Review Article

Open Access, Volume - 2

Risk Factors, Diagnosis, Pathophysiology and Management of Deep

Vein Thrombosis
Gudisa Bereda*
*
Department of Pharmacy, Negelle Health Science College, Guji, Ethiopia.

Received Date : June 08, 2022 *Corresponding Author: Gudisa Bereda, Department of Phar-
Accepted Date : July 04, 2022 macy, Negelle Health Science College, Guji, Ethiopia. Tel:
Published Date : July 26, 2022 +251913118492/+251919622717.
Archived : www.jcmimagescasereports.org Email: gudisabareda95@ gmail.com
Copyright : © Gudisa Bereda 2022

Abstract

Deep vein thrombosis occurs most often in the legs, but can form in the veins of the arms, and in the mesenteric and cerebral
veins. Common risk factors of deep vein thrombosis includes age 40 years or older, being overweight, a personal or family his-
tory of blood clots, birth control pills, hormone replacement therapy, cancer, certain heart cases, stroke, respiratory failure,
varicose veins, pregnancy, surgery including hip, knee, or stomach surgery, restricted mobility due to a long illness, injury, or
surgery. Vascular injury that may result from major orthopedic surgery (e.g., knee and hip replacement), trauma (especially
fractures of the pelvis, hip, or leg), or indwelling venous catheters. The D-dimer blood test measures degraded fibrinogen,
which is raised in patients with a clot. The reference range varies and is set by the laboratory. This test is recommended in
patients with a low or moderate clinical probability of deep vein thrombosis, as calculated by the Wells score. The two main
types of anticoagulants are heparin and warfarin (coumadin) to keep a clot from growing or prevent new clots from forming.
Warfarin interfere with hepatic synthesis of the vitamin K-dependent coagulation factors II, VII, IX and X. Warfarin, a vitamin
K antagonist, is an effective and cheap oral anticoagulant.

Keywords: Deep vein thrombosis; Diagnosis; management; pathophysiology; risk factors.

Abbreviations extremity and right heart [4].

ACCP: American College of Chest Physicians; APTT: Activated Risk factors
Partial Thromboplastin Time; DOACs: Direct Oral Antico-
Risk of DVT associated with long-duration air travel is called
agulants; DVT: Deep Vein Thrombosis; HIP: Heparin Induced
economy class syndrome. It is 3% to 12% in a long-haul flight
Thrombocytopenia; HRT: Hormone Replacement Therapy;
with stasis, hypoxia, and dehydration being pathophysiologi-
INR: International Normalized Ratio; LMWH: Low-Molecular-
cal changes that increase the risk. Genetic risk factors can be
Weight Heparin; NICE: National Institute for Health and Care
divided into strong, moderate, and weak factors. Strong fac-
Excellence; PT: Prothrombin Time; PE: Pulmonary Embolism,
tors are deficiencies of antithrombin, protein C and protein S.
TPA: Tissue Plasminogen Activator; UFH: Unfractionated Hep-
Moderately strong factors include factor V Leiden, prothrom-
arin; VKORC1: Vitamin K–Epoxide Reductase Complex 1
bin 20210A, non-O blood group, and fibrinogen 10034T. Weak
Introduction genetic risk factors include fibrinogen, factor XIII and factor
XI variants. Common risk factors of DVT includes age of 40
The term thrombosis refers to the formation, from constitu- years or older, being overweight, a personal or family his-
ents of blood, of an abnormal mass within the vascular system tory of blood clots, birth control pills, hormone replacement
of a living animal. When this process occurs within the deep therapy (HRT), cancer, certain heart cases, stroke, respiratory
veins, it is referred to as deep vein thrombosis (DVT). Deep failure, varicose veins, pregnancy, surgery including hip, knee,
vein thrombosis (DVT) commonly affects the lower limb, with or stomach surgery, restricted mobility due to a long illness,
clot formation beginning in a deep calf vein and propagating injury, or surgery [5-7].
proximally [1, 2]. Deep vein thrombosis occurs most often
in the legs, but can form in the veins of the arms, and in the Pathophysiology
mesenteric and cerebral veins [3]. DVT is common in lower
Rudolph Virchow described three conditions that predispose
extremities, pelvic venous system, renal venous system, upper
to thrombus, the so-called Virchow’s triad. This triad includes

