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Taiwan Crit. Care Med.2009;10:318-325 Sir-Chen Lin et al. INFECTIVE ENDOCARDITIS AT BICUSPID AORTIC VALVE COMPLICATED WITH SEVERE AORTIC REGURGITATION AND RUPTURE OF INTRACRANIAL INFECTIVE ANEURYSM: REPORT OF A CASE WITH LITERATURE REVIEW Sir-Chen Lin1, Shih-Chi Liu2,3, Chuen-Den Tseng2 Abstract Infective endocarditis may complicate with intracranial infective aneurysm, which carries high mortality rate up to 80% and remain a challenge for critical care providers. We report a 33-year-old man who initially presented with fever, exertional dyspnea, heart murmur and transient focal neurologic deficit. Infective endocarditis over bicuspid aortic valve with severe aortic regurgitation and acute pulmonary edema was diagnosed. Five days after admission to intensive care unit, sudden onset of severe subarachnoid hemorrhage happened. Emergent angiography proved a cerebral aneurysm over left MCA with rupture. Blood culture revealed growth of methicillin-resistant Staphylococcus aureus. Brain edema and coma persisted. No further surgical intervention of brain or heart was done due to rapid downhill clinical course and high perioperative risk. Finally, the patient did not survive because of septic shock, disseminated intravascular coagulation, and multiorgan failure. We discuss such situation of this patient who had infective endocarditis complicated with intracranial infective aneurysm. We reviewed the related literature about the etiology, clinical presentation, diagnosis, clinical prognosis and management. It is believed that intracranial infective aneurysms are caused by septic emboli from vegetations. Its incidence accounts for at least 1% among patients with infective endocarditis. It is estimated that the most common location is the branch of middle cerebral artery. The prodromes of intracranial infective aneurysms can be insidious, which make it hard to diagnose. Once the aneurysm ruptures, the clinical prognosis is poor. It is difficult to decide whether operation should be performed first, brain or heart, because surgical intervention in this setting is highly risky. Nowadays, endovascular treatment for intracranial infective aneurysms may serves as an alternative modality for such complicated case. Key words: Bicuspid aortic valve, Infective endocarditis, Intracranial infective aneurysm Correspondence: Dr. Chuen-Den Tseng Section of cardiology, department of internal medicine, National Taiwan University Hospital; No. 7, Chung Shan South Road, Taipei, Taiwan2 Phone: 886-6-231-23456 ext. 63951; E-mail: [email protected] Department of cardiology, Taipei City Hospital, Renai Branch, No. 10, Jen Ai Road, Sec. 4, Taipei, Taiwan 1 Department of cardiology, Min-Sheng General Hospital, No. 168, Jing Guo Road, TaoYuan, Taiwan3 318 Taiwan Crit. Care Med.2009;10:318-325 Bicuspid aortic valve endocarditis complicated with ruptured intracranial aneurysm Case Report A 33-year-old man came to the emergency room with chief complaints including progressive dyspnea on exertion, intermittent high fever for about 3 months. Right side limbs weakness had ever happened 4 days ago, but it spontaneously subsided during 24 hours. He had ever visited local medical doctors, and only common cold was told. He denied past history of systemic diseases such as hypertension or diabetes mellitus, but he had heavy alcohol consumption. Physical examination revealed: blood pressure = 102/48, bilateral basal rales breath sound, grade VI diastolic murmur over right sternal border. Electrocardiography showed sinus tachycardia and non-specific ST segment change. Chest X-ray disclosed cardiomegaly with bilateral hilar infiltration. Room air pulseoximeter saturation was 88%. Hemogram revealed leukocytosis with left-shift. Echocardiography revealed: a vegetation 3.0X1.8 cm over the non-calcific bicuspid aortic valve with protrusion to left ventricle in diastolic phase (Figs. 1-3), severe aortic regurgitation (Fig. 4), dilated left ventricle with borderline contractility (ejection fraction = 54%), marked diastolic reversal of flow in ascending, thoracic descending and abdominal aorta (Fig. 5). Under the impression of infective endocarditis, severe aortic regurgitation with congestive heart failure, the patient was admitted to intensive care unit. Then he was intubated with ventilator support