기초간호자연과학회지 : 제 11 권제 2 호 2009 J Korean Biol Nurs Sci 2009; 11(2): 99-104 욕창간호중재적용을위한흰쥐의욕창형성예비실험 나연경 1 홍해숙 2 1 경북대학교의학전문대학원박사후연구원, 2 경북대학교간호대학교수 An Experimental Study of Pressure Ulcer Formation for Dressing in Rats Yeon-kyung Na 1, Hae-Sook Hong 2 1 Post-Doctor, School of Medicine, Kyungpook National University; 2 Professor, College of Nursing, Kyungpook National University, Daegu, Korea Purpose: An animal model of pressure ulcers was experimentally-induced with the use of greater trochanter of rats. Methods: Twelve male Sprague-Dawley rats were used in this study and they were randomly divided into 4 groups: Group I (n=3, 120 mmhg, 2 hr), Group II (n=3, 120 mmhg, 3 hr), Group III (n=3, 140 mmhg, 3 hr) and Group IV (n=3, 140 mmhg, 4 hr). The rats were anesthetized with 100 mg/kg of ketamine. The pressure ulcers were induced by using a personally-designed pressing apparatus. After 5 days, the wounds were photographed and excised. Results: After 5 days of induced pressure ulcers, it was observed that Group I and Group II responded with Grade I and Grade II, respectively, while Group III and Group IV responded with Grade III. Conclusion: According to the result of this study, it can be concluded that the pressure ulcers were induced the characteristic grades of pressure ulcer classification by adjusting the degree and the duration of compression. Key Words : Animal model; Pressure ulcer 국문주요어 : 동물모델, 욕창 1. 연구의필요성 서 욕창은신체의특정부위에지속적이고반복적인과도한압박이계속됨으로인해발생된피부와피하조직의괴사를의미하며, 국소적압력이주어진후조직에나타나는현미경적인변화는주로허혈 (ischemia) 에의해발생한다 (Agate, 1977; Herrman, Knapp, Donofrio, & Salcido, 1999; Kathleen & Berecek, 1975; Peirce, Skalak, & Rodeheaver, 2000). 론 Corresponding author : Hae-Sook Hong, Professor, College of Nursing, Kyungpook National University, 101 Dongin-dong 2 ga, Jung-gu, Daegu 700-422, Korea Tel: 82-53-420-4932 Fax: 82-53-421-2758 E-mail: hshong@knu.ac.kr 투고일 : 2009년 9월 10 일게재확정일 : 2009년 11 월 20일 심사의뢰일 : 2009 년 9 월 11 일 욕창을일으키는가장큰요인은중력에의해피부에영향을미치는수직적인힘으로주로신체의뼈돌출부위에가해진지속적인압력에의해혈액순환의장애가유발되어피부와피하조직의허혈상태로조직의괴사가일어나는것을의미하며, 발생의주요원인은압력, 마찰력, 응전력등의외적요인과영양결핍, 감각장애, 감염등의내적요인이있다 (Maklebust, 1987). 인체에가해지는압력은앙와위시천골, 엉덩이, 발뒤꿈치의압력이 40-60 mmhg이고, 복위는무릎에가해지는압력이 50 mmhg이며, 좌위에서는좌골조면에가해지는압력이 75 mmhg 이상이다 (Lindan, Greenway, & Piazza, 1965). Maklebust (1987) 는말초혈관의소동맥혈액정수압은 32, 소정맥은 15 mmhg이며, 압력의강도는소동맥압력이상일때문제가되며, 말초혈관의폐색은산소의결핍과영양결핍을 99
