Leg defect

History –

Particular of patient-

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

Chief complain-

HOPI-

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

Temp-

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

CNS-

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.

Palpation-

Findings of inspection confirmed on palpation.

Wound is …………X ………..in 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 …..cm 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 ……..cm 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 …………..degree of plantar flexion…………..degree 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 …………..degree of plantar flexion…………..degree of dorsal flexion on right side and ……………..degree of plantar flexion…………..degree 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 –

Investigations-

Routine investigation

PAC fitness

Investigations specific to diagnosis-

Wounds c/s

X-ray

Muscle charting

USG Doppler

CT angiography

Management-

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.

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

4cm

6cm

9-12cm

17-19cm

22-24cm

Laterally-from below upwards

4-10 from lateral malleolus tip

10-13

15-20

5-6cm from fibular head

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.

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

4- Anterior, lateral and superficial posterior, deep posterior

What is the different vessels that supply each compartment?

Anterior – anterior tibial artery

Lateral – peroneal artery

Posterior – posterior tibial artery

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

Ponten described its flap in which specific area of the leg?
superomedial aspect of the leg
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

what’s the blood supply of skin?

Ans: Blood supply of skin is through various plexus –

Subepidermal plexus
Subdermal plexus
Subcutaneous plexus
Suprafascial plexus
Subfascial plexus

These plexus can be supplied by various types of perforators –

Direct cutaneous
Septo-cutaneous
Musculo-cutaneous
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.

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.

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

Limitations-

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)

Skin

Laceration with edges that approximate.
Laceration with edges that do not approximate.
Laceration associated with extensive degloving.

Muscle

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

Arterial

No major vessel disruption.
Vessel injury without distal ischemia.
Vessel injury with distal ischemia

Contamination

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

Bone loss

None.
Bone missing or devascularized bone fragments, but still some contact between proximal and distal fragments.
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

Circular

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)

Clamps

Rods

Safe corridors in external fixation in lower leg –

The tibia can conveniently be divided into three segments –

Knee joint line to the neck of fibula
The neck of fibula to the distal metaphyseal flare
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 –

The coronal plane wire
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:

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

Osteomyelitis-

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

Haematogenous,
Contiguous and
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

MRI

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

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.

what is the classification of propeller flap?

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

Subcutaneous pedicled propeller flap is based on a random subcutaneous pedicle and allows for rotations up to 90°
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°.
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.

Advantages of perforator propeller flaps?

Ans:

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.
They represent a simpler and faster alternative to free flaps and expand the possibilities of reconstructing difficult wounds with local tissues.
Their harvest is easy and fast, provided that appropriate dissection technique is applied.
Donor site morbidity is kept very low, avoiding the sacrifice of any unnecessary tissue.

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

Ans: Best perforators is identified based on –

Caliber,
Pulsatility,
Course and orientation,
Number and caliber of accompanying veins, and
Proximity to the defect and to a sensory nerve

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

Peroneal.

Posterior Medial Malleolar.

Nutrient.

Communicating.

Muscular.

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.

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.

Muscular.

Fibular.

Anterior Medial Malleolar.

Anterior Tibial Recurrent.

Anterior Lateral Malleolar.

July 14, 2019 0

Median Nerve Palsy

Anatomy

Contains fibers from C6,7,8 & T1
Composed of lateral and medial roots from lateral and medical cords respectively

In axilla and arm –

Medial and lateral roots join to form Median nerve on the anterolateral side of 3^rd portion of axillary artery
Courses distally in the medial intermuscular septum on anterior surface of brachial artery at middle level of arm
It then lies medial to brachial artery at level of elbow – here it is below the bicipital aponeurosis and superficial to brachialis muscle
(NO branches in arm)

In cubital fossa –

Nerve passes below bicipital aponeurosis and then continues to pass between two heads of Pronator Teres (Here it is separated by ulnar artery by deep (ulnar) head of PT.
Here it gives off muscular branches and AIN
After which it cross ulnar artery and passes beneath the tendinous band between two head of FDS- to enter the septum between FDS and FDP.
From here it continues in midline of forearm.
About 5cms from flexor retinaculum the nerve appears to lateral edge of FDS
It then lies between tendons of FDS & FCR and beneath tendon of PL before entering carpal tunnel

In the Carpal Tunnel

Nerve becomes palmar to tendons of FDS and lies immediately deep to flexor retinaculum
During travel in tunnel for about 2.5-3.0cm the median nerve becomes large and flattened
At distal edge of retinaculum, nerve divides into ulnar and radial terminal trunks
Radial trunk divides into thenar motor branch and 1^st common digital nerve
Ulnar trunk divides into 2^nd, 3^rd and common digital nerve

Anterior Interosseous Nerve (AIN)

Originates from median nerve 5cm distal to medial epicondyle
Passes between FDP & FPL on interosseous membrane and supplies these two muscles
Further it courses between Pronator Quadratus and interosseous membrane and supplies PQ
It ends in articular branches of wrist
(AIN supplies radial side of FDP used for flexion of index and middle fingers]

Surface marking

In arm

with arm abducted, a line can be drawn from a point on the lateral wall of axilla, just posterior to the eminence of coracobrachialis and passing along medial bicipital groove to a point in the distal portion of cubital fossa

In forearm

With elbow extended, a line drawn from distal end of cubital fossa to point between the tendon of FCR and PL at wrist.
Nerve is found along this line

Motor supply of Median Nerve

FCR

FDS

FDP

FPL

Abductor Pollicis Brevis (APB)

FPB (Superficial head)

Lumbrical – 1^st and 2^nd

AIN – Motor supply to FPL and FDS to index and middle

MCNF – Medial cutaneous Nerve of forearm

LCNF- lateral cutaneous nerve of forearm

RN – Radial nerve sensory branch

MN- median nerve sensory branch

PCNF- posterior cutaneous nerve of forearm (Radial nerve)

Palmar cutaneous branch of median nerve –

– given off from radial side of median nerve

– 8.5cm proximal to the wrist crease

– Courses between FCR and PL

– pierces fascia (antebrachial fascia) 4.5cm proximal to wrist crease

– Reaches the wrist- superficial to flexor retinaculum and divides into several branches to supply thenar eminence and palm- central part

Ques-Low vs High Median nerve palsy?

Ans – Median nerve injury is classified into high or low depending on whether injury is proximal or distal to innervation of forearm muscles.

Function lost:

Low median nerve injury:

Loss of thenar function and opposition

High median nerve injury:

Loss of thenar function and opposition
Loss of FDS to all fingers
Loss of FPL
Loss of index FDP

Functional loss

Loss of oppositional and oppositional pinch
Diminished grip strength
Loss of PT and PQ is compensated by shoulder rotation.
FCR is lost, but wrist function maintained by FCU
Loss of fine motor control and prehension

Sensory loss- is in critical area of hand and palm. For this reason, even if motor recovery is not possible and tendon transfers are required, median nerve should be repaired or reconstructed or sensory transfer in hand considered to restore this critical area of sensibility.

Causes of median nerve palsy

Above elbow:

Brachial plexus injury – Trauma, SOL
Humerus Fracture
Ligament of Struthers compression
Crutch Compression
Sleep palsy
Anterior dislocation of humerus

At elbow:

Compression due to joint effusion
Pronator Teres syndrome
Ventral dislocation of radial head

At forearm:

AIN syndrome
Deep laceration

At Wrist:

Carpal tunnel syndrome
Laceration

Other causes:

Aneurysm
Gout
Diabetes
Thyroid disorder
Pregnancy
Genetics

Median nerve injury Signs

Ape-hand deformity: hyperextended and adducted thumb
Thenar hypotrophy
Pointing index finger: inability to flex index on making fist
Inability to make “OK” sign
Pain, paresthesia, numbness in sensory distribution of median nerve
Loss of opposition
Phallen test and Reverse Phallen test: Patient holds wrist in maximum palmar flexion for up to 2 minutes- this increases pressure on carpal tunnel and provokes paresthesia in the area of median nerve
Maximum extension of wrist provokes similar provocation – Reverse Phallen.

Goal of tendon transfer in median nerve injury

Low median nerve injury- Restoration of thumb opposition
High median nerve injury- above + restoration of FPL and index FDP

Biomechanics of thumb opposition

Trapezio-metacarpal joint- Abduction + Flexion + Pronation [AFP]
(Palmar abduction+ Flexion + Pronation)
Prime muscle of Opposition – Abductor Pollicis Brevis
Aided by FPB and OP

History of Opponensplasty

Steindler – 1^st Opponensplasty (radial slip of FPL)
Cook – used EDM
Ney – FCR or PL to EPB
Huber (1921)- ADM
(Nicolayson- 1922)
Bunnell (1924), Camitz (1929) used PL
Royal and Thomson – Superficialis transfer
Caplan and Aguirre (1956) –EIP

Critical points for tendon transfer

Tendon transfer not to be done in unhealed wound
Tendon transfer not to be done in joint function limitation
Tendon transfer should not pass through scarred tissue, and skin graft or skin incision
Other principles of Tendon transfer should be followed

Prevention and preoperative treatment of contracture:

In median nerve palsy and complete thumb intrinsic paralysis- thumb may adopt supinated and adducted position. Thus 1^st web space contracture can occur.

Prevention:

Physiotherapy – passive thumb abduction and opposition

Splint – Abduction splint

Treatment of established first web space contracture:

Two possible causes

Contracture of skin and deep fascia on its exterior surface
Contracture of dorsal capsule of CMCJ (resists opposition but permits abduction)

Treatment:

Physiotherapy
Splint
Surgical release

Surgical release:

Dorsal web space incision
Fascia over Adductor pollicis and FDI released
Skin is widened with SSG or Flap
Capsule contracture of CMCJ- incision over base of joint
Severe contracture- rotational osteotomy at base of 1^st metacarpal and trapezoidectomy

Pulley formation –

Line of lull of transfer should pass parallel to APB muscle
So, all extrinsic opponensplasties should pass around a stout, fixed pulley in the region of pisiform on ulnar border of wrist
Forearm extensor can pass over ulna or through interosseous membrane
Forearm flexor- pulley created on ulnar border of wrist

Insertion for opponensplasty

Single insertion
Double insertion – one for opposition and other for MP joint stabilization or preventing IPJ flexion

Single insertion is better, following single function principles.

Single insertion

into APB
used in isolated median nerve palsy

Dual insertion

APB insertion + Dorsal MP capsule or thumb extensor expansion
Useful in completely intrinsic minus thumb

Four standard opponensplasty

Superficialis ooponensplasty- Royle Thomson technique or Bunnell technique
EIP (Burkhaulter)
Huber transfer (ADM)
Camitz procedure (PL)

Assessment of outcome of opponensplasty

Sundararaj and Mani –

Excellent – Opposition to ring or little finger with IPJ extended

Good – Opposition to middle or index finger with IPJ extended

Fair – IPJ flexes during opposition

Poor – No opposition restored

Superficialis Opponensplasty

Ring finger FDS is widely used.

Ring FDS harvest:

Royle & Thomson divided FDS tendon at its insertion into middle phalanx
North & Littler- suggested division of FDS through a window between A1 and A2 pulley (before its bifurcation)

Drawback of Royle & Thomson method – dividing FDS at its insertion

Involves lot of dissection in flexor sheath – fibrosis
Destroys vincula – disrupts blood supply to FDP
PIP joint capsule may be damaged – contracture

Benefits of North & Littler method

Avoid injury to flexor sheath and PIPJ capsule
Leaves 3cm of FDS tendon that glides freely within the flexor sheath

Complication of donor digit

DIPJ extension lag
PIPJ fixed flexion deformity
Swan neck deformity

These complications are avoided if FDS is harvested through incision in distal palm

Pulley formation –

Options

Passing FDS around FCU- problem of proximal migration
Distally based strip of FCU (based on its attachment to pisiform)
- Problems
  - Raw surface over FCU- will cause adhesion
  - Radial migration can occur (FCU strip can be attached to ECU tendon to prevent radial migration)
- Angle between distal edge of flexor retinaculum and ulnar border of palmar aponeurosis
- Window in flexor retinaculum

Choosing a site of pulley formation-

Transfer’s line of action passes through –

Pisiform – maximum abduction and opposition but small amount of MCPJ flexion

Distal to pisiform – More thumb flexion, less abduction

Proximal to pisiform – more palmar abduction

Superficialis transfer (Royle & Thompson)

Incision 1: 3cm longitudinal incision at the base of the palm on the medial border of hypothenar eminence.

Ulnar border of palmar aponeurosis exposed and retracted radially.

