Types of Wounds

1.acute wound 2.chronic wound

A wound with an etiology that occurs
suddenly, either with or without
intention, but then heals in a timely
manner
A wound that has a slow progression
through the healing phases, or shows
delayed, interrupted, or stalled healing
due to intrinsic and extrinsic factors
that impact the patients and their
wounds.

Types of wounds healing

Primary The healing of wounds whose clean and clear edges are
approximated shortly after trauma (surgical wound)
(normal healing process_)
Secondary The healing of wounds that have gaps between their edges,
Through granulation and epithelization in open wounds
Tertiary Dirty or contaminated wounds such as animal bites
intention Graft or flap is needed
(delayed)
Infection
Contamination: The presence of non-replicating bacteria over a body surface
without causing a disease (no effect on host).
Colonization: Presence of replicating micro-organism in the wound without
wound damage (no effect on host)
Infection: Presence of replicating micro-organism in the wound with injury
of tissues (requires AB).
“The invasion of a microorganism into the host tissues
causing host to be diseased”
 Wound infection occurs when bacteria or other microbes move
1.Local deeper into the wound tissue and proliferate at a rate that
infection invokes a response in the host. Local infection is contained in one
location, system or structure
2.Spreading Spreading infection describes the invasion of the surrounding
infection tissue by infective organisms that have spread from a wound.
Microorganisms proliferate and spread, to a degree that signs and
symptoms extend beyond the wound border. Spreading infection
may involve deep tissue, muscle, fascia, organs or body cavities.
3.Systemic Systemic infection from a wound affects the body as a whole, with
infection Microorganisms spreading throughout the body via the vascular
or lymphatic systems.

Wound Infection Is the presence of replicating microorganism within a wound

leading to host/tissue injury (occur after surgery, trauma or a
disease that interrupt a mucosal or skin surface)
Surgical Site An infection that occurs after surgery in the part of the body
Infection (SSI) where thes urgery took place (with in less than 30 days of
surgery)

Hospital Acquired An infection acquired in the hospital by a patient who was

infection (HAIs) admitted for a reason other than the infection
 Biofilm:
A structured community of microbes with genetic diversity and variable
gene expression that creates behaviour and defences used to produce
unique infections (chronic infections).
Biofilms are characterized by significant tolerance to antibiotics while
remaining protected from host immunity.

Bioflim Cycle
1.Planktonic free-floating, non-attached single microbes attach to a surface or
attachment each other. In this early phase, the attachment is weak and
(reversible) reversible.
2.Irreversible If single microbes that are anchored together or to a surface are
attachement not separated, the attachments becomes stronger and irreversible
3.Cell After attachments become strong and irreversible, microbe cells
proliferation begin proliferating and other microbes become attracted to, and
join, the biofilm colony
4.Growth & The biofilm grows and differentiates. The host’s defenses are
Maturation inadequate to eradicate the biofilm, but recognize its presence
which can cause tissue destruction and increase nutrition
for the biofilm
5.Dispersal Mature biofilm begins reseeding the wound surface with
planktonic microbes as either a passive or active dispersal process
Pathogenesis of Wound Infection:
It is the interaction between:
• Host defense mechanism
• Causitive organism
In the presence of wound
1. Host Defense mechanisms: are the methods by which the
body protects itself from infection:
• Skin
• Chemical barriers as Hcl
• Humoral immunity Abs, complements
• Cellular immunity as macrophages, neutrophils
Failure of host defense mechanism in:
• Wound (interruption of skin)
• Metabolic (Malnutrition, DM….)
• Catabolic disorder(Burn, cancer)
• Iatrogenic (Radiation , chemotherapy, steroid)

2.caustive agents:
 1. Endogenous
- Translocation of normal flora
- Opportunistic Infection
2. Exogenous
- Hospital Acquired Infection

Surgery (wound) Stimulate innate immunity within hours

(sterile inflammatory response) by ROS,
macrophages, and other proteins

neutrophils &Macrophages

Initially beneficial for wound healing, but if unbalanced by

homeostatic anti-inflammatory mechanisms during early
phase, it will suppress the patient's ability to mount an
effective defense mechanism against invading microbes.

Anesthesia Can cause immunosuppression reduce

the patient's ability to resist infections
Surgical site infections

Why is it still a problem?

 Types of SSIs
1.major A wound that either discharge a significant quantities of pus
spontaneously or need a secondary procedure to drain it.

