Outcome of surgical embolectomy in patients with massive pulmonary embolism with and without cardiopulmonary resuscitation

Introduction

Despite advances in diagnostics and therapeutics, pulmonary embolism (PE) is one of the most critical cardiovascular diseases and is associated with high morbidity and mortality [1–4]. Massive PE is a life-threatening condition with a mortality rate of 31–70% [5, 6]. Rapid intervention is necessary to restore pulmonary blood flow and stabilize the hemodynamic state. Pulmonary embolism is usually treated medically with anticoagulation; thrombolysis and surgical embolectomy are other treatments reserved for patients with massive PE and hemodynamically unstable patients [7, 8].
Today surgical embolectomy is a therapeutic option for patients who present with cardiogenic shock, have contraindications to thrombolysis or who have persistent hypotension after initial therapy [9, 10]. Previously, some researchers have reported that surgical embolectomy had a high mortality rate ranging from 16% to 64% [4]. By improvement in surgical techniques and experience of surgeons, recent studies have shown favorable results in massive PE with preserved hemodynamics with evidence of moderate to severe right ventricle (RV) dysfunction on echocardiography [11–17].

Aim

We conducted a retrospective single-center study of patients who underwent surgical embolectomy to investigate the efficacy of this treatment in PE patients.

Material and methods

In this single-center, retrospective study, 36 patients over 18 years old with a definite diagnosis of acute PE who underwent surgical pulmonary embolectomy from January 2011 to January 2016 were included. The study protocol was approved by the Tabriz University of Medical Sciences institutional review boards.
Patients’ clinical records were reviewed and demographic information, initial presentation and symptoms, risk factors, methods of diagnosis, localization of thrombotic material, indication for operation, mortality, and morbidity were recorded. Pulmonary embolism diagnosis was confirmed by 36-slice computed tomography (CT) angiography in all patients. Patients with persistent O2 saturation ≤ 90% and/ or systolic blood pressure (BP) ≤ 90 or a drop of > 40 mm Hg from baseline BP lasting for 15 min or requiring inotropic support with concomitant massive PE findings in computed tomography (CT) angiography (new thrombus formation in the common pulmonary artery trunk or right or left main pulmonary artery) and RV enlargement received fibrinolytic therapy as the first line management and surgical embolectomy was done when dyspnea, low systolic BP and/or O2 saturation ≤ 90% continued after fibrinolytic therapy (defined as fibrinolytic therapy failure) or when there was a contraindication to fibrinolytic therapy. We used intravenous fibrinolytic therapy and interventional angiography was not done for patients. Low molecular weight or unfractionated heparin was administered to normotensive patients with O2 saturation > 90%. A loading dose of 250,000 U of streptokinase over 30 min following 100,000 U/h for 24 h was used for most patients when fibrinolytic therapy was indicated. Recently fibrinolytic therapy protocol in our center has been changed to 15 mg reteplase in two separate stat doses with a 30-minute interval, which has been used in 5 patients.

Surgical technique

The surgery was performed within 72 h of the initial thrombolysis through median sternotomy. After cardiopulmonary bypass a longitudinal incision was performed on the main pulmonary artery trunk, extending the incision into the left pulmonary artery, and additional arteriotomy of the right pulmonary artery was performed when indicated. Using forceps, thrombus removal was started, continuing to extract thrombi inside segmental pulmonary arteries if necessary. In some patients and after inducing moderate hypothermia, extracorporeal circulation was stopped for up to 30 min for better thrombus visualization and its complete extraction.

Post-intervention treatment

All patients received IV unfractionated heparin immediately after surgery or 2–4 h after streptokinase when the activated partial thromboplastin time (aPTT) reached < 80 ms, or 15 min after recombinant tissue plasminogen activator (rTPA) therapy with a therapeutic aPTT ratio of two to three times the control value. Results are expressed as mean ± SD or percentage.

