89 - Venous Thrombosis and Pulmonary Thromboembolism Flashcards
Most common preventable cause of death in hospitalised patients
Pulmonary thromboembolism
Clot
A solid mass composed of blood components which forms after death
Thrombus
Solid mass composed of blood components formed in an artery of vein during life
Where do thrombi often form?
Deep veins of the lower limbs
Deep veins of lower limb 1 2 3 4
Distal to proximal:
Anterior, posterior tibial veins
Popliteal vein
Femoral vein
Iliac vein (in the pelvis)
Most important venous plexus in lower limb
In soleus muscle
Superficial veins of the lower limb
Great and small saphenous veins
Location of formation of venous thrombi
Form upstream of valve.
Become more occlusive, thicker.
Feature of growth of venous thrombi
Can propagate up- and downstream of where thrombus began forming.
Why are venous thrombi red?
Form in an environment of low flow.
Have lots of RBCs.
Structure of venous thrombi
Lines of Zahn.
Alternating layers of red (RBC) and pink (platelets and fibrin)
Thrombi that are often occlusive
Venous thrombi
When are venous thrombi more likely to embolise?
When recently-formed.
Examples of changes to vessel wall that can predispose to thrombi
Trauma from catheterisation.
Bacterial infection of vessel wall.
Polycythaemia
Condition where too many RBCs are produced.
Can’t be cured, only can control symptoms.
Predisposes to thrombosis.
Things that can lead to non-laminar flow, causing thromboses 1 2 3 4 5
Prolonged immobilisation Dehydration Hypotension Congestive cardiac failure Polycythaemia
What cause most arterial thromboses?
Complications of atherosclerosis.
Example of a genetic hypercoagulable state
Factor V Leiden
Factor V Leiden
Point mutation in factor V prevents activated protein C (natural anticoagulant) from binding to a cleavage site.
Proportion of patients with DVT that have factor V Leiden
50%
Uncommon genetic predispositions to hypercoagulable state
1
2
3
(1) Antithrombin III deficiency
(2) Protein C deficiency
(3) Protein S deficiency
Common genetic predispositions to hypercoagulable state
1
2
Factor V Leiden
Prothrombin III deficiency
Examples of secondary predisposing factors to hypercoagulability 1 2 3 4 5 6 7 8
• Surgery
• Massive trauma and burns
• Malignancy – release of thrombogenic substances from
tumours especially mucinous adenocarcinomas
• Obesity – mechanism unknown
• Smoking – probably
• Hyper-oestrogenic states (pregnancy and the OCP)
• Nephrotic syndrome (both cause and effect of renal
vein thrombosis)
• Anti-phospholipid antibody syndrome
Fates of venous thrombi 1 2 3 4
1) Lysis of thrombus
2) Organisation of thrombus (can form scar tissue, forming a stricture on the vessel wall)
3) Recanalisation (most common fate. New blood vessels form, restoring blood flow around thrombus)
4) Embolism (most dangerous outcome)
Embolus
An embolus is a mobile mass of material within the
vascular system able to lodge within a vessel, occlude its lumen and obstruct blood flow.
Thromboembolus
A detached piece of thrombus
What do clinical effects of pulmonary thromboemboli depend on?
Size of occluded vessel
Pulmonary thromboembolus that can cause sudden death
‘Saddle embolus’
Thromboembolus lodges at the bifurcation of the pulmonary artery.
‘Saddle embolus’
Thromboembolus lodges at the bifurcation of the pulmonary artery.
Features of a saddle embolus
Red, with some pale areas.
Lodged at the bifurcation of the pulmonary artery.
Coiled shape, reflecting vein of origin.
Occlusive.
Clinical effects of a saddle embolus
Sudden death - Cardiac arrest with electromechanical dissociation.
Electromechanical dissociation
Electrical activity of heart is continuing in normal fashion, but mechanical activity of heart is prevented from thromboembolus.
Clinical effects of a thromboembolus in a right or left pulmonary artery 1 2 3 4
Sudden death.
Dyspnoea.
Chest pain.
Circulatory failure mimicking myocardial infarction
Thoracic catastrophes presenting with central chest pain, SOB
MI.
Pulmonary thromboembolus
Aortic dissection
Clinical features of a small pulmonary thromboembolus 1 2 3 4 5 6
Share features with other solid-organ infarcts Sharply demarcated infarct Wedge-shaped infarct Pleural base. Red Occluded artery at apex
Clinical features of a small pulmonary thromboembolus
1
2
3
Dyspnoea
Haemoptysis
Pleuritic chest pain
Why are lung infarcts red and not pale?
Dual blood supply (pulmonary circulation and bronchial circulation from descending aorta)
Clinical features of a small pulmonary thromboembolus without infarct
Unexplained tachycardia in a patient with risk factors for pulmonary thromboembolism
What could be occurring if a patient has an unexplained tachycardia, and has risk factors for venous thromboses.
Small pulmonary thromboembolism without an infarct
