Wound Care A Collaborative Practice Manual for Physical Therapists and Nurses
Edited by Carrie Sussman, PT Sussman Phy...
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Wound Care A Collaborative Practice Manual for Physical Therapists and Nurses
Edited by Carrie Sussman, PT Sussman Phys ical Therapy Inc. Torrance, California
Barbara M. Bates-Jensen, MN, RN, CETN Assistant Professor of Clinical Nursing Department of N ursing University of Southern California Los Angeles, California
AN ASPEN PUBLICATION'" Aspen Publishers, In c.
Gaithersburg, Maryland 1998
The au thors have made every effort to ensure the accuracy of the infonnation herem. Ilowever. appropriate information sources should be consulted, especially for new or unfamiliar procedures. It is the responsibility of every practitioner to evaluate the appropriateness of a particular opinion 111 the context of actual clinical situations and with due considerallons to new developments. Authors. editors. and the publisher cannot be held rc!:>ponsible for any Iypogmphical or other errors found in this book library of Congress Catalogmg-In-Publication Data Wound care: a collaborative practice manual for physical therapists and nurses edited by Carrie Sussman. Barbara M. Oates-Jensen p cm. Includes bib liograplucnl references and mdex. ISBN 0-8342-0748-6 1. Wounds and injures Treatment 2. Physical therapy, 3. Nursing. I. Sussman. Carrie, II. Bates-Jensen, Barbara M [DNLM: 1. Wounds and Injuries rehabilitation. 2. Wounds and Injuries nursing, 3. Wounds and Inluries diagnosis. 4. PhYSical therapy methods, WO 700 W93H4 1998] R093 .W683 1998 617.1 dc21 ONLM OLe for Library of Congress 97-40496 CIP Copyright c 1998 by Aspen Ilubllshcrs. Inc All nghts reserved Aspen Publishers. Inc., grants permission for photocopying for limited personal or Internal usc. ThiS consent docs not extend to other kinds of copying. such as copying for general distribution, for advertising or promotional purposes. for ercatlllg new collec tive works, or for resa le. For IIlformation. address Aspen Publishers. Inc .. Permissions Department. 200 Orchard Ridge Onve. SUite 200, Gaithersburg. Maryland 20K78 Orders: (800) 638-8437 Customer Service: (800) 234- 1660
About As pen Publi she rs . For morc than 3S years. A\pcn has been a tellding professional publisher III a variety of disciplincs. A\pcn's \'U!>I inrOrm:1I10n rc!>ourccs arc u\ail,lble in both print amI electronic ronnats. We :Irc cOnlmillcd to providing the highest qual It)' mformation available in thc most appropriate fonnat ror our customers Visit Aspen's Internet sile for more inform:mon resources, directories, article!>" and 1I scurchable vcrs ion of A\pclI's full catalog. including the most rcecn! publications: hUp :llw"". aspcnpub.co m Aspen Publi shers. In c, . The hallmark of quality In pubhshlllg Member of the \\orld\\ ide Wolten; Kluwcr group
I~ dltorial Sen Ices: Ruth Bloom Libmry of Congress Cmalog Card Number: 97-40496 ISBN: 0-8342-0748-6
Printed III tlte U"ited SllIf('.\· or.·lmerlcCl
I 234 5
Table of Contents
Color Plates .. . . . . . . . . . . . . . . . . . . • . . . . . . . . . . . . . . • . . . . . . . . . . . . . . . . • . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Contributors
xi
xiii
Foreword
xv
Prerace ........ .... .... . ......................................................................
xvii
Acknowledgments. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . • . . . . . . . . . . . . . . . . . . . . . . . . . . . .
xix
Introduction:
xxi
The Need for Collaborative Practice. . ...... . . . . ...• . • .•.. ..... . •. . . .. . . . . . . . . . . . . .. Carrie Sussman and Barbara M. BllIes-Jel/sell
PART I- INTRODUCTION TO WOUND DIAGNOSIS Carrie Sussman C hapter I- The Diagnostic Process .......................................... ...................
3
Carrie Sussman, Barbara M. Bmes-Jensen. alld Melisa TljJallY Step I: Assessment Process .... . .......................................... . . ... .... Case Study: Cognitively Impaired Patient with Leg Ulcers ................. . .......... . . . ... Case Study: Example of Patient History Influencing Wound Care Management .... . •. . .... . . . . . Step II : Diagnosis . . .. . . . . . .. .. . . . . .. . . . . . .. .. . . . . . . .. . . . . . . .. .. . . . . . . . .. .. .. . . . . . . .. Step III : Progress and Goals ............ . ........ . ........... . ..... ... . . .............. The Functional Outcome Report ... ..... . ............ . . . . . ......... • . . . , .. . ......... . . . Conclusion ............................................ .. ...... .. . . . . ........ .. .... Appendix I- A: Patient History Form . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. Appendix I- B: Focused Assessment for Wounds .................................. . ..• . .. Appendix 1- : Form HCFA·700 ......................... .. ......... .. ................ Appendix 1- 0 : HCFA·700 Form with FOR Template To Guide Documentation in Italics ......... Appendix I E: Sample Case Report Using HCFA· 700 . . ............................. . .• . . .
111
3 II 14 15 17 22 24 26 27 28 29 30
IV
WOUND CARl
31
Chapter 2- Wound Healing Biology and Chronic Wound Healing Carrie Sussman Wound Healing Models .............................................................. Acute Wound Healing Biology ........................................................ Fetal Wound Healing ................................................................ Chronic Wound Healing. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Conclusion ....... . . . . . .. . . . . .. . . .. . . . . .. . . . . .. . .. . . . .. . . . . .. . . .. . . .. . . .. .. . .
31
32 40 40 45
49
Chapter 3-- Assessment of the Skin and Wound Carrie Sussman
The Assessment Process ............................................................. Assessment of Wound StalUs ......................................................... Case Study: Dangers of Differing Clinical Procedure and Facility Policy ...................... Assessment of the Peri wound and Wound Tissues .............. . ................... Wound Hca ling Phase Diagnosis and Prognosis .................................. . ...... Referral Criteria ......................................................... . ......... Conclusion .......... , ............................................................
. . . . . . .
49 55
56 66 67 81 81
83
C hapter 4- Wound Measurements Carrie Sussman
Baseline Assessment Accepted Measurements ..... Measurement Assessment Forms ...................................................... . Location ......................................................................... .
Wound Size Measurement Accuracy and Reliability ...................................... . Linear Wound Size Measurements . .................................................... .
Wound Photography ................................................................ . Referral Criteria ............................................................. . Referral Sources .... Sci f·Care Teaching Guidelines ........................................................ . Conclusion ....................................................................... .
Resources ........................................................................ .
83 83 83 87 87 88 99 101
101 101
102 102
C hapter 5-- Tools To Measure Wound Healing ....... .. .. .... ............... ......•. ......... ...... Carrie Sussman Gnd Barbara A1. Bates-Jensen
103
Inlroduction .............. ,.... . .................................... . Sussman Wound Healing Tool ....... . ........................................ . The Pressurc Sore Status Tool ............................ . ....................... . Appendix 5- A: Instructions for Pressure Sore Status Tool ................................. .
103 105
C hapter 6-Noninvasive Vascular Testing .. .... . .... .....• ..............•......................•. . Aline Siegel
114 122 125
. .......... .
125
Chief Complaint ............................................................... . Past Medical History ............................................................... . . ............................................. .
125 125 125
. .......•.•..........•..........•............
127
Introduction
............... , . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Physical Examination. . . . . . . . . . . . . .
Pu Isc
EX31TI . . . . . . . . . . . . . . . . . . • . • .
Table a/Colllell/,
Noninvasive Va scular Testing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Case Study: Ankle-Brachial Index. . . . . . . . . . . . . . . . . • . . . . . . . . . . . . . . . . . . . . . . . . . . . Addilional Vascu lar Studies ................. . ............................ . . . . . . . . . . . . . Noninvasive Venous Testing. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Conclusion ........................... . ............................................ Referral Criteria ............... . ...... . .... _ .................... _ . . . . . . . . . . . . . . . . . . Self-Care Teaching Guidelines ........................... .
v
129 132 133 133 133 133 135
PART II- MANAGEMENT BY WOUND CHARACTERISTICS Barbara At!. Bales-Jensell
137
Chapter 7- Managemcnt of Necrotic Tissue .............. _. _ ................ _. _ .. _....... _. _ ...... _ Barhara A1. Bates-Jensen
139
Significance of Necrotic Tissue. . . . . . . . . .
. .............. , ....................... .
Interventions . .................................................................... , .
Mechanical Debridement Procedures ......... , .......... . Entymatic Debridement Procedures .....................
. ..................... .
Sharp Debridement Procedure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ..................... . AUio lylic Dcbridement Procedures ...... .. . .............................. _ . _ ..... . OutconlC M easurcs . . . . . . . . . . . . . . . . . . . . . . . ..... .. ........... . ............... . Referral Criteria .........................................................•....... Self-Care Teaching Guidelines .............. _ . ........ .. ......... . .................... . Appendix 7 A: Debridemem Choices for Chronic Wounds ....................... .. ...... . . Appendix 7 B: Enzymatic Preparalions ......... ... .................................... . Chapter 8- Management of Exudale and Infection Barbara M. Bates-JenseJ/
139 140 140 143 144 146 148 148 148 151 157 159
Significance of Exudate ..................... . .............................. _ ... _... _. Significance of Infection .......................................................... _ . . Procedures for Quantitative Wound Cullure .....................................•...... Management of Exudale and Infeelion ...................•.... . ............... _ . _ . _. . . Outcome Measures. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. ............. Referral Criteria .............. . ....... _. . . . . . . . . . . . . . • . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Self-Care Teac hing Guidelines. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
159 162 165 166 174 176 176
Chapter 9- Management of Edema .. _.......•. • ......... _.... _ ...... _. . . . . . . • . . • • . . . . . • . • . . . . . . Laurel A. Wier.'lema-B,:vol1l
179
Introduction ...................... . Overview of Ihe Problem ............ . Tests and Measurement ............................................... . Modes of Intcrvention and Procedures for Intervention. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Procedures for Managemelll of Edema ................ _ .......................... _ . . Leg Elevation and Exercise ...................... . ...... _ . • . . . . . . . . . . . . . . . . . Compression Wraps (Elastic Bandages) ................. _ . . . . . . . . . . . . . . . . . . . . . . Paste Bandage ................................................................... Four-Layer Bandage . . . . . . . . . . . . . .. ... _ . _ . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Compressio n Stockings ......... . ..... _ ......... . ...... _ . . . . . . . . . . . . . . . . . . . . . . . . . Sequential Compression Pump .. .. .. . . . .. . . . . . . . . .. . . . . . .. .. . . . . . . .. . . . . . . .. . .. .. Referral Cri teria ....... . ..... . ..... . ..... _ ............ _ . _ ...................... _ ... _ Self-Care Teaching Guidelines ... _ .......... _ ................ _ . _ ...................... .
179 179 179 180 185 185 186 187 188 193 195 197 198
VI
W OU, D CARE
Case Study I: A Case for Elastic Bandages. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Case Study 2: Combination Therapy with Sequential Pump and Class I Stockings............... C hapt er 10- Manage m ent of th e Wound Enviro nment Geoffrey Sussmall
199 199 20 1
Introducti on ........ .. ........ . ....... . ...... . .......... . ................. . . .. ..... Inert Wound Dressings.................................. . ............................ Ideal Dressing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Modern Wound Dressings ............................................................ Dressing hoiee ....................... . ................ ................. . .......... Secondary Dressings ................................... . ......... . .... ....... ....... The Usc of Antiseptics in Wounds . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Antiseptics and Acute Wounds. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Antibiotics ............. .. ................. . . . . ... . . ... .. . . . .. ..................... Wou nd Cleansi ng ............................... . ...................................
201 201 20 I 202 209 211 211 2 12 212 2 12
PA RT Ill- MA AGEMENT BYWOU ' D ET IOLOGy.... . ... .... ..... .. .. .... ........ .. .... .. .... . Barbara 1.1. Bates-Jensen
2 15
C hapt er II - Ac ut e Surgical Wound Ma na ge ment ........ . • . • . •.• .. ... . • .• . ..• . ...•. . ..... . • . ...... Barbara M. Bates-Jensen al/d James Wethe
21 9
Acute Surgical Wound Definition .......................... . ... ... ..................... Factors Aflecting Healing in Acute Wounds .... . ...... . .... . .... .. ............ Assessment of the Acute Surgical Wound .. ....... . ................................... Manage ment of the Acute Surgical Wound ......... . . . . ... . . .. . .......................... Secondary and Tertiary Intention Wound Healing . . . . . . . . . . . . . . . . . . . . •. . . . . . . . . . . . . . . . . . . . . Outcome Measures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Case Study: Lack of Innammatory Response Postoperatively ................................ Conclusion ... ... ........ .. ............ _ . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Referral Criteria .................................................................... Self-Care Teaching Guidelines. . . . . . . . . . . .. . . . .... . .. . . . .. . .... . .. . ... ... . . . . ... . .... . . Case tud y: Incisio nal Wound Healing ........ . ..... . ................ . . . .. . ... . . ..• ... ..
219 2 19 224 226 226 227 227 228 228 230 231
C hapt er 12- Press ure Ulcers: Pathophys iology a nd Prevention Barbara /\11. 8t1les-Jel/sell Press ure Ulcer Definition ............................................................ Pressure Ulcer Pathophysiology .... . . . .............. .. ............... . .... . ........... Clinical Prese ntat ion of Press ure Ulccrs ................................................. Press ure Ulcer Staging . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Pressure Ulcer Prediction: Risk Factor Assessment ..................•..................... Press ure Ulcer Prevention: Early Interventions. . . . . . . . . . . • . . . . . . . . . . • . . . . . . . . • . • . . . . . . . . . . Outcome Measures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Referral Criteria .. . ...... . ...... . ....... ...........•.......... ... .. ....... . ....... . . Self-Care Teaching Guidelines . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . ... . . . . . .. . Cha pter 13- Ma nage ment of Pressure by T hera peuti c Positionin g Laurie M. Rapp/ Introduction .............................................•......................... The Diagnostic Process Applied 10 Therapeutic Positioning ........... . ..................... Functional Diagnostic Process. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Rationa le for Intervention in the Sitting Position .............................. : : ..........
235 235 235 238 239 241 252 266 266 266 27 1 27 1 271 274 276
Table oj COli/ellis
VII
Rationale for Intervention in the Recumbent Position ... . . ... .... . . .... ...•.•.... .... ......
290
Case Study: Therapeutic Positioning for Press ure Ulcer Healing. . . . . . . . . . . . . . . • . • . . . • . • . • . . . . Resources . .................................................................•.•....
295 298
C hapter I4-Diagnosis and Management of Vascular Vlcers
Car/os E.
301
D Ollllyre
Introducti on ......................................................•.•....... . ...... Vascular Anatomy of the Lower Ext remities .. . . . . . . . . . . . . . . . . . . . . . . . • . • . • . . . • . • . . . . . . . . . . Occlusive Peripheral Vascular Disease- Signs and Symptoms ..........................•.•.. Diabetes and Foot Ulceratio n . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . • . . . . . . . . . . . . . . . . . . . . • . • . • . . Venous Stasis Ulcers ............................ . ..... . ... .. . . . . ...•.... . •... . ...... Chapt er IS- 1anagcment o f th e Ne uropathic Foot
30 I 30 I 303 305 308 315
Nan(v EI{lman Introduction ................................. . ... • ..... . ........................... Pathogenesis ........................ . ........• . . . ...............•.... . ..... . ....... Medical History .. . ........................... . ... • . • .•. . .......... . . . ...•.•...•....
Systems Review and Examination .. . ..... .... ...... .... ....... ..... ....... ... ......... . Further Visual and Physical Assessments ...•• . ......•...•.•..............•.•...•.•.. . ... Case Study: Charcot Arthropathy .........•..............•.•.•.................. • .•.•.. Inter ventions . ................. . ...... .. ...... .. . . ..•.... ... ....... ... ..... ..... .... Doculncntation ................ , .. , ... . .. .. ... ... . .. , ...................•.•...... , .. .
Self·Care Teaching Guidelines ............•.• . ....... .. ....•. •.•...... .. ..... .•.• .•.. .. Resources ... . ..... . ...................................................... • ........
PART IV- MANAGEMENT OFWOVND HEALI NG WITH PHYSICA L THERAPY TECHNOLOGIES ......... . ........................................................ . Carrie Sussma" Case tudy: Choosing the Appropriate Treatment Intervention .....•.•.• . .. . .......... . . .. ...
315 316 316 318 324
331 332 340 340 343 347 352
Chapter I6--Eloctrical Stimulation for Wound Healing .... ................•......................... Carrie Sussman lIlIll NlIlley Byl
357
Introduction ............................... . ........... . .......... . .....•...•...... Definitions and Terminology . .. .... .... ....... . ........ .. .....•..... .. ................ Theory and Science of Electrica l Stimulation ...... . ........ . ........... ..... ......... . .. .
357 357 361 366 368 374
Clin ical Studies ........................................ . . . . . . .. ................... . Choosing an Intervention : Cl inical Reasoning ................ . . ... . . .................... .
Wound Healing Protocol Selection for Electrica l Stimulation ..........•. •. .................. Protocol for Wound Healing ............................• ..... • . • • .. .• ... • ....... . . . Protocol for Treatment of Ede ma .................................................... . Protocol for Infection Control and Disinfection Protocol for Treatment of Chronic Vcnous InsufTiciency or Chronic Deep Vein Thrombosis .... . . Doculnclltation ......... .. ..... .. .... .... ..... ..... ..... .... ......... .. ............ .
Case Study I: Pressure Ulcer Treated with ES ...•. .. ...........•.•....... . ........ ... .... Case Study 2: Vasc ular Ulcer Treated with ES ... . ...... . ...• .. . . ... . ............•.• . ..•.. Chapter 17- Pulsatile La"age with Co ncurrent Suction
378
380 380 381 382 383 385 389
Itardeff Baugh Loe/m e
Definition .. . .................................•.•................•.•.• .. ......... .. Theory and Science of the Therapy . . . . . . . . . . . . •.• . . . . . . . . . . . . . . • .• . . . . . . . . . . . . . . . . . . • . .
389 389
viii
W OUN D C ARE
Indications for Therapy ...•. .... ...........•................... . .... . ... . .... . ... . ... Precautions ............... . . . ...... . . .. .. . .. . .. . . ..... •.. .. ... ... .. ... ... . ...... . .. Outcome Measures . . . . . . . . . . . . . . . . . . . . . . • . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Frequency and Duration . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Cautions .......................... . ........ .. . . . .. .. . .. . .......... . ............... Vacuum Assisted Closure. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Performance of Pulsati le Lavage with Suction ....•............................ . ... . .... . . How To Use Different Equipment Models .. ....... . .... . ... . ................... . ........ Davo l Simpu lse Plus Procedure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Davol Simpulse Solo/Simpu lse VariCare Procedure . ..................................... Stryker SurgiLav Plus Procedure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Zimmer Pulsavac Procedure .............. . ............ . ......... . ........... . ...... Zimmer Pulsavac III Procedure . . . . . . . . . . . . . .• . . . . . . . . . . . .. . . . . . . . . . . . .. . . . . . .. . . . .•. Zimmer Var-A-Pulse Procedure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ... ... .. . . . ... . . .. . Documentation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ... . . . . . .. . . . . . . Case Study: Gunshot Wound Treated with Pulsatile Lavage with Suction . . . . . . . . . • . . . . . . . . . . . . .
C hapter IS- Pulsed Short Wave Diath ermy a nd Pulsed Radi o Frequ ency Stimulati on Carrie Sussman Introduction .. ... .......................................................... . ....... Definitions and Terminology . . . ... . . .. ..... . ..... . ......... . .......................... T heory and Science of the Therapy ..................... . ... .. .... .. ... . .. . .. . . .. .. . .... Choosing an Intervention: Cli nical Reaso ning ............... . ............ . ..... . ...... . .. Equipment ... ..... .......................... . ...................•............... . . Procedures ...... . .. .... . . .... ... . . . .... .... .. . ..............•...... . ...• .. ....•... Protocols for PSWD ..... . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Magnatherm'" PSWD Protocol . . . .. .... . ...... . ... . ...................•.......... PSWD (Magnatherm"') for Venous Disease ..... . ... . .... . .. ... .. .. . .... .. .. . .. .. . .. Pulsed Radio Frequency Stimulation Protocol ......•. . ......•.................•........ Self-Care Teaching Guidelines . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Documentation ..... . .......................................... . ... . ... .. .. .. . .. ... . Case Study I: Pressure Ulcer Treated with Pulscd Short Wave Diathermy ............. . ........ Case Study 2: Surgical Wound Treated with Pulsed Radio Frequency Stimulation ..... • .......... C hapter 19- Ther apeuti c a nd Diagnostic Ultrasound Carrie Sussman and Mmy Dyson
390 392 393 393 393 394 394 397 397 399 399 400 400 401 401 401
405 405 405 409 414 417 41 8 419 419 42 1 421 422 422 423 424 427
Introductio n ....... . ..... . . . ....... . ..... .. ... .. . . ..... . ........... . ....•.......... Definitions and Terminology ... . .............................. .... .. . ... . .. .. ..... . . .. High-Reso lution Diagnostic Ultrasound .. . . . ........... ..... ..... . . .. .• . ... . ...... . ..... Theory and Science of Ultrasound on Wound I-Iealing ... . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . .. . Choosing an Intervention: Clinical Reasoning ............ . .... . ............. . . .. ..... . ... Procedures ...................................... . .... . .......... . . .. ... .... ... . . .. Self-Care Teaching Guidelines.... .. ..... . ................................... . .. . ..... . Documentation ................ .. ..... . ..... .. . . ..... . ..... . ...•..........•......... Case Study I: Venous Ulcer Treated with US .................... . .... . . .. .. . .... . .. . ... . . Case Study 2: Blood Blister on the Heel Treated with US . ........... . .......... . ...........
427 427 429 432 436 437 442 442 443 444
Chapter 20- Whirlpool ....... .... .... . . . . ....•.... . ....... . .... ... .... . .... ..... ...... .... .... Carrie Sussman
447
Introduction ....... . .................... . ....... .. . . ..... .. ...... . .................
447
Table oj COllle lllS
IX
Theory and Science oflhe Therapy............... ......... ...................... . ...... Therm al EfTects ........... .. ............. .. ........................................ Phys ical and Mechani cal EfTects ........................ .. ..... .•.• . ..•................
44 7 449 450
Choosing an Intervention: Clinica l Reasoning ..................... .. .......... . ..........
45 1
Equ ipment .... . ............. . ................. • ................................... Procedure ............................................................... . .. .. . . ... Ex pected Out comes .. . ...... . ...... . ...... . ........ .. ............................... elf-Ca re Teaching Guidelines. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . •. . . . . . . . . . . . . . . . Case Study: Patient with Esc hars on Both Heels. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
454 454 456 457 457
Appe ndi x A-C uid e to To pical Anlise ptics, Anlifungals, a nd Antibacterials. . . . . . . . . . . . . . . • . • . . . . . . . . . . . .
461
Appe ndi x B-A Quick Reference G uid e 10 Wound Ca re Producl Ca lego ri es . . . ..... • . • . . . . . . . . . . . . . . . . . . Diane Krasner
477
Index ............. .. ... . ..... ... . ... ... ... .. .... . .. .. ...... . ... .... . ....•....................
483
Abo ul lhe Edilors ............. . .................... .. .. .. •.... .. • . • .• .•.. . • . .......... . • . • . • . •.
493
Color Plates
Plates 1-6
Progression through Three Phases of Wound Healing
Pla tes 7-9
Progression through Proliferation Phase
Plates 10- 11
Abnormal Proliferation Phase
Plat e 12
Wound in Remodeling Phase
I' la te 13
Anatomyof
Pla tes 14- 18
Wounding of the Skin
Pla tes 19- 22
Assessment or Darkly Pigmented Skin
Plat es 23- 24
Abnormal Wound Attributes
I' la tes 25-30
Necrotic Tissue Types
Plates 3 1-34
Wound Edges
Plates 35-36
Surgical Dissection for Tunneling
Plates 37- 39
Undermining and Tunneling
Pla tes 40-45
Reading the Dressing: Wound Exudate Assessment
Pla tes 46-48
Arterial Ischemic Wound s
Pl ates 49- 54
Venous Disease
Pl ates 55-56
Wound Healing with Electrical Stimu lation- Chapter 16
Plates 57- 59
Wound Ilcaling with Pulsatile Lavage with
Plates 60-62
Wound I-Iealing with Pulsed Short Wave Diathermy- Case Study I- Chapter 18
Plates 63-64
Wound I-Ieali ng with Pulsed Rad io Frequency Stimulation- Case Study 2
Pla tes 65-67
Wound Hea ling with Ultrasound- Case Study I- Chapter 19
Pla tes 68- 7 1
Wound Ilealing with Ultrasound- Case Study 2-Chapter 19
on Tisslie
L1ction
xi
haptcr 17
Chapter 18
Contributors
Barbara M. Bates-Jensen, MN, RN, CETN
Evonne Fowler, MN, RN, CETN
Assistant Professor of Cli nical Nursing
Wound/Ostomy/Skin Care Specia list
Department of Nursi ng Un iversity of Southern Ca lifornia
Be ll flower Kaiser Hospital
Bell nower, Ca li fornia
Los Angeles. Ca lifornia
Nancy Byl, PhD, PT
Diane Krasner, PhD, RN, CETN
Director Program in Physical Therapy
Consultan t Nursing Care of Patients Wound Care, Ostomies. Incontinence Baltimore. Maryland
University of Cali fornia at San Francisco
Oak land. California
Carlos E, Donayre, M D
Harriett Baugh Loehne, PT
Assistant Professor of Surgery Un iversity of California. Los Angeles School of Medicine Harbor/UCLA Medical Center
Staff Physica l Therapi st The orth Caro lina Baptist Hospital s, Inc. Winston-Sa lem, North Caro lina
Department of Vascular and Genera l Surgery Torrance. Ca li fornia
Laurie M. Rappl, PT Clinica l Support Manager Span-America Medical Systems, Inc.
Mary Dyso n, BSc, PhD, C Biol, M I Bioi Division of Anatomy and ell Bio logy UM DS Medical School Guys Hospital London England
Greenville. SOllih Caroli na
Ann e Siegel, RN, RVT, CVN Vascular
Nancy Elftman, CO, C.Ped.
urgery N urse Coordi nator
University Hospital Los Angeles, Ca lifornia
Certified Orthotist. Certified Pedorthi st Cosmos Extremity Hands on Foot
Carrie Suss man , PT
LaVerne, Ca lifornia
Rancho Los Amigos Medical Center (Reti red)
Sussman Physica l Therapy, Inc.
Downey, Ca li fo rni a
Torrance, Ca li fornia
xiii
xiv
W OUND CARE
Geoffrey Sussman, PhC, MPS, MSHPA, AFAIPM, MSMA,JP Director, Wound Dressing Ed ucatio n and Research Department of Pharmacy Pract ice Victorian Co llege or Pharm acy Monash Uni versi ty Park ville, Victoria, Austra li a
Melisa Tiffany, BSN, RN, CETN Graduate Student ET Nursing Uni versit y of South ern Califo rni a Los Angeles, Ca liforni a
James WeIhe, MD South Bay Plasti c Surge ry Torra nce, Ca lifornia
Laurel A. Wiersema-Bryant, MSN, RN, CS C linica l Nurse Specialist Barnes-Jewish Hos pita l at Washington Uni versity Medica l CCllI cr St. Louis, Missouri
Foreword
Bates-Jensen, MN, CETN, a nu rsc wound care specialist. Both are recognized throughout th e co untry for th eir clin ical knowledge, practical expertise, and unwavering dedi cati on to wou nd care. Both have national reputations HS superb . teachers who emphasize critica l thinkin g/deduct ive reasoning in deci sion making. Their purpose for writing th e book is to provide basic and advanced informati on on wou nd healing and wound ca re therapies, to promote co llabo ra ti ve wound management between nurses and phys ica l therapists by providing a better understanding of the similarities and differences between di sciplines, and to promote an understanding of wound manage ment by challenging the thinking process. The chapters are wrinen by wound ca re specialists from many disciplines, who arc on the fore front of wound healing practice and research. They have joined toge ther to sharc thei r accu mulated knowledge base, wisdom, and divcrse experiences and expertise in wound manage ment. Wound manage ment is multifaceted : th e causes and consequences of non-hcal ing wounds afC complex and multidimensional and resolutions rcquire an agg ressive interdisc iplinary approach to management. The best approach for handling chronic wo unds is management by a multidisciplinary team working in a collaborat ing. support ing manner and using a science-based practice. This wound care manual provides a beginning for a li vi ng reso urce for excellence in wound management .
I was delighted to be given the opportunit y to write a forewo rd to this unique manual about wound care. As a strong support er of collaboration and comm un ity and deep ly embedded in wo und management, I commend the authors for giving us this excellent wound care resource manual. An environmenllhal supports a collaborative spirit allows clinicians from both disciplines to provide their unique perspecti ve to best meet the needs for each individual patient with a wound problem. Chronic wounds are a major problem for the person who has one, for th e significant olhers involved with them, and th e health care providers who care for them . \Vound manage ment is carried out in all cafe settin gs: aClIte and long-term care faciliti es, in the home. and in olltpat ient clinics. In most sett ings, the care is otten provided by health care professional s not formall y educated in wound healing. Howeve r. when wound healin g has not been achieved, the wound is diffi cult to treat, or time consllming and cosIly. onen the patient wi ll be seen by a wound care speciali st. Usually first called is the nu rse wound care specialist or physical therapist wound care specialist. The specia li st may assess the si tuation, and recommend a manage ment plan lIsing advanced care products and techniques or alternati ve methods of managc ment or provide the care. Having a wound care resource manual on hand wo uld be a direct aid to practice. WOllnd Care: II Collaborative Practice Malllla/jor Physical Therapists Gnd Nurses is a much nceded resource for the health care providers who work dai Iy to manage these troublesome wounds. It is a use r-fri endly reso urce vo lume, formatted for quick reference as a guide in any clini cal se ning. The procedures and guidelines included in the chapters provide the clinician with a too l box for dail y practice in wound manage ment . This resource manual is a collaborati ve effo rt . wri tten by Carrie Sussman. PT, a physical therapist, and Barbara M.
El'ol/l/e FOII'Iel; liN. MN. CErN Wound/Ostomy/Skin Care Specialis( Bellflower Kaiser Hospital Belliloll'el; Calijomia
xv
Preface
TI-I E MULTID ISCI PLINA RY TEAM
ca l therapists have used the medical diagnosis of the paricnt to describe the focus of their practice. There is better nu rs-
Writing this book has been a collaborative effort between the two editors and the I J contributors. Early on in the writillg it was recogni zed thaI. just as in the rC ~11 world. the skills and expertise ora multidisciplinary team were needed to provide the scope of information needed for wound management. The writing tcam represents the disciplines usually
ing and physical therapy- re lated termino logy to describe the
found on the wound management team. Our authors include two surgeons. two researchers (one is a physical therapist) ,
five nurses, one certified pcdorthisl. one pharmacist, and three physicallhcmpi sls. What's more, a number of the chapters arc coauthored by representatives ofdifTcrent disc iplines. Two authors arc from outside the United States. Wound l11anagcl11cnI is a global problcm and a multidisciplinary challenge, and collaboration across all borders must be encouraged . Yes. at timcs collaborating was challenging, but it has been very rewarding. Yct it scemed very logical that we should prepare this work as a collaborative effort and thus set the stage for collaborative practice.
impairments, risk factors, and functional deficits for which nurses and physical therapists intervene. As it turns out, terminologics used by nurses and physical therapists arc very similar- all the bCller to foster communication and co llaboration between the two groups. The rest of Part I reviews implementation of the diagnostic process and includes chapters on review of wound healing biology. chronic wound healing, asscssmcnt of the wound and surrounding skin, specific examinations and tes ts for wounds, and the complication factors of vascular disease. These chapters form the assessment foundation for the patient with a wound. Part II describes management of the wound by specific wound characteristics. Recently, the American Physical Therapy Association convened a panel of five integumentary subject matter expert physical therapists to develop pro-
active patterns for management of integumentary impairl11elllS and disabilities. It was the consensus of the panel tha t wounds and burns are managed similarly, and that the factors that affect management of the wound are the depth of the injury (partial versus fu ll thickness and extending into deep tissues) and the wound-associated characteristics ofnecrosis, edema. and infection. Everything else rcvolves around management of the wound environment or the factors influencing healing. Chapters inc lude Management of Necro tic Tissue, Management of Exudate and Infection , Management of Edema, and Management of the Wound Environ ment. Threc wound characteristics. necrotic tissue, exudate and infection. and edema, are the wound characteristics that most often drive interventions and cause concerns for clinicians. Each chapter begins with a definition of the characteristic,
O RGAN IZATION OFTH E BOO K
The book is organized into four parts. Part I reviews the diagnostic process used by both nurses and physical thera-
pists when cva luating thc patient with a wound. Why start with diagnosi s? Nurses and phys ical therapists have exten-
sive education with unique bodies of knowledge and as professionals, have a level of autonomy and self-regulation. The usc ofa process to arrive at a diagnosis for the patient with a wound provides clarity in communication and collaborativc practice. Clear coml11unication assists with accountability and greater professional autonomy. 1-1 istorically. nurses and physixvii
xviii
W OUND CAR l·
the significance oftilc findings, assessment for the characteri sti c. and basic interventions appropriate for the wound characteri sti c. Each chapter ends with outcome measures, self-care teaching guide lines, and referral criteria for th e specific wound characteristic. Where appropriate. procedures and protocol s for interventions arc inc luded. Part III focu ses on management orthe wound by etiology. This sec tion includes chapters on management of acute surgical wou nds, management and prevention of pressure ulccrs, managcment of pressure with thcrapeutic positioning. and management and diagnosis of vascular and neuropathic ulcers. The chapters focus on pathophys iology, prevention, classification. and intervention. Part IV, Management of Wounds with Physical Therapy Technologies. app lies the diagnos tic process to se lec tion of
wound treatment intervention s with ph ys ical th erapy technologies including electrica l stimulation, pul sed shortwave diathermy, pul sed radiofrequcncy stimulation. ultrasOllnd, pul sa til e lavagc with suction, and whirlpool. Each physical therapy technology chap ter begins with a defini tion of the intervention, the science and theory of the intervcntion as it relates to wound healing. and application ofthc diagnostic process to appropriate se lection of candidates for trea tment. Each chapter includes protoco ls and expected outcome re suits for the thera py described, as well as case studi es.
Carrie Sussman Barbara At!. Bares-Jensen
Acknowledgments
We would like to express our apprec iat ion to the many individuals who hm c made this book possible including:
-
- The individua ls who have contribu ted their c1inicHI and academic knowledge, - Mary Anne Langdon. Ruth Bloom, Laura Sm ith , Jan Kortkamp a nd th e rest ort he stall'at Aspen Publi shers fo r their help and support in production, The reviewers and consu ltants whose suggesti ons were invaluable during development: Michelle Cameron, PT, OCS, Linda Frankenberger, MS. PT. Deborth lI ag ler, PT, Robert Kellogg. PhD. PT, Marko Markov, PhD, Gretchc n Swanson. MPII. PT. Eleanor Price, PhD, Nancy A. Stons, EdD, R •
-
Kris Johnson and Erin McEntyre who took care of many or the details associated wi th preparation of th e Inanuscript , The authors, publishers. companies, and colleagues who have allowed us to publish th e ir art work, photographs. and tables 10 illustrate the informat ion.
Our JIlIS/}(IIU/s (llId childrell- Robert Sussman and Ronald Ho lly, and Thomas Jense n, who have swea ted the big and sma ll stufTwith us during the years of development and preparation of th e manuscript and without whom complcti on of thi s projcct wou ld not have been possible.
Carrie Sussma n Barbara NI. Bates-Jensell
XIX
Introduction: The Need for Collaborative Practice Carrie Sussmall and Barbara M. Bales-Jensen
as a team 10 solve patient problems. Payers and hcalth carc settings benefit from fewer duplicated services and better patient outcomes at lower costs. Patients benefit from improved wound healing management. including better wound healing outcomes as a result of hcalth care service intcgration. To practice in a collaborat ive spirit. each discipline must undcrstand the process of wo un d hea ling. chronic wound difficulties, and the skills and services ofTered by e;.ch di scipli ne. Each practitioner has areas ofknowlcdge that by definition are not shared by others. Vet both physical therapy and nursing practice have many similarities. The main purpose of this book is to provide basic information on wound healing and wound care therapies to nurses and physical therapists in a user-fricndly resource volume for clinicians who deal with wounds on a daily basis and who do not have access to a "wound cnre expert." A secondary purpose of this manual is to promote collaborative wound managemcnt berween nurses and physical therapists by providing a better understanding of the similarities and differences between disciplines. This book is for nurses and physical therapists in acu te care, long-term care. outpatient care. and home health care sett ings. The book is forma tted for lise as a quick reference guide in any clinical setting. The book is designed to appea l to severa l groups of Ilurscs . EnteroSlOmal therapy (ET) nurses are ofien consulted on wound care and have additional education in wound care. ET nurses may find the book a direct aid 10 their practice and a va luable educational tool for use with other clinicians involvcd in wound care. Home health care nurses and nurses in long-term care settings in conjunction with physical therapists provide direct wound care in the home and long-term care selling with minimal support or education in new technologies for wound care diagnosis or management. Rehabilitation nurses work with spinal cord- injured patients: these
COLLA BORATION Physical therapy and nursing arc the two health care disciplines Illost often involved in providing care for the patient with a wound. We believe onc key to providing optimal wound care management to individuals with chronic wounds is collaborative practice between the health care disciplines of' nursing and physicallhcrapy. It has been our experience that in clinical practice, true coll aboration is not the standard, and in many instances there exists some level of conflict between nursing and physical therapy. Conflicts may arise from misconceptions about the "other" discipline's ability. education level, or experience with wounds, from interpersonal difTerenccs, or from "turf battles" wherein one discipline is fighting with the other for greater control over the wound care segment of health care. Much of the connict may be related to simple misunderstanding about the true nature of collaborative practice. True interdisciplinary collaboration does not require that one disciplinc "give up control" of wound care. nor does it require that clinicians always agree upon management options for patients. An environment that supports a collaborative spirit allows clinicians frolll both disciplines to provide their unique perspectives to best meet the needs for each individual patienl with a wo un d problem . Collaboration is challenging. The challenges to collaboration include the wide variety of clinical settings in which patients with wounds are managed, the variety of education and experience of clinicians, and the struggles of each discipline to clarify and beller define professional roles. Vet when collaboration is implemcnted successfully, the rewards to clinicians. payers. health care agencies, and patients are numerous. Clinicians benefit from the free exchange of ideas from differing perspectives and the excitement of working xxi
xxii
WOl "'IU CARl
paricnts arc a high-risk group for pressure ulcer wounds, and treatment of pressure ulcers is one of the main points in thc book. Physical therapists will find the text valuable as a refercnce for therapy and also as an educational tool for usc with other health care professiona ls. Physical therapists arc bcing asked to do more in the wound care arena, and many fcclthc need for additional education in this dynamic area.
EDUCATI ON OF NU IlSESAND PHYSICAL HI ERAPI STS Nurses nre licensed health care professionals who diagnose and treat human responses to health and illness.· The nursing profession is committed to the care and nurturing of both healthy and ill people, individually or in groups and communities. There arc four essential features ofcontcmporary nursing practice as defined by the American Nurses' Association Social Policy Statement: " ... Attention to the full range of human experiences and responses to health and illness without restriction to a problem-focused orientation. integration of objective data with knowledgc gained from an understanding of the patient or group's subjective cxperience, application of sc icnti ric know ledge to the processes of diagnosis ~lI1d treatment, and provision ofa caring rela tionship that facilitates health and healing."""") The difference between professional and technica l nurses is the depth and breadth of clinical nursing practice based on the knowledge foundation of the nurse, the nurse's role, and the type ofpatient service. 1 urses study biologic, physical. and social sciences in addition to nursing theory and the science of nursing practice. Nurses acquire knowledge in anatomy. physiology, pathophysiology, pharmacology, microbiology, chemistry, and statistics, as well as nursing science. ursing education includes the traditional focus on illness and acute care clinical practice and the more pressing current focus on health promotion and community nursing. Nurses practice at a variety of educational levels. The vocational or practical nurse education programs arc located in technical or vocational schools. The vocational nurse education program is typically I year in length and leads to a certificate of completion and eligibility to take the state licensure examination to be designated as a licensed vocational nurse (LVN) or a licensed practical nurse (LPN). LPNs and LV s are prepared to work with registered nurses (RNs) and to be supervised by RNs. The purpose of the vocational nurse programs is to prepare assistant licensed nurse workers:' These programs generally do not articulate well with collegiate nursing programs, although LP slLVNs may receive advanced placement in collegiate programs. The first formal nursi ng education in thc Unitcd States was in diploma programs. Diploma programs are typically
hospi tal based and were the predominant model for nursing education in this country. Diploma programs are usually 2 to 3 years in length, and many include summer sessions. Graduates of diploma programs arc eligible to take the RN licensure examination. The purposc of the diploma programs is to prepare clinically competent bedside nurses.' Some diploma programs have now aligned with other academic institutions, and many now offer an assoc iate degree in nursing, ADN or AA.j Associate deg ree programs are community or junior college base~ and the nursing portion is 2 years in length. The purpose of the associate degree nursing programs is to prepare compctent technical bedside nurses for secondary care settings:' Many nurses enter associate degree programs with future intentions of continuing theireducation in nursing at the baccalaureate level. s Some 4-year university programs also otTer combination degree programs to allow flexibility. Baccalaureate programs in nursing are 4 years in length, with the nursing curriculum concentrated at the upper division. Graduates of baccalaureate programs are prepared as nurse generalists to practice nursing in beginning leadership positions in a variety of scttings. In 1965, the Amcrican Nurses' Association designated the bacca laureate degree as the en try level for professiona l nursing prac tice. The majority of programs admit both pre lice nsure st udents and RNs who arc graduates of diploma or associatc degree programs. The general education requirements are the same for all students, and those with prior nursing education or experience arc allowed to progress through the nursing curriculum by designs that capitalize on prior learning. Master's degree education in nursing is typically 2 years in length and builds on the baccalaureate nursing major. Program content usually includes a group of core graduate·level courses. research course work, and specialty nursing courses. Mastcr's-prepared nurses function at an advanced practice level and include nurse anesthetists, nurse midwives, nurse practitioners, and clinical nurse specialists. The degree most often awarded on completion of a master's program is the MSN (master of science in nursing) or the MN (master of nurs ing) degree. The purpose of master's education in nursing is to prepare advanced practice nurses in a specialty area such as psychiatric mental health nursing or nursing management. ~ In addition, advanced practice nurses serve as mentors, consultants. and educators of nurses in basic practice. They conduct research to expand the knowledge base of nursing practice, provide leadership for practice changes, and contribute to the advancement of the profession. health care, and society in general. 1 Doctoral programs in nursing range from 3 to 5 years of full-time study. Doctoral programs include advanced content in concept development, theoretical analysis, research, advanced nursing, and supporting cognates. Doctoral pro-
/IIl1vdll Clioll
grams prepare leaders for programs in education. administration, clinical practice. and resea rch . In addition to formal education programs. many nurses are specialty certified. The necd for specia lizeuion in nursing developed as technologic advances in health care occurred over the last 10 yea rs. Specialty programs arc varied in scope, length of timc. and requirements. Most specialty programs prcpare RNs to take a certification examination as a part of credential ing in th e specialty area. Certifi cation requirements va ry, depending on th e specialt y area, and may inc ludc completion of an education or training program, as wcll as c linical ex perience requirements. National certification examinations arc offe red through professional organizations in a variety of specialties. including wound ca re and ET nursin g. In most states, RN s are required to maintain currency in their practice by co mpletin g specified amounts of continuing educa ti on. Physical th erapi sts (PTs) are licensed health ca re professionals who eva luate and treat people with health problems resulting from disease or injury. The American Phys ical Therapy Association (APTA) is the national organization represe nting the phys ical therapy profession, which accredits education program s for PTs and PT assistants (PTAs). Professional education req uired for PTs includes a minimum 4 yea rs of college or universi ty level training resulting in a baccalaureate degree in physica l therapy from an accredited professional education program. The information explosion in the health-related scie nces has led to current requirements that most therapi ts enter th e profession as master's levelprepared clinicians. and now so me are entering with a professional docto ral degree. FolJowing graduation, PTs mu st pass a national licensi ng examination to qualify for state licensure. Like nurses, PTs may be specialty certified in a variety of areas of practice. Although there is no current spec ialt y certification for wound care, instruction in wound management skills is a requirement for accreditation of phys ical therapist and phys ical therapist assistant programs. The requirements for continuing education for relicensure by PTs varies by state. The fact is that 1110st PTs seek co ntinuing education so as to be at the cutting edge of practice. even though it may not be a mandated requirement. Specialty certifi ca tion in wound manage ment is a targeted goal of the Wound Management Special Interest Group within the Section on Clinical Electrophysiology of theA PTA . The speci al interest group was formed to bring together PTs and PTAs from many practice settings who have special interest in wound management. PTAs arc trained and licensed paraprofessionals with 2 years of educational training in an approved PTA program or who have worked as a phys ical therapy aide for a specific period of time and then passed a qualifying examination. The PTA provides se rvices under the supervi sion of a PT.
XX III
The PTA can perform various tests and measures for which the assistant is trained, such as wound meas urements. tisslle attribute recording. and provision of treatment services with physical agents and electrotherapeutic moda lities. In so me states, the PTA may also perform sharp debridemellt. Both PTs and PTAs are qualified to apply topical agents and dressings to wounds. Many individual s are surpri sed that the PT is included in the wound management team . Re ports of wound management, including burn and wound interventions. by PTs appeared in the physical therapy literature for more than three decades. By education and training, PTs learn anatomy. physiology, and pathophysiology related to body sys tems respo nsible for repair and rege neration of soft tisslie. For example. human cadaver dissection is part of the basic anatomy education o f the PT and provides a foundation for the skills needed in sharp debrideme lll of nonviable ti sslle. Courses in cardiopulmonary and vascular system physiology are required. These two system s are critical to wound healing. Neuropathy plays an important part in development of chronic wounds. PTs take courses in neurology and learn neurologic te sting and eflccts of inse nsitivity on the integumentary system. The PT is expected to examine the integument as part of an overall evaluation . Postsurgical wounds are routinely seen and evaluated by the PT as part of the rehabilitation se rvice. For example, dehi sce nce of a wound on an amputated limb requires wound managemcnt before prosthetic training is initiated . PTs a lso are ski lled in the use of physical agcnts (heal, I ight, so und. and water), electrotherapeutic modalities. and therapelltic exercise, a ll of which are used in wound healing strategies. The PT can manage the wound as well as the prostheti c training and an exercise program to achieve the desired outcomes. PTs are interested in evidence-based hea lth care choices. and many research studies by PTs on wound healing that demonstrate treatment efficacy arc cited in this book. Phys ical therapy is the ca re and services provided by or under the direct supervi sio n of a PT.6 Services provided by others using technologies generically referred to as physica l therapy should not be co nfu sed with the se rvices of a PT. Outcomes research studies show that expected outcomes may not be equivalent. 7 PTs arc important players in the provision of primary care. defined as ''' integratcd accessi ble health care services by clinicians who are accollntable for addressing a large majority ofpersonai health care need, developing a sustained partnership with patients and practicing in the contcxt of family and community." f!\P11.1 1 In 30 states, direct access to physical therapy se rvices from a liccnsed PT is part of the practice acts. PTs play major ro les in seco ndary and tertiary care as well. For example, patients with wounds are often seen initia ll y by another health care practitioner and then referred to the PT. PTs provide tertiary care in highly
XXIV
W OUI\O CARE
specia li zed co mplex . and tec hn ological ly adva nced se tti ngs. In such situatio ns, a patient may have a traumati c wound, surgica l wo und, or burn plus compl icat in g medica l problems, and the PT is ca lled upon to manage th e wound as well as the oth er as pec ts of patient rehabilitation.
3.
Ameri can Nurscs' Associ:l1ion. FacH abouf N/lrsing. Kansas City,
MO; 1987. 4.
lIart SE. Path wuys of nursing educ:nion. In: Crcasia JL. Parkcr B. cds. CfJncepwlll Fowu/mio n5 of Profl'.uionll/ Nllrsing Practice. 2nd cd. 51. Louis. MO: Mosby: 1996:26-45 .
5.
Kozicr Il Erb G. I3111is K. PmfessiOlwl NII":"i,,!: PraClice: Co" cep/~ alltl Perspeclil'f!s. 3rd cd, Men lo Park. CA : Add ison-Wesley: 1997 :
2 27. 6.
America n Physical Therapy Association. A guide to physical therapist practice. I : a descri ption of patient managemenl. Phys Tiler.
1995 ;75:707 764. I.
American urscs' A!isoc iation. Nllnil/g A Social Policy SUlfemenr. K an!>a~ Ci ty. MO : 1980.
7.
American Physical Therapy Association . Olilcomes EffeC/il'e"f!H of Physical Therapy : All Allllou/led IlibUegmp"y, Alex.andria, VA: 1994.
2.
Amcrican Nur!>e~' A!>sociation. Nllr.H·ng ...· Social Wash ington. DC: 1995.
8.
Donaldson M, Yordy K. Vanse low N. Defillillg Primary Care: AIII,,lerim Report. Washington. DC : National Academy Press; 1994.
Poli£~l t
SrMemenl.
P A RT
I
Introduction to Wound Diagnosis Carrie Sussman
Dc\clopmcllt of diagnoses to direct and guide treatment by nurses and physical thcrapi!'lls has been growing over the
last 15 to 20 years. Both disciplines recognize that use or a diagnostic proccss applies the skills and knowledge or the proressional nurse and physical therapist to the appropriatc treatment of client situations they can and shou ld treat lega lly and independently. The role or diagnostician is unramiliar to many. and practice experience in the area of diagnosis varies frol11l1oncxistcnt to full-practice integration for many years. Because the incorporation of diagnosis into the health care professions is still in its infancy, there is much \-ariance in l1nder~landing of the process. Therefore. there arc a number of questions that need to be clarified as the process begins : • What docs a diagnosis really mean? • What kinds of information need to be collected to yield a diagnosis'! • lIow are diagnoses differcntiated from each other? • lIow is a diagnosis tailored to the patient's functional problem or human response to health or illness? • How does diagnosis relate to prognosis and outcOines? • J low docs the nursing or physicalthcrapy diagnosis direct interventions? Ad\anced clinicians who arc more familiar with classification systems and diagnostic methods will ha\c othcr typcs of questions: • Can and should the medical diagnosis be part or the physical therapy diagnostic statement? • What kind of functional diagnostic statement should be \Hittcn for a person at risk for wounds? • What is the dilTcrence between diagnosis and classification'!
Part I begins with an introduction to the diagnostic process. It seeks to answer these questions. including specifics about wound diagnosis. Guidelines for writing functional diagnoses that are meaningful and related to the prognosis and treatment interventions arc included for both disciplines. One of the things that became clear to the authors as Chaptcr I was craned is thai the diagnostic process and the terms of the diagnosis of the nurse and physical therapist arc ve ry simi lar. Both incorporate functional impairment and disability into the diagnostic process. For example. the nurse determines the clients response to health or illness as positive functioning. altered functioning. or at risk for altered functioning. 1 Nurses use a diagnosis that incorportnes risk that could \\ork equally well ror the physicaltherapisl. Nursing diagnosis specifically identiries collaborati, e problems and then the health care practitioner needed for joint management. The most appropriate joint manager for wounds may be the dietitian. the physician. or the physical therapist. Nurses already hm e taxomony for impaired tisslle integ,.ity and impaired skin imegrit): Physical therapists use disablement terminology. including the terms impai,.ment. disahility. and halldicap in their management modcl.;! FUllctional diagnosis requires understanding offu llctional impairment. Functional impairment dilTcrs from the pathogenesis or etiology of the problem and describcs a functional change as physiologic. anatomic. structural, or functional at the tissue. organ. or body system levcl. 1 Functional impairments are the system or organ impairments that prevent normal function :' In impaired wound healing there is a functional impairment of wound healing that occurs at a system, organ. or tissue levcl in the body. Chapter 2 is devoted to understanding the system functions related to wound healing biology and chronic wound healing. Assessment, examinations. tests, and measuremcnts are an integral part of cs-
tabli shing a di ag nosis. Chapte rs 3, 4 ,5, and 6 descri be techniqu es to pe rform th e procedu res and how to interpret the find ings. At the conclusion o f Part I. clinicia ns will bc abl e to pcrform th e tes ts and measures necessary to determ ine functi onal wo und di ag nosis. deve lop a prognosis, a nd stale the expected ourcomc. Thcy wi ll bc able to doc ume nt the diagnosti c process and th e findings with a fun cti onal out comes report. The clinicia n will then be rcady to go to Parts II. III , a nd IV to Ica rn th e man age me nt sk ills fo r diffe rent wound related proble ms and interve nti ons.
I{EFEI{ENCES I.
Carpenito LJ. Nllnillg Dillg1l0.\ /\ Applicatioll 10 Omical Pmclict!. 6th cd. Philadelphia : l B. Lippincott: 1994.
2.
Amcrican Physical Therapy i\:,:,ociaiion . A guidc to phY:'lcal thcmpy p racticc. I : a dcscriptioll of p:ltlcnt munagclllcnt. Pil.\'I Tiler.
3.
World Ilclllth Organization . /lIll!rmlliu1IlIl c/{/\\·i/icalill1l of Impai,.· mell1;" f)imbiIiNe.I', und II{/I/dic(lp~ . Geneva, S'A il7crlnnd: 1980.
4.
kttcAM. Physical disablement concepts lor physica lthcrapy rcsc:lrch and pracllee. Pill"> 711t!r 1994:74:380 ·386.
1995:75:707 764.
