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Human Diseases > W12 38 surgical principles > Flashcards

W12 38 surgical principles Flashcards

1
Q

Wounds can be clean, clean-contaminated, contaminated or dirty. What’s the difference between each?

A

Clean - incision through non-inflamed tissues. Contamination rate (CR) <2%
Clean-contaminated - entry into hollow viscous other than colon, minimal controlled contamination 8-10%
Contaminated - breaching of hollow viscus with spillage eg colon, CR 12-20%
Dirty - gross pus, faecal peritonitis, traumatic wounds >4hrs, CR >25%

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2
Q

How do you sterilise instruments?

A

Autoclave, dry heat, ethylene oxide, low temp steam and formaldehyde, irradiation (gamma rays)

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3
Q

How can skin be disinfected?

A

Aldehydes
Alcohols
Diguanised
Iodophors and iodine

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4
Q

When is antibiotic prophylaxis considered?

A

Where procedure commonly leads to infection
Reducing infection from endogenous sources
Where infection would be devastating

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5
Q

What happens in the inflammation phase of wound healing?

A

Platelets release growth factors eg PDGF
Chemotaxis with pro inflammatory factors eg serotonin, bradykinin
Recruitment and proliferation of neutrophils and macrophages
Endothelial cells swell
IL1 encourage recruitment of T lymphocytes
Lymphocytes release cytokines eg EGF

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6
Q

What occurs in the proliferation phase of wound healing?

A

Macrophages release PDGF and TGF-b causing chemotaxis of fibroblasts.
Type III collagen produced
Some differentiate into myofibroblasts causing wound contraction
Angiogenesis of capillaries occur to sustain proliferation

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7
Q

What happens in the remodelling phase of wound healing?

A

Commences at 2-3 weeks for anything upto 2 years
Fibroblasts organise and cross-link collagen
Type III collagen replaced by type I
No net increase in collagen

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8
Q

What collagen is most abundant in normal dermis?

A

Type I collagen

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9
Q

What collagen is most abundant in maturing scars? (Img pg373)

A

Type III collagen account for 30% in a healing wound but is gradually replaced by type I collagen as scar matures.

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10
Q

What is the difference between keloid scars and hypertrophic scars caused by an excessive inflammatory response?

A

Keloids extend beyond the boundaries of the initial incision
Hypertrophic scars are elevated but do not extend beyond the original boundaries

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11
Q

How can a wound heal?

A

Primary intention
Secondary intention (don’t want this)
Tertiary intention

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12
Q

What is healing by primary intention?

A

Manual approximation of epithelialised edges
Contact inhibition to half cell migration to enable good wound healing
(put edges together)

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13
Q

How can a wound heal via secondary intention?

A

Granulation and re-epithelialisation
Slow healing, more likely to be infected
Poor cosmesis, contraction of wound

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14
Q

How can a wound heal via tertiary intention?

A

Also called delayed primary closure
Wound granulates for a short period
Allows debridement of infected wounds

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15
Q

What systemic factors can interfere with wound healing?

A

Collagen disorders
Anaemia (eg sickle cell)
Chronic steroid use interfering with fibroplasia
Coagulopathy, predisposing to haematoma formation
Malnutrition
Extremes of age
Endocrine abnormalities eg diabetes
Smoking
(all present higher risk of implant failure)

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16
Q

How does smoking affect wound healing?

A

Nicotine is a sympathomimetic with resultant vasoconstriction and hydrogen cyanide poisons intracellular pathways

17
Q

What local factors can impact wound healing?

A

Ischaemia (decreased O2)
Pressure
Radiation
Foreign material/traumatic wounds
Bacterial contamination
Denervated tissue
(all impact success of surgery)

18
Q

What measures are taken to prevent wound sepsis?

A

Careful tissue handling and haemostasis
Minimisation of operation duration
Skin preparation
Prophylactic antibiotics
Saline lavage
Debridement of devitalised tissue
Removal of foreign material
Consider delayed primary closure

19
Q

What are Langar’s lines?

A

Lines of minimal skin tensions

20
Q

Why should skin surgery follow Langar’s lines?

A

As you can place the incisions for them to heal without contractional pull on them which might insite more prolific production and hazard arrangements of collagen during production and more unsightly scars.

21
Q

What types of materials are there for suturing?

A

Resorbable/non-resorbable
Monofilament vs braided etc

22
Q

How do you achieve haemostasis - local measures?

A

Pressure
Bipolar/monopolar cautery
Absorbable haemostatic agents eg surgicel
Identifying and lighting vessels
Selective embolisation

23
Q

How do you achieve haemostasis - systemic measures?

A

Reversing acquired coagulopathy eg vitamin K, FFP, platelets
Discuss with haematologist
Maintaining vitals but consideration of permissive hypotension

24
Q

What does Floseal do?

A

Acts quite far down the coagulation cascade, converting fibrinogen to fibrin without the need for an overall reliance on the coagulation cascade. Bypassed that and promotes impressive haemostasis in even challenging wounds.

25
Q

Describe the reconstruction ladder from simple to complex

A

Secondary healing
Primary closure
Skin graft
Local flaps
Regional flaps
Free flaps

26
Q

How long does a skin graft ‘take’?

A

Adherence (immediately) - fibrin bonds formed to wound bed
Serum imbibition (48hrs) - plasma exudate from host bed capillaries provide serum
Revascularisation phase (after 48hrs) - growth of vessels into graft from host (neovascularisation) or anastomosis between host and graft vessels (inosculation)
Organisation phase - fibrin clot at interface causing adherence infiltrated by fibroblasts (day 8) firmly secures to host bed with vascular supply (day 9)

27
Q

What are the different kinds of grafts?

A

Autografts - from the patient themselves
Isografts - from a genetically identical individual
Allografts - from a non-genetically identical individual
Xenografts - from animals
Alloplastic - synthetic materials

28
Q

What might happen to an infected wound?

A

Resolve
Progress to abscess formation
Ultimately cause fibrosis and scarring

29
Q

What is an abscess?

A

A collection of pus with an actual or potential body cavity:
Plus contains neutrophils and necrotic debris. Inflammatory cells release chemicals and enzymes to cause liquefaction necrosis. Collections of pus track through tissue planes and through the skin (a sinus).

30
Q

How do we manage abscesses/infected wounds?

A

Treat with empirical antibiotics based on local guidelines. Wait for culture and sensitivity results to tailor therapy.

31
Q

What are the most common bacteria causative for infected wounds?

A

Viridans streptococci
Prevotella spp
Staphylococcus spp
Peptostreptococcus spp

Human Diseases (75 decks)

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