You are on page 1of 7

- DVT is caused by vascular endothelial dysfunction, hypercoagulable disorders

and venous blood flow (stasis) which is known as the triad virchow. The clinical
symptoms appear is the swelling of the extremities involved and their pain.
These symptoms are often nonspecific even could not appear. But this is not
handled properly, can be fragmented thrombus and migrate to clogging arteries
leading to the lungs. If this is the case then it would appear highly lethal
pulmonary embolism. DVT is the third most common cardiovascular disorder
after coronary artery disease and stroke. In the UK, 1 in 1000 people suffer from
this disease every year. This figure is expected to continue to rise, it is proved by
the increasing incidence of 30-fold in recent decades than ever before. The
incidence of DVT includes more than half the incidence of venous tromboembili a
whole, where the incidence of venous thromboembolism per year alone reached
0.1% (from 0.01% in young adults to approximately 1% at age above 60 years).
Annual incidence. DVT in Europe and the United States approximately 50 /
100,000 population / year.
DVT risk factors include demographic factors / environment (old age, immobility
time), pathological disorder (trauma, congenital hypercoagulable,
antiphospholipid syndrome, lower extremity varicose veins, obesity, a history of
venous thromboembolism, malignancy), pregnancy, surgery, drug- drugs
(hormonal contraceptives, corticosteroids). Although DVT is generally arise due
to certain risk factors, DVT can occur without clear etiology (idiopathic DVT). To
minimize the risk of fatal pulmonary embolism and panatalaksanaan proper
diagnosis is needed. Death and disability can occur as a result of fault diagnosis,
fault therapy and bleeding due to improper use of anticoagulants, therefore
enforcement diagnosis and appropriate treatment is indispensable

Especially in the venous system of the lower limb is divided into three
subsystems are subsystems surface veins, deep vein subsystems and subsystem
Surface veins located in the subcutaneous tissue and receives venous outflow
from smaller blood vessels in the skin, subcutaneous tissue and legs. the surface
veins system consist of great saphenous vein and saphenous vein parva. Great
Saphenous vein is the longest vein in your body, running from the medial
malleolus up to medial calf and thigh, empties into the femoral vein. Great
Saphenous vein draining blood from the calf and thigh ateromedial. Saphenous
vein parva runs along the lateral side of the ankle through the calf toward the
knee, get blood from the posterolateral calf and flow blood to the popliteal vein,
the meeting point of the two is called safenopoplitea. Among thegreat saphenous
vein and smal saphenous vein many anastomisis obtained, it is the collateral
flow which has an important role during a venous obstruction.

The deep venous system carries most of the blood from the lower extremities
which is located within the muscle compartment. Veins in receiving the
bloodstream from the small venules and veins intramuscular. The deep venous
system tends to run parallel to the arteries of the lower leg and was given the
same name as the artery. As a result, included in this vein is the venous system
anterior and posterior tibial, peroneal, popliteal, femoral, deep femoral veins and
the calf which is not named. Also included in the iliac vein in the lower extremity
venous system because of leg venous flow depending on the vena cava patency
and integrity of these vessels.
Subsystems and surface veins in the channels connected by blood vessels called
veins which form the connecting subsystem liaison lower extremities. Flow
normally from the superficial veins to the deep veins and then into the inferior
vena cava.
In the anatomical structure is obtained venous valves semilunaris one direction
that are scattered throughout the venous system. The valves are folds of the
intima layer consisting of endothelial and collagen, serves to prevent backflow,
stream flow towards the proximal surface of the system into the system through
a liaison. The ability of the valve to function is a very important factor because
the flow of blood from the extremities to the heart goes against gravity.
Physiology of the venous blood flow against gravity is influenced by a factor
called the venous pump. There are two components of the pump that is
peripheral and central veins. Components peripheral vein is the compression of
veins during muscle contractions that push forward flow within the deep venous
system, venous valves work to prevent retrograde flow or reflux for muscle
relaxation and their sinuses small veins that do not berkatup or venules located
in the muscle acts as subsequent blood reservoir will empty its blood into the
deep veins during muscle contraction.
At the pump components that play a role in central venous facilitate venous flow
is a reduction in intrathoracic pressure during inspiration, the reduction in right
atrial pressure and right ventricle after the ventricular ejection phase.

