1、金黃色葡萄球菌腦炎病例討論金黃色葡萄球菌腦炎病例討論實驗室檢查：急診查（1月17號） 血鉀 mmol/l 鈉 mmol/l；白細胞 X109/L,中性粒%，血小板74 X109/L 血沉37s, 血紅蛋白128 g/l, 。1月17日晚查 血鉀 mmol/l 鈉135 mmol/l ； 1月18號：血常規 白細胞 X109/L，中性粒%；血小板60 X 109/L，血紅蛋白132 g/l ，抽血查血培養。乳酸脫氫酶325 U/L 肌酸激酶 U/L ;尿素氮 mmol/l 肌酐 umol/l 血糖 mmol/l 白蛋白 g/l 總膽 umol/l 直膽 umol/l 間膽 umol/l 谷丙48

2、 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.雙側半卵圓中心多發腔梗；3.大腦萎縮，腦白質疏松；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不均勻，性質待定， 實驗室檢查： 腰穿：腦脊液清亮,壓力240mmH2O ,蛋白547 mg/l, 氯113 mmol/l , 糖4.10 mmol/l,白細胞10 X106/L, 紅細胞 X109/L。 1月18日查體較前無明顯變化，自訴無力稍好轉，仍有肌痛，發熱，38度

3、左右； 1月19日體溫度，血壓136/98 mmHg，神志欠清、夜間有講胡話，雙側瞳孔等大、等圓，對光反應靈敏，瞳孔直徑3毫米，水平眼震陽性，伸舌居中，頸抗弱陽性，雙上肢肌力3級，雙下肢肌力3級，肌肉壓痛明顯，病理征陰性。心尖區吹風樣雜音。 20日 體溫度，血壓110/70 mmHg，神志模糊、夜間有講胡話，問話不能準確應答，雙側瞳孔等大、等圓，對光反應靈敏，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，張口費力，伸舌不能，咽反射減退，聲嘶，頸抗陽性，左側肢體肌力3級，右側肢體肌力0級，病理征陰性，四肢肌肉壓痛明顯，心尖區吹風樣雜音。周身散在出血點，前胸及雙側大腿內側明顯。 腰穿：

4、腦脊液清亮,壓力240mmH2O ,蛋白547 1月19號血鉀 mmol/l 鈉 mmol/l ；血常規 白細胞 X109/L，中性粒%；血小板41 X109/L ，紅細胞 X1012/L ,血紅蛋白124 g/l, 結核抗體陰性。20日轉入ICU治療，20日上午血培養報告：金黃色葡萄球菌感染，尿素氮mmol/l ，肌酐umol/l ，白蛋白 g/l ，總膽 umol/l ，直膽 umol/l， 間膽 umol/l， 谷丙 u/l ，谷草 u/l，復查腰穿腦脊液蛋白614 mg/l, 氯117 mmol/l , 糖3.8 mmol/l,白細胞75 X106/L,紅細胞 X109/L；CSF壓力

5、? 頭顱MRI 示腦內多發病變并部分出血合并腦梗死可能；左顳葉軟化灶，腦白質疏松、腦萎縮同前。 頸部CT示甲狀腺右葉改變性質待定：結節型甲狀腺腫？腺瘤？腺癌？建議進一步檢查； 肺部CT雙側胸腔積液；心臟增大（左房、左室增大為主），請結合臨床； 腹部CT兩肺感染；膽囊多發結石；肝及左腎低密度灶性質待定，建議上腹部CT增強掃描；肝多發鈣化灶。 頭顱CT示雙側額葉、左側頂、枕葉及右側小腦半球病變，結合臨床考慮腦炎并出血可能性大，不除外合并部分腦梗死，建議治療后復查。 1月19號血鉀 mmol/l 鈉 mmol/l ；病例特點1 中老年男性病人，突發四肢無力、疼痛，以下肢無力明顯，進行性加重，發展到眼

6、球固定、雙眼瞼下垂，聲音嘶啞，吞咽困難，左側肢體癱瘓。2 發病前有感冒病史，既往有腦外傷、高血壓病史3 胸腹部、大腿內側、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個月，甲狀腺功能示甲減5 實驗室檢查：入院時白細胞總數 X109/L,中性粒%，隨著病情發展，白細胞總數增加，中性粒細胞數增加；入院時血小板減少血小板74 X109/L，第二天血小板60 X 109/L，第三天血小板41 X109/L 病例特點1 中老年男性病人，突發四肢無力、疼痛，以下肢無力明5 血培養示金黃色葡萄球菌感染，以后在尿液、多次血培養均發現金黃色葡萄球菌感染，痰培養克雷柏氏菌。6 腎功能逐漸加重1月18

