VTE Flashcards
Where do thrombi form
USually at site of valves
How does a Thrombus form
Valves become a site of turbulent flow leading to thrombus formation. Valves can be damaged by trauma, stasis and occlusion
Once formed a thrombus grows by successive adherence of platelets and fibrin
Consequences of thrombus formation in a vein
1) lysis and resolution: if small thrombus resolves (fibrinolytic action)
2) Organisation: scar tissue obliterates lumen and blocks it so blood flows through collateral vessels
3) Recanalisation: leads to scar formation and residual thrombus in lumen
4) embolism: fragmentation of thrombus leads causes embolus to travel to vessel
Consequences of emboli
1) Often numerous small emboli may not affect patient and cause damage gradually, resulting in idiopathic pulmonary hypertension.
2) Larger emboli may cause shortness of breath and chest pain; patient is likely to seek medical attention and these may require treatment or resolve on their own.
3) Long emboli which lodge at bifurcation of pulmonary vessels leading to acute outcome e.g. death
Risk factors for thrombus (Virchow’s triad)
Stasis
Hypercoagulable state
vessel wall injury
What increases risk of hyper coagulable state
Oestrogen therapy (hrt, COC) Pregnancy Sepsis Malignancy Congestive heart disease Factor V Lieden (thrombophilia) Antiphospholipid/lupus anticoagulant
What increases risk of stasis of blood
Age Venous insufficiency or varicose veins Obesity Immobility Continuous travel Hospitalisation
What increases vessel wall injury
Trauma or surgery
Indwelling venous catheters
How to take a history for VTE
HPC
SOCRATES
PMH- prior VTE, inflammatory disease, malignancy, thrombophilia
PSH- recent surgery or hospital admission?
Medications- anything with oestrogen, prior need for anticoagulation
Obstetric history- pregnancy, termination, with in past 6 weeks
family history- and VTE or thrombophilia
Travel history- Travel >3h in past 4 weeks
SH- family, dependents, carers, house, smoking and alcohol,
ICE
Presenting complaint of DVT
Unilateral localised pain (throbbing) in one leg Oedema of leg Calf swelling/oedema Tenderness of lower limb Skin changes (redness, warmth) Distension of legs
Diagnostic tool for suspected DVT
Wells score
What test for suspected DVT
D-dimer
-Measures a degradation product released by lysis of a cross-linked fibrin clot
When is d-dimer useful and not useful
D dimer should not be done In those with a high clinical probability of VTE
A negative d-dimer can exclude patients with a low probability of PE
When would you request a doppler ultrasound
Wells score > or equal to 2, high clinical suspicion or a low Wells score but positive D-dimer
When should d-dimer be used
Useful for excluding patients with a low probability of DVT
What is May-Thurner syndrome
Compression of left common iliac vein by the right common iliac artery causes a DvT to form
If there is an unprovoked DVT what would you do
CT
How to emboli travel from leg to lung
Travel up IVC through the right atrium through the right ventricle and into the pulmonary artery
What is a saddle embolism
Consequence of this
A large embolus that straddles the bifurcation of the pulmonary trunk, extending into both the right and left pulmonary arteries
Near-immediate death
Presenting complaint of Pulmonary embolism
Dyspnoea or tachypnoea Pleuritic chest pain Signs of Dot Cough Fever haemoptysis Substernal chest pain
Diagnostic tools in PE
Wells score for PE (2-tier)
PE rule-out criteria (PERC) where clinical suspicion is low (negative d-dimer <15% chance)
What happens if Wells score for PE> 4
Hospital admission for CT pulmonary angiography (CTPA)
If CTPA not immediately available give anticoagulation
What happens if wells score for PE<4
D dimer within 4 hours at gP or send to hospital
If no. d dimer available consider interim anticoagulation
D dimer positive: CTPA (CT pulmonary angiography)
D dimer negative: its not a PE
If pt can’t receive contrast for CTPA egg, for renal failure of anaphylactic contrast allergy - what to use
V/Q scan used.
- Radioactive isotopes delivered by inhaled gas
- Ventilation (v) shows how well air reaches the lung parenchyma
- Perfusion (q) shows how well blood circulates in the lung parenchyma
Can be ECG be used to diagnose PE
no
What findings can be seen in PE
Sinus tachycardia
Dominant R wave in lead V1
T wave inversion in leads V1-v4 or right bundle branch block
Classical ECG finding of a deep, slurred S wave in lead I with a Q wave and T wave inversion in III (S1 Q3 T3) is rare in PE- this indicates cor pulmonale
What is T wave inversion in leads V1-V4 indicate
Right ventricular strain
What is right bundle branch block on ECG indicative of
right ventricular strain
Classification of a massive PE
acute PE with sustained hypotension (systolic <90mmHg) or decrease in baseline SBP of 40mmHg or more than 15 mins or persistent bradycardia <40bpm)
classification of sub-massive PE
Acute PE without hypotension
Signs of right ventricular (RV) dysfunction or myocardial necrosis including:
-Abnormalities on echocardiography (see notes)
-ECG changes: RV strain, ischemic changes, S1 Q3 T3 pattern
-Elevated troponins
Classification of low risk PE
Acute PE without the clinical markers that define massive or sub-massive pulmonary embolism
Low risk PE presentation, bbs and ECG
linical presentation: pleuritic chest pain, shortness of breath, clinical signs of DVT (calf swelling) most likely. Could have any other symptom listed on slide 28. Asymptomatic is also important- don’t forget!
Observations: Tachycardia is most common.
ECG: Sinus tachycardia might be the only abnormality. The ECG might be normal.
Sub-massive PE presentation, obs and ECG
Clinical presentation: this patient is likely to be feeling very unwell- pleuritic chest pain, shortness of breath, clinical signs of DVT (calf swelling) plus other symptoms.
Observations: Tachycardia most likely. Not significantly hypotensive.
ECG: Changes consistent with right ventricular strain and ischaemic changes due to impaired oxygenation of the heart muscle. S1Q3T3 pattern is possible.
Massive PE presentation, obs and ECG
Clinical presentation: clinical presentation of PE with possible signs of DVT. Patient is likely to have symptoms suggestive of haemodynamic compromise (e.g. episode of syncope, loss of consciousness).
Observations: Tachycardia or severe bradycardia. Patient has significant hypotension (systolic <90mmHg or reduced significantly for at least 15 mins).
ECG: same changes as seen in sub-massive PE. May be more likely to have cor-pulmonale.
