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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
PhysiologyPhysiologyDefinition of hyponatDifferent type of hypClinical featuresClinical featuresHyponatremia/DiagnTreatment
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
yponatremiayponatremia
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
PhysiologyPhysiologyDefinition of hyponatDifferent type of hypClinical featuresClinical featuresHyponatremia/DiagnTreatment
tremiaponatremia
nosis
yponatremiayponatremia
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
PhysiologyPhysiologyDefinition of hyponatDifferent type of hypClinical featuresClinical featuresHyponatremia/DiagnTreatment
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.
PhysiologyPhysiologyDefinition of hyponatDifferent type of hypClinical featuresClinical featuresHyponatremia/DiagnTreatment
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
PhysiologyPhysiologyDefinition of hyponatDifferent type of hypClinical featuresClinical featuresHyponatremia/DiagnTreatment
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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INZADE on February 24, 2012. For personal use
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