Department of Surgery Phramongkutklao Hospital

Surgical Infections

Pisake Boontham M.D., Ph.D.Department of Surgery

Phramongkutklao Hospital

Pathogenesis of Infection

•Host defences•Bacterial factors•Bacterial-host interaction•Immune response to infection

Host Defences

FEATURES OF INNATE AND ADAPTIVE IMMUNITY

Innate Immunity Adaptive Immunity

BarriersSkinMucosal epitheliumSecretions (skin surface, gut lumen)

IgA in gut lumen

Humoral components

LysozymeComplement components(C3a, C5a and C3b, C5b)Cytokines

Antibodies (IgG and IgM)Cytokines (Th1, Th2)*

CellsPhagocytic cells (mononuclear cells, polymorphonuclear cells)Natural killer cellsDendritic cells

Dendritic cellsT cells (helper*, cytotoxic, memory)B cells

*Th1: T helper (type 1) cells; Th2: T helper (type 2) cells

Humoral

Acute Phase proteins

Complement

Antibodies

Interferon

Cellular

Neutrophils

Macrophages

Nkcells

B – lymphocytes

T - lymphocytes

Physical Barriers

Skin

Mucus Membranes

Cilia

Gastric Acid

Tears

Urine

HOST DEFENCE SYSTEMS

Host Defences

IMMUNE RESPONSE TO INFECTION

IL-8

TNF-α

IL-1β IL-8

IL-6

The cells and mediators involved in a local acute inflammatory response

Bacterial Factors

• Virulence Factors–Cell Wall Antigens–Serum Resistance–Hemolytic Capability–Growth Dynamics–Iron Scavenging

• Adherence Factors–P Fimbriae–Type 1 Fimbriae–DR Fimbriae

Bacterial Factors

• Microorganisms show Pathogen-Associated Molecular Patterns (PAMPs), which can be recognized, by so-called ‘Pattern-Recognition Receptors’ (PRRs) by the host: example of PAMPs –LPS of Gram-negative bacteria –Glycolipids of mycobacteria –Peptidoglycans (PGs) and Lipoteichoic acids (LTAs) of

Gram-positive bacteria, –Mannans of yeast or fungi–Double-stranded RNAs of viruses –Unmethylated CpG motifs of bacterial DNA

Bacterial-Host Interaction

• Bacterial components activate host immune responses via PRRs, which called Toll-like receptors (TLRs)

• There are ten TLRs (1-10) had been studied.–TLR-1 TLR-2–TLR-3 TLR-4–TLR-5 TLR-6–TLR-7 TLR-8–TLR-9 TLR-10

Akira and Hashino, JID 2003

Microbial Ligands Recognized by TLR family

Cytokine Productions

Sequence of Immune Response

Adaptive Immune Response

SIRS

TRAUMA

BURNS

PANCREATITIS

INFECTION SEPSIS

BACTEREMIA

SEVERE SEPSIS

DEFINITIONS

• Systemic Inflammatory Response Syndrome (SIRS) ≥ 2 of the following:

•Temp > 38°C or < 36°C •Heart rate > 90 bpm•Respiratory rate > 20 bpm•WBC > 12,000, < 4,000 or bands > 10%

• SepsisSIRS + documented infection

Bone, et al. 1992. Chest 101:1644-1655

• Severe sepsis–Sepsis with organ dysfunction, hypoperfusion

or hypotension• Septic Shock

–Sepsis with hypotension and perfusion abnormalities despite adequate volume replacement

• MODS–Presence of altered organ function that need

intervention

Bone, et al. 1992. Chest 101:1644-1655

PATHOGENESIS OF SEPSIS

• Bacterial components (Cell wall)• Host immune responses; 3 major entities

–Cytokine cascade •Proinflammatory cytokines [T helper 1 (Th1)]•Antiinflammatory cytokines [T helper 2 (Th2)]–Mediators: NO, O2

-

–Apoptosis of immune and non-immune cells

ROLE OF CYTOKINES

• Sepsis is associated with the production of many cytokines including:

–Pro-inflammatory cytokines (early phase; SIRS)

: IFN-γ, TNF-α, IL-1β, IL-6, IL-8, IL-12

–Anti-inflammatory cytokines (late phase; CARS)

: IL-4, IL-10, IL-13

• Proinflammatory cytokines activate:–Biochemical systems

•Complement, coagulation, kinin, etc.–Endothelial cells–PMN / platelets–Release of secondary mediators

•NO, prostaglandins, vasoactive agents, endorphins, free-O2 radicals, etc.

