**45. Conclusion**

NTPE continues to pose a diagnostic challenge in clinical medicine despite much advancement in laboratory testing and imaging. Improved awareness along with techniques to allow for more accurate ante-mortem diagnosis may faciltitate early and prompt recognition of these syndromes which may in turn pave the way for better treatment modalities.

### **46. Acknowledgement**

We wish thank Ms. Judy Kammerer (Librarian, UCSF Fresno) for her invaluable contribution in preparation of this chapter.

#### **47. References**


used as insoluble binding agents in oral tablets, are first pulverized, then dissolved in water and injected by intravenous drug users, and may be carried by the bloodstream until they lodge in the pulmonary capillary bed to cause NTPE (Farber et al., 1989; Ferrer et al., 2002;

The advent of modern percutaneous interventional procedures has led to a rise in catheter or fragment related pulmonary embolism. Catheter embolism usually takes place when the catheter is withdrawn from the introducing needle causing the distal portion of the catheter be sheared off (Propp et al., 1988). Spontaneous catheter breakage accounts for 25% of the catheter emboli. Retained catheter fragments have high rate of complications such as arrhythmias, perforations and thrombus formation (Fisher & Ferreyro, 1978; Richardson et

Prostate brachytherapy can also lead to embolization of radioactive seeds. On imaging the radioactive seeds appear as small (Iodine-125 measures 4.8 mm in length and 0.8 mm in diameter) metallic densities, usually detected incidentally. Clinical implications of these embolized radioactive seed implants remain unclear. Patients with arteriovenous malformations undergo therapeutic cerebral embolization with different materials such as cyano-acrylate agents, polyvinyl alcohol foam particles, micro-coils, silk or dacron thread and balloons. Cyano-acrylate has been reported to cause symptomatic pulmonary embolism (Kjellin et al., 2000; Pelz et al., 1995). Intravenous injection of elemental mercury is rare and has typically been reported in relation to psychiatric or suicidal incidents (Givica-Perez et al., 2001). Systemic embolization of mercury has been reported as well (Shareeff et al., 2000; Vas et al., 1980). On imaging, multiple metallic densities are seen. Mercury may remain in the body for a long time and metallic densities may remain visible for years after the

NTPE continues to pose a diagnostic challenge in clinical medicine despite much advancement in laboratory testing and imaging. Improved awareness along with techniques to allow for more accurate ante-mortem diagnosis may faciltitate early and prompt recognition of these

We wish thank Ms. Judy Kammerer (Librarian, UCSF Fresno) for her invaluable contribution

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**6** 

*1Hungary 2Brazil* 

**Pathophysiology, Diagnosis** 

Diana Mühl, Gábor Woth, Tamás Kiss, Subhamay Ghosh and Jose E. Tanus-Santos

*University of Sao Paulo, Ribeirao Preto, SP* 

**and Treatment of Pulmonary Embolism** 

*1Department of Anaesthesia and Intensive Care, University of Pécs, Pécs 2Department of Pharmacology, Faculty of Medicine of Ribeirao Preto* 

**Focusing on Thrombolysis – New approaches** 

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

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 –

**1. Introduction** 

**1.2 Etiology** 

**1.1 Incidence and mortality of pulmonary embolism** 

appropriate treatment (S. Büchner & Th. Hachenberg, 2005).

