1、.,1,金黃色葡萄球菌腦炎病例討論,南華大學(xué)附二醫(yī)院神經(jīng)內(nèi)科 魏麓云主任醫(yī)師,2,.,病例簡(jiǎn)介,李軍 男 62歲，因“四肢乏力、肌肉痛4天”于2012-1-17日17：52入院 。 患者入院4天前漸覺(jué)肢體無(wú)力，雙下肢無(wú)力明顯，尚能行走，無(wú)特殊診治，17日自覺(jué)無(wú)力、肌痛癥狀加重，不能站立，急診入院。既往：近2月來(lái)發(fā)現(xiàn)右側(cè)頸部腫塊，有心臟病、高血壓病、腦外傷史，入院10天前有受涼感冒，自服感冒藥。 入院時(shí)查體：體溫37.90C，血壓150/100mmHg，血糖7.5 mmol/l，神清、語(yǔ)言可，雙側(cè)瞳孔等大、等圓，對(duì)光反應(yīng)靈敏，瞳孔直徑3毫米，眼球運(yùn)動(dòng)正常，伸舌居中，頸抗陰性，雙上肢肌力4級(jí)，雙下

2、肢肌力3級(jí)，病理征陰性，四肢肌肉壓痛明顯，心尖區(qū)吹風(fēng)樣雜音。有胸悶，吸氧，血氧飽和度正常。 右側(cè)頸部可捫及到一腫塊，大約3X4cm大小，質(zhì)地中等,3,.,實(shí)驗(yàn)室檢查： 急診查（1月17號(hào)） 血鉀4.49 mmol/l 鈉135.6 mmol/l；白細(xì)胞7.05 X109/L,中性粒82.3%，血小板74 X109/L 血沉37s, 血紅蛋白128 g/l, 。1月17日晚查 血鉀4.14 mmol/l 鈉135 mmol/l ； 1月18號(hào)：血常規(guī) 白細(xì)胞7.2 X109/L，中性粒79.6%；血小板60 X 109/L，血紅蛋白132 g/l ，抽血查血培養(yǎng)。乳酸脫氫酶325 U/L 肌酸激

3、酶161.3 U/L ;尿素氮11.2 mmol/l 肌酐131.7 umol/l 血糖6.98 mmol/l 白蛋白34.7 g/l 總膽27.3 umol/l 直膽8.9 umol/l 間膽18.4 umol/l 谷丙48 u/l 谷草60 u/l。FT3 1.92 pg/ml FT4 1.37 ng/dl TSH 0.12 uIU/ml。 頭顱頸椎MRI：1.左顳葉腦軟化灶形成；2.雙側(cè)半卵圓中心多發(fā)腔梗；3.大腦萎縮，腦白質(zhì)疏松；4.頸3/4、4/5、5/6、6/7椎間盤膨出并向后方輕度突出；5.頸椎退行性變；6.甲狀腺體積明顯增大且信號(hào)不均勻，性質(zhì)待定，,4,.,腰穿：腦脊液清亮,壓

4、力240mmH2O ,蛋白547 mg/l, 氯113 mmol/l , 糖4.10 mmol/l,白細(xì)胞10 X106/L, 紅細(xì)胞0.5 X109/L。 1月18日查體較前無(wú)明顯變化，自訴無(wú)力稍好轉(zhuǎn)，仍有肌痛，發(fā)熱，38度左右； 1月19日體溫37.7-38度，血壓136/98 mmHg，神志欠清、夜間有講胡話，雙側(cè)瞳孔等大、等圓，對(duì)光反應(yīng)靈敏，瞳孔直徑3毫米，水平眼震陽(yáng)性，伸舌居中，頸抗弱陽(yáng)性，雙上肢肌力3級(jí)，雙下肢肌力3級(jí)，肌肉壓痛明顯，病理征陰性。心尖區(qū)吹風(fēng)樣雜音。 20日 體溫37.2度，血壓110/70 mmHg，神志模糊、夜間有講胡話，問(wèn)話不能準(zhǔn)確應(yīng)答，雙側(cè)瞳孔等大、等圓，對(duì)光

