What is new in

management of
Surgical Infection
Prof. Ravi Kant
Contents:

 Introduction
 Types of surgical infections
 Definition of SSI
 Types SSI
 Recent management of SSI
 sepsis
 Peritonitis
Soft tissue/wound Infictions.

 Third most reported nosocomial

infections
 16% of all reported nosocomial
infections
 Most common surgical patient
nosocomial infection (38%)
Soft tissue/wound Infictions.
 2/3 involved surgical incision
 1/3 deep structures accessed
by incision
 Deaths in patients with
nosocomial infections—77%
related to infection.

EWMA Journal 2005; 5(2): 11-15.

 Introduction

 < 1900= 70-80% mortality for

wound infection
 >1900: Ignaz Semmelweis and
Joseph Lister = antiseptic surgery
 Introduction

 Surgery, trauma, non-trauma

local invasion can lead to
bacterial insult.
 Once present, bacteria, initiate
the host defense processes.
 Inflammatory mediators
(kinins, histamine, etc.) PMN’s
arrive, etc.
 Introduction

 Surgical infections
 surgical wound itself or in

 other systems in the patient.

 They can be initiated not only by

“damage” to the host but also
by changes in the host’s
physiologic state.
 Infections
 Twomain types
 Community-Acquired

 Hospital-Acquired
 Community-Acquired

 Skin/soft tissue
 Cellulitis: Group A strep

 Abcess/furuncle: Staph aureus

 Necrotizing: Mixed

 Hiradenitis suppurativa:Staph aureus

 Lymphangitis: Staph aureus

Cellulitis
Furuncle
Necrotizing
Hiradenitis
Lymphangitis
Breast Abscess
Peri-rectal abscess
Gas Gangrene
Paronychia
Diabetic foot infection
 Biliary Tract
 Usually result from obstruction
 Usual suspects:

E. coli, Klebsiella, Enterococci

 Acute Cholecystitis

 GB empyema
 Ascending cholangitis
 Community-Acquired

 Viral

 Hepatitis

 HIV/AIDS

 Tetanus
 Hospital-Acquired

Post-operative
 At the surgical site

 Systemic.
 Infected Vascular Graft

 Inguinal incision is independent risk

factor
 Length of case and blood loss
 Prosthetic grafts 10%-20%
 S. Aureus
 Gas gangrene

 Beta hemolytic strept

 Clostridial perfringes (gram pos
rods) rare
 50% polymicrobial
 Rapid lysis of tissues with relatively
little response from host
 Endotoxin
 Gas gangrene

 Aggressive debridement &

antibiotics
 Repeat antibiotics
 Catheter Sepsis

 80% of cases, colonized catheters

had been inserted by inexperienced
and experienced residents
 Key is to identify before sepsis
develops
 Stapylococcus epidermis, S. Aureus,
yeast
 Burn Infections

 Necrotic tissue readily colonized

 High bacteria counts are NOT

a reliable indication of an infected burn

 Histological examination to determine
invasiveness
 TX: debridement and antibiotics
 Hospital-Acquired

 Pulmonary
 Pneumonia
Non-ventilator associated

Ventilator associated

Aspiration
 Hospital-Acquired

 Urinary Tract
 Diagnosis

 Usual suspects

Pseudomonas, Serratia,
other
 Hospital-Acquired

 Foreign-body associated
 Sites

Catheters

Lines

Prosthetics/grafts
 Hospital-Acquired

 Wound infection & SSI.

