Department of Anaesthesia And Critical Care. SKIMS.

RECONSTRUCTIVE FREE FLAP SURGERY

Reconstructive Free Flap Surgery involves the transfer of free tissue (e.g. Skin, muscle, bone, bowel or a combination of them) to a distant site using microvascular techniques.
Examples include: Gracilis muscle for lower limb. Latissimus dorsi and Rectus Abdominis for Breast reconstruction. Pectoralis major & radial forearm flap for head and neck reconstruction.

The technique of free tissue transfer is complex and despite the improvements in surgical techniques, hypoperfusion and necrosis can result in failure of the surgery. Consequently anaesthesia plays a crucial role in the success of free tissue transfer by influencing global hemodynamics and regional blood flow. Changes in blood volume, use of vasoactive drugs and regional anaesthesia may influence the blood flow in the free flap's microcirculation.

Circulation Of the Free Flap

Blood flow through the microcirculation is crucial in determining the survival of the Free Flap.
The Microcirculation

What makes Free Flap a special piece of tissue?

1. It has no lymph drainage at least initially 2. It is denervated with respect to sympathetic nervous system but are still able to respond to local factors such as hypoxia, hypercapnia,increases in potassium, osmolality and magnesium, which cause vasodilation as well as to circulating factors such as renin, angiotensin, kinins, prostaglandins and circulating catecholamines. 3. Usually has a single (and damaged) feeder artery and vein.

Stages of Flap Transfer

Initial dissection, flap elevation and clamping of vessels. The free flap is transferred with its accompanying artery and vein, which are then reattached to the vessels at the recipient site using microvascular techniques. Primary ischemia develops as blood flow ceases and intracellular metabolism becomes anaerobic. Reperfusion occurs as arterial and venous anastomosis are completed and clamps released. Secondary ischemia is subsequent to hypoperfusion of the flap due to varied causes, but reperfusion injury being a central component. This can be minimised by appropriate anaesthetic management.

CAUSES OF FLAP FAILURE Inadequate anastomosis:

Dependant on the condition and size of the available vessels, as well as the surgical skill and equipment.

Tests for patency of anastomosis

Clinical tests: 1.Venous patency is mostly evident when the vessel is translucent. 2.Observation of arterial expansive pulsation.

Doppler ultrasound, laser Doppler monitoring, transcutaneous O2 tension monitoring, microdialysis and infrared venous saturation.

Vascular Thrombosis:
The overall thrombosis rate for free flaps is generally reported to be 10-12% although 50-85% can be salvaged by revision surgery or thrombolysis.
The chances of thrombosis are greatest at the site of anastomosis 15-20 minutes following closure. A complete thrombus necessitates resection of the damaged segment and re-anastomosis. Vascular thrombosis is most commonly due to technical error in suture placement or pedicle kinking, or the use of a vessel with a damaged intimal layer. Thrombosis at the venous anastomosis accounts for 9 out of 10 thromboses.

After the first 20 minutes, the next critical period is within the first 3 postoperative days as 90% of vascular thromboses occur during this time.
Neovascularisation may be complete in a short period of time in thin flaps, which have a large surface to volume ratio. Thicker flaps may take several weeks before they are independent of their anastomosed blood supply.

Interestingly, there are a small percentage of very late failures, i.e. years down the line, where the flap remained dependent on the pedicle and sufficient collaterals did not form. This possibility should be kept in mind when anaesthetising and positioning such a patient.

Poor flap Perfusion

Poor flap Perfusion

Arterial: inadequate, thrombosed or in spasm anastomosis.

Venous anastomosis may be defective, in spasm or compressed (e.g. by tight dressings or poor positioning)

Oedema may result from excessive crystalloids, extreme haemodilution, trauma from handling or a prolonged ischemia time. Flap has no lymphatic drainage and is therefore more susceptible to oedema.