5、反應(yīng)靈敏，瞳孔直徑3毫米，眼球固定，左右及上下視不能，眼瞼閉合不全，張口費(fèi)力，伸舌不能，咽反射減退，聲嘶，頸抗陽(yáng)性，左側(cè)肢體肌力3級(jí)，右側(cè)肢體肌力0級(jí)，病理征陰性，四肢肌肉壓痛明顯，心尖區(qū)吹風(fēng)樣雜音。周身散在出血點(diǎn)，前胸及雙側(cè)大腿內(nèi)側(cè)明顯。,5,.,1月19號(hào)血鉀4.28 mmol/l 鈉135.5 mmol/l ；血常規(guī) 白細(xì)胞18.2 X109/L，中性粒80.7%；血小板41 X109/L ，紅細(xì)胞3.84 X1012/L ,血紅蛋白124 g/l, 結(jié)核抗體陰性。20日轉(zhuǎn)入ICU治療，20日上午血培養(yǎng)報(bào)告：金黃色葡萄球菌感染，尿素氮19.0mmol/l ，肌酐214.5umol/l ，

6、白蛋白27.5 g/l ，總膽53.8 umol/l ，直膽27.3 umol/l， 間膽26.5 umol/l， 谷丙51.6 u/l ，谷草95.1 u/l，復(fù)查腰穿腦脊液蛋白614 mg/l, 氯117 mmol/l , 糖3.8 mmol/l,白細(xì)胞75 X106/L,紅細(xì)胞0.5 X109/L；CSF壓力? 頭顱MRI 示腦內(nèi)多發(fā)病變并部分出血合并腦梗死可能；左顳葉軟化灶，腦白質(zhì)疏松、腦萎縮同前。 頸部CT示甲狀腺右葉改變性質(zhì)待定：結(jié)節(jié)型甲狀腺腫？腺瘤？腺癌？建議進(jìn)一步檢查； 肺部CT雙側(cè)胸腔積液；心臟增大（左房、左室增大為主），請(qǐng)結(jié)合臨床； 腹部CT兩肺感染；膽囊多發(fā)結(jié)石；肝及左腎

7、低密度灶性質(zhì)待定，建議上腹部CT增強(qiáng)掃描；肝多發(fā)鈣化灶。 頭顱CT示雙側(cè)額葉、左側(cè)頂、枕葉及右側(cè)小腦半球病變，結(jié)合臨床考慮腦炎并出血可能性大，不除外合并部分腦梗死，建議治療后復(fù)查。,6,.,病例特點(diǎn),1 中老年男性病人，突發(fā)四肢無(wú)力、疼痛，以下肢無(wú)力明顯，進(jìn)行性加重，發(fā)展到眼球固定、雙眼瞼下垂，聲音嘶啞，吞咽困難，左側(cè)肢體癱瘓。 2 發(fā)病前有感冒病史，既往有腦外傷、高血壓病史 3 胸腹部、大腿內(nèi)側(cè)、腳趾有散在的、大小不等出血瘀斑、皰疹。 4 甲狀腺腫塊已有2個(gè)月，甲狀腺功能示甲減 5 實(shí)驗(yàn)室檢查：入院時(shí)白細(xì)胞總數(shù)7.05 X109/L,中性粒82.3%，隨著病情發(fā)展，白細(xì)胞總數(shù)增加，中性粒細(xì)胞

8、數(shù)增加；入院時(shí)血小板減少血小板74 X109/L，第二天血小板60 X 109/L，第三天血小板41 X109/L,7,.,5 血培養(yǎng)示金黃色葡萄球菌感染，以后在尿液、多次血培養(yǎng)均發(fā)現(xiàn)金黃色葡萄球菌感染，痰培養(yǎng)克雷柏氏菌。 6 腎功能逐漸加重1月18號(hào)尿素氮11.2 mmol/l 肌酐131.7 umol/l ，19號(hào)尿素氮19.0mmol/l ，肌酐214.5umol/l ，20號(hào) 7 腦脊液：1月18號(hào)壓力240mmH20,白細(xì)胞10 X106/L,19號(hào)壓力？白細(xì)胞75 X106/L 8 TSH受體抗體（+）GAD抗體（-）丙肝抗體（+） TF3, 2.02,TSH 0.05, D二聚體