7、號尿素氮 mmol/l 肌酐 umol/l ，19號尿素氮mmol/l ，肌酐umol/l ，20號7 腦脊液：1月18號壓力240mmH20,白細胞10 X106/L,19號壓力？白細胞75 X106/L8 TSH受體抗體（+）GAD抗體（-）丙肝抗體（+）TF3, 2.02,TSH 0.05, D二聚體（+）FDP(+)TG-G(-)C反應蛋白，肌鈣蛋白ABO血型 A型，RH血型（+）5 血培養示金黃色葡萄球菌感染，以后在尿液、多次血培養均發現教培用金黃色葡萄球菌腦炎病例討論課件頭部CT,MRI演變頭部CT,MRI演變頭部CT,MRI演變頭部CT,MRI演變頭部CT,MRI演變頭部CT,M

8、RI演變頭部CT,MRI演變頭部CT,MRI演變頭部CT,MRI演變頭部CT,MRI演變頭部CT,MRI演變頭部CT,MRI演變頭部CT,MRI演變頭部CT,MRI演變頭部CT,MRI演變頭部CT,MRI演變多因原發疾病長期用抗生素引起腸道菌群失調所致（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繁殖。The thyroid gland may be enlarged and tender, with tenderness exacerbated by neck extension.它引起的食物中毒癥狀是嘔吐和腹瀉。B CT 監測腦出血情況。The disease is mor

9、e common in individuals with human leukocyte antigen (HLA)Bw35.The gland may not be enlarged, particularly in children who have profound hypothyroidism.4 mm on the downstream side of the bileaflet tilting disk valve.1月19日體溫度，血壓136/98 mmHg，神志欠清、夜間有講胡話，雙側瞳孔等大、等圓，對光反應靈敏，瞳孔直徑3毫米，水平眼震陽性，伸舌居中，頸抗弱陽性，雙上肢肌力3

10、級，雙下肢肌力3級，肌肉壓痛明顯，病理征陰性。它引起的食物中毒癥狀是嘔吐和腹瀉。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。1月19號血鉀 mmol/l 鈉 mmol/l ；A MRI：早期T1出現低信號，T2和flair出現高信號，部位出現在白質或灰白質交界處，要考慮炎性脫髓鞘。后期可見腦、脾、腎等器官栓塞相應體征。隨著病情發展，腦壓進一步增高，白細胞數和紅細胞進一步增多。皮膚可見出血點，但很少融合成片，與腦膜炎球菌腦膜炎不同。病情進行性加重，從一般癥狀如發熱、肢體乏力、肌肉疼痛到出現CNS體征沒有過渡階段。The pain worsens with neck hyperex

11、tension.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。D 腦脊液：早期細胞數不高或稍高，但是，腦壓高，蛋白高，有少量紅細胞（幾個），一定要排除損傷所致。多因原發疾病長期用抗生素引起腸道菌群失調所致（如感冒），抗生甲狀腺CT甲狀腺CT強化的MRI強化的MRI強化的MRI強化的MRI教培用金黃色葡萄球菌腦炎病例討論課件神經影像學點評該病例神經影像學演變有以下幾個特點：1 由于病情發展快，神經影像學變化大，做到實時跟蹤。2 發病第五天第一次頭部MRI平掃，除左側顳葉因腦外傷所致腦軟化灶外，可見右側額葉散在的大小不一類似腦梗死灶。如圖所示。未見出血等其他病灶。神經影像

12、學點評該病例神經影像學演變有以下幾個特點：3 發病第七天頭部MRI平掃，DWI,CT顯示病灶播散、廣泛，小腦、雙側大腦半球白質、灰質均有病灶，出血與類似梗死灶同時存在。但是，中線結構沒有移位，腦室系統內未見出血。腦干未見明顯病灶，與臨床表現不符（眼球固定、雙眼瞼下垂、聲音嘶啞）。此時，已有胸、腹部、大腿內側散在暗紅色皰疹。在ICU搶救后，病情一度有好轉。3 發病第七天頭部MRI平掃，DWI,CT顯示病灶播散、廣泛4 發病后第十天，頭部CT示腦出血，腦室內出血。但是，中線結構仍然沒有移位。病情進行性加重，出現昏迷。4 發病后第十天，頭部CT示腦出血，腦室內出血。但是，中線結5 發病第十三天，頭部

