《胸心外科》全冊配套教學(xué)課件1

《胸心外科》全冊配套教學(xué)課件1早上好胸部損傷ThoracicTrauma概述

一、現(xiàn)狀及意義㈠現(xiàn)狀⒈容易受傷：胸部所占體積大，目標(biāo)明顯；⒉后果嚴(yán)重：兩大生命器官----心臟

和肺（循環(huán)和呼吸）；

⒊死亡率高：外傷是死亡原因的第三位，在外傷的死亡者中，35—50%是胸外傷致死，在創(chuàng)傷致死原因中居第一位。㈡意義由于胸外傷的致死率高，使其診治顯得非常重要，特別是急救方面。

據(jù)統(tǒng)計，經(jīng)及時治療，80%的危重傷員得以存活。

急救方法是學(xué)習(xí)胸外傷的重點。二、胸廓和胸膜腔的

解剖與生理特點⒈胸廓-----骨性支架（胸椎、胸骨及12對肋骨）+肌肉軟組織⒉胸膜腔-----由臟壁層胸膜圍成的完全封閉的潛在性腔隙胸膜腔特點：①完整性②呼吸過程始終是負(fù)壓吸氣相：-8~-10cmH2O

呼氣相：-3~-5cmH2O此二特點是維持呼吸循環(huán)功能，特別是呼吸功能的二個必要條件。由于胸部有心、肺兩大生命器官，任何損傷導(dǎo)致胸膜腔完整性及負(fù)壓發(fā)生改變，均可引起心肺功能（呼吸循環(huán)）變化，甚至危及生命。⒊三個壓力的關(guān)系

┏大氣壓三個壓力┣胸內(nèi)壓（胸膜腔內(nèi)壓）┗肺內(nèi)壓（肺泡內(nèi)壓）

為了便于理解傷后的病理生理變化，現(xiàn)以呼吸過程為例簡述三個壓力的關(guān)系：

吸氣時，胸廓外展，膈肌下降，使胸腔的容積增大，胸內(nèi)壓下降（負(fù)壓值增大至-8~-10cmH2O）；肺亦隨之?dāng)U張，肺容積增大，肺內(nèi)壓下降，當(dāng)肺內(nèi)壓低于大氣壓（設(shè)為0）時，吸氣開始，當(dāng)肺內(nèi)壓等于大氣壓時，吸氣停止?！髿鈮悍蝺?nèi)壓肺內(nèi)壓胸內(nèi)壓胸內(nèi)壓空氣大氣壓

呼氣時，胸廓回縮，膈肌上抬，使胸腔的容積減小，胸內(nèi)壓上升（負(fù)壓值減小至-3~-5cmH2O）；肺亦隨之彈性回縮，肺容積變小，肺內(nèi)壓上升，當(dāng)肺內(nèi)壓高于大氣壓（設(shè)為0）時，呼氣開始，當(dāng)肺內(nèi)壓等于大氣壓時，呼氣停止。↑↑↑←←→→大氣壓肺內(nèi)壓肺內(nèi)壓胸內(nèi)壓胸內(nèi)壓廢氣大氣壓三、胸部損傷分類及致傷原因

分類依據(jù)：⑴是否穿破壁層胸膜⑵胸膜腔是否與外界相通

是否穿破壁層胸膜胸膜腔是否與外界相通致傷原因閉合性損傷

否

否┏第一車禍┓鈍性傷←┫┣→多發(fā)傷┗第二工農(nóng)業(yè)意外┛開放性損傷

是

是┏投射武器┓穿通傷←┫┣→單處傷┗刀子等┛

表胸部損傷分類及致傷原因四、胸部損傷的臨床表現(xiàn)和病理生理變化

Themanifestationandpathophysiologyofthoracictrauma㈠癥狀⒈胸部疼痛------為最主要的臨床癥狀胸壁損傷，肋骨骨折和胸骨骨折等，刺激肋間神經(jīng)引起疼痛。

