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Deep Vein Thrombosis & Pulmonary Embolism > Deep Vein Thrombosis & Pulmonary Embolism > Flashcards

Deep Vein Thrombosis & Pulmonary Embolism Flashcards

1
Q

Venous thromboembolism is very common in those admitted to the hospital, post surgery, trauma or any reason of reduced mobility.

What is venous thromboembolism (VTE)?

A

VTE is a thrombus in the veins.

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2
Q

Thrombosis causes ~25% of worldwide deaths each year.

How is a thrombus formed?

A

Virchow’s triad:
Change in blood flow (stasis or turbulence)
Endothelial dysfunction
Hypercoagulability

A pathogenic thrombus forms within a blood vessel whereas, a physiological blood clot (haemostasis) occurs outside the endothelium.

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3
Q

Thrombosis can occur in both arteries and veins i.e. MI is due to thrombus in coronary arteries, whilst DVT is due to thrombus in a deep vein.

What are the main differences between arterial and venous thrombosis?

A
  1. Arterial thrombus = white because it is made of platelets and fibrin.

Turbulence & vessel-wall dysfunction caused by atheromatous plaques => arterial thrombosis

  1. Venous thrombus = red because it is made of fibrin and red cells.

Stasis and hypercoagulability => venous thrombosis

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4
Q

60% of VTE present with deep vein thrombosis (DVT) and 40% of VTE present with pulmonary embolism (PE).

What is DVT? How is it caused?

A

Most commonly venous thrombosis occurs in deep veins => DVT

Within the pockets of the valves, the flow can be turbulent => localised hypoxia => endothelial dysfunction.

The thrombus may remain localised to leg veins or embolise more proximally i.e. leading to PE

If confined to calf veins = distal DVT

If it reaches popliteal vein or above = proximal DVT

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5
Q

DVT can result in pulmonary embolism (PE).

What is PE? How is a PE caused?

A

Obstruction of pulmonary artery or its branches most likely as a result of an emboli from a DVT

Proximal DVT are larger + more likely to embolise through the large veins of pelvis and abdomen into the right atrium and ventricle
=> into pulmonary artery which further divide into smaller arteries
=> embolus too big = obstructs distal branches from blood flow = PE

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6
Q

How common is PE?

A

i. 3rd most common cause of cardiovascular death after MI and stroke
ii. Most common avoidable cause of death in patients admitted to the hospital
iii. Leading direct cause of death during pregnancy and puerperium.

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7
Q

What are the transient risk factors for VTE?

A
  1. Major surgery i.e. lower limb/pelvis (stasis)
  2. Trauma
  3. Immobilisation >3 days
  4. Plaster cast
  5. Pregnancy / peurperium
  6. Oestrogen i.e. combined pill or hormone therapy
  7. Recent long haul travel >4h
  8. Active cancer
  9. Heparin induced thrombocytopenia
  10. Central venous catheter
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8
Q

What are the persistent risk factors for VTE?

A
  1. Increasing age
  2. BMI >30
  3. Ethnicity
    (highest risk = Africans, intermediate risk = whites and low risk = Asians)
  4. Previous VTE
  5. Inflammatory conditions i.e. IBD, Lupus
  6. Heritable thrombophilia i.e. factor V leiden, deficiency of anti-thrombin, protein C or protein S
  7. Anti-phospholipid syndrome
  8. Lower limb paresis e.g. stroke
  9. Nephrotic syndrome
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9
Q

What are some examples of stasis related risk factors?

What are some examples of hypercoagulability related risk factors?

A

Stasis related:
Surgery, bed rest, plaster cast, immobilisation, pregnancy and long haul travel

Hypercoagulability related:
Cancer, surgery, pregnancy, oestrogen and heritable thrombophilias

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10
Q

Risk factors categorised by likelihood of VTE occurring:

STRONG risk factors increase risk 10-50 fold i.e. major surgery, trauma and bed rest

MODERATE risk factors increase risk 3-10 fold i.e. pregnancy, oestrogen therapy, minor surgery under general anaesthetic and heritable thrombophilias

WEAK risk factors increase the risk up to 3 fold i.e. obesity and long haul travel

A

INFO CARD

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11
Q

What is the clinical presentation of DVT?

A

Unilateral pain and swelling

Red and warm to touch

Tenderness along the course of the deep vein & dilation of superficial veins

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12
Q

70% patients presenting with symptomatic PE have an assoc. DVT and 1/3 of DVT patients have clinically silent PE.

What are the signs and symptoms of PE?

