KULIT

(Anatomi, Terapi, Prevensi)

KARTIKA SOKA RAHMITA 1301-1210-0063

KULIT

ANATOMI
Kulit merupakan organ terbesar dan terberat di

tubuh manusia
Pada orang dewasa, kulit menutupi 2 m2 atau 4-5

kg atau 16% dari total massa tubuh

Ketebalannya berkisar antara 0,5 mm (di kelopak

mata) hingga 4 mm (di tumit)

FISIOLOGI
Proteksi Melindungi tubuh dari lingkungan : abrasi, kehilangan cairan, radiasi sinar UV, mechanical & physical injury, dan mikroorganisme Regulasi panas Mengatur regulasi panas tubuh melalui kelenjar keringat dan pembuluh darah Organ sensoris Memiliki superficial nerve dan sensory endings Membantu produksi vitamin D Kosmetik

HISTOLOGI
Kulit terdiri dari 2 lapisan: Epidermis bagian terluar yang langsung berhubungan dengan dunia luar. Dibentuk oleh sel-sel keratinosit yang menghasilkan keratin (filamentous protein yang berfungsi untuk proteksi)

Dermis bagian dalam yang terdiri dari fibrillar structural protein dan kolagen. Berada diatas panniculus atau subkutis

Epidermis
Lapisan epidermis dari bawah atas : a. Stratum basale / germinativum

Selapis sel columnar/cuboid diatas basal membrane. Mempunyai stem cell yang selalu menghasilkan sel-sel epidermis baru setiap 15-30 hari. Terdapat melanosit yang menghasilkan pigment kulit

b.

Stratum spinosum
Terdiri dari sel cuboid dengan central nucleus dan tonofilaments (keratin filament) utnuk menjaga kohesi sel dan mencegah abrasi. Langerhans cell (star-shaped cell) yang berperan sebagai antigen presenting cell

c.

Stratum granulosum
Terdiri dari 3-5 lapisan sel gepeng poligonal yang sitoplasmanya terdiri dari coarse basophilic granule. Terdiri dari lipid bilayer yang berfungsi sebagai barier terhadap material asing

d.

Stratum lucidum
Translucent, selapis tipis eosinophilic epidermal cells. Sitoplasma terdiri dari keratin filament yang padat

e.

Stratum corneum
Terdiri dari 15-20 lapis sel gepeng berkeratin dengan sitoplasma berisi keratin. Terdapat horny cell yang terdiri dari fibrillar dan amorphous protein serta plasma membrane yang menebal setelah keratinisasi

Dermis
Connective tissue yang menyokong epidermis dan

berikatan dengan jaringan subkutan

Terdiri dari dua lapisan :

Papillary layer

Antara dermis dan epidermis. Terdiri dari jaringan ikat longgar, fibroblast, mast cell, macrophage, dan leukosit yang ekstravasasi

Reticular layer

Untuk menjaga elastisitas kulit. Terdiri dari jaringan ikat pada ireguleri, lebih banyak fiber (kolagen tipe I) dan sedikit sel

Dermis terdiri dari folikel rambut, persyarafan, kelenjar

keringat & minyak

Subkutan
Terdiri dari jaringan ikat yang menghubungkan kulit

dengan organ disekitarnya

PENDARAHAN DAN PERSYARAFAN

Arteri 2 arterial plexus : diantara papillary dan reticular layer; diantara dermis dan subkutan Vena 3 vein plexus : diantara papillary dan reticular layer; diantara dermis dan subkutan; ditengah-tengah dermis Lymphatic 2 lymphatic plexus : diantara papillary dan reticular; diantara dermis dan subkutan Innervasi Free nerve ending receptor di dermis dan subkutan : Vater, Pacini, Meissner, Krause

TRAUMA PADA KULIT

Traumatic injuries Exposure to caustic substances Temperature (hypo- or hyperthermic injuries)

Pressure ulcer
Radiation exposure Infection (bacterial, viral, inflammatory disease ) Malignancies

WOUND HEALING

DEFINISI
Wound healing or cicatrisation is an intricate process

in which the skin ( or another organ-tissue) repairs itself after injury.

TIPE
Primary wound healing
occurrence of mechanical apposition of wound edges and a cascade of

inflammatory cell activation. This recruitment creates a milieu which allows reepithelialization and collagen strengthening to occur

Delayed primary wound healing

the wound healing process is potentially compromised by incipient infection.

