SURGICAL INFECTIONS e.
if there is no infection identified after 3
KEY POINTS:
1. The incidence of surgical site infections can be
reduced by appropriate patient preparation,
timely perioperative antibiotic administration,
maintenance of perioperative normothermia
and normoglycemia, and appropriate wound
management.
2. Principles relevant to appropriate antibiotic
prophylaxis for surgery:
a. select an agent with activity against
common organisms at the site of
surgery,
b. the initial dose of the antibiotic should
be given within 30 minutes of incision,
c. antibiotics should be redosed every 1 to
2 half-lives during surgery to ensure
adequate tissue levels, and
d. antibiotics should not be continued for
more than 24 hours after surgery for
routine prophylaxis.
3. Source control is a key concept in the treatment
of most surgically relevant infections. Infected
or necrotic material must be drained or
removed as part of the treatment plan in this
setting. Delays in adequate source control are
associated with worsened outcomes.
4. Sepsis is both the presence of infection and the
host response to infection (systemic
inflammatory response syndrome, SIRS). Sepsis
is a clinical spectrum, ranging from sepsis (SIRS
plus infection) to severe sepsis (organ
dysfunction), to septic shock (hypotension
requiring vasopressors). Outcomes in patients
with sepsis are improved with an organized
approach to therapy that includes rapid
resuscitation, antibiotics, and source control.
5. When using antimicrobial agents for therapy of
serious infection, several principles should be
followed:
a. identify likely sources of infection,
b. choose an agent (or agents) that covers
likely organisms for these sources,
c. remember that inadequate or delayed
antibiotic therapy results in increased
mortality, so it is important to begin
therapy with broader coverage,
d. when possible, obtain cultures early
and use results to tailor therapy,
days, strongly consider discontinuation
of antibiotics, and
f. stop antibiotics after an appropriate
course of therapy.
6. The keys to good outcomes in patients with
necrotizing soft tissue infection are early
recognition and appropriate débridement of
infected tissue with repeated débridement until
no further signs of infection are present.
7. Transmission of HIV and other infections spread
by blood and body fluid from patient to health
care worker can be minimized by observation of
universal precautions, which include routine use
of barriers when anticipating contact with blood
or body fluids, washing of hands and other skin
surfaces immediately after contact with blood
or body fluids, and careful handling and disposal
of sharp instruments during and after use.
HISTORICAL BACKGROUND
Evolution of Germ theory and antisepsis – aid the
surgeons in the treatment of infection associated with
extremely high rates of morbidity and mortality due to
postoperative infections
“Infection related to surgical wound was the rule rather
than the exception.”
Louis Pasteur: Germ Theory
“All infections are caused by the presence and actions
of a specific microorganism.”
Robert Koch: Koch’s Postulate
1. The suspected pathogenic organism should be
present in all cases of the disease and absent
from healthy animals;
2. The suspected pathogen should be isolated
from a diseased host and grown in a pure
culture in vitro;
3. Cells from a pure culture of the suspected
organism should cause disease in a healthy
animal; and,
4. The organism should be reisolated from the
newly diseased animal and shown to be the
same as the original.
Alexander Fleming: Discovered Penicillin
 The first effective antibacterial agent
 As a result, cases of infections reduced.
Joseph Lister: Father of Antiseptic Surgery
1
  Experimented with the use of a solution of o containment (often leading to the
carbolic acid on the dressings he used on presence of purulence—the hallmark of
patients chronic infection)
o locoregional infection with or w/o
Charles McBurney: distant spread of infection (cellulitis,
 Pioneered the first intra-abdominal operation lymphangitis, and aggressive soft tissue
(appendectomy) infection)
o Treated infection via source control o systemic infection (bacteremia or
(surgical intervention to eliminate the fungemia)
source of infection)  Host defenses may include physical barriers by
o McBurney’s point tissue, substances like lactoferrin that sequester
iron which is a critical bacterial growth factor,
Ignaz Semmelweis: the diaphragmatic pumping mechanism, and
 Required handwashing to reduce puerperal containment by the omentum.
fever (“childbed fever”)
 Infection – identification of microorganisms in
PATHOGENESIS OF INFECTION host tissue or blood stream, plus an
Host Defenses inflammatory response to their presence
 Prevent microbial invasion o Inflammatory response – either local or
 Limit microbial proliferation within the host systemic:
 Contain or eradicate invading microbes  Local manifestations:
 Include site specific (first line of host defenses)  Rubor – redness
defenses  Calor – bodily heat
o Skin – the most extensive physical  Dolor
barrier; harbors nonpathogenic  Systemic manifestations
microorganisms that block the (comprise the Systemic
attachment and invasion of Inflammatory Response
noncommensal microbes Syndrome):
- Diseases of the skin (e.g.,  Elevated temperature
eczema and dermatitis) are  Elevated WBC count
associated with overgrowth of  Tachycardia
skin commensal organisms, and  Tachypnea
barrier breaches invariably lead  SIRS – constellation of signs and symptoms
to the introduction of these brought about by the presence of inflammation;
microbes. not localized
o Respiratory tract – maintain sterility in
the distal bronchi and alveoli under Criteria for Systemic Inflammatory Response
normal circumstances Syndrome
 Circulate throughout the body
o PMN’s General variables