due to aggravated pulmonary edema. Sudden onset of right side limbs weakness happened the next day followed by deep coma and episodes of seizure attack. Brain CT scan revealed diffuse subarachnoid hemorrhage with brain edema (Figs. 6-7). Emergent angiography was done, which showed one cerebral aneurysm over left middle cerebral artery (M1-M2 bifurcation, sized about 4 cm) was demonstrated (Fig. 8). Therefore, intracranial infective aneurysm rupture was confirmed. Blood culture revealed methicillinresistant Staphylococcus aureus growth. Antibiotic treatment with vancomycin was given since the day of admission, but there was still inter- Fig. 1 Fig. 2 Fig. 3 Fig. 4 319 Taiwan Crit. Care Med.2009;10:318-325 Sir-Chen Lin et al. mittent high fever and persistent leukocytosis. His brain edema and consciousness disturbance never improved. Because of fragile consistency of infective aneurysm, possibility of further embolic event and poor heart function and unacceptable high perioperative risk, neither neurology nor cardiovascular surgical interventioin was planned. Later on, septic shock, disseminated intravascular coagulation, with multi-organ failure developed. The patient expired 14 days after admission. Fig. 5 Fig. 6 Fig. 7 320 Taiwan Crit. Care Med.2009;10:318-325 Bicuspid aortic valve endocarditis complicated with ruptured intracranial aneurysm Fig. 8 Discussion bicuspid aortic valve stenosis.3 The important clinical consequences of bicuspid aortic valve disease are valvular stenosis, regurgitation, infective endocarditis, and aortic complications such as dilation and dissection.2 The incidence of infective endocarditis in cohorts of patients with bicuspid aortic valve is 9.5%.5 The incidence of neurological complications of between 20% and 40% in patients with infective endocarditis is remained remarkably constant.6 Neurologic manifestations of infective endocarditis include TIA, embolic CVA, ruptured intracranial infective aneurysm, meningitis, seizure, and nonfocal encephalopathy.7 In published reviews, the frequency of CNS involvement in patients with endocarditis caused by S. aureus has ranged from 53% to 71%, higher than the rates caused by other bacteria. Patients with infection caused by S. aureus have a significantly higher incidence of neurologic sequelae and death.8 Systemic embolization occurs in 22% to 50% of cases of infective endocarditis. Up to 65% of embolic events involve the central nervous system, and 90% of central nervous system emboli lodge in the distribution of the middle cerebral artery. Vegetations >1 cm in diameter are associated with the greatest risk of embolism. 9 Intracranial hemorrhage occurs in about 5% of We reported an unusual case of infective endocarditis with intracranial hemorrhage, probably due to ruptured aneurysm with rapid deterioration. This situation needed early detection and aggressive management. The bicuspid aortic valve is the most common congenital cardiac malformation. The prevalence of bicuspid aortic valve by sex is 7.1/1000 in male neonates and 1.9/1000 in female neonates. Bicuspid aortic valve is likely a genetic disorder. Multiple genes have been implicated including endothelium-derived nitric oxide synthase gene, NOTCH 1, and ubiquitin degradation gene. 3 Echocardiographic screening of first-degree relatives is therefore warranted.2 On echocardiography, aortic valve anatomy can be reliably determined in a short-axis view. Diastolic images can be misleading because the raphe in the larger leaflet of a bicuspid valve may simulate a trileaflet valve in the closed position.4 Inadequate production of fibrillin-1 during valvulogenesis may disrupt the formation of the aortic cusps, resulting in a bicuspid valve and a weakened aortic root.2 The histopathology of a bicuspid aortic valve includes inflammation, fibrosis and calcification. Dyslipidemia appears to be associated with accelerated progression of 321 Taiwan Crit. Care Med.2009;10:318-325 Sir-Chen Lin et al. leukocytes, and elevated protein.9 A large series reported that complaints at the time of admittance are related to SAH in 32.5%, ICH in 25.5%, while 11% of the cases experienced symptoms such as headache, seizure and high fever. 