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Acute Pulmonary Thromboembolism During Mitral Valve Repair
Case Reports
159 CASE REPORTS
Heart, Lung and Circulation 2008;17:146–166
Acute Pulmonary Thromboembolism During Mitral Valve Repair Neerod K. Jha, MD a,∗ , Ahmed I. Rezk, MD a , Ahmad S. Omran, MD b , Arif Hussain, MD c and Hani K. Najm, MD a a
Department of Cardiac Surgery, King Abdulaziz Cardiac Center, National Guard Health Affairs, King Fahad Hospital, Riyadh, Saudi Arabia b Department of Non Invasive Cardiology, King Abdulaziz Cardiac Center, National Guard Health Affairs, King Fahad Hospital, Riyadh, Saudi Arabia c Department of Anaesthesia, King Abdulaziz Cardiac Center, National Guard Health Affairs, King Fahad Hospital, Riyadh, Saudi Arabia
Perioperative pulmonary thromboembolism during cardiac surgery is extremely rare. We report a 55-year-old male, who developed acute pulmonary thromboembolism during mitral valve repair. Intra-operative trans oesophageal echocardiography failed to demonstrate thromboembolus in the pulmonary arteries but it showed the secondary signs of acute pulmonary artery obstruction. Thromoembolectomy was done after high index of suspicion on clinical grounds was found and the patient recovered. The diagnostic accuracy and sensitivity of transoesophageal echocardiography in circumstances with altered haemodynamics is questionable and has not been investigated. Therefore, indirect evidence of pulmonary artery obstruction on echocardiography may have a predictive value and failure to demonstrate pulmonary thromboembolism by this tool should not exclude the possibility of it especially when it is highly suspected. (Heart, Lung and Circulation 2008;17:146–166) © 2007 Australasian Society of Cardiac and Thoracic Surgeons and the Cardiac Society of Australia and New Zealand. Published by Elsevier Inc. All rights reserved. Keywords. Embolism; Pulmonary; Thrombosis; Repair; Mitral
Introduction
Case Report
T
A 55-year-old man, presented with a two-year history of shortness of breath. He was in New York Heart Association symptom class III and was almost confined to bed at home for two weeks before operation. Preoperative 2D echocardiography, TEE and angiocardiography confirmed severe mitral regurgitation, right ventricular systolic pressure of 45 mmHg, ejection fraction 35%, patent foramen ovale (PFO) with a left-to-right shunt and normal coronary arteries. In the operating room, before anaesthesia, his baseline blood pressure (BP) was 110/75 mmHg. The heart rate was 77 beats/min with respiratory rate of 18 breaths/minute. We did not insert Swan Ganz thermodilution catheter but the patient had a probe for TEE assessment. After induction of anaesthesia, systemic BP went down to 65/30 mmHg with a decline in the arterial oxygen saturation up to 75%. The main pulmonary artery was tense and dilated. Cardiopulmonary by-pass (CPB) was initiated immediately and repair of the mitral valve was performed with Cosgrove-Edward annuloplasty band (28 mm, M/s Edward Life Sciences, Irvine, California, USA). After rewarming, weaning from CPB could not be accomplished. On attempt to wean from CPB, the pulmonary artery (PA) pressure (measured by tricuspid regurgitation (TR) jet on Doppler echocardiography) reached 70–80 mmHg with
he incidence of perioperative pulmonary embolism (PE) in patients undergoing non-cardiac surgery ranges from 2–17% and has been associated with fatal outcome in almost half of the cases.1,2 However, perioperative PE during cardiac surgery is extremely rare with only one reported case in the available literature, so far.3 The PE is often diagnosed by pulmonary angiography, spiral CT, or ventilation-perfusion scintigraph. But, these diagnostic techniques are not practical in the setting of massive intraoperative PE or during perioperative period.4–6 Transoesophageal echocardiography (TEE) can provide a useful tool to diagnose PE but may have limitations. We are reporting herein a male, who underwent mitral valve repair and was found to have pulmonary and paradoxical cerebral embolism during surgery.
