The management of lower limb injuries has evolved over the last 20 years from simple wound dressings and amputation to complex surgical attempts at limb salvage involving microsurgical free tissue transfer techniques and technologically advanced dressings. There has also been an increasing emphasis placed on managing lower limb injuries via multidisciplinary teams involving orthopaedic and plastic surgeons. The combined impact of this approach has meant that lower limb injuries previously requiring amputation may now be salvaged to provide a functioning limb.
However, the plastic surgeon is not only involved in injuries involving the lower limb, although this forms the bulk of plastic surgical input. The main areas of plastic surgical involvement in the lower limb apart from significant soft tissue injury requiring a complex soft-tissue coverage solution include: pretibial lacerations, compartment syndrome, reconstruction following cancer extirpation, chronic wounds and infections of the lower limb including ulcers, osteomyelitis and situations where underlying metal work (for example following bony fixation) may extrude or be infected resulting in chronic injury to the overlying soft tissue and lymphoedema.
In this article we will explore each of these areas and look at how each of these defects are managed. When discussing reconstruction of the lower limb it is useful to divide it into distinct anatomical components such as: the upper leg/thigh, knee, tibia and foot. This is because each area presents different reconstructive challenges, the aim in each case being to restore the form and function of the limb. Hence in a final section of this article (Fig 15) we will look at the different flap/free tissue transfer options available for reconstructing each of these regions.
When patients with high energy lower extremity injuries present, it is likely that they may have other concomitant life threatening injuries. In such cases the priority is to ensure that we salvage the patient's life over that of his or her limbs. Initially the patient needs to be assessed in accordance with the principles of advanced trauma life support which involves assessing the airway, breathing and circulation of the patient. Following this, fractures and any other injuries may be assessed. The unstable polytrauma patient may require immediate attention to life threatening injuries, in which case treatment of the extremity involves stabilization of the injury and haemostasis. In clinically unstable patients however, amputation of the mangled extremity may provide better outcomes in terms of overall survival than an attempt at a complex reconstructive procedure to save the extremity.
Once the patient's immediate injuries have been assessed and life threatening injuries addressed, the extremity may be assessed to determine if it is salvageable. Assessment involves a manual and visual examination of the wound, as well as the limb's vascular, bone, soft tissue and neurological status, .
The vascular status is examined by checking for the presence of the pulses, appearance and colour of the limb, temperature and turgor of the limb. An ischaemic limb does not necessarily imply a vascular injury as it may be that the vessels are in spasm or are kinked due to the injury. This can usually be corrected by fracture reduction. If on examination the presence of a vascular injury cannot be confidently determined, doppler examination or angiography of the vessels is in order. The extent of bony injury can be determined by examination of the open wound and more importantly by radiographs. Evaluation of soft tissue injury includes examination of the skin and subcutaneous tissue, muscle and periosteum. The extent of bone and soft tissue viability can usually only be determined once the patient is in the operating room and the full extent of the injury to these structures can be assessed. Finally, neurological assessment involves motor and sensory evaluation of the peroneal and posterior tibial nerves. An injury resulting in the complete loss of both the peroneal and posterior tibial nerves may be a relative contraindication for extremity salvage, and in such cases below-knee amputation maybe the more preferable option to an insensate foot.
Once the patient has been stabilized, the extremity assessed and a decision made to salvage the limb, the primary issue that needs to be resolved is the definitive presence or absence of a vascular injury. If there is a strong suspicion of vascular injury an angiogram needs to be performed. If there is quick access to high quality angiograms in the angio suite, then this would be the preferable option, however if an angiogram would take several hours to be performed in the angio suite, then an on-table angiogram should be performed in the operating room.
The first step in reconstruction of the extremity is stabilization of the bone injury. If the prior angiogram detected the presence of a vascular injury, in this case fracture stabilization needs to proceed quickly or temporary vascular shunts should be considered until stabilization is achieved. Once bone stabilization is achieved, the vascular injury may be repaired if indicated. The rationale behind achieving bony stabilization prior to vascular repair is to ensure that the limb attains maximum length before blood vessels and other soft tissue are repaired. This is to prevent stretching of repaired soft tissue which may occur if bone stabilization was done following soft tissue repair.
