RECONSTRUCTIVE SURGERY

owing to the tight tissue planes, and there may be significant blood
Anaesthesia for loss when used on the scalp. A certain amount of commitment is
required on the part of the patient or parent because of the patient’s
reconstructive surgery increasingly bizarre appearance, but the final results are impres-
sive. This technique can be used to cover alopecia, congenital
Jane Quinlan naevi, burns or defects caused by previous surgery.

Local flaps
Any flap (local, pedicled or free) contains a network of arteries,
capillaries and veins which maintain the perfusion of the flap at
Skin or tissue defects that cannot be closed primarily with simple its recipient site. A local flap is used when tissue adjoining a defect
suturing require skin grafts or flaps to maintain skin integrity is moved laterally to cover the defect (e.g. after excision of a skin
and prevent infection. Tissue defects may be covered using skin cancer). Geometric rearrangements of skin with V–Y plasties or
grafts, tissue-expanded skin, local skin flaps, pedicled flaps, or Z plasties can be used to alter the size and shape of the flap. As
free flaps. with full thickness skin grafts, the size of the local flap is limited
to enable closure of the secondary defect (it could be covered with
a split skin graft, but this compromises the aesthetic result).
Skin grafts and flaps
Skin grafts Pedicled flaps
There are two types of skin graft. While free flaps have their circulation detached and reanastomo-
• Full thickness grafts consist of epidermis and the full thickness sed distantly, pedicled flaps keep their vascular supply, so do not
of dermis. They are typically taken from pre-auricular skin, supra- have an ischaemic insult. Skin and muscle can be used in the
clavicular skin, the antecubital fossa, groin, thigh or abdomen. flap, which is then swung round to cover the defect. They have
These sites have skin laxity so that the donor site can be closed a distinct neurovascular hilum that acts as a pivot point around
directly, but the size of graft taken is limited by the need for pri- which they can be moved. Examples of pedicled flaps are latis-
mary closure. simus dorsi muscle used for breast reconstruction, and pectoralis
• Split skin grafts are made up of epidermis with a variable major used in head and neck cancer reconstruction. Surgery is
proportion of dermis. They are taken by dermatome and can be prolonged with many of the stages being similar to free flap surgery,
almost any size because they can be meshed, thus increasing the but the neurovascular pedicle is not divided and microvascular
surface area of the graft taken. anastomosis is therefore not required. However, there is still a risk
In both cases the graft initially adheres to the recipient bed by of flap failure if the pedicle is twisted, stretched or compressed,
fibrin, while revascularization occurs as capillary buds grow from because this may compromise vascular supply.
the recipient bed into the graft. Fibroblasts produce fibrous tissue
to attach the graft and the tension generated increases, providing Free flap reconstruction
a stable adherence by 4 days. With time, lymphatic link-up and Reconstructive free flap surgery is the most complex method of
nerve supply are re-established. wound closure for large wounds not amenable to linear (primary)
Split skin grafts are extremely painful postoperatively because closure. It involves the transfer of free tissue (skin, muscle, bone,
nerve endings in the dermis are exposed. Patients benefit from a bowel or a combination) to a site of tissue loss where its circula-
local anaesthetic block where possible. For split skin grafts taken tion is restored via microvascular anastomoses. A muscle flap
from the thigh, a lateral cutaneous nerve of thigh block is most produces a more even contour and better aesthetic appearance than
appropriate. EMLA cream (eutectic mixture of local anaesthetic) that achieved by a simple skin graft and provides better defence
applied to the donor site preoperatively or soaking the donor site against infection. The defect may be caused by trauma, infection
dressings (e.g. Kaltostat) in bupivacaine may reduce pain, but the or extensive surgery (e.g. mastectomy, head and neck cancer).
anaesthesia does not extend to the deeper part of the dermis. The site and size of the tissue defect determines which flap is
used. The most commonly used free flaps are the gracilis muscle
Tissue expanders for lower leg trauma; the transverse rectus abdominis muscle for
Saline-filled balloons (Figure 1) are inserted under normal skin and breast reconstruction; and a radial forearm flap for head and neck
inflated at intervals with saline under pressure. The saline is col- reconstruction.
oured blue to avoid confusion with physiological fluids. Expansion In patients with lower third tibulofibular defects, free tissue
occurs weekly for up to 3 months to stretch enough skin to cover transfer is typically required. The bony injury should be repaired
adjacent abnormal skin. The abnormal skin can then be excised, and adequate debridement achieved before skin and muscle cov-
the tissue expanders removed, and the newly stretched skin used erage commences. This should occur within the first 6 days after
to cover the skin defect. Insertion can be painful postoperatively injury before colonization of the wound and the risk of complica-
tions increases. In patients with multiple trauma, any life-threaten-
ing injuries must be addressed first and the patient’s haemodynamic
Jane Quinlan is Consultant Anaesthetist at the Radcliffe Infirmary and the status stabilized before reconstructive surgery is contemplated.
John Radcliffe Hospital, Oxford. She qualified from St Thomas’ Hospital,
London, and trained in anaesthesia in London and Oxford. Her interests Flap transfer
include anaesthesia for plastic surgery and acute pain management. The free flap is transferred with its accompanying artery and vein,

