What you see is what you diagnose: Staging the severity of acute pulmonary embolism with computed tomography pulmonary angiography

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1 What you see is what you diagnose: Staging the severity of acute pulmonary embolism with computed tomography pulmonary angiography Poster No.: A-099 Congress: ECR 2010 Type: Invited Speaker Topic: Emergency Radiology Authors: G. Staskiewicz; Lublin/PL Keywords: pulmonary embolism, rght ventricular dysfunction, computed tomography DOI: /ecr2010/A-099 Any information contained in this pdf file is automatically generated from digital material submitted to EPOS by third parties in the form of scientific presentations. References to any names, marks, products, or services of third parties or hypertext links to thirdparty sites or information are provided solely as a convenience to you and do not in any way constitute or imply ECR's endorsement, sponsorship or recommendation of the third party, information, product or service. ECR is not responsible for the content of these pages and does not make any representations regarding the content or accuracy of material in this file. As per copyright regulations, any unauthorised use of the material or parts thereof as well as commercial reproduction or multiple distribution by any traditional or electronically based reproduction/publication method ist strictly prohibited. You agree to defend, indemnify, and hold ECR harmless from and against any and all claims, damages, costs, and expenses, including attorneys' fees, arising from or related to your use of these pages. Please note: Links to movies, ppt slideshows and any other multimedia files are not available in the pdf version of presentations. Page 1 of 38

2 Learning objectives CTPA allows an objective staging of obstruction of pulmonary arteries in patients with acute pulmonary embolism (PE). It may also indicate the right ventricular dysfunction (RVD) in the course of acute pulmonary embolism, as well as visualize the background of thrombotic event. The presentation covers following topics: Background information about patients, treatment and prognosis in acute PE Scoring systems used for objective staging of obstruction of pulmonary arteries CT signs of right ventricular dysfunction in the course of acute PE. Images for this section: Page 2 of 38

3 Fig. 1 Page 3 of 38

4 Main Acute pulmonary embolism (PE) presents with a wide spectrum of clinical conditions, which range from clinically irrelevant isolated subsegmental embolism, to a lifethreatening central embolism, resulting with hypotension and cardiogenic shock. Right ventricular dysfunction (RVD) is an important prognostic factor in patients with PE, and patients with RVD require an aggressive treatment. Profile of patients with suspected acute PE Figure 1 on page 11 presents CTPA referrals for suspected acute PE in 2009 at I Department of Radiology, Medical University of Lublin. Figure 2 on page 15 shows the age range of patients with suspected PE diagnosed at I Department of Radiology, Medical University of Lublin. Risk factors History of venous thromboembolism (VTE), surgery within the previous 4 weeks, current estrogen use, hypoxemia, active or metastatic cancer, immobilization, age, tachycardia, history of thrombophilia, family history of VTE, female sex, smoking, substernal chest pain, tachypnea and dyspnea [1]. Suspected pulmonary embolism management: Wells score / Revised Geneva score Wells score [2]: Revised Geneva score [3]: Clinical signs and symptoms of deep Age > 65 years: 1 venous thrombosis: 3 Previous DVT/PE 3 An alternative diagnosis likely than PE: 3 Surgery (under general anesthesia) or Heart rate > 100: 1.5 fracture (of the lower limbs) within 1 month: 2 Immobilization or surgery in the previous 28 days: 1.5 Active (considered cured <1 year) malignancy: 2 Previous DVT/PE: 1.5 Unilateral lower limb pain: 3 Hemoptysis: 1 Page 4 of 38

5 Current malignancy on page 12 / treated in the last 6 months / palliative: 1 Hemoptysis: 2 Heart rate bpm: 3 Clinical probability: Heart rate >94 bpm: 5 Low <2 total Pain on lower limb deep venous palpation and unilateral oedema: 4 Intermediate 2-6 total High >6 total Clinical probability: Low 0-3 total Intermediate 4-10 total High >10 total Performance of the prediction scores - percentage of confirmed PE [4]: Wells score: Revised Geneva score: Low risk: 8% Low risk: 0% Medium risk: 26% Medium risk:26% High risk:90% High risk:83% Treatment Class I recommendations of European Society of Cardiology, 2008 [5]: High-risk pulmonary embolism: Treatment with unfractionated heparin should be initiated without a delay in patients with high-risk PE (IA) Systemic hypotension should be corrected to prevent progression of RV failure and death due to PE (IC) Vasopressive drugs are recommended for hypotensive patients with PE (IC) Oxygen should be administered in patients with hypoxaemia (IC) Surgical pulmonary embolectomy is a recommended therapeutic alternative in patients with high-risk PE in whom thrombolysis is absolutely contraindicated or has failed (IC) Page 5 of 38

