Case Study
Mitral valve repair in active infective endocarditis with cerebral infarction
Asian Cardiovascular & Thoracic Annals 21(2) 215–217 ß The Author(s) 2012 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav DOI: 10.1177/0218492312451587 aan.sagepub.com
Kenji Okada, Tomonori Shirasaka, Hiroya Kano and Yutaka Okita
Abstract A 19-year-old woman, who had a recent extensive cerebral infarction caused by a septic embolization in the left-sided territory of the middle cerebral artery, successfully underwent mitral valve repair for severe mitral regurgitation caused by active infective endocarditis, 24 h after the onset of stroke. Anticoagulation during cardiopulmonary bypass was maintained with low-dose heparin and additional nafamostat mesilate. She had no further aggravation of the brain complication and recovered well with midterm mitral valve durability.
Keywords Cardiopulmonary bypass, endocarditis, bacterial, heart valve prosthesis implantation, mitral valve, stroke
Introduction The timing of surgical intervention in patients with active infective endocarditis (IE) complicated by recent extensive brain infarction as been controversial because of the higher risk of promoting brain hemorrhagic infarction. The mode of mitral valve surgery for mitral valve destruction in a young woman is another important issue. We describe our experience of early mitral valve repair in a young woman with destructive mitral valve IE complicated by extensive brain infarction.
Case report A 19-year-old woman was referred to our hospital because of loss of consciousness and right hemiplegia after she had complained of severe headache and fever persisting for 10 days prior to her admission. Preoperative magnetic resonance imaging demonstrated extensive cerebral infarction in the whole left-sided territory of the middle cerebral artery (Figure 1(a)). Transesophageal echocardiography demonstrated a large mobile vegetation on both the anterior (A3) and posterior (P3) leaflets of the mitral valve, measuring 20 14 mm. A blood test showed an elevated white blood cell count (23,100/mL) and C-reactive protein level (25.0 mgdL 1). Blood culture
was positive for methicillin-sensitive staphylococcus aureus. She was diagnosed with active IE accompanied by the neurological deficits of a decreased level of consciousness, motor aphasia, right hemiplegia, and conjugated deviation (Glasgow coma scale E2V1M6). Emergency surgical intervention was planned to prevent further cerebral embolism. Twenty-four hours after admission, we undertook surgery using low-dose heparin and additional nafamostat mesilate (NM) as anticoagulants during cardiopulmonary bypass (CPB), to reduce the risk of hemorrhagic stroke. CPB was established in a routine manner except for the management of anticoagulation: systemic heparinization was carried out with 2500 units (50 Ukg 1) which corresponded to a quarter of the normal dose. NM was administrated continuously through the venous circuit at a rate of 1.5 to 2.0 mgkg 1h 1 and into the cardiotomy reservoir at 0.5 mgkg 1h 1. Additional administration of heparin was not necessary throughout CPB. Department of Surgery, Division of Cardiovascular Surgery, Kobe University Graduate School of Medicine, Kobe, Japan Corresponding author: Kenji Okada, MD, PhD, Department of Surgery, Divisions of Cardiovascular Surgery, Kobe University Graduate School of Medicine, 7-5-2, Kusunoki-Cho, Chuo-Ku, Kobe, Hyogo, 650-0017, Japan. Email: [email protected]
Downloaded from aan.sagepub.com at Freie Universitaet Berlin on May 4, 2015
216
Asian Cardiovascular & Thoracic Annals 21(2)
Figure 1. Brain magnetic resonance images: (a) acute-phase diffusion-weighted image on admission, and (b) T2-weighted image on the day 13th after the operation. Each panel demonstrates extensive cerebral infarction in the left-sided territory of the middle cerebral artery. No exacerbation was observed in panel B.
Figure 2. Schema of the mitral valve repair. (a) Mobile vegetations growing on A2, C2 and P2 leaflets of the mitral valve. (b) Approximation of the medial side of A2 and P2 using 2 stitches of 5/0 polypropylene. (c) Patch repair using an autologous pericardial patch.
We could maintain the activated coagulation time, measured with a coagulation analyzer (Hemocron Response, ITC), at between 300 and 450 s. After cardiac arrest, a right-sided left atriotomy was performed for mitral valve exposure. A 20 14-mm mass of fragile vegetation was attached to the A3, PC, and P3 leaflets of the mitral valve (Figure 2(a)). We carefully resected the vegetation and the infected leaflets (A3, PC and P3) en bloc. The medial side of A2 and P2 was approximated with 5/0 polypropylene (Figure 2(b)), and an autologous pericardial patch (15 30 mm), which had been soaked for 5 min in glutaraldehyde, was sutured over the defect with 4/0 polypropylene suture (Figure 2(c)). Brain magnetic resonance imaging the following day and postoperative day 13 demonstrated no intracranial bleeding or aggravation of brain edema (Figure 1(b)). The patient’s consciousness recovered to a normal level (Glasgow coma scale E4V4M6) on postoperative day 26. She was discharged on postoperative
day 96, and could walk and speak without aphasia. A transthoracic echocardiogram 3 years after the operation demonstrated neither mitral regurgitation nor stenosis (mitral valve area, 2.12 cm2).
