PULMONARY EMBOLISM

DR A HAMMANGABDO FWACP
PROFESSOR AND COSULTANT PULMONOLOGIST
PULMONARY THROMBO
EMBOLISM(PTE)
INTRODUCTION: Acute PE is a form of venous thromboembolism(VTE) that is common
sometimes fatal. The clinical presentation is variable and often non specific making the
diagnosis challenging.
Evaluation of patients with suspected PE should be efficient so that they get early treatment to
reduce morbidity and mortality.
PTE

 DEFINITION:- ‘Pulmonary embolism refers to the obstruction of the pulmonary artery or

one of its branches by material – thrombus, air, tumour or fat that originates elsewhere in
the body’ here we discus venous thromboembolism.
Temporal patterns of presentation of PE:
 Acute- symptoms develop immediately after obstruction of pulmonary vessels.
 Subacute – patients develop symptoms within days or weeks following initial events
 Chronic- patients with chronic PE slowly develop symptoms of pulmonary hypertension
over many years
PTE: epidemiology

 It is estimated that PTE occurs in about 1% of patients admitted to the hospital

 Incidence of PE in general population has increased due to increased screening following
the introduction of D- dimer testing and CT pulmonary angiography in the 1990s.
 Overall the incidence is higher in males than females 56/100000 versus 48/100000
respectively.
 Directly responsible for about 5% of all deaths in hospital
 Thrombus develop in deep veins of the legs
PTE epidemiology contd

 Incidence increases with age esp in females

 In US it accounts for 100000 deaths per year
 It accounts for 300000 deaths per year in Europe
 Overall mortality due to PE is high,
 30days and 1year mortality was 4% and 13% according to one report
 Most clots which cause clinically relevant PE come from pelvic veins and abdominal veins
Risk factors for VTE

 Patient factors  Disease factors

 Age  Surgical procedures esp orthopaedic like
 Obesity pelvic or hip
 Varicose veins  Trauma
 Long air travel  Malignancy
 Immobility .4days bed rest  Stroke
 Pregnancy and puerperium  Cardiac failure
 Previous DVT or PE
 Recent MI, Infarct
 Thrombophilia
 IBD,NS,polycythemia
 Anti thrombin deficiency
 Myeloproliferative disease
 Protein C or S deficiency
 SCA
 homocysteinaemia
pathophysiology

 After PE, lung is ventilated but not perfused

 Impaired gas exchange, after few hours non perfused lung no longer produce surfactant
 Leads to alveolar collapse- >hypoxaemia
 The primary haemodynamic consequence of PE is a reduction in the cross-sectional area of
pul- arterial bed
 This results in elevation of pul- arterial pressure and reduction of cardiac output
 Lung zone that is not perfused may become infarcted, but often it does not because it is
supplied by bronchial circulation and the air ways
Clinical features

 Sudden onset of unexplained dyspnoea is the most common and often the only symptom of
PE
 Pleuritic chest pain and haemoptysis are present only when infarction has occurred
 Many PE are silent but there are 3 typical clinical presentations
 A DVT is not commonly observed, though detailed investigation of lower limb and pelvic
veins will reveal thrombosis in >5% of cases
Clinical features

I. Small/medium PE
Embolus has impacted on a terminal pul vessel, symptoms are:
. Pleuritic chest pain
. Breathlessness, haemoptysis occur in 30% of cases
. Tachypnoea with localised pleural rub, coarse crackles over the area involved
. Exudative plrural effusion, occasionally blood stained
. Fever
Clinical features

 Massive PE:
 Much more rare, because patients don’t make it before reaching hospital, sometimes
diagnosis made at post mortem
 Sudden collapse due to right ventricular out flow tract obstruction
 Severe central cyanosis
 Chest pain-cardiac ischaemia –
 Shock, pale and sweating
 Syncope if cardiac output is transient
 Tachypnoea, tachycardia, hypotension and peripheral shutdown
Clinical features contd:

 Raised JVP, with prominent a’ wave

 Rt ventricular heave, S3 gallop
 Wide split of pul component of S2
 No abnormal chest signs
Clinical features

 Multiple recurrent PE
 Increased breathlessness over weeks or months
 Weakness
 Syncope on exertion
 Occasional angina
 Signs of pulmonary hypertension from multiple occlusion of pul vessels
 Signs of rt ventricular overload with Rt ventricular heave
Diagnosis

