2
ၡāāࢋ
( Heat-related illness )
40
( acute phase response ) ( Thermoregulation ) ( heat-shock proteins )
2 2
( ) 20
ᙯᔣෟĈሤ̚ഁ ( Heat stroke )
݈֏
ܕೀѐϤٺঈ࣏ள૱۞ត̼Ăވड़ᑕ̈́г
ື̼۞યᗟצזࢦෛć͵ࠧЧг۞ঈ၇౹າ
ĂౄјிкЯࠎሤঽ҃Ѫ˸९ּĂд 2003 ѐ ˣ͡มᑝለ߷۞ሤĂҤд 2 ࣎ߐഇ̰ಶౄ
ј˞ 3 ༱ 5 ˼ˠ ( ࠤҌΞਕ྿ 5 ༱ˠ ) ۞Ѫ
˸1,2,3,4Ąሤঽᑕజෛࠎ˘࣎ۤົ̈́ᗁጯ˯۞ࢦ̂
߄ጼĂЯࠎΞഇ۞ֽሤ۞ᐛத̈́ૻޘు
႙ᆧΐ5ĄሤঽΒ߁ሤ൯ăሤຶ౿ăሤა̈́
ᚑࢦ۞ሤ̚ഁĂܕࡁտĈѝдሤა൴
Ϡ۞ТॡĂሤౄј۞Б֗൴ۆͅᑕಶฟؕᔞ
឵Ăтڍॡ࣏՟ѣϲӈϒቁ۞ڼᒚĂΞਕ
ົႊតјሤ̚ഁĂౄјкࢦጡءა̈́Ѫ˸Ą
҃ሤა۞াې఼૱Ϊߏ˘ֱ՟ѣ˘ّ۞ܑ
னĂт˾ഽăিࢽăऴ˧ă൏ᛒăБ̙֗ዋă ᐝຶăᐝ൭ă⪰͕ຏăယФăཛ൭ăཛᕫČ6 , 7ć
็ݭ ( classic ) ሤ̚ഁр൴ٺҁѐˠ̈́ၙّঽଈ ۰Ă̙֭ညྻજݭ ( exertional ) ሤ̚ഁߏдೀ࣎
̈ॡז˘͇۞ॡม̰ᘕ൴Ă็ݭሤ̚ഁ۞൴Ϡ ߏдೀ͇۞ॡม̰ቤၙᔞ឵8Ăܐഇ۞ܑனಶт Тሤა˘ᇹ֭՟ѣপளّĂֱଈ۰Ξਕன
дЧࡊ۞ܝăާ෧̝̚âό൴Ϡሤ̚ഁѪ˸९
ּĂ่̙ߏᗁᒚયᗟ˵ߏ˘࣎ۤົયᗟ̈́ڱޠય ᗟĂώ͛ԯࢦᕇٸдሤ̚ഁ۞ঽăϠந፟ᖼă тңѝഇ෧ᕝăϲӈڼᒚ̈́֨Ą
߹Җঽጯ
आ͇ߏሤ̚ഁ۞р൴؞༼Ăҭ͇˵Ξਕົ
൴Ϡሤ̚ഁĂপҾߏྻજݭሤ̚ഁ˵ѣ൴Ϡд
ޘҲॡ۞ঽּಡӘĄॲፂ˘ีࡁտඕڍĈሤֽ
ॡ઼࡚ݱξ۞ሤ̚ഁ൴ϠதࠎՏ˩༱ˠ 1 7 . 6 ז 2 6 . 5 ˠĂдՒনгܠٛұࠤҌ྿Տ˩༱ˠ 450ז 1800 ˠѨ9,10Ą
έ៉гֲሤĂ็ݭሤ̚ഁ̙֭к֍Ă ҭާ෧ވઊႬ̪ѣঽּ11ĄЯࠎ̙ညྻજݭሤ̚
ഁѣځព۞൴ঽ࿅ĂּтĈ՟ѣ࿅ΝঽΫ۞ѐ ᅅྻજࣶдᅖሤ͇ঈ˭ᆐধྻજޢČć็ݭሤ
̚ഁ۞ঽଈ ( ּтĈ˘ҜܜഇۻԖ۞ҁѐˠĂਖ਼ Ҍާ෧ވॡĂ҅ 39.5 ƨ̈́ຍᙊԼតČ ) टٽᄃ ຏߖ়ّঽćтڍͻᛋᛇĂ૱ڱϲӈᏰ ᙊϩቲ۞পᇈ ( ᒌăھࡓ )ĂЯ҃ౄјࢫ
۞ؼᏵĄЯѩᓜԖᗁरдವԱΞਕ۞ࣧЯТॡĂ ᑕሤ̚ഁЕˢᝥҾ෧ᕝ ( ֍ܑ˘ )8Ă֝ిઇ
ϒቁ۞நĄ
Ϥٺˠߏሤ̚ഁ۞ПᐍཏĂೀͼՏѐౌ
ѣሤ̚ഁ۞९ּ൴ϠĂܕೀѐϤٺ઼ΐૻކጱ
̚ഁ֨ڼ̈́၁߉̚ഁПᐍܼᇴീؠڱ ( тܑ˟ )Ă
ٙͽሤ̚ഁ۞९ּ̈́Ѫ˸தځព˭ࢫĄ
ঽ፟ᖼ
дТᇹ۞ᒖဩ˭ࠎ̦ᆃѣֱˠΪயϠᅅ۞
াېĂҭѣֱˠݒົซणјᚑࢦ۞ሤ̚ഁĉሤ̚
ഁ۞൴ϠߏϤኑᗔăкࢦ۞፟ᖼٙౄј ( ဦ˘ )6Ă
˘ֱአଠࡪ፬৵ ( cytokines )ăҕЯ̄ ( co- agulation proteins ) ሤЃҹకϨܑன۞ૄЯ˵Է
ႊ˞ՙؠّ۞֎Ғ12Ą͔൴၁រဂ൴Ϡሤ̚ഁĂ дЧ࣎͞ࢬ۞ͅᑕܑ̈́னౌᄃˠᙷໂࠎ࠹ҬĂܕ
ೀѐдજۏ၁រ۞јڍĂሤ̚ഁ۞ঽந፟ᖼు႙ జ˞ྋĂ઼̰छጯ۰೩Ξਕ۞፟ᖼтဦ˟
13,14,15
Ąྻજٕሤᒖဩֹ࣎វវ˯̿Ă༊࿅
࣎វਕૉఈ۞ቑಛॡĂົౄјೈᒖა ( Ҳҕ ᑅ )Ăཝҕგލᅪ ( blood brain barrier; BBB ) ఼
ّᆧΐĂౄјཝͪཚ្̰̈́ᑅ̿ăࢫҲཝొ
ڦᑅĂᖐউ۞ඕڍ̂ณயϠҋϤૄ ( free rad- ical )Ăབ఼ّᆧΐĂயϠ̰߲৵ҕাĂ߿̼
Бّ֗൴ۆăҕგ̰ҕͅᑕĂ͔൴ৠགྷ
ࡪצຫăкࢦጡءა̈́࣎វѪ˸Ą
˘ăវአ༼ ( Thermoregulation ) Αਕεड़
༊ྻજ̈́វᆧॡĂϒ૱۞Ϡநត̼тĈ ײӛᆧԣă͕ྯᆧԣă͕ᏮณᆧΐĂҕ߹ົଂ
̰ᖼொҌ̍ү̚۞҉҇Ă҉҇۞ҕ߹ณкΞ ͽᆧΐזЃिॡ۞ 20~40 ࢺĄ༊វ̿ॡ˭ෛ
۞វአ༼̚ᇽົ˭྿΄Ăౄјϩቲ۞ҕგ
ܑ˘ĈᄃຍᙊԼត۞ᝥҾ෧ᕝ
ّ̰Я৵
̚ᇽৠགྷրצຫ ϥېཛྷ̤ซࢲᇷ ຏߖ
ԩჟৠঽᘽۏೋّা࣏ཏ ( neuroleptic malignant syndrome )
ᅝࡪሳ γّЯ৵
ԩᓙែᘽۏ߲̚
ᘽۏ ሤ̚ഁ
ܑ˟Ĉ̚ഁПᐍܼᇴീؠڱ
ПᐍܼᇴП щېڶ ֨͞ڱ
̈ٺ 30 щБ ϒ૱үि
30Ҍ 35 ڦຍ ͪЊྃ·ቁ၁
35Ҍ 40 ᛋԦ ͪЊྃ·ቁ၁ăᔖҺ፬ধᚮԫ
̂ٺ 40 Пᐍ ૻטͪЊྃ·ăწᙯڦវਕېڶ
̳ёĈވγޘ(ƨ)Ůވγ࠹၆ᒅޘ(%) Ű 0.1= Пᐍܼᇴ ဦ˘Ĉሤ͔൴ሤ̚ഁ̝кࢦЯ৵
ᕖૺĂሤ۞ҕ୵ྻਖ਼זϩቲซҖሤĂϩቲ۞
ҕ߹ณΞ྿Տ̶ᛗ 8 ̳̿ĄТॡᖣϤ߹ѭ̈́
ѭ୵۞ᄐ൴ሤณ൴ଫĂᄐ൴ 1 ̳̿۞ѭ୵Ξ ͽ൴ଫ 580 ̂Ι۞ሤณĂ҃֗វ߹ѭณՏ̈ॡ
кਕ྿ז 2~3 ̳̿16ĂҭТॡ֗វ˵߹ε˞̂
ณ۞̶ͪ̈́ྋኳĄࠎ˞ਕሤณϤᙝೈᒖ
൴ଫĂ͕Ꮾณυื೩ĂࠤҌΞͽ྿Տ̶ᛗ 20̳̿17Ăҭߏтڍܜॡม۞ሤᇷᜨĂົౄјᚑ ࢦ۞௲ͪ̈́ៃ̶ಉεĂ௲ͪߏ˘࣎ࢦࢋ۞ПᐍЯ
̄ĂЯࠎࡪ̰ăγ୵۞߹εĂѣड़ೈᒖट᎕
( effective circulating volume ) ˭ࢫĂົᇆᜩࡪ
