1

2 Wound Healing

3 Wound Healing Acute Wound Chronic Wound

6 GENERAL CONSIDERATIONSClinical Wound Healing The Mechanism of Wound Healing Hemostasis and Inflammation Fibroplasia and Matrix Synthesis Angiogenesis Epithelialization Collagen Fiber Remodeling and Wound Contraction Healing of Specialized Tissues Gastrointestinal tract

7 GENERAL CONSIDERATIONSSurgeons often describe wound healing as primary or secondary. Primary healing occurs when tissue is cleanly incised and anatomically reapproximated. It is also referred to as healing by primary intention, and tissue repair usually proceeds without complication. Secondary healing occurs in wounds left open through the formation of granulation tissue and eventual coverage of the defect by migration of epithelial cells. (Granulation tissue) The principles of primary and secondary healing are combined in delayed primary closure, when a wound is left open to heal under a carefully maintained, moist wound healing environment for approximately 5 days and is then closed as if primarily. Wounds treated with delayed primary closure are less likely to become infected than if closed immediately because bacterial balance is achieved and oxygen requirements are optimized through capillary formation in the granulation tissue. Clinical Wound Healing

8 GENERAL CONSIDERATIONSThe Mechanism of Wound Healing Acute wound healing normally proceeds from coagulation and inflammation, through angiogenesis, fibroplasia, matrix deposition (granulation tissue formation), collagen maturation, epithelialization, and finally wound contraction. A chronic wound fails to heal anywhere along this wound healing pathway.

9 GENERAL CONSIDERATIONSFollowing injury, a wound must stop bleeding in order to heal and for the injured host to survive. It is therefore not surprising that cellular and molecular elements involved in hemostasis also signal tissue repair. Immediately after injury, the coagulation products fibrin, fibrinopeptides, thrombin split products, and complement components attract inflammatory cells into the wound. Circulating leukocytes then adhere to the endothelium and migrate into the wounded tissue. Interleukins and other inflammatory components, such as histamine, serotonin, and bradykinin, cause vessels first to constrict for hemostasis and later to dilate, becoming porous so that blood plasma and leukocytes can migrate into the injured area Oxidative stress is an important signal for tissue repair. These conditions trigger reparative processes and stimulate their propagation. Macrophages assume a dominant role in the synthesis of wound healing molecules as coagulation-mediated tissue repair signals fall. Unless the wound becomes infected, the granulocyte population that dominated the first days diminishes. Macrophages now cover the injured surface. Hemostasis and Inflammation

10 GENERAL CONSIDERATIONSFibroplasia Throughout wound healing, fibroplasia (the replication of fibroblasts) is stimulated by multiple mechanisms, starting with PDGF, IGF-1, and TGF-β released by platelets and later by the continual release of numerous peptide growth factors from macrophages and even fibroblasts within the wound. Matrix synthesis Fibroblasts secrete the collagen and proteoglycans of the connective tissue matrix that hold wound edges together and embed cells of the healing wound matrix. These extracellular molecules assume polymeric forms and become the physical basis of wound strength Fibroplasia and Matrix Synthesis

11 GENERAL CONSIDERATIONSAngiogenesis is required for wound healing. It is clinically evident about 4 days following injury but begins earlier when new capillaries sprout from preexisting venules and grow toward the injury in response to chemoattractants released by platelets and macrophages. Numerous growth factors and cytokines are observed to stimulate angiogenesis, but animal experiments indicate that the dominant angiogenic stimulants in wounds are derived first from platelets in response to coagulation and then from macrophages in response to hypoxia or high lactate, fibrin, and its products. Angiogenesis

12 GENERAL CONSIDERATIONSEpithelial cells respond to several of the same stimuli as fibroblasts and endothelial cells within the mesenchymal area of a wound. A variety of growth factors also regulate epithelial cell replication. TGF-α and keratinocyte growth factor (KGF), for instance, are potent epithelial cell mitogens. Squamous epithelialization and differentiation proceed maximally when surface wounds are kept moist. It is clear that even short periods of drying impair the process, and therefore wounds should not be allowed to desiccate. Epithelialization

