Epidemiology
In England, 35,845 hospital admissions for pulmonary embolism (PE) were reported in the 1-year period between 2022 and 2023.[8] The number of deaths due to PE was 7388 between 2019 and 2021.[9]
Of 317,000 deaths related to venous thromboembolism (VTE) in six European Union countries (population 454 million) in 2004, 34% were attributable to sudden fatal PE, 59% from PE-related deaths following undiagnosed VTE, and 7% from correctly diagnosed PE.[10]
Between 2007 and 2009, PE resulted in 277,549 adult (aged ≥18 years) hospitalisations in the US. Of these patients, an average of 19,297 died each year.[11] The annual rate of adult hospitalisations with a discharge diagnosis of PE during 2007 to 2009 was 121 per 100,000 population.[11]
From 1993 to 2012, US National Inpatient Sample recorded an increase in PE admissions from 23 per 100,000 to 65 per 100,000.[12] The rate of both massive PE and mortality increased (1.5 to 2.8 per 100,000, and 1.6 to 2.1 per 100,000, respectively), but not commensurate with the increase in admissions.[12] The proportion of male patients admitted with PE increased from 44.9% in 1993 to 47.3% in 2012. The majority of patients were white (62.1% in 1993, 70.2% in 2012); however, the proportion of black patients admitted increased significantly (from 8.0% to 15.9%).
Among US adults greater than 65 years of age, the adjusted PE hospitalisation rate increased from 129/100,000 person-years in 1999 to 302/100,000 person-years in 2010.[13]
Risk factors
Present in 29% with confirmed PE.[21]
Present in 28% with confirmed PE.[21]
Present in 25% with confirmed PE.[21]
Present in 11% with confirmed PE.[21]
Venous stasis and prolonged bed rest are known to increase the risk of venous thromboembolic event.[36]
Present in 11% to 21% of patients with a venous thromboembolic event (combined DVT/PE incident rate).[58] Heterozygous carriers have an estimated risk for venous thromboembolic event that is 7 times higher than those without the mutation. Homozygous carriers are at 80 times higher risk for venous thromboembolic event than non-affected individuals.[59]
The absolute risk of first pregnancy-associated VTE with heterozygous and homozygous factor V Leiden mutation is 1.1% and 6.2%, respectively.[60]
Patients with factor V Leiden are less likely to have a PE than are people with other inherited thrombophilias. This paradox highlights the differences that exist between the risk factors for DVT and PE.[61][62]
The prevalence of prothrombin G20210A mutation in patients with DVT or PE varies with geography and ethnicity.
In North America, prothrombin gene G20210A carrier rates ranging from 1% in African-Americans to between 6.4% and 10.4% in white people have been reported among those with a history of VTE.[63]
In a Dutch study, the mutation was found in 6.3% of consecutive unselected patients with a first episode of DVT.[64]
Estimated to increase the risk of a venous thromboembolic event by 2 to 5 times that of those without the mutation.[54]
The absolute risk of first pregnancy-associated VTE with heterozygous prothrombin G20210A mutation is 0.9%.[60]
Large variability to the disorder. May not significantly increase the risk of thrombosis in people without a concomitant family history. Fifty percent of patients with antithrombin deficiency and a family history of thrombosis will have a venous thromboembolic event before the age of 40.[54]
The absolute risk of first pregnancy-associated VTE in antithrombin-deficient women is 16.6%.[60]
Found in 1% to 2% of patients presenting with a DVT.
The increase in risk associated with this disorder is not well established; the incidence of venous thromboembolic event is approximately 3.5% per year.[54]
The absolute risk of first pregnancy-associated VTE in protein S-deficient women is 4.8%.[60]
Present in 29% of patients with a diagnosed PE.[21]
More likely to be present in patients who die from PE.