Surgical wounds are healing
by
 1) Primary intention
 2) Secondary intention

 3) Delayed primary intention

 Incidence of SSIs →closure/delayed
closure of an infected wound
Opening and re-closure times Re-infection
rate %
Opening and re-closure at 50
once
Opening and re-closure after 20
two days
Opening and re-closure after 5
four days
Opening and re-closure after 10
nine days
[Gottrup, F. Wound healing and principles of wound closure. In: Holström H, Drzewieck KT (Eds).
The Scandinavian Handbook of Plastic Surgery. Malmoe: Studenterliteraturen, 2005
 Definition of SSI

 The CDC : =< 30 days of

surgery (or within a year in
the case of implants)

Mangram . Guideline for prevention of surgical

site infection, 1999. Infect Control Hosp Epidemiol 1999;
 classificationincisional
surgical site infections

 Superficial

 Deep

 Organ/space
 superficial incisional
surgical site infections
< 30 days of procedure
 involve only the skin or
subcutaneous tissue around
the incision.

Mangram . Guideline for prevention of surgical

site infection, 1999. Infect Control Hosp Epidemiol 1999
 Deep incisional surgical
site infections
 < 30 days of procedure (or one
year in the case of implants)
 are related to the procedure

 involve deep soft tissues, such

as the fascia and muscles.

Mangram . Guideline for prevention of surgical

site infection, 1999. Infect Control Hosp Epidemiol 1999
 ASEPSIS WOUND
SCORING SYSTEM

[ Wilson AP, Lancet 1986

 Southampton wound
scoring system

[Bailey IS, BMJ 1992; 304: 469-71

 Risk Factors

 Surgical factors
 Patient-specific factors

 local

 systemic
 Factors influencing SSIs
Patient Risk Factors

 Local:  Systemic:
 High bacterial  Advanced age
load  Shock

 Wound  Diabetes

hematoma  Malnutrition
 Alcoholism
 Necrotic tissue
 Steroids
 Foreign body
 Chemotherapy
 Obesity
 Immuno-
compromise
 Factors influencing SSIs

Antibiotics
 Prophylactic

 Therapeutic
 Factors influencing SSIs

Surgical Risk Factors

 Type of procedure

 Degree of contamination

 Duration of operation

 Urgency of operation

 skin preparation

 operating room environment

 Antibiotic prophylaxis
EWMA Journal 2005; 5(2): 11-15.
Wound class Definition Example Infection
rate (%)
Clean Nontraumatic, elective Mastectomy 2%
surgery. GI tract, Vascular
respiratory tract, GU tract Hernias
not entered
Clean- Respiratory, GI, GU tract Gastrectomy < 10%
contaminated entered with minimal Hysterectomy
contamination
Contaminated Open, fresh, traumatic Rupture appy 20%
wounds, uncontrolled Emergent
spillage, minor break in bowel resect.
sterile technique
Dirty Open, traumatic, dirty Intestinal 28-70%
wounds; traumatic fistula
perforation of hollow resection
viscus, frank pus in the
field
Berard F, Gandon J, Ann Surg 1964
Reduce hemoglobin A1c levels
to <7% before operation
Evidence
 Class II data
References
 Anderson DJ, Kaye KS, Classen D, et
al. Strategies to prevent surgical site
infections in acute care hospitals.
Infect Control Hosp Epidemiol 2008;
Smoking cessation 30 d
before operation
Evidence
 Class II data
References
 Anderson DJ, Kaye KS, Classen D, et
al. Strategies to prevent surgical site
infections in acute care hospitals.
Infect Control Hosp Epidemiol 2008
Remove hair only if it will interfere with
the operation; hair removal by clipping
immediately before the operation or
with depilatories; no pre- or
perioperative shaving of surgical
Evidence
 Class I data
References
 Kjønniksen I. Preoperative hair removal–
 a systematic literature review. AORN J
2002
Use an antiseptic surgical scrub
or alcohol-based hand antiseptic
for preoperative cleansing of the
operative team members’ hands
and forearms
Evidence
 Class II data
References
 Anderson DJ. Strategies to prevent
surgical site
 infections in acute care hospitals.
Infect Control Hosp Epidemiol 2008;
Prepare the skin around the
operative site with an appropriate
antiseptic agent, including
preparations based on alcohol,
chlorhexidine, or iodine/iodophors
Evidence
 Class II data
References
 Anderson . Strategies to prevent
surgical site
 infections in acute care hospitals.
Infect Control Hosp Epidemiol 2008;
Administer prophylactic antibiotics
for most clean-contaminated and
contaminated procedures, and
selected clean procedures use
antibiotics appropriate for the
potential pathogens
Evidence
 Strong Class I data
References
 Springer R. The Surgical care
improvement project-focusing on infection
control.Plast Surg Nurs 2007;
Administer prophylactic antibiotics within
1 h before incision (2 h for vancomycin
and fluoroquinolones)
Evidence
 Strong Class II data
References
 Springer R. The Surgical care
improvement project-focusing on
infection control.Plast Surg Nurs
2007
Use higher dosages of
prophylactic antibiotics
for morbidly obese patients
Evidence
 Limited Class II data
References
 Springer R. The Surgical care
improvement project-focusing on
infection control.Plast Surg Nurs
2007
Carefully handle tissue, eradicate dead
space, and adhere to standard principles
of asepsis

