Kronična obstruktivna pljučna bolezen

Kronična obstruktivna pljučna bolezen
Centrilobular emphysema 865 lores.jpg
Patologija pljuč z emfizemom centrilobularnega tipa, značilnega za kajenje. Povečava fiksiranega prereza površine pljuč, ki kaže več votlin, obloženih s težkimi sajastimi usedlinami.
Klasifikacija in zunanji viri
MKB-10J40J44, J47
MKB-9490492, 494496
OMIM606963
DiseasesDB2672
MedlinePlus000091
eMedicinemed/373 emerg/99
MeSHC08.381.495.389

Kronična obstruktivna pulmonarna bolezen (KOPB), med drugim znana tudi kot Kronična obstruktivna bolezen pljuč (KOBP) in Kronična obstruktivna bolezen dihalnih poti (KOBDP), je obstruktivno obolenje pljuč, katerega značilnost je kronično slab pretok zraka. Običajno se s časom poslabšuje. Glavni simptomi so zasoplost, kašelj in nastajanje izmečka .[1] Večina ljudi s '"kroničnim bronhitisom imate KOPB.[2]

Kajenje je najpogostejši vzrok za KOPB, s številnimi drugimi dejavniki, kot so onesnaženje zraka in genetika, ki igrajo manjšo vlogo.[3] V državah v razvoju je eden pogostnih vzrokov onesnažen zrak zaradi slabega prezraöevanja med kuho in ob ogrevanju prostorov. Dolgotrajna izpostavljenost tem dražečim vplivom povzroča vnetni odziv v pljučih, zaradi česar prihaja do zoženja malih dihalnih poti in kot emfizem. znanega razkroja pljučnega tkiva.[4] Diagnozo postavimo na osnovi slabega pretoka zraka, ki se ga meri s preskusom delovanja pljuč.[5] Drugače kot je to pri astmi, jemanje zdravil zmanjšanega pretoka zraka ne izboljša bistveno..

KOPB lahko preprečimo z zmanjšanjem izpostavljenosti znanim vzrokom. Gre za prizadevanja, da se zmanjša obseg kajenja in izboljša kakovost zraka v bivališčih in na prostem. Metode za zdravljenje KOPB so med drugim: odvajanje od kajenja, cepljenja, rehabilitacija pljuč, in pogosto vdihavanje brohodilatatornih in s kortikosteroidnih zdravil. Za nekatere ljudi je rešitev dolgoročna terapija s kisikom ali pa presaditev pljuč.[4] Pri prizadetih z obdobji akutnega poslabšanja je lahko da potrebna večja uporaba zdravil in hospitalizacija.

Po vsem svetu KOPB prizadene 329 milijonov ljudi oziroma skoraj 5% prebivalstva. V letu 2012 je bolezen kot tretji najbolj pogosten vzrok smrti terjala življenje več kot threh milijonov ljudi.[6] Število smrtnih žrtev naj bi se v številnih državah zaradi višjih stopenj kajenja in staranja prebivalstva povečalo.[7] Ekonomski stroški bolezni v letu 2010 se cenijo na 2.1 milijard USD.[8]


Znaki in simptomi

Najpogostejši simptomi KOPB so nastajanje izpljuvka, zasoplost in produktiven kašelj.[9] Ti simptomi so prisotni v daljšem časovnem obdobju[2] in se običajno sčasoma slabšajo.[4] Ni jasno, če obstajajo različne vrste KOPB.[3] Doslej so bolezen delili na emfizem in kroničnega bronhitis; pri tem predstavlja emfizem le opis sprememb v pljučih, ne pa bolezni same, kronični bronhitis pa je preprosto opis simptomov, do katerih lahko - ali pa tudi ne - pride pri KOPB.[1]

Kašelj

Kronični kašelj je običajno pojavi kot prvi znak bolezni. To stanje se lahko pojavi, še preden se KOPB v celoti razvije. Količina proizvedenega izmečka se lahko tekom ur ali dni spreminja. V nekaterih primerih kašelj ni prisoten ali pa se pojavlja le občasno in ni nujno produktiven. Nekateri ljudje s KOPB pripisujejo simptome "kašlju kadilcev". Sputum se lahko pogoltne ali pa izpljune, pogosto odvisno od družbenih in kulturnih dejavnikov. Pretiran kašelj ima lahko za posledico polom reber ali kratko izgubo zavesti. Osebe s KOPB imajo pogosto zgodovino "prehladov", ki trajajo dlje časa.[9]

Zasoplost

Zasoplost je pogosto simptom, ki ljudi najbolj moti.[10] Prizadeti jo nabolj pogosto opisujejo takole: "dihati mi je zelo naporno," "Počutim se kot brez sape," ali "Ne morem vdihniti dovolj zraka".[11] Različna kulturna okolja lahko da znake opisujejo drugače.[9] Značilno za zasoplost je, da se ob naporu poslabša, ravno tako se poslabša, če traja dolgo, in pa s časom.[9] V poznejših fazah se pojavi med mirovanjem in je lahko vedno prisotna.[12][13] Pri ljudeh s KOPB predstavlja vir tako anksioznosti kot slabe kakovosti življenja.[9] Veliko ljudi z napredovano obliko KOPB +diha skozi nagubane ustnice, kar pri nekaterih olajša zasoplost.[14][15]