FDS of ring finger identified, as it emerges from carpal tunnel proximal to superficial palmar arch

FDS of ring finger is then divided through a separate transverse incision (2^nd incision) at base of digit.

FDS then delivered into palmar wound, keeping it ulnar to palmar aponeurosis.

Third incision at dorsum of thumb MP joint.

Subcutaneous tunnel created between this and palmar incision

FDS then passed through this tunnel superficial to palmar aponeurosis and carpal tunnel (and hence acting as a pulley for FDS)

This is then inserted into APB.

Tension of suture –

Should be maximum with thumb in full opposition and wrist in neutral

Postop-Immobilization for 4-6 weeks with thumb in full opposition

Bunnell’s technique

Ring FDS harvested as described above.

Distally based FCU pulley is made- distal portion of FCU exposed and split into 2 – for 4 cm proximal to its insertion at pisiform

One part cut and sutured back onto its base at pisiform- forming a loop

Ring FDS is delivered via the wrist incision and passed through FCU pulley and subcutaneous tunnel into insertion to dorsal thumb

FDS passes over EPL over dorsum of thumb and then passes through a drill hole in the base of PP of thumb in ulnar to radio palmar dissection

Transfers’ tension if set with thumb in full opposition and wrist is neutral.

EIP Opponensplasty

Favored by Burkhaulter

Preferred to superficialis transfer as it does not weaken grip

First Incision: Short incision over dorsum of index MP joint. EIP is divided immediately proximal to extensor hood. (EIP is ulnar to EDC)
Second incision: On the ulnar side of distal forearm on the dorsum. EIP is delivered into this incision (EIP tendon is retrieved out of extensor retinaculum)
Third incision: Over dorsoradial aspect of thumb MPJ
Subcutaneous tunnel then created passing from extensor surface of forearm, passing around ulnar border of wrist, across the palm to reach the incision of thumb
EIP then passed through the tunnel and attached to APB tendon (in case of isolated Median nerve palsy)
Suturing done with thumb in maximum opposition and wrist in 30deg flexion.
In combined median and ulnar nerve palsy, transfer is attached sequentially to APB tendon, MPJ capsule, EPL tendon over proximal phalanx (Riordan).
This attachment restricts IPJ flexion and thus helps FPL flex MPJ more effectively substituting FPB function

Post op: Immobilization in wrist in flexion and thumb in full opposition for 3-4 weeks.

ADM opponensplasty (Huber)

This transfer also improves hands appearance by increasing the bulk of thenar eminence.

Incision: Mid-lateral incision over ulnar border of little finger
Incision extended proximally and radially to distal palmar crease and then incision turns ulnarly across as it crosses the distal palmar crease
ADM divided from its insertion (It has 2 insertions- one at base of Proximal phalanx and second into extensor apparatus)
ADM freed of soft tissue attachments by retrograde dissection towards its origin at pisiform
Pitfall- great care must be taken not to damage this neurovascular pedicle which is on its dorso-radial aspect.
Once neurovascular pedicle is isolated ADM is freed up more proximally elevating its origin from pisiform. While retaining an attachment on the FCU tendon by dissecting a slip of FCU proximally
Next incision- over thumb MPJ dorsoradially
Subcutaneous tunnel created to this area immediately proximal to pisiform
This dissection is easier if done through another incision made in the thenar crease at base of thenar eminence
ADM is then turned 180° on its long axis to reduce tension on its neurovascular pedicle (as if turning page of a book)
ADM passed through subcutaneous tunnel and then attached to APB insertion.
Postop immobilization: Thumb in full opposition for 4 weeks
The position of wrist is not critical as transfer does not cross this joint
Difficult transfer
ADM barely reached APB insertion risk of damage to neurovascular bundle
This is to be done when other opponensplasties are not possible.
Origin of ADM at pisiform may be preserved, but then it will require short tendon graft

Palmaris longus opponensplasty –

Described by Camitz
Simple procedure
Done usually in severe carpal tunnel syndrome – leading to loss of abduction and opposition
Procedure can be performed in regional anesthesia
It restores palmar abduction rather than opposition
Not recommended in traumatic median nerve palsy, as PL may be injured as well.
Transfer usually performed with carpal tunnel release- Abduction is restores till the median nerve recovers

Technique:

PL is confirmed (by opposing the thumb to little finger and flexing the wrist)
Incision – longitudinal incision starting 2cm proximal to distal wrist crease and progressing till proximal palmar crease in line of ring finger
Identify and avoid injury to palmar cutaneous branch of median nerve
PL tendon is freed in forearm- into the palm with 1cm wide strip of palmar aponeurosis
2^nd incision over dorsoradial aspect of MP joint
PL is tunneled into the incision and attached to APB tendon insertion
Suturing done with thumb in full opposition, MP joint extended and wrist in neutral

Post-op immobilization:

Light cast holding wrist in neutral and thumb opposed for 4 weeks.
Followed by night splint for 1 week

Other Opponensplasties

ECU
ECRL
EDM
EPL
FPL

Postop management –

Thumb immobilized in opposition for 3 weeks
For EIP transfer – additional wrist flexion is required in immobilization
For FDS- wrist is kept in neutral
If transfer’s tendon is inserted to APB or extensor mechanism then IPJ is kept in full extension
Splint discontinued after 3 weeks
Splint can be continued for longer period if more complex nerve injury.
Combined high median and ulnar nerve injury, Charcot Marie Tooth disease and Leprosy- Splint for 3 months

Preferred Opponensplasties –

PL for CTS (Carpal Tunnel Syndrome)

EIP for other

ADM when others cannot be done

Outcome

Outcome depends on whether
underlying neurologic pathology is progressive or static
Disability attributable to the isolated loss of opposition
Disability attributable to other problems such as sensory loss or other motor loss (More sensory deficit means less likely benefit from reconstructive surgery)

High median nerve palsy –

Aims of tendon transfer –

Restoration of opposition
Restoration of index finger flexion
Restoration of thumb flexion

Extrinsic donor available

ECRL
ECU
BR

Usual transfer

BR to FPL
ECRL to Index FDP (or side to side suturing to other FDP)
ECU to Opponensplasty

Restoration of Opposition

In high median nerve palsy – EPL, EIP, EDM are more readily available

Restoration of index flexion

Side to side suturing of index FDP and conjoint middle, ring and little finger FDP in distal forearm- this restores index finger flexion but does not restore strength
ECRL to index finger FDP- if independent index flexion is wanted and strength is required on radial side of hand
ECRL to index finger FDP should not be too tight- flexion contracture will occur
Tension should be just adequate that tenodesis effect is not restricted

Restoration of thumb flexion

BR to FPL transfer –

BR needs to be extensively released of soft tissue attachments to achieve good excursion
The tension should not be tight- it should be possible to passively extend all three joints of thumb with wrist flexed
BR transfer warrants 45deg elbow flexion during adjustment of tension
Since BR is an elbow flexor primarily, following the transfer to FPL the thumb flexion is maximally achieved when elbow is extended

Postoperative Splintage

For high median nerve palsy-
- wrist 20° flexion
- Thumb palmar abduction and flexion
- Index in intrinsic plus position (Alone if ECRL to FDP transfer, or all fingers in intrinsic plus position if side to side suturing of FDP tendons done)

(Credits : Dr Anoop S (SR, MCh plastic Surgery, VMMC & SJH, New Delhi). Dr. Rohit M (SR, MCh plastic Surgery, VMMC & SJH, New Delhi)- Illustrations)

June 5, 2019 0

Developmental milestones

Periods of growth

Prenatal period –

Ovum – 0-14 days

Embryo – 14 days to 9 weeks

Fetus – 9 weeks to birth

Perinatal period – 22 weeks to 7 days after birth

Postnatal period –

Newborn – first 4 week after birth

Infancy – first year

Toddler – 1-3 yr

Preschool – 3-6 yr

School age – 6-12 yr

Adolescence –

Early – 10-13 yr

Middle – 14-16 yr

Late – 17-20 yr

Approximate anthropometric values by age
Age	Weight (kg)	Length or height (cm)	Head circumference (cm)
Birth	3	50	34
6 m	6 (doubles)	65	43
1 year	9 (triples)	75	46
2 yr	12 (quadruples)	90	48
3 yr	15	95	49
4 years	16	100	50

Key Gross Motor developmental milestone
Age	Milestones
3 m	Neck holding
5 m	Rolls over
6 m	Sits in tripod fashion (sitting with own support)
8 m	Sitting without support
9 m	Stands holding on (with support)
12 m	Creeps well; walks but fails; stands without support
15 m	Walks alone; creeps upstairs
18 m	Runs; explores drawers
2 yr	Walks up and downstairs (2 feet/step); jumps
3 yr	Rides tricycle; alternate feet going upstairs
4 yr	Holds on one foot; alternate feet going downstairs

Key Fine Motor developmental milestone
Age	Milestones
4 month	Bidextrous reach (reaching out for objects with both hands)
6 month	Unidextrous reach (reaching out for objects with one hand); transfers objects
9 month	Immature pincer grasp, probes with forefinger
12 m	Pincer grasp mature
15 m	Imitates scribbling, makes tower of 2 blocks
18 m	Scribbles, makes tower of 3 blocks
2 yr	Tower of 6 blocks, vertical and circular strokes
3 yr	Tower of 9 blocks, copies circle
4 yr	Copies cross, bridge with blocks
5 yr	Copies triangle, gate with blocks

Key Social and Adaptive Milestones
Age	Milestone
2 m	Social smile (smile after being talked to)
3 m	Recongnizes mother; anticipates feeds
6 m	Recognizes strangers; stranger anxiety
9 m	Waves “bye-bye”
12 m	Comes when called, plays simple ball game
15 m	Jargon
18 m	Copies parents in task (eg sweeping)
2 yr	Asks for food, drink, toilet, pulls people to show toys
3 yr	Shares toys, knows full name and gender
4 yr	Plays co-operatively in a group; goes to toilet alone
5 yr	Helps in household tasks, dresses and undresses

Key Language milestones
Age	Milestone
1 m	Alert to sound
3 m	Cooing (musical vowel sounds)
4 m	Laughs loud
6 m	Monosyllables (ba, da, pa); ah-goo sounds
9 m	Bisyllables (mama, baba, dada)
12 m	1-2 words with meaning
18 m	8-10 word vocabulary
2 yr	2-3 word sentences, uses pronous (I, me , you)
3 yr	Asks questions, knows full name and gender
4 yr	Says song or poem; tells stories
5 yr	Asks meaning of words

Upper age limit for attainment of milestone
Milestone	Age
Visual fixation or following	2 m
Vocalization	6 m
Sitting without support	10 m
Standing with assistance	12 m
Hands and knee crawling	14 m
Standing alone	17 m
Walking alone	18 m
Single word	18 m
Imaginative play	3 yr

Timing of Dentition
Primary dentition	Time of eruption , months		Time of fall, years
	Upper	Lower	Upper	Lower
Central incisors	8-12 m	6-10 m	6-7 yr	6-7 yr
Lateral incisors	9-13 m	10-16 m	7-8 yr	7-8 yr
First molar	13-19 m	14-18 m	9-11 yr	9-11 yr
Canine	16-22 m	17-23 m	10-12 yr	9-12 yr
Second molar	25-33 m	23-31 m	10-12 yr	10-12 yr
Permanent teeth	Time of eruption (in years)
	Upper	Lower
First molar	6-7	6-7
Central incisor	7-8	6-7
Lateral incisor	8-9	7-8
Canine	11-12	10-12
First premolar	10-11	10-12
Second premolar	10-12	10-12
Second molar	12-13	11-13
Third molar	17-21	17-21

Further reading – Essential pediatrics, 8th edition

May 17, 2019 0

DISTRACTION OSTEOGENESIS

Q .What is craniofacial distraction or distraction osteogenesis?

A. It is a technique that applies gradual and incremental traction force onto surgically separated bony segments to produce additional bone

(Distraction Histiogenesis – distraction of skeleton also causes enlargement of overlying and surrounding soft tissues)

History

Codivilla – 20^th Century – Femur elongation following osteotomy

Abbot – 1927- Femur elongation following osteotomy

Ilizarov – popularized the distraction osteogenesis in long (endochondral) bone of extremities for limb lengthening and closure of bony defects

McCarthy – 1989 – Craniofacial distraction

Principles

Terminology –

Distraction Zone: The location of bony separation

Latency period: Duration of reparative callus formation in distraction zone

Activation period: Duration during which distraction forces are applied to callus (for elongation)

Distraction degenerate: The newly formed bone following activation

Consolidation period: Period for which external fixation is maintained in position to allow newly formed bone to consolidate

Rhythm: The rate of activation

0.25 mm four times a day or 0.5 mm two times a day

i.e. Total 1 mm /day

Vector: Direction along which forces are applied

Sequence

Bony separation in two segments (osteotomy or corticotomy)
Latency period (5-7 days)
Activation period
Consolidation period (8 weeks)

Process of distraction starts with –

Performing osteotomy or corticotomy.

