Académique Documents
Professionnel Documents
Culture Documents
management of
Surgical Infection
Contents:
Introduction
Types of surgical infections
Definition of SSI
Types SSI
Recent management of SSI
sepsis
Peritonitis
Introduction
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.) PMNs
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 hosts physiologic
state.
Infections
Two
main 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
Biliary Tract
Usually
empyema
Ascending
cholangitis
Community-Acquired
Viral
Hepatitis
HIV/AIDS
Tetanus
Hospital-Acquired
Post-operative
At the surgical site
Systemic.
Gas gangrene
Gas gangrene
Catheter Sepsis
80%
Burn Infections
Necrotic
Hospital-Acquired
Pulmonary
Pneumonia
Non-ventilator
Ventilator
Aspiration
associated
associated
Hospital-Acquired
Urinary
Tract
Diagnosis
Usual suspects
Pseudomonas, Serratia,
other
Hospital-Acquired
Foreign-body
associated
Sites
Catheters
Lines
Prosthetics/grafts
Hospital-Acquired
Wound
Primary intention
2) Secondary intention
3) Delayed primary intention
re-closure at
Re-infection
rate %
50
re-closure after
20
re-closure after
re-closure after
10
[Gottrup, F. Wound healing and principles of wound closure. In: Holstrm H, Drzewieck KT (Eds).
The Scandinavian Handbook of Plastic Surgery. Malmoe: Studenterliteraturen, 2005
Definition of SSI
The
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.
ASEPSIS WOUND
SCORING SYSTEM
Southampton wound
scoring system
Risk Factors
Surgical
factors
Patient-specific factors
local
systemic
Systemic:
bacterial
load
Wound
hematoma
Necrotic tissue
Foreign body
Obesity
Advanced
age
Shock
Diabetes
Malnutrition
Alcoholism
Steroids
Chemotherapy
Immuno-
compromise
prophylaxis
EWMA Journal 2005; 5(2): 11-15.
Class II data
References
Smoking cessation 30 d
before operation
Evidence
Class II data
References
Class I data
References
Evidence
Class II data
References
References
References
Class III
References
Maintain intraoperative
normothermiac
Evidence
References
Discontinue prophylactic
antibiotics
within
24
h
after
the
Evidence
procedure
(48 h for cardiac surgery
Class
I;
meta-analyses
&liver transplant
procedures)
support single
dose
regimens
for prophylaxis
discontinue
prophylactic
References ASHP Therapeutic guidelines on antimicrobial
antibiotics after skin closure
prophylaxis in surgery. Am J Health Syst Pharm 1999
Class II data
References
Treatment of SSI
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.
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
IL6,10
Protease ,PG
PAF
Endothelial
injury
Tissue factor
Coagulopathy
Fibrin
clot
Inhibit activity
Protein C
Antithrombin III
Suppress
fibrinolysis
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
Eliminate
invading object
Maintain
homeostasis
Limit tissue
damage
than adequate
or
Inadequate.
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-10improves survival
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
Sepsis
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,interlukin1,interferon-alpha and interferon gamma in the serum of patients with septic shock.
J Infec Dis 1990;161:982-87
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 :
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
APC action
Anti-inflammatory
Anticoagulant
inactivate Va,VIIa
Low level in sepsis
cytokine-induced
down-regulation of
thrombomodulin
APC
inhibit transcription
NF-kB reducing
proinflammatory
cytokines
APC
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.
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.
PERITONITIS
Classification
1.
Primary peritonitis
2.
Secondary peritonitis
3.
Tertiary peritonitis
Intra-abdominal sepsis...
Diversion
Nutrition
Fluid & Electrolytes
ABG
Antibiotics
Diversion
Small Bowel : ileostomy
Large bowel : colostomy
Nutrition
ANY QUESTION?