Following bony stabilization and vascular repair, all nonviable tissue must be debrided. If there is exposure of vital structures such as bloods vessels and adequate debridment of damaged soft-tissue has been performed, immediate soft-tissue coverage is indicated with microvascular free-tissue transfer. On the other hand, if the zone of injury and the extent of soft-tissue viability is unclear and there are no exposed vital structures, in this case it may be preferable to bring the patient back for a second, or even third debridement, before definitive soft-tissue coverage is achieved. An algorithm for lower limb reconstruction following truamatic injury is presented below:
A number of authors have proposed classification systems for open fractures of the tibia. The two most common systems are those proposed by Gustillo and Anderson and Byrd et al:
Apart from the above classification systems for open tibial fractures, several authors have also attempted to devise scoring systems that help to decide between reconstruction and amputation. These include the Mangled Extremity Severity Score (MESS), the Limb Salvage Index (LSI), the Predictive Salvage Index (PSI) and the AO score. The MESS classification system below is the most commonly used:
A total score of six or less indicates that the limb is salvageable, while a total score of seven or more suggests that the limb would not be a good candidate for salvage. Studies have shown that the MESS score is specific but does not have good sensitivity. For these and other reasons associated with practicality it is not commonly employed in decision regarding salvage of an extremity.
There are three options when it comes to managing complex lower limb fractures, :
Reamed nails: are inserted following reaming of the intramedullary cavity hence providing rigid fixation which enables early mobilization and good fracture reduction and fixation. However this results in obliteration of the entire endosteal blood supply and hence may not be indicated in a massively traumatised lower limb.
Nonreamed nails: do not require obliteration of the entire endosteal network as they do not take up the entire intramedulary cavity, thus they provide a relatively stable fixation while at the same time not compromising bony vascularity.
The use of plates and screws in diaphyseal fractures of the tibia provides relatively good alignment and fixation, however it may require extensive soft tissue and periosteal stripping with the introduction of a considerable amount of foreign body into the wound and hence this method is not commonly used.
This is the fixation of choice in massive lower extremity injuries, (Fig 6). It provides rigid fixation, minimal soft tissue stripping and minimal bone devascularization. It can however obstruct surgery when free flaps are used to cover the soft tissue defects compromising flap options and may also cause infections of the wound via pin tracking.
Fig 6. An external fixator device in situ for fracture stabilization.
This is a type 3 tibial fracture. This defect would require free tissue transfer for adequate coverage due to the extensive zone of injury, .
Management of bone gaps
In situations where lower limb trauma results in the loss of bone, three options are available to reconstruct the bony defect, [1, 4]:
1: Novascularized cancellous bone grafts: this is appropriate for nonunions or bone gaps <4cm with a well vascularized bed for grafting. The usual practice is to wait 6-12 weeks post-trauma prior to introducing non-vascularized bone graft into a defect.
2. Ilizarov techniques: this is used in larger bone gaps where nonvascularized bone graft would not provide good outcomes. It is usually used in defects where the bone gap is between 4-8cm. The Illizarov technique uses the concept of distraction osteogenesis to lengthen bone segments. Essentially it uses the principle of tissue responding to the application of stress by growing.
3. Vascularised bone grafts: these can be used for defects >8cm (theoretically extending upto defects as large as 24cm) and include free fibula or deep circumflex iliac artery (DCIA) flaps.
Soft-tissue coverage in the lower limb
There are four options to cover soft-tissue defects of the lower limb. The size and location of the defect dictates which method is used, [2,4]:
Timing of soft-tissue coverage
This is divided,  into:
Evidence provided by Godina suggests that flap success is best if performed within 3 days of the injury, . If it is not possible to cover the defect within this time period, Arnez et al suggest waiting for more than 3 months before covering the defect to maximise flap success, .
The BAPRAS/BOA Standards for Management of Open Fractures of the Lower Limb suggest that microsurgical reconstruction is best performed within one week of sustaining the injury before the vessels become fibrosed, .
