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.

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

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

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

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

Doppler ultrasound. microdialysis and infrared venous saturation. transcutaneous O2 tension monitoring. 2. . as well as the surgical skill and equipment.Venous patency is mostly evident when the vessel is translucent.Observation of arterial expansive pulsation. laser Doppler monitoring.CAUSES OF FLAP FAILURE Inadequate anastomosis: Dependant on the condition and size of the available vessels. Tests for patency of anastomosis Clinical tests: 1.

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. the next critical period is within the first 3 postoperative days as 90% of vascular thromboses occur during this time. Thrombosis at the venous anastomosis accounts for 9 out of 10 thromboses. Thicker flaps may take several weeks before they are independent of their anastomosed blood supply. Neovascularisation may be complete in a short period of time in thin flaps. Vascular thrombosis is most commonly due to technical error in suture placement or pedicle kinking. which have a large surface to volume ratio. . After the first 20 minutes. A complete thrombus necessitates resection of the damaged segment and re-anastomosis. or the use of a vessel with a damaged intimal layer.

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

thrombosed or in spasm anastomosis.Poor flap Perfusion Poor flap Perfusion Arterial: inadequate. by tight dressings or poor positioning) Oedema may result from excessive crystalloids. trauma from handling or a prolonged ischemia time. extreme haemodilution. in spasm or compressed (e. . Flap has no lymphatic drainage and is therefore more susceptible to oedema.g. Venous anastomosis may be defective.

. The structural and metabolic changes seen in ischemia include: narrowed capillary diameter. “Safe” periods are difficult to determine. with skin and bone being much more resistant than muscle or intestinal mucosa. obligatory ischemia of 1. Although some areas of patchy necrosis are visible in normothermic muscle after 2 hours. Tissues differ in their ability to withstand primary ischemia.Ischemia-Reperfusion (I/R) Injury Tissue damage occurs as a result of ischemia and restoration of blood flow. 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.5 to 3 hours is generally well tolerated.

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 .

Smoking Obesity Collagen vascular disease Coagulopathies are a relative contraindication. . Diabetes and other systemic illnesses such as hypercholesterolemia. The only absolute contraindication for free tissue transfer is a hypercoagulable state. There are a number of patient characteristics which can additively increase the likelihood of failure and must be actively sought. Atherosclerosis. Existing cardiac disease.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.

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. 4. . Measurement of urine output maintained at 1-2 ml/kg/hour.THE PRACTICAL CONDUCT OF ANAESTHESIA. Invasive blood pressure monitoring 2. 5. Blood gas analysis and haematocrit measurement should be carried out at the start of the operation and repeated every 2 hours. Core temperature measurement with peripheral temperature measurement. Central Venous Pressure 3.

INDUCTION Active warming starts before the patient is asleep. while anti-embolism (TED) stockings and compression boots are used intraoperatively. administered through a fluid warmer. The ambient temperature in theatre is raised to about 22–24oC. a regional block is inserted. Fluid. with associated post-operative nausea and vomiting. preferably to cover the free flap recipient site (rather than the donor site) for the full benefit of the sympathetic block. then aspirated and removed at the end of the operation. Subcutaneous heparin or low-molecular-weight heparin is given preoperatively. left on free drainage. Nitrous oxide diffusion into air in the stomach results in gastric distension. If appropriate. A nasogastric tube is therefore sited at intubation. Prophylaxis against deep venous thrombosis is necessary for all patients. is started to compensate for preoperative dehydration. .

MAINTENANCE: Careful positioning of the patient is imperative for such a long operation. The guiding principle of anaesthesia for free flap surgery is the maintenance of optimum blood flow. Eyes are taped and lightly padded to reduce the incidence of corneal abrasion and prevent drying of the cornea. The determinants of flow are summarized by the Hagen–Poiseuille equation: LAMINAR FLOW = ∆P x r4 x π 8x ηxl ∆P = pressure difference across the tube (vessel) r = radius of the tube (vessel) η = viscosity of the fluid (blood) flowing in the tube(vessel). Limbs are positioned and supported to avoid neurological damage or vascular compression. good perfusion pressure and low viscosity. l = length of the tube (vessel) From this we may deduce that the goals of anaesthesia for free flap surgery are vasodilatation. .

