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Leg defect

History –

Particular of patient-

Name, age, sex, r/o, occupation, SES

Chief complain-


Past history

Personal history

Family history


Physical examination-

CCO well oriented to TPP

Attitude of the patient-

Pulse- rate rhythm volume character compared to other site


BP- mmHg arm supine/sitting

CVS- S1S2 heard no murmur

Resp- b/l AE present, no crepts or added sound

PA- soft non-tender, no organomegaly, bowel sounds normally present


Peripheral edema/Lymphadenopathy/Pallor/Cyanosis/clubbing/icterus


LOCAL examination-

Examination of ulcer-

There is a wound of approx size…………… on the …………..aspect of ………leg approximately in the ……third of the leg

Wound has well defined margin with sloping edges having granulation tissue in the floor and ?exposed bone around …….x…….cm .

Wound is having serous/purulent/seropurulent/bloody/serosanguinous foul-smelling discharge from the wound which is scanty/moderate/large in quantity.

Skin around the wound is normal for his skin color/reddish/dark red.

There is granulation tissue present/ or not. Healthy granulation tissue- healthy when bright, beefy red, shiny and granular with a velvety appearance. Unhealthy- pale pink or blanched to dull, dusky red color.

Bone- The exposed bone is lusterless, dry, and yellow in color.

Fixator- There is uiplanar, unidirectional /uniplanar,birectional/ biplanar,unidirectional/ biplanar,bidirectional/ circular fixator present, having …….number of pins above and …..numbers of pins below .


Attitude of the limb-

Patient is lying in supine position/ sitting with

Hip flexed/extended, knee flexed, ankle joint flexed.

Limb externally / internally rotated. Apparent limb shortening.



Findings of inspection confirmed on palpation.

Wound is …………X ……… maximum dimension. ………cm  from tibial tuberosity and …….cm from medial malleolus. ?Medial and lateral margins of the wound.

The wound is tender/ nontender on palpation.

There is no bleeding on touch.

Wound is around …….mm in depth.

Base is formed by ……bone/ muscle.

Wound is not fixed to underlying structures.

There is/no surrounding tissue edema or regional lymphadenopathy.

There fixator has …….number of pins above and …..numbers of pins below Approximately … from tibial tuberosity (each pin distance).


Limb length measurements-

Greater trochanter to medial condyle-   right……. Left…….cm

Tibial tuberosity to medial malleoulus- right………left………cm.

Girth of leg at 15 cm from tibial tuberosity is ………….cm on right side and …………cm on left side.

Girth of thigh 20cm above medial femoral condyle is ………….cm on right side and …… on the left side.

Range of active motion at knee joint is ……….degree flexion……….degree extension on right side and …….on left side.

Range of active motion at ankle joint is ………… of plantar flexion………… of dorsal flexion on right side and ……………..on left side.

Range of passive motion at knee joint is …… degree flexion……….degree extension on right side and …….……….degree flexion……….degree extension on left side.

Range of passive motion at ankle joint is ………… of plantar flexion………… of dorsal flexion on right side and …………… of plantar flexion………… of dorsal flexion on left side.

There is no sensory loss.

Peripheral pulses palpable-

Femoral/ popliteal/ anterior tibial/posterior tibial/ dorsalis pedis.



Diagnosis– post traumatic soft tissue defect over upper/middle/lower third with exposed bone without neurovascular deficit with secondary diagnosis (chronic osteomyelitis) with limb shortening.


Plan –


Routine investigation

PAC fitness

Investigations specific to diagnosis-

Wounds c/s


Muscle charting

USG Doppler

CT angiography



Till the investigations are done, I would do regular dressing of the wound with betadiene or saline.

Once the patient is fit for surgery, I would like to debride the wound with around 0.5 cm margin and underlying bone till healthy normally bleeding bone is found and then cover the defect with muscle flap.



  1. What are the site of perforators?
  2. medially- from below upwards. With reference point – lower border of medial malleolus






Laterally-from below upwards

4-10 from lateral malleolus tip



5-6cm from fibular head


  1. What is the axis of the vessels in leg along which perforators are found?

Ans . Axis of perforator on medial side from post. tibial artery- 4.5 cm medial and parallel to the line joining tibial tuberosity and midmalleolar point.

