PATOFISIOLOGI & PENATALAKSANAAN LUKA TEKAN SECARA MEDIK

Dr.R.Suhartono SpB(K)VVascular dan Endovascular Surgeon

Dalam Seminar KeperawatanPerspektif Medik dan Tradisional Dalam Penatalaksanaan Luka TekanSabtu, 20 Februari 2010 *

OutlineLatar belakangPatofisiologiPencegahanPenatalaksanaan*

ANATOMI KULIT NORMAL*

Apa itu pressure ulcer?Definisi :an area of localised damage to the skin and underlying tissue caused by pressure, shear, friction and/or a combination of theseEuropean Pressure Ulcer Advisory Panel EPUAP (2003) Nama lain bed sores, pressure damage, pressure injuries dan decubitus ulcers.*

Skema konseptual untuk faktor faktor etiologi terjadinya pressure ulcer Mobility Activity Sensory PerceptionExtrinsic FactorsPressure SoreDevelopmentTissue ToleranceIntensity & Duration of PressureMoistureFriction & ShearNutritionAgingLow arteriolar pressureLow oxygen tensionIntrinsic Factors*

Nekrosis kulit terlokalisirDisebabkan olehKompressi Pada Mikrosirkulasi kulit Ref. Kosiak, M., Etiology and pathology of ischemic ulcersJ Arch Phys Med Rehabil. 62-70, 1959PATHOGENESIS*

Faktor PenyebabLama tekanan Besar penekanan Causal factor Nr. 1Causal factor Nr. 2PathogenesisPressureImmobility*

PT: Duration of pressure impactDepends onpatient's mobility

PT* = _____60 = 15 min 4 movements per hour**

*PT= pressure time in minutes*PT= normal time values < 15 minutes** During sleepCausal factor Nr. 1PathogenesisImmobility*

Pressure time: PTPT = Duration of uninterrupted pressure action on a skin area

Ref. Seiler W.O.,Sthelin H.B.; Stoffel F.: Recordings of movement leading to pressure relief of the sacral skin region: identification of patients at risk for pressure ulcer development. Wounds (USA) 1992 4: 256-261 (1992).Causal factor Nr. 1PathogenesisSacral motility scoreNormal value: 15 minutesTissue tolerability: < 1 2 hours*

Besar penekanan Pada kulit tergantung kepada :Support systemLokalisasiBerat dan bentuk tubuh pasien Causal factor Nr. 2PathogenesisPressure*

Loading skin with weightOn a "soft area": muscle padded areae.g. Quadriceps skin areaOn a "hard area" or "pressure point":over a bony prominencee.g. Trochanter skin areaTranscutaneous Oxygen Tension: tcPO2

Ref: Seiler W.O.; Stahelin H.B.: Skin oxygen tension as a function of imposed skin pressure: implication for decubitus ulcer formation. J Am Geriatr Soc 1979 27: 298-301 (1979).Causal Factor Nr. 2PathogenesisPressure*

TcPO2- trochanter areaTcPO2- quadriceps areatcPO25025075100Weight 50g/cm2Weight100g/cm2letal ischemiaminutes246810121416PathogenesisHypoxia*

STAGINGStage I: Kemerahan yang menetap.

Stage II: Kehilangan sebagian tebal kulit.

Stage III: Kehilangan seluruh tebal kulit sampai ke subkutan.

Stage IV: Kehilangan seluruh tebal kulit sampai ke Fasia.*

STAGE I Kulit utuh bewarna kemerahan yang tidak memucat saat ditekan, biasanya diatas tonjolan tulang. Penderita dengan kulit hitam sering tidak terlihat kulit yang memucat, mungkin hanya terjadi perubahan warna kulit.*

STAGE I*

STAGE I*

STAGE II

Kehilangan sebagian tebal kulit, epidermis atau bagian paling atas dari kulit rusak, terlihat sebagai abrasi atau luka terbuka yang tergaung dengan dasar pink atau kemerahan, tanpa jaringan nekrosis. Luka juga bisa terlihat sebagai blister. *

