Presentation mia First

8/14/2019 Presentation mia First

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HYPONATREMIA

BY DR.SYEDOSMANBY DR.SYEDOSMAN


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CASECASE

Mr jagdish aMr jagdish a 49 years49 years old man lecturer byold man lecturer byprofession resident of raichure karnatakaprofession resident of raichure karnataka

K/C/OK/C/O HypertensiveHypertensive onon LosartanLosartan andand

hydrochlorthiazidehydrochlorthiazide Since 15 days presented withSince 15 days presented with

C/OC/O4 episodes of4 episodes ofvomitingsvomitings followed by giddiness andfollowed by giddiness and

slowed mentation since 3 daysslowed mentation since 3 days

H/O Constipation since 4 daysH/O Constipation since 4 days


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No H/O Pain abdomenNo H/O Pain abdomen

No H/O coughNo H/O cough

No H/O sobNo H/O sob

No H/O feverNo H/O fever

No H/O loose motionsNo H/O loose motions

No H/O dysuriaNo H/O dysuria

No H/O seizuresNo H/O seizuresNo H/O loss of conciousnessNo H/O loss of conciousness


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On examinationOn examination

Slurred mentationSlurred mentation

Awake follows commandsAwake follows commandsAfebrileAfebrile

PR = 62/minPR = 62/min

BP = 130/80 mmHgBP = 130/80 mmHgRR = 20/minRR = 20/min

R/S = clearR/S = clear


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SPO2 = 100% On Room AirSPO2 = 100% On Room Air

No Cyanosis Icterus Clubbing Odema LymphadenopathyNo Cyanosis Icterus Clubbing Odema Lymphadenopathy

CVS = S1 S2 + NO murmurCVS = S1 S2 + NO murmur

P/A = soft, Non tender, No organomegalyP/A = soft, Non tender, No organomegaly

CNS = Awake, following commandsCNS = Awake, following commands

No neck stifnessNo neck stifness

No neurological deficitNo neurological deficit

DTR-NormalDTR-Normal


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Plantars down goingPlantars down going


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CBC Normal HB ,TLCCBC Normal HB ,TLC

B Urea ,S Creatinine were normalB Urea ,S Creatinine were normal

Normal LFTNormal LFT

[SGOT,SGPT,T.B,D.B,ALBUMIN{4}][SGOT,SGPT,T.B,D.B,ALBUMIN{4}]

S Electrolytes Na =S Electrolytes Na = 119 mEq /L119 mEq /L

K+ = 4.6 mEq /LK+ = 4.6 mEq /L

Cl- = 84 mEq /LCl- = 84 mEq /L


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CUE -CUE - 8-108-10 Pus CellsPus Cells

SR.Osmolality =SR.Osmolality = 245.22245.22 mOsm/kgmOsm/kg

Urine osmolality =Urine osmolality = 120.09120.09 mOsm/kgmOsm/kg

Urine spot sodium =Urine spot sodium = 4545CT scan brain s/oCT scan brain s/o granulomatous lesion in leftgranulomatous lesion in left

anterior parietal cortexanterior parietal cortex

CSF analysis = normal studyCSF analysis = normal study

TSH = NormalTSH = Normal


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Hyponatremia is defined as a plasmaHyponatremia is defined as a plasma

[Na[Na++]]


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Hypovolemic hyponatremiaHypovolemic hyponatremia

Total body water (TBW) decreases; total bodyTotal body water (TBW) decreases; total body(Na(Na++) decreases to a greater extent.) decreases to a greater extent.

Euvolemic hyponatremiaEuvolemic hyponatremia

TBW increases ; total sodium remains normalTBW increases ; total sodium remains normal..

[ECF increased][ECF increased] without edemawithout edema..

Hypervolemic hyponatremiaHypervolemic hyponatremia

Total body sodiumTotal body sodium increases, and TBW increasesincreases, and TBW increases

to a greater extent.ECF is increased , with theto a greater extent.ECF is increased , with thepresence of edema.presence of edema.


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PathophysiologyPathophysiology

Sr. Na+ regulated bySr. Na+ regulated by thirst, secretion ofthirst, secretion ofADH, feedback of renin-angiotensin-ADH, feedback of renin-angiotensin-aldosterone system, renal handling ofaldosterone system, renal handling ofNa+.Na+.

sr.osmolarity stimulate hypothalamicsr.osmolarity stimulate hypothalamicosmoreceptorsosmoreceptors ,causes thirst ADH.,causes thirst ADH.

