Clinical Profile and Risk Factors of Venous Thrombosis: A Prospective Observational Study from a Tertiary Care Center in South India

Background: Venous thromboembolism (VTE), encompassing deep vein thrombosis (DVT), pulmonary embolism (PE), and cerebral venous thrombosis (CVT), is a major cause of morbidity and mortality. Identifying clinical and laboratory risk factors is crucial for early diagnosis and prevention, particularly in resource-limited settings.

Methods: A prospective descriptive study was conducted over a two-year period (November 2017–November 2019) at a tertiary care teaching hospital in South India. A total of 59 patients with radiologically confirmed venous thrombosis were included. Clinical data, comorbidities, and laboratory parameters, including complete blood count, ESR, CRP, serum homocysteine, and antiphospholipid antibodies, were collected. Statistical analysis was performed using SPSS version 17. Associations were assessed using Chi-square or Fisher’s exact test, and p-values <0.05 were considered significant.

Results: Among 59 patients, the majority were male (≈80%), with peak incidence in the 20–30 and 40–50-year age groups. DVT was the most common presentation (≈60%), followed by CVT (≈20%). Alcohol consumption (35.6%), High BMI (45%), and H/o prior thrombosis (20.3%) were frequent risk factors. Comorbidities included hypertension (30.5%), diabetes mellitus (27%), and chronic liver disease (30.5%). Elevated serum homocysteine (>15 µmol/L) was observed in 78%, and elevated CRP in 81% of cases. Polycythemia (20.3%) and H/o recent surgery (6.8%) were also associated with thrombosis. Significant associations were noted between patients with diabetes and chronic liver disease with pulmonary embolism.

Conclusion: Venous thrombosis in this cohort predominantly affected young to middle-aged males and was frequently unprovoked. Modifiable risk factors such as obesity, alcohol use, and metabolic comorbidities were prevalent. Elevated inflammatory markers and homocysteine levels highlight the role of inflammation and metabolic dysregulation in thrombogenesis.