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Citation: Gudisa Bereda. Risk Factors, Diagnosis, Pathophysiology and Management of Deep Vein Thrombosis. J Clin Med Img
Case Rep. 2022; 2(4): 1200.

endothelial injury, stasis or turbulence of blood flow, and blood Clinical prediction rules
hypercoagulability [8-10]. There are three primary compo-
nents (virchov’s triad) rationale for pathogenesis of DVT such Although none of the symptoms or signs of DVT is diagnostic in
as venous stasis which slowed blood flow in the deep veins isolation, it has been well established that a clinical prediction
of the legs resulting from damage to venous valves, vessel rule that takes into account signs, symptoms and risk factors
obstruction, prolonged periods of immobility and increased can be accurately applied to categorize patients as having low,
blood viscosity; vascular injury that may result from major moderate or high probability of DVT. Alternatively, the same
orthopedic surgery (e.g., knee and hip replacement), trauma rule can be used to categorize cases as “DVT likely” or “DVT
(especially fractures of the pelvis, hip, or leg), or indwelling unlikely.” Patients who are found to be at low pretest prob-
venous catheters and hypercoagulability which include malig- ability can have DVT safely excluded on the basis of a single
nancy; activated protein C resistance; deficiency of protein C, negative ultrasound result. Thus, serial ultrasound testing can
protein S, or antithrombin; factor VIII or XI excess; antiphos- be avoided in this subgroup of patients. The incorporation of
pholipid antibodies; and other situations. Hypercoagulability plasma D-dimer testing into diagnostic algorithms can identify
is an important hallmark of inflammation. Pro-inflammatory patients who do not require ultrasonography [17-20].
cytokines are critically involved in abnormal lot formation and Treatment of deep vein thrombosis
platelet hyperactivation and also play an important role in
the downregulation of important physiological anticoagulant The goal of therapy for DVT are to stop the clot from getting
mechanisms. It has been determined that pro-inflammatory larger, reduce the chance of having another clot develop,
cytokines such as interleukin 6 (IL-6), IL-17A, and tumor necro- prevent the extension of thrombus, acute PE, recurrence of
sis factor reached increased levels in the majority of patients thrombosis, development of late complications such as pul-
with severe outcomes [11, 12]. monary hypertension and post-thrombotic syndromes, re-
duce the chance of the clot breaking off in your vein and mov-
Diagnosis ing to your lungs and to minimize adverse effects and cost of
The clinical presentation of DVT is often non-specific. Hence, treatment [21, 22]. The two main types of anticoagulants are
accurate diagnosis requires sequential integration of clinical heparin and warfarin (coumadin) to keep a clot from growing
features, assessment of pre-test clinical probability, and con- or prevent new clots from forming [23]. The standard initial
firmatory investigations that include D-dimer testing and im- management of deep vein thrombosis has traditionally meant
aging [13]. admission to hospital for continuous treatment with intrave-
nous unfractionated heparin. Treatment then continued with
Symptoms and signs of deep vein thrombosis: Symptoms and a transition to long term use of oral anticoagulants (vitamin K
signs of leg or pelvis DVT include leg pain, swelling, erythema antagonists). Recently a change has taken place, and low mo-
and dilated superficial veins. Arm DVT has similar symptoms lecular weight heparins are being used. Guidelines prepared
localized to the arm. Some DVTs are asymptomatic. Differen- by the haemostasis and thrombosis task force recommend
tial diagnoses for limb DVT include cellulitis, lymphoedema, that patients receive heparin for at least four days and treat-
chronic venous insufficiency, haematoma and, for leg DVT, ment should not be discontinued until the international nor-
ruptured Baker cyst [14]. malized ratio has been in the therapeutic range for two con-
Table 1: Pretest probability assessment (Wells score). secutive days. According to these guidelines, a patient with
a first episode of a proximal vein thrombosis should receive
Variables Points anticoagulants for six months, with a target international nor-
Paralysis, paresis, or recent plaster malized ratio of 2.5 [24, 25].
1
immobilization of the lower extremities
Active cancer (treatment ongoing or within
Direct oral anticoagulants
1
previous 6 months or palliative)
Guidelines from National Institute for Health and Care Excel-
Localized tenderness along the distribution of lence (NICE) and American College of Chest Physicians (ACCP)
1
the deep veins
recommends direct oral anticoagulants (DOACs) as first line
Recently bedridden for 3 days or major
surgery within 12 weeks requiring general or 1
treatment for DVT. DOACs include direct factor Xa inhibitors
regional anesthesia apixaban, rivaroxaban, and edoxaban, and a direct thrombin
Calf swelling 3 cm asymptomatic side inhibitor, dabigatran (oral direct thrombin inhibitor) [26-28].
1
(measured 10 cm below tibial tuberosity)
Warfarin
Entire leg swollen 1
Collateral superficial veins (nonvaricose) 1 Warfarin interfere with hepatic synthesis of the vitamin K-
dependent coagulation factors II, VII, IX and X or warfarin
Pitting edema limited to the symptomatic leg 1
works by inhibiting vitamin K–epoxide reductase complex
Previous DVT 1 1(VKORC1), the enzyme needed to convert vitamin K to the
Alternative diagnosis as likely as or more required active form. Warfarin reduces production of vitamin
-2
likely than DVT
K–dependent clotting factors such as VII, IX, X, and prothrom-
Notes: DVT is unlikely if well score is ≤1; and DVT likely if well score is >2 bin [29, 30]. Warfarin should begin concurrently with UFH or

