ตำราศัลยศาสตร์หลอดเลือด กำพลเลาหเพ็ญแสง,พ.บ. by Thai Vascular Association

VASCULAR SURGERY

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥

°”æ≈ ‡≈“À‡æÁ≠· ß √Õß»“ µ√“®“√¬å ¿“§«‘™“»—≈¬»“ µ√å §≥–·æ∑¬»“ µ√å ¡À“«‘∑¬“≈—¬‡™’¬ß„À¡à, ‡™’¬ß„À¡à 50202

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥

VASCULAR SURGERY »—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥ °”æ≈ ‡≈“À‡æÁ≠· ß √Õß»“ µ√“®“√¬å ¿“§«‘™“»—≈¬»“ µ√å §≥–·æ∑¬»“ µ√å ¡À“«‘∑¬“≈—¬‡™’¬ß„À¡à, ‡™’¬ß„À¡à 50202 ß«π≈‘¢ ‘∑∏‘Ï 2542 À®°. æ’.∫’. øÕ‡√π ∫ÿä§ å ‡´π‡µÕ√å ®”°—¥

°”æ≈ ‡≈“À‡æÁ≠· ß »—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥ 1. SURGERY I. π.æ. °”æ≈ ‡≈“À‡æÁ≠· ß II. °√ÿß‡∑æœ æ’.∫’. øÕ‡√π ∫ÿ§ä å ‡´π‡µÕ√å ®”°—¥ III. Title [DNLM: 1. Surgery Vascular. WG 170 V 3311, 1999 ISBN 974-565-871-5 »—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥

æ‘¡æåµâπ©∫—∫ ≈“¬‡ âπ Õ“√åµ°√“øî§ æ‘¡æå∑’Ë ®—¥æ‘¡æå‡º¬·æ√à

ÿæ—µ√“ ‡ ¡Õ„® √ÿ®‘√“ «ß»å∫ÿ≠µ—π ∏’√– ∑Õß ß ‚√ßæ‘¡æå‡√◊Õπ·°â« æ’.∫’. øÕ‡√π ∫ÿä§ å ‡´π‡µÕ√å ®”°—¥

III

VASCULAR SURGERY

§”π” «—µ∂ÿª√– ß§å¢Õß°“√·µàßÀπ—ß ◊Õ»—≈¬·æ∑¬åÀ≈Õ¥‡≈◊Õ¥‡≈à¡π’È ‡π◊ÕË ß®“°π—°»÷°…“·æ∑¬å, ·æ∑¬åΩ°ñ À—¥, ·æ∑¬åª√–®”∫â“π µ≈Õ¥ ®π·æ∑¬å∑’Ë ‰¥â√∫— °“√Ωñ°Õ∫√¡∑’§Ë ≥–·æ∑¬»“ µ√å ¡À“«‘∑¬“≈—¬‡™’¬ß„À¡à µâÕß°“√„Àâ¡µ’ ”√“À√◊Õ§Ÿ¡à Õ◊ »—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥‡ªìπ¿“…“‰∑¬ ·≈–¡’‚√§∑’Ë‡°’Ë¬«¢âÕß°—∫ºŸâªÉ«¬§π‰∑¬ ‡æ◊ËÕ‡ªìπ·π«∑“ß„π°“√¥Ÿ·≈√—°…“ºŸâªÉ«¬‚√§À≈Õ¥‡≈◊Õ¥´÷Ëßπ—∫«—π°Á®–¡’‡æ‘Ë¡¡“°¢÷Èπ‡√◊ËÕ¬ Ê „π Õ¥’µ‰¡à‡§¬¡’µ”√“À√◊Õ§Ÿà¡◊Õ»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥‡ªìπ¿“…“‰∑¬ ¡’·µà∑“ß»—≈¬»“ µ√å∑—Ë«‰ª ·≈–‰¥â°≈à“«∂÷ß‚√§À≈Õ¥‡≈◊Õ¥∑’Ëπà“ π„® ‡æ’¬ß§√à“« Ê ‰¡à≈ß≈÷° „πª√–‡∑»‰∑¬¡’Õ“®“√¬å·æ∑¬åÀ≈“¬∑à“π®“° ∂“∫—πµà“ß Ê ∑—Èß„π à«π°≈“ß·≈– à«π¿Ÿ¡‘¿“§‰¥â√—∫°“√Ωñ° Õ∫√¡®“°µà“ßª√–‡∑» ·≈–¡’ª√– ∫°“√≥å¥·Ÿ ≈√—°…“ºŸªâ «É ¬‚√§À≈Õ¥‡≈◊Õ¥ ‰¥â°Õà µ—ßÈ ™¡√¡·æ∑¬å‚√§À≈Õ¥‡≈◊Õ¥·Ààßª√–‡∑»‰∑¬¢÷πÈ „πªï æ.». 2539 ‰¥â®¥— °“√Õ¿‘ª√“¬·≈–Ωñ°Õ∫√¡√–¬– —πÈ ∑“ß‚√§À≈Õ¥‡≈◊Õ¥À≈“¬§√—ßÈ „π°“√‡¢’¬πµ”√“·≈–§Ÿ¡à Õ◊ π—πÈ ºŸ‡â ¢’¬πÀ≈“¬∑à“π ‡¢’¬π„π·µà≈–∫∑ °“√∑’Ë®–‰¥â√—∫µâπ©∫—∫§√∫®“°∑ÿ°∑à“π„π‡«≈“∑’Ë°”Àπ¥π—Èπ ‡ªìπ‡√◊ËÕß∑’Ë¬“°≈”∫“°¡“° ‡æ√“–·µà≈–∑à“π¬àÕ¡¡’ß“π √—¥µ—«À“‡«≈“„π°“√‡¢’¬π‰¥â¬“° ‡π◊ÈÕÀ“Õ“®®–‰¡à Õ¥§≈âÕßÀ√◊ÕÕ“®®–´È”´âÕπ°—π ·π«∑“ß„π°“√‡¢’¬π°Á·µ°µà“ß°—π ”À√—∫°“√ ‡¢’¬π‚¥¬ºŸ‡â ¢’¬π§π‡¥’¬« ‡™àπ „πÀπ—ß ◊Õµ”√“»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥‡≈à¡π’È °Á¡¢’ Õâ ®”°—¥‡™àπ°—π §◊Õ ºŸ‡â ¢’¬πÕ“®¡’§«“¡√Ÿ§â «“¡ “¡“√∂ ®”°—¥„π·µà‡©æ“–‡√◊ËÕß∑’Ë ‰¥âΩñ°Õ∫√¡¡“À√◊Õ„π‡√◊ËÕß∑’Ë π„®‡∑à“π—Èπ °“√®–·µàßÀπ—ß ◊Õµ”√“∑—Èß‡≈à¡„Àâ§√Õ∫§≈ÿ¡‡π◊ÈÕÀ“·≈– ¡∫Ÿ√≥å∑ÿ° ¥â“π¬àÕ¡∑”‰¥â≈”∫“° ‡ªìπß“πÀπ—° ¡’¢¥’ ®”°—¥·≈–¢âÕÕÿª √√§¡“°¡“¬ Àπ—ß ◊Õµ”√“‡≈à¡π’ºÈ ‡Ÿâ ¢’¬π‰¥â‡√‘¡Ë ‡¢’¬π·≈–√«∫√«¡√Ÿª¿“æ®“° ‰≈¥å∑∂’Ë “à ¬®“°ºŸªâ «É ¬„πÀÕºŸªâ «É ¬·ºπ°»—≈¬°√√¡ §≥–·æ∑¬»“ µ√å ¡À“«‘∑¬“≈—¬‡™’¬ß„À¡à µ—Èß·µà°àÕπºà“µ—¥ „πÀâÕßºà“µ—¥ ·≈–À≈—ßºà“µ—¥ ‰¥â√«∫√«¡¿“æ√—ß ’·≈–°“√µ√«®«‘π‘®©—¬µà“ß Ê ∂‘µ‘∑’Ëπà“ π„®®“°§≥–·æ∑¬»“ µ√å ¡À“«‘∑¬“≈—¬‡™’¬ß„À¡à ·≈–µà“ß ∂“∫—π ‡√‘Ë¡µâπ®“°æ◊Èπ∞“π∑“ß¥â“π«‘∑¬“»“ µ√å‚√§À≈Õ¥‡≈◊Õ¥ °“√ ª√–‡¡‘πºŸªâ «É ¬ «‘∏°’ “√µ√«®«‘π®‘ ©—¬µà“ß Ê ‚√§∑’æË ∫∫àÕ¬„πª√–‡∑»‰∑¬ °“√¥Ÿ·≈·≈–øóπô øŸºªŸâ «É ¬À≈—ßºà“µ—¥ À≈“¬§√—ßÈ ∑’‡Ë ¢’¬π·≈â«√◊ÕÈ ∑‘Èß‡¢’¬π„À¡à ‡π◊ËÕß®“°¢âÕ¡Ÿ≈ ‡Õ° “√Õâ“ßÕ‘ß µ≈Õ¥®π ‰≈¥å∑’Ë∂à“¬®“°ºŸâªÉ«¬∑’Ë√—∫‡¢â“¡“„πÀÕºŸâªÉ«¬¥’°«à“¢Õß‡¥‘¡ ºŸâ‡¢’¬πÀ«—ß«à“ Àπ—ß ◊Õµ”√“‡≈à¡π’È®–¡’ª√–‚¬™πå „π¥â“π°“√«‘π‘®©—¬‚√§ ·≈–°“√¥Ÿ·≈√—°…“ºŸâªÉ«¬‚√§À≈Õ¥‡≈◊Õ¥ ´÷Ëß„πªí®®ÿ∫—πæ∫‰¥â∫àÕ¬¢÷Èπ„π ‚√ßæ¬“∫“≈∑—«Ë ‰ª ∑—ßÈ „π‚√ßæ¬“∫“≈»Ÿπ¬å·≈–‚√ßæ¬“∫“≈™ÿ¡™π„πª√–‡∑»‰∑¬

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥

¢âÕ∫°æ√àÕß„π°“√‡¢’¬πÀπ—ß ◊Õ‡≈à¡π’ÈÕ“®¡’‰¥âÀ≈“¬ª√–°“√ ∫“ß à«π®“° ”π«π¿“…“∑’Ë „™â¥â«¬§«“¡‡§¬™‘π„π™’«‘µª√–®”«—π ®“°°“√æ‘¡æå·≈–µ√«®∑“πµâπ©∫—∫ √Ÿª¿“æ‰¡à™¥— À√◊Õ·ºπ¿Ÿ¡‰‘ ¡à «¬ ‡¢â“„®¬“° ºŸ‡â ¢’¬π¬‘π¥’πÕâ ¡√—∫øíß‡æ◊ÕË ª√—∫ª√ÿß·≈–·°â ‰¢ à«π¥’ ¢ÕßÀπ—ß ◊Õ‡≈à¡π’È ºŸ‡â ¢’¬π¢ÕπâÕ¡‡°≈â“πâÕ¡°√–À¡àÕ¡∂«“¬‡ªìπæ√–√“™°ÿ»≈·¥àæ√–∫“∑ ¡‡¥Á®æ√–‡®â“Õ¬ŸÀà «— ¿Ÿ¡æ‘ ≈Õ¥ÿ≈¬‡¥™ „π¡À“ ¡ß§≈«‚√°“ ∑’∑Ë √ß‡®√‘≠æ√–™π¡åæ√√…“§√∫√Õ∫ 72 æ√√…“ ·≈–¢ÕπâÕ¡Õÿ∑»‘ ·¥à∫√ÿ æ“®“√¬å∑ß—È À≈“¬∑’Ë ‰¥âª√– ‘∑∏‘ªÏ √– “∑§«“¡√Ÿ∑â ß—È „πÕ¥’µ·≈–ªí®®ÿ∫—π ¢ÕÕÿ∑‘»„ÀâºŸâªÉ«¬„πÀÕºŸâªÉ«¬»—≈¬°√√¡‚√ßæ¬“∫“≈¡À“√“™π§√‡™’¬ß„À¡à Àπ—ß ◊Õµ”√“‡≈à¡π’È®–‰¡à “¡“√∂ ”‡√Á® ≈ÿ≈à«ßÕÕ°¡“‡ªìπ√Ÿª‡≈à¡‰¥â‡≈¬ ∂â“‰¡à ‰¥â√—∫§«“¡√à«¡¡◊Õ®“°Õ“®“√¬å ·≈–·æ∑¬åª√–®”∫â“π ¿“§«‘™“»—≈¬»“ µ√å §≥–·æ∑¬»“ µ√å ¡À“«‘∑¬“≈—¬‡™’¬ß„À¡à §ÿ≥ ÿæµ— √“ ‡ ¡Õ„® ´÷ßË ∑”Àπâ“∑’‡Ë ªìπ‡≈¢“πÿ°“√æ‘¡æåµπâ ©∫—∫®“°≈“¬¡◊Õ∑’ÕË “à π· π¬“° §ÿ≥ß“¡ ®‘µ√§” ·Ààß Àπà«¬‚ µ∑—»π»÷°…“ ∑’∂Ë “à ¬ ‰≈¥åºªŸâ «É ¬∑—ßÈ ·ºπ°ºŸªâ «É ¬πÕ° ÀÕºŸªâ «É ¬ ·≈–„πÀâÕßºà“µ—¥ §ÿ≥√ÿ®√‘ “ §”»√’®π— ∑√å ·ÀàßÀπà«¬‚ µ∑—»π»÷°…“ ∑’Ë ‰¥â«“¥√Ÿªª√–°Õ∫„π‡≈à¡·≈–ÕÕ°·∫∫ª°Õ¬à“ß «¬ß“¡ √Õß»“ µ√“®“√¬å π“¬·æ∑¬å∏’√– ∑Õß ß ∑’ËÕÕ°·∫∫ ®—¥∑”√Ÿª‡≈à¡·≈– Õ“√åµ°√“øî§

°”æ≈ ‡≈“À‡æÁ≠· ß ¿“§«‘™“»—≈¬»“ µ√å §≥–·æ∑¬»“ µ√å ¡À“«‘∑¬“≈—‡™’¬ß„À¡à

ºŸâ·µàß °”æ≈ ‡≈“À‡æÁ≠· ß «.∑.∫., æ.∫., ª√–°“»π’¬∫—µ√™—πÈ Ÿß∑“ß«‘∑¬“»“ µ√å°“√·æ∑¬å§≈‘π§‘ (»—≈¬»“ µ√å), «.«. (»—≈¬»“ µ√å∑«—Ë ‰ª), F.I.C.S., F.R.C.S.T., Cert. in Vascular Surgery (U. of Colorado, U.S.A.) √Õß»“ µ√“®“√¬å ¿“§«‘™“»—≈¬»“ µ√å §≥–·æ∑¬»“ µ√å ¡À“«‘∑¬“≈—¬‡™’¬ß„À¡à, ‡™’¬ß„À¡à 50202 «—π ‡¥◊Õπ ªï ‡°‘¥ 12 °ÿ¡¿“æ—π∏å 2497

VASCULAR SURGERY

“√∫—≠ µÕπ∑’Ë I. æ◊Èπ∞“π∑—Ë«‰ª·≈–°“√ª√–‡¡‘πºŸâªÉ«¬

∫∑∑’Ë 1 »—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥ ª√–«—µ‘»“ µ√å, ªí®®ÿ∫—π ·≈–Õπ“§µ ..........................................................3 ∫∑∑’Ë 2 °“√µ√«®√à“ß°“¬·≈–°“√ª√–‡¡‘πºŸâªÉ«¬‚√§À≈Õ¥‡≈◊Õ¥ ....................................................................9 ∫∑∑’Ë 3 «‘∑¬“»“ µ√åæ◊Èπ∞“π¢Õß‚√§À≈Õ¥‡≈◊Õ¥ .............................................................................................. 37 ∫∑∑’Ë 4 ¬“∑’Ë„™â „π‚√§À≈Õ¥‡≈◊Õ¥ .......................................................................................................................... 43 ∫∑∑’Ë 5 Antibiotics in Vascular Surgery ....................................................................................................... 53 ∫∑∑’Ë 6 Noninvasive Vascular Studies .......................................................................................................... 59 ∫∑∑’Ë 7 °“√µ√«®«‘π‘®©—¬∑“ß√—ß ’«‘∑¬“ ·≈–√—ß ’√à«¡√—°…“ ........................................................................... 71 ∫∑∑’Ë 8 À≈Õ¥‡≈◊Õ¥‡∑’¬¡·≈–°“√µ‘¥‡™◊ÈÕ ............................................................................................................ 81 ∫∑∑’Ë 9 °“√ª√–‡¡‘πºŸâªÉ«¬∑“ßÕ“¬ÿ√°√√¡ .......................................................................................................... 90

µÕπ∑’Ë II ‚√§À≈Õ¥‡≈◊Õ¥·¥ß

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥

∫∑∑’Ë 10 Cerebrovascular disease ................................................................................................................... 93 ∫∑∑’Ë 11 ·¢π¢“¥‡≈◊Õ¥ .......................................................................................................................................... 107 ∫∑∑’Ë 12 Abdominal Aortic Aneurysm (AAA)........................................................................................... 115 ∫∑∑’Ë 13 Aortoiliac Occlusive Disease (AIOD) ........................................................................................ 127 ∫∑∑’Ë 14 °“√√—°…“ Intermittent Claudication (IC) ‚¥¬‰¡àµâÕßºà“µ—¥ .................................................. 137 ∫∑∑’Ë 15 °“√‡ΩÑ“¥Ÿ·≈·≈–æ÷ß√–«—ß„πºŸâªÉ«¬∑’ËµâÕßºà“µ—¥ ................................................................................. 143 ∫∑∑’Ë 16 Renovascular Disease ...................................................................................................................... 149 ∫∑∑’Ë 17 Femoro-Popliteal-Tibioperoneal Occlusive Disease.......................................................... 159 ∫∑∑’Ë 18 Buergerûs Disease (Thromboangiitis Obliterans)................................................................ 167 ∫∑∑’Ë 19 Takayasuûs Arteritis............................................................................................................................ 173 ∫∑∑’Ë 20 Acute Arterial Occlusion ................................................................................................................. 177 ∫∑∑’Ë 21 Infected Aneurysm ............................................................................................................................. 189 ∫∑∑’Ë 22 The Diabetic Foot............................................................................................................................... 199

µÕπ∑’Ë III ‚√§¢ÕßÀ≈Õ¥‡≈◊Õ¥¥”·≈–√–∫∫πÈ”‡À≈◊Õß

207

∫∑∑’Ë 23 Surgical Treatment of Vericose Veins ....................................................................................... 209 ∫∑∑’Ë 24 Venous Thrombosis............................................................................................................................ 221 ∫∑∑’Ë 25 ‚√§¢Õß√–∫∫πÈ”‡À≈◊Õß .......................................................................................................................... 231

VII

VASCULAR SURGERY

µÕπ∑’Ë IV ∑—Ë«‰ª

247

∫∑∑’Ë 26 °“√¥Ÿ·≈ºŸâªÉ«¬À≈—ßºà“µ—¥À≈Õ¥‡≈◊Õ¥∑’Ë¢“ .......................................................................................... 249 ∫∑∑’Ë 27 °“√‡¬Á∫´àÕ¡·≈–µàÕÀ≈Õ¥‡≈◊Õ¥ ........................................................................................................... 253 ∫∑∑’Ë 28 Hemodialysis Access ........................................................................................................................ 261 ∫∑∑’Ë 29 ∫“¥‡®Á∫À≈Õ¥‡≈◊Õ¥ ................................................................................................................................. 273 ∫∑∑’Ë 30 °“√µ—¥π‘È«‡∑â“·≈–¢“„πºŸâªÉ«¬‚√§À≈Õ¥‡≈◊Õ¥ .................................................................................. 291 ∫∑∑’Ë 31 Lumbar Sympathectomy ................................................................................................................. 299

VIII

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥

¢ÕπâÕ¡‡°≈â“πâÕ¡°√–À¡àÕ¡∂«“¬‡ªìπæ√–√“™°ÿ»≈·¥à æ√–∫“∑ ¡‡¥Á®æ√–‡®â“Õ¬ŸàÀ—« ¿Ÿ¡‘æ≈Õ¥ÿ≈¬‡¥™ „π¡À“¡ß§≈«‚√°“ ∑’Ë∑√ß‡®√‘≠æ√–™π¡åæ√√…“ §√∫√Õ∫ 72 æ√√…“ ·≈– ¢ÕπâÕ¡ —°°“√– ·¥à ∫ÿ√æ“®“√¬å∑—Èßª«ß

∫∑∑’Ë 1 ∫∑∑’Ë 2 ∫∑∑’Ë 3 ∫∑∑’Ë 4 ∫∑∑’Ë 5 ∫∑∑’Ë 6 ∫∑∑’Ë 7 ∫∑∑’Ë 8 ∫∑∑’Ë 9

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥ ª√–«—µ‘»“ µ√å, ªí®®ÿ∫—π ·≈–Õπ“§µ °“√µ√«®√à“ß°“¬·≈–°“√ª√–‡¡‘πºŸâªÉ«¬‚√§À≈Õ¥‡≈◊Õ¥ «‘∑¬“»“ µ√åæ◊Èπ∞“π¢Õß‚√§À≈Õ¥‡≈◊Õ¥ ¬“∑’Ë „™â „π‚√§À≈Õ¥‡≈◊Õ¥ Antibiotics in Vascular Surgery Noninvasive Vascular Studies °“√µ√«®«‘π‘®©—¬∑“ß√—ß ’«‘∑¬“ ·≈–√—ß ’√à«¡√—°…“ À≈Õ¥‡≈◊Õ¥‡∑’¬¡·≈–°“√µ‘¥‡™◊ÈÕ °“√ª√–‡¡‘πºŸâªÉ«¬∑“ßÕ“¬ÿ√°√√¡

∫∑∑’Ë 1 ª√–«—µ»‘ “ µ√åª®í ®ÿ∫π— ·≈–Õπ“§µ ¢Õß»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥ ª√–«—µ‘»“ µ√å¢Õß»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥‡°‘¥¢÷Èπæ√âÕ¡°—π °—∫»—≈¬»“ µ√åÕÿ∫—µ‘‡Àµÿ·≈–»—≈¬»“ µ√å∑—Ë«‰ª ‡¡◊ËÕ√“« 800 ªï °àÕπ§√‘ µå°“≈ »—≈¬·æ∑¬å™“«Õ‘π‡¥’¬™◊ËÕ Srushuta ‰¥â‡¢’¬π µ”√“∑“ß»—≈¬°√√¡ Õ∏‘∫“¬∂÷ß«‘∏°’ “√Àâ“¡‡≈◊Õ¥∑’ÕË Õ°®“°∫“¥·º≈ ‚¥¬°“√„™â‡ âπ¥â“¬ºŸ°À≈Õ¥‡≈◊Õ¥À√◊Õ„™âπÈ”¡—π∑’µË ¡â ‡¥◊Õ¥√“¥·º≈ ‡ªìπ°“√ cauterize bleeding(1-5) „π»µ«√√…∑’Ë 2 Antyllus »—≈¬·æ∑¬å™“«‚√¡—π‰¥âÕ∏‘∫“¬∂÷ß«‘∏’°“√ºà“µ—¥√—°…“ aneurysm ‚¥¬°“√ºŸ°À—«∑â“¬·≈â«§«—°‡Õ“ content ÕÕ° „π ¡—¬π—Èπ°“√ ‡¬Á∫´àÕ¡À≈Õ¥‡≈◊Õ¥¥”·≈–À≈Õ¥‡≈◊Õ¥·¥ß‰¡à ‰¥âº≈ ‡π◊ËÕß®“° Õ—µ√“°“√µ‘¥‡™◊ÕÈ ·≈– thrombosis Ÿß¡“°(1,3,5) »—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥ ¡’««‘ ≤ — π“°“√‡√Á«¡“°„π™à«ß 35 ªï∑’Ë ºà“π¡“¢Õß»µ«√√…∑’Ë 20 ·≈–‰¥â·∫àß√–∫∫¢Õß‚√§À≈Õ¥‡≈◊Õ¥ ÕÕ°‡ªìπ(3,6) 1. À≈Õ¥‡≈◊Õ¥·¥ß 2. À≈Õ¥‡≈◊Õ¥¥” 3. ∑àÕπÈ”‡À≈◊Õß ªí≠À“∑’Ëæ∫‰¥â∫àÕ¬∑’Ë ÿ¥§◊Õ ‚√§À≈Õ¥‡≈◊Õ¥·¥ß µàÕ¡“°“√ µ√«®«‘π‘®©—¬æ‘‡»…¥’·≈–·¡àπ¬”¢÷Èπ ®÷ßæ∫·≈–«‘π‘®©—¬‚√§¢Õß À≈Õ¥‡≈◊Õ¥¥” ·≈–√–∫∫‰À≈‡«’¬ππÈ”‡À≈◊Õß‰¥â∫Õà ¬¢÷πÈ „πªï §.». 1902 Alexis Carrel ·≈– Charles Guthrie ‰¥â√“¬ß“π∂÷ß°“√‡¬Á∫µàÕÀ≈Õ¥‡≈◊Õ¥Õ¬à“ß¡’ª√– ‘∑∏‘¿“æ ‚¥¬«‘∏’ triangulation ‚¥¬¡’À≈—°°“√ ”§—≠„π°“√ªØ‘∫—µ‘µàÕÀ≈Õ¥‡≈◊Õ¥ ¥—ßµàÕ‰ªπ’(7)È

1. §’¡®—∫ ·≈–Àâ“¡‡≈◊Õ¥Õ¬à“ßπÿà¡π«≈ ‚¥¬„™â§’¡§’∫À≈Õ¥ ‡≈◊Õ¥∑’Ë ‰¡à∑”„ÀâÀ≈Õ¥‡≈◊Õ¥™È” 2. ≈Õ°™—πÈ adventitia ¢ÕßÀ≈Õ¥‡≈◊Õ¥ÕÕ°‡©æ“–∫√‘‡«≥ ∑’®Ë –‡¬Á∫µàÕ 3. √–«—ß‰¡à „Àâ‡π◊ÕÈ ‡¬◊ÕË —¡º— °—∫Õ“°“»‡¬Áπ·≈–·Àâß 4. „™â«∏‘ °’ “√‡¬Á∫µàÕ·∫∫ three stay sutures À√◊Õ triangulation 5. „™â¥“â ¬‡¬Á∫∑’¡Ë ¢’ π“¥‡≈Á°·≈–‡¢Á¡‡≈Á°‡™àπ°—π 6. ‡¬Á∫µàÕ intimal surface ¢ÕßÀ≈Õ¥‡≈◊Õ¥‡¢â“¡“®√¥°—π ·∫∫ everting suture ‚¥¬‡¬Á∫À≈Õ¥‡≈◊Õ¥∑ÿ°™—πÈ

°“√ºà“µ—¥À≈Õ¥‡≈◊Õ¥„π√–¬–·√° ‡√‘¡Ë µâπ®“° Robert Matas (§.». 1888-1940) ‡ªìπ»—≈¬·æ∑¬å ∑’∑Ë ”°“√ºà“µ—¥À≈Õ¥‡≈◊Õ¥¡“°∑’ Ë ¥ÿ „π¬ÿ§π—πÈ ‚¥¬∑”°“√ºà“µ—¥∂÷ß 620 √“¬ √âÕ¬≈– 80 ‡ªìπ°“√ºŸ°À≈Õ¥‡≈◊Õ¥·¥ß ·≈–√âÕ¬≈– 15 ‡ªìπ°“√‡¬Á∫´àÕ¡·´¡À≈Õ¥‡≈◊Õ¥(6) autogenous vein graft ‡√‘¡Ë π”¡“„™â‡¬Á∫∑¥·∑πÀ≈Õ¥‡≈◊Õ¥ ·¥ß „πªï §.». 1906 ·≈– 1907 ‚¥¬ Goyanes ·≈– Lexor. (8,9) °“√ºà“µ—¥ abdominal aortic aneurysm (AAA) ‚¥¬°“√ µ—¥ÕÕ°·≈–‡¬Á∫∑¥·∑π¥â«¬ human homograft ‡√‘¡Ë ∑”‚¥¬ Gross „πªï §.». 1951 ·≈– 1952

4 „π ß§√“¡‡°“À≈’ ªï §.». 1952(10) »—≈¬·æ∑¬å™“«Õ‡¡√‘°π— ∑’Ë ‡¢â“√à«¡√—°…“∑À“√∑’Ë ‰¥â√∫— ∫“¥‡®Á∫À≈Õ¥‡≈◊Õ¥ ‰¥âæ¬“¬“¡‡¬Á∫ µàÕ´àÕ¡·´¡·≈–„™âÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡∑ÿ°√“¬ ª√“°Ø«à“º≈°“√ √—°…“¥’∂ß÷ √âÕ¬≈– 96 ¡’Õµ— √“°“√µ—¥Õ«—¬«–‡æ’¬ß√âÕ¬≈– 13 ´÷ßË µà“ß®“°ª√– ∫°“√≥å „π ß§√“¡‚≈°§√—ßÈ ∑’Ë 2 ∑’∑Ë ”°“√√—°…“‚¥¬ °“√ºŸ°À≈Õ¥‡≈◊Õ¥‡æ’¬ßÕ¬à“ß‡¥’¬« ¡’Õ—µ√“°“√µ—¥Õ«—¬«– Ÿß∂÷ß √âÕ¬≈– 49 „πµÕππ—Èπ„™âÀπà«¬·æ∑¬å‡§≈◊ËÕπ∑’Ë∑”°“√√—°…“ºŸâ ªÉ«¬∑’‡Ë √’¬°«à“ Mobile Army Surgical Hospital (MASH units) ∑”°“√ºà“µ—¥·≈â« àßºŸªâ «É ¬°≈—∫¡“√—°…“¬—ß·π«À≈—ß „π ß§√“¡ ‡«’¬µπ“¡ °≈ÿ¡à »—≈¬·æ∑¬å ‰¥â®¥— µ—ßÈ Vietnam Vascular Registry √— ° …“ºŸâ ªÉ « ¬∫“¥‡®Á ∫ À≈Õ¥‡≈◊ Õ ¥·¥ß 1,000 √“¬ Õ¬à “ ß¡’ ª√– ‘∑∏‘¿“æ ‚¥¬°“√π”ºŸâªÉ«¬∫“¥‡®Á∫ àßµ—«®“° π“¡√∫ Õ¬à“ß√«¥‡√Á«¡“√—°…“„π‚√ßæ¬“∫“≈∑’Ë¡’»—≈¬·æ∑¬åÀ≈Õ¥‡≈◊Õ¥ æ∫«à“Õ—µ√“°“√µ—¥Õ«—¬«–¡’‡æ’¬ß√âÕ¬≈– 13

«‘«—≤π“°“√ “¢“·æ∑¬åÕ◊Ëπ∑’Ë¡’º≈µàÕ »—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥ µ—«·ª√À≈“¬ª√–°“√∑’Ë¡’º≈µàÕ§«“¡‡®√‘≠°â“«Àπâ“„π “¢“ »—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥ ‡™àπ ¢“¥ anticoagulants ∑’¡Ë ª’ √– ‘∑∏‘¿“æ °“√µ√«®«‘π‘®©—¬∑’Ë ‰¡à¥’æÕ, À≈Õ¥‡≈◊Õ¥‡∑’¬¡‰¡à¥’, °“√µ‘¥‡™◊ÈÕ ·≈– “‡Àµÿ°“√‡°‘¥ atherosclerosis ∑’·Ë ∑â®√‘ß´÷ßË ¬—ß‰¡à∑√“∫™—¥‡®π 1. Arteriography/ Angiography ‡√‘¡Ë µâπ„πªï §.». 1929 À≈—ß®“°§âπæ∫ water soluble organic iodides «‘∏’ °“√„™â “√∑÷ ∫ · ß‡æ◊Ë Õ ∂à “ ¬¿“æ√— ß ’ „ Àâ ¡ Õß‡ÀÁ π °“¬ «‘¿“§·≈–§«“¡º‘¥ª°µ‘¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß ¡’¥ß— µàÕ‰ªπ’È ‡®“–·≈– Õ¥ “¬ «πºà“πÀ≈Õ¥‡≈◊Õ¥°àÕπ©’¥ ’ ‡√‘¡Ë „πªï §.». 1927 translumbar aortic puncture „πªï §.». 1929 ·≈– percutaneous arterial catheterization Õ¥ “¬ «πºà“π‡¢â“∂÷ßÀ≈Õ¥‡≈◊Õ¥∑’ËµâÕß°“√°àÕπ©’¥ ’ „πªï §.». 1953 ´÷ßË ‡ªìπ«‘∏∑’ ª’Ë ≈Õ¥¿—¬∑’ Ë ¥ÿ ·≈– “¡“√∂ ‡ÀÁπ°“¬«‘¿“§ µ≈Õ¥®π§«“¡º‘¥ª°µ‘¢ÕßÀ≈Õ¥‡≈◊Õ¥ ·¥ß‰¥âÕ¬à“ß™—¥‡®π 2. «‘«≤ — π“°“√¢Õß anticoagulants ‡√‘¡Ë „™â heparin „πªï §.». 1937 ”À√—∫°“√√—°…“ deep vein thrombosis(11) ·≈–°“√ºà“µ—¥À≈Õ¥‡≈◊Õ¥·¥ß µàÕ¡“¡’¬“√—∫ª√–∑“π∑’Ë ‰¥âº≈¥’§◊Õ dicurmarol (Coumadin) º≈°“√ºà“µ—¥ À≈Õ¥‡≈◊Õ¥®÷ß¥’¢π÷È ¡“° ‚¥¬∑—«Ë ‰ª·≈â« heparin ®–„Àâ

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥ ºà“π∑“ßÀ≈Õ¥‡≈◊Õ¥¥”‡¢â“ Ÿ√à “à ß°“¬ ·µà „πªí®®ÿ∫π— Low Molecular Weight Heparin (LMWH) „Àâ‡¢â“ Ÿà √à“ß°“¬‰¥â ‚¥¬©’¥‡¢â“„µâº«‘ Àπ—ß 3. ¬“ªØ‘™«’ π– ¡’««‘ ≤ — π“°“√æ√âÕ¡°—π°—∫ anticoagulants ‡æ◊ÕË „™â§«∫§ÿ¡°“√µ‘¥‡™◊ÕÈ ·≈–ªÑÕß°—π graft failure 4. «‘«≤ — π“°“√„π¥â“πÕ◊πË Ê „πªí®®ÿ∫π— ‡√“∑√“∫∂÷ß‚√§∑“ß »—≈¬°√√¡À≈“¬‚√§∑’Ë¡’ à«π‡°’Ë¬«¢âÕß°—∫§«“¡º‘¥ª°µ‘ ∑“ß‡¡µ“‚∫≈‘ ¡å ‡™àπ aneurysm À√◊Õ§«“¡º‘¥ª°µ‘ ∑“ß¬’π å ‡™àπ atherosclerosis ‡§√◊ÕË ß¡◊Õºà“µ—¥™π‘¥„À¡à æ¬“∏‘ √’√¢Õß‚√§µà“ß Ê √«¡∑—Èß«‘∏’°“√ monitor ºŸâ ªÉ«¬∑—ßÈ °àÕπ·≈–À≈—ß°“√ºà“µ—¥

ARTERIAL SURGERY ¬ÿ§„À¡à¢Õß»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥ ‡√‘Ë¡®“°°“√ºà“µ—¥À—«„® „πªï §.». 1938 À≈—ß®“° Gross ∑”°“√√—°…“ PDA ‚¥¬°“√ºŸ°µ—¥ ·≈–„πªï §.». 1944 Blalock & Tausig ºà“µ—¥√—°…“ Tetralogy of Fallot ‚¥¬°“√µàÕ left subclavian artery ‡¢â“°—∫ pulmonary artery ·∫∫ end-toside anastomosis. ·≈–„πªï‡¥’¬«°—π »—≈¬·æ∑¬å™“« «’‡¥π ®“° Stockholm ‰¥âº“à µ—¥·°â ‰¢ Coarctation of the aorta ‰¥â ”‡√Á® §«“¡°â“«Àπâ“∑“ß°“√µ√«®«‘π®‘ ©—¬§◊Õ çnoninvasiveé diagnosis ‡™àπ °“√∑” ultrasound ·≈– ultrasonic duplex scanning «‘∏°’ “√ digital subtraction angiography æ∫«à“≈¥ª√‘¡“≥ °“√„™â “√∑÷∫· ß∑’Ë©’¥ºà“π‡¢â“À≈Õ¥‡≈◊Õ¥·¥ß≈ß ∑”„ÀâÕ—µ√“ ‡ ’¬Ë ßµàÕ°“√·æâ “√·≈–‡°‘¥æ‘…µàÕ‰µπâÕ¬≈ß magnetic resonance arteriography (MRA) ®–‡ÀÁπ direction of blood flow ‚¥¬‰¡àµâÕß©’¥ “√∑÷∫· ß ®–‡ÀÁπ·¡â °√–∑—ËßÀ≈Õ¥‡≈◊Õ¥¢π“¥‡≈Á° à«πª≈“¬·¢πÀ√◊Õ¢“∑’Ë¡’°“√¢“¥ ‡≈◊Õ¥

Occlusive and aneurysmal lesions Gross ·≈–§≥– ‰¥â‡√‘¡Ë ∑” arterial transplantation „πªï §.». 1940 ªï §.». 1951 Dubost ·≈–§≥– ‰¥âµ¥— aneurysmal sac ¢Õß AAA ÕÕ° ·≈–‡¬Á∫∑¥·∑π¥â«¬ homograft µàÕ¡“‰¥â¡’°“√»÷°…“À≈Õ¥‡≈◊Õ¥‡∑’¬¡∑¥·∑π„π√–¬–¬“« ‡æ◊ËÕÀ“«— ¥ÿ∑¥·∑π ‡√‘Ë¡µâπ®“°°“√„™â “√ —ß‡§√“–Àå∑’Ë∂—°„¬§◊Õ

ª√–«—µ‘»“ µ√åªí®®ÿ∫—π·≈–Õπ“§µ¢Õß»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥ Vinyon-N ‚¥¬ Voorhees „πªï §.». 1949(12,13) µàÕ¡“‰¥âπ” polytetra-fluoroethylene (PTFE) ¡“„™â ·≈–‰¥âæ¬“¬“¡ §‘¥§âπª√–¥‘…∞åÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡∑’¡Ë §’ ≥ ÿ ¡∫—µ¥‘ ‡’ ≈‘»¬‘ßË °«à“π’È

Thromboendarterectomy §.». 1946 J Cid dos Santos ‡√‘¡Ë ∑” thrombectomy √à«¡°—∫°“√„Àâ heparin ‚¥¬°“√∑” thrombectomy ®– æ¬“¬“¡≈Õ°‡Õ“™—πÈ intima ·≈– inner media ÕÕ° æ∫«à“‰¥â º≈„π°“√√—°…“¥’ ”À√—∫ carotid arterial occlusion ·≈– AIOD ∑’¡Ë ’ segment ∑’ÕË ¥ÿ µ—πÀ√◊Õµ’∫·§∫„π™à«ß —πÈ Ê ·≈–Õ¬Ÿà localized

The bypass principle ªï §.». 1931 Ernst Jeger ™“«‡¬Õ√¡—ππ’ ‡√‘¡Ë °“√ºà“µ—¥ bypass procedure „π°“√√—°…“ aneurysm ®π°√–∑—ßË §.». 1948 ®÷ß‰¥â‡√‘Ë¡∑” excising lesion ·≈–‡¬Á∫À≈Õ¥‡≈◊Õ¥‡∑’¬¡ ∑¥·∑π §.». 1948 J. Kunlin „™â saphenous vein graft µàÕ ·∫∫ end-to-side anastomosis ‡æ◊ËÕÀ≈’°‡≈’Ë¬ß°“√°√–∑∫ °√–‡∑◊ÕπµàÕÀ≈Õ¥‡≈◊Õ¥·≈–‡ âπª√– “∑√Õ∫¢â“ß √«¡∑—Èß‰¡à „Àâ °√–∑∫°√–‡∑◊ÕπµàÕ collaterals(8) §.». 1950 Robert Linton ®“° Massachusetes General Hospital „™â reversed saphenous vein graft ‡¬Á∫∑¥·∑π‡ªìπ arterial conduit ·≈–‡ªìπ «‘∏°’ “√ºà“µ—¥∑’¥Ë ‡’ ≈‘» ”À√—∫ reconstructive bypass.

Arterial embolectomy ‡√‘Ë¡∑”„πªï §.». 1911 ‚¥¬°“√√’¥À≈Õ¥‡≈◊Õ¥·¥ß√à«¡°—∫ suction º≈°“√√—°…“¬—ß‰¡à§àÕ¬¥’ ‡æ√“–À≈Õ¥‡≈◊Õ¥°√–∑∫ °√–‡∑◊Õπ¡“° ®π°√–∑—ßË ‡√‘¡Ë ∑”‡Õ“ heparin ¡“„™â√«à ¡(11) ·≈– „πªï §.». 1963 Thomas J. Fogarty ‰¥âª√–¥‘…∞å balloon tipped catheter ¢÷Èπ¡“ ∑”„Àâº≈°“√√—°…“¥’¢÷Èπ‡æ√“–¡’°“√°√–∑∫ °√–‡∑◊ÕπµàÕÀ≈Õ¥‡≈◊Õ¥·≈–‡ÕÁπ‚¥∏’‡≈’¬Ë ¡πâÕ¬

Aortic Aneurysm Resection ·≈– Aortoiliac bypass „π°“√√—°…“ AAA ¡—¬‚∫√“≥ Antyllus „™â«∏‘ °’ “√ºŸ°¥â“π ≈à“ß¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß„µâµÕà aneurysm ·≈–ª≈àÕ¬„Àâ‡°‘¥ clot ¿“¬„π aneurysmal sac §.». 1888 Matas „™â«‘∏’ endo-

aneurysmorrhaphy ´÷ßË °àÕπÀπâ“π’¡È «’ ∏‘ °’ “√∑—ßÈ °“√„™â·ºàπ cellophane ÀàÕÀÿ¡â À√◊Õ electro coagulation „πªï §.». 1951 Rene Dubost ‡√‘¡Ë µâπ«‘∏°’ “√ modern repair of AAA §.». 1957 DeBakey ·≈–§≥– „™â Knitted Dacron graft ‡¬Á∫∑¥·∑π aorta À≈—ß∑” aneurysmorrhaphy

Dissecting Aneurysm Gorin „πªï §.». 1935 ·≈– Shaw „πªï §.». 1955 ‰¥â√°— …“ dissecting aneurysm ‚¥¬«‘∏°’ “√ fenestration ·µàºªŸâ «É ¬∑—ßÈ 2 √“¬ ∂÷ß·°à°√√¡®“°¿“«–‰µ«“¬ §.». 1956 De Bakey ·≈– §≥– ‰¥âºà“µ—¥√—°…“ dissecting aneurysm ‡ªìπº≈ ”‡√Á® ‚¥¬„Àâ¬“≈¥§«“¡¥—π‚≈À‘µ®π√–¥—∫§«“¡¥—π‚≈À‘µ≈ß¡“Õ¬Ÿà „π √–¥—∫∑’Ë ‰¡àÕπ— µ√“¬ À≈—ß®“°π—πÈ ®÷ßæ‘®“√≥“ºà“µ—¥√—°…“

Carotid endarterectomy À≈—ß®“° “¡“√∂∑” cerebral arteriography ‰¥â®÷ß∑√“∫ «à“°“√Õÿ¥µ—πÀ√◊Õµ’∫·§∫¢Õß carotid artery ∑”„ÀâºŸâªÉ«¬¡’ Õ“°“√∑“ß ¡Õß §.». 1951 Carrea ºà“µ—¥À≈Õ¥‡≈◊Õ¥·¥ß carotid ‰¥â ”‡√Á® µàÕ¡“ Debakey „πªï §.». 1953 ·≈– Eastcott „πªï §.». 1954 ºà“µ—¥ carotid endarterectomy ‰¥â ”‡√Á® æ∫«à“∂â“ carotid artery µ’∫·§∫√âÕ¬≈– 70-99 °“√ºà“µ—¥∑” carotid endarterectomy ®–ªÑÕß°—π stroke ‰¥â

Femoro-popliteal bypass §.». 1948 Kunlin ‰¥â∑”°“√ºà“µ—¥‰¥â ”‡√Á®„π°“√√—°…“ºŸªâ «É ¬ À≈Õ¥‡≈◊Õ¥·¥ß popliteal µ’∫·§∫ „πªí®®ÿ∫—πæ∫«à“¡’ºŸâªÉ«¬ À≈Õ¥‡≈◊Õ¥·¥ß∑’Ë¢“µ’∫·§∫®”π«π¡“°∑’ËµâÕß°“√ºà“µ—¥√—°…“ ‡π◊ËÕß®“°ªí®®ÿ∫—π®”π«πª√–™“°√ºŸâ ŸßÕ“¬ÿ‡æ‘Ë¡¡“° ·≈–ºŸâªÉ«¬ ‡∫“À«“π¡’¡“°¢÷πÈ

Extra-anatomic bypass „πªï §.». 1952 Freeman ·≈– Leeds Õ∏‘∫“¬∂÷ß«‘∏°’ “√ superficial femoral artery bypass Blaisdell ·≈– Hall Õ∏‘∫“¬∂÷ßÀ≈—°°“√∑” extra cavitary bypass ®“° axillary artery ≈ß¡“¬—ß common femoral artery ‚¥¬‰¡àµÕâ ßºà“µ—¥‡¢â“ ™àÕß∑âÕß ∑” aorto - femoral bypass æ∫«à“«‘∏’°“√π’È

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‡À¡“– ¡ ”À√—∫ºŸªâ «É ¬¢“¢“¥‡≈◊Õ¥∑’¡Ë ’ underlying critically ill diseasesÕ¬Ÿà°àÕπ·≈â«‰¡à§«√ºà“µ—¥„À≠à ‡ªî¥‡¢â“™àÕß∑âÕßÀ√◊Õ ™àÕß∑√«ßÕ° extra-anatomic bypass ‡ªìπ alternative procedures ”À√—∫ intrathoracic À√◊Õ intramediastinal procedures „π°“√ºà“µ—¥√—°…“ occlusive disease ¢Õß aortic arch ·≈–·¢πß

ARTERIOVENOUS FISTULA Guido Guidi (§.». 1500-1559) Õ∏‘∫“¬∂÷ß°≈‰°¢Õß congenital AVM §√—ßÈ ·√° ´÷ßË æ∫‰¥âπÕâ ¬°«à“ traumatic AVM

Vascular access for dialysis „πªï §.». 1943 William Koff ‰¥âª√–¥‘…∞å ‰µ‡∑’¬¡¢÷πÈ ‡ªìπ ‡§√◊ÕË ß¡◊ÕÀ¬“∫ Ê ”À√—∫øÕ°‡≈◊Õ¥ºŸªâ «É ¬‰µ«“¬ µàÕ¡“ Quinton, Scribner ·≈– Dillard „πªï §.». 1960 ‰¥â§¥‘ ª√–¥‘…∞å shunt ∑’‡Ë À¡“– ¡„π°“√∑” dialysis À≈“¬§√—ßÈ ∑”®“°∑àÕ teflon „™â ‰¥â 3-6 ‡¥◊Õπ ¡’¢Õâ ‡ ’¬§◊Õ µ‘¥‡™◊ÕÈ ·≈–‡°‘¥ thrombosis ‰¥âß“à ¬ Appel „πªï §.». 1966 ‡√‘¡Ë ∑” surgically produced AVF ∑’‡Ë √’¬°«à“ Brescia- Cimino fistula ∫√‘‡«≥¢âÕ¡◊Õ ‚¥¬µàÕ cephalic vein ‡¢â“°—∫ radial artery ‰¥âº≈¥’ „™âøÕ°‡≈◊Õ¥‰¥âπ“π·≈– ¿“«–·∑√°´âÕπµà“ß Ê „π°“√„™â¡π’ Õâ ¬ ®÷ß‡ªìπ procedure of choice ”À√—∫ long term dialysis access µàÕ¡“‰¥â¡°’ “√„™â À≈Õ¥‡≈◊Õ¥‡∑’¬¡‡ªìπ bridging graft ”À√—∫ºŸâªÉ«¬∑’Ë ‰¡à “¡“√∂À“À≈Õ¥‡≈◊Õ¥¥”∑’Ë‡À¡“– ¡¡“ µàÕ‡¢â“°—∫À≈Õ¥‡≈◊Õ¥·¥ß∑’·Ë ¢π‰¥â AVF ”À√—∫°“√øÕ°‡≈◊Õ¥ „πºŸªâ «É ¬‰µ«“¬‡√◊ÕÈ √—ß√–¬– ÿ¥∑â“¬ ‡ªìπ°“√ºà“µ—¥»—≈¬°√√¡À≈Õ¥ ‡≈◊Õ¥∑’∑Ë ”∫àÕ¬∑’ Ë ¥ÿ „πªí®®ÿ∫π—

VENOUS SURGERY Venous interruption Virchow (§.». 1846-1856) ‰¥âµß—È ∑ƒ…Æ’æ¬“∏‘ ¿“æ„π°“√ ‡°‘¥ thromboembolism ¢÷πÈ ®“° Virchowûs triad §◊Õ stasis, hypercoagulability ·≈– endothelial injury Bottini „π§.». 1906 ‰¥â∑” IVC interruption ”‡√Á® ‡æ◊ÕË ªÑÕß°—π postoperative pulmonary embolism

§.». 1934 Homan ·π–π”«‘∏°’ “√ IVC ligation ‡æ◊ÕË ªÑÕß°—π pulmonary embolism ‡π◊ÕË ß®“°°“√ºŸ° femoral vein ‰¡à ‰¥â º≈„π°“√ªÑÕß°—π ·µà¡º’ ≈‡ ’¬§◊ÕÕ—µ√“µ“¬ Ÿß√âÕ¬≈– 14 ·≈–‡°‘¥ chronic venous insufficiency µ“¡¡“¿“¬À≈—ß Ÿß∂÷ß√âÕ¬≈– 33 µàÕ¡“‰¥â¡«’ ∏‘ °’ “√∑” IVC plication ‚¥¬„™â ‰À¡≈–≈“¬‚¥¬ Dale ·≈– external vena caval clip ∑”„ÀâÕ—µ√“µ“¬·≈– ¿“«–·∑√°´âÕπ≈¥≈ß¡“°¡“¬ §.». 1960 intraluminal devices ‡™àπ Green field filter ‰¥â‡√‘¡Ë π”¡“„™â ‚¥¬ Õ¥ºà“π femoral À√◊Õ jugular veins ∑”‚¥¬©’¥¬“™“‡©æ“–∑’Ë ‰¡àµÕâ ß¥¡¬“ ≈∫ Õ—µ√“ ‡ ’¬Ë ß®“°°“√ºà“µ—¥·≈–¿“«–·∑√°´âÕπ≈¥≈ß¡“°¡“¬

Ligation and stripping of varicose veins °“√√—°…“‚√§À≈Õ¥‡≈◊Õ¥¥”¢Õ¥¡’¡“µ—Èß·µà ¡—¬‚∫√“≥ ‰¥â ∫—π∑÷°°“√√—°…“‰«â‡¡◊ÕË °àÕπ §.». 370 ªï„π¬ÿ§¢Õß Hippocrates °àÕπ§.». 200 ªï Galen Õ∏‘∫“¬∂÷ß«‘∏°’ “√ stab avulsion °“√ ºà“µ—¥‡Õ“ greater saphenous vein ‚¥¬«‘∏’ stripping ‡√‘¡Ë „πªï 1844 ‚¥¬ Madelung ™“«‡¬Õ√¡—π Travel „πªï§.». 1900 ‰¥â∑” vein ligation ·≈– sclerotherapy §.». 1906 Mayo Õ∏‘∫“¬ ∂÷ß«‘∏°’ “√ extraluminal method ”À√—∫ vein stripping ·≈– Babcock ‰¥âª√–¥‘…∞å plastic intraluminal vein strippers ¢÷πÈ ®÷ß‡ªìπ«‘∏°’ “√ºà“µ—¥√—°…“¡“µ√∞“π¡“µ≈Õ¥ 100 ªï∑º’Ë “à π¡“

SYMPATHECTOMY sympathectomy ‡ªìπ«‘∏’°“√ºà“µ—¥ ”À√—∫‚√§À≈Õ¥‡≈◊Õ¥ À√◊Õ‚√§Õ◊πË Ê ∑’·Ë ¢π·≈–∑’¢Ë “ Julio Diez ™“«Õ“√å‡®πµ‘π“à ‰¥â∑” lumbar sympathectomy „πªï 1924 ´÷ßË °àÕπÀπâ“π’È „πªï §.». 1899 Jaboulay ·≈– Reneû Leriche ‰¥â∑”°“√µ—¥‡≈“– arterial adventitia À√◊Õ«‘∏°’ “√ periarterial sympathectomy ‡æ◊ÕË √—°…“ leg ulcer ·µà ‰¡à ‰¥âº≈‡æ√“–‡¢â“„®∂÷ß°≈‰°„π°“√§«∫§ÿ¡°“√À¥ ·≈–¢¬“¬µ—«¢ÕßÀ≈Õ¥‡≈◊Õ¥º‘¥æ≈“¥ „πªï§.». 1914 Kramer ·≈– Todd Õ∏‘∫“¬∂÷ß√–∫∫ ª√– “∑∑’Ë¡“‡≈’È¬ßÀ≈Õ¥‡≈◊Õ¥·¥ß´÷Ëß¡’º≈µàÕ°“√À¥·≈– ¢¬“¬µ—«¢ÕßÀ≈Õ¥‡≈◊Õ¥ „πªí®®ÿ∫π— revascularization procedures ‰¥âº≈¥’ ∑”„Àâ∫∑∫“∑„π°“√√—°…“‚√§À≈Õ¥‡≈◊Õ¥‚¥¬°“√∑” sympathectomy ≈¥≈ß ·µà°¬Á ß— ¡’∫∑∫“∑„π°“√√—°…“ periph-

ª√–«—µ‘»“ µ√åªí®®ÿ∫—π·≈–Õπ“§µ¢Õß»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥ eral vasospasm ·≈– occlusive disease ∑’Ë ‰¡à “¡“√∂®– revascularize ‰¥â ºŸªâ «É ¬∫“ß√“¬À≈—ß®“°∑” sympathectomy ·≈â«¬—ß°≈—∫¡“¡’ sympathetic activity ‰¥â‡À¡◊Õπ‡¥‘¡ ‡π◊ÕË ß®“°¡’ regeneration ¢Õß preganglionic fibers ·≈– accessory ganglions.

°“√µ—¥Õ«—¬«– ‡ªìπ«‘∏°’ “√√—°…“∑â“¬ ÿ¥‡¡◊ÕË «‘∏°’ “√Õ◊πË ‰¡à ‰¥âº≈ Õ’°·≈â« Syme „πªï§.». 1842 ‰¥âº“à µ—¥‡∑â“ºŸªâ «É ¬®÷ß‡ªìπ∑’¡Ë “ ¢Õß syme amputation ·≈– transmetatarsal amputation ‰¥â∑”„πªï §.». 1949 °“√µ—¥·¢π∂◊Õ‡ªìπ«‘∏°’ “√∑â“¬ ÿ¥„π°“√ √—°…“ºŸªâ «É ¬‚√§À≈Õ¥‡≈◊Õ¥ ‡¡◊ÕË ¡’¢Õâ ∫àß™’µÈ Õâ ßµ—¥∑‘ßÈ ‡æ√“–∂÷ß®– µ—¥‰ª·≈â«°Á¬—ß¡’ ‚Õ°“ ∑’Ë®–„ à·¢πÀ√◊Õ¢“‡∑’¬¡„ÀâºŸâªÉ«¬¡’™’«‘µÕ¬Ÿà „°≈â‡§’¬ß°—∫ ¿“æª°µ‘‰¥â §«√¡’Àπà«¬¥Ÿ·≈ºŸâªÉ«¬µ—¥Õ«—¬«– „Àâ°“√øóπô øŸ °“¬¿“æ∫”∫—¥ µ≈Õ¥®π‡µ√’¬¡·¢π¢“‡∑’¬¡„ÀâºªŸâ «É ¬

√— ° …“ºŸâ ªÉ « ¬°à Õ π°“√ºà “ µ— ¥ , ¢≥–ºà “ µ— ¥ ·≈–À≈— ß ºà “ µ— ¥ ∑“ß »—≈¬°√√¡À≈Õ¥‡≈◊Õ¥é „πªí®®ÿ∫π— ºŸ∑â ¡’Ë ’ ∑‘ ∏‘ Ï Õ∫«ÿ≤∫‘ µ— √§«√®– ºà“π°“√Ωñ°Õ∫√¡µàÕ¬Õ¥∑“ß»—≈¬°√√¡À≈Õ¥‡≈◊Õ¥‰¡àπÕâ ¬°«à“ 1 ªï †À≈—ßç°“√Ωñ°Õ∫√¡»—≈¬°√√¡∑—«Ë ‰ª¡“·≈â« 5 ªï ·≈–ºà“µ—¥ºŸâ ªÉ«¬‚√§À≈Õ¥‡≈◊Õ¥ 80 - 120 √“¬‡ªìπÕ¬à“ßπâÕ¬ „πª√–‡∑»‰∑¬‰¥â¡°’ “√√«¡°≈ÿ¡à »—≈¬·æ∑¬å∑¡’Ë §’ «“¡ π„®·≈– ºà“π°“√Ωñ°Õ∫√¡∑“ß¥â“π»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥®“°µà“ßª√–‡∑» µ—Èß‡ªìπ™¡√¡·æ∑¬å ‚√§À≈Õ¥‡≈◊Õ¥·Ààßª√–‡∑»‰∑¬ À√◊Õ Thai Vascular Society (TVS) „πªï§.». 1996 ‚¥¬¡’ √».πæ. √–«’ æ‘¡≈»“πµ‘Ï ‡ªìπª√–∏“π ·≈– √».πæ. ª√–‡ √‘∞ ‰µ√√—µπ«√°ÿ≈ ‡ªìπ‡≈¢“∏‘°“√ ‰¥â¡’°“√®—¥ª√–™ÿ¡øóôπøŸ·≈– —¡¡π“∑“ß«‘™“°“√ ‚√§À≈Õ¥‡≈◊Õ¥ µ≈Õ¥®π°“√Ωñ°‡™‘ßªØ‘∫µ— °‘ “√ vascular anastomosis ¡’«‘∑¬“°√®“°µà“ßª√–‡∑»¡“√à«¡ª√–™ÿ¡·≈–√à«¡®—¥ °‘®°√√¡∑“ß«‘™“°“√°—∫∑“ß√“™«‘∑¬“≈—¬»—≈¬·æ∑¬å·Ààßª√–‡∑» ‰∑¬¡“µ≈Õ¥ ®πªí®®ÿ∫—π¡’ ¡“™‘°‡æ‘Ë¡¢÷Èπ∂÷ß 200 ∑à“π ®“° ¡“™‘°°àÕµ—Èß‡¥‘¡ 16 ∑à“π „πÕπ“§µ§ß®– “¡“√∂®—¥°“√Ωñ° Õ∫√¡ “¢“‡©æ“–∑“ß»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥‰¥â

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„π™à«ßªï§.». 1961 - 1970 §«“¡‡®√‘≠°â“«Àπâ“∑“ß»—≈¬°√√¡ À≈Õ¥‡≈◊Õ¥ ‡ªìπ‰ªÕ¬à“ß√«¥‡√Á«·≈–µàÕ‡π◊ÕË ß ®π∑”„Àâ»≈— ¬·æ∑¬å °≈ÿ¡à ∑’¡Ë §’ «“¡ π„®∑“ß¥â“ππ’§È ¥‘ «à“§«√®–·¬°‡ªìπ “¢“«‘™“‡™’¬Ë «™“≠ ‡©æ“–‚√§µà“ßÀ“° §.». 1970 „πÕ‡¡√‘°“ ‰¥â¡°’ “√®—¥µ—ßÈ ¡“§¡ ∑’‡Ë °’¬Ë «¢âÕß°—∫»—≈¬°√√¡À≈Õ¥‡≈◊Õ¥§◊Õ The Society of Vascular Surgery ·≈– The International Society for Cardiovascular Surgery ·≈–æ∫«à“»—≈¬·æ∑¬å à«π„À≠à∑’Ëºà“µ—¥√—°…“‚√§ À≈Õ¥‡≈◊Õ¥º≈°“√√—°…“‰¡à¥’ ‡π◊ÕË ß®“°¢“¥§«“¡√Ÿæâ π◊È ∞“π ·π«∑“ß °“√‡¢â“∂÷ßºŸªâ «É ¬·≈–«‘∏°’ “√ºà“µ—¥‰¡à¥’ ∑—ßÈ Õß ¡“§¡®÷ß‰¥â „Àâ§” ·π–π”·≈–ª√÷°…“°—∫ American Board of Surgery «à“§«√®–¡’ °“√Ωñ°Õ∫√¡·æ∑¬åª√–®”∫â“π∑“ß Vascular Surgery ‚¥¬ „ÀâΩñ°Õ∫√¡µàÕ¬Õ¥®“°»—≈¬°√√¡∑—Ë«‰ªÕ’° 1 ªï ¢âÕ‡ πÕπ’È∂Ÿ° ªØ‘‡ ∏„πªï§.». 1972 ·µàÕ’° 10 ªïµàÕ¡“‰¥â¡’°“√Ωñ°Õ∫√¡ ·æ∑¬åª√–®”∫â“π “¢“»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥ ºŸâ∑’Ëºà“π°“√Ωñ° Õ∫√¡·≈–°“√ Õ∫ “¡“√∂„™â«≤ ÿ ∫‘ µ— √ The American Board of General Vascular Surgery ‰¥â ·µà°¬Á ß— ¡’§«“¡¢—¥·¬âß„π¢âÕ∑’Ë °”Àπ¥¢Õß American Board of Surgery Õ¬Ÿ«à “à çºŸ∑â º’Ë “à π°“√ Ωñ°Õ∫√¡»—≈¬»“ µ√å∑«—Ë ‰ª §«√¡’§«“¡√Ÿ§â «“¡‡¢â“„® „π°“√¥Ÿ·≈

„πªí®®ÿ∫π— °“√«‘π®‘ ©—¬‚√§‚¥¬«‘∏°’ “√ noninvasive diagnosis ¡’∫∑∫“∑¡“°¢÷Èπ ‡æ◊ËÕ∑’Ë®–æ‘®“√≥“«à“æ¬“∏‘ ¿“æ¢Õß‚√§À≈Õ¥ ‡≈◊Õ¥∑’æË ∫π—πÈ ¡§«√∑’®Ë –∑”°“√√—°…“À√◊Õ‰¡à ‘ßË ∑’§Ë «√§”π÷ß∂÷ß§◊Õ 1. ‰¡à§«√µ—¥ ‘π„®„π°“√√—°…“‚√§¢ÕßºŸªâ «É ¬®“°°“√¥Ÿ angiogram ‡æ’¬ßÕ¬à“ß‡¥’¬« §«√æ‘®“√≥“√à«¡°—∫ ª√–«—µ‘ ·≈–°“√µ√«®√à“ß°“¬¥â«¬ 2. °“√ºà“µ—¥À√◊Õ∑”À—µ∂°“√„π°“√√—°…“„¥ Ê §«√ª√–‡¡‘π ¡√√∂¿“æ¢Õßµπ‡Õß°àÕπ‡ ¡Õ 3. §«√æ‘ ® “√≥“·≈–µ— ¥ ‘ π „®„π°“√√— ° …“‚¥¬Õ‘ ß ∂‘ µ‘ ∑’Ë ‡™◊ÕË ∂◊Õ‰¥â 4. °“√√—°…“∑’Ëº‘¥æ≈“¥ Õ“®®–∑”„Àâ∂Ÿ°µ—¥¢“À√◊Õ·¢π∑‘Èß ªí®®—¬Õ◊Ëπ∑’Ë§«√π÷°∂÷ß√à«¡¥â«¬§◊Õ ª√–«—µ‘‡°à“ ·≈–ª√–«—µ°‘ “√ºà“µ—¥√—°…“§√—ßÈ °àÕπ 5. °“√µ√«®«‘π®‘ ©—¬‚¥¬«‘∏°’ “√µà“ß Ê §«√æ‘®“√≥“ª√–°Õ∫ °—∫ª√–«—µ·‘ ≈–°“√µ√«®√à“ß°“¬ ‚¥¬°“√¬÷¥À≈—°∑—ßÈ 5 ¢âÕπ’È ®–™à«¬°“√µ—¥ ‘π„®ºà“µ—¥√—°…“ À√◊Õ‰¡à ‚¥¬Õ‘ßÀ≈—°°“√∑“ß®√‘¬∏√√¡√à«¡¥â«¬

AMPUTATIONS

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«‘«—≤π“°“√„À¡à·≈–Õπ“§µ „πªí®®ÿ∫π— noninvasive diagnotic procedures ‰¥â¡§’ «“¡ °â“«Àπâ“·≈–«‘«≤ — π“°“√¡“°¢÷πÈ √«¡∑—ßÈ °“√√—°…“¡—°®–‡ªìπ·∫∫ less invasive surgery techniques ‰¥â¡°’ “√«‘®¬— ·≈–ª√–¥‘…∞å §‘¥§âπÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡∑’Ë¡’ª√– ‘∑∏‘¿“æ¥’°«à“‡¥‘¡ √–À«à“ß§.». 1980 - 1990 ‰¥â¡’°“√π”‡Õ“ laser ¡“√—°…“‚√§∑“ßÀ≈Õ¥ ‡≈◊Õ¥¥”·≈–À≈Õ¥‡≈◊Õ¥·¥ß√à«¡°—∫ balloon angioplasty Endovascular grafting ”À√—∫ AAA ‡ªìπ·π«∑“ß„À¡à „π°“√√—°…“‚√§À≈Õ¥‡≈◊Õ¥ ´÷ßË °”≈—ß‡ªìπ∑’ Ë π„® ‡√‘¡Ë ∑”„πªï §.». 1991 ‚¥¬ Parodi ‚¥¬ Õ¥ stent ºà“π‡¢â“∑“ß femoral artery

William Edward Jr. ‰¥â√“¬ß“π«‘∏°’ “√ endovascular grafting „π°“√√—°…“ AAA ®“°‚√ßæ¬“∫“≈ Nashville, Tenn. Vanderbilt ·≈– St. Thomas „π Annals of Surgery, May 1996. Interventional radiology ¡’∫∑∫“∑„π°“√√—°…“À≈Õ¥ ‡≈◊Õ¥µ’∫·§∫¡“°¢÷πÈ ‚¥¬„™â balloon tipped catheter (Dotter ·≈– Gruntzig „πªï §.». 1974) ‡ªìπ«‘∏’°“√ percutaneous transluminal angioplasty (PTA) ”À√—∫ laser ¡’∫∑∫“∑„π °“√√—°…“ intimal hyperplasia ∑’‡Ë ªìπ “‡Àµÿ¢Õß early restenosis ·µàµâÕß√–«—ß‰¡à „ÀâÀ≈Õ¥‡≈◊Õ¥∑–≈ÿ À≈—ß„™â laser µ—¥‡Õ“ à«π∑’Ë µ’∫·§∫·≈â«§«√„™â angioscope àÕß¥Ÿ«à“À≈Õ¥‡≈◊Õ¥·¥ß∑–≈ÿ À√◊Õ‰¡à

‡Õ° “√Õâ“ßÕ‘ß 1. Dale WA. The beginnings of vascular surgery. Surgery 1974;76:84956. 2. Barker W. A history of vascular surgery. In: Moore WS (ed.). Vascular Surgery: A comprehensive review. Philadelphia: WB Saunders, 1993;1-15. 3. Haimovici H. An historic overview of vascular surgery: Past record and new trends - a vision for the 1990 S. In: Haimovici H. (ed.). Vascular Surgery: Principles and techniques. Cambridge: Blackwell Science, 1996;1-10. 4. Friedman SG. A history of vascular surgery. New York: Futura Publishing, 1989. 5. Wilson S, Veith FJ, Hobson RW, Williams RA. Vascular Surgery: Principles and practice. New York: McGraw-Hill, 1994. 6. Smith LL. Surgeons and the evolution of vascular surgery. Archives of Surgery 1993;128:957-63.

7. Ewards WS, Edward PD. Alexis Carrel: Visionary Surgeon. Charles C. Thomas. Springfield. Illinois 1974. 8. Kunlin J, Treatment of arterial ischemia by long vein grafts. Rev Chir 1951;70:206-13. 9. Dale WA, DeWeese JA, Scott WJM. Autologous venous shunt grafts: Rationale and report of 31 for atherosclerosis. Surgery 1959;46:145-55. 10. Hughes CW. Arterial repair during the Korean War. Ann Surg 1958;147:555-66. 11. Murray G. Heparin in surgical treatment of blood vessels. Arch Surg 1940;40:307. 12. Voorhees AB, Jaretski A, Blakemore AH. The use of tubes constructed from Vinyon-N-cloth in bridging arterial defects. Ann Surg 1952;135:332-341. 13. Smith RB. Arthur B. Voorhees, Jr., pioneer vascular surgeon. J Vasc Surg 1993;18:341-47.

∫∑∑’Ë 2 °“√µ√«®√Ë“ß°“¬·≈–°“√ª√–‡¡‘π ºŸªÈ «Ë ¬‚√§À≈Õ¥‡≈◊Õ¥ ª— ® ®ÿ ∫ — π ‚√§À≈Õ¥‡≈◊ Õ ¥æ∫‰¥È ¡ “°¢÷ È π „πª√–™“°√‰∑¬ ‡π◊ËÕß®“°°“√¥”√ß™’«‘µ·≈–°“√√—∫ª√–∑“πÕ“À“√„°≈È‡§’¬ß°—∫ ∑“ßµ–«—πµ° ·æ∑¬Ï “¡“√∂µ√«®√Ë“ß°“¬·≈–„ÀÈ°“√«‘π®‘ ©—¬‚√§ ‰¥È·µË‡π‘Ëπ Ê Õ¬Ë“ß‰√°Áµ“¡ºŸÈªË«¬‚√§À≈Õ¥‡≈◊Õ¥·¥ß À≈Õ¥ ‡≈◊Õ¥¥”·≈–√–∫∫πÈ”‡À≈◊Õß ¬—ßµÈÕß°“√°“√µ√«®√Ë“ß°“¬æ‘‡»… ·≈–‡©æ“–‡®“–®ß‡æ◊ËÕ„ÀÈ ‰¥È°“√«‘π‘®©—¬‚√§°ËÕπ∑’Ë®–∑”°“√ ◊∫§Èπ·≈–µ√«®«‘π®‘ ©—¬‚¥¬«‘∏°’ “√æ‘‡»…‡©æ“–Õ¬Ë“ßÕ’°µËÕ‰ª „π∫∑π’®È –°≈Ë“«∂÷ß«‘∏°’ “√∑“ß§≈‘π§‘ „π°“√µ√«®√Ë“ß°“¬ºŸªÈ «Ë ¬ ‡©æ“–‚√§À≈Õ¥‡≈◊Õ¥·≈–√–∫∫πÈ”‡À≈◊Õß∑’Ë‡¢È“„®ßË“¬·≈–„™È „π ª—®®ÿ∫—π °“√µ√«®√Ë“ß°“¬·≈–ª√–‡¡‘πºŸÈªË«¬§«√∑”„πÀÈÕß∑’Ë¡’ · ß «Ë“ß·≈–Õÿ≥À¿Ÿ¡∑‘ æË’ Õ‡À¡“–

‚√§¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß I. °“√ª√–‡¡‘π¿“«–‰À≈‡«’¬π‚≈À‘µ¢Õß·¢π·≈–¢“ (µ“√“ß ∑’Ë 2.1 ·≈– 2.2)

1.1 °“√¥Ÿ·≈– —ß‡°µÕ“°“√ ≈—°…≥–¢Õß ’º‘« ºŸÈªË«¬∑’Ëº‘«¢“«´’¥ ®– —ß‡°µ‡ÀÁπ°“√ ‡ª≈’¬Ë π·ª≈ß¢Õß ’º«‘ ‰¥Èß“Ë ¬°«Ë“ºŸªÈ «Ë ¬∑’¡Ë ’ º’ «‘ §≈È” ∂È“¡’ °“√¢“¥‡≈◊Õ¥‰ª‡≈’È¬ß·¢π¢“º‘«®–´’¥¡“°‚¥¬‡©æ“– ª≈“¬π‘È«¡◊Õπ‘È«‡∑È“ ∂È“¡’°“√¢“¥ÕÕ°´‘‡®π√Ë«¡¥È«¬ º‘«

µ“√“ß∑’Ë 2.1 °“√ª√–‡¡‘πºŸªÈ «Ë ¬‚√§À≈Õ¥‡≈◊Õ¥·¥ß —ß‡°µ¥Ÿ ’º«‘ ¢ÕßºŸªÈ «Ë ¬„π¢≥–∑’Ë πÕπ√“∫ ¬°¢“ ·≈–«—¥ vascular angle ÀÈÕ¬¢“≈ß venous filling µ”·ÀπËß°¥∑—∫·≈–´Õ°π‘«È ‡∑È“ §≈” Õÿ≥À¿Ÿ¡¢‘ Õßº‘«Àπ—ß capillary refilling time ™’æ®√∑—«Ë √Ë“ß°“¬ ø—ß bruits „πµ”·ÀπËßµË“ß Ê «—¥§«“¡¥—π‚≈À‘µÀ≈Õ¥‡≈◊Õ¥·¥ß∑’·Ë ¢π ·≈–¢“ reactive hyperemic time

®–°≈“¬‡ªÁπ ’π”È ‡ß‘πÀ√◊Õ¡Ë«ß (purple-blue cyanosis) ‡¡◊ÕË „ÀÈºªÈŸ «Ë ¬πÕπ√“∫ ’¡«Ë ßπÈ”‡ß‘π∫√‘‡«≥ª≈“¬¡◊Õª≈“¬ ‡∑È“ ®–°≈—∫¡“´’¥‡À¡◊Õπ‡¥‘¡¿“¬„π‡«≈“‰¡Ë°«Ë’ π‘ “∑’ Vascular angle À√◊Õ Buergerûs angle §◊Õ¡ÿ¡∑’«Ë ¥— ‰¥È¢≥– ∑’ºË ªÈŸ «Ë ¬πÕπÀß“¬√“∫≈ß°—∫æ◊πÈ ∑’‡Ë √’¬∫ ·≈È«§ËÕ¬ Ê ¬° ¢“¢÷πÈ ®π°√–∑—ßË ‡∑È“´’¥ „π§πª°µ‘®– “¡“√∂¬°‡∑È“∑”¡ÿ¡ 90o ‚¥¬∑’ªË ≈“¬À—«·¡Ë‡∑È“¬—ß¡’ ™’ ¡¿Ÿ‡ªÁπª°µ‘ ·µË∂“È ¡’°“√

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µ“√“ß∑’Ë 2.2 ¢ÈÕ¡Ÿ≈ ”§—≠∑’∫Ë π— ∑÷° ”À√—∫ºŸªÈ «Ë ¬∑’‡Ë ªÁπ‚√§ ∑“ßÀ≈Õ¥‡≈◊Õ¥ ª√–«—µ‘ ∑’§Ë «√´—°«Ë“‡§¬¡’Õ“°“√·≈–Õ“°“√· ¥ß¥—ßµËÕ‰ªπ’ÀÈ √◊Õ‰¡Ë? 1. ‚√§À—«„® Õ“°“√¢Õß angina pectoris, °≈È“¡‡π◊ÕÈ À—«„®¢“¥ ‡≈◊Õ¥¡“‡≈’¬È ß ®—ßÀ«–‡µÈπ¢ÕßÀ—«„®º‘¥ª°µ‘ 2. claudication ∑’‡Ë °‘¥¢÷πÈ ‡°‘¥‡¡◊ÕË ‡¥‘π‰¥È√–¬–∑“ß‡∑Ë“‰√? „π √–¬–‡«≈“‡∑Ë“‰√? ¡’ ischemic rest pain À√◊Õ°“√‡ ◊ËÕ¡ ¡√√∂¿“æ∑“ß‡æ»„π‡æ»™“¬ (impotence) 3. transient ischemic attack (T.I.A) À√◊Õ stroke 4. °“√ Ÿ∫∫ÿÀ√’Ë Ÿ∫¡“π“π‡∑Ë“‰√? °’´Ë ÕßµËÕ«—π? 5. ‚√§‡∫“À«“π ‡ªÁπ¡“π“π‡∑Ë“‰√? √—°…“Õ¬Ë“ß‰√? ∂È“„™ÈÕπ‘ ÿ≈π‘ „™Èª√‘¡“≥‡∑Ë“‰√? 6. §«“¡¥—π‚≈À‘µ Ÿß ‡ªÁπ¡“π“π‡∑Ë“‰√? √—°…“·≈–§«∫§ÿ¡¥È«¬ ¬“Õ–‰√? 7. §«“¡º‘¥ª°µ‘„π°≈‰°°“√·¢Áßµ—«¢Õß‡≈◊Õ¥? ‡§¬‡ªÁπ deep vein thrombosis (DVT) À√◊Õ pulmonary embolism À√◊Õ‰¡Ë? 8. ª√‘¡“≥‰¢¡—π„π‡≈◊Õ¥ Ÿßº‘¥ª°µ‘

¢“¥‡≈◊Õ¥ ¬°∑”¡ÿ¡ 15-30o ‡∑È“°Á®–‡√‘¡Ë ´’¥·≈È« vascular angle ∑’πË ÕÈ ¬°«Ë“ 20o · ¥ß«Ë“¡’°“√¢“¥‡≈◊Õ¥¡“‡≈’¬È ß ¢“¡“° ¡ÿ¡∑’Ë«—¥‰¥È¡—°®–¡’µ—«‡≈¢„°≈È‡§’¬ß°—∫§«“¡¥—π ‚≈À‘µ∑’Ë«—¥‰¥È®“°À≈Õ¥‡≈◊Õ¥·¥ß∑’Ë¢“ ∂È“«—¥§«“¡ Ÿß ‡ªÁπ‡´Áπµ‘‡¡µ√„π√–π“∫‡¥’¬«°—∫°√–¥Ÿ° ‡µÕ√Ïπ—Ë¡∂÷ß Èπ ‡∑È“∑’Ë¬°‰«È ®π°√–∑—Ëß‡∑È“´’¥‡¬Áπ ®–‰¥Èµ—«‡≈¢∑’Ë „°≈È ‡§’¬ß°—∫§«“¡¥—πÀ≈Õ¥‡≈◊Õ¥·¥ß∑’¢Ë “‡ªÁπ¡‘≈≈‘‡¡µ√ª√Õ∑ (√Ÿª∑’Ë 2.1)

°“√µ√«®√Ë“ß°“¬ 1. «—¥§«“¡¥—π‚≈À‘µ ‡ª√’¬∫‡∑’¬∫°—π√–À«Ë“ß·¢π·≈–¢“∑—ßÈ Õß¢È“ß 2. §≈”™’æ®√ §≈”‰¡Ë ‰¥È = 0, §≈”‰¥È‡∫“ Ê = +1, §≈”‰¥È ª°µ‘ = +2, ·√ßº‘¥ª°µ‘ = +3, aneurysm = +4 CAROTID RADIAL FEMORAL POPLITEAL D.PEDIS POST. TIBIAL

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3. µ√«®¥Ÿ§«“¡º‘¥ª°µ‘¢ÕßÀ—«„® 4. ¥Ÿ§«“¡º‘¥ª°µ‘∑·Ë’ ¢π·≈–¢“ ‡™Ëπ perfusion, varicosities, trophic changes, ·º≈‡√◊ÕÈ √—ß, ‡π◊ÕÈ À√◊Õπ‘«È ∑’ÀË ≈ÿ¥ À“¬‰ª 5. abdominal aortic aneurysm (AAA) 6. ankle/ brachial index (ABI) ‡ª√’¬∫‡∑’¬∫√–À«Ë“ß¢È“ß ¢«“·≈–¢È“ß´È“¬ Capillary filling time À≈—ß®“°«—¥ vascular angle ·≈È« „ÀÈºªÈŸ «Ë ¬π—ßË ÀÈÕ¬¢“≈ß°—∫¢Õ∫‡µ’¬ß „π§πª°µ‘º«‘ Àπ—ß®– ‡ªÁπ ’™¡¿Ÿ „πºŸÈªË«¬∑’Ë¢“¥‡≈◊Õ¥¡“‡≈’È¬ß¢“®–‡ª≈’Ë¬π ®“° ’´’¥¡“‡ªÁπ™¡¿Ÿ·≈–·¥ß§≈È”„π∑’Ë ÿ¥ ®“°°“√∑’Ë¡’ ‡≈◊Õ¥¡“§—ËßÕ¬ŸË¿“¬„πÀ≈Õ¥‡≈◊Õ¥ΩÕ¬´÷Ëß¢¬“¬µ—« √–¬– µ—ßÈ ·µË‡√‘¡Ë π—ßË ÀÈÕ¬¢“®π°√–∑—ßË º‘«Àπ—ß°≈“¬‡ªÁπ ’™¡¿Ÿ§Õ◊ capillary filling time ∂È“π“π‡°‘π°«Ë“ 15-30 «‘π“∑’ ·≈–º‘«Àπ—ß¡’ ’·¥ß§≈È” · ¥ß«Ë“À≈Õ¥‡≈◊Õ¥¡“‡≈’È¬ß∑’Ë ¢“πÈÕ¬¡“° «‘∏°’ “√π’§È Õ◊ Buergerûs test (√Ÿª∑’Ë 2.2)

√Ÿª∑’Ë 2.1 °“√«—¥ vascular angle À√◊Õ Buergerûs angle ¡ÿ¡∑’Ë«—¥‰¥È®–¡’§Ë“„°≈È‡§’¬ß°—∫§«“¡¥—πÀ≈Õ¥‡≈◊Õ¥∑’Ë¢“

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√Ÿª∑’Ë 2.2 Buergerûs test „πºŸÈªË«¬∑’Ë¢“¢“¥‡≈◊Õ¥Õ¬Ë“ß√ÿπ·√ß

°. ‡∑È“´’¥¢≥–¬°¢÷πÈ ‡π◊ÕË ß®“°§«“¡¥—π‚≈À‘µ„πÀ≈Õ¥‡≈◊Õ¥·¥ßµË” ‰¡Ë “¡“√∂µÈ“π·√ß¥÷ß¥Ÿ¥¢Õß‚≈°‰¥È ∑”„ÀÈ¢“¥‡≈◊Õ¥‰ª‡≈’¬È ß∑’‡Ë ∑È“ ¢. ‡¡◊ÕË ÀÈÕ¬‡∑È“≈ßÀ≈—ß®“°¬°‡∑È“®–¡’ ’·¥ß§≈È”®“° reactive hyperemia ·≈–¡’‡≈◊Õ¥¡“‡≈’È¬ß¡“°¢÷Èπµ“¡·√ß¥÷ß¥Ÿ¥¢Õß‚≈°

Venous filling „ÀÈºªÈŸ «Ë ¬πÕπ√“∫∫π‡µ’¬ß„πÀÈÕß∑’ÕË ≥ ÿ À¿Ÿ¡‘ æÕ‡À¡“– ∂È“‰¡Ë¡’ª—≠À“°“√¢“¥‡≈◊Õ¥¡“‡≈’È¬ß·¢π¢“ À≈Õ¥‡≈◊Õ¥¥”„µÈº‘«Àπ—ß®–À¬ËÕπ·≈–¡’‡≈◊Õ¥¡“§—Ëßµ“¡ ª°µ‘ ·µË∂È“¡’°“√¢“¥‡≈◊Õ¥¡“‡≈’È¬ßÀ≈Õ¥‡≈◊Õ¥¥” ®– ·ø∫·≈–¡Õß‡ÀÁπ‡ªÁπ√Õ¬ ’πÈ”‡ß‘π®“ß Ê Õ¬ŸË „µÈº‘«Àπ—ß (guttering of the veins) (√Ÿª∑’Ë 2.3) §πª°µ‘¬°¢“¢÷πÈ √–¥—∫ Ÿß°«Ë“À—«„®À≈Õ¥‡≈◊Õ¥¥”„µÈº«‘ Àπ—ß®–§ËÕ¬ Ê ·ø∫ ≈ß ∂È“¡’°“√¢“¥‡≈◊Õ¥ ¬°¢“¢÷πÈ ∑”¡ÿ¡ 10-15o À≈Õ¥‡≈◊Õ¥ ¥”„µÈº«‘ Àπ—ß®–·ø∫·≈–¡Õß‡ÀÁπ‡ªÁπ√Õ¬ ’π”È ‡ß‘π®“ß Ê

Pressure areas §◊Õµ”·ÀπËß∑’∂Ë °Ÿ °¥∑—∫·≈–‡°‘¥·º≈‰¥Èß“Ë ¬ ‡™Ëπ Èπ‡∑È“ µ“µÿ¡Ë ¥È“ππÕ°·≈–„π ªÿ¡Ë ¥È“π¢È“ß π‘«È ‚ªÈß ·≈–π‘ È « °È Õ ¬ ª≈“¬π‘ È « ‡∑È “ ·≈–√Ë Õ ßπ‘ È « ‡∑È “ ΩË “ ‡∑È “ ∫√‘‡«≥‡À≈Ë“π’È¡—°®–‡°‘¥ trophic changes ·º≈·≈– °“√‡πË“µ“¬‡ ¡Õ ‡¡◊ËÕ¡’°“√¢“¥‡≈◊Õ¥ ®– —ß‡°µæ∫«Ë“ Àπ—ß∫√‘‡«≥π—Èπ®–Àπ“ ’¡Ë«ß§≈È” ¡’µÿË¡πÈ” ·º≈‡√◊ÈÕ√—ß ¡’ –‡°Á¥·ÀÈß ’¥”§≈ÿ¡Õ¬ŸË (√Ÿª∑’Ë 2.4)

√Ÿª∑’Ë 2.3 ≈—°…≥–¢Õß¢“∑’¢Ë “¥‡≈◊Õ¥¡“‡≈’¬È ß‡√◊ÕÈ √—ß º‘«Àπ—ßµ÷ß‡ªÁπ¡—π

√Ÿª∑’Ë 2.4 ∫√‘‡«≥¢Õß pressure area ´÷ßË ‡°‘¥·º≈‰¥Èß“Ë ¬ ‚¥¬‡©æ“–

¡’ trophic changes °≈È“¡‡π◊ÈÕ∑’ËπËÕß·ø∫≈’∫ ¡Õß‡ÀÁπ À≈Õ¥‡≈◊Õ¥¥”„µÈº«‘ Àπ—ß·ø∫‡ªÁπ√Õ¬ ’π”È ‡ß‘π®“ß (gutter ing of the veins)

metatarsal head ·≈–ª≈“¬π‘«È ‡∑È“ ‡≈Á∫‡∑È“Àπ“‡ªÁπÀ¬—° ‡ª√“–·µ°ßË“¬ (brittle nail)

»—≈¬»“ µ√ÏÀ≈Õ¥‡≈◊Õ¥

1.2 °“√§≈” Õÿ≥À¿Ÿ¡‘ —ß‡°µ·≈–§≈”‡ª√’¬∫‡∑’¬∫√–À«Ë“ß¢“∑—ßÈ Õß¢È“ß À≈—ß®“°„ÀÈºªÈŸ «Ë ¬Õ¬ŸË„πÀÈÕß∑’¡Ë Õ’ ≥ ÿ À¿Ÿ¡æ‘ Õ‡À¡“–ª√–¡“≥ 5 π“∑’ ¢≥–∑’Ëµ√«®√Ë“ß°“¬‰¡ËµÈÕß„™ÈºÈ“§≈ÿ¡§«√‡ª‘¥„ÀÈ ‚≈Ëß∫√‘‡«≥∑’Ë µÈÕß°“√µ√«® ∫√‘‡«≥¢ÕßºŸÈµ√«®∑’Ë®–„™È —¡º— §«“¡ÕÿËπ‡¬Áπ¢Õß º‘«Àπ—ßºŸªÈ «Ë ¬‰¥È¥§’ Õ◊ À≈—ßπ‘«È ¡◊Õ ‰¡Ë „™ËΩ“Ë ¡◊ÕÀ√◊ÕÕÿßÈ π‘«È ´÷ßË ¡’§«“¡ ÕÿËπ·≈–™◊ÈπÕ¬ŸË ∑”„ÀÈ·ª√º≈º‘¥æ≈“¥‰¥È „™ÈÀ≈—ßπ‘È«¡◊Õ —¡º— º‘«Àπ—ß∑’¢Ë “¢ÕßºŸªÈ «Ë ¬ ∫—π∑÷°√–¥—∫°“√‡ª≈’¬Ë π·ª≈ßÕÿ≥À¿Ÿ¡¢‘ Õß ¢“ Õ¬Ë“¥Ÿ·µË ’º‘«Àπ—ßÕ¬Ë“ß‡¥’¬««Ë“º‘« ’™¡¿Ÿ·≈È«®–µÈÕßÕÿËπ¥È«¬ ∫“ß§√—ßÈ º‘« ’™¡¿Ÿ·µË ¡— º— ·≈È«‡¬Áπ¡“°‡π◊ÕË ß®“°¡’°“√¢“¥‡≈◊Õ¥ Capillary refilling µ√«®‚¥¬„™Èπ«È‘ °¥≈ß∫π‡≈Á∫À√◊ÕÕÿßÈ ¡◊Õ ¢ÕßºŸªÈ «Ë ¬ª√–¡“≥ 2 «‘π“∑’·≈È«ª≈ËÕ¬ ®—∫‡«≈“µ—ßÈ ·µË ’ º‘«®“ß®π°√–∑—ßË °≈—∫¡“‡ªÁπ ’™¡¿Ÿ‡À¡◊Õπ‡¥‘¡«Ë“π“π‡∑Ë“‰√ „π¿“«–ª°µ‘®–‰¡Ë‡°‘π 2 «‘π“∑’ «‘∏’π’È‡ªÁπ°“√ª√–‡¡‘π ‡≈◊Õ¥∑’¡Ë “‡≈’¬È ßÀ≈Õ¥‡≈◊Õ¥ΩÕ¬«Ë“‡æ’¬ßæÕÀ√◊Õ‰¡Ë

°“√§≈”™’æ®√ ∫√‘‡«≥∑’§Ë ≈”™’æ®√‰¥Èß“Ë ¬§◊Õ Ë«π¢ÕßÀ≈Õ¥ ‡≈◊Õ¥·¥ß∑’Ë∑Õ¥¢È“¡°√–¥Ÿ°·≈–Õ¬ŸËµ◊Èπ„µÈº‘«Àπ—ß À≈Õ¥ ‡≈◊ Õ ¥§≈”™’ æ ®√‰¥È § ◊ Õ radial, femoral, brachial popliteal, dorsalis pedis, posterior tibial, carotid (√Ÿª∑’Ë 2.5) Femoral pulse ∫√‘‡«≥¢“Àπ’∫ ®–Õ¬ŸËµ√ß®ÿ¥°÷Ëß°≈“ß √–À«Ë“ß symphysis pubis °—∫ anterior superior iliac spine À≈Õ¥‡≈◊Õ¥®–Õ¬ŸË „µÈº«‘ Àπ—ß¡“°∂÷ß·¡È«“Ë ºŸªÈ «Ë ¬®– ¡’ À ≈Õ¥‡≈◊ Õ ¥·¥ß∑’ Õ ¬Ÿ Ë „ π¿“«– atherosclerosis §≈”™’æ®√‰¡Ë ‰¥È ·µË°Á®– “¡“√∂§≈”À≈Õ¥‡≈◊Õ¥‰¥È·¢Áß ‡ªÁπ≈” Dorsalis pedis pulse ®ÿ¥∑’§Ë ≈”‰¥È§Õ◊ ®ÿ¥°÷ßË °≈“ß√–À«Ë“ß medial malleoli ·≈–√ËÕß√–À«Ë“ß°√–¥Ÿ° metatarsal ∑’Ë 1 ·≈– 2 „π§πª°µ‘æ∫«Ë“§≈” pedal pulse ‰¡Ë ‰¥È√ÕÈ ¬ ≈– 10 ‚¥¬‰¡Ë‡ªÁπ‚√§À≈Õ¥‡≈◊Õ¥

√Ÿª∑’Ë 2.5 °“√§≈”™’æ®√¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß∫√‘‡«≥µË“ß Ê ¢Õß√Ë“ß°“¬

°“√µ√«®√Ë“ß°“¬·≈–°“√ª√–‡¡‘πºŸÈªË«¬‚√§À≈Õ¥‡≈◊Õ¥

√Ÿª∑’Ë 2.6 «‘∏’°“√§≈” popliteal pulse ‚¥¬„ÀÈ º Ÿ È ª Ë « ¬ πÕπÀß“¬

Popliteal pulse §≈”‰¥È§ÕË π¢È“ß¬“° ‡æ√“–‰¡Ë¡·’ π«∑Õ¥ºË“π °√–¥Ÿ° πÕ°®“°π’È¬—ßÕ¬ŸË≈÷°„µÈº‘«Àπ—ß ¡’«‘∏’°“√§≈”¥—ß µËÕ‰ªπ’§È Õ◊ (√Ÿª∑’Ë 2.6) „ÀÈºªÈŸ «Ë ¬πÕπÀß“¬°—∫æ◊πÈ √“∫™—π ‡¢Ë“∑”¡ÿ¡ 135o ‚¥¬ΩË“‡∑È“«“ß√“∫°—∫æ◊πÈ ºŸµÈ √«®„™Èπ«È‘ À—«·¡Ë¡Õ◊ ∑—ßÈ Õß¢È“ß«“ß≈ß∫π tibial tuberosities „™È π‘«È ∑’‡Ë À≈◊Õ§≈”À“·π«¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß´÷ßË Õ¬Ÿ∑Ë “ß¥È“π ≈Ë“ß popliteal fossa ‡¡◊ÕË §≈”‰¥È·≈È«°¥≈ß‡∫“ Ê ∑“∫ °—∫°√–¥Ÿ° tibia ™’æ®√∑’Ë§≈”‰¥È®–™—¥¢÷Èπ «‘∏’π’È®–‰¡Ë “¡“√∂§≈”™’æ®√ popliteal ∑’ Ë ßŸ °«Ë“À—«‡¢Ë“‰¥È ‡æ√“– À≈Õ¥‡≈◊Õ¥∫√‘‡«≥π—ÈπÕ¬ŸË≈÷°„µÈº‘«Àπ—ß¡’°≈È“¡‡π◊ÈÕ·≈– ‡ÕÁπæ—ßº◊¥§≈ÿ¡Õ¬ŸË

∫—π∑÷°§«“¡·√ß¢Õß™’æ®√µ”·ÀπËßµË“ß Ê ¢Õß√Ë“ß°“¬ (√Ÿª∑’Ë 2.7) ‚¥¬∑—«Ë ‰ª·≈È«‡√“·∫Ëß√–¥—∫§«“¡·√ß¢Õß™’æ®√ÕÕ°‡ªÁπ +3 ·√ß°«Ë“ª°µ‘À√◊Õ¡’ aneurysm, +2 ª°µ‘, +1 ‡∫“°«Ë“ª°µ‘ ·≈– 0 §≈”™’æ®√‰¡Ë ‰¥È‡≈¬ °“√«—¥ Ankle Pressure Index „ÀÈºªÈŸ «Ë ¬πÕπÀß“¬∫π‡µ’¬ß√“∫ „πÀÈÕß∑’¡Ë Õ’ ≥ ÿ À¿Ÿ¡æ‘ Õ‡À¡“– æ—π sphygmo cuff √Õ∫µÈπ·¢π §≈”µ”·ÀπËß¢Õß™’æ®√À≈Õ¥ ‡≈◊Õ¥·¥ß brachial ·≈È«„™È‡®≈∑“ „™È doppler probe ·µ–≈ß ∫πµ”·ÀπËß∑’Ë§≈”™’æ®√‰¥È ∑”¡ÿ¡ 45o Ÿ∫≈¡‡¢È“‰ª„π cuff ®π°√–∑—ßË ø—ß‡ ’¬ß°“√‡µÈπ¢ÕßÀ≈Õ¥‡≈◊Õ¥‰¡Ë ‰¥È §ËÕ¬Ê §≈“¬≈¡ÕÕ° ®πø—ß‡ ’¬ß™’æ®√‰¥È ∫—π∑÷°§Ë“ brachial systolic pressure ‰«È

√Ÿª∑’Ë 2.7 ∫—π∑÷°°“√§≈”™’æ®√·≈– ∫√‘‡«≥∑’Ëø—ß‰¥È bruit µ”·ÀπËßµË“ßÊ ∑—Ë«√Ë“ß°“¬

14 §≈”∑’‡Ë ∑È“À“µ”·ÀπËß¢Õß™’æ®√ dorsalis pedis À√◊Õ posterior tibial æ—π sphyg cuff ∫√‘‡«≥πËÕß‡Àπ◊ÕµËÕ¢ÈÕ‡∑È“ ∑“‡®≈≈ß∫π µ”·ÀπËß¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß À√◊Õ posterior tibial ·≈È««“ß doppler probe Ÿ∫≈¡‡¢È“®π°√–∑—Ëßø—ß‡ ’¬ß°“√‡µÈπ¢ÕßÀ≈Õ¥ ‡≈◊Õ¥‰¡Ë ‰¥È À≈—ß®“°π—πÈ ª≈ËÕ¬≈¡ÕÕ°®π°√–∑—ßË ø—ß‰¥È‡ ’¬ß™’æ®√‡µÈπ ∫—π∑÷° ankle systolic pressure „π°“√§”π«≥ ANKLE PRESSURE INDEX (ABI) „ÀÈ‡Õ“ ankle pressure µ—ßÈ À“√¥È«¬ brachial pressure §Ë“ª°µ‘¢Õß ABI ¡—°®–‡°‘π 1 ‡ ¡Õ

»—≈¬»“ µ√ÏÀ≈Õ¥‡≈◊Õ¥ Allen test ‡ªÁπ«‘∏°’ “√µ√«®¥Ÿ«“Ë radial ·≈– ulnar artery µ’∫µ—πÀ√◊Õ‰¡Ë ‚¥¬ºŸµÈ √«®„™Èπ«È‘ °¥≈ßµ√ßµ”·ÀπËß¢Õß radial ·≈– ulnar artery ¢ÕßºŸªÈ «Ë ¬°”·≈–§≈“¬¡◊Õ 3 §√—ßÈ ®π°√–∑—ßË ¡◊Õ´’¥ ·≈–ª≈ËÕ¬π‘«È ∑’°Ë ¥≈ß∫π ulnar artery ∂È“‰¡Ë¡°’ “√µ’∫µ—π‡≈◊Õ¥®–¡“‡≈’¬È ß∑’¡Ë Õ◊ ∑”„ÀÈº«‘ Àπ—ß ’™¡¿Ÿ ·µË∂È“¡’°“√µ’∫µ—π¡◊Õ®–¬—ß§ß¡’ ’´’¥ „™È«‘∏’‡¥’¬«°—π„π °“√µ√«®¥Ÿ°“√µ’∫µ—π¢Õß radial artery

√Ÿª∑’Ë 2.8 °“√«—¥ ANKLE-BRANCHIAL PRESSURE

°“√µ√«®√Ë“ß°“¬·≈–°“√ª√–‡¡‘πºŸÈªË«¬‚√§À≈Õ¥‡≈◊Õ¥ °“√∑”ß“π¢Õß°≈È“¡‡π◊ÕÈ ·≈–‡ Èπª√– “∑ ·¢πÀ√◊Õ¢“∑’¡Ë °’ “√ ¢“¥‡≈◊Õ¥Õ¬Ë“ß‡√◊ÕÈ √—ß º≈∑’µË “¡¡“§◊Õ°≈È“¡‡π◊ÕÈ ®–·ø∫≈’∫ °“√∑”ß“π¢Õß‡ Èπª√– “∑ —¡º— ·≈–‡§≈◊ËÕπ‰À«®–‡≈« ≈ß∑”„ÀÈ¡’°“√™“ ·≈–°“√¢¬—∫‡§≈◊ËÕπ‰À« ∑”ß“π®– ∫°æ√ËÕß‰¡Ë‡ªÁπ‰ªµ“¡¿“«–ª°µ‘

1.3 °“√ø—ß „™ÈÀøŸ ß— ¥È“π diaphragm ø—ßµ√ßµ”·ÀπËßµË“ß Ê ¢ÕßÀ≈Õ¥ ‡≈◊Õ¥∫√‘‡«≥„¥°Áµ“¡∑’Ë ß —¬«Ë“®–¡’°“√µ’∫µ—π ·π∫ÀŸø—ß°—∫ º‘«Àπ—ß‡∫“ Ê Õ¬Ë“°¥·√ß‡°‘π‰ª ‡¡◊ËÕ¡’°“√Õÿ¥µ—π¢ÕßÀ≈Õ¥ ‡≈◊Õ¥®–ø—ß‰¥È‡ ’¬ß bruit ·≈– turbulent flow „µÈµÕË ®ÿ¥∑’µË ∫’ ·§∫ «—¥§«“¡¥—π‚≈À‘µ∑’Ë·¢π∑—Èß Õß¢È“ß·≈–∫—π∑÷°‰«È «—¥§«“¡¥—π ‚≈À‘µ∑’¡Ë “®“°À≈Õ¥‡≈◊Õ¥·¥ß dorsalis pedis À√◊Õ posterior tibial ‚¥¬„™È blood pressure cuff æ—π√Õ∫πËÕßÀ√◊Õ∑’µË πÈ ¢“ (√Ÿª∑’Ë 2.8) ·≈È«ø—ß‚¥¬„™È doppler ultrasound §Ë“¢Õß§«“¡¥—π‚≈À‘µ ´’ ‚µ≈‘ § ∑’ Ë « — ¥ ‰¥È √ –À«Ë “ ß·¢π°— ∫ ¢“®–π”¡“‡ª√’ ¬ ∫‡∑’ ¬ ∫°— π ¿“¬À≈—ß‡ªÁπ ankle branchial index (ABI) ´÷Ëß‡ªÁπ¥—™π’∫Ëß ∫Õ°§«“¡√ÿπ·√ß„π°“√¢“¥‡≈◊Õ¥¢Õß¢“ Reactive hyperemia test “¡“√∂∫Ëß∫Õ°‰¥È∂÷ß§«“¡ √ÿπ·√ß„π°“√¢“¥‡≈◊Õ¥ «‘∏°’ “√µ√«®§◊Õ æ—π blood pressure cuff √Õ∫µÈπ¢“„ÀÈ§«“¡¥—π Ÿß 250 ¡‘≈≈‘‡¡µ√ ª√Õ∑π“π 3 π“∑’ À≈—ß®“°π—πÈ §≈“¬§«“¡¥—π≈ß „π§π ª°µ‘®–‡°‘¥ hyperemia À√◊Õ flushing ¢Õß¢“¢È“ß π—πÈ ¿“¬„π 1-2 «‘π“∑’ ·µË∂“È À≈Õ¥‡≈◊Õ¥·¥ßÕÿ¥µ—π®–„™È ‡«≈“π“π°«Ë“ 2 «‘π“∑’ À√◊Õª≈ËÕ¬·≈È«¢“¬—ß´’¥Õ¬ŸË Exercise test ¡’ª√–‚¬™πÏ „πºŸªÈ «Ë ¬¢“¢“¥‡≈◊Õ¥®“°À≈Õ¥ ‡≈◊Õ¥µ’∫µ—π∑’Ë¬—ß§≈”™’æ®√‰¥È ·µË‡∫“ «‘∏’°“√§◊Õ„ÀÈºŸÈ ªË«¬‡¥‘πÀ√◊Õ«‘ßË ®π°√–∑—ßË ª«¥¢“·≈È«§≈”™’æ®√Õ’°§√—ßÈ Àπ÷ßË ºŸÈªË«¬∑’Ë¡’°“√µ’∫·§∫¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß®–§≈”™’æ®√ ‰¡Ë ‰¥ÈÀ√◊Õ‡∫“≈ß¡“°‡æ√“–°≈È“¡‡π◊ÈÕ¢“®–·∫Ëß‡≈◊Õ¥‡Õ“ ‰ªÀ¡¥ «‘∏°’ “√π’ È “¡“√∂ª√–¬ÿ°µÏ ‰¥È°∫— °“√«—¥ ABI „π ™Ë«ßæ—°·≈–À≈—ß®“°°“√«‘Ëß·≈–‡¥‘π „π§πª°µ‘∑’Ë ‰¡Ë¡’ À≈Õ¥‡≈◊Õ¥Õÿ¥µ—πÀ≈—ß‡¥‘π ABI ®– Ÿß¢÷πÈ °«Ë“‡¥‘¡ „πºŸÈ ªË«¬À≈Õ¥‡≈◊Õ¥·¥ßµ’∫µ—πÀ≈—ß‡¥‘π·≈È« ABI ®–≈¥≈ß À√◊ÕÕ“®®–«—¥‡ª√’¬∫‡∑’¬∫‰¡Ë ‰¥È‡≈¬

II. §«“¡º‘¥ª°µ‘¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß„π°“√‰À≈ ‡«’¬π‚≈À‘µ 2.1 INTERMITTENT CLAUDICATION (IC) À¡“¬∂÷ß¿“«–°“√‡¥‘π°–‡º≈° Ê ‡ªÁπ Ê À“¬ Ê À√◊Õ ≈—∫°—π ‡ªÁπæ—° Ê Õ∏‘∫“¬‰¥È«Ë“‡ªÁπ°“√ª«¥°≈È“¡‡π◊ÈÕ´÷Ëß‡°‘¥¢÷Èπ√–À«Ë“ß °“√ÕÕ°°”≈—ß¢Õß·¢π·≈–¢“´÷ßË ¢“¥‡≈◊Õ¥ ª√–«—µ‘ ¡—°æ∫„π§πÕ“¬ÿ¡“°°«Ë“ 50 ª’ „π§πÕ“¬ÿπÕÈ ¬®–æ∫ ‰¥È „π¿“«– embolism ‚√§À≈Õ¥‡≈◊Õ¥‡™Ëπ Buergerûs disease, Takayasuûs disease À√◊ÕÀ≈Õ¥‡≈◊Õ¥·¥ßµ’∫µ—π¿“¬À≈—ß°“√ ∫“¥‡®Á∫ æ∫„π‡æ»™“¬¡“°°«Ë“‡æ»À≠‘ß ∂È“¡’°“√Õÿ¥µ—π∫√‘‡«≥ aortoiliac ®–¡’°“√‡ ◊ÕË ¡ ¡√√∂¿“æ∑“ß‡æ» (impotence) ¥È«¬ Õ“°“√ª«¥°≈È“¡‡π◊ÈÕ·∫∫ intermittent claudication ¡—°®–‡ªÁπÕ“°“√‡©æ“–∑’¡Ë ¢’ ÕÈ ∫Ëß™’∑È Ë’ ”§—≠¥—ßµËÕ‰ªπ’È 1. ºŸªÈ «Ë ¬®–√Ÿ È °÷ ª«¥°≈È“¡‡π◊ÕÈ ‚¥¬‡©æ“–Õ¬Ë“ß¬‘ßË ∑’πË ÕË ß§≈È“¬ °—∫‡ªÁπµ–§√‘« 2. Õ“°“√ª«¥®–‡°‘¥¢÷πÈ ‡¡◊ÕË ºŸªÈ «Ë ¬‡¥‘πÀ√◊Õ«‘ßË 3. Õ“°“√ª«¥®–À“¬‰ª‡¡◊ÕË À¬ÿ¥‡¥‘πÀ√◊Õ«‘ßË §«“¡√ÿπ·√ß·≈–√–¬–‡«≈“„π°“√ª«¥µË“ß°—π„πºŸªÈ «Ë ¬·µË≈– √“¬¢÷ÈπÕ¬ŸË°—∫µ”·ÀπËß·≈–§«“¡¡“°πÈÕ¬„π°“√Õÿ¥µ—π¢ÕßÀ≈Õ¥ ‡≈◊Õ¥ claudication ‡°‘¥‰¥ÈÀ≈“¬√–¥—∫‡™Ëπ ∑’°Ë πÈ –‚æ° µÈπ¢“ πËÕß·≈–‡∑È“ À√◊ÕÕ“®®–‡°‘¥√«¡ Ê °—π‡π◊ËÕß®“°¡’√–¥—∫°“√Õÿ¥ µ—πÀ≈“¬µ”·ÀπËß¢ÕßÀ≈Õ¥‡≈◊Õ¥ §”Õ∏‘∫“¬∑’ßË “Ë ¬∑’ Ë ¥ÿ ¢Õß claudication §◊ Õ cramping pain ∫√‘ ‡ «≥πË Õ ß´÷ Ë ß ®–‡°‘ ¥ ¢÷ È π ¿“¬À≈—ß°“√‡¥‘π™—Ë«√–¬–‡«≈“Àπ÷Ëß (claudication time) À√◊Õ ™Ë«ß√–¬–∑“ßÀπ÷Ëß (claudication distant) ‡¡◊ËÕæ—°·≈È«®–À“¬ ª«¥·≈–®–ª«¥Õ’°‡¡◊ÕË ‡¥‘π ºŸªÈ «Ë ¬®–¡’§«“¡√Ÿ È °÷ ™“Àπ÷∫ (numbness) ·≈–§≈È“¬°—∫¡’‡¢Á¡‡≈Á° Ê ∑‘¡Ë ·∑ßº‘«Àπ—ßµ≈Õ¥‡«≈“ √Ë«¡ °—∫™“º‘«Àπ—ß‡æ√“–¡’°“√·¬Ëß‡≈◊Õ¥®“°º‘«Àπ—ß‰ª¬—ß°≈È“¡‡π◊ÈÕ ·µËæÕ‡¥‘π‰ª‰¥È °— √–¬–Àπ÷ßË ®–ª«¥°≈È“¡‡π◊ÕÈ ‡π◊ÕË ß®“°¡’ metabolic waste products ·≈–°¥·≈§µ‘§§—ËßÕ¬ŸË „π°≈È“¡‡π◊ÈÕ®”π«π¡“° ·≈–‰À≈‡«’¬π‰¡Ë∑—π ºŸÈªË«¬Õ“®®–æ¬“¬“¡·°È ‰¢Õ“°“√‡À≈Ë“π’È ‚¥¬°“√‡¥‘π„ÀÈ™È“≈ß „π√“¬∑’Ë¡’°“√µ’∫µ—π¡“°¢÷Èπ√–¬–∑“ß·≈– ‡«≈“„π°“√‡¥‘π®– —Èπ≈ß‡√◊ËÕ¬ Ê ‰¡Ë§«√ —∫ π°—∫Õ“°“√ night cramp „π§π™√“´÷Ëß¡’ “‡Àµÿ¡“®“°°“√µÕ∫ πÕßµËÕ√–∫∫ ª√– “∑¢Õß°≈È“¡‡π◊ÕÈ ®“°°“√µ÷ßµ—«¡“°‡°‘π‰ª

16 °“√Õÿ¥µ—π¢ÕßÀ≈Õ¥‡≈◊Õ¥∫√‘‡«≥ aortoiliac ®–∑”„ÀÈºªÈŸ «Ë ¬¡’ claudication ¢Õß°Èπ –‚æ° ·≈–µÈπ¢“‡«≈“‡¥‘π Õ“°“√∑’¡Ë °— ®–æ∫√Ë«¡¥È«¬‡ ¡Õ§◊Õ calf claudication ·µË®–‡°‘¥‰¡Ë√ÿπ·√ß ª√‘¡“≥¢Õß°“√«‘ËßÀ√◊Õ‡¥‘π®π∑”„ÀÈ‡°‘¥Õ“°“√ª«¥‰¡Ë·πËπÕπ ∫“ß§√—ÈßπÕπæ—°·≈È«°Á¬—ß‰¡ËÀ“¬ª«¥ °“√ª«¥À≈—ß√È“«≈ß¢“∑’Ë¡’ “‡Àµÿ®“°°“√µ’∫·§∫¢Õß neurospinal canal √–¥—∫ lumbar „π§π ŸßÕ“¬ÿ Õ“°“√ª«¥Õ“®®–§≈È“¬°—∫ aortoiliac occlusive disease (AIOD) °“√¬◊ π ‡©¬ Ê ®–ª«¥√È “ «≈ß¢“À√◊ Õ ™“ ¡“°°«Ë“°“√‡¥‘π ‡æ√“–‡ªÁπ°“√‡æ‘¡Ë °“√§¥ßÕ¢Õß°√–¥Ÿ° —πÀ≈—ß ºŸÈªË«¬ AOID ¡—°®–¡’°“√‡ ◊ËÕ¡ ¡√√∂¿“æ∑“ß‡æ»√Ë«¡¥È«¬ ‡ ¡Õ„π‡æ»™“¬ venous claudication ¡’ “‡Àµÿ¡“®“°°“√Õÿ¥ µ—π¢ÕßÀ≈Õ¥‡≈◊Õ¥¥”µ√ßµ”·ÀπËß iliofemoral ®“° thrombus ´÷Ëß¡’ collaterals ·≈– recanalization ¬—ß‰¡Ë¥’æÕ ‡«≈“ºŸÈªË«¬ ‡¥‘πÀ√◊Õ«‘ßË ®–¡’°“√‡æ‘¡Ë ¢Õß arterial inflow ·µË venous outflow ‡°‘¥™È“·≈–§«“¡¥—π„πÀ≈Õ¥‡≈◊Õ¥¥”®– Ÿß¡“° À≈Õ¥ ‡≈◊Õ¥¥”∫√‘‡«≥µÈπ¢“®–∫«¡‡ªËß¡“°∑”„ÀÈ‡°‘¥°“√ª«¥µ÷ßÕ¬ŸπË “π (bursting pain) °“√ª«¥®–§ßÕ¬ŸËπ“π ‰¡ËÀ“¬‡√Á«‡À¡◊Õπ°—∫ °“√ª«¥®“°À≈Õ¥‡≈◊Õ¥·¥ßÕÿ¥µ—π

»—≈¬»“ µ√ÏÀ≈Õ¥‡≈◊Õ¥ °“√Õÿ¥µ—π¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ßµ”·ÀπËß∑’µË ”Ë °«Ë“À—«‡¢“≈ß¡“° ¡’ “‡Àµÿ®“°‚√§‡∫“À«“π À√◊Õ Buerger’s disease ¡“°°«Ë“‡°‘¥®“° arteriosclerosis ®–∑”„ÀÈ‡°‘¥°“√ª«¥∫√‘‡«≥À≈—ß‡∑È“·∫∫ drawing À√◊Õ cramping pain ¢≥–‡¥‘π√Ë«¡°—∫°“√™“Àπ÷∫À√◊Õ ∫√‘‡«≥º‘«Àπ—ß™“¥È“π‰√È§«“¡√Ÿ È °÷ —¡º— °“√µ√«®√Ë“ß°“¬ ¥Ÿ ’º‘«Àπ—ß¢Õß‡∑È“‡ª√’¬∫‡∑’¬∫°—π∑—Èß Õß¢È“ß «—¥ vascular angle „ÀÈºªÈŸ «Ë ¬¬°¢“¢÷πÈ æ√ÈÕ¡°—π∑—ßÈ Õß ¢È“ß¢≥–πÕπ√“∫·≈–„ÀÈ¬°Õ¬ŸπË “π®π°√–∑—ßË ºŸªÈ «Ë ¬√Ÿ È °÷ ª«¥ (√Ÿª∑’Ë 2.9) ¢“¢È“ß∑’¢Ë “¥‡≈◊Õ¥¡“‡≈’¬È ß®–ª«¥∑”„ÀÈºªÈŸ «Ë ¬§ËÕ¬ Ê ≈¥¢“ ≈ß¡“µË”°«Ë“¢È“ß∑’ªË °µ‘ ¥Ÿ venous filling µ√«®¥Ÿµ“¡µ”·ÀπËßªŸ¥ ‚ªπ¢Õß°√–¥Ÿ°‡∑È“¥Ÿ«Ë“¡’·º≈°¥∑—∫À√◊Õ‰¡Ë §≈”‡ª√’¬∫‡∑’¬∫ §«“¡‡¬Áπ¢Õßº‘«Àπ—ß ‡∑È“·µË≈–¢È“ß ∫—π∑÷°µ”·ÀπËß·≈–√–¥—∫∑’Ë √Ÿ È °÷ «Ë“‡¬Áπ §≈”™’æ®√‡ª√’¬∫‡∑’¬∫∑—ßÈ Õß¢È“ß «—¥§«“¡¥—π‚≈À‘µ ´’ ‚µ≈‘§¢Õß·¢π·≈–¢“‡¡◊ÕË π”¡“„™È‡ªÁπ ankle brachial ratio ‚¥¬‡©æ“–‡«≈“Õ¬ŸËπ‘Ëß·≈–ÕÕ°°”≈—ß°“¬ µ√«®¥Ÿ°“√≈’∫·ø∫ ¢Õß°≈È “ ¡‡π◊ È Õ πË Õ ß °“√ª«¥πË Õ ß·≈–°≈È “ ¡‡π◊ È Õ ®–µÈ Õ ß·¬° “‡Àµÿ¢Õß‚√§°√–¥Ÿ°·≈–¢ÈÕ µ√«®√–∫∫ª√– “∑Õ¬Ë“ß≈–‡Õ’¬¥ ‡æ◊ËÕ·¬°°“√ª«¥¢“®“°°“√°¥∑—∫‡ Èπª√– “∑∑’Ë¡’ “‡Àµÿ®“° ‚√§°√–¥Ÿ° —πÀ≈—ß (sciatica)

√Ÿª∑’Ë 2.9 „ÀÈºªÈŸ «Ë ¬πÕπ√“∫ ·≈–¬°‡∑È“¢÷πÈ æ√ÈÕ¡°—π∑—ßÈ Õß¢È“ß ¢È“ß ∑’Ë¢“¥‡≈◊Õ¥®–¡’ ’´’¥°«Ë“ ‡¡◊ËÕ¬°‰ª‰¥È√–¬–‡«≈“Àπ÷ËßºŸÈ ªË«¬®–§ËÕ¬ Ê ≈¥¢“¢È“ß∑’Ë¢“¥‡≈◊Õ¥≈ß‡π◊ËÕß®“°ª«¥

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2.2 ISCHEMIC REST PAIN §◊Õ °“√ª«¥¢“∑’‡Ë °‘¥¢÷πÈ µ≈Õ¥‡«≈“∑—ßÈ °≈“ß«—π·≈–°≈“ß§◊π ¡’ “‡Àµÿ®“°¢“¢“¥‡≈◊Õ¥¡“‡≈’È¬ßÕ¬Ë“ß√ÿπ·√ß ºŸÈªË«¬¡—°®–µÈÕßπ—Ëß À√◊ÕπÕπÕ¬Ÿ°Ë ∫— ∑’Ë µË“ß®“° claudication pain ´÷ßË ®–ª«¥¢“°ÁµÕË ‡¡◊ÕË ‡¥‘π «‘ßË À√◊ÕÕÕ°°”≈—ß°“¬ ª√–«—µ‘ ¡—°æ∫„πºŸªÈ «Ë ¬‡æ»™“¬ ŸßÕ“¬ÿ Õ“¬ÿ‡°‘π 60 ª’ „π §πÕ“¬ÿπÕÈ ¬®–¡’ “‡Àµÿ¡“®“°°“√∫“¥‡®Á∫¢ÕßÀ≈Õ¥‡≈◊Õ¥ ®“°Õÿ∫µ— ‡‘ Àµÿ À√◊Õ Buergerûs disease ª√–«—µ∑‘ ´Ë’ °— ‰¥È §◊Õ ºŸÈªË«¬®–∫Ëπª«¥¢“Õ¬ŸËµ≈Õ¥‡«≈“ ®π°√–∑—Ëß‰¡Ë “¡“√∂‡¥‘π‰ª¡“ À√◊ÕπÕπæ—°À≈—∫‰¥Èµ“¡ª°µ‘ ∫√‘‡«≥ ∑’Ëª«¥¡“°§◊Õ π‘È«‡∑È“·≈–À≈—ß‡∑È“„µÈµËÕ malleoli Õ“® ®–æ∫ ischemic ulcer À√◊Õ°“√‡πË“µ“¬¢Õßπ‘È«‡∑È“ √Ë«¡¥È«¬ ‡π◊ÈÕ‡¬◊ËÕ√Õ∫·º≈®–¡’ ’‡∑“‡«≈“·µ–¢Õ∫·º≈ ¢≥–∑”·º≈®–ª«¥· ∫ª«¥√ÈÕπ¡“° ª«¥√ÿπ·√ß·≈– π“π °“√√—∫ª√–∑“π¬“·°Èª«¥®–‰¡Ë∑”„ÀÈÀ“¬ª«¥∑—π∑’ Õ“°“√ª«¥®–≈¥≈ß‰¥È∂È“π—ËßÀ√◊ÕπÕπÀÈÕ¬¢“≈ß ºŸÈªË«¬ ¡—°®–À≈—∫‚¥¬°“√πÕπÀÈÕ¬¢“≈ß®“°‡µ’¬ß À√◊Õπ—ßË À≈—∫ ∫π‡°È“Õ’È °“√ÀÈÕ¬¢“≈ßπ“π Ê ®–∑”„ÀÈÀ≈—ß‡∑È“∫«¡ ºŸÈ ªË«¬∑’ËÀ≈—∫¡—°®–µ◊Ëπ¢÷Èπ¡“‡ÕßµÕπ°≈“ß§◊π®“°°“√ª«¥ ¢“Õ¬Ë“ß√ÿπ·√ß ´÷Ëß “‡Àµÿ¡“®“°°“√≈¥¢Õß cardiac output ¢“¡’‡≈◊Õ¥¡“‡≈’È¬ßπÈÕ¬≈ß ‡®Á∫ª«¥¡“°®πµÈÕß π«¥ª≈“¬‡∑È“ À√◊Õ≈ß¡“‡¥‘π°—∫æ◊Èπ‡¬Áπ„ÀÈÀ“¬ª«¥ °“√√—∫ª√–∑“π¬“·°Èª«¥®–∫√√‡∑“Õ“°“√ª«¥‰¥È∫È“ß ·µË®–µÈÕß‡æ‘¡Ë ª√‘¡“≥¬“„ÀÈ ßŸ ¢÷πÈ ‡√◊ÕË ¬ Ê ∂È“‰¡Ë·°È ‰¢§«“¡ º‘¥ª°µ‘®“°°“√Õÿ¥µ—π¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß Õ“°“√®– ‡≈«≈ß‡√◊ÕË ¬ Ê ºŸªÈ «Ë ¬®–ª«¥¢“¡“° ®π°√–∑—ßË ¢Õ√ÈÕß„ÀÈ ·æ∑¬Ïµ—¥¢“∑‘Èß ·≈–∂÷ß·¡È®–µ—¥¢“‰ª·≈È«ºŸÈªË«¬®–¬—ß¡’ §«“¡√ŸÈ ÷°ª«¥¢“‡À¡◊Õπ°—∫¬—ß¡’¢“Õ¬ŸË ‡ªÁπ Phantom limb sign ´÷Ëß®–µÈÕß„™È‡«≈“π“π„π°“√√—°…“ §«√´—° ª√–«—µº‘ ªÈŸ «Ë ¬«Ë“°ËÕπ∑’®Ë –¡’Õ“°“√¢Õß †ischemic rest pain ºŸªÈ «Ë ¬¡’°“√ª«¥¢“·∫∫ intermettent claudication ¡“°ËÕπÀ√◊Õ‰¡Ë √–¬–‡«≈“π“π‡∑Ë“‰√ ‡§¬¡’ª√–«—µ‘ ‚√§À≈Õ¥‡≈◊Õ¥·¥ß‚§‚√π“√’Ë·∫∫ angina ¡’°≈È“¡‡π◊ÈÕ ÕËÕπ·√ß µ“¡—«¡Õß‡ÀÁπ‰¡Ë™¥— stroke ª√–«—µ‚‘ √§‡∫“À«“π ·≈–ª√–«—µ‚‘ √§À≈Õ¥‡≈◊Õ¥„π§√Õ∫§√—« °“√µ√«®√Ë“ß°“¬∑—«Ë ‰ª ®–æ∫«Ë“ºŸªÈ «Ë ¬ÕËÕπ‡æ≈’¬·≈–ßË«ß´÷¡ µ≈Õ¥‡«≈“ ®“°°“√Õ¥πÕπ‡æ√“–‰¡Ë “¡“√∂À≈—∫‰¥È π‘∑ ‡π◊ËÕß®“°°“√ª«¥ ºŸÈªË«¬ªØ‘‡ ∏∑’Ë®–πÕπ√“∫À√◊Õ¬°

17 «“ß¢π“π°—∫¢Õ∫‡µ’¬ß ·¡È«“Ë ®–‡ªÁπ√–¬–‡«≈“ —πÈ Ê ‡æ√“– ®–ª«¥¢“¡“° §«√µ√«®√Ë“ß°“¬∑—«Ë ‰ªÀ“√ËÕß√Õ¬¢Õß‚√§ ∑’ÕË “®®–æ∫√Ë«¡‰¥È§Õ◊ §«“¡¥—π‚≈À‘µ Ÿß ·≈– bruit °“√µ√«®√Ë“ß°“¬‡©æ“–‚√§À≈Õ¥‡≈◊Õ¥ —ß‡°µÿ¥‡Ÿ ¡◊ÕË ºŸªÈ «Ë ¬ ÀÈÕ¬¢“≈ß ∫√‘‡«≥ª≈“¬‡∑È“®–‡ª≈’¬Ë π‡ªÁπ ’·¥ß§≈È”À√◊Õ‰¡Ë ª≈“¬π‘È«‡∑È“®–‡ªÁπ ’‡∑“À√◊Õ´’¥‡π◊ËÕß®“°‰¡Ë¡’‡≈◊Õ¥‰ª ‡≈’È¬ß‡≈¬ ∫“ß Ë«π¢Õßπ‘È«·≈– Èπ‡∑È“Õ“®®–¡’ ’¥”‡ªÁπ ª◊Èπ®“°°“√‡√‘Ë¡¡’°“√‡πË“µ“¬ ∂È“«“ß¢“„π·π«√“∫®–¡’ ’¢“«´’¥·≈–®ÿ¥¡Ë«ß§≈È”§≈È“¬À‘πÕËÕπ (marble like) À≈Õ¥‡≈◊Õ¥¥”„ÀÈº‘«Àπ—ß·ø∫·≈–¡Õß‡ÀÁπ‡ªÁπ‡ Èπ ’ πÈ”‡ß‘π ¬°¢“∑”¡ÿ¡ (vascular angle) ‰¥È ‰¡Ë‡°‘π 20o ºŸÈ ªË«¬∑’πË ßË— À≈—∫∫π‡°È“Õ’·È ≈–ÀÈÕ¬¢“≈ß À≈—ß‡∑È“®–∫«¡ ºŸÈ ªË«¬∑’πË Õπ√“∫‰¥È º‘«Àπ—ß∑’‡Ë ∑È“®–∫“ß„ ¡’≈°— …≥– atrophic change —ß‡°µÿ¥ºŸ «‘ Àπ—ß∫√‘‡«≥ pressure area ∑’Ë Èπ‡∑È“·≈–√–À«Ë“ßπ‘È«‡∑È“ Õ“®®–æ∫«Ë“‡√‘Ë¡¡’°“√‡πË“ µ“¬À√◊Õ·º≈‡√‘Ë¡¡’°“√Õ—°‡ ∫µ‘¥‡™◊ÈÕ ∫√‘‡«≥∑’Ë¡’°“√µ‘¥ ‡™◊ÕÈ ‰¥Èß“Ë ¬§◊Õ„µÈ‡≈Á∫ §≈”Õÿ≥À¿Ÿ¡¢‘ Õßº‘«Àπ—ß®–√Ÿ È °÷ «Ë“‡¬Áπ ‚¥¬‡©æ“–‡«≈“ÀÈÕ¬‡∑È“ æ∫«Ë“ capillary refilling ™È“ §≈”™’æ®√¢“¢È“ßπ—πÈ ‰¡Ë ‰¥È µÈÕß„™ÈÀøŸ ß— À√◊Õ doppler ultrasound ø—ß™’æ®√À√◊Õ bruit µ”·ÀπËßÀ≈Õ¥‡≈◊Õ¥∑’¢Ë “ ‚¥¬∑—Ë«‰ª·≈È«√–∫∫°≈È“¡‡π◊ÈÕ·≈–°√–¥Ÿ°¢ÕßºŸÈªË«¬¬—ß Õ¬ŸË „π ¿“æ„™Èß“π‰¥È πÕ°®“°®–π—ËßÀ√◊ÕπÕπÕ¬ŸËπ“π ®π°√–∑—ßË ‡°‘¥¿“«– disuse atrophy ¡’ flexion deformity ¢Õß¢ÈÕ –‚æ°À√◊Õ¢ÈÕ‡¢Ë“ √–∫∫ª√– “∑®–‡ªÁπ ª°µ‘∂È“‰¡Ë¡’‚√§‡∫“À«“π√Ë«¡¥È«¬ ´÷Ëß„πºŸÈªË«¬‡À≈Ë“π’È®– ‰¡Ë§ËÕ¬ª«¥¢“‡æ√“–√–∫∫ª√– “∑ —¡º— ‡ ◊ËÕ¡ÀπÈ“∑’Ë ‰ª π“π·≈È«

2.3 PREGANGRENE AND GANGRENE Pregangrene À¡“¬∂÷ß¿“«–«‘°ƒµ‘¢ÕßÕ«—¬«–∑’Ë¡’°“√¢“¥ ‡≈◊Õ¥Õ¬Ë“ß√ÿπ·√ß ®π°√–∑—Ëß‡π◊ÈÕ‡¬◊ËÕ‡√‘Ë¡·ª√ ¿“æ·≈–‡πË“µ“¬ Õ“°“√‡√‘¡Ë µÈπ¢Õß pregangrene §◊Õ rest pain µ“¡∑’°Ë ≈Ë“«¡“ ·≈È«„π¢ÈÕ 2.2 ‚¥¬∑—«Ë ‰ª·≈È«‡π◊ÕÈ ‡¬◊ÕË ∑’¢Ë “¥‡≈◊Õ¥®–°¥‡®Á∫ ºŸªÈ «Ë ¬ ∑’‡Ë √‘¡Ë ¡’Õ“°“√·≈–Õ“°“√· ¥ß¢Õß rest pain · ¥ß«Ë“‡π◊ÕÈ ‡¬◊ÕË Õ¬ŸË√–À«Ë“ßµ“™—Ëß¢Õß‡ªÁπ°—∫µ“¬ ®–µÈÕß√’∫∑”°“√√—°…“·≈– ø◊πÈ øŸ ¿“æÕ¬Ë“ß√’∫¥Ë«π Gangrene À¡“¬∂÷ß °“√µ“¬¢Õß‡π◊ÕÈ ‡¬◊ÕË ∑’¡Ë ’ “‡Àµÿ¡“®“° °“√¢“¥‡≈◊Õ¥ (√Ÿª∑’Ë 2.10) ‡π◊ÈÕ‡¬◊ËÕ∑’Ëµ“¬®–¡’ ’¥”À√◊Õ ’πÈ”µ“≈ §≈È”·≈–®–§ËÕ¬À¥µ—«≈ß‡ªÁπ –‡°Á¥À√◊Õ°ÈÕπ·¢Áß Ê ∂È“‰¡Ë¡’°“√

»—≈¬»“ µ√ÏÀ≈Õ¥‡≈◊Õ¥

√Ÿª∑’Ë 2.10 ‡∑È“ºŸªÈ «Ë ¬∑’ÕË ¬ŸË„π¿“«– ischemic rest pain ‡√‘Ë¡¡’ dry gangrene ¢Õßπ‘È«‡∑È“

‡πË“µ“¬ ≈ÿ°≈“¡ ‡π◊ÕÈ ‡¬◊ÕË ∑’µË “¬·≈È«®–‰¡Ë√ ÈŸ °÷ ‡®Á∫ √Õ¬µËÕ√–À«Ë“ß ‡π◊ÕÈ ‡¬◊ÕË ∑’‡Ë ªÁπ°—∫µ“¬®–µË“ß°—πÕ¬Ë“ß™—¥‡®π ‡ªÁπ line of demarcation ‡π◊ÕÈ ‡¬◊ÕË ∑’µË “¬®–À≈ÿ¥≈Õ°ÕÕ°‰ª‡Õß ‚¥¬‡©æ“–ª≈“¬π‘«È (autoamputation) ‡π◊ÕÈ ‡¬◊ÕË ∑’¬Ë ß— ¥’‡Àπ◊Õ line of demarcation ®–ª«¥·≈–°¥‡®Á∫‡™Ëπ‡¥’¬«°—∫∑’æË ∫„π ischemic rest pain ´÷ßË ·µ°µË“ß®“°°“√‡πË“µ“¬¢Õß‡π◊ÈÕ‡¬◊ËÕ∑’Ë‡°‘¥®“°·√ß°√–·∑°®“° Õÿ∫—µ‘‡Àµÿ‡©æ“–∑’Ë ‡æ√“–‡π◊ÈÕ‡¬◊ËÕ√Õ∫¢È“ß®–‰¡Ëª«¥ ‡π◊ÈÕ‡¬◊ËÕ∑’Ë µ“¬·≈È«¡’°“√µ‘¥‡™◊ÈÕ¿“¬À≈—ß®–°≈“¬ ¿“æ®“° –‡°Á¥·¢Áß‡ªÁπ ∫«¡πÿ¡Ë ¡’ÀπÕß‡´“–Õ¬ŸµË √ß¢Õ∫ line of demarcation ‡√’¬°«Ë“ wet gangrene æ∫‰¥È „πºŸªÈ «Ë ¬‡∫“À«“π

2.4 ISCHEMIC ULCERATION ‡ªÁπ·º≈∑’‡Ë °‘¥®“°°“√¢“¥‡≈◊Õ¥ ®–‡°‘¥„π¿“«– ischemic rest pain ¡’°“√ª«¥¢“Õ¬Ë“ß√ÿπ·√ß ∑’Ë·º≈¡’‡≈◊Õ¥ÕÕ°πÈÕ¬¡’ πÈ”‡À≈◊Õß„ ´÷¡ÕÕ°¡“ ¡—°®–¡’ª√–«—µ‘«Ë“∂Ÿ°¢Õß¡’§¡∫“¥À√◊Õ °√–∑∫°—∫«—µ∂ÿ·¢Áß∑”„ÀÈ‡°‘¥∫“¥·º≈´÷ßË ‰¡ËÀ“¬°≈“¬‡ªÁπ·º≈‡√◊ÕÈ √—ß

∂÷ß·¡È«“Ë ®–¥Ÿ·≈√—°…“‡ªÁπÕ¬Ë“ß¥’ ·º≈®–¡’¢π“¥‚µ·≈–≈÷°¢÷πÈ ‡√◊ÕË ¬ Ê “‡Àµÿ¢Õß ischemic ulcer ¡’‰¥ÈÀ≈“¬‚√§µ“¡µ“√“ß∑’Ë 2.3 ‡™Ëπ atherosclerosis, scleredema, ‡∫“À«“π, ‚√§‰µ, Buerger’s disease, °“√©“¬√—ß ’, °“√∂Ÿ°°¥∑—∫π“π Ê, ∫“¥‡®Á∫À√◊Õ∂Ÿ°‰øøÈ“ ™ÍÕµ ‚¥¬∑—Ë«‰ª·≈È«ºŸÈªË«¬¡’ª√–«—µ‘‡ªÁπ‚√§À≈Õ¥‡≈◊Õ¥·¥ßÕÿ¥ µ—π¡“π“π·≈È« µ√«®æ∫√Ë“ß°“¬æ∫ ischemic ulcer ∑’ªË ≈“¬π‘«È ‡∑È“ ∫√‘‡«≥°¥∑—∫À√◊Õ´Õ°π‘È«‡∑È“ √Õ∫¢Õ∫·º≈®–ª«¥¡“° °“√∑” ·º≈·µË≈–§√—Èßª«¥¡“° ‡π◊ÈÕ‡¬◊ËÕ√Õ∫·º≈´’¥‡¬Áπ ·º≈Õ“®®–¡’ ¢π“¥‡≈Á°·µË≈°÷ „À≠ËÀ√◊Õµ◊πÈ ·∫∫ ·µË≈°— …≥– ”§—≠§◊Õ¢Õ∫·º≈‡ªÁπ punch out lesion ·º≈®–‰¡Ë “¡“√∂ À“¬‰¥È ‚¥¬¢Õ∫·º≈À¥‡¢È“¡“™π°—π °Èπ·º≈¡’‡π◊ÈÕ‡¬◊ËÕ ’‡∑“À√◊Õ ‡À≈◊Õß§≈ÿ¡´÷Ëß®–À≈ÿ¥≈Õ°·≈–µ‘¥‡™◊ÈÕ‰¥ÈßË“¬ º‘«Àπ—ß„°≈È¢Õ∫ ·º≈¡’ π’ ”È ‡ß‘π‡∑“ °Èπ·º≈¡’‡≈◊Õ¥¡“‡≈’¬È ß‰¡ËæÕ∑’Ë granulation tissue ®–‡®√‘≠‰¥È ∫“ß√“¬∑’Ë·º≈‡°‘¥¢÷ÈπÕ¬ŸËπ“π ·º≈®–≈÷°≈ß‰ª ∂÷ß°√–¥Ÿ°·≈–¢ÈÕµËÕ Õ“®®–¡Õß‡ÀÁπ°√–¥Ÿ°À√◊Õ‡ÕÁπæ—ßº◊¥∑’°Ë πÈ ·º≈ ¡’ “√πÈ”„ Ê À√◊Õ¡’ÀπÕßªπ‰À≈´÷¡ÕÕ°¡“®“°°Èπ·º≈ ‡π◊ÕÈ ‡¬◊ÕË

°“√µ√«®√Ë“ß°“¬·≈–°“√ª√–‡¡‘πºŸÈªË«¬‚√§À≈Õ¥‡≈◊Õ¥ µ“√“ß∑’Ë 2.3 “‡Àµÿ¢Õß ISCHEMIC ULCERATION °“√µ’∫·§∫¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß¢π“¥„À≠Ë®“° atherosclerosis embolism °“√Õÿ¥µ—π¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß¢π“¥‡≈Á°®“° Raynaudûs disease Scleredema Embolism ‡∫“À«“π “‡ÀµÿÕπË◊ ‡™Ëπ °“√°¥∑—∫ √—ß ’∫”∫—¥ ‡π◊ÕÈ ‡¬◊ÕË ∫“¥‡®Á∫ ∂Ÿ°‰øøÈ“™ÍÕµ

√Õ∫·º≈¡’°“√¢“¥‡≈◊Õ¥™—¥‡®π §≈”™’æ®√‰¡Ë ‰¥È ª√– “∑ —¡º— Ÿ≠‡ ’¬ °≈È“¡‡π◊ÈÕ·ø∫ÕËÕπ·√ß reflexed ≈¥≈ß §«√µ√«® √–∫∫ª√– “∑ Ë«πª≈“¬√Ë«¡°—∫ ischemic ulcer µÈπµÕ¢Õß °“√‡°‘¥∫“¥·º≈®–¡“®“° sensory neuropathy ‡ ¡Õ (µ“√“ß∑’Ë 2.4, 2.5)

2.5 NEUROPATHIC ULCERATION ‚¥¬∑—Ë«‰ª·≈È«‡π◊ÈÕ‡¬◊ËÕ∑’Ë ‰¥È√—∫°“√∫“¥‡®Á∫À√◊Õ∂Ÿ°°√–∑∫ °√–‡∑◊Õπ®–ª«¥ Õ“°“√ª«¥‡ªÁπ°≈‰°ªÈÕß°—π µ—«∑’Ë ”§—≠¢Õß √Ë“ß°“¬‚¥¬‡©æ“–‡π◊ÈÕ‡¬◊ËÕ∑’Ë∂Ÿ°°¥∑—∫π“π Ê ·≈–¢“¥‡≈◊Õ¥‰ª ‡≈’È¬ß∂È“‡√“π—Ëß ¬◊πÀ√◊ÕπÕπ∑Ë“„¥∑Ë“Àπ÷Ëßπ“π Ê ‡π◊ÈÕ‡¬◊ËÕ Ë«π∑’Ë ∂Ÿ°°¥∑—∫®“°πÈ”Àπ—°¢Õß√Ë“ß°“¬®–¡’°“√ª«¥ ∑”„ÀÈµÕÈ ß¢¬—∫µ—« ‡ª≈’¬Ë πÕ‘√¬‘ “∫∂„ÀÈÀ“¬‡®Á∫À√◊Õ‡¡◊ÕË ¬¢∫ ∂È“‡√“‰¡Ë¢¬—∫‡≈¬‡π◊ÕÈ ‡¬◊ÕË Ë«ππ—πÈ ®–∂Ÿ°°¥∑—∫·≈–‡πË“µ“¬‰¥È¿“¬À≈—ß

µ“√“ß∑’Ë 2.5 §«√®–æ‘®“√≥“∫“¥·º≈µ“¡·π«∑“ß¥—ßµËÕ‰ªπ’È µ—«∫“¥·º≈‡Õß: µ”·ÀπËß¢Õß∫“¥·º≈·≈–®”π«π √Ÿª√Ë“ß·≈–¢π“¥ ¢Õ∫·≈– °Èπ·º≈ §«“¡≈÷°¢Õß∫“¥·º≈ °¥‡®Á∫·≈–Õÿ≥À¿Ÿ¡‡‘ ¬ÁπÀ√◊ÕÕÿπË discharge ∑’Ë ‰À≈´÷¡®“°·º≈ ‡π◊ÕÈ ‡¬◊ÕË √Õ∫·º≈: µ”·ÀπËß„°≈È°∫— Õ«—¬«–∑’ Ë ”§—≠ ≈—°…≥–‡π◊ÕÈ ‡¬◊ÕË µËÕ¡πÈ”‡À≈◊Õß „°≈È‡§’¬ß °“√‰À≈‡«’¬π‚≈À‘µ °“√∑”ÀπÈ“∑’¢Ë Õßª√– “∑ —¡º— ·≈–‡§≈◊ÕË π‰À«

neurotrophic ulcer ¡’ “‡Àµÿ¡“®“°‡π◊ÕÈ ‡¬◊ÕË ∫√‘‡«≥π—πÈ Ÿ≠ ‡ ’¬ª√– “∑ —¡º— √Ë«¡°—∫°“√¢“¥‡≈◊Õ¥¡“‡≈’¬È ß‡©æ“–·ÀËß ·º≈ ®–≈÷°§≈È“¬ ischemic ulcer ·≈–®–‡°‘¥∫√‘‡«≥∑’¡Ë °’ “√°¥∑—∫‡ ¡Õ ‡π◊ÈÕ‡¬◊ËÕ¢Õ∫·º≈¡’≈—°…≥–ª°µ‘·≈–°“√‰À≈‡«’¬π‡≈◊Õ¥¥’ ¡’¢ÈÕ™’È ∫Ëß„π°“√«‘π®‘ ©—¬ neurotrophic ulcer ¥—ßµËÕ‰ªπ’È (µ“√“ß∑’Ë 2.6) 1. ‰¡Ëª«¥·º≈ 2. ‡π◊ÕÈ ‡¬◊ÕË √Õ∫·º≈ Ÿ≠‡ ’¬ª√– “∑ —¡º— ∑”„ÀÈ ‰¡Ë√ ÈŸ °÷ ‡®Á∫ 3. ‡π◊ÕÈ ‡¬◊ÕË √Õ∫·º≈¡’°“√‰À≈‡«’¬π‡≈◊Õ¥‡ªÁπª°µ‘ ºŸ∑È Ë’ ‰¡Ë¡§’ «“¡™”π“≠·≈–‰¡Ë‡§¬‡ÀÁπºŸªÈ «Ë ¬≈—°…≥–π’®È –«‘π®‘ ©—¬ ‚√§‡ªÁπ ischemic ulcer ‡ ¡Õ ®÷ß§«√µ√«®¥Ÿ°“√∑”ß“πª√– “∑ Ë«πª≈“¬¢ÕßºŸªÈ «Ë ¬∑ÿ°√“¬ “‡Àµÿ¢Õß°“√‡°‘¥ neurotrophic ulcer ∑’ Ë ”§—≠§◊Õ 1. §«“¡º‘¥ª°µ‘¢Õß‡ Èπª√– “∑ Ë«πª≈“¬‡π◊ËÕß®“°‚√§ ‡∫“À«“π ∫“¥‡®Á∫¢Õß‡ Èπª√– “∑ ‚√§‡√◊ÕÈ π µ“√“ß∑’Ë 2.6 “‡Àµÿ¢Õß neurotrophic ulcers ´÷ßË ◊∫‡π◊ÕË ß ¡“®“°°“√ Ÿ≠‡ ’¬ª√– “∑ —¡º— Ë«πª≈“¬

µ“√“ß∑’Ë 2.4 “‡Àµÿ∑∑Ë’ ”„ÀÈ‡°‘¥·º≈‡√◊ÕÈ √—ß °“√Õ—°‡ ∫µ‘¥‡™◊ÕÈ ‰¥È√∫— °“√∫“¥‡®Á∫´È”´“° ‡π◊ÕÈ ‡¬◊ÕË ¢“¥‡≈◊Õ¥ ‡π◊ÕÈ ‡¬◊ÕË ∫«¡ Ÿ≠‡ ’¬ÀπÈ“∑’¢Ë Õß‡ Èπª√– “∑ Ë«πª≈“¬ ‚√§‡©æ“–∑’∑Ë ¡Ë’ °’ “√∑”≈“¬‡π◊ÕÈ ‡¬◊ÕË ‡™Ëπ ¡–‡√Áß ·≈–«—≥‚√§

§«“¡º‘¥ª°µ‘¢Õß‡ Èπª√– “∑ Ë«πª≈“¬ ‚√§‡∫“À«“π ‡ Èπª√– “∑∂Ÿ°µ—¥¢“¥ ‚√§‡√◊ÕÈ π §«“¡º‘¥ª°µ‘¢Õß‰¢ —πÀ≈—ß spina bifida tabes dorsalis syringomyelia

»—≈¬»“ µ√ÏÀ≈Õ¥‡≈◊Õ¥

2. §«“¡º‘¥ª°µ‘¢Õß‰¢ —πÀ≈—ß ‡™Ëπ spina bifida, tabes dorsalis, syringomyelia ‚√§‡∫“À«“πÕ“®®–‡ªÁπ “‡Àµÿ∑∑Ë’ ”„ÀÈ‡°‘¥ ischemic ulcer ‰¥È ‚¥¬®–‡°‘¥ atherosclerosis ¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß√Ë«¡°—∫§«“¡ º‘¥ª°µ‘¢Õß‡ Èπª√– “∑ Ë«πª≈“¬ ®÷ß§«√·¬°·¬– “‡Àµÿ¢Õß ∫“¥·º≈„πºŸªÈ «Ë ¬ ‡∫“À«“π„ÀÈ·πËπÕπ °ËÕπæ‘®“√≥“°“√√—°…“

2.6 OCCLUSIVE PERIPHERAL VASCULAR DISEASES Õ◊Ëπ Ê ∑’Ëæ∫‰¥È 2.6.1 THE LERICHEûS SYNDROME æ∫„π™“¬«—¬‡®√‘≠æ—π∏ÿÏ

™Ë«ßª≈“¬ ¡’ª√–«—µ‘ intermittent claudication ∑’°Ë πÈ ·≈–¢“∑—ßÈ Õß¢È“ß §≈”™’æ®√ femoral ‰¡Ë ‰¥È ¢“‡¬Áπ´’¥ °≈È“¡‡π◊ÈÕ≈’∫·ø∫ Õ«—¬«–‡æ»‰¡Ë·¢Áßµ—«µ“¡ª°µ‘ ‚¥¬ ∑—Ë«‰ª·≈È«ºŸÈªË«¬‚√§π’È®–¡’ thrombus ‰ªÕÿ¥µ√ßÀ≈Õ¥ ‡≈◊Õ¥·¥ß iliac ·≈–≈‘Ë¡‡≈◊Õ¥®–¢¬“¬¢π“¥≈ÿ°≈“¡ ®π°√–∑—ßË Õÿ¥∂÷ß®ÿ¥·¬°¢Õß aorta 2.6.2 THROMBOANGITIS OBLITERAN À√◊Õ Buergerûs disease æ∫‰¥È „π°≈ÿË¡§π¬‘« ·≈–™“«‡Õ‡´’¬ ‡æ»™“¬ Õ“¬ÿ‰¡Ë‡°‘π 50 ª’ Ÿ∫∫ÿÀ√’®Ë ¥— °“√¢“¥‡≈◊Õ¥¡—°®–‡√‘¡Ë ∑’Ë ¢“°ËÕπ·¢π ¡’ intermittent claudication µ“¡¥È«¬ º‘«Àπ—ß´’¥ ‡¬Áπ §≈”™’æ®√‰¡Ë ‰¥È ¡’·º≈‡√◊ÈÕ√—ß‡°‘¥¢÷Èπ∑’Ë ª≈“¬π‘È«¡◊Õπ‘È«‡∑È“ ∂È“¬—ß Ÿ∫∫ÿÀ√’ËµËÕ‰ªª≈“¬π‘È«®–‡πË“ µ“¬·≈–À≈ÿ¥≈Õ°‰ª‡Õß„π∑’ Ë ¥ÿ ºŸªÈ «Ë ¬ Buergerûs disease „π√–¬–·√° (inflamumatory phase) ®–æ∫ superficial migratory thrombophlebitis √Ë«¡¥È«¬ 2.6.3 COARCTATION OF THE AORTA ‡ªÁπ§«“¡º‘¥ª°µ‘ ·µË°”‡π‘¥¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß¢π“¥„À≠Ë∑æË’ ∫‰¡Ë∫ÕË ¬ ‡°‘¥ ®“°°“√µ’∫·§∫¢Õß aorta µ”·ÀπËß∑’ÕË ¬ŸµË ”Ë °«Ë“®ÿ¥‡√‘¡Ë µÈπ¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß subclavian ¢È“ß´È“¬ ∂È“ ductus arteriosus ª‘¥„πºŸªÈ «Ë ¬ coarctation of the aorta ®–‰¡Ë¡§’ «“¡º‘¥ª°µ‘¢ÕßÀ—«„®‡À¡◊Õπ°—∫°≈ÿ¡Ë ∑’¡Ë ’ patent ductus arteriosus Õ“°“√ ”§—≠§◊Õ ‡Àπ◊ÕË ¬ÀÕ∫ßË“¬À≈—ß ÕÕ°°”≈—ß ·≈–‡°‘¥ cerebro vascular accident (CVA) ´÷Ëß‡ªÁπº≈¡“®“°§«“¡¥—π‚≈À‘µ Ÿß¢Õß‡≈◊Õ¥·¥ß Ë«π ∫π¢Õß√Ë“ß°“¬ µ√«®√Ë“ß°“¬®–æ∫«Ë“§«“¡¥—π‚≈À‘µ∑’Ë «—¥‰¥È®“°·¢π∑—ßÈ Õß¢È“ß®– Ÿß°«Ë“∑’«Ë ¥— ‰¥È®“°¢“ §≈” ™’æ®√∑’Ë¢“‰¥È‡∫“ ¡’ collaterals ¡Õß‡ÀÁπ‰¥ÈÕ¬ŸË „µÈ

º‘«Àπ—ß∑’Ë ‰À≈Ë ÀπÈ“Õ°·≈–À≈—ß ø—ß‰¥È systolic murmur ∑’ÀË ≈—ßµ√ß left vertebral column ¢Õß T4 ·≈– T5 2.6.4 CEREBROVASCULAR INSUFFICIENCY Õ“°“√∑’æ Ë ∫ ‰¥È§◊Õ§«“¡º‘¥ª°µ‘∑“ß√–∫∫ª√– “∑·∫∫ transient neurologic deficit À√◊Õ transient ischemic attack ‡°‘¥§«“¡º‘¥ª°µ‘∑“ß√–∫∫ª√– “∑¿“¬„π‰¡Ë°’Ë«‘π“∑’ ·≈–‡ªÁπª°µ‘¿“¬„π 24 ™—«Ë ‚¡ß ‡™Ëπ µ“¡Õß‰¡Ë‡ÀÁπ¢È“ß ‡¥’¬«™—Ë«¢≥– (amaurosis fugax) µ“®–¡—«§√÷ËßÀπ÷Ëß ‡À¡◊Õπ¡’¡“Ë π∫—ß Õ“®®–√Ë«¡°—∫Õ—¡æ“µ¢Õß√Ë“ß°“¬¥È“π µ√ß°—π¢È“¡ Õ“°“√¢Õß vertebrobasilar insufficiency (VBI) §◊Õ ¡÷πßß «‘ß‡«’¬π»’√…–·≈–¡Õß‡ÀÁπ‰¡Ë™¥— ∑—ßÈ VBI ·≈– CVA ‡ªÁπº≈¡“®“°°“√µ’∫·§∫À≈Õ¥‡≈◊Õ¥·¥ß∑’Ë ‰ª‡≈’È¬ß ¡ÕßÀ√◊Õ·º≈¢ÕßÀ≈Õ¥‡≈◊Õ¥∑’Ë √È“ß microemboli ·≈È«À≈ÿ¥≈Õ¬µ“¡°√–· ‡≈◊Õ¥‰ªÕÿ¥À≈Õ¥ ‡≈◊Õ¥·¥ß∑’Ë retina ·≈– ¡Õß °“√µ√«®√Ë“ß°“¬§«√ µ√«®¥Ÿ visual field ‚¥¬„™È opthalmoscope ®–¡Õß ‡ÀÁπ√ËÕß√Õ¬§«“¡º‘¥ª°µ‘¢ÕßÀ≈Õ¥‡≈◊Õ¥∑’Ë fundi ´÷Ëß ‡°‘¥®“°°“√Õÿ¥µ—π¢Õß microemboli ¢ÕßÀ≈Õ¥‡≈◊Õ¥ ·¥ß®–µ’∫·§∫‡ªÁπ√–¬– yellow-white exudate √—«Ë ´÷¡®“°À≈Õ¥‡≈◊Õ¥∫“ß®ÿ¥ ¿“«–µ“¡—«¡Õß‰¡Ë‡ÀÁπ™—Ë« ¢≥–µÈÕß«‘π®‘ ©—¬·¬°®“°‚√§µËÕ‰ªπ’§È Õ◊ ‰¡‡°√π, disseminated sclerosis, temporal arteritis ·≈–Œ’ ∑’‡√’¬ §≈”™’æ®√À≈Õ¥‡≈◊Õ¥·¥ß subclavian ∑’Ë§Õ‡Àπ◊ÕµËÕ °√–¥Ÿ° clavicle ∂È“¡’°“√Õÿ¥µ—π¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß vertebral ®–ø—ß‰¥È bruit ∫√‘‡«≥À—«‰À≈Ë ∂È“¡’°“√µ’∫µ—π ¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß innominate À√◊Õ subclavian ®–‡°‘¥ collaterals §≈”™’æ®√‰¥È‡∫“·≈–«—¥§«“¡¥—π ‚≈À‘µ‰¥ÈµË”°«Ë“·¢π¥È“πµ√ß°—π¢È“¡ “‡Àµÿ∑’Ëæ∫‰¥È∫ËÕ¬ ¢Õß cerebrovascular insufficiency §◊Õ arteriosclerosis √Õß≈ß¡“§◊ Õ fibromuscular hyperplasia ¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß carotid ·≈– Takayasuûs artertis 2.6.5 GASTROINTESTINAL ISCHEMIA ºŸªÈ «Ë ¬®–ª«¥∑ÈÕß Õ¬Ë“ß√ÿπ·√ß¿“¬À≈—ß√—∫ª√–∑“πÕ“À“√‰ª‰¥È 15-30 π“∑’ Õ“°“√ª«¥·∫∫π’È§◊Õ çabdominal anginaé ¡—°®– ª«¥∑’ Ë ≈ ‘ È π ª’ Ë · ≈–∑— Ë « ∑È Õ ß ºŸ È ª Ë « ¬¡’ § «“¡°≈— « «Ë “ À≈— ß √— ∫ ª√–∑“πÕ“À“√·≈È « ®–ª«¥∑È Õ ß ®÷ ß ‰¡Ë ° ≈È “ ∑’ Ë ® – √—∫ª√–∑“πÕ“À“√ ∑”„ÀÈºÕ¡≈ß·≈–πÈ”Àπ—°µ—«≈¥≈ß¡“° °“√µ√«®√Ë“ß°“¬∑—«Ë ‰ª®–‰¡Ëæ∫§«“¡º‘¥ª°µ‘ ·µË®–ø—ß‰¥È bruit µ√ß®ÿ¥°÷ßË °≈“ß√–À«Ë“ß –¥◊Õ°—∫°√–¥Ÿ° xiphoid

°“√µ√«®√Ë“ß°“¬·≈–°“√ª√–‡¡‘πºŸÈªË«¬‚√§À≈Õ¥‡≈◊Õ¥ µ”·ÀπËß∑’µË ∫’ ·§∫¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ßÕ“®®–‡°‘¥∑’Ë celiac trunk À√◊Õ superior mesenteric artery «‘π®‘ ©—¬‚√§ ‰¥È ‚¥¬°“√∑” arteriography ·≈–§«√ºË“µ—¥√—°…“ ‡æ√“–∂È“ª≈ËÕ¬∑‘ßÈ ‰«ÈÀ≈Õ¥‡≈◊Õ¥®–Õÿ¥µ—π·≈–‡°‘¥ acute intestinal infraction 2.6.6 SUBCLAVIAN STEAL SYNDROME ∂È“¡’°“√µ’∫·§∫ ¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß subclavian Ë«πµÈπ °“√¢¬—∫ ·¢π¥È“π‡¥’¬«°—π®–·¬Ëß‡≈◊Õ¥∑’ºË “Ë π‰ª¬—ß vertebral artery ≈ß¡“‡≈’¬È ß∑’·Ë ¢π∑—ßÈ À¡¥ º≈∑’µË “¡¡“§◊Õ¢“¥‡≈◊Õ¥ ‰ª‡≈’È¬ß°È“π ¡Õß∑—π∑’∑—π„¥ ºŸÈªË«¬®–¡’Õ“°“√¡÷πßß ·≈–ø—ß‰¥È systolic murmur ∑’§Ë Õ¥È“π≈Ë“ß ·≈–∂È“°¥ common carotid artery ¥È“π‡¥’¬«°—π ®–¡’°“√≈¥¢Õß retrograde vertebral flow (the circle of Willis anastomosis) º≈µ“¡“§◊Õ ™’æ®√ radial ∑’§Ë ≈”‰¥È®–‡∫“≈ß (Õ∏‘∫“¬‚¥¬ Javid) «—¥§«“¡¥—π‚≈À‘µ ®–µË”°«Ë“·¢π ¥È“πµ√ß°—π¢È“¡¡“°°«Ë“ 50 ¡‘≈≈‘‡¡µ√ª√ÕÕ∑ 2.6.7 COSTOCLAVICULAR SYNDROME æ∫‰¥È „π§π™√“ ‡°‘¥ ®“°°≈È“¡‡π◊ÈÕ∑’Ë¬◊¥„ÀÈ°√–¥Ÿ° clavicle Õ¬ŸËÀË“ß®“° °√–¥Ÿ°´’Ë ‚§√ßÀ¬ËÕπµ—«≈ß (°≈È“¡‡π◊ÕÈ trapezius, sternocleidomastoid, levator scapulae) ∑”„ÀÈÀ≈Õ¥ ‡≈◊Õ¥·¥ß subclavian ∂Ÿ°°¥Õ¬Ÿ√Ë –À«Ë“ß°√–¥Ÿ° clavicle °—∫°√–¥Ÿ°´’Ë‚§√ß À√◊Õ¡’√ÕË ßπ’·È §∫Õ¬Ÿ·Ë ≈È«·µË°”‡π‘¥µ√«® √Ë“ß°“¬‚¥¬„ÀÈºŸÈªË«¬¬◊πÀÈÕ¬·¢π≈ß∑—Èß Õß¢È“ß §≈” ™’æ®√‡ª√’¬∫‡∑’¬∫ ·≈È«°“ß·¢π∑”¡ÿ¡©“°®—∫™’æ®√ À≈—ß®“°π—Èπ¬°·¢π¢÷Èπ‡Àπ◊Õ»’√…–®–æ∫«Ë“¢È“ß∑’Ë¡’§«“¡ º‘¥ª°µ‘®–§≈”™’æ®√‰¥È‡∫“≈ß 2.6.8 CERVICAL RIB SYNDROME æ∫‰¥ÈπÕÈ ¬√“« 0.4% ¢Õßª√–™“°√∑—ÈßÀ¡¥ √ÈÕ¬≈– 7 ¢ÕßºŸÈªË«¬æ∫«Ë“‡ªÁπ ∑—Èß Õß¢È“ß Ë«π„À≠Ë®–‰¡Ë¡’Õ“°“√º‘¥ª°µ‘ „π√“¬∑’Ë¡’ Õ“°“√®–æ∫«Ë“¡◊Õ·≈–π‘È«‡¬Áπ´’¥À√◊Õ cyanosis ∂È“¡’ mocroemboli À≈ÿ¥ÕÕ°®“°À≈Õ¥‡≈◊Õ¥·¥ß subclavian ®–Õÿ¥À≈Õ¥‡≈◊Õ¥‡≈Á° Ê Ë«πª≈“¬∑”„ÀÈ¡’°“√‡πË“µ“¬ ¢Õßπ‘«È ¡◊Õ °“√¬°·¢π Ÿß®–∑”„ÀÈÕ“°“√´’¥¢Õß¡◊Õ¥’¢πÈ÷ ·µË∂È“ÀÈÕ¬·¢π≈ß®–‡ªÁπ°“√‡°√Áß°≈È“¡‡π◊ÈÕ scalenus anticus æ∫«Ë“§≈”™’æ®√ radial ‰¥È‡∫“≈ß ø—ß‰¥È subclavian artery murmur §«√µ√«®√Ë“ß°“¬¥Ÿ°“√À—° æ—∫À√◊Õ‚°ËßßÕ¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß subclavian µ√ß thoracic outlet ·≈– supraclavicular fossa ∂È“°¥ ≈ß∫πÀ≈Õ¥‡≈◊Õ¥®–æ∫Õ“°“√¢“¥‡≈◊Õ¥∑—π∑’¢Õß·¢π

21 ¡—°®–§≈”‰¥È cervical rib ∫“ß√“¬®–§≈”‰¥È¬“°∂È“ °√–¥Ÿ°¢π“¥‡≈Á°·≈–¡’‡ÕÁπæ—ßº◊¥¬÷¥‚¥¬√Õ∫ 2.6.9 RAYNAUDûS PHENOMENON Õ“°“√·≈–Õ“°“√· ¥ß ∑’Ë ”§—≠§◊Õ°“√‡ª≈’Ë¬π ’º‘«®“°´’¥‡ªÁπ·¥ß ·≈–·¥ß §≈È”À√◊Õ¡Ë«ß ¿“¬À≈—ß®“° —¡º— °—∫§«“¡‡¬Áπ WBC W=white, B=blue, C=crimson red À≈—ß —¡º— §«“¡ ‡¬Áπº‘«®–´’¥®“°À≈Õ¥‡≈◊Õ¥·¢πß‡≈Á° Ê Ë«πª≈“¬À¥ µ—«Õ¬Ë“ß√ÿπ·√ß ∑”„ÀÈ‡π◊ÈÕ‡¬◊ËÕ¢“¥‡≈◊Õ¥ µËÕ¡“®–°≈“¬ ‡ªÁπ ’πÈ”‡ß‘π®“ßπ‘È«¡◊Õ®–‡¬Áπ™“ Õ∏‘∫“¬ª√“°Ø°“√≥Ï π—Èπ‰¥È«Ë“ deoxygenated blood ‡§≈◊ËÕπºË“πÀ≈Õ¥ ‡≈◊Õ¥ΩÕ¬™È“ Ê √Ë«¡°—∫¡’ venous congestion ®“° °“√À¥µ—«Õ¬Ë“ß√ÿπ·√ß¢ÕßÀ≈Õ¥‡≈◊Õ¥¥” Ë«πª≈“¬ º‘«Àπ—ß ’·¥ßÀ¡“¬∂÷ß¿“«–∑’Ë¡’‡≈◊Õ¥‰À≈ºË“πº‘«Àπ—ß ª√‘ ¡ “≥¡“° (reactive hyperemia) ‡°‘ ¥ ®“°°“√ µ“√“ß∑’Ë 2.7 “‡Àµÿ¢Õß RAYNAUDûS PHENOMENON °“√°√–µÿπÈ ª√– “∑ Ë«πª≈“¬®“° cervical spondylosis ·≈– cervical disc protusion æ∫‰¥È∫ÕË ¬ cervical ribs thoracic outlet syndrome spinal cord diseases poliomyelitis ‡ÕÁ¡‚∫‰≈¢Õß‡°√Á¥‡≈◊Õ¥®“°: subclavian aneurysm (º≈®“°°“√¡’ cervical rib) °“√µ’∫·§∫¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß subclavian °“√∫“¥‡®Á∫¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß subclavian ∑’∑Ë Õ¥ºË“π cervical rib, collagen disease Collagen disease scleredema „™È‡§√◊ÕË ß¡◊Õ∑”ß“π∑’¡Ë °’ “√ —πË –‡∑◊Õπ ‡™Ëπ °“√‡®“–À‘π ‡≈◊ÕË ¬‰øøÈ“ ∑”ß“π∑’ Ë ¡— º— °—∫§«“¡‡¬Áπµ≈Õ¥‡«≈“ §«“¡º‘¥ª°µ‘„π “√ª√–°Õ∫¢Õß‡≈◊Õ¥ ‡™Ëπ cold aggluti nin, cryoglobulin cold sensitivity (primary Raynaudûs disease) ¬“∫“ß™π‘¥ ‡™Ëπ ergot ‚√§Õ◊πË Ê ∑’æË ∫√Ë«¡‰¥È ‡™Ëπ hypothyroidism, ‡∫“À«“π, ∑ÿ‚¿™π“°“√

22 À¬Ë Õ πµ— « ¢Õßºπ— ß À≈Õ¥‡≈◊ Õ ¥À≈— ß °“√À¥µ— « Õ¬Ë “ ß √ÿπ·√ß®–¡’‡≈◊Õ¥¡“§—Ëß¿“¬„πÀ≈Õ¥‡≈◊Õ¥∑’Ë¢¬“¬µ—« √–¬–π’ºÈ «‘ Àπ—ß®–ÕÿπË ·≈–ª«¥π‘«È ¡“° Raynaudûs phenomenon π’È Õ“®®–‡°‘¥¢÷πÈ ‰¥È∑ªË’ ≈“¬π‘«È ‡∑È“ ®¡Ÿ° „∫ÀŸ ·≈–√‘¡Ω’ª“° πÕ°®“°∑’ªË ≈“¬π‘«È ¡◊Õ “‡Àµÿ∑æË’ ∫‰¥È∫ÕË ¬§◊Õ (µ“√“ß∑’Ë 2.7) cervical spondylosis, scleredema, cervical rib ·≈– idiopathic Raynaudûs disease «‘π‘®©—¬‚√§‰¥È®“°ª√–«—µ‘‡æ√“–™Ë«ß∑’Ë ‰¡Ë¡’Õ“°“√ ’ º‘«Àπ—ß®–ª°µ‘Õ“®®–¡’√ÕË ß√Õ¬¢Õß‚√§„ÀÈµ√«®æ∫‰¥È „π cervical spondylosis, scleredema ·≈– cervical rib º≈®“°°“√‡°‘¥ Raynaudûs phenomenon ‡ªÁπ√–¬– ‡«≈“π“πÕ¬Ë“ßµËÕ‡π◊ÕË ß∑”„ÀÈ¡°’ “√À¥µ—«¢Õß digital artery À≈“¬§√—Èß ¡’ emboli Õÿ¥µ—π ‡π◊ÈÕ‡¬◊ËÕª≈“¬µËÕ À≈Õ¥‡≈◊Õ¥∑’ËÕÿ¥µ—π®–‡πË“µ“¬ º‘«Àπ—ß®–·ÀÈß‡ª√“– ‡¬Áπ´’¥·≈–¡’ §’ ≈È”‡ªÁπ®È” Ê ¡’·º≈‡°‘¥¢÷πÈ ·∫∫‡¥’¬«°—∫ ischemic ulcer µ√ßª≈“¬π‘«È ∂È“¡’°“√µ‘¥‡™◊ÕÈ ´È”‡µ‘¡√Õ∫ Ê ÕÿßÈ ‡≈Á∫®–°≈“¬‡ªÁπ paronychia ‡®Á∫ª«¥¡“° Õ“°“√ ”§—≠§◊Õ ischemic rest pain √Ë«¡°—∫°“√‡πË“µ“¬ ¢Õß‡π◊ÕÈ ‡¬◊ÕË primary Raynaudûs disease æ∫„π‡¥Á° “««—¬√ÿπË (teenage) ·≈–‡ªÁπ‚√§∑“ß°√√¡æ—π∏ÿÏ ‡¡◊ËÕ∂Ÿ°§«“¡ ‡¬Áππ‘È«®–∫«¡·≈–‡®Á∫·µËÕ“°“√‰¡Ë√ÿπ·√ß Õ“°“√‡À≈Ë“ π’È®–À“¬‰ª‡¡◊ËÕÕ“¬ÿ¬Ë“ß‡¢È“ 20 ª’ ¡’πÈÕ¬√“¬∑’ËÕ“°“√ §ßÕ¬Ÿ·Ë ≈–√ÿπ·√ß¢÷πÈ µ“¡Õ“¬ÿ∑¡Ë’ “°¢÷πÈ ∂È“Õ“°“√‡À≈Ë“π’È ‡°‘¥¢÷πÈ À≈—ßÕ“¬ÿ 20 ª’ ‰¡Ë „™Ë‡°‘¥¢÷πÈ ™Ë«ß«—¬√ÿπË ‰¡Ëπ“Ë ®–‡ªÁπ primary Raynaudûs disease §«√π÷°∂÷ß‚√§ sclerederma 2.6.10 ACROCYANOSIS ‡ªÁπ¿“«–∑’¡Ë Õ◊ ·≈–‡∑È“¡’ π’ ”È ‡ß‘π·≈– ‡¬Áπµ≈Õ¥‡«≈“ ’º‘«®–‰¡Ë‡ª≈’Ë¬π·ª≈ßµ“¡Õÿ≥À¿Ÿ¡‘∑’Ë ‡æ‘¡Ë ¢÷πÈ À√◊Õ≈¥≈ß ´÷ßË µË“ß®“° Raynaudûs disease º‘« ’π”È ‡ß‘ππ’∫È “ß¢≥–®–À“¬‰ª‡Õß∑”„ÀÈº«‘ Àπ—ß°≈—∫ ¡“‡ªÁπ ’™¡¿Ÿ¥ß— ‡¥‘¡ „π™Ë«ß∑’¡Ë Õ’ “°“√®–‰¡Ëª«¥¡“° ¡◊Õ ∫«¡‡≈Á°πÈÕ¬ 2.6.11 ERYTHROMELALGIA ¿“«–π’‡È °‘¥¢÷πÈ ¿“¬À≈—ß®“°¡◊Õ À√◊Õ‡∑È“°√–∑∫°—∫§«“¡ÕÿËπ º≈∑’Ëµ“¡¡“§◊Õ®–‡°‘¥°“√ ª«¥· ∫ª«¥√È Õ π ¡’ flushing, À≈Õ¥‡≈◊ Õ ¥¥”„µÈ º‘«Àπ—ß‚ªËßæÕß º‘«Àπ—ßπŸπ „πºŸªÈ «Ë ¬∑’‡Ë ªÁπ¡“°‡æ’¬ß·§Ë ÀË¡ºÈ“°Á‡°‘¥Õ“°“√¢÷πÈ ‰¥È 2.6.12 LIVEDO RETICULARIS ®–æ∫«Ë“À≈Õ¥‡≈◊Õ¥„µÈº«‘ Àπ—ß ¡’≈—°…≥–‡ªÁπµ“¢Ë“¬ ’πÈ”‡ß‘π®“ß°√–®“¬Õ¬ŸË∑—Ë«‰ª„µÈ

»—≈¬»“ µ√ÏÀ≈Õ¥‡≈◊Õ¥ º‘«Àπ—ß primary livedo reticularis æ∫„π™Ë«ß«—¬ ‡®√‘≠æ—π∏Ï º‘«Àπ—ß®–‡ªÁπ ’πÈ”‡ß‘π®“ßÕ¬Ë“ß∂“«√ ’ ®–‡¢È ¡ °«Ë “ ‡¥‘ ¡ ∂È “ — ¡ º— °— ∫ §«“¡‡¬Á π À√◊ Õ Õ“√¡≥Ï ‡ª≈’Ë¬π·ª≈ß ‡°‘¥¢÷Èπ∑’Ëª≈“¬¡◊Õª≈“¬‡∑È“∑—Èß Õß¢È“ß æ∫‰¥È∫“È ß∫√‘‡«≥≈”µ—« secondary livedo reticularis ‡°‘¥¢÷Èπ∑’Ëª≈“¬¡◊Õª≈“¬‡∑È“¥È“π„¥¥È“πÀπ÷Ëß°Á ‰¥È ∫“ß §√—ÈßÀ≈Õ¥‡≈◊Õ¥„µÈº‘«Àπ—ß®–·µ°ÕÕ°·≈–°≈“¬‡ªÁπ ·º≈‡√◊ÕÈ √—ß

2.7 ACUTE ARTERIAL OCCLUSION °“√Õÿ¥µ—π¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ßÕ¬Ë“ß‡©’¬∫æ≈—π ¡’ “‡Àµÿ¡“®“° arterial thrombosis, embolism ·≈–®“°°“√∫“¥‡®Á∫µËÕ À≈Õ¥‡≈◊Õ¥ 2.7.1 ACUTE ARTERIAL THROMBOSIS µ”·ÀπËß¢ÕßÀ≈Õ¥ ‡≈◊Õ¥·¥ß∑’Ë®–‡°‘¥°“√Õÿ¥µ—π®“° thrombus ‰¥È∫ËÕ¬ ∑’ Ë ÿ ¥ §◊ Õ femoral artery ®ÿ ¥ ∑’ Ë ∑ Õ¥ºË “ πÕÕ°®“° subsartorial canal Õ“°“√·≈–Õ“°“√· ¥ß¢Õß°“√ ¢“¥‡≈◊Õ¥®“° thrombus Õÿ¥À≈Õ¥‡≈◊Õ¥·¥ß ®–§≈È“¬ °—∫ embolism ¡“° Õ¬Ë“ß‰√°Áµ“¡ºŸªÈ «Ë ¬®–¡’ª√–«—µ‘ intermittent claudication ¡“°ËÕπ Õ“°“√¢Õß°“√ ¢“¥‡≈◊Õ¥®–‰¡Ë√ÿπ·√ß‡π◊ËÕß®“°¡’ collaterals ∑’Ë √È“ß ·≈–‡®√‘≠¡“°ËÕπÀπÈ“∑’®Ë –‡°‘¥ thrombus Õÿ¥µ—π √–¬– ·√°¢Õß°“√Õÿ¥µ—π®–ª«¥·¢π ¢“ º‘«Àπ—ß´’¥ ‡¬Áπ ™“ ·≈–¢¬—∫‰¡Ë ‰¥È §≈”™’æ®√‰¡Ë ‰¥È ´÷ßË °ËÕπÀπÈ“π—πÈ °Á®–§≈” ™’æ®√‰¥È‡∫“À√◊Õ‰¡Ë ‰¥È‡≈¬ ‡π◊ÕË ß®“°¡’ atherosclerosis Õ¬ŸË·≈È« §«√®–§≈”™’æ®√‡ª√’¬∫‡∑’¬∫°—π∑—Èß Õß¢È“ß ·¢πÀ√◊Õ¢“∑’Ë¢“¥‡≈◊Õ¥®–∫«¡µ÷ß ¡’ ’§≈È” ∂È“‰¡Ë ‰¥È ∑”°“√·°È ‰¢√—°…“º‘«Àπ—ß®–¡’µ¡Ëÿ πÈ”·µ°ÕÕ° ¡’°“√‡πË“ µ“¬·≈–Õ—°‡ ∫µ‘¥‡™◊ÈÕ¢Õß‡π◊ÈÕ‡¬◊ËÕµ“¡¡“ Õ“°“√·≈– Õ“°“√· ¥ß¢Õß acute arterial thrombosis ®– ·µ°µË“ß°—π„π·µË≈–µ”·ÀπËß¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß∑’Ë¡’ °“√Õÿ¥µ—π 2.7.2 EMBOLISM §«√ ß —¬„πºŸªÈ «Ë ¬∑’¡Ë ª’ √–«—µ‚‘ √§À—«„®¡“ °ËÕπ‡™Ëπ atrial fibrillation, °≈È“¡‡π◊ÈÕÀ—«„®µ“¬®“° ¢“¥‡≈◊Õ¥ ‡æ√“–ª√–¡“≥√ÈÕ¬≈– 90 ¢Õß mural thrombus ®–¡’µÈπ°”‡π‘¥¡“®“°À—«„® ∑’Ë‡À≈◊ÕÕ“®®–‡°‘¥®“° aneurysm ¢Õß aorta ·≈–À≈Õ¥‡≈◊Õ¥·¥ß Ë«πª≈“¬ Õ“°“√ª«¥¢Õß embolism ´÷Ëß‡ªÁπ≈—°…≥–‡©æ“–§◊Õ ®–ª«¥Õ¬Ë“ß√ÿπ·√ß∑—π∑’∑’Ë¡’°“√Õÿ¥µ—π ‡À¡◊Õπ∂Ÿ°µ’

°“√µ√«®√Ë“ß°“¬·≈–°“√ª√–‡¡‘πºŸÈªË«¬‚√§À≈Õ¥‡≈◊Õ¥ Õ¬Ë“ß√ÿπ·√ß∑’¢Ë “À√◊ÕπËÕß∑”„ÀÈµÕÈ ßπ—ßË ≈ß À¬ÿ¥æ—° À√◊Õ ≈È¡≈ß∑—π∑’ Õ“°“√ª«¥®–≈¥≈ß¿“¬À≈—ß¡’°“√À¥µ—« ¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß·≈–µ“¡¡“¥È«¬°“√¢¬“¬µ—«¢Õß À≈Õ¥‡≈◊Õ¥„π collaterals ·µË¬ß— ¡’ª«¥Àπ÷∫ (numbness) ·≈–·¢π¢“ÕËÕπ·√ß ’º‘«®–§≈È”·≈–º‘«Àπ—ß®–‡¬Áπ µ”·ÀπË ß „µÈ µ Ë Õ °“√Õÿ ¥ µ— π ¢ÕßÀ≈Õ¥‡≈◊ Õ ¥·¥ß §≈” ™’æ®√‰¡Ë ‰¥È À≈—ß°“√Õÿ¥µ—π 1-2 ™—«Ë ‚¡ßº‘«®–¡’ §’ ≈È” ¡’ ®ÿ¥‡ªÁπ®È” Ê (mottling) Õ“°“√¢Õß 5ûP ®–™—¥‡®π¡“° ´÷ßË ª√–°Õ∫¥È«¬ Pulselessness, Pallor, Pain, Poikilothermia, Paresthesia 2.7.3 TRAUMA °“√Õÿ¥µ—π¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß¿“¬À≈—ß®“° ∂Ÿ°·√ß°√–·∑°¿“¬πÕ° ¡—°®–‡°‘¥®“°°√–¥Ÿ°À—°À√◊Õ ¢ÈÕ‡§≈◊ËÕπ¡“°√–∑∫ºπ—ß¢ÕßÀ≈Õ¥‡≈◊Õ¥∑”„ÀÈ¡’°“√©’° ¢“¥À√◊Õ™Õ°™È”¢Õßºπ—ßÀ≈Õ¥‡≈◊Õ¥™—Èπ intima µ“¡ ¡“¥È«¬≈‘¡Ë ‡≈◊Õ¥Õÿ¥µ—π µ”·ÀπËß¢Õß°√–¥Ÿ°À—°·≈–¢ÈÕ‡§≈◊ÕË π∑’∑Ë ”„ÀÈ‡°‘¥°“√ ∫“¥‡®Á∫¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß‰¥È∫ÕË ¬§◊Õ supracondylar fracture of the shaft of the humerus dislocation of the shoulder supracondylar or shaft fracture of the femur dislocation of the elbow dislocation of the knee µ“√“ß∑’Ë 2.8 “‡Àµÿ¢ÕßÀ≈Õ¥‡≈◊Õ¥‚ªËßæÕß (aneurysm)

Õ“°“√·≈–Õ“°“√· ¥ß¢ÕßÀ≈Õ¥‡≈◊Õ¥Õÿ¥µ—π®“° Õÿ∫—µ‘‡Àµÿ®–§≈È“¬°—∫ embolism ¡“° πÕ°®“°®–æ∫ «Ë“¡’°√–¥Ÿ°À—°·≈–¢ÈÕ‡§≈◊ÕË π√Ë«¡¥È«¬

2.8 ANEURYSMAL DISEASE aneurysm §◊Õ °“√‚ªËßæÕß¢ÕßÀ≈Õ¥‡≈◊Õ¥∑’¡Ë ¢’ π“¥‚µ°«Ë“ ‡ ÈπºË“»Ÿπ¬Ï°≈“ßª°µ‘ 1 1/2 ‡∑Ë“ Õ“®®–‡°‘¥¢÷Èπµ≈Õ¥∑—Ë«∑ÿ° ¥È“π¢Õßºπ—ßÀ≈Õ¥‡≈◊Õ¥ À√◊Õ¥È“π„¥¥È“πÀπ÷ßË (√Ÿª∑’Ë 2.11) ∑’æË ∫ ‰¥È∫ËÕ¬§◊Õ congenital aneurysm ‡™Ëπ berry aneurysm „π ¡Õß·≈– arteriovenous fistula acquired aneurysm ¡—°®–‡°‘¥¿“¬À≈—ß°“√∫“¥‡®Á∫ °“√µ‘¥‡™◊ÕÈ degenerative disease (µ“√“ß∑’Ë 2.8) false aneurysm ‡°‘¥¿“¬À≈—ßÀ≈Õ¥‡≈◊Õ¥·¥ß ∂Ÿ°·∑ß∑–≈ÿ¡’™ËÕßµËÕ°—∫≈‘Ë¡‡≈◊Õ¥ ´÷ËßµËÕ¡“≈–≈“¬À¡¥°≈“¬‡ªÁπ ‚æ√ßÀ≈Õ¥‡≈◊Õ¥ µ”·ÀπËß∑’æË ∫‰¥È∫ÕË ¬¢Õß atherosclerotic aneurysm §◊Õ aorta femoral ·≈– popliteal ‡ªÁπ‚√§æ—π∏ÿ°√√¡ æ∫„π‡æ»™“¬¡“°°«Ë“À≠‘ß Õ“¬ÿ¡“°°«Ë“ 50 ª’ (√Ÿª∑’Ë 2.12)

I. TRUE ANEURYSMS

Congenital : weak areas (berry aneurysm) weak walls (Marfanûs syndrome, Ehlers-Danlos syndrome) À≈Õ¥‡≈◊Õ¥·¥ß‚ªËß¢¬“¬µ—«®“° congenital arteriovenous fistula Acquired : Trauma: ®“°°“√∫“¥‡®Á∫¢ÕßÀ≈Õ¥‡≈◊Õ¥ √—ß ’∫”∫—¥ Infection: non-specific bacterial arteritis (mycotic), syphilis Degeneration: atherosclerosis, arteriomegaly, cystic medionecrosis II. FALSE ANEURYSMS À≈—ß°“√∫“¥‡®Á∫

√Ÿª∑’Ë 2.11 ≈—°…≥–µË“ß Ê ¢ÕßÀ≈Õ¥‡≈◊Õ¥‚ªËßæÕß °. Fusiform aneurysm ¢. Saccular aneurysm §. False aneurysm ∑’Ë‡°‘¥¿“¬À≈—ß°“√∫“¥‡®Á∫ ¡’ ‚æ√ß ¢Õß≈‘Ë¡‡≈◊Õ¥ ´÷ËßµËÕ‡¢È“‰¥È°—∫ºπ—ß¢ÕßÀ≈Õ¥‡≈◊Õ¥

»—≈¬»“ µ√ÏÀ≈Õ¥‡≈◊Õ¥

√Ÿª∑’Ë 2.13 De Bakeyûs sign µ”·ÀπËß¢Õß AAA ®–Õ¬ŸËµË”°«Ë“ √Ÿª∑’Ë 2.12 µ”·ÀπËß¢Õß aneurysms ∑’Ëæ∫∫ËÕ¬

Renal arteries ‡ ¡Õ∂È“ºŸÈµ√«® “¡“√∂ Õ¥π‘È«ºË“π‰¥È √–À«Ë“ß¬Õ¥¢Õß aneurysm °—∫ costal margin ¥È“π ´È“¬

abdominal aortic aneurysm (AAA) ∂È“¡’¢π“¥‚µ¢÷Èπ ®–¡’Õ“°“√ª«¥µ◊ÕÈ √È“«‰ª∑’ÀË ≈—ß (√Ÿª∑’Ë 2.13)

°“√µ√«®√Ë“ß°“¬ª√–‡¡‘π‚√§À≈Õ¥‡≈◊Õ¥¥” °“√´—°ª√–«—µ·‘ ≈–µ√«®√Ë“ß°“¬∑’‡Ë °’¬Ë «¢ÈÕß°—∫°“√‰À≈‡«’¬π ‡≈◊Õ¥¥”¢Õß¢“ ®–∑”„ÀÈ ‰¥È¢ÕÈ ¡Ÿ≈‡°’¬Ë «°—∫°“√‰À≈‡«’¬π¢Õß‡≈◊Õ¥ ¥”„π·µË≈–√–∫∫·≈–µ”·ÀπËß µ≈Õ¥®πÀπÈ“∑’Ë°“√∑”ß“π·≈– §«“¡º‘¥ª°µ‘¢Õß≈‘Èπª‘¥‡ª‘¥ (valve) Õ“°“√·≈–Õ“°“√· ¥ß ¢Õß§«“¡º‘¥ª°µ‘∑‡Ë’ °‘¥∫ËÕ¬„πÀ≈Õ¥‡≈◊Õ¥¥”¢Õß¢“§◊Õ ª«¥ ∫«¡ ·≈– ’ µ≈Õ¥®π≈—°…≥–°“√‡ª≈’¬Ë π·ª≈ß¢Õßº‘«Àπ—ß (µ“√“ß∑’Ë 2.9) °“√¥Ÿ (√Ÿª∑’Ë 2.14) „ÀÈºªÈŸ «Ë ¬¬◊πµ√ß∫π‡µ’¬ß·≈–Õ¬Ÿ Ë ßŸ °«Ë“ºŸÈ µ√«® „πÀÈÕß∑’Ë¡’· ß «Ë“ß·≈–Õÿ≥À¿Ÿ¡‘æÕ‡À¡“– —ß‡°µÿ§«“¡ º‘¥ª°µ‘¢ÕßÀ≈Õ¥‡≈◊Õ¥¥”„µÈº‘«Àπ—ßÕ“®®–¡’°“√‚ªËßæÕßÀ√◊Õ §¥ßÕ‰ª¡“ „ÀÈ‡¢’¬π∫—π∑÷°§«“¡º‘¥ª°µ‘¢ÕßÀ≈Õ¥‡≈◊Õ¥¥”„µÈ º‘«Àπ—ß·µË≈–µ”·ÀπËß‡Õ“‰«È §«“¡º‘¥ª°µ‘¢ÕßÀ≈Õ¥‡≈◊Õ¥¥” ∫“ß·ÀËßµÈÕß —ß‡°µÿ„°≈È™‘¥®–æ∫«Ë“¡’®ÿ¥‡≈Á° Ê ’πÈ”‡ß‘πÕËÕπ„µÈ

√Ÿª∑’Ë 2.14 °“√µ√«®‚¥¬„ÀÈºªÈŸ «Ë ¬¬◊π∫π°√–¥“π ÀÈÕß¡’§«“¡ «Ë“ß·≈– Õÿ≥À¿Ÿ¡‘æÕ‡À¡“–

°“√µ√«®√Ë“ß°“¬·≈–°“√ª√–‡¡‘πºŸÈªË«¬‚√§À≈Õ¥‡≈◊Õ¥ µ“√“ß∑’Ë 2.9 °“√ª√–‡¡‘π∑—«Ë ‰ª¢Õß√–∫∫‰À≈‡«’¬πÀ≈Õ¥‡≈◊Õ¥¥” ÀÈÕßµ√«®∑’¡Ë Õ’ ≥ ÿ À¿Ÿ¡æ‘ Õ‡À¡“– „ÀÈºªÈŸ «Ë ¬¬◊π —ß‡°µÿ¥Ÿ µ”·ÀπËß·≈–¢π“¥¢ÕßÀ≈Õ¥‡≈◊Õ¥¥”∑’¡Ë Õß‡ÀÁπ‰¥È °“√¬°·≈–ÀÈÕ¬¢“¡’º≈µËÕÀ≈Õ¥‡≈◊Õ¥¥”Õ¬Ë“ß‰√? ¡’°“√∫«¡∑’¢Ë ÕÈ ‡∑È“À√◊Õ‰¡Ë? ’¢Õßº‘« §≈” µ”·ÀπËß¢Õß‡ÕÁπæ—ßº◊¥∑’¡Ë √’ Õ¬∫ÿ¡Î º‘¥ª°µ‘ µ√ß®ÿ¥ ∑’‡Ë °’¬Ë «¢ÈÕß°—∫À≈Õ¥‡≈◊Õ¥¥” ≈—°…≥–¢Õßº‘«Àπ—ß·≈–‡π◊ÕÈ ‡¬◊ÕË „µÈº«‘ Àπ—ß Trendelenberg test Tourniquet test ‡§“– ‡§“–·≈– —ß‡°µÿ wave conduction µ“¡·π«¢Õß À≈Õ¥‡≈◊Õ¥ ø—ß bruits

º‘«Àπ—ß ‡ªÁπ·ºß¢ÕßÀ≈Õ¥‡≈◊Õ¥¥”¢π“¥‡≈Á°°√–®“¬ÕÕ°®“° À≈Õ¥‡≈◊Õ¥¥”À≈Õ¥Àπ÷Ëß∑’Ë‡√’¬°«Ë“ çvenous starsé ‡ª√’¬∫ ‡∑’¬∫¢π“¥¢Õß¢“∑—Èß Õß¢È“ß«Ë“∫«¡·µ°µË“ß°—πÕ¬Ë“ß‰√ ‡√‘Ë¡ ∫«¡µ—ßÈ ·µË√–¥—∫‰Àπ ¥Ÿ ¢’ Õßº‘«Àπ—ß·≈–§«“¡º‘¥ª°µ‘∑®Ë’ –‡°‘¥¢÷πÈ ‡™Ëπ ’º«‘ §≈È”¥”°«Ë“ª°µ‘ º◊πË §—π ·≈–·º≈‡√◊ÕÈ √—ß °“√§≈” §≈”µ“¡·π««‘ßË ¢ÕßÀ≈Õ¥‡≈◊Õ¥¥”„µÈº«‘ Àπ—ß¥Ÿ«“Ë ºπ—ß À≈Õ¥‡≈◊Õ¥¡’§«“¡µ÷ß·πËπ‡æ’¬ß‰√ §≈”µ√ß saphenofemoral junction ·≈–„ÀÈ º Ÿ È ª Ë « ¬‰Õ‡æ◊ Ë Õ — ¡ º— °— ∫ cough impulse ‡ªÁπ°“√µ√«® competency ¢Õß≈‘πÈ ª‘¥‡ª‘¥„πÀ≈Õ¥‡≈◊Õ¥„µÈº«‘ Àπ—ß (√Ÿª∑’Ë 2.15) §≈”¥È“π„π¢Õß¢“µ”·ÀπËß¢Õß communicating veins ´÷ßË ‡ªÁπ®ÿ¥‡™◊ÕË ¡√–À«Ë“ß deep °—∫ superficial veins (√Ÿª∑’Ë 2.16) °¥º‘«Àπ—ßµ√«®¥Ÿ«Ë“¡’°“√∫«¡ °¥∫ÿÎ¡ À√◊Õ‰¡ËÀ√◊Õ°“√ Õ—°‡ ∫µ‘¥‡™◊ÕÈ ∑’∑Ë ”„ÀÈ°¥‡®Á∫ ’º«‘ Àπ—ß¡’ π’ ”È µ“≈§≈È” (brown pigmentation) ‡°‘¥®“°‡¡Á¥‡≈◊Õ¥·¥ß∑’ÀË ≈ÿ¥·≈–·µ°µ—«¿“¬„π‡π◊ÕÈ ‡¬◊ÕË ∫“ß√“¬®–¡’ºπË◊ §—π·≈–·º≈‡√◊ÕÈ √—ß‡°‘¥¢÷πÈ ∑’¢Ë ÕÈ ‡∑È“

√Ÿª∑’Ë 2.15 °“√µ√«® competency ¢Õß saphenous vein watching finger tapping finger tapping test for saphenous incompetence

√Ÿª∑’Ë 2.16 venous ulcers ·≈– brawny induration „πºŸÈªË«¬ chronic venous insufficiency

I. VENOUS THROMBOSIS Thrombosis ‡°‘¥¢÷πÈ ‰¥È „πÀ≈Õ¥‡≈◊Õ¥¥”√–¥—∫≈÷° (deep) ·≈– √–¥—∫µ◊Èπ (superficial) ¡’‡æ’¬ß√ÈÕ¬≈– 25-40 ¢ÕßºŸÈªË«¬∑’Ë¡’ Õ“°“√·≈–Õ“°“√· ¥ß¢Õß‚√§Õ¬Ë“ß™—¥‡®π ‡æ√“– thrombus Õÿ¥À≈Õ¥‡≈◊Õ¥¥”‡æ’¬ß∫“ß Ë«π‰¡ËÕ¥ÿ µ—πÕ¬Ë“ß ¡∫Ÿ√≥Ï®ß÷ “¡“√∂ À≈ÿ¥≈Õ¬‡¢È“‰ªÕÿ¥µ—π∑”„ÀÈ‡°‘¥ pulmonary embolism ´÷ßË Õ—µ√“ µ“¬ Ÿß¡“° ®÷ß§«√«‘π®‘ ©—¬‚√§ deep vein thrombosis „ÀÈ ‰¥È·µË‡π‘πË Ê ‡æ◊ËÕ∑”°“√√—°…“·≈–ªÈÕß°—π‰¡Ë „ÀÈ‡°‘¥¿“«–·∑√°´ÈÕπ√ÿπ·√ß ¿“¬À≈—ß ºŸªÈ «Ë ¬°≈ÿ¡Ë ∑’‡Ë ’¬Ë ßµËÕ°“√‡°‘¥ venous thrombosis ‡™Ëπ ÕÈ«πº‘¥ª°µ‘ Õ“¬ÿ‡°‘π 40 ª’ ¡’‰¢È ‚¥¬‰¡Ë∑√“∫ “‡Àµÿ ‡ªÁπ‚√§À—«„® ‡§¬ºË“µ—¥„À≠Ë∑“ß™ËÕß∑ÈÕßÀ√◊Õ„ Ë‡À≈Á°¥“¡°√–¥Ÿ° femur °“√ ºË“µ—¥∑’µË ÕÈ ßπÕπæ—°‡ªÁπ√–¬–‡«≈“π“π œ≈œ §«√‰¥È√∫— °“√¥Ÿ·≈Õ¬Ë“ß „°≈È™¥‘ ºŸªÈ «Ë ¬∑’‡Ë ªÁπ deep vein thrombosis (DVT) ®–∫Ëπª«¥µ÷ß ∫√‘‡«≥πËÕß·≈–¢“ ∫“ß√“¬®–‰¡Ë¡Õ’ “°“√· ¥ß °“√µ√«®√Ë“ß°“¬ ∑’ËµÈÕß¢¬—∫‡¢¬◊ÈÕπ·≈–∫’∫°≈È“¡‡π◊ÈÕ Õ“®∑”„ÀÈ thrombus À≈ÿ¥ ÕÕ°®“°ºπ—ßÀ≈Õ¥‡≈◊Õ¥ ≈Õ¬„π°√–· ‡≈◊Õ¥¥”°≈“¬‡ªÁπ emboli ‰¥È °“√µ√«®√Ë“ß°“¬®÷ß§«√°√–∑”¥È«¬§«“¡≈–¡ÿπ≈–¡ËÕ¡ „ÀÈºÈŸ ªË«¬πÕπÀß“¬¡Õß¥Ÿ≈—°…≥–¢“∑—Èß Õß¢È“ß‡ª√’¬∫‡∑’¬∫°—π ¥Ÿ À≈Õ¥‡≈◊Õ¥¥”„µÈº«‘ Àπ—ß∑’πË ÕË ß·≈–À≈—ß‡∑È“«Ë“‚ªËßµ÷ß°«Ë“ª°µ‘À√◊Õ‰¡Ë ¡’°¥∫ÿ¡Î ∫√‘‡«≥À≈—ß‡∑È“‡°‘¥¢÷πÈ À√◊Õ‰¡Ë °“√∑” dorsiflex ¢Õß¢ÈÕ ‡∑È“®–∑”„ÀÈ posterior tibial vein µ÷ß ∂È“¡’ thrombus Õ¬ŸË „πÀ≈Õ¥‡≈◊Õ¥¥”®–√Ÿ È °÷ ª«¥µ÷ß∑’πË ÕË ß Õ“°“√π’§È Õ◊ Homanûs sign ·µË‡™◊ÕË ∂◊Õ‰¡Ë ‰¥È ‚¥¬ ¡∫Ÿ√≥Ï‡æ√“–‚Õ°“ ‡°‘¥º≈∫«°ª≈Õ¡¡’‰¥È ßŸ ®–µ√«®æ∫‰¥ÈÕ“°“√§≈È“¬°—π„π‚√§°≈È“¡‡π◊ÈÕÀ√◊ÕºŸÈªË«¬∑’Ë «¡ √Õß‡∑È“ Èπ Ÿß‡ªÁπª√–®” «‘∏’°“√µ√«®π’È¬‘Ëß‡ ’Ë¬ßµËÕ°“√À≈ÿ¥¢Õß thrombus ¥È«¬ µ√«®∫√‘‡«≥πËÕß„ÀÈºªÈŸ «Ë ¬ßÕ‡¢Ë“ „™Èπ«È‘ ¡◊Õ§≈”µ—ßÈ ·µË Achillis tendon ‰≈Ë¢÷Èπ‰ª®π∂÷ßπËÕß ∂È“°¥‡®Á∫∑’ËπËÕß· ¥ß«Ë“ thrombus Õ“®®–‡°‘¥¢÷πÈ „πÀ≈Õ¥‡≈◊Õ¥¥”∑’ÕË ¬ŸË„π°≈È“¡‡π◊ÕÈ soleus ∑’‡Ë √’¬°«Ë“ soleus plexus ∫√‘‡«≥π’®È –‡°‘¥ thrombosis ‰¥È∫ÕË ¬∑’ Ë ¥ÿ ∫’∫°≈È“¡‡π◊ÕÈ ∫√‘‡«≥ÀπÈ“·¢Èß∂È“‡®Á∫· ¥ß«Ë“¡’ thrombosis ‡°‘¥ ¢÷πÈ „πÀ≈Õ¥‡≈◊Õ¥¥” posterior tibial §≈”·≈–°¥∫√‘‡«≥ popliteal space ¡’°¥‡®Á∫À√◊Õ‰¡Ë ‚¥¬„ÀÈºªÈŸ «Ë ¬πÕπÀß“¬ °¥¥ŸµßÈ— ·µË saphenous opening „µÈµËÕ inguinal ligament ≈ß¡“∂÷ß‡¢Ë“ «—¥ ‡ Èπ√Õ∫«ß¢ÕßπËÕß µÈπ¢“ ·≈–¢ÈÕ‡∑È“∑—Èß Õß¢È“ß„πµ”·ÀπËß ‡¥’¬«°—π ‡æ◊ÕË ‡ª√’¬∫‡∑’¬∫¢π“¥

»—≈¬»“ µ√ÏÀ≈Õ¥‡≈◊Õ¥ 1.1 ACUTE VENOUS THROMBOSIS 1.1.1 Phlegmasia Alba Dolens (whiteleg, milkleg) ‡°‘¥®“°°“√¡’ thrombus Õÿ¥µ—π„πÀ≈Õ¥‡≈◊Õ¥¥” iliofemoral æ∫„πºŸÈªË«¬À≈—ß§≈Õ¥À√◊ÕÀ≈—ßºË“µ—¥„À≠Ë ∑’ËµÈÕßπÕπæ—°‡ªÁπ√–¬–‡«≈“π“π µ”·ÀπËß∑’Ë®–‡√‘Ë¡‡°‘¥ thrombus ‰¥È∫ËÕ¬§◊Õ soleus plexus ·≈–≈‘Èπª‘¥ ‡ª‘¥¢ÕßÀ≈Õ¥‡≈◊Õ¥¥” femoral À√◊ÕÀ≈Õ¥‡≈◊Õ¥¥” „πÕÿßÈ ‡™‘ß°√“π ºŸªÈ «Ë ¬®–¡’‰¢È ª«¥∂Ë«ß∑’¢Ë “Àπ’∫·≈–µÈπ¢“ À≈—ß®“°π—ÈπÕ’°ª√–¡“≥ 12 ™—Ë«‚¡ß µËÕ¡“¢“®–∫«¡ ¢“«´’¥ °¥‡®Á∫µ“¡·π«¢ÕßÀ≈Õ¥‡≈◊Õ¥¥” femoral ®π∂÷ß iliac fossa ‡∑È“‡¬Áπ µËÕ¡πÈ”‡À≈◊Õß∑’¢Ë “Àπ’∫∫«¡‚µ acute phase ®–‡°‘¥¢÷πÈ ¿“¬„π 2-6 —ª¥“ÀÏ·√° ·≈–µ“¡¡“¥È«¬ chronic phase ´÷ßË ®–¡’Õ“°“√· ¥ß∑’ Ë ”§—≠§◊Õ¢“∫«¡ ‡¬Áπ ·≈–ª«¥µ≈Õ¥‡«≈“ ¿“«–·∑√°´ÈÕπ∑’Ë‡°‘¥¢÷Èπ ¿“¬À≈—ß§◊Õ venous ulcer 1.1.2 Phlegmasia Cerulea Dolens ‡°‘¥®“° thrombus ª√‘¡“≥¡“°Õÿ¥À≈Õ¥‡≈◊Õ¥¥” Ë«π ileofemoral „ÀÈµ—π·≈–ª‘¥°—Èπ°“√‰À≈‡«’¬π¢Õß‡≈◊Õ¥°≈—∫ ŸËÀ—«„® Õ¬Ë“ß ¡∫Ÿ√≥Ï Õ“°“√®–‡√‘Ë¡µÈπ®“°°“√ª«¥Àπ÷∫·≈–¡’ §«“¡√ŸÈ ÷°§≈È“¬°—∫¡’‡¢Á¡∑‘Ë¡º‘«Àπ—ßµ≈Õ¥‡«≈“ µ“¡¡“ ¥È«¬ª«¥¢“ ¢“®–‡ª≈’Ë¬π‡ªÁπ ’πÈ”‡ß‘π§≈È”∫«¡ Õ“°“√ ª«¥¢“®–√ÿπ·√ß¡“° º‘«Àπ—ßµ÷ß·¢Áß°¥∫ÿÎ¡‡≈Á°πÈÕ¬ ºŸÈ ªË«¬®–¡’Õ“°“√™ÁÕ§√Ë«¡°—∫ venous gangrene §≈” ™’æ®√∑’Ë¢“‰¡Ë ‰¥È‡æ√“–‡π◊ÈÕ‡¬◊ËÕ∫«¡¡“°√Ë«¡°—∫¡’ reflex spasm ∑”„ÀÈ¡’°“√À¥µ—«¢ÕßÀ≈Õ¥‡≈◊Õ¥Õ¬Ë“ß√ÿπ·√ß Õ“°“√¢“¥‡≈◊Õ¥¢Õß®–√ÿπ·√ß¢÷Èπ ®–µÈÕß√’∫√—°…“‚¥¬ °“√ºË“µ—¥∑” venous thrombectomy °ËÕπ ¢“®– ‡πË“µ“¬„π∑’ Ë ¥ÿ 1.1.3 Superficial thrombophlebitis ‡√‘¡Ë ®“°°“√‡°‘¥ thrombus „πºπ—ßÀ≈Õ¥‡≈◊Õ¥¥”¿“¬À≈—ß°“√Õ—°‡ ∫ æ∫„πºŸªÈ «Ë ¬‚√§À≈Õ¥‡≈◊Õ¥¢Õ¥À√◊Õ‡ªÁπ‚√§¡–‡√ÁßÕ¬Ÿ·Ë ≈È« ‡™Ëπ ¡–‡√ÁßªÕ¥ µ—∫ÕËÕπ ‰µ °√–‡æ“–Õ“À“√ µËÕ¡πÈ” ‡À≈◊Õß Buergerûs disease, polycythemia, polyarthritis œ≈œ (µ“√“ß∑’Ë 2.10) Õ“®®–‡°‘¥‰¥È „π·¢πß¢ÕßÀ≈Õ¥ ‡≈◊Õ¥¥”∑’Ë∂Ÿ°·∑ß‡ Èπ‡®“–‡≈◊Õ¥ „ÀÈ¬“ À√◊Õ„ÀÈ “√πÈ” Õ“°“√·≈–Õ“°“√· ¥ß§◊Õª«¥µ“¡·π«À≈Õ¥‡≈◊Õ¥¥” ¡’°ÕÈ π§≈”‰¥È º‘«Àπ—ß∫√‘‡«≥π—πÈ ∫«¡ ·¥ß√ÈÕπ·≈–°¥‡®Á∫

°“√µ√«®√Ë“ß°“¬·≈–°“√ª√–‡¡‘πºŸÈªË«¬‚√§À≈Õ¥‡≈◊Õ¥

®–‚ªËßæÕß·≈–µ÷ß ¬°·¢π¢÷ÈπÀ≈Õ¥‡≈◊Õ¥¥”®–‰¡Ë·ø∫ §≈”‰¥ÈÀ≈Õ¥‡≈◊Õ¥¥”„µÈ√—°·√È‡ªÁπ≈”·≈–°¥‡®Á∫ §«√ µ√«®§≈”¥ŸµËÕ¡πÈ”‡À≈◊Õß∑’Ë∫«¡‚µº‘¥ª°µ‘∫√‘‡«≥§Õ ‡µÈ“π¡ ·≈–∑ÈÕß

µ“√“ß∑’Ë 2.10 “‡Àµÿ¢Õß superficial thrombophlebitis Varicose veins Occult carcinoma: ‡™Ëπ bronchus, pancreas, stomach, lymphoma Thromboangiitis obliterans (Buergerûs disease) Polycythemia Polyarteritis Idiopathic Iatrogenic: ®“°°“√∫“¥‡®Á∫À√◊Õ©’¥¬“‡¢È“À≈Õ¥‡≈◊Õ¥¥”

1.1.4 Thrombophebitis migrans ‡°‘¥„πÀ≈Õ¥‡≈◊Õ¥ ¥”ª°µ‘ ∂◊Õ‡ªÁπ sinister sign ¢Õß occult malignancy §«“¡‡°’Ë¬«¢ÈÕß¢Õß¡–‡√Áß°—∫ superficial migratory thrombophlebitis π’È ‡√’¬°«Ë“ Trousscanûs sign Õ“®®–æ∫¿“«–π’È ‰¥È „π Buergerûs disease 1.1.5 Mandorûs disease À√◊Õ string phlebitis ‡°‘¥ ¢÷ÈπÀ≈—ß®“°°“√∫“¥‡®Á∫À√◊Õ„™È·¢π„π°“√‡§≈◊ËÕπ‰À« ¡“°°«Ë“ª°µ‘ æ∫„π‡æ»™“¬«—¬√ÿËπ·≈–«—¬°≈“ß§π ®– ª«¥¢ÈÕ»Õ° µÈπ·¢π·≈–∑ÈÕß·¢π ¡◊Õ∫«¡ ·π«∑’ªË «¥§◊Õ ∑“ß¥È“π„π¢ÕßµÈπ·¢π·≈–√—°·√È §≈”º‘«Àπ—ß√ÈÕπ·≈–µ÷ß ¢¬—∫·¢π·≈–¢ÈÕ‰À≈Ë ‰¥ÈπÈÕ¬ ∂È“¡’°“√Õÿ¥µ—π‡°‘¥¢÷Èπ Õ¬Ë“ß√ÿπ·√ß®–∫«¡µ÷ß∑—Èß¢È“ß À≈Õ¥‡≈◊Õ¥¥”„µÈº‘«Àπ—ß

1.2 CHRONIC VENOUS INSUFFICIENCY ®–¡’Õ“°“√∑“ß§≈‘π§‘ ∑’ Ë ”§—≠§◊Õ ¢“∫«¡ º‘«Àπ—ßÀ¥µ—« ¡’‚√§ º‘«Àπ—ßÕ—°‡ ∫‡°‘¥¢÷πÈ ‡√◊ÕÈ √—ß ‚¥¬‡©æ“–¢“¥È“π„π‡Àπ◊Õµ“µÿ¡Ë ¢÷πÈ ‰ª º‘«Àπ—ß®–¡’ §’ ≈È” ¡’°“√Õ—°‡ ∫·≈–‡°‘¥·º≈‰¥Èß“Ë ¬ ·º≈∑’‡Ë °‘¥¢÷πÈ ¡’°“√µ‘¥‡™◊ÕÈ ·≈–≈ÿ°≈“¡‰¥È ‡°‘¥∑—ßÈ cellulitis ·≈– fibrosis ´÷ßË µËÕ¡“®–¡’·º≈‡√◊ÕÈ √—ß√—°…“‰¡ËÀ“¬ (µ“√“ß∑’Ë 2.11, 2.12) ª√–«—µ°‘ ÕË πÀπÈ“∑’®Ë –¡’Õ“°“√‡À≈Ë“π’∑È Ë’ ”§—≠§◊Õ ‡§¬‡ªÁπ DVT ¡“°ËÕπ ¡’°“√∫“¥‡®Á∫¢ÕßÀ≈Õ¥‡≈◊Õ¥¥”∑’Ë¢“Àπ’∫À√◊ÕÕÿÈß‡™‘ß°√“π ¡“°ËÕπ ‡§¬ºË“µ—¥„À≠Ë∑µË’ ÕÈ ßπÕπæ—°‡ªÁπ√–¬–‡«≈“π“π ∂È“¬◊π À√◊Õ‡¥‘ππ“π®–√Ÿ È °÷ ª«¥Àπ—°∂Ë«ß∑’¢Ë “ Õ“°“√ª«¥∫«¡®–∑ÿ‡≈“‡¡◊ÕË ¢“¬° Ÿß ¡’°“√‡¥‘π°–‡º≈°·≈–ª«¥µÿ∫ Ê ‡«≈“‡¥‘ππ“π Ê ´÷ßË ‡ªÁπÕ“°“√¢Õß venous claudication ≈—°…≥–°“√∫«¡®–‡ªÁπ·∫∫ çbrawny edemaé °¥‰¡Ë∫¡Îÿ ‡π◊ÕË ß®“°‡π◊ÕÈ ‡¬◊ÕË ¡’ fibrosis ¿“«– §«“¡¥—π„πÀ≈Õ¥‡≈◊Õ¥¥”∑’¢Ë “ Ÿß°«Ë“ª°µ‘ (venous hypertension) ®–∑”„ÀÈ¡°’ “√‡æ‘¡Ë ¢Õß hydorstatic pressure „πÀ≈Õ¥‡≈◊Õ¥ΩÕ¬ ‡¡Á¥‡≈◊Õ¥·¥ß®–´÷¡ºË“πºπ—ß™—Èπ‡ÕÁπ‚¥≈’‡≈’Ë¬¡¢ÕßÀ≈Õ¥‡≈◊Õ¥‡¢È“ ¡“ ŸË‡π◊ÈÕ‡¬◊ËÕ√Õ∫ Ê hemosiderin pigment ∑’Ë‡°‘¥¢÷Èπ®“°°“√ ≈“¬µ—«·≈– oxidation ®–·∑√°µ—«Õ¬ŸË „π‡π◊ÈÕ‡¬◊ËÕ ¡’≈—°…≥–

µ“√“ß∑’Ë 2.11 ·π«∑“ß„π°“√«‘π®‘ ©—¬·¬°‚√§ºŸªÈ «Ë ¬∑’¡Ë ·’ º≈‡√◊ÕÈ √—ß∑’¢Ë “

Pain Location

Bleeding with manipulation Characteristics Associated findings

ISCHEMIC

STASIS

NEUROPATHIC

Severe,particularly night,relieved by dependency Distally,on dorsum of the feet or toes

Mild,relieved by elevation

None

Lower 1/3 of leg (gaiter area)

Under calluses or pressure points (Plantar aspiects of 1st+5th metaphalangeal joints) May be brisk Punched out with deep sinus Demonstrable neuropathy

Little or none Irregular edge, poor granulation tissue Trophic changes of chronic ischemia

Venous ooze Shallow,irregular shape,granulating edges, Stasis dermatitis

»—≈¬»“ µ√ÏÀ≈Õ¥‡≈◊Õ¥

µ“√“ß∑’Ë 2.12 ·π«∑“ß„π°“√«‘π®‘ ©—¬·¬°‚√§ºŸªÈ «Ë ¬∑’¡Ë ¢’ “∫«¡

Consistency of swelling Relief by elevation Distribution of swelling Pain Bilaterally

VENOUS

LYMPHATIC ORTHOSTATIC

CARDIAC/

LIPIDEMA

Brawny (fat) Complete

Spongy

Pitting

Non-compressible

Mild

Complete

Minimal

Diffused, greatest distally None or heave ache

Diffused, greatest distally

Maximal in ankles, and legs, feet spared Dull ache, cutaneous sensitivity

As often as not

Always but may be unequal

Maximal, in ankles and leg, feet spared Heavy ache, tight or bursting Occasionally, but usually unequal

§≈È“¬ π‘¡‡À≈Á° ∑”„ÀÈ‡π◊ÕÈ ‡¬◊ÕË ·≈–º‘«Àπ—ß∫√‘‡«≥π—πÈ ¡’ π’ ”È µ“≈§≈È” (brownish skin pigmentation) (√Ÿª∑’Ë 2.16) º‘«Àπ—ß∑’ÀË ¥µ—« ‡°‘¥®“°§«“¡¥—π„π‡π◊ÕÈ ‡¬◊ÕË ¡’√–¥—∫ ŸßÕ¬Ÿ‡Ë ªÁπ√–¬–‡«≈“π“π‡°‘¥ fat necrosis ·≈– fibrosis ∫“ß√“¬®–¡’°≈È“¡‡π◊ÈÕ≈’∫º‘«Àπ—ß ∫√‘‡«≥¢ÈÕ‡∑È“√—¥·πËπµ÷ß®–∑”„ÀÈ¢“¡’≈°— …≥–‡ªÁπ çinverted champagne bottleé (√Ÿª∑’Ë 2.16) venous stasis ulcer ®–‡°‘¥∫√‘‡«≥ gaiter area À√◊Õ¢“¥È“π„π‡Àπ◊ÕµËÕµ“µÿË¡‡ ¡Õ Õ“®®–æ∫‰¥È ∑“ß¥È“π¢È“ßÀ√◊ÕÀπÈ“·¢Èß ·º≈°«È“ßµ◊Èπ‰¡Ë≈÷°∂÷ß¢—Èπæ—ßº◊¥ Õ“® µ“√“ß∑’Ë 2.13 “‡Àµÿ¢ÕßÀ≈Õ¥‡≈◊Õ¥¢Õ¥∑’¢Ë “ Primary

“‡Àµÿ∑·Ë’ ∑È®√‘ß¬—ß‰¡Ë∑√“∫·πËπÕπ ¡—°æ∫„π‡§√◊Õ≠“µ‘ Õ“®®–‡π◊ Ë Õ ß¡“®“°§«“¡ÕË Õ π·Õ¢Õßºπ— ß À≈Õ¥ ‡≈◊Õ¥¥”·≈–≈‘Èπª‘¥‡ª‘¥ ®÷ß∑”„ÀÈÀ≈Õ¥‡≈◊Õ¥‚ªËßæÕß ≈‘πÈ ª‘¥‡ª‘¥æ‘°“√ À√◊Õ‰¡Ë¡·’ µË°”‡π‘¥ Secondary ¡’°“√Õÿ¥µ—π¢Õß°“√‰À≈‡«’¬π‡≈◊Õ¥≈‘πÈ À—«„®: ®“°°“√µ—ßÈ §√√¿Ï, ‡π◊ÕÈ ßÕ°„π™Ë«ß∑ÈÕß, ascites, iliac vein thrombosis, µËÕ¡πÈ”‡À≈◊ÕßÕ—°‡ ∫, retroperitoneal fibrosis ≈‘πÈ ª‘¥‡ª‘¥∂Ÿ°∑”≈“¬: ®“° deep vein thrombosis

§«“¡¥—π·≈–¡’‡≈◊Õ¥‰À≈‡«’¬π¡“°¢÷πÈ : arteriovenous fistula

Little or none

Always

®–¡’À≈“¬·º≈·≈–¡’¢π“¥µË“ß°—π ‰¡Ëæ∫·º≈∑’Ëª≈“¬π‘È«‡∑È“ ‡À¡◊Õπ°—∫·º≈∑’Ë‡°‘¥®“°°“√¢“¥‡≈◊Õ¥¡“‡≈’È¬ß (µ“√“ß∑’Ë 2.14) º‘«Àπ—ß√Õ∫·º≈¡’ ’§≈È” ¡’√ËÕß√Õ¬∫“¥·º≈‡°Ë“∑’ËÀ“¬·≈È« °Èπ ·º≈µ◊Èπ°«È“ß§≈ÿ¡¥È«¬‡π◊ÈÕ‡¬◊ËÕ∑’Ëµ“¬·≈È«·≈–≈Õ°À≈ÿ¥‰¥ÈßË“¬ µ“√“ß∑’Ë 2.14 “‡Àµÿ¢Õß°“√∫«¡πÈ”‡À≈◊Õß§—ßË Secondary Neoplastic infiltration of lymph nodes: Secondary carcinoma Primary reticuloses Infection: Filariasis Lymphogranuloma inguinale Tuberculosis Recurrent non-specific infection Iatrogenic Surgical excision and Irradiation of lymph nodes Primary Congenital or acquired deficiency of the lymphatics Dilatation and incompetence of the lymphatics

°“√µ√«®√Ë“ß°“¬·≈–°“√ª√–‡¡‘πºŸÈªË«¬‚√§À≈Õ¥‡≈◊Õ¥ Õ“®®–¡’ cellulitis ‡°‘¥¢÷Èπ√Õ∫¢Õ∫·º≈ ‘Ëß∑’Ë· ¥ß«Ë“·º≈®– ‡√‘¡Ë À“¬§◊Õ vascular granulation tissue „µÈ·º≈ ·≈– epithelium ’™¡¿Ÿµ√ß¢Õ∫·º≈ ·º≈‡√◊ÕÈ √—ßπ“π Ê ∑‘ßÈ ‰«È®–°≈“¬‡ªÁπ ¡–‡√Áßº‘«Àπ—ß™π‘¥ squamous cell (Marjolinûs ulcer) 1.3 VARICOSE VEINS ‡ªÁπ‚√§À≈Õ¥‡≈◊Õ¥¥”∑’æË ∫‰¥È∫ÕË ¬∑’ Ë ¥ÿ ®–æ∫«Ë“¡’°“√¢¬“¬µ—« ¬◊¥¬“« ·≈–§¥¢Õ¥¢ÕßÀ≈Õ¥‡≈◊Õ¥¥”„µÈº«‘ Àπ—ß ‚¥¬‡©æ“– long ·≈– short saphenous veins ·≈– “¢“µË“ß Ê ∑’·Ë ¬°ÕÕ°‰ª ®“°À≈Õ¥‡≈◊Õ¥À≈—° À≈Õ¥‡≈◊Õ¥„µÈº‘«Àπ—ß®–‡™◊ËÕ¡µËÕ°—∫ deep veins ‚¥¬ perforating veins ´÷ßË ·∑ß∑–≈ÿº“Ë π deep fascia long saphenous vein ®–¡’ perforators Õ¬ŸË 3 ™ÿ¥ (√Ÿª∑’Ë 2.17) ™ÿ¥·√°®–Õ¬ŸËµ√ß subsatorial canal ™ÿ¥∑’Ë Õßµ√ß°≈È“¡‡π◊ÈÕ πËÕß·≈–™ÿ¥∑’Ë 3 ‡Àπ◊Õ¢ÈÕ‡∑È“ ∂È“™ÿ¥∑’Ë 3 ¡’ incompetent valves ‡«≈“°≈È“¡‡π◊ÈÕπËÕßÀ¥µ—« ®–¢—∫‡≈◊Õ¥≈ß¡“∑’Ë‡∑È“·∑π∑’Ë®–¬ÈÕπ ¢÷Èπ¥È“π∫πµ“¡ª°µ‘ ∑”„ÀÈ‡°‘¥°“√°√–®“¬¢Õß·¢πßÀ≈Õ¥‡≈◊Õ¥ ¥”¢π“¥‡≈Á°ÕÕ°‰ª∑ÿ°∑‘»∑“ß ®“° perforators ‡Àπ◊Õµ“µÿ¡Ë ‡√’¬°«Ë“ çflare signé À≈Õ¥‡≈◊Õ¥¥”¢Õ¥æ∫‰¥È∑ÿ°°≈ÿË¡Õ“¬ÿ æ∫¡“°„π ‡æ»À≠‘ß«—¬°≈“ß§π Õ—µ√“ Ë«π∑’æË ∫‡æ»À≠‘ß¡“°°«Ë“‡æ»™“¬√“« 10 ‡∑Ë“ „π‡¥Á°®–æ∫√Ë«¡°—∫§«“¡º‘¥ª°µ‘·µË°”‡π‘¥¢Õß‚√§ À≈Õ¥‡≈◊Õ¥Õ◊Ëπ√Ë«¡¥È«¬ °“√¬◊ππ“π∑”„ÀÈ ‚√§π’È‡ªÁπ¡“°¢÷Èπ·µË ‰¡Ë „™Ë “‡Àµÿπ”¢Õß°“√‡ªÁπ‚√§ Õ“°“√§◊Õª«¥µ◊ÈÕ∑’ËπËÕß·≈–¢“ µÕπ‡¬ÁπÀ√◊ÕµÕπ°≈“ß§◊πÀ≈—ß®“°¬◊πÀ√◊Õ‡¥‘π¡“‡ªÁπ√–¬–‡«≈“ π“π Õ“°“√ª«¥®–¥’¢πÈ÷ ∂È“π—ßË À√◊ÕπÕπæ—°‚¥¬¬°¢“ Ÿß ¡’ night cramp ∫“ß√“¬‰¡Ë¡Õ’ “°“√ª«¥·µË®–æ∫À≈Õ¥‡≈◊Õ¥¢Õ¥√Ë«¡°—∫ venous stars, ’º‘«§≈È”, µÿË¡º◊Ëπ§—π·≈–·º≈‡√◊ÈÕ√—ß ∫√‘‡«≥¢ÈÕ ‡∑È“∫«¡µÕπ°≈“ß«—π·µËæÕæ—°·≈–¬°‡∑È“°“√∫«¡®–¬ÿ∫≈ß °“√ µ—Èß§√√¿Ï∑”„ÀÈÀ≈Õ¥‡≈◊Õ¥¢Õ¥‡ªÁπ¡“°¢÷Èπ ∫“ß§√—Èß‚√§π’Èæ∫‰¥È „πºŸªÈ «Ë ¬∑’¡Ë °’ ÕÈ π‡π◊ÕÈ ßÕ°¿“¬„πÕÿßÈ ‡™‘ß°√“π (µ“√“ß∑’Ë 2.13) µ√«®√Ë“ß°“¬‚¥¬„ÀÈºŸÈªË«¬¬◊π ¥Ÿµ—Èß·µË –¥◊Õ≈ß‰ª®π∂÷ß ª≈“¬‡∑È“ ¥Ÿ¥È“πÀ≈—ßµ“¡·π«¢Õß short saphenous vein ∫—π∑÷°≈—°…≥–°“√¢¬“¬µ—« §«“¡§¥¢Õ¥¢ÕßÀ≈Õ¥‡≈◊Õ¥·≈– ·π«∑“ß‡¥‘π µ≈Õ¥®π√ËÕß√Õ¬¢Õß¿“«– venous hypertension ‡™Ëπ ’º«‘ πÈ”µ“≈ (brown pigmentation) º◊πË §—π·≈–·º≈∑’‡Ë °‘¥ ¢÷Èπµ√ß¢“¥È“π„π‡Àπ◊Õµ“µÿË¡ (gaiter area) ¥ŸÀ≈Õ¥‡≈◊Õ¥¥”∑’Ë ¢¬“¬¢π“¥∑’Ë¢“Àπ’∫·≈–∑ÈÕß¥È“π≈Ë“ß§≈”À≈Õ¥‡≈◊Õ¥¥”µ“¡ ·π«∑“ß¢Õß long ·≈– short saphenous veins µ√«®¥Ÿ°“√ §¥¢Õ¥¢ÕßÀ≈Õ¥‡≈◊Õ¥∑’¡Ë Õß‡ÀÁπ®“°¢“∑—ßÈ Õß¢È“ß

√Ÿª∑’Ë 2.17 ∫√‘‡«≥¢“¥È“π„π∑’Ë§≈” perforating veins ‰¥È Cough impulse test ‡ªÁπ°“√µ√«® competency ¢Õß ≈‘πÈ ª‘¥‡ª‘¥¢Õß long saphenous vein µ√ß saphenofemoral junction ‚¥¬„™Èπ«È‘ «“ß≈ß∫π saphenous opening ·≈È«„ÀÈºªÈŸ «Ë ¬‰Õ ∂È“¡’§«“¡√Ÿ È °÷ «Ë“¡’ fluid thrill ¡“°√–∑∫µ√ßª≈“¬π‘«È · ¥ß«Ë“¡’ incompetent valve Trendelenberg test (retrograde filling) ‡ªÁπ°“√µ√«® competency ¢Õß≈‘Èπª‘¥‡ª‘¥„πÀ≈Õ¥‡≈◊Õ¥¥”∑ÿ°√–∫∫¢Õß saphenofemoral veins „ÀÈºªÈŸ «Ë ¬πÕπÀß“¬√“∫∫π‡µ’¬ß ¬°‡∑È“ Ÿß®πÀ≈Õ¥‡≈◊Õ¥¥”·ø∫ „™È “¬¬“ß√—¥ (torniquet) æ—π∑’µË πÈ ¢“ „ÀÈºªÈŸ «Ë ¬≈ÿ°¢÷πÈ ¬◊π·≈– —ß‡°µÿ venous filling „π¿“«–ª°µ‘ venous filling ®–‡√‘¡Ë µÈπ®“°ª≈“¬‡∑È“¢÷πÈ ¡“∂÷ßµÈπ¢“„™È‡«≈“ª√–¡“≥ 35 «‘π“∑’ (√Ÿª∑’Ë 2.18) „π°“√∑’Ë®–¡’‡≈◊Õ¥ºË“π®“°À≈Õ¥‡≈◊Õ¥·¥ß‰ª¬—ß capillary beds ·≈–‡¢È“ ŸË venules º≈¢Õß°“√µ√«®·º≈º≈‰¥È¥ß— µËÕ‰ªπ’È 1. ¡’ filling ¢Õß superficial veins Õ¬Ë“ß√«¥‡√Á«¢≥–∑’√Ë ¥— “¬¬“ß·≈–„ÀÈºŸÈªË«¬¬◊π¢÷Èπ · ¥ß«Ë“¡’ incompetent valves ¢Õß perforators ‡≈◊Õ¥®–‰À≈ºË“π®“° deep veins ‡¢È“ ŸË superficial veins Õ¬Ë“ß√«¥‡√Á« 2. ¡’ filling ¢Õß superficial veins ®“°∫π≈ß≈Ë“ßÕ¬Ë“ß √«¥‡√Á« · ¥ß«Ë“¡’ incompetent valves ¢Õß saphenous veins ·ª≈º≈°“√µ√«®√Ë“ß°“¬‰¥È¥ß— µËÕ‰ªπ’È (√Ÿª∑’Ë 2.19)

»—≈¬»“ µ√ÏÀ≈Õ¥‡≈◊Õ¥

√Ÿª∑’Ë 2.18 The Brodie-Trendelenbug test for venous valvular incompetence

1. 2. 3. 4.