̈́Б֗րΑਕĄӈֹΪߏᅅ۞௲ͪ ( វࢦ۞
1% ) ಶົฟؕᆧΐ͕ҕგ۞ఈćᚑࢦ௲ͪॡĂ
ྻજॡ͕ྯ಼̂ΐԣĂҭ͕Ꮾณڱѣड़ᆧ ΐĂϩቲҕ߹ณ˭ࢫăࢫҲሤזϩቲ۞ਕ
˧Ăଵѭณ˭ࢫăഴҲ֗វሤਕ˧Ăౄјវ
̿Ą࣎វ၆ሤ۞ԡצਕ˧ᄃ͕ҕგր̝ͅᑕ ਕ˧ѣᙯĂ͕ҕგ়ঽ̈́ߙֱົᇆᜩ͕Αਕ۞
ᘽۏĂົࢫҲሤ۞ਕ˧Ăјࠎሤ̚ഁ۞ПᐍЯ
̄Ą
ٺᅖሤ۞ᒖဩ֗̚វਕၙၙ۞ዋᑕĂ೩چ
͕ҕგրΑਕăᆧΐ͕Ꮾณ18Ăᆧΐѭ୵۞
ଵăᆧΐሤ۞ड़தҭഴ͌ѭ୵̚ៃ̶۞߹
ε Ą ᖣ Ϥ ߿ ̼ ඪ ৵ - ҕ გ ќ ᒺ ৵ - ゟ ⟮ ր ဦ˟Ĉሤ̚ഁΞਕ۞൴Ϡ፟ᖼ
( Renin-Angiotensin-Aldosterone System ) ᆧΐඪ
ៃ̶ ( NaCl ) ۞ࢦӛќĂᆧΐೈᒖ̚ҕል۞ณ
̈́ඪක࿅ᕭதĄགྷ࿅ቚ۞ሤዋᑕ۰҉҇۞
ཛྷវ̈́ೈᒖᆧΐĂᆧΐ҉҇۞ֻউณă AT P ( ཛྷ⡊᭐८ˬᒤᅕ ) ۞ᐼх̈́ᔁड़த ( ѣউᔁ )Ă ҭֱ֗វ၆ሤᒖဩ۞ዋᑕͅᑕᅮࢋ 10 ͇זᇴ
࣎ᖃ̖ਕԆј19Ą
ࠎ˞ჯវ۞ޮؠĂயሤ̈́ሤυืܲ
πᏊ ( тဦˬ )Ă࣎πᏊېၗѣᏥ˭ෛ۞វ
አ༼̚ᇽӻгአଠ֗វͅᑕĂтڍனᗼ πᏊ۞Я৵ĂтĈវ̰யሤᆧΐăγдᒖဩᒐሤ
ٕሤਕ˧ࢫҲĂົᗼ࣎πᏊĄ
˟ăഴ͌ሤЃҹకϨ۞யϠ
ሤЃҹకϨߏ˘ཏপҾ۞కϨኳĂ̶ֶ̄ณ ( 7 to 110 kDa ) ̈́Αਕ̙Тֽડ̶Ăт HSP25 ă HSP32ă HSP47 ă HSP60 ă HSP70 ă HSP90 ̈́ HSP110Ą HSP70 ˘ཏҌ͌ಶΒ߁ HSP72 ă H- SP73ă HSP75 ̈́ HSP7820,21ĄሤЃҹకϨజᄮࠎ ߏࡪЯᑕᒖဩត̼̈́צז๋चॡࠎՐϠх۞ͅ
ᑕ͞ёĂ༊ࡪዎצγ˧๋चăሤăউă
ҕăউ̼ăҺࠪ൴ۆČ๋चॡĂሤЃҹకϨົజ
̂ณயϠ22-25ĂٙͽᙷకϨኳ˵Ⴭࠎᑅ˧కϨ
ኳ(stress protein)ĄሤЃҹకϨѣࡪ᜕ܲ ( cyto- protection )ăჯࡪ۞ޮؠېၗ ( cellular home- ostasis ) ̈́೩ሤਕ˧ ( thermotolerance )۞Α ਕĄሤЃҹకϨ۞யϠࡗдצሤޢ 30~60 ̶ᛗĂ
̂Ϡயณࡗд 18 ̈ॡ̰Ą༊צזᒖဩᑅ˧ॡ ( тሤ )ĂϠۏវ̰۞కϨኳΞਕ൴Ϡតّ ( de- naturation )҃εΝүϡĂֱᇃھхдٺৌ८ᄃ
ࣧ८ࡪ̚۞ሤЃҹకϨਕᑒӄᘦؠకϨኳ۞ඕ
ၹĂүࠎιకϨኳ۞٣ࢲ ( chaperon Ăҡᐌక Ϩ )ĂឰకϨኳԶᝑᄏҝ̙ٽצԽᑝĂᔖҺ൴Ϡ
̙Ξਗ਼۞តّĂჯకϨኳ۞߿ّ26Ąдሤ˭
ೀͼٙѣ۞ࡪౌົயϠሤЃҹͅᑕ ( heat shock response ) ᄦౄሤЃҹకϨĂдሤ̚ഁͽ HSP72 ࠎĂтڍԺטሤЃҹకϨ۞Ъјົឰࡪԩሤ ਕ˧ࢫҲĂࠤҌౄјࡪѪ˸Ąજۏ၁រពϯሤ ЃҹకϨ ( পҾߏ HSP72 ) ΞͽᔖҺ࣎វޘ࿅
ă᜕ܲೈᒖր۞ᘦؠĂ᜕ܲࡪҺٺЯ
ሤăউă̰߲৵̈́൴ۆͅᑕٙౄј۞๋चĂፋ វ҃֏Ξͽᆧΐх߿த2 2 , 2 7Ą˘ֱଐڶтĈѐ ᔙăѣঽд֗ăϏዋᑕۆሤᒖဩă௲ͪ̈́পঅૄ
ЯܑனĂֹ࣎វ࿃זሤॡڱ̂ณயϠЃҹక ϨĂ࠹၆ྵटٽႊតјሤ̚ഁ28Ą
ˬăҋϤૄ۞ࡪّ߲̈́উ๋̼च
ሤ̚ഁॡЯೈᒖა̈́ᖐউĂ֗វ ( প Ҿߏཝొ ) ົயϠ̂ณѣࡪّ߲۞ҋϤૄĂт
߿ّউҋϤૄ ( reactive oxygen species,ROS ) - ࿅ উ̼ۏ ( peroxide )Ăউ̼ۏ ( superoxide )̈́߿
ّധҋϤૄ ( reactive nitrogen species,RNS )Ăҋ Ϥૄົ၆ࡪăᖐౄјࡪّ߲̈́উ๋̼चć
ౄјབ۞఼ّᆧΐ̰߲̈́৵ซˢೈᒖ̚Ă֭
͔൴˘ాҚ۞Бّ֗൴ۆ̈́ҕგ̰ҕͅᑕĂ
ౄјкࢦጡءაĂࠤҌ࣎វѪ˸22,29Ą αăБّ֗൴ۆ̈́ҕგ̰ҕͅᑕ
дዎ࿃ሤᒖဩॡ࣎វົயϠާّഇͅᑕĂ
ֹ̰ϩࡪăϨҕ̈́˯ϩࡪ̶کкࡪ
፬৵ ( cytokines )6Ąࡁտពϯࡪ፬৵ߏણᄃሤ̚
ഁ۞ঽந፟ᖼ̝˘Ăధкࡁտѝ̏൴னдλጥ
ࡪ̚Ă̰߲৵ ( endotoxin ) ٙᄵጱ۞൴ۆّࡪ፬
৵ĂтĈሳᗼѪЯ̄-ɗ(Tumor necrosis factor-ɗĂ TNF-ɗ)ă̬Ϩ৵-1 ( Interleukin-1 )30Čົ͔ᚑࢦ۞
Бّ֗൴ۆͅᑕĂ࣎វੵ˞ົ൴፵ăϨҕᆧΐ
Б֗ҕᑅᆐࢫČγĂ˵Ξਕౄјкࢦጡء
აĂ҃ጱЃҹѪ˸31Ąજۏ၁រពϯሤ̚ഁ൴Ϡ ॡĂ൴ۆّࡪ፬৵ົ̂ณயϠĂౄјҕᑅ˭
ࢫă្̰ᑅ˯̿ăཝొڦᑅ˭ࢫ̈́ཝొ๋च32Ą ࡁտពϯĈдᆐধྻજޢҕ୵̚ົன፧
ޘ۞̰߲৵ă൴ۆّࡪ፬৵̈́ާّకϨ33Ą༊
֗វٚצᆐধྻજٕሤॡĂҕ߹ົଂ̰ᖼொ
Ҍ̍ү̚۞҉҇̈́యሤ۞ϩቲĂౄј֗វ
ဦˬĈវአ༼πᏊ
ጡءҕĂքࡪ̈́བҕ۞ඕڍĂౄјѣ चউ̼ҋϤૄ̂ณ۞யϠĂౄјབᕆቯצຫ̈́
Ⴃّ34Ąབᕆቯ۞Ⴃّౄј̰߲৵ę
кᔝ ( lipopolysaccharide ) ซˢೈᒖ̚35Ăೈᒖ
̚۞̰߲৵ົౄјҕ߹જ˧ጯ۞̙ᘦؠăБ֗൴ ۆ̈́ЃҹͅᑕĄ
ҕგ̰ϩࡪ۞ຫ๋̈́ᚢႝّ۞ҕგҕ
