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بسم الله الرحمن الرحيم

بسم الله الرحمن الرحيم. SIADH 23.11.1423. BACKGROUND. # AVP, THE NATURAL HUMAN ADH # SYNTHESTISED IN THE ANT . HYPOTHALAMUS & STORED IN THE POS. PITUITARY # ADH RELEASING RECEPTORS 1.OSMORECEPTORS 2-BARORECEPTORS. ACTION OF ADH.

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بسم الله الرحمن الرحيم

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  1. بسم الله الرحمن الرحيم SIADH 23.11.1423

  2. BACKGROUND #AVP, THE NATURAL HUMAN ADH #SYNTHESTISED IN THE ANT . HYPOTHALAMUS & STORED IN THE POS. PITUITARY #ADH RELEASING RECEPTORS 1.OSMORECEPTORS 2-BARORECEPTORS

  3. ACTION OF ADH #PROMOTES REABSORPTION OF . WATER IN D.T & C.D #ARTERIOLAR VASOCONSTRICTIONANDINCREASE ARTERIAL B.P #NO SIGNIFICANT EFFECT ON Na . REABSORPTION

  4. PATHOPHYSI-OLOGY -EXCESS ADH LEAD TO WATER . RETENTION, VOLUME EXPANTION, DECREASE SERUM OSMOLALITY -THE NATRIURESIS DESPITE . HYPONATREMIA CONTRIBUTES TO HYPONATREMIA -ANP IS PROPABLY THE MEDIATOR . OF NATRIURESIS IN SIADH

  5. OVERVIEW THE SIADH SEC DEFINED BY THE HYPON. &HYPO OSMOLALITY RESULTING FROM INAPPRPRIATE CONTINUED SEC.AND/OR ACTION OF ADH DESPITE NORMAL OR INC. PLASMS VOL. &IT’S THE MOST COM. CAUSE OFEUVOLEMIC HYPONATREMIA IN PED.

  6. DIAGNOSIS • #HYPONATREMIA • #HYPOTONICITY<LESS THAN 280MOSM/KGWATER> • #INAPPROPRIATLY CONCENTRATED URINE<LESS THAN 1OOMOSM/KGWATER • #ELEVATED URINE Na. CON>20MEQ/L

  7. DIAGNOSISCONTINUATION>>>>> • #CLINICAL EUVOLEMIA • #NORMAL RENAL,ADRENAL,AND THYROID FUNCTION

  8. FREQUENCY • *SIADH IS RARE IN PE. POPULATION • *OTHER CAUSES OF HYPONA. ARE MORE COM. • *THE MOST COM. CAUSE OF HYPOTONIC NORMOVOLEMIC HYPONATREMIA.

  9. CAUSES • --EITHER HYPERSEC. OF ADH OR LESS OFTEN BY AN ADH-LIKE SUBSTANCE PRODUCED BY NEOPLASTIC TISSUES • --SIADH IN CHILDREN IS SEEN OST OFTEN IN ASS. WITH INTRACRANIAL DIS. OR INJURY &IN POSTOPERATIVE PATIENTS

  10. CAUSESCONT.>>>>>>> • 1-CNS DISORDERS • -HEAD TRAUMA • -STROKE • -NEONATAL HYPOXIA • -BRAIN TUMOR • -HYDROCEPHALUS • -CEREBRAL ABSCESS • -MENINGITIS

  11. CAUSESCNS DIS. CON.>>>> • -ENCEPHALITIS • -SUBARACHNOID HGE • -G.B SYNDROME -

  12. CAUSESCONT.>>>>> • 2-POST-OPERATIVE PERIOD • 3-PAIN ,NAUSIA &VOMITING • 4-PULMONARY DIS.<LESS COM. CAUSES OF SIADH IN CHILDREN THAN ADULT> PNEMONIA,B.P.,ACUTE RES FAILURE,+VE PREASURE VENT.,BA,T.B.,C.F.,EMPYEMA,ABSCESS, PNEMOTHORAX>

  13. CAUSESCONT.>>>>> • 5-DRUGS<CHEMOTHERAPUETIC DRUGS CAUSES NAUSIA WHICH IS APOWERFUL STIMULUS OF ADH SEC.> • -ANALGESCS<NARCOTIC,NSAIDS> • -ANTI-NEOPLASTICS<VINCRISTINE> • -ANTIB.<AZETHROMYCINE> • -ORAL HYPOGLYCEMIC • -DIURETICS<THIAZIDE>

  14. CAUSESCONT.>>>>>> • -CARBAMAZEPINE,BARBITURATE • -CYCLOPHOSPHAMIDE • -CLOFIBRATE • -ANTI-DEPRESSANTS • -NEUROLEPTICS<PHENOTHIAZINE> • -6-AIDS DUE TO INFECTION OF THE LUNG &CNS