STAGE II*

Stage III Kehilangan seluruh tebal kulit, kerusakan meluas sampai ke dermis subkutan dan jaringan lemak. Mungkin terdapat slough( jaringan nekrotik bewarna kuning atau abu abu)*

STAGE III*

STAGE IV Kehilangan seluruh tebal kulit, kerusakan meluas sampai ke otot bahkan dapat meluas sampai ke tulang. Sering terdapat slough atau eschar yang bewarna hitam kecoklatan pada daerah luka. *

STAGE IV*

Unstageable

Kehilangan jaringan dengan dasar luka ditutupi oleh slough atau eschar.*

Unstagable *

Unstagable*

PENYEBABTekanan dalam jangka lamaLama dan intensitas penekanan.Lokasi penekananLuasnya penekanan yang mengakibatkan hambatan aliran darah kelokasi penekananFriksi (gesekan)Regangan (shear)

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EtiologiPenekanan pada tonjolan tulang mengakibatkan aliran kapiler terhenti ke lokasi penekanan.Jaringan kekurangan oksigen dan nutrisi yang dapat mengakibatkan kematian jaringan.Tekanan yang dapat mengakibatkan terhentinya flow kapiler adalah 32 mmHg.*

EtiologiPengaruh waktu dan besar tekananTekanan > 70 MmHg lebih dari 2 jam menyebabkan cedera yang irreversibelPenekanan yang lebih besar , lebih sedikit waktu yang dibutuhkan untuk cedera.Tekanan lebih rendah, waktu lebih lama.Obesitas, lebih rendah tekanan penyebabnya.*

LokasiSakrum (tersering)Tumit

Lokasi lainTrokanterIskhium*

Penyebab Lain Sepatu.Pelindung tumit (heel protectors).Selang oksigen (oxygen tubing).Stocking.Setiap alat yang dapat mengakibatkan iskemia kulit akibat penekanan.*

Morbiditas dan MortalitasNyeriInfeksiKualitas hidupKematianBiaya*

Mortalitas40% kematian pertahun.60% kematian dalam setahun sesudah keluar rumah sakit.*

Nyeri 59% mengeluh nyeri.Hanya 2 % yang menerima pengobatan.45% mengeluh nyeri hebat.*

Faktor ResikoPerawatan baring di tempat tidur/kursi roda.Inkontinensia urin.Inkontinensia alvi.Kondisi gizi jelek.Riwayat pressure ulcer sebelumnya.Penyakit PAD/ DM.*

Assesmen Faktor ResikoStatus mobilitasKontinensia urinKontinensia alviRiwayat pressure ulcer sebelumnyaFeeding assistance neededKehilangan berat badanTinggi dan berat badanPemeriksaan kulit*

6 Treatment Principles Pressure relieve Debridement Infection Wet dressing Risk factors Surgery

Ref. Seiler W.O.; Stahelin H.B.: Decubitus ulcers: treatment through fivetherapeutic principles. Geriatrics 1985 40: 30-44 (1985).Treatment*

AssessmentDifferensiasi tipe ulkus.Tentukan staging.Tetapkan dan monitor karakteristik ulkus.Monitor kemajuan dan potensial komplikasi.Tangani infeksi jika ada.Assess, treat dan monitor nyeri jika ada.Monitor dressings dan pengobatan.*

Penatalaksanaan Terhadap faktor resikoPerawatan kulitPengurangan tekananPerawatan inkontinensiaIntervensi nutrisi*

Perawatan KulitInspeksi kulit setiap hariPencucian kulitHindari kekeringan dan retakan kulitHindari keringat berlebihan

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Perlindungan kulit dari kelembabanCuci kulit dengan air hangat dan sabun ringanCuci kulit setiap selesai BABGunakan pelembab non alkoholJangan pijat diatas tonjolan tulangbowel and bladder training programGunakan underpad absorbens*

Pengurangan tekananMobilisasi pasienJadwal reposisiPerobahan posisiAlat pengurangan tekananTempat tidurKursi roda/kursi*