Factors affecting response and outcome: Fever [core temp >38.3°C (100.9°F)]
 Initial number of microbes
Hypothermia [core temp <36°C (96.8°F)]
 Rate of microbial proliferation in relation to
containment and killing by host defenses Heart rate >90 bpm
 Microbial virulence
 Potency of host defenses Tachypnea

Altered mental status

Definitions:
 Possible outcome to body’s reactions on Significant edema or positive fluid balance (>20
microbial invasion:
mL/kg over 24 h)
o Eradication
2
 Hyperglycemia in the absence of diabetes o Most severe manifestation of infection

Inflammatory variables Relationship between sepsis and systemic response:

Leukocytosis (WBC >12,000)

Leukopenia (WBC <4000)

Bandemia (>10% band forms)

Plasma C-reactive protein > 2 s.d. above normal

value

Plasma procalcitonin >2 s.d. above normal value

Hemodynamic variables

Arterial hypotension (SBP <90 mmHg, MAP <70, or

SBP decrease >40 mmHg)
SVO2 >70%
Cardiac index >3.5 L/min per square meter
Organ dysfunction variables
Arterial hypoxemia
Acute oliguria
Creatinine increase
Coagulation abnormalities
Ileus
Thrombocytopenia
Hyperbilirubinemia
Tissue perfusion variables
Hyperlactatemia
Decreased capillary filling
 Sepsis – SIRS as caused by infection; mediated
by the production of a cascade of
proinflammatory mediators produced in
response to exposure to microbial products
 Severe sepsis – SIRS + new onset of one or
more organ failure
 Septic Shock – acute circulatory failure with
persistent arterial hypotension [<90 mmHg]
despite adequate fluid resuscitation, and
without other identifiable causes
Figure 1. Relationship between infection and systemic
inflammatory response syndrome (SIRS). Sepsis is the
presence both of infection and the systemic
inflammatory response, shown here as the intersection
of these two areas. Other conditions may cause SIRS as
well (trauma, aspiration, etc.). Severe sepsis (and septic
shock) are both subsets of sepsis.
 PIRO Staging System – a more recent
classification of Sepsis developed to improve
treatment, but is still being investigated for its
clinical utility
o (P)redisposing conditions
o Nature and extent of (I)nfection
o Nature and magnitude of host
(R)esponse
o The degree of concomitant (O)rgan
dysfunction
PIRO Classification Scheme
Domain Means of Classification
Predisposition Premorbid illness that affects
probability of survival
[immunosuppression, age,
genetics]
Infection/Insult Type of Infecting Organism,
location of disease, intervention
(source control)
Response SIRs, other signs of sepsis, shock
tissue markers [C-reactive protein,
IL-6]

3
 Organ Number of failing organs or  Consist of the use of mechanical,
Dysfunction composite score chemical and antimicrobial modalities,
or a combination
a. Mechanical
MICROBIOLOGY OF INFECTIOUS AGENTS OF SURGICAL o Scrubbing – scrubbing from tip
SIGNIFICANCE of fingers to few inches above
Bacteria elbow
 Causing majority of surgical infections
o Hair removal – preferably a
 Identification by Gram stain and growth
clipper rather than a razor
characteristics on specific media
o Bowel prep
 Gram positive bacteria that frequently cause
o Sterile barriers
infections in surgical patients include aerobic
b. Chemical
skin commensals (S. aureus, S. epidermidis,
o Skin prep – use of antiseptic on
Strep. pyogenes) and enteric organisms like E.
faecalis and E. faecium surface
 Gram negative → Family Enterobacteriaceae
II. Source Controls
 Anaerobic organisms → Propionibacterium
acnes  Primary goal of surgical infection
control:
Fungi a. Drainage – of all purulent material
b. Debridement – of all infected,
 Identified by use of special stains (e.g.
devitalized tissue and debris
potassium hydroxide, India ink, methenamine
c. Removal of foreign body – at site of
silver, or Giemsa)
infection
 Cause nosocomial infections in surgical patients
d. Remediation of underlying cause –
o Part of polymicrobial infections or
remove the underlying cause of
fungemia
infection
 C. albicans
o Rare causes of aggressive soft tissue
III. Appropriate Use of Antimicrobial Agents
infections
 Prophylaxis – consists of the
 Mucor, Rhizopus, Absidia spp.
administration of an antimicrobial agent
o Opportunistic pathogens
or agents before initiation of certain
 Aspergillus, Blastomyces,
specific types of surgical procedures to
Cryptococcus
reduce the number of microbes that
enter the tissue or body cavity.
Virus
o Surgery must be planned and not a
 Recent identification of the presence of viral
pressing situation (breast mass vs.
DNA or RNA include PCR
appendicitis)
 Most viral infections in surgical patients occur in
o Organism that is the most probable
immunocompromised host, especially those
cause of infection – Staph. and
with immunosuppresion to prevent solid organ
Strep. – most common on skin
allograft rejection
o Depend upon type, duration and
 Epstein–Barr, adenoviruses, cytomegalovirus,
risk of surgery
HSV, VZV, Hep B, C, and HIV
o Could be at any route as long as
directed toward organism (oral, IV -
PREVENTION AND TREATMENT OF SURGICAL
most common)
INFECTIONS
 Selection of prophylaxis according to
I. Prophylaxis
activity against microbes likely to be
 Maneuvers to diminish the presence of
present at surgical site
exogenous (surgeon and operating
 Limited to the time before and during
room environment) and endogenous
the operative procedure
(patient) microbes

