Boala diareică acută la copilcurs2011

7/27/2019 Boala diareic acut la copilcurs2011

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Boala diareic acut lacopilcurs anul V MG

Simona Dumitra
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Definiie

Emisia frecventa (peste 3) a

unor scaune modificate ca

i consisten

Cronologiccu durata de

maximum 14 zile


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Particulariti

Model de evacuareintestinal particularfiecarui copil

Scaunele nou nscuilor isugarilor alimentai natural

Falsa diaree dinconstipaia cronic


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Redefinire

Modificarea modelului deevacuare intestinal dinultimele 4 sptmni prin

creterea numrului iscderea consisteneiscaunelor, soldate cu

pierdere de ap i

electrolii


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Frecventa

Crescuta, pe tot globul fiind adoua cauza de morbiditate simortalitate le copil.

3 milioane de decese la copii /an

5 copiii mor in fiecare minutcare trece pe intreg globul!

In primii 5 ani de viatamajoritatea copiilor trec prin 2-3episoade diareice


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Etiologie

Principalii germeni implicai n boaladiareic acut bacterian la copil sunt:

1. Shigella: Shigella dysenteriae10 serotipuri; Shigella flexneri14 serotipuri; Shigella boydii - 18 serotipuri; Shigella sonnei1 serotip. 2.Salmonella: Salmonella netyphiaproximativ 2000 de

serotipuri clasificate n grupele A E; Salmonella typhi:

S. paratyphi;

S. schottmuleri; S. hirschfeldii; S. typhimurium.
http://images.google.com/imgres?imgurl=http://www.marlerblog.com/salmonella_typhimurium_300.jpg&imgrefurl=http://www.marlerblog.com/2007/07/&h=315&w=300&sz=49&hl=en&start=12&um=1&tbnid=N2EcNwgyzjnsXM:&tbnh=117&tbnw=111&prev=/images%3Fq%3Dsalmonella%26um%3D1%26hl%3Den%26sa%3DNhttp://rds.yahoo.com/_ylt=A0WTefiJ4QBIXnQBWc2JzbkF;_ylu=X3oDMTBpcWpidGtpBHBvcwM4BHNlYwNzcgR2dGlkAw--/SIG=1e9n7pmp4/EXP=1208103689/**http%3A//images.search.yahoo.com/images/view%3Fback=http%253A%252F%252Fimages.search.yahoo.com%252Fsearch%252Fimages%253Fp%253DShigella%2526y%253DSearch%2526fr%253Dsfp%2526ei%253Dutf-8%2526js%253D1%2526x%253Dwrt%26w=100%26h=100%26imgurl=www.biotrading.com%252Fimg%252Fshigella.jpg%26rurl=http%253A%252F%252Fwww.biotrading.com%252Fen%252Faboutbugs.html%26size=33.8kB%26name=shigella.jpg%26p=Shigella%26type=JPG%26oid=0b6b74142a660614%26no=8&tt=2058


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Etiologie

3. Escherichia Coli: E.Coli enteropatogenEPEC; E. Coli enterotoxigenETEC; E. Coli enteroinvazivEIEC; E. Coli enterohemoragicEHEC E. Coli enteroaderent