Druge značilnosti

Pri KOPB, lahko izdih traja dlje kot vdih.[16] Lahko se pojavi stiskanje v prsih,[9] ki pa ni običajno in katerega vzrok je lahko kaj drugega.[10] Pri osebah z oviranim pretokom zraka je ob pregledu prsnega koša s stetoskopom lahko slišati piskanje ali druge zvoke ob vstopu zraka v pljuča.[16] Prsni koš v obliki soda je za KOPB značilen, čeprav relativno redek znak.[16] S slabšanjem bolezni prizadeti pogosto zavzemajo trinožno lego.[2]

V poznem štadiju KOPB vodi do visokega tlaka v pljučnih arterijah, ki obremenjuje desni prekat srca.[4][17][18] To stanje se imenuje cor pulmonale, in vodi do simptomov v obliki oteklih nog[9] in izbuljenih žil na vratu.[4] KOPB je med obolenji pljuč najpogostejši vzrok za cor pulmonale.[17] Cor pulmonale je postal manj pogost, odkar se od uporablja dodaten kisik.[2]

KOPB se pogosto, deloma zaradi skupnih dejavnikov tveganja, pojavlja skupaj s številnimi drugimi bolezenskimi stanji.[3] To so med drugim: ishemične bolezni srca, visok krvni tlak, diabetes mellitus, oslabitve mišic, osteoporoza, pljučni rak, [[anksiozna motnja] ] in depresija.[3] Bolniki s hudo obliko bolezni imajo pogosto občutek, da so ves čas utrujeni.[9] Betičasti prsti niso specifični za KOPB in bi morali spodbuditi preiskave v smeri pljučnega raka.[19]

Poslabšanje

Kot akutno poslabšanje KOPB je razumeti povečano kratko sapo, povečano količino izmečkov, spremembe njih barve od brezbarvne k zeleni ali rumeni ali poslabšanje kašlja.[16] Lahko se pojavi skupaj s znaki za povečan napor pri dihanju, kot so hitro dihanje, hitro bitje srca, potenje, aktivnost mišic v vratu, modrikast odtenek kože in zmeda, ali pa bojevito vedenje, če gre za zelo hude izbruhe.[16][20] Ob pregledu pljuč s stetoskopom je slišati pokanje.[21]

Vzrok

Primarni vzrok za KOPB je tobačni dim, v nekaterih državah spadata med pomembne vzroke še izpostavljenost pri delu ter onesnažen zrak zaradi odprtih ognjev v bivališčih..[1] Značilno je, da morajo te izpostavljenosti biti prisotne desetletja dolgo, preden se pojavijo simptomi.[1] Genetska slika osebe tudi vpliva na nevarnost.[1]

Kajenje

Odstotek kadilk od konca 1990 st. do zgodnjih 2000
Odstotek kadilcev od konca 1990 do začetka 2000. Uporabljeni lestvici za ženske in moške se med seboj razlikujeta.[22]

The primary risk factor for COPD globally is tobacco smoking.[1] Med kadilci bo okoli 20% dobilo KOPB,[23] med tistimi, ki kadijo že celo življenje, pa okoli polovica.[24] V Združenih državah Amerike in Združenem kraljestvu je med obolelimi za KOPB 80-95% aktivnih ali preteklih kadilcev.[23][25][26] Verjetnost, da se KOPB pojavi, raste z celokupno izpostavljenostjo dimu.[27] Poleg tega so ženske dovzetnejše za škodljive učinke dima kot pa so moški.[26] Pri nekadilcih, je pasivno kajenje vzrok za približno 20% primerov.[25] Tudi druge vrste kajenja, kot je marihuana, cigare in vodna pipa, pomenijo tveganje.[1] Ženske, ki kadijo med nosečnostjo, lahko da povečajo tveganje za KOPB pri otroku.[1]

Onesnaženost zraka

Slabo odzračevani ognji za kuho, pri katerih je pogosto gorivo premog ali biomasa, kot so les in živalski iztrebki, vodijo do onesnaženosti zraka v zaprtih prostorih in so eden od najpogostejših vzrokov za KOPB v državah v razvoju.[28] Ti ognji predstavljajo način, kako skoraj 3 milijarde ljudi kuhajo in grejejo; njih učinki na zdravje je zaradi večje izpostavljenosti večja med ženskami.[1][28] Predstavljajo glavni vir energije v 80% bivališč v Indiji, na Kitajskem in v podsaharski Afriki.[29]

Ljudje, ki živijo v velikih mestih, imajo višjo stopnjo KOPB kot ljudje, ki živijo na podeželju.[30] Urbano onesnaževanje zraka urban je sicer dejavnik pri slabšanju bolezni, vendar njegova celotna vloga kot vzrok za KOPB ni jasna.[1] Območja s slabo kakovostjo zraka na prostem, med drugim zaradi izpušnih plinov imajo na splošno višjo stopnjo KOPB.[29] Za celokupni učinek pa se v primerjavi s kajenjem meni, da je majhen.[1]

Poklicne izpostavljenosti

Intenzivna in dolgotrajna izpostavljenost prahu na delovnem mestu, kemikalijam in hlapom povečuje tveganje za KOPB, tako pri kadilcih kot tudi pri nekadilcih.[31] Za izpostavljenost na delovnem mestu se meni, da je vzrok v 10-20% primerov.[32] Po ocenah je v Združenih državah Amerike z izpostavljenostjo na delovnem mestu povezanih več kot 30% primerov pri bolnikih, ki niso nikoli kadili; tveganje v državah brez zadostnih predpisov je verjetno še večje.[1]

