whom that have sx of swelling leg, painful when walking and raise up leg, redness of leg skin, have history of accident or long journey u are suspected had deep vein thrombosis.

1. NOOR AFIFAH BT ABD
RAHMAN
AZIZAH BT MAJID
MOHD NAQIB B BAJURI
DEEP VEIN
THROMBOSIS

2. Definition
• Deep vein thrombosis is the
formation of a blood clot in one of
the deep veins of the body, usually
in the leg

3. • 2 types of VT
– Superficial
• Occur in tortuous dilated varicose vein ; pregnancy
– Deep
• may be referred to as proximal DVT or distal DVT.
• Occasionally, DVT also occurs in the veins of the
upper extremities.
• DVT can occur spontaneously without known
underlying cause (idiopathic thrombosis) or after
provoking events, such as trauma, surgery or acute
illness (provoked thrombosis).

4. EPIDEMIOLOGY
• Untreated Proximal DVT
– 30-50% risk PE
– 12-15% mortality
• Untreated Proximal
DVT
– 30-50% risk PE
– 12-15% mortality
• Treated DVT
– <8% risk PE
– Mortality <2%

5. RISK FACTORS
• Principal Risk Factors
– Immobilization
– Trauma
– Surgery
– Infection
– Post-partum period
• Other Factors
– Age
– Obesity
– Malignancy
– Previous VTE
– Varicose Veins
– Dehydration
– smoking
– Hormonal Therapy

6. SFJ
SPJ

7. ETIOLOGY
• DVT usually originates in the lower extremity
venous level ,starting at the calf vein level and
progressing proximally to involve popliteal
,femoral ,or iliac system. .80 -90 % pulmonary
emboli originates here .

8. Virchow triad
• More than 100 years ago, Virchow described a
triad of factors of
• venous stasis,
• endothelial damage, and
• hypercoagulable state

9. DVT:
Pathogenesis
Clinical features
Azizah Binti Majid
027653

10. More than 100 years ago, Virchow described a triad of
factors of
venous stasis,
endothelial damage, and
hypercoagulable state
Virchow triad

13. • deficiencies of protein ‘S,
• ’ protein ‘C,’ and
• antithrombin III.Inherited
disorders of
coagulation
• nephrotic syndrome results in urinary
loss of antithrombin III, this diagnosis
should be considered in children
presenting with thromboembolic disease
• Antiphospholipid antibodies accelerate
coagulation and include the lupus
anticoagulant and anticardiolipin
antibodies.
Acquired
disorders of
coagulation

14. The nidus for a clot is often an intimal defect
RBC, WBC, Platelets, and Fibrin adhere (stick together) to
form a clot (thrombus.)
The thrombus enlarges as blood products accumulate
forming a large clot that occludes the vein lumen.
When a clot forms on an intimal defect, the coagulation
cascade promotes clot growth proximally. Thrombus can
extend from the superficial veins into the deep system
from which it can embolize to the lungs.
Clinical Pathophysiology

15. Two different types of thrombus can form:
• Arterial thrombus (white thrombus)
• Venous thrombus (red thrombus)
Arterial and venous thrombi differ in composition
and appearance.
Arterial thrombi are typically composed mainly of
platelet aggregates, giving the appearance of ‘white
thrombi’.
Venous thrombi largely consist of fibrin and red
blood cells so are known as ‘red thrombi’.
Cont…

16. Opposing the coagulation cascade is the endogenous
fibrinolytic system. After the clot organizes or dissolves,
most veins will recanalize in several weeks. Residual clots
retract as fibroblasts and capillary development lead to
intimal thickening.
Venous hypertension and residual clot may destroy
valves, leading to the postphlebitic syndrome- a state
characterized by edema,pain, and skin discoloration most
often as a complication of DVT- which develops within 5-
10 years
Cont…

17. Edema, sclerosis, and ulceration characterize this
syndrome, which develops in 40-80% of patients with DVT.
patients also can suffer exacerbations of swelling and pain,
probably as a result of venous dilatation and hypertension
Pulmonary embolism (PE) is a serious complication of
DVT. Many episodes of pulmonary embolism go
unrecognized, and at least 40% of patients with DVT have
clinically silent PE.
Cont…

18. Clinical feature of DVT and PE
DVT
• Swelling of the leg
• Pain or tenderness in the leg; the
pain is usually in 1 leg and may
only be present when standing or
walking
• Skin that is warm to the touch in
the leg
• Red or discolored skin
• Swelling with pitting oedema
• Swelling below knee in distal
deep vein thrombosis and up to
groin in proximal deep vein
thrombosis
• Superficial venous dilatation
• Cyanosis can occur with severe
obstruction
• Positive Homan’s Sign-pain on
forced dorsiflexion of the foot
when the leg is raised
• Low Grade Fever
• Unequal Leg Measurements???
• Pallor- Phlegmasia Alba Dolens
• Cyanosis-Phlegmasia Cerulea
Dolens
PE
• Unexplained shortness of breath
• Chest pain and/or palpitations
• Anxiety and/or sweating
• Hemoptysis
• Fever
• Fatigue and/or fainting
• tachycardia (common),
• tachypnea
• Massive Emboli- Shock, Pallor,
Severe Dyspnea, Crushing Chest
Pain
Not all people with DVT
have signs or symptoms
If the inferior vena cava is involved – lower
extremities edematous and cyanotic
If the superior vena cava is involved – upper
extremities, back, neck and face show signs

19. • Phlegmasia Alba Dolens
• known as milk leg or
white leg)
• deep vein thrombosis
that progresses to total
occlusion of the deep
venous system.
• sudden (acute) process.
• The leg, then, must rely
on the superficial venous
system for drainage
• Phlegmasia Cerulea Dolens
• painful blue edema,
• occlusion of the superficial
venous system, thereby
preventing all venous
outflow from the extremity
• Sudden occurrence -
edematous cyanotic painful
leg.
• May result in gangrene and
high risk for massive
pulmonary embolism

20. PE
• From the thrombi originating in the deep venous system
of the lower extremities
• Rarely, they may originate in the pelvic, renal, or upper
extremity veins and the right heart chambers.
• Large thrombi lodge at the bifurcation of the main
pulmonary artery or the lobar branches, accumulate and
may cause haemodynamic compromise.
• Smaller thrombi continue distally, occluding smaller
vessels in the lung periphery. These are more likely to
produce pleuritic chest pain by initiating an inflammatory
response adjacent to the parietal pleura.
• Most pulmonary emboli are multiple, and the lower lobes
are involved more commonly than the upper lobes

21. The Wells clinical prediction guide incorporates risk factors, clinical signs, and the
presence or absence of alternative diagnoses

22. Investigation

23. • D-dimer measurement
• Duplex ultrasound
examination after
raised D-dimer
• Filling defects in flow
and a lack of
compressibility
indicate the presence
of a thrombosis

24. • Ascending venography (rarely)
• Pulmonary embolism is diagnosed
by ventilation–perfusion scanning
shows mismatched defects
• Computerised tomographic
(CT) scanning of the
pulmonary arteries,
which can show filling
defects in pulmonary arteries
• Pulmonary angiography (rarely)

25. Management

26. • low molecular weight heparin
• Warfarin
– started at a dose of 10 mg on day one, 10 mg on day
two and 5 mg on day three
• Thrombolysis
– Iliac vein thrombosis
– tissue plasminogen activator administered directly
into thrombus via popliteal vein or by direct puncture
in groin
• stent grafting for iliac vein compression syndrome
• Thrombectomy (rarely)

27. • pulmonary emboli
– Anticoagulation
– severe right heart strain & shortness of breath
need for fibrinolytic treatment