Lecture 24: Cutaneous Wound Healing Flashcards
What are the layers of cutaneous tissues?
Skin:
-Epidermis: protective structure from infection and the elements. Avascular, renews every 28 days, composed of epithelial cells.
-Dermis: Supports and nourishes the epidermis. Loose connective tissue w/ bv and sensory nerve endings. Also has hair follicles, sebaceous glands and sweat glands.
Subcutaneous tissue under the skin: Energy reserves. Thermal protection and shock absorption. Contains pacini corpuscles and other mechanoreceptors.
Skin: 1.5 to 4 mm, depending on region of the body.
Define: A. Hyperkeratosis B. Granulation Tissue C. Maceration D. Fibrin E. Necrotic tissue/slough F. Eschar G. Erythema H. Undermining I. Sinus tract
Define:
A. Hyperkeratosis: abnormal thickening of the stratum corner found on the dermis of people with diabetes.
B. Granulation Tissue: Red, raspberry-like appearance of tissue w/ small blood vessels and collage fibers. Allows for migration of epithelial cells in the epidermis and covering the wound.
C. Maceration: overabundance of humidity in the tissue- whitened skin.
D. Fibrin: Thin yellowish layer, deposit found on the surface of the wound during the inflammatory phase.
E. Necrotic tissue/slough: dead tissue that are yellow, grey, blackish or greenish in appearance.
F. Eschar: Black, hard crust resulting from necrosis of a cutaneous or mucous covering.
G. Erythema: redness found on skin covering more or less intense, disappears w/ pressure.
H. Undermining: skin thickness detached from tissue below
I. Sinus tract Deep anatomical tunnel.
What are the two wound healing models and what are their defining characteristics?
Partial-thickness wounds:
- Healed primarily by epithelialization (resurfacing of a wound by new epithelial cells).
- Partial loss of dermis. So new epithelial cells can surface from the dermal appendages. (islands of epidermis throughout wound surface-speeds up process)
- New epithelial cells from the edge of the wound.
Full thickness wounds:
- Wound extends through all layers of skin (dermis) and some underlying tissue.
- Healing primarily occurs via contraction.
- Epithelialization only occurs at the outer edge of the wound.
What are the stages of wound healing? Key characteristics of each stage?
1: Hemostasis
- stop bleeding/coagulation
- Fibrin clot (platelets and fibrin)
2: Inflammatory
- redness, swelling, warmth, pain
- decreased ROM
- Increased bv permeability leads to oedema
- Autogenic debridement: body uses its own mechanisms to get rid of dead tissue
- Infection control through WBC
3: Proliferative
- Repair phase
- Formation of granulation tissue: Angiogenesis via endothelial cells and collagen formation via fibroblast.
- Wound closes via contraction (myofibroblasts) and epithelialization (mitosis epithelial cells).
4: Remodelling:
- Collagen fibers organize themselves.
What is a chronic wound? Types of chronic wounds?
CW: One that deviates from the expected sequence of repair in terms of time, appearance and response to Rx. 4 to 12 wks +
Pressure Ulcers
Venous Ulcers
Arterial Ulcers
Neuropathic Ulcers
How do pressure ulcers develop?
Localized areas of necrosis that happen when soft tissue is compressed between a bony prominence and an external surface for a prolonged period of time.
Sequence: Pressure exerted by external surface>Pressure in the capillaries->Obstruction of capillary BF->Ischemia->Hypoxia in tissues.
-If pressure stops after 1-2 hours: Blood restored
-If pressure lasts >2 hours: Tissue necrosis.
What are the NPUAP stages of pressure sore classification?
Stage 1:
- Observable pressure-related alteration in intact skin (skin temp, tissue consistency, sensation)
- Well-defined area of redness that does not whiten w/ finger pressure (usually on a bony prominence)
Stage 2:
- Partial-thickness skin loss (epidermis, dermis or both)
- Superficial ulcer (blister, abrasion)
- Bed of sore is light red. No necrotic tissue.
Stage 3:
- Full thickness skin loss (damage or necrosis to subcutaneous tissue-not through ms fascia)
- Ulcer is a deep crater
Stage 4:
-Full-tickness skin loss w/ extensive destruction, tissue necrosis or damage to muscle, bone or supporting structures.
Unspecified:
-Complete tissue loss, bed of wound is covered by humid, necrotic tissue or eschar. (must decried tissue first to determine stage of wound)
How do venous ulcers develop?
Normally ms contraction pumps blood and enhance venous return, w/ unidirectional valves preventing blood from flowing back.
-Venous hypertension can occur, when there is insufficiency in the valve, so blood accumulates in the vein.
Sequence:
Venous distension-> fluid and RBC pop out of bv->swelling and brownish pigmentation-> Skin hardening (dermatosclerosis)-> Lipodermatoscloerosis
What are the causes of venous hypertension?
Valve dysfunction: genetics, previous DVT, trauma, infection and inactivity.
BF obstruction: obesity, pregnancy and thrombosis.
-Pain decreases w/ elevation leg vs arterial ulcers where pain increases w/ elevation of the leg.
How do arterial ulcers occur?
PVD->Insufficient BF to peripheral arteries-> LE do not receive adequate nutrition and oxygen->Tissue necrosis and ulceration.
Necrotic tissue=13-30mmHg
Gangrenous tissue=0-12mmHG
What are predisposing factors to arterial ulcers?
Arteriosclerosis Hypertension Diabetes Smoking Hyperlipidemia
What are the types of neuropathic ulcers and what are their characteristics.
-PN common complication of diabetes.
- Sensory
- sensory deficits (thermal, pain, pressure, tactile) leads to continuous or repetitive mechanical, thermal and chemical trauma. - Motor
-Ms atrophy and imbalances can lead to foot deformities and loss of joint mobility.
This can the lead to points of abnormal pressure (especially during gait in MT heads). (clawed toe or hammer toe deformity)
-Thinning of the fat pad
=Ulceration: Malus performans pedis - Autonomic
Dysfunction of the SNS (decreased sweating, dry skin, fissure) and poor vascular control favours the development of fungal or bacterial infections.
What is the microbial progression in a wound?
Contamination
Colonisation
Critical Colonisation (Topical infection)
-If not treated then a local infection can become a systemic infection.
What are the classes of infection and frequency?
3 Signs and symptoms of each
- Systemic: Tissue near and far from the wound are affected (ex: septicaemia)
SS: Increase WBC, fever, fatigue - Local: Tissues surrounding the wound are affected (Cellulitis)
SS: Swelling, redness, increase temp - Topical Infection: In bed of wound, no surrounding tissue affected (ex: Impetigo)
SS: Increase pain, foul door, wound enlargement, granulation tissue bright red.
1<2<3
-If their is an infection associated w/ a chronic wound, a qualitative wound culture (swab) is taken.
How is the objective appearance of a wound assessed?
- Height (long axis of wound) and width of the wound measure w/ cotton swab then ruler.
- Depth (also sinus and neighbouring space)
- Clock technique to describe where sinuses are.
- Trace area wound.
How is sensitivity of the wound assessed?
- Pressure sensitivity (monofilament)
- Pt at risk of developing diabetic ulcers if they feel <8/10 points
