This document discusses wound healing and wound care. It covers the basic principles of wound healing including regeneration and repair. It describes the different types of tissues based on their regenerative capacity (labile, stable, permanent) and how each type heals. Factors that can influence and delay wound healing are discussed. The document also covers chronic wounds, excessive scarring, wound dressings and their purposes in wound management and care.

1. Wound healing and wound care
Dr Thana Ram Patel
Assistant Professor
Department of General Surgery
Dr SN medical college jodhpur

2. Wound Healing
• BASIC PRINCIPLES
• A. Healing is initiated when inflammation
begins.
• B. Occurs via a combination of regeneration
and repair

3. regeneration
• A. Replacement of damaged tissue with native
tissue; dependent on regenerative capacity of
tissue
• B. Tissues are divided into three types based
on regenerative capacity: labile, stable, and
permanent.

4. Labile tissues
• Labile tissues possess stem cells that
continuously cycle to regenerate the tissue.
• 1. Small and large bowel (stem cells in
mucosal crypts, Fig. 2.5)
• 2. Skin (stem cells in basal layer in epidermis,
Fig. 2.6)
• 3. Bone marrow (hematopoietic stem cells)

5. Stable tissues
• Stable tissues are comprised of cells that are
quiescent (G0) , but can reenter the cell cycle
to regenerate tissue when necessary.
• 1. Classic example is regeneration of liver by
compensatory hyperplasia after partial
resection. Each hepatocyte produces
additional cells and then reenters quiescence.
• stable cells (e.g., fibroblasts, smooth muscle
cells) can replicate.

6. Permanent tissues
• Permanent tissues lack significant
regenerative potential (e.g., myocardium/
cardiac muscle and striated / skeletal muscle,
and neurons).

7. Repair (fibrosis/ scar)
• A. Replacement of damaged tissue with fibrous scar
• B. Occurs when regenerative stem cells are lost (e.g., deep skin cut) or when a
tissue lacks regenerative capacity (e.g., healing after a myocardial infarction, Fig.
2.7)
• C. Granulation tissue formation is the initial phase of repair (Fig. 2.8).
• 1. Consists of fibroblasts (deposit type III collagen), capillaries (provide nutrients),
and myofibroblasts (contract wound)
• D. Eventually results in scar formation, in which type III collagen is replaced with
type I collagen
• 1. Type III collagen is pliable and present in granulation tissue, embryonic tissue,
• uterus, and keloids.
• 2. Type I collagen has high tensile strength and is present in skin, bone, tendons,
• and most organs.
• 3. Collagenase removes type III collagen and requires zinc as a cofactor.

8. • The main components of connective tissue
repair are
• angiogenesis,
• migration and proliferation of fibroblasts,
• collagen synthesis, and
• connective tissue remodeling.

9. • 1 haemostasis
• 2 inflammation
• 3 profliferation
• 4 remodelling.

13. Mechanism of tissue generation and
repair
• MECHANISMS OF TISSUE REGENERATION AND REPAIR
• A. Mediated by paracrine signaling via growth factors (e.g., macrophages secrete
• growth factors that target fibroblasts)
• B. Interaction of growth factors with receptors (e.g., epidermal growth factor with
• growth factor receptor) results in gene expression and cellular growth.
• C. Examples of mediators include
• 1. TGF-α - epithelial and fibroblast growth factor
• 2. TGF-β - important fibroblast growth factor; also inhibits inflammation
• 3. Platelet-derived growth factor - growth factor for endothelium, smooth muscle,
• and fibroblasts
• 4. Fibroblast growth factor - important for angiogenesis; also mediates skeletal
• development
• 5. Vascular endothelial growth factor (VEGF) - important for angiogenesis

