Deep Vein Thrombosis and Pulmonary Embolus Flashcards
define thrombus/thrombosis
pathological intravascular solidification of blood constituents
define embolism and examples of what can form an embolus
vascular obstruction at a site distant from origin of thrombus
eg thrombus which has broken away, fat, air, amniotic fluid
how many deaths does venous thrombo embolism cause per year in UK
25000 deaths/year in UK
DVT incidence/year
1:1000 people per year
proportion of people affected by DVT in lifetime
1/20
% mortality of DVT and explain
21%
not always at time, but later effects: PE, chronic problems eg falling –> hip fracture
what is a pulmonary embolism (PE)
clot of pulmonary artery
% mortality of PE
10-15%
is PE preventable?how is it managed?
yes.
all pts in hospital given LMW heparin, wearing stockings
statements about PE and death risk
- second leading cause of sudden death
- leading cause of preventable in-hospital mortality
- leading cause of death associated with childbirth (6x inc VTE risk during pregnancy)
explain healthy blood flow from leg veins to lungs
superficial veins of leg (greater saphenous v)
–> deep veins of leg (popliteal, femoral)
–> inferior vena cava
–> R atrium –> R ventricle
–> pulmonary artery
THIS MOVEMENT HAPPENS DUE TO DEEP VEINS IN LEG BEING IN MUSCLES –> LEG MOVEMENT CAUSES RETURN OF BLOOD THROUGH VENOUS SYSTEM. WITHOUT THIS MOVEMENT, BLOOD RETURN IS POOR –> INC RISK OF PE WHEN PEOPLE DO NOT MOVE
how does this blood flow change to form a PE?
embolus travels through venous system and heart and lodges in one of the pulmonary arteries
name given to the fatal type of PE and why this is fatal
saddle embolus
lodges at pulmonary trunk –> no blood flow to lungs, pt cannot exchange gases so dies
what is Virchow’s triad about
3 things needed to get a PE
contents of Virchow’s triad and explain
- alterations in blood flow (eg kink, turbulence)
- alterations in blood constituents (eg proteins inc stickiness of blood, more likely for thrombus to form)
- vascular endothelial injury (injury to inside of blood vessel, activates clotting cascade)
explain/examples for 9 risk factors for VTE
- malignancy, esp lung cancer
- surgery esp orthopaedic: hip replacement. +vascular, neurosurgery
- immobility: less venous return legs –> heart
- trauma: to hip/pelvis
- oestrogen: combined pill
- pregnancy: enlarged uterus blocks venous return
- obesity: fat blocks venous return
- previous thromboembolism: 25% recurrence rate
- other chronic illness: tips balance thrombosis > thrombolysis in inflammatory state
examples of chronic illnesses which cause VTE 5 and explain
- heart failure
- inflammatory bowel disease
- nephrotic syndrome
- antiphospholipid syndrome: autoimmune disease against phospholipids –> clots on cell walls
- myeloproliferative disorders (inc number blood cells) eg polycythaemia vera, essential thrombocythaemia
why are venous and arterial diseases different?
venous diseases are LOW PRESSURE
draw clotting cascade
see lecture
function of factor V
converts prothrombin to thrombin
name and description of factor V mutation
Leiden mutation
INCREASES factor V –> not inactivated by protein C, increases clotting cascade
what other gene mutation enhances clotting pathway
prothrombin
increases amount of prothrombin
name 3 deficiencies in clotting cascade which enhance clotting pathway
protein S
protein C
antithrombin III
6 symptoms of DVT
pain tenderness swelling erythema (redness) heat venous engorgement
what other diseases share these symptoms with DVT 7
and how each of them is caused/ looks different to DVT
- cellulitis: staph aureus or strep infection, but localised to surround site of injury
- superficial thrombophlebitis: clots in superficial veins, not harmful but painful
- Baker’s cyst: synovium of joint bulges out (often behind knee) and bursts –> inflammation
- lymphodema: compromise in lymphatic drainage when lymph nodes removed due to tumour.looks v similar to DVT
- muscle strain/tear
- drug-induced oedema: commonly caused by calcium channel blockers
- chronic venous insufficiency: presents as purple/black, hard lower legs. starling forces –> haemosiderin in tissue fluid
investigations to diagose DVT 3, inc which is not used and why
- D dimer (blood test)
- ultrasound/Doppler
- venogram: not used. involves catheter with iodine and x ray. BUT very painful and allergy to contrast common
what is D dimer?