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LMWH therapy. Warfarin, a vitamin K antagonist, is an effec- tion described in young adult patients receiving heparin for
tive and cheap oral anticoagulant [31]. Warfarin remains the longer than ten, skin necrosis at the site of subcutaneous in-
drug of choice for long-term therapy to prevent clot formation jection after several days of treatment, alopecia, hypersensi-
once acute anticoagulation is achieved [32]. Warfarin should tivity reactions, including chills, fever, urticaria, bronchospasm
be administered, with a target INR of 2.0 to 3.0, for 3 months and anaphylactoid reactions, occur rarely, hypoaldosteronism;
to patients with DVT following exposure to a transient risk fac- heparin inhibits aldosterone biosynthesis [45, 46]. Reversal
tor (eg, surgery, trauma, immobility) and for at least 6 months agent of heparin toxicity is protamine sulfate. Protamines are
to patients with unprovoked (or idiopathic) DVT [33]. Adverse basic low-molecular-weight, positively charged proteins that
drug reactions of warfarin are spontaneous haemorrhage, have a high affinity for the negatively charged heparin mol-
rashes, and teratogenesis from use during pregnancy [34]. ecules. The binding of protamine to heparin is immediate and
Reversal agent of warfarin toxicity is vitamin k1 (phytomena- results in the formation of an inert complex [47].
dione). It bypasses inhibition of vitamin k epoxide reductase Table 2: The difference between warfarin and heparin.
enzyme [35].
Heparins Warfarin Heparin
Inhibit synthesis
Heparin inhibits coagulation by activating antithrombin III a of vitamin k
protein that inactivates two major clotting factors: thrombin Mechanism of
dependent Activates antithrombin,
and factor Xa. Production of fibrin is reduced, and hence clot- clotting factors, which then inactivates
action
including thrombin and factor xa
ting is suppressed [36]. Heparin is initially given with warfarin prothrombin and
and stopped after a minimum of 4 to 5 days, at which time the factor x
international normalized ratio (INR) should be within 2.0 to Parenterally (IV/SubQ), but
3.0 (therapeutic range). This overlap with warfarin is essential Route of
Orally (PO) not IM because it causes
administration
because factors II, IX, X will not be affected until after 5 days, painful hematoma
hence the intrinsic clotting pathway is intact. The initial pro-
Onset of action Slow (hours) Rapid (minutes)
longation of INR is mainly due to the effect of depression of
factor VII which has a half-life of 5 to 7 hours [37, 38].
Duration of action Prolonged (days) Brief (hours)
Low-molecular-weight heparin Activated partial
Prothrombin time
Monitoring thromboplastin time
Low molecular weight heparins are fragments of unfractionat- (PT)
(aPTT)
ed heparin created by depolymerisation. The LMWHs increase
the action of antithrombin III on factor Xa but not its action Reversal agent for vitamin k1
protamine sulfate
toxicity (phytomenadione)
on thrombin, because the molecules are too small to bind to
both enzyme and inhibitor, essential for inhibition of factor Xa
but not for that of thrombin [39]. Several LMWH preparations, Thrombolytic (fibrinolytic) therapy
administered once or twice daily by subcutaneous injection,
Fibrinolytic are proteolytic enzymes that enhance the conver-