ROLE OF CYTOKINES

Arya et al, AJS183 (2002); 268-273

CYTOKINE PROFILE IN SEPSIS

IL-8

• Stage 1. In response to injury / infection, the local environment produces cytokines

• Stage 2. Small amounts of cytokines are released into the circulation:• Recruitment of inflammatory cells• Acute Phase Response• Normally kept in check by endogenous anti-

inflammatory mediators (IL-10, PGE2, Antibodies, Cytokine receptor antagonists)

Bone, et al. 1996

Sequential Stages in Sepsis

Sequential Stages in Sepsis• Stage 3. Failure to control inflammatory cascade:

• Loss of capillary integrity• Stimulation of Nitric Oxide Production• Maldistribution of microvascular blood flow• Organ injury and dysfunction

• Stage 4. Compensatory anti-inflammatory response syndrome [CARS]:• Inappropriate and excessive anti-inflammatory responses• Immunosuppression• Multiple organs injuries• Significant morbidity and mortality

Bone, et al. 1996

Appropriate cytokineresponse

Inappropriate cytokineresponse

Low bacterial loadBalanced cytokine

Minimal SIRS

High bacterial loadExcessive cytokine

SIRS or CARS

ROLE OF CYTOKINES

CYTOKINES AND COAGULATION PATHWAY

Gut Liver Axis Theory

Rowlands BJ, 1999

Gut Liver Axis Theory

Rowlands BJ, 1999

Severe sepsis

Clinical hypoperfusion

Gut barrier dysfunction

Influx of bacterial products (e.g. QSSMs) into systemic circulation

Bacterial products inhibit host immunity

Dysfunction of host immunity

MODS

Tissue injuryApoptosis

Septic shock

Apoptosis

MODS

Bacteria Host immune cells

Bacterial products+Cytokines Apoptosis

Bacteria Host immune cells

Antibiotics

Anti-apoptosis

CytokinesApoptosis

Neutralization

Surgical Infection

• Infections that require operative treatment or result from operative treatment

Definition

Specific Surgical Infections

•Surgical Site Infections•Skin and Soft Tissue Infections •Intra-abdominal Infections•Sepsis•Organ specific Infections•Catheter Related Infections•Post-operative Nosocomial Infections

Surgical Site Infection (SSI)

DefinitionAn infection that occurs at the incision site within 30

days after surgery or within 1 year if a prosthetic implant is in place.

Nosocomial PathogensNNIS, Jan. 1990 - Mar. 1996

0

5000

10000

15000

20000

25000

30000

35000

40000

Urinary TractInfection

Surgical SiteInfection

BloodstreamInfection

Pneumonia Other Sites

Num

ber o

f Iso

late

s

Burke JP. N Engl J Med. 2003;348:651-656.

Systematic review of economic analyses of health care-associated infections: AJIC 2005;33:501 – 9.

Attributable costs of HAI

ระยะเวลาที่อยูโรงพยาบาลนานขึ้นเฉลี่ย 12.5 วัน

คายาตานจุลชีพ 4,544 บาท

Impacts of SSIs

Prevalence and Impacts of Nosocomial Infection in Thailand 2001J Med Assoc Thai 2005 Vol. 88 Suppl.10

CLASSIFICATION OF SURGICAL WOUNDS

CLEAN

Uninfected operative wounds in which no inflammation is encountered and the respiratory, alimentary, genital and uninfectedurinary tractare not entered.

CLEAN-CONTAMINATED

Operative wounds in which the respiratory, alimentary, genital or urinary tract is entered under controlled conditions and without unusual contamination.

CONTAMINATED

Includes open, fresh accidental wounds, operations with major breaks in sterile technique or gross spillage from the GI tract and incisions in which acute, non-purulent inflammation is encountered.

DIRTY

Old traumatic wounds with retained devitalised tissue and those that involve existing clinical infection or perforated viscera.