100 나연경 홍해숙 유발한다고하였다. 피부에가해지는압력은허혈상태를유발하여창백하게되지만압력이제거되면피부는다시선홍색을띠는반동성충혈 (reactive hyperemia) 이나타나는데이는욕창발생을막으려는신체방어기전으로대개압력을받은후 2시간이경과하면조직과모세혈관에비가역성변화가나타난다 (Herrman et al., 1999; Patel, Knapp, Donofrio, & Salcido, 1999; Song, 1991). 짧게는 1-2시간부동에의해서도욕창이발생할수있고, 기간이길어지면낮은압력이라할지라도욕창을유발시킬수있으며, 대부분의욕창은병원에입원한지 2주내에생긴다. 그러므로장기간움직임에제한을받거나척수손상등으로기동성장애가있는대상자들은욕창의위험이매우크다. 욕창은기존질환에수반되는증상으로볼수있고, 일단발생하면치료가어려울뿐만아니라합병증이발생할수있으며, 합병증은환자의고통과불편감을증가시켜환자와가족의삶의질을저하시키고이에따른노력과비용이증가된다 (Kim, 1996; Park, 1998). 또한욕창은가정간호대상자의과반수에서발생하고있고욕창의치료에베타딘, 항생제연고, 실바딘크림, 듀오덤크림등을사용하고있다고하였으며 (Kim, Cho, & Park, 1997), Kim (1998) 은욕창에하이드로콜로이드폐쇄드레싱이전통적거즈드레싱보다편리하고효과적이나비용의문제점이있어이러한경제적인부담으로일부대상자는대체요법 ( 느릅나무뿌리등 ) 을사용하고있다고하였다. 욕창치료와간호를위해드레싱, 특히대체요법에대한임상적용전실제적이고체계적인연구가부족한상태이며, 임상적근거가부족한상태에서환자에게직접적용하기어려운점이있어실험동물에게먼저적용해보고자하였으나드레싱적용을위해쥐에게 3기이상의욕창을만드는방법이거의연구가되어있지않은실정이다. 따라서본연구는인간에게접근하기어렵고욕창의종류, 기간등대상자들의특성이다르기때문에먼저쥐에게욕창모델을만들어간호중재의기초자료로제공하고자이연구를시도하였다. 연구방법 1. 연구설계본연구는쥐에 3기 (Europe Pressure Ulcer Advisory Panel, 1998; National Pressure Ulcer Advisory Panel, 1989) 이상의욕창을형성하는실험연구이다. 2. 실험동물본실험의동물은동일한조건으로사육된체중 350 g 내외, 12-14주사이의성숙한수컷흰쥐 (Sprague-Dawley) 12마리를대상으로하였다. 3. 실험방법압력기구는스테인리스강철의재질로서, 가로 30.5 cm, 세로 20.5 cm, 높이 7 cm의상자에혈압계커프를넣고그위에 30 20 cm의스테인리스강철판을얹은다음압력이균등하게주어지도록상자의 4모서리에고정나사를만들었으며, 쥐의대전자 (greater trochanter) 부위에맞닿는압력봉의직경은 1.8 cm로제작하였다 (Figure 1). 연결된혈압계로압력의정도를측정하였다. 피부는 55 mmhg, 피하조직은 80 mmhg의압력에서관류가 0 으로되기시작하고, 100 mmhg의압력에서는근육의혈류에변화가나타나며, 최소한 1시간이상의압력이있어야현미경적변화를확인할수있으므로 (Herrman et al., 1999; Patel et al., 1999; Salcido et al., 1995) 3기이상의욕창형성을위해 120 mmhg, 2시간에서시작하였다. 12마리의실험동물을 3마리씩무작위로 4개의그룹 Group I (120 mmhg, 2시간 ), Group II (120 mmhg, 3시간 ), Group III (140 mmhg, 3시간 ) 및 Group IV (140 mmhg, 4시간 ) 에 2. 연구목적본연구의목적은욕창의치료및간호중재방법을검증하기위한선행연구로서쥐에욕창을만들고자실시하였다. Figure 1. Personallydesigned pressing apparatus.