With this type of healing, the surgeon may opt to leave the soft tissue unapposed and allow native inflammation and external debridement to cleanse the wound. If, on evaluation several days later, the wound appears uninfected, the wound can then be closed and the normal process of primary healing can then be re-initiated

Secondary wound healing

Third is secondary healing, which is recommended for a wound that does not show potential for early closure. The wound can be allowed to close over time by the processes of inflammation, contraction (via myofibroblasts), and eventual reepithelialization

MEKANISME
Proses wound healing secara klasik dibagi mejadi 3

sekuens :
1.

2.

3.

Hemostasis dan inflamasi terjadi beberapa menit setelah truma, ditandai dengan terbentuknya fibrin clot, proses fagositosis, pelepasan faktor-faktor inflamasi Proliferatif angiogenesis, deposisi kolagen, pembentukan jaringan granulasi, epitelialisasi, kontraksi luka Remodeling remodeling collagen dan realignment tension lines, dan apoptosis sel

HEMOSTASIS DAN INFLAMASI

Hemostasis precedes and initiates inflammation with the ensuing release of chemotactic factors from the wound site

Wounding by definition disrupts tissue integrity, leading to division of blood vessels and direct exposure of extracellular matrix to platelets

Exposure of subendothelial collagen to platelets results in platelet aggregation, degranulation, and activation of the coagulation cascade

Platelet granules release a number of wound-active substances, such as platelet-derived growth factor (PDGF), transforming growth factor- (TGF-), platelet-activating factor (PAF), fibronectin, and serotonin

In addition to achieving hemostasis, the fibrin clot serves as scaffolding for the migration into the wound of inflammatory cells such as polymorphonuclear leukocytes (PMNs, neutrophils) and monocytes. Primary role of neutrophils is phagocytosis of bacteria and tissue debris

PROLIFERASI
Tissue continuity is re-established

Fibroblasts and endothelial cells are the last cell populations to infiltrate the healing wound, and the strongest chemotactic factor for fibroblasts is PDGF Upon entering the wound environment : fibroblasts proliferate activated primary function of matrix synthesis remodeling mediated by cytokines and growth factors released from wound macrophages Fibroblasts isolated from wounds synthesize more collagen than non-wound fibroblasts, they proliferate less, and they actively carry out matrix contraction Endothelial cells also proliferate extensively to formation of new capillaries (angiogenesis) under the influence of such cytokines and growth factors as TNF-, TGF-, and VEGF

MATURASI DAN REMODELING

Reorganization of previously synthesized collagen that broken down by matrix metalloproteinases (MMPs) Wound strength and mechanical integrity in the fresh wound are determined by both the quantity and quality of the newly deposited collagen

By several weeks post injury the amount of collagen in the wound reaches a plateau, but the tensile strength continues to increase for several more months. Fibril formation and fibril cross-linking result in decreased collagen solubility, increased strength, and increased resistance to enzymatic degradation of the collagen matrix.
Scar remodeling continues for many (6 to 12) months post injury, gradually resulting in a mature, avascular, and acellular scar This balance of collagen deposition and degradation is the ultimate determinant of wound strength and integrity.

FACTORS AFFECTING WOUND HEALING

SYSTEMIC

LOCAL

Age Nutrition Trauma Metabolic diseases Immunosuppression Connective tissue disorders Smoking

Mechanical injury Infection Edema Ischemia/necrotic tissue Tropical agents Ionizing radiation Low oxygen tension Foreign bodies

TERAPI
Local Care Antibiotics Dressing Skin Replacement
Tetanus prophylaxis Irigasi dan Debridement Suturing

If, evidence of obvious wound infection Topikal dan sistemik

Provide the ideal environment for wound healing Provide hemostasis and limits edema

Conventional skin grafts Skin subtitude Skin flap

Growth Factor Therapy

IMPAIRED WOUND HEALING

If the necessary blood supply to a healing region is compromised, then wound healing can be delayed Similarly, the relative paucity of the basic constituents of inflammatory cytokines or matrix components (vitamins, zinc, copper, iron) may result in structural weakness of the wound Radiation is often an issue for reconstruction of ablative defects. Among other effects, radiation can create local ischemic conditions via microangiopathic damage