CHAPTER
1
The Diagnostic Process Carrie SusslIlan, Barbara M. Bales-Jensen. and Melisa TiffcJIIY
didacy or noncandidacy for serv ices; for nurses. the hi story and systems review determine the direction for the treatment plan. Many physica l therapists retai n the belie f that all referrals automaticall y show candidacy for wo und care. The realit y is that not all patients arc appropriately re re rred ror phys ica l therapy. To some physical therapi sts thi s will sound li ke heresy, but proper ut iliza tion management is mandatory in today's hea lth earc environmcnt. Utili zati on managemcnt is part ofthc process ofpros pccti ve managc ment and is designed to ensure that only medi ca lly necessary, reasonable, and appropriatc services arc providcd. Utili zatiol1managcl11cnt attempts to influencc the treatmcnt path way to cnsure optimal clinical outcomes.' For nurscs. the assessment process provides the framework for planning comprehensive wo und care incorporating uti lization manage ment. and may include making a referral for physical therapy. Utili zation management for the patient with the wound and for comorbidit ies and coimpairment are separate but re lat ed. Co ll aborati ve intcrdi sc iplinary manage mcnt o f comorbid iti cs and coi mpairmcJ1t s will redu ce iatroge ni c cffccts from in appropriate selectio n of intcrve nti ons or handling of thc wound, and will Icsscn extrinsic and intrinsic complications. Chapte r 2 cx plains and di scusses comorbiditi es and co impairments as well as the iat rogenic extrinsic and int rin sic fa ctO rs thai a ffcct wound hcaling. The interdiscipl inary nature inherent in cari ng for the patient with a wound requires clinic ians to carefull y determine candidacy for services be fore initiating rcfcrral or treatment. The assessmcnt process assists in clinica l decision makin g by avoiding undirected care and inappropriate treatment. Assessment with attcntion to utili zation managcmcnt allows selcction of a path for rcferral for another intcrvcnti on or to other hea lth care disc iplines and practitioners. For ex-
Thi s chapter descri bes th e di ag nosti c process for mana gement o f pati ents wit h chronic wounds. N urses and phys ica l therapi sts usc essenti ally th e sam e decision-makin g process in diagnosing pati ent probl ems, although the term s used to
describe the process may differ slightly. Nurses lise the nursing process and nursing diagnosis as the framework for planning and eva luating palient carc. The nursing process includes the following steps: assess ment. diag nosis, goals. interventions. and evaluation. Physical therapy uses a process that inc ludes the steps o f assess ment. cx aminari on. di agnosis.
prognosis, and Olltcomes, To simplify and guide the reader, the diag nost ic process has been broken into four steps, each with two or th ree parts. Step I, assessment. includes review of the reason for re ferral, history, systems rev iew/physical assessment, and wound assess ment. Step II. diagnosis. includes examination strategy, evaluation, and diag nosis. Step III , goals, includes prognosis, goa ls, and outcomes. Step IV, intervent ion. is described in subsequent chapters. Examinations and specific measurements plus special test procedures are found in Chapters 6 and 8. as wcll as in others. STEP I:ASSESSMENT PROCESS The assessment process is the first stcp in wo und care manage mcnt. Assessment is done ror all patients berore determ ining the need fo r special testing examinations and interven tions. For nurses. th is process begins when the patient is admitted to the age ncy. For phys ica l therapi sts. thi s process begins wi th the reason for referral. which is part of the patient hi story. The assessment process involves gathering data from the patie nt history and physica l exam ination. The pati ent hi story determines which relevant systems reviews are needed in the physica l examination. For physical therapists. the history and systems review determine the can-
3
4
WOUND CARr
amp le, the physical th erapist may determine that the patient is not a candidate for whirlpool therapy as ordered by the physician, and sends the findings with an alternative recol11-
mendation to the referring physician . An addi tional example is provided when the history and phys ica l examination of th e wound suggest to th e nurse th at vascular examination
and testing procedures arc needed. The usc of standardi zed fo rm s is the best method of collect ing assessment data quickly and efficiently. thus ensur-
ing that important information is not losl. Use ora form that the c linicia n completes and a form that the patient comp letes e ns ures da ta maintenance from the interview. A sc lf-adm inisrcred patient hislOry form helps the clinician to focu s the interview and can save time. Samples of an assessmen t form for a se lf-administered hi story and an illlcrview form for physical thcnlpi sts and nurses are prcse nted in Appendixes I- A and I B. The forms inc lude reason for admission/ referral, past medical history. physical examina tion findings. and a place to list suggestcd examinations to follow based on the int ake information. Forms may be completed by both the cli ni cian and the patient or significant other. Some informalio n w ill be fo un d in the patient's medical record but many times the paticnt or s ignificant ot her can prov ide additional ins ights ~1I1d informHtionnot o th erw ise avai lab le. Partncring or e ngagi ng th e patient in hi s or her own care from the beginning is esscntial to achieving mutually sati sfactory outcomes.
Itc\'icw ofAdmission/ Rcfcrrul It is essen tial for a physical therapist to know the reason why a patient is referred. This referral is the first step in documen ting patient hi story. The initial referral for wound ca re management is us ually to the nurse; if the nurse determines a need for physical therapy services, the physica l therapist is brought into th e team . It is cri tical for nurses to know ex pec tati ons and projected outcomes from a physical therapy referral in order to refer appropriate ly. In so me health care settings, a wound care team decides the serv ices nece ssa ry for wound management and makes the appropriate referral s. T he patient referred to th e physica l therapist for wo un d healing is usua ll y an individual who has not shown signs of normal wo und repair. Most often other treatment interventions arc in use or have been tried with limited or no success. Phys ica l therapy services usually involve an additional fee. The referra l to physica l therapy is regarded as an attempt to ma xim ize and en hance wound repair. However, expectati o ns of rcfe rra lm pl ying FO R to Form H CFA-700 To become familiar with the diagnostic process and
the FOR method, review the samp le case in Exhibit 1- 2. Physica l therapists arc accustomed to using the Form 1-1 FA-700 (I 1-91) for documentation (see Appendix I-C). The HCFA-700 and the FOR method of reporting were designed to work together. A template added to the I-ICFA-700 (Appendix I -D) guides the physical therapi st through documentation of the diagnostic process and FOR methodology. Appendix I-E is a sample ease report on the I-I CFA-700 using FOR methodology.
I
Clinical Wi sdom Some faci lities have the HCFA-700 form on computer. If a template can be added to the form with the items as listed formatled to fit the computer field, it would help the physical therapist complete the documentation in an orderly and consistent manner. For those using a hard copy of HCFA-700, a template can still be useful to ensure that all items are recorded following the format.
Reevalu ati on Once the target outcomes and goals have been determined the reeva luation process is really quite simple. The clinician uses performance indicators to mcasurc the patient'S progress toward the outcome within the desired time frame. For example, if the target outcome is patielll .'s wOllnd will demollstrate 25% reduction ill si;e lI'ithill 2 lI'eeks. then the clinician simp ly monitors wound size over the 2-wcek period of time and then determines whether the wound has reduced surface area size by 25% at the end of week 2. I f the wound has decreased in size more than 25%, the outcome has been exceeded. I f the wOllnd has just decreased in size by 25%. the outcome has been acceptably met . If the wound has fai led to decrease in size by 25%. the outcome has not been met
and the goals must be adjusted and interventions reviewed. Reevaluation is an ongoing dynamic process that will recur on a regular basis following reexamination of the effects of treatmenLAt that time, goa ls and outcomes may be adjusted, new goals developed, and interventions modified . The PSST and SWI-IT tools described in Chapter 5 are validated methods for monitoring wound hea ling outcomes that are used throughout the evaluation and reevaluation process.The tools provide a quick checkup at regular intervals to determine efficacy of treatment or to alert the clinician to deviations from the expected course. Since utilization management attempts to innuence the clinical path from the beginning so as to reduce devia tion from an expected course and to produce optima l outcomes. th e adjustment of goals and expected outcomes should be minimal. The clinician must make accurate predictions at baseline. Multiple approximations to reach the target outcome will not be tolerated by patients or third-party payers. For example. the APTA Guide to PT Practice l4 lists wound management guidel ines regarding range of visits and length of episode of care by physical therapist s for patients with wounds. This range represents the lower and upper limits of services that it is anticipated that 80% of tile patients/client s with such wounds will need to achieve the predicted goals and outcomes (prognosis) listed. Multiple factors may modify the duration of the episode of care, frequency. and number of visi ts. Wounds extending into fascia. muscle. or bone (integumentary pattern E). for instance, will require 4 to 16 weeks (12-112 visi ts) for an episode of care (all types of etiologies included). The prognosis for wounds of thi s severity is that over the course of 4 to 16 weeks of care by the PT that one of the followin g will occur: o o • •
Wound will be clean and stable. Wound will be prepared for ciosure. Wound will be closed . Immature scar will be cvidcnt.14Ip'6l1~)
CONCLUS ION The diagnostic process described in thi s chapter is intended as a framework for clinicians working with patients with wounds. The information mayor may not be new. but there are limes when review ofmalcrial may be helpful. This chapter is meant to assis t those clinicians new to the diagnostic process or unfamiliar with its usc. Use of clinical judgment with diagnostic reasoning is one oflhe essential prac tice tool s that nurses and physical therapi sts use with the patients they serve.
The Diagnostic Process
REFE RENCES
25
7.
Jette AM . 1lhysical disablement concepts for physical therapy research and practice. Ph),s Ther. 1994;74:380 ·386.
I.
Clifton. Ow, Utilization management: whose Job is it? Rehab Man· age. June/July 1996;38:44.
8.
Swanson G. The IDH Guidebook/or Physica/Therapy. Long Beach. CA: Swanson and Company ; 1995.
2.
Bergstrom N. BcnnclI MA. Carlson C. ct al. Treatment of pressure ulcers. C/imca/ Practice Guideline. No. 15. Rockville. MD: US Department of Health and Human Services, AHCPR Pu blication No. 95-0652. December 1994.
9.
Sussman C. Case presentation: patient with a pressure ulcer on the coccyx . Paper presented at APTA Scientific Meeting and Exposilion, Minneapolis. MN . June 1996.
10.
3.
lI isen lB. White 1)1:: Medical nmnagcmcnt of su rgical patients wilh diabetes, In: Levin ME. O'Neal LW. Bowker JH . cds. 71Ie Diabetic Fool. Chicago: CV Mosby: 1993.
Lazarus GS. Cooper OM. Knigh ton DR . ct al . Definitions and guidelines for assessment of wounds and cvaluation of healing. Arch Dan/lIfOl. 1994; 130:489-493.
I I.
4.
Swanson G. The Guide to Phy.\ ical ThE-rapi!)1 Practice. vol I. Presentation at California cll:I ptcr. APTA. S:1Il Di ego. CA. October 1995 .
Swanson G. What is an outcome? And what docs it mean to you? VI/rohol/lltls. (Ca lifornia Private Practice Spcciallntercst Group Cali/omit! APTA). 1995; 94-51 :7.
12.
Swanson G. Functional outcomc report: The ncxt generation in physical Iherapy reporting in docume nting physica l thcrapy Qutcomes. In : Stuart D. Ablen S. cds. Docume"'ing I'hysical Therapy Outcomes. C hicago: CV Mosby: 1993:101 134.
13.
Staley M, Richard R. et a!. Functional outcomes for the patient wilh burn injuries. J Bllrn Care Rehab. 1996: 17(4):362367.
14.
Guide to physical therapi st pmctice. Phys Ther. 1997;77: 1593 1605.
5.
6.
Amcnc:m Physical Therapy Associalion. A guide to physicallhcrapy practice. I : a description of patient management. Phys Ther, 1995:75 :707 764 Oocnges MD. Moorhouse MF. Burley JT. Applicatioll of Nursillg Process (tnd Vurslllg Diagnosis. 2nd cd. Phil ade lphia: EA . Davis: 1995.
26
WOUND (",\It!
Appendix 1- A: Patient History Form
#___________
Medical Record Name' _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __ Street Addrcss, _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __ City, State, l1p _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __ Telephone Number (-,-,-,--,---_ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _-,-,,---,---_ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __ Sex: M f ___ lIeight ' _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ Wetghl. _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __ Religiolls Preference: _____________________________________________
What is your primary reason ror seeking woulld care today'! ______________ Ilow long has your ""''QUlld existed'! ________________________________________
Who referred yOll hcre? _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __ Who has bl!clllreating you hefore today? _ _ _ _ _ _-,--,---______________________________ Can you describe what you hu\c heen using on your wound'! _______________________________ Who has been helpmg you \.. l1h your wound care? __________________________________ 110\\ have yOll been paYlIlg for your supplies'! ____________________________________ Ilave you l!\cr had surgery'! Type: -,_ _",._________ Other? _ _ _ _ _ _ _ _ _ _ _ _ _ _ __ Do you have rilly allcrgies'! Medications (Sulf'l. PCllIcillin) _________ Packs per day: # of years: _________________ Do YOli smoke" Ilowoflt.,'1l do yOll u~e recreational or illicit drugs? ____________ 110\\ oOen do yOll drink alcohol'! _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __ Do yOll ha\'l~ any palll? ______________________________________- - - - - - - On a scale oro 10 (0 No P;:lin, 10 Sc\"t!fC Pain). what is your p SlcRV ICES ~URNISIII:D LJNDIR TillS I'LAN on Rl,ATMENT AND "'II ILl: UNDER MY CARl' 181 N'A 15 . PIIYSICL\N SIGNArURI.
20
w,
x 4 wkl (n"c I)a/cl
17 C£.RTlflCATION D N 'A fROM TliROU Ii
18 . ON llLE (Prim type physician's name) 116. DATI'
1l\ITIALASSLSS~1LNT (1IIstory.medlcal complications. lc\cI of function al starl or care Rcason ror rererral)
D 19. PRIOR lIOSPITAli/ATION FROM TO
'"
.')\'.\(('/1/,\ N('rI(l
wer~'
Iprnfc"lIlnJI c'!ilhh~hcJ liCK lOduUlOg pml dC'lgnJtlOn)
I CI' RTII Y 1'111' Nl'!'D FOR T II ESE SFRVICLS FURNISIIED UN DI R T i llS PLAN 01 TRLATMI·.NT AND WII ILI UNDER MY CAR l 181 N 'A 15 PIIYSICIAN SIGNATUR I
16 DATE
14 FRFQ DURATION (Due Dale) (: .... . '...... , " .If
"
17. CERTIF ICATION 181 N 'A I ROM TIIROUII 18. ON FILE (print type phys ician s n;:1I11e)
0
1
211
INn IALASSLSSf\II :NT (1IIstory. medical comrlicatlons. le\eI of function at s tMI of ca re . Reason for referral)
Rt'(I\OIl for Rt'fer/ul '''.1'''1
I I \ _ t.-', d
,It'I'
.n
'-,'f, . lI c-alth Can! Fmanc1l1g Adm1llhlr.lll on Medlcarc- .
,
COLOR PLATES PROGRESSION THROLJGH THREE PHASES OFWOLJND HEALING Plates 1-6
The paticm is a 97-year-old nursing home resident with Stage IV pressure ulcers in the bilateral rib cage and sacral area.
t.
3.
Chronic wound converted to acute inflammation phase.
(I) (2) (3) (4)
Yellow, strin gy slough; Edema; Skin color changes (rcd), erythema; Rib bone noted in superior ulcer. Wound healing phase diagnosis: acute inflammation phl.lsc. Wound severity diagnosis : Impaired integumentary in tegri ty secondary to skin involvement extending inlo fascia, muscle, bone. Source: Reprinted with permission, copyright © C. Sussman.
2.
Same wound as in Plate I. ( I) Rolled epidermal ridge around granulation base; (2) Brown hemosiderin staining . Wound healing phase: prolireration phase. Source: Reprinted with permission. copyright ~ C. Sussman.
Same paticni as in Plate I. Chronic wound: converted to acute proliferation phase. This is a sacra l wound with stringy. yellow slough evident. Predomi nant wound hea ling phase diagnosis: Proli reration phase. Wound severity diagnosis : same as in Plate I. Source: Reprinted with permission, copyrig ht rCl C. Sussman.
4.
Same wound as Plate 3 progressing through the prolireration phase or healing. Wound contracting and prolirerating. Note change in size, shape, and depth compa red to Pl ate 3. Source: Reprinted with permission, copyri ght C. Sussman.
Color Plates Page 2
3/31
AL
I!J
S.
Note sustained wound contraction evident between Plates 4 and 5. Wound is in both epithelialization and proliferation phases. Source.' Reprinted with permission, copyright,~ C. Sussman.
6.
The wound is completely resurfaced. II is
In
the remodeling
phase. Source: Reprinted with permiss ion. copyright ·(, C Sussman.
Color Plates Page 3
PROGRESSION THROUGH PROLIFERATION PHASE Plates 7-9 Plates 7 to 9 show a sacral pressure ulcer progressing from chronic inflammation phase through the proliferation phase of wound healing. In Plales 8 and 9 the wound edges demonstrate epithelia l migration with new epidermis clearly visible as bright pink 10 this darkskinned patient In Plales 7 to 9.
7.
Chronic inflammation phase. Note the following wound char-
actenstlcs: ( I ) Sangumeous drainage; (2) (3)
Muscle exposure; Hemosiderin staining surrounding the wound. Sourc:e: Reprinted with permission, copyrightt.. B.M. BatesJensen.
9.
8.
Acute proliferation phase. Note the attached wound edges from the 12-o'c1ock to 6-o'c1ock positions and how granu lation tissue fil ls up onc side of the ulcer. Source: Reprinted with permiSSion, copyright ·c, B.M . BatcsJensen.
All of the wound edges arc now attached to wound base Note the presence of fibrin (yellow) wlthm thc granulation tissue . Ready for eplthcllalization phase. Source: Reprinted with permiSSion. copyright (" B.M Bates-Jensen
Color Pl(l{es Page 4
ABNORMAL PROLIFERATION PHASE Plates 10 and II
10. Acu te proliferation phase . ( 1) Hemosiderin staining; (2) Sanguineous drainage. Source: Reprinled with permission , copyright to S.M . BatesJensen.
WOUND IN REMODELING PHASE Plate 12
10/27/87 Left hip healed
t 2. An example of a wound in the remodeling phase of wound hea ling. ( I) New epitheli um (scar); (2) Hype rpigmcntalion (Hemosiderin-staining). Source: Reprinted with pemli ss ion , copyright © I3.M . BatesJen sen.
1 J. Chro nic proliferation phase with attributes of infection . ( 1) Hemorrhagic area of tTauma; (2) Hypopigmcnlation ; (3) Dull pink gran ulati on tissue. SOl/ree: Reprinted with permission , copyright ~ B.M. BatesJensen.
Color Plales Page 5
ANATOMY OF SOFT T ISSUE Plate 13
13. FullMthickness skin resected from calf. (I) Vascularized dermis; (2) Yellow healthy rat tissue ; (3) White fibrous fasc ia; (4) Dark red muscle tissue; (5) Tendon covered with peritenon: (6) Blood vessel. Source: Reprinted with permission. copyright to 1. Weihe .
WOUNDING OFTHE SK I N Plates 14-18
15. 900 mm J
Stat e of Hydration 24-l-Iour Intake
Note:
rnL
24-Hour Output ___ mL
Thirst. tongue dryness in non- mouth breathers. and tenting orce rvical skin may indicate dehydration. Jugu lar vein disten-
tion may indicate overhydration. [slimaled Nulritional Requiremenl
Estimated Nonpro tein Ca lori es (NPC)
_ _!kg
Estima ted Protein
_ _ (glkg)
Actual NPe
_ _ !kg
Ac tual Protei n
_ _ (glkg)
Recommendalions/Plan I.
2. 3. 4. Source: Reprinted from N. Bergstrom, M.A. Bennett. C.E. Carlson. et al.. Treatment of Pressure Ulcers. Clinical Practice Guideline No. 15. December. 1994. U.S. Department of Health and Human Services. Public Health Service. Agency for Health Care Policy and Research. AHCPR Publication No. 95-0652 .
43
44
WOl
Nil
C,.,
Neuropathy curopathy is a C0l111110n complication of chronic diabetes and alcoholism. Three types of neuropathy are found in individuals with neuropathy: sensory, motor. and autonomic. Neuropathy affects autonomic nervous system function of the sweat and sebaceous glands. resulting in impairments of these sweat and sebaceous glands. When sweat and sebaceo us g land function in the feet is impaired. the skin becomes dry and crackclL providi ng a portal of entry for infection. The skin acidity is also changed resulting in impairment orthe skin's ability to control surface bacteria normally controlled by the skin acidity. Patients with diabetcs also hmc an impairment orthe body's immune system. which is simply unable to generate an inflammatory phase of repair and subscqucntly unable 10 overcome infcction. Combining al l of these functional impairments results in a chronic infected wound in a paticnt with a comorbidity of diabetes. Chaptcr 15 describes the examinations to test for and thc consequences of the trineuropathy, including photos of the consequences.
EX lrinsic Factors in C hronic \Vound I-Iealing ftle(/i(:lIfioll lIlId Imlllull e Suppression
Research Wisdom : Topical Vitamin A to Restart Inflammation
Application of topical Vitamin A will effectively counteract the effects of steroid and restart the inflammation process in chronic wounds and set them back on track. for breakdown and poor hcaling. The cxtel11. dosage. frequcncy. and location of irradiation in rc lation to the wound site will determine the cITect on wound hcaling. The effects of irradiation on tissue arc not easi ly revcrscd:'11 P.\)'(·/r op" ysi%gic Siress
Understanding the role of psychophysiologic stress is allother area of chronic wound research. Psychophysiologic stress has been shown to lengthen Ihe time for wounds to heal. Paraplegics who were college students were found to ha\'c morc skin breakdown during final examination periods than at other times of the school ycar.fII ) Caregivers of chronically ill patients who cxperienced wo unds were found to takc longer to heal than persons not li ving in slich stressfu l situations. The chronica ll y ill patient wi th multiple cOl11orbidit ies has psychophysiologic strcss frol11 multiple discasc processes.
In body systems sufTering immune suppress ion. such as is common in those who have diabetes. human immunodeficiency \irus infection. and acquired immune deficiency syndrome. the body lacks the ability to produce an inflammation phase. \\ hich is the body's immune response to injury. As described above. the inflammatory response sets ofT the cascade of rcpair. Absence or impaimlent of inflammation at the onset of trauma will impair the healing cascade. Medications are ollen prescribed to control inflammatory responses in the body including anticoagulants. immunosuppressive agen ts. antiprostaglandins. and antineoplastics. Steroids are immunosuppression medications that may be applied topica lly or systemica ll y. Steroids arc prescribed for diverse disorders ranging from asthma to polymyalgia rheumf.ltica. Stcroids in hibit macrophage levels and delay wound repair. ~It Application of topical vi tamin A and systcm ic vita m in A suppl ementation have proven efficient in cou nteracting the efTects of steroid medication. Vilamin A shou ld be part of the medical management of the \'.;ound paticnt on steroids. (II
Excessi\'c bioburden from necrotic tissue and infection h3\'c been associated with development of a chronic wound. For example. epidermal cells normally march forward as a sheet and lyse the necrotic debris from the wound edges. but they are impaired in this process of phagocytosis ifobstructed by a large quantity of de\'itali7cd material. De\itali..:cd tissue and foreign matter debris contribute to the proliferation of bacteria in the wound wh ich in turn wi ll overwhelm the body with infection. possibly leading to sepsis. In sllch situations. the body will not be able to clcanse the wo und without intcrvention. It is imperati ve to clean the wound down to hcalthy bleedi ng (issue to restHrt the inflammatory phase and the biologic cascade of hc~lli ng. Blecding creates a new acute batt le zone and signa l source for the respondcr cell s. Il owevcr. thc response may fail to occur or be inadequate to initiate a new inflammation response if there is inadequate circulation .
Irradialio"
Iatrogenic Factors in C hronic \\'ollnd I-Iealing
The purpose of radiation therapy is to kill cells. The damage may not be visible on thc surface. Injuries to the ce ll s of repair. fibroblasts and endothelial cells. and to the vasculature of the area make tisslies that have been irradiated at risk
BiobllrtJell and III/el'lioJl
Isd,emill
Ischcmia is the result of constricting blood suppl y to tissues. Ischemia occurs in differcnt ways. such as from pres-
Wound Healing Biology lI li d Chronic Wound Healing
sure over a bony prominence or an inadequat e vascular functi on, and may result in mi xed ve nous and arte ri a l di sease. If the patie nt is th en inappropriately placed on co mp ression treatm ent, ischemi c tra uma may ensue. 50
Inappropriate ' YOWIt/ Care AI(11lt1gemellt Inappropriate wo und Inanagement, inc luding a misuse of topica l agent s (eg, ant ise pti cs) or poo r technique in appli cati on of dressings and tapes that results in tears and bli sters on surroundin g skin or wound bed, have all bee n implicat ed as factors in development of a chroni c wo und.49.so Wound desiccati on, from lac k o f a dressing or inappropri ate dressing choice, is not uncomn'tO n. Drying Ollt o f the wound inte rferes with th e "current of injury" functi on as we ll as the mitoti c and mig ra tory fun ction o f cell s.!O
T rauma Trauma to wo und ti ss ue occurs frequent ly and impedes wo und repa ir. Tra uma ca n be attributed to many different ca uses. inc luding th e foll owi ng: • High-press ure irrigati on such as in th e whirlpool or with WaterPikn.! or removal of wet to dry dressings used for c leaning granul ating wound s ca n cause trauma. • Imp ropcr pressure to new g ranul ati on ti ss ue traumati zes th e frag ile ti ssue and initiates a new innammatory response, which retards hea lin g and ca uses abnormal sca rfin g. • Improper handlin g during removal of dressings, compression wraps, or stockings, frequentl y results in trauma to vc nous ul ce rs whose surrounding skin is oft en extreme ly frag ile.
Clinical Wisdom: Avoiding Adverse Treatment Effects
I
45
wound healing: innamm ation, proliferation, epit he lial izati on, a nd remode lin g. The chapter has focused on the fo ur phases subdi vided into three co mpa rtm ent s to di fferen ti ate the acti vities occur ri ng in th e wound space, called the bail ie ZOIlC: these are th e signal so urces-chemica l and bioelec tri c produced by th e body a nd by th e res ponder ce ll s. T he inte nt has bee n to descri be key as pects of eac h phase and then conn ect th e re lati onships to th e cl inica l ma nagcment. Much morc has bee n wri tt en abollt th e bio logic process of wo und hea ling than is presented here, and funhcr reading is suggestcd. T he goa l of wo und manageme nt is to provide inte rventi ons that prog ress wo un ds th rough the biologic sequence of re pa ir or regene ra ti on in an orde rl y and time ly manne r. In ord er fo r th e nu rse and phys ica l therapist to have successfu l wound healin g out co mes, it is c riti ca l to und ersta nd and be able to recognize thi s key sequ ence of event s. T he ab ility to recogni ze the benchmarks of wo und phase c ha nge are c ritical 10 monitoring the e ffects o f trea tm ent interven tions and recogni zing whcn the inte rve nti on is successful or not SllCcess ful. Early identifica tio n th at the wou nd has become " stuck" and unable to progress shoul d tri gge r an app rop ri ate response to avo id chro nicit y. Chro nic ity ca n happen du ri ng any phase o f recovery. A wo und ca n a lso have an abse nce of a phase of repair. T his occ urs whe n th e body simpl y fai ls to init iate the phase (eg, when there is inadaq uate ci rcula tion). T hese co nce pts are ex panded in Chapter 3. Assessment of Surroundin g Skin and Wound Tiss ue. In the sectio n on chroni c wounds, three majo r facto rs (i ntrinsic, ex trin sic, a nd ia trogenic) we re descri bed. Care ful assess ment o f th e patient wi th respec t to these three fac tors in conn ec ti on with the wo und are requ ired to ident ify potenti a l interfe rence with th e process of hea ling. T he fo ll owing chapte rs are arranged so as to gui de th e nurse and physica l th erapi st th ro ugh assess ment and diagnos is, ma nage ment strategies to manage the fac LOrs that a re coi mpa innc nts to heali ng, a nd selecti on of inte rve nti ons that will provide optim a l wound healing outco mes. REFEREN CES
Careful evaluat io n of each treatm e nt and technique based on wound assessment can avoid adverse treatmen t effects and change th e co urse of the wound .
I.
Hunt TK. Hussain M. Can wound healing be a paradigm fo r lis,",ue repair? Med Sci Sports E:rerc. J994;26:755 758.
2.
Cohen K. Principles of II olllld lIe(lliflg (video) . Richmond. VA. Wound Healing Center. Medical College of Virginia. Virginia Commonwealth University: t990 .
3.
Coope r D. The physiology of wound heali ng: an overview. tn: Krassner D. cd. Chronic m)tlll(/ C(lre. Ki ng of Prussia. PA : Ilcalth Manage ment J'ubl ication ; 1990: J II .
4.
Winter GO. Epidermal regeneration stud ied in the domestic pIg. In: Hunt T K, Dunphy JE. cds. FIII/dtll/wnwl.'} oj WOllnd Mallagemelll. Ncw York : ApplclOn-Ccntury-Crorts; 1979:71 II I.
5.
Hunt TK , Hcppcnstal t RB. I'ines E. Ro\'cc 0 , cds. Soft "nd Hard Tissue Rep(lir: Biological alld C/illictt/ Aspecls. New York : Pmegar Publishing; t984.
CONCLUSION T he begi nning of thi s chapt er ex plains fi ve methods by whi ch wo unds heal : superfi c ial, partia l thi ckness, primary intenti on. de layed primary intenti on, and secondary intenti on. Biologically they all heal similarly. The bio logic sequence o f healing was described for fo ur phases of ac ute
46
6.
WOUND C'\ltl
lIunt Tf\.. Van Wmlde \\
FIIII"'1I11('I/f(l/'
of
/J()IIlId MmwXi'III/.'II/
III
28
l3arnmco S. Spmlaro J. el ai, In \llro cOCct of weak direct current on staphylococcus aurcu.ifieilllOll nnd 1ll;ltIagelllcnl ellll O,.,IIop. 1975;112 :1.
27
lIinul//'.
Wound Ileafilig
mg A/lerll(llil'£'\ ill \/wwg£'melll 2nd cd. Philadclphia : F.A . Davis:
55.
1995:47 59
SO.
Stott:,. NA. Wipkc-Tc\ is D, Co-faclOrs in Impaired wound healing. O~tomy.IIlJ/lfl(' Mal/llge. Murch 1996:42:44 56.
5 I.
Dean E. Oxygen transport deficit:,. in systcmic discase and implications for physical thcrapy. Phys Ther 1997:77: 187 202.
52.
lIum TK. Rabkin J. \011 Smitten K. Effect.) of edema and anemia on wound healing :lI1d lIl/cction. Cllr,.. S'lld Hemato/ Blood TrailS! 1986:53: 101 111.
53.
McCulloch J\\. Treatmcnt of wounds ca used by vascular insufTicieney. In : McCulloch JM. Kloth LC. Feedcr JA. cds. IIhlllll/ lleaimg A/I£'rll(lI;l'£'\ ill ,\/tlIwgemC'lIt. 2nd cd. Philadelphia : EA. Davis; 1995 : 2 16 217 .
54.
Allmun R~·1. Laprade CA. Noe l LB. ct al. Pressurc sore!> among hO'lpltalizcd patients . .'11/1/ illfern Med. 1987:105:337 342 .
56.
57 .
58. 59. 60.
8iolog~ '
alld Chronic WOllnd Ileafing
47
Berg:,.l rom N. Braden B. A pro'>pectivc sllIdy of pressure sore risk aillong in s titutionalized elderly. .I Am Cerial/" Soc 1992 :4 0 : 747 758 . Breslow RA. Ilallfrisch J. Goldberg A P. r. 1:,lnutrition in wbefed nursing home patient:,. with pressure sores. J P(I/"ellfel" Emera! Nlltr. 1991:15:663 668 . Bergstrom N. Bennet! MA. Carl son C. ct al. Trcatmcnt ofprcsslirc ulcers . Clinica/ Practice Gltideline, no. 15. Rockvi ll e. MD: US Dept of Ilcalth and Il uman $cnices. AIICPR Publication No. 95-0652, December 1994 . Leiebowitch SJ. Ross R. The role of the macrophage in \voll nd rcpair. Am J Parhol. 1975:78:7 1 91. Hunt TK. Vitamin A and wound healing . .I Am Aead DermalOl 1986:15 :8 17. Crenshaw R. Vi:,.tncs L. A decade of press ure sorc research . .I Rehah Re.~ f)l"l'. 1989:26:63 ·74 .
CHAPTER
3
Assessment of the Skin and Wound Carrie Sussman
This chapler continues the methodology of the diagnostic process described in Chapter 1 with step II. the assessment and functional diagnosis of the wo und. Assessment is a process of assigning numbers or grades (0 events systematica lly. Tests arc the instruments or means by which events arc assessed or measured. Examination is the process of detennining the values of the lests. To evaluate something properly or acc urately, ski lis of evaluation are necessary. That is, a backgro und is required in selecting appropriate tests. understanding the significance of the lests and measurements, and kn ow-
two diagnoses- wound severity and biologic phase of wound hea ling. Additional examinations that are related to the wound etiology or coimpairmcnts are described in chapters re latcd to specific problems such as the chapters on noninvasive . vascular testing, management of exudate and infection, management of edema. and therapeutic posi tioning. During the initial assessmcnt, the clinician may find that data co llected triggc r concerns that require another opinion or a difTerent leve l of care. For example. the initial assessment may indicate that the patient is not a candidate for sharp debridement because of concerns about circulatory or med ical status. The nurse or physica l therapist communicates these findings to the referring physician. The term for this is prospecfil>e manogement, and physical therapists and nurses are clinicians who have the ability to do prospective management of wound cases. Utili za tio n manage ment beg ins at baseline and is really prospective management because it is manage ment of services to be de livered to the patient ahead of the actual delivery. Utili zation management continues with every follow-up reassessment. At the end of thi s chapter. referral criteria are discussed. Why li st referral criteria in a chapter on assessment? Utili zation management mandates that at the earliest possible time the patient be diagnosed, appropriate medically necessary services identified and proper referral made. Prospecti ve. appropriate utili zation management of health care services is critical under prospect ive payment and ca pitated delivery systems.
ing how to interpret th em. Both th e examination and th e
eva luation require specific skill s and understanding of the condition. how the information wi ll be used to recognize its importance and va lue. and how to coll ect it appro priately and in an organ ized manner. I Examination and performance of tests are wit hin the scope of practice of both physical therapist assistants and licensed practicaUvocational nurses; however, evaluation of the data is a skill that is the purview of licensed physical thera pists and registered nurses who have some knowledge of wound manage ment. Simple monitoring of tissue attributes can be performed by unskilled persons after instruction and then reported back to the professional. The purpose of this chapter is to instruct the clinician in the why, who. when, where. what, and how to assess wound attributes leading to a functional diagnosis. Accepted tenninology and the significance of each tissue attribute to be assessed are described and illustrated with color plates located in this book. Chapter 4 describes techniques for measurement of size and extent of woundin g. Chapter 5, Tools To Measure Wound Healing. teaches how to use two methods to assign numbers or grades to the attributes described in this chapter. Assessment of the wound and surrounding tissues through examination of various attributes provides data leading to
T HE ASSESSME 'T PROCESS Purpose a nd Freq uency
Wound assessment data are collected for three purposes: (I) to examine the severity of the lesion, (2) to determine the 49
50
WOlNIl CARl
phase of wound healing, and (3) to establi sh a baseline for
the wound and to report observed changes in the wound over
Clinical Wisdom: Monitoring Wound Progress
lime. Assessment data enable clinicians to communicate
clearly about a patient's wound provide for continuity in the pl an of care, and allow evaluat ion of treatment modalities.
Baseline assessment, monitoring. and reassessment arc the keys to establishing the plan of care and evaluating achievement of target outcomes and progress toward goals. Valid
significant tests and measurements should be selected for the assessment process. Usc the tests se lected initially and for each retest throughout the course of care to eva luate progress toward target ou tcomes and to revise the treatm ent plan as required.
Attributes are assessed at the initial or baseline examination and at regular intervals. usually week ly or at most biweekly. to measure progress or deterioration of the ulcer. Rcassessment is done to measure change in either the status of the ulcer or change in risk factors ' One study of stage III
and stage IV pressure ulcers found that the percentage reduction in the ulcer area afler 2 weeks of treatment was predictive of time to h eal. ~ Expect improved status in 2 to 4 weeks.' If the reassessment indicates that the wound has deteriorated or has failed to improve with appropriate treatment afler 2 to 4 weeks. the physician should be notified.
Monitoring is a means of check ing the wound frequently for signs and symptoms that may trigger a full reassessment ~ u c h as increased wound exudate or bruising of the adjacen t or peri wound skin. Monitoring includes gross eva luation for signs and symptoms of wound complications such as erythema (change in color) of peri wound skin and pus sec-
ondary to infection and progress toward wound healing, stich as granu lati on tissue growt h (red co lor) and reepithelialization (new skin). Less skill is required for monitoring than for assessment and may be performed by unskilled caregivers such as the palient's family or a nurse attendant. Monitoring ta kes place at dressing changes or other treatment application times. Different care settings will have different requirements and wi ll designate specific individuals to perform the assessment funct ion. For example. in the home setting the nurse or physical therapist may function as professional wound "case manager" who assesses the findings but they may instruct a nonprofessional caregiver in wound attributes to be monitored. The caregiver would gather the data at dressing changes and predetermined intervals and report changes to the professional wound case manager who would eva luate the results of the treatment plan. The professional wound case manager may see the patient's wound only intermittently for a complete reassessment. In a skilled nursing facility (SNF),
there are lIsually requirements by federal licensing agencies that prescribe interva ls for reassessment. If the patient is in an acute or subacute setting where there are very short lengths of stay, there may be on ly a single assessment.
Teach family and other caregivers to monitor the wound at each dressing change, looking for the following: signs of wound infection such as large amounts of purulent exudate (pus), peri wound erythema (reddish, purplish), warmth, increased tenderness or pain at the site or elevated temperature, and signs of healing characteristics (bright red color and new skin).
Attributes to Assess
Evaluation of the severity of the wound by obscnation of the depth of tissue destruction. tisslle response to injury. and signs of wound healing phase arc presented. These compo~ nellis are used to provide a wound severity diagnosis and wound healing phase diagnosis. Assessment of the wound is separate from the assessment of the etiology of the wound although the examinations chosen for the assessment may relate to or provide clues to the etiology. Wound etiologies are presented in Part III . For example. wounds with an etiology of venous insufficiency wi ll have characteristics of the adjacent and periwound skin that are differelll from those of a pressure ulcer. A patient with a diagnosis of diabetic ulcer and insensitivity will have distinctive adjacent skin and tissue characteristics. Therefore. soft tissues adjacent to the area of wounding should be assessed for attributes of sensation,
circulation, texture, and color. Findings of the adjacent soft tissues will be useful in determining medical necessity. establi shing a treatment plan. and predicting outcomes of care for the wound.Adjacellf refers to tissues extending away from the peri wound. Therefore. it is a good clinical practice 10 include examination of the adjacent skin characteristics as well as peri wound skin characteristics. Assessment encompasses a composite of characteristics. A single characteristic cannot provide the data necessary to determine the treatment plan nor will it allow for monitoring progress or degradation of the wound. The indexes for wound assessment include all of the following: location. size of the wound stage or depth of tissue involvement, presence of undermining or tunneling. presence or absence of tissue attributes not good ror healing (such as necrotic tissue in the wound and erythema of the peri wound tissue), and attributes good for wound healing such as cond ition of the wound edges, granu lation tissue. and epithelialization. For many clinicians, the wound exudate characteristics are also cssential indexes. There are IWO schools of thought regarding tissue assessment. One looks only at the wound tissue. The second examines both the wound tisslie and periwound skin and soft tissue structures. Because the peri wound skin is intimately in-
Assessmellf off/Ie Skill and I1huml
volved in the c ircu lato ry response to wo undin g as well as the risk for infeclio n, il is prudent 10 eva luate both areas. The exa minati on of til c wound and pcriwound skin providcs the data related to th e wound heal ing phase diagnosis desc ribed latcr in th is chapt cr. Wou nd severi ty attributes to assess include determination of tile tissue layers involved in the wound. Wounds that penet rate through more ti ssue layers are more seve re than those th at are less deep. This is th e wo und severity diagnosis. Depth of ti ssue invo lvemen t indicates the wound seve rity a nd has an impact on further wo und assess men t strategies and determinati on o f an approprialc treatment plan. For exam ple. a partia l-thickness wound would not be assessed for tunneling or undermin ing. II a lso has impact on prediction of ri sk for nonh ea ling and on re imbursemcnt . For exam ple. third-party paye rs kn ow lilat a stage IV pressure ul ccr requircs mo re care and a longe r leng th of stay th an a stage II pressure ul cer and th at thc ri sk of com pli ca tion s is g rea ter. The most co mmonly used method of diagnosing wou nd severity is with classification sys tems.
51
ably one of th e most wide ly known wo und classificat ion systems. T he stagi ng system is most onen applied to press ure ulcers, but it is used (sometimes inappropriately) to classify ot her types of wo unds as we ll. It is best lIsed for wo und s with a press ure or ti ss ue perfusion eti ologic fa ctor such as a rte ria l/ischemi c wo unds or diabet ic ne uropath ic ulce rs. The N PUA P and theAgency for Health Care Policy and Research (A HCPR) used the initial pressure ulcer stagi ng system proposed by Shea6 as a basis for recommending a un iversa l fOllrstage systcm for describing press ure ul cers by anatomi c depth a nd soft ti ssuc layers invo lved. The pressure ulcer sta ging system does not descri be the who le wo und and is limited to a desc ripti on of th e anatomi c ti ssue loss and is a diagnosis of seve rity of ti ssuc insult before hea lin g sta rts. The A I-I C PR adopted the NPUA P staging system for use in two sets o f c li nical practice guidelines. '·' ll is wi del y accepted und commonly uscd to com muni cate wound severity, to orga ni zc treatmcnt protocols. and as crite ri a for selectio n and re imburseIll CIll of treatment products for pressure ul cc rs. Table 3- 1 presents the stag ing c riteria for pressure ulcers.
\Vound Classification Systems Table 3-1 Pressure Ulcer Staging Criteria
Allhc prescnt tim e. a va ri ety of wound classification systems is used to describe wou nd seve rit y for different wo und etiol ogy. Allhough the classification systcms were dcsigned and researc hed wit h onc specific wou nd type. they are often (sometimes inappropriately) used for any wo und type. A lthough there are many wou nd c lassification syste ms. such as meth ods of classifyi ng surgica l wo unds and scvcri ty scoring of lower leg ulcers, four wo und c lassifica tion systems are presented in thi s chapter. The Nat ional Press ure Ulcer Advisory Panel (NPUAP) pressure ulcer stagi ng cri teria deve loped for lise wi th pressure ul cers, the Wagner staging system for grading seve rity of dysvasc ular ul ce rs, partialthickness/full -thi ckn ess sk in loss criteria. and Marion Laboratories red/yellowlblack color sys tem arc desc ribed and di scussed."5 The NPUA P pressure ul cer stagi ng systc m and the Wagner stagi ng syste m are c lass ifications based on ti sslie layers and depth of ti ssue destru cti on. The partial-thickness and full-thickness sk in loss classi fi cat ions are tissue layer desc riptions o f skin loss that a re also com monly used. The final method discussed groups wounds based on co lor of the ti ss ue. Marion Laboratori es, in Europe, deve lopcd a system that classifies the wound based on th e color of the wo und surface red. ye ll ow. or black. No wound c lassi fi ca ti on system when lIsed in isolati on is a n appropri ate meth od ofmcasuring wo und hea ling (sec Table 3- 5). NPUA P Pressure Ulcer Sfllgillg System
Classificatio n by stages is used to descr ibe the anatomic depth ofsofl ti ssue damage observed after the path ology has declared itsel f.' The pressure ulcer staging system is prob-
Stage
Definition
I·
Nonblanchable erythema of intact skin , the heralding lesion of skin ulceration. In individuals with darker skin , discoloration of the skin, warmth, edema, induration, or hardness may also be indicators.'
11
Partial-thickness skin loss involving epidermis and/or dermis. The ulcer is superficial and presents clinically as an abrasion, a blister, or a shallow crater.
III
Full-thickness skin loss involving damage or necrosis of subcutaneous tissue that may extend down to, but not through, undertying fascia. The ulcer presents clinically as a deep crater with or without undermining of adjacent tissue.
IV
Full-thickness skin loss with extensive destruction, tissue necrosis or damage to muscle, bone, or supporting structures (eg, tendon , joint capsule).
"In 1997 the NPUAP proposed a new definition of stage I pressure ulcers to reflect better the ethnic diversity of persons With pressure ulcers. The new definition under review is as follows : ~an observable pressure related alter· ation of intact skin whose indicators as compared to an adjacent or OPPOSite area on the body may include changes in skin color (red. blue. purple tones). skin temperature (warmth or coolness), skIn stiffness (hardness. edema) andl or sensation (pain). "!ltPlIlSource: Reprinted with permiSSion from Pressure Ulcer Staging Criteria from Pressure Ulcers: Prevalence, Cost. and Risk Assessment, Consensus Developmenl Conference Statement. 0 1989. National Pres· sure Ulcer Advisory Panel.
52
WOUND CARE
Clinical Wi sdom: Reverse Staging or Back Staging of Pressure Ulcers Once the ulcer is staged, that remains the stage and wound severity diagnosis. Correct terminology is healing stage II, III, or IV.
The pressure ulcer staging system is not an ideal system.
It has many problems. Staging systems measure only one characteristic of the wound and should not be viewed as a comp lete assessment independent of other indicators. Staging classification systems do not assess for criteria in the healing process and hinder tracking of progress because of the inability of the staging system to demonstrate change over tim e. The definition of a stage I pressure ulcer does not account for the severity of soft tissue trauma beneath the unbroken skin such as is seen with purple stage I ulcers.
Stage I lesions vary in presentation and pose validity concerns. Some stage I lesions may be the indicator of deep
tissue damage just beginning to manifest on the skin, and others may indicate only superficial insult where damage is somewhat reversible and not indicative of underlying tissue
death. There are problems with the reliability of assessment of stage I ulcers in dark-skinned patients. In fact, in 1997 the NPUAP proposed a new definition of Stage I pressure ulcers to renecl better the ethnic diversity of persons with pres-
sure ulcers (see footnote to Table 3- 1). Identification and meaningful interpretation of skin color changes in darkly pigmented skin requires special assessment strategies. These strategies arc described in the sect ion on assessment of the peri wound and wound tissues. Stage II pressure ulcers are lesions that are not necessarily caused by pressure and are more likely due to shearing. friction , or incontinence. The latter should be distinguished
and treated in a different manner than pressure ulcers. Theoretically, pressure ulcer trauma starts at the bony tissue interface and works outward, eventually manifesting damage at
the skin. However, stage II lesions are usually caused by fricti on or shearing of the tissues, causing superficial and par-
tial-thickness damage to the epidermis and dermis. Stage II lesions start at the epidermis or skin and may progress to
deeper layers. Staging of pressure ulcers covered by eschar and necrotic tissue cannot be accomplished until removal of necrotic tis-
sue allows determination of the extent of depth of tissue involvement. Pressure ulcers with necrotic tissue filling the
meaningful communication is difficult, as clinicians may not have the experience necessary to recognize the various tissue layers that identify the stage or grade. In addition, clinicians may be defining stages difTerently. Slaging requires practice and a certain amount of skill that develops with time spent examining wounds Unfortunately, the staging system has been misinterpreted and applied in clinical practice as a way to monitor healing.
It was not designed to do this. Biologically wounds do not heal in the manner suggested by reversing the staging system. For example, a stage IV pressure ulcer cannot "heal" and become a stage " pressure ulcer. taging pressure ulcers is lIsed to document the maximum analOmic depth of tissue involved after all necrotic tissue is removed. Staging of pressure ulcers is a diagnostic tool useful to determine the extent of tissue damage only. Staging is a diagnostic tool to aid examination of the wounding severity and not wound healillg. Elimination of reverse staging has left a void in the
system to report and document wound healing quickly and efficiently. The situation has been complicated because ofa
reporting system developed by the Health Care Financing Administration (HCFA) that requires that providers must continue to reverse stage in order to stay in compliance with
HCFA regulations. Specifically. the Minimum Data Set (MDS) developed by HCFA relies on the reverse staging of wounds, both pressure ulcers and ve nous ulcers, to demonstrate progress ofa wound toward healing. This has created a dilemma for the conscientious practitioner. One pragmatic suggestion is to stage for the wound severity at baseline and then on subsequent reassessment report with decreasing
stages as the wound shows attributes of healing (eg, initial stage IV wound has bad-for-healing attributes of eschar, slough, and exposure of tendon. muscle. or bone indicators
progressing to a stage III wound with presence of some goodfor-healing attributes: absence of necrosis and presence of granulation tissue to a stage II recpithelialization beginning
and stage I healed).' While this is a misuse of the staging system, it does have some merit, and until there is broad
acceptance ofa research-based tool to monitor healing and a change in the government reporting system, this may be the
only route open to the thoughtfu l clinician. The MDS documenting system can be supported by using the Pressure Sore Status Tool, or the Sussman Wound Healing Tool, which are research-based tools for monitoring wound healing attributes.
The tools are presented in Chapter 5. Wagller Ufeer Grade Clas.' ijieulioll
wound bed are full-thickness wounds or stage III or stage IV
Thc Wagner Ulcer Grade Classification system is used to
wounds. The clinician cannot determine the level of tissue insult until th e necrotic debris is removed. Another di fTiculty with staging occurs with patients with supportive devices
establish the presence of depth and infection in a wound.
because of the difficulty in accurately assessing the wound without removal of the supportive device. Finally. accurate,
The Wagner grading system was developed for the diagnosis and treatment of the dysvascular foot .' It is common ly used as an assessment instrument in the evaluation of diabetic foot ulcers. It is useful for both neuropathic and artc-
Assessmel1l of the Ski" (Jl1l/ lffJII"d
rial/ischemic ulcer classification. There are six grades progressing from 0 to 5 in order or seve rit y. Table 3- 2 presents the Wagner grading criteria and Figure 3 I shows how the natural history ofbreakdowll in the diabetic, neuropathi c foot corresponds to the Wagner 0 to 5 classification. The 0 classificatioll evaluates for predisposing ractors leading to breakdown and, a long with grades I 10 3, is used for risk managemelll as described in Chapter 15 .
Table 3-2 Wagner Ulcer Grade Classification Grade
Characteristics
o
Preulcerative lesions; healed ulcers; presence of bony deformity Superficial ulcer without subcutaneous tissue involvement
2
Penetration through the subcutaneous tissue; may expose bone, tendon, ligament, or joint capsule
3
Osteitis, abscess or osteomyelitis
4
Gangrene of digit
5
Gangrene of the foot requiring disarticulation
Source: Reprinted With permiSSion from F.E.W. Wagner. The dysvascular foot a system for diagnosis and treatmenl.Foot and Ankle. 2:64-122. 0 1981 . WilUams & Wilkins.
53
CllISSijiClllioll by ThiL'klless of S kill Loss Classification by thickness of skin 1055, parlial- or I'ullthi ckness skin loss. is another classification sys telll and is cOlllmonly used for wounds whose etio logy is ot her than pressure wounds such as skin lears, donor si te s. vascu la r ulcers (venous ulcers in particular), surgical wounds, and burns. Wound thickness refers to partial-thickness or full-thickness loss of the skin with or without penetration into subcu taneous tissue and deeper structures. Partial-thickness wounds extend through the first layer of the skin or epidermi s, and il1lo. but not through. the seco nd layer of th e skin or dermi s. Full-thickness wou nds extend through the epidermis. the dermi s, and beyond. Full-thickness wounds may be further ca tegorized accordi ng 10 dcpth of involvemcn t by using the term slIbclIIlIlleolis tisslle wOUl1ds. Subcut aneolls ti ss ue wounds extend into or through subcutaneous ti ssues and may extend into muscles. tendons, and possibly down to th e bone. Depth of injury classi fication identifies the speci fie anatomic level of tissues involved but does not report their condition or color. Anatomic deplh is predictive of healing.uo Partia l-thick. ness wounds heal by epithe lializ.1Iion and heal faster th an full-thickness and subcutaneous wounds. Full-th ick ness and subcll taneous wounds heal by secondary intention, whic h is a comb ination of f ibroplasia or granulation tissue formation and con traction. Table 3- 3 provides the definitions of partia l- and full-thickness skin loss.
Figure 3- 1 Diabetic neuropathic progression of foot breakdown. Courtesy of William Wagner. MD.
54
WOUND
CARe
Table 3-3 Partial-Thickness and Full-Thickness Skin Loss
Definition
Thickness of Skin Loss
Clinical Examples
Partial-thickness skin loss
Extends through the epidermis, into but not through the dermis
Skin tears, abrasions, tape damage, blisters, perineal dermatitis from incontinence; heal by epidermal resurfacing or epithelialization
Full-thickness skin loss
Extends through the epidermis and the dermis, extending into subcutaneous fat and deeper structures
Donor sites, venous ulcers, surgical wounds; heal by granulation tissue formation and contraction
Subcutaneous tissue wounds
Additional classification level for fullthickness wounds, extending into or beyond the subcutaneous tissue
Surgical wounds, arterial/ischemic wounds; heal by granulation tissue lormation and contraction
Mario" Laboratories Red, J'ellow, BIOl:k ,roulld Classificatioll Classification by color is a popular system because of the simplicity of the concept and th e ease of use of the system. A three-color concept, red, ye llow, or black, is used for assessing the wound surface color. II The three-color system was originally conceived as a tool to direct treatment , with each color corresponding to specific therapy needs. The red
wound is clean, healing, and granulating. Yellow signals possible infection, need for cleaning or debridement, or the presence of necrotic tissue. Finally, the black wound is necrotic and needs cleaning and debridement. Red is considered most desired, yellow less desirable, and black least desirable. I f all three types are present, select the least desirable as the ba sis for treatment. Table 3-4 shows the red, yellow, and black
classification system with clinical manifestations. The four wound classification systems discussed in this section and the type of wound most appropriate for use with each sys tem are presented in Table 3- 5. Wound Severity Diagnosis
Nurses use nursing diagnoses to classify skin and tissue impairments and assist with developing care plans for wound care patients. Nursing diagnoses are expressed as specific diagnostic statements, which include the diagnostic category and the related to stem statement. Impaired (issue iJlfegrity is the broad diagnosis and would be correctly applied to stage III and stage I V pre ssure ulcers, for example. Impaired skill iJlfegri(y is a subcategory and correctly applies to partialthi ckness or full- thi ckness loss of sk in . Impaired skill illtegrity should not be used for surgical incisions or deep ti ssue wounds. The diagnosis risk for infection related to surgical incision is more appropriate because of the di sruption of the
ski n during surgery, making it more vulnerable to infection.
Table 3-4 Red, Yellow, and Black Wound Classification System Color Red Yellow Black
Indication Clean; healing; granulation Possible infection; needs cleaning; necrotic Needs cleaning; necrotic
Source: Data from J.Z . Cunell, The New RYB Color Code, American Journal of Nursing, Vol. 88, pp. 1342-1346, C 1988, American Nurses Association and NA Stotts, Seeing Red & Yellow & Black, The Three Color Concept of Wound Care, Nursing, Vol. 2, pp. 59-61. 0 1990. SpnnghOuse Corporation .
The related to stem statements aid in communicating with other hea lth care professionals and in planning care by targeting the defining characteristics for the diagnostic statement. For example, the diagnosis statement impaired skill illtegrity would be followed by a re lated to stem statement such as impaired skill i11legrity related to frictioll (llld moislUre fivm urillGlY illcolJlinence. For nurses, the related to stem
statement usuall y reflects etiologic factors in wound development and directs the plan of care and specific interven-
tions.12 Physical therapist s will also use a wound severity diagnosis that relates to depth of penetration of wounding. The wound diagnosis statement wi ll have a stem statement impaired ilJlegumentGlY ;11Iegri!y secolldwy 10 - . The ending part of the statement will include the depth of ski n involvement. End statements read superficial ski" ;nvolveme11l or partial-thickness skill illvolvemelltalld scarformation, full-thickness ski" involvemellt and scar formatioll, or involvement extending ;1110 fascia, muscle. or bOlle. A total statement would read impaired illlegumelltmy i11legr"ty secondmy to partial-thickness skill involvemelll and scar formation. Il The statement refers to the functional impairment
Assessmellf o/the Skin alld Wound
55
Table 3-5 Wound Classification Systems and Wound Types Wound Classification Systems
NPUAP pressure ulcer stages
Pressure Ulcers
Venous Ulcers
X
Arterial, Ischemic Ulcers X (Those with pressure component)
Wagner grades
Diabetic Ulcers (Neuropathic) X (Those with pressure component)
X
X
X
Other Wounds
Stage II classification will be appropriate for skin tears and tape damage.