Received 21 July 2006; received in revised form 25 August 2006; accepted 15 December 2006; available online 2 March 2007 ∗
Corresponding author at: Department of Cardiac Sciences, King Fahad Hospital, P.O. Box-22490, Mail Code-1413, Riyadh-11426, Saudi Arabia. Tel.: +966 1 237 9259; fax: +966 1 252 0088x16700. E-mail address: nk [email protected] (N.K. Jha).
© 2007 Australasian Society of Cardiac and Thoracic Surgeons and the Cardiac Society of Australia and New Zealand. Published by Elsevier Inc. All rights reserved.
1443-9506/04/$30.00 doi:10.1016/j.hlc.2006.12.004
160
Case Reports
CASE REPORTS
Figure 1. Pulmonary thromoemboli from the pulmonary arteries.
systemic pressure of 50–60 mmHg. We thought of pulmonary hypertensive crisis and started hyperventilation but there was no improvement. The right ventricle was found to be acutely dilated and the CPB was re-instituted. Intra-operative TEE revealed a competent mitral valve, no clear evidence of thrombo-embolism within the central PAs, but it showed severe right ventricular dysfunction, severe TR and significant right to left shunt through PFO. Although the right ventricular pressure was supra systemic, the left atrial pressure was extremely low (1–2 mmHg) as measured by direct needle puncture. We, therefore, felt that the high PA pressure was very likely due to obstruction in the PA despite negative TEE examination. The weaning from CPB failed despite multiple attempts. Eventually, we explored the PA. On exploration, we found a large thrombus sitting at the bifurcation of the main PA, totally occluding the left and partially occluding the right PA. The morphology of thrombus resembled that of deep vein thrombus of the lower limb (Fig. 1). Histopathology of excised thrombus confirmed it to be chronic in nature. After thromboembolectomy and direct closure of PFO, we could wean the patient from CPB successfully. Postoperatively, the patient had right hemiplegia and computed tomogram of brain revealed multiple left sided cerebral infarctions.
Comments Although practical guidelines introduced by the American Society of Echocardiography strongly recommend TEE for the diagnosis of acute life threatening haemodynamic compromise, the diagnostic accuracy of TEE for diagnosing PE in the intraoperative setting is usually questionable and has not been specifically investigated.1,7,8 Intraoperative TEE has low sensitivity (50%) for direct visualisation of thromboemboli especially in the left pulmonary artery.1 Similarly, on echocardiography, secondary signs of severe PE such as right ventricular dilatation, D-shaped left ventricle, moderate to severe tricuspid regurgitation, leftward
Heart, Lung and Circulation 2008;17:146–166
bowing of the interatrial septum, or right to left shunt through PFO are relatively non-specific indicators and may be difficult to differentiate from the other causes of acute right ventricular failure, including protamine reaction or pulmonary hypertension.1,9 The limited diagnostic ability of echocardiography in diagnosing PE during surgery could be attributed to various reasons. First, the usual echocardiographic evidence of chronic adaptive changes in the pulmonary circulation may not be identified after acute, massive PE. Second, the location of the air-filled trachea, left main bronchus and endotracheal tube may interfere with the ability of ultrasound to visualise PE, especially in the left PA and, last, the operative environment during cardiopulmonary by-pass and altered haemodynamic state may not provide optimal conditions for performing echocardiographic examination.1,4,10 Prolonged immobilisation, obesity, prior history of venous thromboembolism, recent myocardial infarction, congestive heart failure, atrial fibrillation and hypercoagulable state are important risk factors for pulmonary thromoembolism especially in cardiac surgical patients.11 Our patient had physical limitation and congestive heart failure (CHF) before surgery. The CHF was treated by medication including diuretic and fluid restrictions. In this scenario, there might have been a state of haemoconcentration, altered viscosity of blood and resultant hyper coagulation state. Also, we feel that patient mobilisation elevation of legs during cleaning and preparation of the patient in the operating room may contribute towards embolisation of existing thrombus. In conclusion, failure of TEE to directly demonstrate PE should not exclude this possibility, particularly when it is highly suspected on clinical grounds. Successful management of such cases require a high index of suspicion, supportive clinical findings and timely intervention especially in circumstances where it is least expected.1,10
