Pot Pouri: Fat grafting, common derm conditions Flashcards
(35 cards)
1
Q
A
2
Q
List the advantages of using autologous fat as a filler
A
- Tissue properties
- abundant and readily available
- has angiogenic and vasculogenic properties
- biocompatable
- potential for integration
- contains 100-1000x more pluripotent cells then bone marrow
- permanent (after stabilization)
- Technical properties
- ease of harvest
- relatively (comparatively) inexpensive
- does not require cell expansion
3
Q
Describe theories of fat survival
A
- Host replacement: adipocytes are phagocytosed by histiocytes, form foam cells, that replace fat in location and volume
- Cell survival: adipocytes that are revascularized will survive; those that are not revascularized are phagocytosed by histiocytes and resorbed
4
Q
Describe the phases of graft take.
A
- Like graft take: imbibition/inosculation/revascularization
- Imbibition wihtin first 3 days
- extensive infiltration of inflammatory cells; no reaction of adipocytes
- Inosculation at 4 days
- recipient and donor vessel connect antegrade
- Angiogenesis at 4++++ days
- vessels connect bidirectional as adipocytes are revascularized
- if not revascularized then fat degenerates
- btwn day 4 - 60 absorption peaks
- @ 1 yr remaining fat is stable
5
Q
list and briefly describe the options for autologous fat grafting
A
- macrograft
- unaltered adipose tissue & stromal components, taken en bloc
- used for dead space filler for small spaces (H&N, frontal sinus, etc)
- disadv: unpredictable graft take/failure
- dermis-fat graft
- near-full thickness dermis + variable (~ 2cm thick) underlying unaltered fat
- augments small contour defects; interpositional & glide barrier (nerves, tendons & skin)
- around 50% graft loss at 1 yr, risk of graft loss
- micrograft
- adipose harvested with liposuction cannula (manual suction, suction-assisted, other) and therefore stroma is not captured
- useage
- volume:
- small vol: cosmetic facial augmentation, penis
- lg vol: breast, buttock augmentation
- regeneration/reconstruction
- sm vol: cleft lip/palate, scar recontouring, nipple reconstruction, VPI, non-healing ulcer/wound
- lg vol: partial/total breast recon; radiated skin wounds
- volume:
6
Q
Describe the coleman technique for fat transfer
A
- Tumescence
- RL + 1:400,000 epi; 1:1 (superwet technique)
- Blunt cannula, larger bore (3-4mm)
- if small volume, try to do manual (true coleman)
- if large volume, then suction-assisted
- Lipoaspirate
- Centrifuge or sediement; wick the supernatent
- injection
- transferred in 1-3mL aliquots in small tunnel (for small vol)
- use 18g+ needle/cannula
- inject as needle is withdrawn
- multiple passes; criss-cross
- all layers: deep, intramuscular, subfascial, subcutaneous
7
Q
what are the layers in a fat aspirate after it has been allowed to settle (+.- centrifuge)
A
- oil (from ruptured adipocytes)
- fat/adipocytes
- blood, serum, water, infiltrate +/- pellet (if centrifuged)
8
Q
what are the processing methods for aspirated fat
A
- sedimentation
- wick away or decant the serum
- centrifuge
- best is < 3000rpm for 3 min
- washing
- w NS, D5W, RL, sterile H20
- Cotton gauze (telfa) rolling
- other: revolve
9
Q
what are complications of fat grafting
A
- resportion
- under/overcorrection
- contour irregularities
- change over time can be unpredictable/ w weight gain
- infection
- microcyst
- calcifications
- fat necrosis
- migration
- embolism
10
Q
what are current controversies regarding fat transfer to breast
A
- controversy regarding cancer detection and risk
- now ASPS / radiologic groups agree shouldn’t affect cancer detection; microcyst and microcalcifications from fat necrosis should be distinguisable from malignancy
- regarding cancer risk - still controversial
- ASPS supports FG after mastectomy
- controversial still after partial mastectomy (no direct position, say contra-indicated in DCIS)
- no position on augmentation in breast w no history of breast ca
11
Q
describe some guiding principles when considering autologous fat transfer to breast
A
- ASASP/ASPS supports fat transfer after mastectomy, with/without previous breast recon, with/without previous XRT
- note: can improve skin quality after XRT
- low risks, low complications (greatest risk is unpredictabiltiy of resporption)
- undertake rigourous surveillance
- do not use after partial mastectomy & DCIS
- In France, there are some defined contraindications to various scenarios
- Augmentation / benign breast disease contraindications:
- unreasonable expectations (expects large vol augment)
- High risk for malignancy (familial, histologic, genetic)
- Insufficient reserve of fat
- abnormal pre-op breast imaging
- After partial mastectomy for pre/invasive Ca contraindications:
- evidence of local recurrence (remission not achieved)
- Not completed all components of prescribed/indicated treatment
- incomplete resection\
- mets
- < 2 yrs since surgery
- After total mastectomy for pre/invasive Ca contraindications
- local recurrence
- < 2 yrs since surgery when HIGH RISK for recurrence
- mets
*
- Augmentation / benign breast disease contraindications:
12
Q
What is erythema multiforme
A
Def. Self-limiting immune-mediated condition characterized by
- target lesions on the extensor acral surfaces (duscky erythematous center, halo blanched surrounding)
- no epidermal detachment
- affects palms and soles
EM minor = no oral mucosa involvement/corneal involvement
EM major = mucosal involvement
Etiology: MAINLY infection 90% of cases, (bacterial or viral), other drug-related NSAIDS, sulfonamides, antiepilectics, antibiotics
Infection: CMV, mycoplasma
Diagnosis: biopsy to exclude other conditions
Tx: treat underlying condition, stop drug, supportive
13
Q
what is SJS/TENs?