4
 Note the serum half-life of
antimicrobial, as operations exceeding
it, patients may need additional doses
 There is no evidence that
administration of postoperative doses
of an antimicrobial agent provides
additional benefit, and this practice
should be discouraged since it is costly
and is associated with increased drug
resistance
 Empiric therapy – comprise the use of
an antimicrobial agent when the risk of
a surgical infection is high. Based on the
underlying disease process (e.g.,
ruptured appendicitis), or when
significant contamination during
surgery has occurred (e.g., inadequate
bowel preparation or considerable
spillage of colon contents)
o used in critically ill patients in
whom a potential site of infection
has been identified and severe
sepsis or septic shock occurs
o Also if there is significant
contamination during surgery
o If there is already occurring
infection but unsure of causative
organism, could still be guided on
what antibiotics to give
 Treatment of Established Infection
o Manner in which this therapy is
used depends on whther the
infection is monomicrobial or
polymicrobial
 Monocrobial – nosocomial
infections in postoperative
patients (UTIs, pneumonia,
bacteremia)
 Polymicrobial – antimicrobials
given should not depend solely
on culture information, but also
throughout the clinical course
of the patient
o Based on laboratory (staining,
culture, antibiotic sensitivity)
o Based on clinical course - if
infection is responsive to antibiotic
then continue treatment
o Less toxic
o Less expensive
 Duration
o Should be decided at the time the
drug regimen is prescribed
o Prophylaxis limited to single dose
administered immediately before
creating the incision
o Empiric therapy = limit of 3-5 days
or less, and restrict if no presence
of local site or systemic infection
o Standard guidelines in
monomicrobial infections:
 UTIs – 3-5 days
 Pneumonia – 7-10 days
 Bacteremia – 7-14 days
o The least toxic, least expensive
agent to which the organism is
most sensitive should be selected.
o Essential outcome is more closely
linked to the ability of the surgeon
than to the duration of antibiotic
administration
 Allergy
o Important to ascertain if there has
been any type of allergic reaction in
association with administration of a
particular antibiotic
 True allergic s/sx:
urticarial,
bronchospasm
o Penicillin allergy – quite common
o Incidence of cross reactivity highest
in carbapenems and lower for
cephalosporins, none for
monobactam
 Misuse [guidelines to stop]
o Responsible practitioner limits
prophylaxis to the period during the
operative procedure
o Does not convert prophylaxis into
empiric therapy except under well-
defined conditions
o Sets the duration of antibiotic
therapy from the outset
o Curtail antibiotic administration
when there is no evidence of
infection
o Limit therapy to a short course in
every possible instance
INFECTIONS OF SIGNIFICANCE IN SURGICAL PATIENTS
Surgical Site Infections (SSIs)
5
  infections of the tissues, organs, or spaces
exposed by surgeons during performance of an
invasive procedure
 development is related to:
(a) the degree of microbial contamination of
the wound during surgery
(b) the duration of the procedure
(c) host factors (ex. diabetes, malnutrition,
obesity, immune suppression, and presence
of underlying disease states)
 characterized as:
o Incisional SSI - occurs if surgical wound
drains purulent material or if the
surgeon judges it to be infected and
opens it
o Superficial - limited to skin and SQ
tissue
o Deep incisional
o Organ/space specific
Surgical Wounds
 classified based on the presumed magnitude of
the bacterial load at the time of surgery
1. Clean wounds (class I)
o only skin microflora potentially contaminate
the wound
o no hollow viscous that contains microbes is
entered
o No infection is present
o Ex. Hernia repair, breast biopsy
** Class ID wounds - similar to Class I except that a
prosthetic device (e.g., mesh or valve) is inserted.
2. Clean/contaminated wounds (class II)
o indigenous bacterial flora is opened under
controlled circumstances without significant
spillage of contents
o include those in which a hollow viscous
such as the respiratory, alimentary, or
genitourinary tracts with
o Ex. Cholecystectomy, elective GI surgery
(not colon)
3. Contaminated wounds (class III)
o open accidental wounds encountered early
after injury
o due to major breaks in sterile technique
(e.g., open cardiac massage)
o gross spillage of viscus contents such as
from the intestine
o incision through inflamed, nonpurulent,
tissue
o Ex. Penetrating abdominal trauma, large
tissue injury, enterotomy during bowel
obstruction
4. Dirty wounds (class IV)
o traumatic wounds with significant delay in
treatment
o Presence of necrotic tissue
o those created in the presence of overt
infection (presence of purulent material)
o those created to access a perforated
viscous accompanied by a high degree of
contamination
Microbiology of SSIs is reflective of the initial host
microflora:
· SSIs following class I wound are invariable
due to skin microbes found on that part of
the body
· SSIs following class II wound created for
elective colon resection may be caused by
skin microbes/colonic microflora/both.
In healthy individuals, class I and II wounds may be
closed primarily. Skin closure of class III and IV wounds
is associated with high rates of incisional SSIs.
· superficial aspects should be packed open
and allowed to heal by secondary intention
· selective use of delayed primary closure has
been assoc. with reduction in incisional SSI
rates
Single dose of an antimicrobial agent should be
administered immediately before surgery for class ID, II,
