2. Introduction
• Flap Failure as a result of ischemic necrosis occurs in both pedicled
and free flaps
• In Free flaps alone, ischemic necrosis occurs in 5–10% of patients,
even in experienced hands
• Increases the incidence of donor site deformity and/or morbidity,
with devastating effects on the patient
• Additional operating room cost ranges from about $40 000 to $68
000 for each total free flap failure, and the additional surgeon
reimbursement ranges from $5000 to $35 000 for each surgery
6. Surgical Manipulation in augmentation of
pedicle flap viability
• Flap Design in the augmentation
• Surgical delay
• Vascular delay
7. Flap design in the augmentation of flap
viability
• ultimate surviving length of a pedicle flap is
determined by the balance between perfusion
pressure and vascular resistance
• Increasing the width of pedicle flap merely
adds additional vessels of the same type and
the same perfusion pressure and thus cannot
increase the length of flap viability
• increasing the width of the pedicle may
increase the chance of including a large artery
8. Surgical Delay
• In studies with pig random-pattern skin flaps, investigators showed
that surgical delay increased skin flap capillary blood flow between 2
and 7 days of delay
• Mainly in the distal random portion of the delayed skin flap
9. Vascular delay
• Dividing distal perforating arteries at 1–2 weeks prior to raising the muscle
flap
• Division of perforators or one or two dominant arteries that supply blood
to the rectus abdominis muscle 2–3 weeks before flap surgery significantly
augmented viability in TRAM flaps in rats
• In human patients, ligation of the deep inferior epigastric arteries 2–4
weeks before flap surgery augmented skin blood supply and viability in
TRAM flap
• Vascular delay by embolization does not require general anesthesia, but it
requires local anesthesia and catheterization performed in the
interventional radiology
10. Mechanism of surgical delay
• Surgical delay procedure reduces
arteriovenous (AV) shunt flow
• Surgical delay procedure depletes
vasoconstriction and prothrombotic
substances in the skin flap
• Surgical delay procedure induces vascular
territory expansion by opening existing
choke arteries
• Surgical delay procedure induces
angiogenesis
11. Two schools of thought…
• delay conditions tissue to ischemia, allowing it to survive on less
nutrient blood flow than normally needed
• delay improves or increases vascularity.
13. • Braithwaite proposed that the likely mechanism of delay consists of
vascular reorganization and reactive hyperemia acting through
nonlethal ischemia to condition the tissue to survive on less blood
flow, together with an increase in size of the vessels in the
dermovenous plexus
• hyperemia observed when a tubed pedicle is transferred arises from a
vascular debt as a result of increased resistance to venous outflow
14. • Brown and McDowell: to permit gradual hypertrophy of the blood
vessels in the pedicle and possibly to accustom the tissues in the flap
to a lower oxygen tension or poor circulation
• Delayed flaps have adequate blood flow to survive the early stage of
vasoconstriction whereas acute flaps do not
15. • When flaps are delayed, blood vessels and adrenergic nerves are
severed, causing a spontaneous discharge of neurotransmitters, so
that by the time of flap inset there is little release of norepinephrine
and consequent diminution in vasoconstriction of the flap
16. • Seitchik and Kahn
• longitudinal reorientation of small vessels parallel with the long axis of tubed
pedicles at 1 to 7 days post-delay
• increase in size of vessel
• increase in number of small arteries in the subdermal plexus
17. • Pang and colleagues monitored skin capillary blood flow and
angiogenesis in delayed and nondelayed random skin flaps in the pig
• The increase in flow was detectable within 2 days of surgical delay,
increased 100% by day 4, and remained at this plateau until day 14.
There was, however, no significant increase in the density of arteries
between acute and delayed skin flaps
• Delay phenomenon is not dependent on angiogenesis but probably
mediated through locally released neurohumoral substances
18. • Serafin and later by Garcia: both an increase in the number and size
and an ingrowth of new vessels from the surrounding tissue occurred
about 4 to 5 days postoperatively
• Others confirm these findings and suggest that an ischemic tissue
gradient provides the impetus for angiogenesis and leads to greater
viability of delayed flaps
19. • Lopez et al:
• Delayed flaps exhibit an increase in capillaries from 48 hours, and this
continues until 7 days after flap elevation. Their theory of delay holds that
hypoxia accounts for vasodilation and release of neurohumoral substances
• The period of delay offering maximum survival is about 1 week,
whereas the minimum effective time is 2 to 3 days
23. Timing of Flap Division
• German and associates concluded that circulation in flaps was
reestablished considerably earlier than previously thought. They
begandividing their flaps at 14 days post-transfer, and subsequently
shortened the interval to 10 days without deleterious effects on flap
survival
• Flaps can be divided as early as the third day
• The cumulative experience of many surgeons suggests that most flaps
can be divided safely at 10 days to 3 weeks
24. To sum up…
Hoopes’ 5 mechanisms
• sympathectomy
• vascular reorganization
• reactive hyperemia
• acclimatization to hypoxia
• nonspecific inflammatory reaction