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w w w . j c o l . o r g . b r

Journal of

Coloproctology

Original Article

A new theory on the cause of anal fissure impaction theory

Chen Shaoming

a,∗

, Yu Qinghuan

b

aShidongHospitalAffiliatedtoUniversityofShanghaiforScienceandTechnology,Shanghai,PRChina

bYingboHospital,PudongNewArea,Shanghai,PRChina

a r t i c l e i n f o

Articlehistory:

Received3March2020 Accepted21June2020

Availableonline6September2020

Keywords:

Analfissure Etiology

Impactiontheory

a bs t r a c t

Theinternalhemorrhoid,rectaltumor,hypertrophicanalpapilla,andsecretfecalmassare regardedastheblocksembeddedintherectum.Theaboveblockshinderdefecation,which willinevitablyleadtoexcessiveopeningoftheanalcaliber.Oncethelimitisexceeded, theskinoftheanalcanalwilltearandformanalfissure.Basedonthestudyofhistorical evolution,hypothesisreasoning,clinicalverificationandcomparisonwithothertheories,a newconceptofanalfissureetiology–impactiontheoryisproposed.Theso-calledimpaction theoryreferstotheimpaction(variousprimarylesions)inanorectum,whichhindersdefe- cation.Whendefecating,theanalcanalexpandsbeyondthelimit,andthewholelayerof analcanalskinsplits,thatistosay,analfissureisformed.

©2020SociedadeBrasileiradeColoproctologia.PublishedbyElsevierEditoraLtda.This isanopenaccessarticleundertheCCBY-NC-NDlicense(http://creativecommons.org/

licenses/by-nc-nd/4.0/).

Umanovateoriasobreacausadafissuraanal-teoriadaimpactac¸ão

Palavras-chave:

Fissuraanal Etiologia

Teoriadaimpactac¸ão

r e su m o

Ahemorroidainterna,otumorretal,apapilaanalhipertróficaeamassafecalsecretasão consideradososblocosincrustadosnoreto.Osbloqueiosacimaimpedemadefecac¸ão,o queinevitavelmentelevaráaumaaberturaexcessivadocalibreanal.Umavezqueolimite éexcedido,apeledocanalanalrasgaeformaumafissuraanal.Combasenoestudoda evoluc¸ãohistórica,raciocíniodehipóteses,verificac¸ãoclínicaecomparac¸ãocomoutras teorias,umnovoconceitodeetiologiadafissuraanal–ateoriadaimpactac¸ão–éproposto.A chamadateoriadaimpactac¸ãorefere-seàimpactac¸ão(váriaslesõesprimárias)noanorreto, oquedificultaadefecac¸ão.Nadefecac¸ão,ocanalanalseexpandealémdolimiteetodaa camadadapeledocanalanalrasga,ouseja,forma-seafissuraanal.

©2020SociedadeBrasileiradeColoproctologia.PublicadoporElsevierEditoraLtda.Este

´eumartigoOpenAccesssobumalicenc¸aCCBY-NC-ND(http://creativecommons.org/

licenses/by-nc-nd/4.0/).

Correspondingauthor.

E-mails:395276816@qq.com,2813733199@qq.com(S.Chen).

https://doi.org/10.1016/j.jcol.2020.06.006

2237-9363/©2020SociedadeBrasileiradeColoproctologia.PublishedbyElsevierEditoraLtda.ThisisanopenaccessarticleundertheCC BY-NC-NDlicense(http://creativecommons.org/licenses/by-nc-nd/4.0/).

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Background

Thetreatment of intractable anal fissureis generally con- sideredtobemoredifficult,somany operationshavebeen derived,suchaslateralsphincterotomy,ctenophorectomyand soon.However,inmyclinicalwork,Ifoundthatmostofthe patientswithobstinateandoldanalfissurewereaccompanied byotherdiseasesofanorectaldepartment,suchashypertro- phyofanalpapilla,hemorrhoids,prolapseofrectum,outlet obstructionconstipation,etc.Therefore,webelievethatanal fissureisasecondarydisease,whichcannotonlybecuredby operation,butalsobyprimarydisease.Therefore,weputfor- wardanewconceptoftheetiologyofanalfissure–impaction theory.