13 GENERAL CONSIDERATIONSRemodeling of the wound extracellular matrix is also a well-regulated process. First, fibroblasts replace the provisional fibrin matrix with collagen monomers. Progressively, the very early provisional matrix is replaced with a more mature one by forming larger, better organized, stronger, and more durable collagen fibers. The very early wound provisional matrix usually mechanically fails within the matrix itself (days 0-5). Collagen Fiber Remodeling and Wound Contraction

14 WOUND HEALING Normal wound healing follows a predictable pattern that can be divided into overlapping phases defined by characteristic cellular populations and biochemical activities: (a) hemostasis and inflammation, (b) proliferation, and (c) maturation and remodeling The majority of wounds that have not healed in 3 months are considered chronic The cellular, biochemical, and mechanical phases of wound healing

15 Hemostasis and InflammationHemostasis 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 α granules release a number of wound-active substances, such as platelet-derived growth factor (PDGF), transforming growth factor-β (TGF- β), 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. The phases of wound healing viewed histologically. A. The hemostatic/inflammatory phase. B. Latter inflammatory phases reflecting infiltration by mononuclear cells and lymphocytes. C. The proliferative phase, with associated angiogenesis and collagen synthesis

16 Cellular infiltration after injury follows a characteristic, predetermined sequence.PMNs are the first infiltrating cells to enter the wound site, peaking at 24 to 48 hours. Increased vascular permeability, local prostaglandin release, and the presence of chemotactic substances such as complement factors, interleukin-1 (IL-1), tumor necrosis factor-α (TNF-α), TGF-β, platelet factor 4, or bacterial products all stimulate neutrophil migration. The postulated primary role of neutrophils is phagocytosis of bacteria and tissue debris. PMNs are also a major source of cytokines early during inflammation, especially TNF-α which may have a significant influence on subsequent angiogenesis and collagen synthesis

17 The second population of inflammatory cells that invades the wound consists of macrophages, which are recognized as being essential to successful healing. Derived from circulating monocytes, macrophages achieve significant numbers in the wound by 48 to 96 hours postinjury and remain present until wound healing is complete. Macrophages, like neutrophils, participate in wound débridement via phagocytosis and contribute to microbial stasis via oxygen radical and nitric oxide synthesis Macrophages also play a significant role in regulating angiogenesis and matrix deposition and remodeling T-lymphocyte numbers peak at about 1 week postinjury and truly bridge the transition from the inflammatory to the proliferative phase of healing. Though known to be essential to wound healing, the role of lymphocytes in wound healing is not fully defined

18 Proliferation The proliferative phase is the second phase of wound healing and roughly spans days 4 through 12 (see Fig. 9-2C). It is during this phase that 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 Fibroblasts isolated from wounds synthesize more collagen than nonwound fibroblasts, they proliferate less, and they actively carry out matrix contraction. Although it is clear that the cytokine-rich wound environment plays a significant role in this phenotypic alteration and activation, the exact mediators are only partially characterized Endothelial cells also proliferate extensively during this phase of healing. These cells participate in the formation of new capillaries (angiogenesis), a process essential to successful wound healing.

19 Matrix Synthesis Collagen, the most abundant protein in the body, plays a critical role in the successful completion of adult wound healing. Its deposition, maturation, and subsequent remodeling are essential to the functional integrity of the wound. Although there are at least 18 types of collagen described, the main ones of interest to wound repair are types I and III. Type I collagen is the major component of extracellular matrix in skin. Type III, which is also normally present in skin, becomes more prominent and important during the repair process. Glycosaminoglycans comprise a large portion of the “ground substance” that makes up granulation tissue The major glycosaminoglycans present in wounds are dermatan and chondroitin sulfate. Fibroblasts synthesize these compounds, increasing their concentration greatly during the first 3 weeks of healing. The interaction between collagen and proteoglycans is being actively studied. As scar collagen is deposited, the proteoglycans are incorporated into the collagen scaffolding. However, with scar maturation and collagen remodeling, the content of proteoglycans gradually diminishes.