9、（+）FDP(+)TG-G(-) C反應(yīng)蛋白156.40，肌鈣蛋白17.99 ABO血型 A型，RH血型（+）,8,.,.,9,頭部CT,MRI演變,.,10,頭部CT,MRI演變,.,11,頭部CT,MRI演變,.,12,頭部CT,MRI演變,.,13,頭部CT,MRI演變,.,14,頭部CT,MRI演變,.,15,頭部CT,MRI演變,.,16,頭部CT,MRI演變,17,.,.,18,甲狀腺CT,.,19,強(qiáng)化的MRI,.,20,強(qiáng)化的MRI,21,.,.,22,神經(jīng)影像學(xué)點(diǎn)評(píng),該病例神經(jīng)影像學(xué)演變有以下幾個(gè)特點(diǎn)： 1 由于病情發(fā)展快，神經(jīng)影像學(xué)變化大，做到實(shí)時(shí)跟蹤。 2 發(fā)病第五天第一

10、次頭部MRI平掃，除左側(cè)顳葉因腦外傷所致腦軟化灶外，可見(jiàn)右側(cè)額葉散在的大小不一類似腦梗死灶。如圖所示。未見(jiàn)出血等其他病灶。,.,23,3 發(fā)病第七天頭部MRI平掃，DWI,CT顯示病灶播散、廣泛，小腦、雙側(cè)大腦半球白質(zhì)、灰質(zhì)均有病灶，出血與類似梗死灶同時(shí)存在。但是，中線結(jié)構(gòu)沒(méi)有移位，腦室系統(tǒng)內(nèi)未見(jiàn)出血。腦干未見(jiàn)明顯病灶，與臨床表現(xiàn)不符（眼球固定、雙眼瞼下垂、聲音嘶?。?。此時(shí)，已有胸、腹部、大腿 內(nèi)側(cè)散在暗紅色皰疹。 在ICU搶救后，病情 一度有好轉(zhuǎn)。,.,24,4 發(fā)病后第十天，頭部CT示腦出血，腦室內(nèi)出血。但是，中線結(jié)構(gòu)仍然沒(méi)有移位。病情進(jìn)行性加重，出現(xiàn)昏迷。,.,25,5 發(fā)病第十三天，頭

11、部CT沒(méi)有很大變化（與23號(hào)比較），病情有所好轉(zhuǎn)，皮疹消退，輸血小板后，血小板有所恢復(fù)。但是，神經(jīng)系統(tǒng)狀況無(wú)好轉(zhuǎn)。,.,26,結(jié)合文獻(xiàn)討論,27,.,金黃色葡萄球菌簡(jiǎn)介,金黃色葡萄球菌 (Staphyloccocus aureus Rosenbach) 是人類的一種重要病原菌，隸屬于葡萄球菌屬（Staphylococcus），有“嗜肉菌”的別稱，是革蘭氏陽(yáng)性菌的代表，可引起許多嚴(yán)重感染。 金黃色葡萄球菌細(xì)胞壁含90%的肽聚糖和10%的磷壁酸。其肽聚糖的網(wǎng)狀結(jié)構(gòu)比革蘭氏陰性菌致密，染色時(shí)結(jié)晶紫附著后不被酒精脫色故而呈現(xiàn)紫色，相反，陰性菌沒(méi)有細(xì)胞壁結(jié)構(gòu)，所以紫色被酒精沖掉然后附著了沙黃的紅色 。新

12、出現(xiàn)的耐甲氧西林金黃色葡萄球菌，被稱作超級(jí)細(xì)菌，幾乎能抵抗人類現(xiàn)在所有的藥物，但是萬(wàn)古霉素可以對(duì)付它。 典型的金黃色葡萄球菌為球型，直徑0.8m左右，顯微鏡下排列成葡萄串狀。 金黃色葡萄球菌無(wú)芽胞、鞭毛，大多數(shù)無(wú)莢膜，革蘭氏染色陽(yáng)性。金黃色葡萄球菌營(yíng)養(yǎng)要求不高，在普通培養(yǎng)基上生長(zhǎng)良好，需氧或兼性厭氧，最適生長(zhǎng)溫度37C，最適生長(zhǎng)pH7.4,干燥環(huán)境下可存活數(shù)周。平板上菌落厚、有光澤、圓形凸起，直徑12mm。血平板菌落周圍形成透明的溶血環(huán)。金黃色葡萄球菌有高度的耐鹽性，可在1015%NaCl肉湯中生長(zhǎng)?？煞纸馄咸烟?、麥芽糖、乳糖、蔗糖，產(chǎn)酸不產(chǎn)氣。甲基紅反應(yīng)陽(yáng)性，VP反應(yīng)弱陽(yáng)性。許多菌株可分解精