ADH free H2O reabsorption from urineADH free H2O reabsorption from urine

returns sr.osmolarity to normal.returns sr.osmolarity to normal.


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AldosteroneAldosterone released inreleased in hypovolemiahypovolemiaviavia renin-angiotensin-aldosteronerenin-angiotensin-aldosteroneaxis.axis.

Absorbs Na+ atAbsorbs Na+ at distal renal tubuledistal renal tubule..

Na+ retentionNa+ retention free waterfree waterretention,retention, corrects hypovolemia.corrects hypovolemia.KidneyKidney regulates Na+ balanceregulates Na+ balance

independent of ADH /aldosteroneindependent of ADH /aldosterone byby

Na+ absorption atNa+ absorption at distal tubule..distal tubule..


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Hyponatremia free H2O fromHyponatremia free H2O fromvascular space to intracellular space.vascular space to intracellular space.

Cellular edemaCellular edema tolerated by tissues,tolerated by tissues,

not tolerated within rigid bonynot tolerated within rigid bonycalvarium.calvarium.

clinical manifestations related toclinical manifestations related to

cerebral edema.cerebral edema.


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WhenWhen Sr.Na+ slowly,brainSr.Na+ slowly,brain

compensates by extrusion of solutescompensates by extrusion of solutes

and fluidand fluid ..

IfIf rapidly, [24-48 hours],rapidly, [24-48 hours], thisthis

compensation overwhelmed andcompensation overwhelmed and

severe cerebral edema,brainstemsevere cerebral edema,brainstem

herniation and deathherniation and death occursoccurs


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Mortality/MorbidityMortality/Morbidity

Acute hyponatremia (Acute hyponatremia (48 h or


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Chronic hyponatremiaChronic hyponatremia (> 48 h)(> 48 h) mildmild

cerebral edema .cerebral edema .

Brainstem herniation not observed .Brainstem herniation not observed .

Morbidity and deathMorbidity and death due todue to statusstatus

epilepticusepilepticus ( 110 mEq/L or


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SexSex

EqualEqual in males and femalesin males and females

postoperative hyponatremiapostoperative hyponatremia commoncommonin menstruant females.in menstruant females.

AgeAge

Common inCommon in extremes of ageextremes of ageExperienceExperience less thirstless thirst andand less fluidless fluid

intakeintake


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RISK OF HYPONATREMIARISK OF HYPONATREMIA

Infants fedInfants fed tap watertap water inin

gastroenteritisgastroenteritis

Infants fedInfants fed dilute formuladilute formula

Elderly withElderly with diminished thirstdiminished thirst,,

physical infirmity limits access tophysical infirmity limits access to

food and drinkfood and drink


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ClinicalClinicalHistoryHistory

Symptoms withSymptoms with degreedegree ofof

hyponatremia &hyponatremia & rapidityrapidity

When Sr.Na+When Sr.Na+ graduallygradually [days or[days or

weeks] levels 110 mEq/L-weeks] levels 110 mEq/L- minimalminimal

symptomatologysymptomatology


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fall in Na+fall in Na+ in 24-48 Hrsin 24-48 Hrs

overwhelms compensatoryoverwhelms compensatory

mechanisms severemechanisms severe cerebralcerebral

edema, coma, or brainstemedema, coma, or brainstemherniationherniation


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SymptomsSymptoms

Mild anorexia, headache, and muscleMild anorexia, headache, and muscle

cramps, alteration in mental statuscramps, alteration in mental status

,confusion, coma, or status epilepticus,confusion, coma, or status epilepticus..

Associated withAssociated with pulmonary/mediastinalpulmonary/mediastinal,CNS disorders.,CNS disorders.

inin pneumonia, active tuberculosis,pneumonia, active tuberculosis,

pulmonary abscess, neoplasm, or asthma,pulmonary abscess, neoplasm, or asthma,

CNS infection, trauma, or neoplasmCNS infection, trauma, or neoplasm..


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carcinoma of the nasopharynx,carcinoma of the nasopharynx,

duodenum, stomach, pancreas,duodenum, stomach, pancreas,

ureter, prostate, or uterus increasedureter, prostate, or uterus increased

risk.risk.Associated with medicationAssociated with medication


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CLINICAL EXAMINATIONCLINICAL EXAMINATION

Findings - degree & chronicity ofFindings - degree & chronicity of

hyponatremia.hyponatremia.

