Nazal pasajlar\u0131n, orofarinksin, trakea, proksimal ve distal hava yollar\u0131n\u0131n ki\u015finin yak\u0131n \u00e7evresiyle do\u011frudan temas halinde olmas\u0131, o ki\u015finin temas etti\u011fi herhangi bir respiratuar irritant ve sensitize edici akut solunan toksik maddelere kar\u015f\u0131 solunum sisteminin daha savunmas\u0131z kabul edilmesine neden olabilir. Semptomlar bile\u015fiklerin fiziksel \u00f6zellikleri, bireyin maruz kald\u0131\u011f\u0131 \u00e7evredeki maddenin konsantrasyonu ve ma\u011fdurun \u00f6nceden var olan durumuna ba\u011fl\u0131 olarak inhale edilen bir toksine maruz kald\u0131ktan sonraki birka\u00e7 saniye i\u00e7inden birka\u00e7 g\u00fcne kadar ortaya \u00e7\u0131kabilir. Patojenik sonu\u00e7lar, b\u00fcy\u00fck \u00f6l\u00e7\u00fcde havayolunun mukozal tutulumu ve h\u00fccresel d\u00fczeyde respiratuar distress veya \u00f6l\u00fcmle sonu\u00e7lanabilen, haftalarca veya aylarca g\u00f6r\u00fclen sistemik hastal\u0131k veya kronik akci\u011fer hastal\u0131\u011f\u0131n\u0131n geli\u015fmesiyle ortaya \u00e7\u0131kabilir.<\/p>\n
Bir akut toksik inhalasyon; toksik bir maddeye izole olarak maruz kalan bir ki\u015fi veya her biri toksik maddeye farkl\u0131 miktarlarda ve s\u00fcrelerde maruz kalan birden fazla ma\u011fdurun oldu\u011fu toplu bir kaza durumu \u015feklinde prezente olabilir. Yaralanma ayr\u0131ca deri ve konjonktiva ile kontaminasyonu, toksik bir maddenin kazara inhalasyonunu veya yutulmas\u0131n\u0131 kapsayabilir. Duman(sigara), gazlar ve buharlar solunan toksik maddelerin en yayg\u0131n bi\u00e7imleridir, ancak s\u0131v\u0131lar ve kat\u0131lar da toz, aerosol veya sis olarak solunabilir. \u00c7o\u011funlukla ilgili madde kesin olarak bilinmemektedir veya yaln\u0131zca fiziksel \u00f6zellikleri veya deneyimlenen semptomlar\u0131n temel niteli\u011fi a\u00e7\u0131s\u0131ndan tan\u0131mlanabilir.<\/p>\n
“Akut inhalasyon hasar\u0131” terimi tipik olarak yanma reaksiyonu sonras\u0131 yap\u0131s\u0131 bozulmu\u015f \u00fcr\u00fcnlerle kontamine havan\u0131n solunmas\u0131 sonras\u0131nda olu\u015fan sekelleri tan\u0131mlamak i\u00e7in kullan\u0131l\u0131r. Bu formdaki respiratuar yaralanma, akut toksik inhalasyonun en yayg\u0131n \u015feklidir ve akut duman inhalasyonu ile yang\u0131na maruz kalan hastalar\u0131n % 10-20’sinde yan\u0131klar\u0131 komplike hale getirerek morbidite ve mortaliteyi \u00f6nemli \u00f6l\u00e7\u00fcde art\u0131r\u0131r. Yang\u0131nla ili\u015fkili inhalasyonlardan kaynaklanan hava yolu yaralanmas\u0131, supraglottik yap\u0131larda termal yaralanmay\u0131, respiratuar yap\u0131lar\u0131n kimyasal irritasyonunu, karbon monoksit (CO) ve siyan\u00fcr bile\u015fiklerinden (CN) kaynaklanan sistemik toksisiteyi veya bu yaralanmalar\u0131n kombinasyonunu i\u00e7erebilir. Genel bir g\u00f6zlem olarak, termal yaralanmalar tipik olarak supraglottik yap\u0131larda g\u00f6r\u00fcl\u00fcr ve kimyasal yaralanmalar alt solunum yollar\u0131nda izlenir. S\u0131cak buhara maruz kalmay\u0131 i\u00e7eren hava yolu yaralanmalar\u0131, \u00fcst veya alt hava yollar\u0131n\u0131 etkileyebilir. Duman inhalasyonundan kaynaklanan toksisitenin etkilerinin, asfiksinin do\u011frudan bir sonucu, sistemik toksisitenin veya respiratuar mukozan\u0131n do\u011frudan yaralanmas\u0131 nedeniyle oldu\u011fu d\u00fc\u015f\u00fcn\u00fclmektedir.<\/p>\n
TANI ARACI OLARAK GAZLARIN F\u0130Z\u0130KSEL \u00d6ZELL\u0130KLER\u0130<\/strong><\/h2>\nSolunan bir toksik maddenin kesin kimli\u011fi bilinmese bile bir gaz\u0131n fiziksel \u00f6zellikleri, toksik inhalasyonun patolojik etkilerinin temel niteli\u011fini belirlemeye yard\u0131mc\u0131 olabilir. \u0130nhale edilen partik\u00fcllerin boyutu ve inhale edilen maddenin sudaki \u00e7\u00f6z\u00fcn\u00fcrl\u00fc\u011f\u00fc g\u00f6z \u00f6n\u00fcnde bulundurulmas\u0131 gereken de\u011fi\u015fkenler aras\u0131ndad\u0131r. 10 \u00b5m\u2019den daha b\u00fcy\u00fck par\u00e7ac\u0131klar \u00a0nazofarenksi ve \u00fcst hava yolunu etkileme e\u011filimindedir; mukosiliyer bariyer, partik\u00fclleri ba\u011flar ve stabilize eder. Bununla birlikte, bu koruyucu mekanizma yo\u011fun bir maruziyete tabi olundu\u011funda veya istenmeyen inhalasyonun kayna\u011f\u0131 tahliye edilemedi\u011finde genellikle kar\u015f\u0131 konulamaz bir \u015fekilde etkilenir. 5-10 \u00b5m\u2019den daha k\u00fc\u00e7\u00fck partik\u00fcller genellikle distal hava yollar\u0131na kadar solunur; alveolar makrofajlar ve h\u00fccresel d\u00fczeydeki di\u011fer mekanizmalar taraf\u0131ndan ele al\u0131n\u0131r. Bir bile\u015fi\u011fin suda \u00e7\u00f6z\u00fcn\u00fcrl\u00fc\u011f\u00fc, potansiyel kimli\u011fi ile ilgili ipu\u00e7lar\u0131 sa\u011flar. Suda \u00e7\u00f6z\u00fcn\u00fcrl\u00fc\u011f\u00fc daha fazla olan bir bile\u015fik (\u00f6rne\u011fin, amonyak)<\/em>; konjonktiva, nazofaringeal ve orofaringeal mukoza gibi \u00fcst solunum yolunun nemli y\u00fczeylerini h\u0131zla etkileme e\u011filimindedir. Azot oksitleri veya fosgen gibi suda daha az \u00e7\u00f6z\u00fcn\u00fcr bile\u015fikler; \u00fcst solunum yollar\u0131n\u0131 hemen etkilemez ve \u00e7o\u011fu zaman daha fazla pulmoner parankimal hasarla ili\u015fkili daha derin inhalasyonla sonu\u00e7lanan gecikmi\u015f etkilere sahiptir.<\/p>\nAkut toksik inhalasyonlarda g\u00f6z \u00f6n\u00fcnde bulundurulacak di\u011fer fakt\u00f6rler aras\u0131nda solunan maddenin ortam havas\u0131ndaki konsantrasyonu, toplam maruz kalma s\u00fcresi, maddenin yo\u011funlu\u011fu (yani daha a\u011f\u0131r gazlar yere do\u011fru \u00e7\u00f6kme e\u011filiminde olacakt\u0131r)<\/em>, gaz\u0131n rengi (\u00f6rne\u011fin, elementel klor, ortam havas\u0131na maruz kald\u0131\u011f\u0131nda sar\u0131-ye\u015fil g\u00f6r\u00fcnme e\u011filiminde olacakt\u0131r)<\/em>, gaz\u0131n kokusu (\u00f6rne\u011fin k\u00fck\u00fcrt bazl\u0131 bile\u015fiklerin \u00e7\u00fcr\u00fck yumurta kokusu veya klor gaz\u0131n\u0131n rahats\u0131z edici keskin kokusu),<\/em> havaland\u0131rman\u0131n varl\u0131\u011f\u0131 veya yoklu\u011fu, ma\u011fdurun bilincini kaybedip kaybetmedi\u011fi, hastan\u0131n solunum cihaz\u0131 gibi herhangi bir ki\u015fisel solunum arac\u0131 kullan\u0131p kullanmad\u0131\u011f\u0131 ve ya\u015f, sigara i\u00e7me durumu, komorbid hastal\u0131klar (\u00f6rne\u011fin e\u015fzamanl\u0131 kalp hastal\u0131\u011f\u0131 veya \u00f6nceden var olan akci\u011fer rahats\u0131zl\u0131klar\u0131)<\/em> ve genetik duyarl\u0131l\u0131k gibi \u00e7e\u015fitli konak fakt\u00f6rleri yer almaktad\u0131r. Akut toksik inhalasyonu olan bir hastay\u0131 de\u011ferlendirirken dikkate al\u0131nacak de\u011fi\u015fkenler; gazlar\u0131n ve bireye ait de\u011fi\u015fkenlerin fiziksel \u00f6zelliklerinin \u00f6zeti Tablo 1\u2019de \u00f6zetlenmi\u015ftir<\/p>\n![\"\"](\"https:\/\/tatd.org.tr\/tatdtoks\/wp-content\/uploads\/sites\/36\/2021\/10\/tablo-11-1.png\")
