SURGICAL INFECTION

&
ANTIBIOTIC POLICY
QURAISHIA ALYA
NURUL SYAZWANI
ALYA MAZLAN
AZRIAH
NAZIFA
NAIM
SHAHRIMAN

Outline Of Seminar
1. Surgical site infection
2. Post operation wound healing
3. Acute surgical infection

Carbuncle
Necrotizing fasciitis
Infected cyst

4. Classification of surgical wounds

5. Antibiotic policy

Overview
Etiology and pathogenesis of surgical
infection
Etiology and pathogenesis of post
operative wound healing

Wound Healing
Involves 3 overlapping major phases:
1. Inflammation, with cascades of processes that can
be further subdivided into early and late phases.
2. Regeneration
3. Maturation

The key cells that are involved in this process:

. Inflammation: platelets, neutrophils, lymphocytes
and macrophages
. Regeneration and maturation: macrophages and
fibroblasts (myofibroblasts)

 Inflammation:
Early inflammation (first 24 hours)
begins with haemostasis through
vasoconstriction, thrombin formation
and platelet aggregation. Platelets
release cytokines and other factors that
influence leucocyte and monocyte
activity.
Late inflammation(24-72 hours) release
of vasodilators that increase
permeability of local capillary bed for
serum and white cells to be released to
surround the wound in margination and
diapedesis.

 Regeneration
Follows over next few days .
Characterized by increase in fibroblast
mitogenic activity and endothelial cell
mitotic activity , with epithelial cell
migration and synthesis of collagen and
metalloproteinases.

Maturation (remodelling phase)

Can take up to 2 years. Granulation
tissue gradually matures into scar
tissue. Fibroblasts and proteases
maintain balance between deposition
and degradation of tissue.

 Infection is usually prevented by

natural mechanism ; eg: mechanical
barriers (skin), chemical (low gastric
pH), humoral (antibodies), cellular
(phagocytic cells).
May be compromised by surgical
intervention and treatment.
Causes of reduced resistance to
infection:
Metabolic : malnutrition, diabetes,
uraemia, jaundice
Disseminated disease: cancer, AIDS
Iatrogenic: radiotherapy, chemotherapy,

 Risk factors for increased risk of

wound infection
Malnutrition (obesity, weight loss)
Metabolic disease ( diabetes, uraemis,
jaundice)
Immunosuppression ( cancer, AIDS)
Colonisation and translocation in GIT
Poor perfusion (systemic shock, local
ischemia)
Foreign body material
Poor surgical technique (dead space,
hematoma)

Surgical Site Infection (SSI)

Infection that occur in the wound created
by an invasive surgical procedure.
Many of these infections occur after the
patient has been discharged from hospital.
Types:
Incisional
1. Superficial (skin and cutaneous tissue)
2. Deep (fascial and muscles)

Organ space
. eg: intra-abdominal abscess

ETIOLOGY
Classification of sources of infection
1. Primary: present in or on the host and
so acquired from an endogenous
source
(eg: contamination of wound from a
perforated appendix)

2. Secondary or exogenous: acquired

from a source outside the body
(eg: operating theatre-inadequate air
filtration, poor asepsis / the ward- poor hand
washing compliance)

 Microbial factor
Most SSI are contaminated by patients
own endogenous flora (on skin, mucous
membranes, or hollow viscera)
Bacteria involved:
Gram positive cocci :
Streptococci - Streptococci pyogenes
Staphylococci Staphylococcus aureus

Gram negative bacilli

E. coli, Klebsiella spp.

Clostridia
Bacteroides

Pathogenesis
Development of SSI depends on
contamination of wound site at the
end of surgical procedure and
specifically relates to pathogenicity
and inoculum of microorganisms
present, balanced against the hosts
immune response.

Reference
Bailey & Love Short practice of
surgery (26th Edition)
NICE Clinical Guideline 2008 (Surgical
site infection prevention and
treatment of surgical site infection)
https://www.nice.org.uk/guidance/cg74/evide
nce/cg74-surgical-site-infection-full-guide
line2

http://emedicine.medscape.com/articl
e/188988-treatment

SURGICAL SITE
INFECTIONSTYPES, PRESENTATIONS
COMPLICATIONS, &
TREATMENT

PRESENTATIONS

BASED ON SITE OF INFECTIONS

Superficial incisional SSI may produce pus, or
purulent discharge from the wound site along with
atleast one sign of inflammation (pain,

redness,

swelling, local warmth of wound,etc)

Deep incisional SSI puulent discharge may present
but without organ/ space involvement. The wound
site may reopen on its own, or a surgeon may reopen
the wound and find purulent discharge inside the
wound.