Acute hyponatremia symptomatic atAcute hyponatremia symptomatic at

120 mEq/L.120 mEq/L.

Chronic hyponatremia tolerate muchChronic hyponatremia tolerate much

lower levels.lower levels.


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Physical examination [neurologic].Physical examination [neurologic].

Alert comatoseAlert comatose

cognitive impairment ( short-termcognitive impairment ( short-termrecall;orientation to person, place,recall;orientation to person, place,

or time; frank confusion oror time; frank confusion or

depression)depression)


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Focal / generalized seizureFocal / generalized seizure

Acute severehyponatremia

coma

fixed, unilateral, dilated pupildecorticate or decerebrateposturing sudden severe hypertensionand respiratory arrest

Signs of brain stemherniation


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signs of hypovolemia orsigns of hypovolemia or

hypervolemiahypervolemia

hypovolemia:hypovolemia:Dry mucous membranes,Dry mucous membranes,

tachycardia,tachycardia,

diminished skin turgor,diminished skin turgor,

and orthostasisand orthostasis


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Hypervolemic hyponatremia:Hypervolemic hyponatremia:Pulmonary rales, SPulmonary rales, S

33gallop, jugulargallop, jugular

venous distention, peripheral edema, orvenous distention, peripheral edema, orascitesascites (ie, cirrhosis, nephrotic(ie, cirrhosis, nephroticsyndrome, congestive heart failure).syndrome, congestive heart failure).

muscle weakness & cramping.muscle weakness & cramping.

RhabdomyolysisRhabdomyolysis is an occasionalis an occasionalconsequence-muscle tendernesconsequence-muscle tendernes
http://emedicine.medscape.com/article/827738-overviewhttp://emedicine.medscape.com/article/827738-overviewhttp://emedicine.medscape.com/article/827738-overviewhttp://emedicine.medscape.com/article/827738-overview


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Hypovolemic hyponatremiaHypovolemic hyponatremia

Na+ & free H2O are lost and replaced byNa+ & free H2O are lost and replaced byhypotonic fluids, tap water, 1/2NS orhypotonic fluids, tap water, 1/2NS ordextrose in H2O.dextrose in H2O.

Na+ lost renal / nonrenal routes.Na+ lost renal / nonrenal routes.

Nonrenal GI losses, excessive sweating,Nonrenal GI losses, excessive sweating,third space (Ascites, peritonitis,third space (Ascites, peritonitis,pancreatitis, burns) & cerebral salt-wastingpancreatitis, burns) & cerebral salt-wastingsyndrome.syndrome.Excess fluid losses (eg, vomiting, diarrhea,Excess fluid losses (eg, vomiting, diarrhea,

excessive sweating, GI fistulas or drainageexcessive sweating, GI fistulas or drainagetubes, pancreatitis, burns) replaced bytubes, pancreatitis, burns) replaced byhypotonic fluidshypotonic fluids


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Acute or chronic renal insufficiency, in which theAcute or chronic renal insufficiency, in which thepatient may be unable to excrete adequatepatient may be unable to excrete adequateamounts of free wateramounts of free water

Salt-wasting nephropathySalt-wasting nephropathyCerebral salt-wasting syndromeCerebral salt-wasting syndrome seen in patientsseen in patients

with traumatic brain injury, aneurysmalwith traumatic brain injury, aneurysmalsubarachnoid hemorrhage, and intracranialsubarachnoid hemorrhage, and intracranialsurgery.surgery.

Cerebral salt-wasting must be distinguished fromCerebral salt-wasting must be distinguished fromSIADH because both conditions can causeSIADH because both conditions can cause

hyponatremia in neurosurgical patients, and yethyponatremia in neurosurgical patients, and yetthe pathophysiology and treatment are different.the pathophysiology and treatment are different.44


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Prolonged exercise in a hot environment,Prolonged exercise in a hot environment,

especially in patients who hydrateespecially in patients who hydrate

aggressively with hyposmolar fluids duringaggressively with hyposmolar fluids during

exertion.exertion. Severe symptomatic hyponatremia hasSevere symptomatic hyponatremia has

been reported in marathon runners and inbeen reported in marathon runners and in

recreational hikers in the Grand Canyon.recreational hikers in the Grand Canyon.


