Wound healing and management Flashcards
1
Q
First intention
A
Occurs by approximation of wound edges soon after injury
Results in narrow scar formation with superior cosmetic result
Most surgical skin incisions are closed, to heal by first intention
2
Q
4 stages of each intention
A
Haemostasis
Inflammation
Proliferation
Remodelling
(HOW I PERSONALLY RECTIFIED)
3
Q
Haemostasis
A
The action of platelets and cytokines forms a haematoma and causes vasoconstriction, limiting blood loss at the afffected area
The close proxmity of the wound edges allows for ease of clot formation and prevents infection by forming a scab
4
Q
Purpose of inflammation
A
A cellular inflamatory response acts to remove any cell debris and pathogens present
5
Q
Proliferation
A
- Cytokines released by inflammatory cells drive the prolfieration of fibroblasts and the formation of granulation tissue
- Angiogenesis is promoted by the presence of growth mediators(e.g. VEGF), allowing for further maturation of the granulation tissue; the production of collagen by fibroblasts allows for closure of the wound around a week
6
Q
Remodelling
A
- Devascularisation of the region occurs and the fibroblasts undergo apoptosis
7
Q
What happens if the sutures used to close a wound are too loose
A
- Wound edges will not be properly opposed, limiting the primary intention healing and reducing wound strength
8
Q
What happens if the sutures used to close a wound are too tight
A
- Blood supply to the region may become compromised and lead to tissue necrosis and wound breakdown
9
Q
3 phases of wound healing
A
1) Inflammatory phase
2) Reparative Phase
3) Consolidation phase
(I Repair Cuts)
10
Q
Inflammatory phase overview
A
- Acute inflammatory processes cascade in response to cellular injury.
- Clot formation, tissue oedema, and increased vascular permeability occur, with fibrin formed in the wound helping to hold the edges together.
- Clean, healthy surgical incisions are typically approximated with sutures, adhesive strips or glues.
- There is no inherent strength of the wound during this phase, which lasts up to 3 days
11
Q
4 cardinal features of acute inflammation
A
1) Rubor(redness) - secondary to vasodilatation and increased blood flow
2) Calor(heat) - localised increase in temp, also due to increased blood flow
3) Tumour(swelling) - Results from increased vessel permeability, allowing fluid loss into the interstitial space
4) Dolor(pain) - Caused by stimulation of the local nerve endings, from mechanical and chemical mediators
12
Q
Phases of acute inflammation
A
1) Vascular phase
2) Cellular phase
13
Q
Vascular phase of acute inflammation
A
- small blood vessels adjacent to the injury dilate (vasodilatation) and blood flow to the area increases
- The endothelial cells initially swell, then contract to increase the space between them, therebyincreasing the permeabilityof the vascular barrier
- This process is regulated bychemical mediators
- Exudation of fluidleads to a net loss of fluid from the vascular space into the interstitial space, resulting inoedema(tumour)
- The formation of increased tissue fluid acts as a medium for which inflammatory proteins(such as complement and immunoglobulins) can migrate through. It may also help to remove pathogens and cell debris in the area through lymphatic drainage
14
Q
Cellular phase of acute inflammation
A
- Predominant cell of acute inflammation is the neutrophil
- They are attracted to the site of the injury in the presence of chemotaxins, the mediators released into the blood immediately after the insult
- Once in the region,neutrophilsrecognise the foreign body and beginphagocytosis,the process whereby the pathogen is engulfed and contained with a phagosome.
Thephagosomeis then destroyed via oxygen-independent (e.g. lysozymes) or oxygen-dependent (e.g. free radical formation) mechanisms.
15
Q
Stages of neutrophil migration
A
Margination - Cells line up against the endothelium
Rolling - Close contact with and roll along the endothelium
Adhesion - Connecting to the endothelial wall
Emigration - Cells move through the vessel wall ot the affected area
(neutrophils like to Move Rapidly Along Endothelium)
16
Q
Chemical mediators initiating vasodilatation
A
Histamine Bradykinin Complement(C3a, C5a) Leukotrienes(LTC3, LTD4) Prostaglandins(PGI2, PGE2, PGD2, PGF2)
17
Q
Chemical mediators initiating mast cell degranulation
A
Complements (C3a, C5a)
18
Q
Chemical mediators for chemotaxis
A
- Interleukins(IL-8), Platelet activating factor(PAF), Complement(C5a), histamine
19
Q
Chemical mediators for lysosomal granule release
A
- Complement(C5a), interleukins(IL-8), PAF
20
Q
Chemical mediators initiating phagocytosis
A
- Complement C3b
21
Q
Chemical mediators in pain
A
- Prostaglandings(PGE2), Bradykinin, Histamine
22
Q
Chemical mediators in fever
A
- Interleukins(IL-1, IL-6), TNF-alpha, prostaglandins(PGE2)
23
Q
Reparative phase
A
- Formation of new capillaries and collagen is deposited by fibroblasts
- Collagen, fibroblasts and capillaries together are known as granulation tissue
- The wound becomes stronger as collagen aligns and then contracts. Epithelisation occurs
- This phase usually lasts 3 weeks
24
Q
Consolidative phase
A
- The scar matures and becomes paler as vascularity decreases
- Abnormal colllagen deposition can result in hypoertrophic or keloid scar formation. 80% of original tissue tensile strength is regained at 6 months. This phase is completed after 1 year
25
Outcomes of acute inflammation
* Complete resolution – with total repair and destruction of the insult
* Fibrosis and scar formation – occurs in cases of significant inflammation
* Chronic inflammation – from a persisting insult
* Formation of an abscess
26
What is an abscess
- Localised collection of pus surrounded by granulation tissue
27
What is granulation tissue
- New connective tissue and microscopic blood vessels that form on the surfaces of a wound during the healing process
28
What does pus contain
- Necrotic tissue with suspended dead and viable neutrophils and dead pathogens
29
When do we get formation of granulation tissue
- It forms when the primary insult is a pyogenic bacterium and extensive tissue necrosis occurs.