A

Symptoms:

Pleuritic chest pain
Acute breathlessness
Haemoptysis
Syncope (severe)

25% present with isolated breathlessness, sometimes only with exertion

10% present with severe/emergency features i.e. syncope, systolic hypotension, shock or MI assoc. with central chest pain.

Signs:

Pyrexia
Cyanosis
Systolic hypotension (severe)
Tachypnoea + Tachycardia

On auscultation: crackles and a pleural rub over localised area of pulmonary infarction ; 
Right ventricular heave ;
Gallop rhythm ;
Widely split S2 ;
Loud P2
Pleural effusion
Raised JVP (severe)

Cardiac arrest with pulseless electrical activity

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13
Q

What are the differential diagnoses for DVT?

A

Ruptured Baker’s cyst

Superficial vein thrombosis

Post-thrombotic syndrome

Cellulitis

Osteoarthritis, osteomyelitis, synovitis, fracture, tumour

Acute arterial occlusion

Lymphoedema

Musculo-tendinous i.e. trauma, haematoma, myositis, tendonitis

Congestive cardiac failure & hypoalbuminaemia = bilateral leg swelling

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14
Q

What are the differentials diagnoses for PE?

A

Chest infection/pneumonia

Exacerbation of COPD

Asthma

Pneumothorax

Congestive cardiac failure

Acute coronary syndrome

Costocondritis

Musculoskeletal pain or rib fracture

Aortic dissection

Pericardial tamponade

Lung cancer

Primary pulmonary hypertension

Anxiety/hyperventilation

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15
Q

What are the initial investigations carried out for patients with chest pain and breathlessness suspected of PE?

A
  1. ECG: commonly normal or sinus tachycardia

Right ventricle strain pattern = T-wave inversion in inferior leads II, III, AVF and V1-3,

Right axis deviation,

Right bundle branch block,

Deep S-wave in lead I, Q-waves in lead III inverted T-waves in lead III => S1,Q3,T3

  1. Chest X-ray: often normal but may show decreased vascular markings, small pleural effusion, atelectasis
  2. ABG: hypoxia, hypocapnia (poor gas exchange), hyperventilation (low O2, CO2, high pH)
  3. Bloods: FBC, U&E, baseline clotting, D-dimer
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16
Q

Which clinical prediction score test is used to stratify risk for DVT and PE?

A

i. Modified 2-level Wells score for DVT

ii. Modified 2-level Wells score for PE

17
Q

Describe the 9 clinical features used in a Modified 2-level Wells score for DVT?

A

1 point for each clinical feature:

Active cancer

Paralysis, paresis, or recent plaster mobilisation of lower leg

Bedridden >3d or major surgery within 12weeks

Localised tenderness along the deep vein distribution
Entire leg swollen

Calf swelling >3cm vs asymptomatic leg

Pitting oedema in the symptomatic leg

Collateral superficial veins

Previous DVT

Alternative diagnosis as likely as DVT (minus 2 points)

DVT likely = 2 or more points

DVT unlikely = 1 or less points

18
Q

Describe the 7 clinical features used in a Modified 2-level Wells score for PE?

A

Clinical signs & symptoms of DVT = 3 points

Alternative diagnosis less likely than PE = 3 points

Heart rate >100beats/min = 1.5 points

Immobilisation >3days or surgery in previous 4 weeks = 1.5 points

Previous DVT/PE = 1.5 points

Haemoptysis = 1 point

Malignancy = 1 point

PE likely = >4 points

PE unlikely = 4 points or less

19
Q

D-dimer test is sensitive but not specific for DVT i.e. its also increased in pregnancy, malignancy, infection and post-op.

What is a D-dimer?

When is a D-dimer test used?

A

D-dimer is a fibrin degradation product and raised levels of D-dimer indicate activation of the coagulation cascade.

A D-dimer is used when VTE is unlikely based on Well’s score.

20
Q

What should be done following a high D-dimer test?

D-dimer test has a high negative predictive value. What does this mean?

A

A high D-dimer test does not confirm a DVT diagnosis => a high value requires radiological testing to confirm the diagnosis

D-dimer result below the cut-off means DVT is very unlikely because of its high negative predictive value.

21
Q

A high Well’s Score => D-dimer + ultrasound needed => if both positive = DVT confirmed ; both negative = DVT excluded

A high Well’s Score => +ve D-dimer but -ve ultrasound => repeat ultrasound in 1wk

A low Well’s Score => high D-dimer value => Ultrasound => +ve imaging = DVT confirmed

A low Well’s Score => low D-dimer value => DVT excluded

A

INFO CARD

22
Q

When is thrombophilia test indicated?

