Acute Pulmonary Embolism

Introduction

Thrombus, usually formed in the systemic veins or rarely in the right heart (<10% of cases), may dislodge and embolize into the pulmonary arterial system.

Risk factors

Patient factors

• Increasing age
• Obesity
• Varicose veins
• Previous Deep vein Thrombosis( DVT)
• Family history, especially of unprovoked venous thromboembolism (VTE) when young
• Pregnancy/puerperium
• Oestrogen-containing oral contraceptives and HRT
• Immobility, e.g. long distance travel (> 4 hrs)
• IV drug use (femoral vein)

Surgical conditions

• Major surgery, especially if > 30 mins’ duration
• Abdominal or pelvic surgery, especially for cancer
• Major lower limb orthopaedic surgery, e.g. joint replacement and hip fracture surgery

Medical conditions

• Myocardial infarction/heart failure
• Inflammatory bowel disease
• Malignancy
• Nephrotic syndrome
• Pneumonia
• Neurological conditions associated with immobility, e.g. stroke, paraplegia, Guillain–Barré syndrome

Haematological disorders

• Polycythaemia rubra vera
• Essential thrombocythaemia
• Deficiency of anticoagulants: antithrombin, protein C, protein S
• Paroxysmal nocturnal haemoglobinuria
• Gain-of-function prothrombotic mutations: factor V Leiden, prothrombin gene G20210A
• Myelofibrosis

Antiphospholipid syndrome

• Lupus anticoagulant
• Anticardiolipin antibody 

Epidemiology

• The incidence of Pulmonary embolism in the community is unknown;
• It occurs in approximately 1% of all patients admitted to hospital and
• accounts for around 5% of in-hospital deaths.
• It is a common mode of death in patients with cancer, stroke and pregnancy.

Pathophysiology

1. Major haemodynamic effects: ↓cardiac output; acute right heart Failure
2. Occlusion of segmental pulmonary artery → infarction ± effusion
3. Chronic occlusion of pulmonary microvasculature, right heart failure

Clinical features

Acute massive PE

• Faintness or collapse,
• Crushing central chest pain,
• Apprehension,
• Severe dyspnoea
• Major circulatory collapse:
• tachycardia,
• hypotension,
• ↑JVP,
• RV gallop rhythm,
• loud P2,
• Severe cyanosis,
• ↓urinary output
• Varicose vein, unilateral leg swelling

Acute small/medium PE

• Pleuritic chest pain,
• Restricted breathing,
• haemoptysis
• Tachycardia,
• Pleural rub,
• Raised hemidiaphragm,
• crackles,
• effusion (often blood-stained),
• Low-grade Fever

Investigations

1. Chest X-ray-
1. oligaemia,(increased darkness)
2. pleuropulmonary opacities,
3. pl effusion,
4. linear shadows,
5. raised hemidiaphragm
2. ECG: Sinus tachycardia, S1Q3T3, RBBB, RVH, T inversion V1-V4

3. Echocardiogram: small underfilled vigorous LV, dilated RV, exclude left ventricular failure, aortic dissection and pericardial tamponade
4. ABG:  Desaturation on formal exercise testing, ↓PaO2, ↓PaCO2, Metabolic acidosis
5. D-dimer: positive
6. Colour Doppler/ compression USG of the leg veins-DVT
7. CT pulmonary angiography- Emboli; first-line diagnostic test.
8. Ventilation-perfusion scanning – perfusion defect with preserved ventilation

Caution: previous Cardiopulmonary disease may affect result.

Diagnosis

1. D-dimer negative + Risk low= No PE/DVT
2. D- dimer negative + Risk High

Or

D- dimer positive + Risk low= then

1. Colour Doppler/ compression USG of the leg veins
2. CT pulmonary angiogram or
3. V/Q scan

3. D-dimer positive + Risk high = Treat then confirm diagnosis.

D/D

1. Myocardial infarction,
2. Pericardial tamponade,
3. Aortic dissection
4. Pneumonia, pneumothorax,
5. musculoskeletal chest pain
6. Other causes of pulmonary hypertension

Management

1. General
1. Oxygen
2. v. fluid, plasma expander
3. Opiates for pain
4. external cardial message

Caution: Diuretics and vasodilators should also be avoided,

2. Anticoagulation
1. Unfractionated Heparin 5000U i.v. followed by continuous infusion of 20 U/ kg/ hr(APTT after 6 hr then twice daily, aim 1.5 to 2.5 times),

Or

2. LMWH

Enoxaparin sodium 1.5 mg/kg (150 units/kg) every 24 hours

Or

Bodyweight < 46 kg, 7500 units;

46–56 kg, 10 000 units;

57–68 kg, 12 500 units;

69–82 kg, 15 000 units;

>83 kg , 18 000 units daily,

         Or

3. , a synthetic pentasaccharide closely related to heparin, represents an alternative to LMWH.

body-weight < 50 kg, 5 mg;

50–100 kg, 7.5 mg;

> 100 kg, 10 mg every 24 hours;

with oral anticoagulant treatment until adequate oral anticoagulation established; (target INR >2) should continue for at least 5 days,

4. Warfarin – a vitamin K antagonist – remains the most commonly used oral anticoagulant.

The usual adult induction dose of Warfarin is 5–10 mg on the first day;

subsequent doses depend upon INR (international normalised ratio).

The daily maintenance dose of warfarin is usually 3–9 mg (taken at the same time each day).

5. LMWH should not be discontinued until the INR is 2 or more for at least 24 hours.
2. Thrombolytic therapy, Indicated in any patient presenting with acute massive PE accompanied by cardiogenic shock.
3. Surgical pulmonary embolectomy: may be considered in selected patients but carries a high mortality. 
4. Caval filter: If anticoagulation is contraindicated,

And who has suffered massive haemorrhage on anticoagulation,

or recurrent VTE despite anticoagulation,

should be considered for an inferior vena caval filter.

Retrievable caval filters are particularly useful in patients with temporary risk factors.

 Prognosis

• Immediate morality is greatest in those with echocardiographicevidence of right ventricular dysfunction or cardiogenic shock.
• After anticoagulation is started the risk of mortality rapidly falls.
• The risk of recurrence is highest in the first 6–12 months.
• At 10 years around one-third of individuals will have suffered a further event.

Further reading

1. Davidson’s Principles & Practice of Medicine 22^nd
2. Kumar & Clark’s Clinical Medicine 8^th
3. Harrison’s Principles of Internal Medicine 18^th