Operative Technique in Plastic Surgery – Kevin C.Chung

■ Anterior tibial artery runs in the anterior compartment of the leg.
■ Anterior tibial artery is between the anterior tibialis and extensor digitorum
longus muscles.
■ Anterior tibial artery becomes the dorsalis pedis when it crosses the ankle
joint.
■ Dorsalis pedis can be palpated just lateral to extensor hallucis longus on the
dorsum of the foot.
■ Posterior tibial artery carries blood through the posterior compartment of the
leg and plantar surface of the foot.
■ Posterior tibial artery branches into the medial and lateral plantar arteries in
the foot.
■ Posterior tibial artery can be palpated midway between the medial malleolus
and the Achilles tendon.
PATIENT HISTORY AND PHYSICAL FINDINGS
■ Ischemic claudication (ie, arterial perfusion inadequate to meet the demands of
the muscle) leads to cramping, aching pain.
■ Claudication will usually occur one vascular level below the stenosis or
occlusion.
■ Ischemic rest pain (ie, chronic ischemic neuropathy that is positional) is often
described as diffuse aching or burning while legs are up in recumbent position,
which is improved after legs have been put in the dependent position.
■ Vascular and neurogenic claudication must first be differentiated.
■ Infrapopliteal disease is most often going to lead to ankle and foot disease.
■ Patients with tibial disease are more likely to experience rest pain or have
nonhealing wounds rather than claudication symptoms.
■ Ulcers to the medial side of the ankle are more likely due to venous disease.
■ Ulcers to the lateral food and ankle are more likely to be due to arterial
disease.
IMAGING AND OTHER DIAGNOSTIC STUDIES
■ An ankle-brachial index (ABI) may be obtained by dividing the systolic blood
pressure of the lower leg/ankle by the systolic blood pressure of the upper arm
(brachial artery) (FIG 1).
■ An ABI ≤ 0.9 is considered abnormal.
■ ABIs will most commonly be indeterminate because the tibial vessels

become noncompressible and waveforms will be monophasic.
■ Toe-brachial pressures (TBIs) will be more diagnostic in patients with tibial
disease.
■ A TBI < 0.4 will indicate a wound is unlikely to heal without intervention.
■ Arteriography should be performed to evaluate the tibial vessels prior to any
distal lower extremity or foot reconstruction.
■ Patients with diabetes and end-stage renal disease most frequently are
affected by small vessel disease, including tibial vessels and the
microvascular circulation.

FIG 1 • Example of an abnormal ankle-brachial index
study.
SURGICAL MANAGEMENT
■ A patient must first have an appropriate inflow and outflow vessel identified
for reconstruction.
■ Autologous vein has superior rates of patency compared to prosthetic grafts.
■ Vein mapping should be performed preoperatively, assuring at least a 3-mm
conduit.
■ Shorter bypass grafts have better patency.
■ The most distal patent native vessel should be used as the proximal origin of
the bypass graft.

■ For example, if the patient has a patent popliteal artery, this should be chosen
over a femoral artery.
■ Primary patency (the patency of a graft without any adjunctive therapies to
keep it open), secondary patency (the patency rate once the graft has been
completely abandoned and no further interventions are performed to keep it
open), and limb salvage rates are 56.8%, 62.7%, and 78.2%, respectively, at 5
years for pedal revascularizations.
T E C H N I Q U E S
■ Femoropopliteal Bypass
■ Identification of the femoral artery should be within the femoral triangle.
■ Femoral triangle consists of the inguinal ligament superiorly, sartorius
muscle laterally, and the adductor magnus medially.
■ The floor of the femoral triangle consists of the iliacus, psoas major,
pectineus, and adductor magnus.
■ The femoral artery is a continuation of the external iliac artery below the
inguinal ligament.
■ Common femoral artery divides into the profunda femoral artery and the
superficial femoral artery.
■ The profunda femoral gives branches to the thigh and collaterals to the
lower extremity.
■ The superficial femoral artery is a continuation of the common femoral
artery and progresses to the popliteal artery.
■ Longitudinal incision is made over the pulse in the groin, which is usually
located below the inguinal ligament approximately one-third lateral to the
pubic tubercle (TECH FIG 1A).
■ Dissection is taken down through the fascia lata, keeping medial to the
sartorius muscle (TECH FIG 1B).
■ The superior limit of the groin dissection is the inguinal ligament. Retraction
of the ligament exposes the external iliac artery.
■ The inguinal ligament can be further retracted by laterally dissecting along
the ligament releasing all attachments.
■ Once under the ligament, the inferior epigastric vein should be identified and

ligated.
■ Profunda femoral artery divides into the adductor fascia. Dissection along
the anterior surface can be performed, identifying each of its branches
(TECH FIG 1C,D).
■ Care should be taken not to dissect into the deep lateral circumflex femoral
vein, which lies across the proximal profunda.
■ A lateral approach at the profunda can also be performed along the lateral
surface of the sartorius.
■ The sartorius is then retracted medially while the rectus femoris and vastus
medialis are retracted laterally.

TECH FIG 1 • A. Longitudinal exposure of the
common femoral artery. B. A longitudinal incision is
medial to the sartorius muscle allowing exposure. C.
The femoral artery sits in the middle of the femoral
sheath between the nerve and vein. D. Proper
exposure includes vascular control of the common
femoral, superficial femoral, and profunda femoral

artery.
Above-Knee Popliteal Exposure
■ Exposure of the above-knee popliteal artery starts with a longitudinal
incision on the distal medial thigh in the intermuscular groove between the
sartorius muscle and the vastus medialis (TECH FIG 2).
■ Care should be taken not to damage the greater saphenous vein during this
incision.
■ Sartorius is then retracted posteriorly, while the adductor magnus is retracted
anteriorly.
■ Retraction of sartorius and adductor magnus gives exposure to the adductor
canal.
■ Dissection is then performed through the popliteal fat pad allowing exposure
of the popliteal artery and vein.
TECH FIG 2 • A. Exposure of the above-knee

femoropopliteal artery. B. Retraction of the sartorius
muscle posterior and adductor magnus anterior allows
for exposure of adductor canal. C. The geniculate
collaterals should be saved if possible. However, they
can be ligated for higher exposure if necessary. D.
Adductor magnus can also be cut if needed for more
proximal control.
Below-Knee Popliteal Exposure
■ A longitudinal incision should be made on the medial calf from the tibial
condyle distally (TECH FIG 3A).
■ Keeping the medial head of the gastrocnemius posterior (TECH FIG 3B),
the soleus muscle arch will be identified. Superior to the soleus is the
popliteal fat pad where the popliteal neurovascular bundle is located.
■ The paired popliteal veins will be surrounding the artery and will need to be
mobilized (TECH FIG 3C).
■ The soleus muscle can be dissected away from the tibia if more distal control
is needed.
■ Autogenous vein grafts provide the best patency for use in arterial bypass for
all infrainguinal reconstructions, regardless of the distal bypass target.
■ Reverse and in situ vein have equal effectiveness.4
■ If an above-knee bypass is performed, PTFE has equivalent 2- to 3-year
patency rates to autogenous vein.5

TECH FIG 3 • A. The below-knee popliteal artery is
exposed from a medial incision starting at the tibial
condyle and continuing distally. B. The medial head of
the gastrocnemius muscle is then retracted posteriorly
and popliteus muscle anteriorly. C. There are multiple
crossing veins around the popliteal artery that will
need to be controlled during popliteal artery exposure.
■ Vascular Reconstruction for Tibial-Peroneal
Arterial Occlusive Disease
■ Indications include rest pain, ischemic ulcerations, gangrene of the foot, and
highly selected patients with short-distance claudication.
■ Selection of conduit is most important. Autogenous vein should be used if
possible. In general, adequate vein is larger than 3 mm.