-, -ve -, +ve +, -ve +, +ve

ª°µ‘ ¡’ incompetent saphenofemoral valve ¡’ incompetent perforators ¡’ incompetent perforators ·≈– saphenofemoral valve Torniquet test ‡ªÁπ°“√À“µ”·ÀπËß incompetent valves

√Ÿª∑’Ë 2.19 Brodie-Trendelenberg test ·≈–°“√·ª≈º≈

¢Õß pertorator „ÀÈºŸÈªË«¬πÕπ√“∫ ¬°¢“ Ÿß®π°√–∑—ËßÀ≈Õ¥ ‡≈◊Õ¥¥”·ø∫ „™È “¬¬“ß√—¥æ—π 1/3 ¢ÕßµÈπ¢“·≈È«„ÀÈºªÈŸ «Ë ¬¬◊π¢÷πÈ (√Ÿª∑’Ë 2.20) ∂È“À≈Õ¥‡≈◊Õ¥¥”∑’ËµÈπ¢“‡Àπ◊ÕµËÕ®ÿ¥∑’Ëæ—π “¬¬“ß ‚ªËßæÕß·µËµ”Ë °«Ë“ “¬¬“ß∑’√Ë ¥— À≈Õ¥‡≈◊Õ¥·ø∫ · ¥ß«Ë“¡’ incompetency ¢Õß perforators ‡Àπ◊ÕµËÕ®ÿ¥∑’Ë√—¥ “¬¬“ß ∂È“„µÈµËÕ ∑’Ë√—¥ “¬¬“ß À≈Õ¥‡≈◊Õ¥¥”‚ªËßæÕß ·µË¢È“ß∫π·ø∫· ¥ß«Ë“¡’ incompetency ¢Õß perforators „µÈµÕË “¬¬“ß√—¥ ®–‡ª≈’¬Ë π µ”·ÀπËß∑’Ë√—¥ “¬¬“ßµ√ß„¥°Á ‰¥È À√◊Õ®–√—¥‡ªÁπ‡ª≈“–À≈“¬ µ”·ÀπËß°Á ‰¥È ∫√‘‡«≥∑’ Ë ß —¬«Ë“®–¡’ perforator incompetent Feganûs method ‡ªÁπ«‘∏’°“√Àπ÷Ëß∑’Ë „™ÈÀ“µ”·ÀπËß¢Õß incompent perforators µ√«®‚¥¬°“√„™Èª“°°“ ’‡¢’¬π∑” ‡§√◊ËÕßÀ¡“¬ º‘«Àπ—ßµ√ß Ë«π∑’Ë§“¥«Ë“®–‡ªÁπ perforators „ÀÈ ºŸªÈ «Ë ¬πÕπÀß“¬√“∫ ¬°¢“¢÷πÈ „™Èπ«È‘ °¥≈ß∫πµ”·ÀπËß¢Õß perforators ·≈È«„ÀÈºªÈŸ «Ë ¬¬◊π¢÷πÈ ®–§≈”‰¥È√≈Ÿ °÷ ≈ß‰ª®“°™‘πÈ ‡ÕÁπæ—ßº◊¥ ‡¡◊ÕË ª≈ËÕ¬π‘«È ÕÕ°‡≈◊Õ¥®–‰À≈ºË“π‡¢È“ ŸË saphenous vein ∑”„ÀÈ ‡≈◊Õ¥‚ªËßæÕßÕ¬Ë“ß√«¥‡√Á«‡æ◊ËÕ„ÀÈ·πË „®«Ë“„πº≈¢Õß°“√µ√«® §«√∑” Trendelenberg ·≈– torniquet test √Ë«¡¥È«¬ °“√‡§“– „™Èπ«È‘ ‡§“–µ“¡≈”¢ÕßÀ≈Õ¥‡≈◊Õ¥¥”∑“ß¥È“π∫π ‚¥¬„™Èπ«È‘ «“ß¥È“π≈Ë“ß¢ÕßÀ≈Õ¥‡≈◊Õ¥¥” ∂È“¡’ incompetency ¢Õß saphenous vein ®–¡’§«“¡√Ÿ È °÷ «Ë“¡’ transmitted wave ¡“° √–∑∫π‘«È ¥È“π≈Ë“ß °“√ø—ß „™È ‰¥È∑ßÈ— ÀŸøß— ·≈– doppler ultrasound §«√µ√«®„π ºŸªÈ «Ë ¬∑’¡Ë ’ arteriovenous malformation °“√µ√«®√Ë“ß°“¬ Ë«πµË“ß Ê ∑’§Ë «√∑”§◊Õ µ√«®∑«“√Àπ—° ∂È“ ß —¬«Ë“®–¡’‡π◊ÈÕßÕ°‡°‘¥¢÷Èπ„π™ËÕß∑ÈÕßÀ√◊ÕÕÿÈß‡™‘ß°√“π µËÕ¡πÈ”‡À≈◊Õß∫√‘‡«≥¢“Àπ’∫

°“√µ√«®√Ë“ß°“¬·≈–°“√ª√–‡¡‘πºŸÈªË«¬‚√§À≈Õ¥‡≈◊Õ¥

√Ÿª∑’Ë 2.20 Torniquet test

1.4 °“√Õÿ¥µ—π¢Õß VENA CAVA 1.4.1 °“√Õÿ¥µ—π¢Õß superior vena cava (SVC) ®– —ß‡°µæ∫«Ë“ºŸÈªË«¬¡’À≈Õ¥‡≈◊Õ¥¥”∑’Ë§Õ Õ°¥È“πÀπÈ“ ·≈–µÈπ·¢π‚ªËßæÕß (engorgement) ‡ÀÁπ‰¥È™¥— ‡®π ¡’ „∫ÀπÈ“∫«¡ (√Ÿª∑’Ë 2.21) “‡Àµÿ‡π◊ÕË ß¡“®“°°“√¡’ thrombus Õÿ¥µ—πÀ√◊Õ‡π◊ÕÈ ßÕ°„π™ËÕß∑√«ßÕ°·≈–‡¡¥‘·Õ µ‘π¡Ë— °¥ SVC Õ“°“√Õ“®®–‡°‘ ¥ ¢÷ È π Õ¬Ë “ ß√«¥‡√Á « À√◊ Õ §ËÕ¬‡ªÁπ§ËÕ¬‰ª ºŸÈªË«¬∑’Ë¡’Õ“°“√Õ¬Ë“ß‡©’¬∫æ≈—π ÀπÈ“ ·≈–§Õ®–∫«¡¡“° ·≈–¡’®ÿ¥‡≈◊Õ¥°√–®“¬„π‡¬◊ËÕµ“ (blood shed eyes) „π√“¬∑’ÕË “°“√§ËÕ¬‡ªÁπ§ËÕ¬‰ª ®–

√Ÿª∑’Ë 2.21 SVC syndrome

æ∫«Ë“¡’ venous star °√–®“¬Õ¬Ÿ∑Ë «Ë— ‰ª∑’ºË «‘ Àπ—ß∫√‘‡«≥ ÀπÈ“Õ°·≈–§Õ “‡Àµÿ∑’Ëæ∫‰¥È∫ËÕ¬∑’Ë ÿ¥§◊Õ ¡–‡√Áß¢Õß Õ«—¬«–¿“¬„π‡¡¥‘·Õ -µ‘π¡Ë— ∑—ßÈ ª∞¡¿Ÿ¡·‘ ≈–∑ÿµ¬‘ ¿Ÿ¡‘ ‚¥¬ ‡©æ“–µËÕ¡∏—¬√Õ¬¥Ï “‡Àµÿ∑’Ëæ∫√Õß≈ß¡“§◊Õ «—≥‚√§, sarcoidosis, aneurysm of the aortic arch, idiopathic mediastinitis, substernal goiter À√◊ Õ °“√ «π “¬§“‰«È „πÀ≈Õ¥‡≈◊Õ¥¥”„À≠Ë∑∑Ë’ √«ßÕ°π“π Ê 1.4.2 °“√Õÿ¥µ—π¢Õß inferior vena cava (IVC) ‡°‘¥¢÷πÈ ‰¥ÈÕ¬Ë“ß‡©’¬∫æ≈—πÀ√◊Õ§ËÕ¬‡ªÁπ§ËÕ¬‰ª °“√∫«¡·≈– collaterals ∑’Ë‡°‘¥¢÷Èπ∑’Ëº‘«Àπ—ß®–∫Ëß∫Õ°∂÷ß ¿“«–°“√ Õÿ¥µ—π«Ë“¡’¡“°πÈÕ¬‡æ’¬ß‰√ ®–æ∫«Ë“¡’¢“∫«¡∑—Èß Õß ¢È“ß¢÷πÈ ¡“∂÷ß∑ÈÕß·≈– –‚æ° º‘«Àπ—ß∫«¡ µ÷ß °¥∫ÿ¡Î ¡’ collaterals °√–®“¬∑—Ë«‰ª∑’Ë¢“·≈–ÀπÈ“∑ÈÕß ®–·¬° °“√Õÿ¥µ—π¢Õß IVC ®“°°“√Õÿ¥µ—π¢Õß portal vein ‰¥È¬“°‡æ√“–„™È collaterals °≈ÿ¡Ë ‡¥’¬«°—π ¡’«∏‘ °’ “√·¬° ßË“¬ Ê ®“°°“√µ√«® superficial collaterals ∑’Ë‡ÀÁπ ®“°º‘«Àπ—ß ‚¥¬„™Èπ«È‘ ¡◊Õ 2 π‘«È °¥À≈Õ¥‡≈◊Õ¥¥”„ÀÈ·ø∫ ·≈È«ª≈ËÕ¬∑’≈–π‘È« ∂È“‡≈◊Õ¥«‘Ëß¢÷ÈππË“®–‡°‘¥®“°°“√Õÿ¥ µ—π¢Õß IVC ∂È“‡≈◊Õ¥«‘ßË ≈ß®–‡°‘¥®“°°“√Õÿ¥µ—π¢Õß portal vein (Harveyûs test) °“√Õÿ¥µ—π¢Õß IVC ¡’ “‡Àµÿ®“°¡–‡√Áß‰¥È Ÿß∂÷ß√ÈÕ¬≈– 50-60 ∑’Ëæ∫∫ËÕ¬√Õß ≈ß¡“§◊Õ retroperitoneal fibrosis, µËÕ¡πÈ”‡À≈◊Õß Õ—°‡ ∫„πÕÿßÈ ‡™‘ß°√“π, lipomatosis, abdominal aortic aneurysm œ≈œ

1.5 §«“¡º‘¥ª°µ‘¢ÕßÀ≈Õ¥‡≈◊Õ¥¥”·µË°”‡π‘¥ æ∫‰¥ÈπÕÈ ¬ ∑’æË ∫‰¥È¡Õ’ ¬ŸË 2 °≈ÿ¡Ë §◊Õ multiple arteriovenous fistula ·≈–§«“¡º‘¥ª°µ‘‡©æ“–∑’ÀË ≈Õ¥‡≈◊Õ¥¥” 1.5.1 multiple arteriovenous fistula (Robertsonûs giant limb) º≈®“°°“√¡’√øŸ ‘ µŸ≈“Ë √–À«Ë“ßÀ≈Õ¥‡≈◊Õ¥ ¥” ·≈–À≈Õ¥‡≈◊Õ¥·¥ßÀ≈“¬·ÀËß §◊Õ®–¡’‡≈◊Õ¥¡“ ‡≈’È¬ß∑’Ë·¢π ¡◊Õ À√◊Õ¢“¥È“ππ—Èπª√‘¡“≥ Ÿß ¡’°“√‡æ‘Ë¡ ¢Õßª√‘¡“≥‡≈◊Õ¥„π√Ë“ß°“¬·≈– cardiac output (CO) º≈∑’µË “¡¡“§◊Õ¡’Õ“°“√À—«„®«“¬ ·¢π·≈–¢“π—πÈ ®–¬“« ·≈–‚µº‘¥ª°µ‘‡¡◊ÕË ‡∑’¬∫¥È“πµ√ß°—π¢È“¡ º‘«Àπ—ßÕÿπË ·≈– ¡’ ™’ ¡¿Ÿ‡¢È¡Õ“®®–‡°‘¥ venous ulcer ‡√◊ÕÈ √—ß‡À¡◊ÕπºŸªÈ «Ë ¬ venous hypertension º‘«Àπ—ß¡’ stasis change À—«„®·≈–À—«„®«“¬¥È“π´È“¬ °¥°“√‰À≈‡«’¬π¢Õß‡≈◊Õ¥ ∑’ Ë º Ë “ π√Ÿ ø ‘ µŸ ≈ Ë “ ®–∑”„ÀÈ ¡ ’ ° “√‡æ‘ Ë ¡ §«“¡µÈ “ π∑“π„π À≈Õ¥‡≈◊Õ¥ Ë«πª≈“¬ º≈∑’Ëµ“¡¡“§◊Õ™’æ®√®–™È“≈ß ∂◊Õ«Ë“‡ªÁπº≈∫«°¢Õß Branhamûs bradycardia response ´÷ßË ®–æ∫„πºŸªÈ «Ë ¬‚√§π’È 1.5.2 venous abnormalities (Klippel-Trenaunay syndrome) §«“¡º‘¥ª°µ‘¢ÕßÀ≈Õ¥‡≈◊Õ¥¥”¡’‰¥ÈÀ≈“¬√Ÿª ·∫∫ ·µË¡Õ’ “°“√· ¥ßÀ≈—°∑’ Ë ”§—≠§◊Õ 1. ¡’À≈Õ¥‡≈◊Õ¥¥”¢Õ¥∑’¢Ë “¥È“ππÕ° 2. ¡’ cutaneous angiomata À√◊Õ port wine stains 3. ·¢πÀ√◊Õ¢“¢È“ßπ—πÈ ®–¬“«·≈–‚µº‘¥ª°µ‘ ºŸÈªË«¬®–‰¡Ë¡’ arteriovenous fistula À—«„®ª°µ‘·≈– bradycardia test ‰¥Èº≈≈∫

√–∫∫πÈ”‡À≈◊Õß (THE LYMPHATICS) ‚√§ª∞¡¿Ÿ¡‘¢ÕßµËÕ¡πÈ”‡À≈◊Õßæ∫‰¥ÈπÈÕ¬ ∑’Ëæ∫‰¥È∫ËÕ¬§◊Õ ∑ÿµ‘¬¿Ÿ¡‘®“°°“√≈ÿ°≈“¡¢Õß‡π◊ÈÕßÕ° °“√°¥∑—∫À√◊Õ∑”≈“¬∑ËÕ ∑“ß‡¥‘ππÈ”‡À≈◊Õß∑”„ÀÈ‡°‘¥§«“¡º‘¥ª°µ‘„π°“√√–∫“¬πÈ”‡À≈◊Õß Õ“°“√∑’æË ∫‰¥È∫ÕË ¬§◊Õ ∫«¡ °“√µ√«®√Ë“ß°“¬ §«√µ√«®¥Ÿ∑°ÿ √–∫∫°ËÕπ ‡æ◊ÕË ·¬°®“° °“√∫«¡∑’Ë¡’ “‡Àµÿ¡“®“°‚√§‰µÀ√◊Õ‚√§À—«„® severe lymphedema ®–æ∫«Ë“¡’°“√∫«¡¢Õß¬“‡ÀÁπ‰¥È™¥— ‡®π „π mild lymphedema ∂È“‰¡Ë —ß‡°µÿ¥Ÿ®√‘ß®–‰¡Ëæ∫«Ë“¡’¢“∫«¡‡≈Á°πÈÕ¬ §«√¥Ÿ ∑“ß¥È“πÀ≈—ß (√Ÿª∑’Ë 2.22) ®–‡ÀÁπ°“√∫«¡‰¥È™—¥°«Ë“¥Ÿ∑’Ë¢ÈÕ‡∑È“ ·≈–À≈—ß‡∑È“ ®–‰¡Ë‡ÀÁπ≈”¢Õß‡ÕÁπ√ÈÕ¬À«“¬ (tendo achillis con-

»—≈¬»“ µ√ÏÀ≈Õ¥‡≈◊Õ¥ tour) ‡À¡◊Õπ„π¿“«–ª°µ‘ ®–°¥∫ÿÎ¡·µËµÈÕßÕÕ°·√ß „πºŸÈªË«¬∑’Ë ∫«¡‡√◊ÈÕ√—ß®–°¥‰¡Ë∫ÿÎ¡‡æ√“–º‘«Àπ—ß·≈–‡π◊ÈÕ‡¬◊ËÕ®–∫«¡·¢Áß¡’ ≈—°…≥–‡ªÁπ°ÈÕπ‡≈Á° Ê §≈È“¬ cobble stone º‘«Àπ—ß∫√‘‡«≥ π‘È«‡∑È“¡’µÿË¡πÈ”·µ°ßË“¬ ¡’πÈ”‡À≈◊Õß‰À≈´÷¡ÕÕ°¡“ ¡’°“√µ‘¥‡™◊ÈÕ ·∫§∑’‡√’¬·≈–‡™◊ÈÕ√“ §«√‡ª√’¬∫‡∑’¬∫¢π“¥¢“∑—Èß Õß¢È“ß‚¥¬ «—¥‡ Èπ√Õ∫«ß∑’¢Ë “„πµ”·ÀπËßµËÕ‰ªπ’È ‡∑È“ ∑’√Ë –¥—∫ 8 ‡´Áπµ‘‡¡µ√ ‡Àπ◊ÕµËÕ interdigital cleft πËÕß¥È“π≈Ë“ß ∑’√Ë –¥—∫ 8 ‡´Áπµ‘‡¡µ√ ‡Àπ◊ÕµËÕ medial melleolus °≈“ßπËÕß ∑’√Ë –¥—∫ 12 ‡´Áπµ‘‡¡µ√ „µÈµÕË lower border of patella µÈπ¢“ ∑’√Ë –¥—∫ 12 ‡´Áπµ‘‡¡µ√ ‡Àπ◊ÕµËÕ upper border of patella

1. À≈Õ¥πÈ”‡À≈◊ÕßÕ—°‡ ∫ (lymphangitis) ‡¡◊ Ë Õ ‡°‘ ¥ °“√Õ— ° ‡ ∫µ‘ ¥ ‡™◊ È Õ ®“°·∫§∑’ ‡ √’ ¬ Õ¬Ë “ ß√ÿ π ·√ß ·∫§∑’‡√’¬®–·æ√Ë°√–®“¬®“°‡π◊ÈÕ‡¬◊ËÕ‡¢È“ ŸË√–∫∫πÈ”‡À≈◊Õß ∑“ß ∑ËÕπÈ”‡À≈◊Õß‰ª¬—ßµËÕ¡πÈ”‡À≈◊Õß∑’ËÕ¬ŸË „°≈È‡§’¬ß ‡¡◊ËÕ¡’°“√Õ—°‡ ∫ ¢Õß√–∫∫πÈ”‡À≈◊Õß ‚¥¬‡©æ“–À≈Õ¥πÈ”‡À≈◊ÕßÕ—°‡ ∫®–¡Õß ‡ÀÁπ‡ªÁπ‡ Èπ·¥ß∫“ß Ê ·≈–°¥‡®Á∫„µÈº«‘ Àπ—ß∫√‘‡«≥∑’‡Ë °‘¥À≈Õ¥ πÈ”‡À≈◊ÕßÕ—°‡ ∫‰¥È∫ÕË ¬§◊Õ∑’¡Ë Õ◊ ·≈–‡∑È“ ºŸªÈ «Ë ¬®–ª«¥·∫∫‡µÈπµÿ∫ Ê (throbbing pain) µ√ßµ”·ÀπËß∑’Ë¡’°“√‡√‘Ë¡µÈπÕ—°‡ ∫ ·≈– ª«¥µ“¡·π«‡ Èπ·¥ß Ê µ“¡º‘«Àπ—ß¢Õß·¢πÀ√◊Õ¢“¢÷Èπ¡“¬—ß µËÕ¡πÈ”‡À≈◊Õß∑’Ë√—°·√ÈÀ√◊Õ¢“Àπ’∫ µËÕ¡πÈ”‡À≈◊Õß∫√‘‡«≥π—ÈπÕ“® ®–∫«¡‚µ‰¥È ®“°°“√µ√«®√Ë“ß°“¬®–æ∫«Ë“¡’‡ Èπ·¥ßµ“¡·π«¢Õß∑ËÕπÈ”‡À≈◊Õß„µÈº«‘ Àπ—ß º‘«Àπ—ß∫√‘‡«≥π—πÈ ∫«¡µ÷ß ∫“ß§√—ßÈ µ”·ÀπËß∑’‡Ë √‘¡Ë µÈπ°“√Õ—°‡ ∫µ‘¥‡™◊ÈÕ·º≈Õ“®®–‡√‘Ë¡À“¬·≈È«æ∫·µË√Õ¬®“ß Ê ∑’πË «È‘ ‡∑È“À√◊Õ¢È“ß‡≈Á∫ „π‡π◊ÕÈ ‡¬◊ÕË ∏√√¡¥“‡¡◊ÕË ¡’°“√Õ—°‡ ∫¢Õß∑ËÕ πÈ”‡À≈◊Õß®–‰¡Ë≈°ÿ ≈“¡ ·µË∂“È ‡π◊ÕÈ ‡¬◊ÕË √Õ∫¢È“ß∫«¡¡“°·≈–ºŸªÈ «Ë ¬ ¡’§«“¡µÈ“π∑“π‚√§πÈÕ¬ Õ“®®–≈ÿ°≈“¡‡¢È“ ŸË√–¥—∫™—Èπ„µÈº‘«Àπ—ß °≈“¬‡ªÁπ cellulitis ‰¥È

2. °“√∫«¡πÈ”‡À≈◊Õß§—Ëß (lymphedema) §◊Õ°“√¡’π”È ‡À≈◊Õß‰À≈´÷¡®“°∑ËÕπÈ”‡À≈◊Õß‡¢È“‰ª§—ßË Õ¬ŸË„π interstitial tissue “√πÈ”∑’Ë§—ËßÕ¬ŸËπ’È¡’ª√‘¡“≥‚ª√µ’π Ÿß µË“ß®“° “√πÈ”∑’Ë§—Ëß´÷Ëß¡’ “‡Àµÿ¡“®“°‰µ«“¬·≈–À—«„®«“¬ ®–¡’ª√‘¡“≥ ‚ª√µ’πµË” “‡Àµÿ¢Õß°“√∫«¡πÈ”‡À≈◊Õß§—ßË (µ“√“ß∑’Ë 2.14) ¡—° ®–‡°‘¥®“°∑ÿµ‘¬¿Ÿ¡‘§◊Õ‚√§¢ÕßµËÕ¡πÈ”‡À≈◊Õß‡ ¡Õ °“√∫«¡πÈ”

°“√µ√«®√Ë“ß°“¬·≈–°“√ª√–‡¡‘πºŸÈªË«¬‚√§À≈Õ¥‡≈◊Õ¥

√Ÿª∑’Ë 2.22 °. ¢“∫«¡®“°πÈ”‡À≈◊Õß§—Ëß ¥Ÿ∑“ß¥È“πÀπÈ“ º‘«µ÷ß ¡—π ∫«¡ µ—Èß·µËπËÕß ¢ÈÕ‡∑È“ ·≈–À≈—ß‡∑È“ ¢. √Ÿª∑“ß¥È“πÀ≈—ß ®–¡Õß‰¡Ë‡ÀÁπ≈”¢Õß tendo Achillis

ª∞¡¿Ÿ¡‘∑’Ë¡’ “‡Àµÿ¡“®“°§«“¡º‘¥ª°µ‘À√◊Õ∫°æ√ËÕß¢Õß√–∫∫ πÈ”‡À≈◊Õßæ∫‰¥ÈπÕÈ ¬ (µ“√“ß∑’Ë 2.15) ª√–«—µ‘ 1o lymphedema æ∫‰¥ÈµßÈ— ·µË·√°§≈Õ¥ Õ“¬ÿπÕÈ ¬ ·≈–«—¬°≈“ß§π 2o lymphedema æ∫„π«—¬°≈“ß§π·≈– ŸßÕ“¬ÿ ‡æ»À≠‘ßæ∫‰¥È∫ÕË ¬°«Ë“™“¬‚¥¬‡©æ“– 2o lymphedema ‡æ√“– ¡—°®–‡°‘¥¿“¬À≈—ß ¡–‡√Áß√–∫∫ ◊∫æ—π∏ÿÏ∑’Ë·æ√Ë°√–®“¬‰ª¬—ßµËÕ¡ πÈ”‡À≈◊Õß∑’Ë¢“Àπ’∫∑—Èß Õß¢È“ß ¡–‡√Áß‡µÈ“π¡·æ√Ë°√–®“¬‰ª∑’Ë µËÕ¡πÈ”‡À≈◊Õß¢Õß√—°·√È Filariasis ∑’‡Ë °‘¥®“°‡™◊ÕÈ Wuchereria bancrofti ‡ªÁπ‚√§∑’Ëæ∫‰¥È „π·∂∫‡¡◊Õß√ÈÕπ ‡ªÁπ “‡Àµÿ¢Õß‚√§ ‡∑È“™È“ß Õ“°“√∑’‡Ë √‘¡Ë ®–§ËÕ¬‡ªÁπ§ËÕ¬‰ª ¢“À√◊Õ≈Ÿ°Õ—≥±–®–§ËÕ¬ Ê ‚µ¢÷πÈ ‚¥¬‡©æ“– 1o lymphedema ¢“®–∫«¡·≈–‚µ¢÷πÈ ¿“¬„π √–¬–‡«≈“ 3-4 —ª¥“ÀÏ ®–‰¡Ëª«¥ °“√‡§≈◊ÕË π‰À«®–≈”∫“°∂È“ ·¢πÀ√◊Õ¢“¢È“ßπ—Èπ¡’¢π“¥‚µ¢÷Èπ¡“° ‚√§∑’Ë¡—°®–‡ªÁπ√Ë«¡§◊Õ‚√§

º‘«Àπ—ß athelete’s foot ®“°‡™◊ÕÈ √“ tinea pedis ∫√‘‡«≥µ“¡ ´Õ°π‘«È ‡∑È“‡°‘¥·º≈·≈–≈ÿ°≈“¡µ‘¥‡™◊ÕÈ ‰¥Èß“Ë ¬ ‡ªÁπ cellulitis ·≈– septicemia ¡’µ¡Ëÿ πÈ”‡°‘¥¢÷πÈ ·≈È«·µ°‡Õß‰¥È∫ÕË ¬ 1o lymphedema ‡ªÁπ‚√§∑’∂Ë “Ë ¬∑Õ¥‰¥È∑“ß°√√¡æ—π∏ÿÏ (familial disease) °“√µ√«®√Ë“ß°“¬ æ∫«Ë“·¢πÀ√◊Õ¢“π—πÈ ®–∫«¡‚µ¡“° °¥ º‘«Àπ—ß®–∫ÿÎ¡‡≈Á°πÈÕ¬ ·µË®–µÈÕßÕÕ°·√ß°¥¡“° ‰¡Ë∫ÿÎ¡ßË“¬ ‡À¡◊Õπ°“√∫«¡πÈ”®“°‰µ«“¬À√◊ÕÀ—«„®«“¬ º‘«Àπ—ß®–À¥·¢Áß¡’ ≈—°…≥–‡ªÁπ hyperkeratosis ∫“ß§√—Èß®–¡’ –‡°Á¥∑’Ë√«¡µ—«°—π ‡ªÁπ°ÈÕπ¥Ÿ§≈È“¬ÀŸ¥ °ËÕπ«‘π®‘ ©—¬«Ë“ºŸªÈ «Ë ¬‡ªÁπ lymphedema §«√®–·¬°·¬–ÕÕ°®“°ºŸªÈ «Ë ¬‚√§‰µ«“¬ À—«„®«“¬ (general causes) °“√Õÿ¥µ—π¢ÕßÀ≈Õ¥‡≈◊Õ¥¥” (local cause) §«√µ√«® √Ë“ß°“¬ºŸªÈ «Ë ¬∑ÿ° Ë«π·≈–∑ÿ°√–∫∫

»—≈¬»“ µ√ÏÀ≈Õ¥‡≈◊Õ¥

µ“√“ß∑’Ë 2.15 °“√·∫Ëß°≈ÿ¡Ë ¢Õß Primary lymphedema

µ“√“ß∑’Ë 2.16 “‡Àµÿ¢ÕßµËÕ¡πÈ”‡À≈◊ÕßÕ—°‡ ∫

Primary lymphedema 1. lymphedema æ∫‰¥È·µË°”‡π‘¥ 2. lymphedema precox æ∫„π‡¥Á° 3. lymphedema tarda ‡°‘¥¿“¬À≈—ßÕ“¬ÿ 35 ª’

Infection Non-specific Glandular fever Tuberculosis Toxoplasmosis Syphilis Cat scratch fever Filariasis Lymphogranuloma (inguinale) Metastatic tumor Primary reticulosis Sarcoidosis

µËÕ¡πÈ”‡À≈◊Õß µËÕ¡πÈ”‡À≈◊Õß∑’√Ë –∫“¬®“°·¢πÀ√◊Õ¢“∑’¡Ë °’ “√ ∫«¡§—ßË ¢ÕßπÈ”‡À≈◊Õß®–‰¡Ë∫«¡‚µ„π 1o lymphedema ·µË®–∫«¡ ‚µ·≈–·¢Áß∂È“¡’¡–‡√Áß·æ√Ë°√–®“¬‰ª∂÷ß §«√µ√«®¥ŸµÕË ¡πÈ”‡À≈◊Õß ∫√‘‡«≥Õ◊πË ¢Õß√Ë“ß°“¬¥È«¬

3. POSTMASTECTOMY EDEMA °“√∫«¡¢Õß·¢π¿“¬À≈—ßµ—¥‡Õ“‡µÈ“π¡ÕÕ° ‡ªÁπ¿“«– ·∑√°´ÈÕπ∑’æË ∫‰¥È ‚¥¬‡©æ“–„π√“¬∑’¡Ë °’ “√©“¬· ß∫”∫—¥∫√‘‡«≥ axillary nodes ‚¥¬∑—Ë«‰ª·≈È«°“√∫«¡¢Õß·¢π∑’Ë‡°‘¥¢÷Èπ¿“¬À≈—ß°“√ºË“µ—¥ ∑—π∑’À√◊Õ¿“¬„π 2-3 —ª¥“ÀÏ·√° ®–¡’ “‡Àµÿ¡“®“° axillary vein thrombosis ·µË∂È“‡°‘¥¢÷Èπ¿“¬À≈—ß°“√ºË“µ—¥ 1-2 ‡¥◊Õπ ·≈– ·¢π∫«¡‚µ‰«¡“° ®–‡°‘¥®“°·º≈°¥√—¥ ·≈–°¥∑—∫∑—ßÈ axillary vein ·≈–∑ËÕπÈ”‡À≈◊Õß ∂È“¡’°“√∫«¡À≈—ßºË“µ—¥À√◊Õ©“¬· ß‡ªÁπ ‡«≈“À≈“¬‡¥◊ÕπÀ√◊Õª’ „π·¢π¢È“ß∑’Ë‡§¬‡ªÁπª°µ‘¡“°ËÕπ „ÀÈ π÷°∂÷ß°“√°≈—∫‡ªÁπ´È”¢Õß¡–‡√Áß‡µÈ“π¡ ∑’Ë¡’°“√°√–®“¬¡“¬—ß µËÕ¡πÈ”‡À≈◊Õß

4. LYMPHANGIOMA ‡ªÁπ¿“«–∑’æË ∫‰¥È ‰¡Ë§ÕË ¬∫ËÕ¬π—° ºŸªÈ «Ë ¬À√◊Õ¡“√¥“ºŸªÈ «Ë ¬ („π ‡¥Á°‡≈Á°) ®– —ß‡°µÿæ∫«Ë“¡’µ¡Ëÿ πÈ”„ ‡°‘¥¢÷πÈ À√◊Õ¡’°ÕÈ ππÿ¡Ë „µÈº«‘ Àπ—ß ´÷ËßµËÕ¡“‚µ¢÷Èπ·µ°·≈–¡’πÈ”„ À√◊Õ ’πÈ”µ“≈·¥ßÕÕ°¡“ Õ“®®– æ∫¿“«–π’È ‰¥ÈÀ≈—ß§≈Õ¥À√◊Õ„π‡¥Á°∑’Ë ‚µ·≈È« °ÈÕπ®–‚µ¢÷Èπ·≈– ®”π«π¢ÕßµÿË¡πÈ”°Á®–‡æ‘Ë¡¡“°¢÷Èπ¥È«¬ æ¬“∏‘ ¿“æπ’È ‰¡Ë¡’§«“¡ ‡®Á∫ª«¥ ∫√‘‡«≥∑’æË ∫‰¥È§Õ◊ º‘«Àπ—ß µ√ß√Õ¬æ—∫¢Õß·¢π ¢“ §Õ ≈”µ—« °ÈÕπ∑’ÕË ¬ŸË „µÈº«‘ Àπ—ß¡’ fluctuation ·≈– transilluminate §≈È“¬ cystic hygroma

5. µËÕ¡πÈ”‡À≈◊ÕßÕ—°‡ ∫ (LYMPHADENOPATHY) ‡ªÁπ¿“«–∑’æË ∫‰¥È∫ÕË ¬ ¡—°®–‡°’¬Ë «¢ÈÕß°—∫æ¬“∏‘ ¿“æ Õ«—¬«– ¢È“ß‡§’¬ß°—∫µËÕ¡πÈ”‡À≈◊Õß∫√‘‡«≥π—πÈ (µ“√“ß∑’Ë 2.16)

°“√µ√«®√Ë“ß°“¬·≈–°“√ª√–‡¡‘πºŸÈªË«¬‚√§À≈Õ¥‡≈◊Õ¥

‡Õ° “√ÕÈ“ßÕ‘ß 1. Pousti TJ, Wilson SE, Williams RA. Clinical examination of the vascular system. In: Veith FJ (eds). Vascular Surgery. Principles and Practice. 2nd ed. New York: McGraw. Hill; 1994;74-89. 2. Browse NL. The arteries, veins and lymphatics. In: Browse NL ed. Introduction to Symptoms and Signs of Surgical Disease, 2nd ed. London: Edward Arnold, 1991;159-192. 3. Vascular Disorder. In:Burkitt HG, Quick CRG, Gatt D. (eds). Essential Surgery. Problems, and management. Edinburgh: ChurchillLivingston, 1990;483-536.

4. Rutherford RB. The surgical approach for Vascular Problems. In: Rutherford RB(eds). Vascular Surgery 4th ed. Philadelphia: WB Saunders, 1995;1-16. 5. Calligaro KD, Veith FJ. Proper technique of lower extremity pulse examination. Contemp Surg 1992;40:49-51. 6. Veith FJ, Gupta SK, Wengerter KR, et al. Changing arteriosclerotic disease patterns and management strategies in lower-limb threatening ischemia. Ann Surg 1990;212:402-412. 7. Abramson DI. Symptoms and signs of arterial vascular disorders. Surg Clin North Am 1960;40:3-14.

»—≈¬»“ µ√ÏÀ≈Õ¥‡≈◊Õ¥

∫∑∑’Ë 3 «‘∑¬“»“ µ√åæπ◊È ∞“π¢Õß ‚√§À≈Õ¥‡≈◊Õ¥ §«“¡°â“«Àπâ“∑“ß«‘∑¬“°“√„π√–¬– 30 ªï∑’Ëºà“π¡“∑”„Àâ »— ≈ ¬°√√¡À≈Õ¥‡≈◊ Õ ¥·¬°·¢πßÕÕ°®“°»— ≈ ¬°√√¡∑—Ë « ‰ª ‡∑§π‘§°“√µ√«®æ‘‡»…·≈– ◊∫§âπµà“ß Ê °“√ºà“µ—¥ °“√„™â¬“√—°…“ ·≈–«‘«—≤π“°“√¢ÕßÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡¥’¢÷Èπ ·æ∑¬åºŸâ‡°’Ë¬«¢âÕß ·≈–ºŸâ∑’Ë π„®∑“ß‚√§À≈Õ¥‡≈◊Õ¥ §«√¡’§«“¡√Ÿâ‡¢â“„®‡°’Ë¬«°—∫ °≈‰°æ◊πÈ ∞“πæ¬“∏‘ √’√¿“æ¢ÕßÀ≈Õ¥‡≈◊Õ¥ ‡™àπ °“√‡°‘¥ atherosclerosis, aneurysm, °“√À¥µ—«¢ÕßÀ≈Õ¥‡≈◊Õ¥∑’Ë‡ªìπ “‡Àµÿ ¢Õß°“√µ’∫µ—π ·≈–°“√·¢Áßµ—«¢Õß‡≈◊Õ¥ ®–∑”„Àâª√– ‘∑∏‘¿“æ °“√√—°…“‚√§À≈Õ¥‡≈◊Õ¥¥’¢π÷È

¥â“π„π‰¥â√—∫‡≈◊Õ¥¡“‡≈’È¬ß®“°·¢πßÀ≈Õ¥‡≈◊Õ¥∑’Ë´÷¡ ·∑√°ºà“π™—Èπ intima ¥â“ππÕ°‰¥â√—∫‡≈◊Õ¥¡“‡≈’È¬ß®“° vasa vasorum ·¬°®“°™—πÈ πÕ° ÿ¥‚¥¬ external elastic membrance 3. adventitia ™—πÈ πÕ° ÿ¥ª√–°Õ∫¥â«¬ ‰ø‚∫√∫≈“ §Õ≈ ≈“‡®π ·≈–‡π◊ÈÕ‡¬◊ËÕ¬◊¥À¬ÿàπ‡°“–°—πÀ≈«¡ Ê ‡æ◊ËÕ‡ √‘¡ √â“ß§«“¡·¢Áß·√ß„Àâ°∫— À≈Õ¥‡≈◊Õ¥ Intima-endothelial cells

®ÿ≈°“¬«‘¿“§¢ÕßÀ≈Õ¥‡≈◊Õ¥ À≈Õ¥‡≈◊ Õ ¥·¥ß (arteries) ºπ— ß ¢ÕßÀ≈Õ¥‡≈◊ Õ ¥·¥ß ª√–°Õ∫¥â«¬™—πÈ µà“ß Ê ∑’ Ë ”§—≠¥—ßµàÕ‰ªπ’È (√Ÿª∑’Ë 3.1) 1. intima ™—πÈ „π ÿ¥ª√–°Õ∫¥â«¬ ‡ÕÁπ‚¥∑’‡≈’¬Ë ¡´÷ßË ∫“ß§√—ßÈ ®–√«¡µ—«°—∫°≈â“¡‡π◊ÈÕ‡√’¬∫∫“ß Ê ‡ªìπ‡¥’¬«°—π ¡’ ≈—°…≥–‡ªìπ·°π¬“«∑’‡Ë ´≈≈å‡√’¬ßµ—«°—π„π·π« longitudinal ·¬°ÕÕ°®“°™—Èπ media ‚¥¬ internal elastic membrance 2. media ™—Èπ°≈“ß‡ªìπ·°π ”§—≠¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß ª√–°Õ∫¥â«¬°≈â“¡‡π◊ÈÕ‡√’¬∫§Õ≈≈“‡®π Õ’≈“ µ‘π·≈– ‚ª√µ’ ‚Õ°≈—¬·§π ‡√’¬ßµ—«°—π„π·π« circumferential

Lumen

Internal elastic membrane Media -Smooth muscle cells -Collagen -Elastin -Proteoglycans Adventitia -Fibroblasts -Collagen -Elastin

External elastic membrane

Vasa vasorum

√Ÿª∑’Ë 3.1 cross-section anatomy of an artery

38 À≈Õ¥‡≈◊Õ¥¥” ‡ªìπ∑àÕπ”‡≈◊Õ¥®“°À≈Õ¥‡≈◊Õ¥ΩÕ¬ ¢π“¥·≈– ‡ â π ºà “ »Ÿ π ¬å ° ≈“ß®–‚µ¢÷È π √«¡∑—È ß ºπ— ß Àπ“¢÷È π ∂â “ Õ¬Ÿà „ °≈â À— « „® ª√–°Õ∫¥â«¬‡π◊ÕÈ ‡¬◊ÕË µà“ß Ê ‡√’¬ßµ—«°—π‡ªìπ 3 ™—πÈ §◊Õ intima, media ·≈– adventitia ´÷Ëß°“√·¬°™—Èπµà“ß Ê „πÀ≈Õ¥‡≈◊Õ¥¥”®–‰¡à ‡ÀÁπ™—¥‡®π‡À¡◊Õπ°—∫¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß πÕ°®“°À≈Õ¥‡≈◊Õ¥ ¥”„µâº«‘ Àπ—ß∑’¡Ë °’ ≈â“¡‡π◊ÕÈ ·∑√°Õ¬Ÿ¡à “° ‡™àπ greater saphenous vein ‚¥¬∑—«Ë ‰ª·≈â«™—πÈ media ¢ÕßÀ≈Õ¥‡≈◊Õ¥¥”®–‰¡à·¬°‡ÀÁπ ™—¥®“°‡π◊ÕÈ ‡¬◊ÕË ∑’ÀË ¡ÿâ Õ¬Ÿ¿à “¬πÕ° À≈Õ¥‡≈◊Õ¥¥”¢π“¥°≈“ß∑’Ë‚µ°«à“ 2.5 ¡‘≈≈‘‡¡µ√ ∫√‘‡«≥·¢π ¢“®–¡’≈π‘È ªî¥‡ªî¥ (valve) ´÷ßË π”‡≈◊Õ¥‰ª∑“ß‡¥’¬«®“°·¢π¢“‰ª ¬—ßÀ—«„® ≈‘Èπªî¥‡ªî¥®–¡’≈—°…≥–§≈â“¬∂ÿß√Ÿªæ√–®—π∑√å‡ ’È¬«Õ¬Ÿà ¥â “ π„π¢Õßºπ— ß À≈Õ¥‡≈◊ Õ ¥¥” ≈‘È π ªî ¥ ‡ªî ¥ ®–‡√’ ¬ ß°— π ‡ªì π §Ÿà ª√–°Õ∫¥â«¬‡π◊ÈÕ‡¬◊ËÕ¬◊¥À¬ÿàπ„π™—Èπ intima ·≈–§≈ÿ¡¥â«¬‡ÕÁπ‚¥ ∑’‡≈’¬Ë ¡

∑àÕπÈ”‡À≈◊Õß ∑”Àπâ“∑’‡Ë ªìπ∑àÕ√–∫“¬ “√πÈ” ‚ª√µ’π ·≈–Õ’‡≈Á§‚µ√≈—¬µå ∑’Ë Õ¬Ÿà„π extravascular environment ∑àÕπÈ”‡À≈◊Õß¢π“¥‚µ°«à“ 0.2 ¡‘≈≈‘‡¡µ√®–¡’ 3 ™—πÈ §◊Õ intima, media ·≈– adventitia ´÷ßË ·µà≈–™—Èπ®–·¬°ÕÕ°®“°°—π‰¡à™—¥‡®π ¡’≈‘Èπªî¥‡ªî¥‡√’¬ß°—π‡ªìπ§Ÿà „ÀâπÈ”‡À≈◊Õß‰À≈‰ª¥â“π‡¥’¬« ‰¡à ‰À≈¬âÕπ°≈—∫

°≈‰°„π°“√‡°‘¥‚√§À≈Õ¥‡≈◊Õ¥ °“√∑”≈“¬‚§√ß √â“ßª°µ‘¢Õßºπ—ßÀ≈Õ¥‡≈◊Õ¥ ®–∑”„Àâ‡°‘¥ æ¬“∏‘ ¿“æ·≈–‚√§À≈Õ¥‡≈◊Õ¥‰¥âÀ≈“¬™π‘¥ ‘Ëß∑’Ë°√–µÿâπ„Àâ‡°‘¥ §«“¡º‘¥ª°µ‘¢ÕßÀ≈Õ¥‡≈◊Õ¥‰¡à«à“„π·ßà¢Õß à«πª√–°Õ∫À√◊Õ Àπâ“∑’‡Ë ™àπ °“√Õ—°‡ ∫ À√◊Õ atherosclerosis ®–∑”„Àâ‡°‘¥ thrombosis ¢ÕßÀ≈Õ¥‡≈◊Õ¥µ“¡¡“‡ ¡Õ

ATHEROSCLEROSIS ‚√§À≈Õ¥‡≈◊Õ¥∑’‡Ë ªìπªí≠À“ ”§—≠æ∫∫àÕ¬·≈–√—°…“„πªí®®ÿ∫π— §◊Õ atherosclerosis ‡π◊ËÕß®“°æ¬“∏‘ ¿“æ∑’Ë‡°‘¥¢÷Èπ°—∫À≈Õ¥ ‡≈◊Õ¥‡°‘¥‰¥â‡°◊Õ∫∑ÿ°µ”·Àπàß¢ÕßÀ≈Õ¥‡≈◊Õ¥ ‚¥¬‡©æ“–À≈Õ¥ ‡≈◊Õ¥ ”§—≠ ∫“ß§√—ßÈ ®–¡’°“√µ’∫·§∫À≈“¬®ÿ¥„πÀ≈Õ¥‡≈◊Õ¥‡ âπ ‡¥’¬« ∑”„Àâ°“√ºà“µ—¥√—°…“·≈–·°â ‰¢≈”∫“° ®ÿ¥‡√‘¡Ë µâπ„π°“√‡°‘¥ atherosclerosis ¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß §◊Õ°“√°√–∑∫°√–‡∑◊ÕπÀ√◊Õ‡°‘¥°“√∫“¥‡®Á∫µàÕ‡ÕÁπ‚¥∑’‡≈’Ë¬¡ ·≈–¡’µ«— ·ª√ ”§—≠µàÕ‰ªπ’√È «à ¡¥â«¬§◊Õ(1)

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥ 1. °“√ Ÿ∫∫ÿÀ√’Ë æ∫«à“π‘‚§µ‘π¡’º≈µàÕºπ—ßÀ≈Õ¥‡≈◊Õ¥ ∑”„Àâ ¡’°“√À¥µ—«·≈–¢“¥‡≈◊Õ¥¡“‡≈’È¬ß ·≈–∑”„Àâºπ—ßÀ≈Õ¥ ‡≈◊Õ¥Õ—°‡ ∫ 2. ‡∫“À«“π ‡ªìπ “‡Àµÿ∑”„Àâ¡’ÕäÕ°´‘‡®π¡“‡≈’È¬ß‡ÕÁπ‚¥∑’ ‡≈’¬Ë ¡πâÕ¬≈ß 3. «‘∏’°“√√—°…“‚¥¬„™â√—ß ’∫”∫—¥‚√§¡–‡√Áß ®–∑”„Àâ¡’°“√ ‡ª≈’Ë¬π·ª≈ß¢Õß‡π◊ÈÕ‡¬◊ËÕºπ—ßÀ≈Õ¥‡≈◊Õ¥¢“¥ÕäÕ°´‘‡®π ¡“‡≈’¬È ß 4. §«“¡¥—π‚≈À‘µ∑’ Ë ßŸ º‘¥ª°µ‘ ®–‡æ‘¡Ë shearing force µàÕ ºπ—ßÀ≈Õ¥‡≈◊Õ¥¡’°“√∑”≈“¬¢Õß‡ÕÁπ‚¥∑’‡≈’¬Ë ¡ 5. ‰¢¡—π„π‡≈◊Õ¥ Ÿß ®–∑”„Àâ‡¡µ“‚∫≈‘ ¡å¢Õß‡ÕÁπ‚¥∑’‡≈’¬Ë ¡ º‘¥ª°µ‘ 6. °“√∫“¥‡®Á∫¢ÕßÀ≈Õ¥‡≈◊Õ¥´÷ßË ¡’º≈µàÕ‡ÕÁπ‚¥∑’‡≈’¬Ë ¡ ®ÿ¥‡√‘¡Ë ·√°¢Õß°“√‡°‘¥ atherosclerosis ‡°‘¥µ√ßµ”·Àπàß∑’Ë ¡’°“√∫“¥‡®Á∫À√◊ÕÀ≈ÿ¥≈Õ°¢Õß‡ÕÁπ‚¥∑’‡≈’Ë¬¡ ∫√‘‡«≥∑’Ë‡°‘¥‰¥â ∫àÕ¬§◊Õ µ”·Àπàß∑’ËÀ≈Õ¥‡≈◊Õ¥·¬°·¢πßÀ√◊Õ®ÿ¥∑’ËÀ≈Õ¥‡≈◊Õ¥‰¡à “¡“√∂‡§≈◊ÕË π‰À«‰¥âß“à ¬ (fixed point) ∫√‘‡«≥π—πÈ ®–¡’ shearing force ·≈– turbulent flow √ÿπ·√ß¡“° à«π¢ÕßÀ≈Õ¥ ‡≈◊Õ¥„π√à“ß°“¬∑’Ë‡°‘¥ atherosclerosis ‰¥â∫àÕ¬§◊Õ·¢πßÀ≈Õ¥ ‡≈◊Õ¥∑’·Ë ¬°ÕÕ°‰ª®“° aorta ‡™àπ aortic bifurcation, common iliac bifurcation, common femoral bifurcation, common carotid bifucation ·≈– superficial femoral artery (SFA) µ√ß Hunterûs canal ´÷ßË ‡ªìπ fixed point (√Ÿª∑’Ë 3.2) High shear region

Atherosclerotic plaque Low shear region

√Ÿª∑’Ë 3.2

«‘∑¬“»“ µ√åæ◊Èπ∞“π¢Õß‚√§À≈Õ¥‡≈◊Õ¥ °“√‡°‘¥ atherosclerosis ¢Õß aorta ‡ªìπº≈∑”„Àâ¡’°“√ µ’∫·§∫¢ÕßÀ≈Õ¥‡≈◊Õ¥∫√‘‡«≥™àÕß∑âÕß¡“°°«à“∫√‘‡«≥∑√«ßÕ° ‡æ√“–«à“ abdominal aorta ‰¡à¡’ vasa vosorum ‡ÕÁπ‚¥∑’ ‡≈’Ë¬¡®–¢“¥ÕäÕ°´‘‡®π‰¥âßà“¬ °“√∫“¥‡®Á∫·≈–∂Ÿ°∑”≈“¬¢Õß ‡ÕÁπ‚¥∑’‡≈’¬Ë ¡®–¡’º≈Õ¬à“ßµàÕ‡π◊ÕË ßµàÕ‡¡µ“‚∫≈‘ ¡å¢Õß‡°√Á¥‡≈◊Õ¥ °“√ —ß‡§√“–Àå prostaglandin, ∑”„Àâ¡°’ “√À¥µ—«¢Õß°≈â“¡‡π◊ÕÈ ‡√’¬∫„π™—πÈ À≈Õ¥‡≈◊Õ¥º‘¥ª°µ‘ ·≈–‡¡µ“‚∫≈‘ ¡å¢Õß‚§‡≈ ‡µÕ√Õ≈ ‘Ëß‡À≈à“π’È‡ªìπªí®®—¬ ”§—≠∑—Èß ‘Èπ„π°“√‡°‘¥ atherosclerosis æ¬“∏‘ ¿“æ∑’‡Ë °‘¥¢÷πÈ ®–·∫àßÕÕ°µ“¡≈—°…≥–∑’æË ∫‰¥â¥ß— π’È 1. fattly streaks æ∫‰¥â·√°‡√‘¡Ë ®–‡ªìπ®ÿ¥πŸπ ’‡À≈◊Õß ´÷ßË ª√–°Õ∫‰ª¥â«¬ cholesterol ester (lipid) ª√‘¡“≥¡“° √à«¡°—∫ macrophages ·≈–°≈â“¡‡π◊ÕÈ ‡√’¬∫ 2. fibrous plaques ‡ªìπæ¬“∏‘ ¿“æ™—ÈπµàÕ¡“ª√–°Õ∫ ¥â«¬°≈â“¡‡π◊ÕÈ ‡√’¬∫‡ªìπ à«π„À≠à æ¬“∏‘ ¿“æπ’®È –·∑√° µ—«‡¢â“‰ª∂÷ß arterial lumen ‚¥¬¡’‰¢¡—π·≈–‰ø∫√— §≈ÿ¡Õ¬ŸÕà °’ ™—πÈ Àπ÷ßË 3. complicated plaques ‡°‘¥®“°°“√¡’ atherosclerosis ¡“‡ªìπ√–¬–‡«≈“π“π‡¡◊ÕË fibrous plaques ‡√‘¡Ë ¡’ necrosis ‡°‘¥‡ªìπ·º≈À√◊Õ¡’·§≈‡´’¬Ë ¡¡“‡°“– §«“¡ —¡æ—π∏å‡°’¬Ë «¢âÕßµàÕ‡π◊ÕË ß°—π®√‘ß Ê √–À«à“ß¿“«–‰¢¡—π „π‡≈◊Õ¥‡°‘π°—∫°“√‡°‘¥ atherosclerosis ¬—ß‰¡à∑√“∫·πàπÕπ ·µà¡§’ «“¡‡°’¬Ë «¢âÕß°—π·πàπÕπ√–À«à“ß√–¥—∫‚§‡≈ ‡µÕ√Õ≈„π‡≈◊Õ¥ low density preteins ·≈– atherogenesis ‚¥¬¡’À≈—°∞“π π—∫ πÿπ¥—ßµàÕ‰ªπ’È µ“√“ß∑’Ë 3.1 °“√·∫àß “‡Àµÿ¢Õß ARTERIAL ANEURYSMS CONGENITAL

Medical agenesis Marfanûs syndrome Ehlers-Danlos syndrome Genetie defects of elastin and collagen INFLAMMATORY Syphilitic Bacterial Noninfecteous inflammatory disease TRAUMATIC Traumatic aneurysm Anastomotic (post surgical) Poststenotic aneurysm DEGENERATIVE Arteriosclerotic Fibrodysplasia

1. à«πª√–°Õ∫¢Õß plaques à«π„À≠à¡“®“° low density lipoprotein ´÷ßË √«¡µ—«°—π„π atheromatous lesions 2. ¡’À≈—°∞“π∑“ß√–∫“¥«‘∑¬“«à“¿“«–‚§‡≈ ‡µÕ√Õ≈ Ÿß„π ‡≈◊Õ¥ ‡°’¬Ë «¢âÕß°—∫‚√§À≈Õ¥‡≈◊Õ¥À—«„®‚§‚√π“√’ 3. ºŸªâ «É ¬ familial type II hyperlipidemia ‡°‘¥ atherosclerosis ‰¥âß“à ¬ ·¡â®–¡’Õ“¬ÿπÕâ ¬ 4. °“√≈¥√–¥—∫‚§‡≈ ‡µÕ√Õ≈„π‡≈◊Õ¥„ÀâÕ¬Ÿà „π√–¥—∫ª°µ‘ ®–≈¥°“√‡°‘¥ atherosclerosis À√◊Õ‡°‘¥™â“≈ß 5. °“√‡æ‘¡Ë √–¥—∫‚§‡≈ ‡µÕ√Õ≈„π‡≈◊Õ¥®–∑”„Àâ‡°‘¥ atherosclerosis ‚¥¬ √ÿª·≈â«µ—«·ª√ ”§—≠„π°“√‡°‘¥ atherosclerosis „πºŸâ ªÉ«¬‚√§À≈Õ¥‡≈◊Õ¥∑’¡Ë Õ’ “¬ÿπÕâ ¬·≈–∑”„Àâ‡ªìπÕ¬à“ß√ÿπ·√ß§◊Õ 1. ¿“«–‰¢¡—π„π‡≈◊Õ¥‡°‘π 2. §«“¡¥—π‚≈À‘µ Ÿß 3. Ÿ∫∫ÿÀ√’Ë 4. ‚√§‡∫“À«“π 5. ÕÕ°°”≈—ß°“¬πâÕ¬ 6. ‚√§Õâ«π 7. §«“¡‡§√’¬¥ 8. ª√–«—µæ‘ π— ∏ÿ°√√¡

ARTERIAL ANEURYSMS aneurysm À¡“¬∂÷ß°“√‚ªÉßæÕß‡©æ“–∑’¢Ë ÕßÀ≈Õ¥‡≈◊Õ¥‚¥¬ ¡’‡ âπºà“»Ÿπ¬å°≈“ß‚µ¢÷ÈπÕ¬à“ßπâÕ¬ 1.5 ‡∑à“¢Õß‡ âπºà“»Ÿπ¬å°≈“ßª°µ‘ Õ“®®–¡’≈—°…≥–‡ªìπ∂ÿß (saccular) À√◊Õ√Ÿª°√– «¬ (fusiform) °“√‚ªÉßæÕß¢¬“¬¢π“¥¢ÕßÀ≈Õ¥‡≈◊Õ¥∑—ßÈ ≈”‡√’¬°«à“ ectasia ”À√—∫ arteriomegaly §◊Õ °“√¢¬“¬µ—«‚ªÉßæÕß ¢ÕßÀ≈Õ¥‡≈◊Õ¥À≈“¬µ”·Àπàß´÷ßË Õ“®®–‡°’¬Ë «¢âÕß°—∫ multiple aneurysms ¿“«– arteriomegaly æ∫‰¥âπÕâ ¬ ºŸªâ «É ¬∑’‡Ë ªìπ multiple aneurysms ®–æ∫«à“¡’À≈Õ¥‡≈◊Õ¥·¥ßº‘¥ª°µ‘·≈–À≈Õ¥ ‡≈◊Õ¥·¥ß∫“ß à«π‚ªÉßæÕß ‰¡à „™à ‚ªÉßæÕß¢¬“¬¢π“¥∑—ßÈ ≈”‡À¡◊Õπ arteriomegaly “‡Àµÿ¢Õß°“√‡°‘¥ aneurysm ¡’À≈“¬™π‘¥ ¥Ÿ®“°µ“√“ß∑’Ë 3.1 ∑ƒ…Æ’‡¥‘¡‡™◊ÕË °—π«à“ infrarenal abdominal aortic aneurysm (AAA) ‡ªìπ≈—°…≥–Àπ÷Ëß¢Õß atherosclerosis ‡°‘¥®“° intimal degerative process §«“¡·¢Áß·√ß¢Õßºπ—ßÀ≈Õ¥ ‡≈◊Õ¥πâÕ¬≈ß ∑”„Àâ¡°’ “√‚ªÉßæÕß¢ÕßÀ≈Õ¥‡≈◊Õ¥ ·µà ‰¡à “¡“√∂

40 Õ∏‘∫“¬‰¥â«“à ∑”‰¡®÷ß‡°‘¥ aortoiliac occlusive disease ¢÷πÈ ‰¥â ¡’¢Õâ —ß‡°µÿ·≈–À≈—°∞“πÕ◊πË Ê À≈“¬ª√–°“√«à“ atherosclerosis ‰¡à„™à “‡Àµÿπ”„π°“√‡°‘¥ aneurysm(2,3,4) §◊Õ®–‰¡àæ∫«à“‡°‘¥ aneurysm „π —µ«å∑¥≈Õß∑’Ë ‰¥â√∫— atherogenic diet ª√–¡“≥ √âÕ¬≈– 30 ¢ÕßºŸªâ «É ¬ AAA ®–æ∫«à“¡’ peripheral arterial occlusive disease √à«¡¥â«¬ ´÷Ëß°≈ÿà¡ºŸâªÉ«¬ AAA ®–¡’Õ“¬ÿ‚¥¬ ‡©≈’¬Ë ¡“°°«à“ AIOD ª√–¡“≥ 10 ªï ·≈–¡’ºªŸâ «É ¬πâÕ¬√“¬¡“° ∑’‡Ë ªìπ generalized arteriomegaly ·≈– aneurysmosis „π™—πÈ tunical media ¢ÕßÀ≈Õ¥‡≈◊Õ¥®–¡’ elastin, collagen ·≈–°≈â“¡‡π◊ÈÕ‡√’¬∫ elastin ∑”„Àâ‡°‘¥§«“¡¬◊¥À¬ÿàπ¢Õßºπ—ß À≈Õ¥‡≈◊Õ¥∂â“¢π“¥ “√µ—«π’È®–∑”„Àâ‡°‘¥ aneurysm collagen ‡ √‘¡§«“¡·¢Áß·√ß∂â“¡’πâÕ¬®–∑”„ÀâÀ≈Õ¥‡≈◊Õ¥·µ°ßà“¬ ®“° °“√µ√«®∑“ß®ÿ≈æ¬“∏‘«‘∑¬“æ∫«à“ AAA ¡’°“√·µ°°√–®“¬ ·≈–‡√’¬ßµ—«°—π‰¡à‡ªìπ√–‡∫’¬∫¢Õß™—πÈ elastin ¡’ª√‘¡“≥¢Õß elastin ≈¥≈ß ™—πÈ tunica media ∫“ß∑’¡’ elastin πâÕ¬ ¡’‰ø∫√— ·≈– plasma cell ·∑√°Õ¬Ÿ∑à «—Ë ‰ª ´÷ßË ·µ°µà“ß®“° intimal medial thickening ´÷ßË æ∫„π occlusive disease elastin ·≈– collagen —ß‡§√“–Àå®“°°≈â“¡‡π◊ÕÈ ‡√’¬∫¢Õß aorta ·≈–∂Ÿ°∑”≈“¬‚¥¬‡ÕÁπ´—¬¡ å elastase ·≈– collagenase ∂â“¿“«–°“√ √â“ßπâÕ¬°«à“°“√∑”≈“¬®–‡°‘¥ AAA elastase æ∫‰¥â „π neutrophils, macrophages ·≈– pancreatic exocrine cells(5) &-1-trypsin ‡ªìπ elastolytic inhibitor ®–æ∫ πâÕ¬„π‡≈◊Õ¥¢ÕßºŸªâ «É ¬ AAA ·≈– COPD ®“°¢â Õ — ß ‡°µÿ ¥— ß °≈à “ «æÕ®–Õ∏‘ ∫ “¬ “‡Àµÿ ¢ Õß°“√‡°‘ ¥ infrarenal AAA «à“‡ªìπº≈¡“®“°ºπ—ßÀ≈Õ¥‡≈◊Õ¥ à«π infra renal aorta ¡’ elastin πâÕ¬°«à“ ·≈– collagen ¡“°°«à“ thoracic aorta ®÷ß∑”„Àâºπ—ßÀ≈Õ¥‡≈◊Õ¥Àπ“§«“¡¬◊¥À¬ÿàπ °√–· ‡≈◊Õ¥ ‰À≈‡«’¬πµ√ß aorta ‡Àπ◊ÕµàÕ bifurcation ¡’·√ß°√–·∑°√ÿπ·√ß ∑”„Àâºπ—ßÀ≈Õ¥‡≈◊Õ¥∑’·Ë ¢Áß‰¡à¬¥◊ À¬ÿπà ‚ªÉßæÕßÕÕ°‰¥â ‚√§∑“ßÕ‘¡¡Ÿπ Õ“®®–‡°’¬Ë «¢âÕß°—∫ AAA ‰¥â‡æ√“–æ∫«à“¡’ inflammatory cells ¡“° ¡’°“√‡æ‘¡Ë ª√‘¡“≥¢ÕßÕ‘¡¡Ÿ‚π‚°≈∫Ÿ≈π‘ ·≈– cytokines „πºŸâªÉ«¬ AAA ´÷Ëß inflammatory cells ®–‡ªìπµ—«º≈‘µ‡ÕÁπ´—¬¡ å elastase ·≈– collagenase ∑”≈“¬ ºπ—ßÀ≈Õ¥‡≈◊Õ¥Õ¬Ÿà·≈â« πà“®–¡’§«“¡‡°’Ë¬«¢âÕß«à“ AAA ‡ªìπ ‚√§∑“ßæ—π∏ÿ°√√¡(6)

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INTIMAL HYPERPLASIA ºŸâªÉ«¬∑’Ë¡’°“√µ’∫·§∫¢ÕßÀ≈Õ¥‡≈◊Õ¥À—«„®‚§‚√π“√’Ë Õ«—¬«– ¿“¬„π ¡Õß·≈–·¢π¢“ °“√ºà“µ—¥·°â ‰¢¡—°®–„™âÀ≈Õ¥‡≈◊Õ¥ ∑¥·∑π¢ÕßºŸªâ «É ¬‡Õß æ∫«à“À≈—ßºà“µ—¥µàÕ·≈â«ª√–¡“≥√âÕ¬≈– 25 ®–¡’°“√µ’∫·§∫À√◊Õ thrombosis ‡°‘¥¢÷Èπ„πÀ≈Õ¥‡≈◊Õ¥¥” ∑¥·∑π‡Õß(7) “‡Àµÿ¢Õß bypass graft failure ‰¡à “¡“√∂∫àß ∫Õ°‰¥â·πàπÕπ Õ“®®–‡π◊ËÕß¡“®“°À≈Õ¥‡≈◊Õ¥·¥ß∑’ËÕ¬Ÿà‡Àπ◊Õ À√◊ÕµË”°«à“∫√‘‡«≥√Õ¬µàÕ´÷ßË ∑” endarterectomy ‰ª·≈â« ‡°‘¥¡’ progressive atherosclerosis ‡π◊ËÕß®“°°≈‰°°“√À“¬¢Õß ∫“¥·º≈¥’‡°‘π‰ª ¿“«–π’§È Õ◊ intimal hyperplasia ®–æ∫«à“„π™—πÈ intima ¡’°“√§—Ëß¢Õß°≈â“¡‡π◊ÈÕ‡√’¬∫ ·≈–‡π◊ÈÕ‡¬◊ËÕ‰ø∫√‘πµà“ß Ê ¡“°¡“¬ ¬—ß‰¡à∑√“∫·πàπÕπ«à“ growth factors µ—«„¥∑’Ë¡’ ∫∑∫“∑§«∫§ÿ¡§«“¡ ¡¥ÿ≈¬å¢Õß vessel healing ·≈–°“√µ’∫ ·§∫¢ÕßÀ≈Õ¥‡≈◊Õ¥ ∂â“ “¡“√∂«‘®—¬§âπæ∫µ—«·ª√∑’Ë “¡“√∂ §«∫§ÿ ¡ «ß®√‡À≈à “ π’È ‰¥â ®–‰¥â π”¡“§«∫§ÿ ¡ æƒµ‘ ° √√¡¢Õß °≈â“¡‡π◊ÕÈ ‡√’¬∫ ·≈–À“·π«∑“ß„π°“√ªÑÕß°—π°“√‡°‘¥ atherosclerosis ‰¥â

√ÿª „πªí®®ÿ∫π— À≈—°∞“πµà“ß Ê „π∑“ß«‘∑¬“»“ µ√å “¡“√∂æ‘ ®Ÿ πå ‰¥â«à“ atherosclerosis, aneurysm ·≈– vasculitis ‡ªìπ‚√§ ∑’Ë ‰¡à‡°’Ë¬«¢âÕß°—π ¡’ªí®®—¬°“√‡ ’Ë¬ß„π°“√‡°‘¥µà“ß°—π ∫“ß‚√§ Õ“®®–¡’æ—π∏ÿ°√√¡¡“‡°’Ë¬«¢âÕß ∂â“≈¥ªí®®—¬‡ ’Ë¬ß≈ß‰¥â ‚Õ°“ ‡°‘¥‚√§°Á¡‰’ ¥âπÕâ ¬≈ß ¿“«– intimal hyperplasia ´÷ßË ‡ªìπ “‡Àµÿ °“√µ’∫µ—π¢ÕßÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡∑’ËµàÕ‰«â ‡π◊ËÕß®“°°≈‰°°“√À“¬ ¢Õß·º≈¥’‡°‘π‰ª ·≈–¡’ growth factors ∫“ßµ—«¡“‡°’¬Ë «¢âÕß∂â“ ‡√“ “¡“√∂§«∫§ÿ¡ growth factor ‰¥â ®–ªÑÕß°—π°“√‡°‘¥ intimal hyperplasia ·≈– atherosclelrosis ‰¥â

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‡Õ° “√Õâ“ßÕ‘ß 1. White RA. Atherosclerosis and arteriosclerosis: Human pathology and experimental animal methods. Boca Ratons, Fla: CRC Press, 1989. 2. Dobrin PB. Pathophysiology and pathogenesis of aortic aneurysm: Current concepts. Surg Clin North Am 1989;69:687-704. 3. Zarins CK, Glagov S, Vesselinovitch D, et al. Aneuryms formation in experimental atherosclerosis: Relationship to plaque formation. J Vasc Surg 1990;12:246-256.

4. Hollier LH, Stanson AW, Gloviczki P, et al. Arteriomegaly: Classification and morbid implications of diffuse aneurysm disease. Surgery 1983;93:700-708. 5. Cohen JR. Role of the neutrophil in abdominal aortic aneurysm development. Cardiovasc Surg 1993;1:37. 6. Majumder PP. On the inheritance of abdominal aortic aneurysm. Am J Hum Genet 1991;48:164. 7. Varty K, Allen KE, Bell PRF, et al. Infrainguinal vein graft stenosis. Br J Surg 1993;80:823-833.

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∫∑∑’Ë 4 ¬“∑’Ë „™â „π‚√§À≈Õ¥‡≈◊Õ¥ „π°“√√—°…“‚√§À≈Õ¥‡≈◊Õ¥ πÕ°‡Àπ◊Õ®“°°“√√—°…“‚¥¬ °“√ºà“µ—¥·≈â«ºŸâ∑’Ë‡°’Ë¬«¢âÕß„π°“√¥Ÿ·≈√—°…“ºŸâªÉ«¬ §«√¡’§«“¡ √Ÿ§â «“¡‡¢â“„®„π°≈‰°°“√·¢Áßµ—«¢Õß‡≈◊Õ¥ «‘∏°’ “√·°â ‰¢§«“¡º‘¥ ª°µ‘µà“ß Ê ∑’Ë‡°‘¥¢÷Èπ¿“¬„πÀ≈Õ¥‡≈◊Õ¥ „πªí®®ÿ∫—π¡’¬“À≈“¬ °≈ÿà¡À≈“¬™π‘¥∑’Ë¡’∫∑∫“∑„π°“√√—°…“‚√§À≈Õ¥‡≈◊Õ¥ ®÷ß§«√ ‡¢â“„®∂÷ß‡¿ —™«‘∑¬“·≈–°≈‰°„π°“√ÕÕ°ƒ∑∏‘Ï¢Õß¬“ µ≈Õ¥®π º≈¢â“ß‡§’¬ß‡æ◊ÕË ∑’®Ë – “¡“√∂‡≈◊Õ°„™â¬“‰¥â∂°Ÿ µâÕß·≈–ª≈Õ¥¿—¬∑’ Ë ¥ÿ ¬“°≈ÿ¡à µà“ß Ê ∑’Ë „™â „π‚√§À≈Õ¥‡≈◊Õ¥¡’¥ß— µàÕ‰ªπ’È

1. ¬“µâ“π‡°√Á¥‡≈◊Õ¥®—∫°≈ÿà¡ (Antiplatelet agents) 1.1 ·Õ ‰æ√‘π ‡ªìπ¬“µâ“π‡°√Á¥‡≈◊Õ¥∑’¡Ë º’ ≈µàÕ°≈‰° prostaglandin pathway ¢Õß‡°√Á¥‡≈◊Õ¥·≈–‡ÕÁπ‚¥∑’‡≈’Ë¬¡(1) ¡’º≈ ‚¥¬µ√ßµàÕ cyclooxygenase ¬—∫¬—ßÈ °“√‡ª≈’¬Ë π arachidonic acid „Àâ‡ªìπ prostagladin endoperoxide ·≈–¬—∫¬—ßÈ °“√ —ß‡§√“–Àå thromboxane A2 „π‡°√Á¥‡≈◊Õ¥ ‡π◊ËÕß®“°‡°√Á¥‡≈◊Õ¥‰¡à ¡’ π‘«‡§≈’¬ ®÷ß‰¡à “¡“√∂ —ß‡§√“–Àå‡ÕÁπ´—¬¡åµ—«„À¡à ‰¥â º≈¢Õß ·Õ ‰æ√‘πµàÕ‡°√Á¥‡≈◊Õ¥®÷ß‡°‘¥∂“«√ ·¡â®–„Àâ¬“‡æ’¬ß§√—Èß‡¥’¬« ®–∑”„ÀâÀπâ“∑’Ë°“√∑”ß“π¢Õß‡°√Á¥‡≈◊Õ¥‡ª≈’Ë¬π·ª≈ß‰ªÀ≈“¬«—π cyclo-oxygenase ∑’‡Ë ª≈’¬Ë π·ª≈ß‰ª®–∑”„Àâ°“√º≈‘µ prostacyline „π‡ÕÁπ‚¥∑’‡≈’Ë¬¡≈¥≈ß¥â«¬ Õ¬à“ß‰√°Áµ“¡ cyclo-oxygenase “¡“√∂ — ß ‡§√“–Àå ¢÷È π ‰¥â „ À¡à ® “°‡´≈≈å ¢ Õß‡ÕÁ π ‚¥∑’ ‡ ≈’Ë ¬ ¡∑’Ë ¡’

π‘«‡§≈’¬ ¥—ßπ—πÈ √–¥—∫¢Õß prostacyclin ®–§ß√–¥—∫‡¥‘¡Õ¬Ÿªà √–¡“≥ 3-4 ™—«Ë ‚¡ß®÷ß®–≈¥≈ß∑—π∑’ °“√„Àâ¬“§◊Õ„Àâ „πª√‘¡“≥πâÕ¬ °«à“ 600 ¡‘≈≈‘°√—¡§√—ßÈ ‡¥’¬«À√◊Õ·∫àß„Àâ«π— ≈– 2 §√—ßÈ ®– “¡“√∂ ¬—∫¬—Èß°“√ —ß‡§√“–Àå thromboxane A2 ∂â“„Àâª√‘¡“≥ Ÿß®– ¬—∫¬—ßÈ °“√ √â“ß prostacyline „π‡ÕÁπ‚¥∑’‡≈’¬Ë ¡¥â«¬ (√Ÿª∑’Ë 4.1) °“√∫√‘À“√¬“ „Àâ√∫— ª√–∑“π enteric coated aspirin 325 ¡‘≈≈‘°√—¡µàÕ«—πÀ≈—ßÕ“À“√ ‡æ◊ËÕº≈„Àâ°“√¬—∫¬—Èß °“√∑”ß“π¢Õß‡°√Á¥‡≈◊Õ¥ À√◊Õ®–„Àâ 80 ¡‘≈≈‘°√—¡ «—π≈– 2 §√—ßÈ °Á ‰¥âº≈„°≈â‡§’¬ß°—π(2) ªÑÕß°—π°“√µ’∫·§∫¢ÕßÀ≈Õ¥‡≈◊Õ¥ ·Õ ‰æ√‘π„™â ‰¡à‰¥âº≈ „πºŸâªÉ«¬∑’ËÀ≈Õ¥‡≈◊Õ¥Õÿ¥µ—π·≈â«®“° thrombosis ‰¥â º≈ ”À√— ∫ ªÑ Õ ß°— π °“√Õÿ ¥ µ— π ¢ÕßÀ≈Õ¥‡≈◊ Õ ¥‡∑’ ¬ ¡ ¿“¬À≈—ß°“√∑” bypass ≈¥Õ—µ√“°“√‡°‘¥ TIA, stroke, MI(3,4) º≈°“√√—°…“®–¥’¢π÷È ∂â“„Àâ√«à ¡°—∫ dipyridamole °àÕπ·≈–À≈—ß°“√ºà“µ—¥(5) ºŸªâ «É ¬∑’ºË “à µ—¥∑” femorodistal bypass §«√„Àâ√—∫ª√–∑“π·Õ ‰æ√‘π 325 ¡‘≈≈‘°√—¡ «—π≈–§√—ßÈ ‰ªµ≈Õ¥™’«µ‘ æ∫«à“·Õ ‰æ√‘π∑”„Àâ graft patency ¢Õß coronary bypass ¥’¢π÷È (6) ¿“«–·∑√°´âÕπ §◊Õ‡≈◊Õ¥ÕÕ°·≈–µ°‡≈◊Õ¥ßà“¬ §«√√–«—ß „πºŸªâ «É ¬·º≈‡ªìªµ‘§·≈–·æâ¬“ À√◊Õ„Àâ «à π√à«¡°—∫‡Œª“√’π·≈–§Ÿ¡“¥’π °“√√—∫ª√–∑“π·Õ ‰æ√‘π‡ªìπ√–¬–‡«≈“ π“π ®–‡æ‘¡Ë ¬Ÿ‡√’¬·≈–°√¥¬Ÿ√§‘ „π‡≈◊Õ¥·µà ‰¡à√πÿ ·√ß ®π ∑”„Àâ‡ªìπ‚√§‡°ä“∑å

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥

ENDOTHELIAL CELL

PLATELET Stimulus

Cell Membrane

Phospholipids

Phospholipase

Arachidonic Acid

Arachidonic Acid !

! !

Aspirin

(large dose)

Cyclooxygenase

(small and large doses)

Cyclic Endoperoxides

PGI-2 synthetase

TXA-2 synthetase

Prostacyclin

Thromboxane (TXA-2)

! (-inhibits platelet cAMP aggregation & ! vasodilation) !

phosphodiesterase

Persantine

cGMP

(-promotes platelet aggregation & vasoconstiction)

Inactive cAMP

√Ÿª∑’Ë 4.1 µ”·Àπàß¢Õß aspirin and Persantine ∑’ËÕÕ°ƒ∑∏‘ÏµàÕ prostaglandin pathway ¿“¬„π‡ÕÁπ‚¥∑’‡≈’Ë¬¡·≈– ‡´≈≈å¢Õß‡°√Á¥‡≈◊Õ¥

1.2 Dipyridamole ¬“™π‘¥π’®È –∑”„Àâ‡°√Á¥‡≈◊Õ¥‰¡à√«¡ °≈ÿà¡ ‚¥¬¬—∫¬—Èß°“√∑”ß“π¢Õß‡ÕÁπ´—¬¡å phosphodiesterase ´÷ËßµàÕ¡“®–∑”„Àâ¡’ cAMP ‡æ‘Ë¡¢÷Èπ„π‡´≈≈å≈¥≈ß ‡°√Á¥‡≈◊Õ¥®– ‰¡à®∫— °≈ÿ¡à √«¡µ—«°—π (√Ÿª∑’Ë 4.1) ªØ‘°√‘ ¬‘ “Õ◊πË ¢Õß dipyridamole §◊Õ¬—ß¬—Èß°“√º≈‘µ thromboxane A2 ´÷Ëß¡’º≈µàÕ°“√∑”ß“π ¢Õß‡°√Á¥‡≈◊Õ¥ºà“π adenosine ‡™◊ËÕ°—π«à“„Àâ√à«¡·Õ ‰æ√‘π®– ‡ √‘¡ƒ∑∏‘Ï „π°“√µâ“π‡°√Á¥‡≈◊Õ¥®—∫°≈ÿà¡ ·µà¬—ß‰¡à¡’°“√æ‘ Ÿ®πå∑’Ë ·πàπÕπ °“√∫√‘À“√¬“ √—∫ª√–∑“π¢π“¥ 25-50 ¡‘≈≈‘°√—¡ ·∫àß „Àâ«π— ≈– 3-4 §√—ßÈ „π°“√ªÑÕß°—π °“√µ’∫·§∫¢ÕßÀ≈Õ¥‡≈◊Õ¥∑’Ë bypass „Àâ √à«¡°—∫·Õ ‰æ√‘π

¿“«–·∑√°´âÕπ ∑’Ëæ∫‰¥â æ∫ª«¥»’√…–‰¥â√âÕ¬≈– 10 Õ“°“√Õ◊πË ‡™àπ∑âÕß√à«ß ∑”„Àâ‡°√Á¥‡≈◊Õ¥‰¡à®∫— °≈ÿ¡à √«¡°—π ‚¥¬°“√°√–µÿπâ §Õ≈≈“‡®π, platelet-activating factor, Õ¥√’π“≈’π ·≈– ADP(7) „Àâ√∫— ª√–∑“π¬“„π¢π“¥ 125 ¡‘≈≈‘°√—¡ «—π≈– 2 §√—ßÈ ticlopidine ®–≈¥Õ—µ√“°“√‡°‘¥ stroke, MI „™â ‰¥âº≈„π intermittent claudication ‚¥¬®–‡æ‘¡Ë √–¬–∑“ß„π°“√‡¥‘π‰¥â¡“°°«à“‡¥‘¡√âÕ¬≈– 10 ‡¡◊ÕË ‡∑’¬∫°—∫ placebo(8) ¿“«–·∑√°´âÕπ∑’æË ∫‰¥âÀ≈—ß°“√ „Àâ¬“§◊Õ neutropenia, pancytopenia ·≈– agranulocytosis ´÷Ëßæ∫‰¥â√âÕ¬≈– 2 ‡¡◊ËÕæ∫Õ“°“√·∑√°´âÕπ §«√À¬ÿ¥√—∫ª√–∑“π¬“∑—π∑’ (9) 1.4 Dextran ‡ªìπ polysaccharide À√◊Õ long-chain CHO ´÷Ëßº≈‘µ¢÷Èπ¡“µ—Èß·µàªï 1940 ‡æ◊ËÕ„™â‡ªìπ volume expander ·≈–æ∫«à“¡’§ÿ≥ ¡∫—µ‘„π°“√µâ“π‡°√Á¥‡≈◊Õ¥®—∫°≈ÿà¡‡¡◊ËÕªï 1960 ®÷ß‰¥âπ”¡“„™â ”À√—∫ thromboembolic disorder µ—ßÈ ·µàªï 1970(10) ¡’ 2 ™π‘¥∑’Ë „™â „πªí®®ÿ∫π— §◊Õ dextran 70 (πÈ”Àπ—°‚¡‡≈°ÿ≈ ‡©≈’¬Ë 70,000 ¥“≈µ—π) ·≈– dextran 40 (πÈ”Àπ—°‚¡‡≈°ÿ≈‡©≈’¬Ë 40,000 ¥“≈µ—π) ¡’∑ß—È 6% dextran 70 À√◊Õ 10% dextran 40 „π 5% °≈Ÿ‚§ À√◊Õ„ππÈ”‡°≈◊Õ ¡¥ÿ≈¬å ¡’º≈µâ“π‡°√Á¥‡≈◊Õ¥®—∫°≈ÿà¡∑—Èß Õß Ÿµ√ ƒ∑∏‘¢Ï Õß dextran ª√–°Õ∫¥â«¬ plasma volume expansion, µâ“π‡°√Á¥‡≈◊Õ¥®—∫°≈ÿà¡ ·≈–‡æ‘Ë¡ª√‘¡“≥‡≈◊Õ¥‰À≈‡«’¬π„π √–¥—∫ microcirculation ƒ∑∏‘Ï „π°“√‡æ‘¡Ë ª√‘¡“µ√‰À≈‡«’¬π®–‰¡à µà“ß®“° “√πÈ”∑’Ë¡’ macromolecules ∑—Ë«‰ª·µàƒ∑∏‘Ï „π°“√µâ“π ‡°√Á¥‡≈◊Õ¥®—∫°≈ÿ¡à ·≈–‡æ‘¡Ë °“√‰À≈‡«’¬π‡≈◊Õ¥√–¥—∫ microcirculation ‡°‘¥®“° dextran ‡§≈◊Õ∫‡¡Á¥‡≈◊Õ¥·¥ß ¡’°“√‡æ‘¡Ë electronegative membrance potential ¢Õß‡¡Á¥‡≈◊Õ¥·¥ß·≈– ‡ÕÁπ‚¥∑’‡≈’Ë¬¡ ≈¥§«“¡Àπ◊¥¢Õß‡≈◊Õ¥(11) „πºŸâªÉ«¬∫“¥‡®Á∫®“° Õÿ∫µ— ‡‘ Àµÿ °“√„Àâ dextran ®–™à«¬≈¥§«“¡º‘¥ª°µ‘¢Õß plasma fibriolytic activity ´÷ßË ¡—°‡°‘¥À≈—ß°“√∫“¥‡®Á∫‡ ¡Õ dextran 70 ¡’ half-life 24 ™—«Ë ‚¡ß dextran 40 ¡’ half-life 6 ™—«Ë ‚¡ß ƒ∑∏‘Ï „π°“√µâ“π‡°√Á¥‡≈◊Õ¥®—∫°≈ÿ¡à „°≈â‡§’¬ß°—π „π 10% dextran 40 ®–‡æ‘Ë ¡ ª√‘ ¡ “µ√‰À≈‡«’ ¬ π„π‡≈◊ Õ ¥‰¥â ¥’ ° «à “ „πªí ® ®ÿ ∫— π ‡ªì π ∑’Ë ¬Õ¡√—∫„π°“√„™â dextran ªÑÕß°—π°“√‡°‘¥ venous thrombosis(12,13) „π∑“ßªØ‘∫µ— ‘ °“√„Àâ dextran √–À«à“ßºà“µ—¥·≈–À≈—ßºà“µ—¥ ®–™à«¬‰¡à „Àâ small-caliber arterial grafts ·≈– distal lower extremity bypass graft Õÿ¥µ—π‰¥âßà“¬‚¥¬„Àâ dextran 20 ¡‘≈≈‘°√—¡µàÕπÈ”Àπ—°µ—« 1 °‘‚≈°√—¡„π 24 ™—«Ë ‚¡ß·√°·≈–µàÕÕ’° 72

¬“∑’Ë„ ™â „π‚√§À≈Õ¥‡≈◊Õ¥ ™—«Ë ‚¡ßÀ≈—ßºà“µ—¥ ·≈–¬—ß„Àâ‡æ◊ÕË ªÑÕß°—π°“√‡°‘¥ DVT ·≈– pulmonary emboli ‰¥âº≈„°≈â‡§’¬ß°—∫°“√©’¥‡Œª“√’π¢π“¥µË”‡¢â“ „µâº«‘ Àπ—ß(14,15) ¢âÕÀâ“¡„π°“√„™â§Õ◊ ·æâ¬“ À—«„®«“¬ ‰µ∑”ß“π∫°æ√àÕß °≈‰° °“√·¢Áßµ—«¢Õß‡≈◊Õ¥º‘¥ª°µ‘·≈–„π¿“«–∑’Ë°”≈—ßµ°‡≈◊Õ¥ ¡’ ‡≈◊Õ¥ÕÕ°ßà“¬ §«√√–«—ß„π°“√„Àâ dextran √à«¡°—∫¬“µâ“π°“√ ·¢Áßµ—«¢Õß‡≈◊Õ¥ ·≈–¬“µâ“π‡°√Á¥‡≈◊Õ¥®—∫°≈ÿà¡ ®–∑”„Àâ‡≈◊Õ¥ ÕÕ°ßà“¬º‘¥ª°µ‘·≈–À¬ÿ¥¬“° À√◊Õ„Àâ „πºŸªâ «É ¬πÕ° °“√„Àâ¬“ dextran ª√‘¡“≥¡“°‡°‘π‰ª®–∑”„Àâ ‰µ«“¬´÷ßË ‡ªìπº≈¡“®“° osmotic damage µàÕ tubular cells dextran ¡’º≈µàÕ blood typing ·≈– cross matching(16,17) ¿“«–·∑√°´âÕπ∑’‡Ë °‘¥¢÷πÈ ¿“¬À≈—ß°“√„Àâ dextran ∑’æË ∫∫àÕ¬ §◊Õ°“√µ°‡≈◊Õ¥·≈–πÈ”‡°‘π ªÑÕß°—π‰¥â ‚¥¬„Àâ „πª√‘¡“µ√‰¡à‡°‘π √âÕ¬≈– 10 anaphylactic reaction æ∫‰¥â√âÕ¬≈– 0.1 ¿“«– ·∑√°´âÕπ®“°°“√µ°‡≈◊Õ¥·≈–πÈ”‡°‘πæ∫‰¥â®“°°“√„Àâ dextran 70 ¡“°°«à“ dextran 40(18) 1.5 Prostaglandin (PGs) ‡ªìπ 20-carbon unsaturated fatty acids ´÷Ëß∑”Àπâ“∑’Ë‡ªìπ ◊ËÕ„π°“√§«∫§ÿ¡°“√ªØ‘∫—µ‘ß“π ¢Õß‡´≈≈å à«πµà“ß Ê ‡√‘Ë¡®“°‡´≈‡¡Á¡‡∫√π phospholipase ®–∂Ÿ°°√–µÿâπ„Àâº≈‘µ arachidonic acid ®“° phospholipid ·≈–‡√‘¡Ë ¢∫«π°“√º≈‘µ prostaglandin ·π«∑“ßπ’®È –§≈â“¬°—∫°“√ ∑”Àπâ“∑’Ë¢Õß‡°√Á¥‡≈◊Õ¥·≈–‡ÕÁπ‚¥∑’‡≈’Ë¬¡ ·µà end products ®–·µ°µà“ß°—π„π‡´≈≈å‡ÕÁπ‚¥∑’‡≈’¬Ë ¡ end products ®–‡ªìπ thromboxane-A.2 PGI-2 º≈‘µ®“°‡ÕÁπ‚¥∑’‡≈’¬Ë ¡‡ªìπ à«π„À≠à ®–‡æ‘¡Ë ª√‘¡“≥¢Õß cAMP ¿“¬„π‡´≈≈å ´÷Ëß cAMP ®–µâ“π°“√®—∫°≈ÿà¡¢Õß‡°√Á¥ ‡≈◊Õ¥·≈–∑”„ÀâÀ≈Õ¥‡≈◊Õ¥¢¬“¬µ—« TXA-2 º≈‘µ®“°‡°√Á¥‡≈◊Õ¥®–‡æ‘Ë¡√–¥—∫¢Õß cGMP ´÷Ëß cGMP ®–∑”„Àâ‡°√Á¥‡≈◊Õ¥®—∫°≈ÿ¡à ·≈–À≈Õ¥‡≈◊Õ¥À¥µ—« º≈°“√µâ“πƒ∑∏‘°Ï π— √–À«à“ß‡°√Á¥‡≈◊Õ¥·≈–‡ÕÁπ‚¥∑’‡≈’¬Ë ¡∫π™—πÈ Õ‘πµ‘¡“¢ÕßÀ≈Õ¥‡≈◊Õ¥ ®–∑”„Àâ‡°‘¥°“√ ¡¥ÿ≈¬å√–À«à“ßƒ∑∏‘¢Ï Õß PGI-2 ·≈– TXA-2

2. ¬“µâ“π°“√·¢Áßµ—«¢Õß‡≈◊Õ¥ (Anticoagulants)(19) 2.1 ‡Œª“√’π ‡ªìπ “√∑’‡Ë °‘¥¢÷πÈ ‡Õßµ“¡∏√√¡™“µ‘„π√ÿª¢Õßπ‘« ‚§‚æ≈’·´§§“‰√¥å ¡’§ÿ≥ ¡∫—µ‘‡ªìπª√–®ÿ≈∫´÷Ëß “¡“√∂®—∫µ—«‰¥â °—∫æ≈“ ¡à“‚ª√µ’π∑’¡Ë §’ ≥ ÿ ¡∫—µ‡‘ ªìπª√–®ÿ∫«° ‡Œª“√’π °—¥‰¥â®“°

45 mast cells ¢Õß — µ «å ‡™à π ®“°ªÕ¥¢Õß«— « À√◊ Õ ≈”‰ â À ¡Ÿ ª√– ‘∑∏‘¿“æ¢Õß‡Œª“√’π«—¥®“°ª√‘¡“≥‡ªìπ¬Ÿπ‘µ ∫√‘À“√¬“‡¢â“ Ÿ√à “à ß°“¬‰¥â∑“ß„µâº«‘ Àπ—ß·≈–À≈Õ¥‡≈◊Õ¥¥” ¡’ half-life 1 1/2 ™—Ë«‚¡ß ¢—∫ÕÕ°®“°√à“ß°“¬∑“ßªí “«– «—¥ª√– ‘∑∏‘¿“æ·≈– ª√‘¡“≥æÕ‡À¡“–¢Õß¬“∑’Ë„Àâ ‰¥â®“° partial thromboplastin time (PTT) ·≈– activated clotting time (ACT) ´÷ßË §«√Õ¬Ÿà „π√–¥—∫ 1.5-2 ‡∑à“¢Õß§à“ª°µ‘ ‡Œª“√’π¡’º≈µàÕ°“√®—∫µ—« √â“ß‰ø∫√‘π ‚¥¬¡’ƒ∑∏‘µÏ Õà µ”·Àπàß µà“ß Ê ¢Õß°≈‰°°“√·¢Áßµ—«¢Õß‡≈◊Õ¥ (coagulation cascades) ¥—ßµàÕ‰ªπ’È (√Ÿª∑’Ë 4.2) 1. °“√‡ª≈’¬Ë π ¿“æ¢Õß prothrombin ‡ªìπ thrombin ™â“≈ß 2. ‡æ‘¡Ë ª√– ‘∑∏‘¿“æ¢Õß antithrombin III ´÷ßË ‡ªìπµ—«¬—∫¬—ßÈ thrombin µ“¡∏√√¡™“µ‘ antithrombin III ¡’ƒ∑∏‘‡Ï ªìπ cofactor ¢Õß‡Œª“√’π„π°“√≈Õß º≈°√–∑∫¢Õß thrombin µàÕ‰ø∫√‘‚π‡®π„π°“√ ≈“¬‰ø∫√‘π‚π‡®π„Àâ°≈“¬ ‡ªìπ‰ø∫√‘π 3. ≈¥°“√®—∫°≈ÿ¡à ¢Õß‡≈◊Õ¥ ‚¥¬°“√‡æ‘¡Ë electronegative potential ¢Õßºπ—ßÀ≈Õ¥‡≈◊Õ¥ ¿“«–·∑√°´âÕπ¢Õß‡Œª“√’π§◊Õ heparin-Induced-Thrombo cytopenia (HIT) ∂â“„Àâ¡“°‡°‘π®π°√–∑—Ëß‡≈◊Õ¥‰À≈‰¡àÀ¬ÿ¥ ‰¡à ·¢Áßµ—« À√◊Õ¡’ prolonged PTT ·≈– ACT “¡“√∂∑’®Ë – neutralized ƒ∑∏‘Ï¬“‰¥â ‚¥¬°“√„Àâ protamine sulfate ‡¢â“∑“ß À≈Õ¥‡≈◊Õ¥¥”„πª√‘¡“≥ 1 ¡‘≈≈‘°√—¡µàÕ 100 ¬Ÿπµ‘ ¢Õß‡Œª“√’π ¿“«–·∑√°´âÕπ∑’ËÕ“®®–æ∫‰¥â „πºŸâªÉ«¬‡∫“À«“π∑’ËµâÕß©’¥Õ‘π ÿ ≈‘πµ≈Õ¥À≈—ß®“°©’¥ protamine sulfate ‡æ◊ËÕµâ“πƒ∑∏‘Ï¢Õß‡Œ ª“√’π§◊Õ §«“¡¥—π‚≈À‘µ≈¥≈ßÕ¬à“ß√«¥‡√Á« °“√„Àâ‡Œª“√’πÕ ¬à“ßµàÕ‡π◊ÕË ß‡ªìπ√–¬–‡«≈“π“π‡ªìπ “‡ÀµÿÀπ÷ßË ¢Õß osteoporosis ¥â«¬ 2.2 Low melecular weight heparin (LMWH) º≈‘µ ¢÷Èπ‰¥â®“°«‘∏’°“√ depolymerization ¢Õß standard À√◊Õ unfractionated heparing (UFH) ‡ªìπ glycoaminoglycan ¡’ πÈ”Àπ—°‚¡‡≈°ÿ≈ª√–¡“≥ 4,500 ¥“≈µ—π ¡’º≈µàÕ anti Xa activity ¡“°°«à“ anti IIa activity ¡’º≈∑—ßÈ immediate ·≈– prolonged antithrombin action ª√–‡¡‘πª√– ‘∑∏‘¿“æ¢Õß¬“‰¥â®“° plasma anti-Xa activity ¬“®–¡’√–¥—∫ Ÿß ÿ¥¿“¬„πæ≈“ ¡“À≈—ß ©’¥¬“·≈â« 3 ™—«Ë ‚¡ß ¡’ half life 3.5 ™—«Ë ‚¡ß ·≈–¡’ anti-Xa activity ¬“«π“π∂÷ß 18 ™—«Ë ‚¡ß ¡’¢Õâ ∫àß™’È „π°“√„™â§Õ◊ ªÑÕß°—π thromboembolic disorders „π°“√ºà“µ—¥°√–¥Ÿ°·≈–»—≈¬°√√¡ ∑—Ë « ‰ªÀ√◊ Õ „™â „π°“√√—°…“¿“«–‡≈◊Õ¥·¢Áßµ—«º‘¥ª°µ‘·≈–øÕ°

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥

√Ÿª∑’Ë 4.2 µ”·Àπàß¢Õß Coumadin, heparin, streptokinase and urokinase ∑’ËÕÕ°ƒ∑∏‘ÏµàÕ coagulation cascade. ‡≈◊Õ¥„πºŸâªÉ«¬‰µ«“¬‡√◊ÈÕ√—ß ‡π◊ËÕß®“°¬“™π‘¥π’È¡’ fixed dose “¡“√∂∫√‘À“√¬“‚¥¬©’¥‡¢â“„µâº‘«Àπ—ß∫√‘‡«≥ –¥◊Õ ©’¥‡ªìπ¡ÿ¡ µ—ßÈ ©“°°—∫º‘«Àπ—ß ‰¡àæ∫«à“∑”„Àâ‡°‘¥≈‘¡Ë ‡≈◊Õ¥º‘¥ª°µ‘∫√‘‡«≥∑’©Ë ¥’ ¬“ ∂â“‡æ◊ÕË °“√ªÑÕß°—π thromboembolic disorder „Àâ©¥’ 12 ™—«Ë ‚¡ß °àÕπ·≈–À≈—ß°“√ºà“µ—¥·≈–©’¥«—π≈–§√—ßÈ ®π°√–∑—ßË ºŸªâ «É ¬ ambulate ‰¥â ∂â“‡ªìπ°“√√—°…“µâÕß„Àâ¬“Õ¬à“ßµàÕ‡π◊ÕË ß®π§√∫ 10 «—π ‡ªìπÕ¬à“ßπâÕ¬ ®π‡≈¬√–¬–‡«≈“‡ ’¬Ë ßÀ√◊ÕºŸªâ «É ¬ ambulate ‰¥â (20)

∂â“„Àâ¬“ª√‘¡“≥ Ÿß‡°‘π®–¡’°“√µ°‡≈◊Õ¥ µâÕß monitor PTT ·≈–ª√‘¡“≥¢Õß‡°√Á¥‡≈◊Õ¥µâ“πƒ∑∏‘¬Ï “‰¥â¥«â ¬°“√©’¥ protamine sulfate 6 ¡‘≈≈‘°√—¡µàÕ 0.1 ¡‘≈≈‘≈‘µ√ (2,500 ICUAXa) ¢Õß Fraxiparen ¬“∑’ÀË “â ¡„™â√«à ¡‡æ√“–®–∑”„Àâµ°‡≈◊Õ¥ßà“¬¡’ ·Õ ‰æ√‘π, NSAIDS, nadroparin ·≈– ticlopidine Õ“°“√¢â“ß‡§’¬ß¢Õß ¬“∑’ÕË “®®–æ∫‰¥â¡’ thrombocytopenia, cutaneous necrosis ·≈–·æâ¬“

¬“∑’Ë„ ™â „π‚√§À≈Õ¥‡≈◊Õ¥ ¬“π’ÕÈ “®®–„ÀâÕ¬à“ßµàÕ‡π◊ÕË ß‰¥â „πºŸªâ «É ¬∑’‡Ë ’¬Ë ßµàÕ°“√‡°‘¥ DVT ·≈–‡ªìπ´È”∫àÕ¬ Ê ‡æ√“–Õ—µ√“‡ ’¬Ë ßµàÕ°“√‡°‘¥ osteoporosis ·≈– fracture spine πâÕ¬°«à“‡Œª“√’π ¬—ß‰¡à¡À’ ≈—°∞“π¬◊π¬—π·πàπÕπ«à“ ¬“π’¡È º’ ≈ teratogenic effect „πÀ≠‘ß¡’§√√¿å ‰¥â¡°’ “√π”‡Õ“¡“„™â ªÑÕß°—π DVT „πÀ≠‘ß¡’§√√¿å æ∫«à“ LMWH ‰¡àº“à π√°‡¢â“ Ÿ∑à “√° „π§√√¿å ¿“«–·∑√°´âÕπ®“°°“√µ°‡≈◊Õ¥ ·æâ¬“ thrombocytopenia ·≈– osteoporosis πâÕ¬°«à“ unfractionated heparin 2.3 Coumadine (sodium warfarin) ‡ªìπ¬“µâ“π‡≈◊Õ¥ ·¢Áßµ—«∑’Ë∫√‘À“√‡¢â“ Ÿà√à“ß°“¬‚¥¬°“√√—∫ª√–∑“π ¡’ƒ∑∏‘Ï „π°“√ Àâ“¡°“√º≈‘µ¢Õß vitamin K dependent factors „π coagulation cascades (√Ÿª∑’Ë 4.2) §◊Õ factor II (prothrombin), VII, IX ·≈– X ®÷ß¡’™◊ËÕ‡√’¬°Õ’°Õ¬à“ßÀπ÷Ëß«à“ vitamin K antagonist ‡π◊ÕË ß®“°¡’ vitamin K dependent factors À≈“¬µ—« ¡’ half-life π“π ®÷ßµâÕß„™â‡«≈“ 3-5 «—π¿“¬À≈—ß√—∫ª√–∑“π¬“®÷ß®–‰¥â ª√– ‘∑∏‘¿“æ‡µÁ¡∑’Ë „π°“√µâ“π‡≈◊Õ¥·¢Áßµ—« ¬“™π‘¥π’È∂Ÿ°¬àÕ¬ ≈“¬·≈–∑”„Àâ‡ ◊ÕË ¡ ¿“æ‰¥â ‚¥¬ microsomal enzyme syetem ¿“¬„πµ—∫ ¬“µ—«Õ◊Ëπ∑’Ë¬àÕ¬ ≈“¬„πµ—∫‡™àπ°—π ®–¡’º≈ àß‡ √‘¡ À√◊Õ¬—∫¬—Èßƒ∑∏‘Ï¢Õß Coumadine ‰¥â ¡’ half-life 36 ™—Ë«‚¡ß À≈—ß®“°À¬ÿ¥¬“ 1-8 «—π √–¥—∫¢Õß PT ®÷ß®–°≈—∫¡“ª°µ‘‡À¡◊Õπ‡¥‘¡ monitor ª√– ‘∑∏‘¿“æ¢Õß¬“®“°√–¥—∫ PT ∂â“ƒ∑∏‘¬Ï “¡“°‡°‘π ‰ª·°â ‰¢‰¥â ‚¥¬°“√©’¥ Vitamin K ‡¢â“À≈Õ¥‡≈◊Õ¥¥”À√◊Õ„Àâ fresh frozen plasma (FFP) 2.4 Ancrod ‡ªìπ°√¥Õ¡‘‚π∑’¡Ë π’ È”Àπ—°‚¡‡≈°ÿ≈ 37,000 ¥“≈ µ—π ‡ªìπÕπÿæπ— ∏ÿ¢å Õßæ‘…ßŸ™π‘¥ malayan pit viper (Agkistrodon rhodostoma) ¡’ circulatory half lift 3-5 ™—«Ë ‚¡ß Ancrod ·¬°®“° A fibrinopeptides (A, AY ·≈– AP) ‰¥â®“° circulating fibrinogen ‰ø∫√‘π∑’Ë ‰¥â®–‰¡à “¡“√∂‡°‘¥ cross linking ‰·µà ®–‰«µàÕ°“√¬àÕ¬ ≈“¬·≈– phagocytosis ®“° reticuloendothelial system (RES) °«à“‰ø∫√‘π∑—Ë«‰ª πÕ°®“°π’È®–¡’º≈µàÕ °“√·¢Áßµ—«¢Õß‡≈◊Õ¥ ´÷Ëß≈¥ª√‘¡“≥§«“¡‡¢â¡·¢Áß¢Õß‰ø∫√‘π‚π ‡®π„π‡≈◊Õ¥ ≈¥§«“¡Àπ◊¥¢Õß‡≈◊Õ¥·≈–ª√– ‘∑∏‘¿“æ∑“ß rheology ¢Õß‡≈◊Õ¥ Ancrod ‰¡à¡º’ ≈µàÕ‡°√Á¥‡≈◊Õ¥·≈–‚ª√µ’π Õ◊πË Ê ∑’‡Ë °’¬Ë «¢âÕß°—∫°“√·¢Áßµ—«¢Õß‡≈◊Õ¥(20) ∫√‘À“√¬“‡¢â“ Ÿ√à “à ß°“¬‰¥â ‚¥¬°“√©’¥‡¢â“„µâº«‘ Àπ—ßÀ√◊ÕÀ≈Õ¥ ‡≈◊Õ¥¥” °“√„Àâ‡¢â“∑“ßÀ≈Õ¥‡≈◊Õ¥¥”®–§«∫§ÿ¡°“√‡°‘¥¿“«– hypofibrinogenemia ‰¥âß“à ¬(21) ª√‘¡“≥§«“¡‡¢â¡¢âπ¢Õß‰ø∫√‘‚π‡®π ‡æ’¬ß 0.2-0.6 °√—¡/≈‘µ√ °Á “¡“√∂∑”„Àâ‡≈◊Õ¥·¢Áßµ—«‰¥â·≈–ªÑÕß°—π spontaneous thrombosis ‰¥â ®–¡’ª√– ‘∑∏‘¿“æ„π°“√µâ“π ‡≈◊Õ¥·¢Áßµ—« ∂â“„Àâ¬“ 70-100 ¬Ÿπ‘µ (1-2 ¬Ÿπ‘µ/πÈ”Àπ—°µ—« 1

°‘‚≈°√—¡) ¿“¬„π 12-36 ™—«Ë ‚¡ß ®–≈¥√–¥—∫‰ø∫√‘‚π‡®π≈ß¡“‰¥â „ÀâÕ¬Ÿà „π™à«ß 48 ™—«Ë ‚¡ß·√°§«√«—¥√–¥—∫‰ø∫√‘‚π‡®π„π´’√¡—Ë ∑ÿ° 12 ™—«Ë ‚¡ß À≈—ß®“°π—πÈ ‡ªìπ«—π≈–§√—ßÈ ·≈–®—¥ infusion rate „Àâ ‰¥â √–¥—∫¢Õß‰ø∫√‘‚π‡®πµ“¡∑’ËµâÕß°“√ ∂â“„™â Ancord ‡ªìπ√–¬– ‡«≈“π“π°«à“ 4-6 —ª¥“Àå √à“ß°“¬®–µâ“π¬“‚¥¬‡°‘¥¡’ serum proteinase inhibitor ‡¢â“¡“¢÷Èπ°—∫ Ancrod ∑”„Àâª√– ‘∑∏‘¿“æ ¢Õß¬“≈¥≈ß(22) Ancord ‡À¡“– ”À√—∫ºŸªâ «É ¬∑’Ë „Àâ‡Œª“√’π·≈â«‡°‘¥¿“«– Heparin Induced Thrombocytopenia (HIT) ∑’¬Ë ß— µâÕß°“√ƒ∑∏‘Ï ¢Õß¬“„π°“√µâ“π≈‘Ë¡‡≈◊Õ¥ ·≈–µâÕß°“√√—°…“Õ¬à“ßµàÕ‡π◊ËÕß ·≈–„™â ‰¥âº≈„πºŸªâ «É ¬∑’¢Ë “¥ antithrombin III ´÷ßË ¥◊ÕÈ µàÕ°“√„Àâ‡Œ ª“√’π‡æ◊ÕË µâ“π≈‘¡Ë ‡≈◊Õ¥ Ancord „™â ‰¥âº≈¥’„πºŸªâ «É ¬ strokd, DVT, pulmonary embolism ·≈– central retinal thrombosis „™â‡ªìπ¬“µâ“π≈‘¡Ë ‡≈◊Õ¥‰¥â „πºŸªâ «É ¬ hemodialysis, cardio pulmonary bypass ·≈–ºà“µ—¥À≈Õ¥‡≈◊Õ¥∫√‘‡«≥·¢π¢“ ¿“«–·∑√°´âÕπ¢Õß¬“∑’æË ∫‰¥â¡‰’ ¢â·≈–Õ“°“√·æâ¬“ µ°‡≈◊Õ¥ ∂â“°“√µ°‡≈◊Õ¥Õ¬Ÿà „π¿“«–«‘°ƒµ‘√ÿπ·√ß§«√„Àâ cryoprecipitate ®–µâ“πƒ∑∏‘Ï¢Õß Ancord ‰¥â∑—π∑’ ∂â“„Àâ Ancord „πª√‘¡“≥∑’Ë ‡À¡“– ¡®–∑”„Àâ°“√ºà“µ—¥‰¥âµ“¡ª°µ‘‚¥¬‰¡àµâÕß°—ß«≈«à“®–¡’ °“√µ°‡≈◊Õ¥¡“°º‘¥ª°µ‘

3. ¬“‡ √‘¡°“√‰À≈‡«’¬π‡≈◊Õ¥ (circulation - enhancing drugs) 3.1 Hemorrheologic drugs 3.1.1 Pentoxifylline ‡ªìπÕπÿæπ— ∏ÿ¢å Õß theobromide §âπ æ∫‚¥¬π—°«‘∑¬“»“ µ√å™“«‡¬Õ√¡—π„πªï 1930 ‚¥¬‡¢â“„®«à“®– ÕÕ°ƒ∑∏‘‡Ï ªìπ¬“¢¬“¬À≈Õ¥‡≈◊Õ¥ ·µà„π∑“ßªØ‘∫µ— ‡‘ ¡◊ÕË π”¡“„™â®√‘ßÊ ·≈â«‰¡à¡º’ ≈„π°“√¢¬“¬À≈Õ¥‡≈◊Õ¥‡≈¬ „πªï 1973 Hess ·≈–§≥– æ∫«à“¬“™π‘¥π’È¡’º≈„π·ßà¢Õß hemorrheology ®÷ßπ”¡“√—°…“ Intermittent claudication „πª√–‡∑»¬ÿ‚√ª ·≈–µàÕ¡“‰¥âπ” ¡“„™â ‚¥¬Õß§å°“√Õ“À“√·≈–¬“¢Õß À√—∞Õ‡¡√‘°“ (FDA) ‰¥â √—∫√Õß„π°“√„™â¬“π’È „πªï 1980 ¬“π’È¡’º≈ àß‡ √‘¡°“√‰À≈‡«’¬π ‡≈◊Õ¥‚¥¬¡’°≈‰°∑’ Ë ”§—≠¥—ßµàÕ‰ªπ’È (23) 1. ‡æ‘¡Ë lipophosphoprotein „π‡¡Á¥‡≈◊Õ¥·¥ß ∑”„Àâ‡¡Á¥ ‡≈◊Õ¥·¥ß¬◊¥À¬ÿπà ‡§≈◊ÕË π‰À«‰¥âß“à ¬ 2. ≈¥ª√‘¡“≥¢Õßæ≈“ ¡“‰ø∫√‘‚π‡®π 3. ≈¥§«“¡Àπ◊¥¢Õß‡≈◊Õ¥ 4. ≈¥À√◊Õµâ“π°“√®—∫°≈ÿ¡à ¢Õß‡°≈Á¥‡≈◊Õ¥ 5. ‡æ‘Ë¡ª√– ‘∑∏‘¿“æ rhelogic characteristic ¢Õß‡¡Á¥ ‡≈◊Õ¥¢“«

48 °“√√—°…“ IC §«√„Àâ¬“™π‘¥Õ¬à“ßµàÕ‡π◊ËÕß π“π°«à“ 6-8 —ª¥“Àå ®÷ß®–‰¥âº≈ ‡æ‘Ë¡√–¬–∑“ß„π°“√‡¥‘π‰¥â√âÕ¬≈– 25-40 º≈°“√√—°…“®–¥’¢÷Èπ ∂â“„ÀâºŸâªÉ«¬ÕÕ°°”≈—ß°“¬√à«¡¥â«¬ ¿“«– ·∑√°´âÕπ∑’æË ∫‰¥â§Õ◊ §≈◊πË ‰ â Õ“‡®’¬π ·πàπ∑âÕß æ∫‰¥â√Õâ ¬≈– 30 3.1.2 Dextran ®—¥Õ¬Ÿà„π°≈ÿ¡à ¬“‡ √‘¡°“√‰À≈‡«’¬π‡≈◊Õ¥ ‚¥¬ ¡’ƒ∑∏‘‡Ï ªìπ plasma volume expander µâ“π°“√·¢Áßµ—«¢Õß‡≈◊Õ¥ ‚¥¬‡§≈◊Õ∫ºπ—ß¥â“π„π¢ÕßÀ≈Õ¥‡≈◊Õ¥ ·≈–‡¡Á¥‡≈◊Õ¥·¥ß‡ªìπ electromagnetic carpet µâ“π‰¡à „Àâ‡≈◊Õ¥Àπ◊¥ ‰À≈‡«’¬π™â“®π ®—∫°≈ÿà¡‡ªìπ≈‘Ë¡‡≈◊Õ¥ „ÀâÀ≈—ßºà“µ—¥‡æ◊ËÕªÑÕß°—π‰¡à „Àâ‡°‘¥≈‘Ë¡‡≈◊Õ¥ „πÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡∑’µË Õà ‰«âÀ√◊ÕªÑÕß°—π DVT 3.2 ¬“‡ √‘¡‡¡µ“‚¡‚∫≈‘ ¡å (metabolic enhancing agents) 3.2.1 Carnitine ‡ªìπ “√∑’‡Ë °‘¥¢÷πÈ µ“¡∏√√¡™“µ‘‰¡à¡æ’ …‘ ∂÷ß ·¡â«à“®–„Àâ „πª√‘¡“≥∑’Ë Ÿß¡“° ƒ∑∏‘Ï∑“ß™’«‡§¡’ ‚¥¬∑—Ë«‰ª·≈â«®– àß‡ √‘¡‰æ√Ÿ‡«∑„Àâ‡¢â“¡“ „π citric acid cycle ·≈–™à«¬°“√π” àß°√¥‰¢¡—π ∑”„Àâ¡°’ “√‡æ‘¡Ë ATP ·≈–≈¥·≈§‡µ∑„π°≈â“¡‡π◊ÕÈ ¡√√∂¿“æ°“√∑”ß“π¢Õß°≈â“¡‡π◊ÕÈ ®–¥’¢π÷È (24) ®“°°“√»÷°…“„π ªí®®ÿ∫—πæ∫«à“°≈â“¡‡π◊ÈÕ∑’Ë¢“¥‡≈◊Õ¥®–¡’ª√‘¡“≥¢Õß carnitine ≈¥≈ß·≈– ¡√√∂¿“æ‰¡à¥’¢≥–∑’Ë¡’‡¡µ“‚∫≈‘ ¡å·∫∫ anaerobic ‡¡◊ÕË π”‡Õ“ carnitine ¡“√—°…“ºŸªâ «É ¬ IC æ∫«à“‡æ‘¡Ë √–¬–∑“ß„π ∑“ß‡¥‘π·≈–µ—¥‡Õ“°≈â“¡‡π◊ÕÈ ¡“µ√«®®–æ∫ª√‘¡“≥¢Õß carnitine „π°≈â “ ¡‡π◊È Õ ‡æ‘Ë ¡ ¢÷È π ¡’ ° “√≈¥¢Õßª√‘ ¡ “≥·≈§‡µ∑„π‡≈◊ Õ ¥¥” Õ¬à“ß‰√°Áµ“¡¬“™π‘¥π’È¬—ßÕ¬Ÿà „π¢≥–∑¥≈Õß„™â Õß§å°“√Õ“À“√ ·≈–¬“¢Õß À√—∞Õ‡¡√‘°“¬—ß‰¡à√∫— √Õß°“√„™â 3.2.2 Naftidofuryl (praxilene) ‡ªìπ¬“∑’¡Ë ’„™â „πª√–‡∑» ∑“ß¬ÿ‚√ª ‰¡à¡’ „™â „π À√—∞Õ‡¡√‘°“ ¬“™π‘¥π’¡È °’ ≈‰°°“√ÕÕ°ƒ∑∏‘Ï ¥—ßµàÕ‰ªπ’(25-28) È 1. ‡ªìπ 5-HT receptor blockade ®–ªÑÕß°—π‰¡à „ÀâÀ≈Õ¥ ‡≈◊Õ¥∫√‘‡«≥∑’Ë¢“¥‡≈◊Õ¥À¥µ—« ¿“¬À≈—ß°“√∫“¥ ‡®Á∫¢Õß‡ÕÁπ‚¥∑’‡≈’¬Ë ¡·≈–°“√®—∫°≈ÿ¡à ¢Õß‡°√Á¥‡≈◊Õ¥ 2. °√–µÿâπ„Àâ ‰¢¡—π·≈–§“√å ‚∫Œ—¬‡¥√∑‡¢â“ Ÿà triboxylic acid cycle ∑”„Àâ¡’°“√‡æ‘Ë¡ ATP ·≈–≈¥°“√§—Ëß ¢Õß·≈§‡µ∑∫√‘‡«≥∑’¢Ë “¥‡≈◊Õ¥ 3. ‡æ‘Ë¡°“√„™âÕäÕ°´‘‡®π¿“¬„π‡π◊ÈÕ‡¬◊ËÕ∑’Ë¢“¥‡≈◊Õ¥ ‚¥¬ ¡’º≈µàÕ‡¡µ“‚∫≈‘ ¡å ¿“¬„π¡—¬‚µ§√Õπ‡¥’¬ ‡æ‘Ë¡ ª√‘¡“≥ ATP „π°≈â“¡‡π◊ÈÕ ≈¥·≈§‡µ∑ ·≈–æ—¬√Ÿ ‡«∑¿“¬„π°≈â“¡‡π◊ÕÈ ∑’¢Ë “¥‡≈◊Õ¥ ¬“π’È „™â „π°“√√—°…“ IC, ischemic rest pain ·≈– vasospastic disorders

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4. ¬“¢¬“¬À≈Õ¥‡≈◊Õ¥ (vasodilators) ‡ªìπ¬“∑’Ë „™â§«∫§ÿ¡ peripheral vascular tone ‡ÕÁπ‚¥∑’‡≈’¬Ë ¡ ®–¡’∫∑∫“∑ ”§—≠„π°“√§ß§«“¡µ÷ß·≈–À¬àÕπ¢Õßºπ—ßÀ≈Õ¥‡≈◊Õ¥ ¿“¬„π‡ÕÁπ‚¥∑’‡≈’¬Ë ¡®–¡’ receptors ´÷ßË √—∫°“√°√–µÿπâ ®“° vasoactive hormones ‡™àπ norepinephrine, epinephrine ·≈– serotonin πÕ°®“°π’È¬—ß‡ªìπ·À≈àßº≈‘µ prostacycline ´÷Ëß‡ªìπ “√¢¬“¬À≈Õ¥‡≈◊Õ¥¥â«¬ “√∑’‡Ë ÕÁπ‚¥∑’‡≈’¬Ë ¡ —ß‡§√“–Àå ‰¥â¡’ endothelium-derived relaxation factors ´÷ßË ¡’º≈‡ªìπ flow-induced vasodilatation ·≈–¬—ß —ß‡§√“–Àå epinephrine ´÷Ëß ‡ªìπ “√∑’Ë¡’ª√– ‘∑∏‘¿“æ∑”„ÀâÀ≈Õ¥‡≈◊Õ¥À¥µ—«Õ¬à“ß√ÿπ·√ß „π ¿“«–¢“¥ÕäÕ°´‘‡®π√à«¡°—∫°“√°√–µÿâπ„ÀâÀ≈Õ¥‡≈◊Õ¥À¥µ—«‚¥¬ norepinephrine ¬“‡À≈à“π’È¡—°®–„™â¢≥–∑” arteriography ‡æ◊ËÕ„Àâº≈°“√«‘π‘®©—¬‚√§¥’¢÷Èπ ≈¥Õ—µ√“§«“¡‡ ’Ë¬ß„π°“√µ√«® «‘π®‘ ©—¬µ≈Õ¥®π¿“«–·∑√°´âÕπ∑’ÕË “®®–‡°‘¥¢÷πÈ ‰¥â 4.1 Tolazolin hydrochloride (Priscoline, Ciba Pharmaceuticals, Edison, NJ) ¡’º≈µàÕ°≈â“¡‡π◊ÕÈ ‡√’¬∫¢ÕßÀ≈Õ¥ ‡≈◊Õ¥¥” ∑”„ÀâÀ≈Õ¥‡≈◊Õ¥À¬àÕπ·≈–À“¬µ—«¢≥–∑’Ë©’¥ “√∑÷∫ · ß®–‡ÀÁπ°“¬«‘¿“§·≈–æ¬“∏‘ ¿“æ∑’Ëº‘¥ª°µ‘¢ÕßÀ≈Õ¥‡≈◊Õ¥ ™—¥‡®π¡“°¢÷Èπ „™â ”À√—∫ selective arteriography À≈Õ¥ ‡≈◊Õ¥∫√‘‡«≥·¢π portal ·≈– mesenteric venous opacification √–À«à“ß∑” arterial portography ‡æ√“–¢≥–∑’∑Ë ” selective catheterization À≈Õ¥‡≈◊Õ¥·¥ß¡—°®–À¥µ—« „πºŸâ „À≠à „Àâ ¢π“¥ 25 ¡‘≈≈‘°√—¡ ≈–≈“¬„ππÈ”‡°≈◊Õ ¡¥ÿ≈¬å 5-10 ¡‘≈≈‘≈‘µ√ ©’¥‡¢â“∑“ßÀ≈Õ¥‡≈◊Õ¥·¥ß®–ÕÕ°ƒ∑∏‘¿Ï “¬„π 20-30 «‘π“∑’ 4.2 Nitroglycerine ™à«¬≈¥°“√À¥µ—«¢ÕßÀ≈Õ¥‡≈◊Õ¥ ©’¥ ‡¢â“∑“ßÀ≈Õ¥‡≈◊Õ¥·¥ß„πª√‘¡“≥ 100-200u ©’¥´È”‰¥â‡¡◊ÕË µâÕß°“√ 4.3 Papaverine hydrochloride ¡’º≈∑”„Àâ°≈â“¡‡π◊ÕÈ ‡√’¬∫ ∑’ºË π—ß¢ÕßÀ≈Õ¥‡≈◊Õ¥À¬àÕπµ—«≈ß πÕ°®“°®–„™â „π°“√∑” arteriography ·≈â«¬—ß„™â‡ªìπ local application „πºŸâªÉ«¬∑’ËÀ≈—ß µàÕÀ≈Õ¥‡≈◊Õ¥·≈â« À≈Õ¥‡≈◊Õ¥¬—ßÀ¥µ—«Õ¬Ÿà 4.4 Calcium channel blockers „™âªÕÑ ß°—πÀ≈Õ¥‡≈◊Õ¥ À¥µ—«¢≥–∑” selective arteriography À√◊Õ angioplasty ‚¥¬„ÀâÕ¡ Nifedipine ¢π“¥ 10 ¡‘≈≈‘°√—¡„µâ≈π‘È ¬“®–ÕÕ°ƒ∑∏‘Ï ¿“¬„π 10-15 π“∑’ ƒ∑∏‘¢Ï “â ß‡§’¬ß¢Õß¬“°≈ÿ¡à π’§È Õ◊ §«“¡¥—π‚≈À‘µµË”∑—π∑’ ·°â ‰¢ ‚¥¬„Àâ “√πÈ”∑¥·∑π‡¢â“∑“ßÀ≈Õ¥‡≈◊Õ¥¥” ·≈–πÕπ¬°¢“ Ÿß ¬“ ¢¬“¬À≈Õ¥‡≈◊Õ¥¡’º≈∑”„Àâ‡°‘¥ reflex tachycardia ®÷ß§«√ √–«—ß„π°“√„™â°∫— ºŸªâ «É ¬‚√§À—«„®¢“¥‡≈◊Õ¥

¬“∑’Ë„ ™â „π‚√§À≈Õ¥‡≈◊Õ¥

5. ¬“≈–≈“¬≈‘Ë¡‡≈◊Õ¥ (Fibrinolytic agents)

lating plasmin inhibitors ∑”„Àâ¡’ plasmin ‡°‘¥¢÷πÈ ¡“°¡“¬ (exogenous fibrinolysis) „π thrombus ®–¡’ plasminogen ‡ªìπ à«πª√–°Õ∫∑’ Ë ”§—≠ °“√°√–µÿπâ bounded-plasminogen „Àâ°≈“¬‡ªìπ plasmin ∑”„Àâ¡°’ “√≈–≈“¬≈‘¡Ë ‡≈◊Õ¥‡°‘¥¢÷πÈ ‡©æ“–∑’Ë „πªí ® ®ÿ ∫— π µâ Õ ß°“√ “√≈–≈“¬≈‘Ë ¡ ‡≈◊ Õ ¥∑’Ë ¡’ ª √– ‘ ∑ ∏‘ ¿ “æ·≈– ÕÕ°ƒ∑∏‘‡Ï ©æ“–∑’Ë §◊Õ‡°“–·πàπ°—∫ thrombus-bound plasminogen ¡’º≈πâÕ¬∑“ß systemic µàÕ circulating coenzymes æ∫ «à“ tissue plasminogen activator (tPA) ∑’Ë —ß‡§√“–Àå®“° melanosma cell lines π”¡“ recombinant ‚¥¬‡∑§π‘§∑“ß DNA ®–¡’º≈≈–≈“¬≈‘¡Ë ‡≈◊Õ¥‡©æ“–∑’Ë ‰¥â¥¡’ “° ¿“«–¢â“ß‡§’¬ß®“° systemic fibrinolysis πâÕ¬ ‰¡à¡“°‡À¡◊Õπ UK ·≈– SK(30-33) 5.1 Streptokinase (SK) ‡ªìπ nonenzymatic protein ∑’Ë º≈‘µ¢÷πÈ ®“° Lancefiedûs group C strain of beta-hemolytic Streptococci „πªï 1933 Tillet ·≈– Garna æ∫«à“ “√∑’ Ë °—¥ ‰¥âπ¡’È §’ ≥ ÿ ¡∫—µ„‘ π°“√≈–≈“¬≈‘¡Ë ‡≈◊Õ¥ ‚¥¬®–√«¡°—∫ plasminogen „πª√‘¡“≥ 1:1 ‡ªìπ activator complex ´÷ßË streptokinase-plasminogen complex π’®È –°√–µÿπâ fibrinolytic system ‚¥¬°“√‡ª≈’¬Ë π uncomplexed plasminogen „Àâ°≈“¬‡ªìπ plas-

§◊Õ¬“∑’Ë„™â „π°“√°√–µÿπâ fibrinolytic system (√Ÿª∑’Ë 4.3) ·∫àß ÕÕ°‰¥â‡ªìπ direct activators °—∫ indirect activators indirect activators ®–°√–µÿπâ fibrinolytic activity ‚¥¬¡’º≈µàÕ plasminogen in vivo à«π direct activators ®–°√–µÿπâ fibrinolytic activity ‚¥¬¡’º≈µàÕ plasminogen in vitro “√µà“ß Ê ∑’Ë ‡°’Ë¬«¢âÕß°—∫ fibrinolytic activity ‡™àπ °√¥π‘‚§µ‘π‘§·≈–Õ¥√’ π“≈‘π®–°√–µÿπâ ‡ÕÁπ‚¥∑’‡≈’¬Ë ¡„ÀâÀ≈—ßË tPA antidiuretic hormone ¡’ƒ∑∏‘ÏµàÕ√–∫∫π’È‡™àπ°—π ·µàº≈∑“ß√–∫∫À≈Õ¥‡≈◊Õ¥·≈–À—«„® ¡“°°«à“‡™àπ‡¥’¬«°—∫‡ µ’¬√Õ¬¥å ·≈– diguanides (Phenformin) ∂â“©’¥ Stanozol (anabolic hormones) «—π≈–§√—ßÈ Õ¬à“ßµàÕ‡π◊ÕË ß 5 ªï √à“ß°“¬®–¡’°“√°√–µÿâπµàÕ fibrinolytic system „Àâ ∑”ß“πÕ¬à“ßµàÕ‡π◊ÕË ß(29) direct fibrinolytic agents ®–‡ª≈’¬Ë π plasminogen „Àâ ‡ªìπ plasmin ¡’º≈„π°“√≈–≈“¬≈‘¡Ë ‡≈◊Õ¥µ“¡·π«∑“ß¢Õß fibrinolytic system ‡π◊ÕË ß®“° “√π’È ‰¡à¡’ fibrinolytic activity „πµ—«‡Õß ®÷ßµâÕßºà“π plasminogen „Àâ¡’ lytic action π’È “√„π°≈ÿ¡à π’‡È ™àπ Urokinase (UK) ·≈– Streptokinase (SK) ®–¡’ƒ∑∏‘°Ï ¥ circu-

THE FIBRINOLYTIC SYSTEM

Plasminogen + + + +

- Anti-Activators - Blood, Tissue and Urine inhibitors

Fibrinogen

√Ÿª∑’Ë 4.3 Fibrinolytic system

Plasmin

Activated Factor XII Tissue Activator Urokinase Streptokinase-->complex

Fibrin ! + Thrombin

Inhibitors Alpha 2 Anti-plasmin Alpha 2 Mauroglobulin Alpha 1 Antitrypsin Antithrombin III Complement 2 inhibitor Soluble Fibrin Split Porducts

50 min À≈—ß®“°π—Èπ SK °Á®–¡“®—∫µ—«°—∫ plasmin ´÷Ëß®–¡’º≈µàÕ °“√‡ª≈’¬Ë π·ª≈ß¢Õß plasminogen ·≈–®–™à«¬¬àÕ¬ ≈“¬≈‘¡Ë ‡≈◊Õ¥ ¬“∑’Ë „Àâ‡¢â“ Ÿ√à “à ß°“¬®–∂Ÿ° neutralized ‚¥¬ antistreptococcal antibodies ´÷Ëß¡’ „πºŸâªÉ«¬∑’Ë‡§¬µ‘¥‡™◊ÈÕ streptococci ∑”„Àâ ª√‘¡“≥¢Õß SK ∑’®Ë –‰ª®—∫°—∫ circulating plasminogen ≈¥≈ß ®÷ß§«√°–ª√‘¡“≥¬“„Àâ‡æ’¬ßæÕ∑’®Ë –ÕÕ°ƒ∑∏‘≈Ï –≈“¬≈‘¡Ë ‡≈◊Õ¥‰¥â ¡’ half life Õ¬Ÿà 2 ™à«ß §◊Õ 16 ·≈– 83 π“∑’ Õ“°“√¢â“ß‡§’¬ß¢Õß ¬“∑’Ëæ∫‰¥â¡’·æâ¬“ æ∫√âÕ¬≈– 1.7-1.8, serum sickness, leukocytoclastic vasculitis ·≈– delayed hypersensivity 5.2 Urokinase (UK) ‡ªìπ direct activator ∑’Ë ‰¡àµÕâ ß°—∫ °≈ÿ¡à °—∫ “√µ—«Õ◊πË °àÕπÕÕ°ƒ∑∏‘¬Ï Õà ¬ ≈“¬‰ø∫√‘π ‡ªìπ trypsin-like serine protease ∑’Ë °—¥®“°ªí “«–¡πÿ…¬åÀ√◊Õ‡´≈≈å ‰µ¢Õß ‡ÕÁ¡‰∫√‚Õ ¡’§≥ ÿ ¡∫—µ‘ nonantigenic ·≈– nonpyrogenic „Àâ §√—ßÈ ·√°„πª√‘¡“≥ Ÿß‡™àπ‡¥’¬«°—π°—∫ SK ®–‡°“–°—∫‰ø∫√‘ππâÕ¬ ¡“° ‰¡à‡ª≈’¬Ë π·ª≈ß§ÿ≥ ¡∫—µ¢‘ Õß circulating plasminogen ·≈– fibrin- bound plasminogen UK ®–°√–µÿπâ ·≈–·¬° ≈“¬ plasminogen ‚¥¬«‘∏°’ “√ proteolysis „Àâ∑“ßÀ≈Õ¥‡≈◊Õ¥¥”®–ºà“πµ—∫ ¡’ half-life 14 π“∑’ UK ¡’ªØ‘°√‘ ¬‘ “µàÕ‚ª√µ’πµà“ß Ê ‡™àπ‡¥’¬«°—π°—∫ fibrinogen ∑”„Àâ‡°‘¥ fibrinolytic response πâÕ¬°«à“ SK ‚¥¬∑’Ë¡’º≈ endogenous lytic activity „°≈â‡§’¬ß°—π ¿“«– ·∑√°´âÕπ®“°°“√µ°‡≈◊Õ¥πâÕ¬°«à“ SK ‡π◊ÕË ß®“°∑”„Àâª√‘¡“≥¢Õß plasminogen ≈¥≈ß

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥ 5.3 Tissue Plasminogen Activator (tPA) ‡ªìπ serine protease ∑’Ëæ∫‰¥â∑—Ë«‰ª„π‡π◊ÈÕ‡¬◊ËÕ™π‘¥µà“ß Ê ¡’§ÿ≥ ¡∫—µ‘µ“¡ ∏√√¡™“µ‘‡À¡◊Õπ°—∫ plasminogen activator ∑’ºË ≈‘µ®“°‡ÕÁπ‚¥ ∑’‡≈’Ë¬¡¢ÕßÀ≈Õ¥‡≈◊Õ¥ ∂â“‰¡à¡’‰ø∫√‘π tPA ®–‡ªìπ‡ÕÁπ´—¬¡å∑’Ë¡’ ƒ∑∏‘πÏ Õâ ¬ tPA ‡°“–°—∫ plasminogen ¥’¡“°„π¿“«–∑’¡Ë ‰’ ø∫√‘π ®–¬àÕ¬ ≈“¬‰ø∫√‘π„Àâ°≈“¬‡ªìπ plasmin ‚¥¬∑’Ë plasmin ∑’Ë ‡§≈◊Õ∫æ∫‰ø∫√‘π®–°√–µÿπâ °“√¬àÕ¬ ≈“¬ thrombus §ÿ≥ ¡∫—µ‘ ∑’¥Ë ¢’ Õß tPA §◊Õ®–‰¡à®∫— °—∫ circulating plasminogen ®–‰¡à‡°‘¥ plasminogen ·≈– plasmin „π°√–· ‚≈À‘µ∑”„Àâ‡°‘¥¿“«– ·∑√°´âÕπ®“°°“√µ°‡≈◊Õ¥≈¥≈ß (‰¡à¡’ systemic lytic state) tPA §âπæ∫„πªï 1940 ·≈– “¡“√∂ °—¥‰¥â®π∫√‘ ÿ∑∏‘Ï®“°‡π◊ÈÕ‡¬◊ËÕ ¡¥≈Ÿ°·≈– Bowes melanoma cell lines „πªï 1980 ¡’ƒ∑∏‘‡Ï ªìπ direct plasminogen activators ·≈–‡ªìπ fibrin selective agent(34) 5.4 ¬“ ≈“¬≈‘¡Ë ‡≈◊Õ¥ ∑’°Ë ”≈—ßÕ¬Ÿà„π√–¬–§âπ§«â“∑¥≈Õß ·≈– ®–π”¡“„™âµÕà ‰ª„πÕπ“§µ ‡™àπ Acylated Streptokinase Plasminogen Complex (APSAC), Plasmin B-chain Streptokinase Complex, Pro-Urokinase ·≈–«‘∏°’ “√ Immunofibrinolysis

¬“∑’Ë„ ™â „π‚√§À≈Õ¥‡≈◊Õ¥

‡Õ° “√Õâ“ßÕ‘ß 1. OûBrien Jr. Effects of salicylates on human platelets. Lancet 1968;1:779. 2. Turpie AGG. Antiplatelet therapy. Clin Hematol 1981;10:497. 3. Mustard JF, Kinlough-Rathbone RL, Packham MA. Aspirin in the treatment of cardiovascular disease: A review. Am J Med 1983;74:43. 4. Lewis HD Jr, Davies JW, Archibald DG, et al. Protective effects of aspirin against acute myocardial infarction and death in men with unstable angina. N Engl J Med 1983;309:396. 5. Chesebro JH, Fuster V, Elvback LR, et al. Effects on dipyridamole and aspirin on late vein graft patency after coronary bypass operation. N Engl J Med 1984;310:209. 6. Kohler TR, Kaufman JL, Kacoyanis G, et al. Effects of aspirin and dipyridamole on expanded PTFE graft patency. Surgery 1982;92:1016. 7. Brun JJ. The mechanism of action of ticlopidine. Thromb Res Suppl 1983;4:59. 8. Gent M, Blakeley JA, Easton JD, et al. The Canadian American Ticlopidine Study (CATS) in Thromboembolic stroke. Lancet 1989;1:1215. 9. Arcan JC, Blanchard J, Boissel JP, et al. Multicenter double blind study of Ticlopidine in the treatment of intermittent claudication and the prevention of its complications. Angiology 1988;39:802. 10. Collins GJ, Bergentz SV. Dextrans. In: Collin G (ed). Vascular Occlusive Disorders: Medical and Surgical management. Mt Kisco, NY, Futura Publ 1981;393-420. 11. Carin G, Modig J, Saldeen T. Effect of infusion of dextran 70 on fibrinolysis inhibition activity in human serum. Acta Clin Scand 1979;145:129. 12. Moncrief JA, Darin JC, Canizaro PC, et al. Use of dextran to prevent arterial and venous thrombosis. Am Surg 1963;158:533. 13. Rothermed JE, Wessinger JB, Stitchfield FE. Dextran 40 and thromboembolism in total hip replacement surgery. Arch Surg 1973;106:135. 14. Bergentz SE, Eikon O, Gelin LE. Rheomacrodex in vascular surgery. J Cardiovasc Surg 1963;4:388. 15. Rutherford RB, Jones DN, Bergentz SE, et al. The efficiency of dextran 40 in preventing early postoperative thrombosis following difficult lower extremity bypass. J Vasc Surg 1984;1:165. 16. Ring J, Messmer K. Incidence and severity of anaphylactoid reactions to colloid volume substitutes. Lancet 1977;1:466. 17. Gruber UF, Saldeen T, Brokop T, et al. Incidences of fatal postoperative pulmonary embolism after prophylaxis with dextran 70 and low dose heparin: An international multicenter study. Br Med J 1980;1:69.

18. Thomas JM, Silva J. Dextran 40 in the treatment of peripheral vascular disease. Arch Surg 1973;106:138. 19. Nussbaum M, Boschos C. Anticoagulants and anticoagulation. Med Clin North am 1976;60:855. 20. Kappenhagen K, Adolf J, Mattress M. Low molecular weight heparin and prevention of postoperative thrombosis in abdominal surgery. Thromb Hae most 1992;67:627. 21. Cole CW, Bormanis J. Ancord: A practical alternative to heparin. J Vasc Surg 1988;8:59. 22. Pitney WR, Bray C, Holt P, et al. Acquired resistance to ancord. Lancet 1969;1:79. 23. Stergachis A, Sheingold S, Luce BR, et al. Medical care and cost outcomes after Pentoxifylline treatment for peripheral arterial disease. Arch Intern Med 1992;152:1220. 24. Bahl JJ, Bresler RD. The Pharmacology of carnitine. Ann Rev Pharmacol Toxicol 1987;27:257. 25. Burns JG, Galloway DJ, Ledingham IM. Effect of naftidrofuryl on the metabolic response of surgery. Br Med J 1981;7:283. 26. Clyne CAC, Gallard RB, Fox MJ, et al. A controlled trial of naftidofuryl in the treatment of intermittent claudication. Br J Surg 1980;67:347. 27. Greenhalgh RM. Naftidofurly for ischemic rest pain: A controlled trial. Br J Surg 1981;68:265. 28. Waters KJ, Crawford AD, Chamberlain J. The effect of naftidofuryl (Praxilene) on intermittent claudication. Br J Surg 1980;67:349. 29. Bell W, Meck A. Guidelines for the use of thrombolytic agents. N Engl J Med 1979;301:1266. 30. Marder VJ, Sherry S. Thrombolytic therapy: Current status. N Engl J Med 1988;318:1512. 31. Towne JB, Bandyk DF. Application of thrombolytic therapy in vascular occlusive disease: A surgical view. Am J Surg 1987;154:548. 32. McNamara TO, Bomberger RA, Merchant RF. Intra-arterial urokinase as an initial therapy for acutely ischemic lower limbs. Circulation 1991;83: (suppl):1106. 33. Graor RA, Risuus B, Geisinger MA, et al. Thrombolysis with recombinant human tissue plasminogen activity in patients with peripheral artery and bypass graft occlusion. Circulation 1986;74: (suppl .1):1-15.

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥

∫∑∑’Ë 5 ANTIBIOTICS IN VASCULAR SURGERY °“√µ‘ ¥ ‡™◊È Õ ¢ÕßÀ≈Õ¥‡≈◊ Õ ¥‡∑’ ¬ ¡À√◊ Õ ∑’Ë ‡ °‘ ¥ ¢÷È π °— ∫ À≈Õ¥ ‡≈◊Õ¥‚¥¬µ√ß ‡ªìπ¿“«–·∑√°´âÕπ∑’æË ∫‰¥â ‰¡à∫Õà ¬ ·µà‡¡◊ÕË ‡°‘¥¢÷πÈ ·≈â«Õ“°“√¡—°®–√ÿπ·√ß≈ÿ°≈“¡‰ª∂÷ß°“√µ‘¥‡™◊ÕÈ ¿“¬„π°√–· ‡≈◊Õ¥ Õ“®®–µâÕßµ—¥·¢π¢“∑‘ÈßÀ√◊ÕºŸâªÉ«¬Õ“®®–∂÷ß·°à°√√¡‰¥â ‘Èπ ‡ª≈◊Õß¬“∑’Ë „™â√—°…“·≈–µâÕßºà“µ—¥À≈“¬§√—Èß °“√ªÑÕß°—π‰¡à „Àâ¡’ °“√µ‘¥‡™◊ÈÕπ—∫«à“‡ªìπ«‘∏’∑’Ë¥’∑’Ë ÿ¥ ¥’°«à“ª≈àÕ¬„Àâ¡’°“√µ‘¥‡™◊ÈÕ·≈â« √—°…“¿“¬À≈—ß

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‡™◊ÈÕ∑’Ë¥’‡≈‘» ‚¥¬∑—Ë«‰ª·≈â«‚Õ°“ ∑’ËºŸâªÉ«¬®–µ‘¥‡™◊ÈÕ¢÷ÈπÕ¬Ÿà°—∫ƒ∑∏‘Ï ¢Õß·∫§∑’‡√’¬·≈–§«“¡µâ“π∑“π‚√§¢ÕßºŸâªÉ«¬ ºŸâªÉ«¬Õ“®®–¡’ systemic underlying disease Õ¬Ÿà°àÕπ·≈â« ‡™àπ ‡∫“À«“π ‚√§À—«„® œ≈œ °“√ºà“µ—¥„ àÕ«—¬«–‡∑’¬¡‚¥¬‡©æ“–À≈Õ¥‡≈◊Õ¥‡∑’¬¡ ®–∑”„ÀâÕ—µ√“‡ ’Ë¬ßµàÕ°“√µ‘¥‡™◊ÈÕ Staph.aureus ‡æ‘Ë¡¡“°¢÷Èπ ·¢π¢“´÷ßË ‡ªìπ‚√§¢“¥‡≈◊Õ¥‡√◊ÕÈ √—ß‡¡◊ÕË ‰¥â√∫— °“√ºà“µ—¥∑’Ë„™â‡«≈“π“π ¡’°“√‡ ’¬‡≈◊Õ¥¡“° §«“¡µâ“π∑“π‚√§¢Õß√à“ß°“¬®–≈¥≈ß ∑”„Àâ¡’‚Õ°“ µ‘¥‡™◊ÕÈ ‰¥âß“à ¬¢÷πÈ

À≈—°°“√ªÑÕß°—π ∑“ß»—≈¬°√√¡·∫àß·º≈ºà“µ—¥ÕÕ°‡ªìπ 4 °≈ÿ¡à µ“¡Õ—µ√“‡ ’¬Ë ß µàÕ°“√µ‘¥‡™◊ÕÈ ‰¥â¥ß— π’(3)È 1. ·º≈ –Õ“¥ (clean wound) 2. ·º≈ –Õ“¥ªπ‡ªóÕô π (clean contaminated wound) ‡™àπ °“√ºà“µ—¥‡¢â“∂÷ßÕ«—¬«–¿“¬„π™àÕß∑âÕß √–∫∫ªí “«– √–∫∫À“¬„® 3. ·º≈ªπ‡ªóôÕπ (contaminated wound) ‡™àπ °“√ ºà“µ—¥·≈â«¡’°“√√—Ë«‰À≈ÕÕ°¡“¢ÕßÕÿ®®“√–®“°≈”‰ â ‡≈Á°πâÕ¬ 4. ·º≈‡°à“·º≈ °ª√° (dirty wound) ¡’°“√·µ°∑–≈ÿ ¢ÕßÕ«—¬«–¿“¬„π ·º≈µ‘¥‡™◊ÕÈ

54 ·º≈ –Õ“¥ ‚Õ°“ µ‘¥‡™◊ÈÕ¡’‰¥â√âÕ¬≈– 1.8 ·µà∂â“‡ªìπ·º≈ –Õ“¥„π°“√ºà“µ—¥À≈Õ¥‡≈◊Õ¥Õ—µ√“µ‘¥‡™◊ÕÈ Ÿß∂÷ß√âÕ¬≈– 37(4) °“√„Àâ ¬ “ªØ‘ ™’ « π–ªÑ Õ ß°— π °“√µ‘ ¥ ‡™◊È Õ ®–‰¥â º ≈¥’ · ≈–≈¥ Õ—µ√“°“√µ‘¥‡™◊ÕÈ „π·º≈ –Õ“¥ ·º≈ –Õ“¥ªπ‡ªóÕô π·≈–·º≈ªπ ‡ªóôÕπ ”À√—∫·º≈ °ª√°‰¡à®”‡ªìπµâÕß„Àâ¬“ªØ‘™’«π–ªÑÕß°—π §«√„Àâ‡ªìπ°“√√—°…“°“√µ‘¥‡™◊ÈÕ‰ª‡≈¬(1,5) ®–‰¡àæ‘®“√≥“„Àâ¬“ ªØ‘™’«π–ªÑÕß°—π„π°“√ºà“µ—¥∑“ßÀ≈Õ¥‡≈◊Õ¥∑’Ë‡ªìπ·º≈ –Õ“¥ ∂â“‡∑§π‘§ª√“»®“°‡™◊ÈÕ¥’‡≈‘» ¬°‡«âπ„πºŸâªÉ«¬∑’ËµâÕßºà“µ—¥„ à À≈Õ¥‡≈◊Õ¥‡∑’¬¡ ‡ª≈’¬Ë πÕ«—¬«–·≈–„ à≈π‘È À—«„®‡∑’¬¡(6,7) ºŸâªÉ«¬∑’Ë®—¥«à“‡ ’Ë¬ßµàÕ°“√µ‘¥‡™◊ÈÕ·≈–§«√√–«—ß‡¡◊ËÕ®–µâÕß ºà“µ—¥¡’¥ß— µàÕ‰ªπ’È (8,9,10) 1. ¡’°“√ºà“µ—¥™àÕß∑âÕß 2. °“√ºà“µ—¥„™â‡«≈“π“π°«à“ 2 ™—«Ë ‚¡ß 3. ‡ªìπ°“√ºà“µ—¥∑’∑Ë ”„Àâ‡°‘¥·º≈ªπ‡ªóÕô π À√◊Õ·º≈ °ª√° µ‘¥‡™◊ÕÈ 4. ‡ªìπÀ≈“¬‚√§À√◊Õ¡’ underlying systemic disease Õ¬Ÿà °àÕπºà“µ—¥ºŸªâ «É ¬ elective §«√°”®—¥µâπµÕ¢Õß°“√µ‘¥‡™◊ÕÈ µ“¡º‘«Àπ—ß‰¡à«“à ®–‡ªìπ folliculitis À√◊Õ furuncles §«√√—°…“ „ÀâÀ“¬ ·º≈Õ—°‡ ∫µ‘¥‡™◊ÈÕÀ√◊Õ cellulitis ¢Õß¢“∑’Ë¢“¥‡≈◊Õ¥ §«√§«∫§ÿ¡√—°…“°“√µ‘¥‡™◊ÈÕ‰¡à „Àâ≈ÿ°≈“¡°àÕπºà“µ—¥„ àÀ≈Õ¥ ‡≈◊Õ¥‡∑’¬¡(11) °“√‡≈◊Õ°¬“ªØ‘™«’ π–∑’Ë „Àâ§«√‡≈◊Õ°„™â¬“∑’ÕË Õ°ƒ∑∏‘Ï ‡©æ“–‡™◊ÕÈ ·∫§∑’‡√’¬∑’§Ë “¥«à“®–∑”„Àâ‡°‘¥°“√Õ—°‡ ∫µ‘¥‡™◊ÕÈ ¡’ toxicity πâÕ¬ ¢âÕ ”§—≠§◊Õ¡’°“√ÕÕ°ƒ∑∏‘Ï·§∫‡©æ“– (narrowed spectrum) ‰¡à¡’§«“¡®”‡ªìπ∑’Ë®–µâÕß„™â¬“ªØ‘™’«π–∑’ËÕÕ°ƒ∑∏‘Ï §≈ÿ¡°«â“ß (broad spectrum) °“√µ‘¥‡™◊ÕÈ ¢ÕßÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡ ¡—°®–‡°‘¥®“°‡™◊ÈÕ Staph.aureus ·≈– Staph.epidermidis °Á „™â¬“ªØ‘™«’ π–∑’ÕË Õ°ƒ∑∏‘Ï‚¥¬µ√ßµàÕ‡™◊ÕÈ ‡À≈à“π’È (11,12) §«√„™â¬“‡¢â“ ‡¢â“∑“ßÀ≈Õ¥‡≈◊Õ¥®–∑”≈“¬‡™◊ÕÈ ‰¥â¥∑’ ’Ë ¥ÿ

‡™◊ÈÕ·∫§∑’‡√’¬ ‡™◊È Õ ∑’Ë ¡’ ∫ ∑∫“∑ ”§— ≠ ·≈–æ∫‰¥â ∫à Õ ¬µà Õ °“√µ‘ ¥ ‡™◊È Õ ¢Õß À≈Õ¥‡≈◊Õ¥‡∑’¬¡§◊Õ taph.aureus, Staph. epidermidis ·≈– E.coli ∑’æË ∫‰¥â√Õß≈ß¡“§◊Õ Proteus ·≈– Pseudomonas √âÕ¬≈– 33 ‡ªìπ°“√µ‘¥‡™◊ÕÈ √à«¡√–À«à“ß Steph.aureus, Staph. epidermidis ·≈– E.coli(2,12) „πªí®®ÿ∫—πæ∫«à“°“√µ‘¥‡™◊ÈÕ®“° Staph. epidermidis ®–§àÕ¬‡ªìπ§àÕ¬‰ª„™â√–¬–‡«≈“π“π®÷ß®–· ¥ßÕ“°“√ ‡æ“–‡™◊ÈÕ‰¥â¬“°‡æ√“– √â“ß‡¡◊Õ°ÀàÕÀÿâ¡µ—«‰«â ®–‡æ“–‡™◊ÈÕ‰¥âµâÕß µ—¥‡Õ“ à«π¢ÕßÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡ÕÕ°¡“·¬°‡™◊ÈÕ √âÕ¬≈– 75

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥ ¢Õß°“√µ‘ ¥ ‡™◊È Õ ¢ÕßÀ≈Õ¥‡≈◊ Õ ¥‡∑’ ¬ ¡‡°‘ ¥ ®“°°“√µ‘ ¥ ‡™◊È Õ ∑’Ë º‘«Àπ—ß∫√‘‡«≥∑’Ë¡’§«“¡™◊Èπ Ÿß‡™àπ ¢“Àπ’∫ °âπ·≈–√—°·√â ¡’ ‚Õ°“ µ‘ ¥ ‡™◊È Õ ‰¥â Ÿ ß ¡“° «‘ ∏’ ≈ ¥Õ— µ √“°“√µ‘ ¥ ‡™◊È Õ ∑’Ë ‰ ¥â º ≈§◊ Õ ∑”§«“¡ –Õ“¥º‘«Àπ—ß·≈–øÕ°¶à“‡™◊ÕÈ ¥â«¬πÈ”¬“ Povidone iodine §≈ÿ¡º‘«Àπ—ß∫√‘‡«≥∑’®Ë –ºà“µ—¥¥â«¬ Steri-drape(11) ∂â“¡’°“√Õ—°‡ ∫ µ‘¥‡™◊ÕÈ ¢ÕßµàÕ¡πÈ”‡À≈◊Õß∫√‘‡«≥¢“Àπ’∫√à«¡°—∫°“√‡πà“µ“¬¢Õß¢“ ®–‡æ‘¡Ë Õ—µ√“°“√µ‘¥‡™◊ÕÈ „Àâ ßŸ ¢÷πÈ

ª√– ‘∑∏‘¿“æ¢Õß°“√„Àâ¬“ªØ‘™’«π–ªÑÕß°—π §«√„Àâ¬“ªØ‘™’«π–ªÑÕß°—π∑“ßÀ≈Õ¥‡≈◊Õ¥¥”°àÕπ ‡√‘Ë¡ ≈ß¡’¥ºà“µ—¥ 30 π“∑’Ë ‡æ◊ËÕ∑’Ë§«“¡‡¢â¡¢âπ¢Õß¬“„π‡π◊ÈÕ‡¬◊ËÕ®–‰¥â Ÿß·≈–¡’ª√– ‘∑∏‘¿“æ¥’∑ ’Ë ¥ÿ (1) ∂â“‡ªìπ°“√ºà“µ—¥∑’Ë „™â‡«≈“π“π‡°‘π °«à“ 4 ™—«Ë ‚¡ß §«√„Àâ¬“´È”Õ’°§√—ßÈ Àπ÷ßË (14) °“√ºà“µ—¥∫√‘‡«≥Àπâ“ ·≈–§Õ∂◊Õ«à“‡ªìπ∫√‘‡«≥∑’Ë –Õ“¥ ‰¡àµâÕß„Àâ¬“ªØ‘™’«π–ªÑÕß°—π πÕ°®“°¡’§«“¡®”‡ªìπ∑’Ë®–µâÕß„ àÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡ ¬“ªØ‘™’«π– ∑’§Ë «√‡≈◊Õ°„™â§Õ◊ Cefazolin ºŸªâ «É ¬‰µ«“¬‡√◊ÕÈ √—ß∑’®Ë –µâÕßºà“µ—¥∑” vascular access ”À√—∫øÕ°‡≈◊Õ¥ ‚Õ°“ ∑’®Ë –µ‘¥‡™◊ÕÈ Staph. epidermidis ¡’‰¥â ßŸ §«√„Àâ¬“ Cefamandol(15) À≈—ßºà“µ—¥§«√ „Àâ¬“ªØ‘™«’ π–∑“ßÀ≈Õ¥‡≈◊Õ¥¥”Õ’°∑ÿ° 6 ™—«Ë ‚¡ß 3 §√—ßÈ ®π§√∫ 24 ™—Ë«‚¡ß ∂â“‡ ’Ë¬ßµàÕ°“√µ‘¥‡™◊ÈÕ Ÿß§«√„Àâ¬“µàÕÕ’° 3-5 «—π °“√„™â¬“ªØ‘™’«π–º ¡°—∫πÈ”‡°≈◊Õ ¡¥ÿ≈¬å‡™àπ Cepharadine, Kanamycin °—∫ Cephalothin ™–≈â“ß¢≥–ºà“µ—¥À≈Õ¥‡≈◊Õ¥ (topical antibiotics) æ∫«à“ “¡“√∂≈¥Õ—µ√“°“√µ‘¥‡™◊ÈÕ¢Õß·º≈ ºà“µ—¥≈ß‰¥â¡“°(16,17,18)

°“√‡≈◊Õ°„™â¬“ªØ‘™’«π– æ∫«à“°“√µ‘¥‡™◊ÈÕ¢ÕßÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡ à«π„À≠à‡°‘¥®“°‡™◊ÈÕ Staph.aureus, Staph. epidermidis ·≈– E. coli ¬“ªØ‘™«’ π– ∑’Ë‡≈◊Õ°„™â§«√‡ªìπ°≈ÿà¡ Cephalosporin ‡æ√“–®–ÕÕ°ƒ∑∏‘Ï§≈ÿ¡ ‡™◊ÕÈ ‡À≈à“π’È ‰¥âÀ¡¥(19) (µ“√“ß∑’Ë 5.1) Cefazolin ‡ªìπ 1st generation Cephalosporin ¡’ƒ∑∏‘¶Ï “à ‡™◊ÕÈ ·∫§∑’‡√’¬„°≈â‡§’¬ß°—∫ Cephalothin ·µà¡’ half life π“π°«à“ ·≈–§«“¡‡¢â¡¢âπ„π´’√¡—Ë Ÿß°«à“ À≈—ßºà“µ—¥§«√„Àâ Cefazolin µàÕ Õ’° 24 ™—«Ë ‚¡ß ‡ªìπ°“√§√∫°√–∫«π°“√·≈–¢—πÈ µÕπ¢Õß°“√„Àâ ¬“ªØ‘™«’ π–ªÑÕß°—π(14,15) ∂â“‡ªìπ°“√ºà“µ—¥∑’Ë „™â√–¬–‡«≈“π“π°«à“ 4 ™—«Ë ‚¡ß §«√„Àâ¬“Õ’° 1 §√—ßÈ ‡æ◊ÕË „Àâ§«“¡‡¢â¡¢âπ¢Õß¬“„π√–¥—∫ ∑’¡Ë ª’ √– ‘∑∏‘¿“æ ªÑÕß°—π°“√µ‘¥‡™◊ÕÈ (13,15)

ANTIBIOTICS IN VASCULAR SURGERY

µ“√“ß∑’Ë 5.1 °“√‡≈◊Õ°„™â¬“ªØ‘™«’ π– °“√ºà“µ—¥

‡™◊ÕÈ ·∫§∑’‡√’¬

¬“ªØ‘™«’ π–∑’§Ë «√„™â

ºà“µ—¥À≈Õ¥‡≈◊Õ¥ aorta ·≈– À≈Õ¥‡≈◊Õ¥·¥ß∫√‘‡«≥¢“Àπ’∫ ‚¥¬„™âÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡ °“√µ—¥¢“∑’¢Ë “¥‡≈◊Õ¥·≈–‡πà“µ“¬

S.aureus, S. epidermidis enteric, gram-negative bacilli

Cefazolin

S.aureus, S.epidermidis, enteric, gram-negative bacilli,anaerobes

Cefoxitin

∂â“ ß —¬«à“¡’°“√µ‘¥‡™◊ÕÈ Staph. epidermidis ´÷ßË Cephalosporin §√Õ∫§≈ÿ¡‰¥â ‰¡à∑«—Ë ∂÷ß §«√„Àâ Vancomycin √à«¡¥â«¬ ¢≥–ºà“µ—¥ À√◊Õ„π ∂“π°“√≥å∑’Ëæ∫«à“¡’ ‚Õ°“ µ‘¥‡™◊ÈÕ Staph. aureus ∑’µË “â πµàÕ Methicillin §«√‡ª≈’¬Ë π¡“„™â Cefamandol À√◊Õ Vancomycin ·∑π(20)

√ÿª §«√„Àâ¬“ªØ‘™«’ π–ªÑÕß°—π „π°“√ºà“µ—¥À≈Õ¥‡≈◊Õ¥¥—ßµàÕ‰ªπ’È §◊ Õ °“√ºà “ µ— ¥ aorta ·≈–∫√‘ ‡ «≥¢“ ‰¡à ®”‡ªì π µâ Õ ß„Àâ ¬ “ ªØ‘™’«π–ªÑÕß°—π ∂â“‡ªìπ°“√ºà“µ—¥∫√‘‡«≥§Õ·≈–·¢π πÕ°®“° µâÕß„ àÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡ Cefezolin ‡ªìπ¬“∑’‡Ë ≈◊Õ°„™âµ«— ·√°‡ ¡Õ „Àâ „π¢π“¥ 1 °√—¡ ∑“ßÀ≈Õ¥‡≈◊Õ¥¥” 30 π“∑’°Õà π≈ß¡’¥ºà“µ—¥ ∂â“°“√ºà“µ—¥„™â‡«≈“π“π°«à“ 1 ™—Ë«‚¡ß„Àâ¬“‰¥âÕ’° 1 °√—¡ À≈—ß®“°π—Èπ„ÀâÕ’°∑ÿ° 6 ™—Ë«‚¡ß 3 §√—Èß ®π§√∫ 24 ™—Ë«‚¡ß ®π°√–∑—ßË ‡Õ“ “¬ arterial line, “¬ «πªí “«–·≈– endotracheal tube ÕÕ°·≈â« ¢≥–ºà“µ—¥§«√™–≈â“ß·º≈¥â«¬πÈ”‡°≈◊Õ ¡¥ÿ≈¬åº ¡°—∫¬“ªØ‘™’«π– ∂â“‡ªìπ°“√ºà“µ—¥∑’Ë‡ªìπ·º≈ªπ‡ªóôÕπ §«√„ÀâºªŸâ «É ¬√—∫ª√–∑“π¬“ªØ‘™«’ π– 5-7 «—π ºŸªâ «É ¬∑’¡Ë À’ ≈Õ¥‡≈◊Õ¥‡∑’¬¡ΩíßÕ¬Ÿà „π√à“ß°“¬ °“√∑”À—µ∂°“√ µà“ß Ê ‡™àπ °“√∂Õπøíπ «π§“ “¬ªí “«– àÕß°≈âÕß√–∫∫ À“¬„®·≈–∑“ß‡¥‘πÕ“À“√§«√„Àâ¬“ªØ‘™’«π–ªÑÕß°—π 24 ™—Ë«‚¡ß °àÕπ·≈–À≈—ßÀ—µ∂°“√

°“√√—°…“ PRIMARY VASCULAR INFECTIONS °“√µ‘¥‡™◊ÕÈ ª∞¡¿Ÿ¡‘ (primary) ∑’‡Ë °‘¥¢÷πÈ °—∫À≈Õ¥‡≈◊Õ¥æ∫πâÕ¬ ·µàÕµ— √“µ“¬ Ÿß¡“° ‡√“·∫àßµ“¡°“√√—°…“ÕÕ°‰¥â‡ªìπ 1. mycotic aneurysm 2. syphilitic aortitis 3. spontaneous aortoenteric fistulas ∂â“·∫àßµ“¡≈—°…≥–¢Õß°“√µ‘¥‡™◊ÕÈ ®–·∫àßÕÕ°‰¥â‡ªìπ 1. primary infection ‡™àπ microbial arteritis ·≈– traumatic aneurysm 2. secondary infection ‡™àπ infected aneurysm °“√√—°…“°“√µ‘¥‡™◊ÕÈ ª∞¡¿Ÿ¡∑‘ ‡’Ë °‘¥¢÷πÈ °—∫À≈Õ¥‡≈◊Õ¥°“√„Àâ¬“ ªØ‘™«’ π–·≈–°“√ºà“µ—¥‡ªìπÀ≈—° ”§—≠(20) √Ÿª·∫∫°“√‡°‘¥ mycotic aneurysm ·∫àßÕÕ°‰¥â‡ªìπ 1. ‡°‘¥®“° septic emboli ¢Õß cardiac vegetative „π endocarditis À≈ÿ¥¡“‡°“–°—∫ºπ—ßÀ≈Õ¥‡≈◊Õ¥ 2. ‡°‘¥®“°°“√µ‘¥‡™◊ÈÕ¢Õß atherosclerotic aneurysm µ√ß∑’ºË π—ßÕàÕπ∫“ßÀ√◊Õ©’°¢“¥„π™à«ß∑’√Ë “à ß°“¬Õ¬Ÿà „π¿“«– bacteremia 3. ‡°‘¥¿“¬À≈—ß°“√∫“¥‡®Á∫®“°«— ¥ÿ·À≈¡¡’§¡ ∑’Ë¡’°“√ ªπ‡ªóÕô π·∑ß∑–≈ÿÀ≈Õ¥‡≈◊Õ¥ 4. ‡°‘¥®“°µ”·ÀπàßÕ◊πË ¢Õß√à“ß°“¬∑’¡Ë °’ “√µ‘¥‡™◊ÕÈ Õ¬Ÿ·à ≈â«‡™àπ osteomyelitis, µàÕ¡πÈ”‡À≈◊ÕßÕ—°‡ ∫µ‘¥‡™◊ÈÕ, ‚æ√ß ÀπÕß®“°°“√©’¥¬“‡ æµ‘¥ ‡¡◊ÕË ‡°‘¥ mycotic aneurysm ·≈â« ºπ—ßÀ≈Õ¥‡≈◊Õ¥®–∫“ß ≈ß‡√◊ÕË ¬ Ê ·≈–·µ°ÕÕ°„π∑’ Ë ¥ÿ

56 syphilitic aneurysm, tuberculous aneurysm ·≈– true fungal aneurysm ‡ªìπ√Ÿª·∫∫¢ÕßÀ≈Õ¥‡≈◊Õ¥‚ªÉßæÕßµ‘¥‡™◊ÈÕ ´÷ßË æ∫‰¥â ‰¡à∫Õà ¬ °“√µ‘¥‡™◊ÕÈ øíß°— æ∫„πºŸªâ «É ¬∑’¡Ë ¿’ ¡Ÿ §‘ ¡ÿâ °—π∫°æ√àÕß ‡∫“À«“π ºŸªâ «É ¬∑’√Ë ∫— ª√–∑“π¬“°¥¿Ÿ¡§‘ ¡ÿâ °—π ‡™◊ÕÈ ∑’æË ∫‡™àπ Histoplasma capsulatum, Aspergillus fumigatus, Candida albicans ·≈– Penicillium species spontaneous aorta-enteric fistula æ∫‰¥âπÕâ ¬°«à“ graft enteric fistula ‡°‘¥®“° AAA ∑’Ë ‰¡à ‰¥â√—°…“·≈â«¡’°“√∑–≈ÿ√—Ë« ‡¢â“ Ÿà≈”‰ â‡≈Á° ¥Ÿ‚Õ¥’π—Ë¡ ·≈–≈”‰ â „À≠à Õ“°“√‡√‘Ë¡µâπ§◊Õ¡’°“√ µ°‡≈◊Õ¥„π∑“ß‡¥‘πÕ“À“√‡≈Á°πâÕ¬‡π◊ËÕß®“°√Ÿ∑–≈ÿ¬—ß‰¡à°«â“ß ¡’ ≈‘Ë¡‡≈◊Õ¥Õÿ¥‡≈◊Õ¥®÷ßÀ¬ÿ¥‰À≈ µàÕ¡“®–¡’°“√µ°‡≈◊Õ¥´È”ª√‘¡“≥ ¡“°®π™ÁÕ§ §«√ ß —¬„πºŸâªÉ«¬∑’Ë¡’‡≈◊Õ¥ÕÕ°∑“ß‡¥‘πÕ“À“√ ª√‘¡“≥¡“°·≈–§≈”°âÕπ‡µâπ‰¥â∑À’Ë πâ“∑âÕß ∫√‘‡«≥∑’æË ∫ mycotic aneurysm ‰¥â∫Õà ¬§◊Õ aorta À≈Õ¥‡≈◊Õ¥·¥ß femoral mesenteric ·≈–À≈Õ¥‡≈◊Õ¥¢π“¥‡≈Á°∑’Ë·¢π·≈–¢“ ‡™◊ÈÕ·∫§∑’‡√’¬∑’Ë ‡ªìπ “‡Àµÿ§◊Õ Staph.aureus, Salmonella, Streptococci, Pseudomonas ·≈– E.coli “‡Àµÿ¢Õß°“√‡°‘¥ mycotic aneurysm §◊Õ®“°∫“¥·º≈·∑ß∑–≈ÿ·≈–°“√∑”À—µ∂°“√ºà“πÀ≈Õ¥ ‡≈◊Õ¥‡™àπ arteriography ·≈â«‡∑§π‘§ª√“»®“°‡™◊ÈÕ‰¡à¥’æÕ ¡’ °“√ªπ‡ªóÕô π Õ“°“√·≈–Õ“°“√· ¥ß§◊Õª«¥∑âÕß (∂â“‡ªìπ∑’Ë aorta) ¡’‰¢â Ÿß leukocytosis ¡’°âÕπ‡µâπ‰¥â∑“ßÀπâ“∑âÕß ‡æ“–‡™◊ÈÕ ·∫§∑’‡√’¬‰¥â®“°‡≈◊Õ¥ ®“° arteriogram ®–æ∫¡’≈—°…≥–‡ªìπ saccular aneurysm ¡’ petecheae °√–®“¬∑—«Ë ‰ª∫√‘‡«≥º‘«Àπ—ß ¢âÕÕ—°‡ ∫µ‘¥‡™◊ÈÕ®“° CT scan æ∫«à“¡’°ä“´Àÿâ¡Õ¬Ÿà√Õ∫ aorta ¢≥–ºà“µ—¥®–æ∫«à“ºπ—ß¢Õß aneurysm ∫“ß¡“° ¡’√àÕß√“¬ ¢Õß°“√Õ—°‡ ∫ µàÕ¡πÈ”‡À≈◊Õß∫√‘‡«≥„°≈â‡§’¬ß‚µ ¬âÕ¡ ’°√—¡æ∫ ‡™◊ÕÈ ·∫§∑’‡√’¬ ´÷ßË ®–‡ªìπ·π«∑“ß„π°“√„Àâ¬“ªØ‘™«’ π–„π∫“ß√“¬ ¬âÕ¡ ’°ç√—¡‰¡àæ∫‡™◊ÕÈ ·∫§∑’‡√’¬·µà‡æ“–‡™◊ÕÈ ®“°‡≈◊Õ¥‰¥â

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À≈—°°“√√—°…“ ‡¡◊ËÕ‡°‘¥ mycotic aneurysm §«√√—°…“‚¥¬°“√„Àâ¬“ ªØ‘™’«π–™π‘¥ÕÕ°ƒ∑∏‘Ï§≈ÿ¡°«â“ß∑“ßÀ≈Õ¥‡≈◊Õ¥¥”„πª√‘¡“≥∑’Ë ŸßÕ¬à“ßµàÕ‡π◊ËÕß·≈–µ—¥‡Õ“À≈Õ¥‡≈◊Õ¥·≈–‡π◊ÈÕ‡¬◊ËÕ à«π∑’Ë¡’°“√ Õ—°‡ ∫µ‘¥‡™◊ÕÈ ÕÕ° §«√∑” extra-anatomical bypass „Àâ‡≈◊Õ¥ ‰ª‡≈’¬È ß·¢π¢“ à«πª≈“¬‚¥¬ºà“π∫√‘‡«≥∑’Ë ‰¡à¡°’ “√Õ—°‡ ∫µ‘¥‡™◊ÕÈ À≈—ßºà“µ—¥„Àâ¬“ªØ‘™«’ π–µàÕÕ’° 6 —ª¥“Àå °“√µ‘¥‡™◊ÕÈ Salmonella µÕ∫ πÕß¥’µÕà °“√√—°…“¥â«¬ Ampicillin ·≈– Chloramphenical ∂â“‡≈“–µ—¥‡Õ“ mycotic aortic aneurysm ÕÕ°‰ª·≈â«‰¡àæ∫ «à“¡’°“√Õ—°‡ ∫µ‘¥‡™◊ÕÈ √ÿπ·√ß À√◊ÕÀπÕß§—ßË Õ¬Ÿ√à Õ∫ aorta, ¬âÕ¡ ’°√—¡‰¡àæ∫‡™◊ÕÈ Õ“®®–„ àÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡µ√ß∫√‘‡«≥π—πÈ ‡≈¬‰¥â (in situ) ·≈–„™â¬“ªØ‘™«’ π– √—∫ª√–∑“πµàÕÕ’° 8 —ª¥“Àå ·µà∂“â ¡’ °“√ªπ‡ªóôÕπÀ√◊ÕÀπÕß§—ËßÕ¬Ÿà¡“° §«√‡¬Á∫ªî¥ aortic stump ·≈–∑” extra-anatomical bypass Õ—µ√“√Õ¥®“°°“√√—°…“ ª√–¡“≥√âÕ¬≈– 12-87

¬“ªØ‘™’«π–∑’Ë„™â√—°…“¿“«–‡π◊ÈÕ‡¬◊ËÕ‡πà“µ“¬ (gangrene) °“√¡’‡π◊ÕÈ ‡¬◊ÕË ∑’‡Ë πà“µ“¬ ‡ªìπªí≠À“ ”§—≠„π°“√√—°…“ ‰¡à«“à ®–°àÕπÀ√◊ÕÀ≈—ßºà“µ—¥ ‡π◊ÈÕ‡¬◊ËÕ‡πà“µ“¬‡ªìπº≈¡“®“°Õ«—¬«–π—Èπ ¡’°“√¢“¥‡≈◊Õ¥‡√◊ÕÈ √—ß À√◊Õ°“√¢“¥‡≈◊Õ¥‡©’¬∫æ≈—π®“°‡ÕÁ¡‚∫‰≈ ∂â“ºŸâªÉ«¬‡ªìπ‚√§‡∫“À«“πÕ¬Ÿà·≈â« ®–¡’ ‚Õ°“ µ‘¥‡™◊ÈÕ≈ÿ°≈“¡‰¥â ßà“¬¢÷πÈ (21) ∂â“‡ªìπ çdry gangreneé ·≈–‰¡à¡°’ “√Õ—°‡ ∫µ‘¥‡™◊ÕÈ ‰¡à®”‡ªìπµâÕß„Àâ¬“ªØ‘™’«π–√Õ„Àâ·π« demarcation ™—¥‡®π ·≈â«®÷ßµ—¥‡Õ“‡π◊ÈÕ‡¬◊ËÕ∑’Ë‡πà“µ“¬ÕÕ° ∂â“‡ªìπ çwet gangreneé ∑’Ë¡’°“√µ‘¥‡™◊ÈÕº ¡‚√ß¿“¬À≈—ß §«√¬âÕ¡ ’°√—¡¥Ÿ‡™◊ÈÕ·∫§∑’‡√’¬ ‡æ“–‡™◊ÈÕ®“°ÀπÕß „Àâ¬“ªØ‘™’«π–™π‘¥ÕÕ°ƒ∑∏‘Ï§≈ÿ¡°«â“ß∑“ß À≈Õ¥‡≈◊ Õ ¥¥” §◊ Õ Cefoxatime, aminoglycoside ·≈– clindamycin À≈—ß®“°π—πÈ µ—¥‡Õ“‡π◊ÕÈ ∑’‡Ë πà“µ“¬ÕÕ°(22)

ANTIBIOTICS IN VASCULAR SURGERY

‡Õ° “√Õâ“ßÕ‘ß 1. Kaiser AB. Antimicrobial prophylaxis in surgery. N Eng J Med 1986;315:1129-1138. 2. Szilagyi DE, Smith RF, Elliott JB. Infection in arterial reconstruction with synthetic grafts. Ann Surg 1972;176:321-333. 3. Burnakis TG. Surgical antimicrobial prophylaxis: Principles and guidelines. Pharmacology 1984;4:248-271. 4. Crause PJE, Foord R. A five year perspective study of 23, 649 surgical wounds. Arch Surg 1973;107:206-210. 5. Antimicrobial prophylaxis in surgery. Med lett Drugs Ther 1989;31:105-111. 6. Kaiser AB, Clayson KR, Mulberin JL, et al. Antibiotic prophylaxis in vascular surgery. Ann Surg 1976;188:283-289. 7. Hasselgren PO, Ivarsson L, Risberg B. Effects of prophylaxis antibiotics in vascular surgery. Ann Surg 1984;200:86-92. 8. Nichols RL. Surgical wound infection. Am J Med 1991;91:54-61. 9. Nichols RL. Postoperative wound infection. N Engl J Med 1982;307:1701-1706. 10. Windser JA, Hill GL. Weight loss with physiologic impairment: Basic indicator of surgical risk. Ann Surg 1988;207:290-297. 11. Buckel JA, Wilson SE. The prevention and management of prosthetic graft infection. In:Wilson SE, ed. Vascular Surgery. Philadelphia, WB Saunders 1987:889-897. 12. Bandyk DF, Berni GA, Thiele BL. Aortofemoral graft infection due to Staphylococcus epidermidis. Arch Surg 1984;119:102-108.

13. Worning AM, Fuimodf-Moller N, Ostri P, et al. Antibiotic prophylaxis in vascular reconstructive surgery. J Antimicrob Chemother 1986:17:105-113. 14. Bennion RS, Hiatt JR, Williams RA. A randomized prospective study of perioperative antimicrobial prophylaxis for vascular surgery. J Cardiovasc Surg 1985;26:270-274. 15. Fracet G, Brister S, Richard GK, et al. Antibiotic prophylaxis in vascular surgery: Pharmacokinetic study of commonly used cephalosporins. J Vasc Surg 1986;3:535-539. 16. Lord JW, Ross G, Daliana M. Intraoperative antibiotic wound lavage. Ann Surg 1977;185:634-638. 17. Pitt HA, Postier PG, McGowan WAC, et al. Prophylactic antibiotics in vascular surgery, topical, systemic or both?. Ann Surg 1980;192:356-364. 18. Matashek KJ, Rosin E. Pharmacokinetics of Cefazolin applied topically to the surgical wound. Arch Surg 1991;126:890. 19. Abramovicz M. Antimicrobial prophylaxis in surgery. Med lett 1987;29:91-94. 20. Wilson SE, Van Wagenen P, Pessaro E. Arterial infection. Curr Prob Surg 1978;15:6-89. 21. Freier J, Daniel D, Davis C. Fetid foot: Lower extremity infections in patients with diabetes mellitus. Rev Infect Dis 1979;1:210-217. 22. Freischlag J, Ajalat G, Busutil RW. Treatment of necrotizing soft tissue infections: The need for a new approach. Am J Surg 1985;149:751-755.

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∫∑∑’Ë 6 NONINVASIVE VASCULAR STUDIES „π∫∑π’®È –°≈à“«∂÷ßÀ≈—°°“√æ◊πÈ ∞“π ªØ‘∫µ— °‘ “√ °“√·ª√º≈ ·≈–·π«∑“ß„π°“√‡≈◊Õ°„™â noninvasive hemodynamic studies ”À√—∫‚√§À≈Õ¥‡≈◊Õ¥·¥ß·≈–À≈Õ¥‡≈◊Õ¥¥” Õ¬à“ß‰√°Áµ“¡ noninvasive tests ®–‰¡à “¡“√∂∑¥·∑π°“√´—°ª√–«—µ‘·≈– µ√«®√à“ß°“¬ºŸâªÉ«¬Õ¬à“ß≈–‡Õ’¬¥∂’Ë∂â«π ‡æ◊ËÕ‡ªìπ·π«∑“ß°“√ «‘π®‘ ©—¬‚√§ „π∫“ß ∂“π°“√≥å À≈—ß®“°∑” noninvasive tests ·≈â« ¢âÕ¡Ÿ≈∫“ßÕ¬à“ß‰¡à‡æ’¬ßæÕ ®–‡ªìπ·π«∑“ßæ‘®“√≥“µ√«® «‘π®‘ ©—¬Õ◊πË ‡æ‘¡Ë ‡µ‘¡ ‡™àπ arteriogram ·≈– venogram °“√µ√«® noninvasive tests ®–∑”„Àâ‡√“∑√“∫∂÷ß √’√«‘∑¬“æ◊πÈ ∞“π¢ÕßºŸâ ªÉ«¬√–∫∫À≈Õ¥‡≈◊Õ¥°àÕπ∑’Ë®–æ‘®“√≥“„Àâ°“√√—°…“∑’Ë‡À¡“– ¡ ·≈–∑√“∫°“√æ¬“°√≥å ‚√§µàÕ‰ª «‘«≤ — π“°“√¢Õß clinical vascular laboratories ‡°‘¥¿“¬À≈—ß arteriogram, À≈Õ¥‡≈◊Õ¥‡∑’¬¡ ·≈–«‘∏°’ “√ºà“µ—¥‡æ◊ÕË √—°…“ peripheral vasscular disease (PVD) „π™à«ß 25 ªï∑’Ëºà“π¡“ noninvasive tests ¡’∑’Ë „™â·æ√àÀ≈“¬„π»Ÿπ¬å°“√·æ∑¬å ‡ªìπ à«π ”§—≠„π°“√™à«¬«‘π‘®©—¬·≈–µ‘¥µ“¡º≈°“√√—°…“ ·≈–πÕ°®“° π’¬È ß— ™à«¬≈¥§«“¡ ‘πÈ ‡ª≈◊Õß„π°“√µ√«®«‘π®‘ ©—¬‚√§‚¥¬‰¡à®”‡ªìπ

VASCULAR LABORATORY ∂“π∑’ªË Ø‘∫µ— °‘ “√§«√Õ¬Ÿà„π∑’‡Ë ß’¬∫ ß∫ª√“»®“°‡ ’¬ß√∫°«π –¥«°µàÕºŸâªÉ«¬πÕ°·≈–ºŸâªÉ«¬„π ªØ‘∫—µ‘°“√‚¥¬‡∑§π’‡™’Ë¬π ·≈–·ª√º≈‚¥¬·æ∑¬å ‡§√◊ÕË ß¡◊Õµ√«®æ◊πÈ ∞“π∑’®Ë –µâÕß¡’§Õ◊ por-

table continuous-wave Doppler unit ‡æ◊ËÕøíß‡ ’¬ß®“° À≈Õ¥‡≈◊ Õ ¥¥”·≈–À≈Õ¥‡≈◊ Õ ¥·¥ß ·æ∑¬å · ≈–æ¬“∫“≈∑’Ë ‡°’Ë¬«¢âÕß„π°“√√—°…“ºŸâªÉ«¬‚√§À≈Õ¥‡≈◊Õ¥®–µâÕß„™â portable Doppler unit ‡ªìπ§ÿ≥ ¡∫—µ‘∑’Ëæ÷ßª√– ß§å¢Õß‡§√◊ËÕß¡◊Õ∑’Ë „™â „π vascular lab §«√ª√–°Õ∫¥â«¬ 1. ¡’§«“¡·πàπÕπ„π°“√«—¥ª√–‡¡‘π·≈–‡™◊ÕË ∂◊Õ‰¥â 2. ‡ªìπ‡§√◊ÕË ß¡◊Õ¡“µ√∞“π 3. ‰¡à ≈—∫´—∫´âÕπ „™âß“π‰¥âß“à ¬ 4. „™â«¥— §à“ª°µ‘‰¥â∑ß—È °àÕπ·≈–À≈—ß exercise 5. ª√—∫„™â ‰¥â°∫— ‡§√◊ÕË ß∫—π∑÷°™π‘¥µà“ß Ê ‡§√◊ËÕß¡◊Õ‡À≈à“π’È‡À¡“– ¡ ”À√—∫‚√§À≈Õ¥‡≈◊Õ¥·¥ß·≈– À≈Õ¥‡≈◊Õ¥¥”∑—«Ë ‰ª 1. continuous-wave bidirectional Doppler system ¢π“¥ 9 mHz ”À√—∫À≈Õ¥‡≈◊Õ¥·¥ß ·≈– 5 mHz ”À√—∫À≈Õ¥‡≈◊Õ¥¥” 2. plethysmography „™âµ√«®À≈Õ¥‡≈◊Õ¥·¥ß·≈–À≈Õ¥ ‡≈◊Õ¥¥” 3. duplex ultrasound ”À√—∫«‘‡§√“–Àå bruit ·≈– imaging 4. treadmill §«“¡‡√Á« 1.5 ∂÷ß 2.5 ‰¡≈åµÕà ™—«Ë ‚¡ß, 10-25% grade 5. transcutaneous oximetry ”À√—∫«—¥·≈–ª√–‡¡‘π cutaneous perfusion

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DOPPLER ULTRASOUND Doppler flow detector ‡ªì π ‡§√◊Ë Õ ß¡◊ Õ ™π‘ ¥ Àπ÷Ë ß ∑’Ë ¡’ ª√– ‘∑∏‘¿“æ„π°“√∫—π∑÷° blood flow ∑”ß“π‚¥¬ çDoppler effecté À√◊Õ°“√‡ª≈’¬Ë π·ª≈ß wave frequency (sound) °≈—∫ ®“°«—µ∂ÿ∑‡’Ë §≈◊ÕË π∑’Ë (reflector) (√Ÿª∑’Ë 6.1) ´÷ßË ∂â“‡§≈◊ÕË π∑’ÕË Õ°‰ª ®“° probe frequency ®–µË”·µà∂“â ‡§≈◊ÕË π∑’‡Ë ¢â“À“ probe frequency ®– Ÿß „π∑“ßªØ‘∫—µ‘ reflector „π√–∫∫‰À≈‡«’¬π ‡≈◊Õ¥°Á§Õ◊ ‡¡Á¥‡≈◊Õ¥·¥ß (√Ÿª∑’Ë 6.2) Doppler flow defectors ∑’Ë„™â „πªí®®ÿ∫π— ¡’ 2 ·∫∫§◊Õ RBC

Direction

√Ÿª∑’Ë 6.1 Doppler effect §≈◊Ëπ‡ ’¬ß®–‡ª≈’Ë¬π·ª≈ßµ“¡§«“¡‡√Á« „π°“√‡§≈◊ËÕπ∑’Ë¢Õß reflector ”À√—∫„π√–∫∫‰À≈‡«’¬π ‚≈À‘µ ‡¡Á¥‡≈◊Õ¥·¥ß®–‡ªìπ reflector

Probe Skin

‡ âπ‡≈◊Õ¥

√Ÿª∑’Ë 6.2 °“√„™â‡§√◊ËÕß¡◊Õ Doppler µ√«®À≈Õ¥‡≈◊Õ¥·¥ß ‚¥¬°“√ «“ß Doppler probe ≈ß∫πº‘«Àπ—ß∑’ËÕ¬Ÿà‡Àπ◊Õ·π«À≈Õ¥ ‡≈◊Õ¥ ‚¥¬∑“º‘«Àπ—ß¥â«¬ acoustic gel °àÕπ ‡Õ’¬ß probe ·≈–∑”¡ÿ¡‰ª∑“ß‡¥’¬«°—∫°“√‰À≈‡«’¬π‡≈◊Õ¥ Doppler arterial signal ®–¡’≈—°…≥–ª°µ‘§◊Õ‡ªìπ triphasic ·µà ∂â“¡’°“√Õÿ¥µ—πÀ√◊Õµ’∫·§∫®–‡ªìπ monophasic signals

1. continuous-wave Doppler probe ®–·æ√à°√–®“¬ ·≈–√—∫ ultrasound waves Õ¬à“ßµàÕ‡π◊ÕË ß ‚¥¬Õ“»—¬ º≈÷°∑’Ë probe ´÷Ëß “¡“√∂®–√—∫ àß —≠≠“≥‰¥â®“° ‡π◊ÈÕ‡¬◊ËÕ∑ÿ°™π‘¥∑’Ë«“ßÕ¬Ÿà „µâæ◊Èπº‘«¢Õß probe ·æ∑¬å ºŸâ‡™’Ë¬«™“≠„π°“√„™â‡§√◊ËÕß¡◊Õ®–·¬°§«“¡·µ°µà“ß‰¥â √–À«à“ß high pitched arterial signal ·≈– low pitched venous signal πÕ°®“°π’È¬—ß¡’‡§√◊ËÕß¡◊Õ™π‘¥π’È¢π“¥ ‡≈Á°·≈–‡∫“ “¡“√∂æ°µ‘¥µ—«‰ª‰¥â –¥«° „™â§≈◊πË §«“¡∂’Ë 5-10 mHz ∂â“‡ªìπ bidirector ®–«—¥·≈–ª√–‡¡‘π‰¥â∑ß—È direction ·≈– velocity 2. pulsed-wave Doppler flow detector ®– àß·≈– √—∫ ultrasound waves ‡ªìπ™à«ß Ê ‚¥¬∑’Ë piezoelectric crystal µ√ßª≈“¬ probe ®–∑”ß“π‡ªìπ™à«ß Ê pulsed-wave Doppler ®–¡’ duplex scanner Õ¬Ÿ¥à «â ¬ ∑”„Àâ‡ÀÁπ√Ÿª√à“ß¢ÕßÀ≈Õ¥‡≈◊Õ¥ ∑’Ëº‘¥ª°µ‘ √à«¡°—∫ velocity profile ´÷Ëß “¡“√∂·¬°§«“¡·µ° °µà“ß‰¥â√–À«à“ßÀ≈Õ¥‡≈◊Õ¥ª°µ‘°∫— À≈Õ¥‡≈◊Õ¥∑’µË ∫’ ·§∫

PLETHYSMOGRAPHY ‡ªìπ°“√«—¥§«“¡‡ª≈’Ë¬π·ª≈ßª√‘¡“µ√‡≈◊Õ¥∑’Ë ‰À≈‡«’¬π‡¢â“ ·≈–ÕÕ°®“°¢“ arterial plethysmography ®–„™â«¥— pulse volume À√◊Õª√‘¡“µ√‡≈◊Õ¥∑’‡Ë ª≈’¬Ë π·ª≈ß‡ªìπ —¥ à«π„π¢“√–À«à“ß cardiac cycle venous plethysmography ®–„™â «— ¥ ª√‘¡“µ√‡≈◊Õ¥¥”∑’‡Ë ª≈’¬Ë π·ª≈ß∑’πË Õà ß„π™à«ß√–¬–‡«≈“∑’®Ë ”°—¥ «‘∏°’ “√„π∑“ßªØ‘∫µ— ¢‘ Õß plethysmography ¡’À≈“¬Õ¬à“ß‡™àπ water displacement, strain gauge impedance ·≈– air plethysmography ∑’Ë „™â –¥«°·≈–º≈„π°“√«—¥‡™◊ÕË ∂◊Õ‰¥â§Õ◊ air plethysmography ‡ªìπ‡§√◊ËÕß¡◊Õ∑’Ë√Ÿâ®—°·≈–„™â°—π·æ√àÀ≈“¬§◊Õ pulse volume recorder (PVR) «‘∏°’ “√§◊Õ æ—π pneumatic cuff √Õ∫·¢πÀ√◊Õ¢“ À≈—ß®“°π—πÈ inflate cuff „Àâ§«“¡¥—π Ÿß∂÷ß 65 ¡‘≈≈‘‡¡µ√ª√Õ∑ „™â pressure transducer «—¥¥Ÿ§«“¡‡ª≈’Ë¬π ·ª≈ß¢Õß§«“¡¥—π™à«ß cardiac cycle ‚¥¬§«“¡¥—πµË”¢π“¥π’È ®–æ∫«à“ °“√‡ª≈’Ë¬π·ª≈ß√–¥—∫§«“¡¥—π®–‡ªìπ —¥ à«π‚¥¬µ√ß °—∫§«“¡‡ª≈’¬Ë π·ª≈ßª√‘¡“µ√‡π◊ÕÈ ‡¬◊ÕË ∑’ÕË ¬Ÿ¿à “¬„µâ cuff (√Ÿª∑’Ë 6.3) ‚¥¬®–ÕÕ°¡“„π√Ÿª wave form air plethysmography ¡’ ª√–‚¬™πå¡“°„π°“√ª√–‡¡‘π limb perfusion ¢ÕßºŸâªÉ«¬∑’Ë À≈Õ¥‡≈◊Õ¥·¥ß¡’·§≈‡´’¬Ë ¡‡°“–ºπ—ß ∑”„ÀâÀ≈Õ¥‡≈◊Õ¥·¢Áß (æ∫ „πºŸªâ «É ¬‡∫“À«“π) §«“¡¥—π∑’«Ë ¥— ‰¥â®– Ÿß‡°‘π‰ª ‰¡àµ√ß°—∫§«“¡

NONINVASIVE VASCULAR STUDIES

√Ÿª∑’Ë 6.3 Pulse volume recordings ≈—°…≥–ª°µ‘¢Õß PVR §◊Õ§àÕπ¢â“ß·À≈¡ Ÿß ·µà∂â“º‘¥ª°µ‘®–·∫π·≈–§àÕπ¢â“ß®– prolong ‡ªìπ®√‘ß §à“ plethysmography ∑’«Ë ¥— ‰¥â®√‘ß Ê ®–‰¡à¢π÷È °—∫·√ß °¥¿“¬πÕ°À√◊ÕÀ≈Õ¥‡≈◊Õ¥∑’ËÕÿ¥µ—π À≈Õ¥‡≈◊Õ¥·¢Áß®“°¡’·§ ≈‡´’¬Ë ¡‡°“–®–‰¡à¡º’ ≈µàÕ°“√«—¥§à“ plethysmography

1. pulse volume recorder (PVR) §‘¥§âπ¢÷πÈ ¡“‚¥¬ Raines ·≈– Darling ®“° Massachusettes General Hospital „π√Ÿª¢Õß segmental plethysmograph „™â monitor pulsatility ¢Õß¢“∑“ßÕâÕ¡∑”„Àâ∑√“∫∂÷ß blood flow PVR „™â air-filled cuff æ—π√Õ∫¢“„π√–¥—∫µà“ß Ê µ“¡µâÕß°“√ (√Ÿª∑’Ë 6.4) °“√‡ª≈’Ë¬π·ª≈ß¢Õßª√‘¡“µ√„π¢“®–µ√«®æ∫‰¥â ‚¥¬¡’§«“¡¥—π‡ª≈’¬Ë π·ª≈ß„π air-filled cuffs pulse volume changes ®–∂Ÿ°∫—π∑÷°‡Õ“‰«â∫π·∂∫∫—π∑÷°≈—°…≥–‡ªìπ arterial pulse contours ´÷ßË ®–¡’§“à „°≈â‡§’¬ß°—π°—∫ direct intraarterial pressure ∑’«Ë ¥— ‰¥â®“°¢“„π√–¥—∫µà“ß Ê Doppler segmental limb

pressure ®–™à«¬ª√–‡¡‘π°“√¢“¥‡≈◊Õ¥ª≈“¬‡∑â“·≈–π‘«È ‰¥â µà“ß®“° Doppler unit ª°µ‘∑«—Ë ‰ª

2. ocular plethysmography (OPG) „™â „π°“√«—¥ª√‘¡“µ√∑’‡Ë ª≈’¬Ë π·ª≈ß„πµ“∑’‡Ë °‘¥®“° arterial pulsation ‡æ◊ÕË ª√–‡¡‘π°“√Õÿ¥µ—π¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß§“‚√µ‘¥ ¡’ 2 «‘∏’∑’Ë „™â „πªí®®ÿ∫—π§◊Õ Kartchner-McRae OPG methods ®–ª√–‡¡‘π delay in volume filling ¢Õßµ“ ´÷ßË ¡’º≈ ◊∫‡π◊ÕË ß ¡“®“°°“√Õÿ¥µ—π¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß§“‚√§µ‘¥ ∂◊Õ‡ªìπ‡∑§π‘§ ∑’Ë·∑â®√‘ß ”À√—∫ plethysmography OPG-Gee ‡ªìπ°“√„™â °√«¬ Ÿ≠≠“°“»«“ß≈ß∫π sclera ‡æ◊ÕË «—¥ intraocular pressure ‡ªìπ°“√«—¥§«“¡¥—π®“°µ“‚¥¬µ√ß ‰¡à‡°’¬Ë «¢âÕß°—∫ plethysmography ®–‡ªìπ —¥ à«π°—∫°“√Õÿ¥µ—π¢Õß internal carotid artery ®–µ√«®æ∫«à“À≈Õ¥‡≈◊Õ¥·¥ß§“‚√µ‘¥Õÿ¥µ—π‰¥â·¡àπ¬”∂â“¡’°“√ Õÿ¥µ—π¡“°°«à“√âÕ¬≈– 60 (‡ âπºà“»Ÿπ¬å°≈“ß) §«“¡¥—π∑’«Ë ¥— ‰¥â®– ≈¥≈ß ∑—Èß Õß«‘∏’‡ªìπ indirect tests ∑’Ë®–ª√–‡¡‘π°“√Õÿ¥µ—π ¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß§“‚√µ‘¥´÷Ëß§«√ª√–‡¡‘π‰«â°àÕπæ‘®“√≥“∑” direct invasive tests µàÕ‰ª ªí®®ÿ∫π— duplex scan ‡ªìπ°“√ µ√«®«‘π®‘ ©—¬ routine ·≈â« ”À√—∫‚√§À≈Õ¥‡≈◊Õ¥¥”·≈–À≈Õ¥ ‡≈◊Õ¥·¥ß

3. photoplethysmography (PPG) √Ÿª∑’Ë 6.4 °“√æ—π segmental pressure cuffs „πµ”·Àπàßµà“ß Ê µ—Èß·µàµâπ¢“, πàÕß, ¢âÕ‡∑â“ ·≈–π‘È«‡∑â“ ®–æ—πµâπ¢“·∫∫ one-cuff À√◊Õ two-cuff °Á ‰¥â

‡ªìπ direct method „π°“√«—¥ cutaneous blood flow ‚¥¬„™â photoelectric sensor «—¥°“√‡§≈◊ËÕπ‰À«¢Õß‡¡Á ¥ ‡≈◊Õ¥·¥ßµ√ß cutaneous circulation arterial pulsation ·≈– venous congestion ®–‡æ‘¡Ë ª√‘¡“≥¢Õß‡≈◊Õ¥∑’Ë ‰À≈‡«’¬π„π dermal circulation ·≈–«—¥‰¥â®“° PPG

4. impedence plethysmography (IPG) ‡ªìπ°“√«—¥ª√‘¡“µ√∑’Ë‡ª≈’Ë¬π·ª≈ß¢Õß·¢π¢“ ‚¥¬°“√ ‡ª≈’Ë¬π·ª≈ß§«“¡µâ“π∑“π‰øøÑ“ §‘¥§âπ«‘∏’°“√π’È ‚¥¬ Wheeler ·≈–§≥– ‡À¡“–„π°“√«‘π‘®©—¬ acute ·≈– chronic DVT ‚¥¬„™âÀ≈—°°“√¢Õß Ohmûs law voltage = current x resistance ‚¥¬„Àâ‡≈◊Õ¥‡ªìπµ—«π”‰øøÑ“ §«“¡µâ“π∑“π‰øøÑ“®–πâÕ¬∂â“¡’ ‡≈◊Õ¥§—ßË Õ¬Ÿà„π·¢π¢“ª√‘¡“≥¡“° „π DVT ¡’°“√≈¥ venous outflow ‡™àπ‡¥’¬«°—π°—∫ peripheral vasoconstriction, À—«„®«“¬, §«“¡¥—π‚≈À‘µµË” À√◊Õ pulmonary hypertension

5. phleborheography (PRG) „™â air-filled cuffs æ—π√Õ∫·¢π·≈–¢“„πµ”·Àπàß∑’µË Õâ ß°“√ √«¡‡∑â“·≈–∫√‘‡«≥Àπâ“Õ° ‡æ◊ÕË —ß‡°µÿ°“√‡ª≈’¬Ë π·ª≈ßª√‘¡“µ√ „π¢“ ™à«ß°“√À“¬„® æ∫«à“„π DVT ®–¡’°“√≈¥¢Õß respiratory waves „π√–¥—∫∑’Ë „µâµàÕ°“√Õÿ¥µ—π ∂â“¡’°“√Õÿ¥µ—πÕ¬à“ß ¡∫Ÿ√≥å®–‰¡àæ∫ waves ‡≈¬ «‘∏π’ ¡’È §’ «“¡‡™◊ÕË ∂◊Õ‰¥â ßŸ ∂÷ß√âÕ¬≈– 95 ¡’¢Õâ ‡ ’¬§◊Õ §àÕπ¢â“ß¬ÿßà ¬“° ≈—∫´—∫´âÕπ·≈–µâÕß‡√’¬π√Ÿâ „™â ‡§√◊ÕË ß¡◊Õµ≈Õ¥®π°“√·ª√º≈

DUPLEX SCANNING ‡ªìπ«‘∏°’ “√µ√«®«‘π®‘ ©—¬∑’√Ë «¡‡Õ“ real-time B-mode ultrasound image °—∫ pulsed Doppler spectral analysis ‡æ◊ÕË ¥Ÿ flow velocity „™â water soluble acoustic gel ∑“º‘«Àπ—ß ∫√‘‡«≥∑’®Ë –«“ß probe ‡æ◊ÕË ®—∫§≈◊πË ‡ ’¬ß À≈Õ¥‡≈◊Õ¥≈—°…≥–µà“ß Ê ®–¡Õß‡ÀÁπ‰¥âµ“¡æ¬“∏‘ ¿“æ „πÀ≈Õ¥‡≈◊Õ¥·¥ß®–‡ÀÁπ calcified plaques «‘«—≤π“°“√¢Õß‡§√◊ËÕß¡◊Õ„πªí®®ÿ∫—π∑”„Àâ¡Õß ‡ÀÁπ‡ªìπ ’µ“à ß Ê ®“° ultrasound B-mode ®–∫àß∫Õ°∂÷ß blood flow ’·¥ßÀ¡“¬∂÷ß flow ¡“¬—ß probe ’πÈ”‡ß‘π§◊Õ flow ÕÕ° ®“° probe §«“¡‡¢â¡®“ß¢Õß ’∫àß∫Õ°∂÷ß velocity «‘∏’π’È®÷ß ‡À¡“– ”À√—∫°“√«‘‡§√“–Àå carotid bifurcation disease À√◊Õ À≈Õ¥‡≈◊Õ¥‡∑’¬¡∑’ËÕÿ¥µ—π∫√‘‡«≥∑’ËÕÿ¥µ—π®–¡’°“√‡æ‘Ë¡ turbulent flow ’®–§àÕπ¢â“ß ¥„ πÕ°®“°π’·È ≈â«¬—ßπ”¡“„™â „π°“√µ√«® °“√µ’∫·§∫¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß∑’¢Ë “, ≈”‰ â, À≈Õ¥‡≈◊Õ¥¥”·≈– renal arteries ¢âÕ‡ ’¬¢Õß duplex scanning §◊Õ√“§“‡§√◊ÕË ß¡◊Õ§àÕπ¢â“ß Ÿß°«à“ noninvasive test ™π‘¥Õ◊Ëπ µâÕßÕ“»—¬‡∑§π’‡™’Ë¬π¥Ÿ·≈ ·≈–ªØ‘∫µ— °‘ “√·≈–®–µâÕß¡’ª√– ∫°“√≥å„π°“√·ª√º≈

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥

TRANSCUTANEOUS OXIMETRY (TCPO2)

‡ªìπ°“√«—¥ local skin oxygen tension ´÷ßË –∑âÕπ∂÷ß arterial ·≈– capillary perfusion «‘∏’°“√§◊Õ∑”„Àâº‘«Àπ—ß¡’ Õÿ≥À¿Ÿ¡ ‘ ßŸ ¢÷πÈ ‡ªìπ 45o C ∑”„Àâ‡°‘¥ localized hyperemia ·≈– oxygen excess ÕäÕ°´‘‡®π®–´÷¡°√–®“¬‚¥¬ concentration gradient √–À«à“ß capillaries °—∫‡π◊ÈÕ‡¬◊ËÕ√Õ∫¢â“ß ‡™àπ‡¥’¬« °—∫´÷¡ºà“πº‘«Àπ—ß´÷Ëß¡’°“√≈¥¢Õß§ÿ≥ ¡∫—µ‘ electrochemical ·≈–«—¥§«“¡·µ°µà“ß‚¥¬«‘∏’ modified Clark platinum oxygen electrode ‡√‘¡Ë µâπ®“°°“√ standardize vosodilation ‚¥¬„™â Õÿ≥À¿Ÿ¡º‘ «‘ Ÿß°«à“ 43o C æ∫«à“ ratio ¢Õß TcPO2 °—∫ arterial PO2 §ß∑’·Ë ≈–„°≈â‡§’¬ß°—∫§à“ 1.

