A blood clot in a deep vein, usually in the legs.
This condition is serious because blood clots can loosen and lodge in the lungs.
Leg pain or swelling may occur, but there may be no symptoms.
Treatments include medication and use of compression stockings.
3. DEFINITION
Deep Vein Thrombosis is a blood clot forms in a
deep vein. DVT is more common in the deep veins of
lower leg (Calf) & spread up to the veins in thigh. DVT
can also first develop in the deep veins in thigh & more
rarely in other deep veins such as the ones in arm.
Deep veins pass through the centre of leg &
surrounded by a layer of muscle when blood clots from in
the superficial veins, which lie just under skin, the
condition is known as Superficial Thrombophlebitis.
4. INCIDENCE
United states – 2 million people / year
Most of them – 40 yrs (or) older
Upto 600,000 are hospitalized each year
650,o00 persons die each year from pulmonary
embolism, 3rd most cause of death in US.
6. ETIOLOGY
Endothelial Damage;
Recent trauma to the lower body
such as fractures of the bones of hip,
thigh (or) heart surgery
Pacing wires, previous history of
DVT
Central venous catheters
Dialysis access catheters
Local vein damage (I.V drug abuse)
Repetitive motion injury
7. ETIOLOGY
Venous stasis;
Prolonged sitting such as during a
long plane (or) car ride
Prolonged bed rest (or) immobility
such as after injury (or) during illness
(such as stroke)
Obesity
Atrial fibrillation, Chronic heart
failure
History of varicositis, varicose vein
Spinal cord injury, Orthopedic
surgery (lower extremity)
Age > 65yrs, pregnancy, post
partum period
8. ETIOLOGY
Hypercoagulabilty of blood;
Cancer
Pregnancy, Recent child birth
Oral contraceptive use
Presence of congenital protein C & S
Presence of anticardiolipin antibody
Antithrombin III deficiency
Polycythemia
Septicemia
high attitude > 14.000 feet
9. ETIOLOGY
Use of estrogen replacement (or) birth
control pills
Heart attack (or) heart failure
Rare inherited genetic changes in
certain blood clotting factors
DIC, Organ failure
Cigarette smoking
Dehydration (or) Malnutrition
High attitudes
Hormone replacement therapy
Severe anemia
Nephrotic syndrome
10. ETIOLOGY FOR UPPER EXTREMITY
VENOUS THROMBOSIS
Patients with intravenous catheter
Underlying disease that causes
hypercoagulability
Internal trauma to the vessels result
from pacemaker leads, chemotherapy
ports, dialysis catheters,(or) parenteral
nutrition lines
The lumen of the vein may be
decreased as a result of the catheter
(or) from external compression such as
by neoplasms (or) an extra cervical rib
Effort thrombosis of upper extremity
by repetitive motion
11.
12.
13. PATHOPHYSIOLOGY
Due to cause
Veins are inactive (or) the pump is
ineffective
Venous stasis
Localized platelet aggregation & fibrin
entrap RBCs,WBCs & more platelets to form a
thrombosis in the valve cusps of vein
14. PATHOPHYSIOLOGY
Deep vein thrombi – small
If continues
Larger thrombi with a tail
Obstruct the vein
Inflammatory process destroy the valves of the
vein
15. PATHOPHYSIOLOGY
If a thrombus occludes
Major vein small vein partially Fully
Venous pressure Collateral venous Thrombi become Lysis
& volume rise channels covered by endothelial
distally cells & thrombotic decrease
process stops embolization
Firmly organized &
adherent with in
5 to 7 days
16. PATHOPHYSIOLOGY
Fully
firmly organized & adherent with in 5 to 7
days
turbulence of blood flow
detachment of thrombi from vein wall
emboli formation
flow through the venous circulation to the heart
(with in 24 to 48 hrs)
Pulmonary embolus
17. CLINICAL MANIFESTATION
Swelling of the affected leg due to edema
Warm skin, a systemic temperature greater than
100.4*F (38*C)
Pain & tenderness in the affected leg
Homan’s sign
Change in the color of the skin – redness, bluish (or)
whitish discoloration of skin
If inferior vena cava involved – lower extremities may
be oedematous 7 cyanotic
If superior vena cava involved – symptoms in the upper
extremities, neck, back & face.
18.
19.
20. DIAGNOSTIC EVALUATION
History collection
Physical examination
Blood laboratory studies – CT, aPTT, bleeding time,
HB, INR, platelet count
D – dimer test
Non – invasive venous studies
➢ Venous Doppler evaluation
➢ Duplex scanning
➢ Venogram.
➢ CT – Scan.
27. Superficial
Thrombophlebitis
Deep vein thrombosis
Usual location Superficial veins of arms &
legs
Deep vein of arms (such as
auxillary, subclavian veins )
Clinical
findings
Tenderness, redness, warmth,
pain, inflammation &
indurations along the course
of the superficial vein, vein
appears as a palpable cord,
edema rarely occurs
Tenderness to pressure over
involved vein, in duration of
overlying muscle, venous
distention, edema may have
mild to moderate pain, deep
reddish color to area due to
venous congestion
Sequelae Embolization rarely Emboliation may occur,
chronic venous insufficiency
29. COMPLICATION OF DVT
Chronic venous
insufficiency;
valvular destruction leads
to retrograde flow of venous
blood
Persistent edema,
increased pigmentation,
secondary varicositis,
ulceration & cyanosis of the
limb.
