الرحمن الله الرحمن بسم الله بسمالرحيمالرحيمSIADHSIADH23.11.142323.11.1423

BACKGROUNDBACKGROUND

##AVP, THE NATURAL HUMAN ADHAVP, THE NATURAL HUMAN ADH

##SYNTHESTISED IN THE ANT . SYNTHESTISED IN THE ANT . HYPOTHALAMUS & STORED IN THE HYPOTHALAMUS & STORED IN THE

POS. PITUITARYPOS. PITUITARY

##ADH RELEASING RECEPTORSADH RELEASING RECEPTORS

11..OSMORECEPTORSOSMORECEPTORS

22--BARORECEPTORSBARORECEPTORS

ACTION OF ADHACTION OF ADH

##PROMOTES REABSORPTION OF . PROMOTES REABSORPTION OF . WATER IN D.T & C.DWATER IN D.T & C.D

##ARTERIOLAR VASOCONSTRICTIONARTERIOLAR VASOCONSTRICTION ANDAND INCREASE ARTERIAL B.PINCREASE ARTERIAL B.P

##NO SIGNIFICANT EFFECT ON NaNO SIGNIFICANT EFFECT ON Na . . REABSORPTIONREABSORPTION

PATHOPHYSI-OLOGYPATHOPHYSI-OLOGY

--EXCESS ADH LEAD TO WATER . EXCESS ADH LEAD TO WATER . RETENTION, VOLUME EXPANTION, RETENTION, VOLUME EXPANTION,

DECREASE SERUM OSMOLALITYDECREASE SERUM OSMOLALITY

--THE NATRIURESIS DESPITE . THE NATRIURESIS DESPITE . HYPONATREMIA CONTRIBUTES TO HYPONATREMIA CONTRIBUTES TO

HYPONATREMIAHYPONATREMIA

--ANP IS PROPABLY THE MEDIATOR . OF ANP IS PROPABLY THE MEDIATOR . OF NATRIURESIS IN SIADHNATRIURESIS IN SIADH

OVERVIEWOVERVIEW

THE SIADH SEC DEFINED BY THE HYPON. THE SIADH SEC DEFINED BY THE HYPON. &HYPO OSMOLALITY RESULTING FROM &HYPO OSMOLALITY RESULTING FROM

INAPPRPRIATE CONTINUED INAPPRPRIATE CONTINUED SEC.AND/OR ACTION OF ADH DESPITE SEC.AND/OR ACTION OF ADH DESPITE

NORMAL OR INC. PLASMS VOL. &IT’S NORMAL OR INC. PLASMS VOL. &IT’S THE MOST COM. CAUSE OFEUVOLEMIC THE MOST COM. CAUSE OFEUVOLEMIC

HYPONATREMIA IN PEDHYPONATREMIA IN PED..

DIAGNOSISDIAGNOSIS

##HYPONATREMIAHYPONATREMIA##HYPOTONICITY<LESS THAN HYPOTONICITY<LESS THAN

280MOSM/KGWATER280MOSM/KGWATER>>##INAPPROPRIATLY CONCENTRATED INAPPROPRIATLY CONCENTRATED

URINE<LESS THAN URINE<LESS THAN 1OOMOSM/KGWATER1OOMOSM/KGWATER

##ELEVATED URINE Na. CON>20MEQ/LELEVATED URINE Na. CON>20MEQ/L

DIAGNOSISDIAGNOSISCONTINUATIONCONTINUATION>>>>>>>>>>

##CLINICAL EUVOLEMIACLINICAL EUVOLEMIA##NORMAL RENAL,ADRENAL,AND NORMAL RENAL,ADRENAL,AND

THYROID FUNCTIONTHYROID FUNCTION

FREQUENCYFREQUENCY

**SIADH IS RARE IN PE. POPULATIONSIADH IS RARE IN PE. POPULATION**OTHER CAUSES OF HYPONA. ARE OTHER CAUSES OF HYPONA. ARE

MORE COMMORE COM..**THE MOST COM. CAUSE OF THE MOST COM. CAUSE OF

HYPOTONIC NORMOVOLEMIC HYPOTONIC NORMOVOLEMIC HYPONATREMIAHYPONATREMIA..