Ischemia-Reperfusion (I/R) Injury

Tissue damage occurs as a result of ischemia and restoration of blood flow. Tissues differ in their ability to withstand primary ischemia, with skin and bone being much more resistant than muscle or intestinal mucosa. Safe periods are difficult to determine. Although some areas of patchy necrosis are visible in normothermic muscle after 2 hours, obligatory ischemia of 1,5 to 3 hours is generally well tolerated. The structural and metabolic changes seen in ischemia include: narrowed capillary diameter, sequestration of leucocytes and dysfunction of endothelial and general cell membranes. Increase in intracellular calcium adding to upregulation of many other enzyme systems to produce inflammatory mediators.

Ischemia
ATP & pH. intracellular Ca++.

Reperfusion

Leukocyteendothelial interaction

Complex activation and immune complexes

Phospholipase & Lysozymes activation.

Reactive oxygen species

Cell damage

Reversible

More cell damage

Cell necrosis

Irreversible

Ischemia reperfusion injury

ANAESTHETIC MANAGEMENT
Proper anaesthetic management in a case of Free Flap Transfer not only serves to ensure good anaesthetic outcome but also minimises chances of failure by ensuring proper patient selection.
There are a number of patient characteristics which can additively increase the likelihood of failure and must be actively sought.

Diabetes and other systemic illnesses such as hypercholesterolemia. Atherosclerosis.

Existing cardiac disease.

Smoking Obesity Collagen vascular disease Coagulopathies are a relative contraindication. The only absolute contraindication for free tissue transfer is a hypercoagulable state.

THE PRACTICAL CONDUCT OF ANAESTHESIA.

The basic anaesthetic goal is to maintain an optimal blood flow for the vascularised free flap.

Monitoring:
In addition to the basic monitoring these patients require: 1. Invasive blood pressure monitoring 2. Central Venous Pressure 3. Core temperature measurement with peripheral temperature measurement. 4. Measurement of urine output maintained at 1-2 ml/kg/hour. 5. Blood gas analysis and haematocrit measurement should be carried out at the start of the operation and repeated every 2 hours.

INDUCTION
Active warming starts before the patient is asleep. The ambient temperature in theatre is raised to about 2224oC.
If appropriate, a regional block is inserted, preferably to cover the free flap recipient site (rather than the donor site) for the full benefit of the sympathetic block. Nitrous oxide diffusion into air in the stomach results in gastric distension, with associated post-operative nausea and vomiting. A nasogastric tube is therefore sited at intubation, left on free drainage, then aspirated and removed at the end of the operation. Fluid, administered through a fluid warmer, is started to compensate for preoperative dehydration. Prophylaxis against deep venous thrombosis is necessary for all patients. Subcutaneous heparin or low-molecular-weight heparin is given preoperatively, while anti-embolism (TED) stockings and compression boots are used intraoperatively.

MAINTENANCE:
Careful positioning of the patient is imperative for such a long operation. Limbs are positioned and supported to avoid neurological damage or vascular compression. Eyes are taped and lightly padded to reduce the incidence of corneal abrasion and prevent drying of the cornea. The guiding principle of anaesthesia for free flap surgery is the maintenance of optimum blood flow. The determinants of flow are summarized by the HagenPoiseuille equation: LAMINAR FLOW = P x r4 x 8x xl

P = pressure difference across the tube (vessel) r = radius of the tube (vessel) = viscosity of the fluid (blood) flowing in the tube(vessel). l = length of the tube (vessel)

From this we may deduce that the goals of anaesthesia for free flap surgery are vasodilatation, good perfusion pressure and low viscosity.

Vasodilatation:
Vessel radius is the most important determinant of flow, for the vessels supplying the flap as well as those in the flap.

Temperature:
The patient should be kept warm in theatre, the recovery room and the ward for the first 2448 hours. Ambient theatre temperature should be relatively high: 24 - 25C, and the temperature differential between skin and core should be kept to less than 2C.

Fluid
Maintain modest hypervolaemia.
An increase in central venous pressure of 2 cm H2O above the control measurement can double the cardiac output and produce skin and muscle vasodilatation.