13、CT沒有很大變化（與23號比較），病情有所好轉，皮疹消退，輸血小板后，血小板有所恢復。但是，神經系統狀況無好轉。5 發病第十三天，頭部CT沒有很大變化（與23號比較），病情 結合文獻討論 結合文金黃色葡萄球菌簡介 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，是革蘭氏陽性菌的代表，可引起許多嚴重感染。 金黃色葡萄球菌細胞壁含90%的肽聚糖和10%的磷壁酸。其肽聚糖的網狀結構比革蘭氏陰性菌致密，染色時結晶紫附著后不被酒精脫色故而呈現紫色，相反，陰性菌沒有細胞壁結構，

14、所以紫色被酒精沖掉然后附著了沙黃的紅色 。新出現的耐甲氧西林金黃色葡萄球菌，被稱作超級細菌，幾乎能抵抗人類現在所有的藥物，但是萬古霉素可以對付它。 典型的金黃色葡萄球菌為球型，直徑左右，顯微鏡下排列成葡萄串狀。 金黃色葡萄球菌無芽胞、鞭毛，大多數無莢膜，革蘭氏染色陽性。金黃色葡萄球菌營養要求不高，在普通培養基上生長良好，需氧或兼性厭氧，最適生長溫度37C，最適生長pH7.4,干燥環境下可存活數周。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。金黃色葡萄球菌有高度的耐鹽性，可在1015%NaCl肉湯中生長。可分解葡萄糖、麥芽糖、乳糖、蔗糖，產酸不產氣。甲基紅反應陽

15、性，VP反應弱陽性。許多菌株可分解精氨酸，水解尿素，還原硝酸鹽，液化明膠。金黃色葡萄球菌具有較強的抵抗力，對磺胺類藥物敏感性低，但對青霉素、紅霉素等高度敏感。對堿性染料敏感，十萬分之一的龍膽紫液即可抑制其生長。 金黃色葡萄球菌簡介 金黃色葡萄球菌 (Staphyloc教培用金黃色葡萄球菌腦炎病例討論課件流行病學 金黃色葡萄球菌在自然界中無處不在，空氣、水、灰塵及人和動物的排泄物中都可找到。因而，食品受其污染的機會很多。 疾病控制中心報告，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世界性衛生難題，在 由金黃色葡萄球菌腸毒素引起的食物中毒，占整個細菌性食物中毒的3

16、3%，加拿大則更多，占到45%，我國每年發生的此類中毒事件也非常多。 金黃色葡萄球菌的流行病學一般有如下特點：季節分布，多見于春夏季；中毒食品種類多，如奶、肉、蛋、魚及其制品。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，金黃色葡萄球菌可通過以下途徑污染食品：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，或在加工過程中受到了污染，產生了腸毒素，引起食物中毒；熟食制品包裝不密封，運輸過程中受到污染；奶牛患化膿性乳腺炎或禽畜局部化膿時，對肉體其他部位的污染。 金黃色葡萄球菌是人類

17、化膿感染中最常見的病原菌，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、膿毒癥等全身感染。金葡菌還是醫源性感染原因之一金黃色葡萄球菌的致病力強弱主要取決于其產生的毒素和侵襲性酶： 流行病學 金黃色葡萄球菌在自然界中無處不在，空氣、水 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.殺死白細胞素：可破壞人的白細胞和巨噬細胞 c.血漿凝固酶：當金黃色葡萄球菌侵入人體時，該酶使血液或血漿中的纖維蛋白沉積于菌體表面或凝固，阻礙吞噬細胞的吞噬作用。葡萄球菌形成的感染易局部化與此酶有關 d.脫氧核糖核酸酶：金黃色葡萄球菌產生的脫氧核糖核酸酶能耐受