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Euvolemic hyponatremiaEuvolemic hyponatremia implies normalimplies normal

sodium stores and a total body excess ofsodium stores and a total body excess of

free water. This occurs in patients whofree water. This occurs in patients who

take in excess fluids.take in excess fluids.Psychogenic polydipsia, often in psychiatricPsychogenic polydipsia, often in psychiatric

patientspatients

Administration of hypotonic intravenous orAdministration of hypotonic intravenous or

irrigation fluids in the immediateirrigation fluids in the immediatepostoperative periodpostoperative period


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Infants who may have been givenInfants who may have been given

inappropriate amounts of free waterinappropriate amounts of free water

Ingestion of sodium phosphate orIngestion of sodium phosphate or

sodium picosulfates and magnesiumsodium picosulfates and magnesiumcitrate combination as a bowelcitrate combination as a bowel

preparation before colonoscopy orpreparation before colonoscopy or

colorectal surgerycolorectal surgery

SIADHSIADH


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Hypervolemic hyponatremiaHypervolemic hyponatremia occurs whenoccurs when

sodium stores increase inappropriately.sodium stores increase inappropriately.

This may result from renal causes such as acuteThis may result from renal causes such as acute

or chronic renal failure, when dysfunctionalor chronic renal failure, when dysfunctional

kidneys are unable to excrete the ingestedkidneys are unable to excrete the ingested

sodium load.sodium load.

It also may occur in response to states ofIt also may occur in response to states of

decreased effective intravascular volume.decreased effective intravascular volume.


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History of hepatic cirrhosis, congestive heart failure, orHistory of hepatic cirrhosis, congestive heart failure, or

nephrotic syndrome, in which patients are subject tonephrotic syndrome, in which patients are subject to

insidious increases in total body sodium and free waterinsidious increases in total body sodium and free water

storesstores

UncorrectedUncorrected hypothyroidismhypothyroidism or cortisol deficiencyor cortisol deficiency(adrenal insufficiency, hypopituitarism)(adrenal insufficiency, hypopituitarism)

Consumption of large quantities of beer or use ofConsumption of large quantities of beer or use of

the recreational drug MDMA (ecstasy)the recreational drug MDMA (ecstasy)


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Hyponatremia can be caused by manyHyponatremia can be caused by manymedications.medications.

Known offenders includeKnown offenders include acetazolamide,acetazolamide,amiloride, amphotericin,amiloride, amphotericin, aripiprazole,aripiprazole,

atovaquone,atovaquone, thiazide diureticsthiazide diuretics, amiodarone,, amiodarone,basiliximab,basiliximab, angiotensin II receptor blockers,angiotensin II receptor blockers,angiotensin-converting enzyme inhibitorsangiotensin-converting enzyme inhibitors,,bromocriptine, carbamazepine, carboplatin,bromocriptine, carbamazepine, carboplatin,

carvedilol, celecoxib, cyclophosphamide,carvedilol, celecoxib, cyclophosphamide,clofibrate, desmopressin,clofibrate, desmopressin,


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donepezil, duloxetine, eplerenone, gabapentin,donepezil, duloxetine, eplerenone, gabapentin,haloperidol, heparinhaloperidol, heparin, hydroxyurea,, hydroxyurea,indapamide,indapamide, indomethacin, ketorolac,indomethacin, ketorolac,levetiracetam, loop diureticslevetiracetam, loop diuretics, lorcainide,, lorcainide,mirtazapine, mitoxantrone, nimodipine,mirtazapine, mitoxantrone, nimodipine,oxcarbazepine, opiates, oxytocin, pimozide,oxcarbazepine, opiates, oxytocin, pimozide,propafenone,propafenone, proton pump inhibitors,proton pump inhibitors,quetiapine, sirolimus, ticlopidine, tolterodine,quetiapine, sirolimus, ticlopidine, tolterodine,vincristine,vincristine, selective serotonin reuptakeselective serotonin reuptakeinhibitors, sulfonylureasinhibitors, sulfonylureas, trazodone,, trazodone,

tolbutamide, venlafaxine, zalcitabine, andtolbutamide, venlafaxine, zalcitabine, andzonisamidezonisamide


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WorkupWorkup

Laboratory StudiesLaboratory Studies

The diagnosis of hyponatremiaThe diagnosis of hyponatremia

depends on accurate measurementdepends on accurate measurement

of sodium concentration.of sodium concentration.