16 Cerebral angiography is used if CT reveals intracranial hemorrhage.7 Some authors suggested even prodromal signs and symptoms of embolism in patients with infective endocarditis should be considered as indicators for cerebral angiography to detect cerebral bacterial aneurysms before rupture.17 Four vessel angiography remains the standard form of investigation and should be performed if an aneurysm is clinically suspected even if the CT scan is normal.13 Angiography is a reliable test to diagnose aneurysm with a sensitivity of 90%.16 Magnetic resonance angiography seems to have a sensitivity of 86% and a specificity of 100% for intracranial infective aneurysms larger than 3 mm in diameter. 8 The overall mortality rate among infective endocarditis patients with intracranial infective aneurysms is 60%. Among those without rupture, the mortality rate is 30%; this approaches 80% if rupture occurs. 9 Aneurysm rupture is life threatening, producing subarachnoid hemorrhage, intracerebral hemorrhage, or direct intracranial destruction of the brain.18 Aneurysm rupture is the most important factor affecting the prognosis.16 Management of the intracranial infective aneurysms is dependent on factors like the presence or absence of hemorrhage, anatomic location, their numbers, location, and patients’ clinical course. Indications for surgical intervention must be evaluated on individual basis.19 Intracranial infective aneurysms may heal with medical therapy. Generally speaking, the duration of antibiotic treatment is between 4 and 6 weeks in most patients.16 There is evidence that one-third resolve completely with antibiotic therapy alone. One-third will demonstrate no significant change in size. Of the remaining third, half enlarge on treatment while the other half reduce in dimensions.11 Even if regression of the aneurysm is observed in cerebral angiographies of the patients patients with infective endocarditis. There are at least there different mechanisms of intracranial hemorrhage : 1) embolic infarcts with secondary hemorrhagic transformation; 2) acute erosive arteritis with rupture; and 3) subacute aneurysms with rupture.10 Anticoagulation is associated with an increased risk of intracranial hemorrhage and dose not prevent separation of small fragments from the infected vegetations. In an experimental animal model of septic brain embolism, anticoagulation therapy is associated with an increased risk of hemorrhage.8 It is estimated that cerebral infective aneurysm develops in 1% to 12% of patients with infective endocarditis and that 10% of these aneurysms rupture.7 Infected embolic material may reach the adventitial layer of an artery through the vasa vasorum; the resulting destruction of the adventitia and muscularis.8 The arterial pulsation against a weakened wall leads to aneurysm formation.11 Experiments suggest that intracranial infective aneurysm usually forms within 48 hours of embolization.12 The intracranial infective aneurysms most commonly are located on the peripheral branches of the middle cerebral artery (55%)13 Near the surface of the brain, infective aneurysms usually involve the secondary and tertiary branches, especially those located in the region of the Sylvian fissure. 14 Multiple aneurysms are detected with an incidence of 18% to 28% in the literature.13 The most common morphology is saccular type.15 The clinical presentation of patients with intracranial infective aneurysms is highly variable.9 More than 50% of patients with intracranial infective aneurysms have no identifiable prodrome.12 Symptoms of an intracranial infective aneurysm usually are not evident unless the aneurysm ruptures or enlarges before rupture and may manifest as compromised cranial nerve function or as a premorbid phase with headache or nuchal rigidity.8 Some intracranial infective aneurysms leak slowly before rupture and produce mild meningeal irritation. Typically, the spinal fluid in these patients is sterile and contains erythrocytes, 322 Taiwan Crit. Care Med.2009;10:318-325 Bicuspid aortic valve endocarditis complicated with ruptured intracranial aneurysm tions for valve replacement in patients with bacterial endocarditis, there is uncertainty regarding the operative priority in patients with both intracranial aneurysm and acute heart failure. If a craniotomy for direct clipping is performed first, perioperative management could be insufficient to control progressive heart failure. On the other hand, if valve replacement is selected first, cardiopulmonary