Evidence
 Class III
References
 Anderson DJ. Strategies to prevent
surgical site infections in acute care
hospitals. Infect Control Hosp
Epidemiol 2008;
Redose prophylactic antibiotics with
short half-lives intraoperatively if
operation is prolonged (for cefazolin if
operation is >3 h) or if there is
extensive blood loss
Evidence
 Limited Class I, Class II data
References
 Scher K. Studies on the duration of
antibiotic administration for surgical
prophylaxis Am Surg 1997
Maintain intraoperative
normothermiac
Evidence
 Class I; some contradictory Class II
data
References
 Sessler DI, Akca O.
Nonpharmacological prevention of
surgical wound infections.
 Clin Infect Dis 2002
 Discontinue prophylactic
antibiotics within 24 h after the
procedure (48 h for cardiac surgery
&liver transplant procedures)
discontinue prophylactic
antibiotics after skin closure
Evidence
 Class I;
 meta-analyses support single dose
regimens for prophylaxis
 References ASHP Therapeutic guidelines on antimicrobial
prophylaxis in surgery. Am J Health Syst Pharm 1999
Maintain serum glucose
levels <200 mg/dL on PO
Evidence
 Class II data
References
 Anderson DJ. Strategies to prevent
surgical site infections in acute care
hospitals. Infect Control Hosp
Epidemiol 2008
Monitor wound for the
development of SSI
postoperative days 1 and 2d
Evidence
 Class III data
References
 Anderson DJ. Strategies to prevent
surgical site infections in acute care
hospitals. Infect Control Hosp
Epidemiol 2008
 Treatment of SSI

•opening the wound I&D .

• For most patients who have had their
wounds opened and adequately
drained, antibiotic therapy is unnecessary.
Stevens DL. Prguidelines for the diagnosis and management of skin and soft-tissue
infections. Clin Infect Dis 2005actice
 Treatment of SSI
o use antibiotics only when there are
 significant systemic signs of infection
(temperature higher than
38.5Cor heart rate greater than 100
beats/min)
 erythema extends more than 5 cm
from the incision.
Stevens DL. Prguidelines for the diagnosis and management of skin and
soft-tissue infections. Clin Infect Dis 2005actice
 Sepsis

 Sepsis: Commonly called a

"blood stream infection.“
 The presence of bacteria
(bacteremia) or other infectious
organisms or their toxins in the
blood (septicemia) or in other
tissue of the body.
 Sepsis
 Sepsis may be associated with clinical
symptoms of systemic (bodywide)
illness, such as fever, chills, malaise ,
low blood pressure, and mental status
changes.
 Sepsis can be a serious situation, a life
threatening disease calling for urgent
and comprehensive care.
 Sepsis, Septic shock

 Signs of:
 Increased C.O.

 Altered O2 SATURATION.

 Metabolic acidosis (usually)

 Can lead to ---Death.