References 1. Rosenberger P, Shernan SK, Body SC, Eltzschig HK. Utility of intraoperative transesophageal echocardiography for diagnosis of pulmonary embolism. Anesth Analg 2004;99:12–6. 2. Geerts WH, Pineo GF, Heit JA, Bergqvist D, Lassen MR, Colwell CW, Ray JG. Prevention of venous thromboembolism: the seventh ACCP conference on antithrombotic and thrombolytic therapy. Chest 2004;126(Suppl. 3):338S–400S. 3. Cleveand JC, Lebenson IM, Friedman JW. Successful management of massive pulmonary emboli occurring during cardio-pulmonary by pass for mitral valve replacement. Chest 1978;73:236–8. 4. Vieillard-Baron A, Qanadli SD, Antakly Y, Fourme T, Loubieres Y, Jardin F, Dubourg O. Transesophageal echocardiography for the diagnosis of pulmonary embolism with acute cor pulmonale: a comparison with radiological procedures. Intensive Care Med 1998;24:429–33. 5. Pruszczyk P, Torbicki A, Pocho R, Chlebus M, Kuch-Wocial A, Pruszynski B, Gurba H. Noninvasive diagnosis of suspected severe pulmonary embolism: transesophageal echocardiography vs. spiral CT. Chest 1997;112:722–8. 6. Goldhaber SZ. Pulmonary embolism. New England J Med 1998;339:93–104.
7. Practice guidelines for perioperative transesophageal echocardiography: a report by the American Society of Anesthesiologists and the Society of Cardiovascular Anesthesiologists task Force on transesophageal echocardiography. Anesthesiology 1996; 84:986–1006. 8. Cahalan MK, Abel M, Goldman M. American Society of Echocardiography and Society of Cardiovascular Anesthesiologists task force guidelines for training in perioperative echocardiography. Anesth Analg 2002;94:1384–8.
Case Reports
161
9. McIntyre RW, Flezzani P, Knopes KD. Pulmonary hypertension and prostaglandins after protamine. Am J Cardiol 1986;58:857–8. 10. Manji M, Issac JL, Bion J. Survival from massive intraoperative pulmonary thromboembolism during orthotopic liver transplantation. BJA 1998;80:685–7. 11. Shammas NW. Pulmonary embolus after coronary artery bypass surgery: a review of the literature. Clin Cardiol 2000;23:637–44.
Lung Cancer Masquerading as Prosthetic Valve Endocarditis Omar A. Khan ∗ , Vanessa Rogers, Raj Sharma and Sunil K. Ohri Wessex Cardiac Centre, Southampton General Hospital, Southampton, United Kingdom
Although marantic endocarditis secondary to pulmonary adenocarcinoma is well described, it is very unusual for this symptom to be the initial presenting feature of lung cancer. Here we describe such a case in which marantic endocarditis affected not only the patient’s native mitral valve, but also his newly implanted bioprosthetic valve—a phenomenon that has not been previously reported. (Heart, Lung and Circulation 2008;17:146–166) © 2007 Published by Elsevier Inc on behalf of Australasian Society of Cardiac and Thoracic Surgeons and the Cardiac Society of Australia and New Zealand. Keywords. Endocarditis; Lung cancer
Case Report
A
55-year-old male presented with acute-onset expressive dysphasia. The dysphasia resolved over 24 h, however neurological examination revealed right-sided blindness with no focal motor or sensory losses. Examination of the cardiovascular, respiratory and abdominal systems revealed no abnormalities—in particular there was no evidence of splinter haemorrhages in the patient’s nail beds. Laboratory examination revealed a normal haemoglobin, white cell, platelet, prothrombin and partial thromboplastin time together with a raised C-reactive protein level and erythrocyte sedimentation rate. Blood cultures revealed no growth and an immunological screen for influenza, mycoplasma, chlamydia, adenovirus, respiratory syncytial virus, C. Burnetii, enterovirus, Q fever & legionella were all negative. An autoantibody screen for rheumatoid factor, anti-nuclear antibody, complement, ANCA and anti-double stranded DNA antibodies were also negative, however the patient was positive for car-
Received 3 September 2006; received in revised form 12 December 2006; accepted 15 December 2006; available online 2 March 2007 ∗ Corresponding author at: Department of Cardiothoracic Surgery, Southampton General Hospital, Tremona Road, Southampton SO16 6YD, United Kingdom. Tel.: +44 238 077 7222; fax: +44 238 077 7222. E-mail address: [email protected] (O.A. Khan).
