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Pathology

Embolus in the pulmonary vasculature that has classically travelled from a deep vein of the leg (DVT) via the right heart or a right atrial thrombus in AF.

Aetiology

Virchow’s Triad:
Venous stasis e.g. immobility, CCF, dehydration and venous obstruction
Endothelial Injury e.g. trauma, inflammation and previous thrombosis
Hypercoagulable state e.g. malignancy, oestrogen therapy, surgery and  
abnormalities of the clotting cascade

Signs

Acute Minor: hyperventilation, haemoptysis, hypoxia, fever, effusion
Acute Major: As above + hypotension, cyanosis, engorged neck veins and collapse
Sub-Acute/Chronic: hyperventilation, raised JVP

Symptoms

Acute Minor: Pleuritic pain, dyspnoea
Acute Major: Central chest pain, dyspnoea
Sub-Acute/Chronic: Progressive dyspnoea


Investigations

Chest X-Ray: Often normal, elevation of a hemi-diaphragm and linear atelectasis, 
small effusions or wedged shaped infarcts may be present
ECG: Sinus tachycardia, right heart strain or S1Q3T3
ABG: Low PaO2 and PaCO2
D-dimer: If clinical probability is intermediate or low then a negative d-dimer is a 
reliable rule-out of thromboembolic disease
CTPA: Initial investigation for non-massive PE’s
V/Q Scan: Used in those who can not tolerate CT contrast 

Treatment

Thrombolysis: Clinically massive PE and marked haemodynamic compromise
Anticoagulation: Low molecular weight heparin then Warfarin with a target INR of 2.0-3.0. 
LMWH continued until 2 consecutive days of target INR achieved due to initial prothrombotic effect of Warfarin.
IVC filter: Aim to prevent further clot reaching pulmonary vasculature

Prognosis

Massive PE 30-60% mortality, most occur in the first 1-2 hours of care
Pulmonary haemorrhage, pulmonary hypertension, CCF, recurrent episodes

Key Facts

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Key References

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