Vpletenih je več industrij in virov, recimo[29] visoka raven prahu v [[premogovništvo|]premogovništvu], pri pridobivanju zlata, v industriji tekstila iz bombaža, ter poklici, kjer se dela s kadmijem in z izocianati in kjer nastaja dim, kot je varjenje.[31] Delo v kmetijstvu tudi predstavlja tveganje.[29] Za nekatere poklice so ocenili, da je tveganje pri njih enakovredno od pol do dveh škatel cigaret na dan.[33] Izpostavljenost kremenovemu prahu lahko tudi povzroči KOPB, s tveganje zanj ni povezano s tveganjem za silikozo.[34] Zdi se, da se negativni učinki izpostavljenosti prahu in cigaretnemu dimu seštevajo, če ne celo obojestransko krepijo.[33]

Genetika

Genetika igrajo vlogo pri razvoju KOPB.[1] Med sorodniki bolnikov s KOPB, ki kadijo, je bolj pogosta, kot med kadilci, ki si niso v sorodu. [1] Trenutno je edini nesporno deden dejavnik tveganja pomanjkanje alfa 1-antitripsina (AAT).[35] To tveganje je še posebej veliko, če oseba, ki ji alfa 1-antitripsin primanjkuje, tudi kadi.[35] Dejavnik je odgovoren za približno 1-5% primerov[35][36] stanje pa je prisotno pri približno 3-4 osebah na 10.000 ljudi.[2] Drugi genetski dejavniki so trenutno predmet preiskav,[35] verjetno jih je precej. [29]

Drugo

Številni drugi dejavniki so manj tesno povezani s KOPB. Tveganje je večje pri revnih ljudeh, čeprav ni jasno, ali je to zaradi revščine same ali zaradi drugih dejavnikeov tveganja, ki so z revščino povezani, kot sta na primer onesnaženje zraka in podhranjenost.[1] Obstajajo še nepotrjeni dokazi za povečano tveganje za KOPB pri ljudeh z astmo in hiper-reaktivnimi dihalnimi potmi.[1] Porodni dejavniki, kot je nizka teža pri porodu, lahko prav tako igrajo vlogo kot številne nalezljive bolezni, kot recimo HIV / AIDS in tuberkuloza.[1] Okužbe dihal kot pljučnica se zdi tveganjea za KOPB, vsaj pri odraslih, ne povečujejo.[2]

Poslabšanja

Akutno poslabšanje (nenadno poslabšanje simptomov)[37] običajno sprožijo okužbe ali okoljska onesnaževala, včasih tudi drugi dejavniki, kot je nepravilna uporaba zdravil.[38] Razlog za 50 do 75% primerov so zgleda okužbe,[38][39] bakterijskega izvora v 25%, virusnega izvora v 25%, in obojnega izvora v 25% primerov.[40] Okoljska onesnaževala so med drugim slaba kakovost zraka v bivališčih in na prostem.[38] Izpostavljenost lastnemu dimu in pasivno kajenje povečujeta tveganje.[29] Nizke temperature lahko prav tako igrajo vlogo, saj se poslabšanja pojavljajo pogosteje v zimskem času.[41] Osebe z resnejšo obliko obolenja poslabšanja pogosteje doletijo: pri blagi obliki bolezni 1,8 na leto, zmerni 2-3 na leto, in hudi 3,4 na leto.[42] Osebe s s številnimi poslabšanji se delovanje pljuč hitreje slabša.[43] Krvni strdki v pljučih lahko pri oosebah z obstoječo KOPB poslabšajo simptome.[3]

Patofiziologija

Na levi je diagram pljuč in dihalnih poti, vložek kaže podroben prerez običajnih bronhiol in alveol. Na desni pljuča poškodovana zaradi KOPB, vložek kaže prerez poškodovanih bronhiol in alveol

KOPB je vrsta obstruktivne pljučne bolezni, pri kateri obstaja kronično slab pretok zraka, ki je le delno reverzibilen (omejen pretok zraka), in pri katerem prizadeta oseba ni zmožna izdihniti v celoti (uklenjen zrak).[3] Slab pretok je posledica okvare pljučnega tkiva (znan kot emfizem) in kot obstruktivni bronhitis poznane bolezni majhnih dihalnih poti. Deleži teh dveh dejavnikov se razlikujejo med ljudmi.[1] Hudo uničenje malih dihalnih poti lahko vodi do nastanka velikih zračnih žepov—znanih bullae—ki nadomeščajo pljučno tkivo. Ta oblika bolezni se imenuje bulozni emfizem.[44]

Micrograf kaže emfizem (levo - velike praznine) in pljučno tkivo, kjer so alveoli relativno ohranjeni (desno).