Axis of perforator on lateral side from anterior tibial artery- 2.5 cm anterior and parallel to the line joining head of fibula and tip of lateral malleolus.

Axis of perforator on lateral side from peroneal artery- 2.5 cm posterior and parallel to the line joining head of fibula and tip of lateral malleolus.










  1. What is the difference in quality and quantity of perforators in leg?
  2. How many compartments are there in the legs?

4- Anterior, lateral and superficial posterior, deep posterior

  1. What is the different vessels that supply each compartment?

Anterior – anterior tibial artery

Lateral – peroneal artery

Posterior – posterior tibial artery


  1. What is the Ponten flap?

Superiomedial based fasciocutaneous flap in leg is called Ponten flap. Also called superflaps of legs because the length to breadth ratio can be extended beyond the usual 1:1 to up to 3:1

  1. Ponten described its flap in which specific area of the leg?
  2. superomedial aspect of the leg
  3. What is the classification for fasciocutaneous flap?

Cormack & Lamberty classification

Type A- pedicled fasciocutaneous flap dependent on multiple fascio-cutaneous perforators at the base and oriented along long axis of the flap (in prominent direction of the arterial plexus at the level of deep fascia)

Eg- Super flaps of Ponten, Sartorius flap without muscle, upper arm flap

Type B – single sizable and consistent fasciocutaneous perforator feeding a plexus at the level of the deep fascia.

Eg – supraclavicular

Median arm flap

Saphaneous artery flap

Parascapular flap

Type C – ladder type. Skin is supported by fascial plexus which is supplied by multiple small perforators along its length, which passes along septum b/w muscle.

Eg. – Radial forearm flap (Chinese forearm flap)

Type D – osteo-myo-fascio-cutaneous flap

An extension of type C – which takes muscle and bone supplied by the same artery.

Eg. – Radial forearm flap with radius


Mathes Nahai classification –

Type A – direct cutaneous àpedicle travels deep to fascia for a variable distance and then pierces fascia to supply skin à Eg. Groin flap, Temporoparietal fascia flap

Type B – septocutaneous à pedicle courses within intermuscular septum. à Eg. Lateral forearm flap, Radial forearm flap

Type C – musculocutaneous à vascular pedicle runs within the muscle substance and then supply skin à Eg. DIEP flap



  1. what’s the blood supply of skin?

Ans: Blood supply of skin is through various plexus –

  1. Subepidermal plexus
  2. Subdermal plexus
  3. Subcutaneous plexus
  4. Suprafascial plexus
  5. Subfascial plexus

These plexus can be supplied by various types of perforators –

  1. Direct cutaneous
  2. Septo-cutaneous
  3. Musculo-cutaneous
  4. what is the characteristics of artery and perforator through length of leg?

Ans: The size of the peroneal artery decreases as we go from proximal to distal but posterior tibial artery diameter remains almost the same as since it continues as the main vessel of the foot.

The perforators can be classified based on their internal diameter into three groups:

Small= 0.8-1.2 mm;

Intermediate= 1.3-2.0 mm;

Large= more than 2.0mm

The sizeable Perforators to sustain a flap are the intermediate or large ones.


  1. Whats are the limits of fasciocutaneous flap dissection in lower leg?

Ans: for retrograde flaps the lower limit of dissection decides the reach of the flap. Since lower two perforators are approximately within 8 cm from malleoli, that is taken as the safe limit of dissection inferiorly.

The safe upper limit of a retrograde flap is about 10 cm from the joint level in an adult.


  1. What is the Open fracture classification?

Gustilo-Anderson classification-

Type I = an open fracture with a wound < 1 cm long and clean

Type II = an open fracture with a laceration > 1 cm long without extensive soft tissue damage, flaps, or avulsions.

Type IIIA = open fractures with adequate soft tissue coverage of a fractured bone despite extensive soft tissue laceration or flaps, or high-energy trauma regardless of the size of the wound

Type IIIB = open fractures with extensive soft tissue injury loss with periosteal stripping and bone exposure, usually associated with massive contamination

Type IIIC = open fractures associated with arterial injury requiring repair


Classification is limited- almost limitless variety of injury patterns, mechanisms, and severities with a small number of discrete categories.