Results

Thirty-six patients including 14 (38.9%) male and 22 (61.1%) female patients with a mean age of 50.80 ±18.89 years were evaluated. Mean time from admission to embolectomy was 6.58 ±1.13 h. Risk factors for development of PE are presented in Table I. Common risk factors were major surgery within 3 months and deep vein thrombosis. The most common presenting symptoms of patients were dyspnea, followed by chest pain and syncope (Tab. II).
Mean CPKMB, CPK and CTnI were 30.47 ±19.75, 93.58 ±26.82 and 0.45 ±0.16, respectively. Mean systolic and diastolic blood pressure were 95.37 ±16.71 and 59.37 ±11.41 mm Hg, respectively. Mean heart rate was 103.35 ±17.63 bpm.
ECG findings included T invert in V1–V3 (15 cases, 41.7%) and S1Q3T3 pattern (16 cases, 44.4%). Echocardiography findings showed RV enlargement in 29 (80.6%) cases and RV dysfunction in 25 (69.4%). Mean RV size was 4.33 ±0.95. Mean left ventricular ejection fraction (LVEF) was 50.75 ±6.01%.
Mean duration of hospitalization was 14.76 ±8.69 days and mean operation duration was 4.47 ±1.54 h. Indications for surgical embolectomy are summarized in Table III.
Ten (27.8%) patients died during the operation including 3 cases with cardiopulmonary resuscitation (CPR) prior to surgery and 2 cases with severe cardiogenic shock. One patient with active bleeding and one with transit clot in the RV developed severe cardiogenic shock before surgery and the operation was done for them before hemodynamic stability. The mortality rate of surgical embolectomy was 27.7%. After excluding the 5 above-mentioned cases, the mortality rate was 16.1%. Long duration of CPR and cardiogenic shock and their induced ischemic state can result in irreversible cardiac damage and death regardless of successful or unsuccessful embolectomy. We excluded these patients to determine the exact surgical embolectomy mortality. Causes of death were right ventricle failure in all cases except 1 patient with post-operative acute renal failure and preoperative distal emboli resulting in lower extremity gangrene.
Patients who survived were followed for 6 months. The mortality rate during follow-up was 15.4%; all 4 patients died due to metastatic cancer. No recurrent PE was detected.

Discussion

Pulmonary embolism is a challenging medical condition with significant morbidity and mortality. Massive PE is life threatening and requires aggressive management. Thrombolysis is the treatment of choice for massive PE [17]. Today surgical embolectomy is the second choice of treatment, and due to its acceptable outcomes its use is increasing for the management of massive and sometimes sub-massive PE [18, 19].
We evaluated 36 cases with massive PE undergoing primary or rescue surgical embolectomy. Mortality in our study was 27.7%, and after excluding patients under CPR or those with a prolonged state of shock mortality decreased to 16.1%, which are similar to most previous studies. Recent studies have indicated lower mortality and morbidity rates for surgical embolectomy with a mortality rate between 3.6% and 29% [17–19]. While in stable patients mortality is very low, in unstable patients the situation is different. Neely et al. reported the largest case series of surgical embolectomy of 115 patients with submassive and massive PE with a mortality rate of 6.6% for all and 10.2% for massive PE [17]. Alizadeh et al. studied 12 massive PE patients and reported a mortality rate of 16.6%. One of their patients died during the surgery and one in the intensive care unit [11].
It is reported that the mortality rate increases if CPR is required. Patients with massive PE, who presented with cardiac arrest and required CPR, had a mortality of up to 70% within the first hour of presentation [14, 20]. A mortality rate of 57% for patients who required CPR was reported by Dauphine and Omari [20], while Yavuz et al. [14] reported a higher mortality rate of 75% for patients with CPR.
Janata et al. reported a mortality rate of 85–95% in patients with cardiac arrest [21]. Leitner et al. reported that the cause of this high mortality could be coagulopathy similar to disseminated intravascular coagulation (DIC) [22].
Hence, the underlying cause of PE should be evaluated in these patients. In our study, ten patients died during the surgery; three of them had CPR prior to surgery. In fact, the mortality rate for patients requiring CPR before surgery was 100%. Previous reports have noted that preoperative cardiogenic shock is an important predictor of survival after massive PE [8]. In our study also 2 patients with prolonged cardiogenic shock died because of RV failure.
It seems that because of many confounding factors such as duration of CPR, the experience of the CPR team, the time between cardiac arrest and operation [8], the distance of the operating room from the emergency room, and multi-organ damage induced by a state of shock, reporting the exact mortality for surgical embolectomy in very unstable patients is not easy.
Using RV support after embolectomy with delay sternal closure may be helpful in patients with post-operative RV failure – a technique not available in some centers [23]. Most of the patients in our study died because of post-operative RV failure. Right ventricle failure was the main cause of surgical embolectomy failure and mortality in our study. Continuous RV failure despite adequate embolectomy can be explained by several factors. In healthy people, the RV cannot continue contraction against a mean pressure > 40 mm Hg [24]. In some cases a large burden of clot in small distal arteries, not suitable for embolectomy, especially when it affects both lungs, can still prevent RV afterload reduction despite adequate proximal embolectomy.
Right ventricle ischemia seems to be the second most important factor. By increasing RV end diastolic pressure the RV blood supply is decreased. Possible coronary artery obstruction and hypotension aggravate the insufficient blood supply [25]. The key point in this setting is the time. If surgical embolectomy is done when irreversible RV ischemic damage happens, the mortality will be high. Also infarct size is important. La Vecchia et al. found that ctnI was the strongest independent predictor of death in massive PE [26]. Hence, we need more investigations to define the golden time for surgical embolectomy in those with a state of shock and cardiac arrest undergoing CPR.
We observed a success rate of 84.6% during 6-month follow-up. Similar to our findings, Leacche et al. [4] reported 3-year survival of 83% in 47 patients; and Fukuda et al. [27] also reported 10-year survival of 84% in 19 patients.
Prompt removal of emboli can save the life of a patient with acute massive PE. So, rapid evaluation of patients with massive PE, especially before cardiac arrest starts, would possibly increase the success rate.
This study has several limitations. This was a retrospective nonrandomized study and all data were collected from medical records, so in some cases laboratory findings were not available. The study included a small sample size of massive PE and no submassive cases, which limits its generalizability. As an observational study, there were no other nonsurgical groups for comparison.

