Deep vein thrombosis and thromboembolism - presentation, investigation and therapy Flashcards
what is a ‘clot’ made up of
fibrin platelets red blood cells
describe the process of thrombosis
damage to endothelium tissue factor exposure prothrombin converted into thrombin thrombin turns fibrinogen into fibrin cross-linked fibrin
or damage to endothelium - exposure of collagen - platelet adhesion and release - platelet recruitment and activation platelet aggregation platelet-fibrin thrombus
arterial thrombosis:- - mechanism - location of origin - results in - diseases - composition
usually rupture of atherosclerotic plaque in arteries, left heart chambers ischaemia and infarction as a result diseases:-
- Acute coronary syndrome
- Ischaemic stroke
- Limb claudication / ischaemia composition - ‘white thrombus’ - platelets and fibrin
venous thrombosis:- - mechanism - location of origin - results in - diseases - composition
Combination of Virchow’s triad, especially - stasis and hypercoagulability Venous valves and venous sinusoids of muscles results in back pressure deep vein thrombosis pulmonary embolism ‘red thrombus’ RBCs and fibrin
3 categories of Virchow’s triad that are said to cause thrombosis
stasis vessel damage - endothelial damage/dysfunction hypercoagulability - inherited or acquired (pregnancy, cancer or sepsis)
things causing endothelial dysfunction
hypertension smoking high cholesterol
things causing endothelial damage
indwelling venous catheters trauma surgery
examples of venous thromboembolism (4)
Limb deep vein thrombosis (DVT) Pulmonary embolism (PE) Visceral venous thrombosis Intracranial venous thrombosis
epidemiology of venous thromboembolism:- DVT and PE
DVT - 1 in 1000 PE - 1 in 3000-5000 leading cause of direct maternal death in UK incidence increases with age and higher in females
risk factors for VTE
Surgery:-
- Major abdominal/pelvic surgery
- Hip/knee replacement
- Postoperative intensive care
Obstetrics:-
- Late pregnancy
- C-section
Lower limb problems:-
- Fracture
- Varicose veins
Malignancy:-
- Abdominal/pelvic
- Advanced/metastatic
- Reduced mobility
- Hospitalisation Institutional care
Miscellaneous:- Previous proven VTE
Cardiovascular:-
- Congenital heart disease
- Congestive cardiac failure
- Hypertension
- Superficial venous thrombosis
- Indwelling central vein catheter
- Oral contraceptive
- Hormone replacement therapy
- COPD
- Neurological disability
- Occult malignancy
- Thrombotic disorders
- Long distance sedentary travel
- Obesity
symptoms and signs of DVT
Unilateral limb swelling persisting discomfort calf tenderness warmth, redness - erythema, prominant collateral veins, unilateral pitting oedema
potential long-term consequences of DVT
Post thrombotic syndrome - damage to venous valves - 20-60% incidence within 2 years of DVT Swelling Discomfort Pigmentation Ulceration in severe form
Diagnosis of DVT
Clinical assessment
FBC - D-dimer - positive result may indicate the presence of an abnormally high level of fibrin degradation products
imaging: B mode venous compression ultrasound, doppler, ultrasonography
what is a compression ultrasound?
probe put on skin, sound waves are able to construct an image of the tissue that lies beneath
wells criteria scoring
> or equal to 3 = high probability of DVT 1 or 2 = moderate probability < or equal to 0 = low probability
D- dimer sensitivity and specificity for VTE?
high sensitivity low specificity - trauma, malignancy, sepsis, bleeding, cancer, recent surgery
symptoms and signs of PE
Pleuritic chest pain Breathlessness- dyspnoea 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 tongue - cyanosis Tachycardia Low blood pressure Raised jugular venous pressure May cause sudden death
Diagnosis/inestigations for PE
Clinical assessment and pretest probability score (Wells score or Geneva score)
- D-dimer - if negative - no PE
- FBC
- CXR - blunt costophrenic angle
- V/Q scan
- Ultrasound
- CT pulm angiogram/MRI
Potential long-term consequence of pulmonary embolism
Most recover fully Pulmonary arterial hypertension
aims of treatment of VTE? (DVT or PE) (3)
Prevent clot extension Prevent clot embolisation Prevent recurrent clot
treatment options for VTE
Anticoagulation is main treatment Parenteral (not mouth or alimentary canal) options: unfractionated heparin low molecular weight heparin (good for women who are pregnant/child baring age) Enteral options: Warfarin Direct Oral Anticoagulants (DOACs)
when is thrombolysis opted for as treatment option?
severe cases like for massive PE Alteplase
prevention of VTE in hospital (4)
Early mobilisation ‘Anti-embolism stockings’ Other mechanical methods of thromboprophylaxis Pharmacological thromboprophylaxis
how do you develop a pulmonary infarction after a PE
Pulmonary infarction = rare due to dual vascular supply to lungs with anastomoses (linkwith) - Pulmonary vascular system - Bronchial vascular system These circulations supply majority of O2 to lung parenchyma Pre and post capillary anastomoses with pulmonary system 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
Diagnostic algorithm for DVT - see image
why is low molecular weight heparin the better option over warfarin for DVT
You need to be loaded with warfarin before it has a therapeutic effect therefore it would not be the immediate treatment
LMWH (version of heparin) like daltaparin is a safe option during pregnancy a
direct oral anticoagulants have taken the place of which other drugs for treatment of DVT
Direct oral anticoagulants are better option over:-
- warfarin
- LMWH - daltaparin
LMWH is better than warfarin however