III, and IV types of wounds. Effective therapy for
incisional SSIs consists solely of incision and drainage
without the addition of antibiotics. Antibiotic therapy is
reserved for significant cellulitis, or concurrent SIRS.
Intra-Abdominal Infections
Peritonitis
· Microbial contamination of the peritoneal
cavity
· a.k.a. intra-abdominal infection
1. Primary microbial peritonitis
· occurs when microbes invade the normally
sterile peritoneal cavity via hematogenous
dissemination from a distant source of
infection or direct inoculation
· common in patients with ascites and renal
failure (peritoneal dialysis)
· monomicrobial, rarely require surgical
intervention
6
 · ascites with infection diagnosed by:
· diffuse tenderness and guarding w/o
localized findings
· absence of pneumoperitoneum on
abdominal flat plate and upright
roentgenograms
· presence of more than 100 WBCs/mL
· microbes with single morphology on Gram's
stain via paracentesis
· If receiving peritoneal dialysis:
· Subsequent cultures demonstrate gram-
positive organisms
· In other patients, organisms can include E.
coli, K. pneumoniae, pneumococci
· Treatment consists of administration of
antibiotics for 14 to 21 days.
· Removal of indwelling devices (e.g.,
peritoneal dialysis catheter or
peritoneovenous shunt) may be required
for effective therapy
2. Secondary microbial peritonitis
· occurs subsequent to contamination of the
peritoneal cavity due to perforation or
severe inflammation and infection of an
intra-abdominal organ.
· Ex. appendicitis, perforation of any portion
of the GI tract, or diverticulitis.
· colonic perforation - most morbid form
· Treatment:
· source control to resect or repair
the diseased organ
· débridement of necrotic, infected
tissue and debris
· administration of antimicrobial
agents directed against aerobes and
anaerobes (such type of antibiotic
regimen is chosen because mostly,
precise diagnosis cannot be
established until exploratory
laparotomy is performed)
· combination of agents or single
agents with a broad spectrum of
activity can be used
· conversion of a parenteral to an
oral regimen when the patient's
ileus resolves will provide results
similar to those achieved with IV
antibiotics
· Failure of standard therapy can lead
to intra-abdominal abscess, leakage
from a GI anastomosis resulting to
postoperative peritonitis, or tertiary
(persistent) peritonitis.
· E. faecalis and faecium, S. epidermidis, C.
albicans, and P. aeruginosa
· identified in combination
· may be selected based on their lack
of responsiveness to the initial
antibiotic regimen, coupled with
diminished activity of host
defenses.
· intra-abdominal abscesses diagnosed via
abdominal CT and drained percutaneously
· Surgical intervention reserved for:
· multiple abscesses
· those with abscesses in proximity to
vital structure those with ongoing
source of contamination (e.g.,
enteric leak)
Organ-Specific Infections
Hepatic abscesses
· rare (approx. 15 per 100,000 hospital
admissions in the US)
Pyogenic Abscesses
· approx. 80% of cases, the remaining 20%
being equally divided among parasitic and
fungal forms
Pyogenic Liver Abscesses
· caused by pylephlebitis due to neglected
appendicitis or diverticulitis.
Most common aerobic bacteria:
· E. coli, K. pneumoniae, and other enteric
bacilli, enterococci, and Pseudomonas spp.
Most common anaerobic bacteria:
· Bacteroides spp., anaerobic streptococci,
and Fusobacterium spp. C. albicans and
other similar yeasts
· cause the majority of fungal hepatic
abscesses
Treatment:
7
 · Small (<1 cm), multiple abscesses: sampled
and treated with a 4- to 6-week course of
antibiotics
· Larger abscesses: percutaneous drainage,
with parameters for antibiotic therapy and
drain removal similar
Splenic Abscesses
· extremely rare
· treated in a similarly with hepatic abscesses
· Recurrent hepatic or splenic abscesses may
require operative intervention—unroofing
and marsupialization or splenectomy,
respectively.
Secondary Pancreatic Infections
· e.g., infected pancreatic necrosis or
pancreatic abscess
· occur in approx. 10 to 15% of patients who
develop severe pancreatitis with necrosis.
Care of patients with severe acute pancreatitis:
· staging with dynamic, contrast-enhanced
helical CT scan with 3-mm tomographs to
determine the extent of pancreatic necrosis
with one of several prognostic scoring
systems
· Patients who exhibit significant pancreatic
necrosis (grade greater than C) should be
carefully monitored in the ICU and undergo
follow-up CT examination
· Elimination of the routine use of
prophylactic antibiotics for prevention of
infected pancreatic necrosis
· enteral feedings initiated early, using
nasojejunal feeding tubes placed past the
ligament of Treitz - assoc. with decreased
devt of infected pancreatic necrosis
· secondary pancreatic infection should be
suspected if:
· systemic inflammatory response
(fever, elevated WBC count, or
organ dysfunction) fails to resolve
· Sepsis syndrome develops 2-
3weeks after recuperating
· CT-guided aspiration of fluid from the
pancreatic bed for performance of Gram's
stain and culture analysis is of critical
importance
· positive Gram's stain or
culture or identification of
gas mandate operative
intervention
Infections of the Skin and Soft Tissue
· Infections of the skin and soft tissue can be
classified according to whether surgical
intervention is required
· superficial skin and skin structure
infections:
· cellulitis, erysipelas, and
lymphangitis
· treated with antibiotics alone
(drugs that possess activity against
the gram-positive skin microflora)
· Furuncles or boils
· may drain spontaneously or require surgical
incision and drainage
· acquired methicillin-resistant S.aureus
infection