30
When do we get scar tissue
- The initial inflammatory exudate forces the tissue apart, leaving a centre of necrotic tissue with the neutrophils and pathogens
- Over time, the acute inflammation will cease and, if not surgically drained, the abscess will be replaced by scar tissue.
31
Negative effects of an abscess
- An abscess can be a source for systemic dissemination of a pathogen, with the abscess acting as a harbour for the infection.
- It can also cause continually rising pressures within the tissue, resulting in pain and destruction of local structures.
32
Second intention
· Occurs when the sides of the wound are not opposed, therefore healing occurs from the bottom of the wound upwards
33
Haemostasis in second intention
A large fibrin mesh forms, which fills the wound
34
Inflammation in second intention
An inflammatory response acts to remove any cell debris and pathogens present
· There is a larger amount of cell debris present, and the inflammatory reaction tends to be more intense than in primary intention
35
Proliferation in second intention
Granulation tissue forms at the bottom of the wound
· This is an important step, as the epithelia can only proliferate and regenerate once granulation tissue fills the wound to the level of the original epithelium; once the granulation tissue reaches this level, the epithelia can completely cover the wound
36
Remodelling in second intention
The inflammatory response begins to resolve, and wound contraction can occur
37
What are myofibroblasts
· Myofibroblasts are modified smooth muscle cells that contain actin and myosin
· They act to contract the wound; decreasing the space between the dermal edges, they also can deposit collagen for scar healing
38
Local factors affecting wound healing
- Type, size, location of wound
- Local blood supply
- Infection
- Foreign material or contamination
- Radiation damage
39
Systemic factors affecting wound healing
- Increasing age
- Co-morbidities, especially CV disease or DM
- Nutritional deficiencies(especially C)
- Obesity
40
Clean wound
- Elective, non-emergency, non-traumatic, and primarily closed with GI, biliary and GU tracts remaining intact
- Infection rate of 2.1%
- Incisions are made under aseptic conditions where the gastrointestinal (GI), biliary and genitourinary (GU) tracts and respiratory organs are not cut open
- Antibiotic prophylaxis is not usually needed except in operations where prosthetic materials are required, e.g. joint replacement, hernia repair, abdominal aortic aneurysm (AAA) repair
41
Clean-contaminated wound
- Urgent or emergency case that is otherwise clean
- Elective opening of resp, GI, biliary or GU tract with minimal spillage and not encountering infected urine or bile
- 3.3% infection rate
- Operations involve incisions into the GI, biliary, GU or respiratory tracts
- A low level of contamination is expected, e.g. small bowel resection, gallbladder removal. Prophylactic antibiotics are usually indicated
42
Contaminated wounds
- Gross spillage from GI tract or entry into biliary or GU tract(in the presence of infected bile or urine)
- Penetrating trauma < 4 hrs old or a chronic open wound to be grafted or covered
- 6.4% infection rate
- A high bacterial load is encountered during surgery, e.g. perforated peptic ulcer, perforated appendicitis
- Antibiotics are always needed pre- and post surgery
- Broad-spectrum antibiotics are usually given e.g. cefuroxime 750 mg to 1.5 g three times a day IV and metronidazole 500 mg three times a day IV.
- Seek regular adive from microbiologist where severe infection is anticipiated
43
Dirty wounds
- Purulent inflammation(e.g. abscess)
- Preoperative performation of respiratory, GI, biliary, or genitourinary tract or a penetrating trauma > 4 hrs old
- 7.1% infection rate
44
Delayed primay closure purpose
· Suitable for wounds where bacterial contamination is high and wound breakdown likely if closed immediately, e.g. anal surgery for fistula-in-ano
· Healthy-looking wounds are closed after irrigation, debridement and a period of observation have occurred
45
When is skin grafting suitable
· Suitable for large, non-infected, healthy granulating wounds
· Indications - burns, traumatic skin loss, ulcers, and wounds following excision of large skin tumours
46
Optimal environment for wound healing
- Dry
47
What does inadequate control of bleeding cause
- prevents apposition of wound edges, leading to increased fibrous tissue deposition and delayed healing
- may lead to a haematoma which has to be released before the wound edges can be opposed
- increases the risk of postoperative infection – bacteria thrive in a haematoma.
48
Main techniques to stop bleeding
- Compression
- Ligation/clipping of vessels
- Diathermy coagulation
49
How is wound closure achieved
· Suturing
· Adhesive tape
· Staples/glue
· Plastic surgery procedures to close defects which cannot be treated with the above methods, e.g. skin grafting, flap transfer
50
What might contaminated wounds require
· Contaminated wounds require adequate debridement, often in the operating theatre
· Foreign bodies must be extracted along with bits of clothing etc, x-rays to exclude deeper FBs are mandatory
Clean wounds may be primarily sutured but others should be left to granulate