CONT
Organ or space SSI may show a discharge of
pus coming from a drain placed through the skin
into a body space or organ. A collection of
purulent discharge may lead to an abscess (occur
within 30 days of operation)

MAJOR AND MINOR SURGICAL SITE

INFECTIONS
Major wound infections:
Significant quantity of pus
Patients are systemically ill (may have systemic signs
such as tachycardia, pyrexia and raised in white cell
count)

Minor wound infections:

Small quantity pus but NOT associated with excessive
discomfort or any systemic signs

CONT
Other than pus or abscess, patient with SSI may
present with:
Cellulitis and lymphangitis
Bacteremia and sepsis
Gas gangrene

COMPLICATIONS OF WOUND
HEALING

1. infection

4. Incisional hernia
& wound
dehiscence

2. Ugly scar

5. Pigmentation
of the skin

3. Keloid &
hypertrophic scar

6. Marjolins
ulcer

TREATMENT
Suture removal plus incision and drainage should be

performed for SSIs (to allow pus to drain adequately)

Major

surgical

infections

with

systemic

signs

need

treatment with appropriate antibiotics

Minor infections may respond to drainage of pus (for

example, by removal of sutures) and topical antisepsis

The choice of antibiotics is empirical until sensitivities are

available
Empirical therapy should be broad-spectrum and cover

S. aureus, which is the most common cause of SSI after all

 SSIs after clean-contaminated surgery should be

treated with an empirical antibiotic regimen that
includes activity against anaerobic bacteria (eg:
metronidazole, co-amoxiclav, piperacillin-tazobactam or
meropenem).
SSIs in patients known to have, or at risk of
methicillin-resistant S. aureus (MRSA) carriage should be
treated with an empirical antibiotic regimen that includes
activity against locally prevalent strains of MRSA (eg:
first-generation Cephalosporins, vancomycin and
antistaphylococcalpenicillins such as nafcillin,
oxacillin)

REFERENCES
Bailey & Love Short practice of surgery (26th
Edition)
Manipal Manual of Surgery (4th Edition)

https://
www.nice.org.uk/guidance/cg74/evidence/cg74-surgica
l-site-infection-full-guideline2
http://emedicine.medscape.com/article/188988treatment

THANK
YOU!

Acute
Surgical
Infection
NUR ALYA SYAFIQAH BINTI MASGELAN @
MAZLAN
012013100252

Outline
Cellulitis
Furuncle (boil)
Carbuncle
Sebaceous cyst
Necrotising fasciitis

Cellulitis

Definition: It is an
invasive nonsuppurative infection
of the loose
connective tissue
Organism:
-Streptococci
(common)
- Staphylococci
(occasionally)
- Mix

Pathogenesis

Bacteria entering the skin, causing infection.

The acute spreading infection may extend
deeper than the skin and involve the
subcutaneous tissues.

Furuncle (boil)

Definition: It is an
acute infection of
a hair follicle,
usually caused by
Staphylococcus
aureus

Common in
diabetics.

The common
sites: Face, neck
and axilla.

Pathogenesis
There is an inflammatory reaction
occurring in the surrounding and
underlying connective tissue,
including the subcutaneous fat.

Carbuncle

Definition: It is an infective gangrene

of the subcutaneous tissue usually
secondary to infection by
Staphylococcus aureus.
It is common in
immunocompromise
d patients as in
diabetics.
The common sites:
Face, nape of the
neck, and the back

Pathogenesis
Infection usually starts in a hair follicle.
Extends to the subcutaneous fat where other
hair follicles get the infection.
Multiple areas of necrosis and thrombosis of
blood vessels occur.
Patches of skin undergo sloughing and
separate from the underlying granulation
tissue.

Sebaceous Cyst

Definition: Small,
benign bumps
filled with an oily
substance called
sebum

It can be caused
by ruptured
sebaceous gland,
damage to a hair
follicle,
developmental
defect, or heredity

Mainly seen on the

face, trunk, and
neck.

Pathogenesis
Implantation of
epidermal
elements in the
dermis.

Necrotising
Fasciitis

Definition: It is a spreading, destructive,

invasive infection of skin and soft tissues
including deep fascia with relative sparing of
muscle.
Causative organisms:
- Monomicrobial: it is due to group A haemolytic streptococci
- Polymicrobial: it is due to synergistic
combination of anaerobes and coliforms or
non-group A streptococci.
Common site: Lower
extremities
Other sites: Genitalia,
groin, lower abdomen.

Pathogenesis
The infectious process spreads along the
fascial planes and results infectious
thrombosis of the vessels passing between
the skin and deep circulation.
Superficial skin necrosis follows.
Hemorrhagic bullae appear as the first sign of
skin death.
Fascial and subcutaneous fat necrosis
involves wider area than the skin.

