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Awareness to Surgical Site Infection

Teddy O.H. Prasetyono I.C.T.E.C (Indonesian Clinical Training and Education Center) RSCM/ FKUI

Disclosure

Wound Microbiology
Wounds prone to potential infection, but not always infected Stages of condition related to the existance of microbes:

1. Contaminated 2. Colonized 3. Infected


Chronic wound is always contaminated

Colonized wound
Normal flora grows without any clinical sign and symptoms

Infected wound
Bacteria is growing fast with clinical sign of tissue destruction

Infection is tissue destructive and prevents wound healing

By time, normal flora will be substituted by the existence of anaerobic bacteria and even poly-microbes

Cut off point of infection is CFU > 106 per gram tissue

Infection depends on
a. Quantity of bacteria
(Enterococcus and Candida need to be many, but other solitaire specific bacteria will be dangerous hyaluronidase, toxin)

b. Potential (virulensi) (those produce c. Host resistance (depends on local and systemic
factors)

Determinants for infection


host resistance bacterial quantity and virulence

bacterial balance biofilms


Sibbald et al (2000) Dow (2001)

always consider any underlying pathology

SEMMELWEIS
mortality and puerperal sepsis Hand washing before delivery: 1846 1848 11.4% 1.3%

SURGICAL SITE INFECTION


CDC defines as: An infection that occurs at an incision site, or

any part of the anatomy that was opened or manipulated during the procedure
Occurs within 30 days after surgery, or within

1 year in the presence of an implant.

The data

SSI
Can be as high as 15% (of HAI) Depends on indications, site, approach, and instrumentation

Olsen MA, Nepple JJ, Riew KD, Lenke LG, Bridwell KH, Mayfield J, et al. risk factors for surgical site infection following orthopedic spinal operations. J Bone Joint Surg Am. 2008; 90A: 62-9. Roy MC, Perl TM. Basics of surgical site infections surveillance. Infect Control Hosp Epidemiol. 1997; 18: 659-68.

Classification of SSI
According to anatomical location and pathophysiological changes Involving skin, subcutaneous tissue, and deep soft tissue
Horan TC, Gaynes RP, Martone WJ, Jarvis WR, Emori TG. CDC definitions of surgical site infections, 1992: a modification of CDC definitions of surgical wound infection. Infect Control Hosp Epidemiol. 1992;13: 606-8.

Classification of SSI
Superficial incisional SSI Deep incisional SSI Organ space SSI

Superficial SSI
Within 30 days, involving skin or subcutaneous tissue Plus one of the following Purulent drainage Organism isolated from culture At least one: pain, swelling, redness, heat, incisions is deliberately opened

Superficial SSI
The following conditions are not SSI Stitch abscesses (minimal inflammation and discharge confined to the points of suture penetration) Infection of an episiotomy or neonatal circumcision Infected burn wound

Deep SSI
Within 30 days or 1 year related to implants Related to the procedure Involved deep soft tissue, e.g. fascia, muscle

Deep SSI
Plus one of the following Purulent drainage from incision but not from organ/space Spontaneously dehisces or deliberately opened Abscess or infection found on direct exam, histopathologic, or radiologic exam

Organ space SSI


Organ space infection Occurs within 30 days or 1 year with implant Involves anatomic structures not opened or manipulated during the operation and at least one of the following: Purulent drainage from drain placed in space Organisms isolated from fluid from space Identification of abscess at subsequent procedure Diagnosis by surgeon or physician

Risk Factors for SSI


Wound classification National Nosocomial Infections Surveillance

(NNIS) score (depends on wound class, duration of surgery, ASA)


Patient-associated factors Procedure-associated risk factors

Consequences of SSI
Extended hospitalisation of the patient (9.8 days in Europe) Readmission rates to hospital increased Increased care costs (for items such as prescriptions); average 325/day
Gottrup F, Melling A, Hollander DA. An overview of surgical site infections: aetiology, incidence, and risk factors. EWMA J. 2005; 5(2): 11-5.

Consequences of SSI
Delayed on-going treatments Decreased confidence in healthcare setting from local population - audit results in the public domain

Signs of local infection

Signs of local infection


Excessive amount of exudate Sign of inflammation (rubor, kalor, dolor,
edema, nyeri)

Barriers to Healing: Infected Wounds


Is the wound infected?
Local Signs & Symptoms
nPain nP eriwound skin is reddened nPeriwound skin is warm in touch nPeriwound skin or limb is

Systemic Signs & Symptoms


nFever nM alaise nIncreased white blood cell count

oedematous nPeriwound skin is indurated (hard) or macerated nPurulent exudate (green,yellow,..) nExudate has a foul odour

* N.B. To suspect infection, most of the local and systemic S&S listed here need to be present. Reddened periwound skin and fever alone may be a sign of the inflammatory phase of healing.

Micro-biology specimen to be taken in the form of sample of tissue or pus

Wound

Infection

Antimicrobial Therapy

Antibiotics

Antiseptics ?

Non antibiotics or Non chemically active agents

Discuss this . . .

