The Lower Limb

Chapter 6
The Lower Limb



  1. Leg ulcers
  2. Lower limb trauma
  3. Osteomyelitis
  4. Lymphoedema
  5. Pressure ulcers
  6. Further reading

Leg ulcers



  • Most common chronic wounds in developed countries.
  • Affect 1–3% of the British population.

Aetiology



  • Leg ulceration may be caused by ‘VATIMAN’:

    • Venous disease
    • Arterial disease
    • Trauma

      • Insect bites
      • Trophic ulcers
      • Self-inflicted injuries
      • Burns and frostbite
      • Radiation

    • Infection

      • Bacterial
      • Fungal
      • Mycobacterial
      • Syphilis

    • Metabolic disorders

      • Diabetes
      • Necrobiosis lipoidica diabeticorum
      • Pyoderma gangrenosum
      • Porphyria
      • Gout
      • Calciphylaxis

    • Autoimmune diseases

      • Vasculitis
      • Systemic lupus erythematosus (SLE)
      • Systemic sclerosis (scleroderma)
      • Rheumatoid arthritis
      • Polyarteritis nodosa

    • Neoplasia

      • Squamous cell carcinoma (SCC)—Marjolin ulcer
      • Basal cell carcinoma (BCC)
      • Melanoma
      • Kaposi sarcoma
      • Lymphoma.

The leg ulcer patient


Medical history



  • Time and mechanism by which the ulcer started
  • Previous treatment
  • Ambulatory status
  • Type of footwear
  • Symptoms suggestive of a cause, e.g. claudication, rest pain
  • Relevant comorbidities, e.g. diabetes, smoking.

Examination



  1. The ulcer itself

    • Examined for features suggestive of aetiology:

      • Venous ulcers—classically in the gaiter area, sloping edges.
      • Arterial ulcers—usually on toes, feet or ankles, ‘punched out’ edges.
      • Features of malignancy.

  2. State of the circulation

    • Temperature, capillary refill.
    • Peripheral pulses.
    • Varicose veins, oedema, venous eczema, hyperpigmentation—all suggest underlying venous disease.

  3. Sensation

    • ‘Glove and stocking’ sensory loss suggests peripheral neuropathy.

Investigation



  • Microbiology wound swab
  • Ankle brachial pressure index (ABPI)
  • Vascular studies
  • Radiology

    • X-rays, CT and bone scans assess bony involvement.

  • Biopsy of long-standing ulcers to exclude malignancy
  • Onward referral to a rheumatologist for vasculitis or connective tissue disorder.

Venous ulcer disease



  • An area of epidermal discontinuity that persists for four weeks or more, occurring as a result of venous hypertension and insufficiency of the calf muscle pump.
  • Accounts for 80% of lower limb ulceration.
  • Venous hypertension may be caused by:

    • Reflux of venous blood due to valvular incompetence
    • Venous obstruction
    • Insufficiency of the calf muscle pump.

  • May affect the superficial system (long and short saphenous veins), deep system or interconnecting perforators.
  • Valvular incompetence occurs due to thrombophlebitis, previous thrombosis or trauma.
  • Pathogenesis is not fully understood; mooted mechanisms include:

    1. Venous hypertension causes protein-rich exudate to leak into subcutaneous tissue.

      • Forms a pericapillary fibrin cuff, causing local tissue hypoxia.

    2. Venous hypertension causes extravasation of erythrocytes.

      • Triggers an inflammatory response, with deposition of haemosiderin within macrophages.
      • Transforming growth factor (TGF)-β may mediate dermal fibrosis, lipodermatosclerosis and eventual ulceration.
      • Lipodermatosclerosis is characterised by:

        • Scarring
        • Fibrotic, hyperpigmented skin
        • ‘Inverted champagne bottle’ appearance.

Management


Non-operative


  1. Bed rest and leg elevation

    • Impractical for most patients; ulceration tends to recur with ambulation.

  2. Compression

    • Gold standard treatment; used continuously until healing occurs.