EAEC; E. Coli enteroagregantEaggEC

E. Coli difuz aderentDAEC. 4. Campylobacter jejuni/coli 5. Proteus.

6. Aeromonas): Aeromonas salmonicida; Aeromonas hydrophila); Aeromonas caviae; Aeromonas sobria.

7. Plesiomonas Shigeloides. 8. Yersinia enterocolitica. 9. Clostridium difficile. 10. Clostridium perfringens). 11. Brachispyra aalborgi.
http://images.google.com/imgres?imgurl=http://koolielu.edu.ee/kajarahu/veeb/mikroobsed_toiduhaigused/images/Campylobacter%2520jejuni.jpg&imgrefurl=http://koolielu.edu.ee/kajarahu/veeb/mikroobsed_toiduhaigused/%3FMikroobsed_toidunakkused_e._-infektsioonid:Kamp%25FCloos&h=343&w=275&sz=68&hl=en&start=14&um=1&tbnid=gPzaVM1YXDHKwM:&tbnh=120&tbnw=96&prev=/images%3Fq%3DCampylobacter%26um%3D1%26hl%3Den%26sa%3DNhttp://rds.yahoo.com/_ylt=A0WTefgY4QBIDHoB6mWJzbkF;_ylu=X3oDMTBqNzBoY2J0BHBvcwMxNARzZWMDc3IEdnRpZAM-/SIG=1gamp84eb/EXP=1208103576/**http%3A//images.search.yahoo.com/images/view%3Fback=http%253A%252F%252Fimages.search.yahoo.com%252Fsearch%252Fimages%253Fp%253DE%252BColi%2526y%253DSearch%2526fr%253Dsfp%2526ei%253Dutf-8%2526js%253D1%2526x%253Dwrt%26w=250%26h=200%26imgurl=www.h4p-support.com%252Fwebsites%252Fwebesites%252Fdavidllo%252Fjj_e_coli.jpg%26rurl=http%253A%252F%252Fwww.h4p-support.com%252Fwebsites%252Fwebesites%252Fdavidllo%253FM%253DA%26size=19.4kB%26name=jj_e_coli.jpg%26p=E%20Coli%26type=JPG%26oid=f60bc85da43c39e4%26no=14&tt=55056


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Etiologie

12. Listeria monocytogenes. 13. Bacilus Cereus. 14. Klebsiella pneumoniae. 15. Pseudomonas aeruginosa. 16. Vibrio cholerae. 17. Vibrio noncholerae:

Vibrio parahaemolyticus; Vibrio cholerae nonO1; Vibrio vulnificus; Vibrio mimicus; Vibrio hollisae; Vibrio furnisii; Vibrio fluvialis;

Vibrio metschnikovii. 18. Hafnia alvei 19. Stafilococcus aureus. 20. Providencia alcalifaciens . 21. Laribacter Hongkongensis


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Etiologie

ViralRotavirusul

Adenovirusul

NorovirusulEnterovirusul
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Etiologie

Micotic

Candida albicans
http://images.google.com/imgres?imgurl=http://www.medizin-forum.de/prostatitis/candida.jpg&imgrefurl=http://www.medizin-forum.de/prostatitis/fungal-d.html&h=344&w=522&sz=40&hl=en&start=7&um=1&tbnid=imWEIOOQqwNH1M:&tbnh=86&tbnw=131&prev=/images%3Fq%3DCandida%2Balbicans%26um%3D1%26hl%3Den%26sa%3DG


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Etiologie

Parazitar Giardia lamblia
http://images.google.com/imgres?imgurl=http://plantphys.info/organismal/lechtml/images/giardia.jpg&imgrefurl=http://plantphys.info/organismal/lechtml/protista.html&h=783&w=571&sz=129&hl=en&start=7&um=1&tbnid=dxXIWXefZziu6M:&tbnh=143&tbnw=104&prev=/images%3Fq%3DGiardia%26um%3D1%26hl%3Den%26sa%3DNhttp://images.google.com/imgres?imgurl=http://www.3dscience.com/img/Products/3D_Models/Biology/Protozoa/Giardia/supporting_images/3d_model_giardia_web3.jpg&imgrefurl=http://www.3dscience.com/3D_Models/Biology/Protozoa/Giardia.php&h=300&w=300&sz=48&hl=en&start=2&um=1&tbnid=9EoZRgMztU9acM:&tbnh=116&tbnw=116&prev=/images%3Fq%3DGiardia%26um%3D1%26hl%3Den%26sa%3DN


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Credeati ca ai scpat?maiurmeaz.

Etiologie neinfecioas

Alimentar

Alergic

Intolerane alimentare

Diareea postantibiotice

Diareea parenterala


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Factori de risc

Deficite metabolice,

careniale

Nivelul socioeconomic al

familiei


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Patogenie

Se disting patru etape nproducerea bolii diareicebacteriene:

ingestia agenilorpatogeni;

depirea mecanismelorantibacteriene;

ataarea de epiteliu; exercitarea efectului

patogen.