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Laboratory StudiesLaboratory Studies

Consider possibility of sampling error, when theConsider possibility of sampling error, when thereported value are not consistent with thereported value are not consistent with thehistory or physical findings.history or physical findings.Was the patient's blood sampleWas the patient's blood sample properly labeled?properly labeled?Was it obtained from a venous siteWas it obtained from a venous site proximal to anproximal to an

infusion of hypotonic saline or dextrose in water?infusion of hypotonic saline or dextrose in water? Is laboratory measurement orIs laboratory measurement or reporting in error?reporting in error? If an error is suspected, aIf an error is suspected, a second samplesecond sample should beshould be

submitted for testing before therapeutic measures aresubmitted for testing before therapeutic measures areinitiated.initiated.


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In addition to sampling and analysisIn addition to sampling and analysiserrors, several physiologic states exist inerrors, several physiologic states exist inwhich correct laboratory analysis yieldswhich correct laboratory analysis yieldslow serum sodium levels, but these levelslow serum sodium levels, but these levelsdo not reflect a true hyposmolar state.do not reflect a true hyposmolar state.The most common example is serumThe most common example is serum

hyperglycemia.hyperglycemia.Accumulation of extracellular glucose induces aAccumulation of extracellular glucose induces a

shift of free water from the intracellular space toshift of free water from the intracellular space tothe extracellular space.the extracellular space.


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Serum sodium concentration isSerum sodium concentration isdiluted by a factor ofdiluted by a factor of1.6 mEq/L1.6 mEq/L forforeacheach 100 mg/dL100 mg/dL increase aboveincrease abovenormal serum glucose concentration.normal serum glucose concentration.

This hypertonic hyponatremia has noThis hypertonic hyponatremia has nophysiologic significance, and serumphysiologic significance, and serumsodium concentrationsodium concentration corrects ascorrects asnormoglycemia is reestablished.normoglycemia is reestablished.


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An expanded plasma protein or lipidAn expanded plasma protein or lipid

fraction leads to a decrease in thefraction leads to a decrease in the

plasma water fraction in which sodiumplasma water fraction in which sodium

is dissolved..is dissolved..


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Serum osmolarity helpful in diagnosisSerum osmolarity helpful in diagnosisof true hyposmolar hyponatremia.of true hyposmolar hyponatremia.

Serum osmolarity abnormally low inSerum osmolarity abnormally low in

hyposmolar hyponatremiahyposmolar hyponatremiaNormal in pseudohyponatremia -Normal in pseudohyponatremia -

hyperlipidemia or hyperproteinemiahyperlipidemia or hyperproteinemia

Normal or elevated in hypertonicNormal or elevated in hypertonichyponatremia - serumhyponatremia - serumhyperglycemia.hyperglycemia.


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Urine sodium levels are helpful in distinguishing renalUrine sodium levels are helpful in distinguishing renalcauses of hyponatremia from nonrenal causes.causes of hyponatremia from nonrenal causes.Hypovolemic hyponatremia due toHypovolemic hyponatremia due to nonrenal causesnonrenal causes (eg,(eg,

vomiting, diarrhea, fistulas, GI drainage, third spacing ofvomiting, diarrhea, fistulas, GI drainage, third spacing offluids) have renal absorption of tubular sodium andfluids) have renal absorption of tubular sodium and urineurine

sodium levelssodium levels < 20 mEq/L< 20 mEq/L Hypovolemic hyponatremia due toHypovolemic hyponatremia due to renal causesrenal causes (eg,(eg,

diuretics, salt-losing nephropathy, aldosterone deficiency)diuretics, salt-losing nephropathy, aldosterone deficiency)have elevatedhave elevated urine sodium levelsurine sodium levels > 20 mEq/L.> 20 mEq/L.


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Hypervolemic hyponatremia due toHypervolemic hyponatremia due to

decreased effective circulating volumedecreased effective circulating volume

(eg,(eg, cirrhosis, nephrosis, congestive heartcirrhosis, nephrosis, congestive heart

failurefailure) have urine sodium) have urine sodium < 20 mEq/L< 20 mEq/L Renal causesRenal causes of hypervolemicof hypervolemic

hyponatremia or withhyponatremia or with SIADHSIADH have urinehave urine

sodiumsodium > 20 mEq/L> 20 mEq/L..


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Urine osmolarity helpful in diagnosis ofUrine osmolarity helpful in diagnosis ofSIADH.SIADH. In SIADH concentrated urine, with urineIn SIADH concentrated urine, with urine

osmolaritiesosmolarities > 100 mOsm/L.> 100 mOsm/L.