14. repair
• Repair by connective tissue (fibrosis)
• 1. Repair by connective tissue occurs when injury is severe or persistent. Tissue in a third-degree
burn cannot be restored to normal, owing to loss of skin, basement membrane, and connective
tissue infrastructure.
• 2. Steps in normal connective tissue repair
• a. Repair requires neutrophil transmigration (see previous discussion) to liquefy injured tissue and
then macrophages to remove the debris.
• b. Repair requires formation of granulation tissue, the precursor of scar tissue . Granulation tissue
accumulates in the ECM and eventually produces dense fibrotic tissue (scar).
• c. Repair requires the initial production of type III collagen. Type III collagen has poor tensile
strength; hence, the wound can easily be reopened
• d. Dense scar tissue produced from granulation tissue contains type III collagen (weak collagen) that
must be remodeled.
• (1) Remodeling increases the tensile strength of scar tissue.
• (2) Metalloproteinases (collagenases containing zinc) replace type III collagen with type I collagen
(strong collagen), which increases the tensile strength of the wound to ≈70% to 80% of the original
after ≈3 months. Scar tissue after 3 months is primarily composed of acellular connective tissue
that is devoid of inflammatory cells and adnexal structures and is surfaced by an intact epidermis

16. Factors influencing
• B. Delayed wound healing occurs in
• Extrinsic causes
• 1. Infection (most common cause; S aureus is
the most common offender)
• 2. foreign body

18. • 3. Other causes include, ischemia, diabetes.

19. Systemic factors
• Intrinsic causes
• Nutritional deficiencies

20. Nutritional deficiencies that impair
wound healing
• Nutritional deficiencies that impair wound healing
• a. Protein deficiency (e.g., malnutrition)
• b. Vitamin C deficiency - Vitamin C is an important cofactor in the hydroxylation of proline and
• lysine procollagen residues; hydroxylation is necessary for eventual collagen cross-linking.
• c. Trace metal deficiency
• (1) Copper deficiency leads to decreased cross-linking in collagen (also in elastic
• tissue). Copper is a cofactor for lysyl oxidase, which cross-links lysine and
• hydroxylysine to form stable collagen.
• (2) Zinc deficiency leads to defects in removal of type III collagen in wound remodeling.
• Type III collagen has decreased tensile strength, which impairs wound healing. Zinc is a cofactor for
collagenase, which replaces the type III collagen of granulation tissue with stronger type I collagen.

21. glucocorticoids
• a. Interfere with collagen formation and decrease tensile strength
• b. Clinically useful in preventing excessive scar formation
• (1) Dexamethasone is used along with antibiotics to prevent scar formation in
bacterial meningitis. Dexamethasone reduces the amount of cytokines (e.g., TNF-
α and IL-1 in the cerebrospinal fluid) and has been associated with decreased
inflammation, decreased cerebral edema, and lower rates of hearing loss.
• (2) Plastic surgeons inject high-potency steroids into wounds to prevent excessive
scar tissue formation.
• c. Other effects of glucocorticoids
• (1) Inhibit production of cytokines (including IL-1, IL-6, and TNF) and other
inflammatory mediators (e.g., histamine, prostaglandins)
• (2) Reduce vasodilation in response to inflammatory mediators, which reduces the
accumulation of cells and fluid in the interstitial space (reduces swelling).
• (3) Reduce the immune cell response by inducing apoptosis of lymphocytes.

22. Cutaneous wound
• NORMAL AND ABERRANT WOUND HEALING
• A. Cutaneous healing occurs via primary or
secondary intention.
• 1. Primary intention-Wound edges are brought
together (e.g., suturing of a surgical incision);
leads to minimal scar formation
• 2. Secondary intention-Edges are not
approximated. Granulation tissue fills the defect;
myofibroblasts then contract the wound, forming
a scar.

26. Abnormal wound healing
• excessive formation of the repair components,
• deficient scar formation,
• formation of contractures.

27. • Excessive Scarring
• Excessive formation of the components of the repair process can
give rise to hypertrophic scars and keloids.
• The accumulation of excessive amounts of collagen may give rise to
a raised scar known as a hypertrophic scar. These often grow rapidly
and contain abundant myofibroblasts, but they tend to regress over
several months (Fig. 3.31A).
• If the scar tissue grows beyond the boundaries of the original
wound and does not regress, it is called a keloid (Fig. 3.31B, C).
• Keloid formation seems to be an individual predisposition, and for
unknown reasons it is somewhat more common in African
Americans.
• Hypertrophic scars generally develop after thermal or traumatic
injury that involves the deep layers of the dermis.