BAPRAS and BOA joint guidelines on the management of open lower limb fractures, :
In 2009 the British orthopaedic association(BOA) and British association of plastic, reconstructive and aesthetic surgeons (BAPRAS) agreed on and published key recommendations for the management of open lower limb fractures. The key recommendations in managing these complex and rare injuries include:
* 1 *
Specialist centres – these injuries require joint management by senior orthopaedic and plastic surgeons. The unit in which these patients are managed needs to have expertise in management of complex tibial frctures and bone reconstruction, as well as microvascular surgery and vascular reconstruction. Following reconstruction they must also have the necessary rehabilitation facilities from both a physchological perspective as well as a physical perspective (such as artifical limb fitting and rehabilitation for amputees).
* 2 *
Characteristics of open injuries that require referral to a specialist centre for management are based on:
a) Fracture patterns:
- transverse or short oblique tibial fractures with fibular fractures at a similar level
- tibial fracturs with communition / butterfly fragments with fibular fractures at a similar level
- segmental tibial fractures
- fractures with bone loss, either from extrusion at the time of injury or after debridement
b) Soft tissue injury patterns:
- skin loss such that direct tension free closure is not possible following wound excision
- injury to muscles that requires excision devitalised muscles via wound extensions
- injury to one or more of the major arteries of the leg
* 3 *
Timing of wound excision in open fractures – surgery should be performed at normal working hours in the presence of senior orthopaedic and plastic surgeons, unless of course there is a factor necessitating immediate exploration of the wound in theatre. Factors that necessitate immediate exploration in theatre include: gross contamination of the wound, compartment syndrome, a devascularised limb or a multiple injured patient.
* 4 *
Guidelines for wound debridement (excision) – the early excision of devitalised tissue is the most important procedure in the management of open tibial fractures. This is done under tourniquet control which provides a bloodless field for identification of important structures such nerves and blood vessels following the cleansing protocol for contaminated wounds.
* 5 *
Temporary wound dressings – negative pressure dressings are thought to reduce bacterial ingress and tissue desiccation as well as preventing the pooling of serous fluid. These dressings may hence be employed in the temporary coverage of wounds prior to surgery. These dressings are however not an alternative to surgical debridement and where necessary flap reconstruction.
* 6 *
Timing of soft-tissue reconstruction – local flaps may be performed at the same time as skeletal fixation while free flaps should be performed by experienced plastic surgeons after adequate debridement and imaging such as CT scanning or angiography of comminuted fractures. Free flap reconstruction should take place in a specialist centre. As stated earlier free flaps should be performed within seven days of the injury as after this period microvascular repair of vessels is made increasingly difficult as the vessels become fibrosed and friable.
* 7 *
Types of soft tissue reconstruction – all open fractures should be covered with vascularised soft tissue. Relatively low energy tibial fractures may be covered by local fasciocutaneous flaps as long as vascularity has not been compromised by the zone of injury and degloving. It is recommended that diaphyseal tibial fractures with periosteal stripping are best covered by muscle flaps instead of fasciocutaneous flaps while tibial metaphyseal fractures, especially those close to the ankle, are covered by fasciocutaneous flaps and when this is not possible, free flaps.
* 8 *
Compartment syndrome – covered in the section below.
* 9 *
Vascular injuries – a devascularised limb is a surgical emergency. The absence of peripheral pulses is a strong indicator of a poorly perfused limb while capillary refill is not as useful. However, in any case, if the injured limb appears to have a poor circulation compared to the contralateral limb, there is a low threshold for surgical exploration. The aim is to to restore circulation within 3-4 hours of the injury, after which muscle death begins. The maximum accepted delay is 6 hours of warm ischaemia time. In addition, preoperative angiography may be considered a waste of valuable time and the level of injury may be determined via the fracture configuration and any site of dislocation.
[Note: this does not contradict what was mentioned above regarding management of lower limb injuries where vascular reconstruction maybe carried out following bony stabilisation. This guidance is for injuries where there is almost no vascular supply and there is imminent death of muscle].