· suspected if infection persists after
treatment with adequate drainage
and antibiotics
· require more aggressive drainage
and altered antimicrobial therapy
· Aggressive soft tissue infections
· rare, difficult to diagnose, and
require immediate surgical
intervention plus administration of
antimicrobial agents
· Patients at risk:
· elderly, immunosuppressed, or
diabetic
· those with peripheral vascular
disease;
· compromise of fascial blood supply
to some degree
· Result is devastating if coupled with the
introduction of exogenous microbes
· Careful examination should be undertaken
for an entry site:
· small break or sinus in the skin with
grayish, turbid semipurulent
material ("dishwater pus")
· skin changes (bronze hue or brawny
induration)
· blebs, or crepitus
· Pain
· Any of these findings mandates immediate
surgical intervention:
· exposure and direct visualization of
potentially infected tissue (including
deep soft tissue, fascia, and
underlying muscle)
· radical resection of affected areas
8
 · surgical extirpation of infected
tissue frequently entails amputation
· Antimicrobial treatment:
· directed against gram-positive and gram-
negative aerobes and anaerobes (e.g.,
vancomycin plus a carbapenem)
· high-dose aqueous penicillin G (16,000 to
20,000 U/d) to treat clostridial pathogens
· Approximately 50% of such infections are
polymicrobial, the remainder is caused by S.
pyogenes, P. aeruginosa, or C. perfringens
· microbiology of polymicrobial infections is
similar to secondary microbial peritonitis,
but gram-positive cocci are more commonly
encountered
· Hyperbaric oxygen therapy - for patients
with infection caused by gas-forming
organisms (e.g., C. perfringens)
· IV Ig in patients with group A streptococcal
infection with toxic shock syndrome,
hypotension, bacteremia, and for the
elderly
Postoperative Nosocomial Infections
· Surgical patients are prone to develop
nosocomial infections during the post-op
period
· include SSIs, UTIs, pneumonia, and
bacteremic episodes
· related to prolonged use of indwelling
tubes and catheters for urinary drainage,
ventilation, and venous and arterial access
Post-op UTI
· urinalysis demonstrating WBCs or bacteria
· positive test for leukocyte esterase
· >104 CFU/mL of microbes are in
symptomatic patients, > 105 CFU/mL in
asymptomatic individuals
· Treatment for 3 to 5 days with a single
antibiotic that achieves high levels in the
urine
· indwelling urinary catheters removed ASAP
within 1 to 2 days or as soon as patients are
ambulatory
Prolonged mechanical ventilation
· assoc. with increased incidence of
pneumonia
· due to pathogens common in the
nosocomial environment
· highly resistant to many antimicrobial
agents
· Diagnosis of pneumonia :
· purulent sputum, elevated
leukocyte count, fever, and new
chest x-ray abnormality
· presence of two of the clinical
findings, plus chest x-ray findings,
increases likelihood of ventilator-
associated pneumonia
· Surgical patients should be weaned from
mechanical ventilation ASAP based on
oxygenation and inspiratory effort
Infection assoc. with indwelling intravascular catheters
· common problem among hospitalized
patients
· used for physiologic monitoring, vascular
access, drug delivery, and
hyperalimentation
· Many are asymptomatic, often exhibiting
elevated WBC count
· Use of antibacterial or antifungal agents to
prevent catheter infection is
contraindicated.
Sepsis
Response to sepsis:
1. Patients presenting with severe sepsis should
receive resuscitation fluids to attain the ff:
o central venous pressure target of 8-12
mmHg
o mean arterial pressure of ≥65 mmHg
o urine output = 0.5 mL/Kg per Hour or
greater
Delaying the above steps for < 3 hrs until arrival
in the ICU have resulted in poor outcomes
2. Do Early empiric treatment in patients who
develop sepsis or nosocomial infections
o Use broad spectrum antibiotics directed
to most likely organisms
o Must be initiated ASAP
3. Use of institutional and unit specific sensitivity
patterns for nosocomial infection
· Select and appropriate agent for Px
· Early identification and treatment of
septic sources is key for improved outcomes in
Px with sepsis
· For a beautiful elaboration on Sepsis and how
to control it, please refer to Schwartz or
9
 elsewhere, regarding the ‘Surviving Sepsis’ · clindamycin - blocks production of
campaign and its guidelines toxin
· rifampin - penetrates the CNS and
Blood-Borne Pathogens intracellular locations.
· The risk of HIV Transmission from Px to
Surgeon is low Yersinia pestis (Plague)
· Universal Precautions · gram-negative organism
a. Routine use of barriers [gloves, goggles] · transmitted via flea bites from rodents
when anticipating contact with blood or · first biologic warfare agent
body fluids · clinical manifestations:
b. Washing of hands and other skin surfaces · epidemic pneumonia with blood-
immediately after contact with blood or tinged sputum (aerosolized bacteria
body fluids sed)
c. Careful handling and disposal of sharp · bubonic plague (fleas)
instruments during and after use · painful lesion (bubo) assoc. with
· Other viruses that may be transmitted: fever, severe malaise
o Hep B – vaccine available · Diagnosis
o Hep C – though is not transmitted · confirmed via aspirate of the bubo
efficiently through occupational and a direct antibody
exposure to blood · morphology : bipolar safety-pin–
shaped gram-negative organism
BIOLOGIC WARFARE AGENTS · Postexposure prophylaxis for
· infectious used as biologic weapons patients : doxycycline
· typical agent is selected for the ability to be · Treatment : aminoglycosides,
spread via the inhalational route which is doxycycline, ciprofloxacin, and
the most efficient mode of mass exposure chloramphenicol