13、氨酸，水解尿素，還原硝酸鹽，液化明膠。金黃色葡萄球菌具有較強(qiáng)的抵抗力，對(duì)磺胺類藥物敏感性低，但對(duì)青霉素、紅霉素等高度敏感。對(duì)堿性染料敏感，十萬(wàn)分之一的龍膽紫液即可抑制其生長(zhǎng)。,28,.,29,.,流行病學(xué),金黃色葡萄球菌在自然界中無(wú)處不在，空氣、水、灰塵及人和動(dòng)物的排泄物中都可找到。因而，食品受其污染的機(jī)會(huì)很多。美國(guó)疾病控制中心報(bào)告，由金黃色葡萄球菌引起的感染占第二位，僅次于大腸桿菌。金黃色葡萄球菌腸毒素是個(gè)世界性衛(wèi)生難題，在美國(guó)由金黃色葡萄球菌腸毒素引起的食物中毒，占整個(gè)細(xì)菌性食物中毒的33%，加拿大則更多，占到45%，我國(guó)每年發(fā)生的此類中毒事件也非常多。 金黃色葡萄球菌的流行病學(xué)一般有如下

14、特點(diǎn)：季節(jié)分布，多見(jiàn)于春夏季；中毒食品種類多，如奶、肉、蛋、魚(yú)及其制品。此外，剩飯、油煎蛋、糯米糕及涼粉等引起的中毒事件也有報(bào)道。上呼吸道感染患者鼻腔帶菌率83%，所以人畜化膿性感染部位，常成為污染源。 一般說(shuō)，金黃色葡萄球菌可通過(guò)以下途徑污染食品：食品加工人員、炊事員或銷售人員帶菌，造成食品污染；食品在加工前本身帶菌，或在加工過(guò)程中受到了污染，產(chǎn)生了腸毒素，引起食物中毒；熟食制品包裝不密封，運(yùn)輸過(guò)程中受到污染；奶?；蓟撔匀橄傺谆蚯菪缶植炕摃r(shí)，對(duì)肉體其他部位的污染。 金黃色葡萄球菌是人類化膿感染中最常見(jiàn)的病原菌，可引起局部化膿感染，也可引起肺炎、偽膜性腸炎、心包炎等，甚至敗血癥、膿毒癥等全

15、身感染。 金葡菌還是醫(yī)源性感染原因之一 金黃色葡萄球菌的致病力強(qiáng)弱主要取決于其產(chǎn)生的毒素和侵襲性酶：,30,.,a.溶血毒素：外毒素，分、四種，能損傷血小板，破壞溶酶體，引起肌體局部缺血和壞死 b.殺死白細(xì)胞素：可破壞人的白細(xì)胞和巨噬細(xì)胞 c.血漿凝固酶：當(dāng)金黃色葡萄球菌侵入人體時(shí)，該酶使血液或血漿中的纖維蛋白沉積于菌體表面或凝固，阻礙吞噬細(xì)胞的吞噬作用。葡萄球菌形成的感染易局部化與此酶有關(guān) d.脫氧核糖核酸酶：金黃色葡萄球菌產(chǎn)生的脫氧核糖核酸酶能耐受高溫，可用來(lái)作為依據(jù)鑒定金黃色葡萄球菌 e.腸毒素：金黃色葡萄球菌能產(chǎn)生數(shù)種引起急性胃腸炎的蛋白質(zhì)性腸毒素，分為A、B、C1、C2、C3、D、E

16、及F八種血清型。腸毒素可耐受100C煮沸30分鐘而不被破壞。它引起的食物中毒癥狀是嘔吐和腹瀉。此外，金黃色葡萄球菌還產(chǎn)生溶表皮素、明膠酶、蛋白酶、脂肪酶、肽酶等。,31,.,金葡菌引發(fā)各種疾病,1 腸炎： 多因原發(fā)疾病長(zhǎng)期用抗生素引起腸道菌群失調(diào)所致（如感冒），抗生素敏感菌株受到抑制，耐藥的金黃色葡萄球菌株趁機(jī)繁殖。金黃色葡萄球菌為侵襲性細(xì)菌，能產(chǎn)生毒素，對(duì)腸道破壞性大，所以金黃色葡萄球菌腸炎起病急，中毒癥狀嚴(yán)重，主要表現(xiàn)為嘔吐、發(fā)熱、腹瀉。嘔吐常在發(fā)熱前出現(xiàn)，發(fā)熱很高。輕癥大便次數(shù)稍多，為黃綠色糊狀便；重癥大便次數(shù)頻數(shù)，每日可達(dá)數(shù)十次，大便呈暗綠色水樣便，外觀像海水，所以叫海水樣便。粘液多，

