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PULMONARY EMBOLISM SUCCESSFULLY TREATED WITH THROMBOLYSIS
THE ROLE OF TRANSESOPHAGEAL ECHOCARDIOGRAPHY Livio Villa, MD, Department of Cardiac Anaesthesia, Cristina Carro, MD, Department of Cardiovascular Surgery, Claudio Savi, MD, Department of Cardiac Anaesthesia, Paolo Vanelli, MD, Department of Cardiovascular Surgery, Alessandro Cialfi, MD, Department of Cardiology, Annamaria Condemi, MD Department of Cardiac Anaesthesia, “L.Sacco” Hospital, Milan |
ABSTRACTAcute pulmonary embolism (PE) carries a high mortality. The diagnosis can be difficult to establish, especially in critically ill patients presenting with cardiopulmonary arrest. Among the available techniques for the diagnosis of acute PE, transesophageal echocardiography (TEE) is the diagnostic tool of choice in many emergency situations as TEE can identify the thrombotic mass in the pulmonary artery and the detect right ventricular dysfunction.
Thrombolytic treatment has been shown to accelerate the resolution rate of major pulmonary clots and to facilitate a significant hemodynamic improvement within a few hours in patients with a massive pulmonary embolism. TEE can also monitor the effect of thrombolysis.
This is a report of a case of an acute PE detected by TEE which was successfully treated with thrombolysis.
INTRODUCTIONMassive pulmonary embolism is a catastrophic event associated with a high mortality rate [1]. Because clinical signs may be unclear, many deaths occur before the establishment of the diagnosis and before effective treatment can be instituted.
CASE REPORTThe patient was a 67-year-old caucasian woman. Her medical history revealed obesity, dyslipidemia, hypertension, and coronary artery disease. She underwent a CABG operation and had an uneventful postoperative course. After discharge from hospital the patient was readmitted for sternal diastasis. She had been well until the week before her readmission, when she developed weakness, and mild shortness of breath (NYHA II). Her medications included diuretics and Beta-blockers. Antiplatelet therapy with Aspirin had been discontinued during the postoperative period.
Her physical examination was remarkable for sternal instability during coughing and for minimal sternal diastasis. The laboratory findings showed a leukocytosis (WBC: 14,315x103/L). Her blood pressure was 110/65 mmHg and her pulse rate was 90 beats/min. The electrocardiogram showed sinus rhythm and an incomplete right bundle branch block. A chest roentgenogram revealed enlargement of the mediastinum. A computer tomographic thoracic scan detected minimal sternal diastasis without retrosternal fluid or gas collection. A transthoracic echocardiogram showed moderate tricuspid and mitral regurgitation, and biatrial and right ventricular dilatation without signs of pulmonary hypertension .
The patient was scheduled for a sternal operation. No premedication was administered and the procedure was performed under general anesthesia. At the end of the procedure, the patient had a cardiac arrest. During cardiopulmonary resuscitation the femoral artery was cannulated, tracheal intubation was performed, and the patient was ventilated with a FiO2=100mm Hg. The patient recovered some cardiac output with a sinus tachycardia (116 beats/min) and severe hypotension (76/48 mmHg). Capnometry revealed a significant decrease of her end-tidal CO2 (15mmHg). The arterial blood gas disclosed hypoxia (PaO2=65mmHg) and severe hypercarbia (PaCO2=66mmHg) with a pH=7.1. The working diagnosis was PE.
A Swan-Ganz catheter inserted via the right internal jugular vein documented:
A transesophageal echocardiogram documented a large clot trapped in the main trunk of the pulmonary artery (Figure 1) and confirmed the diagnosis of PE.
Figure 1. Transesophageal echocardiographic findings showing the floating thrombus (arrow) into central pulmonary artery
(PA, pulmonary artery; RA, right atrium; Ao, aorta)
Because of her recent open-heart surgery and the risk of injury to the bypass grafts, we chose medical instead of surgical therapy. Thrombolytic treatment was started with a continuous intravenous infusion of 100 mg recombinant tissue-type plasminogen activator (rt-PA Actilyse, Alteplase-Boehringer Ingelheim- Florence. Italy) which was administered for 2 hours into the pulmonary artery through the Swan-Ganz catheter.
An infusion of heparin (25000units/500ml of saline, at a rate of 10ml/hour) was started and maintained for 36 hours. The echocardiogram performed one hour after the beginning of the thrombolytic therapy demonstrated a reduction in size of the clot (Figure 2), and hemodynamic measurements showed a decrease of the pulmonary artery systolic pressure from 70 to 50 mmHg.