Deep soft tissue (fascia & muscle) Deep incisional

SSI

Superficial incisional SSI

Mangram AJ et al. Infect Control Hosp Epidemiol. 1999;20:250-278.

Subcutaneous tissue

Skin

Organ/space SSIOrgan/space

SSI rate in Thailand

Surgical Wound Classification

Risk พ.ศ.2531 (1)

พ.ศ.2535 (2)

พ.ศ.2544 (3)

Clean

Clean-ContaminatedContaminated

Dirty-Infected

1- 5 %

3-11 %

10-17 %> 27%

15.3 %

18.6 %

24.7 %

30.1 %

1.3 %

1.5 %

5.1 %

9.7 %

1.5 %

3.4 %

6.3 %

7.7 %

(3) Prevalence and Impacts of Nosocomial Infection in Thailand 2001J Med Assoc Thai 2005 Vol. 88 Suppl.10

(1) A National Prevalence Study on Nosocomial Infections 1988J Med Assoc Thai July 1989 Vol. 72 Suppl.2 :1-6.

(2) A National Study on Surgical Wound Infections 1992J Med Assoc Thai July 1995 Vol. 78 Suppl.2 :73-77.

NNIS risk index categoryKnight R, et al. Am J Surgery 182 (2001) 682–686

SSI rates of different types of procedures and risk index category

Procedures 75th percentile operation time (min)

NNIS risk index 0

NNIS risk index 1

NNIS risk index 2,3

Craniotomy 130 0.90 1.67 NA

Thyroid surgery 120 0.47 NA NA

Cardiac surgery 250 0.70 1.71 2.21

Other thoracic surgery 150 0.65 1.17 3.07

Vascular surgery 140 0.89 1.74 4.51

Mastectomy 140 1.80 2.48 NA

Inquinal hernia repair 60 0.77 1.90 3.77

Laparotomy 90 1.71 3.29 5.16

Cholecystectomy 60 0.68 1.93 3.33

Appendectomy 60 1.20 2.55 4.85

Gastric surgery 140 2.79 5.02 10.36

Small bowel surgery 140 5.20 7.33 9.38

Colon surgery 140 4.02 5.76 8.73,11.62

Nephrectomy 180 1.13 1.13 1.13

Open reduction of fracture 90 0.73 1.25 3.51

NNIS. CDC. Am J Infect Control. 2001;29:404-421.

American Society of Anesthesiologists(ASA)physical status

1 Normal2 Mild systemic disease3 Severe systemic disease4 Incapacitating systemic disease that

is a constant threaten to life5 Moribund, not expected to survive

for 24 hours with/without operation

SSI – Wound Class vs NNIS Class

Wound Class All NNIS 0 NNIS 1 NNIS 2 NNIS 3

Clean 2.1% 1.0% 2.3% 5.4% N/A Clean contaminated 3.3% 2.1% 4.0% 9.5% N/AContaminated 6.4% N/A 3.4% 6.8% 13.2%Dirty infected 7.1% N/A 3.1% 8.1% 12.8%

All 2.8% 1.5% 2.9% 6.8% 13.0%

NNIS. CDC. Am J Infect Control. 2001;29:404-421.

Risk Factors for Surgical Site Infections

Surgical/ Environmental

Factors

Microbial Factors

AgeProlonged preoperativestayInfection at distal siteMorbid ObesityMalnutritionCancerDiabetesASA classDisease severityImmunosuppression

Nasal/skin carriageVirulenceAdherenceInoculum

Abdominal siteWound classificationDuration of surgeryType of procedureHair removalIntraoperative contaminationProphylactic antibioticsSurgical techniqueSurgical volumeMultiple operationsPoor hemostasisDrain/foreign body Dead spaceUrgency of surgeryHypothermiaOxygenation

Host Factors

Roy MC, et al. Infect Control Hosp Epidemiol 1997;18:659-68.

