Pulmonary Thromboembolism

1. Pulmonary Thromboembolism Prof. Sevda Özdoğan MD Chest Diseases

2. Pulmonary Thromboembolism • Pulmonary embolism is caused by the obstruction of the pulmonary arteries by clots from the veins of the systemic circulation that embolise to lungs • Obstructive material other than blood (fat, amnion fluid etc) can also cause pulmonary embolism in certain cituations but venous thromboembolism (VTE) is the most common cause

3. Epidemiology • In USA there are 300-650.000 new case /year and the incidence rate is higher among older age groups • The mortality rate was reported as 51/100000 in 1995 • Mortality rate is very high in the first hour

4. Among the survivors after the first hour 2/3 of the patients remain undiagnosed • The mortality for this group is around 30% • With the right diagnosis and treatment this rate declines to 3-8% • % 90 of the thrombus comes from the lower extremities

5. Pathophysiology Virchow Triade • Venous stasis • Vascular endothelial (wall) damage • Hypercoagulation

6. Risk factors

8. Testing for genetic risk factors is considered in patients who have: • VTE at a young age • Family history of VTE • No evidence of acquired risk factors • PE that originates from a spontaneous venous thrombosis other than leg vein thrombosis

9. Clinical features and Diagnosis • Clinical suspicion*** • Medical history: • To identify the patient at risk • Family history • Medical or acquired risk factors • Symptomatology:

10. Unexplained acute dyspnea • Tachypnea • Substernal chest discomfort • Pleuretic chest pain • Cyanosis • Shock / sencope • Fever • Hemopthysis • Asymptomatic 97%

11. Physical findings: (nonspecific) • Tachycardia, tachypnea • Pleural rub • Late inspiratory rales, wheese • İncreased pulmonary component of the second heart sound (p2) • Right ventricular S3 • Elevated jugular venous pulse • Tender liver • Fever (in infarction)

12. Diagnostic approach • There are significant difficulties in the accurate diagnosis of pulmonary embolism as there is a broad differential diagnosis. • PE can present in a variety of ways depending on the size, location, number of emboli and the underlying condition of the patient. • Objective diagnostic test result are needed for definite diagnosis of VTE and deep venous thrombosis (DVT)

13. Diagnostic approach • Semptomatology and signs • Chest radiology • Arterial blood gas analysis (ABG) • Electrocardiography • Standard laboratory tests • Echocardiography (Cardiac and venous doppler of the lower extremity) • D-Dimer • Spiral CT • Ventilation / perfusion scan • Pulmoner angiography (gold standard) • MRI

14. Estimating Clinical Probability of Pulmonary Embolism HighRisk factor present(80-100% probable) Otherwise unexplained dyspnea, tachypnea, or pleuriticchest pain Otherwise unexplained radiographic or gas exchange abnormality IntermediateNeither high nor low clinical probability(20-79% probable) LowRisk factor not present(1-19% probable) Dyspnea, tachypnea, or pleuritic pain possibly presentbut explainable by another condition Radiographic or gas exchange abnormality possibly present but explainable by another condition

15. Chest Radiography • Negative chest radiogram is a common presentation so does’t exclude the diagnosis • 80% Abnormal chest radiograph but nonspecific • Peripheral regional oligemia (Westermark’s sign) (7%) • A prominant pulmonary hilus with little tapering of vessels (Fleischner’s sign) (15%) • Peripheral wedge shaped densities (Hampton’s hump) (35%) • Plate like atelectasis • Diaphragmatic elevation (%24) • Pleural effusion (%48)

16. Linear atelectasis Pulmonary infarct

17. Frontal chest radiograph obtained from a patient with an acute pulmonary embolism. The left pulmonary artery is enlarged (small arrow), and a wedge-shaped peripheral opacity is present at the left costophrenic angle (large arrow)

18. ABG Analysis • Hypoxemia, hypocapnia and respiratory alcalosis • PaO2 <%80 • PaO2 may be normal in submassive embolism if no underlying pulmonary disease is present • (A-a)O2 gradientis increased in almost all the patients

19. ECG • Abnormalities of ECG are nonspecific • Acute right ventricular strain in massive embolism • Sinus tachicardia • Negative T wave and/or ST segment depression in leads V1-3 • S1Q3T3 patern (Deep S wave in lead D1, deep Q wave in lead D3, inverted T waves in D3) • Right bundle branch block (complete or incomplete) • P-pulmonale • Changes can be similar to MI

20. Standard laboratory tests • Nonspecific changes • WBC can be slightly elevated • LDH, bilirubine can be slightly elevated • D-Dimer (fibrin degradation product) can be elevated • ELISA or Latex agglutination • Sensitivity % 95-97 but specificity is low • <500 ng/ml PE can be excluded if there is also low clinical probability • Elisa is more sensitive but slow compared to Latex

