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304 - Surgery > Wound healing and management > Flashcards

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

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2
Q

4 stages of each intention

A

Haemostasis
Inflammation
Proliferation
Remodelling

(HOW I PERSONALLY RECTIFIED)

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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

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4
Q

Purpose of inflammation

A

A cellular inflamatory response acts to remove any cell debris and pathogens present

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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
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6
Q

Remodelling

A
  • Devascularisation of the region occurs and the fibroblasts undergo apoptosis
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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
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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
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9
Q

3 phases of wound healing

A

1) Inflammatory phase
2) Reparative Phase
3) Consolidation phase

(I Repair Cuts)

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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
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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

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12
Q

Phases of acute inflammation

A

1) Vascular phase

2) Cellular phase

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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
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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.

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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)

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16
Q

Chemical mediators initiating vasodilatation

A 
Histamine 
Bradykinin 
Complement(C3a, C5a)
Leukotrienes(LTC3, LTD4)
Prostaglandins(PGI2, PGE2, PGD2, PGF2)
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17
Q

Chemical mediators initiating mast cell degranulation

A

Complements (C3a, C5a)

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18
Q

Chemical mediators for chemotaxis

A
  • Interleukins(IL-8), Platelet activating factor(PAF), Complement(C5a), histamine
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19
Q

Chemical mediators for lysosomal granule release

A
  • Complement(C5a), interleukins(IL-8), PAF
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20
Q

Chemical mediators initiating phagocytosis

A
  • Complement C3b
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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
Q

Outcomes of acute inflammation

A
  • Complete resolution–with total repair and destruction of the insult
  • Fibrosis and scar formation– occurs in cases ofsignificant inflammation
  • Chronic inflammation–from a persisting insult
  • Formation of an abscess
26
Q

What is an abscess

A
  • Localised collection of pus surrounded by granulation tissue
27
Q

What is granulation tissue

A
  • New connective tissue and microscopic blood vessels that form on the surfaces of a wound during the healing process
28
Q

What does pus contain

A
  • Necrotic tissue with suspended dead and viable neutrophils and dead pathogens
29
Q

When do we get formation of granulation tissue

A
  • Itforms when the primary insult is a pyogenic bacterium and extensive tissue necrosis occurs.
30
Q

When do we get scar tissue

A
  • The initial inflammatory exudate forces the tissue apart, leaving acentre of necrotic tissuewith the neutrophils and pathogens
  • Over time, the acute inflammation will cease and, if not surgically drained, the abscess will bereplaced by scar tissue.
31
Q

Negative effects of an abscess

A
  • An abscess can be a source for systemic dissemination of a pathogen, with the abscess acting as aharbour for the infection.
  • It can also cause continually rising pressures within the tissue, resulting inpainanddestruction of local structures.
32
Q

Second intention

A

· Occurs when the sides of the wound are not opposed, therefore healing occurs from the bottom of the wound upwards

33
Q

Haemostasis in second intention

A

A large fibrin mesh forms, which fills the wound

34
Q

Inflammation in second intention

A

An inflammatory response acts toremove any cell debris and pathogens present

· There is a larger amount of cell debris present, and theinflammatory reaction tends to be more intense than in primary intention

35
Q

Proliferation in second intention

A

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
Q

Remodelling in second intention

A

The inflammatory response begins to resolve, and wound contraction can occur

37
Q

What are myofibroblasts

A

· 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
Q

Local factors affecting wound healing

A
  • Type, size, location of wound
  • Local blood supply
  • Infection
  • Foreign material or contamination
  • Radiation damage
39
Q

Systemic factors affecting wound healing

A
  • Increasing age
  • Co-morbidities, especially CV disease or DM
  • Nutritional deficiencies(especially C)
  • Obesity
40
Q

Clean wound

A
  • 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
Q

Clean-contaminated wound

A
  • 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
Q

Contaminated wounds

A
  • 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
Q

Dirty wounds

A
  • 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
Q

Delayed primay closure purpose

A

· 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
Q

When is skin grafting suitable

A

· Suitable for large, non-infected, healthy granulating wounds
· Indications - burns, traumatic skin loss, ulcers, and wounds following excision of large skin tumours

46
Q

Optimal environment for wound healing

A
  • Dry
47
Q

What does inadequate control of bleeding cause

A
  • 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
Q

Main techniques to stop bleeding

A
  • Compression
  • Ligation/clipping of vessels
  • Diathermy coagulation
49
Q

How is wound closure achieved

A

· 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
Q

What might contaminated wounds require

A

· 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

304 - Surgery (1 decks)

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