Other hyponatremia urine osmolaritiesOther hyponatremia urine osmolarities


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Adrenal function should be assessed,Adrenal function should be assessed,

viavia random serum cortisolrandom serum cortisol levels orlevels or

adrenocorticotropic hormoneadrenocorticotropic hormone (ACTH)(ACTH)

stimulation teststimulation test, in patients who, in patients whohave recently takenhave recently taken oral steroidsoral steroids oror

in any patient suspected of havingin any patient suspected of having

cortisol deficiencycortisol deficiency


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Imaging StudiesImaging StudiesChest radiograph in a patient withChest radiograph in a patient with

congestive heart failure.congestive heart failure.

head CT scan indicated in alteredhead CT scan indicated in alteredmental statusmental status


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TreatmentTreatment

Establish intravenous access giveEstablish intravenous access give

oxygen to patients with lethargy oroxygen to patients with lethargy or

obtundation.obtundation.


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Seizures unlikely to respond toSeizures unlikely to respond toanticovusants, but should be administeredanticovusants, but should be administereduntil a definitive diagnosis and therapy areuntil a definitive diagnosis and therapy areavailable.available.

Intubate & initiate hyperventilation toIntubate & initiate hyperventilation tointracranial pressure in brainstem herniationintracranial pressure in brainstem herniation(eg, obtundation; fixed, unilateral, dilated(eg, obtundation; fixed, unilateral, dilatedpupil; decerebrate or decorticate posturing)pupil; decerebrate or decorticate posturing)

Avoid hypotonic IV fluids [exacerbateAvoid hypotonic IV fluids [exacerbate

cerebral edema]cerebral edema]


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Emergency Department CareEmergency Department Care

Determining the cause and the chronicityDetermining the cause and the chronicity

Acute hyponatremia is less common thanAcute hyponatremia is less common than

chronic hyponatremiachronic hyponatremia and is seen inand is seen insudden free water loading (eg, patientssudden free water loading (eg, patients

with psychogenic polydipsia, infants fedwith psychogenic polydipsia, infants fed

tap water for 1-2 d, patients giventap water for 1-2 d, patients given

hypotonic fluids in the postoperativehypotonic fluids in the postoperativeperiod).period).


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brainstem herniation when sodium levelsbrainstem herniation when sodium levels

fall < 120 mEq/L.fall < 120 mEq/L.

Serum sodium level rapidly by 4-6 mEq/LSerum sodium level rapidly by 4-6 mEq/L

over the first 1-2 hours.over the first 1-2 hours.

The source of free water must be identifiedThe source of free water must be identified

and eliminated.and eliminated.


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Patients withPatients withseizuresseizures

severe confusionsevere confusion

coma orcoma or

signs of brainstem herniationsigns of brainstem herniationshould receive hypertonic (3%) saline toshould receive hypertonic (3%) saline torapidly correct serum sodium to arrest therapidly correct serum sodium to arrest theprogression of symptoms.progression of symptoms.


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Chronic hyponatremia is more common thanChronic hyponatremia is more common thanacute hyponatremia.acute hyponatremia. mild symptoms , serum sodium of 125 mEq/L .mild symptoms , serum sodium of 125 mEq/L . No history of sudden free water loading.No history of sudden free water loading.

Chronic hyponatremia must be managed withChronic hyponatremia must be managed withextreme care.extreme care. Associated with Osmotic demyelinationAssociated with Osmotic demyelination

syndrome (also known as central pontinesyndrome (also known as central pontinemyelinolisismyelinolisis ) focal demyelination in the pons and) focal demyelination in the pons andextrapontine areas with neurologic sequelae.extrapontine areas with neurologic sequelae.


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Osmotic demyelination develops whenOsmotic demyelination develops whenchronic hyponatremia complicated bychronic hyponatremia complicated byhypoxia .hypoxia .

Meticulous attention to adequateMeticulous attention to adequate

oxygenation and gradual increase inoxygenation and gradual increase inserum sodium level to 120-125 mEq/L.serum sodium level to 120-125 mEq/L. Serum sodium level not allowed toSerum sodium level not allowed to

normal levels or hypernatremic levelsnormal levels or hypernatremic levelswithin the first 48 hours.within the first 48 hours.


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Symptoms of osmotic demyelination (eg,Symptoms of osmotic demyelination (eg,dysarthria, dysphagia, seizures, altered mentaldysarthria, dysphagia, seizures, altered mentalstatus, quadriparesis, hypotension) begin 1-3status, quadriparesis, hypotension) begin 1-3days after correction of serum sodium level.days after correction of serum sodium level.

The condition is irreversible and devastating.The condition is irreversible and devastating.