After which the distraction device will be applied depending on which direction the bone lengthening is desired (vector of distraction).

Following osteotomy a latency period (usually of 5-7 days) is given for callus formation, before activation of the device.

Following latency period, gradual distraction force is applied to separate the segments and thus elongate the intersegmentary callus – this is the activation period.

After, the desired length of bone has been achieved, the activation is stopped and the distraction device in maintained in position to allow consolidation of the newly formed bone- the consolidation period.

Osteotomy – Full thickness bony separation

Corticotomy – Spares the endosteum or marrow space

The most usually done distraction is – transosteotomy (or transcorticotomy) distraction.

Distraction can be done across a open suture (such as in young patient) – trans-sutural distraction.

Three types of Distraction

Unifocal
Bifocal
Trifocal

Bifocal and Trifocal is across a skeletal defect

Unifocal: Single osteotomy

Distraction forces on either side of osteotomy

Bifocal: Single osteotomy

Transport segment (of bone) spanned across the defect using single distraction device

Trifocal: Two osteotomies used to fill skeletal defect in bidirectional manner

When distracting across a skeletal defect the transport segment has a fibro-cartilagenous

cap which needs to be removed after final “docking” and replaced with bone graft.

Histological Analysis

Latency period: Hematoma formation

Migration of inflammatory cells into osseous gaps (PMNs)

Activation Period: Presence of tapered cells similar to fibroblasts

New blood vessels (endothelial cells)

New fibrovascular matrix (Type 1 collagen)

At Day 14 – Osteoid synthesis and mineralization

At day 21 – Calcification of linearly oriented collagen bundle

Appearance of osteoblasts

Formation of bony spicules

(Linear orientation is parallel to distraction vector)

Four Temporal Zones –

Fibrous central zone – mesenchymal proliferation
Transition zone – osteoid formation
Remodeling zone – osteoclasts
Mature bone zone

Biomolecular analysis

Marked increase in TGF-B1 level

TGF-B1: Activates VEGF & bFGF

Increase collagen deposition and non-collagen ECM proteins

Leading to mineralization and remodeling of bone

Osteoclast migration, differentiation and bone remodeling

Biomechanics

Tensile force applied to developing callus causes elongation of callus.

The mechanical forces are converted to cellular signals – termed as mechanical transduction.

This mechanical transduction is mediated by – Integrin mediated signal transduction

Tensile strain: Defined as amount of elongation as a fraction of original bone length

Eg. 1mm elongation in 1mm osteotomy defect- tensile strain 1/1 = 100%

By day 10 the bone gap will be 10mm

So, tensile strain will be 1/10 = 10%

Maximum tensile strain for bone is 1-2%

So, bone formation does not occur in distraction zone until approx. 4 weeks of activation

i.e. 1/30 = 3%

Mechanical environment in distraction zone depends upon –

Stability of distraction device
Applied distraction force
Inherent physiological loading (muscle action)
Properties of all the local soft tissue

For formation of successful (stable) regenerate –

The distraction device must be stable
Latency period should be adequate (not too short or too long)
Distraction should be gradual
Sufficient time should be given for consolidation

Patient factors that can affect regenerate formation –

Age –

In younger patient – better and faster distraction can be achieved. Latency period in children can be as low as 2-3 day (due to rapid callus formation).

Blood supply – adequate neovascularization should occur to support newly forming bone.

Radiation or chemotherapy – patient receiving RT or CT has poor blood supply and impairs osteogenesis.

[Credits : Dr. Anoop S. (Mch, department of burn and plastic surgery, VMMC & Safdarjung Hospital New Delhi)]

April 28, 2019 1

Reconstruction of acquired lip defects

Anatomy-

Philtral column

Philtral groove/dimple

Cupids bow

White roll- junction of vermillion and cutaneous surface

Tubercle

Commissure

Vermillion – the red/pink dry part of lip seen outside

Vermillion is widest in central lip

Philtrum columns are formed by C/L orbicularis oris fibers.

Philtrum columns slightly diverge as then come down.

White roll created by pars marginalis fibers of orbicularis oris.

Upper lip elevators-

Z. major
Z. minor
LLS AN
LLS
LAO

[levator labii superioris anguli nasalis, levator labii superioris anguli, levator anguli oris]

Retractors and depressor of lower lip-

Platysma
Depressor labii
Depressor anguli oris

Lower lip elevator– Mentalis (makes pout)

Nasolabial crease formed by-

Z. major
LLS
LAO

Orbicularis oris-

Two components-

Pars marginalis
Pars peripherlais

Marginalis anterior to peripherialis [Peripheralis- Posterior]

Marginalis mostly deep to vermillion area

Peripheralis mostly deep to cutaneous portion of lip

Muscular sling that presses lip against gingiva and teeth is formed by-

Orbicularis
Risorius
Buccinator
Pharyngeal constrictor

Blood supply-

Facial artery courses through a plane which between two muscle layers.

Muscles anterior/superficial to artery are-

Risorius,
Z major,
Superficial lamina of orbicularis oris (OO)

Muscles that are deep to the artery are-

Buccinator,
LAO,
Deep lamina of OO

Facial artery branches approx- 1.5cm lateral to oral commissure

Into – superior labial and inferior labial a.

Superior labial- found within 10mm of lip margin

Inferior labial- found within 4-13 mm of lip margin

Labial artery lies within or posterior to orbicularis oris muscle but Never anterior to it.

Nerve supply-

Motor-

Zygomatic and buccal branch – lip elevators and retractors

Marginal mandibular- lip depressor

Sensory-

V2 –infraorbital & V3 mental branch of trigeminal nerve

Etiology of lip defect –

Most common cause is – Carcinoma lip. MC type of cancer is Squamous cell ca.

96% lip cancer occur in lower lip

96% is SCC type.

96% of patients are male.

Reconstruction – defect wise

Vermillion-

Defect by definition does not crosses white roll.

So, reconstruction should – Avoid crossing white roll.

Simplest method—undermining of adjacent oral mucosa with defect closure by advancement.

Wilson & Walker – laterally based bipedical mucosal flap

For Full-thickness defect of vermillion –

-lateral vermillion musculomucosal advancement flap (based on labial artery)

-musculocutaneous flap composed of intraoral mucosa and orbicularis advanced from sulcus in V-Y fashion

Other regional flaps-

Unipedicle vermillion lip switch flap from opposite lip -divided after 10-14 days

Random musculomucosal flap

FAMM flap (facial artery myomucosal flap) – buccinators muscle based on facial artery

Tongue flap (from lateral/lower surface) – two stage procedure cumbersome.

Partial thickness defect-

Primary closure

Advancement flap

Transposition flap

Skin graft not routinely used/required

Except, central philtral defect- full thickness graft used instead of STSG.

Small full thickness defect-

Primary closure-

Lower lip- up to 40% defect

Upper lip- up to 25 % defect

Large full thickness defect-

Two resources to recruit extra tissue to fill the defect – opposite lip & adjacent cheek.

Orbicularis oris- better competent stoma. Microstomia a risk.

Cheek- microstomia less common, functionally and aesthetically inferior outcome

Large central upper lip defect-

Abbe flap (based on inferior labial artery) –> flap division after 2-3 weeks

Abbe flap with perioral crescent

Large central lower lip defect-

B/L Karapandzic

Modified Bernard (Webster- Bernard)

Nasolabial flap

Karapandzic

Bernard

Musculocutaneous rotation advancement flap

Neurovascular flap

First 1cm incision full thickness- after that only skin and muscle divided, mucosa is intact

Burrow’s triangle excised

Lateral advancement flap

First 1cm full thickness incision after that only skin and mucosa intraorally

Burrow’s triangle excised

Interdigitating nasolabial flap

Partial thickness random flap

Full-thickness “Gate-flap”- based on facial a

Full thickness flap denervates upper lip.

Large lateral and commissure defect-

Estlander-

Medially based rotation advancement flap from upper lip to lower lip

Reverse Estlander- from lower lip to upper lip

Gillies-fan flap- rotational advancement flap. A quadrilateral flap

McGregor & Nakajima modified fan flap –

Pivotal flap
Stoma size unchanged
Need for vermillion reconstruction

Abbe-Estlander flap-

Preserves commissure

Need second stage of flap division

Temporary microstomia

U/L Karapandzic

U/L Bernard

U/L Nasolabial flap

Total lip reconstruction-

>80% defect-

B/L Bernard or Nasolabial flap

Submental flap (flap based on submental branch of facial artery)

Radial forearm free flap (RAFF)

Karapandzic – will cause microstomia, so not preferred.

RAFF is the best choice for total lip reconstruction.

Palmaris longus tendon can be harvested along with the flap to be weaved into remaining OO muscle or into modulus.

Lip replantation –

Uncommon

Most commonly – by traumatic amputation by dog bite.

Every attempt should be made for reimplant as the aesthetic and functional outcome is better than free tissue transfer.

Main obstacle in reimplant of lip is – poorly formed labial vein.

Algorithm –

Defect size	Defect location	Reconstructive option
Up to 25% – upper lip Up to 40% – lower lip		Primary closure
25-80 %	Upper lateral lip or lower lateral lip	Lip switch (Estlander/Abbe) or Unilateral Karapandzic/ Bernard/ Nasolabial flap
	Central lower lip	Bilateral Karapandzic/ Bernard
	Central upper lip	Abbe flap +/- perioral crescent
>80%		Bilateral Bernard/ Nasolabial flap or Free tissue transfer – RAFF

(further reading – Grabb and Smith Plastic surgery 7th Ed. chapter 34)

April 25, 2019 0

Radial nerve palsy

Course of radial nerve?

Radial nerve is terminal branch of posterior cord, a continuation of it. It receives supply from C5-T1.

It then descends in front of subscapularis and latissimus dorsi and posterior to axillary artery.

At the level of lower border of teres major it courses posterolaterally and passes through triangular interval (between long head of triceps, teres major and humerus).

It then courses in shallow groove on posterior surface of the humerus – between lateral and medial head of triceps where it gives off branches- muscular and cutaneous.

At level of middle and lower 1/3^rd of arm it penetrates lateral intermuscular septum to enter anterior compartment.

It travels between brachialis (medially) and brachioradialis & ECRL (laterally).

At the level of capitulum of humerus it divides into superficial and deep branches.

Deep branch (PIN) passes between two heads of supinator à wraps around lateral aspect of radius to reach back of forearm. [PIN emerges from supinator approx. 8cm distal to elbow joint]

After emerging from supinator it travels between superficial and deep layer of muscles of extensor compartment i.e. it passes/travels over APL & EPB and under the EDC.

It then courses on the dorsal surface of interosseous membrane underneath the EPL and EIP.

At wrist joint it is almost flattened giving sensory fibers to wrist joint and DRUJ.

Superficial branch –

Courses underneath the brachioradialis.

In the proximal third of foreram – it lies on the supinator

In the distal part it travels sequentially over pronator teres àFDS (radial side) à FPL

In the distal forearm – Approx. 7-8cm proximal to the wrist it emerges between BR & ECRL – pierces the deep fascia.

After emerging from BR it winds around radius. Travels over (crosses) the tendons of APL & EPB.

Passes through anatomical snuff box, over the extensor retinaculum and then divides into four or five dorsal digital nerves.

The branches of radial nerve?

Near axilla –

Medial muscular branches – medial and long head of triceps

Cutaneous branches -Posterior cutaneous n of arm (arises in axilla)

In the groove –

Posterior muscular branches – medial and lateral head of triceps

Cutaneous branches – @ the start of groove (originating almost just after first muscular branches) a branch of radial n penetrates lateral head of triceps and overlying fascia and then splits into these two nerves –

Posterior cutaneous n of forearm

Lateral cutaneous n of arm

Lateral muscular branches – branches given after radial nerve, penetrates lateral I/M septum – BR & ECRL

Branches before entering supinator –

ECRB & Supinator

After emerging from supinator –

Short muscular branches – EDC, ECU, EDM

Two long muscular branches –

Medial – EPL & EIP
Lateral – APL & EPB

Sequence of innervation of muscle by radial nerve?