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Enterocit

Dezechilibrul

florei

saprofite

Distrugerea

enterocitului

Mucus

Viloziti

Bariera de mucus de la nivelul intestinului


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Patogenie

Mecanism secretorenterotoxic

Mecanism invaziv

Mecanism sistemic

Mecanism tip aderen


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Mecanism enterotoxic/secretor

- alterarea funciei celulareintestinale cu epiteliu

intestinal integru.

V. HOLERIC ETEC


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Mecanism secretor- structuraenterotoxinei


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LEGARE DE RECEPTOR

Adenilatciclaz Guanilatciclaz

creterea AMPc crete GMPc

Activarea Activarea

proteinkinazei proteinkinazei

A GMPc-dependente

Fosforilarea proteinelor

Modificarea activitii sistemelor de transport

Scderea absorbiei Na, Cl Creterea secreiei de clor

Diaree secretorie


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ECHIL IBRUL ABSORBIE-SECREIE

Enkefalinaze

Enkefaline Prostaglandine

VIP

ATP

c-AMP

K+ H2O Na+

Diminuareaconcentraieiintracelulare de

AMPc prin inhibarea

adenilat-cyclasei este

declanat de:-somatostatin,

-neuropeptidul Y,

-enkefaline, care

astfel inhib secreiade ap i electrolii


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Vrf

Cript

Secreie

++

Hipersecreie

Distrugerea

enterocitelor

d in vrful

vi loz i tilor

Defic i t de

absorbie

datorat ataculu i

viralAbsorbie ++


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Modelul enteroinvaziv

Principalii germeni implicai nacest model sunt: Shigella,EIEC, EHEC, Salmonella,Campylobacter, Yersinia.

Evenimentul iniial l constituieinvadarea mucoasei, urmatde multiplicare i distrugere.Procesul inflamator determinrecrutarea de substane

proinflamatorii (prostaglandine,leucotriene), cu lezareasuprafeei de absorbie .


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Leziunea histologic principaleste reprezentat de ulceraiamucoasei, la care se asociazo reacie inflamatorie acut cu

afectarea laminei propria . Clinic, se exprim prin diaree

inflamatorie (scaun n cantitatemic + mucus + puroi + snge),

dar uneori mbrac i caractereale diareei secretorii


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Se cunosc trei tipuri diferite deverocitotoxin (efect de distrugere peculturi de celule Vero sau HeLa).

VT1 sau Shiga like T1 (SLT1);

VT2 sau Shiga like T2 (SLT2);

VT2C. Subunitatea A a verocitotoxinei este

endocitat dup proteoliz ireducerea punilor disulfidice ielibereaz o enzim intracelular de

aproximativ 27 KD. Aceast enzimcliveaz ARN ribozomal n celuleleafectate declannd suprimareasintezei proteice


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VT2 este de 400 de ori maitoxic dect VT1.


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Modelul sistemic

Este reprezentat de Salmonellacare invadeaz lamina propria,producnd o reacieinflamatorie n poriunea distala intestinului subire i colonului.

Stratul epitelial prezintmodificri moderate.Penetrnd lamina propria,Salmonella ajunge princirculaia limfatic in circulaia

sistemic. Are loc o diseminare rapidhematogen a infeciei sprealte organe


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Modelul tip aderen

Este reprezentat de E. Colienteropatogen-EPEC, E. Colienteroagregant-EAggEC, E. Coli difuzaderentDAEC (208).

EPEC se ataeaz de mucoasa

intestinal ntr-un mod caracteristicproducnd modificri aleultrastructurii acesteia numite leziunide fixare i distrugere (distrugereamicrovililor de la locul contactului ialungirea celor marginali), dnd un

aspect caracteristic de cup saupiedestal.