CT scan computed tomography (CT) ‡ªìπ‡∑§π‘§°“√µ√«®§âπ∑“ß √—ß ’«‘∑¬“Õ¬à“ßÀπ÷Ëß ‚¥¬°“√µ—¥ºà“π√à“ß°“¬„π·π«µà“ß Ê ‡ªìπ series ¢Õß x-ray beams „π¡ÿ¡µà“ß Ê °—π ‡∑§π‘§„À¡à§Õ◊ spiral CT ®–‡ÀÁπÀ≈“¬¡‘µ‘ CT scan µ“¡ª°µ‘®–‡ÀÁπÀ≈Õ¥‡≈◊Õ¥‰¥â ·µà∂â“µâÕß°“√„Àâ™—¥¢÷Èπ§«√®–©’¥ “√∑÷∫· ß‡¢â“À≈Õ¥‡≈◊Õ¥°àÕπ ∂à“¬ CT scans.

MAGNETIC RESONANCE TECHNIQUES ‰¥â¡°’ “√π”‡Õ“§≈◊πË ·¡à‡À≈Á°‰øøÑ“¡“µ√«®«‘π®‘ ©—¬‚√§∑—«Ë ‰ª·≈– ‚√§∑“ßÀ≈Õ¥‡≈◊Õ¥ ¥—ßµàÕ‰ªπ’È 1. magnetic resonance imaging ‰¥â¡°’ “√‡√‘¡Ë π”‡∑§π‘§ ¢Õß nuclear magnetic resonance ¡“µ√«®«‘π®‘ ©—¬ ‚√§µ—ßÈ ·µà §». 1940 ·≈–‡√‘¡Ë π”¡“„™âª√–‚¬™πå®√‘ß Ê ‡¡◊ÕË ªï 1980 „π√Ÿª¢Õß magnetic resonance imaging (MRI) À≈—°°“√¢÷ÈπÕ¬Ÿà°—∫ªØ‘°‘√‘¬“√–À«à“ß hydrogen nuclei ´÷ßË ¢÷πÈ Õ¬Ÿ°à ∫— §≈◊πË ·¡à‡À≈Á°‰øøÑ“·≈– (radiowaves) §≈◊πË «‘∑¬ÿ ∂◊Õ‡ªìπ noninvasive test. 2. magnetic resonance flowmeter ‡ªìπ‡§√◊ÕË ß¡◊Õµ√«® «‘π‘®©—¬∑’Ë „À¡à „π°“√«—¥ arterial flow ´÷Ëß·µ°µà“ß®“° standard MR imagers ¡’¢π“¥‡≈Á°æ°æ“ßà“¬·≈–„™â ”À√—∫µ√«® blood flow ‡∑à“π—πÈ „πÕπ“§µÕ“®®–„™â ·∑π plethysmography 3. magnetic resonance angiography (MRA) ‡ªìπ ‡∑§π‘§∑’∑Ë ”„Àâ¡Õß‡ÀÁπ‡≈◊Õ¥«‘ßË ºà“π‡π◊ÕÈ ‡¬◊ÕË ¢Õß√à“ß°“¬‰¥â

NONINVASIVE VASCULAR STUDIES

laminar flow ®–‡ÀÁπ‰¥â™—¥‡®π°«à“ turbulent flow ‡æ√“–‚¡‡≈°ÿ≈¢Õß‡¡Á¥‡≈◊Õ¥·¥ß‰ª„π·π«‡¥’¬«°—π°—∫ π“¡·¡à‡À≈Á°‰øøÑ“ ∫√‘‡«≥∑’µË ∫’ ·§∫¢ÕßÀ≈Õ¥‡≈◊Õ¥®–¡’ turbulent flow À√◊Õ‰¡à¡’ flow ‡≈¬ MRA “¡“√∂ ¡Õß‡ÀÁπÀ≈Õ¥‡≈◊Õ¥∑’¡Ë ¢’ π“¥‡≈Á° 2 ¡‘≈≈‘‡¡µ√‰¥â

°“√ª√–¬ÿ°µå NONINVASIVE TESTS ¡“„™â°—∫‚√§À≈Õ¥‡≈◊Õ¥ I. LOWER EXTREMITY ARTERIAL OCCLUSIVE DISEASE ºŸªâ «É ¬∑’ªË √–‡¡‘π·∫àßÕÕ°‰¥â 2 °≈ÿ¡à À≈—ß®“°´—°ª√–«—µ·‘ ≈– µ√«®√à“ß°“¬·≈â«§◊Õ intermittent claudication °—∫ severe ischemia (rest pain, nonhealing ulcers, gangrene) noninvasive tests ®–™à«¬ª√–‡¡‘π§«“¡√ÿπ·√ß¢Õß claudication ·≈–‡ªìπÀ≈—°∞“π‰«â ”À√—∫°“√µ‘¥µ“¡¥Ÿ·≈ºŸâªÉ«¬ ·≈–¬—ß ª√–‡¡‘πæ¬“°√≥å ‚√§µ≈Õ¥®π∫àß™’«È “à ºŸªâ «É ¬πà“®–∑” bypass À√◊Õ reconstruct ‡æ◊ÕË revascularization. 1. Intermittent claudication (IC) ºŸªâ «É ¬ IC ∑ÿ°√“¬ §«√®–µ√«®«‘π®‘ ©—¬‚¥¬«‘∏°’ “√µà“ß Ê „Àâ§√∫ ‡√‘¡Ë µâπ®“° Doppler survey ¢Õß ankle ·≈– pedal arterial signals ·≈–«—¥ ankle-brachial pressure indices (ABIs) „π∑à“æ—° ‡™àπ ‡¥’¬«°—∫«—¥§à“ segmental pressures ·≈– plethysmographic wave forms (PVRs) ·≈–«—¥§à“‡À≈à“π’´È È”Õ’°À≈—ß®“° exercise. 1.1 Doppler survey À≈Õ¥‡≈◊Õ¥ à«πª≈“¬∑—ßÈ À¡¥µ√«® ‰¥â ‚¥¬°“√„™â doppler probe arterial signal ∑’ªË °µ‘ ®–¡’ 2-3 components ‡√‘¡Ë ®“° high-pitched sound · ¥ß∂÷ß blood flow ‰ª¥â“πÀπâ“ ¢≥– systole ·≈– component µàÕ¡“®– reversed —πÈ ‡¢â“°—∫ reversal flow „π√–¬– diastole diastole ¢≥–∑’Ë„°≈â®–®∫ forword flow ®–‰¥â¬π‘ third low-pitched sound (√Ÿª∑’Ë 6.2) ∂â“¡’ severe proximal arterial stenosis À√◊Õ occlusion Doppler signal ®–‡ªìπ low-pitched ·≈– monophasic ∂â“°“√Õÿ¥µ—πÀ√◊Õµ’∫·§∫‰¡à√ÿπ·√ß„π ∑à“æ—° Doppler signal ®–ª°µ‘ ·µà∂“â exercise ®–‡ªìπ monophasic °“√‡ª≈’¬Ë π·ª≈ß¢Õß Doppler sound

√Ÿª∑’Ë 6.5 °“√«—¥ ankle systolic pressure ‚¥¬„™â blood pres-

sure cuff ·≈– portable continuous-wave Doppler unit π”‡Õ“ ankle pressure ¡“À“√°—∫ brachial (arm) pressure §”π«≥‡ªìπ§à“ ABI §à“ª°µ‘‡∑à“°—∫ 1, claudication √–À«à“ß 0.5-0.9, ischemic rest pain ·≈– tissue necrosis ®–µË”°«à“ 0.5

®–∫àß∫Õ°∂÷ß°“√µ’∫·§∫¢ÕßÀ≈Õ¥‡≈◊Õ¥·≈–®–· ¥ß „Àâ‡ÀÁπ™—¥¬‘ßË ¢÷πÈ À≈—ß®“° exercise §«√µ√«®·≈–∫—π∑÷° Doppler signals «à“¡’À√◊Õ‰¡à·≈–‡ ’¬ß‡ªìπÕ¬à“ß‰√ ¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß femoral, popliteal, posterior tibial ·≈– dorsalis pedis. 1.2 segmental leg pressures ®– “¡“√∂§“¥«à“µ”·Àπàß ¢ÕßÀ≈Õ¥‡≈◊Õ¥Õÿ¥µ—πÕ¬Ÿ∑à ’Ë „¥ ®“°°“√æ—π pressure cuffs ∑’Ëµâπ¢“, πàÕß ·≈–¢âÕ‡∑â“ «—¥§«“¡¥—π¢≥–ºŸâªÉ«¬πÕπ √“∫∫π‡µ’¬ß (√Ÿª∑’Ë 6.4) „™â Doppler probe À√◊Õ plethysmograph «—¥§«“¡¥—π systolic ‚¥¬¢÷πÈ pressure cuff ·µà≈–∑’Ë à«πµ”·Àπàß∑’Ë«—¥§«“¡¥—π®–µâÕß ‡ªìπ∑’¢Ë Õâ ‡∑â“‡ ¡Õ (√Ÿª∑’Ë 6.5) ·ª√º≈ segmental leg pressures ∑’«Ë ¥— ‰¥â¥ß— µàÕ‰ªπ’È °. §à“ª°µ‘¢Õß systolic ankle pressure §«√®–‡∑à“°—∫ À√◊Õ Ÿß°«à“ systolic arm pressure ¥—ßπ—πÈ §à“ anklebrachial pressure ratio §«√®– Ÿß°«à“ 1.0 ∂â“ ¡’°“√µ’∫·§∫¢ÕßÀ≈Õ¥‡≈◊Õ¥®–Õ¬Ÿ√à –À«à“ß 0.5-0.8 ·≈–∂â“µË”°«à“ 0.5 · ¥ß«à“À≈Õ¥‡≈◊Õ¥Õÿ¥µ—πÀ≈“¬ µ”·Àπàß

64 ¢. §«“¡¥—π∑’«Ë ¥— ‰¥â „π¢“¢â“ß‡¥’¬«°—π√–¥—∫µà“ß°—π ·µà¡’ pressure gradient ¡“°°«à“ 20 ¡‘≈≈‘‡¡µ√ª√Õ∑ · ¥ß«à“¡’°“√µ’∫·§∫¢ÕßÀ≈Õ¥‡≈◊Õ¥„π√–¥—∫∑’µË “à ß°—π §. segmental leg pressures Õ“®®–«—¥§à“‰¥âº¥‘ æ≈“¥ „π°√≥’¥ß— µàÕ‰ªπ’È 1. À≈Õ¥‡≈◊Õ¥·¢Áß¡’·§≈‡´’¬Ë ¡‡°“–ºπ—ß„πºŸªâ «É ¬‚√§ ‡∫“À«“π ®–°¥À≈Õ¥‡≈◊Õ¥‚¥¬ pressure cuffs ‰¡à ‰¥â ∑”„Àâ§“à §«“¡¥—π∑’«Ë ¥— ‰¥â ßŸ °«à“ª°µ‘ 2. collaterals ∑’Ë develop ¥’ À≈—ß¡’°“√Õÿ¥µ—π¢ÕßÀ≈Õ¥ ‡≈◊Õ¥ ®–«—¥ pressure gradient µà“ß√–¥—∫‰¥â πâÕ¬°«à“ 20 ¡‘≈≈‘‡¡µ√ª√Õ∑ 3. superficial femoral artery ∑’ÕË ¥ÿ µ—π °“√«—¥ thigh arm ratio ®–„°≈â‡§’¬ß°—∫À≈Õ¥‡≈◊Õ¥·¥ß iliac Õÿ¥µ—π §«√§≈” femoral pulse ‡æ◊ËÕ·¬° §«“¡·µ°µà“ß ∂â“§≈”‰¥â ‰¡à·µ°µà“ß°—π §«√∑” Doppler blood flow velocity ‘ßË ‡À≈à“π’‡È ªìπ¢’¥®”°—¥¢Õß segmental leg pressures ®÷ßµâÕß∑”√à«¡°—π°—∫°“√µ√«®√à“ß°“¬‡æ◊ËÕ ª√–‡¡‘π µ”·Àπà ßÀ≈Õ¥‡≈◊Õ¥Õÿ ¥ µ— π ∂â “µâ Õ ß°“√ ¢âÕ¡Ÿ≈‡æ‘¡Ë ‡µ‘¡®–µâÕß∑” exercise test, PVRs ·≈– Doppler wave form analysis. 1.3 Pulse volume recordings ¢âÕ¡Ÿ≈∑’Ë ‰¥â®– àß‡ √‘¡ segmental leg pressure ´÷Ëß„™â pressure cuffs ∑’Ë ‡¥’¬«°—π ¥Ÿ PVR tracing ª°µ‘®–¡’ sharp upstroke, pulse peak §ß∑’·Ë ≈–µË”≈ßÕ¬à“ß√«¥‡√Á« ·µà∂“â À≈Õ¥ ‡≈◊Õ¥Õÿ¥µ—π®–æ∫«à“ tracing prolong ·≈–·∫π√“∫ (√Ÿª∑’Ë 6.3) „πºŸªâ «É ¬Õ“¬ÿπÕâ ¬∑’¡Ë ’ IC Õ“®®–‡°‘¥®“° popliteal artery entrapment ®“°°“√√—¥¢Õß medial head of gastrocnemius PVR tracing „π∑à“æ—°®–ª°µ‘ ·µà∂“â exercise °≈â“¡‡π◊ÈÕ gastrocnemius ®–À¥µ—« °¥ popliteal artery ∑”„Àâ PVR tracing ·∫π 1.4 Exercise testing °“√ exercise ¢“∑”„Àâ¡‡’ ≈◊Õ¥¡“ ‡≈’¬È ß¡“°¢÷πÈ ·µà§“à ¢Õß systolic ankle pressure ®– Ÿß¢÷πÈ ‡≈Á°πâÕ¬ µà“ß°—∫°√≥’∑À’Ë ≈Õ¥‡≈◊Õ¥·¥ßÕÿ¥µ—π À≈—ß exercise ·≈â« ankle pressure ®–≈¥≈ß ‡π◊ÕË ß®“°‡Àµÿº≈ 2 ª√–°“√§◊Õ 1) ¡’ flow ºà“π¡“∫√‘‡«≥∑’ÕË ¥ÿ µ—π∑”„Àâ‡°‘¥ turbulent flow ·≈–«—¥§«“¡¥—π®–≈¥≈ß 2) ‡≈◊Õ¥ shunt ºà“π‡¢â“ collateral beds „π°≈â“¡‡π◊ÕÈ ‡ªìπ à«π„À≠à „π °“√µ√«®π’∂È “â ºŸªâ «É ¬‰¡à “¡“√∂ exercise ‰¥â §«√∑” re-

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥ active hyperemia test ‚¥¬‡æ‘¡Ë §«“¡¥—π„π high thigh cuff 50 ¡‘≈≈‘‡¡µ√ª√Õ∑ Ÿß°«à“ arm pressure π“π 5 π“∑’ ·≈â « ®÷ ß §à Õ ¬«— ¥ systolic ankle pressure Õ¬à“ß‰√°Áµ“¡ °“√«—¥ exercise pressure ‚¥¬°“√„ÀâºŸâ ªÉ«¬‡¥‘π∫π treadmill §«“¡‡√Á« 2 ‰¡≈åµÕà ™—«Ë ‚¡ß ·≈– æ◊πÈ √“∫∑”¡ÿ¡ 10 Õß»“ ¿“¬„π√–¬–‡«≈“ 5 π“∑’ ®– ‡ªìπ«‘∏∑’ ‡’Ë ™◊ÕË ∂◊Õ‰¥â·πàπÕπ∑’ Ë ¥ÿ “¡“√∂ test ¥Ÿ claudication ‰¥â ·µàµÕâ ß·πà „®«à“ºŸªâ «É ¬¡’ cardiorespiratory preserve ‡æ’¬ßæÕ πÕ°‡Àπ◊Õ®“°°“√«—¥ ankle pressures ·≈– PVRs À≈—ß exercise ·≈â«§«√∫—π∑÷°¢âÕ¡Ÿ≈¢Õß claudication „Àâ≈–‡Õ’¬¥§◊Õ time of onset, location ·≈–§«“¡ √ÿπ·√ß¢Õß°“√ª«¥ serial treadmill examination ®–„™â¥Ÿ progression ¢Õß‚√§À≈Õ¥‡≈◊Õ¥Õÿ¥µ—π·≈– ª√–‡¡‘π anastomotic stenosis À≈—ßºà“µ—¥‰¥â exercise test ®–·¬° vascular ÕÕ°®“° neurogenic claudication ‰¥âÕ¬à“ß™—¥‡®π ‡π◊ÕË ß®“°ºŸªâ «É ¬ peripheral vascular disease ®–¡’ ‚√§À—«„®√à«¡¥â«¬‡ ¡Õ ®÷ß§«√∑” continual EKG monitoring „π¢≥–∑’∑Ë ” treadmill exercise „π°√≥’∑’Ë 1. ¡’ª√–«—µ‚‘ √§À—«„®¢“¥‡≈◊Õ¥¡“°àÕπ 2. ¡’Õ“°“√¢Õß angina pectoris µâÕßÕ¡ nitrates ·≈â« Õ“°“√®÷ß®–¥’¢π÷È 3. ¡’ COPD 4. ¡’Õ“°“√¢Õß cardiac arrhytmia ¢≥–∑’«Ë ¥— arterial PVR ¢≥–æ—° 5. √—∫ª√–∑“π antiarrhytmic drugs Õ¬à“ßµàÕ‡π◊ËÕß ‡æ◊ÕË §«∫§ÿ¡Õ“°“√ 6. ‡§¬ºà“µ—¥À—«„®¡“°àÕπ 7. ¡’ permanent pacemaker 8. ¡’ª√–«—µ‘ stroke À√◊Õ TIAs ¡“°àÕπ ∂â“‰¡à “¡“√∂ monitor EKG ‰¥â¢≥– exercise ®÷ß ‰¡à§«√∑” treadmill exercise „π°√≥’¥ß— µàÕ‰ªπ’È 1. ¡’ª√–«—µæ‘ ∫ angina pectoris ·¡â«“à ®– exercise ‡æ’¬ß‡≈Á°πâÕ¬ 2. ¡’ª√–«—µ‘°≈â“¡‡π◊ÈÕÀ—«„®¢“¥‡≈◊Õ¥„π™à«ß 6 ‡¥◊Õπ∑’Ë ºà“π¡“ 3. §≈”™’æ®√æ∫ cardiac arrhytmia ´÷ßË ¬—ß‰¡à ‰¥â√°— …“ ¡“°àÕπ

NONINVASIVE VASCULAR STUDIES

Õ¬à“ß‰√°Áµ“¡ ∂÷ß·¡â«“à ®– monitor EKG À√◊Õ‰¡à ·≈â« ∑” treadmill exercise test §«√À¬ÿ¥‡¡◊Ë Õ ºŸâ ªÉ « ¬¡’ Õ“°“√¥—ßµàÕ‰ªπ’È 1. ª«¥·πàπÀπâ“Õ° 2. À“¬„®≈”∫“° 3. ¡÷πßß 4. severe claudication ·≈–§«√À¬ÿ¥ exercise „π°√≥’∑’Ë monitor EKG ·≈â« æ∫«à“ 1. ™’æ®√‰«‡°‘π 120 §√—ßÈ µàÕπ“∑’ 2. æ∫ ventricular arrhythmia 3. æ∫ ST segment depression ‡°‘π 2 ¡‘≈≈‘‡¡µ√ 1.5 Penile/brachial pressure index (PBI) aortoiliac occlusive disease (AIOD) ®–∑”„Àâ‡°‘¥ vasculogenic impotence °àÕπÕ◊πË §«√·¬°§«“¡·µ°µà“ß‰¥â√–À«à“ß vasculogenic °—∫ nonvasculogenic impotence ‚¥¬°“√µ√«®Õ¬à“ß≈–‡Õ’¬¥∑“ß¬Ÿ‚√, ‡ÕÁπ‚¥§√’π ·≈–∑“ß ®‘µ«‘∑¬“ „πºŸâªÉ«¬ AIOD ∑’Ë ‰¡à¡’ªí®®—¬‡ ’Ë¬ßÕ◊Ëπ‡™àπ ‚√§‡∫“À«“πÀ√◊Õ√—∫ª√–∑“π¬“∑’Ë¡’º≈¢â“ß‡§’¬ß∑”„Àâ ¡√√∂¿“æ∑“ß‡æ»≈¥≈ß ∂â“«—¥ PBI ‰¥âµË”°«à“ 0.6 ®– «‘π®‘ ©—¬‰¥â«“à ‡ªìπ vasculogenic impotence ∂â“§à“ border line §◊Õ 0.6-0.7 ®–«‘π®‘ ©—¬‰¥â«“à ‡ªìπ vasculogenic impotence ‡¡◊ÕË 1. rest PBI µË”°«à“ 0.7 ·µà«—¥‰¥â‡∑à“‡¥‘¡À√◊Õ≈¥≈ß ‡≈Á°πâÕ¬À≈—ß standard exercise treadmill testing (SETT) 2. rest PBI Ÿß°«à“ 0.7 À≈—ß SETT ·≈â«µË”°«à“‡¥‘¡ ¡“°°«à“ 0.1 À√◊Õ§à“ PBI ≈¥≈ßµË”°«à“ 0.7

II. SEVERE ISCHEMIA ºŸªâ «É ¬∑’¢Ë “¢“¥‡≈◊Õ¥Õ¬à“ß√ÿπ·√ß ®–¡“æ∫·æ∑¬å¥«â ¬Õ“°“√ ”§—≠¥—ßµàÕ‰ªπ’§È Õ◊ rest pain, nonhealing foot lesions ·≈– gangrene ‰¡à “¡“√∂∑” treadmill exercise ‰¥â ®÷ßµâÕß µ√«®ºŸªâ «É ¬„π∑à“æ—°µ≈Õ¥ §«√µ√«®ºŸªâ «É ¬‚¥¬„™â PVRs ·≈– Doppler system ‡æ◊ÕË „Àâ·πà„®«à“ 1. rest pain ∑’æË ∫¡’ “‡Àµÿ¡“®“°°“√¢“¥‡≈◊Õ¥‰¡à „™à neuropathic ‚¥¬∑—Ë«‰ª·≈â«®“°°“√´—°ª√–«—µ‘·≈–µ√«®√à“ß°“¬ °Á “¡“√∂«‘π‘®©—¬ ischemic rest pain ‰¥â „πºŸâªÉ«¬‡∫“À«“π

65 Õ“°“√ª«¥¢“®–‡°‘¥®“°À≈Õ¥‡≈◊Õ¥·¥ßÕÿ¥µ—π√à«¡°—∫ peripheral neuropathy „πºŸªâ «É ¬‡∫“À«“π∑’«Ë ¥— systolic ankle pressure ‰¥âµË”°«à“ 55 ¡‘≈≈‘‡¡µ√ª√Õ∑·≈–¡’Õ“°“√ª«¥¢“„Àâπ÷°∂÷ß ischemic rest pain ”À√—∫ºŸªâ «É ¬∑’Ë ‰¡à‡ªìπ‡∫“À«“π „™â§“à systolic ankle pressure ∑’µË Ë”°«à“ 35 ¡‘≈≈‘‡¡µ√ª√Õ∑ (À√◊Õ™à«ß √–À«à“ß 35-50 ¡‘≈≈‘‡¡µ√ª√Õ∑) ·≈– ankle PVR ·∫π ¡’ minimal deflection (πâÕ¬°«à“ 5 ¡‘≈≈‘‡¡µ√) §à“ systolic ankle pressure ∑’Ë«—¥‰¥â§à“ Ÿß°«à“ª°µ‘„πºŸâªÉ«¬‡∫“À«“π‡π◊ËÕß®“° À≈Õ¥‡≈◊Õ¥·¥ß·¢Áß ¡’·§≈‡´’Ë¬¡‡°“–Õ¬Ÿà∑’Ëºπ—ß ∑”„Àâ ‰¡à¬◊¥À¬ÿàπ ·≈–∂Ÿ°°¥‚¥¬ pressure cuffs ·µàÀ≈Õ¥‡≈◊Õ¥∫√‘‡«≥π‘È«‡∑â“ ¡—°®–‰¡à·¢Áß®÷ß«—¥ toe pressure ‰¥â ∂â“«—¥‰¥âµË”°«à“ 30 ¡‘≈≈‘‡¡µ√ ª√Õ∑∫àß∫Õ°«à“¢“¢“¥‡≈◊Õ¥ °“√«—¥ TcPO2 °Á™à«¬∫Õ° °“√¢“¥‡≈◊Õ¥‰¥â‡™àπ°—π §à“ª°µ‘§◊Õ Ÿß°«à“ 55 ¡‘≈≈‘‡¡µ√ª√Õ∑ ∂â“µË”°«à“ 30 ¡‘≈≈‘‡¡µ√ª√Õ∑· ¥ß«à“¢“¢“¥‡≈◊Õ¥ ‚¥¬‡©æ“– ∂â“¬°¢“¢÷Èπ·≈â««—¥´È” §à“∑’Ë«—¥‰¥â≈¥≈ß 0-10 ¡‘≈≈‘‡¡µ√ª√Õ∑ ¬‘ßË ∫àß™’™È ¥— ‡®π«à“¡’°“√¢“¥‡≈◊Õ¥®“°À≈Õ¥‡≈◊Õ¥·¥ßÕÿ¥µ—π∑’¢Ë “ 2. ™à«¬ª√–‡¡‘π°“√À“¬¢Õß·º≈∑’‡Ë ∑â“À√◊Õπ‘«È ‡∑â“ ®“°°“√ µ√«®√à“ß°“¬∫“ß§√—Èß·¬°·º≈‡√◊ÈÕ√—ß∑’Ë‡∑â“·≈–π‘È«‡∑â“‰¡à ‰¥â«à“¡’ “‡Àµÿ¡“®“°°“√¢“¥‡≈◊Õ¥, venous disease, diabetic neuropathy, °“√µ‘¥‡™◊ÈÕ, collagen diseases À√◊Õ‚√§Õ◊Ëπ Ê ·º≈®–‰¡àÀ“¬∂â“ ankle pressure πâÕ¬°«à“ 55 ¡‘≈≈‘‡¡µ√ª√Õ∑ „πºŸâ ªÉ « ¬∑’Ë ‰ ¡à‡ªìπ‡∫“À«“π·≈– 80 ¡‘≈≈‘‡¡µ√ª√Õ∑„πºŸâªÉ«¬ ‡∫“À«“π ‡™àπ‡¥’¬«°—π°—∫°“√«—¥ PVR æ∫«à“ tracing ·∫π√“∫ ·≈–¡’ minimal deflection (πâÕ¬°«à“ 5 ¡‘≈≈‘‡¡µ√) ‚¥¬«—¥®“° ¢âÕ‡∑â“À√◊Õπ‘È«‡∑â“ ·º≈¡—°®–‰¡àÀ“¬ ‡™àπ‡¥’¬«°—∫§à“ TcPO2 ∑’«Ë ¥— ‰¥âµË” 20-30 ¡‘≈≈‘‡¡µ√ª√Õ∑ 3. ‡æ◊ÕË §“¥·π«∑’®Ë –µ—¥¢“·≈–æ¬“°√≥å stump healing °“√µ√«®√à“ß°“¬ºŸªâ «É ¬®–™à«¬ª√–‡¡‘π√–¥—∫„π°“√µ—¥¢“‰¥â·πàπÕπ vascular tests ¡’∫∑∫“∑‡æ’¬ß‡≈Á°πâÕ¬‰¡à«“à ®–‡ªìπ PVR À√◊Õ ankle pressure ·µà∂â“ PVR æ∫«à“™’æ®√¢Õßπ‘È«‡∑â“À√◊Õ transmetatarsal ¬—ß¡’Õ¬Ÿà °“√µ—¥π‘È«À√◊Õ‡∑â“∫√‘‡«≥π’È·º≈®– À“¬‰¥âµ“¡ª°µ‘ TcPO2 Ÿß°«à“ 40 ¡‘≈≈‘‡¡µ√ª√Õ∑ ·º≈ stump À≈—ß®“°µ—¥¢“·≈â«®–À“¬‰¥âµ“¡ª°µ‘

III. °“√¥Ÿ·≈·≈–ª√–‡¡‘πºŸâªÉ«¬À≈—ßºà“µ—¥ °“√Õÿ¥µ—π¢ÕßÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡∑’∑Ë ” bypass ‰ª·≈â« ®–∑”„Àâ ºŸâªÉ«¬¡’Õ“°“√ claudication °≈—∫¡“Õ’° ®÷ß§«√µ√«®¥Ÿ graft patency ‡ªìπ√–¬– §«√∑” duplex scanning À√◊Õ„™â real-

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥

time-B-mode imaging ¥Ÿ√Õ¬µàÕ√–À«à“ßÀ≈Õ¥‡≈◊Õ¥«à“¡’°“√ µ’∫·§∫À√◊Õ‰¡à

IV. EXTRACRANIAL CEREBROVASCULAR DISEASE noninvasive tests ”À√—∫°“√µ√«®«‘π®‘ ©—¬ cerebrovascular disease ¬—ß¡’«‘«—≤π“°“√¬—ß‰¡à∂÷ß¢—Èπ∑’Ë‡™◊ËÕ∂◊Õ‰¥â ·≈–„™â ·æ√àÀ≈“¬∑—«Ë ‰ª‡æ√“–¬—ß‰¡à “¡“√∂∑¥·∑π cerebral angiography „π·ßà¢Õß§«“¡·¡àπ¬”¢Õßæ¬“∏‘ ¿“æ·≈–°“¬«‘¿“§ ∂÷ß ·¡â«à“Õ—µ√“‡ ’Ë¬ß·≈–¿“«–·∑√°´âÕπ¢Õß°“√∑” angiography ¡’‡æ’¬ß√âÕ¬≈– 1-2 ·µà§à“„™â®à“¬°Á¬—ß§ß Ÿß·≈–„π∫“ß°√≥’Õ“® ®–‡ÀÁπæ¬“∏‘ ¿“æ‰¡à™¥— ‡®π ‰¡à ‰¥â∫ßà ∫Õ°∂÷ß¿“«–∑“ß hemodynamic ®÷ßµâÕß∑” noninvasive test °àÕπ‡æ◊ÕË æ‘®“√≥“∑” angiography ·≈–æ‘®“√≥“ºà“µ—¥√—°…“µàÕ‰ª

1. ¢âÕ∫àß™’È„π°“√∑” noninvasive cerebrovascular tests °àÕπ∑’®Ë –Õ∏‘∫“¬∂÷ß«‘∏°’ “√¢Õß noninvasive tests ”À√—∫ cerebrovascular disease §«√°≈à“«∂÷ß¢âÕ∫àß™’È∑’Ë‡À¡“– ¡„π °“√∑” ´÷ßË ª√–°Õ∫¥â«¬ 1.1 asymptomatic cervical bruit 1.2 Õ“°“√º‘¥ª°µ‘∑“ßª√– “∑‡≈Á°πâÕ¬ ‡™àπ dizziness 1.3 ‡æ◊ÕË µ‘¥µ“¡¥Ÿ·≈ºŸªâ «É ¬‚¥¬‡©æ“–À≈—ßºà“µ—¥ carotid endarterectomy ¥Ÿ«“à ¡’ restenosis À√◊Õ‰¡à 1.4 µ‘¥µ“¡¥Ÿ·≈ºŸªâ «É ¬ carotid stenosis ∑’ÀË ≈Õ¥‡≈◊Õ¥µ’∫ ·§∫‡≈Á°πâÕ¬ (πâÕ¬°«à“√âÕ¬≈– 50) ·≈–¡’Õ“°“√‡æ’¬ß ‡≈Á°πâÕ¬ 1.5 ºŸâªÉ«¬∑’Ë‡§¬ºà“µ—¥∫√‘‡«≥§Õ·≈–»’√…– ´÷ËßµâÕßºŸ°µ—¥ À≈Õ¥‡≈◊Õ¥·¥ß§“‚√§µ‘¥‰ª¢â“ßÀπ÷ßË 1.6 À≈—ßºà“µ—¥·≈â«ºŸâªÉ«¬¡’Õ“°“√º‘¥ª°µ‘∑“ßª√– “∑ ‡™àπ À≈—ß∑” carotid endarterectomy ·≈â« ß —¬«à“¡’ thrombosis 1.7 ‡ªìπÀ≈—°∞“π∫—π∑÷°‰«â ”À√—∫ºŸªâ «É ¬∑’¡Ë Õ’ “°“√º‘¥ª°µ‘∑“ß ª√– “∑ ºŸªâ «É ¬∑’¡Ë Õ’ “°“√ TIAs ‡¥àπ™—¥ §«√∑” cerebral angiography °àÕπ∑’Ë®–ºà“µ—¥√—°…“µàÕ‰ª »—≈¬·æ∑¬å∫“ß∑à“πÕ“®®– µâÕß°“√¢âÕ¡Ÿ≈°“√µ—¥ ‘π„®√—°…“®“° duplex ultrasound °àÕπ

Õ¬à“ß‰√°Áµ“¡ cerebral angiography °Á “¡“√∂„Àâ√“¬¬≈– ‡Õ’¬¥·°à»—≈¬·æ∑¬å°àÕπºà“µ—¥‰¥â¥’‡ ¡Õ ‰¡à«à“®–‡ªìπÀ≈Õ¥‡≈◊Õ¥ ·¥ßπÕ°À√◊Õ„π ¡Õß intrathoracic origins ¢Õß brachiocephalic arteries °“√Õÿ¥µ—π¡“°πâÕ¬‡æ’¬ß‰√, aneurysm πÕ° ·≈–„π ¡Õß, ulcerative lesions ªí®®ÿ∫π— intravenous-digital subtraction arteriograms (IV-DSAs) À√◊Õ MRA °Á “¡“√∂ „Àâ√“¬≈–‡Õ’¬¥¢Õß√Õ¬‚√§‡°◊Õ∫∑’®Ë –„°≈â‡§’¬ß°—∫ cerebral angiography ∂÷ß·¡â«“à noninvasive tests ®–‰¡à‡ª≈’¬Ë π·ª≈ß¢âÕ∫àß™’È „π °“√∑” cerebral angiography ‰¥â „πºŸªâ «É ¬∑’¡Ë Õ’ “°“√∑“ß√–∫∫ ª√– “∑ ·µà°Á¡’¢âÕ¡Ÿ≈ª√–°Õ∫„π°“√æ‘®“√≥“°“√√—°…“§◊Õ ∑√“∫∂÷ß hemodynamics ¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß ·≈–Õ“®®–„™â „πºŸªâ «É ¬∑’·Ë æâ “√∑÷∫√—ß ’∑©’Ë ¥’ ‡¢â“À≈Õ¥‡≈◊Õ¥ duplex sonography ¬—ß„Àâ¢Õâ ¡Ÿ≈‡°’¬Ë «°—∫ vertebral arteries „πºŸªâ «É ¬∑’¡Ë Õ’ “°“√ posterior cerebral symptoms ®–‡ÀÁπ°“√Õÿ¥µ—π¢ÕßÀ≈Õ¥‡≈◊Õ¥ à«πµâπ‰¥â ‡ÀÁπ direction of flow ¢Õß‡≈◊Õ¥∑”„Àâ«π‘ ®‘ ©—¬‰¥â«“à ‡ªìπ subclavian steal syndrome À√◊Õ‰¡à ºŸªâ «É ¬∑’¡Ë ’ posterior circulation insufficiency Õ“®®–µ√«®«‘π‘®©—¬‚¥¬°“√„™â Transcranial Doppler (TCD) ∑”„Àâ∑√“∫¢âÕ¡Ÿ≈∑“ß hemodynamics ‰¥â

2. Noninvasive carotid artery studies ·∫àßÕÕ°‡ªìπ 2 «‘∏°’ “√ §◊Õ indirect ·≈– direct methods „π√–¬–·√°°“√µ√«®«‘π®‘ ©—¬ à«π„À≠à®–‡ªìπ«‘∏°’ “√ indirect ‡™àπ supraorbital Doppler analysis ·≈– ocular plethysmography ´÷Ëß®–„Àâ¢âÕ¡Ÿ≈‡°’Ë¬«°—∫°“√‰À≈‡«’¬π¢Õß‡≈◊Õ¥·≈–§«“¡¥—π „πÀ≈Õ¥‡≈◊Õ¥„µâµÕà carotid stenosis ·µà«∏‘ π’ ¡’È ¢’ Õâ ®”°—¥§◊Õ ‰¡à “¡“√∂µ√«®æ∫§«“¡º‘¥ª°µ‘¢Õß ulcerative lesions ·≈– ·¬°§«“¡·µ°µà“ß√–À«à“ß°“√Õÿ¥µ—πÀ√◊Õµ’∫·§∫∏√√¡¥“°—∫ tight stenosis ‰¥â „π¢≥–∑’Ë direct methods ®–‡æàß‡≈Áß„π°“√‡ÀÁπ ¿“æ¢Õß extracranial carotid arteries (ultrasonic scans) ·≈–∑√“∫∂÷ß§«“¡√ÿπ·√ß„π°“√Õÿ¥µ—π¢ÕßÀ≈Õ¥‡≈◊Õ¥ (continuous pulsed Doppler spectral analysis) ‚¥¬∑—Ë«‰ª·≈â«‡æ◊ËÕ™à«¬„Àâ°“√«‘π‘®©—¬‚√§·≈–¢âÕ¡Ÿ≈ª√–°Õ∫ ·πàπÕπ·≈–·¡àπ¬”¢÷πÈ ®÷ß§«√∑” test ∑—ßÈ Õß«‘∏’ ‡™àπ duplex scan ‡æ◊ÕË ¥Ÿ°“√Õÿ¥µ—π¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß§“‚√µ‘¥ ·≈– OPG-Gee ‡æ◊ËÕ¥Ÿ°“√‰À≈‡«’¬π·≈–§«“¡¥—π¢ÕßÀ≈Õ¥‡≈◊Õ¥„µâµàÕ∫√‘‡«≥∑’Ë Õÿ¥µ—π

NONINVASIVE VASCULAR STUDIES

2.1 Indirect methods «‘∏°’ “√∑’Ë„™â „πªí®®ÿ∫π— ¡’ Transcranial Doppler ·≈– pneumoplethysmography (OPG-Gee) 2.1.1 Ocular pneumoplethysmography (OPG-Gee) §«“¡¥—π„π opthalmic artery ‰¥â ∑”„Àâ∑√“∫∂÷ß¿“«– hemodynamic ¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß§“‚√µ‘¥·≈–ª√–‡¡‘π ‰¥â«“à ¡’°“√µ’∫·§∫À√◊Õ‰¡à (∂â“°“√µ’∫·§∫‡°‘π√âÕ¬≈– 50) ‚¥¬¡’§«“¡·πàπÕπ∂÷ß√âÕ¬≈– 85-95 «‘∏°’ “√ OPG-Gee ßà“¬µàÕ°“√ªØ‘∫—µ‘·≈–°“√·ª√º≈ ·µà®–‰¡à “¡“√∂ µ√«®æ∫æ¬“∏‘ ¿“æ∑’Ë ‰¡àÕ¥ÿ µ—π ·≈–‰¡à “¡“√∂·¬° ulcerative plaques ‰¥â ∫Õ°§«“¡·µ°µà“ß√–À«à“ß severe stenosis °—∫ occlusion ¢Õß internal carotid artery ‰¡à ‰¥â „π°“√«—¥ OPG-Gee ®–µâÕß«“ß plastic cup ∫π lateral sclera ‡æ◊ËÕ monitor §«“¡¥—π ®÷ß‰¡à·π–π” „Àâ∑”„π 1. ºŸªâ «É ¬∑’·Ë æâ¬“™“À¬Õ¥µ“‡©æ“–∑’Ë 2. ¡’ acute À√◊Õ chronic conjunctivitis 3. ¡’ detached retina 4. ‡§¬ºà“µ—¥µ“¿“¬„π 6 ‡¥◊Õπ 5. ‡ªìπ glaucoma ´÷ßË √—°…“¬—ß‰¡à¥æ’ Õ 6. ‰¥â√∫— ∫“¥‡®Á∫∫√‘‡«≥µ“ 7. „ à‡≈π å‡∑’¬¡ 8. ºŸªâ «É ¬∑’Ë ‰¡à „Àâ§«“¡√à«¡¡◊Õ„π°“√µ√«® °“√µ√«® OPG-Gee ∂◊Õ«à“¡’§“à º‘¥ª°µ‘‡¡◊ÕË 1. §«“¡·µ°µà“ß√–À«à“ß ophthalmic artery pressures ∑—ßÈ 2 ¢â“ß‡°‘π 5 ¡‘≈≈‘‡¡µ√ª√Õ∑ 2. „π¢≥–∑’Ë eye pressures ∑—Èß Õß¢â“ß‡∑à“°—π ‡¡◊ËÕ ‡ª√’¬∫‡∑’¬∫ ratio °—∫ brachial artery pressure

67 ·≈â«µË”°«à“ 0.6 (· ¥ß«à“À≈Õ¥‡≈◊Õ¥·¥ß§“‚√µ‘¥ ∑—ßÈ Õß¢â“ßµ’∫·§∫) 3. §à“·µ°µà“ß 1-4 ¡‘≈≈‘‡¡µ√ª√Õ∑‡¡◊ÕË ratio √–À«à“ß opthalmic °—∫ brachial pressure µË”°«à“ 0.66 §à“ OPG ∑’ËµË”Õ“®®–‡π◊ËÕß¡“®“°°“√µ’∫·§∫¢Õß À≈Õ¥‡≈◊Õ¥ à«πÀπ÷Ëß à«π„¥¢Õß carotid artery °Á ‰¥â ‰¡à«“à ®–‡ªìπ intrathoracic origin, carotid bifurcation, carotid siphon À√◊Õµ—« ophthalmic artery ‡Õß 2.1.2 Transcranial Doppler ‡ªìπ noninvasive method «‘∏’„À¡à ‡ªìπ°“√ª√–‡¡‘π√–∫∫‰À≈‡«’¬π‡≈◊Õ¥¿“¬„π ¡Õß TCD ®–°√–®“¬ pulses ¢Õß ultrasound ®“° 2-MHz probe «“ß probes ≈ßµ”·Àπàßµà“ß Ê ¢Õß°√–‚À≈° »’√…–‡æ◊ËÕµâÕß°“√‡¢â“∂÷ßÀ≈Õ¥‡≈◊Õ¥·¥ß„π ¡Õß ‡™àπ internal carotid artery siphon, anterior cerebral artery, middle ·≈– posterior cerebral artery, opthalmic artery ª√–‚¬™πå∑“ß§≈‘π§‘ ¢Õß TCD ¡’¥ß— µàÕ‰ªπ’È 1. ª√–‡¡‘π intracranial collateral patterns ·≈– hemodynamics À≈—ßÕÿ¥µ—π 2. «‘π®‘ ©—¬‚√§À≈Õ¥‡≈◊Õ¥Õÿ¥µ—π„π ¡Õß 3. «‘π®‘ ©—¬ vasospasm ´÷ßË ®–‡°’¬Ë «¢âÕß°—∫ subarachnoid hemorrhage 4. monitor hemodynamic effects À≈—ß®“°√—°…“ AVM 5. ª√–‡¡‘π‡≈◊Õ¥∑’Ë ‰À≈‡«’¬π„π ¡Õß °àÕπ«‘π‘®©—¬«à“ ¡Õßµ“¬ 6. monitor ºŸªâ «É ¬¢≥–ºà“µ—¥·≈–À≈—ßºà“µ—¥

√Ÿª∑’Ë 6.6 Internal carotid artery

Doppler spectrum patterns „π≈— ° …≥–µà “ ß Ê ª°µ‘, µ’∫·§∫‡≈Á°πâÕ¬ ®π µ’∫·§∫¡“°

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥

2.2 Direct methods ª√–°Õ∫¥â«¬ carotid phonoangiography, continuous-wave Doppler velocity wave form analysis, bruit anslysis, Doppler scans ·≈– duplex scanning ‚¥¬√«¡·≈â«∑—ßÈ À¡¥ duplex scan πà“®–‡ªìπ direct method ∑’™Ë «à ¬ª√–‡¡‘π·≈–«‘π®‘ ©—¬‚√§‰¥â¥∑’ ’Ë ¥ÿ 2.2.1 Duplex scanning ‡ªìπ°“√√«¡§ÿ≥ ¡∫—µ¢‘ Õß Bmode ultrasound image system ‡¢â“°—∫ pulsed Doppler detector ®–∑”„Àâ¡Õß‡ÀÁπÀ≈Õ¥‡≈◊Õ¥·≈– plaque ∑”„Àâ ∑ √“∫°“¬«‘ ¿ “§·≈–æ¬“∏‘ ¿“æ¢Õß À≈Õ¥‡≈◊Õ¥ ·≈–¬—ß∑√“∫ velocity patterns ¥â«¬ flow signals ∑’ËÕà“π‰¥â®–∫àß∫Õ°«à“À≈Õ¥‡≈◊Õ¥·¥ß§“‚√µ‘¥ µ’∫·§∫¡“°πâÕ¬‡æ’¬ß„¥ (√Ÿª∑’Ë 6.6) §«“¡‡™◊ÕË ∂◊Õ‰¥â „π °“√«‘π®‘ ©—¬‚√§ Ÿß∂÷ß√âÕ¬≈– 95-97

V. DEEP VENOUS THROMBOSIS (DVT) ®“°ª√–«—µ·‘ ≈–°“√µ√«®√à“ß°“¬ ¢âÕ¡Ÿ≈∑’Ë ‰¥â ‰¡à·πàπÕπ«à“®– «‘π®‘ ©—¬‚√§ DVT ‰¥â ¢“∫«¡·≈–°¥‡®Á∫Õ“®®–¡’ “‡Àµÿ®“°‚√§Õ◊πË venogram ®–™à«¬«‘π‘®©—¬‚√§‰¥â·πàπÕπ·µà°Á‡ªìπ«‘∏’ invasive ºŸâªÉ«¬®–‡ ’Ë¬ßµàÕ°“√·æâ “√∑÷∫· ß∑’Ë©’¥‡¢â“À≈Õ¥‡≈◊Õ¥À√◊Õ‡°‘¥ phlebitis ‰¥â √âÕ¬≈– 50 ¢ÕßºŸªâ «É ¬∑’«Ë π‘ ®‘ ©—¬·µà·√°«à“‡ªìπ DVT ®“° venogram ®–‰¡àæ∫ ‘Ëßº‘¥ª°µ‘ ¥—ßπ—Èπ„π°“√ª√–‡¡‘πºŸâ ªÉ«¬∑’Ë ß —¬«à“®–‡ªìπ DVT ¢—Èπµâπ§«√∑” invasive tests °àÕπæ‘®“√≥“∑” venography

noninvasive venous studies ª√–°Õ∫¥â«¬ impedance plethysmography, Doppler venous auscultation, I125 fibrinogen scanning, radionuclide phlebography ·≈– Doppler ultrasonic imaging 1. Venous plethysmography ¡’§«“¡·πàπÕπ„π°“√ «‘π®‘ ©—¬‚√§ DVT ‰¥â ßŸ ∫√‘‡«≥‡Àπ◊ÕÀ—«‡¢à“ ·≈–µË”∑’πË Õà ß ‡ªìπ ‡§√◊ÕË ß¡◊Õ∑’æË °æ“‰¥âß“à ¬·≈–π”¡“µ√«®ºŸªâ «É ¬¢â“ß‡µ’¬ß‰¥â plethysmography ∑’Ë „™â¡À’ ≈“¬«‘∏°’ “√ ‡™àπ impedance, mercury strain guage ·≈– volume displacement ª√–¡“≥√âÕ¬≈– 80 ‡≈◊Õ¥¢Õß¢“®–Õ¬Ÿà „πÀ≈Õ¥‡≈◊Õ¥¥” «‘∏’ °“√¢Õß plethysmography „π°“√µ√«® venous obstruction ®“° DVT ∂◊ÕÀ≈—°°“√«à“ ‡¡◊ÕË ¡’°“√Õÿ¥µ—π¢ÕßÀ≈Õ¥‡≈◊Õ¥¥”≈÷° ®–¡’°“√‡ª≈’Ë¬π·ª≈ß¢Õß venous resistance ·≈– outflow ´÷ßË µ√«®æ∫‰¥â®“° plethysmography „π°√≥’ª°µ‘ venous plethysmograph ¢Õß¢“®–§àÕ¬ Ê ‡æ‘¡Ë À≈—ß®“°√—¥¢“¥â«¬ pressure cuff ‚¥¬‡æ‘¡Ë §«“¡¥—π‡ªìπ 45-50 ¡‘≈≈‘‡¡µ√ª√Õ∑ π“π 45 «‘π“∑’ À≈—ß®“°π—πÈ ª≈àÕ¬ cuff tracing ®–§àÕ¬ Ê ≈¥≈ß¡“®π∂÷ß√–¥—∫ª°µ‘ ·π«√“∫¢Õß calf volume À≈—ß inflate cuff ‡√’¬°«à“ venous capacitance (VC) (√Ÿª∑’Ë 6.7) ”À√—∫ª√‘¡“µ√∑’≈Ë ¥≈ß„π«‘π“∑’·√°À≈—ß®“° deflate cuff ‡√’¬° «à“ maximum venous outflow (MVO) ‚¥¬°“√ plot °√“ø √–À«à“ß VC °—∫ MVO °Á®–æÕ∑√“∫‰¥â«à“ deep vein ª°µ‘ À√◊Õ¡’°“√Õÿ¥µ—π

√Ÿª∑’Ë 6.7 A. „Àâ°√–· ‰øøÑ“∑’Ë¡’ high-frequency ·≈– low-in tensity ‰À≈ºà“π√à“ß°“¬√–À«à“ß 2 outer electrodes À≈—ß®“°π—Èπ«—¥§à“ voltage ∑’Ë‡ª≈’Ë¬π·ª≈ß√–À«à“ß 2 inner electrodes thigh cuff ®–„™â ”À√—∫À¬ÿ¥ °“√‰À≈‡«’¬π¢ÕßÀ≈Õ¥‡≈◊Õ¥¥”¢≥–æÕß≈¡ B. IPG tracing ®“°¢“¢«“∑’Ëª°µ‘ (∫π) ·≈–∑’Ëº‘¥ª°µ‘®“°À≈Õ¥‡≈◊Õ¥¥”Õÿ¥µ—π (DVT) (≈à“ß)

NONINVASIVE VASCULAR STUDIES

¢≥–µ√«®§«√„ÀâºªŸâ «É ¬πÕπ¬°¢“¢÷πÈ ‡≈Á°πâÕ¬ ‡æ◊ÕË ≈¥§«“¡ ·µ°µà“ß¢Õß venous pooling °“√∑” external rotation ¢Õß¢“™à«¬„Àâ°≈â“¡‡π◊ÈÕÀ¬àÕπ‡¢à“ßÕ‡≈Á°πâÕ¬ ªÑÕß°—π‰¡à „Àâ¡’°“√ °¥∑—∫¢Õß popliteal vein. ¢âÕ®”°—¥¢Õß plethysmography §◊Õ ‰¡à “¡“√∂µ√«®æ∫ §«“¡º‘ ¥ ª°µ‘ ¢ ÕßÀ≈Õ¥‡≈◊ Õ ¥¥”∑’Ë πà Õ ß À√◊ Õ À≈Õ¥‡≈◊ Õ ¥¥” µ”·Àπàß Ÿß¢÷πÈ ‰ª°«à“π’∂È “â ‰¡à¡°’ “√Õÿ¥µ—π·≈–‰¡à “¡“√∂·¬° acute ÕÕ°®“° chronic occlusion ‰¥â Õ“®®–·ª√º≈‰¥âº‘¥æ≈“¥ ‡ªìπº≈∫«°ª≈Õ¡ „πºŸâªÉ«¬Õ—¡æ“µµâÕßπÕππ“π, µ—Èß§√√¿å „π ™à«ß∑â“¬, À—«„®«“¬, Õâ«π¡“°, „™â‡§√◊ËÕß™à«¬À“¬„® À√◊ÕÀ≈—ß °“√ºà“µ—¥„À≠à 2. Duplex venous ultrasonography ‡ªìπ°“√µ√«® «‘π®‘ ©—¬ ”§—≠¢Õß noninvasive test „π°“√∫Õ°µ”·Àπàß∑’¡Ë ’ °“√Õÿ¥µ—π¢Õß thrombi „πÀ≈Õ¥‡≈◊Õ¥¥”µ”·Àπàßµà“ß Ê ∑—Ë« √à“ß°“¬ ‡™àπ vena cava, jugular, portal veins ·≈–À≈Õ¥ ‡≈◊Õ¥¥”∑’¢Ë “ ∫√‘‡«≥ common femoral ·≈– popliteal veins ®–¡Õß‡ÀÁπ«à“¡’ intraluminal soft tissue mass À√◊Õ‰¡à ·≈–¥Ÿ «à“°¥·≈â«·∫π√“∫À√◊ÕµÕ∫ πÕßµàÕ valsalva maneuver À√◊Õ ‰¡à ∂â“¡’ thrombus Õ¬Ÿ®à –°¥ femoral ·≈– popliteal veins ‰¡à·ø∫ ∂â“¡’°“√Õÿ¥µ—π¢Õß common femoral vein ‡°‘¥¢÷πÈ collaterals ∑’¡Ë ®’ –‰¡à‡æ’¬ßæÕ„π°“√µÕ∫ πÕßµàÕ valsalva maneuver ´÷Ëß„π°√≥’ª°µ‘∑’Ë¡’ competent iliofemoral valves ®–µÕ∫ πÕß‚¥¬°“√À¬ÿ¥ femoral flow venous duplex ‡ªìπ«‘∏’°“√µ√«®«‘π‘®©—¬ DVT À≈Õ¥ ‡≈◊Õ¥¥” à«πµâπ¢“‰¥â·¡àπ¬”·≈–‡™◊ËÕ∂◊Õ‰¥â√âÕ¬≈– 95-98 º≈ °“√µ√«®‰¡à·πàπÕπ ”À√—∫À≈Õ¥‡≈◊Õ¥¥”∑’πË Õà ß ∂â“ noninvasive tests ª°µ‘„π°“√µ√«®À“ DVT ·≈– Õ“°“√∑“ß§≈‘π§‘ ‰¡à‡¥àπ™—¥ ‰¡à§«√∑” venography ¥â«¬‡Àµÿº≈ «à“ºŸªâ «É ¬¢“∫«¡·≈–ª«¥ ·µà∂“â ¡’Õ“°“√∑“ß§≈‘π§‘ ∫àß∫Õ°§«√∑” venography ·µà‡¡◊ËÕπàÕß·≈–µâπ¢“∫«¡√à«¡°—∫º≈∫«°¢Õß noninvasive tests «à“‡ªìπ iliofemoral venous thrombosis §«√¥”‡π‘π°“√√—°…“ DVT ‰¥â ‚¥¬°“√„Àâ anticoagulants ‚¥¬ ‰¡àµÕâ ß∑” venography

√ÿª „π™à«ß 20 ªï°àÕπ ·π«∑“ß„π°“√√—°…“‚√§À≈Õ¥‡≈◊Õ¥ ª√–°Õ∫¥â « ¬°“√´— ° ª√–«— µ‘ · ≈–µ√«®√à “ ß°“¬Õ¬à “ ß≈–‡Õ’ ¬ ¥ À≈—ß®“°π—πÈ °“√µ√«®«‘π®‘ ©—¬À≈—°§◊Õ °“√∑” angiography ·≈– venography ‡æ◊ËÕ„Àâ ‰¥â°“√«‘π‘®©—¬‚√§Õ¬à“ß∂Ÿ°µâÕß ‡æ◊ËÕ∑’Ë®– ∑”°“√√—°…“·≈–æ¬“°√≥å ‚√§µàÕ‰ª °“√µ√«®«‘π®‘ ©—¬∑—ßÈ Õß«‘∏’ ∂◊Õ‡ªìπ invasive methods ®–µâÕß Õ¥ “¬ «π‡¢â“À≈Õ¥‡≈◊Õ¥ ·≈–©’¥ “√∑÷∫· ß°àÕπ©“¬¿“æ√—ß ’ ∑”„Àâ¡’§«“¡‡ ’Ë¬ßµàÕ¿“«– ·∑√°´âÕπ∑’®Ë –‡°‘¥¢÷πÈ ‡™àπ ·æâ “√∑÷∫· ß, ‰µ«“¬, ∫“¥‡®Á∫µàÕ À≈Õ¥‡≈◊Õ¥ œ≈œ ·≈–ºŸâªÉ«¬®”π«π‰¡àπâÕ¬∑’Ë ‰¡à®”‡ªìπµâÕß°“√ ºà“µ—¥√—°…“À√◊Õ∑”À—µ∂°“√Õ◊πË ‡™àπ angioplasty À√◊Õ thrombolytic therapy ™à«ß 20 ªï∑’Ëºà“π¡“‰¥â¡’«‘«—≤π“°“√„π°“√µ√«®«‘π‘®©—¬‚√§ ∑“ßÀ≈Õ¥‡≈◊Õ¥À≈“¬«‘∏’ ‡ªìπ noninvasive methods ∑’Ë ‰¡àµÕâ ß √ÿ°≈È”‡¢â“ Ÿ√à “à ß°“¬ºŸªâ «É ¬ ‰¡àµÕâ ß‡ ’¬Ë ßµàÕ¿“«–·∑√°´âÕπµà“ß Ê ∑’Ë®–‡°‘¥¢÷Èπ ‡ªìπ ‘Ëß∑’Ë¡“‡™◊ËÕ¡√Õ¬µàÕ√–À«à“ß°“√´—°ª√–«—µ‘·≈– °“√µ√«®√à“ß°“¬°—∫ invasive methods æÕ¥’ noninvasive tests ∫“ß™π‘¥‡™àπ duplex scanning πÕ°®“°¡Õß‡ÀÁπ¿“æ ‡ÀÁπ√Õ¬‚√§¢ÕßÀ≈Õ¥‡≈◊Õ¥·≈â« ¬—ß∫Õ° hemodynamics ·≈– velocity of flow ‰¥â¥«â ¬ ∑”„Àâª√–‡¡‘πºŸªâ «É ¬·≈–æ¬“°√≥å ‚√§ ‰¥âÕ¬à“ß·¡àπ¬” ºŸªâ «É ¬®”π«πÀπ÷ßË ‰¡à®”‡ªìπµâÕß∑” angiography À√◊Õ venography ‡æ◊ÕË ºà“µ—¥√—°…“ ºŸâªÉ«¬‡À≈à“π’È√—°…“‚¥¬°“√§«∫§ÿ¡ªí®®—¬‡ ’Ë¬ß √—°…“·∫∫ ª√–§—∫ª√–§Õß·≈–„Àâ¬“ “¡“√∂µ‘¥µ“¡¥Ÿ·≈Õ“°“√‰¥â®“° invasive tests πÕ°®“°π’È·≈â« noninvasive tests ®–‡ªìπ µ—«·ª√„π°“√æ‘®“√≥“µ√«®·≈–«‘π®‘ ©—¬·∫∫ invasive tests µàÕ‰ª «‘∏°’ “√µ√«®«‘π®‘ ©—¬ ‡™àπ magnetic resonance angiography (MRA), Spiral CT scanning, plethysmography, duplex scanning œ≈œ °”≈—ß¡’∫∑∫“∑„π°“√µ√«®«‘π®‘ ©—¬‚√§∑“ßÀ≈Õ¥‡≈◊Õ¥ ∫“ß°√≥’Õ“®®–∑¥·∑π invasive disease ·≈–æ‘®“√≥“ºà“µ—¥ √—°…“ ·æ∑¬åºŸâ‡°’Ë¬«¢âÕß°—∫‚√§À≈Õ¥‡≈◊Õ¥®÷ß§«√»÷°…“À≈—°°“√ «‘∏°’ “√„™â‡§√◊ÕË ß¡◊Õ ·≈–°“√·ª√º≈

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥

‡Õ° “√Õâ“ßÕ‘ß 1. Baker JD. The vascular laboratory. In: Moore WS, ed. Vascular Surgery: A Comprehensive Review. 4th ed. Philadelphia: WB Saunders, 1991;168-85. 2. Fronek A. Noninvasive Diagnostics in Vascular Disease. New York: McGraw-Hill, 1989. 3. Kempzinski KE, Yao JST (eds). Practical Noninvasive Vascular Diagnosis, 2nd ed. Chicago: Year Book, 1987. 4. Zwiebel WJ (ed.). Introduction to Vascular Ultrasonography. 3rd ed. Philadelphia: WB Saunders, 1992.

5. Strandness DE. Duplex Scanning in Vascular Disorders. New York: Raven Press, 1990. 6. Sumner DS. Noninvasive assessment of peripheral arterial occlusive disease. In:Rutherford RB. ed. 3rd ed. Philadelphia: WB Saunders, 1989;61-111. 7. Sumner DS. Objective diagnostic techniques: Role of vascular lab. In: Rutherford RB, ed. 3rd ed. Philadelphia: WB Saunders, 1989;4160.

∫∑∑’Ë 7 °“√µ√«®«‘π®‘ ©—¬ ∑“ß√—ß ’«∑‘ ¬“·≈–√—ß ’√«à ¡√—°…“ °“√µ√«®«‘π‘®©—¬∑“ß√—ß ’«‘∑¬“π—∫«à“‡ªìπ à«π∑’Ë®”‡ªìπ¡“° „π°“√ª√–‡¡‘π·≈–«“ß·ºπ√—°…“ºŸâªÉ«¬‚√§À≈Õ¥‡≈◊Õ¥∑’Ë®–µâÕß ºà“µ—¥√—°…“µàÕ‰ª «‘∏°’ “√µ√«®«‘π®‘ ©—¬∑“ß√—ß ’«∑‘ ¬“„πªí®®ÿ∫π— ¡’ arteriography, venography, ultrasonography (US), computed tomography (CT), digital subtraction angiography (DSA), magnetic resonance imaging (MRI), positron emission tomography (PET) ·≈– angioscopy √—ß ’·æ∑¬åπÕ°®“°®–¡’ ∫∑∫“∑„π°“√µ√«®«‘π®‘ ©—¬·≈â«¬—ß¡’∫∑∫“∑„π√—ß ’√«à ¡√—°…“ (radiological intervention) ¥â«¬ ‡™àπ °“√¢¬“¬∂à“ß (percutaneous angioplasty À√◊Õ PTA) embolization À√◊Õ„Àâ¬“≈–≈“¬ ≈‘¡Ë ‡≈◊Õ¥ (thrombolytic therapy) »—≈¬·æ∑¬å·≈–ºŸâ∑’Ë‡°’Ë¬«¢âÕß¥Ÿ·≈ºŸâªÉ«¬§«√∑√“∫∂÷ß¢âÕ∫àß™’È, ¢âÕ®”°—¥, §«“¡‡ ’Ë¬ß·≈–«‘∏’°“√√—°…“¿“«–·∑√°´âÕπ ∑’ËÕ“®®– ‡°‘¥¢÷πÈ ¿“¬À≈—ßÀ—µ∂°“√¥—ß°≈à“«

I. ARTERIOGRAPHY „π°“√ª√–‡¡‘πºŸâªÉ«¬‚√§À≈Õ¥‡≈◊Õ¥ ª√–«—µ‘·≈–°“√µ√«® √à“ß°“¬®– “¡“√∂ª√–‡¡‘π√–¥—∫°“√µ’∫µ—π §«“¡√ÿπ·√ß ·≈– µ”·Àπàß¢Õß atherosclerosis ‰¥â§√à“« Ê noninvasive test ®–™à«¬„Àâ°“√«‘π®‘ ©—¬‚√§·πàπÕπ¢÷πÈ arteriography ´÷ßË ‡ªìπ invasive diagnostic procedures ‡ªìπÀ—µ∂°“√∑’Ë®”‡ªìπ„π°“√ µ√«®«‘π®‘ ©—¬ºŸªâ «É ¬∑’§Ë “¥«à“®–√—°…“‚¥¬°“√ºà“µ—¥ „πªí®®ÿ∫π— ∑’„Ë ™â

πâÕ¬≈ß‡π◊ËÕß®“°¡’¿“«–·∑√°´âÕπ ·≈– noninvasive test À≈“¬™π‘¥¡’ª√– ‘∑∏‘¿“æ„π°“√«‘π®‘ ©—¬‚√§‰¥â „°≈â‡§’¬ß°—π°—∫ arteriography(1) √—ß ’√«à ¡√—°…“¢—πÈ µÕπµàÕ‰ª¿“¬À≈—ß arteriography Õ“®®–‡ªìπ·§àÀ—µ∂°“√‡≈Á° Ê ‡∑à“π—Èπ ‡™àπ °“√¢¬“¬∂à“ß À≈Õ¥‡≈◊Õ¥ (PTA), atherectomy À√◊Õ°“√„Àâ “√≈–≈“¬≈‘¡Ë ‡≈◊Õ¥ °“√∑” arteriography ®–¡’º≈‡ª≈’Ë¬π·ª≈ß°“√‰À≈‡«’¬π¢Õß ‡≈◊Õ¥¢≥–©’¥ “√∑÷∫· ß·≈–©“¬¿“æ√—ß ’¢ÕßÀ≈Õ¥‡≈◊Õ¥∑’Ë∑Õ¥ ºà“π §ÿ≥¿“æ·≈–§«“¡‡À¡“– ¡„π°“√∑” arteriography ¢÷πÈ Õ¬Ÿ°à ∫— µ—«·ª√À≈“¬™π‘¥§◊Õ °“√‡≈◊Õ°„™â “√∑÷∫· ß °“√®—¥∑à“ºŸâ ªÉ«¬‡«≈“∂à“¬¿“æ·≈–°“√ Õ¥ “¬ «πºà“πº‘«Àπ—ß ‡¢â“À≈Õ¥ ‡≈◊Õ¥·¥ßµ”·Àπàß∑’ËµâÕß°“√ §«√‡≈◊Õ°ª√‘¡“≥ “√∑÷∫· ß Õ—µ√“°“√©’¥·≈–§«“¡‡√Á«¢Õß¿“æ√—ß ’∑∂’Ë “à ¬‡ªìπ√–¬– ‡æ◊ÕË „Àâ ‰¥â º≈ arteriography ¥’∑’Ë ÿ¥ °àÕπ∑”À—µ∂°“√§«√¡’ check list ¥—ßµàÕ‰ªπ’È (µ“√“ß∑’Ë 7.1) “√∑÷∫· ß (contrast media) ∑’Ë„™â „πªí®®ÿ∫π— §◊Õ‡°≈◊Õ‚´‡¥’¬¡ À√◊Õ methylglucamine ¢Õß methylglucamine ¢Õß triiodo2,4,6-benzoic acid ‡π◊ÕË ß®“° “√π’¡È ’ osmolarity Ÿß°«à“‡≈◊Õ¥ ‡«≈“©’¥‡¢â“‡ âπÀ≈Õ¥‡≈◊Õ¥®–¢¬“¬µ—«·≈–¡’§«“¡√Ÿâ ÷°ª«¥· ∫ ª«¥√âÕπ “√π’¢È ∫— ∂à“¬ÕÕ°®“°√à“ß°“¬∑“ß‰µ À≈—ß©’¥ ’‡≈◊Õ¥‰ª ‡≈’È¬ß‰µ≈¥πâÕ¬≈ß™—Ë«¢≥– °“√∑”ß“π¢Õß‰µ®–∫°æ√àÕß™—Ë«¢≥– ®÷ß§«√√–¡—¥√–«—ß„π°“√„™â°∫— ºŸªâ «É ¬‚√§‰µ proteinuria, ‡∫“À«“π ·≈–ºŸâ∑’Ë¢“¥ “√πÈ”„π√à“ß°“¬ ∂â“À≈—ß©’¥·≈â«ªí “«–≈¥≈ß ·°â ‰¢‰¥â ‚¥¬°“√„Àâ “√πÈ”‡¢â“∑“ßÀ≈Õ¥‡≈◊Õ¥¥” ‰µ®–°≈—∫¡“

72 ∑”ß“πµ“¡ª°µ‘¿“¬„π 1 —ª¥“Àå °“√©’¥ “√∑÷∫· ß∑”„Àâ‡°‘¥ Õ“°“√·æâ ‰¥â√Õâ ¬≈– 2-5 ¢ÕßºŸªâ «É ¬∑—ßÈ À¡¥ Õ“°“√∑’æË ∫∫àÕ¬§◊Õ ¡’º◊Ëπ§—π ∂â“√ÿπ·√ß®–‡°‘¥ anaphylactic shock, ™’æ®√™â“, À“¬„®ÀÕ∫¡’‡ ’¬ß wheeze ·≈–∂÷ß·°à°√√¡‰¥â ∂â“¡’ª√–«—µ‘·æâ “√∑÷∫· ß¡“°àÕπ°“√∑” arteriogram §√—ßÈ À≈—ßµàÕ¡“æ÷ß√–«—ß ∂â“¡’§«“¡®”‡ªìπµâÕß∑”®√‘ß Ê §«√‡µ√’¬¡≈à«ßÀπâ“‚¥¬°“√©’¥ steriod ·≈–„Àâ¬“ diphenylhydramine °àÕπ¥—ßπ’È „Àâ prednisolone 50 ¡‘≈≈‘°√—¡∑“ßÀ≈Õ¥‡≈◊Õ¥¥”∑ÿ° 6 ™—«Ë ‚¡ß°àÕπ∑” arteriogram „Àâ√∫— ª√–∑“π diphenylhydramine 1 ™—«Ë ‚¡ß°àÕπ∑” arteriogram(2) “√∑÷∫· ßµ—«„À¡à∑Õ’Ë “®®–π”¡“„™â „πÕπ“§µ§◊Õ Iopamidol ·≈– Iohexol ‡ªìπ nonionic monomer ¡’ osmolarity µË” °«à“‡≈◊Õ¥‡«≈“©’¥‡¢â“‡ âπ®–‰¡àª«¥· ∫ª«¥√âÕπ ·µà√“§“¬—ß Ÿß¡“° °“√·∑ß‡ âπ Õ¥ “¬ «π «‘∏’°“√ ¡—¬‡√‘Ë¡·√°¢Õß°“√∑” arteriography §◊Õ ·∑ß‡¢Á¡ºà“π‡¢â“À≈Õ¥‡≈◊Õ¥‚¥¬µ√ß ·≈â« ©’¥ “√∑÷∫· ß µàÕ¡“‰¥â „™â«∏‘ ’ Õ¥ “¬ «π·∑π “¬ «π∑’Ë „™â®– ¡’·∂∫æ≈“ µ‘°´÷Ëß¡Õß‡ÀÁπ‰¥â®“°°“√©“¬¿“æ√—ß ’ª≈“¬ “¬ «ππÿà¡‚§âßßÕ‰¥â¡’Õ—πµ√“¬πâÕ¬µàÕÀ≈Õ¥‡≈◊Õ¥ «‘∏’°“√¡“µ√∞“π ∑’Ë„™â „πªí®®ÿ∫π— §◊Õ Seldinger technique ·∑ß‡¢Á¡∑’¡Ë √’ ¢Ÿ π“¥‚µ ·≈â« Õ¥ “¬ «πºà“π√Ÿ‡¢Á¡‡¢â“ ŸàÀ≈Õ¥‡≈◊Õ¥µ”·Àπàß∑’ËµâÕß°“√ µ”·Àπà ß ¢ÕßÀ≈Õ¥‡≈◊ Õ ¥∑’Ë “¡“√∂ Õ¥ “¬ «πºà “ π‰¥â §◊ Õ À≈Õ¥‡≈◊Õ¥∑’§Ë ≈”™’æ®√‰¥â ·≈–Õ¬Ÿµà π◊È ®“°º‘«Àπ—ß ‡™àπ femoral “¡“√∂ «π‡¢â“‰ª‰¥â∂ß÷ À≈Õ¥‡≈◊Õ¥ carotid, ·¢π, aorta ·≈– Õ«—¬«–¿“¬„π™àÕß∑âÕß ºŸªâ «É ¬ aortoiliac occlusive disease

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥ (AIOD) ‰¡à “¡“√∂ Õ¥ “¬ «πºà“πÀ≈Õ¥‡≈◊Õ¥·¥ß femoral ‰¥â “¡“√∂ºà“π‡¢â“‰¥â∑“ß brachial À√◊Õ axillary «‘∏°’ “√·∑ß‡¢Á¡ Õ¥ “¬‡¢â“ aorta ºà“π∑“ß lumbar ªí®®ÿ∫π— ‰¡à ‰¥â „™â ∂â“µâÕß °“√¥ŸÀ≈Õ¥‡≈◊Õ¥À—«„®‚§‚√π“√’Ë “¡“√∂ Õ¥ “¬ «πºà“π∑“ß À≈Õ¥‡≈◊Õ¥·¥ß brachial ‰¥â “¬ «π∑’Ë „™â¡’À≈“¬√Ÿª·∫∫À≈“¬≈—°…≥– Õ“®®–¡’√Ÿª√à“ß ‚§âßßÕ À—°ª≈“¬‡ªìπµ–¢Õ “¡“√∂∫—ß§—∫∑‘»∑“ß·≈–°“√‚§âßßÕ ‰¥âµ“¡µâÕß°“√ „Àâ‡¢â“∂÷ßÀ≈Õ¥‡≈◊Õ¥„πµ”·Àπàßµà“ß Ê ·≈â«©’¥ ’ ‡ªìπ highly selective catheterization √«¡∑—Èß “¡“√∂∑” À—µ∂°“√∑“ß√—ß ’√«à ¡√—°…“‰¥â ‡™àπ °“√„Àâ¬“≈–≈“¬≈‘¡Ë ‡≈◊Õ¥ À√◊Õ embolization °“√¥Ÿ·≈ºŸªâ «É ¬À≈—ß∑” arteriogram À≈—ß©’¥ ’·≈â«§«√‡ΩÑ“ — ß ‡°µÿ ¥Ÿ Õ “°“√Õ¬à “ ß„°≈â ™‘ ¥ ∑ÿ ° ™—Ë « ‚¡ßÕ¬à“ßπâÕ¬ 6 ™—Ë«‚¡ß ‡æ√“–¿“«–·∑√°´âÕπ∑’Ë‡°‘¥¢÷Èπ à«π„À≠à¡—°®–‡°‘¥¢÷Èπ„π™à«ßπ’È °“√µ√«®√à“ß°“¬ºŸªâ «É ¬§«√¥Ÿ≈°— …≥–∑—«Ë ‰ª·≈– mental status (‚¥¬‡©æ“–∂â“‡ªìπ°“√©’¥ ’¥ŸÀ≈Õ¥‡≈◊Õ¥∑’Ë§Õ·≈– ¡Õß) ™’æ®√ §«“¡¥—π‚≈À‘µ ¥Ÿ∫√‘‡«≥∑’Ë·∑ß‡ âπ §≈”™’æ®√·¢π¢“ ¥Ÿ√–¥—∫ Œ’¡“‚µ§√‘µ·≈–°“√‡ ’¬‡≈◊Õ¥∂â“¡’ √–¬– 12-24 ™—Ë«‚¡ßÀ≈—ß À—µ∂°“√®–µâÕß·πà „®«à“√à“ß°“¬ºŸâªÉ«¬‰¡à·ÀâßÀ√◊Õ¢“¥ “√πÈ” ‡æ√“– “√∑÷∫· ß∑’Ë©’¥‡¢â“‰ª®–¡’ƒ∑∏‘Ï§≈â“¬¬“ªí “«–¢—∫ “√ πÈ”ÕÕ°®“°√à“ß°“¬ ·≈–¡’æ‘…µàÕ‰µ¥â«¬ ®–µâÕß√–«—ß„πºŸâªÉ«¬∑’Ë ¡’°“√∑”ß“π¢Õß‰µº‘¥ª°µ‘ ·≈–‡ªìπ‡∫“À«“πÕ¬Ÿà·≈â« §«√„Àâ “√πÈ”∑“ßÀ≈Õ¥‡≈◊Õ¥¥” 4-6 ™—«Ë ‚¡ß„Àâ·πà„®«à“ºŸªâ «É ¬‰¡à¢“¥ “√πÈ”

µ“√“ß∑’Ë 7.1 Preangiography Check list °àÕπÕ◊πË §«√Õ∏‘∫“¬§«“¡®”‡ªìπ «—µ∂ÿª√– ß§å ¢âÕ∫àß™’È „π°“√µ√«® §«“¡‡ ’¬Ë ß·≈–¿“«–·∑√°´âÕπ∑’ÕË “®®–‡°‘¥¢÷πÈ °“√´—°ª√–«—µ·‘ ≈–µ√«®√à“ß°“¬ µ√«®√à“ß°“¬√–∫∫‰À≈‡«’¬π‡≈◊Õ¥ ·≈–√–∫∫ª√– “∑Õ¬à“ß≈–‡Õ’¬¥∫—π∑÷°‰«â∂“â ‡°‘¥¿“«–·∑√°´âÕπÀ√◊Õ§«“¡º‘¥ª°µ‘À≈—ß®“°À—µ∂°“√®–‰¥â ∫—π∑÷°·≈–‡ª√’¬∫‡∑’¬∫‰¥â ´—°ª√–«—µ„‘ πÕ¥’µ‡°’¬Ë «°—∫°“√·æâ¬“ ·æâ “√∑÷∫· ß ·≈–‰Õ‚Õ¥’π ¢≥–µ√«®«‘π®‘ ©—¬∑“ß√—ß ’«∑‘ ¬“ 1. ª√–«—µ°‘ “√·æâ “√∑÷∫√—ß ’„π°“√∑” arteriography ·≈–°“√µ√«®«‘π®‘ ©—¬‚√§∑“ß√—ß ’«∑‘ ¬“™π‘¥Õ◊πË Ê °àÕπÀπâ“π’È 2. ª√–«—µ‚‘ √§‰µ °“√∑”ß“π¢Õß‰µº‘¥ª°µ‘À√◊Õ‰µ«“¬ §«√µ√«®¥Ÿ√–¥—∫¢Õß BUN, Cr 3. ª√–«—µ‡‘ ∫“À«“π 4. ‡§¬‡ªìπ‚√§À—«„®¢“¥‡≈◊Õ¥¿“¬„π√–¬–‡«≈“ 3-6 ‡¥◊Õπ°àÕπ 5. §«“¡¥—π‚≈À‘µ Ÿß 6. °≈‰°°“√·¢Áßµ—«¢Õß‡≈◊Õ¥º‘¥ª°µ‘ °“√µ√«®§âπ∑“ßÀâÕßªØ‘∫µ— °‘ “√ §«√µ√«®¥Ÿ°“√∑”ß“π¢Õß‰µ ·≈–√–∫∫°“√·¢Áßµ—«¢ÕßÀ≈Õ¥‡≈◊Õ¥ ¥Ÿ√–¥—∫Œ’‚¡‚°≈∫‘π Œ’¡“‚µ§√‘µ ·≈–‡°√Á¥ ‡≈◊Õ¥ ∂â“µâÕß°“√≈–≈“¬≈‘¡Ë ‡≈◊Õ¥ §«√µ√«®¥Ÿ°“√∑”ß“π¢Õß√–∫∫ fibrinolytic ‡™àπ (fibrinogram ·≈– fibrin degradation products) „∫¬‘π¬Õ¡√—°…“·≈–∑”À—µ∂°“√ Õ∏‘∫“¬∂÷ß«‘∏°’ “√∑”À—µ∂°“√ §«“¡‡À¡“– ¡ ·≈–Õ—πµ√“¬∑’ÕË “®®–‡°‘¥¢÷πÈ ‰¥â °“√‡µ√’¬¡º‘«Àπ—ß ∫√‘‡«≥∑’®Ë –·∑ß‡ âπ Õ¥ “¬ §«√ –Õ“¥·≈–ª√“»®“°‡™◊ÕÈ øÕ°º‘«Àπ—ß„Àâ –Õ“¥¥â«¬ π”¬“ Povidone iodine ·≈– Chlorhexidine

°“√µ√«®«‘π‘®©—¬∑“ß√—ß ’«‘∑¬“·≈–√—ß ’√à«¡√—°…“ ¿“«–·∑√°´âÕπ ·∫àßÕÕ°‰¥â‡ªìπ 2 °≈ÿ¡à §◊Õ °≈ÿ¡à ·√°‡ªìπ ¿“«–·∑√°´âÕπ®“°°“√©’¥ “√∑÷∫· ß °≈ÿà¡∑’Ë Õß§◊Õ¿“«– ·∑√°´âÕπ®“°°“√·∑ß‡ âπ·≈–À≈Õ¥§“ “¬ «π ¿“«–·∑√°´âÕπ®“°°“√©’¥ “√∑÷∫· ß(2) 1. ªØ‘°√‘ ¬‘ “°“√·æâ (allergic reaction) æ∫‰¥âª√–¡“≥√âÕ¬ ≈– 5 ∂â“©’¥ “√∑÷∫· ß„π√–¥—∫§«“¡‡¢â¡¢âπ 1:16,000 ∂÷ß 1:117,000 2. ‡ªìπæ‘…µàÕ‰µ (nephrotoxicity) ‡π◊ÕË ß®“° “√∑÷∫· ß¡’ osmolarity Ÿß°«à“‡≈◊Õ¥ ´÷ßË ¡’ƒ∑∏‘§Ï ≈â“¬¬“¢—∫ªí “«– °≈‰°„π°“√∑”≈“¬‡π◊È Õ ‰µ¬— ß ‰¡à ∑ √“∫·πà π ÕπÕ“®®– ‡°’Ë¬«¢âÕß°—∫ª√‘¡“≥¢Õß¬“∑’Ë „Àâ§«“¡‡¢â¡¢âπ·≈–√–¬– ‡«≈“„π°“√©’¥ ºŸâªÉ«¬∑’Ë¡’§«“¡∫°æ√àÕß¢Õß‰µÕ¬Ÿà°àÕπ ·≈â«‡ªìπ‡∫“À«“π proteinuria À√◊Õ√à“ß°“¬¢“¥ “√πÈ” ‚Õ°“ ‡°‘¥¿“«–‰µ«“¬¡’‰¥â ßŸ ®–µâÕßªÑÕß°—π‚¥¬°“√„Àâ “√πÈ”‡¢â“∑“ßÀ≈Õ¥‡≈◊Õ¥¥”Õ¬à“ß‡æ’¬ßæÕ 3. æ‘…µàÕ√–∫∫À—«„®À≈Õ¥‡≈◊Õ¥·≈–°“√À“¬„® ‡π◊ÕË ß®“° “√ ∑÷ ∫ · ß¡’ §ÿ ≥ ¡∫— µ‘ ¢ ¬“¬À≈Õ¥‡≈◊ Õ ¥ ·≈–°¥°“√ ∑”ß“π¢ÕßÀ—«„® ∂â“©’¥Õ¬à“ßµàÕ‡π◊ËÕßÕ“®®–∑”„Àâ§«“¡ ¥—π‚≈À‘µµË” À—«„®¢“¥‡≈◊Õ¥ ·≈– cerobrovascular accident (CVA) ºŸâªÉ«¬ pheochromocytoma ®–‡°‘¥ hypertensive crisis ∑—π∑’À≈—ß©’¥ ’ ∫“ß√“¬®–‡°‘¥ pulmonary edema 4. æ‘…µàÕ√–∫∫ª√– “∑ ‚¥¬®–‡ª≈’¬Ë π·ª≈ß blood brain barrier À≈—ß°“√©’¥ “√∑÷∫· ß‡¢â“À≈Õ¥‡≈◊Õ¥·¥ß ‚¥¬µ√ß ºŸªâ «É ¬Õ“®®–™—° ¡’Õ¡— æ“µ§√÷ßË ´’° cortical blindness À√◊Õ§«“¡º‘¥ª°µ‘∑“ß√–∫∫ª√– “∑Õ◊πË Ê ¿“«–·∑√°´âÕπ®“°°“√·∑ß‡ âπ·≈– Õ¥§“ “¬ «π (mechanical complications) µ√ß∫√‘‡«≥∑’·Ë ∑ß‡ âπ§◊Õ ¡’°“√µ°‡≈◊Õ¥ ¡“° thrombosis, pseudoaneurysm ·≈– arteriovenous fistula ´÷Ëßæ∫‰¥â 0.5-1% ¿“«–·∑√°´âÕπ‡À≈à“π’È¡—°®–‡°‘¥¢÷Èπ ¿“¬„π™à«ß 6 ™—«Ë ‚¡ß·√°À≈—ß∑”À—µ∂°“√ ∂â“µ√«®æ∫§«√√’∫·°â ‰¢ °“√ Õ¥ “¬ «πºà“πÀ≈Õ¥‡≈◊Õ¥·¥ß brachial æ∫«à“‡°‘¥ thrombosis ‰¥â∫àÕ¬∑’Ë ÿ¥ ∂â“À≈Õ¥‡≈◊Õ¥·¥ß axillary ·µ°À≈—ß Õ¥ “¬·≈–‡°‘¥≈‘Ë¡‡≈◊Õ¥¢π“¥„À≠à§«√ºà“µ—¥≈ß‰ª‡¬Á∫´àÕ¡√Õ¬√—Ë« ·≈–§«—°‡Õ“≈‘¡Ë ‡≈◊Õ¥ÕÕ° ‰¡à„Àâ°¥‡ âπª√– “∑¢â“ß‡§’¬ß °“√Õ—°‡ ∫ µ‘¥‡™◊ÕÈ ∫√‘‡«≥·∑ß‡¢Á¡Õ“®®–æ∫‰¥â∂“â ‡∑§π‘§ª√“»®“°‡™◊ÕË ‰¡à¥æ’ Õ ‡™◊ÈÕ∑’Ëæ∫∫àÕ¬§◊Õ Staph. aureus ·≈– Streptococci √—°…“ ‚¥¬„Àâ¬“ªØ‘™«’ π– ∂â“‡°‘¥‚æ√ßÀπÕß§«√ºà“µ—¥√–∫“¬‡Õ“ÀπÕßÕÕ° √—°…“°“√µ‘¥‡™◊ÕÈ „ÀâÀ“¬¥’°Õà π∑’®Ë –∑”°“√ºà“µ—¥√—°…“µàÕ‰ª

II. Contrast Venography ‡ªìπ«‘∏°’ “√«‘π®‘ ©—¬ æ¬“∏‘ ¿“æ·≈–§«“¡º‘¥ª°µ‘¢ÕßÀ≈Õ¥ ‡≈◊Õ¥¥”‚¥¬°“√©’¥ “√∑÷∫· ß‡¢â“À≈Õ¥‡≈◊Õ¥¥”·≈â«∂à“¬¿“æ√—ß ’ ®–‡ÀÁπ«à“≈‘¡Ë ‡≈◊Õ¥¿“¬„πÀ≈Õ¥‡≈◊Õ¥¥”∑ÿ°√–¥—∫ ¡’¢Õâ ∫àß™’È „π°“√ «‘π®‘ µ©—¬ deep vein thrombosis (DVT) ¢Õß¢“ ·µà „πªí®®ÿ∫π— æ∫«à“¡’∫∑∫“∑πâÕ¬≈ß‡π◊ËÕß®“°„™â Duplex ultrasound ®– «‘π®‘ ©—¬‚√§‰¥â¥°’ «à“ ‰¡à‡ ’¬Ë ßµàÕ°“√©’¥ “√∑÷∫· ß ¡’¢Õâ ∫àß™’ÕÈ π◊Ë §◊Õ „πºŸâªÉ«¬∑’Ë¡’§«“¡º‘¥ª°µ‘¢Õß≈‘Èπªî¥‡ªî¥∑’ËµâÕß°“√ºà“µ—¥·°â ‰¢ À√◊Õ∑” bypass ·≈–À“µ”·ÀπàßÕÿ¥µ—π„πºŸâªÉ«¬∑’Ë·¢π∫«¡À≈—ß ·∑ßÀ≈Õ¥‡≈◊Õ¥¥” subclavian ‡æ◊ÕË Õ¥ “¬ °“√∑” venography ®–¬“°°«à“ arteriography ‡æ√“–®–µâÕßÀ“À≈Õ¥‡≈◊Õ¥ ¥”∫√‘‡«≥À≈—ß‡∑â“∑’®Ë –©’¥ “√∑÷∫· ß √âÕ¬≈– 3-5 ¢ÕßºŸªâ «É ¬∑’∑Ë ” venography ®–¡’¿“«–·∑√°´âÕπ®“°°“√·æâ “√∑÷∫· ß ¡’°“√ √—Ë«∑”„Àâ‡®Á∫À√◊Õ “√∑÷∫· ß∑’Ë¡’§«“¡‡¢â¡¢âπ‡°‘π‰ª®–∑”≈“¬‡ÕÁπ ‚¥∑’‡≈’¬Ë ¡¢ÕßÀ≈Õ¥‡≈◊Õ¥¥” ∑”„Àâ‡°‘¥ thrombophlebitis ¿“¬À≈—ß

III. Ultrasound (US) ·≈– Computed Tomography (CT) ∑—Èß Õß‡ªìπ noninvasive method „π°“√«‘π‘®©—¬‚√§∑“ß À≈Õ¥‡≈◊Õ¥‰¥â¥’ ‚¥¬‡©æ“– aneurysm ·≈–¿“«–·∑√°´âÕπ∑’Ë ‡°‘¥¢÷πÈ ¿“¬À≈—ßºà“µ—¥„ àÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡(3) ·µà¡¢’ Õâ ¥âÕ¬°«à“ arteriography §◊Õ‰¡à “¡“√∂ª√–‡¡‘π°“√µ’∫µ—π·≈–‡ÀÁπ ulcerated plaque ‰¥â ªí®®ÿ∫—π duplex scan ¡’∫∑∫“∑¡“°°«à“ √«¡∑—Èß Magnetic Resonance Imaging (MRI) ®–‡ÀÁπ§«“¡º‘¥ª°µ‘ ∑“ß°“¬¿“æ∑ÿ°·ßà¡¡ÿ ¢ÕßÀ≈Õ¥‡≈◊Õ¥‰¡à«“à ®–‡ªìπ hemangioma, arteriovenous malformations (AVM), À√◊Õ§«“¡º‘¥ª°µ‘¢Õß aortic arch ·µàÕ¬à“ß‰√°Áµ“¡ US ·≈– CT scan °Á¬ß— ‡ªìπ«‘∏’ °“√∑’ Ë “¡“√∂«‘π®‘ ©—¬‚√§∑“ßÀ≈Õ¥‡≈◊Õ¥‰¥â‡ªìπ à«π„À≠à «‘∏°’ “√ ‰¡à´—∫´âÕπ ·≈–‰¡à ‘Èπ‡ª≈◊Õß§à“„™â®à“¬¡“° ∑—Èß Õß«‘∏’¡’Õ—µ√“ ‡ ’¬Ë ßπâÕ¬ ¿“«–·∑√°´âÕπÕ“®®–‡°‘¥¢÷πÈ ‰¥â∂“â ∑” CT scan √à«¡ °—∫°“√©’¥ “√∑÷∫· ß ¢âÕ∫àß™’È „π°“√„™â ¡’¥ß— µàÕ‰ªπ’È 1. ”À√—∫°“√«‘π‘®©—¬ Abdominal Aortic Aneurysm (AAA) ®“°°“√∑” US “¡“√∂∫Õ°¢π“¥·≈– intraluminal thrombus ¡’¢âÕ‡ ’¬§◊ÕÕ“®®–‡ÀÁπ‰¡à ™— ¥ ∂â “ ºŸâ ªÉ«¬Õâ«πºπ—ßÀπ—ß∑âÕßÀπ“ ¡’≈¡„π≈”‰ â·≈–°√–‡æ“–

74 Õ“À“√¡“° ‰¡à “¡“√∂∫Õ°æ¬“∏‘ ¿“æ«à“ AAA Õ¬Ÿà „µâ À√◊Õ‡Àπ◊ÕµàÕ renal artery À√◊Õ≈ß‰ª∂÷ß iliac arteries ∂â“ US ‰¡à “¡“√∂„Àâ§«“¡™—¥‡®π„π°“√«‘π®‘ ©—¬‰¥â§«√∑” CT scan µàÕ‰ª´÷Ëß®– “¡“√∂∫Õ°∂÷ßæ¬“∏‘ ¿“æ¢Õß À≈Õ¥‡≈◊ Õ ¥∑’Ë · ¬°·¢πßÕÕ°‰ª®“° aorta AAA µ”·Àπàß ŸßÀ√◊ÕµË”°«à“ renal artery ·≈–æ¬“∏‘ ¿“æ ¢ÕßÕ«—¬«–¿“¬„π™àÕß∑âÕß¥â«¬ 2. peripheral aneurysms ‚¥¬‡©æ“–À≈Õ¥‡≈◊Õ¥·¥ß femoral ·≈– popliteal 3. deep vein thrombosis ∫√‘‡«≥ iliofemoral veins 4. ¿“«–·∑√°´âÕπ®“°°“√ºà“µ—¥„™âÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡ ®– ‡ÀÁπ‚æ√ßÀπÕß ≈‘¡Ë ‡≈◊Õ¥ °ä“´ ·≈– false aneurysm ∑’‡Ë °‘¥¢÷πÈ ”À√—∫°“√ºà“µ—¥ AAA ·≈–À≈Õ¥‡≈◊Õ¥·¥ß Iliac ∂â“ ß —¬«à“¡’°“√µ‘¥‡™◊ÈÕ¢ÕßÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡ «‘∏’ °“√µ√«®«‘π®‘ ©—¬∑’·Ë πàπÕπ§◊Õ °“√∑” indium - labeled leukouyte scans.

IV. Digital Subtraction Angiography (DSA)(4) ‡ªìπ«‘∏°’ “√∑” arteriography ‚¥¬©’¥ “√∑÷∫· ßºà“π “¬ «π ®“° antecubital vein ‡¢â“‰ª¬—ß superior venacava (SVC) ·≈â « „™â fluoroscope à Õ ß‡©æ“–À≈Õ¥‡≈◊ Õ ¥·¥ß∫√‘ ‡ «≥∑’Ë µâÕß°“√»÷°…“∂à“¬¿“æ√—ß ’À√◊Õ«’¥’∑—»πå ‰«â „π™à«ß√–¬–‡«≈“ 2-3 «‘π“∑’ ®–‡ÀÁπ arteriogram µ√ßÀ≈Õ¥‡≈◊Õ¥∑’ËµâÕß°“√ ·≈–¬—ß “¡“√∂¢®—¥‡ß“¢Õß°√–¥Ÿ°·≈–‡π◊ÈÕ‡¬◊ËÕÕÕ°‰¥â «‘∏’π’È¡’¢âÕ¥’§◊Õ‰¡à µâÕß·∑ß‡ âπ·≈– Õ¥ “¬ «πºà“πÀ≈Õ¥‡≈◊Õ¥·¥ß§à“„™â®“à ¬∂Ÿ°°«à“ conventional arteriography ‡À¡“– ”À√—∫ºŸâªÉ«¬∑’ËÀ“‡ âπ À≈Õ¥‡≈◊Õ¥·¥ß·∑ß Õ¥ “¬‰¡à ‰¥â ¥Ÿæ¬“∏‘ ¿“æ¢ÕßÀ≈Õ¥‡≈◊Õ¥ ·¥ß‰¥â ∑ÿ ° µ”·Àπà ß ·µà ¢â Õ ‡ ’ ¬ §◊ Õ ‡«≈“∑’Ë ©’ ¥ µâ Õ ß„™â “√∑÷ ∫ · ß ª√‘¡“≥¡“° “√∑÷∫· ß®–‡¢â“∂÷ßÀ≈Õ¥‡≈◊Õ¥∑—Ë«√à“ß°“¬‡«≈“ ∂à“¬¿“æ√—ß ’®–´âÕπ°—π√–À«à“ß¢â“ß´â“¬·≈–¢â“ß¢«“ (∂â“∂à“¬ ¥â“π¢â“ß) ∑”„Àâ·ª√º≈≈”∫“° ®÷ß‰¡à “¡“√∂„™â·∑π conventional arteriography ‰¥â „πªí®®ÿ∫π— ¡’«∏‘ °’ “√ intra arterial digital subtraction arteriography (1D-DSA) ´÷ßË ‡ªìπ°“√©’¥ “√∑÷∫· ß ‡¢â“∑“ßÀ≈Õ¥‡≈◊Õ¥·¥ß ª√‘¡“≥¢Õß “√∑÷∫· ß∑’Ë „™â®–πâÕ¬°«à“ ©’¥‡¢â“À≈Õ¥‡≈◊Õ¥¥”

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥

V. Magnetic Resonance Imaging „™âÀ≈—°°“√«à“ hydrogen ion (proton) ‡¡◊ËÕÕ¬Ÿà „π π“¡ ·¡à‡À≈Á° ®–‡§≈◊ËÕπµ—«‰ª∑‘»∑“ß‡¥’¬«°—∫¢—È«·¡à‡À≈Á°‡ ¡Õ „™â ‰¥â °—∫Õ«—¬«–∑’¡Ë °’ “√‡§≈◊ÕË π‰À«¿“¬„πµ≈Õ¥‡«≈“ ‡™àπ À≈Õ¥‡≈◊Õ¥ ´÷Ëß¡’‡¡Á¥‡≈◊Õ¥·¥ß«‘ËßÕ¬Ÿàµ≈Õ¥‡«≈“ µ”·Àπàß¢ÕßÀ≈Õ¥‡≈◊Õ¥∑’Ë¡’ æ¬“∏‘ ¿“æ®–‡ÀÁπ‰¥â™¥— ®“° scan MRI ‡À¡“– ”À√—∫°“√«‘π®‘ © ¬— æ¬“∏‘ ¿“æ¢ÕßÀ≈Õ¥‡≈◊Õ¥„π‡¡¥‘·Õ µ‘π¡—Ë ‚¥¬‡©æ“– aortic dissection ®–‡ÀÁπ√Ÿ√«—Ë ·≈– intimal flap ™—¥‡®π ”À√—∫ aorta ®–¡Õß‡ÀÁπ∑—Èß§«“¡Àπ“ mural thrombus ¢π“¥¢Õß lumen µ≈Õ¥®πÀ≈Õ¥‡≈◊Õ¥∑’·Ë ¬°·¢πßÕÕ°‰ª(5) ¡’¢Õâ ¥’„π°“√«‘π®‘ ©—¬‚√§ ∑“ßÀ≈Õ¥‡≈◊Õ¥§◊Õ‡ªìπ noninvasive test “¡“√∂ª√–‡¡‘π blood flow velocity ‰¥â ‰¡àµâÕß©’¥ “√∑÷∫· ß ·≈–∂à“¬¿“æ√—ß ’‰¥â À≈“¬·π«√–π“∫ (transverse, sagittal ·≈– coronal planes) ¡’¢Õâ ‡ ’¬§◊Õ§à“„™â®“à ¬§àÕπ¢â“ß Ÿß

VI. Duplex Ultrasonography ‡ªìπ«‘∏’°“√µ√«®«‘π‘®©—¬∑’Ë „™â∫àÕ¬·≈–‰¥âº≈¥’¡“°„πªí®®ÿ∫—π ”À√—∫‚√§À≈Õ¥‡≈◊Õ¥¥”‡ªìπ«‘∏’°“√µ√«®«‘π‘®©—¬¡“µ√∞“π¢Õß ‚√§À≈Õ¥‡≈◊Õ¥·¥ß§“‚√µ‘§ aortic arch ·≈– vertebral À√◊ÕÀ≈Õ¥‡≈◊Õ¥∫√‘‡«≥∑’Ë‡¢â“∂÷ß‰¥â¬“°‡™àπ „π ¡Õß ·≈–¬—ß‡ªìπ noninvasive test „™â ‰¥âº≈¥’ „π°“√«‘π‘®©—¬‚√§À≈Õ¥‡≈◊Õ¥·¥ß Õÿ¥µ—π∫√‘‡«≥¢“√à«¡°—∫°“√∑” segment pressure measurement Color Doppler imaging „™â ”À√—∫ª√–‡¡‘π§«“¡√ÿπ·√ß„π°“√ ¢“¥‡≈◊Õ¥¢ÕßºŸªâ «É ¬ claudication ¡’∫∑∫“∑„π°“√ follow up ºŸªâ «É ¬∑’ºË “à µ—¥ reconstruction À≈Õ¥‡≈◊Õ¥‚¥¬‰¡àµÕâ ß∑” arteriography

VII. Positron Emission Tomography (PET) CT ·≈– MRI ‡ªìπ«‘∏’°“√µ√«®«‘π‘®©—¬∑’Ë “¡“√∂¡Õß‡ÀÁπ Õ«—¬«–∑’µË Õâ ß°“√∑√“∫æ¬“∏‘ ¿“æ‰¥â 3 ¡‘µ‘ MR spectroscopy ·≈– PET ®– “¡“√∂∫à ß ∫Õ°°“√∑”ß“π¢Õß‡´≈≈å µà “ ß Ê ¿“¬„π√à“ß°“¬‰¥â ‚¥¬„™â “√™’«‡§¡’ labeled ¥â«¬ positron-emitting isotope ©’¥‡¢â“„π√à“ß°“¬„Àâ°√–®“¬‡¢â“µ“¡‡π◊ÈÕ‡¬◊ËÕ·≈– à«πµà“ß Ê À≈—ß®“°π—πÈ ¿“æ√—ß ’ ‡æ◊ÕË ª√–‡¡‘π ¿“«–°“√≥å‡¡µ“ ‚∫≈‘ ¡å¢Õß‡´≈≈å „π√à“ß°“¬ PET ®–∫àß∫Õ°∂÷ß regional blood

°“√µ√«®«‘π‘®©—¬∑“ß√—ß ’«‘∑¬“·≈–√—ß ’√à«¡√—°…“ flow, oxygen consumption ·≈– substrate (glucose) utilization ´÷ßË ®– “¡“√∂·¬°‡π◊ÕÈ ‡¬◊ÕË ∑’¢Ë “¥‡≈◊Õ¥‰¥â®“°‡π◊ÕÈ ‡¬◊ÕË ª°µ‘ PET ®–ª√–‡¡‘ π metabolic response À≈— ß ºà “ µ— ¥ revascularization

√ÿª „πªí®®ÿ∫π— «‘∏°’ “√µ√«®«‘π®‘ ©—¬·≈– ◊∫§âπ‚√§∑“ßÀ≈Õ¥‡≈◊Õ¥ ‚¥¬«‘∏°’ “√∑“ß√—ß ’«∑‘ ¬“¡“°¡“¬ πÕ°‡Àπ◊Õ®“° arteriography, US ·≈– CT scan »—≈¬·æ∑¬å·≈–√—ß ’·æ∑¬å ®–µâÕß‡≈◊Õ°„™â«∏‘ ’ °“√µà“ß Ê „Àâ‡À¡“– ¡·≈–‡ªìπÕ—πµ√“¬µàÕºŸâªÉ«¬πâÕ¬∑’Ë ÿ¥ noninvasive test À≈“¬™π‘¥‡√‘¡Ë ¡’∫∑∫“∑„π°“√«‘π®‘ ©—¬‚√§¡“°¢÷πÈ ‡™àπ Doppler US ·≈– MRI

ENDOVASCULAR TREATMENT TECHNIQUES «‘∏°’ “√µ√«®«‘π®‘ ©—¬∑“ß√—ß ’«∑‘ ¬“¡’§«“¡°â“«Àπâ“‰ª¡“° ·≈– endovascular treatment °Á‡ªìπÕ’°·¢πß “¢“∑“ß√—ß ’«‘∑¬“∑’Ë °”≈—ß¡’∫∑∫“∑ ”§—≠„π°“√√—°…“‚√§À≈Õ¥‡≈◊Õ¥ ‡ªìπÀ—µ∂°“√ ™π‘¥Àπ÷ßË ´÷ßË ∑”‚¥¬§«“¡√à«¡¡◊Õ√–À«à“ß√—ß ’·æ∑¬å·≈–»—≈¬·æ∑¬å ‡™àπ «‘∏°’ “√ percutaneous transluminal angioplasty (PTA), Thrombolytic therapy, Atherectomy, Angioscopy Intraluminal vascular stent œ≈œ «‘∏’°“√‡À≈à“π’È “¡“√∂∑¥·∑π ·≈–¡’ª√– ‘∑∏‘¿“æ„°≈â‡§’¬ß°—∫°“√ºà“µ—¥√—°…“‡ªìπ∑“ß‡≈◊Õ°Õ’° ·π«∑“ßÀπ÷Ëß ”À√—∫ºŸâªÉ«¬∑’Ë ¿“«–√à“ß°“¬‰¡à‡À¡“– ¡°—∫°“√ ºà“µ—¥(1)

I. Angioscopy ‡Õ° “√Õâ“ßÕ‘ß 1. Dyer R (ed). Handbook of Vascular and Interventional Radiology. Churchill Livingstone, 1993. 2. Bush WH, Swanson DP. Acute ractions to intravascular contrast media: Types, risk factors, recognition, and specific treatment. AJR 1991;157: 1153. 3. Tumch SS, Seltzer SE, Wang A. Computed tomography in Vascular Disorder. In: Loscalzo J, Greager MA, Dzau VJ (eds) Vascular Medicine. Boston: Little, Brown, 1992;81-102. 4. Bettmann MA. Principles of Angiography. In:Loscalzo J, Creager MA, Dzau VJ (eds.), Vascular Medicine. Boston: Little, Brown, 1992;155-173. 5. Glazer HS. The thoracic aorta studied by MR Imaging. Radiology 1985;157:149.

‡ªìπ«‘∏°’ “√ àÕß°≈âÕß¥Ÿ°“¬¿“æ·≈–æ¬“∏‘ ¿“æ¿“¬„πÀ≈Õ¥ ‡≈◊Õ¥·≈–ª√–‡¡‘π«à“®–√—°…“‚¥¬«‘∏’„¥µàÕ‰ª(2) angioscope ∑’Ë „™â „πªí®®ÿ∫π— ¡’‡ âπºà“»Ÿπ¬å°≈“ß 0.5-3.3 ¡‘≈≈‘‡¡µ√ ‡ªìπ fiberoptic “¡“√∂‚§âßßÕ Õ¥‡¢â“‰ª‰¥â∑ÿ° à«π¢ÕßÀ≈Õ¥‡≈◊Õ¥ ¡’· ß «à“ß „Àâ¡Õß‡ÀÁπ‰¥â 3 ¡‘µ‘ ¡’ª√–‚¬™πå¡“°¿“¬À≈—ß∑” thrombectomy ‡æ◊ÕË ¥Ÿ thrombus ∑’‡Ë À≈◊Õ·≈–µ√«®‰¡àæ∫®“°°“√∑” arteriogram «‘∏°’ “√µ√«®À≈Õ¥‡≈◊Õ¥‚¥¬ angioscope ºŸªâ «É ¬‰¡àµÕâ ß‡ ’¬Ë ßµàÕ °“√ —¡º— √—ß ’‡À¡◊Õπ arteriography ¡’¢âÕ‡ ’¬§◊ÕÕ“®®–∑”„Àâ √à“ß°“¬‰¥â√—∫ “√πÈ”‡°‘π§«“¡µâÕß°“√‡æ√“–¢≥– àÕß®–µâÕß «π≈â “ ßÀ≈Õ¥‡≈◊ Õ ¥µ≈Õ¥‡«≈“¥â « ¬πÈ” ‡°≈◊ Õ ¡¥ÿ ≈ ¬å °— ∫ °“√ ∫“¥‡®Á∫µàÕ intima À√◊Õ∂â“æ¬“¬“¡ àÕßÀ≈Õ¥‡≈◊Õ¥∑’Ë¡’¢π“¥ ‡≈Á°°«à“°≈âÕß ®–∑”„Àâ‡°‘¥ spasm ·≈– thrombosis ¡’∫∑∫“∑ ”§—≠À≈—ß®“°∑” angioplasty ·≈–„ à stent „™â Õà ß¥Ÿ«“à À≈Õ¥ ‡≈◊ Õ ¥¢¬“¬¢π“¥‡æ’ ¬ ßæÕÀ√◊ Õ ‰¡à ¡’ ªí ≠ À“·∑√°´â Õ π®“° À—µ∂°“√Õ¬à“ß‰√

II. Percutaneous Transluminal Angioplasty

‡√‘¡Ë π”¡“„™â ‚¥¬ Dotter „πªï 1964(3) ‡ªìπ«‘∏°’ “√ Õ¥ “¬ «π∑’Ë¡’∫—≈≈ŸπÕ¬Ÿàµ√ßª≈“¬ “¡“√∂∑”„Àâ·ø∫·≈–‚ªÉß‰¥â ‡¢â“‰ª ∂÷ßÀ≈Õ¥‡≈◊Õ¥·¥ßºà“πº‘«Àπ—ß‡æ◊ËÕ¢¬“¬∂à“ßÀ≈Õ¥‡≈◊Õ¥∑’Ëµ’∫ ·§∫®“° atherosclerotic plaque ∑”„Àâ‡ âπºà“»Ÿπ¬å°≈“ß¢Õß À≈Õ¥‡≈◊Õ¥‚µ¢÷Èπ °“√¢¬“¬∂à“ßπ’È®–¡’º≈„π°“√∑”≈“¬ ¿“æ ¢Õß°≈â“¡‡π◊ÕÈ ‡√’¬∫„π™—πÈ media ∑’¡Ë ’ elastin ·≈– collagen fibrins À≈Õ¥‡≈◊ Õ ¥∑’Ë ∂Ÿ ° ∂à “ ß¢¬“¬®–¡’ ¢ ∫«π°“√À“¬¢Õß

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥

∫“¥·º≈·≈–‡ âπºà“»Ÿπ¬å°≈“ß¿“¬„π∑’¢Ë ¬“¬¢π“¥‚µ°«à“‡¥‘¡ PTA „™â „π°“√√—°…“°“√µ’∫·§∫¢ÕßÀ≈Õ¥‡≈◊Õ¥ aorta, ·¢π¢“ renal ·≈– mesenteric arteries, subclavian ·≈– coronary arteries √«¡∑—ßÈ hemodialysis fistula Õ“®®–„™â√°— …“·∑π°“√ºà“µ—¥‰¥â „π∫“ß ∂“π°“√≥å ¡’¢âÕ¥’§◊Õ∑”‰¥â ‚¥¬°“√©’¥¬“™“‡©æ“–∑’Ë ‚¥¬ „Àâ ¬ “√–ß— ∫ ª√– “∑‡≈Á ° πâ Õ ¬ ºŸâ ªÉ « ¬Õ“®®–‰¡à µâ Õ ßæ— ° Õ¬Ÿà „ π ‚√ßæ¬“∫“≈ À√◊Õæ—°¥ŸÕ“°“√‡æ’¬ß√–¬– —Èπ §à“„™â®à“¬πâÕ¬ ¿“«–·∑√°´âÕπ¡’πâÕ¬ ‡À¡“– ”À√—∫ºŸâªÉ«¬∑’Ë ¿“æ√à“ß°“¬‰¡à ‡À¡“– ¡ ”À√—∫°“√ºà“µ—¥ ‰¡à¡¿’ “«–·∑√°´âÕπ®“°°“√ºà“µ—¥‡™àπ ∫“¥‡®Á∫µàÕ∑àÕπÈ”‡À≈◊Õß ‡ âπª√– “∑ ·≈–Õ«—¬«–¢â“ß‡§’¬ß “¡“√∂¢¬“¬∂à“ß´È”‰¥â∂“â ∑”§√—ßÈ ·√°·≈â«‰¥âº≈‰¡à¥’ °“√∑” PTA ®–‰¥âº≈¥’∂â“§«“¡¬“« à«π¢ÕßÀ≈Õ¥‡≈◊Õ¥∑’Ë µ’∫·§∫‰¡à‡°‘π 5 ‡´Áπµ‘‡¡µ√ (short segment) ‰¥âº≈¥’„πÀ≈Õ¥ ‡≈◊Õ¥¢π“¥„À≠à‡™àπ iliac ·≈– superficial femoral(4) ∂â“¢¬“¬ ·≈â«§“·°π (stent) ∑‘Èß‰«â º≈°“√√—°…“®–¥’ ‚Õ°“ °≈—∫¡“µ’∫ ·§∫Õ’°§√—ßÈ æ∫‰¥âπÕâ ¬(5) (√Ÿª∑’Ë 7.1) ‰¥âº≈‰¡à§Õà ¬¥’∂“â ¡’°“√µ’∫·§∫ À≈“¬™à«ß À≈Õ¥‡≈◊Õ¥‚µ‚Õ°“ ∑’Ë°≈—∫¡“µ’∫·§∫´È”æ∫πâÕ¬ ‰¥â º≈„π°“√√—°…“√âÕ¬≈– 95 ¡’ 5-year patency √âÕ¬≈– 75-90(6) ”À√—∫À≈Õ¥‡≈◊Õ¥·¥ß‚§‚√π“√’Ë À≈—ß¢¬“¬∂à“ß·≈â«√âÕ¬≈– 30 ®–°≈—∫¡“µ’∫·§∫Õ’°¿“¬„π√–¬–‡«≈“ 6 ‡¥◊Õπ(7) º≈°“√√—°…“‚¥¬ PTA ªí®®—¬ ”§—≠∑’Ë∑”„Àâº≈°“√√—°…“ À≈Õ¥‡≈◊Õ¥µ’∫·§∫‚¥¬«‘∏°’ “√ PTA ‰¥âº≈¥’§Õ◊ (6) 1. ∫√‘‡«≥∑’µË ∫’ ·§∫¡’™«à ß —πÈ ‰¡à‡°‘π 5 ‡´Áπµ‘‡¡µ√ ·≈–‡ªìπ µ”·Àπàß‡¥’¬« 2. ¡’ blood outflow ¥’

3. √—°…“ claudication ®–‰¥âº≈¥’°«à“ limb theratening condition 4. ºŸªâ «É ¬‰¡à ∫Ÿ ∫ÿÀ√’Ë ·≈–‰¡à‡ªìπ‚√§‡∫“À«“π º≈°“√√—°…“æ∫«à“À≈Õ¥‡≈◊Õ¥µ’∫∑’Ë¢“¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß femoral, popliteal ·≈– terminal aorta ‰¥âº≈¥’√Õâ ¬≈– 85-95 ¡’ 5-year patency √âÕ¬≈– 75-90(8) „π°“√√—°…“ Renovascular hypertension (RVH) ∂â“µ’∫·§∫™à«ß —πÈ Ê ®“° fibromuscular dysplasia ®–‰¥âº≈√âÕ¬≈– 87-100 §«“¡¥—π‚≈À‘µ®–≈¥≈ß√âÕ¬ ≈– 57 ·≈–≈¥≈ß®π§ÿ¡ßà“¬¥â«¬¬“√âÕ¬≈– 27(9) ¿“«–·∑√°´âÕπ æ∫‰¥â√Õâ ¬≈– 5-10 Õ—µ√“µ“¬√âÕ¬≈– 0-2 ¡—°‡°‘¥µ√ß∫√‘‡«≥∑’Ë‡®“–À√◊Õ¢¬“¬∂à“ß æ∫«à“‡°‘¥ thrombosis ∫àÕ¬∑’ Ë ¥ÿ µâÕßºà“µ—¥≈ß‰ª‡Õ“ thrombus ÕÕ° À≈Õ¥‡≈◊Õ¥·µ° æ∫πâÕ¬„π¡◊ÕºŸâ™”π“≠°“√ ¿“«–·∑√°´âÕπÕ◊Ëπ∑’Ëæ∫‰¥â®“°°“√ ©’¥ “√∑÷∫· ß§◊Õ ·æâ¬“ ‰µ«“¬ ™ÁÕ§ °“√„Àâ¬“µâ“π‡°√Á¥‡≈◊Õ¥·≈–¬“°—π‡≈◊Õ¥·¢Áßµ—« ®–∑”„Àâ º≈°“√√—°…“¥’¢π÷È §«√¡’·π«∑“ß¥—ßµàÕ‰ªπ’È „Àâ√∫— ª√–∑“π·Õ ‰æ√‘π 81-325 ¡‘≈≈‘°√—¡µàÕ«—π 24-48 ™—Ë«‚¡ß°àÕπ∑” PTA À≈—ß®“° π—πÈ „Àâ¬“√—∫ª√–∑“πµàÕÕ’° 2-3 ¢≥–∑” PTA ©’¥‡Œª“√‘π 2,5005,000 ¬Ÿπµ‘ ∑“ßÀ≈Õ¥‡≈◊Õ¥·¥ß„Àâ√∫— ª√–∑“π Coumadin 1-3 ‡¥◊ÕπÀ≈—ß∑” PTA

III. Atherectomy Devices ∑’Ë¡’ „™â „πªí®®ÿ∫—π§◊Õ Simpson atherectomy cath, The Kensey atherectomy device, The Auth Rotablator ·≈– The transluminal extraction catheter ¡’°≈‰°°“√∑”ß“π

√Ÿª∑’Ë 7.1 °. °“√∑” percutaneous transluminal angioplasty (PTA) ¢¬“¬∂à“ßÀ≈Õ¥‡≈◊Õ¥∑’Ëµ’∫·§∫ ¢. À≈—ß°“√¢¬“¬∂à“ß·≈â« “¡“√∂§“ stent ºà“π∑“ß “¬ «π§È”À≈Õ¥‡≈◊Õ¥ à«π∑’Ëµ’∫·§∫„Àâ¢¬“¬∂à“ß‰¥â

°“√µ√«®«‘π‘®©—¬∑“ß√—ß ’«‘∑¬“·≈–√—ß ’√à«¡√—°…“

V. Thrombolytic Therapy

√Ÿª∑’Ë 7.2 °“√µ— ¥ plaque ¢ÕßÀ≈Õ¥‡≈◊ Õ ¥·¥ßÕÕ°‚¥¬„™â atherectomy catheter

·≈–«‘∏°’ “√„™âµ“à ß°—π(10) ®ÿ¥¡ÿßà À¡“¬À≈—°§◊Õ≈Õ°‡Õ“ atheromatous debris ÕÕ°®“° atherosclerotic arteries (√Ÿª∑’Ë 7.2) «‘∏°’ “√¥—ß°≈à“«æ∫«à“¡’°“√∑”≈“¬‡π◊ÕÈ ‡¬◊ÕË ™—πÈ intima ®–‡°‘¥ intima hyperplasia ·≈–À≈Õ¥‡≈◊Õ¥®–µ’∫µ—π¢÷πÈ Õ’°‰¥â „π¿“¬À≈—ß º≈°“√√—°…“„°≈â‡§’¬ß°—π°—∫ PTA

IV. Laser Angioplasty ™à«ß√–¬–‡«≈“ 10 ªï∑º’Ë “à π¡“‰¥â¡°’ “√π”‡Õ“‡≈‡´Õ√å‡¢â“¡“„™â ”À√—∫‡≈“–µ—¥ atherosclerotic lesions(11,12) ·µàº≈°“√√—°…“ ‰¡à¥’ „πÕπ“§µ§“¥«à“®–¡’°“√ «π Õ¥ “¬ fiberoptic ºà“π º‘«Àπ—ß‡¢â“‰ª∂÷ßÀ≈Õ¥‡≈◊Õ¥∑’¡Ë æ’ ¬“∏‘ ¿“æ „Àâ· ß‡≈‡´Õ√å‡¢â“∂÷ß plaque ·≈–‡√‘¡Ë ¢∫«π°“√ vaporization º≈‘µº≈∑’‡Ë °‘¥®“° laser vaporization §◊ÕÕäÕ°´‘‡®π ‰π‚µ√‡®π·≈–‰Œ‚¥√§“√å∫Õπ ®–∂Ÿ°¥Ÿ¥´÷¡‚¥¬ “√πÈ”·≈–‡π◊ÈÕ‡¬◊ËÕ„π√à“ß°“¬ µ“¡À≈—°°“√·≈â« ¥Ÿ‡À¡◊Õπßà“¬ ·µà „π∑“ßªØ‘∫—µ‘·≈â«¡’¢âÕ®”°—¥·≈–§«“¡´—∫´âÕπ À≈“¬ª√–°“√§◊Õ · ß‡≈‡´Õ√å∑ ’Ë “¡“√∂π”ºà“π “¬ fiberoptic ‰¥â¡’ argon °—∫ eximer «‘∏°’ “√π’È „™â ‰¥â°∫— plaque ∑’ÕË Õà ππ‘¡Ë ‰¡à ‰¥âº≈ °—∫ calcified plaque ·≈–§«“¡√âÕπ∑’Ë‡°‘¥¢÷Èπ®–∑” “¬ºπ—ß À≈Õ¥‡≈◊Õ¥∑’Ëª°µ‘‰ª¥â«¬æ√âÕ¡°—∫°“√∑”≈“¬ plaque Õ“®®– ∑”„ÀâÀ≈Õ¥‡≈◊Õ¥∑–≈ÿ‰¥â §à“„™â®à“¬®“°°“√„™â· ß‡≈‡´Õ√å¬—ß¡’ √“§“ Ÿß (√Ÿª∑’Ë 7.3)

„™â‡ªìπ«‘∏’À≈—°À√◊Õ«‘∏’°“√√—°…“Õ—π¥—∫·√°¢Õß‡ÕÁ¡‚∫‰≈À√◊Õ ∏√Õ¡∫— ÕÕ°®“°À≈Õ¥‡≈◊Õ¥‰¥âÀ¡¥À√◊Õ®“°À≈Õ¥‡≈◊Õ¥ à«π ª≈“¬∑’Ë ‰¡à “¡“√∂ Õ¥‡§√◊ÕË ß¡◊Õ‡¢â“‰¥â∂ß÷ (13,14) “√≈–≈“¬≈‘Ë¡‡≈◊Õ¥∑’Ë „™â „πªí®®ÿ∫—π¡’ streptokinase (SK), Urokinase (UK), ·≈– tissue plasminogen activator (TPA) SK ·≈– UK ‡ªìπ exogenous plasminogen activator ∑’¬Ë Õà ¬ ≈“¬‰ø∫√‘π‚¥¬°√–µÿâπ°≈‰°°“√¬àÕ¬ ≈“¬‰ø∫√‘π„π√à“ß°“¬ ‚¥¬‡ªìπ ◊ËÕπ”„π°“√‡ª≈’Ë¬π plasminogen „Àâ‡ªìπ plasmin ´÷ßË ®–¡’º≈„π°“√¬àÕ¬ ≈“¬ fibrin clots SK ‡ªìπº≈‘µº≈®“°·∫§∑’‡√’¬ streptococci ‡π◊ÕË ß®“°‡ªìπ “√‚ª√µ’π·ª≈°ª≈Õ¡πÕ°√à“ß°“¬ ®÷ß¡’§≥ ÿ ¡∫—µ‡‘ ªìπ antigenic ∑”„Àâ‡°‘¥ªØ‘°‘√‘¬“·æâ ‰¥â UK ‡ªìπ “√∑’Ë °—¥®“°ªí “«–¡πÿ…¬å π”¡“‡æ“–‡≈’¬È ß„π embryonic kidney cell ¡’§√÷ßË Õ“¬ÿ 14 π“∑’ ¡’§≥ ÿ ¡∫—µ‘ nonantigenic ·≈– low pyrogenicity ‚¥¬‡∑§π‘§ recombinant DNA ®– “¡“√∂ —ß‡§√“–Àå recombinant UK ‰¥â „Àâ¡§’ ≥ ÿ ¡∫—µ„‘ °≈â‡§’¬ß°—∫ tissue culture UK ‰¥â TPA ‡ªìπ “√∑’Ëº≈‘µ‰¥â®“°‡∑§π‘§ recombinant DNA ∂÷ß·¡â«à“ “√π’È‡ªìπµ—«°√–µÿâπ∑’Ë ‰¡à§àÕ¬¡’ª√– ‘∑∏‘¿“æµàÕ√–∫∫ ¬àÕ¬ ≈“¬‰ø∫√‘π ∂â“¢“¥‰ø∫√‘π·µà®–‡°“–·≈–√«¡µ—«¥’°∫— plasminogen „π¿“«–∑’Ë ‰ø∫√‘π¡’πâÕ¬·≈–ª√– ‘∑∏‘¿“æ„π°“√¬àÕ¬ ≈“¬ fibrin clot ¥’¡“° ‚¥¬‰¡àµÕâ ß‡ª≈’¬Ë π plasminogen „π æ≈“ ¡à“‡≈¬

√Ÿª∑’Ë 7.3 °“√„™â laser beam ∑–≈«ßÀ≈Õ¥‡≈◊Õ¥∑’Ëµ’∫µ—π„Àâ¡’√ŸæÕ∑’Ë ®– Õ¥ “¬ «π‡æ◊ËÕ¢¬“¬∂à“ß‰¥â

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«‘∏’°“√∫√‘À“√¬“∑’Ë ‰¥âº≈¥’§◊Õ §“ “¬ «π‰«â „πÀ≈Õ¥‡≈◊Õ¥ ·¥ß„Àâª≈“¬ “¬®àÕ‡¢â“°—∫‡ÕÁ¡‚∫‰≈À√◊Õ∏√Õ¡∫— ‚¥¬µ√ß ·≈â«©’¥ UK „πª√‘¡“≥ Ÿß 250,000 ¬Ÿπµ‘ µàÕ™—«Ë ‚¡ß¿“¬„π√–¬–‡«≈“ 2-4 ™—«Ë ‚¡ß µ“¡¥â«¬°“√∑” arteriography ª√–‡¡‘π°“√√—°…“ À√◊Õ Õ’°«‘∏À’ π÷ßË §◊Õ§“ “¬ «π∑‘ßÈ ‰«âπ“π „Àâ UK „π¢π“¥µË”Õ¬à“ßµàÕ‡π◊ÕË ß ª√–‡¡‘πº≈°“√√—°…“‚¥¬°“√∑” arteriography ‡ªìπ√–¬– ¢≥–∫√‘À“√¬“§«√‡®“–‡≈◊Õ¥µ√«®¥Ÿ§«“¡º‘¥ª°µ‘¢Õß°≈‰°°“√ ·¢Áßµ—«¢Õß‡≈◊Õ¥‡ªìπ√–¬–¥Ÿ§«“¡‡À¡“– ¡¢Õß systemic fibrinolysis ·≈–ªÑÕß°—π¿“«–·∑√°´âÕπ∑’ÕË “®®–‡°‘¥¢÷πÈ

VI. Intraluminal Vascular Prostheses «‘∏°’ “√√—°…“„À¡à∑“ß endovascular therapy §◊Õ Õ¥ vascular bypass graft ºà“π‡¢â“∑“ßÀ≈Õ¥‡≈◊Õ¥∑’Ë¡’æ¬“∏‘ ¿“æ ‚¥¬„™â “¬ «π(15,16) ‚¥¬∑—«Ë ‰ª·≈â«°“√ºà“µ—¥„ àÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡ ‡æ◊ÕË ∑” bypass °Á ‰¥âº≈„π°“√√—°…“¥’Õ¬Ÿ·à ≈â« ·µà°‡Á ªìπ°“√ºà “ µ— ¥ „À≠à ´÷ËßÕ“®®–¡’¿“«–·∑√°´âÕπ‰¥â „ πºŸâ ªÉ « ¬∑’Ë ¡’ ‚√§ª√–®”µ—« ‡™àπ ‚√§À—«„®À√◊Õ‡∫“À«“πÕ¬Ÿ·à ≈â« ‰¥â¡«’ ∏‘ °’ “√„™â Intraluminal prostheses „π —µ«å∑¥≈Õß‰¥â º≈¥’ ·≈–π”¡“ªØ‘∫µ— √‘ °— …“¡πÿ…¬å™«à ß 3 ªï∑º’Ë “à π¡“ §“¥«à“«‘∏’ °“√π’È∂â“‰¥âº≈¥’®–‡ª≈’Ë¬π‚©¡Àπâ“·≈–·π«∑“ß„π°“√√—°…“‚√§ À≈Õ¥‡≈◊Õ¥„πÕπ“§µ (√Ÿª∑’Ë 7.4)

√ÿª °“√∑”À—µ∂°“√√—ß ’√«à ¡√—°…“„π‚√§À≈Õ¥‡≈◊Õ¥ ®–µâÕßÕ“»—¬ §«“¡√à«¡¡◊ÕÕ—π¥’√–À«à“ß»—≈¬·æ∑¬å∑“ßÀ≈Õ¥‡≈◊Õ¥°—∫√—ß ’·æ∑¬å µâÕßª√–‡¡‘π«à“ºŸªâ «É ¬‡À¡“– ¡°—∫°“√∑”À—µ∂°“√À√◊Õ‰¡à ∂â“‡°‘¥ ¿“«–·∑√°´âÕπ¢÷Èπ®–·°â ‰¢Õ¬à“ß‰√ „πÕπ“§µ endovascular therapy ®–¡’∫∑∫“∑¡“°„π°“√√—°…“‚√§À≈Õ¥‡≈◊Õ¥µ’∫µ—π·≈– ‚ªÉßæÕß ‚¥¬ºŸªâ «É ¬‰¡àµÕâ ß‡ ’¬Ë ßµàÕ°“√ºà“µ—¥„À≠àÕ°’ µàÕ‰ª

√Ÿª∑’Ë 7.4 «‘∏’°“√ endovascular therapy ‚¥¬°“√ Õ¥ vascular bypass graft ºà“π‡¢â“∑“ßÀ≈Õ¥‡≈◊Õ¥∑’¡Ë æ’ ¬“∏‘ ¿“æ‡™àπ AAA ‚¥¬„™â “¬ «π

°“√µ√«®«‘π‘®©—¬∑“ß√—ß ’«‘∑¬“·≈–√—ß ’√à«¡√—°…“

‡Õ° “√Õâ“ßÕ‘ß 1. Ahn SS, Eton D, Moore WS. Endovascular surgery for peripheral arterial occlusive disease: A critical review. Ann Surg 1992;216: 316. 2. White GH, White GA (eds.). Angioscopy: Vascular and Coronary Applications, Mosby Year Book, 1989. 3. Dotter CT, Judkins MP. Transluminal treatment of atherosclerotic obstruction: Description of a new technique and a preliminary report of its application. Circulation 1964;30:654. 4. Van Andel GJ, van Erp WFM, Krepel VM, et al. Percutaneous transluminal dilatation of the iliac artery: Long term results. Radiology 1985;156:321. 5. Martin ML, Veith FJ, Panetta TF, et al. Transfemoral stent graft treatment of occlusive arterial disease for limb salvage: A preliminary report. Circulation 1993;88:1. 6. Mahler F, Gallino A, Probst P, et al. Factors influencing early and late follow-up result after percutaneous transluminal angioplasty of the lower limb arteries. In:Dotter CT, Grunring A, Schoop W, et al, eds. Percutaneous transluminal Angioplasty. Berlin:Springer, 1983:199. 7. King SB III, Schlumpf M. Ten-year completed follow-up of percutaneous transluminal coronary angioplasty. The early Zurich experience. J Am Coll Cardiol 1993;22:353.

8. Tegtmeyer CJ, Kellum CD, Kron IL, et al. Percutaneous transluminal angioplasty in the region of the aortic bifurcation. Radiology 1985;157:661. 9. Schwarten DE. Transluminal angioplasty of renal artery stenosis: 70 experiences. Am J Roentgenol 1980;135:969. 10. Ahn SS, Eton D, Yeatman LR, et al. Intraoperative peripheral rotary atherectomy: Early and late clinical results. Ann Vasc Surg 1992;6:272. 11. White RA. White GH. Laser angioplasty: Development, current status and future perspectives. Sem Vasc Surg 1989;2:123. 12. Sanborn TA. Peripheral laser assisted balloon angioplasty: Initial multicenter trial in 219 peripheral arteries. Arch Surg 1989;168:121. 13. McNamara TO, Bombergen RA, Merchant RF. Intra-arterial urokinase as the initial therapy of acutely ischemic lower limbs. Circulation 1991;83:1106. 14. Montarjame A. Thrombolytic therapy in acute arterial occlusion and graft thrombosis. Semin Vasc Surg 1989;2:155. 15. Parodi J. Endovascular repair of abdominal aortic aneurysms. In: Advances in Vascular Surgery. Whittemore ET, et al(eds.) MosbyYear Book. 1993:85. 16. Parodi JC, Palmaz JC, Barone HD. Transfemoral intraluminal graft implantation for abdominal aortic aneurysms. Ann Vasc Surg 1992;5:491.

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∫∑∑’Ë 8 À≈Õ¥‡≈◊Õ¥‡∑’¬¡ ·≈–°“√µ‘¥‡™◊ÕÈ „πªí®®ÿ∫—πÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡∑’Ëπ”¡“„™â∑¥·∑πÀ≈Õ¥‡≈◊Õ¥ ·¥ß·≈–¡’§≥ ÿ ¡∫—µ¥‘ ‡’ ≈‘» (µ“√“ß∑’Ë 8.1) §√∫∑ÿ°¥â“π ¬—ß‡ªìπ∑’§Ë πâ §«â“«‘®¬— °—πÕ¬Ÿ‡à æ◊ÕË ∑’®Ë –‰¥âº≈‘µ¢÷πÈ ¡“„™âµÕà ‰ª„πÕπ“§µ „πªï §.». 1906 Carrel ·≈– Guthrie ‰¥âπ”‡Õ“À≈Õ¥‡≈◊Õ¥¥”¢ÕßºŸªâ «É ¬ ¡“‡¬Á∫∑¥·∑π À≈Õ¥‡≈◊Õ¥·¥ß∑’¡Ë ¢’ π“¥„°≈â‡§’¬ß°—π(1) (venous autograph) ·≈–µàÕ¡“‰¥â¡’°“√π”‡Õ“À≈Õ¥‡≈◊Õ¥·¥ß¢Õß —µ«å (xenograft) ¡“‡¬Á∫∑¥·∑π À≈Õ¥‡≈◊Õ¥‡∑’¬¡∫“ß™π‘¥‰¥âº≈¥’ Õ¬Ÿà ‰¥âπ“π ∫“ß™π‘¥°Á‡°‘¥ªØ‘°‘√‘¬“µâ“πµàÕ√à“ß°“¬ ¡’°“√ Ÿ≠ ≈“¬·≈–Õ—°‡ ∫µ‘¥‡™◊ÈÕ ‡ªìπ¿“«–·∑√°´âÕπµ“¡¡“ „πªï §.». 1952 Voorhees ‰¥âπ”‡Õ“ Vinyon-N-cloth ¡“‡¬Á∫‡ªìπÀ≈Õ¥ ‡≈◊Õ¥‡∑’¬¡∑¥·∑π aorta(2) À≈—ß®“°π—Èπ¡“ “√ —ß‡§√“–Àå‡√‘Ë¡¡’ ∫∑∫“∑„π°“√ºà“µ—¥À≈Õ¥‡≈◊Õ¥¡“°¢÷Èπ ®πªí®®ÿ∫—π “¡“√∂„™â À≈Õ¥‡≈◊Õ¥‡∑’¬¡∑’Ë¡’¢π“¥‡≈Á°∂÷ß 4 ¡‘≈≈‘‡¡µ√‰¥â Õ¬à“ß‰√°Áµ“¡ °“√ºà“µ—¥µàÕÀ≈Õ¥‡≈◊Õ¥¢π“¥‡≈Á°∑’ËÕ¬ŸàµË”°«à“À—«‡¢à“≈ß¡“ °“√ „™âÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡®–‰¥âº≈‰¥â ‰¡à¥’‡∑à“°—∫À≈Õ¥‡≈◊Õ¥¥”¢ÕßºŸâ ªÉ«¬‡Õß ‡æ√“–‡°‘¥≈‘Ë¡‡≈◊Õ¥·≈–°“√Õÿ¥µ—π‰¥âßà“¬ Õ“¬ÿ°“√„™â ß“π§àÕπ¢â“ß —πÈ À≈Õ¥‡≈◊Õ¥‡∑’¬¡∑’Ë „™â „πªí®®ÿ∫π— ¡’À≈“¬™π‘¥ (µ“√“ß∑’Ë 8.2)

1. ™’« “√ 1.1 À≈Õ¥‡≈◊Õ¥·¥ß¢ÕßºŸªâ «É ¬ (arterial autografts) ‡ªìπ À≈Õ¥‡≈◊Õ¥∑¥·∑π∑’Ë¥’‡≈‘»„π°“√‡¬Á∫µàÕ‡¢â“‚¥¬µ√ß°—∫À≈Õ¥ ‡≈◊Õ¥·¥ß¢ÕßºŸªâ «É ¬∑’¡Ë ¢’ π“¥·≈–§«“¡Àπ“„°≈â‡§’¬ß°—π(3,4) ¡’∑’Ë „™â

‡™àπ °“√ºà“µ—¥ coronary artery æ∫«à“„™â internal mammary artery ®–‰¥âº≈¥’°«à“„™â saphenous vein graft °“√ºà“µ—¥ renal artery reconstruction „π‡¥Á°æ∫«à“°“√„™â internal liac artery ¢ÕßºŸâªÉ«¬‡Õß¡“‡¬Á∫∑¥·∑π®–¥’∑’Ë ÿ¥‡æ√“–¢π“¥À≈Õ¥‡≈◊Õ¥ „°≈â‡§’¬ß°—π ‰¡à‡°‘¥ aneurysmal dilatation ßà“¬‡À¡◊Õπ°—∫°“√ „™â saphenous vein graft ·µà¡’¢âÕ‡ ’¬§◊Õ‡≈“–À“À≈Õ¥‡≈◊Õ¥ ≈”∫“° À≈Õ¥‡≈◊Õ¥∑’‡Ë ≈“–‰¥â¡°— ®– —πÈ ‡°‘π‰ª„π°“√µàÕ‡™◊ÕË ¡√–À«à“ß aorta °—∫ renal artery 1.2 À≈Õ¥‡≈◊Õ¥¥”¢ÕßºŸªâ «É ¬ (venous autografts) ‡ªìπ «— ¥ÿ∑À’Ë “‰¥âß“à ¬ ·≈–π”¡“‡¬Á∫µàÕ∑¥·∑π‰¥â¥ ’ ”À√—∫À≈Õ¥‡≈◊Õ¥ ·¥ß¢π“¥‡≈Á° ∑’Ë „™â „πªí®®ÿ∫π— ¡’ greater ·≈– lesser saphenous vein, cephalic vein, brachial vein, superficial femoral vein, internal, internal jugular vein œ≈œ µ“√“ß∑’Ë 8.1 §ÿ≥ ¡∫—µ¢‘ ÕßÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡∑’¥Ë ‡’ ≈‘» 1. 2. 3. 4. 5.

‡¢â“°—π‰¥â∑“ß™’«¿“æ°—∫‡π◊ÕÈ ‡¬◊ÕË ¢Õß√à“ß°“¬ ¡’§«“¡¬◊¥À¬ÿπà µâ“π·√ß‡ ’¬¥∑“π·≈–°√–· ‡≈◊Õ¥‰¥â ‰¡à∑”„Àâ‡°‘¥≈‘¡Ë ‡≈◊Õ¥‰¥âß“à ¬ ‰¡à¡‡’ ≈◊Õ¥√—«Ë ´÷¡ÕÕ°®“°À≈Õ¥‡≈◊Õ¥À≈—ß‡¬Á∫µàÕ·≈â« ‡¬Á∫µàÕ°—∫À≈Õ¥‡≈◊Õ¥‰¥âß“à ¬ ¡’À≈“¬¢π“¥„Àâ‡≈◊Õ°„™â ·≈– “¡“√∂∑”„Àâª√“»®“°‡™◊ÕÈ ‰¥â ‚¥¬§ÿ≥ ¡∫—µ‰‘ ¡à‡ª≈’¬Ë π·ª≈ß 6. ‰¡à‡°‘¥°“√Õ—°‡ ∫µ‘¥‡™◊ÕÈ 7. √“§“‰¡à·æß

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µ“√“ß∑’Ë 8.2 ™π‘¥µà“ß Ê ¢ÕßÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡ “√ —ß‡§√“–Àå

™’« “√

“√ —ß‡§√“–Àå √«¡°—∫™’« “√

∑”®“°„¬∂—° (textile) Woven Dacron Knitted Dacron Velour Biological Nontextile Teflon (ePTFE) Polyurethrane Bioabsorbable

Allograft End-to-end Arterial homografts straight graft Venous allografts Sequential grafts Umbilical vein Xenografts Bovine carotid Canine carotid Fibrocollagenous tubes Autogenous Heterogenous

„π°“√µàÕÀ≈Õ¥‡≈◊Õ¥·¥ß∑’ËÕ¬ŸàµË”°«à“¢“Àπ’∫≈ß¡“ °“√„™â greater saphenous vein ∑’‡Ë ≈“–µ—¥¡“®“°¢“¥â“πµ√ß°—π¢â“¡ ®–‰¥âº≈¥’°«à“À≈Õ¥‡≈◊Õ¥‡∑’¬¡™π‘¥Õ◊Ëπ À≈Õ¥‡≈◊Õ¥¥”∑’Ë‡≈“–¡“ ‰¥â °à Õ π∑’Ë ® –π”¡“µà Õ °— ∫ À≈Õ¥‡≈◊ Õ ¥·¥ß®–µâ Õ ß°≈— ∫ ¥â “ π„Àâ °√–· ‡≈◊Õ¥‰À≈‰ª Ÿà¢“‰¥â „π·π«¢Õß≈‘Èπªî¥‡ªî¥ (valve) ¢Õß À≈Õ¥‡≈◊Õ¥¥” (reversed saphenous vein graft) „π°“√„™â À≈Õ¥‡≈◊Õ¥¥”∑¥·∑πÕ’°«‘∏À’ π÷ßË ∑’Ë ‰¥â¥§’ Õ◊ çin situé saphenous vein bypass ‚¥¬„™â greater saphenous vein „π¢“¢â“ß ‡¥’¬«°—π°—∫À≈Õ¥‡≈◊Õ¥·¥ß∑’µË Õâ ß°“√ºà“µ—¥´àÕ¡·´¡ „™â valvulotome µ—¥ venous valve ·≈â«µàÕ saphenous vein ‡¢â“°—∫ À≈Õ¥‡≈◊ Õ ¥·¥ß‡≈¬‚¥¬‰¡à µâ Õ ß°≈— ∫ ¥â “ π æ∫«à “ ¢π“¥¢Õß saphenouse vein ·≈–À≈Õ¥‡≈◊Õ¥·¥ß à«πµâπ·≈– à«πª≈“¬¡’ ¢π“¥„°≈â‡§’¬ß°—π ∑”„ÀâµÕà ‰¥âß“à ¬ ‰¡àµÕâ ß≈ß·º≈ºà“µ—¥¬“«µ≈Õ¥¢“ ·≈–√–¬–‡«≈“∑’Ë „™â „π°“√ºà“µ—¥§àÕπ¢â“ß —πÈ (5) æ∫«à“°“√„™â autogenous reversed saphenous vein graft „π°“√µàÕÀ≈Õ¥‡≈◊Õ¥·¥ß femoral °—∫ politeal ®–¡’Õ“¬ÿ°“√„™â ß“π§àÕπ¢â“ß®–¥’ §◊Õ¿“¬„π 1 ªï ¬—ß„™âß“π‰¥â√Õâ ¬≈– 80-90 ¿“¬„π 5 ªï√Õâ ¬≈– 55-86 ¿“¬„π 10 ªï√Õâ ¬≈– 38-46 ·µà∂“â µàÕ≈ß¡“ ®π∂÷ß√–¥—∫µË”°«à“À—«‡¢à“∑’ÀË ≈Õ¥‡≈◊Õ¥¢π“¥‡≈Á°∑’ÀË ≈Õ¥‡≈◊Õ¥·¥ß tibial æ∫«à“Õ“¬ÿ„™âß“π®–µË”°«à“µàÕ‡Àπ◊ÕÀ—«‡¢à“‚¥¬‡©≈’¬Ë ª√–¡“≥ √âÕ¬≈– 10 °“√ Ÿ∫∫ÿÀ√’Ë∑”„ÀâÕ“¬ÿ°“√„™âß“π¢ÕßÀ≈Õ¥‡≈◊Õ¥ ‡∑’¬¡≈¥≈ß ∂â“„Àâ¬“µâ“π‡°√Á¥‡≈◊Õ¥æ∫«à“Õ“¬ÿ°“√„™âß“π¢Õß À≈Õ¥‡≈◊Õ¥‡∑’¬¡®–¥’¢π÷È (6,7)

¡’À≈“¬√“¬ß“π· ¥ß„Àâ‡ÀÁπ«à“ çin situé saphenous vein bypass ®–¡’Õ“¬ÿ°“√„™âß“π‚¥¬‡©≈’¬Ë Ÿß°«à“ reversed saphenous vein bypass(8,9,10) 1.3 Human umbilical vein grafts (HUVG) º≈‘µ®“° À≈Õ¥‡≈◊Õ¥¥”¢Õß “¬ –¥◊Õ‡¥Á°·√°§≈Õ¥ ´÷ßË ¡’§«“¡¬“«ª√–¡“≥ 50 ‡´Áπµ‘‡¡µ√ ¢π“¥‚µ ¡Ë”‡ ¡Õ 6-7 ¡‘≈≈‘‡¡µ√ ‰¡à¡·’ ¢πß·¬° π”¡“∑”§«“¡ –Õ“¥·™à·¢Áß ·≈–‡§≈◊Õ∫¥â«¬πÈ”¬“ 1% glutaraldehyde Àÿ¡â ¥â«¬„¬∂—° Dacron ¥â“ππÕ°‡æ◊ÕË ‡ √‘¡§«“¡·¢Áß·√ß „™â ”À√—∫‡¬Á∫´àÕ¡À≈Õ¥‡≈◊Õ¥¢π“¥‡≈Á° ‡¬Á∫ßà“¬ ¡’¢Õâ ‡ ’¬§◊Õ¢—πÈ µÕπ„π°“√º≈‘µ¬ÿàß¬“° √“§“·æß¡“° ·≈–¡’°“√¬àÕ¬ ≈“¬„π √à“ß°“¬∑”„ÀâÕ“¬ÿ°“√„™âß“π‰¡à¬“«π“π 1.4 À≈Õ¥‡≈◊Õ¥¢Õß —µ«å (Xenografts) ∑’Ë „™â§Õ◊ À≈Õ¥‡≈◊Õ¥ ·¥ß§“‚√µ‘§¢Õß«—« π”¡“¬àÕ¬ ≈“¬¥â«¬‡ÕÁπ´—¬¡å®π‡À≈◊Õ·µà nonantigenic collagen tube ·≈â«π”¡“‡§≈◊Õ∫¥â«¬ diadehyde starch „Àâ·¢Áß·√ß ¬—ß‰¡à‡ªìπ∑’πË ¬‘ ¡„™â „πªí®®ÿ∫π— 1.5 Fibrocollagenous tubes ‡ªìπ “√™’«¿“æ∑’ºË ≈‘µ®“° ‡π◊ÈÕ‡¬◊ËÕ¢Õß¡πÿ…¬åÀ√◊Õ —µ«å ¡’ªØ‘°‘√‘¬“µàÕ√à“ß°“¬πâÕ¬¡“° ·µà “¡“√∂¬àÕ¬ ≈“¬‰¥â ¬—ßÕ¬Ÿà „π√–¬–∑¥≈Õß §âπ§«â“ «‘®¬— ‰¡à ‰¥â π”¡“„™â∑“ß§≈‘π§‘

æ¬“∏‘«‘∑¬“¢ÕßÀ≈Õ¥‡≈◊Õ¥¥”∑¥·∑π ¿“¬À≈—ß°“√‡¬Á∫µàÕ¿“¬„π 30 «—π·√°·≈â«‰¡à “¡“√∂„™âß“π ‰¥â ¡’ “‡Àµÿ¡“®“°‡∑§π‘§°“√‡¬Á∫µàÕ‰¡à¥’ À√◊Õ¿“«– hypercoagulable ¢ÕßºŸªâ «É ¬‡Õß(7) ∂â“„™âß“π‰¡à ‰¥âÀ≈—ß°“√‡¬Á∫µàÕ 60 «—π ®–¡’ “‡Àµÿ¡“®“° progressive atherosclerosis ¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß µ”·Àπàß∑’ËÕ¬Ÿà ŸßÀ√◊ÕµË”°«à“∑’Ë‡¬Á∫µàÕ Õ¬à“ß‰√°Áµ“¡°“√µ’∫·§∫ ¢ÕßÀ≈Õ¥‡≈◊ Õ ¥¥”∑¥·∑πÕ“®®–¡’ “‡Àµÿ ¡ “®“°°“√ºà “ µ— ¥ ‡µ√’¬¡À≈Õ¥‡≈◊Õ¥‰¡à¥’ ¡’°“√„™â§’¡§’∫À≈Õ¥‡≈◊Õ¥√ÿπ·√ß‡°‘π‰ª ¡’°“√∑”≈“¬¢Õß‡ÕÁπ‚¥∑’‡≈’¬Ë ¡ ¡’ fibrosis ‡°‘¥¢÷πÈ µ√ß≈‘πÈ ªî¥‡ªî¥ ‡°‘¥ atherosclerosis ¢ÕßÀ≈Õ¥‡≈◊Õ¥¥”(11,12) ‡°‘¥ fibrointimal hyperplasia ‰¥â°—∫À≈Õ¥‡≈◊Õ¥¥”∑¥·∑π√âÕ¬≈– 10 ·≈–‡ªìπ “‡Àµÿ°“√µ’∫·§∫‰¥â√Õâ ¬≈– 15-30 ¢Õß coronary artery bypass(13) “‡Àµÿ∑ ’Ë ”§—≠∑’ Ë ¥ÿ ¢Õß fibrointimal hyperplasia §◊Õ °“√∂Ÿ°∑”≈“¬¢Õß‡ÕÁπ‚¥∑’‡≈’Ë¬¡¢≥–‡≈“–À≈Õ¥‡≈◊Õ¥À√◊Õ¢π“¥ ¢ÕßÀ≈Õ¥‡≈◊Õ¥¥”°—∫À≈Õ¥‡≈◊Õ¥·¥ß‰¡àæÕ¥’°π— ∑”„Àâ‡°‘¥ shearing force ¢Õß°√–· ‡≈◊Õ¥∑’Ë ‰À≈ºà“π(14,15) ‡ÕÁπ‚¥∑’‡≈’¬Ë ¡∑’∫Ë „ÿ π™—πÈ „π¢ÕßÀ≈Õ¥‡≈◊Õ¥¡’§≥ ÿ ¡∫—µ„‘ π°“√µâ“π°“√µ‘¥‡™◊ÕÈ ‡≈◊Õ¥·¢Áßµ—« ·≈– “¡“√∂º≈‘µ growth inhibiting factor ‰¥â¥«â ¬ ¢≥– ºà“µ—¥‡≈“–‡≈◊Õ¥¥”®÷ß§«√√–¡—¥√–«—ß‰¡à„ÀâÀ≈Õ¥‡≈◊Õ¥™Õ°™È”®π‡°‘π ‰ª(16,17)

À≈Õ¥‡≈◊Õ¥‡∑’¬¡·≈–°“√µ‘¥‡™◊ÈÕ

2. “√ —ß‡§√“–Àå ∑’Ë„™â „πªí®®ÿ∫π— §◊Õ À≈Õ¥‡≈◊Õ¥‡∑’¬¡ Dacron ·≈–∑’ºË ≈‘µ®“° polytetra fluoroethylene 2.1 Dacron grafts º≈‘µ®“° “√ —ß‡§√“–Àå‡ âπ„¬À≈“¬ ‡ âπ (multifilaments) ¡“∂—°∑Õ°—π‡ªìπ∑àÕ ∂â“‡ªìπ™π‘¥ Woven °“√∂—°∑Õ®–∂’Ë¡“°¡’√Ÿ√—Ë«„Àâ‡≈◊Õ¥´÷¡ÕÕ°¡“πâÕ¬ ·µà¡’¢âÕ‡ ’¬§◊Õ ‡¬Á∫¬“° ™π‘¥ Knitted graft ÕàÕππÿà¡·≈–‡¬Á∫ßà“¬ ¡’√Ÿ√—Ë«„Àâ ‡≈◊Õ¥´÷¡ÕÕ°¡“µâÕß preclotted °àÕπ„™â „πªí®®ÿ∫π— ‰¥â¡°’ “√º≈‘µ double velour Dacron graft ¢÷Èπ¡“„™â ‚¥¬¥â“ππÕ°·≈– ¥â“π„πÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡®–¡’ velour surface ‡ªìπ„¬ —ß‡§√“–Àå ∑’Ë∂—°∑Õ‡ªìπ·π«µ—Èß©“°µàÕ°—π∫ÿÕ¬Ÿà∑”„Àâ‡≈◊Õ¥√—Ë«´÷¡ÕÕ°¡“πâÕ¬ ‰¡àµâÕß preclotted °àÕπ„™â πÕ°®“°π’È¬—ß “¡“√∂‡¬Á∫‰¥âßà“¬‰¡à ≈◊πË ‡Àπ’¬«(18) À≈Õ¥‡≈◊Õ¥‡∑’¬¡™π‘¥Õ◊πË ∑’Ë ‰¡àµÕâ ß preclotted §◊Õ impregnated autoclave Dacron graft ®–‡§≈◊ Õ ∫¥â « ¬ ‚ª√µ’πÀ≈—ß®“°∑”„Àâª√“»®“°‡™◊ÕÈ ·≈â« “¡“√∂π”¡“„™â ‰¥â∑π— ∑’(19) 2.2 Polytetrafluoroethylene (PTFE) grafts º≈‘µ®“° “√ —ß‡§√“–Àå inert polymer ´÷ßË ª√–°Õ∫¥â«¬ solid nodes ¢Õß PTFE °—∫ interconnecting fobrils À≈Õ¥‡≈◊Õ¥‡∑’¬¡™π‘¥π’¡È ’ electronegative surface charge ´÷ßË ¡’§≥ ÿ ¡∫—µ‘ hydrophobic ‡°√Á¥‡≈◊Õ¥‰¡à‡°“–·≈–√«¡µ—«„πÀ≈Õ¥‡≈◊Õ¥„Àâ‡°‘¥≈‘Ë¡‡≈◊Õ¥·≈– µ“¡¡“¥â«¬°“√µ’∫·§∫‰¥âß“à ¬(20)

3. “√ —ß‡§√“–Àå√«¡°—∫™’« “√ (composite grafts) ‡ªìπ∑“ß‡≈◊Õ°∑’¥Ë ’„π°√≥’∑º’Ë ªŸâ «É ¬µâÕß°“√‡¬Á∫µàÕÀ≈Õ¥‡≈◊Õ¥∑” bypass µ—Èß·µà∫√‘‡«≥µË”°«à“¢“Àπ’∫≈ß¡“ ®π∂÷ßÀ≈Õ¥‡≈◊Õ¥

A √Ÿª∑’Ë 8.1 ™π‘¥µà“ß Ê ¢Õß composite graft A. °“√µàÕ·∫∫ end-to-end anastomosis B. composite sequential bypass graft

¢π“¥‡≈Á°∫√‘‡«≥πàÕßÀ√◊Õ¢âÕ‡∑â“·≈–‰¡à “¡“√∂‡≈“–À“À≈Õ¥ ‡≈◊Õ¥¥”∑¥·∑π∑’Ë¡’§«“¡¬“«‡æ’¬ßæÕ‰¥â ®÷ßµâÕß„™âÀ≈Õ¥‡≈◊Õ¥ ‡∑’¬¡‡¬Á∫µàÕ¥â“π∫π ·≈â«µàÕ¥â«¬À≈Õ¥‡≈◊Õ¥¥”(21,22) (√Ÿª∑’Ë 8.1) «‘∏°’ “√π’®È –·°âª≠ í À“À≈Õ¥‡≈◊Õ¥‡∑’¬¡À—°æ—∫ ∫√‘‡«≥¢âÕ‡∑â“‡æ√“–„™âÀ≈Õ¥‡≈◊Õ¥¥”§«“¡¬◊¥À¬ÿπà ·≈–°“√∑π µàÕ°“√‚°àßßÕ®–¥’°«à“ πÕ°®“°π’È¬—ß “¡“√∂‡¬Á∫µàÕ°—∫À≈Õ¥ ‡≈◊Õ¥·¥ß¢π“¥‡≈Á°∑’¢Ë “‰¥â‡π◊ÕË ß®“°¢π“¥‰¡àµ“à ß°—π¡“°

°“√‡≈◊Õ°„™âÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡ Dacron graft „™â ‰¥âº≈¥’„π°“√µàÕ°—∫À≈Õ¥‡≈◊Õ¥¢π“¥‚µ∑’Ë Õ¬Ÿ‡à Àπ◊Õ¢“Àπ’∫ ‡™àπ °“√∑” aortofemoral bypass æ∫«à“Õ“¬ÿ °“√„™âß“π¿“¬„π√–¬–‡«≈“ 5-10 ªï Ÿß∂÷ß√âÕ¬≈– 91 ·≈– 66 ∂â“‡ªìπ axillofemoral bypass Õ“¬ÿ°“√„™âß“π¿“¬„π 5 ªï √âÕ¬≈– 75 femorofemoral bypass Õ“¬ÿ°“√„™âß“π ¿“¬„π 5 ªï √âÕ¬≈– 75-80(23) ∂â“‡ªìπ°“√µàÕÀ≈Õ¥‡≈◊Õ¥¢π“¥‡≈Á°∑’ÕË ¬Ÿµà Ë”°«à“¢“Àπ’∫ ª√– ‘∑∏‘¿“æ·≈–Õ“¬ÿ°“√„™âß“π®–¥âÕ¬°«à“ PTFE ·≈–À≈Õ¥ ‡≈◊Õ¥¥”∑¥·∑π¢ÕßºŸªâ «É ¬‡Õß PTFE graft „™â ‰¥âº≈„°≈â‡§’¬ß°—∫ Dacron graft ∂÷ß·¡â«“à √“§“®– Ÿß°«à“ πÕ°®“°π’È¬—ß “¡“√∂„™âµàÕ°—∫À≈Õ¥‡≈◊Õ¥¢π“¥ °≈“ß·≈–¢π“¥‡≈Á° ∫√‘‡«≥∑’ËµË”°«à“¢“Àπ’∫≈ß¡“ Õ“¬ÿ°“√„™â ß“π‰¡à¥‡’ ∑à“À≈Õ¥‡≈◊Õ¥¥”∑¥·∑π¢ÕßºŸªâ «É ¬‡Õß(24,25) ‡ªìπ∑“ß‡≈◊Õ° Õ’°∑“ßÀπ÷Ëß ”À√—∫ºŸâªÉ«¬∑’Ë ‰¡à¡’ saphenous vein graft ¬“« ‡æ’¬ßæÕ À√◊ÕµâÕß°“√‡°Á∫‰«â ”À√—∫∑” coronary artery bypass graft (CABG) ‡π◊ËÕß®“°¡’§ÿ≥ ¡∫—µ‘∑’Ë ‰¡à§àÕ¬µ‘¥‡™◊ÈÕ·≈–‰¡à‡°‘¥ ≈‘¡Ë ‡≈◊Õ¥Õÿ¥µ—π‰¥âß“à ¬ ®÷ß‡ªìπ∑’πË ¬‘ ¡„™â ”À√—∫°“√ºà“µ—¥∑” vascular access ”À√—∫øÕ°‡≈◊Õ¥„πºŸªâ «É ¬‰µ«“¬‡√◊ÕÈ √—ß

°“√ ¡“πµ—«¢ÕßÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡ (PROSTHETIC GRAFT HEALING) °“√ ¡“πµ—«¢ÕßÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡„Àâ‡¢â“°—∫√à“ß°“¬¢Õß¡πÿ…¬å µà“ß®“°„π —µ«å∑¥≈Õß§◊Õ ®–‰¡à‡°‘¥°“√ ¡“πµ—«Õ¬à“ß ¡∫Ÿ√≥å ®–‰¡à¡‡’ ÕÁπ‚¥∑’‡≈’¬Ë ¡„π™—πÈ intima ‡À¡◊ÕπÀ≈Õ¥‡≈◊Õ¥ª°µ‘∑«—Ë ‰ª ∂÷ß·¡â«à“®–ºà“µ—¥‰ª·≈â«À≈“¬ªï ¡’‡©æ“–µ√ß∫√‘‡«≥„°≈â°—∫√Õ¬ µàÕ‡∑à“π—Èπ ‡≈¬®“°π—Èπ‰ª®–¡’·§à fibrin ª°§≈ÿ¡Õ¬Ÿà(26) ¥—ßπ—Èπ ª√– ‘ ∑ ∏‘ ¿ “æ·≈–Õ“¬ÿ ° “√„™â ß “π¢ÕßÀ≈Õ¥‡≈◊ Õ ¥‡∑’ ¬ ¡®–‰¡à ∑—¥‡∑’¬¡°—∫À≈Õ¥‡≈◊Õ¥¥”∑¥·∑πÀ√◊ÕÀ≈Õ¥‡≈◊Õ¥·¥ß¢ÕßºŸâ ªÉ«¬‰¥â‡≈¬ „πªí®®ÿ∫π— °Á¬ß— ¡’°“√§âπ§«â“«‘®¬— æ¬“¬“¡À“«‘∏’„Àâ‡ÕÁπ‚¥ ∑’‡≈’Ë¬¡µ‘¥°—∫ºπ—ß¥â“π„π¢ÕßÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡‡æ◊ËÕ„Àâ‡°‘¥°“√ ¡“πµ—«Õ¬à“ß ¡∫Ÿ√≥å(27) Õ“¬ÿ°“√„™âß“π®–‰¥âπ“π¢÷πÈ ‡π◊ÕË ß®“°‡°‘¥ °“√µ‘¥‡™◊ÕÈ ·≈–¡’≈¡‘Ë ‡≈◊Õ¥Õÿ¥µ—ππâÕ¬≈ß

¿“«–·∑√°´âÕπ¢ÕßÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡ ¿“«–·∑√°´â Õ π¢ÕßÀ≈Õ¥‡≈◊ Õ ¥‡∑’ ¬ ¡∑’Ë æ ∫‰¥â ∫à Õ ¬§◊ Õ neointimal hyperplasia ∫√‘‡«≥√Õ¬µàÕ´÷Ëß®–π”‰ª‡ªìπ “‡Àµÿ ¢Õß°“√µ’∫µ—π false aneurysm ∫√‘‡«≥√Õ¬µàÕ·≈–°“√µ‘¥‡™◊ÕÈ neointimal hyperplasia ‡°‘¥‰¥â „πÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡∑—Èß™π‘¥ Dacron ·≈– PTFE °“√„Àâ¬“µâ“π‡°√Á¥‡≈◊Õ¥®–™à«¬≈¥°“√‡°‘¥ neointimal hyperplasia „πÀ≈Õ¥‡≈◊Õ¥¥”∑¥·∑π ·≈–‰¥âº≈¥’ ‡™àπ‡¥’¬«°—π‡¡◊Ë Õ π”¡“„™â °— ∫ ºŸâ ªÉ « ¬∑’Ë ºà “ µ— ¥ ‡ª≈’Ë ¬ πÀ≈Õ¥‡≈◊ Õ ¥ ‡∑’¬¡(28,29) false aneurysm ∑’‡Ë °‘¥¢÷πÈ µ√ß√Õ¬µàÕ ¡’ “‡Àµÿ¡“®“°‡∑§π‘§ °“√ºà“µ—¥‰¡à¥’ ‡≈◊Õ°„™â« — ¥ÿ°“√‡¬Á∫‰¡à‡À¡“– ¡ °“√‡ ◊ÕË ¡ ¿“æ ¢ÕßÀ≈Õ¥‡≈◊Õ¥ °“√µ‘¥‡™◊ÕÈ ·≈– compliance mismatch(30,31) √—°…“‚¥¬°“√ºà“µ—¥·°â ‰¢‡ª≈’Ë¬πÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡„À¡à·≈–‡¬Á∫ ´àÕ¡·´¡ °“√µ‘¥‡™◊ÕÈ æ∫‰¥â√Õâ ¬≈– 1-2 ¡’ “‡Àµÿ¡“®“°°“√ªπ‡ªóÕô π¢≥– ºà“µ—¥¡“°°«à“µ‘¥‡™◊ÕÈ ®“°·À≈àßÕ◊πË (32) √—°…“‚¥¬°“√ºà“µ—¥‡Õ“À≈Õ¥ ‡≈◊Õ¥‡∑’¬¡ÕÕ° „Àâ¬“ªØ‘™«’ π– ∑” extra-anatomical bypass „Àâ‡≈◊Õ¥‰ª‡≈’¬È ß·¢π¢“ à«πª≈“¬ ºà“π∫√‘‡«≥∑’ Ë –Õ“¥(33)

À≈Õ¥‡≈◊Õ¥‡∑’¬¡„πÕπ“§µ „πªí®®ÿ∫π— ¬—ß¡’°“√«‘®¬— §âπ§«â“·≈–∑¥≈ÕßÀ“À≈Õ¥‡≈◊Õ¥‡∑’¬¡ ∑’Ë¡’§ÿ≥ ¡∫—µ‘¥’‡≈‘»„°≈â‡§’¬ß°—∫À≈Õ¥‡≈◊Õ¥·¥ß ·≈–æ¬“¬“¡À“ À≈Õ¥‡≈◊Õ¥‡∑’¬¡∑’Ë “¡“√∂µàÕ‡¢â“‰¥â°—∫À≈Õ¥‡≈◊Õ¥¢π“¥‡≈Á° ‚¥¬¡’°“√ ¡“π°—∫‡π◊ÈÕ‡¬◊ËÕ¢Õß¡πÿ…¬å¥’‡≈‘»‡°‘¥°“√µ’∫µ—ππâÕ¬

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥ ·≈–¡’§«“¡¬◊¥À¬ÿàπ¥’(34) ‡π◊ËÕß®“°À≈Õ¥‡≈◊Õ¥‡∑’¬¡¢“¥‡ÕÁπ‚¥∑’ ‡≈’¬Ë ¡∫ÿºπ—ß¥â“π„π‡À¡◊ÕπÀ≈Õ¥‡≈◊Õ¥∑—«Ë ‰ª ®÷ß∑”„Àâ‡°‘¥ thrombus ‰¥âß“à ¬·≈–¡’°“√Õÿ¥µ—π„π∑’ Ë ¥ÿ µ≈Õ¥®πßà“¬µàÕ°“√µ‘¥‡™◊ÕÈ ®÷ß‰¥â ¡’°“√æ¬“¬“¡‡§≈◊Õ∫‡ÕÁπ‚¥∑’‡≈’Ë¬¡‡¢â“°—∫ºπ—ß¥â“π„π¢ÕßÀ≈Õ¥ ‡≈◊Õ¥‡∑’¬¡(35) ¢≥–ºà“µ—¥ ∑”„Àâª√– ‘∑∏‘¿“æ¢ÕßÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡ ¥’¢÷Èπ (endothelial seeding grafts) ‰¥â¡’§«“¡æ¬“¬“¡„™â «— ¥ÿ∑∂’Ë °Ÿ ¥Ÿ¥´÷¡¿“¬„π√à“ß°“¬‰¥â∑“ß™’«¿“æ (biodegradable prostheses) ¡“º≈‘µ‡ªìπ∑àÕµàÕ‡¢â“°—∫À≈Õ¥‡≈◊Õ¥ ´÷ËßµàÕ¡“®–∂Ÿ°¥Ÿ¥ ´÷¡‡¢â“ Ÿà‡π◊ÈÕ‡¬◊ËÕ¢Õß√à“ß°“¬‚¥¬‰¡à¡’ªØ‘°‘√‘¬“„¥ Ê ·≈–‡π◊ÈÕ‡¬◊ËÕ ¢Õß√à “ ß°“¬®–æ¬“¬“¡ √â “ ß∑à Õ π”À≈Õ¥‡≈◊ Õ ¥¢÷È π ¡“„Àâ ¡’ ≈— ° …≥–„°≈â ‡ §’ ¬ ß°— ∫ À≈Õ¥‡≈◊ Õ ¥∑’Ë ÿ ¥ ¡’ ‡ ÕÁ π ‚¥∑’ ‡ ≈’Ë ¬ ¡·≈– °≈â“¡‡π◊ÕÈ ‡√’¬∫ µ≈Õ¥®π‡π◊ÕÈ ‡¬◊ÕË ‰ø∫√— (36,37) ·µà¡¢’ Õâ ‡ ’¬§◊Õ∂â“ ªØ‘°√‘ ¬‘ “¥Ÿ¥´÷¡ ≈“¬¿“¬„π√à“ß°“¬‡°‘¥‡√Á«‡°‘π‰ª ®–∑”„Àâ‡°‘¥ aneurysm πÕ°®“°π’¬È ß— ‰¥â¡§’ «“¡æ¬“¬“¡„π°“√À“ “√∑’¡Ë ¬’ ¥÷ ¬“ªØ‘-™’« π–„Àâµ‘¥°—∫À≈Õ¥‡≈◊Õ¥‡∑’¬¡ (impregnated graft) „™â ”À√—∫ ∫√‘‡«≥∑’µË ¥‘ ‡™◊ÕÈ ‰¥âß“à ¬(36) À√◊Õ¬÷¥‡Œª“√‘π°—∫À≈Õ¥‡≈◊Õ¥‰¡à „Àâ‡°‘¥ ≈‘¡Ë ‡≈◊Õ¥‰¥âß“à ¬¿“¬„πÀ≈Õ¥‡≈◊Õ¥(37) ‡¡◊ÕË ¡’°“√µ‘¥‡™◊ÕÈ S. epidermidis ®– √â“ß‡¡◊Õ°¢÷πÈ ¡“·≈â«Õ“»—¬Õ¬Ÿ·à ≈â«π—πÈ ‡¡◊Õ°™π‘¥π’®È –‡ªìπ µ—«ªÑÕß°—π°≈‰°·≈–ªØ‘°√‘ ¬‘ “¢Õß√à“ß°“¬„π°“√∑”≈“¬‡™◊ÕÈ ·≈–¬“ ªØ‘™«’ π–‰¡à “¡“√∂·∑√°´÷¡ºà“π‡¡◊Õ°‰ª∑”≈“¬‡™◊ÕÈ ·∫§∑’‡√’¬‰¥â

°“√Õ—°‡ ∫µ‘¥‡™◊ÈÕ¢ÕßÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡ Õ“°“√·≈–Õ“°“√· ¥ßºŸªâ «É ¬∑’¡Ë °’ “√µ‘¥‡™◊ÕÈ ¢ÕßÀ≈Õ¥‡≈◊Õ¥ ‡∑’¬¡®–¡“‚√ßæ¬“∫“≈¥â«¬°“√¡’‰¢âÀ√◊Õ°“√µ‘¥‡™◊ÈÕ·æ√à°√–®“¬ ‚¥¬∑’¬Ë ß— À“µâπµÕ‰¡à ‰¥â ¡’ cellulitis ·º≈‡ªìπÀπÕß °¥‡®Á∫ ¢Õß º‘«Àπ—ß à«π∑’§Ë ≈ÿ¡À≈Õ¥‡≈◊Õ¥‡∑’¬¡Õ¬Ÿà ∫“ß√“¬∑’√Ë πÿ ·√ß®–¡’ septic emboli À≈ÿ¥®“°À≈Õ¥‡≈◊Õ¥‡∑’¬¡‰ªÕÿ¥À≈Õ¥ à«πª≈“¬(38-46) °“√«‘π®‘ ©—¬ °“√µ√«®∑“ßÀâÕßªØ‘∫µ— °‘ “√®–æ∫«à“¡’‡¡Á¥‡≈◊Õ¥ ¢“«ª√‘¡“≥ Ÿßº‘¥ª°µ‘ (leukocytosis) ¡’°“√‡æ‘¡Ë ¢Õß erythrocyte sedimentation rate (ESR) °“√µ√«®«‘π®‘ ©—¬∑’¥Ë ∑’ ’Ë ¥ÿ ·≈– „Àâ°“√«‘π®‘ ©—¬∑’·Ë πàπÕπ§◊Õ °“√π”‡Õ“ isotope tagged WBC ®“°ºŸªâ «É ¬·≈â«©’¥°≈—∫‡¢â“‰ª„π√à“ß°“¬ºŸªâ «É ¬Õ’° √à«¡°—∫°“√∂à“¬ ¿“æ√—ß ’·∫∫ nuclear medicine ®–æ∫ WBC ‡°“–µ‘¥Õ¬Ÿà °—∫À≈Õ¥‡≈◊Õ¥‡∑’¬¡∑’Ëµ‘¥‡™◊ÈÕ(47) «‘∏’Õ◊Ëπ∑’Ë ‰¥âº≈¥’∂â“¡’°“√µ‘¥‡™◊ÈÕ ¿“¬„π™àÕß∑âÕß§◊Õ CT scan ·≈– MRI °“√Õ—°‡ ∫µ‘¥‡™◊ÈÕ„π ™àÕß∑âÕß‡™àπ diverticular disease Õ“®®–¡’°“√·æ√à°√–®“¬

À≈Õ¥‡≈◊Õ¥‡∑’¬¡·≈–°“√µ‘¥‡™◊ÈÕ ¢Õß‡™◊ÕÈ ·∫§∑’‡√’¬‡¢â“‰ª„πÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡„π™àÕß∑âÕß‡π◊ÕË ß®“° ‡ªìπ«— ¥ÿ·ª≈°ª≈Õ¡¢Õß√à“ß°“¬Õ¬Ÿ·à ≈â« °“√√—°…“ À≈—°°“√√—°…“§◊Õ æ¬“¬“¡√–∫“¬‡Õ“ÀπÕßÕÕ° „ÀâÀ¡¥ µ—¥‡π◊ÈÕ‡¬◊ËÕ∑’Ë‡πà“µ“¬·≈–µ‘¥‡™◊ÈÕÕÕ°„Àâ¡“°∑’Ë ÿ¥ ºà“µ—¥ ‡Õ“À≈Õ¥‡≈◊Õ¥‡∑’¬¡ÕÕ° º≈‡ ’¬∑’Ë‡°‘¥¢÷Èπµ“¡¡“§◊Õ ·¢π¢“®– ¡’ ° “√¢“¥‡≈◊ Õ ¥‰ª‡≈’È ¬ ß ∂â “ „ à À ≈Õ¥‡≈◊ Õ ¥‡∑’ ¬ ¡‡¢â “ ‰ª„π∑’Ë µ”·Àπàß‡¥‘¡®–‡°‘¥°“√µ‘¥‡™◊ÈÕ¢÷Èπ¡“Õ’° µ“¡À≈—°°“√·≈â«®“° °“√ºà“µ—¥‡Õ“À≈Õ¥‡≈◊Õ¥‡∑’¬¡ÕÕ° §«√„Àâ¬“ªØ‘™’«π–∑“ß À≈Õ¥‡≈◊Õ¥¥”Õ¬à“ßµàÕ‡π◊ÕË ß 7-10 «—π À≈—ß®“°π—πÈ ®÷ß®–ºà“µ—¥∑” revescularization(48,49) „π√–¬–π’°È “√¢“¥‡≈◊Õ¥Õ“®®–√ÿπ·√ß®π ºŸªâ «É ¬‰¡à “¡“√∂∑π‰¥â ·¢π¢“Õ“®®–‡πà“µ“¬ «‘∏°’ “√∑’¥Ë ∑’ ’Ë ¥ÿ §◊Õ „ àÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡„À¡à∑π— ∑’ ªí≠À“ ”§—≠≈”¥—∫µàÕ¡“§◊Õ À≈Õ¥‡≈◊Õ¥‡∑’¬¡„À¡à®–„ à‡¢â“ ∫√‘‡«≥„¥∂â“‡ªìπ∑’·Ë ¢π¢“ “¡“√∂∑’®Ë –∑” extra-anatomical bypass ºà“π∫√‘‡«≥∑’Ë ‰¡à¡°’ “√µ‘¥‡™◊ÕÈ ∂â“·µà‡ªìπ∑’Ë abdominal aorta §«√®–∑”‡ªìπ axillo-bifemoral bypass ´÷ßË Õ—µ√“µ“¬πâÕ¬ ®–∑” in situ bypass °ÁµàÕ‡¡◊ËÕ„π™àÕß∑âÕß¡’°“√Õ—°‡ ∫µ‘¥‡™◊ÈÕ‰¡à √ÿπ·√ßÀ√◊Õ¬âÕ¡ ’°√—¡·≈â«‰¡àæ∫‡™◊ÕÈ (50)

√ÿª „πªí®®ÿ∫π— ¬—ß‰¡à¡À’ ≈Õ¥‡≈◊Õ¥‡∑’¬¡™π‘¥„¥∑’¡Ë §’ ≥ ÿ ¡∫—µ¥‘ ‡’ ≈‘» ”À√—∫°“√ºà“µ—¥µàÕÀ≈Õ¥‡≈◊Õ¥∑ÿ°¢π“¥·≈–∑ÿ°µ”·Àπàß¢Õß √à“ß°“¬ ¬—ß¡’°“√§âπ§«â“«‘®—¬∑¥≈Õß‡æ◊ËÕÀ“À≈Õ¥‡≈◊Õ¥‡∑’¬¡∑’Ë¡’ §ÿ≥ ¡∫—µ‘„°≈â‡§’¬ß°—∫À≈Õ¥‡≈◊Õ¥∑’Ë ÿ¥ ¡’Õ“¬ÿ°“√„™âß“π‰¥âπ“π ‰¡àµ’∫µ—π·≈–µ‘¥‡™◊ÈÕ‰¥âßà“¬ »—≈¬·æ∑¬å§«√¡’§«“¡√Ÿâ§«“¡‡¢â“„® ∂÷ßª√– ‘∑∏‘¿“æ¢ÕßÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡™π‘¥µà“ß Ê ‡æ◊ËÕ∑’Ë®– “¡“√∂‡≈◊Õ°„™â°—∫°“√ºà“µ—¥·µà≈–™π‘¥‰¥â∂Ÿ°µâÕß °“√µ‘¥‡™◊ÈÕ ¢ÕßÀ≈Õ¥‡≈◊ Õ ¥‡∑’ ¬ ¡æ∫‰¥â πâ Õ ¬·µà ‡ ¡◊Ë Õ ‡°‘ ¥ ¢÷È π ·≈â « ¿“«– ·∑√°´âÕπ√ÿπ·√ß¡“° °“√ªÑÕß°—π°“√µ‘¥‡™◊ÈÕµ≈Õ¥®π√–¡—¥ √–«—ß‡°’Ë¬«°—∫‡∑§π‘§°“√ª√“»®“°‡™◊ÈÕ®–‡ªìπ«‘∏’∑’Ë¥’°«à“√—°…“ ¿“«–·∑√°´âÕπµà“ß Ê ∑’‡Ë °‘¥¢÷πÈ ·≈â«¿“¬À≈—ß

‡Õ° “√Õâ“ßÕ‘ß 1. Carrel A, Guthrie CG. Uniterminal and biterminal venous transplantations. Surg Gynecol Obstet 1906;2:266-271. 2. Blakemore AH, Voorhees AB Jr. Use of tubes constructed from vinyon çNé cloth in bridging arterial defects: Experimental and clinical. Ann Surg 1954; 140:325-331. 3. Edwards WS. Arterial grafts, Past, present, and future. Arch Surg 1978; 133:1225-1233. 4. Stoney RJ, Wylie EJ. Arterial autografts. Surgery 1970;67:18-24. 5. Leather RP, Shah DM, Buchbinder D, et al. Further experience with the saphenous vein used in situ for arterial bypass. Am J Surg 1981;142:506-512.’ 6. Taylor LM, Edwards JM, Porter JM. Present status of reversed vein bypass grafting:Five-year results of a modern series. J Vasc Surg 1990;11:193-201. 7. Sonnenfeld T, Cronestrard R. Factors determining outcome of reversed saphenous vein femoropoliteal bypass grafts. Br J Surg 1980;67:642-648. 8. Batson RC, Sottiurai VS. Nonreversed and in situ vein grafts. Ann Surg 1985;201:771-779. 9. Buchbinder D, Singh JK, Karmody AM et al. Comparison of patency rate and structural change of in situ and reversed vein arterial bypass. J Surg Res 1981;30:213-219. 10. Bergamini TM, Towne JB, Bandyk DF, et al. Experience with in situ saphenous vein bypasses during 1981 to 1989:Determinant factors of long-term Patency. J Vas Surg 1991;13:137-141. 11. Fuchs JCA, Mitchener JS III, Hagen P. Postoperative change in autologous vein grafts. Ann Surg 1978;1:188-193. 12. Reifsynyder T, Towne JB, Seabrook GR, et al. Biologic characteristics of long-term autogenous vein grafts: A dynamic evaluation. J Vasc Surg 1993;17:207-212. 13. Atkinson JB, Forman MB, Vaughn WK, et al. Morphologic changes in long-term saphenous vein bypass graft. Chest 1985;88:341-348. 14. Bush HL, McCabo ME, Nabseth DC. Functional injury of vein graft endothelium. Arch Surg 1984;119:770-776. 15. Abbott WM, Wieland S, Austin WG. Structural changes during preparation of autogenous venous grafts. Surgery 1972;76:10311307. 16. Bonchek LI. Prevention of endothelial damage during preparation of saphenous veins for bypass grafting. J Thorac Cardiovasc Surg 1980;79:911-916. 17. LoGerfo FW, Quist WC, Crawshaw HM, Haudenschild C. An improved technique for preservation of endothelium morphology in vein grafts. Surgery 1981;90:1015-1019.

86 18. Goldman M, McCollum CN, Hawker RJ, et al. Dacron arterial grafts: The influence of porosity, velour, and maturity on thrombogenicity. Surgery 1982;92:947-954. 19. Quinones-Baldrich WJ, Moore WS, et al. Development of a çleakproofé Knitted Dacron vascular prostheses. J Vasc Surg 1986;3:895902. 20. Kempczinski RF. Physical characteristics of implanted polytetrafluoroethylene grafts: A priliminary report. Arch Surg 1979;114:917-922. 21. Edwards WS, Gerety E, Larkin J, et al. Multiple sequential femoraltibial grafting for severe inchemia. Surgery 1976;80:722-731. 22. Flinn WR, Ricco JB, Yao JST, et al. Composite sequential grafts in severe ischemia: A comparative study. J Vasc Surg 1984;1:449454. 23. Crawford ES, Bomberger RA, Glaeser DH, et al. Aortoiliac occlusive disease: Factors influencing survival and function following reconstructive operation over twenty-five year period. Surgery 1981;90:1055-1063. 24. Michaels JA. Choice of material for above-knee femoropopliteal bypass graft. Br J Surg 1989;76:7-13. 25. Tilanus HW, Obertop H, Urk HV. Saphenous vein or PTFE for femoropopliteal bypass. A prospective randomized trial. Ann Surg 1985;202:780-788. 26. Sauvage LR, Berger K, Wood SJ, et al. Interspecies healing of porous arterial prostheses: Observations, 1960-1974. Arch Surg 1974;109:698. 27. Graham LM, Burkel WE, Ford JW, et al. Immediate seeding of enzymatically derived endothelium in Dacron vascular grafts. Arch Surg 1980;115:1289. 28. Chesebro JH, Clements IP, Furter V, et al. A platelet inhibitor drug trial in coronary artery bypass operations. N Engl J Med 1982;307:73. 29. Goldman MD, Simpson D, Hawker RJ, et al. Aspirin and dipyridamole reduce platelet deposition on prosthetic femoropopliteal grafts in man. Ann Surg 1983;198(6):713. 30. Szilagyi DE, Smith RF, Elliott JP, et al. Anastomic aneurysms after vascular reconstruction: Problems of incidence, etiology and treatment. Surgery 1975;78:800. 31. Dennis JW, Littooy FN, Greisler HP, et al. Anastomotic pseudoaneurysms. A continuing late complication of vascular reconstructive procedures. Arch Surg 1986;121:314. 32. Bandyk DF. Vascular graft infections: Epidemiology, microbiology, pathogenesis and prevention. In: Bernhard VM, Towne JB (eds). Complications in Vascular Surgery. St Louis, Quanlity Medical Pulbishing. 1991;223-234. 33. Taylor SM, Mills JL, Fujitani RM, et al. The influence of groin sepsis on extra-anatomical bypass patency in patients with prosthetic graft infection. Ann Vasc Surg 1992;6:80.

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥ 34. Sauvage LR, Berger K, Mansfield PB, et al. Future directions in the development of arterial prostheses for small and medium caliber arteries. Surg Clin North Am 1974;54:213. 35. Herring MB, Baughman S, Glover JL, et al. Endothelial seeding of Dacron and poly tetrafluoroethylene grafts: The cellular events of healing. Surgery 1984;96:745. 36. Shue WB, Worosilo SC, Donetz AP, et al. Prevention of vascular prosthetic infection with an antibiotic-bonded Dacron graft. J Vasc Surg 1988;8:600. 37. Esquivel CO, Bjorck C-G, Bergentz S-E, et al. Reduced thrombogenic characteristics of expanded polytetrafluroethylene and polyurethane arterial grafts after heparin bonding. Surgery 1984;95:102. 38. Bandyk DF. Vascular graft infection: epidemiology, bacteriology, and pathogenesis. In:Bernhard VM, Towne JB. (eds) Complications in Vascular Surgery. New York: Grune & Stration, 1985;471-494. 39. Bunt TJ. Synthetic vascular graft infection; I. Graft infection. Surgery 1983;93:733-741. 40. Seabrook GR, Schmitt DD, Bandyk DF, et al. Anastonotic femoral pseudoaneurysm: An investigation of occult infection as an etiologic factor. J Vas Surg 1990;11:629-636. 41. Bandyk DF, Berni GA, Thiele BL, et al. Aortofemoral graft infection to Staphylococcus epidermidis. Arch Surg 1984;119:102. 42. Ernst CB, Campbell HC, Daugherty ME, et al Incidence and significance in intraoperative bacterial culture during abdominal abdominal aortic aneurysmectomy. Ann Surg 1977;185:625-633. 43. Leny MF, Schmitt DD, Edminton CE, et al. Sequential analysis of Staphylococcal colonization of body surfaces of patients undergoing vascular surgery. J Clin Microbiol 1990;28:664-671. 44. MacBeth GA, Rubin JR, McIntyre KE, et al. The relevence of arterial wall icrobiology to the treatment of prosthetic graft infections: Graft infection versus arterial infection. J Vasc Surg 1984;1:750785. 45. Rubin JR, Malone JM, Goldstone J. The role of the lymphatic system in acute arterial prosthetic graft infection. J Vasc Surg 1985;2:92-98. 46. Schmitt DD, Bandyk DF, Pequet AJ, et al. Bacterial adherance to vascular prostheses: A determinant of graft infectivity. J Vasc Surg 1986;3:732-739. 47. Lawrence PF, Dries DJ, Alazraki N, Albo D. Indium 111-labeled leukocyte scanning for detection of prosthetic graft infection. J Vasc Surg 1985;2:165. 48. Lorentzen JE, Nielsen, OM, Arendrup H, et al. Vascular graft infection; An analysis of sixty-two graft infections in 2411 consecutively implanted synthetic vascular grafts. Surgery 1985;98:81. 49. Reilly LM, Ehrenfeld WK, Stoney RJ. Delayed aortic prosthetic reconstruction after removal of an infected graft. Am J Surg 1984;148:234. 50. Turnipseed WD, Berkoff HA, Detmer DE, et al. Arterial graft infections: delayed versus immediate vascular reconstruction. Arch Surg 1983;118:410.

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ment depression · ¥ß∂÷ßπ—¬ ”§—≠¢Õß‚√§À—«„®§«√∑”°“√ µ√«®æ‘‡»…·≈– ◊∫§âπµàÕ‰ª ¢âÕ®”°—¥¢Õß°“√∑” exercise test §◊ÕºŸâªÉ«¬‚√§À≈Õ¥‡≈◊Õ¥¢“¡—°®–‡¥‘π°–‡º≈°·≈–ª«¥¢“‡ ’¬ °àÕπ∑’®Ë –µ√«®æ∫§«“¡º‘¥ª°µ‘¢ÕßÀ—«„® ‰¡à “¡“√∂µ√«®§âπ‰¥â „π ºŸâªÉ«¬∑’Ëµ—¥¢“·≈â«·≈–„ à¢“‡∑’¬¡ ºŸâªÉ«¬∑’Ë√—∫ª√–∑“π¬“¢—∫ ªí “«–·≈– B-blocker °“√·ª≈º≈®–º‘¥æ≈“¥ ªí®®ÿ∫π— exercise test π‘¬¡∑”πâÕ¬≈ß ‡π◊ËÕß®“°¡’«‘∏’µ√«®Õ◊Ëπ´÷Ëß·ª≈º≈‰¥â ·πàπÕπ°«à“‚¥¬∑’ºË ªŸâ «É ¬‰¡àµÕâ ß‡¥‘πÕÕ°°”≈—ß°“¬

2. echocardiography and radionuclide ventriculography ‡ªìπ°“√µ√«®«‘π®‘ ©—¬‡æ◊ÕË ª√–‡¡‘π ejection fraction (EF) ºŸâªÉ«¬∑’Ë¡’ EF º‘¥ª°µ‘®–¡’Õ“°“√·≈–Õ“°“√· ¥ß¢Õß‚√§À—«„® ‡ÀÁπ‰¥â™—¥‡®π„π¢≥–∑”°“√ºà“µ—¥ ‚¥¬‡©æ“–∂â“ EF πâÕ¬°«à“ §à“ª°µ‘√Õâ ¬≈– 35(8,9) ∫“ß§√—ßÈ ºŸªâ «É ¬¡’ EF ª°µ‘·µà¬ß— ¡’ coronary heart disease °“√µ√«®«‘π‘®©—¬™π‘¥π’È¡’ª√–‚¬™πå „π·ßà°“√∑” screen test ‚√§À—«„®∑—«Ë ‰ª°àÕπ∑’®Ë –∑” invasive monitoring ·µà ‰¡à‡À¡“– ¡ ”À√—∫°“√µ√«®«‘π‘®©—¬‚√§À≈Õ¥‡≈◊Õ¥À—«„®‚§ ‚√π“√’Ë

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4. dipyridamole-Thallium Scintigraphy (DTS) ‡ªìπ«‘∏°’ “√µ√«®«‘π®‘ ©—¬∑’Ë „™âÕ¬à“ß·æ√àÀ≈“¬„πªí®®ÿ∫π— „π°“√ ª√–‡¡‘π ‚√§À—«„®¢ÕßºŸªâ «É ¬‚√§À≈Õ¥‡≈◊Õ¥(12) dipyridamole ®– ¡’º≈„π°“√¢¬“¬À≈Õ¥‡≈◊Õ¥ ·≈– “¡“√∂∑¥·∑π°“√ÕÕ°°”≈—ß °“¬‰¥â thallium „™âª√–‡¡‘π cardiac perfusion «‘∏°’ “√§◊Õ©’¥ dipyridamole ‡¢â“À≈Õ¥‡≈◊Õ¥¥”¿“¬„π 4 π“∑’ À≈—ß®“°π—πÈ ©’¥ thallium 201 ·≈–∑” isotope scan ∑—π∑’ °“√·ª≈º≈ scan ®–µâÕßÕ“»—¬°“√‡ª√’¬∫‡∑’¬∫°—π√–À«à“ß scan ∑’Ë‡ÀÁπ§√—Èß·√° °—∫§√—ßÈ ∂—¥¡“ °≈â“¡‡π◊ÕÈ À—«„® à«π∑’ªË °µ‘®–‡ÀÁπ uptake ¢Õß thallium scan ∑—π∑’∫√‘‡«≥∑’Ë ‰¡à‡ÀÁπ uptake §◊Õ∫√‘‡«≥√àÕß√Õ¬ ‡°à“¢Õß°≈â“¡‡π◊ÕÈ À—«„®∑’¡Ë °’ “√¢“¥‡≈◊Õ¥¡“°àÕπ à«π∑’Ë ‰¡à‡ÀÁπ uptake ∑’Ë·√°·µà¡“‡ÀÁπ¿“¬À≈—ß®–¡’ ‚Õ°“ ¢“¥‡≈◊Õ¥¡“‡≈’È¬ß‰¥â ßà“¬®–‰¥â√–¡—¥√–«—ß°àÕπºà“µ—¥ ·≈–æ‘®“√≥“°“√µ√«®«‘π®‘ ©—¬À≈Õ¥

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5. Dobutamine Stress Echocardiography (DSE) ‡ªìπ«‘∏’°“√µ√«®«‘π‘®©—¬·≈–ª√–‡¡‘π‚√§°≈â“¡‡π◊ÈÕÀ—«„®¢“¥ ‡≈◊Õ¥ ·µà¬ß— ‰¡à‡ªìπ∑’πË ¬‘ ¡·æ√àÀ≈“¬(13) dobutamine ‡ªìπ B1 antogonist ´÷Ëß¡’ƒ∑∏‘Ï inotropic ·√ß ·µà chronotropic ÕàÕπµàÕÀ—«„® «‘∏°’ “√§◊Õ©’¥ dobutamine ‡¢â“∑“ßÀ≈Õ¥‡≈◊Õ¥™â“ Ê ·≈–§àÕ¬ Ê ‡√Á«¢÷πÈ ¢≥–‡¥’¬«°—π°Á monitor 2-dimensional echocardiography ‡æ◊ÕË ‡≈◊Õ¥™â“ Ê ·≈–§àÕ¬ Ê ‡√Á«¢÷πÈ ¢≥– ‡¥’¬«°—π°Á monitor 2-dimensional echocardiography ‡æ◊ÕË —ß‡°µÿ¥Ÿ°“√‡§≈◊ËÕπ‰À«¢Õß°≈â“¡‡π◊ÈÕÀ—«„® à«π∑’Ëº‘¥ª°µ‘ ‡π◊ËÕß ®“°¢“¥‡≈◊Õ¥¡“‡≈’¬È ß ∂â“™’æ®√‰«‡°‘π‰ª„Àâ atropine ‡ªìπ antagonist ‰¥â À¬ÿ¥°“√µ√«®‡æ◊ËÕæ∫«à“À—«„®¢“¥‡≈◊Õ¥À√◊Õ™’æ®√‰«â∂÷ß ®ÿ¥∑’ËµâÕß°“√ “¡“√∂„™â ‰ ¥â „πºŸâªÉ«¬ bronchospasm ‡æ√“– dobutamine ‰¡à∑”„ÀâÀ≈Õ¥‡≈◊Õ¥À¥µ—« §«√ß¥¬“æ«° B-blocker °àÕπµ√«®‡æ√“–®–∑”„Àâ°“√·ª≈º≈º‘¥æ≈“¥

6. Cardiac catheterization ‡æ◊ÕË ¥Ÿ§«“¡º‘¥ª°µ‘¢ÕßÀ≈Õ¥‡≈◊Õ¥À—«„®‚§‚√π“√’Ë ¡’¢Õâ ∫àß„™â „πºŸªâ «É ¬∑’∑Ë ” screening test ∑’°Ë ≈à“«¡“·≈â«‰¥âº≈∫«° ¡’ unstable angina ·≈–ºŸªâ «É ¬∑’µË Õâ ß°“√ºà“µ—¥ coronary artery bypass graft (CABG) °àÕπ°“√ºà“µ—¥À≈Õ¥‡≈◊Õ¥

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°“√ª√–‡¡‘πºŸâªÉ«¬∑“ßÕ“¬ÿ√°√√¡ ºŸâªÉ«¬∑’Ë‡ ’Ë¬ßµàÕ¿“«–·∑√°´âÕπ∑“ß√–∫∫À“¬„®¢≥–ºà“µ—¥ ·≈–À≈—ßºà“µ—¥®–µâÕß‡®“–À“§à“ blood gas ·≈–∑” pulmonary function test (PFT) oxygenation ª√–‡¡‘π‰¥â®“° PaO2, alveolar ventilation ª√–‡¡‘π‰¥â®“° PaCO2 Forced Expiratory Volume (FEV1) À¡“¬∂÷ßª√‘¡“µ√¢ÕßÕ“°“»∑’ÀË “¬„®ÕÕ°‰ª„Àâ ‰¥â¡“°∑’Ë ÿ¥¿“¬„π√–¬–‡«≈“ 1 «‘π“∑’ Total volume §◊Õ ª√‘¡“≥¢ÕßÕ“°“»‡ª≈’¬Ë π·ª≈ß¢Õß normal ventilatory cycle ·≈– Functional Residual Capacity (FRC) §◊Õª√‘¡“µ√¢Õß Õ“°“»∑’§Ë “â ßÕ¬Ÿ¿à “¬„πªÕ¥À≈—ßÀ“¬„®ÕÕ°µ“¡ª°µ‘ (µ“√“ß∑’Ë 9.1) Flow rates ®–∫àß∫Õ°∂÷ßª√‘¡“µ√Õ“°“»∑’ËÀ“¬„®ÕÕ° ¿“¬„π√–¬–‡«≈“Àπ÷Ëß °“√«—¥π’È®–¡’ª√– ‘∑∏‘¿“æ‡æ’¬ß„¥¢÷ÈπÕ¬Ÿà °—∫§«“¡ “¡“√∂„π°“√À“¬„®¢ÕßºŸªâ «É ¬ „™â ”À√—∫¥Ÿ obstructive airway disease(14) ∫Õ°§à“‡ªìπ percentage of expected volume „π‚√§À≈Õ¥≈¡¢π“¥‡≈Á°®–æ∫§«“¡º‘¥ª°µ‘¢Õß mid expiratory flow rate (FEF25%-75%) ∫àß∫Õ°∂÷ß§à“°÷ßË °≈“ß¢Õß°“√ À“¬„®‡ªìπ≈‘µ√µàÕπ“∑’ (spirogram) §à“ FEF25%-75% ®–ª°µ‘®– Ÿß°«à“√âÕ¬≈– 80 ¢Õß√–¥—∫∑’§Ë “¥‰«âÀ√◊Õª√‘¡“µ√√–À«à“ß 150200 ≈‘µ√µàÕπ“∑’ Maximal voluntary ventilation §◊Õª√‘¡“≥¢ÕßÕ“°“» ¡“°∑’Ë ÿ¥∑’ËÀ“¬„®‡¢â“ÕÕ°¿“¬„π 1 π“∑’ §à“‡©≈’Ë¬ 150-200 ≈‘µ√µàÕπ“∑’ ¢÷πÈ Õ¬Ÿ°à ∫— ª√– ‘∑∏‘¿“æ°“√∑”ß“π¢Õß°≈â“¡‡π◊ÕÈ À—«„® lung compliance ·≈– dead space tidal volume «‘∏°’ “√ µ√«®π’È · πà π Õπ·≈– “¡“√∂§“¥¿“«–·∑√°´â Õ π∑’Ë ® –‡°‘ ¥ ¢÷È π ¿“¬À≈—ß°“√ºà“µ—¥‰¥â µ“√“ß∑’Ë 9.1 °“√ª√–‡¡‘π°“√∑”ß“π¢ÕßªÕ¥ «‘∏µ’ √«®

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90 ®–º≈‘µ¢÷Èπ®“°µ—∫∂â“ºŸâªÉ«¬¡’¿“«–µ—∫«“¬À√◊Õ‚√§µ—∫‡√◊ÈÕ√—ß®– ∑”„Àâ√–¥—∫¢Õß A-III µË”°«à“ª°µ‘ °“√¢“¥ lupus anticoagulant ·≈– anticardiolipin antibodies ‡ªìπ‚√§„π°≈ÿ¡à antiphospholipid antibody syndromes lupus anticoagulant ‡ªìπ acquired IgG À√◊Õ IgM antibodies ´÷Ë ß «— ¥ ª√‘ ¡ “≥‰¥â ® “° Russel viper venom time anticardiolipin ‡ªìπ IgM antibodies ·≈–«—¥ª√‘¡“≥‰¥â®“° enzyme-linked immunosorbent assay (ELISA) ´÷ßË ¡’ cardiolipin ‡À¡◊Õπ antigen ºŸªâ «É ¬‡À≈à“π’®È –æ∫«à“ prolonged activated PTT ´÷ßË ‡ªìπº≈¡“®“°§«“¡º‘¥ª°µ‘¢Õß antibodies „π phospholipid dependent assay Õ“°“√· ¥ß∑’æË ∫‰¥â∫Õà ¬§◊Õ ‡°‘¥≈‘Ë¡‡≈◊Õ¥‰¥âßà“¬ ∑—Èß„πÀ≈Õ¥‡≈◊Õ¥¥”·≈–À≈Õ¥‡≈◊Õ¥·¥ß «‘∏’ °“√√—°…“§◊Õ„Àâ√—∫ª√–∑“π¬“ Coumadin Õ¬à“ßµàÕ‡π◊ËÕß‡ªìπ √–¬–‡«≈“π“π

√ÿª ºŸªâ «É ¬‚√§À≈Õ¥‡≈◊Õ¥ ŸßÕ“¬ÿ ¡—°®–¡’‚√§∑“ßÕ“¬ÿ√°√√¡Õ◊πË Ê √à«¡¥â«¬‡ ¡Õ °àÕπ∑’Ë®–√—°…“‚¥¬°“√ºà“µ—¥§«√®–ª√–‡¡‘ π ¿“«–µà“ß Ê ¢ÕßºŸªâ «É ¬‡ ’¬°àÕπ ∂â“¡’§«“¡º‘¥ª°µ‘¢Õß‚√§À—«„® ‚√§ªÕ¥·≈–§«“¡º‘¥ª°µ‘„π°“√·¢Áßµ—«¢Õß‡≈◊Õ¥§«√√—°…“·≈– ‡µ√’¬¡æ√âÕ¡‡¡◊ËÕ‡°‘¥¿“«–·∑√°´âÕπÀ≈—ßºà“µ—¥‡æ◊ËÕ∑’Ë®–√—°…“‰¥â ∑—π∑à«ß∑’ ®–≈¥Õ—µ√“∑ÿæ≈¿“æ·≈–Õ—µ√“µ“¬≈ß‰¥â¡“°

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‡Õ° “√Õâ“ßÕ‘ß 1. Hertzer NR. Basic data concerning associated coronary artery disease in peripheral vascular patients. Ann Vasc Surg 1987;1:616. 2. Ouyang P. Frequency and significance of early postoperative silent myocardial ischemia in patients having peripheral vascular surgery. Am J Cardiol 1989;64:113. 3. Wong T, Detsky AS. Preoperative cardiac risk assessment for patients having peripheral vascular surgery. Ann Intern Med 1992;116:743. 4. Coldman L, Cardiac risks and complications of noncardiac surgery. Ann Intern Med 1983;98:504. 5. Cooperman M. Cardiovascular risk factors in patients with peripheral vascular disease. Surgery 1978;84:505. 6. McCabe CJ. The value of electrocardiogram monitoring during treadmill testing for peripheral vascular disease. Surgery 1982;83:183. 7. McPhail NV. The use of preoperative exercise testing to predict cardiac complications after arterial reconstruction. J Vasc Surg 1988;7:60-68. 8. Kazmers A, Cerqueira MD, Zierler RE. The role of preoperative radionuclide ejection fraction in direct abdominal aortic aneurysm repair. J Vasc Surg 1988;8:128. 9. Mosley JG, Clarke JMF, Marston A. Assessment of myocardial function before aortic surgery by radionuclide angiocardio graphy. Br J Surg 1985;72:886. 10. Gewertz BL. Transesophageal echocardio-graphic monitoring of myocardial ischemia during vascular surgery. J Vasc Surg 1987;5:607. 11. Goldman L. Cardiac risks and complications of noncardiac surgery. Ann Intern Med 1983;98:504. 12. Leppo JA. Dipyridamole-thallium imaging:The lazy man’s stress test. J Nucl Med 1989;30:281. 13. McPhai NV. Comparison of left ventricular function and myocardial perfusion for evaluation perioperative cardiac risk of abdominal aortic surgery. Can J Surg 1990;33:224. 14. Diener CF, Burrows B. Further observation on the course and prognosis of chronic obstructive lung disease. Am Rev Respir Dis 1975;111:719-724. 15. Samlaska CP, James WD. Superficial thrombophlebitis. I. Primary hypercoagulable states. J Am Acad Dematol 1990;22:975-989. 16. Donaldson MC, Weinberg DS, Belkin M, et al. Screening for hypercoagulable tates in vascular surgical practice: A preliminary study. J Vasc Surg 1990;11:825-831.

