1) Surgical site infections are caused by contamination of the incision site during surgery by microorganisms from the patient or environment. Staphylococcus aureus is the most common cause. 2) Risk factors for SSIs include longer surgeries, contaminated/dirty wounds, diabetes, obesity, and poor wound care after surgery. Proper antibiotic use, sterile technique, and monitoring wounds post-operatively can help prevent infections. 3) SSIs are classified as superficial, deep, or organ/space based on the involved tissue layers. Treatment involves removing sutures and draining pus from infected sites.

1. Wound Healing and Surgical site
infections
Seblewongel Aseme(MD,FCS(ECASA))

2. • Hemostasis and Inflammation
• release of chemotactic factors from the
wound site
• Wounding disrupts tissue integrity and this
activate hemostasis cascade

3. • a) hemostasisand inflammation,
• (b) proliferation, and
• (c) maturation and remodeling.

4. • Hemostasis precedes and initiates
inflammation with the ensuing release of
chemotactic factors from the wound site
• Hemostasis will be achieved at a wound site
• the fibrin clot serves as scaffolding for the
migration of inflammatory cells (neutrophils
and monocytes).
• PMNs are the first infiltrating cells to enter
the wound site, peak at 24 to 48 hours.

5. • Increased vascular permeability, the
presence of chemotactic stimulate neutrophil
migration.
• The primary role of neutrophils is
phagocytosis of debris and bacteria
• The second population of inflammatory cells
that invades the wound consists of
macrophages,
• 48 to 96 hours postinjury and remain until
wound healing is complete

6. • macrophage’s most pivotal function is activation
and recruitment of other cells via mediators such as
cytokines and growth factors,
• cell proliferation, matrix synthesis, and
angiogenesisremodeling
• , T-lymphocyte numbers peak at about 1 week
postinjury and truly bridge the transition from
• the inflammatory to the proliferative phase of
healing.

7. Proliferation
• The proliferative phase is the second phase
of wound healing
• From days 4 through
• It is during this phase that tissue continuity is
re-established.
• Fibroblasts and endothelial cells are the last
cell populations to infiltrate the wound site
• At this stage collagen formation and
angiogenesis will occur

8. • Matrix Synthesis For wound repair are
types I and III collagen are the main types
• Proteoglycan Synthesis.
Glycosaminoglycans comprise a large
• portion of the “ground substance” that
makes up granulation tissue in a wound
healing

9. • Maturation and Remodeling
• a reorganization of previously synthesized collagen.
• balance between collagenolysis and collagen synthesis.
• re-establishment of extracellular matrix
• composed of a relatively acellular collagen-rich scar.
• . The deposition of matrix at the wound site is in the following
order
• fibronectin and collagen type III
• ; glycosaminoglycansand proteoglycans
• collagen type I is the final matrix.
• the tensile strength continues to increase for several more
months.

10. Epithelization
• Restoration of the epithelial layer is primarily by
proliferation and migration of epithelial cells adjacent
to the wound (Fig. 9-4)
• starts at day 1 of injury
• Re-epithelialization is complete in less than 48
hours in the case of approximated incised wounds,
• Growth factors and cytokines are polypeptides
stimulate cellular migration, proliferation, and
function.
• All wounds undergo some degree of contraction.

12. Ehlers-Danlos syndrome
• defect in collagen formation, genetic defects
collagen type V,
• thin, friable skin with prominent veins, easy
bruising, poor wound healing, atrophic scar
formation, recurrent hernias, and
hyperesxtensible joints.
• Gastrointestinal problems include bleeding,
hiatal hernia, aneurysms, varicosities
• Fragile tissue, making suturing difficult during
surgery.

13. Marfan’s Syndrome
• A defect I a gene which codes for fibrillin, a component of
elastic tissue
• Patients with Marfan’s syndrome have tall stature,
arachnodactyly,
• lax ligaments, myopia, scoliosis, pectus excavatum, and
aneurysmof the ascending aorta.
•
• hernias. Surgical repair of a dissecting aneurysm is difficult,
• as the soft connective tissue fails to hold sutures. Skin may be
• hyperextensible but shows no delay in wound healing.36,37

14. Osteogenesis Imperfecta
• Patients have brittle bones,
• osteopenia, low muscle mass, hernias, and ligament and joint
• laxity.
• a mutation in type I collagen.
• OI subtypes with mild to lethal manifestations.
• Patients experience dermal thinning and increased
bruisability.
• Scarring is normal, and the skin is not hyperextensible.
Surgery
• can be successful but difficult in these patients, as the bones
• fracture easily under minimal stress

15. Healing in Gi tract
• The submucosa is the layer that imparts
• the greatest tensile strength and greatest
suture-holding capacity,
• a characteristic that should be kept in mind
during surgical
• repair of the GI tract.
• Healing phase similar like cutaneous healing