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Anamneza

Nivelul socioeconomic alfamiliei

Calatorii in zone endemice

Colectivitati

Obiceiuri culinare

Focar familial

Utilizarea recenta deantibiotice

Anotimpul internarii


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Tablou clinic

Debut acut

Prodrom

Scaune apoase initial, ulteriormucoase, grunjoase,

modificari de culoare

elemente patologice mucus, puroi sisange

varsaturi,

dureri abdominale,

tenesm,

eritem fesier.

convulsii

modificari in cadrul SAD


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Caracteristicile clinice principale asociate cu ceimai frecveni patogeni enterici

Salmonella Campylobacte

r

Rotavirus Norwalk-like

virus

Giardia

Febra ++++ ++++ ++++ + +

Snge nscaun ++ ++++ + ++ ++

Dureri

abdominale

++++ ++ - + +

Vrsturi + + ++++ ++++ +

>6 scaune/zi + ++++ ++ + +

Durata

simptome

7 7


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Diareea acut

Etiologie Scaune Simptome asociateSalmonella Scaune lichide, urat mirositoare Febr, dureri abdominale

Yersinia enterocolitica Scaune lichide, urat mirositoare

Apendicita acuta

Febr, dureri abdominale

Shigella Scaune mici cu puroi, snge, mucus Febr,tenesme, dureri abdominale

Campylobacter Scaune cu snge i mucus Semne sistemice uoare

E.coli: Invaziv

Enterotoxigen

Enteropatogen

EHEC

Scaune cu snge apoase, voluminoase

Verzi apoase

Verzi voluminoase

Diaree hemoragic

Dureri abdominale, tenesme

Deshidratare grav, rapid !

Diaree persistent

Sindrom hemolitic-uremic

Stafilococ aureu Scaune exploziv apoase Grea, vrsturi, istoric de grup

Vibrion cholerae Apoase, abundente, frecvente Rapid semne de deshidratare grav

Giardia lamblia Scaune foarte urat mirositoare Vrsturi, greuri, distensie abdominal,flatulen, dureri epigastrice


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Diareea viral

Rotavirus

cauz major a BDA la sugarii i copii sub 2 ani; reprezint 30-60% din diareea acut ntre 6-24 luni.

Adenovirus enteric 40, 41 provoac BDA sub 2 ani reprezint 5-10% durat mai lung a sindromului diareic

(aproximativ 10 zile).Virus Norwalk

provoac diaree la copiii peste 4 aniAstrovirus

determin un tablou clinic asemntor rotavirusului.


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Diareea viral

Tablou clinic

Incubaia bolii este de 2-3 zile. Debut i perioad de stare. Debutuleste acut, cu anorexie, vrsturi care preced diareea,

febr moderat , diaree apoas cu grade variate de

deshidratare, dureri abdominale. Evoluiaeste n general benign, autolimitat (7- 10 zile), cu

mortalitate redus, imunitate durabil.

Examene paraclinice coprocultura, coprocitogramanegative;test ELISA (Rotazyme)pozitiv

Profilaxia vaccinarea antirotavirus (vaccin Rotarix).


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Enterocolita cu Salmonella

Etiologie. Exist numeroase serotipuri deSalmonella, iar doza infectant este 106.

Tabloul clinic febr de tip septic, semnede gastroenterit cu sindrom

dizenteriform, scaune apoasemucosanguinolente, grea, vrsturi cuabdomen destins de volum, bradicardie,meningism.

Complicaiile sunt reprezentate demeningit, septicemie, artrite.


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Diareea cu Campylobacter jejuni

Tablou clinic: febr, vrsturi, diareeapoas pn la sanguinolent, dureriabdominale, rar bacteriemie i

sindrom de deshidratare. Evoluia este prelungit, uneori

recidivant. Complicaii: complicatii imunreactive sindrom Guillain-Barr, eritem nodos, artrit reactiv, sindrom Reiter.


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Diareea cu Yersinia enterocolitica

Yersinia enterocolitica diaree acut; Yersinia pseudotuberculosis adenit

mezenteric cu sindrom pseudoapendicular

Tablou clinic. Febra, varsaturi, dureriabdominale in fosa iliaca dreapta, scaune

mucosangvinolente sau apoase Evoluie.Boala este autolimitat, de obicei la

copilul mare. Evoluia poate fi scurt de 2 zilesau mai lung, de 3-4 sptmni.

