A past SAQ (2018, 64% pass rate) on free flap surgery actually pertained to reconstructive breast surgery, rather than head & neck surgery.
The principles of free flap surgery are, however, broadly similar between specialties and this page fulfils the same role across OMFS, breast surgery and plastic surgery sections.
Free flap surgery involves transfer of vascularised tissue to a new site
It is the final step of 'the reconstructive ladder':
Direct closure
Autologous skin grafting e.g. split skin graft or full-thickness skin graft
Locoregional reconstruction inc. pedicled flap
Free flap
Flaps benefit patients by improving skin integrity, function and aesthetics
Indications
To restore function or aesthetic appearance after tissue loss following:
Reconstruction inc. resections e.g. cancer, necrotising fasciitis
Trauma
Burns
Contraindications
Free flaps are contraindicated in diseases states where a hypercoagulable state, anastamotic thrombosis, or (microcirculatory) vascular compromise is likely to occur, causing flap failure
Such conditions include:
Sickle cell disease
Polycythaemia rubra vera (untreated)
Active vasculitis
Peripheral vascular disease with MRA evidence of poor vessel patency at the donor site
Donor sites are often more painful than the flap site, especially in free flaps where the tissue is rendered insensate
Patients may need a skin graft from another site to graft onto the donor site
Head and neck
Radial forearm flap (RFF)
Antero-lateral thigh (ALT flap)
Fibula
Latissimus dorsi
Plastics/Breast
Breast reconstruction
Transverse rectus abdominis muscle (TRAM) flap
Deep inferior epigastric perforator (DIEP) flap
Inferior gluteal artery perforator (IGAP) flap
Gracilise muscle flap for lower leg trauma
Arterioles - resistance vessels
Arteriolar walls contain vascular smooth muscle; constriction or dilation of the arteriolar wall controls resistance to blood flow in the flap
The flap, once dissected, is denervated and therefore loses sympathetically-mediated vasoconstrictor responses
Response to local and humeral factors, however, is maintained
Vasoconstriction will occur in response to catecholamines (inc. pain), hypothermia and the myogenic stretch reflex
Vasodilation occurs in response to features of anaerobic metabolism: hypoxia | hypercarbia | acidosis | potassium | histamine | prostacyclins | kinins
Capillaries - exchange vessels
Precapillary sphincters control flow through capillaries
Oxygen and metabolites diffuse along their concentration gradients
Venules - capacitance vessels
Venules drain blood from the capillary network
They act as a reservoir, although high venous pressure/congestion may impair microcirculatory flow
A lack of lymphatic drainage makes the tissue susceptible to interstitial oedema
Microcirculatory flow
Microcirculatory flow is determined by plasma viscosity and RBC factors such as concentration, deformability and degree of aggregation
Within the microcirculation, viscosity is closely related to haematocrit
The relationship between viscosity and haematocrit is non-linear; above 40% haematocrit there is a steep rise in viscosity
In addition to haemoglobin, viscosity is increased by:
Haemodilution to haematocrit of 30% may improve microvascular blood flow through reduce viscosity, while still providing adequate oxygen delivery
Use of dextrans, which impair platelet adhesiveness and improve flow, is no longer advised; they are associated with increased blood loss and pulmonary oedema
Heparin boluses may be used to improve microcirculatory flow
Primary ischaemia
The flap is elevated and vessels clamped, leading to primary ischaemia
This induces anaerobic metabolism and accumulation of metabolites including potassium, lactate and pro-inflammatory molecules
The response is proportional to duration of anaerobic metabolism, and thus primarily influenced by surgical factors
The rate of oxygen consumption (and therefore time to anaerobic metabolism) is determined by the composition of the flap
Skin (0.2ml/min/100g tissue) consumes much less oxygen than muscle (1ml/min/100g tissue)
Flaps which have greater proportion of muscle (TRAM) are more sensitive to ischaemia than those with less (DIEP)
Secondary ischaemia
Anastomosis of arterial and venous supply should reperfuse the tissue at the recipient site, restoring (aerobic) cellular function
Altered microcirculatory flow may cause secondary ischaemia
Maintaining optimal blood flow in this period is key, and is influenced by conduct of anaesthesia
Failure occurs in 1 - 5% of cases
The highest risk occurs in the first two post-operative days
Flap compromise, if managed in a timely (<6hrs) manner, is salvageable in ∽75% of cases
Definitive management of the failing flap is urgent surgical re-exploration to reinstate microvascular anastomosis
Ischaemia & reperfusion injuries
Prolonged primary ischaemic time intra-operatively
Arterial issues
Inadequate blood flow → ensure normotension and normothermia
Vasospasm → consider calcium channel blockers
Thrombosis
Venous issues
Thrombosis
Excessive extrinsic compression e.g. dressing, tube ties
Venous congestion from excessive crystalloid use, kinking at the vascular pedicle
Oedema e.g. from lack of lymphatic drainage in flap
Reperfusion injury can occur anytime from vessel de-clamping following completion of the microvascular anastomosis, and leads to secondary ischaemia
Wound infection
Inflammatory mediators and oedema impair flap perfusion, leading to failure
Perioperative management of the patient undergoing free flap surgery
MDT assessment should aim to optimise patient fitness and identify modifiable risk factors
Assessment
Full history and examination, with a particular focus on:
Airway assessment including review of previous anaesthetics
Identification of cardiopulmonary risk factors in a patient cohort who are often smokers