17、有腥臭味，有時(shí)可排出片狀偽膜，將偽膜放入生理水，脫落的腸粘膜即漂在水面上，對(duì)診斷幫助很大。體液損失多，患兒脫水、電解質(zhì)紊亂和酸中毒嚴(yán)重，可發(fā)生休克。挑選大便粘液部分涂片，在顯微鏡下檢查可見(jiàn)大量膿細(xì)胞，如經(jīng)革蘭氏染色，顯微鏡檢查可見(jiàn)成堆的大量革蘭氏陽(yáng)性球菌。大便培養(yǎng)金黃色葡萄球菌生長(zhǎng)，即可明確診斷。,32,.,2 亞急性細(xì)菌性心內(nèi)膜炎： 病因 ： 1，病原體侵入血流：引起菌血癥敗血癥或膿毒血癥并侵襲心內(nèi)膜； 2，心瓣膜異常：有利于病原微生物的寄居繁殖； 3，防御機(jī)制的抑制：例如腫瘤患者使用細(xì)胞毒性藥物和器官移植患者用免疫抑制劑時(shí)病因包括各種細(xì)菌真菌及貝納特考克斯體（coxiella burnet

18、tii）等 。,33,.,臨床癥狀 亞急性感染性心內(nèi)膜炎：較急性者為常見(jiàn)且重要 （1）一般表現(xiàn)：大多數(shù)病例起病緩慢，低熱、乏力疲倦、少數(shù)起病急，有寒戰(zhàn)、高熱，或栓塞現(xiàn)象；部分患者起病前有口腔手術(shù)史，呼吸道感染、流產(chǎn)或分娩的病史 。 （2）發(fā)熱：伴全身性感染時(shí)，發(fā)熱最常見(jiàn)，常呈原因不明的持續(xù)發(fā)熱一周以上，不規(guī)則低熱多在38.540之間，也可為間歇熱或弛張熱伴有乏力盜汗，進(jìn)行性貧血，脾腫大，晚期可有杵狀指 （3）精神障礙：患者可伴有輕微的精神癥狀，但極少出現(xiàn)嚴(yán)重的精神錯(cuò)亂或譫妄，若心內(nèi)膜炎并發(fā)蛛網(wǎng)膜下腔出血或腦膜炎，則常會(huì)出現(xiàn)激越行為，精神錯(cuò)亂和意識(shí)障礙，亦可伴有局灶性的神經(jīng)系統(tǒng)體征 未治療的急性

19、患者幾乎均在4周內(nèi)死亡，亞急性者的自然史一般6個(gè)月。預(yù)后不良因素中以心力衰竭最為嚴(yán)重。除耐藥的格蘭陰性桿菌和真菌所致的心內(nèi)膜炎者外，大多數(shù)患者可獲細(xì)菌學(xué)治愈。但本病的近期和遠(yuǎn)期病死率仍較高。,34,.,體證： 原有心臟病雜音，相當(dāng)一部分的病例在病程中雜音的性質(zhì)及強(qiáng)度發(fā)生改變。部分病例有歐氏小結(jié)，也可有詹恩威結(jié)。后期可見(jiàn)腦、脾、腎等器官栓塞相應(yīng)體征。,35,.,Toxic Shock Syndrome（TSS) Author: Ramesh Venkataraman, MBBS; Chief Editor: Michael R Pinsky, MD, CM, FCCP, FCCM 定義： Tox

20、ic shock syndrome (TSS) is a toxin-mediated acute life-threatening illness, usually precipitated by infection with either Staphylococcus aureus or group A Streptococcus (GAS), also called Streptococcus pyogenes,36,.,37,.,臨床表現(xiàn)： It is characterized by high fever, rash, hypotension, multiorgan failure

