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Bilateral multiple brain infarction can occur in

Case 246

5. all


【Discussion】
 Brain infarctions usually arise from occlusive cerebral arteries or carotid arteries. Their lesions occur in hemi-lateral brain. Multiple bilateral brain infarctions are occasionally found on Diffusion WI MRI. They are not related with the lesion from carotid artery and cerebral branch arteries but the lesion from aortic arch, heart and hyper-coagulable-state. The most common cause for bilateral multiple infarctions is atrial fibrillation. The other causes are aortic atheroma, bacterial endocarditis, non-bacterial endocarditis (1, 2), cholesterol embolism after medical procedure such as stent graft or coronary intervention (3) and Trousseau syndrome (hypercoagulable due to tumor or immune disease)(4-6).
 Cancer has four characteristics: growing and invasion, metastasis, vessel remodeling, and coagulation. Trousseau syndrome expresses one of the aspect of cancer characteristics. Trousseau syndrome is defined as thrombo-embolism events underlying malignant tumor. Especially, in case of advanced cancer, it predominantly causes occlusive venous and arterial events; redness and edema due to deep vein occlusion, brain infarction. Trousseau syndrome occurs in approximately 30% as non-bacterial thrombotic endocarditis (4-6). Mechanism of coagulation is that cancer cells secrete thromboplastin (tissue factor) and mucin which cause activation of platelets in the peripheral vessel, producing minute thrombus to migrate in the whole body (6).
 Mitral valve and tricuspid valve can be the barrier in the vessel lumen, implying that tumor cells, bacteria and platelets predominantly adheres to these valves. In other words, bacteria, platelets and tumor are susceptible to stay at these valves and migrate to brain. Our case (Fig.2) had advanced intrahepatic cholangiocarcinoma and received anticancer which was resistant to his cancer. After he experienced bilateral multiple brain metastases, he died twenty days later.
 Approximately a half of all cases with infectious endocarditis had no known history of valvular disease (7, 8). Cardiac valves do not have a dedicated arterial blood supply system. Then, when an organism attaches to the valve, defensive immune system to resist bacteria does not respond effectively. As a result, bacteria proliferate and form a vegetation (bacillus accumulation + clot), travelling to the various parts of the body. Meanwhile, in case of endothelial damage, platelet-fibrin clot, first occurs on the damaged endothelium and thereafter, bacillus from bactremia adheres to the clot, inducing to form a vegetation.
 There exist two routes of septic emboli from left-sided endocarditis and right-sided endocarditis. Namely, when bacillus vegetation is formed on tricuspid valve or right ventricular endothelium, pulmonary septic emboli happen, while when bacillus vegetation is formed on mitral valve, aortic valve, left arterial appendage or left ventricular endothelium, systemic septic emboli happen in various body parts such as brain, retina, spleen, kidney, intestine and extremities (7 – 9). As specific findings observed in septic emboli from left-sided endocarditis, painless hemorrhagic cutaneous lesions on the palm and soles are named Janeway lesions, painful subcutaneous lesions in the distal fingers are named Osler’s nodules and fungus ball in the retina are named Roth’s spots (9). In our case, changes by septic emboli appeared in brain, eye ball and upper and lower extremities including Janeway lesions.
 Although any bacteria possibly cause endocarditis, Staphylococcus and Streptococcus are the main organisms. Staphylococcus infection is known to cause fulminant illness such as valvular fistula previously categorized acute bacterial endocarditis, while Streptococcus infection causes mild to moderate illness previously categorized subacute bacterial endocarditis (8 – 11). In our case, she had bacteremia by methicillin-resistant staphylococcus aureus blood culture revealed. The prompt and appropriate use of antibiotics is imperative to control infectious endocarditis. She was given antibiotics and the symptoms were recovered.


【Summary】
 We presented two cases with bilateral multiple brin infarctions: one case with advanced cholangiocarcinoma and another with bacteria endocarditis of methicillin-resistant staphylococcus aureus. It is borne in mind that thrombo-embolism events underlying malignant tumor are termed as Trousseau syndrome. Activation of platelets arising from cancer producing mucin and thromboplastin. There are four main diseases to cause bilateral multiple infarctions; atrial fibrillation, bacteria endocarditis, non-bacteria endocarditis including cancer-related (Trousseau syndrome) and immune disease-related. Further, from a point of diffusion weighted MRI interpretation, metastatic brain tumor might be better to be listed. Mitral valve and tricuspid valve are barrier in lumen of blood flow and susceptible for thrombus, bacteria and tumor cells to contact, reach and adhere.


【References】
1.Maekawa, M. et al. Multiple Brain Infarction Associated with Cholesterol Embolization Syndrome. Intern Med. 2017; 56: 2531–2533.
2.Altieri M, et al. Multiple brain infarcts: clinical and neuroimaging patterns using diffusion-weighted magnetic resonance. Eur Neurol.1999; 42:76–82.
3.Kronzon I, et al. Cholesterol embolization syndrome. Circulation 122: 631-641, 2010.
4.Ikushima S, et al. Trousseau's syndrome: cancer-associated thrombosis. Jpn J Clin Oncol 2016 ;46(3):204-8
5.Maharaj S et al. Trousseau syndrome. Cleveland Clinic Journal of Medicine April 2020, 87 (4) 199-200
6.Dicke C, et al. Pathophysiology of Trousseau's syndrome. Hamostaseologie 2015;35:52-59.
7.Heiro M, et al. Infective endocarditis in a Finnish teaching hospital: a study on 326 episodes treated during 1980–2004. Heart. 2006; 92: 1457–62. doi:10.1136/hrt.2005.084715. PMC 1861063
8.Morris AM. How best to deal with endocarditis. Curr Infect Dis Rep. 2006 8 (1): 14–22. doi:10.1007/s11908-006-0030-8. PMID 16448596.
9.Kasper DL, Brunwald E, Fauci AS, Hauser S, Longo DL, Jameson JL (2005). Harrison's Principles of Internal Medicine. McGraw-Hill. pp. 731–40. ISBN 0-07-139140-1. OCLC 54501403.
10.Stawicki SP, et al. Septic embolism in the intensive care unit. Int J Crit Illn Inj Sci. 2013 Jan-Mar; 3: 58–63. doi: 10.4103/2229-5151.109423
11.Avery RK, et al. Listeria monocytogenes tricuspid valve endocarditis with septic pulmonary emboli in a liver transplant recipient. Transpl Infect Dis. 1999;1:284–7.

2021.10.11



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