Limited interobserver reliability

Surface injury does not always reflect the amount of deeper tissue damage

Does not account for tissue viability and tissue necrosis


OTA Open Fracture Classification (OTA-OFC)


  1. Laceration with edges that approximate.
  2. Laceration with edges that do not approximate.
  3. Laceration associated with extensive degloving.


  1. No appreciable muscle necrosis, some muscle injury with intact muscle function.
  2. Loss of muscle but the muscle remains functional, some localized necrosis in the zone of injury that requires excision, intact muscle-tendon unit.
  3. Dead muscle, loss of muscle function, partial or complete compartment excision, complete disruption of a muscle-tendon unit, muscle defect does not reapproximate.


  1. No major vessel disruption.
  2. Vessel injury without distal ischemia.
  3. Vessel injury with distal ischemia


  1. None or minimal contamination.
  2. Surface contamination (not ground in).
  3. Contaminant embedded in bone or deep soft tissues or high-risk environmental conditions (eg, barnyard, fecal, dirty water).

Bone loss

  1. None.
  2. Bone missing or devascularized bone fragments, but still some contact between proximal and distal fragments.
  3. Segmental bone loss.



Advantages of External Fixation-

Provides rigid fixation when other forms of immobilization are not feasible. For example, severe open fractures cannot be managed by plaster casts or internal fixation due to risk involved.


Allows compression, neutralization, or fixed distraction of the fracture fragments.

Allows surveillance of the limb and wound status.

Allows other treatments like dressing changes, skin grafting, bone grafting, and irrigation, is possible without disturbing the fracture alignment or fixation.

Allows immediate motion of the proximal and distal joints This aids in reduction of edema and nutrition of articular surfaces and retards capsular fibrosis, joint stiffening, muscle atrophy, and osteoporosis.

Allows limb elevation by suspending frame from overhead frames

Allows early patient ambulation.

Can be done with the patient under local anesthesia, if necessary

External fixators cause less disruption of the soft tissues, osseous blood supply, and periosteum. This makes external fixation excellent choice in

Acute trauma with skin contusions and open wounds

In chronic trauma where the extremity is covered in thin skin grafts and muscle flaps,

Patients with poor skin healing

Ability to fix the bone avoid fixation at the site of fracture or lesion, and still obtained the rigid fixation


Disadvantages of external fixation

Pins inserted in the bones are exposed to internal environment and risk of pin tract infection is always there

Fracture may occur through pin tracts after frame removal. Extended protection may be required.

Assembly of the fixator lies outside the limb, is cumbersome and needs meticulous care.

High degree of compliance and motivation is required

Not suitable for non-cooperative patients

In fixators with pins near the joint or fixators that span joint, joint stiffness can occur.


Types of External Fixators

In strictest sense there are two types of fixators –

Unilateral and


A combination of two is called hybrid fixators.


Uniplanar- fixation in single plane

Biplanar- fixation in two planes

Unilateral-fixation on only one side

Bilateral- fixation on both sides


Parts of fixator-

Pins (Schanz screw)




Safe corridors in external fixation in lower leg –

The tibia can conveniently be divided into three segments –

  1. Knee joint line to the neck of fibula
  2. The neck of fibula to the distal metaphyseal flare
  3. The distal metaphyseal flare to the ankle joint line

Pins or wire can be used for fixation – Half pins (shown as bold arrows), and wire.


At the most proximal level of segment 1, approximately two fingers’ breadth below the knee joint line –

There are two main wire corridors –

  1. The coronal plane wire
  2. The medial face (so called as it parallels the medial subcutaneous face) wire

Half pins (bold arrows) have a wide corridor in this segment – inserted across the palpable anterior surface of the tibial plateau




Segment 2 –

Mid-shaft –

Plane of insertion of half-pins –

Sagittal plane medial to the tibial crest

Perpendicular to the anteromedial surface of the tibia.