Bacillus anthracis (Anthrax) Smallpox

· zoonotic disease in domesticated and wild · Variola : causative agent of smallpox
herbivores · major cause of infectious morbidity and
· Inhalational anthrax develops after a 1- to mortality until its eradication in the late
6-day incubation period 1970s
· nonspecific symptoms : malaise, · used it against native inhabitants by
myalgia, and fever distribution of blankets from smallpox
· symptoms worsen over short victims
period ov time with respiratory · prolonged viability of has been
distress, chest pain, and diaphoresis demonstrated in scabs up to 13 years after
· chest roentgenographic findings : collection even w/o laboratory-preserved
widened mediastinum and pleural virus
effusions · potential for reverse genetic engineering :
· High mortality rate potential biologic weapon
· Resistant to cephalosporins and · highly infectious in the aerosolized form
trimethoprim-sulfamethoxazole · incubation period : 10 to 12 days
· Postexposure prophylaxis: · clinical manifestations :
· ciprofloxacin or doxycycline · malaise, fever, vomiting, and
· If isolate is penicillin-sensitive, headache appear, followed by
switch to amoxicillin development of a characteristic
· Treatment options: centripetal rash (which is found to
· combination therapy with predominate on the face and
ciprofloxacin, clindamycin, and extremities)
rifampin

10
 · Postexposure prophylaxis with smallpox diverticulitis.
vaccine has been noted to be effective for
Today, manipulation of the biliary tract to treat a variety
up to 4 days postexposure
· Treatment: Cidofovir, (acyclic nucleoside of diseases has become a more common cause, although in
phosphonate analogue)
nearly 50% of patients no cause is identified. The most common
Francisella tularensis (Tularemia)
aerobic bacteria identified in recent series include E coli,
· gram-negative, aerobic
· principal reservoir : tick K pneumoniae, and other enteric bacilli, enterococci, and
· proliferates within macrophages after Pseudomonas
inoculation
· Difficult to culture from tissue samples spp., while the most common anaerobic bacteria are
· Has very high infectivity rate after Bacteroides spp., anaerobic streptococci, and Fusobacterium
aerosolization
· Clinical Manifestations (tularemia spp. Candida albicans and other related yeast cause the majority
pneumonia):
· cough of fungal hepatic abscesses. Small (<1 cm), multiple abscesses
· pneumonia on chest should be sampled and treated with a 4 to 6 week course of
roentgenogram
· lymphadenopathy in approx. 85% of antibiotics. Larger abscesses invariably are amenable to
patients percutaneous
· Alternative diagnosis based on
drainage, with parameters for antibiotic therapy and
acute-phase agglutination tests
· Treatment: drain removal similar to those mentioned previously. Splenic
· aminoglycosides
· second-line agents (ex. doxycycline abscesses are extremely rare and are treated in a similar fashion.
and ciprofloxacin)
Recurrent hepatic or splenic abscesses may require operative

intervention—unroofing and marsupialization or splenectomy,

respectively.