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AKUT TOKS\u0130K \u0130NHALASYON YARALANMALARININ PATOF\u0130ZYOLOJ\u0130S\u0130<\/strong><\/h2>\nAkut toksik inhalasyon hasar\u0131 s\u0131ras\u0131nda ve sonras\u0131nda tan\u0131mlanan \u00e7e\u015fitli \u00f6nemli patofizyolojik de\u011fi\u015fiklikler belirlenmi\u015ftir. Is\u0131 ve buhar, trakeobron\u015fiyal a\u011faca do\u011frudan zarar verebilmesine ra\u011fmen; bilinen di\u011fer respiratuar irritanlar yanma reaksiyonu sonucu ortaya \u00e7\u0131kan \u00fcr\u00fcnlerdir. Bunlar akrolein ve formaldehit gibi doymam\u0131\u015f aldehitleri, halojen asitleri gibi bile\u015fikleri i\u00e7erir. Bu maddelerin varl\u0131\u011f\u0131 kona\u011f\u0131n enflamatuar yan\u0131t\u0131n\u0131 tetikler, genellikle trakeobron\u015fiyal mukozan\u0131n soyulmas\u0131na neden olur ve s\u0131kl\u0131kla h\u00fccresel d\u00fczeyde hava yoluna do\u011frudan toksik etkiler bu duruma e\u015flik eder. Havayolu hasar\u0131, duyusal ve vazomotor sinir u\u00e7lar\u0131ndan substance P ve kalsitonin ili\u015fkili peptit gibi n\u00f6ropeptitlerin \u00fcretilmesine yol a\u00e7ar. Ayr\u0131ca bu n\u00f6ropeptitler; bronkokonstr\u00fcksiyonun ind\u00fcklenmesi ve nitrik oksit sentetaz\u0131 stim\u00fcle ederek h\u00fccrelerde toksik etkilere neden olan reaktif oksijen radikallerinin \u00fcretilmesiyle ili\u015fkilendirilmi\u015ftir. N\u00f6ropeptitlerin, ta\u015fikininler gibi i\u015flev g\u00f6rd\u00fckleri tan\u0131mlanm\u0131\u015ft\u0131r; vask\u00fcler permabilitede art\u0131\u015f olu\u015fturmas\u0131, lenfatik ak\u0131\u015f ve vask\u00fcler ge\u00e7irgenlik nedeniyle s\u00fcre\u00e7 pulmoner \u00f6demle sonu\u00e7lan\u0131r. S\u00fcrfaktan d\u00fczeylerinin, interl\u00f6kinler ve TNF-\u03b1 gibi imm\u00fcnmod\u00fclat\u00f6rlerin azalmas\u0131 hasar\u0131n \u00f6nemini belirtir. Bu kaskad ortaya \u00e7\u0131kt\u0131\u011f\u0131nda, h\u00fccresel pulmoner vazokonstr\u00fcksiyon kayb\u0131 ile ekstra lokal h\u00fccresel hasar meydana gelir. Bu da inhalasyon hasar\u0131ndan sadece 20 dk i\u00e7inde bron\u015fiyal kan ak\u0131\u015f\u0131n\u0131n dramatik bir \u015fekilde artmas\u0131na neden olur. Reaktif oksijen radikalleri, mitokondriyal disfonksiyona ve h\u00fccresel apoptoza neden olur; hayvan modellerinde hasar g\u00f6rm\u00fc\u015f solunum epiteli ve alveoler makrofajlar\u0131n ekstrensek koag\u00fclasyon kaskad\u0131n\u0131 tetikledi\u011fi, bunun daha sonra ind\u00fckleyici plazminojen aktivat\u00f6r-I seviyesinde homeostatik koag\u00fclasyon balans\u0131n\u0131 bozdu\u011fu ve dolay\u0131s\u0131yla hiperkoag\u00fclabilite durumu olu\u015fturdu\u011fu g\u00f6sterilmi\u015ftir. Ekstra bron\u015fiyal kan ak\u0131\u015f\u0131, intersitisyumda polimorfon\u00fckleer lenfositleri ve sitokinleri biriktirerek inflamatuar yan\u0131t\u0131 g\u00fc\u00e7lendiriyor gibi g\u00f6r\u00fcnmektedir. Plazma proteinlerinin, kast ve eks\u00fcda olu\u015fumu ile hava yollar\u0131na kaymas\u0131, alveolar kollapsa veya distal hava yollar\u0131n\u0131n tamamen t\u0131kanmas\u0131na neden olur. Bron\u015fiyal kan ak\u0131\u015f\u0131n\u0131 kas\u0131tl\u0131 olarak azaltmak i\u00e7in hayvan deneyleri yap\u0131ld\u0131\u011f\u0131nda, hava yolu t\u0131kan\u0131kl\u0131\u011f\u0131n\u0131n azald\u0131\u011f\u0131, intraparankimal s\u0131v\u0131n\u0131n s\u0131n\u0131rland\u0131\u011f\u0131 ve sonu\u00e7 olarak oksijenasyonun iyile\u015fti\u011fi g\u00f6r\u00fclm\u00fc\u015ft\u00fcr. Yap\u0131lan ilave \u00e7al\u0131\u015fmalarda bir koyun modelinde; kalsitonin ile ili\u015fkili peptit ve P maddesine kar\u015f\u0131 antagonistlerin, s\u0131v\u0131 shiftini ve inflamasyonu yava\u015flatt\u0131\u011f\u0131n\u0131 g\u00f6sterilmi\u015ftir. Akut toksik inhalasyonlar s\u0131ras\u0131nda reaktif oksijen t\u00fcrleri ve peroksinitrit (ONOO\u00a0 \u0304) \u00fcretimi ile hava yoluna n\u00f6trofilik hareket olmas\u0131 anti-inflamatuar tedavilerin hedefi olarak belirlenmi\u015ftir. Peroksinitrit ayr\u0131\u015fma kataliz\u00f6rlerinin, duman inhalasyon hasar\u0131n\u0131 inceleyen hayvan modellerinde sitoprotektif oldu\u011fu g\u00f6sterilmi\u015ftir.<\/p>\n
AKUT TOKS\u0130K AKC\u0130\u011eER HASARININ \u015e\u0130DDET\u0130, TANI VE DERECELEND\u0130RME<\/strong><\/h2>\n\u0130nhalasyon hasar\u0131n\u0131n varl\u0131\u011f\u0131n\u0131 do\u011frulamak ve ciddiyetini belirlemek i\u00e7in \u00e7ok say\u0131da test kullan\u0131lm\u0131\u015ft\u0131r. Duman inhalasyonunun ilk klinik belirtileri genellikle b\u00fcy\u00fck hava yolu epitel hasar\u0131ndan kaynaklan\u0131r. Mukozal hiperemi, \u00f6dem ve \u00fclserasyon, kast olu\u015fumu ve bron\u015fiyal obstr\u00fcksiyon meydana gelir. Flexible bronkoskopi inhalasyon hasar\u0131n\u0131n ciddiyetini de\u011ferlendirmek i\u00e7in standart teknik olarak kabul edilmesine ra\u011fmen, toraks\u0131n bilgisayarl\u0131 tomografik (BT) g\u00f6r\u00fcnt\u00fclemesi, karboksihemoglobin \u00f6l\u00e7\u00fcmleri ve solunum fonksiyon testleri gibi di\u011fer y\u00f6ntemlerin t\u00fcm\u00fc, toksik inhalasyonun ciddiyetine ve do\u011fas\u0131na ba\u011fl\u0131 olarak yard\u0131mc\u0131 ara\u00e7lar olarak kullan\u0131lmaya devam edilecektir. Bronkoskopi, bronkoskopik g\u00f6rselle\u015ftirilmi\u015f bulgular ile ger\u00e7ek \u00f6l\u00fcm oranlar\u0131 aras\u0131ndaki tutars\u0131zl\u0131\u011f\u0131 muhtemelen a\u00e7\u0131klayaca\u011f\u0131 d\u00fc\u015f\u00fcn\u00fclen distal hava yollar\u0131ndaki de\u011fi\u015fiklikleri tespit edemez veya hasar \u015fiddetini belirleyemez. Res\u00fcsitasyondan sonra