Depth of skin loss (partialthickness to full-thickness skin loss)
X If the wound is full thickness, it requires examination of level of deep tissue involvement.
X If the wound is full thickness, it requires examination of level of deep tissue involvement.
X If the wound is fu ll thickness, it requires examination of level of deep tissue involvement.
X If the wound is full thickness, it requires examination of level of deep tissue involvement.
Useful for skin tears, burns, and other skin wounds. If the wound is full thickness, it requires examination of level of deep tissue involvement.
Marion Laboratories red, yellow, and black system
X
X
X
X
Surgical wound is healing by secondary intention.
of the integument and different ti ssues. which has implications for fu nctional impairmelll and disability. Physical therapists use the severity diagnosis to se lect examinations. plan treatment. and predict functional outcomes. Diagnosis statements for bOlh nurses and physical therapists arc similar. Both usc impairmcnt diagnoses that affect function of the involvcd tissues.
tu s. Two tools, th e Pressure Sore Status Too l (PSST) and the Sussman Wound Hea lingTool (SWHT), can bc used to record the findings and to measure each attribu te objectively. Both are described, with forms and instruction provided in Chapter 5. Useful forms for assessment oftissllc wi ll usually include the following items:
• Peri wound skin attributes ASSESSMENT OF WOUND STATUS
• Wound tissue attributes • Wound exudate characteristics
Data Coll ec tion and Documentation Forms Information collection is easier. beller organized. and more consis tent when a form is used as a collection instrument. Forms may be paper-and-pencil instruments or templates on the computer screen. There are many forms bcing used, with the most common being thc skin care now shect used by Illirses. Mcthods of recordi ng assessment data should allow for tracking of each assessment item over tim e in objective and measurable terms that show changes in the wound sta-
Regardless of which instrument is used 10 collect findings. all attributes on the form should be considercd. I f the attribute is not applicable the notation N/A shou ld fill the blank. Ifan attribute is absent, record a O. If present, a grade or check is required. Leaving a blank space on the form impIies the attribute was not considered or assessed. If th e patient 's medical diagnosis suggests possible related impairments associated with th e wound and peri wound sk in (eg. neuropathy or vascular disease), multiple form s may be
56
WOUND
CA.'
req uired to report all the necessary elements that relate to
th e patient's condi ti on. Chapter 6, Noninvasive VascularTcsti ng. and Chapter 15. Management of Ihe Neuropathic Fool. have sample fOfms specific to recording data related to those problems. Documentation requ irements for wound assessment should be part of the facility policies and procedures. Documentation should be accurate and shou ld clearly reOect the patient's condit ion. the examinations performed, the find ings, the care rendered, and proper notification of the physician of sign ificant findings. Documentation of similar findings by practi-
tioners in the same department or facility should be consistent and reflect the facility policics. I " Remember that some
day. maybe 5 years from the time of initial assessment, the medical records may be subpoenaed into court. "Documentation can be either your shield against a potentia l malpractice lawsui t or the sword that strikes you down."I-lIfl401
Case Study: Dangers of Differing Clinical Procedure and Facility Policy A physical therapist (PT) debrided a toenail on a patient with a medical history of neuropathy associated with diabetes. The toe went on to become infected. leading to below-the-knee amputation of the leg. The PTs action was called into question in a malpractice lawsuit. The debridement procedure followed by the PT was acceptable and documented. but it was the facility policy to have a patient with diabetic neuropathy evaluated in the vascular laboratory for transcutaneous oxygen levels before debridement. The PT did not document anything about evaluating the patient for circulatory status prior to performing the procedure. The case is pending.
Observation and Palpation Techniq ues
Observation and palpHtion are classic components ofphysical diagnosis used to determine alteration in soft tisslie characteristics. including the skin. subcutaneous fascia, and muscles leading to a son tissue or structural diagno s is. '~ Proper lightin g and positioning of the patient and tissue to be assessed wilJ improve observation. Begin the examination of tisslies by eva luating for symmelry with th e opposi te side of th e body and adjacent Slruetures by both observation and palpation. Look for consistency of symmetry of tissues in color. texture. contour, hardness/softness. temperature that represent changes in the attributes of the skin, subcutaneous tissue, fascia. and muscle compared with an area of normal sk in and soft tissue.
Palpation requires the use of the hands as important sensitive diagnostic inslruments. The hands shou ld be clean and the fingernails of appropriate length. It is important for the clinician to development a palpatory sense in the hands. For example. difTerent pans of the hands are valuable for difTeren t tests. The back of the hand is more sensitive to temperature. the palms of the hands are best used to detect changes in tissue contours (induration. edema). and the fingerpads are more sensi tive to texture (fibrotic tissues) and fine discrimination. The thumbs are useFul to apply pressure to check for hardness or so ftness at different tissue depths. Techniques of palpation include the usc of slow. light movements. Avoid pressing too hard and trying to cover the area of examination too quickly. This will provide confusing messages to the sensory receptors of the examiner's hands. Palpation skills require practice to refine the practitioner'S palpatory sensc. The first requiremcnt is for the examiner to reduce other sensory inputs in the environment (noise. traffic, conversation) so as to concentrate and focus on the palpation examination. The ncxt requirement is a coml11OI1 language to communicate the findings, in easi ly understood terms. Paired descriptors such as superficial-deep. moist-dry. warm-cold, painful-non painful, rough-smooth. hard-soft. thick-thin are useful. The state of ti ssue changes can be reported as acute. subacute. chronic, or absent. They can also be graded on a scale of 0 to 3+ as a way of diagnosi ng the severity of the problem. A familiar example of thi s type of grading system is pitting edema; another is pulse strength. The use of this type of grading system is also helpful in reporting response to treatment intervention.
Clinical Wisdom: Four Requirements for Palpatory Examination 1. 2. 3. 4.
Concentration Language to communicate findings Light pressure Slow movement
Assess ment of Adjacent Tissues The ti ssues adjacent to and surrounding a closed or open wound provide many clues that identify the health of the skin. the phase of wound healing, and the patient's overall health stat us. For clarity. the term atijacelll is lIsed to separate tile tissues that may not show signs of wounding but that arc predictive ofhca ling from the tissucs immcdiately surrounding the wounded tissue. referred to as periwound skin. Skin or trophic changes arc important predictors of the body's ability to respond to wounding. The attributes of the adja-
Assessmelll oJlh e Skill alld Wound
cent ti ssues th at should be assessed are described in the following sections including: • • • •
Anatomy of the skin Skin texture (eg, dryness, thickness, turgor) Scar ti ssue Callus
• Maceration • Edema • Color • Sensation (pain, th ermal, touch, protective)
about 0.5 mOl thick (Figu re 3- 2). Each of the primary layers is stratified into severa l layers. The dermis is the true skin. It is tough, flexible, and elastic. The thickness of the skin varies from extremely thin over the eyelids to one third of an inch thick over the palms of the hands and sales of the feet.
The epidermis is avascular, whereas the dermis is we ll vascu larized and contains the lymphatics, epithelial cells, connective tissue. musc le, fat , and nerve ti ssue. The vascular supply of the dermis is responsible for nourishing the epidermis and regulating body temperature. The we ll- vascu larized dermis will withstand press ure for longer periods
of time than wi ll subcutaneous tissue or muscle. The col-
• Temperature • Hair distribution
• Toenails • Blisters Allutomy o[tll . Skill
The skin is composed of two primary layers: the epidermis, which is about 0.04 111111 thick, and th e dermis, which is
OpenIngs ot sweat ducls
lagen in the dermis gives the skin its toughness. Hair fo llicles and sebaceous and sweat glands, located in the dermis, contribute epithelial cells for rapid rcepithelialization of partial-thickness wounds. The sebaceous gla nds are responsible for secretions that lubricate the skin and keep it soft and flexible. They are most numerous in the face, and sparse in the palms of the hands and sales of the feet. The sweat gland secretions control skin pH to prevent derma l
Hair shaft Dermal papilla
Sensory nerve ending lor touch
Stratum corneum
Pigmenllayer
l
EPIDERMIS
S',,"um
Stratum germlnatJVum
57
splnosum Stratum basale
Sebaceous (011) gland
II
Hair follicle Aneclor muscle
Paclnlan corpuscle
DERMIS
I
J
Papilla 01flair
Sweat gland SUBCUTANEOUS FATTY TISSUE
Blood vessels ------l~.,
Figure 3- 2 Anatomy o f Lhc skin . Courtesy of Kn oll Pharmaceutical s. Mount Olive. New Jersey.
58
WOUND CARE
infections. They are numerous in the soles of the feet and palms of the hands. The three togeth er are referred to as dermal appendages. The sweat glands, dermal blood vesse ls, and small mu scles in the skin (responsible for goose pimples) control tempera ture on the surface of the body. The nerve endings in th e skin inc lude receptors for pain, touch, heat, and col d. Loss of the nerve endings in the skin increases risk for sk in breakdown by decreasing the tolerance of the tissues to external forces. Nails are a lso considered as appendages of the skin. The deep or reticular layer of the dermis consists of fibroelastic conn ecti ve tissue that is ye ll ow and composed mainly of coll agen. Fibroblasts are present in thi s ti ssue layer. The deep layer of the dermis merges with the subcuta neous fat and fascia and may be confused with yellow slough, but it shou ld be eva luated for texture and vita lity. A healthy reticular layer will be adhered and firm, not soft, mushy, or stringy like slough. Often g ranulati on buds are seen protruding through the mesh of the reticular layer. Color Plate 17 shows the reticular layer of the dermis with the red granu lation buds poking through the mesh layer in a partial-thi ckness wound. Skin color varies greatly in humans. but the structure and th e ski n arc ve ry similar. Melanin produced from melanocytes account for th e varia ti on in pigmentation from very
light to extreme ly dark. Numbers ofmelanocytes in dark and light skin arc similar, bur the size and activi ty of the melanocytes are greater in black skin th an in li ght skin. The melanin pigmentation is concentrated in the stratum corneum layer in a dark horny layer that can be wiped off when washin g clean, black sk in. Of course, this docs not mean that all the color is removed, just th e superficial layer. The thickness of th e stratum corneum in both dark and light skin is the same, but the cell s in dark ski n are morc compact with morc cell layers. For thi s reason, dark skin is more resistant to external irrita nts. Healthy dark skin is usually smooth and dry. Dry dark sk in may have an ashen appearance. 16
Clini cal Wisdom: Care of Darkly Pigmented Skin Care of darkly pigmented skin requires keeping the skin lubricated. Petrolatum, lanolin-based lotions, and sparing use of soaps are recommended. 16
loss of turgor. The areas most affected by loss of subcutaneous fat are the upper and lower extremities. This thinning of subcutaneous fat resu lts in more prominent bony protuberances on the hips, knees, ankles, and bony areas of the feet with a higher risk of pressure ulcer formation . Elderly skin also experiences a loss of elasticity due to shrinkage of both collagen and elastin. There is a weakening of the juncture between the epidermis and dermi s. making the skin layers "slide" across each other and placing the person at ri sk for skin tears. Sebaceous glands and their secretions are diminished, resulting in skin that is dry. often itchy, and easily tom." Impaired circu lation also contributes to changes in the skin; it is usually associated with aging but may be due to a disease process such as neuropathy associated with diabetes. Neuropathy impairs the secretion of swea t and sebaceous glands. Death of sweat and sebaceo us glands co ntributes to slow resurfacing of partial-thickness dermal ulcers. Loss of sweat changes the pH of the skin. making it marc sllsceptibl e to infection and bacterial penetration . To assess skin texture the clinician uses observation and palpation . Observe the skin , looking for evidence of dryness such as flaking or sca ling. To check skin turgor, gently pick up the tissues with thumb and forefinger and observe how th e ti ssllcs respond. For example. in oldcr patients loss of elasticity may be exhibited by the ti ssues' slow rerurn to normal after pinching. In older patients it is best to check for general skin turgor on the forehead or sternal area. Palpate by gently rubbing your fingers across the patienrs skin and feel for sliding of the epidermis away from the dermis.
Clinical Wisdom: Skin Texture Assessment
Observe skin for moisture content; look for evidence of dryness such as flaking , scaling, and excoriations (linear scratches). Palpate the skin to assess turgor; gently grasp the tissues between thumb and forefinger and observe for any delay in the tissues' return to normal position . Finally. rub your fingers across the patient's skin and feel the sliding of the epidermis from the dermis due to weakened epidermal-dermal juncture.
Scar Tissue Skill Textu re Smooth, flexible skin has a feeling of fullness and resistance to ti ssue deformation that is called turgor. Turgor is a sign of ski n heallh. Aging sk in often shows signs of dryness due to atrop hy and thinning of both the epithelia l and fatty layers of tissue in the dermis. The feel of the skin renects a
Inspection of the adjacen t skin should include checking for scar tissue. Check scar for smoothness, ncxibility, thickness, and toughness. Scar tissue that is mature has greater density and toughness and is less resilient than surrounding sk in. New scar tisslie is thinner and more nexible than mature scar and is less resilient to stress. Wounding in an area of scarring will have less ten si le strength when healed than a
Assessment oJthe Skill alld "'ouml
new wound and will be more likely to break down (see Color
Plate 37).
New scar tissue will be bright pink. As the scar tissue matures it will become nearly the same color as the periwollnd skin except in persons with darkly pigmented skin . Hypopigment3tion frequently follows injuries to dark skin. Loss of skin color may create more anxiety for the individual than the wound itself. If the wounding disruption is less than full-thickness loss of the epidermis. rcpigmcnt3tion wi Ilusually occur over lime. However, new skin covering deeper lesions and new lesions will appear pink. IS The area of scar
59
imbalance and subsequent uneven weight distribution along the metatarsal heads resulting in callus formation in those areas. The location of the callus is a clue to the underlying bony pathologic condition.'" Untreated. the ca l lus buildup will continue creating additional shear forces between the bony prominence and so ft ti ssues, resulting in breakdown of the interposing soft tissues. Hemorrhaging seen on a callus indicates probable ulceration beneath. Callus is an indicator of need for further assessment of the foot. Chapter 15 contains more information about callus management, and pictures of ca ll us.
may even turn white. Hypopigmented areas are morc susceptible to sunburn than arc normally pigmented areas. For some individuals. burns and physical trauma may be followed by locali zed areas of hyperpigmentation . Like hypopigmention. hyperpigmcnt3tion leads to anxiety for many individuals. Observe for abnormal sca rring characteristics. Hypertrophic scarring results from excessive collagen deposition , causing a very thick scar mass that remains within the area of the original wound. These scars are ugly and disfiguring and may be bothered by itching or pain that may interfere with functional mobility. The scars are differentiated from keloid scars, which are also thickened scars , but ke loid scars extend beyond the boundaries of the original woulld. 19 Although keloids arc known in persons of all races, scarring is of special concern to persons of the Negro race and some Asians as opposed to other dark-skinned individuals because of frcquency of keloid formation in this popUlation. thus suggesting a genetic factor. Frequency of occurrence is equal among men and women. Keloids are like benign rumor growths. Ke loids continue to grow long afier the wound is closed and may reach large size. Any attempt to cut or use dermabrasion to buffaway the keloid will only result in even more scarring. IS The mechanism of collagen deposition is totally out of control. Areas with keloids may be itchy and may be tender or painful. 16 New therapies are being used to contro l this phenomenon, but if a patient reports having had this problem or reports a familial tendency to form keloids, special attention should be made to address this problem at the time of initial assessment. Hyperkerototic scarring is hypertrophy of the horny layer of the epidermis. It is commonly seen in diabetic patients and may be located in adjacent and periwound tissue (see ColoI' Plate 24).
ClllIllS The most commonly encountered calluses occur on the plantar surface of the foot. They are usually found along the media l side of the great toe, over the metatarsal heads, and around the heel margin. Callus fonnation is a protective function of the skin to shearing forces ofa prominent bone against an unyielding shoe surface. Neuropathy often leads to muscle
Clinic al Wisdom: Observation and Palpation of Cal/us The callus will appear as a thickened area on the sole of the foot and it will usually be lighter in color (often yellow) when compared with the adjacent areas. When palpated, the callus area will feel firm or hard to the touch. There may also be some scaling or flaking, roughness, or cracking of the callus. Cracked callus is a portal for infection . Further examination is recommended.
~lacerll lio ll
Maceration is defined as "the softening ora tissue by soaking unt il the connective tissue fibers are so dissolved that the tissue components can be teased apart."17I PI·Ut l Macerated skin is drained of its pigment and has a white appearance and a very soft, sometimes soggy, texture (see Color Plate 15). The kin is often described as being wrink led l ike a prune. A familiar example is di shpan hands. Softened tissue is easily traumatized by pressure and is a contribu ting factor in the development of pressure ulcers. 17 The source of moisture that soaks and macerates the skin may be perspiration, soaking in a tub. wound exudate. or incontinence, as well as from wound dressing products. Macerated skin wi ll be thinner than adjacent skin. Palpate very gently so as to avoid trauma. Protect from pressure and shear. Edemll Presence of edema may be associated with the inflammatory phase. the re sult of dependency of a Ii Illb or an indication of circulatory impairment or congestive heart failure . Edema is defined as nuid excess in the ti ssues due to overload of interstitial or intracellular Ouici, causing congestion. A consequence of trauma is increased extrace ll ular fluids in the tissues that both blocks the lymphatic sys tem and causes increased capillary permeability. The function of edema fo llowing injury is to block the spread of infection. The resu lt
60
W OUND CARE
is a swe ll ing that is hard, and the app lication of pressure to
lhe swollen area docs not distort the tissues. The term "brawny edema" refers to this type of swelling and is assoc iated with
the inflammatory phase. Traumatic edema is usually accompanied by pain. Swe lling rcsulting from lymphedema or from systemic causes is usually painlcss, 21
There are two types of edcm3- nonpitting and pitting. Nonp itting ede ma is identi fied by skin that is stretc hed and shiny, with hardness of underlying ti ssues. Pitting edema is identified by firml y pressing a fin ge r dow n into the ti ssues and waiting 5 seconds. When pressure is released, if ti ssues fail to resume th e previo us position and an indent ati on re-
mains, there is pitting edema. Pitting edema is observed when there is ti ssue congesti on associated with congesti ve heart
by usi ng wate r di splacement. This is a qui ck and accurate meas urement using a vo lumometer fill ed with wat er. Vo lumometers are made o f a heavy Lucite and come in diffe rent sizes for immersion of a foot and ankle, leg above the knee. and the hand (see Figure 3- 3). They are strong and durable. Both methods work best when edema in a limb is being measured. A simple form , such as Ex hibit 3- 1, either handwritten or preprinted, listing the measurements of both limbs side by side is a useful guide for consistency and completeness of the measurements and to make compari son between baseline and retest measurements qui ck and easy. Change in edema measurements is one way to assess the treatm ent outcomes. The procedure for girth measurements is as follows:
failure, venous insuffic iency. and lymphedema, or dependency ofa limb. It is meas ured on a severity scal e of 0 to 3+, whe re 0 = no t present , 1+= minimal, 2+ = mode rate, and 3+ = severe. Eva lua te for body symm etry wh en examining for edema and also refer to the patient's medical history. Bilateral edema of the lower extre mities can be a sign of a systemic problem such as congesti ve heart failure, cirrhos is, ma lnutrition, or obcsit y or may be caused by depe ndcncy or usc of ce rtain drugs. Drug-induced edema is often pitting edema and may be caused by hormonal drugs, incl uding corti costeroids. estrogcns, progestcrones. and testosterone. Other drugs to consider include nonsteroidal ant inflammatory and antihypertensive drugs. Symptoms usually resolve i f the drug is withdrawn .:!1 Systemic edema may extend from th e lower ex tremiti es up into the abdomen. Unilateral edema of the lower extremity of suddcn onselmay be due to acute deep vein thromboph lebitis and requires immedia te refe rral to th e phys ician. Other cau ses of unilatera l edema are chronic venous insufficien cy, lymph edema, ce lluliti s, abscess , osteo mye liti s, C ha rco t's j o int , po plitea l a ne ur ys m, de pe nd e ncy, and revasc ul ari za ion. Deep vei n thrombophlebiti s, chro ni c venous insufficiency, and lymphedema are th e three most common callses.21 I fin doubt about th e eti ology of th e edema, co nsult with the physic ian before planning furth er testing or an interventi on. If edcma is left in th c ti ssue th e large-protein molecul es will cl og th e lymphatic channels and cause fibrosis. Chapter 9. Ma nagc ment of Edema, descri bes the management of eden1a with compression. IWellSllrelltelll of El/eIlt U. Ti ssue volume increases when edema is present. Edema ca n be evaluated by palpation for change in COlllour of th e ti ssues and by pholOgraphs. Two meth ods used for measurement of th e ex tent of edema formation are girth and volume. Girth measure ment or the limb is th e mosl common meth od used in clinica l practice becau se it is simple to perform . Although limbs are mos t casily measured, th e torso can also be assessed for edema by taking gi rth measurements. Volumetri c measurement is made
I. Mark and record the bony landmark s on the limb to guide th e measurements, includin g the metatarsa l heads, both ma lleoli, 3 cm above the lateral malleolus, 12 Col above th e lateral ma lleolus, 18 cm above the lateral ma lleolus. and th e lowe r edge of the patella. 2. Use a fl ex ible tape measure to measure th e circumference around th ese landmark s. 3. Measure both limbs. 4. Record measurements (for both limbs) side by side. Repeat at nex t assessment. Compare.
Figure 3- 3 Vo lum etric Edema Measuremenl. Source: Reprinted wi th permission frolll G.M. Pennington, D.L. Danl ey, and M.H. Sumko . Pul sed. Non-Thermal, High-Frequency Elec tromagnetic Energy (DI APULSE) in the Trea tment of Grade I and Grade II Ankle Sprains, Military Medicine: The O.Dicial JOll rnal ofAMSOS. Vo l. 158. No. 2, p. 102. 1993, Associa tio n of Milia ry Surgeons of the United States.
.h.H.',\'.\'11/(11II (~rtlte St.ill
E,hibit 3-1 Lo\\cr h.lrcmlly Girth
Mca~lIrements
umllHnmd
61
Form
Dale
-
-
Righi
Len
Righi
Len
Righi
I ell
MclnlJrsI"I"IIi('/WIl flild !In·· Rock\illc. MD .i\g..:nc) rur Ikallh ("MC I'oli!.:)' and Rc· cte\ Illellllu .... In : Le\'lll Mr.. O'Neal LW. Bo\\k..:r JII . cd\ Til(' Dlt/hel/{ fiml ;th cd, SI I.\lUl ". \10: I\1m,by 'IC;lr BI)(II.. . 1993 :225
26.
MI Jlillhogclle~l\ amlmanagemenl of d ... hctle fool lesion" In L~\lI1MI.O·Neall\\.BO\\l..erJII.ed ... ]1,,'Oillhl'fi('/-imt 5th ed, SI L.Otl\\. "10: Mosby Ye;lr Buol..; 1991:I!\ llIlu.11 Wound Management Work0.2 em. Mea,ure Ihe deplh of fullthickness \\.:ounds of greater than 0.2 em depth. When a wound is undergoing debridement of nonvlUble tissue. the wound depth usually increase~; but then a~ the wound bed fills with granulation tissllc. the depth decreases. Reduction in wound depth IS a measurement of progression through the proliferation phase of healing. Measurement of wound volume is difficult and is usually reservcd for rescarch . T".."o mcthods ha\e been reportcd. One method involves filling the wound with a measured amount of normal saline from a syringe. This wo rk s best for wounds that can be positioned hori/onH.llly so liquid doesn"t spill OUI. Anolhcr mel hod is Ihe use of JeIl"'le, an alginale hydrocolloid used by denliSis. II has been rcponed Ihal by pouring the rapidly selling plastic into the wound a mold of the wound can be made. Jell",le is reponed 10 be well loleraled by Ihe wound tisslle." Regardless of \\hlch method of measuring wound volullle is used there will be significant inac.:cura-
Wound A1easilreme11fs
cics. Is it necessary to measure wound volume? At this time, thcrc is qucstionablc value to thc taking ofvolumc measurements. Use of this paramc ter ofmcasurcmcllt appea rs 10 be of most concern in the research arena and should not be of concern to the cli nician.1> Measurement of S urrounding Ski n Eryt hema
Erythema of th e sk in surround ing a wound may be a measure of the inflammation phase of healing or a sign of in fection. Chronic wounds often show a halo of erythema but lack the other signs of inflammation. The peri wound erythema can be identified as unblanchablc redncss or a darkening of the skin in darkly pigmented sk in, See the C linical Wisdom box rcgarding measurcmcnt oferythcma in dark ly pigmented skin. Streaking or significant signs of eryth ema projecting out a distance from the wound may be an indicat ion of celluliti s, and medica l measurcs are needed. Meas uremen t can be taken using the greatest length and greatest width method, or the clock method can be used. The clock method is described.
The Clo('k l\leth od To Mell ,m re Surrounding Skin Erythema I. Measure across th e wound open area at th e 12:00 to the 6:00 position to the outer margin of the periwound erythema. 2. Measure across the wound open area at the 3:00 to the 9:00 position to the ou ter margin of the peri wound erythema , 3. Comp ute th e peri wound area of erythema.
95
Clinical Wisdom: Measurement of Erythema in Darkly Pigmented Skin Skin color changes reported by clinicians and in the literature' indicate that, when inflamed, the skin color of darkly pigmented people darkens to an eggplanV purplish color. It may be difficult to differentiate darkening of imflammation from hemosiderin staining. If this is true, proceed with temperature and edema examinations. For a fu ll description of assessment of darkly pigmented skin, see the section on assessment of darkly pigmented skin in Chapter 3. The following are guidelines for measuring the extent of inflammation/trauma in darkly pigmented skin: • Use natural light or halogen light, not fluorescent light. • Outline the margins of color change on the surrounding skin with a marking pen. • Select a reference point for future measures. • Measure the greatest length and the greatest width or use the clock method. • Calculate the area of color change (as described for all length-by-width measurements).
household plas ti c wrap with a plastic transparency mark ing pen (the ink does not bead up). Tracings taped to a sheet of
paper can be put in th e patient reco rd . However. because raped-o n tracings can come loose or ragged in a chart, the tracing and form can be photocopied and the copy placed in the chart. A tracing is a picture of the wound shape. Repeated tracings show change of size and shape over the course of recovery. Accuracy of measurement with tracing is dependent on how carefully the wound edges are followed as the
Est imated area of erythema: 12:00 to 6:00 length x 3:00 to 9:00 width ~ _ _cm '
Example: 9:0 cm x 6.0 em
= 54 cm 2
"Vound Tracin gs
tracing is drawn. Kloth and Fecdar lO documented measurements for patients in a research study. Sussman II sugge sted use of tracings app lied to a g raph form wi th a key for ti ss ue assessment called wou nd assessmen t form" for c l inical practice report in g wo und healing progression. Foll owing are suggested ways thai tracings can be used : • Tracings show change in the wound perimeter shape over time. Wound shape is a helpful indicator of the rate of
Making a wound tracing is reported to be the most popular and practicalmcthod for measuring wound area. It is easy to learn. inexpensive. and readily ava ilable.s Measuring the wound area from transparency tracings and plac ing it on graph paper to determine size by counting the centimeters have shown high intra- and inte rtester reliability (0.99). Com-
pared with linear measuremcnts with a ruler th ere is less overestimation of the real wou nd arca. a lthough some error can be expected. Using the I-cm graph papcr to coun t sq uares has been reported to be qu ick a nd efficient.\! Tracing can be made on acetate measuring sheets such as those th at are given out free by many companies for measuring wounds or on
healing. As de scribed in Chaptcr 2. linear wounds contract rap id ly. square or rectangular wounds contract at a moderat c pace, and c ircu la r wou nds contract slowly,9 • Tracings can be placed on a metric graph form. This shows th e wo un d size as we ll as shape and provides a three-dimcnsional pictograph of the wound on a IwOdimensional form " (see Exhibit 4- 5). • A tracing can become a "wound map" showing fca tures of the wound bed such as necro ti c tissue and adjacent tissue c haracteristics such as erythema (sec Exhibit 4-6). Household plasti c wrap is better for th is because it is clear.
96
WI)I ""I> (' \RI
E\hibil and th e Wag ner sca le. 7 (see Chapter 4) are approp ria te for determini ng initi al severit y at tiss ue trauma based on depth of tiss ue destructi on. The inform ation that is reported by assigning a stage of severi ty is static as opposed to healing, whic h is dynamic. Stagi ng systems are uscd in many ways; some arc appropriate and oth ers are not. For example, wou nd stagc is used as a criterion for inc lusion or excl usion in research st ud ies. The rei mburscment system uses the staging system as a crit eri on fo r eli gibility for products and services.
Criteria for a Wound l'lea ling Tool Criteria to eva luate th e appropriateness and util it y of a 100 1 include reliability, va lidi ty. res ponsive ness, se nsiti vity to change. and clinica l prac ti ca lit y.8 Validity
Fo r an instrument to be va lid the instrumcnt should measure what it is supposed to measure. Fo r instance, a wound hea ling toolmllst measure change in att ribut es hi ghly correlated with wo und healing. To be use fu l, the meas urements must be Cl/rrellf . In ord er fo r a too l to have pred icti ve va lidit y, the tool I11ust pred ict out comes characteristi c of healin g. Predi ctivc va lidity is of great import ance. Screenin g too ls th at have predictive va lidi ty are based on th e ass umpt ion that after detecting specific varia bles, an in tc rve ntion CB n be applied th at wo uld affect th e prcdi cted outcome.
103
104
W(JlI~()
C!\RI
Table 5-1 Factors and Scoring Methods Used in Wound Healing Tools
Factors
Wound Factors Size DOOth/Staae Ednes Necrotic Tissue
TvDe Amount Siouah Exudate Tvne Amount Odor Infection Granulation Contraction Undermininn Epithelialization
Surrounding Skin Factors Color Edema Induration Maceration Hemorrhaae Other Factors Location Risk of Skin Breakdown Wound Healing Phase Sha,;; Debridement Healed Scoring:
PSST
x x x x x x x x x x x x x x x
x x x
Sessing Scale
PUSH
WHS
SWHT
x x x
x x x x
x x x x
x x
x x x x x x x
x x
x
x
x
x
x x x x x
x
x x x x
x
x x x
x x x x x
Likert scale: 1=best; 5=worst. Scores for 13 items are added. Score changes as wound improves or worsens.
Scale 0-6 Uses the numerical value most closely associated with description . Score by calculating change in numberic value over successive assessments. Positive score = improvement; negative score = worsening .
3 Weighted subscores for: surface area, exudate. and surface appearance are added to obtain total score. Score changes as wound heals or worsens.
Eight letter modifiers are used with the Pressure Ulcer Staging System (eg.4NStage IV necrotic). Method to measure change in status over time not clear.
Scores presence or absence of each of 19 wound attributes. "good for healing" or "not good for healing" and other factors. Measures change by noting change from "not good" to "good for healing" attributes.
Tools To Measure 110 ulltillealillg
Table!>-2 Historical Measures of Pressure Ulcer Improvement Measures Change in ulcer size
Definitions
• Area (length x width) • Depth (for volume) • Perimeter/circumference
Surface appearance
• Red
• Yellow • Black Tissue type
Surrounding skin characteristics
105
tial. Both tool s are in various stages of development and th e ir reliability, validi ty, responsiveness, se nsitivity to change. and clinical practicality for monitoring wound hea ling are still to be determined. There are simi larities in some aspects of the tools: both 100is eva luate tiss ue attributes of the wound and surrounding skin. Methods of evaluat ion and scoring are different. A t thi s time, ncither author knows for certai n that a ll items li sted in the tools are useful. The processes of devclopmcnt and application of the two tools will now bc presented .
• Necrotic • Granulation
• Epithelial • Singly or in combination • Erythema (color change) • Edema • Undermining or Tunneling
$ource.- Sussman C, Swanson GH . The utility of Sussman Wound Heating Tool In predicting wound healing outcomes in physical therapy. Advances in Wound Care , September 1997.
Re/i"hilily
Rcliabili' y Orn tool is its ability to be used with minimum error. There are seve ral kinds of reliabilit y tests for a tool. Intrarater reliability means th at the sa me raler gets the same sco re with repeated measurements . Interraler reliability means that two or more individuals get the same results after administering the sa me instrument. Re!11JOIIS;,'ellesslSeJlsili'lily 10 ChaJlge
Responsiveness or sensitivity to change is the next test criterion for a tool. An appropriate tool or method must be ab le to detect changes in the condi tion of the wou nd over time with repeated administrations. CIi"iclIl Pmclicllfily
Cl in ical pmcti ca lity mcans the tool mu st be simple, easy to learn and to use with clear instructions, and must be reliable with the sa me and multiple lIsers. It must be time efficient and cost effective.
Two Tools To Monitor Wound Healing This chapter desc ribes two tools to monitor wound healing. the Sussman Wound HealingTool (SW HT) and the Pressu re Sore tatus Tool (PSST). each developed by one of the authors of this chapter. Both c linicians recognized many years ago that the ability to monitor hea ling ou tcomes was essen-
SUSSMAN WOUND HEALING TOOL Introduction and Development of the S ussman Wound Hcaling Tool The SW HT was developed by Sussman and Swanson' as a physical th erapy (PT) diagnostic tool to monitor and track the effec ti veness of PT technologies used for press ure ulcer healing. The ability to predict pressure ulcer hea ling and treat ment outcomcs in PT has yet to be done reliably. The monitoring and tracking of healing and treatment outcomes is essentia l for clinical decision making and triage and provides payers and providers improved utilization management. The basis forthe SWHT is the acute wound healing model (see Chapter 2) that desc ribcs the changes in tissue status and size ove r time as the wound progresscs through the biologic phases of wound healing. Some atlributes of the wo und that are observed during each phase are considered related to failure to heal or " not good for healing" and others are co nsidered indicators ofimprovcment or "good for hea ling." For example, a tissue attribute such as necrosis is thought to be negative or not good for healing. whereas wound attributes such as granu lation tissue, which represent s fibroplasia. and ad herence of the wo und edges are cons idered good for hea ling. The concept of the SW HT is to benchmark the wound attributes as it recovers and progresses throughout the healing phases. For example, the "not good" attribute, necrosis, sho uld change over time from preselll to abselll. thus moving from "not good for healing" to "good for heali ng." The "good for healing" attribute, fibroplasia- significant reducti on in depth , sho uld be g ranul ation obse rvcd as th e wou nd heals and changes from absem to presef1l, in-dicating improved tissue status. The initial design of the SWI-IT is a qualitative instrument. meaning that a wound would be described a s having certain ti ssue atlributes. Subsequcntly, th e tool wi ll be refined an d each SW HT variab le will be measured. weighted. and ranked to produce a quantitative tool. In total , 19 attribut es are defined. It is composed of 10 wound attribut es combined wit h 9 descriptive attributes of size. extent of tissue damage plus loca ti on. and acute wou nd healing phase. wh ic h are not
106
WOUND CAR'·
measurable. The 10 wound tissue attributes described were each ass igned a score as prese/JI or abseil! and ranked as /lot good or good for healing. Five attri butes ranked as 1101 good
include hemorrhage. maceration, erythema, undermining. and necrosis. Five attributes ranked as good include adherence at the wound edge. fibroplasia, appearance of co ntrac-
tion , sustained contraction, and epithelial ization. The lists defining and describing each attribute are shown in Exhibit 5- 1. S uss man \Vo und Hea lin g Tool Attribute Definitions Purl I: ThislieAllribufes
The first five attributes described are classi fied as "not good for healing" and the second five listed are classified as "good for hcaling:'Thc "not good for healing" attributes arc
all related to the inflammatory phase of healing.The att ributes that are "good for healing" are re lated to the proliferation and epithelia liLation phases of healing. As the wound at-
tributes change from "not good" to "good" the wound is progressing th rough the phases corresponding to those of (lcute wound healing. I. U emorrllllge. Hemorrhage is defined as a purple ecchymosis of wound tissue or surrounding skin (see Color PI"tes 65 "fld 68). The color plates show the deepening of
tissue color or distingui shable purple ecchymosis whic h is an indicator of significant subcutaneous bleeding or hemorrhage. Wounds with hemorrhage have high probability of tissue death and thus enlargement of the wound. This attribute is classi fied as "not good for healing."
Clinical Wisdom: Assessment of Hemorrhage
3. Ultclermill;IIg/Tlllllle/illC. Underm ining is defined as erosion under the edge of the wound and tunneling is defined as separatio n of the fascial planes leading to sinus tracts, Locat ion of undermining for thi s attribute means undermining at any location arou nd the wound perimetcr. Color Plates 37 to 39 show wounds that arc underminincd or wit h tunneling . The ex tent of the undermining/tunneling is not recorded or included as part of the assessment. on ly the presence or absence of this attribute. If undermining is present, it is an attribute that is classified as "not good for healing:' 4.
£~"Ilrelllll,
Erythema is defined as reddening or dark-
ening of the skin compared wi th surround ing ski n. Erythema following trauma is due to rupture ofsl113 11 venu les and capillaries or may be caused by inflow of blood to start the innammatory process, or both events. Disti nguishing between the two is oftcn difficult. Erythema is usually accompanied by heat. but it may be accompan ied by cooling. indicating dcv italizat ion of tissuc. lU Di stinguishing and assessing erythema in darkly pigmented skin is described in detai l in Chapter 3 (see Color Plate /9). The abi lity to sec the mar-
gins of the change in sk in color is enhanced by lighting and may be seen morc easi ly in a photograph than in the living tisslles. especially in very dark skin tones. Color PI"te.l' 6. 14. "fld /5 show erythema in both lightly and dark ly pig-
mented skin. Erythema is an attribute that is classificd as "not good for hea li ng."
Clinical Wisdom: Differentiation between Erythema and Reactive Hyperemia
Erythema should be assessed after pressure has been relieved from the area for about 20 minutes so as to eliminate effects of reactive hyperemia.
Triggers Further Examination
The presence of hemorrhage would be a trigger for further examination, including temperature testing as described in Chapter 3 to determine tissue vitality. Hemorrhage may trigger vascular consultation. The chapters in Part IV on electrical stimulation, pulsed short wave diathermy/ pulsed radio frequency, and ultrasound describe how these interventions promote absorption of hemorrhagic materiaL
5. Nec:rosis. All types of necrotic tissue, including eschar and slough, arc included when assessing for presence or absence of th is attribu te. Necrosis is defined as dead devitalized tissue. Color may be black, brown, gray. or yellow. Tex-
ture may be dry and leathery, soft, moist, or stringy. Odor may be present or absent. To determine if the tissue being assessed is necrotic, see Chapter 7. Management of Necrotic Tisslle, and Color PI(ltes 3, ]5 to 30. 46, (If1d 47. One com-
2. A1(1('erlltiolt . Maceration is defined as a softening of
mon error in assessing necrotic tissue is to assess all yellow and wh ite tissue as necrot ic. Yellow ti sslle may be either
connecti ve ti ssue fibers by soak ing un til they are soft and friable ." Macerated tissue loses its pigmentation. and even
a tendon . White tiss ue may be connect ive ti ssue. fascia. or a
darkly pigmented skin looks blanched. Th is weakened tis-
ligament. Color PI(lte 13 shows healthy yellow and white
sue is highl y susceptible to trauma, leading to breakdown of the macerated ti ssue and enlargement of the wound. Maceration is an attribute classified as "not good for healing."
tissue. Healthy tissue usually has a gleam not seen in devitalizcd tisslle. Note, however, that the topica l treatmcnt or exudate is not the source of the "gleam." Ilcalthy tissue is
healthy ye llow fa t, the rcticular membrane of the dermis. or
107
Tools To A1easlire WOllnd /-Iealing
not friable and has resilience whe n compressed. Dead tissue tears and does not spring back when compressed. Waiting 24 hours helps to sec if the ti ss ue c hanges color to gray or
brown. indicating loss of vital it y. Reassess. Necrosis is an attribu te that is classified as "not good for healing."
6, Al/herell('e af WOIIIU/ El/ge. Adhere nce at the wound edge means that there is continuity of the wound edge and the base of the wound at any location along the wound perimeter (Cnlor Plales 8, 9, 56, alld 57), A partial-thic kness wound will be adhe red at the wound edge by definition, A
full-thickness or deeper wound will have closed by either granulation or contraction to the point whe re some area of the wound edge will be even with the skin surface. Some wound edges curl under because of epithelial migration over the edge of the wound. Thi s can halt wound contract ion and lead to fibrosi s of the scar tissue. Edges may not adhere when this occurs. and wound healing will not proceed. Adherence of the wound edges is an attribute that is classi fied as "good for healin g," 7. Grtlllll/afitm Tisslle (Fibroplasia-Sigltijic:allf Rel/Ilcfioll ill Depth). Granulation ti sslle formation or fibropla sia
is the action of the fibroblasts laying down collagen matrix during the proliferation phase of healing. The collagen matrix fills the wound.. causing a measurable or significant redu ction in wound depth . For determining the presence of fibroplasia signi fi cant reduction in depth. a linear measurement of thi s attribute is required (sec Chapter 4), A signifi-
cant reduction in depth is at least 0.2 em si nce the prior assessment. Color Plates 7 to 9 show a significant reduct ion in depth. Granulation is an attribute that is classified as "good for healing:' 8. AppellrtlllCe o/Confracfion, The appearance of contraction is defined as the first measurement of the wound drawing together, resulting in reduction of wound open surface area size. 'ompare Color Plate 3 with Color Plares 4 lind 5 to see the onset and progess ion of contraction . It is identified by a change in wound open area size and may be identified as a change in wound shape (eg, from irregular to symmetric, such as the circular or ova l formation and rounding ofT the edges of the wound seen in pressure ulcers; see Color Plate 2). This item is scored at subsequent assessments as the contraction continues or ifit has stopped. Irthe wound enlarges, however. this itcm wou ld change from present to absen t, and a new appearance of contraction would be required to have a score of "present" again. When present, adherence at thc wound edge is an attribute that is classified as "good for healing."
9. SlIsfaillell COllfrlU:lioll, Sustained contraction means there is a continued drawing together of the wound edges that is measured by a reduction in wound surface open area size. It is usuall y accompanied by a change in wound shape.
Color Plales 3 10 5 show the same wound as it goes through wound contraction . Sustained contraction is scored 0 at the appearance of the contraction benchmark and then scored I at subsequent reassessment following the appearance of contraction. Occasionally something interferes with the wound contraction and the wound does not reduce in size or increases. Thi s attribute would be marked O. absent, if the wound size docs not reduce or enlarges after the appearance of contraction. Sustained contraction is an alLribute that is classified as "good for healing,"
/0. Epifhelill/;Zafioll. Epithelia liza tion refers to the appearance of and continuation of resurfacing of the wound with new skin at the wound edges or surface. Color Plate 5 shows the sa me case as Color Plates 3 10 5, now in the epitheliali za tion phase. Epit helializat ion may first be noticed during the innammation or proliferation phase of healing as a lightl y pigmented pink ti ssue, even in individuals with darkly pigmented skin (Color Plates 7 10 9), In partial-thickness wounds, the epithclia l cells may migrate from islands on the wound surrace or from the wound edges. or both. Color Plales 55 alld 56 show an example, Full-thickness and deeper wounds have epithclial migration, usually from the edges only, Color PI",es 5 alld 6 show the sa me full-thickness wound as seen in Color Plates 3 and 4, that is, resurfacing rrom the wound edges. Many peo ple confuse new bright pink scar ti ssue or skin as erythema. Color Plate 22 shows new pink scar tissue in a person with darkly pigmented skin. Epi thelialization is an attribute that is classified as "good for healing." Parf II: Size Locafiollllllli H'oUlli1 Healillg Pllase Measures
Wound depth and underminin g indicate extent of wound. If a wound has a depth less than 0,2 cm it is scored as
°
at all
four points and at general depth . Depth and undermining are two indicators of "'not good for healing." 1/- 15, W"'/Ild Depl", Five items on part I! o f the SWI-IT arc related to presence of depth of 3t least 0,2 c m both in ge neral depth and at the four points of the c lock. 12-. 3-. 6-, and 9-0'clock posi tion s, Depth is meas ured as desc ribed in Chapter 4 , and if it is at least 0,2 c m it is recorded as
present. Extent of depth is not significant for this assessment as lon g as it is at least 0,2 cm, (Sec Color Plales 2, 7, 27, alld 30 for full-thi c kn ess depth ,) /6-19. TUllllelillglUllllermillillg. Undermining and tun-
neling are measured at a ll four points of the c lock. like depth ,
However, the objective measure used to report this attribute is also present or absent. With further testing and analysis this attribute may prove to be redundant with part I. For the present time. it remains a part of the 1001.
Additional Descriptille Attriblltes 'Yound Locution. Wound location is noted as the anatomic description most closely related to the wound site. Because lower torso and lower extremity wounds are most frequently seen, the locations have been broken down into th e common sites for chron ic wounds and they have been clustered together for the upper body. Letters are also used to represent Ihe wound local ion: UB ror upper body, C ror coccyx, T ror troc hanler, I ror isc hial. " ror heel , and F ror root. Wounds in other locat ions can be added to the list if they are commonly seen in the practice setting by using letters on the rorm and adding a local ion descriplor 10 Ihe key (eg, K = knee, A = abdomen, Til = Th igh). One needs 10 be sure 10 include Ihe side orlhe body where Ihe wound is localed, righl or left, by putting an R or an L next to the location leHer. Wound location has been shown to be an indicator of healing. However, the specific locations that indicate healing are slillio be delermined . I¥ol/nd He(lfillg Phase. The wound healing phase refers to the four biologic pha ses of wound heal ing: inflammatory. proliferative. epi th elializa tion. and remodeling. Letters are used to repre sent the current wound healing pha se: I for inflammation, P for proliferation. £ for epithelialization. and R ror remodeling. As described in Chaple r 2 Ihe wo und hea ling phase may be chronic, acute, or absent. A letter is placed berore Ihe phase suc h as Ihe leller C be rore Ihe phase ror chronic. no letter before acute, or the letter L for lacki ng or absent can be used as modifiers of th e current phase. A change in pha se over time is an expected outcome. Chronicity of a pha se should change to an active state of the pha se followcd by progre ssion to the next pha se in the traj ectory. Absence of a pha se indicates need for investi gation as to why thc pha se has not been achicved. This itcm is listed but unscored. Tesling Ihe SW HT One or Ihe rirsl questi o ns applied 10 Ihe SW HT was whether a tool design based on the four phase acu te wound healing model could be applied to chronic wounds such as pressure ulcers. The SWHT is in Ihe process orbeing lesled on a dala sel or I 12 pressure ulcer cases. All or Ihe palienls who were included in the dataset were long-term care residents with prcssurc ulcers. Many experts consider pre ssure ulcers to be chron ic wounds from the time of ol1set.The ana lyses are as yet incomplete.
SWNT for MOllitorillg (Illd Trackillg WOIIIll/ fleldillg The utility of the SWHT in the clinica l setting for monitoring and tracking healing is easy and practical. Each of the
allribules orl he SWHT is scored ir lissue allribules or Ihe wound or surrounding skin are present or absent. The total number orpresenl (I) "nol good" ror healing allribules shou ld diminish as the wound heals, and the total number of prese nt (I) "good" ror healing attribules should increase in number. Change of score measures the change in hea ling and reduced severity of the wound. The scores are al so useful for measuring the level orhea ling indiealing progress. lack orprogress, or regression or healing. The SWHT has proven ulilil y bOlh as a diagnoslic loollhal difTerenliales phases by assess men I of healing attributes and as a tool for measurement ofcJulIIge in ti ssue statu s (eg, ti ssue attribute) and size (eg, change in deplh and undermining) over lime. Thus, Ihe SWHT is designed to monitor and track healing based on the acute wound healing model , and can be applied to acute or chronic wounds such as pressure ulcers.
SWNT Reliability alld Practicality The SWI-IT has been clinica ll y lesled ror reliabilil Y and clinical praeliea lily by phys ieallherapisls and physicallherapi sts ' assistants working in a long-term carc faci lity during ils 5 yea rs or developmenl and round 10 be very reliable ror monitoring and trackin g healing and nonhca ling ofprcssure ulcers. It relies primarily on visual observation skill s. No linear measurements, arithmet ic calculations. or estimates of amount of ti ssue characteristic present arc required. To health care proressionals who treal wounds. Ihe SWHT information communicatcs clea rl y wound progress or risk. Documentation is very simple and outcomes arc visual. For example, it takes the clinician about 5 minutes to complete the assessment. In a trial educat ional session to train new learners 10 use Ihe WHT, a group or 10 physicallherapisls and physical th erapists' assistant s who recei ved I hour of training in the classroom using verbal description and photos 10 teach the method of assessment and definitions of the attributes, fo llowed by 1 hour of clinical pract ice on pressure ulcer patients. learned to use it well. An'essmenf o!Tre(/fmenf Ollfcome~'
Assessment of treatment outcome was the initial reason ror developmenl orlhe SW HT. Mosl palienls arc rererred 10 Ihe physical Iherapi sl by Ihe nurse ror treatmenl arter conventionaltreatI11ents failed to heal the wound. To qualify for an intervention by the phys ical therapi st, the patient and the wound often need to meet a criterion of 110 progress or regression or a halt of healing. Therefore, it is critica l for the physical th erapist and the nurse to be able to set target outcomes and then assess the response to the treatment intervention. A wound assessed with the SW HT as nOI progressing after a course of conven ti onal care by the nurse would meel Ihe crileri on ror referral. Once rererred, Ihe SWHT is use ful for rcporting wo und outcomcs associated with the
Tools To A1ellsllre Wound lIealiug
intcnelllion prescribed by the physical the rapist. s uch as physica l therapy technologies. Response to treatment with these interventions shou ld demonstrate co nsistent c hange in tissue status that co rresponds to th e biologic model for acu te wou nd healing. A change in ti ssue status benchmarks th e heal in g process and becomes a ta rget functional o ut come for reporting purposes. such as the wou nd w ill be hemorrhage free. undermining free. nec rosis free. and so forth. Reviewers ca n quickly determine a c hange in wound tiss ue status during the co urse of care because. as already descri bed, the wound attribul cs sho uld change fro m those "not good for healing" to those "good fo r hea ling."
6.
7. 8.
Usin g th e SW II T
Two Pllrl.' o/SWU T Exhibit 5 I ,how. th e two pans of the SW ill' The SWI IT is a paper-and-pcncil instrument comprising 19 attributes. Part I is th e coll ection form of 10 tissue att ributes. Part II is the list of II other attributes, inc ludin g ex tent. location. and \\Olilld hea lin g phase. All items on the SW HT arc scored c'(cept locatio n and the wo und hea lin g phase. Omission ofa score indicates th at the assessmen t was no t comp leted. Sco ring begins at baseline. week O. The meth od of scoring for the tool is a number I fo r present and a 0 for absent. This reporting format is readily compatible wi th comp utcr tec hnology and simplifies using the tool to build a database such as the one described later. Completi o n of the form rcq uires understanding of the dcfini tions for each of the scored itc rn s (see Exhibit 5 2 for definitions of att ributes). The aSsessmcnt process is visua l except for detcrmining the presence of undermining tunneling. which cannot be seen at the surface. and Il1ca~urement of the open surface area of thc wOllnd.
Proteilllre/or Usil/g I/l e SWII T (see Ex/libil 5- 1) Compl etion of th e Wi lT is by observa tio n an d physical assessment, as follows : I. Each wo und of each pa ti en t needs its own SW HT attrib utcs forl11 . 2. The patient's name a nd medical record number and da te ofasscssmcllt are wrilten at the top of the form . 3. The examiner has a place to sign the document. 4 . As the wound is assessed. th e rarer marks a I or a 0 to signify present or abscnt on thc form nex t to each of the 19 attributes. The squares in the co lumn must be marked \\ ilh one of the two scores. 5. The wo und l oe~lt i on a nd the current wo und hcaling phase arc marked wi th the appropriate letter. Choose the appropria te letter to represent thc ana to mi c loca-
9.
I O.
109
tion of the wound and place it in th e squa re at th e time of the ini tial assessmcnt and subscquclll reasscssments. The locat ion will not change. Letters are a lso used to reprcsent th e current wound healing phase: mark a nI fo r innammati o n, P for proliferatio n. £ for epilh e li aliLa ti on. and R for re modeling. In the a ppropriate box, th e phasc is no ted ini tially a nd at eac h rea ssessment. The wound hea ling phase sho uld chan ge as th e wo und hea ls. Undermining and depth require some physica l assessme nt to determine prese nce or absencc. Open area measurements a rc Illade and li sted o n a separate form (see Chapter 4) and thell co mpared wi th subsequent measurements of these cha racte ri sti cs to detennine contraction and sustained co ntraction. measured as reduction in linear si/e. Scoring part L Add th e number of·· not good for hea ling" at tributes and the number or"good for healing" attribut es li sted. The sco re of "not good for healing" shou ld diminish as the wo und hca ls. and th e sco re of " good for hea ling" attrib utes shoul d increase. A grap hi c representation o f the chan ge is show n in Ex hibit 5-4.
SW I·/T For ms
Two SW HT forms arc shown (Exhibits 5 2A and 5 28). Part I of th e long form (Exhibi t 5- 1) contains the 10 ti " ue attributes. listed in descending o rder ofse\e rity. next to definitions. followed by a co lumn li sting th e rat ing option for the attribute as present o r nOI present. The ncxt column ranks the relatio nship to hea lin g as " not good" o r ·'good ." The last column is where the rating is listed as a score of present or absent. Part II li sts measures and ex ten t. The same scori ng syste m of"p rese nt" or "absent" for 19 attributes o f ex tent is appli ed. The attributes a re th e ge ne ral depth of grea ter than 0.2 e m, th e dc pth at th e four c lock poi nt s. and unde rminin g at the four clock po ints. Date and week of care sho uld be noted o n th e form . The benefit o rlh e lon g fo rm is havi ng the definitions on th e form. This wou ld be he lpful to a nurse or physical thcrapist learning th e system o r for medical reviewers and surveyors looking for information abou t th e rating system used for documentation.