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∫∑∑’Ë 10 Cerebrovascular disease ∫∑∑’Ë 11 ∫∑∑’Ë 12 ∫∑∑’Ë 13 ∫∑∑’Ë 14 ∫∑∑’Ë 15 ∫∑∑’Ë 16 ∫∑∑’Ë 17 ∫∑∑’Ë 18 ∫∑∑’Ë 19 ∫∑∑’Ë 20 ∫∑∑’Ë 21 ∫∑∑’Ë 22

·¢π¢“¥‡≈◊Õ¥ Abdominal Aortic Aneurysm (AAA) Aortoiliac Occlusive Disease (AIOD) °“√√—°…“ Intermittent Claudication (IC) ‚¥¬‰¡àµâÕßºà“µ—¥ °“√‡ΩÑ“¥Ÿ·≈·≈–æ÷ß√–«—ß„πºŸâªÉ«¬∑’ËµâÕßºà“µ—¥ Renovascular Disease Femoro-Popliteal-Tibioperoneal Occlusive Disease Buergerûs Disease (Thromboangiitis Obliterans) Takayasuûs Arteritis Acute Arterial Occlusion Infected Aneurysm The Diabetic Foot

∫∑∑’Ë 10 CEREBROVASCULAR DISEASE »— ≈ ¬·æ∑¬å ‡ ªì π ∫ÿ § §≈Àπ÷Ë ß „π∑’ ¡ ∑’Ë √à « ¡∑”°“√√— ° …“‚√§ À≈Õ¥‡≈◊Õ¥ ¡Õß ‚¥¬‰¥â√∫— °“√ª√÷°…“®“°Õ“¬ÿ√·æ∑¬å „πºŸªâ «É ¬ ‚√§À≈Õ¥‡≈◊Õ¥·¥ß carotid, aortic arch branches ·≈– verterbral arteries ªí≠À“∑’ Ë ”§—≠¢Õß‚√§À≈Õ¥‡≈◊Õ¥·¥ß§◊Õ °“√µ’∫·§∫, ulcerated arterial lesions, aneurysm ·≈–°“√∫“¥‡®Á∫∫√‘‡«≥§Õ(1) „π∫“ß§√—ßÈ »—≈¬·æ∑¬å®–‰¥â√∫— °“√ª√÷°…“‡æ◊ÕË µ—¥ ‘π„®„π°“√√—°…“ ºŸâªÉ«¬∑’ËÀ≈Õ¥‡≈◊Õ¥·¥ß§“‚√§µ‘¥µ’∫·§∫ high grade (>70% stenosis) ·µà ‰¡à¡Õ’ “°“√∑“ß ¡Õß(2) „π∫∑π’®È –°≈à“«∂÷ß‚√§À≈Õ¥‡≈◊Õ¥ ¡Õß∑’æË ∫‰¥â∫Õà ¬„π à«π¢Õß extracranial carotid ·≈– vertebral arterial disease Õ“°“√∑“ß§≈‘π§‘ , °“√«‘π®‘ ©—¬‚√§, ·π«∑“ß„π°“√√—°…“, À≈—°°“√ ºà“µ—¥, °“√¥Ÿ·≈ºŸâªÉ«¬¢≥–·≈–À≈—ß°“√ºà“µ—¥ µ≈Õ¥®π¿“«– ·∑√°´âÕπ∑’‡Ë °‘¥¢÷πÈ À≈—ßºà“µ—¥·≈–«‘∏°’ “√·°â ‰¢

Õ“°“√· ¥ß∑“ß§≈‘π‘§ 1. SYMPTOMATIC CAROTID ARTERY DISEASE 1.1 Transient Cerebral Ischemia Transient Cerebral Ischemia ª√–°Õ∫¥â«¬ transient monocular blindness (TMB) À√◊Õ amaurosis fugax ´÷Ëß

‡ªì π °“√¡Õß‡ÀÁ π ‰¡à ™— ¥ ¥â « ¬µ“¢â “ ß‡¥’ ¬ «™—Ë « ¢≥–·≈â « °≈— ∫ §◊ π ‡À¡◊Õπ¿“«–ª°µ‘ ·≈– lateralizing trasient ischemic attack (TIA) TMB ®–‡ªìπÕ“°“√‡µ◊Õπ ”§—≠¢Õß‚√§À≈Õ¥‡≈◊Õ¥·¥ß §“‚√µ‘¥µ’∫µ—π Õ∏‘∫“¬‰¥â®“°§«“¡º‘¥ª°µ‘„π°“√¡Õß‡ÀÁπ ºŸªâ «É ¬ ®–∫√√¬“¬«à“¡’§«“¡√Ÿ â °÷ ‡À¡◊Õπ°—∫À¡Õ°≈ß À√◊Õ¡’¡“à π§≈ÿ¡§√÷ßË ®Õ µ“ √–¬–‡«≈“∑’‡Ë °‘¥ —πÈ ‡æ’¬ß‰¡à°«’Ë π‘ “∑’À√◊Õπ“∑’·≈â«‡ªìπª°µ‘ “‡Àµÿ‡°‘¥®“° atheroemboli ∑’ÀË ≈ÿ¥ÕÕ°¡“®“° carotid bifurcation Õ“°“√¢Õß TIA Õ“®®–æ∫„π√Ÿª·∫∫¢Õß°“√ ÕàÕπ·√ß·¢π¢“À√◊Õ™“¥â“πµ√ß°—π¢â“¡°—∫À≈Õ¥‡≈◊Õ¥·¥ß§“ ‚√§µ‘¥∑’µË ∫’ µ—π Õ“®®–¡’À√◊Õ‰¡à¡’ speech disturbance √à«¡¥â«¬ √–¬–‡«≈“∑’Ë¡’Õ“°“√πâÕ¬°«à“ 24 ™—Ë«‚¡ß à«π„À≠à®–¡’Õ“°“√ ‰¡à°π’Ë “∑’À√◊Õ‰¡à∂ß÷ ™—«Ë ‚¡ß À≈—ß®“°π—πÈ °≈—∫‡ªìπª°µ‘‚¥¬‰¡à¡’ neurologic deficit Õ“°“√‡À≈à“π’ÈºŸâªÉ«¬Õ“®®–‰¡à‡≈à“„Àâ·æ∑¬åøíß À√◊Õ·æ∑¬å ‰¡à ‰¥â´—°ª√–«—µ‘§√Õ∫§≈ÿ¡ ∑”„Àâ ‰¡àπ÷°∂÷ß·≈–Õ“®®– ∑”„Àâ«π‘ ®‘ ©—¬‚√§º‘¥æ≈“¥ °“√„™âÕ“°“√·≈–Õ“°“√· ¥ß¢Õß TMB ·≈– TIA ‡ªìπ ¢âÕ∫àß™’È „π°“√µ√«®«‘π®‘ ©—¬√à«¡°—∫ cardiovascular status ‡ªìπ ‘ßË ®”‡ªìπ §«√ ◊∫§âπÀ“µ”·Àπàß¢Õß atheroemboli «à“¡“®“° mural thrombus ∑’Ë‡°‘¥¢÷Èπ¿“¬À≈—ß myocardial infarction, vegetation À√◊Õ atherosclerotic debris ®“° valvular heart disease, embolization ®“° carotid atheroma ∂â“·¬°‚√§ À—«„®‰¥â·≈â«§«√‡æàß‡≈Áß∂÷ß‡©æ“– carotid occlusive disease

94 TIA ¡’‚Õ°“ °≈“¬‡ªìπ stroke ‰¥â ßŸ ∂÷ß√âÕ¬≈– 24-29 ¿“¬„π 5 ∂â“¡’ TIA √à«¡°—∫À≈Õ¥‡≈◊Õ¥·¥ß§“‚√µ‘¥µ’∫·§∫¡“°°«à“ √âÕ¬≈– 70 ‚Õ°“ ‡°‘¥ stroke ¡’ ßŸ ∂÷ß√âÕ¬≈– 40 ¿“¬„π 5 ªï(4) „π¢—πÈ ÿ¥∑â“¬°ÁµÕâ ßºà“µ—¥√—°…“ §«√∑” carotid arteriography ‡æ◊ËÕ¥Ÿ«à“À≈Õ¥‡≈◊Õ¥·¥ß§“‚√µ‘¥∑’Ëµ’∫µ—π¡’æ¬“∏‘ ¿“æÕ¬à“ß‰√ ·≈–‡°‘¥∑’µË ”·Àπàß„¥(5) ªï(3)

1.2 Stroke complete stroke À¡“¬∂÷ß focal neurologic deficit ∑’‡Ë °‘¥¢÷πÈ ∑—π∑’∑π— „¥ ·≈–¡’Õ“°“√º‘¥ª°µ‘∑“ßª√– “∑§ßÕ¬Ÿπà “π°«à“ 24 ™—Ë«‚¡ß ‚¥¬‰¡à¡’∑à“∑’«à“®–‡°‘¥¢÷Èπ §«“¡√ÿπ·√ß¢Õß‚√§ ª√–‡¡‘π‰¥â®“° Stroke Severity Scores ºŸªâ «É ¬∑’¡Ë ’ disabling stroke ‡À¡“– ”À√—∫°“√√—°…“‚¥¬°“√∑” carotid endarterectomy(6,4) „π√“¬ acute stroke ·≈–¡’ severe neurolic deficit Õ—µ√“ µ“¬À≈—ß°“√ºà“µ—¥ Ÿß¡“°(7) §«“¡√ÿπ·√ß¢Õß stroke, ¿“«–·∑√°´âÕπ·≈–°“√æ◊πÈ °≈—∫¢Õß Õ“°“√¢÷πÈ Õ¬Ÿ°à ∫— µ—«·ª√‡À≈à“π’§È Õ◊ collateral circulation, ¿“«–¢Õß cardiorespiratory function ·≈–‚√§∑’ºË ªŸâ «É ¬‡ªìπÕ¬Ÿ°à Õà π·≈â«‡™àπ ‚√§À—«„®, ‡∫“À«“π œ≈œ(1,8,9) ”À√—∫ intermediate neurologic syndrome Õ◊πË ∑’æË ∫‰¥â ‡™àπ reversible ischemic neurologic dificit (RIND) ®–¡’ Õ“°“√¢Õß TIA ´÷ßË ∫“ß§√—ßÈ √ÿπ·√ß·µà®–øóπô ‡ªìπª°µ‘¿“¬„π 24 ™—«Ë ‚¡ß À√◊Õ∑’‡Ë √’¬°«à“ stroke-in-evolution À√◊Õ stuttering stroke Õ“°“√∑“ßª√– “∑∑’Ë¥’¢÷ÈπÕ“®®–∂÷ß baseline À√◊Õ‡ªìπ´È”Õ’° ∑”„Àâ¡Õ’ “°“√∑“ßª√– “∑§ß§â“ßÕ¬Ÿà ¡’ stepwise progressive evolution À√◊Õ∑’‡Ë √’¬°«à“ çcrescendo TIAsé §«√ºà“µ—¥√—°…“(10) „π∫“ß ∂“π°“√≥å stroke Õ“®®–‡°‘¥®“°°“√Õÿ¥µ—πÕ¬à“ß ‡©’¬∫æ≈—π¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß§“‚√§µ‘¥ §«√√’∫ºà“µ—¥√—°…“ °“√√—°…“‚¥¬„™â¬“≈–≈“¬≈‘¡Ë ‡≈◊Õ¥ (thrombolytic therapy) ¡’ ¢âÕ‡ ’¬§◊Õ ∑”„Àâ‡°‘¥°“√µ°‡≈◊Õ¥„π ¡Õß‰¥â

2. VERTEBROBASILAR INSUFFICIENCY ‚√§¢Õß vertebral artery æ∫‰¥â√Õâ ¬≈– 2-5 ¢Õß°“√ºà“µ—¥ cerebrovascular occlusive disease Õ“°“√¢Õß VBI ‡°‘¥ ®“°¡’‡≈◊Õ¥¡“‡≈’¬È ß ¡Õß à«π cerebellum ‰¡àæÕ “‡Àµÿ¢Õß VBI ‡°‘¥®“° subclavian steal syndrome À√◊ÕÀ≈Õ¥‡≈◊Õ¥·¥ß vertebral µ’∫·§∫∑—ßÈ Õß¢â“ß(11)

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥ Õ“°“√ ”§—≠¢Õß VBI §◊Õ vertigo, ataxia, paresis, numbness, dysphasia, dysarthia ·≈– diplopia ª√–¡“≥√âÕ¬≈– 5 ¢ÕßºŸªâ «É ¬ VBI ®–¡“¥â«¬Õ“°“√¢Õß TIA ‡π◊ÕË ß®“°¡’°“√ steal À√◊Õ shunt ‡≈◊Õ¥®“° middle cerebral artery ´÷ßË ºŸªâ «É ¬°≈ÿ¡à π’®È –¡’∑ß—È vertebral ·≈– carotid artery occlusive disease «‘π®‘ ©—¬‚√§‰¥â®“° duplex ultrasonography ·≈– arteriography ‚¥¬°“√©’¥ “√∑÷∫· ßºà“π “¬ «π‡¢â“‰ª‡©æ“– À≈Õ¥‡≈◊Õ¥·¥ß subclavian ‡æ◊ÕË ¥Ÿµπâ µÕ·≈–µ≈Õ¥·π«¢Õß vertebral artery °“√√—°…“ VBI ¡’®¥ÿ ¡ÿßà À¡“¬§◊Õ æ¬“¬“¡‡æ‘¡Ë ‡≈◊Õ¥∑’Ë ‰À≈‡«’¬π ‰ª‡≈’È¬ß posterior circulation ª√–¡“≥√âÕ¬≈– 85 ¢ÕßºŸâ ªÉ«¬∑’‡Ë ªìπ∑—ßÈ carotid ·≈– vertebral occlusive disease °“√ ∑” carotid endarterectomy ®–∑”„ÀâÕ“°“√¥’¢π÷È ¡’πÕâ ¬√“¬∑’Ë ®”‡ªìπ®–µâÕß∑” direct vertebral artery reconstruction °“√µàÕ vertebral artery ‡¢â“°—∫ carotid artery °Á‡ªìπÕ’°«‘∏°’ “√Àπ÷ßË ∂â“À≈Õ¥‡≈◊Õ¥·¥ß§“‚√µ‘¥ª°µ‘(12) à«πª√–°Õ∫¢Õß subclavian steal syndrome §◊Õ¡’°“√ Õÿ¥µ—π¢ÕßÀ≈Õ¥‡≈◊Õ¥∑’ÕË ¬Ÿà proximal µàÕ vertebral artery ´÷ßË Õ“®®–‡ªìπ‰¥â∑ß—È À≈Õ¥‡≈◊Õ¥·¥ß subclavian À√◊Õ innominate ·≈–‡°‘¥ reverse flow „π vertebral artery ¿“¬À≈—ß°“√ ÕÕ°°”≈—ß‚¥¬°“√‡§≈◊ËÕπ‰À«·¢π ∫“ß√“¬®–¡’Õ“°“√¢≥–Õ¬Ÿà „π∑à“ª°µ‘‰¡àÕÕ°°”≈—ß °“√√—°…“§◊Õ ºà“µ—¥∑” carotid-subclavian bypass ‚¥¬„™â À≈Õ¥‡≈◊Õ¥‡∑’¬¡µàÕºà“π„µâº«‘ Àπ—ß ‰¡àµÕâ ßºà“µ—¥‡¢â“™àÕß∑√«ßÕ°

3. ASYMPTOMATIC CONTRALATERAL ARTERY STENOSIS ‡¡◊ÕË µ√«®æ∫«à“¡’À≈Õ¥‡≈◊Õ¥·¥ß§“‚√§µ‘¥Õ’°¥â“πÀπ÷ßË µ’∫·§∫ ‚¥¬‰¡à¡Õ’ “°“√∑“ßª√– “∑ À≈—ß®“°ºà“µ—¥∑” carotid endarterectomy ‰ª·≈â«¢â“ßÀπ÷ßË ´÷ßË ºŸªâ «É ¬¡’‚Õ°“ ‡ ’¬Ë ßµàÕ°“√‡°‘¥ TIA ·≈– stroke ¿“¬À≈—ß®“°°“√µ’∫·§∫¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß§“ ‚√µ‘¥¢â“ß∑’¬Ë ß— ‰¡à ‰¥â∑”°“√ºà“µ—¥ §«√√—°…“·∫∫ ª√–§—∫ª√–§Õß‰ª°àÕπ ®–æ‘®“√≥“ºà“µ—¥√—°…“‡¡◊ÕË ¡’Õ“°“√ ·≈–µ’∫·§∫¡“°°«à“√âÕ¬≈– 80(13,14) ‰¡à®”‡ªìπ µâÕßºà“µ—¥√’∫¥à«π §«√ºà“µ—¥ carotid endarterectomy À≈—ß ºà“µ—¥Õ’°¢â“ß·≈â« 5-7 «—π À√◊Õπ“π°«à“π—πÈ

CEREBROVASCULAR DISEASE

4. ASYPTOMATIC ULCERATED LESIONS æ∫‰¥â ‰¡à∫Õà ¬‡π◊ÕË ß®“°Õ—≈µ√“‡´“«π¥å®–‰¡à “¡“√∂µ√«®æ∫ plaque ulceration ‰¥â ·µàÕ“®·¬°·¬–≈—°…≥–¢Õß plaque ‰¥â«“à ‡ªìπ homogeneous À√◊Õ heterogeneous ·µà®–‰¡à‡°’¬Ë « ¢âÕß°—∫·º≈∑’Ë‡°‘¥∫πº‘«¥â“π„πÀ≈Õ¥‡≈◊Õ¥ Õ“®®–‡ÀÁπ‰¥â ‰¡à™—¥ arteriography ≈—°…≥–·º≈µ◊Èπ¢Õ∫‰¡à‡√’¬∫ ®π°√–∑—Ëß·º≈∑’Ë ‡°‘¥¢÷πÈ ∑’Ë stenotic area

5. ASYMPTOMATIC HOLLENHORST PLAQUE °“√ª√–‡¡‘πÕ“°“√·≈–«‘π®‘ ©—¬‚√§ asymptomatic Hollenhorst plaque (cholesterol embolus „π retinal arteriole) ‰¥â ®“°°“√∑” retinoscopy ‚¥¬®—°…ÿ·æ∑¬å °“√µ√«®æ∫ ‘Ëßº‘¥ ª°µ‘„π®Õµ“π’È®–‰¡à‡°’Ë¬«¢âÕß°—∫°“√‡°‘¥ transient À√◊Õ fixed retinal À√◊Õ cerebral symptoms §«√µ√«® screen ‚¥¬„™â duplex scan ∂â“¡’ high-grade stenosis (>80%) §«√ºà“µ—¥ √—°…“æ∫«à“ºŸªâ «É ¬°≈ÿ¡à π’¡È §’ «“¡®”‡ªìπµâÕßºà“µ—¥√—°…“‡æ’¬ß√âÕ¬≈– 15 à«π„À≠à®–√—°…“µ“¡Õ“°“√·≈–„Àâ¬“

6. PULSATILE MASS °âÕπ‡µâπ‰¥â∑§’Ë Õ´÷ßË Õ¬Ÿà „°≈â°∫— À≈Õ¥‡≈◊Õ¥·¥ß§“‚√µ‘¥ ∑’æË ∫‰¥â ¡’ true aneurysm, carotid body tumors, lymphadenopathy À√◊Õ tortuous carotid artery °“√µ√«®‚¥¬„™â sonography, CT scan À√◊Õ Magnetic Resonance Imaging (MRI) ®– ™à«¬·¬°·≈–«‘π®‘ ©—¬‚√§‰¥â∂°Ÿ µâÕß carotid aneurysm æ∫‰¡à∫Õà ¬ ¿“«–·∑√°´âÕπ∑’ Ë ”§—≠§◊Õ °“√·µ°∑–≈ÿ, ‡°‘¥ cerebral embolization, thrombosis ·≈–≈‘¡Ë ‡≈◊Õ¥°¥ ¡Õß, ¡Õß∫«¡ √—°…“‚¥¬°“√ºà“µ—¥ µ“¡¥â«¬ end-to-end anastomosis À√◊Õ interposition graft carotid body tumor °âÕπ‚µ™â“ ·µà ‰¡à „™à¡–‡√Áß √—°…“ ‚¥¬æ¬“¬“¡µ—¥ÕÕ°°„ÀâÀ¡¥‡æ√“–√—ß ’∫”∫—¥‰¡à ‰¥âº≈ „πºŸâªÉ«¬ ŸßÕ“¬ÿ∑’Ë ‰¡à¡’Õ“°“√À√◊Õ‡°‘¥¿“«–·∑√°´âÕπ ¿“«–√à“ß°“¬‡ ’Ë¬ß µàÕ°“√ºà“µ—¥ §«√√—°…“‚¥¬°“√‡ΩÑ“¥ŸÕ“°“√

7. ASYMPTOMATIC CERVICAL BRUITS Õ“°“√ ”§—≠∑’ºË ªŸâ «É ¬∂Ÿ° àßµ—«¡“æ∫·æ∑¬å§Õ◊ µ√«®æ∫ cervical bruit ‚¥¬‰¡à¡’Õ“°“√∑“ß ¡ÕßÀ√◊Õ√–∫∫ª√– “∑ ∫“ß

√“¬¡’Õ“°“√‡æ’¬ß‡≈Á°πâÕ¬ ‡™àπ «‘ß‡«’¬π»’√…– √Ÿ â °÷ À¡ÿπÀ√◊Õµ“ ¡—«„π√–¬–‡«≈“ —πÈ Ê ·≈â«§◊πª°µ‘ ºŸªâ «É ¬‡À≈à“π’§È «√µ√«®«‘π®‘ ©—¬ ‚¥¬°“√∑” cerebrovascular noninvasive testing ∂â“‰¥â º≈∫«°À√◊Õæ∫§«“¡º‘¥ª°µ‘¢ÕßÀ≈Õ¥‡≈◊Õ¥®÷ß®–æ‘®“√≥“∑” arteriography µàÕ‰ª ºŸªâ «É ¬°≈ÿ¡à asymptomatic carotid stenosis æ∫‰¥â√Õâ ¬≈– 10-33 ¢ÕßºŸâªÉ«¬∑’Ëµ√«®æ∫ asymptomatic cervical bruit ®“°°“√∑” direct continuous-wave Doppler(2)

8. CAROTID FIBROMUSCULAR DYSPLASIA (FMD) ‡ªìπ benign disease ∑’æË ∫‰¥â ‚¥¬∫—ß‡Õ‘≠ ‰¡à „™à “‡Àµÿ ”§—≠ ∑’∑Ë ”„Àâ‡°‘¥ ischemic infarction ∂÷ß·¡â«“à carotid FMD Õ“®®– ‡°’¬Ë «¢âÕß°—∫ TIAs ·µàæ∫«à“Õ—µ√“‡°‘¥ stroke πâÕ¬°«à“ atherosclerotic carotid occlusive disease FMD ‡ªìπ “‡Àµÿ ”§—≠¢Õß internal carotid dissection ®–∑”„Àâ‡°‘¥Õ“°“√∑“ß ¡Õß·≈–√–∫∫ª√– “∑√«¡∑—Èßµ“æ√à“¡—« Õ“°“√‡À≈à“π’®È –À“¬‰ª‰¥â‡Õß‚¥¬‰¡àµÕâ ßºà“µ—¥√—°…“·≈–®–‰¡à‡°‘¥ ‡ªìπ´È”Õ’° high-grade symptomatic FMD stenosis §«√ √—°…“‚¥¬°“√„™â∫≈— ≈Ÿπ¢¬“¬∂à“ß internal carotid artery ∂â“¡’ aneurysm ¢π“¥„À≠à§«√µ—¥‡Õ“ÕÕ°·≈–‡¬Á∫´àÕ¡¥â«¬ vein graft interposition

9. SUBCLAVIAN STEAL SYNDROME Left subclavian stenosis À√◊Õ occlusion ‡ªìπº≈¡“®“° atheroclerosis ‚¥¬∑—«Ë ‰ª·≈â«®–‰¡à¡Õ’ “°“√Õ–‰√∑“ß§≈‘π§‘ ∑’‡Ë ¥àπ™—¥ µ√«®√à“ß°“¬æ∫«à“§«“¡¥—π‚≈À‘µ·¢π´â“¬ (brachial pressure) µË”°«à“·¢π¢«“ ∫“ß§√—Èß¡’ left arm claudication ·µàæ∫ ‰¥âπÕâ ¬‡π◊ÕË ß®“° collaterals ¢Õß·¢π¥’ ∂â“°“√Õÿ¥µ—πÀ√◊Õµ’∫ ·§∫‡°‘¥¢÷πÈ µ√ß proximal ¢Õß left subclavian artery Õ“°“√¢Õß subclavian steal syndrome ®–‡¥àπ™—¥ ´÷Ëßª√–°Õ∫¥â«¬ µ√“æ√à“¡—«, ‡«’¬π»’√…–, ataxia ·≈– syncope À≈—ß¢¬—∫·¢π ´â“¬ÕÕ°°”≈—ß °≈‰°‡°‘¥®“°¡’ retrograde flow ¢Õß‡≈◊Õ¥ ®“° left posterior cerebral circulation ºà“π left vertebral artery ¡“¬—ß distal subclavian artery ·≈–·¢π √ÿª§◊Õ¡’°“√·¬àß ‡≈◊Õ¥∑’Ë ‰ª‡≈’¬È ß ¡Õßºà“π‰ª¬—ß·¢π ∑”„Àâ‡°‘¥ intermittent posterior cerebral ischemia

96 æ∫ classic subclavian steal syndrome ‰¥â ‰¡à∫Õà ¬ §«√ ∑” arteriography ·≈– non-invasive evaluation ¢Õß carotid system √—°…“‚¥¬°“√ºà“µ—¥·°â ‰¢ left subclavian stenosis ™à«¬ collateral flow ºà“π circle of Willis ‰ª¬—ß posterior brain arm claudication ·°â ‰¢‚¥¬°“√ºà“µ—¥ carotid-subclavian, subclavian-subclavian, subcla- vain-to-carotid transposition À√◊Õ percutaneous transluminal angioplasty.

·π«∑“ß„π°“√µ√«®«‘π‘®©—¬‚√§ ºŸªâ «É ¬∑’ Ë ß —¬«à“®–¡’ cerebravascular insufficiency §«√ ´—°ª√–«—µ‘·≈–µ√«®√à“ß°“¬„Àâ≈–‡Õ’¬¥‡ªìπ√–∫∫ ‚¥¬‡©æ“–‚√§ ∑’Ë‡ªìπ¡“°àÕπ ‡™àπ ‡∫“À«“π §«“¡¥—π‚≈À‘µ Ÿß, ‚√§À—«„®·≈– peripheral vascular disease (PVD)(15,16) §≈”™’æ®√∑’Ë carotid, superficial temporal, subclavian ·≈– radial ∂â“§≈” carotid pulse ∫√‘‡«≥§Õ‰¡à ‰¥â · ¥ß«à“¡’ √Õ¬‚√§À√◊Õ°“√Õÿ¥µ—πµ√ß aortic arch «—¥§«“¡¥—π‚≈À‘µ ‡ª√’¬∫‡∑’¬∫°—π√–À«à“ß 2 ·¢π ‡æ◊ÕË ™à«¬„π°“√«‘π®‘ ©—¬°“√µ’∫·§∫ ¢Õß subclavian À√◊Õ innominate artery „™â bell stethoscope øíß bruits µ√ß carotid artery, §Õ, √Õ∫°√–∫Õ°µ“, supraclavicular region ·≈–À—«„® µ√«®√–∫∫ª√– “∑„Àâ≈–‡Õ’¬¥ §«√µ√«®§≈◊Ëπ‰øøÑ“À—«„®, §≈◊Ëπ ¡Õß·≈–¿“æ√—ß ’∑√«ßÕ° ∂â“ ß —¬«à“¡’°“√µ°‡≈◊Õ¥„π ¡Õß·≈–‰¢ —πÀ≈—ßÀ√◊Õ intracranial lesions °“√‡®“–À≈—ß‡æ◊ËÕπ”‡Õ“ CSF ¡“µ√«® ®–™à«¬°“√ «‘π®‘ ©—¬‚√§ CT scan ∑’Ë ¡Õß®–™à«¬„π°“√«‘π‘®©—¬ stroke ·¬°‚√§ ÕÕ°®“° cerebral infarction, °“√µ°‡≈◊Õ¥„π ¡Õß, ‡π◊ÕÈ ßÕ° À√◊Õ∂ÿßπÈ”„π ¡Õß πÕ°®“°π’¬È ß— ‡ªìπ·π«∑“ß„π°“√µ—¥ ‘π„®«à“ ®–ºà“µ—¥‡¡◊ÕË ‰√ MRI ®–‡ÀÁπ°“¬«‘¿“§»“ µ√å¢Õß ¡Õß·≈–‰¢ —πÀ≈—ß‰¥â™¥— ‡®π°«à“ CT scan °“√µ√«®«‘π®‘ ©—¬∑’°Ë ”≈—ß®–¡’∫∑∫“∑ µàÕ‰ª„πÕπ“§µ§◊Õ positron emission tomography (PET) ·≈– single position emission computed tomography (SPECT) ‡æ◊ÕË ·¬°§«“¡·µ°µà“ß√–À«à“ß ischemic ·≈– infarcted cerebral tissue ‡æ◊ËÕæ‘®“√≥“À“¢âÕ∫àß™’È·≈–‡«≈“∑’Ë‡À¡“– ¡„π°“√ ºà“µ—¥

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥

Non-invasive Studies noninvasive methods ¡’««‘ ≤ — π“°“√·≈–‡√‘¡Ë ¡’∫∑∫“∑„π°“√ »÷°…“·≈–µ√«®«‘π®‘ ©—¬‚√§¢Õß extracranial circulation «‘∏π’ ’È ‡À¡“– ”À√—∫°“√µ√«®«‘π®‘ ©—¬ asymptomatic carotid lesions ·≈–À≈’°‡≈’¬Ë ß invasive arteriography ∑’Ë ‰¡à®”‡ªìπ Oculopneumoplethysmography (OPG-Gee) ‡ªìπ°“√ «—¥§«“¡¥—π‚≈À‘µ¢Õß opthalmic artery √à«¡°—∫°“√°¥ common carotid artery ®–«—¥ internal carotid stump pressure ‰¥â “¡“√∂ª√–‡¡‘π collateral flow ∑’Ë ‰ª¬—ß cerebral hemisphere ¥â“π‡¥’¬«°—π ‡ªìπ screening method ∑’‡Ë ™◊ÕË ∂◊Õ‰¥â (16) Oculoplethysmography (OPG-Kartchner) ‡ªìπ°“√ ‡ª√’¬∫‡∑’¬∫ timing ¢Õß ocular pulse wave √–À«à“ßµ“ 2 ¢â“ß ‡æ◊ÕË ª√–‡¡‘ππ—¬ ”§—≠∑“ß hemodynamic ¢Õßæ¬“∏‘ ¿“æ∑’Ë internal carotid artery(17) ®–„™â√à«¡°—∫ carotid phonoangiography (CPA) ‡æ◊ËÕ§«“¡·πàπÕπ¬‘Ëß¢÷Èπ„π°“√«‘π‘®©—¬‚√§ ‡ª√’¬∫‡∑’¬∫°—∫ arteriography ·≈â«æ∫«à“«‘∏’π’È§«“¡‡™◊ËÕ∂◊Õ‰¥â Ÿß∂÷ß√âÕ¬≈– 85 ªí®®ÿ∫π— ·æ∑¬åπ¬‘ ¡„™â OPG-Gee ¡“°°«à“ OPGKartchner „πªí®®ÿ∫π— noninvasive test ∑’Ë „™â∫Õà ¬„π°“√«‘π®‘ ©—¬ cerebrovascular disease §◊Õ duplex scan √à«¡°—∫ real time Bmode scanning À√◊Õ√à«¡°—∫ doppler sound spectral analysis(18) (√Ÿª∑’Ë 10.1) duplex scan ‡ªìπ«‘∏°’ “√µ√«®«‘π®‘ ©—¬‚√§∑’¡Ë ’ §«“¡·¡àπ¬”·πàπÕπ „™â«¥— §«“¡‡√Á«¢Õß carotid blood flow ∑ÿ°®ÿ¥ ·≈–‡ âπºà“»Ÿπ¬å°≈“ß¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß∑ÿ°·¢πß B-mode image ®–∫àß∫Õ°≈—°…≥–·≈– à«πª√–°Õ∫¢Õß plaque «à“ soft, dense, calicified, ¡’®¥ÿ ‡≈◊Õ¥ÕÕ°À√◊Õ·º≈ »—≈¬·æ∑¬åÀ≈“¬∑à“π„™â duplex scan „π°“√«‘π‘®©—¬‚√§·∑π arteriography °àÕπ∑” carotid endarterectomy »—≈¬·æ∑¬å∫“ß°≈ÿ¡à °Á„™â∑ß—È 2 «‘∏°’ “√ µ“¡§«“¡‡À¡“– ¡

Arteriography ‡ªìπ definitive diagnostic procedure §«√»÷°…“§«“¡º‘¥ ª°µ‘¢Õß 4-vessels ·≈– aortic arch (√Ÿª∑’Ë 10.2) ∑” serial biplane ‡æ◊ÕË ¥Ÿ cervical ·≈– intracranial vessels(19) computed digital subtraction arteriography (DSA) „™âπÕâ ¬°«à“ conventional arteriography æ∫«à“©’¥ “√∑÷∫· ß‡¢â“À≈Õ¥ ‡≈◊Õ¥·¥ß®–‡ÀÁπ™—¥°«à“©’¥‡¢â“À≈Õ¥‡≈◊Õ¥¥”·≈–„™â „πª√‘¡“≥∑’Ë

CEREBROVASCULAR DISEASE

√Ÿª∑’Ë 10.1 Grag scale images Duplex scan, Color flow images ·≈– Doppler waveforms °. normal internal carotid artery ¢. 50% stenosis of the internal carotid artery §. 90% stenosis of the internal carotid artery

πâÕ¬°«à“ ¿“«–·∑√°´âÕπ®“°°“√∑” cerebral arteriography æ∫πâÕ¬ 0.2-1% Õ“®®–‡°‘¥ stroke, ·æâ “√∑÷∫· ßÀ√◊Õ‰µ«“¬ ‡©’¬∫æ≈—π ‚¥¬∑—«Ë ‰ª·≈â«ºŸªâ «É ¬ TIA À√◊Õ stroke §«√∑” arteriography ‡ªìπÕ—π¥—∫·√°‚¥¬‰¡àµÕâ ß∑” noninvasive test πÕ°®“° duplex scan noninvasive studies ‡À¡“– ”À√—∫ºŸªâ «É ¬∑’Ë ‰¡à ¡’Õ“°“√‡¥àπ™—¥·≈–¡’ª≠ í À“„π°“√µ√«®«‘π®‘ ©—¬ √Ÿª∑’Ë 10.2 Cerebral angiogram · ¥ß„Àâ‡ÀÁπ high grade right internal carotid artery stenosis ·≈– irregularity wall ¢Õß right common carotid artery

Transcranial Doppler Studies (TCD) ‡ªìπ noninvasive study «‘∏°’ “√„À¡à ”À√—∫«‘π®‘ ©—¬‚√§ À≈Õ¥‡≈◊Õ¥·¥ß ¡Õß·≈– collateral circulatin ®–∫Õ°º≈„π√Ÿª flow velocity ‡ªìπ‡´Áπµ‘‡¡µ√µàÕ«‘π“∑’ «‘∏’°“√π’È‡À¡“– ”À√—∫ °“√µ√«®«‘π®‘ ©—¬°àÕπºà“µ—¥∑” carotid endarterectomy(20) TCD ®–ª√–‡¡‘π intracerebral blood flow ∑ÿ°®ÿ¥ collateralization ·≈– degree of cerebral ischemia ´÷ßË ‡ªìπº≈¡“®“° extracranial cerebrovascular disease °“√‡ª≈’¬Ë π·ª≈ß velocity ¢Õß middle cerebral artery ¢≥–ºà“µ—¥ ¢÷πÈ Õ¬Ÿ°à ∫— stump pressure, EEG, shunt fraction, ª√–‡¡‘π«à“‡≈◊Õ¥‡≈’È¬ß ¡Õß¡“° ¢÷ÈπÀ≈—ß∑” carotid endarterectomy TCD °”≈—ß¡’«‘«—≤π“°“√„π∑“ß∑’¥Ë ¢’ π÷È ‡æ◊ÕË π”¡“„™â«π‘ ®‘ ©—¬‚√§‰¥âÕ¬à“ß¡’ª√– ‘∑∏‘¿“æ

°“√√—°…“ °“√√—°…“‚¥¬°“√„Àâ¬“ ¬“∑’Ë „ ™â „πªí®®ÿ∫—π∑’Ë ‰¥âº≈¥’§◊Õ ¬“µâ“π‡°√Á¥‡≈◊Õ¥®—∫°≈ÿà¡ (antiplatelets)(21,22)

1. Aspirin ‡ªìπ¬“µâ“π°“√®—∫°≈ÿ¡à ¢Õß‡°√Á¥‡≈◊Õ¥ „™â „π°“√√—°…“ºŸªâ «É ¬ TIAs À√◊Õ non disabling stroke ‚¥¬∑—«Ë ‰ª·≈â«‡°√Á¥‡≈◊Õ¥®– ¡’ªØ‘°√‘ ¬‘ “°—∫ atheroclerotic plaque ∑”„Àâ®∫— °≈ÿ¡à °—π·≈–À≈ÿ¥ ÕÕ°‡ªìπ‡ÕÁ¡‚∫‰≈ ∑”„Àâ‡°‘¥Õ“°“√∑“ßª√– “∑ ·Õ ‰æ√‘π‡ªìπ ¬“„π°≈ÿà¡ cyclo-oxygenase inhibitor ≈¥°“√®—∫°≈ÿà¡¢Õß ‡°√Á¥‡≈◊Õ¥ ‚Õ°“ ‡°‘¥Õ“°“√∑“ßª√– “∑®“°‡ÕÁ¡‚∫‰≈®–≈¥≈ß ¬◊π¬—πº≈°“√√—°…“π’È ‚¥¬ American Aspirin Study ·≈– Canadian Aspirin Study ≈¥∑—ÈßÕ—µ√“µ“¬®“°‚√§À—«„®·≈–À≈Õ¥ ‡≈◊Õ¥√«¡∑—ßÈ stroke Dipyridamole ´÷ßË ‡ªìπ platelet suppresant °Á¬—ß¡’ª√– ‘∑∏‘¿“æ‰¡à‡¥àπ™—¥‡∑à“°—∫·Õ ‰æ√‘π ¢π“¥π’È „™â¢Õß ·Õ ‰æ√‘π§◊Õ 325 ¡‘≈≈‘°√—¡µàÕ«—π ®–µâ“π°“√®—∫°≈ÿ¡à ¢Õß‡°√Á¥ ‡≈◊Õ¥‰¥â√Õâ ¬≈– 90 ‚¥¬‰¡à≈¥°“√º≈‘µ¢Õß prostacycline ®“° ‡ÕÁπ‚¥∏’‡≈’¬Ë ¡ ¡’ƒ∑∏‘√Ï –§“¬‡§◊ÕßµàÕ√–∫∫∑“ß‡¥‘πÕ“°“√πâÕ¬

2. Ticlopidine ticlopidine hydrocloride ‡ªìπ¬“„À¡à∑¡’Ë ª’ √– ‘∑∏‘¿“æµâ“π °“√®—∫°≈ÿ¡à ¢Õß‡°√Á¥‡≈◊Õ¥ ÕÕ°ƒ∑∏‘Ï‚¥¬°“√√–ß—∫ pathway ¢Õß adenosine diphosphate „π°“√®—∫°≈ÿ¡à ¢Õß‡°√Á¥‡≈◊Õ¥ ·µà®–‰¡à

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥ inhibit cyclo-oxygenase pathway ·≈–‰¡à¬—∫¬—Èß°“√º≈‘µ thromboxane ‚¥¬‡°√Á¥‡≈◊Õ¥·≈– prostacycline ‚¥¬‡ÕÁπ‚¥ ∏’‡≈’Ë¬¡ ticlopidine ®–‡ª≈’Ë¬π°“√∑”Àπâ“∑’Ë¢Õß‡°√Á¥‡≈◊Õ¥ µ≈Õ¥™à « ßÕ“¬ÿ ‡Õ° “√∑“ß«‘ ™ “°“√À≈“¬©∫— ∫ ¬◊ π ¬— π «à “ ticlopidine ¥’°«à“·Õ ‰æ√‘π„π·ßà ‰¡à°¥‰¢°√–¥Ÿ°·≈–‰¡à√–§“¬ ‡§◊ÕßµàÕ√–∫∫∑“ß‡¥‘πÕ“À“√

°“√ºà“µ—¥√—°…“ ®ÿ¥¡ÿßà À¡“¬¢Õß°“√∑” carotid endarterectomy °Á‡æ◊ÕË ≈¥ Õ“°“√∑“ßª√– “∑ªÑÕß°—π°“√‡°‘¥ stroke, ∑”„Àâ§≥ ÿ ¿“æ™’«µ‘ ºŸâ ª«¬¥’¢π÷È ·≈–≈¥Õ—µ√“µ“¬ ·≈–¢âÕ ”§—≠∑’ Ë ¥ÿ §◊Õ ªÑÕß°—π°“√‡°‘¥ stroke ´÷ßË ¡—°®–‡°‘¥®“°(23,24) 1. ‡ÕÁ¡‚∫‰≈∑’Ë‡°‘¥®“°‡°√Á¥‡≈◊Õ¥√«¡°≈ÿà¡∑’Ëºπ—ßÀ≈Õ¥‡≈◊Õ¥ ·¥ß ·≈–À≈ÿ¥≈Õ°‰ªÕÿ¥À≈Õ¥‡≈◊Õ¥„π ¡Õß 2. ‡≈◊Õ¥‰ª‡≈’¬È ß ¡Õß‰¡àæÕ®“°À≈Õ¥‡≈◊Õ¥·¥ßµ’∫µ—π ¢âÕ∫àß™’∑È ’Ë ”§—≠„π°“√ºà“µ—¥∑” carotid endarterectomy §◊Õ transient cerebral ischemia à«π¢âÕ∫àß™’È√Õß≈ß‰ª·≈–®– ∑”„Àâ√“¬∑’§Ë “¥«à“À≈—ßºà“µ—¥·≈â«Õ“°“√®–¥’¢π÷È §◊Õ stable stroke, asymptomatic stenosis ·≈– cerebral ischemia(25,26) (µ“√“ß ∑’Ë 10.1) ¢âÕÀâ“¡„π°“√ºà“µ—¥∑” carotid endarterectomy §◊Õ„πºŸâ ªÉ«¬∑’Ë‡æ‘Ëß‡ªìπ stroke ·≈–Õ“°“√‡≈«≈ß‡√◊ËÕ¬ Ê ¡’æ¬“∏‘ ¿“æ „π ¡Õß À√◊Õ¡’ underlying disease Õ◊πË Ê ´÷ßË ‡ªìπ¢âÕÀâ“¡„π °“√ºà“µ—¥(27) µ“√“ß∑’Ë 10.1 ¢âÕ∫àß™’È „π°“√ºà“µ—¥ Indications for Carotid Endarterectomy in Cerobrovascular Insufficiency Indications Transient cerebral ischemia Stable strokes (selected) Asymptomatic stenoses (selected) Chronic cerebral ischemia (selected)

Contraindications Acute profound strokes Progressing strokes Severe intracranial disease Other severe generalized disorders (e.g. cancer)

CEREBROVASCULAR DISEASE

carotid endarterectomy ‡ªìπ°“√ºà“µ—¥∑’∑Ë ”∫àÕ¬∑’ Ë ¥ÿ „π °“√√—°…“ extracranial cerebrovascular disease ®÷ß§«√∑√“∫ ∂÷ßÀ≈—°°“√ºà“µ—¥ °“√¥Ÿ·≈ºŸâªÉ«¬°àÕπ·≈–À≈—ß°“√ºà“µ—¥ ´÷Ëß À≈—°°“√‡À≈à“π’È „™â ‰¥â°∫— °“√ºà“µ—¥ vertebral ·≈– subclavian artery.

I. °“√‡µ√’¬¡ºŸâªÉ«¬°àÕπºà“µ—¥ ∂â“‡ªìπºŸªâ «É ¬∑’ºË “à µ—¥„π‡«≈“ ‰¡à√∫’ ¥à«π§«√À¬ÿ¥¬“µâ“π‡°√Á¥ ‡≈◊Õ¥·≈– anticoagulant °àÕπºà“µ—¥Õ¬à“ßπâÕ¬ 24 ™—Ë«‚¡ß πÕ°®“°„π√“¬∑’‡Ë ªìπ multiple recent TIAs À√◊Õ¡’ severe carotid stenosis (<2 mm) µâÕß‰¥â√—∫ ‡Œª“√’πÀ√◊Õ·Õ ‰æ√‘π ®π°√–∑—ßË ºà“µ—¥ ∂÷ß·¡â«à“°“√µ‘¥‡™◊ÈÕ·º≈ºà“µ—¥∫√‘‡«≥§Õæ∫‰¥âπâÕ¬ §«√ ∑”§«“¡ –Õ“¥øÕ°º‘«Àπ—ß„Àâª√“»®“°‡™◊ÕÈ µ—ßÈ ·µà§“ß §Õ ®π∂÷ß Àπâ“Õ° „Àâ¬“ªØ‘™’«π–™π‘¥ÕÕ°ƒ∑∏‘Ï§≈ÿ¡°«â“ß°≈ÿà¡‡»ø“‚≈ ªÕ √‘πÀ√◊Õ‡æπ‘»≈‘ ≈‘π ‡¢â“∑“ßÀ≈Õ¥‡≈◊Õ¥¥”°àÕπºà“µ—¥ ß¥Õ“À“√∑“ßª“°À≈—ß‡∑’¬Ë ß§◊π°àÕπºà“µ—¥ „Àâ “√πÈ”‡¢â“∑“ß À≈Õ¥‡≈◊Õ¥¥”‡ªìππÈ”‡°≈◊Õ ¡¥ÿ≈¬å (5% dextrose in Ringerûs solution) „πÕ—µ√“ 100-125 ¡‘≈≈‘≈‘µ√µàÕ™—Ë«‚¡ß ªÑÕß°—π‰¡à „Àâ √à“ß°“¬¢“¥πÈ” √–«—ß„π°“√„™â¬“°≈ÿ¡à narcotic ‡æ√“–®–∑”„Àâ §«“¡¥—πµË” °àÕπºà“µ—¥§«√§“ “¬ arterial line „π√“¬∑’Ë¡’ ªí≠À“‚√§À—«„®§«√ Õ¥ “¬ «π Swan-Ganz §“ “¬ «π ªí “«–

II. À≈—°°“√ºà“µ—¥ ‚¥¬∑—«Ë ‰ª·≈â«®–¥¡¬“ ≈∫·≈â«ºà“µ—¥ ‡æ√“–§àÕπ¢â“ß –¥«° µàÕ»—≈¬·æ∑¬å·≈–ºŸªâ «É ¬ »—≈¬·æ∑¬å∫“ß°≈ÿ¡à Õ“®®–π‘¬¡ºà“µ—¥‚¥¬ „™â regional anesthesia (regional cervical block) √à«¡°—∫ °“√„Àâ¬“™“‡©æ“–∑’Ë °“√ºà“µ—¥‡¢â“∂÷ßÀ≈Õ¥‡≈◊Õ¥·¥ß§“‚√µ‘¥ §«√∑”¥â«¬§«“¡ πÿ¡à π«≈ À≈’°‡≈’¬Ë ß°“√°√–∑∫°√–‡∑◊ÕπµàÕ‡ âπª√– “∑·≈–À≈Õ¥ ‡≈◊Õ¥¢“¥” √–¡—¥√–«—ß„π°“√®—∫µâÕßÀ≈Õ¥‡≈◊Õ¥·¥ß§“‚√µ‘¥ ‡æ√“–Õ“®®–∑”„Àâ plaque À≈ÿ¥≈Õ°‡ªìπ atheroemboli (√Ÿª∑’Ë 10.3) À≈—°°“√·≈–¢âÕ§«√√–«—ß„π°“√ºà“µ—¥∫√‘‡«≥¡’¥ß— π’È (√Ÿª∑’Ë 10.4) 1. ·¢πß¢Õß ansa cervicals (hypoglosis) µ—¥‰¥â‡æ◊ÕË ‡¢â“∂÷ß À≈Õ¥‡≈◊Õ¥·¥ß§“‚√µ‘¥ ‚¥¬‰¡à ¡’ § «“¡º‘ ¥ ª°µ‘ ∑ “ß √–∫∫ª√– “∑

99 2. hypoglossal nerve ®–∑Õ¥¢â“¡À≈Õ¥‡≈◊Õ¥·¥ß§“‚√ µ‘¥µ√ß bifuracation °“√°√–∑∫°√–‡∑◊ÕπÀ√◊Õ¢“¥¢Õß ‡ âπª√– “∑‡°‘¥®“°°“√¥÷ß∂à“ßÀ√◊Õ„™â§’¡Àπ’∫‚¥¬‰¡à ‰¥â √–«—ß ∂â“¡’ hypoglossal nerve injury ≈‘ÈπºŸâªÉ«¬®– ‡Õ’¬ß‰ª¥â“π∑’Ë‡ âπª√– “∑∂Ÿ°µ—¥¢≥–·≈∫≈‘Èπ ∑”„Àâ ‡§’È¬«Õ“À“√·≈–°≈◊πÕ“À“√≈”∫“° ‡ ’¬ßæŸ¥º‘¥ª°µ‘ ∂â “ ‡ â π ª√– “∑ hypoglossal ∂Ÿ ° µ— ¥ ∑—È ß Õß¢â “ ß §àÕπ¢â“ß®–Õ—πµ√“¬‡æ√“–‡¡◊ËÕºŸâªÉ«¬πÕπÀß“¬≈‘Èπ®–µ° ·≈–Õÿ¥∑àÕÀ“¬„® 3. vagus nerve ∑Õ¥ºà“π posterior carotid sheath À≈—ß µàÕÀ≈Õ¥‡≈◊Õ¥·¥ß§“‚√µ‘¥ÕâÕ¡¡“∑“ß¥â“πÀπâ“ µ√ß anterolateral surface ¢ÕßÀ≈Õ¥‡≈◊ Õ ¥·¥ß§“‚√µ‘ ¥ §«√‡≈“– vagus nerve ÕÕ°®“°À≈Õ¥‡≈◊Õ¥·¥ß§“‚√µ‘¥ µ≈Õ¥‡ âπ ·≈â«„™â¥â“¬§≈âÕß‰«â°—π°“√°√–∑∫°√–‡∑◊Õπ À√◊Õµ—¥¢“¥¢≥–ºà“µ—¥ 3.1 °“√°√–∑∫°√–‡∑◊ÕπµàÕ vagus nerve À√◊Õ‡ âπ ª√– “∑∂Ÿ°µ—¥¢“¥ ‚¥¬‡©æ“– recurrent laryngeal nerve ∑’¡Ë ®’ ¥ÿ ‡√‘¡Ë µâπ®“° vagus nerve «‘ßË ¬âÕπ¢÷πÈ ¡“¬—ß vocal cord ∑“ß tracheoesophageal groove recurrent laryngeal nerve ®–«‘ßË ÕâÕ¡ subclavian artery ∑“ß¥â“π¢«“°≈“¬‡ªìπ vagus nerve ∑’§Ë Õ ‚¥¬ºà“πÀ≈—ßµàÕÀ≈Õ¥‡≈◊Õ¥·¥ß§“‚√µ‘¥ 3.2 superior laryngeal nerve Õ¬ŸàÀ≈—ßµàÕ carotid biturcation ‰ª¬—ß vocal cord ‡ âπª√– “∑π’È®– ‡≈’È¬ß°≈â“¡‡π◊ÈÕ cricothyroid ´÷Ëß®–∑”„Àâ√–¥—∫ ‡ ’¬ß„π°“√æŸ¥§ß∑’Ë ªÑÕß°—π°“√°√–∑∫°√–‡∑◊Õπ À√◊Õ∂Ÿ°µ—¥¢“¥¢≥–ºà“µ—¥ ‚¥¬‡≈“–Õ¬à“ß√–¡—¥√–«—ß √Õ∫ external carotid ·≈– superior thyrodal arteries ∂â“‡ âπª√– “∑π’∂È °Ÿ µ—¥√–¥—∫‡ ’¬ßæŸ¥®–‰¡à§ß∑’Ë ‡«≈“æŸ¥À√◊Õ√âÕß‡æ≈ßπ“π Ê ‡ ’¬ß®–À“¬‰ª 4. greater auricular nerve ‡ªìπ sensory nerve ‡≈’¬È ß º‘«Àπ—ß à«π mastoid process, concha ¢Õß auricle ·≈– ear lobe ®–Õ¬Ÿ∫à π anterior surface ¢Õß°≈â“¡‡π◊ÕÈ sternocleidomastoid ®–∑”„Àâ º‘ « Àπ— ß ∫√‘ ‡ «≥∑’Ë ‡ âπª√– “∑¡“‡≈’¬È ß™“ 5. mandibular branches ¢Õß facial nerve «‘ßË ¡“¬—ß angle of mandible ·≈–¢π“πµàÕ mandible ∂â“∂Ÿ°µ—¥ °≈â“¡‡π◊ÕÈ √Õ∫ª“°¢â“ßπ—πÈ ®–À¬àÕπ∑”„Àâ¡¡ÿ ª“°µ°

100

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥

Circle of Willis Carotid syphon

Basilar artery Left internal carotid artery

Right internal carotid artery

Left vertebral artery Facial artery

Right external carotid artery

Lingual artery Superior thyroid artery Right subclavian artery

Left common carotid artery Left vertebral artery Left subclavian artery

Innominate artery

Hypoglossal (XII) n. Ascending cervical a. Facial a. External carotid a.

Sternocleidomastoid m. (cut edges)

Lingual a. Superior thyroid a. Internal carotid a. Vertebral a. Common carotid a. Cerebral blood supply

√Ÿª∑’Ë 10.3 °“¬«‘¿“§¢ÕßÀ≈Õ¥‡≈◊Õ¥∑’Ë¡“‡≈’È¬ß ¡Õß °. ¥â“πÀπâ“ ¢. ¥â“π¢â“ß

101

CEREBROVASCULAR DISEASE

Nodose ganglion Glossopharyngeal nerve Superior laryngeal nerve Heringûs nerve Vagus nerve

Hypoglossal nerve Internal laryngeal nerve External laryngeal nerve Ansa cervicalis Recurrent laryngeal nerve

√Ÿª∑’Ë 10.4 °“¬«‘¿“§¢ÕßÀ≈Õ¥‡≈◊Õ¥·≈–‡ âπª√– “∑∑’ËÕ¬Ÿà„°≈â‡§’¬ß

III. «‘∏’°“√ªÑÕß°—π thromboemboli ∂â“‡ÕÁ¡‚∫‰≈À≈ÿ¥‡¢â“°√–· ‚≈À‘µ·≈–Õÿ¥À≈Õ¥‡≈◊Õ¥„π ¡Õß ∑”„Àâ‡°‘¥Õ“°“√∑“ß√–∫∫ª√– “∑ «‘∏°’ “√ªÑÕß°—π¡’¥ß— µàÕ‰ªπ’È 1. ‰¡à§«√®—∫§≈÷ßÀ√◊Õ∂Ÿ°µâÕß∫√‘‡«≥ carotid bifurcation ∫àÕ¬ Ê ¢≥–ºà“µ—¥ ‡æ√“–®–∑”„Àâ ulcerated À√◊Õ atheromatous plaque À≈ÿ¥‰¥â 2. °àÕπ clamp À≈Õ¥‡≈◊Õ¥·¥ß§“‚√µ‘¥ µâÕß„Àâ‡Œª“√’π 5000 ¬Ÿπµ‘ ∑“ßÀ≈Õ¥‡≈◊Õ¥¥”°àÕπ 5 π“∑’ 3. «π≈â“ß¿“¬„πÀ≈Õ¥‡≈◊Õ¥·¥ß§“‚√µ‘¥À≈—ßºà“µ—¥‡ªî¥ ·≈â«¥â«¬ heparinized saline ‡æ◊ËÕ‡ªìπ°“√™–≈â“ß atheroma ∑’ËÀ≈ÿ¥≈Õ°®“°ºπ—ßÀ≈Õ¥‡≈◊Õ¥√«¡∑—Èß≈‘Ë¡ ‡≈◊Õ¥°àÕπ®– Õ¥ shunt 4. endarterectomy surface ßà“¬µàÕ°“√‡°“–¢Õß‡°√Á¥‡≈◊Õ¥ ®–‡°‘¥ thromboembolism µ“¡¡“¿“¬À≈—ß‰¥â §«√‡√‘¡Ë „Àâ low melecular weight Dextran µ—ßÈ ·µàºªŸâ «É ¬Õ¬Ÿà„π recovery room ‡æ◊ÕË ‡ªìπ antiplatelet ·≈– anticoagulant ‡√‘¡Ë „Àâ§√—ßÈ ·√° 100 ¡‘≈≈‘≈µ‘ √ µ“¡¥â«¬ 20 ¡‘≈≈‘≈‘µ√µàÕ™—«Ë ‚¡ß ®π°√–∑—ßË ºŸªâ «É ¬√—∫ª√–∑“πÕ“À“√‰¥â ®÷ß ‡ª≈’¬Ë π¡“‡ªìπ·Õ ‰æ√‘π√—∫ª√–∑“π 5. °àÕπ‡¬Á∫ªî¥À≈Õ¥‡≈◊Õ¥·¥ß§“‚√µ‘¥ §«√ flush out ‡≈◊Õ¥ ∑’¡Ë ’ loose atheromatous À√◊Õ‡ÕÁ¡‚∫‰≈°àÕπÕÕ°‰ª°àÕπ

∂â“‡√‘Ë¡„Àâ‡≈◊Õ¥‰À≈‡«’¬π§«√„Àâºà“π external carotid artery °àÕπ ‡æ√“–∂â“¬—ß¡’‡ÕÁ¡‚∫‰≈§â“ßÕ¬Ÿà®– flush ‡¢â“‰ª‰¥â ‰¡àÕπ— µ√“¬‡À¡◊Õπª≈àÕ¬‡¢â“‰ª„π internal carotid artery.

IV. °“√ªÑÕß°—π ¡Õß¢“¥‡≈◊Õ¥¢≥–ºà“µ—¥ ¡’ 2 «‘∏°’ “√∑’ Ë ”§—≠§◊Õ §ß√–¥—∫§«“¡¥—π‚≈À‘µ„ÀâÕ¬Ÿà „π√–¥—∫ ª°µ‘ ·≈–„ à shunt ¢≥–∑” carotid endarterectomy(28)

√Ÿª∑’Ë 10.5 °“√«—¥§≈◊Ëπ‰øøÑ“ ¡Õß (EEG) „πÀâÕßºà“µ—¥¢≥–∑” carotid endarterectomy

102

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥

1. cerebral perfusion ¢÷πÈ Õ¬Ÿ°à ∫— systemic blood pressure ‚¥¬µ√ß ¢≥– clamping carotid artery ¢Õ„Àâ «‘ —≠≠’·æ∑¬å§ß§«“¡¥—π‚≈À‘µºŸâªÉ«¬„ÀâÕ¬Ÿà „π‡°≥±åª°µ‘ À√◊Õ Ÿß°«à“ª°µ‘‡≈Á°πâÕ¬ «—¥§≈◊πË ¡Õß (EEG) µ≈Õ¥‡«≈“ §Õ¬ —ß‡°µ¥Ÿ§≈◊πË ¡Õß∑’ºË ¥‘ ª°µ‘ ∂â“æ∫«à“¡’ diffuse slowing pattern ®–µâÕß‡æ‘¡Ë §«“¡¥—π‚≈À‘µ(29) (√Ÿª∑’Ë 10.5) 2. shunting „π√–À«à“ßºà“µ—¥∑” carotid endarterectomy »—≈¬·æ∑¬å∑’Ë™”π“≠·≈–¡’ª√– ∫°“√≥åÕ“®®–ºà“µ—¥ ‚¥¬‰¡àµâÕß„ à shunt ‡æ√“–¡’‡æ’¬ß√âÕ¬≈– 1-3 ∑’Ë¡’ §«“¡º‘¥ª°µ‘∑“ß√–∫∫ª√– “∑À≈—ßºà“µ—¥ ‘Ëß∑’Ë®–™à«¬ ª√–‡¡‘π cerebral perfusion ¢≥– clamp carotid artery ‰¥â§Õ◊ °“√«—¥ stump pressure(30) ·≈–°“√ª√–‡¡‘π §≈◊πË ¡Õß (EEG) ¢≥–ºà“µ—¥(31) ∂â“§≈◊πË ¡Õßº‘¥ª°µ‘ ¢≥–ºà“µ—¥§«√„ à shunt ∂â“‰¡à “¡“√∂ monitor EEG

·≈–«—¥ carotid stump pressure ‰¥âµË”°«à“ 50 ¡‘≈≈‘‡¡µ√ª√Õ∑ §«√„ à shunt πÕ°®“°π’·È ≈â«§«√„ à shunt „π°“√ºà“µ—¥∑’ËÀ≈Õ¥‡≈◊Õ¥·¥ß§“‚√µ‘¥¥â“π∑’Ë¬—ß ‰¡à ‰¥âº“à µ—¥¡’°“√µ’∫·§∫

V. ‡∑§π‘§°“√ºà“µ—¥ carotid endarterectomy ®ÿ¥¡ÿàßÀ¡“¬ ”§—≠¢Õß°“√ºà“µ—¥ carotid reconstruction ª√–°Õ∫¥â«¬ °“√‡Õ“ à«π∑’Ëµ’∫·§∫À√◊Õ‡ªìπ·º≈∫πÀ≈Õ¥‡≈◊Õ¥ ÕÕ°„Àâ ¡∫Ÿ√≥å (√Ÿª∑’Ë 10.7) ·≈–°“√‡¬Á∫ªî¥À≈Õ¥‡≈◊Õ¥‰¡à „Àâ ‡°‘¥°“√µ’∫·§∫´È”Õ’° ∂â“‡ªìπ‰ª‰¥â§«√∑” primary closure ·µà „π√“¬∑’§Ë “¥«à“‡¬Á∫·≈â«®–µ’∫·§∫≈ßÀ√◊Õ repeated endarterectomy §«√∑” patch angioplasty À≈—ßºà“µ—¥ monitor blood flow ºà“π®ÿ¥∑’‡Ë ¬Á∫ªî¥‚¥¬„™â continuous-wave Doppler probe, arteriography ·≈– B-mode ultrasound

™

√Ÿª∑’Ë 10.6 °“√ºà“µ—¥ carotid endarterectomy °. À≈—ß„ à Pruitt - Inahara shunt ¢. ∑” carotid endarterectomy ‚¥¬¡’ shunt §“Õ¬Ÿà §. carotid endarterectomy specimen ª√–°Õ∫¥â«¬ ulcerated plaque §≈ÿ¡¥â«¬ thrombus ´÷Ëß ª√–°Õ∫¥â«¬ fibrin, platelet aggregates ·≈– atherosclerotic debris ß. ‡¬Á∫ªî¥ arteriotomy site ¥â«¬ running suture ‰¡àµâÕß∑” patch angioplasty ‡æ√“–À≈—ßºà“µ—¥À≈Õ¥‡≈◊Õ¥·¥ß°«â“ßæÕ ‰¡àµ’∫·§∫

103

CEREBROVASCULAR DISEASE

VI. °“√‡ΩÑ“√–«—ß¿“«–·∑√°´âÕπ·≈–§«“¡º‘¥ ª°µ‘∑“ß√–∫∫ª√– “∑À≈—ßºà“µ—¥ ‡√‘¡Ë µâπ¢≥–∑’ÕË ¬Ÿà „πÀâÕßºà“µ—¥ À≈—ß®“°«‘ ≠ — ≠’·æ∑¬å‡√‘¡Ë „ÀâºŸâ ªÉ«¬øóπô µ—«·≈–‡Õ“∑àÕ™à«¬À“¬„®ÕÕ° ‡√‘¡Ë µ√«®√à“ß°“¬∑“ß√–∫∫ ª√– “∑ Õ“°“√∑’æË ∫√ÿπ·√ß§◊Õ §«“¡¥—π‚≈À‘µ Ÿß, ª≈ÿ°‰¡à§Õà ¬µ◊πË –≈◊¡ –≈◊Õ ·≈– fine hand movement º‘¥ª°µ‘ À≈—°„π°“√¥Ÿ·≈√—°…“ºŸªâ «É ¬∑’¡Ë §’ «“¡º‘¥ª°µ‘∑“ß√–∫∫ª√– “∑ À≈—ßºà“µ—¥¡’(32,33) 1. µâÕß·πà „®«à“ cardiorespiratory status ¢ÕßºŸªâ «É ¬§ß √–¥—∫ª°µ‘ ´÷ßË ®–ª√–°Õ∫¥â«¬ ™’æ®√, §«“¡¥—π‚≈À‘µ, °“√ À“¬„®·≈–ª√‘¡“≥ÕäÕ°´‘‡®π„π‡≈◊Õ¥ 2. °“√√— ° …“¢÷È π Õ¬Ÿà °— ∫ µ”·Àπà ß §«“¡º‘ ¥ ª°µ‘ ∑ “ß√–∫∫ ª√– “∑

2.1 ∂â“¡’ contralateral hemiparesis “‡Àµÿ‡°‘¥®“° ‡∑§π‘§°“√ºà“µ—¥¢â“ß∑’Ë∑” endarterectomy §«√ √’∫π”ºŸªâ «É ¬‡¢â“ÀâÕßºà“µ—¥‡æ◊ÕË ¥Ÿ√Õà ß√Õ¬§«“¡º‘¥ª°µ‘ §«√∑” arteriography À√◊Õ duplex ultrasound ‡æ◊ÕË ¥Ÿ≈°— …≥–°“√µ—π«à“‡°‘¥®“° thrombi À√◊Õ residual plaque °àÕπºà“µ—¥·°â ‰¢ 2.2 ∂â“‡ªìπ§«“¡º‘¥ª°µ‘√–∫∫ª√– “∑·∫∫ diffuse neurologic deficit ®–‡°‘¥®“° internal capsule stroke ´÷Ëß¡’ “‡Àµÿ‚¥¬µ√ß®“°§«“¡¥—π‚≈À‘µµË” patency ¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß§“‚√µ‘¥ ª√–‡¡‘π®“° OPG À√◊Õ ultrasonography ∂â“¡’°“√Õÿ¥µ—π¢â“ß∑’∑Ë ”°“√ºà“µ—¥ §«√√’∫ºà“µ—¥·°â ‰¢∑—π∑’ ∂â“À≈Õ¥‡≈◊Õ¥·¥ß§“‚√µ‘¥ ª°µ‘∑ß—È Õß¢â“ß §«√¥Ÿ·≈√—°…“µ“¡Õ“°“√ §«√∑” CT scan ∑’»Ë √’ …–¿“¬„π 24 ™—«Ë ‚¡ß·√°‡æ◊ÕË ¥Ÿ cerebral infarction

°“√¥Ÿ·≈ºŸâªÉ«¬À≈—ßºà“µ—¥

√Ÿª∑’Ë 10.7 °“√ºà“µ—¥ carotid endarterectomy ‚¥¬‰¡àµÕâ ß„ à shunt

12-24 ™—«Ë ‚¡ß·√°À≈—ßºà“µ—¥ §«√‡ΩÑ“¥ŸÕ“°“√ºŸªâ «É ¬„πÀâÕß æ—°øóôπÀ√◊ÕÀÕ∫√‘∫“≈ºŸâªÉ«¬Àπ—° ‡æ◊ËÕ¥Ÿ§«“¡º‘¥ª°µ‘∑“ß√–∫∫ ª√– “∑ ·≈– monitor vital signs πÕπ¬°»’√…– Ÿß 30-45 Õß»“‡æ◊ËÕ≈¥ ¡Õß∫«¡·≈–À“¬„®≈÷° ‡√‘Ë¡√—∫ª√–∑“πÕ“À“√«—π √ÿßà ¢÷πÈ “√πÈ”∑’Ë „Àâ∑“ßÀ≈Õ¥‡≈◊Õ¥¥” 24 ™—«Ë ‚¡ß·√°§◊Õ 5% D/W ·≈– half strength NSS „πÕ—µ√“ 1 ¡‘≈≈‘≈µ‘ √µàÕ°‘‚≈°√—¡µàÕ™—«Ë ‚¡ß √–«—ß·≈–À≈’°‡≈’Ë¬ß‰¡à „Àâ‡°‘¥¿“«– hyponatremia ·≈–πÈ”‡°‘π ‡æ√“–®–∑”„Àâ‡°‘¥ ¡Õß∫«¡‰¥â „π√“¬∑’∑Ë ” carotid endarterectomy ∑—ßÈ Õß¢â“ß √–«—ß°“√‡°‘¥ carotid barorecoptor trauma ´÷Ëß®–µ“¡¡“¥â«¬ hypoxia ®–µâÕß monitor «à“ºŸâªÉ«¬¡’§«“¡ ¥—π‚≈À‘µµË”, ™’æ®√™â“·≈– respiratory distress ·≈–®–µâÕß√’∫ ·°â ‰¢ ∑àÕ√–∫“¬∑’Ë „ à‡Õ“‰«âÀ≈—ßºà“µ—¥«—π·√°§«√‡Õ“ÕÕ° À≈—ß®“° π—Èπ¬â“¬ºŸâªÉ«¬°≈—∫µ÷°„Àâ√—∫ª√–∑“πÕ“À“√·≈–≈ÿ°≈ß¡“‡¥‘π®“° ‡µ’¬ß ∂â“‡°‘¥¿“«– hypoxia (PO2 < 60 mmHg) §«√„Àâ¥¡ÕäÕ°´‘‡®πµàÕ·≈–‡®“– blood gas ‡ªìπ√–¬–À¬ÿ¥°“√„Àâ low molecular weight Dextran ∑“ßÀ≈Õ¥‡≈◊Õ¥¥” ‡√‘¡Ë √—∫ª√–∑“π·Õ ‰æ√‘π„π ¢π“¥ 80-325 ¡‘≈≈‘°√—¡µàÕ«—π À≈—ßºà“µ—¥ 2-3 «—π ºŸªâ «É ¬øóπô µ—«¥’·≈â« ∂â“¬—ß§«“¡¥—π‚≈À‘µ ŸßµâÕßª√—∫¢π“¥¬“„Àâ‡À¡“– ¡ µ—¥‰À¡·º≈ºà“µ—¥∑’Ë§Õ 7 «—π À≈—ßºà“µ—¥ «—¥ OPG ´È”À≈—ßºà“µ—¥ „ÀâºªŸâ «É ¬°≈—∫∫â“π·≈–π—¥¡“ µ√«®∑’·Ë ºπ°ºŸªâ «É ¬πÕ° 3-6 —ª¥“ÀåÀ≈—ßºà“µ—¥

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¿“«–·∑√°´âÕπ∑’Ë‡°‘¥¢÷ÈπÀ≈—ßºà“µ—¥(32) I. ¿“«–·∑√°´âÕπ„π√–¬–·√° ∂â“‡°‘¥ TIA À≈—ßºà“µ—¥«—π·√°À√◊Õ«—π∑’ÕË Õ°®“°‚√ßæ¬“∫“≈ §«√∑” CT scan ¡Õß ∂â“º≈≈∫·≈–·πà„®«à“‰¡à¡‡’ ≈◊Õ¥ÕÕ°„π ¡Õß „Àâ‡Œª“√’π·≈–µ“¡¥â«¬√—∫ª√–∑“π·Õ ‰æ√‘π ∂â“ ß —¬«à“ ¡’æ¬“∏‘ ¿“æº‘¥ª°µ‘ §«√∑” cerebral arteriography §«“¡¥—π‚≈À‘µ ŸßÀ≈—ßºà“µ—¥æ∫‰¥â√âÕ¬≈– 20 ∂â“§«∫§ÿ¡ §«“¡¥—π‚≈À‘µ‰¡à ‰¥â°Õà πºà“µ—¥ À≈—ßºà“µ—¥¡—°®–‡°‘¥ªí≠À“ Õ—µ√“ µ“¬·≈–¿“«–·∑√°´âÕπ∑“ß√–∫∫ª√– “∑®–æ∫‰¥â¡“°„πºŸâªÉ«¬ °≈ÿ¡à π’È §«√„Àâ nitro- prusside ·≈–¬“§ÿ¡§«“¡¥—π‚≈À‘µ ≈‘¡Ë ‡≈◊Õ¥¢Õß·º≈ºà“µ—¥∑’§Ë Õ∑”„ÀâÀ“¬„®·≈–°≈◊π≈”∫“° §«√ π”ºŸªâ «É ¬‡¢â“ÀâÕßºà“µ—¥Õ’°§√—ßÈ Àâ“¡‡≈◊Õ¥·≈–§«—°‡Õ“≈‘¡Ë ‡≈◊Õ¥ÕÕ° ∂â“≈‘Ë¡‡≈◊Õ¥¢π“¥‰¡à ‚µ¡“°§«√‡ΩÑ“¥ŸÕ“°“√ 7-14 «—π ·µàµâÕß √–«—ß°“√µ‘¥‡™◊ÕÈ ∂â“‡ªìπ°âÕπ∑’‡Ë µâπ‰¥âµ“¡®—ßÀ«–™’æ®√ Õ“®®–‡ªìπ pseudoaneurysm Õ—πµ√“¬µàÕ‡ âπª√– “∑ ‚¥¬‡©æ“– cranial nerves æ∫ ‰¥â√âÕ¬≈– 5-20 ‡°‘¥®“°°“√¥÷ß∂à“ß¢≥–ºà“µ—¥À√◊Õ„™â§’¡Àπ’∫ ‚¥¬‰¡àµß—È „® ·µà ‰¡àµ¥— ¢“¥ æ∫‰¥â∫Õà ¬°—∫ hypoglossal ·≈– recurrent laryngeal nerves ∂â“‰¡àµ√«®√à“ß°“¬µ“¡√–∫∫ ®– ‰¡àæ∫ ‡æ√“–‰¡à∑”„ÀâºªŸâ «É ¬√”§“≠¡“° ª√–¡“≥ 1/3 ¢ÕßºŸªâ «É ¬∑’¡Ë ’ recurrent laryngeal nerve injury µ√«®æ∫‰¥â®“°°“√∑” direct laryngoscopy °“√∫“¥‡®Á∫¢Õß‡ âπª√– “∑®“°°“√¥÷ß∂à“ß Õ“°“√®–ª°µ‘¿“¬„π 2-6 ‡¥◊Õπ

II. ¿“«–·∑√°´âÕπ„π√–¬–À≈—ß recurrent carotid stenosis æ∫‰¥â√Õâ ¬≈– 1-3 ·≈–„π°≈ÿ¡à π’∑È ’Ë ‰¡à¡Õ’ “°“√æ∫‰¥â√Õâ ¬≈– 10-20 §«√µ‘¥µ“¡Õ“°“√ºŸªâ «É ¬®“° noninvasive carotid tests(34) æ∫¡“°„π‡æ»À≠‘ß ‚Õ°“ ‡°‘¥ stroke ¿“¬À≈—ß¡’πâÕ¬ µ”·Àπàß∑’‡Ë °‘¥°“√µ’∫·§∫´È”‰¥â∫Õà ¬À≈—ßºà“µ—¥§◊Õ µ√ß origin ¢Õß internal carotid artery „°≈â°∫— ∫√‘‡«≥∑’ºË “à µ—¥ carotid endarterectomy ∂â“‡ªìπ early stenosis ®–¡’ “‡Àµÿ®“° neointimal FMD ·≈– surface thrombus ·≈– late restenosis ®“° atherosclerosis „π°≈ÿ¡à π’∂È “â ºŸªâ «É ¬¡’Õ“°“√ §«√∑” carotid arteriography À≈—ß®“°π—πÈ ∑” carotid endarterectomy ·≈– patch angioplasty(35,36)

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥ carotid pseudoaneurysm ‡°‘¥®“°‡∑§π‘§°“√ºà“µ—¥‰¡à¥’ §«√ ºà“µ—¥°àÕπ mural thrombus À≈ÿ¥≈Õ¬µ“¡°√–· ‚≈À‘µ‰ªÕÿ¥ À≈Õ¥‡≈◊Õ¥„π ¡Õß ∂â“ pseudoaneurysm ¢π“¥‚µ¡“° ®– ‡∫’¬¥Õ«—¬«–§â“ß‡§’¬ß

√ÿª atherosclerotic occlusive disease ¢Õß extra cranial carotid artery ‡ªìπ “‡Àµÿ∑’Ë ”§—≠·≈–æ∫∫àÕ¬∑’Ë ÿ¥∑’Ë∑”„Àâ‡°‘¥ stroke „π§π ŸßÕ“¬ÿ „πªí®®ÿ∫π— °“√«‘π®‘ ©—¬‚√§πÕ°®“°ª√–«—µ·‘ ≈– °“√µ√«®√à“ß°“¬Õ¬à“ß≈–‡Õ’¬¥·≈â« ¬—ß¡’«∏‘ °’ “√µ√«®·∫∫ noninvasive tests µà“ß Ê ‡™àπ oculoplethysmography, duplex scan, Transcranial Doppler Studies (TDS), magnetic resonance arteriography (MRA) ´÷ßË „Àâº≈°“√«‘π®‘ ©—¬‚√§∑’·Ë πàπÕπ ∑√“∫∂÷ßµ”·Àπàßæ¬“∏‘ ¿“æ °àÕπ∑’®Ë –∑” arteriography µàÕ‰ª πÕ°®“°π’È noninvasivests ¬—ß‡À¡“– ”À√—∫°“√ follow up ºŸâ ªÉ«¬∑’ºË “à µ—¥ carotid endarterectomy ·≈â« ºŸªâ «É ¬∑’¡Ë Õ’ “°“√‡µ◊Õπ¢Õß√–∫∫ª√– “∑‡™àπ TIA À√◊Õ‰¡à¡’ Õ“°“√·µà¡’ high-grade stenosis (70%) §«√æ‘®“√≥“ºà“µ—¥ carotid endarterectomy ´÷ßË „πªí®®ÿ∫π— Õ—µ√“‡ ’¬Ë ßµàÕ°“√ºà“µ—¥ πâÕ¬≈ß‡π◊ÕË ß®“°¡’«∏‘ °’ “√‡ΩÑ“ —ß‡°µÿ ¡Õß¢“¥‡≈◊Õ¥¢≥–ºà“µ—¥ ®“° °“√ monitor EEG ·≈–∂â“§≈◊Ëπ ¡Õßº‘¥ª°µ‘ §«√„ à shunt „πÀ≈Õ¥‡≈◊Õ¥¢≥–ºà“µ—¥ °“√ºà“µ—¥®–ªÑÕß°—π°“√‡°‘¥ cerebral infarction °“√√—°…“‚¥¬°“√„Àâ¬“§«√æ‘®“√≥“„πºŸªâ «É ¬∑’¡Ë ’ limited life expectancy ¡’ ‚√§À—«„®·≈–À≈Õ¥‡≈◊Õ¥ ‡ªìπ¡–‡√Áß¢—Èπ ÿ¥∑â“¬ À√◊Õ¿“«–√à“ß°“¬∑—«Ë ‰ª‰¡à‡À¡“– ¡°—∫°“√ºà“µ—¥ lesion ‡¢â“∂÷ß ¬“°À√◊Õµ√«®·≈â«‰¡àæ∫æ¬“∏‘ ¿“æ∑’Ëº‘¥ª°µ‘ §«√„Àâ¬“µâ“π ‡°√Á¥‡≈◊Õ¥®—∫°≈ÿ¡à ‡™àπ ·Õ ‰æ√‘π, ticlopidine ∂÷ß·¡â«“à ®–ºà“µ—¥ carotid endarterectomy ‰ª·≈â«ºŸªâ «É ¬°≈ÿ¡à π’È ‚Õ°“ ‡°‘¥ stroke °Á¬—ß¡’‰¥â Ÿß°«à“°≈ÿà¡ª√–™“°√ª°µ‘ §«√„Àâ¬“µâ“π‡°√Á¥‡≈◊Õ¥ ®—∫°≈ÿà¡√—∫ª√–∑“πµ≈Õ¥™’«‘µ √à«¡°—∫°“√§«∫§ÿ¡ªí®®—¬‡ ’Ë¬ß ¢Õß‚√§À≈Õ¥‡≈◊Õ¥ ‡™àπ ß¥ Ÿ∫∫ÿÀ√’,Ë §«∫§ÿ¡§«“¡¥—π‚≈À‘µ∑’ Ë ßŸ , §ÿ¡√–¥—∫πÈ”µ“≈·≈–‰¢¡—π„π‡≈◊Õ¥„ÀâÕ¬Ÿà „π√–¥—∫ª°µ‘

CEREBROVASCULAR DISEASE

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‡Õ° “√Õâ“ßÕ‘ß 1. Ackerman RH, Candia MR. Identifying clinically relevant carotid disease. Stroke 1994;25:1-9. 2. Chambers BR, Norris JW. Outcome in patients with asymptomatic neck bruits. N Engl J Med 1986;315:860-65. 3. Evans BA, Sicks JD, Whisnant JP. Factors affecting survival and occurence of stroke in patients with transient ischemic attacks. Mayo Clin Proc 1994; 69:416-25. 4. North American Symptomatic Carotid Endarterectomy Trial Collaborators. Beneficial effect of carotid endarterectomy in symptomatic patients with high- grade carotid stenosis. N Engl J Med 1991;325:445-53. 5. Toole JF. The Willis lecture: Transient ischemic attacks, scientific method, and new relialities. Stroke 1991;22:99-106. 6. Toole JF. Clinical Advisory, National Institute of Neurological Disorders and Stroke. September 1994; NIH, Bethesda, Maryland. 7. Gertler JP. Carotid endarterectomy for unstable and compelling neurologic conditions: Do results justify an aggressive approach? J Vasc Surg 1994;19:32-42. 8. McCrory DC. Predicting complications of carotid endarterectomy. Stroke 1993;24:1285-93. 9. Berman SS. Critical carotid stenosis: Diagnosis, timing of surgery, and outcome. J Vasc Surg 1994;20:499-510. 10. Wilson SE, Mayberg MR, Yatsu F, Weiss DG and Veteran Affairs Trialists. Crescendo transient ischemic attacks: A surgical imperative. J Vasc Surg 1993;17:249-57. 11. Sypert GW, Alvord EC. Cerebellar infarction: A clinicopathologic study. Arch Neurol 1975;32:357-64. 12. Berguer R. Long-term results of reconstructions of the vertebral artery. In: Long-term Results in Vascular Surgery. Yao JST, Pearce WH (eds.). New York: Appleton & Lange, 1993. 13. Towne JB, Weiss DG, Hobson RW. First phase report of cooperative VA asymptomatic carotid stenosis study. Operative morbidity and mortality. J Vasc Surg 1990;11:252-61. 14. Podore PC, DeWeese JA, May AG, et al. The asymptomatic contralateral carotid artery stenosis: A-five year follow-up study following carotid endarterectomy. Surgery 1980;88:748-52. 15. Chimowitz MI. Cardiac prognosis of patients with carotid stenosis: Long-term clinical evaluation. J Vasc Surg 1993;18:100-8. 16. Gee W, Reed JF IV. Ocular pneumoplethysmorgraphic evaluation of carotid lesion: Gee method. In: Ernst CB, Stanley JC. (eds). Current Therory in Vascular Surgery. 2nd Philadelphia: BC Decker, Inc, 1991;20-4.

17. Kartchner NM, McRae LP. Non-invasive laboratory evaluation. The clinical use of oculoplethysmography and carotid phonoangiography. In: Baker WH (ed). Diagnosis and Treatment of Carotid Artery Disease. New York: Futura Publishing Co, 1991;9-14. 18. Wagner WH, Treiman RL, Cossman DV, et al. The diminishing role of diagnostic arteriography in carotid artery disease; Duplex scanning as definitive preoperative study. Ann Vasc Surg 1991;5:10510. 19. Plum GE, Thompson JE. Cerebral arteriography. In: Neiman HL, Yao JST. (eds). Angiography of Vascular Disease. New York: Churchill Livingstone, 1985;535-98. 20. Schneider PA, Rossman ME, Torem S, et al. Transcranial Doppler in the management of extracranial cerebrovascular disease: Implications in diagnosis and management. J Vasc Surg 1988;7:223-31. 21. Barnett HJM, Eliasziw M, Meldrum HE. Drugs and surgery in the prevention of ischemic stroke. N Engl J Med 1995;332:328-35. 22. Antiplatelets Trialists Collaboration: Collaborative overview of randomized trials of antiplatelet therapy. I Prevention of death, myocardial infarction, and stroke by prolonged antiplatelet therapy in various categories of patients. Br Med J 1994;308:81-106. 23. The CASSANOVA Study Group. Carotid surgery vs. Medical therapy in asymptomatic carotid sterosis. Stroke 1991;22:1229-36. 24. Mayberg MR. Carotid endarterectomy and prevention of cerebral ischemia in symptomatic carotid stenosis. JAMA 1991;266:328994. 25. Whittemore AD, Ruby ST, Couch NP, et al. Early carotid endarterectomy in patients with small, fixed neurologic deficits. J Vasc Surg 1984;1:795-9. 26. Whittemore AD, Mannick JA. Surgical treatment of carotid disease in patients with neurological deficits. J Vasc Surg 1987;5:9103. 27. Greenhalgh RM. Carotid stenosis with unstable fluctuating neurologic deficit. In: Brewster DC. (ed). Common Problems in Vascular Surgery. Chicago: year Book Medical Publishers, 1989;13-21. 28. Imparato AM, Ramirez A Riles T, et al. Cerebral protection in carotid surgery. Arch Surg 1982;117:1073-8. 29. Sundt TM Jr. Sharbough FW, Piepgras DG, et al. Correlation of cerebral blood flow and electroencephalographic changes during carotid endarterectomy. Mayo Clin Proc 1981;56:533-43. 30. Hayes RJ, Levinson SA, Wylie EJ. Intraoperative measurement of carotid back pressure as a guide to operative management for carotid endarterectomy. Surgery 1972;72:953-60.

106 31. Whittemore AD, Kauffman JL, Kohler TK, et al. Routine electroencephalo-graphic monitoring during carotid endarterectomy. Ann Surg 1983;197:707-13. 32. Thompson JE. Complications of carotid endarterectomy and their prevention. World J Surg 1979;3:155-65. 33. Imparato AM. Recognition and management of acute stroke following carotid artery. In:Ernst CB, Stanley JC (eds). Current Therapy in Vascular Surgery 2nd ed. Philadelphia: BC Decker Inc, 1991;10410.

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥ 34. Kremen JE, Gee W, Kaupp HA, et al. Restenosis or occlusion after carotid endarterectomy: A survey with occlar pneumoplethysmography. Arch Surg 1979; 114:608-10. 35. Gagne PJ, Riles TS, Imparato AM, et al. Redo endarterectomy for recurrent carotid artery stenosis. Eur J Vasc Surg 1991;5:135-40. 36. Hertzer NR, Beven EG, O’Hara PJ, et al. A prospective study of vein patch angioplasty during carotid endarterectomy. Three-year results for 801 patients and 917 operations. Ann Surg 1987;206:62835.

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ª√–«—µ‘ √“¬≈–‡Õ’¬¥‡°’¬Ë «°—∫°“√‡®Á∫ªÉ«¬∑’‡Ë °’¬Ë «¢âÕß°—∫‚√§´÷ßË §«√´—° ∂“¡§◊ÕÕ“™’æ°“√ß“π °“√„™â¬“ °’Ã“∑’‡Ë ≈àπª√–®” ·≈–‚√§∑’‡Ë ªìπ Õ¬Ÿà „πªí®®ÿ∫—π ¡’¢âÕ·µ°µà“ß®“°ºŸâªÉ«¬¢“¥‡≈◊Õ¥∑’Ë¢“§◊Õ ºŸâªÉ«¬ ‚√§·¢π¢“¥‡≈◊Õ¥®–¡’Õ“¬ÿπâÕ¬°«à“‰¡à§àÕ¬æ∫«à“ “‡Àµÿ‡°‘¥®“° arteriosclerosis °√√¡°√∑’Ë∑”ß“π°—∫‡§√◊ËÕß®—°√ —Ëπ –‡∑◊Õπ µ≈Õ¥‡«≈“‡™àπ ‡§√◊ÕË ß‡®“–À‘π ®–¡’ vibratory white finger(3) ™à“ß‰¡â∑’ËµâÕß„™â¶âÕπµÕ°µ–ªŸ∫àÕ¬ Ê ®–¡’°“√µ’∫µ—π¢ÕßÀ≈Õ¥

‡≈◊Õ¥·¥ß ulnar ∑’¡Ë Õ◊ ∑”„Àâ‡°‘¥ hypothenar hammer syndrome „π§πÕ“¬ÿπÕâ ¬ “‡Àµÿ·¢π¢“¥‡≈◊Õ¥Õ“®®–¡“®“° Thoracic Outlet Syndrome (TOS) ¡’°“√°¥∑—∫¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß subclavian ®“° cervical rib À√◊Õ°√–¥Ÿ°´’Ë ‚§√ß´’·Ë √°∑’Ë‚§âßßÕº‘¥ª°µ‘ π—°°’Ã“∑’µË Õâ ß„™â·¢π‡À«’¬Ë ßÀ√◊Õ¢«â“ß∫àÕ¬ Ê ´È”´“°‡™àπ ¢«â“ß®—°√ ∑ÿ¡à πÈ”Àπ—° ª“≈Ÿ°∫Õ≈≈å ¡—°®–‡°‘¥°“√∫“¥‡®Á∫µàÕÀ≈Õ¥‡≈◊Õ¥·¥ß subclavian ·≈– axilla(4,5) ¬“À≈“¬™π‘¥∑”„Àâ¡°’ “√¢“¥‡≈◊Õ¥∑’Ë ·¢π∑—ßÈ Õß¢â“ß‡™àπ ¬“‡§¡’∫”∫—¥ dopamine ·≈–Õπÿæπ— ∏å¢Õß ergot “‡Àµÿ¢Õß·¢π¢“¥‡≈◊Õ¥¥Ÿ®“°µ“√“ß∑’Ë 11.1

Õ“°“√·≈–Õ“°“√· ¥ß “‡Àµÿ¢Õß·¢π¢“¥‡≈◊Õ¥‡©’¬∫æ≈—π ¡—°®–‡π◊ËÕß¡“®“° ‡ÕÁ¡‚∫‰≈®“°À—«„®Õÿ¥À≈Õ¥‡≈◊Õ¥·¥ß brachial ®–¡’Õ“°“√ª«¥ ·¢π·≈–‡¬Áπ´’¥∑—π∑’ §«“¡√Ÿ â °÷ —¡º— ·≈–°“√‡§≈◊ÕË π‰À«¢Õß¡◊Õ ·≈–·¢π®–§àÕ¬ Ê ‡ ’¬‰ª «‘π‘®©—¬‚√§‰¥â®“°°“√∑’ËºŸâªÉ«¬¡’‚√§ À—«„®¡“°àÕπ ‡™àπ À—«„®¢“¥‡≈◊Õ¥À√◊Õ®—ßÀ«–°“√‡µâπ¢ÕßÀ—«„® º‘¥ª°µ‘ “‡Àµÿ¢Õß·¢π¢“¥‡≈◊Õ¥‡√◊ÈÕ√—ß¡’‰¥â¡“°¡“¬¢÷ÈπÕ¬Ÿà°—∫ æ¬“∏‘ ¿“æ¢ÕßÀ≈Õ¥‡≈◊Õ¥·µà≈–µ”·Àπàß ∂â“‡ªìπÀ≈Õ¥‡≈◊Õ¥ ª≈“¬π‘È«®–¡’Õ“°“√ Raynaudûs phenomenon ‡¡◊ËÕ —¡º— °—∫ §«“¡‡¬Áπ À√◊Õ ¿“«–®‘µ„®∑’Ë°—ß«≈ µ◊Ëπ‡µâπµ°„® ’º‘«Àπ—ß ª≈“¬π‘È«¡◊Õ®–¡’°“√‡ª≈’Ë¬π·ª≈ß¥—ßπ’È ‡√‘Ë¡®“°´’¥ (pallor) µ“¡¥â«¬¡à«ß§≈È” (blue) ·≈–·¥ß (redness) ‡π◊ÕË ß®“°¡’°“√À¥ µ—«¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß¢π“¥‡≈Á° ¡—°®–‡°’Ë¬«¢âÕß°—∫‚√§µà“ß Ê µ“¡µ“√“ß∑’Ë 11.2 µâÕß·¬°ÕÕ°®“° acrocyanosis ´÷Ëßπ‘È«¡◊Õ

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Deep cervical Vertebral

Transverse scapular Axillary

Thyrocervical trunk Common carotid

Posterior humeral circumflex

Subclavian Interior thoracic (mammary)

Anterior humeral circumflex

Supreme thoracic Thoracoacromial

Brachial

Lateral thoracic Subscapular

Profunda branchii

Superior ulnar collateral Inferior ulnar collateral Radial recurrent

Elbow Common interosseous Dorsal interosseous

Radial

Ulnar Volar interosseous Deep volar arch Superficial volar arch Digital

√Ÿª∑’Ë 11.1 °“¬«‘¿“§»“ µ√å¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß∑’Ë·¢π·≈– collaterals

·¢π¢“¥‡≈◊Õ¥ ®–´’¥¢“¥‡≈◊Õ¥Õ¬à“ß∂“«√·≈–Õ“®®–≈“¡∂÷ß¡◊Õ¥â«¬‡¡◊ËÕ —¡º— §«“¡‡¬ÁπÕ“°“√®–√ÿπ·√ß¡“°¢÷Èπ ‡ªìπ diffuse cyanosis ¡—° ®–¡’·º≈µ“¡º‘«Àπ—ß ”À√—∫ livedo reticularis ®–¡’°“√À¥ µ—«¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ßª≈“¬π‘«È ¡◊Õ·¢π·≈–¢“Õ¬à“ß∂“«√ Õ“°“√ ®–√ÿπ·√ß∂â“ —¡º— §«“¡‡¬Áπ®–‡ÀÁπ ’¡à«ß‡ªìπ®È”∑—Ë«‰ªµ“¡º‘«Àπ—ß (mottled cyanosis) ·¬°‚√§∑—ßÈ 3 ™π‘¥‰¥â®“°µ“√“ß∑’Ë 11.3 µ“√“ß∑’Ë 11.1 “‡Àµÿ¢Õß·¢π¢“¥‡≈◊Õ¥ Atherosclerosis À≈Õ¥‡≈◊Õ¥‚ªÉßæÕß∑’·Ë ¢π Antiphospholipid syndrome À≈Õ¥‡≈◊Õ¥·¥ßÕ—°‡ ∫ (arteritis) 1. Collagen disease dermatomyositis rheumatic arteritis scleroderma systemic lupus erythematosus (SLE) 2. Allergic Necrotizing arteritis 3. Giant cell arteritis 4. Takayasuûs disease Bechetûs syndrome §«“¡º‘¥ª°µ‘¢Õß‡≈◊Õ¥ cold agglutinins cryoglobulins polycythemia vera Thoracic outlet syndrome (TOS) Congenital arterial wall defects Ehlers-Danloss syndrome Pseudoxanthoma elasticum Fibromuscular dysplasia Frosbite Iatrogenic injury °“√‡®“–‡≈◊Õ¥·≈–«—¥§«“¡¥—π‚≈À‘µºà“πÀ≈Õ¥‡≈◊Õ¥ ·¥ß‚¥¬µ√ß arteriography cardiac catheterization ®“°°“√©“¬· ß∫”∫—¥ ¡–‡√Áß ∑’§Ë Õ·≈–‡µâ“π¡ ‚√§‰µ«“¬‡√◊ÕÈ √—ß ¡’ azotemic arteritis À√◊Õ¡’ hemodialysis shunt

109 Raynaudûs disease À¡“¬∂÷ß Raynaudûs phenomenon ∑’Ë ‰¡à¡’ underlying cause ·¬°®“°§«“¡º‘¥ª°µ‘·≈–°“√µ’∫µ—π ¢ÕßÀ≈Õ¥‡≈◊Õ¥µ“¡µ“√“ß∑’Ë 11.1 ‰¥â ‰¡àæ∫«à“∑”„Àâ‡π◊ÕÈ ‡¬◊ÕË ‡πà“ µ“¬ æ∫„π‡æ»À≠‘ß¡“°°«à“‡æ»™“¬ (√âÕ¬≈– 70) ¡’·π«∑“ß„π °“√«‘π®‘ ©—¬ Raynaudûs disease ‰¥â¥ß— µàÕ‰ªπ’È 1. ¡’Õ“°“√¢Õß Raynaudûs phenomenon ∑’·Ë ¢πÀ√◊Õ¢“ ∑—ßÈ Õß¢â“ß 2. ‰¡à¡°’ “√Õÿ¥µ—π¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß¢π“¥„À≠à 3. ‰¡à¡·’ º≈‡√◊ÕÈ √—ßÀ√◊Õ‡π◊ÕÈ ‡¬◊ÕË ‡πà“µ“¬ 4. ‡ªìπ¡“π“π°«à“ 2 ªï ‚¥¬‰¡à®”‡ªìπ systemic disease ∑’∑Ë ”„Àâ‡°‘¥ Raynaudûs phenomenon °“√µ’∫µ—π¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß∫√‘‡«≥µâπ·¢π∑’∑Ë ”„Àâ·¢π¢“¥ ‡≈◊Õ¥‡√◊ÕÈ √—ß Õ“°“√ ”§—≠§◊Õ·¢πÕàÕπ·√ß¿“¬À≈—ß¢¬—∫À√◊Õ∑”ß“π ¡◊Õ‡¬Áπ´’¥ ª«¥®π∑”ß“πµàÕ‰ª‰¡à ‰¥âµ“¡ª°µ‘ ‡ÕÁ¡‚∫‰≈¢π“¥ ‡≈Á°∑’ËÀ≈ÿ¥≈Õ¬¡“Õÿ¥À≈Õ¥‡≈◊Õ¥¢π“¥‡≈Á°ª≈“¬¡◊Õ®–∑”„Àâ ’ º‘«Àπ—ß§≈È”‡ªìπ®È” ·¬°¬“°®“° livedo reticularis ®ÿ¥‡≈◊Õ¥„µâ º‘«Àπ—ßÀ√◊Õ„µâ‡≈Á∫ ·≈–°“√‡πà“µ“¬∫√‘‡«≥ª≈“¬π‘È« ‡ÕÁ¡‚∫‰≈ ¢π“¥‡≈Á° Ê π’È ¡—°®–À≈ÿ¥¡“®“° aneurysm ¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß subclavian À√◊Õ axillary (√Ÿª∑’Ë 11.2)

µ“√“ß∑’Ë 11.2 “‡Àµÿ¢Õß°“√‡°‘¥ Raynaudûs phenomenon Systemic disease Collagen vascular disease ‡™àπ sclerodema Cold hemagglutinin À√◊Õ cryoglobinemia Myxedema Ergotism Macroglobulinemia Nerve compression Carpal tunnel syndrome Thoracic outlet syndrome (TOS) Occupational trauma Pneumatic hammer operation Chainsaw operation Piano playing Typing Arterial occlusive disease

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µ“√“ß∑’Ë 11.3 °“√·¬°‚√§ vasospastic disease

‡æ» Õ“¬ÿ ’º«‘ ∑’‡Ë ª≈’¬Ë π·ª≈ß ∫√‘‡«≥∑’æË ∫ √–¬–‡«≈“∑’‡Ë ªìπ —¡º— §«“¡‡¬Áπ ·º≈∑’ºË «‘ Àπ—ß

Raynaudûs phenomenon

Acrocyanosis

Livido reticularis

‡æ»À≠‘ß√âÕ¬≈– 70-80 Àπÿ¡à “« (15-35 ªï) Pallor, cyanosis, rubor π‘«È ¡◊Õ,π‘«È ‡∑â“ ‡ªìπ™à«ß Ê Õ“°“√¡“°¢÷πÈ æ∫‰¥â∂“â ¡’ “‡Àµÿ ®“° collagen vascular disease ‡™àπ scleroderma

‡æ»À≠‘ß√âÕ¬≈– 90 Àπÿ¡à “« (15-35 ªï) Diffuse cyanosis π‘«È ¡◊Õ, ¡◊Õ ‡ªìπµ≈Õ¥ Õ“°“√¡“°¢÷πÈ ‰¡àæ∫

æ∫‰¥â∑ß—È ™“¬·≈–À≠‘ß ∑ÿ°Õ“¬ÿ Mottle cyanosis or rubor ª≈“¬π‘«È ¡◊Õ ·¢π·≈–¢“ ‡ªìπµ≈Õ¥ Õ“°“√¡“°¢÷πÈ æ∫πâÕ¬

°“√µ√«®√à“ß°“¬ §«√µ√«®√à“ß°“¬„Àâ≈–‡Õ’¬¥µ—Èß·µà∑àÕπ∫π¢Õß√à“ß°“¬·≈– µ√«®æ‘‡»… ”À√—∫ Thoracic outlet syndrome §≈”¥Ÿ∫√‘‡«≥ supraclavicular «à“¡’ aneurysm À√◊Õ‰¡àÀ√◊Õ§≈”‰¥â cervical rib „™âÀŸøíß·π∫µ√ß midclavicular øíß‡ ’¬ß bruit „ÀâºŸâªÉ«¬¢¬—∫ ·¢π„π∑à“ neutral, abduction, external rotation ·≈– hyperabduction §≈”™’æ®√À≈Õ¥‡≈◊Õ¥∑’·Ë ¢π∑ÿ°®ÿ¥·≈–∫—π∑÷°‰«â ∑” Allenûs test ¥Ÿ«“à ¡’°“√µ’∫µ—π¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß radial ·≈– ulnar ∫√‘‡«≥¢âÕ¡◊ÕÀ√◊Õ‰¡à ¥Ÿ capillary refilling time ∑’Ëª≈“¬π‘È«¡◊Õ´÷Ëß§à“ª°µ‘‰¡à§«√π“π‡°‘π 6 «‘π“∑’ ∂â“¡’Õ“°“√ ·¢π¢“¥‡≈◊Õ¥Õ¬à“ß√ÿπ·√ß §«√µ√«®¥Ÿ°“√∑”ß“π¢Õßª√– “∑ ‡§≈◊ÕË π‰À«·≈– —¡º—« §≈”¥Ÿ°≈â“¡‡π◊ÕÈ ·µà≈– à«π¢Õß·¢π«à“·πàπ µ÷ß¥’À√◊Õ‰¡à

°“√µ√«®§âπæ‘‡»…

√Ÿª∑’Ë 11.2 microemboli ∑’ËÀ≈ÿ¥ÕÕ°¡“®“° aneurysm ¢ÕßÀ≈Õ¥

‡≈◊Õ¥·¥ß subclavian À√◊Õ axillary ¡“Õÿ¥À≈Õ¥‡≈◊Õ¥ ¢π“¥‡≈Á°ª≈“¬π‘È«¡◊Õ ∑”„Àâº‘«Àπ—ß§≈È”‡ªìπ®È”À√◊Õ¡’ ’¥”

™π‘¥ noninvasive ‡™àπ °“√∑” Doppler wave form analysis ¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß∑’·Ë ¢π∑—ßÈ Õß¢â“ß «—¥ segmental arterial pressure ¢Õß·¢π∑—È ß Õß¢â “ ß brachial pressure ‡ª√’¬∫‡∑’¬∫°—∫·¢π∑—ßÈ Õß·¢π∂â“√–¥—∫§«“¡¥—πµà“ß°—π°«à“ 1020 ¡‘≈≈‘‡¡µ√ª√Õ∑πà“®–¡’°“√Õÿ¥µ—π¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß subclavian, axillary À√◊Õ brachial finger pressure µà“ß°—π¡“°°«à“ 15 ¡‘≈≈‘‡ ¡µ√ª√Õ∑ „π·µà≈–π‘È«πà“®–¡’°“√µ’∫µ—π¢ÕßÀ≈Õ¥ ‡≈◊Õ¥·¥ß„π palmar arch

111

·¢π¢“¥‡≈◊Õ¥ Duplex US ‚¥¬‡©æ“– color-coded mode ®–∫àß∫Õ°∂÷ß velocity ·≈– image ¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß “¡“√∂«‘π®‘ ©—¬ aneurysm, AVF ·≈–°“√∫“¥‡®Á∫¢Õßºπ—ßÀ≈Õ¥‡≈◊Õ¥®“°°“√ Õ¥ “¬ «π °“√µ√«®∑“ß√—ß ’«‘∑¬“ °“√©“¬¿“æ√—ß ’∫√‘‡«≥·¢πÕ“® ®–æ∫®ÿ¥·§≈‡´’¬Ë ¡·∑√°°√–®“¬Õ¬Ÿµà “¡‡π◊ÕÈ ‡π◊ÕÈ ‡¬◊ÕË „π‚√§ CRCT syndrome (Calcinosis, Cutis, Raynaud’s phenomenon, Sclerodactyly, Telangiectasia) ¡’°“√°√–®“¬¢Õß·§≈‡´’Ë¬¡∑—Ë« ºπ—ßÀ≈Õ¥‡≈◊Õ¥„π‚√§‡∫“À«“π À√◊Õ azotemic arteriopathy ¿“æ√—ß ’∑√«ßÕ°„πºŸªâ «É ¬ TOS ®–æ∫«à“¡’ cervical rib (√Ÿª∑’Ë 11.3) °√–¥Ÿ°´’Ë ‚§√ßÕ—π·√°‚°àßßÕº‘¥ª°µ‘Õ“®®–æ∫«à“°√–¥Ÿ°´’Ë ‚§√ß ·≈–°√–¥Ÿ° clavicle À—° „π scleroderma ®–æ∫ pulmonary fibrosis

°“√µ√«®∑“ßÀâÕßªØ‘∫—µ‘°“√ ºŸªâ «É ¬∑’¡Ë ·’ ¢π¢“¥‡≈◊Õ¥Õ¬à“ß√ÿπ·√ß ‚¥¬‡©æ“–∑’¡Ë Õ◊ ∑—ßÈ Õß ¢â“ß “‡ÀµÿÕ“®‡°‘¥®“° systemic disease §«√∑”°“√µ√«® §âπ∑“ß´’√¡—Ë Õ‘¡¡Ÿ‚π·≈–‚≈À‘µ«‘∑¬“‚¥¬¥Ÿ®“°

1. °“√‡æ‘¡Ë √–¥—∫¢Õß ESR (erythrocyte sedimentation rate) 2. º≈∫«°¢Õß ANA (antinuclear antibodies) 3. §«“¡º‘¥ª°µ‘¢Õß C3/C4 complement test 4. º≈∫«°¢Õß rheumatoid factor

°“√«‘π‘®©—¬‚√§ ‚√§À≈Õ¥‡≈◊Õ¥¢π“¥„À≠à ‰¡à§Õà ¬¡’ª≠ í À“¬ÿßà ¬“°„π°“√«‘π®‘ ©—¬ ‚√§∂â“‡ªìπ‚√§À≈Õ¥‡≈◊Õ¥¢π“¥‡≈Á°∑’Ë¡◊Õ·≈–ª≈“¬π‘È« §«√·¬° „Àâ ‰¥â√–À«à“ß Raynaudûs phenomenon °—∫ Raynaudûs disease ·¬°„Àâ ‰¥â√–À«à“ß‚√§À≈Õ¥‡≈◊Õ¥µâπ·¢π°—∫ª≈“¬·¢π 1. ‚√§À≈Õ¥‡≈◊Õ¥∫√‘‡«≥µâπ·¢π 1.1 Atherosclerosis ∫√‘‡«≥∑’‡Ë °‘¥‰¥â∫Õà ¬§◊Õ à«π·√°¢Õß À≈Õ¥‡≈◊Õ¥·¥ß subclavian √Õß≈ß¡“§◊Õ innominate æ¬“∏‘ ¿“æ∑’‡Ë °‘¥¢÷πÈ Õ“®®–¡’°“√Õÿ¥µ—πæ√âÕ¡°—∫¡’À√◊Õ‰¡à¡’ vertebral artery steal ∂â“¡’ ulcerative plaque Õ“® ®–‡ªìπ®ÿ¥‡√‘Ë¡µâπ„π°“√‡°‘¥‡ÕÁ¡‚∫‰≈ ´÷Ëß®–À≈ÿ¥‰ªÕÿ¥ À≈Õ¥‡≈◊Õ¥ à«πª≈“¬‰¥â¿“¬À≈—ß

√Ÿª∑’Ë 11.3 °. cervical °√–¥Ÿ°´’Ë ‚§√ßÕ—π·√°‚°àßßÕº‘¥ª°µ‘ ∑”„ÀâÀ≈Õ¥‡≈◊Õ¥·¥ß subclavian ‚°àßßÕº‘¥ª°µ‘ ¢. arch arteriography ®–æ∫«à“À≈Õ¥‡≈◊Õ¥·¥ß subclavian ¢â“ß¢«“‚°àßßÕ·≈–À—°æ—∫¡“°°«à“¢â“ß´â“¬

112 1.2 À≈Õ¥‡≈◊Õ¥Õ—°‡ ∫ (arteritis) ‡™àπ Takayasuûs, giant cell arteritis, temporal arteritis ·≈– polymyalgia rheumatica Takayasuûs arteritis ‡ªìπ nonspecific inflammatory process ‰¡à∑√“∫ “‡Àµÿ‡°‘¥¢÷πÈ °—∫ aorta À≈Õ¥‡≈◊Õ¥ ·¥ß ”§—≠∑’·Ë ¬°·¢πßÕÕ°¡“‡™àπ carotid, subclavian, axillary ·≈– pulmonary æ∫„π‡æ»À≠‘ß™à«ßÕ“¬ÿ 1030 ªï ∑” arteriography ®–æ∫°“√µ’∫µ—π‡ªìπ™à«ß À≈“¬µ”·Àπàß¢ÕßÀ≈Õ¥‡≈◊Õ¥·≈– collaterals ¡“°¡“¬ æ∫«à“‡ªìπæ¬“∏‘ ¿“æ∑’Ë pulmonary artery √âÕ¬≈– 45 Giant cell arteritis ‡ªìπ°“√Õ—°‡ ∫∑’‡Ë °‘¥¢÷πÈ °—∫À≈Õ¥ ‡≈◊Õ¥∫√‘‡«≥»’√…–‡™àπ À≈Õ¥‡≈◊Õ¥·¥ß cranial, temporal √«¡∑—Èß subclavian ·≈– axillary æ∫„πºŸâªÉ«¬Õ“¬ÿ ¡“°°«à“ 50 ªï ª«¥µ√ß¢¡—∫°¥≈ß∫π temporal artery ®–‡®Á∫√–¥—∫ ESR Ÿß°«à“ 50m/SEC ®“° arteriogram ®–æ∫°“√µ’∫·§∫‡ªìπ·π«¬“«¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß ≈—∫ °—π°—∫µ”·Àπàß∑’Ëª°µ‘‡ªìπ√–¬– ∫“ß·Ààßµ—π ‰¡àæ∫·º≈ ¢√ÿ¢√–∫πºπ—ßÀ≈Õ¥‡≈◊Õ¥ Temporal arteritis ·≈– polymyalgia rheumatica ®–æ∫‰¥â∫Õà ¬∑’ÀË ≈Õ¥‡≈◊Õ¥·¥ß subclavian ·≈– axillary 1.3 Thoracic outlet syndrome (TOS) æ∫„π§πÀπÿ¡à “« ‡°‘¥®“°°“√µ’∫·§∫·≈–°¥∑—∫¢Õß°≈â“¡‡π◊ÕÈ ·≈– °√–¥Ÿ°µàÕ‰ªπ’È 1.3.1 costoclavicular space ®“°°√–¥Ÿ°´’Ë‚§√ßÕ—π·√° ·≈– clavicle 1.3.2 anterior scalene muscle 1.3.3 ¡ÿ¡√–À«à“ß insertion ¢Õß pertoralis minor tendon ·≈– coracoid process ∫√‘‡«≥ axilla 1.3.4 humerus head ¢≥–∑” external rotation °“√°¥µ√ß thoracic outlet Õ“®®–‡°‘¥®“°°√–¥Ÿ° ´’Ë‚§√ßÕ—π¥—∫·√° cervical rib À√◊Õ hypertrophy ¢Õß scalene muscle π— ° °’ Ã “∑’Ë µâ Õ ß„™â · ¢π¢«â “ ßÀ√◊ Õ ‡À«’Ë¬ß∫àÕ¬ Ê ®–¡’°“√°¥·≈–°√–·∑°¢ÕßÀ≈Õ¥‡≈◊Õ¥ ·¥ß„°≈â‡§’¬ß‡™àπ axillary artery À√◊Õ circumflex humeral artery ∑”„Àâ°≈“¬‡ªìπ aneurysm ‰¥â

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥ ¿“«–·∑√°´âÕπ¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß ‡™àπ aneurysm, poststenotic dilatation, thrombosis ·≈– distal embolization Õ“®®–æ∫ Raynaudûs phenemenon ‰¥â∑¡’Ë Õ◊ ¢â“ß‡¥’¬« 1.4 Radiation injury ‡°‘¥¢÷πÈ ¿“¬À≈—ß°“√©“¬√—ß ’√°— …“ ¡–‡√Áß‡µâ“π¡ ·≈– Hodgkinûs disease À≈Õ¥‡≈◊Õ¥∑’Ë ‡°‘¥æ¬“∏‘ ¿“æ‰¥â∫àÕ¬§◊Õ subclavian ·≈– axillary artery ‚¥¬¡’æ¬“∏‘°”‡π‘¥ 3 ¢—πÈ µÕπ ¥—ßµàÕ‰ªπ’(6)È 1) ¡’°“√∑”≈“¬¢Õß‡ÕÁπ‚¥∑’‡≈’¬Ë ¡·≈–¡’°“√©’°¢“¥¢Õß internal elastic lamina µ“¡¡“¥â«¬°“√‡°‘¥ fibrosis ¢Õß™—πÈ media 2) ¡’°“√Õÿ¥µ—π¢Õß vasa vasorum ®“°°“√À¥µ—«·≈–¡’ hyalin Àπ“µ—«µ√ß™—πÈ intima ·≈–µ“¡¥â«¬°“√‡°‘¥ fibrosis ¢Õß™—πÈ media 3) periarterial fibrosis ∑”„Àâ°“√À¥√—¥™—ÈππÕ°¢Õß À≈Õ¥‡≈◊Õ¥ À≈Õ¥‡≈◊Õ¥®–µ’∫·§∫≈ß Õ“°“√·≈–Õ“°“√· ¥ß¢Õß‚√§·∫àßÕÕ°‰¥â 4 ·∫∫ §◊Õ 1. ¡’°“√·µ°À√◊Õ©’°¢“¥¢ÕßÀ≈Õ¥‡≈◊Õ¥∑—π∑’ ®“° necrosis ¢Õßºπ—ßÀ≈Õ¥‡≈◊Õ¥·¥ß 2. ‡°‘¥ mural thrombosis ¢ÕßÀ≈Õ¥‡≈◊Õ¥µ√ß∑’‡Ë §¬©“¬ √—ß ’√°— …“ ¡—°®–‡°‘¥ thromboembolism ¿“¬„π 5 ªï 3. ¡’ fibrotic occlusion ·≈â«§àÕ¬ Ê ¡’°“√¢“¥‡≈◊Õ¥¿“¬„π 10 ªï 4. ‡°‘¥Õ“°“√À≈—ß©“¬√—ß ’√°— …“ 20 ªï ¡’≈°— …≥–‡ªìπ periarterial fibrosis ·≈– çaccelerated atherosclerosisé °“√«‘π®‘ ©—¬‚√§‰¥â®“°ª√–«—µ‡‘ §¬©“¬√—ß ’√°— …“ ·≈– arteriogram æ∫«à“¡’ diffuse ·≈– long narrowing ¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß 1.5 Fibromuscular dysplasia æ∫πâÕ¬¡“°¢ÕßÀ≈Õ¥ ‡≈◊Õ¥∑’Ëµâπ·¢π ‚¥¬‡©æ“–À≈Õ¥‡≈◊Õ¥·¥ß brachial æ∫„π‡æ»À≠‘ß “‡Àµÿ·∑â®√‘ß¬—ß‰¡à∑√“∫·πàπÕπ ‡ªìπ∑—ßÈ nonarteriosclerosis ·≈– noninflammatory vascular disease ∑’Ë‡°‘¥¢÷Èπ°—∫À≈Õ¥‡≈◊Õ¥¢π“¥°≈“ß·≈– ¢π“¥‡≈Á°

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·¢π¢“¥‡≈◊Õ¥ 2. ‚√§À≈Õ¥‡≈◊Õ¥∑’ªË ≈“¬·¢π·≈–ª≈“¬π‘«È ¡◊Õ 2.1 §«“¡º‘¥ª°µ‘¢Õß‡π◊ÕÈ ‡¬◊ÕË „π√à“ß°“¬ ‡™àπ scleroderma, rheumatoid arteritis SLE, polyarteritis nodosa ·≈– dermatomyositis ¡’Õ“°“√À≈“¬Õ¬à“ß·≈–∑’æË ∫‰¥â∫Õà ¬§◊Õ Raynaudûs phenomenon ∂â“‡ªìπµàÕ‡π◊ËÕßÕ“®®– √ÿπ·√ß∑”„Àâπ‘È«‡πà“µ“¬‰¥â ¡—°®–‡°‘¥°—∫À≈Õ¥‡≈◊Õ¥∑’Ë‡≈’È ¬ßπ‘«È ¡◊Õ·≈– palmar arch 2.2 Buergerûs disease (Thromboangiitis Oblitrans À√◊Õ TAO) ¡’π«‘È ‡πà“µ“¬ ‚¥¬‰¡à¡°’ “√Õÿ¥µ—π¢ÕßÀ≈Õ¥ ‡≈◊Õ¥¢π“¥„À≠à æ∫„π§π¬‘«·≈–∑“ßµ–«—πÕÕ° ‡æ» ™“¬ Ÿ∫∫ÿÀ√’®Ë ¥— ¡—°®–æ∫ migratory thrombophlebitis √à«¡¥â«¬ ®“° arteriogram ®–æ∫«à“¡’°“√Õÿ¥µ—π¢Õß À≈Õ¥‡≈◊Õ¥¢π“¥‡≈Á° 2.3 Blood dyscrasia ‡™àπ cold agglutinin, cryglobulin ·≈– polycythemia vera ‡ªìπ§«“¡º‘¥ª°µ‘¢ÕßÀ≈Õ¥ ‡≈◊Õ¥„π°“√·¢Áßµ—«∑”„Àâ‡°‘¥≈‘Ë¡‡≈◊Õ¥‰¥âßà“¬ ¡—°®–Õÿ¥ À≈Õ¥‡≈◊Õ¥∑’Ë¡“‡≈’È¬ßπ‘È«¡◊Õ∫àÕ¬∑’Ë ÿ¥ ®“°‡ÕÁ¡‚∫‰≈À√◊Õ local thrombosis §«√µ√«®∑“ßÀâÕßªØ‘∫—µ‘°“√‡æ◊ËÕ À“§«“¡º‘¥ª°µ‘¢Õß√–∫∫‡≈◊Õ¥ 2.4 ∫“¥‡®Á∫À≈Õ¥‡≈◊Õ¥®“°°“√ «π§“ “¬ ‡æ◊ËÕµ√«® «‘π‘®©—¬‚√§À≈Õ¥‡≈◊Õ¥À√◊Õ°“√√—°…“ À≈Õ¥‡≈◊Õ¥∑’Ë ‰¥â √—∫∫“¥‡®Á∫∫àÕ¬§◊Õ À≈Õ¥‡≈◊Õ¥·¥ß radial ·≈– brachial 2.5 Vibration syndrome ‡°‘¥¿“¬À≈—ß®“°°“√„™â‡§√◊ÕË ß¡◊Õ ∑’¡Ë §’ «“¡ —πË –‡∑◊Õπ¡“° ‡™àπ ¶âÕπ≈¡ À√◊Õ «à“π‡®“–æ◊πÈ ‡§√◊ÕË ß‡®“–À‘π ∑”„Àâπ«‘È ¢“¥‡≈◊Õ¥¡’ ´’ ¥’ ¢“« ∂â“‡°‘¥∫àÕ¬ Ê ®–¡’æ¬“∏‘ ¿“æ∂“«√µàÕ digital artery 2.6 Hypothenar hammer syndrome ‡°‘¥®“°°“√∑”ß“π ‡™àπ „π™à“ß∑“ ’∑µ’Ë Õâ ß„™âΩ“É ¡◊Õ„π°“√¥—π ∂Ÿ ªî¥ ªÑ“¬ ®– °√–‡∑◊ÕπµàÕÀ≈Õ¥‡≈◊Õ¥·¥ß ulnar à«π∑’∑Ë Õ¥ºà“π hypothenar eminence ∑”„Àâ‡°‘¥°“√µ’∫·§∫¢ÕßÀ≈Õ¥ ‡≈◊Õ¥À√◊Õ°≈“¬‡ªìπ aneurysm ‡ÕÁ¡‚∫‰≈∑’‡Ë °‘¥¢÷πÈ ¿“¬„π aneurysm Õ“®®–À≈ÿ¥≈Õ¬‰ªÕÿ¥À≈Õ¥‡≈◊Õ¥∑’Ëª≈“¬ ·¢π·≈–π‘«È ¡◊Õ‰¥â 2.7 Calciphylactic arteriopathy æ∫„πºŸªâ «É ¬‡∫“À«“π À√◊Õ‰µ«“¬‡√◊ÈÕ√—ß À≈Õ¥‡≈◊Õ¥·¥ß¡’·§≈‡´’Ë¬¡¡“©“∫ ‡§≈◊Õ∫ ∑”„ÀâÀ≈Õ¥‡≈◊Õ¥µ’∫µ—π ·¢π®–¢“¥‡≈◊Õ¥Õ¬à“ß √ÿπ·√ß®–°√–∑—ßË ‡πà“µ“¬‰¥â ¿“æ√—ß ’∫√‘‡«≥·¢π®–‡ÀÁπ ·π«¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß‡ªìπ·§≈‡´’¬Ë ¡µ≈Õ¥ “¬ (pipe stem pattern)

°“√√—°…“ °“√√—°…“Õ“°“√¢“¥‡≈◊Õ¥¢Õß·¢π ·µ°µà“ß°—π‰ª¢÷πÈ Õ¬Ÿ°à ∫— ‚√§∑’ËºŸâªÉ«¬‡ªìπÕ¬Ÿà°àÕπ·≈â« ∂â“‡°‘¥®“°‡ÕÁ¡‚∫‰≈Õÿ¥µ—π§«√„Àâ‡Œ ª“√’π‡¢â“∑“ßÀ≈Õ¥‡≈◊Õ¥¥”µ“¡¥â«¬°“√ºà“µ—¥¥÷ß‡Õ“‡ÕÁ¡‚∫‰≈ ÕÕ°®“°À≈Õ¥‡≈◊Õ¥·¥ß (embolectomy) ∂â“ºŸâªÉ«¬ ¿“æ‰¡à æ√âÕ¡µàÕ°“√ºà“µ—¥Õ“®®–√—°…“‚¥¬°“√„™â “√≈–≈“¬≈‘¡Ë ‡≈◊Õ¥‡™àπ Urokinase À√◊Õ Streptokinase ºà“π‡¢â“ “¬ «π§“À≈Õ¥ ‡≈◊Õ¥·¥ßµ√ß∫√‘‡«≥∑’Ë¡’≈‘Ë¡‡≈◊Õ¥ Thrombolytic therapy ‰¥â º≈¥’®– “¡“√∂≈–≈“¬≈‘Ë¡‡≈◊Õ¥ à«πª≈“¬¡◊Õ∑’Ë ‰¡à “¡“√∂ Õ¥ Fogarty catheter ¥÷ß‡Õ“ÕÕ°¡“‰¥âÀ¡¥ °“√„Àâ corticosteroid ®–∑”„Àâ°“√Õ—°‡ ∫¢ÕßÀ≈Õ¥‡≈◊Õ¥≈¥πâÕ¬≈ß ∂â“ “‡Àµÿ¢Õß°“√ ¢“¥‡≈◊Õ¥¢Õß·¢π¡“®“°¬“§«√À¬ÿ¥¬“·≈–À¬ÿ¥ Ÿ∫∫ÿÀ√’¥Ë «â ¬ À≈Õ¥‡≈◊Õ¥∑’Ë·¢π à«πµâπµ’∫µ—π∑’Ë∑”„Àâ·¢π¢“¥‡≈◊Õ¥Õ¬à“ß √ÿπ·√ß °“√ºà“µ—¥·°â ‰¢‡ªìπ«‘∏’°“√√—°…“∑’Ë¥’∑’Ë ÿ¥ ∂â“‡ªìπ°“√Õÿ¥ µ—π¢ÕßÀ≈Õ¥‡≈◊Õ¥¢π“¥‡≈Á°∑’πË «‘È ¡◊Õ ®–‰¡à “¡“√∂ºà“µ—¥·°â ‰¢‰¥â Õ“®®–√—°…“‚¥¬°“√„Àâ¬“ calcium blocker (Nifedipine) Õ“®®–∑”„ÀâÕ“°“√ºŸªâ «É ¬¥’¢π÷È °“√ºà“µ—¥√—°…“«‘∏’°“√µà“ß Ê ¢÷ÈπÕ¬Ÿà°—∫µ”·Àπàßæ¬“∏‘ ¿“æ¢ÕßÀ≈Õ¥‡≈◊Õ¥‡™àπ ∂â“‡°‘¥°—∫ subclavian artery ¡’ aneurysm ®“° TOS §«√ºà“µ—¥‡Õ“ aneurysm ·≈– cervical rib ÕÕ° ºà“µ—¥∑” bypass À≈Õ¥‡≈◊Õ¥‚¥¬„™â autogenous vein graft ∂â“µ’∫µ—π„π™à«ß·§∫ Ê ∫√‘‡«≥ radial À√◊Õ ulnar artery §«√∑” thrombectomy À√◊Õ endarterectomy À≈—ß®“°π—πÈ ∑” patch angioplasty

°“√æ¬“°√≥å‚√§ °“√ºà“µ—¥∑” bypass ºŸªâ «É ¬∑’¡Ë À’ ≈Õ¥‡≈◊Õ¥µ’∫µ—π∑’·Ë ¢π‰¥âº≈ ¥’‡∑à“°—∫°“√ºà“µ—¥∑’Ë¢“ À≈Õ¥‡≈◊Õ¥¢π“¥‚µ®–‰¥âº≈¥’°«à“À≈Õ¥ ‡≈◊Õ¥¢π“¥‡≈Á° ‰¡à¡§’ «“¡®”‡ªìπ∑’®Ë –µâÕß∑” major amputation ‡À¡◊ÕπºŸªâ «É ¬‚√§À≈Õ¥‡≈◊Õ¥·¥ßµ’∫µ—π∑’¢Ë “

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‡Õ° “√Õâ“ßÕ‘ß 1. Fugitani RM, Mills JL. Acute and chronic upper extremity ischemia I. Large vessel arterial occlusive disease. In: Porter JM, Taylor LM, (eds.). Basic Data Underlying Clinical Decision Making in Vascular Surgery. St Louis: Quality Medical Publishing 1994;159-165. 2. Mills JL, Fugitani RM. Acute and chronic upper extremity ischemia II. Small vessel arterial occlusive disease. In: Porter JM, Taylor LM. (eds.). Basic Data Underlying Clinical Decision Making in Vascular Surgery. St Louis: Quality Medical Publishing 1994;166-170. 3. Palmar RA, Collin J. Vibratory white finger. Br J Surg 1993;80:705. 4. McCarthy WJ. Upper extremity arterial injury in athletes. J Vasc Surg 1989;9:317. 5. Rohrer MJ. Axillary artery compression and thrombosis in throwing athletes. J Vasc Surg 1990;11:761. 6. Butler MS, Lane RHS, Webster JHH. Irradiation injury to large arteries. Br J Surg 1980;67:341.

∫∑∑’Ë 12 ABDOMINAL AORTIC ANEURYSMS (AAA) Aneurysm À¡“¬∂÷ß°“√‚ªÉßæÕß¢¬“¬¢π“¥¢ÕßÀ≈Õ¥ ‡≈◊Õ¥·¥ßÕ¬à“ß∂“«√ ‚µ°«à“‡ âπºà“»Ÿπ¬å°≈“ßª°µ‘ 2 ‡∑à“ ‡ªìπ ‚√§∑’‡Ë °’¬Ë «¢âÕß∑“ßæ—π∏ÿ°√√¡ ®÷ß¡—°®–æ∫„π‡§√◊Õ≠“µ‘·≈–§√Õ∫ §√—«‡¥’¬«°—π æ∫„π‡æ»™“¬¡“°°«à“‡æ»À≠‘ß∂÷ß 4 ‡∑à“(1) ∂â“¡’ bilateral popliteal aneurysms ®–æ∫ AAA √à«¡¥â«¬√âÕ¬≈– 69 ºŸªâ «É ¬ femoral artery aneurysms ·≈– iliac aneurysms ®–æ∫ AAA √à«¡¥â«¬√âÕ¬≈– 92 ·≈– 70 µ“¡≈”¥—∫(1,2,3) AAA ∑’æË ∫¡—°®–Õ¬Ÿµà Ë”°«à“ renal artery ¡’‡æ’¬ß√âÕ¬≈– 2 ‡∑à“π—πÈ ∑’ÕË ¬Ÿà ‡Àπ◊ÕµàÕÀ√◊ÕæÕ¥’°∫— µ”·Àπàß¢Õß renal ·≈– visceral arteries „πªí®®ÿ∫π— ‡π◊ÕË ß®“°¡’«∏‘ °’ “√µ√«®«‘π®‘ ©—¬µà“ß Ê ∑’¡Ë ª’ √– ‘∑∏‘¿“æ ·≈–·¡àπ¬”¡“°¢÷πÈ ∑”„Àâ«π‘ ®‘ ©—¬ asymptomatic AAA ‰¥â¡“° ¢÷πÈ ®ÿ¥¡ÿßà À¡“¬ ”§—≠∑’ Ë ¥ÿ „π°“√√—°…“ AAA §◊Õ ªÑÕß°—π‰¡à „Àâ ¡’ ° “√·µ°‡æ√“–Õ— µ √“µ“¬·≈–∑ÿ æ ≈¿“æ Ÿ ß ¡“° „πªí ® ®ÿ ∫— π πÕ°®“°«‘∏°’ “√µ√«®«‘π®‘ ©—¬‚√§∑“ß√—ß ’«∑‘ ¬“·¡àπ¬”¢÷πÈ ·≈â« °“√ screen ºŸªâ «É ¬°àÕπºà“µ—¥‚¥¬¥Ÿ°“√∑”ß“π¢ÕßªÕ¥ À—«„® °àÕπºà“µ—¥ ‡∑§π‘§°“√ºà“µ—¥ºà“π∑“ß retroperitoneal ∑”„Àâ¥·Ÿ ≈À≈—ßºà“µ—¥ ßà“¬¢÷Èπ ‰¡àµâÕß„™â‡§√◊ËÕß™à«¬À“¬„®π“πÀ≈—ßºà“µ—¥ À≈Õ¥‡≈◊Õ¥ ‡∑’ ¬ ¡∑’Ë „™â¡’§ÿ≥¿“æ¥’¢÷Èπ °“√¥Ÿ·≈·≈– monitor ºŸâªÉ«¬À≈—ß ºà“µ—¥Õ¬à“ß„°≈â™¥‘ ∑”„ÀâÕµ— √“µ“¬·≈–∑ÿæ≈¿“æ≈¥≈ß¡“°

“‡Àµÿ ∑ƒ…Æ’‡°à“‡™◊ÕË «à“ infrarenal AAA ¡’ “‡Àµÿ¡“®“° atherosclerosis √à«¡°—∫ intimal degenerative process ∑”„Àâ¡’ °“√∑”≈“¬‚§√ß √â“ß¢Õß aorta ·≈–®–‡°‘¥°“√‚ªÉßæÕß¿“¬À≈—ß ∑ƒ…Æ’ª®í ®ÿ∫π— ‡™◊ÕË «à“ ¡’°“√∑”≈“¬¢Õß medial structural proteins ®“° proteolytic enzymes ´÷ßË ¡’ª√‘¡“≥ Ÿß¡“°°«à“ª°µ‘ √à«¡°—∫ nonspecific arteriopathy ∑’‡Ë °‘¥¢÷πÈ °—∫ vasa vasorum ‡≈◊Õ¥‰ª‡≈’È¬ßºπ—ß aorta πâÕ¬≈ß §«“¡¬◊¥À¬ÿàπ‡ ’¬‰ª ·≈– ‡π◊ËÕß®“°‡ªìπÕ«—¬«–∑’Ë¡’‡≈◊Õ¥‰À≈ºà“π·≈–‡µâπÕ¬Ÿàµ≈Õ¥‡«≈“ ®÷ß ∑”„Àâ‡°‘¥°“√‚ªÉßæÕß¢÷πÈ (4,5,6) (√Ÿª∑’Ë 12.1) Genetic abnormality in collagen

Atherosclerotic damage to elastin and collagen

Aging and natural degeneration of elastin

Increased proteolytic enzyme activity

√Ÿª∑’Ë 12.1 µ—«·ª√∑’ËÕ“®®–‡ªìπ “‡Àµÿ„π°“√‡°‘¥æ¬“∏‘ ¿“æ¢Õß arterial aneurysms

116 ¡’À≈—°∞“π·≈–¢âÕ —ß‡°µÿÀ≈“¬ª√–°“√ · ¥ß„Àâ‡ÀÁπ«à“ AAA ‡°’Ë¬«¢âÕß°—∫æ—π∏ÿ°√√¡ ¿“æ·«¥≈âÕ¡·≈–µ—«·ª√∑“ß™’«‡§¡’ ‚¥¬‡©æ“–°“√‡¡µ“‚∫≈‘ ¡å¢Õß connective tissue(4,7) ºŸâªÉ«¬ AAA®–æ∫«à“¡’À≈Õ¥‡≈◊Õ¥∫√‘‡«≥Õ◊πË ¢Õß√à“ß°“¬‚ªÉßæÕß√à«¡¥â«¬ ®“°°“√»÷°…“∑“ß‡§¡’æ∫«à“ºŸâªÉ«¬®–¡’ªØ‘°‘√‘¬“°“√∑”ß“π¢Õß ‡ÕÁπ´—¬¡å elastase Ÿß¢÷πÈ ·≈–¡’°“√≈¥≈ß¢Õß alpha-1-antitrypsin (elastase inhibitor) °“√ —ß‡§√“–Àå collagen ∑’Ëº‘¥ª°µ‘°Á¡’ à«π‡°’¬Ë «¢âÕß°—∫°“√‡°‘¥ AAA atheroclerosis ‡ªìπ “‡ÀµÿÀπ÷ßË ¢Õß°“√‡°‘¥ AAA ·¡â«“à ®–‰¡à „™à “‡ÀµÿÀ≈—° à«π “‡ÀµÿÕπ◊Ë ‡™àπ °“√∫“¥‡®Á∫ °“√µ‘¥‡™◊ÕÈ (salmonella ·≈– syphilis) §«“¡º‘¥ ª°µ‘¢Õß connective tissue ‡™àπ Ehlers-Danlos ·≈– Marfanûs syndrome œ≈œ(8,9,10,11) ‡π◊ËÕß®“°‰¡à∑√“∫ “‡Àµÿ∑’Ë·πàπÕπ·∑â®√‘ß„π°“√‡°‘¥ AAA §≥–°√√¡°“√¡“µ√∞“π„π°“√‡ΩÑ“√–«—ß·≈–√“¬ß“π‚√§¢Õß Society for Vascular Surgery ·≈– International Society for Cardiovascular Surgery ®÷ß‰¡à „™â§”«à“ atherosclerotic AAA µàÕ‰ª·µà „™â nonspecific AAA ·∑π

Õ“°“√·≈–Õ“°“√· ¥ß∑“ß§≈‘π‘§ √âÕ¬≈– 75 ¢Õß infrarenal AAA ®–‰¡à¡’Õ“°“√ æ∫‰¥â ®“°°“√µ√«®√à“ß°“¬∑—Ë«‰ª À√◊ÕºŸâªÉ«¬¡“¥â«¬‚√§Õ◊Ëπ∑’Ë ‰¡à „™à ‚√§ ¢ÕßÀ≈Õ¥‡≈◊Õ¥ °“√µ√«®√à“ß°“¬Õ¬à“ß≈–‡Õ’¬¥∂’Ë∂â«π “¡“√∂ «‘π®‘ ©—¬‚√§‰¥â·πàπÕπ√âÕ¬≈– 80 ∂â“ºŸªâ «É ¬‰¡àÕ«â π®π‡°‘π‰ª ‡¡◊ÕË §≈”Àπâ“∑âÕß‰¥â°Õâ π‡Àπ◊Õ –¥◊Õ · ¥ß«à“ AAA Õ¬Ÿ‡à Àπ◊ÕµàÕ aortic bifurcation §≈”‰¥â°âÕπµË”°«à“ epigastrium À√◊Õ∑” DeBakeyûs maneuver ‰¥âº≈∫«° · ¥ß«à“ AAA Õ¬Ÿµà Ë”°«à“ renal arteries Õ¬à“ß‰√°Áµ“¡§«√®–·¬° AAA ÕÕ°®“° tortuous aorta ´÷Ëß§≈”æ∫‰¥â „πºŸâªÉ«¬∑’ËºÕ¡¡“°·≈–°√–¥Ÿ° —πÀ≈—ß §¥ßÕ ¡’À≈—° ”§—≠„π°“√·¬°¥—ßπ’§È Õ◊ AAA ®–§≈”‰¥â°Õâ π∑“ß ¥â“π´â“¬ ∑—∫·π«°÷Ëß°≈“ß¡“¬—ß¥â“π¢«“¢ÕßÀπâ“∑âÕß‡ ¡Õ ·µà tortuous aorta °âÕπ¡—°®–§≈”‰¥â‡ªìπ≈”¢π“¥ª°µ‘∑Õ¥¡“∑“ß ¥â“π´â“¬¢ÕßÀπâ“∑âÕß ‰¡à∑∫— ·π«°÷ßË °≈“ß transmitted pulse ®“° aorta ∑’ºË “à π°âÕπ„π∑âÕß ‡™àπ pancreatic mass ®–¢÷πÈ ≈ß „π·π«‡¥’¬« µà“ß®“° radiated À√◊Õ expansile pulsation ¢Õß infrarenal AAA ´÷Ëß®–°√–®“¬ÕÕ°∑ÿ°∑‘»∑“ß „π§πÕâ«π, ºπ—ßÀπâ“∑âÕßÀπ“, ∑âÕßµ÷ß ¡“ππÈ” ®–§≈”‰¥â AAA ‰¡à™¥— À≈—ß µ√«®√à“ß°“¬·≈â«§«√∫—π∑÷°¢Õ∫‡¢µ·≈–≈—°…≥–¢Õß aorta ∑’Ë §≈”‰¥â §≈”™’æ®√¢Õß¢“‰¥â·√ßª°µ‘¥À’ √◊Õ‰¡à ‡æ√“–ºŸªâ «É ¬ AAA ∫“ß√“¬Õ“®®–§≈”™’æ®√∑’‡Ë ∑â“‰¡à ‰¥â À≈—ß°“√ºà“µ—¥‡π◊ÕË ß®“°‡°‘¥

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥ distal embolization(12) ºŸªâ «É ¬∑’Ë AAA ¡’¢π“¥‚µ¢÷πÈ Õ¬à“ß√«¥‡√Á«®π„°≈â·µ° ®–¡’ triad ∑’ Ë ”§—≠¥—ßµàÕ‰ªπ’§È Õ◊ ª«¥∑âÕß√â“«¡“∑“ß¥â“πÀ≈—ß §≈”‰¥â °àÕπ∑’ÀË πâ“∑âÕß ·≈–§«“¡¥—π‚≈À‘µ≈¥µË”≈ß ‚¥¬ à«π¡“°·≈â«®– ¡“¥â«¬ ruptured AAA Õ“°“√ª«¥∑âÕß∫“ß§√—Èß®–µâÕß·¬° ®“°°“√ª«¥∑âÕß‡©’¬∫æ≈—π∑’¡Ë ’ “‡Àµÿ¡“®“° ·º≈‡ªìªµ‘§, pancreatitis ·≈– renal colic(13) AAA ¡—°®–·µ°∑–≈ÿ‡¢â“ left retroperitoneal ¡“°°«à“‡¢â“„π peritoneal cavity AAA ∑’Ë¡’ ¢π“¥‚µ¡“°Õ“®®–∑”„Àâ‡°‘¥°“√Õÿ¥µ—π¢Õß≈”‰ â ‚¥¬‡©æ“–µ√ß duodenum ¡’°“√µ°‡≈◊Õ¥®“° mucosa ¢Õßºπ—ß duodenum ∑”„Àâπ÷°‰ª∂÷ßæ¬“∏‘ ¿“æÀ√◊Õ‚√§Õ◊Ëπ∑’Ë∑”„Àâ‡°‘¥°“√µ°‡≈◊Õ¥ ¢Õß∑“ß‡¥‘πÕ“À“√ à«πµâπ ∂â“°≈“¬‡ªìπ aorto-duodenal fistula ®–¬‘ßË ∑”„Àâ°“√µ°‡≈◊Õ¥¡“°¢÷πÈ µ”·Àπàß¢Õß duodenum 4th part ‡°‘¥ fistula ‰¥â∫Õà ¬∑’ Ë ¥ÿ „π aortocaval fistula ®–µ√«®æ∫ «à“ºŸªâ «É ¬¡’ abdominal bruit, venous hypertension, ¢“∫«¡ ∑—ßÈ Õß¢â“ß ·≈–À—«„®«“¬(14) ¿“«–·∑√°´âÕπ¢Õß AAA Õ◊πË ∑’æË ∫‰¥â¡’ distal embolization ®“° aortic debris À√◊Õ aortic thrombosis(12) ª«¥À≈—ß ‡°‘¥®“° vertebral erosion ∫“ß§√—ßÈ Õ“®®–∑”„Àâ¡°’ “√Õÿ¥µ—π¢Õß ureter

°“√«‘π‘®©—¬‚√§ «‘∏°’ “√µ√«®«‘π®‘ ©—¬¡’∑ß—È screening ·≈–°“√ª√–‡¡‘πºŸªâ «É ¬ °àÕπºà“µ—¥ ¢âÕ¡Ÿ≈∑’Ë§«√∑√“∫ ”À√—∫ºŸâªÉ«¬ AAA §◊Õ ¢π“¥ ¢Õ∫‡¢µ·≈–æ¬“∏‘ ¿“æ∑’‡Ë °’¬Ë «¢âÕß°—∫À≈Õ¥‡≈◊Õ¥∑’·Ë ¬°·¢πß®“° aorta §ÿ≥ ¡∫—µ¢‘ Õß screening test ∑’¥Ë §’ Õ◊ ¡’§«“¡·¡àπ¬” Ÿß, noninvasine, ‘Èπ‡ª≈◊Õß§à“„™â®à“¬πâÕ¬, ‰¡à —¡º— µàÕ ionizing radiation ·≈– nephrotoxic agents °“√µ√«®«‘π®‘ ©—¬∑’Ë „™â „πªí®®ÿ∫π— ¡’ (15-17) 1. plain abdominal film Õ“®®–æ∫ calcified aneurysmal wall ‡ªìπ·π«∑“ß¥â“π´â“¬¢Õß™àÕß∑âÕß (√Ÿª∑’Ë 12.2) 2. B-mode ultrasonography ®– “¡“√∂«‘π®‘ ©—¬ AAA ‰¥â·πàπÕπ‡°◊Õ∫ 100% (√Ÿª∑’Ë 12.3) Õ“®®–‡ÀÁπ‰¡à™¥— „π°√≥’∑¡’Ë ’ ≈¡„π≈”‰ â¡“°, ºŸâªÉ«¬Õâ«πÀ√◊Õºπ—ßÀπâ“∑âÕßÀπ“ ‰¡à “¡“√∂ ‡ÀÁπ¢Õ∫‡¢µ¢Õß AAA ·≈–À≈Õ¥‡≈◊Õ¥·¥ß∑’·Ë ¬°·¢πßÕÕ°‰ª ‰¥â™¥— ‡®π ‡À¡“– ”À√—∫‡ªìπ screening test À√◊Õ„™â ”À√—∫°“√ follow up ¥Ÿ¢π“¥∑’Ë ‚µ¢÷πÈ ¢Õß AAA ∑’¬Ë ß— ‰¡àµÕâ ßºà“µ—¥ 3. computed tomography (CT) scan ‡ªìπ«‘∏°’ “√ µ√«®«‘π®‘ ©—¬∑’ Ë “¡“√∂„Àâ¢Õâ ¡Ÿ≈√“¬≈–‡Õ’¬¥¢Õß AAA ∂÷ß¢π“¥,

117

ABDOMINAL AORTIC ANEURYSMS (AAA)

√Ÿª∑’Ë 12.2 ®“° plain abdominal film æ∫ calcified aneurysmal wall ∑“ß¥â“π´â“¬¢Õß™àÕß∑âÕß √à«¡°—∫π‘Ë«„π‰µ¢â“ß ¢«“

√Ÿª∑’Ë 12.3 ultrasonography „π·π«µ—¥ ·≈–·π«¢π“π “¡“√∂ «‘π‘®©—¬‚√§·≈–∑√“∫¢π“¥¢Õß abdominal aortic aneurysms ‰¥â

√Ÿª∑’Ë 12.4 CT scan abdomen “¡“√∂ ∑√“∫√“¬≈–‡Õ’¬¥ µ”·Àπàß ¢π“¥ æ¬“∏‘ ¿“æ µ≈Õ¥ ®π∂÷ß leakage ¢Õß aortic aneurysms ‰¥â πÕ°®“° π’È ¬— ß ‡ÀÁ π §«“¡º‘ ¥ ª°µ‘ ¢ Õß Õ«—¬«–¿“¬„π™àÕß∑âÕß

118

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥

¢Õ∫‡¢µ, æ¬“∏‘ ¿“æ¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß∑’Ë·¬°·¢πßÕÕ°‰ª, degree ·≈–µ”·Àπàß¢Õß calcified aortic plaques §«“¡ º‘ ¥ ª°µ‘ ¢ ÕßÕ«— ¬ «–¿“¬„π™à Õ ß∑â Õ ß, extravasation ¢Õß ‡≈◊Õ¥„π√“¬∑’Ë¡’ ruptured À√◊Õ leakage AAA (√Ÿª∑’Ë 12.4) ‡ªìπ«‘∏°’ “√µ√«®«‘π®‘ ©—¬∑’¥Ë ¡’ “° ”À√—∫„πºŸªâ «É ¬∑’¡Ë retroperitoneal ’ fibrosis À√◊Õ inflammatory AAA 4. aortography ‰¡à«“à ®–‡ªìπ«‘∏’ conventional À√◊Õ digital ¬—ß¡’∑’Ë„™â ‚¥¬‡©æ“– biplane aortography „π°“√µ√«®«‘π®‘ ©—¬ ¥Ÿ¢Õâ ¡Ÿ≈√“¬≈–‡Õ’¬¥¢Õß AAA °àÕπºà“µ—¥‡¬Á∫´àÕ¡À≈Õ¥‡≈◊Õ¥ (√Ÿª∑’Ë 12.5) ¢âÕ¥’¢Õß aortography §◊Õ “¡“√∂‡ÀÁπ≈—°…≥–·≈– ¢Õ∫‡¢µ¢Õß AAA ‰¥â™¥— ‡®π ‡ÀÁπ§«“¡º‘¥ª°µ‘¢ÕßÀ≈Õ¥‡≈◊Õ¥ ∑’·Ë ¬°·¢πßÕÕ°‰ª ‡™àπ renal arteries, iliofemoral arteries „π√“¬∑’¡Ë ’ luminal thrombus ®–‰¡à “¡“√∂∫àß∫Õ°¢π“¥∑’·Ë ∑â ®√‘ß¢Õß AAA ‰¥â §«√∑” contrast-enhanced CT complements aortography ¿“«–·∑√°´âÕπ∑’æË ∫‰¥â®“°°“√∑” aortography §◊Õ ·æâ “√∑÷∫· ß, ‰µ«“¬‡©’¬∫æ≈—π, °“√∫“¥‡®Á∫ ·≈–Õÿ¥µ—π¢ÕßÀ≈Õ¥‡≈◊Õ¥®“°°“√·∑ß

preoperative aortography ¡’§«“¡®”‡ªìπ„π°√≥’µÕà ‰ªπ’È 4.1 ß —¬«à“®–¡’ thoracoabdominal aortic aneurysm 4.2 ß —¬«à“®–¡’ renovascular hypertension 4.3 ß —¬«à“ AAA ®– Ÿß∂÷ß√–¥—∫ renal arteries À√◊ÕÕ¬Ÿà Ÿß°«à“π—πÈ 4.4 ¡’Õ“°“√¢Õß visceral angina 4.5 øíß‰¥â bruit ∫√‘‡«≥Àπâ“∑âÕßÀ√◊Õ ’¢“â ß 4.6 §≈” femoral pulse ‰¥â‡∫“≈ß¢â“ß‡¥’¬«À√◊Õ∑—ßÈ Õß¢â“ß 4.7 ¡’Õ“°“√·≈–Õ“°“√· ¥ß¢Õß peripheral vascular occlusive disease 4.8 ¡’ horseshoe Kidney 4.9 ¡’ chronic aortic dissection 4.10 ¡’ iliac artery aneurysm 4.11 ‡§¬ºà“µ—¥ colectomy ¡“°àÕπ §«√µ√«®¥ŸÀ≈Õ¥‡≈◊Õ¥ ·¥ß∑’¡Ë “‡≈’¬È ß≈”‰ â°Õà π ∑” aneurysmorrhaphy ¥Ÿ colonic circulation ªÑÕß°—π°“√‡°‘¥ intestinal ischemia À≈—ßºà“µ—¥ 5. magnetic resonance arteriography ·≈– spiral CT scaning ‡ªìπ noninvasive diagnostic test ∑’ Ë “¡“√∂¡Õß ‡ÀÁπ§«“¡º‘¥ª°µ‘¢ÕßÀ≈Õ¥‡≈◊Õ¥‰¥â∑°ÿ √–π“∫, √–¥—∫ ·≈–·π«

¢âÕ∫àß™’È„π°“√ºà“µ—¥√—°…“

√Ÿª∑’Ë 12.5 Transfemoral aortography “¡“√∂‡ÀÁπ¢Õ∫‡¢µ ·≈– ≈—°…≥–¢Õß aneurysms ‰¥â ™—¥‡®π √«¡∑—Èß°“¬«‘¿“§ ¢Õß·¢πßÀ≈Õ¥‡≈◊Õ¥µà“ß Ê

¢âÕ∫àß™’È „π°“√ºà“µ—¥√—°…“ AAA §◊Õ ‡°‘¥ thrombosis ·≈–¡’ distal embolization AAA ¢π“¥‚µ¡“°°¥¥—πÕ«—¬«–¢â“ß‡§’¬ß ∑”„Àâ¡Õ’ “°“√º‘¥ª°µ‘ ¡’ fistula µàÕ°—∫ vena cava À√◊Õ duodenum ¥—ß∑’°Ë ≈à“«¡“·≈â«‡∫◊ÕÈ ßµâπ«à“√âÕ¬≈– 75 ¢ÕßºŸªâ «É ¬ AAA ®–‰¡à¡Õ’ “°“√º‘¥ª°µ‘Õ–‰√ ·µàµ√«®æ∫«à“¡’°Õâ π‡µâπ‰¥â∑À’Ë πâ“∑âÕß ¢âÕ∫àß™’ È ”§—≠„π°“√ºà“µ—¥ºŸªâ «É ¬ AAA ∑’¬Ë ß— ‰¡à¡Õ’ “°“√§◊Õ ‡æ◊ÕË ªÑÕß°—π°“√·µ°∑–≈ÿ´ß÷Ë ¡’Õµ— √“µ“¬ Ÿß¡“° Õ—µ√“‡ ’¬Ë ß¢Õß°“√·µ° ∑–≈ÿ¢÷ÈπÕ¬Ÿà°—∫¢π“¥¢Õß AAA Õ—µ√“°“√‚µ¢¬“¬¢π“¥ ·≈– Õ“°“√∑’‡Ë °‘¥¢÷πÈ (18,19) Õ—µ√“‡ ’¬Ë ß„π°“√·µ°∑–≈ÿ¢Õß AAA ¢π“¥‡ âπºà“»Ÿπ¬å°≈“ß 4 ‡´Áπµ‘‡¡µ√ §◊Õ√âÕ¬≈– 15 ¿“¬„π√–¬–‡«≈“ 5 ªï ∂â“¢π“¥‚µ 8 ‡´Áπµ‘‡¡µ√ ®–‡ªìπ√âÕ¬≈– 75 ‡ªìπ∑’¬Ë Õ¡√—∫°—π∑—«Ë ‰ª«à“ AAA ¢π“¥ 5-6 ‡´Áπµ‘‡¡µ√¡’Õµ— √“‡ ’¬Ë ß„π°“√·µ°∑–≈ÿ§Õà π¢â“ß Ÿß(19,21,22) ®÷ß §«√ºà“µ—¥·∫∫ elective ¡“°°«à“√Õ„Àâ·µ°∑–≈ÿ·≈â«§àÕ¬ºà“µ—¥ √—°…“‡æ√“–Õ—µ√“µ“¬®– Ÿß¡“° µ—«·ª√∑’‡Ë °’¬Ë «¢âÕß·≈–∑”„ÀâÕµ— √“°“√·µ°∑–≈ÿ¢Õß AAA Ÿß ¢÷πÈ §◊Õ(23)

119

ABDOMINAL AORTIC ANEURYSMS (AAA)

1. ¢π“¥¢Õß AAA ∑’Ë ‚µ‡√Á«‡°‘π°«à“ 4 ¡‘≈≈‘‡¡µ√µàÕªï 2. ¿“«–§«“¡¥—π‚≈À‘µ Ÿß 3. generalized ectasia 4. COPD Õ—µ√“√Õ¥À≈—ß°“√ºà“µ—¥ ruptured AAA ª√–¡“≥√âÕ¬≈– 45 ∂â“¡’™ÕÁ §·≈–°“√·µ°∑–≈ÿ‡¢â“„π™àÕß∑âÕß Õ—µ√“√Õ¥‡À≈◊Õ√âÕ¬≈– 10 „π°“√ºà“µ—¥ elective aneurysmorrhaphy Õ—µ√“µ“¬ ª√–¡“≥√âÕ¬≈– 3-5 ¢÷ÈπÕ¬Ÿà°—∫¿“«–√à“ß°“¬·≈– underlying diseases ¢ÕßºŸªâ «É ¬¢≥–π—πÈ (22) Õ“¬ÿºªŸâ «É ¬‰¡à„™à¢Õâ Àâ“¡„π°“√ºà“µ—¥ ∂â“ AAA ¡’¢π“¥‚µ°«à“ 5 ‡´Áπµ‘‡¡µ√ §«√ºà“µ—¥√—°…“‡æ√“– ‚Õ°“ ·µ°∑–≈ÿ¡’‰¥â Ÿß §«√ºà“µ—¥·∫∫ elective ‡æ√“–Õ—µ√“ µ“¬®–πâÕ¬°«à“ºà“µ—¥©ÿ°‡©‘π¢≥–·µ°∑–≈ÿ ‰¡à§«√ºà“µ—¥ AAA „πºŸªâ «É ¬¥—ßµàÕ‰ªπ’(22) È 1. ‡ªìπ‚√§À—«„® ‡™àπ recent À√◊Õ multiple myocardial infarction, À—«„®«“¬ 2. ‚√§ªÕ¥‡√◊ÕÈ √—ß ‡™àπ COPD ∑’√Ë πÿ ·√ß ·≈–§“¥«à“®–‰¡à “¡“√∂‡Õ“‡§√◊ËÕß™à«¬À“¬„®ÕÕ°‰¥âÀ≈—ßºà“µ—¥ À√◊Õ¡’ dyspnea at rest 4. ‡ªìπ metastatic cancer À√◊Õ‚√§∑’¡Ë ’ limit life expectancy

°“√ª√–‡¡‘πºŸâªÉ«¬°àÕπºà“µ—¥ °àÕπºà“µ—¥§«√ª√–‡¡‘πºŸªâ «É ¬Õ¬à“ß√Õ∫§Õ∫ ‚¥¬‡©æ“–„π√“¬ ∑’ºË “à µ—¥·∫∫ elective ∂â“µ√«®√à“ß°“¬·≈–°“√µ√«®§≈◊πË ‰øøÑ“ À—«„®ª°µ‘ ‰¡àπà“®–¡’ªí≠À“„π°“√ºà“µ—¥ ·µà∂â“§≈◊ËπÀ—«„®‰øøÑ“ º‘¥ª°µ‘§«√ª√–‡¡‘π¥Ÿ coronary heart disease (CAD) ´÷ßË ®– æ∫√à«¡°—∫ AAA ‰¥âª√–¡“≥√âÕ¬≈– 20 CAD ‡ªìπ “‡Àµÿ°“√ µ“¬¢ÕßºŸâªÉ«¬‚√§À≈Õ¥‡≈◊Õ¥∂÷ß√âÕ¬≈– 50 ºŸâªÉ«¬ AAA ∑’Ë µ“¬À≈—ßºà“µ—¥√–¬–·√° ª√–¡“≥√âÕ¬≈– 30 ®–¡’ “‡Àµÿ¡“®“° myocardial infarction(24,25) ∂â“¡’§«“¡º‘¥ª°µ‘¢Õß‚√§À—«„® ·≈– CAD „πºŸªâ «É ¬ AAA §«√®–∑” preoperative noninvasive cardiac evaluation ¥—ßµàÕ‰ªπ’È (26,27,28) 1. dipyridamole scan 2. echocardiography 3. ejection fraction evaluation 4. cardiac catheterization ∂â“æ∫§«“¡º‘¥ª°µ‘¢Õß‚√§À—«„®·≈–À≈Õ¥‡≈◊Õ¥‚§‚√π“√’Ë §«√ºà“µ—¥·°â ‰¢‡ ’¬°àÕπ∑”°“√ºà“µ—¥ AAA

ºŸâªÉ«¬∑’Ë¡’Õ—µ√“‡ ’Ë¬ß Ÿß∑’Ë®–‡°‘¥¿“«–·∑√°´âÕπÀ√◊Õµ“¬ ¿“¬À≈—ß°“√ºà“µ—¥ AAA §◊Õ 1. recent MI 2. inoperable CAD 3. end-stage pulmonary disease 4. ‰µ«“¬‡√◊ÕÈ √—ß °“√ºà“µ—¥√—°…“ AAA „πºŸªâ «É ¬°≈ÿ¡à ¥—ß°≈à“« ¡’¢¥’ ·≈–¢âÕ®”°—¥ ®–æ‘®“√≥“ºà“µ—¥√—°…“µ“¡§«“¡‡À¡“– ¡„π·µà≈–√“¬‰ª ®– √—°…“µàÕ‡¡◊ÕË §“¥«à“ AAA ¡’‚Õ°“ ‡ ’¬Ë ßµàÕ°“√·µ°∑–≈ÿ¿“¬„π 25 ªï ”À√—∫«‘∏°’ “√√—°…“∑’¡Ë Õ’ µ— √“‡ ’¬Ë ßπâÕ¬°«à“°“√ºà“µ—¥§◊Õ(29) 1. external aneurysm wrapping 2. extra-anatomical bypass with ligation of the aneurysm «‘∏°’ “√∑—ßÈ 2 ·∫∫ ‰¡à ‰¥â≈¥Õ—µ√“‡ ’¬Ë ß¢Õß AAA „π°“√·µ° ∑–≈ÿÀ≈—ß√—°…“ °“√ºà“µ—¥°Á¬ß— ‡ªìπ«‘∏°’ “√√—°…“∑’¥Ë ∑’ ’Ë ¥ÿ ·µà§«√¡’ intensive care ·≈– monitor „π√–¬–ºà“µ—¥·≈–À≈—ßºà“µ—¥ «‘∏°’ “√√—°…“∑’¥Ë ’„πªí®®ÿ∫π— ‚¥¬‰¡àµÕâ ßºà“µ—¥§◊Õ intraluminal AAA (√Ÿª∑’Ë 12.6) ‡À¡“– ”À√—∫ºŸªâ «É ¬Õ“°“√Àπ—°, ¡’‚√§·∑√°´âÕπ, ¥¡¬“ ≈∫‰¡à ‰¥â, ‡ ’¬Ë ßµàÕ°“√·µ°∑–≈ÿ ·µà®–µâÕß¡’ iliac artery ¢â“ß„¥¢â“ßÀπ÷Ëßª°µ‘ “¡“√∂ Õ¥ “¬¬“ß·≈–À≈Õ¥‡≈◊Õ¥‡∑’¬¡ ºà“π‡¢â“‰¥â(30) „πªí®®ÿ∫π— æ∫«à“¡’ perigraft leakage ¿“¬„π 12 ‡¥◊Õπ Ÿß∂÷ß√âÕ¬≈– 20 À≈—ß∑” Endovascular Stent Grafting(31) ®÷ßµâÕßª√–‡¡‘π«‘∏°’ “√√—°…“„À¡à

√Ÿª∑’Ë 12.6 «‘∏’°“√ Endovascular Stent Grafting ‚¥¬ºà“π‡¢â“ ∑“ß femoral artery

120

°“√ºà“µ—¥ ºŸâªÉ«¬∑’Ë®–ºà“µ—¥ AAA repair §«√·∑ßÀ≈Õ¥‡≈◊Õ¥¥” ¥â«¬‡¢Á¡‡∫Õ√å‚µ ‡æ◊ÕË „Àâ “√πÈ”·≈–‡≈◊Õ¥‰¥â ¡’ invasive monitoring line (pulmonary ·≈– radial arterial catheters) °àÕπºà“µ—¥ ‡æ◊ÕË ¥Ÿ hemodynamic status æ√âÕ¡∑—ßÈ «π§“ “¬ªí “«–‡æ◊ÕË ¥Ÿª√‘¡“≥ªí “«–∑’ÕË Õ°µàÕ™—«Ë ‚¡ß À¬ÿ¥¬“µâ“π‡°√Á¥‡≈◊Õ¥·≈–¬“ µâ“π‡≈◊Õ¥·¢Áßµ—«Õ¬à“ßπâÕ¬ 7 «—π°àÕπºà“µ—¥ „Àâ¬“ªØ‘™«’ π–°àÕπ ºà“µ—¥‡ªìπ°“√ªÑÕß°—π°“√µ‘¥‡™◊ÈÕ Õÿ≥À¿Ÿ¡‘¿“¬„πÀâÕßºà“µ—¥§«√ æÕ‡À¡“– ‰¡à‡¬ÁπÀ√◊Õ√âÕπ®π‡°‘π‰ª ‡µ√’¬¡‡§√◊ÕË ß¡◊Õºà“µ—¥„Àâæ√âÕ¡ ‡µ√’ ¬ ¡∑”§«“¡ –Õ“¥øÕ°º‘ « Àπ— ß „Àâ ª √“»®“°‡™◊È Õ µ—È ß ·µà Àπâ“Õ°∂÷ß‡¢à“ ‡µ√’¬¡‡§√◊ÕË ß autotransfusion ‰«â „™â‡¡◊ÕË ®”‡ªìπ ≈ß¡’¥ºà“µ—¥Àπâ“∑âÕß„π·π« midline ∂â“µâÕß°“√‡¢â“∂÷ß AAA ∑“ß™àÕß∑âÕß À√◊Õ∂â“®–‡¢â“∑“ß retroperitoneal „Àâ≈ß¡’¥‡ªìπ oblique incision ‚¥¬‡√‘¡Ë µâπ®“°´’Ë ‚§√ß™àÕß∑’Ë 11 „°≈â°∫— ¢Õ∫ ¢Õß°≈â“¡‡π◊ÕÈ rectus abdominis «‘∏’ retroperitoneal approach ®–¡’ª≠ í À“‡¢â“∂÷ßÀ≈Õ¥‡≈◊Õ¥ iliac artery ·≈– renal arteries ∑“ß¥â“π¢«“ §«√„™â retroperitoneal approach „π°√≥’¥ß— µàÕ‰ªπ’(32,33) È 1. aneurysm ‰¡à≈“¡∂÷ß right iliac artery 2. obesity 3. ºŸªâ «É ¬∑’¡Ë ª’ ≠ í À“ pulmonary disease 4. ‡§¬ºà“µ—¥™àÕß∑âÕßÀ≈“¬§√—ßÈ À√◊Õ¡’ colostomy Õ¬Ÿà ¢âÕ¥âÕ¬¢Õß retroperitoneal approach §◊Õ ‰¡à “¡“√∂ ‡ÀÁπæ¬“∏‘ ¿“æ¢ÕßÕ«—¬«–¿“¬„π™àÕß∑âÕß‰¥â ¢âÕ¥’§Õ◊ ‡ªìπ°“√ ºà“µ—¥‡¢â“∂÷ß aorta ‚¥¬µ√ß ‰¡à°√–∑∫°√–‡∑◊ÕπµàÕÕ«—¬«–Õ◊Ëπ ¿“¬„π™àÕß∑âÕß ºŸªâ «É ¬øóπô µ—«‡√Á« √–¬–∑’ÕË ¬Ÿà „π ICU —πÈ °«à“ „™â ‡§√◊ËÕß™à«¬À“¬„®„π√–¬–‡«≈“ —Èπ ¿“«–·∑√°´âÕπ‡°‘¥πâÕ¬°«à“ ºà“µ—¥‡ªî¥™àÕß∑âÕß AAA ª√–¡“≥√âÕ¬≈– 90 ®–Õ¬Ÿµà Ë”°«à“√–¥—∫¢Õß renal arteries ´÷ßË ‚Õ°“ ‡°‘¥¿“«–‰µ«“¬Õ¬à“ß‡©’¬∫æ≈—π¡’πÕâ ¬ ¿“¬À≈—ß cross clamping aorta ·≈â« „π√“¬∑’Ë AAA Õ¬Ÿà „π√–¥—∫‡¥’¬«°—πÀ√◊ÕÕ¬Ÿ à ßŸ °«à“ renal arteries ®”‡ªìπ∑’®Ë –µâÕß cross clamp aorta „π√–¥—∫ Ÿß°«à“π—πÈ °“√ºà“µ—¥µàÕÀ≈Õ¥‡≈◊Õ¥®–µâÕß„™â‡«≈“πâÕ¬°«à“ 30 π“∑’‡æ√“–®– ‡°‘¥¿“«–‰µ«“¬‡©’¬∫æ≈—π‰¥â ∂â“µâÕß°“√„™â‡«≈“ºà“µ—¥π“π°«à“π’È §«√ „™â§«“¡‡¬ÁπÀ√◊ÕπÈ”·¢Áß·™à„π™àÕß∑âÕß ≈¥‡¡µ“‚∫≈‘ ¡å¢Õß‰µ ‚¥¬„Àâ¬“¢—∫ªí “«– mannitol À¬¥„Àâ∑“ßÀ≈Õ¥‡≈◊Õ¥¥”(35,36)

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥ ‚¥¬∑—«Ë ‰ª·≈â«‡√“®– cross clamping iliac arteries °àÕπ cross clamping aorta ‡ªìπ°“√ªÑÕß°—π‰¡à „Àâ emboli À√◊Õ debris À≈ÿ¥≈ß‰ªÕÿ¥À≈Õ¥‡≈◊Õ¥·¥ß∫√‘‡«≥ª≈“¬‡∑â“ ¥Ÿ¥‡Õ“‡≈◊Õ¥ ÕÕ°¡“‡æ◊ËÕ pre-clotting Dacron graft °àÕπ©’¥‡Œª“√’π„Àâ ∑“ßÀ≈Õ¥‡≈◊Õ¥¥”°—π°“√‡°‘¥≈‘Ë¡‡≈◊Õ¥À≈—ß cross clamping ‡ªî¥·∫– AAA ÕÕ° ‡¬Á∫ªî¥√Ÿ lumbar arteries ·≈– inferior mesenteric arteries ·µà∂“â ‡ªìπ meandering artery ®–µâÕß µàÕ°≈—∫‡¢â“°—∫À≈Õ¥‡≈◊Õ¥‡∑’¬¡ Dacron ∂â“‡ªìπ saccular aneurysm ®–„™âÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡™π‘¥µ√ß ‰¥â ·µà∂“â aneurysm ≈ß¡“∂÷ß iliac arteries §«√®–„™â™π‘¥ Y graft ‡¬Á∫ Dacron graft ∑’Ë pre-clotted ·≈â«‡¢â“°—∫ aorta ·≈– iliac arteries À≈—ß®“°π—πÈ ª≈àÕ¬ clamps ∑’Ë iliac arteries ·≈– aorta √–¬–π’ÈµâÕß„Àâ “√πÈ”‡¢â“∑“ßÀ≈Õ¥‡≈◊Õ¥¥”ª√‘¡“≥¡“° ·≈–‡≈◊ Õ ¥Õ¬à “ ß‡æ’ ¬ ßæÕ ‡æ√“–®–‡°‘ ¥ ¿“«–°√¥‡°‘ π ·≈– declamping hypotension µ√«®¥Ÿ √ Õ¬√—Ë « ∫√‘ ‡ «≥√Õ¬µà Õ À≈—ß®“°π—πÈ ‡¬Á∫ aneurysmal sac ¡“§≈ÿ¡ªî¥À≈Õ¥‡≈◊Õ¥‡∑’¬¡ Õ’°∑’Àπ÷ßË (√Ÿª∑’Ë 12.7)

À≈—°°“√‡≈◊Õ°À≈Õ¥‡≈◊Õ¥‡∑’¬¡ ∑’Ë„™â„π°“√ºà“µ—¥ AAA „πªí®®ÿ∫π— Dacron graft ´÷ßË º≈‘µ®“°«— ¥ÿ∑‡’Ë ªìπ„¬ —ß‡§√“–Àå π”¡“∂—°∑Õ‡ªìπ∑àÕ ¬—ßπ‘¬¡„™âÕ¬Ÿà „π°“√ºà“µ—¥ elective ·µà®–µâÕß pre-clotting ¥â«¬‡≈◊Õ¥¢ÕßºŸâªÉ«¬°àÕπ‡¬Á∫µàÕ ªÑÕß°—π‰¡à „ Àâ ‡≈◊Õ¥‰À≈ÕÕ°®“°À≈Õ¥‡≈◊Õ¥‡∑’¬¡ ‡ªìπÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡∑’√Ë “§“ ‰¡à·æß¡“° ·≈–¬—ß„™â ‰¥â¥ ’ ”À√—∫°“√ºà“µ—¥ AAA Õ—µ√“‡ ’¬Ë ßµàÕ °“√µ‘¥‡™◊ÈÕ¡’‡æ’¬ß√âÕ¬≈– 1-2 ∂â“„Àâ¬“ªØ‘™’«π–∑“ßÀ≈Õ¥‡≈◊Õ¥ ¥”°àÕπºà“µ—¥ ·≈–ªŸº‘«Àπ—ß∫√‘‡«≥∑’Ë®–ºà“µ—¥¥â«¬ Steri-drape ªÑÕß°—π contamination „πºŸâªÉ«¬©ÿ°‡©‘π‡™àπ ruptured AAA ·≈–¡’™ÁÕ§√à«¡¥â«¬ °≈‰°°“√·¢Áßµ—«¢Õß‡≈◊Õ¥®–º‘¥ª°µ‘ °“√∑” pre-clotting Dacron graft ®–‰¡à ‰¥âº≈ ‡≈◊Õ¥®–√—Ë«´÷¡ÕÕ°®“°À≈Õ¥‡≈◊Õ¥‡∑’¬¡À≈—ß ‡¬Á∫µàÕ §«√®–„™â Woven Dacron graft ´÷ßË ∑Õ∂—°´âÕπ°—πÀ≈“¬™—πÈ ¡’√√Ÿ «—Ë πâÕ¬ ·µà¢Õâ ‡ ’¬§◊Õ‡¬Á∫¬“° À√◊Õ impregnated Dacron graft ∑’Ë ‡ §≈◊ Õ ∫‚ª√µ’ π À√◊ Õ pre-clotting ¡“‡√’ ¬ ∫√â Õ ¬·≈–∑”„Àâ ª√“»®“°‡™◊ÕÈ “¡“√∂‡¬Á∫µàÕ‰¥â‡≈¬ ‚¥¬‡≈◊Õ¥®–‰¡à´¡÷ √—«Ë (37) ≈¥ °“√‡ ’¬‡«≈“„π°“√ºà“µ—¥®“°°“√ pre-clotting ≈ß„πºŸâªÉ«¬∑’Ë

121

ABDOMINAL AORTIC ANEURYSMS (AAA)

√Ÿª∑’Ë 12.7 «‘∏’ºà“µ—¥ aneurysmorrhaphy ¡“µ√∞“π√à«¡°—∫ Graft Interposition

°. À≈—ß®“°„Àâ‡Œª“√’π‡¢â“∑“ßÀ≈Õ¥‡≈◊Õ¥¥”·≈â« „™â§’¡§’∫À≈Õ¥‡≈◊Õ¥Àπ’∫À≈Õ¥‡≈◊Õ¥·¥ß iliac µ“¡¥â«¬ aorta ·≈– inferior mesenteric artery (IMA) ¢. ‡ªî¥ aneurysm §«—°‡Õ“ thrombus ÕÕ° ‡¬Á∫ back bleeding ®“° lumbar artery ‡°Á∫ IMA ‰«â ”À√—∫ reimplantation §. „™â Dacron graft ∑’Ë‡µ√’¬¡‰«â‡¬Á∫µàÕ‡¢â“°—∫ aorta à«π∑’Ëª°µ‘ µ√«® Õ∫¥Ÿ√Õ¬√—Ë«∫√‘‡«≥‡¬Á∫‚¥¬ª≈àÕ¬ cross clamp aorta ∂â“‰¡à√—Ë«„Àâ‡¬Á∫ distal anastomosis µàÕ‡Õ“∂ÿß aneurysm ‡¥‘¡‡¬Á∫§≈ÿ¡ À≈Õ¥‡≈◊Õ¥‡∑’¬¡À≈—ß reimplant IMA

‡ ’Ë¬ßµàÕ°“√µ‘¥‡™◊ÈÕ “¡“√∂‡§≈◊Õ∫¬“ªØ‘™’«π–≈ß∫πÀ≈Õ¥ ‡≈◊Õ¥‡∑’¬¡‰¥â √“§“¢ÕßÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡∑—ßÈ Woven ·≈– impregnated Dacron graft ®– Ÿß°«à“ Dacron graft ∏√√¡¥“ ª√–¡“≥ 2 ‡∑à“ °“√„™â Polytetrafluoroethylene (PTFE) graft „π°“√‡¬Á∫ aorta ¡’∑’Ë „™â „π∫“ß ∂“∫—π À√◊Õ„π√“¬∑’‡Ë ’¬Ë ßµàÕ°“√µ‘¥‡™◊ÕÈ ®– ∑”„Àâ ‚Õ°“ µ‘¥‡™◊ÕÈ πâÕ¬°«à“ ·µà PTFE graft √“§“ Ÿß°«à“ Dacron graft ª°µ‘ª√–¡“≥ 3 ‡∑à“

§«“¡º‘¥ª°µ‘¢ÕßÕ«—¬«–¿“¬„π™àÕß∑âÕß∑’Ë æ∫‰¥â√à«¡°—∫ AAA §«“¡º‘¥ª°µ‘¢ÕßÕ«—¬«–¿“¬„π™àÕß∑âÕß “¡“√∂µ√«®æ∫‰¥â ®“°°“√ºà“µ—¥‡ªî¥™àÕß∑âÕß‚¥¬µ√ß ´÷ßË ‡ªìπ¢âÕ¥’‡Àπ◊Õ°“√ºà“µ—¥ retroperitoneal approach

1. æ∫ malignant tumor √à«¡‰¥â „π elective repair ª√–¡“≥√âÕ¬≈– 4-5 à«π„À≠à®–‡ªìπ¡–‡√Áß≈”‰ â „À≠à §«√®–ºà“µ—¥ AAA °àÕπ πÕ°®“°¡’¿“«–·∑√°´âÕπ ‡™àπ ≈”‰ â · µ°∑–≈ÿ , µ°‡≈◊ Õ ¥À√◊ Õ Õÿ ¥ µ— π ´÷Ë ß ®–‡ªì π ¿“«– ©ÿ°‡©‘π§«√·°â ‰¢°àÕπ ·≈â«§àÕ¬ºà“µ—¥ AAA ¿“¬À≈—ß 2. æ∫ asymptomatic gall stone ‰¥â√âÕ¬≈– 5-20 ‰¡à §«√ºà“µ—¥√à«¡°—∫ repair AAA ‡æ√“–Õ“®®–‡°‘¥ contamination ¢Õß graft ‰¥â(38) 3. ∂â“æ∫ renovascular hypertension ∑’¡Ë ’ “‡Àµÿ¡“®“° renal artery stenosis “¡“√∂ºà“µ—¥·°â ‰¢‰¥â√à«¡°—∫ repair AAA

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°“√¥Ÿ·≈ºŸâªÉ«¬À≈—ßºà“µ—¥ Õ—µ√“µ“¬¢Õß elective aneurysmal repair ª√–¡“≥√âÕ¬ ≈– 1-5 „π ∂“∫—π¡“µ√∞“π(39,40) “‡Àµÿ°“√µ“¬ à«π„À≠à®–‡°‘¥ ®“° myocardial dysfunction nonfatal MI æ∫‰¥â√Õâ ¬≈– 316(41)¢≥–ºà“µ—¥∂â“¡’‡≈◊Õ¥‰À≈ÕÕ°¡“¡“°∫√‘‡«≥∑’ºË “à µ—¥‡¢â“∂÷ß·≈– ¡’ ¥’ ”§≈È” „Àâπ°÷ ∂÷ß venous injury ‚¥¬‡©æ“–∑’‡Ë °‘¥µàÕ IVC, left renal vein ·≈– iliac vein À≈—ßºà“µ—¥¡’‡≈◊Õ¥‰À≈ÕÕ°¡“°®π ´÷¡∑’Ëª“°·º≈·≈–ºŸâªÉ«¬™ÁÕ§ „Àâπ÷°∂÷ß√Õ¬√—Ë«∫√‘‡«≥∑’ËµàÕ §«√ ºà“µ—¥≈ß‰ª‡¬Á∫´àÕ¡√Ÿ√—Ë« ‰µ«“¬‡©’¬∫æ≈—π∑’Ë‡°‘¥¢÷ÈπÀ≈—ßºà“µ—¥ Õ“®®–¡’ “‡Àµÿ¡“®“° reflex renal vasoconstriction, ¿“«–™ÁÕ§, intrarenal redistribution of blood flow, atheromatous debris ∑’ÀË ≈ÿ¥‰ªÕÿ¥ renal artery, ∫“¥‡®Á∫µàÕ‰µ À√◊Õ temporary suprarenal aortic cross clamping °àÕπ aortic cross clamping §«√„Àâ mannitol ∑“ßÀ≈Õ¥‡≈◊Õ¥¥”°àÕπ‡ªìπ°“√≈¥‡¡µ“‚∫≈‘ ¡å¢Õß‰µ ªÑÕß°—π renal complication ¿“«–·∑√°´âÕπ∑’‡Ë °‘¥¢÷πÈ °—∫√–∫∫∑“ß‡¥‘πÕ“À“√æ∫‰¥â ‰¡à∫Õà ¬ ∑’æË ∫‰¥â¡’ ileus ·≈– colonic infarction(42) adynamic ileus ®– ‡°‘¥¢÷Èπ¿“¬„π 5 «—π·√°À≈—ßºà“µ—¥ hematoma À√◊Õ°“√∫«¡ ∫√‘‡«≥√Õ¬µàÕ¢ÕßÀ≈Õ¥‡≈◊Õ¥Õ“®®–°¥∑”„Àâ‡°‘¥ duodenal obstruction ‰¥â pancreatitis æ∫πâÕ¬Õ“®®–æ∫«à“¡’ hyperamylasemia ®“°µ—∫ÕàÕπ∂Ÿ°°√–∑∫°√–‡∑◊Õπ ¢≥–‡≈“–µ—¥À√◊Õ „™â‡§√◊ÕË ß¡◊Õ¥÷ß¢¬“¬∂à“ßÀπâ“∑âÕß ischemic colitis æ∫‰¥â√Õâ ¬ ≈– 2 ∂◊Õ‡ªìπ¿“«–·∑√°´âÕπ∑’√Ë πÿ ·√ß∑’ Ë ¥ÿ (43) Õ“°“√·√° Ê ¢Õß bowel ischemia §◊Õ bloody diarahea §«√ àÕß colonoscope ¥Ÿ colonic mucosa ∂â“≈”‰ â‡πà“∑–≈ÿ ®–¡’ peritonitis µâÕß ºà“µ—¥‡Õ“≈”‰ â «à π∑’‡Ë πà“ÕÕ° ∑” proximal diverting colostomy ‡¡◊ËÕ ß —¬«à“®–¡’ ischemic colitis ‡°‘¥¢÷Èπ §«√ investigate ·≈–«‘π®‘ ©—¬‚√§„Àâ ‰¥â·µà‡π‘πË Ê ·≈–∑”°“√√—°…“∑—π∑’ ∂â“‡ªìπ‰¡à ¡“°„Àâ‡ΩÑ“¥Ÿ·≈√—°…“·∫∫ª√–§—∫ª√–§Õß ·µà∂â“Õ“°“√√ÿπ·√ß ®π≈”‰ â‡πà“·≈–·µ°∑–≈ÿ Õ—µ√“°“√µ“¬®– Ÿß∂÷ß√âÕ¬≈– 90 lower extremity ischemia ‡ªìπ¿“«–·∑√°´âÕπ∑’Ëæ∫‰¥â ‰¡à∫Õà ¬ ®“°‡∑§π‘§°“√ºà“µ—¥ “‡Àµÿ‡°‘¥®“° distal embolization ¢≥–‡¬Á∫µàÕÀ≈Õ¥‡≈◊Õ¥ À√◊Õ thrombosis ∑’¡Ë º’ ≈ ◊∫‡π◊ÕË ß ¡“®“° blood stasis, intimal flap À√◊Õ crushed atherosclerotic plaque °“√„Àâ heparin ∑“ßÀ≈Õ¥‡≈◊Õ¥¥”°àÕπ cross clamping aorta ®–ªÑÕß°—π°“√‡°‘¥ thrombosis ®“°¿“«– hemostasis À≈—ß‡¬Á∫µàÕÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡·≈â« ß —¬«à“‡≈◊Õ¥ ‰ª‡≈’¬È ß¢“‰¡àæÕ ®“° thromboembolism §«√∑” thromboem-

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥ bolectomy ∂â“ micro emboli ¢π“¥‡≈Á°∑’ÀË ≈ÿ¥®“°ºπ—ßÀ≈Õ¥ ‡≈◊Õ¥ ®–æ∫‡ªìπ potches ¢Õß ischemia ∑’Ëº‘«Àπ—ß ·≈– ª≈“¬π‘«È ‡∑â“¡’≈°— …≥–‡ªìπ çtrash footé ¿“«–·∑√°´âÕπ∑’æË ∫‰¥â ‰¡à∫Õà ¬‡™àπ paraplegia ®“° spinal cord ischemia æ∫À≈—ß°“√‡¬Á∫´àÕ¡ thoraco abdominal aneurysm ¡’°“√°√–∑∫°√–‡∑◊ÕπµàÕ Radicularis artery (À√◊Õ Adam kevicûs artery) °“√√—Ë«´÷¡¢ÕßπÈ”‡À≈◊Õß®“°°“√ ºà“µ—¥∑àÕπÈ”‡À≈◊Õß„π™àÕß∑âÕß¢≥–‡≈“– neck ¢Õß aneurysm ‚¥¬‡©æ“– cysterna chyli ∑’∑Ë Õ¥µ—«Õ¬Ÿ∫à π°√–¥Ÿ° —πÀ≈—ß L2 °“√µ‘¥‡™◊ÈÕ¢ÕßÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡Õ“®®–‡°‘¥À≈—ßºà“µ—¥π“π ‡ªìπ‡¥◊ÕπÀ√◊ÕÀ≈“¬ªï ®–‡°‘¥¿“«–·∑√°´âÕπ‡À≈à“π’Èµ“¡¡“§◊Õ recurrent bacteremia, false aneurysms, intraabdominal infected collection ·≈– graft-enteric fistula(44)

RUPTURED ABDOMINAL AORTIC ANEURYSM (rAAA) rAAA ∂â“‰¡à∑”°“√√—°…“ Õ—µ√“µ“¬®– Ÿß∂÷ß 100% ∂÷ß·¡â«“à ®–ºà“µ—¥√—°…“‰¥â∑π— Õ—µ√“µ“¬°Á¬ß— §ß ŸßÕ¬Ÿªà √–¡“≥√âÕ¬≈– 5080(45,46,47) à«π„À≠à·≈â«®–µ“¬®“°¿“«–·∑√°´âÕπ∑’Ë‡°‘¥¢÷Èπ ¿“¬À≈—ß°“√ºà“µ—¥ ‡™àπ ‰µ«“¬, respiratory failure ·≈– multiple organ failure (MOF) ¥—ßπ—πÈ ®÷ß§«√«‘π®‘ ©—¬‚√§„Àâ ‰¥â·µà‡π‘πË Ê ‡æ◊ÕË ¥”‡π‘π°“√√—°…“‰¥âÕ¬à“ß∑—π∑’ (48)

°“√«‘π‘®©—¬‚√§ 1. ª√–«—µ·‘ ≈–°“√µ√«®√à“ß°“¬ ª√–«—µ ‘ ”§—≠§◊Õª«¥∑âÕß ¡’°âÕπ‡µâπ‰¥â∑’ËÀπâ“∑âÕß¢π“¥‚µ‡√Á« triad ∑’Ë ”§—≠ ”À√—∫ Õ“°“√·≈–Õ“°“√· ¥ß§◊Õ ª«¥∑âÕß, ¡’°Õâ π‡µâπ‰¥â∑À’Ë πâ“∑âÕß ·≈– syncope ∂â“¡’§√∫∂◊Õ«à“‡ªìπ pathognomonic signs §«√√’∫ àßºŸâªÉ«¬‰ª¬—ß∑’Ë “¡“√∂ºà“µ—¥√—°…“‰¥â∑—π∑’ ‰¡à§«√‡ ’¬‡«≈“„π °“√µ√«®«‘π‘®©—¬ ®π°√–∑—ËßºŸâªÉ«¬™ÁÕ§ °“√§≈”™’æ®√∑’Ë¢“ Õ¬à“ß‡¥’¬«®–‰¡à “¡“√∂™à«¬ª√–‡¡‘πæ¬“°√≥å ‚√§‰¥â ‡æ√“–∫“ß √“¬ rAAA ®–·µ°·≈–¡’‡≈◊Õ¥√—Ë«‡¢â“‰ª„π retroperitoneum §«“¡¥—π‚≈À‘µ‰¡à≈¥ ·≈–¬—ß “¡“√∂§≈”™’æ®√‰¥â (49) 2. °“√µ√«®«‘π®‘ ©—¬‡æ‘¡Ë ‡µ‘¡ ·∑∫®–‰¡à®”‡ªìπ‡≈¬ ºŸªâ «É ¬ ∫“ß√“¬Õ“®®–æ∫ leukocytosis √–¥—∫Œ’‚¡‚°≈∫‘π·≈–Œ’¡“‚µ§√‘µ ª°µ‘ °“√µ√«®§≈◊Ëπ‰øøÑ“À—«„®Õ“®®–∫àß∫Õ°§«“¡º‘¥ª°µ‘¢Õß À—«„®‰¥â∫“â ß °“√µ√«®«‘π®‘ ©—¬‡æ‘¡Ë ‡µ‘¡∂â“®”‡ªìπ§«√∑”„πºŸªâ «É ¬∑’Ë vital signs §ß∑’Ë

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ABDOMINAL AORTIC ANEURYSMS (AAA)

2.1 Plain abdomen film ®–æ∫ widened and calcified aorta ·≈–‰¡à‡ÀÁπ psoas shadow 2.2 ultrasound ·ª≈º≈‰¡à ‰¥â·πàπÕπ„π¿“«–©ÿ°‡©‘π Õ“® ®–¡’‡ß“¢Õß≈¡„π≈”‰ â∫ß— ∑”„Àâ‡ÀÁπ‰¥â ‰¡à™¥— 2.3 CT scan ‡ªìπ«‘∏°’ “√µ√«®«‘π®‘ ©—¬∑’·Ë πàπÕπ∑’ Ë ¥ÿ 2.4 aortography ‰¡à§«√∑”‡æ√“–„™â‡«≈“¡“° ‡°‘¥ contamination ¡Õß‰¡à‡ÀÁπ√Õ¬∑–≈ÿ

°“√√—°…“ °“√‡µ√’¬¡ºŸªâ «É ¬°àÕπºà“µ—¥ ‰¡à®”‡ªìπ∑’®Ë –µâÕß„ÀâºªŸâ «É ¬Õ¬Ÿà „π ¿“«– hemodynamic stable °àÕπºà“µ—¥ ‡æ√“–®–‡ ’¬‡«≈“¡“° „π¢≥–∑’Ë∑”°“√‡§≈◊ËÕπ¬â“¬ºŸâªÉ«¬§«√·∑ß‡ âπ¥â«¬‡¢Á¡‡∫Õ√å ‚µ „Àâ “√πÈ”∑“ßÀ≈Õ¥‡≈◊Õ¥¥” ‡®“–‡≈◊Õ¥µ√«® blood chemistry ¥Ÿ√–¥—∫Œ’‚¡‚°≈∫‘π·≈–Œ’¡“‚µ§√‘µ ·≈– Group matching √’∫ π”ºŸâªÉ«¬‡¢â“ÀâÕßºà“µ—¥ ‰¡à®”‡ªìπµâÕß «π “¬ CVP ∂à“¬¿“æ √—ß ’∑√«ßÕ°À√◊Õ‡ ’¬‡«≈“„π°“√µ√«®«‘π®‘ ©—¬∑’Ë‰¡à®”‡ªìπ(50,51,52) ∂â“ ·πà „®„π°“√«‘π‘®©—¬·≈â« ∂÷ß·¡â«à“„Àâ “√πÈ”‡¢â“∑“ßÀ≈Õ¥‡≈◊Õ¥ ¥”·≈â« §«“¡¥—π‚≈À‘µ‡æ‘Ë¡¢÷Èπ°Á¬—ßµâÕßπ”ºŸâªÉ«¬‡¢â“ÀâÕßºà“µ—¥ ‰¡à § «√∑” ER thoracotomy ‡æ◊Ë Õ cross clamp aorta ‡æ√“–º≈‡ ’¬®–¡’¡“°°«à“„π·ßà§«“¡æ√âÕ¡ ‡§√◊ËÕß¡◊Õ·≈–°“√ µ‘¥‡™◊ÕÈ ∂÷ß·¡â«“à ®–∑”‚¥¬»—≈¬·æ∑¬åº¡Ÿâ §’ «“¡™”π“≠ ‡µ√’¬¡ÀâÕßºà“µ—¥ ‡§√◊ËÕß¡◊Õºà“µ—¥‡ªî¥∑√«ßÕ°·≈–™àÕß∑âÕß „Àâæ√âÕ¡ ‡µ√’¬¡ cell saver ‡æ◊ÕË „™â ”À√—∫ autologous blood transfusion „™â‡≈◊Õ¥∑—ßÈ RBC, FFP, cryoprecipitate ·≈– platelets æ¬“¬“¡„ÀâÕÿ≥À¿Ÿ¡‘„πÀâÕßºà“µ—¥·≈–µ—«ºŸâªÉ«¬ Ÿß¢÷Èπ ‡æ◊ËÕ ªÑÕß°—π°“√ Ÿ≠‡ ’¬§«“¡√âÕπ¢Õß√à“ß°“¬ (heat loss ‡ªìπ “‡Àµÿ ”§—≠¢Õß coagulopathy) ¢≥–∑”°“√ºà“µ—¥ ¢≥–Õ¬Ÿà„πÀâÕßºà“µ—¥ §«√ «π “¬ªí “«– «π Õ¥ hemodynamic monitoring equipment ‡µ√’¬¡º‘«Àπ—ß ∑”§«“¡ –Õ“¥µ—ßÈ ·µàÀπâ“Õ° ™àÕß∑âÕß ≈ß‰ª∂÷ß¢“Àπ’∫∑—ßÈ Õß¢â“ß ‡√‘¡Ë ¥¡¬“ ≈∫æ√âÕ¡°—∫≈ß¡’¥ ¢≥–¥¡¬“ ≈∫§«“¡¥—π‚≈À‘µ®–≈¥ ≈ßÕ¬à“ß√«¥‡√Á« ‡π◊ËÕß®“°‡ ’¬ sympathetic tone §«√√’∫ ºà“µ—¥„Àâ‡¢â“∂÷ß ·≈– cross clamping aorta Õ¬à“ß√’∫¥à«π ¢≥–ºà“µ—¥ ºà“µ—¥‡ªî¥™àÕß∑âÕß‡ªìπ·π«¬“«∑“ß midline ‡æ◊ÕË proximal ·≈– distal control aorta °“√‡≈“– iliac arteries ‡æ◊ÕË distal clamp control ®–µâÕß√–«—ß‰¡à „Àâ¡°’ “√∑–≈ÿ¢Õß iliac veins ¢â“ß„µâ‡æ√“–®–Àâ“¡‡≈◊Õ¥≈”∫“° ‡ ’¬‡≈◊Õ¥¡“°·≈–„™â ‡«≈“ºà“µ—¥π“π¢÷Èπ §«√‡≈◊Õ°„™âÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡™π‘¥ Woven

Dacron graft À√◊Õ coated graft ‡æ√“–‰¡à¡’‡≈◊Õ¥√—Ë«´÷¡®“° À≈Õ¥‡≈◊Õ¥‡∑’¬¡ ·≈–‰¡à‡ ’¬‡«≈“„π°“√∑” pre clotting °“√¥Ÿ·≈ºŸªâ «É ¬À≈—ßºà“µ—¥ ¿“«–·∑√°´âÕπ∑’‡Ë °‘¥¢÷πÈ À≈—ßºà“µ—¥ ‡ªìπº≈ ◊∫‡π◊ËÕß¡“®“°°“√‡µ√’¬¡ºŸâªÉ«¬°àÕπºà“µ—¥ ·≈–¢≥– ∑”°“√ºà“µ—¥(53) ®–¡’ª≠ í À“¿“«–·∑√°´âÕπ‡°‘¥¢÷πÈ ¡“° ∂â“‡°‘¥¿“«– prolonged hypotension °“√¥Ÿ·≈ºŸâªÉ«¬À≈—ßºà“µ—¥®–µâÕß √–«—ß¿“«– ¿“«– coagulopathy, hypothermia ¥Ÿ circulatory volume ∑’‡Ë À¡“– ¡ √–«—ß‰¡à „Àâ‡°‘¥¿“«–πÈ”‡°‘π ∂â“¡’ coronary heart disease §«√ monitor ¥â«¬°“√ «π§“ “¬ Swan-Ganz catheter ‰µ«“¬‡©’¬∫æ≈—π‡ªìπ¿“«–·∑√°´âÕπ∑’Ë‡°‘¥¢÷Èπ‰¥â∫àÕ¬∑’Ë ÿ¥ §«√√’∫∑” dialysis ∑—π∑’ °“√¡’πÈ”‡°‘π„π√à“ß°“¬®–∑”„ÀâπÈ”∑’Ë ‡°‘π‰ª§—ßË „πªÕ¥ ‡°‘¥¿“«– ARDS ·≈– CHF ¿“«–·∑√°´âÕπ Õ◊πË Ê ∑’‡Ë °‘¥¢÷πÈ √à«¡ ‡™àπ lower extremity ischemia, ischemic colitis ·≈–‡≈◊Õ¥ÕÕ°¡“°®“°¿“«–°≈‰°°“√·¢Áßµ—«¢Õß‡≈◊Õ¥ º‘¥ª°µ‘ À≈—°„π°“√√—°…“ rAAA §◊Õ early recognition °“√ √Õ¥™’«µ‘ ¢ÕßºŸªâ «É ¬¢÷πÈ Õ¬Ÿ°à ∫— µ—«·ª√À≈“¬ª√–°“√ ‡™àπ °“√¥Ÿ·≈ ºŸªâ «É ¬∑’¥Ë °’ Õà π·≈–À≈—ß°“√ºà“µ—¥ ∂â“™ÁÕ§∑’‡Ë °‘¥¢÷πÈ ‰¡à√πÿ ·√ß·≈–π“π °“√æ¬“°√≥å ‚√§¡—°®–¥’ §π™√“∑’ÕË “¬ÿ¡“°°«à“ 80 ªï ·≈–™ÁÕ§ Õ¬Ÿπà “π ‰µ¡—°®–«“¬·≈–‰¡àøπóô Õ—µ√“µ“¬®– Ÿß¡“°(46-49,53)

√ÿª „πªí®®ÿ∫π— Õÿ∫µ— °‘ “√¢Õß abdominal aortic aneurysms æ∫‰¥â∫àÕ¬¢÷Èπ ‡π◊ËÕß®“°ª√–™“°√∑—Ë«‰ª¡’Õ“¬ÿ¬◊π ªí®®—¬‡ ’Ë¬ßµàÕ °“√‡°‘¥‚√§ √«¡∑—Èß‚¿™π“°“√‡ª≈’Ë¬π·ª≈ß‰ª§≈â“¬°—∫ª√–‡∑» ∑“ßµ–«—πµ° °“√µ√«®«‘π®‘ ©—¬æ‘‡»…µà“ß Ê ‡™àπ ultrasonography, CT scan ·≈– spiral CT scan ∑”„Àâ«π‘ ®‘ ©—¬‚√§‰¥â·¡àπ¬”¢÷πÈ ·π«∑“ß°“√√—°…“ µ≈Õ¥®π°“√¥Ÿ·≈ºŸªâ «É ¬°àÕπ ¢≥–ºà“µ—¥·≈– À≈—ßºà“µ—¥¥’¢π÷È ∑”„ÀâÕµ— √“µ“¬≈¥πâÕ¬≈ß °“√ºà“µ—¥„πºŸªâ «É ¬ ruptured abdominal aortic aneurysm Õ—µ√“µ“¬·≈–¿“«– ·∑√°´âÕπ¬—ß§ß Ÿß §«√ºà“µ—¥ aneurysmorrhaphy „π√“¬∑’¡Ë ’ ¢âÕ∫àß™’·È πàπÕπ ·≈–ºà“·∫∫ elective case °“√ºà“µ—¥‡¢â“∑“ß retro peritoneal ∑”„ÀâºŸâªÉ«¬øóôπµ—«‰«°«à“ºà“µ—¥‡ªî¥‡¢â“∑“ß™àÕß∑âÕß „πªí®®ÿ∫—π‡√‘Ë¡¡’«‘∏’°“√√—°…“‚¥¬‰¡àµâÕßºà“µ—¥§◊Õ Endovascular Stent Grafting ·µàº≈°“√√—°…“§ß®–µâÕßµ‘¥µ“¡¥Ÿ¢âÕ¥’·≈– ¢âÕ‡ ’¬µàÕ‰ª

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‡Õ° “√Õâ“ßÕ‘ß 1. Allardice JT, Allright GT, Watula JMC, et al. High prevalence of abdominal aortic aneurysm in men with peripheral vascular disease. Screeing by ultrasonography. Br J Surg 1988;75:240-242. 2. Schellack J, Smith RB, Perdue GD. Nonoperative management of selected popliteal aneurysms. Arch Surg 1987;122:372-375. 3. Dent TL, Lindenauer SR, Ernst CB, Fry WJ. Multiple arteriosclerotic arterial aneurysms. Arch Surg 1972;105:338-344. 4. Dobrin PB. Pathophysiology and pathogenesis of aortic aneurysms: Current concepts. Surg Clin North Am 1989;69:687-704. 5. Zarins CK, Glagov S, Vesselinovitch D, et al. Aneurysm formation in experimental atherosclerosis: Relationship to plaque formation. J Vasc Surg 1990;12:246-256. 6. Hollier LH, Stanson AW, Gloviczki P, et al. Arteriomegaly: Classification and morbid implications of diffuse aneurysm disease. Surgery 1983;93:700-708. 7. Brophy CM, Tilson JE, Braveman JM, et al. Age of onset, pattern of distribution, and histology of aneurysm development in a genetically predisposed mouse model. J Vasc Surg 1988;8:45-48. 8. Dobrin PB, Baker W, Gley W. Elastolytic and collagenolytic studies of arteries. Arch Surg 1984;119:405-409. 9. Cohen JR, et al. The calcium messenger system and the kinetics of elastase release from human neutrophils in patients with abdominal aortic aneurysms. Ann Vasc Surg 1990;4:570-574. 10. Cohen JR, Mandell C, Margolis I, et al. Altered aortic protease and antiprotease activity in patients with ruptured abdominal aortic aneurysms. Surg Gynecol Obstet 1987;164:355-358. 11. Cohen JR, Safarty I, Wise L. The effec of cigarette smoking on rabbit aortic elastase activity. Presented at the International Society for Cardiovascular Surgery/Society for Vascular Surgery Scientific Meeting, Chicago, June 14, 1988. 12. Baxter BT, McGee GS, Flinn WR, et al. Distal embolization as a presenting symptoms of aortic aneurysms. Am J Surg 1990;160:197201. 13. Crawford ES. Ruptured abdominal aortic aneurysm: An editorial. J Vasc Surg 1991;13:348-350. 14. Salo JA, Verkkala KA, Ala-Kulju KV, et al. Hematuria is an indication of rupture of an abdominal aortic aneurysm into the vena cava. J Vasc Surg 1990; 12:41-44. 15. Quill DS, Colgan MP, Sumner DS. Ultrasonic screening for the detection of abdominal aortic aneurysm. Surg Clin North Am 1989;69:713. 16. LaRoy LL, Gormier PJ, Matalon TAS, et al. Imaging of an abdominal aortic aneurysm. AJR 1989;152:785-792. 17. Weinbaum FI, Dubner S, Turner JW, et al. The accuracy of computed tomography in the diagnosis of retroperitoneal blood in the presence of abdominal aortic aneurysm. J Vasc Surg 1987;6:11-16.

18. Pavone P, Di Cesare E, Di Renzi P, et al. Abdominal aortic aneurysm evaluation: Comparison of US, CT, MRI and angiography. Magn Reson Imaging 1990;8:199-206. 19. Nevitt MP, Ballard DJ, Hallet JW. Prognosis of abdominal aortic aneurysms. N Eng J Med 1989;321:1009-1014. 20. Olsen PS, Schroeder T, Agerskov K, et al. Surgery for abdominal aortic aneurysms: A survey of 656 patients. J Cardiovasc Surg 1991;32:636-643. 21. Szilagyi DE, Smith RF, De Russo FJ, et al. Contribution of abdominal aortic aneurysmectomy to prolongation of life. Ann Surg 1966;164:678-699. 22. Szilagyi DE, Elliott JP, Smith RF. Clinical fate of patient with asymptomatic abdominal aortic aneurysm and unfit for surgical treatment. Arch Surg 1972;104:600-610. 23. Sterpetti AV, Cavallaro A, Cavallari N, et al. Factors influencing the rupture of abdominal aortic aneurysm. Surg Gynecol Obstet 1991;173:175-178. 24. Hertzer NM. Fatal myocardial infarction following abdominal aortic aneurysm resection. Ann Surg 1980;192:667-673. 25. Yeager RA, Weigel RM, Murphy ES, et al. Application of clinically valid cardiac risk factors to aortic aneurysm surgery. Arch Surg 1986;121:278-281. 26. Golden MA, Whitlemore AD, Donaldson MC, et al. Evaluation and management of coronary artery disease in patients undergoing repair of abdominal aortic aneurysms. Ann Surg 1990;212:415-422. 27. Cambria RP, Brewster DC, Abbott WM, et al. The impact of selective use of dipyridamole-thallium scans and surgical factors on the current morbidity of aortic surgery. J Vasc Surg 1992;15:43-51. 28. Hertzer NR, Young JR, Kramer JR, et al. Routine coronary angiography prior to elective aortic reconstruction. Arch Surg 1979;114:1336-1344. 29. Smith PK, Fuchs J CA, Sabiston DC. Surgical management of abdominal aortic aneurysms in patients with severe pulmonary insufficiency. Surg Gynecol Obstet 1980;151:407-411. 30. Chuter TA, Green RM, Ouriel K, et al. Transfemoral endovascular aortic graft replacement. J Vasc Surg 1993;18:185-191. 31. Lumsden AB, Allen ARC, Chaikof EL, et al. Delayed ruptured of aortic aneurysm following endovascular stent grafting. Am J Surg 1995;170:174-178. 32. Cambria RP, Brewster DC, Abbott WM, et al. Transperitoneal versus retroperitoneal approach for aortic reconstruction: A randomized prospective study. J Vasc Surg 1987;5:19-27. 33. Laohapensang K, Pongcheowboon, A, Rerkasem K. The retroperitoneal approach for abdominal aortic aneurysms. J Med Assoc Thai 1997;80:479-485.

ABDOMINAL AORTIC ANEURYSMS (AAA) 34. Veith FJ, Gupta S, Daly V. Technique for occluding the supraceliac aorta through the abdomen. Surg Gynecol Obstet 1980;151:426428. 35. Veith FJ, Gupta SK, Wengerten KW. Emergency abdominal aortic aneurysm surgery and supraceliac aortic control. In: Greenhalgh RM, Mannick JA, (eds). The cause and management of aneurysms. London:WB Saunders 1990;387-400. 36. Cohen JR, Mannick JA, Couch NP, et al. Abdominal aortic aneurysm repair in patients with preoperative renal failure. J Vasc Surg 1986;3:867-870. 37. Freischlag JA, Moore WS. Clinical experience with a collagen impregnated knitted dacron vascular graft. Ann Vasc Surg 1990;4:449454. 38. String ST. Cholelithiasis and aortic reconstruction. J Vasc Surg 1984;1:664-669. 39. Dichl JT, Cali RF, Hertzer NR, et al. Complications of abdominal aortic reconstruction: An analysis of perioperative risk factors in 557 patients. Ann Surg 1983;197:49-56. 40. Johnston JW. Multicenter prospective study of nonruptured abdominal aortic aneurysm II. Variables predicting morbidity and mortality. J Vasc Surg 1989;9:437-447. 41. Brown OW, Hollier LH, Pairolero PC, et al. Abdominal aortic aneurysm and coronary artery disease: A reassessment. Arch Surg 1981;116:1484-1488. 42. Smith RF, Szilagyi DE. Ischemia of the colon as a complication in the surgery of the abdominal aorta. Arch Surg 1960;80:806-821. 43. Hagihara PF, Ernst CB, Griffen WO. Incidence of ischemic colitis following abdominal aortic reconstruction. Surg Gynecol Obstet 1979;149:571-573.

125 44. Seabrook GR, Schmitt DD, Bandyk DF, et al. Anastomotic femoral pseudoaneurysm: An investigation of occult infection as an etiologic factor. J Vasc Surg 1990;11:629-634. 45. Meyer AA, Ahlquist RE Jr, Trunkey DD. Mortality from ruptured abdominal aortic aneurysm: A comparison of two series. Am J Surg 1986;152:27-33. 46. Wakefield TW, Whitehouse WM Jr, WS.C, et al: Abdominal aortic aneurysm rupture:Statistical analysis of factors affecting outcome of surgical treatment. Surgery 1982;91:586-596. 47. Bodily KC, Butorff JD. Ruptured abdominal aortic aneurysm: The Tacoma experience. Am J Surg 1985;149:580-582. 48. Bauer EP, Redaelli C, van Segesser LK, et al. Ruptured abdominal aortic aneurysms: Predictors for early complication and death. Surgery 1993;114:31-38. 49. Rutherford RB, McCroskey BL. Ruptured abdominal aortic aneurysms: Special considerations. Surg Clin North Am 1989;69:859868. 50. Mannick JA, Whittemore AD. Management of ruptured or asymptomatic abdominal aortic aneurysms. Surg Clin North Amm 1988;68:377-384. 51. Hoffanan M, Avellone JC, Plecha FR, et al. Operation for ruptured abdominal aortic aneurysms: A community-wide experience. Surgery 1982;91:597-602. 52. Lawler M Jr. Aggressive treatment of ruptured abdominal aortic aneurysm in a community hospital. Surgery 1984;95:38-44. 53. Ouriel K, Geary K, Green RM, et al. Factors determining survival after ruptured abdominal aortic aneurysm: The hospital, the surgeon, and the patient. J Vasc Surg 1990;11:493-496.

