Wound repair
Effort of tissues to restore normal function and structure after injury To reform barriers to fluid loss and infection Limit further entry of foreign organisms and material Re-establish normal blood and lymphatic flow patterns Restore the mechanical integrity of the injured system
Regeneration
Perfect restoration of the preexisting tissue architecture in the absence of scar formation Ideal in the world of wound healing Only found in embryonic development, in lower organisms, organisms such as the stone crab and the salamander, or in certain tissue compartments, such as bone and liver In wound healing in the adult human
the accuracy of regeneration is traded for the speed of repair
Types of Wound
Clean wound Clean contaminated wound Contaminated wound Dirty or infected wound
Clean wound
Elective surgery No infection/inflammation No opening of GIT/GUT/RT Infection rate: 1-3% E.g. thyroidectomy, breast surgery(excision, lumpectomy, MRM)
9/4/2007
Contaminated wound
Infection/inflammation No obvious purulent material/no fecal material Emergency surgery with no preparation Infection rate: 10-15% E.g. Emerg cholecystectomy for acute cholecystitis; emerg surgery for small bowel perforation (trauma)
Dirty Wound
Presence of purulent/fecal material Emerg surgery for generalized peritonitis Infection rate: 30% E.g. surgery for ruptured appendicitis, diverticulitis, perforated peptic ulcer; trauma surgery with colon perforation
9/4/2007
Secondary Intention
No active intent to seal the wound Use for highly contaminated t i t d wound Close by reepithelialization and contraction of the wound.
Tertiary Intention
Akadelayed primary closure Contaminated wound
initially initially treated with repeated debridement systemic or topical antibiotics closure by suturing, skin graft placement, or flap design, is performed.
9/4/2007
Healing Responses
Inflammatory Phase
Reactive phase Immediate response to injury Limits the amount of damage Prevents further injury
Proliferative Phase
Regenerative or reparative phase Reparative process p Reepithelialization Matrix synthesis Neovascularization to relieve the ischemia of the trauma itself
Healing Responses
Final maturational (or remodeling) phase Period of scar contraction
collagen cross cross-linking linking, shrinking loss of edema.
9/4/2007
Time course of the appearance of the different cells in the wound during healing
Macroph/neutros at inflamm. phase (peaks at days 2 and 3) Lymphocytes peak at day 7 Fibroblasts, proliferative phase
Macrophage
Central to wound healing Orchestrate the release of cytokines Stimulate many of the subsequent processes of wound healing Appear at the same time that neutrophils disappear Macrophages induce PMN apoptosis.
Type of Scar
Ultimately
dictated by the amount of collagen deposition balanced by the amount of collagen degradation
9/4/2007
Preferred orientation for elective skin incisions (A) is parallel to lines of facial expression (B)
Keloid
Excessive collagen deposition vs collagen degradation Grow beyond the borders of the original wounds d Rarely regress with time More prevalent among patients with darker pigmented skin
15% to 20% of African Americans, Asians, and Hispanics
KELOIDS
Genetic predisposition. Tends to occur above the clavicles on the trunk, in the upper extremities, t iti and on the face. Refractory to medical and surgical intervention
Hypertrophic Scars
Raised scars that remain within the confines of the original wound Frequently regress spontaneously Occur O anywhere h on the th body b d Preventable Prolonged inflammation and insufficient resurfacing
9/4/2007