 Sepsis

Sepsis remains a major clinical

problem for 21st century
marginal improvement in the
mortality
antibiotics are cornerstone
10% improvement in mortality
Mac Arthur RD et al.Adequacy of early empiric antibiotic treatment in severe sepsis
experience from MONARCS trial . Clin Infect Dis 2004;38(2):284-88
 Cytokines Release
TNF , IL1 Endothelial
IL6,10 injury
Protease ,PG
PAF

Tissue factor

Coagulopathy

Fibrin
clot

Inhibit activity
Protein C Suppress
fibrinolysis
Antithrombin III
 The aim
Sepsis is condition diagnosed on the
bases of clinical & laboratory parameters

increased level of inflammatory

mediators reflects global dysregulation of
immune response

Examine the latest evidence for the use

of immuno-modulating drugs obtained
from human clinical trials
 immune response is multi-
faceted
Aim :
Eliminate
invading object

Maintain Limit tissue

homeostasis damage
 Sepsis And host response

More than adequate

or
Inadequate.
Inadequate Host response

 Stimulation by Levamisole
 Pro inflammatory Cytokine
interferon y
 Anti- prostaglandins
(immunosuppressive
mediators
 IL-10

 IL- 10 administration
improves survival
following endotoxin
challenge
 Live candida - block IL-10-
improves survival
 More than adequate host
response

 Anti-inflammatory cyotkines
like Interleukin 10
 Agents to neutralise tumor
necrsois factor or interlekin -1
 Severity assessment
 PAC- initially
 Ultra low frequency ossillations in
CO/global end diastolic vol -severity
high
 Lactate levels –good severity predictor

 Low exogenous clearance – very early

predictor of mortality
 C reactive protein – high risk of organ
failure/ too slow to monitor
 Management of Sepsis
 Hemodynamic, respiratory
stability
 Source control in sepsis

 Early enteral feed/intensive

insulin therapy
 stress ulcer prophylaxis, and
deep vein thrombosis
 Daily hemodalysis – better survival
 Early goal-directed therapy (EGDT)

 Oximetric central venous catheters

were placed to measure central
venous pressure
(CVP) & CvO2
 500-mL aliquots of isotonic
crystalloid were given by bolus
infusion to achieve a central venous
pressure greater than 8 mm Hg.
Rivers E, Nguyen B, Havstad S, et al. Early goal-directed therapy in the treatment
of severe sepsis and septic shock. N Engl J Med 2001;
 Early goal-directed therapy (EGDT)

 Mean arterial pressure was

maintained at 65 mm Hg or higher
with vasopressors.
 If the CvO2 saturation was still less
than 70%, blood was transfused to
a hematocritof 30.
 If the CvO2 saturation was still less
than 70%, dobutamine was started.
Rivers E, Nguyen B, Havstad S, et al. Early goal-directed therapy in the treatment
of severe sepsis and septic shock. N Engl J Med 2001;
 Early goal-directed therapy (EGDT)

 Mortality was significantly lower

among patients randomized to
EGDT (48.2% versus
 33.3%, P 5 .01).

Rivers E, Nguyen B, Havstad S, et al. Early goal-directed therapy in the treatment

of severe sepsis and septic shock. N Engl J Med 2001;
 Sepsis

 itis complex process and the

goal of immune therapy is
identifying critical point of
response to modulate it
 TNF

TNF is an important mediator

of sepsis
Serum level correlate with
outcome
Immunotherapy :
- Antibodies
- Blocking receptor
Calandra T et al.Prognostic values of tumor necrosis factor/cachectin,interlukin-
1,interferon-alpha and interferon gamma in the serum of patients with septic shock.
J Infec Dis 1990;161:982-87
 Blockade of tumor necrosis
factor

 Improves outcome in E.
coli septicemia.
 But increased mortality
with cecal ligation and
puncture.
TNF antibody