Short Form The short form (Ex hib its 5 2A and 5 28) of the S WIIT is thc same as the lo ng form except that th e sho rt form lacks the defi nit io ns printed o n the forl11. T he sho rt form lists o nl y the attributes and has co lumns to record data for Illultiplc
Elhibit 5-1 Long Form SWHT o Sussman \\ound lIealing Tool (S\\ Hn \\OL '0 ASSESS'IE'\T FOR;\I
=E
o
'A'IE, _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ ___
\IEDIC \L RECORD
O\TE' ____________________
~O.,
_ _ _ _ _ _ __
EXA \II\"ER: _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __
L Z
",." ~
CIRCLE \\ UK OF CARE, S\\'IIT
Tiss ue Attribute
\ariablc
2
B
3
~
5
6
7
Altribute Definilion ecchYlllosi~
8
9
10
II
12 Relationship 10 Healing
Rating I)rcsent or absent
Not good
Softening of a tissue by soaking until the connectiw tissue fibers afe soft and friable
Present or absent
Not good
UndcrmlRlng
Includes bOlh underOlimng and tunnding
Present or absent
Not good
~
Erythcltlj
Reddening or darkening of the sJ..:in compared to surrounding skin: usually accompanied by heat
Present or absent
i'l'ot good
5
""ecrosis
All types of necrotic tis:-.uc. includIng eschar and slough
Present or absent
1\1ot good
6
Adherence at \\ound edge
Continuity of wound edge and Ihe base of the wound
Present or absent
Good
7
Granulallon (Fibroplasia significant reduction in depth)
Pink red granulation tissue filling wound depth
the wound bed reducing
Present or absent
Good
8
Appearance of contraction (reduced size)
First measurement of the wound drawing together. resulting in reduc tIOn in wound open surface area
Present or absent
Good
9
SusUlined eontmctiol1 (morc reduced sile)
Continued dmwing together of wound edges. measured by reduced wound open surface area
Prl!$ent or nbsent
Good
EpithelialiLation
Appearance and cOnllllualiOIl of resurfacing with nc\\ skin or the wound edges or surface
Present or ab:;cnt
Good
I
Hemorrhage
Purple
2
\-Iaceratlon
3
10
of wound tissue or surrounding skm
10
~car
at
Score
',EASURES A1\D EXTE;r.,'T (Depth and Undermining: 'ot Cood) Oepth/ Location
SCORE
L nderminingi Location
SCORE
12:00
Other
II
GenerJI depth -·0.2 em
16
Underm
'll
12
Geneml depth
17
lindcrm
(j
3:00
Wound healing phase
13
Geneml depth a 3:00 >0.2 em
18
L:ndcrm
/L
6:00
Total "'Jot Good"
14
General depth
1I
6:00 >0.2 cm
19
Lnderrn a 9:00
15
GencrJI depth
(t/
9:00 >0.2 em
ill
12:00 >0.2 cm
-
Leiter
Location
TOlal "Good" -
---
--
Key: Present - 1. \bscnl - O. Location choices: upper body fUB). coccy\: (C). trochanter (T), ischial (lJ. heel (II). loot If): add right or left (R or L). \Vound healing phase' Innammalion Ill. prollfcration (Pl. epitheli.llizalion fE). remodeling tRI. SO/lrcl'.
Copyright
i:'"
1997. Sussman Physical Therapy Inc.
Tools To Measure It blfllll /-Iealillg
II I
Ex hibit 5- 2A SWIIT Short Form Parl I: Wow,d Tissue Allributcs
Namc: _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ Mcd Rec # ________ Examiner: _ _ _ _ _ _ _ _ _ __ \Vct'k
0
I
2
3
4
3
4
I. Ilclllol'rlm gc
2. Ma ceration
3.
Undcrll1inin~
4. Erythcma 5. Necrosis
6. Adherence 7. Granula tion (decreased deth)
8. Appearance of cOlllraction (Reduced size) 9. Sustained contraction (More reduced size)
10. Epilhcliali7tHion Total NO{ Good Total Good Key : Prc . . cnt SOI/I"/.·(':
1 Not preSC11I
CopY right
I
O.
1997. Su . . . . man I'hysical Thcr:tpy Inc.
Exhibit 5-28 SW II T Short Form Part II : Sile. Location. Wound lI ea llll g Phase Measures. and Extent
Date
0
I
2
II. General Depth >0.2 ern I:!. Depth ((/ 12:00 > 0.2 em
13. Depth (a l 3:00 >0.2 em 14. Depth
(ll
6:00 >0.2
CIll
15. Oqllh «(/ 9:00 >0.2 em 16. Undcrrn (al 12:00 >02 ern 17. Undl.!rrn (a l 3:00 >0.2 ern 18. Undenn ({II 6:00 >0.2 em 19. Undcnn
(ll
9:00 >0.2 em
Location Wound healing piw"c K\.'y: Present I Not prc:.cnt O. Location choices: upper body (UB). coccyx (e). troch:Ullcr (T). ischial (I). heel (I I). lllld foot (F); add right or len (R or L) Wound healmg ph:tsl.! : :lbsent (A). chronic (el, inflammation ( I). proliferation (P). epithelialization (E), remodeling (RI. S{l///'('(':
Cupyright
c'
1997. $us-;man Physical Therapy Inc.
Wtalnl!d contraction (mon: reduced sil"l!)
()
(I
()
I
1
I· pJthcllalll" ..lt iol1
()
()
0
I
I
Total "Not Good "
J
2
J
I
I
Total "Good"
()
(I
2
5
5
4 I ryt hema f--5. NeCrthlS f--6. Adherencc
f-
1
I
I---
-
0
r----u,
I\.ey:
Prl'\l'nl
I. \b\l! 1I1
0.
S"un'(' Cupyright, 1997. SII\\milll PhY'l!;ill Therap) Inc.
[,hibil 5-38 SWIIT Part II : Si/c, Location. Wound lI ealing Phase Ml!a'HO cm~ Nonblanchuble crythcma on inlact ,,"til Partial-thie"ne ... s skin It)s~ in\'oh mg epIdermis and or dermi ... htll-thie!-.ne,,:. :.!-.in lu~s ttl\olvUlg damage or nccro ... is of suhcutaneous tts':'lIe: llIay extend dO\'..'11 tu hut not through utulerlying fa"cl;]: andor mi"(cd partial and full thidncss alldor tissue layers ob ...cured by granulation tissue Ob:scurcd by Ilecro.:,j:., rull~thickne ... s ... kin loss \\1Ih cxten\l\e destruction. tbsue necrosis, or damage to muscle. bone, m ... upporting ... trueturcs Indistinct. dilrusc. none clearly \ i... ible DI.,ttllcl. outline ckurly \Isible, all ached e\:en WIth wound base \Vell-defined not attached 10 \\ounJ ba ...e Well-defined not attached to bllse, rolled under. thickencd Well-defined fibrollc, scarred or hypcr!-'cr4 em tn any area Tunneling undior ... inu ... tract formation None visible While gray nonviable Itssue antI or nonudhcrent ycllO\\ slough Loosely adhercnt yellO\\ slough AdhcrCnI. sofi. black cschar Firmly adherent. hard blac" cschar None \ isible 25"" of \\'Ound bed covered 25"" to 50"'0 of wound covcred >50"" and 25°'0 to ~75% dressi ng Large wound ti ss ues bathed in Ouid ; drainage free ly expressed: mayo r may not be evenly distributed in wound: drainage involves >75% of dressing Skin Color S urro undin g \ Vo und : Assess ti ss ues within 4 Clll of wound edge. Dark-skinned perso ns show the colors "bright red" and "dark red" as a deepening of normal ethnic skin color or a purple hue. As healing occurs in dmk· skin ned persons. the new skin is pink and may never darken . Peri phera l T iss ue Ede ma: Asses ti ssues within 4 Clll of wound edge. Nonpining edema appears as skin that is shiny and taut. Identify pitting edema by firmly pressing a finger down into the tissues and waiting for 5 seconds; on release of press ure. ti ssues fail to resume prev ious position and an indentation appears. Crepitus is acculllulation of air or gas in ti ssues. Use a trans parent metric mcasuring guide to determine how far edema extends beyond wound . Pe r ip hera l Tiss ue Ind uratio n : Assess tissues within 4 em of wound edge. Induration is abnormal firmne ss of ti ssues with marg ins. Assess by gently pinching the ti ssues. Induration result s in an inability to pinch the ti ss ues. Use a tran sparent metri c measurin g guide with concentric circles divided into four (25%) pie-shaped quadrant s to determine perce ntage of wound and area involved. Gra nulatio n Tiss ue: Granulation tisslie is the growth of small blood vesse ls and connective ti ssue to fill in fullthi ck ness wounds. Tissue is healthy when bright, beefy red shiny, and granu lar with a velvety appearance. Poor vascular supply appears as pale pink or blanched to dull , dusky red color. E pit heli a li za ti o n : Epithelialization is the process of epiderma l resurfacing and appears as pink or red skin . In partialthi c kness wounds it can occur throughout the wound bed as well as from the wound edges. In full -thickness wounds it occurs from the edges only. Use a transparent metric measuring guide with concentric circles di vided into four (25 %) pic-shaped quadrants to help determine percentage of wound involved and to measure the di stance the epithelial tissue ex tends into thc wound.
C H A P TER
6
Noninvasive Vascular Testing Anne Siegel
INTRODUCTION
What time of the day is the pain experie nced? Describe the pain : ac hing? burning'! constan t? int erm itt e nt ? For exa mpl e, venous ulce rs are not very painfu l and th e pat ie nt may find relief from e leva ti on of th e leg. A rt eria l ulce rs a re ve ry painful because o f the lack of c ircu la tio n. Keep in mind that th ere arc a lways except ions. The patient may have a combina tion o f arte ri a l and ve no us disease. The pmien t can have dia bet ic ncuropat hy and have a n arteria l ulcer wi th ou t a ny pain . Pain o n the plantar as pec t of the foot usually s igna ls a diabetic neuropat hic fool. Art eri al res t pa in is fo und on th e dorsum of the foot and is us ually described as a b urnin g ache type of pain (like a toothache). Sometimes the patient will f ind so mc re li ef w ith depe ndency of the leg. Rcst pain indicates that the patient has s ign if ica nt arterial insufTiciency und w ill need intervention from a vasc ul ar surgeon to hea l the wou nd s. Cla udi ca ti on is exe rcise· induced pa in in th e major mu sc le grou ps th at is rcli eved wi th rest (usua ll y descri bcd as a cra mplikc pai n in the ca lf, th ig h, or b utt ock). Ifthc pat ie nt has a history of c laud icati o n, thi s shoul d guid e the cli ni c ian 's thinking that thc ul cer being eva lua tcd may havc an arte ri al et io logy.
In the pas t decade. many adva nces have been made in the diagnosis and treatm ent of vascul a r di sease. The key to pre-
ven ting deb ilitat ing circulatory prob lems is prevention and early diagnosis. Noni nvasive vascu lar eva luations are lIsed to detect th e presence o r absence o f arterial occlusive o r ve nous disease. They a re lIsed to eva luate the healing po ten-
tial of ul cers/wou nds. as an a id in determining wou nd care management plans. and as a guide in determinin g which patie nt s need refe rral to a vascula r surgeo n for fur-
ther eval uation. T he f irst stcp in a vascul ar eval uat io n is to obtai n 11 CO I11 plete medical his to ry from the patient. Thi s infonnation is imperative in th e overa ll assessment and trea tm en t of the patient's cond it ion. The patient's history prov ides a g uide in determ inin g the etiology of the wo und be ing evaluating. A carefu l. thorough history is th e key in vasc ular assess ment. Thc history shou ld incl ud e th e a reas discussed below.
O Il EF COMPLA I NT PAST ME DI CAL H ISTORY T he ch ief co mplai nt is the combi nat ion of symptoms that prompted the patient to seek med ica l attention. I Focus on the symp toms that co nce rn the pati ent and th en ask th e patient to describe those sympt oms in mo re detail. Spending time liste ning to the patient is as important as the phys ica l exa mination. A detailed pai n hi sto ry is essential in determinin g the urge ncy an d type of treatm en t th e patie nt will receive. Invest igate the pain. Where is the locati on of th e pain? Wh en did the pain start? Wh at factors aggravate o r relieve th e pain: e levation? depe ndency? wa lk ing? restin g? standin g? si ttin g?
Ex hibit 6- 1 lists a reas of mcdi cal hi story qucstio nin g used to ide ntify risk fac tors for vascu lar disease, bot h art eria l and ve no us. It goes beyond th e ge neralmcdical hi sto ry di scussed in C hapter I and focuses 0 11 spec ific vascu la r-re lat ed factors.
PH YS ICAL EXAM INATION A fler obtai nin g a co mplete history from the patient. the next step is th e physical exam. A carefu l phys ica l exa m used
125
126
W OUND CARl
Exhibit 6-1 Past Mcdicai lli story
Risk Fuctors ror Peripheral Vascular Diseuse'
Cardi:.lc hi story
Concom itant illnesses (renal disease, co ll agen vascular disease. arthritis. pulmonary disease. mali gna ncy [type ormallgnancYI back [spine] problems. etc) Family hislOry or arterial disease
• lIeart disease (cardiac catheterization'! results?)
• Hcarl attack (dalc of last event) • Chest pain (note location of the pain. how is pain relieved? ollser!) • Stroke (date of event. nole location of weakness or speec h
deficit) Il ypertcnsion (severity, medications. age at onset, highest blood pressure reading)
Il ypcrlipidcrnia (iasl cholesterol leve l. medication. number of
Risk Faclors for Venous Diseu se Trauma (type. date) Deep vei n thrombosis (date. anti coagu lant s) Prolonged inactivity Pregnancies Family history or \e nous disease Obesity Clolling disorders
years)
Smoking history (number of packs per day x years smoked ... number of p:'lck-ycilrs) (For example: a patient smoking IwO packs per day for 20 years ha s a 40-pack-year smoking hi s-
tory.) (quit? year quit) Diabetes (number of yea rs. medi cations)
in conjunction with a thorough history can usually determine the etiology of the wound and determine the wound ca re plan or establish the need ror rurther vascu lar tesling. The rirst step to the physical exam is inspection of th e extrcmity. Note the presence and location orallY ulcers, wounds, or gangrene. Describe the wound : color. wound bed, drainage (color or drainage). size, and odor. Note Ihe presence or absence or swelling (compare both legs. and docul11ent the location orany swelling).Ask the patient how long the ulcer has been present. Look at th e skin color. Are Ihere any pigl11ent changes? Feel the tcxture of the patient's skin: dry? moist? Feellhe lemperature or ,he skin, comparing both legs. Using th e back of the hand to assess temperature. note the leve l at which the limb is cool or warm. Note the presence or absence or hair (legs. toes). NOle the appearance orthe loenails (thickened?). Check for the presence and distribution of varicose veins.
Pasl Surgical Hislory
or
Vasclliar surgery (date procedure. indicati on) Angiogram/venogram (dates, indi ca tion. interven ti on'!) Gelleral surgcry (date or procedure. indic:'ltion)
Clinical Wisdom: Severe Arteria/Insufficiency If arterial disease is severe, elevating the leg while the patient is supine will cause the patient's leg to become pale, which is known as elevation pal/or. The pale color is due to lack of blood flow in the patient's leg. If the patient then hangs the leg over the side of the examining table, the color of the foot will change to a deep red or purple color, known as dependent rubor. This is also due to the lack of blood flow and vasodi latation of the arterioles. Be careful not to confuse dependent ru bor with cellulitis. If the patient has cellulitis, the leg will not become pale with elevation. 1
VOl1im'll\'II'e I (/Sut/ar n'.\ li"X
Diffcn.'ntiation
hch~cc n
Arterial a nd Venous Ilisease
Patients \\ ith arterial in~ufriciency ha\e classic characterISllcs that will ennblt.! the eX(lJ11l1ler to distingUIsh easily bet\\ecn arterial and 'venous ulcers. Always remember that patienl!-o can have a comhinatlon of arterial and \cnou~ disease,. and Ihe \\ hole clinical piclure may not fll 11110 one speL'ific category. Usc the follmving lists of characterisllcs as a guide. C h 'lraCler i ~ l ic~
• • • •
PULSE EXA ,. The nexl ~tep in the physical c_xaminatlOn is the puIs£' IThe pulse exam mc1ude!-o locatmg and grading bi lat-
l!.HlUI.
erol femoral. popliteal. dorsalIS pedIS. and postenor tibial
artery pulses. The following system shou ld be used to grade pulses: () I+
t--.o pulse Barely felt
Diminished
of \ rtcr ia i llheao,c
Normal pulse (eaSily felt)
Bounding. aneurysmal r'pulse hils you in the
Pain (\\alklllg and'or at rest) I-oot cool or cold Weak or ab!-ocnt pulses :\bscnce of leg hair
face") Pu l1)C Tab le
• S~1I1 ,llIny. dry. pale
• Thickened toell,-lIls • Llcer location: usually belm... ankle (pressure arcas. toes) • Ulcer: m:crotic. 1111nitnal drainage • \nkle-brachlUl II1de\ (1\1l1) Ie" than 0.5 (11I1Ie' If dlabellc. can he greater than I.O) • Flcvation pallor dependent rubor • History of diabetes. hypertension . smoking. claudication • llistory of foot trauma (tight shoes. toenails cut too short. object falllllg on foot)
Clinical Wisdom: Trophic Changes Trophic changes are skin changes that occur over time 1n patients with chronic arterial insufficiency. TrophiC changes Include absence of leg half; shiny, dry. pale skin; and thickened toenails. These symptoms are due to the chroniC lack of nutntlon from a good blood supply to the extremlly. Some of these changes occur naturally in elderly patients.
Cha ractrri'ilic, of \ cnous Oiscas('
• • • • • • •
root \\ arm Edema Brawny :-,kin pigment challge~ Varicose \eill~ Llcer location usually abm,e ankle (l11edI3Imallcolus) Venous ulcer, gcncrally not painful Llcer: granulating. drainage
• I\HI greater than 1.0
• II i~tory of trauma. deep \ CIIl thrombosIs. \aricose \ eiIlS. malignancy
127
\·cllloral
Poplltcal
Dorsal!,
Po~tcrior
I)cdl~
Tibial
RLI III
The pulse exam algorithm (Figure 6 I) is the clinicians gUide to triage patients for appropriate pathways for examination. referral and patient teaching. The lower extremity pulse exam can accurately assess ror the presence, absence. and location of arterial disl':ase. The patient should be supine \\ ith head and legs adequately SllPported. The commoll/('''lOrul urler" (eTA) is easily palpated with the second third and fourth fingers in the groin below and medial to Ihe inguinal ligament. If the patiellt is obese, the CFI\ pulse m"y be difTicult to palpate. If the pulse is
diminished or absent. the palient may have aortieiiliac disease. Figurc 6 2 indicates the location of artcries to palpate and to u~e for malll probe sltcs \\ hen taking Doppler readIngs (described later). The poplileal arIel''' is the most difTicuh to palpate. The artery is located midl1l1c bchll1d the knee 111 the popliteal fossa . 11,,\e the pallent slightly !lex at the knee. Il ave the
clinician place both hands behind the patient's knee in a cupped fashion and ,,110\\ the pu"e to bounce back Into the clll1lcian's hands. \'ore Irthe popliteal pul~c is ca . . y to pa l-
pate. this could indicate a popliteal aneurysm, and fur ther Il1\esligl:ltion is nceded from a vascular lab. The dorsalis pedis p/llse is examined by sitting or standII1g facing the patient. Using the second and third finge rs. palpate the dorsum of the fool. Place the thumb on the plan-
tar surface oflhc foot to anchor the.:: hand. Do not press hard because thc prc!ssure can occlude the artery. Use a light touch. The posterior lihialarle/:\" is palpated at the level of the ,.!Ilk Ie (medial and posterior). While facing the patient, lise the sec-
128
W OUND CAR l
r
Pulse Exam
[
Diminished (1+ , 2+) or absent pulses
Perform ASI and Iranscutaneous partial pressure of oxygen (tcpO,) measurements
ASI :>1.0 tcpO, : > 30 mm Hg (- diabetes)
I
Wound care (debride if needed)
Patient teaching: 1. Wound, foot care 2. Risk factors 3. Orthotics
Fi~u"c
6--1 Pulse exa m.
1
ASI : on APt 1o .. lf1on 0.8.
AT RISK: Polienh who oro ""y old, diabolIC, hype.1en ...., """"en APt 10 .. If10n 1.00 "'IJ9O'b orIerioI d. ...... • Comp"'_ therapy .t.ouId be uMd wolf> _ Tho Ioww the APt the 9'...... the orionoI 'mpo,nnonl
Fi g ure 6- 3 Proced ure fo r pe r fo rmin g ABI. SO llrce: Reprint e d wi th pe rmi ss io n from . Moffatt , The C ha ri ng Cross Approach to Ve nous Ulcers. Nursing Standard, Dec 12.5. No. 12 . pp. 6 9. c 1990. ROY'll College of' N urs ing.
NOllim'(lsil'f! Ih.\'('u/ar Testing
131
Table 6-1 Table of ASI Values
Dopplex · Ankle Pressure Index (API) Guide - _ _ - __ ~__ 10 15-40 045 50 55 ~.6.5 "0 75 80 85 9Q·9.s:l(X)')051101151iOl2jllO~~.J~_~~Z51801!!..!-90195'200 180 16 19 22 2.S 27 30 II 36 J8 .(\ "' j...o .5Ol52 55 58 61 63+66 69" n 75 n eo 8:.3 So 19 n 9.( 9'>' 00 180 17517 20 22:2S:28.j-31.'~:l?:40~4~~~t48:5~ • .s.t~5(~62:6S~·68r.71>" n-- IH I l- IU \( Fl RllIlR ~ 'Il 1I\
I' ~
I·OR
BI;Id. J. Black S Surgleallllanag~I1l":lllllfprc~'un.. ukcr" \/In Clm \"r/II 1m 191..:hnOCIllI.!III an l·"cnll'll ClIlllpUllcnt llf Ir..luIllillll.! "nUllO l.'ilrI.! 'm.! SlIr!: 1971< . 1.1:' -:'1.11< 2 ... 2
5
\gri .. J. ~ptr;1 M l}re, .. un.: ulcer,: pn;\1.!1lI10n ami Ircal mel\l , Clill SIll/II 197 1Ul 2 14
Kl1Ighl DB. Scntt II ("nlllr:tclur..: ,uul prc"urc nCCHl'I" \lelt/a.!!e_ jI)9U;16( 11M) 67
(,
Idllerg I L. ('erll~ K. SliIuO'cr I-S Pn:\..:ntioll and tre;lll11":11I orpr..:,,ur..:
'" Wound Type Pressure sores
Tissue Type Black/brown eschar
Consistency Hard
Adherence Firmly adherent ,
attached to all edges and base of wound
Amount of Debris
Debridement Choices
Rationale and Notes
75%-100% Wound
1. Autolytic-best choice is
covered
May use hydrocolloid or hydrogel; score eschar with scalpel for more rapid results. 2. Enzymatic ointment with
1. Transparent film dressings trap fluid at the wound surface with no absorp-
transparent film dressing.
secondary dressingmust score eschar with scalpel.
tive capabilities , providing
for more rapid hydration of the eschar and facilitating autolysis. Hydrocolloid/ hydrogel dressings have an absorptive capacity and may require more time for autolysis. 2. Enzymatic ointments
effective against collagen and protein may be most effective.
Black/brown eschar or Yellow/tan slough
Soft, soggy Soft, stringy
Adherent, attached to wound bas~,
50%-100% Wound covered
mayor may
not be attached to wound edges
1. Autolytic-best choices are hydrocolloids and hydrogels; composite dressings may also be beneficial. 2. Enzymatic ointment with secondary dressing.
3. Sharp, sequential, or one time-may be used alone or in conjunction with any
of the above methods.
1. Hydrocolloids and hydrogels provide for absorption of mild to moderate amounts of exudate while maintaining a moist wound environ-
ment to facilitate autolysis. 2. Enzymatic ointments
effective against collagen and protein may be most effective. May need to protect intact skin from enzyme and excess exudate.
Yellow/ tan slough
Soft , stringy
Adherent, attached to wound base; mayor may
not be attached to wound edges or loosely adherent to
Less than 50,¥> wound covered
1. Autolytic-best choices are hydrocolloids and hydrogels.
2. Enzymatic ointment with secondary dressing. 3. Sharp, sequential, or one
time-may be used alone or in conjunction with any of the above methods.
1. Hydrocolloids and hydrogels provide for absorption of mild to moderate amounts of exudate while maintaining a moist wound environment to facilitate autolysis .
wound base
continues
:E
c c z
"n>c:
Wound Type
Tissue Type
Consistency
Adherence
Amount of Debris
Debridement Choices
Rationale and Notes 2. Enzymatic ointments
Pressure sores
effective against collagen and protein may be most effective. May need to
(cont.)
protect intact skin from
enzyme and excess exudate. Yellow slough
Mucinous
Loosely adherent to
wound base, clumps scattered throughout wound
50%-100% Wound covered
1. Autolytic-best choices are hydrocolloids and hydrogels. 2. Enzymatic ointment with secondary dressing.
1. Hydrocolloids and hydrogels provide for absorption of mild to moderate amounts of exudate while maintaining
a moist wound environment to facilitate autolysis. 2. Enzymatic ointments effective against collagen and protein may be most effective. May need to protect intact skin from enzyme and excess
exudate. Should be discontinued when wound is predominantly clean.
Venous disease ulcers
Black/brown eschar
Hard
Firmly adherent, attached to ali edges and base of wound
50%-100% Wound covered
1. Autolytic-best choices are hydrocolloids and hydrogels. 2. Enzymatic ointment with secondary dressing.
1. Hydrocolloids and hydrogel dressings have absorptive capacity, which helps prevent maceration of surrounding
tissues and promotes autolysis. 2. Enzymatic ointments
effective against fibrin may be most effective.
-..
"-
~ ~
~
~ -5'., ~
C HA PTE R
8
Management of Exudate and Infection Barbara M. Bales-Jensel/
out of the open ti ssue. This fluid is se rou s or serosanguineous. Evaluation or the wound type, the number and type or organi sms present, and the condition of the patient arc important in determin ing risk for infection. Eva luation of wound type includes assessment of acute versus chronic wounds and necrotic versus clean. nonhealing wounds. The number and type of organisms present in the wound are evaluated for burden on the wound possible bacteria-produced toxins, and pathology of the organisms. Patient condition relates to immune function and local host defenses. In the infected wound, the exudate may thicken , become purulent. and continue to be present in moderate to large amounts. An example of exudate character changes in infected wounds is the presence of Pseudomonas organisms, which produce a thick. malodorous, sweet-smelling, gree n drainage,oI or PlVlelis infection, which may produce an ammonia odor. Wounds with foul-smelling drainage are generally in fected or filled with necrotic debris. and healing time is prolonged as tissue destruction progresses. 5 Wounds wit h significam amounts of necrotic debris will often have a thick, tenacious, opaque, purulent, malodorous drainage in moderate to copious amounts. True wound exudate should be differentiated from necrotic ti ssue sloughing off the wound secondary to debridement efforts. Exudate rrom sloughing necrotic tissue is common ly attached to or connected wi th the necrotic debris. However, frequent ly the only method of differemiation is adeq uate debridement of necrotic tissue from the wound. The solubization of necrotic tissue occurs most often as a result of enzymatic or autolytic debridement. Often the removal of the necrotic ti ssue dramatically reduces the amount and changes the character of the exudate. Wounds can become edematous when excessive amounts of plasma proteins leak from damaged capi llaries and per-
Wound exudate (also known as wound fluid and wound drainage) is an important wound aSSCSSI11CIll feature because
the characteristics of the exudate help the clinician diagnose wound infection. evaluate effectiveness of topical therapy, and monitor wound healing. Wound infection retards wound
healing and mllst be treated. Proper assessment of wound ex udate is also illlportaill because it afTirms the body's brief. normal. inflammatory response to tissue injury. Thus, accurate assessment of wound exudate and diagnosis of infection arc critica l components of effecti ve wound management. SIGN I FICANCE OF EXUDATE The healthy wound normally has some evidence of mois-
ture all its surface. Healthy wound fluid contains enzymes and growth factors, which may playa ro le in promoting reepithelializa tion of the wound and provide nceded growth factors for all phases of wound repair. I The moist environment produccd by wound exudate al lows efficient migration of epidermal cell s and prevents wound desiccation and further injury.~ J In acute wounds healing by primary intention, exudate on the incision line is normal during the first 48 to 72 hours. After that time, the presence or exudate is a sign or impaired healing. In fection and serom3 arc the two most likely causes. In chronic wounds, increased exudate is a response to the inflammatory process or infection . Increased capillary permeability causes leakage of fluids and substrates into the injured ti ssue. When a wound is present, the tissue fluid leaks
Nou~ :
The contributions ofNa ncyA . Stot ts, MN, EdD,arc gmtc-
fully acknow ledged.
159
160
WOLNIJ CARl
vade the wound cnviron mcllI. The fluid of wound edema contains proteolytic en7ymcs. bacteria and bacterial toxins.
CooperO suggests estimating the percentage of exudate in
prostaglandins. and necrotic debris, a ll of which contribute
the wound exudate is thick and can be observed in the wound bed. When wound exudate charactcr is more serous in nature, clinica l observation of the wound alone is insufficient to quantify the amount of drainage. For thinner wound exudate, the amount of drainage is estimated by noting the number of dressings saturated during a period of time. Although not part of exudate assessment. evaluation of the wound dressing provides the clinician with valuable data about the efTcctiveness of treatment. Eva luation of the percentage of the wound dressing involved wi th wound drainage during a specific time frame is helpful for clinicalmanagelllent that includes dressings beyond traditional gau7c. In cstimating thc percentage of the dressing involved with the wound exudate. clinical judgment is quantified. as the clinician must put a number to visua l assessment of the dressing. For example. the clinician might determine that 50'. orthe hydrocolloid dressing was involved with wound drainage over a 4-day wearing period. Based on the above data, the clinician might
to prolonged chronic inflammation. Exudate also drains valuable and needed substrates, slich as growth factors. from the wound bed and impairs the healing process. Excess exudate losses drain substrates and energy that could be used ror wound healing processes:'
Asscssmcnl of\Vo und Ex udate C hara cteristics of exudate arc color, consistency. adherence, distribution in the wound the presence of odor, and the amount prcscnt. lI The color and consistency of wound exudate may vary depending on the type of wound degree
of moisture in the wound the wound recovery cycle. and the presence of organisms in the wOllnd. Table 8- 1 presents \iuiOliS types of \'v'Ound exudate and associated characteristic!'!. Color Plale serie.\ 40 ItJ 45 (reading the dressing and wound exudate characteristics) will help the clinician identify exudate types and make an appropriate assessment of significance. Estimating the amount of exudate in the wou nd is diITicu lt because of wound si7e va riability and topica l dressing types. Certain dressing types interact with or lrap wound nuid to create or mimic certain characterist ics of exudate, such as color and consistency of purulent drainage. For example. both hydrocolloid and alginate dressings mimic a purulent drainage upon removal of the dressing. Preparation ofthc wound site for appropriate exudate assessment involves removal of the wound dressing and cleansing to remove dressing debris in the wound bed. Then cvaluate the wound for true exudate.
the wound by clinical observation. This approach \\orks ir
quantiry judgment for this type or dressing, length or dress-
ing wear time, and wound et iology 3S n "minimal"' amount of exudate. Cli nical judgment of amount of wound drainage requires somc experience with ex pected wound exudate output in relation to phase of wound healing and type of wound and knowledge of absorptive capacity and normal wear lime of topica l dressings. One problem wi th assessment of exudate amount is the size of the wound. What might be considered a large amount of drainage for the sma ller wound may be considercd a small amount for the larger wound, making clinically meaningful assessment of exudate more difficult to obtain.
Tabl e 8-1 Wound Exudate Characteristics Color
Exudate Type
Consistency
Significance
Sanguineous/bloody
Red
Thin, watery
Indicates new blood vessel growth or disruption of blood vessels
Serosanguineous
Light red to pink
Thin, watery
Normal during inflammatory and proliferative phases of healing
Serous
Clear, light color
Thin, watery
Normal during inflammatory and proliferative phases of healing
Seropurulent
Cloudy, yellow to tan
Thin, watery
May be first signal of impending wound infection
PurulenVpus
Yellow, tan, or green
Thick, opaque
Signals wound infection ; may be associated with odor
A/altagemellf (?r EXlldal(' anti /II/i.!ction
Appropriate wound c.xudatc assessment requires consideration of wound etiology. Independent of exudate differences related to etiology of the wound certain characteristics of exudate indicate \",ound degeneration and infection. If SIgns of celluhlls (erythema or skin discoloration. edema. pain. induration. and purulent drainage) arc present at the \\-'ound site. the exudate amount may be copious and seropurulent or purulent in character. The amount of exudate remains high or increases in amount and character may change to frank purulence wl,h further wound degeneration . Wound IOfecllon must be considered 111 these cases regardless of etiology.
161
As the \'enous ulcer heals. edema is lessened and the wound exudate increases . The excess nUld takes the path of least resistance. which in this case is the wound bed! Often venous wounds will appear with yello\\ fibrinous material covering the wound which must be differentiated from true exudate. Pre.\ .\UI"e So,.e!tl
Venous disease wounds lIsually arc highly exudative bOlh on initial prest.!l1tation and throughollt the course of healing.
Pressure sores present \\ ith a variety of \\iOlll1d exudate characteristics and amounts. In parllal-thlckness pressure sores the \\'ound exudate is most likely to be serous or serosanguineous in nature and presents in minimal to moderate amounts. In clean full-thickness pressure sores the wound exudate is similar. with minimal to moderate amounts of scrous to serosanguineolls exudate. As healing progresses in the clean full-thickness pressure sore. the character of the exudate changes and may become bloody if the fragile capillary bed is disrupted and lessens in amount. For full-thickness pressure ulcers with necrotic debris, wound cxudate is dependent on the presence or absence of infecllon and the typc of therapy instituted. Exudate may appear moderate to large. but in fact be rclated to the amount of necrotic tissue present and the liquefaction of the debris in the wound. Typically. the necrotic full-thickness pressure ulcer presents with serous to seropurulent wound exudate in moderate 10 large amounts (Figures 8 IA and 8 (8). With appropriate treatmcnt. the wound exudate amount may also tcmporarily incrcase. although the charactcr gradually assumes a serous nature.
A
B
A rteria/I/.\ chem ito If ollm/.\
Exudate 111 the ischemic wound may vary in amount and character Arterial ischemic wounds arc often dry or have only a scant to small amount of serous exudate present. Veuropllthil' "olilld.\
Neuropathic wounds may present with very little exudate presellt. One pOSSible reason for decreased exudate is a limlied innammation response due to concomitant vascular disease and Immune status changes from diabetes. Generally. the exudate is mll1imal and usually serous or serosanguineous in character. J (!IIOll.\ Di.\(!u.\(! HOI/lid.,·
Fi~urc
8 1 \ :tnd B. Ob\ iou, "gns of mfectton
SIGN IFI CANCE OF I NFECTION
!\1ct h ici II i n-I{csista n t SllIp/ty/Ol'Ol'l'u.\ A II rell.\
Although bacteria colonize all chronic wounds, wound coloni7ation by bacteria is not the same as infection. When host and wound condi ti ons arc favorable. infection can occur. Wound infection extends inflal11matory response. delays collagen sYl1lhcsis. retards cpithclialil.ation. and causes more injury to the tissues as the bacteria compete with fibroblasts and other cclb for limited amounts of oxygcn.~ Large acule wounds generally reaci to bacterial burden in a way different from that in small chrollle ulcerative wounds. ACLIte \\o'ollnds arc marc susceptible lO bacterial invasion by skin flora. in particular those with prolonged inflammatory rcsponscs. ~ Wounds with loss of large amounts of surface area (15 11/0 of body surface area or greater) arc also at a higher risk for bacterial invasion. SufTicient number:; of skin flora organisms will cause acute \vounds like graBs and flaps to fall and, ifuntreated lead to sepsis while a chronic leg ulcer may remain unchanged for months or years with no signs of infection or sepsis with the same or largcr number of organisms presclll.lC Thc same organisms that pose serious threat of infection and sepsis in some acute wounds present entirely difTerent pictures in the sma ll chronic WOUJ1(l which may go on to heal despite the presence of these organisms. Chronic wounds arc oBen contaminated \\ ith skin flora. such as Emerf)cocclis. Stap/ty/ocOCCf/.\, Bacillus, or occasionally gram-negative organisms. 1I Distinguishing between contamination and infection in wound, is orten difTicult. The process of difTerentiating between a contaminated wound and an infected wound is important to better underMand treatment choices. Coloni/ation is the process of a group of organisms living together. whereas infection is the invasion of tissues by microorganisms. resu lting in a systemic reaction. Most clinicians will agree that IO~ to IO~ organisms per gram of tissue indicate wound infection. Some laboratories lise different references, so what Illay be considered colonization in one facility may be considered infection in another facility. In general. the o\-erall condition of the patient also enters into the diagnosis process. Infection is signaled by a systemic reaction to the microorganisllls. and contami nation signals the presence of microorganisms in the wound. II igh leyels of bacteria arc found in chronic wounds with necrotic debris. The number and density of aerobes and anaerobes are greater in necrotic wounds and those with undermining. s The presence of a foul odor is usually associated with anaerobic organisms. Sharp debridement of necrotic tissue virtually eliminates the anaerobic organisms (such as Ba c teroilif!s , Streptococcus, EIIIl'rohucter, and Escherichia coli) and decreases the aerobic organisms (such as Sraphy/ococclI\' lIUf'f!IIS) present in the wound . ~
Methicillin-resistant S lIllH'II\' (MRSA) presents special concerns for patients with wounds. SWphy/ococl"Il.\ lIureliS IS part of normal skill flora and IS on the Skill of approxImately 20 00 to 50°'0 of healthy adults and can persist in wounds.' Patients at highest risk for de\'eloplllg MRSA colonl/ation and IIlfecllon arc those wllh a 111story of injecllon drug abuse, the presence of chronic discase. prc\ious antimicrobial therapy. prc\iou:,,> hospltali/ation. admiss ion to an IIltensi\'e care unit. or a prolonged stay in a health care institution. ln All forms ofSt/un'lI\,. includlllg M RSA. can quickly ill\ade and infect breaks in skin integrity. making woulllb onc of thc most C0l111110n sites of ,\. allrew infection and a site commonly coloni/ed with S 1IIIH' II.'i or M RSA. In the early 1940s. pellicillll1 was found to be cfTectiH! against S 1I111'l'1I.\: howcver. soon after Ih IIlllial usc. some strallb of S (JItreliS began to produce the ell/yme penicillinase. \\ hich lIlacti\·atcs antimicrobial\ slu;h as ampicillin. other pelllcillins. and cephalosp0rlns. MethiCillin was the fir:">t penicillinase-resistant semisynthetic penicillin and was (and is) used to treat S 1I11rellJ infcctions. The late 1960s and early 1970s saw the emergence of MRSA \\ ith the first rcports of outbreaks in both ,lcute and long-term caJ'e facilities.'" In fections caused by MRSA cause conccrn bec~lUsc resistance to I11cthlCllI1ll IS associated \\ IIh resistance to other tlntlllllcrobials. A gene on the bacterial chromosome that codes for abnormal penicillln-biJ1(ilng protein (PI3P) carries resistance to l11ethlcllllll .'" ThiS abnormal PBP has il lower afl'inity for all peniCIllin. so ,cry little methicdlin blllds to It. Therefore. all pel1lcillins. \'vhich mllst bind to the PSP site 111 order 10 kill the bactena, arc incffccth'c. Some strains of MRSA mutate and become resistant to additIOnal anwnicrobials. Of special concern is the recent finding of the potcnllal for MRSA to acquire the gcne-conferring \·ancol11ycin resistance from yancomycin-resistant enterococci (VRE). leading to vancomycin-resistant S UUI'('II\.'l Since yancomycin IS the drug of choice for treating MRSA. resistance to \'),Ufe )'orcs in geriatric patients. JAm G"rillll' Soc. 1983:31'7 10 712
CHAPTER
9
Management of Edema Laurel A. Wiersema-Bryanl
INTRODUCTION
cations, especia lly th e ant ihypertensive age nt s. may ca use leg edema. T hese medi ca ti o ns inc lude calcium c ha nn e l blockers, clo nidine. minoxi dil . guanethidin e mo nosulfate, hydra laz in e , ra uwo lf ia d e ri va ti ves, m e th y ld o pa . a nd di azox ide . l Managi ng a clie nt with mo rbid abe ity requ ires the ass istance of the tea m in directing the clie nt to appropriate exercise and weight manage ment strateg ies. Fitting these clie nt s w ith co mpress ion therapy is a cha ll e nge; in these indi vidua ls we are asking for mult iple li fes tyle adju stm ents to be made to reduce the we ig ht a nd manage the edema. Increased inte rstiti a l vo lume is a noth er reason fo r ede ma. These c li ent s may suffer from a protei n-l os ing entero pathy, li ve r c irrhos is, rena l fa il ure, and/or prote in-cal ori c malnutriti o n. Ca re must be taken to ma nage the frag ile skin. a nd edema manageme nt becomes a s uppo rti ve th era py as the unde rl ying med ical pro ble m is add ressed. A nother category of edema is th at re lated to drug therapy w ith hormo ne replaceme nt. Ho rmo nes in thi s ca tego ry include corti coste ro ids, estrogen, testosterone. and progesterone. Clients ex perie nci ng edema secondary to hormo ne therapy generally respond we ll to leg elevat ion and exerc ise. If compression stoc kings are req uired, the low co mpressio n usua ll y wo rks we ll. Client s with primary lymph edema require aggress ive management and ge nera ll y require compressio n at much hi gher levels than the indi vidua l w ith primary veno us hyperte nsion. Comprehensive management o fl ymphedema is not addressed in thi s chapte r. The reader interested in thi s to pic is enco uraged to obtain info rmati o n from the Nati ona l Lymphedema Netwo rk o r oth er so urces avai lable to th em.:!
In this chapter. the reader w ill f ind a di scussio n of the etiologies associated wi th edema and stra teg ies directed to-
ward the manage ment of edema. Management of edema includes a desc ript ion of the procedures fo r managing edema
and parameters to measure in determining outcome. Emphasis is placed o n th e steps the cl ie nt needs to tak e in o rder to care for himselfo r herself beca use th e manage mcm a nd control of edema requires a n investm ent of lime, energy, and dedi cati on on the part of th e client. At the end of th e chapter two case studi es are d isclissed in an e tTort to appl y th e as-
sessment. management plan, and outcome evaluation of the chapter content.
OVERVIEW OF THE PROBLEM Venous disease w ilh ul cers occ urs in approximatel y 1% of the genera l po pulati on and 3.5% o f pe rso ns ove r the age of 65 years. Edema in the c lient w ith ve no us di sease occurs as a res ult o f sustain ed inc reased ve no us pressure. This ve nous hypert ension may occur primaril y in the dee p ve in system (femora l, popliteal, and tib ial ve ins) o r the supe rfi cial system (t he g reat er and lesse r sapheno us ve ins or the perforator ve ins th at join thc dee p and s uperficia l syste m). These problems may occ ur in isolati o n o r in combinati o n. Respecting th e underlying pathology is criti cal in the man age ment o f these client s. Increased ve no us pressure may be a res ult of chronic venous insuffi c ie ncy (as described above), ca rdiac disease. pe lvic tumors th at place increased pressure on or occl ude veno us a nd lymph atic return , o r mo rbid obesity in whic h the weight of the abdo me n may restri ct venous and lymph ati c return. In clients with ede ma seco ndary to cardi ac disease , manage ment of edema needs to be accomplished in co ncert wi th the ca rd iologist. A number of medi-
TESTS AND MEASUREMENT Meas ure men t of edema and edema control ca n be di vided into two primary ca tegori es of q uantit ati ve and qualit ati ve find ings. Q uant itatively, leg c ircumfe rcnce a nd leg vo lume
179
can bc mcasu red to give a reference range of Icg siL.e: with ca re, pilling edcma can also be measured and quantified. Mcasurin g leg circumference is an easy tool for c linica l usc; mcasuring leg \'olumc is less ··friendly" clinica ll y. but it is a good mcas ure of leg volume. Leg circumference can be measu rcd with a disposable tape. obtaining measures of the calf 10 c m belo\\ the IIlfcrior rim ofthc patella. at the \isually largest portion of the calf ( if different fro m the first measure). and 5 cm above the superior rim of thc lateral mallcolus. These measuremcnts, plottcd over time. pro\ide a refere nce range for leg size and progress toward edema con trol. Leg \01u1l1c measuremcnt requircs a large cylinder. which wi ll hold the c li ent's leg. and a basin to hold the water that is displaced. The cylillder or chamber is filled with water and the clicnt's lower leg is placed in the chamber. allowing th c excess watcr to be displaced O\"cr the top and contained in the reservoir. The volumc of water is then measured: the amo unt displaced will decrease as leg \'olume (ede ma) is dccreascd. Leg circumfercnce is measured wc!ek ly o r with eac h clinic/n ursing \'isit. Measurement of pitting edcma is onen dcscriptivc~ howcver. edema can be quantified by using a simp lc grading sca le as out lined be low:
o to L4-inch pitting ti .. to t/2- inc h pilling t/2 to I-inch pitting > I-inch pitting
I + (mild) 2+ (moderate) 3+ (sc,cre) 4+ (very se,ere)
Clinical Wisdom: Improper Bandagmg of Edematous Foot The foot shown in Figure 9-1 shows pitting at the arch where the bandage was wrapped. This indicates that the bandaging was started up too far on the foot. Bandage should have been started at the toes.
Qualitative measures to follow include the general appearance of the leg. the shi niness of the skill. the amount of drainage frol11 the uiccr(s). ifprcsent. and the client's sense of the heavi ness or \veight of the leg. It is also important to docllment the appearance of the Icg when the \HapS arc rCl110vccl loo king for areas of ridging and bu lging between the layers o r above the level ofthc wrapping. Clients may a lso identify changes ill how their clothing and shoes fecI.
Figuf1.' 9- 1 Pllung ctll.!ma. Source Rt.:pnnlcd \\ IIh rcrnm.... ion from
R.B. Chmnhcrs and N. Unman. Orlhnllc Management Mlhe Neuropathic anrJDY"'''Jsculaf P'lllcnl. 111 Irlu.\ 01"0,.,110.\0 cllld.h.,i.\fII"(, Dnin'.\. 3nl cdnion. 11 Goldberg and lD, 'hu. cds .. p, 450. ( 1997. ,\.lnshy- YC J I/mp 111/('1'1 191(4;5 :6 1) 73. )(HII1£ JB, DubrJ'anslo.l S. I)rcssurc sorcs epidellllology anti I;urrcnt managcment com:epls, f)rI/.I!.\ ,·Ij.!/Ilg 1992;2:42 57. Brown CD, Ilte1li J/\ " rc\ic", of topil.'al agent .. for \\'OUI1(1\ and methods of woundlllg . ./ IkrllWfof SlIr.1! Ol/wl J (1).1; J 9
H27.n 4()
Din: JD. \\el ... h ,\P. A clllllpariMHl of wound Irrlgatiun solution used the emergency department '"" Emt'l".I!, .\It'd June 11}90; 71)4 71)7
111
P A RT
III
Management by Wound Etiology Barbara M. Bales-Jensen
Determining the cause or etiology of a wound is a critical element in creating a co mp rehe nsive trea tm ent pla n for pati ents with wounds. The chapters in Part III foc liS on management by wound etiology. Specific attention to acute surgical wounds, pressure ulcers, vasc ular ulcers, and neuropa thi c ulce rs is prese nted in the chapters in Part III. Em phasis is placed on understanding the pathophysiology involved in the wound type, assess ment methods, and prevention and manage ment of spec ific wound types. Improving and expanding knowledge of wo und eti ology empowers
cli nicians to provide quality comprehensive care in clinical practice. In Chapter II Bates-Jensen and Wethe present management of the acute surgica l wound. Th e chapter begins by defin ing the acu te and chro nic wound. When does an acute woun d become a chronic wound? The easiest and perhaps the least controversial defin ing characteristic of the acute wound tha t becomcs chronic is fa ilure to follow the normal wou nd hea ling tem poral sequence. Better understanding of ac ute wou nds im proves ability to monitor and treat all wounds. Types of surg ical wound healing- primary intention, secondary intention, and tertiary intention- are presented. Extrinsic factors that affect wound hea ling during the preo perati ve, intrao perative, and postoperati ve time periods are described. Surgical wound class ifications are presented and reviewed. Interven tio ns fo r managi ng hypovole mi a. thermoregul ation strategies, and meth ods o f optimizing tissue oxygen perfusion are described. In tri nsic factors affecting hea ling of the acute surgical wo und are those that innuence the person systemically. Examples of intrinsic factors incl ude age, concurrent conditions, nu trit ional stat us, and oxygenation and tissue perfusion. Each intrinsic factor is disc ussed with special attention to the patie nt with diabetes. Examination of the surgical in-
cision includes evaluation of wou nd characteristics such as incision locatio n, length , presence of hea li ng ridge, type and amount of exudate. type of wound closure materials. and approx imation of wound edges. The incisional examination forms the basis of acute surgica l wound assessment and is presented by phase of wo und heal ing (i nflammatory, pro li ferati ve, and remodeling). Management of the surg ica l incision includes atte ntion to factors that affect wound heali ng as addressed in Chapter II , as well as dressing care. The surgical dressing includes the primary and secondary drcss ing. Di scussion inc ludes types of dressings lIsed for pri mary and seconda ry dressings. Wound healing in secondary intention and tertiary in tention wo unds is discussed and cont rasted with pri mary intention incisions. Outcomc measures for eva luati ng heali ng in incisional wounds following the phases of wound hea ling are presented and described. Thi s sectio n includes examples of approp riate documentation of the healing incision. Chapter II concludes with a case study for review of material and self-care teaching guidelines for use wi th other health care prov iders, famil y caregivers, and patients. Chapters 12 and 13 descri be issues related to managemcnt of pressure ulcers. Chapter 12 is devoted to pathophysiology and prevention of pressure ulcers. Pressure ulcers arc areas ofl oea l tissue tra uma that us uall y develop where soft tissues arc compressed betwee n bony prominences and any external surface for pro longed peri ods. Chapter 12 begi ns with a definition of pressure ulcers and an extensive rev iew of the pathophys iology of pressure ulcer development. The re lationship between time and pressure in the deve lopment of pressure ulcers is presented. Clinica l presentatio n of pressure ulceratio n and the 1110st preva lent locations fo r pressure ulcer development are covered. Specific information is i112 15
2 16
W OUND CARE
el uded o n assess ment or the dark-skinn ed ind iv idua l for risk o f pressure ulcera ti on. Pressure ulcers are commo nly classified according to g rading or staging sys tems ba sed on th e depth of ti ssue destructi on. The sta ge is dClCfmincd on initial assessment by noti ng
the deepest layer of tiss ue involved. The history of stag ing systems and th e c urrent system recomm ended by the Age ncy
for Hea lth Care Policy and Research and the National Pressure Ulcer Ad visory Panel are described . The issue of pressure ulcer assess ment and the usc and misuse of staging classi fi cation systems are a subject of debate and cont roversy. Pressure ulcer develo pment docs no t necessa ril y occur fro m
one stage to the nex t, and there may be different etiologic factors f'or va rio us stages. Chapter 12 reviews this issue. Di scussion of press lire ulcer pathophysiology and etiology would not be complete without mention of other interac ting facto rs. Pressure ul cers are phys ica l ev idence of multiple causati ve influences. Factors that contribute to pressure ulcer developmcnt can be th ought of as those that afTcct the prcssure fo rce over the bony prominence and those that affect the tolerance of the tissues to press ure. Mobility, sensory loss, and ac ti vity level are related to the concept of increasing pressure. Ex trinsic factors such as shear, fri ction. and moisture, as well as intrinsic fac tors sllch as nutrition, age. and arteri olar pressure relate to the concept of tissue tolerancc. Each of thc factors is presented and discussed. Particula r attention is given to immobility or severely restricted mobility because it is the 1110st important risk fac tor for all populations and a necessary condition for the deve lopment of pressure ulcers. The most common risk assessment tools, Braden·s Scale for Predicting Pressure Sore Risk, No rt on's sca le. and Gosnell 's scale, are all presented and di scussed. Preve ntion strategies are ta rgeted at reducing risk factors present. Appropri ate prevention intervent ions can be focused on eliminating spec ific ri sk fac tors. Thus, earl y intervention for pressure ulcers is ris k factor- spec ific and prophylactic in natu re.The preve ntion strategies arc presented by risk factors. begi nning with general informat io n and ending with speci fi c strategies for a particular ri sk fac tor. Chapter 12 includes speci fi c information on the use of support surfaces with de finiti ons of pressure-reduci ng and pressure-relieving dev ices, pill ow bridgi ng, and pass ive repositioning. Extensive discussion on nutrition interve ntions and management of incontincnce is included. Skin hygiene interventions and sk in maintcnance interventions round out the prevention strategies. Chapter 12 concludes with outcome measures for eva luating thc success of a pressure ulcer prevention program and extensive sc lf~ca re tcaching guidelines for other health care prov iders. fa mily caregivers. and patients. In Chapter 13, Rappl continues the di scussion of support surfaces that began in Chapter 12. Rappl provides a look
at therapeutic posit io ning for pressure ulcer prevention. Persons who become sitting dependent more than a m~ bu latory and those who use the lying-down or the sitting position for the majorit y of their day are at high risk of skin breakdown. And for the patient with an ex isting pressure ulcer, proper positioning in the most acti ve and fu nctional position possible. both in sitting and in recumbent positions, improves the healing rate of the ulcer and mini mi zes the likelihood of developing new ulcers. Chapter 13 provides an overview of therapeutic positioning kn owledge. The areas the clinician should exam ine in order to determine the need for intervention arc presented and described. The bas ics of therapeut ic positioning and a di scussion of how therapeutic positioning affects body system impa irments is presented. The chapter includes a ta ble on fun ctional diagnosis and relationship to prognosis. interventions. and out comes related to therapeuti c posi tioning. The idea l sitting position is described, and basic seating principles re lated to pelvic co nt ro l, th igh cont ro l, scat dept h, and footrest arc di scussed . Finally, spec ifics in pos itioning the patient with an ex isting ulcer both in sitting and in lying down are described. An extensive di scussion of methods of determining appropriate wheelchai rs and sitt ing pos ition and proccdures for recumbent posit ioning for patients is presented. Donayre provides an in-depth analysis of the diagnosis and management of vascul ar ulcers in Chapter 14. The chapter begins with a review of ge neral anatomy and physiology of the circulatory system and pathophysiology related to lower extremity ulcers. Thorough hi story and physical assessment are essential for the patient wi th a lower leg ulcer, and Donayre prov ides this information for each ulcer type; in addition, risk factors for arteria l/ischemic, ve nous, and diabetic ulcers are discussed. Donayre describes presentation and assessment of common find ings related to lower leg ulcers, such as intermittent claudication, rest pain . altered an kle- brachial index, edema. and tissue changes. Associated diagnostic tests for the lower leg arc described. Differential diagnosis for leg ulcers is a key fac tor in determining appropriate treatment. Treatment that is appropriate for a ve nous ulcer may be contraindicated for an arterial/ischemic ulcer. The presenting clinical manifestations, diagnostic tests, and differential wound assessment are presented for each lower leg ulcer type. Medical and surgical manage ment related to arteria l/ischemic, venous di sease, and diabetic ulcers is described. Special attent ion is given to diagnosing osteomyeliti s in the diabetic and describin g pathophysiology of edema related to ve nous di sease with indications for clinica l manage ment . Part III concludes with Elfiman 's presentation of the neuropathic foot. Chapter 15 opens with a disc ussion of the necessit y of interdisciplinary coll aboration in the management
Par/III
of neuropa th ic ulcers. The neuropat hi c patient ofte n has dysvasc ul ar components Ih at muSI be add ressed by a m ed i ~ ca l tea m ra th er Ih an one specialty. The trineuro pal hy assess ~ ment with allen tion to senso ry, motor, and a ut onom ic neur-
opathy is explained. Gradua l and sudden-onset peripheral neuropa thy are compared for easy differential diagnos is. Diabeti c neuropathy is th e major foca l point of Chaptc r 15. Common infections and derma tologic changes are prese nted. T he definitions of wet and dry ga ngrene are prese nt ed, and the two conditions are compared. Footwear assess ment guidelines and interve nt ions based on th e Wa gner ul cer g rade is
explained. Chapter 15 includes in-depth exp lanatio ns of sensory, pressure, vi bra tory. and root de formit y eval uati on.