CAUSESCAUSES

----EITHER HYPERSEC. OF ADH OR LESS EITHER HYPERSEC. OF ADH OR LESS OFTEN BY AN ADH-LIKE SUBSTANCE OFTEN BY AN ADH-LIKE SUBSTANCE

PRODUCED BY NEOPLASTIC TISSUESPRODUCED BY NEOPLASTIC TISSUES----SIADH IN CHILDREN IS SEEN OST SIADH IN CHILDREN IS SEEN OST

OFTEN IN ASS. WITH INTRACRANIAL OFTEN IN ASS. WITH INTRACRANIAL DIS. OR INJURY &IN POSTOPERATIVE DIS. OR INJURY &IN POSTOPERATIVE

PATIENTSPATIENTS

CAUSESCAUSESCONTCONT>>>>>>>.>>>>>>>.

11--CNS DISORDERSCNS DISORDERS--HEAD TRAUMAHEAD TRAUMA--STROKESTROKE--NEONATAL HYPOXIANEONATAL HYPOXIA--BRAIN TUMORBRAIN TUMOR--HYDROCEPHALUSHYDROCEPHALUS--CEREBRAL ABSCESSCEREBRAL ABSCESS--MENINGITISMENINGITIS

CAUSESCAUSESCNS DIS.CNS DIS. CON CON>>>>.>>>>.

--ENCEPHALITISENCEPHALITIS--SUBARACHNOID HGESUBARACHNOID HGE--G.B SYNDROMEG.B SYNDROME

--

CAUSESCAUSESCONTCONT>>>>>.>>>>>.

22--POST-OPERATIVE PERIODPOST-OPERATIVE PERIOD33--PAIN ,NAUSIA &VOMITINGPAIN ,NAUSIA &VOMITING44--PULMONARY DIS.<PULMONARY DIS.<LESS COM. CAUSES LESS COM. CAUSES

OF SIADH IN CHILDREN THAN ADULT> OF SIADH IN CHILDREN THAN ADULT> PNEMONIA,B.P.,ACUTE RES FAILURE,+VE PNEMONIA,B.P.,ACUTE RES FAILURE,+VE

PREASURE PREASURE VENT.,BA,T.B.,C.F.,EMPYEMA,ABSCESS, VENT.,BA,T.B.,C.F.,EMPYEMA,ABSCESS,

PNEMOTHORAXPNEMOTHORAX>>

CAUSESCAUSESCONTCONT>>>>>.>>>>>.

55--DRUGS<DRUGS<CHEMOTHERAPUETIC DRUGS CHEMOTHERAPUETIC DRUGS CAUSES NAUSIA WHICH IS APOWERFUL CAUSES NAUSIA WHICH IS APOWERFUL

STIMULUS OF ADH SECSTIMULUS OF ADH SEC>.>.

--ANALGESCS<ANALGESCS<NARCOTIC,NSAIDSNARCOTIC,NSAIDS>>

--ANTI-NEOPLASTICS<ANTI-NEOPLASTICS<VINCRISTINEVINCRISTINE>>--ANTIB.<AZETHROMYCINEANTIB.<AZETHROMYCINE>>

--ORAL HYPOGLYCEMICORAL HYPOGLYCEMIC--DIURETICS<DIURETICS<THIAZIDETHIAZIDE>>

CAUSESCAUSESCONTCONT>>>>>>.>>>>>>.

--CARBAMAZEPINE,BARBITURATECARBAMAZEPINE,BARBITURATE--CYCLOPHOSPHAMIDECYCLOPHOSPHAMIDE--CLOFIBRATECLOFIBRATE--ANTI-DEPRESSANTSANTI-DEPRESSANTS--NEUROLEPTICS<PHENOTHIAZINENEUROLEPTICS<PHENOTHIAZINE>>--66--AIDS DUE TO INFECTION OF THE AIDS DUE TO INFECTION OF THE

LUNG &CNSLUNG &CNS

CAUSESCAUSESCONTCONT>>>>>>.>>>>>>.

77--MALIGNANCY<UNCOM. IN CHMALIGNANCY<UNCOM. IN CH>.>.--LEUKEMIA,LYMPHOMA,BRAINLEUKEMIA,LYMPHOMA,BRAIN>>88--MISCELLANEOS----TEMPRAL MISCELLANEOS----TEMPRAL

ARTERITIS,POLY ARTERITIS NODOSA, ARTERITIS,POLY ARTERITIS NODOSA, SARCOIDOSIS,ROCKY MOUNTAIN SARCOIDOSIS,ROCKY MOUNTAIN

SPOTTED FEVER,ALFACTORY SPOTTED FEVER,ALFACTORY NEUROBLASTOMA,H.ZNEUROBLASTOMA,H.Z..

