1.PULMONARY THROMBOEMBOLISM

2. History
Susrutha describes swollen painful leg circa 600-1000 BCE
Giovanni battistamargagni recognized blood clots in pulmonary vessels in patients suffering sudden death in 1761
In mid 1800 jean cruveilheir a french pathologist suggested role of venous inflammation& thrombosis
3. Virchow triad
Intimal vessel injury
Stasis
hypercoagulability
4. The classic description of radiographic findings by westermark in 1938
The description of electrocardiographic corpulmonale by Mcginn and white 1935
Echo in the diagnosis of PE by has its origin in case report by Covarrubias & colleagues in 1977
5. --Modifiable Risk Factors for Venous Thromboembolism
Obesity Metabolic syndrome Cigarette smoking Hypertension Abnormal lipid profile High consumption of red meat and low consumption of fish, fruits, and vegetables
6. --Major Risk Factors for Venous Thromboembolism That Are Not Readily Modifiable
Advancing age Arterial disease, including carotid and coronary disease Personal or family history of venous thromboembolism Recent surgery, trauma, or immobility, including stroke Congestive heart failure Chronic obstructive pulmonary disease Acute infection Air pollution Long-haul air travel Pregnancy, oral contraceptive pills, or postmenopausal hormone replacement therapy Pacemaker, implantable cardiac defibrillator leads, or indwelling central venous catheter
7. Hypercoagulable states Factor V Leiden resulting in activated protein C resistance
Prothrombin gene mutation 20210
Antithrombin deficiency
Protein C deficiency
Protein S deficiency
Antiphospholipid antibody syndrome
8. 9. Symptoms Otherwise unexplained dyspnea Chest pain, either pleuritic or atypical Anxiety CoughSigns Tachypnea Tachycardia Low-grade fever Left parasternal lift Tricuspid regurgitant murmur Accentuated P2 Hemoptysis Leg edema, erythema, tenderness
10. 11. --Simplified Wells Criteria to Assess Clinical Likelihood of Pulmonary Embolism
>1 score point = high probability
1 score point = nonhigh probability
SCORE POINTS
DVT symptoms or signs 1
An alternative diagnosis is less likely than PE 1
Heart rate >100/min 1
Immobilization or surgery within 4 weeks 1
Prior DVT or PE 1
Hemoptysis 1
Cancer treated within 6 months or metastatic 1
12. 13. Massive Pulmonary Embolism
Patients with massive PE are susceptible to cardiogenic shock and multisystem organ failure.
Renal insufficiency, hepatic dysfunction, and altered mentation are common findings.
Thrombosis is widespread, affecting at least half of the pulmonary arterial vasculature.
Clot is typically present bilaterally.
Dyspnea is usually the most noticeable symptom;
chest pain is unusual
transient cyanosis is common, and systemic arterial hypotension requiring pressor support is frequent
14. Moderate to Large (Submassive) Pulmonary Embolism
These patients frequently present with moderate or severe right ventricular hypokinesis as well as elevations in troponin, pro-BNP, or BNP, but they maintain normal systemic arterial pressure. Usually, one third or more of the pulmonary artery vasculature is obstructed.
If there is no prior history of cardiopulmonary disease, they may appear clinically well, but this initial impression is often misleading.
They are at risk for recurrent PE, even with adequate anticoagulation.
15. Most survive, but they may require escalation of therapy with pressor support or mechanical ventilation.
Therefore, especially if moderate or severe right ventricular dysfunction persists, one should consider thrombolytic therapy or embolectomy.
If neither thrombolysis nor embolectomy appears warranted, placement of an inferior vena caval filter is controversial but may be employed as a back-up in case heparin anticoagulation fails.
16. Small to Moderate Pulmonary Embolism
This presentation is characterized by normal systemic arterial pressure,
no cardiac biomarker release
normal right ventricular function.
Patients appear clinically stable.
Adequate anticoagulation results in an excellent clinical outcome.
17. Pulmonary Infarction
This syndromeis characterized by pleuritic chest pain that may be unremitting or may wax and wane.
The pleurisy is occasionally accompanied by hemoptysis.
The embolus usually lodges in the peripheral pulmonary arterial tree, near the pleura.
Tissue infarction usually occurs 3 to 7 days after embolism.
The syndrome often includes fever, leukocytosis, elevated erythrocyte sedimentation rate, and radiologic evidence of infarction.
18. Nonthrombotic Pulmonary Embolism
They include fat, tumor, air, and amniotic fluid
Fat embolism syndrome is most often observed after blunt trauma complicated by long bone fractures.
Air embolus can occur during placement or removal of a central venous catheter.
Amniotic fluid embolism may be catastrophic and is characterized by respiratory failure, cardiogenic shock, and disseminated intravascular coagulation.
Intravenous drug abusers sometimes self-inject hair, talc, and cotton that contaminate the drug they have acquired. These patients also have susceptibility to septic PE, which can cause endocarditis of the tricuspid or pulmonic valves.
19. Differential Diagnosis of Pulmonary Embolism
Anxiety, pleurisy, costochondritis
Pneumonia, bronchitis
Myocardial infarction
Pericarditis
Congestive heart failure
Idiopathic pulmonary hypertension
20. Biomarkers for detecting myocardial injury
BNP & NT- Pro BNP
cTroponin T & I
H-FABP (Heart type)
Growth differentiation factor -15
21. Plasma D-Dimer Assay
This blood screening test relies on the principle that most patients with PE have ongoing endogenous fibrinolysis that is not effective enough to prevent PE but that does break down some of the fibrin clot to d-dimers
Although elevated plasma concentrations of d-dimers are sensitive for the presence of PE, they are not specific.