18、高溫，可用來作為依據鑒定金黃色葡萄球菌 e.腸毒素：金黃色葡萄球菌能產生數種引起急性胃腸炎的蛋白質性腸毒素，分為A、B、C1、C2、C3、D、E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生溶表皮素、明膠酶、蛋白酶、脂肪酶、肽酶等。 a.溶血毒素：外毒素，分、四種，能金葡菌引發各種疾病1 腸炎： 多因原發疾病長期用抗生素引起腸道菌群失調所致（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繁殖。金黃色葡萄球菌為侵襲性細菌，能產生毒素，對腸道破壞性大，所以金黃色葡萄球菌腸炎起病急，中毒癥狀嚴重，主要表現為嘔吐、

19、發熱、腹瀉。嘔吐常在發熱前出現，發熱很高。輕癥大便次數稍多，為黃綠色糊狀便；重癥大便次數頻數，每日可達數十次，大便呈暗綠色水樣便，外觀像海水，所以叫海水樣便。粘液多，有腥臭味，有時可排出片狀偽膜，將偽膜放入生理水，脫落的腸粘膜即漂在水面上，對診斷幫助很大。體液損失多，患兒脫水、電解質紊亂和酸中毒嚴重，可發生休克。挑選大便粘液部分涂片，在顯微鏡下檢查可見大量膿細胞，如經革蘭氏染色，顯微鏡檢查可見成堆的大量革蘭氏陽性球菌。大便培養金黃色葡萄球菌生長，即可明確診斷。 金葡菌引發各種疾病1 腸炎：2 亞急性細菌性心內膜炎：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膜； 2，心瓣

20、膜異常：有利于病原微生物的寄居繁殖； 3，防御機制的抑制：例如腫瘤患者使用細胞毒性藥物和器官移植患者用免疫抑制劑時病因包括各種細菌真菌及貝納特考克斯體（coxiella burnettii）等 。2 亞急性細菌性心內膜炎：臨床癥狀亞急性感染性心內膜炎：較急性者為常見且重要 （1）一般表現：大多數病例起病緩慢，低熱、乏力疲倦、少數起病急，有寒戰、高熱，或栓塞現象；部分患者起病前有口腔手術史，呼吸道感染、流產或分娩的病史 。（2）發熱：伴全身性感染時，發熱最常見，常呈原因不明的持續發熱一周以上，不規則低熱多在38.540之間，也可為間歇熱或弛張熱伴有乏力盜汗，進行性貧血，脾腫大，晚期可有杵狀指 （

21、3）精神障礙：患者可伴有輕微的精神癥狀，但極少出現嚴重的精神錯亂或譫妄，若心內膜炎并發蛛網膜下腔出血或腦膜炎，則常會出現激越行為，精神錯亂和意識障礙，亦可伴有局灶性的神經系統體征 未治療的急性患者幾乎均在4周內死亡，亞急性者的自然史一般6個月。預后不良因素中以心力衰竭最為嚴重。除耐藥的格蘭陰性桿菌和真菌所致的心內膜炎者外，大多數患者可獲細菌學治愈。但本病的近期和遠期病死率仍較高。 臨床癥狀體證：原有心臟病雜音，相當一部分的病例在病程中雜音的性質及強度發生改變。部分病例有歐氏小結，也可有詹恩威結。后期可見腦、脾、腎等器官栓塞相應體征。 體證：Toxic Shock Syndrome（TSS)Au

22、thor: Ramesh Venkataraman, MBBS; Chief Editor: Michael R Pinsky, MD, CM, FCCP, FCCM 定義： Toxic 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 pyogene

23、s Toxic Shock Syndrome（TSS)教培用金黃色葡萄球菌腦炎病例討論課件臨床表現： It is characterized by high fever, rash, hypotension, multiorgan failure (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 inc

24、lude severe myalgia, vomiting, diarrhea, headache, and nonfocal neurologic abnormalities. 臨床表現：金黃色葡萄球菌腦膜炎 一、病因 主要是亞細，其次顱腦損傷、顱腦手術后及腰椎穿刺時消毒不嚴也可并發腦膜炎。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腦膜炎，發病時間多在產后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、發病機制 細菌侵入腦膜可有多種途徑：血源性：經血循環進入腦膜；直接擴散：可以是顱腦外傷從顱外如耳部或鼻部感染向顱內