Ambient theatre temperature should be relatively high: 24 . 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. for the vessels supplying the flap as well as those in the flap. Fluid Maintain modest hypervolaemia. the recovery room and the ward for the first 24–48 hours. Temperature: The patient should be kept warm in theatre.25°C.Vasodilatation: Vessel radius is the most important determinant of flow. and the temperature differential between skin and core should be kept to less than 2°C. .

Guide to fluid management Crystalloids • 10–20 ml/kg to replace preoperative deficit • 4–8 ml/kg/hour to replace insensible losses Colloids • 10–15 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. . Maintain normocapnia. Propofol inhibits platelet aggregation and neutrophil activation which could reduce the risk of thrombosis and ischemia reperfusion injury. Inhalational agents are used more often. Both inhalational and propofol infusions can be readily titrated during the protracted surgery. but there is no clear evidence of benefit over a TIVA technique.

Other advantages of epidural analgesia include a reduction in intraoperative and postoperative blood loss and vessel spasm.Sympathetic blockade : Epidural. . Blood flow to the flap improves as a result of the increased flow through the feeding recipient artery. a lower incidence of deep venous thrombosis. used intraoperatively and postoperatively. brachial plexus or interpleural local anaesthetic infusions. provide sympathetic blockade to further dilate vessels. Good analgesia reduces the level of circulating catecholamines and avoids the vasoconstrictor response to pain. improved diaphragmatic function and more rapid postoperative recovery.

Adequate analgesia .Modalities used to relieve vasospasm: Epidural infusions of local anaesthetics Local infiltration of a) 2% Papaverine b) 10% or 20% Lidocaine c) Chlorpromazine.

Appropriate anaesthetic depth and aggressive fluid management are usually all that is needed. Most inotropes are contraindicated owing to their vasoconstrictive effects. dobutamine and low-dose dopamine could be used.Perfusion pressure: The preservation of a good perfusion pressure with wide pulse pressure is essential to flap survival. . but if required.

Viscosity: Isovolaemic haemodilution to a haematocrit of 30% improves flow by reducing viscosity. Further reductions in haematocrit do not provide much more advantage because the curve of viscosity versus haematocrit flattens off markedly.34) + (PaO2 x 0. which decrease tissue necrosis.003)] A low haematocrit also increases myocardial work. . If the haematocrit falls further. reducing reperfusion injury in muscle and increasing the number of patent capillaries. therefore care should be taken in patients with poor cardiac reserve. 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.

Viscosity versus Haematocrit .

resulting in the destabilization of fibrin polymerization. pulmonary oedema. Hence routine use of Dextran is no longer warranted . pleural effusion and pneumonia. 2.ANTICOAGULATION: The use of various anticoagulants and volume expanders is employed by some to reduce the probability of vascular thrombosis. Heparin – used sytemically and topically in irrigation fluids. It is also a volume expander and decreases blood viscosity. Low molecular weight dextran .Based on a good safety profile. MI.thought to decrease platelet adhesiveness and aggregation by increasing the negative charge of platelets. 3. The complications included: CCF. low dose aspirin is usually recommended for prophylaxis in microvascular free flap surgery. erythrocytes and endothelial cells. Aspirin . A prospective study of 100 consecutive patients showed increase in complication. The three most commonly used substances include 1.

or both. well-filled and sympathetically blocked with a high cardiac output. the patient should be warm.EMERGENCE AND RECOVERY: By the time the flap is reperfused. Analgesia is maintained infusions postoperatively for regional with local anaesthetic patient- blocks. so smooth emergence and extubation are needed. The patient should wake up pain-free. Coughing and vomiting increase venous pressure and reduce flap flow. . intravenous controlled analgesia.

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 30–35% • 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.

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