■ Ipsilateral vein is preferred over contralateral if possible.
■ Inflow should be chosen based on preoperative imaging as well as available
conduit length.
■ Inflow vessels include common femoral, profunda femoris, superficial
femoral artery, and above-knee popliteal artery.
■ Outflow vessel chosen for bypass should be the one with in-line flow to the
pedal vessels. However, peroneal can also be used despite lack of direct
communication.
Anterior Tibial Artery Exposure
■ Longitudinal incision lateral aspect of leg between the anterior tibialis and
the extensor digitorum longus muscles.
■ Dissection should be continued on the lateral aspect of the anterior tibialis
muscle rotating it anterior and medial. The neurovascular bundle will be
identified posterior to this muscle.
■ Tunneling can be performed from a medial or a lateral approach.
■ For a medial approach, a medial incision is made to expose the popliteal
fossa. This is followed by an incision of the interosseous membrane to cross
the conduit into appropriate position.
■ If a lateral approach is used, then the graft is initially brought subsartorius
from the femoral position and lateral through the tensor fascia lata. The
tensor fascia will need to be incised to allow the conduit to come through.
The graft will then lie in the subcutaneous tissue of the lateral thigh and calf.6
■ Care should be taken with the lateral tunneling away from the fibular head to
avoid injury to the peroneal nerve.
Posterior Tibial Artery Exposure
■ Longitudinal incision is made 2 cm below the medial edge of the tibia.
■ The gastrocnemius muscle is kept posterior until the soleus muscle is
identified.
■ Careful dissection is then performed with electrocautery dissecting the
soleus off of the posterior tibia aponeurosis.
■ Crossing tibial veins will need to be identified and ligated to allow the
posterior tibial artery to be exposed.
■ Tunneling for a posterior tibial bypass will be in the same anatomic position
as a femoral popliteal artery bypass but extended down to the location of the

distal exposure.
Peroneal Artery Exposure
■ Longitudinal incision on the medial leg 2 cm below the medial edge of the
tibia
■ The gastrocnemius and soleus are dissected posteriorly to expose the flexor
digitorum longus muscle, which lies on the posterior aspect of the tibia.
■ The fascia of the flexor digitorum longus is opened to enter the deep
compartment. Dissection is carried until the peroneal vascular bundle is
identified on the anterior aspect of the fibula on the flexor hallucis longus
muscle.
Pedal Artery Exposure
■ Exposure of the pedal vessels can be accurately identified with the assistance
of ultrasound or handheld Doppler prior to making an incision.
■ The dorsalis pedis artery will be on the dorsum of the foot just lateral to the
extensor hallucis longus tendon.
■ A longitudinal incision is made directly over the artery. Dissection will go
through the dorsal sheath, and retracting the tendon medially should expose
the dorsalis pedis.
■ For the posterior tibial artery distally, a longitudinal incision is made half
way between the medial malleolus and the Achilles tendon (TECH FIG 4).

TECH FIG 4 • Plantar exposure of the posterior tibial
artery. Incision is made posterior to the medial
malleolus. As the artery starts to cross the arch of the
foot, it will branch into the medial and lateral plantar
arteries.
PEARLS AND PITFALLS
Conduit
condition
■ If performing a vein bypass, always ensure careful handling of the
venous conduit. If there is an area that appears sclerotic or injured, it is
better to remove that segment.
Conduit
length
■ Obtain exposure of the proximal and distal location of your bypass
prior to performing the vein harvest, as you want to make sure you
have adequate length vein as well as an appropriate location for your

proximal and distal anastomosis.
■ Measure the distance of the bypass with the knee extended to ensure
adequate conduit length.
Tourniquet
use
■ A tourniquet can be used for arterial control of the distal anastomosis
and is particularly useful if the patient significantly calcified vessels.
Imaging
■ A completion arteriogram is helpful if there is any question about the
patient’s outflow.
POSTOPERATIVE CARE
■ Average length of stay for a bypass patient is 4 to 6 days.
■ Leg elevation postoperatively is important as the patient will have swelling to
the limb from both reperfusion and resection of the superficial venous system.
■ All patients should be started on a daily 81 mg aspirin following surgery.
Patients should also be restarted on their statin and beta-blocker if on them
preoperatively.1,7
■ Dual therapy with antiplatelet and anticoagulation has demonstrated improved
patency, particularly in patients who have a prosthetic conduit. However, these
patients are also at increased risk of bleeding.
■ Repeat ABIs with graft duplex can be performed at the first postoperative
clinic visit in 2 to 4 weeks.
OUTCOMES
■ Open surgical bypass is accepted as the most durable treatment for critical
limb ischemia.
■ Five-year overall patency rates range from 60% to 80% and limb salvage rate
of 80% to 90% in patients with critical limb ischemia.
■ Venous conduits have better patency than using prosthetic graft below the
knee.
■ Five-year expected patency rates for infrainguinal bypass a vein conduit4,8
■ Femoral to above-knee popliteal—75%
■ Femoral to below-knee popliteal—70%
■ Femoral to tibial artery—65%
■ Five-year expected patency rates for infrainguinal bypass with prosthetic
graft5,8
■ Femoral to above-knee popliteal—50%
■ Femoral to below-knee popliteal—35%

■ Femoral to tibial artery—20%
COMPLICATIONS
■ Patients with vascular disease often have other comorbid conditions. Systemic
complications such as MI, stroke, renal failure, and pneumonia are all potential
risks.
■ Wound complications can occur with either incision but are particularly higher
at the groin incision. Femoral incision complications occur in about 15% to
30% of patients, with underlying graft infection ranging from 1% to 7%
depending on if autogenous vein or prosthetic graft were used.
■ Early graft failures could be multifactorial.9
■ Technical failure due to imperfect anastomosis, or kinking of the conduit due
to compression or graft redundancy.
■ Patients may have an undiagnosed hypercoagulable state.
■ Poor inflow. If depressed velocities with poor waveforms are seen in the
conduit, further evaluation prior to the graft failing should be performed.
REFERENCES
1. Ardati AK, Kaufman SR, Aronow HD, et al. The quality and impact of risk
factor control in patients with stable claudication presenting for peripheral
vascular interventions. Circ Cardiovasc Interv. 2013;5:850-855.
2. Chen DKW, Conte MS, Belkin M, et al. Arterial reconstruction for lower limb
ischemia. Acta Chir Belg. 2001;101:106-115.
3. Taylor LM, Hamre D, Dalman RL, et al. Limb salvage vs amputation for
critical ischemia: the role of vascular surgery. Arch Surg. 1991;126:1251-1258.
4. Belkin M, Know J, Donaldson MC, et al. Infrainguinal arterial reconstruction
with nonreversed greater saphenous vein. J Vasc Surg. 1996;24:957-962.
5. Klinkert P, Schepers A, Burger DHC, et al. Vein versus
polytetrafluoroethylene in above-knee femoropopliteal bypass grafting: five
year results of a randomized controlled trial. J Vasc Surg. 2003;37:149-155.
6. Dardik H, Dardik I, With FJ. Exposure of the tibioperoneal arteries by the
single lateral approach. Surgery. 1974;75:377-382.
7. Schanzer A, Hevelone N, Owens CD, et al. Statins are independently
associated with reduced mortality in patients undergoing infrainguinal bypass
graft surgery for critical limb ischemia. J Vasc Surg. 2008;47:774-781.
8. Twine CP, McLain AD. Graft type for femoropopliteal bypass surgery.
Cochrane Database Syst Rev. 2010;12:CD001487.

