IC4 VTE, DVT & PE Flashcards
When is D-dimer produced?
D-dimer – byproduct of fibrinolysis (more D-dimer, more fibrin mesh to degrade)
Where can thrombus be formed in DVT and what does it suggests?
Thombus location:
- Distal/Calf/below knee – unlikely to embolise
- Proximal/Above knee – liklely to embolise
What are the S&S of DVT?
What are the differential diagnosis?
Deep Vein Thrombosis (DVT)
S&S:
- Unilateral, leg swelling, pain, warmth
- Palpable cord on affected leg, pain in back of knee
- objective testing needs to be done
- Triage: cellulitis, infection, fluid overload due to HF
What are the S&S of PE?
Explain how a patient can die from a PE?
What are the differential diagnosis?
Pulmonary Embolism (PE)
– result in occlusion of blood flow in lungs → impaired gas exchange → necrosis → impaired O2 delivery to other organs could result in fatal circulatory collapse
S&S:
- chest pain, SOB, cough, chest tightness, palpitation, hemoptysis, dizziness, light-headedness, ECG change
o small distal emboli → create areas of alveolar haemorrhage → hemoptysis, pleuritis, and pleural effusion (usually mild) - tachypnea, tachycardia, diaphoretic (sweating heavily), distended neck veins, cyanotic and hypotensive
- cardiac arrest, obstructive shock, persistent hypotension
o PE is the infarction of lung tissues → vessels can’t push blood that well, this causes back damping into heart
o Causes RV strain and congestion → RV failure
o Causes systemic congestion → In turn can cause left congestive HF
o Reduced CO → overt RV failure → then circulatory collapse & shock → die - severe: cardiogenic shock and die
- Triage: MI
What is the Virchow’s triad? Give at least 2 examples each.
RF of VTE (Virchow’s Triad)
- Hypercoagulability (chronic, states which increases clotting factors/clotting)
a. Malignancy, pregnancy, infection, sepsis - Circulatory stasis
a. Immobility, AF, Long haul flights, obese (venous obstruction), pregnancy - Vascular Damage
a. Accident, atherosclerosis, smoking DM
How to diagnose DVT?
When & How to start treatment for VTE
Diagnosis of VTE:
DVT diagnostic algorithm:
Suspect DVT (from S&S)
→ Well’s score
If 2 or less, D-dimer → (P)imaging[CDUS] / (N)rule-out DVT
If 3 or more, imaging → (proximal)immediately start ACG / (distal)consider ACG (if very symptomatic) or surveillance
Note:
Pre-test probability of DVT (Well’s score) – Clinical features of DVT (similar Virchow’s triad)
D-dimer
- +ve does NOT CONFIRM it is DVT
- -ve CONFIRMS that it is not DVT (good negative predictive value)
What are the baseline test and investigations to be ordered after suspecting someone has DVT? (Haven’t diagnose yet)
Baseline test and investigations to be ordered (DVT w/o PE)
Based on the things we want to triage
e.g. cellulitis, infection, fluid overload, HF
- FBC(see if have left shift, meaning have infection)
- Procalcitonin (infection and sepsis)
- Renal panel (SCr to calculate CrCL)
- NTproBNP (natriuretic peptide tests, if suspect have dyspnoea & HF fluid overload)
- +/- D-dimer
What are the acute treatments for proximal and distal DVT respectively?
Acute treatment of VTE algorithm:
-
Proximal DVT
→ look below at choice of ACG
→ DOACs in non-cancer pts and if no CI
→ at least 3 months ACG
→ then evaluate for 3 months e.g. Venous US, risk/benefit, compliance, pts’ preference
→ stop ACG / extend AC -
Isolated Distal DVT
→ look below at choice of ACG
→ high risk recurrence → 3months ACG
→ low risk recurrence → 4-6wks ACG/venous US surveillance
(want to prevent post-phlebitic syndrome, thus start ACG if see DVT worsens/symptoms progresses)
VTE treatment strategies:
- *Apixaban
a. (Acute) 10mg PO BD x 7days
(Early maintenance) 5mg PO BD x 3-6months
(Extension/Prophylaxis) 2.5mg PO BD after 1st 6 months - *Rivaroxaban
a. (Acute) 15mg PO BD x 21days
(Early maintenance) 20mg PO QD x 3-6months
b. (Extension/Prophylaxis) 10mg PO QD after 1st 6 months - UFH/LMWH (SC) x 5days, THEN dabigatran 150mg PO BD x 3-6months / edoxaban 60mg PO QD x 3-6months consider extension
- UFH/LMWH (SC) x 5days AND warfarin INR>=2, target INR=2.5 x 3-6mth
- Alteplase (rTPA)
o HAM, only for high risk PE
o usually dose by weight, *no need to memorise dose, but need to know that dose differs from that in AIS and MI
Choice of ACG
- General population → DOACs over warfarin
- Pros of DOACs:
o Less DDI/FDI
o Fixed dosing, no need titrate
o No initial parenteral agent
- Pros of warfarin:
o Used in renal impairment - Severe renal impairment (CrCL <30mL/min) → UFH/LMWH x 5days AND warfarin INR>=2, target INR=2.5
Name the dosing and duration for all 4 acute treatment for VTE.