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 RECONSTRUCTIVE SURGERY

Use of saline-filled
balloons.
1

which are then reattached to vessels at the recipient site using if factors in the flap are unfavourable. Prolonged ischaemia time
microvascular techniques. or poor perfusion pressure make this more likely. Reperfusion
The stages of flap transfer are: injury occurs when the restored blood flow allows the influx of
• flap elevation and clamping of vessels inflammatory substrates that may ultimately destroy the flap.
• primary ischaemia as blood flow ceases and intracellular Secondary ischaemia occurs after a free flap has been trans-
metabolism becomes anaerobic (this depends on surgical time planted and reperfused. This period of ischaemia is more damaging
and lasts between 60 and 90 min) to the flap than primary ischaemia. Flaps affected by secondary
• reperfusion as the arterial and venous anastomoses are com- ischaemia have massive intravascular thrombosis and significant
pleted and the clamps released interstitial oedema. Fibrinogen and platelet concentrations are
• secondary ischaemia is hypoperfusion of the flap following increased in the venous effluent. Although skin flaps can tolerate
attachment; it can be minimized, peri- and postoperatively, by 10–12 hours of ischaemia, irreversible histopathological changes
appropriate anaesthetic management. in muscle can be seen after 4 hours.
Primary ischaemia – with cessation of blood flow, the flap
becomes anoxic. In the presence of anaerobic metabolism, lactate Causes of flap failure
accumulates, intracellular pH drops, ATP decreases, calcium levels The general causes of poor flap perfusion are arterial, venous or
rise and proinflammatory mediators accumulate. The severity of resulting from oedema. The arterial anastomosis may be inad-
the damage caused by primary ischaemia is proportional to the equate, in spasm or thrombosed. The venous anastomosis may be
duration of ischaemia. Tissues with a high metabolic rate are similarly defective, in spasm or compressed (e.g. by tight dressings
more susceptible to ischaemia, therefore skeletal muscle in a flap or poor positioning). Oedema reduces flow to the flap and may be
is more sensitive to ischaemic injury than skin. At the conclusion a result of excessive crystalloids, extreme haemodilution, trauma
of primary ischaemia, the changes in the flap tissue include: from handling or a prolonged ischaemia time. Flap tissue has no
• narrowed capillaries due to endothelial swelling, vasoconstric- lymphatic drainage and is therefore susceptible to oedema.
tion and oedema
• sequestration of leucocytes ready to release proteolytic enzymes Microcirculation: blood flow through the microcirculation is
and reactive oxygen intermediates crucial to the viability of a free flap. The microcirculation is a
• diminished ability of endothelial cells to release vasodilators series of successive branchings of arterioles and venules from the
and degrade ambient vasoconstrictors central vessels.
• end-organ cell membrane dysfunction and accumulation of Regulation of blood flow and oxygen delivery is accomplished
intracellular and extracellular toxins by three functionally distinct portions of the microcirculation: the
• up-regulation of enzyme systems to produce inflammatory resistance vessels, the exchange vessels and the capacitance ves-
mediators. sels. The resistance vessels are the muscular arterioles that control
Reperfusion begins with the release of the vascular clamps. regional blood flow. Arterioles are 20–50 µm in diameter and
Normally, the re-establishment of blood flow reverses the transient their walls contain a relatively large amount of vascular smooth
physiological derangement produced by primary ischaemia. The muscle. Alterations in vascular smooth muscle tone are responsible
flap recovers with minimal injury and normal cellular metabolism for active constriction and dilation in arterioles and thus control
is restored. However, an ischaemia or reperfusion injury may result resistance to blood flow. The capillaries constitute the network