  15. CAUSESCONT.>>>>>> • 7-MALIGNANCY<UNCOM. IN CH.> • -LEUKEMIA,LYMPHOMA,BRAIN> • 8-MISCELLANEOS----TEMPRAL ARTERITIS,POLY ARTERITIS NODOSA, SARCOIDOSIS,ROCKY MOUNTAIN SPOTTED FEVER,ALFACTORY NEUROBLASTOMA,H.Z. • 9-IDIOPATHIC

  16. HISTORY • *EXCLUDE OTHER DISORDERS CAUSING HYPONATREMIAAS • -CARDIC FAILURE • -HEPATIC DYSF. • -ADRENAL INSUFFICIENCY • -RENAL DISORDER • -THYROID DIS.

  17. CAUSESCONT.>>> • *PT. DIET<FLUID INTAKE,DRUGS,G.I. LOSSES • *SYMPTOMS OF CHRONIC HYPONA. TEND TO BE MORE SUBTLE---VAGUE • *CLINICAL MANIFES. ARE RELATED TO THE DEGREE &RATE OF WHICH HYPONAT. DEVELOPS

  18. HISTORYCONT.>>>> • *SIGNIFICANT SYMPTOMS IF SERUM Na. LESS THAN 115-120 MEQ/L& SERUM OSM.<240MOSM/KGWATER • *RATE OF DEC. OF SERUM Na.>0.5MEQ/L/Hr. IS PARTICULARLY WORRISOME • *THE YOUNGER THE AGE THE MORE LIABILITY TO DEVOLOP SYM

  19. HISTORYCONT.>>>>> • *MANIFESTATION ARE DUE TO CELLULAR SWELLING &CEREBRAL EDEMA DUE TO HYPONa. • *THE MAJORITY OF SYM. ARE VAGUE &NON SPECIFIC AND MOSTLY NEUROPSYCHIATRIC

  20. HISTORYCONT.>>>>>> • *ANEMIA,NAUSEA,VOMITING,HEADACHE BLURRED VISION,LETHARGY,APATHY,AGITA-TION IRRITABILITY.MS. CRAMPS.WEAKNESS,TREMULOUS-NESS,SEIZURE, COMA

  21. PHYSICAL • #ABSCENCE OF DEHYD. &HYPOVOL. • #NO EDEMA CLINICALLY,EVEN THOUGH PT. HAVE AMODEST ICREASE ECF VOL AND A • MAXIMUM WT. GAIN OF 8 PERCENT • #PT. APPEARS EUVOLEMIC-NORMAL SKIN TURGOR &B.P.,

  22. PHYSICALCONT.>>>>> • #DEPRESSED DEEP TEN. REF. • # ATAXIA, GAIT DIST. • #ABN. SENSORIUM • #DELERIUM,PSYCHOSIS • #ASYM. PUPILS,PAPILLEDEMA • #CHEYNE-STOKE RESP. • #MYOCOLONUS • #FOCAL NEUR. SIGNS

  23. D.D • :ADRENAL INSUFF. • :HYPOTHYR.,MYXEDEMA COMA • :D.M.-DKA • :CH. LIVER DIS. • :PIT. INSUFF. • :PURE RT. SIDED C.H.F • :RENAL DIS. • :1RY. POLYDIPSIA,WATER INTOX.

  24. LAB. STUDIES • =S. Na. <130 • =S OSMOL.<280 • =URINARY Na. >20MMOL/L • =URINE OSMOL.>100MOSM/KG(URINE OSMOL US. EXCEEDS THAT OF PLASMA OSMOL.& RANGING FROM 250-1400 MOSM/KG BUT PTS. WITH HYPON. WITH NO SIADH HAVE A URINE THAT IS MAXIMALLY DILUTE (50-80MOSM/KG))

  25. LAB. STUD.CONT.>>> • =BUN, U.ACID ARE US. LOW • =GFR INC. • =NOR. S. BICARB., K • =OTHER TESTS—CXR,BRAIN CT OR MRI,S. PROTEINS, LIPID,PLASMA CORTISOL,THYROID FUN. TESTS,S.ADH

  26. MORT.-MORB. • #SEVERITY OF HYPON. • #ACUTE ONSET. • #PROLONGED HYPON. • #DELAY IN INATIAT. ADEQ. TT • #RAPID CORR. OF HYPON. • #8 PERCENT. MORT. IN CH.WITH ACUTE HYPON.

