SUBJECT SEMINAR

PULMONARY EMBOLISM
18/01/2017
• The term ‘pulmonary embolism’ implies
clinically significant obstruction of a part or the
whole of the pulmonary arterial tree, usually by
thrombus that becomes detached from its site of
formation outside the lung and is swept
downstream until arrested at points of
intrapulmonary vascular narrowing.
 PULMONARY EMBOLISM

Thrombotic Non thrombotic

Embolus from Deep veins Air embolism

Fat embolism
Amniotic fluid
Septic embolism
Tumour embolism
Foreign body
 1,00,000 Deaths/year
( 7% of admission )

Hemodynamically

Stable Unstable
3% 30%
 Autopsy incidence

1% Overall 30% in high risk group

Pathophysiology
Secondary
• Prolonged immobilization
• Myocardial infarction
• Cancer
• Nephrotic syndrome
• Hyperestrogenic state
• Smoking
Clinical features
• Dyspnea is the most frequent symptom, and
tachypnea is the most frequent sign of PE.
• Chest pain
• Cyanosis
• Syncope, hypotension
• Distended neck veins
• Tachycardia
When to suspect ?
• Presence of risk factors for DVT.
• Above clinical features.
• ECG changes.
• ECHO evidence of RV dilatation and
hypokinesia.
ECG
• Sinus tachycardia,
• Atrial arrhythmias,
• Q waves in leads III and aVF (pseudoinfarction),
• S1Q3T3 pattern,
• Qr pattern in V1,
• P pulmonale,
• right-axis deviation and
• Incomplete or complete right bundle-branch
block
2D-ECHO
Diagnosis
• D-Dimer
• Chest Xray
• CT pulmonary angio
• MR pulmonary angio
• Invasive Pulmonary angio
What is the likelihood ?
• Classic Well’s criteria
How to treat ?
• Fibrinolysis
• Embolectomy
• Anticoagulats.
Guidance for the use of thrombolytic therapy for the treatment of venous
thromboembolism; Suresh Vedantham; J Thromb Thrombolysis. 2016; 41: 68–80.
CLASSIFICATION OF PULMONARY
EMBOLISM
• Massive
• Sub massive
• Low risk
Fibrinolysis

• Fibrinolysis refers to the process of fibrin

digestion by the fibrin-specific protease,
plasmin.
Fibrinolytic agents
• Streptokinase- 2,50,000 units over 30 mins

1,00,000 units/Hr for 12 to 24 hours

Adverse effects
• Haemorrhage.
• Allergic reactions
• CVA
Anticoagulation
• Indirect thrombin inhibitors.
• Direct thrombin inhibitors.
• Inhibitors of factor Xa.
• Warfarin.

• Anticoagulation therapy is the cornerstone of PE

treatment and should be initiated immediately,
even while patients with suspected PE are
awaiting the results of confirmatory tests.
Indirect thrombin inhibitors
Heparin
UFH- 80U/Kg Bolus Warfarin 5 mg