Charcot's deformi ty is explained and the method of assess-
2 17
mcnt described . Managemcnt wilh orth otic devices is explained. Specific instrll cti ons for procedures. such as how to make a foam toe se parator are incl uded. Interve nt ions to decrease pressure, such as tota l-contact cas ting. use of splints and insc rt s, and ncurowa lke rs are all di sc ussed. T he chapter concl udes with self-care teac hin g g uide lines ror usc wi th patie nt s and family caregivers and doclimentation req uirements for ne uropath ic ul cers. Although similarities exist in th e treatment ora ny wo und, treatment ap proach va ri es depcndi ng on wo und eti ology. The c hapters in Part III form a foundation on knowledge o f wounds of va ri olls eti ologies. This fou nd ation should provide c linicians with a stron ger and more indi vidualized ap~ proach to th e person with a wou nd .
CHAPTER
11
Acute Surgical Wound Management Barbara M. Bales-Jensen and James WeIhe
ACUTE SURG ICA L WOUND DEFINITION
Acu te wounds arc defined as disruptions in the integrity of the skin and underlying tiss ues that progress through the healing process in a timely and uneventful manner. The acute elective surgical wound is an exampl e of a healthy wound in
which healing can be maxi mi zed. However, not all surgical wounds are uncomplicated, with maximal healing potential or the possibility of uneventful healing. For example, acute surgical wounds can occur in unhealthy tissues, in a compromised host, or as a res ult of unexpected or significant trauma. Surgical wounds may be allowed to heal by one of three methods : primary intention, secondary intent ion. and tertiary intention (Table 11 - 1). Wounds healing by primary intention are wounds with edges approximated and closed. Secondary wounds are wounds left open after surgery. Secondary healing wounds heal wi th scar tissue replacement in the ti ssue defect. Tertiary wound hea I ing, or delayed primary closure, involves aspccts of both primary and secondary wound healing. In tcniary wo und healing the wound is left open ini tiall y and afier a short period of time the edges are approximated and the wound is closed. Wound healing by secondary intention or dchisccd wounds may not follow a timely and uneventful healing course and thus may be considered "chronic" wounds by some clinicians. I When does an acute wo und become a chronic wound? The easiest and perhaps the least controversial defining characte ri stic of the acute wound that becomes chronic is failu re to follow the normal wound healing temporal sequence. In general, the acute surgical wou nd should complete the proli ferative phase of wound healing in 4 weeks. For example, th e wound should have filled with granu lation tissue and be resurfaced with
epithclial tiss ue. Acute surgical wounds that progress at a slower pacc or fail to progress can be considered chronic. The surgical inci sion healing by primary intention might be described as the ideal wound for healing. The wound is controlled with attention to ti ssue handling and proper use of surgi ca l instruments by the surgeon. and the wound edges are apposed and aligned immediately to decrease the risk of infection. The acute surgi ca l incision wound healing by primary intention is the focus of thi s chapter. FACTORS AFFECTING HEALING I N ACUTE WOUNDS
Healing in acute surgical wounds involves the interaction of extrinsic and intrinsic factors. Extrinsic fac tors relate to those agents outside the person , whe reas intrinsic factors are those influencing the person internally or systemically. Extrinsic Factors The physical environment before and during surgery, the surgical preparation , the technique of the surgeon, and types of sutures are all examples of extrinsic fac tors aficct ing acute wound healing. Thus for the surgical woun(~ evaluation of the perioperative period is indicated, as it plays a role in the wound outcomc. Wound infection is the major cause of surgical wounds ' fai lure to progress through th e healing process in a timely and unevcntful manner. Operat ing room protocols, attention to instrumentation, and appropriate surgica l technique are all means of decreasing the risk ofinfecti on and ensuring optimal healing from the outset for the surgica l wound.
219
220
WOUND CARE
Table 11 -1 Types of Surgical Wound Healing Wound Healing Type
Definition
Primary intention
Wound edges approximated and closed at time of surgery
Secondary intention
Wound left open after surgery and allowed to heal with scar tissue replacing the tissue defect
Tertiary or delayed primary closure
After surgery, wound left open initially and after a short period of time the wound edges are approximated and the wound is closed
Preoperlllive I'er;or/ The length oftimc the patient spends in the hospital prior
to surgery innucnccs the rate of surgical wound infection. As the length of hospital time increases prior to surgery, the
risk of wound infection incrcascs. 2 Prcparation orthe operative site also innucnccs the risk of wound infection. Showering immediately prior 10 surgery. lIsi ng a hexachlorophene soap. has been shown to result in a decrease in infection rate, compared with not s howering . ~ Shaving the operative area and the method used to shave the area have also been impli-
cated in surgical wound infection.
Research Wi sdom: Operative Site Preparation
Use of an electric razor, clipping hair, and not shaving the operative area are all associated with wound infection rates lower than those with use of a nonelectric razor to shave the operative area. 2 0espite the research, however, most preparations still include nonelectric shaving, most commonly performed in the operating room. The poor implementation of the research may be due to the absence of electric razors or clippers in the operating room.
contaminated wounds are procedures wherein the gastrointestinal (G I) tract or respiratory tract is entered without signi ficant contamination. A contaminated wound is one in which a major break in ste rile technique or gross spillage from the gastrointestinal tract occurs. Procedures in which acute bacterial inflammation or pus is encountered with devitalized ti ssue or contamination are classified as dirty or infected wounds. Increased length of time for the operative procedure increases the risk for wound infection significantly. One study found that th e infection ratc doubled each hour the surgical procedure continued.:! Strict adherence by operating room personnel to a protocol ha s also resulted in decreased wound infection rates. 4 The surgeon must be concerned with wound tension , vascular supply, and proper surgical technique. If the wound ca nnot be closed without a significant amount of tension or if the vascular supply is poor, there is increased risk of dehiscence and infection.~ Suturing technique can assist with optimal wound healing outcomes. Use of buried sutures ca n improve primary wound healing by decreasing potential dead space underneath the incision, giving ten sile support for 4 to 6 weeks while the wound is still weak. and decreasi ng tension on the apposed wound edges. ~ Surface sutures may provide additional concerns for optimal hea ling because they provide additional "wound s" to heal alongside the incision.
ill frtlOperllfi l'e Periol/
po:,·toperlllive Perioci
Limiting the infection rate intraoperatively is largely under the control of the surgeon . Sometimes infection co ntrol is hard to obtain. For example. the surgeon has limited power over the nature of the problem for which the surgery is performed the operative si te. and the general condition of the patient ; all arc more complicated factors that are not easily controlled. The type of surgical procedure influences the risk ofinfcction. Surgical procedures are classified according to the ri sk of infection .1 Table 11 - 2 prese nts wound classification s for s urgery. Clean wounds are those nontraumatic injuries in which no innalllll1ation is encollntered during the procedure and there is no break in sterile technique. Clcan-
The stress response associated with surgery has also been implicated as a cause of impaired wound hea ling. The stress of surgery is known to stimu late the sympathetic nervous system with a resultant sympathetic nervous syslemmediated vasoconstriction. The effect of high levels of circulating catecholamines in the immediate postoperative period causes the resulting vasoconstriction with factors leading to the trigger of the sympathetic nervou s system, including hypoxia, hypothermia, pain, and hypovolemia.b ln the immediate postoperative period measures of subcutaneous ti ss ue/wound oxygenation arc lower after major operations
Acute Surgical Wound Nlcmagemel11
22 1
Table 11 -2 Surgical Wound Classifications Surgical Label
Definition
Clean
• Nontraumatic injuries • No inflammation found during procedure • No break in sterile technique
II
Clean-contaminated
• Procedures involving GI or respiratory tract • No significant contamination
III
Contaminated
• Major break in sterile technique • Gross spillage from GI tract
IV
Dirty or infected
• Acute bacterial inflammation found • Pus encountered • Devitalized tissue encountered
Wound Classification
and correlate wi th extensive. morc complex surgica l procedurcs.b Attempts to restore ti ssue and wo und oxygen defi cits re late to minimi zing the risks of hypoth ermi a. pain, hypovolemia, and hypoxia si multaneously in the immed iate postoperative period.
Clinical Wisdom: Maximizing Wound Healing Critical measures to maximize wound healing in the immediate postoperative period include all of the following . Keep the patient • Warm • Well hydrated, intravenously or orally • Pain free by use of patient-controlled analgesia if possible • Well oxygenated by use of supplemental oxygen if needed
Thermoregulatory responses are diminished in the surgica l pat ient because th e prolonged exposure to thc co ld
or
Correc tin g hypovolemi a wi th adequate fluid infusion preven ts continuing vasoconstri ction caused by hypovo lemia . Fluid replacement occ urs si multaneollsly with rewarming efforts. Assessment and management of pain and ti ssue perfusion are also recommended to ensure optimal wo und healing.6 Additional factors crucia l to opt imal surgical wound hea ling in th e postoperati ve period are intrinsic factors that can be controlled, which are discussed in th e following sect ion.
In trinsic Factors Intrinsic factors affecting hea ling of th e acute surgica l wound are thosc that influcnce th e person systemically. Intrin sic factors include age, concurren t conditions. nutritional statu s. and oxygena ti on and ti ssue perfusion. Age The physiologic changes that occur wi th aging place the older individual at higher ri sk for poor wound hea ling outcomes. Decreased elastin in the skin and differences in collagen replacement innuence healing in older adults. 7 A de-
operating room environment. Pati ent s treated with active rewa rming by usc of hea ted bl ankets during the recove ry
period respond wi th a faster return of normal tissue/wound oxygen levels th an do those allowed to return to normothermia without rewarming intervcl1tions. 6Routine use of me asures to warm th e patient actively during the surgical procedure, slich as warming blankets and th e lise of warmed intravenous nuids along with active monitoring during sur-
gery, hclp prevent thermoregulatory problems. It is casier to prevent therm oregu latory problems than to remedy th ermoregulatory problems.
Clinical Wisdom: Risk of Delayed Wound Resurfacing in the Older Adult The delay in wound resurfacing puts the older patient at risk for wound infection. Daily wound assessments and use of topical dressings for protection are required for a longer period of ti me than necessary for younger patients.
222
WOuND CARl
creased ratc ofreplaccl11cnt of cells affects the rate of wound healing and. in particular. rccpithclialization of the skin.1 Immune system function declines with age. and this may
Clinical Wisdom: Urine Glucose Levels
account for increased ri sk of infection in o lder adults. The microorganisms proliferate in the wound before they can be removed due (0 the diminished immune response. Older adu lts present with chronic discases. circulalOTY changes. and
Urine glucose levels are not sensitive enough to provide good glucose control because of the high renal threshold for glucose (approximately 180 mg/dL) . The use of blood glucose monitoring for more definitive management is a critical assessment strategy.
nutritional problems. which increase the risk for poor or delayed wound healing. Decreased mOlor coordination and di-
minished sensory function increase the potential for injury. \\,ound complications. and rcpealed wounding at the same
site. COII ('lI rrellf Couditiolls
The presence of certain discases, conditions, or treatments can innuence \.,,'ound healing outcomes. Diabetes mellitus is one condition that interferes with wound hea ling. Diabetcs is associated \\ ith small vessel disease. neuropathy. and problems specific 10 glucose control- all of which predisposc
the person to impaired wound hcaling. Diabetic wound healing problems include increased ri sk of infec tion, delayed epitheliali73tion. impaired or delayed collagen synthesis. and
slowed wound contraction and closure. ~ Hyperglycemia can arrect the cellular response to wounding. There may be a delayed response or impaired functioning of the leukocyte and fibrobla st cell>. both of which are essential for \\ound
repair." The eOcct of surgery on the diabetic patient can bc dramatic. The diabetic responds to the stress of surgery by releasing a series of hormones: epinephrine. glucagon. corti sol. and growth hormone. The stress hormones reduce the amount of ci rculating insulin while increasing circulating glucose. Ele\'ated glucose levels can reduce the errecti\cness ofneutrophils' phagocytotic function and alter the deposition of collagen by fibroblasts, leading to a decrea se in
wound tensile strength .MElevated glucose leyels can also lead to cellular malnutrition. as insulin is the key for allowing nutrient usc in cells. Because glucose is not able to be used as energy, proteins and fats are used as fuel , depleting necessary substrates for wound hea ling. The ability to control the glucose level in the postoperative period is probably advan-
tageolls for positive wound healing outcomes in the diabetic. Maintaining serum glucose levels below 200 mgldL is recol11mended for patients with wounds. ' In the immediate postoperati\e period c lose monitoring of blood glucose and insulin supplements as indicated are required for adequate wound healing. Careful attention to blood glucose levels can assist significantly in positive outcomes and prevent an acute surgical wound from becoming a chronic wound.
Other conditions also affect wound healing. Cardiovascular di sease presents risks for wound healing because of the associated perfusion alterations. impaired blood flow, and vascular disease. Atherosclerosis is a common cause of inadequate perfusion of wounds." Immullocompromi sed patients are an additional group at fisk for poor healing outcomes. The immune system plays a significant role in wound healing, and any impairment (eg. aging. malnutrition. and cancer) can have serious sequelae for the patient with a wound. Treatments that affect \VOlllld healing include steroids. antiinflammatory drugs. antimitotic drugs. and radiation therapy. Steroids inhibit all pha ses of wound healing, affecting
phagocytosis, collagen synthesis. and angiogenesis. The effects of steroids can be reversed with the usc of topical vitamin A. The vitamin A is applied directly to the wound and acts as an inflammatory agent. Vitamin A is approprinte to apply to open wound beds. Wounds healing by primary in-
tention. closed with edges well approximated may not be appropriate candidates for topical \ itamin A.
Clinical Wi sdom: Vitamin A Use for Wounds The usual dose of topical vitamin A is 1,000 U applied three times a day to the open wound bed for 7 to 10 days.
Other anti-innamrnatory dru gs also inhibit wound healing. with errects seen predominantl y in the inflammatory phase. Cancer therapies. antimitotic medications. and radiation therapy work by impeding the normal cell cycle in rapidly dividing cells. The antimitotic activity interferes with new tissue generation in the wound. In addition. radiation therapy has both acute efTects on cellular fun ction and longterm sequelae for healing. The long-tcrm efTects of radi ation therapy on wound healing arc caused by hypoperfusion of
Acute Surgical Wound Manageme"t
ti sslles in the irradiated fi c ld . Hypope rfu sion induced by irradiation is due to damage. deterioriation. and fibrosis of the vasculature. 1
NlIIritiollll/ Statlls Adequate nutriti on is esse nti al fo r wou nd healing. In the hea lthy surgica l patient malnutriti on may no t be an iss ue. Howeve r. with the populatio n aging and more procedures bei ng perform ed on older adults. nutritional statu s is a conccrn for wound healing. Adeq uatc amounts of ca lories I proteins. fa ts. ca rbohydrates. vitamins. and minerals arc all required for wou nd repa ir. Inadequate am ount s of a ny nutri CIll S ncga tive ly influence wo und healin g.1t) Pro tein s are necded for ncovascul arization. fibroblast prolifera ti on. coll agen synthesis, and wound remodelin g. Amino ac ids are the struct ural co mpon ent s of proteins and an.! csse nt ia l paris of deoxyribonuc le ic acid (DNA) and ribo nuc leic ac id (RNA). DNA and RNA provi de the panern for cell milOsis and enzy mes required for ti ss ue generation. Protein malnutrition results in loss of bod y stores of amino acids and insufficient substrates for wound repair and new tissue growth. Carbo hyd rates and fa ts provide necessary energy required forccllular fun ction . When th ere are inadequate amounts o f carbo hydrates and fats (ca lo ri e malnutrition ), the body uses ca tabolism to brea k down prote ins in order to meet energy requircments. G lu cose balance and ava ilable esse ntial fally ac ids are esse ntial substrates for wo und healing. Vitamins and mineral s play an important ro le in wound heal ing. Several vitamins a nd mineral s have specific functi o ns for wound healing. Vitamin A is ~I fat-soluble vi tamin and is responsible fo r suppo rting epithel ia li zation , ang iogenesis, and collagen formation. It is a lso important for th e inflammator y phase of wou nd healing. The wa ter-soluble B vitami ns are co facto rs in enzymatic reaction s. Vitam in C has been associated with wound healing. Vitamin C is essential for an giogene sis and collagen sy nethesis. Vitamin C al so supports fibrobla st function an d is critical for leukocyte functi on. For pati ent s w ith wound s, infection. or significant injury, suppl emental vitamin C is often provided to ass ist in meeting the incrcased metaboli c nceds and wound healing needs. Co nse nsus o n s pecific guidelines for appropriate supplemental doses of vitamin C is not available: howeve r. megadoses of vitamin C have not been proven beneficial. ViUlll1in C usc and elimination increase w ith exercise, stress. injury, increases in metabo li c rate. and smoking. Vita min 0 is requi red for bo ne healing and abso rption of calc ium. wh ich is important in enzyme system s. Vi tam in K is necessary for coagulation and hemosta sis. Vitamin E is used for fat mc-
223
taboli sm ; excess amo unt s are not beneficial to wo und healing.
Clinical Wisdom: Vitamin E and Wound Healing Many people think that vitamin E has healing properties. In fact, vitamin E delays healing and fibrosi s. 1o It is the delay of fibrosis or scarring that may be responsible for decreased scar format ion at the injury site.
Mineral s also playa role in wound hea ling. usually: the minerals of co ncern arc zinc and iron. Zinc plays an esse ntial role in enzy me systems and immune system function and is a cofacto r for co ll age n sy ne th es is. Zinc defi ciency contrib ut es to di srupti on in g ranulati o n ti ssue formation. diminished ten sile strength. dehiscence, and ev isceration . 'o Low levels of z inc are found in o lder adults and low- inco me patients, with losses associated with d iarrh ea. re na l failure, diuretic and la xative use, and paren teral and ente ral nutri tion. 11 lron is a cofactor in coll agcn synthesis and acts to transport oxyge n. Iro n dcficiency may be prese nt in those with c hanges in eat in g habits, intestinal damage. o r inc reased metabolic need s.
Oxygellatioll and Perjilsioll Adeq uate wound oxygcnati o n is essen tial for wound healing. The initia l injury causes hypoxia. and th e resultant growth factor release s upports initial c(lp illary budding. Oxygen is influc l1l ia l in angioge nesis, fibroblast function , e pithe lial ization, and resistance to infccti o nY 14 Ti ssue perfusio n is intertwined with ti ss ue oxygenation . Sati sfactor y ti ss ll c perfusion is essential for oxygenati o n. Ample ci rc ulating blood vo lume ca rri es oxygen- ri c h hemogl obin to the ti ssues. Tiss ue perfu sion a lone, however, does not g uarantee wo und oxyge nation. Probl ems related to tissue perfusion and oxygenati o n may be due to cardiovasc ular or pulmonary disease as well as other conditi ons sllch as hypovolemia. Thus, ma inlaining vascular vol um e is crit ical for ensuring adeq uat c ti sslle pe rfusion. The c linic ian mu st ba lance fluid rep lace ment to prevent both underhydration and overhydrati o n. Excess hydration ca n lead to hypervo lem ia and edema, wh ich may decrease ti ssue oxygenatio n. To optimize oxygenation in the presence of adequate ti ss ue perfusion, use of pulmonary hyg iene interventions, assessment and monitoring of tissue oxygen levels, an d low-fl ow s uppl eme nta l oxygen may be warra nted . IS Pulmo nary hygiene, inc luding incentive spirom-
224
W OUNO CAR'·
amount of time postsurgery, since the hea ling progress of the wound can be measured against the standard time expectations for acu te wound repair. Knowledge of the wo und healing process provides a critica l foundation for assess melll of the acute surgical incision. During the inflam matory process, assessment focuses on identification of signs and symptoms of in flammation, eval ua tion of wound closure materials and wo und dressings. and appraisal of epithelial resurfacing. The central point during the proliferation phase of wound healing is evaluation of collagen deposition. wound exud31e, and tissllcs surrounding the incision. Assessment during the remodeling phase is directed toward exami nat ion of collagen remodel ing at the incisional sitc.
etry, deep brea thing and co ughing, and postura l drainage,
improves the pulmonary toi let and increases the likelihood of adequate oxyge nati on of the wound. Low-now oxyge n cun saturate hemoglobin so that the supply to the ti ssue is
ample. Promoting activity such as repos ition ing and early 3mbulation ca n also be beneficial for periphera l tissue per-
fusion and Qxygcnation,l' Oxygcn3tion and perfusion arc vital to wound hea ling. and postoperative intervent ions (0 improve the ci rculatory and oxygen-carrying capaci ty of the tissues or blood (the oxygen saturation of tissues) can enha nce wound
heali ng. ASSESSMENT OF THE ACUTE SU RCICAL WO UN D
IncisionalAssess ment during th e Innammatory Phase Assessment of the acute surgical wound invo lves physical
examination of the wound site and surrounding wound tis-
The major assessment finding in the first 4 days postoperati vely is the identification of inflammation . The surgical incision may fee l warm 10 the tollch. and there may bc surrounding erythema and edema at the incision site. Signs of inflammation are ex pected and normal during the first 4 days
sues in relation to the wound healing process (Figure II - I ).
Physical examina tio n of the wou nd and the surro unding tissues includes measurement of the incision: observation of the wound ti ssues wilh attent ion 10 epithelia l resurfac ing, wound closure, wou nd exudate, and surroundi ng wo und tissues; and palpation of the incision with attention to coll agen deposition and surround ing tissues. The linear measurement orth e length of the incision and the ana tomic location of the incision provide a baseline measure. Measure the length of the incision in centimetcrs. Observation and palpation of the incision line provides insight to the healing process that occurs in the underlying ti ssues. Healing proceeds in the surgica l inc ision as it does in other wou nds with inflammation- proliferation of new tissues and remodeling. In the surgica l incision the wo und healing processes are not always visible. Thus. the standard for assess ment of healing may be best based on time since the surgica l injury. It is important for clinicians to track the
postoperatively.
Clinical Wisdom: Signs of Inflammation
It is normal to observe signs of inflammation such as warmth, erythema or discoloration, pain, and edema at the incisional wound site during the first few days after surgery.
Pat ients wi th immune system compromise due to age, a disease process. or therapy (such as steroid treatments) may not be able to mount an elTective inflammatory process. thus
rf,
•
,
,.
Figure 11 - 1 Surgical inci sion healing by primary intention. Note the lack of wound edge approximation and no healing ridge at the posterior halfofthe inci sion . SUlures remain present along the posterior incision . Courtesy of Evonne Fowler. MN. RN. CETN. Banning, C'lli fo rni a.
Acute SurgicallVolilld Mallagemem
the signs of innammatiol1 aI the incision are not visible. The lac k of innammat ion at th e incision si te is an indi cat ion of immune system comprom ise. Thus. an ab normal finding during the first 4 days afte r surgery is an incision with no ind ication of innammation. The process of epithelia l resurfaci ng also occu rs during th e innammatory phase of wound healing. In th e ac ute surgical inc isio n, new epidermal ti ss ues are ge nerated quickly because of the prese nce of intact hair folli cles and sebaceo us and swea t gla nds and the short distance th e epi thelia l cells mllst trave l to resurface th e incision. The surgical incision is resurfaced with epithe lium within 72 hours poslsurgery. T he new epidermis provides a barrier to bacterial organisms and to a small degree external tra uma. The tensi le strength of the incision is rela ti ve ly weak and th e incision is not able to withstand force. The astute clini c ian ca n obse rve c hanges in th e new incisio n indicati ng the presence of new epithelia l ti ss ue. The incision is eva luated for the close approximation of th e wo und edges and co lor of the inc ision line. Wound edges should appear we ll aligned wi th no tension observed.
Clinical Wisdom: Incisional Color Changes As the new epithelial tissue migrates across the incision, the color of the incision may change from bright red to pink; although this is not observed in ali patients, it is a useful clinical change that demonstrates maturing epithelial tissue.
A wound dressing is no longer necessary to preven t bacterial contaminat ion of the incision once epithel ial resurfacing has occurred. However, the wo und dress ing has other benefits at thi s point. Some cli ni c ians suggest that the presence of th e dressing at thi s point may be a reminder of the wounds presence and th e need to use care in the wo und area. The dressing provides a physica l barrier to rough edges of clothi ng to limit local irritation , and th e dressing ca n hel p the patie nt to inc lude th e wound in a new body image by allowing gradual view in g of th e wound. Wound closu re materials are assessed for the reacti on of the surrounding incisiona l tissues. The lise of sutures. o f any type, to approximate the wo und edges creates small wo unds alongside the incision wo und. The wo unds frOl1) th e surures increase the innammation at th e wo und site and can ca use ischemia if th e sutures are pulled taut with increased tensio n, e ither from poor technique or wo und edema postoperat ive ly. The continued presence of sutures or stapl es provides additional tensi le strength for th e wound, but th e sutures can also ca use increased ri sk of infection and the potenti al for wound ischcmi a. Use ofSteri strip tapes for wo und
225
c los ure or early remova l of sutures with Steristrip tape replace ment ca n decrease th e problems associated with sutures. Re mova l of the wo und sutures or staples in a timely manne r is a proactive hea lin g intervention. Remova l of sutures in healt hy surgica l patients in 7 to 10 days postoperatively can be lIsed as a genera l gu ideli ne depending on surg ica l site.
Incisiona l Asscss mcll' du ri ng th e Proliferative I>hase Palpation of th e surgical incision rcvea ls th e underlying process o f co llage n deposition. The new coll agen tiss ues ca n be pa lpated as a f irm ness along th e incision, exte ndin g I em on e ither side of the incision: 4 T hi s firmness to the tissues ca used by new collage n deposition in the wound area is ca lled the hea ling ridge. The healing ridge should be palpable along the entire length of the inc ision between day 5 and day 9 postoperati ve ly.' If the healing ridge is not palpable within 5 to 9 days, th e wound is at risk for dehiscence or infec ti on. 4 Eva luati on o f surgical inc is ional wo und exuda te requires knowledge of what wou nd exudate is expected in the co urse of hea ling. The characte r and th e a mount of th e ex udate c hanges as wound heal ing progresses. The wound exudate immediate ly afte r surgery is bloody. Within 48 hours the wou nd dra inage becomes serosa nguineous in nature and finally the ex udat e is serous. The a mount of the wo und ex udat e shou ld gradua ll y decrease throughout the healing peri od. An increase in wound ex udate usua ll y indicates co mpromised wound hea ling ca used by infection. New drainage fro m a previollsly healed incision hera lds wound dehiscence, in fect ion. and in some cases fistula formation . The ti ssues immedia te ly su rround ing th e inc ision should be obse rved and palpated for the presence of ede ma and induration and for color cha nges. T he presence of edema retards the wound hea lin g process. as the excess nu ids in th e ti ss ues provide an obstacl e to angiogenesis and raise the potential for wound ischem ia. Skin color changes may indicate th e presence of bruising or hemato ma formatio n ca used by surgery. T he skin color will appear dark red or purple. Skin color changes may also indicate impending infecti on. Signs of eryt hema, wa rmth , and edema and inc reased pai n at the inc ision wo und a re indicators o f possible wou nd in fecti on. Evaluation of the heali ng ridge, wound exudate, and surrounding inc isiona l ti ss ues provides information on the progress of the pro liferati ve phase of wou nd hea ling.
I ncisional Assess ment d u ri ng th e Remode li ng Phase The remode ling phase of wound hea ling is best assessed in the surgica l incisio n by eva luation o f th e colo r of the incision. As th e sca r ti ssue is remodeled a nd organ ized str uctur-
226
W OUND CARE
ally. th e color o f the tissue changes. The remodeling phase
of wound healing can last I to 2 years. The incision color changes throughout the first yea r, gradually changing from
Securin g the wou nd dressing is usually done with the use of tape. Premature and frequent dress ing changes can damage the tissues surrounding the incisional wound and nega-
bright red or pink to a sil very gray or white. The tensile
tively affect wound healing. Use of Montgomery straps, skin
strength of the wo und gradu ally increases over the first yea r,
sea lants. or hydroco lloid frames aro und the wound and underneath the tape can eliminate sk in stripping around the incision wound from frequent dressing changes. Frequent dressi ng changes are more likely to be a problem with wounds heali ng by secondary intention. tert iary intention. or draining wounds.
eventually ae hi eving approx imately 80% of the ori ginal
strength of the ti ssues. The main focus of int erventi ons at
this stage is to lim it force on the wound site. Interventions to lim it force and tension at the wo und site include teaching the patient to avoid heavy lifting. bending, or straining at the site. MANAGEMENT OF HIE ACUTE SU RGI CAL WOUND
SECON DARY AND TERTIARY INTENTION WOUND HEALING
Managemen t orthe surgica l incision includes attention to fHeloTs that affect wo un d healing as addressed earl ier, as we ll
Surgica l wou nds len open to hea l by secondary or tertiary intention have a reparative trajectory similar to that of chronic wounds. Secondary intention healing is allowing wounds to hea l without surgica l closure. Wounds healing by secondary intent ion must heal by scar tissue replacement. The tissue defect at the wound site must fill with new collagen tissue during the proliferative phase of wo und hea ling. The inflammatory phase of wound hea ling may be prolonged because of the contaminated nature of the wo und. Tertiary intent ion is a combi natio n of both primary and secondary intention wound hea ling. The wound is allov.led
as dressing care. The surgica l dressing includes the primary and secondary dressing.The primary. or first. surgica l dressing is the dressing in direct contact with the wound . The di rect wo und contact requ ires that the primary dressing be nontraumatic to the wound. The primary dressing provides absorption of drainage, ma intains a sterile wo und environment , and serves as a physical barrier to further wound trauma. The primary dressing shou ld be nonad herent to rhe wound si te. The tradi tional ga uze dressing becomes ad herent to the new incision and upon removal causes ncw ti ssue injury. Use of nonadhcrent abso rpti ve dressings c(tn faci li tate wound healing because the nonharm ful nature of the dressings allows wo und healing to proceed. The primary dressing absorbs wound exudate and wicks it away from rhe wou nd site, allowi ng the ex udate to be absorbed into the secondary dressing. Secondary wound dressings provide increased absorpti ve capacity or hold the primary dressing in place. Secondary wo und dressings are applied on top of the primary dressing and may be composed of the sa me materials as the primary dressing. The secondary dressing plays an important role for wo unds when increased amounts of wo und exudate arc anticipated. The secondary dressing absorbs drainage from the primary dressing and wicks the ex udate away from the wou nd bed and into the absorbent material of the dress ing.
Clinical Wisdom: Surgicallncisional Dressings The vast majority of primary intention surgical wound dressings continue to be gauze. Conversion to moist wound healing in the immediate postoperative period may facilitate wound healing and provide for patient com fort when changing dressings. Education of the surg eon on "better" primary wou nd dressings is also helpful.
to heal secondari ly and then primarily closed for final hea ling.' Tertiary wo und hea ling is designed for spec ialized
wounds in which primary intention is pre ferred but nOt possible at the time of wounding. The de lay in primary closure may be to clear infection. allow somc wound contracture. or creat\! a hea lthy gra nulation base for a gran. ~ Most surgical wou nds left to heal by secondary or terti ary intention are those in whic h the risk of infection is increased or the tissue loss is such that thc wound edges cannot be approx imated wi thout unacceptab le tension 0 11 the incision. Reversal of both conditions- in fec tion and extensive tissue loss-can be max im ized in the earl y wee ks following surgery. The ad mini stration of systemi c antibiotics. when appropriate, and careful wound observation and care can lessen infection risk. The process of wo und cont raction and proliferat ion of granulation tisslle occurs as the hea ling response attempts to decrease the IO tal surface area or the woundSand to decrease the ti ssue loss. The primary wo und dressing takes criti ca l importance in th e wo und hea ling by secondary or tertiary intenti on. Nonadherent, absorpti ve dressings optimize wound heal ing for secondary and tertiary intention wou nds. Assessment of the wound for signs and symptoms of infecti on includes
eva luation of the character and amount of wound ex udate and exam ination of the wo und and surroundin g tissues for eryt hema, edema, induration, heat, and pain. Wounds healing by secondary or terti ary intention should be evaluated
AClIIe Surgical Wound MlIllligemel1l
using the same parameters used for chronic wounds. Evaluate the wound size ..md depth. the presence or absence of necrotic tissue. the characteristi cs and amount of exudate, the condition of the surrounding tissues, and the presence of the healing characteristics of granu lat ion and ep it hel ia Iizat ion.
OUTCOME MEASURES Outcome measures for acule surgical incisio ns relate to healing progress according to time since injury. The outcome measures for incisiona l wounds are presented according to the time frame since surgery. Postopenlti\'e Day I t hrough Day 4
The following signs and symptoms represent measures of positive outcomes for acute surgica l incision wounds. The presence of an innal11l1latory response, inc luding erythema or skin discoloration , edema, pain, and inc reased temperature at the incision site during the first 4 days after su rgery is a normal healing respon se. The lack of innammation at the new surgical incision is a negative outco me . Wound ex udate should be bloody in character initially, and toward day 3 and day 4 change to serosanguineolls in nature. The amount of wound exudate should gradually decrease from a moderate amount to scant exudate by day 4. Many surg ical wounds have no exudate past day 2 or 3, especia lly facial wounds. Failure of the wound exudate to decrease in amount and to change in character from bloody to serosanguin eous is a negative indicator for hea li ng. Ep ithe li a l resurfacing shou ld be complete by day 4. The incis ion appears bright pink as opposed to th e initia l red co lor of th e incision. Lack of epithelial resurfacing of lhe surgical incision indicates delayed healing and less than op timal outcomes. One negative outcome that ca n occur at any time during the postoperative course of the patient is th e development of a hematoma (swelling or mass of blood usua ll y c l o tt e(~ confined in the tissues and ca used by a break in a blood vesse l). External evidence of hematoma formation includes swel ling or edema at the site, a soft or boggy fccl to the tissues initially, which may bc followed by induration at the site, and color change of the sk in (sim ilar to bruising). Postoperative Day 5 through Day 9
The major healing outcome in the surgical incision on days 5 through 9 is the presence of the healing ridgc along the entire length of the inc isio n. The healing ridge indicates new collagen deposition in the wound site. Lack of developmen t or incomplete development of the hea ling ridge may be prodromal to wound dehiscence and wo und infection. A defi-
227
Case Study: Lack of Inflammatory Response Postoperatively M.J., a 71-year-old Caucasian woman, was admitted for bowel surgery with resection of the descending colon and low anterior anastomosis. M.J.'s history included long-term steroid therapy for rheumatoid arthritis. On postoperative day 1 her midline incision primary dressing showed evidence of bright red bleeding. The wound edges were well approximated with staples as the closure material. Assessment of the incision on postoperative days 2 and 3 revealed no evidence of any edema, warmth, erythema, or discoloration at the incision site. Exudate was moderate and serosanguineous to seropurulent in nature. By postoperative day 4, the incision was not fully resurfaced with new epithelial tissue, and signs of inflammation, although now present, were diminished and the exudate remained seropurulent and moderate in amount. She showed signs of confusion and agitation (signs of infection in older adults); lab tests con firmed the presence of wound infection. In this case, the absent signs of inflammation were early warning signs of impaired healing and wound infection.
c ient or non existent hea lin g rid ge is a negative ou tcome measure for wound heal ing. \Vound exudate character should change from serosanguineous to serous and gradua ll y disappear over days 4 to 6. The exudate amount should diminish from a minimal amount to none present. Any increase in the amount of wound exudate during days 5 through 9 sho uld be viewed as a negative outcome and heralds probable wou nd infection . The suturc materials shou ld begin to be removed from the incisiona l site during days 5 to 9. Adhesive tape strips or Steristrips may be used to provide additiona l wound tens ile strength. Failure to remove any of the wound suture materi· a ls during days 5 through 9 may indicate a negative outcome for the wound. Continued signs of inflammation at the incision site during days 5 through 9 are indicative of delayed wound healing. igns of erythema or edema. extensive pain. or increased temperalUre at the inc ision wound during this time frame indicate that wound healing is not normal. Prolonged innammati on may occ ur as a result of under lying infection, immunoeompromise, or continued trauma at the wound site. Documentation of a ll characteristics of the incision a nd healing are important for continui ty ofeare throughout the wound recovery period but especially during this time frame. as the patient wi ll likely be changing health care settings. For examp le. the su rgica l patient is often discharged fromlhe acute care hospi tal to the home setting very soo n after surgery.
228
WOCND CARl
Clinical Wisdom: Documentation of Incisional Wound Healing Documentation should include all of the following: • • • • • • • •
Time since surgery in days Location Size in centimeters Closure materials present Color of the incision Type and amount of exudate Presence or absence of epithelial resurfacing Presence or absence of collagen deposition or healing ridge • Actions taken for follow-up or referral as necessary • Primary and secondary dressing as appropriate
Posloperali ve Day 10 Ihrough Day 14
Example: Postop day 6 for a 12-cm midline abdominal incision with Steristrips present. Incision is completely reepithelialized with no exudate present. Incision is bright pink with healing ridge palpable along anterior 10 cm of incision. Posterior 2 cm of incision is soft and boggy to touch with no healing ridge palpable and erythema present. Physician notified of possible impaired healing. Dry gauze 2 x 2-inch dressing applied to posterior aspect of incision for protection of site.
A positive outcome measure at year I for the incisional wound includes lack of significant hypertrophic sca rring or wound
The major outcome measure for day 10 through day 14
is the removal of externa l incision suture materials. Internal or "buried" sutures remain in place. Failure to remove externa l suture material s during this time frame will prolong incision healing. Healing is delayed by increasing the risk of in feC Iion from the suture microwounds and the continued in sult to the tis sue s by the presence of the foreign
objects (the suture materials), prolonging the illnammatory response.
Postop erati ve Day 15 through I to 2 Yea rs
During the end of the proliferative phase of wound healing and throughout the remode ling phase. attention is directed toward the changes in the incisional scar tissue. The collagen deposiled alongside the incision is gradually re-
aligne(L restructured and strengthened. The outcome measure for this time period is predominantly based on the changes in the incisional Scar tissuc color. The color of the incision changes from a bright pink after the initial epithelial resurfacing. gradually fading to pink and eventually turning a pearly gray or si lvery white color. The noticeable induration and firmness associated with the healing ridge gradually soncns during thi s timc frame also. Negative outcomcs include reinjury of the inci siona l linc such as hcrniation orthe wound sitc and complications associated with scarring such as keloid formation or hypertrophic scarring. Functional ability with the scar tissue becomes a key outcome measure for many surgical incisional wounds during this time frame.
herniation, maximal functional abi lity with the Ile\v scar. and acceptable cosmetic results of hea ling with a si lvery white or gray scar line. Tables 11- 3 and 11-4 present the positive and negati ve outcome measures for time frames from the point of surgery to the end of remodeling. CONCLUS ION
There are many strategics clinicians use to optimize wound healing in the aCLIte surgical incision . The astute and attentive clinician may diminish risk of complications, ident ify delayed or impaired hea li ng. and provide for a supportive healing environmcnt. The key to sliccess ful intervention for the patient with an acute surg ical incision is knowledge of normal healing mechanisms and temporal expectations, knowledge of factors that impair wound healing. and vigilant aHemion to both . The case study at thc end of this
chapter helps to demons trate the interaction between knowledge of normal healing and thc timc seq uence associated with wound healing, and factors that interfere with normal healing.
REFE RRAL C RI TE RI A
Watchful assessment of the patient with an acutc surgical incision can innucnce prompt referral to the physician or advanced practice nurse for evaluation and intervention for complications of wound healing. The following critcria are helpful guide lincs for referral of the patient to an-
Acllfe Slirgical WOlilld A1allogement
229
Table 11-3 Positive Outcome Measures for Incisional Wound Healing
Outcome Measure
Days 1-4: Inflammation
Days 5-9: Proliferative
Days 10-14: Proliferative
Day IS-Years 1-2: ProliferativeRemodeling
Incision color
Red,edges approximated
Red, progressing to bright pink
Bright pink
Pale pink, progressing to white or silver in light-skinned patients; pale pink, progressing to darker than normal skin color in darkskinned patients
Surrounding tissue inflammation
Edema, erythema, or skin discoloration; warmth, pain
None present
None present
None present
Exudate type
Bloody or sanguineous, progressing to serosanguineous and serous
None present
None present
None present
Exudate amount
Moderate to minimal
None present
None present
None present
Closure materials
Present, may be sutures or staples
Beginning to remove external sutures! staples
Sutures/staples removed, Steristrips or tape strips may be present
None present
Epithelial resurfacing
Present by day 4 along entire incision
Present along entire incision
Present
Present
Collagen deposition (healing ridge)
None present
Present by day 9 along entire incision
Present along entire incision
Present
other level of health care and to other specialties for their expertise:
• The patient with markedly increased bloody drainage during the imlllediate postoperative period may be at risk of hemorrhage from undetected leaking blood vessels in the surgical rield. • Patients who exhib it a change in exudate characteristics. from bloody or serosanguineous to purulent, should be evaluated for wound infection or abscess formation and treated with appropriate antimicrobia l therapy. • Any increase in alllount of exudate after postoperative day 4 is indicative of wound infection or abscess formation and as above, requires primary care provider evaluation and appropriate antimicrobial therapy. • The absence of a healing ridge along the cntire length of the incision wound by postoperative day 9 indicates
impaired healing and, often, abscess formation. Prompt refcrra l to the primary care provider usually results in drainage of the abscess area. antimicrobial therapy, and a wound len to heal by secondary intention. • The patient wi th the presence of sig ns and symptoms of wound infection. including erythema, edema. elevated temperature, and increased pain along the incision after day 4, andlor signs of systemic infection. including elevated temperature. elevated white blood cell count. or confusion in th e older adult, requires evaluation. These signs and symptoms suggest a wo und infection. and the primary care provider should evaluate and treat appropriately. • The patient with a frank wound dehiscence or fistu la formation requires eva luation by the primary care provider. usually the surgeon, and may nced a referral to an cntcroslomal therapy (ET) nursc (special izing illl1lanagemcnt of draining wou nds) for management.
230
WOUN D
CAR'
Table 11-4 Negative Outcome Measures for Incisional Wound Healing
Outcome
Days 1-4:
Measure
Inflammation
Incision
Red, edges approximated but tension evident on
incision line Surrounding tissue inflammation
No signs of inflammation present: no edema, no erythema or skin
discoloration , no warmth, and minimal pain at incision site; hematoma formation
Days S-9: Proliferative
Days 10-14: Proliferative
Red, edges may not be well approximated; tension on incision line evident
May remain red ,
Edema, erythema, or skin discoloration;
Prolonged inflammatory response with edema, erythema, or skin discolora-
warmth, pain at
incision site;
progressing to bright pink
hematoma
tion ; warmth and
formation
pain ; hematoma formation
Day IS-Years 1-2: Pro/iferativeRemodeling Prolonged epithelial resurfacing, keloid or hypertrophic scar formation If healing by second-
ary intention, may be stalled at a plateau (chronic inflammation or proliferation), with no evidence of healing and continued signs of inflammation
Exudate type
Bloody or sanguineous, progressing to serosanguineous and serous
Serosanguineous and serous to seropurulent
Any type of exudate present
Any type of exudate present
Exudate amount
Moderate to minimal
Moderate to minimal
Any amount present
Any amount present
Closure materials
Present, may be sutures or staples
No removal of any external sutures! staples
Sutures/staples still present
For secondary intention healing, failure of wound contraction or edges not approximated
Epithelial resurfacing
Present by day 4 along entire incision
Not present along entire incision
Not present along entire incision, dehiscence evident
Not present or abnormal epithelialization , such as keloid or hypertrophic scarring
Collagen deposition (healing ridge)
None present
Not present along entire incision
Not present along entire incision, dehiscence evident
Abscess formation with wound left open to heal by secondary intention
SELF-CARE TEAC HI NG GUIDELINES The patient 's and caregiver's instructi on in self-care must be individualized to the type of surgical incision and the individual patient's wound, the specific incisional dressing man-
agement routine. the individual patient's learning style and coping mechanisms. and the ability of the patient/caregiver to perform procedures. The general sci f-care teachin g guidelines in Exhibi, 11 - 1 Illust be individualized for each patient and caregiver.
Acute Surgical Wound Monagemelll
I
231
Case Study: Incisional Wound Healing PL., a 78-year-old African American man, was admitted for radical prostatectomy surgery for prostate cancer. PL. has a history of diabetes mellitus, hypertension, obesity, and peripheral vascular disease. His diabetes is managed with oral hypoglycemic agents and an 1800calorie diabetic diet (with which he is noncompliant). PL. lives alone on a small pension and fixed income and is a smoker. He was admitted with a random blood sugar of 198 mg/ dL.
Postoperative Day 9 PL. was discharged from the hospital to his home with home health care nursing follow-up . Upon discharge from the hospital, PL. 's incision was bright pink with no exudate present. The incision was completely resurfaced with new epithelial tissue present along the entire incision, and half of the staples had been removed . A healing ridge was palpable along the anterior 13 cm of the wound but not palpable at the posterior aspect of the wound.
Preoperatively
Postoperative Day 10 Assessment of PL. revealed several risk factors for impaired healing: uncontrolled diabetes mellitus, obesity, advanced age, hypertension, and peripheral vascular disease. Control of blood sugar level was identified as a goal in the preoperative period, and PL. was started on sliding-scale insulin therapy with blood glucose monitoring. PL. 's history of hypertenSion and peripheral vascular disease put him at risk for poor tissue perfusion; thus, in the immediate postoperative period (days 1 and 2) he was put on supplemental oxygen per nasal cannula to optimize tissue oxygenation. Obesity is a risk factor for excess incision wound tension, which increases potential for poor perfusion of the incision wound due to the presence of excess subcutaneous fat. Postoperative Day 4
p.L. 's 15-cm midline abdominal incision showed evidence of inflammation with edema, skin discoloration, and warmth at the site. There was evidence of epithelial resurfacing, and the incision line was bright pink. There was a continued minimal amount of serous drainage and staples remained in place. The primary gauze dressing was changed daily. Blood sugars ranged from 110 to 132 mg/dL on insulin therapy. Oxygen was administered the fi rst 2 days postoperatively at 2 L per nasal cannula.
The home health nurse evaluated PL.'s incision and found surrounding skin discoloration , increased pain, and edema present at the posterior aspect of the wound. No healing ridge was palpable at the posterior aspect of the wound, although collagen deposition was evident along the anterior 13 cm of the wound. Half of the original staples were still present in the incision line. The physician was notified, and PL. was referred to the physician's office for evaluation of the incision. Postoperative Day 12 The physician removed the remaining staples, performed an incision and drainage (I and 0) of the posterior aspect of the incision in the office, started PL. on systemic antibiotics, and left the posterior aspect of the wound open to heal by secondary intention, using moist saline gauze dreSSings. Postoperative Day 15 PL.'s posterior incision is 75% filled with granulation tissue and there is minimal serous exudate present. The anterior aspect of the incision is well healed and pale pink. PL. 's incision wound went on to heal uneventfully by secondary intention over the next 10 days.
232
WOl'N() ('.\RI
to: "hibit 11 - 1 Self-Care Tcaciullg GUldclim:s
Se lf-Care
G ui dc l i n c~
In st r uct io ns Ch·cn (Dale/) nili a ls)
Spec ific to Ac ut e Surgica l In cis io ns
Dc monstra li o n or Rc \ iew of Ma teri al ( Date!1ni fia ls)
Return Oemonstration or Slates Understa ndin g ( Dal e!) nili a ls)
L Type or incislonal wound and specific C SlIrJ.: Uin Sorl" -/m
J
Stolts r-;A Imp.urcll wuund healing. In C. MO \4o .. by Year Book; 1992. Mulder GD. Jeter KF. ]'airchild PA Cfiniciw/\ Pod.. cI (illitit' til Clmmil" "OUIIl' Rt'pdir Spartanburg. SC Wound Ilcahng Publica lions; 11)92
C H A PTE R
12
Pressure Ulcers: Pathophysiology and Prevention Barbara M. Bafes-Jensell
PRESSURE ULCER DEFIN IT ION
Pressure ulcers arc areas of local tissue trauma usually deve loping where sofl tissucs are com pressed between bony prominences and any external surface for prolonged lime periods. I.! A press ure ulcer is a sign of local tiss ue necrosis and death. Pressure ulce rs arc mos t comI11only found over
bony prominences subject to external pressure. Pressure exerts the greatest force al the bony tissue intcrf"lce; therefore. there may be significant musc le and subcutaneous fat tissue destruction underneath intact skin .
PRESSU RE ULCER l'ATI10P HYS IOLOGY
Press ure ul cers arc the result of mechanical injury to the ski n and underlying tissues. The primary forces involved are pressure and shea r.-1 7 Press ure is the perpendicular force or load exerted on a specific area. causing ischemia and hypoxia of the tissues. I-ligh pressure areas in the supine position are the occiput. sacrum, and heels. In the sitting position, the isc hial tuberosities exert the highest press ure and the trochanters arc affected in the s ide-lying position .-I·II As the amount of son tissue available for compression decreases. the pressure gradient increases. Likewise. as the tiss ue available for compression increases, the pressure gradient decreases: thus most pressure ulcers occur over bony prominences where there is less ti ssue for compression and the press ure gradient within the vasc ular network is altered. 1I Figure 12- 1 demonstrates this relat ionship. The changes in the vascular network allow an increase in the interstitial fluid pressure. which exceeds the venous flow. This results in an additional increase in the pressure and impedes arteriolar circulation. The ca pillary vessels collapse
and thrombosis occurs. Increased capillary arteriole pressure leads to nuid loss through the capillaries, tissue edema, and subseq uent autolysis. Lymphatic now is decreased, allowing further ti ss ue edema and contributing to the tissue necrosis. S.7.9 II Pressure, over time, occludes blood and lymphatic circulation, causing deficient tissue nutrition and bui Idup of waste products due to ischemia. I f press ure is relieved before a critical time period is reached, a normal compensatory mechanism. reactive hyperemia, restores tissue nutrition and compcnsatcs for compromised circulation. Ifpressure is not relicved bcfore the critical time period, the blood vessels collapse and thrombose. The tiss ues arc dcprived of oxygen, nutrients. and waste removal. In the absencc of oxygen, cells use anaerobic pathways for mctabolism and produce toxic byproducts. The toxic byproducts lead to tissue acidosis, increased cell membrane permeability, edema, and eventual cell death .'·' Ti ss ue damage may also be due to reperfu sion and reoxyge nation of the ischemic tissues or post ischemic injury. l~.1l Oxygcn is reintroduced into tis s ues during reperfusion following ischemia. Thi s tri ggc rs oxygen-free radicals known as superoxide anion. hydroxy l radicals, and hydrogen peroxide, which induce endothelial damage and decrease microvasc ular integrity. T ime a nd Press u re
Isc hemia and hypoxia of body tiss ues arc produced whcn capillary blood now is obstructed by localized pressure. How much press ure and what amount oftimc is necessary for ulceration to occur has been a subject or stud y for many years. In 1930 Landi s,I4 us ing single-capil lary microinjeetion techniqucs. determined normal hydrostatic pressure to be 32111111 235
236
W OUND CAR '-
/
,
I
\
BONE
!
I
/ = tissue damage
\
= e xternal pressure from support surfac e
\ SUPfORT SURFACE
\
\
Figure 12- 1 Pressure gradient at the bony prominence.
I-Ig at the arteri o le end and 15
111111
Hg althe venule end. H is
work has bee n th e cri terio n for meas uring occ lusion of ca pilla ry blood fl ow_Ge ne ra ll y, a range fro m 25 to 32 mm Hg is co nsidered norm a l capill ary blood flow and is used as the marker fo r ad eq uate re licfo f presslire on th e tissues. Press ure is the g reatest at the bony prominence and so ft
tissue inte rface and g ra d ually lessens in a co ne-shaped g radi ent to th e pe riphe ry.'-" -" Thus, altho ug h tissue da mage appa re nt o n the skin surface may be minima l, the damage to th e deeper structures ca n be seve re. In add it io n, subcuta neo us fa t and mu scle arc more se ns iti ve than the ski n to isc hemi a. Muscle and fa t tiss ues arc mo re meta bo lically acti ve a nd th us mo re vuln era ble to hypox ia wit h increased s usceptibility to pressure damage_ T he vulnerab ilit y of musc le a nd fa t tissues to press ure fo rces ex pla ins press ure ul ce rs where large a reas of muscle a nd fat tissue a re da maged wi th und ermining du e to necrosis, yet th e ski n ope ning is re lati ve ly sl11 a ll. lO
Intensity and Duration of I')ressure T here is a re lat ionship be tween in tensi ty and d urati o n of press ure in pressure ulcer deve lo pment. Low pressures ove r a lo ng period o ft imc arc as ca pab le of produ cing tiss ue dam-
age as hig h pressures fo r shorter periods of time:' Tissues can tolerate higher cycl ic press ures versus constant pressure. 11 Pressures di ffer in va ri ous body pos itio ns. Pressures are highest (70 mill Hg) o n th e buttocks in the ly in g posi ti o n, and in th e sitting pos itio n ca n be as high as 300 !TIm Hg over lhe ischi all ll berosi t ies.~·II These leve ls are we ll above the nonnal capillary c losi ng press ure and a rc capa ble of ca using tiss ue isc hemi a. When tiss lies have been co mpressed fo r prolonged periods of time, tissue da mage continues to occ ur even after th e pressure is relieved Y T hi s continu ed tissue damage rclatcs to changes at the ccllular levellhat lead to di fTic ult ies with resto ratio n o f pe rfusion. Figure 12- 2 shows the rclati o nship between timc, press ure, and tissue destructi o n. Fo ur levels of skin breakd owll occ ur dependi ng 0 11 the amo unt o ft imc ex poscd to unreli eved press ure . III Hype remia ca n be observed wi thin 30 minut es or less; it is mani fes ted by redness of the sk in a nd diss ipates w ithin I ho ur afte r press ure is relieved. Isc hemi a occurs a ft er 2 to 6 ho urs of continuo us pressure: the erythema is dee per in color and may take 36 ho urs or more to di sappear afier press ure is rel ieved _ Necros is is the th ird level and occ urs a ft er 6 hours of co ntinu o us press ure. The sk in may take o n a bl ue o r g ray color and beco me indu rated. Damage th at has progressed to thi s leve l disappea rs o n an indi vidua l bas is. Ulce ration is the
Pressllre Ulcers: Pathophysiology alld Prel'emiOIl
237
PRESSURE
SKIN
Cellular necrosis and tissue death
TIME
A
PRESSURE
Cellular necrosis and tissue death
TIME
B
PRESSURE
PRESSURE
normal tissue response reactive hyperemia
TIME C
Fig ure 12- 2 Relation ship of limc versus pressure . A. lIi gh pressures over a short period of lime. B. Low pressurcs over a long period oftimc. C. Intcrminent pressure .
238
W OUND CAR.
fourth and final level and may occur within 2 weeks aficr necrosis with potential infection: it resolves on an individual basis. In dark-skinned paticllIs it is often dilTicult to di scern red-
ness or erythema of the sk in . Redness and erythema may appear as a deepening of normal ethnic color or as a purp le hue to the sk in. 1.\,\ and ./illl thickness arc COI11monly used to describe wounds of various skin dt:pths that heal by euher rcgeneration or scar fOfllH1tion. Partl3l-thickness wounds imolve only the epidermis and dermis. hlllthickness wounds invol\'c complcte destruction of the epidermis and dermis and extend IIlIO deeper tissues.
12- 1 Prl.!ssure Llcer Stagll1g Cnteria
Definiti on
Prcs \ure l lce r St:tge
erythcma or IIltacl ,>1..111; Ihe her:tldlllg lc"lon of skill uJccralloll. In II1lIl\lduals \\ IIh darker ... klO. dlscoloral1on of the S1..111. warmth. e(lcma. mdurJl1oll. or hardncs ... may also be indicators.