99--IDIOPATHICIDIOPATHIC

HISTORYHISTORY

**EXCLUDE OTHER DISORDERS EXCLUDE OTHER DISORDERS CAUSING HYPONATREMIAASCAUSING HYPONATREMIAAS

--CARDIC FAILURECARDIC FAILURE--HEPATIC DYSFHEPATIC DYSF..--ADRENAL INSUFFICIENCYADRENAL INSUFFICIENCY--RENAL DISORDERRENAL DISORDER --THYROID DISTHYROID DIS..

CAUSESCAUSESCONTCONT>>>.>>>.

**PT. DIET<PT. DIET<FLUID INTAKE,DRUGS,G.I. FLUID INTAKE,DRUGS,G.I. LOSSESLOSSES

**SYMPTOMS OF CHRONIC HYPONA. SYMPTOMS OF CHRONIC HYPONA. TEND TO BE MORE SUBTLE---VAGUETEND TO BE MORE SUBTLE---VAGUE

**CLINICAL MANIFES. ARE RELATED TO CLINICAL MANIFES. ARE RELATED TO THE DEGREE &RATE OF WHICH THE DEGREE &RATE OF WHICH

HYPONAT. DEVELOPSHYPONAT. DEVELOPS

HISTORYHISTORYCONTCONT>>>>.>>>>.

**SIGNIFICANT SYMPTOMS IF SERUM SIGNIFICANT SYMPTOMS IF SERUM Na. LESS THAN 115-120 MEQ/L& Na. LESS THAN 115-120 MEQ/L&

SERUM OSM.<240MOSM/KGWATERSERUM OSM.<240MOSM/KGWATER**RATE OF DEC. OF SERUM RATE OF DEC. OF SERUM

Na.>0.5MEQ/L/Hr. IS PARTICULARLY Na.>0.5MEQ/L/Hr. IS PARTICULARLY WORRISOMEWORRISOME

**THE YOUNGER THE AGE THE MORE THE YOUNGER THE AGE THE MORE LIABILITY TO DEVOLOP SYMLIABILITY TO DEVOLOP SYM

HISTORYHISTORYCONTCONT>>>>>.>>>>>.

**MANIFESTATION ARE DUE TO MANIFESTATION ARE DUE TO CELLULAR SWELLING &CEREBRAL CELLULAR SWELLING &CEREBRAL

EDEMA DUE TO HYPONaEDEMA DUE TO HYPONa..**THE MAJORITY OF SYM. ARE VAGUE THE MAJORITY OF SYM. ARE VAGUE

&NON SPECIFIC AND MOSTLY &NON SPECIFIC AND MOSTLY NEUROPSYCHIATRICNEUROPSYCHIATRIC

HISTORYHISTORYCONTCONT>>>>>>.>>>>>>.

**ANEMIA,NAUSEA,VOMITING,HEADACHANEMIA,NAUSEA,VOMITING,HEADACHE BLURRED E BLURRED

VISION,LETHARGY,APATHY,AGITA-TION VISION,LETHARGY,APATHY,AGITA-TION IRRITABILITY.MS. IRRITABILITY.MS.

CRAMPS.WEAKNESS,TREMULOUS-CRAMPS.WEAKNESS,TREMULOUS-NESS,SEIZURE, COMANESS,SEIZURE, COMA

PHYSICALPHYSICAL

##ABSCENCE OF DEHYD. &HYPOVOLABSCENCE OF DEHYD. &HYPOVOL..##NO EDEMA CLINICALLY,EVEN THOUGH NO EDEMA CLINICALLY,EVEN THOUGH

PT. HAVE AMODEST ICREASE ECF VOL PT. HAVE AMODEST ICREASE ECF VOL AND AAND A

MAXIMUM WT. GAIN OF 8 PERCENTMAXIMUM WT. GAIN OF 8 PERCENT##PT. APPEARS EUVOLEMIC-PT. APPEARS EUVOLEMIC-NORMAL SKIN NORMAL SKIN

TURGOR &B.PTURGOR &B.P,.,.

