Pulmonary Embolism (PE) Flashcards

1
Q

What is venous thromboembolism?

A

Venous thromboembolism (VTE) is a term used to describe both deep vein thrombosis (DVT) and pulmonary embolism (PE)- disorders caused by thrombus formation.

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2
Q

Briefly describe Virchow’s triad

A

The formation of a thrombus in a patient is dependent on any one of Virchow’s Triad being present:

  • Abnormal blood flow-usually due to recent immobility, such as a long-distance flight or being bed-bound in hospital
    • This is the most common underlying cause of a DVT
  • Abnormal blood components- can be caused by multiple factors, such as smoking, sepsis, malignancy, or even inherited blood disorders (e.g. Factor V Leiden)
  • Abnormal vessel wall- can be from atheroma formation, inflammatory response, or direct trauma
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3
Q

What are the risk factors for VTE?

A

The main risk factors for developing a venous thromboembolism include:

  • Increasing age
  • Previous VTE
  • Smoking
  • Pregnancy or recently post-partum
  • Recent surgery (especially abdominal surgery, pelvic surgery, or hip or knee replacements)
  • Prolonged immobility (> 3 days)
  • Hormone replacement therapy or the combined oral contraceptive pill
  • Current active malignancy
  • Obesity
  • Known thrombophilia disorder (e.g. antiphospholipid syndrome or Factor V Leidin)
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4
Q

What are thrombophilias? And give examples

A

Thrombophilias are conditions that predispose patients to develop blood clots. There are a large number of these:

  • Antiphospholipid syndrome (this is the one to remember for your exams)
  • Antithrombin deficiency
  • Protein C or S deficiency
  • Factor V Leiden
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5
Q

What is a pulmonary embolism (PE)?

A

A pulmonary embolism (PE) refers to a blockage of the pulmonary artery by a substance that has travelled there in the bloodstream.

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6
Q

Give examples of causes of PE

A

Most commonly, this blockage is a thrombosis that has broken off and migrated (such as from a DVT).

Other causes include a right-sided mural thrombus (e.g. post-MI), atrial fibrillation (AF), neoplastic cells, or from fat cells (e.g. following tibial fracture).

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7
Q

How does a PE present?

A

The key clinical features of a PE are sudden onset dyspnoea, pleuritic chest pain, cough, or (rarely) haemoptysis.

Clinically, a patient may have tachycardia, tachypnoea, pyrexia, a raised JVP (rare), or pleural rub or pleural effusion (rare). Remember to examine for any signs of DVT in any patient with suspected PE.

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8
Q

What parameters are assessed when investigating Well’s Score for PE?

A
  • Clinical signs and symptoms of DVT (minimum of leg swelling and pain with palpation of the deep veins)
  • An alternative diagnosis is less likely than PE
  • Heart rate more than 100 beats per minute
  • Immobilisation for more than 3 days or surgery in previous 4 weeks
  • Previous DVT/PE
  • Haemoptysis
  • Malignancy (on treatment, treated in the last 6 months, or palliative)
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9
Q

How does a Wells score dictate further investigations?

A

If pulmonary embolism is suspected in a patient, the PE Wells’ Score should be calculated:

  • Score less than or equal to 4: PE clinically unlikely, requires a further D-dimer test to exclude
  • Score greater than 4: PE clinically likely and a PE diagnosis should be confirmed with a CT Pulmonary Angiography (CTPA) scan (or V/Q scan in those with poor renal function).
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10
Q

What are other causes of raised D-dimers?

A

A D-dimer test is sensitive but not specific; a D-dimer may also be raised following recent surgery or trauma, with ongoing infection or inflammation, concurrent liver disease, or pregnancy, and indeed in any patient with a prolonged hospital stay.

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11
Q

What tests are used to diagnose PE?

A

Pulmonary embolism can be diagnosed with a CT pulmonary angiogram or ventilation–perfusion (VQ) scan.