  27. TT. OF SIADH • -DEPENDS ON • 1-PRESENCE OR ABSENCE OF SYM.S • 2-SEVERITY OF HYPON. • 3-DURATION OF HYPON. • 4- UNDERLYING DIS. • 5-HEMODYNAMIC STATUS • ASYMPTOMATIC PT.S US. ARE TTED WITH WATER RESTRICTION ALONE

  28. TT. OF SIADHCONT.>>>>> • PT.S WITH CNS SYM.S US. REQUIRED MORE RAPID CORR. OF THE HYPON.THAN CAN BE ACHIEVED BY WATER RESTR. ALONE (REST.+HYPERTONIC SALINE) • HYPON. OF <110 NEEDS TT. • HYPERT. SALINE(3PERCENT NACL) FOR SEVERELY HYPON. PT.S WHO ARE COMATOSED,SEIZING OR DISPLAYING NEW –ONSET,CHANGES IN MEN.STATUS

  29. TT. OF SIADHCONT.>>>> • -WHEN URINE OSMOL. <300MOSM/L CORR. WITH ISOTONIC SALINE,BUT IF >300 CONSIDER HYPERTONIC SALINE • -WATER REST. TO 30 -70 PERCENT MAINT. • -IN MOST CHILD. WITH NO SEVERE SYM.S,FLUID REST. IS SUFF. TO CORRECT HYPON. WITHIN 24 HRS. • -FOR SEIZING PT. GIVE 3PERCENT NACL DOSE OVER 10 MINUTES

  30. HYPERTONIC3 PERCENT NACL • -(1/2MMOL/ML) OF Na. CAN PRECIPITATE H. F IN A PT. WHO ALREADY IS VOL. EXPANDED • -THE AIM IS TO RAISE S. Na. BY 10 MMOL/L- • -THE AMOUNT OF MMOL OF Na. TO BE INFUSED IS WT.X0.6X10MMOL/L—EX. 5 KG PT. • 5X0.6X10 =30 MMOL(60 ML)OR 12ML/KG • -GIVE ½ OVER 30-60 MIN.IF NOT SEIZING &THE REST ½ OVER 2-4 HRS • -DON’T CORRECT S. Na. TO >130MMOL/L INITIALLY OR > 15MMOL/L/DAY • IT PROVIDES ONLY TEMPORARY&SYMPIC.

  31. 3%nacl RELIEF UNTIL FLUID RESTR., OR OTHER TT. CAN TAKE EFFECT -1.2-2.4 ML/KG/HR. RAISES S. NA. BY 1-2 MEQ/L/HR. .

  32. TT.OF SIADHCONT.>>>. • FLUID RESTR. REMANS THE MAINSTAY OF TT. • -IF 70% MAINT. NOT HELPFUL IN 6 HRS GO TO 50%MAINT. • MAINTAIN & DON’T RESTRICT NACL INTAKE FOR URINARY LOSSES DURING FLUID RESTR. • -FLUID INTAKE CAN BE INCREASED GRAD. AS S.ELECTROLYTES&OSMOLALITY BECAME NORMAL

  33. DRUGS • 1-LOOP DIURETICS-FUROSEMIDE • 2-ADH ANTAGONISTS • A-LITHIUM CARBONATE • B-DEMECLOCYCLINE • 3-OSMOTIC DIURETICS • A-UREA • B-MANNITOL • C-GLYCERINE • 4-ADH REALESE INHIBITORS ---ETHANOL,PHENYTOIN

  34. IN PT. FOLLOW UP • MONITOR S. ELECT. &URINE 2 HRS AFTER STARTING TT THEN Q4 HRS UNTILL STABILIZED • CHANGE OR STOP THERAPY WHEN S. NA. 120-130,SYMPTOMS RESOLVE, OR S. NA HAS INCREASED >15MEQ/L IN 24 HRS

  35. OUT PT. FOLLOWUP &PROGNOSIS • -- IN CH. SIADH CONSIDER LITHIUM CARBONATE,DEMECLOCYCLINE,OR FUROSEMIDE. • PROMPT RECOVERY US. FOLLOWS WATER RESTRICTION. • PROGNOSIS IS US.RELATED TO UNDERLYING DIS

  36. COMPLICATIONS • ---FLUID OVERLOAD • -ACUTE EXTRACELLULAR HYPOOSMOLALITY • -CEREBRAL EDEMA • -PERMENANT BRAIN DAMAGE-CPM- • -CEREBRAL HERNIATION

  37. MEDECAL-LEGALPITFULLS • -DON’T USE THIAZIDE DIURETICS • -DON’T CORRECT S.NA TOO RAPID(>2MMOL/HR, OR >15-20MMOL/D.WHICH MAY LEAD TO CPM WITHIN SEVERAL DAYS • -CPM IS MORE LIKELY WITH LONG STANDING SEVERE HYPON. THAT IS CORRECTTED TOO RAPIDLY(<24HRS.)

  38. THANKSHAVE A NICE DAY • PRESENTED BY • DR ALHOURANI

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