In order of innervation from proximal to distal (helps in guiding the recovery process) –

BR
ECRL
ECRB ↔ supinator
EDC
ECU
EDM
APL
EPL
EPB
EIP

High or low radial nerve injury?

When injury occur above the elbow there is loss of almost all the function of radial n – this is called high radial nerve injury.

When the injury is distal to the elbow, so that only PIN is injured. In this case innervation to BR, ECRL, ECRB (variable) is preserved and hence wrist extension is preserved. When wrist extension is preserved its called Low radial nerve injury.

The sensory distribution of radial nerve?

In the arm – posteriorly and inferior lateral

In the forearm – posterior

In the hand – radial aspect of half of dorsum of hand, proximal portion of dorsum of radial 3 and ½ finger (excluding the tip)

The deficit that you will notice in radial nerve injury?

In motor loss there will be –

Loss of finger extension at MCPJ
Loss of wrist extension
Loss of thumb extension and abduction
Loss of elbow extension if nerve to triceps if also injured

In sensory, there will be loss noted in –

1^st dorsal web space- also known as the autonomous zone of radial sensory nerve.
Lateral 3 & ½ fingers (except distal phalanx)
Posterior aspect of forearm

Surface marking of radial nerve ?

Mark points –

First point – lateral wall of axilla – lower limit

Second point – junction of upper 1/3rd and lower 2/3rd of line joining lateral epicondyle and insertion of deltoid

Third point – in front of elbow joint below level of LE approx 1 cm lateral to insertion of biceps brachii.

1st point to 2nd point – oblique course in radial groove.

2nd point to 3rd point – anterior compartment course.

In forearm –

4th point – junction of upper 2/3rd and lower 1/3rd of line along lateral border of forearm lateral to radial artery.

5th point – anatomical snuff box

3rd point to 4th point – radial nerve is straight

4th point to 5th point – radial nerve curves backwards.

Planning for nerve injury – nerve exploration vs nerve repair vs tendon transfer?

Nerve grows @ 1mm/day with 30 days of latency period.

In case of closed fracture its prudent to wait till the expected(calculated) time of recovery. Nerve exploration to be done if no recovery seen. if more than 3-6 months has passed from expected time of recovery without any recovery.

If more than 16-18 months has elapsed since time of injury then directly planned for tendon transfer.

When do you time the tendon transfer?

There are two approach for tendon transfer-

“Early” tendon transfer – tendon transfer done simultaneously with nerve repair or before the expected time of reinnervation of muscle.

“Conventional” or late tendon transfer – when reinnervation of most proximal paralysed muscles (BR & ECRL) fails to occur by three months after the expected time of reinnervation.

In early tendon transfer there can be –

“Limited” transfer – which is PT –> ECRB only

Provides for internal splintage (eliminates need for external splintage) while the nerve is recovering,
Provides immediate restoration of power grip (by stabilizing the wrist)
If the nerve recovers it works as a helper by adding power of a normal muscle to innervated muscle.

Complete set of transfer (advocated by Brown) –

This is reasonable approach in case where prognosis of nerve repair is poor –

Nerve gap >4cm
There is large wound or extensive scarring or skin loss over the nerve.

Bevin advocated directly proceeding to tendon transfer without attempting nerve repair – benefit of reduced time of disability. This has not been well accepted.

Historical perspective of development of tendon transfer in radial nerve palsy?

First transfer was described by Franke – FCU to EDC.

Followed by Capellen – FCR to EPL

First complete set of transfer was given by Sir Robert Jones (1906) –

PT –> ECRB & ECRL
FCU –> EDC III-V
FCR –> EPL, EIP, EDC II

He subsequently modified it in 1921 (Jones II) –

And used FCR to additionally to EPB & APL

PT –> ECRB & ECRL
FCU –> EDC III-V
FCR –> EPL, EIP, EDC II, EPB & APL

Starr was firs to use PL to EPL transfer and left one wrist flexor intact.

Zachary convincingly proved that it’s desirable to leave at least one wrist flexor intact.

In 1949, Scuderi refined PL to rerouted EPL transfer.

These studies resulted in what is called “Standard” set of transfer –

PT to ECRB
FCU to EDC II-V
PL to rerouted EPL

Brand proved that FCU should not be used as it is too strong, too short excursion and is prime ulnar stabilizer of wrist. He then, along with Starr described FCR transfer (which was used instead of FCU) –

PT to ECRB
FCR to EDC II-V
PL to rerouted EPL

Boyes reasoned that FCU is a more important wrist flexor to preserve than FCR because the normal axis of movement of wrist movement is dorso-radial to volar-ulnar (a dart-throwing type of movement).

Boyes also reasoned that wrist flexors (FCU & FCR) (33mm) has inadequate excursion compared to finger extensors (50mm), and it’s better to use FDS which has better excursion (70mm).

Boyes described Superficialis transfer –

PT to ECRB & ECRL
FDS IV to EDC
FDS III to EIP & EPL
FCR to APL & EPB.

Aims to achieve by tendon transfer in radial nerve palsy?

Aim is to achieve –

Wrist extension
MCPJ extension
Thumb abduction and extension

The principles of tendon transfer?

One tendon , one transfer
Straight line of pull
Similar amplitude of excursion
Adequate strength (muscle to be transferred should be atleast >85% of its normal strength)
Supple joint
Synergistic muscle
Expendable donor

Example of synergistic muscle – wrist flexor with finger extensor & wrist extensor with finger flexors.

Describe the incision and procedure of FCU set of transfer.

Incision –

First incision – directly over the FCU in distal half of forearm longitudinally. Distal end in J-shaped extension to reach PL.

FCU is transected just proximal to pisiform and freed up as far as possible through that incision.

Second incision – begins 2 cm below the medial epicondyle and angles across the dorsum of proximal forearm directed towards Lister tubercle.

Deep fascia overlying the FCU muscle is incised. Fascial attachments of FCU is completely freed up .

Upper limit of dissection of FCU muscle is 2 inches from its proximal origin where its nerve supply enters.

Third incision – begins on the volar-radial aspect of mid-forearm, passes dorsally around the radial border of forearm in the region of insertion of PT and then angles back on the dorsum.

Tendon of PT is identified in the volar aspect – followed to its insertion on the radius –tendon insertion is freed with a cuff of periosteum around 2-3 cm – muscle tendon unit freed up proximally – PT then transferred around the radius, superficial to BR and ECRL to be inserted to ECRB just distal to musculocutaneous junction .

Through dorsal incision – Kelly’s clamp is passed around the ulnar border to grab FCU and pulled into dorsal wound. (FCU muscle belly may be required to be trimmed if too bulky)

EPL is identified àdivided at its musculotendinous junction à rerouted out of Lister’s canal towards the volar aspect of wrist across anatomical snuffbox à PL transected at the wrist –muscle-tendon unit freed up proximally to allow for straight line of pull.

FCU can alternatively be passed through a window in interosseous membrane.

FCU is sutured to EDC tendons by weaving through all four EDC tendons in end to side fashion at an angle of 45° just proximal to retinaculum.

How will be the tension in tendons adjusted?

1^st suture will be PT to ECRB – to be sutured with wrist in 45° extension with PT in maximum tension.

2^nd suture is FCU to EDC – to be sutured with wrist in neutral position, with FCU in maximum tension with full extension at MCPJ.

After these two sutures – there should be full flexion of fingers with wrist extended and – full extension of digits with wrist flexed.

Final suture is PL to EPL. Both tendons are sutured under resting tension with wrist in neutral position.

Reconstruction is checked again for full movements – finger flexion with wrist extension & finger extension with wrist flexion.

Post-op care following tendon transfer?

Long term splint for immobilization –

Forearm in – 15-30° pronation
Wrist – 45° extension
MCPJ – slight flexion – 10-15°

Thumb in – maximum abduction and extension

Remove sutures after around 6-7 days

Remove cast at 4 weeks – start physiotherapy.

Potential problems after FCU repair?

Excess radial deviation – removing the only remaining ulnar deviator can lead to radial deviation of hand, especially if ECRL is functioning well (PIN only palsy.). this is also more aggravated if PT to ECRL transfer has been done, less so if PT to ECRB transfer.

Solution –

Avoidance – if preoperatively there is already radial deviation present (PIN only palsy) – avoid FCU transfer.

After transfer – reposition ECRL insertion – i) into ECRB; ii) attach PT to ECRB & ECRL and then detach ECRL; iii) detach from 2^nd metacarpal- reroute and inset into 3^rd and 4^th metacarpal bone (Tubiana).

Absence of PL –

Solution – i) Use superficialis transfer; ii) include EPL into FCU to EDC transfer ; iii) include EPL, EPB, APL into FCU to EDC transfer; iv) Use BR (if low radial n palsy) to EPL; v) Use FDS III or IV.

Highlights of Superficialis transfer?

Incision –

Long incision on volar side of the radial aspect of mid-forearm.

Expose PT and ECRB

Remove PT with 2-3 cm of periosteum and interwoven into ECRB.

Exposure of FDS (ring and middle) –

Through transverse incision in distal palm or at base of each finger.

Tendon divided proximal to chiasma- freed up and delivered into forearm.

@ Level just proximal to pronator quadratus, two incision made of size 1 x 2 cm in I/O membrane.

“J-shaped” incision in dorsum of distal forearm –

Transverse limb from radial styloid to ulnar styloid. Vertical limb extends proximally along ulna.

Bring out FDS through I/O membrane. FDS of long finger passed radial to profundus mass and FDS of ring finger passed on ulnar side of profundus mass.

FDS III – attached to EIP & EPL

FDS IV – attached to EDC.

Setting of tension – an assistant holds wrist in 20° extension with fingers and thumb held in a fist, until all transfers are done with reasonable tension.

Transverse incision at base of thumb – free FCR tendon –-> pass it dorsally –-> attach to APL (preferably only to APL or with APL & EPB both).

FCR transfer highlights?

Incision –

Straight longitudinal incision in volar forearm on radial side in distal half b/w FCR & PL.

Both tendons identified, transected near their insertion, freed up to middle of the forearm.

Longitudinal incision on dorsum – extending just distal to retinaculum to mid forearm.

FCR passed around radial border of forearm through subcutaneous tunnel.

EDC tendons are identified and divided at musculotendinous junction – withdrawn distally superficial to intact extensor retinaculum to a point over distal radius and sutured to FCR

Adjusting the tension – wrist and MCPJ in neutral position – FCR sutured in maximum tension.

PT to ECRB & PL to rerouted EPL as described for others.

Nerve transfer option for radial nerve injury.

Median nerve to radial nerve

Fascicles of FDS or FCR to PIN & ECRB.

FDS to ECRB
FCR to PIN

Indications –

Very proximal nerve injury – where proximal stump is not available for repair, or even if available regeneration will take a very long time.
Avoiding an area of scarring
Nerve injury presenting in delayed fashion
Partial nerve injury – presenting with well defined motor function deficit.
Level of injury is unclear (idiopathic, radiation induced injury)

April 1, 2019 0

Foot and ankle reconstruction

Foot and ankle reconstruction is possible with –

Simple reconstruction – 90% cases
Complex flap – 10% cases

Vascular anatomy-

Six angiosomes –

Distal anterior tibial artery – anterior ankle. & The dorsalis pedis artery – the dorsum of the foot
Calcaneal branch of PTA – medial and plantar heel
Calcaneal branch of the peroneal artery (PA) – lateral and plantar heel
Anterior perforating branch of PA – anterolateral ankle
Medial plantar artery – plantar instep
Lateral plantar artery – lateral plantar mid- and forefoot

Plantar heel has dual blood supply –> gangrene of heel means a severe vascular compromise.

Because the foot is an end organ, many arterial-arterial anastomoses provide a duplication of inflow (provides a margin of safety) –

Arterial-arterial anastomoses around the foot and ankle-

Between anterior perforating branch of the peroneal artery and anterior tibial artery

via the lateral malleolar artery @ ankle joint

Dorsalis pedis artery with lateral plantar artery

via direct connection @ Lisfranc joint as the DPA dip in 1^st interspace

This vascular loop is critical in determining the direction of flow within the anterior or posterior tibial arteries.

Between plantar and dorsala metatarsal arteries – via proximal and distal perforators.