bypass with systemic heparinization could cause lethal neurologic deficits.18 Some patients with infective endocarditis require both cardiac valve replacement and intracranial infective aneurysm ligation. Although data are limited in this situation, an approach that uses staged procedures, with the more severe problem dictating the procedure to be performed first, has been suggested. A bioprosthetic valve, which does not require anticoagulant therapy, may be preferable to a mechanical valve in this circumstance.9 In patients whose general condition precludes surgery, a minimally invasive endovascular approach is used to embolize the aneurysm.8 Detachable balloon technique had been proven to be a simple procedure for bacterial aneurysms.20 After Guglielmi introduced the detachable platinum coil in 1989, coil embolization has steadily replaced neurosurgical therapy after publication of a randomized comparison of endovascular and surgical treatments of ruptured aneurysms (International Subarachnoid Aneurysm Trial, ISAT).21 Another new technique is injection of N-butylcyanoacrylate glue into the affected aneurysm.11 The decision to use a coil or cyanoacrylate as an occlusive device depends on the location of the aneurysm. If the aneurysm can be reached with a microcatheter, cyanoacrylate is the logical choice because it permits simultaneous sealing of the aneurysm. A coil may also be used to achieve occlusion of the parent vessel, but the advantage of using detachable coils must be weighed against the elevated risk of perforating the inflamed and fragile aneurysmal wall. 22 The major advantage of the endovascular techniques is that they avoid craniotomy and surgical handling of the swollen brain. Post- under antibiotic treatment, the aneurysm may regrow.16 However, late rupture of intracranial infective aneurysm after otherwise successful treatment of infective endocarditis can occur. 10 Unfortunately, there is no way to predict whether a intracranial infective aneurysm will regress or rupture on appropriate antibiotic treatment. 11 Surgical excision of peripheral aneurysms is made easier after antibiotic therapy, because the aneurysm wall is much thicker and less likely to rupture.13 Patients should undergo neurosurgery for ruptured aneurysms of cerebral arteries when intracranial hematoma is present.8 Traditionally, the neurosurgical management involves evacuation of the hematoma with ligation of the parent artery. The presence of surrounding clot also makes aneurysm identification particularly difficult. Surgery in the acute setting is technically difficult because of the friable nature of the necrotic tissue.11 Cardiac operations should be performed only when neurologic status has stabilized and CT scan reveals resolution of cerebral edema and no ongoing cerebral hemorrhage.7 The approach to the patient with unruptured intracranial infective aneurysms is controversial. Currently, there are no data that precisely identify patients at risk for imminent rupture, and decisions concerning medical versus surgical therapy must be individualized.9 When the location of the aneurysm is at a site where a new neurologic deficit is likely to be introduced by neurosurgery, a surgical approach must be carefully weighed.8 A large proportion of unruptured proximal intracranial infective aneurysms, and aneurysms of the cavernous sinus may resolve under appropriate antimicrobial therapy, leading some authors to recommend carefully clinical follow up and repeat imaging scans and angiography within 7 to 14 days for unruptured intracranial infective aneurysms.9 For aneurysms that remain unchanged or increase in size on antibiotic therapy for 4-6 weeks, surgical or transcatheter intervention is required and may be individualized to the particular case.11 Although progressive heart failure and systemic embolism are well-established indica323 Taiwan Crit. Care Med.2009;10:318-325 Sir-Chen Lin et al. 10. Hart RG, Kagan-Hallet K, Joerns SE. Mechanisms of intracranial hemorrhage in infective endocarditis. Stroke 1987;18:1048-1056. 11. Misser SK, Lalloo S, Ponnusamy S. Intracranial mycotic aneurysm due to infective endocarditis— successful NBCA glue embolisation. S Afr Med J 2005;95:397-9, 403-404. 12. Salgado AV, Furlan AJ, Keys TF. Mycotic aneurysm, subarachnoid hemorrhage, and indications for cerebral angiography in infective endocarditis. Stroke 1987;18:1057-1060. 