Plane of wire insertion –

Medial face wire (from a posteromedial to anterolateral direction) – it goes slightly through gastrosoleus complex – stretch the muscles before inserting the wire.

Coronal plane wire –

Palpate the anterior and posteromedial limits of the subcutaneous surface of the tibia and determine the midpoint—a transverse trajectory from this point in the coronal plane is the position for this wire.

Segment 2 – At the beginning of the metaphyseal flare

Here posterior tibial neurovascular bundle moves from a midline location to posteromedial.

The medial face wire placed a little more anteriorly.


Segment 3 – between the widened metaphysis to the ankle joint –

Two additional wire can be placed other than medial face and coronal plane wire – transfibular and another behind the peroneal tendons but anterior to the lateral edge of the tendo Achilles.

Pins are similar in location, except that the sagittal pin is placed medial to tibialis anterior to avoid injury to ATA.


The hindfoot –

Wire –

One medial wire is placed across the calcaneum posterolaterally just posterior to posterior tibial neurovascular bundle.

Another complementary wire is placed at 45–60°, passing from anterolateral (behind and a little distal to the peroneal tendons) to posteromedial.

Half pins are inserted from lateral to medial in two areas:

  1. The posterior third of the body of the calcaneum (the pin can be inserted from posterior to anterior as an alternative direction)
  2. The neck of the talus




MC causative agent- staph aureus. Others staphylococcus epidermidis and Enterobacter species.

MC causative agent in Sickle cell anemia- Salmonella

MC causative agent in IV drug abuser- Pseudomonas or klebsiella.

Three main routes for spread of osteomyelitis have been described; these are

  1. Haematogenous,
  2. Contiguous and
  3. Direct inoculation.

Haematogenous spread-

Blood-borne organisms, usually bacteria, are deposited in the medullary cavity and form a nidus of infection.

In long bones, the region which is most predisposed to infection is the metaphysis, because it has a large supply of slow-flowing blood.

The metaphysis is also prone to infection because there is discontinuity in the endothelial lining of the metaphyseal vessel walls.

The gaps in the metaphyseal vessels allow bacteria to escape from the bloodstream into the medullary cavity.

In flat bones, the equivalent regions where infection tends to originate are the bony-cartilaginous junctions

Contiguous spread-

Infections originating from soft tissues and joints can spread contiguously to bone.

Direct inoculation-

Direct seeding of bacteria into bone can occur as a result of open fractures, insertion of metallic implants or joint prostheses, human or animal bites and puncture wounds.


Cierny-Mader Staging System of osteomyelitis-

Anatomic type    

Stage 1: Medullary osteomyelitis- involves only medullary cavity

Stage 2: Superficial osteomyelitis- involves only cortex

Stage 3: Localized osteomyelitis- involves both cortical and medullary bone, but not the full thickness

Stage 4: Diffuse osteomyelitis- involves the entire thickness of the bone, with loss of stability, as in infected nonunion.

The Cierny-Mader system adds a second dimension, characterizing the host as either A, B, or C.

A hosts- patients without systemic or local compromising factors.

B hosts- affected by one or more compromising factors.

C hosts – patients so severely compromised that the radical treatment necessary would have an unacceptable risk-benefit ratio.


Osteomyelitis can be divided into acute and chronic stages.

Acute osteomyelitis-

Bacterial proliferation within the bone induces an acute suppurative responseàaccumulation of pus within the medullary cavity leading to raised intramedullary pressure and vascular congestionàdisrupt the intraosseous blood supply.

Reactive bone and hypervascular granulation tissue may form around the intramedullary pus, giving rise to a well-circumscribed intraosseous abscess, also known as a Brodie’s abscess.

The rise in intramedullary pressure may eventually lead to rupture of the bony cortex, producing a cortical defect known as a cloaca.

Intramedullary pus can spread outward through the cloaca and form a subperiosteal abscess. This causes elevation of the periosteum and disrupts the periosteal blood supply to the bone.

Continual accumulation of pus in the subperiosteal space leads to rupture of the periosteum and spread of infection to soft tissues through a channel between the bone and skin surface known as a sinus tract.