Dysfunctional healing can also manifest as abnormal scars. Hypertrophic scars and keloids are manifestations of altered collagen deposition and breakdown
Treatment of scars includes pressure, silicone sheet and gels, and intralesional corticosteroids. Topical vitamins A and E are used for treatment of unsightly scars, but no definitive clinical trials have demonstrated their efficacy. For intractable keloids, radiation therapy in conjunction with surgical excision has led to a 50 to 80% reduction in keloids

KELOID

DEFINISI
Jaringan diatas lapisan kulit, melebar lebih luas dari

tepi luka sebelumnya, dan tidak menghilang secara spontan

Terjadi setelah trauma pada kulit

Bersifat lembut, gatal, dan bisa terjadi sensasi

terbakar

EPIDEMIOLOGI
Terjadi 3 bulan atau lebih setelah trauma kulit 15x lebih sering pada ras berkulit gelap (African) atau

berwarna (Spanish)

Laki-laki : Perempuan sama angka kejadiannya Terjadi setelah operasi, luka bakar, peradangan pada

kulit, jerawat, cacar air, herpes zoster, folliculitis, laserasi kulit, abrasi kulit, tempat tatto, tempat vaksin, tempat injeksi, digigit serangga, tindik telinga, ataupun tumbuh sendiri secara spontan

PATOFISIOLOGI
Mekanisme yang mendasari terjadinya keloid masih

belum diketahui, namun dicurigai berkaitan dengan sistem imun tubuh

Mekanisme lain disebutkan sebagai mechanical

tension dan prolonged irritation/inflammation yang akan menghasilkan abnormal konsentrasi dari sitokin profibrotik

TREATMENT
Tujuan dari treatment pada keloid untuk :

mengembalikan fungsi kulit di area yang terkena, mengurangi gejala, dan mencegah kekambuhan Jenis-jenis terapi :

Eksisi dikombinasikan dengan intralesional corticosteroid injection, topical application of silicone sheets, radiasi atau pressure (penekanan) Operasi debulking lesi luas Aplikasi silikon mencegah rebound hypertrophy Intralesion cortcisteroid injection mengurangi proliferasi fibrosit, serta sintesis kolagen&glycosaminoglycan dalam proses inflamasi Radiasi yang dikombinasikan dengan surgical eksisi Topical retinoids (50-100%) Intralesional injections of INF- mengurangi kolagen tipe I,II,&III dengan mengurangi mRNA dan level TGF-

HIPERTOPIK SKAR

DEFINISI
Jaringan diatas lapisan kulit, yang tidak lebih luas

dari tepi luka sebelumnya, dan dapat menghilang spontan seiring waktu (jarang terjadi penebalan hingga 4mm diatas batas kulit normal)

Terjadi setelah trauma pada kulit

Bersifat lembut, gatal, dan bisa terjadi sensasi

terbakar. Awalnya lesi kemerahan dan menebal, seiring waktu lesi akan menjadi pucat, datar, dan meninggalkan parut

EPIDEMIOLOGI
Terjadi cepat, dalam waktu 4 minggu setelah trauma

kulit
Risiko meningkat bila epitelialisasi lebih lama dari

21 hari (tergantung tempat lesi, usia, dan ras)

TERAPI
Kompresi eksternal secepatnya setelah trauma

dengan tekanan 24-30 mmHg

Berfungsi untuk membantu maturasi kolagen,

mendatarkan jaringan parut, dan mempercepat proses penipisan

KONTRAKTUR

DAFTAR PUSTAKA
1. 2.

3.
4.

5. 6. 7.

Wolff, Klaus., Johnson, Richard Allen. Fitzpatricks Color Atlas & Synopsis of Clinical Dermatology. 5th Edition. McGraw-Hill. 2006. Brunicardi, F. Charles. Schwartzs Principle of Surgery. 8th Edition. McGraw-Hill. 2004. www.wikipedia.com/Wound_healing Arnold, Harry L., Odom, Richard B., James, William D. Andrews Disease of the Skin Clinical Dermatology. 8th Edition. W.B. Saunders Company. 1990. Junqueira, Luiz Carlos., Carneiro, Jose. Basic Histology. 11th Edition. McGraw-Hill. 2005. Moore, Keith L., Dalley, Arthur F. Clinically Oriented Anatomy. 5th Edition. Lippincott Williams & Wilkins. 2006. Tortora, Gerard J., Derrickson, Bryan. Principles of Anatomy and Physiology. 11th Edition. John Wiley & Sons, Inc. 2006.