KOPB se razvija kot pomemben in kroničen vnetni odziv na vdihavanje dražečih snovi.[1] Kronične bakterijske okužbe lahko dodatno vplivajo na to vnetno stanje.[43] Vnetne celice, ki sodelujejo, so med drugim nevtrofilci granulociti in makrofagi, dve vrsti belih krvničk. Pri kadilcih so delujejo tudi TC1 limfociti, pri nekaterih bolnikih s KOPB, podobno kot pri astmi, tudi eozinofilci granulociti. Ta odziv celic je delno posledica vnetnih mediatorjev, kot so kemotaktični dejavniki. Drugi procesi, vpleteni v poškodbe pljuč, so med drugim iz vnetnih celic izhajajoč oksidativni stres kot posledica visoke koncentracije prostih radikalov v tobačnem dimu, in razgrajevanje [[vezno tkivo|vezivnega tkiva] ] pljuč zaradi proteaz, ki jih zaviralci proteaz nwe ihibirfajo v zadostni meri. Uničenje veznega tkiva v pljučih je povod za razvoj emfizema, ki nato prispeva k slabemu pretoka zraka in končno k slabi absorpciji in sprostitvi respiratornih plinov.[1] Splošno propad mišic, ki pogosto spremlja KOPB, je lahko deloma posledica vnwetnih posrednikov, ki jih pljuča sproščajo v kri.[1]

Do zoženja dihalnih poti prihaja zaradi vnetja in zaradi njih brazgotinjenja. Posledica zoženja dihalnih poti je, da prizadeta oseba ni zmožna popolnoma izdihniti. Do zmanjšanja pretoka zraka prihaja največ med izdihom, ko tlak v prsih stiska dihalne poti.[45] To ima lahko za posledico, da ob naslednjem vdihu v pljučih ostane več zraka iz prejšnjega diha, s tem pa povečanje celotnega volumna zraka v pljučih v danem trenutku; proces se imenuje Dihanje#hiperinflacija.[45][46] Hiperinflacija zaradi telesne aktivnosti je pri KOPB povezana z zasoplostjo in kratko sapo, saj je manj udobno vdihniti, če so pljuča deloma že polna.[47]

Nekatere osebe imajo tudi delno hiperodzivnost dihalnih poti na dražila, ki spominja na znake pri astmi.[2]

Do nizke ravni kisika in konec koncev visoke ravni ogljikovega dioksida v krvi lahko pride zaradi slabe plinske izmenjave kot posledice zmanjšane ventilacije zaradi obstrukcije dihalnih poti, hiperinflacije in zmanjšane volje dihati. [1] Med obdobji poslabšanja se tudi poveča vnetje dihalnih poti, kar ima za posledico povečano hiperinflacijo, zmanjšanje pretoka zraka ob izdihu in poslabšan prenos plinov. To lahko privede tudi do nezadostnega prezračevanja in navsezadnje do nizke ravni kisika v krvi.[4] Nizki nivoji kisika, če so prisotni dalj časa, lahko povzročijo zoženje arterij v pljučih, emfizem pa okvare kapilar v pljučih. Obe spremembi imata za posledico povečan tlak krvi v pljučnih arterijah, kar lahko povzroči cor pulmonale.[1]

Diagnoza

oseba sedi in piha v napravo, priključeno na računalnik
Pacient piha v spirometer. Manjše prenosne naprave so na voljo za uporabo v ordinaciji

Diagnozo KOPB je treba imeti v mislih pri vseh osebah, ki so starejše od 35 do 40 let in ki imajo kratko sapo, kronični kašelj, s proizvodnjo izmečka, ki imajo številnejše prehlade pozimi in zgodovino izpostavljenosti dejavnikom tveganja za to bolezen.[9][10] Spirometrija se nato uporabi za potrditev diagnoze.[9][48]

Spirometrija

Spirometrija mero trenutni obseg obstrukcije dihalnih poti in se praviloma izvede po uporabi bronhodilatatorja, to je zdravila za odpiranje dihalnih poti.[48] Za diagnozo se merita dve glavni komponenti: prisilno izdihan volumen v eni sekundi (FEV1), to je največja količina zraka, ki jo je mogoče izdihniti v prvi sekundi diha, in prisiljenavitalna kapaciteta (FVC), ki je največja količina zraka, ki jo lahko olseba izdihne v enem samem velikem dihu.[49] Normalno se v prvi sekundi izdihne 75-80% FVC[49] in razmerje FEV1 / FVC pod 70% pomeni za osebo s simptomi KOPB, da to bolezen tudi ima.[48] Na podlagi teh meritev bi spirometrija privedla do prekomernega diagnostiviranja KOPB pri starejših.[48] Merila, ki jih je postavil Nacionalni inštitut za klinično odličnost, dodatno zahtevajo FEV1 pod 80% napovedanega.[10]

Dokazi, po katerih naj bi spirometrija pri osebah brez simptomov omogočila predhodno diagnosticirati stanje, niso zanesljivi, zato se te metode ne priporoča.[9][48] Konični ekspiratorni pretok (največja hitrost izdiha), ki se pogosto uporablja pri astmi, za diagnozo KOPB ne zadošča.[10]

Resnost

MRC skala za zasoplost[10]
Skor Prizadeta aktivnost
1 Samo naporna aktivnost
2 Živahna hoja
3 Ob normalni hoji
4 Po nekaj minutah hoje
5 Med preoblačenjem
Skor GOLD[9]
Resnost FEV1 % predvideno
Milo(GOLD 1) ≥80
Zmerno(GOLD 2) 50–79
Hudo (GOLD 3) 30–49
Zelo hudo (GOLD 4) <30 ali chronic respiratory failure