ংߏሤ̚ഁځព۞ঽநপҒ36Ăҕგ̰ϩࡪΞ ͽአଠҕგૺ˧̈́ΞّĂአ༼Ϩҕ۞ொજĂ ჯᔌۏኳ ( prothrombotic ) ̈́ԩҕۏኳ ( anticoagulant ) ม۞πᏊĄົֹҕგ̰ϩຫ
๋Ă̈́ҋϤૄౄјҕېၗ̈́ҕგ఼ّ
ᆧΐĄдሤ̚ഁ൴Ϡ۞ТॡĂҕͅᑕ˵Тॡజ
߿̼Ăҕ୵̚னҕ ęԩҕ ǷኑЪۏ ( thrombin anti-thrombin Ƿ complex ) ̈́ញჯకϨ ಏវ ( fibrin monomers )ćకϨኳ C ăకϨኳ S ̈́ ԩҕ Ƿഴ͌Ąॡ࣏ӈֹ͕̚វޭೇϒ
૱Ăҕͅᑕ̪ົᜈซҖĂႊតјᚢႝّ
ҕგ̰ҕ ( DIC )Ąͽ˯۞ன෪ᄃୀҕাॡ۞ܑ
னߏ࠹Т۞Ăֹሤ̚ഁдޝк͞ࢬౌᙷҬୀҕ
া( sepsis )19,37Ą
̣ăሤώ֗၆ࡪ۞ۡତ๋च
જۏ၁រពϯሤົ၆ࡪăᖐౄјۡତ๋
चĂౄј̂ณࡪ̰కϨኳតّ̈́ჸะĂֹࡪ ቯ۞ᒤ ( phospholipids ) ̈́కϨ ( lipoproteins ) ត۞̙ᘦؠĂԼតࡪቯ۞఼ّĂຫचࡪቯ కϨኳ۞ྻਖ਼̈́ࡪቯ˯ତצវ۞Αਕ38Ą๋च
۞ᚑࢦޘפՙٺᇷᜨ۞ޘ̈́ॡมܜൺĂࡁտព ϯˠᙷ۞̂ᓜࠧሤࢨޘ ( critical thermal max- imum ) ࠎ 41.6 ƨז 42 ƨ39ćᇷᜨॡม 45 ̶ᛗז 8
̈ॡĂ࿅ѩࢨޘࡪົצזᗼĂࡪЯࠎត
ّ҃εΝϒ૱ΑਕĂౄјЧጡء۞ຫ๋ ( পҾߏ
̚ᇽৠགྷր )Ăࡪ۞Ѫ˸кΗߏͽࢍ൪ّѪ˸
( apoptosis ) ͞ёซҖĄҭдໂ۞ޘ ( 49-50 ƨ)
˭ĂΪࢋ 5 ̶ᛗಶΞౄјࡪඕၹజᗼăౄј
ࡪᗼѪĂౄј࣎វѪ˸Ą
ፖ৳҉໘ྋাӈ҉҇ࡪᗼѪ֭ࡪ̰ट ۏᛖٸזೈᒖ̚Ăሤ̚ഁ׀൴ፖ৳҉໘ྋা۞፟
ᖼࠎĈ˘ăሤώ֗ಶົౄј҉҇ࡪ۞ᗼć
˟ăࡪቯ۞ᗼ̈́ࡪਕณ ( ATP Ă adenosine triphosphate )۞ਈႽĄࡪቯ఼ّᆧΐౄј
ࡪγทᗓ̄ซˢࡪ̰ć NaŮ/KŮ ᑒ ( ทᗓ
̄ࡪ̈́࿔ᗓ̄ˢࡪ ) Я ATP ਈႽ҃
εΝϒ૱ΑਕĂౄјࡪ̰ทᗓ̄ᆧĄࡪ̰
ทᗓ̄ᆧֹ NaŮ/Ca2Ů ϹೱకϨ ( exchanger protein ) ߿ّᆧΐĂྏဦทᗓ̄ᗓࡪĂҭ
˵Тॡถᗓ̄ซࡪ̰ĄϤٺ A T P ۞ਈ ႽĂถᗓ̄ᑒ˵ТॡεΝϒ૱ΑਕĂถᗓ̄ᑒ
ϒ ૱ ॡ ົ ถ ᗓ ̄ ଵ ࡪ ̈́ д ҉ ል შ ( sarcoplasmic reticulum ) ̰Ă۞ඕڍࡪ̰
ถᗓ̄ᆧΐ֭߿̼ࢫྋᅔ৵ ( degradative enzymes )Ă тᒤ A2 ( phospholipase A2 )ăకϨᅔ৵ ( pro- teases )Ăࢫྋᅔ৵ົᗼ҉ញჯቯ ( sarcolemma )ă
ࡪቯ̈́ࡪ൴፟-ཛྷវĂඕڍԛј˘࣎ೋ
ّೈᒖĂ AT P Հซ˘ՎਈႽĂՀซ˘Վౄј
ࡪ̰ทᗓ̄̈́ถᗓ̄۞ᆧΐČĂѩγࡪ̰Яࠎ ทᗓ̄۞ᆧΐౄј˘࣎ႣᑅېၗĂͪЊซˢ
ࡪౄјࡪ۞ཚණćЯࠎ ATP ۞ਈႽĂࡪ̰
னѣच۞ҋϤૄĄЯࠎͽ˯Ч۞ᗼĂ
ౄј҉҇ࡪ۞Ѫ˸̈́ፖ৳҉໘ྋা۞யϠ40,41Ą
ᓜԖܑன
ሤა۞াې఼૱ߏ˘ֱ՟ѣ˘ّ۞ܑ
னĂтܧ૱˾ഽăিࢽă൏ᛒăБ̙֗ዋăα۳ ͻ˧ă⪰͕ăယФăཛ൭ăཛᕫăᐝ൭ăຶোă ϩቲᒅҽăࢬҒᄔϨăਔຨާిͷऴĄീณវ
ົд 37 ז 40 ƨมĂ҃ሤ̚ഁ۞ؠཌྷࠎ͕̚វ
̂ٺ 40 ƨ ( ѣֱ͛ᚥࠎ 40.6 ƨ )ĂҭొЊ͛ౢ
ޙᛉ෧ᕝሤ̚ഁॡᑕྍ̙ࢋٲڪٺޘĂЯࠎѣ
ֱঽଈ̏གྷତצ࿅ࢫڼᒚĂืТॡ੨Ъᓜ Ԗܑனֽ෧ᕝ4 2Ăঽଈϩቲഴٕ͌ࠤҌઃͤ
ѭĂតᒌࡓሤĂ͕ຨ࿅ిăײӛϺు႙ΐ ԣĄሤ̚ഁ͔۞ጡءຫ๋ࢋะ̚ٺཝొă քăඪă҉҇̈́ҕ୵ҕրĂ૱֍۞׀൴
াтဦαĄ
ሤ̚ഁॡ̚ᇽৠགྷள૱۞ܑன˼ត༱̼Ăт
൏ᇋăᛇă͑ᛇăҿᕝ˧˭ࢫăள૱۞Җࠎă જү̙םአăᓾྖ̙ăຍᙊใă൯̈́ڃ ਜ਼Ąঽଈࡶͽڃਜ਼ֽܑனĂੵሤ̚ഁώ֗ٙౄ
јĂᔘᅮ҂ᇋሤ̚ഁЪ׀ྋኳள૱ăҲҕᎤă քّཝঽតăཝͪཚăཝۛ̈́Яҕள૱͔۞
្̰ҕĂౄјঽଈڃਜ਼Ą
͕Αਕ̈́ҕ߹જ˧ጯ۞ܑனΞ̶ࠎĈ
ҕ߹જ˧ېၗ ( hyperdynamic state ) ̈́Ҳҕ߹
જ˧ېၗ ( hypodynamic state )Ăҕ߹જ˧ېၗ
ॡ͕Ꮾณ ( cardiac output ) ᆧΐҭТॡБ֗ҕგ ܡ˧˭ࢫĂঽଈҕᑅ఼૱ߏϒ૱۞ćҲҕ߹જ˧
ېၗ͕Ꮾณ˭ࢫҭБ֗ҕგܡ˧ᆧΐĂ९
ּົӔனҲҕᑅ۞ېڶĂѣ͕ঽΫ̈́ͪ۞ঽ ଈटٽͽѩܑனĂҲҕ߹જ˧ېၗ˵ຳϯ˞͕҉
ࡪצຫ̈́ঽڶྵᚑࢦ43,44Ą
̚ഁঽଈ૱Ъ׀བࡤҕĂք۞ຫ๋͔
เᓙ̈́քᇴ̿˵ޝ૱֍ĂᘕّքაЪ
׀ཝঽតăҲҕᎤă D I C ̈́ҕྵ͌֍ĄϤ ٺҲҕᑅ̈́ፖ৳҉໘ྋĂঽଈ˵૱׀൴ާّඪ
აĄͽ˯۞׀൴াΞͽТॡனĂԛјሤ̚ഁ
ᚑࢦ۞׀൴া-кࢦጡءຫ๋া࣏ཏ ( multiorgan- dysfunction syndrome )Ą
็ݭሤ̚ഁᄃᇷᜨٺᒖဩ ( тሤ )
ͧྵѣᙯĂ૱֍ٺҁѐˠ̈́ၙّঽଈ۰ć҃ྻજ ݭሤ̚ഁ૱֍ٺᅮ̂ณ߿જ۞ˠĂ۰ᓜԖܑன
ͧྵтܑˬ45Ą
ሤ̚ഁঽଈ۞၁រވᑭߤ൴னĂтܑαĄ͕
ဦ૱൴ன͕ຨ࿅ి̈́՟ѣ˘ّ۞ ST-T ߱ҕ ត̼Ă˵ѣΞਕன็ጱܡ႖( тΠ͚Ձ็ጱܡᕝ