Guide to fluid management

Crystalloids 1020 ml/kg to replace preoperative deficit 48 ml/kg/hour to replace insensible losses Colloids 1015 ml/kg for haemodilution To replace blood loss Blood To maintain haematocrit at 30% Dextran Often given postoperatively

Anaesthesia :
Isoflurane has the advantage over other volatile anaesthetics and propofol that it causes vasodilatation with minimal myocardial depression. Inhalational anaesthetics also help in ischemic preconditioning. Propofol inhibits platelet aggregation and neutrophil activation which could reduce the risk of thrombosis and ischemia reperfusion injury. Both inhalational and propofol infusions can be readily titrated during the protracted surgery. Maintain normocapnia.

Inhalational agents are used more often, but there is no clear evidence of benefit over a TIVA technique.

Sympathetic blockade :
Epidural, brachial plexus or interpleural local anaesthetic infusions, used intraoperatively and postoperatively, provide sympathetic blockade to further dilate vessels. Blood flow to the flap improves as a result of the increased flow through the feeding recipient artery.

Other advantages of epidural analgesia include a reduction in intraoperative and postoperative blood loss and vessel spasm; a lower incidence of deep venous thrombosis; improved diaphragmatic function and more rapid postoperative recovery.
Good analgesia reduces the level of circulating catecholamines and avoids the vasoconstrictor response to pain.

Modalities used to relieve vasospasm:

Epidural infusions of local anaesthetics

Local infiltration of a) 2% Papaverine b) 10% or 20% Lidocaine c) Chlorpromazine.

Adequate analgesia

Perfusion pressure:
The preservation of a good perfusion pressure with wide pulse pressure is essential to flap survival.

Appropriate anaesthetic depth and aggressive fluid

management are usually all that is needed.

Most inotropes are contraindicated owing to their

vasoconstrictive effects, but if required, dobutamine and low-dose dopamine could be used.

Viscosity:
Isovolaemic haemodilution to a haematocrit of 30% improves flow by reducing viscosity, reducing reperfusion injury in muscle and increasing the number of patent capillaries, which decrease tissue necrosis.

Further reductions in haematocrit do not provide much more advantage because the curve of viscosity versus haematocrit flattens off markedly.

If the haematocrit falls further, the marginally improved flow characteristics from a lower viscosity may then be offset by a reduction in oxygen delivery: DO2 = CO x [(Hb x sat x 1.34) + (PaO2 x 0.003)]

A low haematocrit also increases myocardial work, therefore care should be taken in patients with poor cardiac reserve.

Viscosity versus Haematocrit

ANTICOAGULATION:
The use of various anticoagulants and volume expanders is employed by some to reduce the probability of vascular thrombosis. The three most commonly used substances include

1. Heparin used sytemically and topically in irrigation fluids. 2. Aspirin - Based on a good safety profile, low dose aspirin is usually
recommended for prophylaxis in microvascular free flap surgery.

3. Low molecular weight dextran - thought to decrease platelet

adhesiveness and aggregation by increasing the negative charge of platelets, erythrocytes and endothelial cells, resulting in the destabilization of fibrin polymerization. It is also a volume expander and decreases blood viscosity. A prospective study of 100 consecutive patients showed increase in complication. The complications included: CCF, MI, pulmonary oedema, pleural effusion and pneumonia. Hence routine use of Dextran is no longer warranted

EMERGENCE AND RECOVERY:

By the time the flap is reperfused, the patient should be

warm, well-filled and sympathetically blocked with a high

cardiac output. The patient should wake up pain-free. Analgesia is maintained infusions postoperatively for regional with local anaesthetic patient-

blocks,

intravenous

controlled analgesia, or both. Coughing and vomiting increase venous pressure and reduce flap flow, so smooth emergence and extubation are needed.

Principles of perioperative and postoperative care

Maintain high cardiac output Normal arterial blood pressure (systolic >100 mm Hg) Low systemic vascular resistance

Normothermia
High urine output (> 1 ml/kg/hour) Effective analgesia

Haematocrit 3035%
Monitoring of blood flow in flap (Doppler postoperatively).

CONCLUSION
Anaesthesia for free flaps has some unique
problems and challenges, with many

uncertainties regarding the best management. It is also an exciting and expanding field with great promise in improving quality of life for many.