Possible Risk Factors for Postoperative Wound Infections

Host Factors

• Age• Gender• Severity of disease• ASA physical status

classification• Immunocompromising

disease

• Diabetes mellitus• Estimated prognosis• Nutritional status• Serum albumin• Weight• Presence of other

infections• Duration of preoperative

stay

Effect of Aging on Surgical Site Infection

10-year, prospective, cohort studyN = 144,485 patients undergoing surgical proceduresAge ranged from 17 to 108 years

Age was a strong predictor of infection between 17 and 65 years, the rate of infection increased (~ 1%) per decade peaking at 65 years

At 65, the risk of SSI actually decreased in a linear manner for each additional year;

candidate for less risky selected surgical procedures – low risk procedureshardy survivor effectless likely to detect an infection in this patient population

Kaye KS. J Infect Dis 2005;191:1056-1062

Hyperglycemia: Diminished Phagocytic Cell Function

Rayfield et al, Am J Med 1982; 72: 439-450

Hyperglycemia: Impaired Wound Healing - Collagenase

Hennessey et al, J Pediatr Surg 1990; 25: 75-78

Link Between High Blood Glucose and Poor Outcomes: Potential Mechanisms

Copyright 2004 American Diabetes Association. From Clement S, et al. Diabetes Care.2004;27:553–591. Reprinted with permission.

Immune dysfunction Reactive O2 species

Secondary mediators

Transcription factors

Metabolic stress response↑ Stress hormones and peptides

GlucoseInsulin

Infection dissemination

FFAKetonesLactate

Cellular injury/apoptosisInflammationTissue damageAltered tissue/wound repairAcidosisInfarction/ischemia

Prolonged hospital stayDisabilityDeath

Perioperative Glucose Control

0

5

10

15

20

<200 200-249 250-299 >300

% In

fect

ions

Latham R. Infect Control Hosp Epidemiol. 2001;22:607-12

*1,000 cardiothoracic surgery patients

SSIs Reduced By Tight Peri-op Glucose Control

Type of SurgeryType of Surgery PrePre--Tight Tight glycemic controlglycemic control

Post_Tight Post_Tight Glycemic ControlGlycemic Control

CardiothoracicCardiothoracic 4.6%4.6% 2.5%2.5%

VascularVascular 1.9%1.9% 0.83%0.83%

Hip replacementHip replacement 1.0%1.0% 0.7%0.7%

Knee Knee replacementreplacement

1.1%1.1% 1.0%1.0%

BariatricBariatric 17.9%17.9% 5.3%5.3%

Morris Brown MD, Henri Ford Hospital,Morris Brown MD, Henri Ford Hospital,International Anesthesia Research SocietyInternational Anesthesia Research Society

Possible Risk Factors for Postoperative Wound Infections

Surgery Factors

• Emergency vs elective procedure

• Hair removal technique• Hand washing• Surgical skin prep• Perioperative

antibiotics• Site of surgery• Operating room

environment

• Increased O2 tension• Normothermia• Surgeon• Duration of surgery• Drains• Packs & Drapes• Glove puncture• Primary or secondary

closure• Iatrogenic

Hair Removal and SSI

• Presence of hair does not does not increase SSI• Razor blades increase SSI• Hair removal with clippers was found to be safer

and result in a lower incidence of SSI• Hair removal closer to incision time decrease SSI

compared to hair removal the night before surgery.

Alexander et al, Arch surg 1983, 118(3): 347

Shaving, Clipping & SSI

0

0.5

1

1.5

2

2.5

Shave Clip Neither

% Infected

Cruse. Arch Surg 1973; 107:206

Ability of Hand Hygiene Agents to Reduce Bacteria on Hands

99.9 3.0

99.0 2.0

90.0 1.0

0.0 0.0

Baseline

Bac

teria

l Red

uctio

n% log 0 60 180 minutes

Plain soap

Antimicrobial soap(4% Chlorhexidine)

Alcohol-based handrub(70% Isopropanol)

