DVT (Deep vein thrombosis)

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.

2. BY
B KALYAN KUMAR MSC(N)
DEPT OF MSN
DEEP VEIN
THROMBOSIS

3. DEFINITION
DeepVeinThrombosisisabloodclotformsina
deepvein.DVTismorecommoninthedeepveinsof
lowerleg(Calf)&spreaduptotheveinsinthigh.DVT
canalsofirstdevelopinthedeepveinsinthigh&more
rarelyinotherdeepveinssuchastheonesinarm.
Deepveinspassthroughthecentreofleg&
surroundedbyalayerofmusclewhenbloodclotsfromin
thesuperficialveins,whichliejustunderskin,the
conditionisknownasSuperficialThrombophlebitis.

4. INCIDENCE
United states –2 million people / year
Most of them –40 yrs (or) older
Upto600,000 are hospitalized each year
650,o00 persons die each year from pulmonary
embolism, 3
rd
most cause of death in US.

5. ETIOLOGY
VIRCHOW’S TRAID
Endothelial damage
Venous stasis Hypercoagulability

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
Atrialfibrillation, 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 anticardiolipinantibody
AntithrombinIII 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
Nephroticsyndrome

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

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 oedematous7 cyanotic
If superior vena cava involved –symptoms in the upper
extremities, neck, back & face.

20. DIAGNOSTIC EVALUATION
History collection
Physical examination
Blood laboratory studies –CT, aPTT, bleeding time,
HB, INR, platelet count
D –dimertest
Non –invasive venous studies
➢Venous Doppler evaluation
➢Duplex scanning
➢Venogram.
➢CT –Scan.

22. D –dimertest

23. Venous dopplerevaluation

24. Duplex scanning

25. Venogram

26. CT -Scan

27. Superficial
Thrombophlebitis
Deep vein thrombosis
Usual locationSuperficial veins of arms &
legs
Deep vein of arms (such as
auxillary, subclavianveins )
Clinical
findings
Tenderness, redness, warmth,
pain, inflammation &
indurations along the course
of the superficialvein, 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 Embolizationrarely Emboliationmay occur,
chronic venous insufficiency

28. COMPLICATION OF DVT
Pulmonary embolism;
 blood clot block one of the blood vessel of the
lung

29. COMPLICATION OF DVT
Chronic venous
insufficiency;
 valvulardestruction leads
to retrograde flow of venous
blood
 Persistent edema,
increased pigmentation,
secondary varicositis,
ulceration & cyanosis of the
limb.

30. COMPLICATION OF DVT
Phlegmasiacerula
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 emboliticstocking
Vitamins B6, B12 & folic acid

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 Xainhibitors
Action-it does not dissolve the but lysisof the
clot begins spontaneously through the
body’s intrinsic fibrinolyticsystem.

35. MEDICAL MANAGEMENT
Anti
coagulant
Drug Action Route of
administration
Vitamin K
antagonist
Warfarin(coumadin)
Acenocoumarol
Dicumarol
Activation of vitK
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
Hirudinderivatives;
Lepirudin
Bivalirudin
Syntheticthrombotic
inhibitots; Argatroban
Binds with thrombin &
inhibiting its action
ContiuousIV
Factor Xa
inhibitor
Fondaparinux Directly(or) indirectly
produces rapid anti
coagulation
Subcutaneous

36. Contraindication of Anti coagulants
Lack of patient co-operation
Bleeding, Haemorrhagicblood dyscrasias
Aneurysms
Severe trauma
Alcoholism
Recent (or) impending surgery, cerebrovascular
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, simonnitinol,
vena tech (or) TrapEasefilters
inserted through right femoral
(or) right internal jugular veins
which is opened & penetrates the
vessel wall.

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 oestrogenpills
If surgery;
get out of bed several times a day during the recovery
period
Sequential compression devices
LMWH

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

48. SUMMARY
CONCLUSION
ASSIGNMENT
JOURNAL ABSTRACT
THEORY APPLICATION
BIBLIOGRAPHY