* 10 *
When things go wrong with soft tissue – local flap necrosis is managed by an early return to theatre and revision surgery to achieve healthy soft tissue coverage. In situations of venous congestion leech therapy maybe attempted. In terms of free flaps, failure is minimised by careful patient preparation and performing the anastomosis outside the zone of injury,ideally proximally. There is a low threshold for immediate re-exploration of a free flap with suspected circulatory compromise.
* 11 *
Primary amputation – a primary amputation is performed as a damage control measure when there is uncontrollable haemorrhage from an open tibial injury (usually occuring in blast injuries where there are multiple levels of arterial and venous damage) or from crush injuries exceeding a warm ischaemic period of 6 hours. A primary amputation is considered when the injury has one or more of the following characteristics:
- avascular limbs exceeding a 4-6 hour threshold of warm ischaemia
- segmental muscle loss affecting more than 2 compartments
- segmental bone loss greater than one third the length of the tibia
Amputation of the limb is either at the trans-tibial or trans-femoral level (where salvage of the knee is not possible). Through-the-knee amputations are not recommended for adults.
Compartment syndrome is usually defined as a raised interstitial pressure within a muscle compartment over that of the perfusion pressure leading to ischaemia and eventually tissue necrosis. This is a limb-threatening injury and could even be life threatening, leading to renal failure and death.
Compartment syndrome can be subdivided into four categories:
1) Acute – characterized by well-known symptoms such as pain on passive stretch and pain out of proportion with injury
2) Subacute – where the symptoms are not as easily recognised, but it may progress to acute
3) Recurrent – most common in athletes
4) Chronic – unrelieved acute ischaemia progressing to fibrosis and Volkman’s ischaemic contracture.
Aetiology of compartment syndrome
A compartment syndrome can result in any situation where the interstitial pressure of the compartment rises. This can be either due to a decrease in compartment size (such as when a tight bandage is applied) or increase in tissue volume and include:
Vascular injuries including bleeding from fractures, extravastation injuries and reperfusion injury (caused by oxygen free radicals on re-establishing blood flow to an ischaemic limb).
Swelling of soft tissue such as in myositis, nephrotic syndrome, electrical injury, excessive exercise or leukaemic infiltration.
Fractures which result in vascular injury, haemorrhage and soft tissue swelling. Of special relevance in this article is the fact that up to around 6% of Gustillo grade 3B fractures may be complicated by compartment syndrome.
Prolonged extrinsic compression including plaster of paris casts or prolonged lying down in one position.
Symptoms and signs
The symptoms of compartment syndrome include:
As mentioned earlier, pain especially on passive stretch and out of proportion to injury. This is the EARLIEST sign of compartment syndrome!!!
The affected compartment feels hard and tight and maybe swollen.
Paraesthesia or in some cases hyperaesthesia.
The affected limb may appear pale with capillary refill time >2 secs.
The limb maybe pulseless with poikilothermia (late signs).
Weakness of muscles in the affected compartment (late sign).
Blood profile including U+E’s, serum potassium, FBC, CK and clotting screen.
Measurement of the pressure within the involved compartment. A tissue pressure >30mmHg in a normotensive patient and >20mmHg in a hypotensive patient is an indication for fasciotomy.
MRI/Doppler/arteriography, all of which are more useful in subacute forms.
Urinary myoglobin levels (myoglobinuria leads to kidney failure).
It is important to stress that apart from fasciotomy, a number of other supportive measures go hand in hand with dealing with this syndrome. It includes:
Removing any sources of extrinsic compression such as casts etc, and elevating the limb to heart level. Elevating above this level is counterproductive as it reduces arterial pressure and hence perfusion of the limb.
Maintain an urine output of around 1-2ml/kg via IV hydration anticipating the risk of any kidney injury via myoglobinuria due to rhabdomyolysis.
Decompression via fasciotomy. Following this the limb should be splinted in a functional position and elevated.
Definitive wound closure should only be carried out once the swelling has reduced significantly. The wound could be closed directly or via skin grafting.
