- sindroame hemoragice
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sindroame hemoragiceTRANSCRIPT
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SINDROAME HEMORAGICE
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HEMOSTAZA• ansamblu de fenomene biologice al carui scop
final este oprirea rapida a sangerarii la nivelul solutiilor de continuitate ale sistemului vascular.
• 2 etape– 1. hemostaza primara = vasoconstrictia reflexa a
vasului lezat si agregarea tr– 2. coagularea propriu-zisa
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ANOMALIILE HEMOSTAZEIHemostaza primara–faza vasculara
purpure vasculare- faza trombocitara/ plachetara
purpure trombocitare
Coagularea coagulopatii = tulburari de coagulare a
sangelui
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DIATEZE HEMORAGICE PRIN TULBURAREA COAGULARII SANGUINE
• stari patologice de hipocoagulabilitate decompensata
• mecanisme– deficit de factori de coagulare– anticoagulanti circulanti in exces– fibrinoliza excesiva
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SINDROAME HEMORAGICE PRIN DEFICIT DE FACTORI DE COAGULARE
• 25% din totalul sdr hemoragice• simptomatologia clinica depinde de gradul
deficitului• coagulopatii – de productie – de consum
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COAGULOPATII DE PRODUCTIE• Congenitale
– Prin deficit de factor izolat• a/hipo/dis- fibrinogenemie• Fact II – boala Biggs-Douglas• Fact V – parahemofilie Owren• Fact VII – boala Alexander• Fact VIII – hemofilia A• Fact vW – boala von Willebrand• Fact IX – hemofilia B• Fact X – boala Hougie-Barrow• Fact XI – sdr Rosenthal• Fact XII• Fact XIII
– Prin deficite congenitale multiple• Fact V + VIII
• Dobandite
– Hepatopatii severe• Ciroza• Sdr Ray• Intoxicatii
– Avitaminoza K– Hipotiroidism – Boli de colagen– Insuficienta renala
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COAGULOPATII DE CONSUM
• Sdr de coagulare intravasculara diseminata
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HEMOFILIA A
• cea mai comuna coagulopatie ereditara, X-linkata
• transmitere recesiva• afectarea producerii factorului VIII • clinic – hemoragii – forme de gravitate diferite
in functie de importanta diminuarii factorului antihemofilic
• incidenta : 12-13/ 100.000 nasteri• 80 % din sdr hemofilice
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MECANISM DE TRANSMITERE
• Genele – recesive - pentru factorii de coagulare VIII si IX se afla pe cromozomul X
• Hemofilia apare doar la sexul masculin (XhY) care a mostenit gena mutanta (Xh) de la mama purtatoare (XhX) asimptomatica
• 30 % din cazurile de hemofilie provin din mutatii spontane si nu au istoric familial de sangerari
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MECANISM DE TRANSMITERE
• tata – sanatos (XY) , mama – purtatoare (XhX)
50% din baieti – hemofilici (XhY) 50% din fete – purtatoare (XhX)
tata – hemofilic (XhY) , mama – sanatoasa (XX)
toti baietii – indemni (XY) toate fetele – purtatoare (XhX)
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MECANISM DE TRANSMITERE
• tata – hemofilic (XhY) , mama – purtatoare (XhX)
50% din baieti – hemofilie (XhY) 50% din fete – homozigote – hemofilie (XhXh) 50% din fete – purtatoare (XhX)
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FIZIOPATOLOGIE
• Deficitul de factor VIII afecteaza conversia protrombinei in trombina cu formare insuficienta de fibrina
• Tulburarile de coagulare apar numai in cazurile cu scadere importanta a fact VIII
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Manifestari clinico-biologice in hemofilia A in functie de concentratia factorului VIII
Conc Conc fact fact VIIIVIII
Timp de Timp de coagularcoagularee
Manifestari Manifestari cliniceclinice
FormForma a clinicclinica a
SubSub 1%1% prelungiprelungitt
Hemoragii Hemoragii spont spont ,6-8/luna, ,6-8/luna, hemartrozehemartroze
SeverSeveraa
1 -4%1 -4% variabilvariabil Hemoragii Hemoragii spontane, rar spontane, rar hemartrozehemartroze
MedieMedie
5 -25%5 -25% normalnormal Hemoragii Hemoragii posttraumaticeposttraumatice
UsoarUsoara a