Hosp Epidemiol Infect Control, 2nd Edition, 1999

Time after disinfection

Agent Action Gram + Gram - Tbc Fungi Virus Rapidity Residual

activity

toxicity

Alcohol Denature

protein

E E G G G Most rapid None Drying,

Volatile

Chlorhexidine Disrupt cell

membrane

E G P F G Intermediate Excellent Ototoxic,

Keratitis

Iodine /

Iodophore

Oxidation /

substitution

by free

iodine

E G G G G Intermediate Minimal Absroption

from skin,

Irritation

Chlorhexidine

/ Alcohol

Denature

protein

E E G G G Most rapid Excellent Ototoxic,

Keratitis

E-excellent; F-fair; G-good

200000

180000

160000

140000

120000

100000

80000

60000

40000

20000

0

Hallux

Tota

l num

ber o

f bac

teria

l col

onie

s

Toes Controls

Ostrander RV. J. Bone Joint Surg. Am. 2005;87:980-985

Effects of Skin Preparative Agents in Foot and Ankle Surgery

Chlorhexidine /alcohol

Iodophor /alcohol

Chloroxylenol

Antibiotic Prophylaxis

Goals of Surgical ProphylaxisPrevent postoperative infection of the surgical sitePrevent postoperative infectious morbidity and mortalityReduce duration and cost of health careProduce no adverse effectsHave no adverse consequences for the microbial flora of patient or hospital

Probability of Wound Infection

Houang ET, et al. J Hosp Infect 1991;19:181-9.

Guidelines of prophylactic antibiotics

Recommended in:

Some Clean wound*Clean-contaminated woundContaminated woundDirty wound

Documented beneficialin clean wounds

Prosthesis is insertedVascular surgeryNeurosurgeryBone is incised (craniotomy,

sternotomy)High risk patients e.g. old,

DM, co-morbidityControversy on cases of clean surgery of soft tissues (eg,

breast, hernia)

Barie PR, et al. Surg Clin N Am 2005;85:1115–35.

Mangram AJ, et al. Infect Control Hosp Epidemiol 1999;20:247–80.

Which Antibiotics?1st-gen cephalosporin is the preferred agent Clindamycin and vancomycin preferred for patients with a history of anaphylaxis to penicillin*No evidence of routine use of vancomycin for prophylaxisVancomycin prophylaxis is appropriate only in institutions where the incidence of MRSA infection is high (>20% of all SSIs caused by MRSA)Vancomycin should be considered for prophylaxisin patients with known MRSA colonization


*Bratzler DW, et al. Am J Surg 2005;189:395–404.

Procedure-Specific Recommendations for Prophylaxis Procedure Likely organisms Recommended antibiotic Adult dose Cutaneous S. aureus, S. epidermidis No uniform recommendation Head and neck S. aureus, streptococci Cefazolin 1 to 2 g IV Neurosurgery S. aureus, S. epidermidis Cefazolin 1 to 2 g IV Thoracic S. aureus, S. epidermidis Cefazolin 1 to 2 g IV Cardiac S. aureus, S. epidermidis Cefazolin 1 to 2 g IV Gastro-intestinal-Appendectomy

Gram-positive cocci, enteric gram-negative bacilli

High risk: cefoxitin or cefminox Alternative: ampicillin/sulbactam

amoxicillin/clavulanic acid

1 to 2 g IV 3 g IV1.2 g IV

Colorectal Enteric gram-negative bacilli, anaerobes

Oral: neomycin + erythromycin Parenteral: cefoxitin or cefminox Alternative: ampicillin/sulbactam


1 g oral x 3 1 to 2 g IV3 g IV

1.2 g IV

Biliary tract Enteric gram-negative bacilli High risk: cefoxitin or cefminox Alternative: ampicillin/sulbactam


1 to 2 g IV 3 g IV1.2 g IV

Ob-Gynecologic Enteric gram-neg bacilli, anaerobes Cefazolin, cefoxitin or cefminox 1 to 2 g IV

Urologic S. aureus, enteric gram-neg bacilli High risk: ciprofloxacin 400 mg IV

Orthopedic S. aureus, S. epidermidis Cefazolin 1 to 2 g IV

Vascular surgery S. aureus, S. epidermidis Cefazolin 1 to 2 g IV

Breast and hernia S. aureus, S. epidermidis High risk: cefazolin 1 to 2 g IV

The Medical Letter; Dec 2006:83-88

The Medical Letter; Dec 2006:83-88

SSI Rates by Time of Antibiotic Administrations

0

1

2

3

4

5

6

>2 2 1 1 2 3 4 6 7 8 9 >10

SSI R

ate

Classen DC, NEJM 1992; 326:281-6

Single vs Multiple Dose Surgical Prophylaxis: Systematic Review

McDonald. Aust NZ J Surg 1998;68:388

0.01

0.1

1

10

100

All

stud

ies,

fixe

dA

ll st

udie

s, ra

ndom

Mul

ti >

24h

Mul

ti <

24h

Favo

rs m

ultip

le d

ose

Favo

rs s

ingl

e do

se

Antimicrobial DosingAgents Renal half-life, h Infusion

durationStandard

doseWeight-adjusted

Redosinginterval, h

normal ESRD

Cefazolin 1.2–2.5 40–70 3–5 min 1–2 g iv 20–30 mg/kg (>80 kg, 2 g)