21、(involving at least 3 or more organ systems), and desquamation, typically of the palms and soles, 1-2 weeks after the onset of acute illness. The clinical syndrome can also include severe myalgia, vomiting, diarrhea, headache, and nonfocal neurologic abnormalities.,38,.,金黃色葡萄球菌腦膜炎,一、病因 主要是亞細(xì)，其次顱腦損傷、

22、顱腦手術(shù)后及腰椎穿刺時(shí)消毒不嚴(yán)也可并發(fā)腦膜炎。腦膜附近的感染病灶如中耳炎、乳突炎、鼻竇炎等亦可引起該病。新生兒臍帶和皮膚的金葡菌感染也可繼發(fā)腦膜炎，發(fā)病時(shí)間多在產(chǎn)后2周左右。其他易患因素為：糖尿病、靜脈濫用毒品、血液透析及惡性腫瘤等。 二、發(fā)病機(jī)制 細(xì)菌侵入腦膜可有多種途徑：血源性：經(jīng)血循環(huán)進(jìn)入腦膜；直接擴(kuò)散：可以是顱腦外傷從顱外如耳部或鼻部感染向顱內(nèi)擴(kuò)散；逆行性血栓性脈管炎；醫(yī)源性通路：顱腦手術(shù)的污染、腦室引流及造影而將化膿菌直接接種于蛛網(wǎng)膜下腔。細(xì)菌抵達(dá)腦膜引起化腦，其致病機(jī)制和病理改變與腦膜炎球菌腦膜炎相似,39,.,三、臨床表現(xiàn) 起病不太急，常于原發(fā)化膿性感染數(shù)天或數(shù)周后發(fā)病，多有全身

23、感染中毒癥狀。畏寒發(fā)熱，伴持久而劇烈的頭痛，頸強(qiáng)直較一般腦膜炎明顯。除有腦膜炎癥狀外，尚有局部感染病灶，敗血癥患者還可有其他遷徙性病灶。還可出現(xiàn)皮疹，如蕁麻疹樣、猩紅熱樣皮疹或小膿皰疹。皮膚可見(jiàn)出血點(diǎn)，但很少融合成片，與腦膜炎球菌腦膜炎不同。如敗血癥過(guò)程中出現(xiàn)頭痛、嘔吐、神志改變、腦膜刺激征等表現(xiàn)，應(yīng)及時(shí)地進(jìn)行腦脊液檢查。病變以蛛網(wǎng)膜下腔為主，額葉、顳葉、頂葉部位較明顯，病程中可出現(xiàn)硬膜下積液、積膿，顱底粘連，可致腦神經(jīng)損害。并發(fā)腦膿腫者，可發(fā)生肢體癱瘓。,40,.,Thyroiditis Author: Robert P Hoffman, MD; Chief Editor: Stephen

24、Kemp, MD, PhD, Medscape The broad category of thyroiditis includes the following inflammatory diseases of the thyroid gland: (1) acute suppurative thyroiditis, which is due to bacterial infection; (2) subacute thyroiditis, which results from a viral infection of the gland; and (3) chronic thyroiditi

25、s, which is usually autoimmune in nature,41,.,Acute suppurative thyroiditis is rare in childhood because the thyroid is remarkably resistant to hematogenously spread infection. Most cases of acute thyroiditis involve the left lobe of the thyroid and are associated with a developmental abnormality of

26、 thyroid migration and the persistence of a pyriform sinus from the pharynx to the thyroid capsule. The usual organisms responsible include Staphylococcus aureus, Streptococcus hemolyticus, and pneumococcus. Other aerobic or anaerobic bacteria may also be involved.,42,.,History A history of acute il

27、lness, including fever, chills, neck pain, sore throat, hoarseness, and dysphagia, is common. Neck pain is frequently unilateral and radiates to the mandible, ears, or occiput. Neck flexion reduces the severity of the pain. The pain worsens with neck hyperextension. Physical Acute thyroiditis The pa

28、tient may have a fever of 38-40C. Acute illness may be evident. Neck tenderness is present, and the swollen thyroid gland is tender. The swelling and tenderness may be unilateral. Erythemas develop over the gland, and regional lymphadenopathy may develop as the disease progresses. Abscess formation

29、may occur,43,.,Laboratory Studies Acute thyroiditis Laboratory abnormalities in acute thyroiditis reflect the acute systemic illness. Findings include leukocytosis with a left shift and an increased sedimentation rate. Thyroid function test results are within the reference range,44,.,Subacute thyroi