Complicaii:pot apare artrit reactiv, eritemnodos, miocardit, anemie hemolitic.


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Diagnostic de laborator

Coprocitograma

Coprocultura

Culturi virale

Identificarea agentuluicauzal la ME

Teste imunoenzimatice dinscaun

Determinarea lactoferineifecale

Examen coproparazitologic


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Tratamentul igienodietetic

Dieta!!!!- formele uoare i medii rehidratare oral cu

SRO n primele 4 - 6 ore

Formula pentru preparare la domiciliu

La 1 litru de ap fiart i rcit

linguri de sare

1 linguri de bicarbonat

4 lingurie de glucoz

250 ml suc de portocale

Se administreaz 20 ml la interval de 10 -15 minute, n cantitate de 150 ml / kg

Pentru fiecare scaun diareic emis n plusse adaug 50 ml de SRO la sugar i100 ml la copilul peste 1 an


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Sugar sub 6 luni

Alimentatnatural

Continuareaalimentaia la sn!

Alimentatartificial

GreutatenormalIntroducerealaptelui dinainteadiareei

DistrofieIntroducereaUnui lapte delactozat

ziua 1 - 50%

ziua 275%ziua 3 - integral


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Sugar peste 6 luni

Brnz de vaci cu orez pasat +5%glucoz

Carne fiart mixat de pui+morcovi fieri+5% glucoz

Mr rasBanan pasirat

Cereale fr gluten

Introducerea laptelui

ziua 450%ziua 575%

ziua 6 - integral


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Copii peste 1 an

GrisineSrteleOrez fiert cu sareMorcovi fiertiSup de legumeSup de carne de

puiCarne fiart de puiMr ras, BananeBrnz proaspt de

vaciIaurt

Ceai cu glucozAp platDieta BRATbanane

orezsos demerepineprajit

Evitai Smantana

Laptele gras

Apelecarbogazoase

Dulciurile Prjiturile

Mazrea, fasolea,conopida, broccoli,

ceapa, usturoiul


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Tratament

Etiologic

Antibioterapia?Cazuri limitate

Patogenic

AntisecretoriiRacecadotrilum

Diosmectita

Probiotice

ZincTrimebutinum

Subsalicilatul debismut


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TRATAMENTUL ETIOLOGIC

A. Criterii bacteriologice

1. Indicaii absolute: Shigella;

Salmonella typhimurium;

Vibrio cholerae.

2. Indicaii relative (nfuncie de contextul clinic) E.Coli enteropatogen;

Samonelloze non-tifoide;

Yersinia enterocolitica;

Campylobacter jejuni.


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B. Criterii clinice

Sugar < 3 luni;

Denutriiesever;

Deficite imune;

Drepanocitoz; Sindrom toxi-infecios grav;

Diaree muco-sanghinolent > 7 zile;

Hemoculturi pozitive.


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TRATAMENTUL CU ECHILIBRANTE DE FLOR INTESTINAL (EUBIOTICE)

Acioneaz prin competiie pentrureceptorii GP pe care ader i patogenii,prin competiie pentru substratulenergetic, prin refacerea biocenozeinormale a tractului digestiv care este unimportant factor de aprareantiinfecioas i previn instalareadisbiozei postantibioterapie