20 Maturation and RemodelingThe maturation and remodeling of the scar begins during the fibroplastic phase and is characterized by a reorganization of previously synthesized collagen. Collagen is broken down by matrix metalloproteinases (MMPs), and the net wound collagen content is the result of a balance between collagenolysis and collagen synthesis. There is a net shift toward collagen synthesis and eventually the re-establishment of extracellular matrix composed of a relatively acellular collagen-rich scar. Wound strength and mechanical integrity in the fresh wound are determined by both the quantity and quality of the newly deposited collagen. The deposition of matrix at the wound site follows a characteristic pattern: fibronectin and collagen type III constitute the early matrix scaffolding; glycosaminoglycans and proteoglycans represent the next significant matrix components; and collagen type I is the final matrix Scar remodeling continues for many (6 to 12) months postinjury, gradually resulting in a mature, avascular, and acellular scar. The mechanical strength of the scar never achieves that of the uninjured tissue.

21 Epithelialization While tissue integrity and strength are being re- established, the external barrier must also be restored. This process is characterized primarily by proliferation and migration of epithelial cells adjacent to the wound. The process begins within 1 day of injury and is seen as thickening of the epidermis at the wound edge Re-epithelialization is complete in less than 48 hours in the case of approximated incised wounds, but may take substantially longer in the case of larger wounds, where there is a significant epidermal/dermal defect. If only the epithelium and superficial dermis are damaged, such as occurs in split-thickness skin graft donor sites or in superficial second-degree burns, then repair consists primarily of re-epithelialization with minimal or no fibroplasia and granulation tissue formation.

22 Wound Contraction All wounds undergo some degree of contraction. For wounds that do not have surgically approximated edges, the area of the wound will be decreased by this action (healing by secondary intention); the shortening of the scar itself results in contracture. The myofibroblast has been postulated as being the major cell responsible for contraction, and it differs from the normal fibroblast in that it possesses a cytoskeletal structure. Typically this cell contains α-smooth muscle actin in thick bundles called stress fibers, giving myofibroblasts contractile capability. The α-smooth muscle actin is undetectable until day 6, and then is increasingly expressed for the next 15 days of wound healing. After 4 weeks, this expression fades and the cells are believed to undergo apoptosis. A puzzling point is that the identification of myofibroblasts in the wound does not correspond directly to the initiation of wound contraction, which starts almost immediately after injury.

23 CLASSIFICATION OF WOUNDSWounds are classified as either acute or chronic Surgical wounds can heal in several ways. An incised wound that is clean and closed by sutures is said to heal by primary intention. Often, because of bacterial contamination or tissue loss, a wound will be left open to heal by granulation tissue formation and contraction; this constitutes healing by secondary intention. Delayed primary closure, or healing by tertiary intention, represents a combination of the first two, consisting of the placement of sutures, allowing the wound to stay open for a few days, and the subsequent closure of the sutures

24 Factors Affecting Wound HealingAdvanced Age Hypoxia, Anemia, and Hypoperfusion. Steroids and Chemotherapeutic Drugs. Metabolic Disorders. Nutrition. Infections.

25 Cerrahi Enfeksiyonlar, Cerrahi alan Enfeksiyonları, Profilaksi Şeması

26 A – Cerrahi EnfeksiyonlarCerrahi klniklerin yükünü arttıran Yatış süresini uzatan Bazen yeni cerrahi girişim ihtiyacı doğuran Maliyeti arttıran Iş gücü kaynı nedeni Mortalitenin yükselmesi SORUNDUR !