29. Normal and aberrant wound healing
• C. Dehiscence is rupture of a wound; most commonly seen after
abdominal surgery
• D. Hypertrophic scar is excess production of scar tissue that is
localized to the wound (Fig. 2.9).
• E. Keloid is excess production of scar tissue that is out of proportion
to the wound (Fig.2.10).
• 1. Characterized by excess type III collagen
• 2. Genetic predisposition (more common in African Americans)
• 3. Classically affects earlobes, face, and upper extremities

30. Defects in healing – chronic wounds
• These are seen in numerous clinical situations, as a result of local and systemic
factors. The following are some common examples.
• • Venous leg ulcers (Fig. 3.30A) develop most often in elderly people as a result of
chronic venous hypertension, which may be caused by severe varicose veins or
congestive heart failure. Deposits of iron pigment (hemosiderin) are common,
resulting from red cell breakdown, and there may be accompanying chronic
inflammation. These ulcers fail to heal because of poor delivery of oxygen to the
site of the ulcer.
• • Arterial ulcers (Fig. 3.30B) develop in individuals with atherosclerosis of
peripheral arteries, especially associated with diabetes. The ischemia results in
atrophy and then necrosis of the skin and underlying tissues. These lesions can be
quite painful.
• • Diabetic ulcers (Fig. 3.30C) affect the lower extremities, particularly the feet.
There is tissue necrosis and failure to heal as a result of vascular disease causing
ischemia, neuropathy, systemic metabolic abnormalities, and secondary infections.
Histologically, these lesions are characterized by epithelial ulceration (Fig. 3.30E)
and extensive granulation tissue in the underlying dermis

31. • Pressure sores (Fig. 3.30D) are areas of skin ulceration
and necrosis of underlying tissues caused by prolonged
compression of tissues against a bone, e.g., in elderly
patients with numerous morbidities lying in bed
without moving. The lesions are caused by mechanical
pressure and local ischemia.
• When a surgical incision reopens internally or
externally it is called wound dehiscence. The risk
factors for such an occurrence are obesity,
malnutrition, infections, and vascular insufficiency. In
abdominal wounds it can be precipitated by vomiting
and coughing.

32. Parenchymal wound
• Parenchymal fibrosis

33. Wound care
• The aim of wound management is to prevent
the build-up of unwanted tissues types
(necrotic tissue , slough tissue) on the wound
bed, while encouraging the growth of
granulation and epithelial (healing) tissue in
order to repair the wound.

38. dressing
• Hydrating / moisturisinng dressings - Hydrocolloids –
these are hydrating products that can be used on dry
wounds with little or no moisture in order to raise the
exudate levels to a moist environment
• Absorbent dressings - Foams – these are absorbent
dressings intended to reduce exudate levels.
• Films – these products neither absorb moisture nor
hydrate wounds. Used on their own they can only be
used on vulnerable but unbroken skin (e.g. a Grade 1
pressure damage, areas vulnerable to friction, or on
healed wounds that require some protection for a
while).

39. Absorbent primary dressings
• Alginates – these are absorbent primary dressings
• Hydrofibre – this is an absorbent primary dressing
• absorbent primary dressings that require one of
the aforementioned insulating secondary
dressings applied over them. Failure to ‘insulate’
this type of dressing will cause it to dry and
adhere to the wound bed, thereby causing
trauma on removal. This type of dressing is
required for deeper wounds

40. • Non-adherent – these are dressings that don’t
insulate the wound, hydrate nor absorb
moisture and are commonly used for
superficial wounds under other dressing types
to prevent them from adhering to the wound.
Many wound experts consider these dressing
types have little usefulness in wound care and
are therefore most frequently used with
vacuum-assisted closure treatments (topical
negative pressure)