PaO2 \/ FiO2 hesaplamas\u0131ndan ve toraks BT g\u00f6r\u00fcnt\u00fclemesinden yararlan\u0131larak gerekli olacak res\u00fcsitasyon d\u00fczeyini \u00f6l\u00e7mek i\u00e7in mortaliteyi tahmin etme \u00e7abalar\u0131 mevcuttur. Yakla\u015f\u0131k olarak inhalasyon hasar\u0131 olan hastalar\u0131n \u00fc\u00e7te biri, dumana maruz kald\u0131ktan sonraki ilk 3 g\u00fcn i\u00e7inde akut akci\u011fer hasar\u0131 (ALI) geli\u015ftirir. Duman inhalasyonuna verilen bu pulmoner yan\u0131t, inflamatuar bir s\u00fcre\u00e7 ile karakterizedir ve klinik olarak d\u00fc\u015f\u00fck PaO2 \/ FiO2, azalm\u0131\u015f respiratuar kompliyans ve mekanik ventilasyon ihtiyac\u0131 ile kendini g\u00f6sterir. ALI’nin bu klinik belirtileri, bu t\u00fcr akut toksik maruziyetler i\u00e7in ilk duman maruziyetinden sonra tipik olarak 72 saate kadar ortaya \u00e7\u0131kt\u0131\u011f\u0131ndan; son zamanlarda bir koyun modelinde, PET ile \u00f6l\u00e7\u00fclen [\u00b9\u2078F] -florodeoksiglukoz al\u0131m\u0131, daha \u00f6nce duman inhalasyonunun neden oldu\u011fu ALI’yi saptamak i\u00e7in kullan\u0131lm\u0131\u015ft\u0131r. B\u00f6yle bir te\u015fhisin m\u00fcmk\u00fcn olup olmad\u0131\u011f\u0131, akci\u011fer parankimindeki inflamatuar de\u011fi\u015fiklikler ba\u015flad\u0131\u011f\u0131nda bu t\u00fcr de\u011fi\u015fikliklerin invaziv olmayan bir \u015fekilde \u00f6l\u00e7\u00fcl\u00fcp \u00f6l\u00e7\u00fclemeyece\u011fine ba\u011fl\u0131d\u0131r.<\/p>\n
Akut toksik inhalasyonlar\u0131n ciddiyetini derecelendirmek i\u00e7in mevcut mekanizmalar yetersizdir. Woodson bu hasta grubu i\u00e7in, standartla\u015ft\u0131r\u0131lm\u0131\u015f ve do\u011frulanm\u0131\u015f bir \u015fiddet puanlama \u00f6l\u00e7e\u011fi olu\u015fturmak amac\u0131yla b\u00fcy\u00fck \u00e7ok merkezli bir randomize \u00e7al\u0131\u015fman\u0131n y\u00fcr\u00fct\u00fclmesini \u00f6nermi\u015ftir. \u00c7ok merkezli \u00e7al\u0131\u015fmalar halen s\u00fcrmektedir, \u00e7al\u0131\u015fmaya kay\u0131tlar tamamlanm\u0131\u015f ancak veriler hen\u00fcz yay\u0131nlanmam\u0131\u015ft\u0131r.<\/p>\n
AKUT TOKS\u0130K \u0130NHALASYON \u0130LE \u0130LG\u0130L\u0130 SPES\u0130F\u0130K GAZLAR<\/strong><\/h2>\nYan\u0131c\u0131 maddelerden duman inhalasyonunun en yayg\u0131n akut toksik inhalasyon \u015fekli olmas\u0131na ve \u00e7e\u015fitli solunum irritanlar\u0131n\u0131n inhalasyonunu i\u00e7ermesine ra\u011fmen; pratikte end\u00fcstriyel s\u0131z\u0131nt\u0131 ve sa\u00e7\u0131lmalardan, tar\u0131msal kullan\u0131mlardan veya ev kaynaklar\u0131ndan olu\u015fan \u00e7e\u015fitli spesifik toksik gaz inhalasyonlar\u0131 ile kar\u015f\u0131la\u015f\u0131l\u0131r. Akut toksik inhalasyonlara neden olan en yayg\u0131n gazlar\u0131n baz\u0131lar\u0131 ve bunlar\u0131n temel \u00f6zellikleri Tablo 2’de \u00f6zetlenmi\u015ftir.<\/p>\n
![\"\"](\"https:\/\/tatd.org.tr\/tatdtoks\/wp-content\/uploads\/sites\/36\/2021\/10\/tablo-21-1.png\")
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TEDAV\u0130 STRATEJ\u0130LER\u0130<\/strong><\/h2>\nYeterli hava yolu a\u00e7\u0131kl\u0131\u011f\u0131, yeterli torasik hareket, tidal hacimler ve uygun kardiyak tepkiyi sa\u011flamak i\u00e7in yang\u0131n yerinde veya di\u011fer gazl\u0131 inhalasyon kaynaklar\u0131nda primer bak\u0131 yap\u0131l\u0131r. Res\u00fcsitasyon s\u0131v\u0131lar\u0131, intraven\u00f6z yol sa\u011fland\u0131ktan sonra uygulan\u0131r. \u00d6nemli bir akut inhalasyon hasar\u0131ndan sonra 48 saatten fazla bir s\u00fcre, hava yolu \u00f6demi geli\u015fmeyebilece\u011finden erken ent\u00fcbasyonun -tercihen flexible bronkoskop kullan\u0131larak- d\u00fc\u015f\u00fcn\u00fclmesi \u00f6nemlidir. Bron\u015fiyal hijyen, izotonik salin inhalasyonu gibi yard\u0131mc\u0131 tedaviler kullan\u0131larak sa\u011flan\u0131r; ard\u0131\u015f\u0131k terap\u00f6tik bronkoskopiler soyulmu\u015f mukozal doku, kastlar veya di\u011fer yabanc\u0131 cisimleri \u00e7\u0131karmak i\u00e7in kullan\u0131l\u0131r. Belirli vakalarda terap\u00f6tik \u00f6ks\u00fcr\u00fck, g\u00f6\u011f\u00fcs fizyoterapisi, y\u00fcksek frekansl\u0131 perk\u00fcsif ventilasyon, mukus temizleme cihazlar\u0131n\u0131n kullan\u0131m\u0131, derin nefes egzersizleri ve erken ambulasyon da uygulanmaktad\u0131r. Daha ciddi vakalarda, mekanik olarak ventile edilirken ekstrakorporeal membran oksijenasyonu ve prone pozisyonu kullan\u0131ld\u0131\u011f\u0131 bildirilmi\u015ftir. Beta-2 agonistleri, muskarinik resept\u00f6r antagonistleri, rasemik epinefrin gibi farmakolojik ajanlar, N-asetil sistein gibi mukolitik ajanlar ve aerosolize heparin, hava yolu a\u00e7\u0131kl\u0131\u011f\u0131n\u0131 korumak ve akci\u011ferlerin oksijenlenmesini iyile\u015ftirmek i\u00e7in kullan\u0131l\u0131r. Oral veya inhale kortikosteroidler, akut toksik inhalasyonlar\u0131 olan hastalar i\u00e7in nadiren re\u00e7ete edilmese de bu pop\u00fclasyonda d\u00fczenli kullan\u0131m\u0131 destekleyecek herhangi bir veri bulunmamaktad\u0131r.<\/p>\n
TARTI\u015eMA<\/strong><\/h2>\nAkut toksik inhalasyonlar\u0131n de\u011ferlendirilmesi ve tedavisi, \u00f6zellikle solunan bile\u015fik bilinmedi\u011finde veya patlamalar, s\u0131z\u0131nt\u0131lar veya yang\u0131n\u0131n bir sonucu olarak ayn\u0131 anda solunan birden fazla madde oldu\u011funda zordur. Solunan belirli bir toksik gaz\u0131n fiziksel \u00f6zelliklerinin yan\u0131 s\u0131ra daha yayg\u0131n olarak toksisitesi g\u00f6r\u00fclen gazlar\u0131n baz\u0131 temel \u00f6zelliklerini tan\u0131mak klinik uygulamada tedavi hedeflerini belirlemede yard\u0131mc\u0131 olabilir. Akut toksik inhalasyonlar\u0131n \u015fiddeti i\u00e7in derecelendirme \u00f6l\u00e7eklerinin geli\u015ftirilmesi devam etmektedir ve muhtemelen bu durum \u00e7e\u015fitli tedavi stratejilerinin standartla\u015ft\u0131r\u0131lmas\u0131na yard\u0131mc\u0131 olacakt\u0131r. Hava yolunun sa\u011flanmas\u0131 ve desteklenmesi, tedavinin kritik bir bile\u015fenidir; hava yolunu sa\u011flamak i\u00e7in ent\u00fcbasyon e\u015fi\u011finin d\u00fc\u015f\u00fck tutulmas\u0131 \u00f6nemlidir. Destekleyici bak\u0131m i\u00e7in d\u00fc\u015f\u00fcn\u00fclebilecek \u00e7e\u015fitli yard\u0131mc\u0131 y\u00f6ntemler vard\u0131r. Son zamanlarda, imm\u00fcnomod\u00fclasyon ve antiinflamatuar farmakoterap\u00f6tikleri kullanan stratejiler, hayvan modellerinde umut vadetmi\u015ftir ve \u00f6n\u00fcm\u00fczdeki y\u0131llarda klinik uygulamada faydal\u0131 olabilir.<\/p>\n