NOJ1blanchabl~
skin loss l1l\'ol\lng cpldcnl11s or dennis. or both. Thl! ulcer IS superfiCIal and presents clinically as all ·~7 She added skin appearance. medication, diet and nlild balance. and intervention categories to the tool. along with detailed instructions for usc. Gosnell reversed the nUlllerical scaling so that thc higher the score the higher the risk of pressure ulcer development. so a Gosnell score of 5 is the lowest risk and a score of20 is the highest risk (sec F,hibit 123).
Brat/ell:\ SLoa te for Pre//iclillg l're.\slIre So,.e
Nortoll ~' Scale
Ri~k
The Braden Scale was developed in 1987 and
The Norton tool is the oldest rh.k assessment instrument
De,e loped in 1961. it consists of five subseales: physical condition. mental state, activity, mobility. and incontinence. q Each parameter is rated on a scale of I to 4 with the sum of the ratings for all rivc parameters yielding a total score rang-
ing from 5 to 20 (sec Exhibit 12 2). Lov,ler scores indicate
IS
composed
of six subscales that conceptually rencct degrees of sensory perception. moisture. activity. mobility. Illilrition. and friction and shear.!'UUAll subscales are ralCd from I to 4 except for friction and shear. whit;h is rated from I to 3.Thc subscales may be sUlllmed for a lotal score. with a mngc frolll 6 to 23 (sec Exhibit 12-1).
[), hibit 12-2 Norton's Scale
NO RTON RI SK ASSESSMENT SCALE P h ~sical
Me nta l Cond ition
Co ndit ion
Good ,""air Poor V. bad Name
Source
4 3 2
I
Alert
4 Aprllhcllc 3 Confused 2 Stupor I
Activit} Ambulanl Walk help Chalrbound IJed
Incontinent
t\lobilit~
4 3
2 I
full SI. 1II1lIIed V. limited Immobile
4 3 2
NOI
4
Occasionnl J Usually Urine 2 I Doubly I
TOTAL
SCORI
Date
Rcpnlllcd \\ IIh pcnni\~lon from D, Norton. R McLarcn. und A l'\ I 'tlln-Snlllh. 11I IlIl'n/iXlllltlfl III (jailll"/( - \'1If"\/IIg Pmh/(,,,,\ ill 1975. Churchill LI\ ing~tonc
1/0'l1l1tl/.\ RC-I~~uc'
Pre,\Sllrt! Lker\'_ ParllOphys;%gr CInd Pre\ 'el11;Ofl
247
E\hibil 12-3 Go:-.ocll\ Tool
GOSNELL SCALE-PRESSURE SORE RISK ASSESSME T I I). Agc___ Sex Ileight· _ _ _ _ _ _ _ _ 'hclght. _ _ _ _ _ _ __ Dale of Admission _ _ _ _ _ _ _ _ _ _ _ _ _ __
Medical Diagnosis: Pnmary Sccondar} _ _ _ _ _ __ Nur:-.mg Diagl1o,)I,)~
Date of Discharge Instruction s: Complete all categones willull 24 hours of admission and c\cry other day thcreaOcr. Refer to the accompanying gUlddines ror specific fatlllg details. \Ienlal
~taluS
I Alert
Continence
\Iobilit)
Acth il)
hilly Controlled 2. Usuali) Controlled 3. Mmimally Controlled 4. Absence of Control
I Full 2. Sllghlly
I. AmbulalOry
I. Good
2 Walks with
2. Fair
Llilliled 3 Very LlillIted 4 1I111110bi Ie
Asslslance 3. ehalrfast 4 Bedfast
3 Poor
I
2. Armthctlc 3. Confused 4 Siuporous 5. UnconscIous
IHTE
TOTAL SCORE
COLOR
2... -Jlour Fluid B-::: REFER APPROPRlA TELY
DOC '
D ietary Phys ical TIlerapy
IN TERVEN TIONS based 011 idelltified risks Fig ure 12- 7 Whcn to assess patients for risk of pressure ulcer developmcnl.
252
WOUND
CARe
on patients and Exhibit 12- 5 present s a flow diag ram for determining prevention strategies based on ri sk factor assessment.
PRESSU RE UL CE R PR EVENT ION: EARLY INTE RVENT IONS
caregiver education and caregivcr-depcndcnt repositioning. The spinal cord- injured patient requires selr-ca re education and may be able to perfo rm self-reposit ionin g. Thus. the interven tion ror the risk ractor o r immobility is very different ror these two patients. Imm obilit y, Ina ctivit y, a nd Se nso r y Loss
Prevention strategies are targeted at reducing risk factors
present . Appropriate prevention interventions can be focli sed on eli minating specific risk factors. Thus, early intervention for pressure ulcers is risk-factor specific and prophylactic in nature. The prevention strateg ies arc prese nted by risk fac-
Patients with impaired ability to reposi ti o n and who cannot independentl y change body posit io ns must have local pressure alleviated by any orlhe rollowing inlerve nti o n s.N .26.~9
tors. beginning wi th genera l informarion and ending with s pecific strategies for a particular ri sk factor. The Braden Scale is the basis for these prevention interve ntion s. Prevention interventions should be instituted that are appropriate to the patient's leve l or ri sk and spec ific to indi vidual ri sk ractors . ~6 For examp le, the ri sk ractororimmobility is managed very difTcre ntly ror th e co matose patient ve rsus the spinal co rd- injured patient. The comatose patient requires
• Passive repositioning by th e careg ivcr • Pillow bridging • Use or pressure-re lier o r pressure- redu ction s upport surfaces fo r chair and bed In additi o n, meas ures to in crease mobility and activity and to decrease fri cti o n and shear should be institut ed. Overhead bed fram es wi th trapeze bars arc he lpful for pati ent s with
Ex hibit 12- 5 Flow Diagram for Determining Pre\ cm ion Strateg ies Based o n Risk Factor Assess ment
Pre.'iell ce o/tissue trim",,, Ol'er hOlty promilteltce'! (u.m a//o(·atiolls: .wl(·mV(·O(·qcea/. tmcllllllter. i.'ichial tuherosity. "",lIeo/us. heel) NO
YES. provide for wound assessment and treatment plus prc\icn tion strnh.:gics
Patie"t NOT clwir or hed bOlllld altd titus (It JlO or low risk'! (pmie", scores (I I or 2 011 Brat/elt Scale llct;" ily slIhsctllej NO. completc full risk asscssmcnt
YES, do not nced furth er risk assessmen t
Pressure ulcer risk fuctors preSt'III'! Illll1lobi Iit y
Inacti vi ty
Dcc reased Sensory Perception
utrition
Friction and Shear
Moi sture Urinary and Fccal Incontinence
Prel'elltiolt iuterl'elltiolls by risk fa("fors: Immob ilit y. Inacti vity. and Dccreascd Sensory Perception
Malnutritio n
Friction and S hear
Moi sture Incont inence
pass ive reposit ion in g. pillow bridging. pressure-rcducing/relieving su pport surfaces
provide nutrition suppl ement: protei n. ca lori e. vi tam in C. zi nc, iron
cornstarch, lubricants. pad protectors. tran sparent film. thin hyd rocolloi d dress in gs. turning. and draw s hcets
absorben t products. diagnosis o f inco ntincncc. gc neru l skin c:'lre
Pressure Ulcers: Pathophysiology alld Pre\'ellfioll
paraplegia, stroke pat ients wi th upper body streng th. and obese patients and may increase mobil it y and independence with body repositioning. Wheelchair-bound patients with upper body strengt h can be taug ht and encouraged to do whee lchair pushups to relieve pressure and a ll ow for rcperfusion of the ti ssues in th e ischial tuberosi ty reg ion. For patients who are weak from prolonged inactivity, providi ng support and assistance for reconditioning and increasing strcngt h and endurance wi ll he lp prevent future debi lity." Mobility plans for eac h patient sho uld be ind iv idua lized with the goal ofauaini ng the highest level of mobility and activity individually possible. Mobility plans are the responsibi lit y of nurses and physical therapists worki ng together in all health ca re se ttin gs. It is essential th at health care professiona ls train and obse rve home ca reg ivers in the mobility plan and. in particular. passive repositioning techniqucs. Careg ivers in the home arc often left to fend for th emselves for preve nti on interventions and Illay be fra il and wi th health problems th emse lves. A return demonstration of a repositioni ng procedure ca n be very info rm ative to th e health care providcr. The health care provider may need to coach, improvise, a nd think of creative strategies for caregive rs to usc in the home setti ng in order to meet th e patient's need for movement a nd tiss ue reperfusion.
P(u."Ih'e Repositioning by Cllregh'er Turni ng schedules and passive reposit ion ing by caregivers is the normal response for patients wi th immobility risk factors. Typically. turning sc hedul es a re based on time or event. If time based, turning sc hedu les are usually eve ry 2 hours for full body change of position and more often for sma ll shifts in position. Event-based sched ul es relate to typica l events during the day, for exa mpl e, turning the patient aller eac h meal. Fu ll body cha nge of position involves rurning the patient to a new lying position. for example, turnin g the patient from the right sidelying position to the left sidelying position or the sup ine position. When th e sidelying position is used in bed, avoida nce of direct pressure on the trochanter is esse nti al. To avo id placing pressure o n the troc hante r, po it io n the patient in a 30 0 laterally inclined position instead of the com mo nl y lI sed 90 0 s id c lying position , which increases ti ssue comp ression over the trochanter.6 °The 3~' laterally inc l ined position a ll ows for distribution of pressure over a greater area (see Figure 12- 8). Use of diagrams wit h c lock faces and body position of patient are he lpful in reminding staff when and how to position the patientbl (sec Figure 12- 9). Small shifts in position invo lve moving the patient but keeping thc sa me lying position.!:>:! for exa mp le, c hang ing the ang le of the right side lyi ng position o r cha nging the lowe r extremity position in the right side lying position. Both strateg ies are helpful in achieving repe rfusioll of co mpressed tis-
253
30' angle between hips and mattress
Figure 12- 8 Th irty-degree laterally inclined position . SOllrce: Copyright Barbara M. Bates-Jensen and Lynette Mcrrman.
sties but Dilly full body change 0/ position completely relieves pressure. T here arc techniques to make turning pati e nts easie r and less time cons umin g. Turn ing shee ts. draw shee ts, and pi llows are essential for passive movement of patients in bed. Turning sheets are useful in repositioning th e patie nt to a side lyillg position, and draw sheets are used for pulling th e patient up in bed and help prevent draggi ng the patient's skin ove r th e bed surface. Two-person repositioning is a s imple task with th e turning sheet and can be accomplished in a very sma ll amo unt of time with little ri sk of dragging the patient's skin across the bed li nens:
I. Positio n one person on eac h side of th e bed. 2. Bend th e patient's knees and fo ld the pati ent 's arms across the chcst. 3. Ro ll up th e draw sheet nex t to the pat ie nt 'S body and grasp fi rmly. 4. On a prearranged verba l cue. both perso ns lift th e pati e nt and move him o r her up in bed. 5. Nex t. o ne person pulls on th e turn sheet to ro ll th e patienl pass ively toward th e side. 6. The person on the othe r side of the bed immediate ly places pillows behind th e patient's bac k for s upport.
254
W OUNI)
CAR"
SUPINE POSITION
LEFT SIDELYING POSITION
RIGHT SIDE LYING POSITION
RIGHT SIDELYING POSITION LEFT SIDELYING POSITION
SUPINE POSITION
Figure 12- 9 Clock method of determining turn ing sc hedule.
7. Additional pillows are then used for easing pressure on other bony prominences. The recommended time interval for full change of position turning is every 2 hours, depending on the individual palienl profile. Simi lar approaches arc use ful for patients in chairs. Fu ll body change of position invol ves standing th e patient and re sitting him or her in the chair. Small shifts in posi tion for tho se in chairs might be changing lower ex tremit y position . For Ihe chair-bound patienl, il is also helpful 10 use a foolstool to help reduce the pressure on the ischial tuberosities and to distribute the pressure over a wider surface . Attention to proper alignment and posture is essential. Indivi dua ls at ri sk for pressure ulcer developmcnt should avoid uninterrupted sitting in chairs and shou ld be repositioned every hour. The rationale behind Ihe shorter lime frame is the extremely high pre ssures generated on the ischial tuberosities in the sCaled position . I Those patients with upper bod y strength shou ld be taught to shift weight cvery 15 minutes to allow
Clinical Wisdom: One-Person Turning
For one-person turning, the followiog procedure may be helpful: 1. First, remove the pillows previously used to position the patient. 2. Next align the patient's body in a central position . 3. Gently bend the right knee and position the right leg in a crossed position over the left leg , 4. Place the right arm across the body, as if the patient is reaching for the other side of the bed. S. Using the turn sheet from the opposite side of Ihe bed, gently pull the patient's body over to the left sidelying position. 6. Alternatively, from the same side of the bed, with hands on the shoulder and hip, gently push the patient's body over to the left sidelying position. 7. Position pillows at the patient's upper back area, between the knees, between the ankles, and under the feet if appropriate.
Pressure Ulcers: Pathophysiology and Pret'elllioll
for ti ssue reperfusion. Aga in, pillows may be used to help po sition the patient in proper body alignment. Physical therapy and occupational therapy can assist in body alignment strategies with even the most contracted patient. (See Chapter 13 for further di scussion on orthotic devices and sea tin g thempeutic s.)
Pillow Bridgillg Pillow bridging involves the usc of pillows to position patients with minimal tissue compression. The usc of pillows can help prevent pressure ulcers from occurring on the mcdial knees, the medial malleolus, and the heels. Pillows should be placed between the knees. between the ank les. and under th e heels.
Clinical Wisdom: Positioning Pillows
Five pillows can overcome repositioning pressure point difficulties. Use the pillows in the following positions: Pillow Pillow Pillow Pillow Pillow
1: 2: 3: 4: 5:
under legs to elevate the heels between the ankles between the knees behind the back under the head
(Use a small pillow for comfort under the arm in sidelying position .)
Pillow usc is especially important for reducing ri sk of development of hee l ulcers regardless of the support surface in use.!/I The best prevention strategy for eliminating pressure ulcers on the heels is to keep the heels off the surface of the bed. Use of pillows under the lower extremities will keep the heel from making contact with the support surface of the bed. Pillows help to redi stribute the pressure over a larger area. thus red ucing high pressures in one specific area.
Research Wisdom: Donut Pillow Devices
One type of pillow device is not recommended for use. Use of a donut type or ring cushion device is contraindicated . Donut ring cushions cause venous congestion and edema and actually increase pressure to the area of concern. 2iI
I
255
Use of Pressure-Relief or Pres.m re-Rel/u clioll Support Surfilces There are specific guidelines for the use of support surfaces to prevent and manage pressure ulcers. Ui1 .1t4 Regardless of the type of Slip port surface in use with the patient, th e need for written repositioning and turning schedules remains essential. The support surface serves as adjuncts to strategies for positioning and careful monitoring of patients . The type of support surface chosen is ba sed on a multitude of factors, including clinical condition of the patient, type of care se tting, ease of use. maintenance, cost, and characteristi cs of the support surface. The primary concern should be the therapeuti c benefit associated with the surface. Table 12- 1 ca tegori zes the types of support surfaces avai lable and th eir general performance characteri sti cs l ; Exhibit 12 6 presents ideal support surface characteristics. Table 12- 1 and Exhibit 12- 6 are presented as an overview to the remainder of thi s sec tion. The information on support surfaces is organized in the following manner: first. information on tissue interface pressure is presented: second information on pressure-reducing and pressure-relieving support surfaces is presented ; finally, thi s sec tion ends with information and guidelines on how to determine the appropriate surface for specific patients.
Tissue IlIlerface Pressures. Tissue interface pressures are common ly evaluated by using capillary closing pressure (genera lly considered 10 be 12 to 32 111111 Hg) as an indirect l11easure to label effectiveness of support surfaces. The lI SC of capillary closing pressures implies that skin surface interface pressure is equallo capillary closing pressures. Further, as ti ssue interface (skin surface) pressures approach capillary closing pressures (12 to 32 111111 Hg). the support surface is 1110re effective and less likely to occlude blood vessels ( less likely to cause pressure ulcer formation) . One of the difficulties with the use of capillary closing pressures is th e assumption that capillary closing pressures are absolute values. Capillary closing pressures may be more individualized than absolute values imply. Capi llary closing pre ssures assume that skin interface pressures renect pressure at the bony ti ssue interface. Some suggest that pressure on subcutaneous ti ssues may be three to five times higher than skin interface pressure. Interface pressure is a measurement obtained by placing a sensor between the skin and the restin g support surface. It i s usually obtained wi th sOl11e type of electropneumatic pre ssure sensor connected to an inn ation system and gauge. Typically, three or more readings arc obtained and the average of the readings is used as the reported va lue. Instrumentation (size of sensor, shape of sensor, and position of sensor) greatly affects values of pressure readings, so it is difficult if not imposs ible to make cornpari sons between studies.
256
W OUND CARE
Table 12-1 Selected Characteristics for Classes of Support Surfaces
Performance Characteristics Increased support area Low moisture retention Reduced heat accumulation Shear reduction Pressure reduction Dynamic Cost per day
Air Fluidized (High Air Loss) Yes Yes Yes Yes Yes Yes High
Low Air Loss Yes Yes Yes
? Yes Yes High
Alternating Air Static Flotation (Dynamic) (Air or Water) Yes No No Yes Yes Yes Moderate
Yes No No Yes Yes No Low
Foam
Standard Hospital Mattress
Yes No No No Yes No Low
No No No No No No Low
Source: Reprinted from N. Bergstrom , M.A. Bennett, C.E. Carlson, at al., Treatment of Pressure Ulcers, Clinical Practice Guideline No. 15, December, 1994, U.S. Depanment of Health and Human Services, Public Health Service, Agency for Health Care Policy and Research, AHCPA Publication No. 95-0652.
Ex hibi t 12- 6 Ideal Suppo rt Surface C harac teristics
• • • • • • • • • •
Red uces/re li eves pressure under bony prominences Comrols pressure gradi ent in tissue Provides stability No interference wi th we ight shift s No interference with transfers Controls temperature a! in terface Co ntrols moisture at skin su rfn ce Li gh tweigh t Low cost OUnlblc
Source: Reprinted wi th permi ss ion from J. McLean. Pressure reduction or pressure relief: making thc right cho icc. Jot/mal of ET Nflrsillg, Vol. 20. 0 , 5. pp. 2 t I 2 15. (' 1993. Mosby YearBook . Inc.
Pressure- Relludllg Support Su rfilce..·. Pressure-reduction dev ices lower ti ssue interface pressures, but do not consistel/tly mailllain interface pressures below capillary closing pressures in all positions, on all body 10cations. 68 Pressurereducing support surfaces arc indicated for patients who are assessed to be at ri sk for pressure ulcer development, who can be turned, and who have sk in breakdown invo lving ollly onl! sleep slIrjace .N.26 Patients with an existing pressure ulcer who are determined to be still at risk for development of funher skin breakdown should be managed on a pressurereducing support surface. Pressure-reducti on devices can be classified as static or dynamic devices. SUllie devices do not move; they reduce pressure by spreading the load over a large r area. The easy definition of a static support surface is a device that does not require electrici ty to function, usua ll y a mattress overlay (lies on top of the standard hospital mattress). Examples of static devices
are foam, air, or gel mattress overlays and water-filled mattresses. When considering the foam mattress overlays, the health care provider should consider stifTness of the foam and the density and thickness of the foam. Indcntat ion load deflection (ILD) is a mcasure of the stiffness of the foam ; generally, the ILD should be 25% for 30 lb. The density and thickness of the foam relate to the fO ) Passive r..mge of motion exercises and frequency
b. Pdltl\\- britlgll1g
c
(I)
Usc of pillows In protect heels
m
lliUm\-·s bel\\een bony prommences
-
Pressure-reducing rclie\"lIlg support surface (I)
Management of SLIp port surface in use
m
De\ Ices Il)r s1U1I1!;
--(3)
Up
III
cha ir for
hour(s). _ _ time(s) pe r day
J. "iulntion strateglcs tI. Pn.)\ Ide adequate nutrition ( I)
Small frequent (si\. mcals a day) lugh-caloric highprotem meals
(2)
Nutntional "upplclllcnts pnw lded. Give - - olof supplemen t timcs per day.
-
b. 1>1'0\ ale adequate hydration (I)
bght 8-07 glasscs of noncallcillc thuds per day un less contIrO\ Ide \ It; December 199~ "',Ilion,,] Pre ...... urc Ulcer Ad\ lsory I)ancl. Pn'H/II\, l kl.."1".\ I/lCItIt'IKe', \1If'('
1:'("0/101111('\.
Ri\J. IHt·uIIJI.'/l/. ('onwlI\l/\ 1J1.·\·I.'!tJ/II1,('/Il (·onle'n'n(·I.'
We!.t Dundee. IL S·',J PublicaIIOll'>, Inc; 19H93 -4 1),1l11c! RIt'r",fllOl 19K2;6:IOI4 1021
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!.kcJct;(1 rnu!.cle.
AIIII
I lcrT1ande,·~Ii1ldonUt.lo JJ, Teehan I:, I·mnco ('D, Duran WN, Ilob!.on R\\ SupcroxuJe ,IIl10n produellun b) lcukocYles e'<po!.cd 10 po... tIschemic .. kc!elal nlll ..cle. J Ca,.di(lI"f/\c· S/I"g 1992;3J:6t}5 699
14
Landi'" EM Mlcro·lnJccllon ,ludic" of capillary blood prc ... ,ure human ... l..ln. lit,,,,., 193CJ;15:2()t)
I;
I hl!.illIl 1\n c:o ulcer.: 111 paraplegic)' .1.4\/1 1t}5~;166 :761763 Bennett I.. Ka\ ncr D. Icc BY. r ... inor FS, Skin stress and blood flow In slllmg paraplegIC patlenl' /1'('11 Plln ,Ht'd Rl'Il(lhil 19X4;65(4):IX6 190. DIIl:-.dak JM DccubllU\ uker" rotc or pr..::-.surc and friction in causallon, Ir,:11 /'lln Met/ HellII"d 1974;)5: 147 153 Kemp 1\-1(; Protecting the ,kill from mOl ... ture and associated irritanh, ./ Gawllo/ \///"\ 1994;:!0(tJ):X 14
n.. t..:,,-Jcn:-.en \\ltkow~kl
11 Inconllnence manugcmenl. In Parish Le. JA. Crissey JT. cd., TIlt' Oe"IfI1/fII~ l.ker m ('flr/Ie'al
Prat'lin' Berlin. Germany: \pringcr- Verlag; I t)97~ 189 199.
Norton D Calculating the ri .. k rell..:etlOl1'i un Ihe Norton Sc.:aie. 19X9;2(3):14 31
f)l'whitIH.
,'re,sure ,or..: rbk a~'ie,>,m..:nl. a (':"fltlqU":. I the (io'>n..:11 SCille O('('/I/)ill/\ 19S9;2(3):.J2 .J9
56
(jo~ncIlI)J
57.
{jo .. nelll)J.
ri .. k facto'" 5R 59
60
60.
35.
NOTton D. McLaren R. Lxton-Snllth NA III IIIH""nIlIWII til (h,,.IIdlllhurgh . Scotland: Churchdl I iVl1lgstone; 1962
Iltf'l{'\unilln Prohll'III\ illl-lrHpiwl,
61 62
63
Ilr..::-. ... ure ...ore fisk "s:-.c",ment .. cfltiqu..:. 11 an;ll),sl" of O"("Ilbll/I\. 1989:2(3)AO 4.l
Ilraden B. Bergstrom N Clinical utility of the Bmd..:n Scale for predicting pre:-.~ure ~ore ri:-.k f)t'(lIhi(/I\. 19Xt);:!(.'H4 51 Bergstrom N. Braden OJ. Bo)nton I~ Ilruch S l',,'g a rc,>c;trehba,cd as'e,:-.mcnt sC:lle III cl1mcal pr.:lctlce, \-I/n elm \'0/"(11 ·Im 1995 ;30539 Seiler WOo Allen S. Stahclin 1111 Influ..:nc..: of the 30 degr..:e, latcrJlly IIlcJlIl..:d position and the ",uper ,un" 3-pi..:c..: maitre,s 011 skill oxygen tension on arc'" of ma'l:illlulll rre..sure: linplic;lIions for prc .. sur..: ..or..: .. pr,,:\cl1tion (;('rolltollln,y 1986;32: 15X 166. Lowlluan PT. Praeucal nur:-'1I1g: turnll1g clock 'y .. tem 10 pr..:\cnt pres.. ure :-.orc~ \/11"' \Iirmr It)79;14X(21) :30 31 Smith AM. Malone JA Prc\cl1ung pr..:s,urc ulcer... III 1Il:-.lIIulmnall.fed cider.. : a,:-,c'islllg the err..:e,"" of :-.lllalL ul1,chedulcd ,Iult .. III body po~ItIOn, IR'cuhIllH I99(UH )::W 24 \leLcan J Pressure reduction or prc"ur..: relief maklllg the nght chOIce. J £1" 'V/ln 1993:20:211 215. Krouskop TA. Garber Sl. Cullen UIl , I'actur, to cOlhltkr 111 ..clCCI/Ilg a 'iUpport :-.urface, In : Kra;,ner D. cd Chmnic lIilllllil Cllre Kmg
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Bryant RA. Shannon \IL. PlI:per B. ct al I)re"ure ulcer .... In : Bryant RA. ed kU(t· alld Chrollic II(Himl, \UI"';II.1: \!llIIlIxell/el/1. St I.olli at the capillary Ie, el. "hich has been termed the" hite blood cell tntpping hypothcsi s"'1_:l1 Transient clcvations in \enous pressures ha,e been shown 10 decrease capillary blood flo w. resulting in trapping of white blood ce lls at the capi llary level. This occurs to a much greater degree in patients with long-sta nding venous hypertension and liposclerotic ski n. These marginated \\ hitc blood cell s in turn plug capi llary loops. rcsulting in area!o! of local ilcd ischem ia. These cells may also become ac tivated at this level. which in turn causes rcle,lse of ,",uious proteolytic enlymes as well as supcrox ide free radicals and chcmotactic subMunces. Thcse substances ultimntely lead to direct tisslie damagc. thus leading to ulceratiOl1. ~' Differential Diagnosis of Venous Sta sis Ulce rs
All that ulcerates is not \enOliS in origin. The coml11on feature of all ulcerations of the Icgs is an underlying sys-
Medical Treatment of Venous Stasis Ulcers
Definitive treatment of \cnOliS stasis lIlcer~ is depend en on the operative repair of the underlying reason for venou: incompetcnce ofthc affected c\trelllity. This is seldom pos sible. howc\cr. and long-term ~uccess is rarely achie\ed Excision and grafting of the ulcerated area and surroundint scar tissue. even when accompanied by local and region; subfascialligation ofpcrforating \ es!otels. docs not uniforml~ result in returning long-standing skin integrity. Therefore there remain a grcat many patients \\hose \cnous st ~lsis ul cers hmc to bc managed nonopcrath I!ly:l~ Before attcmp t ing a mcdicall11anagcll1ent ofa \enOliS stasis ulccr. the diag nos is mu st bc assured. Noninvasive measurements mus elim inatc a significant ischemic com ponen t to that ct iology TI1C AS I must be at least greater than 0.5 and prcferabl~ greater than 0.75 . If transcutaneous oxygen l1lea s urel1lent~ arc performed, the foot dorsal pressures shou ld exceed 3( Illlll Ifg. I fcmoglobin electrophoresis shou ld eliminate sickh ccll disease and if suspected :I biopsy should eliminatc \ ":lS culitis as thc caliSC of the ulcer. To allow the ulcer to heal by sceondS ApplH:allun of ullr:lsound to thc .. tudy of arterio ... ckf()~i ... nhllter.ms IlIgwlogy 1975;20: I K7 I !N.
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CHAPTER
15
Management of the Neuropathic Foot Nancy Eljimiln
INTRODUCTION
The multidisciplinary cllmc rC{lulrcs speCial tralnlllg 111 treatment of chronic disabilities. Although the lIutl\ Idual training programs of profe!)sionals include 110rmal fOOl anatomy and biomechanics. few describe the neuropathic foot and associated complications. leading to inadequate medical ad\icc or treatment:' In the clinical settlllg no initial prob w lem is too small to addres!'i. The clinical team IS important and must treat minor trauma 1I11111ediately to prc\ ellt deterioration of thc condition. There is a destruct I\"e chain oftraullla surrounding the neuropathiC foot. as follows:
Medical research has pTm'idcd ad,'tUlCements in medication and technology that now extend the lives of patients with previously raral diseases: the prognosis has changed from fatality to chronic complications. I The chronic disease complication addressed in this chapter is neuropathy. The objective ofmanagclllcllt or the problem is to control progression and reduce amputations conservatively. The patient with neuropathy onen has dysvascular components that must be addressed by a medical team rather than onc specialty (sec Chapler 14. Diagnosis and Management of Vascular Ulcers). With the tcam approach the limb can be evaluated treated and monitored through follo\\-up to prm ide continucd alllbul~tion for the paticnt.': The team goal is the prevention or delay of Hmputation andior limb salvage of lower extremities. In the form3tion of clinical teams there has been a trend to include practitioners of several disciplines. including wound carc nurse. advanced practicc nurse. or cllIerostomalthcrapy (ET) nurse. diabctologisl endocrinologist. \'aseular surgeon. physical therapist. orthoIIstpcdorthist. orthopaedic surgeon podiatrist. and dermatologist. The multidisciplinary approach to treating foot problems is an optimum intervenllon for pre\'cnlloll of amputations. The dlsciplmes playing the 1110st nnporl largest-diamcter monofilament indicates KX
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Figure 15- 16 DiagrJlll of accommodauvc Insef! fabricallol1. Source: Repnlllcd wllh permiSSion from R,B. Chamhl.:r.-. and N, Llftman. Orthotic Management of the Ncuropalhic and Dysvascular I)atient. in Allw olOrtJlOse.\' amI I.nis/il'e D('dn',\, J rd . t.!d lIiOIl , Il. Goldberg and J.D. Iisu. ed~., p, 444. l 1997. Mosby-Year Oook, Inc .
334
WOLIN!)
C'RI
High Top
Pillow Back
Lateral Flare
BLUCHER STYLE
DEPTH SHOE
Rocker Figure 15- 17 Depth shoe modifications, Source: Reprinted with permission from R.B. Chambers and N. I:-.lftman. Orthotic Manag~l11el1t orthc Neuropathic and Dysvaseular Patient. in A fh,s oiOrrhoses wICIAssistil 'e D(!\'ic('s. 3rd . edition. B. Goldberg and J.~ . I bu. cds .. p. 443, c 1997. Mosby-Year Book. Inc .
Clinical Wisdom: Choose Crepe Sole Shoes for Pressure Relief Crepe sales, which are full of air cells, provide pressure relief to the plantar surface, whereas air or water "pillows," which are enclosed in an inflexible compartment, create pressure,
Lealher gradually ada piS 10 the slope oflhe fool and will retain shape between wearings. The leather will breathe and absorb perspiration. I,,! The patient should not depend upon the "feel" of a shoe for correct size. The shoe must be full width and girth and allow lh- to %-inch space beyond the longest toe to prevent distal shoe contact through the gait cycle. Standard modi fications of ext.ra-depth shoes for the neuropalhic palienl include siretching orlhe softloe box for clawed toes. nared lateral soles to discourage varus instability, nnd shank/rocker bottom for a partial fool, hallux rigid us, or decreased motion at the metatarsal heads. A rocker bot-
10m should be added to Ihe shoe when metatarsophalangeal extension is to be avoided.:!:' When properly fit, the instep Icather should not be taut. There arc thrce tests 10 determine the proper fit of shoes (sec Figure 15~ 1 S, how to mensure for proper shoe rit) :
I. Length: Allow \12 to % inch of space in front of longest toe. 2_ Ball ,,-;d,": With Ihe palient weighl bearing, grasp Ihe vamp of the shoe and pinch the upper mnterial, if leather cannot be pinched. it is too mllTOw. The ball should be in the widest pan ofthc shoc.n 3. /-led to hal/lenglli : Measure the distance from the palienl-s heel 10 Ihe firsl and fifth metalarsal heads_ Bend the shoe to determine toe break. and repeat measurements on the shoe. They should be close to the same measuremcnts. ~4
The simple addition of shoes instead of barefoot may correct many defor111ities .;~ Laced shoes will give the best control. but Lhey must be broken in slowly. beginning with
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Natural Elongation of the foot lIeel-off stage
Full weight bearing Partial weight bearing
Figure I~ IH lIow to measure for proper shoe fit. SOl/ree: Rc· prITlIcd \\-lIh Jlcrl1liS~IOn from R.B. Chambers and N, Elftman, Orthollc Management of the Neuropathic and Oys\3scular Patient. IIllrlm ofO,.,hows ""dAs\;_~'/iI'e f)el'il'('.\, 3nl cdulon. B. Goldberg and J.D. IIsli. cds .. p. 442. c 1997. Mosby-Year Book, Inc.
2 hOUr> per day and slO\I Iy adding ume." Caution should be taken with cutout sandals for the possibility of irritation along
the borders of the sandal and straps.7hTo evaluate pressures
within a shoe. there is a pressure-sensitive sock that is coated I"th dye-filled lIax capsules. The capsules fracture when a certain pressure threshold is exceeded leaving dye stains in areas of high pressure, to., To protect a healing area in which dressings will be applied. a healing shoe lined with Plastazotc will :1110\\' greater circumference and volume adjustability. Socks for Ihe neuropalillc limb should have no mended arcas or scams over bony promincnces.A cotton/acryli c blend willnssist in the wicking of perspiration away from the fool. ~" The soc~ should be fully cushIOned and have a nonreSlric-
]35
tive top. The partial foot rcquires ~l sod.. that \\ill confllTl1lto the shape without distal prominl!nt S\!HmS or c\cess I11Hlerial at the distal end. For thc actl\"c patient. socks can bi: obtained with silicone over high-stress areas to prevent . . hear for full or parlial feel. The partial foot may require a bloc~ within the shoe lor the area of amputation. The purposc or a block IS to r\!uuce migration of the partial foot und medial luteral shear for the toe amputation. No block or "prosthctic lOC" IS to be used for a central digit amputation. The 10'W pressures applied by a block to central digits calise ischemic ulcerations on opposing surfaces. Medial or lateral amputmions (first and finh lOes) may require a block 10 hold Ihe fOOl in Ihe correci posilion Within Ihe shoe. The lorcfool bloc~ holds Ihe shoe leather away fromlhe distal cnd of the foot and discourages distal migration of the fool. All forms of blocks mllst hnve space from the amputation slle and be an integral part of the insert. not added to an existing orthotic. Forefoot bloc~s require a rigid rocker sole to pn!\'cl1t ulcl:ration to distal end. By utilizing state-of-the-art foams and room tcmpcTilture vulcani7cd (RTV) siliconc elastomers. shear can be reduced in areas of skin grafts, chronic ulcerations, and cnlcancctomies within more rigid orthotics. The viscoelastomer gel is a two-pari gellhat can be adjuSied for durol11cler demed. The mixture can be used for shock absorption and shear reduction. Scar-adherent areas can benefit from a medium duromele r mixture. The disadvantage is weight. so it should be used in small areas. Low-density foams can be designed into orthotics. such as toe breaks and forefoot blocks and rehefs. Reliefs for heel pain can be deSIgned into the insert OT shoe sale as a Sach heel. Snch heels use soft and medium duromcter soling to simulate plantar flexion .md provide shock absorplion al heel s((ike.
Total-Contact Casting The tOlal-conlacl ca.llng (Tee) melhod prOlldcs decreased plantar pressures by increasing weight bearing over the entire Imver Icg. It has been sliccessful as a treatment for plantar ulcerations but requires careful application. close follow-up. and patient compli ance \\ith scheduled appointments to minimize complications.' Brand introduced the 10lal-conlacl casl to Ihe Uniled Siaies III Ihe 1950s 10 redIStribute walking pressures. prevent direct tnwma to the wound redu ce edema. and provide immobili7ation to Joinh and son ti ssuc. The average healing time for ulcerations treated with the healing cast was 6 weeks. 71> This method has been used for patients with and without evidence of severe peripheral vascu lar disease. ~" The cast spreads weight evenly over the lower limb so that no part of the foot takes mOTe than 5 pSI . There is never a \Vindo\'. cut III thc cast OT there may be 10-
336
WOl iJ'\1> C\RI
call/cd swelling. shear stresses, and cventually a secondary \,;ound (sec rigure 15 - 19). Application methods of the total-contact healing cast vary Vr'ith different IIlstlllitions. The healing cast was originally designed \\.po. "Hllln; S'1Il Diego. CA: M.I) 10 June 4. 1997
44
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Ulley R. NutTiliunal faclors associated \\uh wound hcaling in the elderly: the role nf ~oI~I These modalities include alternating, direct, and pulsed current (eg. hi gh-voltage pulsed current. low-voltage pulsed current. and transcutaneous electrical nerve stim ulation [TE S]). Chapters 16 to 20 describe the rationale. device. applicati on of. and case studies fo r six modalities: electrical stimulation. pulsatilc lavage with suction. pu lsed short wave diathermy, pulsed radi o frequency stimulation, ultrasound, and whirlpool.
347
348
W OUND
C A.,
care or ca re by a prov ider olher th an a physical therap ist arc ex plained in each chapter's sectio n on self-care treatment guidelines.
CAN I) ID ACY FO R T HE INTE RVENTION Ca nd idacy for appli ca tion of physic al agent s a nd clcclrolhcrapclIl ic interve nt ions fo llows a th orough di agnostic process described in Chapter 1 to determine those condi tions that wo uld benefit from or preve nt lise of the interve ntion and to determ ine that the body systcms lack the abil ity to pcrrOfmlh c necessa ry process of repair wi th out inte rvention. The clinical decision-mak ing process used for selecting each of the modalities is related to the system impairments it aOccts, as we ll as pract ica l conside ration. Candidates for physica llhcrapy technologies incl ude patients wi th obscrvn blc ac ule inflammation of the tissues. includi ng pain , chro nici ty of or absence of any phase of repair, circulatory comp ro mise and edema. as wc ll as impai rmcnts ofd ifTercnt body orga n systems such as the cardi opulmonary, musculoskeletal. ncuromuscular. and integumentary systcms. Thc mode of interve nt io n best suited to the patient, the treatment selling. and the wo und wi ll be determined by the physical therapist. As a guide, the paticnts should be referred to the physical th e ra pis t for int erve nti on with a ph ysica l age nt or elcctro thcrapeut ic modality whcn the additional followi ng candidacy cri teria are met: • Medica l comorbi di tics ex ist that predict that a wound needs ex tra help to heal (eg, insensitivit y associated with spinal cord injury, diabetes). • Ilealing will be speeded by the thera py. • The wo und has been reca lcitrant to other methods. • There is an acute wo und in a patient wi th a coimpairmcnt such as chro nic obstructive pulmonary disease or imp::t ircd ci rculation, ind icating a high proba bility of nonconforming hea ling. • The ac ute trau matic wo und(s) is associated wi th neuromuscul ar or musculoskeletal prob lems that may require illlmobi lizat ion. • The wo un ds ex tend into subcutaneous tissuc and deeper underl ying structu res and interfere with functional acti vities: eg. the patient is unable to sit up in a wheelchai r beca use of the wo unds over thc ischial tuberosities or coccyx. • The patient s functional status is im pa ired by slow wound healing; eg. gait will be helped if the wound is healed more ra pidly. or patie nt may be ab le to return to wo rk. I~ easo n s
fo r Referra l
The patient referred to the physical therapi st for wo und hea ling is usuall y an indi vidual who has not shown signs of
normal wound repair. Often other treatment interventions are being used or have been tried with lim ited or no success. Actuall y the ve ry best time for intervening with physica l agents or electrotherapeutic modalities is during the first 72 hours immediately aft er injury. Several recent stud ies show that intervention by a physical therapist soon after onset of the problem (eg, stroke,u ac ute musculoskeletal painU) reduces cost. Appropriate early intervention by the physica l therapist has a prove n track record of signi ficantly reducing the development of costly chronic health prob lems. A review of the research literature eiled in the chapters on electrical stimulation, pulsed radi o frequ ency. pulsed short wave diathermy, and ult raso und all cite research that demonstrates optimal effecti ve ness when the treatment interve ntion is applied earl y. However, since in rea lity more chronic wo unds than acute wounds are referred to the physica l therapist, other research cited in the chapters dcmonstrates efficacy of thesc technologies for hca ling of chronic wounds or to alter factors related to chronic wound healing such as circulation, oxygen uptake by cells, and edema. Ex pected outcomes should be based on the reason for the referral, the efTi cacy of the treatment interve ntion selected, and the chro nicity of the wound. Patients, caregivers. and physicians seek carc for a wo und for many reasons. Although it seems as if thc obvious goal of treatment is healing, healing is not the highest priorit y for everyone with a wound, and that assumption should not be madc. It is ve ry important to ask the patient, famil y, physician, and payer the reason for the referral and base the interve ntion selected and ex pected outcomes on meeting those objectives. Most of the time the patient and fa mil y arc looking for a simple fun ctional outcome. For example, the patiellt with a foot ulcer secondary to pressure and insensi ti vity is fearful of amputation and loss of the ability to walk . The patient wa nts to kn ow if the limb can be saved.The family of a debilitated nursing home patient wants thcir loved one with a pressure ulccr to bc comfon able. They may rcalize that closure is not an option. Fea r is a concern and creates a reluctance to come to therapy. All of these issues need to be addressed. The physical therapist's first intervent io n will be to learn as much about the patient and his or her goa ls and then begin education about the treatment options, effects of the treatment. and the ex pected outcomes. Di agnosis The diagnosis is the synthesis of the information gathered. Physical therapists use a fun ctional diagnosis to describe an impairmcnt, disabilit y, or handicap of an associated body fun ction. For examp le, the patient wi th a neuropathy as a consequence of alcoholism, dia betes, or spinal cord injury or the il11mobile or il11l11obil izcd patient could all have
Par/IV
a functional diagnosis of impaired sensa ti on with undue susceptibility to ischemia. ti ssue anoxia. infection. and pressure ulcera tion. The impairmen t is decreased immunity. ti ssue anox ia. infecti on, and cell death , The disability is desellsit ized skin and ri sk for skin breakdown. The handi ca p is inability to maintain normal activit y and mobilit y. Patients with chronic wounds have an abse nce ofprogression through th e phases of repair. that is, a functional impairment to wound hea lin g at th e cellular leve l or the ti ssue level. Ahsence of il!/iammatiull alld il/abilily 10 progress 10 proliferatiou is a functional di agnos is about functional impairment of the process at the cellular leve l or ti ss ue leve l. This could be applied cqually 10 a funclional impairmelll of the prolife rati on phase: abse nce of proliferation or wound contraction with inab ilit y to progress to closure. Chroni c wound edges do not produce functional epidermal cell s to mi gra te across the wound to c lose it. Ahsence oJepitheliali:atioll due 10 impail1l1elll (?f epidermal cell activity is a functional diagnosis ro r abse nce of wound progressio n to closure. A poorly healed wound or a minim ally healed wound has a functional diagnos is of absence of remodelillg due to il1leglll1l e111111)' .~ystem impairmem. Although traditionally patients with non-healin g wounds are referred for physieallherapy. palienls wilh mu sc uloskeletal injuries and so n tissue trauma should also be viewed as patients with a closed wound. Patients with wounds such as ligamentous tears. muscle stra ins, sprains, sk in tears, hematoma s. stage I pressure ulcers. stage 0 vascu lar ulcers. and abrasions that interfere with one's ability to wnlk, work. or co mpete in a sport should be viewed as cand idates for inte rventi on with physical agents and e lec trotherape utic modalities including elec tri ca l stimulati on, pul sed radio freque ncy stimulation. pulscd short wave diathermy, ultraso und and whirlpool. In patients with metabo lic di seases (eg. lupus or diabetes) who sufTe r wounding. acute wounds can. and onen do. become chronic. Also. mi crotrauma resulting from excessive forces and repetition ca n also lead to closed wounds such as tendinitis and nerve e ntrapmcnts. In these patients, the imp3inncnt is also a closed ti ssue wound. The di sability is pain and usua lly limitation in ran ge of moti on. A handi ca p would result from prolonged di sability and the resulting inabilit y to work or pa rticipate in normal ac ti vities of daily living or recrea tion . Ea rl y and e fTecti ve interve ntion to accelerate repair with the listed interven ti ons should be co nsidered. In summ ary. a patient who has a functional diagnosis of impairment or a body system at the cellular. tissue , or organ level (or a combination) related to ti ss ue repair shou ld be co nsidered a candidate for interve ntion with e lectrica l stimulation, pulsed radio frequency stimul at ion, pulsed short wave diathermy. or ultra so und. In addition, patient s with mu sc uloske letal injuries in need o f acce lerated repair should also
349
be co nsidered candidates for the sa me intervcntions used for closed wound healing.
Prognosis The functional diagnosis is predicti ve of the need for the interventi o n . Inter ve ntion with ph ys ica l a ge nt s and electrotherapeutic modalities must have a predicted outcome, or prognosis. that the intervention wi ll reduce the impai rment or alter the consequences oflhe di sease assoc iated with the fun ctional diagnosis. A wound diagnosis of absence of the illJ1ammllfioll phase, for exa mple, is predictive that the wound needs an inflammation phase fo llowed by progression Ihrough Ihe phases of healing 10 reach closure. The prognosis is ;1I;I;al;OI1 oj inflammation fhl/oll'ed by progression oftlte wOllnd through the phases oj healing. Part of a prognosis is th e ex pec ted due date. There is enough information in th e literature to evaluate the expected length of tim e to reac h an outcome. The individual chapters in Part IV provide this informati on. Electrical stimulation . pu lsed radio frequcncy stimulati on, pul sed short wave diathe rmy, ultrasound whirlpool, and pulsalile lavage wilh suclion are all ex pected to re initiate an inflammation phase followed by progressionlhrough Ihe phases of healing. AnOlher example of functional di ag nosis is impairment a/sensation witlt 1II1 due s usceptibility 10 pre.5SI11l1 ulceration. Reflexive neurona l mechanisllls are impaired. and other methods Illust be used to stimulate circulatory responses; the prognosis ror thi s functional diagnosis would beadeqllare circullllOlT peljilsiollJor deli\lelJ' 0/mygell ami nUlrielllS to tisslles tu pmgress thlVugh phases ofl'epail: Multiple fun ctional diagnoses may be made that lead to l11ultipl e interventions, all of which will afTec t the outcome with the phys ical agent or electrotherapeutic modalit y interventi on chosen for th e wound. For instance, the patient with an impairment of se nsation with undue susceptibilit y to pressure ulceration mu st be assessed for pressure ri sk. An interve ntion of press ure relief or elimination the n must be included in the trea tment plan so that the enhanced circulalory perfusion broughl abo ul by Ihe se leeled interventi on can reach the ti ss ues. The phys ical therapist would apply Ihis melhodol ogy 10 predici an ouleome. The progno sis for repa ir of a c losed ti ss ue injury would be acceler(l!ed ah.mrption a/hematoma. acceler(l!ed deposition 0/collagen. aud reslOratioll ofl1ormal range.\' 0/ motiol1. tiss lle extensibility. fiSSile s freng fh forfi mCfiollal activifie,\' (eg, self-ca re, work. leisure, or play). Clinical resea rch studies are very useful to guide the cli nician in predicted outcomes and can function as a guide for a target due date. C lini cal research studics should identify whether the wound s treated are acute or chronic. Because clinical resea rch studies are usually carried out in ideal settings under optimal co nditions, th ey should be considered
350
W OUND CARl
onl y as guidelines that need to be tested in the individual clini ca l settin g to determin e th e outco mes for th e spec ific
program . For example. the literature describes wound healing by closure or improvement. Imp l'Ol'emell l is less cl earl y
defined and usuall y is described by reduction in depth of tissue loss or size and is listed as incompletely hea led. Depth of ti ssue involve ment (severity) will alter the ex pected length oftimc to closure. Parti al-thickn ess wounds heal fas ler than full-thickness and deeper wo unds.' Normal wound healing takes 3 to 4 weeks,' while the defin ition of chronicity is hea ling that has not occurred in the normal tim e fra me. The con-
and exudate that leads to an outcome of wo und hea ling. There are also practica l considerati ons in choosing an intervent ion. These include th e treatm ent setting, th e treatment provider, th e trea tm ent payer. th e tre atm ent avai labilit y, medica l contraind icati ons. and adj uncti ve tre atm ents (dressings,
multiple technologies). Ifthe treatment provider is to be other than a physical therapist or physica l th erapi st assis tant, the
treatment must be safely app lied by a person not trained in physical therapy. This would prec lude use of pu lsed short wave diathermy or ult raso und, for example. The treatment paye r must be agreeable to payi ng for the physical thera py
cept of using physica l age nts and electrotherapeutic modali-
intervcntion selected. For cxamplc. Medicare contractors
tie s is to initiate or acce lerate th e ra te of repair of acute or chro nic wounds. For example, Dyson andYoung8 found th at
have an exc lusion poli cy for payment of ultraviolet light to
appli cati on of low-intensity ultrasound duri ng the earl y inflammatory phase accelerated the inflammatory ph ase of repalT.
Choosing between In tervent ions A frequentl y as ked questi on is, How do I know which intervention to choose? There is no si ngle answer to thi s question. The mechan isms of acti on on th e biologic system are different. but the expected trea tment outcomes of progression through the pha ses of hea ling are sim ilar for each of the deviccs prese nted in Part I V. Somc have optimal tim es fo r application, however. For instance. ult rasound is best deli vered in th e inflammatory pha se--early proli fe rationSor to restart th e inflammatory phasc, but it is not effec ti ve fo r improvement of tensile strength if used in the later proli fe rali ve or epitheli alizati on pha se. 9 Figure I V- I is an algori thm
showing the phases of wound hea ling with a key to highlight whi ch arc the putati ve effec ts on the phase or factor of healing of th e six physical therapy technologies descri bed in Part IV. If one or more of the technologies affects the same biologic aspect of the phase, oth er criteria will be used to choose the modality. For instance, most dev ices desc ribed have th e
ability to increase tissue perfusion. What diffe rs is the degree of tissue perfusion. The th erm al modaliti es heat and increa se circul ati on more vigorously than the nontherm al modal ities. Thi s effect may be suitable for some pati ents who necd a vigorous attcmpt to enhance blood fl ow to reac h ischemic ti ssues. Th e nonthermal dev ices affcct the microcirculation but may not have a vigorous enough effec t on circulation for all patients. Research is highly va lued as the basis for sc lcc ti on of an intervent ion, and conscquently the intcrvention with th e most support ing research may bc given th e nod over less testcd deviccs; however, cli nical ex peri ence still must be valued. For example, whirlpool and pul satil e lavage with sucti on havc no controllcd c lin ical tri als for cfTi cacy of wo und hea ling, yet clinica l experi ence demonstrates that both have the abi lity to clean wounds of debris
treat wo unds. Treatm ent ava ilabi lity is as practical a reality as anything. I f th e preferred intervention is not available and cannot be obtained, th en it is inacccssible and another choice will have to be made. M edical cOJ1traindications ex ist for all of th e different technologies. but the medical contraindication that rul es Ollt the use of one will not necessari Iy rul e out oth ers. For exampl e. a semicomatose pati cnt should not be
seen in the whirlpool. but wound cleansing with pulsatile lavage with sucti on at bedside would be an appropriate al-
ternati ve. The following Casc Study illustrates where thoughtfu l evaluation of the history and systems review narrowed down th e choice of treatment intervention to one appro priate technology aft er considering all th e factors.
Trcatmcnt Outcomcs Ma nage mcnt Clinical managers havc an obl igation to revicw trea tment outcomes systemi cally for wo und patients referred 10 physical therapy. Most oft en the patient population refcrred are those individuals with comp lex wo unds and comorbidities and many arc also vcry debi litated. areful screening and monitoring proced ures arc necessary to utili ze trcatment ef-
fecti vely. Sussman Physical Therapy, Inc. (S PT) is used to illustrate how a clinical program lIsed a wound databa se to do progra m evaluati on and quality improvemcnt, and eva luate program outcomes. SPT trea tcd a popu lation of complex
and debili ta ted nursi ng home patients. SPT developed and conform ed to a se lf-i mposed standard of 50% reducti on in wo und size within a 4-to-6 week peri od using Sussman's noninvasive. surgery-altcrnative trcatm cnt approac h with
physical therapy technologies and debridement. The first requirement was identificati on. fo r the pati ent 'S medi cal manager, wound stability, and the candidacy for surgical and oth er more costly interventi ons. SPT used paper-and-pencil instrum ents to record wo und data information. The information was th en transfcrred to bubble sheets and scanned into a computer databa se. tatisti ca l analysis of the SPT wo und database was performed by Swanson and Co., Inc.lO Findings were th at SPT had cxcellent success wi th chronic
Pari I V
35 1
Injury
I
r
Inflammation Phase l'
Epithelialization Phase
l'
Proliferation Phase
Pain 6....JOX=
6 l'
Immobility 6 0 0 = X
+
l'
Impaired 6 0 0 = X Circulation
Infection Control 6 XX= l'
Edema 6 0 = l'
Oxygenation Nutrition 60=XO
~
Macrophage 600
~ Granulocyte 6
Fibroblast 600 Formation
~
Angiogenesis 600
+
Wound Contraction 60
Hypoxia l'
Necrosis 60 () X
l'
Collagen Lysis
!
• Remodeling Phase .. I 6~
Collagen Synthesis 6 0
j
l'
Wound Recovery
KEY :
6.
Electrical stimulation Ultrasound Pulsed radio frequency stimulation
,~
X )
Unknown • HVPC: Necroti c > Closed o TCC: Neuro/O pen > Closed
Course of Care in Days
Figu re 1\1- 2 Le ngth of stay dependent on wound Iype and procedure .
5,000
$4,500
4,000 3,000
• • • o
2,000
Surg.Debr: Necrotic> Open Hydro: Necrotic> Unknown HVpe: Necrotic> Oosed Tee: NeuralOpen > Oosed
1,000 0
$ Figu re IV- 3 Cost companson for different wound interve ntions and out comes. Physica ilh crapy is co mpeti tive for ccrw in wound s.
35 3
354
WOUN D C ARl
outcome of closure is expected in 84 visits a cost analysis can be done as fol lows: Labor cost at $30/visit x 84 Supply cost at 56.25/visi t x 84 Equipmcnt cost at 0.50 x 84 Total cost Billed charges at S60/ visit x 84 Net profit
52.520 $ 525 = S 42 $3.087 S5.040 $1.953
of healing when wounds were treated with physical therapy technologies. For example. reduction in wound depth is a finding of acute proliferation phase. Reduction in size is a measure of wound contraction and of epithe li a li zat ion. If these benchmarks of healing are not occurring in an orderly manner, thi s may be due to a poor response to treatment or changes in medical status and should trigger a change in the treatment approach. The following are some examp les of situations that trigger a change:
The cost for a different Olilcomc to co nvert the wound to clean and stable may take half the time to closure. Cost to the payer would be reduced by half to 52.520. The case manager for the payer may be morc willing to authorize an interim step for a known cost than an unknown outcome at
unmanaged cost. Utili zat io n a nd Cost Management Utilization and cost Olltcomes management !TIcan that con-
tinued ongoing evaluation of the patient candidacy be reviewed. Candidacy determined ar the initial evaluation may change as the patient experiences a course of care (Figure IV-4). This would initiate a reevaluation (0 assess appropriateness for furthcr treatment. The Sussman Wound Healing Tool. described in Chaptcr 5. was deve loped as a diagnostic (001 to evaluatc progression through the phases
• Failure to progress: If the wound(s) are not progressing through the biologic sequence of repair aner 2 weeks of treatment with high-voltage pulsed current (HVpe). for examp le. the enti re wound management plan needs to be reviewed to determine whet her it is the treatment wi th the HVpe or other factors th at are respons ibl e for failure to progress. Since all wounds have multiple associated interventions, including wound cleansing, topical treatments, dressings, and debridement. along with the HVpe. each intervention should be reviewed to determine whether continuation is appropriate or if there needs to be cha nge in these intcrventions o r with the HVpe protocol. It is standard wisdom that wounds shou ld be progress ing in the rcpair process during a 2-week interval or the treatment should be revised. I;!: • ~"o ull d regressioll: If th e wound has golten larger or deeper and is invading named structures or areas or has
Still Treating: pen- Candidate? Total $ Spent
Discharged: Closed ~--------n ischarged:
Stable & Open Start of Care
Course of Care and Outcome
Fig ure IV....4 Monitor candidacy and outcome throughout course of care.
