Pulmonary embolism (PE) is a relatively common cardiovascular emergency. By occluding the pulmonary arterial bed it may lead to acute life-threatening (3% early mortality rate), but potentially reversible right ventricular failure. PE is a difficult diagnosis that may be missed because of non-specific clinical presentation. Early diagnosis is fundamental, since immediate treatment is highly effective. Depending on the clinical presentation, initial therapy is primarily aimed either at life-saving restoration of flow through occluded pulmonary arteries (PA) or at the prevention of potentially fatal early recurrences
The prevalence among hospitalized patients in cardiology clinics and words accros our country is somewhat around 1-1,6%. The prevalence of PE among hospitalized patients in the United States, according to data collected between 1979 and 1999, was 0.4%. The incidences of VTE and PE were 18.3 (0,18%) and 6.0 (0,06%) /10 000/year respectively, in Brittany and France. The true incidence of PE is difficult to assess in view of its non-specific clinical presentation.
P A T I E N T : male, age 44, sedentary work and lifestyle R I S K F A C T ORS: HTA, DM type II, Obesity (BMP >28) S Y M P TOMS: dyspnea, deconditioning, shortnes of breath at low level of activity for several days S I G N S : tachypnea, tachycardia
Red blood count: Er 5,66; Hgb 166; Htc 0,50; CONTROL: Er 5,30; Hgb 156; Htc 0,47 White cells/platelet: Le 18,5 (Ly 7,4%; Neutr. 85,6%); Pl 264 Control: Le 8,8; Pl: 191 Glicemia 9,9..6,0; urea 9,6; kreatinin 154,8, CONTROL: urea 5,6; kreatinin 73; Bill 28,7; AST 30; ALT 29; Hol 5,27; HDL Hol 1,3; LDL Hol 4,8; Tg 0,68; electrolytes: Na 137; K 4,6; Ca 2,43 Markers of thrombosis: D - dimmers: 4500 4500 3453 2500
P R E D I S P O S I N G F A C T O R STRONG PREDISPOSING FACTORS (ODDS RATIO >10) PATIENT RELATED SETTING RELATED Fracture (hip or leg) / Hip or knee replacement Major general surgery / Major trauma Spinal cord injury MODERATE PREDISPOSING FACTORS (ODDS RATIO 2 9) Arthroscopic knee surgery / Central venous lines / Chemotherapy Chronic heart or respiratory failure Hormone replacement therapy Malignancy Paralytic stroke / Oral contraceptive therapy Previous VTE / Thrombophilia Pregnancy/Postpartum WEAK PREDISPOSING FACTORS (ODDS RATIO <2) Bed rest >3 days Immobility due to sitting (e.g. prolonged car or air travel) Increasing age / Obesity / Varicose veins Laparoscopic Surgery Anderson FA Jr, Spencer FA. Risk factors for venous thromboembolism. Circulation, 2003; Vol. 107, I-9 I-16.
CLINICAL PREDICTION RULES FOR PE: the Wells score and the revised Geneva score Revised Geneva score Wells score variable points variable points Predisposing factors Age >65y Previous DVT or PE Surgery or fracture within 1 month Active malignancy Symptoms Unilateral lower limb pain Haemoptysis Clinical signs Heart rate 75-94/min / 95 Lower limb pain at palpation and unilateral oedema +1 +3 +2 +2 +3 +2 +3 +5 +4 Predisposing factors Previous DVT or PE Recent surgery or imobilisation Cancer Symptoms +15 +15 +1 Haemoptysis +1 Clinical signs Heart rate >100/min Clinical signs of DVT Clinical probability Total Clinical probability Total Low Intermediate High 0-3 4-10 11 Low Intermediate High +15 +3 0-1 2-6 February 1, 2011 7
2D TT ECHOCARDIOGRAPHY LV with normal dimensions, volumes and function, only slight septal hypertrophy, enlarged LA-43mm diameter RV and RA enlarged - dilated (40mm / 41mm diameter); RV/LV ratio <1,0 (0,8);TR 2+; severe PAH (AT 40msec)
64 CT OF THORAX Technical conditions: 1,2mm tick slices,
64 CT OF THORAX Nonoclusive massive thrombi of booth pulmonary arteries and lobar and segmental branches no pulmonary artery CT obstruction index was calculated Main pulmonary artery diameter: enlarged - trunks pulmonalis 33mm; right pulmonary artery 24,9mm, left pulmonary artery 25,5mm