REFERANSLAR VE TAVS\u0130YE ED\u0130LEN OKUMALAR<\/strong><\/h2>\n1. The MSDS HyperGlossary: acute toxicity. Safety Emporium. 2016; Retrieved 12 December 2018.<\/p>\n
2. Acute toxicity. International Union of Pure and Applied Chemistry (IUPAC). http:\/\/goldbook.iupac.org\/html\/A\/AT06800.html. 2018. [Accessed 10 December 2018].<\/p>\n
3. National Occupational Exposure Survey. National Institute for Occupational Safety and Health. Centers for Disease Control and Prevention. https:\/\/ web.archive.org\/web\/20110716084755\/http:\/\/www.cdc.gov\/noes\/. 1990. [Accessed on 15 December 2018].<\/p>\n
4. & United Nations. United Nations globally harmonized system of classification and labelling of chemicals (GHS). 7th rev. ed. New York and Geneva: United Nations; 2017 ; http:\/\/www.unece.org\/trans\/danger\/publi\/ghs\/ghs_rev00\/ 00files_e.html. [Accessed 9 December 2018] This compendium is revised periodically and contains a large international on-line listing of various chemicals and their classifications that may be useful in the process of ascertaining the nature of acute toxic exposures.<\/p>\n
5. Jing J, Schwartz DA. Acute and chronic responses to toxic inhalations. In: Grippi MA, Elias JA, Fishman JA, et al., editors. Fishman\u2019s pulmonary diseases and disorders, 5th ed. New York, NY: McGraw-Hill; 2015.<\/p>\n
6. Metin G, Metin A. Acute inhalation injury. Eurasian J Med 2010; 42:28\u201335.<\/p>\n
7. Dries DJ, Endorf FW. Inhalation injury: epidemiology, pathology, treatment strategies. Scand J Trauma Resusc Emerg Med 2013; 21:31.<\/p>\n
8. Edelman DA, White MT, Tyburski JG, Wilson RF. Factors affecting prognosis of inhalation injury. J Burn Care Res 2006; 27:848\u2013853.<\/p>\n
9. & Walker PF, Buehner MF, Wood LA, et al. Diagnosis and management of inhalation injury: an updated review. Crit Care 2015; 19:351. Although published in 2015, this is a very good comprehensive recent review article with outstanding explanations of the new research ongoing to understand acute toxic inhalation injury of smoke at the cellular level.<\/p>\n
10. MoritzAR, Henriques FC,McLeanR. The effects of inhaled heat onthe air passages and lungs: an experimental investigation. Am J Path 1945; 21:311\u2013331.<\/p>\n
11. Gann RG, Averill JD, Butler KM, et al. International study of the subepithelial effects of fire smoke on survivability and health (SEFS): phase I final report. NIST Technical Note 2001; 1439. http:\/\/fire.nist.gov\/bfrlpubs\/fire01\/PDF\/ f01080.pdf. [Accessed 10 December 2018]<\/p>\n
12. Albright JM, Davis CS, Bird MD, et al. The acute pulmonary inflammatory response to the graded severity of smoke inhalation. Crit Care Med 2012; 40:1113\u20131121.<\/p>\n
13. Fontan JJ, Cortright DN, Krause JE, et al. Substance P and neurokinin-1 receptor expression by intrinsic airway neurons in the rat. Am J Physiol Lung Cell Mol Physiol 2000; 278:L344\u2013L355.<\/p>\n
14. Lange M, Enkhbaatar P, Traber DL, et al. Role of calcitonin gene-related peptide (CGRP) in ovine burn and smoke inhalation injury. J Appl Physiol 2009; 107:176\u2013184.<\/p>\n
15. Kraneveld AD, Nijkamp FL. Tachykinins and neuro-immune interactions in asthma. Int Immunopharmacol 2001; 1:1629\u20131650.<\/p>\n
16. & Gupta K, Mehrotra M, Kumar P. Smoke inhalation injury: etiopathogenesis, diagnosis, and management. Indian J Crit Care Med 2018; 22:180\u2013188. A recent review article that pulls together some of the major issues involved in acute toxic exposure and outlines treatment strategies.<\/p>\n
17. Murakami K, Traber DL. Pathophysiologic basis of smoke inhalation injury. News Physiol Sci 2003; 18:125\u2013129.<\/p>\n
18. Morita N, Enkhbaatar P, Maybauer MO, et al. Impact of bronchial circulation on bronchial exudates following combined burn and smoke inhalation injury in sheep. Burns 2011; 37:465\u2013473.<\/p>\n
19. & Enkhbaatar P, Pruitt BA, Suman O, et al. Challenges in research on the pathophysiology of smoke inhalation injury and its clinical management. Lancet 2016; 388:1437\u20131446.<\/p>\n
20. Lange M, Szabo C, Enkhbaatar P, et al. Beneficial pulmonary effects of a metalloporphyrinic peroxynitrite decomposition catalysts in burn and smoke inhalation injury. Am J Physiol Lung Cell Mol Physiol 2011; 300:L167\u2013L175.<\/p>\n
21. Hamahata A, Enkhbaatar P, Lange M, et al. Administration of a peroxynitrite decomposition catalyst into the bronchial artery attenuates pulmonary dysfunction after smoke inhalation and burn injury in sheep. Shock 2012; 38:543\u2013548.<\/p>\n
22. Hassan Z, Wong JK, Bush J, et al. Assessing the severity of inhalation injuries in adults. Burns 2010; 36:212\u2013216.<\/p>\n
23. Ryan CM, Fagan SP, Goverman J, Sheridan RL. Grading inhalation injury by admission bronchoscopy. Crit Care Med 2012; 40:1345\u20131346.<\/p>\n
24. Cancio LC, Galvez E Jr, Turner CE, et al. Base deficit and alveolararterial gradient during resuscitation contribute independently but modestly to the prediction of mortality after burn injury. J Burn Care Res 2006; 27:289\u2013296.<\/p>\n
25. Park MS, Cancio LC, Batchinsky AI, et al. Assessment of severity of ovine smoke inhalation injury by analysis of computed tomographic scans. J Trauma 2003; 55:417\u2013427.<\/p>\n
26. Mosier MJ, Pham TN, Park DR, et al. Predictive value of bronchoscopy in assessing the severity of inhalation injury. J Burn Care Res 2012; 33:65\u201373.<\/p>\n
27. Musch G, Winkler T, Harris RS, et al. Lung [18F]fluorodeoxyglucose uptake and ventilation\u2013perfusion mismatch in the early stage of experimental acute smoke inhalation. Critical Care Med 2014; 120:683\u2013693.<\/p>\n
28. Woodson LC. Diagnosis and grading of inhalation injury. J Burn Care Res 2009; 30:143\u2013145.<\/p>\n
29. Foster KN. \u2018Burn multicenter proposal: development of an inhalation injury scoring system to predict severity of inhalation injury.\u2019 (Clinical Trials.gov identifier NCT 01194024). Completion date December 2018.<\/p>\n
