Deep Vein Thrombosis and Pulmonary Embolism

thrombus is activation of clotting cascade intravascularly, can happen in artery and in vein

different from blood clot/haematoma

thrombus made up of fibrin, platelets and RBCs

coagulation cascade - intrinsic pathway, internal damage to endothelium, seen more frequently in arterial thrombosis

extrinsic pathway more trauma like putting something into

Intrinsic- Exposure of collagen etc

Extrinsic- release of TF from the adventitia of the the BV

apixaban, rivoroxaban

hypercoagulability - sepsis making thrombosis more likely

white arterial thrombus vs red venous thrombus

symptoms consequence of back pressure in venous thrombosis

long haul flights not the only cause of DVT, it’s associated with other factors e.g. dehydration, alcohol

superficial thrombosis within the veins - thrombophlebitis?

pregnancy associated increased risk of DVT in left leg 3rd trimester - oestregen strong pro thrombotic hormone

adenocarcinoma secrete factors that activate clotting cascade, leading to increased thrombosis

sepsis activated protective inflammatory system activation clotting system leading to thrombosis

pain and swelling in calf, distal leg, majority of DVT in lower limbs

thromboembolism - movement of thrombus along vessel

as supposed to fat embolism if someone had a fracture, fat moves along vessel

air embolism

venous thromboembolism

venous thrombosis can occur in veins of distal colon in some ischaemic colitis, those that present not due to arterial occlusion but due to congestal - frequent in women who are smokers

thrombosis in liver - kiary syndrome, within portal veins leading to infarction of liver

intracranial thrombosis - those pregnant or on contraceptive pill

for venous thromboembolism make diagnosis after CT if presented with stroke like symptoms, most in young female patients

leading cause of maternal death

if left untreated 1 in 3 people die

present with pleuritic chest pain on right, find PE on left in imaging, unrelated to pain on right hand side

more worried about segmental and..

sub-segmental not sure but anticoagulate

risk increases as you get older

younger -common in women

older-common in men

risks

-pregnancy -malignancy -primary pulmonary hypertension -oestrogens -malignancy -lower limb problems

prevention

-early mobilisation

-anti embolism stockings

-other mechanical methods of thromboprophylaxis in patients anaesetised for long period of time to help venous return

-pharmacological thromboprophylaxis

sign guidelines say risk stratification for every patient

signs

-swelling of whole leg, persistent discomfort in calf or groin where the deep veins run, calf tenderness “tight shoes, socks causing discomfort”

-warmth

-redness-erythema

-prominent collateral veins

-unilateral pitting oedema

-very significant DVT leg can be ischaemic

very severe pain is not suspecting of DVT

blueish leg or swollen could be very significant DVT causing significant back pressure compromising arterial supply

well’s score for DVT

low risk - d-dimer, if negative then excluded DVT

high risk -ultrasound

**can’t use well score in pregnant patient or those very high risk e.g. IV patients

GOLD STANDARD TEST: venous limogram?

if ultrasound abnormal -treat

in higher risk do ultrasound, if it’s normal then you do d-dimer, if it is positive you repeat ultrasound in 7 days

as DVT progress above knee- most risk of PE

essential two tests to exclude DVT

well score, d-dimer

and carry on from there

D-dimer very sensitive for VTE

non specific if patient has bruise, bleeding, malignancy, anything that activated clotting cascade can lead to positive D-dimer

high sensitivity, low specificity

symptoms and signs of PE

Pleuritic chest pain

Breathlessness-  dyspnoea

[Blood in sputum- haemoptysis

Rapid heart rate- tachycardia → likely sinus tachycardia some non specific T wave changes

Pleural rub on auscultation- very rarely, usually as pulmonary infarction and consolidation, sounds like walking on fresh snow

usually due to pulmonary infarction

**acute breathlessness

massive PE relatively rare

Severe dyspnoea of sudden onset

Collapse

Blue lips and tongue - cyanosis

Tachycardia

Low blood pressure

Raised jugular venous pressure

May cause sudden death

well score PE also excludes pregnancy but can use in some who are IV drug users

well score positive → d-dimer, if negative stop (low risk), excluded pulmonary embolism

well score positive → CT angiogram (high risk) / isotope ventilation or perfusion scan

^history first and pre test probability

when starting treatment looking at why PE has happened, signs of malignancy?

those with PE can have malignancy in next 12-24 months

provoked DVT is below level that you would give anticoagulant

risk of bleeding from anticoagulant 1-2%

young patients with unprovoked VTE, get VTE analysed in more depth by haematologist to see if inheritance thrombophilias

Consider risk of recurrence

Clinical Risk

Cancer patients

DASH score/ HERDoo2 etc

main treatment is anticoagulation

provoked 3 months because provoked would eventually go away

unprovoked and high risk of reocurrence - lifelong anticoagulation if BMI above 30, cancer, something that won’t go away

patients very obese warfarin instead of DOAC

thrombectomy if causing ischaemia

thrombolysis if PE so big like in cardiac arrest or high risk, reserved for extremist situation e.g. alteplase

lots of effort

aim of treatment

Prevent clot extension

Prevent clot embolization

Prevent recurrent clot

most patients with DVT will have ongoing swelling after that

most recover fully from PE

some develop pulmonary arterial hypertension

some follow up with echo after 3 months or first if they’re breathless

robot