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∫∑∑’Ë 13 AORTOILIAC OCCLUSIVE DISEASE (AIOD) Aortoiliac atherosclerosis ‡ªìπ°“√µ’∫µ—π¢ÕßÀ≈Õ¥‡≈◊Õ¥ µ—ßÈ ·µà infrarenal aorta ·≈– iliac arteries ´÷ßË ‡ªìπ “‡Àµÿ¢Õß °“√‡°‘¥ arterial insufficiency ¢Õß¢“ ‡π◊ÕË ß®“° atherosclerosis ‡ªìπ generalized process °“√µ’∫µ—π¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß ∑’‡Ë °‘¥¢÷πÈ ∫√‘‡«≥ aortoliac ®÷ß¡—°®–√à«¡°—∫°“√µ’∫µ—π¢ÕßÀ≈Õ¥ ‡≈◊Õ¥∑’µË Ë”°«à“π—πÈ ¥â«¬‡™àπ femoral, popliteal ·≈– tibioperoneal arteries (√Ÿª∑’Ë 13.1) æ∫„π§πÕ“¬ÿ 50-65 ªï „π‡æ»™“¬æ∫‰¥â ∫àÕ¬°«à“‡æ»À≠‘ß 10 ‡∑à“(1) „πªí®®ÿ∫—πæ∫„π‡æ»À≠‘ß∫àÕ¬¢÷Èπ ‡π◊ÕË ß®“°°“√ Ÿ∫∫ÿÀ√’Ë ´÷ßË ‡ªìπµ—«·ª√ ”§—≠Õ—πÀπ÷ßË ¢Õß‚√§π’(2)È Õ“°“√ ”§—≠¢Õß‚√§π’§È Õ◊ claudication ∑”„Àâ‡¥‘π·≈–¥”√ß ™’«µ‘ µ“¡ª°µ‘ª√–®”«—π‰¥â ‰¡à –¥«° ºŸªâ «É ¬®÷ß¡“æ∫·æ∑¬å‡æ◊ÕË „Àâ ‰¥â°“√√—°…“∑’Ë‡À¡“– ¡ „π∫∑π’È®–‰¥â°≈à“«∂÷ß·π«∑“ß„π°“√ «‘π®‘ ©—¬‚√§·≈–°“√√—°…“∑’‡Ë À¡“– ¡ ‡æ√“–¡’ºªŸâ «É ¬¡“°¡“¬∑’¡Ë “ ¥â«¬Õ“°“√ª«¥À≈—ß ª«¥¢“ ·≈–‰¥â√∫— °“√√—°…“∑“ß‚√§¢âÕ·≈– °√–¥Ÿ°¡“°àÕπ °“√«‘π®‘ ©—¬‚√§≈à“™â“∑”„ÀâÕ“°“√¢Õß‚√§‡≈«≈ß °“√´—°ª√–«—µ‘ µ√«®√à“ß°“¬ ·≈–°“√µ√«® «‘π®‘ ©—¬«‘∏µ’ “à ß Ê ®–∑”„Àâ‡√“ “¡“√∂∫Õ°°“√æ¬“°√≥å‚√§ ·≈–«“ß·π«∑“ß„π°“√√—°…“∑’‡Ë À¡“– ¡µàÕºŸªâ «É ¬·µà≈–√“¬µàÕ‰ª ‰¡à«“à ®–‚¥¬°“√„Àâ¬“ °“√∑” angioplasty À√◊Õ°“√ºà“µ—¥

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Type III

√Ÿª∑’Ë 13.1 ≈—°…≥–µà“ß Ê ¢Õß Aortoiliac occlusive disease (AOID)

Type I °“√µ’∫·§∫‡°‘¥∫√‘‡«≥ distal aorta ·≈– common iliac arteries æ∫‰¥â√âÕ¬≈– 13 Type II °“√µ’∫·§∫≈ß¡“∂÷ß femoral arteries æ∫‰¥â√âÕ¬≈– 20 Type III °“√µ’∫·§∫‡°‘¥¢÷ÈπÀ≈“¬√–¥—∫ ·≈–≈ßµË”°«à“ inguinal ligament æ∫‰¥â√âÕ¬≈– 67

dication

Õ“°“√

Mild Clau

æ¬“∏‘«‘∑¬“

udication

Cla Moderate

ion

udicat Severe Cla

Ulcer Rest-Pain ion Claudicat

√Ÿª∑’Ë 13.2 ·ºπ¿Ÿ¡‘· ¥ß∂÷ß°“√µ’∫·§∫·≈–Õÿ¥µ—π„πµ”·Àπàßµà“ß Ê ¢ÕßÀ≈Õ¥‡≈◊Õ¥∑’Ë¢“ Õ“°“√¢Õß claudication ®–¥’¢÷Èπ ∂â“ collaterals ‡æ’¬ßæÕ ·µà∂“â ¡’°“√µ’∫·§∫¢Õß collaterals ‡°‘¥¢÷πÈ ·≈â«Õ“°“√®–√ÿπ·√ß¡“°®π∑”„Àâ‡°‘¥ gangrene À√◊Õ·º≈‡√◊ÈÕ√—ß

129

AORTOILIAC OCCLUSIVE DISEASE (AIOD)

√Ÿª∑’Ë 13.3 °. Ulcerated atheroma ®“° aortic aneurysm ∑”„Àâ‡°‘¥ atheroemboli À≈ÿ¥≈Õ¬¡“µ“¡À≈Õ¥‡≈◊Õ¥·¥ß∑’Ë¢“

¢. atheroemboli À≈ÿ¥¡“Õÿ¥À≈Õ¥‡≈◊Õ¥∫√‘‡«≥ª≈“¬π‘È«‡∑â“·≈–º‘«Àπ—ß ∑”„Àâ‡°‘¥ ’§≈È”‡ªìπ®È” ∫√‘‡«≥ º‘«Àπ—ß‡ªìπ≈—°…≥–¢Õß çblue toe syndromeé

°“√«‘π‘®©—¬‚√§ ‡¡◊ËÕÕ“°“√∑“ß§≈‘π‘§¢ÕßºŸâªÉ«¬∫àß∫Õ°«à“‡ªìπ AIOD §«√ µ√«®√à“ß°“¬ºŸâªÉ«¬‚¥¬≈–‡Õ’¬¥ §«√«—¥ doppler pressure ¢Õß¢“∑’ÀË ≈Õ¥‡≈◊Õ¥·µà≈–µ”·Àπàß(5) À≈—ß®“°π—πÈ ®÷ßæ‘®“√≥“∑” aortogram µà Õ ‰ª‡æ◊Ë Õ °“√«‘ π‘ ® ©— ¬ ‚√§∑’Ë · πà π Õπ ·≈–°“√ «“ß·ºπ√—°…“µàÕ‰ª

°“√µ√«®√à“ß°“¬ „π√–¬–·√°¢Õß‚√§∑’Ë¬—ßÕ“°“√‰¡à√ÿπ·√ß ®–¬—ß§≈”™’æ®√ ∫√‘‡«≥¢“Àπ’∫·≈–À≈—ß‡∑â“‰¥â ·µà „π√–¬–∑’‡Ë ªìπ¡“° ®–øíß‰¥â‡ ’¬ß bruit µ√ßµ”·Àπàß¢Õß aorta ·≈– femoral arteries ‡¡◊ÕË „Àâ ÕÕ°°”≈—ß°“¬‚¥¬°“√‡¥‘πÀ√◊Õ«‘Ëß√Õ∫‡µ’¬ßºŸâªÉ«¬ 30-60 «‘π“∑’ ®–æ∫«à“ abdominal ·≈– femoral bruits øíß‰¥â™¥— ‡®π¢÷πÈ ·µà pedal pulse ®–§≈”‰¥â‡∫“≈ßÀ√◊Õ‰¡à ‰¥â‡≈¬ §«√µ√«®√à“ß°“¬ ∑“ß√–∫∫ª√– “∑·≈–°√–¥Ÿ°·≈–¢âÕ„Àâ≈–‡Õ’¬¥‡æ◊ÕË ·¬°‚√§

non-invasive hemodynamic testing «‘∏°’ “√ª√–‡¡‘π hemodynamic ¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ßµ’∫∑’Ë¢“ ßà“¬ Ê ·≈–¡’ ª√– ‘∑∏‘¿“æ§◊Õ °“√«—¥ ankle-brachial blood pressure index (ABI) „π√“¬∑’‡Ë ªìπ‰¡à¡“° §à“ ABI „π¢≥–∑’æË °— Õ“®®– Ÿß°«à“ 1.0 ´÷ßË ∂◊Õ«à“ª°µ‘ ·µà∂“â „Àâ‡¥‘π∫π treadmill ABI ®–≈¥≈ß‡≈Á°πâÕ¬ „πºŸªâ «É ¬∑’¡Ë ’ IC ·≈–§à“ ABI ¢≥–æ—° 0.5-0.8 ∂â“„Àâ‡¥‘π∫π treadmill √–¥—∫¢Õß ABI ®–≈¥≈ß∑—π∑’ ®πÕ“®®–«—¥‰¡à ‰¥â‡≈¬ treadmill excercise ®–∫àß∫Õ°∂÷ßµ”·Àπàß¢Õß√Õ¬‚√§∑’ÀË ≈Õ¥‡≈◊Õ¥ «à“¡’ claudication ‡°‘¥¢÷πÈ ∑’∫Ë √‘‡«≥„¥ (°âπ, µâπ¢“ À√◊ÕπàÕß) ·≈– walking distance §«√µ√«®§≈◊Ëπ‰øøÑ“À—«„®·≈–ª√–‡¡‘π°“√ ∑”ß“π¢ÕßÀ—«„®(1,5) ºŸªâ «É ¬∑’ÕË ¬Ÿà„π¿“«– threatened limb loss §à“ ABI ®–µË”°«à“ 0.5 ·≈– transcutaneous oxygen tension ¢Õßº‘«Àπ—ß ‡∑â“®–µË”°«à“ 20-30 ∑Õ√√å „πºŸªâ «É ¬ blue-toe syndrome ´÷ßË ‡ªìπ embolic ‰¡à „™à occlusive disease §à“ ABI ®–ª°µ‘ ∂÷ß·¡â«“à ®–‡ÀÁπ¡’°“√Õÿ¥µ—π¢ÕßÀ≈Õ¥‡≈◊Õ¥‡≈Á° Ê µ√ß ª≈“¬‡∑â“(4,6)

130

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥ Arm Blood Pressure 115

130-

Arm Blood Pressure 150

-80

150-

Arm Blood Pressure 135

-120

135-

-135

120-

-75

120-

-115

135-

-60

115-

-70

120-

-115

80-

-60

√Ÿª∑’Ë 13.4 °“√«—¥ segmental leg pressures ‡æ◊ËÕª√–‡¡‘πµ”·Àπàß∑’Ëµ’∫·§∫¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß∑’Ë¢“ ¢âÕ®”°—¥¢Õß doppler pressures §◊Õ‰¡à “¡“√∂∫àß∫Õ° µ”·ÀπàßÀ≈Õ¥‡≈◊Õ¥·¥ß∑’ËÕÿ¥µ—π‰¥â·πàπÕπ ‚¥¬‡©æ“–„π√“¬∑’Ë¡’ °“√Õÿ¥µ—πÀ≈“¬µ”·Àπàß „πªí®®ÿ∫π— ‰¥â¡°’ “√π”‡Õ“ duplex ultrasonography ·≈– magnetic resonance (MR) scanning ¡“µ√«®«‘π®‘ ©—¬ æ∫«à“ “¡“√∂∫àß∫Õ°µ”·ÀπàßÀ≈Õ¥‡≈◊Õ¥·¥ß ∑’ÕË ¥ÿ µ—π‰¥â·πàπÕπ ∂÷ß·¡â«“à ®–¡’°“√Õÿ¥µ—πÀ≈“¬√–¥—∫(7,8) ∂â“ºŸªâ «É ¬¡’Õ“°“√¢Õß impotence §«√«—¥§à“ penile-brachial doppler pressure index (PBI) ∂â“µË”°«à“ 0.7 ∫àß∂÷ß«à“¡’ vasculogenic erectile dysfunction §«√∑” treadmill exercise ´È” ·≈â««—¥Õ’°§√—ßÈ Àπ÷ßË ∂â“ PBI µË”°«à“‡¥‘¡¡“° ∫àß∫Õ°∂÷ß AIOD penile duplex sonography ¡’ª√–‚¬™πå „π°“√·¬° √–À«à“ß venogenic ·≈– arteriogenic impotence §«√«—¥√–¥—∫ ABI ¢ÕßºŸªâ «É ¬¢≥–æ—°·≈–À≈—ß®“° exercise ∂â“§à“≈¥≈ß§àÕπ¢â“ß®–∫àß™’È«à“‡ªìπ AIOD §«√®–µ√«®«‘π‘®©—¬ ‚¥¬°“√∑” aortogram µàÕ‰ª

Arteriography standard À√◊Õ digital intra-arterial arteriography ‡ªìπ «‘∏’°“√µ√«®«‘π‘®©—¬¡“µ√∞“π∑’Ë “¡“√∂¡Õß‡ÀÁπ°“¬«‘¿“§ ·≈– æ¬“∏‘ ¿“æ¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß∑’ËÕÿ¥µ—π ∑”„Àâ “¡“√∂∫Õ°°“√ æ¬“°√≥å ‚√§·≈–«“ß·ºπ„π°“√√—°…“µàÕ‰ª‰¥â (√Ÿª∑’Ë 13.5) ¢≥–∑’Ë∑” arteriogram §«√«—¥§«“¡¥—π‚≈À‘µ¢ÕßÀ≈Õ¥‡≈◊Õ¥ ·µà≈–µ”·Àπàß À√◊Õ “¡“√∂∂à“ß¢¬“¬À≈Õ¥‡≈◊Õ¥∫√‘‡«≥∑’Ëµ’∫ ·§∫‰¥â¥«â ¬(9,10,11) arteriogram ∑’¥Ë ’ §«√‡ÀÁπ abdominal aorta ·≈–·¢πß¢ÕßÀ≈Õ¥‡≈◊Õ¥∑’·Ë ¬°ÕÕ°¡“∑—ßÈ À¡¥§◊Õ renal, mesenteric ·≈– pelvic arteries ∑”‡ªìπ biplane aortography ‚¥¬ Õ¥ “¬ «πºà“π femoral À√◊Õ axillary arteries(9,10,11) oblique pelvic views ®–‡ÀÁπ iliac artery ™—¥‡®π ·≈– lateral views ®–‡ÀÁπ celiac ·≈– mesenteric arteries µ≈Õ¥®π persterior wall ¢Õß aorta §«√¡Õß‡ÀÁπ femoral arteries ·≈–À≈Õ¥‡≈◊Õ¥ à«πª≈“¬ ®“°π—πÈ pressure gradients ∑’«Ë ¥— ‰¥â ¢≥–∑” arteriography ∂â “ µà “ ß°— π ¡“°°«à “ 10 mmHg ∂◊Õ«à“¡’π—¬ ”§—≠∑“ß hemodynamic πà“®–¡’°“√µ’∫·§∫¢Õß À≈Õ¥‡≈◊Õ¥·¥ß

131

AORTOILIAC OCCLUSIVE DISEASE (AIOD)

·≈â«Õ“°“√ºŸªâ «É ¬‰¡à¥¢’ π÷È À√◊Õ°“√Õÿ¥µ—π¢ÕßÀ≈Õ¥‡≈◊Õ¥√ÿπ·√ß¡“° §«√æ‘®“√≥“ºà“µ—¥‚¥¬¡’¢Õâ ∫àß™’¥È ß— µàÕ‰ªπ’È (12,13,14) 1. „πºŸªâ «É ¬ threatened limb loss ‚¥¬¡’Õ“°“√¢Õß rest pain, foot sores, gangrene ·≈– blue toe syndrome 2. ¡’ disabling claudication 3. ¡’ vasculogenic impotence

¢âÕÀâ“¡·≈–¢âÕ§«√√–«—ß„π°“√ºà“µ—¥√—°…“ ·≈–¢¬“¬∂à“ßÀ≈Õ¥‡≈◊Õ¥ ¡’¥—ßµàÕ‰ªπ’È

√Ÿª∑’Ë 13.5 Transfemoral arteriography æ∫¡’°“√µ’∫·§∫¢Õß distal aorta

°“√√—°…“¢—πÈ µâπ ºŸªâ «É ¬ AIOD ®–µâÕß‰¥â√∫— °“√¥Ÿ·≈Õ¬à“ß„°≈â™¥‘ ‡ªìπ√–¬–®“° ·æ∑¬åºŸâ√—°…“ §«√≈¥ªí®®—¬‡ ’Ë¬ß„π°“√‡°‘¥‚√§ ‡™àπ §«“¡¥—π ‚≈À‘µ Ÿß √–¥—∫‰¢¡—π·≈–πÈ”µ“≈„π‡≈◊Õ¥ Ÿß µ≈Õ¥®π§«“¡º‘¥ ª°µ‘„π°“√·¢Áßµ—«¢Õß‡≈◊Õ¥ µâÕßß¥°“√ Ÿ∫∫ÿÀ√’Ë·≈–‡√‘Ë¡®—¥ ‚ª√·°√¡„π°“√‡¥‘πÕÕ°°”≈—ß°“¬ ‚¥¬«‘∏’°“√‡À≈à“π’ÈÕ“°“√ ¢ÕßºŸâªÉ«¬®–§ß∑’Ë À√◊Õ¥’¢÷Èπª√–¡“≥√âÕ¬≈– 70-80 §«√«—¥ √–¬–∑“ß·≈–‡«≈“„π°“√‡¥‘π«à“‡æ‘¡Ë ¢÷πÈ ¡“°πâÕ¬‡∑à“‰√„π·µà≈–«—π Õ“®®–„Àâ¬“°≈ÿà¡ hemorrheologic agents √à«¡¥â«¬ ‡™àπ pentoxifylline ·µà®–µâÕß„Àâ¬“„π√–¬–‡«≈“‰¡àµË”°«à“ 8 —ª¥“Àå ∂â“Õ“°“√‰¡à¥¢’ π÷È √–¬–∑“ß·≈–‡«≈“„π°“√‡¥‘π‰¡à‡æ‘¡Ë §«√À¬ÿ¥¬“ (12)

¢âÕ∫àß™’È„π°“√√—°…“‚√§‚¥¬°“√ºà“µ—¥ À√◊Õ¢¬“¬∂à“ßÀ≈Õ¥‡≈◊Õ¥ ‡¡◊ÕË √—°…“‚¥¬«‘∏∑’ °’Ë ≈à“«¡“·≈â«¢â“ßµâπ‚¥¬ ß¥ Ÿ∫∫ÿÀ√’Ë ≈¥ªí®®—¬ ‡ ’Ë¬ß„π°“√‡°‘¥‚√§·≈–®—¥‚ª√·°√¡„π°“√‡¥‘πÕÕ°°”≈—ß°“¬

1. stable claudication ∑’¡Ë °’ “√Õÿ¥µ—π¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß À≈“¬µ”·Àπàß ∑’Ë aortoiliac ·≈– femoropopliteal-tibial „πºŸªâ «É ¬ ŸßÕ“¬ÿ·≈–¡’Õµ— √“‡ ’¬Ë ß Ÿß 2. ¡’ life threatening condition √à«¡¥â«¬‡™àπ ‚√§À—«„® «“¬ 3. ¡’°“√Õ—°‡ ∫µ‘¥‡™◊ÈÕÕ¬à“ß√ÿπ·√ß∫√‘‡«≥¢â“ß‡§’¬ßµàÕ °“√ºà“µ—¥ ´÷Ëß “¡“√∂∑’Ë®–·æ√à°√–®“¬¡“¬—ßÀ≈Õ¥ ‡≈◊Õ¥‡∑’¬¡‰¥â ‡¡◊ÕË µ—¥ ‘π„®«à“®–ºà“µ—¥À√◊Õ∂à“ß¢¬“¬À≈Õ¥‡≈◊Õ¥®–µâÕß·πà„® «à“º≈°“√√—°…“®–µâÕß¥’°«à“‡¥‘¡ ·≈–‰¡à‡°‘¥¿“«–·∑√°´âÕπ ‡™àπ °“√‡°‘¥‡ÕÁ¡‚∫‰≈Õÿ¥À≈Õ¥‡≈◊Õ¥ à«πª≈“¬ °“√µ‘¥‡™◊ÕÈ ¢ÕßÀ≈Õ¥ ‡≈◊Õ¥‡∑’¬¡ À√◊Õµ“¬®“°‚√§À—«„® ®–µâÕß∑√“∫«à“ºŸªâ «É ¬√âÕ¬≈– 1530 ®–µâÕßºà“µ—¥À√◊Õ∑”À—µ∂°“√À≈“¬§√—ßÈ ‚¥¬‡©æ“–„π√“¬∑’¡Ë ’ AIOD √à«¡°—∫ femoropopliteal-tibial disease

°“√ª√–‡¡‘π§«“¡‡ ’Ë¬ß¢ÕßºŸâªÉ«¬µàÕ°“√ºà“µ—¥ °“√ºà“µ—¥√—°…“ ”À√—∫ºŸªâ «É ¬ AIOD ∑’ Ë ßŸ Õ“¬ÿ ¡’‚Õ°“ ‡ ’¬Ë ß µàÕ¿“«–·∑√°´âÕπ∑“ß‚√§ªÕ¥·≈–À—«„®‰¥â ª√–¡“≥√âÕ¬≈– 15 ∂â “ ¡’ AIOD √à « ¡°— ∫ °“√Õÿ ¥ µ— π ¢ÕßÀ≈Õ¥‡≈◊ Õ ¥·¥ß∫√‘ ‡ «≥ femoropopliteal-tibial ·≈â« ‚Õ°“ ∑’®Ë –¡’ coronary atherosclerosis √à«¡¥â«¬®– Ÿß∂÷ß√âÕ¬≈– 30(15,16) ”À√—∫ªí®®—¬‡ ’¬Ë ß∑“ßÕ“¬ÿ√°√√¡∑’®Ë –‡æ‘¡Ë Õ—µ√“µ“¬·≈–∑ÿæ≈ ¿“æ„πºŸªâ «É ¬∑’Ë ‰¥â√∫— °“√ºà“µ—¥ ‡™àπ ¿“«–À—«„®«“¬‡√◊ÕÈ √—ß (ejection fraction πâÕ¬°«à“√âÕ¬≈– 35) COPD (FEV1 πâÕ¬°«à“ 1 ≈‘µ√), ·≈–¿“«–‰µ«“¬‡√◊ÕÈ √—ß (√–¥—∫§√’Õ“µ‘ππ‘ „π´’√¡—Ë Ÿß°«à“ 3.0 mg%) ∂â“¡’¿“«–‡À≈à“π’ÕÈ µ— √“µ“¬®“°°“√ºà“µ—¥®– Ÿß √âÕ¬≈– 710 ´÷ßË „πºŸªâ «É ¬ª°µ‘Õµ— √“µ“¬®–¡’‡æ’¬ß√âÕ¬≈– 2-7(17) ‡π◊ÕË ß®“° coronary heart disease ‡ªìπ “‡Àµÿ°“√µ“¬ Ÿß ÿ¥ ¢ÕßºŸªâ «É ¬ AIOD ¢≥–ºà“µ—¥À√◊ÕÀ≈—ß°“√ºà“µ—¥ ´÷ßË §«√ª√–‡¡‘π ¿“«–∑“ßÀ—«„®¢ÕßºŸªâ «É ¬°àÕπºà“µ—¥„Àâ≈–‡Õ’¬¥(18,19) ∂â“¡’ pro-

132

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥ ®–µâÕß∑” thrombolytic infusion therapy ‡æ◊ËÕ≈–≈“¬≈‘Ë¡ ‡≈◊Õ¥°àÕπ¢¬“¬∂à“ß∫√‘‡«≥∑’µË ∫’ ·§∫ À√◊ÕÕ“®®–√à«¡°—∫°“√„™â hottip laser À√◊Õ atherectomy device ∫√‘‡«≥∑’§Ë “¥«à“Õ“®®– ‡°‘¥°“√µ’∫·§∫´È”Õ’° §«√§“ stent ‰«â(19) PTA ®–‰¥âº≈¥’¡“°∂â“ ∫√‘‡«≥∑’µË ∫’ ·§∫¢Õß common iliac artery §«“¡¬“«‰¡à‡°‘π 3 ‡´Áπµ‘‡¡µ√ ·≈–¡’ run-off ¥’ 5-year survival iliac arteries √âÕ¬≈– 60-70(14) «‘∏°’ “√π’È ‰¡à§Õà ¬‰¥âº≈¥’ ”À√—∫°“√µ’∫·§∫ ¢Õß aorta ·≈– external iliac arteries

2. Aortoiliac Surgical Reconstruction

√Ÿª∑’Ë 13.6 °“√¢¬“¬∂à“ßÀ≈Õ¥‡≈◊Õ¥·¥ß common iliac ∑’Ëµ’∫·§∫ ‚¥¬„™â∫≈— ≈Ÿπ¢¬“¬

gressive unstable angina pectoris §«√®–∑” coronary angiography ·≈–∂â“¡’À≈Õ¥‡≈◊Õ¥·¥ßµ’∫µ—π§«√®–∑” coronary bypass °àÕπ∑’®Ë –ºà“µ—¥ revascularization AIOD ºŸªâ «É ¬∑’¡Ë ª’ √–«—µ‘ MI À√◊Õ¡’ stable angina pectoris §«√®–∑” cardiac stress test ·µàÕ“®®–¡’ª≠ í À“∑”‰¡à ‰¥â „πºŸªâ «É ¬∑’¡Ë ’ severe claudication ®÷ß§«√µ√«®«‘π®‘ ©—¬‚¥¬°“√∑” dipyridamole thallium scan ´÷ßË ®–∫àß∫Õ°«à“∫√‘‡«≥„¥¢ÕßÀ—«„®¢“¥‡≈◊Õ¥ ‡æ◊ÕË ∑’®Ë –∑” coronary angiography °àÕπ∑’®Ë –ºà“µ—¥√—°…“µàÕ‰ª «‘∏°’ “√ non-invasive „π°“√ª√–‡¡‘π‚√§À—«„®§◊Õ 24-hour EKG monitoring ‡æ◊ÕË ¥Ÿ ischemic ST-segment change ºŸâ ªÉ « ¬∑’Ë ‰¡à ¡’ ‚√§À—«„®´÷Ëß‡ ’Ë¬ßµàÕ°“√ºà“µ—¥·≈–¡’¢âÕ∫àß™’È „π°“√ ºà“µ—¥·πàπÕπ ”À√—∫ AOID „Àâ‡µ√’¬¡ºŸâªÉ«¬ ”À√—∫°“√ºà“µ—¥ √—°…“‰¥â

SPECIFIC INVASIVE THERAPIES 1. Percutaneous Transluminal Angioplasty PTA ‡ªìπÀ—µ∂°“√„π°“√√—°…“∑’Ë ‰¥âº≈¥’ „π°“√µ’∫·§∫∫√‘‡«≥ À≈Õ¥‡≈◊Õ¥·¥ß common iliac(10) (√Ÿª∑’Ë 13.6) „π∫“ß√“¬Õ“®

„π advanced AOID °“√ºà“µ—¥√—°…“‡ªìπ ‘ßË ∑’®Ë ”‡ªìπ‰¡à«“à ®–‡ªìπ endarterectomy À√◊Õ bypass grafting (√Ÿª∑’Ë 13.7, 13.8) Õ—µ√“µ“¬®“°°“√ºà“µ—¥·≈–∑ÿæ≈¿“æ ª√–¡“≥√âÕ¬≈– 2-3 ·≈– 5-10 “‡Àµÿ°“√µ“¬¡—°®–‡°‘¥®“°‚√§À—«„®(20-24) À≈—ßºà“µ—¥ Õ“°“√¢Õß claudication ®–¥’¢π÷È √âÕ¬≈– 95 5-year patency ¢Õß aortofemoral bypass ®–ª√–¡“≥√âÕ¬≈– 80-90(20) ¿“«– ·∑√°´âÕπ¢Õß°“√ºà“µ—¥∑’æË ∫‰¥â ¡’ graft thrombosis, femoral anastomotic pseudoaneurysm °“√µ‘¥‡™◊ÈÕ œ≈œ ∂â“¡’°“√ µ’∫·§∫¢ÕßÀ≈Õ¥‡≈◊Õ¥¿“¬„π™àÕß∑âÕß ‡™àπ renal À√◊Õ visceral arteries Õ◊Ëπ Ê §«√∑” revascularization √à«¡¥â«¬°—∫°“√ ºà“µ—¥√—°…“ AIOD

3. Extra-anatomic Surgical Procedure ‡™àπ axillofemoral À√◊Õ femorofemoral bypass graft ¡’∫∑∫“∑ ∫“ß°√≥’„π°“√ºà“µ—¥√—°…“ AIOD(25,26,27) ‚¥¬‡©æ“– ºŸâªÉ«¬∑’Ë ¿“«–∑“ß√à“ß°“¬‰¡à‡À¡“– ¡°—∫°“√ºà“µ—¥„À≠à §◊Õ °“√ºà“µ—¥‡ªî¥Àπâ“∑âÕß‡æ◊ÕË ∑” direct aortoiliac À√◊Õ aortofemoral bypass (√Ÿª∑’Ë 13.9) Õ—µ√“µ“¬·≈–∑ÿæ≈¿“æπâÕ¬°«à“ ·µà‚Õ°“ ‡°‘¥ graft thrombosis ¡’‰¥â ßŸ °«à“(24,26) femoro-femoral crossover bypass ‡À¡“– ”À√—∫ºŸªâ «É ¬∑’¡Ë ’ iliac artery ¢â“ßÀπ÷ßË Õÿ¥ µ—π ·µàÕ°’ ¢â“ß¬—ß¥’Õ¬Ÿà ¡’ 5-year graft patency √âÕ¬≈– 70-80(26,28) axillofemorals bypass §«√„™â „ πºŸâ ªÉ « ¬∑’Ë ¿ “«–√à “ ß°“¬‰¡à ‡À¡“– ¡µàÕ°“√ºà“µ—¥‡ªî¥Àπâ“∑âÕß‡æ◊ÕË ∑” aortoiliac reconstruction ¡’ª®í ®—¬‡ ’¬Ë ß Ÿß ‡™àπ infected aortic graft ¡’ adhesions ¡“°„π™àÕß∑âÕß ‡§¬‰¥â√—∫√—ß ’∫”∫—¥∫√‘‡«≥™àÕß∑âÕß ·≈–¡’ ªí≠À“∑“ß‚√§ªÕ¥·≈–À—«„® „π∫“ß°√≥’Õ“®®–‡≈’¬Ë ß‚¥¬°“√∑” extraperitoneal approach(29) axillofemoral bypass ¡’ 5-year patency √âÕ¬≈– 50-80 ¢÷ÈπÕ¬Ÿà°—∫ femoropopliteal runoff «à“¥’¡“°πâÕ¬‡æ’¬ß„¥(25)

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√Ÿª∑’Ë 13.7 °. aortoiliac reconstruction ‚¥¬°“√ºà“µ—¥‡ªî¥™àÕß ∑âÕß ‡æ◊ËÕ‡¢â“∂÷ß abdominal aorta ¢. Endarterectomy §. Aortic bypass grafting

°“√ºà“µ—¥™π‘¥Õ◊Ëπ√à«¡°—∫ aortoiliac reconstruction

√Ÿª∑’Ë 13.8 Transabdominal aortobifemoral bypass

elective aortoiliac reconstruction ‚¥¬°“√„™âÀ≈Õ¥‡≈◊Õ¥ ‡∑’¬¡ ‰¡à§«√ºà“µ—¥√à«¡°—π°—∫°“√ºà“µ—¥¿“¬„π™àÕß∑âÕß™π‘¥Õ◊πË (30) ‡æ√“–®–‡æ‘Ë¡Õ—µ√“µ“¬·≈–¿“«–·∑√°´âÕπ¡“°¢÷Èπ°«à“°“√∑” aortic grafting Õ¬à“ß‡¥’¬« (√âÕ¬≈– 6-9 ‡∑’¬∫°—∫√âÕ¬≈– 3) ¢âÕ§«√√–«—ß∑’Ë ÿ¥§◊Õ°“√ªπ‡ªóôÕπ·≈–°“√µ‘¥‡™◊ÈÕ¢ÕßÀ≈Õ¥‡≈◊Õ¥ ‡∑’¬¡(31) ®÷ß‰¡à§«√∑” cholecystectomy À√◊Õ herniorrhaphy √à«¡¥â«¬ ®–∑” cholecystectomy °ÁµÕà ‡¡◊ÕË À≈—ßºà“µ—¥·≈â«‡°‘¥ cholecystitis ´÷Ëß√—°…“‚¥¬«‘∏’ª√–§—∫ª√–§Õß·≈–„Àâ¬“ªØ‘™’«π–‰¡à ‰¥âº≈ „πºŸâªÉ«¬∑’Ë∑” aortic reconstruction retroperitoneal approach “¡“√∂ºà“µ—¥‡ªî¥™àÕß∑âÕß‡æ◊ÕË ∑” cholecystectomy ‰¥â ∂â“æ∫«à“„π™àÕß∑âÕß¡’¡–‡√Áß≈”‰ â „À≠à °√–‡æ“–Õ“À“√ À√◊Õ µ—∫ÕàÕπ §«√√Õ‰«â°àÕπ‡æ◊ËÕ„ÀâºŸâªÉ«¬øóôπµ—«®“°°“√ºà“µ—¥ aortic reconstruction ·≈–ª√–‡¡‘πºŸâªÉ«¬µ≈Õ¥®πµ√«®«‘π‘®©—¬‚¥¬ ≈–‡Õ’¬¥·≈â«

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§ √Ÿª∑’Ë 13.9 °. Axillobifemoral bypass graft ¢. Crossover femorofemoral bypass graft §. Unilateral iliofemoral bypass graft

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°“√‡ΩÑ“¥Ÿ·≈ºŸâªÉ«¬À≈—ß°“√ºà“µ—¥ ºŸªâ «É ¬∑’Ë ‰¥â√∫— °“√√—°…“‚¥¬«‘∏°’ “√ PTA À√◊Õºà“µ—¥ aortoiliac reconstruction ‚Õ°“ ∑’Ë®–‡°‘¥°“√µ’∫µ—π´È”À√◊ÕÀ≈Õ¥‡≈◊Õ¥ ‡∑’¬¡µ’∫·§∫Õ’°¡’‰¥â Ÿß ®÷ß§«√π—¥ºŸâªÉ«¬¡“¥ŸÕ“°“√‡ªìπ√–¬– §«√π—¥ºŸªâ «É ¬∑ÿ° 6-8 —ª¥“Àå ‡æ◊ÕË «—¥ ankle Doppler pressure ‡ª√’¬∫‡∑’¬∫√–À«à“ß¢≥–æ—°°—∫ÕÕ°°”≈—ß°“¬ ‡ªìπ√–¬– ∂â“¡’ Õ“°“√º‘¥ª°µ‘ ¢“¢“¥‡≈◊Õ¥ °“√µ‘¥‡™◊ÕÈ ∫√‘‡«≥·º≈ºà“µ—¥ À√◊Õ false aneurysm §«√æ∫·æ∑¬å‚¥¬¥à«π À≈—ßºà“µ—¥ºŸªâ «É ¬¡—°®– µ“¬®“°‚√§À—«„®‰¡à«à“®–‡ªìπ MI, arrhytmia À√◊ÕÀ—«„®«“¬ §«√‡ΩÑ“√–«—ß„Àâ°“√√—°…“∑’∂Ë °Ÿ µâÕß

√ÿª °“√≈¥ªí®®—¬‡ ’¬Ë ß„π°“√‡°‘¥ atherosclerosis ‰¡à«“à ®–‡ªìπ°“√ ß¥ Ÿ∫∫ÿÀ√’Ë ®”°—¥Õ“À“√‡æ◊ËÕ≈¥‰¢¡—π·≈–πÈ”µ“≈„π‡≈◊Õ¥ √—°…“ ‚√§§«“¡¥—π‚≈À‘µ Ÿß πà“®–∑”„Àâ°“√¥”‡π‘π‚√§¢Õß AOID ‰¡à ‡≈«√â“¬®π‡°‘π‰ª ·≈–‡ªìπ°“√ªÑÕß°—π‚√§¥â«¬ „πªí®®ÿ∫—πæ∫«à“ ª√–™“°√‡æ»À≠‘ß Ÿ∫∫ÿÀ√’Ë¡“°¢÷Èπ ∑”„Àâ‡ªìπ‚√§∑“ßÀ≈Õ¥‡≈◊Õ¥ ¡“°¢÷Èπ «‘∏’°“√√—°…“‚√§∑’Ë ‰¥âº≈§◊Õ‚ª√·°√¡°“√ÕÕ°°”≈—ß°“¬ æ∫«à“ PTA ‰¥âº≈¥’ „πºŸâªÉ«¬∑’Ë¡’À≈Õ¥‡≈◊Õ¥µ’∫·§∫∫√‘‡«≥‰¡à ¬“«¡“°π—°∑’Ë common iliac artery °“√ºà“µ—¥‰¡à«“à ®–‡ªìπ endarterectomy À√◊Õ°“√∑” bypass graft ‰¥âº≈¥’‡ ¡Õ ·µà®–µâÕß ª√–‡¡‘π‚√§À—«„®·≈– underlying disease ¢ÕßºŸªâ «É ¬°àÕπºà“µ—¥

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‡Õ° “√Õâ“ßÕ‘ß 1. McDaniel MD, Cronenwett JL. Basic data related to the natural history of intermittent claudication. Ann Vasc Surg 1989;3:273277. 2. Couch NP. On the arterial consequences of smoking. J Vasc Surg 1986;8:303-317. 3. Goodreau JJ, Creasy JK, Flanigan DP, et al. Rational approach to the differentiation of vascular and neurogenic claudication. Surgery 1978;84:749-757. 4. Baumann DS, McGraw D, Rubin BG, et al. An institutional experience with arterial atheroembolism. Ann Vasc Surg 1994;8:258-265. 5. Carter SA, Hamel ER, Paterson JM, et al. Walking ability and ankle systolic pressures: observations in patients with intermittent claudication in a short-term walking exercise program. J Vasc Surg 1989;10:642-649. 6. Karmody AM, Powers FR, Monaco VJ, Leather RP. çBlue toeé syndrome: an indication for limb salvage surgery. Arch Surg 1976;111:1263-1271. 7. Owen RS, Carpenter JP, Baum RA, et al. Magnetic resonance imaging of angiography occult runoff vessels in peripheral arterial occlusive disease. NE J Med 1992;326:1577-1581. 8. Picus D, Hicks ME, Darcy MD, et al. Critical review of: Magnetic resonance imaging of angiographically occult runoff vessels in peripheral arterial occlusive disease. J Cardiovasc Surg 1991;32:8186. 9. Rubin GD, Walker PJ, Dake MD, et al. Three-dimension spiral computed tomographic angiography: An alternative imaging modality for the abdominal aorta and its branches. J Vasc Surg 1993;18:656-665. 10. Van Andel GJ, van Erp WFM, Krepel VM, et al. Percutaneous transluminal dilatation of the iliac artery: Long term results. Radiology 1985;156:321-323. 11. Brewster DC, Cambria RP, Darling RC, et al. Long term results of combined iliac balloon angioplasty and distal surgical revascularization. Ann Surg 1989;210:324-331. 12. Porter JM, Cutler BS, Lee BY, et al. Pentoxifylline efficacy in the treatment of intermittent claudication: Multicenter controlled doubleblind trial with objective assessment of chronic occlusive arterial disease patients. Am Heart J 1982;104:66-72. 13. Brewster DC, Perler BA, Robison JG, Darling RC. Aortofemoral graft for multilevel occlusive disease: predictors of success and need for distal bypass. Arch Surg 1982;117:1593-1600. 14. Johnston KW, Rae M, Hogg-Johnston SA, et al. Five-year results of a prospective study of percutaneous transluminal angioplasty. Ann Surg 1987;206:403-413. 15. Hertzer NR. Basic data concerning associated coronary disease in peripheral vascular patients. Ann Vasc Surg 1988;1:616-620.

16. Taylor LM Jr, Yeager RA, Moneta G, et al. The incidence of perioperative myocardial infarction in general vascular surgery. J Vasc Surg 1991;15:52-61. 17. Hertzer NR, Beven EG, Young JR, et al. Coronary artery disease in peripheral vascular patients: a classification of 1000 coronary angiograms and results of surgical management. Ann Surg 1984;199:223-224. 18. Freeman WK, Gibbons RJ, Shub C. Preoperative assessment of cardiac patients undergoing noncardiac surgical procedures. Mayo Clin Proc 1989;64:1105-1117. 19. Weibull H, Bergqvist D, Jonsson K, et al. Complications after percutaneous transluminal angioplasty in the iliac, femoral and popliteal arteries. J Vasc Surg 1987;5:681-686. 20. Golden MA, Whittemore AD, Donalson MC, et al. Selective evaluation and management of coronary artery disease in patients undergoing repair of abdominal aortic aneurysms: A 16-year experience. Ann Surg 1990;212:415-423. 21. Naylor AR, Ah-See AK, Engeset J. Aortoiliac endarterectomy: An 11-year review. Br J Surg 1990;77:190-197. 22. Inahara T. Eversion of endarterectomy for aortoiliac occlusive disease. Arch Surg 1975;110:1458-1464. 23. Van den Akker PJ, van Schilfgaarde R, Brand R, et al. Aortoiliac and aortofemoral reconstruction of obstructive disease. Am J Surg 1994;167:379-385. 24. Szilagyi DE, Elliott JP Jr, Smith RF, et al. A 30-year survey of the reconstructive treatment of aortoiliac occlusive disease. J Vasc Surg 1986;3:421-436. 25. Donaldson MC, Louras JC, Bucknam CA. Axillofemoral bypass: A tool with a limited role. J Vasc Surg 1986;3:757-763. 26. Fahal AH, McDonald AM, Marston A. Femorofemorals bypass in unilateral iliac artery occlusion. Br J Surg 1989;76:22-29. 27. Harris EJ Jr, Taylor LM Jr, McConnell DB, et al. Clinical results of axillobifemoral bypass using externally supported polytetrafluoroethylene. J Vasc Surg 1990;12:416-421. 28. Kalman PG, Hosang M, Cina C, et al. Current indications for axillounifemoral or axillofemoral bypass grafts. J Vasc Surg 1987;5:828-835. 29. Sicard GA, Freeman MB, Vandar Woude JC, et al. Comparison between the transabdominal and retroperitoneal approach for reconstruction of the infrarenal aorta. J Vasc Surg 1987;5:19-27. 30. Franko E, Cohen JR. General surgical problems requiring operation in postoperative vascular surgery patients. Am J Surg 1991;162:247250. 31. Pitt HA, Postier RG, MacGowan WAL, et al. Prophylactic antibiotics in vascular surgery. Ann Surg 1980;192:356-364.

∫∑∑’Ë 14 °“√√—°…“ Intermittent Claudication (IC) ‚¥¬‰¡àº“à µ—¥ Intermittent Claudication (IC) À¡“¬∂÷ß¿“«–°“√‡¥‘π °–‡º≈° ®“°°“√ª«¥°≈â“¡‡π◊ÈÕ∫√‘‡«≥¢“¿“¬À≈—ß°“√‡¥‘π Õ“°“√ª«¥®–∑ÿ‡≈“À≈—ß®“°À¬ÿ¥‡¥‘π ¿“«– IC ®–‡°‘¥¢÷Èπ‡¡◊ËÕ¡’ ‡≈◊Õ¥‰ª‡≈’È¬ß∑’Ë¢“‰¡à‡æ’¬ßæÕµàÕ‡¡µ“‚∫≈‘ ¡å¢Õß°≈â“¡‡π◊ÈÕ¢≥– ‡¥‘πÀ√◊ÕÕÕ°°”≈—ß°“¬(1,2) ºŸªâ «É ¬ IC ¡’ “‡Àµÿ¡“®“°°“√µ’∫µ—π¢Õß À≈Õ¥‡≈◊Õ¥·¥ß®“° atherosclerosis µ”·Àπàß¢ÕßÀ≈Õ¥‡≈◊Õ¥ ∑’‡Ë Àπ◊ÕµàÕ°≈â“¡‡π◊ÕÈ ∑’ªË «¥(2) IC Õ“®®–‡°‘¥¢÷πÈ ‰¥â „π§π∑’¡Ë ‡’ ≈◊Õ¥¡“ ‡≈’¬È ß„πª√‘¡“≥ª°µ‘ ·µàÕ¬Ÿà„π¿“«– hypoxemia À√◊Õ anemia ∑”„Àâ¡’ÕäÕ°´‘‡®π¡“‡≈’È¬ß∑’Ë°≈â“¡‡π◊ÈÕ¢“‰¡à‡æ’¬ßæÕ°—∫‡¡µ“‚∫≈‘ ¡å∑µ’Ë Õâ ß°“√µ“¡ª°µ‘(3) ¡—°®–§≈”™’æ®√∫√‘‡«≥À≈—ß‡∑â“‡∫“À√◊Õ‰¡à ‰¥â „πºŸªâ «É ¬ IC °“√ª√–‡¡‘π§«“¡√ÿπ·√ß·≈–æ¬“°√≥å¢Õß‚√§ ∑’¥Ë §’ Õ◊ °“√«—¥ ankle-brachial index (ABI) ‡ª√’¬∫‡∑’¬∫°—π¢≥– Õ¬Ÿ‡à ©¬ Ê °—∫‡¥‘πÕÕ°°”≈—ß°“¬(4) „πºŸªâ «É ¬∑’¡Ë À’ ≈Õ¥‡≈◊Õ¥·¥ßµ’∫ µ—πÀ≈—ßÕÕ°°”≈—ß°“¬·≈â«§à“ ABI ®–≈¥≈ß µâÕßæ—° —°§√Ÿà §à“ ABI ®÷ß®–°≈—∫‰ª§ß√–¥—∫„°≈â‡§’¬ß°—∫§à“‡¥‘¡(5) §à“ exercised ABI ®– ∫àß∫Õ°∂÷ß°“√µ’∫µ—π¡“°πâÕ¬·≈–ª√‘¡“≥¢Õß collaleral circulation(4,5) “‡Àµÿ°“√µ“¬∑’ Ë ”§—≠§◊Õ À—«„®¢“¥‡≈◊Õ¥®“°‚√§À≈Õ¥ ‡≈◊Õ¥À—«„®‚§‚√π“√’Ë ´÷ßË æ∫√à«¡¥â«¬°—∫ IC ª√–¡“≥√âÕ¬≈– 1520(6,7) ªí®®—¬∑’‡Ë ’¬Ë ßµàÕ°“√‡ ’¬™’«µ‘ §◊Õ °“√ Ÿ∫∫ÿÀ√’Ë ‚√§‡∫“À«“π ·≈–§«“¡¥—π‚≈À‘µ Ÿß(6,7,8,9)

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µ“√“ß∑’Ë 14.1 ¬“∑’Ë „™â „π°“√√—°…“ Intermittent claudication (IC)

Anticoagulants Vasodilator Cyclandelate Ethaverine Isoxuprine Nicotinic acid Papaverine Phenoxybenzamine Tolazoline Prostaglandins PGE1 PGE2 Antiserotonin agents Ketanserin Metabolic enhancers Naftidofuryl

Antiplatelet agents Aspirin Dipyridamole Sulfinpyrazone Sulotidil Ticlopidine Calcium-channel blocking agents Cinnarizine Darodipine Flunarizine Verapamil Hemorrheologic agents Buflomedil Dextran Pentoxifylline

·µ°µà“ß°—π(13,14) æ∫«à“¬“°≈ÿ¡à calcium channel blocker ®–¡’ º≈∑”„ÀâÀ≈Õ¥‡≈◊Õ¥¢¬“¬µ—«·≈–µâ“π‡°√Á¥‡≈◊Õ¥®—∫µ—«(15,16,17) ¬“ ∫“ßµ—«§“¥«à“®–¡’º≈¢¬“¬À≈Õ¥‡≈◊Õ¥‡™àπ pentoxifylline °≈—∫¡’º≈„π·ßà¢Õß hemorrheology(18-23)

¬“µâ“π‡≈◊Õ¥·¢Áßµ—« ‡ªìπ¬“µ—«·√°∑’Ëπ”¡“√—°…“‚√§À≈Õ¥‡≈◊Õ¥‚¥¬‡™◊ËÕ«à“®–≈¥ ·≈–™–≈Õ°“√‡°‘¥ atherosclerosis ·µàµÕâ ß„™âÕ¬à“ßµàÕ‡π◊ÕË ß √“§“ Ÿß·≈–¡’¿“«–·∑√°´âÕπ®“°°“√„™â¬“‡ªìπ√–¬–‡«≈“π“π(24) ™à«¬ ≈¥°“√Õÿ¥µ—πÀ≈Õ¥‡≈◊Õ¥∑’Ë‡°‘¥®“° thrombus ¬“∑’Ë „™â√—∫ª√–∑“π§◊Õ Warfarin (Vit K antagonist) ´÷ßË ‰¡à ‰¥â¡¢’ Õâ ∫àß™’È „π°“√ „™â‡©æ“–‚√§À≈Õ¥‡≈◊Õ¥™π‘¥„¥ ªí®®ÿ∫—π‰¡à ‰¥â‡ªìπ∑’Ëπ‘¬¡·≈– √—∫√Õß„π°“√„™â ”À√—∫‚√§¢“¢“¥‡≈◊Õ¥

¬“¢¬“¬À≈Õ¥‡≈◊Õ¥ π”¡“„™â‡æ◊ÕË ∑’®Ë –§«∫§ÿ¡°“√¢¬“¬·≈–À¥µ—«¢ÕßÀ≈Õ¥‡≈◊Õ¥ ·µà ‚¥¬ª°µ‘·≈â« ‡ÕÁπ‚¥∑’‡≈’Ë¬¡®–¡’∫∑∫“∑ ”§—≠„π°“√§«∫§ÿ¡ °“√¢¬“¬·≈–À¥µ—«¢ÕßÀ≈Õ¥‡≈◊Õ¥ ‚¥¬®–º≈‘µŒÕ√å‚¡π‡™àπ norepinephrine, epinephrine ·≈– serotonin „ÀâÀ≈Õ¥‡≈◊Õ¥À¥µ—« ·≈– “√∑’∑Ë ”„ÀâÀ≈Õ¥‡≈◊Õ¥¢¬“¬µ—« ‡™àπ prostacycline ·≈– endothelium derived relaxation factors πÕ°®“°π’¬È ß— º≈‘µ en-

dothelium-1 ´÷Ëß∑”„ÀâÀ≈Õ¥‡≈◊Õ¥À¥µ—«„π¿“«–¢“¥ÕäÕ°´‘‡®π ·≈–‡ √‘¡ƒ∑∏‘¥Ï «â ¬ norepinephrine °“√π”‡Õ“¬“¢¬“¬À≈Õ¥‡≈◊Õ¥ ¡“„™â „ πºŸâ ªÉ « ¬‚√§¢“¢“¥‡≈◊ Õ ¥‡π◊Ë Õ ß®“°§«“¡‡¢â “ „®º‘ ¥ ∑’Ë «à “ ∫√‘‡«≥∑’Ë¢“¥‡≈◊Õ¥¡’°“√À¥µ—«¢ÕßÀ≈Õ¥‡≈◊Õ¥ ®“°°“√ —ß‡°µÿ æ∫«à“ºŸâªÉ«¬¢“¢“¥‡≈◊Õ¥®“°ÕÕ°°”≈—ß°“¬ª≈“¬π‘È«·≈–º‘«Àπ—ß ‡¬Áπ´’¥ ®÷ß∑”„Àâ§“¥«à“¡’°“√À¥µ—«¢ÕßÀ≈Õ¥‡≈◊Õ¥ ·µà∑®’Ë √‘ß·≈â« ‡ªìπ°“√°√–®“¬¢Õß‡≈◊Õ¥®“°º‘«Àπ—ß·≈–π‘È«‡∑â“‰ª¬—ßÀ≈Õ¥ ‡≈◊Õ¥∑’Ë¢¬“¬µ—«¿“¬„π°≈â“¡‡π◊ÈÕ ‚¥¬‰¡à¡’°“√À¥µ—«¢ÕßÀ≈Õ¥ ‡≈◊Õ¥‡≈¬ „π¢“¢“¥‡≈◊Õ¥À≈Õ¥‡≈◊Õ¥®–¡’°“√¢¬“¬µ—«Õ¬à“ß ‡µÁ¡∑’ÕË ¬Ÿ·à ≈â« ®“°¿“«–°“√¢“¥ÕäÕ°´‘‡®π·≈–°“√§—ßË ¢Õß “√‡§¡’ ∑’‡Ë °‘¥¢÷πÈ ®“° anaerobic metabolism ∂â“„Àâ¬“¢¬“¬À≈Õ¥‡≈◊Õ¥ º≈∑’Ëµ“¡¡“§◊Õ®–‡°‘¥ çstealé phenomenon ¥÷ß‡Õ“‡≈◊Õ¥ ÕÕ°®“°∫√‘ ‡ «≥∑’Ë ¢ “¢“¥‡≈◊ Õ ¥‰ª¬— ß À≈Õ¥‡≈◊ Õ ¥∑’Ë “¡“√∂ ¢¬“¬µ—«‰¥âÕ’°„π∫√‘‡«≥∑’Ë ‰¡à¡’°“√¢“¥‡≈◊Õ¥ Õ“°“√¢“¥‡≈◊Õ¥®– ‡≈«≈ß‰ªÕ’°(25) Õß§å°“√Õ“À“√·≈–¬“¢Õßª√–‡∑» À√—∞Õ‡¡√‘°“‰¡à √—∫√Õß«à“¡’¬“¢¬“¬À≈Õ¥‡≈◊Õ¥™π‘¥„¥∑’¡Ë ª’ √– ‘∑∏‘¿“æ„π°“√√—°…“ IC

¬“µâ“π‡°√Á¥‡≈◊Õ¥®—∫°≈ÿà¡ ‡ªìπ¬“∑’πË ”¡“„™â‡π◊ÕË ß®“°‡™◊ÕË «à“¡’ «à π‡°’¬Ë «¢âÕß°—∫¢∫«π°“√ ‡°‘ ¥ atherosclerosis À≈— ß ®“°¡’ ° “√À≈ÿ ¥ ≈Õ°·≈–°√–∑∫ °√–‡∑◊Õπ¢Õß‡ÕÁπ‚¥∑’‡≈’¬Ë ¡ ‡°√Á¥‡≈◊Õ¥®–¡“√«¡µ—«‡°“–‡ªìπ°≈ÿ¡à Õ¬Ÿ∫à √‘‡«≥π—πÈ ·≈–ª≈àÕ¬ “√‡§¡’‡™àπ serotonin ·≈– mitogenic ÕÕ°¡“ (platelet-derived growth factor) ®–‡ªìπµ—«‡√‘¡Ë µâπ∑’Ë ∑”„Àâ‡°‘¥ atherosclerosis “√∑’Ë¡’§ÿ≥ ¡∫—µ‘µâ“π°“√®—∫°≈ÿà¡ ¢Õß‡°√Á¥‡≈◊Õ¥πà“®–¡’∫∑∫“∑ªÑÕß°—π¿“«– atherosclerosis(26) ®÷ß ‰¥â¡’°“√π”¬“°≈ÿà¡π’È¡“„™â ‡™àπ Aspirin, Sulfinpyrazole ·≈– Dipyridamole Aspirin (irreversibly) ·≈– Sulfinpyrazole (reversibly) ®–¬—∫¬—Èß°“√∑”ß“π¢Õß‡ÕÁπ´—¬¡å cyclo-oxygenase ªÑÕß°—π°“√°àÕµ—Èß¢Õß postanoids ®“° arachidonic acid (thromboxan A2 ·≈– prostacycline) Dipyridamole ®–¬—ß¬—ßÈ ƒ∑∏‘¢Ï Õß‡ÕÁπ´—¬¡å phosphodiesterase ‡æ‘¡Ë ª√‘¡“≥¢Õß cyclic adenosine monophosphate (cAMP) „π‡°√Á¥‡≈◊Õ¥ ·≈– ¬—∫¬—Èß‰¡à „Àâ·§≈‡´’Ë¬¡‡¢â“„π‡´≈≈å‡°√Á¥‡≈◊Õ¥‚¥¬‡ √‘¡ƒ∑∏‘Ï¢Õß prostacycline (PGI2) ª√– ‘∑∏‘¿“æ„π°“√„™â¬“‡À≈à“π’√È °— …“ IC ¬—ß‰¡à‡ªìπ∑’¬Ë π◊ ¬—π·πàπÕπ æ∫«à“°“√„™â¬“µâ“π‡°√Á¥‡≈◊Õ¥‚¥¬‡©æ“– Aspirin √à « ¡°— ∫ Dipyridamole ®–™à « ¬≈¥Õ— µ √“°“√µ’ ∫ ·§∫¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß∑’¢Ë “ Thromboxane synthetase inhibitors ‡ªìπ imidazole compounds ®–¬—∫¬—ßÈ Àπâ“∑’¢Ë Õß‡ÕÁπ´—¬¡åµ“à ß Ê ‚¥¬∫à“¬‡∫π‡¡

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°“√√—°…“ Intermittent Claudication (IC) ‚¥¬‰¡àºà“µ—¥ µ“‚∫≈‘ ¡å¢Õß arachidonic acid ‰ª‡ªìπ PGI2 ®–¡’º≈„π°“√¢¬“¬ À≈Õ¥‡≈◊Õ¥·≈–µâ“π‡°√Á¥‡≈◊Õ¥®—∫°≈ÿà¡‰¥âº≈„π°“√√—°…“ IC ‚¥¬‡©æ“–„™â√«à ¡°—∫ Aspirin „πª√‘¡“≥µË” Sulotidyl ®–¬—∫¬—ßÈ platelet thrombogenic activity ‡™àπ ‡¥’¬«°—∫¡’º≈„π°“√¢¬“¬À≈Õ¥‡≈◊Õ¥ Ticlopidine ‡ªìπ¬“ µâ“π‡°√Á¥‡≈◊Õ¥µ—«„À¡à ®–¬—∫¬—ßÈ °“√∑”ß“π¢Õß platelet membrane adenosine diphosphate (ADP) receptor ´÷ßË Õ“®®– ‰¥âº≈„π°“√√—°…“ IC ¬“‡À≈à“π’È¡’∫∑∫“∑„π°“√√—°…“‚√§À≈Õ¥‡≈◊Õ¥„π ¡Õß·≈– À≈Õ¥‡≈◊Õ¥À—«„®‚§‚√π“√’¡Ë “° πà“®–π”¡“ª√–¬ÿ°µå„™â „π°“√√—°…“ IC ∑’Ë ‰¡à ‰¥âºà“µ—¥√—°…“À√◊ÕÀ≈—ßºà“µ—¥·≈â« ‚¥¬„Àâ „πª√‘¡“≥∑’Ë ‡À¡“– ¡ ”À√—∫ Aspirin §«√„Àâ√∫— ª√–∑“π„πª√‘¡“≥«—π≈– 325 ¡‘≈≈‘°√—¡

Prostaglandins PGE1 ·≈– PGE2 „™â „π°“√√—°…“‚√§À≈Õ¥‡≈◊Õ¥·¥ßµ’∫·§∫ ‚¥¬¡’§ÿ≥ ¡∫—µ‘¢¬“¬À≈Õ¥‡≈◊Õ¥·≈–µâ“π°“√®—∫°≈ÿà¡¢Õß‡°√Á¥ ‡≈◊Õ¥ µâÕß∫√‘À“√¬“‚¥¬°“√©’¥‡¢â“∑“ßÀ≈Õ¥‡≈◊Õ¥ ·≈–¡’ half life —Èπ¡“°‡æ’¬ß‰¡à°’Ë«‘π“∑’ ·µàº≈¢â“ß‡§’¬ß¢Õß¬“ Ÿß¡“°(27) „π°“√ ∑¥≈Õßæ∫«à“√—°…“·º≈ ischemic ulcer ‰¥â ‰¡àµ“à ß®“° placebo(28) ·µàº≈„π·ßà°“√µâ“π‡°√Á¥‡≈◊Õ¥®—∫°≈ÿà¡¥’¡“° „πÕπ“§µ§«√À“ ¬“„π√Ÿª·∫∫∑’√Ë ∫— ª√–∑“π·≈–ÕÕ°ƒ∑∏‘πÏ “π¡“„™â

¬“‡ √‘¡‡¡µ“‚∫≈‘ ¡å ¬“°≈ÿ¡à π’‡È √‘¡Ë µâπ§âπ§«â“·≈–π”¡“„™â „πª√–‡∑»·∂∫¬ÿ‚√ª ∑’Ë„™â Õ¬Ÿ¡à ’ Naftidrofuryl (Praxilene) ®–‡æ‘¡Ë °“√π”‡Õ“§“√å ‚∫Œ—¬‡¥√∑ ·≈–°√¥‰¢¡— π ‰ª¬— ß ‰¡‚µ§√Õπ‡¥√’ ¬ ¢Õß°≈â “ ¡‡π◊È Õ ´÷Ë ß ¡’ º ≈ ‚¥¬µ√ßµàÕ Kreb cycle „π°“√º≈‘µ ATP º≈„π°“√√—°…“ IC ¬—ß‰¡à·πàπÕπ Õ“®®–™à«¬‡æ‘Ë¡√–¬–∑“ß„π°“√‡¥‘π ∂â“¿“«–∑’Ë¢“ ¢“¥‡≈◊Õ¥«‘°ƒµÀ√◊Õ ischemic rest pain ®–‡æ‘¡Ë tissue oxygenation(29) Carnitine ®– àß‡ √‘¡ aerobic metabolism ‡æ‘¡Ë °“√π”‰æ√Ÿ ‡«∑‡¢â“‰ª¬—ß Kreb cycle ·≈–π” long-chained fatty acid ‡¢â“‰ª¬—ß‰¡‚µ§√Õπ‡¥√’¬ ®–‡æ‘Ë¡ª√‘¡“≥¢Õß ATP ·≈–≈¥°“√ Ÿ≠‡ ’¬‰æ√Ÿ‡«∑ °“√„Àâ carnitine ‡¢â“ Ÿ√à “à ß°“¬∑“ßÀ≈Õ¥‡≈◊Õ¥¥” ®–æ∫«à“‡æ‘Ë¡√–¬–∑“ß‡¥‘π„πºŸâªÉ«¬ IC ‡®“–‡≈◊Õ¥¥”∫√‘‡«≥¢“ ¡“µ√«®æ∫«à“ª√‘¡“≥¢Õß·≈§‡µ∑≈¥≈ß ¡’°“√‡æ‘Ë¡‡≈◊Õ¥‰À≈ ‡«’¬π‰ª∫√‘‡«≥∑’¢Ë “¢“¥‡≈◊Õ¥ ´÷ßË ‡ªìπº≈ ◊∫‡π◊ÕË ß¡“®“°°“√º≈‘µ ATP ¡“°¢÷πÈ (30)

Antiserotonin drugs serotonin‡ªìπ “√∑’¡Ë ƒ’ ∑∏‘∑Ï ”„ÀâÀ≈Õ¥‡≈◊Õ¥À¥µ—«Õ¬à“ß√ÿπ·√ß ®–°√–µÿπâ „Àâ¡°’ “√®—∫°≈ÿ¡à ¢Õß‡°√Á¥‡≈◊Õ¥ ´÷ßË ¡’®¥ÿ ‡√‘¡Ë µâπ¢Õß inflammatory response “√π’æÈ ∫¡“°„π‡°√Á¥‡≈◊Õ¥ Ketanserin ‡ªìπ serotonin antagonist ∑’®Ë ¥— Õ¬Ÿà „π°≈ÿ¡à ¢Õß Serotonin S-2 receptor blocker πÕ°®“°π’È¬—ß∑”„Àâ‡¡Á¥‡≈◊Õ¥·¥ß¡’§«“¡¬◊¥ À¬ÿàπ·ª√√Ÿª “¡“√∂≈Õ¥ºà“πÀ≈Õ¥‡≈◊Õ¥¢π“¥‡≈Á°‰¥â ‡æ‘Ë¡√–¬– ∑“ß„π°“√‡¥‘π¢ÕßºŸªâ «É ¬ IC(31)

Calcium-channel blockers ¬“„π°≈ÿ¡à π’∑È °ÿ µ—«¡’ƒ∑∏‘Ï„π°“√¢¬“¬À≈Õ¥‡≈◊Õ¥·≈–µâ“π‡°√Á¥ ‡≈◊Õ¥®—∫°≈ÿ¡à à«π°≈‰°∑’∑Ë ”„ÀâÕ“°“√¢Õß IC ¥’¢π÷È ®√‘ß Ê ·≈â« ¬—ß‰¡à∑√“∫·πàπÕπ(15,16,17) Verapamil ®–‡æ‘¡Ë °“√¥÷ß‡Õ“ÕäÕ°´‘‡®π ‡¢â“ Ÿà‡´≈≈å¢Õß¢“∫√‘‡«≥∑’Ë¢“¥‡≈◊Õ¥ ‚¥¬‰¡à‡æ‘Ë¡ª√‘¡“≥‡≈◊Õ¥ ‰À≈‡«’¬π Dazopidine ‡ªìπÕπÿæπ— ∏å¢Õß dihydropyridine ´÷ßË ®–¡’º≈∑”„ÀâÀ≈Õ¥‡≈◊Õ¥„π°≈â“¡‡π◊ÕÈ ≈“¬¢¬“¬µ—« Cinnarizine ·≈– Flunarizine ‰¥âº≈∫â“ß„π°“√√—°…“ IC ‡¢â“„®«à“¬“∑—ßÈ Õß ™π‘¥Õ“®®–¡’§≥ ÿ ¡∫—µ∑‘ “ß hemorrheology

Hemorrheologic agents ¬“„π°≈ÿ¡à π’¡È À’ ≈“¬µ—«·≈–¬—ß„™âÕ¬Ÿà „πªí®®ÿ∫π— Dextran ‡ªìπ “√∑’∑Ë ”„Àâ¡°’ “√‡æ‘¡Ë ª√‘¡“µ√¢Õßæ≈“ ¡à“ ≈¥§«“¡Àπ◊¥¢Õß‡≈◊Õ¥ ∑”„Àâ¡’‡≈◊Õ¥‰À≈‡«’¬π¡“°¢÷Èπ„π√–¥—∫¢Õß microcirculation(18) ®“°°“√»÷°…“æ∫«à“ºŸªâ «É ¬ IC ®–Õ¬Ÿà „π¿“«–‡≈◊Õ¥Àπ◊¥‡π◊ÕË ß®“° ¡’‡¡Á¥‡≈◊Õ¥·¥ß¡“°‡°‘π‰ª ‡¡Á¥‡≈◊Õ¥·¥ß·¢Áß¢“¥§«“¡¬◊¥À¬ÿàπÕàÕπµ—« ®—∫°≈ÿà¡°—πßà“¬ ·≈–ª√‘¡“µ√¢Õßæ≈“ ¡à“πâÕ¬ §«“¡·¢Áßµ—«‰¡à¬◊¥À¬ÿàπ¢Õß‡¡Á¥ ‡≈◊Õ¥·¥ß®–∑”„Àâ ‰¡à “¡“√∂π”‡Õ“ÕäÕ°´‘‡®π‰ª‡≈’¬È ß‡´≈≈åµ“à ß Ê „π√à“ß°“¬‰¥âÕ¬à“ß∑—«Ë ∂÷ß ‚¥¬‡©æ“–∫√‘‡«≥∑’¢Ë “¥‡≈◊Õ¥®“°À≈Õ¥ ‡≈◊Õ¥µ’∫µ—π „π¿“«–ª°µ‘‡¡Á¥‡≈◊Õ¥·¥ß¢π“¥ 8 ‰¡§√Õπ®– “¡“√∂ ≈Õ¥ºà“πÀ≈Õ¥‡≈◊Õ¥ΩÕ¬‡ âπºà“»Ÿπ¬å°≈“ß¢π“¥ 5-6 ‰¡§√Õπ ‰¥â‡π◊ÕË ß®“°¡’§«“¡¬◊¥À¬ÿπà ¢Õßºπ—ß‡¡Á¥‡≈◊Õ¥ ·µà∂“â ‡¡Á¥‡≈◊Õ¥·¥ß ·¢Áß¢“¥§«“¡¬◊¥À¬ÿàπ®–‰¡à “¡“√∂≈Õ¥ºà“πÀ≈Õ¥‡≈◊Õ¥ΩÕ¬‰¥â „π¿“«–¢“¢“¥‡≈◊Õ¥®–¡’‡¡µ“‚∫≈‘ ¡å·∫∫ anaerobic ‡≈◊Õ¥‡ªìπ °√¥ ·≈– hyperosmolality ‡¡Á¥‡≈◊Õ¥·¥ß·¢Áß¢“¥§«“¡¬◊¥À¬ÿπà °“√ÕÕ°°”≈—ß°“¬®–∑”„Àâ‡≈◊Õ¥Àπ◊¥¡“°¢÷πÈ °“√π”‡Õ“ hemorrheologic agents ¡“„™â®–™à«¬·°â ‰¢§«“¡º‘¥ª°µ‘‡À≈à“π’(19) È

140 Pentoxifylline ‡ªìπÕπÿæπ— ∏å¢Õß xanthine ·√°‡√‘¡Ë π”¡“„™â ‡æ√“–§‘¥«à“¡’º≈‡ªìπ¬“¢¬“¬À≈Õ¥‡≈◊Õ¥ ·µàæ∫«à“‰¡à¡’ƒ∑∏‘Ï „π °“√¢¬“¬À√◊ÕÀ¥µ—«¢ÕßÀ≈Õ¥‡≈◊Õ¥‡≈¬ ·µà®–‡æ‘¡Ë °“√‰À≈‡«’¬π ¢Õß‡≈◊Õ¥„π microcirculation ‚¥¬∑”„Àâ‡¡Á¥‡≈◊Õ¥·¥ß¡’§«“¡ ¬◊¥À¬ÿπà ≈¥§«“¡Àπ◊¥¢Õß‡≈◊Õ¥ Ehrhy æ∫«à“ ∂â“„™â¬“™π‘¥π’È „πºŸâªÉ«¬∑’Ë¢“¢“¥‡≈◊Õ¥Õ¬à“ß√ÿπ·√ß ®–∑”„Àâ¡’°“√‡æ‘Ë¡ÕäÕ°´‘‡®π „π‡π◊ÈÕ‡¬◊ËÕ∑’Ë¢“¥‡≈◊Õ¥¡“°¢÷Èπ ´÷Ëß‡ªìπº≈¡“®“°°“√≈¥ oxygen tension ¿“¬„π°≈â“¡‡π◊ÕÈ (20,21) Pentoxifylline ‰¥âº≈¥’„π°“√√—°…“ IC ‡ªìπ√“¬ß“π®“°°“√ „™â¬“™π‘¥π’È°—∫ºŸâªÉ«¬„π¬ÿ‚√ª °àÕπ®–π”¡“„™â „πÕ‡¡√‘°“·≈– Õß§å°“√Õ“À“√·≈–¬“√—∫√Õß°“√„™â ·µà®–µâÕß„™â¬“π’Èµ‘¥µàÕ°—π π“π°«à“ 10 —ª¥“Àå ®÷ß®–‡ÀÁπº≈ º≈¢â“ß‡§’¬ß¢Õß¬“∑’æË ∫‰¥â§Õ◊ §≈◊πË ‰ â Õ“‡®’¬π «‘ß‡«’¬π °“√√—°…“ IC §«√‡√‘¡Ë µâπ®“°°“√ß¥ Ÿ∫∫ÿÀ√’Ë ÕÕ°°”≈—ß°“¬ ·≈–„Àâ¬“ pentoxifylline Õ¬à“ßµàÕ‡π◊ÕË ß ‡ªìπ√–¬–‡«≈“ 10-12 —ª¥“Àå(20-23)

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°“√√—°…“ Intermittent Claudication (IC) ‚¥¬‰¡àºà“µ—¥

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‡Õ° “√Õâ“ßÕ‘ß 1. Imparato AM, Kim G, Davidson T, et al. Intermittent claudication: Its natural course. Surgery 1975;78:795-799. 2. McDanield MD, Cronenwett JL. Basic data related to the natural history of intermittent claudication. Ann Vasc Surg 1989;3:273277. 3. Coffman JD. Pathophysiology of intermittent claudication. In: Spittell JA Jr (ed): Pharmacology Approach to Treatment of Limb Ischemia. Philadelphia: American College of Clinical Pharmacology 1983;4352. 4. Reich T. Cyclandelate: effect on circulatory measurements and exercise tolerance in chronic arterial insufficiency of the lower extremity. J Am Geriatr Soc 1977;15:202-205. 5. Sumner DS, Strandness DE Jr. The relationship between calf blood flow and ankle blood pressure in patients with intermittent claudication. Surgery 1969;65:763-771. 6. Hughson WG, Mann JI, Tibbs DJ, et al. Intermittent claudication: factors determining outcome. Br Med J 1978;1:1377-1379. 7. Hughson WG, Mann JI, Garrod A. Intermittent claudication: prevalence and risk factors. Br Med J 1978;1:378-381. 8. Birkenstock WE, Louw JH, Terblanche J, et al. Smoking and other factors aftecting the conservative management of peripheral vascular disease. S Afr Med J 1975;49:1129-1132. 9. Thomas M. Smoking and vascular surgery. Br J Surg 1981;68:601604. 10. Cronenwett JL, Warner KG, Zelenock GB, et al. Intermittent claudication:current results of nonoperative management. Arch Surg 1984;119:430-436. 11. Clifford PC, Davies PW, Haynes JA, et al. Intermittent claudication: is a supervised exercise class worth while? Br Med J 1980;280:15031505. 12. Bylund AC, Hammersten J, Holm J, et al. Enzyme activities in skeletal muscles from patients with peripheral arterial insufficiency. Eu J Clin Invest 1976;6:425-429. 13. Taylor LM Jr. Porter JM. Drug treatment of claudication: vasodilators, hemorrheologic agents and antiserotonin drugs. J Vasc Surg 1986;3:374-381. 14. Boobis LH, Bell PRF. Can drugs help patients with lower limb ischemia? Br J Surg 1982;69 (suppl): 17-23. 15. Bagger JP, Mather R, Paulsen PK, et al. Verapamil induced increment of oxygen extraction in the arteriosclerotic limb. Cardiovasc Res 1985;19:567-569. 16. Staessin AJ. Treatment of peripheral circulatory disturbances with cinnarizine: a multicenter double-blind placebo-controlled evaluation. Proc R Soc Med 1977;70 (suppl 8): 17-20.

17. Emanuel MB. Specific calcium antagonists in the treatment of peripheral vascular disease. Angiology 1979;30:454-469. 18. Groth CG, Thorsen G. The effect of rheomacrodex and macrodex on factors governing the flow properties of the human blood. Acta Chir Scand 1965;130:507-520. 19. Reid HL, Dormandy JA, Barnes AJ, et al. Impaired red cell deformity in peripheral vascular disease. Lancet 1976;1:666-668. 20. Porter JM, Cutler BS, Lee BY, et al. Pentoxifylline efficacy in the treatment of intermittent claudication: multicenter controlled doubleblind trial with objective assessment of chronic occlusive arterial disease patients. Am Heart J 1982;104:66-72. 21. Grean RM, McNamara J. The effects of pentoxifylline on patients with intermittent claudication. J Vasc Surg 1988;7:356-362. 22. Aviado DM, Dettelbach HR. Pharmacology of pentoxifylline: a hemorrheologic agent for the treatment of intermittent claudication. Angiology 1984;34:407-417. 23. Gallos AS, Morley AA, Gleadow F, et al. Intermittent claudication: a double-blind crossover trial of pentoxifylline. Aust NZJ Med 1985;15:402-409. 24. Macke MJ, Doughlas AS. Oral anticoagulants in arterial disease. Br Med Bull 1978;34:177-182.

25. Coffman JD, Vasodilator drugs in peripheral vascular disease. N Engl J Med 1979;303:713-717. 26. Hess H, Mietaschk A, Derchsel G. Drug-induced inhibition of platelet function delays progression of peripheral occlusive arterial disease. Lancet 1985;1:415-419. 27. Cronenwett JL. The use of prostaglandin P6E1 and P6I2 in peripheral arterial ischemia. J Vasc Surg 1986;3:370-388. 28. Cronenwett JL, Zelenocke GB, Whitehouse WM Jr, et al. Prostacycline treatment of ischemic ulcers and rest pain in unreconstructible peripheral arterial occlusive disease. Surgery 1986;100:369-375. 29. Waters KJ, Crawford AD, Chamberlain J, The effect of naftidrofuryl (Praxilene) in the treatment of intermittent claudication. Br J Surg 1980;67:349-351. 30. Brevetti G, Chiariellom, Ferularo G, et al. Increases in walking distance in patients with peripheral vascular disease treated with L-carnitine: a double-blind, cross-over study. Circulation 1988;77:767773. 31. Bounameaux H, Hellemans H, Holditch T, et al. Placebo-controlled double-blind, two center trial of Ketanserin in intermittent claudication. Lancet 1985;2:1268-1271.

142

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blood gases ¡’§«“¡®”‡ªìπ∑’Ë®–µâÕß„™â „π°“√ºà“µ—¥À≈Õ¥ ‡≈◊Õ¥·¥ß carotid ·≈– aorta ´÷Ëß¡’°“√‡ª≈’Ë¬π·ª≈ß§«“¡¥—π ‚≈À‘µ‰¥âß“à ¬ °àÕπ Õ¥ “¬ arterial lines ºà“π radial artery §«√µ√«®√à“ß°“¬∑” Allenûs test ¥Ÿ°Õà π«à“¡’°“√µ’∫µ—π¢Õß radial ·≈– ulnar artery À√◊Õ‰¡à °“√ Õ¥ “¬ arterial line ºà“π brachial artery §«√√–«—ß ‡æ√“–∂â“‡°‘¥°“√Õÿ¥µ—πÀ√◊Õµ’∫·§∫ ¢ÕßÀ≈Õ¥‡≈◊Õ¥∫√‘‡«≥π’È collaterals ‰¡à¥æ’ Õ ®–∑”„Àâ·¢π¢“¥‡≈◊Õ¥ §«√ monitor EKG µ≈Õ¥°“√ºà“µ—¥¥Ÿ§«“¡º‘¥ª°µ‘„π ®—ßÀ«–°“√‡µâπ¢ÕßÀ—«„®∑’ËÕ“®®–‡°‘¥¢÷Èπ√–À«à“ß°“√ºà“µ—¥ µ‘¥ pulse oximeter ∑’ªË ≈“¬π‘«È ‡æ◊ÕË «—¥ arterial oxygen saturation «π§“ “¬ªí “«–‡æ◊ÕË monitor urine output ·≈–ª√–‡¡‘π ª√‘¡“≥ “√πÈ”∑’Ë„Àâ‡¢â“‰ª„π√à“ß°“¬ Õ¥ “¬ NG tube ‡¡◊ÕË ¡’°“√ ºà “ µ— ¥ ºà “ π™à Õ ß∑â Õ ßÀ√◊ Õ retroperitoneum ªÑ Õ ß°— π ‰¡à „Àâ °√–‡æ“–Õ“À“√‚ªÉßæÕß °—π°“√ ”≈—°Õ“À“√‡¢â“∑“ßÀ≈Õ¥≈¡ ·≈–≈¥ postoperative ileus

√Ÿª∑’Ë 15.1

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√Ÿª∑’Ë 15.2

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√Ÿª∑’Ë 15.3

∂â“‡ªìπ°“√ºà“µ—¥∑” axillofemoral bypass µ”·Àπàß∑’Ë ‡µ√’¬¡º‘«Àπ—ß§◊Õ clavicle, ∑√«ßÕ°¥â“πÀπâ“∑—ÈßÀ¡¥∑’ËµË”°«à“ clavicle, ·¢π¢â“ß‡¥’¬«°—π°—∫∑’®Ë –ºà“µ—¥, ’¢“â ß, ¢“Àπ’∫ ·≈–µâπ¢“ ·≈â«ªŸº“â ª√“»®“°‡™◊ÕÈ ‚¥¬√Õ∫ §≈ÿ¡∑—∫¥â«¬ steri-drape (√Ÿª∑’Ë 15.2) °“√ºà“µ—¥‡¢â“∂÷ßÀ≈Õ¥‡≈◊Õ¥‚¥¬∑—Ë«‰ªºŸâªÉ«¬®–Õ¬Ÿà „π∑à“πÕπ Àß“¬ πÕ°®“°‡ªìπ°“√ºà“µ—¥ thoracoabodominal aorta À√◊Õ retroperitoneal approach of the aorta ®÷ß®–®—¥∑”„ÀâºªŸâ «É ¬ πÕπµ–·§ß ∑à“ right lateral decubitus ‚¥¬ –‚æ°Õ¬Ÿà „π·π« √“∫ ®–∑”„Àâºà“µ—¥‡¢â“∂÷ß femoral arteries ‰¥âßà“¬ „™âÀ¡Õπ À√◊Õ‡∫“–≈¡√Õß‡Õ« ·≈–À—«‰À≈à‡æ◊ÕË ªÑÕß°—π brachial nerve palsy (√Ÿª∑’Ë 15.3) ∂â“‡ªìπ°“√ºà“µ—¥‡¢â“∂÷ßÀ≈Õ¥‡≈◊Õ¥„π™àÕß∑âÕßÀ√◊Õ¢“ „ÀâºŸâ ªÉ«¬πÕπÀß“¬ ªŸº“â §≈ÿ¡µ√ß pubis °—π∫√‘‡«≥π’ÕÈ Õ°®“°º‘«Àπ—ß ∑’Ë®–ºà“µ—¥ ∂â“‡ªìπ°“√ºà“µ—¥ abdominal aorta §«√‡µ√’¬¡

°“√®— ¥ ∑à “ ºŸâ ªÉ « ¬„π∑à “ πÕπ µ–·§ß¥â“π¢«“≈ß ‡æ◊ÕË ‡¢â“∂÷ß thoracoabdominal aorta À√◊Õ retroperitoneal aorta

º‘«Àπ—ßµ—Èß·µà∑√«ßÕ°„µâµàÕ√“«π¡≈ß¡“∂÷ßµâπ¢“ (√Ÿª∑’Ë 15.4) ∂â“‡ªìπ°“√ºà“µ—¥ bypass ∑’Ë¢“§«√‡µ√’¬¡º‘«Àπ—ßÀπâ“∑âÕß ¢“ µ≈Õ¥¢â “ ßµ—È ß ·µà ¢ “Àπ’ ∫ ≈ß¡“ ·≈–¢“Àπ’ ∫ ¥â “ πµ√ß°— π ¢â “ ¡ ‡µ√’¬¡‡π◊ÕÈ ∑’Ë ‰«â ”À√—∫∑’®Ë –ºà“µ—¥‡¢â“∂÷ß external iliac ·≈– femoral arteries ¥â “ πµ√ß°— π ¢â “ ¡·≈–À≈Õ¥‡≈◊ Õ ¥·¥ß∑’Ë ª ≈“¬‡∑â “ ‡µ√’¬¡¢“¥â“πµ√ß°—π¢â“¡‰«â ”À√—∫°“√‡≈“– greater saphenous vein ‡¡◊ÕË ¡’§«“¡®”‡ªìπ∑’®Ë –µâÕß„™â ∂â“À≈Õ¥‡≈◊Õ¥¥”∑’¢Ë “‰¡à¥æ’ Õ Õ“®®–„™â cephalic vein À√◊Õ basilic vein ∑’·Ë ¢π·∑π‰¥â

Mechanical Assistants §«√„™â mechanical retractor À√◊Õ çrobot retractorsé ™à«¬„π·ßà continous exposure ¢Õß operative field ¢≥–∑’Ë ‡≈“–µ—¥‡¢â“∂÷ßÀ≈Õ¥‡≈◊Õ¥·≈–‡¬Á∫µàÕ ≈¥°“√™È”¢Õß‡π◊ÈÕ‡¬◊ËÕ ·≈–‡π◊ÈÕ‡¬◊ËÕ®–™È”πâÕ¬°«à“„ÀâºŸâªÉ«¬ºà“µ—¥¥÷ß∂à“ßµ≈Õ¥‡«≈“ ®–

146

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥

√Ÿª∑’Ë 15.4

Omni retractor ”À√—∫°—π Õ«—¬«–¿“¬„π™àÕß∑âÕß·≈– ¥÷ß∂à“ß‡æ◊ËÕ‡¢â“∂÷ß abdominal aorta

√Ÿª∑’Ë 15.5

∫√‘ ‡ «≥∑’Ë µâ Õ ß‡µ√’ ¬ ¡º‘ « Àπ— ß ·≈–ªŸºâ“ª√“»®“°‡™◊ÈÕ √Õ∫ µàÕ∫√‘‡«≥∑’Ë®–ºà“µ—¥ ‡¢â“∂÷ß abdominal aorta ·≈– À≈Õ¥‡≈◊Õ¥¿“¬„π™àÕß∑âÕß

147

°“√‡ΩÑ“¥Ÿ·≈·≈–¢âÕæ÷ß√–«—ß„πºŸâªÉ«¬∑’ËµâÕßºà“µ—¥ ‡°‘¥§«“¡‡¡◊ÕË ¬≈â“ µâÕß¡“®—¥ operative field °—π„À¡à Omni retractor ¥’¡“° ”À√—∫°“√ºà“µ—¥‡¢â“∂÷ß abdominal aorta ·≈–À≈Õ¥‡≈◊Õ¥¿“¬„π™àÕß∑âÕß (√Ÿª∑’Ë 15.5) Single-armed robot retractor „™â expose „π°“√ ºà“µ—¥‡¢â“∂÷ß corotid artery, distal external iliac À√◊Õ proximal common femoral arteries

°“√√–ß—∫§«“¡√Ÿâ ÷° ‚¥¬∑—«Ë ‰ª·≈â«°“√ºà“µ—¥‡¢â“∂÷ß abdominal aorta ®–„™â«∏‘ ’ °“√«“ß¬“ ≈∫ „πªí®®ÿ∫π— ¡’°“√„™â epidural À√◊Õ spinal anesthesia √à«¡ ‡æ√“–‡ªìπ°“√™à«¬≈¥ cardiac stress ”À√—∫°“√ ºà“µ—¥À≈Õ¥‡≈◊Õ¥∫√‘‡«≥¢“ ®–„™â regional anesthesia ‡ ¡Õ „π°“√ºà“µ—¥ carotid artery „™â regional anesthesia ·≈– §Õ¬ —ß‡°µ¥Ÿ§«“¡º‘¥ª°µ‘∑“ßª√– “∑ ∑’ËÕ“®®–‡°‘¥¢÷Èπ∑—π∑’ ‡π◊ÕË ß®“°º≈·∑√°´âÕπ®“°°“√ºà“µ—¥

¬“∑’Ë„™â∫àÕ¬„πÀâÕßºà“µ—¥ Heparin ‡ªìπ¬“∑’Ë„™â∫Õà ¬∑’ Ë ¥ÿ „π°“√ºà“µ—¥À≈Õ¥‡≈◊Õ¥ ¬°‡«âπ°“√ºà“µ—¥ ´àÕ¡·´¡ thoracoabdominal aneurysm ®–µ‘¥µ“¡ anticoagulant effect ¢Õß‡Œª“√’π‰¥â®“°°“√ monitor activated clotting time (ACT) ∂÷ß·¡â«“à partial thromboplastin time (PTT) ®–‡ªìπµ—«∫àß∫Õ°∂÷ß anticoagulant effect ¢Õß¬“π’È ‚¥¬µ√ß ·µà®–µâÕß„™â‡«≈“‡ªìπ™—«Ë ‚¡ß®÷ß®–∑√“∫º≈ „π¢≥–∑’Ë ACT test ∑”„Àâ „πÀâÕßºà“µ—¥ „™â‡«≈“‰¡à‡°‘π 10 π“∑’ §à“ ACT ∑’Ë ‡À¡“– ¡ ”À√—∫°“√ÕÕ°ƒ∑∏‘¢Ï Õß‡Œª“√’πÕ¬à“ß¡’ª√– ‘∑∏‘¿“æ§◊Õ 200-250 «‘π“∑’ (§à“ª°µ‘ 150 «‘π“∑’) ∂â“§à“¢Õß ACT µË”°«à“ 150 «‘π“∑’ §«√„Àâ bolus dose ¢Õß‡Œª“√’π 100 ¡‘≈≈‘°√—¡/ πÈ”Àπ—°µ—« 1 °‘‚≈°√—¡ ∑—π∑’ À≈—°°“√∑—«Ë ‰ª§◊Õ„Àâ‡Œª“√’π 1000 ¬Ÿπµ‘ ∑ÿ°™—«Ë ‚¡ß·µàª√—∫√–¥—∫„Àâ‡À¡“– ¡°—∫§à“ ACT ∂â“‡°‘¥ thrombosis ¢÷πÈ ¿“¬„πÀ≈Õ¥‡≈◊Õ¥·¥ßÀ√◊ÕÀ≈Õ¥‡≈◊Õ¥ ‡∑’¬¡∑—π∑’À≈—ß°“√ºà“µ—¥‚¥¬Õ∏‘∫“¬ “‡Àµÿ°“√‡°‘¥‰¡à ‰¥â ‰¡à¡§’ «“¡ º‘¥æ≈“¥∑“ß‡∑§π‘§ §«√ ◊∫§âπÀ“ “‡Àµÿ¢Õß hypercoagulable states ∂â“„Àâ‡Œª“√’π·≈â«§à“¢Õß ACT Ÿß¢÷Èπ∑—π∑’· ¥ß«à“‰¡à¡’ °“√¢“¥ antithrombin III ‡Œª“√’π®–ÕÕ°ƒ∑∏‘Ï‚¥¬°“√°√–µÿπâ antithrombin III ·≈–¬—∫¬—ßÈ °“√∑”ß“π¢Õß clotting factors ∑”„Àâ§“à ¢Õß ACT Ÿß¢÷πÈ ∂â“„Àâ‡Œª“√’π‰ª·≈â«§à“¢Õß ACT ¬—ß §ß‡¥‘¡ · ¥ß«à“¡’°“√¢“¥ antithrombin III

º≈¢â“ß‡§’¬ß¢Õß‡Œª“√’π§◊Õ Õ“®®–∑”„Àâ‡≈◊Õ¥·¢Áßµ—«‰¥â ∂â“ºŸªâ «É ¬¡’·Õπµ’∫È Õ¥’È ´÷ßË ∂Ÿ°°√–µÿπâ ‰¥â ‚¥¬‡Œª“√’π ·Õπµ’∫È Õ¥’πÈ ®’È – ¡’º≈∑”„Àâ‡°√Á¥‡≈◊Õ¥®—∫µ—«°—πµ“¡¡“¥â«¬°“√‡°‘¥ arterial thrombosis ¿“«– hypercoagulable state π’‡È √’¬°«à“ heparin-induced-thrombocytopenia (HIT) §«√‡®“–‡≈◊Õ¥‡æ◊ËÕµ√«®π—∫ ª√‘¡“≥¢Õß‡°√Á¥‡≈◊Õ¥

Protamine ¡’§≥ ÿ ¡∫—µ∑‘ ®’Ë – reverse anticoagulant effect ¢Õß‡Œª“√’π ‰¥â ¢π“¥∑’Ë „Àâ§Õ◊ 1 ¡‘≈≈‘°√—¡¢Õß‚ª√µ“¡’πµàÕ 100 ¬Ÿπµ‘ ¢Õß‡Œ ª“√’π¿“¬„π 30 π“∑’·√° ·≈– 0.5 ¡‘≈≈‘°√—¡µàÕ 100 ¬Ÿπµ‘ ¢Õß ‡Œª“√’π 30 π“∑’µÕà ¡“ Õ“°“√¢â“ß‡§’¬ß¢Õß°“√„Àâ ‚ª√µ“-¡’π¡’ §«“¡¥—π‚≈À‘µµË” ™’æ®√™â“·≈–À—«„®À¬ÿ¥‡µâπ Õ“°“√‡À≈à“π’È®– æ∫‰¥â „πºŸªâ «É ¬‡∫“À«“π∑’µË Õâ ß„Àâ INH Õ‘π ÿ≈π‘ ‡æ√“–Õ“®‡°‘¥ allergic reaction µàÕ‚ª√µ“¡’π‰¥â (The P in INH strands for protamine)

¬“ªØ‘™«’ π– ª√– ‘∑∏‘¿“æ¢Õß°“√„Àâ¬“ªØ‘™’«π–ªÑÕß°—π°“√µ‘¥‡™◊ÈÕ‡ªìπ à«π ”§—≠Õ—πÀπ÷Ëß ”À√—∫°“√ºà“µ—¥∑“ß»—≈¬°√√¡À≈Õ¥‡≈◊Õ¥ ‡æ√“–®–≈¥Õ— µ √“°“√µ‘ ¥ ‡™◊È Õ ¢Õß·º≈ºà “ µ— ¥ ·≈–À≈Õ¥‡≈◊ Õ ¥ ‡∑’¬¡∑’Ë „™â ‰¥â≈ß¡“° §«√„™â 1st generation cephalosporin ‡™àπ cefazolin „π¢π“¥ 1 °√—¡ ‡¢â“À≈Õ¥‡≈◊Õ¥¥” 30 π“∑’°àÕπ ≈ß¡’¥ºà“µ—¥ ·≈–∑ÿ° 4 ™—«Ë ‚¡ß ∂â“‡ªìπ°“√ºà“µ—¥∑’Ë „™â‡«≈“π“π ∂â“¡’ contamination §«√„ÀâÕ°’ ∑ÿ° 8 ™—«Ë ‚¡ß ®π§√∫ 48 ™—«Ë ‚¡ß ∂â“ºŸâ ªÉ«¬„™â¬“ªØ‘™«’ π–™π‘¥ÕÕ°ƒ∑∏‘§Ï ≈ÿ¡°«â“ßÕ¬Ÿ·à ≈â«®“° foot infection ‰¡à®”‡ªìπ∑’®Ë –µâÕß„Àâ cefozolin ‡ √‘¡Õ’° °“√∑” local wound irrigation ‚¥¬„™â¬“ªØ‘™«’ π–º ¡°—∫πÈ”‡°≈◊Õ ¡¥ÿ≈¬å™–≈â“ß ®– ™à«¬≈¥Õ—µ√“°“√µ‘¥‡™◊ÈÕ¢ÕßÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡∫√‘‡«≥∑’Ë‡ ’Ë¬ßµàÕ °“√µ‘¥‡™◊ÕÈ ‡™àπ ¢“Àπ’∫

“√Àâ“¡‡≈◊Õ¥ ∂â“¬—ß¡’‡≈◊Õ¥√—«Ë ´÷¡ÕÕ°¡“®“°À≈Õ¥‡≈◊Õ¥‡∑’¬¡À≈—ß®“°ª≈àÕ¬ clamp À≈Õ¥‡≈◊Õ¥·≈â«‰¡àÀ¬ÿ¥ §«√ pack ¥â«¬ “√Àâ“¡‡≈◊Õ¥ ‡™àπ thrombin, Gelfoam, Avitene À√◊Õ Surgicel °“√„™â Surgicel ¡’¢Õâ ¥’§Õ◊ –¥«° ßà“¬ ·≈–√“§“‰¡à ßŸ ‡À¡◊Õπ “√Àâ“¡‡≈◊Õ¥µ—«Õ◊πË Ê

°“√‡¬Á∫·º≈ªî¥ À≈—ß®“°°“√Àâ“¡‡≈◊Õ¥∫√‘‡«≥·º≈ºà“µ—¥¥’·≈â« ‡¬Á∫·º≈ªî¥„Àâ ·πàπæÕ‡À¡“–‰¡à „Àâ·πàπµ÷ß‡°‘π‰ª ‚¥¬‡©æ“–∑’ËÀπâ“∑âÕß√–«—ß‰¡à

148 „Àâ‡°‘¥ wound dehiscence „π°“√‡¬Á∫ªî¥·º≈∑’§Ë Õ À≈—ßºà“µ—¥ ∑” carotid endarterectomy ·≈â« „Àâ‡¬Á∫ sternomastoid ‡¢â“¡“™‘¥°—π‚¥¬‡¬Á∫∑’≈–§” ·≈–‡¬Á∫ plastysma ‡¢â“¡“À“°—π ‚¥¬‡¬Á∫Õ¬à“ßµàÕ‡π◊ÕË ß „™â ‰À¡≈–≈“¬ ‡¬Á∫ªî¥º‘«Àπ—ß‚¥¬„™â skin staples ‡æ√“–ßà“¬ –¥«° ‡√Á« ≈¥√–¬–‡«≈“¡π°“√¥¡¬“ ≈∫ ·≈–ºà“µ—¥ ·º≈ «¬ ∂â“µâÕß°“√„Àâ·º≈ «¬ß“¡„Àâ‡¬Á∫ subcuticular sutures ·º≈∑’¢Ë “§«√‡¬Á∫À≈“¬™—πÈ ‡æ◊ÕË §«“¡·¢Áß·√ß ∑—ßÈ ™—πÈ fascia, subcutaneous ·≈–º‘«Àπ—ß ·º≈∫√‘‡«≥¢“Àπ’∫ µ‘¥‡™◊ÈÕ‰¥âßà“¬ §«√‡¬Á∫ªî¥™—Èπµà“ß Ê ¥—ßµàÕ‰ªπ’È crural fascia, Scarpa’s fascia, subcutaneous tissue ·≈–º‘«Àπ—ß §≈ÿ¡ ªî¥·º≈¥â«¬ºâ“°äÕ´°àÕπµ‘¥æ≈“ ‡µÕ√å ·≈–¥÷ßºâ“ª√“»®“°‡™◊ÈÕ ∑’ªË √Ÿ Õ∫·º≈ÕÕ° À≈—ßºà“µ—¥‡ √Á®

√ÿª „π°“√ºà“µ—¥À≈Õ¥‡≈◊Õ¥πÕ°®“°®–µâÕß√–«—ß¿“«–·∑√°´âÕπ ∑’‡Ë °‘¥¢÷πÈ ‡™àπ‡¥’¬«°—∫∑“ß»—≈¬°√√¡∑—«Ë ‰ª ‘ßË ∑’®Ë –µâÕßæ÷ß√–«—ßÕ’° §◊Õ ‡∑§π‘§‡©æ“–∑“ß»—≈¬°√√¡À≈Õ¥‡≈◊Õ¥ °“√„™â¬“À√◊Õ “√ Àâ“¡‡≈◊Õ¥™π‘¥µà“ß Ê ¢≥–ºà“µ—¥ ¿“«–·∑√°´âÕπ∑’ÕË “®®–‡°‘¥¢÷πÈ ‰¥â µ≈Õ¥®π«‘∏°’ “√·°â ‰¢ ∂â“∑ÿ°Õ¬à“ß∂Ÿ°¢—πÈ µÕπ ¡∫Ÿ√≥å·∫∫ ¿“«– ·∑√°´âÕπµà“ß Ê ®–πâÕ¬≈ß º≈°“√ºà“µ—¥√—°…“®–¥’‡ ¡Õ

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥

‡Õ° “√Õâ“ßÕ‘ß 1. Bunt TJ. The role of a defined protocol for cardiac risk assessment in decreasing perioperative myocardial infarction in vascular surgery. J Vasc Surg 1992;15:626-632. 2. Gage AA, Bhayana JN, Balu V, et al. Assessment of cardiac risk in surgical patients. Arch Surg 1977;112:1488-1497. 3. Gersh BJ, Rihal CS, Rooke TW, et al. Evaluation and management of patients with both peripheral vascular and coronary artery disease. J Am Coll Cardiol 1991;18:203-209. 4. Pearce WH. Perioperative monitoring and intensive care of patients undergoing major vascular surgery. In: Rutherford RB ed. Vascular Surgery, 3rd ed. Philadelphia: WB Saunders, 1989;364-374. 5. Robertson JM, Buckberg GB. Cardiovascular monitoring and perioperative management of vascular surgery patient. In: Moore WS. ed. Vascular Surgery: A Comprehensive Review. New York: Grune & Stratton, 1986;317-337. 6. Stacey-Clear A, Jamieson CW. Omnitract retractor. Br J Surg 1987;74:22.

∫∑∑’Ë 16 RENOVASCULAR HYPERTENSION §«“¡¥—π‚≈À‘µ Ÿß ‡ªìπªí≠À“ ”§—≠„πª√–™“°√∑—Ë«‰ª‚¥¬ ‡©æ“–°≈ÿà¡ºŸâ ŸßÕ“¬ÿ ∂â“ª≈àÕ¬ª≈–≈–‡≈¬‰¡à∑”°“√√—°…“ À≈Õ¥ ‡≈◊Õ¥®–‡ ◊ËÕ¡·≈–°≈“¬‡ªìπ atherosclerosis ‡√Á«¢÷Èπ µ“¡¡“ ¥â«¬¿“«–·∑√°´âÕπ¢Õß√–∫∫À—«„®·≈–À≈Õ¥‡≈◊Õ¥ §«“¡¥—π ‚≈À‘µ∑’ Ë ßŸ ¢÷πÈ Õ¬à“ß√«¥‡√Á«Õ¬à“ß«‘°ƒµ‘„π¿“«– malignant hypertension ®–∑”„ÀâÀ≈Õ¥‡≈◊Õ¥·¥ß∑’Ë‡≈’È¬ßÕ«—¬«– ”§—≠·µ° ‡™àπ ¡Õß ∑”„Àâ‡°‘¥ cerebrovascular accident À√◊Õ‰µ«“¬‡©’¬∫æ≈—π ·≈– ischemic nephropathy ∑”„Àâª√– ‘∑∏‘¿“æ¢Õß‰µ„π°“√ ¢—∫ ªí “«–·≈–¢Õß‡ ’¬®“°√à“ ß°“¬‡ ’¬ ‰ª §«√«‘π‘® ©—¬ À“ “‡Àµÿ¢Õß§«“¡¥—π‚≈À‘µ Ÿß·≈–„Àâ°“√√—°…“·µà‡π‘Ëπ Ê ‡æ◊ËÕ ªÑÕß°—π‰¡à „Àâ ‰µ«“¬ ®π°√–∑—ßË Õ¬Ÿà „π¿“«– end-stage renal failure æ∫«à“ª√–¡“≥√âÕ¬≈– 5-15 ¢Õß‚√§§«“¡¥—π‚≈À‘µ Ÿß ¡’ “‡Àµÿ¡“®“°À≈Õ¥‡≈◊Õ¥·¥ß∑’¡Ë “‡≈’¬È ß‰µµ’∫µ—π(1-4)

°“¬«‘¿“§»“ µ√å À≈Õ¥‡≈◊Õ¥·¥ß¢Õß‰µ ‡ªìπÕ«—¬«–∑’ÕË ¬Ÿà„π retropertoneum ‚¥¬∑—Ë«‰ª·≈â«®–‡ªìπ·¢πß‡¥’Ë¬« ·¬°ÕÕ°®“° aorta ∫√‘‡«≥∑’Ë Õ¬Ÿµà Ë”°«à“ superior mesenteric artery (SMA) „π√–¥—∫ L1 - L2 ª√–¡“≥√âÕ¬≈– 25 ¢Õßª√–™“°√∑—Ë«‰ª®–¡’ renal arteries ¡“°°«à“ 2 ‡ âπ „π‰µ¢â“ß‡¥’¬«°—π ´÷ßË Õ“®®–·¬°·¢πß®“° aorta „π√–¥—∫ Ÿß∂÷ß T12 À√◊Õ≈ß¡“µË”∂÷ß common iliac artery (CIA) main renal artery ®–·¬°ÕÕ°‡ªìπ 5 ·¢πß¬àÕ¬ extra parenchymal segmental artery (apical upper, middle, lower ·≈–

posterior) ‰ª‡≈’È¬ß‰µ·µà≈–¢â“ß ·µà≈– segmental arteries ®–·¬°·¢πß¬àÕ¬ÕÕ°‡ªìπ lobar ·≈– interlobar arteries ·∑√°‡¢â“‰ª√–À«à“ß pyramids interlobar arteries ®–‡™◊ÕË ¡ µàÕ°—∫ arcuate artery ´÷ßË ®–µ—ßÈ ©“°·≈–·∑√°Õ¬Ÿ√à –À«à“ß cortex °—∫ medulla ®“° arcuate artery ®–·¬°ÕÕ°‡ªìπ interlobular artery, intralobular artery ·≈–¡“ ‘πÈ ÿ¥∑’Ë afferent glomerular arteriole renal vein ®–∑Õ¥Õ¬ŸàÀπâ“µàÕ artery ‚¥¬¥â“π´â“¬®–¬“«°«à“¥â“π¢«“ºà“π aorta ·≈– superior mesenteric artery ‡¢â“ IVC ·¢πß ”§—≠ 3 ‡ âπ¢Õß left renal vein §◊Õ gonadal, adrenal ·≈– posterior lumbar vein æ∫«à“ posterior lumbar vein ®–‡ªìπ·¢πß„À≠à∑ ’Ë ¥ÿ „π°“√ºà“µ—¥‡æ◊ÕË mobilize renal vein ®–µâÕßºŸ°µ—¥À≈Õ¥‡≈◊Õ¥¥”∑—ßÈ 3 ·¢πßπ’È

æ¬“∏‘°”‡π‘¥ ª√–¡“≥√âÕ¬≈– 75 ¢Õß°“√µ’∫·§∫À≈Õ¥‡≈◊Õ¥·¥ß∑’Ë ‰µ ¡’ “‡Àµÿ¡“®“° atherosclerosis ‚¥¬‡©æ“–µ√ß√Ÿ‡ªî¥ (orifice)(5,6) ”À√—∫ fibromuscular dysplasia (FMD) ∑”„Àâ‡°‘¥ dysplastic ·≈– fibrosing lesions ¢÷πÈ „π™—πÈ intima, media ·≈– adventitia(7,8) ≈—°…≥–¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß∑’Ë ‰µµ’∫·§∫®“° medial FMD ¥Ÿ®“° angiogram ®–‡ÀÁπ‡ªìπ·∫∫ çstring beadé FMD æ∫ „π‡æ»À≠‘ßÕ“¬ÿπÕâ ¬(8) “‡Àµÿ∑·’Ë ∑â®√‘ß¬—ß‰¡à∑√“∫ °“√µ’∫·§∫®– ‡°‘¥¢÷Èπ‰¥âÀ≈“¬µ”·Àπàß„πÀ≈Õ¥‡≈◊Õ¥·¥ß∑’Ë ‰µ ”À√—∫ “‡Àµÿ Õ◊πË ∑’∑Ë ”„Àâ‡°‘¥ RVH ‰¥â‡™àπ aneurysm, emboli, traumatic lesion ·≈– arteriovenous fistula

150

æ¬“∏‘ √’√«‘∑¬“ ‰µ‡ªìπ»Ÿπ¬å§«∫§ÿ¡§«“¡¥—π‚≈À‘µ∑’Ë ”§—≠∑’Ë ÿ¥¢Õß√à“ß°“¬ ‡æ√“–¡’Õ∑‘ ∏‘æ≈„π°“√§«∫§ÿ¡ª√‘¡“µ√¢Õßæ≈“ ¡à“∑’Ë ‰À≈‡«’¬π„π °√–· ‚≈À‘µ ‡™àπ‡¥’¬«°—π°—∫°“√§«∫§ÿ¡ vasomotor tone °“√ µ√«®æ¬“∏‘ √’√«‘∑¬“¢Õß°“√‡°‘¥ RVH ®–µâÕß¥Ÿª√– ‘∑∏‘¿“æ „π°“√∑”ß“π¢Õß‰µ‡ªìπÕ—π¥—∫·√° §«“¡¥—π‚≈À‘µ·≈–ª√‘¡“µ√¢Õß‡≈◊Õ¥∂Ÿ°§«∫§ÿ¡‚¥¬ renin angiotensin -aldosterone system(1,4,9,10) °≈â“¡‡π◊ÕÈ ‡√’¬∫∫√‘‡«≥ afferent arterioles µ√ß juxtaposition ¢Õß renal glomerulus (juxtaglomerular apparatus) ‰«µàÕ°“√≈¥≈ß¢Õß§«“¡¥—π ‚≈À‘µ¡“° §«“¡¥—π‚≈À‘µ∑’ËµË”À√◊Õ perfusion pressure ∑’Ë≈¥ ≈ß®–°√–µÿπâ „Àâ‡´≈≈å‡À≈à“π’ÀÈ ≈—ßË proteolytic enzymes ∑’ Ë ”§—≠§◊Õ renin ÕÕ°¡“ renin ®–∑”ªØ‘°√‘ ¬‘ “°—∫ !-globulin (angiotensin) ´÷ßË º≈‘µ®“°µ—∫„Àâ°≈“¬‡ªìπ angiotensin I angiotensin I ‡ªìπ inactive ·≈– labile decapeptide ®–∂Ÿ° converting enzyme „πªÕ¥ ‡ª≈’¬Ë π„Àâ‡ªìπ angiotensin II ´÷ßË ¡’ƒ∑∏‘‡Ï ªìπ potent vasoconstrictor ∑”„ÀâÀ≈Õ¥‡≈◊Õ¥À¥µ—«·≈–§«“¡¥—π‚≈À‘µ Ÿß¢÷Èπ ·≈–¬—ß°√–µÿπâ „Àâ¡°’ “√À≈—ßË aldosterone ®“° zona glomerulosa ¢Õß adrenal cortex aldosterone ®–∑”„Àâª√‘¡“µ√¢Õß æ≈“ ¡à“‡æ‘Ë¡¢÷Èπ ¡’°“√¥Ÿ¥´÷¡¢Õß “√πÈ”·≈–‚´‡¥’¬¡®“° renal tubules (√Ÿª∑’Ë 16.1) ‚¥¬¢∫«π°“√¥—ß°≈à“«π’È ®“° angiotensin II ®–¡’º≈„Àâ§«“¡ ¥—π‚≈À‘µ, ª√‘¡“µ√¢Õßæ≈“ ¡à“·≈–ª√‘¡“≥¢Õß‚´‡¥’¬¡„π‡≈◊Õ¥ Ÿß¢÷πÈ ‡´≈≈åµ√ß distal convoluted tubules (macula densa) ®–‰«µàÕ§«“¡‡¢â¡¢âπ¢Õß‚´‡¥’¬¡„πæ≈“ ¡à“µ√ß distal tubules ∑’≈Ë ¥≈ßÀ√◊Õ‡æ‘¡Ë ¢÷πÈ ·≈–®–¡’º≈ feed back µàÕ°“√°√–µÿπâ renin „πºŸâªÉ«¬∑’Ë¡’À≈Õ¥‡≈◊Õ¥·¥ß∑’Ë¡“‡≈’È¬ß‰µµ’∫·§∫¢â“ß‡¥’¬« §«“¡¥—π‚≈À‘µ®– Ÿß¢÷πÈ ®“°ƒ∑∏‘¢Ï Õß renin ¡’°“√¥Ÿ¥´÷¡°≈—∫¢Õß πÈ”·≈–‚´‡¥’¬¡ºà“π∑àÕ‰µ¡“°¢÷Èπ À≈—ß®“°π—Èπ‰µ¢â“ß∑’Ëª°µ‘®– æ¬“¬“¡§ß√–¥—∫ª°µ‘¢Õß “√πÈ”„π√à“ß°“¬„Àâ ‰¥â ‚¥¬°“√¢—∫ ‡Õ“ “√πÈ”∑’Ë¡“°‡°‘πÕÕ°®“°√à“ß°“¬ ¥—ßπ—Èπ„π∑’Ë ÿ¥ºŸâªÉ«¬∑’Ë À≈Õ¥‡≈◊Õ¥·¥ß¢Õß‰µµ’∫·§∫¢â“ß‡¥’¬« ®–¡’√–¥—∫¢Õß renin Ÿß¢÷πÈ º‘¥ª°µ‘ „π¢≥–∑’ªË √‘¡“µ√¢Õß “√πÈ”„π√à“ß°“¬§ß√–¥—∫ª°µ‘ ‡ªìπ≈—°…≥–¢Õß renin dependent hypertension ºŸªâ «É ¬´÷ßË ¡’ À≈Õ¥‡≈◊Õ¥·¥ß¢Õß‰µµ’∫·§∫∑—ßÈ Õß¢â“ß ¡’°“√‡æ‘¡Ë °“√À≈—ßË ¢Õß renin ÕÕ°®“°‰µ∑—Èß Õß¢â“ß ª√‘¡“µ√¢Õß “√πÈ”„π√à“ß°“¬®– Ÿß¢÷Èπ‚¥¬‰¡à “¡“√∂¢—∫ÕÕ°‰¥â ®–µ“¡¡“¥â«¬√–¥—∫¢Õß renin

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥ „πæ≈“ ¡à“ª°µ‘À√◊ÕµË”°«à“ª°µ‘‡≈Á°πâÕ¬ ¡’°“√‡æ‘¡Ë ª√‘¡“≥ “√ πÈ”„π‡´≈≈å ·≈–®–Õ¬Ÿà „π volume-dependent hypertension

Õ“°“√· ¥ß∑“ß§≈‘π‘§ ª√–¡“≥√âÕ¬≈– 5-15 ¢ÕßºŸªâ «É ¬§«“¡¥—π‚≈À‘µ Ÿß∑’¡Ë ’ “‡Àµÿ ®“°À≈Õ¥‡≈◊Õ¥ ®–¡’ “‡Àµÿ®“°À≈Õ¥‡≈◊Õ¥·¥ß∑’Ë ‰µµ’∫·§∫ ‚¥¬∑—«Ë ‰ª·≈â« °“√ª√–‡¡‘πºŸªâ «É ¬§«“¡¥—π‚≈À‘µ Ÿßª√–°Õ∫ ¥â«¬°“√´—°ª√–«—µµ‘ √«®√à“ß°“¬ µ√«®√–¥—∫Õ’‡≈Á§‚µ√≈—¬µå „π´’√¡—Ë √–¥—∫µ√’Õ“µ‘ππ‘ µ√«®§≈◊πË ‰øøÑ“À—«„® ‡æ◊ÕË ·¬°‚√§ÕÕ°®“°‚√§ À—«„®‚µ·≈–À—«„®¢“¥‡≈◊Õ¥ °“√‡®“–À“§à“´’√¡—Ë Õ’‡≈Á§‚µ√≈—¬µå·≈– «—¥§à“‚ª·µ ‡´’¬¡‡ªìπ√–¬–®–∫àß∫Õ°‰¥â«“à ºŸªâ «É ¬‡ªìπ 1o aldosteronism À√◊Õ‰¡à ∂â“√–¥—∫¢Õß‚ª·µ ‡´’¬¡„π´’√¡—Ë Ÿß°«à“ 3.0 mg/ dL §«√µ√«®°“√∑”ß“π¢Õß‰µ„Àâ≈–‡Õ’¬¥ ‚¥¬∑—«Ë ‰ª·≈â«°“√´—° ª√–«—µ‘µ√«®√à“ß°“¬·≈–°“√µ√«®æ◊Èπ∞“π∑“ßÀâÕßªØ‘∫—µ‘°“√®– ‰¡à “¡“√∂·¬°‚√§ RVH ÕÕ°®“° essential hypertension ‰¥â Õ“°“√∑“ß§≈‘π‘§∑’Ë®–∑”„Àâ ß —¬«à“ºŸâªÉ«¬‡ªìπ‚√§ RVH ´÷Ëß§«√ ®–æ‘®“√≥“µ√«®«‘π®‘ ©—¬æ‘‡»…µàÕ‰ª ¡’¥ß— π’È (1,2,3,4) 1. §«“¡¥—π‚≈À‘µ Ÿß¢÷πÈ Õ¬à“ß√«¥‡√Á« 2. ºŸªâ «É ¬‡¥Á°À√◊Õ§πÀπÿ¡à “« 3. §«∫§ÿ¡§«“¡¥—π‚≈À‘µ≈ß¡“°‚¥¬°“√„™â¬“ 4. øíß‰¥â‡ ’¬ß abdominal epigastric bruit 5. ‰¡à¡ª’ √–«—µ§‘ √Õ∫§√—«‡ªìπ‚√§§«“¡¥—π‚≈À‘µ Ÿß¡“°àÕπ 6. §«“¡¥—π‰¥·Õ ‚µ≈‘§ Ÿß°«à“ 105 ¡‘≈≈‘‡¡µ√ª√Õ∑

Screening test «‘∏°’ “√∑’¬Ë ß— „™â „πªí®®ÿ∫π— ¡’ 1. intravenous pyelography (IVP) ®–æ∫«à“¡’ delayed function ¢Õß‰µ¢â“ß∑’Ë¡’ªí≠À“ «‘∏’°“√µ√«®π’È¡’§«“¡ ·πàπÕπ„π°“√«‘π‘®©—¬‚√§‰¥â∂÷ß√âÕ¬≈– 75 Õ“®®–·ª√ º≈º‘¥æ≈“¥‰¥â „π RVH ∫“ß√“¬ (√Ÿª∑’Ë 16.2) 2. captopril test ‚¥¬„ÀâºªŸâ «É ¬√—∫ª√–∑“π¬“ captopril (ACE inhibitor) À≈—ß®“°«—¥√–¥—∫ baseline ¢Õß plasma renin activity ·≈–§«“¡¥—π‚≈À‘µ·≈â« ®–æ∫«à“√–¥—∫¢Õß plasma renin ®– Ÿß¢÷πÈ ¡“° ¢≥–∑’§Ë «“¡¥—π‚≈À‘µ≈¥≈ß test π’¡È ’ sensitivity Ÿß∂÷ß 100% ·≈– specificity √âÕ¬≈– 90 ·µà∂“â ºŸªâ «É ¬‰µ«“¬®–·ª√º≈‰¡à ‰¥â 3. captopril renal scaning º≈∫«°∑’Ë ‰¥â®–æ∫«à“¡’°“√ ≈¥¢Õß glomerular filtration rate ·≈–°“√¢®—¥ÕÕ° ®“°√à“ß°“¬¢Õß “√°—¡¡—πµ¿“æ√—ß ’™“â ≈ß(11,12)

RENOVASCULAR HYPERTENSION

√Ÿª∑’Ë 16.1 Renin-angiotensin system

151

152

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥

√Ÿª∑’Ë 16.2 Intravenous pyelography (IVP) æ∫«à“‰µ¢â“ß¢«“¡’ delayed excretory function

√Ÿª∑’Ë 16.3 Arteriography ∑’Ë ¡∫Ÿ√≥å¡Õß‡ÀÁπ aorta ·≈– renal arteries ∑—Èß Õß¢â“ß ¢â“ß¢«“¡’ proximal stenosis µ“¡≈Ÿ°»√™’È

4. duplex ultrasonography «‘∏°’ “√§◊Õ„ÀâºªŸâ «É ¬Õ¥Õ“À“√ 1-2 ™—«Ë ‚¡ß µâÕß«‘π®‘ ©—¬‚¥¬ºŸ∑â ¡’Ë §’ «“¡™”π“≠ Õ“®·ª√ º≈º‘¥æ≈“¥‰¥â®“°≈¡„π≈”‰ â∫ß— (13,14,15) 5. ultrasonography ®–¡Õß‡ÀÁπ¢π“¥·≈– parenchyma ¢Õß‰µ ‰µ∑’ºË ¥‘ ª°µ‘®–¡’¢π“¥‡≈Á°°«à“Õ’°¢â“ßÀπ÷ßË 6. magnetic resonance angiography √“§“ Ÿß¬—ß‰¡à ‡ªìπ∑’πË ¬‘ ¡„™â

«‘∏°’ “√ª√–‡¡‘π∑’Ë ‰¥âº≈·πàπÕπ∑’ Ë ¥ÿ §◊Õ °“√«—¥ baseline renin °àÕπ ·≈–À≈—ß®“°π—πÈ „ÀâºªŸâ «É ¬√—∫ª√–∑“π catapril 25 mg √Õ 30 π“∑’ À≈—ß®“°π—πÈ ¥Ÿ¥‡≈◊Õ¥¥”ÕÕ°¡“ «—¥§à“ renin Õ’°§√—ßÈ Àπ÷ßË ∂â“Õ—µ√“‡ª√’¬∫‡∑’¬∫¢÷Èπ‰ª Ÿß°«à“‡¥‘¡¡“°°«à“ 3 ‡∑à“ · ¥ß «à“°“√ºà“µ—¥·°â ‰¢°“√µ’∫·§∫À≈Õ¥‡≈◊Õ¥·¥ß‰µ®–‰¥âº≈„π°“√ √—°…“ RVH

Renin determination

¬—ß∂◊Õ‡ªìπ gold standard À√◊Õ°“√«‘π®‘ ©—¬À≈—° ”À√—∫°“√ µ’∫·§∫¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß‰µ „πºŸâªÉ«¬∑’Ë§«“¡¥—π‰¥·Õ ‚µ≈‘§ Ÿß°«à“ 120 mmHg (√Ÿª∑’Ë 16.3) §«√∂à“¬¿“æ√—ß ’Õ¬à“ßπâÕ¬ 2 √–π“∫„π·π« lateral ·≈– oblique ‡æ◊ËÕ¥Ÿ§«“¡º‘¥ª°µ‘¢Õß À≈Õ¥‡≈◊Õ¥·¥ß√–¥—∫µà“ß Ê arteriogram ∑’¥Ë §’ «√‡ÀÁπ aorta ·≈– À≈Õ¥‡≈◊Õ¥·¥ß∑ÿ°·¢πß∑’¬Ë π◊Ë ÕÕ°‰ª‡™àπ splenic, hepatic, celiac ·≈– superior mesenteric arteries ‡æ√“–Õ“®®–¡’ °“√µ’∫·§∫√à«¡¥â«¬ À√◊Õ‡µ√’¬¡‡Õ“‰«â ”À√—∫ extra-anatomic reconstruction spiral CT scanning ®–‡ÀÁπ≈—°…≥–¢Õß‰µ·≈–À≈Õ¥ ‡≈◊Õ¥·¥ß∑’µË ∫’ ·§∫‰¥â∂ß÷ 3 ¡‘µ‘ ¡’ sensitivity Ÿß√âÕ¬≈– 90 ·≈– specificity √âÕ¬≈– 80 „π°“√«‘π®‘ ©—¬‚√§(18)

°“√æ∫«à“À≈Õ¥‡≈◊Õ¥·¥ß¢â“ß„¥¢â“ßÀπ÷Ëß¢Õß‰µµ’∫·§∫º‘¥ ª°µ‘¬—ß‰¡à∫àß∫Õ°∂÷ß°“√∑”ß“π∑’Ëº‘¥ª°µ‘¢Õß‰µ §«√ Õ¥ “¬ ¬“ßºà“πÀ≈Õ¥‡≈◊Õ¥¥”‡¢â“∂÷ßÀ≈Õ¥‡≈◊Õ¥¥”¢Õß‰µ ‡æ◊ËÕ¥Ÿ¥‡Õ“ ‡≈◊Õ¥¥”ÕÕ°®“° renal veins ∑—ßÈ Õß¢â“ß·≈– IVC ®ÿ¥∑’ÕË ¬Ÿµà Ë” °«à“ renal veins ÕÕ°¡“‡ª√’¬∫‡∑’¬∫ª√‘¡“≥¢Õß renin(16,17) ∂â“ Õ—µ√“‡ª√’¬∫‡∑’¬∫§à“ Ÿß°«à“ 1.5 µàÕ 1.0 · ¥ß«à“¡’°“√µ’∫·§∫ ¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß∑’Ë¡“‡≈’È¬ß‰µ¡’π—¬ ”§—≠ ∂â“ collaterals ¡’ ¡“°§à“∑’Ëπ”¡“‡ª√’¬∫‡∑’¬∫®–‰¡à·µ°µà“ß°—π¡“°π—° °àÕπ∑”°“√ µ√«®«‘π‘®©—¬§«√„ÀâºŸâªÉ«¬ß¥¬“≈¥§«“¡¥—π‚≈À‘µ ß¥Õ“À“√‡§Á¡ ∑’¡Ë ‡’ °≈◊Õ‚´‡¥’¬¡ ¬“≈¥§«“¡¥—π‚≈À‘µ°≈ÿ¡à beta blocker ®–≈¥ °“√À≈—ßË ¢Õß renin ‡™àπ‡¥’¬«°—π°—∫‚´‡¥’¬¡

Arteriography

153

RENOVASCULAR HYPERTENSION

carbondioxide arteriography ‡ªìπ«‘∏°’ “√µ√«®«‘π®‘ ©—¬∑’®Ë – π”¡“„™âµàÕ‰ª„πÕπ“§µ ‡æ√“–§“√å∫Õπ‰¥ÕäÕ°‰´¥å≈–≈“¬„π´’ √—Ë¡‰¥â¥’°«à“ÕäÕ°´‘‡®π∂÷ß 20 ‡∑à“ ·≈–®–∂Ÿ°¢—∫ÕÕ°®“°√à“ß°“¬ ∑“ßªÕ¥ °“√©’¥§“√å∫Õπ‰¥ÕäÕ°‰´¥å‡¢â“À≈Õ¥‡≈◊Õ¥®–æ∫«à“¡’ §«“¡Àπ◊¥πâÕ¬°«à“ “√∑÷∫· ß∑’Ë„™â°π— „πªí®∫ÿ π— ‚Õ°“ ·æâ “√¡’πÕâ ¬ ¡’¢Õâ ‡ ’¬§◊Õ¡Õß‡ÀÁπ‰¡à™¥— „πÀ≈Õ¥‡≈◊Õ¥∑’¡Ë ¢’ π“¥‡≈Á°(19)

°“√√—°…“ À≈—° ”§—≠§◊Õ‡≈◊Õ°«‘∏’°“√√—°…“„Àâ‡À¡“– ¡°—∫ºŸâªÉ«¬·µà≈– √“¬ ‡π◊ÕË ß®“°ªí®®—¬À√◊Õµ—«·ª√µà“ß°—π‡™àπ Õ“¬ÿ, ‡æ», µ”·Àπàß ∑’ÀË ≈Õ¥‡≈◊Õ¥µ’∫·§∫, æ¬“∏‘ ¿“æ·≈–°“√∑”ß“π¢Õß‰µ·µ°µà“ß °—π„πºŸªâ «É ¬·µà≈–√“¬(2) ºŸªâ «É ¬¡—°®–¡’§«“¡¥—π‚≈À‘µ Ÿß∑’Ë ‰¡à “¡“√∂§«∫§ÿ¡‰¥â¥«â ¬¬“ ª√‘¡“≥ª°µ‘ µâÕß„™âª√‘¡“≥ ŸßÀ√◊Õ¬“À≈“¬¢π“π ·¡â°√–π—Èπ Õ“°“√°Á¬ß— §ß√ÿπ·√ß °“√√—°…“„πªí®®ÿ∫π— ª√–°Õ∫¥â«¬ percutaneous transluminal angioplasty (PTA) ·≈–°“√ºà“µ—¥ «‘∏°’ “√µà“ß Ê (√Ÿª∑’Ë 16.4)

1. Percutaneous transluminal angioplasty (PTA) ‡√‘¡Ë µâπ‚¥¬ Gruntzig „πªï§.». 1978 ‡ªìπ°“√ Õ¥ “¬ «π∑’¡Ë ’ ∫—≈≈ŸπÕ¬Ÿàµ√ßª≈“¬ Õ¥‡¢â“‰ªÀ≈Õ¥‡≈◊Õ¥·¥ß∑’Ë¡’°“√µ’∫·§∫ ·≈â«æÕß∫—≈≈Ÿπ¢÷Èπ‡æ◊ËÕ¢¬“¬∂à“ß ∑”„Àâ‡ âπºà“»Ÿπ¬å°≈“ß¢Õß À≈Õ¥‡≈◊Õ¥·¥ß∑’µË ∫’ ·§∫¡’¢π“¥‚µ¢÷πÈ ‡ªìπ°“√∑”„Àâ atherosclerotic À√◊Õ fibrodysplastic intima ·¬°ÕÕ°®“°°—π ”À√—∫ fibrodysplastic disease º≈°“√¢¬“¬∂à“ß„π°“√√—°…“„°≈â‡§’¬ß °—∫°“√ºà“µ—¥·°â ‰¢ ºŸâªÉ«¬‰¡àµâÕß‡ ’Ë¬ßµàÕ°“√¥¡¬“ ≈∫ºà“µ—¥ º≈°“√√—°…“‰¥âº≈¥’√Õâ ¬≈– 37-60 ¿“«–·∑√°´âÕπ∑’ÕË “®®–æ∫‰¥â¡’ °“√µ°‡≈◊Õ¥, À≈Õ¥‡≈◊Õ¥·µ°∑–≈ÿÀ√◊Õ intimal flap Õÿ¥À≈Õ¥ ‡≈◊Õ¥·¥ß··¢πß¢â“ß‡§’¬ß(20,21) fibromuscular dysplasia (FMD) ∑’≈Ë “¡∂÷ß·¢πßÀ≈Õ¥‡≈◊Õ¥ ¢π“¥‡≈Á° §«√ºà“µ—¥√—°…“ PTA §«√®–„™â „π√“¬∑’√Ë Õ¬µ’∫·§∫ ‡°‘¥¢÷πÈ ∑’Ë main artery ·≈–‰¥âº≈¥’„πºŸªâ «É ¬‡¥Á°

√Ÿª∑’Ë 16.4 ·π«∑“ß„π°“√√—°…“ºŸâªÉ«¬§«“¡¥—π‚≈À‘µ Ÿß·≈– ß —¬«à“®–¡’ “‡Àµÿ®“° renovascular hypertension (RVH)

154

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥ ‡≈◊Õ¥‡∑’¬¡ —ß‡§√“–Àå™π‘¥µà“ß Ê °“√„™â grafts ·µà≈– ™π‘¥¢÷ÈπÕ¬Ÿà°—∫µ—«·ª√À≈“¬Õ¬à“ß ‚¥¬∑—Ë«‰ª·≈â«Õ—π¥—∫ ·√°®–æ‘®“√≥“„™â saphenous vein graft °àÕπ‡æ√“– À≈Õ¥‡≈◊Õ¥·¥ß¢Õß‰µ¡’¢π“¥‡ âπºà“»Ÿπ¬å°≈“ßª√–¡“≥ 4 ¡‘≈≈‘‡¡µ√ („πºŸâ „À≠à) ´÷ßË ¢π“¥æÕ¥’°π— (28) µ—«‡≈◊Õ°µàÕ‰ª π’§È Õ◊ hypogastric artery ∂â“À≈Õ¥‡≈◊Õ¥·¥ß¢Õß‰µ¢π“¥ 6 ¡‘≈≈‘‡¡µ√ §«√„™â PTFE graft (√Ÿª∑’Ë 16.5 °.¢.§.ß.)

”À√—∫ bilateral ostial atherosclerotic lesions PTA √—°…“‰¥âº≈‡æ’¬ß√âÕ¬≈– 14-45 „π√–¬–‡«≈“ 1 ªï ‡æ√“–¡’°“√ µ’ ∫ ·§∫¢ÕßÀ≈Õ¥‡≈◊ Õ ¥·¥ßÀ≈“¬µ”·Àπà ß §«√√–«— ß ¿“«– ·∑√°´âÕπ∑’®Ë –‡°‘¥¢÷πÈ µ“¡¡“¿“¬À≈—ß ‡™àπ cholesterol embolization, vessel thrombosis ·≈–‰µ«“¬(22) 2. °“√ºà“µ—¥√—°…“ ¡’Õ¬ŸÀà ≈“¬«‘∏¥’ ß— µàÕ‰ªπ’È (23-27) 2.1 aortorenal bypass ‚¥¬„™â grafts ¥—ßµàÕ‰ªπ’È autologous saphenous vein hypogastric artery ·≈–À≈Õ¥

√Ÿª∑’Ë 16.5 Aorto renal reconstruction «‘∏’µà“ß Ê °. ¢. §. ß.

unilateral aortorenal bypass graft bilateral aortorenal bypass graft aortorenal bypass ‚¥¬„™â autogenous saphenous vein graft aortic and renal reconstruction

155

RENOVASCULAR HYPERTENSION

2.2 thromboendarterectomy ‡À¡“– ”À√—∫ atherosclerosis ‚¥¬‡©æ“–µ√ß ostia ≈ß¡’¥„π·π« transverse aortotomy ºà“π∫√‘‡«≥∑’µË ∫’ ·§∫®π∂÷ßÀ≈Õ¥‡≈◊Õ¥·¥ß ∑’Ë ‰µ∑—ßÈ Õß¢â“ß ·≈â«∑” endarterectomy (√Ÿª∑’Ë 16.6) 2.3 ex-vivo reconstruction ‡À¡“– ”À√—∫ fibromuscular dysplasia, aneurysms À√◊Õ°“√µ’∫·§∫∑’Ë≈“¡‰ª∂÷ß ·¢πßÀ≈Õ¥‡≈◊Õ¥·¥ß ∑’®Ë ”‡ªìπµâÕß∑” partial resection µâÕßºà“µ—¥¬°‡Õ“‰µÕÕ°¡“∑—ßÈ ¢â“ß ∑” hypothermic perfusion ·≈– reconstruction „™â‡«≈“„π°“√ºà“µ—¥π“π ¡“°(29)

2.4 extra-anatomical renal artery revascularization ‚¥¬ „™â hepatic À√◊Õ splenic artery ‰¥âº≈„π°“√√—°…“¥’ æÕ ¡§«√(30,31) (√Ÿª∑’Ë 16.7) 2.5 nephrectomy ”À√—∫À≈Õ¥‡≈◊Õ¥·¥ß∑’Ë ‰¡à “¡“√∂ reconstruct ‰¥â·≈â« ‰µ∑”ß“πº‘¥ª°µ‘ ‰¡à¡’ excretory function ·≈â« °“√ºà“µ—¥‡Õ“‰µ¢â“ß∑’‡Ë ’¬ÕÕ°®–§«∫§ÿ¡ §«“¡¥—π‚≈À‘µ‰¥â §«√æ‘®“√≥“„π√“¬∑’Ë „™â¬“¢π“¥ Ÿß À≈“¬¢π“π·≈â«¬—ß‰¡à “¡“√∂§«∫§ÿ¡§«“¡¥—π‚≈À‘µ‰¥â „πºŸâªÉ«¬ atherosclerosis ®–æ∫«à“À≈Õ¥‡≈◊Õ¥·¥ß ¢Õß‰µµ’∫·§∫∑—ßÈ Õß¢â“ß√âÕ¬≈– 35 ®÷ß§«√√—°…“·∫∫ conservative Õ¬à“ß‡µÁ¡∑’Ë

°“√æ¬“°√≥å‚√§ ªí≠À“∑’∂Ë °‡∂’¬ß°—π¡“°„πªí®®ÿ∫π— §◊Õ ºŸªâ «É ¬ RVH ·≈–¡’¿“«– ‰µ«“¬√à«¡¥â«¬§«√®–√—°…“‚¥¬°“√„Àâ¬“À√◊Õºà“µ—¥ ¬“≈¥§«“¡ ¥—π‚≈À‘µ ∂â“„Àâ „π¢π“¥ ŸßÕ¬à“ßµàÕ‡π◊ËÕß ®–¡’º≈·∑√°´âÕπµàÕ √–∫∫ª√– “∑∑”„Àâ¡÷πßß §«“¡√Ÿâ ÷°∑“ß‡æ»≈¥πâÕ¬≈ß ·≈– πÕπ‰¡àÀ≈—∫∂÷ß√âÕ¬≈– 15-20 ∑”„ÀâµÕâ ßÀ¬ÿ¥¬“(32,33) ºŸªâ «É ¬‡À≈à“ π’È®–µâÕßøÕ°‡≈◊Õ¥Õ¬à“ßµàÕ‡π◊ËÕß·≈–‚Õ°“ ∑’Ë®–À“¬‡ªìπª°µ‘¡’ ‡æ’¬ß√âÕ¬≈– 50-60 ·µà∂“â ºà“µ—¥√—°…“§«“¡¥—π‚≈À‘µ®–≈¥≈ß Ÿà √–¥—∫ª°µ‘‰¥â√Õâ ¬≈– 75-90 ‰¡àµÕâ ßøÕ°‡≈◊Õ¥Õ’° Õ—µ√“‡ ’¬Ë ßµàÕ°“√ºà“µ—¥„π ∂“∫—π¡“µ√∞“π√âÕ¬≈– 2-3 „πºŸâ ªÉ«¬∑’Ë ‰¡à¡¿’ “«– azotemia ·µà∂“â ´’√¡—Ë §√’Õ“µ‘π Ÿß°«à“ 2 mg/dL Õ—µ√“‡ ’¬Ë ß®–‡æ‘¡Ë ‡ªìπ√âÕ¬≈– 5-7

√Ÿª∑’Ë 16.6 Transaortic renal endarterectomy with patch closure

√Ÿª∑’Ë 16.7 Extra-anatomical renal revascularization ‚¥¬„™â hepatic À√◊Õ splenic arteries

156

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥

√ÿª °“√ºà“µ—¥·°â ‰¢À≈Õ¥‡≈◊Õ¥·¥ß‰µ∑’µË ∫’ ·§∫ ‡ªìπ°“√ºà“µ—¥∑’Ë ¬“°™π‘¥Àπ÷Ëß ”À√—∫»—≈¬·æ∑¬å∑“ßÀ≈Õ¥‡≈◊Õ¥ ‡π◊ËÕß®“° À≈Õ¥‡≈◊Õ¥∑’¡Ë ¢’ π“¥‡≈Á°·≈–‡¢â“∂÷ß¬“°‡π◊ÕË ß®“°Õ¬Ÿ≈à °÷ „π™àÕß∑âÕß Õ¬à“ß‰√°Áµ“¡°Á¬—ß‡ªìπ«‘∏’°“√√—°…“∑’Ë ‰¥âº≈¥’ ”À√—∫ RVH ·≈– ªÑÕß°—π‰¡à„ÀâºªŸâ «É ¬‡°‘¥¿“«–‰µ«“¬µàÕ‰ª “‡Àµÿ¢Õß RVH πÕ°®“° À≈Õ¥‡≈◊Õ¥·¥ßµ’∫·§∫·≈â« Õ“®®–‡°‘¥‰¥â®“° aneurysms, emboli, °“√∫“¥‡®Á∫À√◊Õ arteriovenous fistula „π∫∑π’®È ß÷ °≈à“«∂÷ß °“√«‘π®‘ ©—¬ °“√ª√–‡¡‘πºŸªâ «É ¬ ·≈–¢âÕ∫àß™’È „π°“√∑” PTA ·≈– ºà“µ—¥·°â ‰¢ °≈à“«∂÷ß«‘∏’°“√ºà“µ—¥™π‘¥µà“ß Ê °“√¥Ÿ·≈ºŸâªÉ«¬ ¢≥–ºà“µ—¥·≈–À≈—ß°“√ºà“µ—¥

¡’«‘∏’°“√¡“°¡“¬„π°“√√—°…“ RVH ‰¡à«à“®–‡ªìπ°“√„Àâ¬“ √—ß ’√«à ¡√—°…“ ·≈–°“√ºà“µ—¥ ¬“≈¥§«“¡¥—π‚≈À‘µ°≈ÿ¡à angiotensin-converting enzyme (ACE) inhibitors ·≈– calciumentry blockers “¡“√∂§«∫§ÿ¡§«“¡¥—π‚≈À‘µ Ÿß®“° RVH ‰¥â º≈ √—ß ’·æ∑¬å√°— …“ RVH ‰¥â ‚¥¬°“√∑” PTA ¢¬“¬∂à“ßÀ≈Õ¥ ‡≈◊Õ¥·¥ß∑’µË ∫’ ·§∫‰¥âº≈¥’ °“√ºà“µ—¥√—°…“∑’Ë ‰¥âº≈¡’∑ß—È ex-vivo renal reconstruction ·≈– renal autotransplantation °“√ ºà“µ—¥®ÿ≈»—≈¬°√√¡ “¡“√∂·°â ‰¢§«“¡º‘¥ª°µ‘¢ÕßÀ≈Õ¥‡≈◊Õ¥ ·¥ß‰¥âÕ¬à“ß¡’ª√– ‘∑∏‘¿“æ ∑”„ÀâºªŸâ «É ¬ RVH ‰¡àµÕâ ß≈ß‡Õ¬°“√ √—°…“¥â«¬°“√ºà“µ—¥∑” nephrectomy

RENOVASCULAR HYPERTENSION

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‡Õ° “√Õâ“ßÕ‘ß 1. Goldblatt H. Hypertension of renal origin. Am J Surg 1964;107: 21-5. 2. Chiantella V, Dean RH. Basic data related to clinical decision making in renovascular hypertension. Ann Vasc Surg 1988;2: 92-8. 3. Berglund G, Anderson O, Wilhelmson L. Prevalence of primary and secondary hypertension: Studies in a random population sample. Br Med J 1976;2:554-6. 4. Ram CVS. Renovascular hypertension. Cardiol Clin 1988;6: 483508. 5. Veiball H. Percutaneous transluminal angioplasty versus surgical reconstruction of atherosclerotic renal artery stenosis: A prospective randdomized study. J Vasc Surg 1993;18: 841-8. 6. Zierler RH, Bergelin RO, Isaacson JA, Strandness DE Jr. Natural history atherosclerotic renal artery stenosis: A prospective study with duplex ultrasonography. J Vasc Surg 1994;19: 200-59. 7. Stanley P, Gyepes MT, Olsen DL, Gates GF. Renovascular hypertension in Children and adolescents. Radiology 1978;129:123-31. 8. Zelenok GB. Renal and mesenteric ischemia. Prob Gen Surg 1994;11: 450-62. 9. Robaezewski DL, Dean RH. Pathophysiology of renovascular hypertension. In: Vascular Surgery: Basic science and chinical correlations. White RA, Hollier LH (eds). JB Lippincott, 1994;263-80. 10. Skoggs LT, Dorer FE, Kahn JR, et al. The biochemistry of reninangiotensin system and its role in hypertension. Am J Med 1976;60:737-748. 11. Meier GH. Captopril renal scintigraphy: A new standard for predicting outcome after renal revascularization. J Vasc Surg 1993;17:280-91. 12. Joseph V, Nally JR. Captopril renography in renal vascular disease. In: Novick A, Scoble J, Hamilton G (eds). Renal vascular disease. London: WB Saunders, 1996;195-205. 13. Hansen KJ, Reavis SW, Dean RH. Use of duplex scanning in renovascular hypertension. In: Technologies in Vascular Surgery. Yao JST, Pearce WH (eds). WB Saunders, 1991;174-81. 14. Guzman RP, Zierler RE, Isaacson JA, et al. Renal atrophy and arterial stenosis: A prospective study with duplex ultrasound. Hypertension 1994;23: 346-50. 15. Stracos TA, Parker SH, Yakers WF, et al. Segmental stenosis of the renal artery: Pattern recognition of Tardeus and Pannus abnormalities with duplex sonography. Radiology 1992;184: 487-92. 16. Canzanello VJ, Tertor SC. Noninvasive diagnosis of renovascular disease. Mayo Clin Proc 1994;69: 1172-84. 17. Stanley JC, Fry WJ. Surgical treatment of the renovascular hypertension. Arch Surg 1977;112:1291-7.

18. Rubin GD, Dake MD, Napel S, et al. Spiral CT of renal artery stenosis: Comparison of three-dimensional rendoring techniques. Radiology 1994;190: 181-9. 19. Hawkins IF, Kerns SR. Carbondioxide digital subtraction angiography. In: Cope C (edd.). Current techniques in interventional radiology. Philadelphia:Current Medicine, 1994;11.1-11.7. 20. Miller GA. Percutaneous transluminal angioplasty V.S. surgery for renovascular hypertension. AJR 1985;144: 447-58. 21. Ramsay LF, Waller PC. Blood pressure response to percutanous transluminal angioplasty for renovascular hypertension: An overview of published series. Br Med J 1990;30: 569-72. 22. Bergentz SE, Weibull H, Bergqvist D. Long-term patency after reconstructive surgery and PTA for renal artery stenosis: In: Greenhalgh RM, Hollier L (eds). The maintenance of arterial reconstructions. London: WB Saunders, 1991;384-96. 23. Stanley JC. The evolution of surgery for renovascular occlusive disease. Cardiovasc Surg 1994;2: 195-206. 24. Hansen KJ. Comtemporary surgical management of renovascular disease. J Vasc Surg 1992;16(3): 319-27.

25. Stanley JC, Gerwetz BL, Fry WJ. Renal: Systemic indices and renal vein renin ratio as prognostic indications in remedial renovascular hypertension. J Surg Res 1976;20:149-55. 26. Novick AC. Trends in surgical revascularization for renal artery disease. JAMA 1987;257:498-506. 27. Stanley JC. Surgical interventions in pediatric renovascular hypertension. Clin Nephrol 1992;12:167-76. 28. Dean RH, Wilson JP, Burkett, Foster JH. Saphenous vein aortorenal bypass grafts. Ann Surg 1974;180:469-78. 29. Novick AC. Extra corporeal microvascular reconstruction and autotransplantation for branch renal artery disease. In: Novick A, Scoble J, Hamilton G. (eds.). Renal vascular disease. London: WB Saunders, 1995;497-511. 30. Fergamy A, Kolettis P, Novick AC. The comtemporary, role of extra-anatomic surgical renal revascularization in patients with atheroclerotic renal artery disease. J Urol 1995;153:1798-1802. 31. Reilly JM, Rubin BG, Thompson RW, et al. Long-term effectiveness of extra-anatomical renal artery revascularization. Surgery 1994;110: 984-96. 32. Frishmen WH. B-adrenergic blockers. Med Clin North Am 1988;72:37-81. 33. Erdos EG. Angiotensin converting enzyme and the change in our concepts through the year. Hypertension 1990;16:363-70.

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∫∑∑’Ë 17 FEMORO-POPLITEAL-OCCLUSIVE DISEASE „π∫∑π’®È –°≈à“«∂÷ß°“√µ’∫·§∫¢ÕßÀ≈Õ¥‡≈◊Õ¥∑’¢Ë “ πÕ°‡Àπ◊Õ ®“°°“√µ’∫·§∫ aortoiliac occlusive disease (AIOD) ´÷ßË °≈à“« ‰ª·≈â«„π∫∑∑’Ë 11 µ”·Àπàß¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß∑’Ëµ’∫·§∫∫àÕ¬∑’Ë ÿ¥¢ÕßºŸâªÉ«¬ ∑’¡Ë Õ’ “°“√ Intermittent claudication (IC) §◊Õ superficial femoral artery (SFA) µ√ß Adductor canal (Hunterûs canal) æ∫‰¥â√Õâ ¬≈– 50-60 ¢ÕßºŸªâ «É ¬∑’¡Ë ª’ ≠ í À“ IC ∑—ßÈ À¡¥ √Õß≈ß¡“ §◊Õ popliteal artery “‡Àµÿ‡°‘¥®“° atherosclerosis(1) (√Ÿª∑’Ë 17.1) °“√µ’∫·§∫¢ÕßÀ≈Õ¥‡≈◊Õ¥®–§àÕ¬ Ê ‡°‘¥¢÷πÈ √à«¡°—∫°“√ ‡°‘¥ collaterals √–À«à“ß profunda femoris ·≈– popliteal artery ¥—ßπ—Èπ à«π„À≠à¢ÕßºŸâªÉ«¬∑’Ë¡’À≈Õ¥‡≈◊Õ¥µ’∫µ—π∫√‘‡«≥π’È ¡—°®–‰¡à¡Õ’ “°“√ æ∫«à“¡’ IC ‡æ’¬ß√âÕ¬≈– 3-5 „π§πÕ“¬ÿ¡“°°«à“ 50 ªï(1,2) IC ‡ªìπÕ“°“√∑’æË ∫‰¥â∫Õà ¬∑’ Ë ¥ÿ „πºŸªâ «É ¬ ∑’¡Ë ’ femoro-popliteal occlusive disease ∂â“°“√Õÿ¥µ—π√ÿπ·√ß¡“°¢÷πÈ √à«¡°—∫ AOID ·≈–¿“«– hemodynamic ¢ÕßºŸªâ «É ¬∑’ºË ¥‘ ª°µ‘ ®–æ∫«à“¡’ rest pain, disabling claudication ·≈– gangrene ‡°‘¥¢÷Èπ ®– æ‘®“√≥“∑”°“√ºà“µ—¥√—°…“„πºŸâªÉ«¬∑’Ë¡’ limb-threatening ischemia À√◊Õ severe claudication

Õ“°“√∑“ß§≈‘π‘§ claudication Õ∏‘∫“¬‰¥â«“à ‡ªìπÕ“°“√ª«¥πàÕß‡«≈“‡¥‘π ·≈– ∂â“‰¥âæ—°Õ“°“√ª«¥®–À“¬‰ª „™â√–¬–∑“ß‡¥‘π‡ªìπµ—«°”Àπ¥

√à«¡°—π‡«≈“„π°“√‡¥‘π (claudication distant ·≈– time) πÕ°®“° ª«¥·≈â«Õ“°“√®–¡’Õ“°“√Àπ—°∂à«ßÀ√◊ÕÕàÕπ·√ß ∑”„Àâπ°÷ ∂÷ß neuromuscular disorder ‡ªìπ spinal stenosis ®–µâÕß«‘π‘®©—¬ ·¬°‚√§„Àâ ‰¥â (3,4) ischemic rest pain ®–ª«¥∑’ªË ≈“¬‡∑â“‰¡à „™à∑π’Ë Õà ß ª«¥¡“° ‡«≈“°≈“ß§◊π ™“‡¬Áπ °≈â“¡‡π◊ÈÕ≈’∫ ∂â“ÀâÕ¬‡∑â“≈ß°—∫¢Õß‡µ’¬ß Õ“°“√ª«¥®–≈¥≈ß µâÕß·¬°®“°Õ“°“√ª«¥®“° neuritis ·≈– arthritis gangrene °“√‡πà“µ“¬¢Õß‡π◊ÕÈ ‡¬◊ÕË ¡—°®–‡°‘¥∑’ªË ≈“¬‡∑â“‡ ¡Õ ·µàÕ“®®–‡°‘¥∫√‘‡«≥„¥¢Õß‡∑â“°Á ‰¥â ∫√‘‡«≥ pressure area ‡™àπ º‘«Àπ—ßµ√ß metatarsophalangeal joint ·¬°®“° venous ulcer ´÷ßË ‡°‘¥µ√ß¢âÕ‡∑â“‰¡à‡®Á∫·º≈ ·≈–¡’ venous stasis ·º≈ neurotropic ulcer æ∫„π‚√§‡∫“À«“π µ”·Àπàß∑’‡Ë °‘¥‰¥â∫Õà ¬§◊Õ âπ‡∑â“ metatarsal head ·≈–π‘«È ‡∑â“ blue toe syndrome ®–‡°‘¥®“° microemboli Õÿ¥À≈Õ¥‡≈◊Õ¥¢π“¥‡≈Á°‡™àπ digital arteries ∑”„Àâº«‘ Àπ—ß∫√‘‡«≥π‘«È ‡∑â“‡πà“µ“¬ ·≈–¡’ ¥’ ”§≈È”

°“√µ√«®√à“ß°“¬ ‘ßË ∑’µË √«®æ∫®–∫àß∫Õ°∂÷ß atherosclerotic process °“√ æ¬“°√≥å ‚√§·≈–·π«∑“ß„π°“√√—°…“µàÕ‰ª °“√µ√«®√à“ß°“¬®– æ∫«à“§≈”™’æ®√À≈Õ¥‡≈◊Õ¥·¥ß femoral ‰¥â·µàÀ≈Õ¥‡≈◊Õ¥·¥ß µË”°«à“π—πÈ ®–§≈”‰¥â‡∫“¡“°À√◊Õ‰¡à ‰¥â‡≈¬(5) ABI ®–Õ¬Ÿà „π™à«ß 0.51 ∂â“µË”°«à“ 0.5 ®–∂◊Õ«à“Õ¬Ÿà „π¿“«– threatened limb loss

160

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥

Aorta

Internal iliac External iliac Common femoral Profunda femoris Superficial femoral

Popliteal

Lateral superior genicular Posterior tibial Peroneal Anterior tibial

Popliteal

Highest genicular Medial superior genicular Middle genicular

Lateral inferior genicular Anterior tibial recurrent Anterior tibial

Medial inferior genicular

Posterior tibial Peroneal

√Ÿª∑’Ë 17.1 °“¬«‘¿“§À≈Õ¥‡≈◊Õ¥·¥ß∑’Ë¢“∫√‘‡«≥À—«‡¢à“

FEMORO-POPLITEAL-OCCLUSIVE DISEASE

trophic changes ¢Õß‚√§¢“¥‡≈◊Õ¥‡√◊ÕÈ √—ß ∑’µË √«®æ∫‰¥â‡™àπ ‡≈Á∫Àπ“‡ªìπÀ¬—° ¢π√à«ß º‘«Àπ—ß‡ªìπ¡—πµ÷ß ¡’·º≈‡√◊ÕÈ √—ßÀ√◊Õ gangrene ∫√‘‡«≥ª≈“¬‡∑â“À√◊Õπ‘È«‡∑â“ À≈—ß‡∑â“∫«¡‡π◊ËÕß®“°µâÕß π—ßË À√◊ÕπÕπÀâÕ¬¢“‡ªìπ‡«≈“π“π‡æ◊ÕË ∫√√‡∑“Õ“°“√ª«¥

°“√µ√«®«‘π‘®©—¬ 1. °“√ª√–‡¡‘π systemic factors πÕ°‡Àπ◊Õ‰ª®“°¢“∑’Ë À≈Õ¥‡≈◊Õ¥·¥ßµ’∫µ—π‡√◊ÈÕ√—ß ‡æ◊ËÕ¥Ÿ°“√æ¬“°√≥å ‚√§ ·≈–·π«∑“ß„π°“√√—°…“µàÕ‰ª ‘ßË ‡À≈à“π’®È –ª√–°Õ∫¥â«¬ ª√–«—µ°‘ “√µ√«®√à“ß°“¬ ·≈–°“√µ√«®∑“ßÀâÕßªØ‘∫µ— °‘ “√ ª√–‡¡‘π«à“ºŸâªÉ«¬¡’¿“«– major organ failure √à«¡ ¥â«¬À√◊Õ‰¡à ‡™àπ ‚√§À—«„® ‚√§ªÕ¥ ‰µ ‡∫“À«“π §«“¡¥—π ‚≈À‘µ Ÿß ·≈– CVA ºŸªâ «É ¬ femoro-popliteal occlusive disease ª√–¡“≥√âÕ¬≈– 15-25 ®–¡’ coronary heart disease √à«¡¥â«¬ ´÷Ëß®–‡ªìπ “‡Àµÿ ”§—≠„π °“√µ√“¬™à«ß√–À«à“ß·≈–À≈—ß°“√ºà“µ—¥(6) ®–µâÕßª√–‡¡‘π „Àâ¥«’ “à ‡À¡“– ”À√—∫°“√ºà“µ—¥√—°…“À√◊Õ√—°…“‚¥¬«‘∏Õ’ π◊Ë ªí®®—¬‡ ’¬Ë ß ”À√—∫‚√§À—«„®ª√–°Õ∫¥â«¬ MI, CHF, unstable angina, ‡∫“À«“π·≈–Õ“¬ÿ ßŸ °«à“ 70 ªï 2. Inflow disease ‡™àπ AIOD ∑’Ë‡°‘¥√à«¡°—∫ femoropopliteal occlusive disease §«√®–‰¥â√∫— °“√ºà“µ—¥·°â ‰¢ °àÕπ∑’Ë®–√—°…“ femoropopliteal occlusive disease ‚¥¬‡©æ“–„π√“¬∑’¡Ë ’ ischemic rest pain ·≈– disabling claudication ‡æ√“–∫“ß§√—Èß°“√ºà“µ—¥·°â ‰¢À≈Õ¥ ‡≈◊Õ¥µ’∫ à«π∫π (AIOD) ‰ª·≈â« Õ“°“√‚√§¢Õß femoropopliteal occlusive disease ®–¥’¢π÷È ¡“°®πÕ“®®–‰¡à µâÕßºà“µ—¥·°â ‰¢ 3. °“√«—¥ segmental pressures ·≈– plethysmography ‡ªìπ noninvasive test ∑’Ë „™âª√–‡¡‘π¢—πÈ µâπ ”À√—∫ ºŸªâ «É ¬‚√§À≈Õ¥‡≈◊Õ¥µ’∫µ—π °“√«—¥ segmental arterial pressure ‚¥¬„™â standard pressure cuff À√◊Õ continous-wave doppler probe «—¥§«“¡¥—π´’ ‚µ≈‘§ ∑’µË πâ ¢“ ‡¢à“ πàÕß·≈–¢âÕ‡∑â“ ®–∫Õ°‰¥â§√à“« Ê «à“ À≈Õ¥ ‡≈◊Õ¥·¥ß∫√‘‡«≥„¥∑’¡Ë °’ “√µ’∫µ—π §«“¡¥—π´’ ‚µ≈‘§¢Õß ¢“∑’µË Ë”°«à“ 55 ¡‘≈≈‘‡¡µ√ª√Õ∑ ·≈– pulse-volume recording amplitude πâÕ¬°«à“ 5-10 ¡‘≈≈‘‡¡µ√ ∫àß∂÷ß limb threatening condition ·º≈√— ° …“‰¡à À “¬ §«√æ‘®“√≥“ºà“µ—¥·°â ‰¢(7,8) °“√·ª√º≈Õ“®®–º‘¥æ≈“¥ ∂â“„™â«∏‘ °’ “√π’°È ∫— À≈Õ¥‡≈◊Õ¥·¥ß∑’·Ë ¢Áß ¡’ arterial calcification „π‚√§‡∫“À«“π ®÷ß§«√„™â‡©æ“– Aire pl-

161 ethysmography (pulse-volume recording) 4. Duplex scanning „™â ‰¥âº≈¥’„π°“√«‘π®‘ ©—¬°“√Õÿ¥µ—π ¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß iliac, femoral ·≈– popliteal °àÕπ ∑’Ë®–æ‘®“√≥“∑” invasive studies µàÕ‰ª „πªí®®ÿ∫—π „™â‡ªìπ color duplex scanning “¡“√∂∫àß∫Õ°∂÷ß degree „π°“√µ’∫·§∫¢ÕßÀ≈Õ¥‡≈◊Õ¥‰¥â πÕ°®“°π’È¬—ß “¡“√∂„™âª√–‡¡‘πÀ≈Õ¥‡≈◊Õ¥¥” saphenous ∑’¢Ë “ ´÷ßË ®–π”¡“„™â‡ªìπ interposition graft ”À√—∫„π°“√∑” bypass µàÕ‰ª‰¥â 5. Arteriography ‡ªìπ«‘∏°’ “√µ√«®«‘π®‘ ©—¬∑’∫Ë ßà ∫Õ°√Õ¬ ‚√§·≈–‡æ◊ÕË ‡ªìπ°“√ª√–‡¡‘π«‘∏°’ “√ºà“µ—¥√—°…“ §«√®–‡√‘¡Ë ¥Ÿµ—Èß·µà infra renal aorta ≈ß¡“®π∂÷ßÀ≈Õ¥‡≈◊Õ¥ ª≈“¬‡∑â“ (√Ÿª∑’Ë 17.2) magnetic resonance arteriography (MRA) ‡ªìπ«‘∏’°“√µ√«®«‘π‘®©—¬∑’Ë¥’Õ—πÀπ÷Ëß “¡“√∂¡Õß‡ÀÁπ distal arteries ‰¥â™¥— ‡®π‚¥¬‰¡àµÕâ ß ©’¥ “√∑÷∫· ßºà“π‡¢â“À≈Õ¥‡≈◊Õ¥

√Ÿª∑’Ë 17.2 Arteriogram ¢ÕßÀ≈Õ¥‡≈◊Õ¥∑’Ë¢“ ®“°“√ Õ¥ “¬ «π ºà“π femoral artery ·≈–©’¥ “√∑÷∫· ß æ∫«à“¡’°“√ Õÿ¥µ—π¢Õß superficial femoral artery à«π middle 1/ 3 ·µà¡’ collaterals ®“° profunda femoris ≈ß¡“∂÷ß popliteal artery

162

°“√√—°…“ ºŸªâ «É ¬ femoropliteal stenosis ∑’Ë ‰¡à¡Õ’ “°“√Õ–‰√ ‰¡à®”‡ªìπ µâÕßºà“µ—¥√—°…“ §«√®–æ¬“¬“¡§«∫§ÿ¡ªí®®—¬‡ ’¬Ë ß¢ÕßºŸªâ «É ¬¥—ßπ’È ‡™àπ ß¥ Ÿ∫∫ÿÀ√’Ë §ÿ¡Õ“À“√ ·≈–°“√ÕÕ°°”≈—ß°“¬∑’Ë‡À¡“– ¡ ºŸâªÉ«¬‡À≈à“π’È ¿“¬„π 5 ªï Õ“°“√ IC ®–¥’¢÷Èπ√âÕ¬≈– 10-15 Õ“°“√§ß‡¥‘¡√âÕ¬≈– 60-70 µâÕßºà“µ—¥√—°…“À√◊Õµ—¥¢“‡æ’¬ß√âÕ¬≈– 15-30(2,7) ºŸªâ «É ¬∑’§Ë «√æ‘®“√≥“∑”°“√ºà“µ—¥√—°…“À√◊Õ¢¬“¬∂à“ßÀ≈Õ¥ ‡≈◊Õ¥ §«√¡’¢Õâ ∫àß™’¥È ß— µàÕ‰ªπ’È ∂â“‰¡à¡ª’ ®í ®—¬‡ ’¬Ë ßµàÕ°“√ºà“µ—¥ ‡™àπ ‚√§ªÕ¥À√◊ÕÀ—«„®∑’√Ë πÿ ·√ß(8,9) 1. ¡’ disabling claudication ‡¥‘π‰¥â√–¬–‰¡à ‰°≈ 2. ¡’ ischemic rest pain, ·º≈‡√◊ÕÈ √—ß‰¡àÀ“¬ ·≈– gangrene

°“√√—°…“‚¥¬‰¡àºà“µ—¥ ”À√—∫ºŸªâ «É ¬ Intermittent claudication ∑’ Ë ”§—≠§◊Õ ß¥ °“√ Ÿ∫∫ÿÀ√’Ë ÕÕ°°”≈—ß°“¬·≈–°“√„™â¬“ 1. ß¥°“√ Ÿ∫∫ÿÀ√’Ë °“√ Ÿ∫∫ÿÀ√’¡Ë º’ ≈¡“°µàÕ‚√§À≈Õ¥‡≈◊Õ¥ ‚¥¬‡©æ“– femoropopliteal stenosis °“√ Ÿ∫∫ÿÀ√’¡Ë ’ º≈∑”„ÀâÀ≈Õ¥‡≈◊Õ¥À¥µ—«‡æ‘Ë¡√–¥—∫§“√å∫Õπ¡ÕππÕ° ‰´¥å „π‡≈◊Õ¥ ‡°‘¥ atherosclerosis ¢ÕßÀ≈Õ¥‡≈◊Õ¥‡√Á« ¢÷πÈ °“√∑”ß“π¢Õß‡°√Á¥‡≈◊Õ¥‡¡µ“‚∫≈‘ ¡å¢Õß‰¢¡—π ·≈– ª√– ‘∑∏‘¿“æ¢Õß‡ÕÁπ‚¥∑’‡≈’¬Ë ¡®–≈¥≈ß(10) °“√ß¥ Ÿ∫ ∫ÿÀ√’®Ë –∑”„ÀâÕ“°“√¢Õß IC ¥’¢π÷È „π√“¬∑’ºË “à µ—¥·≈â« graft patency ®– Ÿß¢÷πÈ ‚Õ°“ µ—¥¢“∑‘ßÈ ¡’πÕâ ¬≈ß(11) 2. °“√ÕÕ°°”≈—ß°“¬Õ¬à“ß ¡Ë”‡ ¡Õ „πºŸªâ «É ¬ IC ®–™à«¬ „Àâ√–¬–∑“ß„π°“√‡¥‘π·≈â«‰¡àª«¥¢“‡æ‘Ë¡¡“°¢÷Èπ °“√ ÕÕ°°”≈—ß°“¬®–™à«¬‡æ‘¡Ë collaterals ∑”„Àâ°≈â“¡‡π◊ÕÈ ¡’ ª√– ‘∑∏‘¿“æ¡“°¢÷πÈ „π°“√¥÷ßÕäÕ°´‘‡®π®“°‡≈◊Õ¥(12,13) 3. °“√„™â¬“ æ∫«à“°“√„Àâ¬“¢¬“¬À≈Õ¥‡≈◊Õ¥ ‡™àπ prostaglandins ‰¡à¡’º≈∑”„ÀâÕ“°“√ IC ¢ÕßºŸâªÉ«¬‚√§ À≈Õ¥‡≈◊Õ¥·¥ßµ’∫µ—π‡√◊ÕÈ √—ß¥’¢π÷È ¡’¬“‡æ’¬ßµ—«‡¥’¬«´÷ßË ‡ªìπ hemorrheologic agent „™â ‰¥âº≈§◊Õ Pentoxifylline ®–™à«¬„ÀâÕ“°“√ IC ¥’¢π÷È ‚¥¬≈¥°“√‡°“–µ—«®—∫°≈ÿ¡à ¢Õß ‡°√Á¥‡≈◊Õ¥ ·≈–™à«¬„Àâ RBC ‡ª≈’¬Ë π√Ÿª√à“ß≈—°…≥–‰¥â¥’ “¡“√∂π”‡Õ“ “√Õ“À“√·≈–ÕäÕ°´‘‡®πºà“πÀ≈Õ¥‡≈◊Õ¥ ΩÕ¬‰ª‡≈’¬È ß‡π◊ÕÈ ‡¬◊ÕË à«πª≈“¬‰¥â¥¢’ π÷È (14) °“√∫√‘À“√¬“ ∑’Ë‰¥âº≈§◊Õ√—∫ª√–∑“πµàÕ‡π◊ÕË ß„π√–¬–‡«≈“‰¡àµË”°«à“ 6-8

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥ —ª¥“Àå ∂â“‰¡à ‰¥âº≈§«√À¬ÿ¥¬“ Pentoxifylline ‰¡à ‰¥âº≈ „π°“√√—°…“ rest pain, ischemic ulcer ·≈– gangrene

°“√√—°…“‚¥¬À—µ∂°“√ 1. Angioplasty ‚¥¬«‘∏’ Percutaneous transluminal angioplasty (PTA) ‡ªìπ«‘∏°’ “√¢¬“¬À≈Õ¥‡≈◊Õ¥·¥ß ‚¥¬ «π «πºà“πº‘«Àπ—ß‡¢â“ ŸàÀ≈Õ¥‡≈◊Õ¥ ·≈–„™â∫—≈≈Ÿπ ¢¬“¬∂à“ß à«π∑’Ëµ’∫·§∫ ‰¥âº≈¥’ „πÀ≈Õ¥‡≈◊Õ¥∑’Ëµ’∫ ·§∫§«“¡¬“«‰¡à¡“° ‚¥¬‡©æ“–À≈Õ¥‡≈◊Õ¥·¥ß iliac ∑’µË ∫’ ·§∫§«“¡¬“«‰¡à‡°‘π 3 ‡´Áπµ‘‡¡µ√ ¡’ good runoff ®–æ∫ 5-year patency rates Ÿß∂÷ß√âÕ¬≈– 70 ”À√—∫À≈Õ¥‡≈◊Õ¥·¥ß femoral ·≈– popliteal ‰¥âº≈¥’ √Õß≈ß¡“§◊Õ¡’ 5-year patency rate √âÕ¬≈– 17-68 (√Ÿª∑’Ë 17.3) PTA ¡’¢Õâ ¥’°«à“°“√ºà“µ—¥§◊Õ ‰¡àµÕâ ß¥¡¬“ ≈∫ æ—° Õ¬Ÿà „π‚√ßæ¬“∫“≈‰¡àπ“π §à“„™â®“à ¬‰¡à ßŸ Õ—µ√“µ“¬·≈– Õ—µ√“‡ ’Ë¬ßπâÕ¬°«à“°“√ºà“µ—¥ §«√∑”‚¥¬√—ß ’·æ∑¬å∑’Ë¡’ §«“¡™”π“≠ 2. Femoropopliteal ·≈– femoro distal bypasses ºŸâ ªÉ«¬∑’ÕË ¬Ÿà „π ¿“«– limb-threatening ·≈–¡’Õ“°“√¥—ßµàÕ ‰ªπ’§È Õ◊ disabling claudication, rest pain ·≈– gangrene §«√æ‘®“√≥“∑”°“√ºà“µ—¥√—°…“(15) ‚¥¬°“√∑” femoro popliteal bypass À√◊Õ∂â“À≈Õ¥‡≈◊Õ¥·¥ß popliteal Õÿ¥µ—πÕ“®®–∑” bypass ®“° femoral artery µàÕ≈ß‰ª∂÷ßÀ≈Õ¥‡≈◊Õ¥·¥ß∑’ËÕ¬ŸàµË”°«à“ popliteal arteries ∫√‘‡«≥¢âÕ‡∑â“ (√Ÿª∑’Ë 17.4) À≈Õ¥‡≈◊Õ¥‡∑’¬¡ ∑’Ë „™â§Õ◊ autogenous vein graft ®“° saphenous À√◊Õ caphalic vein ·≈– polytetrafluoroethylene graft(16) „π¿“«– threatened limb loss ∂â“∑” femoropopliteal bypass ®–¡’ 5-year patency rates √âÕ¬≈– 75-80 ·≈– limb salvage rates √âÕ¬≈– 85-90 ·≈–‰¡àæ∫«à“¡’ limb loss (√Ÿª∑’Ë 17.4) À≈Õ¥‡≈◊Õ¥‡∑’¬¡∑’Ë„™â „π°“√∑” bypass ∑’Ë ‰¥âº≈¥’∑ ’Ë ¥ÿ §◊Õ autogenous vein graft ‰¡à«“à ®–‡ªìπ°“√µàÕ‡Àπ◊Õ À√◊ÕµË”°«à“√–¥—∫À—«‡¢à“ º≈°“√ºà“µ—¥¥’‡√’¬ß°—πµ“¡ ≈”¥—∫¥—ßπ’È greater saphenous vein, arm veins, cephalic vein À√◊Õ lesser saphenous vein

163

FEMORO-POPLITEAL-OCCLUSIVE DISEASE

√Ÿª∑’Ë 17.3 °. Stenosis ¢Õß left common iliac artery ¢. left common iliac artery ¢π“¥‚µ¢÷πÈ À≈—ß¢¬“¬∂à“ß ¥â«¬∫—≈≈Ÿπ §. Percutaneous Transluminal Angioplasty (PTA) ¢Õß superficial femoral artery ∑’Ëµ’∫·§∫ºà“π∑“ß common femoral artery ß. PTA ¢Õß superficial femoral artery ºà“π∑“ß popliteal artery

164

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥ √Ÿª∑’Ë 17.4 °“√ºà“µ—¥√—°…“À≈Õ¥‡≈◊Õ¥∑’¢Ë “µ’∫·§∫À≈“¬µ”·Àπàß§◊Õ∑’Ë superficial femoral artery ·≈– distal arteries (tibioperoneal) ‚¥¬«‘∏’°“√ °. sequential bypasses ®“° femoropopliteal ·≈– popliteal distal bypass ¢. femoro distal bypass

µ“√“ß∑’Ë 17.1 ‡ª√’¬∫‡∑’¬∫¢âÕ¥’·≈–¢âÕ‡ ’¬√–À«à“ß°“√„™â Reversed, In-situ ·≈– Nonreversed translocated vein grafts Grafts

«‘∏°’ “√ºà“µ—¥ ”À√—∫ femoro-popliteal ·≈– femorotibial bypass ∑’Ë‰¥âº≈„π°“√√—°…“∑’¥Ë §’ Õ◊ saphenous vein in-situ technique(17) ‚¥¬ Leather ·≈–§≥– «‘∏π’ ’È ‰¡à µâÕß‡≈“–‡Õ“ saphenous vein ÕÕ°·≈â« π”¡“µàÕ °≈—∫¥â“π‡æ◊ÕË ∑” bypass (µ“√“ß∑’Ë 17.1) ª≈àÕ¬ saphenous vein ‡Õ“‰«â „π·π«‡¥‘¡∑’¢Ë “ Õ¥ vulvulotome ºà“π‡¢â“À≈Õ¥‡≈◊Õ¥ µ—¥ valves ºŸ° tributaries vein ·µàµÕà saphenous vein à«πµâπ‡¢â“°—∫ femoral artery ·≈–∑“ß à«πª≈“¬‡¢â“°—∫ popliteal À√◊Õ tibio-peroneal arteries æ∫«à“¢π“¥¢ÕßÀ≈Õ¥‡≈◊Õ¥¥”∑’µË Õà ®–¡’¢π“¥ æÕ¥’°—π°—∫À≈Õ¥‡≈◊Õ¥·¥ß (√Ÿª∑’Ë 17.5) ‡π◊ËÕß®“°‰¡à µâÕß‡≈“–µ—¥À≈Õ¥‡≈◊Õ¥ÕÕ° °“√‡ ◊ÕË ¡ ¿“æ¢Õß autogerous vein ®–πâÕ¬ «‘∏°’ “√π’æÈ ∫«à“¡’ 3 year patency rates Ÿß√âÕ¬≈– 80-90(17)

Reversed

In-situ

¢âÕ¥’ ‰¡àµÕâ ß∑” vulvulotume ´÷ßË ®–∑”„ÀâÀ≈Õ¥‡≈◊Õ¥™È” „™âÀ≈Õ¥‡≈◊Õ¥®“°¢“ ¥â“πµ√ß¢â“¡ µàÕÀ≈Õ¥‡≈◊Õ¥ßà“¬°«à“ √â“ß tunnel „À¡à „ÀâÀ≈Õ¥ ‡≈◊Õ¥ºà“π‰¥â≈°÷ „µâº«‘ Àπ—ß No size mismatch ≈¥ ischemic time À≈Õ¥‡≈◊Õ¥‰¡à™È”¡“°

Nonreversed No size mismatch translocated ! ‡¬Á∫µàÕÀ≈Õ¥‡≈◊Õ¥ saphenous ‰¥âß“à ¬ vein

¢âÕ‡ ’¬ µ—¥ vasa vasorum ∑”„Àâ‡°‘¥ ischemia Size mismatch

‡°‘¥ vulvulotome trauma Vein graft Õ¬Ÿµà π◊È „µâ º‘«Àπ—ßµàÕ¬“°‡π◊ÕË ß®“° À≈Õ¥‡≈◊Õ¥Õ¬Ÿ°à ∫— ∑’Ë ‡§≈◊ÕË π¡“°‰¡à ‰¥â µ—¥ vasa vasorum ∑”„Àâ‡°‘¥ ischemia ‡°‘¥ vulvutome trauma

* Size mismatch À¡“¬∂÷ß §«“¡·µ°µà“ß√–À«à“ß¢π“¥¢ÕßÀ≈Õ¥‡≈◊Õ¥ ·¥ß·≈–À≈Õ¥‡≈◊Õ¥¥”∑’µË Õà ‡¢â“À“°—π ¡’¢π“¥‰¡àæÕ¥’ ‡π◊ÕË ß®“°‚µ°«à“°—π¡“°

165

FEMORO-POPLITEAL-OCCLUSIVE DISEASE

End-to-side anastomosis Valve incision Saphenous vein Tied

Femoral artery

Distal popliteal artery

End-to-side anastomosis saphenous vein

√Ÿª∑’Ë 17.5 ‡∑§π‘§°“√ºà“µ—¥ In Situ saphenous femoropopliteal ·≈– tibial bypass grafting

°. ≈ß¡’¥ºà“µ—¥‡¢â“∂÷ß greater saphenous vein à«πµâπ∫√‘‡«≥¢“Àπ’∫·≈– à«πª≈“¬∫√‘‡«≥¢âÕ‡∑â“¥â“π„π ¢. ‰¡àµâÕß‡≈“– saphenous vein ÕÕ° Õ¥ vulvulotume ºà“πÀ≈Õ¥‡≈◊Õ¥‡æ◊ËÕµ—¥ valves §. ºŸ°·¢πßµà“ß Ê ¢Õß saphenous vein ªÑÕß°—π°“√‡°‘¥ arterio venous fistula µàÕÀ≈Õ¥‡≈◊Õ¥¥” à«π µâπ°—∫ common À√◊Õ superficial femoral artery à«πª≈“¬µàÕ°—∫ popliteal À√◊Õ tibio-peroneal arteries ß. “¡“√∂µàÕÀ≈Õ¥‡≈◊Õ¥¥”‡¢â“°—∫À≈Õ¥‡≈◊Õ¥·¥ß à«πª≈“¬∑’ËÕ¬ŸàµË”°«à“¢âÕ‡∑â“

√ÿª ·π«∑“ß°“√√—°…“ ºŸªâ «É ¬‚√§À≈Õ¥‡≈◊Õ¥·¥ßµ’∫·§∫∫√‘‡«≥ femoropopliteal-tibial ‡™àπ‡¥’¬«°—π°—∫ aortoiliac occlusive diseases (AIOD) §◊Õ‡√‘¡Ë ®“°°“√ÕÕ°°”≈—ß°“¬‡æ◊ÕË ‡æ‘¡Ë collaterals ß¥ Ÿ∫∫ÿÀ√’Ë ≈¥ªí®®—¬‡ ’¬Ë ßµàÕ°“√µ’∫·§∫¢ÕßÀ≈Õ¥‡≈◊Õ¥ ·≈–„Àâ¬“√—∫ª√–∑“π ®–ºà“µ—¥µàÕ‡¡◊ÕË ¡’¢Õâ ∫àß™’∑È ·’Ë πàπÕπ§◊Õ disabling claudication ·≈– ischemic rest pain À√◊Õ gangrene °àÕπºà“µ—¥√—°…“À≈Õ¥‡≈◊Õ¥∑’µË ∫’ ·§∫µË”°«à“ inguinal ligament §«√·°â ‰¢§«“¡º‘¥ª°µ‘¢Õß AOID °àÕπ ·π«∑“ß°“√√—°…“∑“ß À—µ∂°“√Õ“®®–‡√‘Ë¡µâπ®“° PTA ®π°√–∑—Ëß bypass grafting „πªí®®ÿ∫π— “¡“√∂∑” distal bypass µàÕ≈ß‰ª®π∂÷ßÀ≈Õ¥‡≈◊Õ¥ ·¥ß∑’ÕË ¬Ÿµà Ë”°«à“¢âÕ‡∑â“ ‚¥¬«‘∏’ In Situ saphenous vein bypass grafting ®÷ß∑”„Àâº≈°“√√—°…“·≈–°“√æ¬“°√≥å‚√§¥’¡“°¢÷πÈ

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‡Õ° “√Õâ“ßÕ‘ß 1. Boyd AM. The natural course of arteriosclerosis of the lower extremities. Proc Roy Soc Med 1962;55:591-597. 2. Imparato AM. Intermittent claudication: Its natural course. Surgery 1975;78:795-781. 3. Goodreau JJ. Rational approach to the differentiation of vascular and neurogenic claudication. Surgery 1978;84:749-756. 4. Kavanaugh GJ, Svien HJ, Holman CB, Johnson RM, et al. çPseudo claudicationé syndrome produced by compression of the cauda equina. JAMA 1968;206:2477-2483. 5. Calligaro KD, Veith FJ. Proper technique of lower extremity pulse examination. Contemp Surg 1992;40:49-55. 6. Cooperman M, Pflug B, Martin EWJr, Evans WE. Cardiovascular risk factors in patients with peripheral vascular disease. Surgery 1978;84:505-509. 7. Hughson WG, Mann JI, Garrod A. Intermittent claudication: Prevalence and risk factors. Br Med J 1978;1:1379-1386. 8. DeWeese JA, Leather R, Porter J. Practice guidelines: lower extremity revascularizations. J Vasc Surg 1993;18:280-294. 9. Goldsmith J, Franco D, Farrel EA, et al. Advances in the surgical treatment of lower extremity disease. J Am Acad Phys Assist 1991;4:481-487. 10. Lithe IIH, Hedstrand H, Karlsson R. The Smoking habits of men with intermittent claudication. Acta Med Scand 1975;197:473-481.

11. Quick CRG, Cotton LT. The measured effect of stopping smoking on intermittent claudication. Br J Surg 1982;69:524. 12. Dahlloff AG. Peripheral arterial insufficiency: Effect of physical training on walking tolerance, calf blood flow and blood flow resistance. Scan J Rehabil Med 1976;8:19-26. 13. Ekroth R. Physical training of patients with intermittent claudication:Indications, methods and results. Surgery 1978;84:640648. 14. Porter JM. Pentoxifylline efficacy in the treatment of intermittent claudication: Multicenter controlled double-blind trial with objective assessment of chronic occlusive arterial disease patients. Am Heart J 1982;104:66-74. 15. Hobson RW II. Results of revascularization and amputation in severe lower extremity ischemia: A five-year clinical experience. J Vasc Surg 1985;2:174-180. 16. Quinones-Baldrich WJ. Long-term results of infrarenal revascularization with polytetrafluoroethylene: A ten-year experience. J Vasc Surg 1992:16:209-215. 17. Wengerter KR. Prospective randomized multicenter comparison of in situ and reversed vein infrapopliteal bypass. J Vasc Surg 1991;13:189-196.

∫∑∑’Ë 18 Buergerûs disease (Thromboangitis Obliterans) ‚√§π’È√“¬ß“π§√—Èß·√°‚¥¬ Buerger „πªï 1908(1) æ∫«à“ ‡ªìπ°“√Õ—°‡ ∫¢ÕßÀ≈Õ¥‡≈◊Õ¥µ“¡¡“¥â«¬°“√µ’∫·§∫ ®–¡’ ≈—°…≥–·≈–Õ“°“√· ¥ß‡ªìπ·∫∫ çpresenile spontaneous gangreneé ¡’°“√À¥µ—«·≈–‡æ‘Ë¡®”π«π‡´≈≈å „π™—Èπ intima ¡“°¡“¬ æ∫„πºŸªâ «É ¬‡æ»™“¬Õ“¬ÿµË”°«à“ 50 ªï ·≈– Ÿ∫∫ÿÀ√’®Ë ¥— Wessler ·≈–§≥– ‰¥âÕ∏‘∫“¬Õ“°“√∑“ß§≈‘π§‘ ¢Õß‚√§π’È „πªï 1960 µàÕ¡“‰¥â√«∫√«¡Õ“°“√·≈–Õ“°“√· ¥ß‡©æ“–‰«â‡æ◊ËÕ°“√«‘π‘®©—¬‚√§(2) æ∫¡“°„πª√–™“°√·∂∫‡Õ‡´’¬°≈“ß·≈–µ–«—πÕÕ° ¡“°°«à“„π¬ÿ‚√ª·≈–Õ‡¡√‘°“(3,4,5) „π≠’ËªÿÉπæ∫ 5/100,000 ¢Õß ®”π«πª√–™“°√∑—ßÈ À¡¥(6) “‡Àµÿ∑·’Ë ∑â®√‘ß¢Õß‚√§ Buergerûs À√◊Õ Thromboangiitis Obliterans (TAO) ¬—ß‰¡à∑√“∫·πàπÕπ ‡°’Ë¬«¢âÕß°—∫°“√ Ÿ∫ ∫ÿÀ√’Ë‡™àπ‡¥’¬«°—π°—∫‚√§À≈Õ¥‡≈◊Õ¥·¥ß à«πª≈“¬∑—Ë«‰ª °“√ Ÿ∫ ∫ÿÀ√’Ë∑”„ÀâÕ“°“√¢Õß‚√§‡ªìπ¡“°¢÷Èπ·≈–¡’ ‚Õ°“ ‡°‘¥‡ªìπ´È”‰¥â Õ’°À≈—ß®“°À“¬·≈â«(7) ºŸ∑â ‡’Ë ªìπ passive smoker °Á®–æ≈Õ¬‰¥â√∫— º≈°√–∑∫®“°§«—π∫ÿÀ√’∑Ë ”„Àâ‡ªìπ‚√§π’È ‰¥â‡™àπ°—π °“√«—¥√–¥—∫¢Õß cotinine ´÷Ëß‡ªìπ metabolite ¢Õß nicotin „πªí “«–®–∫àß ∫Õ°∂÷ß√–¥—∫¡“°πâÕ¬„π°“√ Ÿ∫·≈– —¡º— µàÕ§«—π∫ÿÀ√’Ë∑—ßÈ ºŸ â ∫Ÿ ·≈– passive smoker(8) ºŸªâ «É ¬·∂∫‡Õ‡´’¬µ–«—πÕÕ°®–‡ªìπºŸâ „™â·√ßß“π °≈“ß·®âß ∞“π–∑“ß‡»√…∞°‘®µË” ¡’¿“«–‡≈◊Õ¥·¢Áßµ—«ßà“¬º‘¥ª°µ‘ (9-12) Õ“®®–‡°’¬ Ë «¢âÕß°—∫‚√§ rickettsiosis, hepatitis B virus À√◊Õ‚√§∑“ßÕ‘¡¡Ÿπ(7,13,14)

√Õ¬‚√§∑“ßæ¬“∏‘ TAO ‡ªìπ inflammatory occlusive disease ∑’‡Ë °‘¥¢÷πÈ °—∫ À≈Õ¥‡≈◊Õ¥¥”·≈–À≈Õ¥‡≈◊Õ¥·¥ß¢π“¥°≈“ß∫√‘‡«≥·¢π¢“ °“√Õ—°‡ ∫π’®È –≈ÿ°≈“¡‰ª∂÷ß‡ âπª√– “∑¢â“ß‡§’¬ß‰¥â‡™àπ°—π(9,12,14,15) ‡√“·∫àßæ¬“∏‘ ¿“æ¢Õß TAO ÕÕ°‰¥â‡ªìπ 1. Early stage À≈Õ¥‡≈◊Õ¥∑’µË ∫’ ·§∫®–∫«¡µ÷ß ¡’°“√Õ—°‡ ∫ ∑ÿ°™—πÈ À≈Õ¥‡≈◊Õ¥·¥ß·∫∫ panvasculitis ¡’°“√∫«¡πÈ” ¿“¬„π √ŸÀ≈Õ¥‡≈◊Õ¥®–¡’ fresh thrombus Õÿ¥Õ¬Ÿ´à ß÷Ë „π thrombus π’®È –¡’ focal infiltration °√–®“¬Õ¬Ÿ∑à «—Ë ‰ª ¿“¬„π®–ª√–°Õ∫¥â«¬ multinucleated giant cells, epithelioide cells ·≈– leukocytes „π√Ÿª¢Õß microabscesses ¡’ lymphocytes ·≈– fibroblasts ·∑√°Õ¬Ÿà „π™—πÈ media ·≈– adventitia ·µà ‰¡àæ∫ necrotizing lesion ¿“¬„π™—πÈ media æ∫«à“ª√‘¡“≥¢Õß‡´≈≈å „π™—πÈ intima ‡æ‘¡Ë ¢÷πÈ ‡≈Á°πâÕ¬ ·µà¬ß— æ∫ internal elastic membrane granulomatous reaction °—∫ giant cells „π thrombus π’®È –æ∫·µà „π TAO ‡∑à“π—πÈ ‰¡àæ∫„π arteriosclerosis obliterans À√◊Õ simple thrombosis ®–‡ÀÁπµ”·Àπàß¢ÕßÀ≈Õ¥‡≈◊Õ¥ ª°µ‘ ≈—∫°—∫À≈Õ¥‡≈◊Õ¥∑’ÕË °— ‡ ∫‡ªìπ™à«ß Ê(16-18) ‰¡à¡’ disruption ¢Õß internal elastic lamina À√◊Õ fibrinoid necrosis ‡À¡◊Õπ°—∫∑’æË ∫„π necrotizing vasculitis 2. Subacute stage ª√‘¡“≥¢Õß‡´≈≈å·≈–°“√‡°‘¥ microabscess ®–≈¥≈ß ‡√‘¡Ë ¡’ recanalization ¢Õß thrombus

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3. Late stage æ∫«à“À≈Õ¥‡≈◊Õ¥∑’ÕË ¥ÿ µ—π®–À¥µ—«·≈–§≈” ‰¥â‡ªìπ™à«ß Ê §≈”‰¥â‡ªìπ≈”·¢Áß„µâº‘«Àπ—ß∑—ÈßÀ≈Õ¥‡≈◊Õ¥¥”·≈– À≈Õ¥‡≈◊Õ¥·¥ß ∂â“‡ªìππ“π®–‡√‘¡Ë ¡’ recanalization ¢Õß thrombus ¡’ fibrous thickening ¢Õß™—πÈ intima æ∫ fibrous tissue ¡“°¡“¬„π™—πÈ media ·≈– adventitia internal elastic membrane ∂Ÿ°∑”≈“¬·µ° ≈“¬·µà√Ÿª∑√ß¢ÕßÀ≈Õ¥‡≈◊Õ¥¬—ß§ß‡ªìπ ª°µ‘ ≈—°…≥–∑“ßæ¬“∏‘«‘∑¬“∑’Ë‡°‘¥¢÷Èππ’È®–æ∫∑—Èß„πÀ≈Õ¥‡≈◊Õ¥ ¥”·≈–À≈Õ¥‡≈◊Õ¥·¥ß ‡°‘¥ fibrosis „πÀ≈Õ¥‡≈◊Õ¥¥”·≈– À≈Õ¥‡≈◊Õ¥·¥ß

Õ“°“√·≈–Õ“°“√· ¥ß∑“ß§≈‘π‘§ Õ“°“√‡√‘Ë¡µâπ∑’Ëæ∫‰¥â∫àÕ¬§◊Õ ª«¥· ∫ª«¥√âÕπµ“¡ª≈“¬ ¡◊Õª≈“¬‡∑â“ ¡’ rest pain ¡’·º≈·≈–°“√‡πà“µ“¬¢Õßº‘«Àπ—ß ·≈–‡π◊ÈÕ‡¬◊ËÕ∑’Ëª≈“¬π‘È«¡◊Õπ‘È«‡∑â“ ´÷Ëß‡®Á∫ª«¥∑√¡“π¡“° ª≈“¬ π‘«È ‡¬Áπ¡’ mottling ·≈– rubor (√Ÿª∑’Ë 18.1) (µ“√“ß∑’Ë 18.1) æ∫¡’ foot claudication À≈—ß°“√‡¥‘πÀ√◊ÕÕÕ°°”≈—ß°“¬ ‡°‘¥®“°

µ“√“ß∑’Ë 18.1 Õ“°“√·≈–Õ“°“√· ¥ß¢ÕßºŸªâ «É ¬ TAO Burning pain on foot and hand Intermittent claudication Chronic ulceration of toe finger Digital gangrene Raynaudûs phenomenon Superficial thrombophlebitis

74.8% 59.8% 53.3% 36.4% 48.6% 10.3%

®“°°“√»÷°…“ºŸâªÉ«¬ 107 √“¬ ‡æ»™“¬ 106 √“¬ ‡æ»À≠‘ß 1 √“¬ ™à«ßÕ“¬ÿ 25-40 ªï π“¬·æ∑¬å√–«’ æ‘¡≈»“πµå ‚√ßæ¬“∫“≈»‘√‘√“™

À≈Õ¥‡≈◊Õ¥·¥ßÕÿ¥µ—π„πµ”·Àπàß∑’ËÕ¬ŸàµË”°«à“ popliteal artery ∂â“‡ªìπ calf claudication À≈Õ¥‡≈◊Õ¥·¥ß∑’ÕË ¥ÿ µ—π®–Õ¬Ÿ à ßŸ °«à“ popliteal artery æ∫«à“¡’ digital gangrene √à«¡¥â«¬‡ ¡Õ ºŸâ ªÉ«¬¡’ Raynaudûs phenomenen √à«¡°—∫ paresthesia ¡—°®– ‡ªìπ¡“°°«à“ 2 extremities ‡ªìπ∑’¢Ë “‰¥â∫Õà ¬°«à“∑’·Ë ¢π(9,15,19) °“√„™â Fontaine stepwise classfication ∑’Ë „™â°—∫‚√§ ¢“¢“¥‡≈◊Õ¥®“°‡≈◊Õ¥µ’∫µ—π arteriosclerosis obliterans „™â ‰¡à ‰¥â°∫— TAO ‡æ√“–°“√‡°‘¥·º≈‡√◊ÕÈ √—ß·≈–‡π◊ÕÈ ‡¬◊ÕË ‡πà“µ“¬ª≈“¬ π‘«È ¡◊Õπ‘«È ‡∑â“ Õ“®®–‡°‘¥¢÷πÈ °àÕπ claudication venous filling time ¢Õß‡∑â“®–π“π‡°‘π°«à“ 20 «‘π“∑’(20) recurrent superficial thrombophlebitis æ∫‰¥â∑¢’Ë “ ‡∑â“ ·≈–·¢π ®–‡ÀÁπº‘«Àπ—ß‡ªìπªóôπ·¥ß °¥‡®Á∫µ“¡·π«¢ÕßÀ≈Õ¥ ‡≈◊Õ¥¥” Õ“°“√Õ—°‡ ∫¢ÕßÀ≈Õ¥‡≈◊Õ¥¥”®–À“¬‡Õß¿“¬„π 2-3 —ª¥“ÀåÀ≈—ß®“°π—Èπº‘«Àπ—ß∫√‘‡«≥π—Èπ®–¡’ ’§≈È”≈ß phlebitis migranes ‡ªìπ pathognomonic sign Õ—πÀπ÷ßË ∑’ Ë ”§—≠¢Õß TAO à«π„À≠à·≈â«ºŸªâ «É ¬®– —ß‡°µÿ‡Õß‰¡àæ∫ À√◊Õ‰¡à ‰¥â‡Õ“„®„ à Õ—µ√“ à«π¢Õß‚√§√–À«à“ß‡æ»™“¬°—∫‡æ»À≠‘ßª√–¡“≥ 98:2 ·¡â«à“ ‡æ»À≠‘ß®– Ÿ∫∫ÿÀ√’¡Ë “°¢÷πÈ „πªí®®ÿ∫π— (6,9) ∫“ß√“¬ß“πæ∫«à“¡’‡æ» À≠‘ß Ÿß∂÷ß√âÕ¬≈– 16-18(21)

°“√«‘π‘®©—¬‚√§

√Ÿª∑’Ë 18.1 °“√Õÿ¥µ—π¢ÕßÀ≈Õ¥‡≈◊Õ¥ superficial femoral à«πª≈“¬ „πºŸâªÉ«¬ TAO ‡ÀÁπ collaterals (cock screw) ‡°‘¥¢÷Èπ √Õ∫ Ê À≈Õ¥‡≈◊Õ¥∑’ËÕÿ¥µ—π

Shionoya ‰¥â«“ß·π«∑“ß„π°“√«‘π®‘ ©—¬‚√§ TAO ∑“ß§≈‘π§‘ ‰«â¥ß— µàÕ‰ªπ’È (9,16,17) 1. ‡æ»™“¬ Ÿ∫∫ÿÀ√’®Ë ¥— 2. ‡°‘¥Õ“°“√§√—ßÈ ·√°‡¡◊ÕË Õ“¬ÿπÕâ ¬°«à“ 50 ªï 3. À≈Õ¥‡≈◊Õ¥∑’ÕË ¥ÿ µ—πÕ¬Ÿµà Ë”°«à“ popliteal artery 4. æ∫ phlebitis migranes ¢ÕßÀ≈Õ¥‡≈◊Õ¥¥”∑’·Ë ¢π·≈– ¢“

169

Buergerûs disease (Thromboangitis Obliterans) µ“√“ß∑’Ë 18.2 °“√‡ª√’¬∫‡∑’¬∫°—π√–À«à“ß Thromboangiitis Obliterans °—∫ Arteriosclerosis Obliterans TAO Õ“¬ÿ µ”·Àπàß√Õ¬‚√§

™à«ßÕ“¬ÿ 25-50 ªï ª≈“¬π‘«È ‡∑â“ ‡∑â“ ¡◊Õ ª≈“¬π‘«È ¡◊Õ ‡°’¬Ë «¢âÕß°—∫‚√§ æ∫√à«¡¥â«¬

Ÿ∫∫ÿÀ√’Ë ªí®®—¬‡ ’¬Ë ß∑’‡Ë °’¬Ë «¢âÕß ∑“ß‚√§À≈Õ¥‡≈◊Õ¥ (Õâ«π, §«“¡¥—π‚≈À‘µ Ÿß. ‰¢¡—π‡°‘π ª√–«—µ§‘ √Õ∫§√—« superficial thrombophlelitis æ∫ >40% Raynaudûs phenomenon æ∫ >40%

AO Ÿß°«à“ 55 ªï Ÿß°«à“¡◊Õ ·≈–‡∑â“ ‡°’¬Ë «¢âÕß æ∫√à«¡¥â«¬

‰¡àæ∫ æ∫πâÕ¬

5. ‰¡à¡’ arteriosclerotic factors Õ◊πË πÕ°®“°°“√ Ÿ∫∫ÿÀ√’Ë °“√∑” arteriography ®–™à«¬„π°“√«‘π®‘ ©—¬‚√§„Àâ·πàπÕπ ¢÷πÈ

°“√«‘π‘®©—¬·¬°‚√§ §«√«‘π®‘ ©—¬·¬°‚√§®“° arteriosclerosis ´÷ßË Õ“®®–‡°‘¥‰¥â „π §πÕ“¬ÿµË”°«à“ 50 ªï ‚¥¬‡©æ“–∑’‡Ë ªìπ‚√§‡∫“À«“π „π‡æ»À≠‘ß µâÕß·¬°®“° collagen disease ‡™àπ scleroderma ·≈– SLE (µ“√“ß∑’Ë 18.2 ·≈– 18.3)

°“√µ√«®«‘π‘®©—¬∑“ßÀâÕßªØ‘∫—µ‘°“√ ‡æ◊ÕË ·¬°®“°‚√§ atherosclerosis, vasculopathy ·≈– hypercoagulability §«√‡®“–‡≈◊Õ¥µ√«® CBC, BUN, FBS ·≈– lipid profile ∂â“ ß —¬«à“®–‡ªìπ rheumatic disease À√◊Õ vasculitis §«√ ‡®“–¥Ÿ√–¥—∫¢Õß erythrocyte sedimentation rate (ESR), antinuclear antibody (ANF), ·≈– rheumatoid factor (RF) ·¬°‚√§®“° hypercoagulable state ‚¥¬‡®“–À“√–¥—∫¢Õß protein C ·≈– S, antithrombin III, lupus anticoagulants ·≈– anticardiolipin antibodies ∂â“ ß —¬¿“«– dysfibrinogenemia Õ“®®–µâÕßµ√«®∑“ßÀâÕßªØ‘∫µ— °‘ “√‡æ‘¡Ë ‡µ‘¡

µ“√“ß∑’Ë 18.3 °“√«‘π®‘ ©—¬‚√§®“° Thromboangiitis Obliterans Atherosclerosis

Connective tissue disease/vasculitis Systemic Lupus Erythematosus Rheumatoid arthritis Scleroderma Polyarteritis nodosa Antiphospholipid antibody syndrome Giat cell or Takayasu’s arteritis Leukocytoclastic vasculitis Miscellaneous Idiopathic arterial thrombosis (i.e.,cancer, infection, ulcerative colitis, congestive heart failure) Blood dyscrasia (polycythemia vera) Ergotamine abuse Occupational hazards (vibratory tools, hypothenar hammer syndrome) Ehlers-Danlos syndrome Pseudoxanthoma elasticum Calciphylaxis Thrombosis of aneurysms.

°“√µ√«®«‘π‘®©—¬æ‘‡»… ‡™àπ°“√«—¥ ABI, ankle ·≈– toe pressure, plethysmography, digital artery flow velocity, thallium-201 perfusion scan „π√“¬∑’¡Ë ·’ º≈‡√◊ÕÈ √—ß ®“°°“√∑” arteriography ®–æ∫«à“ ¡’°“√µ’∫µ—π¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß à«πª≈“¬ ‚¥¬∫√‘‡«≥µâπ¬—ß¥’Õ¬Ÿà À≈Õ¥‡≈◊Õ¥·¥ß¡’≈°— …≥–§¥‡§’¬È «·≈–µ’∫·§∫‡ªìπ™à«ß Ê ‡ªìπ skip area ≈—∫°—∫™à«ßª°µ‘ ∫“ß§√—ÈßÀ≈Õ¥‡≈◊Õ¥·¥ß¢π“¥‡≈Á°À≈Õ¥ „¥À≈Õ¥Àπ÷Ëßª°µ‘µ≈Õ¥·π« collaterals ∑’Ë‡ÀÁπ®–¡’≈—°…≥–‡ªìπ çfree rooté À√◊Õ çcockscrew appearanceé(22,23) (√Ÿª∑’Ë 18.2)

Clinical course ∑’Ë¢“√Õ¬‚√§®–‡√‘Ë¡µâπ®“°À≈Õ¥‡≈◊Õ¥·¥ßª≈“¬π‘È« ·≈– À≈Õ¥‡≈◊Õ¥·¥ß¢π“¥‡≈Á°∑’‡Ë ∑â“µàÕ¡“®–≈“¡∂÷ßÀ≈Õ¥‡≈◊Õ¥„µâÀ«— ‡¢à“ ≈—°…≥–¢Õß√Õ¬‚√§®–·∫àßÕÕ°‰¥â‡ªìπ 2 ·∫∫§◊Õ(23) 1. continuous progression 2. skip progression

170

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥ µ“√“ß∑’Ë 18.4 ·π«∑“ß°“√√—°…“ 1. À¬ÿ¥ Ÿ∫∫ÿÀ√’Ë 2. √—°…“ locial ischemic ulceration 2.1 °“√¥Ÿ·≈‡∑â“ 2.1.1 ∑“º‘«Àπ—ß¥â«¬§√’¡≈“‚π≈‘πÀ√◊Õ‚≈™—πË 2.1.2 ªÑÕß°—π‰¡à„Àâ‡°‘¥·º≈∑’‡Ë ∑â“µ“¡√Õ¬·¬°√–À«à“ßπ‘«È ‚¥¬ „™â ”≈’À√◊Õºâ“πÿ¡à √Õß 2.1.3 √–«—ß‰¡à „Àâ‡°‘¥·º≈∑’‡Ë ∑â“‚¥¬„™â√Õß‡∑â“∑’πË ¡ÿà ·≈–µ—¥ ‡©æ“– 2.2 „™â¬“ calcium channel blocker ‡™àπ nifedipine, nicardipin √à«¡°—∫ pentoxifyllin 2.3 „™â Iloprost 2.4 ∂â“·º≈‰¡àÀ“¬¥’ §«√∑” sympathectomy 3. ∂â“¡’ cellulitis §«√„Àâ¬“ªØ‘™«’ π– ·≈–∂â“¡’ superficial phlebitis §«√„™â NSAIDS 4. µ—¥π‘«È ¡◊Õπ‘«È ‡∑â“ ∂â“‰¡à “¡“√∂ control ischemic rest pain À√◊Õ pain ∑’‡Ë °’¬Ë «¢âÕß°—∫ ischemic ulcer

√Ÿª∑’Ë 18.2 Superficial thrombophlebitis ¢ÕßÀ≈Õ¥‡≈◊Õ¥¥”∫√‘‡«≥

À≈—ß‡∑â“¢ÕßºŸâªÉ«¬ TAO ¡’ ischemic ulcer ‡°‘¥¢÷Èπ∑’Ë ª≈“¬À—«·¡à‡∑â“

clinical course ¢Õß TAO ®–Õ¬Ÿà „π™à«ß 1-2 ªï µ—ßÈ ·µà‡√‘¡Ë ¡’Õ“°“√®π°√–∑—Ëß¡’°“√Õÿ¥µ—π¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß√–¥—∫ Ÿß°«à“ À—«‡¢à“®÷ß®–‡√‘Ë¡¡’ claudication °“√Õÿ¥µ—πÕ“®®–≈“¡¢÷Èπ¡“∂÷ß À≈Õ¥‡≈◊Õ¥·¥ß iliac ´÷ßË ‡ªìπº≈¡“®“° secondary thrombosis √âÕ¬≈– 60 ¢Õß°“√«‘π®‘ ©—¬‚√§§√—ßÈ ·√° ®–¡’°“√Õÿ¥µ—π¢ÕßÀ≈Õ¥ ‡≈◊Õ¥·¥ß„µâÀ«— ‡¢à“ µ√ß femoropopliteal artery √âÕ¬≈– 32 ·≈– aortoiliac √âÕ¬≈– 8(9) ∑’·Ë ¢π °“√Õÿ¥µ—π®–‡°‘¥¢÷πÈ ∑’ÀË ≈Õ¥‡≈◊Õ¥ ª≈“¬π‘«È ¡◊Õ µâπ·¢π ·µà ‰¡àæ∫≈“¡¢÷πÈ ¡“∂÷ßÀ≈Õ¥‡≈◊Õ¥·¥ß brachial(25) πâÕ¬√“¬æ∫«à“ TAO ‡°‘¥¢÷πÈ °—∫À≈Õ¥‡≈◊Õ¥·¥ß„π™àÕß ∑âÕß‡™àπ mesenteric ·≈– renal(18)

°“√√—°…“‚√§ (µ“√“ß∑’Ë 18.4) °“√„™â¬“√—°…“‚√§ TAO ‡ªìπ‚√§¢ÕßÀ≈Õ¥‡≈◊Õ¥ à«πª≈“¬ ∑’Ë§àÕ¬ Ê ≈“¡¢÷Èπ¡“ ºŸâªÉ«¬∑’Ë¡“æ∫·æ∑¬å ‚√§¡—°®–≈ÿ°≈“¡‰ª ¡“°·≈â«‚¥¬‡©æ“–∑’‡Ë ∑â“ π‘«È ¡◊Õπ‘«È ‡∑â“¬—ß®–‰¡à‡πà“µ“¬„π√–¬–·√°

Õ“°“√¢Õß‚√§®–¥’¢÷Èπ∂â“ß¥ Ÿ∫∫ÿÀ√’Ë ∂â“¬—ß Ÿ∫∫ÿÀ√’Ë°“√Õ—°‡ ∫ ¢ÕßÀ≈Õ¥‡≈◊Õ¥®–≈ÿ°≈“¡‰ªÕ¬à“ßµàÕ‡π◊ÕË ß Õ“°“√¢Õß‚√§®–‡≈« ≈ßµ“¡≈”¥—∫ ¡’°“√‡πà“µ“¬∑’Ëª≈“¬π‘È« æ∫·º≈‡√◊ÈÕ√—ß∑’Ë¡◊Õ·≈– ‡∑â“√âÕ¬≈– 25 ·≈–√âÕ¬≈– 25 ®–°≈—∫‡ªìπ´È”‰¥âÕ°’ ∂â“Õ“¬ÿ¡“° ¢÷πÈ ®π‡°‘π 60 ªï §«“¡√ÿπ·√ß¢Õß‚√§®–≈¥πâÕ¬≈ß ®ÿ¥¡ÿßà À¡“¬ „π°“√„Àâ¬“√—°…“‚√§§◊Õ ¬ÿµ‘°“√≈ÿ°≈“¡¢Õß‚√§‰¡à „Àâ¡’°“√Õÿ¥ µ—π¢ÕßÀ≈Õ¥‡≈◊Õ¥¡“°‰ª°«à“π’È °“√„™â¬“¢¬“¬À≈Õ¥‡≈◊Õ¥‰¡à ‰¥â º≈„π°“√‡æ‘¡Ë collaterals °“√„Àâ¬“µâ“π≈‘¡Ë ‡≈◊Õ¥®–™à«¬‰¡à „Àâ‡°‘¥ thrombus ·≈–À≈Õ¥‡≈◊Õ¥Õÿ¥µ—π¡“°¢÷πÈ °“√„Àâ prostaglandin „π√Ÿª¢Õß prostagladin E, (PGE1) ‡¢â“∑“ßÀ≈Õ¥‡≈◊Õ¥·¥ß ®–∑”„ÀâÀ≈Õ¥‡≈◊Õ¥¢¬“¬µ—«Õ¬à“ß¡’ ª√– ‘∑∏‘¿“æ ·≈–¬—ßµâ“π‡°√Á¥‡≈◊Õ¥®—∫°≈ÿ¡à §«√„Àâ „πª√‘¡“≥∑’Ë µË”·≈–‡¢â“∂÷ß∫√‘‡«≥√Õ¬‚√§‚¥¬µ√ß ‰¥âº≈„π°“√√—°…“∂÷ß√âÕ¬≈– 72 ‚¥¬‡©æ“–„π√“¬∑’¡Ë ·’ º≈‡√◊ÕÈ √—ß(26) ªí≠À“ ”§—≠„π°“√√—°…“ TAO §◊ÕÕ“°“√ª«¥ ´÷Ëß‡°‘¥¢÷Èπ √ÿπ·√ß·≈–‡√◊ÕÈ √—ß µâÕß√—∫ª√–∑“π¬“·°âª«¥À≈“¬¢π“π «‘∏°’ “√ √—°…“∑’Ë ‰¥âº≈§◊Õ epidural anesthesia, prostaglandin infusion, °“√„™â¬“≈–≈“¬≈‘¡Ë ‡≈◊Õ¥·≈– hyperbaric oxygenation

171

Buergerûs disease (Thromboangitis Obliterans) µ“√“ß∑’Ë 18.5 °“√ºà“µ—¥√—°…“ºŸªâ «É ¬ TAO ∑—ßÈ À¡¥ Amputation sympathectomy ‰¡à¡’ direct reconstruction

107 √“¬ 107 88

π.æ.√–«’ æ‘¡≈»“πµå √.æ.»‘√‘√“™

°“√ºà“µ—¥√—°…“ (µ“√“ß∑’Ë 18.5) 1. °“√¥Ÿ·≈∫“¥·º≈ ∫√‘‡«≥∑’Ë¡’°“√‡πà“µ“¬·≈–‡°‘¥·º≈ ‡√◊ÈÕ√—ß‚¥¬‡©æ“–ª≈“¬¡◊Õª≈“¬‡∑â“µâÕß§Õ¬∑”§«“¡ –Õ“¥·º≈µ—¥‡Õ“π‘È«∑’Ëµ“¬ÕÕ° ∂â“¡’°“√µ‘¥‡™◊ÈÕ°“√„Àâ ¬“ªØ‘™’«π–‚¥¬°“√©’¥‡¢â“°≈â“¡À√◊Õ∑“ßÀ≈Õ¥‡≈◊Õ¥®– ‰¡à ‰¥âº≈ ‡æ√“–¬“‰¡à “¡“√∂ºà“π‡¢â“∂÷ß∫√‘‡«≥∑’Ë¡’°“√ µ‘¥‡™◊ÈÕ‰¥â §«√„Àâ¬“ªØ‘™’«π–·∫∫ topical §«√√–¡—¥ √–«—ß‰¡à „Àâ‡°‘¥∫“¥·º≈∫√‘‡«≥π‘«È ¡◊Õπ‘«È ‡∑â“ 2. °“√µ—¥π‘«È ‡∑â“ ∑’‡Ë πà“µ“¬ÕÕ° ∂â“‡ªìπ·∫∫ dry gangrene §«√√Õ„Àâ¡’·π«¢Õß demarcation ™—¥‡®π°àÕπ ®– ºà“µ—¥√’∫¥à«π„πºŸâªÉ«¬∑’Ë¡’°“√µ‘¥‡™◊ÈÕ√à«¡¥â«¬ à«π„À≠à ·≈â«ºŸâªÉ«¬ TAO ¡—°®–¡’ªí≠À“·≈–≈ß‡Õ¬¥â«¬°“√µ—¥ π‘«È ∑’‡Ë πà“µ“¬ÕÕ°‡∑à“π—πÈ ‰¡à∂ß÷ °—∫µâÕßµ—¥·¢πÀ√◊Õµ—¥¢“ (major amputation) 3. sympathectomy ‡ªìπ«‘∏°’ “√ºà“µ—¥√—°…“ TAO ∑’Ë ‰¥âº≈ ¥’·≈–‡™◊ÕË ∂◊Õ‰¥â∑ ’Ë ¥ÿ ¡’¢Õâ ∫àß™’È „πºŸªâ «É ¬∑’¡Ë ·’ º≈‡√◊ÕÈ √—ß rest pain ·≈–™“‡¬Áπª≈“¬¡◊Õª≈“¬‡∑â“ æ∫«à“®–™à«¬„Àâ

·º≈À“¬‡√Á«¢÷πÈ ≈¥Õ“°“√‡®Á∫ª«¥(9,17) ®ÿ¥¡ÿßà À¡“¬¢Õß °“√∑” sympathectomy §◊Õ≈¥°“√À¥µ—«¢ÕßÀ≈Õ¥ ‡≈◊Õ¥ª≈“¬·¢π¢“‚¥¬‡©æ“–∑’Ë ‰ª‡≈’È¬ßº‘«Àπ—ß ‰¡à¡’º≈ „π°“√¢¬“¬µ—«¢ÕßÀ≈Õ¥‡≈◊Õ¥„π°≈â“¡‡π◊ÕÈ ®–‰¡à ‰¥âº≈ „πºŸªâ «É ¬¢“¢“¥‡≈◊Õ¥‡√◊ÕÈ √—ß«‘°ƒµ‘ (ABI<0.3) 4. arterial reconstruction ¡—°®–‰¡à ‰¥âº≈‡π◊ËÕß®“°¡’ À≈Õ¥‡≈◊Õ¥·¥ß∑’µË ∫’ µ—π ≈—∫°—π°—∫∫√‘‡«≥∑’ªË °µ‘À≈“¬™à«ß distal run-off ‰¡à¥’ ∂â“ºà“µ—¥‰¥âº≈ ·º≈®–À“¬‡√Á«¢÷πÈ ∂â“ TAO ‡°‘¥°—∫À≈Õ¥‡≈◊Õ¥¢π“¥„À≠à∫√‘‡«≥µâπ¢“Õ“®®– reconstruct ·≈– bypass ‰¥â ‚¥¬°“√„™âÀ≈Õ¥‡≈◊Õ¥ ‡∑’¬¡∂â“‡°‘¥°—∫À≈Õ¥‡≈◊Õ¥∑’ÕË ¬Ÿµà Ë”°«à“À—«‡¢à“ °“√∑” bypass §«√®–„™â saphenous vein graft ·µà®–¡’ª≠ í À“ „™â ‰¡à ‰¥â‡π◊ÕË ß®“°¡’ migratory phlebitis ‰ª·≈â«µâÕßÀ“ À≈Õ¥‡≈◊Õ¥¥”®“°∑’Ë·¢π¡“„™â·∑π æ∫«à“ “¡“√∂ ∑” revascularization „πºŸªâ «É ¬ TAO ‰¥â ”‡√Á®‡æ’¬ß√âÕ¬≈– 10-17.3 ‡∑à“π—πÈ (9-11) à«π„À≠à®–‡ªìπÀ≈Õ¥‡≈◊Õ¥·¥ß∑’ÕË ¬Ÿà ‡Àπ◊ Õ À— « ‡¢à “ ¢÷È π ¡“ ·≈–º≈°“√ºà “ µ— ¥ √–¬–¬“«‰¡à ¡’ ‡π◊ËÕß®“° distal run-off ‰¡à¥’æÕ ‡°‘¥‡ªìπ‚√§´È”·≈– À≈Õ¥‡≈◊Õ¥ saphenous vein ∑’πË ”¡“„™â§≥ ÿ ¿“æ‰¡à¥æ’ Õ

°“√æ¬“°√≥å‚√§ √âÕ¬≈– 20 ¢ÕßºŸâªÉ«¬∑’Ë¡’√Õ¬‚√§‡°‘¥¢÷Èπ∑’Ë‡∑â“ ®–µâÕß ≈ß∑â“¬¥â«¬°“√µ—¥π‘«È ‡∑â“ ·≈–√âÕ¬≈– 20 µâÕßµ—¥‡∑â“(9,11) ∂â“‡ªìπ ∑’·Ë ¢π‚Õ°“ µ—¥·¢π¡’πÕâ ¬‡æ√“–√Õ¬‚√§®–‰¡à≈°ÿ ≈“¡‰ª∂÷ß brachial artery πâÕ¬°«à“√âÕ¬≈– 10 ∑’®Ë –µâÕßµ—¥π‘«È ¡◊Õ(25) Õ“°“√ ¢Õß‚√§®–¥’¢÷Èπ¡“°∂â“ºŸâªÉ«¬ß¥ Ÿ∫∫ÿÀ√’Ë·≈–§«“¡√ÿπ·√ß¢Õß‚√§ ®–≈¥≈ß‡¡◊ÕË ºŸªâ «É ¬Õ“¬ÿ¡“°°«à“ 60 ªï

172

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥

‡Õ° “√Õâ“ßÕ‘ß 1. Buerger L. Thromboangiitis obliterans: a study of lesions leading to presenile spontaneous gangrene. Am J Med Sci 1908;136:567-580. 2. Wessler S, Ming SC, Gurewick V, et al. A critical evaluation of thromboangiitis obliterans:the case against Buerger’s disease. N Engl J Med 1960;262:1149-1160. 3. McKusick VA, Harris WS. The buerger syndrome in the Orient. Bull John Hopkins Hosp. 1961;109:241. 4. Hill GL, Smith AH. Buergerûs disease in Indonesia:clinical course and prognostic factos. J Chronic Dis 1974;27:205. 5. Reddi HTV. Thromboangiitis obliterans and or Buergerûs disease in South India: a review of 70 cases. Int Surg 1974;59:555. 6. Nishikimi N, Shionoya S, Mizuno S, et al. Result of national epidemiological study of Buergerûs disease. J Jpn Coll Angiol 1987;27:1125. 7. Papa M, Bass A. Autoimmune mechanism in Thromboangiitis obliterans (Buergerûs disease):the role of tobacco antigen and the major histocompathbility complex: Surgery 1992;111:527-531. 8. Matsushita M, Shionoya S, Matsumoto T. Urinary cotinine measurement in patients with Buergerûs disease-effects of active and passive smoking on the disease process. J Vasc Surg 1991;14:53. 9. Shionoya S. What is Buergerûs disease? World J Surg 1983;7:544. 10. Mills JL, Taylor LMJ, Porter JM. Buergerûs disease in modern era. Am J Surg 1987;154:123-129. 11. Lie JT II. Thromboangiitis obliterans (Buergerûs disease) revisited. Pathol Annu 1988,23:257. 12. Olin JW, Young JR, Craor RA, et al. The changing clinical spectrum of thromboangiitis obliterans (Buergerûs disease). Circulation 1990;82(Suppl IV):iv-1-iv-7. 13. de Moerloose PH, Jeannet M, Mirimanoff P, Boubier CA. Evidence for an HLA-linked resistance gene in Buergerûs disease. Tissue Antigens 1979;14:169. 14. Gulatism, Madha K, Thusoo TK, et al. Autoantibodies in thromboangiitis obliterans (Buergerûs disease). Angiology 1982;33:642.

15. McKusick VA, Harris WS, Ottesen OE, et al. Buergerûs disease. A distinct clinical and pathologic entity. JAMA 1962;18:15. 16. Nishikimi N, Sakurai T, Shionoya S, et al. Microcirculatory characteristics in patients with Buergerûs disease. Angiology 1992;43:312. 17. Shionoya S. Diagnosis, pathology and treatment of Buergerûs disease. Surgery 1974;75:695. 18. Shionoya S. Pattern of arterial occlusion in Buergerûs disease. Angiology 1982;375:33. 19. Phimolsanti R. Buergerûs disease in Thailand. (Abstract) Presented at Clinical Congress Royal College of Surgeons of Thailand. Pattaya Cholburi. February 12, 1987. 20. McPherson JR, Juergens JL, Gifford RW Jr. Thromboangiitis obleterans and arteriosclerosis obliterans: clinical and prognostic differences. Ann Intern 1963;59:288-296. 21. Lie JT. Thromboangiitis obliterans (Buergerûs disease) in women. Medicine 1987;66:65. 22. Rivera R. Roentgenographic diagnosis of Buergerûs disease. J Cardiovasc. Surg (Torino) O 1973;14:40. 23. Rosenberger R. The angiographic apperance of Thromboangiitis obliterans (Buergerûs disease) in the abdominal vessels. Br J Radiol 1973;46:337. 24. Rutherford RB, Flanigan DP, Gupta SK, et al. Suggested standard for reports dealing with lower extremity ischemia. J Vasc Surg 1986;4:480. 25. Hirai M, Shionoya S. Arterial obstruction of the upper limb in Buergerûs disease: its incidence and primary lesions. Br J Surg 1979;66:124. 26. Fiessinger JN, Shafer M. Trial of Iloprost vs Aspirin treatment for critical limb ischemia of thromboangiitis obliterans. Lancet 1990;335:555-557.

