Wound Assessment Flashcards

1
Q

What is wound healing by primary intention?

A

Primary intention is the healing of a clean wound without tissue loss e.g. surgical incision

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2
Q

What is wound healing by secondary intention?

A

Secondary intention is the healing of a wound with considerable tissue loss and in which the edges cannot be brought together

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3
Q

What are the phases of wound healing?

A
  1. Hemostasis
  2. Inflammation
  3. Proliferation
  4. Remodelling
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4
Q

How long does the substrate (inflammatory) phase of wound healing last for?

A

Up to 5-7 days

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5
Q

Explain the inflammatory phase of wound healing

A

Inflammatory cells migrate into the wound (chemotaxis) and promote the inflammatory phase, which is characterised by the sequential infiltration of neutrophils, macrophages, and lymphocytes.

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6
Q

Explain the proliferative phase of wound healing

A

Once the wound is cleared of devitalised tissue, the arrival of fibroblasts produce collagen (type I and III) within the wound bed which cross-links and imparts strength to the scar. Wound revascularisation also occurs at this time.

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7
Q

What characterises the maturation or remodelling phase of wound healing?

A

A gradual gain in tensile strength due to continued collagen deposition and collagen remodelling (type III collagen is replaced with type I)

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8
Q

How does RhA lead to anaemia?

A

During conditions in which hepcidin level is abnormally high, such as inflammation (e.g. RhA), serum iron falls and this typically leads to anaemia due to an inadequate amount of serum iron being available for developing RBCs

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9
Q

How does anaemia (secondary to RhA, SLE, etc.) or hypoxia (secondary to PVD) affect wound healing?

A

An anemic state decreases the amount of oxygen available to the tissues, which increases the opportunity for bacterial colonisation. In addition to hypoxia, PVD also results in a reduction of nutrients to the tissues and cells necessary to fight bacteria

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10
Q

How does smoking affect wound healing?

A

The nicotine and other chemicals present in tobacco have vasoconstrictive properties, thus inducing hypoxia to the tissues and impeding wound healing

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11
Q

How does infection affect wound healing?

A

Bacteria compete with the newly forming tissue for nutrients and oxygen and leads to eventual tissue starvation (anoxia). Tissue anoxia produced by bacteria results in further tissue breakdown; aerobic bacteria complicate this environment further due to their high oxygen consumption.

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12
Q

Why are WBCs recruited during the inflammatory phase?

A

Neutrophils and monocytes are recruited to debride the wound by phagocytosis

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13
Q

How do glucocorticoids impair wound healing?

A
  1. Recruitment of WBCs in the inflammatory phase is suppressed
  2. Inhibit fibroblastic proliferation
  3. Reduce collagen production
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14
Q

What’s the difference between a hypertrophic and a keloid scar?

A

Hypertrophic scar is a result of unchecked (excessive) proliferation of fibrous tissue but remains confined to the skin injury, whereas a keloid scar invades the surrounding normal skin i.e. beyond the incision scar

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15
Q

What’s gold standard to offload diabetic foot/heel ulcer?

A

Total contact cast (TCC)

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16
Q

Name the stages of bone healing

A
  1. Inflammation
  2. Induction
  3. Remodelling
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17
Q

Describe the inflammation stage of bone healing

A
  • There’s haemorrhage between bone ends
  • Inflammatory cells accumulate (cellular proliferation) at # line and macrophages phagocytose tissue debris
  • Bone necrosis occurs as a result of tearing of blood vessels
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18
Q

Describe the induction stage of bone healing

A

Provisional callus (trabecular and cartilaginous tissue) immobilises bone fragments

19
Q

Describe the remodelling stage of bone healing

A

Collagen initially forms a fibrous union of # gap, which is later remodelled, resorbed and ossified to become bony tissue

20
Q

What are the harvesian systems?

A

Narrow cannals in (cortical) bone containing blood vessels

21
Q

What is Wolff’s law?

A

‘Bone follows function’: bone is laid down where needed and resorbed where not needed.

22
Q

What is the function of PTH (parathyroid hormone)?