Številne metode omogočajo ugotoviti, koliko KOPB vpliva na določenega posameznika.[9] Prilagojeni vprašalnik mMRC ( British Medical Research Council) ali test za oceno KOPB (CAT - COPD assessment test) sta preprosta vprašalnika, ki omogočata ugotoviti, kako resni so simptomi.[9] Rezultati pri CAT iimajo razpon 0-40, čim višji rezultat, tem hujša je bolezen.[50] Spirometrija lahko pomaga ugotoviti, kako resna je omejitev zračnega pretoka.[9] Običajno temelji na FEV1 kot odstotek "normalne" vrednosti za starost, spol, višino in težo osebe.[9] Tako ameriške kot tudi evropske smernice priporočajo, da se zdravljenje delno opira na FEV1.[48] Smernice GOLD predlagajo štiri kategorije, ki temeljijo na oceni simptomov in na omejitvi pretoka zraka.[9] Treba je tudi upoštevati izgubo teže in šibkost mišic, kot tudi prisotnost drugih bolezni.[9]

Drugi testi

Rentgensko slikanje prsnega koša in krvna slika sta med diagnozo lahko koristna zaradi izključitve drugih bolezni.[51] Značilni znaki na rentgenski sliki so pretirano razširjena pljuča, sploščena prepona, povečan retrosternalni zračni prostor, in bule; rentgenska slika tudi pomaga izključiti druga obolenja pljuč, kot so na primer pljučnica, pljučni edem ali pnevmotoraks.[52] Posnetek prsi visoke ločljivosti z računalniško tomografijo lahko pokaže rauzpostranjenost emfizema po celih pljučih, tudi je lahko koristen, če je treba izključiti druge bolezni pljuč.[2] Vendar to le redko vpliva na nadaljnje zdravljenje, razen če je načrtovan kirurški poseg. [2] Analiza arterijske krvi se uporablja za določanje potrebe po kisiku; priporoča se jo pri bolnikih s FEV1 pod 35% napovedane vrednosti, pri bolnikih z nasičenostjo okončin s kisikom pod 92%, in pri bolnikih z znaki kongestivne srčne odpovedi.[9] V predelih sveta s pogostim pomanjkanjem alfa-1 antitripsina, bi bilo treba razmisliti, če se ljudi s KOPB (zlasti ljudi, ki so mlajši od 45 let in pri bolnikih z emfizemom, ki vpliva na spodnji del pljuč) ne bi testiralo.[9]

Diferencialna diagnoza

KOPB je morda treba razlikovati od drugih vzrokov za kratko sapo kot so kongestivna srčna odpoved, pljučna embolija, pljučnica ali pnevmotoraks. Veliko ljudi s KOPB zmotno misli, da imajo astmo.[16] Med astmo in KOPB se razlikuje na osnovi simptomov, na anamnezi kajenja, in glede na to, ali je omejitev pretoka pri spirometriji reverzibilna z bronhodilatatorji.[53] Tuberkuloza se tudi lahko javlja s kroničnim kašljem, kar je treba imeti v mislih na lokacijah, kjer je pogosta.[9] Manj pogosti stanji s podobnimi znaki sta lahko bronhopulmonalna displazija in obliterativni bronhiolitis.[51] Kronični bronhitis se lahko javlja ob normalnem pretoku zraka in v tem primeru ni razvrščen kot KOPB.[2]

Preventiva

Večina primerov KOPB se lahko preprči tako, da se zmanjša izpostavljenost tobačnemu dimu in izboljša kakovost zraka.[29] Letno cepljenje proti gripi pri osebah s KOPB zmanjša verjetnost za poslabšanja, hospitalizacijo in smrt.[54][55] Pnevmokokno cepljenje je lahko tudi koristno.[54]

Konec kajenja

Skrb za to, da ljudi sploh ne začnejop kaditi, je ključni vidik preprečevanja KOPB.[56] Politika vlad, javne zdravstvene ustanove in protikadilske organizacije bi lahko zmanjšale ravni kajenja, ko bi ljudi od odvračale od tega, da začnejo kaditi, oziroma bi jim pomagale, da prenehajo kaditi.[15] Prepoved kajenja na javnih mestih in delovnih mestih so pomembni ukrepi, ki zmanjšujejo izpostavljenost pasivnemu kajenju in čeprav prepoved že mnogokje velja, bi jo bilo vredno še razširiti. [29]

Pri kadilcih je prenehanje kajenja edini ukrep, ki dokazano upočasni slabšanje KOPB.[57] Tudi v pozni fazi bolezni lahko upočasni slabšanje pljučne funkcije in odloži začetek invalidnosti in nastop smrti.[58] Konec kajenja se začne z odločitvijo nehati s tobakom, odločitvi za ta korak sledi poizkus, s kajenjem prenehati.. Pogosto je potrebnih več poskusov, preden se doseže dolgoročna vzdržnost.[59] Poskusi v obdobju 5 let vodijo do uspeha pri skoraj 40% ljudi.[60]

Nekateri kadilci lahko dolgoročno prenehajo kaditi samo s pomočjo močne volje. Tobak pa povzroča visoko stopnjo zasvojenosti[61] in mnogi kadilci potrebujejo dodatno podporo. Podpora okolja, sodelovanje v programu za odvajanje od kajenja in uporaba zdravil, kot so nikotinska nadomestna terapija, bupropion ali vareniklin, povečujejo verjetnost za uspeh.[15][60]