Analfissure,thatistosay,thewholelayeroftheskinof theanal canaliscracked.Thetypicalsymptom isperiodic pain, whichformsspindle ulcerfor along time.Theclini- calmanifestationsarepain, hemorrhage,and constipation.

Theetiologicaltheoriesincludeinfection,trauma,anatomic factors,internalsphinctercontracture,chronicinflammatory stimulation,andanalstenosis.Theauthorbelievesthatthe abovetheoriescannotfullysummarizetheformationofanal fissure.Therefore,accordingtotheresultsofclinicalresearch, anewconceptoftheetiologyofanalfissure–impactiontheory isproposed.

Historical evolution

ChinesetraditionalChinesemedicineliteraturehasamore detailedrecordoftheclinicalmanifestationsandtreatment methodsofanalfissure.Thediseasebelongstothecategoryof hemorrhoids.The24hemorrhoidsinsurgicalDachenginclude hemorrhoidsinsideandoutsidetheanus,brokenseams,such assheepdung, andthosewithpostfecalhemorrhage,foul smell,and greatpain. Inthechapterofthe goldenhemor- rhoidsofYizong,itisrecordedthat“theanusissurrounded, thefoldlinesare broken,and thefireisdry”.Thesepapers vividlydescribethemanifestationofanalfissureandempha- sizethatconstipationisthecauseofthedisease.Thereare seventy-twokindsofhemorrhoidfistulawrittenbyMaPeiin QingDynasty,whichhasbeenrecordedas“splitanalhemor- rhoid”.TheChinesemedicinetreatsthisdisease,advocates treatingthediseasefortheroot,paysattentiontothenon- surgicaltreatment,thishastheobviousdifferencecompared withtheemphasisonthesurgicalmethod.

Some modern theories of anal fissure

Anatomictheory

Theexternalanalsphincterisdividedintotwopartsfromthe tailbonetotherearoftheanalcanal,whichencirclestheanal canalalongboth sidesoftheanal canal;the externalanal sphincterisconnectedtothetwopartsinfrontoftheanal canal,leavingagapinfrontandrearoftheanalcanal.Most ofthelevatoranimuscleisattachedtobothsidesoftheanal canal,lessinthefrontandtheback.Thebackandthefrontof theanalcanalarenotasstrongasthetwosidesandareeasy

tobedamaged.Theanalcanalformsananalandrectalangle downwardand backward,andthebackofthe analcanalis subjecttogreaterfecalpressure.Thebloodsupplyofthepos- teriormedianlineoftheanalcanalislessanditselasticityis less.

Traumafactors

Hard feces can tear the skin ofanus; frequent defecation causessensitiveconstrictionofanalcanal,andnormalcon- sistencyfecescanalsocausedamage.Chronicinflammation ofanalcanal,hyperplasiaoffibroustissue,formationofanal combinduration,hinderingsphincterrelaxation,makinganal canaleasytobedamagedandtorn.Thecausesofanal fis- sureincludeforeignbodyinrectum,impropermethodofanal expansion,analoperation,delivery,congenitalanalstenosis andprococolonitis.Therearetwokindsoftheories1:thethe- ory ofskintear:the firstone isball2 in 1908.Heassumed that anal fissure isa line like wound formed by the anal flap tornbydry hardfecalmassand extendingdownward.