Identification of nutritional and electrolyte issues in a patient cohort who are often drinkers
Optimise risk factors
Anaemia should be addressed; an [Hb] of <100g/L is associated with increased risk of flap failure and thrombosis
Diabetes
Aim HbA1c <69mmol/mol
Aim blood glucose 6-12mmol/L
Smoking
Cessation at least 4-6 weeks prior to surgery reduces risk of vasoconstriction and flap compromise
Benefit of reduced pulmonary complications too
Nicotine replacement therapy is contraindicated as it may reduce blood flow at donor site
Weight loss should be encouraged in obese patients, which improves surgical outcomes
Patients undergoing RRT should have their dialysis timed to minimise fluid overload and reduce uric acid levels
Airway planning
MDT approach to airway planning as shared airway during OMFS surgery
Plans should be explained to patient in advance, including tracheostomies, HDU/ICU care post-op. and other interventions such as NGT, catheters and drains
The aim is to provide optimal blood flow to the flap, achieved via a 'full' hyperdynamic circulation
Factors
Target
Cardiac output
High-normal
SVR
Low-normal
Pulse pressure
Wider
Temperature
Normothermic Core-peripheral gradient <2°C
Monitoring and lines
AAGBI as standard (ECG monitoring may need to be placed in alternative positions depending on surgical site)
Wide-bore access in case of major haemorrhage
Fine-bore access for induction and for post-operative PCA
CVP and/or cardiac output monitoring often not required
Invasive arterial monitoring allows optimisation of blood pressure, but also sampling for acid-base status, [Hb] and haematocrit
Urinary catheter with thermistor for measuring bladder temperature and monitoring UO
Core and peripheral temperature monitoring
A fall in peripheral temperature implies reduce perfusion e.g. hypovolaemia, vasoconstriction
A core - peripheral temperature difference of <2°C implies a warm and well-perfused patient
Positioning
Prolonged procedures increase the risk of pressure-induced injuries to skin, nerves and eyes
Meticulous padding, inflatable mattress and heel supports should be used
Patients should be subtly moved with relative frequency to avoid dependence on particular areas for the whole case
Generally positioned slightly head-up to aid venous drainage and reduce bleeding
Anaesthetic technique
Consider pre-induction warming to reduce the hypothermia that occurs during induction
Induction and airway choice will depend on pre-planned airway management strategy
Maintenance of anaesthesia is with either:
Volatile anaesthesia: sevoflurane may attenuate ischaemic reperfusion injury and isoflurane maintains microcirculatory flow
TIVA: propofol + remifentanil TCI to provide intra-operative analgesia and control of BP
IPPV should be used to provide PEEP and maintain PCO2 control, avoiding:
Hypoxia, which induces catecholamine release and vasoconstriction
Atelectasis from prolonged anaesthesia
Hypocapnoea and peripheral vasoconstriction
Hypercapnoea, which potentiates sympathetic responses and acidaemia-induced decreases in RBC deformability
Fluid and haemodynamic management
Reduce blood loss in the initial (dissecting) phase
Hypotensive anaesthesia e.g. remifentanil infusion, deepening volatile
Head-up positioning to reduce venous pressure
Use of local or regional anaesthesia
Use of adrenaline-containing LA/fluid by surgical team
Avoid β-blockers and other direct vasodilators, which may cause a relative peripheral vasoconstriction and systemic vasodilation; 'steal' phenomenon
Return MAP to >70mmHg at time of flap harvest
Fluid resuscitation using goal-directed therapy (see below)
Judicious use of vasopressors appears safe in the adequately volume-resuscitated patient, with studies suggesting their use does not increase risk of flap failure
Inodilators such as dobutamine/dopexamine are theoretically advantageous
There is a direct relationship between quantity of intra-operative fluid and rate of complications in free-flap surgery
Overly-restrictive fluid strategies may cause hypotension and resultant flap/organ compromise
Overly-liberal fluid strategies, in a bid to raise MAP, can lead to interstitial oedema and without lymphatic drainage compromise microcirculatory blood flow
Use of goal-directed therapy may help strike the balance, e.g.:
SVV <13%
UO >0.5ml/kg/hr
Normal lactate
Bleeding and VTE
Transfusions may be required to improve microcirculatory flow; aim haematocrit 30 - 35%
TXA is popular as it reduces blood loss without increasing VTE risk or significantly increasing the risk of flap complications
Patients are at higher risk of VTE due to prolonged immobilisation
Microvascular thrombosis can also interfere with flap perfusion
VTE risk is addressed via:
Intra-operative mechanical prophylaxis
Peri-operative unfractionated heparin 5000units
Post-operative chemical thromboprophylaxis with either LMWH or UH
Care bundle
Antibiotic prophylaxis as per local guidelines
Temperature management as above (normothermia, core-peripheral gradient <2°C
VTE prophylaxis as above
Analgesia
Donor - site pain is often greater than recipient-site pain as the flap is insensate
Epidural analgesia is in general avoided as it may cause poor graft perfusion through reduced systemic MAP and 'steal' phenomenon
Opioids are the mainstay, helping provide haemodynamic stability
Regional anaesthetic techniques benefit from:
Providing analgesia
Improved blood flow at recipient site via sympathetic block, aiding graft re-perfusion
Reducing sympathetic-associated catecholamine release, which causes vasoconstriction/vasospasm and compromises flap survival
Emergence and extubation
Airway strategy should include plan for extubation
Surges in blood pressure and coughing at emergence increase the risk of haematoma formation