An important point of consideration is the placement of incisions when fasciotomies are performed. The BAPRAS/BOA joint guidelines on the management of lower limb fractures advocates the two incision technique which provides optimal access to all four compartments of the lower limb while also preserving the perforators to enable raising of local fascioutaneous flaps. It involves a postero-medial and an anterolateral incision as shown below:
These include a range of injuries involving the soft-tissue in the pretibial region, and extend from relatively minor superficial skin lacerations to degloving injuries. They are relatively common in those aged over 60 years of age, especially women and may be associated with a number of other comobidities such as diabetes, peripheral odema and peripheral vascular disease.
The pretibial region is prone to injury due to its location and the fact that the skin in this region is relatively tight. The area has little subcutaneous protection and is poorly vascularized meaning that these injuries maybe at times be difficult to manage conservatively.
Classification and management of pretibial lacerations
The following classification system and corresponding management for each rung has been proposed by Dunkin and colleagues, :
* Type 1 - Laceration:
-> Clean, tape without tension, supportive dressing, mobilize immediately.
* Type 2 - Laceration or flap with minimal haematoma and or skin edge necrosis:
-> Clean, debride under LA, excise non-viable skin, evacuate haematoma, dress, mobilise immediately. Review after 7-14 days and assess healing. If poor consider debridement under LA or GA, excise damaged skin and SSG, mobilise immediately.
Type 3 - Laceration of flap with moderate to severe haematoma and or necrosis (Fig 9):
-> Debride under LA or GA, excise damaged skin and SSG, mobilise immediately.
Type 4 - Major degloving injury:
-> Debride and SSG or other reconstruction.
Fig 9. A type 3 pretibial laceration.
Following debridement of necrotic tissue this wound would require a spilt-skin graft for coverage, .
There are a number of causes which lead to ulcers on the lower limb, especially on the foot. Venous ulcers are the commonest type of leg ulcer in the western world accounting for 80-85% of all lower limb ulcers. Apart from venous ulcers, other causes of lower limb ulcers include arterial disease leading to arterial ulcers, diabetes and peripheral neuropathy leading to neuropathic ulcers, ulcers due to vasculitic conditions such as systemic lupus erythematosus and rheumatoid arthritis, ulcers due to haematological causes such as polycythaemia and sickle cell anaemia, and ulcers due to trauma, neoplasia, sarcoidosis and pyoderma gangrenosum. In this section we will look at the pathogenesis,clinical features,investigation and management of venous, arterial and neuropathic ulcers, the three most common types of ulcer encountered in the western world.
* Venous ulcers (Fig 10) *
These occur due to sustained venous hypertension or chronic venous insufficiency secondary to venous disease (such as varicose veins or venous valve malfunction due to previous DVT), impaired function of the calf muscle pump (due to immobility, arthritis, paralysis or severe obesity limiting mobility) or congestive cardiac failure. This leads to repetitive ischaemic reperfusion injury which in turn results in the formation of ulcers.
* Arterial ulcers (Fig 11) *
These are the result of artherosclerosis within the large and medium sized arteries of the lower limb. The significant ischaemia results in the formation of ulcers.
* Neuropathic ulcers (Fig 12) *
These occur in diabetic patients who have peripheral neuropathy. Peripheral neuropathy encompasses sensory, motor and autonomic nerve malfunction. Sensory neuropathy leads to neglect of minor injuries or infections which may progress to ulcers and eventually limb-threatening injuries. Motor neuropathy leads to a gradual denervation of the intrinsic muscles of the foot which in turn lead to loss of the transverse and longitudinal arches of the foot and the foot adopting a characteristic claw-like shape. Autonomic neuropathy results in opening of arterio-venous shunts allowing blood to bypass the skin capillary bed and resulting in an increased flow of blood through bone, which promotes osteoclastic activity. This in turn increases the susceptibility of the foot to fracture with minor trauma and Charcot foot collapse. There are several theories regarding the pathological mechanisms leading to nerve malfunction in peripheral nueropathy, this is however beyond the scope of this article.
Fig 10. A venous ulcer in the gaiter area of the lower limb, .
Fig 11. An arterial ulcer on the dorsal aspect of the foot.
These ulcers are extremely painful and usually give out a pungent odour, .
Fig 12. A neuropathic ulcer at a pressure point on the foot.