* Enterolactil - Enterol* Bactisubtil* Flonivin* Biosun

* Protectis* Ecoflorina* Biotics

Refflor


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Profilaxie

Vaccinuri antirotavirale

Vaccinuri antiholeric

Vaccinuri anti.E Coli

enterotoxigen Vaccin antiClostridium

difficile
http://rds.yahoo.com/_ylt=A0WTefRc2gBIywUAs5aJzbkF;_ylu=X3oDMTBqM3IzZ25kBHBvcwMzMgRzZWMDc3IEdnRpZAM-/SIG=1gq5oj47n/EXP=1208101852/**http%3A//images.search.yahoo.com/images/view%3Fback=http%253A%252F%252Fimages.search.yahoo.com%252Fsearch%252Fimages%253Fp%253Drotavirus%2526ei%253DUTF-8%2526fr%253Dmsgr-buddy%2526xargs%253D0%2526pstart%253D1%2526b%253D19%2526ni%253D18%26w=100%26h=75%26imgurl=www.empowereddoctor.com%252Flibrary%252Fmedia%252FROTAVIRUS_VACCINES.jpg%26rurl=http%253A%252F%252Fwww.empowereddoctor.com%252Flibrary_stories.php%253Fid%253D119%26size=1.8kB%26name=ROTAVIRUS_VACCINES.jpg%26p=rotavirus%26type=JPG%26oid=795be2831968a860%26no=32&tt=1326


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Retineti..

Internarea este necesar nurmtoarele situaii:

Prezena deshidratrii

Vrsturi frecventeDiaree invaziv.

Forme sistemice


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Retineti..

Evitai administrarea dinproprie initiativ aantispasticelor de orice tip,a antiperistalticelor

Loperamidul i in special aANTIBIOTERAPIEI.

Evitati administrarea apei nexces sau a solutiilor

hipotone, pot accentuadeficitul de sodiu i apariiaintoxicaiei cu ap!


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Retineti..

Sa nu uitati de probiotice!

Combinatia Hidrasec,saprosan, probiotic, zinc

pare rezonabila.


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Sindromul acut de deshidratare


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Sindromul acut de deshidratare

Sindrom fiziopatologic de

etiologie variata,

determinat de pierderea

brusca a unei cantitatimari de apa si

electroliti,care determina

un dezechilibru

hidroelectrolitic siacidobazic.


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Cauze favorizante

Continutul proportional mai

mare in apa totala si

extracelulara

Nevoi zilnice mai crescutePierderile de apa mai

accentuate la copii


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Cauze determinante

1. Aport necorespunzator

2. Excreta crescuta

Perspiratie insensibila

Pierderi renale

Pierderi digestive

3. Translocatie de lichide in

seroase si subcutan4. Arsuri


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Consecinte fiziopatologice

SAD

Spoliere hidroelectrolitica

Hipotensiune

Hipoperfuzie renala

Tulburari functionale celulare

Leziuni celulare

Sindrom de disfunctie organica multipla

Deces


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Tulburari functionale celulare

Respiratorii

Cardiorespiratorii

Renale

Nervoase

Hematologice

Metabolice


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Clasificare I

Tip dedeshidratare

Sugar Copilpeste1 an

SAD usoara Sub 5 % 2-4 %

SAD medie 5 -10 % 4-8 %

SAD severa Peste 10 % Peste8 %


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Clasificare II

I. SAD celulara

II. SAD extracelulara

III. SAD mixta


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SAD celulara SADextracelulara

SAD mixta

Pierdere predominant de

lichide

Pierdere predominanta

de sodiu

Pierdere

Proportionala de sodiu siapa

SAD hipertona

Hipernatremie

SAD hipotona

Hiponatremie

SAD izotona

Normonatremie

Fuga apei din celula in SEC

VC scade

Fuga apei in celula

VC scade extrem de mult

Volum circulant scazut

Tulburari neurologice

Tulburari circulatorii atenuate

Tulburari circulatorii

Grave

Manifestarile neurologice

apar tardiv

Asociaza semne de SADcelulara si extracelulara

Febra

Sete vie

Refuzul apei

Convulsii

Coma

Hipotensiune

Puls filiform

FA deprimata

oligoanurie


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Tabloul clinic

Modificarea starii generale Facies incercanat Ochi infundati in orbite FA deprimata Febra Sete vie

Mucoase uscate Turgor redus Pliu lateroabdominal lenes Polipnee Hipotensiune Puls rapid, filiform Tahicardie Oligoanurie Timp de umplere capilara prelungit Convulsii, obnubilare, coma


