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Pulmonary Embolism

• Embolism : Impaction of a thrombus or foreign matter in the


pulmonary vascular bed.
• Infarction : The pathological changes which develop in the lung as a
result of pulmonary embolism.

Pulmonary Thrombo-embolism (PTE):

• Thrombosis of peripheral veins , embolization of pulmonary arteries ,


and pulmonary infarction.
• In most cases PE is a consequence of DVT. Among patients with
proximal DVT, about 50% have an associated, usually clinically
asymptomatic PE at lung scan. In about 70% of patients with PE,
DVT can be found in the lower limbs.

EMBOLUS

• Thrombotic
• Non-thrombotic : Fat, Air, Tumour , Amniotic fluid, IV Drug abusers.

Pathogenesis of Vascular Thrombosis

• Decrease in blood flow below a certain critical level.


• Increase in coagulability of blood.
• Damage of the vessel wall.

RISK FACTORS

• Bed rest • Obesity


• Post-operative • Post-partum
• After severe blood loss and • Malignancy
trauma • DM
• CCP • Pneumonia
• CHF • Debilitating diseases
• Varicose veins • 1ry polycythemia
• Advancing age
Symptoms
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 Dyspnea
 Pleuritic chest pain
 Substernal chest pain
 Cough
 Hemoptysis
 Syncope

Signs

 Tachypnea (≥ 20/min)
 Tachycardia (> 100/min)
 Signs of DVT
 Fever (> 38.5 ºC)
 Cyanosis

Investigation

• ECG :
Signs of RV strain, such as inversion of T waves in leads V1-

V4, a QR pattern I lead V1
 The classic S1Q3T3 type
 Right bundle-branch block
 In a patient with shock or hypotension, the absence of ECG
signs of RV overload or dysfunction excludes PE as a cause of
hemodynamic compromise.
• Echocardiography
• ABG :
 Hypoxemia, Hypocapnia, Non-specific

• Alveolar-Arterial Oxygen Tension Difference:


 Increased Difference
 More Sensitive but Non-specific
• CXR may show:
 Elevated Diaphragm,
 Collapse/ Atelectasis
 Consolidation / Wedge-shaped opacity

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 Small pleural effusion
 Elevated diaphragm
 Pleural based opacities with convex medial margins are also
known as a Hampton's Hump
 Westermark sign : Dilatation of pulmonary vessels proximal
to embolism along with collapse of distal vessels, often with a
sharp cut off.
• Isoenzyme Pattern(Troponin T,I)
 To distinguish PE from MI
• Leucocytic Count:
 < 15 000, If over 15 000, consider Bacterial Sepsis

• Compression ultrasonography and computed tomographic venography


• D-dimer :

 Plasma D-dimer levels, a degradation product of crosslinked


fibrin, are elevated in the presence of an acute clot because of
simultaneous activation of coagulation and fibrinolysis.
 The negative predictive value of D-dimer is high.
 The specificity of fibrin for VTE is poor because fibrin is
produced in a wide variety of conditions, such as cancer,
inflammation, infection and necrosis

• Ventilation-perfusion scintigraphy (V/Q scan)

 The basic principle of the test is based on an intravenous


injection of technetium (Tc)-99m labeled macroaggregated
albumin particles, which block a small fraction of pulmonary
capillaries, and thereby enable scintigraphic assessment of lung
perfusion at tissue level.
 Perfusion scan are combined with ventilation studies for which
multiple tracers, such as xenon (Xe)-133 gas or Tc-99 labeled
aerosols is used.
 A normal V/Q scan excludes pulmonary embolism

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 The combination of a high-probability ventilation-perfusion
scan plus a high clinical suspicion is diagnostic for pulmonary
embolism.
 A low-probability or normal lung scan with a low clinical
suspicion makes the diagnosis of pulmonary embolism unlikely

• Computed tomography

 Since the introduction of multidetector CT (MDCT), CT


angiography has become the method of choice for imaging the
pulmonary vasculature for suspected PE. It has sensitivity and
specificity of about 90% for detecting pulmonary emboli, as it
allows visualization of the pulmonary arteries up to the
segmental level.