⒉呼吸困難（不同程度）

(1)反常呼吸運動；

(2)肺組織受壓；

(3)氣道阻塞；

(4)呼吸運動受限。⒊循環(huán)障礙（不同程度）

(1)失血(復(fù)合傷）；

(2)縱隔隨呼吸而左右來回移位,縱隔和肺門神經(jīng)叢受刺激(胸膜肺休克)；

(3)劇烈疼痛。⒋其它：痰中帶血、咯血、血性泡沫痰等㈡胸部比較特殊的體征

⒈胸壁裂傷；⒉胸廓畸形；⒊骨折征：局部壓痛﹑骨摩擦感、胸廓擠壓征；

⒋反常呼吸運動；⒌皮下氣腫；⒍胸腔積氣、積液征；心包積液征。五、診斷及治療

⒈根據(jù)外傷史+臨床表現(xiàn)一般作出初步診斷不困難，疑診者可行診斷性胸穿或心包穿刺，必要時可行胸部X線檢查；⒉胸部外傷的診療要貫徹“先初步診斷→緊急治療（急救措施）→進(jìn)一步診治”的方案需要緊急處理時不容許進(jìn)行更多檢查(包括X線檢查)⒊治療原則⑴恢復(fù)胸壁的完整性，恢復(fù)和重建胸膜腔負(fù)壓；⑵呼吸支持：①保持呼吸道通暢②維持呼吸功能⑶循環(huán)支持：抗休克治療等；⑷根據(jù)剖胸探查指征積極進(jìn)行開胸手術(shù)；⑸防治感染：鼓勵咳嗽排痰，抗生素等。剖胸探查指征(1)胸膜腔進(jìn)行性出血(2)廣泛肺裂傷或支氣管斷裂，食管裂傷(3)心臟大血管損傷(4)胸腹聯(lián)合傷（Thoraco-abdominalinjury)(5)胸內(nèi)異物存留肋骨骨折

Ribfracture最常見，發(fā)生率占胸外傷的60％以上。㈠12對肋骨發(fā)生骨折的情況

-----與各肋骨解剖部位及特點有關(guān)┏1～3肋：因有鎖骨、肩胛骨和較厚肌肉1~7肋（真肋）┃保護(hù)，很少骨折；若發(fā)生骨折，┃提示暴力非常巨大┗4～7肋：長而固定，缺乏保護(hù)，最易發(fā)生骨折8~10肋（假肋）：雖長，但連接于軟骨肋弓上，有彈性緩沖，不易骨折11~12肋（浮肋）：因前端游離不固定，活動度較大，甚少骨折㈡病因⒈直接暴力

骨折發(fā)生于著力點；向胸內(nèi)彎曲骨折，尖銳的骨折斷端向內(nèi)移位，易發(fā)生合并傷，如可刺破肋間血管、胸膜和肺產(chǎn)生血胸或（和）氣胸。直接暴力著力點⒉間接暴力

骨折發(fā)生于應(yīng)力點；向胸外彎曲骨折，骨折斷端向外移位,不易發(fā)生合并傷，但可刺傷胸壁軟組織,產(chǎn)生胸壁血腫。

間接暴力應(yīng)力點㈢肋骨骨折分類⒈根據(jù)骨折斷端是否穿破皮膚分為：閉合性開放性⒉根據(jù)肋骨骨折的根數(shù)及骨折的處數(shù)分為：┏單根單處┃若有合并傷，治療合并傷顯得更重要；┃若無合并傷則為單純性。┗多根單處┏單根多處：機(jī)會很少。┗多根多處：本身就可引起一系列病理生理變化㈣多根多處肋骨骨折的

病理生理變化多根多處肋骨骨折Multiplebreaksofmultiplefracturesofrib胸壁軟化Malaciaofthechestwall反常呼吸運動Paradoxicalrespiratorymovementofchestwall

縱隔撲動Mediastinalflutter通氣功能障礙循環(huán)功能障礙連枷胸｛什么叫反常呼吸運動？吸氣時，軟化區(qū)的胸壁向內(nèi)陷，呼氣時則反之，軟化區(qū)的胸壁向外凸，這與正常胸廓呼吸運動方向相反。←←→→↓↓↓→←←→↑↑↑多根多處肋骨骨折致縱隔撲動的原理？

正常人不論吸氣相或呼氣相雙側(cè)胸膜腔壓力都是相等的，因此縱隔不會發(fā)生撲動；而在多根多處肋骨骨折時由于反常呼吸運動的出現(xiàn)，而導(dǎo)致呼吸過程中雙側(cè)胸膜腔壓力不等，形成壓力差，縱隔就會發(fā)生撲動。

吸氣時，胸廓外展，健側(cè)胸膜腔壓力降低，即負(fù)壓值增加，如

-8~-10cmH2O；而傷側(cè)由于反常呼吸運動，局部胸壁內(nèi)陷，容積相對減小，壓力就不能降到健側(cè)那樣低，可能只達(dá)到-6~-8cmH2O，這樣雙側(cè)胸膜腔壓力不等，縱隔向壓力低側(cè)，即健側(cè)移位。

呼氣時，胸廓回縮，健側(cè)胸膜腔壓力增高，即負(fù)壓值減少，如

-3~-5cmH2O；而傷側(cè)由于反常呼吸運動，局部胸壁向外鼓出，容積相對增大，壓力就不能升到健側(cè)那樣高，可能只達(dá)到-5~-7cmH2O，這樣雙側(cè)胸膜腔壓力又不等，縱隔向壓力低側(cè)，即傷側(cè)移位。㈤臨床表現(xiàn)