30. COMPLICATION OF DVT
Phlegmasia cerula
dolens (swollen, blue,
painful);
severe lower extremity
DVT – near total occlusion
of venous outflow
sudden, massive
swelling, deep pain 7
intense cyanosis of the
extremity
If untreated gangrene
occurs due to arterial
occlusion
31. COMPLICATION OF DVT
Post thrombotic
syndrome;
DVT damages
the valves in deep
veins – blood pools
in lower leg
long term pain,
swelling & in severe
cases – ulcer on leg
32. MEDICAL MANAGEMENT
Non – pharmacological therapy;
Bed rest with elevation of the extremity
Warm compresses & Anti embolitic stocking
Vitamins B6, B12 & folic acid
33.
34. MEDICAL MANAGEMENT
Drug therapy = Anti coagulants:
Goal – to prevent propagation of the clot,
development of any new thrombi &
embolization
Four major classes;
1. Vitamin K antagonist
2. Indirect thrombin inhibitors
3. Direct thrombin inhibitors
4. Factor Xa inhibitors
Action- it does not dissolve the but lysis of the
clot begins spontaneously through the
body’s intrinsic fibrinolytic system.
35. MEDICAL MANAGEMENT
Anti
coagulant
Drug Action Route of
administration
Vitamin K
antagonist
Warfarin (coumadin)
Acenocoumarol
Dicumarol
Activation of vit K
dependent coagulation
factors II,VII,IX & X
Po
Unfractionated
Heparin (UH)
Heparin
Hepalean
Lipo – hepin
Calciparine
Affects both the
intrinsic & common
pathway of blood
coagulation
Continuous IV
Intermittent IV
Subcutaneous
Low Molecular
Weight Heparin
(LMWH)
Enoxaparin
Tinaparin
Dalteparin
Nadroparin
Certoparin
Shorter heparin chains
have increased affinity
for inhibiting factor xa
Subcutaneous
Direct thrombin
inhibitors
Hirudin derivatives;
Lepirudin
Bivalirudin
Synthetic thrombotic
inhibitots; Argatroban
Binds with thrombin &
inhibiting its action
Contiuous IV
Factor Xa
inhibitor
Fondaparinux Directly (or) indirectly
produces rapid anti
coagulation
Subcutaneous
36. Contraindication of Anti coagulants
Lack of patient co-operation
Bleeding, Haemorrhagic blood dyscrasias
Aneurysms
Severe trauma
Alcoholism
Recent (or) impending surgery, cerebro vascular
hemorrhage
Severe hepatic (or) renal disease
Infections
Open ulcerative wounds
Occupation that involve a significant hazard for injury
Recent delivery of a baby.
37. Increase Anti coagulant effect Decrease anti coagulant effect
Alcohol
Amiodarone
Anabolic steroids
Cephalosporins
Chloral hydrate
Cimetidine
Erythromycin
Flucanazole
Influenza
Isoniazid
Metronidazole, miconazole
Neomycin
NSAID
Omeprazole
Phenytoin
Propafenone
Quinidine
Salicylates
Sulfonamides
Barbiturates
Carbamazepine
Chlordiazepoxide
Cholestyramine
Oestrogens
Ethchlorvynol
Griscofulvin
Itraconazole
Rifampin
Vitamins C & K
Minerals, Iron , Magnesium, Zinc
38. Complication Of Anti coagulants
Bleeding
Thrombocytopenia
Drug interaction
39. Drug therapy
Thrombolytic therapy;
It causes the thrombus to lyse & dissolve in 50% of
patient
e.g; t-PA, reteplase, staphylokinase, urokinase
Advantage;
less long term damage to the venous valves
reduced incidence of post thrombotic syndrome
Disadvantage;
greater incidence of bleeding than heparin
40. SURGICAL MANAGEMENT
Open surgical venous
thrombectomy & inferior
vena cava interruption;
removal of DVT through an
incision in the vein
vena cava interruption devices
such as greenfield, simon nitinol,
vena tech (or) TrapEase filters
inserted through right femoral
(or) right internal jugular veins
which is opened & penetrates the
vessel wall.
41.
42. Complication;
Air embolism, improper placement
Migration of the filter
Perforation of vena cava with retroperitoneal
bleeding
Complete occlusion of vena cava
43. PREVENTIVE MEASURES
Early ambulation
Anti embolism stockings & ICDs
Lose weight
Avoid periods of prolonged immobilty
Keep leg elevated while sitting down (or0 in bed
Avoid high – dose oestrogen pills
If surgery;
get out of bed several times a day during the recovery
period
Sequential compression devices
LMWH
44.
45. PREVENTIVE MEASURES
If travelling;
Short walks
Exercise
Wear loose fitting clothes
Keep hydrated
Avoid too much of alcohol,
sleeping tablets
compression stockings
46. NURSING MANAGEMENT
Assessing & monitoring anti coagulant
therapy
Providing comfort
Applying elastic compression stocking &
ICDs
Positioning the body & encouraging exercise
Identify risk factors predisposing patient to
DVT, reevaluate status frequently
Implement ordered prophylactic regimen
Non-pharmacological & pharmacological
Assess all of the patients extremities on a
regular basis
Encourage early ambulation & active leg
exercise every hr the patient is awake
47. NURSING MANAGEMENT
Perform passive range of motion exercises every shift
if the patient is immobile
Monitor for low grade fever to detect
thrombophlebitis
Encourage fluid intake
Use of knee gatch (or) pillows under the knees.
Patient education