Deep vein thrombosis is a blood clot (thrombus) that forms on the walls of the
veins (deep vein), usually in the lower limbs. , DVT is a venous thrombosis that
occurs in the deep veins, while the veins occurs at superfisila called
Deep vein thrombosis causes only a minimal inflammation. Inflammation that
occurs around the thrombus, accompanied by adhesions thrombus against the
vein wall that is gradually released and becomes an embolus, travels through the
bloodstream and ends on a narrow blood flow, causing blockade to blood flow.
Thrombus occurs because of the slowing of blood flow, abnormalities of the blood

vessel wall, or a blood clotting disorder that is often called the Triassic Virchow.
Some of these factors led to a high incidence of deep venous thrombus. Based
on the venous thrombus venous blood flow is relatively slow, usually red and is
composed of fibrin, erythrocytes, and a small number of platelets, also called the
red thrombus. While the thrombus formed in the lumen of the arteries, the flow is
fast, generally gray and consist of platelets (platelet rich), also called white
DVT occurs in the presence of a clear risk factor is referred to as secondary DVT,
whereas if the risk factors are unclear called primary or idiopathic DVT. DVT in
the pelvis and lower extremities were classified into central DVT (DVT occurs
above v. Popliteal) and peripheral DVT (DVT occurs in v.poplitea and veins in the
distal). Based on the symptoms, signs and severity of disorders of blood flow
drainage, DVT is divided into acute and chronic

The cause is generally of the occurrence of venous thrombus is a dysfunction of

the endothelial wall of the vein, hiperkoagulobilitas, and disruption of flow in the
veins or better known as Virchow's triad. Virchow Trias development will be
influenced by a variety of risk factors.
Risk factors for VTE (Venous Thromboembolism) in general and in particular DVT
can be classified into three, namely: demographic or environmental factors,
process / pathology, and as a result of a particular medical procedure. More
details can be seen there are the table below:
DVT risk factors
Risk factor
1. Demographic factors / environment
Old age, sat for a long (long trips, when a disaster situation)
2. Conditions of pathology
a. Trauma: inferior extremity fractures, spinal cord injury
b. Malignancy
c. Hiperkoagulobilitas congenital: coagulation inhibitor deficiencies
d. Hiperkoagulobilitas income: post-cardiac surgery
e. Inflammatory bowel disease, antiphospholipid syndrome, vasculitis, systemic
lupus erythematosus
f. The veins of the lower extremities
g. Dehydration, polycytemia
h. Obesity, pregnancy, post partum
i. Congenital iliac bands and webs, compressing v. iliac by a. iliac

j. A history of previous thrombosis: venous thrombosis, pulmonary embol

3. medical action
a. Surgery: orthopedics, neurosurgery, digestive surgery
b. Drug: female hormones, corticosteroids, hemostatic
c. Catheterization of blood vessels
d. Bed rest time
3. Medical action of old age, sat for a long (long trips, when a disaster situation)
a. Trauma: inferior extremity fractures, spinal cord injury
b. Malignancy
c. Hiperkoagulobilitas congenital: coagulation inhibitor deficiencies
d. Hiperkoagulobilitas income: post-cardiac surgery
e. Inflammatory bowel disease, antiphospholipid syndrome, vasculitis, systemic
lupus erythematosus
f. The veins of the lower extremities
g. Dehydration, polycytemia
h. Obesity, pregnancy, post partum
i. Congenital iliac bands and webs, compressing v. iliac by a. iliac
j. A history of previous thrombosis: venous thrombosis, pulmonary embol
a. Surgery: orthopedics, neurosurgery, digestive surgery
b. Drug: female hormones, corticosteroids, hemostatic
c. Catheterization of blood vessels
d. Bed rest time
Approximately 47% of patients with DVT have at least Sattu risk factors, the
incidence of VTE increases as more and more risk factors you have. It is said that
the risk of DVT increased from 2.4 in people with one risk faktr to 20 people with
three risk factors.
Cases of DVT in the lower extremities are more common. Developing DVT is
caused by the pressure on v. iliac, use of central venous catheters in the v.
femoral, or bed rest for long. DVT can also occur in other veins such as the neck
and the superior extremity which is usually the cause of iatrogenic due to central
venous catheters in v. subclavian, use of catheters pacemaker, thoracic outlet

Thrombogenesis process was first put forward by Karl Ludwig Rudolf Virchow (a
doctor from Germany) where he explains the three main factors that led to the
development of venous thrombosis, or more famously called sebgai Virchow's
1. Changes in blood flow (stasis, turbulence)
2. Abnormal blood vessel wall / endothelial injury
3. Blood Hiperkoagulobilitas
Static veins often in old age, bedrest more than three days, and the operation
takes a long time. Venous stasis gives local thrombosis predisposition. Stasis
disrupt cleanup active coagulation factor and limit the accessibility of thrombin
in the vein is then attached to trombomodulin. These proteins are found in the
greatest density in the capillaries .. ultrastructural study showed that after a
trauma in the countryside where the leukocytes attached between intercellular
junctions vein endothelial static area. This becomes a nidus for thrombus
formation. If the nidus of thrombus began there in the static area, the substance
which can increase platelet aggregation, ie activated factor X, thrombin, fibrin
and catecholamines remain in high concentrations in the area. Stasis also
provide additional contributions, that forms thrombin by damaging the vein
valves are avascular.
Vascular damage contribute to the growth of venous thrombosis through direct
injury such as fracture and injury to the soft tissues such action intravenous
infusion or substances that irritate such as potassium chloride, chemotherapy or
high doses of antibiotics or endothelial cell activation by cytokines (interleukin-1
and tumor necrosis factor ) were released from the tissue injury and
inflammation. Blood coagulation can be activated through stimulation
intravascular released from distant places (eg damage to the femoral vein when
pelvic surgery) or by cytokine-induced stimulation of endothelial intact. These
cytokines stimulate endothelial cells to synthesize tissue factor and plasminogen
activator inhibitor-1 and the resulting reduction trombodulin, thus reversing the
normal endothelial protective ability. Trombodulin (TM) is an endothelial cell
membrane receptors for thrombin. When thrombin is bound to TM the ability to
break down fibrinogen decreased. Instead ability activates anticoagulants,
protein C increased. Protein C with its cofactor protein S inactivates the active
form procoagulant cofactors, factor Va and VIIIA. Activated protein C also
enhances fibrinolysis. Containing vein endothelial activator that converts
plasminogen to plasmin then plasmin lysis of fibrin. After surgery and injuries,
fibrinolysis system will be inhibited later ekstemitas venous activity under much
reduced compared with the upper limb.
Hirepkoagulabilitas state is a state change of blood helps venous thrombus
formation. The alterations include increased concentrations of both normal and