PHYSICALPHYSICALCONTCONT>>>>>.>>>>>.

##DEPRESSED DEEP TEN. REFDEPRESSED DEEP TEN. REF.. # #ATAXIA, GAIT DISTATAXIA, GAIT DIST..##ABN. SENSORIUMABN. SENSORIUM##DELERIUM,PSYCHOSISDELERIUM,PSYCHOSIS##ASYM. PUPILS,PAPILLEDEMAASYM. PUPILS,PAPILLEDEMA##CHEYNE-STOKE RESPCHEYNE-STOKE RESP..##MYOCOLONUSMYOCOLONUS##FOCAL NEUR. SIGNSFOCAL NEUR. SIGNS

D.DD.D::ADRENAL INSUFFADRENAL INSUFF..::HYPOTHYR.,MYXEDEMA COMAHYPOTHYR.,MYXEDEMA COMA::D.M.-DKAD.M.-DKA::CH. LIVER DISCH. LIVER DIS..::PIT. INSUFFPIT. INSUFF..::PURE RT. SIDED C.H.FPURE RT. SIDED C.H.F::RENAL DISRENAL DIS..::1RY. POLYDIPSIA,1RY. POLYDIPSIA,WATER INTOXWATER INTOX..

LAB. STUDIESLAB. STUDIES

==S. Na. <130S. Na. <130==S OSMOL.<280S OSMOL.<280==URINARY Na. >20MMOL/LURINARY Na. >20MMOL/L==URINE OSMOL.>100MOSM/KGURINE OSMOL.>100MOSM/KG(URINE (URINE

OSMOL US. EXCEEDS THAT OF PLASMA OSMOL.& OSMOL US. EXCEEDS THAT OF PLASMA OSMOL.& RANGING FROM 250-1400 MOSM/KG BUT PTS. WITH RANGING FROM 250-1400 MOSM/KG BUT PTS. WITH

HYPON. WITH NO SIADH HAVE A URINE THAT IS HYPON. WITH NO SIADH HAVE A URINE THAT IS

MAXIMALLY DILUTE (50-80MOSM/KG)MAXIMALLY DILUTE (50-80MOSM/KG)))

LAB. STUD.LAB. STUD.CONTCONT>>>.>>>.

==BUN, U.ACID ARE US. LOWBUN, U.ACID ARE US. LOW==GFR INCGFR INC..==NOR. S. BICARB., KNOR. S. BICARB., K==OTHER OTHER TESTS—CXR,BRAIN CT OR MRI,S. TESTS—CXR,BRAIN CT OR MRI,S.

PROTEINS, LIPID,PLASMA CORTISOL,THYROID FUN. PROTEINS, LIPID,PLASMA CORTISOL,THYROID FUN. TESTS,S.ADHTESTS,S.ADH

MORT.-MORBMORT.-MORB..

##SEVERITY OF HYPONSEVERITY OF HYPON..##ACUTE ONSETACUTE ONSET..##PROLONGED HYPONPROLONGED HYPON..##DELAY IN INATIAT. ADEQ. TTDELAY IN INATIAT. ADEQ. TT##RAPID CORR. OF HYPONRAPID CORR. OF HYPON..#8#8 PERCENT. MORT. IN CH.WITH PERCENT. MORT. IN CH.WITH ACUTE HYPONACUTE HYPON..

TT. OF SIADHTT. OF SIADH

--DEPENDS ONDEPENDS ON11--PRESENCE OR ABSENCE OF SYM.SPRESENCE OR ABSENCE OF SYM.S 22--SEVERITY OF HYPONSEVERITY OF HYPON..33--DURATION OF HYPONDURATION OF HYPON..44 - -UNDERLYING DISUNDERLYING DIS..55--HEMODYNAMIC STATUSHEMODYNAMIC STATUSASYMPTOMATIC PT.S US. ARE TTED WITH ASYMPTOMATIC PT.S US. ARE TTED WITH

WATER RESTRICTION ALONEWATER RESTRICTION ALONE

TT. OF SIADHTT. OF SIADHCONTCONT>>>>>.>>>>>.

PT.S WITH CNS SYM.S US. REQUIRED MORE PT.S WITH CNS SYM.S US. REQUIRED MORE RAPID CORR. OF THE HYPON.THAN CAN BE RAPID CORR. OF THE HYPON.THAN CAN BE ACHIEVED BY WATER RESTR. ALONE (REST.ACHIEVED BY WATER RESTR. ALONE (REST.

+HYPERTONIC SALINE)+HYPERTONIC SALINE)HYPON. OF <110 NEEDS TTHYPON. OF <110 NEEDS TT . .HYPERT. SALINE(3PERCENT NACL) FOR HYPERT. SALINE(3PERCENT NACL) FOR

SEVERELY HYPON. PT.S WHO ARE SEVERELY HYPON. PT.S WHO ARE COMATOSED,SEIZING OR DISPLAYING NEW –COMATOSED,SEIZING OR DISPLAYING NEW –

ONSET,CHANGES IN MEN.STATUSONSET,CHANGES IN MEN.STATUS

TT. OF SIADHTT. OF SIADHCONTCONT>>>>.>>>>.

--WHEN URINE OSMOL. <300MOSM/L CORR. WITH WHEN URINE OSMOL. <300MOSM/L CORR. WITH ISOTONIC SALINE,BUT IF >300 CONSIDER ISOTONIC SALINE,BUT IF >300 CONSIDER

HYPERTONIC SALINEHYPERTONIC SALINE--WATER REST. TO 30 -70 PERCENT MAINTWATER REST. TO 30 -70 PERCENT MAINT..--IN MOST CHILD. WITH NO SEVERE SYM.S,FLUID IN MOST CHILD. WITH NO SEVERE SYM.S,FLUID

REST. IS SUFF. TO CORRECT HYPON. WITHIN 24 HRSREST. IS SUFF. TO CORRECT HYPON. WITHIN 24 HRS . .--FOR SEIZING PT. GIVE 3PERCENT NACL DOSE OVER FOR SEIZING PT. GIVE 3PERCENT NACL DOSE OVER

10 MINUTES10 MINUTES

HYPERTONICHYPERTONIC3 PERCENT NACL3 PERCENT NACL

(-(-1/2MMOL/ML1/2MMOL/ML ) )OF Na. CAN PRECIPITATE H. F IN A OF Na. CAN PRECIPITATE H. F IN A PT. WHO ALREADY IS VOL. EXPANDEDPT. WHO ALREADY IS VOL. EXPANDED

--THE AIM IS TO RAISE S. Na. BY 10 MMOL/LTHE AIM IS TO RAISE S. Na. BY 10 MMOL/L----THE AMOUNT OF MMOL OF Na. TO BE INFUSED IS THE AMOUNT OF MMOL OF Na. TO BE INFUSED IS

WT.X0.6X10MMOL/L—EX. 5 KG PTWT.X0.6X10MMOL/L—EX. 5 KG PT..5X0.6X10 =30 MMOL(60 ML)OR 12ML/KG5X0.6X10 =30 MMOL(60 ML)OR 12ML/KG--GIVE ½ OVER 30-60 MIN.IF NOT SEIZING &THE GIVE ½ OVER 30-60 MIN.IF NOT SEIZING &THE

REST ½ OVER 2-4 HRSREST ½ OVER 2-4 HRS --DON’T CORRECT S. Na. TO >130MMOL/L INITIALLY DON’T CORRECT S. Na. TO >130MMOL/L INITIALLY

OR > 15MMOL/L/DAYOR > 15MMOL/L/DAYIT PROVIDES ONLY TEMPORARY&SYMPICIT PROVIDES ONLY TEMPORARY&SYMPIC..

3%nacl3%nacl

RELIEF UNTIL FLUID RESTR., OR OTHER TT. RELIEF UNTIL FLUID RESTR., OR OTHER TT. CAN TAKE EFFECTCAN TAKE EFFECT

--1.2-2.41.2-2.4 ML/KG/HR. RAISES S. NA. BY 1-2 ML/KG/HR. RAISES S. NA. BY 1-2 MEQ/L/HRMEQ/L/HR..

..

TT.OF SIADHTT.OF SIADHCONTCONT.>>>..>>>.

