Microsurgery:

Free Tissue Transfer

Plastic Surgical Department
Mark Chiu
 Microsurgery
• Surgical specialty requiring magnification
for its completion
• Plastic surgery
• Neurosurgery
• Ophthalmology,
• Orthopedic surgery,urology,otolaryngology,
gynecology
 History
• 1890s to 1990s, approximate blood
vessels in animal or clinical patients
without magnification
• 1902, Alexis Carrel, advocated end-to-side
anastomosis
• 1921, Nylen, first used monocular
microscope
 History
• 1960, Jacobson, reported microscopic
anastomosis in animal with 100% patency
in carotid artery, 1.4 mm diameter
• 1965, Jacobson, 1mm, diameter, in animal
• He emphasized the importance of avoiding
intimal trauma and precise intima-itima
reapproximation
 History
• 1968, Cobbett, transferred a great toe to
the hand
• 1971, antia and Buch, reported successful
transfer of a superficial epigastric artery
skin to the face
• 1971, McLean and Buncke, free transfer of
the omentum to scalp
 History
• 1966, Green, used 9-O Nylon suture, in rat,
aortas (1.3 mm, ave), vena cavas (2.7mm,
ave), patency, 37/40
• 1962, Malt and McKhann, described first
arm replantation in two patients
• 1972, Acland, reported 95% patency in rat
epigastric artery
 History
• 1963, Chinese surgeon, reported hand
replantation at wrist level, radial and ulnar
arteries were anastomosed using short
links of 2.5mm diam polyethylene tubes
• 1963, Kleinert and Kasdan described
digital revascularization in near-amputaed
digit. Stressed the importance of using
vein grafts
 History
• 1964, Nakayama, reported first clinical
series of free-tissue microscopic transfers.
Intestinal transfer to cervical esophagus,
21 patients series
• 1968, Komatsu and Tamai, first successful
replantation of a completely amputated
digit
 History
• 1973, Daniel, Taylor and O’Brien, free-
tissue transfer of groin flaps for lower
extremity reconstruction
• The first human-to-human hand transplant
were performed 17 years ago
• Drawbacks: poor sensory return, acute or
chronic rejection, systemic complications,
immunosupressive therapy, loss of the
transplants
 History
• As the result of surgery became more
predictable and the number of available
free flaps grew, efforts shifted to
minimizing donor site morbidity
• Free flap selection in specific defects is
becoming more standardized.
 Requirements
• Magnification
• Microinstrumentation
• Microsutures
• Microsurgical skills
 Magnification
• Surgical microscope: from 6X to 40X
• Ocular loupe: from 2.0X to 4.0X
 Microinstrumentation
• Forceps
• Scissors
• Needle holder
• Microvascular clamps
• Background
 Microsutures
• 8.0 to 12.0 Nylon
• Needle diameter: 75 to 135 μm
 Microsurgical skills
• It is required
• No one is born with an ability to do
microsurgery
• Training
 End-to-End, End-to-Side
• When size-discrepant vessels are involved,
end-to-side venous repairs have proved to
be significantly better.
• The dynamics of flow in end-to-side
arterial repairs are favorable.
 Basic science concepts in
microsurgery
• As a microvascular surgeon, should
understand the mechanisms of vessels
injury, repair and regeneration, be familiar
with the processes of vasospasm and
thrombosis and their pharmacological
control, be aware of the effects of
ischemia and hypoxia
Vessel injury and Regeneration
• Exposure of the underlying
subendothelium to the blood stream
results in platelet aggregation, which is the
first step in the formation of thrombotic
plug.
• Full-thickness sutures that afforded intimal
continuity provoked the least amount of
anastomotic bleeding and platelet
aggregates
Vessel injury and Regeneration
• Far worse damage was seen with partial
thickness-thickness bites
• Pseudointima forms within the first 5 days
• Approximately 1-2 weeks after injury new
endothelium covers the anastomotic site.
• The layer of platelet cells will not progress
to fibrin deposition and thrombosis if it is
not exposed to the media and the lumen is
not injured.
Vessel injury and Regeneration
• Over the next 24-72 hrs, the platelets
gradually disappear.
• Critical period of thrombus formation: the
first 3-5 days.
• The mechanism of endothelial
regeneration depends on presence or
absence of mechanical injury of the
subendothelial structure.
Vessel injury and Regeneration
• Endothelium injury alone: reconstituted
from the surrounding cells, complete in 7-
10 days
• Damage to the subendothelium:
regenerate by migration and differentiation
of myoendothelial cells.
• Remaining layers: by proliferation of
fibroblasts with collagen deposition.
Vessel injury and Regeneration
• Elastic and muscular elements of the
vessel wall fail to regenerate to the same
degree; do not return to their preinjury
state.
• Exposure of vessels from its bed results
in significant endothelial loss.
• Avoid damage to vessels during dissection,
careful using of bipolar
Vessel injury and Regeneration
• Desiccation leads to endothelial loss and
triggers diffuse platelet aggregation.
• Vasospasm can lead to endothelial slough,
> 2hrs, lose most of their endothelial layer.
• Lidocaine: antispasmatic effect. Most of
the topically applied lidocaine is not fully
absorbed
Vessel injury and Regeneration
• Injury related to clip pressure
• Curved clips or angled clips do more injury
than flat ones
• Vascular clips should remain < 30gm/mm2
Vessel injury and Regeneration
• 20% xylocaine, optimum spasmolytic and
antispasmodic effects, experimentally.
• Clinically, 2% xylocaine has a beneficial
effect on most vessels.
• The most significant damage to vessel
wall is from needle and suture penetration
and technique of placement.
Vessel injury and Regeneration
• Large needle and oblique placed sutures:
major endothelial laceration
• Repeated needle :large platelet plugs at
bleeding site
• Unequal intersuture distance: endothelial
gaps, distortion, constriction, exposed
intimal flaps
Vessel injury and Regeneration
• Reasons of surgical failure:
• Do anastomosis at zone of injury
• External compression of anastomosis by
hematoma
 The Clotting Mechanism
• Aggregation: platelet activated by collagen,
platelet granules are released, in turn
attract more platelets
• Fibrinogen adheres and fibrinogen forms
proteinaceous bridges
• As platelet become activated, fibrinogen
become fibrin, then red clot forms
 The Clotting Mechanism
• Alpha granules: von Willebrand factor,
fibrinogen
• Dense granule: ADP, Ca, serotonin
• All factors promote thrombus formation,
extrinsic pathway of coagulation
 The Clotting Mechanism
• PGE1: like PGI 2: potent vasodilator and
platelet disaggregator
• But higher dose result in hypotension and
decrease blood flow to flap
 The Clotting Mechanism
• Heparin: increase action of anti-thrombin-
3 which inactivate thrombin, decrease
platelet adhesion, hamper conversion of
fibrinogen to fibrin
• Use heparin, hematoma incidence: 12.5%,
in animal model
• In clinic, for saving flap
 The Clotting Mechanism
• Some surgeon feel that heparin does not
improve patency in uncomplicated repair
• So, heparin infusion is used sparingly by
most microsurgeon.
 The Clotting Mechanism
• Aspirin: inhibit initial platelet aggregation
• Mediated by endothelial cyclooxygenase
pathway, subsequent blockage of
thromboxame A2
• Low doses: 325mg daily
 Ischemia