⒈癥狀局部疼痛（特點）+不同程度的呼吸困難↓↑加重畏痛-----→呼吸道分泌物潴留⒉體征

骨折局部壓痛或畸形+骨檫感+胸廓擠壓征（+），反常呼吸運動等胸廓擠壓征-----前后擠壓胸廓，患者既感骨折處疼痛，此即陽性，若不疼痛則為陰性。

⒊檢查X線胸片：明確診斷，了解有無合并傷。㈤治療

⒈單純性肋骨骨折治療原則：止痛和防治并發(fā)癥①止痛：藥物、固定、封閉等②防治并發(fā)癥：鼓勵咳嗽排痰，防止肺不張、肺炎；抗生素的應(yīng)用

對固定不同的看法：①限制呼吸運動，減少潮氣量；②不利于咳嗽排痰和深呼吸；③疼痛因肌肉痙攣而加重。

最好的治療方法是提供有效的解除疼痛的措施，使患者能行深呼吸、擴(kuò)張肺，維持和恢復(fù)全部肺功能。⒉多根多處肋骨骨折治療原則：上2條+最重要的是制止反常呼吸運動制止反常呼吸運動方法：①加壓包扎：適用于現(xiàn)場或范圍較小的胸壁軟化②外牽引固定：適用于大塊胸壁軟化或包扎不能奏效者

③肋骨手術(shù)固定：可用于需要剖胸探查或清創(chuàng)縫合者④呼吸機(jī)輔助呼吸：嚴(yán)重時出現(xiàn)呼吸衰竭，氣管插管或氣管切開，長者要2-3周。又叫呼吸機(jī)內(nèi)固定（internalfixation）。創(chuàng)傷性氣胸

TraumaticPneumothorax

概念：肺組織、支氣管破裂，胸壁傷口穿破胸膜→空氣逸進(jìn)胸膜腔→胸膜腔積氣→氣胸

發(fā)生率：僅次于肋骨骨折，是胸外傷后呼吸困難最常見的原因，其在鈍性傷中約占15

％～50％，在穿透性傷中約占30％～87.6％。分類：通常分為閉合性、開放性和張力性三類。㈠閉合性氣胸

ClosedPneumothorax

⒈病因常見閉合性損傷、胸壁損傷⒉特點氣胸形成后裂口封閉，不再漏氣⒊病理生理變化：對負(fù)壓影響不大：①傷側(cè)肺部分萎陷；②對呼吸循環(huán)功能影響小⒋臨床表現(xiàn)①胸痛、胸悶+氣促；②積氣征（氣管向健側(cè)偏移，傷側(cè)胸部叩診呈鼓音，呼吸音明顯減弱或消失）；③X線：胸腔積氣+肺壓縮（萎陷）⒌治療及急救措施①小量（肺壓縮<30%）不治療，1-2

周內(nèi)吸收，但年齡大，肺功能差者仍應(yīng)酌情治療；②中大量（肺壓縮>30~50%）胸穿抽氣或胸腔閉式引流，促使肺復(fù)張；③應(yīng)用抗生素，預(yù)防感染。㈡張力性氣胸

TensionPneumothorax

⒈病因常見于肺裂傷，也常見于胸壁穿通傷或支氣管損傷。⒉特點肺或支氣管裂口與胸膜腔相通，并形成單向活瓣，吸氣時開放，呼氣時關(guān)閉，空氣不能排出，胸內(nèi)壓愈來愈高，高于大氣壓（正壓）。⒊病理生理變化①傷側(cè)肺完全萎陷，健側(cè)肺受壓，呼吸功能嚴(yán)重?fù)p害。②縱隔向健側(cè)移位，血管扭曲靜脈回流受阻。上述變化導(dǎo)致呼吸循環(huán)衰竭。⒋臨床表現(xiàn)①極度呼吸困難，急性呼吸衰竭，甚至導(dǎo)致窒息（大汗淋漓，極度煩躁不安，瀕死感，青紫）；循環(huán)功能衰竭，甚至導(dǎo)致休克。②積氣征+嚴(yán)重皮下氣腫

(subcutaneousemphysema)，縱隔氣腫（mediastinalemphysema），不宜X線檢查。⒌治療及急救措施⑴緊急處理：緊急排氣減壓⑵針對病因進(jìn)一步治療（強(qiáng)調(diào)剖胸探查指征）。㈢開放性氣胸

OpenPneumothorax⒈病因多見于火器傷，彈片傷。只指胸壁損傷時與外界相通，不指支氣管斷裂與外界相通。⒉特點胸腔與外界相通的裂口，可致空氣自由出入胸膜腔。傷情嚴(yán)重程度主要取決于裂口與氣管口徑的關(guān)系。①裂口＜?xì)夤芸趶健諝獬鋈肓浚己粑敕蝺?nèi)氣體量→傷側(cè)肺還有部分呼吸功能。②裂口＞氣管口徑→空氣出入量＞呼吸入肺內(nèi)氣體量→傷側(cè)肺完全萎陷，呼吸功能喪失→嚴(yán)重呼吸循環(huán)障礙，短時間死亡。⒊病理生理變化①負(fù)壓消失，傷側(cè)肺萎陷；②縱隔撲動：吸氣時，縱隔因健側(cè)胸腔負(fù)壓增加，與傷側(cè)壓力差增大，而向健側(cè)移位；呼氣時，兩側(cè)胸腔壓力差減小，縱隔擺回傷側(cè)。⒋臨床表現(xiàn)①呼吸功能障礙：呼吸困難；不同程度循環(huán)功能障礙，甚至休克；②積氣征；③胸壁有傷口伴氣體進(jìn)出，有時可聞及氣體進(jìn)出時所發(fā)出的聲音。

