S.G.R.

D INSTITUTE OF NURSING, PANDHER, AMRITSAR

SEMINAR
ON
SURGICAL INFECTION & ANTIBIOTIC POLICY

SUBJECT- MEDICAL SURGICAL NURSING

SUBMITTED TO- MRS. SATINDER KAUR
ASSISTANT PROFESSOR
MEDICAL SURGICAL NURSING

SUBMITTED BY- CHARANJIT KAUR

MEDICAL SURGICAL NURSING
M.SC NURSING 1ST YEAR

DATE OF SUBMITTED- 29/08/2020

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.
fig. 2. Hernostasis phaw. At the time of injuy, De fibrin clot forms the provisional wound matrix and platelets releaw mukiple growth facton Dat initi@e
the repair process. (Frnm GrHn€eld, U, editor. Surgery: xientific principle and prani‹e. Philadelphia: J.B. Lippincott, 1991' with nermit‹inn 1
• 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.
F@. 5. Remodellng phæe. The lnltial diarganlzed xar tlsrue lx slowly replaced @ a matrlx that more ctosety
resembles the organized extracellular matrix of normal shin. )Fmm Greenfield, U, editor. Surgcry: srientific
pÑnciples and praŒce. Philadelphia: J.B. Lippincott
• 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
SkĞ

Deeo incisš inel

991

liuue

0e9p soê ti8sue (fasóB 8 mus%)

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 host’s 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 INFECTIONS-
TYPES, 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.
 CON’T

• 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
 CON’T

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 2. Ugly scar 3. Keloid &
hypertrophic scar

4. Incisional hernia & 5. Pigmentation of 6. Marjolin’s

wound dehiscence the skin 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 types of operation
• 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

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

• https://
www.nice.org.uk/guidance/cg74/evidence/cg74-surgica l-site-infection-full-guideline2

• http://emedicine.medscape.com/article/188988- treatment
l

Infection Outline

Cellulitis Furuncle (boil) Carbuncle

Sebaceous cyst
Necrotising fasciitis
Cellulitis
Definition: It is an
invasive non-
suppurative infection
of the loose
connective tissue

Organism:
-Streptococci (common)
- Staphylococci
(occasionally)
- Mix
 Common in
abetics.
hogenesis

There is an inflammatory reaction occurring in the surrounding and

underlying connective tissue, including the subcutaneous fat.
Carbuncle
 Definition: It isItan
Definition: is infective
an infective
gangrene of theofsubcutaneous
gangrene tissue
the subcutaneous
usually secondary
tissue usuallyto infectionto
secondary by
Staphylococcus
infection by aureus.
Staphylococcus
aureus.
 It is common in immunocompromise d
 It is common
patients as in diabetics.

in
• The common sites: Face, nape of the
neck, and the back
immunocompr
omise d
patients as in
diabetics.
• The common
sites: Face, nape
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
 It can be caused
by ruptured
Definition:
sebaceous gland,
damage to a hair
Small, benign
follicle,
bumps filled
developmental
with an oily
defect, or
substance called
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 β- 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
• Cock’s 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. Clean
2. Clean-contaminated
3. Contaminated
4. 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
wound
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 & Love’s 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

treatment
The use of antibiotics
before, during, or after a
diagnostic, therapeutic or
surgical procedure to
prevent infectious
complications.
antibiotic treatment
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 patient’s 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 72–96 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