16. SURGICAL SITE INFECTION
Seblewongel Aseme(Pediatric
Surgeon,MD,FCS)

17. Surgical infection
• Infection
– identification of microorganisms in host tissue or the
bloodstream, plus an inflammatory response
• Surgical Site Infection
– an infection that occurs after surgery in the part of the
body where the surgery took place
• may range from a spontaneously limited wound
discharge within 7–10 days of an operation to a
life- threatening postoperative complication,

19. • SSIs accounted for 14% of Hospital acquired
infections
• 5% of patients who had undergone a surgical
procedure were found to have developed an
SSI.
• it has been reported that over one-third of
postoperative deaths are related to SSI

20. Pathogenesis
• .How are Surgical Infections caused?
– Most surgical site infections are caused by
contamination of an incision with microorganisms
from the patient's own body during surgery
• The development of an SSI depends on
contamination of the wound site at the end of
a surgical procedure and
– the pathogenicity and inoculum of
microorganisms present,
– host’s immune response.

23. • Staphylococcus aureus is themost common
cause of SSIs.
• When a viscus, such as the large bowel, is
opened, It is likely to be multibacterial
contamination

24. The microorganisms that cause SSIs are
• endogenous infection,
– from patient skin or from an opened viscus.
• Exogenous microorganisms
– from instruments or environment contaminate the
site at operation,
urogenital, biliary, pancreatic ductal, and distal
respiratory tracts do not possess resident
microflora

25. Classification of SSI
• •superficial incisionaL
– the skin and subcutaneous tissue. redness, pain, heat or swelling
drainage of pus.
• • deep incisional,
– the fascial and muscle layers.
– pus or an abcess, fever with tenderness of the wound, or a separation
of the edges of the incision exposing the deeper tissues.
• • organ or space infection,
– any part of the anatomy other than the incision that is opened or
manipulated during the surgical procedure, for example joint or
peritoneum. T
• These infections may be indicated by the drainage of pus or the
formation of an abscess detected by histopathological or
radiological examination or during re-operation.

26. • Superficial
• Deep
• Organ/space

27. Clinical feature
• At the site of infection,
– the classic findings of rubor, calor, and dolor in
areas such as the skin or subcutaneous tissue are
common.
• systemic manifestations
– elevated temperature, elevated white blood cell
(WBC) count, tachycardia, or tachypnea. The
systemic manifestations noted above comprise

34. Risk factors of SSI

35. Factors influencing SSIs
Surgical Risk Factors
• Type of procedure
• Degree of contamination
• Duration of operation
• Urgency of operation
• skin preparation
• operating room environment
• Antibiotic prophylaxis
EWMA Journal 2005; 5(2): 11-15.

36. Factors influencing SSIs
Patient Risk Factors
 Local:
 High bacterial
load
 Wound
hematoma
 Necrotic tissue
 Foreign body
 Obesity
 Systemic:
 Advanced age
 Shock
 Diabetes
 Malnutrition
 Alcoholism
 Steroids
 Chemotherapy
 Immuno-
compromise

40. The degree of risk for an SSI is linked to the type of surgical wound you
have. Surgical wounds can be classified in this way:
Wound class Definition Example Infection
rate (%)
Clean Nontraumatic, elective
surgery. GI tract,
respiratory tract, GU tract
not entered
Mastectomy
Vascular
Hernias
2%
Clean-
contaminated
Respiratory, GI, GU tract
entered with minimal
contamination
Gastrectomy
Hysterectomy
< 10%
Contaminated Open, fresh, traumatic
wounds, uncontrolled
spillage, minor break in
sterile technique
Rupture appy
Emergent
bowel resect.
20%
Dirty Open, traumatic, dirty
wounds; traumatic
perforation of hollow
viscus, frank pus in the
field
Intestinal
fistula
resection
28-70%
Berard F, Gandon J, Ann Surg 1964

45. • Antibiotic prophylaxis
– clean-contaminated surgery •
– contaminated surgery.
• Do not use antibiotic prophylaxis routinely for
clean surgery
• give a single dose of antibiotic prophylaxis
intravenously on starting anaesthesia.

46. Discontinue prophylactic antibiotics
within 24 h after the procedure
discontinue prophylactic antibiotics
after skin closure

47. Prevention OF SSI
• The prevention of surgical site infections can be
achieved in the pre-operative, intra-operative,
and post-operative settings.
• Pre-Operative Phase
• prophylactic antibiotics iDo not remove hair
routinely – if necessary do this immediately prior
to surgery with an electric clipper
• Patient advice – encourage weight loss and
smoking cessation, optimise nutrition ensure
good diabetic control

48. • Intraoperative Phase
– Prepare the skin at the surgical site
immediately before the incision using an
antiseptic preparation
– Change gloves or gowns if contaminated
– Wound irrigation at closure and
• Post-Operative Phase
– Monitor wounds closely, especially those
in difficult areas, such as skin creases and

49. Treatement of surgical site infection
• removal of sutures with drainage of pus if
present and
• Many complications of postoperative wounds do
not represent infection but exudation of tissue
fluid or an early failure to heal, which is common
in patients with a high body mass index (BMI).
• Incomplete sealing of the wound - delayed
primary or secondary suture or closure with
adhesive tape,