⒌治療及急救措施急救措施：變開放為閉合。在變開放為閉合后，要特別注意以下兩點：①傷口巨大時，要防止胸壁軟化；②防止發(fā)展為張力性氣胸，因此要密切觀察。進(jìn)一步治療包括：①糾正休克，清創(chuàng)縫合胸壁傷口，并做胸腔閉式引流；②剖胸探查指征；③預(yù)防感染。創(chuàng)傷性血胸

TraumaticHemothorax

胸膜腔積血。閉合性胸外傷中25-75%有血胸。在穿透性傷中約占60％～80％。⒈出血來源

①肺組織裂傷肺循環(huán)的壓力低，出血少而慢，可自行停止。

②肋間血管或胸廓內(nèi)血管體循環(huán)的壓力高，出血快而多，不易自行停止。③心臟大血管出血多而急→失血性休克，短時間內(nèi)死亡。⒉病理生理┏丟失血容量→內(nèi)出血征象（脈搏快弱、血壓下降、┃氣促等低血容量休克癥狀）兩個方面┃┃┗積血壓迫肺、使縱隔移位→影響呼吸循環(huán)功能⒊臨床表現(xiàn)

內(nèi)出血表現(xiàn)+積液征強(qiáng)調(diào)兩點：⑴根據(jù)出血量、速度、病人體質(zhì)不同，臨床表現(xiàn)可有很大差異。年老體弱者，小量出血即可引起循環(huán)呼吸功能障礙，年輕強(qiáng)壯者，出血量較大也不至于引起明顯的循環(huán)呼吸功能障礙。

┏小量<500ml

(平肋膈角)臨床據(jù)出血量分┣中500-1000ml（液平面達(dá)前四肋水平）┗大>1000ml⑵判斷出血是否為進(jìn)行性。有5個觀察要點：①脈搏逐漸增快，血壓持續(xù)下降；②經(jīng)輸血補液后，血壓不回升或升而不穩(wěn)；③Hb、RBC和HCT反復(fù)測定，持續(xù)降低；④連續(xù)X線胸部檢查示胸腔陰影持續(xù)增大；⑤最重要：胸引量：引流量每小時>200ml，持續(xù)3小時；或短時間一次引流量>1000ml（<6小時）。⒋治療原則

不同類型的血胸治療原則不同。⑴非進(jìn)行性血胸：(Nonprogressivehemothorax)①少量可自行吸收；②積血較多，排盡積血（胸穿、胸引），促進(jìn)肺完全復(fù)張；③預(yù)防感染。⑵進(jìn)行性血胸：

(progressivebleedinginhemothorax)2字方針：補：補充血容量；止：剖胸探查止血。⑶凝固性血胸(Clottedhemothorax)

心肺、膈肌運動有去纖維蛋白作用，不凝。短時間內(nèi)大量出血，凝。出血停止、病情穩(wěn)定后手術(shù)清除凝固的血塊。⑷機(jī)化性血胸：（OrganizedHemthorax）凝固性血胸血塊機(jī)化后，形成纖維組織束縛肺和胸廓，限制呼吸運動，損害肺功能。傷后4-6周進(jìn)行纖維組織剝除術(shù)。⑸感染性血胸(InfectedClottedHemthorax)怎樣判斷：①全身中毒癥狀：高熱、寒戰(zhàn)、白分升高②胸液：RBC：WBC<100：1；③胸液涂片或細(xì)菌培養(yǎng)（+）按膿胸處理。心包積血

Hemopericardium

心包腔積血又稱血心包。多為銳器穿破胸壁所致。常見兩種情況：①心包裂口開放通暢者：心臟出血外溢→低血容量休克→死亡②心包裂口小或閉合者：急性心包填塞征，出現(xiàn)Beck三聯(lián)征

急性心包填塞的病理生理變化：心包積血→心包腔壓力↑→壓塞心臟，使回心血量和心排血量↓→靜脈壓↑，動脈壓↓→急性循環(huán)衰竭。

臨床上心包積血100-200ml，甚至50ml即可產(chǎn)生明顯的心包壓塞征象。⒈臨床表現(xiàn)及診斷

Beck三聯(lián)征：①靜脈壓↑>15cmH2O；②動脈壓↓；③心搏微弱，心音遙遠(yuǎn)

我們的經(jīng)驗是：（傷口位置）+靜脈壓↑動脈壓↓脈壓差↓等一派循環(huán)衰竭征象。⒉治療緊急處理：⑴心包穿刺減壓，用于①疑診時確診；②暫時減壓解危，爭取手術(shù)時間）。⑵手術(shù)心包切開減壓，修補心臟裂口。兩種特殊胸外傷一、創(chuàng)傷性窒息

Traumaticasphyxia

突發(fā)強(qiáng)烈暴力擠壓胸部，聲門反射性關(guān)閉，致使胸內(nèi)壓劇烈升高，迫使上腔靜脈血液逆流到頭、頸及肩部，引起毛細(xì)血管破裂，造成血液滲入組織內(nèi)。

可引起頭面頸部，前上胸部局部皮膚出現(xiàn)淤斑和出血點，口腔黏膜和眼結(jié)膜出血斑，眼耳鼻及顱內(nèi)靜脈可破裂出血，導(dǎo)致不同程度功能障礙。治療：針對出血情況（部位及程度）處理+給氧二、肺爆震傷

Blastinjuryofthelung

爆炸引起高壓氣浪或水浪，產(chǎn)生所謂超壓沖擊胸廓，同時經(jīng)氣管傳遞入小支氣管和肺泡，導(dǎo)致肺內(nèi)壓迅速增高，使小支氣管肺泡破裂；另外爆炸后空間一時性負(fù)壓，使肺內(nèi)壓縮氣體急速膨脹，亦導(dǎo)致肺內(nèi)壓迅速增高，亦使小支氣管肺泡破裂。上述變化均可引起肺組織廣泛滲出及出血，產(chǎn)生嚴(yán)重肺水腫。治療：激素+給氧重癥病人呼吸機(jī)呼氣末正壓輔助呼吸等EmpyemaJiangYingjiuDeptofCardiothoracicSurgery胸心外科歡迎你!主任醫(yī)師胸心外科89818339主任醫(yī)師胸心外科1Definition2Etiology

3Pathwayofpathogen4Pathology

5ClinicalclassificationCommonintroductionDefinedasapleuralinfectionandpleuralspacesuppurativefluidcollectionPleuralcavity,pleuralspaceorpleuralsacAnatomy

EmpyemathoracicischaracterizedbypresenceofpusormicroorganisminthepleuralfluidPusinthepleuralcavity.

1Definition2Etiology

3Pathwayofpathogen4Pathology

5ClinicalclassificationCommonintroductionEmpyemaiscausedbyaninfectionofthestructuressurroundingthepleuralspace.Riskfactorsinclude:bacterialpneumoniathemostcommoncauselungabscessthoracicsurgerytraumatothechestthoracentesissubdiaphragmaticinfectionsCausesandriskfactors:ParapneumonicEmpyemaEtiologyAnaerobesareinvolvedinapproximately50%ofempyemasandareusuallyassociatedwithaspiration,anddentalorlungabscessesApproximately25%ofinfectionsarepolymicrobialPost-surgicalempyemasareusuallymonomicrobial,causedbytypicalnosocomialpathogens(Staphylococcusaureus)Pathogenincludethefollowing:

Streptococcuspneumoniae

Streptococcus

Staphylococcusaureus

Escherichiacolibacteria

Bacilluspyocyaneus

Fungus

Anaerobicbacteria

Mycobacterium

Tuberculosis

StreptococcuspneumoniaeStreptococcusStaphylococcusaureusFungusAnaerobicbacteriaMycobacterium,Tuberculosis

1Definition2Etiology

3Pathwayofpathogen

4Pathology

5ClinicalclassificationCommonintroductionDept.CardiothoracicsurgeryPathwayofpathogenintopleuralcavity1.Directinvolvementpneumonia,lungabscess2.Lymphaticdrainageliverabscesssubphrenicabscess

3.Bloodstreamsepticemia,sepsis1Definition2Etiology

3Pathwayofpathogen4Pathology

5ClinicalclassificationCommonintroductionParapneumonicEmpyemaPhysiopathology

Accumulationoffluidinthepleuralcavity,secondarytoaninfectiousprocessofthelung.ExudativePhase:early,acuteFibrino-purulentPhase:late,transitionalFibrinogenicPhase:chronic,organizingPhase1

Exudativephase,acutephaseThisistheimmediateresponsewithoutpouringofthefluid.Thecellularcontentoftheexudatesisrelativelylow.Duringthisstagethefluidisthinandlungsarereadilyre-expandable.Gramstainandcultureisnegativeformicro-organism.Phase1Dept.CardiothoracicsurgeryPhase2Fibrinopurulentphase/transitionalphasePhase2Inthisstagealargenumberofpoly-morphonuclearleukocytesandfibrinaccumulateintheeffusion.Withcontinuedaccumulationofneutro-philsandfibrin,effusionbecomespurulent.Thereisprogressivetendencytowardsloculationsandformationofalimitingmembranes.Gramstainandculturereportsshowmicroorganism.Phase3

Organizingphase,chronicphasePhase3Fibro-blastsgrowintoexudatesonboththevisceralandparietalpleuralsurfaces,producinganinelasticmembrane"thepeel".Thickenedpleuralpeelmaypreventtheentryofanti-microbialdrugsinthepleuralspaceandinsomecasescanleadtodrugresistance.Athickenedpleuralpeelcanrestrictlungmovementanditiscommonlytermedastrappedlung.Calcification,fixedInempyema,pathologicalresponsemaybedividedintothreephases.Thesephasesarenotsharplydistinctivebutgraduallyonephasemergesintoanotherdependinglargelyonthenatureofinfectingorganism.1Definition2Etiology

3Pathwayofpathogen4Pathology

5ClinicalclassificationCommonintroductionAcuteChronicLocalizedDiffuseDept.CardiothoracicsurgeryEmpyema1Definition2Clinicalmanifestationanddiagnosis3TreatmentAcuteEmpyemaExudativephase/acutephase

Thisistheimmediateresponsewithoutpouringofthefluid.Thecellularcontent

oftheexudatesisrelativelylow.

Duringthisstagethefluidis

thinandlungsarereadily

re-expandable.

1Definition2Clinicalmanifestationanddiagnosis3TreatmentAcuteEmpyemaClinicalsignsandphysicalfindingsvarydependingonthetypeoforganismisolated,ageofthepatient,stageoftheempyemaandtypeofpriorantibiotictherapy.Dept.CardiothoracicsurgeryClinicalManifestationandDiagnosis

Commonsymptomschills,fever,dyspnea,chestpainorreferredpain,nightsweat,malaise,coughandincreasedsputumproductionPhysicalexaminationfindingscanvaryaswell.Auscultationrevealsrales,decreasedbreathsoundspossiblyapleuralrub.Physicalexaminationfindings:DullnesstopercussionFocalchestwallheat,erythema,swelling,splintingofthechestorapreferencetolieontheaffectedsidemaybenoticedDeviationoftracheaDept.CardiothoracicsurgeryDept.CardiothoracicsurgeryHematologicalandBiochemicalInvestigationTherecanbeleukocytosiswithpoly-morphonuclearcellspredominance.Patientswithlowerhemoglobin,lowserumalbuminandabnormalliverfunctiontest.Pusexamination

Dept.CardiothoracicsurgeryPussmearPuscultureDept.CardiothoracicsurgeryX-rayChestCTscanCTchestusuallydifferentiatesempyemafromconsolidationandlungabscess.EmpyemaUltrasoundscanUsedtoconfirmpresenceoffluidinpleuralspaceThoracentesis

Needlethoracentesisforchemistryanalysisandcultureisusuallytheinitialdiagnostic(andoccasionallytherapeutic)stepcoincidentwiththeinitiationofintravenousantibiotics.Thinexudatescanoccasionallybecompletelyevacuatedwiththismaneuver.patientisusually"toxic"±productivecoughandchestpainchestX-rayandCTscanmayshowfeaturessuggestiveofapleuraleffusionultrasoundtoconfirmpresenceoffluidinpleuralspaceconfirmationofthediagnosiscanbeobtainedbyaspiratingpus.Diagnosis1Definition2Clinicalmanifestationanddiagnosis3TreatmentAcuteEmpyemaThemanagementofacuteempyemainvolvesthreecoreprinciples:1.Promptinitiationofappropriateantibioticsaccordingtothedrugsensitivityofpathogen2.Completeevacuationofsuppurativepleuralfluid3.PreservationorrestorationoflungexpansionTreatmentforacuteempyemaCloseddrainage(closed-tubethoracostomy)Patientswithpleuraleffusionorfrankpusonthoracentesisshouldundergoimmediateinsertionofadependent,largeclosed-tubedrainagecatheter.Iftheeffusionhasnotyetloculated,fulllungexpansionwithobliterationoftheempyemaspacewillusuallybeachievedfollowingchesttubeinsertion.

Chesttubeinsertiondrainage

isthemostimportanttreatmentforempyemapatients.

RibresectionopendrainagetechniqueUsedinadultsforempyemasnotrespondingtoclosed-tubethoracostomyCurecriterion

ThepusdrainedentirelyTheresidualcavityvanished

Thelungwasfullyreexpanded1Definition2Causes

3Clinicalmanifestationanddiagnosis4TreatmentChronicEmpyemaFibro-blastsgrowintoexudatesonboththevisceralandparietalpleuralsurfaces,producinganinelasticmembrane"thepeel".Thickenedpleuralpeelmaypreventtheentryofanti-microbialdrugsinthepleuralspaceandinsomecasescanleadtodrugresistance.Athickenedpleuralpeelcanrestrictlungmovementanditiscommonlytermedastrappedlung.1Definition2Causes

3Clinicalmanifestationanddiagnosis4TreatmentChronicEmpyemaCausesofchronicempyema

1Failuretoearlyaggressivetreatmentofacuteempyemaleadstochronicityinappropriatedrainage2Neglectedforeignbody3Coexistanceofbronchopleuralfistulaoresophagealfistula4Specificmicroorganisminfectionsuchastuberculosis,fungus,etc.1Definition2Causes

3Clinicalmanifestationanddiagnosis4TreatmentChronicEmpyemaClinicalManifestationandDiagnosis

Chronic“toxic”symptoms:persistentlowfever,lossofappetite,weakness,anemia,lowserumalbuminRespiratorysymptoms:shortnessofbreath,cough,purulentsputumBronchopleuralfistulasymptomsX-rayChestFilmsCTscanfilmsBronchopleuralfistula1Definition2Causes

3Clinicalmanifestationanddiagnosis4TreatmentChronicEmpyemaSurgicalTreatment

Threecoreprinciplesshouldbefollowedforthetreatmentofchronicempyema.1.Toimprovethepatient’sgeneralconditions,tocorrectchronictoxicsymptomsandmalnutrition2.Toeliminatetheprimarychroniccauses3.Toobliteratepurulentspace,restorelungexpansionandpulmonaryfunction.ImprovementofchestdrainageDecorticationThoracoplastyPleura-lungresection(pleura-lobectomyorpleura-neumonectomy)Surgicaltechniquesforchronicempyema

DecoticationDept.CardiothoracicsurgeryDecoticationDecortication,ofcourse,ismoreidealbecauseitcanpreservemorelungfunctionandavoidchestwalldeformity,butitalsohasitscontraindicationthatiswhentherearelunglesionswithfibrosisoflungtissuethathinderslungre-expansion,thendecorticationiscontraindication.Dept.CardiothoracicsurgeryThoracoplastyThoracoplastyOpenthoracotomyalsopermitspleural-lungresectionifnecessaryfornonresponsivenecrotizingpneumonias,fungalpneumonias,andparenchymalabscesses.Pleural-lungresection(lobectomyorpneumonectomy)ThanksPleasewritedowntheclinicalclassificationofempyemaaccordingtoitspathology請寫上姓名、學(xué)號并回答問題Empyema

積膿（胸）JiangYingjiuDeptofCardiothoracicSurgery胸心外科歡迎你!主任醫(yī)師胸心外科89818339主任醫(yī)師胸心外科1Definition2Etiology

3Pathwayofpathogen4Pathology

5ClinicalclassificationCommonintroductionDefinedasapleuralinfection感染andpleuralspacesuppurative

化膿性fluidcollection（均為胸膜腔）Pleuralcavity,pleuralspaceorpleuralsacAnatomy

Empyemathoracic膿胸ischaracterizedbypresenceofpus膿ormicroorganisminthepleuralfluidPusinthepleuralcavity.

1Definition2Etiology

3Pathwayofpathogen4Pathology

5ClinicalclassificationCommonintroductionEmpyemaiscausedbyaninfectionofthestructuressurroundingthepleuralspace.Riskfactorsinclude:bacterialpneumoniathemostcommoncauselungabscess肺膿腫thoracicsurgery胸科手術(shù)traumatothechestthoracentesis胸腔穿刺subdiaphragmaticinfections膈下感染Causesandriskfactors:ParapneumonicEmpyema膿胸EtiologyAnaerobes厭氧菌areinvolvedinapproximately50%ofempyemasandareusuallyassociatedwithaspiration抽吸/倒吸,anddental牙的orlungabscessesApproximately25%ofinfectionsarepolymicrobial多種微生物的Post-surgicalempyemasareusuallymonomicrobial單微生物的,causedbytypicalnosocomial醫(yī)院的pathogens(Staphylococcusaureus金葡菌)Pathogenincludethefollowing:

Streptococcuspneumoniae肺炎鏈球菌

Streptococcus鏈球菌

Staphylococcusaureus金黃色葡萄球菌

Escherichiacolibacteria大腸埃希菌

Bacilluspyocyaneus綠膿桿菌

Fungus真菌

Anaerobicbacteria厭氧菌

Mycobacterium分枝桿菌

Tuberculosis

結(jié)核StreptococcuspneumoniaeStreptococcusStaphylococcusaureusFungusAnaerobicbacteriaMycobacterium,Tuberculosis

1Definition2Etiology

3Pathwayofpathogen

4Pathology

5ClinicalclassificationCommonintroductionDept.CardiothoracicsurgeryPathwayofpathogenintopleuralcavity1.Directinvolvementpneumonia,lungabscess2.Lymphaticdrainageliverabscesssubphrenic膈下abscess

3.Bloodstream流動septicemia敗血癥,sepsis膿毒病1Definition2Etiology

3Pathwayofpathogen4Pathology

5ClinicalclassificationCommonintroductionParapneumonicEmpyemaPhysiopathology

Accumulationoffluidinthepleuralcavity,secondarytoaninfectiousprocessofthelung.ExudativePhase滲出期:early,acuteFibrino-purulentPhase纖維膿性期:late,transitional過渡的FibrinogenicPhase纖維蛋白原期:chronic,organizing組織的Phase1

Exudativephase,acutephaseThisistheimmediateresponsewithoutpouring流出ofthefluid.Thecellularcontentoftheexudatesisrelativelylow.Duringthisstagethefluidisthinandlungsarereadily容易的re-expandable再膨脹.Gramstain革蘭染色andculture培養(yǎng)isnegativeformicro-organism.Phase1Dept.CardiothoracicsurgeryPhase2Fibrinopurulentphase/transitionalphasePhase2Inthisstagealargenumberofpoly-morphonuclearleukocytes分葉核白細(xì)胞andfibrin纖維蛋白accumulateintheeffusion.Withcontinuedaccumulationofneutro-phils中性粒細(xì)胞andfibrin,effusionbecomespurulent.Thereisprogressivetendencytowardsloculations形成小腔andformationofalimitingmembranes.Gramstainandculturereportsshowmicroorganism.Phase3