He comparedit tothe avulsionof the skinofthe parony- chiaand the“sentinelhemorrhoids”causedbyedemaand repeatedabrasions.2Blaisdell’sgridgatetheory3:accordingto theanatomicalarrangementoftheexternalsphincter,Blais- dellpointedoutin1937thatthesuperficialmusclebundleof theexternalsphincterhadaY-shapedbifurcationattherear oftheanusandformedaminortrianglewiththelowerpartof theskin,wheretheskinoftheanalcanallackedmusclesup- portandwasaweakarea.Hethinksthatthelowerpartofthe skinislikeagrid,whichislocatedattheposterioredgeofthe anusandinfrontofthetriangle.Whenthedryhardfecalblock crossesthefront,itiseasytoteartheskin.Headvocatedthe treatmentofanalfissurebycuttingoffthelowerpartofthe externalsphincter.However,ithasbeenfoundthatthebase ofanalfissureisnotthelowerpartoftheexternalsphincter skin,buttheinternalsphincter.Theexternalsphincterisnot thecauseofanalfissure.

Infectionfactors

Acuteandchronicanalsinusitis,analpapilla,internalhemor- rhoids,andpolypsarethemaincausesofinfection.Infection enters the humananal glandthroughthe glandular canal, andabscessesareformedinthesubcutaneoustissueofthe analcanal.Ulcersareformedafterrupture.Smallsuperficial thrombosismaycauseanalfissureduetothrombophlebitis caused by infection.1 The theory of crypt gland infection:

Rankinetal.4proposedin1932thatanalcryptinfectioncan causeanalfissure.Becausetheanalglandsaremostlylocated atthe back oftheanal canal, it seemsthat anal fissureis more likely tooccur inthe midline ofthe anal canal, but the appearanceofthe realulcer causedbyinfection rather than anal fissureiscompletelydifferent. Rankin etal.also pointedoutthatanalfissureisvaricoseulceration.Therea- sonisthat:thesubcutaneousveinofanalcanalisinacurve state, phlebitis can lead to phlebitis, phlebitis can lead to skin lesions, and the damaged skin loses its resistanceto trauma,resultinginanalfissure.Accordingtothistheory,it seemsthatitcanexplainthereasonwhyanalfissureisdif- ficulttoheal,butitcan’texplainwhyanalfissureisproneto

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postnatalposition.Althoughhethinksitiscausedbythesus- ceptibilityofanalrightangletodefecationtrauma,thereis insufficientevidence.2Theoryofresidualepithelialinfection:

in1982,shafik5 triedtoexplainwhyanal fissureischronic fromembryology.Hepointedoutthatduringtheformationof theanalcanalintheembryonicstage,theprocanalandthe hindgutwereintussuscepted.

Internalsphincterspasmtheory

Theanalsphincterisinspasmstatebecauseoftheinjuryor inflammationstimulationoftheanalcanal,resultinginthe enhancementofanalcanalforceandtheeasyinjuryofanal fissure.Thework ofeisenhammer6 inthe1950sgavemod- ernconceptstotheetiologyofanalfissure.Hefirstfoundthat themusclebundleatthebottomoftheanalfissurewasthe internalsphincterratherthanthelowerpartoftheexternal sphincterskin.Heproposedthatthecauseofanalfissurewas spasmorfibrosisoftheinternalsphincterratherthantheso- calledchlamydoscopy;internalsphincterotomy ratherthan chlamydoscopyshouldbeusedtotreatanalfissure.Henot onlycorrectedthemisrepresentationoftheChlamydomonas, but alsoprotectedthe lowerpart ofthe externalsphincter fromdamage.Internalsphincterspasmisthecauseorresult ofanalfissure.Almostallchronicanalfissureisaccompanied byhightension andhigh anal pressureofinternalsphinc- ter.Schoutenetal.7(1996)recentlymeasuredthemeananal MaximumRestingPressure(MARP),whichwassignificantly higherinpatientswithanalfissurethaninthenormalcontrol group(121.07±16.97mmhgand68.78±24.48mmhg).North- mannetal.8(1974)foundthattheinternalsphincterofanal fissurepatientswasnotrelaxedbutovercontractedwhenthe rectumwasinflated.Theabnormalactivityofinternalsphinc- terisusuallyconsideredastheresultofchronicinflammatory stimulationofanalfissureorthereflexreactionofinternal sphinctercausedbypain.Butthishypothesishasnoexper- imentalbasisand may bemisleading.Because thepain of analfissuredisappearedandtheaverageanalMaximumRest- ingPressure(MARP)didnotdecreaseafterlocalanesthesia,it suggestedthatspasmwasnotsecondarytopain.