9. Schanzer A, Hevelone N, Owens CD, et al. Technical factors affecting
autogenous vein graft failure: observations from a large multicenter trial. J
Vasc Surg. 2007;46:1180-1190.

18
CHAPTER
Management of Diabetic
Foot Ulcers
Rahim Nazerali
DEFINITION
■ Foot ulcers are the most common complication affecting patients with diabetes
mellitus.1
■ A result of lower extremity neuropathic disease, trauma, and deformity.
■ May be compounded by ischemia, callus formation, and edema.
ANATOMY
■ Resembles laceration, puncture, or blister with round or oblong shape.
■ May be necrotic, pink, or pale with well-defined smooth edges.
■ Periwound often presents with callus.
PATHOGENESIS
■ Origin and development have several components.
■ Thirty-two unique casual pathways for developing foot ulcers.2
■ Peripheral neuropathy, structural foot problems, and minor trauma are present
in the majority (63%).
■ Other less prevalent causes include edema, callus, and peripheral ischemia.
■ Major common pathways involve pressure/trauma, ischemia/hypoxia,
infection, cellular failure, and chronic inflammation.
NATURAL HISTORY
■ 12.5% individuals with diabetes will develop lower extremity ulceration.3
PATIENT HISTORY AND PHYSICAL FINDINGS
■ Basic history, including state of health, record of diabetic complications, shoe
problems, pain in extremity, medications, glycated hemoglobin level.

■ Risk factor assessment involving absence of protective sensation due to
peripheral neuropathy, vascular insufficiency, structural deformities/callus
formation, autonomic neuropathy, limited joint mobility, long duration of
diabetes, long history of smoking, poor glucose control, obesity, impaired
vision, past history, increased age, male gender, poor footwear.
■ The Wagner scale for foot wound classification based on depth and presence
of osteomyelitis and gangrene is the most widely accepted classification
scheme4 (FIG 1) but does not address the critically important parameters of
ischemia and infection.
■ Grade 0: intact skin
■ Grade 1: superficial without penetration of deep layers
■ Grade 2: deeper reaching tendon, bone, or joint capsule
■ Grade 3: deeper with abscess, osteomyelitis, or tendonitis extending to those
structures
■ Grade 4: gangrene of some portion of the toe, toes, and/or forefoot
■ Grade 5: gangrene involving the whole foot or enough of the foot that no
local procedures are possible
■ Physical exam:
■ Adequate description of ulcer characteristics such as size, depth, appearance,
location, etc.
■ Examine with blunt sterile probe to detect sinus tract, undermining and
dissection into tendon, bone or joints

FIG 1 • Wagner scale for foot wound classification
showing the natural history of dysvascular foot
breakdown.
■ Identify limb-threatening infection defined by cellulitis extending beyond 2
cm from perimeter, abscesses, or osteomyelitis
■ Protective sensation testing with Semmes-Weinstein 5.07 (10-g)
monofilament test or vibration tuning fork test (128 cycles per second) with
on-off method
■ Evaluate for musculoskeletal abnormalities that lead to focal areas of high
pressure
■ Vascular status evaluation via segmental pressures, toe pressures, or
transcutaneous oxygen readings
■ Evaluate skin and nail condition of the affected extremity
■ Footwear evaluation including bulges on outside of shoes, wear patterns on
soles, wearing down heels, worn lining, shoe cushion, and foreign object in
shoe
IMAGING
■ Duplex studies: ABI/TBI (ABI can be falsely elevated due to atherosclerotic
hardened vessels.)
■ X-ray, MRI, or bone biopsy to rule out osteomyelitis
■ Lower extremity angiography
DIFFERENTIAL DIAGNOSIS
■ Peripheral neuropathy
NONOPERATIVE MANAGEMENT
■ Early prevention through careful and frequent inspection is important.
■ Key therapeutic objectives include addressing global factors (glycemic control
and nutritional support) and local factors.
■ Aggressive treatment of infection through targeted antibiotic treatment from
tissue cultures.
■ Establishing if ischemia is present and revascularization is required.
■ Topical wound care by optimizing wound bed moisture balance and
exudate/odor control.
■ Off-loading and redistribution of pressure involving bed rest, wheelchairs,

crutches, surgical shoes, custom sandals, healing shoes, cast shoes, and foam
dressings.
■ Pressure relief of plantar ulcers utilizing orthotics and total contact casting,
which is considered the “standard” treatment for off-loading
■ Adjunctive hyperbaric oxygen treatment can be an important aspect of the
treatment armamentarium. Cochrane Review supported a 95% reduction in
major amputations when adjunctive HBOT (Hyperbaric Oxygen Therapy) was
used to treat chronic diabetic foot ulcers.5
■ Patient has type 1 or type 2 diabetes and has a lower extremity wound.
■ Wound is classified as Wagner grade 3 or higher.
■ Failed adequate course of standard wound therapy.
SURGICAL MANAGEMENT
■ Ensure appropriate blood flow prior to surgical management.
■ Stenting vs bypass coordinated with vascular surgery
T E C H N I Q U E S
■ Aggressive Wound Debridement
■ Initial surgical debridement
■ Removal of free-living bacteria and biofilms
■ Stimulation of growth factors, removal of senescent cells, and removal of
hyperproliferative nonmigratory tissue
■ Maintenance of surgical debridement
■ Weekly debridement depending on the formation of new necrotic tissue.
■ First 4 weeks of treatment reduces median wound area by 54%.
■ Flaps and Grafts
■ Local flaps and grafts described elsewhere in this text can be used for
definitive soft tissue coverage.
PEARLS AND PITFALLS

Blood flow
■ It is critical prior to any surgical intervention that blood
flow/perfusion be determined and optimized.
Adequate
debridement
■ Ensuring adequate debridement of soft tissue and bone is critical
to minimize biofilm and senescent cells.
Off-loading
■ Minimizing pressure to the area of a diabetic foot ulcer helps
ensure adequate perfusion.
Infection
control
■ It is important to address subclinical infections as well as ensure
that the underlying osteomyelitis is appropriately treated for the
successful long-term treatment of diabetic foot ulcers.
Consideration
for hyperbaric
oxygen
■ Studies indicate that Wagner grade 3 wounds benefit from
hyperbaric oxygen therapy.
OUTCOMES
■ 85% of lower limb amputations in diabetics are preceded by unhealed
ulceration.
■ 50% to 75% of lower extremity amputations are caused by nontraumatic
amputations.
■ Five-year mortality after amputation in diabetics is 45%.
REFERENCES
1. Jeffcoate WJ, Harding KG. Diabetic foot ulcers. Lancet. 2013;
361(9368):1545-1551.
2. Reiber GE, Vileikyte L, Boyko EJ, et al. Causal pathways for incident lower-
extremity ulcers in patients with diabetes from two settings. Diabetes Care.
1999;22(1):157-162.
3. Kalish J, Hamdan A. Management of diabetic foot problems. J Vasc Surg.
2010;51(2):476-486.
4. Wagner FW. The diabetic foot. Orthopedics. 1987;10(1):163-172.
5. Kranke P, Bennett MH, Martyn-St James M, et al. Hyperbaric oxygen therapy
for chronic wounds. Cochrane Database Syst Rev. 2015;(6):CD004123.