Occupational health

A number of measures have been taken to reduce the likelihood that workers in at-risk industries—such as coal mining, construction and stonemasonry—will develop COPD.[29] Examples of these measures include: the creation of public policy,[29] education of workers and management about the risks, promoting smoking cessation, checking workers for early signs of COPD, use of respirators, and dust control.[62][63] Effective dust control can be achieved by improving ventilation, using water sprays and by using mining techniques that minimize dust generation.[64] If a worker develops COPD, further lung damage can be reduced by avoiding ongoing dust exposure, for example by changing the work role.[65]

Onesnaženost zraka

Both indoor and outdoor air quality can be improved, which may prevent COPD or slow the worsening of existing disease.[29] This may be achieved by public policy efforts, cultural changes, and personal involvement.[66]

A number of developed countries have successfully improved outdoor air quality through regulations. This has resulted in improvements in the lung function of their populations.[29] Those with COPD may experience fewer symptoms if they stay indoors on days when outdoor air quality is poor.[4]

One key effort is to reduce exposure to smoke from cooking and heating fuels through improved ventilation of homes and better stoves and chimneys.[66] Proper stoves may improve indoor air quality by 85%. Using alternative energy sources such as solar cooking and electrical heating is effective, as is using fuels such as kerosene or coal rather than biomass.[29]

Management

There is no known cure for COPD, but the symptoms are treatable and its progression can be delayed.[56] The major goals of management are to reduce risk factors, manage stable COPD, prevent and treat acute exacerbations, and manage associated illnesses.[4] The only measures that have been shown to reduce mortality are smoking cessation and supplemental oxygen.[67] Stopping smoking decreases the risk of death by 18%.[3] Other recommendations include: influenza vaccination once a year, pneumococcal vaccination once every 5 years, and reduction in exposure to environmental air pollution.[3] In those with advanced disease, palliative care may reduce symptoms, with morphine improving the feelings of shortness of breath.[68] Noninvasive ventilation may be used to support breathing.[68]

Exercise

Pulmonary rehabilitation is a program of exercise, disease management and counseling, coordinated to benefit the individual.[69] In those who have had a recent exacerbation, pulmonary rehabilitation appears to improve the overall quality of life and the ability to exercise, and reduce mortality.[70] It has also been shown to improve the sense of control a person has over their disease, as well as their emotions.[71] Breathing exercises in and of themselves appear to have a limited role.[15]

Being either underweight or overweight can affect the symptoms, degree of disability and prognosis of COPD. People with COPD who are underweight can improve their breathing muscle strength by increasing their calorie intake.[4] When combined with regular exercise or a pulmonary rehabilitation program, this can lead to improvements in COPD symptoms. Supplemental nutrition may be useful in those who are malnourished.[72]

Bronchodilators

Inhaled bronchodilators are the primary medications used[3] and result in a small overall benefit.[73] There are two major types, β2 agonists and anticholinergics; both exist in long-acting and short-acting forms. They reduce shortness of breath, wheeze and exercise limitation, resulting in an improved quality of life.[74] It is unclear if they change the progression of the underlying disease.[3]

In those with mild disease, short-acting agents are recommended on an as needed basis.[3] In those with more severe disease, long-acting agents are recommended.[3] If long-acting bronchodilators are insufficient inhaled corticosteroids are typically added.[3] With respect to long-acting agents, it is unclear if tiotropium (a long-acting anticholinergic) or long-acting beta agonists (LABAs) are better, and it may be worth trying each and continuing the one that worked best.[75] Both types of agent appear to reduce the risk of acute exacerbations by 15-25%.[3] While using both at the same time may offer a benefit, this benefit, if any, is of questionable significance.[76]

There are several short-acting β2 agonists available including salbutamol (Ventolin) and terbutaline.[77] They provide some relief of symptoms for four to six hours.[77] Long-acting β2 agonists such as salmeterol and formoterol are often used as maintenance therapy. Some feel the evidence of benefits is limited[78] while others view the evidence of benefit as established.[79][80] Long-term use appears safe in COPD[81] with adverse effects include shakiness and heart palpitations.[3] When used with inhaled steroids they increase the risk of pneumonia.[3] While steroids and LABAs may work better together,[78] it is unclear if this slight benefit outweighs the increased risks.[82]

There are two main anticholinergics used in COPD, ipratropium and tiotropium. Ipratropium is a short-acting agent while tiotropium is long-acting. Tiotropium is associated with a decrease in exacerbations and improved quality of life,[76] and tiotropium provides those benefits better than ipratropium.[83] It does not appear to affect mortality or the over all hospitalization rate.[84] Anticholinergics can cause dry mouth and urinary tract symptoms.[3] They are also associated with increased risk of heart disease and stroke.[85][86] Aclidinium, another long acting agent which came to market in 2012, has been used as an alternative to tiotropium.[87][88]

Corticosteroids

Corticosteroids are usually used in inhaled form but may also be used as tablets to treat and prevent acute exacerbations. While inhaled corticosteroids (ICS) have not shown benefit for people with mild COPD, they decrease acute exacerbations in those with either moderate or severe disease.[89] When used in combination with a LABA they decrease mortality more than either ICS or LABA alone.[90] By themselves they have no effect on overall one-year mortality and are associated with increased rates of pneumonia.[67] It is unclear if they affect the progression of the disease.[3] Long-term treatment with steroid tablets is associated with significant side effects.[77]