Par' IV
•
•
•
•
•
bccome infcctc(L indicating that another management strategy is nceded (eg. surgcry for incision and drainage or antibiotics). thi s is referred to as wound regression. Although the physical therapist. phys ical therapist assistant, or nurse would not make the decision for the subscq uent therapy. he or she should be able to recogni ze the signs and sy mptoms of di sease and has responsibi lity to make a referral to the appropriate practitioner. ft!lel/icill illslllbili~v: Ifthe paticnt has bccome medically unstable (eg, pneumonia. sepsis, renal failure), the body's ability to heal is impaired. and the si tuation requires a change in ll1ediea lmanagemcn t bcfore continuing wi th physical therapy. The phys ical therapist may determine that the physica l therapy interve ntion may need to be put on hold ulltil the medical conditioll is stabili zed. Other IIIllltllgemellt rel/uired: If the wound has progressed to a clean and stable wound in the proliferat ion phase. it may indica te that the wound is ready for grafting. It may be the best prognosis for the wound and/or for the patient and may have been the reason for referral. the objecti ve of the palicnt, the family. the therapi st, and the physicin n. Uv tllld lIeells less skilled ClIre: The wound is now at a phasc of repair that dcmonstrates that the healing response is slistHined and the wound is clean and stable. Now thc patient/caregiver or nurse can provide standard wound care procedures to keep the wound clean and if body systems support the process of healing, take it to closure. GOlll.~' m et: Sometimes. thc patient and family have reached their goa ls and do not wish to continue or become noncompliant with trcatment. In other cases, the wound has hea led to closure. Closure (111(1 beyond: Wound closure may be the intent of the trcallne llt. but closlIrc does not include rcmode ling. Wounds that arc minimally c losed are at very high ri sk for recurren ce, especially when located over areas of fri ction . shear, and pressure. such as on the seating surfacc or plantar surface o f the foot. Wounds in those areas of hi gh risk would benefit from further stimulali on o f collagen synthesis by electrical stimulation until the minimall y healed scar is acccptably healed. III Acceptable healing is achicved when thcre is a thickening of the sca r formati on and the color of the scar blanches from bright red or pink 10 light pink or white.
Plan of Carer rre:Hment Part IV focuses primaril y on the usc of exte rnally app lied treatments for wound repair and does not address specific
355
dressings and deb ridement, nor does it olltline the specifics of an exercise program. It must be reinforced, however. that all of the described techno logies are supplemental to the traditional wound managemcnt program ofdebridcmcnt. dressings. and medications. In addition to physical therapy technologies. every patient who is able to participate in exerc ise must be instructed in an appropriate exercise program. For so me. traditional strengthening and condition ing exe rc ises would be appropriate (eg, wa lking, running. stationary bike). In others it may be active range of motion of the extremities or isometric exercises. Every physical therapist mu st address the issues of immobilizalion and prevention of demincral ization. atrophy, and contractures. In some cases, so ft ti ss ue mobili za tion techniques could be used arollnd the wound. In all cases. the patients and caregivers must also be educated about hydration, nutrition , and a balanced lifestyle that addresses stress reduction and positive health. The physica l therapist is lIsually the only team member who can manage the electrical stimulation program, the therapelltic exercises, and appropriate soft ti sslle mobili za tion procedures along with the wound care.
CONCLUS ION The rules for selection oftreall11ent interventions includes consideration of the medical tatu s of the patient, th e status of the wound healing phasc, and all treatments lIsed to achieve th e expected outcome. Wounds all rece ivc multiple intervention s. Treatment efTects arc additive. Therefore. all treatment interventions mu st be compatible with the patient, one another, and the wound. They will change during the progressio n ofhcaling. The most universa ltreatll1ent intervention is the wound dressing. Modern wound dressings have specific efTects and times for reapplication. Because wounds need to be cleansed periodically, the wound c leanscr is another common intervention. Topical agents from cnzymes to a ntimicrobia ls are often added to the wound intervention regimen. Depending on the phase of wound healing, one or more of these interventions will be needed , The addition ofa physical agent or an e lec trotherapeutic modality must be co mpatible with the other trea tmcnt interventions. This will require collaboration of the te3mmcl11bers-nurse, physician, pharmacist, and physical therapi st- to select interventions that are compatible and efficacious for wound healing. Ex hibit IV- I li sts three rules of treatment selection. an example of how each is used, and a formu la for selection of treatments to achieve a desire outcome in a prescribed period. The letters "A," " 8," and "C," in the formula represent three treatment interventions. The number of treatmcnts usually give n is often three, but is not limited to three. Each chapter in Part IV will address the issue of treatment interactions and compatibility with other interventions.
356
WOI ' "
Elhibit 1"- 1
I.
C·,.,
Rulc~
~lcdjCltl
REF ERE.\ CES
ofTrcatmcnt Selection
HsseSSl11cn' ilTtd
li~sue :ls~cssmcnl
determines
the ticlcclion of treatment.
Ew"'p/L': Client has a vcnous stasis ulcer in inflammatory phase and has a cardiac pacemaker implant_ \Vhirlpool. li Vre. PRfS and PSWD arc contramdicated. Ultrasound would be a good choice
American PhY"lcal Thcmp,\ ....ociallon A g.ulde to phY"lcal thempi .. 1 praclicc. \"011 a llcscriplion ofpal1cnl m:lOagemcnt Ph,'( Ther 1995;75 :707 · 764
ror local (lpplicallon.
2.
(icncnll Accountlllg Olllce. L, S t"ongres ... reported III PT Ilullelin. American PhysicalTherap), :\ ....OCUlIH.\Il. \'01 12. No. 10. \Iareh 7. 1997.
J
lIa)e .. S. Carroll S. Larl)' IIltencllllOll care III the acule Mrokc patlcnI . lrd/ Plln' \kd He/whit 19H(';i.7:31(j 321
4
LIIHon S. Ilett~lIlg t\. Andcr.. ~on D. A controlled !!Iully of the ct"of carly IIltenentlon on acute museuloskdetal pam problcm .. /1l1ill 199.t54(3):353 3~9
fecl~
2. Treatment changes during the progression of healing
so 115 to affect the
recOHr~
process.
~.
Amcrkan Ph) .. ical Therapy As.. uciatloll. 01111"01111' f:.llt'(·ln·('lIl·n of Phnicul 711l"~IJJ\ III Inl/(JUlln' B;h1/(jW~/p/II' A1cxandria. \"A ·\PTA. 11}sible that the oxygen rather than the polarity is the variable that is rcsponsible for the bactericidal efTects on pathogens. Oxygen Oxygen is critical for wound hea ling. Constalll delivery of oxygen is required to meet high metabolic demands of the tissues, ox idative killing of infectiolls organ isms, protein and col lagen synthesis. and hydroxylation of proline to make useful collagen. Blood flow is the mechanism of oxygen transport to the tissues. Treatment interventions that increase blood flow consequent ly wi ll enhance oxygen delivery to the tissues and improve healing. Electrical stimulation may be one way of enhancing oxygen and nutrient enrichment to the tissues. Increasing oxygenation could be an important reason to use ES. Lack of adcquatc oxygen coul d be a partial explanation for difficulty in hea ling diabetic ulcers. q Baker et a I. 5"}~ measured oxygen enrichment to the cells of wound repair in a study of age-ma tched older normal adu lt s and diabetic subjects. Oximctry readi ngs of the partial pressure of transcutancolls oxygen (tcpO!) were taken 30 minutes prior to stimulation. during 30 minutes ofstimulatio n, and 30 minutes after stimulation. The electrical st imulation waveforms used were monophasic paired spikes wi th negative polarity and a compensated monophasic waveform. Both waveforms were introduced with the cathode over the wound. The older normal adults also showed higher tcpO! levels at the end of 30 minutes of stimulation regardless of wavefo rm used. However. there were differences in response time for the diabetics. The norm al adults showed increased oxygen levels earlier in the treatment period than did the diabetics. Diabetic subjects showed measurable but not significant increases in tcp02at the end of the 30 minutcs of stimulation but did show sign ifica nt increases 30 minutes afte r cessation of (he stimulat ion. Increases occurred with both wavefo rms. but no change occurred when submotor or trace muscle contraction was elicited with the compensated monophasic wave form. For some reason the trace musc le contract ion blunted the tcpO! response in the diabetics. The same effects we re found for both waveforms and with stimulation by ei ther the positive or the negative pole. In another stud y of diabetics, Baker et al. N compared the effects of a monophasic paired spike \\'3\efonn lIsing both negative and positive polarity with a symmetric biphasic waveform. Transcutaneous oxygen pressure from baseline 30 minutes prior to stimulation. during 30 minutes ofstim ulation, and 30 minutes after treatment were compared. The findings showed that the tcpO! levels were significant ly increased rcgardless of waveform or polarity. Increases were
present at the end of the st imulation period and cont inued to rise during the next 30 minutes afte r stimu lation. Therefore. Baker et al.\II concluded that the mechanism of action of ES on increasing transcutaneous oxygen was unrelated to polarity and did not require any net ion flow. Byl et al. 5b found that whcn supplell''ICnta l oxygen was given by mask prior to and during microamperage stimulati on (1 00 ~lA for 45 minutes). there were significant increases in subcutaneous oxygen measurcd . Maximal oxygen saturation may be necessary prior to and during ES in ord er to faci litate the di ssociation of oxygen from the hemoglobin.~b In transferring technology from the lab bench to the bed the physical therapist could take the information from these three research stud ies and formulate and test a protocol for wound heal ing for diabetics. For examp le. nasal supplementation of oxygen could be provided du ring ES treatment for patients with diabetcs to accclef3Lc the oxygcl1uptake.A trial to evaluate the differcnce in wound healing outcomes for diabetics treated with ES whi le brearhing room ai r or supplemental oxygen could yield useful clinical data from these types of studies. The results would be development of a new clinical protocol for trearing diabetic wounds.
Noninvasive electrical stimu lators that stimulate sensory nerves can be classified as TENS ." A large body of literature supports the usc of TENS for both acute and chronic pain management. Techniques for pain modulation can be used along with the wound healing protocol s. For examp le. one electrode may bc placed 011 the painful area, which includes the wound and adjace nt Lissues. and the indifferent electrode over the related spinal nerve. The electrodes call al so be bracketed proximal and distal to the areas of pain arou nd the wou nd such as with a bipolar Lcchniqllc described later in th is chapte r. ~~ Pain management would be a good rcason to lise clectrodes of cqual size so that there would be suO'icicn t current de nsity at the dispersive electrode. Scar Formation
In anima l and human studies, naps and grafts treated wi th monophasic pulsed current electrical stimul ation heal without ischemia and result in natter, thinner scars than in COIltrols.l'Ul CLINICAL STUDIES
Since the 19605 a series of clinical trials has been undertaken to eva luate the effect of electrica l stimulation on wound healing. The early studics arc classics in th is field .
Low Voltage Pulsed Microal1lpcragc Direct C urrent
Studies Direct current was lIsed in three clinical studies. Wolcott eL al.~.l . Gault and Gatens N • and Carley and Wainapel!itl treated ischemic and indolent ulcers. In all three studies a positive (anode) polarity was lIsed after a period of3 or more days at the caLhode. The polarity was reverscd cvery day or every 3 days if wound healing did not progress. Rationale for cathode app lication was the sol ubilization of necrotic tissue '6 and bactericidal efTects.'41 . u The first two studies used an amp litude of 200 to 800 flA and the latcr study 300 to 700 fiA. Duration of treatment was very long: 2 hours. two or three timcs per day. or 42 hours per week for the first two studies, and 20 hours per week for thc later stud y. A combined tOLal or 163 paticnts were trcated and 29 served as controls. In most cases the patient served as his or her own control. Mcan healing timcs reported were 9.6 wceks, 4.7 wceks, and 5.0. respectively. for the threc studies. The diflerencc in healing time between these three studies is not clear. Perhaps in the Wo\con eL al. stud y the wounds were more extensive. Microcurrcnt stimulation has becn studied in animal models in which current was appl ied on ly onc or two times per day for 30 minutcs for I LO 2 weeks; no significant clinical effects were demonstrated on wound healing .l~.6! In another study. there were significant increases in subclltaneous oxygen measurements when supplementa l oxygen was given by mask during the MENS stimulation.:'>b There was no accelerat ion in healing.
Modified Biphasic Stimulation Study Barron et al.b! reported a stud y of six patients with prcsSllre ulcers who wcre Lreatcd threc times a week for 3 weeks for a total of nine treatments with microcurrcnt stimulation. The waveform was a modified biphasic square wave. The treatme nt characteristics were 600 ~A. 50 V. and 0.5 Hl. The electrode probes were placcd 2 cm away from the edge of the ulcer and thcn moved circumferentially arOllnd the ulcer. Each successive placement of the probes was 2 cm from the prior placement. In this small study. two ulccrs healed 100%. three healed 99%, and onc decreased in siLe 55°0.
High-Voltage Pulsed Current Studies Three controlled clinical studies have been rcported by Kloth and Fcedar. b-1 Griffin et al..1>-1 and Unger et al. b~ In the st ud y by Kloth and Fcedar.t'" wounds had a mean hea ling
Electrical Stimulation/iH' H'tJlIl1t1l1ealil1g
timc of7.3 wceks. and 1000 /0 of the treatment group healed. Unger et al.M repo rted on a controlled study of nine subjects in the treatment group and eight con tro ls. The average wound size in the trcatment group was 460 111m!. compared wi th the control group whose average wound size was I 18.5 mm 2 . Me~l11 healing time was 7.3 weeks for the treatment group, with 88.9% completely healed . GrifTin et al." had demonstrated an 80% reduction in si7c in 4 weeks, but ulcers were not treated until healed. UngerM reported an uncontrolled study using II Vpe treatment fo r 223 wounds. The mean healing limes for the 223 wounds in the uncontrolled study was 10.9 weeks. In all studies. the treatment frequency was five to sevcn timcs pcr wcck for 45 to 60 minutes. All treatmcn t protocols began with negativc polarity. After the wounds were clean of infection. polarity was changed to positive cxcept in the study by GrirTin ct al..nJ whcre the polarity was kept at negative for the 4-week stud y period (Table 16- 3). Tv.'o additiona l published uncontrolled studies included 30 patients. Alon ct al. 11 used positive po larity and stimulated wounds three times a week for I hour: 12 of the IS or SO% of the ulcers treated healed. One patient died. one did not respond and the ulcer in one decrcased significantly in size but did not hea l in 21.6 weeks. Akers and Gabrielson h7 published a study that compared ( I ) Ilvrc direct app lication to the wound: (2) application of Ilvrc usi ng the whirlpoolas a large electrode: and (3) whirlpool alone. The di rect application of the active electrode to the wound site had the best outcome. followed by II vpe lIsing the wh irlpool as an electrode. Whirlpool alol1e was the least efTective.
367
Clinical Wisdom: Best Method for Effective HVPC Treatment
Apply HVPC directly to the wound for best expected outcome. Conducting current to the tissues during whirlpool is not recommended because it is less effective, and some clinicians report that stimulator leads
have become entangled in the agitator. There have even been stories of stimulators falling into the water.
more than twice as much as the sham-stimu lated ulcers (49.S% versus 23.4%). healing at a rate of 12.5% per week compared with 5.8% for the sham-stimulated group. Crossover results for 15 of the 19 sham-treated ulcers showed a fourfold greater healing during the 4 weeks of stimulati on compared to 4 weeks of sham treatment. This difference was statistica lly signi fieant. 1.1 Fcedar et al. fill publ ished a study on pressure ulcers. The 61 patients served as their own contro ls. The treatment pha se of the study was preceded by a 4wcek control phase of optimal nonelectrically stimu lated wound care. Only the stage II I or IV ulcers with need of surgical debridement, necrotic/purulent drainage. or exudate seropurulent drainage that did not improve during the control phase went on to the trealmenl phase. After 4 weeks of treatment 58.8% of the wounds had improved . After an average ofS.4 weeks, 23% completely healed and 82% improved significantly.
Lo\\- Volt agc Pul sed Elec tri ca l C urrent Studi es
Biphasic Stimulation Studies Two controlled clinical tria ls with low-voltage pu lsed current. labeled PES. were located in the litera ture. Gentzkow et al. l \ reported a study of40 ulcers in37 patient s. Nineteen pressure ulcers were stimulated and 21 were sham stimulated. The triallastcd for 4 \leeks. The treated ulcers healed
There are reports in the literature by Kaad'-1. ~1 Lundeberg et al.,bQ Stefanovska et al. 70 and Baker ct a1. 7 1.7! of clinica l trials of wound healing with biphasic waveforms. Kaada ~1 and LUl1deberg el nl."" each used biphasic symmetric wave-
Table 16-3 HVPC Clinical Studies
Researchers
No. of Patients
a controls (diabetic)
% Healed
Mean Time to Heal
Alon et al. 17
15 Treated,
Kloth and Feedar"
9 Treated, 7 controls, 3 crossovers
80% 100%
2.6 Months (10.4 weeks) 7.3 Weeks
(mixed wound etiology) 8 Treated, 9 controls (pressure ulcers) 223 Treated , a controls 9 Treated , 8 controls (pressure ulcers)
80% Reduction in size 89.7% 88.9%
4-Week treatment period 10.85 Weeks (54 .25 days) 7.3 Weeks (51.2 days)
Griffin et al.s.
Unger" Unger et al."
368
W OUND
J\RI
form s with signifi ca nt imp roveme nt in both ulcer area and heal ed ul ce rs. Ka'lda" reported resuits o fT E Son 10 subjects, who se rved as th e ir own cont ro ls, with recal c itrant ul ce rs o f di ffe re nt e ti o log ies. Stimul a tio n was prov ided indirec tl y ove r th e we b of th e thumb da ily durin g three 30-minute sessio ns with rests o f 45 minutes betwee n for a total o f I Y2 hours stimul ati on. Stimul ation was be low visible muscle contracti on. LUlldeberg et al. 69 pe rformed a controlled stud y on 64 patie nts with chro ni c di a beti c ulce rs du e to venous sta sis. All pati e nts received standard treatm ent with pas te bandage in addit io n to the sham or T ENS treatme nt. Asy mmetri c biphas ic stimul ati on was determined to produce s igni f ica nt wo und hea ling e lTects. whereas th e othe r wavefo rm s did not inc rease th e hea lin g ra te. The stu dy by Ste fa novs ka et a l. 70 co mpared direct current a nd asy mm etri c biphas ic curre nt. In a noth er study. Baker et al. compared asyml1letric biphas ic. symmetri c biphasic. and mi crocurrent (DC). The t'mwfol Surg ()"ml 19K9;15:1272 1275. BourgUignon ("J. BourgUIgnon IY \\ I'lcetncal smuulat lon or proteUl ami DNA synlheslS In human hbmbla,,,, "'·ISEB J I'JK7; I' .1 ~1J, "'nkl' ~II', Millcr H I'nhanced ~urvI\jl of full-thickness skill grtudy of thc cffect of lugh voltage pulsed current (IIVI)C) on ....'Qund healing. Phn Ther. 199L71("uppl):SI IQ Linger PC" A randomi7ed chnicaltrial of the effect of IIVpe on \-...-aunt! healing. Pln~ Tiler. 1991;71 (suppl):S 118. Akers T. (jabnebon A. The efTect of high \-'ollage galvanic stimulation on the rate of healing of decubItus ulcers. BlOllled Sl"I Im/ruIII .I 19X~ :2099 100. Feedar JA. Kloth LC. Genllkow GD. Chronic dermal ulcer healing enhanced with monophasic pulsed electrical stimulation. Ph\-'_~ Tiler. 1991;7];639649 I undchcrg TCM. Enksson Sv, Mat s M Electrical nerve 5tmlUlalion Improves heullllg of diabetic ulcer~ A"" Pfost Surg 19l)2;21)(4):32K 3JO. Stcl"ano\-ska A. Vodovnik L. et al. Treatment of chronic wounds by me,lIIS of electrical and electromagnetic fields. 2~ value of FES pammetcn. for prcssurc sore treatment. /lfed 8iol £"g CompllI 1991 ;1 1.213 220. Bakcr L I. Kuhayi S. Ct al. Fllecl or electrical stlillulation wavcform on herding of ulcers in human beings with sp inal cord injury. lIiml/{l Hi'!' R('g 1996;421 2M lJaker LL. Chambers R. et al Effects of electrical st llnulatlon on wound hcaling 111 pallen!) With diabetic ulcers. Dillb(,u'.\ Cllre. 1997;20(3). 1 8. I)onayre (' Diugno~i~ and mana!!cment of\-'ascular ulccr~ ; artcrial. \-'cnOl!'> and diabctic. Presen ted at Wound Car~ Managemcnt 96; Torr;lllce, CA. October 1996. Ra"l11us~cn MJ. llayes DL. et ai, Can tmnscutaneous eicctricaillervc ~til11ulation be safely u:.cd in patienl.~' with pcrmanent cardiac paccmakers'l \1111 '00/11 Pm!' 191(8:63 :443445.
75.
Eaglstell1 W. OfT-label uscs III wound care. Paper pre~cnted at thc Sympo~iulll on Ad\anccd Wound (':m!; Atlanta. GA; April 1996.
76
Cook T. Barr Jo. Instrumentation In ; Nelson R. Currier D. eds. Clinical £/(!(·tn>them/w No ....... alk. CT' Appleton & Lange; 1991 II 33.
77
Brown M, Electrical stimulation for \....ound management. In: Gogm PP. cd, Clinical Jl(nmd \f{lfWgl.'ltfCllt Thorof.lre . NJ. Slack. Inc; 1995; 176 183.
78.
Kloth L( Electrical ~tlmulallon for wound henhng. !·'(hibll()r prcsClltatlon at American Physical Thcmpy As~oci:HIOIl Conference: MlI1neapoh:., MN: Junc 1996.
79
Davis S. Thc effect of pulsed elcetncal stimulation on epidermal wound healing, J Inn'\( DermlllOl. 191(8:90:555.
80.
Cummings J. Kloth LC Rolc of light. heat and electromagnetic energy in wound hcaling_ In \1cCulioch J. Kloth L. Fecdar J. eds Ubwul llea/illg Alterlltllll'e,I,' /1/ MlllUl/{('mem 2nd ed Philadelphia F.A Davis: 1995 :275 314.
81
Mycr A Observablc effects on granulallon lissuc u'>lng warmed wound care products_ Prcseilled at Symposia. "I uture Directions in Wound lIealing"; Amcrican PhYSical Therapy A~sociation SCIeillific Meetll1g; June 1997; San Dlcgo. CA
82.
Bellmn. KA. Thacker JG, ct ulimpaci pressures genenued by commercial wound irrigution devices_ Unpublished re,>earch report Charloltc!\ville. VA: Uni ..'cr;ily of Virglllia lIealth SCience (enter; 1994
83.
Bourguignon GL. el 31 Occlusive \-....ound dressing' '>uillible for use with electrical stlmulatioll_ IHmnt!\. 1991 ;3(3): 127
84.
Agren MS. MenL MA Collagcnase during burn wound healing: IIlnuence of a hydrogcl drcsslIlg and pulsed electrical ~lImulalion Pfa~t RenmY/r SlIrg. 1993;94:5 I 8 524
85.
Alon G, Panel discussion. Symposi:l. "Future Directions in Wound lIealing"; Amcrican Physical Therapy Associallon SCIentific Mecting: June 1997; San Diego. C A
86.
Kalinowsl.l DP. Brogan MS, Siceper MI), A practlcallcchnique for disinfectlllg electrical ~t1Il1Ulalion apparatuses lIsed III wound treatment. Phy~ Th(,r. 1996;12:1340 1347_
1(7
Lock I'M The elrcet of temperature on 111110tiS ilt the edge of C~ pen mental wounds_ In : Lundgren A. Sovcr AB. cd:. Srnll'osill on UOlltid /let/Illig: PI{l~/jc, SlIrgicalt/llti DI.'mw/ologic A'pects Sweden: Molndal ; 1980.
88
Myers JA. Wound healing and the u~e ofmodcrn Mlrglcal dre'~lI1g Pharm J 1982;229:103 104
CH A PTE R
17
Pulsatile Lavage with Concurrent Suction Harrielf Bal/gh Loel1l1e
DEFI NIT ION
• It reduces bacte ri a and infectio n. • II promotes granul ati o n a nd epithe lia li zati o n. • Th eory: the nega ti ve pressure o f the sucti o n stimulat es g ranul ati o n o f c lea n wo unds.
Pul satile lavage wi th concurrent slict ion is a method of wo und care that prov ides clea ns ing and debri dement with pulsed irrigation comb ined w ith suctio n. It thu s prov ides nega tive press ure to re move th e irriga nt a nd debris to help reduce in fecti on and to enhance granulati on. Thi s ultimately
Ma nage m e nt o f Infectio n
provides an improved fo unda tion for wo und hea ling.
Wo und infec ti o n is a m ajo r concern in ma nage ment o f wo unds. Dead and dyi ng ti ssue, d ebri s. c lo tted bl ood and fo re ig n bodies a re predi spos ing conditi o ns to wo und infecti o n. Rapid rem ova l o f these co nt ami na nt s has been demo ns trated to speed hea ling. Stud ies in the lit erature re port that hi g h-pressure pul sa tin g irri gati o n dec reases the prese nce o f these co ntamin ant s and res ult s in a lower in c idence o f wound infecti on. Debride ment and ir riga tio n a re impo rt a nt meth od s fo r controllin g infecti o n in wo unds. Differe nt me th ods are desc ribed fo r irrigati o n of wo und s, inc ludin g bulb syri nge. Wale r Pik . s howe r spray. spray bo lll es. and pu lsalil e irri gati o n/ lavage. Irri gati o n pressures va ry w ith usc of th ese differe nt dev ices. If th e press ure used to d elive r th e irriga ti o n so luli o n is 100 low, below 4 po und s per square inc h ( PS I), the lavage will not c lea nse e ffe cti ve ly. Sa fc. e fTecti ve irri gali o n pressures range from 4 10 15 PS I. Ex hibil 17 I indi cates th e irri ga tion pressures o btain ed w ith these co mm o nly used clinical dev i ces. J(r~l) A press ure o f 8 PS I has been fo und to be s ign ifi ca ntl y e fTecti ve in remov in g bacte ri a and infecti o n.'" Irri gati o n at 13 PS I has attributed to reducti o n o f in flammati o n in traumatic wo unds. Irri gati o n pressures exceedin g 15 PS I may traumat ize ti ss ue and dri ve bacte ria into the wo und ti ss li es. s.6 Steve nso n et 31 :' repo rt edl y ca lc ulated and tested co mbinati o ns o f syrin ge and need le s izes to dete rmine wound irrigat ing press ure . Th e pressure produ ced
Bo th conso le and ba tte ry- powered un its a rc ava ilab le. along with a se lectio n o f tips for c lea ns in g and debridement of di ffcrcl1l wound con fi gurat ions. Physicians have used these systems in the operating room s in ce the ea rl y 19805 fo r irrigati on in surgica l procedures and to clean wo unds o f debri s.
Physica l Ih cra pisls (PTs) have used Ihe syslems s in ce Ih e lale 1980s for irri g31io n and debridemenl 10 enh ance hea ling o f son ti ssue wounds.
T I-I EO RY AND SCIENCE OF T I-I E T H ERA PY Whi rlpoo ls tra d iti o na ll y have been th e m os t co mm o n choice fo r hydrolhera py. w ilh j el lavage and bulb syringes
also being used. Just as wi th whirlpool, there is limited research to suppo rt th e use o fpul sa lilc lavage w ith sucti o n for
wound healing. There arc numerous anecdotal reports and case slud ies of bene fil s.' J Haynes el aI. ' repo n ed Ihal Ihe rate of g ranul ati on ti ss ue fo rmati o n was 12.2% per week fo r wo unds trea ted with pulsatil e lavage wi th s ucti o n and 4 .8% per week fo r th ose trea ted w ith wh irlpool. Othe r sc ientifi c and theoreti c rati o na les fo r lISC o f th e th erapy arc as fo llows: • Il c lean ses v ia gentl e pulsa til e lavage to stro nger irri gation and debride ment.
389
390
WOl 'D
C 'Ol
E"hibit 17- 1 Irrigallon Pressures Delivered by Vanous Dc\icc:,
Irr igatio n Impact
Press ure (PS I) Spray bottle Ultra Klclu Bulb syringe Piston irrig.llion syringe (60 IllL) with catheter tip Salll1c ... quec/c bottle (250 mL)
with irrigation cap Wa:cr I)it.. at IO\'Csl selllllg (1)
Irrijcl I)S syringe with lip
12 2.0 "",1
4.5 6.0 7.6
J5-I1lL ...yringc \\ ilh 19-9augc needle or angioc50% NccrOli c Purulent drainage
Sepsis
X X X X X
Full granu lation base
VAC being used Duration
X X X
No increased granulation for I week o decreased nec roti c ti ssue for I week Wound closed
Clinical Wisdom: Prevent Disruption of Clot following Pressure To Stop Bleeding After applying pressure over gauze packing to stop bleeding and bleeding has stopped, leave the bottom layer of gauze in place to avoid disruption of the clot and restarting the bleeding_ Cover with the prescribed dressing.
• Stop and call phys ician in any of the following circumstances: 1_ Patient has an arterial bleeder: notify physician STAT 2_ Bleeding has not stopped aner 10 minutes of pressure. 3_ Abscess is opcncd _ 4. Joint is di sarticulated .
VACUUM ASSISTED CLOSU RE
Kinetic Concepts' VAC is a device that uses a pump, attached by tubing to a sponge placed in the wound, to create a vacuum to remove fluid . The negative pressure on the wound helps reduce cdema, incrcasc blood supply, and decrease bacterial co loni zation . The procedure increases tension among the surrounding ccll s, which cncourages cell growth and division , drawing the edges of the wound to the center and assisting wound closure. It provides a moist wound environment to promote more efTective cellular activity and al so helps prevent contamination of the wound site from out side bacteria .
Ind ications for use are pres sure ulcers, chronic open wound s, and meshed grafts and naps_ The VAC is contraindicated in the presence of fistulas to organs or bod y cavities, osteomyelitis, and malignancy in the wound. Precautions are observed when there is active bleeding, patients are taking anticoagulants, and wound hemostasis is difTicult. The sponge is not changed for meshed grans. It is changed every 12 hours with an infected wound and every 48 hours with a chronic open wound. After the sponge is removed, pulsatile lavage with suction is indicated to irrigate and debride the wound, including tunnel s and undermining, before a new sponge is placed and secured with an adherent. occlusive dressing_ The combination of the VAC and pulsed lavage has healed wounds four times faster than nontreated wound s. producing extraordinary cost savings. PERFORMANCE OF PULSATILE LAVAGE wlnl SUCTIO (Figure 17- 1)
Procedures for Pulsatile Lavage with Suction
Procedure Set-Up Most patients ideally arc treated on a high-low stretcher. bed, or treatment table adjusted to a height that en sures the therapi st's proper body mechanics. Treatment may be delivered in the physical th erapy department or at bedside in the paticnt 's room _A nuid-proof or nuid-resistant pad is placed under the body part with 'he wound, and towcls arc strategically placed around the wound and coverin g adjacent body parlS. A sterile field is set up with treatment and dressing supplies in ea sy reach . A strong light source is important during pul satile lavage and during debridement.
Pulsatile Lal'age with COllcurrellt Suctioll
395
ing. Use basins to contain th e irrigant overnow with treatment of extremity wounds. Disinfect the basin after each lISC. Clean th e dressing cart with an approved disinfectant solution aller each use. Dis pose of all di sposa bles in the appropriate waste stream per Occupational Safety and Health Administrati o n (OSHA) guidelines.
Personal Protet:t;ve Equipment. Secondary to mist and splashing. all staff pre sent during trea tment must wear personal protective equipment , consistin g of the foll owing (sec Fig ure 17- 2) :
figure 17-1 Gunshot wound with tunnel.
Outpatients with foot wounds can be treated seated in a wheelchair wi th an elevating footrest, with towels padding th e footrest. The therap ist sits o n low footstool in fro nt of the patient and in easy reach of th e steril e fie ld sc t-up of trea tment and dressing supplies. A basin may be placed under the foot to catc h any overtl ow of irrigant. An aide is invaluable for efficiency and assistance with difficult body placemcnt in treatment of some wounds. Duties vary depending on th c systemllsed. Connecting the tubing to the power source and suction source. spiking the bags of tluid turning the unit off and on, adjusting the PS I at the th erapi st's direction, and emptying and replacing the fi lled sllction cani sters and new tluid bags are common procedures that can be done by th e :.lide. savi ng the therapi st time and from having ( 0 change gloves during trea tment. After the trea tment is completcd, the aide also can dispose of th e personal protective equipment. old dressings, and disposabl es whil e the therapi st comple tes th e documentation.
• • • • •
Face shields or goggles and musks Fluid-proof gow ns Fluid-res ista nt knee-hig h boots No nsterile/steri le gloves Hair covers
S illgle-Use 01111'. A ll di sposables exce p' o ne di sc ussed below are ma rked single-usc only, Food and Drug Adminis-
Illfection Control Uni1'erstll Pre(,(lIltions. Protocols should adhere to each fac ility 's poli cy. The patient sho uld be treated in a n enclosed area. separate from other pati ents. I f at th e bedside, ask all visitors to leave the room during treatment. If in a semipriva te roo m. cllrtains must be drawn around the patient being treated. Call housekeeping to change the curtains if they are visibly soiled after the treatmcn t. If a home treatment, ask th e family members/visitors to leave th e room during treatmen t: otherwise personal protective equipment must be worn as discllssed below. All exposed linen used to cont ro l splash should be placed in a clea r plastic biohazmd bag aft er trea tm ent for tran sport to the laundry. Clean 'he stretcher/wheelchai r a ller each treat ment if it is used to transport and treat th e patient. Do not use a mattress or cushion with tears in the protecti ve cover-
Figure 17- 2 Perso nal protective equipm en l for hydrotherapy treatment.
396
Wm,,, CAR'
tration and OSIIA mandate compliance. In fact. ifused morc
is allached to a mobile operating room base and stand or a mobile wound care cart. Another product is driven by nitrogen or medical air tanks. which can bc attached to a wound care cart. All product manufacturers have a battery unit thaI
than one time. Medicare and other payers consider the occurrence irwcMigational and not reimbursable. Lcgalliability is possible if disposables are reused. Daval has a suction di\crtcr lip that allows the same hand piece to be used multiple times with Ihe ,mUle patient. Otherwise. units cannOI be cleaned wilhoul damaging the product
is completely disposable.
Sterile debridement tips include a fan spray1shower head for soft tissue debridement and general irrigation. ilnd open tract tips for undcrmining tracts. and tunnels (E.\hibil 17 6). Muhiple olher lips arc 3\';:lilablc. depending on the manufac-
or being assured that all contaminants and'or disinfection IlHlIcria l is removed.
Latex
CO lltellt
The latex content of the product used (sec Exhibit 17-4)
E \ hibi t 17-4 Latc\ Contcnt ofProduch
is important for latex-sensitive and hllcx-allergic patients. especially those with myelodysplasia, \\ ho mllst be treated in a latex-free environment. t~
J)~l\o l
Latc\ Present
Power Ullit
!\jot prl!scnt
Prodllct~
Zimmcr
Simpulsc Plus
N \
Pulsa\'ac.:
VariCarc
SurglLa\
Pulsa\'ure ulcer). Unnssislcd. the body can take Sc\ crOll \\eeks to clear this material from the tisslies. US can accelerate the absorption. Color PIa/£'\ ()5 {hrough 7(} shO\\ case e\.amples or absorption or hemorrhagic material rollowing the usc or us. In both cases 110 other (re:.llment II1tcncnllon was gl\'cn.
Therapeuric and Diagnostic Ultrasollnd
435
comparing clean ulcers with infected ulcers, the mean healing time for the clean ulccrs was 30 days versus 40 days for the infected ulcers. This was a hea ling rate ratio of2.7, suggesting that the clean so res healed nearly three times more quickly than the infected sores. This result is statist ica ll y significant. implying that the major factor influencing healing is whether the ulcer is clean or infected. The effect of healing in the US-treated group of clean sores was not statistica lly significant. However, there appeared to be a signifi-
Clinical Wi sdom: US and Absorption of Hematoma Stage I pressure ulcers are histologically the rupture of small capillaries and venules, producing a hematoma in the tissue.3 \ Treatment with US promotes absorption of hematoma after two to four treatments. Depending on depth of tissue involvement and size of the area, the hematoma resolves in about 2 weeks without ulceration . Protocol: 1 MHz, 0.5 W/ cm' (SA, TP), pulsed 20% for 5 to 10 minutes depending on size of area sana ted. Apply with conductive gel/ lotion five to seven times per week for 1 to 2 weeks or until color returns to that of surrounding skin.18
cant efTect of US on the healing of the infected sores .
Dosimetry for treatment with US is an area that lacks conse nsus. To learn more about dosage and wound hea li ng, Byl et al. '" made inci sional wounds in miniature Yucatan pigs and treatment was applied at different doses for different lengths of time. The ten si le strength of wounds treated with
Cli nica l St udies
Ultrasound was lIsed as a pcriwollnd Ireallllcnt for a COIltrolled trial for patients with chronic varicose ulcers by Dyson et al. 12 Two groups received either sonalion or sham sonation three times per week for 4 weeks. Treatment parameters for the US treatment were 3 MHz. 1.0 W/cm' (SA, TP). pul se duration 2 milliseconds was delivered to the tisslies every 10 milliseconds for up to 10 minutes. The treatment technique involved moving the head of the device over the skin immediately adjacent to the ulcer. At the end of 4 weeks. the experimental, sonated group h'ld statistically significant reduction in wound siLe compared with the control group (experimental group 66.4
± 8.8°.: control group 91.6 ± 8.9%).
No
adverse effects of treatment were found .·1! Based on the sc ientific evidence that therapeutic US affccts the biologic processes of repair through stable cavitation and/or acoustic streaming desc ribed above, a study was undertaken by McDiarmid et al .11 to determine whethe r these nonthermal therapeutic effects could be used 10 treat son tissue wounds. Patients with partial-thickness skin loss caused by pressure ulcers but not extending beyond the dermis were selected. Forty patients were cntcred into the study and randomized into a US treatment and a sham US treatment group. Treatment parameters for the US treatment were 3 M117. 0.8 W /cm' (SA, TP). pulse duration 2 mi ll iseconds, duty cycle 20... SATA intensity, 0. 16 W/cm', efTective radiating surface area 5.2 cml. Treatment duration was a minimum of 5 minutes for all pressure ulcers up to 3 C1l1 2. One additional minute was added for each 0.5-cml area for a maximum of 10 minutes. Frequency was three times per week . The insonated ulcers tended to heal more quickly. but the diHcrence was not sta tistical ly significant. However, when
dinercnt in tensities. called high- and low-dose US. was tested. Two variables were evaluated: the breaking strength of the incision and the deposition of hydroxyproline. which is a measure of collagen deposition . l ligh-dose US was classified as 1.5 W/cm 2 • continuous mode. Low-dose US was 0.5 W/cm'. pulsed mode. 20% duty cycle. Both treatment groups received a frequency of I MHz for 5 minutes. The wounds were sonated approximately 1.25 min /cm of inci sional length. beginning 24 hours after surgery. The
wounds were covered with a moisture- and vapor-penneablc adhesive dressing (Tegaderm. 3M Medical-Surgical Division, S!. Paul , Minnesota) tha t was left in place for up to I week.
The dressing was found to permit transmission of US energy and could be left in place avoiding disruption of the wound between treatment sessions. Forty-eight wounds were made and the wounds were divided into three groups: 12 for control. and 18 each for high-dose US and low-dose US. The groups were subdivided into two groups of 12 that received low dose or high dose for 5 days and two groups of six that received high dose or low dose for 10 days. Results
were that the tensi le strength for all trcatment groups was significantly higher than that of the controls. but there was no difference in hydroxypro line deposition. A significant interact ion was found between the number of days of treatment and the US dose. Hydroxyproline deposition was sig-
nificantly higher and the breaking strength was higher for the low-dose group compared wi th the high-dose group af-
ter 10 days oftreatmcnt. During the first week the study rindings suggest that either a low or a high dose will enhance wound breaking strength. but to racilitate collagen deposition and wound strength low-dose US should be used if treat-
ment is to continue for 2 weeks or lllore. 14 Nussbaum et al.l~ conducted a comparison study ofnursing care alone, Ilursing care wi th laser, and Ilursing care with
436
WOUN!) CARl
an alternating protocol of U and ultraviolet C (UVC) was
carried out on 20 spinal cord injured patients '\ ith 22 pressure ulcers. Of the initial group four subjects dropped out. Icaving 16 with 18 wounds who werc considered for the analysis. ursing care consisted ofmoisl dressings and continuous pressure relief. The laser regimen was provided three times per week. The USfUVC regimen consisted ofU treatment five times weekly. alternating the US and UVC daily 5 days per week. If the ulcer had purulent drainage. the UVC was Ll sed three times per week: if not, US was used three times per week. US protocol was frequency 3 MHz. and an intensity (SATA) of 0.2 W lcm' (1:4 pulse ratio) for 5 minutes per 5 cm 2 of wound area delivered to the peri wound area. Results showed that the USfUVC treatment had a greater effect on wound healing than did the other treatment regimens. The ITlCan treatment lime to wound closure was 4. 1 weeks. The trend was for ulcers to heal faster in sites where wound contraction was the primary mode ofcJosure (ego over the coccyx). The conc lusion was that this regimen of U I UVC may decrease the healing time for spinal cord injured patients with pressure ulcers. This was a small study and combined t\\O interventions. Further stud y would determine whether the combination was essential and the efl'ects of each. Pre ssure ulcers werc the subjec t of another study using US by ter Riet et al. " Eight y-e ight subj ects were randomizcd into two groups. 45 for the treatment group and 43 for the control group. The trials lasted 12 weeks. ixteen ulcers were stage IV. extending into muscle ti ssue; 72 had less depth of tissue involvemcnt. Treatment was given directly to the wound surface and to an extended radius 0.75 cm beyond the wound edge. Treatment parameters were frequency 3.28 M117. pulse duration 2 milliseconds. SATA. 0. 1 W /em'. B ' R
CHOOSI NG AN I NTE RVENTION: CLIN ICAL REASON I NG
The prior section of this chapter evaluates the efTieacy of US on the phases of wound recovery and in clinical trials. To summari.le, the studies looked at seven important physiologic
efTects of US therapy that the physical thcrapi .. should consider when selecting US inter\'cntion . Uhmsound has thc following effects: • It afTee ts all phases of wound recO\ery at the cellular leve l if applied during the inflammmion phase. • It accelerates the rate of progression through the phases of repair. • It afTects difTerent tissue types diflcrently according to the ti ssues' ability to absorb energy. More ti ssue absorption requires lower-intensity applicmion . • It promotes absorption of hemorrhagic materials. • It increases circulation and tcpO~ if the patient is well hydrated and oxyge nated. • It raises the threshold of pain . • It enables noninvasive. nontraumatic treatment of deep or superficial tissuc. depending on frequency. Informa ti on about the effects of US on wound healing is less clear because of the limited number of clinical trial s. the difTerent parameters used for each study. the small sa mple sizes. and perhaps because the intervention wa~ not appropriately applied: for example. it was applied to chronic wounds at intensities that would 110t restart the inflammatory phase of healing leading to progression through the phases of repair. One stud y included two interventions. US and UVC. with good outcomes. Two studies included subjects who had pressure ulcers: one Mudy included patients with venous ulcers. The biologic effects described are independent of the wound etiology. The pressure ulcers ranged from partial thickness to full thickness extending to musc le levels of tissue involvement. Partial-thickness ulcers heal by reepithelialization, deep ulcers by contraction. The results for infected ulcers were better than those for clean ulcers. Infected ulcers are usually in an inflammatory phase of healing. which is when US is known to be most effccti\e. Would a different protocol be better for a difTerent phase of healing and would that affect the outcome'? More evaluation of the dosimetry parameters on the efTieacy of US arc still required. In the meantime. US may be the treatment of choice for some patients. Two examples arc described in th e case studi es at the end of thi s chapter. Ca ndid 11CY for th e Intervention With any interactive treatment. the benefit to the patient must outweigh any possible ri sk. The phys ical therapi .. must therefore be able 10 assess both benefit and risk . The potential benefits have been desc ribed above. Kno\\ ledge of the mechanisms by which US interacts with ti sslie aids the physical therapist in risk assessment. There is a long list of contraindications in the literature. 1 and the excellent safety
Therapellfic and DiagnostiC Ultrasollnd
record of US owes much to the constraints on treatment that these have engendered (Exhibit 19- 1). Howe ve r. not all contraindications li sted have been ve rifi ed experimenta lly, and it is possible that some patients who co uld have benefited from US treatment have been denied it. To ensure continued sa fe use. basic precautions must be considered (Exhibit 19- 2). Basic precautions start by selection of the right candidates for the treatment. The medica l hi story of the patient, the 011set dalc. locat ion of th e injury. depth of th e injury, and size of the area to be treated will all guid e th e phys ica l th erapist in the selection of US. For exa mple, review the medical history for information about the circulatory system. Look for information about art eri osc lero ti c vessels. isc hem ia, and occlusion from reports of vascu lar studi es. or plan to do a noninvasive vasc ular cxarnillatioll. Uultrasound is not recolllmend ed over dee p vein thrombosis or thombophl ebitis because of th e risk of dis lodging thrombi . Likewi se. hemophiliacs shou ld not be treatcd with US because of the ri sk of dist urbin g clot formation . (Sec Chapter 6 for nonin vasive vasc ula r testing.) Check for inform ation about diabetes mellitus. type I or type II : patien ts with type I diabetes arc likely to have vasc ula r impai rments and se nsory impairments. Diabetes is an impairment to th e repair process; expect slower healing. Ultrasound should be used in the pu lsed mode over areas of poor circulati on. Loss of sensation due to many pathologic causes (eg. spinal cord injury and alcoho lic neu-
E~hibit
19- 1 Contraindicati ons ror USI
1)0 NOT USE US
Over (he ut eru s during pregnancy
0\ er the gonads Over mali gnanc ies and precancerous lesio ns Over tissues previously treated wi th dee p X-my o r irradi a-
lion On pati ent s with vascu lar abno rm alities
437
Ex hibit 19- 2 Precaution s for Usc of US l
EXERCISE CAUTION I N USE OF US
In acul c inrcclion s Over subcu taneous bony prominenccs Over epiphyseal plates Over subcutaneo us major ncn cs Over the craniulll Over anesthetic areas
ropathy: see Chapter 15 for a more comp lete li st) 111eans that the patient is no t a candidate for thermal US . Treatment over anesth eti c areas is a risk because malfunction of the equ ipment could lead to exposure to intensities that wou ld normally induce pain and be indicative of ti ss ue damage. The insensate patient wi ll not be able to indicate pain during the treatment: th erefo re, pulsed low-dose US shou ld be used for th ose cases. I f the patient has a history of spinal laminectomy. do not treat with US over that area because of effects on the spinal cord that have not ye t been determined but may be harmful . A hi story of ma lignant or precancerous lesions or tum ors in the area to be treated would be a cOlHraindicalion because th era pelltic levels of US cou ld stimulate cellular proliferation . Sometimes injuries occ ur aro llnd the eye. but this is a location that shou ld 110t be treated wi th US because th e sensiti ve retin a may be alTected by it. Metal implants, incl udin g foreign objects, are orten described in th e medical history or by the pat ient. Use onl y kilohert z US ove r metal implants. Do nOt treat over th e uterus during pregnancy, to ensure thnt no embryo or fetlls is exposed to the intensities used in therapeutic US. which are higher than those used diagnostically. Do not treat over the gonads. After a thorough review. consider whether US therapy is indicated. I f in doubt , do not irradiate. I'ROCE DURES Protocol Co nsiderations
Deep ve in thrombosis Emboli Severe atherosclerosis Over the cardiac area in advanced heart di sease Over the eye Over the stellate ga nglion Fo r hemophiliacs
nOI
covered by fa ctor
Over the spinal cord aftcr laminectolllY
repl~l ce ment
Review the history for onset of the wound and prior treatment interventions. Thi s will determi ne both the candidacy and the appropriate treatment parameters. If th e wou nd is acute, make use of the nOlllhennal effects of US. If chroni c. use a protocol of one upper-medium- intens it y treatment and subsequently treat at lower intensity. If th e wo und is located over a bony prominence. the physica l therapist mllst co nsider a meth od of sonation th at will avo id increasing periosteal temperature. There arc several ways to accomplish this objective: ( I) select a hi gh frequency (3 MH z), which is ab-
438
WOl,N D
CAR'
sorbed in th e more superfic ial tissues; (2) move the treat-
Expected Outcomes
ment head continuously to avoid stand ing waves; (3) treat through water for a morc uniform far field; or (4) for deeper wou nds, se lec t a lowcr frequency, I Mllz. If the loca l circlIlati o n is poor. lI SC pulsed US to avoid excessive heat ing because it wi ll take longer for heat to be dissipated from the area. Asse ss th e size of the area to be treated. Usc thi s assess ment to determine the duration of th e treatment and the size orthe app li cator to select. Note that an applicato r with a
larger ERA will allow treatmen t ofa large wound more rapidly than ifan app licator with a smaller ERA is used. Small applicators. however. a rc ve ry lIse ful for being morc se lecti ve in treating specific tissues. Se lect the coupling medium depending on whet her the skin is int act or broken . Coupling medi a are described later. Intensity se lection for aClIte conditions is the upper end of the low range~ for chronic conditions. the middle range (see later). The anmomic location of the wo und is a vc ry important consideration when using US. For examp le. be aware of the location of major subcuta neous nerves, whi ch absorb US energy very wc ll and can become overhcatccl and cpiphyseal plates. if treating young people pri or to the termination of growth of thc plate concerned. This varies with th e bone and with the sex. There are also ra cial differences. To ensure the conti nued safe lise of US. thc fo llowing basic precautions arc recommended:
Ultrasound is most effect ive when treating in th c acu te inflammatory phase of healing. During this phase expect an acce lerat ion of the inflammation and early progression to the proliferation and epit helializa tion phases of healing (Exhibit 19- 3). In chronic wounds the first ou tco mcs to treatment will be increased perfusion. observed as warmth. edema. and darkening of tissue color compared to adjacent skin color tones (Exhibit 19-4). In necrotic wo unds. expect to sec autolysis of the necrotic tissue: the outcome will be a clcan wound bed . Wounds in two clinical trials progressed 10 closure in a mean time of 4 to 6 weeks. n'\~ Thesc times cou ld be longer for patients with intrinsic and extrinsic factors that limit healing. Published research is a valuable gu ide 10 the clinician in prediction of olltcomes. but it Illust be supported by th e experience oftllc program where the treatment is used. Reassessment should confirm the predicted ou tcomes. If the wound docs not change phase and/o r reduce the size of surface area or overall size es timate wi thin 2 to 4 weeks. the treatment regimcn must change. There arc severn I changes to US treatment to consider: en hance the inflammation phase
Exhibit 19- 3 Outcomes: Acule Wound
• Use US only ifadequately trained to do so. • Use US on ly to trea t paticnts wi th conditions known to respond favorably to US th erapy, unless it is being lIsed experimentally wi th the understanding and approval of th e patient, his or her medical advisors. and the local medical ethi cs committee. • Usc Ihc lowest inlensity that produces Ihe required effect, s ince hi ghcr intensities may be damaging. Burns, for examp le. occur when the intensity is too high or the frequ ency is low, but the trea tm ent head is not moved co ntinuous ly or is moved too slowly. • Move the app lica tor constantly throughout treatment. 10 avoid th e damaging effects of standing waves and of hi gh-intensity regions when treating in the nonuniform ncar field. • Make sure that there is adequa te couplant and that it is free of air bubbles. • Make sure tha t the equipment is ca librated regularly. A broken crysta l. for inslH ncc, may occur if the applicator head is dropped . Staff must report any dropping of the applicator head so that it can be tested before reuse. A faulty piece ofequipmcnt can result in inadcquHte treatmcnt for the patient or can produce shear waves and standin g waves that can cause burns or oth er harmful effects.'
/l(Jllnti hetlling plta'ie ditlgl/usi\ :
ClC.·II(('
in/loflllllClrioll
Expected outcome: Skin color: change to Ihal of surrounding ski n Temperature: change to that of adjacent tisslles or sallle area on corresponding OPPOSlIC side of the body Edema frec Necrosis free Wound progressed to proliferation phase
Exhibil 19-4 Outcomes: Chronic Wound
/l hlllul !tellling phase diagnosis: clmJ/lic ill/la",,,,,,lioll Expectcd outcome: lI yperemia: change in skin color to reddish blue or pu rplish depending on color of' surrounding ski n Temperature: increased tcmper:.lIure of li ssue due 10 enhan ced perrusion Edema: hardness, tightness. and shiny skin Wound progresscd to proliferation phase
Therapeutic alit! Diagnostic Ultra .w lInd
or restart it wi th the protocol for chronic wounds: change th e frequency of the transducer: usc a difTerent size tran sduccr for bClIcr ERA, or increase the treatment time; or recalcu late the area ifthc wo und has bcen debrided and wo und is larger than initial size.
