deep venois

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DEEP VEIN THROMBOSIS

• WANDWI- HKMU MD3 LECTURES 2021/22/23

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DEEP VEIN THROMBOSIS

• Definition
• Pathophysiology/causes
• Clinical presentation
• Diagnosis
• Management
• Complications

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DEFN/Aetiology

• CLOT - THROMBUS IN DEEP VENOUS SYSTEM
• The deep venous system lower limb
• common femoral,
• femoral (or superficial femoral),
• deep femoral,
• popliteal,
• tibial veins
• The deep venous system upper limb
• Subclavian, Axillary, or Brachial vein

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DEFN/Aetiology

• CLOT - THROMBUS IN DEEP VENOUS SYSTEM
• Incidence DVT about 250,000 p.a.
• 200,000 pulmonary embolism
• Secondary to CVI

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DEFN./Etiology

• Risk factors
• Age,
• Malignancy,
• Immobilization,
• Surgery and trauma,
• Oral contraceptives,

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DEFN./Etiology

• Risk factors
• Hormone replacement,
• Pregnancy,
• Neurologic disease (spinal cord injury),
• Cardiac disease,
• Obesity,
• Genetic hypercoagulable state

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Pathogenesis -lower limb

• Thrombus formation gt acute and chronic
  inflammatory response gt organization, and
  recanalization, often with vein wall and valve
  damage.

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Presentation

• Unilateral leg pain and swelling,
• Positive Homans sign (pain on passive
  dorsiflexion of foota nonspecific physical
  finding),
• PE

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Diagnosis

• 50 of patients with acute DVT may be
  asymptomatic.
• Duplex ultrasound imaging - test of choice, with
  greater than 95 sensitivity and specificity.
• Differential diagnosis of lower extremity pain
  and swelling
• Muscle strain
• Contusion,
• Cellulitis, Baker cyst,
• Iliac vein obstruction due to retroperitoneal
  tumor or mass,
• Systemic causes of swelling and edema (such as
  congestive heart failure or venous insufficiency)

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Management

• TREATMENT FOR ACUTE DVT IS ANTICOAGULATION.
• Initial IV unfractionated heparin (UFH), or
  subcutaneous low-molecular- weight heparin
  (LMWH), such as enoxaparin.
• Heparin is administered continuously, requiring
  inpatient treatment.
• Response partial thromboplastin time monitoring
  response 2x
• In renal failure pts
• LMWH
• Predictable with greater bioavailability.
• Twice a day.
• LMWH should be avoided in patients with renal
  failure.
• No routine blood monitoring is required

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Management

• TREATMENT FOR ACUTE DVT IS ANTICOAGULATION.
• Systemic or catheter directed thrombolysis,-
  streptokinase or enaplase
• Surgical extraction or thrombectomy in patients
  with massive DVT at risk of limb gangrene
  secondary to venous occlusion.
• Streptokinase Bacterial origin (antigenic),
  binds plasminogen to make plasmin, not o ten
  used.
• Urokinase From renal parenchyma,
  directly activates plasminogen,.
• Tissue plasminogen activator
  (tPA) From vascular endothelium, directly
  activates plasminogen.
• Reteplase Recombinant tPA,
  catalyzes cleavage of endogenous plasminogen to
  or plasmin

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Management

• TREATMENT FOR ACUTE DVT IS ANTICOAGULATION

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Management

• Ambulation with DVT does not increase the risk of
  PE and does decrease the incidence and severity
  of chronic venous disease after DVT. Ambulation
  and sequential compression therapy are encouraged
  in the management of DVT

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Management

• Long-term treatment involves anticoagulation
  usually with vitamin K antagonist (warfarin).
• Patient with a first episode of DVT and
  underlying reversible risk factor should receive
  3 months Rx.
• Patients with a first episode of idiopathic DVT
  should receive treatment for 6 to 12 months and
  should be considered for indefinite anticoagulant
  therapy.

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Management

• Patients with DVT and malignancy should receive 3
  to 6 months of LMWH, and indefinite
  anticoagulation.
• Patients with a first episode of DVT and
  antiphospholipid antibodies, or two or more
  thrombophilic conditions, should receive 12
  months of therapy and be considered for
  indefinite treatment.