Figure 2. Transesophageal echocardiographic shows the reduction in size of the clot (arrow)
(PA, pulmonary artery; RA, right atrium; Ao, aorta)
Another TEE was performed 2 days later showed almost a complete resolution of the thrombus. The postoperative outcome was complicated by hypoxia and persistent post-anoxic cerebral damage characterized by a state of neurological impairment (5-6 GCS). Neurological evaluation showed signs of brain dysfunction affecting mainly the right hemisphere with hypotonia of the arms and hypertonia of the lower limbs. A cerebral computed tomographic scan performed 5 days later was negative, another scan performed 13 days later detected a hemorrhagic infarction located in the basal nuclei; this finding was absent 28 days after the operation. Due to difficulty with respiratory weaning, the patient required a tracheostomy and was discharged from the ICU after 26 days. She was then transferred from the hospital 60 days later to a rehabilitation center.
DISCUSSIONIn this case the non-specific symptoms and signs before the arrest and the presence of preexisting cardiopulmonary disease made the establishment of the correct diagnosis difficult. At the arrest there was supportive evidence for PE (risk factors such as obesity, a recent surgical procedure, right ventricular dilatation, and the findings from capnometry), but it was only after TEE that we confirmed the diagnosis and started the treatment. Although surgery was immediately available, the patient hemodynamically stablized, and was not considered to be a candidate for emergency pulmonary thromboembolectomy. A thoracotomy was felt to represent a high-risk because of her recent cardiac surgery and adhesions which increased the chance of injury to the bypass grafts. Thrombolytic therapy was considered the best choice .
Pulmonary embolism (PE) is a common disease, which is often misdiagnosed, especially in hospitalized elderly patients. Risk factors include obesity and a prolonged postoperative recovery. The incidence of PE after coronary artery bypass operations (CABG) is 3-2% [2]. In patients with fatal PE, the hospital mortality ranges from 43 to 80% within the first two hours, with 85% of the patients dying within the first six hours [3]. An accurate diagnosis and early treatment reduces in-hospital mortality (up to 30%) to 8% [4]. Langdon and Coll. [17] reported the successful use of rt-PA in a patient with cardiac arrest due to PE with 10 mg of rt-PA infused centrally followed by 90 mg by a peripheral route.
TEE visualizes the central pulmonary arteries and evaluates right ventricular function. TEE is an effective tool in detecting clinically unsuspected central pulmonary thromboemboli [5], can be very helpful for establishing the diagnosis [9] and excluding life threatening conditions such as ventricular septal rupture, aortic dissection, or cardiac tamponade. TEE is recommended as an initial test in suspected massive PE or unexplained hypotension in patients admitted to the intensive care unit [10]. Wittlich and Coll [6] reported TEE detection of an embolus in the pulmonary artery in 58% of 60 patients with a pulmonary embolism with cardiac arrest. In critically ill patients with a suspicion of PE TEE is sensitive, specific, and safe [5]. Wittlich and Erbel reported a sensitivity of 76% to 96.7% and a specificity of 86% to 100% in identifying central pulmonary embolism as compared to pulmonary angiography and computed tomography [6, 7]. Although the right ventricle may show no dysfunction in patients with extensive acute PE [8], TEE can still detect thrombus and can monitor clot lysis.
Conventional therapy for acute PE is the administration of intravenous heparin. Some randomized trials have compared thrombolysis with rt-PA with conventional heparin treatment. These trials have demonstrated that rt-PA treatment compared with heparin alone accelerates clot lysis, improves pulmonary reperfusion and reduces pulmonary artery pressures [11]. Thrombolytic therapy compared to heparin anticoagulation accelerates the resolution rate of pulmonary occlusion [13] and improves right ventricular function [14]. These effects are seen within 24 hours [15], as opposed to two weeks or more with heparin alone [16]. Thrombolytic agents are used for patients with hemodynamic instability or with echocardiographic findings of right ventricular failure [12]. Since thrombolytic agents promote the dissolution of clots and the restoration of cardiovascular hemodynamics, patients with massive PE with hemodynamic derangement should be considered for this treatment.
Thrombolytic agents can be administered centrally or peripherally . Both routes of administration have similar rates of lysis, induction of a systemic lytic state and bleeding [11]. The complications of throbolysis include a 1.2% risk of cerebral bleeding[11] which may have been the case with our patient.
In conclusion, in acute massive PE, TEE can both speed the establishment of a diagnosis and in those patients treated with throbolysis monitor thrombolytic efficacy .
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Acknowledgement:
We thank Dr. Neil Colman of the Respiratory Division of the McGill University Health Care Center for reviewing this case report.