VENOUS THROMBOEMBOLISM IN ORTHOPAEDIC SURGERY
Dr Odunsi
Faith Specialist Hospital
What is VTE?
Venous thromboembolism (VTE)
Deep Vein Thrombosis (DVT)
Pulmonary Embolism (PE)
DEFINITION
It is the formation of solid
substances from the fluid
components of Blood in
the deep veins of a Living Body.
INTRODUCTION
One of the most difficult and serious problems in modern medicine
Early recognition and appropriate treatment can save many lives
DVT and PE are aspects of the same disease
About half of patients with proven DVT and no clinical PE have had undiagnosed PE
⅔ of patients with proven PE have no symptoms of DVT
⅓ of the time, original site of DVT is found at autopsy
All currently available diagnostic tests are more sensitive in
Symptomatic disease
Obstructive disease
Thigh thrombus (Likely to miss thrombus above groin or below knee)
EPIDEMIOLOGY
Prevalence is underestimated (relies on clinical disease)
Many cases are clinically inapparent
Apparent cases are often misdiagnosed
A 30 year prospective study of men born in 1913 showed that for every 100,000 person years
387 cases of recognised DVT
285 diagnosed PE
107 fatal PE
EPIDEMIOLOGY
Clinically recognised disease accounts for 1 in 20 deaths in patients above 50 years
Autopsy shows that ≈ 80% DVT & PE are undiagnosed
Prevalence highest in
Hospitalised patients
Patients in bed
Severe co-existing illness
EPIDEMIOLOGY
Incidence in ambulatory outpatients is not insignificant
Emergency patients whose symptoms include pleuritic chest pain have a PE rate of 21%
Consequences of DVT
Death
Pulmonary Embolism
Post-thrombotic Syndrome (chronic V HT)
Venous stasis
Leg pain and swelling
Hyperpigmentation
Leg ulcers
Recurrent Venous Thromboembolism
ETIOLOGY
All recognised risk factors arise from the components of Virchow’s Triad
Venous Stasis
Hypercoagulabilty
Vessel Intimal Injury
Presence of risk factors increases likelihood
Single most powerful risk factor is previous occurrence
Almost certain to occur in post op patients with previous occurrence without prophylaxis
ETIOLOGY
Immobility
Pregnancy &Peuperium: Commonest non-traumatic cause
Local trauma & Stasis (Leg Cast)
Smoking
Obesity
Prolonged Immobility (Coach class travel)
Anaesthesia: GA=500% increased risk compared to Epidural for the same procedure
ETIOLOGY
Auto-Immune Disease: 9% SLE pt develop spontaneous DVT
Blood Surface Antigens: Blood gp A ass with levels of Antithrombin III & factor VIII than gp O
Cancer:
Spontaneous DVT may occur
In 38% of cases of cancer with DVT, DVT is detected 1st
16% of patients with proven PE are diagnosed with cancer within 2 years
ETIOLOGY
Strokes & Neurotrauma
50% develop DVT within 5 days without prophylaxis
Head injury Defibrination DIC DVT
Stroke patient develop DVT in 60% paralised legs but 7% of non paralised legs
Chemotherapy
Coagulopathy: Esp. when DVT/PE occurs in younger patients
Impaired fibrinolysis
ETIOLOGY
Heart disease
Hyperlipideamia
Increasing Age
Oral Estrogens
Polycythaemia & Thrombocytosis
Surgery
70% after non-elective hip surgery
48% after elective hip surgery
12% after elective general surgery
Tissue Antigens: Cw4, Cw5, Cw6 associated with frequency of DVT
RELEVANT ANATOMY
Peripheral venous sys acts as both reservoir and conduit
Veins, unlike arteries, have only one tissue layer
Only larger veins have internal elastic membranes
Contains a sys of valves and pumps
Collecting veins of lower extremity are thin walled and distensible & mostly suprafascial
Can accommodate extra blood without loss in function
RELEVANT ANATOMY
Secondary conduit veins have thicker walls, are less distensible & mostly subfascial
Deep veins
Anterior Tibial (draining dorsum of foot)
Posterior Tibial ( draining sole of foot)
Peroneal ( Lateral aspect of foot)
Popliteal – Femoral Common femoral
Profunda femoris
External iliac
Common Iliac
IVC
Left Atrium
Pulmonary Arteries
RELEVANT ANATOMY
Muscle pumps function like a “Peripheral heart”
Valves ( when competent) prevent backflow
Muscle contraction forces blood upward
PATHOPHYSIOLOGY
Virchow’s Triad (1846) is still the primary mechanism for development of DVT
Relative importance of each factor is still debated
Formation, propagation & dissolution of venous thrombi represent a balance between thrombogenesis & circulating inhibitors of coagulation & fibrinolysis
PATHOPHYSIOLOGY
Minor endothelial injury accumulation of macroscopic thrombi
Inhibition of fibrinolysis causes extension of thrombus to areas of normal epithelium
Usually begins in the deep veins of the calf around the cusps or within the soleal plexus
May arise in femoral vessels due to injury e.g. pelvic/hip surgery or catheter placement
PATHOPHYSIOLOGY
Most calf vein thrombi resolve spontaneously
About 20% propagate proximally
Propagation usually precedes embolization
Adherence & organization of venous thrombus begins 5-10 days after thrombus formation
Until this is fully established the non-adherent, disorganized thrombus may propagate or embolize
Propagation & organization destroys valves venous outflow obstruction stasis worsened risk of thrombus formation
PATHOPHYSIOLOGY
Spontaneous lysis & complete recanalization occurs in fewer than 10% of patients even with anticoagulation
In patients with symptomatic DVT nearly 100% have calf vein thrombosis
Its already propagated above the knee in about 87% before diagnosis is made
Most patients with upper leg or thigh thrombus already have a PE (even if asymptomatic)
PATHOPHYSIOLOGY
Fatal PE often arises from thrombus originating in
Axillary veins
Subclavian veins
Pelvic veins
Indwelling venous catheters
DVT in orthopaedics?