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Halucinatiile deshidratariiTylerMcPherson


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SAD grad ISete, mucoase uscate

SAD grad II

Deprimarea fontanelei anterioare

HipotensiunePliu lenes

Turgor flasc

Oligoanurie

SAD grad IIIanurie, obnubilare, coma,

convulsii,


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Deshidratarea celulara(hipernatremica)

Cauze: Aport scazut

Pierderi excesive apa

Consum exagerat (metabolic)

Mecanism: Hipertonie extracelulara + scaderea volumului

hidric extracelular


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VAS CELULA

Deshidratarea e tracel lara (hiponatremica)


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Deshidratarea extracelulara (hiponatremica)

Pierderi de saruri (varsaturi, scaun, urinare,diuretice)

Sectorul extracelular devine hipoton(presiunea osmotica extracelulara )

Apa trece in celula hiperhidratare Volumul plasmatic scade (hipovolemie

hemoconcentratie)

Scade debitul circulator TA colaps

Scade FG IRF, oligoanurie, hiperazotemie,acidoza metabolica


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VAS CELULA


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Examinari paraclinice

Ionograma sangvina

Parametrii acidobazici

Uree

Glicemie

Hemoleucograma completa

Teste pt. precizarea etiologiei


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Diagnosticul SAD

Diagnostic etiologic

Gradul SAD

Tipul deshidratarii

Diagnosticul perturbariloracidobazice

Aprecierea functiei renaleEX = SAD gradul III prin Gastroenterocolita

acuta infectioasa, SAD hipotonahiponatremica cu AM decompensata siIRA functionala


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SAD grad III

Copil cu tulburari digestive grave insotite de fenomeneneurologice

Stare generala alterata

Prodrom cu manifestari toxi-infectioase: facies toxic,

privire fixa, incercanata Clipit rar, reflex corneean diminuat, depuneri

albicioase pe cornee

Pierdere ponderala > 10% in 24-48 h

Inert, aton, obnubilat-somnolent, tipa stins Convulsiihipertonie musculara

Babinski +


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Examenul obiectiv

Tegumente uscate pliu lenes (consistenta

aluatului)

tahipnee, dispnee sine materia

(acidoza metabolica) tahicardie, hipotensiune

arteriala, extremitati reci, timpde recolorare > 3 sec

hepatomegalie

meteorism

edem cerebral


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Diferentiere clinica

Deshidratare intracelulara Hiper Na > 150 mEq/l

Mucoase uscate, aderentela spatula

Febra, sete vie

turgor de coca

Tulburari senzorialecoma

Hemoragie intracraniana


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Investigatii biologice

Hemoleucograma:hemoconcentratie, Ht>35%

Ionograma Nanormal 135-142 mEq/l

Hiponatremie manifesta clinicsub 130 mEq/l

Hipernatremie peste 150 mEq/l(encefalopatie cuhiperosmolaritate)

Izonatremie


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.

ECHILIBRUL ACIDOBAZIC

Este explorat prin dozarea HCO3-,

rezervei alcaline, pH.

VN (HCO3

-): 20-30 mEq/l

VN (rezerva alcalin): 20-27 vol%

VN (pH): 7,30-7,40

Aparatul Astrup permite n plus:studiul gazelor sangvine, deficitul i excesulde baze.


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EXAMINRI COMPLEMENTARE:

coproculturi repetate;

secreii faringiene;

uroculturi;

hemoculturi;

hemograme.


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Tratamentul SAD forma severa

Monitorizare clinica

Monitorizare paraclinica

Alegerea caii de rehidratare

Cunoasterea solutiilorutilizate

Respectarea algoritmului de

tratament


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Calea intraosoasa

Sugari si copii sub 6 ani

Permite administrarea demedicamente, lichide, sange

Necesita ace de perfuzie

intraosoasa/ ace de aspiratiemedulara

Zona de acces = suprafataplata anteromediala a tibiei la

1- 3 cm sub tuberozitateatibiala


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Calea intravenoasa

Algoritm de tratament in SAD


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Algoritm de tratament in SADforma severa

1.Stabilirea cantitatii de lichidepierdute

2. Stabilirea electrolitilor pierduti

3. Stabilirea necesarului lichidian

pentru pacientul respectiv

4. Stabilirea necesaruluielectrolitic pentru pacientulrespectiv

5. Stabilirea cantitatii totale delichid de perfuzat si a totaluluide electroliti de adaugat in PEV


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Ritmul de administrare

Colaps

20 ml/kg in 30 de min.