CLINICAL MARKERS MARKERS OF RV DYSFUNCTION MARKERS OF MYOCARDIAL INJURY -Shock -Hypotension -RV dilatation, hypokinesis or pressure overload on echocardiography -RV dilatation on spiral computed tomography -BNP or NT-proBNP elevation -Elevated right heart pressure at RHC Cardiac troponin T or I positive Guidelines on the diagnosis and management of acute pulmonary embolism, 2008, European Heart Journal, Vol 29, 2276 2315
Guidelines on the diagnosis and management of acute pulmonary embolism, 2008, European Heart Journal, Vol 29, 2276 2315
PATIENT TREATMENT: 1. Treatment in acute phase: Fibrinolytic therapy: Actylise a 100 mg as 2h i.v. infusion, followed by 25000 IE Heparin (as 24 hour infusion ) 8 days, oral Vit K antagonists (Acenocumarol). CONTROL OF HEMOSTASIS: Prolongation of Protrombine, Trombine and Kaolin-Cephalin time for 2-3 times INR 1,6 2,3. 2. AT DISCARGE: Th: oral Vit K antagonists (Acenocumarol), ASA, ACE inhibitor, Ca channel blocker INR 1,5-2,5
first ECG-acute phase
F O L L O W U P E C H O C A R D I O G R A P H Y - to observe complete resolution of RV function- LV FUNCTION: hypetrofied LV walls, slightly increased LV volumes (158/76ml), normal LV dimensions anf systolic function, dyastolic dysfunction RV FUNCTION: RV short axis diameter 30mm, without PAH, complete resolution of RV function, TR (Vmax 2,90m/sec, PG 33mmHg). FOLLOW UP BYOCHEMICAL ANALYSES: -to observe complete deactivation of activated intravascular fubrinolysis/ to exclude congenital protrombotic states D dimers 727..265, Protrombotic factors -Antitrombin III, proteins C,S (in normal ranges) FOLLOW UP CT PULMONARY ANGIOGRAM - To determine the resolution of pulmonary emboli in individual vessels, and/or complete resolution skadualed for later
F O L LOW U P E C H OCARDIOGRAPHY - at one mounth-complete resolution of RV function- LV FUNCTION: hypetrofied LV walls, slightly increased LV volumes (158/76ml), normal LV dimensions anf systolic function, dyastolic dysfunction RV FUNCTION: RV short axis diameter 30mm, without PAH, complete resolution of RV function, TR (Vmax 2,90m/sec, PG 33mmHg).
T W O R E A S O NS W H Y W E SELECTED T H I S C A S E F O R P R E S ENTATION? 1. BECOUSE OF THE USE OF FIBRINOLYTIC THERAPY (which is not recommended in all APE cases) Normotensive patients (without haemodynamic compromise). generally have a favourable short-term prognosis and they are considered to have non-high-risk PE. The bleeding risk of thrombolysis appears to outweigh the clinical benefits. However, within this group, some may have evidence of right ventricular dysfunction (echocardiography or CT), or of myocardial injury (elevated cardiac biomarkers - troponin I or T, heart-type fatty acid-binding protein). These patients have an intermediate risk of an adverse outcome in the acute phase of PE. Existing data suggest that this intermediate-risk PE patients may benefit from early thrombolytic treatment, particularly if they have a low bleeding risk (Stavros Konstantinides; Thromb Haemost. 2010). 2. BECOUSE WE USED CT FOR DIAGNOSIS (which is not diagnostic procedure performed on regular basis in our institution aldough it is recommended as first line test in APE guidelines) For patients in whom APE might have been suspected, the most common tests are: echocardiography (26% of the patients), CT (11%), ventilation-perfusion scintigraphy (6.9%), and duplex ultrasound (7.3%). For inpatient diagnosis of APE, the most common tests are: CT (49%), duplex ultrasound (18%), echocardiography (10.9%), and ventilation-perfusion scintigraphy (10.9%). (Bhargavan M, Sunshine JH, Lewis RS, Jha S, Owen JB, Vializ J. AJR Am J Roentgenol. 2010)