In this article, Prof James Ker introduces us to haemodynamically stable venous thromboembolism. Next issue, he examines strategies to manage the condition.

About 20% of patients with a VTE event will die within a year of diagnosis

Venous thromboembolism (VTE), consisting of deep venous thrombosis (DVT), and pulmonary embolism (PE), affects about 10 million people globally with an annual incidence of 1-2 cases per 1000 of the population and this incidence rises with increasing age.1

Globally, acute VTE is the third most common acute cardiovascular syndrome after acute myocardial infarction and stroke.2 VTE events can occur up to 50% in patients during or shortly after hospitalisation.3 About 10% of all hospital-associated deaths are associated with VTE. About one third of all patients with a VTE event will have a recurrence of the VTE event within the next 10 years.3 There are some indications that the incidence of in-hospital deaths due to VTE are declining.

CONSEQUENCES OF VTE

There is an increased risk of death during the acute episode of VTE. About 20% of patients with a VTE event will die within a year after diagnosis, often of an underlying co-morbidity.

  1. Major bleeding associated with anticoagulant therapy
  2. Post-thrombotic syndrome such as post-phlebitic leg with venous insufficiency
  3. Post-embolism syndrome, such as chronic thromboembolic hypertension and persisting functional limitations such as dyspnoea and poor physical performance and a reduced quality of life
  4. Large healthcare economic burden.

The above consequences indicate the necessity of early diagnosis of VTE and adequate early treatment.

PATHOPHYSIOLOGY

VTE is a multicausal complex disease triggered by provoking factors. Provoking or risk factors are traditionally associated with Virchow’s triad consisting of conditions of stasis, hypercoagubility, and abnormalities of the blood vessel. VTE is also now regarded as a cardiovascular continuum in which the traditional cardiovascular risk factors for atherosclerotic disease also increase the risk of VTE.4 The proposed mechanism for the development of venous thrombosis is a complex interaction between coagulation and inflammation in which activating the coagulation cascade stimulates the immune system and in turn, innate immune cells then contribute to thrombus formation in a process called immunothrombosis.5 Leucocytes are the primary source of procoagulant tissue factor-positive microparticles that stimulate thrombus formation and growth. Neutrophils produce neutrophil extracellular traps (NETs) that provide a scaffold for red cells, platelets and procoagulant molecules to promote thrombus formation. Platelets help induce the formation of NETs and augment the procoagulant activity of the innate immune cells.

RISK FACTORS FOR VENOUS THROMBOEMBOLISM1,2

Strong risk factors that are persistent:

  • Active cancer
  • Antiphospholipid syndrome.

Strong risk factors that are transient:

  • Major surgery of longer than 30 minutes
  • Major trauma or fracture
  • Joint replacement and spinal cord surgery
  • Caesarean section
  • Hospitalisation for acute illness and prolonged immobility (longer than three days).

Weak risk factors that are persistent include chronic inflammatory conditions, infection, obesity, nursing home confinement, personal positive family history of VTE, oestrogen therapy, minor trauma or fracture, pacemaker placement, pregnancy or puerperium, surgery less than 30 minutes, blood transfusion and platelet transfusion.
 

REFERENCES:

  1. Khan F, Tritschler T, Khan SR, Rodger MA. Venous thromboembolism. Lancet 2021;398: 64-77.
  2. 2019 ESC Guidelines for the diagnosis and management of acute pulmonary embolism developed in collaboration with the European Respiratory Society (ERS). European Heart J 2020; 41: 543-603.
  3. Heit JA. Epidemiology of venous thromboembolism. Nat Rev Cardiol 2015; 12(8): 464-474.
  4. Goldhaber SZ. Risk factors for venous thromboembolism. J of the American College of Cardiology. 2010; 56(1): 1-7.
  5. Engelmann B, Massberg S. Thrombosis as an intravascular effector of innate immunity. Nat Rev Immunol2013; 13: 34-45.