2.minor A wound that may discharge pus or infected serous fluid but should not be
associated with excessive discomfort, systemic signs, or delay in return
home.
Factors determining extent of infection
•Organism…virulence, dose
•Wound….blood supply, foreign bodies
•Medications…antibiotics
Bacteriology
❑Criteria of infective agent:
1-in considerable number in septic focus
2-possible to be isolated , cultured in other media
3- Able to produces similar lesion if injected in
another host
❑Types
(G +ve ,G –ve)(Aerobes) (Anaerobes)
• Streptococci: G +ve , 5-10% of population in pharynx, Cellulitis
,post bowel surgery, skin infection, sesitive to penicillins
• Staphylococci: the commonest organism seen clinicaly , G+ve,
15% of population in naso-pharenx, localized skin
infection….MRSA
• Clostridia: G +ve spore forming, anaerobes ,Tetani, gas
gangrene
• Escherichia coli & pseudomonas : G-ve , intestine
• Bacteroides: non spore forming large bowel, vagina,
metronidazole & cefotaxime

Surgical Site Infection

 Levels of SSIs

Classes of Wounds
Risk factors of SSIs
 Clinical Presentation of SSIs
• Appears usually between fifth and tenth days postoperatively
• Wound pain and fever
• Swollen wound ,tender and red
• Fluctuation and crepitation
• Wound discharge (purulent discharge)
Diagnosis of SSIs:

Wound Dressing:
 Recommendations to minimize SSIs
The patient • Correction of any predisposing factor , control DM , stop
smoking and nutritional support
• Operations should be avoided in patients with active
infections
• Shaving or clipping hair just before skin incision , clipping is
preferred
• Skin preparation with antiseptic
The surgeon •Short nails and should scrub properly
•Meticulous surgical technique by adequate
hemostasis , gentle handling of tissues , avoid tight
sutures , or leaving dead space
•Delayed primary closure of heavily contaminated
wounds

Prophylactic •Indicated in clean contaminated or contaminated

antibiotics surgery and with implants
•Given preoperatively or intraoperative (according to
half life of the AB)
•Cephazolin (first generation cephalosporin) is the
commonest to be used or according to the infection
control program of the hospital
Treatment •Liberal drainage
•Antibiotics guided by culture and sensitivity
 PART 2
Specific Wound
Infection
 1.acute abscess
• It is a localized collection of pus in a cavity lined by
granulation tissue, covered by pyogenic membrane.
• Pus contains dead WBC’s, multiplying bacteria, toxins
and necrotic material.
•Pathogenesis: localized suppurative inflammation.
• Abscesses contain hyperosmolar materialthat draws in
fluid.
• This increases the pressure and causes pain.
• If they spread, they usually track along planes of least
resistance and point towards the skin, so they discharge
spontaneously, or may need drainage through a
surgical incision.
• Most abscesses relating to surgical wounds take 7–10
days to form after surgery.
• Pathology Grossly abscess formed of 3 zones
• Central zone of coagulative necrosis (pus )
• Intermediate zone of granulation
• peripheral zone of acute inflamation
Complications • spread of infection
• fistula & sinus
• necrosis & gangrene
• suppressed wound healing
• immune suppression
• Multiple organ failure
Causative Organism • Pyogenic organisms, predominantly Staphylococcus
aureus, & Streptococci are usually the causative agents
of acute abscesses
• Other includes Mycobacterium & Actinomyces
Clinical Picture • Constitutional symptoms (fever, fatigue, anorexia, malaise)
• Local sings of inflammation (erythema, redness, hotness,
pain)
• Draining lymph node enlargement
Investigations • Lab (CBC, culture & Sensitivity)
• Imaging (US, or CT)

Treatment • Incision & Drainage

• Excision
• Antibiotics
• General supportive measures
Prophylaxis 1- defense mechanisms should be improved (anemia, DM)
2- Prophylactic antibiotics (in contaminated &clean
contaminated)
3-Sound surgical principles (gentle tissue handling ,…..)
4- Colon preparations
5- Wound drainage
 2. Cellulitis
• Cellulitis is a common bacterial skin infection.
• It is an acute bacterial infection causing
inflammation of the deep dermis and surrounding subcutaneous
tissue.
• The infection is without an abscess or purulent discharge.