      • Mean time to healing is 5 months.
      • Ulcer recurrence rate 30% in 5 years.

    • Four-layer bandaging enables the shortest time to healing.

      • The four layers are applied from toes to knee and consist of:

        • Orthopaedic wool
        • Crêpe bandage
        • Elastic bandage
        • Cohesive retaining layer.

    • Compression stockings are easier to use; there is limited evidence of their superiority over bandaging.

      • Stockings are classified as:

        • Class 1 (light): 14–17 mmHg
        • Class 2 (medium): 18–24 mmHg
        • Class 3 (strong): 25–35 mmHg.

  3. Local treatments
  4. Pentoxifylline (unlicensed indication).

Operative


  • Venous ulceration is not usually managed surgically.
  • Indications for surgery may include:

    • Intractable pain
    • Failure of non-operative treatment
    • Surgically treatable venous disease.

  • Surgery addresses both the underlying venous disease and the ulcer.

Treatment of venous disease


  • Ablation of superficial and perforating veins.

    • Achieved by open surgery or endovenous laser ablation.

  • Subfascial endoscopic perforating vein surgery (SEPS).
  • Reconstruction of the deep venous system.

Treatment of the venous ulcer


  • Debridement and skin grafting.

    • High recurrence rate if underlying venous pathology is not corrected.

  • Excision with flap reconstruction.

    • In exceptional circumstances, pedicled or free flaps are used after ulcer excision.

Arterial ulcer disease



  • Results from reduced blood supply to the lower limb.
  • Most common cause is atherosclerosis, risk factors for which include:

    • Age
    • Family history
    • Smoking
    • Diabetes
    • Hypertension
    • Hyperlipidaemia
    • Obesity.

  • Generalised changes in the limb:

    • Dusky erythema
    • Lower surface temperature
    • Lack of hair growth
    • Thin, brittle, atrophic skin
    • Thickened or missing toenails
    • Absent peripheral pulses.

  • Ulceration may develop after seemingly trivial trauma.

    • Patients should be taught how to care for their skin.

Management



  • Combination of operative and non-operative methods.
  • Debridement or negative pressure wound therapy may enlarge the area of ischaemia.

Non-operative management


  • Control of modifiable risk factors, e.g. diabetes, smoking
  • Graded exercise regime
  • Foot care
  • Infection prevention
  • Cilostazol or pentoxifylline.

Operative management


  • Indications for invasive treatment:

    • Non-healing ulceration
    • Gangrene
    • Rest pain
    • Progression of disabling claudication.

  • Aim to improve blood flow into the affected limb.

    • This accelerates healing time.
    • Achieved by reconstructive vascular surgery or angioplasty.

Lower limb trauma


Epidemiology



  • Annual incidence of open lower limb fractures is approximately 5 per 100,000 population.
  • Analysis of open tibial fractures treated by the Edinburgh Orthopaedic Trauma Unit (1988–1990) revealed:

    • 21% Gustilo type I injuries.
    • 19% Gustilo type II.
    • 60% Gustilo type III.

      • Of type III fractures: 27% type IIIA, 60% type IIIB, 8% type IIIC.

  • Average age 42 years.
  • Most common mechanisms of injury:

    • Fall from height
    • Motor vehicle collision
    • Interpersonal violence.

Classification of open fractures



  • Numerous classifications have been described:

    • Gustilo and Anderson (1976)
    • Hannover Fracture Scale-97 (HFS-97) (1982)
    • Byrd and Spicer (1985)
    • Predictive salvage index (PSI) (1987)
    • Mangled Extremity Severity Score (MESS) (1990)
    • The AO soft tissue grading system (1991)
    • Limb salvage index (LSI) (1991)
    • Nerve injury, ischemia, soft tissue, skeletal, shock and age of patient (NISSSA) (1994)
    • Ganga hospital score (2006)
    • Bastion classification (2012).

Gustilo and Anderson



  • Widely used; relatively simple to apply.
  • Based on a retrospective study of long bone fractures.
  • Open fractures are best classified after wound excision.
  • Poor inter-observer reliability.
  • No account is taken of fracture characteristics or nerve/muscle injury.