Theoryofanalnarrowprimaryschool

Analskininthedevelopmentofslow,resultinginnarrowanal canal,easytodamageintoanalfissure.Atpresent,scholars thinkthatanalsinusitis,internalsphincterspasmandanal stricturearethesecondarydiseasesofanalfissure.

Analysis of current theories

Thetheoryofanatomicalfactorsofanalfissure:theanatom- icalstructureofanorectumisthecongenitalconditionthat analfissureiseasytooccurinthespecialpartofanus.Itis notthedirectcauseofanalfissure.

Accordingtothe traumatheory, trauma isalinkinthe processofanalfissure,butnotthecause.

Infectioustheoryofanalfissure:theauthorbelievesthat infectioncanoccuraftertheformationofanalfissure;itisthe conditionforthetransformationofanalfissuretochronicand

pathologicalchanges,anditmayalsooccurbeforetheforma- tionofanalfissure,whichistheconditionfortheaggravation ortransformationofhemorrhoids.

Infection ofhemorrhoids, inflammation ofanal papilla, constipation→dysdefecation,formationofnewanalfissure

→newanalfissure(freshwound)→infection→nonhealing ofwound→spasmofanalsphincter→hypertrophyofanal papilla,hyperplasiaofinternalhemorrhoids,constipationdue topainandfearofstool(increasedimpactionfactor).

Factorssuchasinternalsphincterspasmandanalstenosis arepathologicalchangesintheprocessofanalfissureforma- tionanddevelopment,notthecauseofanalfissure.Clinical experimentsconfirmedthat7:hightensionofsphinctercan induceanorectalskinischemia,resultinginanalfissurefor- mation;ifthetensionofsphincterisreducedandtheblood supplyofanalskinisrestored,theanalfissurewillbehealed.

Thehightensionofsphinctermustbecausedbythefactor ofimpaction.Therefore,internalsphincterspasmisapatho- logicalchangeinthedevelopmentofanalfissure.Therewasa negativecorrelationbetweenMARPandADBF.In1986,gibbons andread9proposedthatthespasmofinternalsphincter,i.e.

theincreaseofanalinternalpressure,canleadtotheischemia ofskinareaofanalcanal.Schouten10simultaneously mea- sured178patientswithvariousanaldiseasesincludinganal fissurewithDopplerlaserskinbloodflowmeterandanorec- talpressuremeter.TheresultssupportedGibbons’conclusion thatthe skinblood flowinthe fourquadrantsofthe front, back,leftandrightoftheanalcanalinhealthypeoplewere (1.5±0.7)V,(0.7±0.3)V,(1.7±0.8)V,(1.6±0.5)V,respectively, Thebloodperfusionpressureintheposterioranalcommis- sureareawassignificantlylowerthanthatinotherareasof theanalcanal.TheMARPofchronicanalfissurepatientswas significantlyhigherthanthatofthecontrolgroupandother analdiseasespatients.

Fromtheaboveanalysis,wecanseethateachtheoryisrel- ativelylimitedandcannotcomprehensively summarizethe pathogenesisanddevelopmentfactorsofanalfissure.There- fore,weputforwardanewtheoryofanalfissure–impaction theory.

New concept of anal fissure etiology–impaction theory

Impactiontheory

Inviewoftheshortcomingsofthetraditionaltheoryofanal fissure etiology, the author repeatedly studies and breaks thetraditionalconceptsandideasinclinicalwork,putsfor- wardanewconceptofanalfissureetiology–impactiontheory, the birth of the new theory, fills the defects of the tradi- tionaltheory,cancomprehensivelysummarizethecausesand pathologicalchangesofanalfissure,easytounderstandand guideclinicaltreatment.