Kasur Khusus*

Penatalaksanaan LukaCuci luka dengan NaCl atau air biasaJangan gunakan skin cleanser atau anti septikGunakan tekanan yang tepat saat pencucianJaga luka tetap lembabJaga sekitar luka tetap bersih dan keringHindaridead space*

Tipe DressingKasaFilm transparanHidrokoloidHidrogelAlginatesFoamcomposite*

Pemilihan DressingGunakan pertimbangan klinis yang tepat.Jaga bed luka tetap lembab.Jaga jaringan sekitarnya tetap kering.Perawat luka (caregiver).*

DebridementBuang semua jaringan mati, karena dapat menghambat penyembuhan luka Methods:SurgicalMechanicalAutolyticEnzymatic

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Surgical DebridementConsiderations:Mengubah luka kronik menjadi luka akut

Cepat dan selektif Adequate perfusionTissue-bone culturesTidak direkomendasi pada pasiendengan kondisi jelek dan compromised Diperlukan Analgesia/anesthesiaTenaga terlatih(surgeon)Mempercepat penyembuhan luka 4Steed et al (1996)

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Mechanical DebridementDefinition: The removal of foreign material and dead or damaged tissue by the use of physical forces.MethodsHydrotherapyIrrigationWet-to-dry dressings

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Wet to Dry Dressings - The Gold Standard?Painful20% slower healingCools wound bedIncreased infection ratesDisperses aerosolized bacterial on removalLabor and Cost intensive*

Pulsatile Lavage*

Mechanical DebridementAB*

Definition Penggunaan agent topikal kimia untuk menghancurkan jaringanYang sering digunakan Papain-UreaCollagenase Hypertonic Saline Enzymatic Debridement*

Treatment of Pressure UlcersUse adjunctive therapies in Stage III and IV Recalcitrant wounds (A)Growth factors (A)Electrical stimulation (A)Negative pressure (A)Mist ultrasound (A)Hyperbaric (A)Bioburden Control (A)Pertimbangkan tindakan operasi pada sdtage III dan IV (C)Eliminasi dan kontrol nyeri (C)

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Antiseptik yang sering digunakan pada perawatan lukaIodineDakins solutionSilver compoundsMethylene Blue/Gentian Violet*

In vivo Evaluation of Antiseptics Bennett LL et al. An in vivo comparison of topical agents on wound repair. Plast Reconstr Surg 2001 Sep 1;108(3):675-87.5 common antiseptic agents compared in porcine wound modelSulfamylon solutionBetadine 0.25% Dakins3% hydrogen peroxide 0.25% acetic acid Analyzed multiple wound healing effects:

Reepithelialization was not significantly influenced by any agent tested.

All treatments except hydrogen peroxide significantly increased fibroblast proliferation.*

Treatment of Pressure UlcersConsider operative repair for Stage III and IV ulcers (C)

Eliminate and control pain (C)

Educate patient, family and healthcare providers involved about prevention, management and factors contributing to pressure ulcers (C)

Monitor vigilantly for recurrence once healed (C)

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How to avoid the whole mess!Communicate!Talk to the patient.Discuss progress within limits with the family.Nothing should be a surprise.Document conversations with the patient and family.*

Thank you*

*NOTES FOR PRESENTERSSLIDE FOR ALL

*When thinking about wound bed preparation there are four methods of debridement surgical, mechanical, autolytic and enzymatic. While there are advantages and disadvantages for each method, there are also clinically appropriate indications for each method. It is important to consider the patients overall condition and the goals for care when selecting the method of debridement.

