pass for cardiac surgery, it usually occurs in the 2nd postoperative week; and to the ... The patient had undergone left saphenous vein stripping 20 years before.
Case Reports
Massive Pulmonary Embolism 3 Hours after Cardiopulmonary Bypass An Exceedingly Rare Case
Paolo Masiello, MD Generoso Mastrogiovanni, MD Severino lesu, MD Antonio Panza, MD Franco Triumbari, MD Giuseppe Di Benedetto, MD
A 70-year-old woman underwent an aortocoronary bypass. Three hours later, she experienced severe pulmonary embolism, diagnosed by transesophageal echocardiography and followed by cardiac arrest. Resuscitation maneuvers were unsuccessful. Autopsy confirmed the diagnosis. When pulmonary embolism occurs after cardiopulmonary bypass for cardiac surgery, it usually occurs in the 2nd postoperative week; and to the best of our knowledge, the literature contains no other reports of cases that occurred during a shorter postoperative interval. Prevention of pulmonary embolism in high-risk patients is mandatory. When embolism occurs, transesophageal echocardiography is an essential tool in making the diagnosis and in guiding the surgeon during intervention. (Texas Heart Institute Journal 1994;21:314-6)
sassive pulmonary embolism after cardiopulmonary bypass for cardiac operation is rare and has a high mortality rate. Usually, it occurs in the 2nd postoperative week, and to the best of our knowledge the literature contains no other reports of cases that occurred during a shorter postoperative interval. We describe a case of a 70-year-old woman who died of massive pulmonary embolism 3 hours after extracorporeal circulation for coronary artery bypass. Diagnosis was made by transesophageal echocardiography and confirmed M
by
postmortem examination.
Case Report a 70-year-old woman was admitted to our unit for myocardial revascularization. For 13 months she had suffered from stable angina, which had worsened in the 3 weeks prior to admission. During those 3 weeks she had developed resting angina that had required emergency hospitalization for cardiac catheterization and the administration of intravenous nitrates (to which the patient had responded). The patient had undergone left saphenous vein stripping 20 years before. For 10 years, she had suffered from diabetes, which was well controlled by oral therapy. Both parents had died of cardiac ischemia, at 69 and 72 years of age. Physical examination was unremarkable except for obesity, and varicose veins of the right leg. Blood tests showed type II hyperlipidemia, prolonged prothrombin time due to anticoagulant therapy, hyperfibrinogenemia, and a high platelet
In March of 1994,
Key words: Cardiopulmonary bypass; coronary artery bypass; echocardiography, transesophageal; hyperlipidemia; pulmonary embolism
count.
From: The Department of Cardiac Surgery, Hospital San Leonardo, 84131 Salerno, Italy Address for reprints: Paolo Masiello, MD, Piazza Vittorio Veneto 39 int. 11, 84100 Salerno, Italy 314
Electrocardiography was negative for myocardial necrosis and showed inverted in leads V2 through V5. Echocardiography was negative for myocardial dyskinesia and the presence of organized thrombi. Cardiac catheterization showed normal left ventricular function. However, left coronary arteriograms revealed critical stenosis of the left anterior descending coronary artery (LAD) distal to its first diagonal branch, which showed an 85% stenosis. The posterolateral branch of the circumflex artery showed a 90% stenosis at its origin. Right coronary arteriograms revealed critical stenosis of the posterior interventricular branch.
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Two days after catheterization, the patient underwent myocardial revascularization. The left internal mammary artery was anastomosed to the LAD, and saphenous vein grafts were placed to the 1st diagonal coronary artery and, sequentially, to the posterolateral branch of the circumflex and to the posterior descending branch of the right coronary artery. The operation was uneventful, and the patient was transferred to the intensive care unit with normal cardiac function and no signs of ischemia. In accordance with our protocol, a Protamine Sulfate Injection (0.5 mg for each mg of heparin) was administered to keep the activated clotting time between 170 and 190 seconds at the end of cardiopulmonary bypass. Two hours later, the patient experienced hypotension (systemic arterial pressure, 80/45 mmHg), which was reversed immediately by inotropic support and systemic fluid administration. One hour later, another episode of hypotension, which could not be reversed by therapy, caused us to perform transesophageal echocardiography that showed floating masses passing through the right atrium (Fig. 1). The right ventricle was dilated and hypokinetic; and the left ventricle was hypokinetic. The hemodynamic situation quickly deteriorated, and cardiac arrest ensued. Resuscitation maneuvers were unsuccessful, and the patient died before reoperation could be performed. Autopsy revealed massive pulmonary embolism, including old organized thrombi in the main pulmonary artery and all over the pulmonary tree (Fig. 2).
