Deep vein thrombosis and plumonary embolism Flashcards
What is a ‘clot’ made up of?
- Fibrin
- Platelets
- Red blood cells
How is a clot formed?
Damage to endothelium etc > Tissue factor > X reacts with Prothrombin to produce Thrombin > Thrombin reacts with Fibrinogen to produce Fibrin which reacts with factor XIII to produce cross-linked fibrin
Mechanisms in Arterial vs Venous thrombosis
Arterial
- Usually rupture of atherosclerotic plaque
Venous
- Combination of Virchow’s triad, especially stasis and hypercoagulability
Location of origin in Arterial vs Venous thrombosis
Arterial
- Arteries, left heart chambers
Venous
- Venous valves and venous sinusoids of muscles
Results in Arterial vs Venous thrombosis
Arterial
- Ischaemia and infarction
Venous
- Back pressure
Disease in Arterial vs Venous thrombosis
Arterial
- Acute coronary syndrome
- Ischaemic stroke
- Limb claudication/ischaemia
Venous
- Deep vein thrombosis
- Pulmonary embolism
Composition in Arterial vs Venous thrombosis
Arterial
- “white thrombus”
- Platelets and fibrin
Venous
- “red thrombus”
- Red blood cells and fibrin
Features of Virchow’s Triad
- Stasis
- Hypercoagulability
- Endothelial damage
What is an embolism?
Intravascular material that migrates from its original location to a distal vessel
E.g. blood clot, fat, air, tumour
What is a thromboembolism?
Movement of blood clot along a vessel
Examples of venous thromboembolism (VTE)
- Limb deep vein thrombosis (DVT)
- Pulmonary embolism (PE)
- Visceral venous thrombosis
- Intracranial venous thrombosis
Epidemiology of venous thromboembolism
- DVT: 1 in 1000 patients
- PE: 1 in 3000-5000 patients
- Leading cause of direct maternal death in UK
- Case fatality rate: 1 to 5% - untreated PE: 30%
- PE in 20% of autopsies
Risk factors for VTE
- Major abdominal/pelvic surgery
- Hip/knee replacement
- Late pregnancy
- Fracture
- Malignancy
- Congenital heart disease
- Hypertension
- COPD
- Obesity
Symptoms and signs of DVT
- Unilateral limb swelling
- Persistent discomfort
- Calf tenderness
- Warmth
- Redness-erythema
- Prominent collateral veins
- Unilateral pitting oedema
May be clinically silent!!
What is a potential long-term consequence of DVT?
Post Thrombotic Syndrome
- Damage to venous valves
- Incidence of 20-60% within 2 years of DVT
- Swelling
- Discomfort
- Pigmentation
- Ulceration in severe form
Diagnosis of DVT
- Clinical assessment and pretest probability score (Wells score)
- Blood test: D-dimer if low pre-test probability score
- Imaging: compression ultrasound if positive D-dimer or high pre-test probability score
Learn wells score for DVT
kinda know about it
What is a D-Dimer?
- Breakdown product of cross-linked fibrin: produced during fibrinolysis
- High sensitivity for VTE
- Low specificity for VTE: trauma, malignancy, sepsis, bleeding, cancer, recent surgery
How is a D-Dimer formed?
Plasmin combines with Fibrin producing fibrin degradation products (FDPs), including D-dimer
Symptoms and signs of pulmonary embolism
- Pleuritic chest pain
- Breathlessness (dyspnoea)
- Blood in sputum (haemoptysis)
- Rapid heart rate (tachycardia)
- Pleural rub on auscultation: usually due to pulmonary infarction
Symptoms and signs of massive pulmonary embolism
- Severe dyspnoea of sudden onset
- Collapse
- Blue lips and tongur (cyanosis)
- Tachycardia
- Low blood pressure
- Raised jugular venous pressure
- May cause sudden death!!
Diagnosis methods of pulmonary embolism
- Clinical assessment and pretest probability score (Wells score or Geneva score)
- Blood test: D-dimer if low pre test probability score
- Imaging: If D-dimer positive or high pre test probability score: Isotope ventilation/perfusion scan, CT pulmonary angiogram
Look over Wells score for PE
Do it
What is a potential long-term consequence of pulmonary embolism?
- Pulmonary arterial hypertension
- Most recover fully
What is the aims of treatment of VTE?
- Prevent clot extension
- Prevent clot embolisation
- Prevent recurrent clot
What are the treatment options for VTE?
Anticoagulation is the main treatment
- Parental options: unfractionated heparin, low molecular weight heparin
- Enteral options: warfarin, direct oral anticoagulants (DOACs)
Thrombolysis is reserved for massive PE: e.g. Alteplase
Prevention methods of VTE in hospital
- Early mobilisation
- ‘Anti-embolism stockings’ - help with the flow of blood
- Other mechanical methods of thromboprophylaxis
- Pharmacological thromboprophylaxis
Summary learning outcomes
- VTE is common and deadly
- Aim to prevent VTE in patients at significant risk
- Need to be aware of suggestive symptoms and signs
- Apply diagnostic and treatment pathway
How do you develop a pulmonary infarction after a PE?
Pulmonary infarction = rare due to dual vascular supply to lungs with anastomoses
- Blockage to a branch of the pulmonary artery = increase in pressure within pulmonary vasculature
- Force within bronchial artery may be insufficient to overcome this
- ‘Leakage’ of blood into alveolar space occurs, and leads to infarction