25、擴散；逆行性血栓性脈管炎；醫源性通路：顱腦手術的污染、腦室引流及造影而將化膿菌直接接種于蛛網膜下腔。細菌抵達腦膜引起化腦，其致病機制和病理改變與腦膜炎球菌腦膜炎相似 金黃色葡萄球菌腦膜炎 一、病因三、臨床表現 起病不太急，常于原發化膿性感染數天或數周后發病，多有全身感染中毒癥狀。畏寒發熱，伴持久而劇烈的頭痛，頸強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。還可出現皮疹，如蕁麻疹樣、猩紅熱樣皮疹或小膿皰疹。皮膚可見出血點，但很少融合成片，與腦膜炎球菌腦膜炎不同。如敗血癥過程中出現頭痛、嘔吐、神志改變、腦膜刺激征等表現，應及時地進行腦脊液檢查。病變以蛛網

26、膜下腔為主，額葉、顳葉、頂葉部位較明顯，病程中可出現硬膜下積液、積膿，顱底粘連，可致腦神經損害。并發腦膿腫者，可發生肢體癱瘓。 三、臨床表現 ThyroiditisAuthor: Robert P Hoffman, MD; Chief Editor: Stephen Kemp, MD, PhD, Medscape The broad category of thyroiditis includes the following inflammatory diseases of the thyroid gland: (1) acute suppurative thyroiditis, which

27、is due to bacterial infection; (2) subacute thyroiditis, which results from a viral infection of the gland; and (3) chronic thyroiditis, which is usually autoimmune in nature Thyroiditis Acute suppurative thyroiditis is rare in childhood because the thyroid is remarkably resistant to hematogenously

28、spread infection. Most cases of acute thyroiditis involve the left lobe of the thyroid and are associated with a developmental abnormality of thyroid migration and the persistence of a pyriform sinus from the pharynx to the thyroid capsule. The usual organisms responsible include Staphylococcus aure

29、us, Streptococcus hemolyticus, and pneumococcus. Other aerobic or anaerobic bacteria may also be involved. Acute suppurative thyroidHistory A history of acute illness, including fever, chills, neck pain, sore throat, hoarseness, and dysphagia, is common. Neck pain is frequently unilateral and radiat

30、es to the mandible, ears, or occiput. Neck flexion reduces the severity of the pain. The pain worsens with neck hyperextension. Physical Acute thyroiditis The patient may have a fever of 38-40C. Acute illness may be evident. Neck tenderness is present, and the swollen thyroid gland is tender. The sw

31、elling and tenderness may be unilateral. Erythemas develop over the gland, and regional lymphadenopathy may develop as the disease progresses. Abscess formation may occurHistory Laboratory Studies Acute thyroiditis Laboratory abnormalities in acute thyroiditis reflect the acute systemic illness. Fin

32、dings include leukocytosis with a left shift and an increased sedimentation rate. Thyroid function test results are within the reference rangeLaboratory Studies Subacute thyroiditis is generally thought to be due to viral processes and usually follows a prodromal viral illness. Various viral illness

33、es may precede the disease, including mumps, measles, influenza, infectious mononucleosis, adenoviral or Coxsackievirus infections, myocarditis, or the common cold. Other illnesses or situations associated with subacute thyroiditis include catscratch fever, sarcoidosis, Q fever, malaria, emotional c

34、risis, or dental work. The disease is more common in individuals with human leukocyte antigen (HLA)Bw35. Subacute thyroiditis is geHistory Subacute thyroiditis Neck tenderness and swelling may occur. Occasionally, the initial symptoms are those of hyperthyroidism. Systemic symptoms such as weakness,

35、 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, including increased pulse rate, widened pulse pressure, fidgeting, tremor, nervousness, tongue fasciculatio

36、ns, 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.History Laboratory Studies Subacute thyroiditis The primary laboratory abnormalities are consistent with abnormal t

37、hyroid 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 hypothyroidism may develop. The WBC count is usually within the reference range but may be mildly elevat

38、ed. High-sensitivity C-reactive protein levels are usually elevated in subacute thyroiditis. Laboratory Studies Because chronic thyroiditis in children is usually due to an autoimmune process, it is HLA-associated, similar to other autoimmune endocrine diseases. The specific alleles in the atrophic

39、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. Follicular thyroid cells may be small or hyperplastic. The degree of fibrosis among patient

40、s 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 also frequently part of the polyglandular autoimmune syndromes. Because chronic thyroidHi

41、story 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 larger. The patient, parent, or physician may discover the goiter. Symptom

42、s 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 parent may not notice other signs of hypothyroidism, including consti

43、pation, 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 stools. History 20日 體溫度，血壓110/70 mmHg，神志模糊、夜間有講胡話，問話不能準確應答，雙側瞳孔等大、等圓，對光