Patients with stage III/IV COPD have a higher risk of VTE compared with those without COPD (HR 1.61, 95% CI 0.90 to 2.93).[26]
COPD severity (defined by airflow limitation or medication usage), rather than frequency of exacerbations, may be associated with VTE events in people with COPD.[27]
Present in 12% with confirmed PE.[21]
Risk of incident DVT is significantly increased in people with varicose veins compared with those without (6.55 vs 1.23 per 1000 person-years).[35] Findings regarding PE are less clear.
Long-duration travel is a weak risk factor for the development of VTE.[36]
The incidence of VTE in flights >8 hours' duration is approximately 0.5% in travellers at low to intermediate risk for development of VTE.[36]
Multiple pathophysiological factors have been attributed to increased risk including immobility, relative hypoxia in the pressure-controlled cabin, and dehydration.[37]
Individual risk factors for long-duration travel-related VTE also play an important role. Age >40 years, female sex, women who use oral contraceptives, people with chronic venous insufficiency and/or varicose veins in the lower limbs, obesity, and genetic thrombophilia are strong modulators of VTE attributed to long-distance travel.[38]
In a small prospective study of patients with severe sepsis and septic shock, VTE incidence was 37.2% despite thromboprophylaxis.[42]
A prospective cohort study using data from the National Surgical Quality Improvement Program database of the American College of Surgeons (ACS-NSQIP) found that preoperative sepsis in patients undergoing a surgical procedure increased the risk of postoperative venous thrombosis compared with patients without any systemic inflammation (odds ratio [OR] 3.3, 95% CI 3.2 to 3.4).[43]
Current exposure to a combined oral contraceptive (COC) is associated with an increased risk of VTE (adjusted OR 2.97, 95% CI 2.78 to 3.17) compared with no exposure during the previous year.[47]
The risk of VTE associated with different COCs appears to be influenced by progestogen type. COCs containing levonorgestrel, norethisterone, or norgestimate have the lowest risk (5-7 events per 10,000 women per year), whereas those containing drospirenone, desogestrel, or gestodene have the highest risk (9-12 events per 10,000 women per year). European Medicines Agency: combined hormonal contraceptives Opens in new window
Observational studies of the combined ethinylestradiol and norelgestromin transdermal patch have reported a similar, or increased, level of VTE risk compared with COCs containing second-generation progestogens. Faculty of Sexual & Reproductive Healthcare: statement - venous thromboembolism (VTE) and hormonal contraception Opens in new window
Progestogen-only methods of contraception do not appear to be associated with an increased risk of VTE. Faculty of Sexual & Reproductive Healthcare: statement - venous thromboembolism (VTE) and hormonal contraception Opens in new window
Oral HRT preparations containing oestrogen, or combined oestrogen-progestogen, increase the risk of VTE.[48] Risk is greater with increased oestrogen dose.
The risk of VTE is increased in patients with inflammatory bowel disease compared with those who do not have inflammatory bowel disease.[49]
More likely to be seen in those who die with a PE, with an adjusted mortality ratio double that of unaffected individuals.[20]
Serological abnormalities found in inactive Crohn's disease and ulcerative colitis, including abnormalities in fibrinolysis, may increase risk of PE.
Nephrotic syndrome increased the risk of VTE in a case-control study (OR 2.89, 95% CI 2.26 to 3.69).[50] The association was strongest within the first 3 months.
Severe nephrotic syndrome leads to hypercoagulability, resulting in thromboembolism at sites such as the renal and pulmonary vasculature.
Estimates of thrombotic events in Behcet's disease vary from 10% to 30%.[51] VTEs appear to be more common in males.
An 8-year audit in one hospital in Turkey found that venous thromboembolic events occurred in 12.8% of patients with the disease.[52]
This association may be linked to hyperhomocysteinaemia.
Prospective studies indicate that hyperhomocysteinaemia is associated with increased risk of VTE.[53]
Homocysteinaemia may increase the relative risk of venous thromboembolic event 2.5-fold.[54]
One pooled analysis of case-control and cohort studies found that the methylenetetrahydrofolate reductase (MTHFR) C677T genetic variant (encoding a thermolabile enzyme that is less active at higher temperatures) is not independently associated with VTE risk.[55]
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