욕창간호중재적용을위한흰쥐의욕창형성예비실험 101 할당하였다. 실험동물모두 ketamine 100 mg/kg을복강내주사하여마취시킨후대전자부위의털을깎고복위 (prone position) 로한다음 protocol에따라 120 mmhg 또는 140 mmhg 압력을 2시간, 3시간, 4시간동안가하였다. 연구결과 1. 육안적변화욕창부위의육안적피부변화를확인하기위해욕창유발 5일째에욕창유발부위를근거리육안사진촬영을하였다. 압력의정도와시간에따라형성된욕창의단계는 Table 1에서보는바와같다. 120 mmhg의압력을가한군중 2시간동안압력을가한군에서는모두욕창이유발되지않았고, 3시간동안압력을가한군은 2기의욕창이형성되었으며, 140 mmhg 의압력을 3시간또는 4시간을가한군에서는모두가피 (crust) 로덮여진 3기의욕창이확인되었다 (Figure 2, 3). 2. 조직학적변화욕창유발후 5일에욕창이형성된부위를조직생검후 hematoxylin과 eosin으로염색하여궤양, 염증세포침윤정도, 부종, 출혈의정도를광학현미경으로관찰하였다. Group I에서는표피가잘보존되어있었고염증반응이거의나타나지않아욕창의 1기로확인되었다. Group II에서는진피나표피부위에서만경미하거나중등도의염증세포침윤과약간의부종을확인할수있었으나궤양과출혈은나타나지않아표피와진피를침범하는부분층결손단계인욕창 2 기의특징을볼수있었다. Group III에서는표피및진피의표층에궤양이일어나염증세포와괴사된조직이가피를형성하여궤양부위를덮고있었으며, 진피의광범위한염증세포침윤과피하지방조직및일부근육조직까지염증세포의침윤이나타났다 (Figure 4, 5). Group IV는육안적으로 Group III와유사한형태의응고된피부와삼출물및괴사조직인가피가형성되어궤양부위를덮고있었고, 진피에는호중구, 림프구, 단핵구같은염증세포가광범위하게침윤되어있으 Table 1. Results of Induced Pressure Ulcer Formation Degrees of Grade of pressure ulcer compression Compression time 2 hr Compression time 3 hr Compression time 4 hr 120 mmhg Group I Group II 1 2 3 1 2 3 Grade I Grade I Grade I Grade II Grade II Grade II Group III Group IV 140 mmhg 1 2 3 1 2 3 Grade III Grade III Grade III Grade III Grade III Grade III Grade I=No ulcer formed; Grade II=A pressure ulcer formed but subsequently healed; Grade III=Experimental area developed flare, edema, and ulceration that progress to necrosis and skin separation without healing. Figure 2. The wound in rat at 5 days after experimentally-induced pressure ulcer (covered crust, Group III). Figure 3. The wound in rat at 5 days after experimentally-induced pressure ulcer (covered crust, Group IV).
102 나연경 홍해숙 Figure 4. Light microphotograph of wound in rat skin at 5 days after induced pressure ulcer (Group III). The skin shows surface ulcer and focal hemorrhage of covering of necrotic tissue in superficial dermis (H&E, 40). Figure 6. Light microphotograph of wound in rat skin at 5 days after induced pressure ulcer (Group IV). The skin shows ulcer and hemorrhage of surface with covering of necrotic tissue and acute inflammatory cells (H&E, 40). Figure 5. Light microphotograph of wound in rat skin at 5 days after induced pressure ulcer (Group III). Intradermal heavy infiltration of acute inflammatory cells are marked (H&E, 100). 며, 침윤범위는피하지방조직및근육조직까지퍼져있었다. 두개체에서는근육조직의광범위한염증세포침윤과더불어경미하지만근섬유의괴사가유발된곳도있었다. Group III 와 IV 두그룹모두진피의기질조직에서광범위한부종이확인되었고, 궤양이있는진피의표층에는국소적으로출혈이일어난곳도있었다 (Figure 6, 7). 이상의광학현미경적소견을요약하면 Figure 8과같다. 논 의 욕창은일정한신체부위에가해지는지속적인압박에의해 Figure 7. Light microphotograph of wound in rat skin at 5 days after induced pressure ulcer (Group IV). Heavy and diffuse infiltration of acute inflammatory cells in dermis are noted (H&E, 100). 혈액순환장애로생긴조직의괴사로서 4기로나눈다. 1기는 30분내에사라지지않은홍반이있으나표피는잘보존되어있고가역적인상태이며, 2기는표피와진피를침범하는부분층결손단계로서홍반을동반한수포로나타날수있으며, 3기는진피를거쳐피하조직까지도달하는전층결손단계이며, 4기는피하조직부터근막, 근육, 뼈, 관절을침범하는심부조직파괴수준을말한다 (National Pressure Ulcer Advisory Panel, 1989). 쥐에게압력과온도에따른피부의관류상태를측정한결과 18 mmhg까지는관류가증가되었으나, 그이후감소되어압력이 55 mmhg를초과하였을때관류가 0 이되었고 (Patel et al., 1999), 피하조직관류는 80 mmhg