An(sep(cs
Jenis An(sep(k Keterangan An8sep8k kulit praoperasi Dapat digunakan untuk mukosa Kontak yang lama akan menyebabkan luka bakar kimiawi - Ha8-ha8 jika digunakan pada pasien dengan riwayat hipersensi8tas iodin Riwayat penyakit 8roid Riwayat penggunaan lithium

Povidon Iodin (aqua) - Povidon iodin 10% b/v, kompleks - iodin & polivinilpirolidon -

Tinktur Iodin Iodin 0,5% dalam isopropil alkohol 70%

- - -

An8sep8k kulit praoperasi Mudah terbakar Mengandung preparat iodin

Chlorhexidin aqua Chlorhexidin glukonat 0,05% b/v

- - -

Chlorhexidin alkohol - Chlorhexidin glukonat 0,05% b/v dalam isopropil alkohol 70% - -

An(sep(k praoperasi Larutan (dak stabil Hanya untuk kulit luar, (dak untuk mukosa An8sep8k praoperasi atau bahan pencuci tangan Dapat terbakar Hanya untuk kulit luar, 8dak untuk mukosa

Chlorhexidin + cetrimid Chlorhexidin glukonat 0,015% b/v dalam cetrimid PhEur 0,15% b/v

chlorhexidine polyhexamethylene polyhexanide aqueous and alcoholic biguanides

povidone iodine

aqueous and alcoholic

triclosan

aqueous and suture coating

hexachlorophane cetrimide benzalkonium

aqueous phenolic aqueous cationic surfactant

We cant do without them

Although reports of resistance are limited, misuse and abuse of an8sep8cs must be avoided.

Moisture control

Exudate management Maintaining moist environment

Do not depend only on an8sep8cs for wound treatment!

Antiseptic dressings

Reduce bioburden and impact of bacteria on healing Debridement with lower toxicity than hypochlorites Aid in infection control (act as a barrier?)

Antiseptic dressings

Reduce infection and associated costs Action on biofilms can we define them?

Bacterial killing
(resistance)

antibiotics are specific


.cell wall, nucleus, DNA

antiseptics are not


..all cell components

An(bio(cs
Bacterial load has a direct impact on wound healing The management of the bacterial load by either local or systemic therapy is important in wound management

There is no existing evidence to support the use of systemic antimicrobial agents for chronicwound healing
Meara SO, Cullum N, MajidM, Sheldon T. Systematic review of wound care management: (3) antimicrobial agents for chronic wounds; (4) diabetic foot ulceraton. Health Tech Asses. 2000; 4(21)

Conservative treatment, including prolonged, culture-guided parenteral and oral antibiotics, is successful without amputation in a large proportion of diabetic patients admitted for a foot skin ulcer or suspected osteomyelitis
Pittet D, Wyssa B, Herter-Claver C, Kursteiner K, Vaucher J, Lew D. Outcome of diabetic foot infections treated conservatively. Arch Intern Med. 1996 Apr; 159: 851-6.

The development of an8bio8cs during the 20th century marked the decline of many former remedies, but the emergence of an8bio8c resistant strains of pathogens has led to the need to nd alterna8ve treatments.

MRSA and HAIs (mostly SSIs) (caused by antibiotic abuse?)

Largest epidemic of modern times


HAIs cause 50,000 deaths/year 5-6 district general hospitals 7-8000 bacteraemias MRSA
(UK by Leaper)

Why do Patients Still Die of Infection?

Overuse of powerful antibiotics Mis-targeting of broad-spectrum empiric therapy Inadequate source control Delayed onset of therapy Increased incidence of side effects Few options for drug-resistant infections Increasing prevalence of resistant pathogens

Micro-organisms causing SSI


(all categories 2002-07; HPA England data)
Anaerobic cocci 2% Anaerobic bacilli 2% Streptococcus spp. 3% Other bacteria 6% Pseudomonas 9% Acinetobacter spp. 1%

synergy opportunists contaminants and transients host defence


MRSA 25%

MSSA 14% Enterococcus spp 9% CNS 9% Enterobacteriaceae 21%

Num ber of organism s = 4034

biofilm production

SSI care bundle

Preoperative Phase
Give antibiotic prophylaxis to patients before:

clean surgery involving the placement of a prosthesis or implant clean-contaminated surgery contaminated surgery dirty surgery (?)

Consider single dose!

Methods to reduce bacterial resistance


Outbreak management Terminal room cleaning
o o o In-service housekeeping Utilization of check lists for cleaning All surfaces (high touch surfaces, lights, equipment, walls, etc) cleaned

Rupp ME. Infect Control Hosp Epidemiol 2001;22:301-303 Falk PS. Infect Control Hosp Epidemiol 2000;21:575-582 Sehulster LM, HICPAC Guidelines for Environmenatal Infection Control in Healthcare Settings

Methods to reduce bacterial resistance


Outbreak management Terminal room cleaning
o o Quaternary ammonium disinfecting solutions Change of curtains

Contact isolation
o Unit-wide isolation of all patients

Rupp ME. Infect Control Hosp Epidemiol 2001;22:301-303 Falk PS. Infect Control Hosp Epidemiol 2000;21:575-582 Sehulster LM, HICPAC Guidelines for Environmenatal Infection Control in Healthcare Settings

I.C.T.E.C RSCM/ FKUI