30. Venus B, Matsuda T, Cplozo JB, Mathru M. Prophylactic intubation and continuous positive airway pressure in the management of inhalation injury in burn victims. Crit Care Med 1981; 9:519\u2013523.<\/p>\n
31. Micak RP, Suman OE, Herndon DN. Respiratory management of inhalation injury. Burns 2007; 33:2\u201313.<\/p>\n
32. Hale DF, Cannon JW, Batchinsky AI, et al. Prone positioning improves oxygenation in adult burn patients with severe acute respiratory distress syndrome. J Trauma Acute Care Surg 2012; 72:1634\u20131639.<\/p>\n
33. Lange M, Hamahata A, Traber DL, et al. Preclinical evaluation of epinephrine nebulization to reduce airway hyperemia and improve oxygenation after smoke inhalation injury. Crit Care Med 2011; 39:718\u2013724.<\/p>\n
34. Palmieri TL, Enkhbaatar P, Bayliss R, et al. Continuous nebulized albuterol attenuates acute lung injury in an ovine model of combined burn and smoke inhalation. Crit Care Med 2006; 34:1719\u20131724.<\/p>\n","protected":false},"excerpt":{"rendered":"
Akut toksisite; bir maddeyle ya tek bir kar\u015f\u0131la\u015fmadan ya da k\u0131sa bir s\u00fcre i\u00e7inde bir maddeye birden fazla maruz kalmaktan\u00a0(genellikle 24 saatten…<\/p>\n","protected":false},"author":1,"featured_media":2022,"comment_status":"open","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"_acf_changed":false,"inline_featured_image":false,"_lmt_disableupdate":"","_lmt_disable":"","footnotes":""},"categories":[10014,10019],"tags":[37,42,401],"class_list":["post-1090","post","type-post","status-publish","format-standard","has-post-thumbnail","hentry","category-akademik-blog-yazisi","category-tft","tag-akut-inhalasyon-hasari","tag-akut-toksik-inhalasyon","tag-toksik-inhalasyon"],"acf":[],"_links":{"self":[{"href":"https:\/\/tatd.org.tr\/toksikoloji\/wp-json\/wp\/v2\/posts\/1090","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/tatd.org.tr\/toksikoloji\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/tatd.org.tr\/toksikoloji\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/tatd.org.tr\/toksikoloji\/wp-json\/wp\/v2\/users\/1"}],"replies":[{"embeddable":true,"href":"https:\/\/tatd.org.tr\/toksikoloji\/wp-json\/wp\/v2\/comments?post=1090"}],"version-history":[{"count":0,"href":"https:\/\/tatd.org.tr\/toksikoloji\/wp-json\/wp\/v2\/posts\/1090\/revisions"}],"wp:featuredmedia":[{"embeddable":true,"href":"https:\/\/tatd.org.tr\/toksikoloji\/wp-json\/wp\/v2\/media\/2022"}],"wp:attachment":[{"href":"https:\/\/tatd.org.tr\/toksikoloji\/wp-json\/wp\/v2\/media?parent=1090"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/tatd.org.tr\/toksikoloji\/wp-json\/wp\/v2\/categories?post=1090"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/tatd.org.tr\/toksikoloji\/wp-json\/wp\/v2\/tags?post=1090"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}
Akut toksik inhalasyonlarda g\u00f6z \u00f6n\u00fcnde bulundurulacak di\u011fer fakt\u00f6rler aras\u0131nda solunan maddenin ortam havas\u0131ndaki konsantrasyonu, toplam maruz kalma s\u00fcresi, maddenin yo\u011funlu\u011fu (yani daha a\u011f\u0131r gazlar yere do\u011fru \u00e7\u00f6kme e\u011filiminde olacakt\u0131r)<\/em>, gaz\u0131n rengi (\u00f6rne\u011fin, elementel klor, ortam havas\u0131na maruz kald\u0131\u011f\u0131nda sar\u0131-ye\u015fil g\u00f6r\u00fcnme e\u011filiminde olacakt\u0131r)<\/em>, gaz\u0131n kokusu (\u00f6rne\u011fin k\u00fck\u00fcrt bazl\u0131 bile\u015fiklerin \u00e7\u00fcr\u00fck yumurta kokusu veya klor gaz\u0131n\u0131n rahats\u0131z edici keskin kokusu),<\/em> havaland\u0131rman\u0131n varl\u0131\u011f\u0131 veya yoklu\u011fu, ma\u011fdurun bilincini kaybedip kaybetmedi\u011fi, hastan\u0131n solunum cihaz\u0131 gibi herhangi bir ki\u015fisel solunum arac\u0131 kullan\u0131p kullanmad\u0131\u011f\u0131 ve ya\u015f, sigara i\u00e7me durumu, komorbid hastal\u0131klar (\u00f6rne\u011fin e\u015fzamanl\u0131 kalp hastal\u0131\u011f\u0131 veya \u00f6nceden var olan akci\u011fer rahats\u0131zl\u0131klar\u0131)<\/em> ve genetik duyarl\u0131l\u0131k gibi \u00e7e\u015fitli konak fakt\u00f6rleri yer almaktad\u0131r. Akut toksik inhalasyonu olan bir hastay\u0131 de\u011ferlendirirken dikkate al\u0131nacak de\u011fi\u015fkenler; gazlar\u0131n ve bireye ait de\u011fi\u015fkenlerin fiziksel \u00f6zelliklerinin \u00f6zeti Tablo 1\u2019de \u00f6zetlenmi\u015ftir<\/p>\n Akut toksik inhalasyon hasar\u0131 s\u0131ras\u0131nda ve sonras\u0131nda tan\u0131mlanan \u00e7e\u015fitli \u00f6nemli patofizyolojik de\u011fi\u015fiklikler belirlenmi\u015ftir. Is\u0131 ve buhar, trakeobron\u015fiyal a\u011faca do\u011frudan zarar verebilmesine ra\u011fmen; bilinen di\u011fer respiratuar irritanlar yanma reaksiyonu sonucu ortaya \u00e7\u0131kan \u00fcr\u00fcnlerdir. Bunlar akrolein ve formaldehit gibi doymam\u0131\u015f aldehitleri, halojen asitleri gibi bile\u015fikleri i\u00e7erir. Bu maddelerin varl\u0131\u011f\u0131 kona\u011f\u0131n enflamatuar yan\u0131t\u0131n\u0131 tetikler, genellikle trakeobron\u015fiyal mukozan\u0131n soyulmas\u0131na neden olur ve s\u0131kl\u0131kla h\u00fccresel d\u00fczeyde hava yoluna do\u011frudan toksik etkiler bu duruma e\u015flik eder. Havayolu hasar\u0131, duyusal ve vazomotor sinir u\u00e7lar\u0131ndan substance P ve kalsitonin ili\u015fkili peptit gibi n\u00f6ropeptitlerin \u00fcretilmesine yol a\u00e7ar. Ayr\u0131ca bu n\u00f6ropeptitler; bronkokonstr\u00fcksiyonun ind\u00fcklenmesi ve nitrik oksit sentetaz\u0131 stim\u00fcle ederek h\u00fccrelerde toksik etkilere neden olan reaktif oksijen radikallerinin \u00fcretilmesiyle ili\u015fkilendirilmi\u015ftir. N\u00f6ropeptitlerin, ta\u015fikininler gibi i\u015flev g\u00f6rd\u00fckleri tan\u0131mlanm\u0131\u015ft\u0131r; vask\u00fcler permabilitede art\u0131\u015f olu\u015fturmas\u0131, lenfatik ak\u0131\u015f ve vask\u00fcler ge\u00e7irgenlik nedeniyle s\u00fcre\u00e7 pulmoner \u00f6demle sonu\u00e7lan\u0131r. S\u00fcrfaktan d\u00fczeylerinin, interl\u00f6kinler ve TNF-\u03b1 gibi imm\u00fcnmod\u00fclat\u00f6rlerin azalmas\u0131 hasar\u0131n \u00f6nemini belirtir. Bu kaskad ortaya \u00e7\u0131kt\u0131\u011f\u0131nda, h\u00fccresel pulmoner vazokonstr\u00fcksiyon kayb\u0131 ile ekstra lokal h\u00fccresel hasar meydana gelir. Bu da inhalasyon hasar\u0131ndan sadece 20 dk i\u00e7inde