Discussion Previous studies reported that surgical intervention in patients with recent onset (44 weeks) of brain infarction or hemorrhage was associated with the risk of exacerbation of cerebral complications.1 Angstwurm and colleagues2 calculated that the risk of neurological deterioration in cases of brain infarction was 20% within 3 days, 20%–50% between days 4 and 14, but declined to
Mitral valve repair in active infective endocarditis with cerebral infarction
Asian Cardiovascular & Thoracic Annals 21(2) 215–217 ß The Author(s) 2012 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav DOI: 10.1177/0218492312451587 aan.sagepub.com
Kenji Okada, Tomonori Shirasaka, Hiroya Kano and Yutaka Okita
Abstract A 19-year-old woman, who had a recent extensive cerebral infarction caused by a septic embolization in the left-sided territory of the middle cerebral artery, successfully underwent mitral valve repair for severe mitral regurgitation caused by active infective endocarditis, 24 h after the onset of stroke. Anticoagulation during cardiopulmonary bypass was maintained with low-dose heparin and additional nafamostat mesilate. She had no further aggravation of the brain complication and recovered well with midterm mitral valve durability.
Keywords Cardiopulmonary bypass, endocarditis, bacterial, heart valve prosthesis implantation, mitral valve, stroke
Introduction The timing of surgical intervention in patients with active infective endocarditis (IE) complicated by recent extensive brain infarction as been controversial because of the higher risk of promoting brain hemorrhagic infarction. The mode of mitral valve surgery for mitral valve destruction in a young woman is another important issue. We describe our experience of early mitral valve repair in a young woman with destructive mitral valve IE complicated by extensive brain infarction.
Case report A 19-year-old woman was referred to our hospital because of loss of consciousness and right hemiplegia after she had complained of severe headache and fever persisting for 10 days prior to her admission. Preoperative magnetic resonance imaging demonstrated extensive cerebral infarction in the whole left-sided territory of the middle cerebral artery (Figure 1(a)). Transesophageal echocardiography demonstrated a large mobile vegetation on both the anterior (A3) and posterior (P3) leaflets of the mitral valve, measuring 20 14 mm. A blood test showed an elevated white blood cell count (23,100/mL) and C-reactive protein level (25.0 mgdL 1). Blood culture
was positive for methicillin-sensitive staphylococcus aureus. She was diagnosed with active IE accompanied by the neurological deficits of a decreased level of consciousness, motor aphasia, right hemiplegia, and conjugated deviation (Glasgow coma scale E2V1M6). Emergency surgical intervention was planned to prevent further cerebral embolism. Twenty-four hours after admission, we undertook surgery using low-dose heparin and additional nafamostat mesilate (NM) as anticoagulants during cardiopulmonary bypass (CPB), to reduce the risk of hemorrhagic stroke. CPB was established in a routine manner except for the management of anticoagulation: systemic heparinization was carried out with 2500 units (50 Ukg 1) which corresponded to a quarter of the normal dose. NM was administrated continuously through the venous circuit at a rate of 1.5 to 2.0 mgkg 1h 1 and into the cardiotomy reservoir at 0.5 mgkg 1h 1. Additional administration of heparin was not necessary throughout CPB. Department of Surgery, Division of Cardiovascular Surgery, Kobe University Graduate School of Medicine, Kobe, Japan Corresponding author: Kenji Okada, MD, PhD, Department of Surgery, Divisions of Cardiovascular Surgery, Kobe University Graduate School of Medicine, 7-5-2, Kusunoki-Cho, Chuo-Ku, Kobe, Hyogo, 650-0017, Japan. Email: [email protected]
Downloaded from aan.sagepub.com at Freie Universitaet Berlin on May 4, 2015
216
Asian Cardiovascular & Thoracic Annals 21(2)
Figure 1. Brain magnetic resonance images: (a) acute-phase diffusion-weighted image on admission, and (b) T2-weighted image on the day 13th after the operation. Each panel demonstrates extensive cerebral infarction in the left-sided territory of the middle cerebral artery. No exacerbation was observed in panel B.
Figure 2. Schema of the mitral valve repair. (a) Mobile vegetations growing on A2, C2 and P2 leaflets of the mitral valve. (b) Approximation of the medial side of A2 and P2 using 2 stitches of 5/0 polypropylene. (c) Patch repair using an autologous pericardial patch.
We could maintain the activated coagulation time, measured with a coagulation analyzer (Hemocron Response, ITC), at between 300 and 450 s. After cardiac arrest, a right-sided left atriotomy was performed for mitral valve exposure. A 20 14-mm mass of fragile vegetation was attached to the A3, PC, and P3 leaflets of the mitral valve (Figure 2(a)). We carefully resected the vegetation and the infected leaflets (A3, PC and P3) en bloc. The medial side of A2 and P2 was approximated with 5/0 polypropylene (Figure 2(b)), and an autologous pericardial patch (15 30 mm), which had been soaked for 5 min in glutaraldehyde, was sutured over the defect with 4/0 polypropylene suture (Figure 2(c)). Brain magnetic resonance imaging the following day and postoperative day 13 demonstrated no intracranial bleeding or aggravation of brain edema (Figure 1(b)). The patient’s consciousness recovered to a normal level (Glasgow coma scale E4V4M6) on postoperative day 26. She was discharged on postoperative
day 96, and could walk and speak without aphasia. A transthoracic echocardiogram 3 years after the operation demonstrated neither mitral regurgitation nor stenosis (mitral valve area, 2.12 cm2).
Discussion Previous studies reported that surgical intervention in patients with recent onset (44 weeks) of brain infarction or hemorrhage was associated with the risk of exacerbation of cerebral complications.1 Angstwurm and colleagues2 calculated that the risk of neurological deterioration in cases of brain infarction was 20% within 3 days, 20%–50% between days 4 and 14, but declined to