ٕ QT มؼܜ )Ąཝᕝᆸٕ८ჃВॎᑭߤд൴ ঽܐഇ۞൴னкߏ˘ֱ˘ّ۞ඕڍтĈཝͪ
ཚăୟٕҕćሤ̚ഁݭ۞ᇆညጯܑனࠎ
̈ཝᒺ ( cerebellar atrophy )Ăܑ࣎ன఼૱ߏࢋ
дᇴ͡זᇴѐޢГᖸᇆညᑭߤॡ̖ົ൴ன46,47Ą
ڼᒚ
ԧࣇᕩৼڼᒚሤ̚ഁ۞͞੫т˭Ĉ
˘ăௐ˘ॡมăѣड़۞ࢫ
ሤ̚ഁ൴Ϡॡᑕঽଈொז఼ࢲౚ୲ăྋ
ੵҗۏăᑕଳݻ๕Ăͽ྿ז̂ሤࢬ᎕Ă
֭Ξ֨Яຍᙊ̙ယФॡĂౄјײӛܡٕ
ӛˢّ۱ۆćТॡϲӈેҖனಞΞᒔ۞ࢫ͞
ёĄௐ˘ॡมăѣड़۞ࢫߏڼᒚሤ̚ഁঽଈ
ࢦࢋ۞ᙯᔣĂᓜԖ˯тڍѣᘃႷሤ̚ഁ۞Ξਕ
ّĂซ˘ՎᝥҾ෧ᕝᄃ᎕ໂࢫᑕТॡซҖĄ
ࢍྤफ़ពϯĈሤ̚ഁ൴Ϡޢົ̙ົயϠ̙Ξਗ਼۞
ຫ๋ăࠤҌѪ˸۞ᙯᔣߏॡม48Ą Yuval Heled ඈ ˠ೩ڼᒚሤ̚ഁঽଈ۞ņเܛڼᒚഇ ( Golden hours )Ň49ĂՀซ˘Վనঽ൴ޢ۞݈ 2 ࣎̈ॡ ߏࢦࢋॡมĂࡶঽଈϏਕд 2 ̈ॡ̰זዋ༊
۞ڼᒚĂ఼૱ޢߏ࠹༊म۞50Ą
ѣड़۞ࢫυืਕሤณԣి۞ଂ֗វ൴ Ҍᒖဩ̚Ă̏జ೩۞ࢫ͞ёܧ૱۞кĂ֭՟
ѣࣹ˘࣎ࢫ͞ڱజٙѣˠᄮؠߏѣड़۞Ąҭ ࡁտពϯዋЪ۞͞ёᑕྍߏ̚ഁ൴ϠனಞΞͽ ϲӈેҖ۞ࢫ͞ёĄͽҒЕฤд࿅Νೀ˩ѐ มેҖ˘࣎னಞΞҖ۞ࢫ͞ёĈϡ̂ณ۞ҋֽ
ͪ ( 20~40 ̳̿ ) ᜈሐᒅঽଈ֭ϡૻ˧ࢲैĂπ Ӯࢫ۞ిޘΞͽ྿ז 0.14 ƨ/min Ă˵ಶߏᄲ дඈޞା᜕֘۞ 10 ̶ᛗĂϡᖎಏ۞ࢫ͞ڱಶΞ ͽវࢫҲ 1.4 ƨĂּт 41 ƨࢫҌ 39.6 ƨĂᔵ ဦαĈሤ̚ഁ׀൴া
ܑˬĈ็ݭሤ̚ഁᄃྻજݭሤ̚ഁͧྵ
็ݭሤ̚ഁ পᇈ ྻજݭሤ̚ഁ
ѣ֗វ়ঽ ઉېၗ ઉ
кҁˠ ѐࡔ кѐᅅˠ
̷ ᄃᅖሤᒖဩ۞ᙯܼ ЧޘᒖဩౌѣΞਕ
ྵ͌ ߿જ ᆐধ߿જ
ăሤăѭ ෧ᕝॡϩቲܑன ăሤĂҭ૱ᔘѣѭ
̙૱֍ ᚢႝّҕგ̰ҕ ૱֍
̙૱֍ ፖ৳҉໘ྋ ૱֍
̙૱֍ ާّඪა ૱֍
̙૱֍ ֯ᅕ߲̚ ૱֍
̙૱֍ Ҳҕ࿔ ૱֍
̚ޘ Ԍᅕҕা ᚑࢦ
૱֍ ײӛែ ̙૱֍
ྵ Ѫ˸த ྵҲ
Ϊߏ 1 . 4 ƨҭ၆ঽଈ۞ޢಶѣՙؠّ۞̙
ТĄซ˘Վͧྵϫ݈ᇃࠎତצ۞࣎͞ڱĈᄐ
൴ ( ֗វሐᒅТॡֹϡૻ˧۞ࢲै ) ̈́ওڽҽͪ
( ٕДͪ )Ăᄐ൴ࢫిޘߏ 0.034 ז 0.31 ƨ/min Ă ওڽДͪࢫిޘߏ 0.15 ז 0.35 ƨ/min51Ą
ᄐ൴ࢫॡืࢋϡ̂ณ۞ͪ ( ҋֽͪăᚩߵ
ٕͪͪದĂޘΞͽߏ 1 2 Ƃ 3 0 ƨ ) ֗វሐ ᒅĂϡͪജኳ̰җăᓠԖజಏٕͨ̑ওᒅ֭ᑡ ᇳ֗វĂֹϡૻ˧ࢲैٕТॡֹϡᇴࢲैĂд
ା᜕֘˯ᑕ͗χฟĂ఼ܲࢲ̖ਕ֝ిሤ
ᗓĄ
ওڽҽͪ ( ٕДͪ ) ࢫΞͽԣࢫҲ
ޘĂҭυืπॡಶѣ౯ĂΞͽֹϡિ۞ቱ ଡ଼ĂڦˢΗ႕۞ͪٸдౚ୲ĂТॡय़ᙝᑕ౯ѣ ДఠٕДĂ༊ѣᅮࢋॡΞͽ֝ిࢫҲͪĂֹ
ϡॡͪᑕܲ 7 Ƃ 1 4 ƨĄ၁ᅫፆүଐԛࠎ
జಏٕͨ̑ٸཉٺঽଈඨ˭â࣎ӄ͘ٺঽ ଈ֗ޢঽଈؠĂᔖҺፋ࣎ˠଫˢͪ̚Ăੵ˞
ᐝొγ֗វᑕጐณওڽٺͪ̚Ăកજֹͪܲ
߹જĄ᎕ໂࢫ۞ТॡᑕႾീֆĂࡶࢫҌ 39 ƨ ӈᑕྍઃͤ᎕ໂࢫĂᔖҺயϠҲវ48Ą
͞ётϡДఠઇ̂જਔડ ( ᐚొăඨ
˭Ăཛ۵ ) ۞ࢫĂтڍдனಞΞҖ۞ଐڶ˭
ᑕซҖᐖਔᏮ୵ྃ·ڼᒚĂޙᛉ݈ 2 ࣎̈ॡගඈ
ૺ໘୵ ( normal saline ) 1 ז 1.5 ̳̿Ă̝ޢՏ̈ॡ ග̟ 250 ml Ă࿅к۞Ꮾ୵Ξਕົౄј͕აăཝ
ͪཚ̈́۱ͪཚ4 3ĄЯࠎሤ̚ഁঽଈ૱Ъ׀Ҳҕ
ᎤĂᏮ୵۞ᙷᑕӣཬᎤĄӈֹдᖼਖ਼࿅̚
ᑕڦຍା᜕֘۞఼ࢲͷᑕᜈ᎕ໂࢫĂග̟উ ঈ ( 4L/min ) ܲউঈޘ̂ٺ 90% Ą
дݑΙᘲֽৼэ۞࡚ঔౙጼฤቚ̚
͕ĂдซҖቚॡౌ౯ѣД̈́ྻᏮ̍âό ˠࣶனሤঽ۞াېϲӈณֆ֭ٺனಞฟؕග
̟ࢫڼᒚĂ֭ޢਖ਼ܢܕ۞ЪүᗁੰĂᖼਖ਼࿅
̚ ̪ ᎕ ໂ ࢫ Ą ᗁ ੰ ާ ෧ ވ ̰ ѣ ˘ ม ࢫ ވ ( cold room )Ă౯ѣДͪ ( 1 Ƃ 5 ƨ ) ওڽ̈́ާା
న౯Ăྍੰࢍ 10 ѐมᓁВѣ 80 ࣎९ּĂΪѣ˘
ּѪ˸ͷܜഇ׀൴াໂҲĄওڽДͪд˘ቔࡁ տ̚జᄮࠎߏਕԣిࢫҲޘͷѪ˸தҲ52Ą ၁ᅫ˯кᇴᗁੰާ෧ވ֭ٙᏜņcold roomŇ
ٕДͪওڽన౯Ăͷڃਜ਼˫ײӛა۞ঽଈĂ֗
˯ிк۞გྮ˵ࢨט˞Дͪওڽࢫ۞ΞҖّĄ
҃ͷֹϡДͪওڽࢫĂࡶֹϩቲ۞ޘҲٺ 30ƨ ົ͔ϩቲҕგќᒺ̈́ᝫԪĂᝫԪົயϠ ሤ ( 250 ̂Ι/m2hr )ĂЯࠎওڽٺДͪ̚ܧ૱̙න ڇĂຍᙊ۞ঽଈ૱ົଲ͙ĂѩγДͪওڽࢫ
ᔘѣΞਕົ͔ឩ⿔݄̈́ېજਔҕგ൯(va- sospasm)51Ăֱͅᑕౌ̙ӀٺࢫĂͅ៍ওڽ ҽͪ ( 7 Ƃ 14 ƨ ) ࢫĂͧྵ՟ѣ˯ᕇĄࡶ
൴ϠᝫԪΞͽԼϡͪ ( 40 ƨ ) ᑡĂТॡ
ᇝϩቲĂҹڇܑϩҕგќᒺ۞ͅᑕ֭ΐԣሤ
ిޘćࡶࢫ࿅யϠឩ⿔ΞͽֹϡBenzodiazepines
ֽڼᒚĄЯࠎДͪওڽࢫѣӀѣၑĂٙͽྵΞ Җ۞ޙᛉࠎĈДͪওڽࢫዋϡٺѐᅅă՟ѣ˘
ܑαĈሤ̚ഁ۞၁រވᑭߤ൴ன
ᑭߤ ඕڍ ᄲځ
જਔঈវ̶ژ ૱֍ײӛّែ߲̈́̚ᔁّᅕ߲̚ ็ݭሤ̚ഁঽଈன֯ᅕ߲͔̚۞ᔁّᅕ߲̚ߏ˘̙࣎р۞ޢᇾ