THANK
YOU

Acute Surgical
Infection (cont.)
NUR AZRIAH BINTI KAMARZAMAN
012013100256

OUTLINE
Clinical features
Complication/ Risk factor
Treatment

CELLULITIS

CLINICAL FEATURES
The affected area is red,indurated,hot and
painful
It spreads rapidly with ill defined edge
The skin may be the seat of blisters
Fever
Lymphangitis in the form of red streaks
No suppuration
In severe cases patches of skin necrosis with
sloughing of subcutaneous tissues

COMPLICATION

Septicaemia
Abscess
Necrotising fasciitis
meningitits

TREATMENT
Gram positive cover. Used broad spectrum for
immune compromised/ diabetic patient
Cephalosporins (cephalothin, cephalexin) for
antistaphylococcal coverage except for MRSA

FURUNCLE (BOIL)

CLINICAL FEATURES
Swelling which is raised, red,with discharging pus
through one punctum with central filling of
necrotic tissue.
site of friction, occlusion, and perspiration (neck,
axilla, buttocks)
Tender, hot swelling, non-mobile
Firm at first then become fluctuant

COMPLICATION
Cavernous sinus thrombosis
Systemic sepsis in uncontrolled diabetes

TREATMENT
Heal spontaneously
Some cased incision and drainage needed (done
under local anaesthesia)
Remove necrotic centre/slough and continue
drassings till heals completely
Control of diabetes if present

CARBUNCLE

CLINICAL FEATURES
Typically in diabetic patient
Severe pain and swelling in the nape of the neck
Constitutional symptoms such as fever with chills
and rigors are severe
Surface is red, angry looking like red hot coal
Surrounding area is indurated
Later, skin on the centre of carbuncle softens and
peripheral satellite vesicles appear, which rupture
discharging pus and giving rise to a cribriform
appearance
The end result Is development of large
crateriform ulcer with central slough

COMPLICATION
Worsening of the diabetic status resulting in
diabetic ketoacidosis
Extensive necrosis of skin overlying carbuncle.
Hence, it is included under acute infective
gangrene
Septicaemia, toxaemia

TREATMENT
Diabetic control, preferably with injected insulin
Appropriate parenteral antibiotics are given till
complete resolution occur
Improve general health of the patient
If carbuncle does not show any evidence of
healing
Not incised
Left open to exterior or saline dressings may
be applied to reduce oedema complete
resolution within 10-15 days
Surgery required when there is pus
Cruciate incision is preferred

SEBACEOUS CYST

CLINICAL FEATURES

Single/multiple
Site: can be anywhere except palm and sole.
Common site: scalp, neck, axilla, groin, scrotum
Size: 5mm-2cm
Shape: spherical
Smooth surface with well defined margin
Consistency: firm
Skin: usually normal but when infected may cause
redden skin and tender/ increase temperature on
palpation
Associated features: punctum where foul-smelling
cheesy exudates (sebum) can be squeezed out/
sebaceous horn
Not comprissible/reducible

COMPLICATIONS

Infection
Ulceration
Rupture and sinus formation
Calcification
Cocks peculiar tumor
Sebaceous horn

TREATMENT
Removal of entire cyst wall together with the
punctum by ecliptical incision to prevent
recurrence
Intralesional steroid at 5mg/m to control small
inflamed symptomatic lesion
If cyst is infected- incision and drainagewith
antibiotic to cover S.aureus
If cyst ruptured/ infected- drainage and curatage
done

NECROTISING FASCIITIS

CLINICAL FEATURES
Sudden pain in the affected area with gross
swelling of the limbs
The part is swollen, red, erythematous and
oedematous with skip lesion of skin necrosis
and ulceration
Skin changes: bronze hue, brawny induration,
blebs or crepitus
High degree fever, jaundice, renal failure can
occur soon in untreated cases

RISK FACTOR

Diabetes mellitus,
Malnutrition
Obesity
Corticosteroid
Immune deficiency

TREATMENT
Medical emergency
Supportive treatment
Hospitalization
Adequate hydration
Broad spectrum antibiotics vancomycin +
carbapenem
In type ll cases (streptococcal) : high dose penicillin
+ clindamycin

Surgical treatment
Involves wide excision, generous debridement
followed by skin grfating, a few days or weeks later

Classification of
Surgical Wounds

Nazifa Nusral
012012050561


1.
2.
3.
4.

Clean
Clean-contaminated
Contaminated
Dirty

Clean wound

. Uninfected operative wound.

. No inflammation.
. Respiratory, alimentary, genital, or uninfected
urinary tract is not entered.
. No viscus opened.
. Primarily closed, if necessary, drained with closed
drainage.
. 1-2 % infection rate.
. Rate before prophylaxis is the same.
. Eg: Breast biopsy.

