Venous Thrombosis And Pulmonary Embolism Flashcards
Thrombosis
Pathological clot formation within a blood vessel
Embolism
Part of a clot breaks off and travels through circulation until obstructed by vessels of smaller diameter
What colour are venous thrombi
Red
What colour are arterial thrombi
White - platelets and fibrin, few RBCs
Are venous or arterial thrombi more common
Venous
Deep vein thrombosis
Thrombus formed in deep vein
Where does a distal deep vein thrombosis form
Calf veins
Where does a proximal deep vein thrombosis form
Popliteal vein or above
What I’d the most common DVP site
Popliteal vein
Pulmonary embolism
Dislodged thrombus migrating to pulmonary vasculature
Embolus
Dislodged thrombus
How does leg muscle contraction aid venous return from legs
Muscle contraction squeezes vein opening proximal valve and pushing blood to heart
What happens if leg muscles don’t contract for a prolonged period
Valves remain closed and blood between them becomes stagnant, causing clotting above and below valved
What can dislodge a clot after a period of extended immobility
Muscle contraction
What is the most common route a clot may take to the brain
Through patent foramen ovale
Why do emboli often get stuck in pulmonary arteries
Arteries get smaller as they branch, before this arteries as getting bigger as the clot moves centrally
Saddle embolism
Large pulmonary embolus gets stuck in bifurcation of pulmonary trunk
Factors in Virchow’s triad
Endothelial injury
Stasis or turbulence of blood flow
Blood hypercoagulability
How does flowing blood prevent platelet adhesion to wall and clotting
Stimulates endothelium to release anticoagulants inc NO and prostacyclin
Risk factors for decr blood flow in deep veins
Immobilisation
Long haul flights
Obesity
Sickle cell disease
What does heparin sulphate and what does it do
Sulphide containing polysaccharide on luminal surface of endothelial cells
Form feathery projections into blood vessel lumen to prevent platelet adhesion
What can cause vessel wall damage
Chronic inflammatory disease
Smoking
Obesity
Diabetes
How can chronic inflammatory disease increase clot formation
Damage endothelial wall and decr amount of attached heparin
What can cause hypercoagulability
Antithrombin III deficiency
Protein C deficiency/resistance
Protein S deficiency/resistance
What is the most common DVT/PE risk in younger people
Factor V Leiden mutation - causes resistance to activated protein C
Thromboembolism risk factors
Pregnancy
Prolonged immobilisation
Previous VTE
Contraceptive pill
Long haul travel
Cancer
Heart failure
Obesity
Surgery
HRT
Thrombophilia
Severe burns
Age
How does pregnancy increase thromboembolism risk
Coagulant factor production increases in liver
DVT signs and symptoms
Pain
Erythema
Tenderness
Warmth
Superficial venous dilation
May be asymptomatic
DVT differential diagnoses
Musculo-tendinois injury
Superficial thrombophlebitis
Cellulitis
Compression of iliac veins
Congestive cardiac failure
Lymphoedema
Lymphangitis
What is used to estimate probability of DVT and PE in a patient
Wells’ scores
What are the 2 risk categories for DVT and PE
Likely - wells score 2+
Unlikely - wells score 1 or less
DVT clinical features - Wells score
Active cancer
Paralysis, paresis, or recent plaster immobilisation of lower extremities
Recently bedridden for 3+ days or major surgery within 12wks needing anaesthesia
Localised tenderness along distribution of the deep venous system
Entire leg swollen
Calf swelling 3cm larger than asymptomatic side
Pitting oedema confirmed to symptomatic leg
Collateral superficial veins
Previously undocumented DVT
When is a proximal leg vein ultrasound scan offered to a patient
Wells score 2 points or more
What test should be done if a proximal leg vein ultrasound scan is negative in a patient with a wells score over 2
