DVT and PE Flashcards
two commonest presentations of venous thrombosis
PE and DVT
VTE occurs due to
virchows triad:
- alteration in blood flow (venous stasis)
- injury to the blood vessel wall (vascular endothelial injury)
- hypercoagulable state (inherited or acquired)
things that might cause a hyper coagulable state
sepsis
inflammation
oestrogens
malignancy
inherited thrombophilia
things that might cause vascular damage
cannula
atherosclerosis
trauma or surgery
things that might cause venous stasis
AF
immobility
venous obstruction
venous insufficiency or varicose veins
factor V leiden mutation
point mutations in the F5 gene which encodes for factor V in clotting cascade
mutations make factor V resistant to activated protein C (natural anticoagulant) = patient is more likely to clot
clinical presentation of DVT
usually unilateral leg
leg erythema
warmth
swelling
pain
DDx for DVT
muscle strain/tear
baker’s cyst
cellulitis
lymphatic obstruction
venous insufficiency
leg oedema (heart failure or others)
D-dimer is
is a product of clot breakdown
released upon breakdown of polymerised cross linked fibrin
high D-dimer levels indicate
that coagulation has been activated
fibre clot has formed, and clot degradation by plasmn has occurred
if D-dimer is negative (low)
high negative predictive value
if negative, a blood clot is highly unlikely
causes of elevated D-dimer
not just clotting
also:
- severe infection and sepsis
- trauma
- cancer
- thrombolytic therapy
- surgery
- pregnancy
- liver or kidney disease
- DIC
doppler ultrasound
if a vein cannot be collapsed or compressed, a DVT diagnosis is made on the assumption that a clot is preventing the collapse
the flow of blood changes the sound waves reverberated via the Doppler effect
an absence of blood flow indicates a blood clot
how does warfarin work
prevents vit K dependant coagulation factors from being activated
which are the vit K dependant anticoagulation factors
2,7,9,10 (the good analog tv channels)
heparin acts on
antithrombin
most emboli come from
lower limb proximal veins
iliac, femoral, popliteal
how does a PE form
emboli comes from the lower limb proximal veins
clot travels through the right ventricle to pulmonary arteries and lodges
once a PE emboli has lodged
results in
1. decreased gas exchange due to mechanical obstruction of the vascular bed. ventilation/perfusion mismatch causes hypoxia
2. infarction in 10% of people where the slot lodges in smaller pulmonary arteries. pleuritic chest pain
3. cardiovascular compromise depending on the clot burden, there can be compromised cardiac output = hypotension
saddle PE
if the embolus is large enough
it can lodge in the main pulmonary artery and obstruct flow from the right ventricle to the lung
life threatening
clinical presentation of PE
dyspnoea
cough
chest pain
maybe also haemoptysis or calf pain or swelling (due to concurrent DVT)
examination findings of PE
tachypnoea
tachycardia
hypoxia
signs of DVT
if ssaddle PE or massive PE: low BP, signs of right heart failure, raised JVP, leg swelling
DDx of PE
heart failure
MI
pneumonia
exacerbation of chronic lung disease
pericarditis
MSK pain
investigations for PE
blood tests: FBC, U&E, troponin (MI?), d-dimer
CXR: look for another diagnosis
ECG: most commonly you see a tachycardia
V/Q scan
ventilation/perfusion scan - nuclear medicine
need to have a normal CXR first
looks at distribution of blood flow compared to alveolar ventilation
pulmonary artery occlusion leads to ventilated areas without perfusion (dead space) leading to V/Q mismatch
CTPA
CT pulmonary angiogram
most sensitive and specific test
contrast injected into vein - CT lung to capture contrast moving through the pulmonary arteries
thrombophilia screen
protein tests
protein C, ATII levels: reduced in acute thrombosis, anticoagulation
prothrombin gene mutation and factor V Leiden gene mutation
lupus anticoagulant (affected by anticoagulation), antiphospholipid antibodies
indication for thrombophilia screen
a patient with unexplained VTE
a patient with strong family history of VTE if it will change management
family Hx of thrombophilia in young women considering COCP
do not do protein C, S and ATII in acute thrombosis and anticoagulation and the levels will be affected
choice of treatment for VTE
DOAC: apixaban, rivaroxaban, dabigatran are treatment of choice in most cases
warfarin
LMWH: low molecular weight heparin, may be used in short term initially if in hospital, used in pregnancy
treatment duration for VTE
minimum 3 months and then assess ongoing risk factors for thrombosis at the end of three months