27 Cerrahi EnfeksiyonlarCerrahi girişimi izleyen dönemde cerrahi alanı ilgilendiren (yara enfeksiyonu, karın içi apseler vb.) Tedavisi için cerrahi girişim ihtiyacı duyulan enfeksiyonlar (meme apsesi, panaris vb.) Diğer bir grup ise nasokomial enfeksiyonlar Bu başlık altınca inceleyeceğiz konular

28 Tarihçe Lister asepsi ve antisepsi alanında gözlem ve deneyimleriSemmelweis’ın elleri hipoklorid solüsyonu ile yıkaması sonrası fark ettiği puerperal sepsistedi azalma Erlich ile başlayan ve İan Fleming ile ortaya çıkan antibiyotikler Halstedt’in lastik eldiven kullanımı Günümüzdeki cerrahi profilaksi ve tedavinin kilometre taşlarıdır.

29 Cerrahi EnfeksiyonlarEnfeksiyonun klasik kardinal belirtilerinin takibi ve gözlemlenmesi çok önemlidir; kızarıklık, ağrı, lokal ısı artışı, şişlik Ayrıca; ameliyat sonrası hastanın iştahının kesilmesi, uykusuzluk çekmesi, etraf ile ilgisinin azalması, karında gerginlik, susuzluk hissi, dil kuruluğu, idrar miktarında azalma uyarıcı olmalıdır. Yapılması gerekenler; hastanın gün içinde bir kaç kez gözlenmesi, iletişişm kurulması, hastanın tüm koşullarda gözlenmesi gibi bir protokol oluşturulmalıdır. Yani cerrah beş duyusunu açık tutmalıdır.

30

31 Relative Percentage by Site of InfectionHastane Enfeksiyonlarında En sık Mikroorganizmalar (NNIS 1989–1998) Medikal & Cerrahi Relative Percentage by Site of Infection Pathogen All Sites BSI Pneumonia SSI n=235,758 n=50,091 n=64,056 n=22,043 Coag-neg Staph S aureus Enterococci spp P aeruginosa Enterobacter spp E coli C albicans K pneumoniae Others Examination of data from the NNIS from 1989 through 1998 documents that Gram-positive organisms are the most common pathogens associated with nosocomial infections in the intensive care unit. This study, which evaluated more than 235,000 isolates in both medical and surgical ICU patients, demonstrated that coagulase-negative Staphylococcus and S aureus were the two most common pathogens isolated from all nosocomial infections. These two organisms also accounted for the majority of bloodstream and surgical site infections in the ICU. BSI=bloodstream infection; SSI=surgical site infection. Fridkin SK et al. Clin Chest Med. 1999;20:

32 Patogenez Cerrahi enfeksiyonların oluşması için doğal savunma engeli olan cilt-mukoza epitel devamlılığının bozulması Enfeksiyon etkeninin/etkenlerinin bulaşması Potansiyel virulansın aktif hale gelmesi gerekir. Kısacası; saldırı-savunma dengesinin saldıran lehine bozulması ile enfeksiyonlar ortaya çıkar.

33 Konak direncinde azalmaBakteri dozu Virülans Konak direncinde azalma Enfeksiyon Riski In a nonsurgical infection, the virulence of the pathogen, bacterial dose, and impaired host resistance are all equivalent to one another. However, in a surgical infection, the bacterial dose and impaired host resistance play the major roles in infection, while virulence is less of a factor.

34 Patogenez Enfeksiyon etkeni Organizmaya ait faktörler Lokal faktörlerEnfeksiyonun derecesini, yaygınlığını, mortalite ve morbiditeyi belirler.

35 Patogenez – 1) Enfeksiyon etkeniKlostridium, stafilokok, streptekok türleri ekzotoksinleri ile doku harabiyetine yol açarken, özellikle gram negatif bakteriler daha çok endotoksinleri ve sitokinler ile olayları başlatırlar. Endotoksik şok; hipotansiyon, pıhtılaşma bozuklukları, karaciger ve böbrek yetmezliği, sonunda multipl organ yetmezliği ile sonuçlanabilen tablodur.