6 Thrombolytic therapy should be used in patients with high-risk PE presenting with cardiogenic shock and/or persistent arterial hypotension (IA) Non-high-risk pulmonary embolism Anticoagulation should be initiated without delay in patients with high or intermediate clinical probability of PE while diagnostic workup is still ongoing (IC) Use of LMWH or fondaparinux is the recommended form of initial treatment for most patients (IA) In patients at high risk of bleeding and in those with severe renal dysfunction, unfractionated heparin with an aptt target range of times above normal is a recommended form of initial treatment (IC) Initial treatment with unfractionated heparin, LMWH or fondaparinux should be continued for at least 5 days and may be replaced by vitamin K antagonists only after achieving target INR levels for at least 2 consecutive days (IA, IC) CTPA protocol for suspected PE [6, numbers in brackets show parameters used at I Department of Radiology, Medical University of Lublin]: 16-MDCT Pulmonary 64-MDCT Pulmonary Angiography Protocol Angiography Protocol Parameter Normal-sized Patient Large Patient Normal-sized >113kg Patient Large Patient >113kg Collimation 1.25/ / / /1.25/2.5 Table speed/ rotation (mm) Pitch 1.375: : : :1 Peak kilovoltage [120] 140[120] Milliamperes [mA modulation] 380[mA modulation] time Rotation (s) Multidetector scanners allow modification on page 12 of the typical protocol, with inclusion veins of lower limbson page 13, abdominal scanning on page 13 or triple rule out on page 14 protocol. Page 6 of 38

7 CTPA-related workload in clinical setting [7]: Figure 8 on page 15 presents number of CTPA examinations for an acute PE performed at I Department of Radiology, Medical University of Lublin. Figure 9 on page 16 presents a summary of CTPA findings in 500 consecutive patients, referred to I Department of Radiology for CTPA due to suspected acute and chronic pulmonary embolism between 2002 and A decrease in confirmed acute PE cases is observed. Alternative diagnoses [7]: pneumonia on page 16 and/or pleuritis on page 17: 12.8% circulatory failure on page 18: 12.8% advanced emphysema on page 19: 6.3% pulmonary fibrosis on page 20: 6.1% neoplasm on page 21: 5.0% other on page 22: 2.1% Additional diagnoses [7] (decreasing frequency within groups): A. Lungs (32% patients): nodules, emphysema, postinflammatory, COPD, tuberculosis, post Rtx on page 23, fibrosis B. Pleura (13% pts): small effusion, focal/generalized thickening, calcification C. Heart and vessels (39%) - cardiac enlargement, coronary / great vessels calcifications, pericardial effusion, LV enlargement, venous thrombosis, intracardiac thrombi on page 24, anomalies, tumors (left atrium on page 25, right atrium on page 26) D. Musculoskeletal (51%): spondyloarthrosis, scoliosis, osteoporosis, posttraumatic, tumors, congenital, thoracic outlet syndrome E. Other (51%): lymphadenopathy, hiatus hernia, thyroid / hepatic / splenic / adrenal pathologies, breast lesions Scoring systems used for objective staging of obstruction of pulmonary arteries Miller score on page 26 [8] Qanadli score on page Mastora score on page 27 [9] 28 [10] Page 7 of 38