21. ECHOCARDIOGRAPHY (Doppler) • Can be performed rapidly at the bedside • Features that suggest acute massive PE include • A dilated, hypokinetic right ventricle • With the absence of right ventricular hypertrophy • Distortion of the interventriculer septum toward the left ventricle • Tricuspit regurgitation the elevation of pulmonary artery pressure • Identified trombi in the central pulmonary arteries • Absence of significant pathologic left ventricular conditions

22. Spiral Computed Tomography Angiography (SCTA) • Allows rapid investigation of the pulmonary vasculature at peak contrast opasification within a single breath hold • Three dimentional reconstruction is possible • Sensitivity and specificity is around 90% up to subsegmental defects • May demonstrate or exclude other abnormalities in the lung • Bolus contrast is used for the visualization of the pulmonary vasculature • Filling defects are diagnostic

23. Partial filling defect in right middle lobe and lover lobe artery Wedge shaped infiltration on the right upper lobe posterior segment

24. Sagital-oblique CT image showing thrombus narrowing left lover lobe pulmonary artery

26. Ventilation-Perfusion Scintigraphy • Detection of the perfusion abnormalities subsequent to the embolic event • Classically to display that a segment distal to an obstructing embolus is not perfused but is still ventilated • 99Tc is usually used for perfusion and 133Xe for ventilation scaning. The two studies are analysed together. • In clinical practice the results of V/Q scintigraphy are interpreted together with the clinical estimate of the likelihood of acute PE • A normal V/Q virtually excludes clinically relevant PE

27. Patient with multiple embolisms in both lungs: segmental mismatch defect in left lung was detected by both SPECT (A and B) and planar scintigraphy (C and D). Defects are marked by arrows in B and D. Subsegmental mismatch defects are present in right lung. CT angiography found thrombotic clots in branches of middle lobe artery and both lower lobe arteries

28. Estimate of the likelihood of PE • Normal Perfusion (Q): exclude PE • Q defects—Ventilation (V) is normal on these regions: (V/Q mismatch defect) High probability of PE • If Chest x ray is normal on the regions of V/Q mismatch: higher probability • If V/Q mismatch areas are segmental or larger: higher probability • Q defects—V defect on these regions: (V/Q match defect) Low probability, undetermined

29. MRI • Magnetic resonance angiography with the use of contrast material can demonstrate the pulmonary arteries beyond the segmental level • A potential advantage is that it allows the study of the pulmonary arteries and the deep veins of the lower extremities within a single examination

30. Pulmonary Angiography (gold standard) • Detects emboli in the subsegmental or even more peripheral arteries • Unfortunately it is invasive and there is lack of availability in an urgent investigation • Can be used if V/Q scan is nondiagnostic and the clinical probability is high • Not performed if perfusion scintigraphy is normal • Mortality %0,5 • Major complications %0,4

31. Deep Venous Thrombosis (DVT) • Compression ultrasound • Doppler ultrasonography • Venography (gold standard)

32. Suspect Pulmonary Embolism ? Give heparin IV and order V/Q scan BT Low V/Q probability,low clinical probability Intermediate V/Q probability, Low or high V/Q prob with discordant clinical probability High V/Q probability +high clinical probability BT (-) BT (+) BT (-) high cl prob. _ + No treatment Leg Ultrasound Treat + PulmonaryAngiography Probability V/Q Clinical 3. Low High 4. Mid Mid / High 5. High Low / Mid Probability V/Q Clinical 1. Low Mid 2. Mid Low Am J Respir Crit Care Med. Vol 159: 1-14; 1999

33. Treatment of PTE and DVT • Supportive treatment • Oxygen • Intravenous fluid • Vasopressor agents • Resuscitary measures depending on the clinical status of the patient • Anticoagulant therapy • Unfractionated heparin (UFH) • Low molecular weight heparin (LMWH) • Oral anticoagulants (Warfarin) • Thrombolytic treatment • Vena Cava Filters • Surgical treatment

34. Treatment duration • Reversible risk factor, first event, age<60 : 3-6 months • Reversible risk factor, first event, age>60: 6-12 months • First event, unknown risk factor: 6-12 months • Recurrent event: >12months- life long • Irreversible risk factor, first event: >12 months- life long

35. Primary Prevention • Determined by the thrombotic risk of the clinical situation in conjunction with the patients profile of risk factors • Ortopedic surgery (post-traumatic) • ICU • Neurosurgery carry the highest risk • LMWH or UFH can be used • LMWH’s can be used preoperatively safely • Prophylaxis should be continued up to 4 weeks after surgery

36. Patients with congenital risk factors: • Homozygot : Lifelong anticoagulation • Heterozygot: During the periods of high risk • Recurrent embolism or continious risk factor: lifelong anticoagulation

37. Non medical Prophylaxis • Graduated compression stockings • İntermittent pneumatic compression • Foot impulse pumps Can be used for patients who have contraindications to anticoagulants.