Conclusions

Although surgical embolectomy is performed mostly for high-risk patients, it has good in-hospital and excellent mid-term outcomes.

Disclosure

Authors report no conflict of interest.

References

1. Casazza F, Becattini C, Bongarzoni A, Cuccia C, Roncon L, Favretto G, Zonzin P, Pignataro L, Agnelli G. Clinical features and short term outcomes of patients with acute pulmonary embolism. The Italian Pulmonary Embolism Registry (IPER). Thromb Res 2012; 130: 847-852.
2. Lankeit M, Konstantinides S. Thrombolysis for pulmonary embolism: past, present and future. Thromb Haemost 2010; 103: 877-883.
3. Agnelli G, Becattini C. Acute pulmonary embolism. N Engl J Med 2010; 363: 266-274.
4. Leacche M, Unic D, Goldhaber SZ, Rawn JD, Aranki SF, Couper GS. Modern surgical treatment of massive pulmonary embolism: results in 47 consecutive patients after rapid diagnosis and aggressive surgical approach. J Thorac Cardiovasc Surg 2005; 129: 1018-1023.
5. Wu AS, Pezzullo JA, Cronan JJ, Hou DD, Mayo-Smith WW. CT pulmonary angiography: quantification of pulmonary embolus as a predictor of patient outcome: initial experience. Radiology 2004; 230: 831-835.
6. Santos Martinez LE, Uriona Villarroel JE, Exaire Rodriguez JE, Mendoza D, Martínez Guerra M, Pulido T, Bautista E, Castańón A, Sandoval J. Massive pulmonary embolism, thrombus in transit, and right ventricular dysfunction. Arch Cardiol Mex 2007; 77: 44-53.
7. Vohra HA , Whistance RN, Mattam K, Kaarne M, Haw MP, Barlow CW, Tsang GM, Livesey SA, Ohri SK. Early and late clinical outcomes of pulmonary embolectomy for acute massive pulmonary embolism. Ann Thorac Surg 2010; 90: 1747-1752.
8. Goldhaber SZ. Surgical pulmonary embolectomy: the resurrection of an almost discarded operation. Tex Heart Inst J 2013; 40: 5-8.
9. Kearon C, Akl EA, Comerota AJ, Prandoni P, Bounameaux H, Goldhaber SZ, Nelson ME, Wells PS, Gould MK, Dentali F, Crowther M, Kahn SR. Antithrombotic therapy for VTE disease: antithrombotic therapy and prevention of thrombosis, 9th ed: American College of Chest Physicians evidence-based clinical practice guidelines. [Published erratum appears in Chest 2012; 142: 1698-704]. Chest 2012; 141 (2 Suppl): e419S-e496S.
10. Konstantinides SV, Torbicki A, Agnelli G, Danchin N, Fitzmaurice D, Galiè N, Gibbs JS, Huisman MV, Humbert M, Kucher N, Lang I, Lankeit M, Leka- kis J, Maack C, Mayer E, Meneveau N, Perrier A, Pruszczyk P, Rasmussen LH, Schindler TH, Svitil P, Vonk Noordegraaf A, Zamorano JL, Zompatori M; Task Force for the Diagnosis and Management of Acute Pulmonary Embolism of the European Society of Cardiology (ESC). 2014 ESC Guidelines on the diagnosis and management of acute pulmonary embolism. Eur Heart J 2014; 35: 3033-3069.
11. Alizadeh K, Tabari M, Shirinzadeh Feizabadi A, Izanloo A. A report on emergent pulmonary embolectomy. J Cardiothorac Med 2016; 4: 411-414.
12. Yi I, Park JC, Cho KS, Kim BS, Kim SC, Kim DH, Kim JH, Youn HC. Pulmonary thromboembolectomy for acute pulmonary thromboembolism. Korean J Thorac Cardiovasc Surg 2011; 44: 343-347.
