Burns Flashcards

(38 cards)

1
Q

Complications of burns

A

Systemic- Secondary to SIRS, MODS
Specific organ injuries - acute lung injury, AKI, endocrine complications (hypernatremia, hypokalemia, hypomagnesemia, hypocalcemia, hypophosphatemia), gastrointestinal (paralytic ileusm, Curling’s ulcer, bacterial translocaiton)

Local- adverse scarring and contractures

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2
Q

At what TBSA do systemic complications of burns manifest

A

> 25%

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3
Q

Prospective scar management begins with:

A

early excision and grafting in the initial phase to prevent post-burn hypertrophic scarring and contracture

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4
Q

Techniques for formed scars and contractures

A

Techniques include excision and grafting, scar release and joint release, local and regional flaps, skin substitutes, and tissue expansion.

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5
Q

Non-surgical techniques for scar management

A

intralesional corticosteroid injection, cryotherapy, laser treatment, radiotherapy and 5-fluorouracil.

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6
Q

All electrical burns have:

A

Entry and exit wounds

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7
Q

MCC of large electrical burns

A

Lightning strikes
Contact with high voltage power lines.

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8
Q

Cx of electrical burns

A

Arrhythmias and myoglobinuria

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9
Q

Mng of electrical burns

A

A to E
ECG
Renal function
CK levels

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10
Q

Mng of contractures secondary to electrical burns

A

early fasciotomy

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11
Q

Types of cold injuries

A

Freezing/frostbite
Non freezing/ trench foot

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12
Q

Mng of cold injuries

A

Remove wet clothing- replace with dry blankets
Gradual rewarming - affected extremity placed in circulating water bath 37-39 degrees until tissues soften and become a red/purple color.
If patient has hypothermia, rewarming should be warm IVF.

IV analgesia
+/- tetanus ppx

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13
Q

Mng of trench foot

A

Treatment involves washing, air-drying, rewarming, elevating and resting the feet, to prevent progression to gangrene. It can take up to six months to recover and there may be persistent cold insensitivity.

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14
Q

When are skin grafts and flaps used

A

when a defect cannot be closed by primary or secondary intention

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15
Q

Differences between skin graft and flap

A

The key differences between a graft and a flap is in regards to its blood supply; a skin graft receives its blood supply from the recipient site though the vascular bed, whilst a skin flap brings its blood supply from the flap donor site.

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16
Q

Contraindications to skin grafts and flaps

A

infections, known skin cancer, immunosuppression, current smoker, poorly controlled diabetes

17
Q

Indications for using skin grafts

A

extensive skin damage, such as those caused from deep burns, following large skin excision procedures, or poorly healing ulcerating lesions

18
Q

2 types of skin grafts

A

Split-skin thickness skin graft (SSG) – does not contain the whole dermis
Full-thickness skin graft (FTSG) – contains the whole dermis (also transplanting hair follicles)

19
Q

Reasons for skin graft failure

A

including hematoma or seroma formation under the graft, infection (commonly Streptococcus spp.), shearing forces, an unsuitable bed (e.g. avascular wound beds, such as tendons or bone), or technical error.

20
Q

Signs of skin graft failure

A

pallor or discoloration at the graft site, skin graft non-adherence to the wound bed, and evidence of localised infection, systemic features (malaise, lethargy), or even full thickness necrosis* (occurs 1-2 weeks after grafting)

21
Q

When are full thickness skin grafts used

A

used to cover areas with optimal vascular availability

22
Q

When are split thickness grafts used

A

plit thickness grafts are commonly used for skin defects that are too large for a full thickness graft.

23
Q

most commonly used donor site for split thickness graft

24
Q

Skin flap principles

A

A skin flap is where tissue is transferred from a donor site to recipient site along with its corresponding blood supply.

Skin flaps are thought to provide better cosmetic results than skin grafting (Fig. 5), as the skin tone and texture are usually better matched. Additionally, they have a reduced chance of failure in comparison to skin grafts.

However, flap failure remains a potential complication of the procedure*. This can occur due to issues with either the arterial supply, presenting with signs of pallor and reduced perfusion, or venous supply, presenting with features of venous congestion.