욕창간호중재적용을위한흰쥐의욕창형성예비실험 103 Finding Group I II III IV Ulcer - - + + Inflammatory infiltration -~± +~++ +++ +++ Muscle-inflammation - - + +~+++ Edema - ±~+ ++ +++ Hemorrhage - - + + Ulcer: +=present, -=absent; Inflammatory infiltration: ±=trace, +=mild infiltration, ++=moderate infiltration, +++=heavy infiltration; Muscle inflammation: +=scattering of inflammatory cells around muscle fibers, ++=scattering of inflammatory cells with muscle necrosis, +++=scattering of inflammatory cells with muscle loss; Edema: -=absent, +=focal edema, ++=moderate edema, +++=diffuse edema; Hemorrhage: -= absent, +=present. Figure 8. Light microscopic findings of ischemic rat skin after induced pressure ulcer. 의압력에서 0 이되기시작하였으며, 100 mmhg의압력에서는근육의혈류에변화가나타났다고하였다 (Salcido et al., 1995). 돼지에게압력을가한후압력과시간을증가시키는실험을한결과 30 mmhg에서혈류량이줄어들기시작하였으며 (Daniel, Wheatley, & Priest, 1985), 토끼의귀에 0, 50, 100, 150, 200, 300 mmhg의압력을 10분동안가하여혈액의흐름을관찰한결과 100 mmhg 이상의압력에서혈액의흐름이차단되었다 (Niitsuma, Yano, & Togawa, 2003) 고하였으므로욕창부위의간호중재효과를검증하기위해 3기이상의욕창을유발하고자 120 mmhg의압력부터시작하였다. 본연구에서 120 mmhg 압력을 2시간가한군에서는욕창이유발되지않았고 3시간동안가한군에서는 2기의욕창이형성되었다. 이는대개압력을받은후 2시간이경과하면조직과모세혈관의비가역성변화가유발된다 (Herrman et al., 1999; Patel et al., 1999) 는것과유사한결과가나타났으므로욕창을유발하기위해서는최소한 2시간이상의압력시간이필요한것으로생각된다. 본연구의실험결과 140 mmhg의압력을 3시간가한군에서는 3기의욕창이유발되었고 4시간을가한군에서한개체는 Group III와유사한결과가나타났으나다른두개체에서는비록같은 3기의욕창이라하더라도더심한조직손상이나타났으므로 Niitsuma 등 (2003) 이토끼의귀에 50, 100, 300 mmhg의압력을 6시간또는 12 시간동안각 3회씩처치한결과 50 mmhg의압력하에서는욕창이유발되지않았고, 100 mmhg의압력에서는 2기의욕창이유발되었다가자연치유되었으며, 300 mmhg의압력에서는 3기또는귀가천공된 4기의욕창을형성한실험결과와비교해볼때비록개 체의특성, 압력의강도및시간의차이는있으나쥐에도압력의강도와시간을달리하면 4기의욕창을유발할수있을것으로생각된다. 조직의재생과정은일반적으로염증기 (inflammatory phase), 증식기 (proliferative phase), 성숙기 (maturational phase) 의 3단계를거치고, 상처의크기, 깊이, 감염여부등상처의상태에따라치유양식이달라질수있다 (Korean Society of Pathologists, 1998; Martin, 1997). 특히 3기이상의욕창은개방된창상에서현저한조직의결손이나괴사또는감염을유발할수있으므로이차유합에의한치유과정이일어나며 (Kumar, Abbas, & Fausto, 2005), 염증기는손상직후반응이유발되어 2-5일정도지속되지만괴사조직이있으면상처치유기간이길어질수있고, 응고된피부와삼출물및괴사조직인가피는혈액순환장애를유발하고미생물을번식시키는장소가될수있다 (Kim, 1987) 고하였다. 본실험에서 Group III와 IV 에형성된 3기욕창은궤양부위에형성된가피와광범위하고심한염증세포의침윤및부종이나타났으므로욕창유발 5일후에도염증기가지속된것으로생각된다. 본연구의제한점은동물모델을이용하여형성된욕창은실제환자에서발생한욕창과의차이점을배제하지못할것으로생각된다. 따라서쥐에서욕창을유발하고자할경우 140 mmhg, 3 시간의 protocol 적용하면 3기이상의욕창을형성하는욕창모델을만들수있을것으로사료되며, 근거중심의간호에효과적으로적용될수있을것으로생각된다. 결론및제언본연구는욕창의치료및간호중재의효과를검증하기위한선행연구로서쥐에욕창모델을시도하였다. 실험방법은체중 350 g 내외, 12-14주사이의성숙한수컷흰쥐 (Sprague-Dawley) 12 마리를무작위로 4개의그룹에각각 3마리씩할당, ketamine 100 mg/kg으로마취한후연구자가제작한압력기구를이용하여쥐의대전자 (greater trochanter) 부위에욕창을유발하였다. 욕창부위의육안적변화가나타나기시작한욕창유발후 5일에욕창의육안적변화와조직학적검사결과는다음과같다. Group I (120 mmhg, 2 hr) 에서는욕창이형성되지않았으며, Group II (120 mmhg, 3 hr) 는 2기의욕창이유발되었다. Group III (140 mmhg, 3 hr) 와 Group IV (140 mmhg,