∫∑∑’Ë 19 TAKAYASUûS ARTERITIS

arteritis À¡“¬∂÷ß°≈ÿà¡Õ“°“√Õ—°‡ ∫¢ÕßÀ≈Õ¥‡≈◊Õ¥∑’Ë¡’ “‡Àµÿ‡ªìπ·∫∫ transmural necrosis ´÷Ëß “‡Àµÿ∑’Ë·∑â®√‘ß¬—ß ‰¡à∑√“∫·πàπÕπ vasculitis À¡“¬∂÷ß°≈ÿ¡à Õ“°“√¢Õß‚√§∑’‡Ë °‘¥®“° necrosis ·≈– occlusions ¢ÕßÀ≈Õ¥‡≈◊Õ¥¥”·≈–À≈Õ¥‡≈◊Õ¥ ·¥ß∑’¬Ë ß— ‰¡à “¡“√∂Õ∏‘∫“¬∂÷ßæ¬“∏‘ ¿“æ‰¥â (1) ·µàÕ“®®–‡°‘¥®“° ‚√§Õ‘¡¡ŸπÀ√◊Õ hypersensitivity reaction (µ“√“ß∑’Ë 19.1) Takayasuûs arteritis ‡ªìπ‚√§∑’Ë¡’°“√Õ—°‡ ∫‡√◊ÈÕ√—ß∑’Ë‡°‘¥ ¢÷πÈ °—∫À≈Õ¥‡≈◊Õ¥·¥ß ∑”„Àâ¡°’ “√µ’∫·§∫¢Õß aorta ·≈–À≈Õ¥ ‡≈◊Õ¥·¥ß∑’·Ë ¬°·¢πßÕÕ°‰ª æ∫„π‡æ»À≠‘ß∑’ÕË “¬ÿπÕâ ¬°«à“ 35 ªï ™à«ßÕ“¬ÿ∑æ’Ë ∫‰¥â∫Õà ¬§◊Õ 10-30 ªï ™◊ÕË Õ◊πË ∑’‡Ë √’¬°‚√§π’È pulseless disease, nonspecific aortoarteritis, arteritis in young women, atypical aortic coarctation ·≈– middle aorta syndrome(2-5) ‚√§π’‡È ªìπ‚√§∑’æË ∫‰¥â „πª√–™“°√™“«‡Õ‡´’¬(6-9) æ∫‰¥âπÕâ ¬„π ∑«’ªÕ◊πË (10,11) “‡Àµÿ¢Õß‚√§∑’·Ë ∑â®√‘ß¬—ß‰¡à∑√“∫ Õ“®®–‡π◊ÕË ß¡“ ®“°‚√§∑“ßÕ‘¡¡Ÿπ∑’‡Ë °‘¥¢÷πÈ ‡©æ“–‡®“–®ß°—∫À≈Õ¥‡≈◊Õ¥ À√◊Õ¡’°“√ Õ—°‡ ∫‡√◊ÕÈ √—ß(12) µ”·Àπàß¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß∑’æË ¬“∏‘ ¿“æ‰¥â∫Õà ¬ §◊Õ aortic arch ·≈–·¢πß¢ÕßÀ≈Õ¥‡≈◊Õ¥∑’·Ë ¬°ÕÕ°‰ª √Õß ≈ß¡“§◊Õ à«πµâπ¢Õß abdominal aorta ‚¥¬‡©æ“–À≈Õ¥‡≈◊Õ¥ ∑’Ë‰ª‡≈’¬È ßÕ«—¬«–¿“¬„π™àÕß∑âÕß ∂â“‡°‘¥°—∫À≈Õ¥‡≈◊Õ¥∑’Ë ‰ª‡≈’¬È ß‰µ ®–∑”„Àâ§«“¡¥—π‚≈À‘µ Ÿß ∂â“‡°‘¥∑’Ë pulmonary artery ·≈–¡’ °“√µ’∫µ—π ®–‡°‘¥¿“«– pulmonary hypertension ·≈–µ“¡ ¡“¥â«¬À—«„®«“¬(2-5,12) Õ“®æ∫‰¥â∑À’Ë ≈Õ¥‡≈◊Õ¥À—«„®‚§‚√π“√’Ë

°“√·∫àß™π‘¥¢Õß Takayasuûs disease µ“¡§«“¡√ÿπ·√ß¢Õß ‚√§·∫àßÕÕ°‰¥â‡ªìπ 4 ™π‘¥¥—ßπ’§È Õ◊ (12,13) (√Ÿª∑’Ë 19.1) ™π‘¥∑’Ë 1 √Õ¬‚√§æ∫·µà∑’Ë aortic arch ·≈– “¢“À≈Õ¥‡≈◊Õ¥ ∑’·Ë ¬°ÕÕ°‰ª æ∫‰¥â√Õâ ¬≈– 9 ™π‘¥∑’Ë 2 æ∫√Õ¬‚√§∑’Ë descending aorta, abdominal aorta ·≈–À≈Õ¥‡≈◊Õ¥∑’·Ë ¬°·¢πßÕÕ°‰ª æ∫‰¥â √âÕ¬≈– 11 ™π‘¥∑’Ë 3 √Õ¬‚√§ æ∫∑’Ë aortic arch ·≈– “¢“√à«¡°—∫ abdominal aorta ·≈– “¢“ æ∫‰¥â√Õâ ¬≈– 65 ™π‘¥∑’Ë 4 æ∫‰¥â∑°ÿ µ”·Àπàß¢Õß aorta ·≈– “¢“√à«¡°—∫√Õ¬ ‚√§∑’Ë pulmonary artery æ∫‰¥â√Õâ ¬≈– 15

™π‘¥∑’Ë I

™π‘¥∑’Ë II

™π‘¥∑’Ë III

™π‘¥∑’Ë IV

√Ÿª∑’Ë 19.1 ™π‘¥µà“ß Ê ¢Õß Takayasuûs arteritis

174 æ¬“∏‘ ¿“æ À≈Õ¥‡≈◊Õ¥∑’ÕË °— ‡ ∫®–¡’ patchy granulomatous inflammation ∑’Ë adventitia, vasa vasorum ·≈– media ¡’ lymphocytes, histiocytes ·≈– multinucleated giant cells ·∑√°∑—«Ë ∑ÿ°™—πÈ ¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß¢π“¥„À≠à∑¡’Ë √’ Õ¬‚√§≈—°…≥– ·∫∫ panarteristis ∑”„ÀâÀ≈Õ¥‡≈◊Õ¥·¥ß‡ ’¬§«“¡¬◊¥À¬ÿπà (12) „π√–¬–∑â“¬®–¡’ reactive hyperplasia ¢Õß™—πÈ intima ·≈– adventitia æ√âÕ¡°—∫°“√∫“ßµ—«¢Õß™—Èπ media √–¬–π’È°“√ Õ—°‡ ∫®–≈¥≈ß À≈Õ¥‡≈◊Õ¥·¥ß®–‡°‘¥ sclerosis ·≈–¡’ calcification À≈Õ¥‡≈◊Õ¥·¥ßÕ“®®–µ’∫·§∫À√◊Õ‚ªÉßæÕß°≈“¬‡ªìπ aneurysm ‰¥â (4,512)

Õ“°“√· ¥ß∑“ß§≈‘π‘§ „π√–¬– acute phase ºŸªâ «É ¬®–¡’‰¢â ÕàÕπ‡æ≈’¬ ‡∫◊ÕË Õ“À“√ πÈ”Àπ—°≈¥ ª«¥‡¡◊ÕË ¬µ“¡¢âÕ·≈–°≈â“¡‡π◊ÕÈ √–¬–·√°®–¡’Õ“°“√ ‡ªìπ Ê À“¬ Ê µàÕ¡“Õ“°“√®–‡¥àπ™—¥¢÷πÈ „π·µà≈–Õ«—¬«– ‡π◊ÕË ß®“° À≈Õ¥‡≈◊Õ¥∑’ÕË °— ‡ ∫®–‡√‘¡Ë µ’∫µ—π®π‡°‘¥Õ“°“√¢“¥‡≈◊Õ¥(2) „π√–¬– ‡√◊ÕÈ √—ßÕ“°“√µà“ß Ê ¢Õß‚√§®–¢÷πÈ Õ¬Ÿ°à ∫— À≈Õ¥‡≈◊Õ¥∑’µË ∫’ µ—π¡’‰¥â ∑—ßÈ §«“¡¥—π‚≈À‘µ Ÿß CVA À—«„®«“¬ ·≈– claudication ‡≈◊Õ¥‰ª ‡≈’¬È ß ¡Õß‰¡àæÕ®–∑”„Àâ‡°‘¥ syncope µ“¡—« ¡Õß‡ÀÁπ‰¡à™¥— ·≈– dementia §«“¡¥—π‚≈À‘µ Ÿß‡°‘¥®“° coarctation of the aorta À√◊ÕÀ≈Õ¥‡≈◊Õ¥·¥ß∑’Ë ‰ª‡≈’È¬ß‰µµ’∫µ—π(3,4,14) À—«„®«“¬‡°‘¥®“° À≈Õ¥‡≈◊Õ¥ pulmonary artery µ’∫·§∫ ºŸâªÉ«¬∑’Ë¡’Õ“°“√¡“°·≈â«®–§≈”™’æ®√∫√‘‡«≥·¢π¢“‰¡à ‰¥â øíß‰¥â‡ ’¬ß bruit À√◊Õ systolic murmur °≈â“¡‡π◊ÕÈ ≈’∫·ø∫ «—¥ §«“¡¥—π‚≈À‘µ ·¢π∑—ßÈ Õß¢â“ß‰¥â ‰¡à‡∑à“°—π ¡’ retinal arteriovenous anastomosis, visual field deficits ª«¥»’√…–∫àÕ¬ Ê À—«„®‚µ ™’æ®√‰«(5)

°“√µ√«®∑“ßÀâÕßªØ‘∫—µ‘°“√ µ√«® CBC æ∫«à“√âÕ¬≈– 50 ®–¡’À≈Õ¥‡≈◊Õ¥®“ß≈—°…≥– ‡ªìπ·∫∫ normochromic normocytic anemia ºŸâªÉ«¬∑’Ë¡’ §«“¡¥—π‚≈À‘µ Ÿß®–æ∫«à“¡’À—«„®‚µ®÷ßÕ“®®–æ∫‰¥â®“°¿“æ√—ß ’ ∑√«ßÕ° §≈◊πË ‰øøÑ“À—«„®º‘¥ª°µ‘ (LVH, LAE) √–¥—∫¢Õß erythrocyte sedimentation rate (ESR) ®–‡ªìπ marker Õ¬à“ß¥’∑’Ë ∫àß∫Õ°«à“À≈Õ¥‡≈◊Õ¥¬—ß¡’°“√Õ—°‡ ∫Õ¬ŸÀà √◊Õ‰¡à(5,5)

°“√µ√«®∑“ß√—ß ’«‘∑¬“ ∑’Ë ”§—≠∑’Ë ÿ¥§◊Õ°“√∑” arteriography ®–∫àß∫Õ°∂÷ß§«“¡ √ÿπ·√ß·≈–≈—°…≥–°“√µ’∫·§∫¢ÕßÀ≈Õ¥‡≈◊Õ¥ §«√¥Ÿµß—È ·µà aor-

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥ tic arch ·≈– “¢“·¬° pulmonary artery, abdominal aorta ·≈– “¢“·¬°(15,16)

°“√√—°…“ ·∫àßÕÕ°‡ªìπ°“√√—°…“‚¥¬„Àâ¬“ ·≈–°“√ºà“µ—¥√—°…“ °“√„™â¬“√—°…“(17) „π acute phase ∑’¡Ë Õ’ “°“√„Àâ°“√√—°…“‰¥â ‚¥¬°“√„™â NSAIDs ·≈– steroid ‚¥¬∑—«Ë ‰ª·≈â«„Àâ steroid „π√Ÿª¢Õß prednisolone „π¢π“¥ 40-60 ¡‘≈≈‘°√—¡µàÕ«—π µÕπ‡™â“§√—ßÈ ‡¥’¬«À√◊Õ·∫àß„Àâ«π— ≈– 3 §√—ßÈ ∂â“„Àâ·µà‡π‘πË Ê ™’æ®√Õ“®®–°≈—∫¡“§≈”‰¥â À≈—ß®“°π—πÈ 46 —ª¥“Àå ‡¡◊ÕË Õ“°“√¥’¢π÷È ≈¥¢π“¥¬“≈ß‡ªìπ 2-4 —ª¥“Àå®π ß¥¬“„π∑’ Ë ¥ÿ Õ“°“√ºŸªâ «É ¬®–¥’¢π÷È À√◊Õ‰¡à monitor ‰¥â®“° ESR „π√“¬∑’Ë„Àâ steroid ·≈â«‰¡à ‰¥âº≈Õ“®®–µâÕß‡ª≈’¬Ë π¡“„™â cytotoxic drugs ‡™àπ cyclophosphamide À√◊Õ cyclosporin Õ¬à“ß‰√ °Áµ“¡°“√√—°…“‚¥¬„™â¬“°¥Õ‘¡¡Ÿπ ®–‰¡à “¡“√∂¬—∫¬—ßÈ °“√‡ª≈’¬Ë π ·ª≈ß∑“ßæ¬“∏‘ ¿“æ¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß®“°‚√§ Tasayasu ‰¥â µ“√“ß∑’Ë 19.1 Nonatherosclerotic vascular conditions Inflammatory conditions Arteritis Takayasuûs arteritis Giant cell arteritis Polyarteritis nodosa Hypersensitivity arteritis Kawasakiûs disease Bechetûs disease Buergerûs disease Noninflammatory conditions Fibromuscular conditions Inherited dysplasia Marfan syndrome Ehlers-Danlos syndrome Pseudoxanthoma elasticum Congenital and development disease Abdominal aortic coarctation Persistent sciatic artery Adventitial cystic disease Popliteal artery entrapment

175

TAKAYASUûS ARTERITIS

°“√ºà“µ—¥√—°…“ ∂â“¡’§«“¡¥—π‚≈À‘µ Ÿß®“°°“√µ’∫·§∫ coarctation of the aorta À√◊ÕÀ≈Õ¥‡≈◊Õ¥·¥ß∑’¡Ë “‡≈’¬È ß‰µ §«√ºà“µ—¥·°â ‰¢´àÕ¡·´¡ °“√¢¬“¬∂à“ß¥â«¬∫—≈≈Ÿπ‰¡à ‰¥âº≈¥’ endarterectomy ¢ÕßÀ≈Õ¥ ‡≈◊Õ¥∑’µË ∫’ ·§∫‰¡à§«√∑”‡æ√“–‰¡à§Õà ¬‰¥âº≈ ¡—°®–°≈—∫¡“µ’∫·§∫Õ’° æ∫«à“°“√ºà“µ—¥∑” bypass ‰¥âº≈¥’∑’Ë ÿ¥·µà®–µâÕßµàÕ°—∫À≈Õ¥ ‡≈◊Õ¥·¥ß∑’Ë ‰¡à¡æ’ ¬“∏‘ ¿“æ ·≈–ºŸªâ «É ¬‰¡àÕ¬Ÿà„π√–¬– acute phase „π™à«ßºà“µ—¥ ª√‘¡“≥¢Õß prednisolone ∑’Ë „Àâ®–µâÕßπâÕ¬∑’Ë ÿ¥ À√◊ÕÀ¬ÿ¥¬“‰ª·≈â«(18-22)

°“√æ¬“°√≥å‚√§ °“√ºà“µ—¥∑” bypass ‰¥âº≈¥’„πºŸªâ «É ¬ Takayasu’s disease ∑’√Ë Õ¬‚√§∑’Ë ‰¡à≈°ÿ ≈“¡‰ª°«à“π’È æ∫«à“°“√ºà“µ—¥¡’ 6-year survival rate Ÿß∂÷ß√âÕ¬≈– 98 „πºŸªâ «É ¬∑’‡Ë ªìπ¡“°Õ—µ√“µ“¬ Ÿß∂÷ß√âÕ¬≈– 45 „πÕπ“§µ°“√√—°…“¥â«¬¬“√à«¡°—∫°“√ºà“µ—¥πà“®–‰¥âº≈¥’(23,24)

‡Õ° “√Õâ“ßÕ‘ß 1. Conn DL, Hunder GG. Necrotizing vasculitis. In: Kelly WN, Hanis ED, Ruddy S, Sledge CB, eds. Textbook of Rheumatoly. 3rd ed. Philadelphia: WB Saunders, 1989:1137. 2. Lupi-Herrera E, Sanches-Torres G, Marcustiamer J, et al. Takayasuûs arteritis: Clinical study of 107 cases. Am Heart J 1997;93:94-103. 3. Hall S, Buchbinder R. Takayasuûs arteritis. Rheum Dis Clin North Am 1990;16:411. 4. Sekiguchi M, Suzuki J. An overview of Takayasuûs arteritis. Heart Vessels 1992(Suppl);7:6-10. 5. Deyu Z, Digun F, Lisheng L. Takayasuûs arteritis in China:A report of 530 cases. Heart Vessels 1992(Suppl);7:32-36. 6. Deyu Z, Digun F, Ligheng L. Takayasuûs arteritis in China:A report of 530 cases. Heart Vessels 1992(Suppl);7:32-36. 7. Koide K. Takayasuûs arteritis in Japan. Heart Vessels 1992 (Suppl);7:48-52. 8. Piyachon C, Suwanwela N. Takayasuûs arteritis in Thailand. Heart Vessels 1992(Suppl);7:60-67. 9. Rosenthal T, Morag B, Itzchak Y. Takayasuûs arteritis in Israel. Heart Vessels 1992(Suppl);7:44-47. 10. Halls, Ban W, Lie JE, et al. Takayasuûs arteritis: A study of 32 North American patients. Medicine 1985;64:89-99. 11. Hotchi M. Pathological studies on Takayasuûs arteritis. Heart Vessel 1992 (Suppl);7:11-17. 12. Arend WP. The American College of Rheumatology 1990 criteria for the classification of Takayasuûs arteritis Rheum 1990;33:1129.

13. Takayasu U. A case with unusual changes of the central vessels of the retina. Acta Soc Ophthalmol Jap 1908;12:554. 14. Park YB, Hong SK, Choi KT, et al. Takayasuûs arteritis in Korea: Clinical and angiographic features. Heart Vessels 1992(Suppl);7:5559. 15. Cho YD, Lee KT. Angiographic characteristics of Takayasuûs arteritis. Heart Vessels 1992(Suppl);7:97-101. 16. Ito I. Medical treatment of Takayasuûs arteritis. Heart Vessels 1992 (Suppl);7:133-137. 17. Weaver FA, Yellin AE. Surgical treatment of Takayasuûs arteritis. Heart Vessels 1992(Suppl);7:154-158. 18. Tada Y, Sato O, Oshima A, et al. Surgical treatment of Takayasuûs arteritis. Heart Vessels 1992(Suppl);7:159-167. 19. Robbs JV, Human RR, Rajaruthnam P. Operative treatment of nonspecific aortoarteritis (Takayasuûs arteritis). J Vasc Surg 1986;3:605. 20. Scott D. Surgical repair of visceral artery occlusions in Takayasuûs disease. J Vasc Surg 1986;3:904. 21. Weaver FA. Surgical porcedures in the management of Takayasuûs arteritis. J Vasc Surg 1990;12:429. 22. Ishikawa K. Survival and mortality after diagnosis of occlusive thromboarthrophasty (Takayasuûs disease) Am J Cardiol 1981;47:10261032. 23. Morwaki R, Numano F. Takayasuûs arteritis: follow up studies for 20 years. Heart Vessels 1992(Suppl);7:138-145.

176

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥

∫∑∑’Ë 20 ACUTE ARTERIAL OCCLUSION Thomas J. Fogarty ‰¥âª√–¥‘…∞å balloon catheter ‰«â „π °“√ºà“µ—¥À≈Õ¥‡≈◊Õ¥ „πªï 1963 ‚¥¬„™â¥ß÷ ‡Õ“ arterial emboli À√◊Õ thrombi ÕÕ°®“°À≈Õ¥‡≈◊Õ¥·¥ß ‡ªìπ«‘∏°’ “√∑’ßË “à ¬µ√ß‰ª µ√ß¡“·≈–°√–∑∫°√–‡∑◊ÕπµàÕ‡ÕÁπ‚¥∑’‡≈’Ë¬¡¢ÕßÀ≈Õ¥‡≈◊Õ¥ πâÕ¬∑’ Ë ¥ÿ (1) ºŸªâ «É ¬·µà≈–√“¬‰¡à ‰¥â¡ª’ ≠ í À“µ√ß‰ªµ√ß¡“‡ ¡Õ ·µà≈– √“¬¡’ª≠ í À“ ≈—∫´—∫´âÕπ∑’µË Õâ ß¥Ÿ·≈‡Õ“„®„ à ‚¥¬‡©æ“– Õ—µ√“µ“¬ ·≈–Õ—µ√“ survival of limb °Á·µ°µà“ß°—π ºŸªâ «É ¬ acute limb ischemia ¡—°®–¡’ªí≠À“‚√§∑’Ë‡ªìπÕ¬Ÿà°àÕπ·≈â« ‡™àπ ‚√§À—«„®, ‚√§ªÕ¥, ‡∫“À«“π À√◊Õ peripheral vascular disease

“‡Àµÿ

“‡Àµÿ¢Õß°“√‡°‘¥ acute arterial occlusion ¡’‰¥â®“°(2) 1. Arterial embolism ‡°‘¥®“°‡ÕÁ¡‚∫‰≈∑’¡Ë “®“°À—«„®À√◊Õ À≈Õ¥‡≈◊Õ¥ à«πµâπ‡§≈◊ÕË π¡“Õÿ¥µ—πÀ≈Õ¥‡≈◊Õ¥ à«πª≈“¬ ∑”„Àâ¡Õ’ “°“√¢“¥‡≈◊Õ¥Õ¬à“ß‡©’¬∫æ≈—π 1.1 cardiac causes ‡ªìπ “‡Àµÿ∑æ’Ë ∫‰¥â∫Õà ¬∑’ Ë ¥ÿ ª√–¡“≥ √âÕ¬≈– 90 ¡—°®–‡°‘¥®“° atherosclerotic heart disease ´÷Ëß®–∑”„Àâ‡°‘¥ atrial fibrillation „πºŸâ ªÉ«¬°≈â“¡‡π◊ÈÕÀ—«„®¢“¥‡≈◊Õ¥‡©’¬∫æ≈—π ¡—°®–‡°‘¥ ‡ÕÁ¡‚∫‰≈∑’Ëºπ—ßÀ—«„® 2-3 —ª¥“ÀåµàÕ¡“ ·≈â«®÷ß À≈ÿ¥≈Õ¬¡“µ“¡°√–· ‚≈À‘µ ‚√§À—«„®Õ◊Ëπ Ê ∑’Ë ∑”„Àâ‡°‘¥‡ÕÁ¡‚∫‰≈‰¥â‡™àπ cardiomyopathy, left ventricular aneurysm, ‚√§√Ÿ¡“µ‘§, endocarditis ·≈– atrial myxoma

1.2 atheroembolization ‡°‘¥®“°‡ÕÁ¡‚∫‰≈¢π“¥‡≈Á°∫π atherosclerotic plaque ¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß à«πµâπ ≈—°…≥–‡ªìπ microscopic stenosis ¡’ thrombosis ‡°‘¥¢÷πÈ ‡π◊ÕË ß®“°¿“«– hypotension, dehydration, À—«„®«“¬, polycythemia, hyperviscosity ·≈– hypercoagulable states ‡ªì π “‡Àµÿ ¢ ÕßÀ≈Õ¥ ‡≈◊Õ¥·¥ßÕÿ¥µ—π‡©’¬∫æ≈—π‰¥â√Õâ ¬≈– 5-8 À≈—ß‡°‘¥ thrombosis ·≈â« ≈‘Ë¡‡≈◊Õ¥∑’Ë·¢Áßµ—«®–≈“¡‰ª¬—ß ¥â“π∫π·≈–≈à“ßµàÕÀ≈Õ¥‡≈◊Õ¥∑’ÕË ¥ÿ µ—π ·≈–≈“¡‡¢â“∂÷ß collaterals 2. In-situ arterial thrombosis ´÷ßË ‡°‘¥®“° arteriosclerotic stenosis À√◊Õ dissecting aneurysm (√Ÿª∑’Ë 20.1) 3. “‡ÀµÿÕπ◊Ë ∑’æË ∫‰¥â ‰¡à∫Õà ¬ ‡™àπ vasculitis, §«“¡º‘¥ª°µ‘ ∑“ß‚≈À‘µ«‘∑¬“, ®“°“√∫“¥‡®Á∫, graft occlusion ·≈– cervical rib syndrome

æ¬“∏‘ √’√«‘∑¬“ ∑’‡Ë °‘¥¢÷πÈ ¿“¬À≈—ßÀ≈Õ¥‡≈◊Õ¥·¥ßÕÿ¥µ—π‡©’¬∫æ≈—π¡’¥ß— µàÕ‰ªπ’È cardiac emboli ∑’ÀË ≈ÿ¥ÕÕ°®“°À—«„® ¡—°®–Õÿ¥µ—πµ√ß·¢πß ·¬°¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß À≈Õ¥‡≈◊Õ¥·¥ß∑’¡Ë °’ “√Õÿ¥µ—π‰¥â∫Õà ¬§◊Õ superficial femoral artery (SFA) ®“°°“√Õÿ¥µ—π∑’Ë common femoral artery (CFA) °“√Õÿ¥µ—π¡—°®–‡°‘¥µ√ßµ”·Àπàß∑’‡Ë √‘¡Ë ¡’ °“√‡ª≈’¬Ë π·ª≈ß¢π“¥À≈Õ¥‡≈◊Õ¥ ·≈–À√◊Õ∫√‘‡«≥ bifurcation ∑’¢Ë “‡°‘¥‰¥â∫Õà ¬°«à“∑’·Ë ¢π ·≈– visceral arteries(3,4,5) (√Ÿª∑’Ë 20.2)

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√Ÿª∑’Ë 20.1 °. mural thrombus ∑’Ë‡°‘¥¢÷Èπ„π infrarenal abdominal aortic aneurysm

¢. mural thrombus ®“° AAA „π√Ÿª∑’Ë 20.1 °. °≈“¬‡ªìπ‡ÕÁ¡‚∫‰≈À≈ÿ¥¡“Õÿ¥µ—π∑’Ë left popliteal artery

‡ÕÁ¡‚∫‰≈∑’Ë‡°‘¥®“° aorto-iliac ulcerated plaque À√◊Õ aneurysms ¡—°®–Õÿ¥µ—π∑’Ë popliteal ·≈– tibioperoneal arteries ·µà∂â“¡’¢π“¥‡≈Á°¡“°‡ªìπ microemboli ®–Õÿ¥µ—πÀ≈Õ¥ ‡≈◊Õ¥¢π“¥‡≈Á° ‡™àπ digital arteries ∑”„Àâ‡°‘¥ blue toe syndrome(6,7) À≈Õ¥‡≈◊Õ¥·¥ß∑’¡Ë °’ “√µ’∫·§∫Õ¬Ÿ·à ≈â« ¿“«– hypotension, dehydration, polycythemia, hyperviscosity, hypercoagulable state ·≈–À—«„®«“¬®–∑”„Àâ‡°‘¥ thrombosis „πÀ≈Õ¥ ‡≈◊Õ¥·¥ß·≈–¡’°“√Õÿ¥µ—π‡°‘¥¢÷Èπ∑—π∑’ À≈—ß®“°π—Èπ≈‘Ë¡‡≈◊Õ¥∑’Ë ·¢Áßµ—«®–≈“¡‰ª¥â“π∫π·≈–≈à“ßµàÕÀ≈Õ¥‡≈◊Õ¥∑’ÕË ¥ÿ µ—π ·≈–‡¢â“∂÷ß collaterals ∑”„ÀâÕ“°“√¢“¥‡≈◊Õ¥√ÿπ·√ß¡“°¢÷πÈ (8) À≈—ß‡°‘¥°“√Õÿ¥µ—π ®–¡’°“√À¥‡°√Áßµ—«¢Õß°≈â“¡‡π◊ÕÈ ‡√’¬∫„π À≈Õ¥‡≈◊Õ¥ à«πª≈“¬µàÕ∫√‘‡«≥∑’ÕË ¥ÿ µ—π∑—π∑’À≈“¬™—«Ë ‚¡ß ®π°√–∑—ßË sympathetic tone ‡ ’¬‰ª®“°¿“«– hypoxia °≈â“¡‡π◊ÕÈ ®÷ß®– §≈“¬µ—«À¬àÕπ≈ß „π√–¬–π’È®–‡°‘¥¡’ secondary thrombus

¢÷Èπ∑—Èß à«πµâπ·≈–ª≈“¬µàÕÀ≈Õ¥‡≈◊Õ¥·¥ß∑’ËÕÿ¥µ—π ·≈–®–≈“¡ ‰ªÕÿ¥ collaterals µàÕ¡“®–¡’°“√À≈—ßË “√∑’¡Ë §’ ≥ ÿ ¡∫—µ§‘ ≈â“¬Œ’ µ“¡’π∑”„ÀâÀ≈Õ¥‡≈◊Õ¥¢¬“¬µ—« ¡’°“√‡æ‘Ë¡ permeability ¢Õß capillary system µ“¡¡“¥â«¬ interstitial edema ·≈– erythrocyte sludging ‡°‘¥ intravascular coagulation ·≈– hemolysis ®–‡°‘¥ venous thrombosis „πÀ≈Õ¥‡≈◊Õ¥¥”¢π“¥„À≠à ‡π◊ËÕß®“°¿“«– hypercoagulability µ“¡À≈—ß embolism ‡ âπª√– “∑ à«πª≈“¬®–∑πµàÕ¿“«–¢“¥‡≈◊Õ¥·≈–ÕäÕ°´‘‡®π‰¥â ‰¡à°™’Ë «—Ë ‚¡ß °“√Õÿ¥µ—π¢Õß vasa vasorum ®–µ“¡¡“¥â«¬ degeneration of amyelinic fibrous type C ´÷Ëß¡’Àπâ“∑’Ë ”§—≠„π°“√√—∫√Ÿ§â «“¡√âÕπ‡¬Áπ·≈–§«“¡‡®Á∫ª«¥ motor nervous system ®–‡°‘¥ degeneration ¿“¬„π 6 ™—«Ë ‚¡ß(9) °≈â“¡‡π◊ÕÈ ®–∑πµàÕ¿“«–°“√¢“¥‡≈◊Õ¥·≈–ÕäÕ°´‘‡®π‰¥â√–¬– Àπ÷Ëß ‡æ√“–„π°≈â“¡‡π◊ÈÕ®–¡’ anaerobic metabolism ¿“«– anoxia ®– àß‡ √‘¡„Àâ¡’°“√À≈—Ëß¢Õß acid radicals ¡’°“√

179

ACUTE ARTERIAL OCCLUSION

Upper Extremity 14%

Visceral 7% Aortoiliac 22% Femoral 36%

Popliteal 15%

Other 6%

‡ª≈’¬Ë π·ª≈ß¢Õß cell membrance permeability ¡’°“√ª≈àÕ¬ ‚ªµ— ‡´’Ë¬¡·≈–¡—¬‚Õ‚°≈∫‘π cutaneous tissue ®–∑πµàÕ ¿“«–°“√¢“¥‡≈◊Õ¥‰¥âπ“π°«à“ 24 ™—«Ë ‚¡ß §«“¡√ÿπ·√ß¢Õß¿“«–°“√¢“¥‡≈◊Õ¥¢÷ÈπÕ¬Ÿà°—∫µ—«·ª√À≈“¬ ª√–°“√ ‡™àπ(8,10,11,12,13) 1. µ”·Àπàß¢Õß°“√Õÿ¥µ—π «à“‡ªìπÀ≈Õ¥‡≈◊Õ¥„¥ 2. percentage of lumen obstruction 3. √–¬–‡«≈“¢Õß°“√¢“¥‡≈◊Õ¥¡“‡≈’¬È ß 4. state of collateral circulation 5. degree of thrombus propagation 6. cardiac output 7. blood viscosity 8. ª√– ‘∑∏‘¿“æ„π°“√√—°…“«à“∑—π∑à«ß∑’À√◊Õ‰¡à

√Ÿª∑’Ë 20.2 µ”·ÀπàßÕÿ¥µ—π¢Õß cardiac emboli ¢ÕßÀ≈Õ¥ ‡≈◊Õ¥·¥ß∑—Ë«√à“ß°“¬¢Õß ‚√ßæ¬“∫“≈¡À“√“™π§√ ‡™’ ¬ ß„À¡à 74 √“¬ √– À«à“ßæ.». 2533-2535

ºŸâ ªÉ « ¬∑’Ë À ≈Õ¥‡≈◊ Õ ¥·¥ßÕÿ ¥ µ— π ‡©’ ¬ ∫æ≈— π ·≈–¡’ ° “√¢“¥ ‡≈◊Õ¥Õ¬Ÿπà “π ®–¡’ª≠ í À“¡“°‡√◊ÕË ß metabolism ∑’‡Ë °‘¥¢÷πÈ ¿“¬À≈—ß ®“° revascularize ·≈â« ®–‡°‘¥ reperfusion syndrome “√æ‘…µà“ß Ê ∑’‡Ë °‘¥¢÷πÈ ®–∂Ÿ°ª≈àÕ¬‡¢â“ Ÿà systemic circulation ·≈–¡’º≈µàÕÕ«—¬«– ”§—≠¢Õß√à“ß°“¬‡™àπ À—«„® ªÕ¥ ‰µ·≈– ¡Õß ¢÷πÈ Õ¬Ÿ°à ∫— degree of tissue necrosis ‡°‘¥¿“«–‰µ«“¬‡©’¬∫æ≈—π, respiratory distress syndrome ·≈– multiple organ failure(9,13,14)

Õ“°“√·≈–Õ“°“√· ¥ß „π√–¬–·√°∑’¡Ë °’ “√¢“¥‡≈◊Õ¥ º‘«Àπ—ß®–‡¬Áπ´’¥ µàÕ¡“Õ’° 812 ™—Ë«‚¡ß ®–‡°‘¥ vasospasm ∑”„Àâº‘«Àπ—ß¡’ ’§≈È”‡ªìπ®È” Ê (mottling) ¡’ poor capillary filling ·≈– collapsed ¬“®–‡¬Áπ

180

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µ“√“ß∑’Ë 20.1 condition ¢Õß ischemic lower limb ·∫àß ÕÕ°‡ªìπ 1. early ischemia ®–¡’ paresthesia, pallor ·≈– pulselessness ´÷ßË ∫àß∫Õ°«à“ limb viable 2. advanced ischemia ®–¡’ paralysis ·≈– rigor ∫àß∫Õ° «à“‡°‘¥¿“«– non-viable limb

´’¥ (poikilothermia) ´÷ßË ∫àß∫Õ°«à“‡π◊ÕÈ ‡¬◊ÕË ‡πà“µ“¬‰¡àøπóô (√Ÿª∑’Ë 20.3) Õ“°“√· ¥ß∑’ Ë ”§—≠¢Õß°“√¢“¥‡≈◊Õ¥Õ¬à“ß‡©’¬∫§◊Õ 6 Pûs ¡’ pain, pallor, paresthesia, pulselessness, paralysis ·≈– poikilothermia °“√ª«¥®–§ß∑’Ë·≈–®–ª«¥¡“°¢÷Èπ‡¡◊ËÕ¢¬—∫¢“ °“√™“À¡“¬∂÷ß¡’°“√¢“¥‡≈◊Õ¥´÷Ëß¡’º≈µàÕ‡ âπª√– “∑ —¡º— à«πª≈“¬ À≈—ßÀ≈Õ¥‡≈◊Õ¥·¥ßÕÿ¥µ—π¢“®–‡¬Áπ´’¥ª√–¡“≥ 1 joint µË”°«à“ √–¥—∫¢ÕßÀ≈Õ¥‡≈◊Õ¥∑’ÕË ¥ÿ µ—π (√Ÿª∑’Ë 20.2) „π√“¬ advanced ischemia ·≈–¡’‡π◊ÕÈ ‡¬◊ÕË µ“¬®“°°“√¢“¥ ‡≈◊Õ¥ ®–¢¬—∫π‘«È ‡∑â“À√◊Õ∑” ankle dorsiflex ‰¡à ‰¥â Õ“®®–‡°‘¥ complete foot paralysis ‰ª‡≈¬ §«√æ‘®“√≥“µ—¥¢“ ‡æ√“–∂÷ß ·¡â«à“®– revascularization ·≈â« motor function ®–‰¡à§◊π °≈—∫¡“‡≈¬ muscle rigor °Á∫ßà ∫Õ°∂÷ß nonviable extremity (µ“√“ß∑’Ë 20.1) „π arterial thrombosis Õ“°“√·≈–Õ“°“√· ¥ß®–§≈â“¬°—∫ ºŸªâ «É ¬∑’ÀË ≈Õ¥‡≈◊Õ¥·¥ßÕÿ¥µ—π®“° embolism ·µà®–¡’ª√–«—µ‘ claudication ¡“°àÕπÀπâ“π’È À√◊Õ‚√§À—«„®√à«¡¥â«¬ Õ“°“√ª«¥®– πâÕ¬°«à“ embolism §«√µ√«®√à“ß°“¬¥Ÿ≈—°…≥–¢Õß¢“«à“¡’ trophic skin changes, ¢π√à«ß, ‡≈Á∫À¬—°‡ªìπ™—πÈ À√◊Õº‘«Àπ—ß ·ÀâßÀ√◊Õ‰¡à (15,16)

°“√«‘π‘®©—¬‚√§ ‡æ◊ÕË „Àâ ‰¥âº≈„π°“√√—°…“∑’¥Ë ’ §«√æ¬“¬“¡·¬°·¬–À“ “‡Àµÿ √–À«à“ß embolization À√◊Õ in-situ thrombosis ‚¥¬∑—«Ë ‰ª·≈â« ª√–«— µ‘ · ≈–°“√µ√«®√à “ ß°“¬®– “¡“√∂∫Õ°‰¥â § √à “ « Ê ¡’ ª√–¡“≥√âÕ¬≈– 5-20 (15%) ∑’Ë ‰¡à “¡“√∂∫Õ° “‡Àµÿ‰¥â®“° ª√–«—µ·‘ ≈–°“√µ√«®√à“ß°“¬ ‡æ√“–‰¡à‡§¬¡’ª√–«—µ‘ Intermittent claudication À√◊ÕÕ“°“√¢“¥‡≈◊Õ¥‡√◊ÈÕ√—ß¡“°àÕπ °“√µ√«® «‘π®‘ ©—¬æ‘‡»…®– “¡“√∂™à«¬·¬°·¬–‚√§‰¥â 1. °“√µ√«®∑“ßÀâÕßªØ‘∫µ— °‘ “√ ‡æ◊ÕË ¥Ÿ¿“«–°“√¢“¥ “√πÈ” °“√π”ÕäÕ°´‘‡®π¢Õß‡¡Á¥‡≈◊Õ¥·¥ß«à“¡’ª√– ‘∑∏‘¿“æ¥’ ‡æ’¬ß„¥ °“√∑”ß“π¢ÕßÀ—«„® ‰µ ·≈–°“√∂Ÿ°∑”≈“¬

¢Õß°≈â“¡‡π◊ÕÈ ¿“æ√—ß ’∑√«ßÕ°®–∫àß∫Õ°∂÷ßÀ—«„®À√◊Õ ‰¡àÀ√◊Õ‡ÀÁπ thoracic aortic disease √–¥—∫Œ’¡“‚µ§√‘µ∫àß∫Õ°«à“¡’¿“«– polycythemia À√◊Õ‰¡à µ√«® ªí “«–æ∫ myoglobinuria „πªí “«–À√◊Õ‰¡à ‡®“– ‡≈◊Õ¥æ∫ creatinine phosphokinase ∑’¡Ë √’ –¥—∫ Ÿß¢÷πÈ ®“°°“√∑’Ë°≈â“¡‡π◊ÈÕµ“¬ EKG ¥Ÿ®—ßÀ«–°“√‡µâπ·≈– ¿“«–º‘¥ª°µ‘¢ÕßÀ—«„® 2-dimensional echocardiography ®– “¡“√∂∫Õ°¢π“¥¢Õß™àÕßÀ—«„® ejection fraction °“√∑”ß“π¢Õß≈‘πÈ À—«„® ºπ—ßÀ—«„® thrombus À√◊Õ°âÕπ¡–‡√Áß∑’‡Ë °‘¥¢÷πÈ „πÀ—«„® ¿“«– ASD °“√∑” ultrasound ∫√‘‡«≥™àÕß∑âÕßÕ“®®–æ∫ AAA ∫√‘‡«≥ πàÕßÕ“®®–æ∫ popliteal artery aneurysm (µ“√“ß∑’Ë 20.2) 2. Arteriography „πºŸªâ «É ¬ advanced ischemia §àÕπ¢â“ß·πà „®«à“ “‡Àµÿ°“√¢“¥‡≈◊Õ¥‡°‘¥®“° embolism ·≈–§“¥µ”·Àπàß·πàπÕπ‰¥â §«√π”‰ªºà“µ—¥∑” embolectomy ∑—π∑’ „π√“¬∑’¬Ë ß— ‰¡à·πà„®„π°“√«‘π®‘ ©—¬‚√§√–À«à“ß embolism °—∫ thrombosis §«√∑” arteriography ¿“æ√—ß ’∑’Ë ‰¥â®–∫àß∫Õ°∂÷ß√Õ¬‚√§ ∂â“°“√Õÿ¥µ—π¢Õß À≈Õ¥‡≈◊Õ¥‡°‘¥®“°‡ÕÁ¡‚∫‰≈ ®–æ∫«à“À≈Õ¥‡≈◊Õ¥·¥ßª°µ‘ ·µà∫√‘‡«≥∑’ÕË ¥ÿ µ—π®–¡’≈°— …≥–‡ªìπ sharp, convex-appearing cutoff (√Ÿª∑’Ë 20.5) ∂â“‡ªìπ thrombosis À≈Õ¥‡≈◊Õ¥®–¡’√Õà ß√Õ¬¢Õß atherosclerosis ∑—«Ë ‰ª ¡’ collaterals ∫√‘‡«≥∑’ËÕÿ¥µ—π®–¡’≈—°…≥–‡ªìπ irregular tapering (√Ÿª∑’Ë 20.6) 3. Duplex scanning ‡ªìπ«‘∏°’ “√µ√«®«‘π®‘ ©—¬‚√§À≈Õ¥ ‡≈◊Õ¥·¥ßÕÿ¥µ—π ·∫∫ noninvasive “¡“√∂∫Õ°‰¥â∂ß÷ distal outflow tract ·≈–¥Ÿ‰¥â∂÷ß§«“¡º‘¥ª°µ‘„π À≈Õ¥‡≈◊Õ¥¥”‰¥â«“à ‡°‘¥ venous thrombosis √à«¡¥â«¬ µ“√“ß∑’Ë 20.2 °“√µ√«®«‘π®‘ ©—¬∑“ßÀâÕßªØ‘∫µ— °‘ “√ µ√«®√–¥—∫Œ’¡“‚µ§√‘∑, PT/PTT ·≈–‡°√Á¥‡≈◊Õ¥ Electrolytes, BUN, Creatinine ·≈–πÈ”µ“≈„π‡≈◊Õ¥ µ√«®ªí “«–¥Ÿ myoglobinuria CPK ·≈– isoenzymes ¿“æ√—ß ’∑√«ßÕ° EKG Two-dimensional echocardiogram

181

ACUTE ARTERIAL OCCLUSION

√Ÿª∑’Ë 20.3

¢“ºŸâªÉ«¬∑’Ë¢“¥‡≈◊Õ¥‡©’¬∫æ≈—π ®“°‡ÕÁ¡‚∫‰≈Õÿ¥À≈Õ¥‡≈◊Õ¥·¥ß ¡’ ° “√‡πà “ µ“¬‰¡à øóô π æ∫«à “ ¡’ blebs, mottling, superficial skin necrosis ·≈–¢“‡¬Áπ´’¥

If nutritional changes above knee then occlusion is at aortic bifurcation Common femoral occlusion Superficial femoral occlusion minimal nutritional changes if distal bed open Popliteal artery occlusion

Distal block to popliteal bifurcation

√Ÿª∑’Ë 20.4 µ”·Àπà ß ¢ÕßÀ≈Õ¥‡≈◊ Õ ¥·¥ß∑’Ë Õÿ ¥ µ— π ·≈– ∫√‘ ‡ «≥º‘ « Àπ— ß ∑’Ë ‡ ¬Á π ®–µË” °«à “ À≈Õ¥‡≈◊ Õ ¥ ·¥ß∑’ËÕÿ¥µ—π 1 ¢âÕ‡ ¡Õ

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√Ÿª∑’Ë 20.5 ≈—°…≥–¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ßÕÿ¥µ—π‡©’¬∫æ≈—π®“°‡ÕÁ¡‚∫‰≈

√Ÿª∑’Ë 20.6 ≈—°…≥–À≈Õ¥‡≈◊Õ¥·¥ßÕÿ¥µ—π‡©’¬∫æ≈—π®“° thrombosis

∑’Ë‡ÀÁπ®“° arteriography À≈Õ¥‡≈◊Õ¥·¥ßª°µ‘∫√‘‡«≥∑’Ë Õÿ¥µ—π®–‡ÀÁπ‡ªìπ sharp, convex-appearing cutt-off

∑’Ë‡ÀÁπ®“° arteriography À≈Õ¥‡≈◊Õ¥·¥ß¡’√àÕß√Õ¬¢Õß atherosclerosis ∑—Ë«‰ª ¡’ collaterals ∫√‘‡«≥∑’Ë Õÿ¥µ—π ‡ªìπ irregular tapering

À√◊Õ‰¡à ·≈–¬—ß “¡“√∂ª√–‡¡‘πÀ≈Õ¥‡≈◊Õ¥¥” saphenous ∑’®Ë –π”¡“„™â∑” bypass ‰¥â¥«â ¬ „πÕπ“§µ duplex scanning ®–‡ªìπ«‘∏’°“√µ√«®«‘π‘®©—¬‚√§À≈Õ¥‡≈◊Õ¥ ·¥ßÕÿ¥µ—π‡©’¬∫æ≈—π ∑’Ë¡’∫∑∫“∑¡“°¢÷Èπ·≈–¬—ß™à«¬„π °“√µ‘¥µ“¡ºŸªâ «É ¬À≈—ß°“√√—°…“Õ’°¥â«¬

¬Ÿπµ‘ µàÕ™—«Ë ‚¡ß §«∫§ÿ¡„Àâ√–¥—∫¢Õß partial thromboplastin (PTT) Õ¬Ÿà∑’Ë 1.5-2 ‡∑à“¢Õß√–¥—∫ª°µ‘®÷ß®–‰¥âº≈¥’∑’Ë ÿ¥ °≈‰°¢Õß √à“ß°“¬À≈—ßÀ≈Õ¥‡≈◊Õ¥·¥ßÕÿ¥µ—π ®–À≈—ßË inflammatory factors ∑’Ë∑”„ÀâÀ≈Õ¥‡≈◊Õ¥ à«πª≈“¬À¥µ—« ªÑÕß°—π distal clot propragation Õÿ¥À≈Õ¥‡≈◊Õ¥ à«πª≈“¬ ·µà°Á¡’¢âÕ‡ ’¬§◊Õ∑”„Àâ ‡°‘¥°“√À¥µ—«¢Õß collaterals ·µàÀ≈—ß®“°„Àâ anticoagulants „πª√‘¡“≥∑’Ë‡À¡“– ¡·≈â« °“√À¥µ—«¢ÕßÀ≈Õ¥‡≈◊Õ¥®–≈¥≈ß À≈Õ¥‡≈◊Õ¥®–¢¬“¬µ—« ∑”„Àâ collaleral flow ¥’¢π÷È Õ“°“√ª«¥ ®–≈¥≈ß √–¥—∫¢Õß ischemic demarcation ®–≈¥√–¥—∫µË” ≈ß°«à“‡¥‘¡ ∂â“„π√–¬–·√°¢Õß°“√¢“¥‡≈◊Õ¥Õ¬à“ß‡©’¬∫æ≈—π ‡°‘¥¢÷Èπ·≈–¬—ß‡ªìπ viable limb °“√„Àâ anticoagulants „πª√‘¡“≥∑’‡Ë À¡“– ¡ ®–∑”„Àâ ‰¡àµÕâ ßºà“µ—¥©ÿ°‡©‘π “¡“√∂‡ª≈’¬Ë π ‡ªìπ°“√ºà“µ—¥·∫∫ elective ‰¥â(4,5,10,11,15,16) (µ“√“ß∑’Ë 20.3)

°“√√—°…“ ºŸªâ «É ¬∑ÿ°√“¬∑’ÕË ¬Ÿà„π¿“«– limb-threatening ®“°À≈Õ¥‡≈◊Õ¥ ·¥ßÕÿ¥µ—π‡©’¬∫æ≈—π §«√„Àâ‡Œª“√’π∑“ßÀ≈Õ¥‡≈◊Õ¥¥”∑—π∑’‡æ◊ËÕ ªÑÕß°—π°“√‡°‘¥ distal clot propragation ‡Œª“√’π‡ªìπ¬“∑’Ë ÕÕ°ƒ∑∏‘Ï ‰¥â ‰« ∂â“„Àâ‡¢â“∑“ßÀ≈Õ¥‡≈◊Õ¥¥” ‡¡µ“‚∫‰≈ å ‰«·≈–·°â ƒ∑∏‘Ï ‰¥â¥«â ¬‚ª√µ“¡’π´—≈‡øµ ‡√‘¡Ë „Àâ‡Œª“√’π 5,000 ¬Ÿπµ‘ ‡¢â“À≈Õ¥ ‡≈◊Õ¥¥”∑—π∑’ ·≈â«À¬¥‡¢â“À≈Õ¥‡≈◊Õ¥¥”µàÕ‡π◊ËÕß¢π“¥ 1,000

ACUTE ARTERIAL OCCLUSION

µ“√“ß∑’Ë 20.3 À≈—°°“√√—°…“¿“«–¢“¢“¥‡≈◊Õ¥‡©’¬∫æ≈—π 1. ªÑÕß°—π°“√‡°‘¥ propragation of clotting ‚¥¬°“√„Àâ loading dose ¢Õß heparin ∑“ßÀ≈Õ¥‡≈◊Õ¥¥” 2. «‘π®‘ ©—¬‚√§„Àâ ‰¥â«“à ‡°‘¥®“° “‡ÀµÿÕ–‰√ ®“°ª√–«—µ°‘ “√µ√«® √à“ß°“¬, doppler US, EKG ·≈– arteriography ·¬°®“° ‚√§¥—ßµàÕ‰ªπ’È arterial embolism acute thrombosis atherosclerotic artery atherosclerotic aneurysm dissecting aneurysm phlegmasia cerulea dolens 3. ·°â ‰¢¿“«–§«“¡º‘¥ª°µ‘¢Õß√à“ß°“¬∑—π∑’‡™àπ dehydration, ¿“«–À—«„®∑’‡Ë µâπº‘¥ª°µ‘ ‚¥¬‰¡à delay operation 4. ‰¡à§«√‡ ’¬‡«≈“„π°“√ºà“µ—¥‰ª°—∫°“√„™â vasodilators, sympathetic blockers À√◊Õ°“√µ√«®«‘π®‘ ©—¬∑’Ë ‰¡à®”‡ªìπ 5. ºà “ µ— ¥ √— ° …“Õ¬à “ ß∂Ÿ ° µâ Õ ßÀ≈— ß ®“°·πà „®„π°“√«‘π‘®©—¬ „π √–¬–‡«≈“∑’Ë‡À¡“– ¡ ·≈–≈ß·º≈ºà“µ—¥µ”·Àπàß∑’Ë‡¢â“∂÷ß √Õ¬‚√§Õ¬à“ß∂Ÿ°µâÕß‡æ◊ÕË repurfusion Õ“®®–‚¥¬°“√∑” embolectomy, arterial repair, venous thrombectomy œ≈œ ·≈– proof distal patency ‚¥¬°“√§≈”™’æ®√ øíß¥â«¬ doppler US À√◊Õ∑” intraoperative arteriography

∂â“ºŸâªÉ«¬¡“æ∫·æ∑¬å¿“¬„π 4-6 ™—Ë«‚¡ßÀ≈—ßÀ≈Õ¥‡≈◊Õ¥ ·¥ßÕÿ¥µ—π‡©’¬∫æ≈—π ¡’Õ“°“√¢Õß pain, paralysis ·≈– paresthesia ´÷Ëß∑”„Àâ ß —¬«à“¬—ß¡’ limb viability À√◊Õ‰¡à §«√ √’∫∑”°“√ºà“µ—¥√—°…“∑—π∑’ ·µà§«√√–«—ßªí≠À“°“√µ°‡≈◊Õ¥À≈—ß ºà“µ—¥ „πºŸâªÉ«¬∑’Ë ‰¥â√—∫ anticoagulants „πª√‘¡“≥∑’Ë Ÿß „πºŸâ ªÉ«¬∑’§Ë “¥«à“°“√¢“¥‡≈◊Õ¥¡’ “‡Àµÿ®“° thrombosis ·µà¬ß— ¡’ limb viable §«√„Àâ anticoagulants „πª√‘¡“≥ Ÿß‡æ◊ÕË „Àâ collaterals ¥’¢π÷È √–¥—∫¢Õß°“√¢“¥‡≈◊Õ¥¥’¢π÷È ·≈–§ß∑’Ë À≈—ß®“°π—πÈ ®÷ßºà“µ—¥ revascularization ·∫∫ elective µàÕ‰ª(17,18) ‰¡à§«√ºà“µ—¥©ÿ°‡©‘π„πºŸâªÉ«¬∑’Ë¢“¥‡≈◊Õ¥π“π‡°‘π 8 ™—Ë«‚¡ß ‡æ√“–„π√–¬–‡«≈“π“π¢π“¥π’È °≈â“¡‡π◊ÕÈ ®–‡πà“µ“¬‰¡à°≈—∫øóπô ·≈â« ‡™àπ‡¥’¬«°—π°—∫ºŸªâ «É ¬∑’ Ë ßŸ Õ“¬ÿ·≈–¡’ underlying diseases Õ◊πË Õ¬Ÿ·à ≈â«‡™àπ COPD, CHF ‰µ«“¬ œ≈œ °“√ºà“µ—¥ revascularization ¢Õß·¢π¢“∑’¢Ë “¥‡≈◊Õ¥ ®–∑”„Àâ ischemic waste products ºà“π‡¢â“ Ÿà central circulation ∑”≈“¬Õ«—¬«– ”§—≠„π√à“ß°“¬ ‡™àπ ªÕ¥ À—«„® µ—∫ ‰µ ºŸâªÉ«¬∑’Ë√à“ß°“¬·¢Áß·√ß‡∑à“π—Èπ∑’Ë®–

183 “¡“√∂∑πµàÕ reperfusion syndrome ‰¥â °“√„Àâ high full dose ¢Õß‡Œª“√’π„π√–¬–·√°®–¡’º≈∑”„Àâ‡°‘¥°“√µ°‡≈◊Õ¥‰¥âßà“¬ §«√√–«—ß‚¥¬‡©æ“–„πºŸªâ «É ¬∑’®Ë ”‡ªìπ∑’®Ë –µâÕß∑” arteriography À≈— ß ®“°‰¥â ‡ Œª“√’ π ·≈â « Õ“°“√∑“ß§≈‘ π‘ § ¢ÕßºŸâ ªÉ « ¬®–¥’ ¢÷È π —ß‡°µ‰¥â®“° Õÿ≥À¿Ÿ¡‘¢Õß·¢π·≈–¢“®–Õÿàπ¢÷Èπ à«π∑’Ë‡¬Áπ®– ‡≈◊Ë Õ πµË” ≈ß‰ª Ÿà ª ≈“¬·¢π·≈–¢“ ª√– “∑ — ¡ º— ·≈–°“√ ‡§≈◊ÕË π‰À«¢Õß°≈â“¡‡π◊ÕÈ ®–¥’¢π÷È ∂â“°¥º‘«Àπ—ß·≈â«¬—ß¡’ blanching · ¥ß«à“º‘«Àπ—ß¬—ß viable ·µà∂“â º‘«Àπ—ß ’§≈È”¡’æ√“¬®È”·≈– °¥‰¡à¡’ blanding · ¥ß∂÷ß non-viable ‡°‘¥°“√µ“¬¢Õß ‡π◊ÈÕ‡¬◊ËÕº‘«Àπ—ß·≈â« °“√µ°‡≈◊Õ¥‡ªìπ¿“«–·∑√°´âÕπ∑’Ë√ÿπ·√ß∑’Ë ‡°‘¥¢÷Èπ¿“¬À≈—ß°“√„Àâ‡Œª“√’π´÷Ëßæ∫‰¥â ‰¡à∫àÕ¬π—° ·¡â«à“ºŸâªÉ«¬ ®–¡’·º≈ºà“µ—¥ §«“¡º‘¥ª°µ‘„π°“√·¢Áßµ—«¢Õß‡≈◊Õ¥À√◊Õ„π√“¬ ∑’Ë ‰¥â‡Œª“√’π„π dose ∑’ Ë ßŸ ¡“° «—π·√° Ê °“√µ°‡≈◊Õ¥¡—°®–‡°‘¥ ¢÷πÈ À≈—ß®“°‰¥â‡Œª“√’π¡“®π∂÷ß«—π∑’Ë 5 ´÷ßË ‡ªìπº≈¡“®“° heparininduced thrombocytopenia ®÷ß§«√„Àâ‡Œª“√’π„π dose ∑’ Ë ßŸ 3-4 «—π·√°·≈â«§àÕ¬≈¥ dose ≈ß¡“Õ¬Ÿà „π therapeutic level ∑“ßÀ≈Õ¥‡≈◊Õ¥¥” À√◊Õ‡ª≈’Ë¬π¡“©’¥‡¢â“„µâº‘«Àπ—ß´÷Ëß –¥«° ·≈–ª≈Õ¥¿—¬°«à“ À≈—ß«—π∑’Ë 7 §«√‡ª≈’¬Ë π‡ªìπ oral anticoagulant À≈—ß«—π∑’Ë 7 ‰ª·≈â«∑’Ë ‰¥â√∫— anticoagulant ·¢πÀ√◊Õ¢“∑’Ë ¢“¥‡≈◊Õ¥ ®– viable À√◊Õ¡’ partial necrotic ®÷ß®–æ‘®“√≥“ °“√√—°…“µàÕ‰ª«à“®– amputate, revascularize À√◊Õ„Àâ¬“ anticoagulant Õ¬à“ßµàÕ‡π◊ÕË ß ‚¥¬«‘∏’°“√‡√‘Ë¡„Àâ anticoagulant „πºŸâªÉ«¬∑’Ë¡’Õ“°“√·¢π ¢“¢“¥‡≈◊Õ¥Õ¬à“ß‡©’¬∫æ≈—π∑—π∑’ æ∫«à“ “¡“√∂≈¥Õ—µ√“µ“¬ ·≈–∑ÿæ≈¿“æ®“°°“√µâÕßµ—¥·¢π¢“≈ß‰¥â¡“°°«à“°“√µ—¥ ‘π„® ºà“µ—¥√—°…“∑—π∑’(19) „πºŸªâ «É ¬∑’¡Ë “¥â«¬ ischemic viable limbs §«√µ—¥ ‘π„®∑” thromboembolectomy À√◊Õ revascularization ¿“¬À≈—ß®“°„Àâ adequate dose ¢Õß anticoagulant ‡æ◊ÕË ªÑÕß°—π thrombus propragation ·≈â« „π√“¬∑’Ë¡’°≈â“¡‡π◊ÈÕ·≈– º‘«Àπ—ß‡πà“µ“¬·≈â«À≈—ß®“°„Àâ anticoagulant ·≈â«§«√∑” amputation ºŸâªÉ«¬∑’Ë¡’Õ“°“√·¢π¢“¢“¥‡≈◊Õ¥Õ¬à“ß‡©’¬∫æ≈—π∑’Ë¡“À≈—ß ‡°‘¥Õ“°“√ 48 ™—«Ë ‚¡ß ·µà·¢π¢“¬—ß viable §«√„Àâ anticoagulant „π dose ∑’ Ë ßŸ √Õ®π collaterals ¥’ À≈—ß®“°π—πÈ ∑” arteriography ‡æ◊ËÕ∑’Ë®–æ‘®“√≥“ºà“µ—¥ revascularize µàÕ‰ª „π √“¬∑’¿Ë “«–√à“ß°“¬‰¡à‡À¡“– ¡µàÕ°“√ºà“µ—¥ Õ“®®–√—°…“µàÕ¥â«¬ °“√„Àâ Warfarin (Coumadin) √—∫ª√–∑“πÀ√◊Õ©’¥‡Œª“√’π‡¢â“ „µâº«‘ Àπ—ß

184

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‡∑§π‘§°“√∑” embolectomy ºŸªâ «É ¬∑’·Ë ¢Áß·√ß¥’ ‰¡à¡’ underlying disease ·≈–Õ—µ√“‡ ’¬Ë ß µàÕ°“√ºà“µ—¥‰¡à ßŸ ·¢πÀ√◊Õ¢“¢“¥‡≈◊Õ¥¡“„π√–¬–‡«≈“‰¡àπ“π‡°‘π 8 ™—«Ë ‚¡ß ·≈–„Àâ°“√«‘π®‘ ©—¬™—πÈ µâπ«à“ “‡Àµÿ‡°‘¥®“°‡ÕÁ¡‚∫‰≈ §«√ æ‘®“√≥“ºà“µ—¥∑” embolectomy ‚¥¬ local À√◊Õ regional anesthesia(1) ≈ß¡’¥ºà“πº‘«Àπ—ß∫√‘‡«≥·¢π·≈–¢“‡æ◊ÕË ‡¢â“∂÷ßÀ≈Õ¥ ‡≈◊Õ¥·¥ß Õ¥ “¬ Fogerty balloon tip catheter ‡¢â“ À≈Õ¥‡≈◊Õ¥ºà“π≈‘Ë¡‡≈◊Õ¥À√◊Õ‡ÕÁ¡‚∫‰≈‡æ◊ËÕ¥÷ß≈“°ÕÕ°¡“®“° À≈Õ¥‡≈◊Õ¥ ‡∑§π‘§∑’¥Ë §’ Õ◊ §«√∑” proximal ·≈– distal control À≈Õ¥‡≈◊Õ¥·¥ß¥â«¬§’¡Àπ’∫À≈Õ¥‡≈◊Õ¥°àÕπ arteriotomy „ à “√πÈ”À√◊Õ≈¡‡¢â“„π∫—≈≈Ÿπ„Àâ¡ª’ √‘¡“≥æÕ‡À¡“–‰¡à¥ß÷ ·√ß‡°‘π‰ª®π Õ‘π∑‘¡“À≈ÿ¥≈Õ°À√◊ÕÀ≈Õ¥‡≈◊Õ¥™È” back bleeding ·≈–°“√§≈” distal pulsation ‰¡à ‰¥âÀ¡“¬§«“¡«à“¥÷ß‡Õ“ clot ÕÕ°À¡¥ clot ∑’Ë¥÷ßÕÕ°¡“‰¥â§«√‡ªìπ‡ âπ¬“«≈—°…≥–‡À¡◊Õπ·¢πßÀ≈Õ¥‡≈◊Õ¥ ·≈–‰¡à¢“¥ (√Ÿª∑’Ë 20.7) ∂â“‰¡à·πà „®«à“¥÷ß‡Õ“ clot ÕÕ°À¡¥À√◊Õ ‰¡à §«√∑” arteriography(20)

√Ÿª∑’Ë 20.7 ‡ÕÁ¡‚∫‰≈∑’Ë¥÷ßÕÕ°¡“®“°À≈Õ¥‡≈◊Õ¥·¥ß ‚¥¬°“√„™â Fogarty balloon tip catheter ¥÷ß≈“° ®–‰¥â‡ªìπ‡ âπ ¬“« ·≈–¡’·¢πß·¬°ÕÕ°¡“§≈â“¬À≈Õ¥‡≈◊Õ¥

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ACUTE ARTERIAL OCCLUSION

1. “¡“√∂¡Õß‡ÀÁπ·≈–∑√“∫µ”·Àπàß∑’·Ë πàπÕπ¢Õß clot 2. “¡“√∂§«∫§ÿ¡·π«∑“ß¢Õß∫—≈≈Ÿπ·≈–°“√ inflate ‰¥â ∑”„Àâºπ—ßÀ≈Õ¥‡≈◊Õ¥‰¡à™È”¡“° 3. ‡Õ“ clot ∑’§Ë “â ßÕÕ°‰¥âÀ≈—ß∑” blind embolectomy 4. “¡“√∂ Õ¥ “¬ª≈“¬ “¬ catheter ‡¢â“À≈Õ¥‡≈◊Õ¥ ·¢πß∑’µË Õâ ß°“√‰¥â 5. ‰¡àµÕâ ß∑” angiogram ‰¡àµÕâ ß√Õøî≈¡å x-ray ∑”„Àâ°“√ ºà“µ—¥π“π 6. ‡¢â “ ∂÷ ß À≈Õ¥‡≈◊ Õ ¥¢π“¥‡≈Á ° ‡™à π popliteal ·≈– tibioperoneal arteries ‰¥â ‚¥¬‰¡à®”‡ªìπ∑’Ë®–µâÕß≈ß ·º≈ºà“µ—¥‡æ‘¡Ë À≈—ßºà“µ—¥ 24 ™—«Ë ‚¡ß·√°§«√¥Ÿ·≈ºŸªâ «É ¬Õ¬à“ß„°≈â™¥‘ „π ICU ¥Ÿ‡≈◊Õ¥∑’Ë ‰À≈‡«’¬π‰ª‡≈’¬È ßª≈“¬¡◊Õª≈“¬‡∑â“«à“¥’À√◊Õ‰¡à ∂â“Õ“°“√ ‡≈«≈ß À¡“¬§«“¡∂÷ß‡°‘¥ rethrombosis À√◊Õ recurrent emboli §«√√’∫π”ºŸâªÉ«¬‡¢â“ºà“µ—¥´È”∑—π∑’ ∂â“‡°‘¥¿“«–·∑√°´âÕπ ¢Õß√–∫∫µà“ß Ê ‡™àπ À—«„® À√◊Õ‰µ §«√√—°…“∑—π∑’ ¿“«–·∑√° ´âÕπ¢Õß revascularization ∑’æË ∫‰¥â¡¥’ ß— µ“√“ß∑’Ë 20.4

Thrombosis ∂â“ “‡Àµÿ¢Õß°“√¢“¥‡≈◊Õ¥‡©’¬∫æ≈—π‡°‘¥®“° thrombosis ·π«∑“ß°“√√—°…“®–·µ°µà“ß®“° emboli ´÷ßË µâÕßºà“µ—¥∑” embolectomy ∑—π∑’À≈—ß®“°‰¥â anticoagulant „πª√‘¡“≥∑’‡Ë À¡“– ¡ (11,16,17,27,28,29) „π thrombosis À≈—ß®“°‰¥â anticoagulant ·≈â« §«√√—°…“·∫∫ conservative πÕ°®“°°“√¢“¥‡≈◊Õ¥Õ¬Ÿà „π¿“«– «‘°ƒµ‘®√‘ß Ê ·≈â«®÷ßæ‘®“√≥“∑”°“√ºà“µ—¥ revascularization à«π „À≠à·≈â«ºŸªâ «É ¬ thrombosis Õ“°“√®–¥’¢π÷È À≈—ß®“°‰¥â censervative management À≈—ß®“°π—πÈ ®÷ß∑” arteriogram ¥Ÿµ”·Àπàß ∑’ÕË ¥ÿ µ—π ‡æ◊ÕË ºà“µ—¥ revascularize µàÕ‰ª µ“√“ß∑’Ë 20.4 ¿“«–·∑√°´âÕπ¢Õß Revascularization °“√µ°‡≈◊Õ¥ Thrombosis Recurrent emboli Pulmonary emboli Microembolic acute respiratory distress syndrome ·¢π¢“∫«¡ ‰µ«“¬‡©’¬∫æ≈—π ‚√§À—«„® ‡™àπ myocardial infarction, arrhytmias Mesenteric infarction

Postoperative Anticoagulation À≈—ßºà“µ—¥§«√„Àâ‡Œª“√’π∑“ßÀ≈Õ¥‡≈◊Õ¥¥”µàÕ‡π◊ÕË ßÕ¬à“ßπâÕ¬ 72 ™—«Ë ‚¡ß ·≈–§àÕ¬ Ê ≈¥¢π“¥≈ß ‡√‘¡Ë „Àâ Coumadin (Warfarin) ‡¡◊ÕË ºŸªâ «É ¬√—∫ª√–∑“π‰¥â (30) ¿“«–·∑√°´âÕπ∑’æË ∫‰¥â®“°°“√ „Àâ‡Œª“√’π §◊Õ°“√µ°‡≈◊Õ¥ Õ“®®–æ∫‡ªìπ melena, hematuria, ecchymosis,¡’≈‘Ë¡‡≈◊Õ¥∑’Ë·º≈ºà“µ—¥ ºŸâªÉ«¬∑’Ë ‰¥â√—∫‡Œª“√’π§«√ monitor √–¥—∫Œ’¡“‚µ§√‘µ, platelet count ·≈– partial thromboplastin time (PTT) ∂â“¿“«–·∑√°´âÕπ®“°°“√‰¥â‡Œª“√’π ‰¡à√πÿ ·√ß §«√√’∫‡ª≈’¬Ë π‡ªìπ¬“√—∫ª√–∑“π ·µà∂“â ‡°‘¥¢÷πÈ √ÿπ·√ß ¡’°“√µ°‡≈◊Õ¥·≈–‡≈◊Õ¥‰À≈‰¡àÀ¬ÿ¥ §«√„Àâ¬“µâ“π§◊Õ Protamine ¿“«–·∑√°´âÕπ√ÿπ·√ß∑’‡Ë °‘¥®“°°“√„Àâ‡Œª“√’π§◊Õ ‡≈◊Õ¥‰À≈‰¡àÀ¬ÿ¥ µâÕß„Àâ‡≈◊Õ¥, CVA, pulmonary infarction ·≈–≈‘¡Ë ‡≈◊Õ¥¢π“¥ ‚µ∑’·Ë º≈ºà“µ—¥ °“√„Àâ‡Œª“√’πÀ≈—ßºà“µ—¥ ®–≈¥Õ—µ√“°“√‡°‘¥ recurrent emboli ·≈– thrombi ≈ß‰¥â¡“°(31)

Fasciotomy ·¢π¢“∫«¡À≈—ß revascularization ®–¡’º≈∫’∫√—¥À≈Õ¥‡≈◊Õ¥ ∑”„Àâ ‡ ≈◊ Õ ¥À¡ÿ π ‡«’ ¬ π‰À≈‰ª¬— ß ª≈“¬¡◊ Õ ª≈“¬‡∑â “ ‰¥â ‰¡à ¡’ ª√– ‘∑∏‘¿“æ °“√∑” fasciotomy ®–™à«¬≈¥§«“¡¥—π∑’Ë‡°‘¥ ¢÷Èπ Ÿß¿“¬„π muscle compartments ‡≈◊Õ¥®–‰À≈‡«’¬π‰ª ª≈“¬¡◊Õª≈“¬‡∑â“‰¥â¥¢’ π÷È (32) À≈—ß∑” fasciotomy ®–‡ ’¬Ë ßµàÕ°“√ µ‘¥‡™◊ÕÈ ‰¥âß“à ¬ ‡æ√“– necrotic muscle ®–≈’∫·≈–§àÕ¬ΩÉÕ‰ª‡Õß ·µà∂“â ∑” fasciotomy ·≈â«®–‡ ’¬Ë ßµàÕ°“√µ‘¥‡™◊ÕÈ ‰¥âß“à ¬ ‡π◊ÕË ß®“° ‡ªìπ media ∑’¥Ë ’„π°“√‡®√‘≠‡µ‘∫‚µ¢Õß·∫§∑’‡√’¬ §«√∑” fasciotomy ‡¡◊ÕË ¡’¢Õâ ∫àß™’ÀÈ ≈—ß¡’°“√‡æ‘¡Ë §«“¡¥—π„π compartments §◊Õ °“√∫“¥‡®Á∫µàÕ‡π◊ÈÕ‡¬◊ËÕ‚¥¬µ√ß°“√µ°‡≈◊Õ¥„π°≈â“¡‡π◊ÈÕ·≈– venous obstruction À≈—ß°“√∑” fasciotomy ·≈â«®–µâÕß∑√“∫«à“ necrotic muscle ®–‰¡àøπóô °≈—∫¡“ Ÿà „π ¿“«–ª°µ‘‰¥â

Fibrinolytic Therapy ‡√“®–‰¡à‡√‘Ë¡µâπ√—°…“ºŸâªÉ«¬∑’Ë¡’·¢π¢“¢“¥‡≈◊Õ¥Õ¬à“ß‡©’¬∫ æ≈—π∑’Ë‡ªìπ advanced ischemia ‚¥¬ Fibrinolytic therapy ‡æ√“–®–µâÕß„™â‡«≈“ 12-24 ™—«Ë ‚¡ß µ—«¬“®÷ß®–ÕÕ°ƒ∑∏‘Ï ‰¥â‡µÁ¡∑’Ë ´÷ßË ¿“¬„π 6-8 ™—«Ë ‚¡ß°≈â“¡‡π◊ÕÈ °Á®–‡πà“µ“¬·≈â« ·µà∂“â ‡ªìπ subacute ischemia ´÷ßË ¡’ “‡Àµÿ®“° thrombi ¡“°°«à“ emboli °“√„™â Fibrinolytic therapy ‡√‘¡Ë „Àâ¬“∑“ßÀ≈Õ¥‡≈◊Õ¥¥” ®÷ßµâÕß„Àâ „π ª√‘¡“≥ Ÿß‡æ◊ËÕ∑’Ë®–≈–≈“¬ clot æ∫«à“¡’ªí≠À“·∑√°´âÕπ®“° °“√µ°‡≈◊Õ¥¡“° (µ“√“ß∑’Ë 20.5) ªí®®ÿ∫π— «‘∏°’ “√∑’Ë ‰¥âº≈¥’·≈– ¿“«–·∑√°´âÕπ®“°°“√µ°‡≈◊Õ¥πâÕ¬§◊Õ °“√„Àâ plasminogen

186

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µ“√“ß∑’Ë 20.5 ¿“«–·∑√°´âÕπ¢Õß Fibrinolytic Therapy Intracranial hemorrhage Arterial site hematoma Distal embolization ¡’‡≈◊Õ¥´÷¡ÕÕ°®“°√Ÿ¢ÕßÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡‡π◊ÕË ß®“°¡’ lysis ¢Õß pseudointima ∫π Dacron graft Retroperitoneal hemorrhage ·æâ¬“

activator ºà“π “¬ «π∑’Ë Õ¥ºà“πº‘«Àπ—ß‡¢â“À≈Õ¥‡≈◊Õ¥·¥ß ·≈–ª≈“¬ “¬ «πÕ¬Ÿµà √ßµ”·Àπàß¢Õß thrombus æÕ¥’ (33,34,35) Streptokinase (SK) ‡ªìπ nonenzymatic protein ¢Õß group C B-hemolytic streptococci ´÷ßË ®–®—∫µ—«°—∫ plasminogen °≈“¬‡ªìπ active enzymatic complex ∑’ Ë “¡“√∂‡ª≈’¬Ë π plasminogen „Àâ‡ªìπ plasmin ‰¥â ∂â“„Àâ∑“ßÀ≈Õ¥‡≈◊Õ¥·¥ß „Àâ ‰¥â „π¢π“¥µË”§◊Õ 5,000-10,000 IU/h ¿“¬„π 12-48 ™—«Ë ‚¡ß ∑” arteriography ‡ªìπ√–¬–¥Ÿ«“à thrombus ≈–≈“¬À¡¥À√◊Õ‰¡à ¿“«–·∑√°´âÕπ∑’Ëæ∫‰¥â∫àÕ¬®“°°“√„Àâ SK §◊Õ ¡’‰¢â¢÷Èπ ´÷Ëß‡ªìπ ªØ‘°‘√‘¬“¢Õß√à“ß°“¬ ®“° antigen-antibody interaction ∑’Ë ‡°‘¥¢÷πÈ ®“° Streptokinase ∑’∑Ë ”„Àâ‡°‘¥ streptococcal antibodies Urokinase ‡ªìπ “√∑’ Ë °—¥‰¥â®“° human renal cells „π tissue culture ·≈–‰¡à „™à “√ antigenic ¡’≈°— …≥–‡ªìπ trypsin like protease ®–‡ª≈’¬Ë π plasminogen „Àâ‡ªìπ plasmin „Àâ ∑“ßÀ≈Õ¥‡≈◊Õ¥·¥ß„π¢π“¥ 20,000 IU/h ¡’√“§“·æß°«à“ SK ¡“° Fibrinolytic therapy ®–‰¥âº≈¥’ ”À√—∫ fresh thrombus ¡“°°«à“ organized thrombus ·≈–§«√®–‡√‘¡Ë µâπ°“√√—°…“∑—π∑’ °àÕπ∑’Ë®–‡°‘¥ clot propation ¢≥–∑’Ë „Àâ SK ‡æ◊ËÕ≈–≈“¬ clot §«√„Àâ‡Œª“√’π√à«¡¥â«¬ ‡æ◊ËÕªÑÕß°—π°“√‡°‘¥ clot „À¡à ·≈– ‡ªìπ°“√‡æ‘¡Ë collaterals ¥â«¬ „π¢≥–∑’Ë fibrinolytic agent ®–

≈–≈“¬ clot ™â“ Ê ∂÷ß·¡â«à“®–„Àâ¬“„π¢π“¥µË”·µà°Á®–¡’°“√ ‡ª≈’Ë¬π·ª≈ß¢Õß systemic fibrionolysis ‡°‘¥¢÷Èπ‰¥â ®÷ß§«√ monitor Thrombin time, platelet counts, √–¥—∫Œ’¡“‚µ§√‘∑ ·≈– fibrin split products ‡æ◊ËÕªÑÕß°—π·≈–‡ΩÑ“√–«—ß¿“«– ·∑√°´âÕπ®“°°“√µ°‡≈◊Õ¥ ‚¥¬‡©æ“–„π√“¬∑’Ë„Àâ anticoagulant √à«¡¥â«¬

√ÿª ºŸªâ «É ¬∑’¡Ë ª’ ≠ í À“·¢πÀ√◊Õ¢“¢“¥‡≈◊Õ¥Õ¬à“ß‡©’¬∫æ≈—π ®–µâÕß «‘π‘®©—¬„Àâ ‰¥â«à“¡’ “‡Àµÿ®“° emboli À√◊Õ thrombi ‡æ√“– ·π«∑“ß°“√√—°…“µ≈Õ¥®π∂÷ß°“√æ¬“°√≥å ‚√§µà“ß°—π ‡√‘Ë¡µâπ √—°…“Õ—π¥—∫·√°§◊Õ „Àâ‡Œª“√’π‡¢â“À≈Õ¥‡≈◊Õ¥¥”„π¢π“¥ Ÿß ‡æ◊ÕË ªÑÕß°—π clot propagation ∂â“·πà„®«à“ “‡Àµÿ‡°‘¥®“° emboli §«√√’∫∑” embolectomy ·µà∂“â ·¢πÀ√◊Õ¢“¢â“ßπ—πÈ ¡’ rigor ·≈– paralysis ·πà „®«à“‡°‘¥°“√‡πà“µ“¬·≈â«§«√µ—¥∑‘Èß ‰¡à§«√ revascularize °“√∑” embolectomy ®–∑”„Àâ√–¥—∫„π°“√µ—¥ ¢“À√◊Õ·¢π≈¥≈ß‰¡àµÕâ ßµ—¥ Ÿß¡“° ”À√—∫ thrombosis §«√∑” arteriography ™à«¬°“√«‘π‘®©—¬‚√§·≈–‰«â ”À√—∫«“ß·ºπ„π °“√ºà“µ—¥√—°…“µàÕ‰ª à«π„À≠à·≈â« acute thrombosis Õ“°“√ ®–¥’¢÷ÈπÀ≈—ß®“°‰¥â anticoagulant ‰ª„π√–¬–‡«≈“Àπ÷Ëß·≈â« ·≈– “¡“√∂ºà“µ—¥·∫∫ elective ‰¥â ·µà∂“â ‡ªìπ thrombosis ∑’Ë Õ¬Ÿà „π¿“«– limb threatening condition §«√®–√’∫ºà“µ—¥√—°…“ Õ“®®– revascularize ‚¥¬°“√∑” bypass operation ·µà®– µâÕß√–«—ß¿“«–·∑√°´âÕπ∑’Ë®–‡°‘¥¢÷Èπ¿“¬À≈—ß§◊Õ reperfusion syndrome ·≈– compartment syndrome ´÷Ëß®–µâÕß„Àâ°“√ √—°…“∑—π∑’ ¡’µ—«·ª√¡“°¡“¬„π°“√µ—¥ ‘π„®√—°…“ºŸâªÉ«¬·¢π¢“¢“¥ ‡≈◊Õ¥‡©’¬∫æ≈—π ¢÷ÈπÕ¬Ÿà°—∫ severity of ischemia, ¿“«– √à“ß°“¬¢ÕßºŸªâ «É ¬, ·æ∑¬åº∑Ÿâ ”°“√√—°…“«à“®–√—°…“‚¥¬°“√ºà“µ—¥, „Àâ‡Œª“√’πÀ√◊Õ fibrinolytic therapy ”À√—∫ºŸâªÉ«¬ cardiac emboli §«√„Àâ anticoagulants ‰ªµ≈Õ¥ ®π°√–∑—ßË ºà“µ—¥·°â ‰¢ §«“¡º‘¥ª°µ‘¢ÕßÀ—«„®·≈â«

ACUTE ARTERIAL OCCLUSION

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‡Õ° “√Õâ“ßÕ‘ß 1. Fogarty TJ, Cranley JJ, Krause RJ, et al. A method of extraction of arterial emboli and thrombi. Surg Gynecol Obstet 1963;116:241250. 2. Haimovici M. Acute atherosclerotic thrombosis. In: Vascular Emergencies. New York: Appleton-Century-Croft 1982;213-223. 3. Elliot JP, Hageman JH, Szilagyi E, et al. Arterial embolization: Problems of source, multiplicity, recurrence, and delayed treatment. Surgery 1980;88:833-845. 4. Eglund R, Magee HR. Peripheral arterial embolism: 1961-1985. Aust N2 J Surg 1987;57:27. 5. Baxter-Smith D, Ashtib F, Stanley G. Peripheral arterial embolism: a 20 year review. J Cardiovasc Surg 1988;29:453. 6. Kempczinski RF. Lower extremity arterial embolus from ulcerating atherosclerotic plaques. JAMA 1979;241:807. 7. Lord JW Jr, Rossi G, Daliana M, et al. Unsuspected abdominal aortic aneurysm as the cause of peripheral arterial occlusive disease. Ann Surg 1973;177:767. 8. Jivegerd L, Holm J, Schersten T. Acute limb ischemia due to arterial embolism or thrombosis: Influence of limb ischemia versus pre-existing cardiac disease on postoperative mortality rate. J Cardiovasc Surg 1988;29:32. 9. Haimovici H. Metabolic complications of acute arterial occlusions. J Cardiovasc Surg 1979;20:349-357. 10. Lusby RJ, Wylie EJ. Acute lower limb ischemia: Pathogenesis and management. World J Surg 1983;7:340. 11. Tawes RL, Harris EJ, Brown WH, et al. Arterial thromboembolism: A 20-year perspective. Arch Surg 1985;120:595. 12. Jivegard L. Selective conservation and routine early operation in acute limb ischemia. Br J Surg 1987;74:798-801. 13. Caruana JA, Cutierrez IZ, Anderson MN, et al. Factors that affect the outcome of peripheral arterial embolization. Arch Surg 1981;116:423-425. 14. Haimovici H. Muscular, renal and metabolic complications of acute arterial occlusions: Myonephropathic-metabolic syndrome. Surgery 1979;85:461-468. 15. Blaisdell F, Steele M, Allen R. Management of acute lower extremity arterial ischemia due to embolism and thrombosis. Surgery 1978;84:822-831. 16. Dale A. Differential management of acute peripheral arterial ischemia. J Vasc Surg 1984;1:269-276. 17. Mills JL, Porter JM. Basic data related to clinical decision-making in acute lime ischemia. Ann Vasc Surg 1991;5:96-98. 18. Yeager RA, Moneta GL, Taylor LM, et al. Surgical management of severe acute lower extremity ischemia. J Vasc Surg 1992;15:38539.

19. Blaisdell FW, Stells M, Allen RE. Management of acute lower extremity arterial ischemia due to embolism and thrombosis. Surgery 1978;84:822-829. 20. Mavor GE, Walker MG, Dhall DP. Routine operative arteriography in arterial embolectomy. Br J Surg 1972;59:482-484. 21. Schweitzer DL, Aguam AS, Wilder JR. Complications encountered during arterial embolectomy with the Fogarty balloon catheter. Vasc Surg 1976;10:144-156. 22. Foster JH, Carter JW, Graham CP, et al. Arterial injuries secondary to the use of the Fogarty catheter. Ann Surg 1970;171:971-978. 23. Short D, Vaughn GD III, Jachimczyk J, et al. The anatomic basis for the occasional failure of transfemoral balloon catheter thromboembolectomy. Ann Surg 1979;190:555. 24. Gupta SK, Samson RH, Veith FJ. Embolectomy of the distal part of the popliteal artery. Surg Gynecol Obstet 1981;153:255. 25. Wyffells PL, DeBord JR. Increased limb salvage. Distal tibial/ peroneal artery thrombectomy embolectomy in acute lower extremity ischemia. Am Surg 1990;56:468-475. 26. White GH, White RA, Kopchok GE, et al. Angioscopic thromboembolectomy: Preliminary observations with a recent technique. J Vasc Surg 1988;7:318-325. 27. Cambria RP, Abbott WM. Acute arterial thrombosis of the lower extremity. Its natural history contrasted with arterial embolism. Arch Surg 1984;119: 784-787. 28. McPhail NV, Fratesi SJ, Barber GG, et al. Management of acute thromboembolic limb ischemia. Surgery 1983;93:381-385. 29. Field T, Littooy FN, Baker WH. Immediate and long term outcome of acute arterial occlusion of the extremities. Arch Surg 1982;117:1156-1160. 30. Holm J, Schersten T. Anticoagulant treatment during and after embolectomy. Acta Chir Scand 1972;138:683. 31. Tawes RL, Beare JP, Scribner RG, et al. Value of postoperative heparin therapy in peripheral arterial thromboembolism. Am J Surg 1983;146:213. 32. Patman RD, Thompson JE. Fasciotomy in peripheral vascular surgery. Arch Surg 1970;101:663. 33. Hallett JW, Yrizarry JM, Greenwood LH. Regional low dosage thrombolytic therapy for peripheral arterial occlusions. Surg Gynecol Obstet 1983;156:148. 34. Hargrove WC, Barker CF, Bergowitz HD, et al. Treatment of acute peripheral arterial and graft thrombosis with low-dose streptokinase. Surgery 1982;92:981. 35. Marder VJ, Sherry S. Thrombolytic therapy: Current status. NEngl J Med 1988;318:1585.

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∫∑∑’Ë 21 INFECTED ANEURYSMS

„πªï §.». 1885 Sir William Osler §âπæ∫§«“¡ —¡æ—π∏å √–À«à“ß≈‘ÈπÀ—«„®∑’Ëº‘¥ª°µ‘¢ÕßºŸâªÉ«¬°—∫°“√µ‘¥‡™◊ÈÕ¢Õß·∫§∑’‡√’¬ ∑’Ë‰¡à„™à‡°‘¥®“°‡™◊ÕÈ √“ ‚¥¬¬°µ—«Õ¬à“ßºŸªâ «É ¬ bacterial endocarditis çfungus vegetationsé ®÷ß„Àâ§”π‘¬“¡°“√Õ—°‡ ∫µ‘¥‡™◊ÈÕ ™π‘¥π’«È “à ‡ªìπ éMycotic aneurysmsé(1) ´÷ßË „πªí®®ÿ∫π— ‡ªìπ∑’‡Ë ¢â“„® °—π«à“‡°‘¥®“°°“√µ‘¥‡™◊ÈÕ®“°·∫§∑’‡√’¬™π‘¥„¥°Á ‰¥â ‰¡à „™à®“° ‡™◊ÕÈ √“‡ ¡Õ‰ª(2,3) ªí®®ÿ∫π— ‰¡à§Õà ¬æ∫ syphylitic aneurysms ·µà®–æ∫ arterial infection ®“°‡™◊ÈÕ·∫§∑’‡√’¬À≈“¬™π‘¥´÷Ëß¡’ “‡Àµÿ®“°°“√ ©’¥¬“‡ æµ‘¥‡¢â“À≈Õ¥‡≈◊Õ¥ æ∫πâÕ¬«à“¡’ “‡Àµÿ¡“®“° bacterial endocarditis ‡π◊ËÕß®“°„πªí®®ÿ∫—π¬“ªØ‘™’«π–¡’ª√– ‘∑∏‘¿“æ¥’ °«à“°àÕπ¡“° °“√µ‘¥‡™◊ÕÈ ¢Õß atherosclerotic À√◊Õ aneurysmal arterial lesions æ∫‰¥â∫Õà ¬«à“‡ªìπ “‡Àµÿ¢Õß mycotic aneurysm(4,5)

¢âÕ ”§—≠„π°“√«‘π‘®©—¬‚√§ 1. ‡ªìπ°“√µ‘¥‡™◊ÕÈ ¢Õßºπ—ßÀ≈Õ¥‡≈◊Õ¥·¥ß∑ÿ°¢π“¥ 2. ºπ—ßÀ≈Õ¥‡≈◊Õ¥·¥ß∑’µË ¥‘ ‡™◊ÕÈ ‡ ’¬§«“¡¬◊¥À¬ÿπà ∑”„ÀâæÕß µ—«¬◊¥ÕÕ°‡ªìπ aneurysm 3. ‡æ“–‡™◊ÕÈ ‰¥â®“°ºπ—ßÀ≈Õ¥‡≈◊Õ¥ 4. ∂â“∑‘ßÈ ‰«â ‰¡à∑”°“√√—°…“ ®–·µ°ÕÕ° ·≈–¡’°“√µ°‡≈◊Õ¥ ”À√—∫·À≈àßÀ√◊ÕµâπµÕ¢Õß°“√µ‘¥‡™◊ÈÕ¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß Õ“®®–¡“®“° (µ“√“ß∑’Ë 21.1)

1. classic mycotic organisms ®“°°“√À≈ÿ¥¢Õß≈‘Èπ À—«„®∑’¡Ë ‡’ ™◊ÕÈ ·∫§∑’‡√’¬‡ªìπ micro À√◊Õ macroemboli ‰ª¬—ßÀ≈Õ¥‡≈◊Õ¥·¥ßµ”·Àπàßµà“ß Ê ∑—«Ë √à“ß°“¬ 2. extravascular ®“° osteomyelitis, pneumonia, abscesses À√◊Õ°“√Õ—°‡ ∫µ‘¥‡™◊ÕÈ Õ◊πË Ê πÕ°À≈Õ¥‡≈◊Õ¥ ‡°‘¥‰¥â∑ß—È ®“° bacteremia ·≈– local spread °“√ Õ—°‡ ∫µ‘¥‡™◊ÕÈ „°≈âÀ≈Õ¥‡≈◊Õ¥‡™àπ spinal osteomyelitis ·≈â«∑”„Àâºπ—ß¢ÕßÀ≈Õ¥‡≈◊Õ¥‡ ’¬§«“¡¬◊¥À¬ÿàπ æÕß ÕÕ°‡ªìπ aneurysm 3. direct inocculation ®“°°“√©’¥¬“‡ æµ‘¥ ·≈â«¡’°“√ ªπ‡ªóÕô π π”‡Õ“‡™◊ÕÈ ·∫§∑’‡√’¬‡¢â“ Ÿ√à “à ß°“¬ À√◊Õ∫“¥‡®Á∫ À≈Õ¥‡≈◊Õ¥®“°∂Ÿ°¬‘ßÀ√◊Õ∂Ÿ°·∑ß ‚¥¬∑—«Ë ‰ª·≈â«ºπ—ßÀ≈Õ¥‡≈◊Õ¥ª°µ‘∑¡’Ë ‡’ ÕÁπ‚¥∏’‡≈’¬Ë ¡ª°§≈ÿ¡Õ¬Ÿà ®–¡’§«“¡µâ“π∑“πµàÕ°“√Õ—°‡ ∫µ‘¥‡™◊ÈÕ‰¥â Ÿß ∂â“¡’°“√Õ—°‡ ∫ µ‘¥‡™◊ÈÕ‡°‘¥¢÷Èπ · ¥ß«à“ª√‘¡“≥À√◊Õ®”π«π¢Õß‡™◊ÈÕ·∫§∑’‡√’¬®– µâÕß Ÿß¡“° atherosclerotic intima ®–ª√–°Õ∫¥â«¬ ulcerated plaque, necrotic cellular debris ·≈– thrombus ´÷ßË ‡ªìπ media ∑’¥Ë ’ ”À√—∫°“√‡®√‘≠‡µ‘∫‚µ¢Õß‡™◊ÕÈ ·∫§∑’‡√’¬ ‡™àπ‡¥’¬«°—π°—∫ mural thrombus „π aneurysms ‡™◊ÕÈ ·∫§∑’‡√’¬∑’‡Ë ªìπ “‡Àµÿ ¢Õß°“√µ‘¥‡™◊ÕÈ ∑’æË ∫‰¥â∫Õà ¬§◊Õ Salmonella, Staphylococcus ·≈– Streptococcus à«π‡™◊ÕÈ √“∑’æË ∫‰¥â¡’ Candida ·≈– Aspergillus(4,6)

190

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥

µ“√“ß∑’Ë 21.1 Classification of vascular infections Source of Infection Intrinsic endocarditis or other intravascular infection Extrinsic osteomyelitis, pneumonia, or other infection by local spread or bacteremia Inoculation inadvertent during medical procedures, unhygienic injections, infecting drug use Affected Vessel Normal resistant except in high virulence or large inoccula Atherosclerotic susceptible, especially to Salmonella and Staphylococcus Aneurysmal many more culture positive than infections Causative Microorganism Salmonella - most common, 65% involve aorta Staphylococcus - next most common Streptococcus - seen especially with endocarditis Other unusual organisms - as seen in unhygienic injections, IV drug abuse and in immune deficiency

„πªí®®ÿ∫π— Õ—µ√“∑’æË ∫¢Õß arterial infections ·≈– infected aneurysms Ÿß¢÷πÈ ‡π◊ÕË ß®“° ª√‘¡“≥¢ÕßºŸªâ «É ¬ immune suppressed hosts ‡™àπ°“√µ‘¥‡™◊ÈÕ HIV, ºŸâªÉ«¬‡ª≈’Ë¬πÕ«—¬«–∑’Ë µâÕß√—∫ª√–∑“π¬“°¥¿Ÿ¡§‘ ¡ÿâ °—π·≈–µ‘¥¬“‡ æµ‘¥¡’¡“°¢÷πÈ √«¡∑—ßÈ À—µ∂°“√µà“ß Ê ∑’≈Ë °ÿ ≈È”‡¢â“‰ª∂÷ßÀ≈Õ¥‡≈◊Õ¥·¥ß ‡™àπ hemodynamic monitoring ·≈– arteriography(7-12)

°“√·∫àß™π‘¥¢Õß infected aneurysms „πªí®®ÿ∫π— °“√·∫àß™π‘¥¢Õß infected aneurysms ÕÕ°‰¥â (µ“√“ß∑’Ë 21.2) 1. mycotic aneurysms ¡’ “‡Àµÿ¡“®“° septic arterial emboli 2. microbial arteritis ·≈â«µ“¡¡“¥â«¬°“√‡°‘¥ aneurysms ¿“¬À≈—ß 3. °“√µ‘¥‡™◊ÕÈ ¢Õß aneurysms ´÷ßË ¡’Õ¬Ÿ°à Õà πÀπâ“π’·È ≈â« 4. infected false aneurysm ∑’‡Ë °‘¥À≈—ß trauma ‚¥¬µ—¥‡Õ“ spontaneous aortoenteric fistula ·≈–°“√µ‘¥ ‡™◊ÕÈ ¢ÕßÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡ÕÕ°‰ª ‡ªìπ(4,13,14)

MYCOTIC ANEURYSMS Õÿ∫µ— °‘ “√ æ∫‰¥â∑ß—È „πÀ≈Õ¥‡≈◊Õ¥·¥ß∑’ºË π—ßÀ≈Õ¥‡≈◊Õ¥ª°µ‘ ·≈–∑’‡Ë ªìπ atherosclerosis ‡ªìπº≈¡“®“° embolization À√◊Õ direct extension ¢Õß septic valvular vegetation „πºŸªâ «É ¬ infective endocarditis(1,4) °àÕπÀπâ“∑’®Ë –¡’¬“ªØ‘™«’ π– mycotic

µ“√“ß∑’Ë 21.2 ≈—°…≥–∑“ß§≈‘π§‘ ∑’·Ë µ°µà“ß°—π¢Õß Infected Aneurysms ·µà≈–™π‘¥ Mycotic Aneurysm

Microbial Arteritis

Infected Existing Aneurysm

Post-traumatic Infected

“‡Àµÿ

Endocarditis

Bacteremia

Bacteria

Õ“¬ÿ(ªï) Õÿ∫µ— °‘ “√ µ”·Àπàß¢Õß À≈Õ¥‡≈◊Õ¥·¥ß ∑’æË ∫ ‡™◊ÕÈ ·∫§∑’‡√’¬∑’æË ∫

30-50 æ∫πâÕ¬ Aorta Visceral Intracranial °√—¡∫«°§Õ§‰§

¡“°°«à“ 50 æ∫πâÕ¬ -Infrarenal Aorta

Õ—µ√“µ“¬

25%

¡“°°«à“ 50 æ∫∫àÕ¬ Atherosclerotic Aortoiliac Intimal defects Salmonella Õ◊πË Ê 75%

„™â‡¢Á¡©’¥¬“‡ æµ‘¥ ‡¢â“À≈Õ¥‡≈◊Õ¥ Õÿ∫µ— ‡‘ Àµÿ πâÕ¬°«à“ 30 æ∫‰¥â∫Õà ¬ -Femoral -Carotid

Staphylococcus Õ◊πË Ê 90%

Staphylococcus aureus 5%

INFECTED ANEURYSMS

aneurysms §◊Õ arterial infection ∑’æË ∫‰¥â∫Õà ¬∑’ Ë ¥ÿ (3) „πªï §.». 1923 Stengel ·≈– Wolferth æ∫«à“√âÕ¬≈– 87 ¢ÕßºŸªâ «É ¬ mycotic aneurysms ¡’ “‡Àµÿ¡“®“° endocardial infection ∑’æË ∫‰¥â√Õß≈ß¡“§◊Õ pulmonary infection ·≈– osteomyelitis(3) √âÕ¬≈– 13 ¢ÕßºŸªâ «É ¬ endocarditis ®–¡’ “‡Àµÿ°“√µ“¬ ®“° ruptured mycotic aneurysms ¬“ªØ‘™«’ π–¡’∫∑∫“∑„π°“√√—°…“‚√§µ‘¥‡™◊ÕÈ „π√–¬–À≈—ß ∑” „ÀâÕµ— √“°“√µ“¬·≈–¿“«–·∑√°´âÕπ¢Õß bacterial endocarditis ≈¥≈ß¡“° Õÿ∫µ— °‘ “√¢Õß mycotic aneurysms °Á≈¥≈ß¡“° ‡™àπ°—π ªí®®ÿ∫π— °Á¬ß— æ∫ºŸªâ «É ¬ bacterial endocarditis Õ¬Ÿà ·≈– ¬—ß‡ªìπ “‡Àµÿ¢Õß septic arterial complications ®“°√“¬ ß“π„πªï§.». 1967 æ∫«à“ 10 „π 16 infected aneurysms ¡’ “‡Àµÿ¡“®“° bacterial endocarditis(15) ®“° 25 √“¬¢Õß mycotic aneurysms æ∫«à“ 9 √“¬ ¡’ “‡Àµÿ¡“®“° bacterial endocarditis ·≈– 7 „π 9 ¡’ aneurysms ‡°‘¥¢÷πÈ À≈“¬µ”·Àπàß ¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß ºŸªâ «É ¬∑’‡Ë æ¬“‡ æµ‘¥‚¥¬°“√©’¥¬“‡¢â“‡ âπ ‚√§ AIDS ·≈–¿Ÿ¡§‘ ¡ÿâ °—π∫°æ√àÕß ¡’‚Õ°“ ‡ªìπ infected aneurysms ¡“°¢÷πÈ (16,17) æ¬“∏‘«∑‘ ¬“ mycotic aneurysms ¡’µπâ µÕ “‡Àµÿ°“√µ‘¥‡™◊ÕÈ ¡“®“°≈‘ÈπÀ—«„®∑’Ë‡ªìπ bacterial endocarditis ‚¥¬≈ÿ°≈“¡µ‘¥ ‡™◊ÈÕ‰ª¬—ßÀ≈Õ¥‡≈◊Õ¥¢π“¥„À≠à∑’ËÕ¬Ÿà „°≈âÀ—«„®‡™àπ ascending aorta(18,19) ·≈–À≈ÿ¥‡ªìπ emboli ‰ª‡°“–∑’µË ”·Àπàßµà“ß Ê ¢Õß À≈Õ¥‡≈◊Õ¥·¥ßµ√ß vasa vasorum ·≈–À≈Õ¥‡≈◊Õ¥·¥ß·¢πß ‡≈Á° Ê „π∫“ß√“¬°“√Õ—°‡ ∫µ‘¥‡™◊ÈÕ®“° vasa vasorum ®– °≈“¬‡ªìπ intramural abscess ‚¥¬∑’Ë intima ¬—ß§ß‡¥‘¡(20-22) Infected emboli ®–∑”„Àâ‡°‘¥ thrombosis ¢Õß vasa vasorum ∑”„Àâºπ—ßÀ≈Õ¥‡≈◊Õ¥¢“¥‡≈◊Õ¥¡“‡≈’È¬ß √à«¡°—∫°“√µ‘¥‡™◊ÈÕ ∑”„Àâºπ—ßÀ≈Õ¥‡≈◊Õ¥‡ ’¬§«“¡¬◊¥À¬ÿπà ∑”„Àâ ‚ªÉßæÕßÕÕ°°≈“¬‡ªìπ aneurysm(23) ‡°‘¥‰¥âµß—È ·µà aorta, visceral ·≈– peripheral arteries µ√«®‡π◊ÈÕ‡¬◊ËÕ∑“ß histology ¥Ÿ ®–æ∫«à“¡’°“√Õ—°‡ ∫¢Õß À≈Õ¥‡≈◊Õ¥·¥ß∑’ªË °µ‘„°≈â°∫— aneurysm „π infected aneurysm æ∫ªØ‘°√‘ ¬‘ “°“√Õ—°‡ ∫¢Õß‡π◊ÕÈ ‡¬◊ÕË √ÿπ·√ß°«à“ mycotic aneurysm ≈—°…≥– ”§—≠¢Õß mycotic aneurysm §◊Õ¡’°“√À≈ÿ¥≈Õ°¢Õß ™—πÈ intima ‡π◊ÕÈ ‡¬◊ÕË ™—πÈ internal elastic lamina ∂Ÿ°∑”≈“¬ ¡’ periarteritis À√◊Õ mesoarteritis ∂â“°“√Õ—°‡ ∫≈¥≈ß®–æ∫ plasma cells ·≈– lymphocytes ¡“°¢÷Èπ„π‡π◊ÈÕ‡¬◊ËÕºπ—ß À≈Õ¥‡≈◊Õ¥ °“√Õ—°‡ ∫®–æ∫¡“°√Õ∫ vasa vasorum

191 MICROBIAL ARTERITIS WITH ANEURYSM ¬ÿ§°àÕπ∑’®Ë –¡’°“√„™â¬“ªØ‘™«’ π–∑’¡Ë ª’ √– ‘∑∏‘¿“æ æ∫Õÿ∫µ— °‘ “√ ¢Õß microbial arteritis √âÕ¬≈– 14 ¢Õß infected aneurysms ∑—ßÈ À¡¥(3) „πªí®®ÿ∫π— ‚√§√Ÿ¡“µ‘§·≈– bacterial endocarditis æ∫πâÕ¬≈ß ∑”„ÀâÕ∫ÿ µ— °‘ “√¢Õß microbial artertis ‡æ‘¡Ë ¡“°¢÷πÈ ·≈–æ∫‰¥â∫Õà ¬°«à“ mycotic aneurysms(25) “‡Àµÿ∑ ’Ë ”§—≠Õ¬à“ß Àπ÷Ëß§◊Õ §π ŸßÕ“¬ÿ¡’¡“°¢÷Èπ ´÷Ëß à«π„À≠à®–¡’ atherosclerosis ¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß∑—Ë«√à“ß°“¬ ·≈–ßà“¬µàÕ°“√µ‘¥‡™◊ÈÕ¢Õß À≈Õ¥‡≈◊Õ¥ ºπ—ßÀ≈Õ¥‡≈◊Õ¥ª°µ‘∑’Ë¡’ intima §≈ÿ¡®–¡’§«“¡ µâ“π∑“πµàÕ°“√µ‘¥‡™◊ÕÈ ∫√‘‡«≥ atherosclerotic arteries ∑’Ë ‰¡à¡’ intima §≈ÿ¡ ®–¡’ blood-borne bacterial ¡“‡°“– ∑”„Àâ‡°‘¥ °“√µ‘¥‡™◊ÕÈ ‡©æ“–∑’Ë suppuration, localized perforation ·≈– false aneurysm „π∑’ Ë ¥ÿ (√Ÿª∑’Ë 21.1) aorta ‡ªìπµ”·Àπàß∑’‡Ë °‘¥ microbial arteritis ‰¥â∫Õà ¬∑’ Ë ¥ÿ (13,26,27) ºŸªâ «É ¬∑’¡Ë ’‚√§¿Ÿ¡§‘ ¡ÿâ °—π ∫°æ√àÕß ¡’‚Õ°“ µ‘¥‡™◊ÕÈ ·≈–‡ªìπ microbial arteritis ‰¥âß“à ¬

√Ÿª∑’Ë 21.1 arteriography ¢ÕßºŸªâ «É ¬ Staphylococcus aureus microbial arteritis with aneurysm ®“°¿“æ√—ß ’‡ÀÁπ saccular aneurysm ¢Õß right renal artery

192

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥

‡™◊ÕÈ ·∫§∑’‡√’¬∑’‡Ë ªìπ “‡Àµÿ∑æ’Ë ∫‰¥â∫Õà ¬¡’ Salmonella, Staphylococcus, Escherichia coli ·≈– Bacteroides fragilis(4,28,29) ∑’‡Ë æ“–‡™◊ÕÈ ‰¡à¢π÷È ¡’√Õâ ¬≈– 25 ´÷ßË Õ“®®–‡ªìπ anaerobic bacteria Salmonella ‡ªìπ‡™◊ÕÈ ·∫§∑’‡√’¬∑’∑Ë ”„Àâ‡°‘¥°“√µ‘¥‡™◊ÕÈ µàÕ diseased aorta ”À√—∫ species ∑’æË ∫‰¥â∫Õà ¬§◊Õ S. choleraesuis ·≈– S. typhimurium ª√–¡“≥√âÕ¬≈– 62(29) INFECTION OF PREEXISTING ANEURYSMS Õÿ∫µ— °‘ “√·≈–µ”·Àπàß¢ÕßÀ≈Õ¥‡≈◊Õ¥∑’æË ∫ æ∫°“√µ‘¥‡™◊ÕÈ „π atherosclerotic aneurysms ‰¥âª√–¡“≥ √âÕ¬≈– 3.4(5) Ernst ·≈–§≥–æ∫«à“ºŸªâ «É ¬ AAA ∑ÿ°√“¬∑’Ë ‰¥â√∫— °“√ºà“µ—¥®–‡æ“–‡™◊ÕÈ ·∫§∑’‡√’¬‰¥â√Õâ ¬≈– 15(30) ∂â“‡ªìπ ruptured ®–æ∫ Ÿß∂÷ß√âÕ¬≈– 38 æ∫«à“ abdominal aorta ‡ªìπµ”·Àπàß ∑’Ë‡°‘¥°“√µ‘¥‡™◊ÈÕ·∫§∑’‡√’¬‰¥â∫àÕ¬∑’Ë ÿ¥ √Õß≈ß¡“§◊Õ thoracic aorta(4,31) (√Ÿª∑’Ë 21.2) ‡™◊ÕÈ ·∫§∑’‡√’¬∑’æË ∫ æ∫«à“‡ªìπ™π‘¥°√—¡∫«°√âÕ¬≈– 59 °√—¡ ≈∫√âÕ¬≈– 35 ‡™◊ÕÈ ∑’æË ∫∫àÕ¬§◊Õ Staphylococcus (√âÕ¬≈– 41)(32) √“¬ß“πÀ≈—ß¡“π’æÈ ∫«à“‡ªìπ°√—¡∫«°√âÕ¬≈– 81 °√—¡≈∫√âÕ¬≈– 19 ·≈–‡™◊ÕÈ ∑’æË ∫∫àÕ¬∑’ Ë ¥ÿ §◊Õ S. epidermidis (√âÕ¬≈– 53)(30)

POST-TRAUMATIC INFECTED FALSE ANEURYSMS Õÿ∫µ— °‘ “√·≈–µ”·Àπàß∑’æË ∫ ‡ªìπ infected aneurysms ∑’Ë æ∫‰¥â∫Õà ¬∑’ Ë ¥ÿ ¡’ “‡Àµÿ¡“®“°°“√‡ æ¬“‡ æµ‘¥‚¥¬„™â‡¢Á¡∑’Ë ‰¡à –Õ“¥©’¥‡¢â“‡ âπ µ”·Àπàß∑’æË ∫‰¥â∫Õà ¬§◊Õ µ√ß¢“Àπ’∫ ‡π◊ÕË ß®“° ‰¡à¡’‡ âπ∑’Ë®–©’¥‡¢â“‰¥â·≈â«∫√‘‡«≥·¢π (√Ÿª∑’Ë 21.3) °“√©’¥¬“ ‡ æµ‘¥‡Õß∫√‘‡«≥¢“Àπ’∫æ≈“¥‡¢â“À≈Õ¥‡≈◊Õ¥·¥ß ¡’°“√µ‘¥ ‡™◊ÕÈ ·≈–µ“¡¡“¥â«¬ false aneurysm(33) À≈Õ¥‡≈◊Õ¥·¥ß femoral ·≈– external iliac ®–‡ªìπµ”·Àπàß∑’æË ∫∫àÕ¬∑’ Ë ¥ÿ √Õß≈ß¡“§◊Õ carotid(34,35) À—µ∂°“√µà“ß Ê „π°“√«‘π‘®©—¬·≈–√—°…“√à«¡∑“ß√—ß ’ ‡™àπ arteriography percutaneous angioplasty À√◊Õ monitoring procedures µà“ß Ê Õ“®®–∑”„Àâ‡°‘¥ post-traumatic infected false aneurysm µ“¡¡“¿“¬À≈—ß‰¥â(12,36) ‡™◊ÕÈ ·∫§∑’‡√’¬∑’æË ∫ ∑’æË ∫∫àÕ¬∑’ Ë ¥ÿ §◊Õ S. aureus (√âÕ¬≈– (25) 30) ´÷ßË √âÕ¬≈– 48 ®–‡ªìπ™π‘¥ methicillin resistant ª√–¡“≥ √âÕ¬≈– 33 ®–æ∫‡™◊ÕÈ À≈“¬™π‘¥ªπ°—π ‡™àπ S. aureus, E. coli, S. faecalis, Pseudomonas aeruginosa œ≈œ(34)

√Ÿª∑’Ë 21.2 CT scan abdomen ‡ÀÁπ salmonella infection ¢Õß preexisting small AAA ¡’ fluid §—ËßÕ¬Ÿà „π wall ¢Õß aneurysm

193

INFECTED ANEURYSMS

√Ÿª∑’Ë 21.3 °. arteriograms · ¥ß∂÷ß infected false aneurysm ¢Õß superficial femoral artery ¢. arteriograms · ¥ß∂÷ß infected false aneurysm ¢Õß right external ilialc artery ®“°°“√©’¥¬“‡ æµ‘¥∫√‘‡«≥¢“Àπ’∫ æ∫ «à“¡’ collateral ºà“π≈ß‰ª∂÷ß femoral arteries æÕ‡æ’¬ß

Õ“°“√· ¥ß∑“ß§≈‘π§‘ Õ“°“√·≈–Õ“°“√· ¥ß∑“ß§≈‘π§‘ ¢ÕßºŸªâ «É ¬ infected aneurysms ¢÷πÈ Õ¬Ÿ°à ∫— “‡Àµÿ·≈–µ”·Àπàß ¢ÕßÀ≈Õ¥‡≈◊Õ¥ ‡™àπ ª«¥∑âÕß, ¡’‰¢â, leukocytosis, ‡æ“–‡™◊ÕÈ ‰¥â®“°‡≈◊Õ¥, §≈”‰¥â°âÕπÀ√◊Õ¡’°“√·µ°∑”„Àâµ°‡≈◊Õ¥ æ∫‰¥â „π ∑ÿ°™à«ßÕ“¬ÿ ∑’æË ∫‰¥â∫Õà ¬§◊Õ §π ŸßÕ“¬ÿ∑À’Ë ≈Õ¥‡≈◊Õ¥·¥ß¡’ atherosclerosis(5,20) ºŸªâ «É ¬ infected aortic aneurysm Õ“®®–«‘π®‘ ©—¬ ‚√§‰¥â≈”∫“°®“°Õ“°“√·≈–Õ“°“√· ¥ß ‡æ√“–Õ“®®–¡“¥â«¬‰¢â ∑’Ë ‰¡à∑√“∫ “‡Àµÿ °“√«‘π‘®©—¬‚√§®–ßà“¬¢÷Èπ∂â“§≈”‰¥â°âÕπ∑“ß Àπâ“∑âÕß (ª√–¡“≥√âÕ¬≈– 40 ®–§≈”°âÕπ‰¡à ‰¥â) ‡æ“–‡™◊ÈÕ‰¥â ®“°‡≈◊Õ¥, ¡’ erosion ¢Õß lumbar vertebrae, ‡æ»À≠‘ßæ∫ uncalcified aneurysm À√◊Õ‡°‘¥ aneurysm ¢÷πÈ ¿“¬À≈—ß®“°¿“«– sepsis(32,37) ∫“ß√“¬®–¡“¥â«¬ ruptured aneurysm(38) ”À√—∫ infected aneurysms ∑’‡Ë °‘¥¢÷πÈ ∑’§Ë Õ·≈–¢“Àπ’∫ ®–«‘π®‘ ©—¬‚√§ ‰¥âß“à ¬ ‡æ√“–§≈”°âÕπ‰¥â ¡’ª«¥ ∫«¡ ·¥ß √âÕπ °âÕπ·µ°‰¥âß“à ¬ ∫“ß§√—ßÈ ¡’‡≈◊Õ¥‰À≈´÷¡ÕÕ°¡“À√◊Õ¡’ sepsis(38)

°“√µ‘¥‡™◊ÕÈ √“∑“ßÀ≈Õ¥‡≈◊Õ¥æ∫‰¥âπÕâ ¬¡“° Õ“®®–æ∫„πºŸâ ªÉ«¬∑’‡Ë ªìπ‚√§¿Ÿ¡§‘ ¡ÿâ °—π∫°æ√àÕß‰¥â√∫— ¬“°¥Õ‘¡¡ŸπÀ≈—ßºà“µ—¥‡ª≈’¬Ë π Õ«—¬«– À√◊Õ‡ªìπ‡∫“À«“π Õ“°“√ ”§—≠¢ÕßºŸªâ «É ¬°≈ÿ¡à π’§È Õ◊ ‰¢â ¡’ gangrene ¢Õß·¢π¢“®“° distal embolization(10,39,40) ‰¡à«“à infected aneurysms ®–‡°‘¥¢÷πÈ °—∫À≈Õ¥‡≈◊Õ¥·¥ß ∫√‘‡«≥„¥¢Õß√à“ß°“¬ Õ“°“√·≈–Õ“°“√· ¥ß∑“ß§≈‘π§‘ Õ“®®– ·µ°µà“ß°—π ·µà ‚Õ°“ ∑’®Ë –‡°‘¥ sepsis ·≈–À≈Õ¥‡≈◊Õ¥·µ°∑–≈ÿ ®π°√–∑—Ëßµ°‡≈◊Õ¥‡ªìπ‰¥â‡™àπ°—π ‡¡◊ËÕ ß —¬„Àâµ√«®«‘π‘®©—¬„Àâ ‰¥â ·µà‡π‘πË Ê ‡æ◊ÕË «“ß·π«∑“ß„π°“√ºà“µ—¥√—°…“‰¥â∂°Ÿ µâÕß

°“√«‘π‘®©—¬‚√§ ∑“ßÀâÕßªØ‘∫µ— °‘ “√ ®“°°“√‡®“–‡≈◊Õ¥µ√«®ºŸªâ «É ¬ infected aneurysms ®–æ∫«à“¡’ leukocytosis „π∫“ß√“¬®–æ∫«à“¡’ erythrocyte sedimentation rate (ESR) Ÿß¢÷πÈ (28,32) æ∫«à“‡æ“–‡™◊ÕÈ

194

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥

‰¥â®“°‡≈◊Õ¥ª√–¡“≥√âÕ¬≈– 50(7) ·µà∑‡’Ë æ“–‡™◊ÕÈ ®“°‡≈◊Õ¥‰¡àæ∫°Á ‰¡à ‰¥âÀ¡“¬§«“¡«à“‰¡à „™à infected aneurysms ®–µâÕßÕ“»—¬ «‘∏°’ “√µ√«®«‘π®‘ ©—¬Õ◊πË Ê ‡æ‘¡Ë ‡µ‘¡Õ’° ¢≥–ºà“µ—¥§«√π”‡Õ“ÀπÕß, ºπ—ßÀ≈Õ¥‡≈◊Õ¥·≈– thrombus ‰ª¬âÕ¡ ’°√—¡‡æ“–‡™◊ÕÈ ∑—ßÈ aerobic ·≈– anaerobic ‡æ◊ÕË „™âæ®‘ “√≥“„π°“√„Àâ¬“ªØ‘™«’ π–√—°…“ µàÕ‰ª æ∫«à“„π infected aneurysms √âÕ¬≈– 69 ‡æ“–‡™◊ÕÈ ™‘πÈ ®“°‡≈◊Õ¥ ·≈–√âÕ¬≈– 92 ‡æ“–‡™◊ÕÈ ™‘πÈ ®“°ºπ—ßÀ≈Õ¥‡≈◊Õ¥ √âÕ¬ ≈– 50 æ∫‡™◊ÕÈ ®“°°“√¬âÕ¡ ’°√—¡(32) °“√«‘π®‘ ©—¬∑“ß√—ß ’«∑‘ ¬“ aortic aneurysms ∑’æË ∫«à“∑”„Àâ ‡°‘¥ vertebral body erosion ·≈–‰¡à¡’ calcification „Àâ ß —¬ «à“®–‡ªìπ infected aneurysm ‡ ¡Õ ∂â“√à«¡°—∫Õ“°“√·≈– Õ“°“√· ¥ß∑“ß§≈‘π‘§ ¿“æ√—ß ’ª°µ‘Õ“®®–‰¡à™à«¬°“√«‘π‘®©—¬∑’Ë ·πà™¥— ¡“°π—° §«√®–µâÕß∑”°“√µ√«®«‘π®‘ ©—¬æ‘‡»…‡æ‘¡Ë ‡µ‘¡ ‡™àπ CT scan ·≈– digital subtraction angiography (DSA) °“√∑” sonography ®–∑”„Àâ∑√“∫¢π“¥·≈–µ”·Àπàß¢Õß aneurysm ·µà®–‰¡à∫ßà ™—¥‡®π«à“‡ªìπ infected aneurysm(41) sonography ¡’ª√–‚¬™πå¡“°„π°“√«‘π®‘ ©—¬ infected femoral artery false aneurysm (√Ÿª∑’Ë 21.4) °“√«‘π®‘ ©—¬‚√§∑’§Ë «√∑”§◊Õ digital subtraction angiography ‡æ√“–º≈°“√«‘π‘®©—¬‚√§·πàπÕπ·≈– –¥«°°«à“ conventional angiography(42)

µ“√“ß∑’Ë 21.3 CT Findings of Infected Aneurysms Saccular aneurysm Irregular aneurysm lumen Absence of calcification Gas within aortic wall Perianeurysmal gas Perianeuryamal fluid Encasing or contiguous mass Associated paraaortic or psoas abscess Vertebral osteomyetitis

°“√∑” angiography ‰¡à«“à ®–‡ªìπ conventional angiography À√◊Õ DSA ®–™à«¬°“√«‘π®‘ ©—¬‚√§ infected aneurysms ‰¥â ∂â“æ∫ ‘ßË µàÕ‰ªπ’È (43) 1. saccular aneurysm ∑’‡Ë °‘¥∫πÀ≈Õ¥‡≈◊Õ¥·¥ß∑’ªË °µ‘ 2. multilobulated aneurysm 3. aneurysm ≈—°…≥–·ª≈° Ê ´÷ßË ¡’ narrow neck contrast-enhanced CT scan (µ“√“ß∑’Ë 21.3) ·≈– Magnetic resonance imaging (MRI) ®–™à«¬°“√«‘π®‘ ©—¬ aneurysm ‚¥¬‡©æ“–„π√“¬∑’¡Ë ’ leakage À√◊Õ rupture ·µà∂“â ®–«‘π®‘ ©—¬ «à“¡’°“√Õ—°‡ ∫µ‘¥‡™◊ÕÈ µàÕ aneurysm ∑’·Ë πàπÕπ §«√∑” indium111-labeled white blood cell scanning.(44)

°“√√—°…“

√Ÿª∑’Ë 21.4 ultrasonography ∫√‘‡«≥¢“Àπ’∫ · ¥ß„Àâ‡ÀÁπ false aneurysm ¢Õß common femoral artery

°“√‡µ√’¬¡ºŸªâ «É ¬°àÕπºà“µ—¥ ‡¡◊ÕË ß —¬«à“‡ªìπ infected aneurysm °“√√— ° …“„π√–¬–·√°‰¡à ®”‡ªì π µâ Õ ß∑√“∫‡™◊È Õ ·∫§∑’‡√’¬∑’Ë·πàπÕπ §«√„Àâ¬“ªØ‘™’«π–™π‘¥ÕÕ°ƒ∑∏‘Ï§≈ÿ¡°«â“ß ‡¢â“∑“ßÀ≈Õ¥‡≈◊Õ¥¥”‰¥â∑π— ∑’ °àÕπ·≈–À≈—ßºà“µ—¥(45) ¬“∑’Ë „Àâ§«√ ®–¡’ƒ∑∏‘Ï§≈ÿ¡‡™◊ÈÕ Salmonella ¥â«¬„π√“¬∑’Ë©’¥¬“‡ æµ‘¥§«√ ©’¥¬“°—π∫“¥∑–¬—°√à«¡¥â«¬ ∂÷ß·¡â „π√“¬∑’¡Ë ’ ruptured infected aneurysm ¡“·≈â« °Á§«√„Àâ¬“ªØ‘™’«π–°àÕπ∑’Ë®–∑”°“√ºà“µ—¥ √—°…“µàÕ‰ª(34) °“√ºà“µ—¥√—°…“ ¡’À≈—°°“√„π°“√ºà“µ—¥√—°…“¥—ßµàÕ‰ªπ’È 1. §«∫§ÿ¡°“√µ°‡≈◊Õ¥®“° ruptured À√◊Õ leakage aneurysms „Àâ ‰¥â 2. «‘π‘®©—¬‚√§„Àâ ‰¥â·πàπÕπ«à“¡’°“√µ‘¥‡™◊ÈÕ®“°°“√¬âÕ¡ ’ °√—¡¢ÕßÀπÕß, thrombus ºπ—ßÀ≈Õ¥‡≈◊Õ¥ ·≈–‡æ“– ‡™◊ÕÈ ‰¡à«“à ®–‡ªìπ anaerobic, aerobic À√◊Õ fungus

195

INFECTED ANEURYSMS

3. ºà“µ—¥§«∫§ÿ¡°“√µ‘¥‡™◊ÈÕ ‚¥¬µ—¥‡Õ“‡π◊ÈÕ‡¬◊ËÕ∑’Ëµ‘¥‡™◊ÈÕ ·≈–‡πà“µ“¬ÕÕ°‰ª„Àâ¡“°∑’Ë ÿ¥ «π≈â“ß¥â«¬πÈ”‡°≈◊Õ º ¡¬“ªØ‘™«’ π–·≈–«“ß∑àÕ√–∫“¬ 4. ¥Ÿ·≈·º≈ºà“µ—¥ ‚¥¬°“√∑”·º≈∫àÕ¬ Ê ·≈–µ—¥‡π◊ÕÈ ‡¬◊ÕË ∑’µË “¬ÕÕ° 5. „Àâ¬“ªØ‘™«’ π–µàÕ‡π◊ÕË ßÀ≈—ßºà“µ—¥ π“πæÕ∑’®Ë –§«∫§ÿ¡°“√ µ‘¥‡™◊ÕÈ ¢Õß·∫§∑’‡√’¬·µà≈–™π‘¥ 6. arterial reconstruction ¢ÕßÀ≈Õ¥‡≈◊Õ¥ ”§—≠ ‚¥¬ ºà“π∫√‘‡«≥∑’Ë ‰¡à¡°’ “√µ‘¥‡™◊ÕÈ ·≈–æ¬“¬“¡„™â autologous vessels °àÕπ∑’Ë®–‡≈◊Õ°„™âÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡∑’Ëº≈‘µ®“° “√ —ß‡§√“–Àå µ”·Àπàßµà“ß Ê ¢ÕßÀ≈Õ¥‡≈◊Õ¥ ”§—≠∑—«Ë √à“ß°“¬ ”À√—∫°“√ ∑” arterial reconstruction ¡’°“√ºà“µ—¥√—°…“µà“ß°—π¥—ßπ’È aorta ¡’·π«∑“ß„π°“√ºà“µ—¥√—°…“‡™àπ‡¥’¬«°—π°—∫ infected aortic prostheses ‚¥¬µ—¥‡Õ“ infected aneurysm ·≈– ‡π◊ÕÈ ‡¬◊ÕË √Õ∫¢â“ß∑’¡Ë °’ “√µ‘¥‡™◊ÕÈ ÕÕ°„ÀâÀ¡¥ «“ß∑àÕ√–∫“¬·≈– arterial reconstruction «‘∏’∑’Ë§àÕπ¢â“ß®–ª≈Õ¥¿—¬§◊Õ axillobifemoral bypass (√Ÿª∑’Ë 21.5) À≈’°‡≈’¬Ë ß°“√∑” çin situ interposition aortic grafté „π∫√‘‡«≥‡¥‘¡∑’¡Ë °’ “√µ‘¥‡™◊ÕÈ ·≈–¡’ÀπÕß (32,46) ‡π◊Õ Ë ß®“°‡ ’¬Ë ßµàÕ°“√µ‘¥‡™◊ÕÈ ´È”·≈–µâÕßºà“µ—¥‡Õ“ graft ÕÕ°

‚¥¬‡©æ“–∂â“°“√µ‘¥‡™◊ÕÈ ‡°‘¥®“°·∫§∑’‡√’¬™π‘¥°√—¡≈∫(47) Õ“®®– ∑”‰¥â „π√“¬∑’Ë ‰¡à¡’ gross sepsis À√◊Õ infected aneurysm ∫√‘‡«≥∑’ÀË ≈’°‡≈’¬Ë ß°“√∑” interposition grafting ‰¡à‰¥â ‡™àπ aortic arch, thoracic aorta ·≈– suprarenal abdominal aorta.(25,31,45) femoral artery °“√√—°…“∑’‡Ë À¡“– ¡§◊Õ arterial excision Õ¬à“ß‡¥’¬« À√◊Õ√à«¡°—∫ arterial reconstruction „π√“¬∑’Ë ®”‡ªìπ ´÷ßË ¡’«∏‘ °’ “√ºà“µ—¥À≈“¬«‘∏’ (√Ÿª∑’Ë 21.6) ∂â“ “‡Àµÿ¢Õß infected aneurysm ‰¡à„™à®“°°“√©’¥ “√‡ æ µ‘¥ §«√∑” obturator bypass À√◊Õ interposition grafting ºŸâ ªÉ«¬©’¥ “√‡ æµ‘¥‰¡à‡À¡“– ”À√—∫°“√ºà“µ—¥ arterial reconstruction ‚¥¬‡©æ“–°“√„™âÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡ ‡æ√“–®–°≈—∫‰ª©’¥ “√ ‡ æµ‘¥Õ’° ∑”„ÀâÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡µ‘¥‡™◊ÕÈ ‰¥â (7,11,48) ∂â“¡’§«“¡®”‡ªìπ ∑’Ë®–µâÕßºà“µ—¥ arterial reconstruction ®√‘ß Ê µâÕß§«∫§ÿ¡ °“√µ‘¥‡™◊ÈÕ∫√‘‡«≥¢“Àπ’∫„Àâ ‰¥â‡ ’¬°àÕπ ·≈–À≈’°‡≈’Ë¬ß°“√„™â À≈Õ¥‡≈◊Õ¥‡∑’¬¡∑’ºË ≈‘µ®“° “√ —ß‡§√“–Àå „™â autogenous vein ®–¥’∑ ’Ë ¥ÿ à«π„À≠à·≈â«ºŸªâ «É ¬ infected femoral false aneurysm À≈—ßºà“µ—¥‡Õ“ aneurysm ÕÕ°‰ª·≈â«‰¡à®”‡ªìπµâÕßºà“µ—¥ arterial reconstruction ‡π◊ÕË ß®“° collaterals ‡æ’¬ßæÕ ®π‰¡à ∑”„Àâ¢“¢“¥‡≈◊Õ¥(11,48,49,50) À≈—ßºà“µ—¥§«√„Àâ¬“ªØ‘™«’ π–µàÕÕ’°‡ªìπ √–¬–‡«≈“π“π(49,50)

Closed aortic stump

Axillobifemoral graft

√Ÿª∑’Ë 21.5 °“√ºà“µ—¥∑” axillobifemoral bypass ”À√—∫ºŸâªÉ«¬ infected abdominal aortic aneurysm ·≈–°“√«“ß∑àÕ√–∫“¬∫√‘‡«≥∑’Ë¡’°“√ µ‘¥‡™◊ÈÕ

196

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥

√Ÿª∑’Ë 21.6 °“√ reconstruct femoral artery ¿“¬À≈—ßºŸ°µ—¥ ‚¥¬°“√∑” °. obturator bypass ¢. lateral femoral bypass

√ÿª º≈°“√ºà“µ—¥√—°…“ infected aneurysm ®–¥’À√◊Õ‰¡à¢π÷È Õ¬Ÿà °—∫™π‘¥¢Õß aneurysm µ”·Àπàß·≈–‡™◊ÕÈ ·∫§∑’‡√’¬ √«¡∑—ßÈ condition ∑—Ë«‰ª¢ÕßºŸâªÉ«¬·≈–Õ“°“√· ¥ß∑“ß§≈‘π‘§ „πªí®®ÿ∫—π º≈°“√√—°…“¥’°«à“ ¡—¬°àÕπ¡“° ‡π◊ËÕß®“°¡’«‘∏’°“√µ√«®«‘π‘®©—¬ æ‘‡»…∑’¥Ë ∑’ ”„Àâ«π‘ ®‘ ©—¬‚√§‰¥â‡π‘πË Ê «‘∏°’ “√ºà“µ—¥·≈–¬“ªØ‘™«’ π–¡’ ª√– ‘∑∏‘¿“æ¥’¢÷Èπ¡“° Õ—µ√“µ“¬¢Õß infected aneurysms ™π‘¥µà“ß Ê ¡’¥ß— µàÕ‰ªπ’È mycotic aneurysm √âÕ¬≈– 25 microbial arteritis √âÕ¬≈– 75 infected preexisting aneurysm √âÕ¬≈– 75 ·≈– post-traumatic infected false aneurysm √âÕ¬≈– 10(4) Õ—µ√“°“√µ—¥¢“À≈—ß°“√√—°…“ infected femoral artery false aneurysm Õ¬Ÿ√à –À«à“ß√âÕ¬≈– 11-25(7,48,49,50) ∂â“¬—ß§«∫§ÿ¡°“√ µ‘¥‡™◊ÈÕ¢Õß·º≈∫√‘‡«≥¢“Àπ’∫‰¥â¬—ß‰¡à¥’ ‰¡à§«√∑” revascularization.

INFECTED ANEURYSMS

197

‡Õ° “√Õâ“ßÕ‘ß 1. Osler W. The Gustanian Lectures on malignant endocarditis. Br Med J 1885;1 467-471. 2. Lewis D, Schrager J. Embolomycotic aneurysms. JAMA 1909;63:1808-1814. 3. Stengel A, Wolferth CC. Mycotic (bacterial) aneurysms of intravascular origin. Arch Intern Med 1923;31:527-536. 4. Wilson SE, Van Wagenen P, Passaro E Jr. Arterial Infection. Curr Probl Surg 1978;15:5. 5. Sommerville RI, Allen EV, Edwards JE. Bland and Infected arteriosclerotic abdominal aortic aneurysms: A clinicopathologic study. Medicine 1959;38:207. 6. Wilson SE, Gordon E, Van Wagenen PB. Salmonella arteritis. Arch Surg 1978;113:1163-1171. 7. Anderson CB, Butcher HR Jr. Mycotic aneurysms. Arch Surg 1974;109: 712-721. 8. Eshaghy B, Scanlon RJ, Amirparviz F, et al. Mycotic aneurysm of brachial artery: A complication of retrograde catheterization. JAMA 1974;228: 1574-1581. 9. Gouny P, Valverde, A, Vincent D. Human immunodeficiency virus and infected aneurysm of the abdominal aorta: Report of three cases. Ann Vasc Surg 1992;6: 239-246. 10. Kyriakides GK, Simmons RL, Najarian JS. Mycotic aneurysms in transplant patients. Arch Surg 1976;111: 472-481. 11. Padberg F, Hobson RII, Lee B, et al. Femoral pseudoaneurysm from drug of abuse: Ligation or reconstruction? J Vasc Surg 1992;15: 642-652. 12. Soderstrom CA, Wasserman DJ, Ransom KT, et al. Infected false femoral artery aneurysms secondary to monitoring catheters. J Cardiovasc Surg 1983;24: 63-70. 13. Patel S, Johnston KW. Classification and management of mycotic aneurysms. Surg Gynecol Obstet 1977;144: 691-702. 14. Mcnamara MF, Roberts AB, Bakshi KR. Gram-negative bacterial infection of aortic aneurysms. J Cardiovasc Surg 1987;24:453-462. 15. Perdue GDm, Smith RB III. Surgical treatment of mycotic aneurysms. South Med J 1967;60: 848-852. 16. Dean RH, Meacham PW, Weaver FA, et al. Mycotic embolism and embolomycotic aneurysms: Neglected lessons of the past. Ann Surg 1986;204: 300-311. 17. Dupont J, Bonavita JA, Digiovanni RJ, et al. Acquired immunodeficiency syndrome and mycotic abdominal aortic aneurysms: A new challenge? Report of a case. J Vasc Surg 1989;10: 254-262. 18. Wang Y, Chester E, Korns ME, edwards JE. Mycotic aneurysms of left ventricle and ascending aorta. Minn Med 1968;51: 395-401. 19. Thompson TR, Tilleli J, Johnson DE, et al. Umbilical artery catheteriztion complicated by mycotic aneurysms in neonates. Adv Pediatr 1980;27: 275-286.

20. Benette DE. Primary mycotic aneurysms of the aorta. Arch Surg 1967;94: 758-763. 21. Smith G, Hutchinson HE. Lymph borne infection and aneurysm formation. Surg Gynecol Obstet 1957;104:722-731. 22. Buxton RW, Holderfer WF. Primary mycotic aneurysms. Am Surg 1963;29: 86323. McCrae J. A case of multiple mycotic aneurysms of the first part of the aorta. J Pathol Bacteriol 1905;10: 373-382. 24. Brown SL, Busutil RW, Baker JD, et al. Bacteriologic and surgical determinants of survival in patients with mycotic aneurysm. J Vasc Surg 1984;1:541-549. 25. Bennett DE, Cherry JK. Bacterial infection of aortic aneurysm: A clinicopathologic study. An J Surg 1967;113: 321-332. 26. Parkhurst GF, Decker JP. Bacterial aortitis and mycotic aneurysm of the aorta. Am J Pathol 1955;31:821-830. 27. Reddy DJ, Shepard AD, Evans JR, et al. Management of infected aortoiliac aneurysms. Arch Surg 1991;126: 873-882. 28. Suddleson EA, Katz SG, Kohl RD. Mycotic suprarenal aortic aneurysm. Ann Vasc Surg 1987;1:426-432. 29. Ernst CB, Campbell C Jr, Daugherty ME, et al. Incidence and significance of intra-operative bacterial cultures durign abdominal aortic aneurysmectomy. Ann Surg 1977;185: 626-635. 30. Triratvorakul P, Sriphojanart S, Sathapatayavongs B. Abdominal aortic aneurysms infected with salmonella: Problems of treatment. J Vasc Surg 1990;12: 16-24. 31. Jarrett F, Darling RC, Mundth ED, et al. Experience with infected aneurysms of the abdominal aorta. Arch Surg 1975;10:1281-1290. 32. Huebl HC, Read RC. Aneurysmal abscess. Minn Med 1966;49:1118. 33. Johnson JR, Ledgerwood AM, Lucas CE. Mycotic aneurysm: New concepts in surgery. Arch Surg 1983;118:577-584. 34. Ledgerwood AM, Lucas CE. Mycotic aneurysm of the carotid artery. Arch Surg 1974;109: 496-503. 35. Baker WH, Moran JM, Dormer DB. Infected aortic aneurysm following arteriography. J Cardiovasc Surg 1979;20: 313-319. 36. Vozelgang RL, Sohaey R. Infected aortic aneurysms: CT appearance. J Comput Assist Tomogr 1988;12(1): 109-118. 37. Mundth ED, Darling RC, Alvarodo RH, et al. Surgical management of mycotic aneurysms and the complications of infections. in vascular reconstructive surgery. Am J Surg 1980;191: 47-56. 38. Mendelowitz DS, Ramstedt R, Yao JST, et al. Abdominal aortic salmonellosis. Surgery 1979;85: 514-521. 39. Miller BM, Waterhouse G, Alford AH, et al. Histoplasma infection of abdominal aortic aneurysms. Ann Surg 1983;197: 157-164.

198 40. Reddy DJ, Smith RF, Elliott JP Jr, et al. Infected femoral artery false aneurysms in drug addicts: Evolution of selective vascular reconstruction. J Vasc Surg 1986;3: 718-726. 41. Shetty PC, Krasicky GA, Sharma RP, et al. Mycotic aneurysms in intravenous drug abusers: The utility of intravenous digital subtraction angiography. Radiology 1985;155: 319-326. 42. Weintraub RA, Abrams HL. Mycotic aneurysm. Am J Roentgenal 1968;102:354-361. 43. Brunner MC, Mitchell RS, Baldwin JC, et al. Prosthetic graft infection: Limitations of indium white blood cell scanning. J Vasc Surg 1986;3: 42-51. 44. Chan FY, Crawford ES, Coselli JS, et al. In situ prosthetic graft replacement for mycotic aneurysms of the aorta. Ann Thorac Surg 1989;47: 193-202.

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥ 45. Taylor LM Jr, Deitz DM, McConnell DB, Porter JM. Treatment of infected abdominal aneurysms by extraanatomical bypass, aneurysm excision and drainage. Am J Surg 1988;155: 655-664. 46. Ewart JM, Burke ML, Bunt TZ. Spontaneous abdominal aortic infections: Essentials of diagnosis and management. Am Surg 1983;49:37. 47. Reddy DJ, Smith RF, Elliott JP jr, et al. Infected femoral artery false aneurysms in drug addicts: Evolution of selective vascular reconstruction. J Vasc Surg 1986;3:718-724. 48. Feldman AJ, Berguer R. Management of an infected aneurysm of the groin secondary to drug abuse. Surg Gynecol Obstet 1983;157: 519-528. 49. Johnson JR, Ledgerwood AM, Lucas CE. Mycotic aneurysm: New concepts in surgery. Arch Surg 1983;118: 577-585.

∫∑∑’Ë 22 THE DIABETIC FOOT

‡∫“À«“π‡ªìπ‚√§¢Õß√–∫∫µàÕ¡‰√â∑àÕ∑’Ëæ∫‰¥â∫àÕ¬ ‡ªìπ “‡Àµÿ ”§—≠¢Õß‰µ«“¬‡√◊ÕÈ √—ß ‚√§À—«„®·≈–À≈Õ¥‡≈◊Õ¥ µ“∫Õ¥ ‚√§‡ ◊ÕË ¡¢Õß‡ âπª√– “∑ à«πª≈“¬·≈–°“√µ—¥¢“∑‘ßÈ (1) °“√µ‘¥ ‡™◊ÈÕ∑’Ë‡∑â“„πºŸâªÉ«¬‚√§‡∫“À«“π∂◊Õ‡ªìπ¿“«–·∑√°´âÕπ∑’Ë√ÿπ·√ß ·≈–∑”„ÀâºŸâªÉ«¬µâÕßæ—°√—°…“„π‚√ßæ¬“∫“≈‡ªìπ√–¬–‡«≈“π“π ¡—°®–æ∫„πºŸªâ «É ¬Õ“¬ÿ¡“°°«à“ 50 ªï ‡ªìπ·∫∫ Type II (Insulin dependent) ¡“π“π°«à“ 18 ªï·≈â«(2) ‚¥¬∑—«Ë ‰ªºŸªâ «É ¬‡∫“À«“π∑’Ë ¡’ª≠ í À“°“√µ‘¥‡™◊ÕÈ ∑’‡Ë ∑â“®–µâÕßæ—°øóπô √—°…“„π‚√ßæ¬“∫“≈π“π°«à“ 1 ‡¥◊Õπ ·≈–ª√–¡“≥√âÕ¬≈– 44 µâÕßæ—°Õ¬Ÿà„π‚√ßæ¬“∫“≈π“π °«à“ 3 ‡¥◊Õπ ∑”„Àâ π‘È ‡ª≈◊Õßß∫ª√–¡“≥„π°“√¥Ÿ·≈√—°…“¡“°¡“¬ ‡ªìπªí≠À“‡√◊ÈÕ√—ß¢ÕßºŸâªÉ«¬·≈– —ß§¡ °“√„Àâ§«“¡√Ÿâ·°àºŸâªÉ«¬„π °“√¥Ÿ·≈µπ‡Õß ªÑÕß°—π µ√«®§âπæ∫æ¬“∏‘ ¿“æ·√°‡√‘¡Ë ¡“æ∫ ·æ∑¬å·≈–‰¥â√∫— °“√√—°…“·µà‡π‘πË Ê ®–‡ªìπº≈¥’°«à“

°“¬«‘¿“§·≈– √’√«‘∑¬“¢Õß‡∑â“ √’√«‘∑¬“‡∑â“‡ªìπÕ«—¬«–∑’µË Õâ ß‡§≈◊ÕË π‰À«·≈–„™âß“πµ≈Õ¥«—π πÕ°®“°‡«≈“πÕπÀ≈—∫ ®÷ß¡’ ‚Õ°“ ∫“¥‡®Á∫·≈–µ‘¥‡™◊ÈÕ‰¥âßà“¬ °«à“Õ«—¬«– à«πÕ◊πË ¢Õß√à“ß°“¬(3) ‡∑â“µâÕß∑πµàÕ·√ßÕ—¥ ·√ß‡ ’¬¥ ∑“π·≈–·√ß∫‘¥µ≈Õ¥«—π º‘«Àπ—ßΩÉ“‡∑â“ ‡π◊ÈÕ‡¬◊ËÕ™—Èπ„µâº‘«Àπ—ß ·≈–‰¢¡—π∫√‘‡«≥ plantar foot pad ®–∑”Àπâ“∑’Ë‡ªìπ‡∫“– √Õß√—∫°“√°√–·∑°∑’¥Ë ·’ ≈–¡’ª√– ‘∑∏‘¿“æ Ÿß ÿ¥(4) ºŸªâ «É ¬‡∫“À«“π ∑’ Ë ≠ Ÿ ‡ ’¬ª√– “∑ —¡º— ®–‡°‘¥·º≈·≈–°“√∫“¥‡®Á∫∑’‡Ë ∑â“‚¥¬‰¡à√µŸâ «— ‡¡◊ËÕª≈àÕ¬ª≈–≈–‡≈¬‰¡à¥Ÿ·≈‡Õ“„®„ à®–‡ªìπµâπµÕ¢Õß¢∫«π°“√ Õ—°‡ ∫µ‘¥‡™◊ÕÈ µàÕ¡“‰¥â

°“¬«‘¿“§»“ µ√å °àÕπ∑’®Ë –∑”°“√√—°…“ºŸªâ «É ¬ ®–µâÕß‡¢â“„®∂÷ß°“¬«‘¿“§»“ µ√å ¢ÕßΩÉ“‡∑â“ ·≈–æ¬“∏‘ ¿“æ∑’Ë‡°‘¥¢÷Èπ°—∫∫√‘‡«≥µà“ß Ê ¢Õß‡∑â“ ‡¡◊ÕË ‡°‘¥°“√µ‘¥‡™◊ÕÈ plantar compartment ·∫àßÕÕ°‰¥â‡ªìπ 3 à«π §◊Õ medial, central ·≈– lateral (√Ÿª∑’Ë 22.1) æ◊πÈ ∑’√Ë Õß∑—ßÈ 3 compartment §◊Õ plantar fascia à«π¥â“π∫π®–‡ªìπ metatarsal bones ·≈– interosseous fascia ‡¡◊ËÕ¡’°“√∫«¡‡°‘¥¢÷Èπ ¿“¬À≈—ß°“√Õ—°‡ ∫µ‘¥‡™◊ÈÕ compartments ‡À≈à“π’È®–¢¬“¬ ÕÕ°‰¡à ‰¥â ∑”„Àâ¡’§«“¡¥—π¿“¬„π Ÿß¢÷Èπ µàÕ¡“®–‡°‘¥°“√¢“¥ ‡≈◊Õ¥·≈–‡πà“µ“¬¢Õß‡π◊ÈÕ‡¬◊ËÕµà“ß Ê ∑’ËÕ¬Ÿà „π compartments °“√Õ—°‡ ∫µ‘¥‡™◊ÈÕ‡¡◊ËÕ‡°‘¥¢÷Èπ„πΩÉ“‡∑â“®–°√–®“¬Õ¬à“ß√«¥‡√Á« „π·µà≈– compartments ‰¥â∑“ß intercompartmental septa °“√·æ√à‡™◊ÈÕ¡—°®–‡√‘Ë¡®“° deep space infection ·≈â«°√– ®“¬¡“∑“ßÀ≈—ß‡∑â“·≈–∑“ß¥â“π¢â“ß ºŸâªÉ«¬Õ—°‡ ∫µ‘¥‡™◊ÈÕ∑’Ë¡’ À≈—ß‡∑â“∫«¡®÷ß¡—°®–‡°‘¥ deep space infection ¡“°àÕπ·≈â« Õ“°“√®÷ß√ÿπ·√ß¡“° °“√·æ√à°√–®“¬¢Õß‡™◊ÈÕ·∫§∑’‡√’¬¿“¬„π compartment ¢Õß‡∑â“®–°√–®“¬®“° plantar surface À√◊Õ web spaces ¢Õß‡∑â“‰ª¬—ß¢âÕ‡∑â“À√◊Õ¢“‰¥â

æ¬“∏‘ √’√«‘∑¬“ °“√Õ—°‡ ∫µ‘¥‡™◊ÈÕ∑’Ë‡∑â“„πºŸâªÉ«¬‡∫“À«“π‡ªìπ “‡Àµÿπ”∑’Ë ”§—≠ „π°“√µ—¥¢“‰¡à«“à ®–‡ªìπ°“√µ—¥„µâ‡¢à“ (BK amputation) À√◊Õ°“√µ—¥‡Àπ◊Õ‡¢à“ (AK amputation) ª√–¡“≥√âÕ¬≈– 3

200

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√Ÿª∑’Ë 22.1 Plantar compartment ¢Õß‡∑â“·∫àßÕÕ°‰¥â‡ªìπ 3 à«π „µâΩÉ“‡∑â“ medial compartment ¡’ intrinsic muscles ¢ÕßÀ—«·¡à‡∑â“ central compartment ¡’ intrinsic muscle ¢Õßπ‘È«°≈“ß, extrinsic flexor tendons, vascular arch ·≈– plantar nerves lateral compartments ¡’ intrinsic muscles ¢Õßπ‘È«°âÕ¬ °“√Õ—°‡ ∫ µ‘¥‡™◊ÈÕ∑’Ë‡°‘¥¢÷Èπ∫√‘‡«≥π’È®–≈“¡¢÷Èπ∑’Ë¢“ºà“π flexor tendons ·≈– neurovascular bundles

¢ÕßºŸâªÉ«¬‡∫“À«“π∑’ËµâÕßµ—¥¢“ ·µà√âÕ¬≈– 50 ¢ÕßºŸâªÉ«¬∑’Ë ®”‡ªìπµâÕßµ—¥¢“∑’Ë ‰¡à „™à “‡Àµÿ®“°Õÿ∫µ— ‡‘ Àµÿ‡ªìπºŸªâ «É ¬‡∫“À«“π(5) ª√–¡“≥√âÕ¬≈– 60 ¢ÕßºŸªâ «É ¬∑’µË ¥— ¢“·≈–™à«¬‡À≈◊Õµ—«‡Õß‰¡à ‰¥â ®–∂÷ß·°à°√√¡¿“¬„π√–¬–‡«≈“ 5 ªï(6) ª∞¡‡Àµÿ·≈–µ—«·ª√∑’ Ë ”§—≠ „π°“√µ‘¥‡™◊ÈÕ∑’Ë‡∑â“¢ÕßºŸâªÉ«¬‡∫“À«“π§◊Õ ¢“¢“¥‡≈◊Õ¥·≈–‚√§ ¢Õß‡ âπª√– “∑

‚√§À≈Õ¥‡≈◊Õ¥ ºŸªâ «É ¬∑’‡Ë ªìπ‚√§‡∫“À«“π¡“π“π‡°‘π°«à“ 10-15 ªï ¡—°®–¡’ ‚√§À≈Õ¥‡≈◊Õ¥√à«¡¥â«¬ª√–¡“≥√âÕ¬≈– 50(7) √âÕ¬≈– 22 ®–æ∫ «à“¡’·§≈‡´’¬Ë ¡‡°“–Õ¬Ÿ°à ∫— ºπ—ßÀ≈Õ¥‡≈◊Õ¥®“°¿“æ√—ß ’ª°µ‘ √âÕ¬≈– 13 ®–§≈”™’æ®√∫√‘‡«≥¢âÕ‡∑â“‰¡à ‰¥â ºŸªâ «É ¬‡∫“À«“π®–‡°‘¥ atherosclerosis ‰¥â ‡ √Á « °«à “ §πª°µ‘ ∑—Ë « ‰ª„πÀ≈Õ¥‡≈◊ Õ ¥¢π“¥ °≈“ß·≈–À≈Õ¥‡≈◊Õ¥¢π“¥‡≈Á°∫√‘‡«≥ª≈“¬‡∑â“(6,8) ∫√‘‡«≥∑’ÕË ¬Ÿµà Ë” °«à“À≈Õ¥‡≈◊Õ¥·¥ß popliteal ≈—°…≥–¢Õß°“√Õÿ¥µ—π·≈–µ’∫ ·§∫®–‡ªìπ™à«ß Ê Õ¬ŸàÀ≈“¬™à«ß ≈—∫°—π °“√Õÿ¥µ—πÕ“®®–≈“¡ ≈ß‰ª∂÷ß metatarsal arteries(9) ∑”„Àâ°“√´àÕ¡·´¡·≈–ºà“µ—¥„Àâ

¡’‡≈◊Õ¥¡“‡≈’¬È ß‰¡à ‰¥âº≈ ”À√—∫Õÿ∫µ— °‘ “√·≈–≈—°…≥–¢Õß°“√‡°‘¥ aortoliac occlusive disease (AIOD) ‰¡àµ“à ß°—π√–À«à“ßºŸªâ «É ¬ ∑—Ë«‰ª°—∫ºŸâªÉ«¬∑’Ë‡ªìπ‡∫“À«“π microangiopathy ‡ªìπæ¬“∏‘ ¿“æÕ—πÀπ÷ßË ¢ÕßÀ≈Õ¥‡≈◊Õ¥∑’æË ∫‰¥â „πºŸªâ «É ¬‡∫“À«“π(10) ºŸâªÉ«¬‡∫“À«“π∑’Ë¢“¢“¥‡≈◊Õ¥·≈–πÈ”µ“≈„π‡≈◊Õ¥ ŸßÕ¬Ÿà·≈â« ‡¡◊ËÕ‡°‘¥∫“¥·º≈‡≈Á°πâÕ¬∑’Ë¢“ ®–‡°‘¥°“√Õ—°‡ ∫µ‘¥‡™◊ÈÕ≈ÿ°≈“¡ ‰¥âßà“¬ °“√§«∫§ÿ¡πÈ”µ“≈„π‡≈◊Õ¥„ÀâÕ¬Ÿà „π√–¥—∫∑’Ë‡À¡“– ¡®– ™à«¬„Àâ∫“¥·º≈À“¬¥’¢÷Èπ ·≈–≈¥Õ—µ√“°“√µ‘¥‡™◊ÈÕ≈ß °“√¢“¥ ‡≈◊Õ¥¢Õß¢“¡’µ—«·ª√¡“°¡“¬∑’Ë¡’ à«π‡°’Ë¬«¢âÕß‡™àπ °“√Õÿ¥µ—π À≈“¬™à«ß¢Õß°√–· ‡≈◊Õ¥ ‡¡µ“‚∫≈‘ ¡å¢Õß°≈Ÿ‚§ ºà“π sorbital pathway ·∑π∑’®Ë –ºà“π glycolytic pathway ®–∑”„Àâ‡°‘¥¿“«– hyperglycemia induced pseudohypoxia °“√„™âÕäÕ°´‘‡®π ¢Õß‡´≈≈å®–º‘¥ª°µ‘ §«“¡º‘ ¥ ª°µ‘ ¢ Õß‡ â π ª√– “∑ à « πª≈“¬ æ∫„πºŸâ ªÉ « ¬ ‡∫“À«“π√âÕ¬≈– 50 ·≈–Õ—µ√“®– Ÿß¡“°¢÷Èπ∂â“‡ªìπ‡∫“À«“π ‡ªìπ√–¬–‡«≈“π“π(11,12) ‡√‘¡Ë ®“°™“·≈–µàÕ¡“®–‰√â§«“¡√Ÿ â °÷ —¡º— §«“¡º‘¥ª°µ‘¢Õß‡ âπª√– “∑¡’ “‡Àµÿ¡“®“° progressive distal axonopathy À√◊Õ‡ âπª√– “∑∫“ß®ÿ¥∂Ÿ°°¥∑—∫Õ¬Ÿàπ“π ª√– “∑ —¡º— ∑’ËΩÉ“‡∑â“®–À“¬‰ª °≈â“¡‡π◊ÈÕ intrisic „πΩÉ“‡∑â“ ®–≈’∫·ø∫ °“√¬◊¥¢Õß‡ÕÁπæ—ßº◊¥º‘¥ª°µ‘ °√–¥Ÿ° metmatarsal ®–‚ªÉß (√Ÿª 22.2) ‡«≈“‡¥‘π®–‡°‘¥·º≈®“°·√ß°√–·∑°‰¥âßà“¬ ¡’·º≈®–‰¡à√ Ÿâ °÷ ‡®Á∫∂÷ß·¡â«“à ®–¡’°“√Õ—°‡ ∫≈ÿ°≈“¡‰ª·≈â« √–∫∫ ª√– “∑ autonomic Ÿ≠‡ ’¬‰ª º‘«Àπ—ß®–·µ°·Àâß‡ªìπ –‡°Á¥ ‡°‘¥·º≈µ‘¥‡™◊ÕÈ ‰¥âß“à ¬(12) (√Ÿª∑’Ë 22.3) °“√Õ—°‡ ∫µ‘¥‡™◊ÈÕ¢Õß‡∑â“ ºŸâªÉ«¬‡∫“À«“π¢“¢“¥‡≈◊Õ¥ ·≈–‡ âπª√– “∑ —¡º— Ÿ≠‡ ’¬§«“¡√Ÿâ ÷° —¡º— °“√∫“¥‡®Á∫∑’Ë ‡°‘¥·º≈‡æ’¬ß‡≈Á°πâÕ¬®–≈ÿ°≈“¡®π¡’°“√µ‘¥‡™◊ÕÈ √ÿπ·√ß‰¥â ºŸªâ «É ¬ ∫“ß√“¬Õ“®®–≈–‡≈¬°“√¥Ÿ·≈√—°…“§«“¡ –Õ“¥¢Õß‡∑â“ „ à√Õß ‡∑â“§—∫À√◊ÕÀ≈«¡‡°‘π‰ª∑”„Àâ‡°‘¥·º≈‰¥âßà“¬ (√Ÿª∑’Ë 22.4) °“√ µ‘¥‡™◊ÈÕÕ“®®–‡°‘¥®“°‡™◊ÈÕ√“∑’Ë´Õ°‡≈Á∫·≈–≈ÿ°≈“¡°≈“¬‡ªìπµ‘¥ ‡™◊È Õ ·∫§∑’ ‡ √’ ¬ ∑’Ë √ÿ π ·√ß®π°√–∑—Ë ß ¡’ ° “√‡πà “ µ“¬¢Õß‡π◊È Õ ‡¬◊Ë Õ ·æ∑¬åºŸâ√—°…“§«√«‘π‘®©—¬‚√§„Àâ ‰¥â·µà‡π‘Ëπ Ê ‡æ◊ËÕ∑’Ë®–∑”°“√ √—°…“‰¥â∑π— ∑’ (2) ºŸªâ «É ¬‰¡à “¡“√∂ —ß‡°µÿ·≈–∫Õ°‡≈à“Õ“°“√·≈– æ¬“∏‘ ¿“æ‰¥â‡π◊ËÕß®“° “¬µ“‰¡à¥’ ¡Õß‰¡à‡ÀÁπ ·≈– Ÿ≠‡ ’¬ ª√– “∑ —¡º— ·º≈∑’Ë‡°‘¥¢÷Èπ¡—°®–À“¬™â“®÷ß§«√µ√«®¥Ÿ«à“¡’‚√§ À≈Õ¥‡≈◊Õ¥µ’∫µ—π√à«¡¥â«¬À√◊Õ‰¡à ‡æ√“–∂â“ “¡“√∂ºà“µ—¥·°â ‰¢ §«“¡º‘¥ª°µ‘¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß‰¥â °“√À“¬¢Õß∫“¥·º≈®–‡ªìπ ª°µ‘

201

THE DIABETIC FOOT

Ischemia due to tibial/peroneal artery occlusive disease

Toes curled in claw position

Cavas deformity with increased pressure under metatarsal heads

Diminished sensation

√Ÿª∑’Ë 22.2 ªí≠À“¢Õß‡∑â“„πºŸâªÉ«¬‡∫“À«“π ‡ªìπº≈ ◊∫‡π◊ËÕß®“°æ¬“∏‘ ¿“æ neuropathy, ischemia ·≈– infection Acute Soft Tissue Infections √Õ¬·¬°¢Õßº‘«Àπ—ß À√◊Õ ·º≈∫“¥‡®Á∫‡æ’¬ß‡≈Á°πâÕ¬ ®–‡ªìπ®ÿ¥‡√‘¡Ë µâπ„π°“√Õ—°‡ ∫µ‘¥‡™◊ÕÈ (√âÕ¬≈– 10) „πºŸªâ «É ¬‡∫“À«“π¡—°®–‡√‘¡Ë ®“° nail plate (√âÕ¬≈– 30) À√◊Õ√àÕß√–À«à“ßπ‘«È (√âÕ¬≈– 60)(13) ‡π◊ÕË ß®“°µ√ß√àÕß√–À«à“ß π‘«È ‡∑â“‡ªìπ∫√‘‡«≥∑’¡Ë §’ «“¡™◊πÈ Ÿß µ√ß nail plates ¡’ Keratin ·≈– debris – ¡Õ¬Ÿà¡“° ‡ªìπ media ∑’Ë¥’ ”À√—∫°“√µ‘¥‡™◊ÈÕ °“√ µ‘¥‡™◊ÕÈ ∑’‡Ë ∑â“®–¡’§«“¡√ÿπ·√ß‡√’¬ßµ“¡≈”¥—∫¥—ßπ’È (µ“√“ß∑’Ë 22.1) ‡√‘Ë¡®“° acute cellulitis ®π°√–∑—Ëß∂÷ß necrotizing fascitis ´÷ßË ∂â“‰¡à§«∫§ÿ¡√—°…“ºŸªâ «É ¬®–∂÷ß·°à°√√¡‰¥â µ“√“ß∑’Ë 22.1 °“√Õ—°‡ ∫µ‘¥‡™◊ÕÈ ¢Õß‡∑â“∑’æË ∫‰¥â∫Õà ¬ ACUTE INFECTIONS

CHRONIC INFECTIONS

Localized cellulitis Neurotrophic ulcers Septic arthritis of Osteomyelitis metatarsophalangeal joint Necrotizing cellulitis or fascitis Deep space infections Gangrene (clostridial or nonclostridial)

acute cellulitis ‡√‘¡Ë ®“°√àÕß√–À«à“ßπ‘«È ∂â“‰¡à√°— …“§«∫§ÿ¡ ®–≈“¡‰ª∂÷ß¢—πÈ tendon °≈“¬‡ªìπ deep space infection ·≈– necrotizing fascitis „π∑’ Ë ¥ÿ ‚Õ°“ ∑’®Ë –∂Ÿ°µ—¥‡∑â“¡’‰¥â ßŸ ‡æ√“– ∂â“°“√Õ—°‡ ∫≈ÿ°≈“¡¡“∂÷ß¢—Èππ’È·≈â«°≈â“¡‡π◊ÈÕ·≈–‡ÕÁπæ—ßº◊¥®– ‡πà“µ“¬À¡¥ ºŸªâ «É ¬ acute necrotizing ®–¡’Õ“°“√·≈–Õ“°“√ · ¥ß¥—ßµàÕ‰ªπ’§È Õ◊ ‰¢â ßŸ ÕàÕπ‡æ≈’¬ §≈◊πË ‰ â Õ“‡®’¬π ·≈–¡’ ketoacidosis ∂â“‡°‘¥¢÷πÈ ∑’ÀË ≈—ß‡∑â“ ®–æ∫«à“À≈—ß‡∑â“∫«¡ deep space infection ®–‡√‘¡Ë ®“° central compartment ¢Õß‡∑â“°àÕπ‡ ¡Õ°àÕπ®–≈“¡¡“∑’Ë lateral ·≈– medial compartment °“√‡πà“µ“¬¢Õß interosseous fascia ®–∑”„Àâ‡™◊ÈÕ ·∫§∑’‡√’¬·æ√à°√–®“¬ deep compartment ‰ª¬—ßÀ≈—ß‡∑â“·≈– flexor tendon ≈“¡‰ª∂÷ßπàÕß·≈–¢“ ‡π◊ÕË ß®“°¢“¢“¥‡≈◊Õ¥Õ¬Ÿ·à ≈â« °“√µ‘¥‡™◊ÈÕ®÷ß≈ÿ°≈“¡‰¥âßà“¬ ‡π◊ÈÕ‡¬◊ËÕ„π compartment ®– ∫«¡¡’§«“¡¥—π Ÿß µ÷ßµ—« ®÷ß∑”„Àâ‡πà“µ“¬‚¥¬‡©æ“– intrinsic muscles °“√¡’µÿà¡πÈ”æÕß∑’Ë∫√‘‡«≥ΩÉ“‡∑â“∂◊Õ‡ªìπÕ“°“√√–¬– ∑â“¬· ¥ß«à“ plantar vessels µ’∫µ—πÀ¡¥·≈â« ‡π◊ÕÈ ‡¬◊ÕË ‡πà“µ“¬ ·≈â«

202

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥

0 I II III IV V √Ÿª∑’Ë 22.3 Grading of Diabetic Foot Ulcer Grade O Grade I Grade II Grade III Grade IV Grade V

No ulcer but high-risk foot Superficial ulcer Deep ulcer, No bony involvement Abscess with bony invovlement Localized gangrene (toes, heel) Gangrene - whole foot

°“√∂à“¬¿“æ√—ß ’ ∂â“æ∫¡’øÕßÕ“°“»·∑√°°√–®“¬Õ¬Ÿàµ“¡ ‡π◊ÈÕ‡¬◊ËÕ · ¥ß«à“¡’°“√µ‘¥‡™◊ÈÕ¢Õß·∫§∑’‡√’¬™π‘¥ clostridium À√◊Õ™π‘¥°√—¡≈∫∑’ºË ≈‘µ°ä“´‰¥â À√◊ÕÀ≈—ß°“√µ‘¥‡™◊ÕÈ ·≈â«ºŸªâ «É ¬‰¡à√Ÿâ ÷°µ—«¬—ß‡¥‘πÕ¬Ÿà ∑”„ÀâøÕßÕ“°“»°√–®“¬‡¢â“‰ª„π‡π◊ÕÈ ‡¬◊ÕË µà“ß Ê §«√π”‡Õ“ÀπÕß‰ª¬âÕ¡ ’°√—¡·¬°‡™◊ÈÕ°àÕπ„Àâ¬“ªØ‘™’«π– °“√ µ‘¥‡™◊ÈÕ¢Õß·∫§∑’‡√’¬ clostridium ¡—°®–≈ÿ°≈“¡‡√Á«‡ ¡Õ ºŸâ ªÉ«¬®–¡’Õ“°“√Õ◊πË √à«¡¥â«¬‡ ¡Õ‡À¡◊Õπ°—∫ sepsis ‡√“ “¡“√∂«‘π®‘ ©—¬·¬°‚√§√–À«à“ß acutely inflamed diabetic foot infection ®“° gouty arthritis ·≈– Charcotûs joint ‰¥â ‚¥¬ gouty arthritis ®–¡’°“√Õ—°‡ ∫‡°‘¥¢÷πÈ √Õ∫ metatarsophalangeal joint ·≈–π‘«È ·¡à‡∑â“‰¡à¡Õ’ “°“√Õ◊πË ¢â“ß‡§’¬ß √–¥—∫¢Õß °√¥¬Ÿ√‘§ Ÿß„π‡≈◊Õ¥ ‡®“–¥Ÿ¥πÈ”∫√‘‡«≥¢âÕ∑’ËÕ—°‡ ∫®–æ∫º≈÷° ¢Õß°√¥¬Ÿ√‘§ Charcotûs joint æ∫‰¥â√âÕ¬≈– 2.5 ¢ÕßºŸâªÉ«¬ ‡∫“À«“π‡°‘¥®“°°“√∫“¥‡®Á∫À√◊Õ°√–∑∫°√–‡∑◊Õπ´È”´“°µàÕ‡∑â“ ¡’°“√Õ—°‡ ∫‡°‘¥¢÷ÈπÕ¬à“ß‡©’¬∫æ≈—π ‡°‘¥µ√ß metatarsophalangeal, metatarsotarsal, intratarsal ·≈– interphalangeal

joints ®–‡√‘¡Ë ®“°¡’∫«¡·¥ß¢âÕ‡¢à“¡’πÈ”§—ßË ´÷ßË ®–∑”„Àâ‡¢â“„®º‘¥«à“ ‡ªìπ¢∫«π°“√Õ—°‡ ∫µ‘¥‡™◊ÈÕ‚¥¬‡©æ“–‡¡◊ËÕ¡’·º≈‡√◊ÈÕ√—ß∑’Ë‡∑â“ Charcotûs joint ·µ°µà“ß®“°°“√Õ—°‡ ∫µ‘¥‡™◊ÕÈ ¢Õß‡∑â“§◊Õ‰¡à¡’ Õ“°“√·∑√°∑—«Ë ‰ª ¡’Õ“°“√‡©æ“–∑’√Ë –¥—∫¢Õß‡¡Á¥‡≈◊Õ¥¢“« ·≈– ESR ‰¡à ßŸ Neurotrophic ulcer °“√Õ—°‡ ∫µ‘¥‡™◊ÕÈ Õ“®®–‡°‘¥µ√ß neurotrophic ulcer ‰¥â „πºŸâªÉ«¬‡∫“À«“π ·º≈π’È‡°‘¥®“°æ¬“∏‘ ¿“æ¢Õßª√– “∑ à«πª≈“¬‰¡à ‰¥â¡ ’ “‡Àµÿ¡“®“°‚√§À≈Õ¥‡≈◊Õ¥ æ¬“∏‘ √’√«‘∑¬“„π°“√‡°‘¥ neurotrophic ulcer §◊Õ¡’æ¬“∏‘ ¿“æ¢Õß‡ âπª√– “∑§«∫§ÿ¡°“√‡§≈◊ÕË π‰À« ∑”„Àâ¡’ claw toe deformity °√–¥Ÿ°µ√ß metatarsal head ®–‚ªÉßÕÕ°¡“¡“° ∑”„Àâ¡°’ “√‡æ‘¡Ë plantar pressure(14) ¡’°“√∫“¥‡®Á∫°√–·∑°´È”´“° µàÕ∫√‘‡«≥π’Èº‘«Àπ—ß®–°≈“¬‡ªìπ keratosis ¡’°“√∫«¡·≈– Õ—°‡ ∫¢Õß plantar tissue à«π≈÷° ·º≈¡—°®–‡°‘¥µ√ß metatarsal head Õ—π∑’Ë 1, 2 ·≈– 5 ∂÷ß·¡â«“à callus ·≈– neurotrophic ulcers ®–‡°‘¥µ√ß∫√‘‡«≥„¥¢Õß‡∑â“°Á ‰¥â

THE DIABETIC FOOT

√Ÿª∑’Ë 22.4 ∫√‘‡«≥¢Õß‡∑â“∑’Ë¡’°“√°¥∑—∫‡ ’¬¥ ’´÷Ëß‡°‘¥·º≈‰¥âßà“¬ ·º≈∑’Ë‡ÀÁπ®–¡’¢Õ∫‡√’¬∫ ·µà≈÷° °“√∑”≈“¬¢Õß‡π◊ÈÕ‡¬◊ËÕ®– ≈÷ ° ≈ß‰ª®π∂÷ ß ¢â Õ ·≈–‡ÕÁ π æ— ß º◊ ¥ ∂â “ ¡’ ° “√µ‘ ¥ ‡™◊È Õ ‡°‘ ¥ ¢÷È π ®– ≈ÿ°≈“¡‰ª∂÷ß plantar surface ‰¥âßà“¬¡“° ·º≈‡√◊ÈÕ√—ß∫√‘‡«≥ ‡∑â“¡—°®–‡°‘¥®ÿ¥‡√‘¡Ë ¢Õß°“√‡°‘¥ osteomyelitis ‡ ¡Õ ‡æ√“–¡’√Ÿ sinus ®“°·º≈ neurotrophic ulcer ‰ª¬—ß deep compartment ·≈–®–¡’°“√Õ—°‡ ∫¢Õß deep compartment „π∑’Ë ÿ¥ °“√ «‘π®‘ ©—¬‚√§ osteomyelitis ®“°¿“æ√—ß ’‰¡à·πàπÕπ(15,16) ‡æ√“–∂â“ ‡°‘¥¿“¬„π 14 «—π·√°®–‰¡à‡ÀÁπ°“√∑”≈“¬¢Õß‡π◊ÕÈ °√–¥Ÿ° ·≈– „πºŸâªÉ«¬‡∫“À«“π®–·ª≈º≈¬“° ‡π◊ËÕß®“°°√–¥Ÿ°æ√ÿπºÿÕ¬Ÿà·≈â« „π∫“ß√“¬∑’®Ë ”‡ªìπ CT scan ·≈– MRI ®–™à«¬„π°“√«‘π®‘ ©—¬ osteomyelitis ·≈–°“√Õ—°‡ ∫µ‘¥‡™◊ÕÈ ¢Õß‡π◊ÕÈ ‡¬◊ÕË µà“ß Ê(17) °“√¥Ÿ·≈√—°…“‡∑â“ Õ“°“√ª«¥‡∑â“·≈–¢“‡ªìπªí≠À“ ”§—≠„π ºŸªâ «É ¬‡∫“À«“π ·≈–‚√§À≈Õ¥‡≈◊Õ¥·¥ßÕÿ¥µ—π∑’¢Ë “ ®“° atherosclerosis ‡æ√“–Õ“®®–‡°’Ë¬«¢âÕß°—∫°“√Õ—°‡ ∫µ‘¥‡™◊ÈÕ·≈– ‡π◊ÈÕ‡¬◊ËÕ‡πà“µ“¬≈ÿ°≈“¡®“°·º≈‡≈Á° Ê ∑’Ë ‰ ¡à ‰¥â¥Ÿ·≈‡Õ“„®„ à µ—Èß·µà·√° ∂â“°“√µ‘¥‡™◊ÈÕ√ÿπ·√ß‡π◊ÈÕ‡¬◊ËÕ‡πà“µ“¬¡“°®–µâÕß ≈ß∑â“¬¥â«¬°“√µ—¥¢“∑‘Èß °“√¥Ÿ·≈√—°…“‡∑â“∑’Ë¥’®–ªÑÕß°—π¿“«– ¥—ß°≈à“«‰¡à „Àâ‡°‘¥¢÷Èπ ·æ∑¬å·≈–æ¬“∫“≈∑’Ë√—°…“‡∑â“µàÕºŸâªÉ«¬ ª√–¡“≥√âÕ¬≈– 50 ¢ÕßºŸâªÉ«¬‡∫“À«“π∑’Ëµ—¥¢“‰ª®–∂Ÿ°µ—¥¢“ Õ’°¢â“ßÀπ÷ßË ¿“¬À≈—ß(18) ºŸªâ «É ¬‡∫“À«“π∑’¡Ë À’ ≈Õ¥‡≈◊Õ¥·¥ßÕÿ¥µ—π ∫“¥·º≈∑’Ë‡°‘¥¢÷Èπ®–À“¬™â“¡“° ‚¥¬‡©æ“–ª√– “∑ —¡º— ·≈– ‡§≈◊ËÕπ‰À«∫°æ√àÕß æ¬“∏‘ ¿“æÀ√◊Õ·º≈‡≈Á° Ê ∑’Ë‡∑â“®–∂Ÿ° ª≈àÕ¬ª≈–≈–‡≈¬ ‡™àπ µÿ¡à ÀπÕß ·º≈·µ° √Õ¬·¬° ·≈–‡≈Á∫À¬—ßË

203 ∫“ß§√—Èß‡À¬’¬∫µ–ªŸ∑–≈ÿ‡∑â“¬—ß‰¡à√Ÿâ ÷° ºŸâªÉ«¬∑’Ë¡’ retinopathy µ“¡Õß‡ÀÁπ‰¡à™—¥ ‡∑â“°√–∑∫µàÕ·ßà¡ÿ¡·≈–¢Õß·À≈¡‡«≈“‡¥‘π ∑”„Àâ‡°‘¥·º≈‰¥âß“à ¬ ¡Õß‰¡à‡ÀÁπ·º≈∑”„Àâ ‰¡à‡Õ“„®„ à‡∑â“∫√‘‡«≥ ∑’Ë¡’°“√‡ ’¬¥ ’À√◊Õ∂Ÿ°°¥∑—∫®–‡°‘¥·º≈‰¥âßà“¬ (√Ÿª∑’Ë 22.4) º‘«Àπ—ß∫√‘‡«≥´àπ‡∑â“∑’ËÀπ“µ—«®–‡°‘¥√Õ¬·¬°‰¥âßà“¬ ‡π◊ÈÕ‡¬◊ËÕ„µâ º‘«Àπ—ß®–‡πà“µ“¬¡’°“√Õ—°‡ ∫µ‘¥‡™◊ÈÕ‡ªìπ‚æ√ßÀπÕß À√◊Õ·º≈ ‡√◊ÈÕ√—ß∑’Ë√—°…“‰¡àÀ“¬¢“¥ ¿“«–¢“¢“¥‡≈◊Õ¥®–∑”„Àâ·º≈À“¬™â“ ‚¥¬‡©æ“–∂â“ ankle pressure ‰¥âµË”°«à“ 80 mmHg „πºŸªâ «É ¬ ∑—«Ë ‰ª ·≈– 55 mmHg „πºŸªâ «É ¬‡∫“À«“π ·º≈∑’πË «‘È ‡∑â“®–À“¬ ™â“∂â“§«“¡¥—π‚≈À‘µ∑’¢Ë Õâ ‡∑â“«—¥‰¥âµË”°«à“ 30 †mmHg ç·≈– transcutaneous oxygen (TcO2) tenson µË”°«à“ 10-20 torr(19) °“√ªÑ Õ ß°— π ‰¡à „Àâ ‡ °‘ ¥ °“√µ‘ ¥ ‡™◊È Õ ¢Õß‡∑â “ Õ¬à “ ß√ÿ π ·√ß ª√–°Õ∫¥â«¬ °“√¥Ÿ·≈·≈– —ß‡°µÿ§«“¡º‘¥ª°µ‘¢Õß‡∑â“∑ÿ°«—π «¡√Õß‡∑â“∑’¡Ë ¢’ π“¥æÕ¥’·≈–„ à ∫“¬°“√ÕÕ°°”≈—ß°“¬ ¡Ë”‡ ¡Õ ·≈–°“√¥Ÿ·≈æ¬“∏‘ ¿“æ∑’‡Ë °‘¥¢÷πÈ ‡∫◊ÕÈ ßµâπ 1. °“√¥Ÿ·≈·≈– —ß‡°µÿ§«“¡º‘¥ª°µ‘¢Õß‡∑â“∑ÿ°«—π 1.1 ≈â“ß‡∑â“∑ÿ°«—π¥â«¬πÈ”∑’ËÕÿàπæÕ¥’ ·≈–øÕ°¥â«¬ ∫ŸàÕàÕπ ‰¡à§«√®ÿà¡„Àâ‡ªï¬°‚™° ‡æ√“–®–‡°‘¥·º≈·¬°·≈–√Õ¬ ‰À¡â ‰¥â ‚¥¬‡©æ“–πÈ”∑’Ë√âÕπ‡°‘π‰ª ºŸâªÉ«¬∑’Ë¡’ª√– “∑ —¡º— ∫°æ√àÕß Õ“®®–‰¡à√ Ÿâ °÷ √âÕπÀ√◊Õ‡¬Áπ À≈—ß≈â“ß‡∑â“ ·≈â«‡™Á¥¥â«¬ºâ“·Àâß„Àâ –Õ“¥ √–«—ß‰¡à „Àâ¡’°“√‡ªï¬°™◊Èπ µ“¡√àÕßπ‘«È ‡æ√“–®–‡ªìπµâπ‡Àµÿ∑∑’Ë ”„Àâ¡°’ “√µ‘¥‡™◊ÕÈ √“‰¥â 1.2 ¥Ÿ§«“¡º‘¥ª°µ‘∑‡’Ë °‘¥¢÷πÈ µÿ¡à πÈ” ‡≈Á∫À¬—ßË ’º«‘ ∑’ºË ¥‘ ª°µ‘ √Õ¬·µ°·¬°µà“ß Ê ∫√‘‡«≥´àπ‡∑â“ ∂â“ºŸâªÉ«¬µ“¡Õß ‡ÀÁπ‰¡à™¥— ‡®π§«√„Àâ≠“µ‘À√◊ÕºŸâ „°≈â™¥‘ ™à«¬¥Ÿ 1.3 ∂â“º‘«·Àâß‡°‘π‰ª ®–‡°‘¥√Õ¬·¬°·≈–·º≈‰¥âßà“¬ §«√ ∑“¥â«¬πÈ”¬“∫”√ÿßº‘« ‡™àπ Lanolin, Eucarin ‰¡à§«√ ∑“„Àâ™¡ÿà ‡°‘π‰ª‚¥¬‡©æ“–µ“¡´Õ°π‘«È ‡æ√“–®–µ‘¥‡™◊ÕÈ √“‰¥â ·ªÑß∑’Ë „™â ‚√¬§«√„™â·ªÑß°—π‡™◊ÕÈ √“ ‡™àπ Desenex 1.4 ∂â“¡’‡≈Á∫À¬—ßË §«√¥Ÿ·≈§«“¡ –Õ“¥µ—¥‡≈Á∫„Àâ‡ ¡Õ°—π ‰¡à ∫“¥‡¢â“‡π◊ÕÈ ¢â“ßπ‘«È ‡∑â“§«√µ—¥‡≈Á∫À≈—ß®“°·™à‡∑â“„ππÈ”Õÿπà ‡æ√“–‡≈Á∫®–πÿ¡à ·≈–µ—¥ßà“¬ 1.5 corns ·≈– calluses ∫√‘‡«≥ªÿ¡É °√–¥Ÿ°‡°‘¥®“°°“√‡ ’¬¥ ’ ·≈–·√ß°¥¢Õß√Õß‡∑â“ ∂â“¥Ÿ·≈√—°…“‰¡à¥’®–°≈“¬‡ªìπ ·º≈‡√◊ÕÈ √—ß ·≈–°≈“¬‡ªìπ osteomyelitis §«√‡≈Á¡‡Õ“ÕÕ° 1.6 ¥Ÿ·≈π‘È«‡∑â“‰¡à „Àâ‡∫’¬¥·≈–‡ ’¬¥ ’°—π ‚¥¬„™âºâ“π‘Ë¡À√◊Õ ”≈’«“ßµ“¡√àÕßπ‘«È °àÕπ «¡√Õß‡∑â“ 1.7 ªÑÕß°—π‰¡à „Àâ‡°‘¥·º≈∑’Ë‡∑â“ √–«—ß§«“¡√âÕπ·≈–‡¬Áπ®—¥ °“√æ—π·∂∫ºâ“¬“ß¬◊¥À√◊Õæ—π·º≈·πàπ‡°‘π‰ª œ≈œ

204 2. √Õß‡∑â“ 2.1 ºŸâ ªÉ « ¬‡∫“À«“π∑’Ë ¡’ ‚√§À≈Õ¥‡≈◊Õ¥µ’∫ ·≈–ª√– “∑ —¡º— ∫°æ√àÕß‰¡à§«√‡¥‘π‡∑â“‡ª≈à“ 2.2 «¡∂ÿß‡∑â“·≈–√Õß‡∑â“µ≈Õ¥‡«≈“„Àâ‡°‘¥§«“¡Õ∫Õÿπà 2.3 √Õß‡∑â“§«√¡’¢π“¥æÕ¥’ «¡„ à ∫“¬‰¡à§—∫À√◊ÕÀ≈«¡ ‡°‘π‰ª 3. °“√ÕÕ°°”≈—ß°“¬ ¡Ë”‡ ¡Õ ®–™à«¬„Àâ collateral circulation ¥’¢π÷È 3.1 °“√‡°‘¥ÕÕ°°”≈—ß°“¬∑’Ë¥’∑’Ë ÿ¥§◊Õ °“√‡¥‘π ·µà®–µâÕß «¡√Õß‡∑â“∑’¡Ë ¢’ π“¥æÕ¥’°∫— ‡∑â“ 3.2 §«√‡¥‘ π ∑ÿ ° «— π ∂â “ ¡’ Intermittent claudication ‡√‘Ë¡®“°‡¥‘π™â“ Ê ∂â“ª«¥„ÀâÀ¬ÿ¥æ—°æ¬“¬“¡‡æ‘Ë¡√–¬– ‡«≈“„π°“√‡¥‘π∑ÿ° —ª¥“Àå 3.3 ‡¡◊ËÕª«¥¢“¡“°„ÀâÀâÕ¬¢“≈ß ·µàÕ¬à“ÀâÕ¬π“π‡°‘π‰ª ‡æ√“–À≈—ß‡∑â“®–∫«¡ ·º≈∑’‡Ë °‘¥¢÷πÈ ®–À“¬™â“ 4. °“√¥Ÿ·≈¢—Èπµâπ ‡¡◊ËÕ —ß‡°µÿ«à“¡’°“√ª«¥À√◊Õ¡’∫“¥·º≈ ‡≈Á°πâÕ¬∑’ Ë “¡“√∂¥Ÿ·≈√—°…“‡Õß‰¥â 4.1 ≈â“ß·º≈¥â«¬πÈ”Õÿπà ·≈– ∫ŸÕà Õà π ‰¡à§«√®ÿ¡à „ππÈ”√âÕππ“π Ê ‡æ√“–®–‡°‘¥·º≈‰À¡â ‰¥â 4.2 ‰¡à§«√„™âπÈ”¬“¶à“‡™◊ÕÈ ∑’¡Ë ƒ’ ∑∏‘√Ï πÿ ·√ß°—¥º‘«Àπ—ß·≈–‡π◊ÕÈ ‡¬◊ÕË ∂â“®”‡ªìπ§«√„™â bacitracin ointment 4.3 æ—π·º≈¥â«¬·∂∫ºâ“¬“ß¬◊¥ ‰¡à·πàπ®π‡°‘π‰ª ‰¡à§«√√—¥ ¥â«¬æ≈“ ‡µÕ√å √—¥·∂∫ºâ“°äÕ´·πàπ‡°‘π‰ª 4.4 ·º≈‰¡à¥’¢÷ÈπÀ√◊ÕÕ“®®–‡°‘¥¿“«–·∑√°´âÕπ„Àâª√÷°…“ ·æ∑¬å °“√√—°…“·º≈¢π“¥‡≈Á°°«à“ 2 ‡´Áπµ‘‡¡µ√ µ◊πÈ corns ·≈– calluses √«¡∑—Èß‡≈Á∫À¬—Ëß §«√√—°…“·∫∫ºŸâªÉ«¬πÕ°‚¥¬°“√∑” ·º≈·≈–„Àâ¬“ªØ‘™«’ π–√—∫ª√–∑“π ∂â“ ß —¬«à“®–‡ªìπ osteomyelitis ‡π◊ËÕß®“°√—°…“π“π°«à“ 2 —ª¥“Àå·≈â«·º≈‰¡à¥’¢÷Èπ§«√ àß¿“æ√—ß ’¥æŸ ¬“∏‘ ¿“æ¢Õß°√–¥Ÿ° ·º≈Õ—°‡ ∫‡ªìπ‚æ√ßÀ≈Õ¥ §«√ºà“√–∫“¬‡Õ“ÀπÕßÕÕ° §«√æ‘®“√≥“√—∫ºŸâªÉ«¬‰«â√—°…“„π ‚√ßæ¬“∫“≈‡¡◊ÕË ‡ªìπ cellulitis, ¡’ ‚æ√ßÀπÕß¢π“¥„À≠à °“√µ‘¥ ‡™◊ÈÕ≈ÿ°≈“¡ √—°…“·º≈·≈â« 3 —ª¥“Àå¬‘Ëß‰¡à¥’¢÷Èπ µ√«®√à“ß°“¬ §≈”™’æ®√¢Õß‡∑â“‰¥â‡∫“ §«√∑” arteriogram ‡æ◊ËÕ«“ß·ºπ ºà“µ—¥À≈Õ¥‡≈◊Õ¥(20)

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205

THE DIABETIC FOOT

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√Ÿª∑’Ë 22.5 °“√ºà“µ—¥√–∫“¬ÀπÕßÕÕ°®“°‡∑â“

°. Plantar incision: ≈ß¡’¥°√’¥·º≈‡ªìπ√Ÿª¢π¡‡ªï¬°ªŸπµ“¡ web space ∑’Ë âπ‡∑â“∑“ß medial ·≈– lateral compartments ‡Àπ◊Õ µàÕ plantar surface µ√ß toe pulp „Àâ≈ß¡’¥µ“¡·π« longitudinal ¢. Dorsal incisions: ≈ß¡’¥°√’¥·º≈‡ªìπ√Ÿª¢π¡‡ªï¬°ªŸπµ“¡·π«¢Õß dorsal web space ¥—ß√Ÿª æ¬“¬“¡‡≈’Ë¬ß venous arcade ·π«≈ß¡’¥∑“ß lateral compartment ·≈– âπ‡∑â“§«√Õ¬Ÿà‡Àπ◊Õ plantar surface

major amputation (AK or BK) ®–æ‘®“√≥“‡¡◊ÕË ¡’°“√µ‘¥ ‡™◊ÕÈ ≈ÿ°≈“¡ Ÿß¢÷πÈ ‰ª ·≈–‡√‘¡Ë °√–®“¬‡¢â“°√–· ‡≈◊Õ¥ À≈—ßºà“µ—¥ major amputation ·≈â « ºŸâ ªÉ « ¬®–¡’ §ÿ ≥ ¿“æ™’ «‘ µ ‡≈«≈ß ™à«¬‡À≈◊Õµ—«‡Õß‰¡à ‰¥â‡π◊ÕË ß®“°¡’‚√§·∑√°´âÕπ®“° retinopathy ·≈–À—«„®«“¬Õ¬Ÿà·≈â« Õ—µ√“µ“¬·≈–∑ÿæ≈¿“æ®– Ÿß¡“° ®÷ß§«√ æ¬“¬“¡ºà“µ—¥‡°Á∫§«“¡¬“«¢Õß¢“∑’µË ¥— „Àâ ‰¥â¡“°∑’ Ë ¥ÿ (28) ‡æ◊ÕË „Àâ ºŸâªÉ«¬ “¡“√∂‡¥‘π‰¥â‡Õß‚¥¬„™â√Õß‡∑â“‰¡àµâÕß„™â¢“‡∑’¬¡À√◊Õ ‰¡â‡∑â“§È”¬—π °“√ºà“µ—¥√–∫“¬ÀπÕßÕÕ°®“°™àÕß‡∑â“ §«√≈ß¡’¥À≈“¬√Õ¬ µ“¡·π«∑’Ë®– “¡“√∂√–∫“¬ÀπÕßÕÕ°¡“‰¥â æ¬“¬“¡À≈’°‡≈’Ë¬ß neurovascular bundles (√Ÿª∑’Ë 22.5) µ“√“ß∑’Ë 22.2 °“√ºà“µ—¥ªÑÕß°—π ”À√—∫ºŸªâ «É ¬‡∫“À«“π Keller bunionectomy Claw toe correction Metatarsal head resection Dorsal wedge osteotomy of the metatarsal shaft Partial calcanectomy

Preventive operations ‡ªìπ°“√ºà“µ—¥ªÑÕß°—π ·≈–≈¥ mechanical trauma µàÕ‡∑â“ ·º≈ ·≈– plantar surface ‡™àπ °“√∑” metatarsal osteotomies À√◊Õµ—¥‡Õ“ metatarsal head ÕÕ° ®–≈¥°“√°“√‡°‘¥·º≈·≈–µ‘¥‡™◊ÕÈ ∫√‘‡«≥ plantar surface ‰¥â(29,30) (µ“√“ß∑’Ë 22.2)

√ÿª °“√Õ—°‡ ∫µ‘¥‡™◊ÕÈ ‡ªìπªí≠À“ ”§—≠∑”„ÀâºªŸâ «É ¬µâÕßæ—°√—°…“„π ‚√ßæ¬“∫“≈‡ªìπ√–¬–‡«≈“π“π °“√√—°…“·º≈‡∫“À«“π‰¥âº≈‰¡à ¥’‡π◊ËÕß®“°ºŸâªÉ«¬‰¡à ‰¥â¥Ÿ·≈‡Õ“„®„ àµ—«‡Õß‡æ’¬ßæÕ µ≈Õ¥®π ·æ∑¬å∑’Ë√—°…“‰¡à‡¢â“„®∂÷ß°≈‰°°“√‡°‘¥æ¬“∏‘ ¿“æ °“√√—°…“∑’Ë ∂Ÿ°µâÕß·≈–¥’∑’Ë ÿ¥§◊Õ°“√ªÑÕß°—π‰¡à „Àâ‡°‘¥·º≈‡∫“À«“πµ‘¥‡™◊ÈÕ ®–™à«¬≈¥Õ—µ√“µ“¬ °“√µ—¥¢“ ·≈–∑ÿæ≈¿“æ≈ß‰¥â¡“° §ÿ≥¿“æ ™’«µ‘ ¢ÕßºŸªâ «É ¬®–¥’¢π÷È ·æ∑¬åºŸâ¥Ÿ·≈√—°…“§«√‡¢â“„®∂÷ßæ¬“∏‘ √’√«‘∑¬“¢Õß°“√‡°‘¥ ·º≈‡∫“À«“π ‡¡◊ËÕ¡’·º≈‡°‘¥¢÷Èπ§«√„Àâ°“√√—°…“∑—π∑’ ª√–‡¡‘π ¿“«–§«“¡∫°æ√àÕß¢Õßª√– “∑ À≈Õ¥‡≈◊Õ¥·¥ßÕÿ¥µ—π ·≈– ‡π◊ÕÈ ‡¬◊ÕË µà“ß Ê ·æ∑¬åÀ≈“¬ “¢“§«√¥Ÿ·≈√—°…“√à«¡°—π

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‡Õ° “√Õâ“ßÕ‘ß 1. Maser RE. Cardiovascular disease and arterial calcification in insulindependent diabetes mellitus: Interrelations and risk factor profiles. Arterioscler Thrombos 1991;11:958. 2. Leichter SB. Clinical characteristisc of diabetic patients with serious pedal infections. Metabolism (Suppl 1) 1988;37:22. 3. Wright DG, Desai SM, Henderson WH. Action of the subtalar and ankle joint complex during the stance phase of walking. J Bone Joint Surg 1964;46:361. 4. Bojsen-Moller F. Anatomy of the forefoot: Normal and pathologic. Clin Orthop 1979;142:10. 5. Bouton AJM. Detecting the patient at risk for diabetic foot ulcers. Practical Cardiology 1983;9:135. 6. Penn I. The impact of diabetes mellitus on extremity ischemia. In: Kempczinski RF (ed.). The Ischemic leg. Chicago. Year Book Medical Publishers 1985;56-69. 7. Brandman O, Redisch W. Incidence of peripheral vascular changes in diabetes mellitus. Diabetes 1953;2:194. 8. Haimovici H. Peripheral arterial disease in diabetes mellitus. In: Ellenberg M, Rifkin H (eds.). Diabetes Mellitus: Therory and Practice. New York: McGraw-Hill 1970;890-911. 9. Ferrier TM. Comparative study of arterial disease in amputated lower limbs from diabetics and nondiabetics (with special reference to feet arteries). Med J Aust 1967;1:5. 10. Strandness DE Jr, Priest RE, Gibbons GE. Combined clinical and pathologic study of diabetic and nondiabetic peripheral arterial disease. Diabets 1964;13:366. 11. Edmonds ME, Watkins PJ. Management of the diabetic foot. In:Dyck JP, Thomas PK, Lambert Elt, et al (eds.). Diabetic Neuropathy. Philadelphia: WB Saunders 1987;212. 12. Thomas PK, Eliassan SG. Diabetic Neuropathy 2nd ed. Philadelphia: WB Saunders 1984;1773-1810. 13. Bose K. Surgical approach for the infected diabetic foot. In Orthop 1979;3:177. 14. Harrison MJ, Faris IB. The neuropathic factor in the etiology of diabetic foot ulcers. J Neurol Sci 1976;28:217. 15. Park HM. Scintigraphic evaluation of diabetic osteomyelitis: Concise communication. J Nucl Med 1982;23:569.

16. Sach W, Kanat IO. Radionucleotide scanning in osteomyelitis. J Foot Surg 1986;25:311. 17. Erdman WA, Tamburro F, Jayson HT, et al. Osteomyelitis. Characteristics and pitfalls of diagnosis with MR imaging. Radiology 1991;180:533. 18. Laing P. Diabetic foot ulcers. Am J Surg 1994;167:318. 19. Cina C. Utility of transcutaneous oxygen tension measurements in peripheral arterial occlusive disease. J Vasc Surg 1984;1:362. 20. Mueller MP, Wright J, Klein SR. Diabetes and Peripheral Vascular Disease. In:Veith FJ, Hobson RWII, Williams RA, Wilson SE (eds.). Vascular Surgery (2nd ed.). New York: McGraw-Hill 1994;514-522. 21. Arcieri G, Griffith E, Gruenwaldt G, et al. Ciprofloxacin: An update on clinical experience. Am J Med 1987;82:381. 22. Ingram C, Eron LJ, Goldenberg RI, et al. Antibiotic of osteomyelitis in outpatients. Med Clin North Am 1988;72:723. 23. Lipsky BA, Pecoraro RE, Larson SA, et al. Outpatient management of uncomplicated lower-extremity infections in diabetic patients. Arch Intern Med 1990;150:790. 24. Sapico FL, Witte JL, Canawati HN, et al. The infected foot the diabetic patient: Quantitative microbiology and analysis of clinical features. Rev Infect Dis 1984;6:S171. 25. Wheat LJ, Allen SD, Henry M, et al. Diabetic foot infections: Bacteriologic analysis. Arch Intern Med 1986;146:1935. 26. Hughes CE, Johnson CC, Bamberger DM, et al. Treatment and Long-term follow-up of foot infections in patients with diabetes or ischemia: A randomized, prospective, double blind comparison of cefoxitin and ceftizoxime. Clin Ther 1987;10(Suppl A):36. 27. Tsukayama DT, Guay DR, Gustilo RB, et al. The efffect of anaerobiosis on antistaphylococcal antibiotics. Orthopedics 1988;11:1285. 28. Fylling CP, Knighton DR. Amputation in the deabetic population: Incidence, causes, cost, treatment and prevention. J Enterostomal Ther 1989;16:247. 29. Frykberg RG. Podiatric problems in diabetes. In: Koza KGP, Campbell C, Hoar CS Jr, et al (eds.). Management of Diabetic Foot Problems. Philadephia: WB Saunders 1984;58-67. 30. Jacobs RI. Hoffman procedure in the ulcerated diabetic neuropathic foot. Foot Ankle 1982;3:142.

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∫∑∑’Ë 23. Surgical Treatment of Vericose Veins ∫∑∑’Ë 24. Venous Thrombosis ∫∑∑’Ë 25. ‚√§¢Õß√–∫∫πÈ”‡À≈◊Õß

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∫∑∑’Ë 23 SURGICAL TREATMENT OF VARICOSE VEINS ·π«∑“ß„π°“√ºà“µ—¥√—°…“ varicose veins (vv) ‰¡à ‰¥â ·µ°µà“ß‰ª®“°‡¡◊ÕË 20 ªï°Õà π¡“°π—°(1-4) „πÀπ—ß ◊Õ«“√ “√°≈à“« ∂÷ß«‘∏’°“√ºà“µ—¥√—°…“·π«„À¡à·≈–°“√‡°‘¥‡ªìπ´È”πâÕ¬¡“°‡¡◊Ë Õ ‡∑’¬∫°—∫‚√§Õ◊πË ∑“ßÀ≈Õ¥‡≈◊Õ¥(5) »—≈¬·æ∑¬å·µà≈– ∂“∫—π¡’«∏‘ °’ “√ ºà“µ—¥√—°…“·≈–¥Ÿ·≈ºŸªâ «É ¬µà“ß°—π Õ¬à“ß‰√°Áµ“¡‚Õ°“ °≈—∫‡ªìπ´È” (recurrent rate) ≈¥µË”≈ß ‡π◊ÕË ß®“°»—≈¬·æ∑¬å‡¢â“∂÷ß°“¬«‘¿“§ »“ µ√å, æ¬“∏‘ √’√«‘∑¬“¢Õß°“√‡°‘¥‚√§ “¡“√∂„Àâ°“√√—°…“‰¥â µ√ß®ÿ¥‡ªÑ“À¡“¬(6-10) °“√ºà“µ—¥√—°…“πÕ°®“°®–∑”„ÀâÕ“°“√Õ—π ‰¡àæ÷ßª√– ß§å·≈–‚√§·∑√°´âÕπ∑’Ë‡°‘¥¢÷Èπ‡™àπ ª«¥¢“, ¢“∫«¡ ·≈–·º≈‡√◊ÈÕ√—ßÀ“¬·≈â« ®–µâÕß§”π÷ß∂÷ß§«“¡ «¬ß“¡¢Õß·º≈ ºà“µ—¥·≈–ªÑÕß°—π‰¡à „Àâ‡°‘¥¿“«–·∑√°´âÕπ®“°°“√ºà“µ—¥¥â«¬

„π°“√ºà“µ—¥√—°…“ 1o vv ‘Ëß∑’Ë®–µâÕß§”π÷ß∂÷ß¡’ 1. superficial venous insufficiency ‡ªìπº≈¡“®“°§«“¡ º‘¥ª°µ‘¢Õß√–∫∫Àπ÷ßË √–∫∫„¥¢ÕßÀ≈Õ¥‡≈◊Õ¥¥”∑’¢Ë “ §◊Õ superficial veins (long saphenous ·≈– short saphenous) ·≈– perforating veins(11) 2. ≈—°…≥–§«“¡º‘¥ª°µ‘¢Õßº‘«Àπ—ß·≈– subcutaneous tissue ∫√‘‡«≥¢âÕ‡∑â“·≈–πàÕß∫àß∫Õ°∂÷ß§«“¡º‘¥ª°µ‘À√◊Õ æ¬“∏‘ ¿“æ∑’‡Ë °‘¥¢÷πÈ °—∫ perforating veins 3. ∂â“º‘«Àπ—ß∫√‘‡«≥¢âÕ‡∑â“·≈–πàÕß¡’≈°— …≥–¢Õß venous hypertension ‡™àπ edema, fibrosis, induration, ’

¥”§≈È”º‘¥ª°µ‘ °“√ºà“µ—¥ºà“πº‘«Àπ—ß∫√‘‡«≥π’È®–µâÕß √–«—ß°“√À“¬¢Õß∫“¥·º≈´÷Ëß®–À“¬™â“º‘¥ª°µ‘ §«√ À≈’°‡≈’¬Ë ß°“√≈ß¡’¥ºà“µ—¥∫√‘‡«≥π’È «‘∏°’ “√ºà“µ—¥√—°…“∑’Ë ¥’ ”À√—∫ incompetent perforators §◊Õ endoscopic subfascial ligation ‚¥¬≈ß¡’¥‡ªìπ·º≈¢π“¥‡≈Á°ºà“π º‘«Àπ—ßª°µ‘„µâÀ—«‡¢à“·≈â« àÕß°≈âÕßºà“π„µâ™—Èπ fascia ‡¢â“‰ª®π‡ÀÁπ perforating veins ·≈â«„™â clip Àπ’∫ 4. ·º≈‡√◊ÈÕ√—ß venous ulcers ∑’Ë‡°‘¥¢÷Èπ∫√‘‡«≥¢âÕ‡∑â“ ¥â“ππÕ° ‡°‘¥®“° incompetent lesser saphenous vein ·≈– perforating veins ∑“ß¥â“π¢â“ß °“√ºà“µ—¥√—°…“ºŸªâ «É ¬ vv ·µà≈–√“¬¡’«∏‘ °’ “√·µ°µà“ß°—π¢÷πÈ Õ¬Ÿ°à ∫— æ¬“∏‘ ¿“æ∑’‡Ë °‘¥¢÷πÈ °—∫ perforating veins ·≈– superficial vein µ”·Àπàß¢ÕßÀ≈Õ¥‡≈◊Õ¥¥” ·≈–≈—°…≥–∑“ß§≈‘π§‘ ¢Õß ºŸªâ «É ¬(1,2-15)

«‘∏’°“√ºà“µ—¥√—°…“¡’¥—ßµàÕ‰ªπ’È 1. high ligation and stripping of the long saphenous vein 2. stripping of the short saphenous vein 3. subcutaneous removal of varicosities 4. subfascial ligation of perforating veins

210

¢âÕ∫àß™’È„π°“√ºà“µ—¥ ¢âÕ∫àß™’È „π°“√ºà“µ—¥ vv ∑’ Ë ”§—≠¡’¥ß— µàÕ‰ªπ’È 1. ‡æ◊ÕË ≈¥Õ“°“√¢Õß varicosis ‡™àπ ª«¥∂à«ß∑’¢Ë “·≈–πàÕß , ¢“∫«¡, night cramps ·≈– restless leg 2. ‡ªìπ°“√√—°…“¿“«–·∑√°´âÕπ¢Õß varicosis ‡™àπ hemorrhage, thrombophlebitis dermatitis, pruritus ·≈– painful ulcers ´÷ßË ‡°‘¥®“° exposure µàÕ nerve endings 3. ‡æ◊ÕË §«“¡ «¬ß“¡ (cosmetic considerations) Õ¬à“ß‰√°Áµ“¡ „π°“√ºà“µ—¥√—°…“§«√®–ºà“µ—¥·°â ‰¢‡©æ“– ∫√‘‡«≥∑’¡Ë æ’ ¬“∏‘ ¿“æ¢ÕßÀ≈Õ¥‡≈◊Õ¥¥”¢Õ¥‡À≈◊ÕÀ≈Õ¥‡≈◊Õ¥¥”∑’Ë non-varicose ‡Õ“‰«â ·≈–®–µâÕß§”π÷ß∂÷ß§«“¡ «¬ß“¡¢Õß ·º≈ºà“µ—¥¥â«¬

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I. High ligation and stripping of the long saphenous vein À≈—ß¥¡¬“ ≈∫À√◊Õ„™â epidural anesthesia ®—¥∑”„ÀâºªŸâ «É ¬ πÕπÀß“¬ øÕ°∑”§«“¡ –Õ“¥º‘«Àπ—ß ¢“ ®“°ª≈“¬‡∑â“®π∂÷ß¢“ Àπ’∫ ªŸº“â ª√“»®“°‡™◊ÕÈ µ√ß genitalia §≈ÿ¡ª≈“¬‡∑â“·≈–π‘«È ‡∑â“ ¥â«¬∂ÿß¡◊Õª√“»®“°‡™◊ÈÕ °“ß¢“ºŸâªÉ«¬ÕÕ°·≈–„ÀâºŸâªÉ«¬Õ¬Ÿà „π∑à“ »’√…–µË” ‡∑â“ ŸßÀ√◊Õ Trendelenberg position ‡ªìπ°“√≈¥°“√ ‡ ’¬‡≈◊Õ¥®“°°“√ºà“µ—¥∑’¢Ë “ ≈ß¡’¥„µâµÕà inguinal ligament 2 ‡´Áπµ‘‡¡µ√¢π“π‡ªìπ·π«¬“« 10 ‡´Áπµ‘‡¡µ√‡æ◊ÕË ‡¢â“∂÷ß saphenofemoral junction ‡≈“–„Àâ‡ÀÁπ tributaries ∑—ßÈ 5 ·¢πß∑’·Ë ¬° ÕÕ°®“° long saphenous vein (√Ÿª∑’Ë 23.2,.3,.4) ºŸ°·≈–µ—¥ tributaries ∑—ßÈ 5 ·¢πß„ÀâÀ¡¥ ªÑÕß°—π°“√‡ªìπ´È” ·¢πß∑’ÀË “¬“°∑’ Ë ¥ÿ §◊Õ inferior epigastric vein §«√‡≈“– long saphenous vein ®π∂÷ß 5 ‡´Áπµ‘‡¡µ√ Àà“ß®“° saphenofemoral junction ∂â“‡®Õ·¢πß

1. ºŸªâ «É ¬‡ªìπ‚√§‡√◊ÕÈ √—ßÕ◊πË ∑’√Ë °— …“‰¡àÀ“¬ µâÕßπÕπÕ¬Ÿ°à ∫— ‡µ’¬ß À√◊Õ ¿“æ√à“ß°“¬∑—«Ë ‰ª ‰¡à “¡“√∂∑πµàÕ°“√ºà“µ—¥‰¥â 2. Õâ«π¡“° ‡§≈◊ÕË π‰À«≈”∫“° ‰¡à “¡“√∂ amublate ‰¥â ∑—π∑’À≈—ßºà“µ—¥ 3. ¡’ chronic arterial insufficiency ¢Õß¢“´÷ßË ®–∑”„Àâ ·º≈À“¬™â“·≈–‡ªìπ¢âÕÀâ“¡„π°“√æ—π elastic bandage 4. active postphlebitic conditions 5. active superficial thrombophlebitis 6. ºŸâªÉ«¬µ—Èß§√√¿å ‡æ√“–À≈—ß§≈Õ¥·≈â« vv ®–À“¬À√◊Õ Õ“°“√¥’¢π÷È ¡“° 7. ¡’·º≈µ‘¥‡™◊ÕÈ ∑’‡Ë ∑â“ 8. ¡’°Õâ π‡π◊ÕÈ ßÕ°¢π“¥„À≠à „π™àÕß∑âÕß∑’¬Ë ß— ‰¡à ‰¥â√°— …“

°“√‡µ√’¬¡ºŸâªÉ«¬°àÕπºà“µ—¥ À≈—ß®“°µ√«®√à“ß°“¬ºŸªâ «É ¬¥â«¬ Brodie-trendelenberg test ·≈– Perthes test ®π·πà „®«à“‰¡à¡§’ «“¡º‘¥ª°µ‘¢Õß deep veins ·≈â« „ÀâºªŸâ «É ¬Õ¬Ÿà „π∑à“¬◊π „™âª“°°“ ’‡¢’¬π∫πº‘«Àπ—ßµ”·Àπàß¢Õß À≈Õ¥‡≈◊Õ¥¢Õ¥∑’ËµâÕß°“√®–ºà“µ—¥(16) ‡¢’¬π·π«≈ß¡’¥∫√‘‡«≥ groin, popliteal fossa ·≈–¢âÕ‡∑â“ ∂â“µâÕß°“√ºà“µ—¥∑” local excision ∫√‘‡«≥∑’Ë®–µâÕß∑” subfascial ligation §«√∑” ‡§√◊ËÕßÀ¡“¬°“°–∫“¥À√◊Õ‡ªìπ√Ÿª¥“«‡Õ“‰«â ‡æ◊ËÕ∑’Ë®–≈ß¡’¥ ‡¢â“∂÷ß·≈–ºŸ°‰¥â∑π— ∑’ (√Ÿª∑’Ë 23.1)

√Ÿª∑’Ë 23.1 „™âª“°°“ ’«“¥·π«¢ÕßÀ≈Õ¥‡≈◊Õ¥¥”¢Õ¥∑’®Ë –ºŸ°µ—¥ °àÕπ ºà“µ—¥‚¥¬„ÀâºŸâªÉ«¬Õ¬Ÿà „π∑à“¬◊π

SURGICAL TREATMENT OF VARICOSE VEINS

211

√Ÿª∑’Ë 23.2 ·π«≈ß¡’¥„µâ·≈–¢π“πµàÕ inguinal ligament ‡æ◊ËÕ‡¢â“∂÷ß long saphenous vein

√Ÿª∑’Ë 23.3 ‡≈“– long saphenous vein „Àâ‡ÀÁπ tributaries ∑—Èß 5 ·¢πß§◊Õ inferior epigastric, superficial iliac circumflex, pudendal, medial ·≈– lateral femoral veins.