fibrin degradation product (FDP)
formed when plasminogen activates plasmin to break down fibrin clot. D dimer is a part of the fibrin clot
when are there high levels of D dimer
when a large clot has just been broken down
problems of D dimer
any inflammatory state increases D dimer –> false positive readings
what may give false positive D dimer results 5
- inflammation
- malignancy
- trauma
- pregnancy
- recent surgery
what may give false negative D dimer results
- tested too early after thrombus formation (has not yet been broken down)
- tested after several days: anti-coagulants may have stopped thrombus extension
compare % of D dimer sensitivity and specificity
sensitivity: 93-95%
specificity: 50%
when to use D dimer test and why
only when there is no alternative explanation for inc D dimer
otherwise if D dimer is raised (for another reason) you are obliged to do further testing –> unpleasant for pt, wasting resources
3 possible sequelae of DVT
- venous insufficiency
- recurrent DVT
- PE (worst one)
3 symptoms of venous insufficiency and explain
- hyper pigmentation: haemosiderin out of blood vessels
- limb pain and swelling: nerve damage, hydrostatic pressure
- dermatitis, ulcers, gangrene
define PE
obstruction of pulmonary artery or one of its branches
what usually causes PE
what else can cause it
embolus from proximal DVT (femoral, ileac, pelvic vv)
could also be from tumours, air, fat etc
4 ways to classify PE
- temporal pattern (acute, subacute, chronic)
- haemodynamic stability
- anatomical location: saddle, lobar, segmental, subsegmental
- presence/absence of symptoms
explain difference between PE symptoms:
a. acute
b. subacute
c. chronic
explain difference between PE symptoms:
a. acute: sudden, severe
b. subacute: minor changes eg out of breath walking
c. chronic: caused by pulmonary hypertension: heart pumps harder to remove obstruction in pulmonary a –> fails (muscle exhaustion) –> dilates –> back pressure in rest of body –> R sided heart failure (swollen legs, peripheral oedema, sacral oedema, fluid on belly)
how to measure haemodynamic stability
any drop of 40mmHg systolic bp
tachycardia
7 presenting factors of PE and explain
- collapse
- pleuritic (from lungs) chest pain
- dyspnoea (difficulty breathing)
- tachypnoea (fast breathing, less oxygen transferred to blood –> hypoxia)
- tachycardia (heart trying to compensate hypoxia)
- cough, possible haemoptysis (blood)
- pleural rub (lung pleura stick together –> sounds crunchy thru stethpscope)
how to tell pleuritic from MI chest pain
pleuitic: often one-sided, worse at the end of inspiration (when lungs are fully stretched)
MI: not localised, constant with breathing
6 ways to investigate/diagnose PE and how they work
- D Dimer
- ABG (arterial blood gas, measures arterial oxygen levels)
- ECG (look for arrythmia, commonly AF)
- Chest x ray (look for pleural affusion, dilated pulmonary aa, wedge infarct- tissue has died and there is an inflammatory reaction)
- V/Q scan: breathe in radio-labelled gas and record on ventilation scan. inject IV technicium and record on perfusion scan. look for differences between perfusion and ventilation
- CT scan (best one): inject contrast to see circulation of lungs
when would VQ scan be used
if CT scan cannot be used
eg kidney problems (cannot take contrast) or contrast allergy
what do blood and clots look like on CT scans
blood: white
clot: black
what scoring system is used to justify investigation for VTEs
what score means gives 60% chance of having VTE
Wells scoring
>6 points
how to treat major PE 3
- systemic thrombolysis: use plasminogen activators alteplase/streptokinase
- catheter embolectomy with local thrombolysis
- surgical embolectomy (rare)
absolute indications with PE 2
hypotension
systemic hypoperfusion
relative indications of PE 3
right ventricular dysfunction
pulmonary hypertension
extensive DVT
treatment of uncomplicated, non-major PE
- LMW heparin (enoxoparin) as subcutaneous injection. given to everyone as prophylactic dose or treatment dose. works immediately
- warfarin. takes 5-7 days to work. dose according to risk
why is LMW heparin used over heparin
easy to use (subcutaneous injection)
heparin is IV and needs more monitoring
how long will warfarin be prescribed for pt
a. first episode DVT
b. first episode PE
c. lots of risk factors/ previous VTE
how long will warfarin be prescribed for pt
a. first episode DVT: 3 months
b. first episode PE: 6 months
c. lots of risk factors/ previous VTE: poss life
explain 4 ways to prevent VTE
- TEDS (thrombo-embolic deterrent stockings): prevent venous pooling around lower leg
- calf pumps: move leg muscles for you, given to immobile people
- LMW heparin
- early mobilisation, eg physios after surgery
how to treat PE in pt who is already on warfarrin and not major urgency 2
increase warfarrin (3-4 INR) IVC filter
what is an IVC filter
filter in inferior vena cava that catches clots coming up from legs
2 times IVC filter should be used
- PE with contraindication to anticoagulation
- recurrent PE despite adequate anticoagulation
why are novel oral anti-coagulants (NOACs) being used?
minimal monitoring- no monthly checks or INRs –> acceptable to pt
problems with NOACs
cannot be reversed
name 3 NOACs and how they work
- dabigatran: direct thrombin inhibitor
- rivaroxaban +
- apixaban: direct factor Xa inhibitors
how to treat VTE pt differently as dentist
check INR ratio (must be below 4)
inc risk of bleeding
may need stitches, extractions in hospital setting