8 Miller score defines the 10 segmental arteries are right PA as having nine evaluated for both lungs: major segmental branches: three to the upper lobes three to the two to middle upper lobe lobe or lingula two to middle five to lower lobe lobes. four to the lower lobe A filling defect in segmental Regarding left PA, seven artery is scored 1 point, main branches are and a weighting factor is assessed: assessed for each point, according to perfusion four to the distal to the embolus: upper lobe (two to superior 0 = no distal segments, and filling defect two to lingula) 1 = partial three to the occlusion upper lobe. 2 = complete occlusion. In Miller score, each filling defect of segmental artery is scored 1 point. If a filling defect is proximal to segmental arteries, it receives a score equal to number of segmental arteries distal to the obstruction. A subsegmental embolus is scored as partial occlusion of segmental artery, and is scored 1 point. If a filling defect proximal to segmental arteries, it receives a score equal to number of segmental arteries distal to the Maximum obstruction score obstruction. is 16. Maximum obstruction index is 40. Each element of pulmonary artery is scored separately. Following arteries are assessed: five mediastinal arteries: PA trunk, right PA, left PA and right and left interlobar PAs six lobar arteries (upper lobes, middle lobe or lingula, lower lobes) 20 segmental arteries. Severity of arterial obstruction is weighed with 5-points scale, from 1 (<25% obstruction) to 5 (100% obstruction). Mastora score allows evaluation of central obstruction score (mediastinal and lobar arteries), peripheral score (segmental arteries) and total pulmonary obstruction score. Maximum total obstruction score is 155. Qanadli score (pulmonary obstruction index) above 60% = higher 2-weeks mortality rate[11] pulmonary index below 40% to be a significant prognostic factor of a 3months survival[12] Page 8 of 38

9 Risk of death within 3-months period is 20% in patients with obstruction score of 60%, and 40% in patients with obstruction score of 80-90% obstruction score according to Qanadli and Mastora[13] limited relation between pulmonary obstruction score and patient outcome[14] CT signs of right ventricular dysfunction in the course of acute pulmonary embolism RV short axis diameter and RV/LV ratio on page 30 RV = 40mm vs. 55mm in patients with RVD, 0.83 sensitivity and 0.66 specificity at 43.5mm[15] RV = 40mm: 5% 3-months mortality; RV = 69mm :50% mortality[13] RV/LV > 0.9: high risk of complications in the course of PE [16] RV/LVL > 0.9: one of key risk factors of 30-days mortality [17] RV/LVL = 1.3: a risk of 3-months death is 10% and 50% when RV/LVL equals 2.3 [13] RV/LVL < 1.0 a positive predictive factor of 3-months survival [12] Bowing of the interventricular septum on page 30 to the left observed in massive PE, predictive of subsequent admission to the intensive care unit [18] predictive of short-term death due to PE (low sensitivity, high interobserver variability)[19] indicates PASP of 70mmHg or more [20] Pulmonary artery diameter on page 31 PA in RVD: 38mm, vs. 29mm in normal PASP; sensitivity and specificity for RVD: 0.55, 0.75 respectively at 34mm diameter [15] No significant difference of PA diameters between 3-months survivors and non-survivors [13] useful in a follow-up of pulmonary pressure monitoring in patients with chronic PE after thrombarterectomy [21] Superior vena cava on page 32 SVC = 22mm vs. 28mm in patients with RVD, 0.74 sensitivity and 0.79 specificity at 25mm[15] Page 9 of 38

10 significant difference of SVC diameters between acute pulmonary embolism 3-months survivors and non-survivors mm and 18.9mm, respectively [22] Azygos vein on page 33 AV= 9.25mm vs. 12.5mm in patients with RVD, 0.65 sensitivity and 0.85 specificity at 10mm [15] Mortality significantly higher in patients who died in the course of acute PE, with a risk increased at 13.1mm diameter [13] A recognized sign of pulmonary hypertension in a chronic PE [23]. Coronary sinus diameter on page 34 - a new sign of RVD[15]? CS measure 10mm in normal, and 16mm in RVD, with a cutoff value of 12.5mm possessing 0.94 sensitivity and 0.75 specificity [15] coronary sinus compression on CT is an early specific indicator of cardiac tamponade [24] coronary sinus is wider in patients with atrioventricular nodal re-entry tachycardia comparing to other types of arrhythmia [25] Summary Multislice computed tomography not only allows a reliable imaging of embolic obstruction of pulmonary arteries, but also consists a useful tool for identification of the signs of the right ventricular dysfunction (RVD). The advantage of such approach is, that both RVD and PE signs may be examined during the same examination, while the exposure of to ionizing radiation is not increased. Acknowledgements Grateful acknowledgements are due to Dr. El#bieta Czekajska-Chehab, MD, PhD, for her guidance, steady and critical help with preparing this presentation. I am deeply grateful to Dr. Luiza Grzycka-Kowalczyk, MD, PhD for permission to use her data on additional and alternative diagnoses in patients with suspected PE. Figures are modified schemes from presentation Shortest guide to anatomy of pulmonary arteries evaluated in multislice computed tomography angiography by G. Staskiewicz et al., awarded with Certificate of Merit at ECR 2007 (C-270). Page 10 of 38