• Pulmonary angiography

 Pulmonary angiography is a reliable but invasive test and is


useful when results of non-invasive imaging are equivocal.

• MRI / MR Angiogram

 Very good to visualize the blood flow ,Almost similar to


angiogram

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Diagnostic strategies

Suspected high-risk and non-high-risk PE are two distinct situations that


differ in diagnostic strategies.

Suspected high-risk pulmonary embolism:

☼ It is an immediately life-threatening situation and usually patients


present with shock or hypotension (systolic ≤90).

☼ The clinical probability is high and the differential diagnosis includes:


• Myocardial Infarction.
• Dissecting Aortic Aneurysm.
• Peumothorax.
• Major Pulmonary Collapse.
• Shock.
• Perforating Peptic Ulcer.
• Acute Pancreatitis.

Hence, the most useful initial test is ECG, which will usually show indirect
signs of acute pulmonary hypertension and right ventricular overload if
acute PE is the cause of hemodynamic consequences.

Suspected non high-risk pulmonary embolism:


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☼ Clinical Probability of PE
• High Probability ( 90% ):

 Presence of at least one of three symptoms ( Sudden onset


Dyspnea, Chest Pain, or Fainting ) not explained otherwise and
associated with :

 (1) Any two of the following abnormalities:

o ECG signs of RV overload,


o Radiographic signs of Oligemia, Amputation of
hilar artety, or Pulmonary consolidations
compatible with infarction;

 (2) Any one of the above three radiographic abnormalities.

• Intermediate Probability (50%):

 Presence of one of the above symptoms, not explained


otherwise
 But not associated with the above ECG and Radiographic
abnormalities, or associated with ECG signs of RV overload
only.

• Low Probability (10%):

 Absence of the above three symptoms,


 Or identification of an alternative diagnosis that may account
for their presence (e.g.,exacerbation of COPD, Pneumonia,
Lung Edema, Pneumothorax, Myocardial Infarction, and
others).

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Treatment
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☼ Thrombolysis

Heparin should not be infused concurrently with streptokinase or urokinase,


but it can be given during alteplase administration.

☼ Contraindications of fibrinolytic therapy

☼ Surgical pulmonary embolectomy:

It has been reserved for:


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 Patients with PE who may necessitate cardiopulmonary resuscitation,
 Patients with contraindications or inadequate response to thrombolysis

☼ Percutaneous catheter embolectomy:

 Catheter embolectomy of proximal pulmonary artery clots may be


considered as an alternative to surgical treatment in high-risk PE
patients when thrombolysis is absolutely contraindicated or has failed.

Initial anticoagulation:

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 Anticoagulation with parenteral anticoagulants should be continued
for at least 5 days and vitamin K antagonists (VKA) should be
initiated as soon as possible and preferably on the same day as the
initial anticoagulant.

 Parenteral anticoagulants should be stopped when the international


normalized ratio (INR) lies between 2 and 3 for at least two
consecutive days.

 If warfarin is used, a starting dose of 5 or 7.5 mg is preferred

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☼ Long term anticoagulation and secondary prophylaxis:

☼ Venous filters:

 Venous filters may be used when there are absolute contraindications


to anticoagulation and a high risk of VTE recurrence.
 Permanent IVC may provide lifelong protection against PE, however
they are associated with complications (eg, thrombosis and recurrent
DVT )
 At present, the systematic use of venous filters is not recommended in
the general population with VTE.

Specific problems
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Pregnancy

 Plasma D-dimer levels increase physiologically throughout


pregnancy. A normal D-dimer level has the same exclusion value for
PE in pregnant women

 The radiation dose of chest CT delivered to the fetus is lower than that
of the perfusion lung scintigraphy in the first or second trimesters and
that it can be performed safely.

 The treatment of PE in pregnancy is based mainly on heparin, either


unfractionated or LMWH, neither of which crosses the placenta nor is
found in the breast milk.

 The heparin treatment should be given throughout the entire


pregnancy.

 VKA antagonists crosses placenta and are associated with a well-


defined embryopathy.