19
CHAPTER
Nerve Repair and
Reconstruction—Peroneal
Nerve
Shawn Moshrefi and Catherine M. Curtin
DEFINITION
Peroneal Nerve Injury
■ Peroneal nerve injuries vary in severity, mechanism, and needed treatment.
■ The nerve injury type dictates the treatment and prognosis.
■ Types of nerve injury1
• Neuropraxia: conduction delay with no axonal injury. These injuries will
recover spontaneously without intervention.
• Axonotmesis: axonal injury resulting in disruption of the axons; however,
the supporting nerve scaffolding is intact. In these injuries, distal nerve
segment will undergo Wallerian degeneration and proximal fibers will
regenerate. Spontaneous recovery is possible.
• Neurotmesis: complete disruption of the nerve. In these injuries,
spontaneous regeneration will not occur.
• Neuroma in continuity: disruption of the axons though the scaffolding
seems to be intact. However, at the injury site, there is internal fibrosis,
which prevents axons from regeneration. In these injuries, spontaneous
regeneration will not occur.
• Mixture of injury types: nerve patterns can be complex, and one nerve can
have several different levels of injury.
ANATOMY
■ The common peroneal nerve fibers originate from L4 to S3 nerve roots (FIG
1).

■ The common peroneal nerve branches from the sciatic nerve in the popliteal
fossa.
■ The motor component of the peroneal nerve innervates the anterior and lateral
lower leg compartment muscles as well as some intrinsic muscles of the foot.
■ The sensory component of the peroneal nerve supplies the first dorsal web
space of the foot and the top of the foot.
■ The peroneal gives off the lateral sural cutaneous branch, which joints the
medial sural cutaneous branch (contributed from tibial nerve) to form the sural
nerve.
■ The common peroneal nerve crosses from posterior to anterolateral around the
neck of the fibula.
■ The peroneal nerve is susceptible to compression as it wraps around the
fibula.
■ Once the nerve crosses anterior to the fibula, it branches into the superficial
peroneal and deep peroneal nerves.
■ The superficial peroneal nerve passes straight down the lateral compartment.
■ The superficial peroneal nerve supplies motor to the lateral compartment
(peroneus longus and peroneus brevis).
■ The superficial peroneal nerve supplies sensation to the top/lateral portion of
the foot.
■ The nerve transitions from within the muscle to a more superficial
subcutaneous position at the junction of the middle and distal thirds of the
lower leg. This transition site can be a point of compression.
■ The deep peroneal nerve turns acutely around the fibular neck to enter the
anterior compartment of the leg. The deep peroneal nerve then passes under the
intermuscular septum between the anterior and lateral compartments to
eventually course down between the tibialis anterior and extensor hallucis
longus alongside the anterior tibial artery.
■ The deep peroneal motor nerve supplies the anterior compartment of the leg
as well as some of the small foot extensor muscles: tibialis anterior, extensor
digitorum longus, peroneus tertius, extensor hallucis longus, extensor
digitorum brevis, and extensor hallucis brevis.
■ The deep peroneal nerve supplies sensation to the first web space of the foot.

FIG 1 • Anatomy of the peroneal nerve.
PATHOGENESIS
■ Direct trauma can injure the nerve along its course.
■ Fibular fracture can lacerate the nerve or result in neuropraxia.
■ Knee dislocation can result in a stretch injury or even a rupture of the
peroneal nerve.2
■ Iatrogenic injuries that occur include prolonged tourniquet time, laceration of
nerve during hardware placement, and compression of nerve from operative
positioning.
■ Swelling and compression can cause injury along the course of the peroneal
nerve.
■ Ankle swelling can cause superficial peroneal nerve entrapment and resulting
pain.

■ Compression from tight splints or casts can result in common peroneal nerve
injury.
■ Soft tissue masses
■ Cysts, especially Bakers cysts, or other nerve compressing structures can
result in peroneal nerve injury.
■ Neural tumors such as schwannomas can result in nerve deficits.
PATIENT HISTORY AND PHYSICAL FINDINGS
■ A complete and thorough history detailing patient’s history of present illness,
current injuries, history of prior injuries, prior surgeries (including spinal,
buttock, and lower extremity procedures), comorbidities, occupation, and other
case-by-case considerations should be obtained.
■ Inspection
■ Is the leg/foot swollen?
■ Are there vascular changes?
■ Is there atrophy?
■ Is there a gait abnormality or foot drop?
■ Vascular exam should assess for palpable pulses distally, temperature, and
capillary refill of the foot.
■ Sensory exam
■ Ten test: this quick test uses the contralateral area of normal sensation as a
reference. The patient is lightly touched in the contralateral healthy
distribution, and this normal sensation is a “ten.” Then, both the healthy and
affected side are lightly touched at the same time, and the patient is asked to
grade the affected side using the scale 0 to 10.3
■ Motor exam
■ Consists of testing the respective muscles that the peroneal nerve: extension
of the foot and ankle.
■ Each muscle can be tested individually and compared to the contralateral
side. Comparing to the healthy side allows for identification of subtle motor
deficits seen in compression.
■ Motor examination remember mnemonic PED = Peroneal Everts and
Dorsiflexes or more correctly noted, Extends.
■ Scratch collapse test4
■ This test can identify site of nerve entrapment.

FIG 2 • Large peroneal nerve schwannoma.
■ Directly over the suspected nerve compression, the examiner gently scratches
the skin. Then, the examiner immediately tests arm external rotation by
applying force to the patient’s dorsal forearm. The patient attempts to resist.
■ A positive test on the scratch collapse test is when the patient briefly has
decreased external rotation strength and “collapses” under the examiner’s
pressure.
■ Tinel test
IMAGING
■ X-rays are useful for suspected bony injury.
■ Angiography may be required in complex trauma patients.
■ This is particularly important as the deep peroneal nerve runs intimately with
anterior tibial artery.
■ MRI
■ Standard MRI can assess for soft tissue masses such as Baker cysts,
schwannomas, or tumors.
• FIG 2 shows a large peroneal nerve schwannoma with its typical smooth
bright appearance.
■ MRI neurogram can identify areas of nerve compression and enhancement
(FIG 3).
■ Nerve conduction studies and electromyelography.
■ For acute injuries, perform the first nerve testing at least 1 month after injury.
■ Studies can be repeated at 12 weeks, if there is no signs of recovery on
physical examination.

■ Nerve conduction studies may be normal for nerve compression that has not
resulted in any axonal injury.
FIG 3 • MRI showing inflamed deep peroneal nerve and
superficial peroneal nerve.
DIFFERENTIAL DIAGNOSIS
■ Lumbar spinal pathology
■ Sciatic pathology
■ If on physical examination, both peroneal nerve and tibial nerve distributions
are involved, then sciatic pathology should be suspected.
■ Nerve studies should help differentiate.
■ Neurologic problem
■ Peripheral neuropathy
■ Motor neuron disease
■ Double crush5
■ A nerve may have more than one site of entrapment: for example, common
peroneal at the fibular head and superficial peroneal at middle third of lower
leg.
■ The theory is that an axon injured in one area may be more susceptible to
secondary sites of injury.
■ Missing secondary sites of pathology will result in limitation of recovery if
only one site is treated.
NONOPERATIVE MANAGEMENT
■ For closed nerve injuries, nonoperative management is appropriate initially.