Se poate repeta

In primele 2 ore 50 ml/kgIn primele 8 ore din lichide

si electrolitii pierduti

Restul de lichide si electrolitiin 16 ore

Schema Thieffry de rehidratare si


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Schema Thieffry de rehidratare sicombatere a acidozei

Avantaje:

24 ore pentru deshidratare10% din G

Restabileste volemia Combate acidoza

Compenseaza pierderile

Asigura hidratarea


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I. REHIDRATAREA

Primele 4 ore: se administreaza din pierderi: 15combaterea colapsului

Dextran 70%10 ml/kgc

Formula: pierderi % x G

Creste rapid volumul plasmatic intravenos Ramane in spatiile intravasculare

45combaterea acidozei NaHCO3 1,4% sol. izotona15 ml/kgc

3 orerehidratare glucoza 5% + ser fiziologic 9 in parti egale 15-20 ml/kgc


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II. NEVOI DE INTRETINERE

Urmatoarele 20 ore100ml/kgc

Ser glucozat 5% - 100 ml/kgc

NaCl 5,85% - 5 mEq/kgc

KCl 7,45% - 3 mEq/kgc

Ca gluconic1 mEq/kgc


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II. NEVOI DE INTRETINERE

din cantitate in 8 ore:

din cantitate in 12 ore:

SG 5% - 50 ml/kgNaCl 5,85% - 2,5 mEq/kg

KCl 7,45% - 1,5 mEq/kg

Ca gluconic 10% - 1 ml =

0,5 mEq

SG 5% - 50 ml/kg

NaCl 5,85% - 2,5 mEq/kg

KCl 7,45% - 1,5 mEq/kgCa gluconic 10% - 1 ml = 0,5

mEq


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Solutii utilizate

Solutiicristaloideizotone

Ser fiziologic

Ringer lactat Ieftine,

nonalergice,

Solutii coloidalesintetice

Dextran

Expansioneza

optim VP Scumpe,

alergice


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Solutii utilizate

Solutii electroliticeEchimolare

NaCL 5,85 % 1 ml=1mEq

KCl 7,45 % 1 ml=1mEq

Semimolare

Ca glu 10 % 1 ml=0,5 mEq

Trimolare

MgSO4 20 % 1 ml=3 mEq

Glucoza 5%, 10%


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Acidoza

Solutie de bicarbonat Molara 8,4%: 1 ml = 1 mEq

Semimolara 4,2%: 2 ml = 1mEq

Izotona 1,4%: 6 ml = 1 mEq


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Atentie

Administrarea K

Max. 20 ml la 500 ml de

perfuzat

Max. 0,3 mEq/kg/oraMax. 3 mEq/kg/zi

Bicarbonatul de sodiu

1 ml solutie= 20 picI ml Dextran=13 pic


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Complicatii

Oligo-anurie (IRO) Complicatii renale: tromboza,

necroza corticala

Convulsii hipoglicemice,hipocalcemice, hiponatremice,

hematoame-tromboze (hiper Na)

CID

Infectii de cateter


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Atentie!!!!!!

rehidratarea excesiv care se manifestprin edeme periferice, edem cerebral;

utilizarea soluiilor sracen sodiu cureintrarea brutal a H2On celule;

inducerea hipopotasemiei si

hipocalcemiei prin corectarea brusca a

acidozei


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Va multumesc!


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Masaru Emoto

i


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Imagine

L


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Love

R


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Ruga


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L d i ti


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Love and appreciation


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Th k !


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Thank you!

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