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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
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