A
- SJS-TENs is a non-autoimmune severe exfoliative disease, that affects only stratified squamous keratinocytes (not columnar, cuboidal)
- = extensive necrosis and epidermal detachment
14
Q
describe the pathophysiology of SJS/TENs
A
- complex interaction of genetic pre-disposition, environmental exposure and cell-mediated immune response
- CD8+T cells produce cytolytic proteins CD95+ Fas-Ligand and granulysin
- Fas-Ligand couples w. Fas Receptor on Keratinocyte, induces apoptosis
- Initiates shedding/exfoliation just above basement membrane
15
Q
how do you make the diagnosis of SJS/TEN?
A
- combination of clinical features and definitive diagnosis established with pathologic review (after biopsy)
- SJS/TEN differentiated by TBSA (< 10 = SJS; 10-30 = SJS/TEN overlap; >30 = TEN)
- classic prodrome / crescendo phase build-up to skin findings (erythema, papules, bullae +/- widespread involvement and Nikolsky’s sign + and > 2 sites of mucosal involvement
- biopsy shows absence of inflammatory infiltrate, cleave plane above BM, large sheets of necrotic keratinocytes, presence of CD8+T cells & macrophages in dermis
16
Q
what is the etiology of SJS/TENs?
A
- DRUGS > 50-80%
- antibiotics: penicillins, sulfa, fungal
- anticonvulsant: phenytoin, phenobarb, carbemazepine, valproate
- antiinflammatory: ibuprofen, naproxen, allopurinol
- Infection: bacterial, viral (measles, herpes), fungal
- Immunosuppression: GVHD, BMT, lymphoma, leukemia
- Idiopathic
17
Q
how do you prognosticate TEN?
A
- SCORTEN
- cancer
- HR (high)
- age
- TBSA
- bicarb (low)
- urea (high)
- glucose (high)
18
Q
how do you treat STS/TEN
A
- remove causative agent
- define diagnosis (biopsy) & transfer to burn unit
- ACLS/ABLS
- supportive care
- airway & breathing (oral cavity, upper aerodigestive tract involvement –> secure airway & breathing)
- circulation: no directed fluid resuscitation, follow usual measures (consider 1/2 parkland)
- determination of TBSA
- analgesia
- management of mucosal surfaces
- ophtho consult, conjunctival sweeping
- feed assist (NG)
- foley, rectal tube, perineal care
- management of skin
- derm consult
- debride blsiters if partially deroofed - leave if intact
- if early, cover w/ biobrane
- if contaminated, use jelonet,acticoat or allograft * avoid Ag sulfadiazine
- systemic medical management
- no good evidence to support prophylactic antibiotics, steroid or IVIG/cyclosporin/cyclophosphamide (controversial); derm to decide
19
Q
what is long term sequellae of SJS/TEN
A
- Skin: hyperpigmentation is biggest issue, nail deformities, hyperhidrosis
- Ocular: cicatricial deformity/synechiae, photophobia, visual impairment, blindness,
- Resp: Long-term pulmonary dysfunction
- GI: esophageal stenosis
GU: urethral stricture, phimosis, vaginal synechia, vaginal stenosis
20
Q
how do you differentiate between SJS/TEN and erythroderma multiforme?
A
- clinically they differ:
- EM prodrome is absent or mild and onset of rash is abrupt; whereas in SJS/TEN prodrome for 3-5 days prior to onsent of rash
- EM rash is characteristic target sign, where SJS/TEN is erythema, papules then blisters and exfoliation, with charactristic Nikolsky sign
- EM typically has no mucosal involvement (EM major can have 1 site of involvement, usually oral) whereas SJS/TEN requires > 2 sites for diagnosis (usually oral, ocular, GIT, GU, resp)
- biopsy will definitively discern between processes
- EM shows +++ inflammatory infiltrates, and small areas of keratinocyte apoptosis and vacuoles, from partial to total epidermal thickness
- SJS/TEN shows sheets of necrotic keratinocytes with cleavage plane above BM, presence of CD8+T cells and macs in dermis
21
Q
what are autoimmunue bullous disease?
