**1. Introduction**

118 Pulmonary Embolism

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#### **1.1 Incidence and mortality of pulmonary embolism**

Pulmonary embolism (PE) is not a disease by itself but may have a venous thrombotic source and is therefore more precise if classified as venous thromboembolism (VTE). According to the international registry, the frequency of VTE is 150-200 new cases diagnosed per 100,000 inhabitants per year. Out of this, one third is diagnosed as primary PE (Oger, 2000; Walther et al., 2009). Following the diagnosis the average mortality is 11% in the first two months (Goldhaber et al., 1999). In the ICOPER study, the total mortality of PE in the first 3 months was 17.5%. However, in the long run the recurrent embolic episodes and lack of revascularisation caused progressive pulmonary hypertension (Goldhaber et al., 1999). The mortality of untreated PE is 30% and with adequate treatment can be reduced to 2-8% (Goldhaber, 1998). The hospital mortality of haemodynamically stable PE patients is overall 10% in general, 4% in the first 24 hours (Kline et al., 2003). Mortality of PE with respiratory and cardiovascular failure on hospital admission can be up to 95%. Hospital mortality is 80% in patients requiring mechanical ventilation and 77% in those who need cardiopulmonary resuscitation in the first 24 hours (Janata et al., 2002). Only 29% of fatal PE cases (verified at hospital autopsies) were previously diagnosed clinically. Based on these facts, the primary goal in PE management is a rapid and clear diagnosis followed by the appropriate treatment (S. Büchner & Th. Hachenberg, 2005).

#### **1.2 Etiology**

The source of PE in majority of cases can be due to the postoperative state, trauma injury, long term immobilization causing deep vein thrombosis (DVT), or congenital/acquired coagulation defect (Goldhaber & Morrison, 2002; Schürmann et al., 1992; Spöhr et al., 2005; Tapson, 2008). There are congenitally predisposed and non-influenced factors in the aetiology of VTE. Most important ones are: old age, family predisposition, genetic defects –

Pathophysiology, Diagnosis and Treatment of Pulmonary

**risk**

**Inter mediate 3-15%**

**Non**

**high**

*Clinical signs* 

*Probability of PE* 

Table 2. Clinical probability score

**1.4 Pulmonary embolism diagnostic strategy** 

improve survival of this critical condition.

**Low <1%**

**High>15% + (+) (+)**

Table 1. Risk stratification according to the ESC 2008 guidelines.

**The clinical probability of pulmonary embolism in outpatients**

normal RV pressure group (Torbicki et al., 2008).

**Mortality Mortality Risk markers markers**

**shock/hypo tension**

Embolism Focusing on Thrombolysis - New approaches 121

**RV dysfunction dysfunction**

(+) Presence of shock/hypotension it is not necessery confirm RV dysfunction

(Wells et al., 2001) **Score** 

Deep vein thrombosis (DVT) +3.0 Pulmonary embolism (PE) suspected from other signs or symptoms +3.0 Hearth rate >100 / min +1.5 Operation, immobilization, bed rest in the last 4 weeks +1.5 Former DVT or PE +1.5 Hemoptysis +1.0 Malignancy (active or confirmed in the last 6 months) +1.0

Small < 2.0 Medium 2.0-6.0 High > 6.0

Acute PE, in the presence of shock/hypotension, RV dysfunction and myocardial injury causes high mortality risk. Rapid and clear diagnosis and appropriate therapy may help to

The prognosis of the increased RV pressure (intermediate risk) group is worse than the

**home treatment treatment- - -**

**admission - <sup>+</sup> -**

**Myocardial Myocardial injury**

**- -**

**+ +**

**Early discharge dischargeor**

**Hospital Hospital**

**Thrombolysis Thrombolysisor embolectomy embolectomy**

**Potential treatment treatment**

activated protein C resistance (Dahlbäck, 1995), 20210A mutation of factor II (Poort et al., 1996), hyperhomocysteinaemia (den Heijer et al., 1996), antithrombin III, protein C and protein S deficiency (Demers et al., 1992).

Aetiology can be divided into two groups:

*a/ Congenital risk factors:* Lack of anti-thrombin III (0.2%), lack of protein C (0.8%), lack of protein S (1.3%), Leiden point-mutation of factor V (3.0%), mutation of prothrombin G20210 A (2.3%) (Ageno et al., 2006).

*b/ Acquired risk factors*: DVT, phlebitis, immobilization, bed rest, post-traumatic and operative state, sepsis, diabetes, smoking, hypovolaemia, diuretic treatment, elevated plasma/blood viscosity, coagulation disorders (disseminated intravascular coagulation, heparin induced thrombocytopenia (HIT), drug induced coagulopathy (anticoncipient, oestrogen), obesity, sedentary lifestyle, pregnancy, postnatal state, cardiac insufficiency, heart valve disorders, artificial valves, central venous catheter, pacemaker electrode, tumour, old age, nephrosis syndrome (Goldhaber et al., 1997).