diolipin antibody. Chest X-ray and abdominal ultrasound revealed no abnormalities; however a CT scan of the brain showed regions of infarction in the left frontal, left parietal and right occipital lobes with haemorrhagic transformation of the occipital ischaemic infarct. Trans-thoracic and trans-oesophageal echo (TOE) revealed a 1 cm vegetation on the posterior mitral valve leaflet together with a thickened anterior valve leaflet and moderate mitral valve regurgitation. A clinical diagnosis of infective endocarditis was made and the patient underwent emergency tissue mitral valve replacement with a 25 mm Perimount valve. In view of the risks of further haemorrhagic transformation of his ischaemic infarcts, the patient was not systemically anticoagulated following surgery. Post-operatively, he initially recovered well, however, five days following surgery, he became acutely short of breath. TOE revealed restricted movement of the mitral cusps, together with a mean gradient of 15 mmHg across the bioprosthetic valve (see Fig. 1a). Emergency surgery was performed, the patient was placed on cardiopulmonary bypass and the left atrium opened. The prosthetic valve was noted to be obstructed with laminar thrombus (see Fig. 1b), and was replaced with a 27 mm St Jude valve. Twenty-four hours following his second procedure the patient developed emboli in both feet. TOE revealed debris in the left ventricle together with new vegetations on the aortic and tricuspid valves. The patient was systemically heparinised, and commenced on oral anticoagulation, however despite adequate anticoagulation, the
© 2007 Published by Elsevier Inc on behalf of Australasian Society of Cardiac and Thoracic Surgeons and the Cardiac Society of Australia and New Zealand.
1443-9506/04/$30.00 doi:10.1016/j.hlc.2006.12.006
CASE REPORTS
Heart, Lung and Circulation 2008;17:146–166
159 CASE REPORTS
Heart, Lung and Circulation 2008;17:146–166
Acute Pulmonary Thromboembolism During Mitral Valve Repair Neerod K. Jha, MD a,∗ , Ahmed I. Rezk, MD a , Ahmad S. Omran, MD b , Arif Hussain, MD c and Hani K. Najm, MD a a
Department of Cardiac Surgery, King Abdulaziz Cardiac Center, National Guard Health Affairs, King Fahad Hospital, Riyadh, Saudi Arabia b Department of Non Invasive Cardiology, King Abdulaziz Cardiac Center, National Guard Health Affairs, King Fahad Hospital, Riyadh, Saudi Arabia c Department of Anaesthesia, King Abdulaziz Cardiac Center, National Guard Health Affairs, King Fahad Hospital, Riyadh, Saudi Arabia
Perioperative pulmonary thromboembolism during cardiac surgery is extremely rare. We report a 55-year-old male, who developed acute pulmonary thromboembolism during mitral valve repair. Intra-operative trans oesophageal echocardiography failed to demonstrate thromboembolus in the pulmonary arteries but it showed the secondary signs of acute pulmonary artery obstruction. Thromoembolectomy was done after high index of suspicion on clinical grounds was found and the patient recovered. The diagnostic accuracy and sensitivity of transoesophageal echocardiography in circumstances with altered haemodynamics is questionable and has not been investigated. Therefore, indirect evidence of pulmonary artery obstruction on echocardiography may have a predictive value and failure to demonstrate pulmonary thromboembolism by this tool should not exclude the possibility of it especially when it is highly suspected. (Heart, Lung and Circulation 2008;17:146–166) © 2007 Australasian Society of Cardiac and Thoracic Surgeons and the Cardiac Society of Australia and New Zealand. Published by Elsevier Inc. All rights reserved. Keywords. Embolism; Pulmonary; Thrombosis; Repair; Mitral
Introduction
Case Report
T