The lateral edge of the foot has inward pressure exerted on it by footwear such as shoes which may contribute to the ulceration, .
* Venous Ulcers *
These are usually located in the gaiter area just proximal to the medial or lateral malleous within an area of lipodermatosclerosis or haemosiderosis. They are usually painless and it maybe possible to notice varicose veins proximal to the area of ulceration.
* Arterial ulcers *
These are usually located distally over and between the toes or in pressure points such as the heels or malleoli. They are usually very painful and have a pungent smell. The limb maybe appear pale. Palpation of pulses will usually reveal a diminished pulse and the capillary refill maybe prolonged >2 seconds.
* Neuropathic ulcers *
These are characteristically associated with a warm foot with palpable pulses. Ulcers maybe located at points of repetitive trauma. Looking at how ones shoe fits onto the foot and the contact points between the foot and footwear may reveal the mechanism of injury. In certain situations there maybe concomitant arterial insufficiency leading to absent/reduced pulses.
Examination & Investigations
* Venous ulcers *
Pure superficial venous incompetence based ulcers maybe treated with varicose vein stripping. These ulcers respond well to surgery and may heal within 4 weeks of the operation. On the other hand patients who are unfit for surgery or who have deep venous incompetence are best treated conservatively with occlusive dressings covered by compression bandages worn from the foot to the knee. These patients require weekly dressing change and sometimes ulcer debridement. Topical applications such as antibiotic and antiseptic creams have not shown to reduce ulcer healing time. Treated in this way 80-90% of ulcers heal by 1 year. It is recommended that patients wear compression stockings for life to prevent recurrence.
* Arterial ulcers *
As these ulcers are usually very painful they require analgesia. They need to be dressed, but compression should be avoided as this may worsen tissue ischaemia. In diabetic patients, good glycaemic control should be advocated. Smokers should be advised to stop smoking. The ulcers should be debrided of necrotic tissue. If there is significant arterial disease revascularization should be considered.
* Nueropathic ulcers *
X-rays to assess the bones of the foot and to rule out foreign bodies, osteomyelitis, fractures, gas or bone collapse. The patient should be adivsed to regularly visit the chiropodist to aid early recognition of problems with regular debridement of ulcers if already present. Ulcers in pressure areas that are not infected may be treated with pressure relieving footwear such as a total-contact cast which distributes pressure on ambulation over the entire surface area of the foot. The cast needs to be changed every 48 hours to ensure a snug fit, and then weekly for 8-10 weeks until the ulcer is healed. Any infected or gangrenous ulcers should be treated promptly with surgical debridement if necessary and broadspectrum IV antibiotic therapy. If an ischaemic component is suspected, revascularization should be considered as the ulcers are unlikely to heal in this circumstance.
Lymphoedema involves the accumulation of protein and lipid rich interstitial fluid in subcutaneous tissues while the deep muscle compartments remain uninvolved. This maybe due to a maldevelopment of lymphatic channels or via an acquired obstruction to the flow within these channels.
It is divided into primary and secondary types (Fig 14). Primary lymphoedema is a diagnosis of exclusion and should only be made when no precipitating cause can be found.
Primary lymphoedema is classified according to age of onset:
* Lymphoedema congenita *
Occurs at birth and is responsible for approximately 20% of cases of primary lymphoedema. More common in girls and affects the lower limb in 60% of cases. 30% of cases are bilateral. Affected patients have a family history of the condition which shows an association with Turner's syndrome. Lymphangiography usually shows a lack of proper lymph vessel development i.e. the vessels are anaplastic.
* Lymphoedema praecox *
Occurs in adolescence and is the most common form of primary lymphoedema accounting for around 80% of cases. Lymph vessels appear hypoplastic on lymphangiography.
* Lymphoedema tarda *
Occurs later in life becoming apparent after about 35 years of age. Lymph vessels appear hyperplastic on lymphangiography i.e. characterized by an increase in size and number of lymphatic channels.
Secondary lymphoedema is classified according to its cause and include:
* Neoplasia *
Tumours obstructing flow of lymph within vessels which maybe primary tumours of the lymphatic system or secondary tumours invading the lymphatic system.