ҕᎤ ૱֍ҲҕᎤ পҾனٺྻજݭሤ̚ഁ̈́ᘕّքა
ҕท ૱֍ҕท னٺͪঽଈĂҭࡶៃ̶࿅ޘ߹ε˫ྃ·Ҳૺ໘୵ΞனҲҕท
ҕ࿔ ૱֍Ҳҕ࿔ ሤ̚ഁѝഇ૱னҲҕ࿔Ăҭனፖ৳҉໘ྋॡΞ൴னҕ࿔
ҕถ ૱֍Ҳҕถ ҕถඕЪٺצຫ۞҉҇
ҕᒤ ૱֍Ҳҕᒤ ЯԌᒤ͔ҲҕᒤĂҭனፖ৳҉໘ྋॡΞ൴னҕᒤ
քΑਕ ( AST/ALT ) ˯̿ 48̈ॡז 2 ฉॡ྿זᕇ ඪΑਕ ( BUN/Cr ) ˯̿
Ξ֍ٺ׀൴ާّඪაঽଈ
Ԍᅕ ˯̿
ᓁᓙࡓ৵ ˯̿ քაޢ 36-72 ̈ॡ࣏ன
ҕ୵૱ఢ ள૱ ϨҕᆧΐĂҕ̈ڕҲ˭
CPK,LDH,myoglobin ˯̿ Ξ֍ٺ׀൴ፖ৳҉໘ྋĂ CPK ࠤҌΞ྿ 100,000 IU/mL
̂ુგྮă՟ѣ׀൴া۞ঽଈćࡶߏѐࡔ
̂ăѣ͕ҕგ়ঽ۞ଈ۰ᑕྍଳפ۞ڼ
ᒚ͞ڱ51,53Ą
ܬˢّ۞ࢫ͞ётДͪ߾ࡤăབٕཛቯ
߾Ăѣሕд۞ࢲᐍĂт̶ͪ࿅кĄ Broessner ඈˠ೩ֹϡҕგ̰ࢫ͞ё۞ಡӘĂሤϹೱ ጱგ ( CoolGard® and CoolLine® ) ཉˢ˭ටᐖਔ
̰ĂҽͪڦˢጱგĂೈᒖޢሤณĂጱგ ߏދౕਫ਼ྮĂ̙ͪົ߹ˢҕ୵̚54Ąҭֱ͞ё
֭՟ѣ̂ݭ۞ࡁտಡӘពϯᐹٺܧܬˢّ۞ࢫ
͞ёĂٙͽ̪̙ޙᛉ૱ఢֹϡ51Ą
˟ă੫၆ຫ๋۞ጡءઇّ͚ᒚڱĂჯЧጡء ΑਕĄ
дΐ᜕ঽٗΞֹϡДദᜈࢫĂࢫి
ޘ̙тওڽДٕͪᄐ൴Ăྵ̙ٽயϠҲវĂΩ γ˘࣎рߏΞͽჯ˘࣎ᒌ۞үຽᒖဩĂ̙
ᅮࢋঽଈዎԘᒅĄޢᜈ۞ڼᒚࠎ੫၆ຫ๋۞
ጡءઇّ͚ᒚڱĂჯЧጡءΑਕ ( тܑ̣ )6Ă
̂ొ̶۞Ҳҕᑅдග̟᎕ໂࢫ̈́Ꮾ୵ޢਕԼ චĂ᎕ໂᏮ୵ڼᒚॡᑕႾീԌณ͕̈́̚ᐖਔᑅ ( CVP ) ٕ۱જਔແᑅ ( PCWP )ĂᔖҺЯ࿅кᏮ
୵ౄј۱ͪཚ43ĄࡶҲҕᑅ՟ѣԼචΞਕߏБ֗
൴ۆͅᑕ͔۞ҕგᕖૺ͕̈́҉ࡪצຫౄј͕
აٙĄ͕Αਕ۞ෞҤ̈́ႾീΞͽϡܬˢ
ّ۱જਔጱგႾീ۱જਔແᑅĂֹٕϡܧܬˢّ
۞͞ёę͕ࢰگֽෞҤĂ͕ࢰگΞͽᖎ ಏѣड़۞ෞҤ͕Αਕ֭ລ੨͕̚ᐖਔᑅֽႾീ
វ୵ېၗĄҕᑅᑕనڱჯπӮજਔᑅ ( mean ar- terial pressure ) ̂ٺ 60 mmHg ĂͽჯЧጡء۞
ҕ߹ڦ̈́উঈֻගĂࠎ྿ѩϫᇾΞͽֹϡچᑅ
( vasopressor )Ăҭυืڦຍณ۞چᑅົ
ౄ ј ᙝ ҕ გ ќ ᒺ Ă ̙ Ӏ ٺ ሤ Ą ѩ γ 3 % NaClăϟᜨዔ ( mannitol )Ăҕልᕖૺ ( plasma expanders )ĂтϨకϨ ( human albumin )ă✴˙ૄ
፥ৰ ( hydroxyethyl starch ) 15Ăдજۏ၁រ̚Ξͽ
̿πӮજਔᑅăࢫҲ្̰ᑅ ( intracranial pres- sureĂ ICP )ă೩ཝొڦᑅ ( cerebral perfusion pressureĂ CPP )ăԼචཝొͪཚ̈́ҕଐڶ֭ഴ
͌ৠགྷր۞๋चĄϟᜨዔТॡ˵ߏҋϤૄੵ
ۏ ( free radical scavenger )ĂΞͽഴ͌ҋϤૄ۞
ࡪّ߲̈́উ๋̼च22Ą
ˬăܡٕͤԼචৠགྷΑਕຫޢাĄ
˘όሤ̚ഁ൴ϠޢĂԯޘࢫҲҌϒ૱វ
̙֭ਕಶѩܡͤ൴ۆͅᑕăҕͅᑕ۞ซҖ̈́ޢ ᜈкࢦጡءა۞൴Ϡć˘ό൴Ϡ̙Ξਗ਼۞ৠགྷ Αਕຫϫ݈֭ѣड़۞ڼᒚ͞ёĄԧࣇ၆ሤ̚
ഁ۞൴ঽ፟ᖼѣܐՎ۞˞ྋ̝ޢĂдજۏ၁រ˯
ࡁտтңአ༼֗វ۞൴ۆͅᑕĂт̬Ϩ৵-1 ତצ វԩ ( interleukin-1 receptor antagonists )ă̰
߲৵ԩវ ( antibodies to endotoxin )ăԩউ̼ ( an- tioxidant agents )ă˘উ̼ധЪј ( nitric oxide synthase,NOS ) ܡᕝ̈́ϩኳᙷዔĂֹϡдજ ۏ˯Ξͽഴᅅৠགྷăೈᒖր۞ຫ๋ĂԼචх߿
தĂҭдˠវ۞үϡإϏࡁտ6,15ĄְАͽሤăྻ
જ̈́ၙّউдҁဂ֗˯ᄵֹሤЃҹకϨயϠĂ Ξͽѣ᜕ܲ۞ड़ڍĂഴᅅሤ̚ഁॡ۞๋चĄ
Ϥٺሤ̚ഁдޝкܑன˯ޝညᚑࢦୀҕাĂ ٺߏѣࡁտڼᒚୀҕা۞͞ڱဘྏдሤ̚ഁ
˯Ąሤ̚ഁॡົ߿̼ҕგ̰ҕ̈́ញჯకϨ໘ྋ ( fibrinolysis ) ͅᑕ͔̈́൴ᚢႝّҕგ̰ҕ ( dis- seminated intravascular coagulation )Ăᚑࢦୀҕা
۞ঽଈྃ·ૄЯࢦ۞߿ّకϨኳ C ( human re-
ܑ̣Ĉሤ̚ഁ۞ّ͚ᒚڱ
ېڶ ڼᒚ
វ ᜈࢫĂႾീֆ̈́ϩቲޘćܲֆŴ 39.4 ƨăϩቲޘ 30-33 ƨ ឩ⿔ ܲײӛၰ఼ĂΞග̟ Benzodiazepines ڼᒚ
ײӛა ࡶঽଈүယͅड ( gag reflex ) ٕݜမͅडĂӈᑕ̟ͽঈგ̰გ೧გĂ᜕ܲײӛ֭ܲউঈޘ̂ٺ 90 Ʀ
Ҳҕᑅ Ⴞീ͕̚ᐖਔᑅĂග̟Ꮾ୵̈́ҕგќᒺĂܲπӮજਔᑅ ( mean arterial pressure ) ̂ٺ 60 mmHg ͽჯЧጡءҕ୵ڦ
̈́উঈֻᑕ
ፖ৳҉໘ྋ ͽ̟Ꮾ୵ăӀԌăϟᜨዔ ( mannitol )Ăᆧΐඪҕ߹ăᅕ୰ท ( sodium bicarbonate ) ែ̼Ԍ୵ кࢦጡءა ͚ᒚڱĂޭೇЧጡءΑਕ
combinant protein C ) ΞͽࢫҲҕგ̰ҕăБ֗