The so-called impaction theory refers to the impaction factors (various primary lesions) inanorectum that hinder defecation,causeexcessiveanaldilatationwhendefecating, exceedtheanaldilatationlimit,andopenthewholelayerof analskin.Thetypicalsymptomsareperiodicpain,repeated

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analdilatationortear,andfusiformulcercausedbywound infection,namelyanalfissure.

Pathologicalevolution

Pathological evolution: due to the “impaction factor” hin- deringdefecation,theanalcanalcaliberisenlargedbeyond thelimit.Duetotheweaknessoftheanalcanal,theblood perfusionpressureintheposterioranaljunctionareaissig- nificantlylowerthanthatinotherareasoftheanalcanal.9So itwastornfirst.Analfissureoftenoccursbetweentheanal flapandtheanalmargin,thelowestsuperficialsurfaceofthe internalsphincter.Attheinitialstage,itwas onlythe skin fissureoftheanalcanal,someofwhichreachedthesubcu- taneoustissue or sphincter. If the anal canalis opened,it willberoundoroval.Theedgeisneat,thebottomisshal- lowand elastic, andthe longitudinalmuscle separatesthe splitbottomfromtheinternalsphincter.Ifpropertreatmentis given,itcanbecured.Becausetheinternalsphincterisoften spasmodic and contracted, the blood supply of the fissure islack,andit iscontinuouslystimulatedbythe“impaction factor”and secondary infection.The edgeofthe fissure is thickened,thesurrounding iscongested,andthebottomis hard.Theannularfiberoftheinternalsphinctercanbeseen.

Thereareabundantnervesinthefissure,whicharesensitive tosensation.Slightstimulationcancause severepain. The skinatthelower end ofthe fissurewasinflamed, andthe superficialveinsandlymphcirculationwereblocked, caus- ingedemaandfibrosis,formingtheconnectivetissueexternal hemorrhoids.Theanalflapatthe upperendofthe fissure, edemaandfibrosisoftheanalpapillamaketheanalpapilla furtherhyperplasia andhypertrophy(thatis,theimpaction factor isintensified),formingavicious circle.Thefibers of thelateralmarginofthefissurebecamehard,andabscesses occurredinthesurroundingtissues,whichbrokeintotheanal canalandformedfistulas.Theinternalsphincterofthefis- surebasewasdeformedobviously,inaspasmstate,andthe analpressureincreased.Therefore, thereare 6pathological changes such as fissure, external hemorrhoids ofconnec- tivetissue,analsinusitis,hypertrophicanalpapilla,internal sphincter,and branchingfibersofcombinedmuscle,which arestimulatedbyinflammationforalongtime.Itcanbeseen thatthetheoriesoftrauma,anatomicalstructure,infection andinternalsphincterspasmareonlythephysiologicaland anatomicalfactorsorpathologicalevolutionofacertainlink inthedevelopmentofanalfissure,andthemostfundamen- talpathologicalfactoristhe“impactionfactor”intheprimary anorectum.

Reasoning

Conditions: Ablock isembedded inthe anorectum, which hindersdefecation.Ifdefecationisnecessary,effortsmustbe made.Theexternalforcewillmaketheanalcaliberlargerthan thephysiologicallimit.Theskinoftheanalcanalwillbetorn andtheanalfissurewillbeformed.Iftheblockingfactoris notremoved,theanalcanalwillbedamagedrepeatedlyevery time.Thewoundsurfaceoftheanalfissurewillberepeat- edlystimulated,orsecondaryinfection willforma chronic ulcer.Theanalfissurewillchangefromtheacutestagetothe

chronicstage.Becausetheinternalsphincterhasthenatureof nonrandomcircularmuscle,itiseasytospasm.Thespasmis mostlyattheoutletofanalcanal.Ifthespasmcontinues,itcan leadtopermanentanalcanalstenosis.Itisaviciouscycleof pathology.Theinternalsphincterspasmandcontractionform chronicanalfissure.Thebranchingfibersofinternalsphincter andcombinedmusclewerestimulatedbyinflammationfora longtime.

Hypothesis:Theinternalhemorrhoid,rectaltumor,hyper- trophicanalpapilla,andthefecalmassofthesecretknotare regardedastheblockofrectalimpaction.