Levels are elevated for at least 1 week postoperatively and are increased in patients with myocardial infarction, sepsis, cancer, or almost any other systemic illness.
Therefore, the plasma d-dimer assay is ideally suited for outpatients or emergency department patients who have suspected PE but no coexisting acute systemic illness.
This test is generally not useful for acutely ill hospitalized inpatients because their d-dimer levels are usually elevated. A normal d-dimer assay appears to be as diagnostically useful as a normal lung scan to exclude PE.
patients with a low clinical probability of PE who had negative d-dimer results, additional diagnostic testing was not necessary.
22. Electrocardiographic Signs of Pulmonary Embolism
Sinus tachycardia
Incomplete or complete right bundle branch block
Right-axis deviation
T wave inversions in leads III and aVF or in leads V1-V4
S wave in lead I and a Q wave and T wave inversion in lead III (S1Q3T3)
QRS axis greater than 90 degrees or an indeterminate axis
Atrial fibrillation or atrial flutter
23. Chest Radiography
A near-normal radiograph in the setting of severe respiratory compromise is highly suggestive of massive PE.
Major chest radiographic abnormalities are uncommon.
Focal oligemia (Westermark sign) indicates massive central embolic occlusion.
A peripheral wedge-shaped density above the diaphragm (Hampton hump) usually indicates pulmonary infarction.
Subtle abnormalities suggestive of PE include enlargement of the descending right pulmonary artery.
The vessel often tapers rapidly after the enlarged portion. PE.
24. 25. Echocardiographic Signs of Pulmonary Embolism
Right ventricular enlargement or hypokinesis, especially free wall hypokinesis, with sparing of the apex (the McConnell sign)
Interventricularseptal flattening and paradoxical motion toward the left ventricle, resulting in a D-shaped left ventricle in cross section
Tricuspid regurgitation
Pulmonary hypertension with a tricuspid regurgitant jet velocity >2.6m/sec
Loss of respiratory-phasic collapse of the inferior vena cava with inspiration
Dilated inferior vena cava without physiologic inspiratory collapse
Direct visualization of thrombus (more likely with transesophageal echocardiography)
26. Chest Computed Tomography
Size, location, and extent of thrombus Other diagnoses that may coexist with PE or explain PE symptoms:
Pneumonia Atelectasis Pericardial effusion Pneumothorax Left ventricular enlargement Pulmonary artery enlargement, suggestive of pulmonary hypertension
Age of thrombus: acute, subacute, chronic
Location of thrombus: pulmonary arteries, pelvic veins, deep leg veins, upper extremity veins
Right ventricular enlargement
Contour of the interventricular septum: whether it bulges toward the left ventricle, thus indicating right ventricular pressure overload
Incidental masses or nodules in lung
27. 28. 29. Magnetic Resonance Imaging
Gadolinium-enhanced magnetic resonance angiography (MRA) is far less sensitive than CT for the detection of PE.
However, unlike chest CT or catheter-based pulmonary angiography, MRA does not require ionizing radiation or injection of iodinated contrast agent.
In addition, magnetic resonance pulmonary angiography can assess right ventricular size and function.
Three-dimensional MRA can be carried out during a single breath-hold and may provide high resolution from the main pulmonary artery through the segmental pulmonary artery branches.
30. Pulmonary Angiography
Invasive pulmonary angiography was formerly the reference standard for diagnosis of PE, but it is now rarely performed.
It is an uncomfortable and potentially risky procedure.
However, pulmonary angiography is required when interventions are planned, such as suction catheter embolectomy, mechanical clot fragmentation, or catheter-directed thrombolysis.
In cases of chronic thromboembolic PE, pulmonary arteries appear pouched. The thrombus usually organizes with a concave edge.
Bandlike defects called webs may be present, in addition to intimal irregularities and abrupt narrowing or occlusion of lobar vessels.
31. Lung scans depend on expert interpretation, and there is a great deal of interobserver variability even among experts.
Only three indications to obtain a lung scan exist: (1) renal insufficiency,
(2) anaphylaxis to intravenous contrast agent that cannot be suppressed with high-dose corticosteroids
(3) pregnancy (lower radiation exposure to the fetus).
32. Contrast Venography
Although contrast phlebography was once the reference standard for DVT diagnosis, venograms are now rarely obtained
. Venography is costly, invasive, and potentially harmful.
It can cause contrast-induced renal failure, anaphylaxis, or chemical phlebitis.
Furthermore, difficulty in interpretation of contrast venograms causes considerable disagreement among experienced readers.
Invasive contrast phlebography is required, of course, for interventional procedures such as catheter-directed thrombolysis, suction embolectomy, angioplasty, stenting, and placement of an inferior vena caval filter.
In patients undergoing total hip or knee replacement, contrast venography is more sensitive than venous ultrasonography for the diagnosis of acute DVT.
33. 34. The Pulmonary Embolism Severity Index
PREDICTORSCORE POINTS
Age,per year Age, in years
Male sex10
History of cancer 30
History of heart failure10
History of chronic lung disease10
Pulse 110/min 20
Systolic blood pressure