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USA
> 650,000 known cases of PE per year and
50,000 - 200,000 fatalities annually,
PE =the third leading cause of death in the
United States.
Additionally, estimates > 400,000 PE diagnoses
are missed annually.
2/3 of patients die within 1 hour of symptom
onset;
This first hour is known as the golden hour.
If PE is diagnosed and treated within this first
hour, the mortality rate drops to 3% - 8%.
Fiziopatologie
Reducerea functionala (reflex vasoconstrictor pulmo-
pulmonar) si anatomica (prin amputare) a patului casc.pulm .
HTAP brutal instalata) suprasolicitare brutala a VD
Dilatarea acuta a VD IT staza retrograda
Scaderea FEjVD umplere redusa a VS debit redus a VsHipoTA
Bombarea SIV umplere redusa a VS debit redus a VsHipoTA
Tulb distributie circ pulm: Zona tributara arterei ocluzionate = ventilata dar
neirigata nu mai secreta surfactant colaps alveolar (ATELECTAZIE)
INFARCT PULMONAR (daca nu supleaza circulatia bronsica)
PREZUMTIA CLINICA
1.Fondul pe care survine
1. Stri primare de hipercoagulabilitate
sugerate de:
AHC tromboembolice
tromboze recurente fr cauze aparente
tromboze la vrst tnr, n plin sntate apa-rent;
cauzate de:
deficien de antitrombin III (principalul inhibi-tor al trombinei)
deficien de protein C (consum factorii Va i VIIIa i stimuleaz
fibrinoliza)
deficien de protein S (cofactor al proteinei C activate)
fibrinoliz deficitar (fie prin defect de elibera-re, fie prin exces de
inhibitori ai activatorului ti-sular al plasminogenului tPA), ceea ce
perturb echilibrul fin dintre coagulare i fibrinoliz.
Stari primare de
hipercoagulabilitate
Mutatia genei fact V Leiden fact V devine
rezistent la inactivarea determinata de proteina C
activata tripleaza riscul
Mutatia genei fact II (protrombina) creste
protrombinemia
Deficienta sintezei de proteina S (cofactor al
proteinei C)
Hiperhomocisteinemia tripleaza riscul TVP
Ac antifosfolipidici
PREZUMTIA CLINICA
Fondul pe care survine
2. Stri secundare de hipercoagulabilitate
TRIADA VAQUEZ:
Durere pleuretica
Dispnee /tahipnee
Tuse + Expect. hemoptoica
80
TRIADA LDH crescut + TGO=N + Hiperbilirubinemie ARE SENSIBILITATE MODESTA DAR SPECIFICITATE INALTA
Echocardiografia
Scintigrafia pulmonara
Scintigrafia pulmonara
Computer-Tomografia cu baleiaj
helicoidal
Angiografia pulmonara
Diagnostic diferential
TRATAMENTUL PREVENTIV
MOBILIZARE PRECOCE POST-OPERATOR / POST-PARTUM
TRATAMENT ANTICOAGULANT PRE- SI POSTOPERATOR LA
PACIENTII CU RISC
VARSTA > 40 ANI
INTERVENTII CHIRURGICALE LABORIOASE (> 1 h)
OBEZITATE
NEOPLAZII
A.P. TROMBO-EMBOLICE
HEPARINE GMJ:
TROMBOLITICE + ANTICOAGULANTE in
caz de IMA
IN IMOBILIZARI PRELUNGITE:
COMPRESIE PNEUMATICA INTERMITENTA A
GAMBELOR
CIORAPI CU COMPRESIE GRADATA
ANTICOAGULARE PREVENTIVA cu
acenocumarol
FbA preECV
Protezati valvulari / vasculari
Cardiomegalie (CMD)
TRATAMENTUL CURATIV
REPAUS ABSOLUT LA PAT (mn 3-5 zile) pt. a preveni noi emboli
HEPARINE GMJ
NADROPARINA (FRAXIPARINA) 100ui/kgcorp la 12h
ENOXAPARINA (LOVENOX) 100 ui(1mg)/kgcorp / 12h
DALTEPARINA (CLIVARIN) 100 ui/kgcorp/12h
TINZAPARINA (INNOHEP)
Apoi,
ACENOCUMAROL x mn 6 luni,daca persista factorii favorizanti,
sub control IQ(25-35%) sau INR (2 - 3, respectiv 3 - 4,5 in caz de risc inalt)
Rivaroxaban = oxazolidinone derivat inhibitor de factor Xa, 20mg/zi p.o., fara control INR
Dabigatran (Pradaxa Boehringer Ingelheim.) p.o. = direct thrombin inhibitor ; 150/ 220 mg once daily
Apixaban (Eliquis Pfizer & Bristol-Myers Squibb) = anticoagulant oral= a direct factor Xa inhibitor
TRATAMENTUL ANTICOAGULANT
SUPRADOZAJ CU HEPARINA
PROTAMINA cate 1mg pt fiecare 1mg de heparina sodica la ultima
adm) in caz de adm. Intermitenta i.v. lent (altfel risc de
bronhiolospasm sever HPAP CPA, consecutiv eliberarii masive de
tromboxan)
SUPRADOZAJ DE ACENOCUMAROL
- PLASMA PROASPATA CONGELATA
- PPSB 0,5-1ml/KGCORP
- Vit K1 (hidrosolubila) 5 -10mg i.v. lent
Tratamentul trombolitic
GAZOMETRICA
SaO2
BIOLOGICA
Coagulabilitatea( Timpul de coagulare, APPT, INR (zilnic)
Trombocitele (la 2 -3zile)
Fibrinogen
ECG (zilnic)
Radiografia toracica
Echo Doppler