Conclusion: All of the above blocks hinder defecation, whichwillinevitablyleadtoexcessiveopeningofanalcaliber.

Oncetheyexceedthelimit,theskinofanalcanalwilltearand formanalfissure.

Reasoning: Inother words,why can’tweregard hemor- rhoids,rectal tumors,hypertrophicanal papillae,and fecal massofsecretknotsasakind ofrectal impaction?Thisis thenewconceptofanalfissureetiology.

Clinical experience

Inthelong-termclinicalpractice,theauthorclassifiesalarge number of casesofanal fissure nomatter whatkind, and takes the“impactiontheory” asthe guidanceand“Tongas theuse”asthetreatmentprinciple,thoroughlytreatstheroot causesofinternalhemorrhoids,hypertrophicanalpapilla,rec- talpolyp,rectalprolapse,constipation,enteritis,diarrhea,etc.

–eliminates the “impaction factor”. For those with chronic analfissurewiththeformationofthepatternbelt,theauthor appropriatelyusestheanalexpansiontherapyI.Thesecond timelaxationwasperformed,allofthemreceivedsatisfactory effect,andnofailureoccurred.

Anyanorectalspecialist,intheclinicaltreatmentofcases ofinternalhemorrhoids,rectalpolyps,anal papillaryfertil- izer,oftenfoundthesecaseswithanal fissure.Also,inthe treatmentofpatientswithanal fissure,thereareoftenpri- maryinternalhemorrhoids,constipation,rectaltumor,rectal prolapse,thatis,“impactionfactor”.Iftheprimarydiseases ofthese casesare noteliminated,the simpletreatmentof analfissurewillnotwork,thatis,temporarysymptomrelief, inashortperiodoftimewillstillrecurandthediseasewill worsen.

From1975to1977,Chinamadeageneralsurveyofindus- trialandmining,governmentagencies,schools,troops,urban residents in service industries, rural fishing grounds, etc.

thetotalnumberofpeopleexaminedwas76,692,including children, adults and the elderly. There are 57,292 casesof completeanorectalinformation,and33,837casesofanorectal disease, with a total incidence rate of 59%–10%. Theinci- dence rate ofmale is 53.9%,and female incidence rate is 67%.Theincidencerateofmale andfemale ishigher than thatofmen.Theincidencerateofanalfissureishigherthan thatofmale.Themainreasonisthatwomenhavefertility, and their activities afterpregnancy are reduced,intestinal peristalsis weakened,and uterusiscompressedto rectum.

This shows that impaction is the root cause of anal fis- sure.

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Clinical significance

The“impactiontheory”isusedtosummarizethepathological factorsofanalfissureandtoexplaintheoccurrence,develop- ment,andpathologicalchangesofanalfissure.

Thetheoryofanatomicalfactorsofanalfissurecanonly explainthecongenitalconditionsofanalfissureoccurringin specialpartsofanus,but notthedirectfactors ofanal fis- sureformation.Thatis,without“impactionfactor”,thereis nodirectfactorofanalfissure,andanalfissurewillnotoccur.

Accordingtothetheoryoftrauma,impactionisthecon- ditionand sourceoftrauma, whiletraumais the resultof impactionhinderingdefecation.

In the Institute of infection of anal fissure, the author believes that infection can be secondary to the formation ofanal fissure, which is the condition forthe anal fissure tobecomechronic and pathological,whilebefore the anal fissure,itistheaggravationofhemorrhoidsanditstransfor- mationinto“impactionfactor”.

Internal sphincter spasm theory, chronic inflammatory stimulationand analstenosis arethe pathologicalchanges inthedevelopmentofanalfissure,notthecauseofanalfis- sure.

Usingthetheoryofimpactiontostudytheformationand treatmentofanalfissurehashighacademicandclinicalvalue.