A

Stimulated by low calcium: decreases renal excretion and stimulates vitamin D by increasing GI absorption of calcium and osteoclastic activity from bone to release calcium

23
Q

List common types of sutures and describe their main features

A
  1. Monocryl - monofilament (non-braided) and absorbable
  2. Vicryl (coated) - multifilament (braided) and absorbable
  3. Ethilon - monofilament and non-absorbable
  4. Polypropylene - monofilament and non-absorbable
24
Q

What are the differences/benefits between mono- and multifilament and absorbable and non-absorbable sutures?

A
  • Single-stranded sutures resist harbouring of micro-organisms, tie easily and [due to its smooth surface] provides less resistance to passage through tissue
  • Braided sutures are stronger and more pliable but increase drag (friction) through tissues and have a higher affinity to harbour bacteria
25
Q

How are sutures absorbed?

A

They are broken down by the action of hydrolysis and phagocytosis by inflammatory cells

26
Q

Outline the four types of wounds

A

Type 1 wounds (clean)
Type 2 wounds (clean contaminated)
Type 3 wounds (contaminated)
Type 4 wounds (dirty)

27
Q

What are type 1 wounds?

A

Clean wounds made in a sterile environment (operating theatre)

28
Q

What are type 2 wounds?

A

Minimally contaminated wounds created with a sharp, clean instrument in a non-sterile environment

29
Q

What are type 3 wounds?

A

Contaminated wounds created in a dirty environment. There is no frank infection and minimal dead tissue

30
Q

What are type 4 wounds?

A

Infected wound/grossly contaminated or devitalised wound

31
Q

How does pulse oximetry work?

A

One side of the probe contains LEDs and the other a light sensor that measures changes in light absorbed. It works on the principle that the amount of light absorbed by a solution (i.e. oxyhaemoglobin and deoxyhaemoglobin present within blood) is proportional to the concentration (i.e. oxygen saturation).

32
Q

What is the function of neutrophils in the wound-healing process?

A

The clearance of invading microbes and cellular debris in the wound area. N.B. these cells also produce substances such as ROS that cause some additional damage.

33
Q

What is the function of macrophages in the wound-healing process?

A

Macrophages release cytokines that promote the inflammatory response by recruiting additional leukocytes. They’re also responsible for clearing apoptotic cells (incl. neutrophils) for the resolution of inflammation. As macrophages clear these apoptotic cells they stimulate keratinocytes, fibroblasts, and angiogenesis to promote tissue regeneration (i.e. they promote the transition to the proliferative phase of healing).

34
Q

Explain the hemostatic phase of the wound healing process

A

Hemostasis begins immediately after wounding, with vascular constriction, platelet aggregation and fibrin clot formation (thrombus). The clot and wound tissue release pro-inflammatory cytokines and growth factors

35
Q

How does oxygenation influence healing?

A

Temporary hypoxia after injury triggers wound healing: hypoxia induces cytokine (promoters of angiogenesis) and growth factor production (from macrophages). However, prolonged or chronic hypoxia delays healing as oxygen is important for cell metabolism to sustain the healing process.

36
Q

How does stress influence healing?

A

Stress upregulates glucocorticoids and reduces the levels of proinflammatory cytokines at the wound site: the glucocorticoid cortisol functions as an anti-inflammatory

37
Q

How does diabetes influence healing?

A

The impaired healing that occurs in individuals with diabetes involves:

  1. Hypoxia (insufficient perfusion as small blood vessels are dysfunctional or occluded in patients with diabetes).
  2. Dysfunction in fibroblasts (fibroblasts have limited reproductive capability in the presence of hyperglycaemia, thus resulting in abnormal amount of collagen).
  3. Impaired angiogenesis and neovascularisation.
  4. Decreased host immune resistance as hyperglycaemia decreases phagocytosis/the killing of bacteria by white blood cells.
  5. Neuropathy.
38
Q

How do glucocorticoid steroids influence healing?

A
  • They inhibit wound repair via global anti-inflammatory effects and suppression of cellular wound responses incl. fibroblasts proliferation and collagen synthesis.
  • Beyond effects on repair, systemic corticosteroids may increase the risk of wound infection
39
Q

How do chemotherapeutic drugs influence healing?