Chronic osteomyelitis-

Pathological features of chronic osteomyelitis are a result of osteonecrosis, caused by disruption of the intraosseous and periosteal blood supply during the acute stage of disease.

A fragment of dead infected bone becomes separated from viable bone and is known as a sequestrum.

In an attempt to wall off the sequestrum, an inflammatory reaction characterised by osteoclastic resorption and periosteal new bone formation occurs. The sequestrum becomes surrounded by pus, granulation tissue and a reactive shell of new bone known as an involucrum.


Age-dependent differences-

Mechanism of infection-

Haematogenous spread is the predominant mechanism of infection in children.

Adult osteomyelitis is most commonly caused by contiguous spread from soft tissue infections or direct inoculation.

In adults, haematogenous spread is less common and when it does occur, usually leads to vertebral osteomyelitis.


Intraosseous vascular anatomy-

Below 18 months of age, growth plate is not ossified. Metaphyseal and epiphyseal vessels anastomose via transphyseal vessels that perforate the growth plate. So, osteomyelitis originating in metaphyses can migrate to epiphysis. This may result in slipped epiphyses, growth impairment and joint destruction.


In children older than 18 months of age (18m-16yrs), the growth plate ossifies and forms a barrier between the metaphysis and epiphysis, limiting the spread of infection from the metaphysis.

In adulthood (16yrs), the growth plate is reabsorbed, removing the barrier between the metaphyseal and epiphyseal vessels. These vessels reanastomose, once again allowing spread of infection into the epiphysis and joint space.


Subperiosteal abscess formation-

Subperiosteal abscesses are more common in children than in adults for two main reasons-

In children, the cortical bone is thinner and more easily ruptured, leading to spread of infection from the medullary cavity to the subperiosteal space.

The periosteum in children is also more loosely attached to the surface of the cortex and is easily separated.


Plain radiography-

Low sensitivity and specificity for detecting acute osteomyelitis.

Bone marrow edema, which is the earliest pathological feature, is not visible on plain films.

The features of acute osteomyelitis that may be visible include

A periosteal reaction secondary to elevation of the periosteum

A well-circumscribed bony lucency representing an intraosseous abscess and

Soft tissue swelling.

Regional osteopaenia

Periosteal reaction/thickening (periostitis): variable, and may appear aggressive including formation of a Codman’s triangle

Focal bony lysis or cortical loss

Endosteal scalloping

Loss of bony trabecular architecture

New bone apposition

Eventual peripheral sclerosis

Brodies abscess.

In chronic osteomyelitis, a sequestrum may be visible on plain radiographs as a focal sclerotic lesion with a lucent rim.


Codman triangle– it is a triangular area of new subperiosteal bone that is created when a lesion, often a tumour, raises the periosteum away from the bone.



Other investigations-

CT scan


Bone scintigraphy- 99mTc-MDP (methylene diphosphonate)- delayed bone scan shows increased uptake in affected bone.


  1. what is definition of a propeller flap?

Ans. It’s an islanded flap that reaches its recipient site through axial rotation.

It is different from other pedicled flap as the rotation is Axial around its pedicle.

  1. what is the classification of propeller flap?

Ans . They can be classified according to the type of nourishing pedicle- Tokyo consensus, 2009.

  1. Subcutaneous pedicled propeller flap is based on a random subcutaneous pedicle and allows for rotations up to 90°
  2. Perforator pedicled propeller flap is based on a skeletonized perforator pedicle. This is the most commonly used type of propeller flap and can be rotated up to 180°.
  3. Supercharged propeller flap is modification of the perforator pedicled propeller flap- a superficial or perforating vein of the flap is anastomosed to a recipient vein or an extra artery is anastomosed to a second arterial pedicle of the flap, to increase venous outflow or arterial inflow.

Recently, the “axial propeller flap” has been described that includes propeller flaps based on known vessels (e.g., suprathrochlear artery and lingual artery) and not on a perforator.