18U/Kg/Hr infusion

aPTT- 60-80 sec/ 24 hours INR 2-3

1.5 – 2.5 times control
• A plasma concentration of heparin of 0.2–0.4
unit/mL (by protamine titration) or 0.3–0.7
unit/mL (anti-Xa units) is considered to be the
therapeutic range for treatment of venous
thromboembolic disease.
Adverse effects
• Bleeding
• Hair loss
• Osteoporosis
• Mineralocorticoid deficiency
• Heparin-Induced Thrombocytopenia
Heparin induced thrombocytopenia
• Immune mediated activation of platelet and its
consumption.
• Thrombocytopenia within 5–10 days of exposure
to heparin.
• Decline in baseline platelet count of 50% or
greater.
• Stop heparin.
• Start direct thrombin inhibitors.
Contraindication
• HIT,
• Hypersensitivity
• Active bleeding,
• Hemophilia,
• Significant thrombocytopenia,
• Purpura,
• Severe hypertension,
• Intracranial hemorrhage,
• Ulcerative lesions of the gastrointestinal tract,
• Threatened abortion,
• Advanced renal disease,
• Heparin should be avoided in patients who have
recently had surgery of the brain, spinal cord, or
eye.
Protamine sulfate
• Highly basic
• Positively charged peptide
• 100 units of heparin - 1 mg of protamine sulfate
the rate of infusion should not exceed 50 mg in
any 10-minute period.
• Protamine will not reverse the activity of
fondaparinux.
Mechanism
• Coumarin anticoagulants block the γ-
carboxylation of several glutamate residues in
prothrombin and factors VII, IX, and X as well
as the endogenous anticoagulant proteins C and
S.
• Warfarin prevents reductive metabolism of the
inactive vitamin K epoxide back to its active
hydroquinone form.
Monitoring of warfarin
• Usual starting dose is between 2.5 to 7.5 mg.
• Start along with heparin.
• Not to be started alone.
• Therapeutic INR 2-3
• Duration atleast for 3 months in the presence of
a precipitating event.
• INR once in 2 weeks for 1 month, atleast once in
6 weeks later on.
Direct factor Xa inhibitors
• Fixed dose.
• Monitoring not required.
• Rapid onset of action.
• Short half life.
• Metabolised by cytochrome enzymes in liver.
• Lesser incidence of major bleed.
• Potency same as warfarin.
Limitation
• No antidote.
• Compliance is very important, Therapeutic level
of drug decrease even if single dose is missed.
• Contraindicated if CrCl is < 30ml/min.
• Rivaroxaban T1/2- 5 to 9 hours
• Apixaban T1/2 – 12 hours.
• Edoxaban.
Direct thrombin inhibitors
• Lepirudin – Discontinued in 2012.
• Bivalirudin Parenteral
• Argatroban

• Dabigatran Oral
Dabigatran
• 150mg BD.
• Initial 5 to 7 days of parenteral anticoagulation
is necessary.
• Half life – 15 hours.
• Require no monitoring.
• No antidote.
• Overdose – Hemodialysis.
• Avoided in renal impairment.
Newer modality of treatment
• Catheter directed Thrombolysis and
fragmentation.
Pulmonary Embolism Response to Fragmentation, Embolectomy, and
Catheter Thrombolysis (PERFECT), CHEST 2015; 148 ( 3 ): 667 –
673.
Study done on 101 patients with massive and sub massive
pulmonary embolism.
Differential diagnosis
• Pneumonia,
• Asthma,
• Chronic obstructive pulmonary disease
• Congestive heart failure
• Pericarditis
• Pleurisy
• Costochondritis
• Musculoskeletal discomfort
• Rib fracture
• Pneumothorax
• Acute coronary syndrome
• Anxiety
Venous air embolism
• Indwelling catheters, invasive neck surgeries,
RTA.
• Direct aspiration through central catheter.
• Closed chest cardiac massage.
• 100% oxygen.
• Hyperbaric oxygen therapy.
Fat embolism
Long bone fracture, Liposuction, Lipoinjection
procedures.

Petechiae, Seizures and focal neurologic deficits.

• Although a variety of treatments have been

suggested (e.g., intravenous ethanol, albumin,
dextran, heparin), none has proved effective.
• Supportive care.
Amniotic fluid embolism
• 2.0 per 100,000 deliveries.
• Advanced maternal age, multiparity, premature
placental separation, fetal death, and meconium
staining of amniotic fluid have been associated
with increased risk of amniotic fluid embolism.
 Amniotic fluid
(Thromboplastic activity)

Extensive fibrin deposition in pulmonary

vascular bed

Consumptive coagulopathy
• Treatment is mainly supportive.

• Mortality can be as high as 80%.

Tumour embolism
• Breast, lung, prostate, stomach, and liver cancer.

• Pulmonary microvascular cytology on specimens

aspirated through a wedged pulmonary artery
catheter may demonstrate malignant cells.
• Surgical lung biopsy - In the setting of a primary
malignancy for which effective
chemotherapeutic options are available.

• Treatment is supportive.
References
• Robbins basic pathology, 9th edition.
• Braunwald’s Heart disease, 10th Edition.
• Goldman- Cecil Medicine, 25th edition.
• Fishman’s Pulmonary diseases and disorders, 5th
edition.
• Basic and clinical pharmacology,13 edition.
• CMDT 2016.
THANK YOU