൴ۆͅᑕ̈́Ѫ˸தĂٕధ၆ሤ̚ഁ۞९ּ˵ົѣ ड़36Ą
જۏࡁտពϯͪᅕៃ ( Salicylate ) ̈́
ܧᙷዔԩ൴ۆᘽۏ ( NSAIDs ) Ξͽ͔൴ࣲ֯ᙷ જۏࡪயϠՀк۞ሤЃҹకϨ55Ăᆧΐ၆ሤ۞
צޘ̈́ࡪ᜕ܲүϡĂҭ࿅к۞ሤЃҹకϨݒ
˫ົܡᕝࡪૄώ۞ྻүΑਕĄٙͽᔘᅮซ˘Վ ࡁտтңΝአ༼֗វ۞൴ۆ̈́ᑅ˧ͅᑕĂҭ˫̙
̒ᕘૄώ۞Һࠪ፟ᖼĄϫ݈֭՟ѣࡁտᙋ၁ֹ
ϡ NSAIDs ࢫ၆ٺሤ̚ഁঽଈ̝ڼᒚ̈́ޢѣ ᑒӄĂڶͷ NSAIDs ࢫ۞፟ᖼߏࢫҲ˭ෛ۞
ૄޘ ( set-point )Ăҭሤ̚ഁ۞ঽଈវ̿
ߏϤٺវአ༼Αਕεड़Ă֭ܧૄޘ۞̿
Ą NSAIDs ᔘѣઘүϡĂтքّ߲ăࢫҲ࿔
ᗓ̄۞ଵڴ̈́ Aspirin Ξਕೋ̼ҕΑਕள૱ඈĂ
ٙͽNSAIDsϫ݈̙ޙᛉֹϡٺሤ̚ഁঽଈ51Ą ሤΞͽו፬ҕ̈ڕะ̈́ᛖٸౄјҕგќᒺ
۞ҕ৵͔൴ҕგќᒺĂБّ֗۞ҲڼᒚΞͽ ഴ͌ཝొৠགྷ۞ຫ๋Ăҭѣ̙͌ᚑࢦ۞ઘүϡĂ
ٙͽᏴፄّ۞ཝొࢫߏ̙࣎۞ᏴፄĄજۏ၁ រ̚ͽ 4 ƨϠநࢴៃͪགྷᐚᐖਔਗ਼ҖّซҖཝొ
ࢫ ( retrograde jugular vein flush ) Ξͽഴ͌ཝҕ გ۞εਕăкࢦጡءεਕăБّ֗൴ۆͅᑕ̈́
ҕېၗĂԼචх߿த13Ąࡁտពϯ၆ᐚજਔග
̟ࢫΞͽౄјҕგනૺĂഴ͌ৠགྷຫ๋56Ą ᔘѣՀкજۏ၁រࡁտ̚۞͞ڱĂтᑅউ ( hyperbaric oxygen )ăνჟঊᅕ ( L-arginine )ă
ᅬ፬৵ ( estrogen )ăˠᙷᖜҕࡪ6,15,57ČĂԧ ࣇ̪ืՀᒢྋ়ঽ۞፟ᖼĂซ˘ՎࡁտࢫҲѪ˸
த̈́ܡͤϖ˳ৠགྷጯޢা۞൴ϠĄ
Ѫ˸த̈́ޢ
ࡶਕזዋ༊ͷ᎕ໂ۞ڼᒚĂঽଈ۞̚ᇽৠ གྷրΑਕᑕਕдࢫ۞࿅̚ు႙ޭೇĂߏ
˘࣎ѣ̙ޢ۞рᇈЏĄҭߏ่Ѩٺ͕ҕ გ়ঽ̈́γ๋၆̚ᇽৠགྷౄј๋च۞ௐˬ̂୭
͘Ăӈֹᒔዋ༊۞ڼᒚĂࢍ˯̪ѣѺ̶̝
20۞ঽଈົѣϖ˳۞ৠགྷΑਕຫ58Ą̈ཝߏཝ
ొटٽצሤ๋च۞ొҜĂઊ҃ົѣ̈ཝা࣏ཏ ( cerebellar syndrome ) ۞ঽּಡӘĂᓜԖ۞ܑன ࠎྻજεአ ( ataxia)ăᝫԪ ( tremor )ăၹࢰள૱
( dysarthria )ăᅅឨ ( paresis ) ٕ˭Η֗ឨႼ ( para- plegia )59Ą
ѣᙯሤ̚ഁѪ˸த۞ࢍඕڍमள࠹༊̂Ă
ଂ 10% ז 50% ౌѣĂдՒনгܠٛұሤ̚ഁ۞
Ѫ˸தࠎ 5 0 % ĂҭдݑΙᘲֽৼэ۞࡚ঔ
ౙጼฤቚ͕̚ซҖ۞ࢍĂѪ˸தΪѣ 1.25%
( 80࣎९ּĂ 1 ּѪ˸ )52,60Ă̶ژࣧЯពϯĈт ڍ၆ሤ̚ഁѣ֖ૉ۞ᄮᙊă·̶۞౯ăѝഇ෧ ᕝ̈́ϒቁ֝ి۞ڼᒚĂሤ̚ഁ˵Ξͽѣ̙۞
ޢĄ
֨
тڍԧࣇਕ၆ሤ̚ഁѣ֖ૉ۞ᄮᙊĂಶਕࢫ Ҳሤ̚ഁ۞Ѫ˸தĂࠤҌ֨ሤ̚ഁ۞൴ϠĄЯ
ܑ̱Ĉᗼវአ༼πᏊ۞Я৵
Я৵ ᄲځ
វ̰யሤᆧΐ
൴፵়ٕঽ̈́ϥېཛྷ፟ਕ̤ซ າౘᔁిதᆧΐ
ᆐধ۞߿જ ᆧΐវ̰ሤณ۞யϠĂΞ྿ 1000 ̂Ι/̈ॡ
ᘽۏĈщܧăΟߟែăԩჟৠঽᘽۏăӛˢّ౫ዕăԩ͐ܛͩাᘽۏ γдᒖဩᒐሤ
ሤሗᒅΞͽጱᒖဩޘ۞᎕Ăঈ྿ז 33ƨͽ˯ॡĂटٽ̚ഁĄ
ሤਕ˧ࢫҲ
௲ͪ ͍௲ͪ࿅ 3% ۞ॡ࣏
͕ҕგ়ঽ ڱዋ༊ᆧΐ͕Ꮾณ
ϩቲঽٕ̙ዋ༊۞җڇ ˠវ 97% ۞ሤౌߏ൴Ϡдϩቲܑᆸ˯
ᘽۏĈӀԌă˙ݭܡᕝăถᗓ̄ܡᕝăԩᖐăԩᓙែă੧ჟăˬᒖԩ
ѩሤ̚ഁ۞֨ڼᑕΒ߁Ĉ
˘ă࿅Чგᜈିֈϔிᄮᙊሤ̚
ഁĈ̬ሤ̚ഁ۞ПᐍЯ̄ăٽܳ൴ሤ̚ഁ۞ᘽ ۏ ( ܑ̱ ) ̈́Пᐍཏ ( ܑ˛ )ćିጱтң֨̈́
ᖎಏ۞ҋାă̢ାĄ
˟ăྃ·֖ૉ۞̶ͪăៃ̶Ĉࡶ̶ͪྃ·̙
֖ĂΞਕдాᜈೀ͇̰ు႙г௲ͪĂтѣវࢦд ᇴ͇̰ۡቢ˭ࢫ۞ଐڶĂᑕΐͽຍĄ˘ਠࢴۏ
۞ᛷפ֖̏ૉྃ·߹ε۞ៃ̶Ăੵܧޝᆐধ۞ྻ
જă̂ณ۞߹εĂΞͽಅංᛖ۞ྋኳफ़ֽྃ
·Ą
ˬăᔖҺٺሗᒅăۆሤ۞͇ঈүᆐধ۞߿
જĈдሗᒅăۆሤ۞͇ঈ྆Ăሤณ̙टٽ൴Ă ࠤҌՏ̶̣ᛗ͕̚វΞͽ˯̿ 1 ƨĂጐณᔖҺ
፬ধٕܜॡม۞ྻજĂ߿જᑕጐณщଵٺވ̰ٕ
ዌวĂ͗γ߿જрщଵдѝ˯ٕเڃޢĄ αăሤዋᑕ ( Acclimatization )Ĉѣࢍ൪۞ు
႙ዋᑕᅖሤ͇ঈĂՏ͇࣎̈ॡ۞ྻજĂᅮࢋ 7 Ƃ 10 ͇̖ਕ၆ሤ۞ᒖဩயϠዋᑕĄ
̣ă็ݭሤ̚ഁр൴ٺҁˠĂপҾߏا
̈́ၙّঽଈ۰Ă၆ٺ็ݭሤ̚ഁ۞֨ڼĂᑕϤ
ۤڇˠࣶٕۤ̍ޙϲЩΊᖸĂдഇপҾؠ ഇଣణă೩ֻםӄٕ֖ૉ۞ͪĂѣυࢋॡ
щཉٺΞͽ೩ֻҽঈ۞፟ၹ61Ą
ඕኢ
Ϊࢋԧࣇ၆ሤ̚ഁѣ֖ૉ۞ᄮᙊĂሤ̚ഁߏ Ξͽ֨۞Ċሤ̚ഁޢᜈົЪ׀ᚑࢦ۞׀൴াĂ
૱ᅮࢋ̂ݭ۞ᗁᒚੰ̖ٙਕ೩ֻዋ̷۞ڼᒚĂҭ ᙯܼঽଈޢࢦࢋ۞ᙯᔣ၁ߏଂ൴ঽזᖼਖ਼ זᗁੰ۞֤ 1~2 ࣎̈ॡĂঽଈ˘ฟؕΞਕజҌ
൴ঽனಞܢܕ۞ЇңᗁੰĂЯѩٙѣᓜԖᗁरӮ
ᑕ˞ྋሤ̚ഁ۞ڼᒚĄሤ̚ഁ۞ڼᒚᑕྍѣᇅ
ّăЯгטآĂᖎಏă၁ᅫΞҖҭѣड़۞ࢫ͞
ڱಶߏр۞͞ڱ62Ă̙֭ᅮࢋӧᙱஎ۞͞ڱ
̈́Аซڀෳ۞న౯ĄࠤҌтڍ̚ഁ൴Ϡனಞѣዋ
༊۞̍үˠࣶ ( тฤᗁăགྷ࿅ቚ̝ቚࣶ )Ăᑕྍ
ࢋАࢫăГޢਖ਼ ( cool firstĂ transport second )48Ą ϫ݈۞ᗁᒚ̏གྷΞͽሤ̚ഁ۞Ѫ˸தࢫҲᔌܕ ٺ 0 Ăҭߏϖ˳ّৠགྷጯޢা۞൴Ϡͧத̪
