Surgical infection

History
• In 1846, Ignaz Semmelweis  teaching hospital

• Louis Pasteur  germ theory

• Joseph Lister  in 1859  postoperative infection

Pathogenesis of infection
• The mammalian host possesses several layers of endogenous
defense mechanisms that serve to prevent microbial invasion,
limit proliferation of microbes within the host, and contain or
eradicate invading microbes
• Entry of microbes into the mammalian host is precluded by
the presence of a number of barriers :
• Epithelial (integument)  block physicly, sebaceous
• Mucosal (respiratory, gut, and urogenital)
• Respiratory  mucus
• Gut  acidity of gaster, low motility, comensal, low oxygen of colon
• Microbes also immediately encounter a series of host
defense mechanisms that reside within the vast majority
of tissues of the body. These include resident
macrophages and low levels of complement (C) proteins
and immunoglobulins

• Macrophages initiated by genome encode pattern

regonition, pathogen-associated molecular patterns
(PAMPs) and endogenous danger-associated molecular
patterns (DAMPs)
• Macrophage cytokine synthesis is upregulated.
Secretion of tumor necrosis factoralpha (TNF-α),
of interleukins (IL)-1β, 6, and 8; and of gamma
interferon (IFN-γ) occurs within the tissue milieu,
and, depending on the magnitude of the host
defense response, the systemic circulation
Defenition
Infection is defined by the presence of microorganisms in host
tissue or the bloodstream

• At the site of infection the classic findings of rubor, calor, and dolor
in areas such as the skin or subcutaneous tissue are common

• Infection manifestation 
• Local
• Systemic  elevated temperature, WBC, tachycardia, tachypnea

• The systemic manifestations noted previously comprise the systemic

inflammatory response syndrome (SIRS).
• A documented or suspected infection with some of the findings of
SIRS define sepsis
• Severe sepsis is characterized as sepsis (defined previously)
combined with the presence of new-onset organ failure
PREVENTION AND TREATMENT OF
SURGICAL INFECTIONS
General Principles
Manuvers to diminish the presence of exogenous (surgeon and
operating room environment) and endogenous (patient)
microbes are termed prophylaxis, and consist of the use of
mechanical, chemical, and antimicrobial modalities, or a
combination of these methods.
Source Control
The primary precept of surgical infectious disease therapy
consists :
• drainage of all purulent material,
• débridement of all infected,
• devitalized tissue, and debris,
• and/or removal of foreign bodies at the site of infection, plus
remediation of the underlying cause of infection

Other treatment modalities such as antimicrobial agents, albeit

critical, are of secondary importance to effective surgery with
regard to treatment of surgical infections and overall outcome
Appropriate Use of Antimicrobial Agents
Agents are selected according to their activity against microbes
likely to be present at the surgical site, based on knowledge of
host microflora.
INFECTIONS OF SIGNIFICANCE
IN SURGICAL PATIENTS
Surgical Site Infections
• Surgical site infections (SSIs) are infections of the tissues,
organs, or spaces exposed by surgeons during performance of
an invasive procedure.
• SSIs are classified into incisional and organ/space infections,
and the former are further subclassified into superficial
(limited to skin and subcutaneous tissue) and deep incisional
categories
• The development of SSIs is related to three factors :
• The degree of microbial contamination of the wound during
surgery
• Duration of procedure
• Host factors : diabetes, malnutrition, obesity, immune
suppression and other disease states
Surgical wounds are classified based on the presumed
magnitude of the bacterial load at the time of surgery
• SSIs are associated with considerable morbidity and occasional
lethality  consider antibiotic prophylaxis  still controversial
 not use in routine circumtances
Intra-Abdominal Infections
• Microbial contamination of the peritoneal cavity is termed
peritonitis or intra-abdominal infection, and is classified
according to etiology.

• Primary microbial peritonitis occurs when microbes invade

the normally sterile confines of the peritoneal cavity via
hematogenous dissemination from a distant source of
infection or direct inoculation