Cell menbrane

Arachidonic acid

Cyclooxygenase
Endoperoxides

PGI-2 TXA-2 synthetase

synthetase Prostaglandins

Prostacyclin ( Pgi-2) Thromboxane TAX-2

 The Clotting Mechanism
• Dextran: 70000, Dextran 70 and 40000,
Dextran 40
• Anti-platelet and anti-fibrin function
• Elevated negative charge on platelet,
inactivation of von Willebrand factor
• Loading dose:40-50ml, maintain dose: 25-
50ml/hr
 The Clotting Mechanism
• Complications: bleeding with subsequent
vessel compression, acute renal failure
secondary to Dextran use
 The Clotting Mechanism
• Proteolytic enzymes:
• Streptokinase and Urokinase
• Streptokinase:produced by group C beta-
hemolytic streptococci
• Urokinase: produce by human kidney cells
• Both convert plasminogen to plasmin
• Plasmin: highly specific fibronolytic
enzyme
 The Clotting Mechanism
• Tissue plasminogen activator (tPA)
• Produced by human vascular endothelium
• Activating plasminogen
• Next horizon: monoclonal antibody
regulation of platelet aggregation
 The Clotting Mechanism
• There are no definite indications for
anticoagulation or antifibrinolytic therapy
when mechanical and vascular factors are
optimal, eg, during elective free flap
transfers
 The Clotting Mechanism
• When there is evidence of thrombosis in
the post-operative microvascular
anastomosis, flap reexploration and
treatment with fibrinolytic therapy and
anticoagulation seem prudent. Flap
reexploration is the essential step.
 The Clotting Mechanism
• Anticoagulation or fibrinolytic therapy may
be indicated in clinical situations where
mechanical or metabolic factors are not
favorable and cannot be improved.
Tissue Response to Ischemia and
Hypoxia
Tissue Warm Cold
Skin and subcutaneous 4-6h up to 12h
tissue

Musccle <2h 8h

bone <3h 24h

 Tissue Response to Ischemia and
Hypoxia
• Skin and subcutaneous tissue are
relatively resistant to the effect of anoxia.
• Mammalian skeletal muscle is relatively
less tolerant to ischemia than skin.
• Connective tissue rich in fibroblasts,
chondroblasts, osteoblasts is relatively
resistant to prolong hypoxia.
 Tissue Response to Ischemia and
Hypoxia
• Neuromuscular junctions are most
sensitive to ischemia
 Reperfusion injury and the No-
Reflow Effect
• Ischemic organs fail to reperfuse after their
blood supply has been reestablished, and this is
called no-reflow phenomenon.
• Mechanism: cellular swelling in the vascular
endothelium, subsequent intravascular platelet
aggregation and adhesion of white cells to the
endothelium, increase in endothelium
permeability, occlusion of small capillary bed, AV
shunting, lack of tissue perfusion, flap loss
 Reperfusion injury and the No-
Reflow Effect
• In summary, the common denominator in
failure of microvascular anastomosis is
endothelial disruption with exposure of
subendothelial collagen-containing
surfaces to which platelets adhere.
 Reperfusion injury and the No-
Reflow Effect
• If platelets aggregation reaches a certain
mass, it will trigger fibrin deposition that
leads to vasospasm, stenosis, and
eventual thrombosis of the vessel. As the
blood flow rate through the anastomosis
falls below the critical level, the flap fails.
Flaps
Anterolateral Thigh (ALT) Flap
Anterolateral Thigh (ALT) Flap
Radial Forearm flap
Radial Forearm flap
Postoperative Care
 Monitoring
• Doppler ultrasound flowmeter
• Temperature monitoring
• Pulse oxymetry: digital replantation
• Clinical observation
 Wound Care
• Avoid pressure as possible on vessels
• Avoid excess exercise: splinting, bed rest..
• Smoking is prohibited
Thank You