25
Classifications of skin flaps
Classification Flaps can be classified via their tissue type, blood supply, or location. Tissue Type For tissue types, this is based on the compositions that are utilised in the flap, including cutaneous flap, fasciocutaneous flap, musculocutaneous flap, or muscle flaps Blood Supply Based on blood supply, three definitive types of flap are possible: Axial flap – a designated subcutaneous artery that runs beneath the flaps longitudinal axis (the artery can be a direct, facsiocutaneous, or musculocutaneous artery) Random flap – no designated named artery that provides blood supply to the flap; blood supply via the subdermal plexus Pedicled (or perforator) flap – the tissue is completely raised on a named vessel from the donor site and then transferred to the recipient site; this can be as a pedicled flap or free flap Location Subtypes When defined by location, flaps can be classified as either local, regional, or free flaps Local flaps are harvested from a contiguous site and are commonly used for facial defects (Fig. 6), fingertip injuries, or defects on the limb. These can be further classified into: Advancement flap – The skin is moved directly forward Rotation flap – The skin is rotated around a pivot point to cover an adjacent defect Transposition flap – Moves laterally in relation to the pedicle to cover an adjacent defect Regional (or pedicled) flaps are harvested from the same anatomical region but not directly adjacent. The attached skin (or pedicle) will be tunnelled under the intact tissue, or laid over intact skin forming what is known as a skin bridge, which can then detached from the donor site in a second procedure. Free (or distant) flaps are harvested from a different anatomical region entirely. The tissue and named fasciocutaneous artery are separated from the donor site before being reattached at the recipient site using microsurgical techniques. Examples of free flaps are seen in Table 2.
26
What cell type does BCC arise from
Pluripotent cells of the stratum basale layer of the epidermis
27
RF BCC
Long term UV exposure Psoriasis Fitzpatrick type 1 skin Immunosuppression Genetic sydrome- xeroderma pigmetosa, gorlinsyndrome
28
Subtypes of BCC and their features
Nodular – most common (50-60%), commonly a pink pearly nodule with telangiectasia, and can become ulcerated or encrusted; subtypes include cystic, pigmented, or keratotic Superficial – (10-15%) erythematous scaly plaques with a thread-like border, and may bleed or ulcerate Morphoeic – more uncommon, presenting as thickened and sclerosing plaques with poorly defined borders; highest risk of incomplete excision and often prone to recurrence after treatment Basosquamous – a mixed basal cell and squamous cell malignancy, with an infiltrative growth pattern and often are more aggressive
29
BCC differentials
Trichoepithelioma (a rare benign tumour of the hair follicle), Keratoacanthoma (rapidly-growing tumour of the skin derived from the glands surrounding a hair follicle), or a cutaneous Squamous Cell Carcinoma
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Mng BCC
Factors such as tumour subtype, size, anatomical location, and histological diagnosis will impact how a BCC is managed: Low-risk BCCs are small, well-circumscribed lesions superficial type lesions that do not meet any of the high-risk criteria High-risk BCCs include those occurring in the young (<25yrs) or immunocompromised patients, recurrent lesions, lesions on the nose, lips, ears, or around the eyes, lesions with poorly defined margins, and all non-nodular subtypes of BCC Multiple management options are available BCCs. Superficial disease can often be treated with non-surgical options alone, which include: Cryotherapy (or CO2 ablation) Curettage and electrodissection – 75% cure rate (95% for smaller lesions <2cm) Immune response modulator – Topical imiquimod 5% cream (for superficial BCCs) Topical chemotherapy – 5-fluorouracil 5% cream (for superficial BCCs) Photodynamic therapy – Uses light therapy together with a topical photosensitising agent (for superficial BCCs) Radiotherapy – usually reserved for the older age group, achieves ~90% cure rates Surgical Management The mainstay of surgical management is with excision biopsy. The margins required are between 3-5mm, depending on how demarcated the border is and the location of the lesion. Higher excision margins are required for recurrent BCCs (5mm) or high-risk histological subtypes. If there is sufficient skin laxity in the region, the defect can be closed directly. However, some may require local, regional or free flap or skin grafts. Lesions which are close to vital anatomical structures, have indistinct margins, or are recurrent should be considered for Mohs’ micrographic surgery.
31
What cell type does cutaneous SCC arise from
malignant tumour of keratinocytes, arising from the epidermal layer of the skin
32
RFs for SCC
Cumulative prolonged exposure to UV light, such as excessive sunbed use Chronic wounds and inflammation A SCC arising in chronic ulcers and scars (particularly burns scars) is known as a Marjolin’s ulcer Immunosupression Pre-malignancy conditions, such as Bowen’s disease or actinic keratoses Smoking (particularly in lip SCC)
33
Differentials for SCC
other forms of skin cancer, such as BCC or melanoma. Other differentials to consider include pre-malignant conditions (e.g. Bowen’s disease or Actinic Keratosis, Fig. 3), Keratoacanthoma (rapidly growing keratinising nodules, well-demarcated), verrucous carcinoma, or cutaneous horns.
34