(Proximal perforators are at Lisfranc joint, distal perforators are at digital web space)

Posterior tibial artery and peroneal artery are directly connected

(Deep to the distal Achilles tendon by one to three connecting arteries)

Motor and sensory anatomy –

Sciatic nerve –> Tibial nerve &

Common peroneal nerve –> deep peroneal nerve &

Superficial peroneal nerve

Tibial nerve –

Innervates muscle of deep and superficial posterior compartment (except gastrocnemius)

Tibial nerve trifurcates deep to flexor retinaculum into –

Calcaneal nerve
Medial plantar nerve
Lateral plantar nerve

All these nerve supplies all intrinsic muscles of the foot (except Extensor digitorum brevis, EDB).

Deep peroneal nerve –

Innervates extensor muscles in the Anterior compartment and then EDB.

Superficial peroneal branch –

Innervates the everting peroneal muscles of the lateral compartment

And then it pierces the fascia to become subcutaneous and provide sensibility to the lateral lower leg and dorsum of the foot.

Sensory supply –

Superficial peroneal nerve (L4, 5, and S1) –

Anterolateral skin in the upper third of the leg

It becomes subcutaneous approximately 10 to 12 cm above the lateral ankle and travels anterior to the extensor retinaculum to supply the dorsum of the foot and skin of all the toes.

Except the lateral side of the fifth toe (sural nerve) and the first web space (deep peroneal nerve).

Deep peroneal nerve (L4, LS. and S1) –

Exits the anterior compartment deep to the extensor retinaculum.

Supply and ankle and mid-foot joints, sinus tarsi, and the first web space.

The sural nerve (LS and S1) –

Provides sensibility to the posterior and lateral skin of the leg’s distal third and

The skin of the dorsolateral foot and fifth toe.

Posterior tibial nerve –

Has three branches in the tarsal tunnel –

Calcaneal branch (S1 and S2) – supplies the medial aspect of the heel pad

Lateral plantar nerve (51 and 52) supplies the lateral two thirds of the sole and the fifth and lateral fourth toes

Medial planter nerve (L4 and L5) supplies the medial one third of the sole and the first; second, third, and medial fourth toes.

Wound comorbidities-

Diabetes-

Lifetime risk of ulcer in diabetic – 15%

Major cause of diabetic foot wounds – Diabetic peripheral polyneuropathy.

>80% of diabetic foot ulcers arise in the setting of neuropathy.

↑Sorbitol level intra-neurally –> principle mechanism of nerve damage.

Damaged nerve swells –> in tight anatomical compartment this can cause further damage —- “Double crush syndrome”

This can be partially reversed by nerve release surgery.

↑ Glucose –> ↑ Advanced glycosylated end products –> causes microvascular injury.

↓insulin and ↓neurotrophic factors –> ↓ed maintenance or repair of nerve.

All these factors lead to peripheral neuropathy.

Other potential causative factor of peripheral neuropathy –

Altered fat metabolism,
Oxidative stress, and
Abnormal levels of vasoactive substances such as nitric oxide

Diabetes and infection –

↑ Glucose –> diminished ability of PMNs to destroy bacteria

Diminished ability to coat bacteria with antibiotics

Diabetics are especially prone to – Streptococcus and Staphylococcus

In patient with diabetic neuropathy – 80-95% of amputation are preceded by non-healing ulcer.

Arterial disease (usually located in infra-popliteal region) significantly increases risk of ulceration and amputation. Arterial disease is present in 50% cases of diabetic foot ulcers.

Although peripheral vascular disease is frequently present, peripheral neuropathy is the primary cause of foot wounds in the diabetic population.

Neuropathic Changes –

Autonomic neuropathy – loss of pseudomotor function –> anhydrosis and hyperkeratosis –> fissuring of skin –> infection.

Charcot deformities (neuroarthropathy) of the joints – 0.1% – 2.5% of diabetic population

MC joints involved – tarsometatarsal joints 30% = metatarsophalangeal joints 30% > intertarsal joints 24%> IP joints in 4%

Possible etiology –

Neurotraumatic – joint collapse from damage that has accumulated because of insensitivity to pain.
Osteopenia triggered by abnormalities in the RANK1/RANK-ligand/osteoprotegerin system.

Pathogenesis –

Ligamentous soft-tissue injury + Synovitis + Effusion –>

Distention of the joint capsule leads to –> ligament distortion, resulting in joint instability –>

Articular cartilage erosion, with debris being trapped within the synovium.

(These changes occur due to continued use of limb due to lack of pain sensation)

Collapse of the medial longitudinal arch –> Altered biomechanics of gait –>

Heterotopic bone formation and eburnation of load-bearing surfaces

Causes overload specific parts of the foot –>

Increased focal stress –> ulceration, infection, gangrene, and limb loss.

Motor component of neuropathy –

Intrinsic foot muscle becomes atrophied and fibrotic –> leads to MTPJ extension and IPJ flexion –> excessive pressure on metatarsal head and end of toes.

Ischemia –

Atherosclerotic disease is a common cause of non-healing foot ulcers.

Hypercholesterolemia, hypertension, and tobacco use are additional risk factors.

Other causes of ischemia in the foot –

Thromboangiitis obliterans (Buerger disease, generally seen in young smokers),
Vasculitis,
Thromboembolic disease.

Before planning revascularization procedure – MUST accurately diagnose which angiosome ulcer belongs to.

If the affected angiosome is directly revascularized – wound healing increases by 5O% and the risk of major amputation decreases fourfold.

Site of ulcer	Arteriosome to be revascularized
Dorsum of the ankle and foot	Anterior tibial artery or dorsalis pedis (posterior tibial artery- If connection b/w the dorsalis pedis and the lateral plantar artery is intact)
Heel ulcers	Posterior tibial artery or Peroneal artery
Mid- and forefoot plantar wounds	Posterior tibial artery (Dorsalis pedis – If connection b/w the dorsalis pedis and the lateral plantar artery is intact)

If the ideal vessel is not available – >15% chance of failure

Patient with significant peripheral vascular disease presents with gangrene – the timing of revascularization versus debridement is critical –

Stable dry gangrene without cellulitis – revascularization first.

Wet gangrene with or without cellulitis – wound debridement first followed by revascularization urgently.

Following revascularization –> wound coverage attempted only when wound shows signs of healing (appearance of new, healthy granulation tissue and neoepithelialization).

Wound healing starts to occur by 4 – 10 days following bypass and 4 weeks following endovascular procedure.

Connective Tissue Disorders-

CTD causes recalcitrant vasculitis ulcers.

e.g., systemic lupus, rheumatoid arthritis, and scleroderma

Treatment includes – steroids and immunosuppressive agents.

Wound-retarding effects of steroids are mitigated with oral vitamin A (10,000 U/d while the wound is open). Topical vitamin A is also effective.

Almost half of patients with vasculitic ulcers also have coagulopathy leading to a hypercoagulable state.

MC are – antithrombin III, Leiden factor V, protein C, protein S, and homocysteine.

Investigation should include a – coagulation profile.

Treatment of these ulcers is principally medical.

Underlying abnormalities are identified and corrected. Wound healing adjuncts are used to cause healing.

Evaluation and diagnosis of the wound –

Etiology of foot and ankle wounds is often traumatic.

MC systemic comorbidities –

Diabetes,
Peripheral vascular disease,
Venous hypertension
Connective tissue disorders

(Accompanying disease processes include infection, ischemia, neuropathy, venous hypertension, lymphatic obstruction, immunologic abnormality, hypercoagulability, vasospasm, neoplasm, self-induced wound).

Diagnostic Studies-

History –

Etiology,
Duration
Previous treatment of the wound(s),
Comorbid conditions
Current medications,
Allergies
Nutritional status
Assess the patient’s current and anticipated level of activity

If patient likely to used limb and procedure medically tolerable and technically feasible then plan – Limb salvage.

Otherwise – consider amputation.

Physical examination –

General physical examination

Examine wound – length, breadth, depth

Examine tissue involved – epithelium, dermis, subcutaneous tissue, fascia, tendon, joint capsule, and/or bone

(If bone can be felt through wound with metal probe, it is most likely to be involved.)

(Diabetic ulcer >2 cm² –> 90% chance of underlying osteomyelitis)

Assess vascular status – PTA , DPA. If these are palpable then the blood supply is adequate.

If not palpable –> Doppler should be used.

Doppler findings-

Triphasic flow – indicates excellent blood £low
Biphasic sound – indicates adequate blood flow
Monophasic sound – warrants further investigation

(Monophasic tone does not necessarily reflect inadequate blood flow.)

If the pulses are non-palpable or monophasicà noninvasive arterial Doppler studies are done.

PVRs (pulse volume recordings) at each level is obtained –

PVR amplitude <10 mmHg – indicates Ischemia.

Toe arterial pressure is <30 mm Hg – indicates ischemia

Tissue oxygen pressure levels <40 mm Hg – insufficient local blood flow to heal a wound.

Skin perfusion pressure <50 mm Hg – indicates insufficient blood flow to heal a wound.

If all these noninvasive tests suggest ischemia –> an arterial imaging study is obtained to decide – whether a vascular inflow and/or vascular outflow procedure is required.

The gold standard for revascularization- bypass surgery.

Endovascular techniques are also very effective in treating stenosed or obstructed arteries by dilation, recanalization, or atherectomy with or without stenting. These are also less invasive than bypass surgery.

Sensory examination-

Performed with a 5.07 Semmes-Weinstein filament that represents 10 g of pressure.

If patient cannot feel the filament –> protective sensation is absent

Vibration sensation tested using 128-Hz tuning fork

Pinprick sensation, or

Ankle reflexes

Motor examination –

Looking at the resting position of the foot

Strength and active range of motion of the ankle, foot, and toes.

Bone architecture –

Evaluate if the arch is stable, collapsed, or disjointed.
Look for bony prominences.
X-ray series of foot- AP, Lateral, Oblique.
X-ray appearance of osteomyelitis lags behind the clinical appearance by up to 3 weeks.
Earlier detection of osteomyelitis- best by MRI.
MRI also differentiates between osteomyelitis and Charcot collapse.
Bone scans are of no value in evaluation of osteomyelitis when there is an ulcer present (as increased uptake will be seen due to ulcer).

Evaluate Achilles tendon –

If the ankle cannot be dorsiflexed 10° to 15° beyond neutral –> the Achilles tendon is tight.

If the patient cannot dorsiflex his or her foot with the knee bent or straight –>

Both the gastrocnemius and soleus portions of the tendon are tight.

If the patient can dorsiflex his or her foot only when the knee is bent –>

Then the gastrocnemius portion of the Achilles tendon is tight.

Preparing the Wound for Reconstruction –

Goal of treating any wound is to promote healing in a timely fashion.

First step – establish a clean and healthy wound base.

Acute wound is defined as a recent wound that has yet to progress through the sequential stages of wound healing.

Chronic wound is a wound that is arrested in one of the wound-healing stages (usually the inflammatory stage) and cannot progress further.

Acute wound –

Wound is usually well vascularized.

Simple debridement f/b

Immediate closure or NPWT

Chronic wound (aims to convert it to acute wound)–

Correction of medical abnormalities
Restoration of adequate blood flow,
Antibiotics if infection is present,
Aggressive debridement of the wound
Debridement includes removal of the senescent cells along the edge of the wound (3 to 4 mm of the wound edge)

If the wound responds this therapy –

Healthy granulation appears,
Edema decreases, and
Neoepithelialization appears at the wound edge

Negative-pressure wound therapy (NPWT) is a useful post-debridement dressing for the uninfected, well-vascularized wound – it accelerates the formation of granulation tissue, decreases wound edema and keeps the bacterial countdown.

Measuring the wound area weekly to monitor progress – the rate of normal healing is a – 10%-15% decrease in surface area per week.

At this stage, if the wound healing is not as per expected rate – adjunct to wound healing (such as growth factors, cultured skin, and/or hyperbaric oxygen) can be used.

Surgical debridement-

Must be done thoroughly.

It is mostly under-performed – leaving dead or infected tissue or bone leads to persistent infection.

Biofilm is present in over 90% of chronic wounds. It penetrates every aspect of the wound and can be found up to 4mm deep to its base (as it spreads along the perivascular plane of arterioles feeding the wound bed).

Debridement should be considered complete only when normal bleeding tissue remains.

Colors of the tissue can be used as a guide for debridement –

Muscle – red/pink, contracting
Fat – yellow
Bone, tendon, fascia – white

Debridement should be done till such normal appearing tissue are reached.

Debridement can also be aided by painting the base of wound with blue dye and then removing all the painted tissue.

Sequential removal of thin layers of tissue till the normal tissue is reached – is the most effective way of debridement.

Skeletal fixation –

Stabilizing – by splinting or external fixation (monoplanar frame or Ilizarov frame).

llizarov frame provides superior immobilization, allows for bone transport, and minimizes the risk of pin track infection because of the thin wire pins.

Tissue culture – Deep uncontaminated tissue cultures pre- and postdebridement should be obtained during the initial and subsequent debridement to guide antibiotic therapy.

Effective dressings should be done following debridement.

Clean and well vascularized – a moist dressing or NPWT.

Suspected unclean wound – dressing with topical antibiotics and/or biocides

Biologic debriding agents -maggots are useful in patients too ill for anesthesia.

Maggots consume all bacteria (antibiotic resistant also VRE, MRSA), as well as biofilm.

After initial debridement to clean the tissue – its important to keep the wound clean – i.e. prevent biofilm from reestablishing itself, prevent a subsequent buildup of metalloproteases (MMPs destroy the naturally produced growth factors) à this is done by – regular scrubbing or wet-to-dry dressing.

If the wound still doesn’t heals even if bed is healthy and vascularity is good then next step is adding – local wound healing growth factors such as PDGF or cultured skin or inert dermis.

Level-one evidence has demonstrated that systemic hyperbaric oxygen can also be used to convert a non-healing wound into a healthy granulating wound.

When wound shows signs of healing (healthy granulation tissue, neoepithelialization at the skin edge) – then its appropriate to close the wound (not before).

Reconstructive techniques –

Lower Leg and Ankle Flaps-

Lower leg muscles are poor pedicled flaps as most of them are type 4 muscles (segmental minor arterial pedicles).

Muscle of leg	Distance up to which defect can be closed
EHL	As distal as 2 cm from medial malleolus
Extensor digitorum longus Peroneus tertius	As distal as 2 cm from medial malleolus
Peroneus brevis	As distal as 4 cm from medial malleolus
Flexor digitorum longus	As distal as 6 cm from medial malleolus
Soleus muscle (type 2 muscle)	anterior lower leg defects as distal as 6.6 cm above the medial malleolus

Local Muscle flaps are not frequently used in lower leg, ankle and foot –

For defect that are small in size fasciocutaneous flap are better – better coverage without loss of function.

For large defects – free flaps are better.

Fasciocutaneous flaps are useful for reconstruction around the foot and ankle (the donor site always requires skin grafting).

Retrograde peroneal flap –

Useful for ankle, heel, and proximal dorsal foot defects.
Blood flow is retrograde.
Similarly retrograde anterior tibial artery fasciocutaneous flap can be used.
Both peroneal and anterior tibial artery can be isolated as a perforators (saving the main arteries).

Retrograde sural nerve flap –

Neurofasciocutaneous flap

Useful for ankle and heel defects.

Receives retrograde flow from a peroneal perforator 5cm above the lateral malleolus.

Artery first courses above the fascia and then penetrates deep to the fascia at mid-calf.

A common problem with the flap is venous congestion- problem with venous drainage.

Venous congestion – can be minimized if the pedicle is harvested with 3 cm of tissue on either side of the pedicle and with the overlying skin intact.

Venous congestion – can be minimized – if the flap is delayed, 4 to 10 days earlier, by ligating the proximal lesser saphenous vein and sural artery.

Inset of flap is critical to avoid kinking of the pedicle.

Splinting is necessary to avoid pressure on the pedicle.

Major donor deficit – the loss of sensibility along the lateral aspect of the foot.

Depression at donor site can be problematic if patient subsequently requires BK amputation.

Donor site deficit can be minimized if the flap is harvested as a perforator flap.

Supramalleolar flap –

Used for lateral malleolar, anterior ankle, and dorsal foot defects.
Harvested either with the overlying skin or as a fascial layer.
Donor site can be closed primarily.
Flap reach is limited, but can be expanded by applying delay approach.

Foot flaps –

Muscles in foot are – type 2.

Useful for coverage of relatively small defects.

ADM –

Coverage of small mid- and posterior lateral defects of the sole of the foot and lateral distal and plantar calcaneus.

Dominant pedicle is medial to the muscle’s origin at the calcaneus and the muscle has a thin distal muscular bulk.

AHB –

Larger muscle than ADM

Used to cover medial defects of the mid- and hindfoot, medial distal ankle.

Dominant pedicle – is at the takeoff of the medial plantar artery

Flexor digiti minimi brevis –

Small muscle

Used to cover defects over the proximal fifth metatarsal

lt receives its dominant pedicle at the lateral plantar artery takeoff of the digital artery to the fifth toe.

Flexor hallucis brevis –

Can be raised on a longer pedicle as an island flap on the medial plantar artery – can reach up to proximal ankle.

EDB muscle –

Very little bulk.

Can be used for local defect over sinus tarsi or lateral calcaneum.

FDB –

Used to cover plantar heel defects.

Medial plantar flap –

Most versatile flap of the foot.

Ideal tissue for coverage of plantar defects.

It can also reach medial ankle defects.

Can be harvested to a size as large as 6 cm x 10 cm.

It is a sensate flap.

Has a wide arc of rotation if harvested till proximal part of medial plantar artery.

Flap can be raised on either of – deep or superficial branch of MPA.

Flap is easier to raise on deep branch, but raising the flap on superficial branch disturbs less of blood supply of foot.

When harvested with retrograde flow – it is based on the deep branch of the medial plantar artery.

Lateral calcaneal flap –

Useful for postetior calcaneal and distal Achilles defects.
Length of the flap can be increased by harvesting it as an L-shaped flap. L-shaped extension below and posterior to lateral malleolus.
It is harvested with sural nerve and saphenous vein.

Dorsalis pedis flap –

Can be either proximally or distally based
Used for coverage of ankle and dorsal foot defects.
Width of flap >4cm require skin grafting for closure
Now rarely used – exposes vulnerable extensor tendons, and vascular structures.

Filet of the toe flap –

Useful for small forefoot web space ulcers and distal forefoot problems

Reach of the flap is always less than expected.

The technique involves removal of the nail bed, phalangeal bones, extensor tendons, flexor tendons, and volar plates while leaving the two digital arteries intact.

A variation is the toe island flap, where a part of the toe pulp is raised directly over the ipsilateral digital neurovascular bundle and then brought over to dose a neighboring defect.

Treatment Options –

Guiding principle – coverage of a wound should be performed as quickly and efficiently as possible.

Once the wound is clean and well vascularized – one of the following technique is used for reconstruction –

Healing by secondary intention
Wound closed primarily
Split- or full-thickness skin graft and or neodermis is applied
Local random flap is transposed or advance
Pedicled or island flap
Microvascular free flap

Biomechanics of foot should be taken care during reconstructive procedure – which may require- bone rearrangement, partial joint removal or fusion, or tendon lengthening or transfer.

Method of soft-tissue reconstruction depends on –

Patient’s medical condition,
Surgeon’s experience,
Size of the wound,
Vascular status of the foot.
Exposed structures (tendon, joint And or bone), and
Access to the wound (i.e., an ilizarov frame limits the access to the foot)

Any procedure chosen aims for – restoration of a biomechanically sound foot (to prevent recurrent breakdown).

No tendon, joint, or bone involved –> Simple coverage (secondary intention, delayed primary closure, or simple skin graft and/or neodermis).

Even some of the complex wound with exposed tendon, bone or joint can be managed by wound care and then simple coverage – With NPWT, granulation tissue forms over tendon, bone, or joints.

It is critical to immobilize the wound over a moving joint and to offload the wound (to prevent shearing forces from disrupting the healing process).

More than 85% of all wounds can be dosed by simple techniques, while less than 15% require flaps.

Delayed primary closure – is planned once edema has subsided. NPWT is helpful in reducing edema.

In some region wound may heal by simpler method but can result in problematic with normal activity – such as over a joint, plantar foot and posterior heel – soft tissue is a better option.

Most foot and ankle wounds – can be closed by skin grafting.

Healthy granulating bed is the necessary prerequisite for STSG.

If the granulation bed contains bacteria/biofilm – it should be removed before placing the skin graft.

Wound can be then pulse lavaged and then skin grafted with 1:1 meshing.

NPWT can be used on low continuous suction as a temporary dressing for the first 3 to 5 days – helps absorb excess fluid and ensure fixation of the skin graft to the underlying bed and minimizes possible skin graft-recipient bed disruption from shear forces.

Ideal graft donor site for a plantar wound is – the glabrous skin from the plantar instep.

Flaps for foot reconstruction should be accurately assessed – vascular pedicle should be dopplerable.

Local flaps are useful for coverage of foot and ankle defect because they only need to be large enough to cover the exposed tendon, bone, or joint while the rest of the wound is skin grafted.

Local flaps and their variation are most commonly used to cover lower leg and foot defect – because pedicled, perforator or free flaps are difficult to plan due to access problem in patient having external fixators.

Pedicled flaps are more difficult to dissect, have higher perioperative complication rate but equally good long-term success as free flaps.

Free flaps in the foot and ankle carry the highest failure rate of free flaps in any anatomic location – most probably because the anastomosis is near zone of trauma.

Postsurgical Care –

No weight bearing for 6 weeks if plantar surface is involved.

Offload specific parts.

Reconstructive options by location of defect –

Forefoot Coverage –

Toe ulcers and gangrene – limited amputation

Ulcer under metatarsal head causes –

Principal abnormal biomechanical force is a tight Achilles tendon.
Bony abnormality (plantar-prominent metatarsal head)
Ulcer present without any abnormality

Patient cannot dorsiflex his or her foot with the knee bent or straight –> both the gastrocnemius and soleus portions of the tendon are tight.

If the patient can dorsiflex his or her foot only when the knee is bent –> only the gastrocnemius portion of the Achilles tendon is tight –> in this case gastrocnemius recession should correct the problem.

In addition the posterior capsule of the ankle joint may be tight.

Treatment require release of Achilles tendon and if it foot still does not dorsiflex then additional posterior capsular release is performed.

Release of the Achilles tendon –> forefoot pressure drops dramatically and if underlying bone is not involved forefoot ulcer within 6 weeks post release.

The lengthening of a tight Achilles tendon has decreased the ulcer recurrence rate in diabetics by half at 2 years.

Patient has normal ankle dorsiflexion, but bony abnormality causing planter ulcer –

Plantar-prominent metatarsal head –> the affected metatarsal head is elevated with osteotomies and internal fixation. The metatarsal head is shifted 2 to 3 mm superiorly –> pressure is relieved –> ulcer to heal by secondary intention.

Ulcer without any bony abnormality –

Small size – heals by secondary intention.

Large ulcer with metatarsal head and shaft involvement –> single metatarsal involved – Ray amputation.

If ulcers are present under several metatarsal –> pan-metatarsal head resection

If >2 toes with the accompanying metatarsal heads have to be resected –> then a trans-metatarsal amputation.

While doing trans- metatarsal amputation – maintain normal parabola of with the second metatarsal being the longest.

Equinus deformity can result –> to prevent this –> extensor and flexor tendons of 4^th & 5^th toe is tenodesed with the ankle in the neutral position and/or the Achilles tendon lengthened.

The most proximal forefoot/distal midfoot amputation is – Lisfranc amputation where all the metatarsals are removed. To prevent equinus deformity – anterior tibial tendon is split and lateral aspect inserted on to cuboid bone. Also, achillis tendon is lengthened.

Post-operatively foot is placed in neutral position, until wound heals.

Midfoot coverage –

Defect on medial aspect (non-weight bearing area) – treated with SSG.

Small defects – V -to-Y flap, the bilobed flap, the rhomboid flap, and the transposition flap, pedicled abductor hallucis flap medially or an abductor digiti minimi flap laterally.

Slightly larger defects – large V-to-Y flaps, random, large, medially based rotation flaps, pedicled medial plantar fasciocutaneous flap.

Larger defects – free muscle flaps covered by skin grafts.

Ulcers in midfoot are usually caused by Charcot collapse of the mid foot plantar arch –

If the underlying fragmented bone has healed and is stable (Eichenholz stage 3) à then the excess bone is shaved à the ulcer heals by secondary intention or is covered with a glabrous skin graft or a local flap.

If the midfoot bones are unstable (Eichenholz stage 1 or 2) à then bone is excised using a wedge excision and the arch reconstituted by fusing the proximal metatarsals to the talus and calcaneus.

Hindfoot Coverage –

Among the most difficult of all wounds to treat.

Usually also reflect severe vascular disease.

They are result of the patient being in a prolonged decubitus position.

Partial calcanectomy (preferably vertical) – can create soft tiisue to cover defect.

Collapsed bone or bone spur can cause ulcer – needs to be shaved.

Distally based V-to-Y flap or larger medially based rotation flaps.