A 55-year-old man, presented with a two-year history of shortness of breath. He was in New York Heart Association symptom class III and was almost confined to bed at home for two weeks before operation. Preoperative 2D echocardiography, TEE and angiocardiography confirmed severe mitral regurgitation, right ventricular systolic pressure of 45 mmHg, ejection fraction 35%, patent foramen ovale (PFO) with a left-to-right shunt and normal coronary arteries. In the operating room, before anaesthesia, his baseline blood pressure (BP) was 110/75 mmHg. The heart rate was 77 beats/min with respiratory rate of 18 breaths/minute. We did not insert Swan Ganz thermodilution catheter but the patient had a probe for TEE assessment. After induction of anaesthesia, systemic BP went down to 65/30 mmHg with a decline in the arterial oxygen saturation up to 75%. The main pulmonary artery was tense and dilated. Cardiopulmonary by-pass (CPB) was initiated immediately and repair of the mitral valve was performed with Cosgrove-Edward annuloplasty band (28 mm, M/s Edward Life Sciences, Irvine, California, USA). After rewarming, weaning from CPB could not be accomplished. On attempt to wean from CPB, the pulmonary artery (PA) pressure (measured by tricuspid regurgitation (TR) jet on Doppler echocardiography) reached 70–80 mmHg with
he incidence of perioperative pulmonary embolism (PE) in patients undergoing non-cardiac surgery ranges from 2–17% and has been associated with fatal outcome in almost half of the cases.1,2 However, perioperative PE during cardiac surgery is extremely rare with only one reported case in the available literature, so far.3 The PE is often diagnosed by pulmonary angiography, spiral CT, or ventilation-perfusion scintigraph. But, these diagnostic techniques are not practical in the setting of massive intraoperative PE or during perioperative period.4–6 Transoesophageal echocardiography (TEE) can provide a useful tool to diagnose PE but may have limitations. We are reporting herein a male, who underwent mitral valve repair and was found to have pulmonary and paradoxical cerebral embolism during surgery.
Received 21 July 2006; received in revised form 25 August 2006; accepted 15 December 2006; available online 2 March 2007 ∗
Corresponding author at: Department of Cardiac Sciences, King Fahad Hospital, P.O. Box-22490, Mail Code-1413, Riyadh-11426, Saudi Arabia. Tel.: +966 1 237 9259; fax: +966 1 252 0088x16700. E-mail address: nk [email protected] (N.K. Jha).
© 2007 Australasian Society of Cardiac and Thoracic Surgeons and the Cardiac Society of Australia and New Zealand. Published by Elsevier Inc. All rights reserved.
1443-9506/04/$30.00 doi:10.1016/j.hlc.2006.12.004
160
Case Reports
CASE REPORTS
Figure 1. Pulmonary thromoemboli from the pulmonary arteries.
systemic pressure of 50–60 mmHg. We thought of pulmonary hypertensive crisis and started hyperventilation but there was no improvement. The right ventricle was found to be acutely dilated and the CPB was re-instituted. Intra-operative TEE revealed a competent mitral valve, no clear evidence of thrombo-embolism within the central PAs, but it showed severe right ventricular dysfunction, severe TR and significant right to left shunt through PFO. Although the right ventricular pressure was supra systemic, the left atrial pressure was extremely low (1–2 mmHg) as measured by direct needle puncture. We, therefore, felt that the high PA pressure was very likely due to obstruction in the PA despite negative TEE examination. The weaning from CPB failed despite multiple attempts. Eventually, we explored the PA. On exploration, we found a large thrombus sitting at the bifurcation of the main PA, totally occluding the left and partially occluding the right PA. The morphology of thrombus resembled that of deep vein thrombus of the lower limb (Fig. 1). Histopathology of excised thrombus confirmed it to be chronic in nature. After thromboembolectomy and direct closure of PFO, we could wean the patient from CPB successfully. Postoperatively, the patient had right hemiplegia and computed tomogram of brain revealed multiple left sided cerebral infarctions.
