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Venous Thromboembolism
Venous Thromboembolism
Venous Thromboembolism
Classification[edit]
Common forms
Superficial venous thromboses cause discomfort but generally not serious
consequences, as do the deep vein thromboses (DVTs) that form in the deep veins of
the legs or in the pelvic veins. Nevertheless, they can progress to the deep veins
through the perforator veins or, they can be responsible for a lung embolism mainly if the
head of the clot is poorly attached to the vein wall and is situated near the sapheno-
femoral junction.
When a blood clot breaks loose and travels in the blood, this is called a venous
thromboembolism (VTE). The abbreviation DVT/PE refers to a VTE where a deep vein
thrombosis (DVT) has moved to the lungs (PE or pulmonary embolism).[1]
Since the veins return blood to the heart, if a piece of a blood clot formed in a vein
breaks off it can be transported to the right side of the heart, and from there into
the lungs. A piece of thrombus that is transported in this way is an embolus: the process
of forming a thrombus that becomes embolic is called a thromboembolism. An embolism
that lodges in the lungs is a pulmonary embolism (PE). A pulmonary embolism is a very
serious condition that can be fatal depending on the dimensions of the embolus. Venous
thromboembolism (VTE) refers to both DVTs and PEs.
Rare forms
While venous thrombosis of the legs is the most common form, venous thrombosis may
occur in other veins. These may have particular specific risk factors:[2]
Risk Factors
VTE does not discriminate. It affects people of all ages, races and ethnicities, and
occurs in both men and women. Certain factors and situations can increase the risk
of developing potentially deadly blood clots.
Strong Risk
Moderate Risk
Age (60+)
Personal or family history of blood clots, recent stroke
Cancer/chemotherapy
Trauma
Using estrogen-based medication (e.g., oral contraceptives or hormone
replacement therapy)
Other Factors
Obesity
Pregnancy or recent birth
Smoking
Alcohol consumption
Warning Signs and Symptoms
VTE can occur without any warning signs or symptoms and can go unrecognized
and undiagnosed by a healthcare professional. Symptoms that do appear may be
associated with either DVT or PE.
What are the most common tests my care team may order to see if I have a
blood clot?
Pathophysiology
In contrast to the understanding for how arterial thromboses occur, as with heart attacks,
venous thrombosis formation is not well understood With arterial thrombosis, blood
vessel wall damage is required for thrombosis formation, as it initiates coagulation, but
the majority of venous thrombi form without any injured epithelium.
Red blood cells and fibrin are the main components of venous thrombi,and the thrombi
appear to attach to the blood vessel wall endothelium, normally a non-thrombogenic
surface, with fibrin.Platelets in venous thrombi attach to downstream fibrin, while in
arterial thrombi, they compose the core.As a whole, platelets constitute less of venous
thrombi when compared to arterial ones.The process is thought to be initiated by tissue
factor-affected thrombin production, which leads to fibrin deposition.
The valves of veins are a recognized site of VT initiation. Due to the blood flow pattern,
the base of the valve sinus is particularly deprived of oxygen (hypoxic). Stasis
excacerbates hypoxia, and this state is linked to the activation of white blood cells
(leukocytes) and the endothelium. Specifically, the two pathways of hypoxia-inducible
factor-1 (HIF-1) and early growth response 1 (EGR-1) are activated by hypoxia, and they
contribute to monocyte and endothelial activation. Hypoxia also causes reactive oxygen
species (ROS) production that can activate HIF-1, EGR-1, and nuclear factor-κB (NF-
κB), which regulates HIF-1 transcription.
HIF-1 and EGR-1 pathways lead to monocyte association with endothelial proteins, such
as P-selectin, prompting monocytes to release tissue factor-filled microvesicles, which
presumably initiate fibrin deposition (via thrombin) after binding the endothelial surface.
Treatment
DVT and PE are serious, life-threatening conditions that require immediate medical
attention. Treatment can differ by patient but typically includes blood thinning
medication to break up clots and prevent new ones from forming. Depending on
specific conditions, a patient might need:
Early diagnosis and treatment can often lead to recovery, but long-term
complications, such as post-thrombotic syndrome and chronic thromboembolic
pulmonary hypertension may occur.
Not everyone who is diagnosed with VTE needs treatment. In some cases, your doctor will
detect a clot and decide to monitor it instead of treating it right away. Doctors usually
recommend medicines to treat VTE, but a vena cava filter may be used if you cannot take the
medicine.
-Venous Thromboembolism
Catheter-assisted thrombus removal
Medicines
- Venous Thromboembolism
Catheter-assisted thrombus removal
Some people who cannot take blood thinners may need a vena cava filter to
treat their deep vein thrombosis. The filter is inserted inside a large vein
called the vena cava. The filter catches blood clots before they travel to the
lungs, which prevents pulmonary embolism. However, the filter does not stop
new blood clots from forming. A filter is not usually recommended if you
have taken blood thinners.
Prevent a first VTE event
If you are preparing to go to the hospital for a procedure or have other risk
factors for VTE, talk with your doctor about a plan for preventing blood clots
from forming. Doctors may suggest three ways to help prevent VTE: