【医学课件大全】急性胰腺炎 acute pancreatitis

AcutePancreatitisXUEHuiping Pancreatitisisaninflammatoryprocessinwhichpancreaticenzymesautodigestthegland Theglandcansometimeshealwithoutanyimpairmentoffunctionoranymorphologicchanges Thisprocessisknownasacutepancreatitis Itcanrecurintermittently contributingtothefunctionalandmorphologiclossofthegland thepathologicalchangereferredtoaschronicpancreatitis Acutepancreatitisreferstoanattackinvolvingapreviouslynormalpancrease Chronicpancreatisisappliedtoanattackinvolvingapreviously permanentlydamagedpancrease Acutepancreatitisisanacuteinflammatoryprocessofthepancreas withvariableinvolvementofotherregionaltissueorremoteorgansystems Althoughpancreaticfunctionandstructureusuallyreturntonormal theriskofrecurrentattacksis20to50 unlesstheprecipitatingcauseisremoved Thediseaseincludesabroadspectrumofpancreaticdisease whichvariesfrommildparenchymaledematoseverehemorrhagicpancreatitisassociatedwithsubsequentgangreneandnecrosis 急性胰腺炎 acutepancreatitis 是指胰酶在胰腺内激活后引起胰腺组织自身消化的急性化学性炎症 Asensibleclassificationsystemseparatespancreatitisintomildandseverediseasebasedonphysiologicfindings laboratoryvalues andradiologicimaging Mildpancreatitisisnotassociatedwithorgandysfunctionorcomplications andrecoveryisuneventful Severepancreatitisisassociatedwithdecreasedfunctionofthepancreas localandsystemiccomplications andacomplicatedrecovery 轻型急性胰腺炎是指仅有很轻微的脏器功能紊乱 没有明显腹膜炎体征及严重代谢紊乱等临床表现 临床恢复顺利者 该型病理上绝大多数为水肿型胰腺炎 少数也可有胰腺实质坏死 Severepancreatitisisdefinedasalocalcomplicationand ororganfailure 重症急性胰腺炎是指急性胰腺炎伴有脏器功能障碍 或出现坏死 脓肿或假性囊肿等局部并发症 或两者兼有 该型病理上绝大多数为坏死型胰腺炎 但少数情况下水肿型胰腺炎也可表现为重症胰腺炎 Localcomplicationsaredefinedas 1 acutefluidcollections 2 pancreaticnecrosis 3 pancreaticabscess 4 pancreaticpseudosyst Theclinicalpresentationofacutepancreatitisisvariable fromepisodesofmildabdominaldiscomfortalonetoasevereillnessassociatedwithhypotension metabolicderangements sepsis fluidsequenstration multipleorganfailureorevendeath Itisalwaysaccompaniedbyanincreasedconcentrationsofpancreaticenzymesinbloodandinurine EtiologyApproximately70 80 ofpatientseitherhavegallstonesorahistoryofsustainedalcoholabuse Choledocholithiasis 胆总管石病 andethanolabuseaccountfor70to80 ofallcases GallstonesmaycausepancreatitisbyimpactingintheampullaofVater Theincidenceofgallstone associatedpancreatitisparallelsthatofcholelithiasis 胆石症 itpeaksatages50to70 andwomenoutnumbermenby2to1 CausesofAcutePancreatitisObstruction Biliarytractdisease cholelithiasis tumor ascarid stenosispancreaticductobstruction neoplasms cysts pancreasdivisumannularpancreasampullarystenosis duodenaldiverticulumDuodenalobstructionAlcoholHyperlipidemiaHypercalcemiaHereditaryTrauma external operative ERCPIschemia hypotension cardiopulmonarybypass atheroembolism vasculitisInfectiouscauses parasticbacterialviralfungalDrugs steroids azathioprine6 mercaptopurine Idiopathic ObstructiveCauses Choledocholithiasis胆总管石病AmpullaryobstructionbytumororsphincterofOddihypertensionCholedochocele胆总管囊肿Periampullaryduodenaldiverticulum 憩室 Pancreasdivisum annular 环状的 pancreasPrimaryormetastaticpancreatictumorParasitesinpancreaticduct Clonorchis 支睾吸虫 Ascaris Drugs azathioprine硫唑嘌呤 6 mercaptopurine6 巯基嘌呤 valproicacid丙戊酸 estrogens雌激素 metronidazole灭滴灵 甲硝唑 loopdiuretics includingthiazides噻嗪类 furosemide速尿 pentamidine sulfonamides includingsulfasalazine methyldopa L asparaginase tetracyclines etc Pathogenesis1 Acomplicatedpathophysiologicprocess2 Enzymeautoactivationandself digestion keypoint 3 Manyagentsparticipatingintheprocess4 Completemechanismremainingunknown Pancreaticself protectivemechanism1 mucopolysaccharideonpancreaticductepithelia2 proenzyme3 pancreatininhibitor4 acinusmetabolismactivity5 Anti refluxmechanism oddi ssphincterpancreaticductsphincter InitiationfactorinEarlierperiod 1 PancreaticEnzymeAbnormallyActivated BilerefluxBilecommonchannelpancreaticduct1 hypertensioninpancreaticduct2 prematureactivationofpancreaticenzymes3 injurytotheliningofthepancreaticductspancreaticedemaornecrosisMODS DuodenalRefulxduodenalenterokinasepancreaticducttrypsinogentrypsinelastasnogenelastasephospholipasogenphospholipaselecithinlysolecthin 2 AlcoholToxicity stimulatethepancreastosecretepancreatichypertentiontinypancreaticductandacinusrupturepancreaticjuicespillage spasmofthesphinctorofoddi directinjurytopancreas 3 PancreaticMicrocirculationDisorder systemichypotension hyperlipidemia triglycerideslipasefreeacidfattyacidsinjurepancreaticmicrocirculation artheroembolism vasculitis Aggravatiingfactorsinlaterperiod Infection pancreaticabscess Intestinalbacteriatranslocation CytokineandsystemicinflammationreactionsyndromeTNFIL 1IL 6PAFMSOF Freeradicals PATHOGENESIS Prematureactivationofzymogens 酶原 andtheescapeofactivatedenzymesfromacinarcellsandpancreaticductssetthestagefortheautodigestiveprocessthatrepresentsacutepancreatitis PATHOGENESIS Proteases 蛋白酶 releasedintothebloodareinactivatedbycirculatinginhibitors including 2 macroglobulin 巨球蛋白 1 antitrypsin 抗胰蛋白酶 andtheC1 esterase 酯酶 inhibitor Inaddition trypsin 胰蛋白酶 activateskallikrein 激肽释放酶 apeptidase 肽酶 whichthencleavesseveralpeptides includingbradykinin 缓激肽 andkallidin 胰激肽 fromtheirinactiveprecursorsinbloodplasma PATHOGENESIS PATHOGENESIS Thesepeptides termedkinins 激肽 havevariousdeleteriouseffectsincludingvasodilatation increasedvascularpermeability pain andneutrophil 嗜中性粒细胞 accumulation Twomechanismsmaytriggerpancreaticautodigestion zymogenactivationwithinthepancreaticacinarcell increasedpancreaticductpermeability PATHOGENESIS Aftertheacinarcellistriggered itprovokesanintenseinflammatoryresponseinthepancreas Weepingofpancreaticjuiceintotheperipancreaticspaceormicroperforationsofthepancreaticductalsystemcanleadtopseudocystformation PATHOGENESIS Subsequenthypoperfusiontotheglandcanconvertmildedematous interstitialpancreatitistonecrotizingpancreatitis Atthispoint releaseoftoxicfactorsintothesystemiccirculation suchastrypsin elastase phospholipaseA2 andplateletactivatingfactororothercytokines canleadtocardiovascularandpulmonarycollapse Thenecroticpancreascanbecomesecondarilyinfectedfromhematogenousortransperitonealsources 重症胰腺炎是一多因素 累及多环节的疾病 首先是几种致病因素引发胰腺腺泡的损伤 释放多种受激活的胰酶及炎症细胞因子 有多种细胞的过度激活和相互作用 产生氧自由基和炎症介质引起胰腺 腹膜和一些主要器官 肺 脑 的血管通透性增加 最后导致了重症胰腺炎及其并发症的发生 Pathology1 Edematouspancreatitis interstitialedema inflammatorycellinfiltrationoftheglandparenchyma2 Hemorrhagicornecrotizingpancreatitis extensivepancreaticandperipancreaticfatnecrosis parenchymalnecrosis Overviewofthepancreaticgland Thepancreaticglandcontainsthreemajortypesofcells Theductcellsmakeupabout10 ofthepancreasandsecretesolutionsrichinbicarbonate Theacinarcellscompriseover80 ofthepancreasandtheysynthesizeandsecretepancreaticenzymes Overviewofthepancreaticgland Theisletcellsmakeupabout10 ofthepancreasandformtheendocrineportionofthepancreas Thefourmajortypesofisletcellssecretethehormonesinsulin glucagon somatostatin andpancreaticpolypeptide Interstitial Thegrossarchitectureoftheglandispreserved butitisedematous Hemorrhageisabsent Interstitialedemaandinflammatorycellswithintheparenchymaareprominent Disruptionofthenormalacinarcellarchitectureiscommonandmaycontributetocharacteristicallyreducedenzymesecretion Interstitialedemaandinflammatorycellswithintheparenchyma Hemorrhagic Macroscopically markedtissuenecrosisandhemorrhageareapparent Surroundingareasoffatnecrosisarealsoprominent Thesearechalky白垩的areasofdeadadiposetissuethatarefoundwithintheperipancreatictissueandthroughouttheabdomen Largehematomas血肿oftenarelocatedintheretroperitoneal腹膜后的space Hemorrhagic Themicroscopicappearanceofthepancreasparallelsthegrosschanges withmarkedfatandpancreaticnecrosis Vascularinflammationandthrombosisarecommon Fatnecrosis Fatnecrosisseenatsurgeryisassociatedwithperipancreaticreleaseoflipase withhydrolysisoftriacylglycerols triglycerides totoxicfattyacids ClinicalPresentation Steady dull orboringmidepigastricpainassociatedwithnauseaandvomitingistheclassicpresentationofacutepancreatitis Abdominalpain predominantclinicalfeaturemidepigastrium intherightorleftupperquadrantsThepainreachespeakintensitywithin15minutesto1hourfromonset incontrasttothemoreabruptonsetofpainwithaperforatedviscus apenetratingpain radiatingtotheback Itradiatesstraighttothemidlineofthelowerthoracicvertebralregioninabout50 ofpatientsandisusuallyworseinthesupineposition Abdominalpain rarepatientswithoutabdominalpainbutwithaseveresystemicillness hypotension hypoperfusionanddepressionofmentalstatus Painlessacutepancreatitisisveryrarebutcarriesagraveprognosisbecausethepatientsfrequentlypresentinshock ClinicalPresentation NauseaandvomitingAbdominalDistentionresultingfromaparalyticileusarisingfromretroperitonealirritationorascitesoraretroperitonealphlegmonJaundicedistalcommonbileductobstructionbygallstones compressionofthedistalCBDbypancreaticheadedemaorbyotheruncommonfindings AbdominalDistention Paralyticileus 麻痹性肠梗阻 withabdominaldistentionmaydevelopduringthefirstfewdays signifyingextensionoftheinflammatoryprocessintothesmallintestinalandcolonic 结肠的 mesentery 肠系膜 ClinicalPresentationofSeverPancreatitis CirculatoryDerangements hypotention hypovolemia hypoeffusion circulatingmyocardialdepressantfactor decreasedpreloadtotheheart reducedsystemicvascularresistance sepsis likesyndromehyperdynamicstateelevatedcardiacoutputloweredsystemicvascularresistanceloweredarteriovenousoxgendifference ClinicalPresentationofSeverPancreatitis leftpleuraleffusionpulmonaryfailuretachypnea dyspneaandcyanosiscerebralabnormalitiesbelligerence confusion psychosisandcomaTurnersignandCullensignabluishcolorintheflanksoraroundtheumbilicus representingblooddissectingtothoseareasfromtheretroperitoneumnearthepancreasalongfascialplanes Oneto2weeksaftertheonset largeecchymoses 瘀斑 mayappearintheflanks侧腹 GreyTurner ssign ortheumbilicalarea Cullen ssign Oneto2weeksaftertheonset largeecchymoses 瘀斑 mayappearintheflanks侧腹 GreyTurner ssign ortheumbilicalarea Cullen ssign Oneto2weeksaftertheonset largeecchymoses 瘀斑 mayappearintheflanks侧腹 GreyTurner ssign ortheumbilicalarea Cullen ssign PhysicalExamination Initialphysicalexaminationrevealsmildfeverandtachycardia 心动过速 Hypotensionispresentin30to40 ofpatients PhysicalExamination epigastriatenderness rigidityandreboundtenderness Thereismarkedtendernesstodeeppalpationoftheupperabdomen butsignsofperitonealirritationarefrequentlyabsent bowelsoundsdecreasedorabsentpalpablemassswollenpancreasPseudocystabscess LaboratoryTest SerumAmylase Totalserumamylaseactivityisthetestmostfrequentlyusedtodiagnoseacutepancreatitis Thelevelrises6to12hoursafteronsetofsymptomsandremainselevatedfor3to5daysinmostcases hyperamylasemiaisobservedwithin24 48hrs graduallyreturntonormalvaluesduringthesubsequent2 5days SerumAmylase Valuesmorethan3timestheupperlimitofnormalarehighlyspecificforacutepancreatitisbutarefoundinonly80to90 ofcases Themagnitudeoftheriseinserumamylasedoesnotcorrelatewiththeseverityoftheattack nordoesprolongedhyperamylasemiaindicatedevelopingcomplications theabsenceofhyperamylasemiacan texcludethediagnosisofacutepancreatitis extensivepancreaticnecrosis DisordersAssociatedwithhyperamylasemiaIntra AbdominalExtra AbdominalPancreaticdisordersSalivaryglanddisordersacutepancreatitismumpschronicpancreatitisparotitistraumatraumacarcinomacalculipseudocystirradiationsialoadenitispancreaticascitesimpairedamylaseexcretionabscessrenalfailureNonpancreaticdisordersmecroamylasemiabiliarytractdiseaseMiscellaneusintestinalobstructionpneumoniamesentericinfarctionpancreaticpleuraleffusionperforatedpepticulcermediastinalpseudocystperitonitiscerebraltraumaafferenloopsyndromesevereburnsacuteappendicitisdiabeticretoacidosiseupturedectopicpregnancypregnancysalpingitisdrugsrupturedaorticaneurysmbisalbuminemia UrinaryAmylase asensitiveindexofthepancreatitiselevationspersistforalongerperiodthanserumamylasesomeotherdiseasesalsomanifesthyperamylasuriaanormalurinaryamylasecan tprecludethepancreatitis Separationoftotalserumamylaseintoitspancreatic P andsalivary S isoenzymesandmeasurementsofurinaryamylaseoutputaddlittletothediagnosticinformation Theamylase creatinineclearanceratio ACR theratioofamylaseconcentrationinurineoverplasma dividedbythecorrespondingvaluesforcreatinine isusefulindiagnosingasymptomaticmacroamylasemia inwhichaggregatesofcirculatingamylaseescapeglomerularfiltrationandtheACRisabnormallylow 淀粉酶 这一古老的检查方法虽已应用了半个多世纪 但对胰腺炎的诊断仍不失为良好而简便可行的手段 由于胰酶在胰管内逆流入血或渗出液重吸收入血 则在急性胰腺炎时血 尿的淀粉酶有所升高 血淀粉酶正常值 温氏单位 256单位 苏氏单位 500单位 急性胰腺炎 轻型 发作后6 12小时即升高 48 72小时逐渐恢复正常 尿淀粉酶约在发病后12 24小时升高 要持续3 5天 但急性重型胰腺炎升高的时间要提前 临床上对淀粉酶值的变化要作全面的分析 再结合临床其他症状才能做出正确的判断 淀粉酶 血淀粉酶值正常 有两种情况 其一表明病已痊愈 血淀粉酶值恢复正常 同时全身情况良好 无腹部体征 其二在重症急性胰腺炎的初检或治疗中 淀粉酶也可不升高 说明病情会进行性加重恶化 因为胰腺腺泡大量坏死 崩溃 已不能分泌淀粉酶 即所谓的 枯竭 现象 这一现象在急性重症胰腺炎中时有发生 应予以高度重视 淀粉酶 血淀粉酶升高 有时病人出现腹痛 并伴血淀粉酶升高 但临床的症状 体征并不支持胰腺炎 这时就应考虑到血清淀粉酶检测往往是非特异性的 临床常见的一些急腹症也可伴有血淀粉酶升高 如胆囊炎 胆石症 胆道梗阻 肠梗阻 消化性溃疡病穿孔 肠系膜血栓形成以及使用吗啡后 胆石症时可能是由于排石对Oddi括约肌的刺激 使之痉挛 血淀粉酶一过性升高 消化性溃疡穿孔 特别是十二指肠球部穿孔 时 含有大量胰液的肠内容物进入腹腔后 淀粉酶被腹膜吸收则血淀粉酶值升高 肠梗阻后 肠腔内肠液淤积 淀粉酶通过受损的肠壁渗入腹腔而被吸收 因此 对血淀粉酶的升高必须结合临床进行判断 决不可因单纯血淀粉酶升高而诊断为胰腺炎 淀粉酶 巨淀粉酶血症 是一罕见病症 其原因不明 可能是由于病人血中的淀粉酶与大分子物质形成复合物 从而不能通过肾小球滤过 将其贮存在血中 特点是血淀粉酶虽高 但尿淀粉酶正常或偏低 血淀粉酶升高可持续数月乃至数年 淀粉酶 重症胰腺炎往往伴有腹腔大量炎性腹水 应做腹腔穿刺测定腹水淀粉酶 穿刺物多为血性混浊的液体 其淀粉酶含量可以相当高 淀粉酶 肌酐肾廓清率比值 ACR ACCR的正常比值为3 8 5 3 若比值 5 6 则提示急性胰腺炎 ACCR在急性胰腺炎以外的疾患亦可升高 如慢性肾衰 糖尿病酸中毒 烧伤 严重肝衰等 因此只有在排除以上诸疾患时 才有价值 ACCR一方面可用来确诊急性胰腺炎 另一方面亦可用来排除非胰腺炎的高淀粉酶血症 ACCR的计算公式是 尿淀粉酶 血清淀粉酶 血清肌酐 尿肌酐 100 SerumLipase amoreaccurateindicatorofacutepancreatitislipaseissolelyofpancreaticoriginTheserumlipaselevelstendtoremainelevatedlongerthantheamylaselevelsduringthehealingphaseofpancreatitis someotherdiseasesalsomanifestelevatedserumlipaseperforatedpepticulceracutecholecystitisintestinalischemiaThecombinationofserumamylaseandlipasedeterminationsismoreaccuratethaneithertestalone Hypocalcemia theconsequenceofdilutionalhypoalbuminemiacalciumdespositioninareasoffatnecrosisresistanceofskeletalbonetoparathyroidhormonestimulationTheionizedcalciumconcentrationremainsnormal andsymptomsoftetany 手足抽搐 areextremelyrare OtherlaboratoryTest Elevatedwhitecellcount 10000cellspermm3Leukocytosis 白细胞增多 Hyperglycemia Mildazotemia氮质血症 relatedtofluidsequestration Abnormalitiesofliverfunctiontest Serumtriglyceridelevelsshouldbeobtainedinallpatientsbecauseoftheiretiologicimplicationsandtohelpinterpretunexpectedlynormalserumamylaseandlipaselevels Elevatedalanine 丙胺酸 aminotransferase 转氨酶 ALT andalkalinephosphatasevaluessuggestgallstone associatedpancreatitis Theserumaspartate 天 门 冬氨酸 aminotransferase AST iselevatedinapproximately50 ofpatients owingtoalcoholicliverdiseaseortothepancreaticinflammationitself ImagingTests1 AplainAbdominalFilm notspecific dilatationofanisolatedloopofintestineadjacenttothepancreas calcificationinthepancreas leftpleuraleffusionsPlainfilmsshouldbeobtainedroutinelytoruleoutthepresenceoffreeaircausedbyperforationofaviscus 2 UltrasoundExamination notrauma pancreaticandperipancreaticedemaoffluidcollection pseudosyst dilationofpancreaticduct GBstoneandCBDstone Ultrasoundexaminationshowingtwolargepancreaticpseudocysts Bothcystsareindicatedbythelargewhitearrows 3 CTScans confirmdiagnosisofpancreatitis confirmdiagnosisofcomplicationssuchasabscessorpseudocyst revealextensionofinflammationandnecrosis implyprognosis aneedleaspirationunderCTguide Withrapidintravenousbolusinjectionofcontrastmaterial adynamicCTscanwillrevealextensionofperipancreaticinflammation involvementofadjacentorgans venousthrombosis andfluidcollections Mostimportantly pancreaticnecrosiscanbeidentifiedandquantitatedbythelackofcontrastmediumenhancementafterthebolusinjection TheabdominalCTscanmaybenormal however inabout10 ofpatientswithearly mildpancreatitis ComputedTomographicFindingsinAcutepancreatitispancreaticchangesnonspecificfindingsparenchymalenlargementboweldistentiondiffusepleuraleffusionfocalmesentericedemaparenchymaledemanecrosisperipancreaticchangesblurringoffatplanesthickeningoffascialplanespresenceoffluidcollections ThisCTscanshowspoorperfusionofthepancreas AbdominalUltrasonography US andComputedTomography CT USisthemethodofchoicefordetectingcholelithiasis 胆石症 andfordeterminingthediameteroftheextrahepaticandintrahepaticbileducts DilatationoftheseductssuggestsrecentorpersistingimpactionofastoneinthedistalcommonbileductortheampullaofVater Whentheclinicaldiagnosisismade theCTscanisfarsuperiortoUSforassessingtheextentandlocalcomplicationsofpancreatitis Twopancreaticpseudocysts arrows Computedtomographyfollowingtheintravenousadministrationofcontrastmaterialdemonstratesfoursharplymarginated fluid filledcollections Largearrowindicatesinflamedpancreas Smallarrowdenotesareasofperipancreaticinflammationextendingtowardthehilumofthespleen Alargepseudocyst openarrows whichisbeingpercutaneouslydrained closedarrow Pseudocyststhatdevelopinchronicpancreatitisaremostcommonlycausedbyductobstruction withtheformationofa retention cystintheupstreamductorsidebranch Unlikethepseudocystsassociatedwithacutepancreatitis thesepseudocystsdonotcontainactivatedenzymes andareusuallynotareflectionofanecrotizinginflammatoryprocess Thesepseudocystsarelesslikelytoproducecomplicationsthanthoseassociatedwithacutenecrotizingpancreatitis buttheyareparadoxicallyalsolesslikelytoresolve Manyofthesepseudocystsremainasymptomatic buttheymaybecomplicatedbyinfection ruptureorleak bleeding orobstructionofaneighboringhollowviscus eg duodenum bileduct colon orureter amongothers Pseudocystsmayalsoworsenchronicpainoreveninitiateawastingsyndrome Recentclinicalexperiencesuggeststhatinpatientswithpseudocystssmallerthan6cm ifthereisamaturepseudocystwallonradiographicimagingthatdoesnotresembleacysticneoplasm minimalsymptoms andnoevidenceofactivealcoholabuse theriskofcomplicationsisextremelysmall 10 Thesepatientsmaybesafelyobservedwithlittleriskofseriouscomplication Computedtomogramofapatientwithpancreaticabscess Thepancreasisdiffuselyinvolved anditsmarginsaredifficulttodefinebecauseofthemassiveperipancreaticinflammation whichisreflectedinthestreakingseeninthisscan Towardthetailofthepancreas numeroussmallandlargebubblesarenoted arrows intheperipancreaticinflammatorymass Bubbles causedbygas formingmicroorganisms indicatethatthepancreaticabscessisinfected 4 Diagnostic