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Principles of delay

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Principles of delay
Delay is any preoperative maneuver that results in increased flap survival
Observed changes: anatomical; haemodynamic and metabolic
a) anatomical changes
1) increased size of subdermal vessels
2) longitudinal reorientation of vessels
b) haemodynamic changes
1) flow at flap tip initially low, but increases
2) little evidence of A-V shunting
c) metabolic changes
1) hypoxia
2) glucose consumption in ischaemic tip increases by 3 days & normal by
7 days
3) lactate production increases, tissue glycogen & glucose decrease,
cAMP decreases but reverts in 12hrs if viable
4) sympathetic catecholamines disappear 18-30hrs
5) increased production superoxide radicals secondary to xanthine
metabolism
6) decreased viscosity
7) ischaemia leads to decreased fibrinolysis
8) ischaemia increases thromboxane
End result is delay conditions tissue to ischaemia
Callegari and colleagues (1992), after their numerous experiments, arrived at the
following conclusions:
1. the survival length of flaps is related to the distance between perforators
2. the necrosis line of a flap usually appears in the zone of choke vessels connecting
adjacent territories
3. a surgical delay results in dilatation of existing vessels with maximal effect in the
zone of the choke arteries
4. the most effective delay is obtained by elevating the flap in stages from the base
and not detaching the tip until last
5. tissue expansion is a form of delay, particularly in terms of vessel hypertrophy
6. similar changes occur when a muscle is delayed
Classical Theories
1) increased axiality of blood flow
a. German in 1933 established that a delay procedure will increase the
number and size of small arteries in tubed skin grafts.
b. Cutting found that total blood flow in the delayed flap markedly
increased, suggesting that the most significant hemodynamic event
occurring during the delay period is the development of vascular
collaterals.
2) opening of choke vessels
a. Morris and Taylor postulated that the increased perfusion was due to
opening of choke vessels between vascular territories.
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b. They found that the maximal effect of this perfusion change occurred
between 48 and 72 hours after surgical delay.
c. histologic analysis revealed an increase in the diameter of the vessels
and a decrease in vessel wall thickness compared with the control
vessels.
d. Stages
i. Vessel spasms for 3 hours
ii. Increased caliber of choke vessels with wall thinning (24-72
hours)
iii. Dilation and thickening of wall (72hrs-1 week)
iv. Choke vessels open permanently
Tolerance to ischaemia
a. In 1965, McFarlane stated that the delay procedure conditions flaps to
survive on diminished nutrient blood flow, resulting in increased flap
survival.
b. In 1972, Myers theorized that the improvement in flap circulation was
dependent on the degree of ischemia produced by the initial delay
procedure.
c. Now known to be mediated by heat shock proteins
Sympathectomy vasodilatation theory
a. Divided sympathetics at the borders of the flap
b. Does not explain why maximal effect is delayed and why delay
requires weeks.
Interflap shunting hypothesis
a. Sympathectomy dilates the AVAs more than precapillary sphincters
resulting in increased blood bypass
b. Delay results in less sympathetic fibers cut and therefore less of a
reduction in non-nutritive flow
Hyperadrenergic state
a. Surgery results in rise in local and systemic vasoconstrictive
substances (Adrenaline and noradrenaline)
b. As the effect of these chemicals gradually diminishes (4 to 12 hours),
vessels in the flap begin to dilate. Over the next 24 to 72 hours, an
active process further dilates the vessels.
Unifying theory (Pearl 1981)
a. elevation of flap produces a hyperadrenergic state lasting 18-30 hrs.
b. This results in vasoconstriction.
c. Recovery from hyperadrenergic state follows over next few days as the
flap is exhausted of noradrenaline. Thus when flap finally elevated,
adverse vasoconstriction is avoided.
Current Theory
Induction of Heat Shock Proteins
 Supraphysiologic stress induces a heat shock response, which may exert
protection against ischemic necrosis.
 Delay preconditions the tissue at risk prior to surgery to induce heat shock
proteins (HSPs) by exposure to physical or pharmacologic stressor
 Experimentally, the heat shock response has been demonstrated to have a positive
effect on flap survival by protecting tissue from ischemia or ischemia–reperfusion
injury.
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HSPs are a superfamily of highly conserved intracellular proteins that protect cells
and whole organisms from various stresses.
Mechanism of action
1) Tolerance to ischaemia
a. act as molecular chaperones, escorting proteins targeted for other
cellular compartments
b. prevent misfolding of newly synthesized proteins
2) improving microcirculatory blood flow on an arteriolar and capillary level
a. vasodilatory action of carbon monoxide
Of interest are heat-shock protein (HSP) 70 and HSP-32 [haem oxygenase 1]
HSP-32 has been identified as heme oxygenase (HO)-1, the rate-limiting enzyme
in the catabolism of heme to biliverdin, free iron, and carbon monoxide.
HSP-32 is the main endogenous source of carbon monoxide
In mouse studies, induction of HSP-32 after repetitive local heat preconditioning
of the skin significantly preserves endangered myocutaneous ischemic tissue from
apoptotic and necrotic cell death.
This protection from ischemic tissue loss seems to be the result of the HSP-32mediated vasoactive action of carbon monoxide, improving microcirculatory
blood flow on an arteriolar and capillary level rather than increasing ischemic
tolerance of the tissue.
Delay may be
1) Surgical
a. Dividing margins of flap
b. Classically, lateral borders are divided and flap totally undermined
(bipedicled flap)
2) Vascular
a. Dividing perforators/axial vessels
3) Laser
4) Chemical
a. Alpha-adrenoreceptor blocker
i. Phenoxybenzamine
ii. Phentolamine
iii. Daxozocin
b. Adrenergic neuron blocking
i. Guanethidine
c. Noradrenaline depletion
i. Reserpine
d. Free radical scavengers
i. Superoxide dismutase
ii. Allupurinol
e. Cytokines
i. VEGF
1. preoperative intramuscular injection of VEGF increases
skin paddle survival (rat model) alone or in conjunction
with surgical delay
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