Other medication

Long-term antibiotics, specifically those from the macrolide class such as erythromycin, reduce the frequency of exacerbations in those who have two or more a year.[91][92] This practice may be cost effective in some areas of the world.[93] Concerns include that of antibiotic resistance and hearing problems with azithromycin.[92] Methylxanthines such as theophylline generally cause more harm than benefit and thus are usually not recommended,[94] but may be used as a second-line agent in those not controlled by other measures.[4] Mucolytics may be useful in some people who have very thick mucous but are generally not needed.[54] Cough medicines are not recommended.[77]

Oxygen

Supplemental oxygen is recommended in those with low oxygen levels at rest (a partial pressure of oxygen of less than 50–55 mmHg or oxygen saturations of less than 88%).[77][95] In this group of people it decreases the risk of heart failure and death if used 15 hours per day[77][95] and may improve people's ability to exercise.[96] In those with normal or mildly low oxygen levels, oxygen supplementation may improve shortness of breath.[97] There is a risk of fires and little benefit when those on oxygen continue to smoke.[98] In this situation some recommend against its use.[99] During acute exacerbations, many require oxygen therapy; the use of high concentrations of oxygen without taking into account a person's oxygen saturations, may lead to increased levels of carbon dioxide and worsened outcomes.[100][101] In those at high risk of high carbon dioxide levels, oxygen saturations of 88–92% are recommended, while for those without this risk recommended levels are 94-98%.[101]

Surgery

For those with very severe disease surgery is sometimes helpful and may include lung transplantation or lung volume reduction surgery.[3] Lung volume reduction surgery involves removing the parts of the lung most damaged by emphysema allowing the remaining, relatively good lung to expand and work better.[77] Lung transplantation is sometimes performed for very severe COPD, particularly in younger individuals.[77]

Poslabšanja

Acute exacerbations are typically treated by increasing the usage of short-acting bronchodilators.[3] This commonly includes a combination of a short-acting inhaled beta agonist and anticholinergic.[37] These medications can be given either via a metered-dose inhaler with a spacer or via a nebulizer with both appearing to be equally effective.[37] Nebulization may be easier for those who are more unwell.[37]

Oral corticosteroids improve the chance of recovery and decrease the overall duration of symptoms.[3][37] In those with a severe exacerbation, antibiotics improve outcomes.[102] A number of different antibiotics may be used including: amoxicillin, doxycycline or azithromycin; it is unclear if one is better than the others.[54] There is no clear evidence for those with less severe cases.[102]

Non-invasive positive pressure ventilation in those with acutely raised CO2 levels (type 2 respiratory failure) decreases the probability of death from or needing intensive care admission for mechanical ventilation.[3] Additionally, theophylline may have a role in those who do not respond to other measures.[3] Less than 20% of exacerbations require hospital admission.[37] In those without acidosis from respiratory failure, home care ("hospital at home") may be able to help avoid some admissions.[37][103]

Prognoza

invalidnosti prilagojena življenje leto za kronične obstruktivne pljučne bolezni na 100.000 prebivalcev v letu 2004.[104]
  ni podatkov
  ≤110
  110–220
  220–330
  330–440
  440–550
  550–660
  660–770
  770–880
  880–990
  990–1100
  1100–1350
  ≥1350

KOPB se običajno postopoma slabša s časom in se lahko konča s smrtjo. Ocenjuje se, da je 3% vseh invalidnosti povezano s KOPB.[105] The proportion of disability from COPD globally has decreased from 1990 to 2010 due to improved indoor air quality primarily in Asia.[105] The overall number of years lived with disability from COPD, however, has increased.[106]

The rate at which COPD worsens varies with the presence of factors that predict a poor outcome including: severe airflow obstruction, little ability to exercise, shortness of breath, significantly underweight or overweight, congestive heart failure, continued smoking, and frequent exacerbations.[4] Long-term outcomes in COPD can be estimated using the BODE index which gives a score of zero to ten depending on FEV1, body-mass index, the distance walked in six minutes, and the modified MRC dyspnea scale.[107] Significant weight loss is a bad sign.[2] Results of spirometry are also a good predictor of the future progress of the disease but not as good as the BODE index.[2][10]

Epidemiologija

Globally, as of 2010, COPD affected approximately 329 million people (4.8% of the population) and is slightly more common in men than women.[106] This is as compared to 64 million being affected in 2004.[108] The increase in the developing world between 1970 and the 2000s is believed to be related to increasing rates of smoking in this region, an increasing population and an aging population due to less deaths from other causes such as infectious diseases.[3] Some developed countries have seen increased rates, some have remained stable and some have seen a decrease in COPD prevalence.[3] The global numbers are expected to continue increasing as risk factors remain common and the population continues to get older.[56]

Between 1990 and 2010 the number of deaths from COPD has decreased slightly from 3.1 million to 2.9 million.[109] Overall it is the fourth-leading cause of death.[3] In some countries, mortality has decreased in men but increased in women.[110] This is most likely due to rates of smoking in women and men becoming more similar.[2] COPD is more common in older people;[1] it affects 34-200 out of 1000 people older than 65 years, depending on the population looked at.[1][52]