* Infection *
The most common cause of lymphoedema worldwide is filariasis caused by the parasite wuchereria bancrofti. The condition is referred to as elephantiasis in this cases. Other less common infective causes include turberculosis and lymphogranuloma.
* Inflammation *
Due to snake or insect bites.
* Iatrogenic *
Includes causes such as elective lymph node dissection and varicose vein stripping.
* Irradiation *
Causing damage to lymph vessels.
In lymphoedema the skin eventually becomes thick and brawny, and fissuring and ulceration result. Initially there is a pitting oedema which eventually becomes non-pitting due to fibrosis of tissues. It may be associated with pain. In addition there is 10% probability of developing lymphangiosarcoma in those afflicted by this condition for a period >10 years.
It is important to distinguish lymphoedema from other similar conditions which cause a swollen, oedematous looking limb such as:
-> Klippel-Trenaunay syndrome – consisting of vascular malformations, limb oedema, varicose veins and limb elongation.
-> Venous hypertension – due to deep/superficial venous malfunction.
-> Odema due to renal, hepatic or cardiac causes.
A simple oedema may be distinguished from a lymphoedema in the following ways:
* Lymphoedema is usually non-pitting.
* Oedema usually may improve within hours of elevation.
* The skin of a limb affected by lymphoedema may be thick and hyperkerototic.
* Secondary lymphoedema usually has factors suggestive of its aetiology in the history.
The following tests may be used to investigate the cause of lymphoedema:
* Lymphangiography *
Involves the injection of dye into the first webspace of the foot. This dye is then absorbed into the lymphatic system allowing their identification. One identified, the lymph trunks are cannulated and a radio-opaque contrast medium injected into them. This then enables the lymph channels to be imaged radiologically. Lymphangiography has been preceded by lymphscintigraphy as it may lead to worsening of lymphoedema by damaging valves and inducing fibrosis.
* Interstitial lymphangiography *
In this investigation dye is injected into the interstitial space which is then preferentially absorbed into the lymphatic system. This in turn enables radiological identification of the lymphatic vessels.
* Lymphscintigraphy *
In this investigation technetium labelled antimony (a high molecular weight metal) is injected into the venous system. It is preferentially taken up by the lymphatic channels which are then imaged radiologically.
* CT or MRI *
Management of lymphoedema
The management of lymphoedema can be divided into medical management and surgical management. It must be emphasized that either form of treatment is not curative and that surgical management is not commonly indicated.
Medical management includes:
Elevation of the oedematous limb with the use of foot pumps to encourage lymphatic drainage.
Meticulous skin care to prevent ulceration and infections, especially fungal.
Treatment of lymphangitis and celulitis.
Pharmacological treatments such as diethycarbamazepine to treat filariasis. This maybe effective in reducing lymphoedema in early stages of the disease when the parasitic worms are small. Benzopyrone, a coumarin derative on the other hand, binds interstial proteins and induces phagocytosis.
Complex regional physiotherapy, which involves techniques to encourage lymphatic drainage such as massage of the affected limb and then maintainence and optimization post-drainage such as wearing elastic compression garments.
Is divided into excisional techniques and physiological techniques. Excisional techniques focus on the excision of lymphoedematous tissue while physiological techniques focus on improving lymphatic drainage from the affected limb.
Excisional techniques include:
* Charles technique *
Lymphoedematous tissue is excised in a circumferential manner and a split-skin graft is applied to the fascia. It is now possible to resurface the fascia with a graft harvested from the excised skin. However the application of grafts to fascia results in unstable grafts with poor aesthetic outcome. Thus this technique is only employed in situations where lymphoedema has lead to severe skin ulceration.
* Thompson technique*
In this technique subcutaneous tissue is excised and a dermal flap is tunnelled through the fascia into a muscular compartment of the leg. The aim is to create a theoretical lymphatic communication allowing drainage of the dermal flap via the deep compartment. However the capacity of the muscle compartment to act as a route for the drainage of lymph has not been substantiated and there is a paucity of studies in this area. Hence this technique is rarely performed.
