general points, random & local flaps Flashcards
1
Q
list ways to address a discrepancy when undertaking an arterial anastomosis
A
- Dilate small vessel
- Oblique transection
- end-to-side
- telescoping, sleeve and cuff
- spatulation
- venous coupler (for vein)
- interpositional vein graft (reversed)
2
Q
how do you define a flap?
A
- a composite of tissue that is transferred to a new location with its vascular pedicle (or by reconstituting its vascular pedicle)
- a unit of tissue (any combination of skin, fat, muscle, bone, tendon, nerve, or fascia) that is transferred from a donor site to a recipient site while maintaining (or reconstituting) a blood supply through a vascular pedicle
3
Q
how do you classify flaps?
A
Cormac and Lamberty suggested the 6 C’s:
- Circulation: a) random; b direct / axial; c) indirect / perforator (fascio-, septo-, musculo- cutaneous)
- Conformation / Vascular Directionality – normograde / anterograde, retrograde / reversed, flow -through
- Constituents: cutaneous, fasciocutaneous, musculocutaneous, osseomyocutaneous, etc
- Construction / Transfer Method – advancement, rotation, transposition, interpolation, distant transfer
o Advancement flap – move in a direction directly forward without any lateral movement
o Rotation flaps – semicircular flaps that rotate about a pivot point into an adjacent defect
o Transposition flaps – usually rectangular and move laterally about a pivot point into an adjacent defect
o Interpolation flaps – transfer skin above or deep to an intervening skin bridge to a non-adjacent defect
o Distant Transfer – tubed pedicle or free tissue transfer
- Contiguity – Relationship to defect (local/regional/distant/free)
- Conditioning – delay, tissue expansion
4
Q
Describe the 5 plexuses of skin and subcutaneous tissue
A
- Subepidermal
- Dermal
- Subdermal
- Subcutaneous
- Fascial
- larger prefascial
- smaller subfacial
- intrafascial – very minor
5
Q
Describe an angiosome
A
- Angiosomes (40 in total) – 3D units of skin & underlying deep tissue supplied by a single source artery (ateriosome) & associated venosome
- Single source vessel may supply multiple angiosomes (ie perforasomes)
- Defines flap boundaries
- Can be linked by true anastamotic arteries or choke anastamotic vessels
- Territories are dynamic and depend on intravascular pressure & caliber of choke vessels
6
Q
Describe the 3 ways that reverse flow flaps work:
A
- Two systems of venous arcades with NO VALVES
- Macrovenous connections (no valves) criss-cross between venae commitantes and provide a mechanism whereby the valves of the venae commitantes are bypassed
- Microvenous connections (no valves), surround the artery as the vena arteriosa and also provide a connection to the venae commitantes
- Increased venous hydrostatic pressure within the flap causes a dilatation of the venae commitantes which may cause the valves to become incompetent
- Surgical sympathectomy may also provide the necessary venous dilatation
7
Q
what is a suspected mechanism of perfusion of venous flaps?
A
- Plasmic imbibition
- Perfusion pressure
- Sites of AV anastomosis
- V-v connections
- Circumvent valves
8
Q
what are the advantages and disadvantages of venous flaps?
A
- Advantages – smaller, thinner, no artery needed, fast and easy to raise, no donor site mobdiity, anatomically constant pedicle (e.g. saphenous)
- Disadvantages – Poorly understood physiology, limited size, inconsistent survival, potential hemodynamic complications from creating the AV shunt
9
Q
describe the physiology of skin microcirculation
A
- Systemic
- Neurologic regulation
- Adrenergic –> SNS control of smooth muscle (vasoconstriction = alpha, vasodilation = beta)
- Cholinergic –> parasympathetic = vasodilation
- Humoral regulation (important in surgical sympathectomy)
- Vasoconstriction = adrenalin/serotonin/thromboxane, prostaglandin F2 (PGF2)
- Vasodilation = histamine, bradykinin, PGE2
- Local
- Metabolic factors (↑PCO2, [K+], ↓PO2, pH) –> vasodilation
- Physical factors – temperature, viscosity (↓ flow with hct >.45)
10
Q
what are the 3 physiologic processes that occur during acute flap elevation?
A
Early flap hemodynamics rely on the balance of these 3 processes:
Increased Vascular Resistance
- Severing of cutaneous vessels - incr flap ischemia
- Ischemia and surgical trauma - incr inflammation, capillary permeability and endothelial cell edema
- Interstitial and endothelial cell edema - decr intraluminal diameter and incr vascular resistance
- cap permeability - incr blood viscosity and contributes to vascular resistance
Vasoconstriction
- Surgical sympathectomy – initial release terminal neurotransmitters (adrenaline and noradrenaline) –> vasoconstriction
- Sympathetic re-innervation takes about 4 weeks (by then, your flap has vascular ingrowth)
- Surgical trauma also results in release of platelet-derived vasoconstrictors (Serotonin & TxA2)
Vasodilatation
- Sympathectomy eventually results in vasodilatation (and insensitivity to plt-derived v-const)
- Surgical trauma & anaerobic metabolism = release of local vasodilators (eg. bradykinin, histamine, and prostaglandins)
11
Q
Describe the temporal changes in vascularity of a flap after elevation
A
- 0-12 hours: vasoconstriction, marked congestion and edema in the 1st 24 hours
- 12-24 hours: vasodilatation
- 1-3 days: ↑ choke vessels (size and number), axial reorientation of flow
- 4-7 days: ↑ circulatory efficiency
- Week 1: inosculation
- Week 2: return to normal perfusion efficiency (can divide pedicle 10-21 days)
- Week 3: inosculation complete, flow 90-100% normal
12
Q
Define vascular delay
A
- surgical PARTIAL disruption to the blood supply of a flap at a preliminary stage prior to transfer
13
Q
How does vascular delay work?
A
- Early
- Sympathectomy (with vasodilation, increased flow, and decreased AV shunting)
- Vascular reorganization via increase size and longitudinal re-orientation of choke vessels (into true anastomoses)
- Ischemic pre-conditioning via early metabolic response: Metabolic tolerance to hypoxia and ischemia
- Others: reactive hyperemia
- Late
- Tissue metabolism: blunted secretion of vasoconstrictive cytokines (TXF2) and increased secretion of vasodilatory cytokines (TXE2)
- Neovascularization
14
Q
describe the crane principle
A
- Technique of transforming an ungraftable bed to a graftable one
- Stage 1 – pedicled flap placed in defect
- Stage 2 – superficial portion replaced to original place; subcutaneous tissue in defect now can accept a graft
15
Q
describe the pathophysiology of acute flap failure
A
- Intrinsic factors – arterial insufficiency (tip nec = vasodil @ tip/vasocon at bas), venous insufficiency
- Extrinsic factors – systemic (transient: hypotension, caffeine; preexisting: PAD, DM) , local (tension/pressure/dressing)
- Ischemia-reperfusion injury
- ATP stores broken down –> xanthine –> PMNs then release O2 free rad –> inc cell adhesion + more PMN –> ++ proimflammatory cytokines/cell injury/death vascular permeability/inc cell adhesion/microthrombosis
- No Reflow – never flows d/t irrev vascular damage with prolonged ischemia time