 The symptoms and signs of small and medium PE are subtle and non- specific, so
diagnosis is often delayed or completely missed.
 PE should be suspected or considered if patients present with symptoms of unexplained
cough, chest pain, haemoptysis, new onset AF or other tachycardia or signs of pulmonary
hypertension, if no other cause can be found
Investigations

 Small/medium PE
 CXR often normal, linear atelectasis, blunting of costophrenic angles-these develop only after
sometime
 Raised hemidiaphragm
 Wedge shaped pul infarct, abrupt cut off of a pulmonary artery
 Previous infarcts may be seen as opaque linear scars
investigations

 ECG-normal or sinus tachycardia, AF or evidence of RV strain

 Blood tests:-
 Pulmonary infarcts results in increased PMN leucocytes or WBC
 Increased ERS,LDH
 Thrombophilia check immediately prior to anti coagulant use
 Plasma D-dimer- if undetectable-excludes the diagnosis of PE
Radionuclide
 ventilation/perfusion scan:
 Pul Tc Scintigraphy
investigations

 Ultrasound scanning of pelvis or ilio-femoral veins for clots

 Spiral CT scanning chest scan with IV contrast (CT pul angiography)-good sensitivity and
specifity for medium sized PE, multiple slices for small sized PE
 MRI scan similar to CT angiography
Investigations- :
massive PE
 CXR : pulmonary oligemia, dilatation of pulmonary artery in hilar
 ECG:-
 Rt atrial dilatation
 Tall peaked P waves in lead II, RV strain and dilatation-gives to Rt axis deviation
 RBBB. T waves inversion in R precordial leads
 Classic ECG pattern is S in lead I,Q waves and inverted T waves in lead III (SI,T3QIII)
investigations

 Arterial blood gases:- arterial hypoxaemia with low pCO2 ie type I respiratory failure
 Echo: vigorously contracting LV ,dilated RV, clots in RV outflow tract
 Pulmonary angiography:-filling defects or obstructed vessels may be seen

 Massive recurrent PE:-

 CXR oligaemic lung fields,
 ECG signs of pul HTN
 Leg imaging;-ultrasound and venography, show thrombi
 V/Q scanning evidence of infarcts
treatment

 Acute pulmonary Embolism (PE) is a common and sometimes fatal disease

 Variable clinical presentation
 Treatment be administered in a timely fashion to prevent recurrent thromboembolism and
death
Treatment of PE

 Initial approach and resuscitation

 Stabilize the patient, while clinical evaluation and definitive diagnostic testing are ongoing, risk
stratification is crucial.
 Assess haemodynamic stability;- the initial approach to patients with suspected PE depends
whether the patient is haemodynamically stable or not
Treatment of PE contd

 Haemodynamically unstable PE(massive PE) is that which present with hypotension –

systolic BP < 90 mmHg for a period of > 15 minutes, hypotension requiring vasopressors,
or clear evidence of shock
 Haemodynamically stable PE is defined as PE that does not meet the definition of unstable
PE
 Majority of patients with PE are haemodynamically stable on presentation
 Peripheral IV access
 Oxygen supplementation
 Empiric anticoagulation- depending on suspicion for PE, risk of bleeding and expected timing of
definitive diagnostic tests
Treatment of PE contd-

 Haemodynamically unstable- small % of patients

 Restoring perfusion with IVF resuscitation
 Vasopressor support
 Oxygenation
 Stabilizing airways with intubation
 Mechanical ventilation
 Immediate anticoagulation after patients are stable in whom there is high suspicion of PE
 Prompt imaging (CTPA)
 Initial therapies;-
 Respiratory support, supplemental Oxygen, target O2 sat >90%
 Haemodynamic support-
 IVF
 Vasopressors- norepinephrine, dopamine, epinephrine, dobutamin
 Empiric anticoagulation
 Dissolution of the thrombus
 Fibrinolytic therapy such as streptokinase 250000 iu by IV infusion over 30 min
 Then streptokinase100000 iu IV up to 12- 72 hrs
 Surgical embolectomy
PTE

 Differential diagnosis
 Pneumothorax
 Pneumonia
 Empyema/pleural effusion
 Aortic dissection
 Dressler’s syndrome
 Pericardial tamponade
 Acute pericarditis, AMI
 asthma
Thank you