Plantar heel defects – pedicled flaps –

Medial plantar fasciocutaneous flap
Flexor digiti minimi muscle flap
Extended lateral calcaneal fasciocutaneous flap
Retrograde sural artery fasciocutaneous flap

Large defect – free muscle flap with SSG.

Underlying bone – if osteomyelitis – bone needs to be debrided.

Hindfoot amputations –

Chopart – leaves an intact talus and calcaneus while removing the mid- and forefoot bones of the foot

Symes – tibia and fibula are cut just above the ankle mortise and the deboned heel pad is anchored to the anterior portion of the distal tibia to prevent posterior migration.

Symes amputation is done if –

There is insufficient tissue to primarily close a Chopart amputation.
There is insufficient arterial blood supply for a free flap, or
If the talus and calcaneus are involved with osteomyelitis.

Dorsum of the Foot –

Most wound treated with – SSG

Small local flaps

EDB muscle flap works well for sinus tarsi defects.

Supramalleolar flap can be used over the lateral proximal dorsal foot.

Larger defect – free fasciocutaneous flap eg. Free radial forearm flap with palmaris tendon to reconstruct extensor tendons.

Ankle Defects –

If wounds granulating – SSG.

NPWT can be used to promote granulation.

Local flaps can be used to cover critical areas (tendon, bone or joint) while rest of area can be skin grfted.

Local flaps – rotation or transposition flaps based on posterior tibial and peroneal arterial perforators.

Pedicled flaps –

Supramalleolar flap,
Retrograde sural artery flap,
Medial plantar flap,
Abductor hallucis muscle flap,
Abductor digiti minimi muscle flap,
EHL, and
EDB muscle flap.

January 29, 2019 0

Muscle attachments

Trapezius –

Origin –

Medial third of superior nuchal line
External occipital protuberance
Nuchal ligament
Spinous process of C7 to T12

Insertion –

Lateral third of clavicle
Acromian process
Spine of scapula

Innervation –

Spinal accessory nerve (CN 9)
Cervical nerves C3-C4

Movement –

Descending part – elevates scapula
Transverse part – retracts scapula
Ascending part – depresses scapula
Descending and ascending working together – superior rotation of scapula

Pectoralis major –

Origin –

Clavicular head – anterior surface of medial half of clavicle
Sternocostal head – anterior surface of sternum, superior six costal cartilages
Abdominal part – aponeurosis of external oblique

Insertion –

Crest of greater tubercle of intertubercular sulcus (lateral lip of bicipital groove)

Innervation –

Lateral and medial pectoral nerves

Action –

Adducts and medially rotates humerus
Draws scapula anteriorly and inferiorly
Clavicular head alone – flexes humerus
Sternocostal head alone – extends humerus from flexed position.

Pectoralis minor –

Origin –

3^rd to 5^th ribs near their costal cartilages

Insertion –

Medial border and superior surface of coracoid process of scapula.

Innervation –

Medial pectoral nerve (C8-T1)

Function –

Stabilizes scapula by drawing it inferiorly and anteriorly against chest wall

Serratus anterior –

Origin –

External surface of lateral part of 1^st to 8^th-9^th ribs

Insertion –

Anterior surface of medial border of scapula

Innervation –

Long thoracic nerve (C5, 6, 7)

Action –

Protracts scapula and holds it against thoracic wall
Rotates scapula

Latissimus dorsi –

Origin –

Spinous process of inferior six thoracic vertebrae (T7-T12)
Thracolumbar fascia
Iliac creast
Inferior 3 or 4 ribs

Insertion –

Intertubercular sulcus (bicipital groove) of humerus

Innervation –

Thoracodorsal nerve (C6-8)

Action –

Extends, adducts and medially rotates humerus

Rectus abdominis –

Origin –

Pubic symphysis and pubic crest

Insertion –

Xiphoid process and 5^th -7^th costal cartilages

Innervation –

Thoracoabdominal nerves and anterior rami of inferior thoracic nerves

Action –

Flexes trunk and compresses abdominal viscera.

Gracilis –

Origin –

Body of pubis and inferior pubic ramus

Insertion –

Superior part of medial surface of tibia

Innervation –

Obturator nerve

Action –

Adducts thigh, flexes leg and rotates leg medially.

Gastrocnemius –

Origin –

Lateral head – lateral aspect of lateral condyle of femur
Medial head – superior to medial condyle

Insertion –

Posterior surface of calcaneus with calcaneal tendon (tendoachillis)

Innervation –

Tibial nerve

Action –

Plantarflex ankle when knee is extended
Raises heel during walking
Flexes leg at knee joint.

Soleus –

Origin –

Posterior aspect of head of fibula
Superior fourth of posterior surface of fibula
Soleal line and medial border of tibia

Insertion –

Posterior surface of calcaneus with calcaneal tendon (tendoachillis)

Innervation –

Tibial nerve

Action –

Plantar flexes ankle (independent of knee position)
Steadies leg on foot

January 11, 2019 0

Hemifacial atrophy/ Romberg disease

Introduction

Progressive hemifacial atrophy (PHA) has no definite pathogenesis – may be a lymphocytic neurovasculitis or a variant of localized scleroderma.

Also called Romberg’s disease.

Most commonly confused with – localized scleroderma (especially in the forehead) as the “en coup de sabre” (ECDS) or saber mark.

Historical perspective –

Dr. Caleb Hillier Parry – first description of the disease.

Dr. Moritz Heinrich Romberg – further described the clinical manifestations of hemifacial atrophy.

Albert Eulenburg, a German neurologist – coined the term “progressive hemifacial atrophy” or PHA

Blair, Sarnat, Greeley and Neumann in the 1950s all described the use of local flaps to augment the soft-tissue deficiency.

Campbell, and later Converse, described the use of onlay iliac bone graft to augment areas of atrophy.

Wallace et al. described the use of an omental free flap for soft-tissue augmentation.

Jurkiewicz described the use of free vascularized tissue for patients with PHA.

Siebert and Longaker used- free parascapular tissue for the treatment of this disorder.

Patient selection and treatment –

Factors to be considered –

Age of the patient
Nature and complexity of the deformity (i.e., which tissue types are affected)
Presence of associated disorders and conditions
Patient’s understanding of the problem and the options for treatment.

Timing of the surgery – best performed after the disease has “burned itself out” (delay up to 2 years following what looks like the end of progression).

Etiopathogenesis –

Exact etiology of PHA is not well understood.

But, has a strong autoimmune and neurogenic component – and a combination of the two been described as a “lymphocytic Neurovasculitis.

Possible etiologies –

Autoimmune process
Neurogenic process
Infection hypothesis
Trauma

Autoimmune process –

PHA is likely a variant of the autoimmune disease localized scleroderma, specifically the subtype of linear scleroderma that affects the face, termed ECDS “en coup de sabre” or sabre mark.

Thought to be different spectra of the same disease.

Similar characteristics – age of onset, female preponderance, neurological involvement, lymphocytic infiltrate on biopsy, and a clinical course of evolution.

Histologic findings –

Findings similar in PHA & ECDS –

A perivascular infiltrate of mononuclear cells, mostly lymphocytes and monocytes in the dermis – surrounding the dermal neurovascular bundles, termed “lymphocytic neurovasculitis”

Degenerative alterations of the vascular endothelia on electron microscopy

Findings different from ECDS –

	PHA	ECDS
Dermal collagen fibrils	Closely packed	Homogenized and fragmented
Elastic fibers	Preserved	Destruction of elastic fibers
Dermal appendages (hair follicles and sebaceous glands)	Hypoplastic	Atrophy

Neurogenic process –

Clinical manifestations supporting a neurogenic origin –

Distribution of facial atrophy typically follows a dermatome of the trigeminal nerve. (Unilateral in 95%, rarely crossing the midline)
Dermal lymphocytic infiltrate centered around neurovascular bundles in the dermis
Clinically – CNS involvement are found in approximately 8–20% of patients.
Radiologically – atrophy and calcinosis, multiple or diffuse brain lesions.
CSF analysis – findings consistent with an inflammatory process – presence of oligoclonal bands and elevated IgG levels.

Infection hypothesis –

The most notorious suspect for both PHA and ECDS was Borrelia burgdorferi (not substantiated).

Other agents – Epstein–Barr virus.

These can be mere incidental findings than causative etiology.

Trauma –

Role of trauma inducing PHA is quite controversial.

Epidemiology –

Incidence – not well defined.

Estimated incidence of 5 per 1 000 000 people.

Prevalence of 8 per 100 000 people.

No racial predilection of PHA

Slight female predominance – F: M = 2-3 :1

Median age of onset -is 10 years old (range of 5–15 years)

Most cases of are sporadic, few familial cases have been reported.

Clinical manifestations –

(Cutaneous, subcutaneous, muscle, bone and cartilage)

Initial clinical manifestations include both cutaneous findings and subcutaneous atrophy.

Subcutaneous atrophy typically evolves first on the cheek or temple and later extends to the brow, angle of mouth, and/or neck.

Later in course – atrophy or growth arrest of the underlying bone and cartilage – facial deformity.

Facial muscles – atrophic, but normal function.

The disease typically progresses slowly over several years (2–10 years) and then tends to enter a stable phase.

Cutaneous and subcutaneous involvement –

Hyperpigmentation and hypopigmentation
Dermal atrophy
Subcutaneous atrophy and
Skin thickening/fibrosis
Alopecia of the scalp, eyebrow, and eyelashes

Pigmentary changes –

Hyperpigmentation – “bluish” discoloration – most likely due to increased vascularity during the active or inflammatory phase.

Later on lesion might become hypopigmented.

Discolorations – dermatomal distribution along the trigeminal nerve.

When skin lesion becomes fibrotic (thickened skin) or atrophic and forms a well-demarcated linear depression (groove) in the frontoparietal or hemifacial distribution – considered to be ECDS morphea or linear scleroderma of the head.

Musculoskeletal involvement –

Facial muscle – atrophy and thinning – mostly affecting masseteric muscles, tongue, and palatal muscles.

Function of muscles are usually preserved.

Degree of skeletal hypoplasia is dependent upon the age of onset. Onset younger than 10 yrs – highest risk.

Maxilla and mandible are most often involved – both sagittal and vertical undergrowth.

Bony involvement is also unilateral – profound tilting of the occlusal plane.

When PHA involves the V1 distribution – enophthalmos is common.

Enophthalmos is due to atrophy of the periorbital subcutaneous tissues rather than skeletal hypoplasia.

CNS involvement –

Occur in approximately 8–21% of patients.

Manifestations – Seizures, hemiparesis, migraine headaches, neuropsychiatric disturbances, ischemic stroke, and intellectual deterioration

The most common CNS manifestation is – localization-related seizures.

Brain lesions of PHA appear to be more epileptogenic (than MS and other autoimmune disorder of CNS).

Brain imaging is – often abnormal, 90% cases.

Lesions observed are – T2 hyperintense lesions, intraparenchymal calcifications and brain atrophy.

The brain atrophy “respects” the midline – does not cross the midline.

Not a direct correlation between brain lesion and degree of severity of skin and subcutaneous involvement.

Many patients may be neurologically asymptomatic in spite of visible brain lesions.

Brain biopsies – brain parenchymal inflammation with a perivascular lymphocytic cuffing. (Sclerosis, fibrosis, gliosis of brain parenchyma, meninges, and vasculature have also been reported.)

CSF findings – oligoclonal bands and elevated IgG levels.

Ocular involvement –

The MC findings – uveitis, optic neuritis, and globe retraction.

Other findings – Ocular muscle paralysis, ptosis, Horner syndrome, heterochromia iridis, and dilated fixed pupil.

Slit lamp examination is recommended.

Oral involvement –

Tongue and upper lip of the affected side of the face are often markedly atrophic.

Maxilla and mandible hypoplastic – resulting in malocclusion (unilateral posterior crossbite) and altered dentition.

An abnormally skewed high-arched palate.

Laboratory findings and prognostic indicators –

↑ WBC – 10%

↑ ESR – 20%

Autoantibodies +ve – 40-50% –

Anti-single-stranded DNA (ss-DNA) – a/w disease severity and progressive disease features.

Ant- histone – – a/w disease severity and progressive disease features.
Anti-double-stranded DNA,
Anti-centromere,
Anti-Scl-70 antibodies

Clinical prognostic indicator – age of onset <10yrs – a/w profound skeletal dysplasia.

Differential diagnosis –

Congenital hemifacial atrophy
ECDS subtype of localized scleroderma
Lipodystrophy

Congenital hemifacial atrophy – present since birth. Not progressive.