■ Physical modalities
■ Edema prevention with lightly compressive wraps/garments and direct hands
on physical therapy can be helpful.
■ Strategic splinting to prevent contractures.
■ Ankle-foot orthoses help improve mobility and stability in patients with a
foot drop.
■ Gentle range of motion exercises to allow the nerve to glide and limit
potential scarring in an injured soft tissue bed.
■ Desensitization to minimize pain and reeducate the nociceptive pathways.
SURGICAL MANAGEMENT
■ Exploration and repair is indicated for open nerve injuries or closed injuries
that are not showing signs of recovery.
■ Nerve laceration
■ Urgent repair is indicated.
■ Blast injuries should be explored no sooner than 6 weeks.
■ These injuries can have a surprising amount of recovery and should be
followed until recovery plateaus before surgery.
■ Intraoperative nerve monitoring is critical to define the zone of injury.
■ Traction injury should be explored if no signs of recovery at 3 months.
FIG 4 • Patient positioning for decompression of
common peroneal and superficial peroneal nerves.
■ Intraoperative nerve monitoring is critical to define the zone of injury.
■ Be prepared for the need for long nerve grafts.

■ Release of compressed common peroneal nerve (or branches) can be
performed after thorough workup and no signs of recovery at 3 months.
■ If injured superficial peroneal nerve resulting in painful neuroma in ankle or
foot region, consider resection of nerve at junction of middle/distal third of the
leg.
■ This will trade numbness for pain.
■ It will allow the surgeon to be out of the zone of injury.
■ Allows new placement of the neuroma deep in muscle and not crossing a
joint.
Preoperative Planning
■ Definitive fracture fixation should be performed prior to nerve repair.
■ Arterial injury should be addressed prior to nerve repair.
■ If possible, use a lower extremity tourniquet to aid in visualization of the
nerve.
■ If intraoperative nerve monitoring to be utilized, inform anesthesia team to not
use paralytics.
■ If pain is a concern, consider a more aggressive perioperative pain strategy.
■ 900 mg of gabapentin preoperatively6
■ Intraoperative ketamine
■ Regional block
■ Multimodal postsurgical pain management strategy
■ If planning nerve resection of superficial peroneal nerve
■ Preoperative diagnostic block of the nerve at planned level of resection.
■ Ensure patient has significant relief of pain for hour after block.
■ Ensure patient will tolerate the numbness felt at the time of the block for the
decrease in pain.
Positioning
■ Positioning depends on level of injury (above knee, at level of knee, or below
knee).
■ Access to popliteal area is easiest when the patient is in the prone position.
■ Access to the lateral leg is managed either supine with a hip bump or a
“sloppy” lateral with the unaffected side down. FIG 4 shows positioning for
decompression of common peroneal and superficial peroneal nerves.
■ Access to compression sites at the extensor retinaculum is managed with the

patient supine.
T E C H N I Q U E S
■ Common Peroneal Nerve Decompression
■ Regional or general anesthesia
■ If no intraoperative nerve monitoring is required, regional anesthesia with a
pain pump can provide several days of pain relief reducing opioid use.
■ Thigh tourniquet is placed.
■ Hip bump or slight lateral decubitus positioning to internally rotate the leg.
■ Oblique incision 2 cm distal to the fibular head (on thin patients, you can
palpate the nerve and design your incision above the nerve).
■ Skin and subcutaneous tissue are divided down to the overlying fascia of the
anterior lower leg muscles. Careful hemostasis is obtained as the dissection
proceeds.
■ Begin proximal and identify the nerve just posterior to the biceps femoris
tendon.
■ The nerve is visualized with gentle longitudinal spread with a dissecting
scissor.
■ A vessel loop is placed around the nerve.
■ The dissection proceeds distally releasing the fascia overlying the nerve. The
fascia that overlies the muscles in the lateral muscle compartment is released.
Then, the muscle fibers are spread/retracted allowing visualization of the
thick fascia overlying the nerve, which is released (TECH FIG 1).
■ The nerve will start dividing at the level of the fibular neck. In addition to
the superficial and peroneal branches, the genicular branch that loops back
proximal to the joint.
■ Under direct visualization, follow the branches distally to ensure there are no
unreleased fascial bands. The intermuscular septum can cause compression
so inspect for any overlying compressive bands.
■ This dissection can be performed with an incision that only goes about 2 cm
anterior to the fibular head.
■ Release tourniquet, achieve hemostasis, and close skin.
■ Soft bulky dressing is placed.

TECH FIG 1 • Visualization of the peroneal nerve.
■ Common Peroneal Nerve Traction Injury (Knee
Dislocation)
■ General anesthesia is required as patient will be prone and intraoperative
nerve monitoring will be used.
■ Thigh tourniquet.
■ Prone positioning.
■ Intraoperative nerve monitoring available.
■ Incision is angled from the center of popliteal fossa laterally toward the
fibular head.
■ The dissection is taken down to the level of the muscle fascia.
■ The common peroneal nerve is identified as it branches off the sciatic nerve.
■ A vessel loop is placed on the nerve, and the dissection is taken distally.
■ The nerve is released from the overlying scar (often a very challenging
dissection). The dissection is taken around the fibular head releasing the
anterior muscle fascia.
■ Intraoperative nerve monitoring is performed. Start with somatosensory
evoked potentials can help establish the proximal level of intact nerve.
Nerve-to-nerve monitoring can identify neuroma in continuity.
■ If the nerve is ruptured or neuroma in continuity is identified, resect
damaged nerve until two healthy nerve ends are revealed.
■ Ensure that the proximal nerve is healthy by using the assistance of your
neuromonitoring.

■ For the nerve gap, harvest sural nerve graft.
■ Cable the graft and suture in place with a few 9-0 sutures using microscopic
technique. The repair should be tension free to allow for knee motion.
■ Augment repair by sealing coaptation site with fibrin glue.
■ Close wound.
■ Superficial Peroneal Nerve Compression Release
and/or Neurectomy
■ Thigh tourniquet.
■ Regional anesthesia.
■ Supine position.
■ Approximately 3 cm longitudinal incision over seam between anterior and
lateral compartments at juncture of middle and distal third of the leg.
■ The dissection is taken down to the level of the muscle fascia.
■ Identify the thin raphe located between the lateral and anterior compartments
of the lower leg.
■ Of note, there is a wide fat stripe anterior to the superficial peroneal nerve. If
you find this first, look about a 1 cm posterior and you will find the seam that
contains the nerve.
■ Release overlying fascia proximally and distally.
■ If performing neurectomy for damaged superficial peroneal nerve, the
approach to the nerve is the same.
■ Once the nerve is identified, divide nerve distally and free up the proximal
nerve for several centimeters.
■ Place nerve stump deep within peroneus longus muscle. Bury the nerve
stump in the muscle bed without tension.
■ Close wound and place bulky dressing.
■ Nerve Laceration
■ The nerve is identified using the existing wounds or the approaches
described above.
■ The nerve can be directly coapted using microsurgical technique if a tension-
free repair is possible.

