**2.6 Diagnostic and treatment challenges**

102 Deep Vein Thrombosis

mesenteric systems (Mammen et al., 1992), hepatic veins (Singh et al., 2000), and peripherally in the extremities with associated pulmonary emboli (Northup et al., 2006). The prothrombotic state may be involved in other sequelae of chronic liver disease, including hepatic parenchymal extinction, fibrosis and portopulmonary hypertension. Thus, a prolonged prothrombin time does not adequately portray the levels of other clotting factors, particularly factors VIII, X and II that can be more than adequate to promote clot formation (Violi et al., 1995). As well, it is known that the coagulation disorders associated with falling liver can induce further hepatic damage, namely, parenchymal extinction. Wanless et al (Wanless et al., 1995) have clearly demonstrated the histopathologic evidence of the secondary hepatic damage caused by circulatory disturbances due to thrombotic occlusion

Deep vein thromboses in the lower extremity are common in the general medicine population without liver disease and range from 4% to 12% in inpatients (Anderson et al., 1991, Stein et al., 2002). Patients with cirrhosis share many of the same risk factors as hospitalized general medicine inpatients, including prolonged immobility, obesity, recent surgical procedures and malignancies. The presence of anticardiolipin and antiphospholipid antibodies have also been documented in patients with cirrhosis (Violi et al., 1994) and hepatitis C (Prieto et al., 1996). Hyperfibrinolysis, perhaps related to persistence of tissue plasminogen activator, is also prevalent in decompensated cirrhosis (Gunawan et al., 2006). It is not commonly symptomatic that DVT events may occur in patients with liver cirrhosis despite the coagulopathy of liver disease and clinical experience suggests this is the case. Several studies have shown lower levels of antithrombin, protein C and protein S in cirrhosis patients compared with controls (Mammen EF et al., 1992, De Caterina et al., 1993, Vukovich et al., 1995, Walker et al., 1990, Zurborn et al., 1988). Indeed, the diminution in the circulating levels of these inhibitors was noted in the early stages of liver disease and well before the setting of its chronic stages as in liver cirrhosis (Al-Ghumlas et., 2005, Abdo et al.,

The literature is sparse in the area of clinical DVT in cirrhosis and is limited to case reports and a single case-controlled study (Ben Ari et al., 1997) comparing hospitalized cirrhotic patients with and without DVT. In this retrospective study, a new DVT or PE was diagnosed in appropriately 0.5% of all inpatients with documented cirrhosis despite 21% of these patients being on some form of DVT prophylaxis. While the rate of VTE is lower than expected in the general medicine population, these data show that patients with liver cirrhosis are not immune to VTE. It is plausible that this underestimates its true incidence. This could be explained as symptoms of VTE in the decompensated liver cirrhosis patients, particularly edema and dyspnea are common and not specific. Diagnosis requires a high

The symptoms of DVT in the decompensated cirrhotic patient, edema, and dyspnea are common and not specific; those patients have similar risk factors as medical inpatients. Patients with liver disease can present to medical services with complaints of leg edema, leg

of intrahepatic blood vessels (microvascular thrombosis).

2010),

**2.5 Clinical presentation** 

pain dyspnea, and abdominal pain.

**2.4 The prevalence of deep vein thrombosis in liver disease** 

index of suspicion and accurate radiologic testing methods.

Diagnosing DVT in patients with liver disease need high level suspicion, presence of laboratory investigation such as D-dimer and radiological procedure of Duplex ultrasound; thus elevation of coagulation markers such as the prothrombin time and partial thromboplastin time does not safeguard against thrombotic events. Serum albumin level was independently associated with the occurrence of thrombosis (Ben Ari et al., 1997, Senzolo et al., 2009).