* Homans technique *
Subcutaneous tissue segments are excised in a longitudinal fashion while overlying skin flaps are preserved and trimmed back when the edges are ready to be sutured together. This procedure is usually done in a staged manner i.e. medial side and then lateral side. This technique gives good results and hence is the most commonly performed excisional technique in lymphoedema surgery.
* Lymphangioplasty *
Aims to improve lymphatic drainage by implanting silk threads into subcutaneous tissue.
* Omental tranfer *
Here a protion of omentum is transposed to the affected limb.
* Enteromesenteric flap *
In this technique transected illiac or inguinal nodes are covered with a segment of ileum.
* Lymphovenus shunts *
Lymphatic vessels are anastomosed to veins.
* Lympholymphatic anastomosis *
Autologus lymphatic grafts are used to bypass obstructed lymphatic segments.
In this section we will consider some of the general principles of lower limb reconstruction which could be applied in any situation requiring soft-tissue reconstruction of the lower limb. We will start by considering some of the aspects that make the lower limb unique and how these factors affect the choice of reconstruction.
Unique aspects of the lower limb
Principles of lower limb reconstruction
Plastic surgeons manage a number of conditions affecting the lower limb including soft tissue trauma, chronic wounds (such as the ulcers mentioned above) and lymphoedema.
The primary aim of reconstructive surgery is to improve function of the lower limb and prevent life threatening infection of the wound site, such as osteomyelitis. This is followed by aesthetic considerations. A primary reconstruction that has a poor aesthetic result can always be revised once healing has taken place.
Significant lower limb trauma with bone involvement and significant soft tissue damage require joint management between orthopaedic and plastic surgeons. There is still much debate with regards to how best to manage trauma to the lower limb. The joint guidelines on the management of open tibial fractures issued by BAPRAS and BOA are an attempt to formulate an organised approach to management of these injuries. However it must be stressed that they are still guidelines and where necessary could be breached based on the individual intricacies of each patient’s needs.
The soft tissue reconstructive options of the lower limb include skin grafts (both spilt thickness and full thickness), local fasciocutaneous and muscle flaps, going all the way up the reconstructive ladder to include free tissue transfer.
 Kasabian AK, Karp NS. Lower-extremity reconstruction. In: Thorne CH, Beasley RW, Aston SJ, Bartlett SP, Gurtner GC, Spear SL editors. Grabb and Smith's plastic surgery 6th ed. Philadelphia: Lippincott Williams and Wilkins;2007. Pg 676-688.
 Gustillo RB, Mendoza RM, Williams DN. Problems in the management of type III(severe) open fractures. J Trauma 1984;34(8):742-6.
 Byrd HS, Spicer TE, Cierney G. Management of open tibial fractures. Plast. Reconstr Surg 1985;76(5):719-30.
 Chiu TW. Stone's plastic surgery facts and figures.Cambridge:Cambridge University Press;2011.
 Morgan SJ,Newman J, Ozer K et al. Salvage of a below the knee amputation level following a type 3B open tibial fracture. A case report. J Bone Joint Surg Am.2007; 89(12):2769-78
 Giele H, Cassell O. Plastic and reconstructive surgery. Oxford:Oxford University Press;2008.
 Godina M. Early microsurgical reconstruction of complex trauma of the extremities. Plast. Reconstruct Surg 1986;78(3):285-92.
 Arnez ZM. Immediate reconstruction of the lower extrmity – an update. Clin Plast Surg 1991;18(3):449-57.
 Standards for the management of open fracture of the lower limb(BAPRAS/BOA) avialable from:www.bapras.org.uk/downloaddoc.asp?id=379
 Dunkin C, Elfleet D, Ling CA et al. A step-by-step guide to managing pretibial injuries. Nurs Times 2003;99(21):58-61.
 http://www.surgical-tutor.org.uk/default-home.htm system/vascular/venous_hypertension.htm~right
 Tahernia A, Levin S. Reconstruction of the lower extremity. In:Evens GRD, Wirth GA editors. General reconstructive surgery.Philadelphia:Elsevir:2009. Pg 47-58.
Fastbleep © 2019.