2–5

Cefuroxime 1–2 15-22 3–5 min 1.5 g iv 50 mg/kg 3-4

Cefoxitin 0.5–1.1 6.5–23 3–5 min 1–2 g iv 20–40 mg/kg 2-3

Clindamycin 2–5.1 3.5–5.0 10–60min (not>30 mg/

min)

600–900mg iv

<10 kg, at least 37.5mg; >10

kg, 3–6 mg/kg

3–6

Vancomycin 4-6 44.1–406.4

1 g > 60min

1 g iv 10–15 mg/kg (adult)

6-12

Dale W, et al. Clin Infect Dis 2004;38:1706–45.

Principles of Antibiotic Prophylaxis


Preop administration, serum levels adequate throughout procedure with a drug active

against expected microorganisms.

High Serum Levels1. Pre-op timing2. IV route3. Highest dose

of drug4. Long half-life

Re-doses when:1. Operation time

more than 2 half-life of drug

2. Long procedure3. Large blood loss

Duration1. None after wound

closed2. 24 hours maximum

Prolongation of Antibiotic Prophylaxis

Harmful and no benefitClostridium difficile-associated diseaseIncreases ris k of later nosocomial infections unrelated to surgical site

Pneumonia and catheter-related infection

Emergence of multi-drug resistant pathogensMRSA, ESBL

StaphylococcusStreptococcusStaphylococcusStaphylococcusStreptococcusStreptococcus

Gram-negative

bacilli

Gram-negative

bacilliAnaerobesAnaerobes

Distribution of Bacteria from Superficial to Deep Infection

Superficial infection

Deep infection

Microorganism of SSI

Major Pathogen in SSI%

of i

nfec

tions

NNIS 2003

Microbiology of SSI in Ramathibodi Hospital (47 isolates)

MRSAEnterococci

A. baumanniiP. aeruginosa K. pneumoniae (inc. ESBL)E. coli (inc. ESBL)Proteus spp. Stenotrophomonas spp.Enterobacter spp. (ESBL)

Treatment of SSI

Incision and drainage and evacuate infected material of the SSITissue specimens or pus collected aseptically (no routine swabs of fluid)Antibiotics is not required for uncomplicated SSI

Minimal surrounding evidence of invasive infection and minimal systemic signs of infectionObservation-dressing changes-opening the incision site

Antibiotics may be indicated in SSI with the presence of systemic toxicity


Stevens DL, et al. Clin Infect Dis 2005;41:1373-405.

Empiric Antibiotic Therapy

Findings of Gram stain and results of culture of the wound contentsType and site of surgeryResident flora of surgical environmentColonization flora of specific hospitalStatus of patients’ immune system


Coverage against gram-positive cocci is indicated in most circumstances

Antibiotic Treatment Regimens

Type of infection Common infecting bacteria Antibiotic therapy

Superficial wound and surgical incisioninfections

Strep, staph Not used routinely; if needed, 1st

gen ceph or oxacillin

Deep wound infections other than GI, female genital tract, or oropharyngealsurgery

Strep, staph, Gram- negative enteric bacteria

1st-gen ceph or cloxacillin; if mixed infections are suspected, 2nd or 3rd

gen ceph or amoxicillin/clavulanate, ampicillin/sulbactam, or piperacillin/tazobactam (imipenem or meropenem)

GI, female genital tract, or oropharyngeal surgery

Same as for other deep wound infections, with addition of Bacteroides species, other anaerobes,enterococci

Same as for mixed infection, above

Nichols RL, et al. Clin Infect Dis 2001;33:S84-93.