Comments Although practical guidelines introduced by the American Society of Echocardiography strongly recommend TEE for the diagnosis of acute life threatening haemodynamic compromise, the diagnostic accuracy of TEE for diagnosing PE in the intraoperative setting is usually questionable and has not been specifically investigated.1,7,8 Intraoperative TEE has low sensitivity (50%) for direct visualisation of thromboemboli especially in the left pulmonary artery.1 Similarly, on echocardiography, secondary signs of severe PE such as right ventricular dilatation, D-shaped left ventricle, moderate to severe tricuspid regurgitation, leftward
Heart, Lung and Circulation 2008;17:146–166
bowing of the interatrial septum, or right to left shunt through PFO are relatively non-specific indicators and may be difficult to differentiate from the other causes of acute right ventricular failure, including protamine reaction or pulmonary hypertension.1,9 The limited diagnostic ability of echocardiography in diagnosing PE during surgery could be attributed to various reasons. First, the usual echocardiographic evidence of chronic adaptive changes in the pulmonary circulation may not be identified after acute, massive PE. Second, the location of the air-filled trachea, left main bronchus and endotracheal tube may interfere with the ability of ultrasound to visualise PE, especially in the left PA and, last, the operative environment during cardiopulmonary by-pass and altered haemodynamic state may not provide optimal conditions for performing echocardiographic examination.1,4,10 Prolonged immobilisation, obesity, prior history of venous thromboembolism, recent myocardial infarction, congestive heart failure, atrial fibrillation and hypercoagulable state are important risk factors for pulmonary thromoembolism especially in cardiac surgical patients.11 Our patient had physical limitation and congestive heart failure (CHF) before surgery. The CHF was treated by medication including diuretic and fluid restrictions. In this scenario, there might have been a state of haemoconcentration, altered viscosity of blood and resultant hyper coagulation state. Also, we feel that patient mobilisation elevation of legs during cleaning and preparation of the patient in the operating room may contribute towards embolisation of existing thrombus. In conclusion, failure of TEE to directly demonstrate PE should not exclude this possibility, particularly when it is highly suspected on clinical grounds. Successful management of such cases require a high index of suspicion, supportive clinical findings and timely intervention especially in circumstances where it is least expected.1,10
References 1. Rosenberger P, Shernan SK, Body SC, Eltzschig HK. Utility of intraoperative transesophageal echocardiography for diagnosis of pulmonary embolism. Anesth Analg 2004;99:12–6. 2. Geerts WH, Pineo GF, Heit JA, Bergqvist D, Lassen MR, Colwell CW, Ray JG. Prevention of venous thromboembolism: the seventh ACCP conference on antithrombotic and thrombolytic therapy. Chest 2004;126(Suppl. 3):338S–400S. 3. Cleveand JC, Lebenson IM, Friedman JW. Successful management of massive pulmonary emboli occurring during cardio-pulmonary by pass for mitral valve replacement. Chest 1978;73:236–8. 4. Vieillard-Baron A, Qanadli SD, Antakly Y, Fourme T, Loubieres Y, Jardin F, Dubourg O. Transesophageal echocardiography for the diagnosis of pulmonary embolism with acute cor pulmonale: a comparison with radiological procedures. Intensive Care Med 1998;24:429–33. 5. Pruszczyk P, Torbicki A, Pocho R, Chlebus M, Kuch-Wocial A, Pruszynski B, Gurba H. Noninvasive diagnosis of suspected severe pulmonary embolism: transesophageal echocardiography vs. spiral CT. Chest 1997;112:722–8. 6. Goldhaber SZ. Pulmonary embolism. New England J Med 1998;339:93–104.
7. Practice guidelines for perioperative transesophageal echocardiography: a report by the American Society of Anesthesiologists and the Society of Cardiovascular Anesthesiologists task Force on transesophageal echocardiography. Anesthesiology 1996; 84:986–1006. 8. Cahalan MK, Abel M, Goldman M. American Society of Echocardiography and Society of Cardiovascular Anesthesiologists task force guidelines for training in perioperative echocardiography. Anesth Analg 2002;94:1384–8.
Case Reports
161
9. McIntyre RW, Flezzani P, Knopes KD. Pulmonary hypertension and prostaglandins after protamine. Am J Cardiol 1986;58:857–8. 10. Manji M, Issac JL, Bion J. Survival from massive intraoperative pulmonary thromboembolism during orthotopic liver transplantation. BJA 1998;80:685–7. 11. Shammas NW. Pulmonary embolus after coronary artery bypass surgery: a review of the literature. Clin Cardiol 2000;23:637–44.