36 Patogenez – 1) Enfeksiyon etkenStafilokoklar; kasık, perine, koltuk altı deri florasını oluşturur. Daha çok nekroz ve cerahatlenmeye, apseleşmeye neden olur.(fronkülit, karbonkül, meme ve perine apseleri, yağ kisti enfeksiyonları gibi)

38 Paronişi

44 Patogenez – 1) Enfeksiyon etkenYanık ünitelerinde streptekok infeksiyonlarına sıklıkla rastlanılır. Ayrıca çocuk cerrahisinde splenektomi sonrası sepsisin başlıca nedenidir. Strep. Faecalis ise özellikle kolon cerrahisi ve üriner sistem kateterizasyonunda ağır enfeksiyon tablosuna yol açtığı bilinir.

45 Patogenez – 2) Organizmaya ait faktörlerDeri ve mukoza enfeksiyon etkenlerinin dokuya girişimlerine karşı ilk engeli oluştururlar. Ayrıca ek olarak epitelden salgılanan lipid yapısındaki maddeler, mide asidi gibi bariyerlerde etkendir.

46 Patogenez – 2) Organizmaya ait faktörlerCerrahi kesi bu bariyeri ortadan kaldırır. vücudun doğal direnç mekanizması devreye girer. Opsonin, kompleman sistemi devreye girer, fagositoz için makrofajlar, PLN,monositler kesi yerine ulaşır. Daha önce bu etkenlerle karşılaşmış ise B lenfositlerin oluşturduğu IgM, IgG yapısındaki antikorlar, T lenfositleri devreye girer. Ayrıca; Kompleman sitemi, pıhtılaşma mekanizmaları, kinin, lökotrşenler, sitokinlerin aktivasyonu vücud direncinde rol alır.

47 Patogenez – 2) Organizmaya ait faktörlerVücud direncini etkileyen faktörler Beslenme bozuklukları Cerrahi girişim Travma Yanıklar Kanserler Kemoterapi Transplantasyonda kullanılan ilaçlar ve steroidler Ek hastalıklar(DM, Kalp hast, otoimmun hast, KOAH vb.)

48 Patogenez – 3) Lokal faktörlerYabancı cisim varlığı Ölü doku varlığı Sıvı toplanması, ödem Periferik arter ve ven bozuklukları Şok tablosu

49 Patogenez – 3) Lokal faktörlerWilliam Halsted çağından bu yana enfeksiyon oluşmadan doku tamiri, yani primer yara iyileşmesinin olmazsa olmazları tariflenmiştir: Dokuya kibar davranma, zedelememe Ölü boşluk ve ölü doku bırakmama Potansiyel boşlukları drene etme Anastomozda gerginliğe, dolayısıyla hipoksiye yol açmamak Canlılığı olan, kanlanması mevcut dokularda cerrahi yapma

50 B- Cerrahi Alan Enfeksiyonu (CAE)CAE cerrahi girişimden sonra, implant yoksa 30 güne kadar gelişen enfeksiyonlar, eğer implant konulmuşsa 1 yıla kadar gelişen enfeksiyonlardır. (Awad et al. (2009). Çoğu CAE cerrahiden sonra ilk 2-3 haftada olur. (Ramos et al. 2008).

51 Cerrahi Alan Enfeksiyonları (CAE)Hastane enfeksiyonlarının en sık 2.nedeni (14%–16%) Cerrahi hastalarda en sık hastane enfeksiyonu nedeni (38%) 2/3 insizyonel 1/3 cerrahi sırasında girilen organ veya boşluk 7.3 postop ek hastane günü ve ek $3,152 maliyet Surgical site infections are the third most common type of nosocomial infection accounting for 14% to 16% of all infections. Among surgical patients, however, SSIs are the most common nosocomial infection, observed in 38% of cases. Two-thirds of these infections are due to the incision, whereas one-third are due to infection of the organs or spaces during surgery. Surgical site infections result in an additional 7.3 postoperative days at an added cost of $3,152. Mangram AJ et al. Infect Control Hosp Epidemiol. 1999;20:

52 Hastane Enfeksiyonlarının MaliyetiRate per 100 admits Proportion of all HAIs Excess Hospital Days Proportion of costs of all HAIs UTI 2.5 35% 1-2 15% SSI 1.5 20% 7 50% Pneumonia 1.0 10 30% BSI 10-12 5%

53 Yüzeyel İnsizyonel CAEEnfeksiyon, cerrahi girişimden sonraki 30 gün içinde gelişir ve sadece insizyon bölgesinde deri ve subkutan dokuları içerir. Yüzeyel insizyonel CAE Deri Subkutan doku The first type of surgical site infection is the superficial incisional surgical infection which occurs within 30 days post-op and involves only the skin or subcutaneous tissue. Mangram AJ et al. Infect Control Hosp Epidemiol. 1999;20:

54 Derin İnsizyonel CAE Enfeksiyon, implant yoksa cerrahiden sonraki 30 gün içinde gelişir; veya implant konmuşsa 1 yıl içinde gelişebilir. Enfeksiyon cerrahi ile ilişkili görülür ve derin yumuşak dokuları, (fassia ve kas tabakaları) içerir. Derin insizyonel CAE Yüzeyel insizyonel CAE A more serious SSI is a deep incisional surgical infection, which extends past the superficial layer. The infection occurs within 30 days post-op only if no implant is left in place or within 1 year if implant is in place and the infection appears to be related to the operation and the infection involves the deep soft tissue, which include the fascia and muscle layers. Derin yumuşak doku (fassia & kas) Mangram AJ et al. Infect Control Hosp Epidemiol. 1999;20:

55 Organ/Boşluk CAE Enfeksiyon, implant yoksa cerrahiden sonraki 30 gün içinde gelişir; veya implant konmuşsa 1 yıl içinde gelişebilir. Enfeksiyon cerrahi ile ilişkili görülür ve cerrahi sırasında açılan/manipüle edilen insizyon dışında anatominin herhangi bir parçasını içerebilir. Yüzeyel insizyonel CAE Derin insizyonel CAE The most extensive of these surgical infections involves the organs and the space surrounding the organs. These infections can occur within 30 days post-op if no implant is left in place or within 1 year if an implant is in place and the infection appears to be related to the operation and the infection involves any part of the anatomy, other than the incision, which was opened or manipulated during the operation. Organ/boşluk CAE Organ/boşluk Mangram AJ et al. Infect Control Hosp Epidemiol ;20:

56 CAE – Yara Sınıflaması 1- TEMİZ YARA İnflamasyon olmayanSolunum,Sindirim,Genital Sistemlere veya Enfekte Üriner Sisteme girilmeyen 2- TEMİZ-KONTAMİNE Kontrollü olarak Solunum,Sindirim,Genital Sistemlere veya Üriner Sisteme girilen Sıradışı kontaminasyonun olmadığı

57 CAE – Yara Sınıflaması 3- KONTAMİNESteril teknik açısından problemli olan ameliyatlarda Sindirim sisteminden akıntı olan Akut pürülan olmayan inflamasyonlu yaralar 4- KİRLİ-ENFEKTE Cansız doku içeren Enfeksiyonlu, travmatize yaralardır

58 CAE – Yara Sınıflaması Sınıf 1 = Temiz Sınıf 2 = Temiz kontamineSınıf 3 = Kontamine Sınıf 4 = Kirli, enfekte Profilaktik Antibiyotik endike Surgical site infections are categorized into four classes depending on wound type. Class 1 is a clean wound, class 2 is a clean contaminated wound, class 3 is a contaminated wound, and class 4 is a dirty infected wound. Terapötik antibiyotik Mangram AJ et al. Infect Control Hosp Epidemiol. 1999;20:

59 CAE – Yara sınıfı vs NNIS SınıfıYara sınıfı Tüm NNIS 0 NNIS 1 NNIS 2 NNIS 3 Temiz 2.1% 1.0% 2.3% 5.4% N/A Temiz kontamine 3.3% 2.1% 4.0% 9.5% N/A Kontamine 6.4% N/A 3.4% 6.8% 13.2% Kirli enfekte 7.1% N/A 3.1% 8.1% 12.8% Tümü 2.8% 1.5% 2.9% 6.8% 13.0% This chart compares the wound class for surgical site infections with the NNIS classes. Although the risk of infection increases within the wound classification, it has been shown to be also dependant within each wound class on the NNIS classification. NNIS. CDC. Am J Infect Control. 2001;29:

60 CAE Önleme Yaklaşık 40%–60% CAE önlenebilirAmeliyatlarda fazla, az, uygunsuz, zamansız, yanlış antibiyotik kullanımı var. It is estimated that 40% to 60% of surgical site infections are preventable. The overuse, underuse, improper timing, or misuse of antibiotics occurs in 25% to 50% of operations. Mangram AJ et al. Infect Control Hosp Epidemiol. 1999;20:

61 Antibiyotik Profilaksi PrensipleriPreop uygulama, serum düzeyleri işlem boyunca yeterli, beklenen mikroorganizmalara karşı aktif antibiyotik Yüksek Serum Düzeyleri Preop zamanlama IV yol İlacın yüksek dozu İşlem süresinde Uzun yarı ömür Uzun işlemde ikinci doz Fazla kan kaybında yeni doz Süre Yara kapandıktan sonra verilmez En fazla 24 saat Mangram AJ et al. Infect Control Hosp Epidemiol. 1999;20:

62 Zamanlama Son zamanlarda yayınlanan bir meta analizde 250 klinik 4809 hastada profilaktik antibiyotik etkisi 23 cerrahi operasyonda araştırılmış. Is antibiotic prophylaxis in surgery a generally effective intervention? Testing a generic hypothesis over a set of meta-analyses. Ann Surg. 2009;49:551–556.

63 Zamanlama En iyi koruma insizyondan 30 dk önce yapılan antb görülmüş.Vancomycin ve diğer uzun etkili antb zamanlama farklı hastada koroner arter bypass, op da optimal vancomycin zamanı dakika.

64

65 Normal vücut ısısını koruCerrahi Enfeksiyon Önlenmesi Uygun antibiyotik kulan Alanı traş etme Oksijen basıncını optimize et Normal vücut ısısını koru Normal kan glukozunu koru

66 Tetanoz Özellikle toprakta yoğun bir şekilde bulunan, anaerob, spor yapan bir bakteri olan clastridium tetani’ninnyol açtığı mortlitesi yüksek klinik bir tablodur. Bilinen antiseptiklere dirençli olması dikkat çekicidir. Bir nörotoksin olan tetanospazmin salgılar. Bu madde kan yoluyla omurilik ön boynuzuna yerleşir ve hastalığı ana ögesi olan kas spazmlarına neden olur.

67 Tetanoz Opistotonus; bel,sırt, uyluk kaslarının spazmı ile baş ve topuklar yatağa değecek şekilde yatma poziyonu gelişir. Sfinkter spazmı ile beraber idrar ve dışkı retansiyonu gelişir. Sesli ve ışıklı uyarılar ile artan konvülziyonlar gelişir.

68 Tetanoz Ilk yapılacak şey yaranın temizliğidir.Yara bol su ve oksijenli suyla yıkanır. Nekrotik dokular ve varsa yabancı cisimler çıkarılır. Tetanoz açısı toksoid aşıdır. Pediatrik DT, yetişkin Td formları ve pediatrik DTaP, yetişkin TdaP formu bulunur(hem difteri toksoidi hemde aselüler boğmaca aşısı ile beraber) Yaranın özelliği, yaralanmadan sonra geçen süre, kişinin immun durumu göz önüne alınarak aşı ve/veya TIG uygulanabilir.

69 Travmalı hastada yaranın değerlendirilmesi

70 Aşı takvimi Tig; ünite

71 TEŞEKKÜR EDERİM