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MANIFESTARI CLINICE
• comune celor 2 forme de hemofilie• F VIII si F IX nu traverseaza bariera
transplacentara sangerarile pot fi prezente la nastere :– hemoragie la nivelul cordonului ombilical– cefalhematom voluminos– hemoragie meningocerebrala la nn
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Caracterele definitorii ale manifest hemoragice
1. Caracter intotdeauna provocat, uneori in urma unor trumatisme minore
2. Debutul uneori tardiv al hemoragiei, dupa ore sau zile de la traumatism
3. Durata prelungita a sangerarilor exteriorizate, fara tendinta la oprire spontana
4. Sediul profund al hemoragiilor: im, intravisceral, intraarticular
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Caracterele definitorii ale manifest hemoragice
5. Evolutie cronica, ondulanta, in pusee de agravare de 3 - 4 sapt
6. Absenta petesiilor7. Dintre sangerarile exteriorizate, cele mai
frecvente sunt cele din plagile bucale, dentare, linguale, epistaxisul
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HEMARTROZELE• caracteristice bolii• frecvente la varste mici• afecteaza artic mari : genunchi/ cot/ glezna/
sold• clinic: durere, tumefactie, caldura locala,
limitarea miscarilor– in timp, prin repetarea lor, apar leziuni sinoviale
cronice si lez distructive osoase– anchiloze totale => atrofii musculare
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HEMATOAMELE• manifestari extrem de precoce si foarte frecvente
dupa ce copilul incepe sa mearga• localizare– subcutanate– intramusculare
• complicatii – localizare/ dimensiuni– cap, gat/ planseu bucal/ orbitar, periorbitar/fosa axilara sau
poplitee• COMPRESII vasculo-nervoase sau de cai resp
– intramusc => ANEMII ACUTE– hemat de psoas # apendicita acuta
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HEMORAGII EXTERIORIZATE
• plagi cutanate• hemoragii bucale si dentare– plagi ale limbii– plagi ale partilor interne ale obrajilor– extractii dentare
• epistaxisuri• hematurii ± colici nefretice• hemoragii digestive
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ALTE SANGERARI
• ale SNC – subarahnoidiene– meningocerebrale
• la nivelul organelor de simt– ochi– ureche interna
• intraoperatorii– bilant preoperator
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EXAMENE DE LABORATOR
• Valori normale-hemograma-testele care exploreaza
hemostaza primara– TS/ TC pe lama/ TQ/
retractia cheagului
• Valori modificate- TC in eprubeta- Tp Howell- PTT- PTTA
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EXAMENE DE LABORATOR
• DIAGNOSTIC DE CERTITUDINE• Dozarea specifica a factorilor antihemofilici– VIII – hemofilia A– IX – hemofilia B
• Determinare cantitativa
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FORME CLINICE
• gravitatea depinde de deficitul biologic– severa <1%– moderata 1-5%– minora 5-25%
• nu exista intotdeauna o concordanta stricta intre manifestarile hemoragice si nivelul factorului antihemofilic
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HEMOFILIA B
• boala Christmas• mecanism de transmitere asemanator• mai putin frecventa decat hemofilia A• manifestari clinice identice• diferenta : biologica – fact IX
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TRATAMENT
• obiective– oprirea hemoragiilor– tratament substitutiv : concentrate de factori de
coagulare – iv – reducerea afectarii musculo-scheletale
• se contraindica:– injectiile im– medicamentele cu actiune antiagreganta
plachetara – aspirina
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TRATAMENTUL SUBSTITUTIV
• produse de sange uman– plasma proaspata– plasma liofilizata– crioprecipitat– concentrat de fact VIII
• Fact VIII si IX recombinant – inginerie genetica
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TRATAMENTUL SUBSTITUTIV
• necesarul de fact VIII : G *( %F VIII ideal - %F VIII actual) ----------------------------------------- 2
1 U F VIII / kg corp iv asigura cresterea % de F VIII circulant cu 2%adm iv in bolus / PEV continua
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TRATAMENTUL SUBSTITUTIV