30、ditis is generally thought to be due to viral processes and usually follows a prodromal viral illness. Various viral illnesses may precede the disease, including mumps, measles, influenza, infectious mononucleosis, adenoviral or Coxsackievirus infections, myocarditis, or the common cold. Other illne

31、sses or situations associated with subacute thyroiditis include catscratch fever, sarcoidosis, Q fever, malaria, emotional crisis, or dental work. The disease is more common in individuals with human leukocyte antigen (HLA)Bw35.,45,.,History Subacute thyroiditis Neck tenderness and swelling may occu

32、r. Occasionally, the initial symptoms are those of hyperthyroidism. Systemic symptoms such as weakness, fatigue, malaise, and fever are usually low grade. Physical Subacute thyroiditis The patient may have signs of systemic illness, such as low-grade fever and weakness. Signs of hyperthyroidism, inc

33、luding increased pulse rate, widened pulse pressure, fidgeting, tremor, nervousness, tongue fasciculations, brisk reflexes (possibly with clonus), weight loss, and warm moist skin, may be present. The thyroid gland may be enlarged and tender, with tenderness exacerbated by neck extension.,46,.,Labor

34、atory Studies Subacute thyroiditis The primary laboratory abnormalities are consistent with abnormal thyroid function. Initially, the thyroid-stimulating hormone (TSH) level is suppressed, and the free thyroxine (T4) level is increased. As the disorder progresses, transient or sometimes permanent hy

35、pothyroidism may develop. The WBC count is usually within the reference range but may be mildly elevated. High-sensitivity C-reactive protein levels are usually elevated in subacute thyroiditis.,47,.,Because chronic thyroiditis in children is usually due to an autoimmune process, it is HLA-associate

36、d, similar to other autoimmune endocrine diseases. The specific alleles in the atrophic and goitrous forms of the disease vary. The histologic disease picture varies, but lymphocytic thyroid infiltration is the hallmark of the disease and frequently obliterates much of the normal thyroid tissue. Fol

37、licular thyroid cells may be small or hyperplastic. The degree of fibrosis among patients also widely varies. Children usually have hyperplasia with minimal fibrosis. The blood contains autoantibodies to thyroid peroxidase and, frequently, autoantibodies to thyroglobulin. Autoimmune thyroiditis is a

38、lso frequently part of the polyglandular autoimmune syndromes.,48,.,History Chronic autoimmune thyroiditis is observed in the following 3 patterns: Goiter that is usually diffuse and nontender: Systemic illness is not evident. The thyroid gland is frequently 2-3 times its normal size and may be larg

39、er. The patient, parent, or physician may discover the goiter. Symptoms of hypothyroidism: In children, this frequently includes poor growth or short stature. Adolescent girls may have primary or secondary amenorrhea. Boys may have delayed puberty. Because the disease develops slowly, the patient or

40、 parent may not notice other signs of hypothyroidism, including constipation, lethargy, and cold intolerance. The child with diabetes may have decreasing insulin requirement. Symptoms of hyperthyroidism: These may include poor attention span, hyperactivity, restlessness, heat intolerance, or loose s

41、tools.,49,.,Physical Chronic autoimmune thyroiditis Initially, an enlarged, lumpy, bumpy, and nontender thyroid is often present. The gland may not be enlarged, particularly in children who have profound hypothyroidism. Signs of hypothyroidism include slow growth rate, weight gain, slow pulse, cold

42、dry skin, coarse hair and facial features, edema, and delayed relaxation of the deep tendon reflexes. Signs of hyperthyroidism are occasionally present early in the disease,50,.,Laboratory Studies Chronic thyroiditis Laboratory abnormalities reflect thyroid function abnormality and evidence of autoi

43、mmunity. TSH levels are increased in children with subclinical and overt hypothyroidism. Free T4 levels are within the reference range in the former and low in the latter. In children with hyperthyroidism, TSH levels are suppressed. Many children have normal thyroid function and normal TSH levels. A

44、ntithyroid peroxidase (antithyrocellular, antimicrosomal) antibody levels elevated above the reference range are the most sensitive indicator of thyroid autoimmunity. Many children also have antithyroglobulin antibodies, although this is less sensitive and less specific.,51,.,staphylococcus aureus e