104 나연경 홍해숙 4 hr) 에서는가피가형성되어궤양부위를덮고있는 3기이상의욕창이형성되었다. 본연구의결과를토대로다음과같은제언을하고자한다. 1) 욕창을 3기와 4기로분류하기위해서는실험대상의수, 압력의시간및강도를늘려검증할필요가있다. 2) 유발된욕창에욕창치료및간호중재효과를검증하기위해여러가지드레싱을적용하는추후연구가필요하다. 참고문헌 Agate, J. (1977). Pressure sores-mechanical and medical factors. Nursing Mirror, 144, 17. Daniel, R. K., Wheatley, D., & Priest, D. (1985). Pressure sores and paraplegia: An experimental model. Annals of Plastic Surgery, 15, 41-49. Europe Pressure Ulcer Advisory Panel. (1998). Pressure ulcer prevention guidelines. Br J Nurs, 7, 888-889. Herrman, E. C., Knapp, C. F., Donofrio, J. C., & Salcido, R. (1999). Skin perfusion responses to surface pressure-induced ischemia: Implication for the developing pressure ulcer. J Rehabil Res Dev, 36, 109-120. Kathleen, H., & Berecek, M. S. (1975). Etiology of decubitus ulcers. Nurs Clin North Am, 10, 157-170. Kim, J. A. (1987). A study on the nosocomial infection in one burn unit. J Korean Acad Nurs, 17, 227-240. Kim, K. S. (1998). Comparison of traditional gauze dressing and occlusive hydrocolloid dressing in 2nd stage over decubitus ulcer treatment in regional home care setting. J Korean Acad Fundam Nurs, 5, 181-195. Kim, K. S., Cho, N. O., & Park, Y. S. (1997). Decubitus ulcer in home care patients who received regional home care services. J Korean Acad Fundam Nurs, 4, 43-60. Kim, K. Y. (1996). Identification of pressure ulcer risk factors. Nur Sci, 8, 29-48. Korean Society of Pathologists. (1998). Text book of pathology (3rd ed.). Seoul: Komoonsa Press. Kumar, V., Abbas, A. K., & Fausto, N. (2005). Pathologic Basis of Disease (7th ed.). Elsevier Saunders, 107-114. Lindan, O., Greenway, R. M., & Piazza, J. M. (1965). Pressure distribution on the surface of human body, evaluation in lying and sitting position using a bed of springs and nails. Arch Phys Med Rehabil, 46, 378-385. Maklebust, J. (1987). Pressure ulcers: Etiology and prevention. Nurs Clin North Am, 22, 359-377. Martin, P. (1997). Wound healing-aiming for perfect skin regeneration. SCI, 276, 75-81. National Pressure Ulcer Advisory Panel. (1989). Pressure ulcers prevalence, cost and risk assessment: Consensus development conference statement. Decubitus, 2, 24-28. Niitsuma, J., Yano, H., & Togawa, T. (2003) Experimental study of decubitus ulcer formation in the rabbit ear lobe. J Rehabil Res Dev, 40, 67-72. Park, S. M. (1998). The effect of the calcium alginate dressing on the pressure sore and it s cost. Unpublished master s thesis, Seoul National University of Korea, Seoul. Patel, S., Knapp, C. F., Donofrio, J. C., & Salcido, R. (1999). Temperature effects on surface pressure-induced change in rat skin perfusion: Implications in pressure ulcer development. J Rehabil Res Dev, 36, 189-201. Peirce, S. M., Skalak, T. C., & Rodeheaver, G. T. (2000). Ischemiareperfusion injury in chronic pressure ulcer formation: A skin model in rat. Wound Repair Regen, 8, 68-76. Salcido, R., Steve, B., Fisher, S. B., Donofrio, J. C., Bieschke, M., Knapp, C., et al. (1995). An animal model and computer-controlled surface pressure delivery system for the production of pressure ulcers. J Rehabil Res Dev, 32, 149-161. Song, K. A. (1991). Effects of immobility: Pressure sore and its management. Korean Nurs, 30(2), 32-40.