NEROCEPT :
reduction of mortality 1st 3
days - dose dependant

INTERSEPT :
-reduce progression of sepsis
- rapid resolution of shock
 TNF antireciptor:

Recombinant receptor :
- dose dependant increase
in mortality
- deleterious effect in
human clinical trial

Fisher CJ et al.Treatment of septic shock with the tumot necrosis factor receptor.Fc
fusion protein .N Engl J Med 1996;334:1697-702
 Steroids
Most widely known and used
immunotherapy
Blunt & potent anti-inflammatory
Action :
 Prevent complement activation
 inhibit nitrous oxide synthatase
 Decrease proinflammatory
cytokines
 inhibit neutrophil aggregation
 stabilise lysosomal membrane
 1960-90S No advantage
1997 increase mortality with high dose
Beneficial for patient with adrenal
insufficiency
Currently “ 2nd generation trials” :
- low & physiological dose
- long duration
- vasopressor dependant pt
- no difference among
corticotrophic
dependant or non dependant
Minneci PC et al Meta analysis:the effect of steroids on survival & shock during sepsis
depend on the dose. Ann Intern Med 2004;141:47-57
 Inhibit thrombin and factor Xa
low during sepsis d/t
- impaired synthesis
- consumption by DIC
- degradation by elastase
Abraham E et al.Efficacy and safety of tifacogen in severe sepsis: randomised
controlled trial .JAMA 2003;290:238-47
 APC action
Anti-inflammatory
Anticoagulant inhibit transcription
APC NF-kB reducing
inactivate Va,VIIa pro-inflammatory
Low level in sepsis cytokines
cytokine-induced
down-regulation of
thrombomodulin
Esmon CT. Inflammation & thrombosis : mutual regulation by protein C.
Immunologist 1998;6:84-89
 APC
48hrs /reduces mortality
iv 24 ug/ kg/hr x 96hrs
Recombinant APC “ Dotrecogin alfa” :
- Significant reduction of mortality
- faster resolution cardiovascular &
respiratory dysfunction
PROWESS ( protein c worldwide evaluation in severe sepsis)
multicentre study,2001
 Vasopressor/ Inotropics

 The Surviving Sepsis guidelines

recommended
dopamine or norepinephrine as first
line agents.
 Vasopressin should be considered an
important adjunct vasopressor.
 Epinephrine may be considered as a
second line agent.
Matthew C. Byrnes, MDa,b,*, GregJ. Beilman, MDa
 INTENSIVE
GLUCOSEMANAGEMENT
 Current international
recommendations have been made
to maintain blood glucose levels
lower than150 mg/dL.
 Maintenance of blood glucose
between 80 and 110 mg/dL may
carry a significant risk of
hypoglycemia.
All of the mentioned immunotherapeutic
strategies worked in animal models of sepsis
but not always converted into patient
Comorbidity
 Extreme ages
 organ dysfunction
 genetic polymorphism
 site of infection
cautious multi-centre studies !

- differences resources
- availability of intensive care bed
Only APC has been shown to improve
outcome in septic patient

low steroid dose also worthy , should not

restricted to corticotrophin hypo-
responsive patient

Sprung CL et al.Influence of alterations in foregoing life sustaining treatment

practices on a clinical sepsis trial.Critical Care Medicine 1997;25:383-7
most effective management of septic
patient remains recognition support of
organ dysfunction

antibiotics remain the cornerstone of

management
PERITONITIS
 Classification

1. Primary peritonitis

2. Secondary peritonitis

3. Tertiary peritonitis
Secondary peritonitis is the most

common form for surgeons

 Intra-abdominal sepsis...

Diversion
 Nutrition
 Fluid & Electrolytes

 ABG

 Antibiotics
 Diversion

 Small Bowel : ileostomy

 Large bowel : colostomy

More important than

antibiotics
 Nutrition

 Enteral or parenteral (TPN)

ANY QUESTION?