44、反應靈敏，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，張口費力，伸舌不能，咽反射減退，聲嘶，頸抗陽性，左側肢體肌力3級，右側肢體肌力0級，病理征陰性，四肢肌肉壓痛明顯，心尖區吹風樣雜音。腰穿：腦脊液清亮,壓力240mmH2O ,蛋白547 mg/l, 氯113 mmol/l , 糖4.Subacute thyroiditis國外注意到DWI能區別硬膜下小膿腫。金黃色葡萄球菌具有較強的抵抗力，對磺胺類藥物敏感性低，但對青霉素、紅霉素等高度敏感。多因原發疾病長期用抗生素引起腸道菌群失調所致（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繁殖。新出現的耐甲氧西林金黃色葡萄

45、球菌，被稱作超級細菌，幾乎能抵抗人類現在所有的藥物，但是萬古霉素可以對付它。熟食制品包裝不密封，運輸過程中受到污染；1）一般癥狀：發熱、肌肉疼痛、四肢乏力。Axial cNECT and cMR images on admission (A+B, E-H) and 4 days after onset of neurological symptoms (C+D).新出現的耐甲氧西林金黃色葡萄球菌，被稱作超級細菌，幾乎能抵抗人類現在所有的藥物，但是萬古霉素可以對付它。(466 U/l), serum troponin T (0.金黃色葡萄球菌細胞壁含90%的肽聚糖和10%的磷壁酸。E 腎功能和肝

46、功能惡化，肌酶譜增高。Laboratory StudiesPhysical 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,

47、slow pulse, cold 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 disease20日 體溫度，血壓110/70 mmHg，神志模糊、夜間有Laboratory Studies Chronic thyroiditis Laboratory abnormalities reflect thyroid f

48、unction abnormality and evidence of autoimmunity. 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

49、thyroid function and normal TSH levels. Antithyroid 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 le

50、ss specific. Laboratory Studies staphylococcus aureus encephalitis staphylococcus aureus encephal教培用金黃色葡萄球菌腦炎病例討論課件教培用金黃色葡萄球菌腦炎病例討論課件教培用金黃色葡萄球菌腦炎病例討論課件 教培用金黃色葡萄球菌腦炎病例討論課件 After acute development of a left sided palsy a 57-year-old Caucasian German woman was referred to us with a preceding 4-day hist

51、ory of high-grade fever, coughing andgeneral weakness. Due to mechanical replacement of theaortic valve 11 months ago, ampicillin and sulbactam hadbeen selected for antibiotic treatment. Initial chest X-ray,transthoracic echocardiography, abdominal ultrasound,and cultures of blood and urine had all

52、been negative forsigns of infection. After acute developme The neurological exam revealed left facial weakness, slurriness of speech, left-sided hemi-paresis and hemihypaesthesia whereas clinical examina-tion was normal apart from minor respiratory distress. Blood tests showed a normal white cell co

53、unt, a lowplatelet count (60 109/l), elevations of creatine kinase(466 U/l), serum troponin T (0.04 g/l), and an elevatedCRP (471 mg/l) while coagulation tests demonstrated anINR of 2.4 (under coumarine treatment) that was normal-ized rapidly thereafter. The neurological exam reThe initial brain CT

54、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 protein 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 ceft

55、riax-one, gentamicin and linezolid. Complementary transoeso-phageal echocardiography showed two major vegetations on the mechanical aortic valve and the development of an aortic ring abscess (Figure 1, I+J). These findings pointedconclusively to a septic embolic encephalitis due to IE.The initial br

56、ain CT and A severe deterioration of the patient s clinical conditioncaused by additional intracranial bleedings four days later(Figure 1, C+D) prevented a surgical replacement of theaortic valve. All blood cultures revealed a Staphylococcusaureus bacteriaemia resistant to the formerly appliedampici

57、llin but sensitive to gentamicine and linezolid.Although medical therapy was intensified, the patientfinally died from cardiac failure.A severe deterioration of the Figure 1. Axial cNECT and cMR images on admission (A+B, E-H) and 4 days after onset of neurological symptoms (C+D). (A+B) NECT images s

58、how 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 infarction are visible. (E+F) Axial FLAIRweighted 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. Transoesophagealechocardiogram examination shortly after admission (I+J). (I) Demonstration of two large oscillating vegetation