Lung Cancer Masquerading as Prosthetic Valve Endocarditis Omar A. Khan ∗ , Vanessa Rogers, Raj Sharma and Sunil K. Ohri Wessex Cardiac Centre, Southampton General Hospital, Southampton, United Kingdom
Although marantic endocarditis secondary to pulmonary adenocarcinoma is well described, it is very unusual for this symptom to be the initial presenting feature of lung cancer. Here we describe such a case in which marantic endocarditis affected not only the patient’s native mitral valve, but also his newly implanted bioprosthetic valve—a phenomenon that has not been previously reported. (Heart, Lung and Circulation 2008;17:146–166) © 2007 Published by Elsevier Inc on behalf of Australasian Society of Cardiac and Thoracic Surgeons and the Cardiac Society of Australia and New Zealand. Keywords. Endocarditis; Lung cancer
Case Report
A
55-year-old male presented with acute-onset expressive dysphasia. The dysphasia resolved over 24 h, however neurological examination revealed right-sided blindness with no focal motor or sensory losses. Examination of the cardiovascular, respiratory and abdominal systems revealed no abnormalities—in particular there was no evidence of splinter haemorrhages in the patient’s nail beds. Laboratory examination revealed a normal haemoglobin, white cell, platelet, prothrombin and partial thromboplastin time together with a raised C-reactive protein level and erythrocyte sedimentation rate. Blood cultures revealed no growth and an immunological screen for influenza, mycoplasma, chlamydia, adenovirus, respiratory syncytial virus, C. Burnetii, enterovirus, Q fever & legionella were all negative. An autoantibody screen for rheumatoid factor, anti-nuclear antibody, complement, ANCA and anti-double stranded DNA antibodies were also negative, however the patient was positive for car-
Received 3 September 2006; received in revised form 12 December 2006; accepted 15 December 2006; available online 2 March 2007 ∗ Corresponding author at: Department of Cardiothoracic Surgery, Southampton General Hospital, Tremona Road, Southampton SO16 6YD, United Kingdom. Tel.: +44 238 077 7222; fax: +44 238 077 7222. E-mail address: [email protected] (O.A. Khan).
diolipin antibody. Chest X-ray and abdominal ultrasound revealed no abnormalities; however a CT scan of the brain showed regions of infarction in the left frontal, left parietal and right occipital lobes with haemorrhagic transformation of the occipital ischaemic infarct. Trans-thoracic and trans-oesophageal echo (TOE) revealed a 1 cm vegetation on the posterior mitral valve leaflet together with a thickened anterior valve leaflet and moderate mitral valve regurgitation. A clinical diagnosis of infective endocarditis was made and the patient underwent emergency tissue mitral valve replacement with a 25 mm Perimount valve. In view of the risks of further haemorrhagic transformation of his ischaemic infarcts, the patient was not systemically anticoagulated following surgery. Post-operatively, he initially recovered well, however, five days following surgery, he became acutely short of breath. TOE revealed restricted movement of the mitral cusps, together with a mean gradient of 15 mmHg across the bioprosthetic valve (see Fig. 1a). Emergency surgery was performed, the patient was placed on cardiopulmonary bypass and the left atrium opened. The prosthetic valve was noted to be obstructed with laminar thrombus (see Fig. 1b), and was replaced with a 27 mm St Jude valve. Twenty-four hours following his second procedure the patient developed emboli in both feet. TOE revealed debris in the left ventricle together with new vegetations on the aortic and tricuspid valves. The patient was systemically heparinised, and commenced on oral anticoagulation, however despite adequate anticoagulation, the
© 2007 Published by Elsevier Inc on behalf of Australasian Society of Cardiac and Thoracic Surgeons and the Cardiac Society of Australia and New Zealand.
1443-9506/04/$30.00 doi:10.1016/j.hlc.2006.12.006
CASE REPORTS
Heart, Lung and Circulation 2008;17:146–166