• sangerare importanta / hematoame profunde / hemoragie meningo cerebrala– doza initiala de 40 UI/kgc F VIII => ↑ nivelul circ la 80%– se repeta la interval de 8 ore doze de 20-30
UI/kgc pt a mentine nivelul seric la > 50%– durata trat – fctie de tipul de accident
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TRATAMENTUL SUBSTITUTIV
• hemoragii minore: hemartroze la debut /plagi superficiale /sangerare dentara– 20-40 UI/kgc F VIII– repetarea dozelor – fctie de localizarea sangerarii
si de posibilitatile de hemostaza locala
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TRATAMENTUL SUBSTITUTIV
• pentru interventiile stomatologice
– cu 5 – 10 min preoperator se adm 15-20 U/kgc– se repeta doza la 12 – 24 ore
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TRATAMENTE ADJUVANTE
• hemartroze – imobilizare– kinetoterapie
• corticosteroizii– trat antiinflamator –
• terapia durerii– paracetamol 30-60 mg/kgc
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CARNET DE SANATATE
• Tipul de hemofilie• Severitatea deficitului• Grupul sg si Rh• Prezenta de aglutinine• Adresa celui mai apropiat centru de
hematologie care asigura tratamentul de urgenta
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EVOLUTIE SI PROGNOSTIC
• mult imbunatatita datorita trat substitutiv – risc de infectii
• rezervat – la purtatorii de anticoagulant circulant
• interventii chirurgicale la hemofilici necunoscuti
• accidente inevitabile
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PURPURA TROMBOCITOPENICA IDIOPATICA
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• Diateza hemoragica de cauza plachetara / trombocitara
• Cea mai frecventa trombocitopenie diagnosticata la varsta copilariei
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DEFINITIE
• boala a copilului si adultului tanar caracterizata:– clinic : manifestari hemoragice cutaneo-mucoase
si viscerale– trombocitopenie < 50.000/mmc – prin
distrugerea exagerata in periferie printr-un mecanism imunologic
– hiperproductie compensatorie in MO => cresterea nr de megacariocite
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ETIOPATOGENIE
• proces imunologic – formarea de Ac antitrombocitari - splina– in forma cronica – autoAc– corticoterapie
• infectii virale – actiune lezionala directa asupra trombocitelor
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CLINIC
• varsta de debut : 2 -6 ani• nu exista predominanta legata de sex• 50-80% din cazuri sunt precedate de un
episod infectios aparent viral cu 1 – 6 saptamani inainte – IACRS
• mai frecventa in sezoanele reci• debut dramatic aparent in plina stare de
sanatate
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CLINIC
• debut brusc : echimoze si petesii– afecteaza orice regiune a tegumentului, dar mai
ales membrele inferioare– hemoragii spontane sau la traumatisme minime
• aspect de “copil batut”• hemoragii la nivelul mucoaselor:– gingivoragii– epistaxis– bule hemoragice la nivelul cavit bucale
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CLINIC
• in formele clinice grave– hemoragii genitale / digestive
• in formele clinice extrem de grave– hemoragii oculare / cerebrale
• nu apar:– hemartroze– hematoame intramusculare
• splenomegalia 5-10% / minora• nu exista adenopatii / hepatomegalie
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SEMNE DE GRAVITATE
1. Difuziunea rapida a purpurei2. Aparitia de bule hemoragice la nivelul
palatului cavitatii bucale3. Prezenta hemoragiilor retiniene4. Anemia acuta severa5. Nr trombocite < 3.000/mmc6. Menometroragii la o adolescenta care face
o PTI acuta
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SEMNE BIOLOGICE• nr trombocite < 50.000 / mmc• 2/3 cazuri < 20.000 / mmc• aspect normal ± megatrombocite• nr leucocite / hematii – normal• medulograma exclude aplaziile medulare si
leucemiile acute la debut– MO normala– megakariocitele – nr normal / crescut
• teste de coagulare normale
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EVOLUTIE
1. PTI acuta / autolimitate vindecare spontana sau accelerata de terapie