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 RECONSTRUCTIVE SURGERY

of vessels primarily responsible for the exchange function in the recovery room and the ward for the first 24–48 hours. This is best
circulation. Small bands of vascular smooth muscle, the precapil- achieved by raising the ambient temperature in theatre and by
lary sphincters, are located at the arterial end of many capillaries using a warm air blanket. Active warming should begin before the
and are responsible for the control of blood flow in the capillaries. start of anaesthesia because patients cool rapidly after induction
The venules act as the capacitance vessels, which collect blood of anaesthesia. In an awake patient, the central core temperature
from the capillary network and function as a reservoir for blood is higher than that of peripheral tissue and skin temperature. After
in the circulation. induction of anaesthesia, vasodilatation modifies the thermal
The vascular bed of skeletal muscle has rich adrenergic innerva- balance between compartments. The volume of the central com-
tion and therefore has a marked vasoconstrictor response to neural partment enlarges, leading to a decrease in its mean temperature,
stimulation, primarily through the resistance vessels. Precapillary while the temperature of the peripheral and skin compartments
sphincters constrict in response to sympathetic stimulation, but increases. At thermoregulation, the size of the central compart-
are also sensitive to local factors, such as hypoxia, hypercapnia, ment becomes smaller owing to vasoconstriction, which leads to
and increases in potassium, osmolality and magnesium, which an increase in the mean temperature, though the peripheral and
may then cause relaxation. Other vasoactive hormones (e.g. skin temperatures fall.
renin, vasopressin, prostaglandins, kinins) also have a role in In addition to vasoconstriction, hypothermia also produces a
microvascular control. Transplanted vessels in a free flap have no rise in haematocrit and plasma viscosity, the aggregation of red
sympathetic innervation but are still able to respond to local and blood cells into rouleaux, and platelet aggregation. These effects
humoral factors, including circulating catecholamines. may reduce microcirculatory blood flow in the flap.
Rheology – the flow behaviour (rheology) of blood in the Fluid – peripheral vasoconstriction owing to an underestimation
microcirculation is determined by the red cell concentration, of fluid losses is common. There are two operating sites in free flap
plasma viscosity, red cell aggregation and red cell deformability. transfer: the donor site and the recipient site. Both have insensible
Following all surgery under general anaesthesia, the changes in fluid losses and both may have blood losses. A warm theatre envi-
blood rheology include: ronment also increases fluid loss. Modest hypervolaemia reduces
• increased platelet aggregation and adhesion sympathetic vascular tone and dilates the supply vessels to the
• an impairment of red cell deformability flap. An increase in central venous pressure of 2 cm H2O above
• an increase in whole blood viscosity the control measurement can double cardiac output and produce
• increased clotting factors skin and muscle vasodilatation. A guide to fluid management is
• increased plasma fibrinogen and red cell aggregation given in Figure 2.
• disturbance of fibrinolysis. Anaesthesia – isoflurane causes vasodilatation with minimal
Normal levels of 2,3–diphosphoglycerate (2,3-DPG) are required myocardial depression, unlike other volatile anaesthetics and pro-
for optimal red cell deformability. After blood transfusion, this pofol. Propofol inhibits platelet aggregation, which could reduce
deformability is impaired owing to the negligible amount of 2,3- the risk of thrombosis. This may be caused by an effect of intralipid
DPG in stored blood. on the interaction between platelets and erythrocytes, and by the
increased synthesis of nitric oxide by leucocytes.
Vasospasm of the transplanted vessels may occur after surgi-
Physiology
cal handling or after damage to the intima of the vessels, and
The physiological status of the patient has a major influence on can happen during surgery or postoperatively. Surgeons may use
the viability of the transferred tissues, therefore the conduct of topical vasodilators (e.g. papaverine, lidocaine, verapamil) during
anaesthesia and the postoperative management have a direct effect the operation to relieve the vasospasm.
on outcome. Surgery is long (often 6–8 hours) with multiple sites Sympathetic blockade – epidural, brachial plexus or interpleural
for tissue trauma, resulting in extensive blood and fluid losses, local anaesthetic infusions, used intraoperatively and postop-
as well as heat loss. The resulting hypovolaemic vasoconstriction eratively, provide sympathetic blockade to dilate vessels further.
and hypothermia, if not corrected, compromise blood flow to Concerns have been raised that the sympathetically denervated
the flap and result in flap failure. Even with good fluid manage-
ment, blood flow to a flap may decrease by 50% for 6–12 hours
postoperatively. The guiding principle of anaesthesia for free flap Guide to fluid management
surgery is the maintenance of optimum blood flow. The determi-
nants of flow are summarized by the Hagen–Poiseuille equation Crystalloids
for laminar flow: ∆Pr4π • 10–20 ml/kg to replace preoperative deficit
8ηl • 4–8 ml/kg/hour to replace insensible losses
where ∆P is the pressure difference across the tube, r is the radius Colloids
of the vessel, η is viscosity and l is the length of the tube. From this • 10–15 ml/kg for haemodilution
we may deduce that the goals of anaesthesia for free flap surgery • To replace blood loss
are vasodilatation, good perfusion pressure and low viscosity. Blood
• To maintain haematocrit at 30%
Vasodilatation Dextran
Vessel radius is the most important determinant of flow, for the • Often given postoperatively
vessels supplying the flap as well as those in the flap.
Temperature – the patient should be kept warm in theatre, the 2