D dimer test
D dimer
Fibrin degradation product
When is d dimer released into the blood
Thrombus degraded by fibrinolysis
Inflammation
Cancer
Pregnancy
Pulmonary embolism symptoms
Dyspnea
Pleuritic chest pain
Cough
Sub sternal chest pain
Haemoptysis
Fever (but <39*c)
Syncope
Unilateral leg pain
Chest wall tenderness
When is pleuritic pain worst
Inspiration
Haemoptysis
Coughing up blood
Syncope
Fainting
Pulmonary embolism signs
Tachypnoea
Rales
Decreasing breath sounds
Accentuated second heart sound
Tachycardia
Fever
Diaphoresis
SIgns and symptoms suggesting thrombophlebitis
Lower extremity oedema
Cardiac murmur
Central cyanosis
Why is pulmonary embolism difficult to diagnose
Patients may have mild or no signs and symptoms
Pulmonary embolism differential diagnoses
Pneumothorax
Pneumonia
Myocardial infarction
Pericarditis
Pleurisy
Musculo skeletal chest pain
Pulmonary embolism investigations
Blood gases
Chest x ray - exclude other diagnoses
ECG - rule out CVD
Classic PE ECG
deep S wave lead I
Q wave lead iii
Inverted t wave lead iii
What 2 level PE wells score suggests PE is likely
More than 4 points
What 2 level PE wells score suggests PE is unlikely
4 or less points
PE clinical features on 2 level wells score
Clinical signs and symptoms of DVT
Alternative diagnosis less likely than PE
heart rate >100 bpm
Immobilisation more than 3 days or surgery in prev 4wks
Previous DVT/PE
Haemoptysis
Malignancy
PE imaging
Pulmonary angiography
Ventilation perfusion lung scintigraphy
CT pulmonary angiography
PE causes of death
Acute right ventricular overload
Respiratory failure
Pulmonary infarction
PE treatment
Immediate subcutaneous low molecular weight heparin
Oral anticoagulant
How does heparin prevent clot formation
Binds to and Activates antithrombin -> activated complex inactivates factor Xa -> prevents conversion of prothrombin to thrombin
How does heparin decrease PE mortality
Stops thrombus propagation in pulmonary arteries
Stops thrombus propagation at emboli source
Reduces frequency of further pulmonary embolism
Heparin complications
Increased risk of bleeding
Heparin induced thrombocytopenia
High risk PE patients
Haemodynamic support
Respiratory support
Exogenous fibrinolytics
Percutaneous catheter directed thrombectomy
Surgical pulmonary embolectomy
How long are patients put on oral anticoagulants for PE
Identifiable temporary risk factor - 3 months
Active cancer - 6 months
No identifiable risk factor - indefinitely
Why are direct oral anti coagulants DOACs increasingly being prescribed instead of warfarin
Lower risk of bleeding
How does warfarin reduce plasma levels of factors II, VII, IX, and x
Vitamin K+ antagonist
Why must treatment be started with heparin instead of just giving warfarin
Warfarin has a delayed onset of actiom
Why can warfarin not be given in pregnancy
Tetarogenic
Can cause material bleeding
Why must warfarin dose be changed if patient put on antibiotics
Antibiotics kill vitamin k producing bacteria in gut, leading to decr coagulation and bleeding
Dabigatran
Orally active direct thrombin inhibitor
Rivaroxaban and apixaban
Orally active factor Xa inhibitors
What are rivaroxaban and apixaban used to treat
DVT
PE
reduce risk of recurrent DVT and PE
Prophylaxis of DVT
Prevent blood clots in atrial fibrillation
When can rivaroxaban and apixaban not be used
Significant liver disease
End stage kidney disease
How can venous thromboembolism be treated during pregnancy
Low molecular weight heparin
How can venous thromboembolism be treated while breastfeeding
Low molecular weight heparin
Warfarin
How are patients with active cancer and associated thrombosis treated
Low molecular weight heparin more effective than warfarin
DOACs
Treatment reviewed after 3-6 mo
How are patients who can’t take anti coagulants treated for venous thromboembolism
Umbrella filter