Pathogensis • The skin acts as a protective barrier that prevents normal skin
flora and other microbial agents from reaching the subcutaneous
tissues & lymphatic system.
• When a wound (break in the skin) occurs, it allow the entery of
pathogens to the subcutaneous tissue causing acute superficial
infection.
• Nonsuppurative Invasive infection in loose connective of tissue
Causative • Mainly Streptococci (streptococcus pyogens)
Organism • Staphylococci
• Clostridium perfringens

Clinical ❑Pain
Presentation ❑Fever
❑Skin oedema
❑Poor Localization of inflammation
❑Non-suppurative
❑Skin blisters
Treatment • TTT of Mild Cellulitis: Antibiotics covering Streptococcal
species (for a minimum of 5 days)
• TTT of purleunt cellulitis (MRSA): IV antibiotics with sulfa
• Hospitalization: indicated in patients with MRSA or patients
showing signs of systemic infection
• If untreated: Bacteremia
3. Acute Lymphangitis & lymphadenitis
• Acute It is an acute nonsuppurative infection and spreading
Lymphangitis: inflammation of lymphatics of skin and subcutaneous
tissues due to beta hemolytic streptococci, staphylococci,
clostridial organisms.
• Acute Acute nonsuppurative
Lymphadenitis: infection of the draining lymph nodes

Clinical • Painful red streaks in affected

Presentation lymphatics
• Painful enlarged lymph nodes
• Pain & Tenderness
• Usually accompanied with cellulitis
• Fever is common
Treatment • Treatment of the cause
• Antibiotics (IV)

4.Bacteremia 5.Septicemia
• Circulating Bacteria • Circulating bacteria & toxins
• Bacteremia is common after
anastomotic breakdown It can also
follow procedures under(deep space
SSI). taken through infected tissues
(particularly instrumentation in
infected bile or urine),or through
bacterial colonization of indwelling
intravenous cannula.
 6.(SIRS)Systemic Inflammatory Response
syndrome
• Systemic inflammatory response syndrome (SIRS) is a systemic manifestation
of sepsis, although the syndrome may also be caused by multiple trauma, burns
or pancreatitis without infection.
• SIRS should not be confused with bacteremia although the two may coexist.
• It may cause multiorgan failure and death
Two of:
• Hyperthermia (>38°C) or hypothermia (<36°C)
• Tachycardia (>90/min, no B-blockers) or tachypnoea
(>20/min)
• White cell count >12 X 109/l or <4 X 109/l

7.Gas gangrene
0.1% of SSIs
Clostridium perfringens (Trauma) (80-90%)
Clostridium novyi (40%)
Clostridium septicum (GI abnormalities) (10%)
Clostridium histolyticum (Trauma) (20%)
Pathophysiology Clostriduim species (gas producing organism)
produce alpha & theta toxins that cause
extensive damage to the tissues
Treatment 1- Surgical debridement & Fasciotomy
2- Aggressive ABs
3- IV fluid resuscitation
4- ICU monitoring
5- Hyperbaric oxygen therapy
 8.Necrotizing Fasciitis
• Infection of the soft tissue, which start in the
superficial fascia and progresses rapidly to the deep
fascia resulting in occlusion of the small blood vessels that
supply the overlying skin and subsequently skin necrosis
• If untreated ----- systmeic inflammatory response
syndrome & spetic shock
Epidemiology • 26.1% NF are related to trauma
• 4.3% of NF are related to surgical site infection
Risk Factors • Diabetes mellitus
• Severe peripheral vascular
disease
• Alcoholism
• Trauma
• Malignancy
• Reduced immunity
• NSAIDs
Classification Type I
Caused by polymicrobial organisms (aerobic and
anaerobic organisms) which commonly originates from the
bowel flora.
…………………………………….
Type II
caused by group A Streptococcus pyogens Staphylococcus
aureus, Vibrio vulnificus, Vibrio damsel, Aeromonas
hydrophila and anaerobic Streptococci.
 Group A streptococci

collagenase & hyaluronidase

enzymes Liquefactive necrosis of fat and fascia

..Separation of the skin from the underlying tissues,

thrombosis of the small blood vessels, tissue necrosis,
decreased oxygen saturation and growth of anaerobic

presentation *Pain (earliest sign & disappear as disease progress)

*Fever (40%)
*skin manifestation
Stage I (early stage):
Warmness, tenderness, erythema, swelling and indurated
wooden skin
Stage II (intermediate):
Blisters & Bullae
Stage III (Late):
Hemorrhagic bullae, crepitus, skin anesthesia and necrosis
Bullae & Necrosis

Surgical debridment
Broad spectrum AB
Fluid resuscitation & wound care
Hyperbaric oxygen / IV immunoglobulin