Slow,correction of serum sodium level andSlow,correction of serum sodium level andmaintenance of adequate oxygenation .maintenance of adequate oxygenation .

hypokalemia, female gender, or history ofhypokalemia, female gender, or history ofalcoholism or liver transplant prone to developalcoholism or liver transplant prone to developosmotic demyelination.osmotic demyelination.

Caution in treating hyponatremia in theseCaution in treating hyponatremia in thesesubgroups.subgroups.


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osmotic demyelination minimal if chronicosmotic demyelination minimal if chronichyponatremia is corrected at a rate < 10-12hyponatremia is corrected at a rate < 10-12mEq/L in first 24 hours ,18mEq/L in the firstmEq/L in first 24 hours ,18mEq/L in the first48 hours.48 hours.

Chronic hyponatremia and severe symptomsChronic hyponatremia and severe symptoms

(eg, severe confusion, coma, seizures) should(eg, severe confusion, coma, seizures) shouldreceive hypertonic saline to raise serumreceive hypertonic saline to raise serumsodium level by 4-6 mEq/L and to arrestsodium level by 4-6 mEq/L and to arrestseizure activity.seizure activity.Anecdotal reports suggest that therapeuticAnecdotal reports suggest that therapeutic

relowering of the serum sodium level with hypotonicrelowering of the serum sodium level with hypotonicfluids and desmopressin (DDAVP) may help avertfluids and desmopressin (DDAVP) may help avertneurologic sequelae in patients whose chronicneurologic sequelae in patients whose chronichyponatremia is inadvertently corrected too quickly.hyponatremia is inadvertently corrected too quickly.


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In chronic hyponatremia , consider the cause ofIn chronic hyponatremia , consider the cause ofthe hyponatremic state.the hyponatremic state.

Patients classified as hypovolemic, euvolemic, orPatients classified as hypovolemic, euvolemic, orhypervolemic hyponatremia based on historicalhypervolemic hyponatremia based on historical

,physical examination.,physical examination.must be monitored and corrected no faster thanmust be monitored and corrected no faster than

10-12 mEq/L in the first 24 hours and 18 mEq/L in10-12 mEq/L in the first 24 hours and 18 mEq/L inthe first 48 hours.the first 48 hours.


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Hypovolemic hyponatremia:Hypovolemic hyponatremia: Patients havePatients havedecreased total body sodium stores.decreased total body sodium stores.

o If symptoms are mild to moderately severe, treatIf symptoms are mild to moderately severe, treatwithwith isotonic salineisotonic saline

Hypervolemic hyponatremia:Hypervolemic hyponatremia: Patients havePatients have

increased total body sodium stores.increased total body sodium stores.o Treatment consists ofTreatment consists ofsodium and water restrictionsodium and water restriction

and attention to the underlying cause.and attention to the underlying cause.o The vasopressin receptor antagonistsThe vasopressin receptor antagonists conivaptanconivaptan

(Vaprisol) and tolvaptan (Samsca) are now(Vaprisol) and tolvaptan (Samsca) are nowapproved for use in hospitalized patients withapproved for use in hospitalized patients with

hypervolemic hyponatremia,hypervolemic hyponatremia, though clinicalthough clinicalexperience is scant.experience is scant.


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Euvolemic hyponatremia:Euvolemic hyponatremia: normal sodiumnormal sodiumstores and total body excess of free water.stores and total body excess of free water.oTreatment Treatment freefree 2 2 restriction andrestriction and

correction of the underlying conditioncorrection of the underlying condition..oAVP receptor antagonists (eg, conivaptan,AVP receptor antagonists (eg, conivaptan,

tolvaptan)tolvaptan) show promise as effective &show promise as effective &well-tolerated IV therapy for SIADHwell-tolerated IV therapy for SIADH

o Further studies are needed to better defineFurther studies are needed to better definetheir role in treatment of hyponatremiatheir role in treatment of hyponatremiaassociated with SIADH.associated with SIADH.


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MedicationMedication Treatment on classification of hyponatremia, concomitantTreatment on classification of hyponatremia, concomitant

disease , severity of symptoms,severity of hyponatremiadisease , severity of symptoms,severity of hyponatremia

Electrolyte supplementsElectrolyte supplements Hypertonic saline used to rapidly increase serum Na+ inHypertonic saline used to rapidly increase serum Na+ in

severe acute or chronic hyponatremia, manifested bysevere acute or chronic hyponatremia, manifested bysevere confusion, coma, seizures, or evidence of brainstemsevere confusion, coma, seizures, or evidence of brainstemherniation.herniation.