    • Grade IIIB is therefore a diverse group.

  • Open fractures were originally classified into three categories:

Type I


  • Open fracture with a wound <1 cm long and clean.

Type II


  • Open fracture with a laceration >1 cm long without extensive soft tissue damage, flaps or avulsions.

Type III


  • Either open segmental fracture, open fracture with extensive soft tissue damage or traumatic amputation.

    • This key point is often overlooked: all high energy pattern injuries are Type III.

  • Special categories in Type III:

    • Gunshot injuries
    • Any open fracture caused by a farm injury
    • Any open fracture with accompanying vascular injury requiring repair.

  • In 1984, Gustilo et al. subclassified type III injuries:

Type IIIA


  • Adequate soft tissue coverage of a fractured bone despite extensive soft tissue laceration or flaps.
  • High energy trauma irrespective of the size of the wound.

Type IIIB


  • Extensive soft tissue injury with periosteal stripping and bony exposure.

    • This is usually associated with massive contamination.

Type IIIC


  • Open fracture associated with arterial injury requiring repair.

MESS



  • Designed to predict whether a lower limb is salvageable.
  • Total score ≤6 is consistent with a salvageable limb, using modern multidisciplinary surgical reconstruction techniques.
  • May aid decision making when primary amputation is considered.
  • Does not replace experienced clinical judgement.

A. Skeletal/soft tissue injury


  • Low energy (stab, simple fracture, civilian gunshot wound): 1
  • Medium energy (open or multiple fractures, dislocation): 2
  • High energy (close-range shotgun, military gunshot wound, crush injury): 3
  • Very high energy (above + gross contamination, soft tissue avulsion): 4

B. Limb ischaemia (double the score for ischaemia >6 h)


  • Pulse reduced or absent but perfusion normal: 1
  • Pulseless, paraesthesias, diminished capillary refill: 2
  • Cool, paralysed, insensate, numb: 3

C. Shock


  • Systolic blood pressure always >90 mmHg: 0
  • Hypotensive transiently: 1
  • Persistent hypotension: 2

D. Age (years)


  • <30: 0
  • 30–50 years of age: 1
  • >50 years of age: 2.

NISSSA



  • Aims to address MESS’s shortcomings by including nerve injury, and more detailed information about muscle and soft tissue injuries.
  • Applies only to open tibial fractures.
  • More sensitive and specific than MESS.

AO system



  • The most comprehensive soft tissue classification.
  • However, it is very complex; usually reserved for research or coding.

Bastion classification



  • Named after Camp Bastion, the main British military base in Afghanistan.
  • Classifies lower limb injuries caused by improvised explosive devices.

Initial management of lower limb trauma



  • As with all trauma, initial assessment is an ATLS-style primary survey.
  • The purpose of the primary survey is to identify and treat all immediately life-threatening problems.
  • The <C>ABC approach, adopted by the military, may be appropriate.

    • This attends to <C>, catastrophic haemorrhage, early on in the algorithm.
    • A tourniquet may be required to stop bleeding.

History



  • Mechanism of injury is a guide to the level of energy transferred.
  • Factors suggestive of high energy injury:

    • High speed motor vehicle accidents, particularly pedestrian.
    • Falls from significant height
    • Missile wounds
    • Any injury involving crushing.

Examination



  • Establish the neurovascular status:

    • Capillary refill time.
    • Dorsalis pedis and posterior tibial arterial pulse.
    • Active movement of toes and ankle (common peroneal and tibial nerves).
    • Sensation on the sole of foot (tibial nerve) and first webspace (deep peroneal nerve).
    • Re-examine neurovascular status regularly, particularly after fracture manipulation.

  • Factors suggestive of high energy injury:

    • Transverse or segmental fracture pattern with comminution
    • Associated injuries
    • Large soft tissue defect
    • Closed degloving, where skin is intact but perforating vessels are divided.
    • Tyre prints.

