This document discusses recent management of surgical site infections. It begins with an introduction on the history and types of surgical infections. It then defines surgical site infections and classifies them as superficial, deep or organ/space infections. Risk factors for surgical site infections include patient factors like diabetes as well as surgical factors like procedure type and duration. Recent management involves measures to prevent infections like controlling blood sugar, administering prophylactic antibiotics appropriately, and maintaining normothermia in the operating room. For treating existing infections, strategies include opening and draining wounds along with targeted antibiotic therapy only in significant infections. The document also discusses sepsis, a serious complication, and its immune mediated pathophysiology as well as approaches for assessment and management.

1. What is new in
management of
Surgical Infection

2. Contents:
 Introduction
 Types of surgical infections
 Definition of SSI
 Types SSI
 Recent management of SSI
 sepsis
 Peritonitis

3. Soft tissue/wound Infictions.
 Third most reported nosocomial
infections
 16% of all reported nosocomial
infections
 Most common surgical patient
nosocomial infection (38%)

4.  2/3 involved surgical incision
 1/3 deep structures accessed
by incision
 Deaths in patients with
nosocomial infections—77%
related to infection.
Soft tissue/wound Infictions.
EWMA Journal 2005; 5(2): 11-15.

5. Introduction
 < 1900= 70-80% mortality for
wound infection
 >1900: Ignaz Semmelweis and
Joseph Lister = antiseptic surgery

6. 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.

7. 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.

8. Infections
 Two main types
Community-Acquired
Hospital-Acquired

9. Community-Acquired
 Skin/soft tissue
Cellulitis: Group A strep
Abcess/furuncle: Staph aureus
Necrotizing: Mixed
Hiradenitis suppurativa:Staph aureus
Lymphangitis: Staph aureus

10. Cellulitis

11. Furuncle

12. Necrotizing

13. Hiradenitis

14. Lymphangitis

15. Breast Abscess

16. Peri-rectal abscess

17. Gas Gangrene

18. Paronychia

19. Diabetic foot infection

20. Biliary Tract
Usually result from obstruction
Usual suspects:
E. coli, Klebsiella, Enterococci
Acute Cholecystitis
GB empyema
Ascending cholangitis

21. Community-Acquired
 Viral
Hepatitis
HIV/AIDS
 Tetanus

22. Hospital-Acquired
Post-operative
 At the surgical site
 Systemic.

23. Infected Vascular Graft
 Inguinal incision is independent risk
factor
 Length of case and blood loss
 Prosthetic grafts 10%-20%
 S. Aureus

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

25. Gas gangrene
 Aggressive debridement &
antibiotics
 Repeat antibiotics

26. 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

27. 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

28. Hospital-Acquired
 Pulmonary
Pneumonia
Non-ventilator associated
Ventilator associated
Aspiration

29. Hospital-Acquired
 Urinary Tract
Diagnosis
Usual suspects
Pseudomonas, Serratia,
other

30. Hospital-Acquired
 Foreign-body associated
Sites
Catheters
Lines
Prosthetics/grafts

31. Hospital-Acquired
 Wound infection & SSI.

32. Surgical wounds are healing
by
 1) Primary intention
 2) Secondary intention
 3) Delayed primary intention

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

34. 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;

35. classificationincisional
surgical site infections
 Superficial
 Deep
 Organ/space

36. 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

37. 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

38. ASEPSIS WOUND
SCORING SYSTEM
[ Wilson AP, Lancet 1986

41. Southampton wound
scoring system
[Bailey IS, BMJ 1992; 304: 469-71

43. Risk Factors
 Surgical factors
 Patient-specific factors
local
systemic

44. Factors influencing SSIs
Patient Risk Factors
 Local:
 High bacterial
load
 Wound
hematoma
 Necrotic tissue
 Foreign body
 Obesity
 Systemic:
 Advanced age
 Shock
 Diabetes
 Malnutrition
 Alcoholism
 Steroids
 Chemotherapy
 Immuno-
compromise

45. Factors influencing SSIs
Antibiotics
 Prophylactic
 Therapeutic

46. 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.