Orthopaedic patients are most at risk of all patients in hospital1
Total Joint Arthroplasties
Major Trauma
Hip Fractures
DVT Pathophysiology
Virchow’s Triad
Endothelial injury
Surgery
Venous stasis
Tourniquet
Immobilisation
Delayed ambulation
Casting
Change in blood constituents
↑ platelets
↑ clotting
↑ viscosity
Risk factors
Increased in orthopaedics:
Immobilisation
Major surgery
Tourniquet
Other non orthopaedic
Obesity BMI >30 (often in arthroplasties)
History of prior DVT
Female
Smoking
OCP
Genetic (many)
Course of DVT illness
Determined by the site of thrombosis1
Calf
Where DVTs start
50% resolve in 3/7
Rarely causes PE in isolation
25% extend proximally within 1 week
Proximal
Symptomatic
50% have PE at Dx
only 1 in 5 of those is symptomatic of PE
CLINICAL FEATURES
Many are asymptomatic
Incomplete obstruction
Collateral drainage
Many non-thrombotic conditions may mimic DVT
History
Unilateral leg swelling (MAY BE BILATERAL!)
Pain
Calf Tenderness
Warmth or Erythema
Correlate poorly with size location and extent
CLINICAL FEATURES
Chest pain. May be pleuritic
Back, Shoulder, Upper abdominal pain
Chest wall tenderness
Syncope
Haemoptysis
Shortness of breath
Painful respiration
New onset of wheezing
Unexplained thoracic symptoms
CLINICAL FEATURES
Symptoms are non specific
May be seizures, fever, productive cough, hiccoughs, DIC
Of patients who die from PE
Only 60% have dyspnoea
17% have chest pain
3% have haemoptysis
Signs
Edema
Tenderness
Homan’s Sign
CLINICAL FEATURES
Signs
Venous distension with prominence of subcutaneous veins
Superficial thrombophlebitis
Fever
Phlegmesia cerulea dolens
Phlegmesia alba dolens
Lipodermatosclerosis
CLINICAL FEATURES
Signs
Tachypnoea
Tachycardia
Chest wall tenderness
Accentuated second heart sound
Atelectasis (due to loss of pulmonary surfactant) may mimic pneumonia
Wheezing
Pleural Rub
Hypotension
CLINICAL FEATURES
Signs
Fever
Diaphoresis
S3 or S4 Gallop
Cardiac murmur
Cyanosis
Differentials include
Asthma
CCF
MI
Pneumonia
ARDS
INVESTIGATIONS
PCV: Polycythaemia may point to cause
Tests of clotting function do not correlate well
Even full anticoagulation with corresponding clotting profiles do not exclude DVT/PE
WBC & ESR may point to underlying cause
Progressive thrombocytopaenia should alert to new onset thromboembolism
Arterial Blood Gases
Arterial-Alveolar Oxygen gradient is more sensitive
INVESTIGATIONS
Imaging Studies
Duplex Ultra Sound (Observer dependent)
Contrast Venography
May miss recanalised thrombus
Eccentric thrombi (viewed perpendicular to defect)
Time consuming
Magnetic Resonance Venography
Most sensitive and specific available test
Also identifies alternative diagnoses
INVESTIGATIONS
Nuclear Venography
CT Venography
Chest X-ray
Westermark Sign: Proximal arterial dilation with distal collapse, sometimes with sharp cut-off
Atelectasis Effusion Elevated Hemi-diaphragm
Focal infiltrates similar to pneumonia
Hampton Hump: Pulmonary Infarction with triangular pleural based infiltrate with apex toward hilum often adjacent to diaphragm
Nuclear Scintigraphic Ventilation-Perfusion Scan
INVESTIGATIONS
CT Angiography
Pulmonary Angiography
ECG
Tachycardia
Non-Specific ST-T wave abnormalities
P pulmonale: Tall peaked T waves in lead II
Right axis deviation
RBBB
Atrial fibrillation
Echocardiography
TREATMENT
Pre-hospital Care
Immediate Transport
Oxygen
IV fluids may be needed especially in rapidly deteriorating hemodynamic status
Presumptive fibrinolysis especially in patients known to be on treatment for DVT
