6mg/dl

What type of hyponpatient have?

/D for 4 days

ambulance

251 mosmol/kg7 mosmol/kg

natremia does this

Hyponatremia How will you Tx her?

Calculate the total body wate 0.5 x weight = 37.5 L

What rate of correction do o What rate of correction do yo 8 to 10 mEq/L in 6 to 8 hours

What fluid will you use? 3% Saline

How will you calculate the am ΔSNa = {[Na + K] SNa} ÷ (T ΔSNa = {[Na + K]inf − SNa} ÷ (T

How will her sodium increase a By 10.8 mEq/L to 118.8 mEq/L

er

o ant?ou want?

mount of sodium to give her?BW + 1)BW + 1)

after 1 liter of 3% saline?

ey points ey points Hyponatraemia is the most common yp

clinical practice and its most commorelease of arginine vasopressin

In the elderly hyponatraemia predisp In the elderly, hyponatraemia predispmay worsen cognitive impairment; in hyponatraemia reflects severe haemassociated with worse morbidity and y

In patients with liver cirrhosis, hyponatincreased mortality, hepatorenal syndencephalopathy and reduced qualiencephalopathy, and reduced quali

electrolyte disturbance in yn mediator is the nonosmotic

poses to falls and fractures and poses to falls and fractures and patients with heart failure, odynamic alterations and is mortality y

traemia is associated with drome, hepatic ty of life ty of life

ey points ey points Hyponatraemia carries a worse progn

kidney disease including those with ekidney disease, including those with e Syndrome of inappropriate secretion

(SIADH) is classified as euvolaemic hyh l i h l i hypovolaemic or hypervolaemic caube excluded

In addition to fluid restriction, vasoprenow available in some countries to trefailure, cirrhosis

nosis in patients with chronic end stage renal disease end-stage renal disease of antidiuretic hormone ponatraemia, and therefore

f h t i d t uses of hyponatremia need to

essin-receptor antagonists are eat hyponatremia in heart

EuropeanEuropeanJournal ofEndocrinogy(2014) 170(2014) 170G1–G47

chrier, R. W. et al. Nat. Rev. Nephrol. 9, 37–50 (0 November 2012; doi:10.1038/nrneph.2012.24

(2013); published online 46

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Clinical practice guideline on diagnosis ... - edc.mui.ac.ir practice guideline on... · congestive heart failure, GI loss, yg pypychogenic polydipsya H enal from renal causes Physiology