VTE treatment strategies:
-
Apixaban
a. (Acute) 10mg PO BD x 7days
→ (Early maintenance) 5mg PO BD x 3-6months
→ (Extension/Prophylaxis) 2.5mg PO BD after 1st 6 months -
Rivaroxaban
a. (Acute) 15mg PO BD x 21days
→ (Early maintenance) 20mg PO QD x 3-6months
→ (Extension/Prophylaxis) 10mg PO QD after 1st 6 months - UFH/LMWH (SC) x 5days, THEN dabigatran 150mg PO BD x 3-6months / edoxaban 60mg PO QD x 3-6months → consider extension
- UFH/LMWH (SC) x 5days AND warfarin INR>=2, target INR=2.5 x 3-6mth
- Alteplase (rTPA)
o HAM, only for high risk PE
o usually dose by weight, **no need to memorise dose, but need to know that dose differs from that in AIS and MI
What is the choice of ACG for the general population and those who are severely impaired respectively?
Choice of ACG
- General population → DOACs over warfarin
- Pros of DOACs:
o Less DDI/FDI
o Fixed dosing, no need titrate
o No initial parenteral agent
- Pros of warfarin:
o Used in renal impairment - Severe renal impairment (CrCL <30mL/min) → UFH/LMWH x 5days AND warfarin INR>=2, target INR=2.5
How to diagnose someone with PE?
PE diagnostic algorithm:
Same as DVT but criteria is >4 = PE likely
Suspect PE (from S&S)
Modified Well’s score
If 4 or less, D-dimer → (P)imaging[CTPA] / (N)rule-out PE
If 5 or more, imaging → immediately start ACG (need to look at severity & risk stratification → determines drug choice)
Severity & Risk Assessment:
1. Haemodynamically unstable
2. Clinical parameters of PE severity and/or comorbidity
3. RV dysfunction on TTE/CTPA
4. Increase troponin levels (cardiac muscles dies)
Risk stratification of PE into high, intermediate and low risk
High risk → all 4
intermediate risk → 1-3
What is the acute treatment for high risk, intermediate risk PE, and reperfusion treatment for PE?
- High risk PE
a. UFH + Thrombolytics + inotropes + fluid replacement for 3 months → stop ACG / extend AC
i. Use UFH instead of LMWH here becos easily reversible → impt esp if haemodynamically unstable
ii. Use thrombolytics here as high risk of mortality > risk of bleeding/clumps embolizing - Intermediate/low risk PE
a. SC LMWH / DOAC (no preference btw the 1st 2, choose either 1) / SC LMWH + warfarin until INR 2.5 for 3 months → stop ACG / extend AC
b. DOACs NOT for VTE treatment in
i. Severe renal impairment (use LMWH/warfarin)
ii. Pregnancy and lactation (LMWH)
iii. Antiphospholipid antibody syndrome (warfarin) - Reperfusion treatment for PE
a. Rescue Thrombolytics recommended for pts with haemodynamic deterioration on ACG treatment → thus use UFH as the ACG too as it is quickly reversible
b. If pts are well, switch from infusion UFH to SC LMWH or PO DOACs, becos less nursing time
What do you need to think about when considering extending therapy? (3)
List the conditions and whether should stop or extend.
What are the follow up/TCU labs during ACG prevention therapy?
[Prevention/Prophylaxis] When to stop / extend beyond 1st 6 months?
At 3month, analyse RF of VTE:
- Characteristics & nature of the VTE:
a. provoke/unprovoked? (unprovoked is worse, since can’t remove cause)
b. If provoked, is it transient/irreversible RF?
c. Link back to Virchow’s triad
d. Proximal/distal DVT? Have PE?
e. 1st symptomatic unprovoked DVT worse than 1st unprovoked PE - Bleeding risk (hard to get risk score)
- Patient’s preference
- Usually send them to Ultrasound, if clot is still there will continue ACG
At 6month, if want to extend:
- Reduce dose of rivaroxaban/apixaban OR ensure warfarin INR at 2-3
- If patient has IHD/stroke before this event + don’t want to continue ACG, possible to use single antiplatelet (but if only for VTE prophy. Then single antiplatelet not good)
IF:
- Provoked VTE by transient RF (proximal DVT or PE) / 1st unprovoked isolated distal DVT
→ stop treatment after 3months - 1st unprovoked proximal DVT / PE / 1st symptomatic unprovoked DVT
→ consider bleeding risk + patients agreement → extend therapy
→ if choose to stop ACG, consider low dose aspirin - Chronic irreversible RF e.g. malignancy
→ treat at least 6 months + extend therapy - Unprovoked recurrent VTE
→ lifelong
→ warfarin recommended for Antiphospholipid antibody syndrome (chronic RF)
Follow up/TCU for pts on extended ACG for VTE prophylaxis on regular intervals (similar DOAC monitoring for SPAF)
- Drug tolerance & adherence
- Hepatic & renal function
- Bleeding risk
what is excessive bleeding?
* black tarry stools (dangerous)
* coffee brown vomitus (upper GI bleeding, e.g. PUD)
* trauma to any part of their body, fell
* Per Rectal bleeding
common site of bleeding for any ACG used?
* GIT, and butt when passing motion :)
* odorous stools (because of oxidised blood)
* blood is a laxative, so can cause diarrhea
* fresh blood in stool, suggest Lower GIT bleeding, piles
* epistaxis - nosebleed
When have a bleed?
* go to the doctor (don’t say stop, if not they will just stop and dont go see dr)
When should VTE prophylaxis should be considered? What are the relevant risk scores?
*When should VTE Prophylaxis be considered
- Medically ill (Padua risk score) → e.g. septic, HF exacerbation, stuck in bed, limited mobility >3days
- Surgical patients (Caprini risk score) → e.g. high stress major surgery
- Cancer patients (Khorona)
What are the other common risk factors of getting VTE during pregnancy?
Other common RF of getting VTE during pregnancy:
- Obesity
- Medical comorbidity
- Stillbirth
- Pre-eclampsia
- Post-partum haemorrhage
- Caesarean section
VTE risk is high in pregnant women → increases during pregnancy → peaks during postpartum period