Throughclinicalobservation,wecanturnitintoatheory, and use thecorrect theoryto guide thework. Thegeneral principleforthetreatmentofanalfissureis“tousethegen- eralprinciple”,tocorrectlyjudgethecausesofanalfissure, tothoroughlytreattheprimarydisease,and toremovethe

“impactionfactor”,wecanobtaingoodtreatmenteffect.We can’tcuttheinternalsphincter,cuttheChlamysband,pur- suetheoperationtoomuchandbecomeasimple“surgeon”.

Inthisrespect,traditionalChinesemedicineadvocatestreat- ingdiseases forthe root,andit isworthlearningfromthe wholeconcept.Inthelong-termclinicalwork,thetreatmentof chronicanalfissureundertheguidanceofthe“impactionthe- ory”,thetreatmentofprimarydiseases,theinternalsphincter isnotcut,theChlamysbandisnotremoved,throughthelong- termclinicalobservation,thepatientsarecured,thepainof surgeryisreduced,thecourseoftreatmentisshortened,and thecomplicationsofsurgeryareavoided.Therefore,usingthe theoryofimpactiontostudytheformationofanalfissureand guidethe treatmentofanalfissurehashigh academicand clinicalvalue.

IntermsofinternaladministrationoftraditionalChinese medicine,xiaodaorunzaoisthemaindrug.Preventionofthis syndrome first,use Tongli medicine.In the treatment, the

theoryof“generalprincipledoesnothurt”,“topassforuse”

and“plugforpass”isfollowed.AccordingtotraditionalChi- nese medicine, the cause of this disease is large intestine drynessandheat,blockofQiandmachine,crisscrossQiand blood,crisscrossmeridiansandcollaterals,andbleedingwith doors.

ModernChinesemedicinedevelopstheessenceoftradi- tional medicine,absorbs theadvantagesofworldmedicine andWesternChina,attachesimportancetotheorganicinte- grationofmacroscopicandmicroscopicaspects,carriesout researchonregionalanatomy,embryology,pathology,cytol- ogy,andneurology.UnderthepremiseoftraditionalChinese medicine,itintegratesmodernmedicalscienceandtechnol- ogy, and activelydevelops EPHminimally invasive surgery.

Analfissurerecovered.

Conflict of interest

Theauthorsdeclarenoconflictsofinterest.

references

1.ChenShaoming,etal.TherapeuticsofModernChinese AnorectalDiseases,PublishedByPeople’sHealthPress, December20191bALLC.TheRectum,ItsDiseases,And DevelopmentalDefects.London:HodderandStoughton;1988.

2.BlaisdellPC.Pathogenesisofanalfissureandimplicationsas totreatment.Surg.Gynecol.Obstet.1937;65:672–7.

3.HananelN.Re-examinationofclinicalmanifestationsand responsetotherapyoffissure-in-ano.Dis.Colon.Rectum.

1997;40:229.

4.FwRankin,BargenJA,BaieLA.TheColon,Rectum,AndAnus.

Phtiladelphia:WBSaunders;1932.p.584–93.

5.ShafikA.Anewconceptoftheanatomyofanalsphincter mechanismandthephysiologyofdefecation:chronicanal fissure:anewfherorvofpathogenesis.Am.J.surg.

1982;144:262.

6.EisenhammerS.Theevaluationoftheinternalanalsphincter otomy.Operationoftheinternalanalsphincterotomy operationwithspecialreferencetoanalfissure.Surg.Gyn.

Obst.1959;109:583.

7.SchoutenWR,BrielJW,AuwerdaJJ,DeGraafEJ.Ischaemic natureofanalfissure.Br.J.Surg.1996;83:63.

8.NorthmanBJ,SchusterMM.Internalanalsphincter derangementwithanalfissure.Gastroenterol.1974;67.Two hundredandsixteen.

9.GibbonsCP,ReadNW.Analhypertoniainfissures:causeor effect?Br.J.Surg.1986;73:443.

10.SchoutenWR,BrielJW,AuwerdaJJ.Relationship.between analpressureandanodermalbloodflow.Dis.Colon.Reetum.

1994;7:664–9.

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