TREATMENT
Emergency Department Care
Immediate rapidly acting fibrinolytic (except contra-indicated)
Heparin: Slows/Halts clot progression
Oxygen
IV Fluids: WITH CAUTION! May worsen patients condition
Emergency Cardiopulmonary Bypass With extracorporeal membrane oxygenation may be life saving in massive PE esp in cardiac arrest
Emergency immediate bilateral thoracotomy with massage of pulmonary vessels has been reported to dislodge a saddle embolus
TREATMENT
Gradient Compression stockings with 30-40mmHg pressure gradient limit or prevent extension of thrombus
Reduce capacitance venous volume by 70%
Increase velocity of venous blood flow by a factor of 5 or more
Anti-coagulation
Heparin-Warfarin
TREATMENT
Unfractionated Heparin 333units/kg subcut followed by 250 units/kg twice daily
Enoxaparin 1 mg/kg 12h hourly
Enoxaparin 1.5 mg/kg daily
Tinzaparin 175 IU/kg daily
Dalteparin 100 IU/kg 12hourly
Dalteparin 200 IU/kg daily
TREATMENT
Fibrinolysis
Now mainstay of therapy esp in early presentation
However large thrombi and recent surgery are unsuitable
Two forms of recombinant tissue plasminogen activator
t-PA (alteplase)
r-PA (reteplase)
Urokinase
Streptokinase
TREATMENT
Surgical Treatment
To reduce rethrombosis heparin anticoagulation is initiated before surgery & continued till 6-12 months afterward
Surgical Therapy
Preservation of patency AND valve function are the main goals
Venous thrombectomy with Fogarty catheter
Angioscopic thromboembolectomy
Aspiration thromboembolectomy
With/without adjunctive fibrinolytic infusion
TREATMENT
Filters
IVC barriers were first suggested by Trousseau in 1868
Current benchmark is Greenfield filter
Maintains patency
Traps emboli
Preserves prograde caval flow
Avoids stasis
Enhances thrombolysis of trapped emboli
Compression stockings
Ambulation (controversial)
TREATMENT
Continued close monitoring is important as many patients may re-thrombose or re-embolise or propagation may continue
FOLLOW-UP
Admitted patients on Unfractionated heparin, aPTT must be monitored at least 6 hourly until dose is stabilised in therapeutic range
Platelet count must be monitored. Discontinue Heparin or LMWH if count > 75,000
For Warfarin: Monitor PT, INR (daily or alternate days) till target is achieved. Then weekly, then monthly
Selected patients qualify for out-patient monitoring with LMWH
FOLLOW-UP
Treat 1st episode for 3-6 months
Recurrent episodes for at least a year
Investigate ALL bleeding thoroughly as anticoagulation may unmask pre-existing disease
COMPLICATIONS
Haemorrhage
May require stopping drug
Give Protamine or Vitamin K
Chronic Venous insufficiency
Post phlebitic syndrome
Pulmonary infarction
Pulmonary Fibrosis (esp. with repeated small emboli)
PREVENTION
Primary prophylaxis is likely to be more effective, less expensive, and is the prophylaxis of choice in most clinical circumstances. Secondary prevention by screening should never replace primary prophylaxis, and is reserved for those patients in whom effective primary prophylaxis is either contraindicated or unavailable” Hull RD, Raskob GE and Hirsh J (1986) Chest 89, 3745-3835
PREVENTION
Mechanical methods
Early mobilisation
Graded Compression Stockings
Intermittent Pneumatic Leg Compression
Pharmacological Agents
Aspirin
Heparin
Warfarin
Dextran
CONCLUSION
Serious but preventable health care problem
Vigilance, pro-activeness, high index of suspicion and prompt initiation of appropriate therapy is life-saving
THANK YOU
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