bron\u015fiyal kan ak\u0131\u015f\u0131n\u0131n dramatik bir \u015fekilde artmas\u0131na neden olur. Reaktif oksijen radikalleri, mitokondriyal disfonksiyona ve h\u00fccresel apoptoza neden olur; hayvan modellerinde hasar g\u00f6rm\u00fc\u015f solunum epiteli ve alveoler makrofajlar\u0131n ekstrensek koag\u00fclasyon kaskad\u0131n\u0131 tetikledi\u011fi, bunun daha sonra ind\u00fckleyici plazminojen aktivat\u00f6r-I seviyesinde homeostatik koag\u00fclasyon balans\u0131n\u0131 bozdu\u011fu ve dolay\u0131s\u0131yla hiperkoag\u00fclabilite durumu olu\u015fturdu\u011fu g\u00f6sterilmi\u015ftir. Ekstra bron\u015fiyal kan ak\u0131\u015f\u0131, intersitisyumda polimorfon\u00fckleer lenfositleri ve sitokinleri biriktirerek inflamatuar yan\u0131t\u0131 g\u00fc\u00e7lendiriyor gibi g\u00f6r\u00fcnmektedir. Plazma proteinlerinin, kast ve eks\u00fcda olu\u015fumu ile hava yollar\u0131na kaymas\u0131, alveolar kollapsa veya distal hava yollar\u0131n\u0131n tamamen t\u0131kanmas\u0131na neden olur. Bron\u015fiyal kan ak\u0131\u015f\u0131n\u0131 kas\u0131tl\u0131 olarak azaltmak i\u00e7in hayvan deneyleri yap\u0131ld\u0131\u011f\u0131nda, hava yolu t\u0131kan\u0131kl\u0131\u011f\u0131n\u0131n azald\u0131\u011f\u0131, intraparankimal s\u0131v\u0131n\u0131n s\u0131n\u0131rland\u0131\u011f\u0131 ve sonu\u00e7 olarak oksijenasyonun iyile\u015fti\u011fi g\u00f6r\u00fclm\u00fc\u015ft\u00fcr. Yap\u0131lan ilave \u00e7al\u0131\u015fmalarda bir koyun modelinde; kalsitonin ile ili\u015fkili peptit ve P maddesine kar\u015f\u0131 antagonistlerin, s\u0131v\u0131 shiftini ve inflamasyonu yava\u015flatt\u0131\u011f\u0131n\u0131 g\u00f6sterilmi\u015ftir. Akut toksik inhalasyonlar s\u0131ras\u0131nda reaktif oksijen t\u00fcrleri ve peroksinitrit (ONOO\u00a0 \u0304) \u00fcretimi ile hava yoluna n\u00f6trofilik hareket olmas\u0131 anti-inflamatuar tedavilerin hedefi olarak belirlenmi\u015ftir. Peroksinitrit ayr\u0131\u015fma kataliz\u00f6rlerinin, duman inhalasyon hasar\u0131n\u0131 inceleyen hayvan modellerinde sitoprotektif oldu\u011fu g\u00f6sterilmi\u015ftir.<\/p>\n \u0130nhalasyon hasar\u0131n\u0131n varl\u0131\u011f\u0131n\u0131 do\u011frulamak ve ciddiyetini belirlemek i\u00e7in \u00e7ok say\u0131da test kullan\u0131lm\u0131\u015ft\u0131r. Duman inhalasyonunun ilk klinik belirtileri genellikle b\u00fcy\u00fck hava yolu epitel hasar\u0131ndan kaynaklan\u0131r. Mukozal hiperemi, \u00f6dem ve \u00fclserasyon, kast olu\u015fumu ve bron\u015fiyal obstr\u00fcksiyon meydana gelir. Flexible bronkoskopi inhalasyon hasar\u0131n\u0131n ciddiyetini de\u011ferlendirmek i\u00e7in standart teknik olarak kabul edilmesine ra\u011fmen, toraks\u0131n bilgisayarl\u0131 tomografik (BT) g\u00f6r\u00fcnt\u00fclemesi, karboksihemoglobin \u00f6l\u00e7\u00fcmleri ve solunum fonksiyon testleri gibi di\u011fer y\u00f6ntemlerin t\u00fcm\u00fc, toksik inhalasyonun ciddiyetine ve do\u011fas\u0131na ba\u011fl\u0131 olarak yard\u0131mc\u0131 ara\u00e7lar olarak kullan\u0131lmaya devam edilecektir. Bronkoskopi, bronkoskopik g\u00f6rselle\u015ftirilmi\u015f bulgular ile ger\u00e7ek \u00f6l\u00fcm oranlar\u0131 aras\u0131ndaki tutars\u0131zl\u0131\u011f\u0131 muhtemelen a\u00e7\u0131klayaca\u011f\u0131 d\u00fc\u015f\u00fcn\u00fclen distal hava yollar\u0131ndaki de\u011fi\u015fiklikleri tespit edemez veya hasar \u015fiddetini belirleyemez. Res\u00fcsitasyondan sonra PaO2 \/ FiO2 hesaplamas\u0131ndan ve toraks BT g\u00f6r\u00fcnt\u00fclemesinden yararlan\u0131larak gerekli olacak res\u00fcsitasyon d\u00fczeyini \u00f6l\u00e7mek i\u00e7in mortaliteyi tahmin etme \u00e7abalar\u0131 mevcuttur. Yakla\u015f\u0131k olarak inhalasyon hasar\u0131 olan hastalar\u0131n \u00fc\u00e7te biri, dumana maruz kald\u0131ktan sonraki ilk 3 g\u00fcn i\u00e7inde akut akci\u011fer hasar\u0131 (ALI) geli\u015ftirir. Duman inhalasyonuna verilen bu pulmoner yan\u0131t, inflamatuar bir s\u00fcre\u00e7 ile karakterizedir ve klinik olarak d\u00fc\u015f\u00fck PaO2 \/ FiO2, azalm\u0131\u015f respiratuar kompliyans ve mekanik ventilasyon ihtiyac\u0131 ile kendini g\u00f6sterir. ALI’nin bu klinik belirtileri, bu t\u00fcr akut toksik maruziyetler i\u00e7in ilk duman maruziyetinden sonra tipik olarak 72 saate kadar ortaya \u00e7\u0131kt\u0131\u011f\u0131ndan; son zamanlarda bir koyun modelinde, PET ile \u00f6l\u00e7\u00fclen [\u00b9\u2078F] -florodeoksiglukoz al\u0131m\u0131, daha \u00f6nce duman inhalasyonunun neden oldu\u011fu ALI’yi saptamak i\u00e7in kullan\u0131lm\u0131\u015ft\u0131r. B\u00f6yle bir te\u015fhisin m\u00fcmk\u00fcn olup olmad\u0131\u011f\u0131, akci\u011fer parankimindeki inflamatuar de\u011fi\u015fiklikler ba\u015flad\u0131\u011f\u0131nda bu t\u00fcr de\u011fi\u015fikliklerin invaziv olmayan bir \u015fekilde \u00f6l\u00e7\u00fcl\u00fcp \u00f6l\u00e7\u00fclemeyece\u011fine ba\u011fl\u0131d\u0131r.<\/p>\n Akut toksik inhalasyonlar\u0131n ciddiyetini derecelendirmek i\u00e7in mevcut mekanizmalar yetersizdir. Woodson bu hasta grubu i\u00e7in, standartla\u015ft\u0131r\u0131lm\u0131\u015f ve do\u011frulanm\u0131\u015f bir \u015fiddet puanlama \u00f6l\u00e7e\u011fi olu\u015fturmak amac\u0131yla b\u00fcy\u00fck \u00e7ok merkezli bir randomize \u00e7al\u0131\u015fman\u0131n y\u00fcr\u00fct\u00fclmesini \u00f6nermi\u015ftir. \u00c7ok merkezli \u00e7al\u0131\u015fmalar halen s\u00fcrmektedir, \u00e7al\u0131\u015fmaya kay\u0131tlar tamamlanm\u0131\u015f ancak veriler hen\u00fcz yay\u0131nlanmam\u0131\u015ft\u0131r.<\/p>\n Yan\u0131c\u0131 maddelerden duman inhalasyonunun en yayg\u0131n akut toksik inhalasyon \u015fekli olmas\u0131na ve \u00e7e\u015fitli solunum irritanlar\u0131n\u0131n inhalasyonunu i\u00e7ermesine ra\u011fmen; pratikte end\u00fcstriyel s\u0131z\u0131nt\u0131 ve sa\u00e7\u0131lmalardan, tar\u0131msal kullan\u0131mlardan veya ev kaynaklar\u0131ndan olu\u015fan \u00e7e\u015fitli spesifik toksik gaz inhalasyonlar\u0131 ile kar\u015f\u0131la\u015f\u0131l\u0131r. Akut toksik inhalasyonlara neden olan en yayg\u0131n gazlar\u0131n baz\u0131lar\u0131 ve bunlar\u0131n temel \u00f6zellikleri Tablo 2’de \u00f6zetlenmi\u015ftir.