• Secondary microbial peritonitis occurs subsequent to

contamination of the peritoneal cavity due to perforation or
severe inflammation and infection of an intra-abdominal
organ
Organ-Specific Infections
Hepar
• Hepatic abscesses are rare
• 15 per 100,000 hospital admissions in the United States.
• Pyogenic abscesses account for approximately 80% of cases,
• the remaining 20% being equally divided among parasitic and fungal
forms
• The most common aerobic bacteria : E coli, K pneumoniae, and other
enteric bacilli, enterococci, and Pseudomonas
• the most common anaerobic bacteria: Bacteroides spp., anaerobic
streptococci, and Fusobacterium spp.
• Candida albicans and other related yeast cause the majority of fungal
hepatic abscesses
• Small (<1 cm), multiple abscesses should be sampled and treated with a
4 to 6 week course of antibiotics
• Larger abscesses invariably are amenable to percutaneous drainage,
with parameters for antibiotic therapy and drain removal similar to
those mentioned previously
• Pancreatic Infections
• Secondary pancreatic infections (e.g., infected pancreatic necrosis or
pancreatic abscess) occur in approximately 10% to 15% of patients
who develop severe pancreatitis with necrosis
• Current care of patients with severe acute pancreatitis includes
staging with dynamic, contrast material enhanced helical CT scan to
evaluate the extent of pancreatitis
• Enteral feedings initiated early, using nasojejunal feeding tubes
placed past the ligament of Treitz, have been associated with
decreased development of infected pancreatic necrosis
• The approach of open necrosectomy with repeated debridements,
although life saving, is associated with significant morbidity and
prolonged hospitalization
• Infections of the Skin and Soft Tissue
• These infections can be classified according to whether or not
surgical intervention is required. For example, superficial skin and
skin structure infections such as cellulitis, erysipelas, and
lymphangitis invariably are effectively treated with antibiotics
alone
• Aggressive soft tissue infections are rare, difficult to diagnose,
and require immediate surgical intervention plus administration
of antimicrobial agents
• Postoperative Nosocomial Infections
• Surgical patients are prone to develop a wide variety of
nosocomial infections during the postoperative period, which
include SSIs, UTIs, pneumonia, and bacteremia.
Sepsis
• Patients presenting with severe sepsis should receive
resuscitation fluids to achieve a central venous pressure target
of 8-12 mm Hg, with a goal of mean arterial pressure of ≥ 65
mHg and urine output of ≥ 0.5 mL/kg/h. Delaying this
resuscitative step for as little as 3 hours until arrival in the ICU
has been shown to result in poor outcome. Typically this goal
necessitates early placement of central venous catheter.
Blood-Borne Pathogens
• HIV
• surgeons were one of the lower risk groups (compared to nurses
at 60 cases and nonsurgeon physicians at 19 cases
• needlestick from a source with HIV-infected blood is estimated at
0.3%.
• Postexposure prophylaxis for HIV has significantly
• decreased the risk
• Hepatitis B
• Hepatitis C
BIOLOGIC WARFARE AGENTS
• Surgeon must know other infection from entities for potential use as
biologic weapons

• Bacillus anthracis (Anthrax)

• Anthrax is a zoonotic disease occurring in domesticated and wild
herbivores
• 1800 in england
• 1979 sverdlovsk russia
• Inhalational anthrax develops after a 1- to 6-day incubation period, with
nonspecific symptoms, including malaise, myalgia, and fever. Over a
short period of time, these symptoms worsen, with development of
respiratory distress, chest pain, and diaphoresis
• widened mediastinum and pleural effusions
• Treatment options include combination therapy with ciprofloxacin,
clindamycin, and rifampin; clindamycin added to block production of
toxin, while rifampin penetrates into the central nervous system and
intracellular locations.
• Yersinia pestis (Plague)
• Gram-negative organism Yersinia pestis
• transmitted via flea bites from rodents
• first biologic warfare agent, and was used in the Crimean city of
Caffa by the Tartar armyfirst
• clinical manifestation :
• Epidemic pneumonia with blood tinged sputum
• Painful enlarged lymph node “bubo’
• Fever
• Malaise
• Diagnosis is confirmed via aspirated of bubo
• Postexposure prophylaxis  doxycycline.
• Treatment of the pneumonic or bubonic/septicemic : streptomycin,
an aminoglycoside, doxycycline, ciprofloxacin, levofloxacin, or
chloramphenicol
Smallpox
• Variola, the causative agent
• Variola virus is highly infectious in the
aerosolized, incubation period of 10 to 12
days, clinical manifestations of malaise, fever,
vomiting, and headache appear, followed by
development of a characteristic centripetal
rash (which is found to predominate on the
face and extremities).
• The fatality rate may reach 30%.
• prophylaxis effective to 4 days post exposure
• Cidofovir, an acyclic nucleoside phosphonate
analogue, has demonstrated activity in animal
models of poxvirus infections and may offer
promise for the treatment of smallpox
• Francisella tularensis (Tularemia)
• The principal reservoir of this Gram-negative aerobic organism
is the tick.
• bioterrorist threat due to a very high infectivity rate after
aerosolization.
• Patients with tularemia pneumonia develop a cough and
demonstrate pneumonia on chest roentgenogram. Enlarged
lymph nodes occur in approximately 85% of patients.
• The organism can be cultured from tissue samples, but this is
difficult, and the diagnosis is based on acute-phase
agglutination tests.
• Treatment of inhalational tularemia consists of administration
of an aminoglycoside or second-line agents such as
doxycycline and ciprofloxacin.
Terima Kasih