Clean-contaminated
wound

. An operative wound where respiratory,

alimentary, genital, or urinary tracts are entered
under controlled conditions and without unusual
contamination.
. Viscus opened, minimal spillage.
. <10% infection rate.
. Rate before prophylaxis for gastric surgery is up
to 30% and biliary surgery is up to 20%.
. Eg: Biliary tract, appendix, vagina, and
oropharynx.

Contaminated wound

. Open, fresh, accidental wounds.

. Open viscus with spillage or inflammatory
disease.
. 15-20% infection rate.
. Rate before prophylaxis is variable but up to
60%.
. Eg: Penetrating wounds.

Dirty wound

. Old traumatic wounds with retained devitalized

tissue and those that involve existing clinical
infection or perforated viscera.
. Pus or perforation, or incision through an
abscess.
. Organism causing postoperative infection were
present in the operative field before operation.
. <40% infection rate.
. Rate before prophylaxis is up to 60% or more.
. Eg: Perforated bowel.

References

. Bailey & Loves Short Practice of Surgery.

. Medscape.com
. CDC.gov

THANK YOU

COMMONLY USED
ANTIBIOTICS

TARGETED TREAMENT

DEFINITION
A type of treatment that uses drugs or other
substances to identify and attack specific types of
cancer cells with less harm to normal cells

TYPE

HOW IS IT DETERMINED WHETHER

A PATIENTS IS A CANDIDATE?
The use of a targeted therapy may be restricted
to patients whose tumor has a specific gene
mutation that codes for the target :
patients who do not have the mutation would
not be candidates because the therapy would
have nothing to target
E.g : BCR-ABL gene in CML

a condition that cannot be treated by surgery.

cancer did not respond to other therapies

SIDE EFFECT
most common side effects therapies
diarrhea
liver problems, such as hepatitis and elevated liver
enzymes.

Other side effects

Skin problems (acneiform rash, dry skin, nail changes,
hair depigmentation)
Problems with blood clotting and wound healing
High blood pressure
Gastrointestinal perforation

PROPHYLAXIS
ANTIBIOTIC

DEFINITION
Antibiotics used for prevention of infection
complications
Prophylactic antibiotic
Therapeutic antibiotic
treatment
treatment
The use of antibiotics before,
during, or after a
diagnostic, therapeutic or
surgical procedure to
prevent infectious
complications.

The use of substances that

reduce the growth or
reproduction of bacteria,
including eradication therapy.
This term is used to describe
antimicrobial therapy
prescribed to clear infection by
an organism or to clear an
organism that is colonising a
patient but is not causing
infection.

GENERAL PRINCIPLE

Active against common surgical wound pathogen

Proved efficacy in clinical trials
Shortest course of administration
Newer-broad spectrum are reserved for
resistance
Least expensive of antibiotic

EMPIRICAL TREATMENT

DEFINITION
ANTIBIOTIC THAT FREQUENTLY USED
BEFORE THE PATHOGEN RESPONSIBLE FOR A
PARTICULAR ILLNESS TO A PARTICULLAR
ANTIBIOTIC IS KNOWN
EARLY INTERVENTION THAT WILL IMPROVE
THE OUTCOMES

APPROACH TO EMPIRIC THERAPY

1. FORMULATE A CLINICAL DIAGNOSIS
2. OBTAIN SPECIMEN FOR LABROTARY
EXAMINATION
3. FORMULATE CLINICAL DIAGNOSIS
4. DETERMINE THE NECESSITY FOR EMPIRIC
TREATMENT
5. INSTITUTE TREATMENT

GENERAL PRINCIPLES
Cultures of presumed infected site(s) should always
be obtained Initial empiric therapy should be chosen based
on most likely
pathogens,
hospital susceptibility patterns,
cost-effective therapy,
impact on development of resistance.

Alteration patients flora by previous and recent therapy

should taken to account when choosing

 Greater severity of illness state suggest to use broader

antimicrobial

A history of PCN-allergy should be carefully evaluated as it does

not always suggest to use of non-beta-lactam antibiotics.
In patients with less severe PCN allergies the use of cephalosporins /

carbapenems may be possible based on risk/benefit.

If any doubt exists, discussion with Infectious Diseases (ID) is recommended.

Reassess all antibiotic therapy in 7296 hours.

Once culture results are obtained, antibiotic therapy should be modified to
target identified pathogen(s) and to narrow the spectrum of activity if
possible.

 Discontinue vancomycin if no methicillin-resistant S. aureus

(MRSA) /resistant gram-positive organisms identified.

A switch to oral therapy should be considered following

clinical improvement where possible to complete the
recommended course of therapy.

Recommendations for duration of therapy are provided

based on clinical syndromes and usual clinical course.
Duration may be altered by clinical course