surgical site infections

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,