■ If there is tension, a bridging nerve graft is required.
■ Nerve repair is done using microsurgical technique and should be tension
free.
■ Use 9-0 suture and the minimal amount of sutures needed.
■ Fibrin glue can be used to seal the repair site and to hold cabled nerve grafts
together.
■ The wounds are closed.
■ Repairs are protected for 3 weeks if concern about the repair with
splints/braces to limit mobility at adjacent joints.
PEARLS AND PITFALLS
Nerve repair
■ Nerve coaptation must be without tension. If a 9-0 suture cannot
hold the repair, there is too much tension and a graft is required.
Diagnosis of
entrapment
site
■ Confident location of entrapment can be made if the patient has a
positive Tinel sign, positive scratch collapse, and sensory changes
in the appropriate distribution.
■ Double crush is a risk so assess if nerve entrapped at both the
superficial and common peroneal entrapment sites.
Intraoperative
monitoring
■ Communication between neurology and anesthesia team is critical
to ensure that patient does not receive medications that will hinder
intraoperative monitoring.
■ SCD machine and warming machines can cause background that
interferes with intraoperative monitoring.
■ Do not use prolonged tourniquet if planning intraoperative
monitoring.
Meticulous
hemostasis
■ If not using a tourniquet, preinject incision with bupivacaine with
epinephrine before prepping.
■ To improve visualization, a mix of 1 ampule of epinephrine with
100 cc of saline can be used to moisten gauze pads. These can be
dabbed in the wound and improve visualization and minimize the
need for cautery adjacent to the nerve.
POSTOPERATIVE CARE
■ Medications

■ If neuropathic pain is a significant concern, consider multimodal pain control,
which can include acetaminophen, NSAIDs, gabapentin, and opioids.6
■ Therapy
■ At 2 to 3 weeks, consider therapy for scar management, nerve gliding, and
desensitization.
■ Nerve repair
■ Nerve repairs with slight tension need to be protected from disrupting forces
for 3 weeks postoperatively. This can be performed through an immobilizer or
splint. However, if reconstructed with a graft with some redundancy, early
mobilization is possible.
■ Nerve decompression
■ Soft dressing and early mobilization will prevent scarring and tethering of the
nerve.
OUTCOMES
■ Studies show approximate 80% functional nerve recovery in patients with a
multitude of methods of common peroneal nerve injuries.7
■ Other studies indicate a vastly significant difference in prognosis from
incomplete nerve palsy (highly favorable functional outcome) to complete
peroneal nerve palsy (less than 40% functional recovery).2
■ Complete peroneal nerve injuries after knee dislocation still have poor
functional outcomes with less than 40% recovering extension despite
treatment.2
■ Release of the superficial peroneal nerve has resulted in high rates of pain
resolution.8,9
COMPLICATIONS
■ Most severe complication is iatrogenic nerve injury though this is very rare
■ Bleeding
■ Infection
■ Fibrosis of the release site requiring revisionary surgery
REFERENCES
1. Seddon HJ. A classification of nerve injuries. Br Med J. 1942;2:237-239.
2. Woodmass JM, Romatowski NP, Esposito JG, et al. A systematic review of
peroneal nerve palsy and recovery following traumatic knee dislocation. Knee
Surg Sports Traumatol Arthrosc. 2015;23(10):2992-3002.

3. Strauch B, Lang A, Ferder M, et al. The ten test. Plast Reconstr Surg.
1997;99(4):1074-1078.
4. Gillenwater J, Cheng J, Mackinnon SE. Evaluation of the scratch collapse test
in peroneal nerve compression. Plast Reconstr Surg. 2011;128(4):933-939.
5. Upton AR, McComas AJ. The double crush in nerve entrapment syndromes.
Lancet. 1973;2(7825):359-362.
6. Carroll I, Hah J, Mackey S, et al. Perioperative interventions to reduce chronic
postsurgical pain. J Reconstr Microsurg. 2013;29(4):213-222.
7. Emamhadi M, Bakhshayesh B, Andalib S. Surgical outcome of foot drop
caused by common peroneal nerve injuries; is the glass half full or half empty?
Acta Neurochir. 2016;158(6):1133-1138.
8. Styf J, Morberg P. The superficial peroneal tunnel syndrome. Results of
treatment by decompression. J Bone Joint Surg Br. 1997; 79(5):801-803.
9. Franco MJ, Phillips BZ, Lalchandani GR, et al. Decompression of the
superficial peroneal nerve: clinical outcomes and anatomical study. J
Neurosurg. 2017;126(1):330-335.

20
CHAPTER
Achilles Tendon
Reconstruction
Hani Sbitany
DEFINITION
■ Achilles tendon is the most frequently ruptured tendon in the body, with
incidence reported as high as 34/100 000, most commonly seen in males in
their 30s.1
■ The male-to-female ratio of this injury is 20:1.
■ Classically seen when less active males engage in a new sport, without
significant previous experience.
ANATOMY
■ Most common site of rupture is 3 to 6 cm above the os calcis (ie, the
calcaneus):
■ This area is a watershed zone in terms of blood supply.
■ Achilles tendon is made up of gastrocnemius and soleus muscles, along with
the plantaris tendon (FIG 1).
■ This tendon begins in the midportion of the calf (superficial posterior
compartment) and narrows to approximately 4 cm width at its insertion on the
calcaneus bone.
■ Achilles tendon helps to produce plantar flexion of the foot, which is powered
through associated muscle innervation by the tibial nerve.

FIG 1 • The Achilles tendon is formed by the
convergence of the medial, lateral gastrocnemius, and
soleus muscles.
PATHOGENESIS
■ With aging, there is an increase in type 3 collagen content on the Achilles
tendon and a reduction in type 1 collagen content.2
■ Increasing age is also accompanied by decreased orderly collagen cross-
linking.
■ All this results in reduced tensile strength of the tendon.
NATURAL HISTORY
■ In addition to aging, there are numerous other risk factors associated with
Achilles tendon rupture:

■ Hypercholesterolemia
■ Rheumatoid arthritis
■ Hypercholesterolemia
■ Long-term dialysis
■ Renal transplantation
■ Chronic steroid use
PATIENT HISTORY AND PHYSICAL FINDINGS
■ A history of pain and weakening on plantar flexion is usually indicative of
Achilles tendon rupture.
■ On physical exam, there is usually a palpable defect in the tendon, in 75% of
patients.
■ Up to 25% of tendon injuries can be missed when only clinical assessment is
used for diagnosis.
■ Simmonds/Thompson test: the patient lies face down with feet hanging off the
edge of the bed. If there is no plantar flexion of the foot on squeezing the calf,
then there is likely rupture of the Achilles tendon.
■ O’Brien test: insert 25-gauge needle at right angle through the skin of calf
muscle just medial to midline at a point 10 cm proximal to superior border of
calcaneus. The needle should be within the substance of the tendon. Movement
of the needle in a direction opposite that of the tendon during passive extension
and flexion of the foot confirms an intact tendon distal to the level of needle
insertion.
■ Copeland test: the patient is prone with the feet hanging off of the exam table.
A sphygmomanometer is placed around the calf with the foot in plantar flexion
and inflated to 100 mm Hg. If the tendon is intact, then extension of the foot
will lead to a pressure increase to 140 mm Hg. If the tendon is ruptured, then
the pressure does not change.
IMAGING
■ Imaging is always recommended when there is clinical concern for Achilles
tendon rupture.