ا̙˭Ăԧࣇ၆ٺሤౄјཝৠགྷր๋च۞ۢᙊ
̪ѣࢨĂՀк۞ࡁտਕᑒӄԧࣇᒢྋ়ঽ۞፟
ᖼĂซ˘ՎࢫҲϖ˳ّৠགྷጯޢা۞൴ϠதĄ
ણ҂͛ᚥ
1.Tom K. The 2003 European Heat Waves. Euro Surveill 2005;
10: 118-49.
2.Johnson H, Kovats RS, McGregor G, Stedman J, Gibbs M, Walton H. The impact of the 2003 heat wave on daily mortali- ty in England and Wales and the use of rapid weekly mortality estimates. Euro Surveill 2005; 10: 168-71.
3.Fouillet A, Rey G, Laurent F, Pavillon G, et al. Excess mortali- ty related to the August 2003 heat wave in France. Int Arch Occup Environ Health 2006; 80: 16-24.
4.Patz JA, Campbell-Lendrum D, Holloway T, Foley JA. Impact of regional climate change on human health. Nature 2005; 438:
310-7.
5.Easterling DR, Meehl GA, Parmesan C, Changnon SA, Karl TR, Mearns LO. Climate extremes: observations, modeling, and im- pacts. Science 2000; 298: 2068-74.
6.Bouchama A, Knochel JP. Heat Stroke. N Engl J Med 2002; 346:
1978-88.
7.Hassanein T, Razack A, Gavaler JS, Van Thiel DH. Heatstroke:
its clinical and pathological presentation, with particular atten- tion to the liver. Am J Gastroenterol 1992; 87: 1382-9.
8.Glazer JL. Management of heatstroke and heat exhaustion. Am Fam Physician 2005; 71: 2133-40.
9.Jones TS, Liang AP, Kilbourne EM, et al. Morbidity and mor- tality associated with the July 1980 heat wave in St. Louis and Kansas City, Mo. JAMA 1982; 247: 3327-31.
10.Ghaznawi HI, Ibrahim MA. Heat stroke and heat exhaustion in pilgrims performing the Haj (annual pilgrimage) in Saudi Arabia. Ann Saudi Med 1987; 7: 323-6.
11.ౘୁරĄ็ݭ̚ഁĄᓜԖᗁጯ 2001; 47: 76-80.
12.Lin MT, Liu HH, Yang YL. Involvement of interleukin-1 re- ceptor mechanisms in development of arterial hypotension in rat heatstroke. Am J Physiol 1997; 273: H2072-7
13.Hsu SF, Niu KC, Lin CL, Lin MT. Brain cooling causes attenu- ation of cerebral oxidative stress, systemic inflammation, acti- vated coagulation, and tissue ischemia/injury during heatstroke.
Shock 2006; 26: 210-20.
ܑ˛ĈПᐍཏ
ҁˠ ࿅ࢦĞ̂ٺ85̳͝ğ
̈ޅ វਕָ̙
͗γ̍ˠ ၆ሤᒖဩإϏዋᑕ
ˠ(͍ߏາһ) Ⴢ্ăᒉዳ̙֖
ྻજᏴ͘
ၙّჟৠ়ঽଈ۰ ੧ჟăᘽۏᑿϡ۰
14.Chang CK, Chang CP, Chiu WT, Lin MT. Prevention and repair of circulatory shock and cerebral ischemia/injury by various agents in experimental heatstroke. Curr Med Chem 2006; 13:
3145-54.