Treatment



  • Current UK Standards recommend this initial treatment:

    1. Analgesia.
    2. Restore limb alignment; splint using plaster of Paris backslab.
    3. Remove gross contamination.
    4. Photograph the wound.
    5. Cover the wound with sterile, saline-moistened gauze covered with semi-occlusive film dressing.
    6. Repeat neurovascular examination.
    7. Intravenous antibiotics—co-amoxiclav or cefuroxime 8 hourly:

      • Continue until definitive soft tissue cover or 72 hours, whichever is sooner.
      • Additional ‘single shot’ gentamicin 1.5 mg/kg at the time of debridement.
      • Additional ‘single shot’ gentamicin and either teicoplanin or vancomycin at the time of skeletal stabilisation and definitive soft tissue closure.
      • Penicillin allergy: give clindamycin instead of coamoxiclav/cefuroxime.

    8. Tetanus prophylaxis if required.
    9. X-ray—two views, including the joints above and below the fracture.

Surgical management



  • Summarised as:

    • Debridement
    • Skeletal stabilisation
    • Soft tissue cover.

Timing



  • The traditional ‘6-hour rule’ of open fracture surgery was based on the doubling time of Staphylococcus.

    • This is the time it takes one bacterium to reach an infective load of 105 organisms.

  • However, many studies fail to demonstrate a relationship between the timing of debridement and outcome.
  • UK Standards recommend primary surgery within 24 hours of injury by senior plastic and orthopaedic surgeons.
  • Exceptions mandating immediate surgery:

    1. Gross contamination
    2. Compartment syndrome
    3. Devascularised limb
    4. Another injury requiring immediate surgery.

Primary surgery



  • A major aim of primary surgery is to convert a contaminated traumatic wound into a clean surgical wound.
  • This is achieved by three ‘Es’:

    1. Extend
    2. Explore
    3. Excise.

  • Use of a thigh tourniquet is preferred by some surgeons.

Wound extension


  • Extend along lines of election for fasciotomy to assess the entire zone of trauma.

    • Should not injure perforators that supply local fasciocutaneous flaps.

Degloving injuries


  • Degloving is avulsion of skin and subcutaneous tissue from underlying muscle or bone.
  • Degloving is classified by Arnež:

    • Pattern 1—Limited degloving with abrasion/avulsion

      • Tissue loss due to abrasion/avulsion and limited degloving of remaining skin.
      • Typically occurs around bony prominences; may expose bone or joint.

    • Pattern 2—Non-circumferential degloving

      • Most skin remains as a flap or undermined area, usually just superficial to muscle fascia.

    • Pattern 3—Circumferential single-plane degloving

      • More extensive than pattern 2; skin does not usually survive.

    • Pattern 4—Circumferential multiplane degloving

      • Similar to pattern 3, but with additional breach of muscle fascia.
      • Degloving can run between muscles and between muscle and periosteum.
      • Indicative of high energy transfer.

  • The margins of excision following degloving can be difficult to determine.
  • Findings suggestive of non-viable skin:

    • Fixed staining and thrombosis of subcutaneous veins.
    • Circumferential degloving.
    • Poor perfusion, demonstrated by intravenous fluorescein and a Wood’s lamp.
    • Newer technologies using indocyanine green (ICG) fluorescence have been reported.

Muscle


  • Muscle viability is assessed by four Cs:

    1. Colour (pink)
    2. Contraction
    3. Consistency (dead muscle tears easily in the jaws of forceps)
    4. Capacity to bleed.

Bone


  • Deliver the ends of the fracture out of the wound.

    • This allows complete assessment and debridement of the wound and bone.
    • The deep posterior compartment can be inspected this way.

  • Loose bone fragments that fail the ‘tug test’ are removed.

    • Large articular fragments that can be fixed with absolute stability are preserved.

  • Bone viability is determined by its capacity to bleed:

    1. Punctate bleeding from exposed cortical surfaces (paprika sign).
    2. Extent of periosteal stripping and muscle/fascia connections.

  • Following excision, irrigate the wound with large volumes of warm saline.