MNG SCC
The first line management for resectable SCC is surgical; non-surgical options are only used as adjuncts or where surgery is not feasible. Surgical Treatment The standard surgical treatment is with an excision biopsy, with the peripheral margins taken dependent on the risk status of the patient: low risk ≥ 4mm high risk ≥ 6mm very high risk ≥ 10mm The deep margins taken should be the next clear surgical plane (or in scalp lesions, down to the galea) Further wide local excision (with likely delayed reconstruction), Mohs micrographic surgery, or adjuvant radiotherapy may be offered to patients with one or more involved or close margins if there are any high risk factors. Dermatologists may perform curettage and cautery for immunocompetent patients who have small (<1cm), clinically low risk SCC Non-Surgical treatment Multiple non-surgical options are also available to patients with SCC in certain cases. Primary radiotherapy may be a treatment option if surgery is not feasible or would result in an unacceptable functional or aesthetic outcome. Adjuvant radiotherapy is used for patients with close or involved margins if further surgery is not possible, or for patients with clear margins but multiple high risk factors where the chance of local recurrence is high. Immune Checkpoint Inhibitors can be used in locally advanced SCC where curative surgery or radiotherapy is not no reasonable, or in cases of metastatic SCC. Chemotherapy is often used as a third line, in people who are not suitable for immune checkpoint inhibitors, however is often poorly tolerated in frailer or co-morbid patients, and usually has a short lived response.
35
Histological subtypes of melanoma
https://teachmesurgery.com/plastic-surgery/skin-cancer/melanoma/
36
RFS for melanoma
UV exposure – both recreational (e.g. sunbed use) and occupational Age – the majority of melanomas occur in patients aged >50yrs Previous melanoma – represents an 8-10x increased risk Skin tone – incidence is highest in Caucasian groups (although prognosis in darker skin is worse due to delayed diagnosis) Most commonly affects Fitzpatrick Type 1 and 2 skin, the two palest skin types Family history – approximately 10% of patients will have a positive family history for melanoma Predisposing conditions – albinism, xeroderma pigmentosum, atypical mole syndrome, >50 typical naevi, immunosuppression (i.e. organ transplant recipient)
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Mng melanoma
Patients with a tissue diagnosis of melanoma should be referred to the specialist skin MDT (ssMDT), where definitive excision margins, further investigations, and treatment are determined. In all cases of melanoma, ongoing sun protection advice should be given, with concurrent Vitamin D supplementation and advice on prevention (see Prognosis). Wide Local Excision A wide local excision refers to excision of a larger area of tissue from the original site of the melanoma. Its aim is to improve local control of melanoma by removing micrometastases. It is indicated is nearly all cases of melanoma, including those with clear histological margins on the excision biopsy. The exact peripheral margin used in the wide local excision is guided by the Breslow thickness (Table 2). The deep margin should always be down to the deep fascia Breslow Thickness Sentinel Lymph Node Biopsy Sentinel lymph node biopsy (SLNB) aims to identify whether or not there is any melanoma in the primary draining lymph node(s) within a regional lymph node basin. Current NICE guidelines recommend offering SLNB to patients with melanoma with a Breslow thickness >1 mm, without clinically apparent nodal or metastatic disease. If the lymph nodes are clinically suspicious (i.e. palpable) or radiologically suspicious (i.e. enlarged on imaging) then fine needle aspiration cytology (FNAC) should be performed. When obtaining patient content for SLNB, it is important to emphasis that it is a staging and prognostic procedure only. It is usually performed at the same time as the wide local excision. Staging Imaging should be performed in patients with stage IIc melanoma who have not had SLNB, or stage III and IV melanoma. Typically, this involves a CT chest-abdomen-pelvis and MRI brain (or whole body PET-CT with additional imaging of the brain). Melanoma is staged using the TNM classification; the clinical TNM (cTNM) stage is then updated with information after surgery to give the pathological stage (pTNM). The AJCC staging (Table 3) groups the TNM stages to guide treatment and prognosis Metastatic Disease Unfortunately, metastatic disease is relatively common in melanoma. Both regional and distant metastases can be managed using various immunotherapy and chemotherapy agents. The immunotherapy agents most commonly used are: Ipilimumab – a monoclonal antibody that inhibits cytotoxic T lymphocyte antigen 4 (CTLA 4), which would normally down regulate T cell activation Pembrolizumab and Nivolumab – monoclonal antibodies that attach to the PD1 receptor on T cells so that the T cells cannot be switched off and remain active Vemurafenib and Dabrafenib – both are BRAF kinase inhibitors that block the activity of the BRAF V600E mutation which otherwise causes persistent MAPK pathway activation leading to uncontrolled cell proliferation Talimogenelaherparepvec (TVEC) – an oncolytic immunotherapy derived from herpes simplex virus type-1 which causes tumour lysis and the release of tumour-derived antigens; it is injected directly into the metastasis
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