A

Before commencing anticoagulant conduct a thrombophilia test if:

i. No predisposing factor for DVT
ii. Recurrent DVT
iii. DVT in unusual site

23
Q

Which imaging confirms the diagnosis of DVT?

A

Ultrasound confirms diagnosis for DVT.

Ultrasound is very sensitive for proximal DVTs but less for distal DVTs.

A +ve scan confirms diagnosis for both proximal and distal DVTs.

A -ve scan for proximal DVT excludes DVT but a -ve scan for distal DVT does not exclude a DVT diagnosis.

24
Q

A high PE Wells score (>4 points) => PE likely
=> immediate CT pulmonary angiography or empirical treatment with LMWH if delay

A low PE Wells Score (<4 points) = PE unlikely

=> do a D-dimer:

if +ve immediate CT pulmonary angiography ;

if -ve excludes PE, consider alternative diagnosis

A

INFO CARD

25
Q

Which imaging confirms the diagnosis of PE?

A

CT pulmonary angiography (CTPA) = sensitive & specific for high risk PE patients or low risk with +ve D-dimer test => 1st choice imaging

It can provide alternative diagnosis if PE is excluded.

2nd choice imaging: Ventilation/perfusion (V/Q) scan if CTPA unavailable

26
Q

What is the treatment for VTE (DVT & PE)?

A

Low molecular weight heparin (LMWH) i.e. enoxaparin or fondaparinux (subcutaneous or IV) => provides immediate anticoagulation

Warfarin (oral vitamin K antagonist) alongside LMWH => takes at least 5 days to provide full anti-coagulation

Stop LMWH once INR 2 or more on 2 consecutive days => treat for 3 months then reassess

DOACs
i. Direct factor Xa inhibitor: rivaroxaban ; apixaban
=> used at a higher dose, no parenteral anti-coagulant needed

ii. Direct thrombin inhibitor: dabigatran
=> first 5 days by parenteral anticoagulant i.e. LMWH then straight switch to Dabigatran on day 6

Inferior vena cava filters used to prevent PE in active bleeding or when anticoagulant fails

27
Q

CONTRAINDICATION:

Warfarn and DOACs cross the placenta & cause abnormalities in the foetus 6 weeks onwards = should not be used in pregnancy

Recognise pregnancy early

If already on anti-coagulant, switch to LMWH before 6 weeks of pregnancy.

LMWH safer in pregnancy => taken until delivery

A

INFO CARD

28
Q

Cancer patients: LMWH more effective than warfarin for VTE treatment

A

INFO CARD

29
Q

What is the difference between anticoagulant and thrombolysis agents?

A

Anticoagulants help prevent further thrombus and recurrence.

Thrombolysis helps dissolve clots.

30
Q

When is thrombolysis indicated in PE?

Why is thrombolysis rarely used?

A
  1. Haemodynamically unstable i.e. massive PE with systolic hypotension = high risk of early death

=> thrombolyse i.e. I.V. Alteplase => restoring pulmonary perfusion

  1. Rarely used as thrombolysis has a major risk of bleeding than anti-coagulant.
31
Q

What do you do in unprovoked PE with no known provoking risk factors?

Which other underlying factors are important to consider?

A

Consider possibility of malignancy - full hx, examination (inc breast), bloods (FBC, LFT, calcium), urinalysis and chest x-ray.

> 40 years consider pelvic CT and mammography in women.

Consider anti-phospholipid and thrombophilia testing if family Hx +ve

32
Q

What preventative measures can be taken for DVT?

A

Stop combined contraceptive pills 4 wks before pre-op

Mobilise early

LMWH for high risk patients

Thromboembolic deterrent (TED) stockings

Intermittent pneumatic compression devices reduces DVT by 70% in surgical patients

33
Q

What preventative measures can be taken for PE?

A

Give heparin to all immobile patients

Stop HRT and combined contraceptive pill 4wks before pre-op (switch to another form of contraception)

34
Q

What are the complications of VTE?

A
  1. Mortality - rate is lower in patients presenting with DVT than PE.
  2. Assoc. cancer => hypercoagulability directly from cancer, surgery/chemotherapy, reduced mobility.
    Cancer + thrombosis = poor prognosis
  3. Post-thrombotic syndrome in 40% people following DVT.
    Symptoms i.e. pain, swelling, venous claudication on exercise — reduces physical functions & mobility
  4. Pulmonary hypertension due to incomplete resolution of pulmonary embolism — suspected in those with persisting symptoms.

Deep Vein Thrombosis & Pulmonary Embolism (1 decks)

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