Organizingphase,chronicphasePhase3Fibro-blasts成纖維細(xì)胞growintoexudatesonboththevisceralandparietalpleuralsurfaces臟壁胸膜表面,producinganinelasticmembrane非彈性膜“thepeel皮".Thickenedpleuralpeelmaypreventtheentryofanti-microbialdrugsinthepleuralspaceandinsomecasescanleadtodrugresistance.Athickenedpleuralpeelcanrestrict限制lungmovementanditiscommonlytermedas稱為trappedlung陷閉肺.Calcification鈣化,fixedInempyema,pathologicalresponsemaybedividedintothreephases.Thesephasesarenotsharplydistinctive有特色的butgraduallyonephasemergesinto并入anotherdependinglargelyonthenatureofinfectingorganism.1Definition2Etiology

3Pathwayofpathogen4Pathology

5ClinicalclassificationCommonintroductionAcuteChronicLocalized局限D(zhuǎn)iffuse擴(kuò)散Dept.CardiothoracicsurgeryEmpyema1Definition2Clinicalmanifestationanddiagnosis3TreatmentAcuteEmpyemaExudativephase/acutephase

Thisistheimmediate即刻responsewithoutpouring流出ofthefluid.Thecellularcontent

oftheexudatesisrelativelylow.

Duringthisstagethefluidis

thinandlungsarereadily

re-expandable.

1Definition2Clinicalmanifestationanddiagnosis3TreatmentAcuteEmpyemaClinicalsignsandphysicalfindingsvarydependingonthetypeoforganismisolated隔離,ageofthepatient,stageoftheempyemaandtypeofprior先前的antibiotictherapy.Dept.CardiothoracicsurgeryClinicalManifestationandDiagnosis

Commonsymptomschills,fever,dyspnea,chestpainorreferredpain,nightsweat盜汗,malaise萎靡,coughandincreasedsputumproductionPhysicalexaminationfindingscanvaryaswell.Auscultation聽診revealsrales啰音,decreasedbreathsoundspossiblyapleuralrub胸膜摩擦音.Physicalexaminationfindings:Dullness濁音topercussionFocal病灶chestwallheat,erythema紅斑,swelling,splinting夾板固定ofthechestorapreferencetolieontheaffectedsidemaybenoticedDeviationoftrachea氣管偏向Dept.CardiothoracicsurgeryDept.CardiothoracicsurgeryHematologicalandBiochemicalInvestigationTherecanbeleukocytosis白細(xì)胞增多withpoly-morphonuclearcellspredominance優(yōu)勢.Patientswithlowerhemoglobin,lowserumalbumin血清白蛋白andabnormalliverfunctiontest.Pusexamination

Dept.CardiothoracicsurgeryPussmear涂片PuscultureDept.CardiothoracicsurgeryX-rayChestCTscanCTchestusuallydifferentiatesempyemafromconsolidation合并（？）andlungabscess.EmpyemaUltrasoundscanUsedtoconfirmpresenceoffluidinpleuralspaceThoracentesis胸腔穿刺術(shù)

Needlethoracentesisforchemistryanalysisandcultureisusuallytheinitialdiagnostic(andoccasionallytherapeutic治療的)stepcoincident一致的withtheinitiationofintravenous靜脈注射antibiotics.Thinexudatescanoccasionallybecompletelyevacuated排出withthismaneuver機(jī)動/演習(xí)（？）.patientisusually"toxic"±productivecoughandchestpainchestX-rayandCTscanmayshowfeaturessuggestiveofapleuraleffusionultrasoundtoconfirmpresenceoffluidinpleuralspaceconfirmationofthediagnosiscanbeobtainedbyaspirating吸pus.Diagnosis1Definition2Clinicalmanifestationanddiagnosis3TreatmentAcuteEmpyemaThemanagementofacuteempyemainvolvesthreecoreprinciples:1.Prompt迅速initiationofappropriateantibioticsaccordingtothedrugsensitivityofpathogen2.Completeevacuationofsuppurativepleuralfluid3.Preservation保留orrestorationoflungexpansionTreatmentforacuteempyemaCloseddrainage閉式引流(closed-tubethoracostomy閉管胸廓造口術(shù))Patientswithpleuraleffusionorfrankpusonthoracentesisshouldundergoimmediateinsertionofadependent,largeclosed-tubedrainagecatheter導(dǎo)管.Iftheeffusionhasnotyetloculated有分隔的,fulllungexpansionwithobliteration閉塞oftheempyemaspacewillusuallybeachievedfollowingchesttubeinsertion.

Chesttubeinsertiondrainage

isthemostimportanttreatmentforempyemapatients.

Ribresection肋骨切除術(shù)opendrainagetechniqueUsedinadultsforempyemasnotrespondingtoclosed-tubethoracostomyCurecriterion

ThepusdrainedentirelyTheresidual剩余的cavityvanished

消失Thelungwasfullyre-expanded1Definition2C