ECDS is difficult to distinguish and sometime argued to be spectrum of same disease.

Lipodystrophy can occur due to –

Congenital diseases – progeria, Dunnigan syndrome, and Kobberling syndrome.

Endocrine disorders – hyperthyroidism and diabetes

Autoimmune diseases – systemic sclerosis and dermatomyositis

Drug-induced atrophy – protease inhibitors of ART.

Hemifacial microsomia.

Treatment/surgical technique –

Immunosuppression –

Few patients can be considered candidate for immunosuppression –

Patients having any cutaneous features of localized scleroderma
The appearance of a demarcated line, as in ECDS

Drugs – corticosteroids + disease modifying agents such as Methotrexate.

Duration of treatment – usually 3-5 years.

Reconstruction planned when disease is stable “off” the immunosuppression – typically after 1 year.

Nonsurgical intervention –

Alloplastic filling agents –

Advantage – absence of a donor site and their abundant supply.

Disadvantage – Susceptibility to local tissue responses, including capsule formation, seroma development, infection, extrusion, and cost.

Examples – silicone gel, hydroxyapatite beads, and hyaluronic acid.

Structural fat grafting –

Easily harvested, No donor site morbidity, No functional loss.

Atrophy of some portion of fat can occur.

Surgical intervention –

Currently offer the largest amount of tissue with excellent safety.

Can be used in conjunction with fillers to provide the best possible result.

Local pedicle flap –

Provides small amount of tissue.

Most obvious choice of flap – superficial temporal pedicle. It can be used in combination with fat grafting or dermal fat to increase the bulk.

Free flap –

Gracilis & Radial forearm adipofascial flap – for small volume augmentation
Deep inferior epigastric perforator – more soft tissue bulk.
Omentum – lacks internal structure – can lead to soft tissue decent with time.
Superficial inferior epigastric flap
Transverse rectus abdominis muscle flap
Deltopectoral flap
Anterolateral thigh adipofascial flap
Scapular and parascapular flap

Scapular and parascapular adipofascial flap based on the circumflex scapular pedicle are the most useful flaps for restoring facial volume.

Advantages – relatively straightforward harvest, posterior-torso donor scar, and minimal functional deficit.

Disadvantage – positioning in either a prone or lateral decubitus to harvest,

Technique of soft-tissue augmentation –

Mark the defect on face of patient with patient standing.
Make a transparency of the defect using an X-ray film.
Use the transparency to mark the defect on the planned flap.
Procedure begins with creation of the subcutaneous pocket on the face – extent of the dissection must extend beyond the borders of the atrophy.
Suitable recipient vessels are identified for the anastomosis. Achieve hemostasis. Pack the area with counted sponges.
Harvest the flap.
Flap is inset.
Terminal flap ends should be contoured and fixed to the skin with overlying bolsters.
Drains are placed at donor and recipient site.
Hourly monitoring of flap done with audible Doppler for 24 hours, and then 2 hourly for next 24 hours.
Patient is kept NPO for first night, then gradually allowed orally.

Outcomes –

Outcomes from soft-tissue augmentation are usually good.

Secondary procedures –

Revision of flap is almost always required and should be part of the plan of management.

First revision is planned after 6 months following flap placement.

Contents written by – Dr. Kamlesh Kumar (MBBS, AIIMS, New Delhi, MS(Surgery), AIIMS, New Dehi, MCh (Burns, Plastic & Maxillofacial Surgery) VMMC & Safdarjung hospital, New Delhi), 2019.

January 4, 2019 1

WOUND HEALING: NORMAL AND ABNORMAL

Introduction

Wound healing may be best understood as an organism’s global response to injury.

Wound healing represents the response of an organism to a physical disruption of a tissue/organ to re-establish homeostasis of that tissue/organ and stabilize the entire organism’s physiology.

Essentially two processes (for re-establishment of homeostasis)-

Substitution of a different cellular matrix as a patch to immediately re-establish both a physical and physiologic continuity to the injured organ. This is the process of scar formation.
Recapitulation of the developmental processes that initially created the injured organ. By reactivating developmental pathways, the architecture of the original organ is re-created. This is the process of

Balance between- Scarring ↔Tissue regeneration

Different tissue shows different proportion of these two process. One more than the other.

Eg. Nerve tissue – Scarring >>>Tissue regeneration

Liver and bone- Scarring <<<Tissue regeneration

Healing is different in different species- eg. Limb amputation in newts results in limb regeneration, whereas in humans, only scarring can occur.

Undesirable or dysfunctional response to injury in a tissue or organ system can occur due to any of the two processes.

It is important to establish which process is responsible for the undesirable effect and which portion of the wound is showing that effect.

Acute wound- wound that is present for less than 3-4weeks

Chronic wound- wound that persists beyond 4-6 weeks. (These wounds also called as non-healing, delayed healing, recalcitrant).

Phases of wound healing-

Three distinct but overlapping phases-

Inflammatory phase (0-4 days)
Proliferative phase (4-21 days)
Remodeling phase (21days – years)

Inflammatory Phase-

Primary purpose- to remove devitalized tissue and prevent invasive infection.

Functional priorities`-

Attainment of hemostasis
Removal of devitalized tissues
Prevention of colonization and invasive infection by microbial pathogens

Attainment of hemostasis-

Coagulation cascade activated- ultimately leading to formation of fibrin mesh (fibrinogen –> fibrin –> fibrin mesh). This fibrin mesh is called the provisional matrix.

Formation of platelet plug- during formation of formation of platelet plug, platelets also degranulate releasing growth factors – PDGF, TGF-β.

Other two functions are done by neutrophils and macrophages.

Inflammatory cells are attracted by-

Activation of the complement cascade

TGF-β released by degranulating platelets

Bacterial degradation products such as lipopolysaccharide.

Neutrophils-

These are the first inflammatory cells to be recruited.

Prominent type for first 2 days.

Function-

Remove dead tissue by phagocytosis
Prevent infection by oxygen-dependent and oxygen-independent killing mechanisms.
Release a variety of proteases to degrade remaining ECM (to prepare the wound for healing)

Neutrophils play a role in decreasing infection but, their absence does not appear to prevent the overall progress of wound healing.

Instead, there prolonged presence has been proposed to be a primary factor in the conversion of acute wounds into non-healing chronic wounds.

Monocyte/macrophages-

Follows after neutrophils. Appear 48 to 72 hours post-injury.
MCP-1 attracts these monocyte/macrophage to the site of injury.
By day 3, they are the predominant cell type.
Macrophages phagocytize debris and bacteria.
Produces growth factors necessary for the production of the ECM by fibroblasts and the production of new blood vessels in the healing wound.
Unlike the neutrophil, the absence of monocyte/macrophages has severe consequences for healing wounds.

Lymphocyte-

Last cell to enter the wound. [Last- Lymphocytes]

Enters between days 5 and 7 post-wounding. Its role in wound healing is not well defined.

Proliferative Phase-

Occur from days 4 to 21 following injury.

Re-epithelialization probably begin almost immediately following injury.

Injury –> Regression of the desmosomal connections between keratinocytes and basement membrane –> formation of actin filaments in the cytoplasm of keratinocytes –> keratinocytes actively migrate into the wound –> Keratinocytes proceed between the desiccated eschar and the provisional fibrin matrix beneath (this movement is via interactions with ECM proteins (such as fibronectin, vitronectin, and type I collagen) via specific integrin mediators)

Provisional fibrin matrix is gradually replaced by granulation tissue.

Granulation tissue is largely composed of three cell types- [EFM-G]

Endothelial cells
Fibroblasts
Macrophages

Granulation tissue begins to appear by about day 4 post-injury.

Fibroblasts are the workhorses during this time –> they produce the ECM that fills the healing scar and provides a scaffold for keratinocyte migration.

Macrophages produces –> PDGF and TGF-β1 –> stimulates fibroblast –> they proliferate, migrate and produces ECM. PDGF and TGF-β1 –> Stimulates endothelial cells –> produces new blood vessels.

Provisional matrix is replaced by type 3 collagen during proliferative phase.

Type 3 collagen will then be replaced by type 1 collagen during remodeling phase.

Endothelial cells- produce new blood vessels.

Hypoxia –> induces hypoxia inducible factor-1 (HIF-1) –> ↑ Proangiogenic factors released by macrophage (VEGF, FGF-2, angiopoietin 1, and thrombospondin.) –> angioneogenesis.

Remodeling phase –

Longest phase of wound healing

Day 21 – 1 year (years)

Begins with the programmed regression of blood vessels and granulation tissue.

Two process that define remodeling phase are – Wound contraction & Collagen remodeling.

Wound contraction occurs by – myofibroblast.

Myofibroblasts are – fibroblasts with intracellular actin microfilaments capable of force generation and matrix contraction.

Myofibroblasts contract the wound through specific integrin-mediated cell-matrix interactions with the dermal environment.

Collagen remodeling – replacement of type III by type I

Collagen remodeling is a slow remodeling phase which is largely mediated by a class of enzymes known as – matrix metalloproteinases

At 3 weeks wound strength is – 20% [wound strength – 21% @ 21 DAY]

Finally, wound strength is around – 70%- 80% @ 1 year.

Abnormal response-

Inadequate regeneration –
1. CNS injury
2. Bone non-union
3. Corneal ulcer
Inadequate scar formation –
1. Diabetic foot ulcer
2. Pressure sore
3. Venous stasis ulcer
Excessive regeneration –
1. Hyperkeratosis
Excessive scar –
1. Keloid
2. Hypertrophic scar

Keloids-

Are less common – <6% of population

Have genetic component

Overgrowth of dense fibrous tissue beyond the borders of the original wound

Large thick collagen fibers composed of numerous fibrils closely packed together

Hypertrophic scars are also characterized by the formation of dense collagen fibers following injury but, in contrast to keloids, do not extend beyond the original wound margins.

Etiology and pathophysiology – unknown

Treatment Modalities –

Steroid injections,
Pressure therapy with silicone sheeting, and
External beam irradiation

Recurrence rates – 75%.

December 31, 2018 0

Anatomy

In axilla and arm –

In cubital fossa –

In the Carpal Tunnel

Anterior Interosseous Nerve (AIN)

Surface marking

Motor supply of Median Nerve

Palmar cutaneous branch of median nerve –

Function lost:

Median nerve injury Signs

Goal of tendon transfer in median nerve injury

Biomechanics of thumb opposition

History of Opponensplasty

Critical points for tendon transfer

Prevention and preoperative treatment of contracture:

Pulley formation –

Insertion for opponensplasty

Four standard opponensplasty

Superficialis Opponensplasty

Bunnell’s technique

EIP Opponensplasty

ADM opponensplasty (Huber)

Palmaris longus opponensplasty –

High median nerve palsy –

Extrinsic donor available

Usual transfer

Restoration of Opposition

Restoration of index flexion

Restoration of thumb flexion

Postoperative Splintage

Developmental milestones

Approximate anthropometric values by age

Key Gross Motor developmental milestone

Key Fine Motor developmental milestone

Key Social and Adaptive Milestones

Key Language milestones

Upper age limit for attainment of milestone

Timing of Dentition

Q .What is craniofacial distraction or distraction osteogenesis?

History

Principles

Sequence

Process of distraction starts with –

Three types of Distraction

Histological Analysis

Four Temporal Zones –

Biomolecular analysis

Biomechanics

Mechanical environment in distraction zone depends upon –

For formation of successful (stable) regenerate –

[Credits : Dr. Anoop S. (Mch, department of burn and plastic surgery, VMMC & Safdarjung Hospital New Delhi)]

Anatomy-

Blood supply-

Nerve supply-

Etiology of lip defect –

Reconstruction – defect wise

Vermillion-

Partial thickness defect-

Small full thickness defect-

Primary closure-

Large full thickness defect-

Large central upper lip defect-

Large central lower lip defect-

Large lateral and commissure defect-

Course of radial nerve?

The branches of radial nerve?

Sequence of innervation of muscle by radial nerve?

High or low radial nerve injury?

The sensory distribution of radial nerve?

The deficit that you will notice in radial nerve injury?

Surface marking of radial nerve ?

Planning for nerve injury – nerve exploration vs nerve repair vs tendon transfer?

When do you time the tendon transfer?

Historical perspective of development of tendon transfer in radial nerve palsy?

Aims to achieve by tendon transfer in radial nerve palsy?

The principles of tendon transfer?

Describe the incision and procedure of FCU set of transfer.

How will be the tension in tendons adjusted?

Post-op care following tendon transfer?

Potential problems after FCU repair?