Hypertonic (3%) salineHypertonic (3%) saline Contains 513 mEq/L of NaCl. Volume of hypertonic salineContains 513 mEq/L of NaCl. Volume of hypertonic saline

administered depends on current and desired serumadministered depends on current and desired serumsodium levels and patient's weight.sodium levels and patient's weight.


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AdultAdult Sodium Requirement (mEq) = TBW (Desired NaSodium Requirement (mEq) = TBW (Desired Na

- Serum Na) where TBW = Body Weight X 0.6- Serum Na) where TBW = Body Weight X 0.6

Volume of Hypertonic Saline = Na RequirementVolume of Hypertonic Saline = Na Requirement

(mEq) X 1000 / Infusate Na Concentration(mEq) X 1000 / Infusate Na Concentration(mEq/L)(mEq/L)


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In general, 200-400 mL of 3% NaCl inIn general, 200-400 mL of 3% NaCl in

most adult patients with severemost adult patients with severe

symptomatic hyponatremiasymptomatic hyponatremia

Give IV over first 1-2 h untilGive IV over first 1-2 h untilresolution of seizures or herniationresolution of seizures or herniation

PediatricPediatric

Administer as in adultsAdminister as in adults


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Arginine vasopressin antagonistsArginine vasopressin antagonistsTreating hyponatremiaTreating hyponatremia V2 antagonism ofV2 antagonism of

AVP in renal collecting ductsAVP in renal collecting ducts. Causes. Causesaquaresis[excretion of free H2O]aquaresis[excretion of free H2O]

Conivaptan (Vaprisol)Conivaptan (Vaprisol)Arginine vasopressin antagonist (VArginine vasopressin antagonist (V1A1A , V, V22) in) in

euvolemic (dilutional) and hypervolemiceuvolemic (dilutional) and hypervolemichyponatremia.hyponatremia.

urine free H2O, with little electrolyte loss.urine free H2O, with little electrolyte loss.


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AdultAdult 20 mg IV loading dose (30 min), 20 mg via continuous IV20 mg IV loading dose (30 min), 20 mg via continuous IV

infusion [24 h] treatment for 1-3 d as 20-mg/d continuousinfusion [24 h] treatment for 1-3 d as 20-mg/d continuousIV infusion [titrate up to 40 mg/d]IV infusion [titrate up to 40 mg/d]

Tolvaptan (Samsca)Tolvaptan (Samsca) SelectiveSelective vasopressin Vvasopressin V

22-receptor antagonist-receptor antagonist..

In hypervolemic & euvolemic hyponatremia (SrIn hypervolemic & euvolemic hyponatremia (SrNa+


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AdultAdult 15 mg PO qd initially; increase at 24-h15 mg PO qd initially; increase at 24-h

intervals to 30 mg/d; not to exceed 60 mg/dintervals to 30 mg/d; not to exceed 60 mg/d

Follow-upFollow-up Further Inpatient CareFurther Inpatient Care Admit severely symptomatic hyponatremiaAdmit severely symptomatic hyponatremia

manifested by coma, recurrent seizures, ormanifested by coma, recurrent seizures, or

evidence of brainstem dysfunction to ICU &evidence of brainstem dysfunction to ICU &monitor Sr.Na+monitor Sr.Na+


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Clozapine treatment of schizophrenicClozapine treatment of schizophrenicpatients with compulsive H2O drinking.patients with compulsive H2O drinking.

Discontinue medications associated withDiscontinue medications associated withhyponatremia.hyponatremia.

Thiazide diuretics cause profoundThiazide diuretics cause profoundhyponatremia, in elderly patients, shouldhyponatremia, in elderly patients, shouldbe discontinued in all admitted patientsbe discontinued in all admitted patients


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ComplicationsComplications

Rhabdomyolysis, seizures, permanent neurologicRhabdomyolysis, seizures, permanent neurologic

sequelae due to ongoing seizures or cerebralsequelae due to ongoing seizures or cerebral

edema, respiratory arrest, and death.edema, respiratory arrest, and death.

Complications -therapy of hyponatremia - fluidComplications -therapy of hyponatremia - fluid

overload & osmotic demyelination syndrome.overload & osmotic demyelination syndrome.


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PrognosisPrognosisDependent on underlying condition andDependent on underlying condition and

severity of disease.severity of disease.


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Thank

you

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