activated coagulation factors, reduced levels of inhibitors in the circulation,

impaired fibrinolytic system function, their platelet hyperactivity,
hypercoagulability and static factors work together to form venous thrombus.
Although the development of science shows that the causes of DVT is
multifactorial, but the components of Virchow's triad remains an important
element of the pathogenesis of thrombosis. In 1970, Stewart Gwendylen propose
a new theory about the relationship between thrombosis and inflammation.
Stasis of blood flow, although important, is not enough to trigger the formation of
thrombus, but it requires a certain factor to begin the process of thrombogenesis.
Normal vein endothelial antithrombotic character with a variety of mechanisms:
1. producing trombomodulin and then activates protein C, 2. Removing heparin
sulfate and dermatan sulfate which will accelerate the activity of antithrombin
and heparin cofactor activity, 3. regulate the expression of tissue factor pathway
inhibitor (TFPI) and 4. producing tissue pl asminogen activator (tPA). In addition,
joint work between NO, prostacylin and interleukin (IL) -10 is regulated by
endothelial inhibiting leukocyte adhesion and activation. Conversely, when an
interruption in the endothelium, both physical disorder (trauma) or functional
(sepsis), endothelial it is prothrombotic and proinflammatory. Endothelial will
issue plat Elet activating factor (PAF) and endothelin-1 that triggers
vasoconstriction, Von Willebrand factor (vWF), tissue factor (TF), plasminogen
activator inhibitor (PAI) -1, and factor V which will enlarge the process of
thrombosis. Endothelial will also express P-selectin or E-selectin on their surfaces
that will trigger leukocyte adhesion and activation.
Inflamed cells that are not only capable of initiating thrombosis but also able to
improve the process of thrombosis. Interleukin-1 (IL-1) and tumor necrosis factor
(TNF) will trigger the deposition of fibrin through the mechanism of the
expression of endothelial procoagulant and depressed fibrinilisis. TNF also
perform trombomodulin downregulation of the expression, would ultimately
change the nature of antithrombotic endothelial be prokoagulan.Disini Virchow's
triad can be seen that happen but at the molecular level.
Most thrombus occurs in veins with a slow stream. Compared with a pulsating
flow, the flow will slow and static berubungan with hypoxia on endothelial in
venous valves and will trigger the endothelial injury. Hypoxia also stimulates the
production of cytokines and the expression of leukocyte adhesion molecules that
stimulate. Furthermore, the state of stasis of blood flow allows the accumulation
of a pro-coagulant factors and reduced antitrombisis factor.
The combination of stasis of blood flow to the endothelial damage both at macro
and micro levels, without the activation of the coagulation system can not start
the process of thrombogenesis. Activation of the coagulation system alone
without the other two factors above will not be able to start the process of
thrombosis. Already activated coagulation factors, in normal conditions would
rapidly dissolve in the bloodstream, but if it terlokalisassi in stasis regions
trombosisi then the process will quickly occur.
Venous thrombosis any underlying stimulus will increase the resistance of the
lower extremity venous flow, with increased resisitensi, emptying the vein will be
disrupted, causing an increase in blood volume and venous pressure. Thrombosis
may involve the bag valve to impair the function of the valve. The valves are not

functioning or incompetent facilitate the accumulation of static and diekstremitas

In the course of time, with the maturity of a thrombus will become increasingly
organized and attached to the walls of blood vessels. As a result, the risk of
embolization becomes greater in earlier phases trombisis, however, the end of
the fixed clot can break off and become emboli during the organization phase.
Besides the expansion of a thrombus can form the end of a long and smoking
can further be separated into emboli to the pulmonary circulation. Progressive
expansion also increases the degree of venous obstruction and involves
additional areas of the vein system. In the end, lumen patency may be stabilized
to some degree or direkanalisasi with clot retraction and lysis by endogenous
fibrinolytic system. But some residual damage remains