45、ncephalitis,52,.,53,.,54,.,55,.,56,.,After acute development of a left sided palsy a 57-year-old Caucasian German woman was referred to us with a preceding 4-day history of high-grade fever, coughing and general weakness. Due to mechanical replacement of the aortic valve 11 months ago, ampicillin an

46、d sulbactam had been selected for antibiotic treatment. Initial chest X-ray, transthoracic echocardiography, abdominal ultrasound, and cultures of blood and urine had all been negative for signs of infection.,57,.,The neurological exam revealed left facial weakness, slurriness of speech, left-sided

47、hemi-paresis and hemihypaesthesia whereas clinical examina-tion was normal apart from minor respiratory distress. Blood tests showed a normal white cell count, a low platelet count (60 109/l), elevations of creatine kinase (466 U/l), serum troponin T (0.04 g/l), and an elevated CRP (471 mg/l) while

48、coagulation tests demonstrated an INR of 2.4 (under coumarine treatment) that was normal- ized rapidly thereafter.,58,.,The initial brain CT and MRI revealed two secondarily haemorrhaged infarcted areas (Figure 1). The analysis of the cerebrospinal fluid displayed a cell count of 127/ l, a total pro

49、tein of 1.36 g/l and lactate concentration of 3.5 mmol/l. Because of the severe septic clinical course antibiotic therapy was changed to ceftriax-one, gentamicin and linezolid. Complementary transoeso-phageal echocardiography showed two major vegetations on the mechanical aortic valve and the develo

50、pment of an aortic ring abscess (Figure 1, I+J). These findings pointed conclusively to a septic embolic encephalitis due to IE.,59,.,A severe deterioration of the patient s clinical condition caused by additional intracranial bleedings four days later (Figure 1, C+D) prevented a surgical replacemen

51、t of the aortic valve. All blood cultures revealed a Staphylococcus aureus bacteriaemia resistant to the formerly applied ampicillin but sensitive to gentamicine and linezolid. Although medical therapy was intensified, the patient finally died from cardiac failure.,.,60,Figure 1. Axial cNECT and cMR

52、 images on admission (A+B, E-H) and 4 days after onset of neurological symptoms (C+D). (A+B) NECT images show initially small cortical bleedings left frontal and right occipital and swollen cortex sections right occipital. (C+D) 4 days later the haemorrhage is enlarged, and multiple zones of infarct

53、ion are visible. (E+F) Axial FLAIR weighted images demonstrate bilaterally multiple cortical and subcortical signal hyperintensities representing multiple ischemic lesions. (G+H) Axial T2*GRE MR images show microbleedings and haemorrhages within infarcted lesions. Transoesophageal echocardiogram exa

54、mination shortly after admission (I+J). (I) Demonstration of two large oscillating vegetations (arrows), one of 4.5 2 mm on the upstream side and one of 4.3 7.4 mm on the downstream side of the bileaflet tilting disk valve. (J) Closer examination of the mechanical aortic valve shows relevant thicken

55、ing of the aortic root indicating an evolving ring abscess (arrow).,61,.,AJNR Am J Neuroradiol 27:217990 Nov-Dec 2006 2179,62,.,63,.,小 結(jié),一、該病例特點(diǎn) 1 基礎(chǔ)疾?。?1）自身免疫性疾?。杭谞钕倌[塊（性質(zhì)待定），TSH受體抗體（+），GAD(-)。 丙肝抗體（+） 2 ）腦外傷、高血壓。 2 誘因：感冒，自服感冒藥后發(fā)病。 3 發(fā)病后早期癥狀： 1）一般癥狀：發(fā)熱、肌肉疼痛、四肢乏力。 2）神經(jīng)系統(tǒng)癥狀：雙下肢無(wú)力，但是能站立， 體征：神清，顱神經(jīng)陰性，雙上肢肌力4級(jí)，雙下肢肌力3級(jí)，肌肉壓痛。未見(jiàn)皮膚出血點(diǎn)。心臟可聞吹風(fēng)樣雜音。,64,.,4 病情進(jìn)展 病情進(jìn)行性加重，從一般癥狀如發(fā)熱、肢體乏力、肌肉疼痛到出現(xiàn)CNS體征沒(méi)有過(guò)渡階段。不像金葡菌腦膜炎或其他細(xì)菌性腦膜炎，有一個(gè)最后形成腦膿腫短暫的過(guò)渡階段（幾天或幾周）。 其原因： A 亞