FIG 2 • A. Normal Achilles ultrasound image. B. Ankle
MRI (T1-weighted image) showing a distal Achilles
tendon rupture. (From Labib S. Open Achilles tendon
repair. In: Wiesel S, ed. Operative Techniques in
Orthopaedic Surgery. 2nd ed. Vol. 4. Philadelphia, PA:
Wolters Kluwer Health; 2015:4967-4973.)
■ Ultrasound is a useful first-line imaging technique, with sensitivity of 100%
(FIG 2A).
■ Ultrasound tendon gap greater than 4 mm with patient in equinus (plantar
flexion) indicates the need for surgical repair.
■ Ultrasound can differentiate partial vs complete tear:
• This is more difficult with a tear at the proximal musculotendinous junction,
in which sensitivity is much lower.
■ MRI is the best imaging modality for Achilles tendon rupture, with sensitivity
of 100% (FIG 2B).
■ MRI should always be obtained if any uncertainty exists regarding location,
completeness, or length of tear.
DIFFERENTIAL DIAGNOSIS
■ Achilles tendon peritendinitis
■ Gastrocnemius tear or strain
■ Calcaneus fracture
■ Posterior tibialis tendon injury
■ Posterior tibialis stress syndrome

NONOPERATIVE MANAGEMENT
■ Nonoperative treatment of Achilles rupture is only an option in cases of acute
rupture, with immediate diagnosis.
■ In cases of delayed diagnosis, scarring and retraction of tendon ends make
conservative management less effective and unlikely to heal properly.
■ The purpose of nonoperative management is to appose the ruptured Achilles
ends, in stable fashion, such that healing can occur.
■ Treatment regimen consists of immobilizing the extremity below the knee,
with a brace or rigid cast.
■ The foot is initially placed in full plantar flexion.
■ Ankle is slowly brought into neutral position over 8 to 12 weeks.
■ Knee immobilization is not necessary for reapproximation of the tendon edges.
■ Early, gradual weight bearing has also been shown to confer protection against
repeat rupture in the future.
■ Many nonoperative regimens now advocate early weight bearing in a custom
or Sheffield splint.
■ This is particularly beneficial in frail patients for whom joint contracture is at
high risk.
■ The Sheffield splint is a specialized device worn on the lower leg and foot
that allows for early controlled mobilization of the Achilles tendon.
■ Early weight bearing also facilitates faster resumption of mobility after
complete healing.
■ One preferred conservative regimen:
■ Patient in full equinus (30 degrees) with touch weight bearing for 2 weeks
■ Ankle then placed in partial equinus (15–20 degrees) with partial weight
bearing for 2 weeks
■ Finally, placed in neutral (0 degrees) with full weight bearing for 2 weeks
SURGICAL MANAGEMENT
■ Operative treatment is used for the majority of acute tendon ruptures in
younger patients, as well as in all patients with chronic rupture or delayed
diagnosis.
■ This is the only treatment option when there has been scarring and retraction
of the tendon ends, resulting in a lack of apposition.
Preoperative Planning

■ As previously mentioned, ultrasound and MRI assessment of the injury is
important, to identify the location of the rupture relative to the
musculotendinous junction and the length of the gap.
■ The patient’s physical examination should also include a workup of mobility
potential and strength, to ensure that early mobilization and weight bearing will
be possible.
Positioning
■ Surgical repair is commonly performed with the patient in the supine position,
the hips abducted, and the knees flexed (frog leg position) (FIG 3).
■ The operation can also be performed with the patient in the prone position, for
easier, direct access to the posterior ankle.
Approach
■ Open surgical repair is performed with a direct longitudinal incision, directly
over the Achilles to expose the entire tendon.
FIG 3 • Patient is placed in the prone position with both
legs prepared and draped for surgery. (From Labib S.
Open Achilles tendon repair. In: Wiesel S, ed. Operative
Techniques in Orthopaedic Surgery. 2nd ed. Vol. 4.
Philadelphia, PA: Wolters Kluwer Health; 2015:4967-
4973.)
T E C H N I Q U E S

■ Percutaneous Repair
■ Performed with patient in prone position.
■ Skin incision is first made over site of rupture.
■ Second skin incision made 4 cm proximal to initial incision.
■ Third incision made 4 cm distal to rupture (TECH FIG 1A).
■ The track of the entire tendon is defined under the skin and spread open.
■ For this repair, a suture is first passed on a needle through middle incision
and through tendon at this point (TECH FIG 1B).
■ A monofilament, permanent suture is used for this.
■ Needle is then passed proximal and brought out through proximal incision
(see TECH FIG 1B).
■ At this proximal incision, the suture is then passed through the proximal
cut edge of the Achilles tendon.
■ The needle is then passed back through the tunnel, brought out the middle
incision, passed through the distal stump of the tendon, and brought out the
distal end (TECH FIG 1C).
■ Traction is then applied to ensure proper tension (TECH FIG 1D).
TECH FIG 1 • A-D. Pattern for suture passage for
percutaneous repair of Achilles tendon rupture.
■ Open Direct (End-to-End) Suture Repair

■ Performed in cases of acute rupture, less than 6 weeks old.
■ Achilles tendon exposed along the entire length through vertical skin
incision.
■ Multiple figure-of-8 sutures are used to repair tendon at proper tension
(TECH FIG 2).
■ Similar to percutaneous, a large monofilament, permanent suture is used
for repair.
TECH FIG 2 • End-to-end suture repair of Achilles
tendon rupture.
■ Reconstruction With VY Advancement
■ Used to repair chronic ruptures with defect less than 3 cm between tendon

ends.
■ The entire posterior compartment, from the calcaneus to the midportion of
the calf, is exposed with the incision.
■ The gastrocnemius/soleus/Achilles junction is exposed posteriorly from the
prone position.
■ An inverted V incision is planned along the posterior superficial surface of
the muscular complex, with the apex of the V placed at the proximal portion
of the myotendinous junction.
■ The medial and lateral limbs of the V exit through the sides of the Achilles
tendon.
■ The inverted V is incised through the tendinous, superficial portions of the
tissue, leaving underlying muscle intact.
■ Then, the tendon ends are sutured to each other across the rupture, using
permanent suture.
■ Can use monofilament or braided suture.
■ Done with locking knots, at least five suggested.
■ Tension is set with gentle traction, such that the muscle is not disrupted.
■ Finally, the limbs of the inverted V are rerepaired with suture.
■ Flexor Hallucis Longus Transfer
■ Used to repair chronic ruptures with defect greater than 3 cm between
tendon ends.3
■ Requires a functional tibial nerve.
■ The flexor hallucis longus (FHL) tendon can be harvested through the same
posterior Achilles incision used for injury exposure.
■ The dissection is carried down into the deep posterior compartment fascia,
and underneath this, the FHL muscle and tendon sit.
■ The FHL muscle belly extends more distal than others in this compartment,
usually to the level of tibiotalar joint, which is the method of identification:
■ The muscle is confirmed by retracting manually and seeing flexion of the
hallux.
■ Medial to the FHL tendon, the neurovascular bundle of tibial nerve and
posterior tibial artery is identified.
■ The muscle is dissected distally, around the medial malleolus, taking care not

to injury the neurovascular bundle.
■ Then, the FHL is transected as distal as possible, along its tendinous portion,
with the ankle held in flexion and muscle under traction.
■ Based on FHL tendon diameter, a bone tunnel is drilled into the calcaneus
(posterior tubercle), just anterior to the area of Achilles tendon insertion on
the bone.
■ The length of the FHL muscle and tendon is set, after the tendon is passed
through the tunnel using a suture and passer (TECH FIG 3).
■ At this length, the tendon is fixed into the calcaneus after passing through
the tunnel, with an interference screw.
■ The final resting tension, after repair, is compared to the contralateral
uninjured side.
■ Gentle extension is applied to test the repair, and then the skin is closed.4
TECH FIG 3 • Flexor hallucis longus tendon used to
augment Achilles tendon repair. (From Labib S. Open
Achilles tendon repair. In: Wiesel S, ed. Operative
Techniques in Orthopaedic Surgery. 2nd ed. Vol. 4.
Philadelphia, PA: Wolters Kluwer Health; 2015:4967-
4973.)
POSTOPERATIVE CARE
■ For most repair techniques, the ankle is splinted in equinus for 2 weeks.
■ Strict nonweight bearing is employed for 6 to 8 weeks.