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.

The surgical treatment of this disorder was pioneered by Bradley

and Allen, who noted significant improvements in outcome for

patients undergoing repeated pancreatic débridement of infected

Organ-Specific Infections
pancreatic necrosis.63 Current care of patients with severe acute
Hepatic abscesses are rare, currently accounting for
approximately pancreatitis includes staging with dynamic, contrast
materialenhanced
15 per 100,000 hospital admissions in the United States.
helical CT scan to evaluate the extent of pancreatitis
Pyogenic abscesses account for approximately 80% of cases,
(unless significant renal dysfunction exists in which case one
the remaining 20% being equally divided among parasitic and
should forego the use of contrast material) coupled with the
fungal forms.62 Formerly, pyogenic liver abscesses mainly were
use of one of several prognostic scoring systems. Patients who
caused by pylephlebitis due to neglected appendicitis or
11
exhibit clinical signs of instability (e.g., oliguria, hypoxemia,
large-volume fluid resuscitation) should be carefully monitored
in the ICU and undergo follow-up contrast enhanced CT
examination
when renal function has stabilized to evaluate for development
of local pancreatic complications (Fig. 6-3). A recent
change in practice has been the elimination of the routine use
of prophylactic antibiotics for prevention of infected pancreatic
necrosis. Enteral feedings initiated early, using nasojejunal
feeding tubes placed past the ligament of Treitz, have been
associated with decreased development of infected pancreatic
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CHAPTER 6 SURGICAL INFECTIONS
necrosis, possibly due to a decrease in gut translocation of
bacteria.
These topics have been recently reviewed.64,65
The presence of secondary pancreatic infection should be
suspected in patients whose systemic inflammatory response
(fever, elevated WBC count, or organ dysfunction) fails to
resolve, or in those individuals who initially recuperate, only to
develop sepsis syndrome 2 to 3 weeks later. CT-guided aspiration
of fluid from the pancreatic bed for performance of Gram’s
stain and culture analysis can be useful. A positive Gram’s stain
or culture from CT-guided aspiration, or identification of gas
within the pancreas on CT scan, mandate surgical intervention.
The approach of open necrosectomy with repeated
debridements, although life saving, is associated with significant
morbidity and prolonged hospitalization. Efforts to
reduce the amount of surgical injury, while still preserving the
improved outcomes associated with debridement of the infected
sequestrum have led to a variety of less invasive approaches.66
These include endoscopic approaches, laparoscopic approaches
and other minimally invasive approaches. There are a limited
number of randomized trials reporting the use of these new
techniques
currently. An important concept common to all of these
approaches, however, is the attempt to delay surgical intervention,
since a number of trials have identified increased mortality
when intervention occurs during the first two weeks of illness.
Data supporting the use of endoscopic approaches to this
problem include nearly a dozen case series and a randomized
trial.67,68 The reported mortality rate was 5%, with a 30%
complication
rate. Most authors noted the common requirement
for multiple endoscopic debridements (similar to the open
approach), with a median of 4 endoscopic sessions required.
Fewer series report experience with the laparoscopic approach,
either transgastric or transperitoneal, entering the necrosis
through the transverse mesocolon or gastrocolic ligament. The
laparoscopic technique is carefully described in a recent
publication.
69 Laparoscopic intervention is limited by the difficulty
in achieving multiple debridements and the technical
expertise required to achieve an adequate debridement. Mortality
in 65 patients in 9 case series reported was 6% overall.
Debridement of necrosis through a lumbar approach has
been advocated by a number of authors. This approach, developed
with experience in a large number of patients, 70 has been
recently subjected to a single center randomized prospective
Figure 6-3. Contrast-enhanced CT scan of pancreas 1ó weeks after
presentation showing large central peripancreatic fluid collection.
trial.71 This approach includes delay of intervention when possible
until 4 weeks after the onset of disease. Patients receive
transgastric or preferably retroperitoneal drainage of the
sequestrum.
12
If patients do not improve over 72 hours, they are treated
with video-assisted retroperitoneal drainage (VARD), consisting
of dilation of the retroperitoneal drain tract, placement of
and irrigation, and debridement of the pancreatic bed (Fig. 6-4).
Repeat debridements are performed as clinically indicated,
with most patients requiring multiple debridements. In the
trial reported, patients randomized to VARD (n=43) compared
to those randomized to the standard open necrosectomy (n=45)
had a decreased incidence of the composite endpoint of
complications
and death (40% vs. 69%), with comparable mortality rate,
hospital, and ICU lengths of stay. Patients randomized to VARD
had fewer incisional hernias, new-onset diabetes, and need for
pancreatic enzyme supplementation.
It is apparent that patients with infected pancreatic necrosis
can safely undergo procedures that are more minimal than
the gold-standard open necrosectomy with good outcomes.
However, to obtain good outcomes these approaches require an
experienced multidisciplinary team consisting of interventional
radiologists, gastroenterologists, surgeons, and others. Important
concepts for successful management include careful preoperative
planning, delay (if possible) to allow maturation of
the fluid collection, and the willingness to repeat procedures as
necessary till the majority if not all nonviable tissue has been
removed.
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,
although a search for a local underlying source of infection
should
be undertaken. Generally, drugs that possess activity against the
causative gram-positive skin microflora are selected. Furuncles
or boils may drain spontaneously or require surgical incision and
drainage. Antibiotics are prescribed if significant cellulitis is
present
or if cellulitis does not rapidly resolve after surgical drainage.
Community-acquired methicillin resistant Staphylococcus aureus
(MRSA) infection should be suspected if infection persists after
treatment with adequate drainage and administration of first line
antibiotics. These infections may require more aggressive
drainage
and altered antimicrobial therapy.72
Aggressive soft tissue infections are rare, difficult to diagnose,
and require immediate surgical intervention plus administration
of antimicrobial agents. Failure to do so results in an
extremely high mortality rate (~80%–100%), and even with
rapid recognition and intervention, current mortality rates are
high (16%–24%).73 Eponyms and classification in the past have
been a hodgepodge of terminology, such as Meleney’s synergist
gangrene, rapidly spreading cellulitis, gas gangrene, and
necrotizing fasciitis, among others. Today it seems best to
delineate
these serious infections based on the soft tissue layer(s)
of involvement (e.g., skin and superficial soft tissue, deep soft
tissue, and muscle) and the pathogen(s) that cause them.
Patients at risk for these types of infections include those
who are elderly, immunosuppressed, or diabetic; those who
suffer from peripheral vascular disease; or those with a
combination
of these factors. The common thread among these host
factors appears to be compromise of the fascial blood supply
to some degree, and if this is coupled with the introduction of
13