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Management

• Patients with two or more documented episodes of
  DVT should receive indefinite treatment
• Vena caval interruption via filter placement
  should be considered when anti- coagulation is
  contraindicated, PE recurs on anticoagulation, or
  a complication develops from use of
  anticoagulation

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Pathogenesis -upper limb

• Thrombus formation gt acute and chronic
  inflammatory response gt organization, and
  recanalization, often with vein wall and valve
  damage.
• Usually associated with central venous catheters
  or other instrumentation
• Compression in the thoracic outlet, also known as
  Paget Schroetter syndrome or effort thrombosis
• Signs and symptoms are edema, dilated collateral
  circulation, and pain
• Diagnosis is clinical with venous duplex

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Management

• Generally, removal of foreign body is sufficient.
• Treatment may be similar to lower extremity DVT.
  However, the level of evidence for this course is
  lower than for lower extremity DVT..
• Thrombolysis with 3 to 6 months of
  anticoagulation is indicated

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POSTPHLEBITIC SYNDROME AND CHRONIC VENOUS
INSUFFICIENCY

• Postphlebitic (postthrombotic) syndrome is
  symptomatic chronic venous insufficiency after
  deep venous thrombosis (DVT). Incidence
• PTS develops in 20 to 50 of patients after
  documented DVT.
• In the absence of DVT, this constellation of
  symptoms is referred to as chronic venous
  insufficiency (CVI).
• Developing venous ulcers.
• Pathology. Development of CVD may be related to
  venous obstruction, valvular insufficiency, or
  calf muscle pump malfunction

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POSTPHLEBITIC SYNDROME AND CHRONIC VENOUS
INSUFFICIENCY

• Clinical Features Symptoms
• Chronic postural dependent swelling, pain, local
  discomfort, and venous ulceration at the ankle.
• Superficial venous insufficiency that may appear
  as spider vein, telangiectasias, or varicosities.
• Pain, hyperpigmentation, stasis dermatitis, or
  venous ulcers (CVD).
• Venous ulcers that tend to form just above the
  medial malleolus.
• Venous claudication pain associated with walking
  from increased swelling and prominence of the
  superficial venous system usually observed in the
  setting of both venous obstruction and venous
  incompetence.

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POSTPHLEBITIC SYNDROME AND CHRONIC VENOUS
INSUFFICIENCY

• Diagnosis
• Venous duplex ultrasonography - imaging of veins
  as well as analysis of blood flow.
• Plethysmography uses an air-filled cylinder
  fitted over the extremity to analyze changes in
  the extremity with position change and exercise.
• Venography has no significant role in diagnosis
  of acute or chronic disease, but may be used to
  complement noninvasive testing when considering
  intervention in the deep venous system or in
  research protocols

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POSTPHLEBITIC SYNDROME AND CHRONIC VENOUS
INSUFFICIENCY

• Management
• Maintain adequate hydration (important if using
  mechanical bowel preparation)
• Stop smoking tobacco, encourage healthy
  lifestyle
• Stop alcohol consumption
• education on DVT, risk factors and how to
  decrease the risks

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POSTPHLEBITIC SYNDROME AND CHRONIC VENOUS
INSUFFICIENCY

• Management
• Elastic compression stockings should be used for
  2 years following DVT and for symptom improvement
  in the setting of PTS or CVD.
• Conservative medical therapy includes
• compressive stockings (30 to 40 mm Hg at the
  ankle),
• avoiding prolonged periods of standing,
• elevating legs intermittently through the day,
• elevating the foot of the bed at night,
• and exercising.

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POSTPHLEBITIC SYNDROME AND CHRONIC VENOUS
INSUFFICIENCY

• Management
• Sclerotherapy - isolated varicosities,
  telangiectasias, and varicosities remaining after
  saphenous stripping.
• Surgery Vein stripping/ablation, as well as
  endovascular laser or radiofrequency abla- tion,
  act by disrupting the great saphenous vein,
  usually at the saphenofemoral junction, with
  removal of the vein to the level of the knee or
  below. This is indicated for treatment of
  saphenous vein insufficiency.
• Perforator vein ligation can be performed for
  treatment of isolated perforator vein incompetence