FLUID RESTR. REMANS THE MAINSTAY OF TTFLUID RESTR. REMANS THE MAINSTAY OF TT..--IF 70% MAINT. NOT HELPFUL IN 6 HRS GO TO IF 70% MAINT. NOT HELPFUL IN 6 HRS GO TO

50%MAINT50%MAINT..MAINTAIN & DON’T RESTRICT NACL INTAKE FOR MAINTAIN & DON’T RESTRICT NACL INTAKE FOR

URINARY LOSSES DURING FLUID RESTRURINARY LOSSES DURING FLUID RESTR . .--FLUID INTAKE CAN BE INCREASED GRAD. AS FLUID INTAKE CAN BE INCREASED GRAD. AS

S.ELECTROLYTES&OSMOLALITY BECAME NORMALS.ELECTROLYTES&OSMOLALITY BECAME NORMAL

DRUGSDRUGS

11--LOOP DIURETICS-FUROSEMIDELOOP DIURETICS-FUROSEMIDE22--ADH ANTAGONISTSADH ANTAGONISTSA-LITHIUM CARBONATEA-LITHIUM CARBONATEB-DEMECLOCYCLINEB-DEMECLOCYCLINE33--OSMOTIC DIURETICSOSMOTIC DIURETICS A-UREAA-UREAB-MANNITOLB-MANNITOL C-GLYCERINEC-GLYCERINE44--ADH REALESE INHIBITORS ---ETHANOL,PHENYTOINADH REALESE INHIBITORS ---ETHANOL,PHENYTOIN

IN PT. FOLLOW UPIN PT. FOLLOW UP

MONITOR S. ELECT. &URINE 2 HRS AFTER MONITOR S. ELECT. &URINE 2 HRS AFTER STARTING TT THEN Q4 HRS UNTILL STARTING TT THEN Q4 HRS UNTILL

STABILIZEDSTABILIZED CHANGE OR STOP THERAPY WHEN S. NA. CHANGE OR STOP THERAPY WHEN S. NA.

120-130,SYMPTOMS RESOLVE, OR S. NA HAS 120-130,SYMPTOMS RESOLVE, OR S. NA HAS INCREASED >15MEQ/L IN 24 HRSINCREASED >15MEQ/L IN 24 HRS

OUT PTOUT PT. . FOLLOWFOLLOW UP &PROGNOSISUP &PROGNOSIS

-- --IN CH. SIADH CONSIDER LITHIUM IN CH. SIADH CONSIDER LITHIUM CARBONATE,DEMECLOCYCLINE,OR CARBONATE,DEMECLOCYCLINE,OR

FUROSEMIDEFUROSEMIDE..PROMPT RECOVERY US. FOLLOWS WATER PROMPT RECOVERY US. FOLLOWS WATER

RESTRICTIONRESTRICTION..PROGNOSIS IS US.RELATED TO UNDERLYING PROGNOSIS IS US.RELATED TO UNDERLYING

DISDIS

COMPLICATIONSCOMPLICATIONS

------FLUID OVERLOADFLUID OVERLOAD--ACUTE EXTRACELLULAR HYPOOSMOLALITYACUTE EXTRACELLULAR HYPOOSMOLALITY--CEREBRAL EDEMACEREBRAL EDEMA--PERMENANT BRAIN DAMAGE-CPMPERMENANT BRAIN DAMAGE-CPM----CEREBRAL HERNIATIONCEREBRAL HERNIATION

MEDECAL-LEGALMEDECAL-LEGALPITFULLSPITFULLS

--DON’T USE THIAZIDE DIURETICSDON’T USE THIAZIDE DIURETICS--DON’T CORRECT S.NA TOO DON’T CORRECT S.NA TOO

RAPID)>2MMOL/HR, OR RAPID)>2MMOL/HR, OR >15-20MMOL/D.WHICH MAY LEAD TO >15-20MMOL/D.WHICH MAY LEAD TO

CPM WITHIN SEVERAL DAYSCPM WITHIN SEVERAL DAYS--CPM IS MORE LIKELY WITH LONG CPM IS MORE LIKELY WITH LONG

STANDING SEVERE HYPON. THAT IS STANDING SEVERE HYPON. THAT IS CORRECTTED TOO RAPIDLY)>24HRS.(CORRECTTED TOO RAPIDLY)>24HRS.(

THANKSTHANKSHAVE A NICE DAYHAVE A NICE DAY

PRESENTED BYPRESENTED BY DR ALHOURANIDR ALHOURANI