6
152
PART I BASIC CONSIDERATIONS
B as they delay surgical intervention and frequently provide
C confusing information. Unfortunately, surgical extirpation
Figure 6-4. Infected pancreatic necrosis. (A) Open necrosectomy
specimen with pancreatic stent in situ. It is important to gently
debride only necrotic pancreatic tissue, relying on repeated operation
to ensure complete removal. (B) For video-assisted retroperitoneal
debridement (VARD), retroperitoneal access is gained through
radiologic placement of a drain, followed by dilation 2-3 days later.
(C) Retroperitoneal cavity seen through endoscope during VARD.
exogenous microbes, the result can be devastating. However, it
is of note that over the last decade, extremely aggressive
necrotizing
soft tissue infections among healthy individuals due to
streptococci have been described as well.
Initially, the diagnosis is established solely upon a constellation
of clinical findings, not all of which are present in every
patient. Not surprisingly, patients often develop sepsis syndrome
or septic shock without an obvious cause. The extremities,
perineum, trunk, and torso are most commonly affected, in that
order. Careful examination should be undertaken for an entry site
such as a small break or sinus in the skin from which grayish,
turbid semipurulent material (“dishwater pus”) can be expressed,
as well as for the presence of skin changes (bronze hue or brawny
induration), blebs, or crepitus. The patient often develops pain
at the site of infection that appears to be out of proportion to
any of the physical manifestations. Any of these findings
mandates
immediate surgical intervention, which should consist of
exposure and direct visualization of potentially infected tissue
(including deep soft tissue, fascia, and underlying muscle) and
radical resection of affected areas. Radiologic studies should not
be undertaken in patients in whom the diagnosis seriously is
considered,
of infected tissue frequently entails amputation and/or disfiguring
procedures; however, incomplete procedures are associated
with higher rates of morbidity and mortality (Fig. 6-5).
During the procedure a Gram’s stain should be performed
on tissue fluid. Antimicrobial agents directed against
Grampositive
and Gram-negative aerobes and anaerobes (e.g., vancomycin
plus a carbapenem), as well as high-dose aqueous penicillin
G (16,000,000 to 20,000,000 U/d), the latter to treat clostridial
pathogens, should be administered. Approximately 50% of such
infections are polymicrobial, the remainder being caused by a
single
organism such as Streptococcus pyogenes, Pseudomonas
aeruginosa,
or Clostridium perfringens. The microbiology of these
polymicrobial infections is similar to that of secondary microbial
peritonitis, with the exception that Gram-positive cocci are more
commonly encountered. Most patients should be returned to the
operating room on a scheduled basis to determine if disease
progression
has occurred. If so, additional resection of infected tissue
and debridement should take place. Antibiotic therapy can be
refined based on culture and sensitivity results, particularly in the
case of monomicrobial soft tissue infections. Hyperbaric oxygen
therapy may be of use in patients with infection caused by
gasforming
organisms (e.g., Clostridium perfringens), although the
evidence to support efficacy is limited to underpowered studies
14
and case reports.In the absence of such infection, hyperbaric
oxygen

therapy has not shown to be effective. 74

15