  1. Advantages of perforator propeller flaps?


  1. They allow for a great freedom in design and choice of the donor site, based on the quality and volume of soft tissue required and on scar orientation.
  2. They represent a simpler and faster alternative to free flaps and expand the possibilities of reconstructing difficult wounds with local tissues.
  3. Their harvest is easy and fast, provided that appropriate dissection technique is applied.
  4. Donor site morbidity is kept very low, avoiding the sacrifice of any unnecessary tissue.



  1. How to choose best perforator if more than one can be identified?

Ans: Best perforators is identified based on –

  1. Caliber,
  2. Pulsatility,
  3. Course and orientation,
  4. Number and caliber of accompanying veins, and
  5. Proximity to the defect and to a sensory nerve


  1. what is the course of posterior tibial artery?

Ans: The posterior tibial artery (Fig. 551) begins at the lower border of the Popliteus, opposite the interval between the tibia and fibula; it extends obliquely downward, and, as it descends, it approaches the tibial side of the leg, lying behind the tibia, and in the lower part of its course is situated midway between the medial malleolus and the medial process of the calcaneal tuberosity. Here it divides beneath the origin of the Adductor hallucis into the medial and lateral plantar arteries.

Relations.—The posterior tibial artery lies successively upon the Tibialis posterior, the Flexor digitorum longus, the tibia, and the back of the ankle-joint. It is covered by the deep transverse fascia of the leg, which separates it above from the Gastrocnemius and Soleus; at its termination it is covered by the Abductor hallucis. In the lower third of the leg, where it is more superficial, it is covered only by the integument and fascia, and runs parallel with the medial border of the tendo calcaneus. It is accompanied by two veins, and by the tibial nerve, which lies at first to the medial side of the artery, but soon crosses it posteriorly, and is in the greater part of its course on its lateral side.

Branches.—The branches of the posterior tibial artery ar


Posterior Medial Malleolar.




Medial Calcaneal

The peroneal artery -is deeply seated on the back of the fibular side of the leg. It arises from the posterior tibial, about 2.5 cm. below the lower border of the Popliteus, passes obliquely toward the fibula, and then descends along the medial side of that bone, contained in a fibrous canal between the Tibialis posterior and the Flexor hallucis longus, or in the substance of the latter muscle. It then runs behind the tibiofibular syndesmosis and divides into lateral calcaneal branches which ramify on the lateral and posterior surfaces of the calcaneus.

It is covered, in the upper part of its course, by the Soleus and deep transverse fascia of the leg; below, by the Flexor hallucis longus.


  1. what is the course of anterior tibial artery ?

Ans: The anterior tibial artery commences at the bifurcation of the popliteal, at the lower border of the Popliteus, passes forward between the two heads of the Tibialis posterior, and through the aperture above the upper border of the interosseous membrane, to the deep part of the front of the leg: it here lies close to the medial side of the neck of the fibula. It then descends on the anterior surface of the interosseous membrane, gradually approaching the tibia; at the lower part of the leg it lies on this bone, and then on the front of the ankle-joint, where it is more superficial, and becomes the dorsalis pedis.

Relations.—In the upper two-thirds of its extent, the anterior tibial artery rests upon the interosseous membrane; in the lower third, upon the front of the tibia, and the anterior ligament of the ankle-joint. In the upper third of its course, it lies between the Tibialis anterior and Extensor digitorum longus; in the middle third between the Tibialis anterior and Extensor hallucis longus. At the ankle it is crossed from the lateral to the medial side by the tendon of the Extensor hallucis longus, and lies between it and the first tendon of the Extensor digitorum longus. It is covered in the upper two-thirds of its course, by the muscles which lie on either side of it, and by the deep fascia; in the lower third, by the integument and fascia, and the transverse and cruciate crural ligaments.                  2

The anterior tibial artery is accompanied by a pair of venæ comitantes which lie one on either side of the artery; the deep peroneal nerve, coursing around the lateral side of the neck of the fibula, comes into relation with the lateral side of the artery shortly after it has reached the front of the leg; about the middle of the leg the nerve is in front of the artery; at the lower part it is generally again on the lateral side.

Branches.—The branches of the anterior tibial artery are:            6

Posterior Tibial Recurrent.



Anterior Medial Malleolar.

Anterior Tibial Recurrent.

Anterior Lateral Malleolar.




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