    • High pressure pulse lavage is not recommended

      • Associated with deep bacterial inoculation and tissue damage.

  • Second look within 24–48 hours is occasionally indicated; multiple serial debridements are associated with worse outcomes.

Fracture stabilisation


  • Provisional stabilisation is achieved with a spanning external fixator.

    • Indicated when definitive stabilisation and soft tissue cover cannot be achieved at primary surgery.
    • Pins are inserted through ‘safe corridors’ to avoid neurovascular structures.
    • The construct should allow access to the wound for soft tissue cover.
    • If conversion to definitive internal fixation is planned, UK Standards recommend this occurs within 72 hours of primary surgery.

  • Definitive stabilisation is usually achieved by internal fixation (intramedullary nail, plate, screws).

    • Internal fixation should not be placed if immediate soft tissue cover cannot be achieved.
    • Orthopaedic implants within open wounds are associated with higher infection rate.

Vascular injury



  • Limb devascularisation requires emergency surgical exploration.
  • Muscle suffers irreversible ischaemic damage in 3–4 hours.

    • The maximum acceptable delay is 6 hours of warm ischaemia.

  • Diagnosed by absent dorsalis pedis or posterior tibial pulse on palpation or Doppler.

    • Capillary refill in the toes can be misleading.

  • Preoperative angiography unnecessarily prolongs ischaemia time.

    • The level of vascular injury is predicted by the fracture or dislocation.

  • Management of vascular injuries:

    1. Direct exploration of the suspected site of injury.
    2. Immediate revascularisation by temporary shunts, e.g. Javid, Pruitt-Inahara or Sundt.

      • Venous injury at, or proximal to, the popliteal vein is also shunted.
      • Risk of cardiovascular events as toxic metabolites enter the systemic circulation.
      • Renoprotective measures may prevent complications of myoglobinuria.

    3. Once circulation is restored, reasses the limb.
    4. If salvageable, stabilise the skeleton with an external fixator.
    5. Replace shunts with reversed vein grafts.
    6. Fasciotomy is required following revascularisation—muscle tends to swell post-operatively.

      • If not done, compartment pressure monitoring should be performed repeatedly.

Wound cover



  • The decision to proceed with definitive soft tissue cover at primary surgery depends on:

    1. Immediate definitive bony stabilisation possible?

      • Is the fracture configuration fully understood?

        • May require further imaging with CT.

    2. Plastic surgeon available?
    3. What flaps are available?
    4. Zone of injury well defined?
    5. Recipient vessels available?

      • May require CT angiography.

    6. Patient stable enough to withstand long surgery?

Temporary


  • Topical negative pressure dressing

    • Should not be used instead of definitive vascularised soft tissue cover.
    • Use for >7 days associated with increased risk of deep infection.

  • Antibiotic bead pouch

    • Supplies higher local concentrations of antibiotics than systemic administration.
    • Polymethylmethacrylate (PMMA) cement is impregnated with an antibiotic—usually gentamicin or tobramycin.
    • PMMA beads are placed in the wound, then covered with a semi-occlusive film dressing.
    • Antibiotic elutes from the cement; can remain effective for 21 days.

Definitive


  • Definitive cover requires vascularised soft tissue.
  • UK Standards state this be done by senior specialist teams on a semi-elective basis within 7 days of injury.

    • Evidence favours early closure to avoid infection.
    • Delay >7 days increases likelihood of friable/fibrotic recipient vessels.

Local or regional fasciocutaneous and muscle flaps


  • Reserved for low energy injuries with limited zone of trauma.
  • Fasciocutaneous flaps are typically raised on septocutaneous or myocutaneous vessels from peroneal or posterior tibial arteries.

    • Can be located with hand-held Doppler to aid flap planning.

  • The pedicled medial sural artery perforator flap and reverse flow sural neurocutaneous flap can cover defects over the proximal and distal tibia, respectively.
  • Anterolateral thigh flap can be pedicled distally for proximal tibial wounds.
  • Common pedicled muscle flaps for lower leg coverage:

    • Medial gastrocnemius for knee and proximal third.
    • Medial hemisoleus for middle third.
    • Bipedicled tibialis anterior for middle third.