In England, an estimated 0.84 million people (of 50 million) have a diagnosis of COPD; translating into approximately one person in 59 receiving a diagnosis of COPD at some point in their lives. In the most socioeconomically deprived parts of the country, one in 32 people were diagnosed with COPD, compared with one in 98 in the most affluent areas.[111] In the United States approximately 6.3% of the adult population, totaling approximately 15 million people, have been diagnosed with COPD.[112] 25 million people may have COPD if currently undiagnosed cases are included.[113] In 2011, there were approximately 730,000 hospitalizations in the United States for COPD.[114]

Zgodovina

Giambattista Morgagni who made one of the earliest recorded descriptions of emphysema in 1769

The word "emphysema" is derived from the Greek ἐμφυσᾶν emphysan meaning "inflate" -itself composed of ἐν en, meaning "in", and φυσᾶν physan, meaning "breath, blast".[115] The term chronic bronchitis came into use in 1808[116] while the term COPD is believed to have first been used in 1965.[117] Previously it has been known by a number of different names including: chronic obstructive bronchopulmonary disease, chronic obstructive respiratory disease, chronic airflow obstruction, chronic airflow limitation, chronic obstructive lung disease, nonspecific chronic pulmonary disease, and diffuse obstructive pulmonary syndrome. The terms chronic bronchitis and emphysema were formally defined in 1959 at the CIBA guest symposium and in 1962 at the American Thoracic Society Committee meeting on Diagnostic Standards.[117]

Early descriptions of probable emphysema include: in 1679 by T. Bonet of a condition of "voluminous lungs" and in 1769 by Giovanni Morgagni of lungs which were "turgid particularly from air".[117][118] In 1721 the first drawings of emphysema were made by Ruysh.[118] These were followed by pictures by Matthew Baillie in 1789 and descriptions of the destructive nature of the condition. In 1814 Charles Badham used "catarrh" to describe the cough and excess mucus in chronic bronchitis. René Laennec, the physician who invented the stethoscope, used the term "emphysema" in his book A Treatise on the Diseases of the Chest and of Mediate Auscultation (1837) to describe lungs that did not collapse when he opened the chest during an autopsy. He noted that they did not collapse as usual because they were full of air and the airways were filled with mucus. In 1842, John Hutchinson invented the spirometer, which allowed the measurement of vital capacity of the lungs. However, his spirometer could only measure volume, not airflow. Tiffeneau and Pinelli in 1947 described the principles of measuring airflow.[117]

In 1953, Dr. George L. Waldbott, an American allergist, first described a new disease he named "smoker's respiratory syndrome" in the 1953 Journal of the American Medical Association. This was the first association between tobacco smoking and chronic respiratory disease.[119]

Early treatments included garlic, cinnamon and ipecac, among others.[116] Modern treatments were developed during the second half of the 20th century. Evidence supporting the use of steroids in COPD were published in the late 1950s. Bronchodilators came into use in the 1960s following a promising trial of isoprenaline. Further bronchodilators, such as salbutamol, were developed in the 1970s, and the use of LABAs began in the mid-1990s.[120]

Družba in kultura

Glej tudi: COPD Awareness Month

COPD has been referred to as "smoker's lung".[121] Those with emphysema have been known as "pink puffers" or "type A" due to their frequent pink complexion, fast respiratory rate and pursed lips,[122][123] and people with chronic bronchitis have been referred to as "blue bloaters" or "type B" due to the often bluish color of the skin and lips from low oxygen levels and their ankle swelling.[123][124] This terminology is no longer accepted as useful as most people with COPD have a combination of both.[2][123]

Many health systems have difficulty ensuring appropriate identification, diagnosis and care of people with COPD; Britain's Department of Health has identified this as a major issue for the National Health Service and has introduced a specific strategy to tackle these problems.[125]

Gospodarstvo

Globally, as of 2010, COPD is estimated to result in economic costs of $2.1 trillion, half of which occurring in the developing world.[8] Of this total an estimated $1.9 trillion are direct costs such as medical care, while $0.2 trillion are indirect costs such as missed work.[126] This is expected to more than double in the next 20 years.[8] In Europe, COPD represents 3% of healthcare spending.[1] In the United States, costs of the disease are estimated at $50 billion, most of which is due to exacerbation.[1] COPD was among the most expensive conditions seen in U.S. hospitals in 2011, with a total cost of about $5.7 billion.[114]

Raziskave

Glej tudi: COPD: Journal of Chronic Obstructive Pulmonary Disease

Infliximab, an immune-suppressing antibody, has been tested in COPD but there was no evidence of benefit with the possibility of harm.[127] Roflumilast shows promise in decreasing the rate of exacerbations but does not appear to change quality of life.[3] A number of new long acting agents are under development.[3] Treatment with stem cells is being studied.[128] While generally safe and with promising animal data there is little data in humans as of 2014.[129]

Druge živali

Chronic obstructive pulmonary disease may occur in a number of other animals and may occur from exposure to cigarette smoke.[130][131] Most disease, however, is relatively mild.[132] In horses it is also known as recurrent airway obstruction and is typically due to an allergic reaction to straw containing fungus.[133] KOPB je pogosto najti pri starih pseh.[134]

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