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 RECONSTRUCTIVE SURGERY

transplanted vessels would be unable to dilate after lumbar epi-

Practical conduct of anaesthesia
dural blockade, resulting in a ‘steal’ effect reducing flap blood
flow. In fact, providing any hypotension due to the sympathetic Monitoring
block is treated appropriately, blood flow to the flap improves as In addition to basic monitoring, these patients require invasive
a result of the increased flow through the feeding recipient artery. blood pressure monitoring to enable safe manipulation of the
Other advantages of epidural analgesia include a reduction in intra- perfusion pressure.
operative and postoperative blood loss and vessel spasm; a lower Direct measurement of arterial pressure gives a continuous
incidence of deep venous thrombosis; improved diaphragmatic record of the pressure and is more accurate than non-invasive
function and more rapid postoperative recovery. Good analgesia, indirect techniques. An arterial cannula also provides access to
by any route, reduces the level of circulating catecholamines and blood-gas analysis and haematocrit estimations.
avoids the vasoconstrictor response to pain. Central venous pressure reflects cardiac filling pressures and
can be manipulated to increase cardiac output.
Perfusion pressure Core temperature measurement is essential when active
The preservation of a good perfusion pressure with wide pulse warming is instituted. A nasopharyngeal or rectal probe is used
pressure is essential to flap survival. Appropriate anaesthetic depth intraoperatively for a continuous reading, while intermittent tym-
and aggressive fluid management is usually all that is needed. panic or axillary measurements are used in the recovery and ward
Most inotropes are contraindicated owing to their vasoconstric- areas.
tive effects, but if required, dobutamine or low-dose dopamine Peripheral temperature is also measured because a fall in skin
could be used. temperature can reflect hypovolaemia and vasoconstriction. A dif-
ference of less than 2°C between core and peripheral temperatures
Viscosity indicates a warm, well-filled patient. The temperature of the skin
Isovolaemic haemodilution to a haematocrit of 30% improves flow flap is sometimes monitored postoperatively because a drop in
by reducing viscosity, reducing reperfusion injury in muscle and temperature may herald flap failure. However, this is not a sensi-
increasing the number of patent capillaries, which decrease tissue tive test, because by the time the temperature has fallen the flap
necrosis. Further reductions in haematocrit do not provide much will have suffered sufficient vascular damage to render it virtually
more advantage because the curve of viscosity versus haematocrit unsalvageable.
flattens off markedly (Figure 3). If the haematocrit falls further, the Urine output is another indicator of volume status. A urine
marginally improved flow characteristics from a lower viscosity output of 1–2 ml/kg/hour should be maintained intraoperatively
may then be offset by a reduction in oxygen delivery: and postoperatively with appropriate fluid management. Diuretics
are contraindicated in these operations because volume depletion
DO2 = CO x [(Hb x sat x 1.34) + (PaO2 x 0.003)] compromises flap survival.