11 Images for this section: Fig. 1: CTPA referrals for suspected acute PE in 2009 at I Department of Radiology, Medical University of Lublin. Page 11 of 38

12 Fig. 2: Age range of patients referred for suspected acute PE between to I Department of Radiology, Medical Univeristy of Lublin. Fig. 3: Active malignancy: patient with pheochromocytoma. Page 12 of 38

13 Fig. 4: Modifications of standard CTPA protocol. Fig. 5: CTPA modified by inclusion of venous phase for lower limbs examination. Arrows - venous thrombosis. Page 13 of 38

14 Fig. 6: CTPA range modified by inclusion of abdominal scanning. PE, renal cell carcinoma (white arrow) and infiltration of IVC (green arrows). Page 14 of 38

15 Fig. 7: Triple rule out protocol in patient with alcoholic cardiomyopathy. Concomitant acute pulmonary embolism and obstruction of mesenteric artery with small bowel ischemia. White arrow - PE, green arrow - superior mesenteric artery.curved MPR. Page 15 of 38

16 Fig. 8: Number of CTPA examinations for an acute PE performed at I Department of Radiology, Medical University of Lublin. Fig. 9: A summary of CTPA findings in 500 consecutive patients, referred to I Department of Radiology for CTPA due to suspected acute and chronic pulmonary embolism between 2002 and Page 16 of 38

17 Fig. 10: Pneumonia in patient with suspected PE. Frontal MPR. Page 17 of 38

18 Fig. 11: Pleuritis and lymphadenopathy in patient with chronic circulatory insufficiency, with suspected PE. Page 18 of 38

19 Fig. 12: Pulmonary edema in patient with chronic circulatory insufficiency, with suspected PE. Page 19 of 38

20 Fig. 13: Emphysema in patient with suspected PE. Page 20 of 38

21 Fig. 14: Fibrosis in patient with with suspected PE. Page 21 of 38

22 Fig. 15: A. Breast cancer and pleural effusion in the female patient, with suspected PE. B. Tracheal metastasis. Page 22 of 38

23 Fig. 16: ASD, superior sinus venosus type in the patient with suspected PE. Page 23 of 38

24 Fig. 17: Pulmonary tumour recurrence - infiltration of the left atrium and pulmonary fibrosis following radiotherapy in the patient with PE. Page 24 of 38

25 Fig. 18: A large thrombus in the aneurysm of the left ventricle in the patient with acute PE. Page 25 of 38

26 Fig. 19: Myxoma of the left atrium and mitral valve in the female patient with acute peripheral pulmonary PE. Fig. 20: Pathological mass of RA in a patient with acute PE. Page 26 of 38

27 Fig. 21: Miller score. Explanations in the text. Page 27 of 38

28 Fig. 22: Qanadli score. Explanations in the text. Page 28 of 38

29 Page 29 of 38

30 Fig. 23: Central (a) and peripheral (b) obstrucion score according to Mastora et al. Explanations in the text Fig. 24: Right and left ventricular short axes measured on a reformatted four-chamber view are defined as the largest distance between the interventricular septum and the free wall of ventricle. Page 30 of 38

31 Fig. 25: Frequency of normal configuration interventricular septum, flattening and leftsided bowing in 50 patients with acute PE (own study). (a) Left-sided bowing of IVS in the patient with severe PE (b) The same patient after treatment. Page 31 of 38

32 Fig. 26: Diameter of pulmonary artery measured proximal to its bifurcation. Page 32 of 38

33 Fig. 27: Diameter of superior vena cava measured at the level of arch of azygos vein. Page 33 of 38

34 Fig. 28: Diameter of azygos vein measured at its arch, lateral to the right tracheal wall. Page 34 of 38

35 Fig. 29: Diameter of coronary sinus measured in the axial plane, proximal to its opening, at the level of the right margin of the interventricular septum. Page 35 of 38