212

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√Ÿª∑’Ë 23.4 ºŸ°µ—¥·¢πß∑—Èß 5 ·≈–ºŸ°µ—¥ long saphenous vein ÕÕ°®“° femoral vein

√Ÿª∑’Ë 23.5 saphenous nerve «‘Ëß§Ÿà¢π“π¡“°—∫ long saphenous vein ∑’ËÀ—«‡¢à“·≈–¢“¥â“π„π ¡’ ‚Õ°“ ∂Ÿ°°√–∑∫°√–-‡∑◊Õπ¢≥–∑” venous stripping

SURGICAL TREATMENT OF VARICOSE VEINS

√Ÿª∑’Ë 23.6 ‡ âπª√– “∑ saphenous nerve ¢“¥À≈—ß°“√ºà“µ—¥®–∑”„Àâº‘«Àπ—ß∫√‘‡«≥„µâÀ—«‡¢à“¥â“π„π ·≈–¢âÕ‡∑â“™“ ‰√â§«“¡√Ÿâ ÷°

√Ÿª∑’Ë 23.7 A. «‘∏’°“√ Õ¥ “¬ stripper ºà“π long saphenous vein ºà“π¢âÕ‡∑â“¢÷Èπ‰ª®π∂÷ß∫√‘‡«≥ groin B. ºŸ°À—« stripper °—∫ª≈“¬À≈Õ¥‡≈◊Õ¥¥”∑’Ë¢“Àπ’∫ µàÕª≈“¬≈à“ß¢Õß stripper ‡¢â“°—∫ T-bar

213

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√Ÿª∑’Ë 23.8 ºŸâªÉ«¬®–ºà“µ—¥∑” short saphenous vein stripping §«√Õ¬Ÿà„π∑à“πÕπÀß“¬À√◊ÕπÕπµ–·§ß ≈ß¡’¥„π·π«¢π“π„µâµàÕ®ÿ¥°÷Ëß°≈“ß ¢Õß popliteal fossa

√Ÿª∑’Ë 23.9 sural nerve ®–«‘ßË §Ÿ¢à π“π¡“°—∫ short saphenous vein ∫√‘‡«≥πàÕß

SURGICAL TREATMENT OF VARICOSE VEINS

215

√Ÿª∑’Ë 23.10 ‡≈“–À“ short saphenous vein ´÷ËßÕ¬Ÿà „µâ™—Èπ fascia ºŸ°µ—¥ short saphenous vein „µâµàÕ Giacomini vein

√Ÿª∑’Ë 23.11 ≈ß¡’¥„π·π«¢π“πÀ≈—ßµàÕ lateral malleolus ‡¢â“∂÷ß à«πª≈“¬¢Õß short saphenous vein Õ¥ “¬ stripper ®“°∫π≈ß≈à“ß ≈“° ‡Õ“ short saphenous vein ®“°≈à“ß¢÷Èπ∫π °¥Àâ“¡‡≈◊Õ¥ ‡¬Á∫·º≈ªî¥ ·≈â«æ—π¥â«¬ elastic bandage ®“°ª≈“¬‡∑â“®π∂÷ßÀ—«‡¢à“

216 À≈Õ¥‡≈◊Õ¥¥”„Àâº°Ÿ µ—¥„ÀâÀ¡¥ ‡¬Á∫ºŸ°·≈–µ—¥·¬° long saphenous vein ÕÕ°®“° femoral vein ‚¥¬„ÀâÀ“à ß®“°®ÿ¥·¬° 0.51.0 ‡´Áπµ‘‡¡µ√ (flush ligation) ªÑÕß°—π‰¡à „ÀâÀ≈Õ¥‡≈◊Õ¥¥” µ’∫·§∫À√◊Õ‡°‘¥ venous injury clamp Àπ’∫À≈Õ¥‡≈◊Õ¥ long saphenous vein à«πª≈“¬®“°∫√‘‡«≥∑’ºË °Ÿ µ—¥‡Õ“‰«â ≈ß¡’¥„π·π«¢π“π°—π°—∫¢âÕ‡∑â“¥â“π„π¬“« 2-3 ‡´Áπµ‘‡¡µ√ ‡æ◊ËÕ‡¢â“∂÷ß long saphenous vein à«πª≈“¬∫√‘‡«≥¢âÕ‡∑â“ æ¬“¬“¡·¬° saphenous nerve ´÷ßË «‘ßË ¢π“π¡“°—∫ long saphenous vein(17) (√Ÿª∑’Ë 23.5) ‡æ√“–∂â“‡ âπª√– “∑¢“¥À√◊Õ‰¥â√∫— ∫“¥‡®Á∫¢≥–∑” stripping ®–‡°‘¥°“√™“¢Õßº‘«Àπ—ß™—Èπ∑’Ë ∫√‘‡«≥¢âÕ‡∑â“·≈–„µâµÕà À—«‡¢à“¥â“π„π(18) (√Ÿª∑’Ë 23.6) ‡¬Á∫ºŸ°À≈Õ¥ ‡≈◊Õ¥¥” long saphenous ∑“ß¥â“π≈à“ß Õ¥ “¬ stripper ºà“πÀ≈Õ¥‡≈◊Õ¥¥”®“°∑“ß¥â“π≈à“ßµ“¡·π«¢ÕßÀ≈Õ¥‡≈◊Õ¥¥” ¢÷πÈ ‰ª®π∂÷ß groin (√Ÿª∑’Ë 23.7A) ‡Àµÿº≈∑’ Ë Õ¥ “¬ stripper ®“°≈à“ß¢÷πÈ ∫π§◊Õ(18,19) 1. ‚Õ°“ ∑’®Ë – Õ¥ “¬æ≈“¥‡¢â“·¢πßÀ≈Õ¥‡≈◊Õ¥¥”∑’·Ë ¬° ®“° long saphenous vein ¡’πÕâ ¬ °“√ Õ¥ “¬®“° ∫π≈ß≈à“ß ¡ÿ¡√–À«à“ßÀ≈Õ¥‡≈◊Õ¥¥” main trunk °—∫ ·¢πß∑’Ë·¬°ÕÕ°‰ª·§∫¡—°®– Õ¥æ≈“¥‡¢â“·¢πßÀ≈Õ¥ ‡≈◊Õ¥‰¥âß“à ¬‚¥¬‰¡àº“à π≈ß main trunk ‰ª∂÷ß¢âÕ‡∑â“ 2. °“√ Õ¥ “¬®“°≈à“ß¢÷πÈ ∫π ∂â“ºà“π perforators „Àâ≈ß¡’¥ ºà“πº‘«Àπ—ß∫√‘‡«≥π—Èπ‡¢â“∂÷ß perforators ·≈–ºŸ°µ—¥ ‡ ’¬°àÕπ ®÷ß§àÕ¬ Ê Õ¥ “¬ tripper ºà“π¢÷πÈ ‰ª‡√◊ÕË ¬ Ê 3. ∂â“„™âÀ—« stripper ‰¡à ‚µ¡“° ·≈– Õ¥®“°≈à“ß¢÷Èπ∫π ‚Õ°“ ∑’®Ë –°√–∑∫°√–‡∑◊Õπ·≈–∑”„Àâ saphenous nerve ·≈– lymphatic ©’°¢“¥ ¡’πÕâ ¬°«à“‡«≈“∑” stripping „™â¥“â ¬‡∫Õ√å 2-0 ºŸ°À—« stripper °—∫ª≈“¬À≈Õ¥‡≈◊Õ¥¥”∑“ß ¢“Àπ’∫ (√Ÿª∑’Ë 23.7B) µàÕª≈“¬≈à“ß¢Õß stripper °—∫ T-bar ·≈â«§àÕ¬ Ê ¥÷ß stripper ≈“°‡Õ“ long saphenous vein ºà“π „µâº‘«Àπ—ß≈ß¡“®π∂÷ß¢âÕ‡∑â“ „™âºâ“°äÕ´°¥Àâ“¡‡≈◊Õ¥µ“¡·π« ¢ÕßÀ≈Õ¥‡≈◊Õ¥ long saphenous vein ‡ªìπ°“√Àâ“¡‡≈◊Õ¥ ‡¬Á∫ªî¥ fascia ¢Õß·º≈ºà“µ—¥∑’Ë¢“Àπ’∫¥â«¬‰À¡≈–≈“¬ ·≈–‡¬Á∫ªî¥ º‘«Àπ—ß¥â«π‰π≈àÕπÀ√◊Õ staple suture ·º≈∫√‘‡«≥¢âÕ‡∑â“‡¬Á∫ ªî¥º‘«Àπ—ß¥â«¬‰π≈àÕπ À≈—ß®“°π—Èπæ—π¢“ºŸâªÉ«¬¥â«¬ elastic bandage µ—Èß·µà ª≈“¬‡∑â“®π∂÷ß¢“Àπ’∫ ·≈– «¡∂ÿß‡∑â“¬“«∑—∫Õ’°™—πÈ Àπ÷ßË

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥ µàÕ®ÿ¥°÷Ëß°≈“ß¢Õß popliteal fossa short saphenous vein ®–Õ¬Ÿà „µâµÕà fascia ‰¡à ‰¥âÕ¬Ÿà „π™—πÈ subcutaneous ®–µâÕßµ—¥ºà“π fascia ‡¢â“‰ª∂÷ß Õ¬à“‰ª‡ ’¬‡«≈“‡≈“–À“ short saphenous vein „π™—Èπ subcutanous §«√æ¬“¬“¡·¬° sural nerve ∑’Ë«‘Ëß ¢π“π¡“¥â«¬°—π (√Ÿª∑’Ë 23.9) ‰¡à®”‡ªìπµâÕß‡≈“– short saphenous vein ≈ß‰ª®π∂÷ß sapheno popliteal junction µ”·Àπàß∑’Ë ºŸ°µ—¥À≈Õ¥‡≈◊Õ¥§«√Õ¬Ÿµà Ë”°«à“ Giacomini vein (√Ÿª∑’Ë 23.10) ∑“ß à«πª≈“¬¢Õß short saphenous vein ‡¢â“∂÷ß‚¥¬≈ß¡’¥„π ·π«¢π“πÀ≈—ßµàÕ lateral malleoulus Õ¥ “¬ stripper ®“°∫π≈ß≈à“ß‰¥â‡æ√“– short saphenous vein ¡’ tributaries ‰¡à°·’Ë ¢πß ‚Õ°“ Õ¥ “¬æ≈“¥‰ª‡¢â“·¢πßÕ◊πË ¡’πÕâ ¬ ∑” stripping ≈“° vein ®“°≈à“ß¢÷πÈ ∫π °¥Àâ“¡‡≈◊Õ¥ ‡¬Á∫·º≈ªî¥·≈â« æ—π¥â«¬ elastic bandage µ—ßÈ ·µàª≈“¬‡∑â“®π∂÷ßπàÕß (√Ÿª∑’Ë 23.11)

III. Subcutaneous removal of varicostics (stab avulsions) ≈ß·º≈ºà“µ—¥¢π“¥‡≈Á° Ê µ“¡·π« skin crease À√◊Õ·π« ¢π“π‡¢â“∂÷ßÀ≈Õ¥‡≈◊Õ¥∑’ËµâÕß°“√ºà“µ—¥‡Õ“ÕÕ° ·µà≈–·º≈‰¡à §«√¡’§«“¡¬“«‡°‘π 1 ‡´Áπµ‘‡¡µ√ „™â arterial forcep ‡≈“–¥÷ß ‡Õ“À≈Õ¥‡≈◊Õ¥¥”¢÷πÈ ¡“®“°º‘«Àπ—ß·≈â«ºŸ°µ—¥(20) (√Ÿª∑’Ë 23.12) «‘∏’

II. Stripping of the short saphenous vein ¥¡¬“ ≈∫ºŸªâ «É ¬ À√◊Õ„™â epidural anesthesia ®—¥∑à“„ÀâºŸâ ªÉ«¬πÕπ§«Ë”À√◊ÕπÕπµ–·§ß (√Ÿª∑’Ë 23.8) ≈ß¡’¥„π·π«¢π“π„µâ

√Ÿª∑’Ë 23.12 stab avulsions of varices

217

SURGICAL TREATMENT OF VARICOSE VEINS

°“√π’‡È À¡“– ”À√—∫À≈Õ¥‡≈◊Õ¥ tributaries ¢Õß saphenous veins ∑’Ë ‰¡à “¡“√∂„™â stripper ¥÷ßÕÕ°‰¥âÀ√◊Õ perforators ∫√‘‡«≥¢“ ∂â“¡’‡≈◊Õ¥ÕÕ°¡“„Àâ°¥‡Õ“‰«â ‡≈◊Õ¥®–À¬ÿ¥‡Õß ¢≥–ºà“µ—¥§«√„Àâ ºŸâªÉ«¬Õ¬Ÿà „π∑à“ Trendelenberg ‡≈◊Õ¥®–ÕÕ°πâÕ¬ à«π„À≠à®– À¬ÿ¥‡ÕßÀ≈—ßºà“µ—¥‡ √Á®·≈–æ—π¥â«¬ bandage ·≈â«ªî¥·º≈‚¥¬ °“√‡¬Á∫·º≈¥â«¬‰π≈àÕπ·∫∫ mattress suture ·≈–æ—π¢“¥â«¬ elastic bandage

IV. Subfascial ligation of perforating veins ≈ß¡’¥∑“ß medial side ¢Õß¢“ 1 ‡´Áπµ‘‡¡µ√ À≈—ßµàÕ¢Õ∫ ¢Õß tibia ¡“‡ªìπ·π«¬“« 15 ‡´Áπµ‘‡¡µ√ ®π∂÷ß medial malleoulus °√’¥ºà“π™—πÈ subcutaneous ≈ß®π∂÷ß fascia ‰¡à µâÕß‡≈“–µ—¥‡Õ“ superficial varicosities ∫√‘‡«≥π’ÕÈ Õ° ∂â“‡≈◊Õ¥ ÕÕ°¡“°„Àâ°¥‡Õ“‰«â‡≈◊Õ¥®–À¬ÿ¥¿“¬À≈—ß‰¥â „µâ fascia ®–æ∫ dilated perforating veins „Àâº°Ÿ ·≈–µ—¥ À≈—ßºà“µ—¥‰¡à§«√‡¬Á∫ ªî¥º‘«Àπ—ß ∂â“∫√‘‡«≥¢âÕ‡∑â“®π∂÷ßπàÕß∫«¡µ÷ß ¡—π ¡’ §’ ≈È” ≈—°…≥– ·∫∫ browny induration §«√‡≈’Ë¬ß°“√≈ß¡’¥ºà“µ—¥∫√‘‡«≥π’È ‡æ√“–·º≈®–À“¬™â“ §«√≈ß¡’¥„µâµÕà À—«‡¢à“¥â“π„π ·≈–∑” endoscopic subfascial ligation ®–¥’°«à“(23)

°“√¥Ÿ·≈ºŸâªÉ«¬À≈—ßºà“µ—¥ °“√æ—π elastic bandage ‡ªìπ ‘ßË ®”‡ªìπÀ≈—ß°“√ºà“µ—¥ varicose veins ∑ÿ°«‘∏’ ‡æ√“–‡ªìπ°“√Àâ“¡‡≈◊Õ¥®“°·º≈·≈–°“√≈¥ ∫«¡(24) §«√æ—π·º≈®“°ª≈“¬‡∑â“∂÷ßÀ—«‡¢à“ ∂â“‡ªìπ°“√ºà“µ—¥ ∫√‘‡«≥¢“ ·≈–æ—π∂÷ß¢“Àπ’∫À≈—ßºà“µ—¥∂÷ßµâπ¢“·≈–¢“Àπ’∫∑‘Èß ‰«â®π°√–∑—ßË µ—¥‰À¡À√◊Õ‡Õ“ metallic clip ÕÕ° ·π–π”„ÀâºªŸâ «É ¬ „™â compressive stocking µÕπ°≈“ß«—π·≈–‡Õ“ÕÕ°µÕπ °≈“ß§◊πÕ’° 6-8 —ª¥“Àå ∂â“¬◊πÀ√◊Õ‡¥‘π¡“° „Àâπß—Ë æ—°·≈–¬°‡∑â“ Ÿß

¿“«–·∑√°´âÕπÀ≈—ß°“√ºà“µ—¥ ¿“«–·∑√°´âÕπ®“°°“√ºà“µ—¥À≈Õ¥‡≈◊Õ¥¥”∑’¢Ë “æ∫‰¥â ‰¡à∫Õà ¬ ·≈–Õ“°“√‰¡à§Õà ¬√ÿπ·√ß ¿“«–·∑√°´âÕπ∑’ÕË “®®–æ∫‰¥â¡’ 1. Bleeding ¡—°®–æ∫‡ªìπ ecchymosis ‡ªìπªóπô µ“¡º‘«Àπ—ß À≈—ßºà“µ—¥ 3-5 «—π ‡≈◊Õ¥∑’§Ë ß—Ë ®–∂Ÿ°¥Ÿ¥´÷¡·≈–√Õ¬™È”®– À“¬‰ª¿“¬„π 3-4 —ª¥“Àå À≈—ßºà“µ—¥∑—π∑’∂â“¬—ß¡’°“√ µ°‡≈◊Õ¥®“°·º≈∑’‡Ë ¬Á∫ªî¥·≈â« §«√æ—π elastic bandage

5. 6. 7.

·πàπ·≈–πÕπ¬°¢“ Ÿß 3-4 ™—«Ë ‚¡ß À≈—ß®“°π—πÈ §≈“¬ elastic bandage „ÀâÀ≈«¡ ∂â“ ecchymosis ‚µ¢÷πÈ ·≈–¡’ °“√Õ—°‡ ∫µ‘¥‡™◊È §«√ºà“µ—¥√–∫“¬‡Õ“ÀπÕßÕÕ° ‡∑§π‘§ °“√ºà“µ—¥Àâ“¡‡≈◊Õ¥∑’¥Ë ’ ¬°¢“ºŸªâ «É ¬ Ÿß‡Àπ◊Õ√–¥—∫»’√…– ¢≥–ºà“µ—¥ ·≈–æ—π elastic bandage À≈—ßºà“µ—¥®– ∑”„Àâ‡°‘¥ ecchymosis ·≈– hematoma πâÕ¬ Edema ¢“∫«¡À≈—ßºà“µ—¥æ∫‰¥â∫Õà ¬ ¡—°®–¬ÿ∫∫«¡‡Õß À√◊ÕÀ≈—ß®“°æ—π elastic bandage ‰ª‰¥â 3-4 —ª¥“Àå ∂â“¬—ß∫«¡Õ¬ŸÕà “®¡’ “‡Àµÿ®“°°“√‰ªµ—¥‡Õ“ lymphatic drainage Nerve Damage æ∫‰¥âÀ≈—ß°“√∑” venous stripping ‡°‘¥®“°°“√∫“¥‡®Á∫À√◊Õ©’°¢“¥¢Õß saphenous nerve ®–∑”„Àâ¡°’ “√™“∫√‘‡«≥¢âÕ‡∑â“¥â“π„π·≈–„µâÀ«— ‡¢à“¥â“π„π ∂â“‡ªìπ sural nerve ®–¡’°“√™“∫√‘‡«≥πàÕß ªÑÕß°—π ‚¥¬°“√ dissect vein „Àâ‡ÀÁπ™—¥®“° nerve ∑” stripping ‚¥¬°“√¥÷ß®“°∫√‘‡«≥ groin ≈ß¡“∑’¢Ë Õâ ‡∑â“ „™âÀ«— stripper ¢π“¥‡≈Á°‡ ¡Õ ∂â“‡ªìπ neurapraxia Õ“°“√ ™“∑’Ëº‘«Àπ—ß®–À“¬‡Õß¿“¬„π 3-4 ‡¥◊Õπ ·µà∂â“‡ âπ ª√– “∑∂Ÿ°µ—¥¢“¥®–¡’°“√™“Õ¬à“ß∂“«√ Wound Infection æ∫πâÕ¬°«à“ 1.1% ·µà∂“â ‡ªìπ°“√ ∑” stripping À√◊Õºà“µ—¥„πºŸªâ «É ¬∑’¡Ë ·’ º≈‡√◊ÕÈ √—ß∑’‡Ë ∑â“·≈– ¡’°“√µ‘¥‡™◊ÈÕ Õ“®®–¡’°“√µ‘¥‡™◊ÈÕ≈“¡∂÷ß·º≈ºà“µ—¥ ·º≈®–À“¬™â“ §«√∑”°“√ºà“µ—¥À≈—ß®“°√—°…“°“√µ‘¥ ‡™◊ÕÈ ¢Õß·º≈À“¬¥’·≈â« Thromboembolic Disease ‡™àπ DVT æ∫‰¥â ‰¡à∫Õà ¬ ‡À¡◊Õπ°“√ºà“µ—¥À≈Õ¥‡≈◊Õ¥¥”Õ◊Ëπ Ê ªÑÕß°—π‰¥â ‚¥¬ °“√„ÀâºªŸâ «É ¬¡’ early ambulation À≈—ß°“√ºà“µ—¥ Induration of the stripper tract ¡’√Õ¬‡ªìπ·π« µ“¡√Õ¬¥÷ß´÷Ëß‡°‘¥®“° fibrous formation ®–§≈”‰¥â ‡ªìπ‡ âπ·¢Áß ·≈–À“¬‡Õß¿“¬„π 1-2 ‡¥◊Õπ Deep vein or arterial stripping ‡°‘¥®“°°“√ Õ¥ “¬≈÷°‡°‘π‰ª ºà“π perforator ‡¢â“ deep vein À√◊Õ ∑–≈ÿ‡¢â“À≈Õ¥‡≈◊Õ¥·¥ß ®–¡’¿“«–·∑√°´âÕπ∑’Ë√ÿπ·√ß ‡°‘¥¢÷πÈ ¡“°¡“¬µ“¡¡“

218

√ÿª·≈–«‘®“√≥å °“√ª√–‡¡‘πºŸªâ «É ¬·≈–°“√µ√«®√à“ß°“¬Õ¬à“ß≈–‡Õ’¬¥∂’∂Ë «â π ‡ªìπ ‘ßË ”§—≠°àÕπ∑’®Ë –«“ß·ºπ„π°“√√—°…“ varicose veins µàÕ‰ª §«√‡≈◊Õ°«‘∏’°“√ºà“µ—¥„Àâµ√ß°—∫æ¬“∏‘ ¿“æ¢ÕßºŸâªÉ«¬ »—≈¬·æ∑¬å „πªí®®ÿ∫π— ≈—ß‡≈∑’®Ë –ºà“µ—¥‡Õ“ varicose veins ÕÕ° À√◊Õ ∑” venous stripping ‚¥¬æ¬“¬“¡‡°Á∫ saphenous vein ‡Õ“‰«â ”À√—∫ bypass „π vascular disease ·≈– coronary heart disease Õ¬à“ß‰√°Áµ“¡ varicose veins ∑’¡Ë Õ’ ¬Ÿ‡à ªìπÀ≈Õ¥‡≈◊Õ¥∑’¡Ë ’ §«“¡º‘¥ª°µ‘∑ß—È valves ·≈–ºπ—ßÀ≈Õ¥‡≈◊Õ¥‰¡à§«√π”¡“„™â bypass §«√„™âÀ≈Õ¥‡≈◊Õ¥¥”∑’Ëª°µ‘∫√‘‡«≥·¢π®–¥’°«à“ ‰¥â¡’°“√ æ¬“¬“¡∑”·§à high ligation ¢Õß long saphenous vein

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥

·≈â«‡°Á∫À≈Õ¥‡≈◊Õ¥¥”‰«â ª√“°Ø«à“À≈Õ¥‡≈◊Õ¥¥”¢Õ¥‰¡àÀ“¬ ¢“¥ ·≈–Õ—µ√“°≈—∫‡ªìπ´È” Ÿß(25) °“√ºà“µ—¥‡Õ“À≈Õ¥‡≈◊Õ¥¥”¢Õ¥ ÕÕ°‡ªìπ«‘∏°’ “√√—°…“∑’¥Ë ∑’ ’Ë ¥ÿ ”À√—∫ºŸªâ «É ¬∑’¡Ë Õ’ “°“√‚√§·∑√°´âÕπ ¢ÕßÀ≈Õ¥‡≈◊Õ¥¥”¢Õ¥∑’¢Ë “ ºŸªâ «É ¬∑’‡Ë À¡“– ¡„π°“√ºà“µ—¥§◊Õ primary varicose vein (primary incompetent symptomatic veins without skin complications) ‡∑§π‘§°“√ºà“µ—¥∑’Ë¥’ ®–∑”„Àâº≈°“√√—°…“¥’‡ ¡Õ·≈–‚Õ°“ °≈—∫‡ªìπ´È”¡’‰¥âπÕâ ¬ °“√ µ‘¥µ“¡¥Ÿ·≈ºŸâªÉ«¬À≈—ßºà“µ—¥§«√µ‘¥µ“¡¥Ÿ·≈√–¬–¬“«‰¡à „™à√–¬– —πÈ ‡æ’¬ß 3 ‡¥◊Õπ 6 ‡¥◊Õπ §«√Õ∏‘∫“¬„ÀâºªŸâ «É ¬‡¢â“„®«à“¡’‚Õ°“ ∑’Ë®–‡°‘¥‡ªìπÀ≈Õ¥‡≈◊Õ¥¢Õ¥‰¥âÕ’°„π∫√‘‡«≥Õ◊Ëπ πÕ°‡Àπ◊Õ®“° ∫√‘‡«≥∑’ºË “à µ—¥‰ª·≈â« ´÷ßË “¡“√∂√—°…“‰¥âß“à ¬‚¥¬°“√©’¥ sclerosing agent À√◊Õºà“µ—¥ local stab avulsions ‰¥â¿“¬À≈—ß

SURGICAL TREATMENT OF VARICOSE VEINS

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‡Õ° “√Õâ“ßÕ‘ß 1. Rivlin S. The surgical cure of primary varicose veins. Br J Surg 1975;62:913-917. 2. Samuels PB. Technique of varicose vein surgery. Am J Surg 1981;142:239-244. 3. Bergan JJ. Surgical procedures for varicose veins: Axial stripping and stab avulsion. In: Bergan JJ, Kistner RL (eds). Atlas of Venous Surgery. Philadelphia: WB Saunders, 1992. 4. Bergan JJ. New developments in surgical treatment of venous disease. Cardiovasc Surg 1993;25:141. 5. Bergan JJ, New developments in surgical treatment of venous disease. Cardiovasc Surg 1993;1:624. 6. Rose SS, Ahmed A. Some thoughts on the aetiology of varicose veins. J Cardiovasc Surg 1986;27:534-543. 7. Beadlehole R. Incidence and risk factors: Epidemiology of varicose veins. World J Surg 1986;10:898. 8. Clarke GH. Venous wall function in the pathogenesis of varicose veins. Surgery 1992;111:402. 9. Sadick NS. Predisposing factors of varicose and telangiectatic leg veins. Phlebology 1992;18:883. 10. Goren G, Yellin AE. Primary varicose veins:Topographic and hemodynamic correlation. J Cardiovasc Surg 1990;31:672. 11. Thompson H. The surgical anatomy of superficial and perforating veins of the lower limb. Ann R Coll Surg Engl 1979;61:118. 12. Rose SS. Surgical techniques in the treatment of varicose veins. In: Greenhalgh RM (ed). Vascular Surgical Techniques, An Atlas. Philadelphia: WB Saunders, 1989:374-382. 13. Bergan JJ, Goldman MP (eds). Varicose Veins and Telangiectasias: Diagnosis and Treatment. Quality Med Publishing, 1993.

14. Hobbs JT. The management of varicose veins. Surg Ann 1980;12:169. 15. Bergan JJ, Yao JST (eds). Venous Disorders Philadelphia: WB Saunders, 1991. 16. Semrow CM, Laborde A, Buchbinder D, et al. Preoperative mapping of varicositics and perforating veins. J Vasc Tech 1990;14:7274. 17. Ramasastry SS. Anatomy of the saphenous nerve:Relevance to saphenous vein stripping. Am Surg 1987;53:277. 18. Cox SJ, Wellwood JM, Martin A. Saphenous nerve injury caused by stripping of the long saphenous vein. Br Med J 1974;1:415. 19. Keith LM Jr, Smead WL. Saphenous vein stripping and its complications. Surg Clin North Am 1983;63:1303. 20. Goren G, Yellin AE. Ambulatory stab avulsion phlebectomy for truncal varicose veins. Am J Surg 1991;162:166. 21. Dodd H. The diagnosis and ligation of incompetent perforating veins. Ann R Coll Surg Engl 1964;34:186-196. 22. Field P, van Boxel P. The role of Linton flap procedure in the management of stasis, dermatitis and ulceration in the lower limb. Surgery 1971;70:920-926. 23. Pierik EGJM, Wittens CHA, van Urk H. Subfascial Endoscopic Ligation in the treatment of Incompetent Perforating Veins. Eur J Vasc Endovasc Surg 1995;9:39-41. 24. Shouler PJ, Runchman PC. Varicose veins: Optimum compression after surgery and sclerotherapy. Am R Coll Surg Engl 1989;71:402. 25. Hammarsten J, Pedersen P, Cederlund CG, et al. Long saphenous vein saving for varicose veins: A long-term follow up. Eur J Vasc Surg 1990;4:361-364

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»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥

∫∑∑’Ë 24 VENOUS THROMBOSIS

‚√§¢ÕßÀ≈Õ¥‡≈◊Õ¥¥”∫√‘‡«≥¢“∑’Ëæ∫‰¥â∫àÕ¬ ¡’ venous thrombosis, valvular incompetence ·≈– pulmonary embolism ®–µâÕß‡¢â“„®∂÷ß°“¬«‘¿“§¢ÕßÀ≈Õ¥‡≈◊Õ¥¥”∑’¢Ë “ µ≈Õ¥ ®πæ¬“∏‘ √’√«‘∑¬“„π°“√‡°‘¥‚√§ ®÷ß®– “¡“√∂«“ß·π«∑“ß„π °“√√—°…“‚√§‰¥âÕ¬à“ß∂Ÿ°µâÕß

°“¬«‘¿“§¢ÕßÀ≈Õ¥‡≈◊Õ¥¥”∑’Ë¢“ ºπ—ßÀ≈Õ¥‡≈◊Õ¥¥”·∫àßÕÕ°‡ªìπ 3 ™—πÈ ‡™àπ‡¥’¬«°—π°—∫À≈Õ¥ ‡≈◊Õ¥·¥ß ·µà¡¢’ Õâ ·µ°µà“ß§◊Õ ‡ÕÁπ‚¥∏’‡≈’¬Ë ¡ „π™—πÈ Õ‘π∑‘¡“¢ÕßÀ≈Õ¥ ‡≈◊Õ¥¥”®–À≈—ßË “√ factor XIII, prostacycline ·≈– fibrinolytic activates ∑”„Àâ ‰¡à¡’≈‘Ë¡‡≈◊Õ¥‡°‘¥¢÷Èπ„πºπ—ßÀ≈Õ¥‡≈◊Õ¥¥” ºπ—ß À≈Õ¥‡≈◊Õ¥¥”∫“ß°«à“ºπ—ßÀ≈Õ¥‡≈◊Õ¥·¥ß 10 ‡∑à“ ¡’ elastic tissue πâÕ¬°«à“ „π™—πÈ media ¢ÕßÀ≈Õ¥‡≈◊Õ¥¥” à«π superficial ®–¡’°≈â“¡‡π◊ÈÕ¡“° ¢≥–∑’Ë venules ¡’°≈â“¡‡π◊ÈÕ·∑√°Õ¬Ÿà „π™—Èπ ¡’‡¥’¬πâÕ¬¡“° ·≈–„πÀ≈Õ¥‡≈◊Õ¥¥”¢π“¥„À≠à∑’ËÕ¬Ÿà≈÷° ™—Èπ adventia ®–¡’ collagen ·≈– elastin ‡ªìπ à«π„À≠à ∂÷ß·¡â«“à À≈Õ¥‡≈◊Õ¥¥”®–¡’ vasa vasorum ‡™àπ°—π ·µà®–‰¡à‡¢â“∂÷ß∑ÿ° ™—Èπ¢Õßºπ—ßÀ≈Õ¥‡≈◊Õ¥¥” Õ“À“√∑’Ë¡“‡≈’È¬ßÀ≈Õ¥‡≈◊Õ¥¥”®–‰¥â ®“°°“√¥Ÿ¥´÷¡®“°°√–· ‡≈◊Õ¥ºà“π‡¢â“™—Èπµà“ß Ê ¢Õßºπ—ß À≈Õ¥‡≈◊Õ¥¥” µ“¡¿“¬«‘¿“§»“ µ√å¢ÕßÀ≈Õ¥‡≈◊Õ¥¥” §«“¡º‘¥ª°µ‘∑‡’Ë °‘¥ ¢÷Èπ°—∫ valves ¢ÕßÀ≈Õ¥‡≈◊Õ¥¥”®–∑”„Àâ‡°‘¥æ¬“∏‘ ¿“æ·≈– ‚√§µà“ß Ê valves ∑—Ë«‰ªµ“¡ª°µ‘¡’≈—°…≥–‡ªìπ biuspid ®–

‡ªî¥„Àâ‡≈◊Õ¥‰À≈ºà“π¬âÕπ°≈—∫‡¢â“ ŸàÀ—«„® ·≈–®–ªî¥‡æ◊ËÕªÑÕß°—π °“√¬âÕπ°≈—∫¢Õß‡≈◊Õ¥ valves ∫√‘‡«≥¢“®–¡’À≈“¬Õ—π ·µàæÕºà“π inguinal ligament ·≈â«®–¡’®”π«π≈¥≈ß „π external iliac vein ®–¡’ valve Õ—π‡¥’¬« ·≈–„π IVC ‰¡àæ∫‡≈¬ À≈Õ¥‡≈◊Õ¥¥”∑’¢Ë “·∫àßÕÕ°‡ªìπ 2 √–∫∫§◊Õ superficial °—∫ deep system ´÷ßË ®–µàÕ‡™◊ÕË ¡°—π¥â«¬ perforators superficial veins ¡’ºπ—ß§àÕπ¢â“ßÀπ“ ·≈–¡’°≈â“¡‡π◊ÕÈ ·∑√°Õ¬Ÿ¡à “° ¡’Àπâ“∑’Ë thermoregulation ª√–°Õ∫¥â«¬ greater ·≈– lesser saphenous veins ´÷ßË Õ¬Ÿµà √ß anteromedial ·≈– posterior ¢Õß¢“ À≈Õ¥‡≈◊Õ¥¥”‡À≈à“π’È®–«“ßÕ¬Ÿà∫π™—Èπ fascia ·≈–¡’ valves À≈“¬Õ—π ·∑ß∑–≈ÿ™π—È fascia ·≈–‡™◊ÕË ¡µàÕ°—∫ deep venous system ¥â«¬ perforators (√Ÿª∑’Ë 24.1) ‡≈◊Õ¥¥”∑’Ë ‰À≈‡«’¬π∑’¢Ë “®–¡’ ª√‘¡“≥√âÕ¬≈– 10 ¢Õß‡≈◊Õ¥∑’Ë ‰À≈‡«’¬π∑—«Ë √à“ß°“¬ deep venous system ºπ—ß∫“ß ª√–°Õ∫¥â«¬ superficial ·≈– deep femoral, popliteal, anterior ·≈– posterior tibial √«¡∑—ßÈ peroneal veins ‚¥¬®–«‘ßË §Ÿ¢à π“π°—∫À≈Õ¥‡≈◊Õ¥·¥ß À≈Õ¥‡≈◊Õ¥¥”„µâÀ«— ‡¢à“®–¡’ 2 À≈Õ¥«‘ßË ¢π“π§Ÿà ‰ª°—∫À≈Õ¥‡≈◊Õ¥·¥ßÀ≈Õ¥‡¥’¬« (venous concomitants) (√Ÿª∑’Ë 24.2) ‡≈◊Õ¥¥”∑’Ë ‰À≈‡«’¬π„µâÀ«— ‡¢à“®–¡’ª√‘¡“≥ √âÕ¬≈– 90 ¢Õßª√‘¡“≥‡≈◊Õ¥‰À≈‡«’¬π∑’¢Ë “ deep veins ®– form ‡ªìπ sinusoids Õ¬Ÿà „π°≈â“¡‡π◊ÕÈ ∑’ Ë ”§—≠§◊Õ soleus sinusoids ∑’πË Õà ß ´÷ßË ®–√–∫“¬‡≈◊Õ¥‡¢â“ Ÿà posterior tibial vein (√Ÿª∑’Ë 24.3) ‡ªìπµ”·Àπàß∑’‡Ë °‘¥≈‘¡Ë ‡≈◊Õ¥‰¥âß“à ¬·≈–‡ªìπ®ÿ¥‡√‘¡Ë µâπ¢Õß deep vein thrombosis ‰¥â∫Õà ¬∑’ Ë ¥ÿ perforators ®–∑–≈ÿ™π—È fascia ‡™◊ÕË ¡

222

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥ Femoral

Superficial epigastric

Superficial circumflex iliac

Femoral External pudendal

Saphenofemoral junction

Great saphenous

Lateral femoral

Medial femoral

Great saphenous

Popliteal Small saphenous

Perforators

√Ÿª∑’Ë 24.1 °“¬«‘¿“§¢Õß greater ·≈– lesser saphenous veins ·≈–·¢πßÀ≈Õ¥‡≈◊Õ¥¥”¢Õß greater saphenous vein ∫√‘‡«≥ saphenofemoral junction

Saphenofemoral junction Thigh perforators Lateral thigh perforator Long saphenous vein

Saphenopopliteal junction

Boydûs perforator

Short saphenous vein Mid calf perforator

Ankle perforators

√Ÿª∑’Ë 24.2 °“¬«‘¿“§¢Õß perforating veins ∑“ß¥â“π medial ·≈– posterolateral

Soleal perforator

223

VENOUS THROMBOSIS

µ“√“ß∑’Ë 24.1 ªí®®—¬‡ ’¬Ë ßµàÕ°“√‡°‘¥ venous thrombosis

Giacomini vein Popliteal vein Short saphenous vein Gastrocnemius vein Mid-calf perforator

√Ÿª∑’Ë 24.3 °“¬«‘¿“§¢Õß lesser saphenous vein ·≈– perforator ∑’ËµàÕ‡¢â“°—∫ gastrocnemius vein

√–À«à“ß superficial π”‡≈◊Õ¥‡¢â“ Ÿà deep system ºà“π one-way valves ´÷ßË ªÑÕß°—π‡≈◊Õ¥‰À≈¬âÕπ°≈—∫ ‡¡◊ËÕ°≈â“¡‡π◊ÈÕ∑’Ë¢“À¥µ—« ®–¥—π‡≈◊Õ¥¥”°≈—∫‡¢â“ ŸàÀ—«„® °≈â“¡‡π◊ÕÈ À¥µ—«·µà≈–§√—ßÈ ®–¡’§«“¡¥—π Ÿß∂÷ß 200 ¡‘≈≈‘‡¡µ√ª√Õ∑ ·À≈àß∑’¡Ë ‡’ ≈◊Õ¥¥”§—ßË Õ¬Ÿ¡à “°§◊Õ soleus ·≈– gastrocnemius sinusoids ¢Õß°≈â“¡‡π◊ÕÈ ∑’πË Õà ß §«“¡º‘¥ª°µ‘¢Õß muscle pump function ∫√‘‡«≥πàÕß‡°‘¥®“°°≈â“¡‡π◊ÕÈ ÕàÕπ·√ß ¡’°“√Õÿ¥µ—π¢Õß deep veins ·≈– incompetent ¢Õß valves ∑’ÀË ≈Õ¥‡≈◊Õ¥∑ÿ° √–∫∫À√◊Õ√–∫∫„¥√–∫∫Àπ÷ßË

VENOUS THROMBOSIS æ∫‰¥â∫Õà ¬‡ªìπ “‡Àµÿ°“√µ“¬Õ¬à“ß‡©’¬∫æ≈—π‰¥â §«√ªÑÕß°—π ‰¡à „Àâ‡°‘¥À√◊Õ«‘π‘®©—¬‚√§‰¥â·µà‡π‘Ëπ Ê ·≈–∑”°“√√—°…“‰¡à „ Àâ ≈ÿ°≈“¡¡“°¢÷Èπ æ¬“∏‘ ¿“æ¢Õß°“√‡°‘¥ venous thrombosis ‡ªìπ‰ªµ“¡ Virchowûs triad (1856) ¥—ßµàÕ‰ªπ’È venous stasis, epithelial injury ·≈– hyper coagulability(1,2) (µ“√“ß∑’Ë 24.1) venous stasis ‡°‘¥¢÷Èπ‰¥â∫àÕ¬„πºŸâªÉ«¬∑’ËµâÕßπÕππ“πÀ≈—ß ºà“µ—¥ ªí®®—¬‡ ’Ë¬ßÕ◊ËπµàÕ°“√‡°‘¥‡™àπ °“√≈¥°“√‰À≈‡«’¬π¢Õß ‡≈◊Õ¥¥” ®“°¡’°âÕπ‡π◊ÈÕßÕ°‡∫’¬¥À≈Õ¥‡≈◊Õ¥¥” À√◊Õ valvular incompetence, endothelium À≈ÿ¥≈Õ°À≈—ßºà“µ—¥À√◊Õ‰¥â√—∫ ∫“¥‡®Á∫ ¿“«– hypercoagulability ·≈–§«“¡º‘¥ª°µ‘ ‡≈◊Õ¥ ·¢Áßµ—«‰«·µà°”‡π‘¥(1-5)

Õ“¬ÿ¡“°°«à“ 40 ªï πÕππ“π‰¡à‡§≈◊ÕË π‰À« ‡§¬¡’ª√–«—µ‡‘ ªìπ deep-vein thrombosis ·≈– pulmonary embolism Õâ«π¡“° ‡ªìπ varicose veins ‚√§¡–‡√Áß µ—ßÈ §√√¿å À√◊ÕÀ≈—ß§≈Õ¥ √—∫ª√–∑“π¬“§ÿ¡°”‡π‘¥°≈ÿ¡à estrogen Polycythemia Thrombocytopenia Connective tissue disease Congenital coagulation disorders

°“√«‘π‘®©—¬‚√§ ¿“«– venous thrombosis ·∫àßÕÕ°‡ªìπ 2 °≈ÿ¡à „À≠à¥ß— π’È 1. Deep Venous Thrombosis (DVT) æ∫‰¥â∫àÕ¬ ∂â“ «‘π‘®©—¬‰¥â§«√√’∫∑”°“√√—°…“ ‡æ√“–‚Õ°“ ∑’Ë®–‡°‘¥ ¿“«–·∑√°´âÕπ√ÿπ·√ß ∑”„ÀâºªŸâ «É ¬∂÷ß·°à°√√¡‰¥â 2. Superficial Venous Thrombosis Õ“°“√‰¡à√πÿ ·√ß √—°…“·∫∫ª√–§—∫ª√–§Õß‡ªìπºŸâªÉ«¬πÕ°‰¥â πÕ°®“° ®–‡ªìπ∑’Ë greater saphenous vein

Õ“°“√·≈–Õ“°“√· ¥ß °“√«‘π®‘ ©—¬‚√§ DVT ®“°ª√–«—µ·‘ ≈–°“√µ√«®√à“ß°“¬‡™◊ÕË ∂◊Õ ‰¥â‡æ’¬ß√âÕ¬≈– 50 ∑’æË ∫‰¥â¡¢’ “∫«¡¢â“ß‡¥’¬« ª«¥À√◊Õ°¥‡®Á∫∑’Ë πàÕß ª«¥πàÕß‡«≈“∑” dorsiflex ¢âÕ‡∑â“ (Homanûs sign) °¥‡®Á∫À√◊Õ§≈”À≈Õ¥‡≈◊Õ¥‰¥â‡ªìπ≈”µ√ßπàÕßÀ√◊Õ¢“Àπ’∫ √âÕ¬≈– 50 ¢ÕßºŸªâ «É ¬ DVT ‰¡à¡Õ’ “°“√ Õ“®®–æ∫ superficial venous thrombosis √à«¡¥â«¬ §≈”À≈Õ¥‡≈◊Õ¥„µâº‘«Àπ—ß‰¥â‡ªìπ≈”·¢Áß „π·π«¢Õß greater ·≈– lesser saphenous vein(2,6-9)

°“√µ√«®«‘π‘®©—¬ ∑’Ë„™â „πªí®®ÿ∫π— ¡’(9-13) 1. Doppler ultrasonography ‡ªìπ‡§√◊ÕË ß¡◊Õ∑’Ë „™âµ√«® Õ∫°“√‰À≈‡«’¬π¢ÕßÀ≈Õ¥‡≈◊Õ¥¥”∑’¢Ë “ ∑”ß“π‚¥¬„™â À≈—°°“√¢Õß doppler °“√‡§≈◊ÕË π‰À«¢ÕßÕπÿ¿“§‡≈Á° Ê ‡™àπ ‡¡Á¥‡≈◊Õ¥·¥ß®–¡’º≈µàÕ§≈◊Ëπ‡ ’¬ß ∑”„Àâ¡’°“√

224

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥ ‡ª≈’¬Ë π·ª≈ß¢Õß§≈◊πË ‡ªìπ™à«ß·µ°µà“ß°—π · ¥ßÕÕ°‰¥â ‡ªìπ retrieving wave ·≈–‡ ’¬ß∑’Ëøíß‰¥â °àÕπÕ◊Ëπ®– µâÕßøíß‡ ’¬ß·¬°„Àâ ‰¥â√–À«à“ßÀ≈Õ¥‡≈◊Õ¥·¥ß·≈–À≈Õ¥ ‡≈◊Õ¥¥”∑’«Ë “ßÕ¬Ÿà „°≈â°π— ≈—°…≥–¢Õß venous flow ∑’Ë øíß‰¥â®–‡√Á«¢÷Èπ™à«ßÀ“¬„®ÕÕ° ·≈–™â“≈ß‡¡◊ËÕÀ“¬„®‡¢â“ ≈—°…≥–‡©æ“–¢Õß venous flow ®–øíß‰¥â‡ªìπ‡ ’¬ß ‡À¡◊Õπ°—∫≈¡∑’Ëæ—¥Õ¬Ÿà „π∂È” µ”·Àπàß¢ÕßÀ≈Õ¥‡≈◊Õ¥¥” ∑’Ë§«√„™â doppler ultrasound øíß§◊Õ anterior ·≈– posterior tibial, popliteal ·≈– femoral ∂â“¡’°“√ Õÿ¥µ—π®–øíß‡ ’¬ß‰¡à™¥— À≈—°°“√ ”§—≠„π°“√„™â doppler ultrasound ”À√—∫À≈Õ¥‡≈◊Õ¥¥”∑’¢Ë “§◊Õ 1.1 §«√øíß‡ª√’¬∫‡∑’¬∫µ”·Àπàß‡¥’¬«°—π√–À«à“ß À≈Õ¥‡≈◊Õ¥¥”∑’¢Ë “∑—ßÈ Õß¢â“ß 1.2 øíß flow ¢≥–À“¬„®‡¢â“·≈–À“¬„®ÕÕ° 1.3 øíß flow ¢≥–∑’∫Ë ∫’ °≈â“¡‡π◊ÕÈ ∑’πË Õà ß·≈–ª≈àÕ¬ §«“¡·πàπÕπ„π°“√«‘π‘®©—¬‚√§ DVT ‚¥¬°“√„™â doppler US ¡’ ßŸ ∂÷ß√âÕ¬≈– 80-85 ¢÷πÈ Õ¬Ÿ°à ∫— ª√– ∫°“√≥å ·≈–§«“¡™”π“≠¢Õß·æ∑¬å ®–‰¥âº≈·πàπÕπ„πÀ≈Õ¥ ‡≈◊Õ¥¢π“¥‚µ ‡™àπ femoral ∂â“¢π“¥‡≈Á°‡™àπ soleal veins ®–øíß‰¥â ‰¡à™—¥ ·≈–‰¡à·πàπÕπ ”À√—∫°“√Õÿ¥µ—π‡æ’¬ß ∫“ß à«π µâÕß„™â°“√µ√«®«‘π®‘ ©—¬«‘∏Õ’ π◊Ë

2. Impedance Plethysmography (IPG) ‚¥¬°“√«—¥ maximal venous output (MVO) ·≈– venous capacitant §à“ venous capacitant §”π«≥‰¥â®“°°“√ ‡ª≈’¬Ë π·ª≈ß¢Õß calf circumference ´÷ßË «—¥‰¥â®“° strain guage ∑’æË π— √Õ∫πàÕßÀ≈—ß®“°æ—π·∂∫ºâ“«—¥§«“¡¥—π‚≈À‘µ „™â§«“¡¥—π 50 ¡‘≈≈‘‡¡µ√ª√Õ∑∫√‘‡«≥µâπ¢“ ºŸªâ «É ¬ DVT ®–¡’§à“ venous capacitance µË”‡æ√“–∫«¡Õ¬Ÿà·≈â« ª√‘¡“µ√¢Õß‡≈◊Õ¥∑’Ë ‰À≈‡«’¬π®–‡ª≈’Ë¬π·ª≈ß‰¡à¡“°π—° ¢≥–∑’Ë inflate cuff (√Ÿª∑’Ë 24.4) §”π«≥MVO ‰¥â®“° slope ¢Õß curve À≈—ß®“° deflate cuff ºŸªâ «É ¬ DVT ®–¡’ slope ∑’Ë·∫π ‡æ√“– outflow ®–™â“≈ßÀ≈—ß®“° delfate cuff IPG „™â«π‘ ®‘ ©—¬ DVT ‰¥â·πàπÕπ√âÕ¬≈– 85-95 ‰¡à ‰¥âº≈„π°“√«‘π‘®©—¬ thrombi ∑’Ë‡°‘¥¢÷Èπ°—∫ À≈Õ¥‡≈◊Õ¥¥”∫√‘‡«≥πàÕßÀ√◊Õ‰¡àÕ¥ÿ µ—π 3. Duplex scanner ªìπ‡§√◊ÕË ß¡◊Õ¡“µ√∞“πÕ—πÀπ÷ßË „π°“√ «‘π®‘ ©—¬‚√§ DVT ‚¥¬°“√π”‡Õ“ B-mode ultrasound ¡“√«¡°—∫ Doppler flowmeter “¡“√∂¥Ÿ‰¥â∑—Èß°“¬ «‘¿“§¢ÕßÀ≈Õ¥‡≈◊Õ¥ ¢Õ∫‡¢µ·≈–™π‘¥¢Õß≈‘Ë¡‡≈◊Õ¥ “¡“√∂§”π«≥Õ—µ√“‰À≈‡«’¬π¢Õß‡≈◊Õ¥„π√–¥—∫µà“ß Ê ‚¥¬„™â§Õ¡æ‘«‡µÕ√å ‰¥â ·¬°≈‘¡Ë ‡≈◊Õ¥«à“‡°à“À√◊Õ‰¡à ‡°“– µ‘¥°—∫ºπ—ßÀ√◊Õ float ·≈–¥Ÿ°“√∑”ß“π·≈–°“√‰À≈ ¬âÕπ°≈—∫∑’Ë valve ‰¥â (√Ÿª∑’Ë 24.5) §«“¡·¡àπ¬”„π°“√ «‘π®‘ ©—¬‚√§ Ÿß ”À√—∫À≈Õ¥‡≈◊Õ¥¥”¢π“¥„À≠à ‡™àπ iliac ·≈– femoral veins À√◊Õ IVC ·µà∂â“µË”≈ß‰ª°«à“ √–¥—∫‡¢à“·≈â«‰¡à·πàπÕπ

√Ÿª∑’Ë 24.4 «‘∏’°“√ Impedance Plethysmography (IPG) À≈—ß®“° æ—π pneumatic cuff ∫√‘‡«≥µâπ¢“ („™â§«“¡¥—π 50 ¡‘≈≈‘‡¡µ√ª√Õ∑ 45 «‘π“∑’) ‡æ◊ËÕ‡æ‘Ë¡ª√‘¡“µ√‡≈◊Õ¥¥” „π ¢“·≈–«—¥ venous capacity À≈—ß®“°π—Èπ≈¥§«“¡¥—π„π cuff ≈ß ·≈–«—¥ª√‘¡“µ√¢Õß‡≈◊Õ¥¥”„π¢“Õ’°§√—ÈßÀπ÷Ëß ®–æ∫«à“ª√‘¡“µ√¢ÕßÀ≈Õ¥‡≈◊Õ¥¥”®–≈¥≈ßÕ¬à“ß√«¥‡√Á« ¬°‡«âπ„πºŸâªÉ«¬ DVT

225

VENOUS THROMBOSIS

√Ÿª∑’Ë 24.5 Duplex scan ¢Õß common femoral vein °. ¡’‹ thrombus „π lumen ∑”„Àâ‡≈◊Õ¥‰¡à ‰À≈‡«’¬π (∫√‘‡«≥ ’¥”) ¢.‹ „™â probe °¥‰¡à·ø∫‡π◊ËÕß®“°¡’ thrombus „π lumen

4. Venogram ‡ªìπ°“√©’¥ “√∑÷∫· ß‡¢â“∑’ÀË ≈Õ¥‡≈◊Õ¥¥” ∫√‘‡«≥À≈—ß‡∑â“ ·≈–„Àâ “√∑÷∫· ß‰À≈‡«’¬π‡¢â“À≈Õ¥ ‡≈◊Õ¥¥” ¥Ÿ venous flow fluoroscopy ·≈–∂à“¬¿“æ √—ß ’‡ªìπ√–¬– º≈®–‡ªìπ∫«° ∂â“æ∫«à“¡’ termination of dye column, ¡’ filling defects, collaterals ‡°‘¥¡“° À√◊Õµ”·Àπàß∑’§Ë «√®–¡’¢ÕßÀ≈Õ¥‡≈◊Õ¥¥”À“¬‰ª‡ªìπ∫“ß à«π (√Ÿª∑’Ë 24.6) «‘∏°’ “√π’ÕÈ µ— √“‡ ’¬Ë ß Ÿß‡æ√“–‡ªìπ invasive diagnostic procedure Õ“®®–·æâ “√∑÷∫ · ßÀ√◊Õ¡’ thrombophlebitis ¢ÕßÀ≈Õ¥‡≈◊Õ¥∫√‘‡«≥©’¥ ·µà°Á¬—ß‡ªìπ«‘∏’°“√µ√«®«‘π‘®©—¬∑’Ë‡™◊ËÕ∂◊Õ‰¥â·πàπÕπ∑’Ë ÿ¥ ∂÷ß√âÕ¬≈– 95-100 ∂◊Õ‡ªìπ çgold standardé ‡¡◊Ë Õ ‡ª√’¬∫‡∑’¬∫°—∫«‘∏°’ “√µ√«®«‘π®‘ ©—¬™π‘¥Õ◊πË Ê

5. I125-labelled fibrinogen uptake test ‡ªìπ°“√»÷°…“ uptake ¢Õß circulating radioactive fibrinogen ∑’‡Ë ¢â“®—∫°—∫ thrombus ∑’‡Ë æ‘ßË ‡°‘¥¢÷πÈ „À¡à «‘∏°’ “√§◊Õ ©’¥ labeled human fibrinogen ‡¢â“√à“ß°“¬·≈– screening ¥Ÿ uptake „π√“¬∑’Ë ‰¥âº≈∫«°®–æ∫«à“¡’ uptake ¡“°°«à“√âÕ¬≈– 20 ‡¡◊ÕË ‡ª√’¬∫‡∑’¬∫°—∫¢“¥â“πµ√ß°—π¢â“¡ ¡’¢âÕ¥’§◊Õ«‘π‘®©—¬‰¥â·¡àπ¬” „π°√≥’∑’Ë thrombi ¢π“¥ ‡≈Á°‡°‘¥¢÷πÈ „π soleal veins ¢âÕ‡ ’¬§◊Õ sensitivity Ÿß ‡°‘π‰ª detect thrombi ∑’Ë ‰¡à®”‡ªìπµâÕß√—°…“ ‚Õ°“ «‘π‘®©—¬º‘¥æ≈“¥¡’‰¥â „πºŸâªÉ«¬ºà“µ—¥∑’Ë¡’·º≈µ‘¥‡™◊ÈÕÀ√◊Õ ¡’≈¡‘Ë ‡≈◊Õ¥§â“ß ‰¡à®∫— °—∫ old thrombi ®÷ß„™â ‰¥âº≈¥’ „π °“√«‘π®‘ ©—¬ acute DVT ∑’‡Ë °‘¥¢÷πÈ ¿“¬„π√–¬–‡«≈“ 1224 ™—«Ë ‚¡ß‡∑à“π—πÈ ‰¡à„™â‡ªìπ screening test „π°“√«‘π®‘ ©—¬ DVT (√Ÿª∑’Ë 24.7)

√Ÿª∑’Ë 24.6 Venogram ¢Õß left superficial femoral vein æ∫¡’ partial obstruction ®“° thrombus

√Ÿª∑’Ë 24.7 I125-labelled fibrinogen uptake test

226

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥

√Ÿª∑’Ë 24.8 ®“° Doppler ultrasonography æ∫ DVT ¢Õß

left ilieofemoral vein °. ·π« longitudinal ¢. ·π«‹ transverse √à«¡°—∫ probe compression

6. Doppler ultrasonography ‡ªìπ«‘∏°’ “√∑’ßË “à ¬ –¥«° ·≈–„™â‡«≈“πâÕ¬∑’Ë ÿ¥„π°“√«‘π‘®©—¬ DVT ‚¥¬°“√„™â continous wave Doppler ultrasonography ”À√—∫ À≈Õ¥‡≈◊Õ¥¥” femoral, superficial femoral, popliteal ·≈– tibioperoneals ∂â“‰¡à¡’ spontaneous wave flow À≈—ß®“° calf ·≈– thigh compression ‚¥¬°“√µ—¥‡Õ“ variation ∑’‡Ë °‘¥¢÷πÈ ®“°°“√À“¬„®‡¢â“ÕÕ°‰ª·≈â« ®–‰¥â º≈„π°“√«‘π®‘ ©—¬ DVT ·πàπÕπ √âÕ¬≈– 23-88 Õ“® ®–«‘π‘®©—¬º‘¥æ≈“¥ ”À√—∫ thrombi ∑’Ë‡°‘¥°—∫À≈Õ¥ ‡≈◊Õ¥¥”∫√‘‡«≥πàÕß À√◊ÕÕÿ¥µ—π‡æ’¬ß∫“ß à«π ‰¡à‡À¡“– ”À√—∫°“√«‘π®‘ ©—¬ recurrent DVT À√◊Õ postthrombotic syndrome ‡æ√“–®–‰¡à “¡“√∂∫Õ°§«“¡·µ°µà“ß‰¥â √–À«à“ß thrombi ‡°à“°—∫∑’‡Ë °‘¥¢÷πÈ „À¡à (√Ÿª∑’Ë 24.8)

‡ âπ„ÀâπÈ”‡°≈◊Õ √—°…“‚¥¬°“√ºŸ°µ—¥‡Õ“À≈Õ¥‡≈◊Õ¥¥” greater saphenous ÕÕ° „Àâ anticoagulant ‡æ◊ÕË ªÑÕß°—π‰¡à „Àâ thrombus ≈“¡‡¢â“‡°‘¥‡ªìπ deep thrombophlebitis ∂â“Õ“°“√‰¡à√πÿ ·√ß ≈ÿ°≈“¡¡“° √—°…“‚¥¬°“√„Àâ¬“µâ“πÕ—°‡ ∫ ª√–§∫∫√‘‡«≥π—Èπ ¥â«¬§«“¡√âÕπ·≈–¬“·°âª«¥ „ÀâÕÕ°°”≈—ß°“¬‰¥â À≈—ß®“°π—πÈ 72 ™—«Ë ‚¡ßµ√«®¥â«¬ duplex scan «à“¡’°“√≈“¡¢Õß thrombus ‡¢â“ Ÿà perforator ·≈– deep venous systems À√◊Õ‰¡à suppurative thrombophlebitis ¡—°®–‡°‘¥¢÷πÈ À≈—ß·∑ß‡ âπ ©’¥¬“ „ÀâπÈ”‡°≈◊Õ À√◊ÕÀ≈—ßÕÿ∫—µ‘‡Àµÿ ∂â“ºŸâªÉ«¬¡’‰¢âÀπ“« —Ëπ°¥‡®Á∫µ“¡·π«À≈Õ¥ ‡≈◊Õ¥¥” „Àâπ÷°∂÷ß suppurative thrombophlebitis ‡™◊ÈÕ∑’Ëæ∫ ‰¥â∫Õà ¬§◊Õ Staph. aureus √—°…“‚¥¬°“√„Àâ¬“ªØ‘™«’ π–·≈–‡≈“– µ—¥‡Õ“À≈Õ¥‡≈◊Õ¥¥”‡ âπ∑’¡Ë Õ’ “°“√Õ—°‡ ∫µ‘¥‡™◊ÕÈ ÕÕ°„Àâ‡√Á«∑’ Ë ¥ÿ

°“√√—°…“

À≈—°°“√„π°“√√—°…“∑’ Ë ”§—≠§◊Õ(14) 1. ªÑÕß°—π‰¡à „Àâ‡°‘¥ thrombi ¢÷πÈ ¡“Õ’° 2. ‰¡à „Àâ‡°‘¥ thrombus propragation 3. ≈¥°“√°√–∑∫°√–‡∑◊ÕπµàÕ venous valve „ÀâπÕâ ¬ ∑’ Ë ¥ÿ ª√–°“√ ”§—≠∑’ Ë ¥ÿ „π°“√√—°…“§◊Õ ªÑÕß°—π‰¡à„Àâ‡°‘¥ pulmonary embolism (PE) ‡æ√“–Õ—µ√“µ“¬ Ÿß¡“° ª√–¡“≥√âÕ¬≈– 5 ¢ÕßºŸâªÉ«¬ DVT ®–‡°‘¥ PE ∂÷ß·¡â«à“®–„Àâ°“√√—°…“Õ¬à“ß ‡µÁ¡∑’°Ë µÁ “¡ ∂â“‰¡à√°— …“‡≈¬Õ—µ√“‡°‘¥‡ªìπ PE ®– Ÿß∂÷ß√âÕ¬≈– 25

Thrombophlebitis «‘π®‘ ©—¬‚√§ superficial thrombophlebitis ‰¥â®“°°“√µ√«® √à“ß°“¬ ‚¥¬§≈”‰¥âÀ≈Õ¥‡≈◊Õ¥¥”‡ªìπ·∑àß„µâº‘«Àπ—ß ·≈–°¥ ‡®Á∫µ“¡·π«¢ÕßÀ≈Õ¥‡≈◊Õ¥¥” greater ·≈– lesser saphenous √à«¡°—∫º‘«Àπ—ß·¥ß√âÕπ Õ“°“√®–‰¡à√ÿπ·√ß·≈–À“¬‰¥â‡Õß ·µà∂“â ‡ªìπ suppurative thrombophlebitis À√◊Õ thrombosis ∑’Ë‡°‘¥¢÷Èπ≈“¡®π∂÷ß saphenofemoral junction µ“¡·π«·∑ß

Deep Vein Thrombosis (DVT)

227

VENOUS THROMBOSIS

‡¡◊ÕË ß —¬«à“ºŸªâ «É ¬®–‡ªìπ‚√§ DVT µâÕß√’∫√—°…“‚¥¬°“√„Àâ anticoagulant(14,15) ¢âÕÀâ“¡„π°“√„Àâ anticoagulant ¡’¥ß— π’È ºŸâ ªÉ«¬∑’°Ë ”≈—ß¡’ª≠ í À“„π°“√µ°‡≈◊Õ¥À√◊Õ‡ ’¬‡≈◊Õ¥ ‡§¬ºà“µ—¥¡“°àÕπ „π√–¬–‡«≈“„°≈â°Õà πÀπâ“π’È ·≈–ºŸªâ «É ¬∑’‡Ë ªìπ‚√§¡–‡√Áß ‡√‘¡Ë „Àâ bolus dose ¢Õß heparin „π¢π“¥ 5,000-10,000 ¬Ÿπµ‘ ‡¢â“∑“ß À≈Õ¥ ‡≈◊Õ¥¥”§√—ßÈ ·√° µ“¡¥â«¬°“√„ÀâÕ¬à“ßµàÕ‡π◊ÕË ß„π¢π“¥∑’æË Õ‡æ’¬ß ®π°√–∑—ßË √–¥—∫¢Õß partial thromboplastin time (PTT) Õ¬Ÿ∑à ’Ë 1.5-2.0 ‡∑à“¢Õß§à“∑’Ë ‰¥â§√—ßÈ ·√° ‡®“–‡≈◊Õ¥π—∫ª√‘¡“≥¢Õß‡°√Á¥ ‡≈◊Õ¥∑ÿ°«—π „Àâ√–«—ß Heparin-Induced-Thrombocytopenia (HIT) ´÷ßË ‡ªìπ¿“«–·∑√°´âÕπ∑’ÕË “®®–æ∫‰¥â „π°“√„Àâ¬“µ—«π’(16,17) È À≈—ß®“°π—Èπæ¬“¬“¡ª√—∫‡ª≈’Ë¬π°“√„™â¬“©’¥‡¢â“∑“ßÀ≈Õ¥ ‡≈◊Õ¥¥”¡“‡ªìπ¬“√—∫ª√–∑“π·∑π(18) ‚¥¬„Àâ Warfarin √—∫ª√–∑“π 3-7 «—π À≈—ß®“°ºŸªâ «É ¬‰¥â√∫— heparin „π¢π“¥‡µÁ¡∑’·Ë ≈â« monitor ¢π“¥¢Õß Warfarin ∑’‡Ë À¡“– ¡‚¥¬§ß√–¥—∫¢Õß prothrombin time (PT) 1.5-2.0 ‡∑à“¢Õß§à“∑’Ë ‰¥â§√—Èß·√°°àÕπ√—∫ª√–∑“π¬“ √–¬–‡«≈“∑’ËºŸâªÉ«¬§«√‰¥â√—∫ anticoagulant §◊Õ 3-6 ‡¥◊Õπ ‡æ◊ËÕ√Õ„Àâ¡’ recanalization ·≈– collaterals ¢ÕßÀ≈Õ¥‡≈◊Õ¥ ¥”∑’ÕË ¥ÿ µ—π µ‘¥µ“¡‡ΩÑ“¥Ÿ°“√‡ª≈’¬Ë π·ª≈ß‚¥¬„™â duplex scanning ª√–‡¡‘π¥Ÿ«à“ thrombus ‡√‘Ë¡¡’°“√≈–≈“¬À√◊Õ ≈“¬µ—« ¡“°πâÕ¬‡æ’¬ß‰√ °“√√—°…“‚¥¬„™â¬“ ≈“¬≈‘¡Ë ‡≈◊Õ¥ (thrombolytic therapy) ‡™àπ Urokinase, Streptokinase ·≈– tissue plasminogen activator „π°“√√—°…“ DVT ®–‰¥âº≈¥’ „π√–¬–·√° ·µàº≈°“√ √—°…“√–¬–¬“«¬—ß‰¡à·πàπÕπ µâÕß∫√‘À“√¬“∑“ßÀ≈Õ¥‡≈◊Õ¥¥” monitor ¬“‚¥¬¥Ÿ®“°√–¥—∫¢Õß fibrinogen ·≈– fibrinolytic products ¡’¢Õâ Àâ“¡„π°“√„™â¬“ (µ“√“ß∑’Ë 24.2) ·≈–®–µâÕß√–«—ß ¿“«–·∑√°´âÕπ∑’®Ë –‡°‘¥¢÷πÈ ®“°°“√µ°‡≈◊Õ¥´÷ßË æ∫‰¥â∫Õà ¬(19,20) ºŸªâ «É ¬∑’¡Ë Õ’ “°“√¢Õß pulmonary emboli ∂÷ß·¡â«“à ®–‰¥â√∫— anticoagulant ¡“‡æ’¬ßæÕ·≈â« §«√√—°…“‚¥¬°“√„ à IVC filter ªÑÕß°—π‰¡à „Àâ embolizing clot ®“°¢“¢÷πÈ ‰ªÕÿ¥ pulmonary artery à«π„À≠à·≈â« emboli ®–¡’µâπµÕ‡°‘¥µ√ß pelvic veins ‡°“–°—∫ºπ—ßÀ≈Õ¥‡≈◊Õ¥¥”À≈«¡ Ê À≈ÿ¥ßà“¬ «‘∏°’ “√„ à Intraluminal Greenfield filter §◊Õ Õ¥ºà“πº‘«Àπ—ß‡¢â“∑“ßÀ≈Õ¥‡≈◊Õ¥¥” femoral À√◊Õ jugular(21) (√Ÿª∑’Ë 24.9) «‘∏°’ “√Õ◊πË §◊Õ ºà“µ—¥‡¢â“‰ª „™â cavel clips À√◊ÕºŸ° IVC(23) °“√ºà“µ—¥„πºŸªâ «É ¬∑’Ë ‰¥â√∫— anticoagulant Õ¬à“ß‡µÁ¡∑’Ë·≈â« ‡ªìπ«‘∏’∑’Ë§àÕπ¢â“ß®–‡ ’Ë¬ßµàÕ°“√ µ°‡≈◊Õ¥ ·≈–‡°‘¥ venous insufficiency ‰¥â ®÷ß‡ªìπ«‘∏’∑’Ë ‰¡à§Õà ¬„™â „πªí®®ÿ∫π—

µ“√“ß∑’Ë 24.2 ¢âÕÀâ“¡„π°“√„Àâ systemic thrombolytic therapy

Absolute ¡’°“√µ°‡≈◊Õ¥¢ÕßÕ«—¬«–¿“¬„π ‡ªìπ CVA ºà“µ—¥µ“ ¡’æ¬“∏‘ ¿“æ„π ¡Õß Relative ºà“µ—¥„À≠à ∫“¥‡®Á∫À≈“¬√–∫∫ ºà“π°“√ CPR ·º≈‡ªìªµ‘§ §«“¡¥—π‚≈À‘µ Ÿß∑’¬Ë ß— §ÿ¡‰¡à ‰¥â µ—ßÈ §√√¿å diabetic hemorrhagic retinopathy

°“√Õÿ¥µ—π¢Õß thrombus µ√ß ileofemoral vein ®–∑” „Àâ¢“∫«¡¡“° ª«¥·≈–°¥‡®Á∫ ∂â“¡’Õ“°“√¡“°®–°≈“¬‡ªìπ Phlegmasia Cerulea Dolens (PCD) º‘«Àπ—ß®–¡’ ¥’ ”§≈È” ·≈–‡πà“ µ“¬„π∑’ Ë ¥ÿ ∂â“‰¡à√∫’ √—°…“(23) Phlegmasia Alba Dolens (PAD) ‡ªìπÕ’°√Ÿª·∫∫Àπ÷ßË ¢Õß°“√Õÿ¥µ—π∫√‘‡«≥ ileofemoral vein ´÷ßË Õ“°“√ ”§—≠√à«¡¥â«¬πÕ°®“°¢“∫«¡·≈â«¬—ß®–‡°‘¥ arterial spasm ∑”„Àâ§≈”™’æ®√ª≈“¬‡∑â“‰¡à ‰¥â ¢“®–‡¬Áπ ´’¥ ∑—ßÈ 2 °√≥’§Õ◊ PCD ·≈– PAD ‡ªìπ¢âÕ∫àß™’È „π°“√ºà“µ—¥ venous thrombectomy √à«¡°—∫°“√„Àâ anticoagulant À≈—ßºà“µ—¥(23,24) ‡π◊ÕË ß®“° venous thrombosis ®–‡°‘¥´È”‰¥âÕ°’ ®÷ß§«√∑” distal arteriovenous fistula ‡ªìπ°“√‡æ‘Ë¡ª√‘¡“≥‡≈◊Õ¥‰À≈‡«’¬π¿“¬„π À≈Õ¥‡≈◊Õ¥¥”(25)

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Right renal vein

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2. Intermittent pneumatic calf compression (IPCC) °“√ «¡∂ÿß‡∑â“¬“ß¬◊¥∑’Ë¢“∑—Èß 2 ¢â“ß ®–™à«¬≈¥Õ—µ√“ °“√‡°‘¥ DVT ≈ß‰¥â®“°√âÕ¬≈– 25 ‡ªìπ√âÕ¬≈– 9.3 ‡æ√“–®–™à«¬°“√‰À≈‡«’¬π°≈—∫ ŸÀà «— „®¢Õß‡≈◊Õ¥¥” ∂â“ „™â IPCC ®–π«¥°≈â“¡‡π◊ÕÈ πàÕß‡ªìπ√–¬–∑”„Àâ‡≈◊Õ¥‰À≈ ‡«’ ¬ π°≈— ∫ À— « „®¥’ ¢÷È π ‡æ‘Ë ¡ fibrinolytic activity Õ—µ√“°“√‡°‘¥ venous thrombosis ®–≈¥≈ß¡“° ·≈– ®–‡°‘¥πâÕ¬¡“°∂â“„Àâ IPCC √à«¡°—∫°“√©’¥ low-dose heparin ‡¢â“„µâº«‘ Àπ—ß 3. Low molecular weight heparin (LMWH) º≈‘µ®“° fractionated heparin ´÷ßË ¡’ƒ∑∏‘¢Ï Õß anti-factor Xa §àÕπ¢â“ß Ÿß ‰¥âº≈¥’„π°“√ªÑÕß°—π°“√‡°‘¥ venous thrombosis ·≈–¿“«–·∑√°´âÕπ®“°°“√µ°‡≈◊Õ¥¡’πâÕ¬ ©’¥ ‡¢â“„µâº«‘ Àπ—ß∑ÿ° 12 ™—«Ë ‚¡ß ‡ªìπ fixed dose ·≈–‰¡àµÕâ ß monitor ¥â«¬ a PTT(28,29,30) 4. Warfarin „™â „π°≈ÿ¡à ∑’°Ë “√ªÑÕß°—π venous thrombosis ¥â«¬ low-dose subcutaneous heparin ‰¡à ‰¥âº≈ ‡À¡“– ”À√—∫ºŸâªÉ«¬°≈ÿà¡‡ ’Ë¬ß¡“° ‡™àπ ºà“µ—¥¢âÕ‡∑â“ ‡ªìπ¡–‡√Áß´÷ßË ®–°√–µÿπâ „Àâ‡°‘¥¿“«– prethrombotic state ‰¥â §«√„Àâ Warfarin Õ¬à“ßµàÕ‡π◊ÕË ß ·≈– monitor ¥â«¬ PT ¿“«–·∑√°´âÕπ∑’Ë ”§—≠§◊Õ°“√µ°‡≈◊Õ¥∂â“‡°‘¥¢÷Èπ µâÕß„Àâ Vitamin K ‡ªìπ antagonist ‡¢â“∑“ßÀ≈Õ¥ ‡≈◊Õ¥¥” À√◊Õ„Àâ fresh frozen plasma ¿“«–·∑√°´âÕπÕ◊πË Ê ∑’æË ∫‰¥â¡’ dermatitis, alopecia, Õ“°“√·æâ, Õ“‡®’¬π, §≈◊πË ‰ â ·≈–∑âÕß√à«ß Àâ“¡„™â „πºŸªâ «É ¬µ—ßÈ §√√¿å ‡æ√“–¬“ ºà“π placenta ‰¥â skin necrosis æ∫„πºŸªâ «É ¬∫“ß√“¬ §«√À≈’°‡≈’¬Ë ß°“√„Àâ loading dose

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‡Õ° “√Õâ“ßÕ‘ß 1. Anderson FA. A population-based perspective of the hospital incidence and casefatality rates of deep vein thrombosis and pulmonary embolism: The Worcestor DVT study. Arch Intern Med 1991;151: 933-945. 2. Alpert JS, Dalen JE. Epidemiology and Natural History of Venous Thromboembolism. Prog Cardiovasc Surg 1994;36: 417-422. 3. Piccioli A, Prandoni P, Ewenstein BM, Goldhaber S2. Cancer and Venous Thromboembolism. Am Heart J 1996;132: 850-855. 4. Toglia M, Weg JG. Venous Thromboembolism During Pregnancy. New Engl J Med 1996;335:108-114. 5. Nachman RL, Siverstein R. Hypercoagulable States. Ann Int Med 1993;119:819-827. 6. Prandoni P, Lensing AWA, Cago A, et al. The Long-term Clinical Course of Acute Deep Venous Thrombosis. Am Coll Phys 1996;125:17. 7. Coon WW. Epidemiology of venous thromboembolism. Ann Surg 1977;186: 149-156. 8. Kakkar VV. Natural history of postoperative deep-vein thrombosis. Lancet 1969;2: 230-242. 9. Kakkar VV, Lawrence D. Hemodynamic and clinical assessment after therapy for acute deep vein thrombosis. Am J Surg 1985;150: 54-62. 10. Oliver MA. Duplex scanning in venous disease. Bruit 1985;9:206214. 11. Cornus J, Pearson SD, Creager MA, et al. Importance of Findings on the Initial Evaluation for Cancer in Patients with Symptomatic Idiopathic Deep Venous Thrombosis. Ann Int Med 1996;125:785793. 12. Hirsh J, Hoak J. Management of Deep Vein Thrombosis and Pulmonary Embolism: A Statement for Health care Professionals. Circulation 1996;12: 2212-2245. 13. Comerota AJ. Venous duplex imaging: Should it replace hemodynamic tests for deep venous thrombosis? J Vasc Surg 1990;11: 5361. 14. Ginsberg JS. Management of Venous Thromboembolism. New Eng J Med 1996;335: 1816-1828. 15. Hirsh J, Raschke R, Warkentin TE, et al. Heparin: Mechanism of Action, Pharmacokinetics, Dosing Considerations, Monitoring, Efficacy and Safety. Chest 1995;108: 2585-2755.

16. Warkentin TE, Chong BH, Greinacher A. Heparin-induced Thrombocytopenia: Towards Consensus. Thrombosis and Hemostasis 1998;79: 1-7. 17. Laster J. The heparin-induced thrombocytopenia syndrome: An update. Surgery 1987;102:763-771. 18. Hirsh J, Dalen JE, Deykin E, et al. Oral Anticoagulants: Mechanism of Action, Clinical Effectiveness and Optimal Therapeutic Range. Chest 1995;108: 2315-2465. 19. Comerota AJ, Aldridge SC. Thrombolytic therapy for acute deep vein thrombosis. Can J Surg 1992;36: 359-371. 20. Molina JE, Hunter DW, Yedlicka JW. Thrombolytic therapy for iliofemoral venous thrombosis. Vasc Surg 1992;26: 630-642. 21. Greenfield LJ. Intraluminal techniques for vena caval interruption and pulmonary embolectomy. World J Surg 1978;3:45-59. 22. Silver D, Sabiston DC. The role of vena caval interruption in the management of pulmonary embolism. Surgery 1975;77:1-10. 23. Haimovici H. Ischemic forms of venous thrombosis: Phlegmasia cerulea dolens and venous gangrene. Heart Bull 1967;16:101-110. 24. Edward WH. Iliofemoral venous thrombosis: The role of theombectomy. In: Vascular Surgery. Rutherford RB (ed.) 4th ed. Philadelphia: WB Saunders 1977;19-95. 25. Rutherford RB. Role of surgery in iliofemoral venous thrombosis. Chest 5 (Suppl.) 1989;434. 26. Eklof B, Einarsson E, Phate G. Role of thrombectomy and temporary arteriovenous fistula in acute iliofemoral venous thrombosis. In: Surgery of the Veins. Bergen JJ, Yao JST (eds.). London: Grune and Stratton 1985;131-144. 27. Clagett GP, Anderson FA Jr, Helt J, et al. Prevention of Venous Thrombo- embolism. Chest 1995;108:3125-3345. 28. Kearon C, Hirsh J. Management of Anticoagulation Before and after Elective Surgery. N Engl Med 1997;336: 1506-1511. 29. Kakkar VV, Murray WJ. Efficacy and safety of low-molecular-weight heparin (CY216) in preventing postoperative venous thromboembolism: A co-operative study. Br J Surg 1985;72:786-793. 30. Ninno MA. Pharmaco therapy: Low Molecular Weight Heparin: Pharmacokinetics. Current Surgery 1996;53: 225-230.

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√Ÿª∑’Ë 25.2 °“¬«‘¿“§¢Õß√–∫∫πÈ”‡À≈◊Õß∑’Ë¢“

dermal plexus ®–√–∫“¬πÈ”‡À≈◊Õß‡¢â“ Ÿà main lymphatic trunks ∑’ÕË ¬Ÿµà √ß à«πº‘«¢Õß°≈â“¡‡π◊ÕÈ ·≈–‡ÕÁπæ—ßº◊¥ ‚¥¬ collecting channels ∑àÕπÈ”‡À≈◊Õß‡À≈à“π’®È –¡Õß‡ÀÁπ‰¥â®“° lymphangiograms deep lymphatic systems ·µà≈– à«π®–·¬°°—π‡ªìπÕ‘ √– √–∫“¬πÈ”‡À≈◊Õß‡¢â“ Ÿ·à µà≈– compartments ·≈–·µà≈– channels ∑’ÕË ¬Ÿà „°≈â°√–¥Ÿ° deep ·≈– superficial systems ®–·¬° À√◊Õ√«¡°—π„π¿“«–º‘¥ª°µ‘‡™àπ ¡’°“√Õÿ¥µ—π¢Õß∑àÕÀ√◊ÕµàÕ¡πÈ” ‡À≈◊Õß(2) deep vessels ®–¡’¢π“¥§ß∑’·Ë ≈–¡’ valves ∑ÿ°™à«ß 1 ‡´Áπµ‘ ‡¡µ√ ª√–¡“≥ 4 ∑àÕ®–√–∫“¬πÈ”‡À≈◊Õß‡¢â“ ŸàµàÕ¡πÈ”‡À≈◊Õß popliteal ∑’¢Ë Õâ ‡¢à“¥â“πÀ≈—ß 6-8 ∑àÕ√–∫“¬‡¢â“ Ÿµà πâ ¢“∑“ß medial ‡¢â“∂÷ß deep inquinal nodes.

superficial systems ‡ÀÁπ‰¥âß“à ¬®“° lymphangiography «‘ßË §Ÿ¢à π“π¡“°—∫ greater ·≈– lesser saphenous veins. §π ª°µ‘®–¡’ª√–¡“≥ 8 ‡ âπ Õ¬Ÿ∑à “ß¥â“π„π¢Õßµâπ¢“ (√Ÿª∑’Ë 25.2) ¥Ÿ®“° lymphangiography ®–æ∫«à“πÈ”‡À≈◊Õß®“°µâπ¢“·≈– ™—πÈ „µâº«‘ Àπ—ß·≈–º‘«Àπ—ß∫√‘‡«≥π’®È –√–∫“¬‡¢â“ Ÿà superior inguinal nodes ¢“¥â“π≈à“ß√–∫“¬‡¢â“ Ÿà inferior inguinal nodes(3) ¥â«¬ ‡Àµÿπ’È®÷ßÕ∏‘∫“¬‰¥â«à“ºŸâªÉ«¬ acquired lymphedema ∫“ß√“¬ ¢“®–∫«¡·µà „µâÀ«— ‡¢à“ inguinal nodes ·∫àßÕÕ°‰¥â 2 °≈ÿ¡à §◊Õ superficial Õ¬Ÿ√à Õ∫ fossa ovalis ·≈– deep Õ¬Ÿ√à Õ∫ fatty fissue ¢Õß femoral sheath ·≈–®–√–∫“¬πÈ”‡À≈◊Õß‡¢â“ Ÿµà Õà ¡√Õ∫ iliac vessels(4) √–∫∫πÈ”‡À≈◊Õß∑’·Ë ¢π ¡’°“¬«‘¿“§§≈â“¬°—∫∑’¢Ë “ ‚¥¬®–¡’ 2 °≈ÿ¡à §◊Õ basilic (medial aspect) ·≈– cephalic (lateral aspect) «‘Ëß¢π“π§Ÿà°—∫À≈Õ¥‡≈◊Õ¥¥” Õ“®®–√«¡°—π∫“ß·Ààß°àÕπ √–∫“¬‡¢â“ Ÿà axillary nodes (√Ÿª∑’Ë 25.3)

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√Ÿª∑’Ë 25.3 °“¬«‘¿“§¢Õß√–∫∫πÈ”‡À≈◊Õß∑’Ë·¢π

√’√«‘∑¬“¢Õß√–∫∫πÈ”‡À≈◊Õß Àπâ“∑’ÀË ≈—°¢Õß√–∫∫πÈ”‡À≈◊Õß§◊Õ °“√π” àß “√πÈ”®“° interstitial space °≈—∫‡¢â“ Ÿà√–∫∫‰À≈‡«’¬π‚≈À‘µ ‚¥¬¡’Àπâ“∑’Ë ”§—≠Õ◊πË ¥—ßµàÕ‰ªπ’È 1. ¥÷ß‡Õ“‚ª√µ’π∑’Ë¡’ ‚¡‡≈°ÿ≈¢π“¥„À≠à°≈—∫®“°√–∫∫‰À≈ ‡«’¬π¢ÕßÀ≈Õ¥‡≈◊Õ¥ΩÕ¬ 2. °”®—¥·∫§∑’‡√’¬·≈– “√·ª≈°ª≈Õ¡µàÕ√à“ß°“¬ ‚¥¬∑” Àπâ“∑’‡Ë √‘¡°—∫√–∫∫¿Ÿ¡§‘ ¡ÿâ °—π√à“ß°“¬ 3. π” “√ ”§—≠∑’®Ë ”‡ªìπµàÕ√à“ß°“¬ ‡™àπ ‚ª·µ ‡´’¬¡®“° √–∫∫∑“ß‡¥‘πÕ“À“√ ∑àÕπÈ”‡À≈◊Õß√–¥—∫ capillary ®– permeable ·≈–§«“¡¥—π ‰Œ‚¥√ ·µµ‘§µË”‡¡◊ÕË ‡∑’¬∫°—∫ interstitial fluid(5,6) πÈ”‡À≈◊Õß®– ‰À≈ºà“π∑àÕ¢÷πÈ ∑“ß¥â“π∫π‡ ¡Õ‡π◊ÕË ß®“°¡’ valves ·≈–‰¡à§ß—Ë Õ¬Ÿà „π interstitial spaces „π¿“«–ª°µ‘ πÈ”‡À≈◊Õß¡’≈—°…≥–‡ªìπ ultrafiltrate §≈â“¬°—∫æ≈“ ¡à“ §≈â“¬ transudate ¡’§«“¡¥—π ‰Œ‚¥√ ·µµ‘§ Ÿß®“° arterial system ¿“¬„π 24 ™—«Ë ‚¡ß√âÕ¬≈–

50 ¢ÕßÕ—≈∫Ÿ¡π‘ ∑’Ë ‰À≈‡«’¬πÕ¬Ÿà „π√à“ß°“¬®– Ÿ≠‡ ’¬‰ª®“° arterialcapillary system ‚ª√µ’π∑’ Ë ≠ Ÿ ‡ ’¬‰ª®–∂Ÿ°¥¥÷ß°≈—∫‡¢â“ Ÿà venules ‚¥¬·√ß¥—πÕÕ ‚¡µ‘§·≈–‰Œ‚¥√ ·µµ‘§ ¡’‡æ’¬ß√âÕ¬≈– 0.1 ‡∑à“ π—πÈ ∑’¬Ë ß— §ß§â“ßÕ¬Ÿà √–∫∫πÈ”‡À≈◊Õß®–¥Ÿ¥´÷¡∑’‡Ë À≈◊Õ√âÕ¬≈– 0.1 π’È πÈ”‡À≈◊Õß∑’Ë·¢π·≈–¢“®–¡’ ‚ª√µ’π 0.1-0.5 °√—¡µàÕ 100 ¡‘ ≈ ≈‘ ≈‘ µ √ ‡¡◊Ë Õ ‡∑’ ¬ ∫°— ∫ ‚ª√µ’ π „π‡≈◊ Õ ¥´÷Ë ß ¡’ Ÿ ß ∂÷ ß 6 °√— ¡ ª√‘¡“≥¢Õß‚°≈∫Ÿ≈π‘ „ππÈ”‡À≈◊Õß®– Ÿß°«à“Õ—≈∫Ÿ¡π‘ °“√‰À≈‡«’¬π¢ÕßπÈ”‡À≈◊Õß ¢÷πÈ Õ¬Ÿ°à ∫— (6,7,8) 1. interstitial pressure 2. negative ·≈– positive fluctuation „π™àÕß∑âÕß·≈–™àÕß ∑√«ßÕ° 3. °“√°¥®“°®—ßÀ«–°“√‡µâπ¢ÕßÀ≈Õ¥‡≈◊Õ¥·≈–°“√À¥ µ—«¢Õß°≈â“¡‡π◊ÕÈ 4. valves 5. °“√À¥·≈–¬◊ ¥ µ— « ¢Õß°≈â “ ¡‡π◊È Õ ‡√’ ¬ ∫¿“¬„πÀ≈Õ¥ πÈ”‡À≈◊Õß

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LYMPHEDEMA ‡°‘¥®“°§«“¡º‘¥ª°µ‘„π°“√·≈°‡ª≈’¬Ë π “√πÈ”√–¥—∫ capillary ·≈–°“√√–∫“¬πÈ”‡À≈◊Õß ∑”„Àâ¡π’ È”‡À≈◊Õß§—ßË ·¢πÀ√◊Õ¢“ ®–∫«¡ §—ßË ¥â«¬ “√πÈ”∑’¡Ë ’‚ª√µ’π„πª√‘¡“≥ Ÿß „π chronic lymphedema ª√‘¡“≥‚ª√µ’π®– Ÿß∂÷ß 5 °√—¡µàÕ 100 ¡‘≈≈‘≈µ‘ √ ‡∑’¬∫°—∫ ¿“«–ª°µ‘ 0.1-0.5 °√—¡ ·≈– 0.9 °√—¡„π¿“«–À—«„®«“¬ fibrosis ¢Õß·¢π·≈–¢“‡°‘¥‰¥â®“°ªí®®—¬ ”§—≠§◊Õ(9,10) 1. “√πÈ”∑’Ë§—ËßÕ¬Ÿà¡’ª√‘¡“≥‚ª√µ’π Ÿß √à«¡°—∫¡’°“√§—Ëß¢Õß metabolic products ‡™àπ fibrin ·≈– fibrous tissue 2. ¡’°“√≈¥ª√– ‘∑∏‘¿“æ¢Õß macrophages ∑”„Àâ collagen lysis ≈¥≈ß

Õ“°“√·≈–Õ“°“√· ¥ß∑“ß§≈‘π‘§ ¢âÕ¡Ÿ≈ ”§—≠„π°“√«‘π®‘ ©—¬‚√§ lymphedema (µ“√“ß∑’Ë 25.3) 1. progressive painless swelling ¢Õß·¢πÀ√◊Õ¢“ 2. nonpitting edema 3. º‘«Àπ—ß¡’≈°— …≥–¢Õß hyperkeratosis, ¡’√Õ¬·¬°·≈– onychomycosis (µ‘¥‡™◊ÕÈ √“) 4. çbuffalo humpé edema ∫√‘‡«≥À≈—ß‡∑â“ 5. çStemnerûs signé À√◊Õ squared toes.

µ“√“ß∑’Ë 25.3 Õ“°“√· ¥ß∑“ß§≈‘π§‘ ¢Õß lymphedema Õ“°“√ Limb swelling Heaviness Recurrent lymphangitis Skin changes Fungal infections

Õ“°“√· ¥ß Limb edema Dorsal buffalo hump Elephantine distribution Pink flushed skin color Lichenification Peau dû orange Subcutaneous tissue lacking resilience

∂â“‡ªìπ chronic lymphedema º‘«Àπ—ß®–·¢Áß§≈â“¬Àπ—ß —µ«å ·≈–¡’≈°— …≥– Peu dû Orange appearance „π°“√«‘π®‘ ©—¬‚√§°àÕπÕ◊πË ®–µâÕß·∫àß«à“¡’ “‡Àµÿ¡“®“° primary (congenital) À√◊Õ secondary (acquired) „π acquired Õ“®®–¡’ “‡Àµÿ¡“®“°°“√µ‘¥‡™◊ÕÈ À√◊Õª√ ‘µ ‡™àπ filariasis, °“√ ∫“¥‡®Á∫, °“√ºà“µ—¥·≈–√—ß ’∫”∫—¥, ¿Ÿ¡·‘ æâÀ√◊Õ¡–‡√Áß

√Ÿª∑’Ë 25.4 lymphangitis ∑’Ë‡°‘¥¢÷Èπ„π lymphedema ¡—°®–‡√‘Ë¡®“°ª≈“¬π‘È«‡∑â“ À√◊ÕÀ≈—ß‡∑â“‡ªìπ√Õ¬·¥ß ≈“¡¢÷Èπ¡“∫√‘‡«≥πàÕß·≈–¢“

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√Ÿª∑’Ë 25.5 lymphedema „π√–¬–·√°®–∫«¡‡ªìπ·∫∫ pitting

√Ÿª∑’Ë 25.6 ºŸâªÉ«¬√“¬‡¥’¬«°—π°—∫√Ÿª∑’Ë 25.5 À≈—ß®“°‡°‘¥ recurrent

edema πÕπ¬°¢“ ¢âÕ®–¬ÿ∫∫«¡ °“√∫«¡®–‡√‘Ë¡µâπ ®“°¢âÕ‡∑â“·≈–À≈—ß‡∑â“≈“¡¢÷Èπ¡“‡√◊ËÕ¬ Ê

lymphangitis À≈“¬§√—Èß„π 2 ªï °≈“¬‡ªìπ chronic lymphedema ¢“∫«¡¡“° º‘«Àπ—ß·¢Áß °¥‰¡à∫ÿã¡

‰¡à«à“®–‡ªìπ primary À√◊Õ secondary lymphedema Õ“°“√·≈–Õ“°“√· ¥ß®–‰¡àµà“ß°—π¡“° ‡√‘Ë¡®“°°“√∫«¡·≈– ¿“«–·∑√°´âÕπ‡À¡◊Õπ°—π§◊Õ ‡ªìπ cellulitis ·≈– lymphangitis ´È”·≈â«´È”Õ’° (√Ÿª∑’Ë 25.4) Õ“®®–°≈“¬‡ªìπ lymphangiosarcoma „π√–¬–·√°®–‡ªìπ°“√∫«¡·∫∫ pitting edema ‡√‘Ë¡∫«¡®“° ¢âÕ‡∑â“¢÷πÈ ¡“‡√◊ÕË ¬ Ê ¢“‚µπÈ”Àπ—°‡æ‘¡Ë ¢÷πÈ ‡√◊ÕË ¬ Ê ∑”„Àâ≈“â °“√ §—Ëß¢Õß‚ª√µ’π·≈–πÈ”‡À≈◊Õß‡ªìπ ◊ËÕ∑’Ë¥’ „π°“√‡®√‘≠‡µ‘∫‚µ¢Õß ·∫§∑’‡√’¬ °“√µ‘¥‡™◊ÕÈ ´È”·≈â«´È”Õ’°∑”„Àâ¡’ fibrosis „π connective tissue ™—Èπº‘«Àπ—ß‡æ‘Ë¡¡“°¢÷Èπ ∂â“‡√‘Ë¡°≈“¬‡ªìπ chronic lymphedema º‘«Àπ—ß®–Àπ“ ¡’ hyperkeratosis ·≈–°≈“¬‡ªìπ non-pitting edema „π∑’ Ë ¥ÿ (√Ÿª∑’Ë 25.6, 25.7) primary lymphedema ·∫àßÕÕ°µ“¡Õ“¬ÿ∑’Ë‡°‘¥¢÷Èπ‰¥â‡ªìπ (µ“√“ß∑’Ë 25.2)

1. congenital lymphedema æ∫‰¥âµ—Èß·µà·√°§≈Õ¥‡™àπ Milroyûs disease 2. lymphedema praecox æ∫‰¥â „π™à«ßÀπÿ¡à “« 3. lymphedema tarda æ∫„π«—¬°≈“ß§πÀ√◊ÕÕ“¬ÿ¡“°°«à“ 35 ªï benign tumor of lymphatics ·∫àßÕÕ°‡ªìπ 1. lymphangioma simplex ª√–°Õ∫¥â « ¬∑à Õ πÈ”‡À≈◊Õß¢π“¥‡≈Á°‡∑à“°—∫À≈Õ¥‡≈◊Õ¥ΩÕ¬®”π«π¡“° 2. cavernous lymphangioma ª√–°Õ∫¥â « ¬ ∑à Õ πÈ”‡À≈◊Õß∑’¢Ë ¬“¬„À≠à·≈–§≈ÿ¡¥â«¬ fibrous adventitia 3. cystic lymphangioma À√◊Õ cystic hygroma acquired lymphedema ‡°‘¥®“°°“√ºà“µ—¥‡Õ“ÕÕ°À√◊Õ Ÿ≠ ‡ ’¬Àπâ“∑’Ë¢Õß axillary ·≈– inguinal nodes ®“°°“√ºà“µ—¥

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µ“√“ß∑’Ë 25.4 °“√·¬°√–À«à“ß venous °—∫ lymphatic edema

Venous 1. ª√–«—µ‘

‰¡à¡ª’ √–«—µ‘

Firm ‰¡à¬∫ÿ ∫«¡ À≈—ß®“°πÕπ¬°¢“ Ÿß º‘«Àπ—ß‡ª≈’¬Ë π·ª≈ß·µà ‰¡à¡·’ º≈

4. 5.

√Ÿª∑’Ë 25.7 ºŸâªÉ«¬√“¬‡¥’¬«°—π°—∫√Ÿª∑’Ë 25.6 · ¥ß„Àâ‡ÀÁπ çbuffalo humpé edema ∫√‘‡«≥À≈—ß‡∑â“ ·≈– çstemnerûs signé À√◊Õ squared toes ¢Õßπ‘È«‡∑â“

√—ß ’∫”∫—¥ ¡–‡√Áß·æ√à°√–®“¬ °“√Õ—°‡ ∫µ‘¥‡™◊ÕÈ À√◊Õª√ ‘µ ‡™àπ Wuchereria bancrofti ∑”„Àâ‡°‘¥‚√§‡∑â“™â“ß √âÕ¬≈– 10-15 ¢ÕßºŸªâ «É ¬¡–‡√Áß‡µâ“π¡∑’µË Õâ ßºà“µ—¥ radical mastectomy À≈—ß ºà“µ—¥®–‡°‘¥ postmastectomy lymphedema ·≈–Õÿ∫—µ‘ °“√≥å®– Ÿß¢÷πÈ ∂â“√à«¡°—∫√—ß ’∫”∫—¥

°“√«‘π‘®©—¬·¬°‚√§ ®“°ª√–«—µ·‘ ≈–°“√µ√«®√à“ß°“¬(11) lymphedema ®–æ∫ «à“¡’ gradual onset of edema ‡√‘¡Ë ®“°¢âÕ‡∑â“≈“¡¢÷πÈ ¡“‡√◊ÕË ¬ Ê „π‡æ»À≠‘ß®–æ∫™à«ßµ—Èß§√√¿åÀ√◊Õª√–®”‡¥◊Õπ„°≈âÀ¡¥ µâÕß ·¬°®“°§«“¡º‘¥ª°µ‘·µà°”‡π‘¥ ´÷ßË ‡ªìπ vascular malformation ‡™àπ Klippel-Trenauney syndrome ·≈– Parkes-Weber syndrome „π venous edema ®–¡’°“√≈¥≈ß¢Õß capillary perfusion º‘«Àπ—ß ’§≈È” ¡’·º≈‡√◊ÈÕ√—ß∫√‘‡«≥¢âÕ‡∑â“ πÕπ¬°¢“ Ÿß ®–¬ÿ∫¿“¬„π«—π·√° µà“ß®“° lymphedema ´÷ËßπÕπ¬°¢“ Ÿß À≈“¬«—π®÷ß¬ÿ∫∫«¡ (µ“√“ß∑’Ë 25.4) «‘π®‘ ©—¬‚√§·≈–·¬°‚√§‰¥â ‚¥¬°“√∑” venography, lymphangiography CT scan ®–æ∫

‡§¬‡ªìπ phlebitis ¡“°àÕπ °“√µ√«®√à“ß°“¬ πÿ¡à µàÕ¡“ firm, °“√∫«¡®–¬ÿ∫≈ß ∂â“πÕπ¬°¢“ Ÿß Õ“°“√· ¥ßÕ◊πË √à«¡ Varicosities, pigmentation ·º≈‡√◊ÕÈ √—ß∫√‘‡«≥ ¢âÕ‡∑â“ Phlebography + result Lymphangiography rusults

Lymphatic

çhoney combé pattern ∫√‘‡«≥ compartments „µâº‘«Àπ—ß ·≈–§«√·¬°‚√§®“° hematoma, obesity, Bakerûs cyst, osteoarthritis, trauma induced reflex sympathetic dystrophy ·≈– lipidemia µâÕß·¬°‚√§®“° Yellow Nail Syndrome (YNS) ´÷Ëß‡°‘¥®“°°“√√–∫“¬πÈ”‡À≈◊Õß∫√‘‡«≥™àÕßßà“¡π‘È«‰¡à ¥’ Õ“°“√·≈–Õ“°“√· ¥ß∑’ Ë ”§—≠¢Õß YNS ¡’ (12) 1. yellow dystrophic À√◊Õ clubbing of the nail 2. primary lymphedema 3. bilateral effusion

°“√µ√«®«‘π‘®©—¬ noninvasive studies ‚¥¬°“√«—¥¢π“¥‡ âπ√Õ∫«ß¢Õß·¢π ·≈–¢“ ·≈– water volume displacement ‡ª√’¬∫‡∑’¬∫°—∫ ¢â“ß∑’Ëª°µ‘ °“√«—¥‡ âπ√Õ∫«ß§«√«—¥µÕπ‡¬ÁπÀ≈—ß®“°‡¥‘πÀ√◊Õ ∑”ß“π¡“Õ¬à“ß‡µÁ¡∑’·Ë ≈â« imaging studies 1. Lymphoscintigraphy ‡ªìπ«‘∏‡’ ≈◊Õ°„π°“√«‘π®‘ ©—¬‚√§ lymphedema «‘∏°’ “√Àπ÷ßË ·≈–‡ªìπ noninvasive study –¥«°µàÕºŸªâ «É ¬·≈–ºŸµâ √«® «‘∏°’ “√§◊Õ„ÀâºªŸâ «É ¬πÕπÀß“¬ ©’¥ radiolabeled antimony trisufide À√◊Õ human serum albumin (HSA) ‡¢â“„π™—πÈ interstitial space

238 µ√ßßà“¡π‘«È ·≈–∂à“¬¿“æ√—ß ’·¢πÀ√◊Õ¢“ ‚¥¬„™â dual head gamma counter ¥Ÿ°“√°√–®“¬¢Õß radiolabelled colloid „π∑àÕπÈ”‡À≈◊Õß «à“¡’§«“¡º‘¥ª°µ‘ Õ¬à“ß‰√∫â“ß ¡’§«“¡·πàπÕπ„π°“√«‘π®‘ ©—¬ lymphedema ‰¥â√Õâ ¬≈– 92-100(13) lymphoscintigram ®–∂◊Õ«à“º‘¥ª°µ‘µÕà ‡¡◊ÕË (14,15) 1. °“√°—¡¡—πµ¿“æ√—ß ’ ‰¡à‡®◊Õ®“ß≈ßÀ√◊Õ‡®◊Õ®“ß≈ß ‡≈Á°πâÕ¬∫√‘‡«≥©’¥ 2. ¡’ dermal backflow (cutaneous pattern) À√◊Õ collaterals 3. ‰¡à ¡’ ° “√ uptake ¢Õß “√°— ¡ ¡— π µ¿“æ√— ß ’ „ π µàÕ¡πÈ”‡À≈◊Õß¢â“ß‡§’¬ß 4. ¡’ abnormal tracer accumulation ®÷ßÕ“®®–‡°‘¥ extravasation, lymphocele À√◊Õ lymphangiectasia. 2. Computed tomography À√◊Õ CT scan ‡æ◊ÕË µ√«® «‘π‘®©—¬„Àâ·πàπÕπ«à“§«“¡º‘¥ª°µ‘¢Õß√–∫∫πÈ”‡À≈◊Õß ‡°‘¥®“° °âÕπ‡π◊ÕÈ ßÕ°„π™àÕß∑âÕßÀ√◊Õ∫√‘‡«≥¢“Àπ’∫°¥∑—∫ „π lymphedema lime ®“° CT scan ®–‡ÀÁπ‡ªìπ honeycomb appearance „π™—πÈ subcutaneous 3. Magnetic resonance imaging (MRI) ‡ªìπ«‘∏°’ “√ µ√«®«‘π®‘ ©—¬·∫∫ noninvasive ‡À¡“– ”À√—∫·¬°°“√ ∫«¡πÈ”‡À≈◊Õß®“°°âÕπ‡π◊ÕÈ ßÕ°‡∫’¬¥∑—∫°—∫ secondary lymphedema ‡æ√“–§«“¡‰«·≈–§«“¡·πàπÕπ Ÿß„π °“√«‘π®‘ ©—¬ vascular malformation ·≈– soft tissue tumor(16,17) „™â „π°“√«‘π®‘ ©—¬·¬°‚√§ lipedema ·≈– chronic venous edema ÕÕ°®“° lymphedema ®“° MRI ®–‡ÀÁπµàÕ¡·≈–∑àÕπÈ”‡À≈◊Õß∑’ËÕ¬Ÿà‡Àπ◊ÕµàÕ∫√‘‡«≥ ∑’∂Ë °Ÿ ‡∫’¬¥∑—∫ ´÷ßË Õ“®®–‰¡à‡ÀÁπ®“° lymphoscintigraphy 4. Lymphangiography ‡ªìπ direct lymphangiography „™â ‰¡à∫Õà ¬„π°“√«‘π®‘ ©—¬‚√§ ¡’¢Õâ ∫àß™’‡È æ◊ÕË „™â¥°Ÿ “¬ «‘¿“§¢Õß∑àÕπÈ”‡À≈◊Õß„πºŸªâ «É ¬∑’«Ë “ß·ºπ®–∑”microvascular lymphatic reconstruction À√◊Õ lymphangiectasia chylous reflux À√◊Õ chylous ascites ¥Ÿ abdominal lymph ·≈– thoracic duct(18) «‘∏°’ “√§◊Õ ‡√‘¡Ë µâπ®“°°“√©’¥ 5 ¡‘≈≈‘≈µ‘ √¢Õß‡¡∏‘≈π’ ∫≈Ÿ º ¡°— ∫ ≈‘ ‚ ¥‡§π„π∫√‘ ‡ «≥‡∑à “ °— ∫ µ√ßßà “ ¡π‘È « √Õ®π °√–∑—Ëß‡ÀÁπ dermal lymphatic outline „™â¡’¥°√’¥ º‘«Àπ—ß‡¢â“∂÷ß∑àÕπÈ”‡À≈◊Õß ·≈â«·∑ß¥â«¬‡¢Á¡¢π“¥‡≈Á°

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥ ‡∫Õ√å 27-30 À≈—ß®“°π—πÈ ©’¥ “√∑÷∫· ß (Ethiodized oil À√◊Õ Ethidol) ‡¢â“‰ª™â“ Ê ∑’¢Ë “„™â 10 ¡‘≈≈‘≈µ‘ √∑’·Ë ¢π„™â 5 ¡‘≈≈‘≈‘µ√ À≈—ß®“°π—ÈπÕ’° 24 ™—Ë«‚¡ß ∂à“¬¿“æ√—ß ’ ·¢π·≈–¢“À≈“¬∑à“‡æ◊ÕË ¥Ÿ∑Õà πÈ”‡À≈◊Õß ‚¥¬∑—«Ë ‰ª·≈â« deep ·≈– superficial lymphatic system ®–‰¡àµ¥‘ µàÕ°—π ∂â“µâÕß°“√¥Ÿ deep system µâÕß ©’¥ ’‡¢â“ deep lymphatic ´÷ßË Õ¬ŸÀà ≈—ßµàÕ medial malleolus ´÷ßË Õ¬Ÿà „°≈â°∫— posterior tibial vessels. ¿“«–·∑√°´âÕπ®“°°“√∑” lymphangiogram §◊Õ lymphangitis, ·º≈µ‘¥‡™◊ÕÈ , cellulitis, ·æâ “√∑÷∫· ß, pulmonary embolism, ¡’ ’µ‘¥º‘«Àπ—ßπà“‡°≈’¬¥ œ≈œ Õ“®®–æ∫«à“¡’‰¢â, Àπ“« —πË , §≈◊πË ‰ âÕ“‡®’¬π, ª«¥»’√…– ·≈–ª«¥¢âÕ

NONOPERATIVE MANAGEMENT ª√–¡“≥√âÕ¬≈– 90 √—°…“‰¥â ‚¥¬‰¡àµÕâ ßºà“µ—¥ (µ“√“ß∑’Ë 25.5) ∂â“¡’°“√Õ—°‡ ∫µ‘¥‡™◊ÈÕ‡°‘¥¢÷Èπ √—°…“‚¥¬°“√„Àâ¬“ªØ‘™’«π– ¬° ¢“ Ÿß·≈– compression ∂â“‡°‘¥®“°ª√ ‘µ‡™àπ W. bencrofti ·≈– Brugia malayi §«√√—°…“‚¥¬°“√„Àâ diethylcarbamazine (Ivermectin) √à«¡°—∫¬“µâ“π°“√Õ—°‡ ∫·≈– antihistamine ‡æ◊ËÕªÑÕß°—π°“√‡°‘¥ irreversible fibrosis ‚¥¬∑—Ë«‰ª·≈â« À≈—°°“√√—°…“‚√§ lymphedema §◊Õ °“√¬°·¢πÀ√◊Õ¢“ Ÿß√à«¡°—∫ compression ·≈–ªÑÕß°—π°“√Õ—°‡ ∫µ‘¥‡™◊ÈÕ Õ“®®–„™â ‰¡âÀπÿπ √Õß âπ‡∑â“ Ÿß 15 ‡´Áπµ‘‡¡µ√ ·≈–æ—π¢“¥â«¬ elastic stocking ¬“«®“°ª≈“¬‡∑â“(19) ¬“¢—∫ªí “«–®–≈¥°“√∫«¡πÈ”‰¥â ·µà ‰¡à§«√ „™âÕ¬à“ßµàÕ‡π◊ÕË ß‡æ√“–®–∑”„Àâ‡≈◊Õ¥¢âπ §«√„™â long-acting thiazide ≈—∫°—π°—∫ potassium sparing diuretics. benzopyrones ®–°√–µÿπâ °“√∑”ß“π¢Õß tissue macrophages ∑”„Àâ ‚ª√µ’π·≈– collagen „π‡π◊ÈÕ‡¬◊ËÕ∑’Ë∫«¡πÈ”‡À≈◊Õß ≈“¬µ—« ·¢πÀ√◊Õ¢“∑’Ë µ“√“ß∑’Ë 25.5 Nonoperative Treatment of Primary Lymphedema

1. Elevation - foot or bed raised 6 inches. 2. External compressin - elastic stocking in termittent compression unit. 3. Diuretics 4. Avoidance of infection - foot hygine (cleansing, antifungal agent): antibiotics early.

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‚√§¢Õß√–∫∫πÈ”‡À≈◊Õß ∫«¡®–πÿ¡à ·≈–¡’¢π“¥≈¥≈ß µâÕß„™â¬“Õ¬à“ßµàÕ‡π◊ÕË ß‰¡àµË”°«à“ 10 ‡¥◊Õπ ®÷ß®–‰¥âº≈(20) °“√µ‘¥‡™◊ÕÈ ¢Õß‡π◊ÕÈ ‡¬◊ÕË ∑’∫Ë «¡πÈ”‡À≈◊Õß‡°‘¥®“°‡™◊ÕÈ streptococcus §«√¥Ÿ·≈‡Õ“„®„ à·≈–∑”§«“¡ –Õ“¥‡∑â“ ªÑÕß°—π°“√ µ‘¥‡™◊ÈÕ ‡√‘Ë¡µâπ°“√√—°…“‚¥¬„Àâ penicillin °“√µ‘¥‡™◊ÈÕ∑’Ë‡°‘¥¢÷Èπ ·µà≈–§√—ßÈ ®–∑”„Àâ tissue fibrosis ‡°‘¥¡“°¢÷πÈ mechanical reduction „π chronic lymphedema ®– ‡°‘¥ fibrosis ·≈– brawny edema „π‡π◊ÕÈ ‡¬◊ÕË ∑’∫Ë «¡πÈ”‡À≈◊Õß Õ¬à“ß∂“«√ ∂÷ß·¡â«à“®–∑”„Àâ¢π“¥¢Õß¢“∑’Ë∫«¡≈¥≈ß®“° mechanical reduction °“√√—°…“∑’Ë ‰¥âº≈§«√„ÀâºŸâªÉ«¬æ—°Õ¬Ÿà „π ‚√ßæ¬“∫“≈ ¬°¢“ Ÿß∑”¡ÿ¡ 45o C ‚¥¬¡’µ“√“ß°“√π«¥¢“Õ¬à“ß µàÕ‡π◊ËÕßÀ√◊Õ manual lymphatic drainage (MLD) ®– ∑”„ÀâπÈ”‡À≈◊Õß‰À≈‡«’¬π·≈–‡π◊ÕÈ ‡¬◊ÕË πÿ¡à ¢÷πÈ §«√π«¥∑—ßÈ 4 quadrants ¢Õß¢“ ‡√‘¡Ë ®“°ª≈“¬‡∑â“¢÷πÈ ¡“∂÷ß¢“Àπ’∫ —ª¥“Àå≈– 2-3 §√—ßÈ µ“¡¥â«¬ external compression §◊Õ «¡ elastic stocking ∑’¡Ë §’ «“¡¥—π 40-50 ¡‘≈≈‘‡¡µ√ª√Õ∑ µ—ßÈ ·µàª≈“¬‡∑â“¢÷πÈ ¡“®π∂÷ß ¢“Àπ’∫ sequential air compression ®–™à«¬√’¥°“√∫«¡®“°¢“ ∂â“„™â pneumatic boot π«¥Õ¬à“ßµàÕ‡π◊ÕË ß ®–π«¥‰¥â∑ß—È 4 compartments „™â§«“¡¥—π„π cuff 90-100 ¡‘≈≈‘‡¡µ√ª√Õ∑ ·≈– —¥ à«π√–À«à“ß compression: decompression ‡∑à“°—∫ 1:3 „πºŸâªÉ«¬æ—°„π‚√ßæ¬“∫“≈ 2-3 «—π π«¥«—π≈– 6-8 ™—Ë«‚¡ß ¿“¬„π√–¬–‡«≈“ 3-6 ‡¥◊Õπ æ∫«à“‰¥âº≈„π°“√√—°…“√âÕ¬≈– 80 (¢π“¥≈¥≈ß√âÕ¬≈– 20) ¡’¢Õâ Àâ“¡„™â „πºŸªâ «É ¬∑’¡Ë °’ “√Õ—°‡ ∫µ‘¥‡™◊ÕÈ , DVT ·≈–Õ¬Ÿà „π¿“«–À—«„®«“¬ SURGICAL TREATMENT ¡’‡æ’¬ß√âÕ¬≈– 5-10 ¢ÕßºŸªâ «É ¬ lymphedema ∑’¡Ë §’ «“¡®”‡ªìπ ∑’®Ë –µâÕß√—°…“‚¥¬°“√ºà“µ—¥‚¥¬¡’¢Õâ ∫àß™’¥È ß— µàÕ‰ªπ’(21) È (µ“√“ß∑’Ë 25.5) 1. ·¢πÀ√◊Õ¢“∫«¡‚µ¡“°®π°√–∑—Ëß‰¡à “¡“√∂‡§≈◊ËÕπ‰À« ∑”ß“πÀ√◊ÕªØ‘∫µ— °‘ ®‘ «—µ√ª√–®”«—π‰¥âµ“¡ª°µ‘ 2. ¡’°“√Õ—°‡ ∫µ‘¥‡™◊ÕÈ cellulitis ·≈– lymphangitis ´È” À≈“¬§√—ßÈ 3. ¡’ intractable pain 4. °≈“¬‡ªìπ lymphangiosarcoma °“√ºà“µ—¥·∫àßÕÕ°‡ªìπ 2 «‘∏§’ Õ◊ excisinal procedures °—∫ lymphatic reconstruction

µ“√“ß∑’Ë 25.5 ·π«∑“ß°“√√—°…“‚√§√–∫∫πÈ”‡À≈◊Õß 1. ‡æ‘¡Ë tissue tension ‚¥¬°“√æ—π·∂∫ºâ“¬“ß¬◊¥À√◊Õ «¡ ∂ÿß‡∑â“¬“ß¬◊¥ 2. gravitational drainage of fluid 3. dehydration ‚¥¬°“√„™â¬“¢—∫ªí “«– 4. ªÑÕß°—π°“√µ‘¥‡™◊ÕÈ ‚¥¬„™â¬“ªØ‘™«’ π– 5. ºà“µ—¥‡Õ“‡π◊ÕÈ ‡¬◊ÕË ∑’‡Ë ªìπ‚√§ÕÕ° 6. surgical reconstruction of the lymphatic drainage

1. Excisional operations ‡ªìπ°“√ºà“µ—¥‡≈“–‡Õ“‡π◊ÕÈ ‡¬◊ÕË ∑’∫Ë «¡πÈ”‡À≈◊ÕßÕÕ°‚¥¬„Àâ¡º’ «‘ Àπ—ß§≈ÿ¡¢“‰«â‡À¡◊Õπ‡¥‘¡ 1.1 Charleûs operation ‡ªìπ«‘∏º’ “à µ—¥∑’µË Õâ ßµ—¥‡Õ“º‘«Àπ—ß ·≈– subcutaneous tissue ÕÕ°®“° tibial tuberosity ≈ß¡“®π∂÷ß malleoli (√Ÿª∑’Ë 25.8) ∂â“ deep fascia ¡’ fibrosis °ÁµâÕß‡≈“–ÕÕ°¥â«¬ ¥â“π‡Àπ◊Õ·≈–„µâµàÕ ∫√‘‡«≥∑’Ëµ—¥ÕÕ°µâÕß‡¬Á∫®’∫‡¢â“À“°—π‰¡à „Àâπà“‡°≈’¬¥ ‡Õ“º‘«Àπ—ß¢“¥â“πµ√ß°—π¢â“¡¡“ª≈Ÿ°·∫∫ STSG À√◊Õ full thickness ªí≠À“∑’Ëæ∫∫àÕ¬®“°°“√ºà“µ—¥«‘∏’π’È§◊Õ º‘«Àπ—ß∑’Ëª≈Ÿ°‰«â®–À≈ÿ¥≈Õ°‰¥âßà“¬ ‚¥¬‡©æ“–ºŸâªÉ«¬∑’Ë ‡§¬¡’°“√Õ—°‡ ∫µ‘¥‡™◊ÕÈ ´È”À≈“¬§√—ßÈ ·º≈‡ªìππà“‡°≈’¬¥ ‡ªìπ‚√§º‘«Àπ—ß‰¥âß“à ¬ ‡À¡“– ”À√—∫ºŸªâ «É ¬∑’ºË “à µ—¥∑” lymphatic reconstruction À√◊Õ flap procedures ‰¡à ‰¥â º≈°“√√—°…“„π√–¬–¬“«§àÕπ¢â“ß¥’

·π«≈ß¡’¥∑’Ëº‘«Àπ—ß ‡¬◊ËÕ„µâº‘«Àπ—ß∑’Ëµ—¥ÕÕ°

√Ÿª∑’Ë 25.8 Charleûs operation ‡ªìπ°“√ºà“µ—¥‡Õ“º‘«Àπ—ß·≈– subcutaneous tissue ÕÕ° ·≈â«‡Õ“º‘«Àπ—ß®“°¢“¥â“π µ√ß°—π¢â“¡ª≈Ÿ°§≈ÿ¡‡π◊ÈÕ‡¬◊ËÕ∑’Ë∂Ÿ°µ—¥ÕÕ°‰ª

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»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥

Touniquet

3 πâ‘«¡◊Õ„µâ °√–¥Ÿ° –∫â“

·π«≈ß¡’¥∑’Ëº‘«Àπ—ß º‘«Àπ—ß·≈–‡¬◊ËÕ„µâº‘«Àπ—ß∑’Ëµ—¥ÕÕ° µ—¥‡¬◊ËÕ„µâº‘«Àπ—ßÕÕ°Õ¬à“ß‡¥’¬«

√Ÿª∑’Ë 25.9 Homanûs operation ‡ªìπ«‘∏’°“√ºà“µ—¥‡Õ“ fibrosed subcutaneous tissue ÕÕ° ·µà ‡ °Á ∫ º‘ « Àπ— ß ‡Õ“‰«â ”À√—∫‡¬Á∫§≈ÿ¡°≈—∫

1.2 Modified Homanûs procedure ‡ªìπ«‘∏’µ—¥‡Õ“ fibrosed subcutaneous tissue ÕÕ° ·µà‡°Á∫º‘«Àπ—ß ‡Õ“‰«â „™â pneumatic torniquet æ—π√—¥µâπ¢“¢≥– ºà“µ—¥®–™à«¬≈¥°“√‡ ’¬‡≈◊Õ¥≈ß medial skin incision ®“° 1 ‡´Áπµ‘‡¡µ√À≈—ß tibial border ‡ªìπ·π«¬“« µ—¥‡Õ“ subctuaneous tissue ÕÕ°„ÀâÀ¡¥ ‡À≈◊Õº‘«Àπ—ß 1-1.5 ‡´Áπµ‘‡¡µ√ ‡¬Á∫ skin flap ·∫∫ interrupt „Àâµ¥‘ °—∫ facia (√Ÿª∑’Ë 25.9) «“ß∑àÕ√–∫“¬‰«â À≈—ßºà“µ—¥Õ“®®– °≈—∫‡ªìπ´È”‰¥â ®÷ß§«√ «¡ elastic stocking µàÕÕ’° √–¬–Àπ÷ßË ·≈–§ÿ¡Õ“À“√ «‘∏°’ “√ºà“µ—¥π’√È °— …“‰¥âº≈√âÕ¬≈– 65-80 ¢π“¥¢Õß¢“®–‡≈Á°≈ß¡“° ∑”„Àâ‡¥‘π‰¥â –¥«° 1.3 Thompsonûs procedure ‡ªìπ°“√ºà“µ—¥¬â“¬‡π◊ÕÈ ‡¬◊ÕË ∑’¡Ë ∑’ Õà πÈ”‡À≈◊Õßª°µ‘ ‰ª¬—ß∫√‘‡«≥∑’¡Ë ª’ ≠ í À“ §◊Õ subcutaneous flap procedure µ—¥‡Õ“‡π◊ÕÈ ‡¬◊ÕË ∑’¡Ë ª’ ≠ í À“ÕÕ°‰ª √â“ß longitudinal dermis flap À≈—ß®“°µ—¥™—πÈ subcutaneous flap ÕÕ°·≈â«‡¬Á∫¢Õ∫ flap µ‘¥°—∫ deep muscular compartment (√Ÿª∑’Ë 25.10) ‡æ◊ËÕ®ÿ¥¡ÿàßÀ¡“¬ „π°“√ √â“ß∑àÕ‡™◊ÕË ¡µàÕπÈ”‡À≈◊Õß„À¡à√–À«à“ß subdermal lymphatic plexus °—∫ deep lymphatic channels º≈°“√ºà“µ—¥√—°…“‰¡à¥‰’ ª°«à“ Homanûs procedure 2. Lymphatic reconstruction °“√∑”„Àâ√–∫∫°“√∂à“¬ πÈ”‡À≈◊Õß¥’¢π÷È ‡ªìπ«‘∏°’ “√√—°…“∑’¥Ë ∑’ ’Ë ¥ÿ ”À√—∫ lymphatic obstruction ºŸªâ «É ¬∫“ß√“¬®–¡’ spontaneous lymphovenous anas-

tomosis ‡°‘¥¢÷πÈ ‡Õß «‘∏°’ “√‡°à“ Ê §◊Õ omentel implantation À√◊Õ„™â segment ¢Õß≈”‰ â‡≈Á°‰Õ‡≈’¬Ë ¡ ¡“‡¬Á∫ patch (mesenteric bride operation) ‡æ◊ËÕ √â“ß∑àÕ‡™◊ËÕ¡µàÕ√–∫“¬πÈ”‡À≈◊Õß ¢÷Èπ¡“„À¡à µàÕ¡“‰¥â¡’°“√ºà“µ—¥∑“ß®ÿ≈»—≈¬°√√¡‡æ◊ËÕ √â“ß·≈– ·°â ‰¢§«“¡º‘¥ª°µ‘¢Õß∑àÕπÈ”‡À≈◊Õß‚¥¬µ√ß „π primary lymphedema ®–‡ªìπ diffuse disease ∑àÕπÈ”‡À≈◊Õß‰¡à ‚µæÕ∑’Ë®– ºà“µ—¥·°â ‰¢§«“¡º‘¥ª°µ‘À√◊ÕµàÕ‡™◊ÕË ¡‰¥â 2.1 lymphovenous anastomosis ‡√‘¡Ë ®“°°“√ —ß‡°µÿæ∫ «à“ºŸªâ «É ¬ chronic lymphedema ∫“ß√“¬®–¡’ spontaneous lymphovenous anastomosis ¥Ÿ®“° lymphangiography æ∫«à“‡ªìπ compensatory mechanism §«√ºà“µ—¥√—°…“°àÕπºŸªâ «É ¬®–¡’ subcutaneous fibrosis ·≈–°“√µ’∫·¢Áßµ—«¢Õß∑àÕπÈ”‡À≈◊Õß ºà“µ—¥‚¥¬«‘∏’°“√ ∑“ß®ÿ≈»—≈¬°√¡(22,23) ¢âÕ∫àß™’ È ”À√—∫°“√ºà“µ—¥«‘∏π’ ¡’È π’ Õâ ¬ ºŸªâ «É ¬®–µâÕß‡ªìπ secondary lymphedema „π√–¬–·√° ‰¡à‡§¬‡ªìπ cellulitis ·≈– lymphangitis ·µà‡§¬√—°…“ ·∫∫ conservative ¡“°àÕπÀπâ“π’·È ≈â« §«√∑” lymphangiography ¥Ÿ∑Õà πÈ”‡À≈◊Õß·≈– CT scan ¥Ÿ°âÕπ‡π◊ÈÕßÕ°∑’Ë°¥∑—∫∑àÕπÈ”‡À≈◊Õß ¢âÕÀâ“¡ ”§—≠„π°“√ºà“µ—¥«‘∏π’ §’È Õ◊ ¿“«– venous hypertension °àÕπºà“µ—¥„ÀâºªŸâ «É ¬πÕπæ—°„π‚√ßæ¬“∫“≈ 24-48 ™—«Ë ‚¡ß ¬°¢“ Ÿß√à«¡°—∫ intermittent compression „Àâ¢“¬ÿ∫ ∫«¡≈ß∫â“ß ‰¥âº≈„π°“√√—°…“√–¬–¬“«√âÕ¬≈– 42(24,25) 2.2 lymphatic grafting ‰¥âº≈¥’°«à“ lymphovenous anastomosis ‚¥¬‡©æ“– postmastectomy lymphedema(26) ‡≈“–‡Õ“∑àÕπÈ”‡À≈◊Õß®“°∫√‘‡«≥¢“¡“µàÕ∑’·Ë ¢π ‚¥¬«‘∏∑’ “ß®ÿ≈»—≈¬°√√¡

PRIMARY CHYLOUS DISORDERS πÈ”‡À≈◊Õß¡’§≥ ÿ ¡∫—µª‘ √“»®“°‡™◊ÕÈ , ‰¡à¡°’ ≈‘πË , ¡’ƒ∑∏‘‡Ï ªìπ¥à“ß ª√‘¡“≥‚ª√µ’π 1 °√—¡µàÕ‡¥´‘≈µ‘ √ (100 ¡‘≈≈‘≈µ‘ √) ·≈–‰¢¡—π 0.44 °√—¡µàÕ‡¥´‘≈µ‘ √ °“√¡’πÈ”‡À≈◊Õß§—ËßÕ¬Ÿàµ“¡∫√‘‡«≥µà“ß Ê ∑—Ë«√à“ß°“¬ πÕ° ∑àÕπÈ”‡À≈◊Õß∂◊Õ«à“º‘¥ª°µ‘ primary chylous disorders ‡°‘¥‰¥â®“° congenital lymphangiectasia À√◊Õ megalymphatics √à«¡°—∫°“√Õÿ¥µ—πÀ√◊Õ∂Ÿ°°¥∑—∫¢Õß∑àÕπÈ”‡À≈◊Õß (thoracic duct À√◊Õ main lymphatic trunk) Primary chylous disorders ª√–°Õ∫¥â«¬ chylous reflux, chylous ascites, ·≈– chylothorax (µ“√“ß∑’Ë 25.6) „π

241

‚√§¢Õß√–∫∫πÈ”‡À≈◊Õß

Tibialis ant. m.

Ext. hallucis longus m.

√Ÿª∑’Ë 25.10 Buried dermis flap (Thompsonûs procedure) ‡ªìπ«‘∏’°“√µ—¥‡Õ“‡π◊ÈÕ‡¬◊ËÕ∑’Ë¡’ªí≠À“ÕÕ° √â“ß longitudinal demis flap ·≈â«‡¬Á∫ ¢Õ∫ flap °—∫ deep muscular compartment

242 µ“√“ß∑’Ë 25.6 Primary Chylous Disorders. Essential of Diagnosis 1. Protein - rich, fatty lymph (chyle) accumulations in a body cavities. 2. Chylous fluid with specific gravity greater than 1.012 g/dL, protein greater than 3 g/dL, and fat content 0.4-4 g/dL. 3. Incompetent lymphatic valve. 4. Dilatation of lymphatics (lymphangiectasia). 5. Chylorrhea lymph - filled vesicles in the lower extremity or perineum.

ºŸªâ «É ¬‡À≈à“π’ÕÈ “®®–¡’ valvular incompetent ¢Õß∑àÕπÈ”‡À≈◊Õß ∑”„ÀâπÈ”‡À≈◊Õß‰À≈¬âÕπ°≈—∫§—ßË √«¡°—π∑’¢Ë “ ≈Ÿ°Õ—π±– ·≈– perineum °“√¡’πÈ”‡À≈◊Õß§—ËßÕ¬Ÿàµ“¡∫√‘‡«≥¥—ß°≈à“«∑”„ÀâºŸâªÉ«¬ √”§“≠¡“° °“√‰À≈∑âπ¬âÕπ°≈—∫¢ÕßπÈ”‡À≈◊Õß„π‰µ®–∑”„Àâ‡°‘¥ chyuria ∂â“‡¢â“„π™àÕß∑âÕßÀ√◊Õ∑√«ßÕ°®–‡ªìπ chyloperitoneum À√◊Õ chylothorax ∫√‘‡«≥∑’ËπÈ”‡À≈◊Õß§—Ëß‰¥â‡™àπ ªÕ¥ ™àÕß‡¬◊ËÕ Àÿâ¡À—«„® tracheobronchial tree °“√‡ ’¬πÈ”‡À≈◊Õß„π∑“ß‡¥‘π Õ“À“√Õ¬à“ßµàÕ‡π◊ÕË ß®–∑”„Àâ‡°‘¥¿“«– protein-losing enteropathy Secondary chylous disorders ‡°‘¥®“°Õÿ∫—µ‘‡Àµÿ°“√ ∫“¥‡®Á∫À√◊Õ¡–‡√Áß ‚√§ lymphoma ∑”„Àâ‡°‘¥°“√Õÿ¥µ—π¢Õß∑àÕ πÈ”‡À≈◊Õß §«“¡º‘¥æ≈“¥„π°“√ºà“µ—¥Õ“®®–∑”„Àâ‡°‘¥ Chylous ascites ·≈– chylothorax ‰¥â

Õ“°“√· ¥ß∑“ß§≈‘π‘§ ∂â“¡’°“√ Ÿ≠‡ ’¬πÈ”‡À≈◊Õß®“°∑àÕπÈ”‡À≈◊Õß‡¢â“ Ÿà ‚æ√ßµà“ß Ê ¢Õß√à“ß°“¬ ‡™àπ ™àÕß∑âÕß À√◊Õ™àÕß∑√«ßÕ°Õ¬à“ßµàÕ‡π◊ÕË ß ®– ∑”„Àâ√à“ß°“¬¡’°“√‡ª≈’Ë¬π·ª≈ß∑“ß‡¡µ“‚∫≈‘ ¡å·≈–∑ÿ‚ ¿™π“°“√Õ¬à“ß¡“° ‚¥¬‡©æ“–°“√‡ ’¬‰¢¡—π·≈–‚ª√µ’π πÕ°®“° ¿“«–∑ÿ‚¿™π“°“√·≈â«®–‡°‘¥¿“«– hypocalcemia, hypocholesterolemia, lymphopenia ·≈–‚≈À‘µ®“ß §«“¡µâ“π∑“π‚√§®– ≈¥≈ß ‡°‘¥°“√µ‘¥‡™◊ÈÕ‚√§√–∫∫∑“ß‡¥‘πÀ“¬„®·≈–∑“ß‡¥‘π ªí “«–‰¥âßà“¬ ∂â“πÈ”‡À≈◊Õß§—ËßÕ¬Ÿà∫√‘‡«≥„¥∫√‘‡«≥Àπ÷Ëß®–¡’µÿà¡ πÈ”„µâº«‘ Àπ—ß‡°‘¥¢÷πÈ ‡ªìπ vesicles „π chylous ascites ∑àÕ®– ·πàπµ÷ß¡“° ‡®“–¥Ÿ¥πÈ”ÕÕ°¡“µ√«®æ∫«à“‡ªìππÈ”‡À≈◊Õß‡™àπ ‡¥’¬«°—∫¿“«– chylothorax πÈ”∑’‡Ë ®“–ÕÕ°¡“‰¥â§«√∑” Sudan fat

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥ stain ‡æ◊ËÕ«‘π‘®©—¬«à“¡’‰¢¡—πÕ¬Ÿà „ππÈ”‡À≈◊Õß®√‘ßÀ√◊Õ‰¡à °“√∑” contrasty lymphangiography ®–∑”„Àâ¡Õß‡ÀÁπ√Õ¬√—Ë«À√◊Õ ∫√‘‡«≥∑’ÕË ¥ÿ µ—π¢Õß∑àÕπÈ”‡À≈◊Õß „π primary chylous ascites §«√∑” CT scan À√◊Õ MRI À“¥Ÿµ”·Àπàß¢Õß°âÕπ‡π◊ÕÈ ßÕ°°àÕπ ∑”°“√√—°…“

°“√«‘π‘®©—¬·¬°‚√§ chylous vesicles ∑’æË ∫µ“¡º‘«Àπ—ß‡°‘¥®“° valvular incompetent „π∑àÕπÈ”‡À≈◊Õß §«√·¬°®“°‚√§¿Ÿ¡‘·æâÀ√◊Õ°“√µ‘¥‡™◊ÈÕ ‚¥¬‡®“–¥Ÿ¥πÈ”ÕÕ°¡“¬âÕ¡ ’°√—¡ ·≈–‡æ“–‡™◊ÕÈ chylous ascites À√◊Õ chylothorax §«√‡®“–¥Ÿ¥πÈ”‡À≈◊ÕßÕÕ°¡“µ√«®∑“ß‡§¡’¥Ÿ à«πª√–°Õ∫¢Õß‰¢¡—π ‚ª√µ’π·≈–‡´≈≈å∑º’Ë ¥‘ ª°µ‘ ascites ·≈– pleural effusion Õ“®®–¡’ “‡Àµÿ¡“®“°¿“«–À—«„®«“¬, ¡–‡√Áß ·≈–°“√µ‘¥‡™◊ÕÈ §«√·¬°‚√§ÕÕ°„Àâ ‰¥â

°“√√—°…“ ∑“ßÕ“¬ÿ√°√√¡ ®ÿ¥¡ÿßà À¡“¬§◊Õ ≈¥°“√º≈‘µπÈ”‡À≈◊Õß ‚¥¬ ≈¥Õ“À“√∑’¡Ë ’‚¶‡≈ ‡µÕ√Õ≈·≈–‰¢¡—π √—∫ª√–∑“πÕ“À“√∑’¡Ë ’ medium-chain triglyceride À√◊Õ„Àâ TPN ‡ªìπ°“√§«∫§ÿ¡°“√ º≈‘µ·≈–°“√∑—π°—∫¢ÕßπÈ”‡À≈◊ÕßÕÕ°®“°∑àÕ §«√∑¥·∑π°“√ ‡ ’¬‚ª√µ’π·≈–·§≈‡´’¬Ë ¡„π chylous ascites ·≈– chylothorax Õ“®®–Õ÷¥Õ—¥·πàπ∑âÕßÀ√◊ÕÀ“¬„®≈”∫“° §«√‡®“–¥Ÿ¥‡Õ“πÈ”‡À≈◊Õß ÕÕ°‡ªìπ§√—ßÈ §√“« ∑“ß»—≈¬°√√¡ §◊Õ°“√‡≈“–‡Õ“ÕÕ°À√◊ÕºŸ°µ—¥∑àÕπÈ”‡À≈◊Õß∑’Ë ¡’ª≠ í À“ °àÕπºà“µ—¥ 4 ™—«Ë ‚¡ß„ÀâºªŸâ «É ¬√—∫ª√–∑“πÕ“À“√∑’¡Ë ‰’ ¢¡—π Ÿß ‡æ◊ÕË ∑’®Ë –¥Ÿµ”·Àπàß√Õ¬√—«Ë ¢Õß∑àÕπÈ”·¢Áß ®–µâÕß‡ÀÁπ∑àÕπÈ”‡À≈◊Õß Õ¬à“ß™—¥‡®π‡ ’¬°àÕπ®÷ß®–ºŸ°µ—¥ Intractable, recurring primary chylous ascites ‡ªìπ¢âÕ ∫àß™’È ”§—≠„π°“√ºà“µ—¥ ºŸâªÉ«¬°≈ÿà¡π’È°“√æ¬“°√≥å ‚√§§àÕπ¢â“ß¥’ ∂â“‡ÀÁπ√Õ¬√—Ë«¢Õß∑àÕπÈ”‡À≈◊Õß ∂â“∑àÕπÈ”‡À≈◊Õß¡’ fibrosis √Õ¬√—«Ë À≈“¬·Ààß À√◊Õ hypoplasia ®–ºŸ°µ—¥‰¥â¬“° °“√ºà“µ—¥ √—°…“‰¡à§Õà ¬‰¥âº≈ §«√„™â peritoneal-venous shunt (Lee Veen) chylothorax §«√ºŸ°µ—¥∑àÕπÈ”‡À≈◊Õß∂â“∑”‰¡à ‰¥â®√‘ß Ê §«√∑” mechanical pleurodesis À√◊ÕµàÕ thoracic duct ‡¢â“°—∫ azygos vein.

243

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LYMPHATIC COMPLICATIONS OF VASCULAR SURGERY ‡π◊ËÕß®“°∑àÕπÈ”‡À≈◊ÕßÕ¬Ÿà™‘¥°—∫À≈Õ¥‡≈◊Õ¥·¥ß·≈–À≈Õ¥ ‡≈◊Õ¥¥” ¢≥–ºà“µ—¥À≈Õ¥‡≈◊Õ¥®÷ß‡°‘¥°“√°√–∑∫°√–‡∑◊Õπ‰¥âß“à ¬ À√◊Õ∂Ÿ°µ—¥¢“¥ ‡™àπ‡¥’¬«°—π°—∫µàÕ¡πÈ”‡À≈◊Õß ∂â“∫“¥‡®Á∫‡æ’¬ß ‡≈Á°πâÕ¬∑àÕπÈ”‡À≈◊Õß®– regenerate ‰¥âÕ¬à“ß√«¥‡√Á«·≈–∑” Àπâ“∑’Ë ‰¥âµ“¡ª°µ‘ ·µà∂â“∑àÕπÈ”‡À≈◊Õß¡’¢π“¥„À≠à·≈–∂Ÿ°µ—¥¢“¥ ¢≥–ºà“µ—¥ ®–‡°‘¥ postbypass edema, lymphocele (∫√‘‡«≥ ¢“Àπ’∫·≈– retroperitoneum) À√◊Õ lymphatic fistula ‡ªìπ ¿“«–·∑√°´âÕπ‰¥â chylous ascites ·≈– chylothorax ‡ªìπ ¿“«–·∑√°´âÕπ∑’æË ∫‰¥âÀ≈—ß°“√ºà“µ—¥À≈Õ¥‡≈◊Õ¥„À≠à ‡™àπ aorta À√◊Õ SVC ·≈– IVC ∫√‘‡«≥∑√«ßÕ°·≈–™àÕß∑âÕß Postbypass edema æ∫‰¥â∫Õà ¬À≈—ß°“√ºà“µ—¥ infra inguinal bypass ºŸªâ «É ¬®–‡√‘¡Ë ¡’¢“∫«¡À≈—ß®“°‡√‘¡Ë ‡¥‘π µ√«®æ∫ °“√∫«¡¡’≈°— …≥–‡ªìπ∫«¡™π‘¥°¥‰¡à∫¡ÿà ‰¡à‡®Á∫ §«√∑” duplex scan ‡æ◊ÕË ·¬°®“°‚√§ DVT √—°…“‚¥¬°“√‰¡àº“à µ—¥ πÕπ¬°¢“ Ÿß·≈– «¡ compressive stocking ∑’¡Ë §’ «“¡¥—π 30-40 ¡‘≈≈‘‡¡µ√ª√Õ∑µ√ß¢âÕ‡∑â“ ·µà®– µâÕß√–«—ß‰¡à „Àâ°¥ bypass graft „µâº«‘ Àπ—ß °“√√—°…“‚¥¬„™â¬“ ¢—∫ªí “«–, mannitol À√◊Õ corticosteroid ‰¡à ‰¥âº≈ Lymphatic fistula ¡’πÈ”‡À≈◊Õß‰À≈ÕÕ°®“°·º≈ºà“µ—¥∑’¢Ë “ Àπ’∫Õ¬à“ßµàÕ‡π◊ÕË ß‰À≈‡≈Õ–‡∑Õ–‡ª√Õ–‡ªóÕô π‡ ◊ÕÈ ºâ“À≈—ßºà“µ—¥∑—π∑’ ∂â“‡°‘¥¢÷πÈ ¿“¬À≈—ßºà“µ—¥À≈“¬‡¥◊Õπ„Àâπ°÷ ∂÷ß°“√µ‘¥‡™◊ÕÈ implanted prosthetic graft «‘π®‘ ©—¬‚√§®“° CT, white cell scan À√◊Õ lymphoscintography(27) ‡√‘¡Ë µâπ°“√√—°…“‚¥¬«‘∏°’ “√ª√–§—∫ª√–§Õß ∑”§«“¡ –Õ“¥ ·º≈ „Àâ¬“ªØ‘™«’ π–∑“ßÀ≈Õ¥‡≈◊Õ¥¥” ∂â“πÈ”‡À≈◊Õß‰¡à≈¥À≈—ß°“√ √—°…“À≈“¬«—π §«√ºà“µ—¥ºŸ°∑àÕπÈ”‡À≈◊Õß ‡√‘¡Ë ®“°©’¥ isosulfan blue dye ‡¢â“„µâº«‘ Àπ—ß√–À«à“ßßà“¡π‘«È ‡∑â“∑’Ë 1-3 ¥Ÿ∑Õà πÈ”‡À≈◊Õß ‡ªî¥·º≈ºà“µ—¥µ√ß¢“Àπ’∫ ¥Ÿ«“à ¡’ π’ È”‡ß‘π‰À≈ÕÕ°®“°∑àÕπÈ”‡À≈◊Õß ∫√‘‡«≥„¥ ‡¬Á∫ºŸ°®π°√–∑—ßË ·πà „®«à“πÈ”‡À≈◊ÕßÀ¬ÿ¥‰À≈ Lymphocele ‡ªìπ°“√§—Ëß¢ÕßπÈ”‡À≈◊Õß‡©æ“–∑’Ë√à«¡°—∫¡’ pseudocapsule Àÿâ¡ §≈”‰¥â°âÕππÿà¡ °¥‰¡à‡®Á∫∫√‘‡«≥¢“Àπ’∫ À≈—ßºà“µ—¥ bypass(28) ∂â“„™â‡¢Á¡‡®“–¥Ÿ¥∫àÕ¬ Ê ®–‡°‘¥√Ÿ∑–≈ÿ°≈“¬ ‡ªìπ fistula ∂â“ lymphocele ¡’¢π“¥„À≠à®–·πàπµ÷ß ‡®Á∫ ∑”„Àâ ·¢π¢“∫«¡ lymphocele ®–¡’∑Õà µàÕ°—∫πÈ”‡À≈◊Õßµà“ß®“° seroma

°“√∑” lymphoscintigraphy ®–™à«¬«‘π®‘ ©—¬‚√§ ultrasonography ®–™à«¬·¬°·¬– lymphocele ÕÕ°®“° hematoma À√◊Õ soft tissue infection ∂â“ lymphocele ‡°‘¥¢÷πÈ À≈—ßºà“µ—¥À≈“¬ªï ®–µâÕßπ÷°∂÷ß graft infection ‡ ¡Õ √—°…“‚¥¬„™â‡¢Á¡¥Ÿ¥‡®“–‡Õ“ “√πÈ”ÕÕ°¡“¬âÕ¡ ’°√—¡¥Ÿ«à“¡’ ‡™◊ÕÈ ·∫§∑’‡√’¬À√◊Õ‰¡à ∂â“‡ªìπ´È” §«√ºà“µ—¥√—°…“ °àÕπºà“µ—¥ ©’¥ isosulfan blue ¥Ÿ√√Ÿ «—Ë °àÕπ ‡¬Á∫ºŸ°·≈–µ—¥‡Õ“ lymphocele ÕÕ° ∂â“¡’ exposed prosthetic graft §«√À“‡π◊ÈÕ‡¬◊ËÕ °≈â“¡‡π◊ÈÕ À√◊Õº‘«Àπ—ß‡¬Á∫§≈ÿ¡‰«â chylous ascites ‡°‘¥®“°°“√ºà“µ—¥À√◊ÕÕÿ∫µ— ‡‘ Àµÿ µ—¥‡Õ“ intra-abdominal ·≈– mesentenic lymphatic channels ¢≥–ºà“µ—¥ aortic reconstruction(28) ‡ªìπ¿“«–·∑√°´âÕπ∑’æË ∫ ‰¥â ‰¡à∫àÕ¬ À≈—ßºà“µ—¥ºŸâª«¬®–Õ◊¥·πàπ∑âÕß §≈◊Ëπ‰ â Õ“‡®’¬π «‘π®‘ ©—¬‚√§‰¥â®“° CT scan ·≈–‡®“–™àÕß∑âÕß¥Ÿ¥‡Õ“πÈ”‡À≈◊Õß ÕÕ°¡“µ√«®∑“ß‡§¡’ √—°…“‚¥¬°“√‰¡àºà“µ—¥ §«∫§ÿ¡Õ“À“√·≈–‡®“–∑âÕß¥Ÿ¥‡Õ“ πÈ”‡À≈◊ÕßÕÕ°‡ªìπ√–¬– ‡¡◊ËÕ·πàπÕ◊¥∑âÕß ∂â“‰¡à ‰¥âº≈ ®÷ßºà“µ—¥ ‡¢â“‰ªºŸ°‡¬Á∫∑àÕπÈ”‡À≈◊Õß chylothorax ‡°‘¥®“°°“√∫“¥‡®Á∫µàÕ∑àÕπÈ”‡À≈◊Õß„À≠à ¿“¬„π∑√«ßÕ° À≈—ß°“√ºà“µ—¥„À≠à ‡™àπ °“√µ—¥À≈Õ¥Õ“À“√À√◊Õ aorta «‘π‘®©—¬‚√§®“°¿“æ√—ß ’ªÕ¥·≈–‡®“–¥Ÿ¥‡Õ“πÈ”‡À≈◊Õß ÕÕ°¡“µ√«®∑“ß‡§¡’ √—°…“‚¥¬°“√„ à∑àÕ√–∫“¬∑√«ßÕ°·≈–µàÕ°—∫¢«¥√–∫∫ªî¥ §«∫§ÿ¡Õ“À“√∑’Ë¡’‰¢¡—π ∂â“Õ“°“√‰¡à¥’¢÷Èπ¿“«–‡¡µ“‚∫≈‘ ¡å¢Õß √à“ß°“¬º‘¥ª°µ‘ ‡ ’¬Õ’‡≈Á§‚µ√≈—¬µåª√‘¡“≥¡“° §«√ºà“µ—¥‡¢â“‰ªºŸ° thoracic duct ∫√‘‡«≥∑’‡Ë ¢â“∂÷ß∑àÕ‰¥âß“à ¬§◊Õ à«π∑’™Ë ¥‘ °—∫°√–∫—ß ≈¡ √à«¡°—∫°“√∑” mechanical pleurodesis chemical pleurodesis ‰¡à ‰¥âº≈„π°“√√—°…“ chylothorax.

«‘∏’ªÑÕß°—π°“√‡°‘¥¿“«–·∑√°´âÕπ‡À≈à“π’È °“√ºà“µ—¥∫√‘‡«≥¢“Àπ’∫§«√≈ß·º≈ lateral µàÕ femoral artery æ¬“¬“¡‰¡à „Àâ°√–∑∫°√–‡∑◊ÕπµàÕ∑àÕπÈ”‡À≈◊Õß∫√‘‡«≥ femoral sheath ¥÷ß∑àÕπÈ”‡À≈◊Õß‰ª∑“ß medial ∂â“ºà“µ—¥‡¢â“∂÷ß popliteal ·≈– tibioperoneal arteries §«√≈ß·º≈ºà“µ—¥„π·π« vertical ‡≈“–‡æ’¬ß‡≈Á°πâÕ¬°Á®–∂÷ßÀ≈Õ¥‡≈◊Õ¥ ∂â“µ—¥∑àÕπÈ”‡À≈◊Õß §«√®’¥È «â ¬‰øøÑ“À√◊Õ‡¬Á∫ºŸ° ∂â“‡®“– saphenous vein harvesting ‰¡à§«√≈ß·º≈¬“« §«√≈ß·º≈‡≈Á° Ê À≈“¬Õ—π ‡ªìπ™—πÈ Ê

244 °“√ºà“µ—¥∫√‘‡«≥™àÕß∑âÕß·≈–∑√«ßÕ° §«√√–«—ß‰¡à„Àâ°√–∑∫ °√–‡∑◊ÕπµàÕ cisterna chyli ∑’ÕË ¬Ÿµà √ß√–¥—∫ L1-L2 ·≈–∑Õ¥Õ¬Ÿà √–À«à“ß IVC ·≈– abdominal aorta ∂â“µ—¥ thoracic duct À√◊Õ cisterna chyli §«√‡¬Á∫´àÕ¡¥â«¬¥â“¬‡¬Á∫‡∫Õ√å 7-0 ∂â“ ‡ªìπ∑àÕπÈ”‡À≈◊Õß¢π“¥„À≠à∑’Ë‡¬Á∫´àÕ¡À√◊ÕµàÕ‰¡à ‰¥â§«√‡¬Á∫ºŸ° À√◊ÕÀπ’∫¥â«¬ metallic clip.

√ÿª ¿“«– lymphedema ‡°‘¥¢÷πÈ ‡¡◊ÕË ¡’§«“¡∫°æ√àÕß„π°“√‰À≈ ‡«’¬π°≈—∫¢ÕßπÈ”‡À≈◊Õß ´÷Ëß¡’ª√‘¡“≥¢Õß‚ª√µ’π Ÿß ‰À≈‡«’¬π °≈—∫‡¢â“ Ÿà√–∫∫πÈ”‡À≈◊Õß‰¡à ‰¥â µ“¡ª°µ‘ πÈ”‡À≈◊Õß∑’Ë§—ËßÕ¬Ÿà „π ‡π◊ÕÈ ‡¬◊ÕË µà“ß Ê ‡À≈à“π’È µàÕ¡“®–∑”„Àâ‡°‘¥ subcutaneous edema µ“¡¡“¥â«¬ brawny edema ·≈–º‘«Àπ—ß¡’°“√‡ª≈’Ë¬π·ª≈ß °“√√—°…“∑’ Ë ”§—≠ ”À√—∫‚√§π’§È Õ◊ external compression ·≈– ªÑÕß°—π°“√µ‘¥‡™◊ÕÈ „π√“¬∑’¡Ë °’ “√Õÿ¥µ—π¢Õß∑àÕπÈ”‡À≈◊Õß ·µà∑Õà à«πª≈“¬¬—ßª°µ‘¥’Õ¬Ÿà §«√æ‘®“√≥“ºà“µ—¥√—°…“‡æ√“–º≈°“√ √—°…“πà“®–¥’∑ ’Ë ¥ÿ „π√“¬∑’‡Ë ªìπ‡√◊ÕÈ √—ß√–¬–‡«≈“π“π¢“∫«¡‚µ¡“° ‡§≈◊ËÕπ‰À«‰¡à –¥«°À√◊Õ‡°‘¥°“√µ‘¥‡™◊ÈÕ´È”À≈“¬§√—Èß µâÕß„™â¬“ ªØ‘™«’ π–À≈“¬¢π“π §«√æ‘®“√≥“√—°…“‚¥¬°“√ºà“µ—¥ excisional procedures

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‡Õ° “√Õâ“ßÕ‘ß 1. Crockett DJ. Lymphatic anatomy and Lymphoedema. Br J Plast Surg 1965;18:12-21. 2. Malek P, Belan A, Kocandrle VL. The superficial and deep lymphatic system of the lower extremities and their mutual relationship under physiological and pathological conditions. J Cardiovase Surg 1964;5:586-94. 3. Rodbard S, Feldman P. Functional anatomy of the lymphatic fluids and pathways. Lymphology 1975;8:49-56. 4. Larson DL. Deep lymphatic system of the lower extremity. Am J Surg 1967;2:217-26. 5. Casley-Smith JR. The fine structure and functioning of tissue channels and lymphatics. Lymphology. 1980;13:177-88. 6. Guyton AC, Barber BJ. The energetics of lymph formation lymphology 1980;13:173-81. 7. Olszewski WL, Engaset A. Intrinsic contractility of prenodal lymphatic vessels and lymph flow in human leg. Am J Physio/ 1980;239:H775. 8. Vang G, Zhang S. Experimental study of lymphatic contractility and its clinical importance. Ann Plast Surg 1985;15:278-88. 9. Pflug JJ, Calnan JS. The normal anatomy of the lymphatic system in the human leg. Br J Surg 1971;58:925-31. 10. Knight KR, Collopy PH, McCann JJ, et al. Protein metabolism and fibrosis in experimental canine obstructive lymphedema. J Lab Clin Med 1987;110:55811. Dale WA. The swollen leg. Cerr Probl Surg 1973:140:1-152. 12. Gupta AK, Davies GM, Haberman HF. Yellow nail syndrome. Cutis 1986;37:37113. Gloviczki P, Calcagno D, Schirger A, et al. Noninvasive evaluation of the swollen extremity: Experiences with 190 lymphoscintigraphic examinations. J Vasc Surg 1989;9:683-690. 14. Cambria RC. Noninvasive evaluation of the lymphatic system with lymphoscintigraphy: A prospective, semiquantitative analysis in 386 extremities. J Vasc Surg 1993;18:773-81. 15. Weissleder H, Weissleder R. Lymphedema: Evaluation of quantitative 2 and qualitative lymphoscintigraphy in 238 patients. Radiology 1988;167:729-35.

16. Haaversted R, Nilsen G, Myhre HO, et al. The use of MRI in the investigation of leg oedema. Eur J Vasc Surg 1992;6:124-29. 17. Case TC, Wittle CL, Witte MH, et al. Magnetic resonance imaging in human lymphedema: Camparison with lymphangioscintigraphy. Magn Reson Imaging 1992;10:549-58. 18. Asby ER, Abdou S, Miller TA. Lymphedema and tumors of the lymphatics. In: Vascular Surgery: A Comprehensive review, 4th ed. Moore WS (ed.). Philadelphia:WB Saunders, 1993;688-98. 19. Pappas GT, O’Donnell TF Jr. Long-term results of compression treatment for lymphedema. J Vasc Surg 1992;16:555-64. 20. Casley-Smith JR, Morgan RG, Piller NB. Treatment of lymphedema of the arms and legs with 5,6-bengo-alpha-pyrone. N Engl J Med 1993;329:1158-63. 21. Servelle M. Surgical treatment of lymphedema: A report on 652 cases. Surgery 1987;101:485-95. 22. Baumeister RG, Siuda S. Treatment of Lymphedemas by microsurgical lymphatic grafting: What is proved? Plast reconstr Surg 1990;85:64-75. 23. Gloviczki P. Microsurgical lymphovenous anastomosis for treatment of lymphedema: A critical review. J Vasc Sug 1988;7:647-52. 24. Gloviczki P. The natural history of microsurgical lymphovenous anastomosis: An experimental study. J Vasc Surg 1986;4:148. 25. OûBrien BMC, Mellow CG, Khazanchi RK, et al. Long term results after microlymphaticovenous anastomoses for the treatment of obstructive lymphedema. Plast Reconst Surg 1990:85:562-71. 26. Brennan MJ. Lymphedema following surgical treatment of breast cancer: A review of pathophysiology and treatment. J Pain Symptom Manage 1992;7:110-16. 27. Kalman PG, Walker PM, Johnston KW. Consequences of groin lymphatic fistulae after vascular reconstruction. J Vasc Surg 1991;25:210. 28. Garrett HE Jr. Retroperitoneal lymphocele after abdominal aortic surgery. J Vasc Surg 1989;10:245-56.

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‡Õ° “√Õâ“ßÕ‘ß 1. Rutherford RB, Jones DN, Bergentz SE, et al. The efficacy of dextran 40 in preventing early postoperative thrombosis following difficult lower extremity bypass. J Vasc Surg 1984;25:765-773. 2. Flinn WR, Rohrer MJ, Yao JST, et al. Improved long-term patency of infragenicular polytetrafluroethylene grafts. J Vasc Surg 1988;7:685690. 3. Veith FJ, Weiser RK, Gupta SK, et al. Diagnosis and management of failing lower extremity arterial reconstructions prior to graft occlusion. J Cardiovasc Surg 1984;25:381-384. 4. Goldsmith J, Fraco CD, Farrel EA, et al. Advances in the surgical treatment of lower extremity vascular disease. J Am Acad Phys Assist 1991;4:481-487. 5. Veith FJ. Gupta SK, Samson RH, et al. Progress in limb salvage by reconstructive arterial surgery combined with new or improved adjunctive procedures. Ann Surg 1981;194:386-401. 6. Calligaro KD, Veith FJ, Schwartz ML, et al. When is it safe to leave an infected prosthetic arterial graft in place? In: Veith FJ, ed. Current Critical Problems in Vascular Surgery, Vol 4. St Louis: Quality Med Publ 1992;365-370.

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À≈Õ¥‡≈◊Õ¥∑’Ë©’°¢“¥∫“ß à«π À≈Õ¥‡≈◊Õ¥∑’©Ë °’ ¢“¥∫“ß à«π‚¥¬‡©æ“–∑“ß¥â“π¢â“ß ®–∑”„Àâ ¡’°“√‡ ’¬‡≈◊Õ¥Õ¬à“ßµàÕ‡π◊ËÕß ∂â“‡ªìπÀ≈Õ¥‡≈◊Õ¥·¥ß¢π“¥„À≠à ®–∑”„ÀâºŸâªÉ«¬™ÁÕ§‰¥â «‘∏’°“√Àâ“¡‡≈◊Õ¥∑’Ë ‰À≈®“°À≈Õ¥‡≈◊Õ¥∑’Ë Õ¬Ÿà ‰¡à≈÷°®“°º‘«Àπ—ß§◊Õ „™âπ‘È«°¥≈ß∫π®ÿ¥∑’Ë¡’‡≈◊Õ¥‰À≈ÕÕ° ‰¡à §«√„™â “¬¬“ß¬◊¥ (torniquet) √—¥‡ªìπ°“√Àâ“¡‡≈◊Õ¥ ‡æ√“–∂â“ √—¥·πàπ‡°‘π‰ª®–∑”„Àâ‡π◊ÈÕ‡¬◊ËÕ√Õ∫¢â“ßµ“¬ ·µà∂â“√—¥‰¡à·πàπæÕ ‡≈◊Õ¥®–‰À≈´÷¡ÕÕ°®“°∫“¥·º≈¡“°°«à“ª°µ‘®“°À≈Õ¥‡≈◊Õ¥¥” ¢âÕ∫àß™’È „π°“√„™â “¬¬“ß√—¥Àâ“¡‡≈◊Õ¥∑’Ë ‰À≈ÕÕ°®“°À≈Õ¥‡≈◊Õ¥ ·¥ß§◊Õ „π√“¬∑’Ë¡’‡≈◊Õ¥‰À≈ÕÕ°®“°∫“¥·º≈¢ÕßÀ≈Õ¥‡≈◊Õ¥ ·¥ß∑’ËÕ¬Ÿà≈÷°¡“°‰¡à “¡“√∂À¬ÿ¥‡≈◊Õ¥‰¥â ‚¥¬°“√°¥ À√◊Õ·¢π¢“ ∑’Ë∫“¥‡®Á∫√ÿπ·√ß‰¡à “¡“√∂ºà“µ—¥´àÕ¡·´¡‰¥â ·≈–‡µ√’¬¡®–µ—¥ ∑‘ßÈ Õ¬Ÿ·à ≈â« ‰¡à§«√„™â§¡’ Àπ’∫À≈Õ¥‡≈◊Õ¥ §«“π‡¢â“‰ª„π∫“¥·º≈ ·≈–§’∫À≈Õ¥‡≈◊Õ¥∑’Ë¡’‡≈◊Õ¥‰À≈ÕÕ°¡“·∫∫‡¥“ ÿà¡ ‡æ√“–Õ“® ®–‰ª§’∫‡Õ“À≈Õ¥‡≈◊Õ¥ ‡ âπª√– “∑ ·≈–‡π◊ÈÕ‡¬◊ËÕ¢â“ß‡§’¬ß„Àâ °√–∑∫°√–‡∑◊Õπ‚¥¬‰¡à®”‡ªìπ

∂â“ “¡“√∂Àâ“¡‡≈◊Õ¥‰¥â ‚¥¬°“√°¥®ÿ¥ ¢¬“¬∫“¥·º≈„Àâ°«â“ß ¢÷Èπµ“¡·π«¢ÕßÀ≈Õ¥‡≈◊Õ¥‡≈“–À≈Õ¥‡≈◊Õ¥ÕÕ°®“°‡π◊ÈÕ‡¬◊ËÕ √Õ∫¢â“ß·¢πß “¢“‡≈Á° Ê (branches) ¢ÕßÀ≈Õ¥‡≈◊Õ¥∑’Ë ‰¡à ”§—≠ “¡“√∂ºŸ°µ—¥‰¥â ‡æ◊ËÕ∑’Ë®–¢¬—∫À≈Õ¥‡≈◊Õ¥‰¥âßà“¬ –¥«°„π°“√ ‡¬Á∫´àÕ¡ ‡¡◊ËÕ‡≈“–À≈Õ¥‡≈◊Õ¥‰¥â§«“¡¬“«‡æ’¬ß æÕ·≈â« „™â§’¡ Àπ’∫À≈Õ¥‡≈◊Õ¥ Àπ’∫À≈Õ¥‡≈◊Õ¥ à«πµâπ·≈–ª≈“¬µàÕ∫√‘‡«≥∑’Ë ¡’·º≈©’°¢“¥ (√Ÿª∑’Ë 27.1)

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√Ÿª∑’Ë 27.2 „™â°√√‰°√µ—¥À≈Õ¥‡≈◊Õ¥ ‡≈Á¡‡Õ“¢Õ∫∑’¢Ë “¥°–√ÿßà °–√‘ßË ·≈– ‡π◊ÕÈ ‡¬◊ÕË à«π∑’µË “¬ÕÕ°

√Ÿª∑’Ë 27.3 ‡¬Á∫´àÕ¡À≈Õ¥‡≈◊Õ¥‚¥¬„™â¥“â ¬‡¬Á∫ polyproprylene ‡¬Á∫ Õ¬à“ßµàÕ‡π◊ËÕß

„™â°√√‰°√µ—¥À≈Õ¥‡≈◊Õ¥ ‡≈Á¡‡Õ“¢Õ∫∑’¢Ë “¥°√–√ÿßà °√–√‘ßË À√◊Õ ‡π◊ÕÈ ‡¬◊ÕË à«π∑’µË “¬ÕÕ° (√Ÿª∑’Ë 27.2) ‡¬Á∫´àÕ¡À≈Õ¥‡≈◊Õ¥‚¥¬„™â¥â“¬„¬ —ß‡§√“–Àå™π‘¥‡ âπ‡¥’Ë¬«∑’Ë º≈‘µ®“° polyproprylene ‡∫Õ√å 5-0, 6-0 À√◊Õ 7-0 ”À√—∫À≈Õ¥ ‡≈◊Õ¥∫√‘‡«≥·¢πÀ√◊Õ¢“∑—«Ë ‰ª ¢÷πÈ Õ¬Ÿ°à ∫— ¢π“¥¢ÕßÀ≈Õ¥‡≈◊Õ¥ ®– ‡¬Á∫·∫∫∑’≈–§√—ßÈ (interrupted technique) À√◊Õ‡¬Á∫Õ¬à“ßµàÕ‡π◊ÕË ß (continous over and over technique) (√Ÿª∑’Ë 27.3) °Á ‰¥â ∂â“À≈Õ¥‡≈◊Õ¥©’°¢“¥·À«àßÕÕ°‰ª¡“° °“√‡¬Á∫´àÕ¡‚¥¬µ√ß ®–∑”„ÀâÀ≈Õ¥‡≈◊Õ¥º‘¥√Ÿª∑√ß‰ª®“°‡¥‘¡ ¡’°“√µ’∫·§∫¡“° (√Ÿª∑’Ë 27.4 A,B) §«√‡¬Á∫´àÕ¡‚¥¬°“√„™âÀ≈Õ¥‡≈◊Õ¥¥”¢ÕßºŸªâ «É ¬ (autogenous vein graft) ¡“·µ–ªî¥·≈–‡¬Á∫´àÕ¡ (patch graft) (√Ÿª∑’Ë 27.5) À≈—ß®“°‡¬Á∫´àÕ¡À≈Õ¥‡≈◊Õ¥·≈â« ‰¡à§«√ºŸ°ª¡∑—π∑’ ª≈àÕ¬ §’¡§’∫À≈Õ¥‡≈◊Õ¥ „Àâ‡≈◊Õ¥‰À≈ºà“π·≈–‰≈à≈¡ÕÕ°®“°√Õ¬µàÕ ‡™Á§¥Ÿ√Õ¬√—Ë«∫√‘‡«≥∑’ËµàÕ √Õ„ÀâÀ≈Õ¥‡≈◊Õ¥µ÷ß¢¬“¬µ—«‡µÁ¡∑’Ë®÷ß ºŸ°ª¡„Àâ·πàπª√–¡“≥ 4-8 ª¡

À≈Õ¥‡≈◊Õ¥∑’Ë∂Ÿ°µ—¥¢“¥ÕÕ°®“°°—π

À≈Õ¥‡≈◊Õ¥∑’Ë∂Ÿ°µ—¥¢“¥ÕÕ°®“°°—π ‡≈◊Õ¥®–À¬ÿ¥‰À≈‡Õß ‡π◊ËÕß®“°ª≈“¬À≈Õ¥‡≈◊Õ¥∑’Ë¢“¥®–À¥·≈–Ωíßµ—«Õ¬Ÿà „π°≈â“¡‡π◊ÈÕ À√◊Õ‡π◊ÈÕ‡¬◊ËÕ√Õ∫¢â“ß ·≈–®–¡’≈‘Ë¡‡≈◊Õ¥¡“Õÿ¥µ√ßª≈“¬ ¢¬“¬ ∫“¥·º≈ÕÕ°„Àâ°«â“ß¢÷πÈ ‡æ◊ÕË „Àâ‡¢â“∂÷ßÀ≈Õ¥‡≈◊Õ¥µ“¡·π« „™â§¡’ §’∫À≈Õ¥‡≈◊Õ¥ à«πµâπ·≈– à«πª≈“¬ µ√«®¥Ÿ·º≈∫πÀ≈Õ¥‡≈◊Õ¥ ∂â“‡ªìπ∫“¥·º≈ –Õ“¥®“°«—µ∂ÿ¡’§¡„Àâ‡≈Á¡µ—¥¢Õ∫ª≈“¬À≈Õ¥ ‡≈◊Õ¥ÕÕ°‡≈Á°πâÕ¬°àÕπ‡¬Á∫µàÕ‡¢â“À“°—π ·µà∂â“‡ªìπ°“√©’°¢“¥

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√Ÿª∑’Ë 27.5 °“√‡¬Á∫´àÕ¡À≈Õ¥‡≈◊Õ¥∑’Ë¡’°“√©’°¢“¥À√◊Õ·À«àß¡“° ‚¥¬«‘∏’ patch graft ®–‰¡à∑”„Àâ√Ÿª∑√ß¢ÕßÀ≈Õ¥‡≈◊Õ¥‡ª≈’Ë¬π·ª≈ß‰ª¡“°

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√Ÿª∑’Ë 27.6 À≈Õ¥‡≈◊Õ¥∑’Ë™È”¡“°µâÕßµ—¥ÕÕ° ·≈–‰¡à “¡“√∂¥÷ß¡“‡¬Á∫µàÕ°—π‰¥â §«√„™âÀ≈Õ¥‡≈◊Õ¥¥”‡¬Á∫µàÕ∑¥·∑π (autogenous saphenous vein graft interposition)

®“°°√– ÿπªóπÀ√◊Õ°√–¥Ÿ°À—°°√–·∑° ∑”„Àâ¡’√Õ¬™È”¡“° §«√ µ—¥À≈Õ¥‡≈◊Õ¥„ÀâÀ“à ß®“°√Õ¬™È” 2-3 ‡´Áπµ‘‡¡µ√ „π°√≥’π®’È –‰¡à “¡“√∂¥÷ßÀ≈Õ¥‡≈◊Õ¥‡¢â“¡“‡¬Á∫µàÕ°—π‚¥¬µ√ß‰¥â ®–µâÕß„™â À≈Õ¥‡≈◊Õ¥¥”∑¥·∑π ‚¥¬‡©æ“– autogenous saphenous vein graft interposition ¡“‡¬Á∫µàÕ∑¥·∑πÀ≈Õ¥‡≈◊Õ¥ à«π∑’¢Ë “¥À“¬‰ª (√Ÿª∑’Ë 27.6) „™â Fogarty balloon catheter ≈“°‡Õ“≈‘Ë¡ ‡≈◊Õ¥ÕÕ°®“°À≈Õ¥‡≈◊Õ¥ à«πµâπ·≈– à«πª≈“¬ ©’¥‡Œª“√’π ´÷ßË ∑”„Àâ‡®◊Õ®“ß„ππÈ”‡°≈◊Õ ¡¥ÿ≈¬å „πÕ—µ√“ à«π 1:100 ‡¢â“∑“ß À≈Õ¥‡≈◊Õ¥ à«πµâπ·≈– à«πª≈“¬°—π‰¡à „Àâ‡≈◊Õ¥·¢Áßµ—« ·≈–„™â §’¡§’∫À≈Õ¥‡≈◊Õ¥§’∫À≈Õ¥‡≈◊Õ¥ à«πµâπ·≈– à«πª≈“¬´È”

À≈Õ¥‡≈◊Õ¥∑’®Ë –µàÕ‡¢â“À“°—π¡’¢π“¥‡≈Á°°«à“ 5 ¡‘≈≈‘‡¡µ√ §«√ ∫“°ª≈“¬ (beveled) ¢ÕßÀ≈Õ¥‡≈◊Õ¥∑—ßÈ Õß¢â“ß ∑”¡ÿ¡ 45 Õß»“ ∑”„Àâ‡ âπºà“»Ÿπ¬å°≈“ß¢ÕßÀ≈Õ¥‡≈◊Õ¥∑’Ë®–µàÕ‚µ¢÷Èπ ‡æ◊ËÕ„Àâ à«π ∑’µË Õà ‰¡àµ∫’ ·§∫À≈—ß®“°‡¬Á∫µàÕ‡¢â“À“°—π (√Ÿª∑’Ë 27.7) ∂â“‡ªìπ°“√‡¬Á∫·∫∫µàÕ‡π◊ÕË ß §«√„™â¥“â ¬‡¬Á∫ polyproprylene ‡∫Õ√å 6-0 À√◊Õ 7-0 ‡¬Á∫∑”¡ÿ¡Àà“ß°—π 180 Õß»“ ·≈â«‡¬Á∫ ‡¢â“À“°—π∑“ß¥â“πÀπâ“·≈–¥â“πÀ≈—ß (√Ÿª∑’Ë 27.8) “¡“√∂¢¬—∫ §’¡§’∫À≈Õ¥‡≈◊Õ¥∑”¡ÿ¡ 180 Õ“»“ ‡æ◊ÕË §«“¡ –¥«°„π°“√‡¬Á∫ µàÕÀ≈Õ¥‡≈◊Õ¥µ“¡·π«¥â“πÀπâ“·≈–¥â“πÀ≈—ß °“√‡¬Á∫À≈Õ¥ ‡≈◊Õ¥µâÕß‡¬Á∫∑ÿ°™—Èπ (all layer) ‡¢â“À“°—π Õ¬à“ß‰√°Áµ“¡°“√

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√Ÿª∑’Ë 27.7 °“√∫“°ª≈“¬ (beveled) ¢ÕßÀ≈Õ¥‡≈◊Õ¥∑—Èß Õß¢â“ß∑”¡ÿ¡ 45 Õß»“ ∑”„Àâ‡ âπºà“»Ÿπ¬å°≈“ß¢ÕßÀ≈Õ¥‡≈◊Õ¥∑’Ë®–µàÕ‚µ¢÷Èπ ‡«≈“‡¬Á∫µàÕ ®–‰¡àµ∫’ ·§∫

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√Ÿª∑’Ë 27.8 °“√‡¬Á∫À≈Õ¥‡≈◊Õ¥·∫∫µàÕ‡π◊ËÕß (continuous suture)

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√Ÿª∑’Ë 27.9 °“√‡¬Á∫µàÕÀ≈Õ¥‡≈◊Õ¥¢π“¥‡≈Á°‚¥¬„™â Carrel’s triangle ∑”¡ÿ¡ 120 Õß»“ À≈Õ¥‡≈◊Õ¥®–‰¡àµ’∫·§∫À≈—ß‡¬Á∫µàÕ

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260

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥ °“√‡¬Á∫µàÕÀ≈Õ¥‡≈◊Õ¥¢Õß‡¥Á°´÷Ëß¡’¢π“¥‡≈Á° ·≈–¡’‚Õ°“ ‡®√‘≠‡µ‘∫‚µµàÕ‰ªÕ’° §«√‡¬Á∫·∫∫ horizontal mattress ·≈– ºŸ°ª¡„Àâ·πàπæÕ ¡§«√ „Àâ¢Õ∫¢ÕßÀ≈Õ¥‡≈◊Õ¥‡¢â“¡“™‘¥°—π‚¥¬ ∫“πÕÕ°‡≈Á°πâÕ¬∑“ß¥â“ππÕ° (√Ÿª∑’Ë 27.10)

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√Ÿª∑’Ë 27.10 °“√‡¬Á∫µàÕÀ≈Õ¥‡≈◊Õ¥¢π“¥‡≈Á°À√◊Õ¢Õß‡¥Á° ·∫∫ horizontal mattress suture

‡¬Á∫·∫∫µàÕ‡π◊ÕË ß§«√∑”„πÀ≈Õ¥‡≈◊Õ¥∑’¡Ë ¢’ π“¥‚µ°«à“ 5 ¡‘≈≈‘‡¡µ√ ‚¥¬ºŸ¡â §’ «“¡™”π“≠·≈–‰¥â√∫— °“√Ωñ°Ωπ¡“·≈â« ”À√—∫ºŸ∑â ¬’Ë ß— ‰¡à¡§’ «“¡™”π“≠„π°“√‡¬Á∫µàÕÀ≈Õ¥‡≈◊Õ¥À√◊Õ À≈Õ¥‡≈◊Õ¥¡’¢π“¥‡≈Á°°«à“ 5 ¡‘≈≈‘‡¡µ√ §«√‡¬Á∫´àÕ¡·∫∫∑’≈–§” ·≈–„™â Carrelûs triangle ‚¥¬«‘∏’°“√‡¬Á∫√—Èß¢Õ∫À≈Õ¥‡≈◊Õ¥ Àà“ß°—π∑”¡ÿ¡ 120 Õß»“ (√Ÿª∑’Ë 27.9)

‡Õ° “√Õâ“ßÕ‘ß 1. Rutherford RB, ed. Atlas of Vascular Surgery: Basic Technique and Exposures. Philadelphia: WB Saunders, 1993. 2. Van Way CW III. Vascular Suture Technique. In: Moore EE, ed. Critical decisions in Trauma. St. Louis: CV Mosby, 1984;648-652. 3. ‡°…’¬√ ¿—ß§“ππ∑å. °“√µàÕ‡ âπª√– “∑·≈–À≈Õ¥‡≈◊Õ¥. §Ÿà¡◊Õºà“µ—¥‡≈Á°. æ‘¡æå §√—Èß∑’Ë 2, °√ÿß‡∑æœ: ‡Õ™ ‡Õπ °“√æ‘¡æå 2531;181-188. 4. Veith FJ. Vascular Surgical Techniques. In: Veith FJ, ed Vascular Surgery. 2nd ed. New York: McGraw-Hill, 1994;1134-1205. 5. Bergan JJ, Yao JST, eds. Techniques in Arterial Surgery. Philadelphia: WB Saunders, 1990.

À≈Õ¥‡≈◊Õ¥¥”¡’ºπ—ß∫“ß ·µà¢π“¥‚µ°«à“À≈Õ¥‡≈◊Õ¥·¥ß„π √–¥—∫‡¥’¬«°—π ∂â“¡’°“√©’°¢“¥‡æ’¬ß‡≈Á°πâÕ¬ “¡“√∂‡¬Á∫´àÕ¡ ∑“ß¥â“π¢â“ß‰¥â·π∫ lateral venorrhaphy ´÷Ëß®–∑”„ÀâÀ≈Õ¥ ‡≈◊Õ¥¥”µ’∫‡æ’¬ß‡≈Á°πâÕ¬ ·µà¬—ß “¡“√∂∑”Àπâ“∑’Ë ‰À≈‡«’¬π‰¥â µ“¡ª°µ‘ ‡¡◊ËÕ¡’°“√∫“¥‡®Á∫µàÕÀ≈Õ¥‡≈◊Õ¥¥” §«√æ¬“¬“¡‡¬Á∫ ´àÕ¡·´¡ ∂÷ß·¡â«à“®–µâÕß„™âÀ≈Õ¥‡≈◊Õ¥¥”∑¥·∑πÀ√◊ÕÀ≈Õ¥ ‡≈◊Õ¥‡∑’¬¡µàÕ à«π∑’Ë¢“¥À“¬‰ª ‰¡à§«√‡¬Á∫ºŸ°‡≈¬ ∂÷ß·¡â«à“°“√ ‡¬Á∫´àÕ¡·´¡À√◊ÕµàÕÀ≈Õ¥‡≈◊Õ¥¥”®–¡’Õ—µ√“Õÿ¥µ—πÀ√◊Õµ’∫·§∫ ¿“¬À≈—ß§àÕπ¢â“ß Ÿß ·µà collateral circulation °Á®–‡°‘¥¢÷πÈ √Õ∫ Ê ·≈â« ·≈–‡æ’¬ßæÕµàÕ°“√‰À≈‡«’¬π‡≈◊Õ¥·≈â« ∂â“µ—¥ ‘π„®ºŸ° À≈Õ¥‡≈◊Õ¥¥”∑’Ë ‰¥â√∫— ∫“¥‡®Á∫‚Õ°“ ·¢πÀ√◊Õ¢“®–∫«¡¡’∂ß÷ √âÕ¬≈– 50 ∂â“‡ªìπ·¢πß„À≠à·≈–¡’§«“¡ ”§—≠„π°“√√–∫“¬‡≈◊Õ¥°≈—∫ Ÿà À—«„®

∫∑∑’Ë 28 HEMODIALYSIS ACCESS „πªí®®ÿ∫—π∂÷ß·¡â«à“°“√ºà“µ—¥ª≈Ÿ°∂à“¬‰µ®–‰¥âº≈¥’ ¿“«– ·∑√°´âÕππâÕ¬ ·µà vascular access °Á¬—ß‡ªìπ à«π ”§—≠Õ’° Õ—πÀπ÷Ëß„π°“√¥Ÿ·≈√—°…“ºŸâªÉ«¬‰µ«“¬ µ—Èß·µà¢—Èπ‡©’¬∫æ≈—π‰ª®π °√–∑—ßË ‡√◊ÕÈ √—ß ”À√—∫°“√øÕ°‡≈◊Õ¥(1,2)

¢âÕ∫àß™’È„π°“√øÕ°‡≈◊Õ¥ ºŸªâ «É ¬‰µ«“¬‡©’¬∫æ≈—πÀ√◊Õ‡√◊ÕÈ √—ß®–¡’¢Õâ ∫àß™’‡È ¡◊ÕË ¡’ª≠ í À“‡À≈à“ π’‡È °‘¥¢÷πÈ 1. ¿“«– uremia ‡ªìπ¢âÕ∫àß™’ È ”§—≠ ”À√—∫‰µ«“¬‡√◊ÕÈ √—ß ‡¡◊ÕË √–¥—∫ BUN ·≈–§√’Õ“µ‘π‘π Ÿß¢÷ÈπÕ¬à“ß√«¥‡√Á« ‚¥¬ ∑—«Ë ‰ª·≈â«∂â“√–¥—∫ BUN µË”°«à“ 100 mg/dl Õ—µ√“µ“¬ ·≈–∑ÿæ≈¿“æ®–≈¥≈ß¡“° Õ“°“√∑“ß√–∫∫ª√– “∑∑’Ë µâÕß°“√øÕ°‡≈◊Õ¥¡’‡°√Áß°√–µÿ°, ™—°, myoclonus, asterixis, peripheral neuritis ·≈– uremic pericarditis 2. ¿“«– hyperkalemia ∑’¡Ë √’ –¥—∫¢Õß‚ªµ— ‡´’¬¡ Ÿß‡°‘π°«à“ 6 mEq/L √à«¡°—∫¡’§«“¡º‘¥ª°µ‘¢Õß§≈◊ËπÀ—«„® §«“¡ º‘¥ª°µ‘À√◊Õæ¬“∏‘ ¿“æ¢Õß√–∫∫ª√– “∑·≈–°≈â“¡‡π◊ÕÈ °“√§«∫§ÿ¡Õ“À“√·≈–„Àâ K-bonding resin √—∫ª√–∑“πÀ√◊ Õ «π‡°Á ∫ ®–™à « ¬≈¥√–¥— ∫ ¢Õß‚ªµ— ‡´’ ¬ ¡„π °√–· ‡≈◊Õ¥ 3. ¿“«–πÈ”‡°‘π ∂÷ß·¡â«“à ®–„Àâ¬“¢—∫ªí “«–¥÷ßπÈ”ÕÕ°®“° √à“ß°“¬·≈â«°Á¬ß— ‰¡à ‰¥âº≈ 4. drug overdose „π¿“«–©ÿ°‡©‘π

°“√ºà“µ—¥∑” hemodialysis access ∂◊Õ«à“‡ªìπ life saving procedure Õ—πÀπ÷Ëß‡æ√“–¡’§«“¡®”‡ªìπ∑’Ë®–µâÕß„™âøÕ°‡≈◊Õ¥„π ºŸâªÉ«¬‰µ«“¬‡√◊ÈÕ√—ß ‰¡à«à“®–√Õ‰µ°àÕπ°“√ª≈Ÿ°∂à“¬À√◊ÕÀ≈—ß°“√ ∑”ºà“µ—¥ª≈Ÿ°∂à“¬‰µ·≈â« vascular access ∑’Ë¡’Õ¬Ÿà®–µâÕß„™â „π °“√øÕ°‡≈◊Õ¥∫àÕ¬§√—ßÈ º≈∑’µË “¡¡“À≈—ß°“√„™âß“π§◊Õ ‡°‘¥¿“«– ·∑√°´âÕπ®π°√–∑—Ëß‰¡à “¡“√∂„™âß“πµàÕ‰ª‰¥â °Á®–µâÕßºà“µ—¥ ¬â“¬∑’Ë „À¡à °“√‡≈◊Õ°∑” vascular access ®–µâÕß§”π÷ß∂÷ß°“¬ «‘¿“§»“ µ√å §«“¡ –¥«°µàÕºŸªâ «É ¬ ¿“«–·∑√°´âÕπ∑’ÕË “®®–‡°‘¥¢÷πÈ ‡∑§π‘§·≈–°“√«“ß·ºπ°“√ºà“µ—¥‰¡à¥’®–∑”„Àâ „™âß“π‰¡à ‰¥âµâÕß ºà“µ—¥À≈“¬§√—Èß °àÕπ·≈–À≈—ß°“√ºà“µ—¥§«√¡’°“√ª√÷°…“·≈– ¥Ÿ·≈√à«¡°—π√–À«à“ß»—≈¬·æ∑¬å∑“ß‚√§‰µ µ≈Õ¥®π∫ÿ§≈“°√∑’Ë¡’ à«π‡°’Ë¬«¢âÕß°—∫°“√„™â vascular access »—≈¬·æ∑¬å∑’Ëºà“µ—¥ vascular access §«√¡’§«“¡ “¡“√∂„π°“√ºà“µ—¥´È”‡æ◊ËÕ°Ÿâ „Àâ vascular access ∑’Ë „™âß“π‰¡à ‰¥â°≈—∫¡“„™âß“π‰¥â¥—ß‡¥‘¡·≈– ∑”°“√ºà“µ—¥ vascular access ∫√‘‡«≥„À¡à ‰¥â ∂â“∫√‘‡«≥‡¥‘¡‰¡à “¡“√∂„™âß“π‰¥â·≈â« °“√∑” revise failed access ∑”‰¥â ‚¥¬ °“√ºà“µ—¥´È” À√◊Õ√—ß ’√«à ¡∫”∫—¥ (invasive radiologic technique) ‡æ√“–®ÿ¥¡ÿàßÀ¡“¬§◊ÕµâÕß°“√°Ÿâ ¿“æ¢Õß vascular access µ”·Àπàß‡¥‘¡„Àâ „™âß“π‰¥âÕ°’ ‡ªìπ√–¬–‡«≈“π“π(1,2,3) ¢âÕ∫àß™’È „π°“√„™â vascular access ¡’¥ß— µàÕ‰ªπ’§È Õ◊ hemodialysis, plasmapheresis, ultrafiltration, charcoal hemoperfusion, „Àâ “√Õ“À“√∑“ßÀ≈Õ¥‡≈◊Õ¥¥” ‡®“–‡≈◊Õ¥µ√«® ·≈–„Àâ “√‡§¡’∫”∫—¥(3)

262

µ“√“ß∑’Ë 28.1 ·ºπ°“√„π°“√∑” Hemodialysis Access ”À√—∫ºŸªâ «É ¬‰µ«“¬

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥

263

HEMODIALYSIS ACCESS

¿“«–‰µ«“¬‡©’¬∫æ≈—πµâÕß°“√øÕ°‡≈◊Õ¥Õ¬à“ß©ÿ°‡©‘π‰¡à °’Ë §√—ßÈ °àÕπ∑’Ë ‰µ®–øóπô ¿“æ hemodialysis ∑’Ë „™â®ß÷ ‡ªìπ™π‘¥™—«Ë §√“« ∑’Ë „ ™â „πªí®®ÿ∫—π§◊Õ Õ¥ “¬ «πºà“πº‘«Àπ—ß‡¢â“À≈Õ¥‡≈◊Õ¥¥” ¢π“¥„À≠à “¡“√∂øÕ°‡≈◊Õ¥‰¥â∑—π∑’ ·≈–¥÷ßÕÕ°‰¥â‡¡◊Ë Õ ‰¡à µâÕß°“√„™â·≈â« ºŸªâ «É ¬∑’§Ë “¥«à“‰µ®–«“¬·≈–°≈“¬‡ªìπ«“¬‡√◊ÕÈ √—ßµàÕ¡“ §«√ «“ß·ºπ∑’®Ë –∑” hemodialysis access ·µà‡π‘πË Ê ‚¥¬æ¬“¬“¡ ‡°Á∫√—°…“À≈Õ¥‡≈◊Õ¥¥”„µâº‘«Àπ—ß∑’Ë·¢π‰«â Àâ“¡‡®“–‡≈◊Õ¥·∑ß ‡ âπÀ√◊Õ„Àâ “√πÈ”‚¥¬‡¥Á¥¢“¥ ®–æ‘®“√≥“«à“ºŸâªÉ«¬µâÕß°“√ øÕ°‡≈◊Õ¥Õ¬à“ßµàÕ‡π◊ËÕß‡¡◊ËÕ√–¥—∫§√’Õ“µ‘π’π¢÷Èπ Ÿß°«à“ 6mg/dl ·≈–§à“ creatinine clearance µË”°«à“ 10 ml/min À≈—ßºà“µ—¥ ·≈â«§«√√Õ®π°√–∑—ßË hemodialysis access matured °àÕπ„™âß“π

§”π‘¬“¡∑’Ë§«√∑√“∫ Dialysis catheter §◊Õ “¬ «π¢π“¥‚µ¡’ 2 √Ÿ·∑√ºà“πº‘«Àπ—ß ‡¢â“ ŸàÀ≈Õ¥‡≈◊Õ¥¥” central vein √Ÿ¥â“πÀπ÷Ëß®–‡ªìπ∑“ßÕÕ°‰ª ¬—ß‡§√◊ÕË ßøÕ°‡≈◊Õ¥ Õ’°√ŸÀπ÷ßË ®–‡ªìπ∑“ß‡¢â“®“°‡§√◊ÕË ßøÕ°‡≈◊Õ¥ Ÿµà «— ºŸªâ «É ¬ Arteriovenous fistula (AVF) ª√–°Õ∫¥â«¬À≈Õ¥‡≈◊Õ¥¥” „µâº«‘ Àπ—ß∑’µË Õà ‡¢â“°—∫À≈Õ¥‡≈◊Õ¥·¥ß∫√‘‡«≥„°≈â‡§’¬ß°—π ‡ªìπ high flow circuit À≈—ßµàÕ·≈â« 4-6 —ª¥“Àå À≈Õ¥‡≈◊Õ¥¥”®–¡’¢π“¥ ‚µ·≈–ºπ—ßÀπ“¢÷πÈ “¡“√∂·∑ß‡ âπ·≈–øÕ°‡≈◊Õ¥‰¥â Arteriovenous graft (AVG) §◊ÕÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡∑’Ë¡’ §ÿ≥ ¡∫—µ‘‡ªìπ∑àÕ (conduit) µàÕ√–À«à“ßÀ≈Õ¥‡≈◊Õ¥¥”·≈– À≈Õ¥‡≈◊Õ¥·¥ß ∂â“µâÕß°“√øÕ°‡≈◊Õ¥®–·∑ß‡¢Á¡ºà“πÀ≈Õ¥ ‡≈◊Õ¥‡∑’¬¡π’È ™π‘¥¢ÕßÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡∑’Ë „™â‡ªìπ AVG ∫àÕ¬§◊Õ polytetrafluoroethylene (PTFE) graft Arteriovenous shunt (AVS) ‡ªìπ externalized communication √–À«à“ßÀ≈Õ¥‡≈◊Õ¥¥”°—∫À≈Õ¥‡≈◊Õ¥·¥ß Õ¬ŸàπÕ° º‘«Àπ—ß‚¥¬„™â silastic tube ¥â“πÀπ÷ßË µàÕ°—∫À≈Õ¥‡≈◊Õ¥¥” ·≈– Õ’°¥â“πÀπ÷ËßµàÕ°—∫À≈Õ¥‡≈◊Õ¥·¥ß ‡«≈“®–„™â°Á‡Õ“ “¬·µà≈– ¥â“πµàÕ‡¢â“°—∫‡§√◊ËÕßøÕ°‡≈◊Õ¥ „™âøÕ°‡≈◊Õ¥™—Ë«§√“«„π‰µ«“¬ ‡©’¬∫æ≈—π

Access Axioms °“√øÕ°‡≈◊Õ¥®–¡’ª√– ‘∑∏‘¿“æ¥’ ∂â“¡’‡≈◊Õ¥‰À≈ºà“π‡§√◊ËÕß øÕ°‡≈◊Õ¥Õ¬à“ßπâÕ¬π“∑’≈– 300-400 ¡‘≈≈‘≈‘µ√ „π°“√øÕ° ‡≈◊Õ¥®–µâÕß¡’ arterialized vein, À≈Õ¥‡≈◊Õ¥‡∑’¬¡ ·≈– central

vein ‰«â ”À√—∫·∑ß‡ âπ ‚¥¬∑—«Ë ‰ª·≈â«µ”·Àπàß∑’®Ë –·∑ß‡ âπ§«√ Õ¬Ÿàµ◊Èπ„µâº‘«Àπ—ß ‰¡àÕ¬Ÿà „°≈âÕ«—¬«– ”§—≠‡™àπ À≈Õ¥‡≈◊Õ¥À√◊Õ ‡ âπª√– “∑ ·¢π‡ªìπµ”·Àπàß∑’Ë‡À¡“– ¡∑’Ë ÿ¥°«à“¢“‡æ√“– ¥Ÿ·≈ßà“¬‰¡à‡ ’¬Ë ßµàÕ°“√µ‘¥‡™◊ÕÈ autologous fistula ®–¥’°«à“ implanted graft ‡æ√“–√–¬–‡«≈“°“√„™âß“ππ“π°«à“¿“«–·∑√°´âÕπ ¡’πÕâ ¬(1,2,3) „π∑“ßªØ‘∫µ— ª‘ ®í ®ÿ∫π— ¡’°“√„™â∑ß—È arteriovenous shunt (AVS) ·≈– arteriovenous fistula (AVF) ∑’Ë „™â∫Õà ¬§◊Õ Brescia-Cimino AVF „πºŸªâ «É ¬∑’√Ë Õ°“√ª≈Ÿ°∂à“¬‰µÀ√◊Õ‰¡à “¡“√∂®–ºà“µ—¥‰¥â ‡™àπ ‡ªìπ¡–‡√Áß ŸßÕ“¬ÿ À√◊Õ¡’°“√µ‘¥‡™◊ÕÈ √ÿπ·√ß(4) °“√‡≈◊Õ° access ∑’‡Ë À¡“– ¡°—∫ºŸªâ «É ¬·µà≈–√“¬ ®–µâÕß¥Ÿ °“¬«‘¿“§»“ µ√å·≈–«‘∏’°“√ºà“µ—¥¥Ÿ«à“ºŸâªÉ«¬µâÕß°“√øÕ°‡≈◊Õ¥ ·∫∫„¥ (µ“√“ß∑’Ë 28.1) ‚¥¬®–·∫àßÕÕ°‡ªìπ 1. acute short-term dialysis access 2. acute as well as eventual chronic hemodialysis access 3. chronic dialysis access without a requirement for immediate access

I. ACUTE DIALYSIS ACCESS 1.1 direct single-lumen percutaneous puncture ‚¥¬ Õ¥ “¬ «πºà“πº‘«Àπ—ß‡¢â“‰ª¬—ß femoral artery ·≈– femoral vein access ∑’Ë „™â§Õ◊ Sheldon femoral catheters ªí®®ÿ∫—π‡≈‘°„™â·≈â«‡π◊ËÕß®“°¿“«–·∑√°´âÕπ Ÿß ‡°‘¥°“√∫“¥‡®Á∫µàÕÀ≈Õ¥‡≈◊Õ¥∫√‘‡«≥¢“Àπ’∫ (thrombosis, pseudoaneurysm, arterivenous fistula) À√◊Õ °“√Õ—°‡ ∫µ‘¥‡™◊ÕÈ ‰¥âß“à ¬ 1.2 non-cuffed dual-lumen dialysis catheters Õ¥ “¬ «πºà“πº‘«Àπ—ß‡¢â“‰ª∂÷ßÀ≈Õ¥‡≈◊Õ¥¥”¢π“¥‚µ (√Ÿª∑’Ë 28.1) ∑’¡Ë ’„™â§Õ◊ Shiley, Quinton À√◊Õ VasCath catheters “¡“√∂∑”À—µ∂°“√ Õ¥ “¬ «π‰¥â¢â“ß‡µ’¬ßºŸâ ªÉ«¬‚¥¬„™â‡∑§π‘§ª√“»®“°‡™◊ÈÕ‰¡àµâÕß∑”„πÀâÕßºà“µ—¥ §“ “¬ «π∑‘ßÈ ‰«â‡æ◊ÕË „™âß“π‰¥âπ“π°«à“ 2 ‡¥◊Õπ ∂â“‰¡à¡’ °“√µ‘¥‡™◊ÈÕÀ√◊Õ thrombosis ‡°‘¥¢÷Èπ ¢≥– Õ¥ “¬ «π§«√√–«—ß¿“«–·∑√°´âÕπµàÕ‰ªπ’´È ß÷Ë Õ“®®–‡°‘¥¢÷πÈ ‰¥â pneumothorax, ·∑ß “¬ «π‡¢â“À≈Õ¥‡≈◊Õ¥·¥ß·≈– °“√µ‘¥‡™◊ÕÈ

264

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥

Internal Jugular v.