A

Most chemotherapeutic drugs are designed to inhibit cellular metabolism and rapid cell division

  1. These medications inhibit DNA, RNA, or protein synthesis, resulting in decreased neovascularisation (angiogenesis), and lower collagen production and fibroblast proliferation
  2. Delay cell migration into the wound
  3. Inhibit contraction of wounds
  4. Weaken immune functions of the patient and thereby impede the inflammatory phase of healing and increase the risk of wound infection.
  5. Induce neutropenia, anaemia, and thrombocytopenia, thus leaving wound vulnerable to infection, causing less oxygen delivery to the wound.
40
Q

How does obesity influence healing?

A

Higher rate of complications (e.g. wound infection, wound dehiscence) due to:

  1. Hypoperfusion and ischaemia that occurs in subcutaneous adipose tissue
  2. Increased tension in wound edges contributes to wound dehiscence. 3. Wound tension also increases tissue pressure, reducing microperfusion and the availability of oxygen to the wound.
41
Q

How does alcohol influence healing?

A

Alcohol impairs wound healing and increased the incidence of infection by:

  1. Suppressing pro-inflammatory cytokine release in response to an inflammatory challenge i.e. impaired early inflammatory response
  2. Decreased neutrophil recruitment and phagocytic function
  3. Decreased angiogenic capacity (up to 60 %): this decrease in wound vascularity causes increased wound hypoxia and oxidative stress
  4. Decreased collagen production
42
Q

How does smoking influence healing?

A
  1. In the inflammatory phase, smoking impairs WBC migration, resulting in lower numbers of monocytes and macrophages in the wound site, and reduces neutrophil bactericidal activity. These effects result in poor wound healing and an increased risk of opportunistic wound infection.
  2. In the proliferative phase of wound healing, smoking decreases fibroblast migration and proliferation
  3. Nicotine interferes with oxygen supply by inducing tissue ischaemia as nicotine decreases tissue blood flow via its vasoconstrictive effects: nicotine stimulates sympathetic nervous activity, resulting in the release of epinephrine, which causes peripheral vasoconstriction.
  4. Carbon monoxide also causes tissue hypoxia: carbon monoxide aggressively binds to haemoglobin with an affinity 200 times greater than that of oxygen, resulting in a decreased fraction of oxygenated haemoglobin in the bloodstream.
  5. Hydrogen cyanide, a component of cigarette smoke, impairs cellular oxygen metabolism, thus compromising oxygen consumption in the tissues.
  6. Beyond these direct effects, smoking increases the individual’s risk for atherosclerosis and COPD, two conditions that might also lower tissue oxygen tension.
43
Q

How does nutrition influence healing?

A
  1. A deficiency of protein can impair capillary formation, fibroblast proliferation, proteoglycan synthesis, collagen synthesis (collagen is a major protein component of connective tissue), and wound remodelling.
  2. A deficiency of protein also affects the immune system, with resultant decreased leukocyte phagocytosis and increased susceptibility to infection.
  3. Collagen synthesis also requires co-factors such as ferrous iron and vitamin C. Impaired wound healing results from deficiencies in any of these co-factors.
  4. Arginine is a semi-essential amino acid and sufficient levels are needed to support collagen deposition, angiogenesis, and wound contraction. Arginine also improves immune function.
  5. Omega-3 fatty acids improve the systemic immune function, thus reducing infectious complications
  6. Vitamin C deficiency results in impaired healing in part due to decreased collagen synthesis and fibroblast proliferation, and decreased angiogenesis. Vitamin C deficiency also leads to an impaired immune response and increased susceptibility to wound infection.
  7. Vitamin A deficiency leads to impaired wound healing as its properties include anti-oxidant activity, increased fibroblast proliferation, and increased collagen synthesis.
  8. Vitamin E, an anti-oxidant, maintains cellular membrane integrity by providing protection against destruction by oxidation. Vitamin E also has anti-inflammatory properties and has a role in decreasing excess scar formation. Topical vitamin E has been promoted as an anti-scarring agent.
  9. Magnesium functions as a co-factor for many enzymes involved in protein and collagen synthesis.
  10. Copper is required for the optimal cross-linking of collagen.
  11. Zinc deficiency impairs wound healing.
  12. Iron is required for the hydroxylation of proline, so, severe iron deficiency can result in impaired collagen production.