15.Chen SH, Niu KC, Lin MT. Cerebrovascular dysfunction is an attractive target for therapy in heat stroke. Clin Exp Pharmacol Physiol 2006; 33: 663-72.
16.Buono MJ, Sjoholm NT. Effect of physical training on periph- eral sweat production. J Appl Physiol 1988; 65: 811-4.
17.Rowell LB. Cardiovascular aspects of human thermoregulation.
Circ Res 1983; 52: 367-79.
18.Horowitz M. Matching the heart to heat-induced circulatory load: heat-acclimatory responses. News Physiol Sci 2003; 18:
215-21.
19.Knochel JP. Catastrophic medical events with exhaustive exer- cise: white collar rhabdomyolysis. Kidney Int 1990; 38: 709-19.
20.Wheeler DS, Wong HR. Heat shock response and acute lung in- jury. Free Radic Biol Med 2007; 42: 1-14.
21.Kregel KC. Heat shock proteins: modifying factors in physio- logical stress responses and acquired thermotolerance. J Appl Physiol 2002; 92: 2177-86.
22.Chang CK, Chang CP, Liu SY, Lin MT. Oxidative stress and is- chemic injuries in heat stroke. Prog Brain Res 2007; 162: 525- 46.
23.Hahn GM, Li GC. Thermotolerance and heat shock proteins in mammalian cells. Radiat Res 1982; 92: 452-7.
24.Pockley AG. Heat shock proteins as regulators of the immune response. Lancet 2003; 362: 469-76.
25.Welch WJ. Heat Shock Proteins as Biomarkers for Stroke and Trauma. Am J Med 2001; 111: 669-70.
26.Welch WJ. Mammalian stress response: cell physiology, struc- ture/function of stress proteins, and implications for medicine and disease. Physiol Rev 1992; 72: 1063-81.
27.Lee WC, Wen HC, Chang CP, Chen MY, Lin MT Heat shock protein 72 overexpression protects against hyperthermia, circu- latory shock, and cerebral ischemia during heatstroke. J Appl Physiol 2006; 100: 2073-82.
28.Moseley PL. Heat shock proteins and heat adaptation of the whole organism. J Appl Physiol 1997; 83: 1413-7.
29.Babior BM. Phagocytes and oxidative stress. Am J Med 2000;
109: 33-44.
30.Lu KC, Wang JY, Lin SH, Chu P, Lin YF. Role of circulating cy- tokines and chemokines in exertional heatstroke. Crit Care Med 2004; 32: 399-403.
31.Jean-Baptiste E. Cellular mechanisms in sepsis. J Intensive Care Med 2007; 22: 63-72.
32.Giulian D, Lachman LB. Interleukin-l stimulation of astroglial proliferation after brain injury. Science 1985; 228: 497-9.
33.Pedersen BK, Hoffman-Goetz L. Exercise and the immune sys- tem: regulation, integration, and adaptation. Physiol Rev 2000;
80: 1055-81.
34.Hall DM, Buettner GR, Oberley LW, Xu L, Matthes RD, Gisolfi CV. Mechanisms of circulatory and intestinal barrier dysfunc-
tion during whole body hyperthermia. Am J Physiol Heart Circ Physiol 2001; 280: H509-21.
35.Gathiram P, Wells MT, Raidoo D, Brock-Utne JG, Gaffin SL.
Portal and systemic plasma lipopolysaccharide concentrations in heat-stressed primates. Circ Shock 1988; 25: 223-30.
36.Bouchama A, Hammami MM, Haq A, Jackson J, al-Sedairy S.
Evidence for endothelial cell activation/injury in heatstroke. Crit Care Med 1996; 24: 1173-8.
37.Bouchama A, Bridey F, Hammami MM, et al. Activation of co- agulation and fibrinolysis in heatstroke. Thromb Haemost 1996;
76: 909-15.
38.Tek D, Olshaker JS. Heat illness. Emerg Med Clin North Am 1992; 10: 299-310.
39.Bynum GD, Pandolf KB, Schuette WH, et al. Induced hyper- thermia in sedated humans and the concept of critical thermal maximum. Am J Physiol 1978; 235: R228-36.
40.Sauret JM, Marinides G, Wang GK. Rhabdomyolysis. Am Fam Physician 2002; 65: 907-12.
41.Allison RC, Bedsole DL: The other medical causes of rhab- domyolysis. Am J Med Sci 2003; 326: 79-88.
42.Mustafa S, Thulesius O, Ismael HN. Hyperthermia-induced vasoconstriction of the carotid artery, a possible causative fac- tor of heatstroke. J Appl Physiol 2004; 96: 1875-8.
43.Shaul A, Ehud R, Tiberio R. Transient cardiac dysfunction and pulmonary edema in exertional heat stroke. Mil Med 2003; 168:
67.
44.Dahmash NS, al Harthi SS, Akhtar J. Invasive evaluation of pa- tients with heat stroke. Chest 1993; 103: 1210-4.
45.Barrow MW, Clark KA. Heat-related illness. Am Fam Physician 1998; 58: 749-56, 759.
46.Yaqub BA, Daif AK, Panayiotopoulos CP. Pancerebellar syn- drome in heat stroke: clinical course and CT scan findings.
Neuroradiology 1987; 29: 294-6.
47.Albukrek D, Bakon M, Moran DS, et al. Heat-stroke-induced cerebellar atrophy: clinical course, CT and MRI findings.
Neuroradiology 1997; 39: 195-7.
48.Casa DJ, Anderson JM, Armstrong LE, Maresh CM. Survival strategy: Acute treatment of exertional heat stroke. J Strength Cond Res 2006; 20: 462.
49.Heled Y, Rav-Acha M, Shani Y, Epstein Y, Moran DS. The
"Golden Hour" for Heatstroke Treatment. Mil Med 2004; 169:
184-6.
50.Yeo TP. Heat stroke: a comprehensive review. AACN Clin Issues 2004; 15: 280-93.
51.Hadad E, Rav-Acha M, Heled Y, Epstein Y, Moran DS. Heat stroke : a review of cooling methods. Sports Med 2004; 34: 501- 11.
52.Kark JA, Burr PQ, Wegner CB, Gastaldo E, Gardner JW.
Exertional heat illness in Marine Corps recruit training. Aviat Space Environ Med 1996; 67: 354-60.
53.Smith JE. Cooling methods used in the treatment of exertional heat illness. Br J Sports Med 2005; 39: 503-7.
54.Broessner G, Beer R, Franz G, et al. Case report: severe heat
stroke with multiple organ dysfunction - a novel intravascular treatment approach. Crit Care 2005; 9: R498-501.
55.Ishihara K, Yamagishi N, Hatayama T. Suppression of heat- and polyglutamine-induced cytotoxicity by nonsteroidal anti-in- flammatory drugs. Eur J Biochem 2004; 271: 4552-8.
56.Thulesius O. Thermal reactions of blood vessels in vascular stroke and heatstroke. Med Princ Pract 2006; 15: 316-21.
57.Kuo JR, Lin CL, Chio CC, Wang JJ, Lin MT. Effects of hyper- tonic (3%) saline in rats with circulatory shock and cerebral is- chemia after heatstroke. Intensive Care Med 2003; 29: 1567-73.
58.Sharma HS. Heat-related deaths are largely due to brain dam- age. Indian J Med Res 2005; 121: 621-23.
59.Lu KC,Wang TL. Heat Stroke. Ann Disaster Med 2004; 2: 97- 109.
60.Cantor RM: Heat illness from mild to malignant. Emerg Med 1991; 000: 93-100.
61.Bernard SM, McGeehin MA. Municipal heat wave response plans. Am J Public Health 2004; 94: 1520-2.
62.Hadad E, Moran DS, Epstein Y. Cooling heat stroke patients by available field measures. Intensive Care Med 2004; 30: 338.
Heat Stroke
Chich-Chiang Wang2, Ming-Kai Tsai1, I-Hung Chen1, Chao-Wen Hsueh2, and Jeng-Chuan Shiang1
Heat-related illness includes heat cramps, heat syncope, heat exhaustion and heatstroke. Untreated heat exhaustion can progress to heatstroke, a life-threatening illness characterized by an elevated core body tem- perature (ŵ 40 ƨ) and dysfunction of central nervous system, which results in delirium, convulsions, or coma.
Hyperthermia associated with the acute physiological alterations, thermoregulatory failure, systemic inflamma- tory response, attenuated heat-shock response and the cytotoxicity of heat leading to progression of heat stroke.
The prognosis of heat stroke in patients is directly related to the duration of hyperthermia. The prognosis is poor- est when treatment is delayed ŵ 2 hours. Therefore, the most important feature in the treatment of heat stroke is rapid cooling. The prognosis is optimal when heat stroke is diagnosed early and management with effective and easy cooling measures (including immersion in water, evaporative cooling) begins promptly. Long-term neu- rologic sequelae occur in approximately 20% of patients. New approaches to reduce mortality and complication of heat stroke are being studied. ( J Intern Med Taiwan 2008; 19: 136- 147 )
1Division of Nephrology, 2Department of Internal Medicine, Kaohsiung Armed Forces General Hospital, Kaohsiung, Taiwan, R.O.C.