2. PTI cu recaderi3. PTI cronica < 20 %
dupa 6 luni de evolutie
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TRATAMENT
• PTI = urgenta in patologia hemoragica la copil• internare obligatorie• sunt contraindicate:– injectiile im– masurarea temperaturii rectal– adm de aspirina
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TRATAMENT DE URGENTA
• primele 5 – 7 zile• trat substitutiv : concentrate plachetare– nr trombocite < 15.000/mmc
• trat patogenic– corticoterapie in “bolus” – dupa efectuarea
mielogramei SoluMedrol 5 -10 mg/kgc/zi– preparate cortizonice per os Metilprednisolon 2 mg/kgc/zi 4 – 6 sapt
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TRATAMENT• Imunoglobuline – 400 mg/kgc/zi iv – 5 zile– 800 mg/kgc/zi iv – 3 zile– accelereaza vindecarea – prin suprasaturarea
sistemului imun– rezultate comparabile cu corticoterapia– risc de transmitere a unor infectii virale– indicatii• esec al corticoterapiei• imposibilitatea efectuarii mielogramei
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TRATAMENT
• Splenectomia– indicatie majora – formele cu evolutie cronica– vaccinare preoperatorie antimeningococica/
pneumococica/ Hi• Imunosupresoare– postsplenectomie , daca apar recaderi=> prognostic rezervat
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PURPURA HENOCH-SCHONLEIN
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• Purpura reumatoida sau anafilactoida• Diateza hemoragica de cauza vasculara =
vasculita• Cea mai frecventa purpura in perioada
copilariei• 4 – 7 ani• Mai frecventa la baieti• Incidenta sezoniera, toamna-iarna
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PATOGENIE
• Mecanism imunologic– Depozite de Ig A la nivelul peretilor vaselor mici– fibrina, C3, Ig M– In faza acuta a bolii – cresterea nivelului de Ig A
seric• Leziunile caracteristice apar la nivelul vaselor
mici fara perete muscular
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PATOGENIE
• Depozite mezangiale de Ig A, Ig M, properdina si complement– Complicatii renale– Studii histochimice
• Factori ereditari – cazuri familiale– HLA Bw 35
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DIAGNOSTIC• Clinic
• Debut dupa– Infectii virale– Vaccinari– Adm de medicamente
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TRIADA SIMPTOMATICA1. PURPURA
Aspect petesial, maculo-papulos, pseudourticarian, rar necrotic
Distributie simetrica, ½ inf a corpului Topografie periarticulara Respecta trunchiul, fata si mucoasele Uneori insotita e edem Evolutie in pusee, declanste de ortostatism
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TRIADA SIMPTOMATICA
2. MANIFESTARI ARTICULARE 60% Artrita / artralgii Articulatii mari Vindecare fara sechele
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TRIADA SIMPTOMATICA
3. MANIFESTARI DIGESTIVE 60 – 80% Nespecifice: varsaturi, dureri abdominale Hemoragii digestive Abdomen acut pseudochirurgical
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ALTE MANIFESTARI
• RENALE– Tardive– 22 – 36% – Hematurie, proteinurie, edeme, HTA– Sdr nefrotic, IR– = complicatii – grefeaza prognosticul
• Pulmonare• Cardiace• Nervoase
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COMPLICATII
• DIGESTIVE– Ocluzii prin invaginatie intestinala ileo-ileala– Perforatie intestinala– Peritonita – Volvulus
• RENALE– Nefrita intrainfectioasa – Sdr nefrotic secundar
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DIAGNOSTIC DE LABORATOR
• HLG– Leucocitoza cu neutrofilie– Hb / trombocite normale
• Probe inflamatorii crescute / ASLO • Complement seric normal / crescut• Teste de coagulare normale, cu exceptia rezistentei
capilare – testul garoului pozitiv• Ex de urina• IRA
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TRATAMENT
• Nespecific • Simptomatic – Repaus la pat– Antihistaminice– Trofice vasculare
• Corticoterapia – controversata– Forme abdominale nechirurgicale– Nu impiedica recaderile
• Imunosupresive – nefropatiile severe
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EVOLUTIE SI PROGNOSTIC
• Vindecare – 1-2 saptamani• Recaderi cutanate• Afectare renala