Free tissue transfer


  • Mainstay of treatment for high energy open tibial fractures.
  • Ongoing debate about fasciocutaneous versus muscle flap superiority.
  • There is little robust, high quality evidence to support use of one flap over another.
  • Proponents of fasciocutaneous flaps say:

    • Aesthetically superior.
    • Easier to re-elevate for secondary bony reconstruction.
    • May be sensate.
    • Minimal donor site morbidity.

  • Proponents of muscle flaps say:

    • Conform better to cavities.
    • Act as ‘muscle macrophages’, reducing likelihood of infection.
    • Experimental data demonstrates improved bone healing.
    • Muscle thins over time to provide a good aesthetic result.

  • Recipient vessels in the lower leg:

    • Posterior tibial artery

      • Approached medially between flexor digitorum longus and soleus.

        • The neurovascular bundle is between soleus and tibialis posterior.

      • Also approachable posteriorly, known as the ‘Godina split’:

        • Posterior mid-calf incision deepened between the heads of gastrocnemius and through soleus.

    • Anterior tibial artery

      • Approached just lateral to the subcutaneous border of the tibia.
      • The neurovascular bundle is on the interosseous membrane, between tibialis anterior and long toe extensors.

  • More proximal recipients include popliteal and superficial femoral vessels.

    • Often requires interposition vein grafts.

  • Long and short saphenous veins provide additional drainage options if venae comitantes are unsuitable.
  • A ‘single vessel leg’ can support a free flap by anastomosing end-to-side.

    • Reconstruction of the other injured vessels with vein grafts is considered.

Management of segmental bone defects


Primary bone shortening


  • Can be done for segmental defects <5 cm.
  • Acute shortening >5 cm may cause circumferential full thickness necrosis of a doughnut-shaped block of adjacent soft tissue.

    • May also kink vessels, resulting in distal ischaemia.

Temporary placement of a spacer


  • Antibiotic-impregnated PMMA spacers bridge bony defects and maintain limb length.

    • They are subsequently removed and the defect reconstructed by other means.

  • The Masquelet technique relies on the ‘induced membrane’ that forms around the cement spacer to revascularise morsellised cancellous bone graft, placed at a second stage.

Bone grafting


  • Delayed cancellous bone grafting is usually performed 6 weeks after injury, when soft tissues have healed.

Primary bone shortening and subsequent lengthening


  • Bone lengthening is accomplished by a circular frame.

    • Examples: Ilizarov, Taylor Spatial Frame™.

  • Lengthening at the site of fracture is bone distraction.
  • Lengthening by corticotomy at a remote site is bone transport.
  • The bone is lengthened by turning special screws on the frame.

    • Lengthening usually proceeds at 1 mm/day.

  • After lengthening, the frame is left in situ for a period of consolidation.

Reconstruction with vascularised bone


  • Common sources include the free fibula and deep circumflex iliac artery (DCIA) flap.

    • Ribs are usually too thin.

  • Up to 18 months or more is required for bone strengthening and hypertrophy.

    • During this period, full weight-bearing risks fracture.

Acute compartment syndrome



  • Compartment syndrome is elevation of interstitial pressure in a closed osseofascial compartment that results in microvascular compromise.
  • It is a surgical emergency.
  • Missed diagnosis causes irreversible neuromuscular ischaemia and significant long-term morbidity.
  • Compartment syndrome can be caused by:

    • Fractures, both closed and open

      • Never assume open fractures concomitantly decompress compartments.

    • Soft tissue trauma
    • Arterial injury
    • Prolonged limb compression in an obtunded patient
    • Burns.

  • Anterior and deep posterior compartments of the lower leg are most affected.

    • These are also the most frequently missed during fasciotomy.

Pathophysiology

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Mar 12, 2016 | Posted by in General Surgery | Comments Off on The Lower Limb

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