SSI organism Antibiotic susceptibilityStaphylococcus aureus •90% remain susceptible to cloxacillin,

macrolides and clindamycin Skin wound at any site

Beta-haemolytic streptococci

•90% remain susceptible to penicillins, macrolides and clindamycin

Head and neck surgery

Oral anaerobes •95% remain susceptible to metronidazole and amoxi/clav. •Penicillin can no longer be relied upon.

Anaerobes •95% remain susceptible to metronidazole and amoxi/clav.

Abdominal surgery

E. coli and other enterobacteriaceae

•Complex resistance problems. However, 90% of E. coli remain susceptible to 2nd generation cephalosporins or BL/BIs, or gentamicin

Insertion of a prosthesis, graft or shunt

Coagulase negative Staphylococci (CNS)Staphylococcus aureus

•90% of S. aureus remain susceptible to cloxacillin, macrolides or clindamycin. Although 2/3 of CNS are methicillin-resistant, prophylaxis with beta-lactam antibiotics is still appropriate.

►

Environmental controlsOperating room environment

Maintain > 15 air changes per hour Maintain positive-pressure ventilation with laminar flowFilter all air, recirculated and fresh, through the appropriate filters Keep operating room doors closed

►

• Double-blind, randomized, controlled trial• 3 hospitals (2 in Austria, 1 in Germany)• N=500, colorectal resection (cancer, IBD)• July 1996-October 1998• FiO2 0.8 vs 0.3 during and 2 hours postop• SSI during 14 days postop

Greif R et al. Greif R et al. N Engl J MedN Engl J Med. 2000;342:161. 2000;342:161--167.167.

Greif R et al. Greif R et al. N Engl J MedN Engl J Med. 2000;342:161. 2000;342:161--167.167.

Supplemental Perioperative Oxygen and the Risk of Surgical Wound Infection

A Randomized Controlled Trial

• Double-blind, randomized, controlled trial• 14 Spanish Hospitals• N=300,Colorectal surgery, general anesthesia• March 2003- October 2004• FiO2 0.8 vs 0.30 during and 6 hours postop• SSI : 35 (24.4%) vs 22 (14.9%), p=0.04

Belda et al, JAMA, 2005; 194: 2035

Hypothermia

Low Oxygen TensionVasoconstriction

↓Oxidative Killing by neutrophils

↓Collagen deposition

Impaired immune function

Effects of Hypothermia and Hypoxia on Wound Healing

Perioperative normothermia

Normothermic Hypothermic Temperature 36.6+0.5 34.7+0.6 Infections (%) 6 19 Hospitalization (Days)

12.1+4.4 14.7+6.5

Melling et al., Lancet 2001;358:876

*200 colorectal surgical patients

Clinical Wound Infections

Blood transfusion–Avoid blood transfusion

–Prospective cohort study 2003: transfusion of more than 4 units of packed red blood cells was associated with a 9.28-fold increased risk of infection

Hill GE, et al. J Trauma 2003;54:908–14.

SurgeonHand washingGloves: double gloves

20% of surgical gloves fail during operationOther barriers

CapsMasksGowns

0

10

20

30

40

50

60

cfu/

m3

90 minutesTest Interval

180 minutes

No Mask - HealthySurgical Mask - HealthyNo Mask - RhinorrheaSurgical Mask - Rhinorrhea

Impact of Surgical Masks on Prevention of Microbial Nasopharyngeal Shedding in Healthy Individuals (N = 22)

and Subjects with Symptoms of Rhinorrhea (N = 8)

NS

NS

p<0.05

p<0.05

Edmiston et al, Surgery 2005; 138:572-583

Surgical techniquesGentle tissue handlingRemoval of devitalized tissue or blood or other substancesUsing drain appropriatelyAvoid extensive cauterizationAvoid anastomosis of intestine under tension

Postoperative wound care

• Sterile dressing for 24-48 hrs postoperatively

• Wash hands before and after dressing changes

• Changed with sterile technique

• Educate patient and family regarding proper incision care, symptoms of SSI, and need to report

PreoperativeIntraoperativePostoperative Surveillance


AimsReduce the inoculums of bacteriaImprove the host defences

Infection surveillance

Good surveillance program lowered wound infection rate from 4.9 to 1.9 %

Mangram AJ, et al. Infect Control Hosp Epidemiol 1999;20:247–80.

Thank you

Documents

Department of Surgery Phramongkutklao Hospital