Inflammation, Wound Healing, and Infection

Anne McConville, MD

Why do we care?

Wound infection and failure remain common complications

Prolong hospitalization Increased resource consumption Increased costs Increased mortality Influenced by patient factors and

perioperative management

Infection Control: Hand Hygiene

Hand Hygiene Often neglected Semmelweis first noted in with 1847: puerperal

infections Resident vs. Transient flora Even “clean” procedures can result in

contamination

Infection Control:Hand Hygiene

Various Hand Hygiene Products Plain soap and water Alcohol-based rinses and gels Chlorhexidine Iodine and iodophors

Choice depends on expected pathogen, acceptability of HCW’s, and cost (usually $1/patient day).

Infection Control: Hand Hygiene

Barriers to hand hygiene Skin irritation Inaccessibility HCW acceptance

Infection Control:Antisepsis

Masks Caps Sterile gloves Drapes Decrease OR traffic Site of line placement

Infection Control:Antibiotic Prophylaxis

Miles et. al used guinea pig model as proof of principle for antibiotic prophylaxis

Knighten et. al assessed the use of high inspired oxygen alone and in addition to prophylactic antibiotics

Classen et. al prospective human study showed same results as Miles.

Standard for surgeries in which greater than minimal risk of infection

Infection Control:Antibiotic Prophylaxis

THA, TKA, extradural ortho and neuro spine, CT, vascular, kidney transplant: Cefazolin

Cranial and intradural spine: Ceftriaxone Liver transplantation: Ceftriaxone Colon surgery: Cefotetan Vaginal and abdominal Hysterectomy: Cefazolin or

Cefotetan (if bowel involved) Dosing depends on weight, redosing interval depends on

durgs used. Discontinued by 24 hours postoperatively

Surgical Site Infections

Superficial Incisional (SSI) Deep Incisional SSI Organ/Space SSI

Mechanism of Wound Repair

Inflammation Matrix production Angiogenesis Epithelization Remodeling

Initial Response to Injury

Starts with skin incision creating a wound Phases: hemostasis, inflammation,

proliferation, and remodeling Each phase is mediated by contaminants,

interaction between cells, cytokines, and other chemical mediators

Initial Response to Injury: Hemostasis

Platelet aggregation and degranulation Release of chemoattractants and growth

factors Coagulation results

Initial Response to Injury: Inflammation

Bradykinin, complement and histamine released by mast cells

PMN’s arrive almost immediately followed by macrophages in 1-2 days

WBC’s continue cycle of inflamamtion Characterized by erythema and edema of

wound edges

Proliferation

Begins about 4 days after injury Neovasularization

Angiogenesis Vasculogenesis

Collagen and Extracellular Matrix Deposition Oxygen dependent process

Epithelization

Maturation and Remodeling

Ongoing remodeling of granulation tissue and increasing tensile wound strength

Wound will never achieve tensile strength of uninjured skin/tissue

Hypertrophic and keloid scars

Wound Perfusion and Oxygenation

Ischemic or hypoxic tissue susceptible to infection and poor healing

Wound tissue oxygenation dependent on: Perfusion Arterial oxygen tension Hemoglobin dissociation conditions Local oxygen consumption Carrying capacity

Wound Perfusion and Oxygenation

Avoid vasoconstrictors Keep patient warm

Preoperative Management

Address modifiable risk factors Optimize cardiopulmonary function Treat vasoconstriction Treat existing infection Administer appropriate antibiotics Glucose control

Intraoperative Management

Administer appropriate antibiotics and re-dose at indicated intervals

Maintain normothermia Elevate PaO2 Gentle surgical technique Keep wound moist Antibiotic irrigation Delay closure for contaminated wounds Use appropriate suture and dressings Judicious fluid administration

Postoperative Management

Pain control Maintain adequate blood volume Keep patient warm Avoid vasoactive substances Maintain PaO2 Maintain glycemic control

Summary

Anesthesiologists have opportunity to enhance wound healing during perioperative management