 Epidural anesthesia cannot be used unless LMWH is discontinued at


least 12 hours before an epidural approach and treatment can be
resumed 12-24 hours after withdrawal of the epidural catheter.

 After delivery, heparin may be replaced by VKA. Anticoagulant


treatment should be administered for at least 3 months after delivery
and VKA can be given even to breast-feeding mothers.

 Streptokinase does not cross the placenta and at the time of delivery,
thrombolytic treatment should not be used except in extremely severe
cases and if surgical embolectomy is not available.

 Indications for cava filters in pregnant women are similar to those in


other patients with PE.

Malignancy

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 Malignancy is a major predisposing factor for the development and
recurrence of VTE.
 In cancer patients with confirmed PE, LMWH should be considered
for the first 3-6 months of treatment and anticoagulant treatment
should be continued indefinitely.

Right heart thrombi

 Thrombolysis and embolectomy are probably both effective whereas


anticoagulation alone appears less effective.

Heparin-induced thrombocytopenia (HIT)

 It is caused by immunoglobulin G directed against the platelet factor


4-heparin complex.
 It is type II immunological reaction and usually occurs between 5 and
14 days after exposure to heparin or earlier in cases of re-exposure.
 Treatment consists of discontinuation of heparin and the patient
should be switched an alternative anticoagulant, if anticoagulation, is
still required.
 Direct thrombin inhibitors, such as lepirudin and argtroban are
effective agents.
 Fondaparinux may be used in the management of HIT type II.

Chronic thromboembolic pulmonary hypertension (CTEPH)

 Pulmonary endarterectomy should be considered as a first-line


treatment whenever possible. Drugs targeting the pulmonary
circulation are currently being assessed.

Non-thrombotic pulmonary embolism


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Septic embolism

 Septic pulmonary emboli are most commonly associated with tricuspid


valve endocarditis, mainly occurring in drug addicts.
 Typically, patients presented with fever, cough and hemoptysis.

Intravascular foreign bodies

 They include broken catheters, guidewires and vena cava filters and more
recently coils for embolization
 Intravascular retrieval using snares is frequently successful.

Fat embolism

 It is associated with trauma and several other surgical and medical


conditions.
 The presentation may be fulminating but more usually, the onset is gradual
with hypoxemia, neurological symptoms, fever and a petechial rash,
typically 12-36 hours after injury.
 Treatment is non-specific and supportive.

Venous air embolism

 Patients should be placed in the left lateral decubitus head-down position.

Amniotic fluid embolism

 Dyspnea, cyanosis and shock that are abrupt in onset classically progress to
cardiopulmonary collapse.
 The diagnosis is one of exclusion and treatment is supportive.

Talc embolism

Usually in intravenous drug addicts.

Tumor embolism

 Pulmonary tumor embolism radiologically mimics pneumonia, tuberculosis


or interstitial lung disease.
 There are reports of limited success with chemotherapy.

NB:
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PE , Clinical Features

• Massive Pulmonary Embolism ( MPE )


• Pulmonary Infarction ( PI )
• Obliterative Pulmonary Hypertension

Pulmonary Infarction, Pathology

• Blood Vessels: Engorgement, Hemorrhage from distended necrotic


capillaries, Granulation tissue repair , Fibrous scar
• Bronchioles: usually survive, may turn bronchiactatic
• Bacterial Infection : Abscess Source : embolus, blood-borne, bronchi
• Pleural Complications : Pleurisy, Pleural effusion, Empyema.

C/P
• Pleuritic chest pain, Pleural rub, Pleural effusion
• Hemoptysis: in only 50% of cases
• Tachcardia( more than 100/ min ) Tachypnoea
• Jaundice, Cyanosis
• Locally: No Physical Findings, Consolidation, Diminished Intensity
of Breath Sounds, Crepitus, Wheezing Chest
• Pleural Rub
• Signs of Pleural Effusion
• With Infection: Worsening of the Clinical Status: Abscess or
Empyema
• Persistent Fever, Malaise, Sweating
• Increasing Pulse Rate
• Leucocytosis more than 20 000
• Chest X-Ray

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