A low haematocrit also increases myocardial work, therefore care Induction

should be taken in patients with poor cardiac reserve. Active warming starts before the patient is asleep. The ambi-
ent temperature in theatre is raised to about 22–24oC, a level
Viscosity versus haematocrit high enough to reduce patient heat loss, but not too hot to be
uncomfortable for the theatre staff. The patient is covered with a
10
hot air blanket before induction of anaesthesia and this remains
9
in place while the patient is prepared for theatre. Once in theatre,
8 the blanket is moved to enable surgical access, but with as much
surface area covered as possible.
Viscosity (water = 1)

7
Regional block – if appropriate, a regional block is inserted,
6
preferably to cover the free flap recipient site (rather than the donor
5 site) for the full benefit of the sympathetic block. The patient is
4
intubated and ventilated; and a large gauge peripheral line, central
line, arterial line, urinary catheter and core temperature and skin
3
temperature probes are positioned.
2 Nasogastric tube – nitrous oxide diffusion into air in the stom-
1
ach combined with gastric stasis results in gastric distension, with
associated postoperative nausea and vomiting. A nasogastric tube
0
is therefore sited at intubation, left on free drainage, then aspirated
0 10 20 30 40 50 60 70 and removed at the end of the operation.
Haematocrit (%) Fluid warmer – fluid, administered through a fluid warmer,
is started in the anaesthetic room to compensate for preoperative
Source: MacDonald D J F. Br J Anaesth 1985; 57: 904–21.
dehydration.
© The Board of Management and Trustees of the British Journal of
Anaesthesia. Reproduced by permission of Oxford University Press/British
Journal of Anaesthesia. Maintenance
Positioning – careful positioning of the patient is imperative
3 for such a long operation. The limbs are positioned and supported

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 RECONSTRUCTIVE SURGERY

Controlled hypotension is useful during the initial dissection

Principles of perioperative and postoperative care and is most easily achieved using epidural local anaesthetic and/or
isoflurane. An infusion of glyceryl trinitrate may be added if needed.
• Maintain high cardiac output Fluid management – crystalloids are used to replace the preop-
• Normal arterial blood pressure (systolic >100 mm Hg) erative fluid deficit from starvation and to cover intraoperative
• Low systemic vascular resistance insensible losses. The latter are high because the warm theatre
• Normothermia increases evaporative losses from the two operating sites. Exces-
• High urine output (>1 ml/kg/hour) sive use of crystalloid may precipitate oedema in the flap.
• Effective analgesia Hypervolaemic haemodilution is achieved using colloids.
• Haematocrit 30–35% Blood gas analysis and haematocrit measurement should be
• Monitoring of blood flow in flap (Doppler, postoperatively) carried out at the start of the operation and repeated every 2 hours.
By the time the flap is reperfused, the patient should be warm,
4 well-filled and sympathetically blocked with a high cardiac
output.
to avoid neurological damage or vascular compression. The eyes
are taped and lightly padded to reduce the incidence of corneal Emergence and recovery
abrasion and prevent drying of the cornea. The patient should wake up free of pain. Analgesia is maintained
Deep venous thrombosis prophylaxis is necessary for all postoperatively with local anaesthetic infusions for regional blocks,
patients. Subcutaneous heparin or low molecular weight heparin intravenous patient-controlled analgesia, or both. Coughing and
is given preoperatively, while anti-embolism (TED) stockings and vomiting increase venous pressure and reduce flap flow, so smooth
compression boots are used intraoperatively. emergence and extubation are needed. The principles of periopera-
Normocapnia – the patient is ventilated to normocapnia. Hypo- tive and postoperative care are given in Figure 4. 
capnia increases peripheral vascular resistance and reduces cardiac
output, while hypercapnia causes sympathetic stimulation. If the FURTHER READING
surgeon uses the microscope for vessel preparation or anastomosis MacDonald D J F. Anaesthesia for microvascular surgery. Br J Anaesth
on the chest or abdomen, the tidal volume is reduced to minimize 1985; 57: 904–21.
movement in and out of the surgeon’s field of vision. The respira- Sigurdsson G H, Thomson D. Anaesthesia and microvascular surgery:
tory rate is then increased to maintain minute ventilation. clinical practice and research. Eur J Anaesthesiol 1995; 12: 101–22.

ANAESTHESIA AND INTENSIVE CARE MEDICINE 7:1 35 © 2006 Elsevier Ltd