ports have documented incidences of postoperative pulmonary embolism ranging from 0.52% to 3.5%,I-4 and mortality rates ranging from 0 to 38%. 1.25 The relatively low rate of pulmonary embolism after cardiac operation has been attributed to many factors. Clot formation can be retarded by the consumption of coagulation factors, platelet dysfunction, hemodilution, and thrombocytopenia.6 Intraoperative heparinization and the use of postoperative anticoagulative or antiplatelet therapy also seem to reduce the occurrence of pulmonary embolism.2 Old age, female sex, bed rest, preoperative hospital stay, myocardial infarction, diabetes, varicose veins, obesity, cardiac catheterization from the groin, etc. have been identified as risk factors for pulmonary embolism,"- and many of these were present in our patient. Because of a related hypercoagulability state, type II hyperlipidemia has been associated with a high incidence of pulmonary embolism (7% of all cardiac operations in patients with that condition);2 our patient suffered from type II hyperlipidemia. Usually, postoperative pulmonary embolism occurs during the 2nd postoperative week,' and there
Discussion Pulmonary embolism is an unusual complication of cardiac operation that has a high mortality rate.' Re-
Fig. 1 Thrombi passing through the right atrium at the time of transesophageal echocardiography.
Texas Heart Institutejournal
Fig. 2 Presence of old, organized thrombi all over the pulmonary tree.
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appear to have been no reports of cases occurring in a shorter interval between the operation and the event. In our patient, a documented episode of pulmonary embolism occurred only 3 hours after a cardiac operation. We think that our patient had many risk factors, and probably formed deep venous thrombi during the long period of bed rest. Suddenly, the thrombi were mobilized after the operation, despite heparinization. This is the only case of symptomatic pulmonary embolization that has occurred since our hospital practice started (1 of 388 cardiopulmonary bypasses, or a rate of 0.26%). In conclusion, we think it reasonable to undertake pulmonary embolism prophylaxis in any high-risk patient: venous Doppler testing should be performed routinely in these cases; and a caval filter could be inserted preoperatively and left in place for approximately a week after the operation. Although the occurrence of pulmonary embolism immediately after surgery appears not to have been reported before now, this case demonstrates the possibility. Whenever massive pulmonary embolism occurs, transesophageal echocardiography is an essential technique for prompt diagnosis and for rapid decisions on surgical intervention. Transesophageal echocardiography can also be used at the time of embolectomy, to guide the surgeon.8
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References 1. Gillinov AM, I)avis EA, Albert Aj, Rykiel M, Gardner TJ, Cameron DE. Pulmonary embolism in the cardiac surgical patient. Ann Thorac Surg 1992;53:988-91. 2. Hanson EC, Levine FH. Hyperlipoproteinemia as a significant risk factor for pulmonary embolism in patients undergoing coronary artery bypass grafting. Ann Thorac Surg 1982;33:593-8. 3. Dorros G, Lewin RF, Daley P, Assa J. Coronary artery bypass surgery in patients over age 70 years: report from the Milwaukee cardiovascular data registry. Clin Cardiol 1987;10: 377-82. 4. Hutchinson JE III, Green GE, Mekhjian HA, Kemp HG. Coronary bypass grafting in 376 consecutive patients, with three operative deaths. J Thorac Cardiovasc Surg 1974;67:7-16. 5. Rao G, Zikria EA, Miller WH, Samadani SR, Ford WB. Incidence and prevention of pulmonary embolism after coronary artery surgery. Vasc Surg 1975;9:37-45. 6. Bagge L, Lilienberg G, Nystrom S-O, Tyd&n H. Coagulation, fibrinolysis and bleeding after open-heart surgery. Scand J Thorac Cardiovasc Surg 1986;20:151-60. 7. Hirsh J, Hull RD, Raskob GE. Epidemiology and pathogenesis of venous thrombosis. J Am Coll Cardiol 1986;8:104B13B. 8. Deleuze P, Saada M, De Paulis R, Brochard L, Mazzucotelli JP, Rotman N, et al. Intraoperative transesophageal echocardiography for pulmonary embolectomy without cardiopulmonary bypass. Ann Thorac Surg 1991;52:137-8.
Volume 21, Nzimber 4, 1994