13. Corr P, Wright M, Handler LC. Endocarditis-related cerebral aneurysms: radiologic changes with treatment. AJNR Am J Neuroradiol 1995;16:745-748. 14. Masuda J, Yutani C, Waki R, Ogata J, Kuriyama Y, Yamaguchi T. Histopathological analysis of the mechanisms of intracranial hemorrhage complicating infective endocarditis. Stroke 1992;23:843-850. 15. Kannoth S, Iyer R, Thomas SV, Furtado SV, Rajesh BJ, Kesavadas C, Radhakrishnan VV, Sarma PS. Intracranial infectious aneurysm: Presentation, management and outcome. J Neurol Sci 2007;256:3-9. 16. Sarica FB, Erdogan B, Tufan K, Cekinmez M, Kizilkilic O, Sen O, Altinors MN. Endovascular treatment of primary infectious aneurysm in childhood: a case report. Turk Neurosurg 2008;18:47-51. 17. Yamada M, Miyasaka Y, Takagi H, Yada K. Cerebral bacterial aneurysm and indications for cerebral angiography in infective endocarditis. Neurol Med Chir (Tokyo) 1994;34:697-699. 18. Utoh J, Miyauchi Y, Goto H, Obayashi H, Hirata T. Endovascular approach for an intracranial mycotic aneurysm associated with infective endocarditis. J Thorac Cardiovasc Surg 1995;110:557-559. 19. Kong KH, Chan KF. Ruptured intracranial mycotic aneurysm: a rare cause of intracranial hemorrhage. Arch Phys Med Rehabil 1995;76:287-289. 20. Micheli F, Schteinschnaider A, Plaghos LL, Melero M, Mattar D, Parera IC. Bacterial cavernous sinus aneurysm treated by detachable balloon technique. Stroke 1989;20:1751-1754. 21. Fiehler J, Byrne JV. Factors affecting outcome after endovascular treatment of intracranial aneurysms. Curr Opin Neurol 2009;22:103-108. 22. Chapot R, Houdart E, Saint-Maurice JP, Aymard A, Mounayer C, Lot G, Merland JJ. Endovascular treatment of cerebral mycotic aneurysms. Radiology 2002; 222:389-396. 23. van der Schaaf I, Algra A, Wermer M, et al. Endovascular coiling versus neurosurgical clipping for patients with aneurysmal subarachnoid haemorrhage. Cochrane Database Syst Rev 2005:CD003085. intervention recovery is less complicated and usually quicker. 11 A recent systematic review identified three randomized trials comparing clipping and coiling of intracranial aneurysms. After 1 year of follow-up, the relative risk of poor outcome for coiling vs. clipping was 0.76.23 Urgent cerebral angiography and an endovascular approach to intracranial infective aneurysms, especially for solitary and peripheral lesions, is an acceptable option for some patients with active endocarditis and severely damaged hearts. 18 Moreover, endovascular treatment should also be preferred in patients who use anticoagulant drugs due to heart valve replacement.16 References 01. Erdogan HB, Erentug V, Bozbuga N, Goksedef D, Akinci E, Yakut C. Endovascular treatment of intracerebral mycotic aneurysm before surgical treatment of infective endocarditis. Tex Heart Inst J 2004; 31:165-167. 02. Fedak PW, Verma S, David TE, Leask RL, Weisel RD, Butany J. Clinical and pathophysiological implications of a bicuspid aortic valve. Circulation 2002; 106:900-904. 03. Aboulhosn J, Child JS. Left ventricular outflow obstruction: subaortic stenosis, bicuspid aortic valve, supravalvar aortic stenosis, and coarctation of the aorta. Circulation 2006;114:2412-2422. 04. Lewin MB, Otto CM. The bicuspid aortic valve: adverse outcomes from infancy to old age. Circulation 2005;111:832-834. 05. Ward C. Clinical significance of the bicuspid aortic valve. Heart 2000;83:81-85. 06. Patel RL, Richards P, Chambers DJ, Venn G.. Infective endocarditis complicated by ruptured cerebral mycotic aneurysm. J R Soc Med 1991;84:746-747. 07. Gillinov AM, Shah RV, Curtis WE, Stuart RS, Cameron DE, Baumgartner WA, Greene PS. Valve replacement in patients with endocarditis and acute neurologic deficit. Ann Thorac Surg 1996;61:1125-1129. 08. Tunkel AR, Pradhan SK. Central nervous system infections in injection drug users. Infect Dis Clin North Am 2002;16:589-605. 09. Bayer AS, Bolger AF, Taubert KA, Wilson W, Steckelberg J, Karchmer AW, Levison M, Chambers HF, Dajani AS, Gewitz MH, Newburger JW, Gerber MA, Shulman ST, Pallasch TJ, Gage TW, Ferrieri P. Diagnosis and management of infective endocarditis and its complications. Circulation 1998;98:29362948. 324 Bicuspid aortic valve endocarditis complicated with ruptured intracranial aneurysm Taiwan Crit. 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