<\/p>\n Yeterli hava yolu a\u00e7\u0131kl\u0131\u011f\u0131, yeterli torasik hareket, tidal hacimler ve uygun kardiyak tepkiyi sa\u011flamak i\u00e7in yang\u0131n yerinde veya di\u011fer gazl\u0131 inhalasyon kaynaklar\u0131nda primer bak\u0131 yap\u0131l\u0131r. Res\u00fcsitasyon s\u0131v\u0131lar\u0131, intraven\u00f6z yol sa\u011fland\u0131ktan sonra uygulan\u0131r. \u00d6nemli bir akut inhalasyon hasar\u0131ndan sonra 48 saatten fazla bir s\u00fcre, hava yolu \u00f6demi geli\u015fmeyebilece\u011finden erken ent\u00fcbasyonun -tercihen flexible bronkoskop kullan\u0131larak- d\u00fc\u015f\u00fcn\u00fclmesi \u00f6nemlidir. Bron\u015fiyal hijyen, izotonik salin inhalasyonu gibi yard\u0131mc\u0131 tedaviler kullan\u0131larak sa\u011flan\u0131r; ard\u0131\u015f\u0131k terap\u00f6tik bronkoskopiler soyulmu\u015f mukozal doku, kastlar veya di\u011fer yabanc\u0131 cisimleri \u00e7\u0131karmak i\u00e7in kullan\u0131l\u0131r. Belirli vakalarda terap\u00f6tik \u00f6ks\u00fcr\u00fck, g\u00f6\u011f\u00fcs fizyoterapisi, y\u00fcksek frekansl\u0131 perk\u00fcsif ventilasyon, mukus temizleme cihazlar\u0131n\u0131n kullan\u0131m\u0131, derin nefes egzersizleri ve erken ambulasyon da uygulanmaktad\u0131r. Daha ciddi vakalarda, mekanik olarak ventile edilirken ekstrakorporeal membran oksijenasyonu ve prone pozisyonu kullan\u0131ld\u0131\u011f\u0131 bildirilmi\u015ftir. Beta-2 agonistleri, muskarinik resept\u00f6r antagonistleri, rasemik epinefrin gibi farmakolojik ajanlar, N-asetil sistein gibi mukolitik ajanlar ve aerosolize heparin, hava yolu a\u00e7\u0131kl\u0131\u011f\u0131n\u0131 korumak ve akci\u011ferlerin oksijenlenmesini iyile\u015ftirmek i\u00e7in kullan\u0131l\u0131r. Oral veya inhale kortikosteroidler, akut toksik inhalasyonlar\u0131 olan hastalar i\u00e7in nadiren re\u00e7ete edilmese de bu pop\u00fclasyonda d\u00fczenli kullan\u0131m\u0131 destekleyecek herhangi bir veri bulunmamaktad\u0131r.<\/p>\n Akut toksik inhalasyonlar\u0131n de\u011ferlendirilmesi ve tedavisi, \u00f6zellikle solunan bile\u015fik bilinmedi\u011finde veya patlamalar, s\u0131z\u0131nt\u0131lar veya yang\u0131n\u0131n bir sonucu olarak ayn\u0131 anda solunan birden fazla madde oldu\u011funda zordur. Solunan belirli bir toksik gaz\u0131n fiziksel \u00f6zelliklerinin yan\u0131 s\u0131ra daha yayg\u0131n olarak toksisitesi g\u00f6r\u00fclen gazlar\u0131n baz\u0131 temel \u00f6zelliklerini tan\u0131mak klinik uygulamada tedavi hedeflerini belirlemede yard\u0131mc\u0131 olabilir. Akut toksik inhalasyonlar\u0131n \u015fiddeti i\u00e7in derecelendirme \u00f6l\u00e7eklerinin geli\u015ftirilmesi devam etmektedir ve muhtemelen bu durum \u00e7e\u015fitli tedavi stratejilerinin standartla\u015ft\u0131r\u0131lmas\u0131na yard\u0131mc\u0131 olacakt\u0131r. Hava yolunun sa\u011flanmas\u0131 ve desteklenmesi, tedavinin kritik bir bile\u015fenidir; hava yolunu sa\u011flamak i\u00e7in ent\u00fcbasyon e\u015fi\u011finin d\u00fc\u015f\u00fck tutulmas\u0131 \u00f6nemlidir. Destekleyici bak\u0131m i\u00e7in d\u00fc\u015f\u00fcn\u00fclebilecek \u00e7e\u015fitli yard\u0131mc\u0131 y\u00f6ntemler vard\u0131r. Son zamanlarda, imm\u00fcnomod\u00fclasyon ve antiinflamatuar farmakoterap\u00f6tikleri kullanan stratejiler, hayvan modellerinde umut vadetmi\u015ftir ve \u00f6n\u00fcm\u00fczdeki y\u0131llarda klinik uygulamada faydal\u0131 olabilir.<\/p>\n 1. The MSDS HyperGlossary: acute toxicity. Safety Emporium. 2016; Retrieved 12 December 2018.<\/p>\n 2. Acute toxicity. International Union of Pure and Applied Chemistry (IUPAC). http:\/\/goldbook.iupac.org\/html\/A\/AT06800.html. 2018. [Accessed 10 December 2018].<\/p>\n 3. National Occupational Exposure Survey. National Institute for Occupational Safety and Health. Centers for Disease Control and Prevention. https:\/\/ web.archive.org\/web\/20110716084755\/http:\/\/www.cdc.gov\/noes\/. 1990. [Accessed on 15 December 2018].<\/p>\n 4. & United Nations. United Nations globally harmonized system of classification and labelling of chemicals (GHS). 7th rev. ed. New York and Geneva: United Nations; 2017 ; http:\/\/www.unece.org\/trans\/danger\/publi\/ghs\/ghs_rev00\/ 00files_e.html. [Accessed 9 December 2018] This compendium is revised periodically and contains a large international on-line listing of various chemicals and their classifications that may be useful in the process of ascertaining the nature of acute toxic exposures.<\/p>\n 5. Jing J, Schwartz DA. Acute and chronic responses to toxic inhalations. In: Grippi MA, Elias JA, Fishman JA, et al., editors. Fishman\u2019s pulmonary diseases and disorders, 5th ed. New York, NY: McGraw-Hill; 2015.<\/p>\n 6. Metin G, Metin A. Acute inhalation injury. Eurasian J Med 2010; 42:28\u201335.<\/p>\n 7. Dries DJ, Endorf FW. Inhalation injury: epidemiology, pathology, treatment strategies. Scand J Trauma Resusc Emerg Med 2013; 21:31.<\/p>\n 8. Edelman DA, White MT, Tyburski JG, Wilson RF. Factors affecting prognosis of inhalation injury. J Burn Care Res 2006; 27:848\u2013853.<\/p>\n 9. & Walker PF, Buehner MF, Wood LA, et al. Diagnosis and management of inhalation injury: an updated review. Crit Care 2015; 19:351. Although published in 2015, this is a very good comprehensive recent review article with outstanding explanations of the new research ongoing to understand acute toxic inhalation injury of smoke at the cellular level.<\/p>\n 10. MoritzAR, Henriques FC,McLeanR. The effects of inhaled heat onthe air passages and lungs: an experimental investigation. Am J Path 1945; 21:311\u2013331.<\/p>\n 11. Gann RG, Averill JD, Butler KM, et al. International study of the subepithelial effects of fire smoke on survivability and health (SEFS): phase I final report. NIST Technical Note 2001; 1439. http:\/\/fire.nist.gov\/bfrlpubs\/fire01\/PDF\/ f01080.pdf. [Accessed 10 December 2018]<\/p>\n 12. Albright JM, Davis CS, Bird MD, et al. The acute pulmonary inflammatory response to the graded severity of smoke inhalation. Crit Care Med 2012; 40:1113\u20131121.<\/p>\n 13. Fontan JJ, Cortright DN, Krause JE, et al. Substance P and neurokinin-1 receptor expression by intrinsic airway neurons in the rat. Am J Physiol Lung Cell Mol Physiol 2000; 278:L344\u2013L355.<\/p>\n 14. Lange M, Enkhbaatar P, Traber DL, et al. Role of calcitonin gene-related peptide (CGRP) in ovine burn and smoke inhalation injury. J Appl Physiol 2009; 107:176\u2013184.