are currently approved for the initial treatment of DVT. Low-
sion of plasminogen to plasmin, which subsequently degrades
molecular-weight heparin preparations have several advan-
the fibrin matrix. It is given to remove thrombi that have al-
tages over unfractionated heparin for treatment of DVT such
ready formed [48]. These are streptokinase, urokinase and
as greater bioavailability, predictability and dose-dependent
alteplase.
plasma level, less risk of bleeding, lower incidence of heparin-
induced thrombocytopenia, lower risk of heparin-induced os- Alteplase: is a thrombolytic drug, used to treat acute myo-
teoporosis, no need for laboratory monitoring, can be safely cardial infarctions (heart attacks) and other severe conditions
administered in outpatient and duration of anticoagulant ef- (ischemic stroke) caused by blood clotting by breaking up the
fect is longer, permitting once- or twice-daily administration blood clots that cause them. The recommended treatment
[40-42]. dose of alteplase is 0.9 mg/kg (not to exceed 90 mg total treat-
ment dose) infused over 60 minutes. 10% of the total treat-
Unfractionated heparin ment dose should be administered as an initial bolus over 1
Unfractionated heparin is a heterogeneous mixture of poly- minute. The remaining treatment dose should be infused
saccharide chains. The anticoagulant effect of UFH is medi- intravenously over 60 minutes [49-51]. Catheter-directed
ated through a specific pentasaccharide sequence on the thrombolysis involves the percutaneous insertion of a cathe-
heparin molecule that binds to antithrombin, provoking a con- ter and infusion of a thrombolytic typically recombinant tissue
formational change [43]. Outpatient treatment of DVT with plasminogen activator (tPA) directly to the DVT [52].
twice-daily subcutaneous unfractionated heparin injections
Conclusion
is efficacious and safe, based on level I evidence. Laboratory
monitoring is required, however, with aPTT testing 6 hours Deep vein thrombosis (DVT) commonly affects the lower limb,
after each daily morning dose. As with intravenous heparin with clot formation beginning in a deep calf vein and propagat-
therapy, subcutaneous heparin doses are adjusted to achieve ing proximally. Rudolph Virchow described three conditions
a target aPTT of 1.5 to 2.0 times the control aPTT. One advan- that predispose to thrombus, the so-called Virchow’s triad.
tage of unfractionated heparin is that it is less expensive than This triad includes endothelial injury, stasis or turbulence of
LMWH [44]. Adverse drug reactions of heparin are bleeding, blood flow, and blood hypercoagulability. The goal of therapy
thrombocytopenia, HIP (heparin Induced Thrombocytopenia), for DVT are to stop the clot from getting larger, reduce the
osteoporosis and vertebral collapse; this is a rare complica- chance of having another clot develop, prevent the extension

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of thrombus, acute PE, recurrence of thrombosis. Guidelines bolism management practices and knowledge of guidelines:
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DVT. 11. Lim W, Le Gal G, Bates SM, et al. American Society of He-
matology 2018 guidelines for management of venous throm-
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