Dacron felt cuff

√Ÿª∑’Ë 28.1 non-cuffed dual lumen dialysis catheter 1.3 cuffed dialysis catheter ∑’¡Ë ’„™â§Õ◊ Perm cath À√◊Õ VasCath catheters (√Ÿª∑’Ë 28.2) °“√ Õ¥ “¬ «π®– µâÕß∑”À—µ∂°“√·∫∫ venous cut down À√◊Õ„™â¡¥’ °√’¥ ºà“πº‘«Àπ—ß ∫“°‡ªìπ√Õ¬‡≈Á° Ê ·≈â« Õ¥ “¬ «π ‡¢â “ ‰ª∂÷ ß À≈Õ¥‡≈◊ Õ ¥¥” “¡“√∂„™â ø Õ°‡≈◊ Õ ¥‰¥â ∑— π ∑’Ë “¬ «πº≈‘µ®“°«— ¥ÿ∑’ËÕàÕπ¬◊¥À¬ÿàπ‰¥â·≈–‰¡à¡’ªØ‘°‘√‘¬“ µàÕ√à“ß°“¬ ®÷ß§“ “¬ «π∑‘Èß‰«â ‰¥â‡ªìπ√–¬–‡«≈“π“π ¿“«–·∑√°´âÕπ∑’ÕË “®®–‡°‘¥¢÷πÈ ‰¥â¡°’ “√µ‘¥‡™◊ÕÈ thrombosis ‡¡◊ÕË ‡°‘¥¿“«–·∑√°´âÕπ¢÷πÈ §«√¥÷ß‡Õ“ “¬ «πÕÕ°

Cephalic vein

Radial artery Arteriovenous fistula

√Ÿª∑’Ë 28.3 wrist fistula (left arm)

Venous adaptor (blue)

Arterial adaptor

√Ÿª∑’Ë 28.2 cuffed dialysis catheter

II. CHRONIC HEMODIALYSIS 2.1 autologous arteriovenous fistula æ∫«à“ direct AVF ∑’Ë „™âÀ≈Õ¥‡≈◊Õ¥¥”„µâº‘«Àπ—ß∫√‘‡«≥·¢πµàÕ‡¢â“ °—∫À≈Õ¥‡≈◊Õ¥·¥ß„°≈â‡§’¬ß ¡’ª≠ í À“·≈–¿“«–·∑√°´âÕπ (5-8) πâÕ¬∑’ Ë ¥ÿ 3-year patency Ÿß∂÷ß√âÕ¬≈– 70 ´÷ßË ¥’°«à“ AVG ´÷ßË ¡’ patency ‡æ’¬ß√âÕ¬≈– 50 ·≈–‡°‘¥ pseudoaneurysm ‰¥âß“à ¬(9-11) 2.1.1 wrist fistula (√Ÿª∑’Ë 28.3) ∂â“À≈Õ¥‡≈◊Õ¥¥”„µâº«‘ Àπ—ß‚¥¬‡©æ“– cephalic vein Õ¬Ÿà „π ¿“æ∑’¥Ë ’ ·≈–À≈Õ¥‡≈◊Õ¥·¥ß∑’¡Ë “‡≈’¬È ßΩÉ“¡◊Õ ª°µ‘¥∑’ ß—È Õß‡ âπ §«√∑” radial artery to cephalic vein fistula (AVF) À√◊Õ Cimino-Brescia fistula ·¢π¢â“ß∑’Ë ‰¡à∂π—¥¢ÕßºŸªâ «É ¬ Õ“®®–µàÕ·∫∫ endto-side À√◊Õ side-to-side æ∫«à“«‘∏°’ “√µàÕ end-vein to-side artery ¥’∑ ’Ë ¥ÿ ‡°‘¥¿“«– venous hypertension πâÕ¬(12)

265

HEMODIALYSIS ACCESS

Axillary artery & vein Brachial artery Cephalic vein Radial artery

Basillic vein Antecubital arteriovenous fistula

Ulnar artery

√Ÿª∑’Ë 28.4 antecubital fossa

Brachial artery Transposed brachial vein

Normal position of brachial vein

Arteriovenous fistula

√Ÿª∑’Ë 28.5 transposed vein arteriovenous fistula

2.1.2 antecubital fistula (√Ÿª∑’Ë 28.4) §«√æ‘®“√≥“∑”‡¡◊ËÕÀ≈Õ¥‡≈◊Õ¥¥”„µâº‘«Àπ—ß∫√‘‡«≥ ∑âÕß·¢π‡ ◊ËÕ¡ ¿“æ®“°°“√‡®“–‡≈◊Õ¥·∑ß‡ âπ„Àâ “√πÈ” ‰¡à “¡“√∂∑” CB fistula ‰¥â cephalic vein ∫√‘‡«≥ antecubital fossa ®–¬—ß¥’Õ¬Ÿà ∂÷ß·¡â«à“ µ”·Àπàß·∑ß‡ âπøÕ°‡≈◊Õ¥∫√‘‡«≥µâπ·¢π®– —Èπ‰ª ÀπàÕ¬ ·µà „™âß“π‰¥âº≈¥’ §«√ºŸ° tributaries vein ¢â“ß‡§’¬ß‡æ◊ÕË ªÑÕß°—π venous outflow ‡¢â“‰ª Ÿà deep vein 2.1.3 transposed vein arteriovenous fistula (√Ÿª∑’Ë 28.5) ∂â“À≈Õ¥‡≈◊Õ¥¥”„µâº«‘ Àπ—ß∑’·Ë ¢πΩÉÕ·≈–‡ ◊ÕË ¡ ¿“æ Õ“®®–„™â brachial À√◊Õ basillic vein ¡“∑¥·∑π cephalic vein ‰¥â ‚¥¬‡≈“–À≈Õ¥‡≈◊ Õ ¥ √â “ ß ‚æ√ß„µâº‘«Àπ—ß∫√‘‡«≥µâπ·¢π·≈â«µàÕÀ≈Õ¥‡≈◊Õ¥ µ“¡¡“„Àâ ‡ ¢â “ °— ∫ brachial artery æ∫«à “ «‘ ∏’ π’È §àÕπ¢â“ß¬ÿàß¬“°·≈–‰¡à¥’°«à“ standard AVF §«√ ®–„™âÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡®–¥’°«à“·≈–≈¥‡«≈“„π°“√ ºà“µ—¥≈ß‰¥â¡“°

266

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Antecubital vein

Cephalic vein Radial artery

Brachial artery Basilic vein Straight forearm graft

Ulnar artery

√Ÿª∑’Ë 28.6 straight fore-arm graft 2.2 dialysis access grafts ®–æ‘®“√≥“ºà“µ—¥‡¡◊ÕË À≈Õ¥‡≈◊Õ¥¥”„µâº«‘ Àπ—ß∫√‘‡«≥·¢π ‡ ◊ËÕ¡ ¿“æ‰¡à‡À¡“–µàÕ°“√∑” direct AVF ¢âÕ¥âÕ¬ ¢Õß°“√„™âÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡‡¡◊ËÕ‡∑’¬∫°—∫À≈Õ¥‡≈◊Õ¥¥” ¢ÕßºŸâ ªÉ « ¬„π°“√∑” conduit §◊ Õ °“√‡°‘ ¥ µ‘ ¥ ‡™◊È Õ thrombisis pseudoaneuarysm µ≈Õ¥®π¿“«– ·∑√°´âÕπÕ◊πË Ê ‰¥â∫Õà ¬°«à“(11,15,16) §«√‡√‘¡Ë µâπ∑”®“° ·¢π à«πª≈“¬ ”À√—∫À≈Õ¥‡≈◊Õ¥‡∑’¬¡∑’Ë „™â·∑ß‡ âπ ‡æ◊ÕË øÕ°‡≈◊Õ¥ PTFE ®–¡’ª√– ‘∑∏‘¿“æ¥’°«à“ tanned bovine carotid artery, Human umbilical vein graft (HUVG) À√◊Õ cryopreserved vein 2.2.1 fore-arm arteriovenous fistula 2.2.1.1 straight fore-arm graft (√Ÿª∑’Ë 28.6) ‚¥¬„™â À≈Õ¥‡≈◊Õ¥‡∑’¬¡µàÕ√–À«à“ß radial artery µ√ß ¢âÕ¡◊Õ°—∫À≈Õ¥‡≈◊Õ¥¥”∫√‘‡«≥ antecubital fossa (basilic, cephalic À√◊Õ antebrachial veins) ¢âÕ‡ ’¬¢Õß straight graft §◊Õµ”·Àπàß∑’Ë®– ·∑ß‡ âπ¡’πÕâ ¬ ∑”„ÀâµÕâ ß·∑ßµ”·Àπàß‡¥‘¡´È”´“° ®–∑”„Àâ‡°‘¥¿“«–·∑√°´âÕπ·≈–Õ“¬ÿ°“√∑”ß“π πâÕ¬ „πºŸªâ «É ¬‡∫“À«“π À≈Õ¥‡≈◊Õ¥·¥ß∫√‘‡«≥ ¢âÕ¡◊Õ®–µ’∫ßà“¬ ‚¥¬‡©æ“– radial artery

Õ“®®–¡’°“√µ’∫·§∫‡ªìπ™à«ß Ê ∑”„ÀâµàÕ¬“° À√◊Õ·¡â«à“µàÕ·≈â«‡≈◊Õ¥®–‰À≈ºà“π√Ÿ fistula ‰¡à ‡æ’¬ßæÕ ”À√—∫°“√øÕ°‡≈◊Õ¥·≈–®–µ—π‰ª„π∑’ Ë ¥ÿ 2.2.1.2 fore-arm loop graft (√Ÿª∑’Ë 28.7) µàÕ®“° distal branchial artery ‰ª¬—ßÀ≈Õ¥‡≈◊Õ¥ ¥”∫√‘‡«≥ antecubital fossa ‚§âß‡ªìπ√Ÿª Ucurve „µâº‘«Àπ—ß∑âÕß·¢π æ∫«à“¡’‡≈◊Õ¥‰À≈ ºà“π‡¢â“‰ªÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡¥’¡“°®“° brachial artery ´÷Ëß¡’¢π“¥‚µ°«à“ radial artery §«“¡ ¬“«·≈–µ”·Àπà ß ∑’Ë ® –·∑ß‡ â π øÕ°‡≈◊ Õ ¥¡’ ¡“°°«à“™π‘¥µ√ß 2.2.2 upper arm graft ∑”‡¡◊ÕË access ‡¥‘¡∫√‘‡«≥ ∑âÕß·¢π‡ ◊ÕË ¡ ¿“æ‰¡à “¡“√∂„™âøÕ°‡≈◊Õ¥‰¥â·≈â« 2.2.2.1 curved upper arm graft (√Ÿª∑’Ë 28.8) µàÕ ®“° brachial artery „°≈â°∫— antecubital fossa ºà“π‚æ√ß„µâº«‘ Àπ—ß∑Õ¥¢â“¡ dorsal ·≈– lateral aspect ¢Õßµâπ·¢π µàÕ‡¢â“°—∫ cephalic, basilic À√◊Õ axillary veins µ√ßÀ—«‰À≈àÀ√◊Õµâπ·¢π À√◊Õ®–µàÕ°≈—∫¥â“π®“° axillary artery ∑’Ëµâπ ·¢π‰ª¬—ß brachial vein ∫√‘‡«≥ antecubital fossa °Á ‰¥â

267

HEMODIALYSIS ACCESS

Brachial artery Cephalic vein Forearm loop graft Radial artery

Basillic vein Antecubital vein Ulnar artery √Ÿª∑’Ë 28.7 forearm loop graft

Curved upper arm access graft Cephalic vein

Axillary vein

Basillic vein

√Ÿª∑’Ë 28.8 loop upper arm graft

Brachial artery

268

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Axillary artery

Loop upper arm graft

Axillary vein

√Ÿª∑’Ë 28.9 looped upper arm graft 2.2.2.2 looped upper arm graft (√Ÿª∑’Ë 28.9) µàÕ À≈Õ¥‡≈◊Õ¥‡∑’¬¡‡¢â“°—∫ à«πµâπ¢Õß axillary artery ·≈– vein ‚¥¬„Àâ à«π‚§âß¢Õß U-curve Õ¬Ÿà‡Àπ◊ÕµàÕ antecubital fossa æ∫«à“¡’‡≈◊Õ¥ ‰À≈ºà“πÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡‡æ’¬ßæÕ ·≈–¡’‡π◊ÈÕ∑’Ë ‡À≈◊Õ‡øóÕ ”À√—∫·∑ß‡ âπ

III. CHRONIC DIALYSIS CATHETER cuffed dialysis catheter (√Ÿª∑’Ë 28.2) ‡ªìπ dual-lumen catheter Õ¥ “¬ºà“πº‘«Àπ—ß‰ª¬—ßÀ≈Õ¥‡≈◊Õ¥¢π“¥‚µ‡™àπ internal jugular À√◊Õ subclavian veins À√◊Õ°“√ cut down ºà“π‡¢â“∑“ß upper cephalic À√◊Õ jugular veins æ∫«à“‡°‘¥ thrombosis ‡ªìπ¿“«–·∑√°´âÕπ∑’Ëæ∫‰¥â∫àÕ¬·°â ‰¢‰¥â ‚¥¬°“√ ©’¥ “√≈–≈“¬≈‘¡Ë ‡≈◊Õ¥ Urokinase 5,000-10,000 ¬Ÿπµ‘ ºà“π‡¢â“ ∑“ß “¬¬“ß∑—ßÈ Õß¥â“π ¿“«–·∑√°´âÕπÕ◊πË Ê ∑’ÕË “®®–‡°‘¥¢÷πÈ ‰¥â ¡’‡≈◊Õ¥‰À≈ºà“ππâÕ¬À√◊Õ –¥ÿ¥‡ªìπ™à«ß Ê central vein thrombosis ·≈–°“√µ‘¥‡™◊ÕÈ ¢Õß “¬ «π

°“√‡µ√’¬¡·≈–¥Ÿ·≈ºŸâªÉ«¬°àÕπºà“µ—¥ I. °“√ª√–‡¡‘π·≈–‡≈◊Õ¥À≈Õ¥‡≈◊Õ¥¥”∑’®Ë –π”¡“„™â µ≈Õ¥ ®π°“√‡≈◊Õ°«‘∏º’ “à µ—¥ venous outflow ‡ªìπ à«π ”§—≠∑’ Ë ¥ÿ ¢Õß hemodialysis access ¥—ßπ—Èπ ®÷ß§«√‡≈◊Õ°À≈Õ¥‡≈◊Õ¥¥”„Àâ ‡À¡“– ¡§«√ª√–‡¡‘π ¿“æÀ≈Õ¥‡≈◊Õ¥¥”„µâº‘«Àπ—ß∫√‘‡«≥·¢π

∂â“¡’°“√‚ªÉßæÕß §¥‡§’¬È « À√◊Õ·¢π∫«¡ Õ“®®–¡’°“√Õÿ¥µ—π¢Õß À≈Õ¥‡≈◊Õ¥¥”¢π“¥„À≠à∫√‘‡«≥µâπ·¢π §«√∑” venogram À√◊Õ duplex scan µ√«®¥Ÿ§«“¡º‘¥ª°µ‘À√◊Õ°“√Õÿ¥µ—π¢ÕßÀ≈Õ¥ ‡≈◊Õ¥¥”°àÕπºà“µ—¥∑” hemodialysis access ‡æ√“–∂â“À≈Õ¥ ‡≈◊Õ¥¥”µ’∫µ—π·≈â« ∂â“µàÕ‰ª°Á „™âß“π‰¡à ‰¥â Õ“®®–‡°‘¥¿“«– ·∑√°´âÕπ∑”„Àâ·¢π∫«¡¡“°¢÷πÈ Õ’° µ√«®À≈Õ¥‡≈◊Õ¥¥”„µâº«‘ Àπ—ß∫√‘‡«≥·¢π ‚¥¬„™â “¬¬“ß√—¥ µâπ·¢π §≈” cephalic vein ´÷ßË ∑Õ¥ºà“π¢âÕ¡◊Õ¥â“ππÕ°∂÷ß antecubital fossa ∂â“ cephalic vein ·≈– radial artery ¥’ §«√®–‡√‘Ë¡µâπ®“°°“√∑” CB fistula ∫√‘‡«≥¢âÕ¡◊Õ ∂â“À≈Õ¥ ‡≈◊Õ¥¥”∫√‘‡«≥∑âÕß·¢π·ø∫≈’∫ À≈Õ¥‡≈◊Õ¥¥”∫√‘‡«≥ antecubital fossa ·≈– cephalic vein µ√ßµâπ·¢π¬—ß¥’Õ¬Ÿà §«√ æ‘®“√≥“∑” antecubital AVF (brachial artery to antecubital or cephalic veins) ∂â“§≈” basilic vein ‰¥â™¥— ®π∂÷ß¢âÕ¡◊Õ§«√∑” ulnar artery to basilic vein AVF ·µà∫√‘‡«≥π’È®–·∑ß‡ âπ Õ¥‡¢Á¡‡æ◊ËÕøÕ°‡≈◊Õ¥‰¥â≈”∫“° ºŸâªÉ«¬«“ß·¢πµ“¡·π«√“∫‰¡à –¥«° ∂â“À“À≈Õ¥‡≈◊Õ¥¥”∑’·Ë ¢π‰¡à¡À’ √◊Õæ¬“∏‘ ¿“æ®π„™â°“√ ‰¡à ‰¥â §«√æ‘®“√≥“„™âÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡·∑π °àÕπºà“µ—¥∑” hemodialysis access À≈—ß®“°‡≈◊Õ°À≈Õ¥ ‡≈◊Õ¥¥”∑’‡Ë À¡“– ¡∑’®Ë –µàÕ‰¥â·≈â«Àâ“¡‡®“–‡≈◊Õ¥·∑ß‡ âπ„Àâ “√πÈ” ·¢π¢â“ßπ—πÈ ∂â“¡’§«“¡®”‡ªìπ®√‘ß Ê §«√„™âÀ≈Õ¥‡≈◊Õ¥¥”„µâº«‘ Àπ—ß ∫√‘‡«≥À≈—ß¡◊Õ·∑π

269

HEMODIALYSIS ACCESS

II. ª√–‡¡‘πª√‘¡“≥°“√‰À≈‡«’¬π¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß∂â“¡’ ‡≈◊Õ¥‰À≈ºà“ππâÕ¬ hemodialysis access ∑’Ë √â“ß‰«â®–‡ ◊ËÕ¡ ¿“æ‡√Á« ¡’°“√µ’∫µ—π®π„™âß“π‰¡à ‰¥â ‰¡à¡’ maturation ·¢π ¢“¥‡≈◊ Õ ¥®“° arterial steal syndrome §«√§≈”™’ æ ®√ ‡ª√’¬∫‡∑’¬∫√–À«à“ß·¢π∑—Èß Õß¢â“ß ·≈–«—¥§«“¡¥—π‚≈À‘µ ∂â“ §≈”™’æ®√¢â“ßÀπ÷Ëß‰¥â‡∫“°«à“·≈–§«“¡¥—π´’ ‚µ≈‘§µË”°«à“·¢π Õ’°¢â“ß‡°‘π 10 torr πà“®–¡’æ¬“∏‘ ¿“æ°“√µ’∫µ—π¢ÕßÀ≈Õ¥ ‡≈◊Õ¥·¥ß ·¢π¢â“ßπ—πÈ ‰¡à§«√ºà“µ—¥∑” hemodialysis access

°“√ºà“µ—¥ ‚¥¬∑—«Ë ‰ª·≈â«°“√ºà“µ—¥ AVF ∫√‘‡«≥¢âÕ¡◊Õ·≈–∑âÕß·¢π·∫∫ direct arteriovenous anastomosis “¡“√∂∑”‰¥â ‚¥¬°“√ ©’¥¬“™“‡©æ“–∑’Ë ·µà∂â“∑’Ë¡’§«“¡®”‡ªìπ∑’Ë®–µâÕß„™âÀ≈Õ¥‡≈◊Õ¥ ‡∑’¬¡§«√„™â regional anesthesia °àÕπºà“µ—¥§«√„Àâ¬“ªØ‘™«’ π– Vancomycin ‡¢â“À≈Õ¥‡≈◊Õ¥¥” ‚¥¬‡©æ“–ºŸâªÉ«¬‡∫“À«“π °“√®—∫µâÕß‡π◊ÈÕ‡¬◊ËÕ§«√√–¡—¥√–«—ß‰¡à „Àâ™È”¡“° √â“ß‚æ√ß„µâº‘« Àπ—ß¢π“¥æÕ¥’„ÀâÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡ºà“π √–«—ß‰¡à „Àâ‡°‘¥≈‘Ë¡‡≈◊Õ¥ ¢π“¥„À≠àÀ√◊ÕÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡À—° ‚°àß ßÕ æ—∫ Àâ“¡‡≈◊Õ¥∑’Ë ‰À≈ ´÷¡„ÀâÀ¬ÿ¥ π‘∑°àÕπ∑’®Ë –‡¬Á∫·º≈ªî¥

°“√¥Ÿ·≈ºŸâªÉ«¬À≈—ßºà“µ—¥ —ß‡°µÿ·≈–µ√«®¥Ÿ«“à AVF À√◊Õ AVG ¬—ß∑”ß“πª°µ‘·≈–¡’ ‡≈◊Õ¥‰À≈‡«’¬πºà“πÀ√◊Õ‰¡à‚¥¬®–§≈”‰¥â thrill µ√ß venous anastomosis §≈”™’æ®√ à«πª≈“¬µàÕ AVF ‰¥â µ√«®¥Ÿ°“√∑”ß“π ¢Õß√–∫∫ª√– “∑ à«πª≈“¬«à“¬—ß‡ªìπª°µ‘¥’Õ¬ŸàÀ√◊Õ‰¡à Õÿ≥À¿Ÿ¡‘ ¢Õß·¢π∑—Èß Õß¢â“ß·≈– capillary refill §«√‡∑à“°—π ∂â“¡’ Õ“°“√ª«¥·¢π¡“°Õ“®®–‡°‘¥°“√µ’∫µ—π¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ßÀ√◊Õ steal syndrome À≈—ßºà“µ—¥„ÀâºªŸâ «É ¬¬°·¢π Ÿß‡Àπ◊Õ√–¥—∫À—«„® ‡æ◊ËÕ„Àâ·º≈¬ÿ∫∫«¡ Àâ“¡æ—π·º≈·πàπÀ√◊Õ«—¥§«“¡¥—π‚≈À‘µ·¢π ¢â“ßπ—πÈ ∂â“¡’≈¡‘Ë ‡≈◊Õ¥¢π“¥„À≠à‡°‘¥„π·º≈§«√§«—°‡Õ“ÕÕ° À≈—ß ºà“µ—¥‡√‘¡Ë „ÀâºªŸâ «É ¬¢¬—∫·¢π·≈–π‘«È ‰¥â ªÑÕß°—π‰¡à „Àâ‡°‘¥ stiffness Fistula and graft maturation §«√√Õª√–¡“≥ 2 —ª¥“Àå AVG °Á mature æÕ∑’®Ë –„™âøÕ° ‡≈◊Õ¥‰¥â·≈â« ºπ—ßÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡®–‡°“–µ‘¥·πàπ°—∫‡π◊ÕÈ ‡¬◊ÕË √Õ∫ ¢â“ß ‡«≈“·∑ß‡ âπÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡®–‰¡àÀ≈ÿ¥≈Õ°·≈–‡°‘¥≈‘Ë¡ ‡≈◊Õ¥¢π“¥‚µ„µâº«‘ Àπ—ß À√◊Õ thrombosis ”À√—∫ AVF ®–„™â √–¬–‡«≈“ª√–¡“≥ 2-3 ‡¥◊Õπ ªí®®—¬µàÕ‰ªπ’¡È º’ ≈∑”„Àâ hemodialysis access ‡ ◊ÕË ¡ ¿“æÀ√◊Õ‰¡à “¡“√∂„™âß“π‰¥âµ“¡ª°µ‘ (17)

1. °“√µ’∫·§∫¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß à«π∑’ÕË ¬Ÿ‡à Àπ◊ÕÀ√◊Õ„µâµÕà √Õ¬µàÕ 2. ‡≈◊Õ¥‰À≈‡«’¬πºà“π‡¢â“À≈Õ¥‡≈◊Õ¥¥”‰¡à‡æ’¬ßæÕ À√◊Õ¡’ °“√µ’∫µ—π¢ÕßÀ≈Õ¥‡≈◊Õ¥¥”∫√‘‡«≥‡Àπ◊Õ√Õ¬µàÕ 3. ¡’À≈Õ¥‡≈◊Õ¥¥”µàÕ√–À«àßÀ≈Õ¥‡≈◊Õ¥¥”∑’ºË «‘ Àπ—ß°—∫deep vein (perforators)

°“√¥Ÿ·≈ dialysis access grafts µ”·Àπàß∑’·Ë ∑ß‡ âπ§«√°√–®“¬„Àâ∑«—Ë µ≈Õ¥‡ âπ ‰¡à·∑ß´È”´“° Õ¬Ÿ∫à √‘‡«≥„¥∫√‘‡«≥Àπ÷ßË ‡∑à“π—πÈ ªÑÕß°—π°“√©’°¢“¥ µ’∫µ—π À√◊Õ pseudoaneurysm µâÕß‡§√àß§√—¥„π‡∑§π‘§ª√“»®“°‡™◊ÕÈ ¢≥–·∑ß ·∑ß‡¢Á¡„Àâ∑–≈ÿºπ—ßÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡¥â“πÀπâ“‡∑à“π—Èπ‰¡à·∑ß∑–≈ÿ ‡≈¬‰ª®π∂÷ßºπ—ß¥â“πÀ≈—ß √–«—ß‰¡à „ÀâºŸâªÉ«¬™ÁÕ§À√◊Õ§«“¡¥—π ‚≈À‘µµË”‡ªìπ√–¬–‡«≈“π“π ‡æ√“–®–‡°‘¥ thrombosis ‰¥â À≈—ß øÕ°‡≈◊Õ¥·≈â« °“√¥÷ß‡Õ“‡¢Á¡ÕÕ°®–µâÕß°¥∫√‘‡«≥∑’·Ë ∑ß‡¢Á¡„Àâ ·√ß·≈–„™â‡«≈“π“πæÕ¥’ ªÑÕß°—π°“√‡°‘¥≈‘¡Ë ‡≈◊Õ¥ psudo-aneurysm ·≈–°“√Õÿ¥µ—π

ªí≠À“·≈–¿“«–·∑√°´âÕπ∑’Ëæ∫‰¥â∫àÕ¬¢Õß hemodialysis access(17-23) 1. À≈Õ¥‡≈◊Õ¥¥”·≈–Õÿ¥µ—π®“°°“√§“ “¬ «π‡ªìπ√–¬– ‡«≈“π“π æ∫‰¥âª√–¡“≥√âÕ¬≈– 7-20 “‡Àµÿπ”§◊Õ°“√ ‡°‘¥ª≈Õ°‰ø∫√‘πÀÿâ¡√Õ∫ “¬ «π·≈–µàÕ¡“¡’≈‘Ë¡‡≈◊Õ¥ ¡“‡°“– ÿ¡°—π®πÕÿ¥µ—π„π∑’Ë ÿ¥ °“√Õÿ¥µ—π‡°‘¥¢÷Èπ‰¥â∑—Èß subclavian, internal jugular vein À√◊ Õ SVC ·°â ‰¢‰¥â ‚¥¬°“√©’¥ “√≈–≈“¬≈‘Ë¡‡≈◊Õ¥ Urokinase 5,000-10,000 ¬Ÿπ‘µ ‡¢â“„π “¬ «π·µà≈–¥â“π ≈‘Ë¡ ‡≈◊Õ¥®–∂Ÿ°≈–≈“¬·≈– “¡“√∂„™â “¬ «πøÕ°‡≈◊Õ¥µàÕ ‰ª‰¥â ∂â“ºŸâªÉ«¬¡’·¢π∫«¡®–∫àß∫Õ°∂÷ß°“√Õÿ¥µ—π¢Õß central vein §«√¥÷ß‡Õ“ “¬ «πÕÕ° „Àâ¬“≈–≈“¬≈‘¡Ë ‡≈◊Õ¥·≈–¬°·¢π Ÿß„Àâ¬ÿ∫∫«¡ Àâ“¡∑”°“√ºà“µ—¥ AVF À√◊Õ AVG µ≈Õ¥®π·∑ß‡ âπ Õ¥ “¬‡¢â“ subclavian ¢Õß·¢π¢â“ßπ—πÈ ‚¥¬‡¥Á¥¢“¥ 2. ª√– ‘∑∏‘¿“æ°“√∑”ß“π¢Õß hemodialysis access º‘¥ª°µ‘ ®“°°“√¡’‡≈◊Õ¥‰À≈ºà“ππâÕ¬°«à“ 300 ¡‘≈≈‘≈µ‘ √ µàÕπ“∑’À√◊Õ¡“°°«à“π’È √âÕ¬≈– 15 ¡—°‡°‘¥®“°°“√µ’∫ ·§∫∫√‘‡«≥ venous outflow tract, arterial inflow À√◊Õ∫πÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡‡Õß ∂â“§≈”™’æ®√°“√‡µâπ¢Õß À≈Õ¥‡≈◊Õ¥‡∑’¬¡‰¥â·√ß¡“°· ¥ß«à“°“√Õÿ¥µ—πÕ¬Ÿàµ√ß

270 venous outflow ·µà∂“â §≈”‰¥â‡∫“®–∫àß∫Õ°∂÷ß inflwo stenosis §«√∑” arteriography À√◊Õ fistulography ‡æ◊ËÕÀ“ “‡Àµÿ·≈–¥Ÿµ”·Àπàß¢ÕßÀ≈Õ¥‡≈◊Õ¥∑’Ëµ’∫·§∫ °«à“ª°µ‘ ·°â ‰¢‚¥¬°“√„™â∫—≈≈Ÿπ¢¬“¬∂à“ßÀ√◊Õºà“µ—¥ ´àÕ¡·´¡ 3. ¡’°“√Õÿ¥µ—πÕ¬à“ß‡©’¬∫æ≈—π¢ÕßÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡À√◊Õ fistula °“√Õÿ¥µ—π∑’‡Ë °‘¥¢÷πÈ ∑—π∑’¿“¬À≈—ß°“√ºà“µ—¥æ∫‰¥â ‰¡à∫Õà ¬ “‡Àµÿ‡°‘¥®“° outflow stenosis À√◊Õ‡∑§π‘§ °“√ºà“µ—¥µàÕÀ≈Õ¥‡≈◊Õ¥‰¡à¥’§«√√’∫∑”°“√ºà“µ—¥·°â ‰¢ ∑—π∑’„πÀâÕßºà“µ—¥ À≈Õ¥‡≈◊Õ¥‡∑’¬¡Õÿ¥µ—π∑—π∑’¿“¬À≈—ß°“√ºà“µ—¥ ‡°‘¥ ®“°‡∑§π‘§°“√ºà“µ—¥‰¡à¥’ ‡™àπ ¡’°“√‚°àßßÕ¢ÕßÀ≈Õ¥ ‡≈◊Õ¥‡∑’¬¡ thrombus Õÿ¥µ—π, inadequate outflow vein §«√√’∫ºà“µ—¥·°â ‰¢´àÕ¡·´¡„À¡à∑π— ∑’ “‡ÀµÿÕπ◊Ë ¢Õß graft failure ∑’æË ∫‰¥â‡™àπ °“√Õ—°‡ ∫µ‘¥‡™◊ÕÈ §«“¡¥—π‚≈À‘µµË” ·≈–‡≈◊Õ¥¢âπ‡Àπ’¬«µ—«‡°‘π‰ª (hypercoagulability) 4. °“√µ’∫µ—πÀ√◊Õ„™âß“π‰¡à‰¥â¿“¬À≈—ß°“√ºà“µ—¥ ‚¥¬∑—«Ë ‰ª ·≈â«ª√– ‘∑∏‘¿“æ¢Õß°“√∑”ß“π¢Õß hemodialysis access ∑’®Ë –‰¡à‡æ’¬ßæÕ (dysfunction) °àÕπ∑’®Ë –¡’°“√Õÿ¥ µ—π ≈—°…≥–∑’‡Ë °‘¥¢÷πÈ ®–§≈â“¬°—∫À≈Õ¥‡≈◊Õ¥‡∑’¬¡∑’µË Õà ∑” bypass ¢ÕßÀ≈Õ¥‡≈◊Õ¥∑’Ë·¢π¢“ ∂â“‡°‘¥¢÷Èπ¿“¬À≈—ß °“√ºà“µ—¥√–¬–‡«≈“‰¡àπ“π ·°â ‰¢‰¥â ‚¥¬°“√©’¥¬“≈–≈“¬ ≈‘Ë¡‡≈◊Õ¥ Urokinase ºà“π “¬¬“ß‡¢â“‰ª¬—ß∫√‘‡«≥∑’Ë¡’ ≈‘¡Ë ‡≈◊Õ¥Õÿ¥µ—πÀ√◊Õºà“µ—¥·°â ‰¢ °“√Õÿ¥µ—π¢ÕßÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡∑’‡Ë °‘¥¢÷πÈ „π√–¬–À≈—ß (late graft occlusion) ‡ªìπº≈¡“®“° perianastomotic neointimal hyperplasia µ√ß venous outflow æ∫ ∫àÕ¬À≈—ßºà“µ—¥ 6 ‡¥◊ÕπÀ√◊Õ 2 ªï À≈—ßºà“µ—¥§√—Èß·√° ∂â“π“π‡°‘π°«à“ 2 ªï “‡Àµÿπà“®–‡°‘¥®“°À≈Õ¥‡≈◊Õ¥ ‡∑’¬¡‡Õß§◊Õ ¡’ fibrous ingrowth µ√ß®ÿ¥∑’·Ë ∑ß‡ âπ∫àÕ¬ Ê ·°â ‰¢‰¥â ‚¥¬°“√ºà“µ—¥‡ª≈’Ë¬πÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡‡ âπ „À¡àµ√ß®ÿ¥∑’¡Ë ª’ ≠ í À“ 5. arterial steal syndrome ‡°‘¥®“° low resistance venous outflow ®–∑”„Àâ‡°‘¥®“°À≈Õ¥‡≈◊Õ¥·¥ßºà“π‡¢â“ fistula ‡¢â“‰ª Ÿà low resistance venous outflow ‡ªìπ à«π„À≠à ‚¥¬ à«ππâÕ¬®–ºà“π‰ª¬—ßÀ≈Õ¥‡≈◊Õ¥·¥ß ∑’ÕË ¬Ÿà „µâµÕà fistula Õ“°“√¢“¥‡≈◊Õ¥¢Õß·¢π à«πª≈“¬ ·≈–¡◊Õ®–√ÿπ·√ß¡“°‡¡◊ËÕ fistula mature ∂â“„™âπ‘È« °¥≈ß∫π fistula À√◊ÕÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡®–æ∫«à“™’æ®√

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥ §≈”‰¥â®“°À≈Õ¥‡≈◊Õ¥ª≈“¬µàÕ fistula À√◊ÕÀ≈Õ¥ ‡≈◊Õ¥‡∑’¬¡®–æ∫«à“™’æ®√∑’§Ë ≈”‰¥â®“°À≈Õ¥‡≈◊Õ¥ª≈“¬µàÕ fistula ®–‡∫“≈ß·≈– perfusion ‰¡à ¥’ ∫ √‘ ‡ «≥·¢π à«πª≈“¬·≈–¡◊Õ Õ“°“√¢Õß steal syndrome §◊Õ¡’ ¡◊Õ‡¬Á∫·≈–™“ª≈“¬¡◊Õ ∂â“Õ“°“√√ÿπ·√ß®–¡’ ischemic rest pain ª≈àÕ¬∑‘Èß‰«â ‰¡à√—°…“π‘È«®–‡πà“µ“¬ √–∫∫ ª√– “∑ à«πª≈“¬®– Ÿ≠‡ ’¬ª√– ‘∑∏‘¿“æ √—°…“‚¥¬ °“√ºà“µ—¥∑” bandaging À√◊ÕºŸ°√Ÿ fistula µ√ß outflow tract ¢ÕßÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡„Àâ√‡Ÿ ≈Á°≈ß 6. highflow AVF ∂â“ AVF ¡’‡≈◊Õ¥‰À≈‡«’¬πºà“π‡ªìπ ª√‘¡“≥∑’ Ë ßŸ ‡°‘π‰ª ®–¡’º≈µàÕ√–∫∫‰À≈‡«’¬π¢Õß√à“ß°“¬ ‡™àπ ™’æ®√‰« À—«„®«“¬ ·≈– hypertrophic cardiomyopathy ‚¥¬∑—Ë«‰ª·≈â«°“√ºà“µ—¥„™âÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡ ®–‰¡à‡°‘¥ªí≠À“π’È¢÷Èπ ‡æ√“–À≈Õ¥‡≈◊Õ¥‡∑’¬¡®–¡’¢π“¥ §ß∑’Ë ‰¡à¢¬“¬ÕÕ° ¡’ fixed flow resistant ∂â“‡°‘¥¿“«– high outflow AVF ·°â ‰¢‰¥â ‚¥¬°“√∑” bandaging ºŸ°∑”„Àâ√Ÿ fistula ‡≈Á°≈ß À√◊Õ‡¬Á∫ªî¥‰ª‡≈¬ ∂â“¡’ ªí≠À“¡“°µàÕ√–∫∫‰À≈‡«’¬π‡≈◊Õ¥¢Õß√à“ß°“¬ 7. °“√Õ—°‡ ∫µ‘¥‡™◊ÕÈ æ∫«à“ direct autogenous AVF ‰¡à ¡’ªí≠À“°“√Õ—°‡ ∫µ‘¥‡™◊ÈÕÀ√◊Õæ∫πâÕ¬¡“° °“√Õ—°‡ ∫ µ‘¥‡™◊ÈÕ∑ÿµ‘¬¿Ÿ¡‘¢Õß AVF ‡°‘¥®“°À≈—ßºà“µ—¥·≈â«¡’≈‘Ë¡ ‡≈◊Õ¥´÷ßË ‡ªìπ media ∑’¥Ë ’„π°“√‡®√‘≠‡µ‘∫‚µ¢Õß·∫§∑’‡√’¬ §—Ë ß Õ¬Ÿà „µâº‘«Àπ—ß∫√‘‡«≥·º≈ºà“µ—¥ °“√µ‘¥‡™◊ÈÕÕ“®®– ‡°‘ ¥ µ√ß·º≈ºà “ µ— ¥ À√◊ Õ °√–®“¬¡“®“°·À≈à ß Õ◊Ë π °Á ‰ ¥â °“√„™âÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡À√◊Õ “¬¬“ß§“ «πÕ—µ√“°“√ Õ— ° ‡ ∫µ‘ ¥ ‡™◊È Õ §à Õ π¢â “ ß Ÿ ß ‡π◊Ë Õ ß®“°«— ¥ÿ ∑’Ë „ ™â ‡ ªì π ‘Ë ß ·ª≈°ª≈Õ¡µàÕ√à“ß°“¬ “‡Àµÿ∑’Ë ”§—≠∑’Ë ÿ¥„π°“√µ‘¥ ‡™◊ÈÕ´÷Ëß¡—°®–‡°‘¥¢÷Èπ„πÀâÕßºà“µ—¥§◊Õ ‡∑§π‘§∑’Ëª√“»®“° ‡™◊ÈÕ‰¡à ¡∫Ÿ√≥å‡æ’¬ßæÕ ∑”„Àâ‡™◊ÈÕ Staph.aureus ·≈– Staph.epidermidis ºà“π®“°º‘«Àπ—ß‡¢â“‰ª Ÿà hemodialysis access §«√∑”§«“¡ –Õ“¥¥Ÿ·≈ “¬∑’ Ë «π§“‰«â∑°ÿ «—π „™âπÈ”¬“¶à“‡™◊ÕÈ ∑“·≈–ªî¥·º≈¥â«¬ºâ“°äÕ´ ‰¡à§«√„™â ·ºàπæ≈“ µ‘° ¬÷¥·ª–∑—∫·º≈‡æ√“–®–‡°‘¥§«“¡™◊Èπ„π ·º≈‡ªì π ¿“æ·«¥≈â Õ ¡∑’Ë ∑”„Àâ ‡ ™◊È Õ ·∫§∑’ ‡ √’ ¬ ‡®√‘ ≠ ‡µ‘∫‚µ‰¥â¥’ ∂â“¡’°“√µ‘¥‡™◊ÈÕ∑’Ë ‰¡à√ÿπ·√ß¢Õß “¬ «π§√—Èß ·√°§«√√—°…“‚¥¬°“√„Àâ¬“ªØ‘™«’ π–‡¢â“∑“ßÀ≈Õ¥‡≈◊Õ¥ ¥” ·µà∂“â °“√Õ—°‡ ∫µ‘¥‡™◊ÕÈ √ÿπ·√ß §«√¥÷ß‡Õ“ “¬ «π§“ ÕÕ° °“√µ‘¥‡™◊ÕÈ ¢Õß dialysis access ∫“ß§√—ßÈ ®–‡°‘¥ ¢≥–∑”°“√ºà“µ—¥∑—π∑’ ·µà «à π„À≠à·≈â«‡°‘¥®“°°“√ªπ

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HEMODIALYSIS ACCESS

‡ªóôÕπ√–À«à“ß°“√·∑ß‡ âπøÕ°‡≈◊Õ¥´÷Ëß‡∑§π‘§ °“√ ª√“»®“°‡™◊ÈÕ‰¡à ¡∫Ÿ√≥å‡æ’¬ßæÕ ‚¥¬‡©æ“–¡’°“√·∑ß ´È”´“°À≈“¬§√—Èß ·≈–‡°‘¥≈‘Ë¡‡≈◊Õ¥ À≈—ßºà“µ—¥∂â“‡°‘¥ cellulitis ∑—π∑’√—°…“‚¥¬°“√„Àâ¬“ªØ‘™’«π–∑“ßçÀ≈Õ¥ ‡≈◊Õ¥¥” ·µà∂“â „Àâ „π√–¬–‡«≈“Àπ÷ßË ·≈â«Õ“°“√‰¡à¥¢’ π÷È „Àâ π÷°∂÷ß°“√Õ—°‡ ∫µ‘¥‡™◊ÕÈ ¢ÕßÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡ ∂â“°“√Õ—°‡ ∫µ‘¥‡™◊ÈÕ¢ÕßÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡≈ÿ°≈“¡ √ÿπ·√ß¡“° ‡™◊ÈÕ®–‡¢â“°√–· ‡≈◊Õ¥ §«√ºà“µ—¥‡Õ“ À≈Õ¥‡≈◊Õ¥‡∑’¬¡∑’Ëµ‘¥‡™◊ÈÕÕÕ° ‡ªî¥·º≈ºà“µ—¥∑‘Èß‰«â√Õ ®π°“√µ‘¥‡™◊ÈÕ≈¥πâÕ¬≈ß ·º≈ –Õ“¥¥’§àÕ¬‡¬Á∫ªî¥·º≈ °“√µ‘¥‡™◊ÈÕ¢ÕßÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡∫“ß§√—Èß®–∑”„Àâ‡°‘¥≈‘Ë¡ ‡≈◊Õ¥Õÿ¥µ—π¿“¬„π∑àÕÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡ ·≈–∑”„ÀâÀ≈Õ¥ ‡≈◊Õ¥‡∑’¬¡À≈ÿ¥≈Õ°‡≈“–ÕÕ°ßà“¬®“°‡π◊ÕÈ ‡¬◊ÕË ∂â“°“√Õ—°‡ ∫µ‘¥‡™◊ÕÈ ‡°‘¥‡©æ“–∑’ÀË √◊Õ‡ªìπ‚æ√ßÀπÕß À√◊Õ cellulitis ∑’Ë ‰¡à≈°ÿ ≈“¡ §«√ºà“µ—¥√–∫“¬‡Õ“ÀπÕß ÕÕ° ·≈–„Àâ¬“ªØ‘™’«π–∑“ßÀ≈Õ¥‡≈◊Õ¥¥” ‰¡à®”‡ªìπ∑’Ë ®–µâÕß¥÷ßÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡ÕÕ°∑—ßÈ ‡ âπ 8. aneurysm ·≈– pseudoaneurysm ∑’æË ∫‰¥â∫Õà ¬§◊Õ aneurysm ¢Õß AVF øíß¥Ÿ«“à ¡’ high velocity turbulent flow À√◊Õ‰¡à ®–æ∫«à“°“√‡°‘¥‡ªìπ aneurysm ¢Õß

AVF ®–‡°‘¥¢÷πÈ ‰¥â∑°ÿ ™—πÈ ¢ÕßÀ≈Õ¥‡≈◊Õ¥ à«π„À≠à®–‚µ ™â“·≈–‰¡à¢¬“¬‡æ‘Ë¡¢÷ÈπÕ’° ´÷Ëß‰¡à®”‡ªìπ∑’Ë®–µâÕßºà“µ—¥ √—°…“§«√‡≈’Ë¬ß‰ª·∑ß‡ âπ∫√‘‡«≥Õ◊Ëπ·∑π °“√‚ªÉßæÕß ∫“ß®ÿ¥¢ÕßÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡‡°‘¥®“°°“√·∑ß‡ âπ´È”´“° „πµ”·Àπàß‡¥‘¡ ºπ—ß¢Õß pseudoaneurysm ®–ª√–°Õ∫ ¥â«¬ organized thrombus ·≈– subcutaneous tissue ®–¢¬“¬‚µ¢÷ÈπÕ¬à“ß√«¥‡√Á«·≈–·µ°ßà“¬ §«√√’∫ ºà “ µ— ¥ √— ° …“‚¥¬°“√‡¬Á ∫ ´à Õ ¡·´¡À√◊ Õ ‡ª≈’Ë ¬ πÀ≈Õ¥ ‡≈◊Õ¥‡∑’¬¡„À¡àµ√ß®ÿ¥æ¬“∏‘ ¿“æ

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272

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‡Õ° “√Õâ“ßÕ‘ß 1. Bennion RS, Wilson SE. Hemodialysis and Vascular Access. In:Moore WS (ed). Vascular Surgery: A Comprehensive Review. 4th ed. Philadelphia:WB Saunders 1993;606-625. 2. Bennion RS, Kempe DA. Arteriovenous Access. In: Strandness ED, van Breda A. (eds). Vascular Disease: Surgical and Interventional Therapy. New York: Churchill Livingtone 1994;1045-1106. 3. Wilson ES. Vascular Access Surgery. Chicago:Year Book Medical Publishger 1988. 4. Byrne C, Vernon P, Cohen JJ. Effects of age and diagnosis on survival of older patients begining chronic dialysis. JAMA 1994;271:24-31. 5. Brescia MJ, Cimino JE, Apple IC, et al. Chronic hemodialysis using venipuncture and surgically created arteriovenous fistula. N Engl J Med 1996;275:1089-1092. 6. Laohapensang K, Lumlertkul D, Pongcheowboon A. Complications of Vascular Access Surgery. Thai J Surg 1992;13:86-90. 7. Ehrenfeld WK, Gransz H, Wylie EJ. Subcutaneous arteriovenous fistulas for hemodialysis. Am J Surg 1972;124:200-206. 8. Zibari GB, Rohr MS, Landreneau MD, et al. Complications from permanent hemodialysis access. 9. Bell DD, Rosenthal JJ. Arteriovenous graft lift in chronic hemodialysis: A need for prolongation. Arch Surg 1988;123:1169-1172. 10. Palder SB, Kirkman RL, Whittemore AD, et al. Vascular access for hemodialysis: Patency rates and results of revisions. Ann Surg 1985;202:235-239. 11. Kherlakian GM, Roedersheimer LR, Arbaugh JJ, et al. Comparison of autogenous fistula versus expanded polytetrafluoroethylene graft fistula for angioaccess in hemodialysis. Am J Surg 1986; 152:238-243. 12. Wedgwood KR, Wiggins PA, Gillou PA. A prospective study endto-side v.s. side-to-side arteriovenous fistula for hemodialysis. Br J Surg 1984;71:640-642.

13. Rivers SP, Scher LA, Sheehan E, et al. Basilic vein transposition: An underused autologous alternative to prosthetic dialysis angioaccess. J Vas Surg 1993;18:391-397. 14. Lo Gerfo FW, Menzoian JO, Kumaki DJ, et al. Transposed basilic vein brachial arteriovenous fistula: A reliable secondary access procedure. Arch Surg 1978;113:1008-1010. 15. Bhat DJ, Tellis VA, Kohlberg WI, et al. Management of sepsis involving expanded polytetrafluoroethylene grafts for hemodialysis access. Surgery 1980;87:445-450. 16. Tordoir JH, Herman JM, Kwan TS, et al. Long-Term follow up of the polytetrafluoroethylene (PTFE) prosthesis as an arteriovenous fistula for hemodialysis. Europ J Vasc Surg 1988;2:3-7. 17. Thomsen MB, Deurell SI, Elfstrom J. What cause the failures in surgically constructed arteriovenous fistulas? Act Chir Scand 1983;149:371-376. 18. Laohapensang K, Salvage of the failing vascular access. J Int Coll Surg Thailand 1992;13:86-90. 19. Zeit RM, Cope C. Failed hemodialysis shunts: One year of experience with aggressive treatment. Radiology 1985;154:353-356. 20. Leny SS, Sherman RA, Nosher SL. Value of clinical for detection of asymptomatic hemodialysis vascular access stenoses. Angiology 1992;43:421-424. 21. Mattson WJ. Recognition and treatment of vascular steal secondary to hemodialysis prostheses. Am J Surg 1987;154:198-201. 22. Bone GE, Momajzl MJ. Management of dialysis fistula thrombosis. Am J Surg 1979;138:901-906. 23. Corry RJ, Patel NP, West JC. Surgical management of complications of vascular access for hemodialysis. Surg Gynecol Obstet 1980;151:49-53.

∫∑∑’Ë 29 ∫“¥‡®Á∫À≈Õ¥‡≈◊Õ¥ Õÿ∫µ— ‡‘ Àµÿ‡ªìπ “‡Àµÿ ”§—≠¢Õß°“√∫“¥‡®Á∫ ∑ÿæ≈¿“æ·≈–µ“¬ Õ—µ√“¢Õß°“√∫“¥‡®Á∫„πªí®®ÿ∫—π¡’·π«‚πâ¡ Ÿß¢÷Èπ¡“°∑ÿ°ªï®“° Õÿ∫µ— ‡‘ Àµÿ¬«¥¬“πæ“Àπ–·≈–°“√∑”√â“¬√à“ß°“¬ (civilian injury) ‡°‘¥„π°≈ÿà¡«—¬‡®√‘≠æ—π∏ÿåæ∫«à“∫“¥‡®Á∫À≈Õ¥‡≈◊Õ¥°Á¡’Õ—µ√“‡æ‘Ë¡ ¢÷πÈ ¥â«¬ ®“° ∂‘µ¢‘ Õß‚√ßæ¬“∫“≈¡À“√“™π§√‡™’¬ß„À¡à æ∫«à“ ∫“¥‡®Á∫À≈Õ¥‡≈◊Õ¥‡æ‘¡Ë ®“° 32 √“¬ „πªïæ.». 2533 ‡ªìπ 48 √“¬ „πæ.». 2536 (µ“√“ß∑’Ë 29.1) §«“¡√ÿπ·√ß¢Õß°“√∫“¥‡®Á∫ Ÿß ¢÷Èπ®“°¬«¥¬“πæ“Àπ–¡’§«“¡‡√Á« Ÿß °√– ÿπªóπ·≈–«—µ∂ÿ√–‡∫‘¥ ∑’Ë „™â¡’Õ”π“®∑–≈ÿ∑–≈«ß Ÿß Iatrogenic injury ®“°°“√µ√«® «‘π‘®©—¬∑“ß√—ß ’«‘∑¬“¢Õß‚√§À≈Õ¥‡≈◊Õ¥·≈–À—µ∂°“√‡°’Ë¬«°—∫ À≈Õ¥‡≈◊Õ¥‡™àπ °“√‡®“– blood gas °Á‡æ‘¡Ë Ÿß¢÷πÈ

“‡Àµÿ·≈–°≈‰°¢Õß°“√∫“¥‡®Á∫ ®“°°“√√«∫√«¡ ∂‘µ‘°“√∫“¥‡®Á∫À≈Õ¥‡≈◊Õ¥¢Õß√.æ.¡À“√“™π§√‡™’¬ß„À¡à√–À«à“ßªïæ.». 2533-2536 ∑—ßÈ À¡¥ 142 √“¬ ‡ªìπ∫“¥‡®Á∫®“°·√ß°√–·∑° 45 √“¬ (31.7%) ®“°·º≈·∑ß∑–≈ÿ 87 √“¬ (61.3%) ®“°«—µ∂ÿ√–‡∫‘¥ 5 √“¬ (3.5%) ·≈–®“°°“√ ∑”À—µ∂°“√„πÀÕºŸªâ «É ¬ 5 √“¬ (3.5%) (µ“√“ß∑’Ë 29.2) ·º≈·∑ß∑–≈ÿ∂â“‡°‘¥®“°«— ¥ÿ¡’§¡‡™àπ ¡’¥ °“√∫“¥‡®Á∫®– ‰¡à√ÿπ·√ß·≈–‡π◊ÈÕ‡¬◊ËÕ®–‰¡à™È”¡“°µà“ß®“°·º≈·∑ß∑–≈ÿ∑’Ë‡°‘¥

µ“√“ß∑’Ë 29.1 ∂‘µº‘ ªŸâ «É ¬∫“¥‡®Á∫À≈Õ¥‡≈◊Õ¥ ‚√ßæ¬“∫“≈ ¡À“√“™π§√‡™’¬ß„À¡à æ.».2533-2536

æ.». 2533 2534 2535 2536

®”π«πºŸªâ «É ¬ 32 42 39 48

µ“√“ß∑’Ë 29.2 °≈‰°°“√∫“¥‡®Á∫À≈Õ¥‡≈◊Õ¥ºŸªâ «É ¬ 142 √“¬ ¢Õß‚√ßæ¬“∫“≈¡À“√“™π§√‡™’¬ß„À¡à æ.». 2533-2536

°≈‰°°“√∫“¥‡®Á∫ ·√ß°√–·∑° (blunt) ·º≈·∑ß∑–≈ÿ (penetrating) ·√ß√–‡∫‘¥ (blast) Iatrogenic

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31.7 61.3 3.5 3.5

274

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Inflammatory reaction

Spasm

Extrinsic compression (dislocation of knee)

Thrombosis Intimal injury

Intimal tear

√Ÿª∑’Ë 29.1 °“√‡§≈◊ÕË π¢Õß¢âÕ‡¢à“‰ª∑“ß¥â“πÀ≈—ß®“°Õÿ∫µ— ‡‘ Àµÿ∑”„Àâ‡°‘¥ °“√∫“¥‡®Á∫µàÕÀ≈Õ¥‡≈◊Õ¥·¥ß·≈–¥” popliteal ´÷Ëß ≈—°…≥–°“√∫“¥‡®Á∫¢ÕßÀ≈Õ¥‡≈◊Õ¥∑’æË ∫‰¥â¡∑’ ß—È subintimal hematoma, intimal tear ·≈– thrombosis Subintimal hematoma

275

∫“¥‡®Á∫À≈Õ¥‡≈◊Õ¥ ®“°°√– ÿπªóπ ∂â“‡ªìπ°√– ÿπ∑’Ë„™â „π ß§√“¡ ®–‡ªìπ high velocity missle ´÷ßË §«“¡‡√Á« Ÿß (>2,500 øÿµ/«‘π“∑’) Õ”π“®°“√∑”≈“¬ ·≈–∑–≈ÿ∑–≈«ß Ÿß¡“° ‡π◊ÈÕ‡¬◊ËÕµà“ß Ê ·≈–À≈Õ¥‡≈◊Õ¥®–∂Ÿ° ∑”≈“¬‡ªìπæ◊πÈ ∑’°Ë «â“ß ∫“¥·º≈∑–≈ÿ®“°°√– ÿπ≈Ÿ°ª√“¬ (shot gun wounds) ‡°‘¥®“°°√– ÿπ∑’Ë§«“¡‡√Á«µË” (<2,000 øÿµ/«‘π“∑’) ‡π◊ÈÕ‡¬◊ËÕ®–∂Ÿ°∑”≈“¬¥â«¬°√– ÿπ´÷Ëß¡’À≈“¬™π‘¥ ∂â“¬‘ß„π√–¬– Àà“ß·π«°√– ÿπ®–°√–®“¬ ·µà∂“â ¬‘ß„π√–¬–‡º“¢π°√– ÿπ®–√«¡ ‡ªìπ°√–®ÿ° À¡Õπ°√– ÿπΩíß„π‡π◊ÈÕ‡¬◊ËÕ∑’Ë∂Ÿ°∑”≈“¬®–®”°—¥Õ¬Ÿà ‡©æ“–·π«∑’≈Ë °Ÿ °√– ÿπºà“π ∫“¥‡®Á∫®“°¬«¥¬“πæ“Àπ–∑”„Àâ‡°‘¥·√ß°√–·∑° ‡ªìπ “‡Àµÿ∑”„Àâ¡’°√–¥Ÿ°À—°·≈–¢âÕ‡§≈◊ËÕπµ“¡¡“¥â«¬°“√∫“¥‡®Á∫¢ ®ÕßÀ≈Õ¥‡≈◊Õ¥∑’∑Ë Õ¥µ—ßÈ Õ¬Ÿà„π·π«¢Õß°√–¥Ÿ°·≈–¢âÕ µ—«Õ¬à“ß‡™àπ posterior dislocation ¢Õß¢âÕ‡¢à“®–‡°‘¥°“√∫“¥‡®Á∫µàÕÀ≈Õ¥ ‡≈◊Õ¥¥”·≈–À≈Õ¥‡≈◊Õ¥·¥ß popliteal (√Ÿª∑’Ë 29.1) ≈—°…≥–°“√∫“¥‡®Á∫¢ÕßÀ≈Õ¥‡≈◊Õ¥∑’Ë‡°‘¥¢÷Èπ®“°°√–¥Ÿ°À—° ·≈–¢âÕ‡§≈◊ÕË π ®–∑”„Àâºπ—ßÀ≈Õ¥‡≈◊Õ¥©’°¢“¥ ¡’ intimal disruption ·≈– thrombosis ‡»…°√–¥Ÿ°∑’Ë·µ°À—°·≈–¡’§«“¡ ·À≈¡§¡ Õ“®®–∑‘¡Ë „ÀâÀ≈Õ¥‡≈◊Õ¥∑–≈ÿ‡ªìπ√Ÿ·≈–¡’‡≈◊Õ¥‰À≈ÕÕ°¡“ ®”π«π¡“° (√Ÿª∑’Ë 29.2)

ªí®®ÿ∫—π∫“¥‡®Á∫À≈Õ¥‡≈◊Õ¥®“°°“√∑”À—µ∂°“√‡°’Ë¬«°—∫ À≈Õ¥‡≈◊Õ¥·≈–°“√µ√«®«‘π®‘ ©—¬∑“ß√—ß ’«∑‘ ¬“æ∫‰¥â∫“â ß ·µàæ∫ «à“‡°‘¥®“°°“√©’¥¬“‡ æµ‘¥‡¢â“‡ âπ¡’¡“°¢÷πÈ ®–‡ÀÁπ«à“∫“¥‡®Á∫À≈Õ¥‡≈◊Õ¥®–‡°‘¥¢÷πÈ °—∫∫√‘‡«≥·¢π·≈–¢“ ∫àÕ¬∑’Ë ÿ¥ (√Ÿª¿“æ∑’Ë 29.3) ‡π◊ËÕß®“°À≈Õ¥‡≈◊Õ¥ à«ππ’È¡’√–¬– ∑“ß¬“«Õ¬Ÿàµ◊Èπ®“°º‘«Àπ—ß ‡¡◊ËÕµ°„®À√◊ÕªÑÕß°—πÕ—πµ√“¬ºŸâ∂Ÿ° ∑”√â“¬¡—°®–¬°·¢πÀ√◊Õ¢“ªÑÕß°—πµ—«°àÕπ‡ ¡Õ ‡™àπ‡¥’¬«°—π ∫“¥‡®Á∫®“°¬«¥¬“πæ“Àπ–¡—°®–‡°‘¥°—∫·¢π¢“°àÕπ‡ ¡Õ »—≈¬·æ∑¬å∑’Ë¥Ÿ·≈ºŸâªÉ«¬∫“¥‡®Á∫ §«√¡’§«“¡‡¢â“„®‡°’Ë¬«°—∫ æ¬“∏‘ √’√«‘∑¬“¢Õß°“√∫“¥‡®Á∫™π‘¥µà“ß Ê ∑’‡Ë °‘¥¢÷πÈ °—∫À≈Õ¥‡≈◊Õ¥ ‡æ◊ÕË ∑’®Ë –‰¥â«“ß·π«∑“ß„π°“√µ√«®«‘π®‘ ©—¬·≈–√—°…“‰¥âÕ¬à“ß∂Ÿ°µâÕß

≈—°…≥–°“√∫“¥‡®Á∫¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß ®ÿ¥¡ÿßà À¡“¬ ”§—≠„π°“√√—°…“∫“¥‡®Á∫À≈Õ¥‡≈◊Õ¥ ®–‡æàß‡≈Áß ∂÷ßæ¬“∏‘ ¿“æ¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß°àÕπ‡ ¡Õ ¡“°°«à“À≈Õ¥ ‡≈◊Õ¥¥” ‡æ√“–°“√¢“¥‡≈◊Õ¥®–∑”„Àâ‡π◊ÈÕ‡¬◊ËÕµ“¬„π√–¬–‡«≈“ Õ—π —Èπ À√◊Õ¡’‡≈◊Õ¥ÕÕ°¡“°®π™ÁÕ§ ∫“¥‡®Á∫À≈Õ¥‡≈◊Õ¥¥”Õ“® ®–µ√«®‰¡àæ∫ ·µàµÕà ¡“À≈Õ¥‡≈◊Õ¥¥”Õ“®®–µ’∫·§∫∑”„Àâ‡°‘¥¿“«– chronic venous insuffciency ¢÷Èπ‰¥â¿“¬À≈—ß ¡’°≈‰°À≈“¬

√Ÿª∑’Ë 29.2 °√–¥Ÿ°∑’ÀË °— ª≈“¬ à«π∑’·Ë À≈¡®–∑‘¡Ë „ÀâÀ≈Õ¥ ‡≈◊Õ¥©’°¢“¥ ∑–≈ÿ‡ªìπ√Ÿ ¡’‡≈◊Õ¥‰À≈ ‡°‘¥ intimal disruption ·≈– thrombosis

276

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Subclavian 7 Thoracic aorta 5 Axillary 7 Branchial 19

Radial & Ulnar 8 Common iliac 2

S. femoral 18

Popliteal 20 Ant. and post. tibial 11

Jugular 9 Subclavian 1 Brachial 2

Innominate 1 Axillary 2 IVC 8 Renal 2 Meseneric 1

Iliac 2 Femoral 2

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Popliteal 8 Tibial 1

∫“¥‡®Á∫À≈Õ¥‡≈◊Õ¥

277

™π‘¥∑’Ë∑”„Àâ‡°‘¥°“√∫“¥‡®Á∫µàÕÀ≈Õ¥‡≈◊Õ¥ ∑”„Àâ‡°‘¥≈—°…≥– °“√∫“¥‡®Á∫µàÕÀ≈Õ¥‡≈◊Õ¥ ∑”„Àâ‡°‘¥≈—°…≥–°“√∫“¥‡®Á∫µà“ß Ê ∑’æË ∫‰¥â¥ß— µàÕ‰ªπ’È 1. Contusion °“√™È”¢Õßºπ—ßÀ≈Õ¥‡≈◊Õ¥√à«¡°—∫°“√¡’ intramural hematoma ‡ªìπº≈¡“®“°·√ß°√–·∑°‚¥¬µ√ß À√◊Õ°“√‡©’Ë¬«¢Õß°√– ÿπªóπ hematoma ∑’Ë‡°‘¥¢÷Èπ®– ∑”„Àâ√ŸÀ≈Õ¥‡≈◊Õ¥·§∫≈ß·≈–µ—π„π∑’Ë ÿ¥ ®ÿ¥∑’Ëºπ—ß À≈Õ¥‡≈◊Õ¥™È”Õ“®®–‡ª√“–·≈–·µ°ÕÕ°‡ªìπ pseudoaneurysm ‰¥â¿“¬À≈—ß ®“° arteriogram ®–æ∫«à“¡’ °“√µ’∫·§∫º‘¥ª°µ‘¢Õß contrast column 2. Intimal disruption ‡°‘¥®“°·√ß°√–·∑°‚¥¬µ√ßµàÕ À≈Õ¥‡≈◊Õ¥·≈â«¡’°“√¥÷ß√—ÈßÀ√◊Õ·√ß°√–·∑°¢Õß°√– ÿπ ªóπ √Õ¬‚√§À√◊Õ°“√∫“¥‡®Á∫¢ÕßÀ≈Õ¥‡≈◊Õ¥®–‰¡à‡ÀÁπ ®“°¿“¬πÕ° °“√∑” arteriogram ®–‡ÀÁπ«à“¢Õ∫„π ¢ÕßÀ≈Õ¥‡≈◊Õ¥‰¡à‡√’¬∫ ‡ÀÁπ√Õ¬©’°¢“¥‡ªìπ intimal flap 3. √Õ¬·∑ß∑–≈ÿ ®“°«— ¥ÿ¡§’ ¡ ‡™àπ ¡’¥ –‡°Á¥°√– ÿπ À√◊Õ °“√µ√«®«‘π®‘ ©—¬∑“ß√—ß ’«∑‘ ¬“‡™àπ °“√∑” arteriogram

√Õ¬∑–≈ÿ®–¡’‡≈◊Õ¥‰À≈´÷¡ÕÕ°¡“ ∂â“‰¡à “¡“√∂°¥®ÿ¥ Àâ“¡‡≈◊Õ¥®–°≈“¬‡ªìπ expanding pseudoaneurysm ´÷ßË ®–‡ÀÁπ‰¥â™¥— ®“° arteriogram 4. √Õ¬©’°¢“¥∑“ß¥â“πÀ≈—ß °“√∂Ÿ°«—µ∂ÿ¡§’ ¡ª≈“¬·À≈¡ ‡©◊Õπ ‡π◊ÕË ß®“°‰¡à∂°Ÿ µ—¥¢“¥À≈Õ¥‡≈◊Õ¥®–‰¡àÀ¥µ—«·≈–¡’ thrombus ¡“Õÿ¥ ‡≈◊Õ¥®–‰À≈ÕÕ°®“°√Ÿ·º≈π‘È«Õ¬à“ß µàÕ‡π◊ÕË ß µ“¡®—ßÀ«–™’æ®√ ∂â“¡’√∑Ÿ –≈ÿÕÕ°πÕ°º‘«Àπ—ß¿“¬ πÕ°®–‡ ’¬‡≈◊Õ¥¡“°®π™ÁÕ§ ·µà∂â“‰¡à¡’√Ÿ∑–≈ÿÕÕ°®– °≈“¬‡ªìπ pulsatile hematoma ·≈– pseudoaneurysm „π∑’ Ë ¥ÿ (√Ÿª∑’Ë 29.4) ∂â“∑‘ßÈ ‰«â®–·µ°‰¥â¿“¬À≈—ß 5. arterial spasm ‡ªìπ°“√À¥µ—«¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß∑—ßÈ ‡ âπ¿“¬À≈—ß°“√∫“¥‡®Á∫ ®“°∂Ÿ°°√–·∑°À√◊Õ·√ß‡©’¬Ë « ®“°°√– ÿπªóπ ·µàµ«— À≈Õ¥‡≈◊Õ¥‡Õß‰¡à‰¥â√∫— ∫“¥‡®Á∫ (√Ÿª∑’Ë 29.5) ¥Ÿ®“°¿“¬πÕ°·≈–µ√«®√à“ß°“¬‡À¡◊Õπ¡’∫“¥‡®Á∫ µàÕÀ≈Õ¥‡≈◊Õ¥·¥ß‡æ√“–§≈”™’æ®√‰¡à ‰¥â ·¢π¢“‡¬Áπ´’¥ ∂â“∑” arteriogram ®–‡ÀÁπæ¬“∏‘ ¿“æ¥—ß°≈à“« µàÕ ¡“À≈Õ¥‡≈◊Õ¥·¥ß®–¢¬“¬µ—«‡ªìπª°µ‘¿“¬À≈—ß

√Ÿª∑’Ë 29.4 pseudoaneurysm ¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß superficial

√Ÿª∑’Ë 29.5 °“√À¥µ—«¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß arterial spasm ¿“¬ À≈—ß

femoral artery ¿“¬À≈—ß∂Ÿ°·∑ß∑–≈ÿ

°“√∫“¥‡®Á∫ À≈Õ¥‡≈◊Õ¥·¥ß®–§≈“¬µ—«µ“¡ª°µ‘¿“¬À≈—ß

278

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Hardûs signs

√Ÿª∑’Ë 29.6 ·º≈·∑ß∑–≈ÿ√–À«à“ßÀ≈Õ¥‡≈◊Õ¥¥”·≈–À≈Õ¥‡≈◊Õ¥·¥ß superficial femoral ¿“¬À≈—ß‡°‘¥‡ªìπ arteriovenous fistula

6. arteriovenous fistula ‡°‘¥®“°·º≈·∑ß∑–≈ÿº“à πÀ≈—ß À≈Õ¥‡≈◊Õ¥¥”·≈–À≈Õ¥‡≈◊Õ¥·¥ß∑”„Àâ¡√’ ∑Ÿ –≈ÿµ¥‘ µàÕ°—π arteriogram ®–æ∫ early venous filling (√Ÿª∑’Ë 29.6) 7. Transection °“√∂Ÿ°µ—¥¢“¥ÕÕ°®“°°—πÕ¬à“ß ¡∫Ÿ√≥å À≈Õ¥‡≈◊Õ¥∑—Èß Õßª≈“¬®–À¥µ—« ·≈–¡’ thrombus ¡“Õÿ¥µ√ßª≈“¬∑”„Àâ‡≈◊Õ¥ÕÕ°πâÕ¬≈ß ªí≠À“ ”§—≠§◊Õ ·¢π·≈–¢“ à«πª≈“¬µàÕÀ≈Õ¥‡≈◊Õ¥∑’Ë ‰¥â√—∫∫“¥‡®Á∫®– ¢“¥‡≈◊Õ¥ arteriogram ®–æ∫«à“À≈Õ¥‡≈◊Õ¥Õÿ¥µ—π π‘∑

°“√«‘π‘®©—¬‚√§ Õ“°“√·≈–Õ“°“√· ¥ß ª√–«—µ‘·≈–°“√µ√«®√à“ß°“¬‡ªìπ ªí®®—¬ ”§—≠„π°“√ª√–‡¡‘ π ºŸâ ªÉ « ¬∑’Ë ß — ¬ «à “ ®–¡’ ° “√∫“¥‡®Á ∫ À≈Õ¥‡≈◊Õ¥ §«√´—°ª√–«—µ‘„Àâ∑√“∫·πàπÕπ∂÷ß°≈‰°¢Õß°“√ ∫“¥‡®Á∫ª√‘¡“≥‡≈◊Õ¥∑’Ë‡ ’¬‰ª §«“¡º‘¥ª°µ‘¢Õß√–∫∫ª√– “∑ °“√´—° ª√–«— µ‘° “√µ√«®√à“ ß°“¬Õ¬à“ ß≈–‡Õ’¬ ¥∂’Ë∂â « π®–∑”„Àâ «‘π‘®©—¬‚√§‰¥âÕ¬à“ß·¡àπ¬”°àÕπ«“ß·ºπ„π°“√µ√«®«‘π‘®©—¬·≈– √—°…“‚√§µàÕ‰ª

¡’Õ“°“√ ”§—≠§◊Õ 1. ¡’‡≈◊Õ¥ÕÕ°ª√‘¡“≥¡“°®“°∫“¥·º≈ 2. ¡’Õ“°“√¢Õß°“√¢“¥‡≈◊Õ¥Õ¬à“ß‡©’¬∫æ≈—πµàÕÕ«—¬«–∑’Ë ‰¥â √—∫∫“¥‡®Á∫ À√◊Õ¡’ 6 Pûs (pulselessness, pallor, paresthesia, pain, paralysis ·≈– poikilothermia) 3. ¡’°Õâ π‡≈◊Õ¥ (hematoma) ∑’¢Ë ¬“¬¢π“¥‚µ¢÷πÈ Õ¬à“ß√«¥‡√Á« 4. §≈”‰¥â thrill À√◊Õøíß‰¥â bruit ∑”„Àâ ß —¬«à“®–‡°‘¥ pseudonaneurysm À√◊Õ arteriovenous fistula ºŸâªÉ«¬∑’Ë¡’ hard signs „π°√≥’√’∫¥à«π®–µâÕß√’∫π”ºŸâªÉ«¬ ‡¢â“ÀâÕßºà“µ—¥‡¬Á∫´àÕ¡·´¡À≈Õ¥‡≈◊Õ¥ ‚¥¬‰¡à µâ Õ ß√Õµ√«® «‘π‘®©—¬æ‘‡»…®“° arteriography ‡æ√“–§àÕπ¢â“ß®–·πà „®«à“¡’ °“√∫“¥‡®Á∫¢ÕßÀ≈Õ¥‡≈◊Õ¥·¥ß®“°Õ“°“√·≈–Õ“°“√· ¥ß∑’Ë ‡¥àπ™—¥¥—ß°≈à“« §«√√—°…“Õ“°“√™ÁÕ§´÷Ëßæ∫√à«¡°—∫°“√∫“¥‡®Á∫ À≈Õ¥‡≈◊Õ¥√âÕ¬≈– 30-40 °àÕπºà“µ—¥‡¬Á∫´àÕ¡À≈Õ¥‡≈◊Õ¥(1-3) Soft signs ‡ªìπÕ“°“√·≈–Õ“°“√· ¥ß„πºŸªâ «É ¬∫“¥‡®Á∫´÷ßË Õ“®®–æ∫À√◊Õ‰¡àæ∫∫“¥‡®Á∫¢ÕßÀ≈Õ¥‡≈◊Õ¥√à«¡¥â«¬ 1. ª√–«—µ¢‘ Õß°“√¡’‡≈◊Õ¥‰À≈ÕÕ°®“°∫“¥·º≈‰¡à·πàπÕπ„π ∑’‡Ë °‘¥‡Àµÿ 2. °âÕπ‡≈◊Õ¥‚µ‰¡à¡“° ‰¡à¢¬“¬¢π“¥·≈–‰¡à‡µâπµ“¡™’æ®√ 3. ·π«¢Õß∫“¥·º≈Õ¬Ÿà „°≈â°—∫µ”·Àπàß∑’ËÀ≈Õ¥‡≈◊Õ¥∑Õ¥ ºà“π 4. ™ÁÕ§∑’Ë ‰¡à “¡“√∂Õ∏‘∫“¬ “‡Àµÿ‰¥â 5. ¡’§«“¡º‘¥ª°µ‘¢Õß√–∫∫ª√– “∑À≈—ß°“√∫“¥‡®Á∫ ºŸâªÉ«¬∑’Ë¡’ soft signs ∂â“π”‰ªºà“µ—¥®–‰¡àæ∫°“√∫“¥‡®Á∫ À≈Õ¥‡≈◊Õ¥„πÕ—µ√“∑’ Ë ßŸ ∂÷ß√âÕ¬≈– 75-80 ®÷ß§«√µ√«®«‘π®‘ ©—¬ ‚¥¬°“√∑” arteriogram „Àâ·πà„®·≈–À“√àÕß√Õ¬¢Õß°“√∫“¥‡®Á∫ °àÕπæ‘®“√≥“ºà“µ—¥√—°…“ ‡√“‰¡à “¡“√∂„™â°“√§≈”™’æ®√ ª√–‡¡‘π°“√∫“¥‡®Á∫¢Õß À≈Õ¥‡≈◊Õ¥‰¥â‡ ¡Õ‰ª‡π◊ÕË ß®“°≈—°…≥–°“√∫“¥‡®Á∫¢ÕßÀ≈Õ¥‡≈◊Õ¥ ·¥ß¡’À≈“¬™π‘¥¥—ß∑’Ë°≈à“«¡“·≈â« æ∫«à“√âÕ¬≈– 10-30 ¢ÕßºŸâ ªÉ«¬∑’Ë¡’∫“¥‡®Á∫À≈Õ¥‡≈◊Õ¥·¥ß¬—ß “¡“√∂§≈”™’æ®√‰¥â (1,2,4) ‡æ√“–∫“¥‡®Á∫À≈Õ¥‡≈◊Õ¥·¥ß∑’‡Ë °‘¥¢÷πÈ ‡ªìπ·∫∫©’°¢“¥∫“ß à«π ¡’ intimal tear À√◊Õ arteriovenous fistula

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∫“¥‡®Á∫À≈Õ¥‡≈◊Õ¥ °“√«‘π‘®©—¬∫“¥‡®Á∫À≈Õ¥‡≈◊Õ¥·¥ß∫√‘‡«≥·≈–≈”µ—«∑”‰¥â ¬“°°«à“∑’·Ë ¢π·≈–¢“ ‡æ√“–‰¡à “¡“√∂µ√«®√à“ß°“¬‚¥¬°“√§≈” ‡¢â“∂÷ßÀ≈Õ¥‡≈◊Õ¥·¥ß„π∫√‘‡«≥¥—ß°≈à“« ®–µâÕß¥Ÿ®“°°“√‡ ’¬ ‡≈◊Õ¥¢ÕßºŸâªÉ«¬ Õ“°“√· ¥ß ”§—≠∑’Ë®–æ∫‰¥â∂â“¡’°“√‡ ’¬‡≈◊Õ¥ ®“°À≈Õ¥‡≈◊Õ¥¢π“¥„À≠à§Õ◊ ™ÁÕ§ À—«„®À¬ÿ¥‡µâπ cardiac tamponade ‡¡¥‘·Õ µ‘π—Ë¡°«â“ß ·≈–¡’‡≈◊Õ¥‰À≈ÕÕ°¡“Õ’°§√—Èß À≈—ß®“°À¬ÿ¥‰À≈·≈â«„πµÕπ·√° ∫“¥·º≈·∑ß∑–≈ÿ®–∑”„Àâ¡’ °“√µ°‡≈◊Õ¥„π mediastinum ·≈– hemothorax ‰¥â∫Õà ¬∑’ Ë ¥ÿ ´÷Ëß®–æ∫‰¥âÀ≈—ß„ à∑àÕ√–∫“¬∑√«ßÕ° „πºŸâªÉ«¬∑’Ë —≠≠“≥™’æ®√ ª°µ‘Õ“®®–∑”°“√µ√«®«‘π‘®©—¬°“√∫“¥‡®Á∫À≈Õ¥‡≈◊Õ¥‰¥â ‚¥¬ °“√∑” arteriogram À√◊Õ CT scan(5,6) °“√µ√«®«‘π®‘ ©—¬∑’™Ë «à ¬«‘π®‘ ©—¬°“√∫“¥‡®Á∫À≈Õ¥‡≈◊Õ¥·¥ß‰¥â §◊Õ °“√«—¥§«“¡¥—π‚≈À‘µ´’ ‚µ≈‘§¢Õß·¢π·≈–¢“·µà≈–¢â“ß ‡ª√’¬∫‡∑’¬∫°—π‡ªìπ§à“ ABI ·≈–°“√„™â duplex scan

ARTERIOGRAPHY ®ÿ¥¡ÿßà À¡“¬„π°“√∑” arteriography §◊Õ(7) 1. ‡æ◊ÕË À≈’°‡≈’¬Ë ß°“√ºà“µ—¥∑’Ë ‰¡à®”‡ªìπ 2. ‡æ◊ÕË «‘π®‘ ©—¬°“√∫“¥‡®Á∫„Àâ·πàπÕπ (exclusive arteriography) „πºŸªâ «É ¬∑’ÕË “°“√·≈–Õ“°“√· ¥ß¢Õß°“√∫“¥‡®Á∫ ”À√—∫«“ß·ºπ„π°“√ºà“µ—¥√—°…“µàÕ‰ª 3. ‡æ◊ÕË À“µ”·Àπàß·πàπÕπ¢Õß°“√∫“¥‡®Á∫ ”À√—∫«“ß·ºπ „π°“√ºà“µ—¥√—°…“µàÕ‰ª ¢âÕ∫àß™’È „π°“√∑” arteriography §◊Õ(8) 1. ∫“¥‡®Á∫À≈“¬√–¥—∫ ‡™àπ ∂Ÿ°¬‘ß¥â«¬ªóπ≈Ÿ°´Õß (shot gun) ∂Ÿ°·∑ßÀ≈“¬·º≈À√◊Õ°√–¥Ÿ°À—°À≈“¬·Ààß„π·¢πÀ√◊Õ ¢“¢â“ß‡¥’¬«°—π 2. ·π«∫“¥·º≈„°≈â°∫— ∫√‘‡«≥∑’ÀË ≈Õ¥‡≈◊Õ¥ ”§—≠∑Õ¥ºà“π 3. §≈”™’æ®√‡∫“À√◊Õ‰¡à ‰¥â‡¡◊ÕË ‡∑’¬∫°—∫¥â“πµ√ß°—π¢â“¡ 4. ¡’√Õ¬™È”À√◊Õ°âÕπ‡≈◊Õ¥¢¬“¬¢π“¥‚µ¢÷πÈ 5. ¡’‡≈◊Õ¥ÕÕ°´È”®“°·º≈‡¥‘¡∑’Ë‡§¬¡’‡≈◊Õ¥ÕÕ°·≈â«À¬ÿ¥ ‰À≈‰ª §«√∑” arteriography „πºŸªâ «É ¬∑’¡Ë ’ ≠ — ≠“≥™’æ§ß∑’Ë ‚¥¬¬÷¥ À≈—°°“√·≈–¢âÕ∫àß™’È¥—ß∑’Ë°≈à“«¡“·≈â« æ∫«à“ºŸâªÉ«¬∑’Ë ß —¬«à“®– ¡’∫“¥‡®Á∫À≈Õ¥‡≈◊Õ¥·¥ß∑—ÈßÀ¡¥¡’‡æ’¬ß√âÕ¬≈– 20-30 ‡∑à“π—Èπ ¡’§«“¡®”‡ªìπ∑’Ë®–µâÕß∑” arteriography ·≈–§«“¡·πàπÕπ„π °“√«‘π®‘ ©—¬‚√§ Ÿß∂÷ß√âÕ¬≈– 92(9) ∂â“ arteriogram ·≈â«¬—ß‰¡à·πà „® ·µà ß —¬«à“®–¡’∫“¥‡®Á∫À≈Õ¥‡≈◊Õ¥ §«√µ—¥ ‘π„®ºà“µ—¥µ√«®¥Ÿ

À≈Õ¥‡≈◊Õ¥‰ª‡≈¬ ºŸâªÉ«¬∑’Ë —≠≠“≥™’æº‘¥ª°µ‘¡’™ÁÕ§¡’‡≈◊Õ¥‰À≈ Õ¬à“ßµàÕ‡π◊ÕË ß®“°∫“¥·º≈‰¡à§«√‡ ’¬‡«≈“√Õ∑” arteriography §«√π”ºŸâªÉ«¬‡¢â“ÀâÕßºà“µ—¥∑—π∑’ °“√µ√«®«‘π‘®©—¬·∫∫ßà“¬ Ê §◊Õ°“√∑” single shot arteriography ∑’ËÀâÕßª∞¡æ¬“∫“≈ ‡ªìπ°“√©’¥ “√∑÷∫· ß‡¢â“À≈Õ¥‡≈◊Õ¥·≈â«∂à“¬¿“æ√—ß ’‡æ’¬ß ¿“æ‡¥’¬« ‡ªìπ«‘∏°’ “√µ√«®«‘π®‘ ©—¬∑’ßË “à ¬·≈–„™â‡«≈“πâÕ¬(10)

°“√√—°…“ °“√ª√–‡¡‘πºŸªâ «É ¬·≈–√—°…“„π¢—πÈ µâπ ºŸªâ «É ¬∑’¡Ë ’ çsoft signsé §«√‰¥â√—∫°“√µ√«®«‘π‘®©—¬„Àâ·πàπÕπ«à“¡’∫“¥‡®Á∫À≈Õ¥‡≈◊Õ¥ ‚¥¬°“√∑” arteriography „πºŸªâ «É ¬∑’¡Ë ’ çhard signsé §«√√’∫ π”‡¢â“ÀâÕßºà“µ—¥∑—π∑’Ë °“√Àâ“¡‡≈◊Õ¥„π√–¬–·√°§«√„™â°“√°¥ ®ÿ¥Àâ“¡‡≈◊Õ¥ ‰¡à§«√„™â “¬¬“ß torniquet √—¥‡æ√“–®–∑”„Àâ ‡≈◊Õ¥∑’Ë ‰À≈ºà“π collaterals ≈¥πâÕ¬≈ß∑”„Àâ·¢π¢“¢“¥‡≈◊Õ¥ √ÿπ·√ß¢÷πÈ Õ’° ∂â“¡’§«“¡®”‡ªìπ∑’®Ë –µâÕß∑” arteriography Õ“® ®–∑”·∫∫ single shot arteriography ¿“¬„πÀâÕßºà“µ—¥°Á ‰¥â °“√Àâ“¡‡≈◊Õ¥‚¥¬„™â§’¡§’∫À≈Õ¥‡≈◊Õ¥§«“πÀ“À≈Õ¥‡≈◊Õ¥·∫∫ ‡¥“ ÿà¡·≈–§âπ®ÿ¥‡≈◊Õ¥ÕÕ°‡¢â“‰ª„π·º≈ ‡ªìπ ‘Ëß∑’Ë ‰¡à § «√∑” ‡æ√“–Õ“®®–∑”„Àâ‡°‘¥°“√∫“¥‡®Á∫µàÕ‡ âπª√– “∑·≈–‡π◊ÈÕ‡¬◊ËÕ ¢â“ß‡§’¬ß ¡’¥∑’Ëªí°§“·º≈‰«â ‰¡à§«√¥÷ßÕÕ°∑—π∑’‡æ√“–Õ“®®– ∑–≈ÿ‡¢â“‰ª„πÀ≈Õ¥‡≈◊Õ¥¡’ tamponade effect ∑”„Àâ‡≈◊Õ¥À¬ÿ¥ ‰À≈Õ¬Ÿà·≈â« ∂â“¥÷ß‡Õ“ÕÕ°‡≈◊Õ¥Õ“®®–‰À≈ÕÕ°®“°∫“¥·º≈ ®”π«π¡“°§«√¥÷ß‡Õ“ÕÕ°„πÀâÕßºà“µ—¥ °“√√—°…“‚¥¬«‘∏°’ “√‰¡àº“à µ—¥ ∫“¥‡®Á∫À≈Õ¥‡≈◊Õ¥∑ÿ°√“¬‰¡à ®”‡ªìπµâÕßºà“µ—¥√—°…“ °“√Õÿ¥µ—π¢ÕßÀ≈Õ¥‡≈◊Õ¥ “¢“‡≈Á° Ê à«πª≈“¬Õ“®®–√—°…“‰¥â ‚¥¬°“√µ‘¥µ“¡¥Ÿ·≈Õ“°“√ ‡™àπ °“√ Õÿ¥µ—π¢Õß tibial arteries ‡ âπ‡¥’¬«À√◊Õ‡ âπ„¥‡ âπÀπ÷ßË √–À«à“ß radial À√◊Õ ulnar arteries ”À√—∫∫“¥‡®Á∫‡≈Á°πâÕ¬¢ÕßÀ≈Õ¥ ‡≈◊Õ¥∑’Ë ‰¡à¡°’ “√Õÿ¥µ—π ‡™àπ √Õ¬∑–≈ÿ®“°°“√·∑ß‡¢Á¡ Õ¥ “¬ «π À√◊Õ intimal disruption ®“°°“√ Õ¥ “¬∫—≈≈Ÿπ¢¢“¬∂à“ß ¡—° ®–À“¬‡Õß‰¥âæ¬“∏‘ ¿“æ‡À≈à“π’È‡ΩÑ“¥Ÿ·≈‰¡à®”‡ªìπµâÕßºà“µ—¥ ∂â“ distal circulation ¬—ß¥’Õ¬Ÿà ‰¡à¡’‡≈◊Õ¥‰À≈ÕÕ°®“°∫“¥·º≈ ®”π«π¡“°(11) 1. intimal defect ¢π“¥‡≈Á° 2. pseudoaneurysm ∑’¡Ë ¢’ π“¥‚µ‡ âπºà“»Ÿπ¬å°≈“ß‰¡à‡°‘π 5 ¡‘≈≈‘‡¡µ√ 3. intimal flap ´÷ËßÕ¬Ÿà „π·π«‡¥’¬«°—∫°√–· ‡≈◊Õ¥‰¡àµâ“π °√–· ‡≈◊Õ¥

280 æ¬“∏‘ ¿“æ‡À≈à“π’È§«√‡ΩÑ“¥Ÿ·≈Õ“°“√·≈–µ√«®¥Ÿ´È”‚¥¬„™â duplex scan À√◊Õ arteriography ∫“¥‡®Á∫À≈Õ¥‡≈◊Õ¥∫“ß ™π‘¥ “¡“√∂√—°…“‰¥â ‚¥¬°“√∑” transluminal embolization ¿“¬À≈—ß°“√∑” dianostic arteriography ‰¥â‡™àπ(12) 1. low-flow arteriovenous fistula 2. pseudoaneurysm 3. active bleeding ®“°À≈Õ¥‡≈◊Õ¥ à«πª≈“¬∑’Ë ‰¡à§Õà ¬¡’ §«“¡ ”§—≠‡™àπ distal profunda femoris ·≈– muscular branches ¢ÕßÀ≈Õ¥‡≈◊Õ¥µà“ß Ê 4. À≈Õ¥‡≈◊Õ¥∑’ºË “à µ—¥‡¢â“∂÷ß≈”∫“° ‡™àπ ·¢πß¢Õß external carotid artery vertebral ·≈– hypogastric artery °“√ºà“µ—¥√—°…“ ‡¡◊ÕË ∑√“∫·πàπÕπ·≈â««à“¡’°“√∫“¥‡®Á∫À≈Õ¥ ‡≈◊Õ¥ §«√∑”°“√‡¬Á∫´àÕ¡„πÀâÕßºà“µ—¥ ∂â“ºŸªâ «É ¬‡ ’¬‡≈◊Õ¥¡“°§«√ resuscitate °àÕπ‚¥¬„Àâ “√πÈ”·≈–‡≈◊Õ¥∑“ßÀ≈Õ¥‡≈◊Õ¥¥” ®π°√–∑—Ëß —≠≠“≥™’æÕ¬Ÿà „π‡°≥±åª°µ‘·≈–§ß∑’Ë °àÕπºà“µ—¥§«√ ©’¥¬“ªÑÕß°—π·≈–∫“¥∑–¬—°·≈–„Àâ¬“ªØ‘™’«π–™π‘¥ÕÕ°ƒ∑∏‘Ï §≈ÿ¡°«â“ß ‡µ√’¬¡º‘«Àπ—ß∫√‘‡«≥∑’®Ë –ºà“µ—¥‡¢â“∂÷ß„Àâª√“»®“°‡™◊ÕÈ ‰¡à«“à ®–‡ªìπ·¢π ¢“ À√◊Õ≈”µ—« øÕ°∑”§«“¡ –Õ“¥·≈–ºâ“ª√“»®“°‡™◊ÕÈ √Õ∫∫√‘‡«≥∑’∑Ë ”°“√ºà“µ—¥„Àâ°«â“ßæÕ∑’®Ë –≈ß¡’¥‡¢â“∂÷ß‡æ◊ÕË proximal ·≈– distal control À≈Õ¥‡≈◊Õ¥∑’Ë∫“¥‡®Á∫ ∂â“‡ªìπ ∫“¥‡®Á∫À≈Õ¥‡≈◊Õ¥·¥ß∑’Ë¢“§«√‡µ√’¬¡º‘«Àπ—ß¢“¥â“πµ√ß°—π ¢â“¡„Àâª√“»®“°‡™◊ÕÈ ‡º◊ÕË «à“®–‡≈“–‡Õ“ saphenous vein graft ¡“„™â‡¡◊ËÕ¡’§«“¡®”‡ªìπ ‡Àµÿº≈∑’Ë „™â saphenous vein graft ®“°¢“¥â“πµ√ß°—π¢â“¡§◊Õ µâÕß°“√ preserve superficial venous drainage ¢Õß¢“∑’Ë ‰¥â√—∫∫“¥‡®Á∫À≈Õ¥‡≈◊Õ¥·¥ß „π°√≥’∑’ËÕ“® ®–‡°‘¥ deep vein thrombosis „π¢“¢â“ßπ—Èπ ∂â“¡’∫“¥‡®Á∫ À≈Õ¥‡≈◊Õ¥·¥ß¢“∑—Èß Õß¢â“ßÀ≈Õ¥‡≈◊Õ¥¥”∑¥·∑π∑’Ë “¡“√∂ „™â ‰¥â§Õ◊ cephalic vein ∑’‡Ë ≈“–‰¥â®“°·¢π ·º≈ºà“µ—¥∑’Ë·¢π·≈–¢“§«√≈ß·π«¬“«¢π“π°—∫µ”·Àπàß∑’Ë À≈Õ¥‡≈◊Õ¥∑Õ¥µ—«Õ¬Ÿà „Àâ∂÷ß à«πµâπ·≈– à«πª≈“¬µàÕµ”·Àπàß ∫“¥‡®Á∫À≈Õ¥‡≈◊Õ¥·≈– “¡“√∂„™â§’¡§’∫À≈Õ¥‡≈◊Õ¥‰¥âßà“¬‚¥¬ ‰¡à¢«“ß∫√‘‡«≥∑’Ë®–‡¬Á∫´àÕ¡ ∂â“‡ªìπ∫“¥‡®Á∫À≈Õ¥‡≈◊Õ¥∑’Ë∑âÕß §«√≈ß¡’¥„π·π«°÷Ëß°≈“ß ®– “¡“√∂‡¢â“∂÷ßÕ«—¬«–¿“¬„π™àÕß ∑âÕß‰¥â∑ß—È À¡¥ ∫“¥‡®Á∫À≈Õ¥‡≈◊Õ¥„π∑√«ßÕ°Õ“®®–‡¢â“∂÷ß‰¥â „π ·π« median sternotomy À√◊Õ lateral thoracotomy

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥ ∫“¥‡®Á∫Õ¬à“ß√ÿπ·√ß¢Õß·¢π¢“ ‰¡à ‰¥â¢÷ÈπÕ¬Ÿà°—∫∫“¥‡®Á∫ ¢ÕßÀ≈Õ¥‡≈◊Õ¥‡æ’¬ßÕ¬à“ß‡¥’¬« ·µàª√–°Õ∫¥â«¬∫“¥‡®Á∫¢Õß º‘«Àπ—ß ‡ âπª√– “∑ °√–¥Ÿ° °≈â“¡‡π◊ÈÕ·≈–‡ÕÁπæ—ßº◊¥ µ—«·ª√ ”§—≠„π°“√µ—¥ ‘π„®µ—¥·¢π¢“ ·∑π∑’Ë®–‡¬Á∫´àÕ¡À≈Õ¥‡≈◊Õ¥ ·≈–‡π◊ÕÈ ‡¬◊ÕË µà“ß Ê ¢÷πÈ Õ¬Ÿ°à ∫— ∫“¥‡®Á∫¢Õß°≈â“¡‡π◊ÕÈ ·≈–°√–¥Ÿ°(13) ¢âÕ§«√æ‘®“√≥“„π°“√µ—¥·¢π¢“∑’∫Ë “¥‡®Á∫¡“°√à«¡°—∫°“√ ∫“¥‡®Á∫À≈Õ¥‡≈◊Õ¥(13-16) 1. ‡ âπª√– “∑¢“¥ÕÕ°®“°°—π‚¥¬ ¡∫Ÿ√≥å ∑”„Àâª√– “∑ —¡º— ·≈–‡§≈◊ÕË π‰À«‡ ’¬‰ª (anesthetic and paralyzed limb) 2. ¡’∫“¥‡®Á∫µàÕ°√–¥Ÿ°Õ¬à“ß√ÿπ·√ß ®π°√–¥Ÿ°¢“¥À“¬‰ª‡°‘π °«à“ 6 ‡´Áπµ‘‡¡µ√ °√–¥Ÿ°À—°À≈“¬™‘Èπ·∫∫‡ªî¥ ´÷Ëß¡’ ªí≠À“„π°“√ºà“µ√÷ß°√–¥Ÿ° ·≈–°“√Õ—°‡ ∫µ‘¥‡™◊ÈÕ¿“¬ À≈—ß 3. ∫“¥‡®Á∫µàÕ‡π◊ÕÈ ‡¬◊ÕË µà“ß Ê Õ¬à“ß√ÿπ·√ß ®“°°“√°¥∑—∫ (crush) À√◊Õ¢“¥‡≈◊Õ¥¡“‡≈’¬È ßπ“π‡°‘π°«à“ 6-8 ™—«Ë ‚¡ß °≈â“¡‡π◊ÈÕµ“¬·≈â« ·º≈ °ª√°ªπ‡ªóôÕπ¡“° º‘«Àπ—ß À≈ÿ¥À“¬‰ª·∫∫ degloving 4. ∫“¥‡®Á∫À≈“¬√–∫∫ ´÷ßË µâÕß°“√ºà“µ—¥∫√‘‡«≥Õ◊πË ‡™àπ ∑âÕß À√◊Õ∑√«ßÕ°Õ¬à“ß√’∫¥à«π°àÕπ°“√ºà“µ—¥À≈Õ¥‡≈◊Õ¥ ∑”„Àâ°“√√—°…“∫“¥‡®Á∫À≈Õ¥‡≈◊Õ¥≈à“™â“ ·¢πÀ√◊Õ¢“ ¢“¥‡≈◊Õ¥π“π°«à“ 6-8 ™—«Ë ‚¡ß °“√µ—¥ ‘π„®„π°“√µ—¥·¢π¢“ §«√∑”„πÀâÕßºà“µ—¥À≈—ß¥¡ ¬“ ≈∫·≈â«µ√«®¥Ÿ§«“¡√ÿπ·√ß‡π◊ÈÕ‡¬◊ËÕ∑’Ëµ“¬·≈–¡’°“√ªπ‡ªóôÕπ ¡“°πâÕ¬‡æ’¬ß„¥ Vascular control À≈—ß°“√ºà“µ—¥‡¢â“∂÷ßÀ≈Õ¥‡≈◊Õ¥∑’∫Ë “¥‡®Á∫ µ”·Àπà ß ∑’Ë „™â§’¡¢’∫À≈Õ¥‡≈◊Õ¥Àπ’∫ §«√Õ¬Ÿà‡Àπ◊Õ·≈–„µâµàÕ µ”·Àπàß∑’Ë∫“¥‡®Á∫¢ÕßÀ≈Õ¥‡≈◊Õ¥Àπ’∫ §«√Õ¬Ÿà‡Àπ◊Õ·≈–„µâµàÕ µ”·Àπàß∑’Ë∫“¥‡®Á∫¢ÕßÀ≈Õ¥‡≈◊Õ¥°àÕπ‡¬Á∫´àÕ¡ „π√“¬∑’Ë¡’ ‡≈◊Õ¥‰À≈ÕÕ°®“°·º≈Õ¬à“ßµàÕ‡π◊ËÕßª√‘¡“≥¡“°®– “¡“√∂ Àâ“¡‡≈◊Õ¥„ÀâÀ¬ÿ¥‚¥¬„™âπ«‘È À√◊Õ sponge stick °¥µ”·Àπàß¢Õß À≈Õ¥‡≈◊Õ¥‡Àπ◊Õ·≈–„µâµÕà ∫√‘‡«≥·º≈ À√◊Õ„™â Foley’s catheter «π§“·≈–¢¬“¬∂à“ß∫—≈≈Ÿπµ√ßª≈“¬‡ªìπ°“√Àâ“¡‡≈◊Õ¥∑’ËÕÕ° ®“°À≈Õ¥‡≈◊Õ¥ à«πµâπ·≈– à«πª≈“¬

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¡’‡≈◊Õ¥‰À≈‡«’¬π‰ª·¢π¢“∑’Ë¢“¥‡≈◊Õ¥ ‡ªìπ°“√≈¥ warm ischemic time “¡“√∂∑”À—µ∂°“√Õ◊Ëπ ‡™àπ °“√µ√÷ß °√–¥Ÿ°°àÕπ‡¬Á∫´àÕ¡À≈Õ¥‡≈◊Õ¥¿“¬À≈—ß

À≈Õ¥‡≈◊Õ¥·¥ß à«π∑’Ë¢“¥°–√ÿàß°–√‘Ëß·≈–¡’‡π◊ÈÕµ“¬ „™â °√√‰°√À√◊Õ¡’¥µ—¥‡≈Á¡ÕÕ°®π∂÷ß‡π◊ÕÈ ¥’·≈–¢Õ∫‡√’¬∫ „™â Fogarty catheter ¥÷ß‡Õ“≈‘¡Ë ‡≈◊Õ¥ÕÕ°®“°À≈Õ¥‡≈◊Õ¥ à«πµâπ·≈– à«πª≈“¬ ©’¥πÈ”‡°≈◊Õ ¡¥ÿ≈¬å∑’Ëº ¡‡Œª“√’π 1:100 ‡¢â“„πÀ≈Õ¥‡≈◊Õ¥°—π ‡≈◊Õ¥·¢Áßµ—«‡ªìπ≈‘Ë¡ ¥÷ßÀ≈Õ¥‡≈◊Õ¥∑—Èß Õßª≈“¬‡¢â“¡“À“°—π ‡æ◊ÕË ‡¬Á∫µàÕ (√Ÿª∑’Ë 29.7) ∂â“À≈Õ¥‡≈◊Õ¥∂Ÿ°µ—¥¢“¥‡ªìπ§«“¡¬“« ‡°‘π°«à“ 2 ‡´Áπµ‘‡¡µ√ ‰¡à§«√¥÷ß‡¢â“¡“‡¬Á∫µàÕÀ“°—π‡æ√“–®–µ÷ß ¡“°·≈–µ’∫·§∫„π∑’Ë ÿ¥ §«√À“À≈Õ¥‡≈◊Õ¥∑’Ë¡’¢π“¥‡ âπºà“ »Ÿπ¬å°≈“ß‡≈Á°°«à“ 4 ¡‘≈≈‘‡¡µ√ §«√µàÕ‚¥¬„™â¥“â ¬‡¬Á∫ Polyproprylene ‡∫Õ√å 7-0 ‡¬Á∫∑’≈–§” (interrupted suture) À≈Õ¥ ‡≈◊Õ¥®–‰¡àµ∫’ ·≈–¢¬“¬¢π“¥‰¥â ∂â“À≈Õ¥‡≈◊Õ¥‚µ°«à“π’ È “¡“√∂ ‡¬Á∫´àÕ¡À≈Õ¥‡≈◊Õ¥·≈â« À“°≈â“¡‡π◊ÈÕ·≈–º‘«Àπ—ß‡¬Á∫§≈ÿ¡ À≈Õ¥‡≈◊Õ¥‡Õ“‰«â ‚¥¬∑—«Ë ‰ª·≈â««— ¥ÿ∑¥·∑πÀ≈Õ¥‡≈◊Õ¥∑’¥Ë ‡’ ≈‘»§◊Õ saphenous vein graft ∑’Ë‡≈“–‰¥â®“°¢“¥â“πµ√ß°—π¢â“¡ √Õß ≈ß¡“§◊Õ hypogastric artery ´÷ßË «‘∏º’ “à µ—¥¬ÿßà ¬“°µâÕß‡¢â“™àÕß∑âÕß ∂â“À≈Õ¥‡≈◊Õ¥¥”∑’Ë¢“‰¡à “¡“√∂π”¡“„™â ‰¥â ‡π◊ËÕß®“°¡’∫“¥‡®Á∫ À≈Õ¥‡≈◊Õ¥¢“∑—Èß Õß¢â“ß “¡“√∂‡≈“–‡Õ“ cephalic vein ®“°·¢π¡“„™â∑¥·∑π‰¥â „π°√≥’∑’Ë ‰¡à “¡“√∂À“ autogenous vessels ‰¥â ‰¡à¡‡’ «≈“ ‡≈“–À≈Õ¥‡≈◊Õ¥‡æ√“–µâÕßºà“µ—¥Õ¬à“ß√’∫¥à«π ¢“À√◊Õ·¢π¢“¥ ‡≈◊Õ¥‡ªìπ√–¬–‡«≈“π“π ¢π“¥À≈Õ¥‡≈◊Õ¥‡ âπºà“»Ÿπ¬å°≈“ß‚µ°«à“

8 ¡‘≈≈‘‡¡µ√ §«√„™âÀ≈Õ¥‡≈◊Õ¥‡∑’¬¡∑’ºË ≈‘µ®“°«— ¥ÿ ß— ‡§√“–Àå‡™àπ polytetrafluoroethylene (PTFE) ‡¬Á∫·∑π æ∫«à“Õ—µ√“‡ ’Ë¬ß µàÕ°“√µ‘¥‡™◊ÕÈ æ∫πâÕ¬ ‡æ’¬ß√âÕ¬≈– 1-5(17,18) ∂â“¡’°“√À—°¢Õß°√–¥Ÿ°À√◊Õ¢âÕ‡§≈◊ËÕπ √à«¡°—∫∫“¥‡®Á∫¢Õß À≈Õ¥‡≈◊Õ¥¥” À≈Õ¥‡≈◊Õ¥·¥ß‡ âπª√– “∑·≈–‡π◊ÈÕ‡¬◊ËÕÕ◊Ëπ Ê §«√¡’À≈—°°“√„π°“√µàÕ°≈—∫§◊π‡√’¬ßµ“¡≈”¥—∫µàÕ‰ªπ’È ∂â“√–¬– ‡«≈“∑’ËºŸâªÉ«¬‰¥â√—∫∫“¥‡®Á∫·≈â«¡“∂÷ß‚√ßæ¬“∫“≈·≈– “¡“√∂π” ‡¢â“ÀâÕßºà“µ—¥‰¥â∑—π∑’Ë ·¢π¢“¢“¥‡≈◊Õ¥‰¡àπ“π §«√µàÕ°√–¥Ÿ° À√◊Õµ√÷ß¢âÕ°àÕπµ“¡¥â«¬À≈Õ¥‡≈◊Õ¥¥” À≈Õ¥‡≈◊Õ¥·¥ß ‡ âπ ª√– “∑·≈–‡π◊ÈÕ‡¬◊ËÕÕ◊Ëπ µ“¡≈”¥—∫ ∂â“√–¬–‡«≈“„π°“√¢“¥ ‡≈◊Õ¥π“πæÕ ¡§«√„°≈â‡§’¬ß°—∫ 6-8 ™—Ë«‚¡ß §«√µàÕÀ≈Õ¥ ‡≈◊Õ¥¥”·≈–À≈Õ¥‡≈◊Õ¥·¥ß°àÕπ À√◊Õ„ à intraluminal shunt „Àâ¡’‡≈◊Õ¥‰À≈‡«’¬π‰ª¬—ß à«πª≈“¬∑’Ë¢“¥‡≈◊Õ¥°àÕπ (√Ÿª∑’Ë 29.8) µ“¡¥â«¬µ√÷ß°√–¥Ÿ°·≈–´àÕ¡‡ âπª√– “∑ °“√„ à intraluminal shunt ®–∑”„Àâ¡’‡≈◊Õ¥‰À≈‡«’¬π‰ª¬—ß à«π∑’Ë¢“¥‡≈◊Õ¥‡æ’¬ßæÕ °“√‡¬Á ∫ ´à Õ ¡À≈Õ¥‡≈◊ Õ ¥®–‰¡à √’ ∫ ¥à « π¡“∑”¿“¬À≈— ß ®“°µ√÷ ß °√–¥Ÿ°°Á ‰¥â §«√∑” fasciotomy ∑ÿ°√“¬ „πºŸâªÉ«¬∑’Ë¡’¢“¢“¥ ‡≈◊Õ¥‡ªìπ√–¬–‡«≈“π“π À≈—ß‡¬Á∫´àÕ¡À≈Õ¥‡≈◊Õ¥·¥ß·≈â« §«√∑” intraoperative arteriography µ√«®¥Ÿ§«“¡‡√’¬∫√âÕ¬¢ÕßÀ≈Õ¥‡≈◊Õ¥∑’Ë‡¬Á∫ ´àÕ¡·≈–µàÕ‡Õ“‰«â ∂â“¡’°“√µ’∫·§∫§«√‡¬Á∫´àÕ¡„À¡à distal arterial spasm ∑’Ëæ∫§«√√—°…“‚¥¬°“√©’¥¬“¢¬“¬À≈Õ¥‡≈◊Õ¥‡™àπ papaverine À√◊Õ tolazoline ‡¢â“∑“ßÀ≈Õ¥‡≈◊Õ¥·¥ß·µàµâÕß ·¬°„Àâ ‰¥â°∫— arterial spasm ∑’‡Ë °‘¥®“° compartment syndrome ∫“¥‡®Á∫µàÕÀ≈Õ¥‡≈◊Õ¥¥” “¡“√∂√—°…“‰¥â ‚¥¬°“√ºŸ°‡ªìπ «‘∏’∑’Ëª≈Õ¥¿—¬∑’Ë ÿ¥ ®–‡¬Á∫´àÕ¡°ÁµàÕ‡¡◊ËÕºŸâªÉ«¬¡’ —≠≠“≥™’æ§ß∑’Ë ‰¡àµÕâ ß∑”°“√ºà“µ—¥Õ◊πË Ê ∑’Ë „™â‡«≈“π“π ∫“¥‡®Á∫¢Õß IVC À√◊Õ iliac veins §«√‡¬Á∫´àÕ¡À√◊ÕµàÕ¥â«¬À≈Õ¥‡≈◊Õ¥‡∑’¬¡ PTFE À≈Õ¥‡≈◊Õ¥¥”∫√‘‡«≥¢“§«√‡¬Á∫´àÕ¡À√◊ÕµàÕ‚¥¬„™â saphenous vein graft ®“°¢“¥â“πµ√ß°—π¢â“¡ ∂â“‰¡à “¡“√∂‡¢â“∂÷ß‡æ◊ÕË ‡¬Á∫ ´àÕ¡‰¥âßà“¬ §«√µ—¥ ‘π„®ºŸ°‰ª‡≈¬ ·µà®–µâÕß√–«—ß°“√∫«¡¢Õß ¢“·≈–·¢π∑’ËÕ“®®–‡°‘¥¢÷Èπ‰¥â¿“¬À≈—ß·≈–®–¡’º≈µàÕ°“√À“¬ ¢Õß∫“¥·º≈ À≈—ßºà“µ—¥§«√πÕπ¬°¢“ Ÿß ‡¡◊ÕË venous collaterals ‡æ’¬ßæÕ·≈â«¢“®–¬ÿ∫∫«¡‡Õß ¿“«–·∑√°´âÕπ∑’ËÕ“®®–‡°‘¥¢÷Èπ À≈—ßºŸ°À≈Õ¥‡≈◊Õ¥¥”¢π“¥„À≠à∑¢’Ë “§◊Õ venous hypertension ·≈– stasis ºŸâªÉ«¬®–¡’¢“∫«¡¡’·º≈‡√◊ÈÕ√—ß∑’Ë‡∑â“·≈–Õ—°‡ ∫µ‘¥ ‡™◊ÕÈ ‰¥âß“à ¬

282

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√Ÿª∑’Ë 29.8 À≈—°„π°“√‡¬Á∫´àÕ¡À≈Õ¥‡≈◊Õ¥·¥ß∑’Ë ‰¥â√∫— ∫“¥‡®Á∫ À≈—ßµ—¥‡≈Á¡À≈Õ¥‡≈◊Õ¥∑’¢Ë “¥°–√ÿßà °–√‘ßË ÕÕ°„Àâ‡√’¬∫ ·≈â« „™â Fogarty balloon catheter ≈“°≈‘Ë¡‡≈◊Õ¥ÕÕ°®“°À≈Õ¥‡≈◊Õ¥ à«πµâπ·≈– à«πª≈“¬ ©’¥ πÈ”‡°≈◊Õ ¡¥ÿ≈¬åº ¡‡Œª“√’π„πÕ—µ√“ à«π 1:100 ª√–¡“≥ 10-15 ¡‘≈≈‘≈‘µ√ ‡¢â“À≈Õ¥‡≈◊Õ¥·¥ß à«π µâπ·≈– à«πª≈“¬À≈—ßµàÕÀ√◊Õ‡¬Á∫´àÕ¡À≈Õ¥‡≈◊Õ¥·¥ß·≈â« §«√∑” intraoperative arteriography

COMPARTMENT SYNDROME °≈ÿ¡à ¢Õß°≈â“¡‡π◊ÕÈ À≈Õ¥‡≈◊Õ¥·≈–‡ âπª√– “∑∫√‘‡«≥·¢π¢“ ®–∂Ÿ°ÀàÕÀÿâ¡¥â«¬ fascial sheath √«¡°—π‡ªìπ compartment ‡¡◊ÕË ¡’°“√¢¬“¬ª√‘¡“≥¢Õß‡π◊ÕÈ ‡¬◊ÕË ™π‘¥„¥™π‘¥Àπ÷ßË ¿“¬„π compartment ´÷ßË ‰¡à¡∑’ ¢’Ë ¬“¬ÕÕ°‰ª‰¥â §«“¡¥—π¿“¬„π®– Ÿß‡æ‘¡Ë ¢÷πÈ (√Ÿª∑’Ë 29.9) compartment syndrome §◊Õ°≈ÿ¡à Õ“°“√∑’‡Ë °‘¥¢÷πÈ ¿“¬À≈—ß°“√‡æ‘Ë¡§«“¡¥—π¢Õß‡π◊ÈÕ‡¬◊ËÕ∑’ËÕ¬Ÿà „π∫√‘‡«≥∑’Ë®”°—¥¢Õß √à“ß°“¬ ´÷ßË Õ“®°àÕ„Àâ‡°‘¥§«“¡º‘¥ª°µ‘∑“ß¥â“π°“√‰À≈‡«’¬π‡≈◊Õ¥ ·≈–Àπâ“∑’¢Ë Õß‡π◊ÕÈ ‡¬◊ÕË „π à«ππ—πÈ ‚¥¬‡©æ“–√–∫∫ª√– “∑ à«πª≈“¬ °≈ÿà¡Õ“°“√‡À≈à“π’ÈÕ“®®–‡°‘¥¢÷Èπ‰¥âÕ¬à“ß‡©’¬∫æ≈—π ‡¡◊ËÕ¡’°“√ ‡æ‘¡Ë §«“¡¥—π¿“¬„πÕ¬à“ß√«¥‡√Á« ®÷ß§«√«‘π®‘ ©—¬‚√§„Àâ ‰¥â·µà‡π‘πË Ê ‡æ◊ÕË √’∫∑”°“√√—°…“°àÕπ∑’‡Ë π◊ÕÈ ‡¬◊ÕË ®–µ“¬Õ¬à“ß∂“«√(19,20)

“‡Àµÿ ªí®®—¬ ”§—≠∑’∑Ë ”„Àâ‡°‘¥ compartment syndrome §◊Õ 1. ¡’°“√‡æ‘Ë¡¢Õßª√‘¡“µ√·≈–§«“¡¥—π¿“¬„π compartment ‡Õß ‡™àπ ∫“¥‡®Á∫µàÕ‡π◊ÈÕ‡¬◊ËÕ¡’‡≈◊Õ¥§—Ëß®“°°“√ ©’°¢“¥¢ÕßÀ≈Õ¥‡≈◊Õ¥ ∂Ÿ°°¥∑—∫ ¿“«–™ÁÕ§π“π ¡’°“√ Õÿ¥µ—π¢ÕßÀ≈Õ¥‡≈◊Õ¥¥”„À≠à reperfusion injury ®“°

·¢π¢“∑’Ë¢“¥‡≈◊Õ¥√–¬–‡«≈“π“πÀ≈—ß®“°¡’‡≈◊Õ¥‰À≈ ‡«’¬π®–ª≈àÕ¬ oxygen-derived free radicals ‡¢â“ Ÿà °√–· ‡≈◊Õ¥ ∑”≈“¬ cell membrance ∑”„Àâ‡´≈≈åµ“¬ °≈â“¡‡π◊ÈÕ®–∫«¡·≈–‡πà“µ“¬ °“√Õÿ¥µ—π¢ÕßÀ≈Õ¥ ‡≈◊Õ¥¥”„À≠à®–∑”„Àâ‡°‘¥ venous hypertension ·≈– ‡π◊ÕÈ ‡¬◊ÕË ∫«¡¡“° 2. ®“°·√ß°¥¿“¬πÕ° ‡™àπ ‡ΩóÕ°∑’√Ë ¥— µ÷ß®π‡°‘π‰ª °“√√—¥ ºâ“ ¬“ß¬÷¥À√◊Õ·∂∫ºâ“·πàπ‡°‘π‰ª °“√„™â MAST-G-SUIT

Õ“°“√·≈–Õ“°“√· ¥ß∑“ß§≈‘π‘§ ∑’ Ë ”§—≠§◊Õª«¥·¢π·≈–¢“¢â“ßπ—πÈ ¡“° ª«¥µ≈Õ¥‡«≈“ ‰¡à‡ªìπ —¥ à«π°—∫°“√µ√«®√à“ß°“¬∑’æË ∫ ∂â“ª«¥®“°°√–¥Ÿ°À—° À≈—ß®“° ®—¥°√–¥Ÿ°‡¢â“∑’·Ë ≈â«®–ª«¥πâÕ¬≈ß ·µà „π compartment syndrome ®–¬—ßª«¥Õ¬Ÿà æ∫«à“¡’°“√ÕàÕπ·√ß¢Õß°≈â“¡‡π◊ÕÈ ¢≥–∑” passive stretching ª«¥√ÿπ·√ßµ“¡·π«‡ âπª√– “∑∑’∑Ë Õ¥ºà“π compartment ·≈–°¥‡®Á∫∫π‡ÕÁπæ—ßº◊¥∑’ÀË ¡ÿâ °≈â“¡‡π◊ÕÈ „π compartment º‘«Àπ—ß‰¡à¡’°“√‡ª≈’Ë¬π·ª≈ß„Àâ‡ÀÁππÕ°®“°‡ªìπ¡“ π“π„π√–¬–∑â“¬

283

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Superficial peroneal nerve

Lateral fasciotomy

Fascia deep department Anterior fasciotomy

Deep posterior fasciotomy

Intermuscular septum

Superficial posterior fasciotomy

Tibia

Saphenous vein & nerve

Fascial septum

Superficial peroneal nerve

Lateral View

Medial View

√Ÿª∑’Ë 29.9 «‘∏’°“√∑” fasciotomy ¢Õß¢“

«‘π®‘ ©—¬‚√§ ‰¥â®“°Õ“°“√·≈–Õ“°“√· ¥ß∑“ß§≈‘π§‘ arteriogram ®–æ∫ «à“¡’ arterial spasm «—¥§«“¡¥—π„π compartment ‰¥â ßŸ °«à“ 40 ∑Õ√√å ´÷Ëß§à“ª°µ‘‰¡à§«√‡°‘π 20 ∑Õ√√å ®–µâÕß„Àâ°“√√—°…“ Õ¬à“ß√’∫¥à«π „π√“¬∑’Ë‡ªìπ¡“π“π®π°√–∑—Ëß°≈â“¡‡π◊ÈÕ‡πà“µ“¬ ®–æ∫«à“¡’™ÕÁ § myoglobinuria ‰µ«“¬‡©’¬∫æ≈—π ¿“«–°√¥‡°‘π ·≈– hyperkalemia

°“√√—°…“ ºŸªâ «É ¬∑’¡Ë Õ’ “°“√·≈–Õ“°“√· ¥ß™—¥‡®π ·≈–«—¥§«“¡¥—π„π compartment ‰¥â ßŸ °«à“ 40 ∑Õ√√å §«√√’∫∑” decompressive fasciotomy °àÕπ∑’‡Ë π◊ÕÈ ‡¬◊ÕË µà“ß Ê ®–‡πà“µ“¬(21) ¢âÕ∫àß™’È ”À√—∫°“√∑” prophylatic fasciotomy ¡’ ¥—ßµàÕ‰ªπ’È 1. √–¬–‡«≈“µ—ßÈ ·µà‡√‘¡Ë ∫“¥‡®Á∫®π°√–∑—ßË ºà“µ—¥√—°…“π“π‡°‘π °«à“ 6 ™—«Ë ‚¡ß

2. ¡’°“√∫“¥‡®Á∫∑—ßÈ À≈Õ¥‡≈◊Õ¥¥”·≈–À≈Õ¥‡≈◊Õ¥·¥ß 3. ¡’™ÕÁ §√à«¡¥â«¬ 4. ‡π◊ÕÈ ‡¬◊ÕË ∫√‘‡«≥·¢π¢“∑’Ë ‰¥â√∫— ∫“¥‡®Á∫™Õ°™È”¡“° 5. ¡’°“√∫«¡·¢π¢“ À≈—ß°“√‡¬Á∫´àÕ¡À≈Õ¥‡≈◊Õ¥ 6. À≈—ß°“√ºà“µ—¥∑’¡Ë °’ “√ºŸ°À≈Õ¥‡≈◊Õ¥¥”„À≠à∫√‘‡«≥¢“ fasciotomy À¡“¬∂÷ß°“√ºà“µ—¥°√’¥‡ÕÁπæ—ßº◊¥∑’ËÀÿâ¡Õ¬Ÿà√Õ∫ compartment ‡æ◊ËÕ„Àâ‡π◊ÈÕ‡¬◊ËÕµà“ß Ê ∑’Ë∂Ÿ°ÀàÕÀÿâ¡Õ¬Ÿà “¡“√∂ ¢¬“¬µ—«ÕÕ°‰¥âÕ¬à“ß‡ªìπÕ‘ √–∑ÿ°∑‘»∑“ß §«“¡¥—π∑’Ë Ÿß®–≈¥≈ß °“√∑” fasciotomy ∑’Ë¥’®–µâÕß≈ß¡’¥°√’¥∑—Èßº‘«Àπ—ß·≈–‡ÕÁπ æ—ßº◊¥ÕÕ°‡ªìπ·π«¬“«æ√âÕ¡°—π ‡æ√“–∂â“‰¡à°√’¥º‘«Àπ—ß‡π◊ÕË ‡¬◊ÕË ∑’ÀË “¬ÕÕ°À≈—ß°√’¥‡ÕÁπæ—ßº◊¥ ®–∂Ÿ°º‘«Àπ—ß√—¥‡Õ“‰«â(22-24) ∫√‘‡«≥πàÕß¡’∑ß—È À¡¥ 4 compartment (√Ÿª∑’Ë 29.10) „π°“√ ∑” fasciotomy ®–µâÕß°√’¥„Àâ∑«—Ë ∂÷ß 4 à«π ‡æ◊ÕË §«“¡¥—π®–‰¥â ≈¥≈ß∑—ßÈ À¡¥(25) ∑“ß¥â“π„π‡√‘¡Ë ®“°µ”·Àπàß 2 ‡´Áπµ‘‡¡µ√ À≈—ß µàÕ°√–¥Ÿ° tibia ‡ªìπ·π«¬“«≈ß¡“‡æ◊ËÕ decompress ”À√—∫ superficial ·≈– deep posterior compartments ‡«≈“°√’¥

284

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Anterior tibial art. and vein

Tibia

Anterior compartment Superficial peroneal nerve Interosseous septum Deep posterior compartment

Flexor digitorum longus muscle

Lateral compartment Fibula

Posterior tibial art. and vein

Flexor hallucis longus muscle

Tibial nerve

Peroneal art. and vein Superficial posterior compartment

√Ÿª∑’Ë 29.10 °“¬«‘¿“§¢Õß°≈â“¡‡π◊ÈÕ ·≈– compartments ∑—Èß 4 ¢Õß¢“ µâÕß√–«—ß‰¡à „Àâµ—¥∂Ÿ° saphenous vein ·≈– nerve À≈—ß‡ªî¥ º‘«Àπ—ß·≈– subcutaneous tissue ·≈â«°√’¥¡’¥ºà“π‡ÕÁπæ—ßº◊¥¢Õß superficial posterior compartment ‡ªìπ·π«¬“«·π«‡¥’¬« °—∫º‘«Àπ—ß ‡ªî¥ origin ¢Õß°≈â“¡‡π◊ÕÈ soleus ∑’‡Ë °“–°—∫°√–¥Ÿ° tibia ‡¢â“‰ª‡æ◊ÕË µ—¥‡ÕÁπæ—ßº◊¥¢Õß deep posterior compartment ·º≈ºà“µ—¥∑’Ë Õß≈ß∑“ß‡¥‘π¢â“ß¢“√–À«à“ß tibia ·≈– fibula °√’¥‡ÕÁπæ—ßº◊¥∑’ÀË ¡ÿâ anterior compartment µ—¥ intermuscular septum ‡æ◊ÕË decompress lateral compartment ¢≥–ºà“µ—¥ µâÕß√–«—ß‰¡à „Àâµ¥— ∂Ÿ° superficial peroneal nerve ‡æ√“–Õ¬Ÿ¢à “â ß septum ∑’·Ë ¢π®–¡’‡æ’¬ß 2 compartments §◊Õ volar ·≈– dorsal ´÷ßË Õ¬Ÿµà ¥‘ °—π “¡“√∂∑’®Ë – decompress ‰¥â∑ß—È Õß compartments ‚¥¬≈ß¡’¥„π·π« volar (√Ÿª∑’Ë 29.11) ‡√‘¡Ë ®“°µ√ß‡Àπ◊ÕµàÕ medial epicondyle ¢Õß humerus ºà“π antecubital fossa ¡“ ∑“ß aspect ¢Õß∑âÕß·¢π≈ß¡“∂÷ß¢âÕ¡◊Õ

µ—¥‡ÕÁπæ—ßº◊¥µ“¡·π«º‘«Àπ—ß∑’≈Ë ß¡’¥ æÕ¡“∂÷ß¢âÕ¡◊Õµ—¥ flexor retinaculum ‡æ◊ÕË ‡ªî¥ carpal tunnel decompress median nerve ∂â“ dorsal compartment ¬—ßµ÷ßÕ¬Ÿà „Àâ≈ß¡’¥„π·π« dorsal ‚¥¬‡√‘Ë¡®“° lateral epicondyle ≈ß¡“∂÷ß·¢π¥—ß°≈à“« “¡“√∂∑” fasciotomy ‰¥â‡æ◊ÕË ≈¥§«“¡¥—π ·º≈ fasciotomy “¡“√∂‡¬Á∫ªî¥‰¥â¿“¬À≈—ß‡π◊ÕÈ ‡¬◊ÕË µà“ß Ê ¬ÿ∫∫«¡≈ß·≈â«‡¡◊ËÕ·πà „®«à“‰¡à¡’°“√µ‘¥‡™◊ÈÕ´È”´âÕπ °≈â“¡‡π◊ÈÕ∑’Ë µ“¬ “¡“√∂µ—¥ÕÕ°‰¥âÀ≈“¬§√—Èß®π°√–∑—Ëß·πà „®«à“¥’æÕ·≈â« ∂â“ º‘«Àπ—ß‡À≈◊Õ¡“°æÕ§«√¥÷ß‡¬Á∫‡¢â“À“°—π ·µà∂â“µ÷ß¡“°§«√µ—¥ º‘«Àπ—ß®“°∫√‘‡«≥Õ◊πË ¡“ª≈Ÿ°∑¥·∑π Õ“°“√∑’√Ë πÿ ·√ß¢Õß compartment syndrome ¡—°®– ◊∫‡π◊ÕË ß ¡“®“°°“√¡’°≈â“¡‡π◊ÈÕµ“¬ º≈∑’Ëµ“¡¡“§◊Õ ‰µ«“¬‡©’¬∫æ≈—π ºŸâ ªÉ«¬§«√¡’ªí “«–ÕÕ°Õ¬à“ß‡æ’¬ßæÕ§«√„Àâ “√πÈ”∑“ßÀ≈Õ¥ ‡≈◊Õ¥®”π«π¡“° √à«¡°—∫„Àâ¬“ªí “«–™π‘¥ loop diuretics ‡™àπ furosemide ·≈– mannitol ‚¥¬‡©æ“– mannitol ®–¡’ƒ∑∏‘‡Ï ªìπ

285

∫“¥‡®Á∫À≈Õ¥‡≈◊Õ¥

Anterior fasciotomy Flexor digitorum superficialis muscle

Flexor carpi radialis muscle

Investing fascia Radius Ulna Extensor digitorum muscle

Extensor digitorum minimi muscle Posterior fasciotomy

Volar

Dorsal

√Ÿª∑’Ë 29.11 «‘∏’°“√∑” fasciotomy ¢Õß·¢π free radical scavenger ®—∫°—∫Õπÿ¡Ÿ≈Õ‘ √–∑’Ë·µ°µ—«ÕÕ°¡“ ®“°°≈â“¡‡π◊ÕÈ ∑’µË “¬„π°“√√—°…“ reperfusion injury §«√∑”„Àâ ªí “«–¡’ƒ∑∏‘Ï‡ªìπ¥à“ß‚¥¬„Àâ§“√å∫Õ‡πµ∑“ßÀ≈Õ¥‡≈◊Õ¥¥”‡ªìπ √–¬–ªÑÕß°—πæ‘…¢Õß myoglobin ∑’®Ë –‡°‘¥¢÷πÈ °—∫‰µ

¿—¬Õ—πµ√“¬®“°°“√©’¥¬“‡¢â“‡ âπ ∫“¥‡®Á∫À≈Õ¥‡≈◊Õ¥Õ“®‡°‘¥®“° °“√©’¥¬“À√◊Õ “√‡§¡’‡¢â“ ∑“ßÀ≈Õ¥‡≈◊Õ¥‡°‘¥¢÷Èπ‰¥â∑—ÈßÀ≈Õ¥‡≈◊Õ¥¥”·≈–À≈Õ¥‡≈◊Õ¥·¥ß Õÿ∫—µ‘°“√∑’Ëæ∫‰¥â∫àÕ¬§◊Õ°“√©’¥¬“‡ æµ‘¥‡™àπ ‡Œ‚√Õ’π‡¢â“∑“ß À≈Õ¥‡≈◊Õ¥¥” ·≈–°“√„Àâ¬“∑“ßÀ≈Õ¥‡≈◊Õ¥¥”‚¥¬·∑ß‡ âπ º‘¥æ≈“¥‡¢â“À≈Õ¥‡≈◊Õ¥·¥ß ∫“¥‡®Á∫À≈Õ¥‡≈◊Õ¥¥” ‡°‘¥®“°°“√©’¥¬“À√◊Õ “√‡§¡’‡¢â“ À≈Õ¥‡≈◊Õ¥¥”µ”·Àπàß‡¥‘¡´È”´“°∑”„Àâ‡°‘¥ªØ‘°‘√‘¬“√–§“¬‡§◊Õß µàÕ‡ÕÁπ‚¥∑’‡≈’¬Ë ¡ µ“¡¡“¥â«¬ sclerosis ·≈– thrombosis ‡°‘¥

‰¥â∑—ÈßÀ≈Õ¥‡≈◊Õ¥„µâº‘«Àπ—ß·≈–À≈Õ¥‡≈◊Õ¥∑’ËÕ¬Ÿà≈÷° °“√©’¥¬“ ‡¢â“µ√ß femoral vein ®–∑”„Àâ‡°‘¥ deep vein thrombosis ‰¥â √—°…“‰¥â ‚¥¬°“√„Àâ¬“µâ“π‡≈◊Õ¥·¢Áßµ—« ∂â“¡’°“√Õ—°‡ ∫µ‘¥‡™◊ÕÈ ‡ªìπ septic thrombophlebitis ´÷ßË ¡—°®–‡°‘¥®“°‡™◊ÕÈ Staph. aureus §«√„Àâ¬“ªØ‘™’«π–∑“ßÀ≈Õ¥‡≈◊Õ¥¥”√à«¡°—∫¬“¥â“π‡≈◊Õ¥·¢Áßµ—« ∂â“‰¡à ‰¥âº≈®÷ß∑” thrombectomy À√◊Õµ—¥‡Õ“À≈Õ¥‡≈◊Õ¥¥” ∫√‘‡«≥∑’Ë¡’°“√µ‘¥‡™◊ÈÕÕÕ° femoral vein pseudoaneurysm √—°…“‚¥¬°“√ºŸ°À≈Õ¥‡≈◊Õ¥¥”∑“ß¥â“πÀ—«·≈–∑â“¬√à«¡°—∫°“√ µ—¥‡Õ“ pseudoaneurysm ÕÕ° mycotic aneurysms ‡°‘¥®“°°“√·∑ß‡ âπÀ≈Õ¥‡≈◊Õ¥ ¢≥–©’¥ “√‡ æµ‘¥‡¢â“À≈Õ¥‡≈◊Õ¥¥”·≈â«‡¢â“À≈Õ¥‡≈◊Õ¥·¥ß À≈“¬§√—ßÈ µ‘¥µàÕ°—π µ“¡¡“¥â«¬°“√µ‘¥‡™◊ÕÈ ·∫§∑’‡√’¬ ºπ—ßÀ≈Õ¥ ‡≈◊Õ¥Õ“®®–°≈“¬‡ªìπ pseudoaneurysm ‡Õß‰¥â ‚¥¬‰¡àµÕâ ß¡’√∑Ÿ –≈ÿ ∂â“°“√Õ—°‡ ∫µ‘¥‡™◊ÕÈ ≈ÿ°≈“¡®“°µ”·Àπàßµâπ‡Àµÿ À√◊Õ®“° bacterial

286 emboli ‡§≈◊ËÕπµ—«‰ªÕÿ¥ vasa vasorum ¢ÕßÀ≈Õ¥‡≈◊Õ¥ µ”·Àπàßπ—πÈ ºπ—ßÀ≈Õ¥‡≈◊Õ¥®–∂Ÿ°∑”≈“¬·≈–‚ªÉßÕÕ° √âÕ¬≈– 50 ¢Õß mycotic aneurysm ®–§≈”°âÕπ‡µâπ‰¥â °“√‡°‘¥ bruit À√◊Õ§≈”™’æ®√ à«πª≈“¬‡∫“ ‡ªìπÕ“°“√∑“ß§≈‘π§‘ ∑’æË ∫‰¥â·πàπÕπ æ∫ AV fistula √à«¡¥â«¬√âÕ¬≈– 5 ¿“«–·∑√°´âÕπ∑’ÕË “®®–‡°‘¥ ¢÷πÈ ‰¥â§Õ◊ aneurysm ·µ°·≈–¡’°“√µ°‡≈◊Õ¥ thrombosis ·≈– distal embolization(26,27) √—°…“‚¥¬°“√„Àâ¬“ªØ‘™«’ π–∑“ßÀ≈Õ¥‡≈◊Õ¥¥” µ—¥‡Õ“‡π◊ÕÈ ‡¬◊ÕË ∑’ Ë °ª√°·≈–µ‘¥‡™◊ÕÈ ÕÕ°‚¥¬∑—«Ë ‰ª·≈â«°“√∑” revascularization ∑—π∑’‰¡à®”‡ªìπ‡æ√“–¡’‡≈◊Õ¥¡“‡≈’¬È ß·¢π¢“æÕ‡æ’¬ßÕ¬Ÿ·à ≈â«„π√“¬∑’Ë ¡’§«“¡®”‡ªìπµâÕß∑”§«√„™â autogenous vein graft ·∑πÀ≈Õ¥ ‡≈◊Õ¥‡∑’¬¡ ‡æ√“–Õ—µ√“µ‘¥‡™◊ÕÈ πâÕ¬°«à“°—π¡“° §«√∑”·∫∫ extra-anatomical bypass ‡≈’¬È ß∫√‘‡«≥ºà“µ—¥‡¥‘¡∑’¡Ë °’ “√µ‘¥‡™◊ÕÈ (28) „π√“¬∑’Ë ‰¡àµÕâ ß°“√∑” revascularization ∑—π∑’ ‡ªî¥·º≈∑‘ßÈ ‰«â∑”·º≈„Àâ –Õ“¥·≈–‡¬Á∫ªî¥·º≈¿“¬À≈—ß ∂â“¡’Õ“°“√¢“¥ ‡≈◊Õ¥ “¡“√∂ºà“µ—¥∑” revascularization ‰¥â¿“¬À≈—ß(29) Arterial injection °“√©’¥¬“æ≈“¥‡¢â“À≈Õ¥‡≈◊Õ¥·¥ß ∑”„Àâ ‡°‘¥¿“«–·∑√°´âÕπµà“ß Ê ¢÷πÈ °—∫ºŸªâ «É ¬ ‚¥¬‡©æ“–°“√¢“¥‡≈◊Õ¥ Õ¬à“ß‡©’¬∫æ≈—πµ“¡¥â«¬°“√µ“¬¢Õß‡π◊ÈÕ‡¬◊ËÕÀ≈Õ¥‡≈◊Õ¥∑’Ë‡°‘¥ intra-arterial injection ¢÷πÈ ‰¥â∫Õà ¬§◊Õ radial ·≈– branchial arteries º≈¢Õß°“√©’¥¬“À√◊Õ “√‡§¡’æ≈“¥‡¢â“À≈Õ¥‡≈◊Õ¥ ·¥ß®–∑”„Àâ™π—È ‡ÕÁπ‚¥∑’‡≈’¬Ë ¡∂Ÿ°∑”≈“¬ ∑”„ÀâÀ≈Õ¥‡≈◊Õ¥À¥µ—« ·≈–‡°‘¥ thrombosis À≈—ß©’¥¬“æ≈“¥‡¢â“À≈Õ¥‡≈◊Õ¥·¥ßª√“ °Æ°“√≥å∑’Ë®–‡°‘¥¢÷Èπ∑—π∑’§◊Õ ¡’ thrombosis ¢ÕßÀ≈Õ¥‡≈◊Õ¥ ¥”¢π“¥‡≈Á° µ“¡¡“¥â«¬°“√‡æ‘¡Ë capillary hydrostatic pressure “√πÈ”®–§—ßË Õ¬Ÿµà “¡‡π◊ÕÈ ‡¬◊ÕË µà“ß Ê §«“¡¥—π„π‡π◊ÕÈ ‡¬◊ÕË Ÿß¢÷πÈ tissue perfusion ‡≈«≈ß ∑”„Àâ¢“¥‡≈◊Õ¥·≈–‡πà“µ“¬„π∑’Ë ÿ¥ thrombosis ®–≈“¡®“°À≈Õ¥¥”‡¢â “ ¡“„πÀ≈Õ¥‡≈◊ Õ ¥·¥ß ¢π“¥‡≈Á°(30) À≈—ß©’¥¬“æ≈“¥‡¢â“À≈Õ¥‡≈◊Õ¥·¥ß ºŸâªÉ«¬®–√Ÿâ ÷°ª«¥¡“° ∑—π∑’ °“√‰À≈‡«’¬π‡≈◊Õ¥®–‡ ’¬¡’°“√·¢Áßµ—«¢ÕßÀ≈Õ¥‡≈◊Õ¥µ“¡ ¡“¥â«¬ cyanosis ·¢π¢“¥‡≈◊Õ¥∑”„Àâ‡π◊ÕÈ ‡¬◊ÕË ¢“¥ÕäÕ°´‘‡®π¡“ ‡≈’¬È ß·¢π®–‡¬Áπ·≈–¡’§«“¡∫°æ√àÕß¢Õß√–∫∫ª√– “∑®–‡≈«≈ß®π °√–∑—ßË ¡’‡π◊ÕÈ ‡¬◊ÕË ‡πà“µ“¬ §≈”™’æ®√∑’¡Ë ·’ ≈–‡∑â“¬—ß‰¥â ·µà∂“â ∑” arteriogram ·≈â«®–æ∫«à“¡’ thrombosis ‡°‘¥¢÷πÈ „π digital arteries °“√√—°…“ ¡’·π«∑“ß¥—ßµàÕ‰ª(31,32) 1. „Àâ ‡Œª“√’π 100,000 ¬Ÿπµ‘ ∑—π∑’∑“ßÀ≈Õ¥‡≈◊Õ¥¥” ·≈– „ÀâµÕà ‡π◊ÕË ß®π°√–∑—ßË √–¥—∫ PTT Ÿß°«à“§à“ª°µ‘ 1.5-2.5 ‡∑à“§à“ª°µ‘‡¥‘¡ ªÑÕß°—π thrombus propragation

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥ 2. „Àâ dexathethasone 4 ¡‘≈≈‘°√—¡∑“ßÀ≈Õ¥‡≈◊Õ¥¥”∑ÿ° 6 ™—«Ë ‚¡ß 3. „Àâ low molecular weight dextran (Dextran 40) „πÕ—µ√“ 20 ¡‘≈≈‘≈µ‘ √µàÕ™—«Ë ‚¡ß ≈¥°“√®—¥µ—«‡°“–°≈ÿ¡à ¢Õß‡°√Á¥‡≈◊Õ¥„πÀ≈Õ¥‡≈◊Õ¥¢π“¥‡≈Á° 4. „Àâ¬“·°âª«¥ 5. ¬°·¢πÀ√◊Õ¢“¢â“ßπ—Èπ¢÷Èπ Ÿß‡Àπ◊Õ√–¥—∫À—«„®‡æ◊ËÕ≈¥°“√ ∫«¡ 6. æ¬“¬“¡ÕÕ°°”≈—ß·¢πÀ√◊Õ¢“∑—π∑’ À≈—ß®“°Õ“°“√¥’ ¢÷πÈ ªÑÕß°—π contracture ·π«∑“ß°“√√—°…“π’È®–™à«¬≈¥æ¬“∏‘ ¿“æ¥—ß°≈à“«‰¡à „ Àâ ‡π◊ÈÕ‡¬◊ËÕ‡πà“µ“¬¡“°¢÷Èπ „Àâ°“√√—°…“ 3-8 «—π √Õ®π°√–∑—Ëß Õ“°“√¥’¢π÷È ®÷ßµ—¥‡Õ“‡π◊ÕÈ ‡¬◊ÕË ∑’‡Ë πà“µ“¬ à«πª≈“¬ÕÕ°

IATROGENIC INJURIES ªí®®ÿ∫π— ¡’«∏‘ °’ “√µ√«®«‘π®‘ ©—¬·≈–√—°…“µ≈Õ¥®π°“√ monitor µà“ß Ê ‚¥¬°“√ «π “¬§“„πÀ≈Õ¥‡≈◊Õ¥ æ∫«à“À—µ∂°“√µà“ß Ê ∑”„Àâ‡°‘¥°“√∫“¥‡®Á∫¢ÕßÀ≈Õ¥‡≈◊Õ¥¡’°“√µ°‡≈◊Õ¥ ‡°‘¥≈‘Ë¡ ‡≈◊Õ¥Õÿ¥µ—π pseudoaneurysm ·≈– A-V fistula(33-36) ¿“«– ·∑√°´âÕπ‡À≈à“π’È∂â“‡°‘¥√ÿπ·√ß„πºŸâªÉ«¬∑’Ë¡’‚√§À≈Õ¥‡≈◊Õ¥À—«„® Õ¬Ÿà·≈â«Õ“®®–∑”„ÀâºŸâªÉ«¬∂÷ß·°à°√√¡‰¥â Õ—µ√“°“√∫“¥‡®Á∫¢Õß À≈Õ¥‡≈◊Õ¥®“°À—µ∂°“√µà“ß Ê „π‚√ßæ¬“∫“≈¡“µ√∞“πæ∫‰¥â√Õâ ¬ ≈– 1-2(36,37) À≈Õ¥‡≈◊Õ¥∑’∫Ë “¥‡®Á∫§◊ÕÀ≈Õ¥‡≈◊Õ¥·¥ß branchial ·≈– femoral ‡°‘ ¥ ®“°°“√∑” cardiac catheterization °“√©’¥ ’µ√«®«‘π®‘ ©—¬À√◊Õ¢¬“¬∂à“ßÀ≈Õ¥‡≈◊Õ¥ “¬ «πÕ“®®– ∑”„ÀâÀ≈Õ¥‡≈◊Õ¥·µ°À√◊Õ©’°¢“¥ °“√„™â¬“‡Œª“√’π ·Õ ‰æ√‘π À√◊Õ “√≈–≈“¬≈‘Ë¡‡≈◊Õ¥®–∑”„ÀâºŸâªÉ«¬µ°‡≈◊Õ¥ßà“¬¢÷Èπ ·µà∂â“‰¡à „™â‡Œª“√’π‚Õ°“ ‡°‘¥ thrombosis °Á¡‰’ ¥â ßŸ (36-39) æ¬“∏‘ ¿“æ¢Õß°“√∫“¥‡®Á∫®“°°“√§“ “¬ «π∑’æË ∫‰¥â¡’ 1. intimal disruption À√◊Õ dissection µ√ßµ”·Àπàß∑’ Ë «π §“ “¬ ∑”„Àâºπ—ßÀ≈Õ¥‡≈◊Õ¥∑–≈ÿ ¡’ thrombus ‡°‘¥ ¢÷πÈ Õÿ¥À≈Õ¥‡≈◊Õ¥ 2. intima ulceration ®“° “¬ «π∑’Ë§“‰«â§√Ÿ¥°—∫ºπ—ß À≈Õ¥‡≈◊Õ¥ ‡ªìπ√–¬–‡«≈“π“π 3. thrombus ¢â“ß “¬ «π∑’§Ë “‰«â ‡¡◊ÕË ¥÷ß “¬ «πÕÕ°®– Õÿ¥À≈Õ¥‡≈◊Õ¥

∫“¥‡®Á∫À≈Õ¥‡≈◊Õ¥

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‡Õ° “√Õâ“ßÕ‘ß 1. Laohapensang K, Prathnadi P. Traumatic arterial injuries of the upper extremity. Thai J Surg 1993;14: 39-42. 2. Feliciano DV, Bitonde CG, Mattox KL, ed al. Civilian trauma in the 1980ûs. Ann Surg 1984;199:717-724. 3. Munoz E, Cohen J. Epidemiology and the economics of vascular trauma. In: Civilian Vascular Trauma. Flanigan DP, Schuller JJ, Meyers JP (eds.) Lea & Febiger, 1992. 4. Drapanas T, Hewitt RL, Weichert RF, et al. Civilian vascular injuries: A critical appraisal of three decades of management. Ann Surg 1970;172: 351-360. 5. Stiles QR. Management of injuries of the thoracic and abdominal aorta. Am J Surg 1985;150:132. 6. Weaver FA. Injuries to the ascending aorta, aortic arch and great vessels. Surg Gynecol Obstet 1989;169:27. 7. Applebaum R. Role of routine arteriography in blunt lower-extremity trauma. Am J Surg 1990;160:221. 8. Schwartz MR, Weaver FA, Bauer M, et al. Refining the indications for arteriography in penetrating extremity trauma: A prospective analysis. J Vasc Surg 1993;17:16-221. 9. King TA, Perse JA, Marmem C, Darvin HI. Utility of arteriography in penetrating extremity injuries. Am J Surg 1991;176:172-174. 10. OûGorman RB, Feliciano DV, Bitondo CG, et al. Emergency center arteriography in the evaluation of suspected peripheral vascular injuries. Arch Surg 1984;119:568-573. 11. Frykberg ER, Vines FS, Alexander RH. The natural history of clinically occult arterial injuries: A prospective evaluation. J Trauma 1989;29:577. 12. Stain SC. Selective management of nonocclusive arterial injuries. Arch Surg 1989;124:1136. 13. Gregory RT, Gould RJ, Peclet M, et al. The mangled extremity syndrome (M.E.S.): A severity grading system for multisystem injury of the extremity. J Trauma 1985;25:1147. 14. Lange RH, Bach AW, Hansen ST Jr, et al. Is limb loss avoidable in civilian vascular injuries? Am J Surg 1987;154:202. 15. Whitman GJR, McCroskey BL, Moore EE, et al. Traumatic popliteal and trifurcation injuries-determinants of limb salvage. Am J Surg 1987;154:681. 16. Alexander JJ, Piotrowski JJ, Craham D, et al. Outcome of complex vascular and orthopedic injuries of the extremity. Am J Surg 1991;162:111-116. 17. Feliciano DV, Mattox KL, Graham JM, et al. Five year experience with PTFE grafts in vascular wounds. J Trauma 1985;25:71-82.

18. Feliciano DV. Use of prosthetic vascular grafts in civilian vascular trauma. In: Civilian Vascular Trauma. Flanigan DP (ed) Philadelphia: Lea & Febiger 1992;364-372. 19. Mubarak SJ, Hargens AR. Acute compartment syndromes. Surg Clin North Am 1983;63:539-565. 20. Hayden JW. Compartment syndromes: Early recognition and treatment. Postgrad Med 1983;74:191-202. 21. Mubarak SJ, Owens CA, Hargens AR, et al. Acute compartment syndromes: Diagnosis and treatment with the aid of Wick catheter. J Bone Jt Surg 1978;60:1091-1095. 22. Feliciano DV, Cruse PA, Spjut-Patrainely V, et al. Fasciotomy after trauma to the extremities. Am J Surg 1988;156:533-536. 23. Mubarak SJ, Owen CA. Double incision fasciotomy of the leg for decompression in compartment syndromes. J Bone Jt Surg 1977;59:184-187. 24. Patman RD. Fasciotomy techniques. In: Civilian Vascular Trauma. Flanigan DP (ed). Philadephia: Lea & Febiger 1992;346-354. 25. Nghiem DD, Bolard JP. Four compartment fasciotomy of the lower extremity without fibulectomy: A new approach. Am Surg 1980;46:414-417. 26. Reedy DJ, Smith RF, Elliott JP, et al. Infected femoral artery false aneurysms in drug addicts: Evolution of selective vascular reconstruction. J Vasc Surg 1986;3:718-724. 27. McIlroy MA, Reddy DJ, Markowitz N, et al. Infected false aneurysms of the femoral artery in intravenous drug addicts. Rev Infect Dis 1989;11:578-585. 28. Patel KR, Semel L, Clauss RH. Routine revascularization with resection of infected femoral pseudoaneurysm from substance abuse. J Vasc Surg 1988;8:321-328. 29. Johnson JR, Ledgerwood AM, Lucas CE. Mycotic aneurysm: New concepts in therapy. Arch Surg 1983;118:577-582. 30. Ellertson DG, Lazarus HM, Auerbach R. Patterns of acute vascular injury after intraarterial barbiturate injection. Am J Surg 1973;30:813817. 31. Buckspan GS, Franklin JD, Novak GR, et al. Intraarterial drug injury: Studies of etiology and potential treatment. J Surg Res 1978;24:294-301. 32. Treiman GS. An effective treatment protocol for intraaterial drug injection. J Vasc Surg 1990;12:456. 33. Cragg AH, Nakagawa N, Smith TP, et al. Hematoma formation after diagnostic angiography: Effect of catheter size. J Vasc Intervent Radiol 1991;2:231-233.

∫“¥‡®Á∫À≈Õ¥‡≈◊Õ¥ 34. Altin RS, Flicker S, Naidech HJ. Pseudoaneurysm and arteriovenous fistula after femoral artery catheterization: Association with low femoral punctures. AJR 1989;152:629-631. 35. Kaufman JL. Pelvic hemorrhage after percutaneous femoral angiography. AJR. 1984;143:335-336. 36. Sigstedt B, Lunderquist A. Complications of angiographic examinations. AJR 1978;130:455-460.

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√Ÿª∑’Ë 30.1 Toe amputation

2. ¢âÕ∫àß™’È„π¿“«–∑’Ë‰¡à√’∫¥à«π 2.1 ¢“¢“¥‡≈◊Õ¥‡√◊ÈÕ√—ß ‚¥¬∑—Ë«‰ª·≈â«ºŸâªÉ«¬∑’ËÕ¬Ÿà „π¿“«– chronic limb threatening ischemia ‡ªìπ¢âÕ∫àß™’È „π °“√ºà“µ—¥ revascularization ºŸªâ «É ¬∑’ªË «¥¡“°®“° ischemic rest pain ®π‰¡à “¡“√∂æ—°ºàÕπ‰¥âÀ√◊ÕµâÕß „Àâ¬“·°âª«¥„πª√‘¡“≥ Ÿß ¡’·º≈‡√◊ÕÈ √—ß ≈ÿ°≈“¡‡πà“µ“¬ ®π∂÷ß®ÿ¥∑’Ë‡π◊ÈÕ‡¬◊ËÕµàÕ°√–¥Ÿ° tarsal §«√µ—¥¢“ÕÕ° À√◊Õºà“π°“√ºà“µ—¥∑” revascularization ·≈â«À≈“¬ §√—ßÈ Õ“°“√‰¡à¥¢’ π÷È (7,8) 2.2 ¿“«–·∑√°´âÕπ¢Õß‚√§‡∫“À«“π ‡™àπ °“√‡°‘¥ neurotrophic ulcer ®÷ ß √— ° …“‰¡à À “¬¢“¥∑’Ë ‡ ∑â “ °“√ æ‘®“√≥“µ—¥‡æ◊ÕË ªÑÕß°—π°“√µ‘¥‡™◊ÕÈ ≈ÿ°≈“¡¿“¬À≈—ß

°“√ª√–‡¡‘π√–¥—∫°“√µ—¥ ¡’«∏‘ °’ “√À≈“¬Õ¬à“ß∑’πË ”¡“„™â‡æ◊ÕË ‡≈◊Õ°·≈–ª√–‡¡‘π√–¥—∫¢Õß °“√µ—¥¢“·≈–π‘«È ‡∑â“ ®ÿ¥¡ÿßà À¡“¬°Á§Õ◊ µâÕß°“√„Àâ·º≈µ√ßµÕÀ“¬¥’ °“√µ—¥ ‘π„®µ—¥‚¥¬Õ“»—¬≈—°…≥–∑“ß§≈‘π‘§Õ¬à“ß‡¥’¬«‰¥âº≈¥’ √âÕ¬≈– 80 ”À√—∫°“√µ—¥√–¥—∫„µâÀ«— ‡¢à“·≈–√âÕ¬≈– 90 ”À√—∫ °“√µ—¥‡Àπ◊ÕÀ—«‡¢à“ ∂â“§≈”™’æ®√‰¥â‡Àπ◊ÕµàÕ∫√‘‡«≥∑’Ë®–µ—¥°Á §àÕπ¢â“ß®–·πà „®«à“·º≈∑’µË Õ®–À“¬¥’ °“√À“¬¢ÕßµÕ∫√‘‡«≥µË” °«à“¢âÕ‡∑â“¬“°®–§“¥°“√≥å ‰¥â ‚¥¬°“√§≈”™’æ®√Õ¬à“ß ‡¥’¬« §«√¡’«∏‘ °’ “√ noninvasive test ™à«¬√à«¡„π°“√µ—¥ ‘π„®¥â«¬ À≈—°°“√ ”§—≠„π°“√µ—¥¢“·≈–ª√–‡¡‘π√–¥—∫„π°“√µ—¥ ‚¥¬ ‡©æ“–„π¿“«–©ÿ°‡©‘π§◊Õ(9,10,12)

1. µ—¥‡Õ“‡π◊ÕÈ ‡¬◊ÕË ∑’µË “¬ ªπ‡ªóÕô π ·≈–µ‘¥‡™◊ÕÈ ÕÕ°„ÀâÀ¡¥ 2. perfusion µ√ß√–¥—∫∑’µË ¥— ¥’‡æ’¬ßæÕ∑’®Ë –∑”„Àâ·º≈À“¬‰¥â 3.µÕ∑’‡Ë À≈◊Õ “¡“√∂À“Õ«—¬«–‡∑’¬¡¡“ «¡„ à·≈–ªØ‘∫µ— À‘ πâ“∑’Ë ‰¥â¥¿’ “¬À≈—ß ”À√—∫ noninvasive test ∑’Ë „™â „πªí®®ÿ∫π— ‡æ◊ÕË ™à«¬µ—¥ ‘π„® ª√–‡¡‘π√–¥—∫°“√µ—¥¢“·≈–π‘«È ‡∑â“ ¡’¥ß— µàÕ‰ªπ’È (12-17) 1. segmental blood volume ·≈– pulse volume recording (PVR) ‚¥¬„™â doppler ultrasound «—¥ pulsatile blood flow √à«¡°—∫°“√ —ß‡°µÿ PVR tracing 2. skin blood flow testing ‚¥¬„™â laser doppler velocimetry local skin fluorescence ·≈–°“√«—¥√–¥—∫‰Õ‚´‚∑∫ ‡æ◊ËÕª√–‡¡‘πª√‘¡“≥¢Õß‡≈◊Õ¥∑’Ë¡“‡≈’È¬ßº‘«Àπ—ß °àÕπ ª√–‡¡‘π√–¥—∫°“√µ—¥ magnetic resonance (MR) limb blood flow scanning „™â ”À√—∫¥Ÿ perfusion ¢Õß∑—ßÈ ¢“·≈–‡≈◊Õ¥∑’Ë ‰À≈ ºà“πÀ≈Õ¥‡≈◊Õ¥·µà≈–À≈Õ¥ 3. °“√«—¥Õÿ≥À¿Ÿ¡º‘ «‘ ‡™◊ÕË ∂◊Õ‰¡à ‰¥â‡≈¬„π°“√ª√–‡¡‘π√–¥—∫ ‚¥¬‡©æ“–„πºŸâªÉ«¬∑’Ë¡’°“√Õ—°‡ ∫µ‘¥‡™◊ÈÕ∫√‘‡«≥π—Èπ ·µà thermographic mapping πà“®–∫àß∫Õ°‰¥â™—¥‡®π °«à“∂÷ß°“√‰À≈‡«’¬π¢Õß‡≈◊Õ¥∑’ºË «‘ Àπ—ß 4. transcutaneous oxygen pressure measurment (TCPO2) ‡ªìπ«‘∏°’ “√„À¡à∑’Ë „™âª√–‡¡‘π√–¥—∫°“√µ—¥‰¥âº≈¥’ ∂â“µË”°«à“ 25 ¡‘≈≈‘‡¡µ√ª√Õ∑·º≈®–‰¡àÀ“¬¥’

«‘∏’°“√°“√µ—¥π‘È«‡∑â“·≈–¢“(18-22) 1. °“√µ—¥π‘«È ‡∑â“ (toe ampulation) „™â¡¥’ °√’¥º‘«Àπ—ß„°≈â µÕ¢Õßπ‘È«‡∑â“‡ªìπ«ß‚¥¬√Õ∫ (√Ÿª∑’Ë 30.1) ‚¥¬°√’¥≈ßºà“π ‡π◊ÕÈ ‡¬◊ÕË ∑ÿ°™‘πÈ ≈ß‰ª®π∂÷ß°√–¥Ÿ° „™â periosteal elevator ∂“°‡Õ“ periosteum ÕÕ°®“°°√–¥Ÿ° µ—¥°√–¥Ÿ°π‘È«‡∑â“„πµ”·Àπàß∑’ËÕ¬Ÿà ª≈“¬µàÕ metatarsophalangeal joint ‚¥¬„™â§¡’ µ—¥°√–¥Ÿ°·≈– ¢≈‘∫‡»…°√–¥Ÿ°ÕÕ°„Àâµ√ßª≈“¬‡√’¬∫¥â«¬ Ronguer §«√√–«—ß ‰¡à „Àâ°√–¥Ÿ°‚º≈àÕÕ°¡“πÕ°·º≈ ‡æ√“–°“√À“¬¢Õß∫“¥·º≈ ∫√‘‡«≥π’È ‰¡à¥π’ °— ‡π◊ÕË ß®“°‡ªìπ∫√‘‡«≥∑’¡Ë ‡’ ≈◊Õ¥¡“‡≈’¬È ßπâÕ¬ °–„Àâ ¢Õ∫¢Õßº‘«Àπ—ßæÕ¥’‰¡àµ÷ßÀ√◊ÕÀ¬àÕπ®π‡°‘π‰ª ‡«≈“‡¬Á∫ªî¥ ∂â“ ‰¡à¡’°“√Õ—°‡ ∫µ‘¥‡™◊ÈÕ¡“°àÕπ„Àâ‡¬Á∫ªî¥º‘«Àπ—ß™—Èπ‡¥’¬«¥â«¬‰π ≈àÕπ‡¬Á∫·∫∫∑’≈–§” (interrupted vertical mattress) 2. Ray amputation ¡’¢Õâ ∫àß™’È „π°“√ºà“µ—¥§◊Õ ¡’°“√Õ—°‡ ∫ µ‘¥‡™◊ÕÈ ≈ÿ°≈“¡¢÷πÈ ¡“®π‡°◊Õ∫∂÷ß metatarsophalangeal crease

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√Ÿª∑’Ë 30.2 Ray amputation

√Ÿª∑’Ë 30.3 Ray amputation of great toe

≈ß¡’¥„π·π««ß°≈¡µ√ß metatarsophalangeal crease (√Ÿª∑’Ë 30.2A) µ—¥π‘«È ‡∑â“·≈–°√–¥Ÿ° phalanx ÕÕ°„ÀâÀ¡¥ „™â periosteal elevator ∂“° tendon ÕÕ°®“° metatarsophalangeal head „™â Ronguer ¢≈‘∫ metatarsal head µ—¥ tendon ∑’¬Ë “«‡°‘πÕÕ° ≈â“ß·º≈„Àâ –Õ“¥¥â«¬πÈ”‡°≈◊Õ ¡¥ÿ≈¬å ‡¬Á∫º‘«Àπ—ßªî¥¥â«¬‰π ≈àÕπ∑’≈–§” (√Ÿª 30.2B) ∂â“‡ªìπ°“√µ—¥π‘«È À—«·¡à‡∑â“ ‡∑§π‘§°“√ ºà“µ—¥®–§≈â“¬°—π (√Ÿª∑’Ë 30.3)

3. Transmetatarsal amputation ¡’¢Õâ ∫àß™’È „π°“√„™â§Õ◊ ¡’°“√‡πà“µ“¬¢Õß‡π◊ÕÈ ‡¬◊ÕË ≈“¡‡≈¬ metatarsal crease º‘«Àπ—ß ¥â“πΩÉ“‡∑â“¬—ß¥’Õ¬Ÿà‡æ◊ËÕ∑’Ë®–„™â‡¬Á∫µ≈∫¡“‡ªìπ posterior flap ≈ß¡’¥„π·π«‚§âß∫πÀ≈—ß‡∑â“Àà“ß®“°®ÿ¥°÷ßË °≈“ß¢Õß metatarsal shaft 5-10 ¡‘≈≈‘‡¡µ√ (√Ÿª∑’Ë 30.4) °√’¥ºà“πº‘«Àπ—ß‡∑â“¥â“ππÕ° ·≈–¥â“π„π ∑”¡ÿ¡©“°·≈â«°√’¥ºà“π metatarsophalangeal crease ¢ÕßΩÉ“‡∑â“ °√’¥¡’¥„Àâ≈°÷ ∂÷ß°√–¥Ÿ° „™â‡≈◊ÕË ¬µ—¥°√–¥Ÿ°„Àâ π—È æÕ¥’ ‰¡à‡≈¬ÕÕ°πÕ°¢Õ∫º‘«Àπ—ß µ—¥ tendon ∑’¬Ë “«‡°‘πÕÕ° ¥÷ß plantar flap ‡¢â“¡“À“À≈—ß‡∑â“ ‡¬Á∫‡π◊ÈÕ‡¬◊ËÕ™—Èπ subcutaneous ·≈–º‘«Àπ—ß∑’≈–™—πÈ ·∫∫∑’≈–§”

A B

√Ÿª∑’Ë 30.4 Transmetatarsal amputation

√Ÿª∑’Ë 30.5 Symeûs amputation

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4. Symeûs amputation (ankle disarticulation) À≈—ß°“√µ—¥‡∑â“«‘∏’π’Èæ∫«à“ –¥«°µàÕ°“√∑”°“¬¿“æ∫”∫—¥ ≈ß¡’¥∫πÀ≈—ß‡∑â“µàÕ ankle crease ‡≈¬µ“µÿ¡à ¥â“ππÕ°·≈–„π (√Ÿª∑’Ë 30.5)°√’¥¡’¥µàÕ‡ªìπ‡ âπµ√ß¡“∑“ß¥â“πÀ≈—ß∂÷ßºŸ°À≈Õ¥‡≈◊Õ¥·¥ßπ’È µ√ßµ”·Àπàß∑’®Ë –·¬°‰ª‡ªìπ medial ·≈– lateral tarsal branches ≈ß¡’¥ºà“π°√–¥Ÿ° talus ≈ß¡“®π∂÷ß¢âÕ‡∑â“ ºŸ°À≈Õ¥‡≈◊Õ¥·¥ß anterior tibial µ—¥ tendon √Õ∫¢â“ß‡æ◊ÕË ‡¢â“∂÷ß talotibial joint µ—¥ medial ·≈– lateral collateral ligaments ‡æ◊ÕË ‡¢â“∂÷ß joint capsule disarticulate °√–¥Ÿ° talus ‡≈“– calcaneus ÕÕ° ®“°‡π◊ÕÈ ‡¬◊ÕË √Õ∫¢â“ß „™â‡≈◊ÕË ¬µ—¥ à«πª≈“¬¢Õß°√–¥Ÿ° tibia ·≈– fibula „Àâµ√ß ¥—π heel flap ¡“∑“ß¥â“πÀπâ“‡¬Á∫æ—ßº◊¥¥â“πÀ≈—ß „Àâµ¥— °—∫æ—ßº◊¥¥â“πÀπâ“¢Õß tibia „™â ‰π≈àÕπ‡¬Á∫ªî¥º‘«Àπ—ß∑’≈–§”

Anterior compartment

5. Below-knee (BK) amputation ‡ªìπ«‘∏’°“√µ—¥¢“‚¥¬°“√‡°Á∫¢âÕ‡¢à“‡Õ“‰«â «‘∏’∑’Ë¥’§◊Õ long posterior myocutaneous flap µ”·Àπàß¢Õß°√–¥Ÿ° tibia ∑’µË ¥— §◊Õ 12 ‡´Áπµ‘‡¡µ√ ‡≈¬ tibial tuberosity ·π«≈ß¡’¥∑“ß¥â“πÀπâ“ ®–Õ¬Ÿ‡à ≈¬·π«°√–¥Ÿ°∑’µË ¥— 1 ‡´Áπµ‘‡¡µ√ °√’¥º‘«Àπ—ßºà“π¡“∑“ß ¥â“π„π·≈–¥â“π¢â“ß¢ÕßπàÕß (√Ÿª∑’Ë 30.6) ª√–¡“≥§√÷ßË πàÕß·≈– ∑”¡ÿ¡‚§âß µ—¥·≈–ºŸ° greater ·≈– lesser saphenous vein µ—¥ sural verve „Àâ Ÿ ß ‡≈¬µÕªÑ Õ ß°— π °“√‡°‘ ¥ neuroma µ— ¥ °≈â“¡‡π◊ÕÈ ∑“ß¥â“π anterior compartment ‡æ◊ÕË ‡¢â“∂÷ß anterior tibial neurovascular bundles ‡æ◊ÕË ºŸ°µ—¥ ‡≈“–°≈â“¡‡π◊ÕÈ ÕÕ° ®“°°√–¥Ÿ° µ—¥°√–¥Ÿ° tibia „Àâ π—È °«à“·π«º‘«Àπ—ß 2 ‡´Áπµ‘‡¡µ√ ∫“°°√–¥Ÿ°∑“ß¥â“πÀπâ“∑”¡ÿ¡ 45o °—∫·π«¢«“ß µ—¥°√–¥Ÿ° fubula

Tibia

Anterior tibial vessels and deep peroneal n. Lateral compartment Peroneal vessels Posterior tibial vessels and tibial n.

√Ÿª∑’Ë 30.6 Below-knee amputation

Greater saphenous v. Posterior compartment Lesser saphenous v.

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Rectus femoris tendon

Vastus medialis m. Popliteal a and v.

Vastus lateralis m.

Adductor magnus tendon Saphenous nerve

Femur

Sartorius m.

Biceps femoris m.

Greater saphenous v.

Tibial n. Common peroneal n. Semitendinous m.

Gracilis m. Semimembranosus m.

√Ÿª∑’Ë 30.7 Above-knee Ÿß°«à“ tibia 2 ‡´Áπµ‘‡¡µ√ ‡¢â“∂÷ß posterior group muscles ‡æ◊ËÕºŸ°µ—¥ posterior tibial ·≈– peroneal neurovascular bundles µ—¥°≈â“¡‡π◊ÕÈ ºŸ° soleal veins ∑”„Àâ posterior flap ∫“ß≈ß‚¥¬∫“°°≈â“¡‡π◊ÕÈ ‡ªìπ√Ÿªª“°©≈“¡ À√◊Õµ—¥‡Õ“°≈â“¡‡π◊ÕÈ soleus ÕÕ° ≈â“ß·º≈„Àâ –Õ“¥¥â«¬πÈ”‡°≈◊Õ ¡¥ÿ≈¬å ‡¬Á∫‡ÕÁπ æ—ßº◊¥¢Õß flap ¥â“πÀπâ“·≈–À≈—ß‡¢â“¡“®√¥°—π‚¥¬„™â ‰À¡ ≈–≈“¬‡¬Á∫∑’≈–§” «“ß∑àÕ√–∫“¬·∫∫ªî¥µ√ßª≈“¬µÕ ‡¬Á∫ º‘«Àπ—ßªî¥‚¥¬„™â ‰π≈àÕπ‡¬Á∫∑’≈–§” µ—¥‰À¡‡¡◊ËÕ·º≈∑’ËµÕ·Àâß ·≈–À“¬Õ’° 3 —ª¥“Àå

6. Above-knee (AK) amputation ¡’¢Õâ ∫àß™’È „πºŸªâ «É ¬∑’Ë §“¥«à“µ—¥¢“·∫∫ BK amputation ·≈â«‰¡à‡æ’¬ßæÕ ‡π◊ÕË ß®“°¡’ °“√µ‘¥‡™◊ÕÈ ≈ÿ°≈“¡À√◊Õ¢“¢“¥‡≈◊Õ¥√–¥—∫ Ÿß §«√‡°Á∫°√–¥Ÿ° femur ‡Õ“‰«â „Àâ¬“«∑’Ë ÿ¥ ‡æ√“–®–™à«¬≈¥æ≈—ßß“π¢Õß√à“ß°“¬∑’Ë®–„™â „π¢≥–∑”°“√¿“æ∫”∫—¥‡æ◊ËÕÀ—¥‡¥‘π ≈ß¡’¥√Õ∫µâπ¢“„Àâ·π« ¢Õßº‘«Àπ—ß¬“«°«à“µ”·Àπàß¢Õß°√–¥Ÿ° femur ∑’Ë®–µ—¥ 2-3 ‡´Áπµ‘‡¡µ√ ‡Àπ◊ÕµàÕ°√–¥Ÿ° patella ·≈– femoral condyles (√Ÿª∑’Ë 30.7) ºŸ°µ—¥ greater saphenous vein µ—¥°≈â“¡‡π◊ÈÕ∑“ß ¥â“πÀπâ“·≈–µ√ß°≈“ß ºŸ°µ—¥ femoral vessels µ—¥°≈â“¡‡π◊ÈÕ ∑’‡Ë À≈◊ÕÕÕ° µ—¥°√–¥Ÿ° femur Àâ“¡‡≈◊Õ¥∑’ÕË Õ°®“°°√–¥Ÿ°‚¥¬„™â bone wax Õÿ¥≈â“ß·º≈„Àâ –Õ“¥¥â«ππÈ”‡°≈◊Õ ¡¥ÿ≈¬å «“ß∑àÕ √–∫“¬·∫∫ªî¥µ√ßª≈“¬µÕ·≈â«‡¬Á∫ªî¥·º≈∑’≈–™—πÈ

296

°“√¥Ÿ·≈ºŸâªÉ«¬À≈—ßºà“µ—¥ °“√ºà“µ—¥„À≠à ‡™àπ AK À√◊Õ BK amputation À≈—ßºà“µ—¥ §«√„™â soft À√◊Õ ragid dressing ‚¥¬‡©æ“– immediate postoperative prostheses (IPOP) À≈—ß‡¬Á∫ªî¥·º≈∑’ËµÕ·≈â« √Õß·º≈¥â«¬ºâ“∫“ß Ê ·≈– ”≈’À√◊ÕøÕßπÈ”∑’πË ¡ÿà „™â∂ßÿ §≈ÿ¡ «“ß À¡Õπ‡≈Á° Ê Àπÿπµ√ßª¡°√–¥Ÿ° ·≈–Àÿ¡â ¥â«¬ªŸπæ≈“ ‡µÕ√åÀ√◊Õ ‰ø‡∫Õ√å°≈“ Õ’°™—πÈ Àπ÷ßË §«√¡’ “¬§“¥√—¥‡Õ“°—π‡§≈◊ÕË π µ—¥ plate µ√ßª≈“¬‡æ◊ËÕµàÕ‡¢â“°—∫¢“‡∑’¬¡Ωñ°¬◊π·≈–‡¥‘π‰¥â∑—π∑’À≈—ßøóôπµ—« ®“°°“√ºà“µ—¥ ¢âÕ¥’¢Õß IPOP §◊ÕµÕ‰¡à∫«¡ ªÑÕß°—π°“√ßÕæ—∫ ¢Õß¢âÕ‡¢à“·≈–°“√°√–∑∫°√–‡∑◊Õπ¢Õß·º≈·≈–µ—¥‰À¡ ‰¡à “¡“√∂¥Ÿ§«“¡º‘¥ª°µ‘·≈– —ß‡°µÿ°“√‡ª≈’¬Ë π·ª≈ß¢Õß∫“¥·º≈‰¥â °“√‡§≈◊ËÕπ‰À«À√◊Õ¢¬—∫¢âÕ≈”∫“°‡π◊ËÕß®“°¡’ dressing æ—π Àπ“«‘∏’·≈–·π«∑“ßªØ‘∫—µ‘∑’Ë¥’§◊Õ§«√°–¢π“¥¢Õß¢“‡∑’¬¡∑’ËæÕ¥’ ·≈–„ à „πÀâÕßºà“µ—¥∑—π∑’ À≈—ßºà“µ—¥§«√πÕπ¬°ª≈“¬µÕ„Àâ Ÿß °—π∫«¡ ¢âÕ‡ ’¬¢Õß rigid dressing §◊Õ §«∫§ÿ¡°“√∫«¡¢Õß µÕ‰¡à ‰¥â ‡°‘¥°“√ßÕ·≈–µ√÷ß¢Õß¢âÕ‡¢à“‰¥âß“à ¬ µ“¡À≈—°°“√·≈â« §«√®–„Àâ stump mature °àÕπ∑’®Ë –„ à¢“‡∑’¬¡·≈–À—¥‡¥‘π ∂â“‡ªìπ soft dressing ®–¥Ÿ·≈·≈–∑”°“¬¿“æ∫”∫—¥‰¥âß“à ¬°«à“

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¿“«–·∑√°´âÕπÀ≈—ßºà“µ—¥ Phantom limb pain ·≈–°“√ª«¥‡√◊ÕÈ √—ß¢Õß·º≈∫√‘‡«≥µÕ æ∫‰¥â√âÕ¬≈– 5-30 æ∫„πºŸâªÉ«¬µ—¥¢“®“°°“√∫“¥‡®Á∫À√◊ÕºŸâ ªÉ«¬∑’Ë¢“¢“¥‡≈◊Õ¥¿“«–«‘°ƒµ¡“‡ªìπ√–¬–‡«≈“π“π µâÕß∑π ∑ÿ°¢å∑√¡“π®“°°“√ª«¥¢“À≈—ß®“°°“√µ—¥¢“‰ª·≈â«ºŸâªÉ«¬°Á¬—ß ¡’§«“¡√Ÿâ ÷°«à“¬—ß¡’¢“Õ¬Ÿà·≈â«ª«¥¡“°´÷Ëß°“√ª«¥Õ“®®–¡’ “‡Àµÿ ®“°µ√ßª≈“¬‡ âπª√– “∑∑’∂Ë °Ÿ µ—¥ √—°…“¬“°¡“°„™â‡«≈“π“π°«à“ ®–À“¬ °“√∑”°“¬¿“æ∫”∫—¥®–∑”„ÀâºªŸâ «É ¬≈¥Õ“°“√‡®Á∫≈ß‰¥â (23) ≈‘Ë¡‡≈◊Õ¥∑’Ë§—Ëß∫√‘‡«≥µÕÀ√◊Õº‘«Àπ—ß„µâ·º≈·≈–°≈â“¡‡π◊ÈÕ‡°‘¥®“° ‡∑§π‘§°“√ºà“µ—¥·≈–Àâ“¡‡≈◊Õ¥‰¡à¥’ ∂â“‰¡à·πà „®§«√«“ß∑àÕ√–∫“¬ §«√„Àâ¬“ªØ‘™’«π–°àÕπ·≈–À≈—ßºà“µ—¥‚¥¬‡©æ“–√“¬∑’Ë‡ ’Ë¬ßµàÕ °“√µ‘¥‡™◊ÈÕ®–™à«¬≈¥Õ—µ√“°“√µ‘¥‡™◊ÈÕÀ≈—ßºà“µ—¥‰¥â¡“° Õ—µ√“ µ“¬¢Õß°“√ºà“µ—¥æ∫‰¥â√âÕ¬≈– 10 ”À√—∫ AK amputation ·≈–√âÕ¬≈– 40 ”À√—∫ BK amputation ´÷ßË ¡’ “‡Àµÿ¡“®“°‚√§ À≈Õ¥‡≈◊Õ¥À—«„®‚§‚√π“√’Ë ´÷ßË ºŸªâ «É ¬‡ªìπÕ¬Ÿ°à Õà π·≈â«

√ÿª °“√µ—¥π‘«È ‡∑â“·≈–¢“‡ªìπÀ—µ∂°“√∑’®Ë ”‡ªìπ ”À√—∫»—≈¬- °√√¡ À≈Õ¥‡≈◊Õ¥ ∫“ß§√—ÈßºŸâªÉ«¬¢“À√◊Õπ‘È«‡∑â“¢“¥‡≈◊Õ¥‡ªìπ√–¬– ‡«≈“π“π ®π°√–∑—ßË ¡’°“√‡πà“µ“¬¢Õß‡π◊ÕÈ ‡¬◊ÕË ®÷ß¡’§«“¡®”‡ªìπ µâÕßµ—¥ÕÕ°‰¡à „Àâ¡°’ “√µ‘¥‡™◊ÕÈ ≈ÿ°≈“¡ À√◊Õ„π°√≥’∑ª’Ë «¥¡“°®“° Õ“°“√¢“¥‡≈◊Õ¥‡√◊ÕÈ √—ß ·≈–‰¡à “¡“√∂µàÕ‡ √‘¡ √â“ßÀ≈Õ¥‡≈◊Õ¥ ‡æ◊ÕË „Àâ‡≈◊Õ¥‰À≈‡«’¬π¡“¬—ß∫√‘‡«≥π—πÈ ‰¥â °“√µ—¥π‘«È ‡∑â“À√◊Õ¢“„π √–¥—∫µà“ß Ê §«√¡’¢Õâ ∫àß™’∑È ·’Ë πà™¥— °√≥’„¥∑’®Ë –‡¬Á∫ªî¥À√◊Õ‡ªî¥µÕ‰«â ‡¡◊ËÕ„¥®÷ß®–„ÀâºŸâªÉ«¬≈ß¡“‡¥‘πÀ√◊Õ°“¬¿“æ∫”∫—¥‰¥â °“√„™â Õ«—¬«–‡∑’¬¡∑’Ë‡À¡“– ¡ ·≈–§«√ª√–‡¡‘πºŸâªÉ«¬«à“¡’°”≈—ßæÕ∑’Ë ®–¡’™’«‘µµ“¡ª°µ‘¥â«¬¢“‡∑’¬¡À√◊Õ‰¡à ‡æ√“–°“√„™â¢“‡∑’¬¡®– µâÕß„™âæ≈—ßß“π¡“°°«à“‡¥‘¡ ∫“ß√“¬∑’Ë¡’‚√§·∑√°´âÕπ∑“ßÀ—«„® ·≈–ªÕ¥°“√„™â æ ≈— ß ß“π¢Õß√à “ ß°“¬‡°‘ π °«à “ ª°µ‘ ® –‡ªì π Õ—πµ√“¬§«√„ÀâºŸâªÉ«¬π—Ëß wheel chair πÕ°®“°π’È§«√∑√“∫ ‡°’Ë¬«°—∫¿“«–·∑√°´âÕπµà“ß Ê ¢ÕßÀ—µ∂°“√°“√µ—¥π‘È«·≈–¢“ «‘∏µ’ “à ß Ê ‡æ◊ÕË ∑’®Ë –‰¥â«“ß·π«∑“ß„π°“√√—°…“Õ¬à“ß∂Ÿ°µâÕßµàÕ‰ª

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297

‡Õ° “√Õâ“ßÕ‘ß 1. Barros DûSa AAB. Upper and lower limb vascular trauma, In: Vascular Techniques: An Atlas, 2nd ed. Greenhalgh RM (ed). London: WB Sanundens 1989;47:65. 2. Whitman JR, McCroskey BL, Moore EE, et al. Traumatic popliteal and trifurcation vascular injuries: determinants of functional limb alvage. Am J Surg 1987;154:681-683. 3. Dajani OM, Haddael FF, Fajj HA, et al. Injury to the femoral vessels:the Lebanese war experience. Eur J Vasc Surg 1988;2:293-296. 4. Barros Dû Sa AAB. How should we manage acute ischaemia associated with trauma. In:Limb salvage and Amputation for Vascular Disease. Greenhalgh RM, Jamiesen CW, Necolaides AN (eds.) London: WB Saunders, 1988;135:150. 5. Baros Dû SA AAB. The rationale for arterial and venous shunting in the management of limb vascular injuries. Eur Vasc Surg 1989;3:471474. 6. Barros Dû Sa AAB. Combined arterial and venous intraluminal shunting in major trauma of the lower limb. Eur J Vasc Surg 1989;3:577581. 7. Robbs JV. Basic principles in the surgical management of vascular trauma In:Vascular Surgical Techniques: An Atlas, 2nd ed. Greenhalgh RM (ed.). London:Wb Saunders, 1989;28-40. 8. White GH. Amuptations in the dysvascular patient. Vasc Surg 1987;71:898-903. 9. Fierer J, Daniel D, Davis C. The fetid foot: Lower extremity infections in patients with diabetes mellitus. Rev Infected Dis 1979;1:210217. 10. Gibbons GW. Management of pre-and postoperative infections in the diabetic patients. Host Pathogen News 1983;1:1-5. 11. Malone JM, Moore WS, Leal JM, et al. Rehabilitation for lower extremity amputation. Arch Surg 1981;116:93-101. 12. Barnes RW, Shanik GO, Slaymaker EE. An index of heshing in below-knee amputation: Leg blood pressure by doppler ultrasound. Surgery 1976;79:13-20.

13. Cheng EY. Lower extremity amputation level using noninvasive hemodynamic methods of evaluations. Arch Phys Med Rehabil 1982;63:475-481. 14. Holloway GAJr, Burgess EM. Cutaneous blood flow and its relation to healing of below knee amputation. Surg Gynecol Obstet 1978;146:750-757. 15. Burgess EM, Matsun FA, Wyss CR, et al. Segmental transcutaneous measurement of PCO2 in patients requiring below knee amputation for peripheral vascular insufficiency. J Bone Joint Surg (Br) 1982;64:378-382. 16. Katsumouris A, Brewster DC, Magermen J, et al. Trancutaneous oxygen tension in selection of amputation level. Am J Surg 1984;147:510-515. 17. White RA, Nolen L, Hanley P, et al. Non-invasive evaluation of peripheral vascular disease using transcutaneous oxygen tension. Am J Surg 1982;144:68-74. 18. Sizer JS, Wheelock FC. Digital amputations in diabetic patients. Surgery 1972;72:980-986. 19. Roon AJ, Moore WS, Goldstone J. Below-knee amputation: A modern approach. Am J Surg 1977;134:153-160. 20. Fearon J, Campbell DR, Hoar CS, et al. Improved results with diabetic below-knee amputations. Arch Surg 1985;120:777-782. 21. Lipski BA, pecoraro RE, Larson SA, et al. Out patient management of uncomplicated lower-extremity infections in diabetic patients. Arch Intern Med 1990;150:790-794. 22. Larsson U, Andersson GBJ. Partial amputation of the foot for uncomplicated lower-extremity infections in diabetic patients. Arch Intern Med 1990;150:790-796. 23. Sherma RA, Tippens JK. Suggested guidelines for treatment of phantom limb pain. Orthopedics 1982;5:1595-1601.

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∫∑∑’Ë 31 LUMBAR SYMPATHECTOMY „πªï §.». 1727 du Petit æ∫«à“ vascular tone ·≈–°“√ À¬àÕπµ—«¢Õßºπ—ßÀ≈Õ¥‡≈◊Õ¥¢÷ÈπÕ¬Ÿà°—∫°“√§«∫§ÿ¡¢Õß sympathetic nervous system „πªï §.». 1924 Royle ‰¥â∑” lumbar sympathectomy ‡æ◊ÕË √—°…“¿“«– spastic paralysis(1) ·≈–¿“¬„π ªï‡¥’¬«°—π Julio Diez ‰¥â∑” sympathectomy ‡æ◊ÕË √—°…“ arterial occlusive disease ¢Õß¢“ À≈—ß®“°π—πÈ ¡“®π∂÷ßªï §.». 1950 ·≈– 1960 sympathectomy ‡ªìπÀ—µ∂°“√ ”§—≠„π°“√√—°…“ limb ischemia ®“° atherosclerotic occlusive disease(2) ®π°√–∑—ßË ¡’°“√∑” femorodistal bypass „π°“√√—°…“ severe limb ischemia „πªï §.». 1970 ‰¥âº≈¥’ À≈—ß®“°π—πÈ ∫∑∫“∑¢Õß°“√∑” sympathectomy ‡√‘Ë¡≈¥≈ß „πªí®®ÿ∫—π sympathectomy ∑“ß»—≈¬°√√¡À≈Õ¥‡≈◊Õ¥®–¡’∫∑∫“∑„π°“√‡æ‘Ë¡ cutaneous blood flow ‡∑à“π—πÈ

°“¬«‘¿“§»“ µ√å lumbar sympathetic trunk ‡¢â“ Ÿ™à Õà ß∑âÕß‚¥¬Õ¬ŸÀà ≈—ßµàÕ medial arcuate ligament ·≈–®–Õ¬Ÿà extraperitoneum µ≈Õ¥·π« ∑Õ¥Õ¬ŸÀà πâ“µàÕ psoas fascia ·≈– lumbar segmental vessels À≈—ß®“°π—πÈ ∑Õ¥ºà“π medial border ¢Õß psoas ·≈â«‡¢â“¡“™‘¥°—∫ lumbar vertebrae ·≈– transverse process (√Ÿª∑’Ë 31.1) ¥â“π¢«“®–Õ¬ŸÀà ≈—ßµàÕ IVC ¥â“π´â“¬ Õ¬Ÿ∑à “ß¥â“π¢â“ß aorta „π∑âÕß®–¡’¢“â ß≈– 4 lumbar ganglia πÕ°®“° visceral

branches ·≈â«¬—ß¡’ somatic branches °√–®“¬¡“∂÷ß lower abdominal wall ·≈–¢“

º≈®“°°“√∑” sympathectomy °“√∑” sympathectomy ®–∑”„Àâª√– “∑ à«π°≈“ß Ÿ≠ ‡ ’¬°“√§«∫§ÿ¡°“√‰À≈‡«’¬π¢Õß‡≈◊Õ¥∫√‘‡«≥·¢π¢“ À≈—ß∑” sympathectomy ®–¡’ ‡ ≈◊ Õ ¥‰À≈‡«’ ¬ π‡æ‘Ë ¡ ¢÷È π ∑’Ë º‘ « Àπ— ß ∑— π ∑’ „ π —ª¥“ÀåµÕà ¡“®–≈¥≈ß‡À≈◊Õ‡æ’¬ß 1/3 ¢ÕßÀ≈—ßºà“µ—¥·≈–§àÕ¬ Ê ≈¥≈ß¡“ ®π∂÷ß√–¥—∫∑’Ë¡“°°«à“ºà“µ—¥‡æ’¬ß‡≈Á°πâÕ¬(3-8) lumbar sympathectomy ¡’º≈µàÕÀ≈Õ¥‡≈◊Õ¥¢π“¥„À≠à·≈–¢π“¥°≈“ß πâÕ¬¡“° À≈—ßºà“µ—¥Õ“°“√¢Õß Intermittent claudication ®–‰¡à¥¢’ π÷È ‡≈¬ vasomotor activity ¢ÕßÀ≈Õ¥‡≈◊Õ¥∑’¢Ë “¢÷πÈ Õ¬Ÿ°à ∫— L2 - L3 ®–§«∫§ÿ¡∑“ß¥â“πÀ≈—ß¢Õßµâπ¢“, ¢“·≈–‡∑â“ (√Ÿª∑’Ë 31.2) L1 ganlia ®–§«∫§ÿ¡°“√À≈—ËßπÈ”°“¡ (ejaculation) ∂â“µ—¥ÕÕ°∑—Èß Õß¢â“ß®–¡’ªí≠À“§◊Õ À≈—ËßπÈ”°“¡¬âÕπ∑“ß¢÷Èπ‰ª„π°√–‡æ“– ªí “«–(9) L1 Õ¬Ÿà „µâ crus of diaphragm ‰¡à “¡“√∂ºà“µ—¥‡¢â“∂÷ß ‰¥âß“à ¬ ‚¥¬∑—«Ë ‰ª®–æ∫ ganglia ¢â“ß≈– 4 (Õ“®®–æ∫‰¥âµß—È ·µà 28) µ”·Àπàß∑’§Ë ß∑’§Ë Õ◊ L2 ·≈– L4 ‚¥¬∑’Ë L4 ®–Õ¬ŸÀà ≈—ß®ÿ¥‡√‘¡Ë µâπ ¢Õß iliac vessels L1 ·≈– L2 Õ“®®–Õ¬Ÿµà ¥‘ °—π∑”„Àâ‡«≈“ºà“µ—¥ L2 ®–µ—¥‡Õ“ L1 ÕÕ°‰ª¥â«¬∫“ß à«π „π‡æ»™“¬ °“√µ—¥ L2 ·≈– L3 ganglia °ÁæÕ‡æ’¬ß·≈â«„π°“√≈¥ vasomotor tone ·≈–∑”„Àâ

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LUMBAR SYMPATHECTOMY

À≈Õ¥‡≈◊Õ¥∑’‡Ë ∑â“¢¬“¬µ—«(10) ®–æ∫ anatomical variation ‚¥¬ °“√¡’ crossover ¢Õß nerve fibers ∑—ßÈ Õß¢â“ß‰¥â√Õâ ¬≈– 15 ∑”„Àâº“à µ—¥∑” sympathectomy ¢â“ß‡¥’¬«·≈â«‰¡à‰¥âº≈ ∂â“µ—¥ ganglia —πÈ ‡°‘π‰ªÕ“®®–‡°‘¥ regeneration ¢Õß nerve fibers ‰¥â ∑”„Àâ°“√ºà“µ—¥√—°…“‰¡à ‰¥âº≈ complete sympathectomy ‡Àß◊ËÕ®–À¬ÿ¥‰À≈ æ‘ Ÿ®πå ‰¥â ‚¥¬°“√∑” iodine starch test „™â°√–¥“…°√Õß™ÿ∫ cobalt À√◊Õ triketohydrinedene hydrate (Ninhydrin) (11) ‚¥¬ √ÿª·≈â«º≈∑“ß √’√«‘∑¬“∑’¡Ë µ’ Õà °“√∑” sympathectomy ¡’¥ß— µàÕ‰ªπ’È (3-8,12,13) 1. ¡’°“√‡æ‘Ë¡‡≈◊Õ¥‰À≈‡«’¬π‰ª‡≈’È¬ß·¢π¢“‡π◊ËÕß®“°¡’°“√ ¢¬“¬µ—«¢Õß arterioles ∫√‘‡«≥ cutaneous vascular beds ‡≈◊Õ¥®–ºà“π‡¢â“¡“∂÷ß AVM ∑’‡Ë °‘¥¢÷πÈ µ“¡∏√√¡™“µ‘ 2. ¡’°“√‡æ‘¡Ë ¢Õß nutritive flow µ√ß distal cutaneous beds ∑”„Àâ·º≈‡√◊ÕÈ √—ß∫√‘‡«≥ª≈“¬‡∑â“À“¬ 3. ≈¥ ischemic rest pain ®“° non vascular effect ¢Õß sympathectomy ‚¥¬¡’°“√‡ª≈’¬Ë π·ª≈ß¢Õß O2 demand: supply ratio ´÷ßË ®–¡’º≈µàÕ pain receptor.

°“√‡≈◊Õ°ºŸâªÉ«¬ ”À√—∫ºà“µ—¥ ¢âÕ∫àß™’È „π°“√ºà“µ—¥∑” sympathectomy ¡’ 1. causalgia À¡“¬∂÷ß¿“«– reflex dystrophy √à«¡°—∫¡’ °“√ª«¥· ∫ª«¥√âÕπ, hypesthesis, ∫«¡ ·≈–¡’‡Àß◊ÕË ÕÕ°¡“°¢Õß·¢π¢“ „π√“¬∑’ÕË “°“√√ÿπ·√ß®–¡’ trophic change ¢Õßº‘«Àπ—ß·≈–°√–¥Ÿ°(14) ª√–¡“≥√âÕ¬≈– 4060 √—°…“‰¥âº≈‚¥¬„Àâ¬“·°âª«¥, °“¬¿“æ∫”∫—¥, „Àâ¬“ tricyclic antidepressants, ¬“°—π™—° ·≈– alpha2-adrenergic blockers ∂â “ √— ° …“¥â « ¬¬“π“π°«à “ 3 ‡¥◊Õπ‰¡à ‰¥âº≈ ®÷ß∑” multiple translumbar sympathetic block ∂â“°“√µÕ∫ πÕß¥’®÷ßæ‘®“√≥“ºà“µ—¥∑” sympethectomy(15) 2. Inoperable arterial occlusive disease ‰¡à “¡“√∂ ∑”ºà“µ—¥ reconstruct À√◊Õ bypass ‰¥â (16) 2.1 rest pain ‚¥¬¡’ criteria ¥—ßµàÕ‰ªπ’È 1. §à“ A.B.I. ¡“°°«à“ 0.3 2. ‰¡à¡’ neuropathy 3. Õ“°“√ª«¥∑ÿ‡≈“≈ßÀ≈—ß∑” sympathetic block

2.2 limited tissue loss ‚¥¬¡’ criteria ¥—ßµàÕ‰ªπ’È 1. §à“ A.B.I. ¡“°°«à“ 0.3 2. ‰¡à¡’ neuropathy 3. ¡’·º≈¢π“¥‡≈Á° À√◊Õ gangrene π‘«È „¥π‘«È Àπ÷ßË 4. ‰¡à¡’ major deep infection 3. lower extremity vasospasm(17) °“√∑” lumbar sympathectomy √à«¡°—∫ aortoiliac À√◊Õ femoropopliteal bypass ‰¡à™«à ¬∑”„Àâº≈°“√√—°…“¥’¢π÷È (18) ºŸâ ªÉ«¬‡∫“À«“π°“√∑” sympathectomy „π°“√√—°…“¿“«– ischemia ®–‰¡à ‰¥âº≈ ‡π◊ÕË ß®“°¡’ degeneration ¢Õß√–∫∫ª√– “∑ ‰ª·≈â«(19) Smithwick test ¡’§«“¡ ”§—≠„π°“√æ‘®“√≥“‡≈◊Õ°ºŸªâ «É ¬ ”À√—∫∑” sympathectomy «‘∏’°“√§◊Õ ¬°¢“ºŸâªÉ«¬¢â“ß∑’Ë¢“¥ ‡≈◊Õ¥¢÷πÈ Ÿß®π°√–∑—ßË ‡°‘¥ maximal tissue anoxia ·≈– vasodilatation À≈—ß®“°π—ÈπÀ¬àÕπ¢“≈ß ∂â“ collaterals ‡æ’¬ßæÕ ®–æ∫«à“ capillary refilling time ®–„™â‡«≈“ 20-30 «‘π“∑’ °“√∑” sympathectomy ®–‰¥âº≈„π°“√√—°…“ºŸªâ «É ¬ ·µà∂“â Smith wick test ‰¥âº≈≈∫§◊Õ ‰¡à¡’ capillary refilling time ‡≈¬ À√◊Õπ“π‡°‘π 30 «‘π“∑’ · ¥ß«à“ arterial ·≈– capillary reserve ‰¡à‡æ’¬ßæÕ °“√∑” sympathectomy ®–‰¡à ‰¥âº≈„π°“√√—°…“ºŸªâ «É ¬(2)

CHEMICAL SYMPATHECTOMY ∑”‚¥¬°“√ Õ¥‡¢Á¡¬“«ºà“πº‘«Àπ—ß ‚¥¬©’¥¬“™“‡©æ“–∑’Ë ·≈– „™â x-ray control ·∑ß‡¢Á¡≈ß„π·π«®ÿ¥°÷ßË °≈“ß√–À«à“ß spinous process ¢Õß L2 ·≈– L3 3 ‡´Áπµ‘‡¡µ√ Àà“ß®“° midline Õ¥ “¬ canula ¡“∑“ß anteromedially ®π°√–∑∫°—∫ lumbar vertebral body À≈—ß®“°π—πÈ À—°¡ÿ¡‡≈Á°πâÕ¬¡“∑“ß¥â“π¢â“ß ®π ª≈“¬‡¢Á¡Õ¬ŸàÀπâ“µàÕ body ¢Õß vertebra ¥Ÿ¥°√–∫Õ°¬“®π ·πà „®«à“ª≈“¬‡¢Á¡‰¡àÕ¬Ÿà „πÀ≈Õ¥‡≈◊Õ¥¥” ©’¥ Phenol ∂â“‰¥âº≈ Õÿ≥À¿Ÿ¡¢‘ Õß¢“®–Õÿπà ¢÷πÈ (20,21) «‘∏°’ “√∑’ßË “à ¬§◊Õ„ÀâºªŸâ «É ¬Õ¬Ÿà„π∑à“π—ßË ©’¥¬“™“‡©æ“–∑’·Ë ≈– Õ¥ ‡¢Á¡‡¢â“‰ª∂÷ß√–¥—∫ L3 ©’¥ contrast media ·≈– x-ray ¥Ÿ„Àâ ·πà „®«à“ª≈“¬‡¢Á¡Õ¬Ÿµà √ßµ”·Àπàß∑’µË Õâ ß°“√ Õ“®®–„™â CT needle guidance À≈—ß®“°π—πÈ ©’¥ 7.5 ¡‘≈≈‘≈µ‘ √ ¢Õß 7.5% Phenol „π 50% glycerine µ√ß¢Õ∫∫π¢Õß L3 „ÀâºªŸâ «É ¬π—ßË À≈“¬™—«Ë ‚¡ß ‡æ◊ÕË „Àâ Phenol µ°≈ß‰ª‡§≈◊ Õ ∫ sympathetic chain ¿“«– ·∑√°´âÕπ¢Õß chemical sympathectomy ∑’Ëæ∫‰¥â¡’°“√∂Ÿ° ∑”≈“¬¢Õß somatic nerve Õ¬à“ß∂“«√ ·≈– paresis(22)

302

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‡∑§π‘§°“√ºà“µ—¥ °“√‡µ√’¬¡ºŸâªÉ«¬ ¥¡¬“ ≈∫ºŸâªÉ«¬·≈â«®—¥„ÀâÕ¬Ÿà „π∑à“πÕπ Àß“¬ „™âÀ¡Õπ∑√“¬¢π“¥‡≈Á°Àπÿπ°âπ ¢â“ß∑’Ë®–ºà“µ—¥„Àâ Ÿß¢÷Èπ øÕ°∑”§«“¡ –Õ“¥º‘«Àπ—ß∫√‘‡«≥Àπâ“∑âÕß, ¢“Àπ’∫ ·≈–µâπ¢“ ¢â“ß‡¥’¬«°—π ªŸºâ“ª√“»®“°‡™◊ÈÕ‚¥¬√Õ∫ ·≈–„™â steri-drape ªî¥º‘«Àπ—ß∫√‘‡«≥∑’®Ë –ºà“µ—¥ Incision ≈ß¡’¥„π·π«¢π“πÀà“ß®“° –¥◊Õ 3 ‡´Áπµ‘‡¡µ√ ·≈– ‡ªìπ·π«¬“«ºà“πºπ—ßÀπâ“∑âÕß 15 ‡´Áπµ‘‡¡µ√

°“√ºà“µ—¥ 1. ·¬°°≈â“¡‡π◊ÕÈ external oblique µ“¡·π«·º≈ºà“µ—¥ ·≈–µ—¥ lateral 1/3 ¢Õß anterior rectus sheath (√Ÿª∑’Ë 31.3)

External oblique muscle

2. ¥—π°≈â“¡‡π◊ÕÈ rectus ¡“∑“ß¥â“π medial ·≈–‡ªî¥ lateral margin ¢Õß posterior rectus sheath ‡æ◊ÕË ‡¢â“∂÷ß extraperitoneal plane ¥—π peritoneum ®“° deep surface ¢Õß°≈â“¡‡π◊ÕÈ transversus abdominis ‚¥¬ «‘∏’ blunt dissection ¥â«¬ peanut ·≈– sponge stick ¢≥–∑’µË ¥— °≈â“¡‡π◊ÕÈ internal oblique ·≈– transversus abdominis §«√√–«—ß‰¡à„Àâ neurovascular bundles ©’°¢“¥ 3. free peritoneum ¥â“π lateral ·≈–¥—π‰ª∑“ß¥â“π medial ‚¥¬„™â sponge stick ®π°√–∑—ßË ‡ÀÁπ°≈â“¡‡π◊ÕÈ psoas ∂â“¡’°“√©’°¢“¥¢Õß peritoneum §«√‡¬Á∫ªî¥∑—π∑’ ¥—π ureter „Àâµ¥‘ ‰ª°—∫ peritoneum ∂â“‰¡à·πà „®„™â forcep §’∫‡∫“ Ê ·≈â«ª≈àÕ¬ ∂â“‡ªìπ ureter ®–¡’ peristalsis

External oblique aponeurosis

Rectus muscle

√Ÿª∑’Ë 31.3 ·π«≈ß·º≈ºà“µ—¥ ”À√—∫ right lumbar sympathectomy

303

LUMBAR SYMPATHECTOMY

‡ âπª√– “∑ genitofemoral ∑’«Ë “ßÕ¬Ÿ∫à π°≈â“¡‡π◊ÕÈ psoas Õ“®®–‡¢â“„®º‘¥«à“‡ªìπ sympathetic trunk ‰¥â ·µà®–Õ¬Ÿà lateral ¡“° (√Ÿª∑’Ë 31.4) ·≈–‰¡à¡’ ganglia 4. „™âπ‘È«§≈” lumbar trunk ´÷Ëß®–§≈”‰¥â‡ªìπ‡ âπ¡’§«“¡ ¬◊¥À¬ÿπà §≈â“¬ “¬‰«‚Õ≈‘π¥â“π´â“¬Õ¬Ÿà lateral µàÕ aorta ·≈–¥â“π¢«“Õ¬ŸàÀ≈—ßµàÕ IVC ‡¢â“∂÷ß∫√‘‡«≥∑’Ë∑”°“√ ºà“µ—¥„Àâ™¥— ¢÷πÈ ‚¥¬„™â Deaver retractor ∂à“ß¥÷ß √–«—ß ‰¡à „Àâ·√ß‡°‘π‰ª ®π°¥ IVC ©’°¢“¥ 5. mobilize L2 ·≈– L3 „™â nerve hook §≈âÕß sympathetic trunk ·≈– forcep §’∫ (√Ÿª∑’Ë 31.5) À≈—ß®“°π—πÈ clip ¥â«¬ metallic clips „™â°√√‰°√µ—¥ sympathetic trunk ·≈–§’∫¥÷ßÕÕ°¡“ 6. ∂â“Àâ“¡‡≈◊Õ¥‰¥â¥’ ‰¡àµâÕß„ à∑àÕ√–∫“¬ À≈—ß®“°π—Èπ‡¬Á∫ ªî¥°≈â“¡‡π◊ÕÈ ·≈–º‘«Àπ—ß

¢âÕ§«√√–«—ß¢≥–∑”°“√ºà“µ—¥ ¢≥–ºà“µ—¥‡¢â“∂÷ß sympathetic chain Õ“®®–¡’‡≈◊Õ¥ÕÕ° ®“° lumber vessels ∑’©Ë °’ ¢“¥ ´÷ßË Àâ“¡‡≈◊Õ¥‚¥¬°“√°¥·≈– packing ∂â“¬—ß‰¡àÀ¬ÿ¥§«√Àπ’∫¥â«¬ metallic clips √–«—ß‰¡à „Àâ ‡§√◊ÕË ß¡◊Õ¢¬“¬∂à“ß°¥À√◊Õ∑”„Àâ IVC ©’°¢“¥ √«¡∑—ßÈ aorta ·≈– iliac vessels ´÷ßË ®–∑”„Àâ‡ ’¬‡≈◊Õ¥¡“° ·≈–®–µâÕß‡¬Á∫´àÕ¡√Õ¬ ©’°¢“¥ ·¬° ureter ÕÕ°®“° peritoneum „Àâ‡ÀÁπ™—¥ ∂â“ peritoneum ©’°¢“¥ §«√‡¬Á∫´àÕ¡∑—π∑’ ¢≥–ºà“µ—¥ºà“π°≈â“¡‡π◊ÈÕ Àπâ“∑âÕß √–«—ß‰¡à„Àâ°√–∑∫°√–‡∑◊ÕπµàÕ neurovascular bundles ∑’∑Ë Õ¥ºà“π °“√‡¢â“„®º‘¥µ—¥‡Õ“ genitofemoral À√◊Õ iliolumbar nerve ÕÕ°‰ª·∑π sympathetic chain πÕ°®“°®–∑”„Àâ °“√√—°…“‰¡à ‰¥âº≈·≈â«®–‡°‘¥ neuritic pain ¿“¬À≈—ß‰¥â ‰¡à§«√∑” lumbar sympathectomy „πºŸªâ «É ¬∑’ÕË «â π¡“° ¡’ retroperitoneal fibrosis ·≈–‡§¬ºà“µ—¥∑“ß™àÕß∑âÕßÀ≈“¬§√—Èß ∑”„Àâ¡’ adhesions ¡“° ·≈–‡¢â“∂÷ß sympathetic chain ‰¥â≈”∫“°

Inferior vena cava

Nerve hook

Psoas muscle

√Ÿª∑’Ë 31.4 °“√ºà“µ—¥‡¢â“∂÷ß sympathetic chain

304

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°“√¥Ÿ·≈ºŸâªÉ«¬À≈—ßºà“µ—¥ °“√ºà“µ—¥∑’Ë ‰¥âº≈§◊Õ À≈—ßºà“µ—¥‡∑â“®–Õÿπà ·≈–º‘«Àπ—ß®–·Àâß Õ“°“√ª«¥·º≈·≈– rest pain ∑’√Ë πÿ ·√ß®–∑ÿ‡≈“ ·º≈‡√◊ÕÈ √—ß®– §àÕ¬ Ê À“¬¿“¬„π 6 ‡¥◊Õπ À≈—ßºà“µ—¥‚¥¬‰¡àµÕâ ßµ—¥‡∑â“·≈–¢“

(23,24)

À≈—ßºà“µ—¥∑—π∑’Õ“®®–¡’°“√µ÷ß·πàπ¢Õß∑âÕß®“° paralytic ileus ∑”„ÀâºªŸâ «É ¬Õ÷¥Õ—¥ 2-3 «—π·√° √à«¡°—∫°“√ «π¥â«¬ rectal tube ‡ªìπ√–¬– ®π°√–∑—ßË ≈”‰ â‡√‘¡Ë ∑”ß“π

¿“«–·∑√°´âÕπÀ≈—ßºà“µ—¥ ∑’æË ∫‰¥â¡’ 1. postsympathectomy neuralgia ‡ªìπÕ“°“√ª«¥∑’Ë ‡°‘¥¢÷ÈπÀ≈—ßºà“µ—¥ 10-14 «—π ®–ª«¥µ—Èß·µàµâπ¢“≈ß‰ª ®π∂÷ßª≈“¬‡∑â“ ª«¥¡“°µÕπ°≈“ß§◊π hypesthesia ®–æ∫‰¥â∫√‘‡«≥ anterolateral ¢Õß¢“Àπ’∫·≈–µâπ¢“ Õ“°“√ª«¥®–∑ÿ‡≈“·≈–À“¬‰ª‡ÕßÀ≈—ßºà“µ—¥ 6 —ª¥“Àå ®–‰¡àæ∫√à«¡°—∫§«“¡º‘¥ª°µ‘¢Õßª√– “∑ sensory ·≈– motor §«√„Àâ¬“·°âª«¥µ“¡§«“¡‡À¡“– ¡

2. °“√µ—¥‡Õ“ L1 ganglia ÕÕ°∑—Èß Õß¢â“ß ∑”„Àâ‡°‘¥ §«“¡º‘¥ª°µ‘„π°“√À≈—ßË πÈ”°“¡ (ejaculation) „π‡æ»™“¬ ‚¥¬®–¡’°“√À≈—ßË πÈ”°“¡¬âÕπ°≈—∫‡¢â“°√–‡æ“–ªí “«– 3. sympathetic regeneration ∑”„Àâ°“√√—°…“‰¡à ‰¥âº≈ ºŸªâ «É ¬¬—ß§ß¡’ sympathetic activity ‡À¡◊Õπ‡¥‘¡ §«√ µ—¥ sympathetic trunk „Àâ¡’§«“¡¬“« ·≈– clip ª≈“¬∑’µË ¥— ¥â«¬ metallic clip

√ÿª sympathectomy ¡’∫∑∫“∑πâÕ¬„π°“√√—°…“ neurovascular pain „π∫“ß√“¬®–æ∫«à“À≈—ßºà“µ—¥·≈â« ®–¡’‡≈◊Õ¥‰À≈‡«’¬π √«¡∑—ßÈ cutaneous nutritive flow ¡“¬—ßª≈“¬‡∑â“¥’¢π÷È ∑”„Àâ ·º≈‡√◊ÕÈ √—ßÀ“¬ ·≈–≈¥ ischemic pain perception ‰¥âº≈¥’„π °“√≈¥ª«¥¢Õß causalgia ·≈–∑”„ÀâÀ≈Õ¥‡≈◊Õ¥¢¬“¬µ—«„π coldinduced vasospasm „πÕπ“§µ®–µâÕß∑”°“√«‘®¬— ·≈–»÷°…“µàÕ«à“ sympathectomy ¡’º≈Õ¬à“ß‰√µàÕ microcirculatory hemodynamics „πºŸªâ «É ¬ end-stage arterial occlusive disease ´÷ßË æ∫«à“„™â¬“°≈ÿ¡à prostacycline analogues √—°…“‰¥âº≈

√Ÿª∑’Ë 31.5 µ—¥ sympathetic chain ¥â«¬°√√‰°√·≈–§’∫¥÷ßÕÕ°

LUMBAR SYMPATHECTOMY

305

‡Õ° “√Õâ“ßÕ‘ß 1. Royle ND. A new operative procedure in the treatment of spastic paralysis and its experimental basis. Med J Aust 1924;1: 27-81. 2. Thimming RF, Smith MB, Sullivan JM. Lumbar sympathectomy in the treatment of arteriosclerotic peripheral vascular disease. Surg Clin North Am 1958;38: 1081-1092. 3. Rutherford RB, Velenta J. Extremity blood flow and distribution: The effects of arterial occlusion, sympathectomy, and exercise. Surgery 1971;69: 332-344. 4. Moore WS, Hall AD. Effects of lumbar sympathectomy on skin capillary blood flow in arterial occlusive disease. J Surg Res 1973;14: 151-157. 5. Collins GJ Jr, Rich NM, Clagett PG, et al. Clinical result of lumbar sympathectomy. Am Surg 1981;47: 31-35. 6. Persson AV, Anderson LA, Padberg FT Jr. Selection of patients for lumbar sympathectomy. Surg Clin North Am 1985;65: 393-402. 7. Welch GH, Lieberman DP. Cutaneous blood flow in the foot following lumbar sympathectomy. Scand J Clin Lab Invest 1985;46: 621626. 8. Walsh JA, Glynn CJ, Cousins MJ, et al. blood flow, sympathetic activity and pain relief following lumbar sympathetic blockade or surgical sympathectomy. Anesth Intensive Care 1985;13: 18-25. 9. Quale JB. Sexual function after bilateral lumbar sympathectomy and aortoiliac bypass surgery. J Cardiovasc Surg 1980;21: 215-224. 10. Callow AD, Simeone FA. The Grimonster symposium. Arch Surg 1978;113:295-301. 11. Benzon HT, Cheng SC, Avram MJ, et al. Sign of complete sympathetic blockade: Sweat test in sympathogalvanic response. Anesth Analg 1987;122: 668-673. 12. Cronenwett JL, Lindenauer SM. Hemodynamic effects of sympathectomy in ischemic canine hind limbs. Surgery 1980;87: 417-424.

13. Cross FW, Cotten LT. Chemical lumbar sympathectomy for ischemic rest pain: A randomized, prospective controlled clinical trial. Am J Surg 1985; 150: 341-349. 14. Schwartzman RJ, McLellan TL. Reflex sympathetic dystrophy: A review. Arch Neurol 1984;41: 821-830. 15. Mockus MR, Rutherford RB, Rosales C, Pearce WH. Sympathectomy for causalgia: Patient selection and long-term results. Arch Surg 1987;122: 668-677. 16. Rutherford RB, Shannon FL. Lumbar sympathectomy: Indication and Technique. In: Rutherford RB (ed.). Vascular Surgery 4th ed. Philadelphia: WB Saunders, 1995;874-883. 17. Janoff KA, Phinney ES, Porter JM. Lumbar sympathectomy for lower extremity vasospasm. Am J Surg 1985;150: 147-158. 18. Lee BY, Thoden WR, Madden JL, et al. Long-term follow-up of bypass procedures with and without lumbar sympathectomy. Contemp Surg 1982;20: 51-59. 19. Danalle MJ, Bauman FG, Mintzer R, et al. Limited success of the lumbar sympathectomy in the prevention of ischemic limb loss in the diabetic patients. Surg Gynecol Obstet 1981;152: 784-792.20. Hoxton HA. Paravertebral block with aqeous phenol in the treatment of vascular disease. Angiology 1953;4: 268-279. 21. Reid W, Kennedy Watt J, Gray TG. Phenol injection of the sympathetic chain. Br J Surg 1973;57: 45-56. 22. Smith RC, Davidson NM, Ruckly CV. Hazard of chemical sympathectomy. Br J Med 1978;1: 552-561. 23. Yao J ST, Bergan JJ. Predictability of vascular reactivity relative to sympathetic ablation. Arch Surg 1973;107: 676-680. 24. Walker PM, Johnston KW. Predicting the success of a sympathectomy: A prospective study using discriminant function and multiple regression analysis. Surgery 1980;87: 216-224.

306

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¥√√™π’ A abdominal angina 20 above-knee (AK) amputation 295 acquired aneurysm 23 acquired lymphedema 235, 236 acrocyanosis 22 acute arterial occlusion 177 acute arterial thrombosis 22 acute cellulitis 201 acute limb ischemia 177 acutely inflamed diabetic foot infection 202 Adam kevicûs artery 122 adductor canal 159 air plethysmography 60 aldosterone 150 Allenûs test 110, 144 alpha-1-antitrypsin 116 alpha-globulin 150 amaurosis fugax 20, 93 Ancrod 47 aneurysm 115, 271 aneurysmorrhaphy 119 angioscopy 75, 184 angiotensin 150 angiotensin I 150 angiotensin II 150 angiotensin-converting enzyme (ACE) inhibitors 156 ankle disarticulation 294 ankle Pressure Index 13 ankle-brachial index (ABI) 137 ankle-brachial pressure indices 63 antecubital fistula 265 anticoagulants 45 antiplatelet agents 43 antiserotonin drugs 139 aorto-duodenal fistula 116 aortocaval fistula 116

aortoiliac surgical reconstruction 132 aortorenal bypass 154 arterial autografts 81 arterial infection 189 arterial lines 143 arterial plethysmography 60 arterial spasm 277 arterial steal syndrome 270 arteriomegaly 39 arteriovenous fistula 278 arteriovenous fistula (AVF) 263 arteriovenous graft (AVG) 263 arteriovenous O2 gradient 137 arteriovenous shunt (AVS) 263 arteritis 173 aspirin 138 asymptomatic AAA 115 asymptomatic carotid stenosis 95 asymptomatic Hollen-horst plaque 95 atherectomy devices 76 autogenous reversed saphenous vein graft 82 autogenous saphenous vein graft interposition 256 autologous fistula 263 autotransfusion 120 axillofemoral bypass 132 B bacterial endocarditis 189 balloon catheter 177 balloon tipped catheter 5 below-knee (BK) amputation 294 berry aneurysm 23 biplane aortography 118, 130 blue toe syndrome 127, 159, 178 Branhamûs bradycardia response 32 brawny edema 27 Brescia- Cimino fistula 6 Brescia-Cimino AVF 263

308 Brodie-trendelenberg test 210 brown pigmentation 25 brownish skin pigmentation 28 Brugia malayi 238 Buergerûs angle 9 Buergerûs disease 167 buffalo hump 235

C calcium-channel blockers 139 calf claudication 168 capillary filling time 10 capillary refilling 12 capillary refilling time 110, 301 captopril renal scaning 150 captopril test 150 carbondioxide arteriography 153 cardiac catheterization 88, 286 cardiac tamponade 279 carotid barorecoptor trauma 103 carotid body tumor 95 carotid endarterectomy 98 carotid pseudoaneurysm 104 causalgia 287, 301 caval filter 229 caval interruption 229 cavernous lymphangioma 236 cerebro vascular accident 20 cervical rib 110 cervical rib syndrome 21 Charleûs operation 239 chemical sympathectomy 301 chronic venous insufficiency 27 chylothorax 243 chylous ascites 243 circulation - enhancing drugs 47 claudication distant 15 claudication time 15 claw toe deformity 202 clinical vascular laboratories 59 coarctation of the aorta 20 cobble stone 32 cockscrew appearance 169 color duplex scanning 161 compartment syndrome 281 compressive stocking 217 congenital aneurysm 23 congenital lymphangiectasia 240 congenital lymphedema 235

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥ continuous-wave Doppler probe 60 contrast venography 73 contrast-enhanced CT complements aortography 118 contusion 277 conventional arteriography 74 costoclavicular syndrome 21 cough impulse test 29 cramping pain 15 CRCT syndrome 111 crescendo TIAs 94 CT scan 62 cuffed dialysis catheter 264 curved upper arm graft 266 cutaneous angiomata 32 cystic lymphangioma 236

D Dacron grafts 83 DeBakeyûs maneuver 116 declamping hypotension 120 decompressive fasciotomy 283 deep lymphatic systems 233 deep space infection 199, 201 deep thrombophlebitis 226 deep vein thrombosis 26 deep venous thrombosis (DVT) 223 delayed nerve ischemia 287 demarcation 171 dermal plexus 233 Dextran 44, 229 dialysis access grafts 266 dialysis catheter 263 diethylcarbamazine 238 digital subtraction angiography 74 Dipyridamole 44 dipyridamole 138 dipyridamole-Thallium scintigraphy 88 direct single-lumen percutaneous puncture 263 disabling claudication 159 Dobutamine stress echocardiography 88 Doppler survey 63 Doppler ultrasonography 226 double velour Dacron graft 83 duplex scanner 224 duplex ultrasonography 74 duplex venous ultrasonography 69

309

¥√√™π’ E

early graft failure 250 echocardio-graphy (2-dimension) 180 echocardiography and radionuclideventriculograph 88 ejection fraction 88 EKG monitoring (24-hr) 132 electrographic monitoring 88 embolism 22 endoscopic subfascial ligation 209, 217 endothelial seeding grafts 84 endovascular stent grafting 119 endovascular therapy 78 ER thoracotomy 123 erythrocyte sedimentation rate (ESR) 174 essential hypertension 150 ex-vivo reconstruction 155 excisinal procedures 239 exercise testing 64 exercised ABI 137 expanding pseudoaneurysm 277 expansile pulsation 116 extra-anatomic surgical procedure 132 extra-anatomical renal artery revascularization 155

gaiter area 29 gangrene 17 Giacomini vein 216 giant cell arteritis 112 glycolytic pathway 200 gouty arthritis 202 graft failure 89 guillotine amputation 291 guttering of the veins 11

F failing graft 250 fasciotomy 185, 281 Feganûs method 30 femoro-femoral crossover bypass 132 femoro-popliteal occlusive disease 159 femorofemoral bypass graft 132 fibrinolytic agents 49 fibrinolytic therapy 185 fibrointimal hyperplasia 82 fibromuscular dysplasia 149 fistula and graft maturation 269 fistulography 270 flare sign 29 Fogarty balloon catheter 256 Fogerty balloon tip catheter 184 Fontaine stepwise classfication 168 foot claudication 168 fore-arm arteriovenous fistula 266 fore-arm loop graft 266 free root 169 fungus vegetations 189

H hard signs 278 Harveyûs test 31 hemodialysis access 261 hemorrheologic drugs 47 heparin 147 heparin-induced-thrombo cytopenia 45 heparin-induced-thrombocytopenia (HIT) 147, 227 high velocity missle 275 highflow AVF 270 highly selective catheterization 72 Homanûs sign 26, 223 human umbilical vein grafts 82 Hunterûs canal 38, 159 hyperkeratosis 33, 236 hypothenar hammer syndrome 107

I I125-labelled fibrinogen uptake test 225 ICU psychosis 249 idiopathic Raynaudûs disease 22 immediate postoperative prostheses (IPOP) 296 impedance plethysmography 224 impedence plethysmography 62 implanted graft 263 impregnated autoclave Dacron graft 83 impregnated Dacron graft 120 in situ interposition aortic graft 195 in situ saphenous vein bypass 82 incompetent perforators 209 indium-111-labeled white blood cell scanning 194 infected false aneurysm 190 inferior inguinal nodes 233 inflammatory AAA 118 intermittent claudication 15 intermittent claudication (IC) 137 intermittent pneumatic calf compression 229

310 intermittent posterior cerebral ischemia 95 interventional radiology 8 intimal disruption 275, 277 intimal hyperplasia 40 intra arterial digital subtraction arteriography 74 intraluminal AAA 119 intraluminal Greenfield filter 227 intraluminal shunt 281 intraluminal vascular prostheses 78 intraoperative arteriography 281 inverted champagne bottle 28 iodine starch test 301 ischemic demarcation 182 ischemic rest pain 17 ischemic ulcer 17 ischemic waste products 183 IVC plication 6 Ivermectin 238

J juxtaglomerular apparatus 150

K Klippel-Trenaunay syndrome 32

L laser angioplasty 77 lateral venorrhaphy 260 lateralizing trasient ischemic attack (TIA) 93 Lericheûs syndrome 20, 127 limb-threatening ischemia 159 livedo reticularis 22, 109 ooped upper arm graft 268 low melecular weight heparin 45 low molecular weight dextran 249 low molecular weight heparin 229 low-dose heparin 227 lumbar sympathectomy 6 lumbar sympathetic trunk 299 lymphadenopathy 34 lymphangiography 233 lymphangioma 34 lymphangioma simplex 236 lymphangiosarcoma 236 lymphangitis 32 lymphatic grafting 240 lymphatic reconstruction 239, 240 lymphedema 32, 33, 235

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥ lymphedema praecox 236 lymphedema tarda 236 lymphocele 243 lymphovenous anastomosis 240

M magnetic resonance angiography 62 magnetic resonance arteriography 118 magnetic resonance arteriography (MRA) 161 magnetic resonance flowmeter 62 magnetic resonance imaging 62, 74 magnetic resonance techniques 62 malignant hypertension 149 Mandorûs disease 27 manual lymphatic drainage (MLD) 239 Marjolinûs ulcer 29 MAST-G-SUIT 282 mechanical reduction 239 mechanical retractor 145 medium-chain triglyceride 242 megalymphatics 240 microangiopathy 200 microbial arteritis 190 Milroyûs disease 236 Mobile Army Surgical Hospital (MASH units) 4 Modified Homanûs procedure 240 multilobulated aneurysm 194 multiple organ failure 179 mycotic aneurysms 189 myoglobinuria 180

N Naftidrofuryl 139 necrotizing fascitis 201 nephrectomy 155 neurologic deficit 20 neurotrophic ulcer 19, 202 neurotropic ulcer 159 non-cuffed dual-lumen dialysis catheters 263 non-pitting edema 236 noninvasive hemodynamic studies 59 noninvasive tests 59 nonspecific arteriopathy 115

O ocular plethysmography 61 Omni retractor 147 open amputation 291

311

¥√√™π’ P

penile/brachial pressure index 65 Pentoxifylline 47, 140 percutaneous arterial catheterization 4 percutaneous transluminal angioplasty 75, 132 percutaneous transluminal angioplasty (PTA) 153 perianastomotic neointimal hyperplasia 270 peritoneal-venous shunt (Lee Veen) 242 Perthes test 210 Peu dû Orange appearance 235 Phantom limb pain 296 Phantom limb sign 17 phlebitis migranes 168 phleborheography 62 phlegmasia alba dolens 26 phlegmasia alba Dolens (PAD) 227 Phlegmasia Cerulea Dolens 227 phlegmasia cerulea dolens 26 plantar compartment 199 plantar foot pad 199 polycythemia 180 polytetrafluoroethylene (PTFE) graft 121, 263 port wine stains 32 portable Doppler unit 59 positron emission tomography 74, 96 postmastectomy edema 34 postmastectomy lymphedema 237 postsympathectomy neuralgia 304 postthrombotic syndrome 226 Praxilene 139 pre-clotting Dacron graft 120 pregangrene 17 presenile spontaneous gangrene 167 primary chylous disorders 240 primary livedo reticularis 22 primary lymphedema 235, 236 primary Raynaudûs disease 22 primary vascular infection 55 progressive distal axonopathy 200 prophylatic fasciotomy 283 prostaglandin 45, 139 protamine 185 pseudoaneurysm 271 pulmonary embolism 26, 221 pulmonary embolism (PE) 226 pulmonary hypertension 173 pulse volume recorder 60, 61 pulse volume recordings 64 pulsed-wave Doppler flow detector 60

radicularis artery 122 Ray amputation 292 Raynaud's phenomenon 21 Raynaudûs disease 109 Raynaudûs phenomenon 22, 109 reactive hyperemia test 15, 64 recurrent carotid stenosis 104 recurrent DVT 226 recurrent superficial thrombophlebitis 168 renin -angiotensin -aldosterone system 150 renin dependent hypertension 150 renin determination 152 reperfusion syndrome 179 retroperitoneal approach 121 reversible ischemic neurologic dificit (RIND) 94 Robertsonûs giant limb 32 robot retractors 145 ruptured abdominal aneurysm (AAA) 122

S saccular aneurysm 120, 194 saphenous nerve 216 saphenous vein in-situ technique 164 secondary chylous disorders 242 secondary livedo reticularis 22 secondary lymphedema 235 segmental leg pressure 63 Seldinger technique 72 self-retaining retractor 143 sequential air compression 239 severe claudication 159 severe crush injury 291 shot gun wounds 275 single position emission computed tomography 96 single shot arteriography 279 single-armed robot retractor 147 Smithwick test 301 soft signs 278 soleus sinusoids 221 sorbital pathway 200 spastic paralysis 299 spiral CT scaning 118 stab avulsions 216 steal phenomenon 138 steal syndrome 269 Stemnerûs sign 235 straight fore-arm graft 266 streptokinase 77, 186

312 string phlebitis 27 stripping of the short saphenous vein 216 stroke 94 stump pressure 102 subclavian steal syndrome 21, 94, 95 subcutaneous removal of varicostics 216 subfascial ligation of perforating veins 217 Sudan fat stain 242 Sulotidyl 139 superficial thrombophlebitis 26 superficial venous thrombosis 223 superior inguinal nodes 233 suppurative thrombophlebitis 226 sural nerve 216 syme amputation 7 Symeûs amputation 294 sympathectomy 171, 287, 299 sympathetic block 287 sympathetic regeneration 304

T Takayasuûs arteritis 112, 173 temporal arteritis 112 Thompsonûs procedure 240 thoracic outlet syndrome (TOS) 107 threatened limb loss 127 thromboangiitis obliterans (TAO) 167 thromboangitis obliteran 20 thromboendarterectomy 155 thrombophebitis migrans 27 thrombophlebitis 226 Ticlopidine 139 tissue plasminogen activator 77 toe ampulation 292 toe pressure 65 tolazoline 281 Torniquet test 30 tortuous aorta 116 transcranial Doppler 67 transcranial Doppler studies 98 transcutaneous oximetry 62 transection 278 transient cerebral ischemia 93 transient ischemic attack 20 transient monocular blindness 93 transient neurologic deficit 20 translumbar aortic puncture 4 transmetatarsal amputation 7, 293

»—≈¬»“ µ√åÀ≈Õ¥‡≈◊Õ¥ transmitted pulse 116 transmural necrosis 173 transposed vein arteriovenous fistula 265 trash foot 122 Trendelenberg test 29

U ultrasound 73 ultrasound B-mode 62 upper arm graft 266 urokinase 77, 186

V valvular incompetence 221 varicose veins 29, 209 vascular access 261 vascular angle 9 vasodilators 48 venogram 225 venous autografts 81 venous filling 11 venous gangrene 26, 229 venous hypertension 27, 264 venous plethysmography 60, 68 venous stars 25 venous stasis ulcer 28 venous thrombosis 221 venous ulcers 209 vertebrobasilar insufficiency 20, 94 vibratory white finger 107 Vietnam Vascular Registry 4 Virchowûs triad 223 volume-dependent hypertension 150

W W. bencrofti 238 Warfarin 227, 229 Woven Dacron graft 120 wrist fistula 264

X xenografts 82

Y Yellow Nail Syndrome (YNS) 237 lymphangioma simplex 236