47. Wound class Definition Example Infection
rate (%)
Clean Nontraumatic, elective
surgery. GI tract,
respiratory tract, GU tract
not entered
Mastectomy
Vascular
Hernias
2%
Clean-
contaminated
Respiratory, GI, GU tract
entered with minimal
contamination
Gastrectomy
Hysterectomy
< 10%
Contaminated Open, fresh, traumatic
wounds, uncontrolled
spillage, minor break in
sterile technique
Rupture appy
Emergent
bowel resect.
20%
Dirty Open, traumatic, dirty
wounds; traumatic
perforation of hollow
viscus, frank pus in the
field
Intestinal
fistula
resection
28-70%
Berard F, Gandon J, Ann Surg 1964

48. 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;

49. 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

50. 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

51. 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;

52. 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;

53. 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;

54. 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

55. 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

56. 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;

57. 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

58. 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

59. 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

60. 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

61. 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

62. • opening the wound I&D .
• For most patients who have had their
wounds opened and adequately
drained, antibiotic therapy is unnecessary.
Treatment of SSI
Stevens DL. Prguidelines for the diagnosis and management of skin and soft-tissue
infections. Clin Infect Dis 2005actice

63. 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
Treatment of SSI

64. 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.

65. 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.

66. Sepsis, Septic shock
 Signs of:
Increased C.O.
Altered O2 SATURATION.
Metabolic acidosis (usually)
 Can lead to ---Death.

67. 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

68. Cytokines Release
TNF , IL1
IL6,10
Protease ,PG
PAF
Endothelial
injury
Coagulopathy
Tissue factor
Fibrin
clot
Inhibit activity
Protein C
Antithrombin III
Suppress
fibrinolysis

69. 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

70. immune response is multi-
faceted
Aim :
Eliminate
invading object
Maintain
homeostasis
Limit tissue
damage

71. Sepsis And host response
More than adequate
or
Inadequate.

72. Inadequate Host response
 Stimulation by Levamisole
 Pro inflammatory Cytokine
interferon y
 Anti- prostaglandins
(immunosuppressive
mediators

73. IL-10
 IL- 10 administration
improves survival
following endotoxin
challenge
 Live candida - block IL-10-
improves survival

74. More than adequate host
response
 Anti-inflammatory cyotkines
like Interleukin 10
 Agents to neutralise tumor
necrsois factor or interlekin -1

75. 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

76. 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

77. 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;

78. 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;

79. 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;

80. Sepsis
 it is complex process and the
goal of immune therapy is
identifying critical point of
response to modulate it

82. 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

83. Blockade of tumor necrosis
factor
 Improves outcome in E.
coli septicemia.
 But increased mortality
with cecal ligation and
puncture.

84. TNF antibody
NEROCEPT :
reduction of mortality 1st 3
days - dose dependant
INTERSEPT :
-reduce progression of sepsis
- rapid resolution of shock

85. 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

86. 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
Steroids

87. 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

89. 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

91. APC action
Anticoagulant
Anti-inflammatory
inhibit transcription
NF-kB reducing
pro-inflammatory
cytokines
APC
inactivate Va,VIIa
Low level in sepsis
cytokine-induced
down-regulation of
thrombomodulin
Esmon CT. Inflammation & thrombosis : mutual regulation by protein C.
Immunologist 1998;6:84-89

93. 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
APC

94. 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

95. 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.

97. 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

98. cautious multi-centre studies !
- differences resources
- availability of intensive care bed

100. 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

101. most effective management of septic
patient remains recognition support of
organ dysfunction
antibiotics remain the cornerstone of
management

102. PERITONITIS

103. Classification
1. Primary peritonitis
2. Secondary peritonitis
3. Tertiary peritonitis

104. Secondary peritonitis is the most
common form for surgeons

105. Intra-abdominal sepsis...
Diversion
 Nutrition
 Fluid & Electrolytes
 ABG
 Antibiotics

106. Diversion
 Small Bowel : ileostomy
 Large bowel : colostomy
More important than
antibiotics

107. Nutrition
 Enteral or parenteral (TPN)

108. ANY QUESTION?