13. He C, Von Segesser LK, Kappetein PA, Mestres CA, Smith JA, Choong CKC. Acute pulmonary embolectomy. Eur J Cardiothorac Surg 2013; 43: 1087-1095.
14. Yavuz S, Toktas F, Goncu T, Eris C, Gucu A, Ay D, Erdolu B, Tenekecioglu E, Karaagac K, Vural H, Ozyazicioglu A. Surgical embolectomy for acute massive pulmonary embolism. Int J Clin Exp Med 2014; 7: 5362-5375.
15. Hartman AR, Manetta F, Lessen R, Pekmezaris R, Kozikowski A, Jahn L, Akerman M, Lesser ML, Glassman LR, Graver M, Scheinerman JS, Kalimi R, Palazzo R, Vatsia S, Pogo G, Hall M, Yu PJ, Singh V. Acute surgical pulmonary embolectomy: a 9-year retrospective analysis. Tex Heart Inst J 2015; 42: 25-29.
16. Azari A, Bigdelu L, Moravvej Z. Surgical embolectomy in the management of massive and submassive pulmonary embolism: the results of 30 consecutive ill patients. ARYA Atheroscler 2015; 11: 208-213.
17. Neely RC, Byrne JG, Gosev I, Cohn LH, Javed Q, Rawn JD, Goldhaber SZ, Piazza G, Aranki SF, Shekar PS, Leacche M. Surgical embolectomy for acute massive and submassive pulmonary embolism in a series of 115 patients. Ann Thorac Surg 2015; 100: 1245-1251.
18. Aymard T, Kadner A, Widmer A, Basciani R, Tevaearai H, Weber A, Schmidli J, Carrel T. Massive pulmonary embolism: surgical embolectomy versus thrombolytic therapy – should surgical indications be revisited? Eur J Cardiothorac Surg 2013; 43: 90-94.
19. Greelish JP, Leacche M, Solenkova NS, Ahmad RM, Byrne JG. Improved midterm outcomes for type A (central) pulmonary emboli treated surgically. J Thorac Cardiovasc Surg 2011; 142: 1423-1429.
20. Dauphine C, Omari B. Pulmonary embolectomy for acute massive pulmonary embolism. Ann Thorac Surg 2005; 79: 1240-1244.
21. Janata K, Holzer M, Domanovits H, Mullner M, Bankier A, Kurtaran A, Bankl HC, Laggner AN. Mortality of patients with pulmonary embolism. Wien Klin Wochenschr 2002; 114: 766-772.
22. Leitner JM, Jilma B, Spiel AO, Sterz F, Laggner AN, Janata KM. Massive pulmonary embolism leading to cardiac arrest is associated with consumptive coagulopathy presenting as disseminated intravascular coagulation. J Thromb Haemost 2010; 8: 1477-1482.
23. Konstantinov IE, Saxena P, Koniuszko MD, Alvarez J, Newman MAJ. Acute massive pulmonary embolism with cardiopulmonary resuscitation: management and results. Texas Heart Inst J 2007; 34: 41-46.
24. Matthews JC, McLaughlin V. Acute right ventricular failure in the setting of acute pulmonary embolism or chronic pulmonary hypertension: a detailed review of the pathophysiology, Diagnosis, and management. Curr Cardiol Rev 2008; 4: 49-59.
25. Brooks H, Kirk ES, Vokonas PS, Urschel CW, Sonnenblick EH. Performance of the right ventricle under stress: relation to right coronary flow. J Clin Investig 1971; 50: 2176-2183.
26. La Vecchia L, Ottani F, Favero L, Spadaro GL, Rubboli A, Boanno C, Mezzena G, Fontanelli A, Jaffe AS. Increased cardiac troponin I on admission predicts in-hospital mortality in acute pulmonary embolism. Heart 2004; 90: 633-637.
27. Fukuda I, Taniguchi S, Fukui K, Minakawa M, Daitoku K, Suzuki Y. Improved outcome of surgical pulmonary embolectomy by aggressive intervention for critically ill patients. Ann Thorac Surg 2011; 91: 728-732.