■ After 2 weeks, once the healing skin is confirmed on examination, the patient
is converted to postsurgical boot that gradually allows for passive extension in
increasing increments over the next 4 weeks.
■ At 6 to 8 weeks, patient is examined and tested for Achilles repair persistence,
and weight bearing is started in ankle boot brace.
■ Physical therapy also started at this point.
■ Three sessions of PT for 8 weeks.
■ PT focuses on passive Achilles stretching and gait training.
■ At 12 weeks, if the ankle is neutral alignment on exam, the patient is allowed
to resume activity slowly.
COMPLICATIONS
■ Bleeding
■ Infection
■ Tendon rerupture
REFERENCES
1. Heckman DS, Gluck GS, Parekh SG. Tendon disorders of the foot and ankle,
part 2: Achilles tendon disorders. Am J Sports Med. 2009;37(6):1223-1234.
2. Padanilam TG. Chronic Achilles tendon ruptures. Foot Ankle Clin.
2009;14(4):711-728.
3. Worth N, Ghosh S, Maffulli N. Management of acute Achilles tendon ruptures
in the United Kingdom. J Orthop Surg (Hong Kong). 2007;15(3):311-314.
4. Den Hartog BD. Flexor hallucis longus transfer for chronic Achilles
tendonosis. Foot Ankle Int. 2003;24(3):233-237.

21
CHAPTER
Excision of Soft Tissue
Tumors of the Lower Leg
Raffi S. Avedian and Robert J. Steffner
DEFINITION
■ Soft tissue tumors of the lower leg may be benign or malignant (soft tissue
sarcoma) and exhibit a variable natural history ranging from latency to rapid
growth.
■ Tumors located entirely above the muscle fascia are considered superficial,
whereas tumors involving the fascia or deep to it are considered deep.
ANATOMY
■ The lower leg is made up of the tibia and fibula and four muscle
compartments: anterior, lateral, deep posterior, and superficial posterior (FIG
1).
■ Three principal arteries travel in the lower leg.
■ The posterior tibial artery is located in the deep posterior compartment on the
surface of the tibialis posterior.
■ The anterior tibial artery is in the anterior compartment located deep to the
muscles on the surface of the interosseous membrane.
■ The fibular artery travels in the deep posterior compartment medial to the
fibula under the flexor hallucis longus; it sends branches to the lateral and
anterior compartments and a nutrient vessel to the fibula.
■ The deep peroneal nerve travels with the anterior tibial artery. The superficial
peroneal nerve is located in the lateral compartment; in the distal one-third of
the leg, it travels between the peroneus muscles and extensor digitorum longus
and pierces the deep fascia to become a cutaneous nerve.

FIG 1 • Cross-sectional anatomy of lower leg showing
the contents of the anterior, lateral, superficial posterior,
and deep posterior compartments.
PATHOGENESIS
■ The mechanism for soft tissue tumor formation is not known.
■ Risk factors for sarcoma development include radiation exposure,
radiotherapy, pesticide exposure, and hereditary conditions including Li-
Fraumeni syndrome and retinoblastoma gene mutation.
NATURAL HISTORY
■ All soft tissue sarcomas have the potential for local recurrence and metastasis.1
■ Soft tissue sarcomas exhibit a spectrum of natural history from slow-growing
low-grade tumors with low risk of metastasis to high-grade sarcoma that may
grow rapidly and pose a high risk of metastasis.

■ Lungs are the most common site of metastasis. Lymph node involvement is
rare.
■ Angiosarcoma, clear cell sarcoma, epithelioid sarcoma, rhabdomyosarcoma,
myxofibrosarcoma, and synovial sarcoma are associated with increased risk of
lymph node spread compared to other sarcomas.2
■ Benign tumors by definition do not have metastatic potential but can grow to
large sizes and cause symptoms.
PATIENT HISTORY AND PHYSICAL FINDINGS
■ A thorough history and examination are important to assess duration of
symptoms, comorbidities, physical dysfunction, organ involvement, overall
health, and patient expectations in order to best tailor treatment strategy for the
individual patient.
■ Many sarcomas may be asymptomatic with the only patient complaint being
the presence of a mass.
■ Neurovascular examination is mandatory for any extremity tumor.
IMAGING
■ Magnetic resonance imaging is the principal imaging modality used to
characterize tumors, formulate differential diagnosis, define local tissue
infiltration, and formulate surgical plan.
■ Plain radiographs are used if there is concern for bone involvement or to
demonstrate mineralization within a tumor such as vascular malformations.
■ Staging for soft tissue sarcomas consists primarily of lung imaging.
DIFFERENTIAL DIAGNOSIS
■ The differential diagnosis for a soft tissue tumor includes benign tumors,
sarcomas, lymphoma, infection, and inflammatory lesions (eg, rheumatoid
nodules).
■ There are over 50 sarcoma subtypes. Common histology types include
pleomorphic undifferentiated sarcoma, synovial sarcoma, leiomyosarcoma,
malignant peripheral nerve sheath tumor, liposarcoma.
SURGICAL MANAGEMENT
■ The appropriate treatment for any musculoskeletal tumor is based on its
diagnosis and natural history.
■ Biopsy incisions are considered contaminated and must be resected at the time

of definitive surgery. Care should be taken to place the biopsy in a location that
does not interfere with the final surgical plan.3
■ Simple marginal excision is appropriate for most benign tumors, and wide
resection with a clean margin is performed for soft tissue sarcomas.
■ Given the relatively low volume of tissue in the lower leg and ankle, soft
tissue reconstruction with local or free flaps is often needed.
Preoperative Planning
■ A patient is considered ready for surgery after completion of staging and
multidisciplinary review of pertinent imaging, pathology, and treatment
strategy.
■ The surgical plan is created by thorough study of the preoperative MRI scan.
Fluid-sensitive sequences and fat-suppressed contrast images show the extent
of disease that must be accounted in the excision. T1 fat-sensitive images show
the normal anatomy best including fat planes between tumor and critical
structures such as nerves and vessels.
■ When tumor abuts, but does not encase blood vessels or nerves, they can be
dissected free by leaving adventitia and epineurium on the tumor as the
margin.4
Positioning
■ Patient positioning is based on the surgeon’s assessment of the critical
anatomy of the surgery and how best to visualize it during surgery.
■ Supine is the most common position for tumor excision of the lower leg. A hip
bump may be used to access more lateral tumors; conversely, frog legging the
extremity facilitates medial and posterior visualization.
■ If a flap is to be used, the harvest must be performed using a separate back
table and instruments and the surgical sites completely isolated to avoid
contamination.
Approach
■ The surgical approach varies based on location of the tumor.
■ Previous biopsy and surgical scars are considered contaminated and must be
excised en bloc with the tumor.