36 References 1. Courtney DM et al. Risk factors among patients diagnosed for PE... Ann Emerg Med Dec 31. [Epub ahead of print] 2. Wells PS et al. Derivation of a simple clinical model to categorize patients probability of pulmonary embolism: increasing the models utility with simplired D-dimer. Thromb Haemost 2000; 83: Ten Cate-Hoek AJ, Prins MH. Management studies using a combination of D-dimer test result and clinical probability to rule out venous thromboembolism: a systematic review. J Thromb Haemost 2005; 3: Calisir C et al. Performance of the Wells and Revised Geneva scores for predicting pulmonary embolism. Eur J Emerg Med. 2009;16(1): Torbicki A et al. Guidelines on the diagnosis and management of acute pulmonary embolism; Eur Heart J. 2008; 29, Wittram C. How I Do It: CT Pulmonary Angiography. AJR 2007; 188: Grzycka-Kowalczyk L. Application of multislice CT in patients with clinically suspected PE. PhD thesis. Medical University of Lublin, Miller GA, Sutton GC, Kerr IH et al. Comparison of streptokinase and heparin in treatment of isolated acute massive pulmonary embolism. Br Med J 1971;2: Qanadli SD, El Hajjam M, Vieillard-Baron A et al. New CT index to quantify arterial obstruction in pulmonary embolism: comparison with angiographic index and echocardiography. AJR Am J Roentgenol 2001;176: Mastora I, Remy-Jardin M, Masson P et al. Severity of acute pulmonary embolism: evaluation of a new spiral CT angiographic score in correlation with echocardiographic data. Eur Radiol 2003;13: Wu AS, Pezzullo JA, Cronan JJ et al. CT pulmonary angiography: Quantification of pulmonary embolus as a predictor of patient outcome-initial experience. Radiology 2004: 230: van der Meer RW, Pattynama PMT, van Strijen MJL. Right ventricular dysfunction and pulmonary obstruction index at helical CT: Prediction of clinical outcome during 3 - month follow-up in patients with acute pulmonary embolism. Radiology; 2005: 235: Page 36 of 38

37 13. Ghaye B, Ghuysen A, Willems V et al. Severe pulmonary embolism: Pulmonary artery clot load scores and cardiovascular parameters as predictors of mortality. Radiology 2006; 239(3): Pech M, Wieners G, Dul P et al. Computed tomography pulmonary embolism index for the assessment of survival in patients with pulmonary embolism. Eur Radiol 2007; 17: Staskiewicz G, Czekajska-Chehab E, Przegalinski J et al. Widening of coronary sinus in CT pulmonary angiography indicates right ventricular dysfunction in patients with acute pulmonary embolism. Eur Radiol Jan 13.[Epub ahead of print] 16. Quiroz R, Kucher N, Schoepf UJ et al. Right ventricular enlargement on chest computed tomography prognostic role in acute pulmonary embolism. Circulation 2004; 109: Schoepf UJ, Kucher N, Kipfmueller F et al. Right ventricular enlargement on chest computed tomography: a predictor of early death in acute pulmonary embolism. Circulation 2004; 110: Araoz PA, Gotway MB, Trowbridge RL et al. Helical CT pulmonary angiography predictors of in-hospital morbidity and mortality in patients with acute pulmonary embolism. J Thorac Imaging 2003;18: Araoz PA, Gotway MB, Harrington JR et al. Pulmonary embolism: prognostic CT findings. Radiology 2007;242(3): McLure LER, Peacock AJ. Cardiac magnetic resonance imaging for the assessment of the heart and pulmonary circulation in pulmonary hypertension. Eur Respir J 2009; 33: Heinrich M, Uder M, Tscholl D et al. CT scan findings in chronic thromboembolic pulmonary hypertension. Predictors of hemodynamic improvement after pulmonary thromboendarterectomy. Chest 2005; 127; Ghuysen A, Ghaye B, Willems V et al. Computed tomographic pulmonary angiography and prognostic significance in patients with acute pulmonary embolism. Thorax 2005; 60: Coche E, Verschuren F, Hainaut P et al. Pulmonary embolism findings on chest radiographs and multislice spiral CT. Eur Radiol 2004; 14: Gold MM, Spindola-Franco H, Jain VR et al. Coronary sinus compression: an early computed tomographic sign of cardiac tamponade. J Comput Assist Tomogr. 2008; 32: Page 37 of 38

38 25. Ong MG, Lee PC, Tai CT et al. Coronary sinus morphology in different types of supraventricular tachycardias. J Interv Card Electrophysiol 2006;15: Personal Information Grzegorz Sta#kiewicz I Department of Radiology, Department of Human Anatomy, Medical University of Lublin, Poland grzegorz.staskiewicz@gmail.com Page 38 of 38