A
- Pemphigus vulgaris
- Bullous pemphigoid
- Epidermolysis bullosa
22
Q
what is your differential diagnosis for SJS/TEN?
A
- blistering skin conditions:
- EM
- pemphigus vularis
- bullous pemphigoid
- epidermolysis bullosa
- Infectious blistering skin conditions
- staph scalded skin syndrome
- toxic shock syndrome
- pustular psoriasis
23
Q
define bullous phemphigoid
A
Bullous pemphigoid is a chronic, inflammatory, subepidermal, blistering disease. No mucosal involvement. Tense blisters
IgG autoantibodies bind to the skin basement membrane
Tx: steroids and immunosuppression
24
Q
what is pemphigus vulgaris?
A
PV = autoimmune, intraepithelial, blistering disease affecting the skin and mucous membranes. Flaccid blisters
- mediated by circulating autoantibodies directed against keratinocyte cell surfaces. A potentially life-threatening disease if no immunosuppressive therapy
- onset rapid with mucosal ulceration as presenting symptom
25
what is epidermolysis bullosa?
* Epidermolysis bullosa (EB) is a group of inherited bullous disorders characterized by blister formation in response to mechanical trauma.
* EB dysfunctional D-E jx and intraepidermal adhesion proteins
* EBsimplex - cleavage within BM
* EB junctional - cleavage at DEjx and lamina lucida
* EB dystrophic - cleavage in dermis, sub lamina lucida
26
what are extra-cutaneous manifestations of epidermolysis bullosa?
Extracutaneous manifestations:
* Mucosal surfaces
* Infection (sepsis),
* SCC (well diff, aggressive, unresponsive to Rx, high mets, death within 5 yrs of 1st SCC),
* Melanoma (slight risk)
* Mitten deformity of hand
KEY is to promote wound healing, manage non-healing areas, prevent infection, diagnose cutaneous malignancy,
27
what is acne?
* inflammation of the pilosebaceous unit,
Etiologies
* Androgens
* increase response to DHT w release of FFA and sebum which blocks pores
* Bacteria
* propionebacterium acnes
* lives in pilosebaceous unit
28
Is there any risk of cutaneous malignancy / malignant transformation associated w/ chronic acne?
rhinophyma associated w/ malignant transformation BCC in 15-30%
29
list congenital disorders of premature aging? which disorders are presumed safe for elective surgery?
* cutis laxa - safe
* pseudoxanthoma elasticum - safe
* progeria - not recommended
* Ehler's Danlos - not recommeded
* Elastoderma - not recommended
30
Define and describe cutis laxa. Why is it safe to perform elective surgery?
* Cutis laxa is an inherited disorder whereby elastin loses its elastic recoil property due to degenerative changes in elastin
* There are three types; the autosomal dominant type has findings localized to elastin in dermis
* The autosomal recessive and x-linked types have localized and systemic findings, whereby elastin in other structures can be affected as well (GI, cardio, pulmonary etc)
* Elective surgery is safe because the normal processes of wound healing are not impaired.
31
Define and describe pseudoxanthoma elasticum. Why is it safe or not safe to do elective surgery?
* pseudoxanthoma elasticum is a hereditary connective tissue disorder whereby the elastin fibres become mineralized, typically affecting the skin, vessels and eyes.
* elective surgery is not specifically contraindicated, but patients may have slower wound healing, hypertrophic or keloid scarring, and extrusion of calcinosis
32
Define and describe Ehler's Danlos. Describe why it is safe or not safe to do elective surgery
* Ehlers Danlos is a congenital, heritable disorder of collagen synthesis and structure, characterized by joint hypermobility, cutaneous fragility, and hyperextensibility
* There are over 10 different types, and the clinical manifestions within and between types can be quite variable.
* In general, the disorder affects to a different degree the skin and soft tissue, bone and vessels
* Elective surgery is typically avoided due to impaired wound healing, due to a probably fibroblast dysfunction and abnormal collagen
33
Define and describe progeria. Describe why elective surgery is safe or not safe
* progeria is a rare congenital hereditory disorder that affects skin, MSK and vasculature that is characterized by features of accellerated aging, including atherosclerosis, loss of subcutaneous fat and muscle, skin atrophy, osteoporosis, arthritis, poor growth, and alopecia
* given the severe atherosclerosis and microangiopathy, wound healing is abnromal elective surgery is not indicated
34
Describe which lasers you would choose to treat which pigments for tattoo removal.
§ QSR --\> black, blue, green, brown (DON’T USE ON RED –WILL TURN BLACK)
§ Nd/YAG: good for black, red
§ QSA excellent for darker tattoos
§ Er-YAG: good for light-colours
§ CO2 laser: good for flesh-colours
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