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12
Q

How may a PE present on and ECG?

A

Less commonly, a PE may present on ECG with a:

  • Right bundle branch block (RBBB)
  • RV strain (inverted T waves in V1-V4 and / or leads AvF-III)
  • Rare S1Q3T3 (deep S wave in Lead I, pathological Q wave in Lead III, and inverted T wave in Lead III)
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13
Q

Briefly describe CT pulmonary angiogram (CTPA)

A

CT pulmonary angiogram (CTPA) involves a chest CT scan with an intravenous contrast that highlights the pulmonary arteries to demonstrate any blood clots.

This is usually the first choice for investigating a pulmonary embolism as it tends to be more readily available, provides a more definitive assessment and gives information about alternative diagnoses such as pneumonia or malignancy.

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14
Q

Briefly describe ventilation-perfusion (VQ) scan

A

Ventilation-perfusion (VQ) scan involves using radioactive isotopes and a gamma camera to compare the ventilation with the perfusion of the lungs. They are used in patients with renal impairment, contrast allergy or at risk from radiation where a CTPA is unsuitable.

First, the isotopes are inhaled to fill the lungs and a picture is taken to demonstrate ventilation. Next a contrast containing isotopes is injected and a picture is taken to demonstrate perfusion. The two pictures are then compared. With a pulmonary embolism there will be a deficit in perfusion as the thrombus blocks blood flow to the lung tissue. This area of lung tissue will be ventilated but not perfused.

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15
Q

How does a PE present on an ABG?

A

Patients with a pulmonary embolism often have a respiratory alkalosis when an ABG is performed.

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16
Q

Briefly describe VTE prophylaxis

A

Every patient admitted to hospital should be assessed for their risk of venous thromboembolism (VTE).

If they are at increased risk of VTE they should receive prophylaxis with low molecular weight heparin such as enoxaparin unless contraindicated. Contraindications include active bleeding or existing anticoagulation with warfarin or a NOAC.

Anti-embolic compression stockings are also used unless contraindicated. The main contraindication for compression stockings is significant peripheral arterial disease.

17
Q

What is the immediate treatment for DVT?

Note: no renal impairment, active cancer, antiphospholipid syndrome or haemodynamic
instability

A

Direct oral anticoagulants (DOACs) are now recommended as as first line treatment for DVT.

Caution is advised in those with chronic renal impairment or if taking potentially interacting medications.

Offer apixaban or rivaroxaban.

18
Q

What is the mechanism of action of DOACs?

A

Direct factor Xa inhibitors: apixaban, rivaroxaban and edoxaban

Direct thrombin inhibitor: dabigatran

19
Q

How long should anticoagulation be offered for following a PE?

A

Anticoagulation treatment should be continued for 3 months in those with a provoked DVT.

However in those with a proximal DVT and a persistent risk factor or high risk of DVT recurrence may require lifelong anticoagulation.

20
Q

If DOACs are contraindicated (e.g. in active cancer or renal impairment), what alternative treatment can be given in DVT?

A

If DOAC is not suitable offer LMWH.

Examples include dalteparin and enoxaparin.

21
Q

Briefly describe the use of inferior vena cava filters

A

Inferior vena cava filters are devices inserted into the inferior vena cava designed to filter the blood and catch any blood clots traveling from the venous system towards the heart and lungs. They act like a sieve, allowing blood to flow through whilst stopping larger blood clots. They are used in unusual cases of patients with recurrent PEs or those that are unsuitable for anticoagulation to prevent emboli traveling to the lungs.

22
Q

Why does a PE present with respiratory alkalosis?

A

This is because the high respiratory rate causes them to “blow off” extra CO2. As a result of the low CO2, the blood becomes alkalotic.

It is one of the few causes of a respiratory alkalosis, the other main cause being hyperventilation syndrome. Patients with a PE will have a low pO2 whereas patients with hyperventilation syndrome will have a high pO2.