*The primary advantage of surgical debridement is that it allows you to remove large amounts of necrotic tissue quickly. This method is considered selective because there is minimal damage to healthy tissue. A vascular assessment to determine the adequacy of perfusion is indicated prior to surgical debridement of wounds in the lower extremities. It also creates the opportunity to obtain tissue and bone cultures.This method is not recommended for patients with bleeding disorders or who are severely compromised.Sharp debridement may be uncomfortable and/or painful for the patient. A pain assessment should occur prior to debridement. In complicated cases the patient may require anesthesia.Sharp debridement also requires the use of sterile instruments which may not be readily available in some settings. Surgical debridement requires specialized training and licensure. The regulations pertaining to sharp debridement vary state to state.During the clinical trials for recombinant human platelet derived growth factor frequent sharp debridement was independently associated with improved healing of DFU.Steed DL, Donohoe D, Webster MW, Lindsley l, and the Diabetic Ulcer study Group. Effect of Extensive Debridement and Treatment on the Healing Diabetic Foot Ulcer. Journal of the American College of Surgeons 1996;183:61-64.*Mechanical debridement is defined as the removal of foreign material and dead or damaged tissue by the use of physical forces.The methods often thought of in this category are hydrotherapy and irrigation. However, wet-to-dry dressings are also categorized as mechanical debridement.

*There are times when mechanical debridement is appropriate. In this case this woman had chronic venous insufficiency for a number of years without compression therapy. Chronic dermatitis and edema resulted in the accumulation of the scale seen in panel A. After six hydrotherapy session there was dramatic improvement in her skin condition and she was fitted for compression stockings.*

Over the years enzymatic agents have been used to debride necrotic tissue from the wound bed and their use has become a well established practice among wound care providers.Enzymatic debridement is defined as the use of proteolytic substances, applied topically to the wound, to stimulate the breakdown of necrotic tissue.Enzymatic debriders use chemical agents which are biologically capable of degrading eschar, protein and other nucleic acids.

There are several preparations on the market for example Collagenase and Papain Urea.

*Commonly used topical antiseptics in wound management include iodine solutions, acetic acid, sodium hypochlorite or Dakins solution, and silver compounds.

We will briefly review each of these antiseptics. *Antiseptics have often been cited as delaying wound healing because their antimicrobial effects may also damage endogenous cells in the wound. Most data to support this contention is based on in vitro studies of the effects of large amounts of antiseptic solutions on cells in test tubes not in wounds.A recent study evaluated the effects of five different antiseptic solutions on the healing of partial thickness wounds in a pig model. Various parameters of wound healing were analyzed. It was interesting that for the parameter of wound re-epithelialization the point at we judge wounds to be clinically healed none of the antiseptic agents had any effect compared to control (saline).Bennett LL, Rosenblum RS, Perlov C, Davidson JM, Barton RM, Nanney LB. An in vivo comparison of topical agents on wound repair. Plast Reconstr Surg 2001 Sep 1;108(3):675-87Selection of the ideal antiseptic or antimicrobial treatment for contaminated wounds remains a controversial decision. Clinical decisions are often made on the basis of in vitro studies and personal preference. Although topical solutions are widely used, their comparative in vivo effects on wound healing are largely unreported. A porcine wound model was used to compare five commonly used topical agents-5% mafenide acetate (Sulfamylon solution), 10% povidone with 1% free iodine (Betadine), 0.25% sodium hypochlorite ("half-strength" Dakin), 3% hydrogen peroxide, and 0.25% acetic acid-with a control group. Reepithelialization, angiogenesis, neodermal regeneration, fibroblast proliferation, collagen production, and bacterial colony counts were analyzed at 4 and 7 days after wounding (n = 4). Reepithelialization was not significantly influenced among the various treatment modalities tested. Sulfamylon and Dakin solutions significantly increased neodermal thickness (p < 0.05), whereas hydrogen peroxide and acetic acid significantly inhibited neodermal formation (p < 0.001). All treatments except hydrogen peroxide significantly increased fibroblast proliferation. Sulfamylon and Betadine significantly enhanced angiogenesis (p < 0.05). Sulfamylon proved most effective in maintaining an aseptic environment while concomitantly increasing angiogenesis, fibroblast proliferation, and dermal thickness compared with control.These data show that selection of a particular topical treatment can affect various aspects of wound repair in an animal model. These results suggest that the selection of topical treatments in the clinical setting should be carefully tailored to match unique wound situations and therapeutic endpoints.

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