<\/p>\n 15. Kraneveld AD, Nijkamp FL. Tachykinins and neuro-immune interactions in asthma. Int Immunopharmacol 2001; 1:1629\u20131650.<\/p>\n 16. & Gupta K, Mehrotra M, Kumar P. Smoke inhalation injury: etiopathogenesis, diagnosis, and management. Indian J Crit Care Med 2018; 22:180\u2013188. A recent review article that pulls together some of the major issues involved in acute toxic exposure and outlines treatment strategies.<\/p>\n 17. Murakami K, Traber DL. Pathophysiologic basis of smoke inhalation injury. News Physiol Sci 2003; 18:125\u2013129.<\/p>\n 18. Morita N, Enkhbaatar P, Maybauer MO, et al. Impact of bronchial circulation on bronchial exudates following combined burn and smoke inhalation injury in sheep. Burns 2011; 37:465\u2013473.<\/p>\n 19. & Enkhbaatar P, Pruitt BA, Suman O, et al. Challenges in research on the pathophysiology of smoke inhalation injury and its clinical management. Lancet 2016; 388:1437\u20131446.<\/p>\n 20. Lange M, Szabo C, Enkhbaatar P, et al. Beneficial pulmonary effects of a metalloporphyrinic peroxynitrite decomposition catalysts in burn and smoke inhalation injury. Am J Physiol Lung Cell Mol Physiol 2011; 300:L167\u2013L175.<\/p>\n 21. Hamahata A, Enkhbaatar P, Lange M, et al. Administration of a peroxynitrite decomposition catalyst into the bronchial artery attenuates pulmonary dysfunction after smoke inhalation and burn injury in sheep. Shock 2012; 38:543\u2013548.<\/p>\n 22. Hassan Z, Wong JK, Bush J, et al. Assessing the severity of inhalation injuries in adults. Burns 2010; 36:212\u2013216.<\/p>\n 23. Ryan CM, Fagan SP, Goverman J, Sheridan RL. Grading inhalation injury by admission bronchoscopy. Crit Care Med 2012; 40:1345\u20131346.<\/p>\n 24. Cancio LC, Galvez E Jr, Turner CE, et al. Base deficit and alveolararterial gradient during resuscitation contribute independently but modestly to the prediction of mortality after burn injury. J Burn Care Res 2006; 27:289\u2013296.<\/p>\n 25. Park MS, Cancio LC, Batchinsky AI, et al. Assessment of severity of ovine smoke inhalation injury by analysis of computed tomographic scans. J Trauma 2003; 55:417\u2013427.<\/p>\n 26. Mosier MJ, Pham TN, Park DR, et al. Predictive value of bronchoscopy in assessing the severity of inhalation injury. J Burn Care Res 2012; 33:65\u201373.<\/p>\n 27. Musch G, Winkler T, Harris RS, et al. Lung [18F]fluorodeoxyglucose uptake and ventilation\u2013perfusion mismatch in the early stage of experimental acute smoke inhalation. Critical Care Med 2014; 120:683\u2013693.<\/p>\n 28. Woodson LC. Diagnosis and grading of inhalation injury. J Burn Care Res 2009; 30:143\u2013145.<\/p>\n 29. Foster KN. \u2018Burn multicenter proposal: development of an inhalation injury scoring system to predict severity of inhalation injury.\u2019 (Clinical Trials.gov identifier NCT 01194024). Completion date December 2018.<\/p>\n 30. Venus B, Matsuda T, Cplozo JB, Mathru M. Prophylactic intubation and continuous positive airway pressure in the management of inhalation injury in burn victims. Crit Care Med 1981; 9:519\u2013523.<\/p>\n 31. Micak RP, Suman OE, Herndon DN. Respiratory management of inhalation injury. Burns 2007; 33:2\u201313.<\/p>\n 32. Hale DF, Cannon JW, Batchinsky AI, et al. Prone positioning improves oxygenation in adult burn patients with severe acute respiratory distress syndrome. J Trauma Acute Care Surg 2012; 72:1634\u20131639.<\/p>\n 33. Lange M, Hamahata A, Traber DL, et al. Preclinical evaluation of epinephrine nebulization to reduce airway hyperemia and improve oxygenation after smoke inhalation injury. Crit Care Med 2011; 39:718\u2013724.<\/p>\n 34. Palmieri TL, Enkhbaatar P, Bayliss R, et al. Continuous nebulized albuterol attenuates acute lung injury in an ovine model of combined burn and smoke inhalation. Crit Care Med 2006; 34:1719\u20131724.<\/p>\n","protected":false},"excerpt":{"rendered":" Akut toksisite; bir maddeyle ya tek bir kar\u015f\u0131la\u015fmadan ya da k\u0131sa bir s\u00fcre i\u00e7inde bir maddeye birden fazla maruz kalmaktan\u00a0(genellikle 24 saatten…<\/p>\n","protected":false},"author":1,"featured_media":2022,"comment_status":"open","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"_acf_changed":false,"inline_featured_image":false,"_lmt_disableupdate":"","_lmt_disable":"","footnotes":""},"categories":[10014,10019],"tags":[37,42,401],"class_list":["post-1090","post","type-post","status-publish","format-standard","has-post-thumbnail","hentry","category-akademik-blog-yazisi","category-tft","tag-akut-inhalasyon-hasari","tag-akut-toksik-inhalasyon","tag-toksik-inhalasyon"],"acf":[],"_links":{"self":[{"href":"https:\/\/tatd.org.tr\/toksikoloji\/wp-json\/wp\/v2\/posts\/1090","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/tatd.org.tr\/toksikoloji\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/tatd.org.tr\/toksikoloji\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/tatd.org.tr\/toksikoloji\/wp-json\/wp\/v2\/users\/1"}],"replies":[{"embeddable":true,"href":"https:\/\/tatd.org.tr\/toksikoloji\/wp-json\/wp\/v2\/comments?post=1090"}],"version-history":[{"count":0,"href":"https:\/\/tatd.org.tr\/toksikoloji\/wp-json\/wp\/v2\/posts\/1090\/revisions"}],"wp:featuredmedia":[{"embeddable":true,"href":"https:\/\/tatd.org.tr\/toksikoloji\/wp-json\/wp\/v2\/media\/2022"}],"wp:attachment":[{"href":"https:\/\/tatd.org.tr\/toksikoloji\/wp-json\/wp\/v2\/media?parent=1090"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/tatd.org.tr\/toksikoloji\/wp-json\/wp\/v2\/categories?post=1090"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/tatd.org.tr\/toksikoloji\/wp-json\/wp\/v2\/tags?post=1090"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}<\/p>\nAKUT TOKS\u0130K \u0130NHALASYON YARALANMALARININ PATOF\u0130ZYOLOJ\u0130S\u0130<\/strong><\/h2>\n
AKUT TOKS\u0130K AKC\u0130\u011eER HASARININ \u015e\u0130DDET\u0130, TANI VE DERECELEND\u0130RME<\/strong><\/h2>\n
AKUT TOKS\u0130K \u0130NHALASYON \u0130LE \u0130LG\u0130L\u0130 SPES\u0130F\u0130K GAZLAR<\/strong><\/h2>\n
<\/p>\nTEDAV\u0130 STRATEJ\u0130LER\u0130<\/strong><\/h2>\n
TARTI\u015eMA<\/strong><\/h2>\n
REFERANSLAR VE TAVS\u0130YE ED\u0130LEN OKUMALAR<\/strong><\/h2>\n