439
Table 19-1 Intensity Levels for Therapeutic Ultrasound ' Intensity Levels
Low Med ium Hig h
Range
Area
1.2-3.0
W/cm 2 W/Cm2 W/cm2
Dyson Protocol
Acute 'Vow"ls Onset. Begin as soon as possible. idea lly within a few hours of inj ury, but always during the inflammatory phase of hea ling. when treHlmcnl with mcgahcrtz US has been shown to result in th e liberation of stimulatory growth factors from platelet s. mast cells, and macrophages wi th th e result that inflammation is accelerated, the proliferative and remodeling phases occur earlier, and the scar ti ssue is stronger th an th at of controls (Ex hibit 19-5). If trea tm ent is delayed beyond the infl ammatory phase, th e strength of the scar tissue is not afTected. 21 Duration . Duration is usually based empirically on the surface area to be treated. The area is divided into zones, eac h 1.5 times the area of th e ERA of the app licator, with I to 2 minutes being allowed for treating each zone. Some physical therapists recommend I min/em'. For th e sa ke o f th e th erapi st, th e maximum treatment time should be no longer than 15 minutes. I f th e wound is large, two sessions per day, one to each section of th e wo und, would be preferable. Three treatment s per week have been found to be effective. II/Iel/sil)'. In the interests or sare ty. the lowest I(SATA ) should be used. This is usua lly near the uppe r end of th e low range (see Table 19- 1). Note that 10 obtain a sign ifica nt increase in temperature a n I(SATA) of at least 0.5 W/cm' is req uired, but th at primarily nont hermal effects can be obta ined wi th lower SATA intensities, obtain ed by pu lsin g I(SATP) 0.5 W/cm' at, for exa mpl e. 2 milliseconds on, 8
Ethibit 19- 5 NOll lh ermal US PrOlocol: Acute Inflammation
Frequency
t or3 MHz
Pulsed du ty cycle
20"'t and :tccur:I\c method for ca lculating the fractal :.tg nalure of tcxture III rmlcror:tdiogmph .. of o .. tcollnhnus knec!>. Me(/ Illf 1991 ;2:241 251 \\,illial1l~ PL. et at Gml" ;'·,fllll/mlll'. 38th cd. Edinburgh, Scotland: Churchi ll -LI\ rng~tone: 1995:417. 00n7:lle7 RC WlIltl P. [)lgH:lllmage processing . In: Gonlale/. RC. Wimer XX. cd ... Dlgilul IIII1Ige Flllltia/l/£'lIw/l. Reading. ~ I A : Addison-We~Ic), 1987: 13 59. Bamber JC. Trt.,tam M. The physic!> of medical imaging. In : Webb S. cd. Oit/foIIOWl" (/I/"{/\()llIId Bmto!. Eng land : Adam Il ilgcrl: 1981t) 19 3~6. Forn.lge IJD. Deslmyes JL. Ultr::tsound of normal )okin. J Clill UImHO/tilt!. [1J!!6 :14:6 19. \\"Imlon RJ. et al Application of high frequency ultmsound to the obJeeu\e as.. e.... mcnl ofhc:lllIlg. \\ound ... In: PIYJl"eeC/illg\ offhe 211t! COI//"ert'IIl"l' 011 o4dl'tlll('('.1 ill H i ll/lid IItllHlgelllelll . London : MacmIllan Pre .. s; 1992:26 29. Young SR. et al. Ultrasound l111a£lOg: a non-iO\a'roduci Na me(s)
Acetic aCid Irrigation Alulllllllll11 S~IItS
Burow's so lution. Domcboro '
ChlorhcxldlllC giliconatc Ilcx:.Ichlorophcnc
pliisoHex
Ilypochiorilcs
Dakin's solution. chloraminc-T
OXldlL.ing agents
Il ydrogcl1 peroxide, 1.5%, 3% 13ctadinc™. Efodinc"
PO\ idonc-lOdint.: Quaternaryammonillill
lIibiclcns'. Exidinc' skin
Dermatologic lotion 0.10'0 Irrigant 0.25%. 60 mL Vosol 2% (Wallace Labs), 15 mL (multipack), 30 mL (multipack) Othcr manufacturers of acetic acid: Kcndall McGaw; Baxter Labs; Abbott Labs.
Zep hiran "
compound
ALUM INUM SALTS (BU ROW 'S SOLUT ION, DO~I E BORO ')
ACETI C AC II) IRRI GATION Description Description
A sterile solution of glacial acetic acid in water i~ lIsed for irrigation . The pll range IS between 2.9 and 3.3.
Aluminum salts have strong antibacterial effects. The general solutions containing aluminum salls arc I ~o aluminum chlorhydrate. 10% aluminum acetate, 300 "0 aluminum chloride hexahydrate. and 5% aluminum diaeetate.
Action
Action The exact mechanism ofactiol1 is unknown. Microorganisms wi ll not prolifcrntc at low pH , and all acids arc bacteriostatic at low concentrat ions and bacteriocidal at higher con centralions.
A mild astringent solution is madc wi th lets or powder.
DOl11cboro ~
tab-
Indications Indi c~ltio ll
Acetic ((cid is used to discourage bacterial infections in surgical wounds and to suppress growth by Pseudomonas ael'lIgillosa in extensive burns: it is also a component in several dermatologic preparations. Adverse ll.euc1io ns
Acetic acid C~1I1 cause irritation and inflammation. A soluti on of 0.25% acctic acid decreased bacterial sur vival by on ly 20% in cu ltured human fibroblasts. I The 0.25% acet ic acid solu ti on proved to be more damaging 10 fibrob lasts than to bacteria whenever a di fTerence in toxicity was observed. I
Relief of inflammatory condition. One percent aluminum ehlorhydntle, 10 0 0 aluminum acetale. and 30°'0 aluminum chloride hexahydrate comp lctely inhibit representative dermatophytcs. yeasts. and gram-positive and gram-negative bacteria in vitro. Twenty percent aluminum chlorhydrate. 10°'0 to 20% aluminum acetate. and 20%. to 30 0 0 aluminum chlorhydrate salt are the 1110st potent in vivo. The recommended concentrations (I :20 and I :40) of 5"0 aluminum diacetate (Burow's solution) exert no in vivo bacteriostatic or bactericidal efTects. PrCC~l ut ions
Mo~ t physicians use acetic acid irrigant for wet-to-dry dressings. Acetic acid irrigant of a 0 .25% solution is commonly used for bladder irrigation.
Do not lise plastic or other impervious material to prevent evaporation. For externa l use on ly. The cI1I.:ymc activity of topical collagenase may be inhibited by aluminum acetate solution because of the metal ion and low pit. Cleanse the wound thoroughly with normal saline before applying enzymes.
Packaging
Direct ion s
Most institutional pharmaci sts prepare as a I % surgica l dressing.
Thirty milliliters of U P solution is diluted to I or 2 L with water, or Domeboro ' tablets or powder may be dissolved
Dosage
Appelldix A
in 0.5 to I L ofw3ler. Domeboro ll tablets make a modified Burow's solution equ ivalent to 1:40.
Packaging Pharmacy prepares Burow's solution . DOl11eboro' 2.2-g packets of powder or tablets (Mil es, Inc .) Blue Boro' 2.2-g packets o f powder o r tablets (Herbert) Burow's solution (J.J. Balan, Inc.), 4 80- mL so luti o n (Paddock Labs), 480-mL sol uti o n, 3,840-mL so luti o n (Wisconsin Pha rl11 .), 480-I11L so luti o n, 3,840-mL so lution
CHLORH EX I DI NE C LUCONA TE (H I BI CLENS~, EX IDENE* SKI N)
Desc riptio n Chl orhexidine gi uconate was introduced in th e United States fro m Europe in 1977 as Hibicl e ns. which is 4 % chl orh ex idine glueonate with 4% isopropyl alcohol in a sudsing ba se. Hibitane is a chlorh ex idine tinct ion for use as a skin preparation. h is an anti septic and antimicrobial.
Action Bacteri ci dal on contac t. Antiseptic ac tivity and a persistent ant imicrob ial effec t with rapid bactericidal activity agai nst a wide range of microorganisms, including gral11positive bacteria and gram-nega ti ve bacteria as Pseudomonas aerllginosll.
Indications
463
Direct ions Thoroughly rinse wo und with steril e wa ter. App ly s uffic ie nt Hibic le ns and wash ge ntly. Rin se thoro ug hly. Pac kagin g Hibi c lens sk in c leanse r (Stuart Ph arm .) (4% chl o rh exid ine gluconate in a sudsing ba se), 120 mL Hibi stat germi cida l hand rin se (S tuart Pharm .) (0.5% chl orhexi dine in 70% iso propy l alcohol) , 120 mL Hibiclens anti septic antimicrobial skin (Stuart Phann.) (4% in sudsing base ), 120 I11L, 240 mL, Y, ga l, I ga l Ex idine s kin (yttri um ) (4% w ith 4 % isopropy l a lco ho l)
H EXAC HLO RO PH ENE (PHI SO H EX' )
Desc ription Hexachlorophene is a chlorinated phenolic compound.
Action Antibacterial cleanser. Its antibacterial act ion is unknown.
Ind ica tions Active pri marily against gram-posi tive bacteria. including staphy lococci. Pea k antibacterial e ffe ct o f hexac hl orophene is obtained only by repeated scrubs on successive days. It has very little effect on gram-negati ve bacteria or spore s.
Preca utions
Effective again st a wide variety of gram-positive and graI1lnegati ve bacteria, molds. yeasts and viruses. Sporicidal only at elevated temperature s. Rapid acting- th e reducti on of bac terial fl ora on the skin occurs immed iately. Repeated use produces further reducti ons. Safe 10 use on the skin . No signi ficant problems with irritation. allergy, or photosensitivity. No evidence of tox icity if absorbed, and does not appear to be absorbed due to th e protein-binding characteri sti c, which cau ses reten tion in the stratllm corneum. It does not lose its effecti veness in th e presence of whole blood.
Tends to leave a residual film on the skin that can persist for seve ral days. Protec ti ve film ca n be eas ily di srupted by alco ho l. It can be abso rbed throu gh the sk in . Once in th e blood stream, there is potential for toxicity to the central nervous syste m. Up to 3. 1% o f to pi ca ll y applied hexac hl oro ph ene co uld be absorbed thro ugh the skin. Hexachlorophene contamination with gram-negati ve bactcria, Klehs iella species. Pseudomonas aerllgillosa, Escherichia coli, and Calldida albicllm' is poss ible. Contraindicated for usc on burned or denuded skin as an occlusive dressing, wet pack, or loti on. or on any mucous membrane. Do not usc in deep wounds.
Precauti ons
Direction s
For external usc only. Avoid contact with the meninges. ot recommended for full -thickness wounds.
Clean area for 3 minutes with pHi so Hcx M and rin se thoro ug hly.
464
WOUND CARl
Packaging PHiso Hex' 3% (Winthrop-B reo n), 5-oz bon Ie, I pt , I ga l Sept i-Soft ' 0.25% (Ves tal), liquid, 240 mL Septi-Sol' 0.25% (Vestal), solution, 240 mL HYI'OC HLORIT ES (DAKI N'S SO L UTIO N, C HLORAM INE-T)
Description
Sodium hypochlorite has germicida l, deodorizing, and bleac hing properties. Henry D. Dakin, U.S. chemist, 18801952, developed this solution for cleansing wounds during World War I as a very dilute neutral solution (0.45% to 0.5%) of sodium hypochlorite and 0.04% boric acid.
Directions Most physicians order wounds packed with Dakin 's solution and gauze three or four times daily.
Ac tion The exact mechanism of action
Chloramine-T, an aq ueous hypoch lorite antiseptic agent. relards the development of collage n in hea ling skin defects and prolongs th e acute innamma tory response; therefore. hea ling is delayed . It is toxic to granu lation tissue, leading to completc and irreversible capi ll ary shutdown . Rcepithelialization at wound edges is dclayed in wounds treated with hypochlorite solutions. Sodium hypoch lorite solutions disso lve blood clots. delay clotting, and are irritating to the skin. II has been suggested that the use of hypoch lorites can cause endotoxi ns to be rcleased from gram-negative bac teria in chronic wounds such as pressure ulcers, which can initiate a clinical respon se varying from mild pyrexia to acute oliguric rcnal failurc .
by which free ch lorine
destroys microorganisms has not been establi shed. The postu lated mechanism is inhibit ion of some key enzymatic reacti ons w ithin the ce ll , protein dena turati on, and inactiva-
tion of nucleic acids.
Indicatio ns For prophylaxi s of epidermophytos is, diluted sodi um hypochlorite solution is sometimes employed as a foot bath. It is employed in full strength. as a freshly prepared solution, in the management of suppurating wo unds, often
by con-
Packagi ng
Most pharmacists prepare Dakin 5 solution as a 0.5% sodium hypoch lorite so lution. Even at thi s concentration, the soluti on is toxic to native cells. There is 110 safe concentration of Dakin's solution for use in open wounds. Dakin's solution is prepared as a topical solution cOlllaining 0. 15% to 0.5% of aOCL. The full- stre ngth solution contains 0 .5% NaOCL. To prepare th e 0.15% solution. it should be diluted 1:3. Dakin's solution (Century Pharm .). 5% ga llon solution Chl oramine-T (A.A. Spectrum ), 250 g, 1,000 g. 2.500 g
tinuous irrigation (Carrel technique). It is lIseful in the dissolving of necrotic ti ssue.
OXIDIZING AGE TS
Prec~lUtion s
Hydro ge n Pe roxid e Solution USP
Cellular damage occurs at concen trati ons of Dakin's soluti on formerly thought to be safe fo r use in open wounds (0.5%). Even at lowe r concentrat ions (0.25%), sig nifican t damage is seen in fibroblasts and e ndothelial cells' Significant damage occurs at morc dilute concentralions of 0 .00 I % and 0.000010/0. In experiments done by Roben Kozo l, c ultured fibroblasts and endothelial cells exposed to Dakin's solution (2.5 x 10 l or 2.5 x 10 I) for 30 minutes showed a marked increase in cell injury characterized by convoluted nuc lei, cytoplasmic vacllolation, dilated endoplasmic reti culum, and swo llen mitochondria. They also found Dakin's solution to have an inhibitory effect on random and stimulated migration of neutrophi ls, a functional re spon se rather than as a result of cellul ar dal11age.2
Contact with tissues releases molecu lar oxygen. and there is a bricfpcriod of an timicrobial ac tion. There is no penetration of tissues. It has been repofted that th c instillation of peroxide into wound cavi ti es under pressure can result in oxygcn passing into the blood Stream. causing a life-threatening embolus. \ Hydrogen peroxide has been documcnted to liberate oxygen th at can spread along fa scial planes. which causes swclling and crepi tation and is frequcntly misdiagnosed as invasion by gas-forming bacteria .1A It is toxic to exposed fibrobla sts unless it is diluted more than I: I 00.'
P{J(:kagillg A.A. Spectrum, 3% so lution in water, 500 mL. 4.000 !TIL J.J. Balan , J% so lution in water, 480 mL
Appendix A
Hydro us Benzoyl Peroxide USP Can be bactericidal (0 microorganisms. When applied as a lotion. it is also keratolytic. antiscborrheic. and an irritant. May produce contact dermatiti s. Its principal use is in the treatment of acne and seborrhea .
PotassiuJII Perrnan ga nate US P
Consists of purple crystals that di sso lve in water to give decp purple solutions. Tends to slain tissue and c lothing brown. A I: 10.000 dilution applied in inert surfaces kills many microorganisms in I hour. Il igher concentrations arc irritating to the tissues. lis principal use is in treatment of weeping ski n lesions with questionable justification. Packllgi"g
A.A. Spectrum. granules. 454 g lIumco Lab. Inc .. granules. 120 g. 420 g. 454 g. 2.270 g l'ovmONE-IODI E Descri ption
Yellow-brown acidic water-so luble solution made of the polymer polyvi nylpyrrolidone and iodine. creating a watersoluble agent that slowly releases free iodine. Action
Potent antiseptic with a broad spectrum of anrimicrobial activity, although its exact mechanism of action is unknown . Povidone-iodine is inactivated in the presence of blood and organic matter.
Indica lions
Pov idone-iodine kill s gram-positi ve and gram-negati ve bacteria, fungi. viruses. protozoa, and yeasts. Spore destruction is achic\'ed only with moist contact for more than 15 l11inutes. ~ A 10°0 solution of povidone-iodine (1% of available iodine) kills 85"" of cutaneous bacteria. Clinica ll y indicated for prevention and treatment of surface infections. as well as to degefm the skin prior to invasive procedures.
Precautions Stinging and burning of the tisslle is a common side effect. One percent povidone-iodinc is indiscriminatc in toxic
465
cfTcets at full strength. A dilution of I: 1.000 is identified where no fibroblast toxicit y occurs. whi le remaining bactericidal in in vi tro studies. l In vivo studies showed that povidone-iodine surgical scrub so lution significantly potentiated (P < 0.002) the development of wound infection when compared with the incidence of infection in wounds treated with 0.9% sa line sol ution.1I It is important to know that the Food and Drug Administration has not approved povido ne-iodine anti septic so lution or povidone-iodine surgica l scrub solution for use in wounds.1I For an antimicrobial agcnt to climinate bacterial contamination , it must reach the bactcria in an active form . Because of the insolubility of iodine in water and its rapid complex formation with tissue and body Ouids. its ability to reach and kill bactcria in a wound or tissue is highl y suspect." Adverse lloeactions A continuous irrigation with Betadinc'IM in a 72-ycar-old woman, postsurgical debridement ofa hip wound resultcd in death 10 hours latcr. Her scrum total iodine level at autopsy was 7,000 ~g1dL. while the normal va lue is 5 to 8 !lg/dL.' Povidone-iodine has been reported to causc acidosis in burn patients. Lasting systemic side etTects identi fied include cardiovascular toxicity, renal toxicit y, hepatoxicity, and neuropathy.s Povidonc-iodinc's toxicity directly interfcres with wound healing at the cellular level and places the patient at a greater risk for wound infection.Q Rodeheaver's studies showed that both aqueous iodine and povidone-iodine solutions significantly impair the wound's ability to fi ght infection ." In se parate studies it was found that povidonc-iodinc inhibits wound healing at the cellular leve l, and that the incidence and potential for infection arc greater than jf wounds are irrigated on ly with normal salinc." Rodehcaver found that cven th ough povidone-iodine solution significantly lowered contHininants in the wound, the wound was still heavily contam inated. Ilc al so found that povidonc-iodine surgical scrub did not reduce the leve l of bacteria in the wound. 6
Dosage
Topical : 0.5% to 10% to the skin Solution: 0.5% to I % to the skin
Packaging
Purdue Frederick. 10% solution. 8 07 Ge neric. 10% solution. 8 oz. 480-mL, 3.840-mL
466
WOUND CARE
QUATE I{NARY AMMON I UM COMPOUN D (ZE PH I RAN' )
Descripti on Be nzalkonium chloride (BAC) is a quate rnary ammonium compound co mmon ly known as Zephiran . It is a ca ti onic
surfactant. The quaternaries arc organically substituted ammonium compou nds in which the nitrogen mom has a va-
lence of 5. Ac ti on
The bactericidal acti on has been attributed to the inactivati on of energy-producing enzymes, denaturation of essential cell pro teins. and disruption of the ce1\ membrane.
I INDEX TO TOPICAL ANTIFUNGALS Ge neric Name Amp hotcricin B Ciclopirox olamine Clotri mazolc Econazole nitrate 1% l-I aJoprogin Ketoconazolc Miconazo le nitrate Nystatin Tolnaftate
I
Prod uct Na me(s) Fungil.onc' Loprox "" Lotrimin ' . Mycclcx ' Spcct370lc" lIalotcx· Nizoral ' Monistat·Dcrm Mica till' . MOlli s tat ~ Mycostalin ' . Nilstat ' Tinactill "
AM PH OTE lll CI N B (FUNG I ZONE* )
Description Indication Effective against some gram-positive and gram -negative
Yellow-orange. odorl ess: may stain ski n. A polyene an ti fungal for topical usc, produced by a stain of Streptomyces lIodoSIIS .
bacteria , some fungi, and protozoa. Many bacteria grow in
its presence. It is not effec ti ve against A1ycobacierilllll 1lIberculosis, Pseudomonas aerug;llosa , spores, and viruses.
Prccn utio ns It is inactivated by anionic compounds such as soaps and detergents. Any residual detergent on the skin will neutralizc thc anti septic efTecl. It is inact ivated by blood and othe r organ ic matter. There arc reports of contam inati on wi th Ps e lldomonas cepac ia, Ellterobacter cloacae, E agg/omeralls. and Serratia l11arcescens.
Act ion Am photericin B binds sterols in the cell membrane with an altera ti on in permeability that results in leakage of intracellular materials.
Indica ti ons Superfic ial Candida a/bieal/s, histoplasmosis, coccidiomycosis, and crytococcoc is. It has no significanl effect agains t gram-positive or gram-ncgat ivc bacteria or viruses.
Preca utions
Direct ions Rin se anionic detergents and soaps from the area first so that the ant ibacteri al activi ty of BAC will not be reduced. Minor wounds and lacera tions usc 1:750 tincture or spray. Deep, infected wounds use I :30,000 to I :20,000 aqueous sol ut io n. Wct drcssings use I :5,000 or less solution.
Packaging Germiein ' (CMC). 50% sol uti on, I pt, I gal Benz" (Cc ntury Pharm.), I :750 so lution, 60 mL, 120 mL Zep hira n' (Winth ro p-Breon) Aqueous solution 1:750,240 mL, I ga l Disinfectant concclllration 17%, 120 mL, I gal Tincture spray 1:750, 30 glga l, 80 glga l Tincture I :750, I ga l
Ineffective against dcrmatophytes. May stain sk in. Rash may develop. Lotion may have a drying effect on some skin .
Ve hi cle Cream : aqueous base contai ning titanium dioxide, thimerosal propylene glycol, cetyl alcohol, ceteareth-20, white petro lat um, methylparaben, propylparaben , sorbitol solution, glycerylmonos tea rate, polyethylenc glycol monostearate, simcthicone, and sorbi c acid. LOfioll: aq ueous base containing th imerosal, titan ium dioxide, guargull1, propylene g lyco l, cetyl alco hol, stearyl alcoho l. so rb itan mOllopalmitatc, polysorbate 20, g lyeery l monostearate , polyethylene glycol monostca ratc, simethicone, sorbic acid, sodium citra te, methylparaben, and propylparaben .
Appelldix A
467
Oill(lI/ell(: Plast ibase' (plasticized hydrocarbon gel). A polyethylene and mineral oi l gcl base wi th titanium dioxide.
Vehicle
Dosage
water US P. cocamide DEA, octyldodec.nol E minera l oil US P, stearyl alco hol NF. cetyl alcoho l NE polysorbate 60 NF, myristyl alcoho l NF. sorbitan monoste.rate NF. lac tic acid US P. and benzyl alcohol NF (1%) as preservative.
Lotion: wate r-m isc ibl e lotion base consist ing of purified
Apply two to four times a day. Apply li berally to candida I lesions. Duration of thera py depends on individual response to treatment. May require 2 to 4 weeks of th erapy.
I'ackaging Fungizonc' (Squibb Pharm .) 3% cream and ointment, 20 g 3% lotion. 30 mL ClCLOPIROX OLAMINE (LO PROX )
Cream: water-miscible vanishing cream base consistin g
of purified water USp. octyldodeeanol NF. mineral oil US P. stearyl alcohol NF, cetyl alcohol N~~ coc.mide DEA. polysorbate 60 NF. myristyl alcohol NF. sorbitan monostearate NF. lactic acid US P, and benzyl alcohol NF (1%) as prescrvativc. Packaging Loprox ' (Hoechst-Rousell Pharm .) I% cream. 15 g, 30 g, 90 g 1% lotion. 30 mL
Description CLOT RIMAZOLE (LOTRIMIN ", MYCELEX ' ) EfTect ive broad-spectrum hydroxpyrimidinone antifunga l agent Ihal inh ibits the growth of pathogenic dcmatophytcs. yeasts. and Malasseziajlll/Ilr.
Description
Actio n
Syntheti c im idazole agent that is an odorl ess. whi te crystalline and practically insoluble in water.
Inhibi ts the uptake of precursors of macromolecu lar synthesis.Acts by impairing transmembrane tran sport, thus pre-
Action
venting essential amino acids and electrolytes from entering the ccl l.
M echanism of action is unclear but probably involves damage to the ce ll wa ll , resulting in loss of intrace llular elec trolytes, similar to that of the polyenc an tibactcria ls.
Indications Ti nea pedis. cruris. corporis due to Trichophyton rubrllUl, T melllagrophyfes. Epidermophytoll 110('cOSIII11, and Microsporum ca"is. Cutaneous candidiasis (moniliasis) caused by Camlitia albiclms and pityriasis (tinea) versicolor, due to
Microsporum clIllis.
Advo rse Roact ions Burning. sti nging. pruritis, and eryth ema are reported side effects. Avoid eye contact.
Indications Indi cated for superficial fungal in fectio ns, Ca lldida
albiclIl1S infections. yeasts. and A1alasse=ia furfur. Inh ibits growth of most dermatophyte specie s as we ll as of some gram-positive bacteria. In high concentra tion clotrimazo le is active against Trichomonas species. Also aClive against tinea pedis. cruris. corporis caused by Trichophytoll rllhrlllll. T melllagrophyles. EpidermophYlO1l 110(,(,OSIII11, and IH i-
crosporul11 c{l IIis . Adverse Reaction s
Dosago Gently massage into afTcclCd area and surrounding skin .
Usc twice-daily application (morning and evening). Treatment should last from 2 to 4 weeks. Avoid use of occl usive wrappings or dressings. There is only minimal absorp tion
(1.3%) when applied topically to intact or broken sk in.
Occasiona l eryth ema at site of applicati on has been rcport ed along with urticaria, burning. edcma. pee ling. blisterin g, and Slingi ng. Do not use in first trimester of pregnancy. Nore: Lotrisonc is not thc same as Lotrimin . Lotrisone contains a steroid.
Ve hicle
Adve rse Reactions
Cream: vanishing cream base of sorbitan monostearate, po lysorbate 60, cetyl ester wax. cetyl alcohol, 2-octy ldodccanol. purified water. and, as preserva tive, benzyl alcohol (1%). Lotio,,: cmulsion composed of sorbitan monostearate, polyso rbate 60, cetyl ester wax, cetyl alcoho l, 2-octyldodecanol, purificd water, benzyl alcohol (I %), and, as preservati vc. sodium phosphate dibasic sod ium biphosphate to adjust pH . SO/lilian: nonaqueous vehic le of polyethylene glycol 400.
Three percent of patients complain of burning, stinging, pruritus, and erythema after 3 to 4 days of treatment. Avoid eye contact.
Ve hicle Cream : water-miscible base consisting orpegoxol F stearate, peglicol 5 oleate, minera l oil, benzoic acid, butylatcd hydroxyanisolc. and purified water.
Dosage
Dosage
Twice daily until eruption clears. Gently rub into the affected areas morning and evening. Clinical improvement should be evident in 1 week. Continue treatment for 4 weeks. Reevaluate after 4 weeks if no improvement. Use the solution four times daily.
Twice daily (morn ing and evening) for 2 or more weeks. There is only minima l absorption when applied topically to intact or broken sk in . Occ lusive dressings slightly increase the amount of absorpti on.
Packagin g Lotrimin ' (Shering Corp .) I % c ream. 15-g tube. 30-g tube, 45-g tubc. 90-g tube 1% solution. 10 mL, 30 mL Mycelex ' (Milex, Inc.) I % c ream. 15-g tube, 30-g tube, 90-g tube
Packaging Spectazole ' (Ortho Pharm ., Dermatological Divisio n). 1% cream. 15 g, 30 g. 85 g
I-I A LOPROG I N (IMLOTEX )
Description ECONAZOLE NITRATE 1% (S PECT AZO L E$)
Synthetic chlorinated ildopropynyl tri chlorophenyl ether.
I)cscripti o n Ac ti on Syn thetic imidazole. The exact mechanism of action is unknown . Ac ti on
Interferes with the biosynthesis of ergosterol (chemical needed by fungi to maintain cell wall integrity), result ing in the disorganization of the funga l plasma cell membrane. Indica ti ons For the topi ca l treatment of tinea pedis. tinea cruris, tinea corporis (ringworm of the body). cutaneous candidias is (caused by Calldida a/hicalls), and pity riasis (tinea) ve rsico lor; efTective against A1icrosporlllll gypsellm . EfTective agai nst TrichophYIOI1 rlliJrulfI. T memagroplzYles. T IOIlSl/I'(IIIS. A4icrosporuIII c(lllis. A1 audouillii. and Epidermophyton jlOCCOSIII1l.
Ind icati ons Topical treatm ent of dermatophyte infections and tinea vcsicolor caused by Ma/asse=ia!ur!lIr. Active in vitro against staphylococci, streptococci, and Candida a/hieans. Indicated ror tinea pedi s. tinea cruris, tinea corpori s, and tinea Illanuum caused by Triehophyloll EpidermophylOll jloccoslim.
Ad,'e rsc Reactions Local irritations. burning sensa tion, pruritus, erythema, scaling, folluculitis, vesicle formation are reported.
Appelldix A
469
Ve hicle
Dosage
Cream: waler-dispersible base composed ofpolyelhylene glycol 400, polyelhylcne glycol 4,000. dielhyl sebacalc, and polyvinylpyrrol idonc. SO/lIlioll: 75% alcoho l and dielhy l sebacale.
Apply 2% cream over affected area and the irnmediate surrounding area once daily for 2 weeks.
1J0sage Twice daily gcnl ly massagc Ihe I % cream liberally onlo Ihe affocled arca for 2 10 3 wocks' duralion. Inlerdigilallcsions may require 4 weeks.
Packa gin g Nizoral ~
(Janssen Pharm.), 2% cream, 15-g tube. 30-g 11Ibe, 60-g Illbe
MI CONAZO L E NITRATE (M O NI STAT-IJERM"', M ICA Tl N~, M O NI ST AT"') Description
Pac kaging
Synthetic imidazole antifungal.
Halolex ' (WcSlwood Pharm ., Inc.) I % cream, 15 g, 30 g I % solution, 10 !TIL K ETOCONAZOLE (N I ZORA L~) Description Water-soluble imidazole derivative. Acti on
Affects fungi by mechanisms involving increased membrane permeabilily, inhibilion ofuplakc ofpreclIrsors of RNA
Acti on
Deslr0Ys fllngi presllmably by inhibiling cell wall synlhesis. Indicati ons EfTective against most dermatophyte species and against cutaneous candidiasis caused by Calldie/a albicalls. Effective against tinea pedis, cruris, and corporis caused by Trichophytol/ rubr""" T mellwgrophYfes, and Epidermophylon jIOCCOSlIl1I, the yeast like fungus . Effective against Ma/assezia /111'/111', the organism responsible for tinea versicolor.
and D A. and synthesis of oxidative and perioxidativc en-
zymes.
Adverse Reac ti ons
Indications High ly effective in chronic dermatophyte infections, including those resistant to Clilldida species. C,yplococClis lle%rmclIIs. Coccidioides immiris. Histoplasma capsula/um , Blastomyces dermolilidis, and pa thogenic dermatophytes. EfTcctive for treatment of Illllcocutaneous candidiasis. Used in Ihe treatmcnt of tinea corporis. tinea cruris, and tinea versicolor.
May cause irritation, burning, erythema, macerat ion, and allergic contact dermatitis. Avoid eye contact.
Ve hicle Cream alld 10lioll: water-miscible base consisting of pegoxol 7 Slcaratc, pcglicol 5 oleare, mineral oil, benzoic acid, and blllyialed hydroxyanisole, and purified wa ler.
Adverse Reactions Stinging, irritation, and pruritus arc reportcd.
Vc hicle
Propylene glycol, Slcaryl and cClyl alcoho ls, so rbilan monostearate, polysorbate 60, isopropyl myrislate, sodium sui file anhydrous, polysorbale 80, and purified waler.
Dosage Apply twice daily until eruption clears. Cream should be genlly rllbbed in Ihorollgh ly (10 avoid macera l io n) on Ihe alTeeled areas and surrounding skin morning and evening. Clinical improvemenl should be evidcl1I (relicf of prllrilis) within I week. Continue treatment for 2 to 4 weeks.
470
W OUND CARL
TOLNM- rATE
Packagin g Moni stat- Dcrm ' (O rlho Defm . Div.), 2% c rea m, 15 g. 28 g, 85 g Micatin ' (O rth o), 2% c rea m, 15 g, 30 g Monistat-7 ' (O rth o Pha rm ), lotion, crea m, 45 gltube with applica tor NYSTA TI N (I\1YCOSTATlN~.
N ILSTA ~)
Oescrilltion Polye ne antimi c robia l de ri ved from a species of the ord er Actinomyceta les. Streptomyces II olirsei .
Action
Binds (0 sterols in fungal cellmcmbrancs, causing a change in the pe rm ea bili ty of cell membranes and lea kage o f cell co mponents.
(TiNACT I N ~)
Desc ription
Fung istati c and fun gicidal age nt. Action Mec hanism o f ac ti oll is unknown. Indica tion s
Effecti ve aga inst Trichophy ton ruhrllUl. T mel1lagmphyles. T IOIlSlIrtl IlS, and va ri ous MicmsporliUl and Aspergillu.\· species. Effective aga inst intradermal demmtophytic infec tions. Commonl y used to trea t tinea pedi a (a thl ete's foot), tinea cruri s Uoc k itch). tinea co rporis (ringwo rm o f the body). and tinea manuul11 when ca used by the above fun gal pat hogens. It is inefTecti ve against Calldida albicalls, C'TPtocoCClis neojol'malls. and Aspergillus jil1l1igallis. and agai nst bacteri a. protozoa, and viruses.
Indications
Cand ida l infecti ons of skin and mucous membranes. Adverse Reac ti ons None kn own.
Vehicle Ni lstat" 's ve hic le is composed o f lig ht minera l oi l a nd Plasti base ' 50 W. Dosngc
Apply tw ice daily and gently massage into affected arca. I>ackaging O intme nt and crea m. 100,000 U/g Mycos tatin ' (Sq uibb ). 15 g Ni lsta t ' (Lederi e). 15 g Gene ri c. 15 g Ni lsta tin ( Lcdcrlc ). 0. 1% tri a mc ino lone ace tonide c ream and ointment Myeo log (Sq uibb ). 15 g Gene ri c. 15 g
Adverse llo cac tion s
Essent ially none. although local irrit ati on and burnin g have been repon ed when applied 10 exco ri ated skin or lesions ca used by l11ultiple pathoge ns. Avoid eye co nt ac t. Dosage Dry the alTccted area first. then apply a small amount and ge ntl y massage into th e area until th e medi cati on disa ppea rs. Appl y twice daily for seve ral weeks (may be req uired ove r 6 wee ks with long-standin g in fec ti ons), Clini ca l improve men t should be noted in 2 or J days. Only sma ll amount s of th e crea m are necessary for therapy. J>ackagi ng Tinactin' (S he rrin g- Plough Healthca re Products) I% cream. 15-g tube I% powder. 45-g co nt ainer I % powder, 120-g aeroso l co nt ai ner 1% solution. 10- mL container Ge neric I% crea m. 15-g tube I% powder, 45-g co ntainer
Appendix A
INDEX TO TOPICAL ANTIBACTERIALS Generic Na me
Bacitracin Gentamicin sulfate Metronida zole Mupirocin Neomyc in sulfate
Nitrofurazone Polymyxin B Sil ver sulfadia 7inc Zi nc bacitracin
I'rod ucl Na l11 c(s) Baciguem
Ge ntam icin. Gon Ilf '1lher sulfadlMlIle, flO\ idone-Iolhne and physioll~IC .. aline III thc Ire.Hmenl uf chmllic pressure ulcer.. ,/ ,4111 G('r Soc 19XL29:2J2 2J5
10 11
4
Oberg MS. IUHbcy 11 Do not put hydrogen peroxide or povidone 1Wllle Intll \\()untb.! IJJ)(
5.
19K7:141:2728.
SIr.Khan ( Anllblotlc prophyla,is in "clean" surgical procedures Hill-h/ ,I S/lrg 1972;6:273 2~().
Thomas ( '\urslllg akr1. \\-llund healing halted \\ Ilh the U'IC or pO\idonc-iodlllc , O~/mJJ\' lIimllel 1/1111 Spnng 19XK:3() 33
10
I[erher! L. Subculancou ... gas frolll hydrogen perox-
Ide adll1l1H'>trallon under prcs,;urc. lm
Kodehc,l\er G, et al !3:II.:1em:ldal :II::II"'U)" and 111"'11)' or lothnecontallling solutions III "ounds ' r"'l SlIrg 19R2; 117; IXI IX5
Chl'lIIlI
(I/JI"('J/\
IQX-l ,:!5:422.
'rdl
/)t'I"lIl
f)t'nll
~tlck
A p PEN DI X
B
A Quick Reference Guide to Wound Care Product Categories Diane Krasner
This listing of wound care products highlights the impor-
Clean sers
tance of generic product categories. Under each generic product category. up to four product examples arc given (a mix of old and new produCIS), 10 help familiarize Ihe reader wilh each category.
0
endorsement of any product or manufac-
turer is intended. Within each category, products must be individually evaluated. All products within a category do not necessari ly perform equally. Combination products may be listed in morc than one category. Refer to rnanufacturers' instructions for specifics regarding product usage.
Absorp tive A nt im ic robia l Dressi ngs Product Nfam!{tu:llIrer
Isosorb ' lodonex"t
Heahhpoinl Medical I-Ieahhpoinl Medica l
Prodlicl
M a /lli/ac III r eI'
a. Saline b. Hydrogen Peroxide c. Skin Cleansers Peri-Wash ' Royl-DermTM Skin Cleanser Triple Care™ d. Wound Cleansers Constant-Clens™ Curasol™ Dennagran · Spray RadiaCare™ Klenz
Muhiple Muhiple
Algina te Orcss in gs
Dermacca™ Alginate Restore Calcicare Seasorb™ Sorbsan™ Biosy nt het ic Dressi ngs ProdllCl
Biobranell' Silon ·
Sherwood - Davis & Geck Heahhpoinl Medical Derma Sciences Carrington Laboratories
Co llage n Dressings Producl
Pmdllcl
Coloplasl Sween Acme Uniled Memor Urology milh & Nephew Uniled
ChroniCure™ Fibracol ' (Collagen! A Iginale) MedifiIT" kinTempTM
Mal/lllaClllrer Sherwood - Davis & Geck I-Iollisler Coloplast Sween Dow Hickam Pharmaceutica ls
MalllifaClurer Derma Sciences Johnson & Johnson Medica l Bio ore BioCore
Manu/aclurer Dow Hickam Phannaceutical s BioMcd Sciences
NOIe: A11 product names should be considered copyri ghted or trademarked regard less of the absence of ~1n ® or nl. SOllrce: CI 1997. Diane Krasner.
4 77
478
WOU", CARL
Ga uze Dress in gs (also see C omposite Dressings)
Co mposit e Dress in gs PIVduCf
Alldress ' CombiDERM'" ACDT"
CovaDcrm™/ CovaDcrm rM Plus Odor-Absorbcnt Drcssing
A10llujaclurer SCA Molnlycke ConvaTec DeRoyal Wound Care Hollister
Co nta c t Laye rs PlTJdu{'/
"'aml/acllIre,.
Mcpitel ' CA Molnlycke Pro fore Smith & ephew United Tegapore 3M Health Care VCIltCX™ Vented Dressing Kendall Healthcare Products Enzy m es! Deb ridin gAge nl s Pmtiuc( A-lamt/aclUrer AcclI7yme1M Healthpoint Medical Elase ' (Fibrinolysin! Fujisawa USA desox yri bon uclease) Panifil ' Ointment Rystan (Papain) Santyl ' (Collagenase) Knoll Laboratories Foam Dress in gs
Prodllct Allcvyn '
Cutinma ' cavity! foam/thin Flcxzan™ Lyofoam '!Lyofoam ' T
Alaml/ac1l1re,. Smith & ephew United Beiersdort-10bst
Dow Hickam Pharmaceuticals Acme United
Prot/IICf
A1ol1l1!aclllrer
a. Woven b. Non-woven EXC ILON ' ATURALON'" NU GAUZE General Usc Sponges SOF-WICK'" c, Packing/Packing Strips (Non-impregnated) Kerlix Il/Kerlix k Lite NU-BREDE'" Packing Strips (Plain) TENDERSORB ' d. ConforminglWrapping
Multiple
Conform ~
Elastomull ' Kerlix l/Kerlix · Lite KLING'" c. Debriding U-BREDE'" TENDERSORB ' f. Impregnated Gauze
Dressings DermagranT\l Wet Dressing (Saline) GentelP">' Hydrogel Dressing GRx Saline Wet Dressing Vaselinc ~
Kcndall Healthcare Products Kendall Healthcare Products 10hnson & 10hnson Medical 10hnson & 10hnson Medical
Kendall Healthcare Products 10hnson & 10hnson Medical Multiple Kendall Healthcare Products Kendall ll ealthcare Products Beiersdorf-10bst Kendall ll e.lthcare Products 10hnson & 10hnson Medical 10hnson & 10hnson Medical Kendall Healthc.rc Products
Derma Sciences
MKM Healthcare Geritrcx Corporation
Kendall ll e.lthc.re Products
Petrol arum
g. Non-adherent Gauze
Primapore ' Release ' Telf. ' h. Specialty Absorptive
Smith & Nephew United 10hnson & 10hnson Medical Kendall i lealthcare Products
Gauze
EXU-DRY ' SURGIPAD Combine Dressings TE DERSORB ' Wet-Pruf Abdominal Pad
Exu-Dry Wound Care Products 10hnson & 10hnson Medic.1
Kendall He.lthcarc Products
Appelldix B
Hyd rocolloid J)ressi ngs Pruduct Repl iCare" M Restore"M/CX/ Extra Thin
SignaDress™ Tegasorb™
Nfanlljacflirer
Smi th & Nephew Un ited Hol li ster
ConvaTec 3M HealLh Care
Hyd rogel Dressings (. Iso see Impregnated Cauze Dress ings) Product Mallujacrurer
SlJm CarraSorb™ M
Carrington Laboratories
EI.sto-GeI™
So uthwest Technologies MKM 1-lea lLhcare Bard Medic.1
Gentcll™ Vig il on ~
AmorvluJIIs
Carrington Gel Wound DrcssingTM
Carrington Laboratories
DuoDERM ' Hyd roaetive Ge l (Hydrogel! Hydrocolloid) Hypergel ' IntraSite' Gel
ConvaTec
SCA Miilnlycke Smith & Nephew Un ited
Leg Ulcer Wraps Co mpression Ba nda ges/Wraps Product Manufacturer Coban ' 3M HealLh Care Dome Paste ' Miles Elastoplas t' Beiersdorf-Jobst SeLOpress' Acme United Multilayered Systems PlVducf
NfallufaCfllrer
Circulon™ ystem Proforc -
ConvaTec Smith & Nephew Uni ted Gle nwood
Unna-Pak Skin Sea lants ProdllCI
MalllljacfUrer
Prcppics™ Skin PrcpHl
Kendall Healthcare Products Smith & Nephew United Mentor Urology 3M Health Ca re
Skin Shield' 3M No Sting Skin
Protcctant
479
Transparent Film Dressings Pmdllci Mallujacrurer BIOCLU IVEn, Joh nson & Johnso n Med ical
Flexfilm™
Dow Hickman Phannaccuticals
OpSite ' lFlexifix/ Flexigrid TegadermT"/ H P
Smith & Nephew United 3M HealLh Ca re
\Vound Fillers: l:ta stes, Powders, Beads, etc. Prodllct Manufacturer Bard ' Absorpti on Bard Medical
Dressing DuoDERM ' Paste OsmoCyte™ Pillow
Wound Dressing Triad™
COllvaTcc ProCytc
Coloplast Sween
Wound Pou ches Afanlijaclllrer Product Wound Drainage Collector 1101 lister Wound ManagcrTM ConvaTec Mu lliple AdulL and Pediatric Sized OSLOmy Pouc hes
Not Otherwise C lassified (NOC) Product Categories Adhesives Adhesive Removers Adhesive S kin Closures Adhesive Tapes Antibiotics Antimicrobials Antiseptics Bandages Creams Dressing Cove rs Growth Factors Healthcarc Perso nne l Handrin ses Lubricating/Stimulating Sprays Moisture Barrier Ointlllcnts/C rea nlS/S kin Protect'lnl Pastes Moisturizers Ointment s Perinea l Cleansing foams Sterile Fields Surgical Scrubs Surgical Tapes
480
W OUND CAKL
WOUND AN D SK IN CA RE PROD UCT MANUFACTUREI{S 3M Hea lth Cllre 3M Center, Bldg. 275-4E-0 1 SI. Paul. Minnesota 55 144-1000 (6 12) 736-1723 or (800) 228-3957 Fax (612) 737-7678
DeRoyal Wound Ca re, A Oil'. of DeRoyallndustries, Inc. 200 DeBusk Lane Powell , Tennessee 37849 (423) 938-7828 or (800) 25 1-9864 Fax (423) 938-6655
Acme United Corporatio n
75 Kings Highway CutotT Fairfield Connecticut 06430 800-TEL-ACM E. (800) 835-2263 Fax (203) 576-0007 Bard MediclIl Di v., C. I{. Ba rd, Inc. 8 195 Industrial Bl vd. Covington. Georgia 30209 (770) 784-6100 or (800) 526-4455 Fax (770) 784-62 18 Beiersdorf-Jobst, Inc, 5825 Carnegie Bl vd. Charlotte, No rth Carolina 28209 (704) 554-9933 or (800) 876-3664 Fax (704) 55 1-858 1 BioCorc, In c.
1605 SW 41 st Street Topeka, Kansas 66609 (913) 267-4 800 or (800) 577-480 1 Fax (913) 267- 1900 Ca rrin gton Laboratories, Inc.
2001 Walnut Hill Lane Irving. Texas 75038 (214) 5 18- 1300 or (800) 358-5213 Fax (2 14) 5 18- 1020 Colorplast Sween C orp. 1955 West Oak Circle Mari etta, Georgia 30062-2249 (770) 426-6362 or (800) 533 -0464 Fax (770) 422-4324 Co nvaTcc
Customer Service. P.O. 5250 Princeton, New Jersey 08543-5250 (800) 325-8005 Fax (800) 523-2965 Derma Sc ie nces, In c.
12 1 West Grace Street Old Forge. Pennsy lva nia 185 18 (717) 457-1232 or (800) 825-4325 Fax (7 17) 457- 1793
Dow Hickam Pharm aceuticals, Inc. 10410 Corporate Drive Sugar LaJ1(~ Texas 77487 (713) 240- 1000 or (800) 231 -3052 Fax (713) 240-0003 EXU- DRY Wound Care Products, Inc. 3830 Boston Road Bronx , New York 10475 (718) 231-5200 or (800) 544-4325 Fax (718) 88 1-49 17 Fujisawa USA, Inc. Three Parkway Nort h Deerfield, Illinois 60015-2548 (847) 317-8800 or (800) 888-7704 Fax (847) 317-7296 G lenwood, In c.
82 North Summit Street Tenany, New Jersey 07670 (20 I) 569-0050 or (800) 542-0772 Fax (20 1) 567-4443 Hea lthpoint Med ical 2400 Handley-Ederville Road Fort Worth, Texas 76118 (817) 595-0394 or (800) 441 -8227 Fax (817) 595-092 1 Hollister, Inc. 2000 Holli ster Drive Libertyville, Illinois 60048 (847) 680- 1000 or (800) 323-4060 Fax (847) 918-3994 Johnson & Johnson Medical, Inc. 2500 Arbrook Bl vd. Arlington, Texas 760 14 (8 17) 465-3 14 1 or (800) 255-2500 Fax (817) 784-5459
Appendix 8
Kendall Healthcare Products Co. 15 Hampshire Slreet Mansrield, Massachusetts 02048 (508) 261-8000 or (800) 346-7 197 Fax (508) 26 1-8271 Knoll Laboratorics,A Oiv. of Knoll Pharmaceutical Co. 3000 Continenta l Drive - North Mount Olive. New Jersey 07828-1234 (20 I) 426-5655 or (800) 3-SANTYL Fax (20 I) 426-5660 Mentor Urology 5427 Hollister Avenue Santa Barbara. Calirorn ia 93 111 (805) 681-6000 or (800) 328-3863 Fax (805) 68 1-6 166
Rysta n Co., Inc. 47 Center Avenue
Little Falls, New Jersey 07424 (20 1) 256-3737 Fax (20 I) 256-4083 SCA Miilnlycke 500 Baldwin Tower Eddystone, Pennsylvania 19022 (610) 499-3700 or (800) 992-9939 Fax (6 10) 499-3396 Sherwood - Davis & Geck 19 15 Olive Street SI. Louis, Missouri 63103 (314) 241-5700 or (800) 325-7472 Fax (314) 24 1-3 127 Smith & Nephew United, Inc.
MKM I-Iealthcare Corporat ion 1957 Pioneer Road Bldg. H Huntindon Valley, Pennsylva nia 19006 (2 15) 957-1400 or (800) 462-3395 Fax (800) 888-1508
I 1775 Starkey Road, P.O. Box 1970 Largo, Florida 34649- 1970 (813) 392- 126 1 or (800) 876-1261 Fax (813) 399-3498
ProCyte Corporation 12040 115th Aven ue, NE, Suite 2 10 Kirkland, Washington 98034 (206) 820-4548 or (800) 848-3668 Fax (206) 820-4111
Southwest Tech nologies, Inc. 1746 Levee Road North Kansas City, Missouri 64 11 6 (8 16) 22 1-2442 or (800) 247-9951 Fax (8 16) 221-3995
481
Index
\ Ab"cc~s. palpation. 73 Absorpli\c antimicrobial dressing. 477 Accllt.: 3CII1 4(,2
Acute )urgical wound management, 21 Q 232 age. 221 222 en ..c \Iud)', 227. 231 concurrent conditIOns. 222 dcr1l1cd 219 document,lIlOn, 22H drc .... lIlg. 22()
factOr.. nrre!';lIng heallOg. 219 224 heahng Iypes. 21urfacc, 294 Algmate drcsslIlg. 206 207.477 AlglIl:ltc h)'dmcollOid combmation. 208 Alternallng current. 360 \!ununum \alt\. 462 463 Amerie;m PhYSIcal Thcmpy Association, '!(Xi Ampcmge. 357 35~ Amphotcricln 0.466 467 AmplltwJc. 357 Ankle-braehi'll mdc;(. 304 procedure. 129. 130. 13 I. ! J2
\Ignificancc of values. 129. 131 AnlibactcnaL 47 1-476 defined 171 exudate. 171 172 infection. 171 172 Antibiotic. 212 defined 171 Antifungal. 466 470 defined 171 exudate. 173 lIlfectlon. 173 Antimicrobial definelIiolllng. 273 274 Cardiovascular system. 9 phYSIcal assessment, 9 Carrier frequency. 406 Ccllulills. infection. 163 Cerebro\ascular :Iccidcnl. 12 CertIficatIOn c~amlllatlOn. XXI Charcot arthropathy case ~lUdy. 331
484
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'I)
CARl
ncuropatluc 1001. DO
:n I
('Iud cnrnplallli. 5 6, 125 Chl(lrlu:'odmc gluconuITu.:IClh':). clcclnt.:al .. 11I11ulall()ll.
:un
3M2
pulsed ... hllft wa\c diathermy. chM:lcteri\tic .. comp,tr, .. , -tfl, 41 Chronil.: \\ounr..I hCOI11T1g. -to 45. M), 67 ah,cnl ph ....c. M. (,7 .y ... lern. 274 recumbent po\111U1l ilctlvilie .. of dail)· Ii\ IIlg e,aminatlon. 292 ;ur·IlUldl/ed .. urface. 29 .. cardiopulmonary ga .. trllillte ... tlnal .. y... tems. 291
cOed .. of lying dO\\,;n on prc... .. ure ulcer furmatlOn. 2110 29\ elJuiprncl1l selectIOn. 2'n 211.. e)("11111111110n ,lIld c\laluallun. 291 29) IIllegumelltary sy ... tcm e-.;allunatlon. 2112 2111 mallre ..... replacement. 2111 motur I\II1Cllon and ergUlllllllll':" el(amll1allon. 292 Ilonptmercd dynamiC maltfC ..... replacemenl. 29.. overlay, :.N3 ]1U"ltlOl1l11g supplie ... 21)" 298 pO\\'Cfed dynamic mallrcs," replacement. 293 2t }" mnge uf mouon cumUlation. 192 r.ttlonalc fur IOtencflllon. 21)() 291 relle\ IIItcgrit) el(ammallon. 29 I 21)2 ,cn ..ury eXallllnatu. lI1. 291
~tallC
mall res .. replacement. 291
Slttlllg
acce"orles. 2M72M9 actl\IU" of daily !i\lIIg e~amlllation. 279 back support. 286 2M7. 2MM ergonomics el(3mlOation. 27X 279 footre'l. 2M I funcllonal diagno~tie procclI!>. 275 276 IIItcgul1lentar)' el(ammallon. 280 Interface pres!ourc el(umlnation. 280 Intcf\eniion using prinCiple .. of scaling. 2XO 2X9
JOInl integrity el(amin3tiOIl. 271) 2MO motor function. 27M 271) pchH': ,"ontrol. 2M I ro ... turc el(anllnation and e\aluallon. 17X 1XO
runge of mOllon. 279 2MO rationale for illlen,cllllOll. 276 2KI) rene)( inlegnly C:ot311l1lHltioll. 278 ,e,1t cu .. hion. 284 286. 2R7 ,e,1t depth. 2M I ..elf·eare trealment guidelines. 289 \en ... ur) Cl(anunatlon. 278 .. hcar and friction cl(3nunation. 279 ,kelclal deformnies Cl(a1lU113110n. 2NO !>.upplicr'\. 289 thlg.h conlrol. 281 whec1chiur me3!ouremcnl. 282 whcclchutr... or mobility buses. 282 284 ,a ...cular "y"lem. 273 274 Thermal ..en ..atlon. 64 Thrombo ....... electrical sllmulatlon. ~M 165 TI ..sue blop"';,-. 1M. 165 Toen.ul. 66 Tolnaliate. "7() Topical anllbacteri:11. 471 476 Toplc.. l antifungal. 466-47() Toplc;tI 'II1theptic ... 62-466 Topical dr" ... ing el(ud'lIe. In 174 Infection. 173 17.. Topical \ 11,1111111 A. IIIllammatlon ...4 Tot'll·contact ankle-foot onho .. ls. neuropathic fool. BM Total-coll ... ct castillg. ncutop.llhie loot. )); ))6 Tnll1 ..cut;lIleou .. ol(ygen measurement. I J2 133 Tr.. n.. parent film drcsC~ ... mcnt, I J 14 ilcule "ul):lcal \\llund manilgemenl.
.224 22h
"~4
lixu,cd a .....e ...... l1\enl Ii.lr \\ound .... 27 ncuropiithlC foot • .\24 Wound a ......e ..~mcnl form. 96, 9~ 91) \\('Iund traclIIg 95. 'n \\ound bed 11 ..... ue ah",CIlCC of mnammatl(lIl. 70. 71 cplthdwit ...atlon, ,lcuIC. 77 7X \\llund car..:, end· ... tagc i1lne:'> .... 10 Wound cla~ .. lflealion ... yMcm. 51 54, 5~ S,·t· 111\0 SpeCific Iype acutc .. urglcal wound m,lIlugcment. 221 by thickne ..... of ... }..III 1m, .... 53. 54. 55 \\-ound c!calhlng. 212 Wound cOnlrat:llOn. lT1)ollbrobla ... t. 37 38 \\ound culture. 164 1M Wound deplh. Su ...... man Wound Healing Tool. 107 \\. 8.\, X.. dC(llh.94 doc}.. method ~'" 95 grC'ale~1 lenglh hy grealc ... t \\ Idth method XX. K9 IIncar ... I.. C. X8 ~9 method. K9 ",up(lhe ... XI) locatl()Il, ~7, XX reliability, K7 ...elf·care tCilching guideline .... 101 1112 !-Jurroundll1g ... 1..111 erythemll. 95 clock method. ()~ tunneling. 9() 93 undcrmllllng. 9() 93 Wound outcome. 21 Wound pholog raph~, 99 I fll) Wound pouch. 479 Wound (lroduct. manur.. tiurer" .. 80 4X I Wound prognO~I"'. O(lllon~. I K 19 Wound 'pace hYPo\l ... IIlllanun.ulon. 3.t Wound Sucl.. Tunneler. ~ I Wound Suck \\