Pathology: Embolusin the pulmonary vasculature that has classically travelled from a deep vein ofthe leg (DVT) via the right heart or a right atrial thrombus in AF.
Aetiology: Virchow’sTriad:
Venous stasise.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 clottingcascade
Symptoms: Acute Minor: Pleuritic pain, dyspnoea
Acute Major: Central chest pain, dyspnoea
Sub-Acute/Chronic:Progressive dyspnoea
Signs: Acute Minor: hyperventilation,haemoptysis, hypoxia, fever, effusion
Acute Major: As above + hypotension, cyanosis, engorgedneck veins and collapse
Sub-Acute/Chronic: hyperventilation, raised JVP
Investigations: Chest X-Ray: Often normal, elevation ofa 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 lowthen a negative d-dimer is a
reliable rule-out of thromboembolicdisease
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 andmarked haemodynamic compromise
Anticoagulation: Low molecular weight heparin thenWarfarin with a target INR of 2.0-3.0.
LMWHcontinued until 2 consecutive days of target INR achieved due to initialprothrombotic effect of Warfarin.
IVC filter: Aim to prevent further clot reaching pulmonaryvasculature.
Complications: Pulmonaryhaemorrhage, pulmonary hypertension, CCF, recurrent episodes
Prognosis: MassivePE 30-60% mortality, most occur in the first 1-2 hours of care
